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"explanation": "An ABG performed in a patient with simple hyperventilation would likely show low PaCO<sub>2</sub> levels (due to losses in expiration) with normal PaO<sub>2</sub> (no pathology present to cause hypoxia). This may cause a respiratory alkalosis if hyperventilation is maintained for long enough, not an acidosis. Additionally, there would be a change in the metabolic axis (i.e. bicarbonate) due to the acuity of the respiratory derangement",
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"explanation": "This patient is acidotic, however a low bicarbonate level would be expected if this were metabolic in origin. Additionally, respiratory compensation for a metabolic acidosis would involve hyperventilation in order to reduce PaCO<sub>2</sub> levels - in this ABG example both the bicarbonate and PaCO<sub>2</sub> are elevated",
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"label": "d",
"name": "Metabolic acidosis with partial respiratory compensation",
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"explanation": "In chronic type 2 respiratory failure there is hypoxia with hypercapnia (as is the case here) - however, as this is a chronic process you would expect the pH to be largely corrected by metabolic compensatory processes (pH normal/close to normal with elevated bicarbonate)",
"id": "33324",
"label": "b",
"name": "Chronic type 2 respiratory failure",
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"explanation": "In type 1 respiratory failure there is hypoxia without hypercapnia. In this example, the PaCO<sub>2</sub> is raised",
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"name": "Type 1 respiratory failure",
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"explanation": "In acute-on-chronic type 2 respiratory failure the usual compensatory metabolic processes have been overwhelmed by the additional acute respiratory insult. The resultant pattern on ABG is a marked increase in PaCO<sub>2</sub> with significant respiratory acidosis, alongside a highly elevated HCO3 that is not adequate to normalise/nearly normalise the pH. Therefore, this patient is likely to need bilevel positive airway pressure (BiPaP) non-invasive ventilation to aid clearance of the CO<sub>2</sub> and improve the acidosis as part of their treatment plan",
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"explanation": "### Mean pressures in pulmonary circulation \n\n- Pulmonary artery 12-15mmHg\n- Left atrium 5mmHg\n- Pressure gradient 7-10mmHg\n\n### Ventilation perfusion ratio\n\nV/Q ratio - the ratio of alveolar ventilation (V) to alveolar blood perfusion (Q).\n\n- To attain efficient gaseous exchange, ventilation and perfusion must be matching.\n- The normal V/Q ratio is 0.8, which means that alveolar ventilation has to be at least 80% of pulmonary blood flow.\n\t- 4L/min of air enters the alvoeli\n\t- 5L/min of blood flows through the lungs\n\nV/Q ratio is different across different lung zones:\n\n- Zone 1 (upper zones, lung apices) has the lowest ventilation and perfusion;\n- Zone 3 (lower zone, lung bases) has the highest ventilation and perfusion due to gravity.\n- However, the regional differences in ventilation are less marked than perfusion, resulting in a higher V/Q ratio in zone 1 (3.3 apically) and lower in zone 3 (0.63 basally).\n\nThe significance of the V/Q ratio lies in its influence on the partial pressure of oxygen (PO2) and the partial pressure of carbon dioxide (PCO2).\n\n- At a high V/Q ratio, the gaseous exchange is more efficient, so PO2 is higher and PCO2 is lower, and vice versa.\n- Normal PO2 in arterial blood is 100mmHg, while normal PCO2 in arterial blood is 40mmHg when the V/Q ratio is at its optimum value, which is 0.8.\n\n### Right-to-left shunt \n\nWhen there is a right-to-left shunt or airway obstruction, where there is no ventilation to a well-perfused alveolus, V/Q = 0; hence, gaseous exchange does not occur. PO2 and PCO2 in the arterial blood remain the same as that in the venous blood, which are 40mmHg and 46mmHg, respectively.\n\n### Dead space \n\nWhen there are alveoli which are well-ventilated but not perfused, this is termed a physiological dead space. V/Q = ∞; hence, gaseous exchange does not occur. An example of this is a pulmonary embolism. PO2 and PCO2 in the alveoli remain the same as that in the inspired air, which are 150mmHg and 0mmHg, respectively.",
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"question": "A 73-year-old woman with a history of chronic obstructive pulmonary disease (COPD) comes in via ambulance to the emergency department with worsening shortness of breath.\n\n\nAn arterial blood gas (ABG) is performed as part of her assessment:\n\n\n||||\n|--------------|:-------:|------------------|\n|pH|7.27|7.35 - 7.45|\n|PaO₂|7.1 kPa|11 - 15|\n|PaCO₂|9.47 kPa|4.6 - 6.4|\n|Bicarbonate|43 mmol/L|22 - 30|\n|Lactate|1.1 mmol/L|0.6 - 1.4|\n\n - Inspired oxygen 28%\n\n\nWhat is the most likely explanation for this blood gas result?",
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"explanation": "Once an ectopic pregnancy has been ruled out, this patient's history is strongly suggestive of appendicitis. An abdominal CT scan can be a valuable investigation, particularly in patients with a longer history of pain or a palpable mass in the right iliac fossa (where there may be concern of an appendicular abscess or underlying malignancy), as well as in cases where a previous ultrasound has been indeterminate. However, it is important to remember that appendicitis can also be a clinical diagnosis and many patients go straight to theatre without any confirmatory imaging",
"id": "33330",
"label": "c",
"name": "Computed tomography (CT) abdomen",
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"explanation": "An erect CXR can play a role in assessment of patients presenting with acute abdominal pain – if the x-ray demonstrates pneumoperitoneum (air under the diaphragm) this is in keeping with a perforated viscus. However, this finding is not that sensitive - many cases of perforation occur in the absence of any identifiable pneumoperitoneum. There are other more valuable investigations at the stage of the patient's assessment",
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"name": "Erect chest x-ray (CXR)",
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"explanation": "This would play an important role in determining the severity of any infection, as well as the patient's response to any antibiotic treatment. However, this is a relatively non-specific test and there are other more urgent considerations to be addressed, particularly the patient's pregnancy status",
"id": "33331",
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"name": "Blood tests for inflammatory markers",
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"explanation": "In women of child-bearing age a urine pregnancy test should be prioritised to rule out the possibility of an ectopic pregnancy. This is a priority in early stages of patient assessment as the rupture of an ectopic is a surgical emergency, with high levels of mortality if not rapidly identified and treated. Additionally, it would be important to know about a viable pregnancy too, as this may alter the plan for further investigation and treatment of the pain",
"id": "33328",
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"name": "Urinary beta-HCG",
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"explanation": "Once an ectopic pregnancy has been ruled out, this patient's history is strongly suggestive of appendicitis. An abdominal ultrasound is an important diagnostic investigation in appendicitis, particularly if there are concerns regarding radiation dose for the patient, i.e. in pregnancy or childhood/for young adults. However, it is important to remember that appendicitis can also be a clinical diagnosis and many patients go straight to theatre without any confirmatory imaging",
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"explanation": "# Summary\n\nThe acute abdomen, a common presentation in clinical practice, refers to the sudden onset of severe abdominal pain. It is often a medical and/or surgical emergency, requiring prompt evaluation and intervention. Causes of an acute abdomen can be divided into surgical and medical causes, and while investigations and management of these are specific to the underlying cause, there are broad principles which should always be followed. This section explores the diverse aetiologies and clinical manifestations of acute abdominal conditions, emphasising the importance of timely diagnosis and management. \n\n# Epidemiology\n\nWhile prevalence varies geographically, acute abdomen accounts for a substantial proportion of emergency department admissions worldwide. A broad spectrum of age groups is affected, with appendicitis being more common in younger individuals, while conditions like diverticulitis and cholecystitis are prevalent in older populations. Additionally, comorbidities and lifestyle factors, including smoking and diet, may contribute to the incidence of acute abdominal conditions. \n\n# Differential Diagnosis\n\n## Surgical Acute Abdomen\n\nHere's a summary table with surgical differential diagnoses for each of the specified types of abdominal pain. It's important to note this is a guide and not all of these pathologies can only present with one type of pain, and there can be overlap with atypical presentations.\n\n\n| Type of Abdominal Pain | Surgical Differential Diagnoses |\n|-----------------------------|-----------------------------------------------------------------------|\n| **Central Abdominal Pain** | - Mesenteric ischemia <br /> - Acute pancreatitis (complicated) <br /> - Aortic dissection <br /> - Appendicitis <br /> - Intestinal obstruction <br /> - Perforated viscus <br /> - Abdominal wall hernia (strangulated) <br /> - Ruptured AAA |\n| **Epigastric Pain** | - Acute pancreatitis (complicated) <br /> - Perforated peptic ulcer <br /> - Cholecystitis (with gallbladder perforation) <br /> - Gastro-oesophageal perforation <br /> - Aortic dissection <br /> - Abdominal aortic aneurysm (AAA) <br /> - Gastric or duodenal ulcer (complicated) |\n| **Left Upper Quadrant Pain** | - Gastrointestinal perforation <br /> - Left-sided diverticulitis <br /> - Left renal pathology (e.g. abscess) <br /> - Perforated gastric or duodenal ulcer <br /> - Abdominal aortic aneurysm (AAA) <br /> - Spleen-related conditions (e.g. splenic infarction, rupture, abscess) <br /> - Gastric or duodenal ulcers (complicated) |\n| **Left Iliac Fossa Pain** | - Diverticulitis (complicated) <br /> - Gynecological emergencies (e.g. ovarian torsion, ovarian cyst rupture, ectopic pregnancy) <br /> - Left ureteral stone (with obstruction) <br /> - Ulcerative colitis <br /> - Perforated sigmoid diverticulitis <br /> - Ischaemic colitis (left-sided) <br /> - Left renal pathology (e.g. abscess) <br /> - Ileocecal tuberculosis (rare) <br /> - Sigmoid volvulus <br /> - Left-sided appendicitis (rare) |\n| **Right Upper Quadrant Pain** | - Acute cholecystitis <br /> - Biliary colic <br /> - Ascending cholangitis <br /> - Perforated peptic ulcer (anterior) <br /> - Liver pathology (e.g. hepatic abscess) <br /> - Right renal pathology (e.g. abscess) <br /> - Right-sided diaphragmatic hernia (e.g. Morgagni hernia) <br /> - Subphrenic abscess <br /> - Appendicitis (retrocecal) |\n| **Right Iliac Fossa Pain** | - Appendicitis <br /> - Caecal diverticulitis (rarely) <br /> - Right-sided gynecological emergencies (e.g. ovarian torsion, ovarian cyst rupture, ectopic pregnancy) <br /> - Right ureteral stone (with obstruction) <br /> - Ileocecal tuberculosis (rarely) <br /> - Right renal pathology (e.g. infarction, abscess) <br /> - Gastrointestinal perforation (e.g. perforated appendicitis) <br /> - Crohn's disease (terminal ileitis) |\n| **Suprapubic Pain** | - Acute appendicitis (atypical presentation) <br /> - Diverticulitis (with involvement of sigmoid) <br /> - Bladder pathology (e.g. bladder rupture) <br /> - Right ureteral stone (with lower migration) <br /> - Urethral pathology (e.g. urethral diverticulum) <br /> - Colonic pathology (e.g. ischaemic colitis) <br /> - Testicular torsion <br /> - Inguinal hernia (rare) <br /> - Pubic osteomyelitis (rare) |\n\n## Medical Acute Abdomen\n\nUnless otherwise specified, these causes can often present with very generalised abdominal pain which is often poorly localised.\n\n- Myocardial infarction (especially inferior MI which can present with epigastric pain)\n- Pericarditis\n- Pulmonary embolism\n- Gastroenteritis\n- Pneumonia (left/right lower lobes)\n- Mesenteric adenitis\n- Vasculitis (such as Henoch-Schonlein purpura)\n- Diabetic ketoacidosis\n- Addison's disease\n- Hypercalcaemia\n- Acute intermittent porphyria\n- Abdominal migraine\n- Irritable bowel syndrome\n- UTI and urinary retention (often suprapubic pain)\n- Sickle cell crisis\n\n# Investigations\n\n### Bedside\n- Blood glucose and ketones \n- Urine (urine dip, cultures and **pregnancy test in all females of childbearing age**\n- Stool (culture, faecal calprotectin), FIT testing in primary care (less urgent in acute setting)\n- ECG (looking for ischaemic changes)\n\n### Blood tests\n- VBG (raised lactate may indicate ischaemia, metabolic disturbances can be indicative of several medical causes such as DKA, addison's disease and hypercalcaemia)\n- FBC (anaemia may indicate haemorrhage, underlying malignancy; raised infection markers), CRP, U+E, LFTs, coagulation profile and group and save (especially if surgical intervention is likely), amylase/lipase, beta-HCG, troponin/d-dimer **(if indicated)**, blood cultures\n- Less urgent blood tests include tumour markers (CEA, CA 19-9)\n\n### Imaging\n- AXR +/- erect CXR (to assess for pneumoperitoneum and perforation)\n- USS of abdomen/renal tract/pelvis/testes\n- CT abdomen pelvis/urinary tract, CT angiogram (if ischaemia/AAA rupture suspected)\n- MRI may be indicated if e.g. looking for abscesses\n- MRCP (gallstones)\n- Endoscopy - OGD/colonoscopy/flexible sigmoidoscopy which may also be therapeutic\n\n# Management\n\nThough specific management strategies will depend on the underyling cause (see separate sections on each differential diagnosis), here are broad principles which will be applicable to the majority of the above differentials:\n\n- Conservative management - IV fluids +/- NG tube insertion ('drip and suck'), analgesia, anti-emetics, anti-spasmodics (such as hyoscine butylbromide), nutritional support (e.g. pabrinex)\n- Medical management - oral/IV antibiotics if suspected infectious cause, PPI (e.g. omeprazole)\n- Surgical management - may include but not limited to: endoscopy, ERCP, laparoscopic intervention.\n\n\n# NICE Guidelines\n\nNICE CKS Summaries:\n\n- [Acute pancreatitis](https://cks.nice.org.uk/topics/pancreatitis-acute/)\n- [Diverticular disease](https://cks.nice.org.uk/topics/diverticular-disease/)\n- [Appendicitis](https://cks.nice.org.uk/topics/appendicitis/)\n- [Ectopic pregnancy](https://cks.nice.org.uk/topics/ectopic-pregnancy/)\n- [Cholecystitis](https://cks.nice.org.uk/topics/cholecystitis-acute/)\n- [Gallstones](https://cks.nice.org.uk/topics/gallstones/)\n- [Crohn's disease](https://cks.nice.org.uk/topics/crohns-disease/)\n- [Ulcerative colitis](https://cks.nice.org.uk/topics/ulcerative-colitis/)\n\n",
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"question": "A 23-year-old female presents to the emergency department with severe abdominal pain. This started 24 hours ago and was generalised in location but has now become markedly worse overnight, alongside migration of the pain to be more focussed in her right iliac fossa. She also reports some associated nausea, but no vomiting.\n\nWhich of the following is the next best step in the management of this patient?",
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"explanation": "Ascites can develop in patients with decompensated chronic liver disease and is primarily due to portal hypertension. It presents with abdominal distension, with evidence of shifting dullness, reflecting excess fluid within the abdominal cavity. In acute liver failure these mechanisms have not taken place, so ascites is significantly less common",
"id": "33335",
"label": "c",
"name": "Ascites",
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"explanation": "Gynaecomastia develops in chronic liver disease because of impaired testosterone breakdown within the liver, leading to a rise in oestrogen levels (more testosterone is converted to oestrogen) which can stimulate breast tissue development",
"id": "33334",
"label": "b",
"name": "Gynaecomastia",
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"explanation": "Splenomegaly can develop in chronic liver disease because of blood pooling in the spleen, secondary to portal hypertension",
"id": "33337",
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"name": "Splenomegaly",
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"explanation": "Tender, smooth hepatomegaly suggests an acute liver pathology, with potential causes including acute viral hepatitis, hepatic vein thrombosis (Budd Chiari syndrome) and right heart failure with portal congestion. In chronic liver disease there is usually a degree of liver cirrhosis over time, which causes a reduction in organ size because of fibrosis. The caveat to this is in cases of malignancy where they may be hepatomegaly due to presence of a mass, but this is usually irregular in nature and not classically tender",
"id": "33333",
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"explanation": "Spider naevi (sometimes also called spider angiomas) are a particular form of telangiectasia representing another manifestation of the imbalance of testosterone and oestrogen occurring in chronic liver disease. On examination, spider naevi can be identified as spider-like vessels, which fill from a central arteriole (i.e. when you apply pressure, they blanch (fade), and refill from the centre)",
"id": "33336",
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"explanation": "# Summary\n\nLiver failure can manifest acutely or chronically, with various causes including infections, drugs, toxins, and chronic liver diseases. Clinical features range from hepatic encephalopathy to abnormal bleeding and jaundice. In hepatic encephalopathy, cerebral oedema arises from the accumulation of ammonia, leading to neurological symptoms. Investigations involve blood tests, ultrasound, and ascitic fluid analysis. Management includes addressing the underlying cause, monitoring closely, and providing supportive care such as lactulose for encephalopathy and vitamin K for coagulopathy. Liver transplantation may be necessary in severe cases. Complications include infections, cerebral oedema, bleeding, and multi-organ failure.\n\n\n# Definition\n\nLiver failure refers to the loss of liver function and the development of complications including coagulopathy, jaundice or encephalopathy. It can occur acutely if onset of symptoms in less than 26 weeks with a previously healthy liver and subdivided into hyperacute (< 7 days), acute (8-21 days), or subacute (4-26 weeks) liver failure. Chronic liver failure occurs on a background of liver cirrhosis.\n\n# Epidemiology\n\nLiver failure is a significant global health concern, with varying incidence rates worldwide. In the United Kingdom, chronic liver diseases represent a substantial portion of liver failure cases, with alcohol-related liver disease and non-alcoholic fatty liver disease being prominent contributors. The incidence of acute liver failure is relatively low but can occur rapidly and unpredictably, leading to severe morbidity and mortality if not promptly managed.\n\n\n# Aetiology\n\nAcute liver failure can arise from various causes, including:\n\n- **Viral Hepatitis:** Hepatitis A, B, and E infections can lead to acute liver failure, particularly in cases of fulminant hepatitis.\n \n- **Drug-Induced Liver Injury:** Overdose or adverse reactions to medications like paracetamol (acetaminophen), halothane, isoniazid, and certain antibiotics can precipitate acute liver failure.\n\n- **Toxic Exposures:** Exposure to hepatotoxic substances such as Amanita phalloides mushrooms or industrial chemicals like carbon tetrachloride can cause acute liver damage.\n\n- **Vascular Disorders:** Conditions like Budd-Chiari syndrome, characterised by hepatic vein obstruction, can result in rapid liver failure.\n\nChronic liver failure typically develops over an extended period due to ongoing liver damage. Common causes include:\n\n- **Alcohol Misuse:** Chronic alcohol consumption is a leading cause of liver cirrhosis and subsequent liver failure.\n\n- **Chronic Viral Hepatitis:** Persistent infection with hepatitis B or C viruses can progress to cirrhosis and liver failure if left untreated.\n\n- **Non-Alcoholic Fatty Liver Disease (NAFLD):** Accumulation of fat in the liver, often associated with obesity and metabolic syndrome, can lead to inflammation, fibrosis, and ultimately liver failure.\n\n- **Autoimmune Liver Diseases:** Conditions such as autoimmune hepatitis, primary biliary cholangitis (formerly primary biliary cirrhosis), and primary sclerosing cholangitis can cause chronic inflammation and scarring of the liver.\n\n- **Hereditary Conditions:** Genetic disorders like haemochromatosis, Wilson's disease, and alpha-1 antitrypsin deficiency can result in progressive liver damage and failure over time.\n\n# Signs and Symptoms \n\n- Hepatic encephalopathy\n- Abnormal bleeding\n- Jaundice\n\nIf the cerebral oedema is severe, raised intracranial pressure may develop. This is more common in fulminant hepatic failure and has a high mortality rate.\n\nIt is important to separate the signs of liver failure from the signs of chronic liver disease. The presence of both indicates a de-compensation of chronic liver disease.\n\n### Pathophysiology of Hepatic Encephalopathy\n\n- In liver failure, nitrogenous waste (ammonia) accumulates in the circulation.\n- This small molecule is able to cross the blood-brain barrier, and once in the cerebral circulation it is detoxified by astrocytes which form glutamine through the amidation of glutamate.\n- The excess glutamine disrupts the osmotic balance and the astrocytes begin to swell, giving rise to cerebral oedema.\n\n### Four stages of hepatic encephalopathy\n\n1. Altered mood and behaviour, disturbance of sleep pattern and dyspraxia\n2. Drowsiness, confusion, slurring of speech and personality change\n3. Incoherency, restlessness, asterixis\n4. Coma\n\n# Investigations \n\n- Blood tests assessing synthetic function of the liver:\n\n- INR to look for coagulopathy and establish a diagnosis of liver failure\n- Liver Function Tests including albumin to check liver enzymes, bilirubin levels and to further assess synthetic function of the liver\n- Full blood count to look for leucocytosis (possible infective cause), thrombocytopaenia (in chronic liver disease) and anaemia (normocytic could indicate haemolytic anaemia as in Wilson's or a GI bleed from oesophageal varices, macrocytic could indicate B12 and folate deficiency as in alcohol excess)\n- Urea and electrolytes to establish baseline renal function and to look for hepato-renal syndrome or any electrolyte abnormalities (such as hypokalaemia which can worsen encephalopathy and should be corrected)\n- Tests to determine cause such as:\n - Paracetamol level (paracetamol overdose)\n - Hepatitis\n - Epstein-Barr virus\n - Cytomegalovirus serology (viral infection)\n - Iron studies (haemochromatosis)\n - α-1 anti-trypsin (α-1 antitrypsin deficiency)\n - Caeruloplasmin level (Wilson's disease)\n - Iron studies (hereditary haemochromatosis)\n - Auto-antibodies (autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis)\n\nImaging/Invasive:\n\n- If ascites is present, a peritoneal tap should be taken for microscopy and culture to look for spontaneous bacterial peritonitis.\n- Abdominal ultrasound\n- Doppler ultrasound would be of use in identifying Budd-Chiari syndrome\n- OGD may be required if concerns over varices/variceal bleeding\n\n# Management\n\n- Treat the underlying cause if possible\n- Monitor observations closely including blood glucose\n\n\n- For encephalopathy:\n - Firstly, the stage of encephalopathy should be graded (see table below)\n - Lactulose is given to help nitrogenous waste loss through the bowels (reducing encephalopathy). Constipation is an important precipitant of encephalopathy in patients with chronic liver disease.\n - Rifaximin is a 2nd line antibiotic which reduces nitrogen forming micro-organisms in gut \n - IV mannitol can be given to reduce cerebral oedema in encephalopathy\n\n\n| Grade | Symptoms |\n|---------|-------------------------------------------------------------|\n| Grade 1 | Altered mood and behaviour, disturbance of sleep pattern, dyspraxia |\n| Grade 2 | Drowsiness, confusion, slurring of speech, personality change |\n| Grade 3 | Incoherency, restlessness, asterixis |\n| Grade 4 | Coma |\n\n \n- For coagulopathy\n - Vitamin K may need to be given IV - helps production of coagulation factors\n - Fresh frozen plasma can be given if patient is bleeding\n\n \n- Spontaneous bacterial peritonitis\n - Broad spectrum antibiotics - IV Piperacillin-Tazobactam is usually first-line\n \n- Hepatorenal syndrome - triad of cirrhosis, ascites and renal failure\n- Portal hypertension leads to release of vasoactive mediators which leads to splanchnic vasodilation, which reduces perfusion to kidneys, sensed by macula densa cells in JGA and leads to the activation of RAS.\n- There are two types: 1. Rapidly progressive, often managed with terlipressin 2. Slowly progressive, usually managed with Midodrine\n - May require haemofiltration\n - If patient required fluid resuscitation, human albumin solution rather than crystalloid fluid.\n-\tA TIPSS procedure may be necessary but note immediately after this can worsen hepatic encephalopathy\n\n- Liver transplantation may be necessary as this is the only definitive management for chronic liver failure - indications are set out below.\n\n## King's College Hospital Criteria for Liver Transplant\n\nThe King's College Hospital criteria are designed to predict poor outcome in acute liver failure and are therefore an indication of patients that should be considered for urgent liver transplantation.\n\nKing's College Hospital Criteria for Liver Transplant (paracetamol induced):\n\nThe criteria for **paracetamol** induced liver failure are as follows:\n\n- Arterial pH <7.3 24h after ingestion **OR**\n - Pro-thrombin time >100s\n - **AND** creatinine >300µmol/L\n - **AND** grade III or IV encephalopathy.\n\nKing's College Hospital Criteria for Liver Transplant (non-paracetamol liver failure):\n\nThe criteria for non-paracetamol liver failure are as follows:\n\n- Prothrombin time >100s **OR**\n- **Any three of**:\n - Drug-induced liver failure\n - Age under 10 or over 40 years\n - 1 week from 1st jaundice to encephalopathy\n - Prothrombin time >50s\n - Bilirubin ≥300µmol/L.\n\n\n# Complications \n\n- The most common complication of acute liver failure is **infection**.\n\nBacterial infection occurs in up to 80% of patients, and fungal infection in around 30%. This is thought to result from decreased phagocyte action, reduced complement levels and multiple medical interventions which are often invasive. Patients often present atypically, with no fever or raised white cell count.\n\nOther complications include:\n\n- Cerebral oedema ± raised intracranial pressure\n- Bleeding (where there is a source, for example during the introduction of intracranial pressure monitors)\n- Hypoglycaemia (easily treated with glucose)\n- Multi-organ failure\n\n\n# NICE Guidelines\n\n[NICE CKS - Cirrhosis](https://cks.nice.org.uk/topics/cirrhosis/)\n\n\n\n",
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"question": "A 57-year-old male presents to the Emergency Department with confusion and abdominal pain. He is unable to give any information about his medical history, due to his confusion. Blood tests identify significantly deranged liver function tests.\n\nOn examination, what clinical sign may suggest that this is an acute rather than chronic form of liver disease?",
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"explanation": "Aortitis is a form of vasculitis and is a **rare** but serious complication that can arise **late** in the disease course of ankylosing spondylitis. It can cause severe fatigue and shortness of breath, but is more classically associated with symptoms of fever or chest pain",
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"explanation": "A recent course of non-steroidal anti-inflammatory (NSAID) medication, alongside a change in bowel habit to dark stool and symptoms of anaemia (fatigue and shortness of breath) is concerning for an upper GI bleed, likely from a peptic ulcer. The dark stool likely represents melaena. NSAIDs are gastric irritants and when prescribed at higher doses or in longer courses, a proton pump inhibitor (PPI) or other gastro-protective medication should be given in addition to prevent this",
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"explanation": "# Summary\n \nAn upper gastrointestinal bleed (UGIB) is a common emergency presentation, with the main symptoms being haematemesis, coffee-ground vomiting and melaena. Haemorrhage can be anywhere in the oesophagus, stomach or duodenum and common causes include peptic ulcer disease, variceal bleeding, Mallory-Weiss tears and angiodysplasia. Management involves resuscitation with IV fluids and blood products, and identification of the likely cause which may be treatable via an endoscopic approach. \n \n# Definition\n \nAn UGIB is defined as any haemorrhage of the gastrointestinal tract between the oesophagus and the duodenum at the ligament of Treitz (the anatomical landmark that differentiates upper from lower GI bleeds).\n \n# Epidemiology\n \n- Acute UGIB is a common medical emergency, accounting for 50,000-70,000 admissions to hospital in the UK per year\n- In hospital mortality is approximately 10%\n- Older patients and those with comorbidities are more likely to experience higher morbidity and mortality than young fit patients with more physiological reserve\n- Men are more affected than women\n- The most common cause identified is peptic ulcer disease\n \n# Aetiology\n\n**Bleeding from the oesophagus:**\n\n- **Oesophageal varices:** usually secondary to portal hypertension due to hepatic cirrhosis\n- **Oesophagitis:** inflammation may be due to gastro-oesophageal reflux, infections (especially in immunocompromised patients), or medications such as bisphosphonates\n- **Mallory-Weiss tear:** longitudinal mucosal lacerations that occur after severe vomiting or retching\n- **Oesophageal cancer:** friable blood vessels in the tumour may cause chronic or acute bleeds\n \n\n**Bleeding from the stomach:**\n\n- **Peptic ulceration:** usually secondary to Helicobacter pylori infection or chronic NSAID use\n- **Gastric varices:**: also associated with portal hypertension\n- **Gastritis:** may be due to H. pylori infection, NSAIDs, alcohol or stress-related mucosal inflammation\n- **Gastric cancer:** tumours may ulcerate or erode blood vessels\n- **Vascular malformations:** a Dieulafoy lesion is a dilated submucosal artery that erodes the gastrointestinal mucosa resulting in massive bleeding\n \n**Bleeding from the duodenum:**\n\n- **Peptic ulceration:** as per ulceration in the stomach\n- **Aortoenteric fistula:** a rare but life-threatening condition where an abnormal connection forms between the aorta and the gastrointestinal tract, usually following abdominal aortic aneurysm repair\n\n# Classification\n\nThere are two main scoring systems used to classify patients as high or lower risk:\n\n- The Glasgow-Blatchford score is used as an initial assessment to determine how urgently endoscopy is indicated\n - It takes into account haemoglobin, urea, systolic blood pressure, tachycardia, melaena, syncope, heart failure and liver disease\n - Patients scoring 0 are considered to be low-risk and may be discharged for an outpatient OGD \n- The Rockall score can be calculated both pre and post-endoscopy but NICE recommends using it post-endoscopy to help with risk stratification\n - The following table shows how this is calculated (with only the first three parameters used in the pre-endoscopy scoring)\n \n\n | | 0 points | 1 point | 2 points | 3 points |\n | ----------------------------------------- | ------------------------- | ------------------- | ---------------------------------------------------------- | ------------------------------------------ |\n | Age (years) | <60 | 60-79 | >80 | |\n | Systolic blood pressure/pulse rate (mmHg) | SBP>100, HR<100 | SBP>100, HR>100 | SBP<100 | |\n | Comorbidities | None | | Ischaemic heart disease or cardiac failure | Liver failure, renal failure or metastatic cancer |\n | Post endoscopy diagnosis | Mallory-Weiss tear | All other diagnoses | Upper GI malignancy | |\n | Signs at endoscopy | No blood or dark red spot | | Blood in upper GI tract, spurting vessel or adherent clot |\n \n\n# Signs & Symptoms\n\nThe most common symptoms are **haematemesis** (vomiting blood) which is seen in 50% of patients, and **melaena** (black, sticky and tarry stool) which is seen in 70%.\n\nOther symptoms include:\n\n- \"Coffee-ground\" vomiting (dark digested blood)\n- Lightheadedness\n- Syncope\n- Abdominal pain\n- Symptoms of anaemia in subacute or chronic bleeds\n - Fatigue\n - Shortness of breath\n - Decreased exercise tolerance\n - Palpitations\n \nSigns include:\n\n- Tachycardia\n- Hypotension\n- Prolonged capillary refill time\n- Altered mental state\n- Abdominal tenderness\n- Melaena or haematochezia (fresh red blood) on rectal examination\n- Stigmata of chronic liver disease in patients with cirrhosis, e.g.\n - Spider naevi\n - Gynaecomastia\n - Palmar erythema\n - Caput medusae\n\n# Investigations\n \n**Bedside tests:**\n\n- **Venous blood gas** to obtain urgent haemoglobin, lactate may be raised if shocked\n- **ECG** as cardiac ischaemia may complicate haemorrhage (type 2 myocardial infarction), screen for arrhythmias if tachycardic\n\n**Blood tests:**\n\n- **Full blood count** for haemoglobin (note that there may be a delay in this falling due to haemoconcentration so do not be falsely reassured if normal)\n- **U&Es** - classically urea is disproportionately raised due to digestion of blood\n- **LFTs** to screen for liver cirrhosis (increased risk of variceal bleeding)\n- **Coagulation screen** so that abnormalities might be corrected to reduce bleeding\n- **Group and save** in case blood transfusion is required\n- **Cross-match** so that matched blood can be given when needed\n\n\n**Imaging/special tests:**\n\n- **Oesophago-gastroduodenoscopy** (OGD) \n - Also referred to as an upper GI endoscopy\n - Usually the definitive diagnostic test to look for a cause of bleeding\n - Allows risk stratification with the Rockall score\n - Facilitates endoscopic treatment (see Management section)\n- **Chest X-ray** to look for evidence of aspiration or perforation (e.g. pneumomediastinum or free air under the diaphragm)\n\n\n# Management\n \n**Resuscitation:**\n\n- Take an A to E approach as in any medical emergency and activate the **major haemorrhage protocol** for any significant bleed\n- Consider if **airway support** required (e.g. in an unconscious patient) and position to reduce aspiration risk if ongoing vomiting\n- Ensure adequate **IV access** (2x wide bore cannulae in the antecubital fossae ideally) and take urgent bloods including a blood gas\n- **Resuscitation** with IV fluids and/or blood \n - Give a **fluid bolus** if unstable\n - In a massive bleed follow local transfusion protocols\n - **Transfuse red blood cells** if Hb < 70, targeting a Hb of 70-100\n - Consider transfusion at a higher Hb in patients who are unstable or have ischaemic heart disease\n - **Transfuse platelets** if these are below 50 \n- **Correct any coagulopathy** or **anticoagulant** medication (may require haematology input)\n- In suspected variceal bleeds, give **terlipressin** and **prophylactic antibiotics**\n- **Immediate endoscopy** is required in severe UGIB; all other patients should have an endoscopy within 24 hours of admission\n - Non-variceal bleeds can be treated mechanically (e.g. **clipping**), with **thermal coagulation** or with **fibrin or thrombin** (plus adrenaline)\n - Oesophageal variceal bleeds should be treated with **band ligation**\n - Gastric variceal bleeds should be treated with N-butyl-2-cyanoacrylate injections (**sclerotherapy**)\n- **Proton pump inhibitors** (PPIs) should **not** be given prior to endoscopy - if the OGD shows a non-variceal UGIB with stigmata of recent haemorrhage (e.g. a peptic ulcer) high-dose IV or PPIs should be started\n- **Review medications** with associated bleeding risks\n - Hold DOACs\n - Hold warfarin\n - Hold P2Y12 inhibitors (e.g. clopidogrel, ticagrelor) - discuss with cardiology if the patient has coronary artery stents \n - Aspirin can be continued\n \n \n# Complications\n\n- **Rebleeding** is a major complication which can occur after endoscopic therapy\n - Repeat endoscopy should be offered +/- endoscopic treatment\n - Patients may require additional treatment to stop bleeding which may be via an interventional radiology or a surgical approach \n - Options for varices that continue to bleed include Sengstaken-Blakemore tube insertion (a bridging therapy) or a transjugular intrahepatic portosystemic shunt (a definitive treatment to reduce portal pressure in appropriate patients)\n- **Aspiration** of haematemesis or coffee-ground vomit may cause aspiration pneumonia or pneumonitis - risk is increased in patients with reduced levels of consciousness\n- **Complications of endoscopy** e.g. perforation\n- **Death** occurs in 10% of patients admitted with an UGIB; mortality is especially high in those who rebleed and require salvage surgery\n\n# NICE Guidelines\n\n[NICE - Acute upper gastrointestinal bleeding in over 16s](https://www.nice.org.uk/guidance/cg141/)\n\n# References\n \n[British Society of Gastroenterology - Acute upper GI bleed care bundle](https://www.bsg.org.uk/clinical-resource/bsge-acute-upper-gi-bleed-care-bundle)\n\n[RCEM Learning - Upper Gastrointestinal Haemorrhage](https://www.rcemlearning.co.uk/reference/upper-gastrointestinal-haemorrhage/)\n\n[Patient UK - Upper Gastrointestinal Bleeding](https://patient.info/doctor/upper-gastrointestinal-bleeding-includes-rockall-score)",
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"question": "A 22-year-old male presents to the emergency department (ED) with severe fatigue and shortness of breath on exertion. On review of symptoms he also reports some associated nausea and a change in bowel habit to darker stools over the past five days.\n\nHe was recently diagnosed with ankylosing spondylitis and three weeks ago was started on 500mg twice daily of naproxen from his GP for this reason. He is otherwise well with no regular medications.\n\nWhat is the most likely diagnosis?",
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"explanation": "Pain from pericarditis is worse when laying flat, with most patients noting significant relief from positional adjustment to sitting forwards. However, it would not only occur at night, nor would it explain the halitosis",
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"explanation": "# Summary\n\nGastro-oesophageal reflux disease (GORD) is characterised by the reflux of gastric contents into the oesophagus due to a defective lower oesophageal sphincter. Key signs and symptoms include dyspepsia, sensation of acid regurgitation, and potentially more atypical symptoms such as epigastric pain and laryngitis. Alarm symptoms include weight loss and persistent vomiting. Key investigations include a trial of proton pump inhibitor therapy and oesophagogastroduodenoscopy (OGD) if certain symptoms are present. Management strategies include lifestyle interventions, proton pump inhibitor therapy, and in refractory cases, anti-reflux surgery.\n\n# Definition\n\nGastro-oesophageal reflux disease (GORD) is a clinical diagnosis based on the presence of typical symptoms (dyspepsia, \"\"heartburn\"\" or \"\"acid reflux\"\") resulting from the reflux of gastric contents into the oesophagus caused by a defective lower oesophageal sphincter.\n\n# Epidemiology\n\nIn the UK, about 10% of adults experience symptoms of GORD daily, with a higher prevalence observed in individuals over 50 years of age.\n\n# Aetiology\n\nGORD is caused by a defective lower oesophageal sphincter, which enables the reflux of gastric contents into the oesophagus.\n\nRisk factors contributing to the development of GORD include obesity, alcohol use, smoking, and intake of specific foods (e.g. coffee, citrus foods, spicy foods, fat).\n\n\n# Signs and symptoms\n\nTypical symptoms:\n\n- Dyspepsia (\"\"heartburn\"\")\n- Sensation of acid regurgitation \n\nAtypical symptoms:\n\n- Epigastric or chest pain\n- Nausea\n- Bloating\n- Belching\n- Globus\n- Laryngitis\n- Tooth erosion\n\nAlarm symptoms:\n\n- Weight loss\n- Anaemia\n- Dysphagia\n- Haematemesis\n- Melaena\n- Persistent vomiting\n\n# Differential Diagnosis\n\nConditions that may present similarly and should be considered in the differential diagnosis include:\n\n- Gastric ulcers: These may present with epigastric pain, nausea, vomiting, and weight loss.\n- Oesophageal cancer: This may present with dysphagia, weight loss, and potentially haematemesis.\n- Functional dyspepsia: This condition may present with similar gastrointestinal symptoms without a clear organic cause.\n- Hiatus hernia: Often coexists with GORD but can cause pain without significant reflux.\n\n\n# Investigations\n\n- Urea (13C) breath test, Stool Helicobacter Antigen Test (SAT), or laboratory-based serology **if** symptoms suggestive of H.pylori infection.\n- Oesophagogastroduodenoscopy (OGD) if alarm features or atypical, persistent or relapsing symptoms are present.\n- Oesophageal manometry\n\n**Referral criteria for urgent (within 2 weeks) OGD to investigate for oesophageal and gastric cancer:**\n\n- Aged 55 years and over with weight loss + dyspepsia/reflux\n\nReferral criteria for non-urgent OGD:\n\nAged 55 years and over plus\n\n- Treatment-resistant dyspepsia\n \nOR\n\n- Raised platelet count + dyspepsia/reflux\n- Nausea/vomiting + dyspepsia/reflux\n\n# Management\n\n- Lifestyle interventions - weight loss, dietary changes, elevation of the head of the bed at night, avoidance of late-night eating.\n- Proton pump inhibitor therapy. For patients <40 years old who present with typical symptoms and no red flags, commence treatment with a standard-dose PPI for 4 weeks in combination with lifestyle changes.\n\t- If the patient meets criteria for urgent OGD, they should only be commenced on PPI therapy after this has been done\n- Antacids for symptomatic relief.\n- Anti-reflux surgery for refractory cases.\n- Treatment for H.pylori infection if confirmed (PPI + antibiotics), with retesting using the urea breath test\n\t- It should not be performed within 2 weeks of treatment with a proton pump inhibitor or within 4 weeks of antibacterial treatment, as this can lead to false negatives.\n\n# Complications\n\nPotential complications of GORD include:\n\n- Oesophageal ulcer\n- Oesophageal stricture\n- Barrett's oesophagus\n- Adenocarcinoma of the oesophagus\n\n# NICE Guidelines \n\n- [NICE: Gastro-oesophageal reflux disease and dyspepsia in adults: investigation and management](https://www.nice.org.uk/guidance/cg184)\n\n# References\n\n- [BMJ Best Practice: Gastro-oesophageal reflux disease](https://bestpractice.bmj.com/topics/en-gb/82)\n- [European Association of Endoscopic Surgery: Recommendations for the management of gastroesophageal reflux disease](https://link.springer.com/article/10.1007/s00464-014-3431-z)",
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"question": "A 30-year-old man presents to his GP complaining of 2 weeks of burning chest pain which he experiences only when laying down in bed at night. His partner has also told him he has notable halitosis in recent months, which he finds embarrassing.\n\nWhat is the most likely diagnosis?",
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"explanation": "GORD would usually be described as causing more of a burning epigastric/chest pain, rather than a sharp pain. It would also usually be improved with dietary modification such as eating smaller meals or cutting out spicy foods",
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"explanation": "Pain from gastric ulcers is classically exacerbated by food, and maximal within 30 minutes to an hour of eating a meal. In addition, this pathology is not easily identified on ultrasound, and would usually require an oesophageal-gastroduodenoscopy (OGD)",
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"explanation": "In biliary colic the pain is more cramping/\"colic-y\" in nature and is exacerbated specifically by fatty foods. In addition, patients may have a history of gallstones, most of which can be visualised on ultrasound",
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"explanation": "Pain from pancreatitis may radiate to the back and is also frequently accompanied by vomiting. In addition, most patients have a history that can identify a potential trigger, such as known gallstones, alcohol excess or pregnancy etc. (although it can be idiopathic!)",
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"explanation": "Pain from duodenal ulcers is classically exacerbated by hunger and alleviated by food. This is thought to be due to acid levels in the duodenum, which is effectively \"diluted\" by the presence of food",
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"explanation": "# Summary\n\nPeptic ulcer disease, encompassing both duodenal and gastric ulcers, is a condition where the stomach lining's self-protection mechanisms fail, often due to the presence of external factors like H. Pylori. Key signs and symptoms include pain, nausea, vomiting and loss of appetite. The primary investigation tool is endoscopy, which allows for a direct visual inspection of the ulcers. Management strategies include both pharmaceutical interventions, such as PPI treatment, and lifestyle changes, like cessation of smoking and dietary adjustments.\n\n# Definition\n\nPeptic ulcer disease refers to painful sores or ulcers in the lining of the stomach or the first part of the small intestine, known as the duodenum. The frequency of duodenal ulcers is four times higher than that of gastric ulcers. It is an endoscopic diagnosis (NB: dyspepsia is a clinical diagnosis). Peptic ulcer disease can be uncomplicated, or complicated (perforation, bleeding).\n\n# Epidemiology\n\nPeptic ulcer disease is a common condition, with the prevalence of duodenal ulcers being four times that of gastric ulcers. It's noteworthy that approximately 90% of duodenal ulcers are caused by H. Pylori infection.\n\n# Aetiology\n\nThe primary cause of duodenal ulcers is the infection by H. Pylori. Other factors contributing to the development of these ulcers include:\n\n- NSAIDs\n- Chronic use of steroids\n- SSRIs\n- Increased secretion of gastric acid\n- Smoking\n- Blood group O\n- Accelerated gastric emptying \n\nFor gastric ulcers, the risk factors include:\n\n- NSAIDs\n- H. Pylori infection\n- Smoking\n- Delayed gastric emptying\n- Severe stress\n\n# Signs and Symptoms\n\nPatients with peptic ulcer disease may present with:\n\n- Abdominal pain\n- Nausea\n- Vomiting\n- Loss of appetite\n- Unexplained weight loss\n- Patients with complicated peptic ulcer disease may present with coffee ground vomiting (bleeding), and can be haemodynamically unstable due to perforation\n\nDuodenal ulcers typically present with epigastric pain typically relieved on eating (closure of pyloric sphincter, less acid irritating ulcerated surface). Symptoms of gastric ulcers on the other hand are often worsened by eating - stomach increases acid production in response to food and irritates ulcerated surface.\n\n# Differential Diagnosis\n\nThe symptoms of peptic ulcer disease can mimic those of other conditions, including:\n\n- Gastritis: inflammation of the stomach lining, presenting with nausea, vomiting, and abdominal discomfort.\n- Gastro-oesophageal reflux disease (GORD): chronic acid reflux, characterized by heartburn, regurgitation, and swallowing difficulties.\n- Stomach cancer: may cause similar symptoms, but often accompanied by significant weight loss, loss of appetite, and anemia.\n\n# Investigations\n\n- Patients >55 with weight loss and dyspepsia should be referred for an urgent OGD (within 2 weeks) to investigate for oesophageal and gastric cancer\n- Patients should be investigated for H.pylori infection with C-13 urea breath test (ensure the person has not taken a PPI in the past 2 weeks, or antibiotics in the past 4 weeks)\n- Investigation tools for peptic ulcer disease primarily include endoscopy, which allows a direct visual inspection of the ulcers. Biopsies may be taken to rule out malignancy.\n\n# Management\n\nManagement of H. Pylori-negative peptic ulcer disease involves a 4-8 week course of full-dose PPI treatment in conjunction with lifestyle advice, such as:\n\n- Smoking cessation\n- Reducing alcohol intake\n- Regular, small meals and avoiding eating 4 hours before bedtime\n- Avoidance of acidic, fatty or spicy foods, and coffee\n- Weight loss if overweight \n- Stress management\n- Avoidance of NSAIDs, steroids, bisphosphonates, potassium supplements, SSRIs, and crack cocaine\n- Over-the-counter antacids\n\n\n- If the patient is H.pylori positive with a proven gastric/duodenal ulcer which is:\n\t- Associated with NSAID use: 8 week PPI therapy followed by first-line eradication therapy - PPI (omeprazole/lansoperazole) + amoxicillin + clarithromycin/metronidazole for 7 days\n\t\t- If penicillin allergic, offer: PPI + clarithromycin + metronidazole for 7 days \n\t- Not associated with NSAID use: eradication therapy with PPI (omeprazole/lansoperazole) + amoxicillin + clarithromycin/metronidazole for 7 days\n\t- If the person is allergic to pencillin and has had previous exposure to clarithromycin, offer a 7-day quadruple therapy regimen of:\nPPI + metronidazole + tetracycline hydrochloride + bismuth subsalicylate\n\n- For patients with gastric ulcers, a repeat endoscopy 6-8 weeks following the start of PPI treatment is recommended to ensure ulcer healing and rule out malignancy, as well as H.pylori re-testing (C-13 urea breath test first-line, stool antigen test second line) if appropriate.\n- Complicated peptic ulcer disease requires urgent surgical intervention with OGD for underunning of ulcers and haemostasis\n\t- Perforated peptic ulcers present initially with localised epigastric pain which later becomes generalised and peritonitic. These patients require an AXR and erect CXR to look for pneumoperitoneum. \n\n# NICE Guidelines\n\n[Click here to see more information NICE CKS on peptic ulcer disease](https://cks.nice.org.uk/topics/dyspepsia-proven-peptic-ulcer/management/management-proven-peptic-ulcer/)",
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"question": "A 22-year-old female presents to her GP with a three month history of sharp upper abdominal pain occurring shortly after eating. She has lost 5 kilograms in the last month due to limiting her food intake to minimise her pain. She has also tried to cut out various foods from her diet, including gluten, lactose, spicy foods and fatty foods, but has not managed to identify any triggers.\n\nShe was previously referred for an abdominal ultrasound, which has come back with no abnormality detected.\n\nWhat is the most likely diagnosis?",
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"explanation": "Colonoscopy, including views of the ileum (which is the most common site of disease) is the definitive diagnostic test for Crohn's disease. Classic findings on colonoscopy include skip lesions and a cobblestone appearance. Other findings may include strictures and fistulae (due to transmural inflammation)",
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"explanation": "In IBS patients experience cramping abdominal pain, classically associated with bloating and relieved with defecation. Colonoscopy would show no abnormality",
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"name": "Irritable bowel syndrome (IBS)",
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"explanation": "In UC the disease is isolated only in the large bowel, therefore the ileum would not affected (unless this is representing back-wash ileitis which can happen in patients with pancolitis). Additionally, inflammation in UC occurs in a continuous process – there would be no areas of separating normal bowel (skip lesions)",
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"name": "Ulcerative colitis (UC)",
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"explanation": "Diverticulitis is a common disease of the older person. It would be rare to have developed in an 18-year-old, particularly to the extent of causing significant symptoms. Diverticular disease would also be easily identified on a colonoscopy. Of note – colonoscopy should not be performed where acute diverticulitis is suspected as this can increase fragility of the bowel and increase risk of perforation during the procedure (guidelines recommend waiting six weeks post-acute episode)",
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"explanation": "Infectious colitis can be the cause of acute gastrointestinal upset, often in those returning from travel abroad. There is no history of other infective symptoms in this stem, such as fever, nor of recent travel. In addition, this patient has been experiencing these symptoms on and off for several years – too long a history for infectious colitis, which is acute in presentation",
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"label": "e",
"name": "Infectious colitis",
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"explanation": "# Summary\n\nCrohn's disease (CD) is a chronic, relapsing inflammatory bowel disease (IBD) characterized by transmural granulomatous inflammation. Key signs and symptoms include gastrointestinal and systemic symptoms, such as crampy abdominal pain, diarrhoea, weight loss, and fever. The disease is diagnosed primarily through blood tests and endoscopy with imaging. Management strategies include monotherapy with glucocorticoids, azathioprine, mercaptopurine, and biological agents for severe cases. Surgical management is rarely curative and should be maximally conservative.\n\n# Definition\n\nCrohn's disease (CD) is a chronic relapsing inflammatory bowel disease (IBD). It is characterised by transmural granulomatous inflammation which can affect any part of the gastrointestinal tract ('from mouth to anus', most commonly the terminal ileum, leading to fistula formation or stricturing.\n\n# Aetiology\n\nThe exact cause is unknown, but it is thought to be an inappropriate reaction to gut flora in a susceptible person. Important risk factors include:\n\n- Family history - 10-25% of patients have a first-degree relative who also suffers from Crohn's disease\n- **Smoking** - x3 increased risk\n- Diets high in refined carbohydrates and fats have been implicated\n\n# Epidemiology\n\nIn Europe the incidence of Crohn's disease is 5.6 per 100, 000 at ages 15-64. The disease is more common in northern climates and developed countries. In the last 60 years the incidence of Crohn's disease has increased in Europe and North America, and is now approximately equal to that of ulcerative colitis.\n\nCrohn's disease has a bimodal age of onset: the most common age of onset is between 15 and 40 years old, but there is a smaller secondary peak between 60-80 years.\n\nCrohn's disease is more common in Caucasian people than in Asian and black people. Ashkenazi Jews have a 2-4 fold higher risk of Crohn's disease.\n\n\n# Signs and Symptoms\n\nSymptoms: \n\n- Gastrointestinal symptoms (crampy abdominal pain and non-bloody diarrhoea)\n- Up to 50% have perianal disease\n- Systemic symptoms (weight loss and fever)\n\nSigns: \n\n- General appearance: cachectic and pale (secondary to anaemia), clubbing.\n- Abdominal examination: aphthous ulcers in the mouth, right lower quadrant tenderness and a right iliac fossa mass.\n- PR examination to check for perianal skin tags, fistulae, or perianal abscess.\n\n[lightgallery] \n\n**Extra-gastrointestinal manifestations include:**\n\nDermatological manifestations:\n\n- Erythema nodosum (painful erythematous nodules/plaques on the shins)\n- Pyoderma gangrenosum (a well-defined ulcer with a purple overhanging edge)\n\n[lightgallery1] [lightgallery2]\n\nOcular manifestations:\n\n- Anterior uveitis (painful red eye with blurred vision and photophobia)\n- Episcleritis (painless red eye).\n\nMusculoskeletal manifestation:\n\n- Enteropathic arthropathy (symmetrical, non-deforming)\n- Axial spondyloarthropathy (sacro-iliitis), \n\nHepatobiliary manifestations:\n\n- Gallstones (these are more common in Crohn's disease than in ulcerative colitis) - reduced bile acid reabsorption and increased calcium loss predisposes to gallstones\n\nHaematological and renal manifestations:\n\n- AA amyloidosis (secondary to chronic inflammation) and renal stones (more common in Crohn's disease than in ulcerative colitis)\n\n# Investigations \n\n- Bedside:\n\t- Stool culture is necessary to exclude infection (MC&S and ovas/cysts/parasite).\n\t- **Faecal calprotectin** (an antigen produced by neutrophils) will be raised (this helps distinguish inflammatory bowel disease from irritable bowel syndrome).\n\n- Blood tests:\n - Raised white cell count\n - Raised ESR/CRP\n - Thrombocytosis\n - Anaemia (secondary to chronic inflammation)\n - Low albumin (secondary to malabsorption)\n - Haematinics and iron studies including (B12, folate) due to terminal ileum involvement\n\n\n- Imaging:\n\t- Endoscopy with imaging is required for diagnosis. Small bowel video capsule endoscopy can be used for proximal disease\n\t- MRI can be used for suspected small bowel disease.\n\t- Upper GI series may show the 'string sign of Kantour'. This is used to describe the string-like appearance of contrast-filled narrowed terminal ileum, and is suggestive of Crohn's disease.\n\t- Colonoscopy with biopsy will reveal:\n\t\t- Intermittent inflammation **('skip lesions')**\n\t\t- Cobblestone mucosa (due to ulceration and mural oedema)\n\t\t- Rose-thorn ulcers (due to transmural inflammation), ± fistulae or abscesses.\n\t\t- Non-caseating granulomas\n\n# Management\n\n- As a general management point, it is paramount to advise patients with Crohn's who are smokers to **stop smoking** as this is known to strongly impact disease activity\n\n## Inducing remission\n\n- The first step of treatment is inducing remission in patients having a flare\n- Patients should be offered monotherapy with glucocorticoids (oral prednisolone, or IV hydrocortisone if first presentation is severe flare necessitating admission).\n- There is an increasing role for biologics for acute management of severe flares\n\n## Maintaining remission\n\n- Azathioprine or mercaptopurine may be added on to induce remission if there are 2 or more exacerbations in a 12-month period or the glucocorticoid cannot be tapered.\n\n - It is important to assess for thiopurine methyltransferase (TPMT) activity before offering azathioprine or mercaptopurine. If there is underactivity, this greatly increases the risk of profound bone marrow suppression if the above medications are given\n\n- Methotrexate may be considered in patients who are intolerant/have a contraindication to azathioprine or mercaptopurine or who do not respond to azathioprine or mercaptopurine monotherapy.\n- Biological agents (such as infliximab or adalimumab) are recommended in patients with severe Crohn's disease who fail to respond to the above.\n\t- These patients should have a CXR before treatment initiation due to the risk of re-activation of latent TB\n\n\n## Surgical management\n\nSurgical management is rarely curative in Crohn's disease (unlike in ulcerative colitis) because disease can occur anywhere along the GI tract, however 50-80% of Crohn’s patients end up requiring surgery at some point.\n\nSurgical options will depend on the part of the GI tract that is affected, and is indicated in those who have failed medical therapy or in those with severe stricturing or fistulating disease:\n\r\n-\tControl fistulae \r\n-\tResection of strictures\r\n-\tRest/defunctioning of the bowel\r\n\n\n### Management of peri-anal fistulae\n\n- Drainage seton is the management of choice for high (trans-sphincteric) fistulae. A seton is a thread passed through the fistula tract, forming a ring between the internal and external openings. It is used in the management of high trans-sphincteric fistulae, to prevent division of the anal sphincter muscles and incontinence. Closure of the fistula occurs by the formation of granulation tissue.\n- Fistulotomy is the management of choice for low (submucosal) fistulae. Fistulotomy involves dissecting the superficial tissue and opening the fistula tract. This is not a treatment option for high fistulae due to the risk of incontinence.\n- 'Sphincter saving' methods include fibrin glue and fistula plug - these are still under investigation and have not yet been approved in mainstream management.\n\n### Management of peri-anal abscess\n\n- The patient should be started on intravenous antibiotics e.g. ceftriaxone + metronidazole.\n- Patients typically require examination under anaesthetic and incision and drainage. An incision is made in the affected region, the pus is broken up, the infected tissue material is excised, and anti-septic soaked packs are inserted. Healing occurs by secondary intention.\n\n# Complications\n\n- **Fistulas:**\n - Formation of abnormal connections between different parts of the digestive tract or between the digestive tract and other organs.\n - Commonly involves the small intestine and other structures like the bladder or skin.\n\n- **Strictures:**\n - Narrowing or tightening of the intestinal walls.\n - Can lead to bowel obstruction and difficulties with the passage of stool.\n\n- **Abscesses:**\n - Collection of pus within the abdomen, often near areas of inflammation.\n - Presents with localized pain, swelling, and may require drainage.\n\n- **Malabsorption:**\n - Impaired absorption of nutrients due to inflammation and damage to the intestinal lining.\n - Can lead to nutritional deficiencies and weight loss.\n\n- **Perforation:**\n - Formation of a hole or tear in the intestinal wall.\n - Can result in peritonitis, a serious and potentially life-threatening condition.\n\n- **Nutritional Deficiencies:**\n - Chronic inflammation can affect nutrient absorption.\n - Common deficiencies include vitamin B12, vitamin D, and iron.\n\n- **Increased Risk of Colon Cancer:**\n - Prolonged inflammation may elevate the risk of developing colorectal cancer, particularly in long-standing disease involving the colon.\n\n- **Osteoporosis:**\n - Reduced bone density due to chronic inflammation and corticosteroid use.\n - Increases the risk of fractures.\n\n- **Intestinal Obstruction andToxic Megacolon:**\n - Severe inflammation can lead to the dilation of the colon.\n - Presents as abdominal distension, fever, and can be a medical emergency.\n\n\n# Comparison with Ulcerative Colitis\n\nPlease see below a summary table comparing Crohn's disease and Ulcerative colitis:\n\n| Characteristic | Crohn's Disease | Ulcerative Colitis |\n|------------------------------------|---------------------------------------|-------------------------------------|\n| **Location** | Any part of the digestive tract, from the mouth to the anus (most commonly affects the terminal ileum and colon) | Limited to the colon and rectum |\n| **Inflammation Pattern** | Patchy, skip lesions | Continuous, involves the entire colon|\n| **Depth of Inflammation** | Full thickness (transmural) | Limited to the inner lining (mucosa and submucosa)|\n| **Symptoms** | Abdominal pain, non-bloody diarrhoea, weight loss | Bloody diarrhoea, abdominal cramps |\n| **Complications** | Fistulas, strictures, abscesses | Toxic megacolon, colon cancer risk |\n| **Extraintestinal Manifestations** | Joint pain, skin problems, eye inflammation | Joint pain, skin problems, eye inflammation |\n| **Endoscopy Findings** | Cobblestone appearance, deep ulcers | Continuous colonic inflammation, ulcers |\n| **Diagnostic Imaging** | Transmural inflammation visible on imaging (e.g, MRI) | Limited to the colonic mucosa and submucosa, visible on colonoscopy |\n| **Treatment Approach** | Individualised, may involve medications (e.g. steroids, immunosuppressants) and surgery | Medications (e.g. aminosalicylates, steroids, immunosuppressants), surgery (in severe cases) |\n| **Prognosis** | Variable, chronic condition with periods of remission and exacerbation | Variable, can be chronic with periods of remission, may require surgery in some cases |\n\n\n# NICE Guidelines\n\n[Click here to see information on NICE CKS on Crohn's disease](https://cks.nice.org.uk/topics/crohns-disease/)\n\n",
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"question": "An 18-year-old female presents to the GP with a three-year history of intermittent cramping abdominal pain and loose stools. She has decided to seek medical advice on this occasion as last week she noted some streaked fresh red blood, as well as some mucous, in her stool.\n\nShe undergoes a colonoscopy with results as follows: there are multiple, small, discrete areas of inflamed mucosa scattered throughout the large bowel, with interspersed regions of normal mucosal appearance. The most significant pathology was identified in the distal ileum, where there were multiple deep and discrete ulcers in a cobblestone appearance.\n\nWhat is the most likely diagnosis?",
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"explanation": "T1DM most commonly develops in younger patients and does not share the same risk factors of obesity and hypercholesterolaemia as T2DM. Instead, it is autoimmune in nature",
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"explanation": "Malignancy can certainly present with fatigue, as well as having the ability to suppress the immune system and make the patient more prone to infections. In addition, late in the course of prostate cancer - and more commonly, following prostate cancer treatments - erectile dysfunction can occur. However this diagnosis is not as common, nor as directly related to his metabolic risk factors, as T2DM",
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"explanation": "# Summary\n\nType 2 Diabetes Mellitus is a chronic metabolic disorder characterised by pancreatic beta-cell insufficiency and insulin resistance. The resulting hyperglycaemia leads to symptoms such as polyuria, polydipsia and if chronic can have microvascular and macrovascular complications. Key investigations include random and fasting blood glucose, 2-hour glucose tolerance, and HbA1C tests, and diagnosis is based on the results of these +/- symptoms. Management of type 2 diabetes primarily revolves around lifestyle modifications, hypoglycaemic agents, and insulin therapy when necessary, as well as reducing risks for serious complications such as cardiovascular and cerebrovascular disease. Other complications from chronic hyperglycaemia involve the gastrointestinal system, nervous system, peripheral arteries, foot infections, sexual dysfunction, and cardiac system. \n\n# Definition\n\nType 2 Diabetes Mellitus (T2DM) is a chronic metabolic condition characterized by inadequate insulin production from pancreatic beta cells, resulting in insulin resistance. This leads to an elevation in blood glucose levels, causing hyperglycaemia.\n\n# Epidemiology\n\nT2DM generally manifests in adults, and it is often associated with a strong familial predisposition. It accounts for approximately 90-95% of all diagnosed cases of diabetes.\n\n# Aetiology\n\nT2DM results from a combination of genetic and environmental factors. Known contributors include:\n\n- Poor dietary habits\n- Lack of physical activity\n- Obesity\n\n# Signs and symptoms\n\nIndividuals with T2DM may initially be asymptomatic, but over time, they may develop:\n\n- Polyuria\n- Polydipsia\n- Unexplained weight loss\n- Blurry vision\n- Fatigue\n\n# Differential diagnosis\n\nThe primary differentials for T2DM include Type 1 Diabetes Mellitus, Maturity Onset Diabetes of the Young (MODY), and Secondary Diabetes Mellitus. The main distinguishing features of these differentials are:\n\n- Type 1 Diabetes Mellitus: Early onset (typically in childhood or adolescence), often presents with ketoacidosis, and requires insulin therapy from diagnosis.\n- MODY (Maturity Onset Diabetes of the Young):\n\t- MODY 3 is the commonest cause, occurring due to a mutation in HNF1A. It is characterised by a very high blood sugar (10-20), and is very sensitive to sulphonylureas (e.g. gliclazide.) Insulin is the next line of treatment if it doesn't respond.\n\t- MODY 2 is the second commonest cause, occurring due to a glucokinase mutation. Blood sugars rarely rise above 7-8, over many years. Patients are generally well with few complications and the diabetes often responds to diet alone.\n\t- MODY 5 is associated with HNF1 beta mutation, and is associated with pancreatic atrophy, renal cycsts (causing palpable kidneys), epidydymal cysts, a bicornuate uterus, and abnormal LFTs\n- Secondary Diabetes Mellitus: Often presents with other signs of pancreatic disease (e.g., pancreatitis, cystic fibrosis), or due to certain medications (e.g., glucocorticoids, antipsychotics).\n\n# Investigations\n\nIf symptomatic, one of the following results is sufficient for diagnosis:\n\n- Random blood glucose ≥ 11.1mmol/l\n- Fasting plasma glucose ≥ 7mmol/l\n- 2-hour glucose tolerance ≥ 11.1mmol/l\n- HbA1C ≥ 48mmol/mol (6.5%)\n\nIf the patient is asymptomatic, two results are required from different days.\n\n# Management\n\nManagement of T2DM involves patient education, lifestyle modifications, pharmacological interventions, and close monitoring of glucose levels:\n\n- Lifestyle modifications: Advice on diet, regular physical activity, and smoking cessation\n- Pharmacological interventions: \n\t- Initial drug treatment is usually metformin, with consideration of other agents like Pioglitazone, DPP‑4 inhibitors, sulphonylureas, or SGLT-2 inhibitors for those who cannot take metformin.\n\t- If on monotherapy HbA1c >58mmol/mol consider dual therapy with metformin, pioglitazone, a DPP‑4 inhibitor or a sulphonylurea (such as gliclizide).\n\t- If dual therapy has not controlled drug glucose, triple therapy using the above medications can be considered. Otherwise, starting insulin may be necessary.\n- Close Monitoring: Measure HbA1c levels at 3-6 month intervals. If the patient is on insulin or is at risk of hypoglycaemia, self-monitoring of glucose at home is necessary.\n\n\n**Insulin Therapy**\n\nNICE guidance recommends basal insulin therapy with isophane (NPH) insulin as the first type to be used as it is most cost effective eg. Insulatard. Quick acting insulin analogues eg. Humalog, Novorapid, may be added in with meals if there is a big post meal glucose excursion.\n\nLong acting insulin analogues include Levemir, Lantus, Insulin Degludec and Abasaglar (a biosimilar insulin).\n\nMixed insulin combination which contain varying proportions of short and intermediate acting insulin such as Novomix 30 (30% short acting, 70% intermediate acting insulin) are more convenient because of fewer injections per day but may not be as successful.\n\n**Blood Pressure targets in Diabetes**\n\n- Blood pressure control needs to be strict in diabetes because these patients are at higher risk of macro- and microvascular complications.\n- NICE Hypertension Guidance [CG136] sets the same blood pressure targets as those who do not have diabetes, however in diabetics with HTN, ACE-inhibitors are first line as they are reno-protective\n\n# Complications\n\nComplications of diabetes are diverse, affecting multiple systems:\n\n### Macrovascular:\n\n* **Cardiac Complications** - diabetes significantly increases the risk of cardiovascular disease, contributing to major morbidity and mortality.\n* **Peripheral Arterial Disease (PAD)** - patients present with foot discolouration, gangrene, intermittent claudication, rest pain, night pain and absent peripheral pulses (confirmed on doppler).\n* **Cerebrovascular disease** - patients with diabetes are at significantly increased risk of TIAs and stroke and as such it is paramount to address the main risk factors (lipids, BP, smoking, obesity) for these as a broader part of management\n\n\n### Microvascular:\n\n* **Diabetic retinopathy** - characterised by vascular occlusion and leakage in the retinal capillaries, leading to potential sight loss if unmanaged, it is the leading cause of visual loss in adults. See separate section.\n* **Diabetic nephropathy** - a leading cause of chronic kidney disease, it is characterised by proteinuria. Prevention of this complication is achieved with ACE inhibitors/ARBs (by managing blood pressure) and SGLT-2 inhibitors.\n\t* Histological changes include Kimmelstiel-Wilson nodules which are the spherical, eosinophilic, sclerotic nodules characteristic of nodular diabetic glomerulosclerosis \n* **Diabetic neuropathy** - the primary causative factor is chronic hyperglycaemia, which leads to several distinct types neuropathy. See separate section.\n\t* **Autonomic Neuropathy** - may lead to postural hypotension and associated symptoms like dizziness, falls, and loss of consciousness.\n\t* **Gastrointestinal Complications: Gastroparesis** - a result of poor glycaemic control leading to nerve damage of the autonomic nervous system. Characterized by delayed gastric emptying, early satiety, abnormal stomach wall movements, and morning nausea.\n\t* **Foot Complications: Diabetic Foot Infections** - patients with vascular and neuropathic complications are at high risk for diabetic foot ulceration and subsequent infection.\n* **Sexual Dysfunction** - caused by a combination of factors including poor glycaemic control, neuropathy, microvascular complications, obesity, hypertension, depression, medication side effects, etc.\n\n# 'Sick day' rules\n\n1. **Temporary Medication Adjustments**: During acute illness, consider temporarily stopping certain medications until the person is eating and drinking normally for 24–48 hours. \n\t- **Angiotensin-Converting Enzyme Inhibitors (ACEIs), Diuretics, and NSAIDs**: Stop treatment if there is a risk of dehydration to reduce the likelihood of acute kidney injury (AKI).\n\n3. **Metformin**: Stop treatment if there is a risk of dehydration to lower the risk of lactic acidosis.\n\n4. **Sulfonylureas**: Be cautious, as they may increase the risk of hypoglycemia, especially if dietary intake is reduced.\n\n5. **SGLT-2 Inhibitors**: Check for ketones and stop treatment if acutely unwell and/or at risk of dehydration due to the risk of euglycemic diabetic ketoacidosis (DKA).\n\n6. **GLP-1 Receptor Agonists**: Stop treatment if there is a risk of dehydration to reduce the risk of AKI.\n\n7. **Insulin Therapy**: Do not stop insulin treatment; instead, consider adjusting the dose with guidance from the specialist diabetes team.\n\n8. **Blood Glucose Monitoring (if indicated)**: \n - Increase monitoring frequency to at least every 3–4 hours, including overnight.\n - Adjust insulin doses based on results.\n - Continue careful monitoring until blood glucose levels return to baseline.\n - Seek urgent medical advice if blood glucose remains uncontrolled.\n\n9. **Ketone Monitoring (Blood or Urinary)**: \n - Check ketone levels regularly (at least every 3–4 hours, including overnight).\n - Seek immediate medical advice if urine ketone level is greater than 2+ or blood ketone level is greater than 3 mmol/L.\n\n10. **Maintain Normal Meal Pattern**: Encourage maintaining regular meals and fluids, including carbohydrates, if appetite is reduced.\n\n11. **Fluid and Carbohydrate Replacement**:\n - If unable to eat or vomiting, replace meals with carbohydrate-containing drinks (e.g. fruit juices, sugary drinks).\n - Adjust fluid intake based on blood glucose levels (sugar-free fluids for high levels, sugary fluids for low levels).\n\n\n\n# NICE Guidelines\n\n[Click here for NICE CKS on T2DM](https://cks.nice.org.uk/topics/diabetes-type-2/)\n",
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"question": "A 52-year-old man presents to his GP complaining of feeling tired all the time. In recent months, he has been prescribed two courses of antibiotics for urinary tract infections, and has also been seen regarding erectile dysfunction. His past medical history includes hypercholesterolaemia and obesity.\n\nWhat is the most likely unifying diagnosis?",
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"explanation": "T1DM is characterised by an absolute lack of insulin, unlike Type 2 diabetes where there is insulin resistance. For this reason, the insulin that the body is lacking must be replaced directly with subcutaneous insulin injections",
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"explanation": "Glucagon injections are used in the acute management of severe episodes of hypoglycaemia. It acts to raise sugar levels by triggering conversion of glycogen to glucose in the liver. It is not used to manage hyperglycaemia",
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"explanation": "A pancreas transplant is not a first line treatment due to the significant risks of both transplants and major surgery in general. It is considered in some patients with T1DM who have severe renal disease (and may be carried out at the same time as a kidney transplant) or those with hypoglycaemic episodes that are unmanageable and pose significant risk to warrant the surgery",
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"explanation": "Gliclazide is a sulphonylurea, which acts to enhance secretion of pancreatic insulin. In T1DM where there is an inherent lack of insulin (due to destruction of the secretory beta cells within the pancreas) Gliclazide would be ineffective and is not used - its role is in type 2 diabetes treatment",
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"explanation": "Metformin acts to reduce hyperglycaemia by reducing hepatic gluconeogenesis and over time, can help increase insulin sensitivity. It is the first line anti-diabetic medication for adults with type 2 diabetes where lifestyle measures are unable to control sugar levels. In T1DM the fundamental problem is an absolute lack of insulin, so without replacing this directly there would be little or no effect on glycaemic control",
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"explanation": "\n\n# Summary\n\nType 1 diabetes mellitus (T1DM) is an autoimmune condition involving the destruction of insulin-producing pancreatic cells, resulting in insulin deficiency. It presents with signs such as polyuria, polydipsia, and weight loss, and mostly affects children and young adults. It's often associated with other autoimmune conditions such as thyroid disease and coeliac disease. Diagnostic tests involve assessing blood glucose, HbA1c, and urine ketones, as well as testing for the presence of auto-antibodies (e.g. anti-GAD, ICA, IAA). Management strategies involve tailored insulin therapy, close monitoring of blood glucose levels, and addressing both short-term and long-term complications.\n\n# Definition\n\nType 1 diabetes mellitus (T1DM) is an autoimmune condition characterized by the destruction of the insulin-producing beta cells within the pancreas, leading to insulin deficiency. \n\n# Epidemiology\n\nT1DM predominantly affects children and young adults but can occur at any age. The incidence varies worldwide, with higher rates observed in northern Europe and in individuals with a family history of T1DM or other autoimmune diseases.\n\n# Aetiology\n\nT1DM is thought to be caused by a combination of genetic predisposition and environmental triggers. Genes associated with the human leukocyte antigen (HLA) system contribute to susceptibility. Environmental triggers, such as viral infections, are proposed but not definitively identified.\n\n# Signs and Symptoms\n\nPatients with T1DM often present with classic symptoms of insulin deficiency:\n\n- Polyuria\n- Polydipsia\n- Weight loss - a distinguishing factor between T1DM and T2DM\n\nIn severe cases, patients may present with diabetic ketoacidosis (DKA), characterised by hyperglycemia, metabolic acidosis, and ketonemia.\n\n# Differential Diagnosis\n\nOther conditions presenting with similar symptoms include:\n\n- Diabetes insipidus: Presents with polyuria and polydipsia, but without hyperglycemia or glucosuria.\n- MODY (Maturity Onset Diabetes of the Young):\n\t- MODY 3 is the commonest cause, occurring due to a mutation in HNF1A. It is characterised by a very high blood sugar (10-20), and is very sensitive to sulphonylureas (e.g. gliclazide.) Insulin is the next line of treatment if it doesn't respond.\n\t- MODY 2 is the second commonest cause, occurring due to a glucokinase mutation. Blood sugars rarely rise above 7-8, over many years. Patients are generally well with few complications and the diabetes often responds to diet alone.\n\t- MODY 5 is associated with HNF1 beta mutation, and is associated with pancreatic atrophy, renal cycsts (causing palpable kidneys), epidydymal cysts, a bicornuate uterus, and abnormal LFTs\n- Hyperthyroidism: Can present with weight loss and increased appetite, but usually also includes symptoms such as tachycardia, tremor, and heat intolerance.\n\n# Investigations\n\nDiagnosis involves first confirming diabetes and then identifying the underlying cause as type 1. Diabetes can be diagnosed either with or without symptoms:\n\nIf symptomatic, one of the following results is sufficient for diagnosis:\n\n- Random blood glucose ≥ 11.1mmol/l or Fasting plasma glucose ≥ 7mmol/l\n- 2-hour glucose tolerance ≥ 11.1mmol/l\n- HbA1C ≥ 48mmol/mol (6.5%)\n\nIf the patient is asymptomatic, two results are required from different days.\n\nTo confirm T1DM, the following investigations can be done:\n\n- Autoantibody testing: Identification of specific antibodies (e.g. anti-GAD, ICA, IAA) contributes to confirming the autoimmune nature of T1DM.\n- C-peptide levels: Evaluation of C-peptide production helps assess endogenous insulin secretion.\n- Urine ketone testing: Presence of ketones may suggest concurrent DKA.\n\n# Management\n\n\n- **Insulin Therapy**: Individualised insulin regimens are essential. Short-acting insulin is administered after meals and snacks, while long-acting insulin is typically given at night-time. Regular adjustments are necessary to maintain blood glucose within target ranges (see below).\n\n- **Glycemic Control**: Tight glycemic control is crucial for preventing complications. Target ranges for blood glucose and HbA1c levels should be individualized but typically aim for:\n\n - Pre-meal blood glucose: 4-7 mmol/L (72-126 mg/dL)\n - Bedtime blood glucose: 6-10 mmol/L (108-180 mg/dL)\n - HbA1c: Less than 7% (53 mmol/mol) for most adults; individualised targets for children, elderly patients, and those at risk of hypoglycemia.\n\n- **Lifestyle Interventions**: Patients should receive guidance on nutrition, exercise, and alcohol consumption. Dietitians and diabetes educators play a crucial role in helping individuals make informed choices.\n\n- **Blood Glucose Monitoring**: Regular self-monitoring of blood glucose (SMBG) is essential. Patients should check their blood glucose levels multiple times a day, especially around meals and before bedtime.\n\n- **Continuous Glucose Monitoring (CGM)**: In some cases, CGM systems may be recommended to provide continuous real-time data on blood glucose levels and trends.\n\n- **Hypoglycemia Management**: Hypoglycemic episodes should be promptly treated with sugary drinks or snacks for conscious patients. For unconscious individuals, intramuscular glucagon or intravenous dextrose administration is necessary.\n\n- **Regular Follow-Up**: Patients should receive ongoing care and education from diabetic specialist nurses and healthcare providers. Monitoring HbA1c levels at least every three months is crucial to assess long-term glycemic control.\n\n- **Psychosocial Support**: Diabetes can have a significant emotional impact. Patients should have access to psychosocial support and resources to cope with the challenges of living with T1DM.\n\n- **Comprehensive Care**: T1DM management should address both short-term and long-term complications. Regular screening for microvascular complications (e.g. retinopathy, nephropathy, neuropathy) and macrovascular complications (e.g. cardiovascular disease) is essential.\n\n- **Blood Pressure Control**: Stricter blood pressure targets are recommended for individuals with T1DM, aiming for values of less than 135/85 mmHg, or less than 130/80 mmHg in the presence of end-organ damage. Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) are often preferred as first-line agents.\n\nThese management strategies, combined with a patient-centered and holistic approach, aim to optimise glycemic control, improve quality of life, and reduce the risk of complications in individuals living with T1DM.\n\n\n## The honeymoon period\n\nImmediately after diagnosis, insulin requirements may be very low if the pancreas is still able to produce a significant amount of insulin. This is known as the 'honeymoon period'. It is important that children are closely monitored during this time. This is because insulin requirements can suddenly increase as the remaining beta cells are destroyed. Additionally, as the blood glucose may be normal in this period on very low insulin doses, parents may incorrectly think that the condition has gone away.\n\n# 'Sick day' rules\n\n1. **Temporary Medication Adjustments**: During acute illness, consider temporarily stopping certain medications until the person is eating and drinking normally for 24–48 hours. \n\t- **Angiotensin-Converting Enzyme Inhibitors (ACEIs), Diuretics, and NSAIDs**: Stop treatment if there is a risk of dehydration to reduce the likelihood of acute kidney injury (AKI).\n\n\n7. **Insulin Therapy**: Do not stop insulin treatment; instead, consider adjusting the dose with guidance from the specialist diabetes team.\n\n8. **Blood Glucose Monitoring (if indicated)**: \n - Increase monitoring frequency to at least every 3–4 hours, including overnight.\n - Adjust insulin doses based on results.\n - Continue careful monitoring until blood glucose levels return to baseline.\n - Seek urgent medical advice if blood glucose remains uncontrolled.\n\n9. **Ketone Monitoring (Blood or Urinary)**: \n - Check ketone levels regularly (at least every 3–4 hours, including overnight).\n - Seek immediate medical advice if urine ketone level is greater than 2+ or blood ketone level is greater than 3 mmol/L.\n\n10. **Maintain Normal Meal Pattern**: Encourage maintaining regular meals and fluids, including carbohydrates, if appetite is reduced.\n\n11. **Fluid and Carbohydrate Replacement**:\n - If unable to eat or vomiting, replace meals with carbohydrate-containing drinks (e.g. fruit juices, sugary drinks).\n - Adjust fluid intake based on blood glucose levels (sugar-free fluids for high levels, sugary fluids for low levels).\n\n\n# Associations\n\n- Growth and pubertal development (delay in puberty and obesity)\n- Associated illnesses:\n - Thyroid disease (most associated; screening recommended)\n - Coeliac disease\n\n# NICE Guidelines\n\n[NICE CKS - T1DM](https://cks.nice.org.uk/topics/diabetes-type-1/)\n\n# References \n[NHS choices - T1DM](https://www.nhs.uk/conditions/type-1-diabetes/)\n\n[Diabetes UK - T1DM](https://www.diabetes.org.uk/diabetes-the-basics/what-is-type-1-diabetes)",
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"question": "A 19-year-old man presents to the GP with lethargy. After a period of investigation, a new diagnosis of type 1 diabetes mellitus (T1DM) is made.\n\nWhat is the most appropriate first line treatment for this patient?",
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"explanation": "This is an appropriate test for this patient as hypercortisolism can cause hyperglycaemia which may need treatment. However this test would not help to establish the **cause** of these symptoms",
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"explanation": "This patient has many symptoms pointing towards hypercortisolism. The first step in investigation here would be to confirm this clinical suspicion. An overnight 1mg dexamethasone suppression test is a suitable first line investigation in patients with suspected Cushing's syndrome. 1mg of dexamethasone is given at midnight and cortisol levels are checked at 8 am. An 8 am cortisol result of <50 nmol/L is normal (as the axis should be suppressed) and >50 nmol/L is abnormal. This requires further investigation (to confirm the result and classify into ACTH dependent vs ACTH independent)",
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"explanation": "An adrenal CT may be appropriate further into this patients work up, if it is confirmed that she has ACTH-independent hypercortisolism - a solitary secretory adrenal adenoma is the most common cause",
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"explanation": "# Summary\n\nCushing's syndrome is an endocrine disorder characterised by excess glucocorticoids, which can have ACTH-dependent or independent origins. Clinically, patients may present with symptoms such as proximal myopathy, obesity, hypertension, and various dermatological changes. Diagnosis is made through investigations such as a 24-hour urinary free cortisol test and low-dose dexamethasone suppression test, alongside imaging for localisation. Management includes medical therapy to reduce cortisol levels, surgery, radiotherapy, and the need for post-operative steroid replacement in successful cases.\n\n# Definition\n\nCushing's syndrome is an endocrine disorder characterised by excess glucocorticoids, often resulting in distinctive clinical symptoms and signs. It is important to distinguish Cushing's syndrome from **Cushing's disease,** which specifically refers to glucocorticoid excess caused by an adrenocorticotropic hormone (ACTH)-secreting pituitary tumour.\n\n# Epidemiology\n\nCushing's syndrome is a relatively rare condition, estimated to affect 2 to 3 per million people each year. It is more common in adults, particularly women, with a peak incidence between 25-40 years.\n\n# Aetiology\n\nThe causes of Cushing's syndrome can be divided into ACTH-dependent and ACTH-independent:\n\n- **ACTH-dependent disease:** This is caused by excessive production of ACTH, most often due to a pituitary tumour (Cushing's disease) or ectopic ACTH-producing tumours (e.g. lung carcinoids, thymic carcinoids, and others).\n- **ACTH-independent:** This arises from primary adrenal diseases, such as adrenal adenomas or adrenal carcinomas, which produce excess cortisol independently of ACTH stimulation. Exogenous steroids can also cause ACTH-independent Cushing's.\n\n# Signs and Symptoms\n\nClinical features of Cushing's syndrome may include:\n\n- Proximal myopathy\n- Striae and easy bruising\n- Osteoporosis and fractures\n- Glucose intolerance or diabetes mellitus\n- Obesity, particularly truncal or \"centripetal\" obesity\n- Hypertension\n- Hypokalaemia\n- Facial changes, such as moon face and acne\n- Hirsutism in women\n- Fat redistribution leading to interscapular and supraclavicular fat pads\n- Thin extremities due to muscle wasting\n- Thin, fragile skin\n- Erectile dysfunction in men\n- Psychological issues, such as depression or cognitive dysfunction\n- Osteopenia or osteoporosis\n\n[lightgallery]\n\n[lightgallery1]\n\n\n# Differential Diagnosis\n\nKey differentials include conditions that may cause similar clinical features, such as:\n\n- Metabolic syndrome\n- Polycystic ovary syndrome\n- Adrenal insufficiency\n- Alcohol excess\n- Depression. \n\nDistinguishing these conditions often relies on biochemical and imaging investigations.\n\n# Investigations\n\nTo confirm the diagnosis and identify the cause:\n\nBiochemical evidence of cortisol excess:\n\n- 24-hour urinary free cortisol test\n- Low-dose Dexamethasone suppression test:\n - Not suppressed by low dose - Cushing’s syndrome (e.g. exogenous steroid use)\n - Not suppressed by low dose but suppressed by high dose - Cushing’s disease (pituitary source)\n - Not suppressed by low dose or by high dose dexamethasone – ectopic ACTH (not under axis control, likely ACTH-producing tumour)\n\nLocalisation of the source:\n\n- Plasma ACTH levels to distinguish between ACTH-dependent and independent causes\n- High-dose dexamethasone suppression test for suspected Cushing's disease\n- Inferior petrosal sinus sampling for suspected pituitary cause\n- MRI of the pituitary and/or CT of chest and abdomen for tumour localisation\n\n\n# Management\n\nManagement of Cushing's syndrome varies according to the underlying cause and may involve a combination of medical, surgical, and radiotherapy options:\n\n- **Medical Management:** Initial therapy often involves medications to decrease cortisol levels. These include Metyrapone, an inhibitor of cortisol synthesis; Ketoconazole, an adrenolytic agent; Mifepristone, a glucocorticoid receptor antagonist; and Pasireotide, a somatostatin analog.\n\n- **Surgical Management:** Resection of the pituitary tumour is the treatment of choice for Cushing's disease, often after initial control of hypercortisolaemia with medical therapy to improve surgical outcomes.\n - NB: Old treatment for Cushing's disease used to be bilateral adrenalectomy, which has risk of developing into Nelson syndrome - enlarging of an adrenocorticotropic hormone-producing tumour in the pituitary gland.\n\n- **Radiotherapy:** May be considered for cases where hypercortisolaemia persists post-surgery, or in cases where surgery is not possible or declined.\n\nSuccessful treatment of Cushing's disease leads to cortisol deficiency and subsequently, steroid replacement post-operatively is essential. Patients need to carry a steroid card and ideally wear a medic alert bracelet in case of acute illness or emergency situations.\n\nPatients unfit for surgery or with unresectable lesions are managed with medical therapy alone.\n\n# References\n\n[BNF - Cushing's syndrome](https://bnf.nice.org.uk/treatment-summaries/cushings-syndrome/#:~:text=Cushing's%20syndrome%20results%20from%20chronic,%2C%20ectopic%20ACTH%2Dsecreting%20tumours.)",
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"question": "A 30-year-old woman attends to see her GP with concerns about her fertility. For the past two years, she has noted increasingly irregular menses. This is in addition to 15 kilograms of weight gain with notable purple striae across her abdomen.\n\nOn examination, the patient is noted to have hyperpigmentation in her palmar folds, multiple unexplained bruises across her arms and facial plethora.\n\nWhat is the most appropriate first line test to investigate the cause of these symptoms?",
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"explanation": "Bone mineral deficiency may occur as a late complication of renal failure that is unlikely to occur in someone with CKD stage 3 (GFR 30-59). In addition, her biochemical profile is normal",
"id": "33376",
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"name": "Bone mineral deficiency secondary to chronic kidney disease",
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"explanation": "Paget's disease of the bone is a form of metabolic bone disease where there is excessive osteoclastic bone destruction alongside high levels of bone deposition (often with poor integrity). An isolated raised ALP is typically seen on blood testing",
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"explanation": "In osteoporosis, all of the above parameters are classically normal - the weakened bone is caused by low bone mineral **density** and atypical bone architecture, rather than any biochemical disturbance. This patient has risk factors for osteoporosis in both her demographic (older, white female, likely post-menopausal) and her history of poorly controlled asthma, which suggests she may have had a significant amount of steroid exposure",
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"explanation": "In normal metabolism, PTH is released in response to low calcium levels in the blood. In primary hyperparathyroidism excess production of PTH causes recruitment of excess calcium from bone, which can damage the bones integrity. There would be a raised PTH, hypercalcaemia, and resultant hypophosphataemia (via homeostatic control) on blood testing",
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"explanation": "Multiple myeloma can damage to bone integrity, however this is through the mechanism of calcium recruitment from bone (via osteoclast activation and bone destruction) and as a result you classically see hypercalcaemia on blood testing",
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"explanation": "# Summary \r\n\r\nOsteoporosis is a chronic condition characterised by low bone density and increased propensity to sustain fragility fractures. It is diagnosed with a dual-energy X-ray absorptiometry (DEXA) scan if a patient's T-score is less than -2.5. It is very common in older patients, especially post-menopausal women, with other risk factors including long-term corticosteroid use, low body weight and immobility. Other key investigations include checking calcium and vitamin D levels as these may require supplementation if low. Treatment is with bone-sparing treatment, with bisphosphonates being the first-line option in the majority of patients. Lifestyle changes such as smoking cessation, taking regular exercise and maintaining a healthy diet are important. Falls risk assessment is also key to reducing the risk of fragility fractures, especially in older patients. \r\n\r\n# Definition\r\n\r\nOsteoporosis refers to a state of low bone density with structural deterioration of bones. This causes bones to weaken, increasing the risk of fragility fractures (defined as a fracture sustained due to a fall from standing or without any trauma). \r\n\r\nPatients are defined as having osteoporosis if their bone mineral density (BMD) is at least 2.5 standard deviations below the mean peak mass of young healthy adults. This is measured with a dual-energy X-ray absorptiometry (DEXA) scan which gives BMD for the lumbar vertebrae and the femur. \r\n\r\n# Epidemiology\r\n\r\n- In the UK, around 2 million people are estimated to have osteoporosis\r\n- Post-menopausal women are particularly at risk due to accelerated bone loss secondary to decreased oestrogen production\r\n- Prevalence also increases significantly with age\r\n- Almost 50% of 80 year old women have osteoporosis\r\n- White ethnicity is also a risk factor\r\n- There are approximately 300,000 fragility fractures per year in the UK, with osteoporosis often being undiagnosed at the time of presentation\r\n\r\n# Aetiology\r\n\r\nRisk of fragility fractures increases as bone density declined, however there are many other factors that increase fracture risk:\r\n\r\n| Risk factors reducing bone density | Risk factors that do not reduce bone density |\r\n|----------|----------|\r\n| Low body weight | Older age |\r\n| Menopause | Inflammatory arthritis (e.g. rheumatoid arthritis) |\r\n| Immobility | Prolonged use of oral corticosteroids |\r\n| Chronic disease e.g. chronic kidney disease, chronic obstructive pulmonary disease, chronic liver disease | Smoking |\r\n| Malabsorption e.g. coeliac disease, inflammatory bowel disease, pancreatic insufficiency | Alcohol excess |\r\n| Endocrine disease e.g. hyperparathyroidism, hyperthyroidism | History of fragility fracture |\r\n| Certain medications (proton pump inhibitors, selective serotonin reuptake inhibitors, carbamazepine) - mixed evidence | Parental hip fracture |\r\n\r\n# Signs and Symptoms\r\n\r\nOsteoporosis itself is asymptomatic and so is usually diagnosed either with screening of people at high risk (e.g. those on long-term corticosteroids) or when someone presents with a fragility fracture.\r\n\r\nThe most common fragility fractures seen are:\r\n\r\n- Vertebral body\r\n- Neck of femur (hip)\r\n- Distal radius\r\n- Proximal humerus\r\n- Pelvis\r\n\r\nSome osteoporotic fractures (e.g. vertebral fractures) may also be asymptomatic acutely. Loss of height and kyphosis may occur due to multiple vertebral fractures, with severe kyphosis leading to reduced mobility and function.\r\n\r\nOther common symptoms of fragility fractures include acute severe pain, difficulty weight-bearing (e.g. for a hip fracture) and mobilising. \r\n\r\nSigns include deformities, such as a shortened and externally rotated leg due to a hip fracture or a \"dinner fork\" deformity in a Colles' wrist fracture.\r\n\r\nThe area around the fracture may be bruised, swollen and tender to touch. \r\n\r\n# Differential Diagnosis\r\n\r\n- **Bone metastases** may lead to pathological fractures, either in patients with known malignancies or as a first presentation of cancer (especially lung, prostate, breast, kidney and thyroid)\r\n- **Osteomalacia** usually occurs secondary to severe vitamin D deficiency and increases fracture risk due to bone weakening; other symptoms include bone pain, muscle pain and proximal weakness with a waddling gait\r\n- **Multiple myeloma** also is associated with pathological fractures, as well as hypercalcaemia, renal impairment, anaemia and bone pain\r\n- **Paget's disease** increases the risk of fracture due to abnormal bone remodelling, leading to features of bone pain and bowing of the long bones\r\n- **Osteogenesis imperfecta** is a genetic condition that commonly presents in childhood with fragility fractures, bowing of the long bones, short stature and blue sclera\r\n- **Avascular necrosis** may mimic a spontaneous fracture with severe pain after no or minimal trauma, commonly affecting the femoral head\r\n\r\n# Investigations\r\n\r\n- The diagnostic investigation for osteoporosis is a **dual-energy X-ray absorptiometry scan (DEXA)**\r\n- This measures **bone mineral density (BMD)**\r\n- A T-score of -2.5 or less is considered diagnostic of osteoporosis\r\n- If the T-score is between -1 and -2.5 this is referred to as osteopenia\r\n- Z-score is also reported (this compares bone density to a age, sex and ethnicity matched population rather than healthy young adults) - below -2 is low for their age\r\n- The following patients should be offered a DEXA scan as the initial step in assessment\r\n- Aged over 50 presenting with a fragility fracture\r\n- Aged under 40 with a major risk factor for fragility fracture (e.g. long-term steroids) \r\n- Those about to start treatment that will rapidly decrease bone density (e.g. hormone deprivation in breast cancer) - consider\r\n- All other patients with risk factors should have their fracture risk assessed as the initial step\r\n- **QFracture** and **FRAX** are the two online assessment tools used\r\n- These both predict a patient's 10-year risk of hip and major osteoporotic fractures\r\n- QFracture is interpreted based on whether the risk score is greater or less than 10%\r\n- FRAX plots fracture risk versus age on a graph that stratifies people into low/intermediate/high risk\r\n- With QFracture, those at approximately 10% risk or more at 10 years should have a DEXA scan \r\n- With FRAX, patients at intermediate or high risk of fracture should have a DEXA\r\n- In women over the age of 75 with a history of fragility fractures, a clinical diagnosis of osteoporosis may be appropriate (if a DEXA is unfeasible)\r\n\r\nOther investigations required in all patients include:\r\n\r\n- **Vitamin D** to check for deficiency; this is needed prior to starting bisphosphonate treatment\r\n- **Bone profile** to check serum calcium as this may also require supplementation\r\n- **X-rays** or other imaging modalities (e.g. CT or MRI) may be required to diagnose and assess fragility fractures\r\n\r\nIf an underlying cause is suspected, the following investigations may be appropriate:\r\n\r\n- **Full blood count** which may show anaemia in malabsorption or malignancy, and leukocytosis in malignancy or inflammatory disease\r\n- **Liver function tests** for chronic liver disease\r\n- **U&Es** for chronic kidney disease\r\n- **ESR** or **CRP** which may be raised in inflammatory disease or malignancy\r\n- **Thyroid function tests** if hyperthyroidism is suspected\r\n- **Testosterone** and **sex hormone-binding globulin** if hypogonadism is suspected in men\r\n- **Anti-TTG antibodies** for coeliac disease if there is evidence of malabsorption\r\n\r\n# Management\r\n\r\n**Conservative management:**\r\n\r\n- Identification and treatment of any underlying condition contributing to osteoporosis\r\n- Optimisation of risk factors e.g. smoking cessation, alcohol reduction\r\n- Advise patients to take regular weight-bearing exercise to improve muscle strength, including walking, strength training and balance and flexibility training\r\n- Advise patients to eat a balanced diet and assess their calcium intake\r\n- Assess falls risk and consider measures to reduce this, including referral to multidisciplinary falls teams \r\n- Referral to specialist services for patients with very high fracture risk (e.g. T score less than -3.5, multiple vertebral fractures)\r\n\r\n**Medical management:**\r\n\r\n- Prescribing vitamin D supplementation for patients not exposed to adequate sunlight\r\n- Prescribing calcium supplements to patients with an inadequate dietary calcium intake\r\n- For patients at high risk of fragility fracture, prescribe bone-sparing treatment\r\n- Treatment should be started promptly after a fragility fracture to reduce the risk of another fracture\r\n- Oral bisphosphonates are the first-line treatment in the majority of patients \r\n- Options include alendronate and risedronate, which can be given either daily or weekly\r\n\t- These must be taken on an empty stomach, at least 30 minutes before food or other medications\r\n\t- Tablets need to be swallowed whole with a glass of water whilst the patient is upright; they should stay upright for at least 30 minutes after this\r\n\t- Common side effects include nausea, dyspepsia, gastritis, abdominal pain and musculoskeletal pains\r\n\t- Rarer side effects include oesophagitis or ulceration, stricturing or erosions, osteonecrosis of the jaw or external auditory canal and atypical stress fractures\r\n\t- To minimise risk of osteonecrosis of the jaw, patients with poor dentition or malignancy should have a dental check-up (and any work required performed) before starting bisphosphonates\r\n\t- They should also continue to have routine dental checks and maintain good oral hygiene during treatment \r\n\t- Contraindications include severe chronic kidney disease, hypocalcaemia or vitamin D deficiency, and oesophageal abnormalities such as stricture or achalasia \r\n\t- Patients with recent peptic ulceration, upper gastrointestinal bleeding or surgery, dysphagia, gastritis or duodenitis should be prescribed bisphosphonates with caution\r\n- If oral bisphosphonates are not tolerated or unsuitable, options for bone-sparing treatment include:\r\n\t- Parenteral bisphosphonates (e.g. zoledronate)\r\n\t- Denosumab\r\n\t- Raloxifene hydrochloride\r\n\t- Strontium ranelate\r\n\t- Hormone replacement therapy should be considered for younger women experiencing menopausal symptoms as this will also reduce their fragility fracture risk\r\n\t- Teriparatide and romosozumab are other bone-sparing treatments that may be recommended first-line in women with severe osteoporosis - these are then followed by bisphosphonate treatment\r\n\r\n**Surgical management:**\r\n\r\n- Fragility fractures may require surgical fixation or joint replacement (e.g. hip arthroplasty for a fractured neck of femur)\r\n\r\n# Complications\r\n\r\n- Hip fractures are high-consequence injuries and lead to permanent disability in 50% and death in 20% of patients \r\n- Vertebral fractures may lead to disabling and painful kyphosis which may in turn cause difficulty breathing and gastrointestinal problems such as dyspepsia\r\n- Wrist fractures can significantly affect independence and functional ability\r\n- Many patients experience a \"fracture cascade\" where further fractures occur in the years following the initial one\r\n- Pain from fractures can lead to poor sleep, low mood and reduced quality of life\r\n- Complications of treatment may be significant (e.g. osteonecrosis of the jaw or oesophageal ulceration with bisphosphonates)\r\n\r\n# Prognosis\r\n\r\n- There is no cure for osteoporosis\r\n- In general however, prognosis is good with effective treatment\r\n- Bisphosphonate treatment should be reviewed after 3-5 years\r\n- If patients remain at high risk of fracture it may be continued for up to 7-10 years\r\n- Patients with previous hip or vertebral fractures, those aged 70 or older or those who sustain another fragility fracture whilst on bone protection often require longer durations of treatment\r\n- Repeat DEXA may be appropriate to aid decision making\r\n- If bone protection is stopped, fracture risk should be reassessed 18 months to 3 years later\r\n\r\n# NICE Guidelines\r\n\r\n[NICE CKS: Osteoporosis - prevention of fragility fractures](https://cks.nice.org.uk/topics/osteoporosis-prevention-of-fragility-fractures/)\r\n\r\n[NICE - Osteoporosis: assessing the risk of fragility fracture](https://www.nice.org.uk/guidance/cg146)\r\n\r\n# References\r\n\r\n[National Osteoporosis Guideline Group - Prevention and Treatment of Osteoporosis](https://www.nogg.org.uk/full-guideline)\r\n\r\n[BNF Treatment Summary - Osteoporosis](https://bnf.nice.org.uk/treatment-summaries/osteoporosis/)\r\n\r\n[Radiopaedia - Dual-energy x-ray absorptiometry](https://radiopaedia.org/articles/dual-energy-x-ray-absorptiometry-1?lang=gb)\r\n\r\n[WHO - Fragility fractures](https://www.who.int/news-room/fact-sheets/detail/fragility-fractures)\r\n\r\n[International Longevity Centre UK report on Osteoporosis](https://ilcuk.org.uk/wp-content/uploads/2018/10/OsteoporosisUK.pdf)\r\n\r\n\r\n",
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"question": "A 62-year-old Caucasian woman presents to the emergency department with a fracture of her distal radius. This is her third fracture in the last nine months. She has a past medical history of poorly controlled asthma and chronic kidney disease (CKD) stage 3.\n\n\nSpecific blood tests are shown below:\n\n\n||||\n|---------------------------|:-------:|------------------------------|\n|Calcium|2.35 mmol/L|2.2 - 2.6|\n|Phosphate|1.1 mmol/L|0.8 - 1.5|\n|Alkaline Phosphatase (ALP)|63 IU/L|25 - 115|\n|Parathyroid Hormone|4.8 pmol/L|1.6 - 8.5|\n|Vitamin D|110 nmol/L|>50|\n\n\n\nWhat is the most likely cause of these repeated fractures?",
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"explanation": "When assessing a patient with low urine output, flushing the catheter to check patency is always a reasonable pragmatic step that should be taken. However, given that some urine is draining from the catheter, it does not appear to be completely blocked. Additionally, in the history there is a clear explanation for why the patient's urine output might be low, making a simple blocked catheter less likely to be responsible",
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"explanation": "Intrinsic or \"renal\" causes of AKI include iatrogenic insult from nephrotoxic agents (commonly medications or intravenous contrast) or rarer causes such as rhabdomyolysis, interstitial nephritis or vasculitides",
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"explanation": "Post-renal AKI refers to renal impairment secondary to obstruction of the urine drainage system, most commonly from renal stones, a very large prostate, ureteric strictures, or more rarely neurological causes such as an atonic bladder",
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"explanation": "This patient likely has an acute kidney injury (AKI) secondary to sepsis and associated hypotension/hypovolaemia. Dividing causes of AKI into pre-renal, renal/intrinsic and post-renal/obstructive causes is a helpful approach to a topic that can otherwise be daunting",
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"explanation": "In chronic kidney disease, there would be deranged renal function in the previous blood test results. However, here we can see that three months ago, the patient had normal renal function, indicating that this is an acute insult",
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"comment": "bad explanation",
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"comment": "urea : creatine ratio is 1:80 suggesting a normal or post renal cause no?",
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"comment": "I did the exact same calculation and ruled pre-renal out based off this lmao",
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"comment": "What about the ratio urea:creatinine? Doesn’t this rule out pre renal cause? Got confused :/",
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"comment": "Bullshit, sepsis can also cause ATN which is intrinsic and suggested by the urea:creatinine ratio",
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"explanation": "# Summary\n\nAcute kidney injury (AKI) refers to a sudden deterioration in kidney function which may lead to oliguria, electrolyte imbalance, and accumulation of urea and other waste products. It is characterised by increased serum creatinine levels and reduced urine output. Causes are typically categorised as pre-renal, renal and post-renal, with most cases being pre-renal. Initial investigations include a urine dip, U&Es and a bladder scan. If there is no obvious cause, common next steps involve an ultrasound of the kidneys, ureters and bladder to look for post-renal causes (i.e. obstruction) and bloods to look for renal causes. Management involves treating the underlying cause as well as addressing complications such as hyperkalaemia.\n\n# Definition\n\nAn acute kidney injury is characterised by a decline in renal function that happens rapidly (over hours to days). It is diagnosed based on the Kidney Disease: Improving Global Outcomes (KDIGO) criteria as below:\n\n- Increase in serum creatinine by >26.5 mmol/l within 48 h, or\n- Increase in serum creatinine > 1.5x the baseline within the last 7 days, or\n- Urine output < 0.5 ml/kg/h for 6 hours\n\nUnlike chronic kidney disease (CKD), AKI is typically reversible, at least in part. \n\n# Epidemiology\n\nAKI is common, affecting approximately 20% of patients admitted to hospital and up to 50% of critically unwell patients in intensive care.\n\nIt is a marker of severe illness, with a 90-day mortality rate of approximately 25%. \n\nPatients at increased risk of AKI include:\n\n- Patients with CKD\n- Elderly patients\n- Previous AKI \n- Malignancy\n- Medical conditions increasing risk of urinary obstruction (e.g. benign prostatic hyperplasia)\n- Cognitive impairment and disability (may be reliant on others for fluid intake) \n- Recent use of medications such as NSAIDs or ACE inhibitors\n- Recent administration of iodine-containing contrast media\n\n# Aetiology\n\nCauses AKI are categorised into pre-renal, renal, and post-renal causes:\n\n**Pre-renal causes** are the most common, and occur due to decreased renal perfusion e.g. due to:\n\n- Hypovolaemia (e.g. dehydration, haemorrhage, gastrointestinal losses, burns)\n- Renovascular disease (e.g. renal artery stenosis)\n- Medications reducing blood pressure or renal blood flow (e.g. NSAIDs, ACE inhibitors, ARBs, diuretics)\n- Hypotension due to reduced cardiac output (e.g. heart failure, sepsis)\n\n**Renal causes** occur due to structural damage to the kidneys, which may affect:\n\n- The glomeruli (e.g. acute glomerulonephritis, nephrotic syndrome)\n- The tubules (e.g. acute tubular necrosis due to ischaemia or toxins, rhabdomyolysis)\n- The interstitium (e.g. acute interstitial nephritis secondary to drugs)\n- The renal vessels (e.g. renal vein thrombosis, vasculitis)\n\n\n**Post-renal causes** involve obstructed to urinary flow anywhere along the urinary tract, which may be:\n\n- Luminal (e.g. ureteric stones or a blocked catheter) \n- Intramural (e.g. urethral or ureteric strictures, ureteric carcinomas) \n- Due to external compression (e.g. an abdominal or pelvic tumour, benign prostatic hyperplasia)\n\n# Classification\n\nAKIs are staged according to the KDIGO criteria as follows:\n\n**Stage 1 - any of:**\n\n- Creatinine rise of 26 micromol/L or more within 48 hours\n- Creatinine rise to 1.5-1.99x baseline within 7 days\n- Urine output < 0.5 mL/kg/hour for more than 6 hours\n\n**Stage 2 - any of:**\n\n- Creatinine rise to 2-2.99x baseline within 7 days \n- Urine output < than 0.5 mL/kg/hour for more than 12 hours\n\n**Stage 3 - any of:** \n\n- Creatinine rise to 3x baseline or higher within 7 days\n- Creatinine rise to 354 micromol/L or more with either\n- Acute rise of 26 micromol/L or more within 48 hours or\n- 50% or more rise within 7 days \n- Urine output < than 0.3 mL/kg/hour for 24 hours\n- Anuria for 12 hours\n\n# Signs and Symptoms\n\nAn AKI may be asymptomatic and be detected on blood tests only, or may be diagnosed due to a fall in urine output.\n\nSymptoms may be seen especially in severe cases where uraemia occurs, and include:\n\n- Nausea and vomiting \n- Fatigue\n- Confusion\n- Anorexia\n- Pruritus \n\nOn examination, look for:\n\n- Hypertension (a complication of AKI)\n- Bladder distension due to urinary retention\n- Hypotension and dehydration (in many pre-renal causes)\n- Signs of fluid overload (e.g. raised jugular venous pressure, pulmonary and peripheral oedema) as a complication of AKI\n- Signs related to the underlying cause (e.g., fevers in sepsis, rashes in vasculitis)\n- Pericardial rub (in uraemic pericarditis)\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urinalysis** - urine dip may show blood and protein in glomerular disease, increased white blood cells may suggest infection or interstitial nephritis\n- **ECG** to screen for complications of hyperkalaemia\n- **Blood gas** to look for acidosis as a complication of AKI, allows rapid potassium measurement\n\n**Blood tests:**\n\n- **U&Es** to get creatinine for diagnosis (compare to baseline if available) and check for hyperkalaemia\n- **Full blood count** may show anaemia in vasculitis or raised white cells in infection\n- **LFTs** may be deranged in severe hypotension causing ischaemic hepatitis \n- **Clotting** as a baseline in case a renal biopsy is later required (rare)\n- **Bone profile** to screen for hypercalcaemia (seen in myeloma which can cause renal AKI)\n- **Creatinine kinase** to look for rhabdomyolysis\n- **CRP** may be raised in infection or vasculitis\n\n**Imaging:**\n\n- **Bladder scan** if urinary retention is suspected\n- **Ultrasound KUB (kidneys, ureters and bladder)** if a post-renal cause is suspected, may show hydronephrosis. The next line of imaging would be a **CT KUB** as this is a more sensitive modality.\n\nIf initial investigations do not reveal a cause, bloods for an acute **renal screen** may be done, including:\n\n- ANA\n- Double-stranded DNA\n- Anti-nuclear cytoplasmic antibodies\n- Anti-GBM antibodies\n- Erythrocyte sedimentation rate\n- Serum immunoglobulins\n- Serum electrophoresis\n- Serum free light chains\n- Complement levels (C3 and C4)\n- HIV screening\n- Hepatitis B and C serology\n\nIf the diagnosis is still unclear and a renal cause is suspected, a **renal biopsy** may be indicated.\n\n# Management\n\n- The key to AKI management is identification and treatment of the underlying cause\n- The **most common cause of AKI is dehydration,** and so for many patients IV fluid resuscitation will be required \n- Careful assessment of fluid status is crucial though, as in certain cases where the patient is fluid overloaded diuretic treatment rather than fluids may be required\n- Fluid balance should be monitored closely with consideration of catheterisation to monitor urine output \n- A catheter may be the definitive treatment in some cases (e.g. post-renal AKI due to urethral obstruction)\n- Screen for complications of AKI (e.g. hyperkalaemia, acidosis, pulmonary oedema) and instigate treatment promptly\n- Involve the renal team early in severe or complicated AKIs, where the cause is unclear or where a renal cause is suspected\n- Review regular medications and **suspend any nephrotoxic drugs** (e.g. NSAIDs, aminoglycosides, ACE inhibitors, ARBs) and review those that may cause complications in cases of renal impairment (e.g. opiates, metformin)\n- Low-risk patients with an uncomplicated stage 1 or 2 AKI may be considered for discharge if there is an identifiable cause that can be managed in the community\n- The following should prompt referral for consideration of renal replacement therapy with dialysis or haemofiltration (remembered by the AEIOU mnemonic): \n\t- **A**cidosis (severe metabolic acidosis with pH of <7.20)\n\t- **E**lectrolyte imbalance (resistant hyperkalaemia)\n\t- **I**ntoxication (AKI secondary to certain drugs or poisons)\n\t- **O**edema (refractory pulmonary oedema)\n\t- **U**raemia (uraemic encephalopathy or pericarditis)\n\n# NICE Guidelines\n\n[NICE CKS - Acute Kidney Injury](https://cks.nice.org.uk/topics/acute-kidney-injury/) \n\n[NICE: Acute kidney injury: prevention, detection and management](https://www.nice.org.uk/guidance/ng148) \n\n# References\n\n[KDIGO - AKI guideline](https://kdigo.org/guidelines/acute-kidney-injury/) \n\n[Patient UK - Acute Kidney Injury](https://patient.info/doctor/acute-kidney-injury-pro)",
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"question": "A 41-year-old male presents to the emergency department with shortness of breath and high-grade fever. He is found to have sepsis secondary to a severe community acquired pneumonia. As part of his management, he is catheterised and noted to have low urine output.\n\n\nSpecific blood tests from today, and three months previously, are found below.\n\n\nToday:\n\n||||\n|---------------------------|:-------:|--------------------|\n|Sodium|147 mmol/L|135 - 145|\n|Potassium|5.4 mmol/L|3.5 - 5.3|\n|Urea|27.1 mmol/L|2.5 - 7.8|\n|Creatinine|336 µmol/L|60 - 120|\n|eGFR|17 mL/min/1.73m<sup>2</sup>|> 60|\n\n\n 3 months previously:\n\n\n||||\n|---------------------------|:-------:|--------------------|\n|Sodium|139 mmol/L|135 - 145|\n|Potassium|4.1 mmol/L|3.5 - 5.3|\n|Urea|7.1 mmol/L|2.5 - 7.8|\n|Creatinine|104 µmol/L|60 - 120|\n|eGFR|>90 mL/min/1.73m<sup>2</sup>|> 60|\n\n\nWhat is the most likely cause of this patient's low urine output?",
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"explanation": "The calculation for GFR is based on a patients gender, age and creatinine. Creatinine is ultimately a waste product from muscle turnover, so higher levels would naturally be found in people with increased muscle mass. This man has a raised BMI but describes a healthy lifestyle and works as a personal trainer - this should highlight that he is likely to be very muscular which is the most likely cause of his raised Creatinine. ",
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"explanation": "# Summary\n\nChronic Kidney Disease (CKD) is a condition characterised by abnormal kidney function for over three months, with a decrease in glomerular filtration rate (GFR) and/or markers of kidney damage such as proteinuria. Classification is based on the cause of CKD, GFR and heaviness of proteinuria. Common causes include diabetes, hypertension and age-related decline. Most patients are asymptomatic in the early stages; signs and symptoms that may develop include lethargy, breathlessness, anorexia and oliguria. First-line investigations include blood tests for U&Es to determine serum creatinine and estimated GFR (eGFR), urine albumin:creatinine ratio and investigations to screen for a cause (e.g. renal tract ultrasound to look for structural abnormalities or obstruction). Management involves regular monitoring for complications (such as anaemia or bone disease), optimising risk factors such as blood pressure and diabetic control, and considering options for renal replacement therapy (RRT) in patients who have end-stage renal disease.\n\n# Definition\n\nCKD is defined by KDIGO as abnormal kidney function or structure for over 3 months, with implications for health. \n\nGlomerular filtration rate (GFR) refers to the volume of fluid filtered by the kidney's nephrons per minute. This can be estimated (eGFR) from serum creatinine although this may be less reliable in patients with extremes of muscle mass.\n\nA GFR below 60 ml/min/1.73m<sup>2</sup> is considered significantly abnormal kidney function.\n\nExamples of abnormal kidney structure include:\n\n- Urinary albumin:creatinine ratio > 3 mg/mmol\n- Urinary sediment abnormalities e.g. haematuria, pyuria or casts\n- Biochemical abnormalities (e.g. acidosis, electrolyte disturbance) due to tubular disorders\n- Histological abnormalities e.g. glomerulosclerosis, tubular atrophy\n- Structural abnormalities e.g. polycystic kidneys or reflux nephropathy\n- Previous renal transplant\n\n# Epidemiology\n\n- CKD is very common, with an estimated global prevalence of 9%\n- Diabetes is the commonest cause, accounting for up to 50% of cases\n- As the early stages of CKD are often asymptomatic, many cases are likely undiagnosed\n- Prevalence is rising due to the ageing population and increased prevalence of chronic diseases such as diabetes and hypertension\n- 50% of people over the age of 75 have CKD\n- Risk factors include:\n\t- Family history of CKD\n\t- Black or Hispanic ethnicity\n\t- History of acute kidney injury (AKI)\n\t- Older age\n\n# Aetiology\n\n- Diseases causing intrinsic kidney damage:\n\t- Diabetes\n\t- Hypertension\n\t- Glomerulonephritis, which may be primary or secondary\n\t- Conditions causing urinary tract obstruction:\n\t- Recurrent urolithiasis\n\t- Structural abnormalities (e.g. ureteropelvic junction obstruction)\n\t- External compression (e.g. from a pelvic mass)\n\t- Bladder voiding problems (e.g. benign prostatic hyperplasia, neurogenic bladder)\n- Iatrogenic causes:\n\t- Radiotherapy\n\t- Nephrotoxic drugs, e.g. aminoglycosides, lithium, NSAIDs\n- Renal involvement secondary to multisystem diseases:\n\t- HIV\n\t- Myeloma\n\t- Vasculitis\n\t- Systemic lupus erythematosus (lupus nephritis)\n\t- Amyloidosis\n\t- Genetic kidney diseases\n\t- Autosomal dominant polycystic kidney disease (ADPKD)\n\t- Alport's syndrome\n\t- Tuberous sclerosis\n\t- Cystinosis\n\t- Recurrent urinary tract infections\n\t- Often secondary to vesico-ureteric reflux or other anatomical defects\n\t- Leads to chronic pyelonephritis which may lead to end-stage renal disease\n\n# Classification\n\nThe KDIGO classification is used to stratify patients by risk of adverse outcomes from CKD based on their GFR and urinary albumin:creatinine ratio (ACR).\n\n||A1 - normal to mildly increased ACR (< 3 mg/mmol)|A2 - moderately increased ACR (3 to 30 mg/mmol)|A3 - severely increased ACR (over 30 mg/mmol)|\n|---------------|-----------|---------------|-----------|\n|**G1 - normal or high GFR (> 90 ml/min/1.73m<sup>2</sup>)**|Low risk/not CKD if no other markers of kidney damage|Moderate risk|High risk|\n|**G2 - mild reduction in GFR (60 - 89 ml/min/1.73m<sup>2</sup>)**|Low risk/not CKD if no other markers of kidney damage|Moderate risk|High risk|\n|**G3a - mild to moderate reduction in GFR (45 - 59 ml/min/1.73m<sup>2</sup>)**|Moderate risk|High risk|Very high risk|\n|**G3b - moderate to severe reduction in GFR (30-44 ml/min/1.73m<sup>2</sup>)**|Moderate risk|High risk|Very high risk|\n|**G4 - severe reduction in GFR (15 - 29 ml/min/1.73m<sup>2</sup>)**|High risk|Very high risk|Very high risk|\n|**G5 - renal failure (< 15 ml/min/1.73m<sup>2</sup>)**|Very high risk|Very high risk|Very high risk|\n\n\n# Signs and Symptoms\n\nCKD is often asymptomatic, however especially in later stages patients may have non-specific symptoms such as:\n\n- Lethargy\n- Anorexia\n- Headaches\n- Weight loss (or gain due to fluid overload)\n- Nausea and vomiting\n- Itching (uraemic pruritus)\n- Shortness of breath (due to anaemia, pulmonary oedema, pleural effusion or acidosis)\n- Muscle cramps, especially at night\n- Bone pain (due to renal osteodystrophy)\n- Taste changes\n- Cognitive impairment\n- Urinary symptoms: \n- Polyuria or oliguria may occur\n- Nocturia\n- Frothy urine (due to proteinuria)\n\nExamination findings may include:\n\n- Hypertension\n- Pallor (due to anaemia)\n- Abnormal fluid status\n- Fluid overload with peripheral and/or pulmonary oedema\n- Dehydration\n- Cachexia\n- Ammonia-like smelling breath due to uraemia\n- Tachypnoea (due to anaemia, pulmonary oedema, pleural effusion or acidosis \n- Flank mass(es) may be palpable due to malignancy or renal cysts (e.g. in ADPKD)\n- Patients on renal replacement therapy may have additional signs such as:\n- Arteriovenous fistula (AVF)\n- Peritoneal dialysis catheter\n- Renal transplant scar (usually right iliac fossa)\n- Parathyroidectomy scar may be present in patients requiring surgical management of secondary or tertiary hyperparathyroidism\n\n# Differential Diagnosis\n\n- **Acute kidney injury (AKI)** is the main differential \n\t- It may be difficult to differentiate AKI from CKD based on investigations showing renal impairment at a single point in time \n\t- To diagnose CKD markers of kidney damage or an eGFR of < 60mL/min/1.73m_ need to be present on two occasions at least 3 months apart\n\t- Abnormal kidneys on imaging (atrophy e.g. in chronic pyelonephritis, or enlarged kidneys e.g. in ADPKD) are indicative of CKD rather than AKI\n\t- Complications of CKD such as anaemia or secondary hyperparathyroidism may also be useful in differentiating the two\n\t- The two may co-exist if there is an acute insult causing AKI in a patient with pre-existing CKD (whether this is diagnosed or not)\n- **False-positive low eGFR results** may occur due to high serum creatinine results, for example in patients with high muscle mass, or after consumption of meat\n- **Urinary ACR** may also be high due to menstruation, strenuous exercise, orthostatic proteinuria or UTI\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urine dipstick** to screen for haematuria and proteinuria\n- Urine positive for haematuria should be sent for **MC&S** to screen for infection\n- Malignancy should also be considered in patients with persistent unexplained haematuria\n- **Early morning albumin:creatinine ratio** should be done in all patients \n- If this is between 3 and 70 mg/mmol it should be repeated within 3 months for confirmation\n\n**Blood tests:**\n\n- **U&Es** for creatinine, eGFR, urea and electrolytes\n- Patients should be advised not to eat meat 12 hours prior to the test\n- If eGFR is < 60 mL/min/1.73m_, this should be repeated within 2 weeks\n- If it remains low with no evidence of ongoing AKI, U&Es should be repeated in 3 months to diagnose CKD\n- **Full blood count** looking for anaemia secondary to CKD, which is usually normochromic and normocytic\n- **LFTs** may show a raised ALP due to bone disease; albumin may be low due to malnourishment or nephrotic syndrome\n- **Bone profile** may show an abnormal calcium; phosphate is usually high\n- **HbA1c** to screen for diabetes as a cause of CKD\n- **Bicarbonate** may be low due to metabolic acidosis\n- **Lipid profile** as dyslipidemia is common in CKD and is a modifiable risk factor for cardiovascular disease\n- **Clotting screen** in case renal biopsy is required\n- **Parathyroid hormone** often rises as renal function declines (secondary or tertiary hyperparathyroidism)\n- **HIV and hepatitis B and C serology** especially in patients for whom renal replacement therapy is being considered\n- **An autoimmune screen** may be sent if an underlying autoimmune condition is suspected\n\t- Antinuclear antibodies\n\t- ANCA antibodies\n\t- dsDNA antibodies\n\t- Anti-GBM antibodies\n\t- Serum complement \n- **Myeloma screen** i.e. immunoglobulins, protein electrophoresis and serum free light chains if this is suspected\n\n**Imaging:**\n\n- **Renal tract ultrasound** is not required in all patients, but should be offered to the following patients:\n- Accelerated progression of CKD (sustained decrease in GFR of 15 ml/min/1.73m_ per year **or** 25% or more **and** a change in GFR category within 12 months)\n- GFR < 30ml/min/1.73m_\n- Patients planned for renal biopsy\n- Suspected urinary tract obstruction\n- Persistent or visible haematuria\n- Family history of polycystic kidney disease\n- Kidneys are usually atrophic in advanced CKD\n- Large kidneys are seen in polycystic kidney disease and in the initial stages of diabetic nephropathy\n- **CT KUB** is the most sensitive imaging modality if renal stones are suspected\n- **CT or MRI angiography** may be indicated for suspected renal artery stenosis - **radionuclide scanning** is also an option\n\n**Special tests:**\n\n- **Renal biopsy** is not required in every case of CKD but may be indicated after initial investigations have been completed, for example if the cause of renal impairment is unclear, where there is rapid progression of CKD or where glomerulonephritis is suspected\n- Important contraindications include active pyelonephritis, uncontrolled hypertension or coagulopathy; biopsying a patient with a single kidney should be avoided where possible due to the (very rare) risk that a nephrectomy may be required to treat complications\n\n# Management\n\n**Conservative management:**\n\n- Patients with CKD are often managed in primary care, however the following should prompt referral to secondary care renal services:\n\t- End-stage renal disease\n\t- Rare or genetic cause for CKD known or suspected (e.g. ADPKD)\n\t- Suspected renal artery stenosis\n\t- Diagnostic uncertainty\n\t- Complications of CKD e.g. malnutrition, hyperkalaemia, anaemia, mineral and bone disorder, acidosis\n\t- Uncontrolled hypertension despite four antihypertensives\n\t- 5-year risk of needing RRT > 5% (see references for calculator)\n\t- Accelerated progression of CKD\n\t- Urinary ACR > 70 mg/mmol (or > 30 mg/mmol with persistent haematuria)\n\t- Patient with obstructive causes of CKD should be referred to urology\n\t- Individualised education on CKD including safety netting regarding complications and risk of AKI\n- Some patients may require additional counselling e.g. genetic counselling and advice regarding screening family members in ADPKD\n- Lifestyle advice should be provided, including:\n\t- Smoking cessation\n\t- Moderating alcohol intake\n\t- Maintaining a healthy weight with regular exercise\n\t- Maintaining a healthy diet\n\t- Avoid over-the-counter nephrotoxics e.g. NSAIDs, dietary supplements and herbal remedies\n- Dietician input may be required for end-stage renal disease (e.g. reducing phosphate, salt and potassium intake)\n- Regular monitoring of eGFR, urinary ACR and for any complications should be undertaken, more frequently in patients with more advanced CKD\n- Patients may benefit from education and/or support groups \n- In the later stages, psychological support and/or access to specialist nurse input may be helpful\n- Many patients with end-stage renal disease may not want or not be suitable for RRT - in these cases - conservative management is an important alternative (also referred to as \"supportive care\")\n\n**Medical management:**\n\n- Treat the underlying cause of CKD e.g. optimise diabetic control; specialist input for immunosuppressive treatments in autoimmune conditions\n- Review medications and consider reducing or stopping nephrotoxic drugs (e.g. NSAIDs, diuretics)\n- Treat hypertension with up to four antihypertensives \n- Aim for a target blood pressure of <140/90 if ACR is < 70 mg/mmol\n- Aim for < 130/80 if ACR is > 70 mg/mmol\n- Patients over 80 with type 1 diabetes should aim for < 150/90\n- An ACE-inhibitor or angiotensin-receptor blocker (ARB) should be first line if ACR is > 30 mg/mmol (if less then manage as per usual hypertension guidelines)\n- ACE-inhibitors or ARBs may be initiated in patients with diabetes and ACR > 3 mg/mmol in the absence of hypertension\n- However these should be avoided in patients with a potassium of > 5 mmol/L \n- They should be stopped if potassium rises to > 6 mmol/L on treatment\n- Consider starting a statin (usually atorvastatin 20mg) in all patients with CKD - the dose should be uptitrated to achieve effect lipid-lowering\n- Consider an antiplatelet (e.g. aspirin) for secondary prevention of cardiovascular disease (balanced against bleeding risk)\n- Sodium-glucose cotransporter-2 (SGLT-2) inhibitors may be considered in some patients on maximal ACE-inhibitor or ARB treatment who meet certain criteria (based on presence of type 2 diabetes, ACR and eGFR)\n- Ensure patients are up to date with vaccinations:\n- Annual influenza vaccine\n- 5-yearly pneumococcal vaccine (PPV23)\n- Covid vaccination as per national guidance\n- Medical management is often required for complications of CKD - see \"Complications\" section for more details\n\n**Surgical/interventional management:**\n\n- Renal replacement therapy is covered in detail in another chapter\n- Options include haemodialysis, peritoneal dialysis (which may be automated and mainly done overnight, or continuous and ambulatory) and renal transplant\n- Patients should be referred for consideration of RRT ideally at least a year before this is anticipated to be required\n- Indications include:\n- eGFR approximately 5-7 ml/min/1.73m_\n- Symptomatic uraemia affecting quality of life\n- Refractory fluid overload\n- Refractory biochemical abnormalities\n- Various options exist for dialysis access which may require surgical formation (e.g. an arteriovenous fistula)\n- Other surgical interventions may be required to treat complications of CKD, for example parathyroidectomy may be indicated in some patients with refractory hyperparathyroidism\n\n# Complications\n\n- **Anaemia** is often multifactorial, due to reduced erythropoietin production, iron deficiency and reduced red blood cell survival\n\t- Other contributing factors include B12 and folate deficiency, haemolysis due to dialysis and the underlying cause of CKD (e.g. myeloma, sickle cell disease)\n\t- Typically anaemia is normocytic and normochromic\n\t- Patients should be investigated if haemoglobin (Hb) is < 110 g/L or if symptomatic\n\t- If eGFR is > 60 ml/min/1.73m_, anaemia is unlikely to be due to CKD\n\t- Other investigations may be required to rule out other causes of anaemia (e.g. gastrointestinal bleeding, B12/folate deficiency)\n\t- All patients should be investigated for iron deficiency with percentage of hypochromic red blood cells being first-line (> 6% indicates functional iron deficiency)\n\t- Ferritin < 100 mcg/L is also indicative of iron deficiency\n\t- Iron supplementation may be either oral or IV (with IV usually preferred for patients on haemodialysis)\n\t- Ferritin should be monitored and iron supplements stopped before ferritin increases over 800 mcg/L\n\t- Once iron stores are replete, erythropoiesis-stimulating agent (ESA) treatment should be considered\n\t- These are usually given subcutaneously, with examples of ESAs including epoetin or darbepoetin\n\t- Roxadustat is a new oral alternative to ESAs which also acts to stimulate erythropoiesis (it is a hypoxia-inducible factor prolyl hydroxylase inhibitor)\n\t- Blood transfusion should be avoided, especially in patients who may require a renal transplant (due to the risk of allosensitization)\n\t- Target Hb is 100-120 g/L\n- **Mineral and bone disorder (MBD)** occurs due to abnormal metabolism of phosphate, vitamin D, calcium and parathyroid hormone\n\t- There is a spectrum of disease that involves abnormal bone turnover and mineralisation as well as vascular and soft tissue calcification\n\t- Risk of CKD-MBD increases once eGFR is < 60 mL/min/1.73m_\n\t- Phosphate retention occurs due to renal dysfunction -> calcitriol (active form of vitamin D) is downregulated, and is also decreased due to reduced renal activation of vitamin D -> calcium falls -> PTH rises (secondary hyperparathyroidism) -> calcium is released from bone\n\t- Tertiary hyperparathyroidism may also occur if there is longstanding secondary hyperparathyroidism (both may be treated with parathyroidectomy)\n\t- \"Renal osteodystrophy\" refers to a range of bone abnormalities seen in CKD including bone resorption, osteosclerosis and osteopenia\n\t- There is an increased risk of fracture - bone density assessment (e.g. DEXA scanning) and bone protection should be considered\n\t- Patients with at least stage 3a CKD should be regularly monitored with serum calcium, phosphate and PTH levels \n\t- Management involves normalising serum phosphate via dietary restriction of phosphate and phosphate binders (e.g. calcium carbonate, sevelamer)\n\t- Severe hyperparathyroidism may be treated with calcitriol and cinacalcet (a calcimimetic)\n\t- Vitamin D supplementation with ergocalciferol or cholecalciferol may be considered\n\t- Dialysis settings can be adjusted to remove excess phosphate and calcium\n- **Cardiovascular risk** is significantly increased, including myocardial infarction, stroke, peripheral arterial disease and heart failure\n\t- There is a high prevalence of comorbid conditions increasing cardiovascular risk (e.g. hypertension, hypercholesterolaemia, diabetes)\n\t- Patients also have additional CKD-related risk factors, including vascular calcification due to CKD-MBD, uraemia, oxidative stress and anaemia\n\t- Dialysis further increases the risk of cardiovascular disease, including ischaemic heart disease, valvular disease and hypertensive cardiomyopathy\n- **Uraemia** typically becomes symptomatic in patients with end-stage renal disease\n\t- Symptoms include nausea, vomiting, anorexia, taste disturbance, confusion, muscle cramps, pruritus and restless legs\n\t- Complications include pericarditis, neuropathy and encephalopathy\n\t- Symptomatic uraemia is an indication for renal replacement therapy\n- **Hyperkalaemia** is a common issue in CKD due to impaired potassium excretion\n\t- Medications such as ACE-inhibitors and ARBs also contribute to hyperkalemia\n\t- Dietary intake of potassium should be limited\n\t- Medical treatment with potassium binders may be required (e.g. sodium zirconium cyclosilicate (Lokelma), calcium resonium or patiromer)\n\t- Treatments such as sodium bicarbonate (for metabolic acidosis) and diuretics (for fluid overload) may also help to reduce serum potassium\n- **Metabolic acidosis** is common due to reduced renal acid excretion once eGFR < 50 ml/min/1.73m_\n\t- Chronic metabolic acidosis further increases kidney injury and fibrosis, bone demineralisation and muscle wasting and risk of cardiovascular events\n\t- Oral sodium bicarbonate should be considered for patients with an eGFR < 30 ml/min/1.73m_, or if serum bicarbonate is < 20 mmol/litre\n- **Fluid overload** with both pulmonary and peripheral oedema may occur in the later stages of CKD\n\t- Fluid restriction may be advised\n\t- Diuretics may also be used, with loop diuretics (e.g. furosemide) being first-line in most cases\n- **Malnutrition** is common, especially as CKD progresses\n\t- Uraemia may cause anorexia and taste disturbance\n\t- Low mood may also contribute to poor oral intake\n\t- Protein catabolism is promoted by acidosis and chronic inflammation\n\t- Patients should be regularly screened for malnutrition\n\t- Specialist renal dietician input should be offered for patients at risk of malnutrition\n\t- Oral nutritional supplements may be indicated in some cases (or less commonly enteral tube feeding or parenteral nutritional support) \n- **Acute kidney injury** - patients with CKD are at increased risk of AKI\n\t- Risk increases in patients with an eGFR of < 60 mL/min/1.73m_\n\t- There is also a risk of increased CKD progression with episodes of AKI\n\t- Triggers include intercurrent illness, especially with diarrhoea and vomiting, medications e.g. NSAIDs, antibiotics and urinary tract obstruction\n- **Increased risk of malignancy** especially of renal and thyroid cancers\n\t- Immunosuppressive medications further increase malignancy risk (e.g. after renal transplant)\n\t- Chronic uraemia is also a contributing factor\n- **Hypertension** both contributes to the development of CKD and is caused by CKD\n\t- Mechanisms include sodium dysregulation, upregulation of the renin angiotensin aldosterone system, and sympathetic nervous system hyperactivity\n\t- Regular monitoring of blood pressure and effective treatment is therefore key to minimising progression of CKD as well as other adverse cardiovascular events\n- **Reduced quality of life**, especially in patients with more severe CKD\n\t- As with any chronic disease, depression and anxiety are common\n\n# Prognosis\n\n- Prognosis is dependent on the underlying cause of CKD, for example ADPKD tends to progress more rapidly than other diseases\n- CKD is typically a progressive disease, although most patients die before reaching end-stage renal disease\n- Approximately 2% of patients with CKD develop end-stage renal disease\n- Progression can be slowed through modification of risk factors such as hypertension and proteinuria\n- The leading cause of death in CKD is cardiovascular disease\n\n# NICE Guidelines\n\n[NICE CKS - Chronic Kidney Disease](https://cks.nice.org.uk/topics/chronic-kidney-disease/)\n\n[NICE - Chronic kidney disease: assessment and management](https://www.nice.org.uk/guidance/ng203)\n\n[NICE - Renal replacement therapy and conservative management](https://www.nice.org.uk/guidance/ng107)\n\n[NICE technology appraisal - Roxadustat for treating symptomatic anaemia in chronic kidney disease](https://www.nice.org.uk/guidance/ta807/)\n\n# References\n\n[Patient UK - Chronic kidney disease](https://patient.info/doctor/chronic-kidney-disease-pro)\n\n[Patient UK - Anaemia in chronic kidney disease](https://patient.info/doctor/anaemia-in-chronic-kidney-disease)\n\n[UK Kidney Association eCKD guide](https://ukkidney.org/health-professionals/information-resources/uk-eckd-guide) \n\n[Kidney Failure Risk Equation]( https://www.kidneyfailurerisk.co.uk/)\n\n[KDIGO CKD Evaluation and Management](https://kdigo.org/guidelines/ckd-evaluation-and-management/)\n\n[KDIGO CKD Mineral and Bone Disorder guideline](https://kdigo.org/guidelines/ckd-mbd/)\n\n[Radiopaedia - Renal osteodystrophy](https://radiopaedia.org/articles/renal-osteodystrophy?lang=gb)\n\n[The Renal Association - Undernutrition in Chronic Kidney Disease Guideline](https://ukkidney.org/sites/renal.org/files/FINAL-Nutrition-guideline-June-2019-RNG-endorsed.pdf)\n\n[NHS Kidney Care - Chronic Kidney\nDisease in England: The Human and Financial Cost](https://www.england.nhs.uk/improvement-hub/wp-content/uploads/sites/44/2017/11/Chronic-Kidney-Disease-in-England-The-Human-and-Financial-Cost.pdf)",
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"question": "A 25-year-old man has some routine blood tests through his GP when registering as a new patient. He is asymptomatic and has no past medical history. He describes his lifestyle as very healthy, and he works as a personal trainer. His body mass index (BMI) is 31.\n\n\nHis renal function is reported as deranged (see results below):\n\n||||\n|---------------------------|:-------:|--------------------|\n|Sodium|142 mmol/L|135 - 145|\n|Potassium|4.6 mmol/L|3.5 - 5.3|\n|Urea|6.9 mmol/L|2.5 - 7.8|\n|Creatinine|130 µmol/L|60 - 120|\n|eGFR|58 mL/min/1.73m<sup>2</sup>|> 60|\n\n\n\nWhat is the most likely explanation for these results?",
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"explanation": "The E. Coli grown is resistant to nitrofurantoin, which explains why the first course did not resolve the patient's symptoms. Extending the course will not alter the resistance and will not benefit the patient",
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"explanation": "Trimethoprim is the only sensitive result for this E. Coli that would be suitable for use alongside a penicillin allergy",
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"explanation": "# Summary\n\nVesicoureteral reflux (VUR) is a congenital condition where urine flows backwards from the bladder into the ureters and kidneys, increasing the risk of recurrent urinary tract infections (UTIs). Symptoms include recurrent UTIs, fevers, and abdominal pain, with severe cases leading to renal scarring and hypertension. Diagnosis can involve ultrasound, MCUG, MAG reflux test, and DMSA scan. Management includes prophylactic antibiotics, monitoring, and possibly surgery for severe cases. Complications include UTIs, pyelonephritis, and chronic kidney disease.\n\n# Definition\n\nVesicoureteral reflux (VUR) is a condition where urine flows backwards from the bladder into the ureters and potentially the kidneys, rather than the usual one-way flow from the kidneys to the ureters and then to the bladder. This condition is typically present from birth and can lead to recurrent UTIs, as the backward flow of urine can carry bacteria up into the kidneys, causing an infection. It is a significant risk factor for atypical UTIs and recurrent infections.\n \n\n# Epidemiology\n \n\nVUR affects around 1-3% of all children and can occur in all age groups. It is more commonly diagnosed in children with UTIs, especially if these UTIs are recurrent or atypical. A familial predisposition is often present.\n \n\n# Pathophysiology\n\nThe abnormal flow of urine in VUR can occur due to a variety of reasons, including a shortened intravesical ureter (the part of the ureter that passes through the bladder wall), an improperly functioning valve where the ureter joins the bladder, or a neurological disorder affecting the bladder.\n \n\n# Signs and Symptoms\n \nVUR is often asymptomatic and may only be detected when investigating recurrent or atypical UTIs. \n\nSymptoms can include:\n\n- Recurrent UTIs or persistent bacteriuria\n- Unexplained fevers\n- Abdominal or flank pain\n- In severe cases, renal scarring can occur leading to hypertension and chronic kidney disease\n \n\n# Investigations\n \n\nIn children with recurrent or atypical UTIs, investigations considering VUR include:\n \n- Ultrasound of the kidneys and bladder is often performed initially \n - Used to detect hydronephrosis, dilatation of renal pelvis or incomplete bladder voiding \n- Micturating Cystourethrogram (MCUG) \n - Contrast is passed into the bladder, and the patient passes urine whilst x-rays are taken.\n - This enables the refluxing of urine to be visualised \n- MAG (mercapto acetyl triglycine 3) reflux test \n - IV contrast recorded on x-ray whilst the child passes urine, to enable any reflux to be visualised \n- Dimercaptosuccinic acid (DMSA) scan\n - This can detect scarring or damage to the kidneys as a result of VUR\n \n\n# Management\n \n\nThe management of VUR can be conservative or surgical, depending on the severity of the condition, the age of the patient, and the risk of kidney damage. \n\n- Conservative management:\n - Prophylactic antibiotics to prevent UTIs\n - Regular monitoring of kidney function and growth\n - Treatment of constipation if present\n- Surgical treatment, such as ureteral reimplantation, may be considered in severe cases or when conservative management fails.\n \n\n# Complications\n\nPotential complications of VUR include:\n \n\n - Recurrent UTIs\n - Pyelonephritis\n - Renal scarring and Chronic Kidney Disease (CKD)\n - Hypertension\n \nThis highlights the importance of early detection and management of VUR, especially in children with recurrent or atypical UTIs.\n \n# NICE Guidelines \n\n[NICE Guideline Urinary tract infection in under 16s: diagnosis and management](https://www.nice.org.uk/guidance/ng224/chapter/Recommendations-for-research) \n \n# References\n\n[Kidney Research UK Vesicoureteral reflux](https://www.kidneyresearchuk.org/conditions-symptoms/vesico-uretal-reflux/)",
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"question": "A 35-year-old woman presents to her GP with no improvement in symptoms following a three day course of nitrofurantoin for a urinary tract infection (UTI). She has ongoing dysuria and urinary frequency. She is allergic to penicillin (rash).\n\nA urine culture result is now available:\n\nModerate growth of E. Coli\n\n- Amoxicillin - R\n- Nitrofurantoin - R\n- Cefalexin - S\n- Co-amoxiclav - S\n- Trimethoprim - S\n- Ciprofloxacin - R\n\nNB: R = Resistant and S = Sensitive\n\nWhat is the most appropriate antibiotic choice to treat this woman's UTI?",
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"explanation": "Muscular back pain would not be expected to cause infective symptoms, such as a high fever",
"id": "33395",
"label": "c",
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"explanation": "Although kidney stones can act as a focus for infection, they more commonly present with **pain as the primary symptom**. The pain is characteristically very severe and radiates in a \"loin to groin\" pattern",
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"label": "b",
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"explanation": "This patient has recently been treated for a urinary tract infection. This treatment was likely insufficient, and she has now gone on to develop pyelonephritis - an upper urinary tract infection that involves infection/ inflammation of the kidney itself. This commonly presents with nausea, vomiting, fever and flank pain",
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"name": "Urinary tract infection",
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"explanation": "Pyelonephritis is an upper urinary tract infection involving infection/ inflammation of the kidney itself. This commonly presents with nausea, vomiting, fever and flank pain - this patient has all of the classic symptoms. There is also the additional clue of recent treatment for UTI via the GP - this treatment was likely insufficient, and the infection has now tracked up the urinary tract to the kidney",
"id": "33393",
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"explanation": "A psoas abscess would also present with flank pain and fever, however, this patient has none of the classic risk factors (underlying immunosuppression, intravenous drug use, recent local surgery or trauma). Additionally, the recent history of urinary tract infection is more suggestive of pyelonephritis. A psoas abscess may also present with a limp, or pain that is exacerbated by movement of the ipsilateral limb",
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"explanation": "# Summary \n\nLower urinary tract infections (LUTIs), often manifesting as cystitis, typically involve the infection of the bladder. Primarily caused by transurethral ascent of colonic commensals like E. coli, symptoms include urinary frequency, dysuria, urgency, foul-smelling urine, and suprapubic pain. Investigations are generally limited to a urine dipstick test for leucocytes and nitrites, while management involves oral nitrofurantoin or trimethoprim, and conservative measures. A key differential diagnosis is pyelonephritis, a urinary tract infection affecting the kidneys. Pyelonephritis exhibits more severe symptoms like fever, malaise, loin pain, and vomiting, and requires hospital admission and intravenous antibiotics.\n\n# Definition \n\nA lower urinary tract infection (LUTI) is generally defined as an infection of the bladder, often manifesting as cystitis.\n\n# Aetiology \n\nLUTIs are caused by the transurethral ascent of colonic commensals, most commonly **E. coli**.\n\n# Signs and symptoms\n\nPatients with LUTIs generally present with:\n\n- Urinary frequency\n- Dysuria\n- Urgency\n- Foul-smelling urine\n- Suprapubic pain\n- Clinical examination may be normal or reveal suprapubic tenderness.\n\nRed flag symptoms such as haematuria, loin pain, rigors, nausea, vomiting, and altered mental state may indicate more serious infection, and these patients may have/are at risk of developing pyelonephritis (see below) and likely need referral to A&E.\n\n\n# Investigations\n\nFor LUTIs:\n\n- Urine dipstick is positive for leucocytes and nitrites in most cases.\n- In uncomplicated cases, no further investigations are required.\n- In children, men, and pregnant women a mid-stream urine sample should be sent.\n\nNB: Urine dipstick is unreliable in women aged older than 65 years and those who are catheterised.\n\nIf being managed in secondary care due to red flag symptoms consider:\n\n- If there are signs of systemic upset consider routine blood tests such as FBC, U+E, and CRP.\n- For uncomplicated UTIs, imaging is rarely required, but if there are concerns over antecedents/complications such as urinary retention/obstruction, an USS bladder/kidney scan would be the first port of call.\n\n# Management \n\n[lightgallery]\n\n[lightgallery1]\n\nFor LUTIs:\n\n- First line management is with oral nitrofurantoin or trimethoprim. Antibiotic duration can vary (see below) however in women the standard course length is 3 days.\n- The patient should be advised on conservative measures to reduce the risk of further infection e.g. regular fluid intake, post-coital voiding.\n\n## Specific situations\n\n**UTI in Men:**\n\n- Empirical antibiotic drug treatment (if no cultures with sensitivities) with trimethoprim or nitrofurantoin for **7 days.**\n- Refer to urology if there are ongoing symptoms despite treatment, if there is an underlying risk factor for UTIs (e.g. urinary calculi, suspected obstruction, previous GU surgery), or if there are recurrent episodes of UTI.\n\n**UTI during Pregnancy (with no haematuria):**\n\n- First-line antibiotics are nitrofurantoin (but *avoid at term),* for **7 days.**\n- If nitrofurantoin is not suitable due to e.g. renal function, or there is no improvement in symptoms, consider second-choice antibiotics such as amoxicillin/cefalexin for 7 days.\n\n\n# NICE Guidelines\n\n[Click here for NICE CKS on urinary tract infection (lower) - women](https://cks.nice.org.uk/topics/urinary-tract-infection-lower-women/)\n\n[Click here for NICE CKS on pyelonephritis - acute](https://cks.nice.org.uk/topics/pyelonephritis-acute/)\n",
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"question": "A 25-year-old female presents to the Emergency Department feeling generally unwell, with nausea, vomiting and a high fever. She has no significant past medical history, but completed a 3 day course of antibiotics (trimethoprim) for a urinary tract infection yesterday.\n\nOn examination her abdomen is soft, but there is significant tenderness in her left flank.\n\nWhat is the most likely diagnosis?",
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"__typename": "QuestionChoice",
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"explanation": "Pain in fibromyalgia is generally more diffuse than the pain experienced in polymyalgia rheumatica. In addition, there is not usually the characteristic shoulder stiffness",
"id": "33402",
"label": "e",
"name": "Fibromyalgia",
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"explanation": "Osteoarthritis is not an inflammatory condition. The associated stiffness does not follow this classic \"worse in the morning for more than 1 hour\" pattern - there still tends to be morning stiffness, but this resolves more quickly, and the pain is often described as being worse after periods of physical activity. Additionally, this patient has had a relatively acute onset of these symptoms, whereas symptoms related to OA tend to be more insidious in onset over many months - years",
"id": "33399",
"label": "b",
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"__typename": "QuestionChoice",
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"explanation": "Adrenal insufficiency is associated with long term steroid use. PMR is treated with steroids, and therefore, these patients are at high risk of developing insufficiency during periods of intercurrent illness. However, at this point, the patient is yet to be diagnosed and commenced on any treatment",
"id": "33400",
"label": "c",
"name": "Adrenal insufficiency",
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"explanation": "PMR most commonly occurs in women over 50. The most characteristic symptoms include shoulder and hip girdle **stiffness and pain** - both of which can affect patients ability to do their daily activities - and which classically inhibit a patient from standing from a seated position. Other common features of the condition which are mentioned in this stem include fatigue and low-grade fever. PMR is a systemic inflammatory condition - the associated stiffness is worse in the morning (lasting for 1 hour or more) - as is the case for most inflammatory rheumatological conditions",
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"explanation": "GCA is an _associated condition_ often co-occurring in patients with polymyalgia. It presents with unilateral symptoms of jaw claudication, headache and scalp tenderness which can progress to visual loss if not identified and treated",
"id": "33401",
"label": "d",
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"comment": "but she has muscle pain how is that pmr?",
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"comment": "Muscle pain and stiffness are possible presentations, the key differentiator between myositis and PMR is functional weakness",
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"explanation": "# Summary\n\nPolymyalgia rheumatica is a systemic inflammatory condition characterised by pain and stiffness of the neck, shoulders and pelvis. It is primarily a disease of older age, and particularly affects people of Northern European descent. Systemic symptoms include weight loss, low-grade fevers, fatigue and anorexia. Diagnosis is essentially clinical and is supported by responsiveness of steroid treatment, however patients should all have baseline bloods and a urine dipstick to rule out differentials. Most patients can be managed in primary care with oral prednisolone, however those with atypical features or a poor response to steroids should be referred to rheumatology for further assessment. \n\n# Definition\n\nPolymyalgia rheumatica (PMR) is a chronic inflammatory condition which presents with stiffness and pain of the proximal large joints. \n\n# Epidemiology\n\n- PMR has a prevalence of approximately 1% in the UK\n- Incidence increases with age, peaking in those aged 70-80 years old\n- PMR is very rare in the under 50s\n- Women make up the majority of cases\n- Incidence is significantly higher in patients with Northern European ancestry \n- Approximately 15-20% of patients with PMR develop giant cell arteritis (see separate topic), and PMR affects up to 60% of patients with giant cell arteritis\n\n# Signs and Symptoms\n\n- The key symptom is bilateral shoulder, neck and pelvic girdle pain \n- Joints feel stiff, especially after rest or sleep, and movement worsens pain\n- Pain may radiate to the elbows or knees\n- Systemic symptoms are common, including:\n- Low-grade fevers\n- Loss of appetite \n- Weight loss\n- Malaise\n- Depression\n- On examination, muscle power is usually preserved (unless there is disuse atrophy from prolonged symptoms)\n- Active range of motion may be limited by pain and stiffness\n- Some patients may have associated swelling and pain in peripheral joints (e.g. wrists and ankles) - this is usually asymmetrical \n- Hands and feet may be swollen with pitting oedema\n- Carpal tunnel syndrome may be present\n\n# Differential Diagnosis\n\n- **Myositis** is often painless but associated with prominent muscle weakness on examination; skin changes are seen in dermatomyositis and CK will be significantly increased\n- **Rheumatoid arthritis** causes joint deformities, primarily affecting the small joints of the hands and feet rather than the larger proximal joints affected in PMR\n- **Malignancy** can cause similar systemic features of weight loss and low-grade fevers; an apical lung cancer may cause shoulder pain (Pancoast tumour) and bone pain is seen in myeloma\n- **Osteoarthritis** also causes joint pain and stiffness, more likely to involve hands, knees, hips and spine\n- **Frozen shoulder** may sometimes be bilateral and causes pain and stiffness with limited range of motion\n- **Chronic infections** such as tuberculosis or infective endocarditis cause similar systemic features and may present non-specifically\n- **Hypothyroidism** also causes fatigue and myalgia; other symptoms include weight gain and constipation\n- **Osteomalacia** causes bone pain and proximal muscle weakness due to vitamin D deficiency\n\n# Investigations \n\nPMR is fundamentally a clinical diagnosis which is supported by resolution of symptoms with steroid treatment.\n\nHowever, given the wide variety of differentials, basic investigations should be undertaken in all patients as follows:\n\n- **Urine dipstick** may be positive for blood due to myoglobin released in myositis\n- **ESR** and/or **CRP** are usually moderately raised in PMR\n- **FBC** - raised white cells may indicate infection, anaemia may be seen in malignancy or due to chronic disease\n- **U&Es** may show renal impairment in myeloma or infection\n- **LFTs** may be deranged e.g. due to metastatic cancer or a high ALP in osteomalacia\n- **Bone profile** may show high calcium in myeloma, or low calcium in osteomalacia\n- **Creatine kinase** will be raised in myositis \n- **Thyroid function tests** for hypo or hyperthyroidism\n- **Protein electrophoresis** to screen for myeloma; **urine Bence Jones protein** should be considered\n- **Rheumatoid factor** as a screen for rheumatoid arthritis, **ANA** and **anti-CCP** antibodies should also be sent if there is clinical suspicion\n- **HbA1c** prior to starting steroids due to their impact on blood glucose control\n- **Chest X-ray** may be indicated if there is suspicion of tuberculosis or lung cancer\n\n# Management\n\n- Patients with core symptoms of PMR, no atypical features and no suspicion of differentials after initial investigations should be started on steroids in primary care\n- 15mg of oral prednisolone once a day is the usual regimen\n- Patients should be reassessed after a week to assess treatment response, and ESR/CRP should be rechecked at 3-4 weeks\n- Consider weaning steroids at 3 weeks - this should be done slowly with close monitoring \n- Usually patients require steroids for 1-2 years\n- Safety-net patients for the risk of giant cell arteritis and advise them to seek urgent medical attention if symptoms develop\n\nImportant management considerations when starting long-term steroids include:\n\n- Give patients a steroid card\n- Advise never to stop steroids suddenly due to the risk of adrenal insufficiency\n- If they are unable to take tablets (e.g. due to vomiting) they need to seek urgent medical advice\n- Explain the risk of immunosuppression and check vaccination status - advise seeking urgent medical advice in patients not immunised if they are exposed to chickenpox, shingles or measles\n- Consider starting bone protection with bisphosphonates +/- vitamin D and calcium supplementation; this should be continued for the duration of steroid treatment before reassessing fragility fracture risk\n- Assess the risk of peptic ulceration and consider starting a proton pump inhibitor for gastric protection\n- Monitor blood pressure and glucose (as hypertension and hyperglycaemia are common side effects)\n\nThe following patients should be referred to rheumatology:\n\n- Atypical clinical features:\n- Aged under 60\n- No shoulder/pelvic girdle pain\n- No stiffness lasting > 45 minutes on waking/after rest\n- Chronic onset of symptoms\n- Red flag signs or symptoms e.g. weight loss or night pain\n- Atypical inflammatory markers i.e. normal or very high (ESR > 100 mm/hour)\n- Limited or no response to steroid treatment\n- Steroids required for over 2 years\n- Unable to wean steroids without relapses\n- Significant adverse effects (or high risk of these) with steroids\n- Suspected giant cell arteritis (ideally requires same day assessment with same day ophthalmology assessment also if there is visual loss)\n\nSecondary care management options for PMR include methotrexate and azathioprine, and physiotherapy may also be of benefit.\n\n# Prognosis\n\n- Generally prognosis is good, with most patients rapidly responding to steroids\n- However relapse is common when steroids are weaned\n- Usually patients require 1-2 years of steroids \n- Some may need many years or even lifelong steroid treatment\n\n# NICE Guidelines\n\n[NICE CKS - Polymyalgia Rheumatica](https://cks.nice.org.uk/topics/polymyalgia-rheumatica/)\n\n# References\n\n[Patient UK - Polymyalgia Rheumatica](https://patient.info/doctor/polymyalgia-rheumatica-pro)\n\n[British Society for Rheumatology - Treatment of polymyalgia rheumatica](https://academic.oup.com/rheumap/article/8/1/rkae002/7606885)",
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"question": "A 59-year-old woman presents to the GP with two weeks of stiffness in her shoulders and hips which she describes as worse in the morning. Initially, she recalls thinking she had the flu, as she had myalgia, a low-grade fever and significant fatigue. However, these symptoms have not improved, and she is now anxious that there may be something more sinister going on. The stiffness and muscle pain is so severe she can no longer stand from sitting independently, or open the top cupboards in her kitchen.\n\nWhat is the most likely diagnosis?",
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"explanation": "This patient does have some risk factors for gout, in that the condition is more common in men of an older age. However, gouty pain tends to have a more acute course of onset, often coming on over several hours - days rather than months. In addition, you would expect some mention of the joint being red or hot, as is the case in flares of crystal arthropathies. Gout can affect any joint, but it most commonly affects the first metatarsophalangeal joint (great toe)",
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"explanation": "Osteoarthritis is a disease of \"wear and tear\". It is more common in those aged over 50 with risk factors that increase weight loading strain on the joint - these include obesity, sports/occupation and previous trauma to the joint. It most commonly affects the knees, hips, hands and spine. It can be differentiated from rheumatoid arthritis (RA) when occurring in the hands by its tendency to spare the metacarpophalangeal (MCP) joints",
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"explanation": "Structural damage to the soft tissues in the knee are generally acute injuries associated with a trauma event. This is not the case in this history. Additionally, you would have to be unlucky to injure your menisci in both knees simultaneously!",
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"explanation": "RA is an inflammatory arthritis and is, therefore, most classically associated with morning stiffness lasting longer than 1 hour. Additionally, RA tends to be distributed differently, having a strong propensity for affecting the hands, in particular, the metacarpophalangeal (MCP) joints, whilst sparing the distal interphalangeal (DIP) joints. This is compared to OA, which tends to occur more in weight-bearing joints, including the hips and knees, spine and hands (in a different distribution to RA)",
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"explanation": "Psoriatic arthritis is again inflammatory in nature and associated with morning stiffness lasting longer than 1 hour. It is associated with psoriasis; however, arthritis can occur without any skin involvement - it would be important to look for associated family history also. It is also associated with nail changes not present in other forms of arthritis, including pitting of the nails and onycholysis",
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"comment": "Is Osteoarthrititis symmetric?",
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"comment": "yes bro\n",
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"explanation": "# Summary\n\nOsteoarthritis (OA) is a chronic, degenerative joint disease characterised by loss of articular cartilage, remodelling of bone with osteophyte formation and mild synovitis. The main risk factor is older age, although obesity, joint injury and genetics also contribute. Presentation is with gradual onset pain that is worse with activity, with associated functional limitations. The most commonly affected joints are the knees, hips and small joints of the hands. Diagnosis is clinical, and severity of disease on X-ray does not correlate well with severity of symptoms. Management should be individualised, with important components being exercise, simple analgesia and optimisation of risk factors (such as maintaining a healthy weight). Where there is ongoing pain and disability, options include intra-articular steroid injections and surgical intervention (such as joint replacement).\n\n# Definition\n\nOsteoarthritis (OA) is the commonest form of arthritis, which is characterised by degenerative changes affecting the entirety of joints affected. Cartilage is lost, the subchondral bone becomes sclerosed with formation of osteophytes and subchondral cysts and there is inflammation of the synovial membrane lining the joint capsule (synovitis). \n\n# Epidemiology\n\n- Approximately 10 million people in the UK have osteoarthritis\n- More women than men are affected\n- Average age of onset is 55 \n- The commonest joint affected is the knee, followed by the hip then the hand\n\n# Aetiology\n\nOsteoarthritis develops due to a combination of factors, with important contributors including:\n\n- Older age\n- Female sex\n- Overweight or obesity\n- Family history of OA\n- Previous joint injury\n- Joint damage due to inflammation (e.g. in patients with inflammatory arthritis)\n- Physical inactivity and reduced muscle strength\n- Low bone density \n- Deformities such as development dysplasia of the hip or leg length discrepancy\n- Stresses on joints due to occupational factors (e.g. repetitive squatting or kneeling) or exercise\n\n# Signs and Symptoms\n\nKey symptoms include:\n\n- Pain in the affected joint exacerbated by use\n- Pain may radiate e.g to the thigh, knee and ankle in hip OA, or to the wrist in hand OA\n- Joints may feel stiff (although prolonged morning stiffness is suggestive of inflammatory arthritis)\n- Functional limitations such as difficulty opening jars (hand OA) or mobilising (knee or hip OA)\n- Locking or giving way of the knee\n\nExamination findings include:\n\n- Restricted and painful range of motion (e.g. in hip OA internal rotation with the hip flexed is particularly painful)\n- Crepitus (friction between bone and cartilage) \n- Affected joints may appear swollen or enlarged\n- A small effusion may form, especially when the knee is affected\n- Synovitis may present with mild soft tissue swelling, tenderness and warmth\n- Muscle wasting and weakness can result from disuse atrophy\n- Joint instability\n- An antalgic gait (\"limping\") in knee OA\n- Trendelenburg gait in hip OA (due to weak abductors patients lurch towards the affected hip)\n- Deformities, including:\n- Heberden's nodes (bony nodules over the distal interphalangeal joints) \n- Bouchard's nodes (bony nodules over the proximal interphalangeal joints) \n- Fixed flexion of the first carpometacarpal joint with hyperextension of the distal joints\n- This may lead to squaring of the joint with subluxation and remodelling\n- Ulnar or radial deviation of joints in the hand may occur\n- In severe hip OA the leg may be shortened due to fixed flexion and external rotation\n- Varus (most commonly) or valgus deformities of the knees \n\n# Differential Diagnosis\n\n- **Inflammatory arthritis** such as rheumatoid arthritis, ankylosing spondylitis; pain that improves with activity and morning stiffness lasting over 30 minutes are differentiating factors, systemic symptoms such as malaise and weight loss may be present\n- **Septic arthritis** is an important differential for all patients presenting with an acutely painful swollen joint (which may occur in an acute flare of osteoarthritis); patients may be systemically unwell with fevers\n- **Fracture** e.g. of the tibial plateau may mimic OA symptoms of pain and limited mobility; usually the patient is unable to weight bear with swelling of the affected area; a history of trauma should be elicited\n- **Malignancy** including bone metastases, multiple myeloma or sarcoma may cause mechanical pain leading to functional limitations; red flags include weight loss, night sweats, persistent pain not relieved by rest and night pain\n- **Greater trochanteric pain syndrome** most commonly occurs in middle-aged women and causes lateral hip pain and tenderness worsened by activity; it may also radiate to the lateral knee\n- **Iliotibial band syndrome** presents with lateral knee pain worse with activity, which is often accompanied by clicking or clunking sounds when the knee is moved; occurs most commonly due to repetitive knee flexion e.g. cyclists or runners \n- **Meniscal tear** may occur after an injury involving a twisting or pivoting movement; similar symptoms of pain, swelling, locking and giving way of the knee and range of motion may be limited on examination\n- **Trigger thumb** may mimic OA of the hand with pain, clicking and catching when the thumb is flexed; a nodule may be palpable in the tendon\n- **Ganglion cysts** occur more commonly in people with OA and present as soft tissue swellings e.g. at the base of the thumb; often asymptomatic but may cause pain and limit movement of the joint\n\n# Investigations\n\nDiagnosis of OA is clinical and can be made without any investigations in a patient of 45 or older if there are no features suggesting another underlying cause of symptoms.\n\nIf there is diagnostic uncertainty or a rapid deterioration in symptoms, **X-rays** of affected joints may be of use. Typical findings can be remembered with the mnemonic \"LOSS\":\n\n- **L**oss or narrowing of joint space due to thinning of cartilage\n- **O**steophytes i.e. formation of new bony spurs at the joint margins\n- **S**ubchondral sclerosis i.e. increased bone density beneath the cartilage\n- **S**ubchondral cysts which are fluid-filled sacs in the subchondral bone\n\n[lightgallery]\n\nHowever, severity of OA features on X-ray may not correlate well with severity of clinical disease.\n\nOther investigations if the diagnosis is in doubt should be targeted to the differential suspected, and may include:\n\n- Further imaging such as MRI to look for ligament or cartilage damage (e.g. a meniscal tear)\n- Joint aspiration with synovial fluid analysis to exclude septic arthritis or crystal arthritis\n- Blood tests for inflammatory markers, rheumatoid factor and anti-CCP (for example) if rheumatoid arthritis is suspected\n\nBaseline bloods for renal function and full blood count should be considered in all patients starting NSAID treatment, especially older patients who are at higher risk of adverse effects.\n\n# Management\n\n**Conservative management:**\n\n- Patient education and advice on self-care e.g. appropriate footwear\n- Weight loss advice and signposting to services in patients with excess body weight\n- Exercise has many benefits including strengthening muscles, improving fitness, reducing pain and improving function\n- Options include online fitness programmes designed for people with arthritis, physiotherapy and supervised exercise sessions\n- Physiotherapy services may also be able to offer manual therapies and joint supports such as braces or splints to reduce load and improve instability\n- Occupational health input may be needed in patients with functional impairment to assess their working environment and suggest adaptations\n- Patients should be asked about psychosocial stressors and support offered e.g. for associated depression and anxiety\n- Occupational therapy input may be helpful to advise on aids and devices to assist with activities of daily living (e.g. walking sticks, sock aids, grab rails, tap turners)\n- Podiatry input may be useful to assess the biomechanics of joint pain and advise on orthotic devices such as insoles\n- Referral to a pain management service may be appropriate for patients who have not responded to maximal medical (and if appropriate, surgical) management of OA\n- Assess falls risk and consider referral to specialist services for patients at risk (e.g. those with abnormal gait or balance, or who have had a fall in the last year)\n\n**Medical management:**\n\n- First-line analgesia is with topical NSAIDs (such as ibuprofen gel) - patients should be made aware that some systemic absorption may occur\n- If this is ineffective or unsuitable, oral NSAIDs should be considered (with a PPI for gastroprotection if there are risk factors for gastrointestinal side effects)\n- Paracetamol or weak opioids (e.g. codeine) may also be used in the short-term\n- Topical capsaicin is another option, especially for knee OA\n- Intra-articular steroid injections may be considered if other treatments are not effective, and/or to enable therapeutic exercise\n\n**Surgical management:**\n\n- Patients with OA of the hip, knee or shoulder who have symptoms significantly impacting quality of life despite optimal medical management should be considered for orthopaedic referral\n- The usual operation offered is an arthroplasty (joint replacement)\n- Rehabilitation before and after surgery is key to optimising outcomes\n\n# Complications\n\n- Joint deformities (as above)\n- Increased risk of falls\n- Functional limitations, e.g. hand OA may making writing, turning keys or fasting buttons challenging\n- Reduced mobility \n- Sleep difficulties\n- Low mood and anxiety\n- Chronic pain\n\n# Prognosis\n\n- Not all cases of OA are progressive and the disease course is variable\n- OA of the hands generally has a good prognosis, especially interphalangeal joint involvement\n- Hip OA has a poorer prognosis with many patients requiring arthroplasty\n- Knee arthroplasties for OA are also common however many patients' symptoms improve or remain stable with time \n- Intermittent flares of OA may occur, where symptoms increase in intensity suddenly\n- Flares tend to last for a few days before improving\n\n# NICE Guidelines\n\n[NICE CKS - Osteoarthritis](https://cks.nice.org.uk/topics/osteoarthritis)\n\n[NICE - Osteoarthritis in over 16s: diagnosis and management](https://www.nice.org.uk/guidance/ng226/)\n\n# References\n\n[WHO fact sheet - Osteoarthritis](https://www.who.int/news-room/fact-sheets/detail/osteoarthritis)\n\n[BNF Treatment Summaries - Osteoarthritis](https://bnf.nice.org.uk/treatment-summaries/osteoarthritis/)\n\n[Patient UK - Osteoarthritis](https://patient.info/doctor/osteoarthritis-pro)",
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"question": "A 63-year-old man presents to his GP with worsening pain in both knees over a period of 6 months. The pain is worse on physical activity and limits his independence as he lives in a second-floor flat and now struggles to get up and down the stairs. He has a past medical history of type 2 diabetes, hypercholesterolaemia and a body mass index (BMI) of 36.\n\nWhat is the most likely diagnosis?",
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"explanation": "In early psoriatic arthritis, there may be no visible change on radiograph, except for some soft tissue swelling due to the inflammatory nature of the condition. Late in the disease course, there is classical osteolysis with new bone formation around the joint margins, which causes a \"pencil-in-cup deformity\". Over time the arthritis can progress into \"arthritis mutilans\"",
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"label": "b",
"name": "Psoriatic arthritis",
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"explanation": "SLE can cause arthritis, particularly of the hands and feet, however this is classically \"non-deforming\" which means you would not see these destructive changes on imaging",
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"label": "e",
"name": "Systemic lupus erythematosus (SLE)",
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"explanation": "X-rays of patients with RA may show loss of joint space with peri-articular osteopenia, bony erosions around the joint margins and associated soft tissue swelling. Late on in the disease course, they may reveal joint subluxation. In this radiograph, you can see evidence of all of these features - in keeping with the history of a delayed presentation and relatively advanced disease. Characteristic of rheumatoid, there is also resultant ulnar deviation at the metacarpophalangeal joints and Z thumb deformity",
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"name": "Rheumatoid arthritis (RA)",
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"explanation": "Ankylosing spondylitis tends to present with inflammatory **back pain** in young patients, usually in their late teens and early 20s. It is also more common in men, compared to RA which is more common in women",
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"explanation": "X-rays in OA show **L**oss of joint space, **O**steophytes, **S**ubchondral cysts and **S**ubarticular sclerosis (helpful acronym to remember these features is **LOSS**). It does not cause the classic ulnar deviation or erosive changes as seen in rheumatoid arthritis",
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"comment": "Is this the correct XR for this question? Can't seem to see any of the signs, especially not any ulnar deviation, unless I'm just being really dumb haha",
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"comment": "Spend more time on x rays",
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"comment": "Another unhelpful smartass.\n\nThis is a tricky question which require close examination of the XR to see the points made. If you don't have a particularly bright screen this may be a problem. \n\nIn this case it might have been better to also weight the decision more based on the patient history. ",
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"explanation": "# Side effects of corticosteroids\n\n**Corticosteroids** (think CORTICOSTEROIDS):\n\n- Cushing's syndrome\n- Osteoporosis\n- Retardation of growth\n- Thin skin, easy bruising\n- Immunosuppression\n- Cataracts and glaucoma\n- Oedema\n- Suppression of HPA axis\n- Teratogenic\n- Emotional disturbance (including psychosis\n- Rise in BP\n- Obesity (truncal)\n- Increased hair growth (hirsutism)\n- Diabetes mellitus\n- Striae\n\n# Side effects of NSAIDs\n\n- Indigestion\n- Peptic ulcer disease,\n- Increased risk of venous thrombo-embolus\n- Peripheral oedema\n- Slightly increased risk of stroke and heart attack\n\n# Side effects of Methotrexate\n\n- Gastro-intestinal disturbance\n- Folate deficiency - anaemia\n- Immunosuppression\n- Pulmonary fibrosis\n- Liver toxicity\n- Interstitial pneumonitis\n- Rash\n- Teratogenicity - Methotrexate is contraindicated during conception and pregnancy. The recommendation is a washout of a few months (at least 3 months) before conception. In the event of a disease flare, low-dose steroids are thought to be relatively safe. Note that high doses are associated with a small increased risk of the child having a cleft palate.\n\n# Side effects of Sulfasalazine\n\n- Myelosuppression\n- Nausea\n- Rash\n- Oral ulcers\n- Decreased sperm count\n\n# Side effects of Hydroxychloroquine\n\n- Retinopathy\n- Rash\n\n# Side effects of Biologic therapy (e.g. etanercept, infliximab, adalimumab)\n\n- Immunosuppression\n- Reactivation of TB\n- Allergic reaction, reaction at infusion site\n\n# Side effects of Gold\n\n- Myelosuppression\n- Renal toxicity (Nephrotic syndrome)\n- Mouth ulcers\n- Photosensitivity\n- Chrysiasis (skin discolouration)",
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"question": "A 52-year-old woman presents to her GP with worsening pain and deformity in both her hands. The patient has recently moved to the UK and previously had poor access to healthcare. The pain first started 15 years ago and is worse in the morning, with associated stiffness which does not ease until the middle of the day.\n\nA plain x-ray of her right hand is shown below:\n\n[lightgallery]\n\nWhat is the most likely diagnosis?",
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"explanation": "The patient will need to be admitted and will receive at least 48 hours of intravenous antibiotics, however, this is not the best option - it does not address the need for other items within the sepsis 6, including taking blood cultures and giving fluids",
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"name": "Admit patient to complete a minimum of 48 hours of intravenous antibiotics",
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"explanation": "Giving beta-blockers to lower the heart rate would be unhelpful here acutely - it would not address the cause of the tachycardia which is ultimately sepsis from severe infection. In some circumstances infection can trigger tachyarrhythmias which do require rate control, however nothing in the stem suggests that this has occurred",
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"name": "Give beta-blockers to help control his tachycardia",
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"explanation": "Young patients often do receive significant volumes of fluid resuscitation quickly when unwell, however, this is not the single best answer here. This option does not address the need for other items within the sepsis 6, including taking blood cultures and giving intravenous antibiotics",
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"name": "Give 1 litre of 0.9% sodium chloride over 1 hour and then return to reassess the patient",
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"explanation": "This patient is clearly very unwell and triggering as potentially septic within all of his observation parameters - he requires inpatient admission, intravenous antibiotics and careful monitoring during this stage of his illness. Additionally, it's important to be aware that young patients can tend to underscore on the CURB-65 model for assessing CAP severity - in these circumstances, it is important to also look at any oxygen demand and consider co-morbidities when assessing their risk of deterioration",
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"explanation": "This patient has a diagnosis of community acquired pneumonia (CAP) from his history and chest x-ray. Respiratory rate of >20 breaths per minute, heart rate of >90 beats per minute, low oxygen saturations and hypotension are all markers of sepsis, and this patient's presentation should prompt immediate action with \"sepsis 6\". The sepsis 6 involves taking **blood cultures** and a blood gas for a **lactate** measurement, giving **oxygen** and **intravenous antibiotics and fluids**, as well as careful monitoring of **fluid input/output** (usually with a catheter) all within 1 hour of recognition of sepsis. This is evidence-based and shown to improve mortality",
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"name": "Perform the \"sepsis 6\" within the next 1 hour",
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"comment": "But his CURB-65 is 0 = outpatient care??",
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"comment": "Man is septic \n",
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"comment": "Did you look at his Obs Acute Botox???????????",
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"comment": "what is that on his XR",
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"comment": "right middle lobe consolidation indicative of CAP",
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"explanation": "# Summary\n \nSepsis is a syndrome characterised by life-threatening organ dysfunction that occurs due to a dysregulated response to infection. Key signs and symptoms include fever, altered mental state, tachycardia, hypotension and dehydration, as well as localising signs of infection. The \"Sepsis Six\" bundle is used to guide care in the first hour following recognition of sepsis; this involves taking blood tests including cultures, a blood gas to measure lactate and monitoring urine output, and giving oxygen, IV broad-spectrum antibiotics and IV fluids.\n \n# Definition\n\nThe terminology used to describe sepsis has changed, with terms like \"severe sepsis\" and SIRS (systemic inflammatory response syndrome) no longer in use.\n\n**Sepsis** is defined as a syndrome of life-threatening organ dysfunction due to a dysregulated host response to infection.\n\n**Septic shock** is another term used to describe some patients with sepsis who are at greater risk of death. To be classified as having septic shock, patients need to be persistently hypotensive, requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more **and** have a lactate of over 2 mmol/L despite adequate fluid resuscitation. \n\n# Epidemiology\n\n- Due to variations in coding and definitions, statistics related to admissions to hospital with sepsis tend to be inconsistent\n- Approximately 200,000 people are admitted to hospital with sepsis per year\n- Approximately 20% of these (40,000 per year) require intensive care admission\n- Mortality is also approximately 20%, with deaths estimated at up to 48,000 per year in the UK\n- Men are more commonly affected than women\n- Patients at the extremes of age (infants under a year and people aged over 75) are more at risk\n\n# Aetiology\n\n- The commonest sources of infection are respiratory, genitourinary, renal and gastrointestinal \n- Most causative pathogens are bacteria, although fungal, parasitic and viral infections can also lead to sepsis\n- The commonest organisms identified are Staphylococcus aureus, Escherichia coli and Pseudomonas species\n- In 50% of sepsis cases, no causative pathogen is identified \n\n**Risk factors** for sepsis include:\n\n- Pregnancy\n- Recent miscarriage or abortion\n- Frailty\n- Immunocompromise due to chronic comorbidities e.g. HIV, diabetes, sickle cell disease\n- Immunosuppression secondary to medications e.g. chemotherapy, steroids\n- Recent surgery or trauma\n- Skin breaks or infections\n- Drug or alcohol misuse\n- Indwelling lines or catheters\n\n# Signs and Symptoms\n\nSymptoms include:\n\n- General malaise\n- Fevers, sweats or chills\n- Localising signs of infection e.g. rashes, dysuria\n- Decreased urine output\n- Confusion\n- Breathlessness\n- Nausea and vomiting\n- Myalgia\n \nOn examination, signs include:\n \n- Tachycardia\n- Hypotension\n- Pyrexia or hypothermia\n- Dehydration e.g. dry mucous membranes\n- Altered mental state including delirium\n- Irritability\n- Respiratory distress e.g. tachypnoea, accessory muscle usage\n- Cyanosis and hypoxia\n- Delayed capillary refill time\n- Cool extremities\n- Skin appears mottled or ashen\n\n# Differential Diagnosis\n\n- **Acute alcohol withdrawal** causes altered mental state, tachycardia and sweating; patients are usually tremulous and may have withdrawal seizures if severe\n- **Acute haemorrhage** may cause hypovolaemic shock with signs of shock including tachycardia, hypotension, delayed capillary refill and cool extremities; differentiated by signs of bleeding which may be overt or more subtle (e.g. abdominal pain)\n- **Diabetic ketoacidosis** causes malaise, tachypnoea (with Kussmaul breathing), dehydration and confusion; metabolic acidosis may be seen in both but in diabetic ketoacidosis glucose will be very high\n- **Pulmonary embolism** may cause tachycardia, hypotension, respiratory distress and a low-grade fever; may have haemoptysis and pleuritic chest pain (which could also be seen in sepsis secondary to pneumonia) - CTPA can be used to differentiate if unclear\n- **Thyrotoxicosis** produces similar symptoms of confusion and fevers and signs of tachycardia; thyroid function testing shows high T4 and suppressed TSH\n- **Drug reactions** e.g. neuroleptic malignant syndrome - shares features of fever, confusion, labile blood pressure and sweating; differentiated by a recent history of antipsychotic use, no localising signs of infection\n\n# Investigations \n\nThe **Sepsis Six** involves taking three key measures (as well as giving three key treatments):\n\n- **Blood cultures** ideally prior to antibiotic administration\n- **Lactate** (i.e. a blood gas - venous or arterial)\n- **Urine output** (which may involve inserting a urinary catheter)\n\nOther **bedside tests** should include:\n\n- **Capillary blood glucose** as hypo or hyperglycaemia may contribute to confusion\n- **Urine pregnancy test** in women of childbearing age\n- **Urine dip** and send for **MC&S** looking for evidence of urinary tract infection\n- **ECG** as in any acutely unwell patient, looking for arrhythmias and ischaemic changes\n\n**Blood tests** should include:\n\n- **FBC** and **CRP** for inflammatory markers\n- **U&Es** looking for evidence of acute kidney injury\n- **LFTs** as a baseline prior to giving antibiotics, may be deranged in sepsis\n- **Coagulation screen** as this may be deranged in sepsis\n\n**Imaging** should include:\n\n- **Chest X-ray** as part of a septic screen\n\nOther investigations should be targeted at a suspected underlying cause, e.g. respiratory or wound swabs, other imaging e.g. a CT abdomen or echocardiogram or special tests e.g. lumbar puncture when stable.\n\n# Management \n \nThe three things that should be given as part of the **Sepsis Six** are:\n\n- IV fluid resuscitation (usually a 500ml bolus over 15 minutes initially)\n- Supplementary oxygen to target saturations of 94-98% (88-92% if at risk of type 2 respiratory failure)\n- Broad-spectrum IV antibiotics (as per local guidelines)\n\nOther **conservative** management considerations involve:\n\n- Close monitoring of observations, fluid balance, clinical condition and bloods including serial lactate measurement\n- Early escalation for senior review and inform intensive care as may require interventions such as inotropes or vasopressors\n\nOther **medical** management involves:\n\n- Modify antibiotic therapy if a source of infection is identified or microbiological results become available\n- Further IV fluids may be required however this should be done with careful fluid balance monitoring\n\n**Surgical** management involves:\n\n- Source control, e.g. draining abscesses or debriding infected tissue\n- Infected devices may need to be removed\n \n# Complications\n\n- **Multi-organ failure** including renal failure, heart failure, acute respiratory distress syndrome and cholestasis\n- **Coagulopathy** including disseminated intravascular coagulation\n- **Delirium** which may be associated with long-term cognitive impairment e.g. difficulty concentrating and memory loss\n- **Mental health impacts** including anxiety, depression and post-traumatic stress disorder\n- **Secondary infections** which are often hospital-acquired\n- **Polyneuropathy** i.e. critical illness polyneuropathy, characterised by generalised weakness and sensory loss\n- **Death**\n\n# Prognosis\n\n- Overall mortality has been estimated at around 20-30%\n- This increases to 64% in patients aged over 85 years\n- Patients with septic shock also have higher mortality (40-60%) \n- Risk of death in survivors remains raised after recovery (15% of sepsis survivors die within a year of discharge, with 6-8% more dying each year for the following 5 years) \n\n# NICE Guidelines\n\n[NICE - Sepsis: recognition, diagnosis and early management](https://www.nice.org.uk/guidance/ng51)\n\n[NICE CKS - Sepsis](https://cks.nice.org.uk/topics/sepsis/)\n\n# References \n \n[UK Sepsis Trust](https://sepsistrust.org/)\n\n[Patient UK - Sepsis](https://patient.info/doctor/sepsis-septicaemia-pro)",
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"question": "A 31-year-old man presents to the Emergency Department with shortness of breath, fever and a cough productive of green sputum. This has been worsening over the course of 3 days, however, today he has been feeling very weak and faint, so decided to seek medical attention. His observations are as follows:\n\nRespiratory rate 24 breaths per minute, oxygen saturations 95% on 2 litres of oxygen by nasal cannula, heart rate 123 beats per minute, blood pressure 91/63 and temperature 38.4. His Glasgow Coma Score (GCS) is 15.\n\nHis chest x-ray is displayed below:\n\n[lightgallery]\n\nWhat is the most appropriate next step in the management of this patient?",
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"explanation": "Ischaemic leg pain or \"claudication pain\" is like angina of the leg, and classically would occur on walking and be alleviated by rest. There is no mention of the pain being exertional in the stem",
"id": "33422",
"label": "e",
"name": "Intermittent claudication",
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"explanation": "In a ruptured popliteal cyst you would usually expect a more acute onset of symptoms following cyst rupture. Additionally, there may also be more localisation of the pain to the popliteal region, or some mention of a swelling within the popliteal region preceding the lower leg swelling",
"id": "33421",
"label": "d",
"name": "Ruptured popliteal cyst (Baker's cyst)",
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"explanation": "In a simple muscular injury, the patient would experience pain but would be unlikely to have significant swelling or redness in the affected limb. There would also likely be a notable trauma associated with this, in that a certain movement or event would likely have happened, followed by sudden onset of the pain. This is not the case in DVT, where symptoms develop more slowly",
"id": "33420",
"label": "c",
"name": "Muscular injury to the calf",
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"explanation": "Cellulitis can cause swelling and redness in the lower limb, however you would expect further evidence of infection. Examples of other features you may see to suggest cellulitis include fever, the leg being hot to touch, a mention of the redness spreading progressively or the patient feeling generally unwell",
"id": "33419",
"label": "b",
"name": "Cellulitis",
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"explanation": "The patient has a risk factor for thrombus formation here in his history, in that he has recently returned from Australia, which would be via a long haul flight. The symptoms he is experiencing, of leg pain and swelling alongside some redness, are classic for DVT and must be identified promptly to avoid delay in treatment",
"id": "33418",
"label": "a",
"name": "Deep Vein Thrombosis (DVT)",
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"explanation": "# Summary\n\nDeep Vein Thrombosis (DVT) refers to intra-luminal occlusion of a deep vein with a blood clot, obstructing blood flow. Commonly these occur in the legs although other veins may be affected. DVTs are categorised as \"provoked\" if a transient risk factor such as pregnancy or surgery is identifiable, and \"unprovoked\" if not. Key signs and symptoms include leg pain, unilateral erythema, warmth and swelling and distention of superficial veins. The Wells score is commonly used to assess how likely a DVT is based on clinical findings and risk factors; this guides whether a D-dimer blood test or a Doppler ultrasound should be offered first-line. Management is usually with anticoagulation; in rare cases other strategies such as mechanical thrombectomy and IVC filters may be required.\n \n# Definition\n \nA deep vein thrombosis (DVT) is a blood clot or thrombus that blocks a deep vein, commonly in the legs or pelvis. \n \n# Epidemiology\n \n- Venous thromboembolism (which includes both DVT and pulmonary embolism) is common, affecting 1-2 per 1000 people per year\n- Two-thirds of cases are DVTs and one-third are pulmonary emboli (PE), with DVT being the main risk factor for PE\n- It is particularly common in unwell patients in hospital, with an incidence of up to 37% in critically ill patients\n\n# Aetiology\n \nRisk factors for DVT can be remembered with the mnemonic **THROMBOSIS:**\n \n\n * **T**hrombophilia\n * **H**ormonal (COCP, pregnancy and the postpartum period, HRT)\n * **R**elatives (family history of VTE)\n * **O**lder age (>60)\n * **M**alignancy\n * **B**one fractures\n * **O**besity\n * **S**moking\n * **I**mmobilisation (long-distance travel, recent surgery or trauma)\n * **S**ickness (e.g. acute infection, dehydration)\n\n# Signs and Symptoms\n \n- Unilateral erythema, warmth, swelling and pain in the affected area\n- Pain on palpation of deep veins\n- Distention of superficial veins\n- Difference in calf circumference if the leg is affected\n - This should be measured 10cm below the tibial tuberosity\n - > 3cm difference between the legs is significant\n\n# Differential Diagnosis\n\n- **Cellulitis** also causes erythema, warmth, swelling and pain and often affects the legs, patients may have other signs of infection e.g. fevers and there may be an obvious wound or discharge\n- **Calf muscle tear** also causes swelling, erythema and pain; there will usually be a history of trauma immediately preceding the development of symptoms\n- **Superficial thrombophlebitis** often occurs in the lower limbs in association with varicose veins, however pain is localised to a thrombosed vein rather than there being generalised pain and swelling of the limb\n- **Compartment syndrome** can be differentiated by severe pain out of proportion to clinical signs, often preceded by traumatic injury\n\n# Investigations\n \nThe two-level DVT Wells score is used to risk-stratify patients into patients likely or unlikely to have a DVT as follows:\n\n**Add one point** for each of:\n\n- Active cancer (treatment within the last 6 months or palliative)\n- Paralysis, paresis, or recent plaster immobilisation of the legs\n- Recently bedridden for 3 days or more, or major surgery within the last 12 weeks\n- Localised tenderness along the distribution of the deep venous system\n- Entire leg is swollen.\n- Calf swelling at least 3 cm larger than asymptomatic side\n- Pitting oedema confined to the symptomatic leg\n- Collateral superficial veins\n- Personal history of DVT\n\n**Minus 2 points** if an alternative cause is considered at least as likely as a DVT.\n\nIf the score is **2 or more**:\n \n- DVT is **likely** and an ultrasound doppler of the proximal leg veins should be done within 4 hours\n- If this isn't possible within 4 hours, do a D-dimer test, start interim anticoagulation and arrange the doppler to happen within 24 hours\n \nIf the score is **1 or less**:\n \n- DVT is **unlikely** and a D-dimer should be sent\n- If the results cannot be obtained within 4 hours, offer interim anticoagulation whilst awaiting results\n- If the D-dimer is positive, do an ultrasound doppler of the proximal leg veins \n- If it is negative, anticoagulation should be stopped if it was started and an alternative diagnosis considered\n\n[lightgallery] \n\nD-dimer is not a specific test and is often raised in infection, trauma, malignancy, post-surgery or haemorrhage. \n\nNote that separate guidelines exist for pregnant and postpartum women - linked below in references.\n\n**Baseline blood tests** should be taken when anticoagulation is started, including a FBC, U&Es, LFTs and a coagulation screen. \n\n# Management\n \n- First-line anticoagulant medications are **DOACs** (e.g. apixaban, rivaroxaban)\n- If these are not suitable, second-line options include low molecular weight heparin (LMWH) for at least 5 days followed by dabigatran or edoxaban, or LMWH bridging with warfarin (with a target INR of 2.5)\n- Treatment duration should be at least 3 months for all patients, and 3-6 months for people with active cancer\n- At this point the risk of VTE recurrence should be weighed against the risks of continuing anticoagulation to make a decision about whether to continue\n- In cases of provoked DVTs (where a major transient risk factor is identifiable e.g. surgery), anticoagulation would usually be stopped at 3 months\n- In cases of unprovoked DVTs, consider testing for thrombophilia with antiphospholipid antibodies in patients who are stopping anticoagulation\n- Patients with unprovoked DVTs should be reviewed with baseline blood tests and an examination to investigate the possibility of an undiagnosed cancer - further investigations should be guided by the patient's signs or symptoms\n\n[lightgallery1]\n \n# Complications\n\n- Pulmonary embolism\n- Post-thrombotic syndrome (chronic venous hypertension post-DVT that may cause significant morbidity)\n- Complications of anticoagulation e.g. gastrointestinal bleeding\n\n \n# NICE Guidelines\n \n[NICE CKS - DVT](https://cks.nice.org.uk/topics/deep-vein-thrombosis/)\n\n[NICE - Venous thromboembolic diseases](https://www.nice.org.uk/guidance/ng158/)\n \n# References\n\n[RCEM Learning - Deep Vein Thrombosis](https://www.rcemlearning.co.uk/reference/deep-vein-thrombosis)\n\n[RCOG - Thromboembolic Disease in Pregnancy and the Puerperium](https://www.rcog.org.uk/media/wj2lpco5/gtg-37b-1.pdf)",
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"question": "A 40-year-old man presents to his GP with pain in his left leg which has been progressively worsening for two days. He has recently returned from a diving holiday in Australia and wonders if he injured the leg during diving, although he does not recall any particular episode of trauma.\n\nOn examination, the left calf is swollen and measures 4.5cm greater in diameter than the right calf. The left calf also appears slightly red.\n\nWhat is the most likely diagnosis?",
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"explanation": "In patients who have taken a staggered overdose first line treatment is with N-acetylcysteine regardless of the time from ingestion",
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"explanation": "Haemodialysis to remove the paracetamol and associated toxins from the blood may be needed rarely in very critical cases of extreme overdose",
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"explanation": "This is the correct course of action in patients with an overdose of <150mg/kg that has been ingested within a 1 hour period - not staggered, as is the case in this patient. In these circumstances, you can wait until you have a blood paracetamol level and treat only if this is above the \"treatment line\" on the paracetamol overdose nomogram. If any doubt remains about the dosage or timescale of the overdose, the safest option is always to treat empirically with N-acetylcysteine",
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"explanation": "Activated charcoal can be considered in patients who present very soon following ingestion of their overdose (within 1 hour of ingestion); however it should not be given in patients where there is any concern regarding their airway (if they have a reduced Glasgow Coma Score of <8 this indicates they cannot protect their own airway, or if they present as very drowsy)",
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"explanation": "As per the Kings College Criteria, a hyper-acute liver transplant is indicated in patients with significant acidosis of pH <7.30 **OR** all 3 of: coagulopathy with INR >6.5 **AND** creatinine of >300umol/L **AND** grade III or IV encephalopathy",
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"comment": "Is charcoal a standalone treatment? Thought as she took last tablets an hour ago she could be given charcoal whilst NAC was being put up. Quesmed got me overthinking these easy marks...",
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"explanation": "# Summary\n \nParacetamol overdose accounts for 44% of all adult self-poisoning cases in the UK and results in approximately 150,000 hospital admissions annually. Some patients may be asymptomatic, or present with nausea, vomiting, abdominal pain, jaundice or altered mental state. Investigations should include baseline bloods including a clotting and a blood gas, as well as a paracetamol level. Management depends on the dose taken, timing of ingestion and the patient's clinical condition, with N-acetylcysteine being the mainstay of treatment. The decision to treat is often guided by a nomogram although in certain situations N-acetylcysteine should be started immediately.\n \n# Definition \n \nParacetamol overdose refers to when a potentially toxic dose of paracetamol is taken, either accidentally or in the context of a self-harm or suicide attempt. \n \n# Epidemiology \n \nParacetamol is the most common agent ingested in the context of intentional self-harm in the UK. Paracetamol overdose accounts for 44% of all adult self-poisoning cases in the UK, with approximately 150,000 people admitted to hospital each year due to poisoning.\n \n\n# Aetiology\n \n- The pathophysiology of paracetamol toxicity involves the build-up of its toxic metabolite NAPQI (N-acetyl-p-benzoquinone-imine). \n- Normally, NAPQI is inactivated by glutathione in the blood, but in a paracetamol overdose, glutathione stores are rapidly depleted. \n- NAPQI therefore accumulates, unmetabolised, and binds to cellular proteins, causing cell death.\n- This causes both severe hepatotoxicity and nephrotoxicity that can lead to liver and kidney failure. \n\n# Classification\n \n - **Acute overdose** - excessive paracetamol taken in less than 1 hour, usually in the context of self-harm\n - **Staggered overdose** - excessive paracetamol ingested over longer than 1 hour, usually in the context of self harm\n - **Therapeutic excess** - excessive paracetamol taken with the intent to treat pain or fever and without self-harm intent, ingested at a dose greater than 75mg/kg/24 hours.\n\n\n# Signs and Symptoms\n \n- These depend on how long has passed since the overdose was taken\n- In the first 24 hours patients may be asymptomatic or have nausea and vomiting\n- After this, up to around 72 hours, right upper quadrant pain and hypotension may develop\n- From 72 to 96 hours patients may develop liver and renal failure with resulting metabolic acidosis, encephalopathy and coagulopathy, with symptoms of:\n - Confusion\n - Drowsiness\n - Reduced urine output\n - Loin pain\n - Jaundice\n - Bleeding diathesis\n\n# Differential Diagnosis \n\n - **Acute gastroenteritis:** has similar symptoms of nausea, vomiting and abdominal pain; may have diarrhoea and history of unwell contacts\n - **Renal colic:** may also present with haematuria, nausea and vomiting; pain more likely to be \"loin to groin\" rather than right upper quadrant\n - **Decompensation of chronic liver disease:** can present with jaundice, abdominal pain and encephalopathy\n - **Sepsis:** can lead to a lactic acidosis and acute kidney injury; patients are often febrile and may have localising signs or symptoms of infection\n \n# Investigations\n \nBlood tests for paracetamol levels should be taken at least 4 hours after ingestion, as this is when plasma paracetamol concentration peaks so an earlier blood test may underestimate levels\n\nOther important blood tests include:\n \n - Full Blood Count (FBC)\n - Urea and Electrolytes\n - Clotting Screen\n - Liver Function Tests\n - Venous Blood Gas (may show metabolic acidosis)\n - Blood glucose (could also do a bedside capillary blood glucose)\n - Salicylate levels (to look for a mixed overdose with aspirin)\n\n# Management\n \n**Conservative:**\n\n- Weigh patient (important for determining dose of paracetamol taken per kg and to calculate N-acetylcysteine dosing)\n- Consider if any other substances may have been taken with paracetamol\n- If overdose was intentional, refer to liaison psychiatry for a mental health assessment\n - Consider if 1:1 observations are required for high-risk patients\n - Assess risk to self and ongoing suicidal ideation\n - Discharge planning and assess need for ongoing psychiatric input\n- Treat any other self-harm\n\n**Medical:**\n\nDecisions on medical treatment are guided by a nomogram which plots paracetamol levels against time from ingestion. \n\nThe management of paracetamol overdose is dependent on the timing of ingestion, the dose taken, and the patient's clinical condition:\n \n - **Ingestion less than 1 hour ago + dose >150mg/kg**: Administer activated charcoal\n - **Ingestion 1-4 hours ago**: Wait until 4 hours to take a level and treat with N-acetylcysteine (NAC) based on level\n - **Ingestion within 4-8 hours + dose >150mg/kg**: Start NAC immediately if there is going to be a delay of ≥8 hours in obtaining the paracetamol level, otherwise wait for level and treat if level high (above the treatment line on the nomogram)\n - **Ingestion within 8-24 hours + dose >150mg/kg**: Start NAC immediately\n - **Ingestion >24 hours ago**: Start NAC immediately if the patient has jaundice, right upper quadrant tenderness, elevated ALT, INR >1.3 or if the paracetamol concentration is detectable\n - **Staggered overdose**: Start NAC immediately\n \nNAC is given as an IV medication - it acts by increasing glutathione levels thereby preventing toxicity. \n\nThere are two ways to give NAC:\n\n- Standard regimen of 3 consecutive infusions totalling 21 hours in duration \n- The newer SNAP protocol (now recommended by Royal College of Emergency Medicine as standard) where the same dose of NAC is given over 12 hours in two infusions\n- If after either of these are completed, bloods show deranged LFTs, clotting or renal function NAC infusions should be continued and the patient discussed with local liver transplant services\n- Anaphylactoid reactions are a common side effect of NAC, characterised by urticaria, angioedema, nausea and vomiting, tachycardia and bronchospasm but rarely shock\n- These are managed by suspending treatment and giving chlorphenamine and salbutamol nebulisers before restarting (possibly at a slower rate)\n \n**Surgical:**\n\nPatients who develop acute liver failure may require an urgent liver transplant as a life-saving measure - the following groups of patients should be transferred to a liver transplant centre:\n\n- INR > 3 at 48 hours or > 4.5 at any time\n- Oliguric or creatinine > 200\n- pH < 7.3 despite fluid resuscitation\n- Hypotension (systolic blood pressure < 80mmHg)\n- Severe thrombocytopenia\n- Encephalopathy\n \nThe King's College Criteria is used to predict mortality from paracetamol overdose and to identify those patients who would potentially benefit from liver transplantation. It advises consideration of liver transplantation if:\n \n- Blood pH < 7.3\n \n\nOr **all** of:\n \n- Serum creatinine > 300 µmol/L\n- INR > 6.5 (Prothrombin time > 100s)\n- Grade III or IV hepatic encephalopathy\n\n# NICE Guidelines\n\n[NICE CKS - Poisoning or overdose](https://cks.nice.org.uk/topics/poisoning-or-overdose/)\n\n# References\n\n[BNF - Poisoning](https://bnf.nice.org.uk/treatment-summary/poisoning-emergency-treatment.html)\n\n[MHRA - Treating paracetamol overdose with intravenous acetylcysteine](https://www.gov.uk/drug-safety-update/treating-paracetamol-overdose-with-intravenous-acetylcysteine-new-guidance)\n\n[RCEM - SNAP Protocol Position Statement](https://rcem.ac.uk/wp-content/uploads/2021/11/Use_of_SNAP_for_Treatment_of_Paracetamol_Toxicity_Nov_2021.pdf)\n\n[Life in the Fast Lane - liver transplanation for paracetamol toxicity](https://litfl.com/liver-transplantation-for-paracetamol-toxicity/)",
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"question": "A 19-year-old female with a history of severe depression presents to the Emergency Department at 7 pm after taking an overdose of paracetamol. She describes taking 36 500mg tablets of paracetamol over the course of the afternoon, between 2 pm and 6 pm.\n\nWhat is the first line treatment for this patient?",
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"explanation": "Anaemia of chronic disease refers simply to anaemia which occurs in the context of long term illness. This includes chronic infections, many inflammatory conditions and some malignancies. The underlying process is related to reduced red blood cell production, which is felt to be mediated by inflammation - on differential blood count, you would see a relatively low reticulocyte count reflecting this",
"id": "33430",
"label": "c",
"name": "Anaemia of chronic disease",
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"__typename": "QuestionChoice",
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"explanation": "Pernicious anaemia is a form of autoimmune disease which results in antibodies forming against gastric parietal cells and ultimately causes a lack of intrinsic factor - this means that B12 cannot be absorbed from the diet. The resultant anaemia would be macrocytic, as per other forms of B12 deficiency anaemia",
"id": "33432",
"label": "e",
"name": "Pernicious anaemia",
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"__typename": "QuestionChoice",
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"explanation": "Haemolysis is the breakdown of red blood cells - it can cause anaemia when this process is happening more rapidly than the red cells can be replaced. This is classically a normocytic anaemia, as there is nothing wrong with the red cells themselves (no deficiencies etc.), simply that they are being broken down more rapidly than intended. If you were to perform a blood film in a haemolytic anaemia, you would likely see schistocytes (broken/fragmented red cells). On differential blood count, you may also see a raised reticulocyte count, as the body works hard to rapidly replace the red cells that have been lost",
"id": "33431",
"label": "d",
"name": "Haemolytic anaemia",
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"explanation": "Macrocytic anaemias are most commonly caused by simple dietary B12 or folate deficiency, or more rarely, pernicious anaemia. A macrocytosis (with or without associated anaemia) also commonly occurs in chronic alcoholism",
"id": "33429",
"label": "b",
"name": "Macrocytic anaemia",
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "Iron deficiency causes a microcytic, hypochromic anaemia. Iron is an important component for the production of haemoglobin - the molecule responsible for the oxygen carrying capacity of red blood cells",
"id": "33428",
"label": "a",
"name": "Microcytic anaemia",
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"comment": "Can someone explain why it causes a microcytic hypochromic anaemia ??????????????",
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"explanation": "# Summary \n\nMicrocytic anaemia, characterised by abnormally small red blood cells with a reduced mean corpuscular volume (MCV), encompasses various causes. Iron deficiency anaemia (IDA) is the most common, often arising from inadequate iron intake, chronic blood loss, or malabsorption. Thalassaemias result from genetic factors affecting globin chain production, while anaemia of chronic disease is linked to inflammation. Lead poisoning, particularly in children, and sideroblastic anaemias are additional aetiologies. Clinical features include fatigue, pallor, and cold intolerance. Diagnosing microcytic anaemia requires thorough investigations, including iron studies and haemoglobin electrophoresis. Management is directed at the underlying cause, involving iron supplementation, transfusions, and treatment of any associated conditions.\n\r\n# Definition\n\nMicrocytic anaemia is defined by the presence of RBCs that are smaller than normal, with a mean corpuscular volume (MCV) typically below the reference range (around <76 fl).\n\n\n\n\r\n# Epidemiology \n\nMicrocytic anaemia can affect individuals across all age groups and demographics. The prevalence of specific causes may vary based on factors such as geographical location, socioeconomic status, dietary habits, and the presence of underlying medical conditions.\n\n\n\n\r\n# Signs and Symptoms \n\n- Fatigue and Weakness\n- Pallor\n- Shortness of Breath\n- Palpitations\n- Cold intolerance\n- Iron-deficiency anaemia specific: \n\t- Nail changes such as koilonychia (spoon-shaped nails)\n\t- Atrophic glossitis\n\t- Angular stomatitis\n\t- Pica: Iron-deficiency anaemia may manifest as pica, with cravings for non-food substances like ice (pagophagia) or clay (geophagia).\n\n# Differential Diagnosis\n\nThe causes of microcytic anaemia encompass a diverse range of conditions:\n\n- **Iron Deficiency Anaemia (IDA):** IDA is the most common cause of microcytic anaemia. It results from insufficient iron intake, malabsorption, chronic blood loss (e.g. gastrointestinal bleeding), or increased iron requirements (e.g. pregnancy).\n- **Thalassaemias:** Thalassaemias are a group of inherited haemoglobin disorders characterized by reduced production of normal globin chains, leading to microcytosis.\n- **Anaemia of Chronic Disease (ACD):** Chronic inflammatory conditions, such as rheumatoid arthritis and chronic infections, can cause ACD, which often presents as microcytic anemia.\n- **Lead Poisoning:** Exposure to lead, often through contaminated sources, can lead to microcytic anaemia, particularly in children.\n- **Sideroblastic Anaemia:** Sideroblastic anaemias are a heterogeneous group of conditions characterized by defective haem synthesis and the accumulation of iron within the mitochondria of erythroid precursors.\n\n\r\n\r\n# Investigations \n\n* Investigations all patients should have include:\n\t- Full Blood Count (FBC): The CBC provides essential information, including hemoglobin levels, red blood cell count, hematocrit, and mean corpuscular volume (MCV). In microcytic anaemia, the MCV is typically lower than the reference range.\n\t- Peripheral Blood Smear Examination: A peripheral blood smear allows visual examination of red blood cells. It can reveal microcytosis, hypochromia (reduced hemoglobin content), and, in certain cases, abnormal cell morphology.\n\t- **Iron Studies:** Iron studies consist of several key parameters:\n\t - Serum Iron: Measures the concentration of iron in the blood. In microcytic anaemia, serum iron may be decreased.\n\t - Ferritin: Ferritin is an intracellular protein that stores iron. Low ferritin levels are indicative of iron deficiency.\n\t - Transferrin Saturation: This parameter assesses the percentage of transferrin (a protein that transports iron) saturated with iron. Reduced transferrin saturation is consistent with iron deficiency.\n- Specific tests to investigate for underlying causes include:\n\t- Haemoglobin Electrophoresis: Helps distinguish thalassaemias from other causes of microcytic anaemia by identifying abnormal hemoglobin variants.\n\t- Serum Lead Levels: When lead poisoning is suspected, measuring blood lead levels is essential for diagnosis.\n\t- Bone Marrow Examination: In selected cases, particularly when there is diagnostic uncertainty or unusual clinical features, a bone marrow examination may be warranted. This invasive procedure allows a detailed assessment of the bone marrow, including cell morphology, iron stores, and other relevant findings.\n\n\n# Management\n\n* **Iron Supplementation:** In cases of IDA, oral or intravenous iron supplementation is often prescribed. Important considerations of oral iron supplementation (usually a 3 month course) include:\n\t* Side effects - diarrhoea, constipation, black stools, abdominal pain, nausea\n\t* Iron supplements should be taken on an empty stomach (preferably one hour before a meal) with a drink containing vitamin C, such as a glass of orange juice or another juice drink with added vitamin C. This aids absorption.\n\t* Oral iron decreases the absorption of oral Levothyroxine. Therefore if both are prescribed, advise patients to take at least 4 hours apart.\n\n- Blood Transfusions: Severe or symptomatic anaemia may require blood transfusions to rapidly restore haemoglobin levels.\n- Thalassaemia Management: Thalassemias may necessitate specialized care, including regular blood transfusions and chelation therapy for iron overload.\n- Addressing Underlying Conditions: Treating the underlying chronic disease is essential in cases of ACD.\n\n# Complications\n\nUntreated or chronic microcytic anaemia can lead to complications such as cardiac issues, developmental problems (particularly in children), and impaired quality of life due to fatigue and reduced exercise tolerance.\n\n# NICE Guidelines\n\n[NICE CKS - Iron-deficiency anaemia](https://cks.nice.org.uk/topics/anaemia-iron-deficiency/)\r\n\r\n\n\n",
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"explanation": "Inherited causes of anaemia such as thalassaemia or sickle cell are unlikely to present for the first time in adulthood, usually being identified at a young age (most commonly through screening programmes). Screening for thalassaemia trait is offered to all pregnant women in England. Additionally, the newborn blood spot test includes haemoglobinopathy testing for both thalassaemia and sickle cell disease",
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"explanation": "There is no mention of menorrhagia in the stem, although this is an important potential cause of anaemia to consider in people who menstruate. Anaemia from menorrhagia would usually be normocytic or microcytic",
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"explanation": "Conditions of the gastrointestinal (GI) tract such as coeliac disease or inflammatory conditions can cause malabsorption of multiple nutrients which can result in anaemia. However, in this stem there is no mention of any GI symptoms and given the patients vegan diet, dietary insufficiency is more likely to be responsible for any deficiencies than malabsorption",
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"explanation": "# Summary \n\nMacrocytic anaemia is a type of anaemia characterized by the presence of larger-than-normal red blood cells (RBCs). It can be classified into megaloblastic and non-megaloblastic types. Megaloblastic anemia is primarily associated with impaired DNA synthesis, often due to deficiencies in vitamin B12 or folate, leading to the enlargement of RBC precursors and hypersegmented neutrophils on blood film. Non-megaloblastic macrocytic anaemia can be caused by various factors, and sometimes a patient may present with non-megaloblastic macrocytosis, without anaemia such as in pregnancy. Key investigations include FBC, blood film and measurement of specific vitamins such as folate and B12, and management centres on the underlying cause of the anaemia. For example, vitamin supplementation in B12/folate deficiency.\n\n\r\n# Definition\n\nMacrocytic anaemia refers to a condition in which red blood cells are larger than normal. It can be further classified into two main categories: megaloblastic and non-megaloblastic. Megaloblastic macrocytic anaemia is characterized by slow or impaired DNA synthesis, leading to delayed maturation of RBCs and, notably, hypersegmented neutrophils on blood film. Non-megaloblastic macrocytic anaemia may manifest as macrocytosis without the presence of anaemia.\n\n\n\r\n# Epidemiology \n\nThe epidemiology of macrocytic anaemia varies depending on the underlying cause. Megaloblastic macrocytic anaemia is often associated with vitamin B12 or folate deficiencies and is more prevalent in older adults. Non-megaloblastic macrocytic anaemia, on the other hand, can occur at any age and may be linked to factors such as alcohol consumption or pregnancy.\n\n\r\n# Classification\n\nMorphologically, macrocytic anaemia is usually typified by large RBCs due to abnormal RBC development, giant metamyelocytes and hypersegmented neutrophils (in the peripheral circulation). Macrocytic anaemia may be megaloblastic or non-megaloblastic.\n\n## Causes of megaloblastic anaemia \n\n* **B<sub>12</sub> deficiency** \n * reduced intake (eg. dietary) \n * reduced absorption (eg. pernicious anaemia, inflammatory bowel disease, gastrectomy)\n* **Folate deficiency**\n* Drugs\n * hydroxycarbamide (previously called hydroxyurea)\n * azathioprine\n * cytosine arabinoside\n * azidothymidine\n\n\n## Causes of non-megaloblastic/normoblastic macrocytic anaemia\n\n* Liver disease\n* Alcohol \n* Hypothyroidism\n* Myelodysplastic syndrome\n* Hypothyroidism\n* Pregnancy (usually a mild macrocytosis)\n\n\r\n# Signs and Symptoms \n\n- Fatigue and Weakness\n- Pallor\n- Shortness of Breath\n- **Glossitis and \"Beefy Tongue\":** A distinctive sign of megaloblastic anaemia, glossitis, is the inflammation of the tongue, giving it a swollen and reddened appearance, often referred to as a \"beefy tongue.\"\n- **Neurological Symptoms:** Severe vitamin B12 deficiency can affect the nervous system, leading to neurological symptoms such as paresthesias (tingling and numbness), ataxia (impaired coordination), and cognitive impairment.\n- Symptoms of associated conditions:\n\t- **Autoimmune Conditions:** Megaloblastic anemia, particularly pernicious anemia, is associated with autoimmune conditions such as autoimmune thyroid disease, type 1 diabetes, and autoimmune gastritis. Therefore, patients may present with features of these conditions.\n\t- **Hypothyroidism Symptoms:** In cases where megaloblastic anaemia is secondary to hypothyroidism, patients may exhibit classic hypothyroidism symptoms like fatigue, weight gain, cold intolerance, and changes in skin and hair.\n\n# Differential Diagnosis\n\n\n- **Megaloblastic Anaemia (Vitamin B12 or Folate Deficiency):** The primary differential diagnosis within the realm of macrocytic anaemia is megaloblastic anaemia, specifically caused by vitamin B12 or folate deficiency. Careful evaluation of vitamin levels, clinical symptoms, and peripheral blood smears can aid in the distinction.\n\n- **Non-Megaloblastic Macrocytic Anaemia:** Macrocytosis, without the typical features of megaloblastic anemia, may result from various non-megaloblastic causes, including alcohol consumption, liver disease, or pregnancy. These cases may present as isolated macrocytosis without the broader clinical picture of anaemia.\n\n- **Haemolysis:** Haemolytic anaemias, both inherited and acquired, can lead to an increase in reticulocyte count and macrocytosis, albeit for different reasons. Evaluating markers of haemolysis, such as elevated bilirubin levels or increased lactate dehydrogenase, can assist in distinguishing haemolytic anaemias from megaloblastic anaemias.\n\n- **Liver Disease:** Patients with liver disease, particularly alcohol-related liver disease, can exhibit macrocytosis. Evaluation of liver function tests and consideration of underlying liver pathology is necessary in such cases.\n\n- **Medications:** Certain medications, such as antiretroviral drugs and chemotherapy agents, can cause macrocytosis. A thorough medication history is important in identifying potential drug-induced macrocytosis.\n\n- **Bone Marrow Disorders:** In rare cases, macrocytic anaemia can be associated with underlying bone marrow disorders, including myelodysplastic syndromes (MDS) and myeloproliferative neoplasms (MPNs). A bone marrow biopsy may be warranted to evaluate these conditions.\n\n\r\n\r\n# Investigations \n\n* Investigations all patients should have include:\n\t* Full Blood Count (FBC): This reveals anaemia and macrocytosis. The presence of hypersegmented neutrophils in the blood film is characteristic of megaloblastic anemia.\n\t* Haematinics: Serum vitamin B12 and folate levels should be assessed to identify deficiencies.\n\t* Blood Film: A peripheral blood smear can show macrocytosis and the presence of hypersegmented neutrophils.\n* Specific tests to investigate for underlying causes include:\n\t* TFTs to look for hypothyroidism\n\t* LFTs to assess liver function\n\t* Antibodies to intrinsic factor +/- gastric parietal cells, seen in pernicious anaemia\n\t* Markers of haemolysis - bilirubin, DAT testing, LDH\n\n# Management\n\n* **Megaloblastic Anaemia:** In pernicious anemia, intramuscular hydroxocobalamin is typically administered to replace vitamin B12. \n* It is important to address vitamin B12 deficiency before folate replacement (if both are deficient) to avoid exacerbating neurological symptoms and precipitating subacute degeneration of the spinal cord (SACD). \n* In cases of folate deficiency, oral folate supplements are provided.\n* **Non-Megaloblastic Anaemia:** The management of non-megaloblastic macrocytic anemia depends on the underlying cause, such as addressing alcohol consumption or providing support during pregnancy.\n\n# NICE Guidelines\n\n[NICE CKS - B12/Folate-deficiency anaemia](https://cks.nice.org.uk/topics/anaemia-b12-folate-deficiency/)\r\n\r\n\n\n",
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"question": "A 23-year-old female presents to the GP with fatigue. She describes herself as very healthy, following a vegan diet and exercising four times a week - although the fatigue is now making this more challenging to maintain. She has no past medical history.\n\nBlood tests reveal:\n\n- Hb 94 (135-175g/dL)\n- MCV 106 (80-96 fl)\n\nWhat is the most likely cause of the patient's anaemia?",
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"explanation": "Anaemia of chronic disease does cause a normocytic anaemia. However, this often occurs in elderly patients or those with significant underlying physical health problems. Whilst this patient is clearly not in a good physical condition, from the information given in the stem there is no evidence to suggest any long term illnesses",
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"explanation": "This patient likely does have an element of folate deficiency contributing to his anaemia, however folate deficiency alone would cause a macrocytic picture, therefore something else must also be contributing. In this patient where their diet is very poor **overall**, it is unlikely that he would be lacking in one specific nutrient alone",
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"explanation": "Additionally, there are no risk factors for autoimmune haemolytic anaemias identified in this stem (such as a history of/signs on examination suggestive of other autoimmune disease)",
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"explanation": "This patient likely does have an element of iron deficiency contributing to his anaemia, however iron deficiency alone would cause a microcytic picture, therefore something else must also be contributing. In this patient where their diet is very poor **overall**, it is unlikely that he would be lacking in one specific nutrient alone",
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"explanation": "# Summary\n\nMalnutrition refers to deficiencies, excesses, or imbalances in a person’s intake of energy and/or nutrients. It can result in significant morbidity and mortality, particularly among vulnerable populations such as the elderly, children, and those with chronic illnesses. Early identification and management are critical to improving health outcomes.\n\n# Definition\nMalnutrition is defined as a state of nutrition in which a deficiency, excess, or imbalance of energy, protein, and other nutrients causes measurable adverse effects on tissue/body form (body shape, size, composition), function, and clinical outcome.\n\nNICE define **malnourishment** as:\n\n* A body mass index (BMI) of less than 18.5 kg/m2.\n* Unintentional weight loss greater than 10% within the last 3–6 months.\n* A BMI of less than 20 kg/m2 and unintentional weight loss greater than 5% within the last 3–6 months.\n\n# Epidemiology\nMalnutrition is a common issue worldwide, affecting both developed and developing countries. In the UK, it is estimated that over 3 million people are malnourished or at risk of malnutrition, with the majority being elderly or chronically ill. Hospital and care home residents are particularly susceptible, with malnutrition affecting 30-40% of these populations.\n\n# Aetiology\nThe causes of malnutrition can be multifactorial and include:\n\n1. **Inadequate intake:**\n - Poor dietary intake due to socio-economic factors, poor appetite, or food availability.\n - Physical difficulties in eating, such as dysphagia or dental issues.\n\n2. **Increased requirements:**\n - Growth in children and adolescents.\n - Pregnancy and lactation.\n - Acute or chronic illnesses that increase metabolic demands.\n\n3. **Malabsorption:**\n - Gastrointestinal diseases such as Crohn’s disease, coeliac disease, and chronic pancreatitis.\n - Post-surgical states affecting the gut.\n\n4. **Chronic diseases:**\n - Cancer, chronic kidney disease, heart failure, and chronic obstructive pulmonary disease (COPD).\n\n5. **Socioeconomic factors:**\n - Poverty, lack of access to nutritious food, and social isolation.\n\n# Classification\nMalnutrition can be classified into two types:\n\n1. **Undernutrition:**\n - Protein-energy malnutrition: Includes conditions such as marasmus and kwashiorkor.\n - Micronutrient deficiencies: Deficiencies in vitamins and minerals, such as iron, iodine, vitamin A, and zinc.\n\n2. **Overnutrition:**\n - Obesity and related conditions such as metabolic syndrome.\n\n# Signs and Symptoms\n- **General signs:**\n - Weight loss or failure to gain weight (in children).\n - Fatigue, weakness, and lethargy.\n - Poor concentration and mental function.\n - Decreased immunity and frequent infections.\n\n- **Specific signs:**\n - Muscle wasting.\n - Oedema (in cases of protein deficiency).\n - Brittle hair and nails.\n - Dry, scaly skin.\n - Delayed wound healing.\n - Growth retardation in children.\n\n# Differential Diagnosis\n- **Anorexia nervosa:** Characterised by intentional restriction of food intake and an intense fear of gaining weight.\n- **Chronic illnesses:** Such as cancer, chronic kidney disease, and COPD, which can cause weight loss and nutritional deficiencies.\n- **Gastrointestinal disorders:** Conditions like coeliac disease, Crohn’s disease, and irritable bowel syndrome that affect nutrient absorption.\n- **Infections:** Chronic infections like tuberculosis or HIV/AIDS can lead to significant weight loss and malnutrition.\n- **Depression:** Can result in reduced appetite and subsequent weight loss.\n\n# Investigations\n- **Bedside:**\n - Nutritional screening tools (e.g., MUST – Malnutrition Universal Screening Tool).\n - Anthropometric measurements (height, weight, BMI, mid-arm circumference).\n\n- **Bloods:**\n - Full blood count (FBC) to check for anaemia.\n - Serum albumin and prealbumin levels.\n - Electrolytes, urea, and creatinine.\n - Liver function tests.\n - Vitamin and mineral levels (e.g., iron studies, vitamin D, vitamin B12, folate).\n\n- **Imaging:**\n - Dual-energy X-ray absorptiometry (DEXA) scan for body composition analysis.\n\n- **Invasive:**\n - Endoscopy and biopsy for suspected malabsorptive disorders.\n\n# Management\n- **General measures:**\n - Nutritional support: Oral nutritional supplements, fortified foods, and dietary modifications.\n - Treat underlying causes: Addressing chronic illnesses, infections, or socioeconomic issues.\n\n- **Specific interventions:**\n - Enteral nutrition: Tube feeding for those unable to eat adequately by mouth.\n - Parenteral nutrition: Intravenous feeding for severe cases where the gastrointestinal tract cannot be used.\n - Micronutrient supplementation: Specific vitamins and minerals based on identified deficiencies.\n\n- **Monitoring and follow-up:**\n - Regular assessment of nutritional status and dietary intake.\n - Adjustments to the nutritional plan based on progress and any new medical issues.\n\n# Complications\n- Increased risk of infections due to impaired immune function.\n- Delayed wound healing and recovery from illnesses.\n- Muscle weakness and decreased functional capacity.\n- Developmental delays in children.\n- Increased morbidity and mortality.\n\n\n# NICE Guidelines\n\n[NICE CKS - Malnutrition](https://cks.nice.org.uk/topics/adult-malnutrition/)",
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"question": "A 40-year-old male presents to the Emergency Department. He appears unkempt, cachectic and on questioning it is identified that he is experiencing homelessness. He describes a very poor diet consisting of donated food when this is available, and otherwise mainly eats scraps from bins. He is noted to be very pale and his full blood count results demonstrate a normocytic anaemia.\n\nWhat is the most likely cause of this anaemia?",
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"explanation": "Anaemia can cause shortness of breath and hypoxia, but it is unlikely that this would develop only after the transfusion - if the anaemia were significant enough to cause these symptoms, you would expect them to have been present both **before** _and after_ the transfusion",
"id": "33446",
"label": "d",
"name": "Persistent anaemia requiring further transfusion",
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"explanation": "In older, more frail patients, extra care and caution must be taken to avoid fluid overload when giving any infusion. We are used to considering this and adapting our prescriptions accordingly when giving simple fluids, but this can be overlooked when giving blood products. It is important to remember that blood products can have similar effects to fluids, particularly when multiple units are required. You can reduce the risk of transfusion associated circulatory overload by giving the blood products more slowly (i.e. giving 1 unit over 4 or 5 hours, instead of 2 or 3) or by giving a small dose of furosemide between each unit",
"id": "33443",
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"explanation": "Complications of transfusions that are classified as \"delayed\" occur days to weeks following the transfusion event. As the onset of the patient's symptoms started only 2 hours after completing the transfusion, this would not be classified as a 'delayed' reaction. Additionally, there is no evidence in the stem to point you towards haemolysis (features of a haemolytic reaction may include jaundice, fever, elevated lactate dehydrogenase +/- bilirubin, a newly positive direct antiglobulin test on blood testing and haemoglobinuria)",
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"name": "Delayed haemolytic transfusion reaction",
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"explanation": "There is no mention in the stem of infective symptoms to meet criteria for sepsis, such as fever, tachycardia or hypotension. With modern screening of blood products, acquiring an infection from a transfusion is rare. Although it is always important to consider when reviewing a patient with complications from a transfusion, it is not the most likely cause of this patients symptoms",
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"name": "Transfusion associated sepsis",
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"explanation": "Anaphylactic reactions to blood products are rare. If this were to be the case, you would expect more of a focus on key anaphylactic symptoms, including the airway being affected (new wheeze, stridor, airway swelling) or features of anaphylactic shock, including significant hypotension. The biggest risk factor for transfusion associated anaphylaxis is IgA deficiency, following receipt of transfused plasma containing normal IgA levels",
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"explanation": "# Summary\n\nBlood comprises two core components: cellular elements and plasma. Cellular components consist of white blood cells (neutrophils, eosinophils, basophils, monocytes, lymphocytes), red blood cells (RBCs or erythrocytes), and platelets (thrombocytes). Plasma encompasses clotting factors, albumin, and immunoglobulins. Blood groups, notably ABO and Rh, influence transfusion compatibility, with group O individuals universal donors. Acute and late transfusion reactions require vigilant monitoring and management. Iron overload can result from frequent transfusions, necessitating interventions to lower iron levels.\n\n# Blood Components\n\nBlood is made of two main components: cells and plasma\n\n- The cellular components of blood include: \n - white blood cells (neutrophils, eosinophils, basophils, monocytes, lymphocytes)\n - RBCs (erythrocytes) \n - platelets (thrombocytes)\n\n- Plasma consists of: \n - clotting factors\n - albumin \n - immunoglobulins\n\n## Lifespan of components\n\nThe normal lifespan of the following cellular components of blood is:\n\n- RBCs, 90–120 days\n- platelets, 10 days\n- neutrophils, 4 days\n\n## Products for transfusion\n\nFour products are readily transfusable:\n\n- **Red blood cells**\n - Generally **stored at 4 °C** for up to 35 days \n - In vivo, RBCs typically have a lifespan of about 120 days; however, it is important to note that transfused red cells last around 50–60 days\n\n\n- **Fresh frozen plasma** (FFP)\n - **Stored at –30 °C**, with a shelf life of a year\n - Used in patients with coagulopathy (impaired blood coagulation) to replace clotting factors\n - The type of FFP used depends on the patient's blood group\n\n\n- **Platelets**\n\n - **Stored at room temperature** for up to 7 days\n - Have a lifespan of 10 days before they are phagocytosed in the spleen and liver\n - 1 pool of platelets comes from 4 donors\n \n \n - Platelets are given if levels are <10 x 10<sup>9</sup>/l in patients with thrombocytopenia due to marrow failure from chemotherapy and radiotherapy – This threshold can be increased if there is sepsis or bleeding, or for a planned surgical procedure \n \n \n - Platelet transfusions should not be used in conditions where there is immune destruction of platelets (eg. immune thrombocytopenia unless there is a haemorrhagic emergency)\n \n \n - Platelet transfusion is also contraindicated in TTP or HUS as it can contribute to the microvascular occlusion in the brain and kidneys that is associated with these conditions\n \n\n\n- **Cryoprecipitate**\n\n - Cryoprecipitate is made by thawing FFP overnight at 4–8 °C\n - It has a shelf life of 1 year **stored at –30 °C**\n - It contains fibrinogen, factor VIII and von Willebrand factor\n - It is generally used in patients with massive bleeding and low fibrinogen\n\n# Blood Groups\n\n* Blood groups, defined as antigens on the surface of red blood cells, are critical in determining blood compatibility for transfusions. \n* There are over 400 blood groups but the ABO and Rh blood groups are the most important, each with distinct inheritance patterns. \n* The ABO antigens develop on red cells 16 weeks after birth, meaning neonates do not require blood cross-matching for transfusions. \n* Adults with group O red cells can universally donate due to the absence of A or B antigens, and group AB plasma can be universally donated due to the lack of anti-A or anti-B antibodies.\n* The A and B genes show co-dominant inheritance, whereas the O gene is recessive.\n\n# Antigens and Compatibility\n\n* **Rhesus antigen** - The Rh group includes 5 main antigens with Rhesus D being the most important. The Rhesus D antigen has an autosomal dominant mode of inheritance.\n- **ABO antigens** - not expressed on red cells until 16 weeks after birth. Therefore, in neonates, there is no need to cross-match for blood transfusions as antibodies are not yet made.\n\nPlease see the summary table below on blood group compatibility and donation:\n\n\n| Blood Type | Can Receive From | Can Donate To |\n|------------|-----------------|--------------|\n| A+ | A+, A-, O+, O- | A+, AB+ |\n| A- | A-, O- | A+, A-, AB+, AB- |\n| B+ | B+, B-, O+, O- | B+, AB+ |\n| B- | B-, O- | B+, B-, AB+, AB- |\n| AB+ | All Blood Types | AB+ |\n| AB- | AB-, A-, B-, O- | AB+, AB- |\n| O+ | O+, O- | A+, B+, AB+, O+ |\n| O- | O- | All Blood Types |\n\n# Acute Transfusion Reactions\n\n## Allergy \n\n- Presentation ranges from urticaria to angioedema and anaphylaxis\n- Management – stop the transfusion if concerns over anaphylaxis (if mild urticaria, can slow the transfusion and give antihistamine), give saline, adrenaline (in case of anaphylaxis), chlorphenamine, and hydrocortisone\n\n## Acute haemolytic transfusion reaction \n\n- Caused by giving an incompatible blood bag to a patient\n- Early signs include fever, abdominal pain, hypotension and anxiety\n- Late complications include generalised bleeding secondary to DIC\n- Management – stop the transfusion, give saline, treat DIC\n\n## Febrile non-haemolytic transfusion reaction \n\nBritish Society for Haematology guidelines recommend that: \n\n- In patients with a **mild** reaction:\n\n - A temperature rise of 1 - 2°C leading to pyrexia ≥38°C, but <39°C\n - And/or pruritus or a rash\n - WITHOUT other features\n\nThe transfusion can be continued with appropriate treatment (oral paracetamol 500 - 1000mg) and direct observation. If a rash/pruritis is also present, slow the transfusion)\n \n- In patients who develop **moderate** reactions:\n - Temperature ≥39°C OR a rise of ≥2°C from baseline\n - AND/OR systemic symptoms such as chills, rigors, myalgia, nausea or vomiting)\n\nSymptomatic treatment should be considered. If symptoms settle, the transfusion can be resumed. If symptoms are sustained, bacterial contamination or a haemolytic reaction should be considered.\n\n## Transfusion-related acute lung injury (TRALI)\n\n- Presents with pulmonary oedema and can cause acute respiratory distress syndrome (ARDS)\n\n- Management – stop the transfusion, give saline, treat ARDS and give supplementary oxygen as needed\n\n## Transfusion-associated circulatory overload (TACO)\n\n- Presents with fluid overload\n\n- Management – Slow the transfusion, give furosemide and supplementary oxygen as needed\n\n# Late Transfusion Reactions\n\n## Delayed haemolytic transfusion reaction \n\n- Caused by an exaggerated response to a foreign red cell antigen that the patient has been exposed to before\n- Patients present with jaundice, anaemia, and fever, usually on day 5 post-transfusion\n\n## Transfusion-associated graft-versus-host disease \n\n- Caused by donor blood lymphocytes attacking the recipient's body \n- Rare but carries a high risk of mortality\n\n## Iron Overload\n\n- Iron overload may be related to the pathophysiology of the condition (eg. haemochromatosis) or iatrogenic (eg. related to a blood transfusion or excess oral iron) \n - There is no secretion pathway for iron and approximately 1 mg of iron is lost via gut mucosal cells\n - Absorption of luminal iron is mediated by enterocytes, which respond to iron stores in the body\n - The enterocyte is modulated via its transferrin receptor, which regulates transferrin uptake from the plasma\n - In turn, the HFE protein modulates transferrin receptor activity\n- Iron overload usually becomes an issue after 20 units have been given or if serum ferritin rises above 1000 µg/l \n- Subcutaneous desferrioxamine is required regularly to lower iron levels\n\n# References\n\n[Click here to see more information on Patient UK about transfusion reactions](https://patient.info/doctor/blood-transfusion-reactions)\n\n[Click here to see more information on the British Society for Haematology guidelines on acute transfusion reactions](https://onlinelibrary.wiley.com/doi/full/10.1111/bjh.18789)",
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"question": "A 69-year-old male requires a 3 unit blood transfusion following a road traffic accident. He has no past medical history but appears physically very frail, weighing 49 kilograms with a body mass index of 17.\n\nTwo hours after the transfusion, he becomes increasingly short of breath and develops an oxygen requirement, needing 2 litres to maintain saturations of 96%.\n\nWhat is the most likely cause of his respiratory symptoms?",
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"explanation": "Delirium is a reversible form of cognitive impairment characterised by its **acute** onset, **fluctuating** course and propensity to cause **inattention**. PINCH ME is a helpful acronym to remember common causes of delirium - Pain, Infection, Nutrition, Constipation, Hydration, Medication and Environment (unfamiliar). In this patient, there is a clearly identifiable trigger preceding the onset of the confusion - constipation",
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"explanation": "Hypoglycaemia in this patient is a valid concern - with her confusion, constipation and vomiting, she may be having very minimal oral intake. Hypoglycaemia can cause confusion and vomiting; however, it would not be in keeping with this patients 5-day history of agitation and disorientation - it would present much more acutely, coming on over minutes to hours, not days",
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"explanation": "Though bowel cancer can present for the first time with bowel obstruction, which may be the case here with the patients marked constipation and subsequent vomiting, it would not explain the rapid onset of the confusion. You may also experience other associated red flag symptoms to be present such as a change in bowel habit for more than 6 weeks, blood in the stool or weight loss",
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"label": "e",
"name": "Malignancy",
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"explanation": "In the elderly, depression can often manifest with cognitive impairment. Additionally, depression and dementia are common co-existing conditions. However, the very acute nature of this confusion and the lack of any affective symptoms points away from depression as the cause",
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"name": "Depression",
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"explanation": "Cognitive impairment in dementia is gradual in onset, over many months to years. It would not progress suddenly over the course of 5 days. Additionally, the clear trigger of constipation here makes a primary neurological cause much less likely",
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"comment": "Is this really DTs? or just ordinary Delirium?",
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"explanation": "# Summary\n\nDelirium tremens (DT) is a severe form of alcohol withdrawal that presents with acute confusion, hallucinations, autonomic hyperactivity, and, in rare cases, seizures. Typically occurring around 72 hours after the cessation of alcohol intake, DT necessitates immediate medical attention and management. The first-line treatment is lorazepam, administered either orally or parenterally, followed by maintenance management strategies.\n\n# Definition\n\nDelirium tremens is a life-threatening condition characterized by a rapid onset of confusion often precipitated by alcohol withdrawal. It generally develops around 72 hours after the cessation of alcohol intake and can persist for several days. This condition is marked by extreme autonomic hyperactivity and neuropsychiatric symptoms.\n\n# Aetiology\n\nThe primary cause of delirium tremens is abrupt withdrawal or a significant reduction in alcohol intake in a person with prolonged, heavy alcohol use. Other factors that can precipitate DT include infection, trauma, or illness in a person with a history of chronic alcoholism.\n\n# Signs and Symptoms\n\nSymptoms typically peak between the 4th and 5th day post-withdrawal. The clinical features of delirium tremens include:\n\n- Confusion and disorientation\n- Hallucinations, which can be visual or tactile (e.g., formication – the sensation of crawling insects on or under the skin)\n- Autonomic hyperactivity, manifesting as sweating and hypertension\n- Rarely, seizures\n\n\n# Differential Diagnosis\n\nDelirium tremens must be distinguished from other conditions that can present with similar symptoms:\n\n- **Alcohol withdrawal syndrome:** Features include anxiety, insomnia, anorexia, tremor, and autonomic hyperactivity, but without the severe confusion or hallucinations seen in DT.\n- **Wernicke-Korsakoff syndrome:** This condition is characterized by ataxia, ophthalmoplegia, and confusion but lacks the autonomic instability of DT.\n- **Encephalitis:** Features include fever, headache, altered mental status, and focal neurological signs which are not typically observed in DT.\n- **Meningitis:** This presents with fever, neck stiffness, and altered mental status but without the characteristic hallucinations seen in DT.\n\n\n\n# Investigations\n\nInvestigations largely aim to rule out other conditions. These include:\n\n- Routine Blood panel including B12, Folate, Thyroid Function\n- Infection screen: Chest Xray, Urine dip, Blood Cultures\n- CT Head to assess for evidence of a structural brain lesion e.g. subdural haemorrhage in patients presenting with an unwitnessed fall while intoxicated\n- Lumbar Puncture if meningitis or encephalitis are suspected\n\n\n# Management\n\nNICE guidelines suggest offering oral lorazepam as the first-line treatment. \n\nIf symptoms persist, or oral medication is declined, offer parenteral lorazepam or haloperidol.\n\nFor maintenance management of alcohol withdrawal, the following steps are recommended:\n\n- Administer Chlordiazepoxide. Eventually this can be tapered according to **Clinical Institute Withdrawal Assessment for Alcohol (CIWA)** scoring\n- Ensure adequate hydration with fluids\n- Provide anti-emetics to manage nausea\n- Pabrinex to replenish vitamins\n- Refer the patient to local drug and alcohol liaison teams for further support and management\n\nWhen patients present with seizures, sometimes they remain in hospital for inpatient detoxification. This is however rare and the evidence shows that community detoxification is more effective.\n\n# NICE Guidelines\n\n[NICE CKS - Alcohol-use disorders](https://www.nice.org.uk/guidance/cg100/chapter/Recommendations)",
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"question": "A 71-year-old female patient is brought into the Emergency Department from a care home with worsening confusion and vomiting. She has not opened her bowels in 7 days and has been increasingly agitated, disorientated and difficult to engage in conversation for the past 5 days.\n\nWhat is the most likely cause of this patients confusion?",
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"explanation": "In FTLD, the first symptoms are often personality change or inappropriate social behaviour, prior to any significant impact in memory (cognitive decline comes later in the disease course). As the name suggests, this is due to the specific area of the brain that is affected. FTLD tends to develop in younger patients, classically <65 years of age, compared with the other forms of dementia which increase in incidence with increasing age",
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"explanation": "Alzheimer's dementia follows a much more gradual course and would not cause these distinct episodes of sudden, marked deterioration in memory",
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"explanation": "In some elderly patients, depression can present by causing cognitive impairment, which can mask as a neurodegenerative disorder. Once treated, the cognitive impairment is often reversible. It is always important to consider and address mood in a patient presenting with memory loss, as **depression rates are very high in patients experiencing true forms of dementia**, and identifying and treating this appropriately can improve cognition and quality of life",
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"explanation": "Alzheimer's dementia follows a much more gradual course and would not cause these distinct episodes of sudden, marked deterioration in memory",
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"explanation": "# Summary\n\nVascular dementia (VaD) is a cognitive impairment resulting from cerebrovascular disease, often presenting with progressive stepwise cognitive deterioration over months or years. Typical presentations are stroke-related vascular disease, subcortical vascular dementia, and mixed dementia. Diagnosis is established via comprehensive history, formal cognitive screening, medication review, exclusion of reversible organic causes, and neuroimaging, preferably MRI. Management revolves around symptomatic treatment, detection and control of cardiovascular risk factors, and advanced care planning.\n\n# Definition\n\nVascular dementia is an umbrella term denoting a collection of cognitive impairment syndromes caused by cerebrovascular disease.These include stroke-related vascular disease, subcortical vascular dementia, and mixed dementia —a combination of Alzheimer's disease and vascular dementia.\n\n# Epidemiology\n\nVascular dementia (VaD) is the second most common type of dementia after Alzheimer's disease, accounting for around 15-20% of all dementia cases.\n\nPrevalence of VaD increases with age, being rare before the age of 65 but significantly rising thereafter. \n\nThe incidence of VaD is higher in males than in females, and higher in individuals with cardiovascular risk factors.\n\n# Aetiology\n\nThe primary cause of vascular dementia is ischemic or hemorrhagic cerebrovascular disease, which leads to brain damage. \n\nVarious vascular events or conditions can lead to VaD, including multi-infarct dementia, single-infarct dementia, subcortical vascular dementia (also known as Binswanger's disease), and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).\n\nRisk factors for VaD mirror those for stroke and other cardiovascular diseases: hypertension, diabetes mellitus, hyperlipidemia, smoking, and atrial fibrillation are significant risk factors. \n\nLess common causes include inflammatory and immunological vascular disorders, genetic conditions, and infections that affect the brain's blood vessels.\n\n# Signs and Symptoms\n\nThe hallmark of vascular dementia is a progressive, **stepwise** deterioration in cognition. This typically occurs over a span of several months to years. Patients may present with a history of strokes, which may be accompanied by stepwise cognitive decline or sudden changes in cognitive function, as well as stroke-like symptoms:\n\n- Visual disturbance\n- Sensory or motor symptoms\n- Difficulty with attention and concentration\n- Seizures\n- Memory disturbance\n- Gait/speech/emotional disturbance\n\nTo compare with Alzheimer's dementia, there is less impairment in episodic memory and more in visual skills, semantic memory and executive functioning.\n\n# Differential Diagnosis\n\nThe differential diagnosis for vascular dementia includes, but is not limited to:\n\n- **Alzheimer's disease**: Predominant memory impairment, slower and continuous decline, usually lack of significant vascular risk factors or neuroimaging evidence of cerebrovascular disease.\n- **Lewy body dementia**: Fluctuating cognition, visual hallucinations, Parkinsonism, and REM sleep behavior disorder are the core features.\n- **Frontotemporal dementia**: Prominent changes in personality and behavior or language difficulties with relative sparing of memory.\n- **Normal pressure hydrocephalus**: Gait disturbance, urinary incontinence, and cognitive impairment (triad of Hakim-Adams).\n\n# Investigations\n\nThe investigations for vascular dementia generally include:\n\n- Comprehensive history and examination.\n- Formal cognition screening, such as MMSE (Mini-Mental State Examination) or MoCA (Montreal Cognitive Assessment).\n- Medication review to exclude medication-induced cognitive impairment.\n- Exclusion of reversible organic causes such as vitamin B12 or folic acid deficiency, hypothyroidism, or normal pressure hydrocephalus.\n- MRI Head, to identify vascular changes, infarcts, or white matter hyperintensities indicative of cerebrovascular disease. The hallmark of vascular dementia is extensive white matter change and infarcts evident on MRI imaging.\n\n[lightgallery]\n\n# Management\n\nThe management of vascular dementia involves:\n\n- Detection of and addressing cardiovascular risk factors such as hypertension, diabetes, hyperlipidemia, and smoking to slow disease progression.\n- Cognitive stimulation programmes, music and art therapy, etc. to help with cognitive impairment. \n- Symptomatic treatment, including cognitive enhancers such as cholinesterase inhibitors or memantine - if there is evidence of co-existent AD, Parkinson's dementia, or dementia with Lewy bodies. Management of neuropsychiatric symptoms.\n- Advanced care planning to prepare for progressive cognitive and physical decline.\n\n# NICE Guidelines\n\n[NICE CKS - Dementia](https://cks.nice.org.uk/topics/dementia/)",
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"question": "A 74-year-old man is brought to the GP by his wife, concerned about his deteriorating memory over the past 3 years. She reports several episodes of marked decline, with the most recent occurring when he woke up and failed to recognize his children. \n\nHe has a past medical history of hypertension and atrial fibrillation, for which he takes amlodipine, ramipril and apixaban. He also had a stroke ten years previously and has some residual visual deficit and right arm weakness from this.\n\n\nWhat is the most likely diagnosis?",
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"explanation": "This patient has had a simple faint, or vasovagal syncope. This is commonly positional, such as here following a long period of standing on the tube, and is often described as being preceded by tunnel vision or vision \"closing in\". A short period of convulsions can be normal. It can be differentiated from proper seizure activity by the lack of a post-ictal phase",
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"explanation": "If this were an epileptic seizure, it might last longer than 15 seconds, be accompanied by classic seizure indicators such as incontinence or tongue biting and be followed by a post-ictal period. The positional nature of this episode, combined with the short course of the convulsions and rapid recovery of the patient to GCS 15, makes an epileptic event very unlikely",
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"explanation": "If a patient has severe enough hypoglycaemia to cause a collapse, you would expect some residual drowsiness, reflected in reduced GCS. Symptoms would also be expected to come on more gradually than in this stem",
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"explanation": "In syncope relating to arrhythmia, the history would usually elude to some preceding symptoms such as palpitations, chest pain or shortness of breath to indicate a cardiac origin. In this context, an arrhythmogenic collapse would be a much less likely cause than a simple faint",
"id": "33460",
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"explanation": "If this patient has been sat down on the tube for a prolonged period and had then stood up prior to collapsing, postural hypotension could be a possible explanation",
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"explanation": "# Summary\n \nSyncope means a transient loss of consciousness and is a common emergency presentation. There are many causes with important differentials being reflex syncope, orthostatic hypotension and cardiac syncope. The term \"blackouts\" is commonly used to refer to a loss of consciousness, and includes differentials such as seizures. A thorough history (including a collateral if available) is important to help to differentiate the above, followed by examination including a lying-standing blood pressure. Initial investigations include an ECG, a blood glucose and consideration of a basic set of bloods to screen for abnormalities such as hyponatraemia that could trigger seizures. Emergency management encompasses ruling out serious causes, treating any injuries sustained during the episode and referral on for specialist investigations and management as appropriate.\n\n# Definition \n\nBlackouts refer to episodes of transient loss of consciousness, which occur for a variety of reasons. Syncope refers to a transient loss of consciousness secondary to cerebral hypoperfusion, with syncopal presentations making up the majority of cases of blackouts.\n \n# Epidemiology \n \nBlackouts are common, with an estimated 50% of the population experiencing at least one in their lifetime. 3% of emergency department presentations and 1% of hospital admissions in the UK are due to blackouts.\n \n# Aetiology\n \n**Causes of cardiac syncope:**\n\n- Structural\n - Acute myocardial infarction \n - Aortic stenosis \n - Ischaemic cardiomyopathy\n - Hypertrophic obstructive cardiomyopathy\n - Cardiac tamponade\n- Electrical \n - Tachyarrhythmias e.g. superventricular tachycarcia (SVT), ventricular tachycardia (VT), ventricular fibrillation (VF)\n - Bradyarrhythmias e.g. sick sinus syndrome, heart block\n - Inherited channelopathies e.g. Brugada syndrome\n\n**Causes of reflex syncope:**\n \n - Vasovagal syncope (\"fainting\")\n - Situational syncope e.g. following defecation, post-exercise, or straining to pass urine\n - Carotid sinus syndrome - occurs due to hypersensitivity of the carotid sinus baroreceptor\n\n**Other causes of syncope:**\n \n - Orthostatic hypotension\n - Pulmonary embolism\n - Occult haemorrhage e.g. subarachnoid haemorrhage, GI bleeding, ruptured aortic aneurysm\n - Head trauma\n - Hypoglycaemia\n\n **Non-syncopal causes of blackouts:**\n \n - Seizures\n - Psychogenic pseudosyncope\n - Psychogenic non-epileptic seizures\n\n# Symptoms and Signs\n \nWhen taking a history and examining a patient after a blackout, there are several additional symptoms and signs to elicit that can help identify the likely cause. If the blackout was witnessed, take a collateral history also. \n\n**Questions to ask about before the blackout:**\n\n- What were they doing/any triggers?\n - Exertional syncope (cardiac)\n - After exercise (vasovagal/orthostatic hypotension)\n - Head movements/pressure on neck (carotid sinus syndrome)\n - Prolonged standing (orthostatic hypotension)\n - Pain (vasovagal)\n - Repeated episodes after defecation/micturition/swallowing/coughing (situational syncope)\n - After a meal (vasovagal or orthostatic hypotension)\n- Prodromal symptoms?\n - Feeling warm/hot, sweating, nausea (vasovagal)\n - Déjà vu or jamais vu (epilepsy)\n- Intercurrent illness?\n - e.g. diarrhoea and vomiting leading to dehydration and hypotension\n- Associated symptoms?\n - Palpitations/chest pain/shortness of breath (cardiac/PE)\n - Headache (subarachnoid haemorrhage)\n - Visual disturbance (if worse on standing may be orthostatic hypotension/vasovagal)\n - Lightheadedness (orthostatic hypotension/vasovagal)\n \n**Questions to ask about during the blackout:**\n \n- Any protective measures taken?\n - e.g. hands outstretched to break fall \n - It can be difficult to ascertain whether the patient lost consciousness\n - If protective measures were observed may be a fall rather than a blackout\n - Patients having a vasovagal may lower themselves to the floor\n- Tongue biting?\n - Lateral tongue typical in epilepsy\n - Tip of tongue typical in vasovagal\n- Incontinence of bowels or bladder? (epilepsy)\n- Duration of loss of consciousness\n - Less than 30 seconds (suggests syncope)\n - Over 1 minute (suggests epilepsy)\n - Over 5 minutes (psychogenic causes more likely)\n- Seizure activity observed?\n - Myoclonic jerks are common in vasovagal syncope\n - Prolonged limb jerking and abnormal posturing suggests a seizure\n- Appearance during blackout e.g. pallor, eyes closed or open? \n \n\n**Questions to ask about after the blackout:**\n\n- Any injuries sustained during the blackout?\n - Ask about site and severity\n- Confusion or amnesia after conciousness regained?\n - If lasts minutes may indicate post-ictal state after a seizure\n- Focal neurological signs (e.g. weakness down one side)\n\n**Other important questions:**\n\n- Any previous blackouts/similar events?\n- Past medical history e.g. any heart disease?\n- Medications (may contribute to orthostatic hypotension)\n- Family history including sudden cardiac or unexplained death in young relatives\n- Recreational drug and alcohol use (alcohol may exacerbate orthostatic hypotension)\n\n**On examination:**\n\n- Do a full set of observations including a lying standing blood pressure to assess for a postural drop\n - A fall in systolic blood pressure by 20mmHg or more or diastolic by 10mmHg or more, or a fall in the systolic to <90mmHg with symptoms indicates orthostatic hypotension\n- Full systems examination focusing on the heart (e.g. any murmurs or abnormalities of the pulse?)\n- Neurological examination including cognitive function (may be abnormal in the post-ictal state)\n \n# Investigations\n \nInitial investigations as follows should be carried out in the emergency setting; patients should also be referred for further specialist investigations (e.g. EEG for epilepsy, Holter monitoring for suspected arrhythmias) as appropriate.\n\n- **Blood glucose** for hypoglycaemia\n- **ECG** looking for arrhythmias, ischaemic changes or evidence of structural abnormalities (e.g. left ventricular hypertrophy in severe aortic stenosis)\n- **Blood tests** looking for electrolyte abnormalities that could trigger seizures or arrhythmias, anaemia in haemorrhage, raised inflammatory markers in intercurrent illness, AKI in dehydration\n- **Transthoracic Echocardiography** should be done in suspected structural heart disease (e.g. aortic stenosis)\n- **24 hour ambulatory blood pressure monitoring** with an activity diary may be useful to assess for e.g. post-prandial hypotension\n \n# Management\n \n- Specific emergency management may be required for any serious cause identified (e.g. head injury, ruptured aortic aneurysm).\n- Investigate for and treat any injuries resulting from the collapse and provide analgesia.\n- Some patients can be discharged with reassurance and advice e.g. uncomplicated vasovagal episode, situational syncope.\n- Patients with suspected epilepsy should be referred to a first fit clinic.\n- Patients with suspected psychogenic causes of blackouts should also be referred for neurology assessment as these can be difficult to differentiate from epilepsy\n- Patients with suspected cardiac syncope (e.g. abnormal ECG, exercise-induced syncope, heart murmur, heart failure, new/unexplained breathlessness or family history of sudden cardiac death in the young/inherited cardiac condition) should be referred for specialist review within 24 hours.\n- Consider urgent referral for cardiovascular review in all patients over 65 with syncope and no prodromal symptoms.\n- All patients with syncope of unclear cause should be referred for specialist cardiovascular review (with urgency based on the clinical picture)\n\n **Driving advice for patients with syncope:**\n\n- Patients with unexplained syncope must inform the DVLA and their licence will be revoked for 6 months (12 months if Group 2) \n- Patients with a vasovagal whilst standing can drive and need not inform the DVLA if they are Group 1 drivers (Group 2 drivers must not drive and should inform the DVLA)\n- Patients with cardiac syncope must not drive and should inform the DVLA - group 1 drivers may be allowed to drive after 4 weeks if a cause is identified and treated\n- Full guidance including for seizures can be found in the references section\n \n# NICE Guidelines\n \n[NICE CKS Guidance on Blackouts](https://cks.nice.org.uk/topics/blackouts/)\n\n[NICE: Transient loss of consciousness ('blackouts') in over 16s](https://www.nice.org.uk/guidance/cg109)\n \n# References \n \n[DVLA guidance on transient loss of consciousness](https://www.gov.uk/guidance/neurological-disorders-assessing-fitness-to-drive#transient-loss-of-consciousness-blackouts--or-lostaltered-awareness)",
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"question": "A 23-year-old female experiences rapid \"closing in\" of her vision and then collapses when travelling as a standing passenger on a busy tube train. Passers-by witness convulsing movements of her arms and legs for approximately 15 seconds following the collapse. She regains consciousness immediately after and has a Glasgow Coma Scale (GCS) of 15.\n\nWhat is the most likely diagnosis?",
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"explanation": "This would be the last resort treatment option in refractory status epilepticus where the seizure activity is unable to be controlled with other agents",
"id": "33467",
"label": "e",
"name": "Rapid sequence induction of anaesthesia",
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"explanation": "Intravenous sodium valproate is an anticonvulsant drug; however, it is less appropriate agent in this context. The patient is known to be on levetiracetam normally to good effect, is any anticonvulsant were to be given, it should be the patient's usual medication. Additionally, valproate should be avoided where possible in women of child-bearing age",
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"name": "Intravenous sodium valproate",
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"explanation": "The patient is usually on levetiracetam, and this may be given intravenously if the seizure cannot be terminated with benzodiazepines alone; however, it is not a first-line agent for the management of status epilepticus",
"id": "33465",
"label": "c",
"name": "Intravenous levetiracetam",
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"explanation": "This may be used in the community, and family members can be trained to administer this if loved ones are prone to having seizures. Where the patient is in hospital and has intravenous access, lorazepam would be more appropriate",
"id": "33464",
"label": "b",
"name": "Rectal diazepam",
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"explanation": "Benzodiazepines are the first-line agents for terminating seizures. They can be given in the form of intravenous lorazepam, buccal midazolam or rectal diazepam, depending on the context, access and availability of medication. Where possible, intravenous lorazepam should be the first choice. A second dose can be given if the seizure does not terminate within 10 minutes of the first dose",
"id": "33463",
"label": "a",
"name": "Intravenous lorazepam",
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"comment": "Surely it isn't status since it has been more than 5 mins since the termination of her first seizure?",
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"comment": "not sure but maybe being post ictal implies that she had incomplete resolution from the first seizure in which case it would be status ? ",
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"comment": "i think recent guidelines have changed so that you administer a second dose of BZD if the seizure does not terminate within 5 minutes of the first dose",
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"comment": "I think it's IV Lorazzy if you already have access.",
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"explanation": "# Summary\n\nStatus Epilepticus is defined as a seizure lasting 5 minutes or more, or multiple seizures occurring within a 5-minute window without regaining full consciousness between episodes. It is a medical emergency, and treatment should begin promptly at the 5-minute mark. Initial management involves administering benzodiazepines, such as rectal diazepam, buccal midazolam, or intravenous lorazepam. If there is no response to two doses of benzodiazepines, second-line treatments include levetiracetam, phenytoin, or sodium valproate. Refractory cases may require general anesthesia with agents like propofol or midazolam. Investigations include blood tests, toxicology screen as well as neuroimaging and CSF analysis if the cause remains unclear\n\n# Definition\n\nStatus epilepticus is defined as a seizure lasting 5 minutes or more OR multiple seizures over 5 minutes without returning to a full level of consciosuness between episodes.\n\nIt should be assumed at 5 minutes and appropriate treatment and investigations initiated.\n\n# Acute management of status epilepticus\n\nEmergency AED therapy for convulsive status epilepticus [NICE guidelines](https://www.nice.org.uk/guidance/ng217/chapter/7-Treating-status-epilepticus-repeated-or-cluster-seizures-and-prolonged-seizures):\n\n\n\n\n**Premonitory stage (0-10 minutes)** \n\n- Diazepam 10−20 mg given rectally, repeated once 15 minutes later if status continues to threaten, or midazolam 10 mg given buccally. If seizures continue, treat as below.\n\n**Early status (0-30 minutes)** \n\n- If in the community:\n\t- Buccal Midazolam or Rectal Diazepam \n- If IV access is obtained and resuscitation facilities are available:\n\t- Lorazepam (intravenous) 0.1 mg/kg (usually a 4 mg bolus, repeated once after 10−20 minutes; rate not critical). \n\n**Established status (0-60 minutes)** \n\n- If not responding to 2 doses of benzodiazepine, give any of the following as second-line treatment\n\t- Levitiracetam\n\t- Phenytoin\n\t- Sodium Valproate\n\n**Refractory status (30-90 minutes)**\n\n- General anaesthesia, with one of:\n\n\t- Propofol (1–2 mg/kg bolus, then 2–10 mg/kg/hour) titrated to effect\n\t- Midazolam (0.1–0.2 mg/kg bolus, then 0.05–0.5 mg/kg/hour) titrated to effect\n\t- Thiopental sodium (3–5 mg/kg bolus, then 3–5 mg/kg/hour) titrated to effect; after 2–3 days infusion rate needs reduction as fat stores are saturated\n\t- Anaesthetic continued for 12−24 hours after the last clinical or electrographic seizure, then dose tapered.\n\n\n# Investigations\n\n- Arterial Blood Gas\n- Routine Blood tests including FBC, U&E, LFT, CRP, Clotting, Bone Profile \n- Toxicology screen (urine)\n- Anti-epileptic drug levels (if appropriate)\n- If the underlying cause is unclear, further investigations can include:\n\t- CT/MRI Brain Imaging\n\t- Lumbar Puncture \n\n\n# References\n\n[Click here for the NICE guidelines on managing status epilepticus](https://www.nice.org.uk/guidance/ng217/chapter/7-Treating-status-epilepticus-repeated-or-cluster-seizures-and-prolonged-seizures)",
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"question": "A 27-year-old female with a history of epilepsy is brought into the Emergency Department by ambulance following a seizure at home 20 minutes ago. She usually takes levetiracetam. She is post-ictal and has intravenous access established by the ambulance crew. During your assessment, she starts having a second seizure.\n\nWhat is the first-line agent to stop this patients seizure?",
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"explanation": "Over the counter analgesia, particularly paracetamol is the most common cause of analgesia overuse headache due to its use being relatively unrestricted. It is an important differential to consider in patients presenting with chronic/recurrent headaches. The criteria to consider this diagnosis is the use of the medication on 2-3 days per week and 10 or more days per month for at least 3 months - these episodes are only happening once per week and have the characteristic quality of a migraine",
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"explanation": "The headache experienced in a SAH is often described as a \"thunderclap\" headache, referring to the sudden onset and severe quality of the pain, which patients often describe as \"the worst headache of my life\"",
"id": "33470",
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"explanation": "Cluster headaches are a rare form of headache disorder compared with migraine and tension headaches. They are most common in younger male patients, and the pain is classically very extreme, acute in onset (comes on to maximal intensity within minutes) and is localised around one eye (which can become red). Episodes are short compared with migraines, with the pain lasting less than 3 hours (compared to migraines which last between 4-72 hours). The patient often experiences restlessness and agitation during episodes due to the intensity of the pain. They are called \"cluster headaches\" as they tend to occur in clusters, with periods of frequent attacks (can be several attacks per day) interspersed with periods of no headaches, which can even extend for years",
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"explanation": "Tension headaches tend to occur across the frontal/forehead region, typically bilaterally and do not have the characteristic throbbing/ pounding character of a migraine. They are also not strongly associated with nausea and are not as disabling, with patients usually able to continue with their work/ activity despite the pain",
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"explanation": "The POUND criteria for migraine highlight the key symptoms of the condition, all of which are being experienced by this patient. The headache is **P**ulsatile in nature, and each episode lasts between 4-72 h**O**urs. The pain is **U**nilateral, associated with **N**ausea +/- vomiting and is significantly **D**isabling for the patient, preventing them from going about their usual daily activities. Patients may also experience a preceding aura, with either visual or sensory symptoms. Generally, migraines are not _fully_ responsive to simple analgesia such as paracetamol and ibuprofen - specific relief can be achieved with the use of an antiemetic and sumatriptan. In patients where migraines are occurring very frequently, prophylaxis can be considered with medications including propranolol or topiramate",
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"comment": "O for hOurs lol",
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"explanation": "# Summary\r\n\r\nMigraine is a common neurological disorder characterised by recurrent, unilateral, throbbing headaches often preceded by an aura such as visual or sensory symptoms. Migraines can last between 4-72 hours and often result in photophobia and phonophobia. Key signs and symptoms include a unilateral headache, a pulsating character, impairment or worsened by daily activities, and presence of nausea, vomiting or photophobia. Diagnosis is often based on clinical history, focusing on the presence of an aura. Management strategies include avoidance of triggers, prophylaxis with medications such as Propranolol, Topiramate or Amitriptyline, and managing acute attacks with oral triptans alongside Paracetamol or an NSAID.\r\n\r\n# Definition\r\n\r\nMigraine is a primary headache disorder characterised by intense episodes of debilitating headaches, usually unilateral and pulsating in nature. Symptoms may be preceded by an 'aura' which manifests as visual disturbances or sensory changes. The pain usually lasts from 4-72 hours and can be accompanied by nausea, vomiting, photophobia, and phonophobia.\r\n\r\n# Epidemiology\r\n\r\nMigraines are one of the most prevalent neurological disorders worldwide, affecting roughly 12% of the global population. It is more common in women, with a male to female ratio of approximately 1:3, likely related to hormonal influences. The peak incidence occurs between the ages of 30-39.\r\n\r\n# Aetiology\r\n\r\nThe exact cause of migraines is not fully understood, but it is likely a combination of genetic and environmental factors. \n\nThe triggering factors are variable and can include certain foods, changes in weather, stress, hormonal changes, and certain medications such as oral contraceptives.\r\n\r\n# Signs and Symptoms\r\n\r\n- Aura (usually visual or sensory symptoms preceding the headache)\r\n- Unilateral throbbing headache\r\n- Photophobia and phonophobia\r\n- Nausea and/or vomiting\r\n\r\nThe International Headache Society criteria for migraine without aura:\r\n\r\n| Criteria | Description |\r\n| -------- | ------------------------------------------------------------ |\r\n| A | At least five attacks fulfilling criteria B-D |\r\n| B | Headache attacks lasting 4-72 hours (untreated or unsuccessfully treated) |\r\n| C | Headache has at least two of the following four characteristics: <br>1. Unilateral location <br>2. Pulsating quality <br>3. Moderate to severe pain intensity <br>4. Aggravation by or causing avoidance of routine physical activity |\r\n| D | During headache, at least one of the following: <br>1. Nausea and/or vomiting <br>2. Photophobia and phonophobia |\r\n| E | Not better accounted for by another ICHD-3 diagnosis |\r\n\r\n# Differential Diagnosis\r\n\r\nMigraines must be differentiated from other conditions that present with severe headache. Some of these include:\r\n\r\n- Tension-type headache: Bilateral, band-like pressure or tightness, not worsened with physical activity, no associated nausea or vomiting.\r\n- Cluster headache: Severe, unilateral, orbital, supraorbital and/or temporal pain lasting 15-180 minutes, occurring up to 8 times a day, associated with autonomic symptoms like ptosis, miosis, lacrimation.\r\n- Subarachnoid hemorrhage: Sudden-onset severe headache, often described as \"the worst headache of my life\", associated with nausea, vomiting, and possible loss of consciousness.\r\n- Giant cell arteritis: New headache in a person over 50 years, scalp tenderness, jaw claudication, visual disturbances, elevated ESR and CRP.\r\n\r\n# Investigations\r\n\r\nDiagnosis is primarily clinical, based on the history and examination. \n\nA headache diary is important to help identify triggers and response to treatment.\n\nIf secondary causes of headaches are suspected, further investigations may be warranted, such as neuroimaging (MRI or CT) or blood tests (ESR, CRP for giant cell arteritis).\r\n\r\n# Acute Management\r\n\n- **Avoidance of triggers**: \n - Identify and avoid potential triggers like certain foods, stress, and poor sleep.\n- **Medications for acute attacks**: \n - **Triptans** (e.g., Sumatriptan) – avoid in patients with ischaemic heart disease.\n - **Paracetamol** or an **NSAID** (e.g., Ibuprofen) can be used in combination with triptans.\n - **Anti-emetics** (e.g., Metoclopramide)\n- **Special considerations**:\n - Female patients with migraine with aura should avoid the **combined oral contraceptive pill** due to increased risk of ischaemic stroke.\n\n# Prophylaxis\n\n- Medications:\n - **Propranolol** (contraindicated in asthma).\n - **Topiramate**.\n - **Amitriptyline**.\n - **Candesartan**.\n- Injections:\n\t- Greater Occipital Nerve Block\n\t- Botulinum Toxin Injection \n- **Newer treatments**:\n - **Rimegepant** (per NICE guidance, May 2023):\n - Used for preventing episodic migraine.\n - Suitable when at least 3 preventive treatments have failed.\n - Indicated for adults with 4-15 migraine attacks per month.\n\nRegular use of acute migraine medications (e.g., triptans, NSAIDs) more than 10-15 days per month can lead to **medication overuse headache (MOH)**.\n\nPatients should be counseled on limiting the use of acute treatments to prevent MOH.\n\n## References\r\n\r\n[Click here for NICE Clinical Knowledge Summaries on Migraines](https://cks.nice.org.uk/topics/migraine/)",
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"question": "A 31-year-old female presents to her GP with headaches. She describes these as \"pounding\" and located across her temple unilaterally, usually lasting for around 10 hours. These headaches are associated with significant nausea and are quite debilitating - when they occur, she has to take the day off work which is impacting her career progression. She has been taking regular paracetamol and ibuprofen during episodes with only moderate relief. She is having 1 episode per week at present.\n\nWhat is the most likely diagnosis?",
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"explanation": "Migraine aura can be in the form of visual or sensory phenomena. Patients describe different experiences, which can including blurring of vision, seeing flashes or floaters or the sensation of pins and needles/ tingling in the arms +/- legs or face. These symptoms can mimic stroke; however, in migraine, they would typically be followed by other migraine symptoms such as nausea/vomiting, aversion to lights (photophobia) and characteristic unilateral headache",
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"explanation": "In stroke, the deficit would not self-resolve as described in the stem",
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"explanation": "GCA most commonly affects women over 50 and is not associated with poor vascular health. Symptoms of GCA classically include a characteristic headache with tenderness over the temple region and jaw claudication pain. _It can cause amaurosis fugax_ but it would not present as the sole symptom of the condition, as can be the case in the context of a TIA. Visual loss in GCA can be irreversible, which is why it is important to promptly treat the condition with corticosteroids to prevent this from occurring",
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"explanation": "Patients with angle-closure glaucoma get an acutely red and painful eye. Their vision can become blurred, and patients often report seeing haloes around lights. If the condition is not treated in time and total visual loss occurs, this is **irreversible**",
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"explanation": "Amaurosis fugax refers to painless temporary loss of vision (classically monocular, though more rarely can be binocular) and, in this instance, is reflective of a form of TIA. A TIA is defined as a sudden neurological deficit that entirely resolves within a 24-hour window and classically lasts only minutes. It often reflects carotid artery stenosis. This patient has significant vascular risk factors and a history of a previous vascular event which makes this option even more likely",
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"explanation": "# Summary\n\nA Transient Ischaemic Attack (TIA), colloquially known as a \"mini-stroke\", represents a sudden focal neurological deficit of vascular origin, characterised by symptom resolution typically within an hour. The absence of an acute infarct on imaging differentiates it from a stroke. Key signs and symptoms include speech difficulty, or arm/leg weakness or sensory changes. Important differential diagnoses include focal seizures, migraine, and intracranial bleeding. Investigations primarily involve neuroimaging, while management aims at reducing future stroke risk with lifestyle changes, control of vascular risk factors, and initiation of antiplatelet therapy. NICE guidelines recommend immediate referral for individuals with suspected TIA for assessment within 24 hours.\n\n# Definition\n\nA transient ischaemic attack (TIA) is a sudden-onset focal neurological deficit with a vascular aetiology, typically resolving symptoms within less than 1 hour. \n\n# Epidemiology\n\nTIA is a significant health concern worldwide due to its association with future stroke risk. \n\nThe incidence is 230 cases per 100000 person-years.\n\nRisk factors include:\n \n* Hypertension\n* Diabetes mellitus\n* High cholesterol\n* Atrial fibrillation\n* Carotid stenosis\n* Smoking\n* Family history of cardiovascular disease/stroke\n* History of cardio-embolic events\n\n# Signs and Symptoms\n\nPatients typically present with a sudden onset of focal neurological deficits which may include:\n\n- Speech difficulty (dysphasia)\n- Arm or leg weakness\n- Sensory changes \n- Ataxia, vertigo or loss of balance\n- Visual disturbance: Homonymous hemianopia, diplopia \n\nSymptoms of TIA are transient, with most resolving within 1 hour.\n\n# Differential Diagnosis\n\nIn assessing for a TIA, clinicians should consider the following differential diagnoses:\n\n- **Stroke**: Persistent symptoms with evidence of ischaemia on MRI imaging\n- **Focal motor seizures**: These might be suggested by positive symptoms preceding the weakness, such as shaking.\n- **Migraine with aura**: Characterized by a preceding aura which may present with visual disturbances, tingling, or numbness, followed by headache.\n\n\n# Investigations\n\nTo confirm the diagnosis and assess the extent of vascular disease, the following investigations are generally recommended:\n\n- Neuroimaging \n\t- The preferred modality is MRI to assess for any evidence of ischaemia, haemorrhage or consider alternative pathologies\n- Carotid ultrasound (looking for carotid stenosis\n- Echocardiogram (looking for cardiac thrombous)\n- 24 hour tape (looking for atrial fibrillation)\n- Blood tests (including glucose, lipid profile, clotting factors)\n\n\n# Management\n\nPatients who have had a suspected TIA should be referred for immediate assessment, ideally to be seen **within 24 hours** of onset of symptoms. The aim of management is to reduce the future risk of stroke and includes:\n\n- Lifestyle modifications (smoking cessation, regular exercise, healthy diet)\n- Control of vascular risk factors (hypertension, diabetes, dyslipidaemia)\n- Initiation of antiplatelet therapy (e.g., aspirin, clopidogrel) unless contraindicated\n- In selected cases, endarterectomy or stenting of the carotid artery might be indicated:\n\t- > 70% stenosis according European Carotid Surgery Trialists' Collaborative Group criteria (ECST) or\n\t- > 50% according to North American Symptomatic Carotid Endarterectomy Trial criteria (NASCT)\n\n# References\n\n[Click here for NICE Clinical Knowledge Summaries](https://cks.nice.org.uk/topics/stroke-tia/management/suspected-transient-ischaemic-attack/)",
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"question": "A 52-year-old man presents to the Emergency Department following a temporary loss of vision in his right eye. He was cleaning the kitchen and suddenly lost vision in his right eye. This returned within approximately 5 minutes. The left eye was not affected, and there were no other associated symptoms. He has a past medical history of hypercholesterolaemia, type 2 diabetes, hypertension, obesity and has had a previous myocardial infarction 18 months ago.\n\nWhat is the most likely diagnosis?",
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"explanation": "An intracranial neoplasm can cause focal neurological symptoms depending on its location; however, you would expect this to have a more gradual/ insidious onset, accompanied by more classic symptoms of malignancy such as weight loss. The symptoms would be highly unlikely to start suddenly, as is the case in this stem",
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"explanation": "Neurological symptoms can be due to psychosomatic causes; however, this is a diagnosis of exclusion and cannot be assumed to be the most likely cause of a new, sudden neurological deficit. Classically in these cases, the neurological signs and symptoms are inconsistent with one another, not fitting into one vascular territory and unable to be localised",
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"explanation": "The patient's wife has called the ambulance as she noted his behaviour and symptoms as atypical for him. That patient drinks to excess daily - it is unlikely that his wife is unable to recognise his behaviour whilst intoxicated. Additionally, the history notes the new symptoms being present on waking, which suggests he is likely to be at his most sober",
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"explanation": "Dysphasia and unilateral motor disturbance (either weakness or total paralysis) are common symptoms of a stroke. They are included in the 'FAST' (face, arms, speech, time) pneumonic, which forms part of early recognition advertising campaigns. This patient also has multiple risk factors for vascular disease, as well as atrial fibrillation, which also poses a risk of thrombus formation, particularly given that he is known to have poor compliance with his medications (including his anticoagulation)",
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"explanation": "Wernicke's encephalopathy refers to thiamine deficiency (classically relating to a long history of alcohol excess) which can cause a typical tried of Confusion, Ophthalmoplegia and ATaxia (helpful pneumonic - COAT). Although this patient does have a history of alcohol excess, which would put him at an increased group of developing the condition, this stem does not mention any eye signs of gait disturbance, two key parts of the syndrome",
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"comment": "Could this not be Saturday night palsy?",
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"explanation": "# Summary\n\nAn ischaemic stroke is a medical emergency characterised by a sudden onset of focal neurological deficit secondary ischaemia. Depending on the affected cerebral area, symptoms can range from contralateral motor and sensory deficits, homonymous hemianopia, to higher cerebral dysfunction (such as aphasia and neglect). Initial management of suspected stroke necessitates urgent neuroimaging, primarily via non-contrast CT scan, to differentiate between ischaemic and haemorrhagic types. Further investigations such as carotid ultrasound, CT/MR angiography, echocardiogram, and various blood tests (e.g., serum glucose and lipids) help define the cause of stroke and quantify vascular risk factors. Acute management of ischaemic stroke involves thrombolysis in selected patients (usually within 4.5 hours of symptom onset), provided there are no contraindications, or mechanical thrombectomy for eligible patients. Long term management usually involves antiplatelet therapy, risk factor optimisation and multidisciplinary rehabilitation.\n\n\n# Definition\n\nAn ischaemic stroke describes a sudden onset focal neurological deficit secondary to focal brain ischaemia, with symptoms lasting >24 hours (or with evidence of infarction on imaging).\n\n# Aetiology\n\n85% of strokes are ischaemic while 15% are haemorrhagic.\n\nIschaemic stroke occurs when blood supply in a cerebral vascular territory is reduced secondary to stenosis or complete occlusion of a cerebral artery.\n\nThe ischaemic penumbra describes the cerebral area surrounding the ischaemic event where there is ischaemia without necrosis. This area is amenable to recovery with thrombolysis.\n\nIn terms of underlying aetiology of ischaemic stroke: \n\n- 25% are caused by intracranial small vessel atherosclerosis.\n- 50% are caused by large vessel atherosclerosis e.g. carotid artery stenosis.\n\t- Typically results from thrombus formation on the atherosclerotic plaque, and subsequent embolism of the thrombus to a smaller cerebral artery.\n- 20% of ischaemic strokes are cardio-embolic \n\t- e.g. in atrial fibrillation there is stasis of blood flow in the left atrium, predisposing to thrombus formation in the left atrium, and subsequent embolisation to the brain.\n\t- Rare causes of ischaemic stroke include primary vascular causes (such as vasculitis and arterial dissection) and haematological causes (prothrombotic states).\n\n\n\n# Stroke risk factors\n\n- Age\n- Male Sex\n- Family History\n- Hypertension\n- Smoking\n- Diabetes \n- Atrial fibrillation\n- High cholesterol\n- Obesity\n- Migraine \n\n# Stroke classification \n\nThe **Bamford/Oxford Stroke Classification System** is the most common classification system for ischaemic stroke. Although it is not used frequently in clinical practice, it is a helpful aide memoire to remember the localisation of common stroke syndromes.\n\nA total anterior circulation infarct (TACI) is defined by:\n\n- Contralateral hemiplegia or hemiparesis, AND\n- Contralateral homonymous hemianopia, AND\n- Higher cerebral dysfunction (e.g. aphasia, neglect)\nA TACI involves the anterior AND middle cerebral arteries on the affected side.\n\nA partial anterior circulation infarct (PACI) is defined by:\n\n- 2 of the above, OR\n- Higher cerebral dysfunction alone.\n- A PACI involves the anterior OR middle cerebral artery on the affected side.\n\nA lacunar infarct (LACI) is defined by: a pure motor stroke, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis or dysarthria-clumsy hand syndrome.\nA LACI affects small deep perforating arteries, typically supplying internal capsule or thalamus.\n\nA posterior circulation infarct (POCI) is defined by:\n\n- Cerebellar dysfunction, OR\n- Conjugate eye movement disorder, OR\n- Bilateral motor/sensory deficit, OR\n- Ipsilateral cranial nerve palsy with contralateral motor/sensory deficit, OR\n- Cortical blindness/isolated hemianopia.\n\nA POCI involves the vertebrobasilar arteries and associated branches (supplying the cerebellum, brainstem, and occipital lobe).\n\n[lightgallery]\n\n# Posterior Stroke Syndromes\n\nThere are a number of different posterior stroke syndromes that you should be aware of:\n\n- Basilar artery occlusion is more likely to present with locked in syndrome (quadriparesis with preserved consciousness and ocular movements), loss of consciousness, or sudden death.\n\n- Anterior inferior cerebellar artery results in lateral pontine syndrome, a condition similar to the lateral medullary syndrome but with additional involvement of pontine cranial nerve nuclei. It leads to cerebellar ataxia, vertigo, hearing loss as well as ipsilateral facial weakness\n- Wallenberg's syndrome (lateral medullary syndrome) causes ipsilateral Horner's syndrome, ipsilateral loss of pain and temperature sensation on the face, and contralateral loss of pain and temperature sensation over the contralateral body.\n- Weber's syndrome/medial midbrain syndrome (paramedian branches of the upper basilar and proximal posterior cerebral arteries): causes an ipsilateral oculomotor nerve palsy and contralateral hemiparesis.\n\n# Acute management of ischaemic stroke\n\n\n- Patients should be approached in the DR ABCDE manner.\n- CT Head should be perfomed on arrival to the emergency department to distinguish ischaemic from haemorrhagic stroke. \n- If no evidence of ischaemic stroke, a CT Angiogram and CT perfusion (in select patients) should be performed to assess for evidence of large vessel occlusion and a salvageable ischaemic penumbra\n- Thrombolysis with Alteplase (tissue plasminogen activator) is considered if:\n\t- The patient presents within 4.5 hours of symptom onset (Up to 9 hours in select patients with good baseline and favourable perfusion imaging) \n\t- No contraindications such as:\n\t\t- Recent head trauma\n\t\t- Recent surgery\n\t\t- Systolic lood Pressure above 185 \n\t\t- Currently taking oral anticoagulation\n\t\t- Raised INR (local guidelines vary)\n- Mechanical Thrombectomy is usually considered in patients with:\n\t- Anterior Circulation Stroke (evidence base is poorer for posterior circulation stroke)\n\t- Evidence of large vessel occlusion (ideally proximal up to distal M1)\n\t- Good functional baseline\n\t- Favourable perfusion criteria indicating salvageable tissue\n\t- Presenting within 6 hours (Up to 24 hours in select patients with good baseline and favourable perfusion imaging)\n\nIf hyper-acute treatments are not offered, patients are started on an antiplatelet agent such as Aspirin or Clopidogrel (local guidelines vary).\n\nIf hyper-acute treatments are offered, antiplatelets are usually started 24 hours after the treatment following a repeat CT Head that excludes any haemorrhagic transformation.\n\n# Stroke investigations (Post-acute)\n\nMRI Head with Diffusion Weighted Imaging (DWI) is the gold standard test to confirm the presence of an acute ischaemic stroke, which can be present within a few minutes of stroke onset. Due to logistical challenges of acute MRI scanning, this is normally performed within 24 hours following initial hyperacute treatment.\n\nInvestigations in the post-hyperacute phase aim to further define the cause of the stroke and to quantify vascular risk factors.\n\nThese include:\n\n- Carotid ultrasound (to identify critical carotid artery stenosis)\n- 24 to 72 hour cardiac monitoring to assess for evidence of atrial fibrillation\n- CT/MR angiography (to identify intracranial and extracranial stenosis)\n- Echocardiogram (if a cardio-embolic source is suspected). \n- In young patients further investigation e.g. a vasculitis screen or thrombophilia screen may be necessary.\n- HbA1c and Serum Lipids to optimise other cardiovascular risk factors \n\n\n# Stroke management (Chronic)\n\nRehabilitation and supportive management will include an **MDT approach** with involvement of physiotherapy, occupational therapy, speech and language therapy, and neurorehabiliation.\n\n\nThe key steps in secondary stroke prevention can be remembered by the mnemonic HALTSS:\n\n- Hypertension: \n\t- Studies show there is no benefit in lowering the blood pressure acutely (as this may impair cerebral perfusion) unless there is malignant hypertension (systolic blood pressure >180 mmHg). Anti-hypertensive therapy should, however, be initiated 2 weeks post-stroke.\n- Antiplatelet therapy:\n\t- Patients should be administered Clopidogrel 75 mg once daily for long-term antiplatelet therapy. In patients with ischaemic stroke secondary to atrial fibrillation, however, warfarin (target INR 2-3. or a direct oral anticoagulant (such as Rivaroxaban or Apixiban) is initiated 2 weeks post-stroke.\n- Lipid-lowering therapy:\n\t- Patients should be prescribed high dose atorvastatin 20-80 mg once nightly (irrespective of cholesterol level this lowers the risk of repeat stroke).\n- Tobacco\n\t- Offer smoking cessation support.\n- Sugar:\n\t- Patients should be screened for diabetes and managed appropriately.\n- Surgery:\n\t- Patients with ipsilateral carotid artery stenosis more than 50% should be referred for carotid endarterectomy. Patients with over 70% stenosis have the most benefit from endarterectomy\n\n\n\n# References\n\n[Click here for NICE Clinical Knowledge Summaries](https://cks.nice.org.uk/topics/stroke-tia/)\r\n\r\n[Click here for Radiopedia](https://radiopaedia.org/articles/lacunar-stroke-syndrome?lang=gb)",
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"question": "A 71-year-old man presents to the Emergency Department via ambulance. On waking this morning, his wife noted he had incoherent speech with an inability to move his right arm. He has a past medical history of hypercholesterolaemia, type 2 diabetes, atrial fibrillation, and alcohol excess. His regular medications include atorvastatin, metformin, bisoprolol and apixaban. He still drinks heavily - his wife estimates 1 litre of whiskey most days - and has poor compliance with his medications.\n\nWhat is the most likely diagnosis?",
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"explanation": "Migraine can cause a headache with classical photophobia and significant nausea and vomiting. Alcohol can also act as a trigger for migraines. However, if this were a migraine, it would usually have resolved within 24 hours, but more rarely can persist for up to 72 hours. The headache would usually be noted as being unilateral and pulsatile in nature. Migraines are not usually associated with significant neck stiffness or infective symptoms",
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"explanation": "A gastrointestinalgastrointestinal infection could cause significant vomiting and infective symptoms of fever and rigors; however, this would usually also be associated with some accompanying abdominal pain or diarrhoea. It would be uncommon for this condition to present with headache as the primary symptom",
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"explanation": "Student populations are one of the higher risk groups for bacterial meningitis, and it is vital to always consider this diagnosis in patients of this cohort presenting with headache or vomiting so as not to miss a potentially fatal infection. This patient has several key signs of meningitis, including headache, photophobia, vomiting and neck stiffness, as well as symptoms that sound like fevers and rigors overnight. Neisseria meningitidis is the classical organism causing meningitis in student populations",
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"explanation": "SAH can also cause a severe headache with photophobia, vomiting and neck stiffness. However, in SAH, you may expect a history of more sudden onset \"thunderclap\" headache, with the severity of the pain being the primary symptom, with patients often describing it as the \"worst pain I've ever felt\". This diagnosis would also not explain the notable infective sounding symptoms of fevers and rigors overnight. Additionally, in this population, meningitis would be a more common cause of these symptoms",
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"explanation": "Though it does happen, it would be rare for a simple hangover to cause severe enough symptoms for a patient to present to the hospital. Additionally, it would be rare for this to be causing such severe symptoms for more than 24 hours with no improvement. A hangover would not cause infective symptoms. Neck stiffness is quite a specific symptom that should point you towards significant central nervous system pathology (indicating inflammation of the meninges)",
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"explanation": "# Summary\n \nMeningitis is a potentially life-threatening condition characterised by the inflammation of the meninges, the membranes enveloping the brain and spinal cord. Its causes span from infectious agents, such as bacteria, viruses, fungi, and parasites, to non-infective causes like malignancy and certain medications. Symptoms are often non-specific, necessitating accurate differential diagnoses and prompt investigations. Timely management, including empirical antibiotics and targeted therapy post-identification of causative agent, is crucial to mitigate complications and improve patient outcomes. \n \n \n# Definition\n \n \nMeningitis is an inflammation of the meninges, which are composed of three layers: the dura mater, arachnoid mater, and pia mater. This inflammation may arise from both infective and non-infective aetiologies. \n \n \n# Epidemiology\n \n \nBacterial meningitis, while not the most common form of meningitis, is particularly significant due to its high morbidity and mortality rates. \n \nViral meningitis, predominantly caused by enteroviruses, is more common but typically less severe. Fungal and parasitic causes are relatively rare, except in immunosuppressed individuals. \n \nIn the United States, the annual incidence of bacterial meningitis is approximately 1.38 cases/100,000 population with a case fatality rate of 14.3%.\n\n# Aetiology\n \n \nInfective causes of meningitis include:\n \n \n - Bacterial: **Streptococcus pneumoniae (most common bacterial cause),** Neisseria meningitidis, Haemophilus influenzae, Listeria monocytogenes, among others.\n - Viral: **Enteroviruses are overall most common** (Echoviruses, Coxsackie viruses A and B, poliovirus), herpes viruses (HSV2, HSV1), Paramyxovirus, measles and rubella viruses, Varicella Zoster Virus, Arboviruses, Rabies virus.\n - Fungal: Particularly Cryptococcus neoformans, mainly affecting the immunosuppressed population.\n - Parasitic: Amoeba (Acanthamoeba), Toxoplasma gondii.\n \n \nNon-infective causes of meningitis encompass:\n \n \n - Malignancies such as leukaemia, lymphoma, and other tumours\n - Chemical meningitis\n - Certain drugs, including NSAIDs and trimethoprim\n - Systemic inflammatory diseases such as sarcoidosis, systemic lupus erythematosus, Behcet's disease.\n \n \n# Signs and Symptoms\n \n \nThe cardinal features of meningitis include:\n \n \n- Headache\n- Fever\n- Neck stiffness\n- Photophobia\n- Nausea and vomiting\n- Focal neurology\n- Seizures\n- Reduced conscious level\n- Features of overwhelming sepsis, such as non-blanching petechial rash indicative of impending Disseminated Intravascular Coagulation (DIC). \n \nSpecific signs suggestive of meningeal irritation (and therefore not specific to meningitis) include:\n \n \n1. **Kernig's sign:** Kernig's sign is a test performed to evaluate the presence of meningeal irritation and stiffness in the hamstrings and lower back. To perform this test, the patient is positioned lying on their back with the hip and knee flexed at 90 degrees. The examiner then attempts to extend the patient's knee. If the patient experiences pain and resistance to knee extension, especially when attempting to straighten the leg, it is considered a positive Kernig's sign. This sign suggests meningeal irritation or inflammation.\n \n \n2. **Brudzinski's sign:** Brudzinski's sign is another manoeuvre used to assess for meningeal irritation. This test involves passive neck flexion, where the examiner gently flexes the patient's neck forward toward the chest while the patient is lying on their back. If the patient involuntarily flexes their hips and knees in response to neck flexion, it is considered a positive Brudzinski's sign. This involuntary movement indicates irritation of the meninges.\n \n \n \n \n# Differential Diagnosis\n \nThe key differentials for meningitis often present with overlapping symptoms. These include:\n \n \n- **Encephalitis**: Headache, fever, altered consciousness, seizures, focal neurological signs, behaviour changes.\n- **Subarachnoid hemorrhage**: Sudden severe headache, nausea and vomiting, neck stiffness, altered consciousness, seizures.\n- **Brain abscess**: Headache, fever, nausea and vomiting, focal neurological deficits, seizures, altered mental status.\n- **Sinusitis**: Headache, fever, facial pain, nasal congestion.\n- **Migraine**: Recurrent headaches, often unilateral and throbbing, accompanied by nausea/vomiting, photophobia, phonophobia.\n \n \n# Investigations\n \n \nDiagnostic investigations for suspected meningitis include:\n \n \n - Blood tests: Full Blood Count, Urea and Electrolytes, Clotting, Glucose, PCT\n - Arterial Blood Gas\n - Blood cultures\n - Bacterial throat swab for meningococcus\n - PCR for meningococcus & pneumococcus\n - HIV test\n - Imaging: CT Head if there are signs of raised intracranial pressure (ICP)\n - Lumbar puncture for Cerebrospinal Fluid (CSF) analysis, once confirmed there are no signs of raised ICP.\n \n \n## CSF Findings \n \n \nAnalysis of the cerebrospinal fluid in acute meningitis can provide important clues as to the underlying aetiology. Once establishing that it is safe to do so, a CSF sample should be taken via lumbar puncture and the opening pressure should be measured.\n \n \nThis can be examined macroscopically, and then sent for haematology, biochemistry, and microbiological microscopy, culture and sensitivities, as well as PCR.\n \n| | **Appearance** | **Predominant cell type** | **Culture** | **Protein** | **Glucose** |\n|---------------------------|-------------------------------------|---------------------------------------------------|--------------------------------------------------------|-------------|-------------|\n| **Bacterial meningitis** | Clear or turbid | **Polymorphonuclear** cells (i.e. neutrophils) | Positive | Raised | **Reduced** |\n| **Aseptic (viral) meningitis** | Clear or slightly turbid | **Lymphocytes** | Negative | Raised | **Normal** |\n| **Tuberculous meningitis** | Clear or slightly turbid ± fibrin web | **Lymphocytes** + polymorphonuclear cells | Negative gram stain; acid-fast bacilli positive (auramine staining) | Raised | **Reduced** |\n\n \nN.b. Cryptococcal meningitis may give any of the above results, so should be considered as a differential in any HIV or immunocompromised patient. Classically the opening pressure is very high, and this is a poor prognostic sign. If suspected, request cryptococcal antigen or India Ink staining.\n \n \n# Management\n \n \n- Empirical antibiotic therapy for suspected bacterial meningitis typically includes 2g of IV ceftriaxone twice daily to ensure CNS penetration, with IV amoxicillin added in patients at age extremes for listeria coverage.\n- In primary care, IM benzylpenicillin or ceftriaxone should be given while awaiting urgent transfer to hospital, especially if meningococcal disease is suspected.\n- Dexamethasone should be given if bacterial meningitis is strongly suspected in the absence of a rash\n\t- This has been shown to reduce neurological sequelae in bacterial meningitis but not meningococcal meningitis\n- In cases of suspected viral encephalitis, IV aciclovir should also be administered. For patients allergic to penicillin, alternatives such as chloramphenicol may be used. \n- It's important to note that any empirical antibiotic regimen should be adjusted based on culture results when available.\n \n **Additional notes**\n \nClose contacts of the patient should receive prophylactic antibiotics. This will be guided by specialists but may be a single dose of oral ciprofloxacin, or rifampicin.\n \nBacterial meningitis is a notifiable disease and any suspected cases should be reported to the local health protection team.\n \n \n# Complications\n \n \nMeningitis may lead to severe complications if not promptly treated, such as:\n \n - Septic shock\n - Disseminated Intravascular Coagulation\n - Coma\n - Subdural effusions\n - Syndrome of inappropriate antidiuretic hormone secretion\n - Seizures\n - Delayed complications: Hearing loss, cranial nerve dysfunction, hydrocephalus, intellectual deficits, ataxia, blindness\n - Death\n \n \n# NICE guidelines\n \n [NICE CKS: Meningitis - bacterial meningitis and meningococcal disease](https://cks.nice.org.uk/topics/meningitis-bacterial-meningitis-meningococcal-disease/)\n \n [NICE: meningitis (bacterial) and meningococcal disease: recognition, diagnosis and management](https://www.nice.org.uk/guidance/ng240/resources/meningitis-bacterial-and-meningococcal-disease-recognition-diagnosis-and-management-pdf-66143949881029)\n \n# References\n \n [BNF: Ciprofloxacin](https://bnf.nice.org.uk/drugs/ciprofloxacin/)",
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"question": "An 18-year-old female student presents to the emergency department on a Monday morning with 24 hours of severe headache and vomiting.\n\nOn Saturday, she went on a night out clubbing, and when she woke up on Sunday morning, she felt extremely unwell with headache, photophobia, nausea and vomiting. This has persisted, and she feels no better this morning. Her neck is also feeling stiff and painful - she wonders if this may be due to her excessive vomiting over the past 24 hours. Overnight she also reports waking up very sweaty and shaky.\n\nWhat is the most likely diagnosis?",
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"explanation": "In femoral shaft fractures, the area over the fracture site (the thigh) is often visibly deformed. Additionally, you would expect the pain to be located primarily at this site rather than in the hip",
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"name": "Left femoral shaft fracture",
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"explanation": "Posterior dislocations account for 90% of hip dislocations – in these cases, the leg may be observed to be flexed at the hip, internally rotated and adducted. In anterior hip dislocations, which are rarer, the leg can be positioned as externally rotated, but this is usually accompanied by significant abduction, which is not present in this patient. Both forms of dislocation can cause variable amounts of leg shortening",
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"explanation": "A simple soft tissue injury would not cause shortening and external rotation of the leg (it would not cause any deformity of the leg) but may present with bruising and swelling. Weight-bearing would usually be possible, although it may still be uncomfortable for the patient",
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"explanation": "In fracture of the pubic rami the leg rarely presents as shortened and externally rotated (the leg itself is not involved in the fracture so should not be deformed or displaced significantly)",
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"explanation": "This patient is above the age of 65 and has risk factors for osteoporosis (steroid use and levothyroxine use) – this puts her at high risk of hip fracture. She has presented following a fall from standing, which is also the most common mechanism of injury for hip fracture in this cohort. Displaced hip fractures cause shortening of the leg due to bone overlap, and external rotation occurs due to the non-anatomical action of muscle groups pulling on the now discontinuous femur. Difficulty in weight-bearing and significant bruising over the area are also common following hip fracture",
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"explanation": "# Summary\n\nA fracture of the neck of the femur is a break occurring in the upper part of the femur, just below the ball-and-socket hip joint. This fracture is common among the elderly population, particularly those with osteoporosis. Notable symptoms include severe hip or groin pain, an inability to bear weight on the affected leg, and external rotation and shortening of the affected leg. Diagnosis typically involves X-rays, though CT scans or MRI may be employed for more complex cases. Management is primarily surgical, with options including cannulated screw fixation, dynamic hip screw, hemiarthroplasty, and total hip arthroplasty, chosen based on factors such as the patient's age, health, and the type of fracture. Complications can include non-union, avascular necrosis, deep vein thrombosis, and pulmonary embolism.\n\n# Definition\n\nA fracture of the neck of the femur is a type of hip fracture that specifically involves the upper part of the femur, just below the ball of the hip's ball-and-socket joint.\n\n# Types of Neck of Femur Fracture\n\nFractures of the neck of the femur are generally classified into two types based on their location in relation to the hip joint capsule:\n\n- **Intracapsular Fractures**: These fractures occur within the joint capsule. They are further subdivided into displaced and non-displaced fractures. Displaced fractures carry a high risk of avascular necrosis due to possible disruption of the blood supply to the femoral head.\n \n- **Extracapsular Fractures**: These fractures occur outside the joint capsule and include intertrochanteric and subtrochanteric fractures. They have a better prognosis due to a lower risk of avascular necrosis.\n\n# Epidemiology\n\nFractures of the neck of the femur are a common injury, particularly in older individuals. This is largely attributed to the increased prevalence of osteoporosis in this population, which makes the bones more susceptible to fractures.\n\n# Aetiology\n\nThe main cause of a fracture to the neck of the femur is a fall, often in the elderly and those with weakened bones due to osteoporosis. Other potential causes can include high-energy trauma such as car accidents, especially in younger individuals.\n\n# Signs and Symptoms\n\nPatients with a fractured neck of femur commonly present with:\n\n- Severe pain in the hip or groin\n- Inability to bear weight on the affected leg\n- Shortening and external rotation of the affected leg\n- Swelling or bruising over the hip area\n\n# Differential Diagnosis\n\nThe differential diagnosis for a fractured neck of femur should include other injuries that could present with similar symptoms:\n\n- **Intertrochanteric Fracture**: Another type of hip fracture, characterised by pain in the hip or groin, inability to bear weight, and often shortening and external rotation of the affected leg.\n- **Pelvic Fracture**: Can be caused by falls or high-energy trauma. Symptoms can include severe pain in the hip or groin, inability to bear weight, and possible signs of internal bleeding.\n- **Hip Dislocation**: Usually a result of high-energy trauma, symptoms include severe hip pain, inability to move the leg, and a visibly deformed hip.\n\n# Investigations\n\nThe primary investigation for a suspected fractured neck of femur is a hip X-ray, which typically reveals the fracture and its severity. In cases where the fracture is not clear on X-ray, a CT scan or MRI may be necessary.\n\n[lightgallery]\n\n# Management\n\nManagement of a fractured neck of the femur is primarily surgical. The choice of surgical intervention depends on several factors, including the type of fracture, the patient's age, general health, and mobility prior to the injury.\n\n- **Cannulated Screw Fixation**: This is often used for non-displaced intracapsular fractures. The procedure involves the insertion of screws across the fracture line to stabilise it.\n \n- **Dynamic Hip Screw (DHS)**: This technique is usually used for stable, extracapsular fractures. It involves the insertion of a single large screw into the femoral head, combined with a side plate fixed to the femoral shaft.\n \n- **Hemiarthroplasty**: This involves replacing the femoral head and neck with a prosthesis. It is typically performed for displaced intracapsular fractures in older patients with lower activity levels, as these fractures have a high risk of non-union and avascular necrosis.\n \n- **Total Hip Arthroplasty (THA)**: This procedure involves the replacement of both the femoral head and the acetabulum with prosthetic components. It is typically used for displaced intracapsular fractures in younger, more active patients or older patients with pre-existing osteoarthritis.\n \n\n# Complications\n\nPotential complications from a fracture of the neck of the femur include:\n\n- Non-union of the fracture\n- Avascular necrosis due to interruption of blood supply to the femoral head\n- Deep vein thrombosis (DVT)\n- Pulmonary embolism (PE)\n- Infection\n- Dislocation of the hip prosthesis, in cases where arthroplasty has been performed\n\n# References\n\n[Click here to read more about fractures of the neck of femur](https://teachmesurgery.com/orthopaedic/hip/femoral-neck-fractures/)",
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"question": "A 69-year-old woman presents to the Emergency Department following a fall at home. She reports standing up from her chair and then falling forwards. She did not injure her head or lose consciousness following the fall, but does have significant pain in her left hip and is unable to weight bear. She has a past medical history of hypothyroidism and polymyalgia rheumatica, and current medications include levothyroxine and prednisolone.\n\nOn inspection, there bruising over the lateral aspect of the left hip and the left leg appears shortened and externally rotated, though there is no visible deformity.\n\nWhat is the most likely diagnosis?",
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"explanation": "# Summary\n\nHyperkalaemia is a potentially life-threatening electrolyte abnormality, defined as a serum potassium concentration greater than 5.5mmol/L. A potassium of 6.0-6.5 mmol/L is classed as moderate hyperkalaemia, and > 6.5 mmol/L is classed as severe. Causes include acute or chronic renal impairment, medications such as ACE inhibitors, adrenal insufficiency and rhabdomyolysis. Pseudohyperkalaemia is also common and occurs when there is haemolysis of the blood collected that causes potassium to leak from cells. Key investigations include an ECG, a blood gas to confirm hyperkalaemia is true, and U&Es for renal function. Management depends on the severity of hyperkalaemia and may include calcium gluconate or calcium carbonate to stabilise the myocardium and insulin-dextrose infusion to drive potassium into the cells, as well as treating the cause of hyperkalaemia. Potassium binders such as sodium zirconium cyclosilicate (Lokelma) may also be used. The main complication is cardiac conduction abnormalities, with possible findings including tall tented T waves, flattened P waves, bradyarrhythmias and QRS widening with bizarre morphology. \n\n# Definition\n\nHyperkalaemia is a common electrolyte abnormality that is defined as an abnormally high serum potassium. The normal range is 3.5-5.0 mmol/L, with a level of > 5.5 mmol/L generally described as hyperkalaemia. It is seen in around 1-10% of hospital inpatients and is often asymptomatic.\n\n# Aetiology\n\n- Impaired excretion of potassium\n - Acute kidney injury\n - Chronic kidney disease\n - Medications (ACE inhibitors, potassium sparing diuretics, NSAIDs, heparin, trimethoprim, ciclosporin)\n - Type 4 renal tubular acidosis\n - Hypoadrenalism (e.g. Addison's disease)\n- Increased potassium intake\n - Oral intake (especially if combined with impaired excretion)\n - Excessive IV potassium\n- Increased cellular release \n - Metabolic acidosis\n - Hyperglycaemia\n - Rhabdomyolysis\n - Tumour lysis syndrome\n - Packed red blood cell transfusion\n - Digoxin toxicity\n - Beta blockers\n - Severe burns\n - Hyperkalaemic periodic paralysis\n\n# Classification\n\nThe European Resuscitation Guidelines stratify severity of hyperkalaemia as follows:\n\n||Serum potassium (mmol/L)|\n|--------------------------|------------------------------------|\n|**Mild**|5.5–5.9|\n|**Moderate**|6.0–6.4|\n|**Severe**|≥6.5|\n\n# Signs and Symptoms\n\nHyperkalaemia is often asymptomatic and only detected on blood tests - there may be symptoms or signs of the underlying cause however (e.g. dark urine in rhabdomyolysis)\n\n**Symptoms include:**\n\n- Palpitations\n- Fatigue\n- Chest pain\n- Shortness of breath\n- Paralysis\n\n**Signs include:**\n\n- Arrhythmias (e.g. bradycardia)\n- Reduced muscle power +/- flaccid paralysis\n- Hyporeflexia\n\n# Differential Diagnosis\n\n**Pseudohyperkalaemia** is common and refers to an artifactual increase in potassium in the sample tested - causes of this include:\n\n- Prolonged tourniquet time\n- Difficult venepuncture\n- Excessive fist clenching\n- Delayed specimen processing\n- Contamination with potassium EDTA anticoagulant in FBC bottles\n- Thrombocytosis\n- Leukocytosis\n\n# Investigations\n\n- **Blood gas** to confirm hyperkalaemia rapidly and check acid-base status and lactate\n- **ECG** to look for cardiac conduction abnormalities associated with hyperkalaemia. ECG changes include tall-tented T waves, PR prolongation, p wave flattening and QRS broadening.\n- **U&Es** to confirm hyperkalaemia, check sodium (may be an associated hyponatraemia e.g. in adrenal insufficiency) and renal function\n\n# Management \n\n**Conservative management:**\n\n- Stop any potassium-containing fluids\n- Address any underlying causes e.g. stop any contributing medications where possible, manage constipation\n- Consider advising the patient on a low potassium diet (e.g. in patients with chronic kidney disease) - dietician referral may be helpful\n- Patients with ECG changes may require cardiac monitoring\n- Mild-moderate cases of hyperkalaemia without ECG changes may be managed by addressing the underlying cause alone\n\n**Medical management:**\n\n- Patients with ECG changes or severe hyperkalaemia require treatment\n- Give 10 ml of IV 10% calcium carbonate or 30ml of IV 10% calcium gluconate immediately\n- This does not reduce serum potassium but acts to stabilise the myocardium and reduce the risk of arrhythmias\n- Further doses may be given if required\n- Give an insulin and glucose infusion (e.g. 10 units of Actrapid in 50 ml of 50% glucose over 15-30 minutes\n- This reduces serum potassium by shifting potassium into cells, however does not eliminate potassium from the body\n- Nebulised salbutamol may be given in addition which has the same effect\n- Potassium binders may be considered to eliminate potassium via the gut, especially in patients with chronic or refractory hyperkalaemia\n- Newer agents such as sodium zirconium cyclosilicate (Lokelma) are better tolerated than older resins (e.g. sodium polystyrene sulfonate)\n- Furosemide may also be useful to increase urinary potassium excretion especially in patients with fluid overload\n- Consider sodium bicarbonate for patients with acidosis and hyperkalaemia\n- Medical treatment may be required to correct the cause of hyperkalaemia (e.g. IV fluids for a pre-renal AKI or rhabdomyolysis)\n\n**Interventional management:**\n\n- Refractory hyperkalaemia despite medical therapy is an indication for emergency dialysis\n\n# Complications\n\nThe main complication of hyperkalaemia is cardiac conduction abnormalities and arrhythmias which in the most severe cases may cause cardiac arrest - changes in order of increasing severity are:\n\n1. Tall tented T-waves\n2. Flattened P-waves\n3. Prolonged PR interval\n4. Widened QRS complexes\n5. Idioventricular rhythms (bradycardia of ventricular origin)\n6. Sine wave pattern (pre-terminal rhythm)\n7. Ventricular fibrillation/asystole\n\n# References\n\n[BNF Treatment Summary - Hyperkalaemia](https://bnf.nice.org.uk/treatment-summaries/hyperkalaemia/)\n\n[The Renal Association - Treatment of Acute Hyperkalaemia in Adults](https://www.ukkidney.org/sites/default/files/RENAL%20ASSOCIATION%20HYPERKALAEMIA%20GUIDELINE%20-%20JULY%202022%20V2_0.pdf)\n\n[Patient UK - Hyperkalaemia in adults](https://patient.info/doctor/hyperkalaemia-in-adults)\n\n[Whittington Hospital Hyperkalaemia Guideline](https://www.whittington.nhs.uk/document.ashx?id=6250)\n\n[Life in the Fast Lane - Hyperkalaemia](https://litfl.com/hyperkalaemia-ecg-library/)",
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"question": "A 49-year-old male presents to the Emergency Department with palpitations and nausea. He has a past medical history of hypertension, migraine and gout. His regular medications include amlodipine, ramipril, indapamide, propranolol and allopurinol.\n\n\nBlood tests reveal hyperkalaemia at 6.4 mmol/L (normal range 3.5-5.3 mmol/L).\n\n\nWhich of his regular medications should be suspended during treatment of his hyperkalaemia?",
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"explanation": "# Summary\n\nHyponatraemia is defined as a serum sodium concentration of less than 135 mmol/L. It may develop acutely or chronically, and is often asymptomatic especially in mild cases. There are many causes which may be classified by whether the patient is hypovolaemic, euvolaemic or hypervolaemic. Symptoms are more likely in severe hyponatraemia and where serum sodium has fallen acutely, including headache, nausea and vomiting and confusion. Key investigations include U&Es for sodium, potassium and renal function, cortisol and thyroid function to rule out other causes of hyponatraemia and urinary sodium and osmolality. Management differs depending on the cause of hyponatraemia - what may improve hyponatraemia in some cases may worsen it in others. In severe cases where more rapid correction of sodium is required, hypertonic saline may be administered with close monitoring of sodium levels.\n\n# Definition\n\nNormal serum sodium is between 135-145 mmol/L, and so levels below 135 mmol/L are classified as hyponatraemia. This may be mild (130-135 mmol/L), moderate (125-129 mmol/L) or severe (< 125 mmol/L). Acute cases develop within 48 hours, with most cases considered to be chronic (i.e. over 48 hours duration) if the onset is unclear. \n\n# Epidemiology\n\n- Hyponatraemia is the commonest electrolyte disorder seen in clinical practice\n- Approximately 15-20% of hospital inpatients are hyponatraemia\n- Incidence increases with age and is particularly common in older people who are nursing home residents or in hospital\n- Other risk factors include:\n- Medications (e.g. diuretics, antidepressants)\n- Comorbidities (e.g. chronic kidney disease, heart failure)\n\n# Aetiology\n\n## Hypovolaemic hyponatraemia\n\nBoth sodium and water are lost (but more sodium than water)\n\n- Diarrhoea\n- Vomiting\n- Medications (e.g. thiazide diuretics)\n- Adrenal insufficiency\n- Burns\n- Excessive sweating\n- Cerebral salt-wasting (rare cause of hyponatraemia that occurs due to intracranial disease, e.g. subarachnoid haemorrhage or traumatic brain injury)\n- Salt-wasting nephropathy (e.g. Bartter syndrome)\n- Third space losses (e.g. sepsis, pancreatitis, bowel obstruction)\n\n## Euvolaemic hyponatraemia\n\nNo loss of sodium but total body water increases causing a dilutional effect\n\n- Syndrome of Inappropriate ADH release (SIADH)\n- Beer potomania (alcohol excess combined with low solute intake)\n- Primary polydipsia\n- Hypothyroidism\n- Secondary adrenal insufficiency\n- Exercise-induced hyponatraemia \n- Hypotonic intravenous fluids\n\n## Hypervolaemic hyponatraemia\n\nBoth total body water and sodium increase, with a greater increase in water resulting in oedema\n\n- Heart failure\n- Chronic liver disease\n- Renal disease (nephrotic syndrome, chronic kidney disease or acute kidney injury)\n\n# Signs and Symptoms\n\nMany patients, especially those with mild and/or chronic hyponatraemia are asymptomatic and detected incidentally.\n\nSymptoms and signs include:\n\n- Lethargy\n- Anorexia\n- Headache\n- Nausea and vomiting\n- Muscle cramps\n- Drowsiness\n- Confusion\n- Seizures\n\nPatients may also have features of either dehydration (in hypovolaemic hyponatraemia) or fluid overload (in hypervolaemic hypernatraemia - see separate chapters for details.\n\n# Differential Diagnosis\n\n- **Pseudohyponatraemia** refers to a falsely low serum sodium reading due to an increase in serum lipid or protein content\n- Serum osmolality will usually be normal or high (unlike in true hyponatraemia where it is low)\n- Causes include:\n- Hypertriglyceridemia\n- Hypercholesterolemia\n- Hyperglycaemia\n- Paraproteinaemia (e.g. in multiple myeloma)\n\n# Investigations\n\n**Bedside:**\n\n- **Venous blood gas** to confirm hyponatraemia - if there is a significant discrepancy between the sodium on the gas and the U&Es, suspect pseudohyponatraemia\n- **Urine osmolality** is used to assess ADH activity - it will be high (i.e. urine is concentrated) if ADH is acting, e.g. in SIADH, and low (i.e. urine is dilute) if ADH is not acting, e.g. in polydipsia\n- **Urine sodium** can be used to help determine the cause of hyponatraemia; in patients who are hypovolaemic:\n- If urine sodium is appropriately low, this indicates extrarenal salt loss - consider vomiting/diarrhoea/third spacing\n- If urine sodium is high (> 30 mmol/L), this indicates renal salt loss - consider diuretics, adrenal insufficiency or cerebral salt-wasting\n- NB urine osmolality and sodium cannot be interpreted in patients taking diuretics and so these may need to be stopped prior to investigations\n- **Urine dip** looking for blood and protein if renal disease is suspected\n\n**Blood tests:**\n\n- **U&Es** to confirm hyponatraemia and to check potassium and renal function\n- **Serum osmolality** should be low in true hyponatraemia - if this is normal or raised suspect pseudohyponatraemia (hypertonic fluids such as mannitol may cause a true hyponatraemia with a raised serum osmolality)\n- **Thyroid function tests** to exclude hypothyroidism as a cause of hyponatraemia\n- **9am serum cortisol** to exclude adrenal insufficiency as a cause of hyponatraemia\n- **NT-proBNP** if heart failure is suspected\n- **Liver function tests** if cirrhosis is suspected (e.g. in patients with ascites)\n\n# Management\n\n**Conservative:**\n\n- Identify and treat the underlying cause (e.g. stopping causative medications where possible)\n- Patients with hyponatraemia which is severe, acute or symptomatic should usually be admitted to hospital for treatment\n- Consider referral to the appropriate speciality for advice on management of the underlying cause of hyponatraemia (e.g. cardiology for heart failure, endocrinology for adrenal insufficiency)\n- Closely monitor sodium levels and ensure these are corrected no faster than 8-10 mmol/L per 24 hours \n- Fluid restriction is the first-line management for SIADH and may also be used in some cases of hypervolaemic hyponatraemia\n\n**Medical:**\n\n- Severe hyponatraemia should be treated with hypertonic saline, usually in the intensive care setting\n- Hypovolaemic hyponatraemia is treated with IV normal saline\n- In some cases of SIADH tolvaptan may be considered - this is a vasopressin V2-receptor antagonist\n- Correction of endocrine abnormalities may be required e.g. levothyroxine for hypothyroidism; corticosteroids for adrenal insufficiency\n\n# Complications\n\n- **Cerebral oedema** may complicate severe and/or acute hyponatraemia and may be life-threatening - patients develop raised intracranial pressure with symptoms of vomiting, headache, seizures and coma\n- **Central pontine myelinolysis** is a complication of rapid correction of hyponatraemia - patients may present with confusion, ataxia, spastic quadriparesis and pseudobulbar palsy with dysphagia and dysarthria\n- Chronic hyponatraemia, especially in the elderly, increases the risk of **falls** as well as **cognitive impairment**\n\n# NICE Guidelines\n\n[NICE CKS - Hyponatraemia](https://cks.nice.org.uk/topics/hyponatraemia/)\n\n# References\n\n[Life in the Fast Lane - Hyponatraemia](https://litfl.com/hyponatraemia/)\n\n[Whittington Hospital Hyponatraemia Guideline](https://www.whittington.nhs.uk/document.ashx?id=6089)",
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"question": "A 76-year-old female presents to the Emergency Department. She has been brought in by her carers, who feel she is more confused and drowsy than normal. She has a past medical history of type 2 diabetes, hypertension and depression. Her regular medications include metformin, gliclazide, ramipril, amlodipine and sertraline.\n\n\nBlood tests reveal hyponatraemia at 125 mmol/L (normal range 135-145 mmol/L).\n\n\nWhich medication is most likely contributing to this patients hyponatraemia?",
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"explanation": "Pulmonary embolism classically presents with pleuritic chest pain, breathlessness, tachycardia, haemoptysis and the presence of a deep vein thrombosis (although their presentation can often be very non-specific in reality). This patient presented only with tachypnoea and had none of the classical risk factors for pulmonary embolism (for example long haul flights, history of cancer, surgery, prolonged immobility). Although pulmonary embolism can present with raised troponins, given the whole clinical picture, myocardial infarction is more likely",
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"explanation": "This is the typical presentation of a myocardial infarction. This is a 65 year old man with significant cardiovascular risk factors. Central, crushing chest pain is the characteristic description of a myocardial infarction and this classically radiates down the left arm. Although myocardial infarctions often present with ECG changes, the absence of ECG changes does not rule out a myocardial infarction. Raised troponins are very suggestive of myocardial infarction in this clinical history, as this confirms myocardial cell lysis. In this case, the specific diagnosis would be classified as a non-ST elevation myocardial infarction (NSTEMI)",
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"explanation": "Pneumonia typically presents with pyrexia, a productive cough, tachypnoea and pleuritic chest pain. This patient only presented with tachypnoea out of these features and this chest pain fits the classical description of cardiac chest pain. Pneumonia does not tend to cause a rise in troponin levels unless the patient is septic and very unwell",
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"explanation": "Unstable angina and myocardial infarction are both subtypes of acute coronary syndrome (ACS). This is used to generally describe an episode of myocardial chest pain and as such, unstable angina and myocardial infarction present very similarly. To differentiate these, it is best to look at troponins. A raised troponin means the myocardial tissue is infarcted, as the myocardiocytes die and release troponins into the blood. In unstable angina, there is no myocardial death, so there is no associated troponin rise. Therefore, in the presence of raised troponins, it is more likely to be a myocardial infarction",
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"explanation": "Stable angina is defined by the presence of at least 2 of the following criteria:\n\n- constricting chest/jaw/arm pain\n- pain triggered by exercise\n- pain relieved by rest for 5 minutes or glyceryl trinitrate\n\nAlthough this patient has chest pain typical in nature, they have not had a clear history of their pain being exercise induced and more importantly, this pain is still present after 45 minutes. In addition, stable angina does not cause raised troponins as there is no associated myocardial death as this tissue is ischaemic, not infarcted. Overall, this makes a diagnosis of myocardial infarction more likely",
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"explanation": "# Summary\r\n\r\nAcute coronary syndrome (ACS) refers to a set of symptoms and signs that occur due to reduced blood flow to the heart at rest. It encompasses 3 distinct diagnoses: unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). In the case of infarction, this is a medical emergency requiring urgent treatment. ACS is most commonly caused by the rupture of atherosclerotic plaques in coronary arteries leading to further narrowing, and potentially complete occlusion, of these critical blood vessels. Diagnosis involves clinical evaluation, ECGs, and troponin levels. Treatment strategies differ for STEMI and NSTEMI/unstable angina but include oxygen therapy if hypoxic, antiplatelet medication, glyceryl trinitrates, morphine, and percutaneous coronary intervention (PCI). Post-MI management includes aspirin, dual antiplatelet therapy, beta-blockers, ACE inhibitors, high-dose statins, and cardiac rehabilitation. There are many complications to be aware of post-ACS and these include arrhythmias, heart failure, and cardiac tamponade, and others.\r\n\r\n# Definition \r\n\r\nAcute coronary syndrome is a set of symptoms and signs that occur due to decreased blood flow to the heart at rest. It broadly refers to three distinct diagnoses: unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI). \r\n\r\n# Epidemiology \r\n\r\nIn the UK, there are over 80,000 hospital admissions due to ACS every year. Coronary artery disease remains the largest cause of death in the UK. \r\n\r\n# Pathophysiology\r\n\r\nCoronary artery disease refers to the narrowing of coronary arteries by atherosclerosis and plaque formation. In stable angina, when the demand for myocardial oxygen increases with exertion, narrowed coronary arteries cannot meet this increased demand leading to myocardial ischaemia and pain. Conversely, in ACS, the symptoms occur at rest. This is because there is sudden plaque rupture and clot formation in the narrowed coronary arteries. If there is partial occlusion of the coronary artery this leads to ischaemia and chest pain at rest (unstable angina). If the coronary artery becomes more occluded or fully occluded this leads to significant hypoperfusion of the myocardium and ultimately leads to infarction (death) of the myocardial tissue (NSTEMI or STEMI). \r\n\r\n# Risk Factors\r\n\r\nCoronary artery disease and the development of plaques can be attributed to non-modifiable and modifiable risk factors. Modifiable risk factors must be addressed in the management of IHD. \r\n\r\n* Non-modifiable:\r\n * Age\r\n * Male sex\r\n * Family history\r\n * Ethnicity (particularly South Asians)\r\n* Modifiable:\r\n * Smoking\r\n * Hypertension\r\n * Hyperlipidaemia\r\n * Hypercholesterolaemia\r\n * Obesity\r\n * Diabetes\r\n * Stress\r\n * High fat diets\r\n * Physical inactivity\r\n\r\n# Classification \r\n\r\nAcute coronary syndrome can be split up into three distinct diagnoses: \r\n\r\n1. **Unstable angina**: caused by partial occlusion of a coronary artery. Troponin negative chest pain with normal/abnormal ECG signs. \r\n2. **Non-ST Elevation Myocardial Infarction**: caused by severe but incomplete occlusion of a coronary artery. Troponin positive chest pain without ST elevation. \r\n3. **ST-Elevation Myocardial Infarction**: caused by complete occlusion of a coronary artery. Troponin positive chest pain with ST elevation on ECG. \r\n\r\n*Myocardial Ischaemia vs. Myocardial Infarction and the Release of Troponin*\r\n\r\nIt is important at this stage to distinguish between angina (stable angina is on exertion and unstable angina is at rest) and myocardial infarction. Angina refers to myocardial ischaemia that causes chest pain but does not lead to the death of myocardial tissue and does not lead to a troponin rise. In myocardial infarction, the hypoperfusion of the myocardium is so profound that it leads to the death of myocardial tissue. It is when there is myocardial tissue death that troponin is released into the bloodstream and a troponin rise is found on blood tests.\r\n\r\n*Type 2 Myocardial Infarction* \r\n\r\nIt is also important to mention that some patient may have myocardial infarctions due to cardiac hypoperfusion for other reasons (e.g. severe sepsis, hypotension, hypovolaemia or coronary artery spasm). These are usually termed type 2 myocardial infarctions and may not require the conventional treatment outlined below. \r\n\r\n# Symptoms and Signs\r\n\r\n* Chest pain - the classical presentation can be considered in terms of the SOCRATES mnemonic:\r\n * Site - Central/left sided\r\n * Onset - Sudden\r\n * Character - Crushing ('like someone is sitting on your chest')\r\n * Radiation - Left arm, neck and jaw\r\n * Associated symptoms - Nausea, sweating, clamminess, shortness of breath, sometimes vomiting or syncope\r\n * Timing - Constant\r\n * Exacerbating/relieving factors - Worsened by exercise/exertion and may be improved by GTN\r\n * Severity - Often extremely severe\r\n* Atypical presentations may include:\r\n * Epigastric pain\r\n * No pain (more common in elderly and **patients with diabetes**):\r\n * Acute breathlessness\r\n * Palpitations\r\n * Acute confusion\r\n * Diabetic hyperglycaemic crises\r\n * Syncope\r\n\r\n# Differential Diagnoses\r\n\r\nIt is important to remember that there are non-MI causes of chest pain and these should be considered when making a diagnosis:\r\n\r\n* Cardiac\r\n * Myocarditis\r\n * Pericarditis\r\n * Cardiomyopathy\r\n * Valvular disease\r\n * Cardiac trauma\r\n* Pulmonary\r\n * PE\r\n * Pneumonia\r\n * Pneumothorax\r\n* Vascular\r\n * Aortic dissection\r\n* GI\r\n * Oesophageal spasm\r\n * Oesophagitis\r\n * Peptic ulcer\r\n * Pancreatitis\r\n * Cholecystitis\r\n* MSK\r\n * Rib fracture\r\n * Costochondritis\r\n * Muscle injury\r\n * Herpes zoster\r\n\r\n# Diagnosis of ACS \r\n\r\nDiagnosis depends on a combination of clinical, ECG and biochemical findings which helps distinguish between the various types of ACS.\r\n\r\n* Unstable angina - cardiac chest pain at rest + abnormal/normal ECG + **normal troponin**.\r\n* NSTEMI - cardiac chest pain at rest + abnormal/normal ECG (but not ST-elevation) + **raised troponin**\r\n* STEMI - cardiac chest pain at rest + **persistent ST-elevation/new LBBB** (note that there is no need for a troponin in this case).\r\n\r\n## Diagnosis of STEMI\r\n\r\n* ST segment elevation **>2mm** in adjacent chest leads\r\n* ST segment elevation **>1mm** in adjacent limb leads\r\n* New left bundle branch block (LBBB) with chest pain or suspicion of MI\r\n\r\n## Diagnosis of NSTEMI\r\n\r\nDiagnosis of NSTEMI requires two of the following:\r\n\r\n* Cardiac chest pain\r\n* Newly abnormal ECG which does not demonstrate ST-elevation e.g. ST depression, T wave inversion or non-specific changes. \r\n* Raised troponin (with no other reasonable explanation)\r\n\r\n# Investigations\r\n\r\n## Bedside \r\n\r\n* ECG \r\n\t* Looking for ST-elevation, LBBB or other ST abnormalities\r\n\t* This is the most important investigation and should not be delayed for other investigations (e.g. bloods) because this will define immediate management.\r\n\t* If an ECG shows STEMI then troponin is essentially irrelevant and the patient requires immediate treatment.\r\n\r\n## Bloods \r\n\r\n* Troponin: performed **at least 3 hours** after pain starts. It will also need to be repeated (usually 6 hours after the first level) in order to demonstrate a dynamic troponin rise. \r\n* Renal function: good renal function is required for coronary angiogram +/- PCI due to the use of contrast. \r\n* HbA1c and lipid profile: looking for modifiable risk factors for coronary artery disease. \r\n* FBC and CRP - rule out infectious causes of chest pain\r\n* D-dimer - may be used in _appropriate_ patients to rule out PE. *Be very careful about who you do a D-dimer on!*\r\n\r\n## Imaging \r\n\r\n* CXR: should be completed in all those presenting with a chest symptoms. It will help to rule out other causes of chest pain (e.g. pneumothorax) and look for complications of a large MI (e.g. pulmonary oedema in acute heart failure). \r\n\r\n# ECG Interpretation - Cardiac Territories and Affected Vessels\r\n\r\nThe importance of a 12-lead ECG is that it allows one to view electrical activity of the heart from different \"views\". In MI (particularly STEMI) this allows you to understand which territory (and therefore which vessel) is being affected.\r\n\r\n| Location of ST elevation | Area of myocardium | Coronary artery |\r\n| -------------------------- | ------------------ | -------------------- |\r\n| II, III, aVF | Inferior | RCA |\r\n| V1-2 | Septal | Proximal LAD |\r\n| V3-4 | Anterior | LAD |\r\n| V5-6 | Apex | Distal LAD/ LCx/ RCA |\r\n| I, aVL | Lateral | Lcx |\r\n| V7-V9 (ST depression V1-3) | Posterolateral | RCA/ LCx |\r\n\r\n\r\nRCA: right coronary artery, LAD: left anterior descending, LCx: Left circumflex\r\n\r\n[lightgallery]\r\n\r\n[lightgallery2]\r\n\r\n[lightgallery3]\r\n\r\n[lightgallery4]\r\n\r\n\r\nNSTEMIs may also show T wave abnormalities (such as ST depression and T wave inversions) in vascular territories as above. However, changes can also often not include all the specific leads of that territory in an NSTEMI.\r\n\r\n# Troponin Interpretation\r\n\r\nTroponin is a myocardial protein that is released into the bloodstream when cardiac myocytes are damaged. Serum levels typically rise **3 hours** after myocardial infarction begins.\r\n\r\nDifferent hospitals have differing guidelines (and assays) for interpretations of results. In general there are three groups of troponin levels:\r\n\r\n* Low - definitely no myocardial cell death. The patient is not having an MI although they may be experiencing unstable angina.\r\n* Mildly raised - This is an equivocal result and may be due to other non-MI related factors (see below). These patients usually need a <u>6-12 hour repeat test</u>.\r\n * If repeat troponin is raised on the repeat they are having an MI.\r\n * If repeat troponin is stable or falling then they are unlikely to be having an MI.\r\n* Definitely raised with sequential dynamic troponin rises - MI confirmed (be aware of the possibility of a Type 2 MI)\r\n\r\n## Non-ACS causes of a raised troponin\r\n\r\nAlthough troponin is often used diagnose myocardial infarction, there are in fact many causes of a raised troponin:\r\n\r\n* Myocardial infarction\r\n* Pericarditis\r\n* Myocarditis\r\n* Arrythmias\r\n* Defibrillation\r\n* Acute heart failure\r\n* Pulmonary embolus\r\n* Type A aortic dissection\r\n* Chronic kidney disease\r\n* Prolonged strenuous exercise\r\n* Sepsis\r\n\r\nIt is therefore critical to have good clinical grounds to test a troponin in order to avoid unnecessary treatments and investigations.\r\n\r\n# Management\r\n\r\nAcute management depends on the type of acute coronary syndrome. It is broadly split into the management of STEMI and the management of NSTEMI/unstable angina. \r\n\r\n# Management of STEMI\r\n\r\n[lightgallery5]\r\n\r\nFor emergencies, always follow A-E structure. \r\n\r\n1. Targeted oxygen therapy (aiming for sats >90%)\r\n2. Loading dose of **PO aspirin 300mg**\r\n - Note that some hospital protocols will also call for a loading dose of a second anti-platelet agent such as clopidogrel (300mg) or ticagrelor (180mg)\r\n - For those going on to have PCI, NICE guidance suggests adding prasugrel (if not on anti-coagulation) or clopidogrel (if on anti-coagulation)\r\n3. **Sublingual GTN spray** - for symptom relief\r\n4. **IV morphine/diamorphine** - in addition this causes vasodilation reducing preload on the heart\r\n5. Primary percutaneous coronary intervention (PPCI) for those who:\r\n - Present **within 12 hours of onset of pain** AND\r\n - Are **<2 hours** since <u>first medical contact</u>\r\n\r\nRemember that (particularly in STEMI) _time is heart_ therefore urgent treatment, escalation, and delivery of PPCI is critical to good outcomes.\r\n\r\n# Management of NSTEMI/Unstable Angina\r\n\r\n[lightgallery6]\r\n\r\nFor emergencies, always follow A-E structure. \r\n\r\n1. Targeted oxygen therapy (aiming for sats >90%)\r\n2. Loading dose of **PO aspirin 300mg** and fondaparinux\r\n * Patients should have their 6 month mortality score (often the GRACE score) calculated as early as possible - all those who are anything other than lowest risk should also be given **prasugrel or ticagrelor** unless they have a high risk of bleeding where **PO clopidogrel 300mg** is more appropriate.\r\n3. **Sublingual GTN spray** - for symptom relief\r\n4. **IV morphine/diamorphine** - in addition this causes vasodilation reducing preload on the heart\r\n5. Start antithrombin therapy such as **treatment dose low molecular weight heparin** or **fondaparinux** if they are for an immediate angiogram\r\n6. Patients with <u>high 6 month risk of mortality</u> should be offered an angiogram within 96 hours of symptom onset.\r\n\r\nNote that management of unstable angina is similar to that of NSTEMI with aspirin for all patients and fondaparinux and early angiography for those at high risk.\r\n\r\n# Post-MI management\r\n\r\n[lightgallery7]\r\n\r\n* ALL patients post-MI patients should be started on the following 5 drugs:\r\n 1. **Aspirin 75mg OM** + second anti-platelet (**clopidogrel 75mg OD** or **ticagrelor 90mg OD**)\r\n 2. **Beta blocker (normally bisoprolol)**\r\n 3. **ACE-inhibitor (normally ramipril)**\r\n 4. **High dose statin (e.g. Atorvastatin 80mg ON)**\r\n* All patients should have an **ECHO** performed to assess systolic function and any evidence of heart failure should be treated.\r\n* All patients should be referred to **cardiac rehabilitation**.\r\n* Patients who have been treated without angiography should be considered for ischaemia testing to assess for inducible ischaemia. \r\n\r\n# Complications\r\n\r\n* Ventricular arrhythmia\r\n* Recurrent ischaemia/infarction/angina\r\n* Acute mitral regurgitation\r\n* Congestive heart failure\r\n* 2nd, 3rd degree heart block\r\n* Cardiogenic shock\r\n* Cardiac tamponade\r\n* Ventricular septal defects\r\n* Left ventricular thrombus/aneurysm\r\n* Left/right ventricular free wall rupture\r\n* Dressler's Syndrome\r\n* Acute pericarditis\r\n\r\n## Ventricular Arrhythmias\r\n\r\n* Ventricular arrhythmias can occur as a consequence of MI, during cardiac catheterisation, or after reperfusion.\r\n* Most post-MI ventricular arrhythmias are short lived and self-resolve.\r\n* However if sustained VT or VF occurs they should be treated as per the Advanced Life Support protocols.\r\n\r\n## Recurrent Ischaemia/Infarction/Angina\r\n\r\n* Occasionally inserted stents can thrombose requiring reintervention.\r\n* New infarcts can occur in different vascular territories - this is less likely in the age of PCI where all territory are imaged during the procedure.\r\n* Angina and chest pain can continue for some time after an MI and is more common in NSTEMI patients.\r\n\r\n## Congestive Heart Failure\r\n\r\n* Heart failure can occur as a consequence of impairment heart muscle function secondary to ischaemia.\r\n* It should be treated as any other acute heart failure.\r\n* Ventricular function may improve over months as the heart muscle recovers.\r\n\r\n## Heart Block\r\n\r\n* Various levels of heart block are common - particularly following **inferior** infarcts (because the right coronary artery supplies the SAN).\r\n* These may be treated with:\r\n * Simple observation (as many will revert back to sinus rhythm)\r\n * Transcutaneous/venous pacing (if symptomatic)\r\n * Permanent pacing (if failing to resolve)\r\n\r\n## Left Ventricular Thrombus/Aneurysm\r\n\r\n* Aneurysm can occur following an anterior MI where the myocardium can be susceptible to wall stress leading to an aneurysm.\r\n* It may be silent, cause arrhythmias or embolic events.\r\n* It is definitely diagnosed on ECHO but ECG may show persisting ST elevation.\r\n* Thrombus can form either within an above described aneurysm or around hypokinetic regions of the myocardium.\r\n* Thrombi can embolise causing complications such as stroke, acute limb ischaemia and mesenteric ischaemia.\r\n\r\n## Left/Right Ventricular Free Wall Rupture\r\n\r\n* Necrosis of the free walls of either ventricle can lead to rupture allowing blood into the pericardial space.\r\n* This leads to a rapid tamponade and normally leads to cardiac arrest/death within seconds.\r\n* Treatment includes pericardiocentesis and surgery but prognosis is extremely poor.\r\n\r\n## Acute Mitral Regurgitation\r\n\r\n* This can occur because of papillary muscle rupture and carries a poor prognosis. Occurs commonly due to infero-osterior MI. \r\n* This presents with:\r\n * Pansystolic murmur heard best at the apex\r\n * Severe and sudden heart failure\r\n* It is diagnosed on echocardiogram and may require surgical correction.\r\n\r\n## Ventricular Septal Defect\r\n\r\n* Interventricular septal rupture is a short-term complications of myocardial infarction.\r\n* Rupture caused by an anterior infarct is generally apical and simple.\r\n* Rupture caused by an inferior infarct is generally basal and more complex.\r\n* Without reperfusion, septal rupture typically occurs within the first week after the infarction.\r\n* Features of septal rupture include:\r\n * Shortness of breath\r\n * Chest pain\r\n * Heart failure\r\n * Hypotension\r\n * Harsh, loud pan-systolic murmur along the left sternal border.\r\n * Palpable parasternal thrill.\r\n* Diagnosis is with echocardiogram.\r\n* Patients are managed with emergency cardiac surgery.\r\n\r\n## Dressler's syndrome\r\n\r\n* Dressler's syndrome or post-infarction pericarditis typically presents with persistent fever and pleuritic chest pain **2-3 weeks** or up to a few months after an MI.\r\n* Note that patients can get pericarditis immediately following MI which is NOT considered Dressler's syndrome.\r\n* Symptoms usually resolve after several days.\r\n* Occasionally it can also present with features of pericardial effusion and has become relatively uncommon since the introduction of PCI.\r\n* Management: **high dose aspirin**\r\n\r\n# Prognosis \r\n\r\nDue to the development of PPCI and post-MI care (cardiac rehabilitation) the mortality rates following myocardial infarction continue to decline. Those patients who go on to develop heart failure after myocardial infarction have a significantly worse prognosis than those who do not. \r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines for Unstable Angina and NSTEMI](https://www.nice.org.uk/guidance/cg94)\r\n\n[NICE Guidelines for STEMI](https://www.nice.org.uk/guidance/cg167)\r\n\r\n# References\r\n\r\n[Patient UK Information on Acute Coronary Syndrome](<https://patient.info/doctor/acute-coronary-syndrome-pro>)",
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"explanation": "This ECG does not show atrial flutter. Characteristic ECG changes seen in atrial flutter include a sawtooth baseline, an atrial rate of 300/min and a ventricular rate that is an exact ratio of the atrial rate. As there is rapid atrial contraction (300/min), not every p wave is conducted. This creates a atrioventricular conduction ratio of either 2:1 (most common), 3:1, 4:1, 5:1 (least common). This will be seen on the ECG as a ventricular rate of 150/min, 100/min, 75/min and 60/min respectively. The rate of the ECG shown is ~90/min, making it unlikely to be atrial flutter. In addition, it is an irregularly irregular rhythm, while atrial flutter has a regular rhythm",
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"explanation": "This patient is presenting with atrial fibrillation. They are presenting with typical clinical symptoms (including breathlessness, palpitations and lightheadness) and a typical ECG. ECG features include an irregularly irregular rhythm with the absence of P waves. Management options available to this patient include long term anticoagulation, rate control (e.g. with bisoprolol) and rhythm control (e.g. with chemical or electrical cardioversion). The preferred management options would depend on whether the patient is clinically stable, whether there is a reversible underlying cause and how long she has been in atrial fibrillation for",
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"explanation": "# Summary \r\n\r\nAtrial fibrillation (AF) is the most common arrhythmia characterised by irregular and uncoordinated atrial contraction at a rate of 300-600 beats per minute. Its prevalence increases with age, and it can be caused by various cardiac and non-cardiac factors. Symptoms of AF include palpitations, chest pain, shortness of breath, lightheadedness, and syncope. Diagnosis is confirmed by an ECG showing the absence of p waves and an irregularly irregular rhythm. Management depends on the acute or chronic nature of the AF and involves rate or rhythm control strategies. Anticoagulation is essential to mitigate the risk of stroke in chronic AF. Complications include heart failure, embolism, and bleeding. With appropriate management, AF has a favourable prognosis.\r\n\r\n# Definition \r\n\r\nAtrial fibrillation (AF) is characterised by irregular, uncoordinated atrial contraction usually at a rate of 300-600 beats per minute. Delay at the AVN means that only some of the atrial impulses are conducted to the ventricles, resulting in an irregular ventricular response.\r\n\r\n# Epidemiology \r\n\r\nAF is the commonest sustained cardiac arrhythmia. The prevalence of AF roughly doubles with each advancing decade of age, from 0.5% at age 50 years to almost 9% at age 80 years.\r\n\r\n# Pathophysiology\r\n\r\nThe exact pathophysiology of AF is unclear, but factors that cause atrial dilatation through inflammation and fibrosis leads to disorganised electrical impulses (which originate near the pulmonary veins) that overwhelm the SAN. These disorganised electrical impulses are usually at a rate of 300-600 beats per minute and are intermittently conducted through the AVN leading to irregular activation of the ventricles. \r\n\r\n# Classification \r\n\r\n* Acute: lasts <48 hours\r\n* Paroxysmal: lasts <7 days and is intermittent\r\n* Persistent: lasts >7 days but is amenable to cardioversion\r\n* Permanent: lasts >7 days and is not amenable to cardioversion\r\n\r\nAtrial fibrillation can also be classified as to whether it is 'fast' or 'slow'. Fast AF refers to AF that is at a rate of =>100bpm. Slow AF refers to AF that is at a rate of <=60bpm. \r\n\r\n# Causes \r\n\r\nCardiac:\r\n\r\n* Ischaemic heart disease: most common cause in the UK. \r\n* Hypertension\r\n* Rheumatic heart disease (typically affecting the mitral valve): most common cause in less developed countries.\r\n* Peri-/myocarditis\r\n\r\nNon-cardiac:\r\n\r\n* Dehydration\r\n* Endocrine causes e.g. hyperthyroidism\r\n* Infective causes e.g. sepsis \r\n* Pulmonary causes e.g. pneumonia or pulmonary embolism\r\n* Environmental toxins e.g. alcohol abuse\r\n* Electrolyte disturbances e.g. hypokalaemia, hypomagnesaemia \r\n\r\n# Symptoms\r\n\r\n* Palpitations\r\n* Chest pain\r\n* Shortness of breath\r\n* Lightheadedness\r\n* Syncope\r\n\r\n# Signs\r\n\r\n* Irregularly irregular pulse rate with a variable volume pulse.\r\n* A single waveform on the jugular venous pressure (due to loss of the a wave - this normally represents atrial contraction).\r\n* An apical to radial pulse deficit (as not all atrial impulses are mechanically conducted to the ventricles).\r\n* On auscultation there may be a variable intensity first heart sound.\r\n* Features suggestive of the underlying cause e.g. hyperthyroidism, alcohol excess, sepsis\r\n* Features suggestive of complications resulting from the AF e.g. heart failure.\r\n\r\n# Differential Diagnoses \r\n\r\nImportant differentials for atrial fibrillation include other common causes of narrow and broad complex tachycardias. Tachycardias may present with palpitations, shortness of breath, and dyspnoea. \r\n\r\n* **Atrial Flutter** \r\n\t* **Similarities**: atrial flutter may have a regular peripheral pulse or may be irregularly irregular if the flutter has variable block. Atrial fibrillation leads to an irregularly irregular peripheral pulse on palpation.\r\n\t* **Differences**: distinguishing between the two requires an ECG. Atrial fibrillation on ECG shows a fibrillating baseline with no visible p waves. Atrial flutter characteristically has a sawtooth baseline. \r\n\r\n* **Supraventricular Tachycardia**\r\n\t* **Similarities**: atrial flutter is a type of SVT, and other types including AVNRT and AVRT may present identically. \r\n\t* **Differences**: distinguishing between different types of SVT requires an ECG. \r\n\r\n* **Ventricular Tachycardia**\r\n\t* **Similarities**:both may present similarly. \r\n\t* **Differences**: the ECG patterns differ tremendously. \r\n\r\nFor palpitation histories, it is also important to consider whether the presentation is being driven by anxiety. However, it is important as a rule of thumb to rule out organic causes first. \r\n\r\n# Investigations\r\n\r\n## Bedside\r\n\r\n**Definitive diagnosis: 12-lead ECG** shows absence of p waves with an irregularly irregular rhythmn. \r\n\r\n[lightgallery]\n\n- If a person has a suspected diagnosis of paroxysmal AF which is not detected on standard ECG, arrange ambulatory electrocardiography or cardiology referral, depending on the frequency and duration of symptoms and local referral pathways\r\n\r\n## Bloods \r\n\r\nRoutine bloods: to look for reversible causes including infection (raised WCC or CRP), hyperthyroidism (raised T3/T4) or alcohol use (raised MCV and GGT).\r\n\r\n## Imaging\r\n\r\nEchocardiogram: can be used to see if there is a cardiac cause of the AF e.g. left atrial dilatation secondary to mitral valve disease. \r\n\r\n# Management\n\nConsider emergency admission or Cardiology referral if a patient presents with:\n\n- New-onset AF within the past 48 hours and is haemodynamically unstable\n- Severe symptoms of AF due to rapid (bpm > 150 ) or very slow (bpm < 40) ventricular rate\n- Concomitant acute decompensated heart failure\n- Complications of AF, such as TIA/stroke\n- An acute, potentially reversible trigger such as pneumonia/sepsis or thyrotoxicosis\n\nIf they do not require acute management or emergency admission, they can be considered for anticoagulation and rate-control treatment in primary care.\r\n\r\n## Management of Acute or New-onset Atrial Fibrillation\r\n\r\nFor emergencies, always follow an A-E structure. Identify reversible causes (dyselectrolytaemias, drugs, cardiac causes etc.) \r\n\r\n*If there are adverse signs (e.g. shock, syncope, heart failure, myocardial ischaemia):* \r\n\r\n* **1st line** = **synchronised DC cardioversion +/- amiodarone.**\r\n\r\n*If there are no adverse signs:* and the rhythm is irregular it is likely atrial fibrillation. \r\n\r\n* **If the patient is stable and onset of AF <48 hours**: \r\n\t* Rate or rhythmn control.\r\n\t* Rhythm control with DC cardioversion (+ sedation) or pharmacological anti-arrhythmics (fleicanide if no structural heart disease, amiodarone if history of structural heart disease). \r\n\t* If DC cardioversion is delayed then heparin will be required to anticoagulate the patient. \r\n\r\n* **If the patient is stable and onset of AF >48 hours/unclear time of onset**: \r\n\t* Rate control only. \r\n\t* Rate control with beta-blockers, diltiazem or digoxin. \r\n\t* Need to anticoagulate for 3/52 prior to attempting cardioversion due to the risk of throwing off a clot. You can also perform a TOE to exclude a mural thrombus. \r\n\r\nIf AF persists or reversible causes are not present then decisions should be made about rate control, rhythm control or electrical cardioversion.\r\n\r\n## Management of Chronic AF \r\n\r\nThe cornerstones of managing chronic AF are related to symptom control and mitigating stroke risk. \r\n\r\n## Symptom Management of Chronic AF \r\n\r\n### Rate vs. Rhythm Control \r\n\r\n#### Rate-Control\r\n\r\nThe aim of rate control is to reduce a patient's heart rate in order to reduce symptoms.\r\n \r\n* First line in most patients. See below for patients who should undergo rhythm control. \r\n* **1st line medications:** beta-blocker (bisoprolol) or rate-limiting calcium channel blocker (diltiazem). \r\n* **2nd line medications**: dual therapy (under specialist guidance) \r\n* Digoxin monotherapy may be considered in those with non-paroxysmal AF who are sedentary. \r\n \r\n#### Rhythm Control\r\n\r\nThe aim of rhythm control is to revert a patient back into sinus rhythm. \r\n \r\nRhythm control should be offered to patients who have: \r\n\r\n* AF secondary to a reversible cause\r\n* Heart failure thought to be caused by AF\r\n* New-onset AF\r\n* Or those for whom a rhythm control strategy would be more suitable based on clinical judgement. \r\n\r\nRhythm control can be achieved via two methods:\r\n\r\n* Electrical cardioversion\r\n* Pharmacological cardioversion: amiodarone, fleicanide or sotalol. \r\n\r\nThe moment of return to sinus rhythm poses the highest stroke risk. Therefore, rhythm control should only be attempted if the onset of AF <48 hours, a patient has undergone 3/52 of anticoagulation or has had a TOE to exclude a mural thrombus. \r\n\r\nNote that patients in chronic AF or those who have failed cardioversion before are unlikely to be successfully cardioverted so this would not be considered in most of these cases.\r\n\r\n#### Catheter Ablation \r\n\r\nA final option for rhythm control is catheter ablation of the arrhythmogenic focus between the pulmonary veins and left atrium. Even if teh foci is ablated, this does not reduce stroke risk and the patient must be anticoagulated. There is a high risk of recurrence (50% have recurrent AF). \r\n\r\n## Medications used for Rate Control \r\n\r\n### Beta-blockers\r\n\r\n* The most commonly used beta-blocker in AF is bisoprolol.\r\n* Commonly used medication for acute treatment and chronic management.\r\n* Technically it is contraindicated in COPD and asthma (in reality unless the conditions are considered _brittle_ it is not a problem). \r\n* Cannot be used in hypotension because it will drop blood pressure.\r\n* Note that sotalol CANNOT be used as a rate control agent because of its rhythm control action.\r\n\r\n### Non-dihydropyridine calcium channel blockers\r\n\r\n* Calcium channel blockers used in AF are diltiazem or verapamil.\r\n* They are not frequently used in hospital settings because they are negatively ionotropic and therefore they are contraindicated in heart failure.\r\n\r\n### Digoxin\r\n\r\n* Usual for patients who are hypotensive or who have co-existent heart failure.\r\n* Should be avoided in younger patients because it increases cardiac mortality.\r\n* Often used second-line in conjunction with beta-blockers if fast AF remains refractory.\r\n\r\n## Medications used for Rhythm Control\r\n\r\n* Flecainide\r\n * Can be either given regularly or as a \"pill in the pocket\" when symptoms come on.\r\n * Is preferred in _young patients_ who have _structurally normal hearts_ because it can induce fatal arrhythmias in those with structural heart disease.\r\n\r\n* Amiodarone\r\n * Extremely effective drug in controlling both rate and rhythm.\r\n * However it comes with a massive list of significant side-effects so should normally only be given to _older, sedentary patients_.\r\n\r\n* Sotalol\r\n * This is a beta blocker with additional K channel blocker action.\r\n * Used for those that don't meet the demographics for either flecainide or amiodarone.\r\n\r\n## Mitigating Stroke Risk in Chronic AF \r\n\r\nIn atrial fibrillation, the lack of organised atrial contraction can lead to blood stasis in the left atrium. Due to the left atrial appendage, blood clots easily here and if part of this clot embolises it can lead to a stroke. Therefore, if a patient has any history of atrial fibrillation or atrial flutter the need for anticoagulation must be considered. \r\n\r\nPatients need to be considered according to their stroke risk (CHADS2VASc score) and their bleeding risk (ORBIT score) to determine whether anticoagulation is appropriate. \r\n\r\n### CHADS2VASc Score\r\n\r\nPatients should be risk stratified using the CHADS2VASc score:\r\n\r\n* C: 1 point for congestive cardiac failure.\r\n* H: 1 point for hypertension.\r\n* A2: 2 points if the patient is aged 75 or over.\r\n* D: 1 point if the patient has diabetes mellitus.\r\n* S2: 2 points if the patient has previously had a stroke or transient ischaemic attack (TIA).\r\n* V: 1 point if the patient has known vascular disease.\r\n* A: 1 point if the patient is aged 65-74.\r\n* Sc: 1 point if the patient is female.\r\n\r\n#### Interpretation of the CHADS2VASc score\r\n\r\nThe minimum score is 0 (associated with 0% annual stroke risk) and maximum score is 9 (15% annual stroke risk).\r\nMales who score 1 or more or females who score 2 or more should be anticoagulated (as long as the risk of stroke outweighs the risk of bleeding). \r\n\r\n#### ORBIT Score\r\n\r\nRisks of anticoagulation also need to be considered. Historically the HASBLED score stratified bleeding risk:\r\n\r\n* H: Hypertension 1 point\r\n* A: Abnormal renal or liver function 2 points if both are present\r\n* S: Stroke (previous) 1 point\r\n* B: Major bleed (previous) 1 point\r\n* L: Labile INR 1 point\r\n* E: Elderly (>65) 1 point\r\n* D: Drugs/alcohol 1 point for drug or alcohol use (2 points if both are present)\r\n\r\nIn their 2021 AF guidelines NICE suggested the use of the ORBIT score which takes into account:\r\n\r\n* Sex\r\n* Haemoglobin (<13mg/Dl in males, <12mg<dL in females) 2 points\r\n* Age (>74) 1 point\r\n* Bleeding history 2 points\r\n* Renal function (eGFR <60) 1 point\r\n* Concomitant use of anti-platelets 1 point\r\n\r\n#### Interpretation of the HASBLED and ORBIT scores\r\n\r\nIn reality very little guidance exists about how to weigh up the stroke and bleeding risks when making a decision on anticoagulation. Choice of long term anticoagulation is generally a decision led by patient choice and clinical judgement.\r\n\r\n### Anticoagulation options in AF\r\n\r\n* **Direct oral anticoagulants (DOACs)**:\r\n * Considered first line for anticoagulation in AF. \r\n * Examples of DOACs are edoxaban, apixaban, rivaroxaban & dabigatran\r\n * **Do not** require monitoring\r\n * Generally associated with fewer bleeding risks compared to warfarin.\r\n * Most have approximately 12 hour half-lives therefore if a patient misses a dose they are not covered.\r\n\r\n* **Warfarin**:\r\n * Requires cover with LMWH for 5 days when initiating treatment (because warfarin is initially _prothrombotic_).\r\n * Requires regular INR monitoring.\r\n * INR can be affected by a whole host of drugs and foods.\r\n * Has 40 hour half-life therefore anticoagulant effect lasts days.\r\n * Is the only oral anticoagulant licenced for **valvular AF**.\r\n* **Low Molecular Weight Heparin (LMWH)**:\r\n * An example of a LMWH is enoxaparin.\r\n * A rare option in patients who cannot tolerate oral treatment.\r\n * Involves daily _treatment dose_ injections.\r\n\r\n# Complications\r\n\r\nMost complications are either from uncontrolled heart rate, embolism or from anticoagulation. They include:\r\n\r\n* Heart failure\r\n* Systemic emboli:\r\n * Ischaemic Stroke\r\n * Mesenteric ischaemia\r\n * Acute limb ischaemia\r\n* Bleeding:\r\n * GI\r\n * Intracranial\r\n \r\n# Prognosis \r\n\r\nIf patients are anticoagulated and are on either rhythm or rate control AF can remain a benign cardiac arrhythmia. \r\n\r\n# NICE Guidelines\r\n\n[Click here to see information on NICE CKS guidance for AF](https://cks.nice.org.uk/topics/atrial-fibrillation/)\r\n\r\n# References\r\n \r\n[Live Life in the Fast Lane AF ECG Summary](https://litfl.com/atrial-fibrillation-ecg-library/)",
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"question": "A 64 year old woman presents to the emergency department with breathlessness, palpitations and lightheadedness. She has a ECG taken, which is shown below:\n\n[lightgallery]\n\nWhat is the most likely diagnosis?",
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"explanation": "This is not a normal ECG. There are no discernible P waves and the QRS complexes are very broad",
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"explanation": "This a typical ECG showing monomorphic ventricular tachycardia. This is characterised by regular, wide QRS complexes of equal amplitude (monomorphic) with an absence of P waves. This patient is conscious (and would have a pulse if felt for) so they are not in cardiac arrest, however they do require urgent management. This patient would need urgent escalation to a senior colleague, with consideration for agents such as amiodarone to cardiovert them back to normal rhythm",
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"explanation": "This ECG does not show atrial fibrillation. Atrial fibrillation is characterised by an irregularly irregular rhythm and absent P waves. Although this ECG does not have P waves, the rhythm is regular. This is also a broad complex tachycardia, whereas atrial fibrillation presents with narrow complexes",
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"explanation": "Torsades de pointes is also known as polymorphic ventricular tachycardia. Monomorphic and polymorphic ventricular tachycardia are both broad complex tachycardias with a regular rhythm. However, polymorphic ventricular tachycardia has QRS complexes of varying amplitude, whereas monomorphic ventricular tachycardia has QRS complexes with no significant difference in amplitude (as shown in this question)",
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"explanation": "Cardiac tamponade can occur after myocardial infarction, and is associated with rupture of the ventricular wall. However this question does not mention the characteristic features of Beck's triad (muffled heart sounds, hypotension, raised jugular venous pressure (JVP)) and this ECG does not show electrical alternans (the amplitude of the QRS complexes swapping between beats)",
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"explanation": "# Summary \r\n\r\nBroad complex tachycardia refers to dysrhythmias with a heart rate greater than 100 beats per minute and a QRS complex broader than 120 milliseconds. This term encompasses life-threatening rhythms such as ventricular tachycardia (VT) and ventricular fibrillation (VF). VT is a regular, broad complex tachycardia and may be with or without a pulse. In contrast, VF is irregular and is always pulseless. Pulseless VT and VF must be managed according to the ALS algorithm and require immediate defibrillation and administration of medications like adrenaline and amiodarone, whilst managing pulsed VT involves synchronised shocks and amiodarone. SVT with aberrancy, a condition where supraventricular tachycardia occurs in the presence of bundle-branch block, can mimic VT and should be treated cautiously.\r\n\r\n# Definition \r\n\r\nBroad complex tachycardias are dysrhythmias that have a heart rate greater than 100bpm and a QRS complex that is greater than 120ms. The most common broad complex tachycardias are ventricular tachycardia or ventricular fibrillation. \r\n\r\n# Ventricular Tachycardia (VT)\r\n\r\nA regular broad complex tachycardia. It can occur with a pulse or it may be pulseless. \r\n\r\nECG features include: \r\n\r\n* Tachycardia (>100 beats per minute)\r\n* Absent p waves\r\n* Monomorphic regular broad QRS complexes (>120ms)\r\n\r\n[lightgallery]\r\n\r\n# Management of VT \r\n\r\n## Pulseless VT \r\n\r\nIf there is no pulse the patient should be managed according to the Advanced Life Support algorithm. \r\n\r\n* Pulseless VT is a shockable rhythm so a 200J bi-phasic **unsynchronised** shock should be administered. \r\n* IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock.\r\n* Adrenaline should be administered every 3-5 minutes thereafter. \r\n\r\n## Pulsed VT with Adverse Features\r\n\r\nIf the patient has a pulse but is demonstrating adverse features (shock, syncope, myocardial ischaemia, or heart failure) the patient should be managed according to Resuscitation Council Tachyarrhythmia algorithm. \r\n\r\n* Administer synchronised DC shocks (up to 3 attempts). If the patient is conscious this will require sedation or anaesthesia. \r\n* Expert help should guide amiodarone administration (300mg IV over 10-20 minutes followed by 900mg infusion over 24 hours). \r\n\r\n## Pulsed VT with No Adverse Features \r\n\r\nIf the patient has a pulse and is not demonstrating adverse features then the Resuscitation Council Tachyarrhythmia algorithm should be followed. \r\n\r\n* Amiodarone 300mg IV over 10-60 minutes. \r\n* If this is ineffective then administer synchronised DC shocks (up to 3 attempts). If the patient is conscious this will require sedation or anaesthesia. \r\n* *N.B. if there has been a previous certain diagnosis of SVT with aberrancy treat as for regular narrow complex tachycardias*\r\n\r\n# Ventricular fibrillation (VF) \r\n\r\nAn irregular broad complex tachycardia. This is always a pulseless rhythm.\r\n\r\nECG features include: \r\n\r\n* Tachycardia >100bpm \r\n* QRS complexes are polymorphic and irregular (>120ms)\r\n\r\n[lightgallery1]\r\n\r\n# Management of VF\r\n\r\nThe patient should be managed according to the Advanced Life Support algorithm. \r\n\r\n* VF is a shockable rhythm so a 200J bi-phasice **unsynchronised** shock should be administered. \r\n* IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock.\r\n* Adrenaline should be administered every 3-5 minutes thereafter.\r\n\r\n# Other Broad Complex Tachycardias \r\n\r\nInclude: \r\n\r\n* Torsades des pointes: see section. \r\n* SVT with aberrancy: occurs when a patient with a bundle-branch block goes into SVT. It can be difficult to distinguish between VT and an SVT with aberrancy. The safest approach is to treat as VT. \r\n\r\n[lightgallery2]\r\n\r\n# NICE Guidelines\r\n\n[NICE CKS Guidelines for Cardiac Arrest and ALS](<https://cks.nice.org.uk/topics/cardiac-arrest-out-of-hospital-care/management/advanced-life-support-adult/>)\r\n\r\n# References\r\n[Resuscitation Council UK Adult Tachycardia Algorithm](<https://www.resus.org.uk/sites/default/files/2021-04/Tachycardia%20Algorithm%202021.pdf>)\r\n\r\n[Resuscitation Council UK Adult ALS Algorithm](<https://www.resus.org.uk/sites/default/files/2021-04/Adult%20Advanced%20Life%20Support%20Algorithm%202021.pdf>)",
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"question": "A 67 year old patient is on the cardiology ward following a myocardial infarction. They received percutaneous coronary intervention six hours ago. They now feels breathless and dizzy, and their current ECG trace is shown below:\n\n[lightgallery]\n\nWhat is the most likely diagnosis?",
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"explanation": "This ECG does not show second degree heart block, mobitz type 1. An ECG of second degree heart block, mobitz type 1 typically shows progressive elongation of the PR interval followed by non-conduction of the P wave and a skipped QRS. This is not shown in this ECG, which shows complete non-conduction of the P waves",
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"label": "c",
"name": "Second degree heart block, mobitz type 1",
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"explanation": "This ECG does not show atrial fibrillation. An ECG in atrial fibrillation would be irregularly irregular with absent P waves. This ECG is regular and although P waves can be difficult to observe, they are visible on more detailed inspection of the ECG",
"id": "33527",
"label": "e",
"name": "Atrial fibrillation",
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"explanation": "This ECG does not show second degree heart block, mobitz type 2. An ECG of second degree heart block, mobitz type 2 typically shows occasionally dropped QRS complexes (due to non-conduction of P waves) in the absence of progressive prolongation of the P-R interval. This can either be somewhat random or in a fixed ratio e.g. 2:1. This is in contrast to this ECG where no P waves are conducted, making it more in keeping with complete heart block",
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"label": "b",
"name": "Second degree heart block, mobitz type 2",
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"explanation": "Complete heart block is caused by failure of the atrioventricular node, preventing the electrical impulses generated by the sinoatrial node reaching the ventricles. This leads to a complete dissociation of the ventricles from the atria. In this case, this was caused by the combination of a beta blocker with a non-dihydropyridine calcium channel blocker, which should never be given in combination due to the risk of bradyarrhythmia and complete heart block. This is a typical ECG of complete heart block, with complete dissociation of the P waves from the QRS complexes. P waves are around the normal atrial rate of around 100-180/min and the QRS complexes are at ventricular escape rhythm which is around 20-40/min. If this patient remains untreated they are at significant risk of asystole and death",
"id": "33523",
"label": "a",
"name": "Complete heart block",
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"explanation": "This is not a normal ECG. In a normal ECG, every P wave is followed by a QRS and every QRS is preceded by a P wave",
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"explanation": "# Summary\r\n\r\nHeart block refers to an obstruction in the electrical conduction system of the heart. This obstruction can occur at various points in the conduction system, including the sinoatrial node, atrioventricular node, Bundle of His, or bundle branches. Atrioventricular heart block specifically affects the conduction between the atria and ventricles. The severity of heart block can range from first degree, which is generally benign, to second degree (Mobitz Type I and II), to complete (third degree) heart block, which requires immediate management with a permanent pacemaker due to the risk of asystole. The underlying causes and management strategies differ for each type of heart block.\r\n\r\n# Definition \r\n\r\nHeart block occurs due to an obstruction in the electrical conduction system of the heart. It can occur anywhere along the conduction system of the heart from the sinoatrial node to the atrioventricular node to the Bundle of His or within the bundle branches themselves. \r\n\r\nSinoatrial node block rarely leads to symptoms as the atrioventricular node acts as a secondary pacemaker. Bundle branch blocks are a form of heart block but they are discussed in a separate section. The rest of this section will discuss atrioventricular block in more detail. \r\n\r\nPatients with atrioventricular heart block may be asymptomatic or may present with fatigue, lightheadeness, syncope, shortness of breath and most seriously in cardiac arrest or with sudden death. \r\n\r\n# First Degree Heart Block\r\n\r\n## Definition\r\n\r\nThis is caused by prolonged conduction of electrical activity through the AV node. It can be identified on ECG by finding a PR interval >200ms.\r\n\r\n[lightgallery]\r\n\r\n## Causes\r\n\r\n* High vagal tone: e.g. athletes\r\n* Acute inferior MI\r\n* Electrolyte abnormalities: e.g. hyperkalaemia\r\n* Drugs: e.g. NHP-CCBs, beta-blockers, digoxin, cholinesterase inhibitors\r\n\r\n## Management\r\n\r\nFirst degree heart block itself is benign and does not need treating. However, any pathological underlying cause should be reversed.\r\n\r\n# Second Degree Heart Block \r\n\r\nSecond degree heart block is split into Mobitz Type I and Mobitz Type II heart block. \r\n\r\n# Mobitz Type I\r\n\r\n## Definition\r\n\r\nWenckebach phenomenon or Mobitz type I is a type of second degree heart block that is usually due to reversible conduction block at the AV node. It is characterised by progressive lengthening of the PR interval which results in a P wave that fails to conduct a QRS.\r\n\r\n[lightgallery1]\r\n\r\n## Causes\r\n\r\n* MI (mainly inferior)\r\n* Drugs such as beta/calcium channel blockers, digoxin\r\n* Professional athletes due to high vagal tone\r\n* Myocarditis\r\n* Cardiac surgery\r\n\r\n## Management\r\n\r\nIt is generally asymptomatic and does not require any specific management as the risk of high AV block/complete heart block is low. If symptoms do arise, ECG monitoring may be required, precipitating drugs must be stopped and if they are bradycardic with adverse features they should be treated with atropine.\r\n\r\n# Mobitz Type II\r\n\r\n## Definition\r\n\r\nMobitz type II block is a type of second degree AV block where there are intermittent non-conducted P waves. The _PR interval is constant_ (may be normal or prolonged) and there may no pattern or fixed ratios such as 2:1 or 3:1 block. It is usually caused by conduction system failure, especially at the His-Purkinje system.\r\n\r\nIn most cases there is a broad QRS indicating a distal block in the His-Purkinje system and many patients have pre-existing left bundle branch block/bifascicular block.\r\n\r\n[lightgallery2]\r\n\r\n## Causes\r\n\r\n* Infarction: particularly anterior MI which damages the bundle branches\r\n* Surgery: mitral valve repair or septal ablation\r\n* Inflammatory/autoimmune: rheumatic heart disease, SLE, systemic sclerosis, myocarditis\r\n* Fibrosis: Lenegre's disease\r\n* Infiltration: sarcoidosis, haemochromatosis, amyloidosis\r\n* Medication: beta-blockers, calcium channel blockers, Digoxin, amiodarone\r\n\r\n## Management\r\n\r\nDefinitive management is with a permanent pacemaker as these <u>_patients are at risk of complete heart block_</u> and at risk of becoming haemodynamically unstable.\r\n\r\n# Complete (Third degree) Heart Block\r\n\r\n## Definition\r\n\r\nComplete heart block occurs when atrial impulses fail to be conducted to the ventricles. Sufficient cardiac output may be secondary to a ventricular or junctional escape rhythm.\r\n\r\nECG shows severe bradycardia and complete dissociation between the P waves and the QRS complexes. These patients are at high risk of asystole, ventricular tachycardia and cardiac arrest. \r\n\r\n[lightgallery3]\r\n\r\n## Causes\r\n\r\n* Myocardial infarction: especially inferior\r\n* Drugs acting at the AVN: beta blockers, dihydropyridine calcium channel blockers, or adenosine\r\n* Idiopathic fibrosis\r\n\r\n## Management\r\n\r\nManagement of complete (third degree) heart block is via the acute bradycardia guideline (see below). Permanent pacemaker insertion is eventually required due to the risk of sudden death.\n\nAcute management:\n\nFor emergencies, always follow an A-E structure. Identify reversible causes (dyselectrolytaemias, drugs, cardiac causes etc.) \r\n\r\n*If there are adverse signs (e.g. shock, syncope, heart failure, myocardial ischaemia):* \r\n\r\n* **1st line** = **500 micrograms atropine IV**\r\n * Atropine blocks the vagal nerve which increases firing rate of the SAN. \r\n* **2nd line** = if the first dose of atropine is not working can consider giving additional doses of atropine 500mcg up to 3mg until response. Alternatively, **transcutaenous pacing** or **isoprenaline** or **adrenaline** or **alternative drugs** including aminophylline, adrenaline, glucagon (in beta-blocker or calcium channel blocker overdose). \r\n\r\n*If there are no adverse signs but a risk of asystole, or a satisfactory response to 500mcg atropine:*\r\n\r\n* Risk of asystole: recent asystole, mobitz type II block, complete heart block + broad QRS, ventricular pauses >3s. \r\n* **1st line** = administer **500 micrograms atropine IV**. Alternatively, **transcutaenous pacing** or **isoprenaline** or **adrenaline** or **alternative drugs** including aminophylline, adrenaline, glucagon (in beta-blocker or calcium channel blocker overdose). \r\n\r\n*If there are no adverse signs and there is no risk of asystole*\r\n\r\n* Observe\r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines on Pacing](<https://www.nice.org.uk/guidance/ta88/chapter/2-clinical-need-and-practice>) \r\n\r\n# References\r\n\r\n[Life in the Fast Lane Heart Block ECG Summary](https://litfl.com/heart-block-and-conduction-abnormalities/)\r\n\r\n[Resuscitation Council Adult Bradycardia Algorithm](<https://www.resus.org.uk/sites/default/files/2020-05/G2015_Adult_bradycardia.pdf>)",
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"question": "A 27 year old patient attends the GP with physical symptoms of anxiety. They are subsequently started on Propanolol. They present to the emergency department the same day with severe breathlessness and lightheadedness. They have a past medical history of cluster headaches for which they take verapamil for prophylaxis. Their ECG is shown below:\n\n[lightgallery]\n\nWhat is the most likely diagnosis?",
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"explanation": "COPD can present with exertional breathlessness and is a good differential to consider in anyone presenting with exertional breathlessness and a significant smoking history. However, this would not explain the associated chest pain, which is more in keeping with angina. This patient's smoking history is also not specified in this question",
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"explanation": "This is a classical description of stable angina pectoris. This patient is present with all 3 diagnostic criteria for stable angina: constricting chest/jaw/arm pain, exercise as a trigger for the pain and rest for 5 minutes/glyceryl trinitrate resolving the pain. This is a typical history of angina and the next steps would involve basic investigations (bloods including full blood count and thyroid function tests), confirmation of the diagnosis (usual first line investigations is a CT coronary angiography) via referral to cardiology and initiation of treatment. Treatment includes symptomatic treatment (usually with glyceryl trinitrate), prophylaxis of attacks (usually with a cardioselective beta blocker or a calcium channel blockers) and drugs for secondary prevention of cardiovascular disease (e.g. statin, aspirin)",
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"explanation": "Although panic disorder can present with chest pain, breathlessness and sweating, this chest pain is more cardiac in nature (crushing with radiation to jaw). This patient also doesn't mention any features of worrying or panicking and his symptoms have a clear association with exercise which would be not be likely to trigger an anxiety attack by itself",
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"explanation": "Acute coronary syndrome will also present with a similar chest pain as both conditions are associated with myocardial ischaemia. However, in stable angina this is related to coronary artery atherosclerosis making it more difficult to meet the demand of the myocardium during exercise, whereas many causes of acute coronary syndrome are related to thrombi in the coronary arteries. As a result, the main differentiating clinical feature is that stable angina will resolve within 5 minutes, whereas acute coronary syndrome will last longer. Stable angina is a risk factor for acute coronary syndrome and it is important to give patients specific advice around this (if getting anginal chest pain: rest and use 2 GTN sprays, wait 5 minutes, use 2 GTN sprays, wait 5 minutes, if symptoms are still there they must ring an ambulance)",
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"explanation": "Ludwig's angina, also known as cellulitis of the floor of the mouth, is an oral infection causing swelling of the mouth which can lead to airway compromise. It is usually associated with a dental abscess. Although this would present with pain around the jaw, this would not explain the chest pain. The root of the word \"angina\" means \"strangling\", which is why the word is used to describe two seemingly unrelated conditions",
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"explanation": "# Summary\r\n\r\nStable angina, characterised by chest pain triggered by myocardial ischemia, is most commonly caused by coronary artery disease. Typical anginal chest pain is described as an exertional chest discomfort that may radiate to the jaw/neck/arm and that is alleviated by rest (<5 minutes) or with GTN spray. Diagnosis involves investigations such as ECG, blood tests, and CT coronary angiogram. Management includes conservative measures to optimise cardiovascular risk factors, medical treatment with anti-anginal medications, and revascularisation options like coronary artery bypass graft or percutaneous coronary intervention in cases not controlled by medical therapy.\r\n\r\n# Definition \r\n\r\nTypical anginal chest pain is defined by the following 3 features:\r\n\r\n1. Constriction/heavy discomfort to chest that may radiate to the jaw/neck/arm.\r\n2. Brought on by exertion.\r\n3. Alleviated by rest (<5 minutes) or GTN spray. \r\n\r\n3/3 features = typical angina pain \r\n\r\n2/3 features = atypical angina pain\r\n\r\n0-1/3 features = non-anginal pain \r\n\r\n# Epidemiology \r\n\r\nA 2020 Health Survey for England estimated prevalence in all UK adults as 3%, increasing to a prevalence of 10–12% in women aged 65–84 years and 12–14% in similarly aged men. \r\n\r\n# Pathophysiology\r\n\r\nStable angina occurs as a result of a mismatch of myocardial oxygen supply and demand. Most commonly, stable angina is due to coronary artery disease. Coronary artery disease refers to the narrowing of coronary arteries by atherosclerosis and plaque formation. When demand for myocardial oxygen increases with exertion, narrowed coronary arteries cannot meet this increased demand leading to myocardial ischaemia and pain. \r\n\r\nOther rarer causes of stable angina include anaemia, aortic stenosis, or hypertrophic cardiomyopathy.\r\n \r\n# Classification \r\n \r\nStable angina pain can be considered by its limitations on day-to-day activity:\r\n\r\n* Class I: no angina with normal physical activity. Strenuous activity may cause symptoms. \r\n* Class II: angina pain causes slight limitation on normal physical activity. \r\n* Class III: angina causes marked limitation on normal physical activity. \r\n* Class IV: angina occurs with any physical activity and may occur at rest (see unstable angina). \r\n\r\n# Symptoms and Signs\r\n\r\n* Central, constricting chest pain that radiates to neck/jaw/arm. \r\n* Exertional chest pain that is relieved on rest/GTN. \r\n* Associated symptoms: nausea, vomiting, clamminess or sweating. \r\n\r\nStable angina may have no clinical signs on examination at rest.\r\n\r\n# Differential Diagnoses \r\n\r\n* **Acute Coronary Syndrome (ACS)** \r\n\t* **Similarities**: cardiac-sounding chest pain as a presenting complaint for both. Similar patient profile with significant risk factors for coronary artery disease. \r\n\t* **Differences**: stable angina only occurs on exertion and is alleviated by rest. ACS chest pain occurs at rest. \r\n\r\n* **Gastro-oesophageal reflux disease (GORD)** \r\n\t* **Similarities**: both may present with central chest discomfort/pain. \r\n\t* **Differences**: discomfort in stable angina commonly described as a squeezing or pressure-like pain brought on by exertion. GORD-related chest discomfort often described as a burning sensation that is triggered by certain foods, alcohol, or lying down. \r\n\r\n* **Costochondritis** \r\n\t* **Similarities**: both present with chest pain. \r\n\t* **Differences**: costochondritis refers to inflammation of the cartilage connecting ribs to the sternum. The pain is described as sharp and can be reproduced by pressing on the chest wall. \r\n\r\n* **Pleuritic Chest Pain e.g. Pulmonary Embolism, Pneumonia** \r\n\t* **Similarities**: both present with chest pain or discomfort. \r\n\t* **Differences**: pleuritic chest pain is often described as sharp and worse on inspiration. Pleuritic chest pain will also be accompanied by clinical features relating to the underlying cause e.g. productive cough, fevers, risk factors for VTE, or a hot swollen calf. \r\n\r\nOther differential diagnoses include anxiety, aortic dissection (radiates to the back), and other causes of musculoskeletal chest pain. \r\n\r\n# Investigations\r\n\r\nOnce atypical/typical anginal pain is suspected: \r\n\r\n**Routine investigations in primary care**: \r\n\r\n* ECG - to assess for ischaemic changes or previous MI. \r\n* Bloods - FBC and TFTs (to exclude anaemia and hyperthyroidism respectively which can exacerbate angina symptoms).\r\n* Consider cardivascular risk factors: hypertension, hypercholesterolaemia, diabetes mellitus, smoking. \r\n\r\n**1st line investigations**\r\n\r\n* CT coronary angiogram (CT CA)- indicated if typical/atypical angina pain or if ECG shows ischaemic changes in chest pain with <2 angina features.\r\n\r\n**2nd line investigations** \r\n\r\nIf CTCA is inconclusive the patient may undergo functional imaging: \r\n\r\n* Stress echocardiogram \r\n* Myocardial perfusion SPECT \r\n* Cardiac MRI\r\n\r\n**3rd line investigations**\r\n\r\nInvasive coronary angiography can be performed if there are inconclusive results from non-invasive testing.\r\n\r\n# Management\r\n\r\n## Conservative management\r\n\r\nConservative management involves the optimisation of cardiovascular risk factors to reduce the atherosclerotic process. \r\n\r\n* Smoking cessation\r\n* Glycaemic control\r\n* Hypertension\r\n* Hyperlipidaemia\r\n* Weight loss\r\n* Alcohol intake \r\n\r\n## Medical management \r\n\r\n* Secondary prevention: aspirin 75mg OD and statin 80mg ON. \r\n* GTN spray for symptom relief: inform patient of side-effects (headache, flushing, dizziness) and to repeat dose if pain not stopped after 5 minutes. \r\n\r\n*Emergency help should be sought if pain not subsided after 2 doses of GTN as this may indicate acute coronary syndrome.* \r\n\r\n**Anti-anginal medications**\r\n\r\n**1st line** = beta-blocker (bisoprolol) OR calcium channel blocker (verapamil or diltiazem). *Do not combine due to risk of heart block*. \n\nIf taking a beta-blocker and symptoms are uncontrolled, switch to, or add, a long-acting dihydropyridine calcium-channel blocker (CCB), such as amlodipine, modified-release nifedipine. If taking a non-dyhydropyridine calcium channel blocker already, switch to a beta blocker.\r\n\r\nIf neither can be tolerated, consider a long-acting nitrate (ISMN), ivabradine, nicorandil or ranolazine. \r\n\r\n**2nd line** = beta-blocker (bisoprolol) AND long-acting dihydropyridine calcium channel blocker (amlodipine or nifedipine)\r\n\r\n**3rd line** = beta-blocker (bisoprolol) AND long-acting dihydropyridine calcium channel blocker AND long-acting nitrate.\r\n\r\nA 3rd medication should only be added if the patient is symptomatic despite 2 anti-anginal drugs. At this stage, revascularisation with PCI or CABG must be considered. \r\n\r\n## Revascularisation\r\n\r\nRevascularisation with coronary artery bypass graft (CABG) or percutaneous coronary intervention (PCI) must be considered in patients with: \r\n\r\n* Symptoms which are not controlled by optimal medical management.\r\n* Complex 3 vessel disease and/or significant left main stem on CTCA. \r\n\r\n# NICE Guidelines\n\r\n[NICE Guidance on Cardiac-Sounding Chest Pain](<https://www.nice.org.uk/guidance/cg95/chapter/Recommendations>) \r\n\n[NICE Guidance on Stable Angina](<https://www.nice.org.uk/guidance/cg126/chapter/Guidance>) \r\n\r\n# References\r\n\r\n[Patient UK Information on Stable Angina](<https://patient.info/doctor/stable-angina-2>) ",
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"question": "A 67 year old male presents to the GP with intermittent chest pain. He describes a crushing chest pain that comes on while he is gardening that goes away when he sits down for 4 minutes. He has also noticed jaw pain, breathlessness and sweating that comes on at the same time and also completely resolves with rest.\n\nWhat is the most likely diagnosis?",
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"explanation": "This a typical presentation of aortic stenosis. Older age is a risk factor, as the aortic valve becomes more calcified over time. Mild to moderate aortic stenosis is generally asymptomatic, but severe aortic stenosis can present with anginal chest pain, syncope, exertional breathlessness and heart failure. An ejection systolic murmur heard in the 2nd intercostal space at the right sternal edge is the classic murmur heard in aortic stenosis. This murmur also radiates to the carotid areas, so can be heard upon auscultation here. Symptomatic aortic stenosis generally has poor outcomes, so are usually considered for repair via open aortic valve replacement or transcatheter aortic valve implantation (TAVI)",
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"explanation": "Aortic regurgitation does not present with this murmur. The murmur heard in aortic regurgitation is an early diastolic murmur heard loudest over the left sternal edge. This is not the murmur in this case and is therefore more likely to be aortic stenosis",
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"label": "c",
"name": "Aortic regurgitation",
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"explanation": "Angina is a feature of severe aortic stenosis. Although it may seem sensible to choose this answer, there is a clear cause of angina in this case as this patient has other symptoms and examination findings suggesting aortic stenosis. Therefore, aortic stenosis is the single best answer",
"id": "33536",
"label": "d",
"name": "Stable angina pectoris",
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"explanation": "Mitral regurgitation does not present with this murmur. The murmur heard in mitral regurgitation is a pansystolic murmur heard loudest in the 5th intercostal space midclavicular line, which radiates to the axilla. This is not the murmur in this case and is therefore more likely to be aortic stenosis",
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"name": "Mitral regurgitation",
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"explanation": "Mitral stenosis does not present with this murmur. The murmur heard in mitral stenosis is a mid diastolic murmur heard loudest in the 5th intercostal space midclavicular line, with or without an audible opening click. This is not the murmur in this case and is therefore more likely to be aortic stenosis",
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"explanation": "# Summary\r\n\r\nAortic stenosis (AS) is characterised by the narrowing of the aortic valve, which restricts blood flow from the left ventricle to the aorta and the rest of the body. It is a common valvular pathology, with severe aortic stenosis having an estimated prevalence of 3% in those over 75 years old. The condition can be caused by senile calcification, congenital bicuspid valve, rheumatic heart disease, or supravalvular stenosis. Mild-to-moderate aortic stenosis may be asymptomatic, but severe cases present with symptoms such as syncope, angina, and dyspnoea. Diagnosis is confirmed through echocardiography. Management of asymptomatic AS is usually conservative and patients require regular echocardiograms. Symptomatic AS requires medical treatment to optimise symptoms and consideration for surgical or interventional interventions. Severe, symptomatic aortic stenosis carries a high risk of mortality without intervention, and prompt treatment is crucial. \r\n\r\n# Definition \r\n\r\nAortic stenosis (AS) refers to the narrowing and tightening of the aortic valve leading to reduced blood flow from the left ventricle into the aorta and ultimately to the rest of the body. \r\n\r\n# Epidemiology \r\n\r\nFor individuals over 75 years old, the prevalence of severe aortic stenosis is estimated at 3%. It is a common valvular pathology. \r\n\r\n# Pathophysiology\r\n\r\nNormally, the aortic valve opens to allow blood to be pumped from the left ventricle into the aorta and to the rest of the body during systole. In aortic stenosis, there is a narrowing of the aortic valve which means that the left ventricle has to generate more pressure to enable sufficient blood to cross the aortic valve and pass into the aorta. Initially, this leads to left ventricular hypertrophy as the left side of the heart compensates for the narrowing. Over time, the left ventricle can no longer compensate and the left ventricle will start to enlarge, the ejection fraction will reduce, and this will ultimately leads to reduced cardiac output.\r\n\r\n# Cause \r\n\r\nCauses of AS include: \r\n\r\n* Senile calcification: most common cause in those >65y/o. \r\n* Congenital bicuspid valve: most common cause in those <65y/o.\r\n* Rheumatic heart disease \r\n* William's syndrome: supravalvular stenosis \r\n\r\n# Symptoms\r\n\r\nLike with all valvular pathologies, mild-to-moderate aortic stenosis may be asymptomatic and may be picked up incidentally on cardiac auscultation or on echocardiogram. \r\n\r\nThe symptoms of severe AS can be remembered by the mnemonic 'SAD'. \r\n\r\n* **S**yncope \r\n* **A**ngina \r\n* **D**yspnoea \r\n\r\nOther symptoms include: pre-syncope, palpitations, left ventricular heart failure symptoms (exertional dyspnoea, orthopnoea, PND) or can present in cardiac arrest/sudden cardiac death. \r\n\r\n# Signs\r\n\r\n* Slow-rising carotid pulse\r\n* Narrow pulse pressure\r\n* Heaving, non-displaced apex beat (can be displaced if there is left ventricular hypertrophy)\r\n* Ejection systolic murmur\r\n * Heard best at the second intercostal space on the right\r\n * Can be described as \"harsh\"\r\n * Radiates to the carotids\r\n* Soft S2 heart sound: absent S2 corresponds with severity\r\n* Ejection click may be heard in some cases (early systolic)\r\n\r\n# Investigations\r\n\r\n## Bedside\r\n\r\n* **ECG:** LVH, left axis deviation, and poor R wave progreesion. \r\n\r\n## Imaging\r\n\r\n* **CXR:** cardiomegaly and evidence of pulmonary oedema. Occasionally, a calcified aortic valve is visible. \r\n* **Echocardiogram: definitive diagnosis**. \r\n\t* Definitive diagnosis of aortic stenosis. \r\n\t* Severity of AS can be quantified with doppler echocardiography. AS is classified as severe if it meets the following parameters: \r\n\t\t* Peak gradient > 40 mmHg (note, in severe left ventricular dysfunction, a low peak gradient can be falsely reassuring)\r\n\t\t* Valve area < 1.0cm x<sup>2</sup>\r\n\t\t* Aortic jet velocity >4 m/s\r\n* **Exercise testing:** may be used in physically active patients to assess the true severity of asymptomatic patients with echocardiography confirmed AS. \r\n* **Cardiac MRI:** can be used to provide additional, more details information regarding valve morphology, dimensions of the aortic root and the extent of valve calcification. \r\n\r\n# Management\r\n\r\n## Conservative \r\n\r\nTiming of intervention is crucial as many cases remain asymptomatic and stable and may not require treatment at all. \r\n\r\nPatients who do not meet the criteria for intervention should have regular echocardiography follow-up, with severe AS being monitored every 6 months, mild-to-moderate AS monitored yearly, and younger patients can be monitored every two to three years.\r\n\r\n## Medical \r\n\r\nMedical management of AS involves symptom management of left ventricular failure with diuretics and optimising heart failure medications with beta-blockers and ACE-I etc. Isolated medical therapy should only be used in those who are not suitable for intervention. \r\n\r\n## Surgical and Interventional \r\n\r\nIntervention in AS is indicated in the following patients:\r\n\r\n* All patients with symptomatic aortic stenosis \r\n* Asymptomatic patients with a left ventricular ejection fraction (LVEF) < 55%\r\n* Asymptomatic patients with an LVEF > 50% who are physically active, and who have symptoms or a fall in blood pressure during exercise testing\r\n* Asymptomatic patients with an LVEF > 50% who have the following risk factors\r\n * Aortic valve peak velocity > 5m/s x<sup>2</sup>\r\n * Severe calcification and peak velocity progression >= 0.3m/s x<sup>2</sup>\r\n * Markedly elevated BNP levels (more than twice upper limit) without other explanation\r\n * Severe pulmonary hypertension (pulmonary artery systolic pressure > 60mmHg)\n * Aortic valve area less than 0.6 cm<sup>2 \n\r\n\r\nChoices of intervention are **transcatheter aortic valve implantation (TAVI)** or **surgical aortic valve replacement (SAVR)**.\r\n\r\n* TAVI is favoured with patients with severe comorbidities, previous heart surgery, frailty, restricted mobility, and those older than 80 years of age.\r\n* SAVR is favoured for patients who are low risk and younger.\r\n\r\n# Complications\r\n\r\nAortic stenosis if left untreated can lead to LV failure. It is also implicated in sudden cardiac death. \r\n\r\n# Prognosis \r\n\r\nSevere, symptomatic AS patients are at a very high risk of sudden-death. It is estimated that these patients have a mortality rate of 50% at 1 year. It is essential that these patients are identified and treated swiftly. \r\n\r\n# Aortic sclerosis\r\n\r\nAortic sclerosis is an asymptomatic condition that can be incidentally revealed through physical examination or via echocardiogram. It is caused by age-related senile degeneration of the valve.\r\n\r\n## Clinical findings\r\n\r\nClassic findings are an ejection systolic murmur that _does not radiate to the carotids_, there is normal S2, pulse character and volume.\r\n\r\nIt can be defined as an irregular aortic leaflet thickening and focal increased echogenicity, but is distinguished from aortic stenosis because there is no impairment of valve leaflet excursion, and peak doppler velocities are normal or only minimally elevated (markedly elevated in stenosis)\r\n\r\n# NICE Guidelines\n\r\n[NICE Guidelines for Valvular Heart Disease](https://www.nice.org.uk/guidance/ng208/chapter/recommendations##References:)\r\n\r\n# References \r\n\r\n[BMJ Aortic Stenosis Summary](<https://www.bmj.com/content/380/bmj-2022-070511>)",
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"question": "An 88 year old man presents to the GP with exertional chest pain, breathlessness and occasional syncope. On auscultation, an ejection systolic murmur is heard in the 2nd intercostal space at the right sternal edge. No other murmurs are heard.\n\nWhat is the most likely diagnosis?",
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"explanation": "This ECG is not in keeping with someone who is presenting with anxiety. Anxiety can present with palpitations, however they would have a normal ECG or sinus tachycardia. In this case, the ECG is abnormal meaning anxiety is not the single best answer",
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"explanation": "This ECG does not show ventricular tachycardia. Ventricular tachycardia is a broad complex tachycardia (QRS complexes >120ms) whereas this ECG is a narrow complex tachycardia (QRS complexes <120ms). Therefore this ECG is more in keeping with supraventricular tachycardia",
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"explanation": "This ECG does not show atrial fibrillation. While supraventicular tachycardia and atrial fibrillation can both be classified as narrow complex tachycardias and both have absent P waves, the key difference is that atrial fibrillation is an irregularly irregular rhythm and supraventricular tachycardia is a regular rhythm. As the rhythm of this ECG is regular, this is more in keeping with a supraventricular tachycardia",
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"explanation": "This is a typical ECG demonstrating supraventricular tachycardia. Key features in keeping with supraventricular tachycardia are a ventricular rate >100, regular ventricular rhythm, QRS complexes <120ms and the absence of P waves. This condition is also relatively common in young patients with no underlying cardiac disease",
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"explanation": "This ECG does not show Wolff-Parkinson-White syndrome. The triad of features in Wolff-Parkinson-White syndrome are delta waves (slurred upstroke in the QRS), wide QRS and a short PR interval. Although Wolff-Parkinson-White syndrome is associated with supraventricular tachycardia, there is nothing that suggests this patient has an underlying diagnosis of Wolff-Parkinson-White syndrome in the question. Therefore, the single best answer is supraventricular tachycardia",
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"explanation": "# Summary\r\n\r\nNarrow complex tachycardia is a term used to describe a dysrhythmia with a heart rate greater than 100bpm and a narrow QRS complex (<120ms) on an ECG. It can be categorised as regular or irregular. Regular narrow complex tachycardias include sinus tachycardia, atrial flutter, atrioventricular re-entry tachycardia (AVRT), atrioventricular nodal re-entry tachycardia (AVNRT), and junctional tachycardia. Irregular narrow complex tachycardias include atrial fibrillation, atrial flutter with variable block, and multifocal atrial tachycardia. Symptoms may include palpitations, lightheadedness, dyspnoea, chest pain, and syncope. Management involves identifying and addressing reversible causes, performing vagal manouevres, administering medications like adenosine or beta-blockers, and performing synchronised DC cardioversion in those presenting with adverse features. Long-term management may involve cardiac ablation. Complications may include heart failure and cardiac arrest, but the prognosis is generally good.\r\n\r\n# Definition \r\n\r\nA narrow complex tachycardia refers to a dysrhythmia that has a heart rate greater than 100bpm and a QRS complex that is less than 120ms. \r\n\r\nAn important distinction to make is between a supraventricular tachycardia (SVT) and a sinus tachycardia. Sinus tachycardias frequently change rate and gradually speed up or slow down over seconds to minutes. On the other hand, an SVT starts suddenly then stays at the same rate until it ends.\r\n\r\n[lightgallery]\r\n\r\n# Epidemiology \r\n\r\nNarrow complex tachycardias are common. \r\n\r\n# Pathophysiology\r\n\r\nThe pathophysiology of different narrow complex tachycardias is diverse and discussed further below.\r\n\r\n# Classification \r\n\r\nNarrow complex tachycardias can be classified according to whether the rhythm is regular or irregular. \r\n\r\n## Regular Narrow Complex Tachycardias \r\n\r\n* **Sinus tachycardia**: physiological or pathological (secondary to pain, sepsis or illness). \r\n* **Focal atrial tachycardia**: autonomous atrial cells acting like the sino-atrial node. There is abnormal p wave morphology. \r\n* **Atrial flutter**: characterised by a **sawtooth baseline**. The electrical activity in the atria is at 300bpm. The AVN acts as a safety mechanism and filters through this high frequency and usually gives a ventricular rate of 150bpm or 75bpm (see below for atrial flutter with variable block). \r\n* **Atrioventricular re-entry tachycardia (AVRT)**: there is an accessory pathway between the atria and the ventricles that is not filtered by the AVN. Associated with Wolff-Parkinson White. \r\n* **Atrioventricular nodal re-entry tachycardia (AVNRT)**: there are re-entrant circuits within or near to the AVN causing a supraventricular tachycardia. \r\n* **Junctional tachycardia**: atrioventricular node becomes the pacemaker and causes ventricular contraction greater than 100bpm. \r\n\r\n## Irregular Narrow Complex Tachycardias\r\n\r\n* **Atrial Fibrillation**: irregularly irregular rhythm with no discernible p waves.\r\n* **Atrial Flutter with Variable Block**: atrial flutter but the atrioventricular node has a variable block of the high frequencies generated by the atria leading to an irregular rhythm. \r\n* **Multifocal atrial tachycardia**: similar to atrial tachycardia but there are multiple groups of autonomous atrial cells acting as the sino-atrial node leading to an irregular rhythm. It is commonly found in those with severe COPD. \r\n\r\n# Symptoms\r\n\r\n* Palpitations \r\n* Lightheadedness \r\n* Dyspnoea\r\n* Chest pain \r\n* Syncope \r\n\r\n# Signs \r\n\r\n* Tachycardic: regular or regularly irregular or irregularly irregular. \r\n* Haemodynamic instability: shock, chest pain, heart failure or syncope. \r\n\r\n# Investigations\r\n\r\n## Bedside\r\n\r\n* **ECG**: hallmark for investigation of narrow complex tachycardias. Sometimes the tachycardia can obscure the underlying rhythmn. \r\n* **24 hour tape**: narrow complex tachycardias are often paroxysmal and so 24 hour tapes are used to capture dysrhythmias. \r\n\r\n## Bloods \r\n\r\n* **FBC, TFTs, dyselectrolytaemias**: used to identify any clear precipitant for sinus tachycardia or other dysrhythmias. \r\n\r\n## Imaging\r\n\r\n* **Echocardiogram**: useful in identifying structural heart disease that prediposes to arrhythmia e.g. dilated left atrium predisposes to atrial fibrillation. \r\n* **Loop recorder**: small device inserted subcutaneously to monitor heart rate and rhythmn continuously. They look like a USB stick on CXR! \r\n* **Cardiac catheterisation**: electrophysiologists can identify arrhythmogenic foci and ablate them. \r\n\r\n# Management\r\n\r\nManagement of narrow complex tachycardias is according to the Resuscitation Council Adult Tachycardia Algorithm (2021).\r\n\r\n## Initial management\r\n\r\nFor emergencies, always follow an A-E structure. Identify reversible causes (dyselectrolytaemias, drugs, cardiac causes etc.) \r\n\r\n*If there are adverse signs (e.g. shock, syncope, heart failure, myocardial ischaemia):* \r\n\r\n* **1st line** = **synchronised DC cardioversion +/- amiodarone.**\r\n\r\n*If there are no adverse signs:* consider whether the rhythmn is regular or irregular. \r\n\r\n*Regular*\r\n\r\n* **1st line** = **vagal manouevres** including Valsalva manouevre and carotid sinus massage. Increasing vagal input can help terminate the SVT. \r\n* **2nd line** = **IV adenosine**. Initially give a 6mg bolus. If this is unsuccessful give 12mg. If this is still unsuccessful give 18mg. \r\n* **3rd line** = **verapamil or beta-blocker** \r\n* **4th line** = **synchronised DC cardioversion**\r\n\r\n*Irregular*\r\n\r\n* Probable atrial fibrillation and to treat with **beta-blockers**. \r\n* If there are signs of heart failure **digoxin** may be trialled. \r\n* If onset >48h the patient will need to be anticoagulated. \r\n\r\n## Further management \r\n\r\nLonger-term other treatments for persistent, recurrent SVT may be trialled including cardiac ablation of arrhythymogenic foci. \r\n\r\n# Complications\r\n\r\nParoxysmal SVT can lead to unpleasant symptoms for patients. Over time, paroxysmal SVT can lead to weakening of the heart muscles and lead to heart failure. SVT with adverse signs can lead to cardiac arrest and death. \r\n\r\n# Prognosis \r\n\r\nSVT is commonly a benign condition that does not shorten life expectancy. \r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines for Palpitations](https://cks.nice.org.uk/topics/palpitations/management/current-palpitations/)\r\n\r\n# References\r\n\r\n[Click here to see the flowchart on the Resus Council website about managing peri-arrest rhythms](https://www.resus.org.uk/library/2021-resuscitation-guidelines/adult-advanced-life-support-guidelines)\r\n\r\n[BNF Arrhythmias Treatment Summary](https://bnf.nice.org.uk/treatment-summaries/arrhythmias/)",
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"question": "A 28 year old female presents to the emergency department with palpitations. Her ECG is shown below:\n\n[lightgallery]\n\nWhat is the most likely diagnosis?",
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"explanation": "Pulseless electrical activity presents as discernable P waves and QRS complexes in the absence of a pulse. There are no discernable P waves or QRS complexes, therefore they do not have pulseless electrical activity",
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"explanation": "Asystole appears as a 'flatline' on the ECG, where the heart has no electrical activity. It has a very poor mortality and is the most serious form of cardiac arrest. This ECG has electrical activity and is therefore not asystole",
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"explanation": "This patient has no discernible P waves or QRS complexes and they are unconscious and pulseless. They are in cardiac arrest",
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"explanation": "This patient has a typical ECG showing ventricular fibrillation. Their ECG shows chaotic, polymorphic, irregular deflections with no discernible QRS complexes. This is a medical emergency that should be managed with unsynchronised DC cardioversion",
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"explanation": "ECG signs of ventricular tachycardia include regular, wide QRS complexes of equal amplitude (monomorphic) with an absence of P waves. This is not the case with this ECG as the rhythm and amplitude are not regular",
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"comment": "Huh? This is VF? But it looks like normal sinus rhythm??",
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"comment": "This looks nothing like VF. Even with PEA you wouldn't expect to see a normal looking ECG like this ",
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"comment": "I think it looks like normal sinus rhythm. Has the correct rhythm strip been put in?",
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"comment": "I think this looks sinus too! \n",
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"explanation": "# Summary \r\n\r\nBroad complex tachycardia refers to dysrhythmias with a heart rate greater than 100 beats per minute and a QRS complex broader than 120 milliseconds. This term encompasses life-threatening rhythms such as ventricular tachycardia (VT) and ventricular fibrillation (VF). VT is a regular, broad complex tachycardia and may be with or without a pulse. In contrast, VF is irregular and is always pulseless. Pulseless VT and VF must be managed according to the ALS algorithm and require immediate defibrillation and administration of medications like adrenaline and amiodarone, whilst managing pulsed VT involves synchronised shocks and amiodarone. SVT with aberrancy, a condition where supraventricular tachycardia occurs in the presence of bundle-branch block, can mimic VT and should be treated cautiously.\r\n\r\n# Definition \r\n\r\nBroad complex tachycardias are dysrhythmias that have a heart rate greater than 100bpm and a QRS complex that is greater than 120ms. The most common broad complex tachycardias are ventricular tachycardia or ventricular fibrillation. \r\n\r\n# Ventricular Tachycardia (VT)\r\n\r\nA regular broad complex tachycardia. It can occur with a pulse or it may be pulseless. \r\n\r\nECG features include: \r\n\r\n* Tachycardia (>100 beats per minute)\r\n* Absent p waves\r\n* Monomorphic regular broad QRS complexes (>120ms)\r\n\r\n[lightgallery]\r\n\r\n# Management of VT \r\n\r\n## Pulseless VT \r\n\r\nIf there is no pulse the patient should be managed according to the Advanced Life Support algorithm. \r\n\r\n* Pulseless VT is a shockable rhythm so a 200J bi-phasic **unsynchronised** shock should be administered. \r\n* IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock.\r\n* Adrenaline should be administered every 3-5 minutes thereafter. \r\n\r\n## Pulsed VT with Adverse Features\r\n\r\nIf the patient has a pulse but is demonstrating adverse features (shock, syncope, myocardial ischaemia, or heart failure) the patient should be managed according to Resuscitation Council Tachyarrhythmia algorithm. \r\n\r\n* Administer synchronised DC shocks (up to 3 attempts). If the patient is conscious this will require sedation or anaesthesia. \r\n* Expert help should guide amiodarone administration (300mg IV over 10-20 minutes followed by 900mg infusion over 24 hours). \r\n\r\n## Pulsed VT with No Adverse Features \r\n\r\nIf the patient has a pulse and is not demonstrating adverse features then the Resuscitation Council Tachyarrhythmia algorithm should be followed. \r\n\r\n* Amiodarone 300mg IV over 10-60 minutes. \r\n* If this is ineffective then administer synchronised DC shocks (up to 3 attempts). If the patient is conscious this will require sedation or anaesthesia. \r\n* *N.B. if there has been a previous certain diagnosis of SVT with aberrancy treat as for regular narrow complex tachycardias*\r\n\r\n# Ventricular fibrillation (VF) \r\n\r\nAn irregular broad complex tachycardia. This is always a pulseless rhythm.\r\n\r\nECG features include: \r\n\r\n* Tachycardia >100bpm \r\n* QRS complexes are polymorphic and irregular (>120ms)\r\n\r\n[lightgallery1]\r\n\r\n# Management of VF\r\n\r\nThe patient should be managed according to the Advanced Life Support algorithm. \r\n\r\n* VF is a shockable rhythm so a 200J bi-phasice **unsynchronised** shock should be administered. \r\n* IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock.\r\n* Adrenaline should be administered every 3-5 minutes thereafter.\r\n\r\n# Other Broad Complex Tachycardias \r\n\r\nInclude: \r\n\r\n* Torsades des pointes: see section. \r\n* SVT with aberrancy: occurs when a patient with a bundle-branch block goes into SVT. It can be difficult to distinguish between VT and an SVT with aberrancy. The safest approach is to treat as VT. \r\n\r\n[lightgallery2]\r\n\r\n# NICE Guidelines\r\n\n[NICE CKS Guidelines for Cardiac Arrest and ALS](<https://cks.nice.org.uk/topics/cardiac-arrest-out-of-hospital-care/management/advanced-life-support-adult/>)\r\n\r\n# References\r\n[Resuscitation Council UK Adult Tachycardia Algorithm](<https://www.resus.org.uk/sites/default/files/2021-04/Tachycardia%20Algorithm%202021.pdf>)\r\n\r\n[Resuscitation Council UK Adult ALS Algorithm](<https://www.resus.org.uk/sites/default/files/2021-04/Adult%20Advanced%20Life%20Support%20Algorithm%202021.pdf>)",
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"question": "A 70 year old patient who has been admitted on the cardiology ward has been found unconscious. They are not breathing and have no pulse on palpation. Their current ECG strip is shown below:\n\n[lightgallery]\n\nWhat is the most likely diagnosis?",
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"explanation": "Heart failure can lead to exertional breathlessness and polyphonic wheeze (referred to as cardiac asthma). However, this patient has no orthopnoea or paroxysmal nocturnal dyspnoea, no peripheral oedema and no obvious cause for heart failure",
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"explanation": "Chronic obstructive pulmonary disease (COPD) presents as shortness of breath, chronic productive cough and polyphonic wheeze. This diagnosis is very rare in patients under the age of 35 and this patient does not have any significant smoking history mentioned in this question",
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"explanation": "Cystic fibrosis can cause breathlessness, however they are more likely to have presented earlier and with additional features. Other expected features would include failure to thrive, malabsorption, diabetes mellitus and frequent chest infections, none of which are present in the case. There is also no clear family history of cystic fibrosis which, although not essential, would be supportive of cystic fibrosis",
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"explanation": "This is a typical presentation of asthma. Breathlessness, dry cough and polyphonic wheeze are typical symptoms and common triggers include exercise. Symptoms of asthma also tend to get worse at night. A history of atopy (e.g. allergic rhinitis, atopic eczema) is characteristic of asthma",
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"explanation": "Alpha-1 antitrypsin deficiency is a rare autosomal recessive condition that causes early onset liver fibrosis and chronic obstructive pulmonary disease (COPD). However, given the variability in this patient's symptoms and history of atopy, asthma is a more likely diagnosis",
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"explanation": "# Summary\n\nAsthma is a common disease of the airways, involving reversible bronchoconstriction, hyperreactivity and chronic inflammation. When bronchoconstriction is triggered (an “asthma attack”), patients experience episodes of wheeze, dyspnoea, cough and chest tightness. Initial investigations for all adults with suspected asthma are fractional exhaled nitric oxide (FeNO) or a full blood count looking for eosinophilia. If neither of these are confirmatory, patients should be assessed with spirometry including bronchodilator reversibility. Management involves a stepwise approach to medications, starting with “reliever therapy” (usually short-acting beta-2 agonists such as salbutamol inhalers) in combination with “preventer therapy” medications including inhaled corticosteroids, leukotriene receptor antagonists and long-acting beta-2 agonist inhalers. Allergen avoidance, smoking cessation, regular peak flow monitoring and inhaler technique are all key to good asthma control.\n\n# Definition\n\nAsthma is a common disease in both adults and children, characterised by intermittent \"asthma attacks\" with wheeze, cough, shortness of breath and chest tightness. There are several underlying mechanisms that centre around reversible bronchoconstriction, hyperreactivity and chronic inflammation.\n\n# Epidemiology\n\nIn the UK, approximately 8 million people have been diagnosed with asthma, of which 5.4 million are on treatment. Onset is usually in childhood and some find symptoms remit with age, although relapse is possible after long periods of being well.\n\nOn average, three people die from an asthma attack each day in the UK. The majority of these deaths are preventable, with an estimated 7/10 people with asthma not receiving basic preventative care such as inhaler technique checks and a personalised asthma plan.\n\nPeople experiencing socioeconomic deprivation are more likely to have asthma and to have worse outcomes (e.g. higher rates of hospitalisation). This is multifactorial, with these groups more likely to be exposed to triggers such as smoking and air pollution, and to have lower health literacy and access to healthcare.\n\n# Pathophysiology\n\nAsthma is often associated with a personal and/or family history of atopy, including the atopic triad of asthma, allergic rhinitis, and eczema. In asthma, there is an exaggerated response to a wide range of triggers. These include:\n\n- Cold air and exercise\n- Pollution and cigarette smoke\n- Allergens such as animal dander, dust mites and pollen\n- Irritants such as perfumes, paints or air fresheners\n- Medications such as NSAIDs or beta-blockers\n\nThese trigger a type 1 hypersensitivity reaction which is mediated by IgE. T Helper 2 cells produce IL4, IL5 and IL13 cytokines which activate the humoral immune system, leading to the proliferation of eosinophils, mast cells and dendritic cells. These cells then produce more inflammatory mediators such as leukotrienes and histamine.\n\nThis inflammation contributes to airway hyperresponsiveness leading to bronchospasm, as well as mucus hypersecretion that also obstructs airways. Over time in severe asthma, airway remodelling mediated by fibroblasts causes chronic obstruction and thickening of smooth muscle.\n\n# Risk factors\n\n- Family history of asthma or atopy\n- Personal history of atopy (eczema, allergic rhinitis, allergic conjunctivitis)\n- Exposure to smoke, including maternal smoking in pregnancy\n- Respiratory infections in infancy\n- Prematurity and low birth weight\n- Obesity\n- Social deprivation\n- Occupational exposures (e.g. flour dust, isocyanates from paint)\n\n# Symptoms\n\n- Wheeze\n- Dyspnoea\n- Cough\n- Chest tightness\n\nThe above symptoms should be episodic and usually show **diurnal variation** (worse at night or in the early morning). The patient may be able to identify specific triggers as listed above.\n\n# Signs\n\nIn between asthma exacerbations, clinical examination may be normal. If asthma is poorly controlled or during an exacerbation, signs include:\n\n- Tachypnoea\n- Increased work of breathing\n- Hyperinflated chest\n- Expiratory polyphonic wheeze throughout the lung fields\n- Decreased air entry (if severe)\n\n\n# Differential diagnosis\n\n- **Bronchiectasis** - usually associated with a productive cough, patients get frequent chest infections and coarse crackles rather than wheeze predominate on examination.\n- **Vocal cord dysfunction** - shares many triggers with asthma, inspiration more difficult than expiration, may have stridor.\n- **Chronic obstructive pulmonary disease** - patients usually >35 years old with a significant smoking history, may overlap with asthma in some.\n- **Gastro-oesophageal reflux disease** - microaspiration of stomach acid due to reflux can cause episodes of cough and wheeze which mimic asthma (although these may coexist and reflux can trigger asthma exacerbations). Symptoms are often postural and related to eating.\n- **Eosinophilic Granulomatosis with Polyangiitis** (Churg-Strauss syndrome) - small vessel vasculitis associated with pANCA, aside from asthma symptoms include nasal polyps, sinusitis, purpuric rashes and peripheral neuropathy.\n\n# Investigations \n\n- **FeNO (fractional exhaled nitric oxide) testing:** offer this **or** blood eosinophil count to all adults to confirm eosinophilic airway inflammation, asthma can be diagnosed if this is >50 parts per billion.\n- **Full blood count** to check **eosinophil count:** offer this **or** FeNO first-line to all adults - asthma can be diagnosed if this is above the normal reference range.\n- If neither of these confirm asthma, **spirometry** with **bronchodilator reversibility** should be offered to confirm airway obstruction (i.e. FEV1/FVC<70%). A bronchodilator (e.g. salbutamol inhaler) is given and spirometry repeated to assess response to treatment. An improvement in FEV1 of 12% or more or 200ml is diagnostic of asthma.\n- If spirometry is delayed or not available, patients may be asked to monitor their peak flow twice a day for 2 weeks and keep a diary of the readings. This is then used to assess **peak flow variability** (the difference between the highest and lowest readings as a percentage of the average PEF). Variability >20% is a positive result.\n- If none of the above are confirmatory, patients may be referred to specialist services for a **direct bronchial challenge test**, where histamine or metacholine is inhaled to trigger bronchoconstriction. Airway hyperresponsiveness is assessed by looking at the concentration of the triggering medication required to cause a 20% decrease in FEV1 - 8mg/ml or less is a positive result.\n\nNote: All of the above tests may be falsely negative in patients treated with inhaled corticosteroids.\n\n# Management of Chronic asthma\n\nThe aim of chronic asthma management is to achieve complete control over symptoms, with no need for rescue medications and no restrictions on physical activity. All patients should have a personalised asthma action plan which should be reviewed at least annually. Components of management include:\n\n## Non-pharmacological\n\n- Teach good inhaler technique and review this regularly\n- Spacer devices can be used to optimise medication delivery\n- Regular peak flow monitoring\n- Smoking cessation\n- Advice on avoiding triggers where possible (e.g. allergens, certain medications)\n- Ensure vaccinations are up to date, including annual influenza vaccination\n- Assess for occupational asthma by asking if symptoms are better when the patient is away from work and arrange specialist referral if this is suspected\n\n## Pharmacological\n\n- Prescribe all patients a combination inhaler with a **long-acting beta-2 agonist** (LABA) i.e. formoterol and a low-dose **inhaled corticosteroid** (ICS) i.e. budesonide to use as a reliever inhaler (i.e. PRN) - this is referred to as anti-inflammatory reliever (AIR) therapy.\n- Patients who do not respond adequately to AIR therapy, who are highly symptomatic at presentation or who present with a severe asthma exacerbation should be started on a low-dose **maintenance and reliever therapy inhaler** (MART). MART is a combination inhaler with ICS and a fast-acting LABA (e.g. beclomethasone + formoterol which is also known as Fostair), which is used as both a reliever inhaler (PRN) and as maintenance treatment (usually twice daily).\n- The next step would be increasing the ICS dose from low to **moderate** in the MART inhaler.\n- At this stage if asthma is not controlled, check FeNO and blood eosinophil count and refer to specialist asthma services if either are raised.\n- If neither are raised, consider adding either a **leukotriene receptor antagonist** (LTRA) such as montelukast (this is a tablet taken every night) or a **long-acting muscarinic agonist** (LAMA) such as tiotropium.\n- One of these should be trialled for 8-12 weeks alongside the moderate-dose MART - if asthma is well-controlled it can be continued.\n- If there is some improvement in control but this is still inadequate, the other medication can be trialled in addition (i.e. moderate dose MART + LTRA + LAMA).\n- If control has not improved, stop the medication and try the other one - if this is not successful refer to specialist services.\n- Options in specialist clinics include therapies such as **biologics** (e.g. omalizumab, which targets IgE).\n\nOther than patients who are not responding to treatment, the following situations shold also prompt a secondary care referral:\n\n- Uncertainty regarding diagnosis\n- Suspected occupational asthma\n- Severe or life-threatening asthma requiring admission to hospital\n- Multiple exacerbations requiring oral steroid treatment per year\n\n# Acute asthma\n\nAcute asthma exacerbations are graded in severity as below:\n\n\n| Severity | Clinical Features |\n|-----------------------|-----------------------------------------------|\n| Moderate | PEFR > 50% of predicted or best |\n| | No features of severe/life-threatening asthma |\n| Severe | PEFR 33-50% of predicted or best |\n| | Heart rate > 110 |\n| | Respiratory rate > 25 |\n| | Unable to complete sentences in one breath. |\n| | Accessory muscle use |\n| Life-threatening | PEFR < 33% of predicted or best |\n| | Oxygen saturation < 92% or cyanosis |\n| | Altered conciousness/confusion |\n| | Exhaustion/poor respiratory effort |\n| | Cardiac arrhythmia |\n| | Hypotension |\n| | Silent chest |\n\n\n## Investigations \n\n- **Peak expiratory flow rate (PEFR)** to help assess severity as per the classification above and monitor response to treatment.\n- **Arterial blood gas** if the patient is hypoxic to assess oxygenation and ventilation in patients - CO2 is expected to be low due to hyperventilation and if this is raised this indicates the asthma attack is near fatal.\n- **Portable chest X-ray** if a trigger such as pneumonia or a complication such as pneumothorax is suspected clinically.\n\n## Management \n\n- Recognise that this may be a medical emergency, assess using an ABCDE approach and escalate early to senior colleagues/critical care if not responding to treatment\n- Titrate oxygen to maintain saturations of 94-98%\n- Nebulised salbutamol driven by oxygen (if out of hospital, give up to 10 puffs of inhaled salbutamol and call an ambulance if not responding)\n- If the attack is severe or life-threatening or if response to salbutamol has been poor, add nebulised ipratropium bromide\n- Give prednisolone 40-50mg orally, or IV hydrocortisone if the patient is unable to swallow\n- Can consider IV magnesium sulphate and/or aminophylline if the patient is not responding to nebulisers\n- If the patient continues to deteriorate despite maximal therapy, they may require intubation and ventilation in an intensive care setting (for example in cases of severe hypoxia or exhaustion)\n\nFollow up after an acute asthma attack is crucial, with NICE guidelines stating that patients should be reviewed within 2 days of discharge from hospital to assess their symptoms, inhaler technique and current management.\n\n# NICE Guidelines\n\n[NICE - Asthma: diagnosis, monitoring and chronic asthma management](https://www.nice.org.uk/guidance/ng245)\n\n# References\n\n[NICE CKS](https://cks.nice.org.uk/topics/asthma/)\n\n[Report on health inequalities and asthma](https://www.asthmaandlung.org.uk/sites/default/files/2023-03/auk-health-inequalities-final.pdf)\n\n[Guideline on severe asthma in primary care](https://www.pcrs-uk.org/sites/default/files/pcru/articles/2019-Autumn-Issue-18-SevereAsthmaReferral.pdf)\n\n\n\n",
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"question": "A 19 year old female presents to the GP with a 4 month history of breathlessness on exertion. She also has a dry cough that mainly occurs at night, which affects her sleep. She has a past medical history of allergic rhinitis and atopic eczema. On auscultation a widespread polyphonic wheeze is heard, with normal heart sounds.\n\nWhat is the most likely diagnosis?",
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"explanation": "Heart failure often presents with exertional breathlessness. However it less typically presents with a productive cough in the morning, which is more characteristic of COPD. Wheeze can also be a feature of heart failure, but it is more commonly associated with COPD. Features like orthopnoea, paroxysmal nocturnal dyspnoea and peripheral oedema are also more characteristic of heart failure but are absent from this question. Although recent myocardial infarction can be a risk factor for heart failure, this presentation is more suggestive of COPD and their significant smoking history is also risk factor for myocardial infarction",
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"explanation": "Asthma can cause exertional breathlessness and a cough, but this will typically be a dry cough. Although it is possible for someone to have first presentation of asthma at 66 years old, it is less typical of asthma. Given the significant smoking history and the clinical presentation, a diagnosis of COPD is more likely",
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"explanation": "Lung cancer is a good differential to consider in anyone presenting with a new onset cough for longer than 3 weeks, especially in anyone with a significant smoking history. However, this is typically a non-productive cough. In addition, this patient does not any red flag symptoms (e.g. haemoptysis, weight loss, hoarse voice, Horner's syndrome). This makes COPD the more likely diagnosis. Lung cancer should still be high on the differential diagnosis given the clinical history and a chest x-ray should be performed to look for evidence of chest malignancy",
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"explanation": "Pulmonary fibrosis can also present with exertional breathlessness. However it usually presents with a dry cough, whereas the cough in this case is productive. Other features that pulmonary fibrosis presents with includes finger clubbing and fine inspiratory crepitations on auscultation. This presentation is more in keeping with COPD, particularly in the context of this person's smoking history",
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"explanation": "COPD typically presents in patients over the age of 40 years old with a significant smoking history, as there is in this case. Typical features include exertional breathlessness, a productive cough and wheeze on auscultation, which are all present in this case. This patient will require spirometry to confirm the diagnosis and a chest x-ray and ECG to look for supporting features and rule out other differentials like lung cancer and heart failure. A full blood count could also be taken to rule out secondary polycythaemia. First line treatment would consist of a short acting ß2 agonist or short acting muscarinic agonist, with escalations of treatment where necessary",
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"explanation": "# Summary\n\nChronic obstructive pulmonary disease (COPD) is a chronic obstructive disease of the airways with the two main components being chronic bronchitis and emphysema. It usually develops due to smoking, with other risk factors including occupation exposures and air pollution. Patients present with breathlessness, a chronic productive cough and wheeze. Key investigations are spirometry (to confirm obstruction), full blood count (to identify anaemia or polycythaemia) and a chest X-ray to exclude lung cancer or other causes of symptoms. Management includes smoking cessation, pulmonary rehabilitation, consideration of long term oxygen therapy, inhaled or nebulised medical treatment and consideration of other medications e.g. mucolytics. Acute exacerbations of COPD may be infective or non-infective, and can be treated by increasing bronchodilator therapy, oral prednisolone and antibiotics (if an infective cause is suspected).\n\n# Definition\n\nChronic obstructive pulmonary disease (COPD) involves airway obstruction that is usually progressive. It encompasses both emphysema (where alveolar wall destruction leads to enlargement of the distal airspaces) and chronic bronchitis (persistent or recurrent productive cough usually due to mucus hypersecretion). \n\n# Epidemiology\n\nIn the UK 1.2 million people have a diagnosis of COPD, with an estimated 2 million people living with it undiagnosed. It is the 5th commonest cause of death in the UK, causing almost 30,000 deaths per year. \n\nAround 90% of COPD cases in the UK are caused by smoking, with household pollution being a bigger contributing factor in low and middle income countries.\n\n# Risk Factors\n\n- Tobacco smoking and passive smoke exposure\n- Marijuana smoking \n- Occupational exposure to dusts and fumes\n- Household air pollution from wood or coal burning\n- Alpha-1 antitrypsin deficiency\n\nPrognosis is variable, with the following factors associated with higher morbidity and mortality:\n\n- Poor exercise tolerance\n- Smoking\n- Low body mass index\n- Multi-morbidity and frailty\n- Exacerbations requiring admission to hospital or frequent exacerbations\n- Severe obstruction on spirometry (as measured by a lower FEV1)\n- Chronic hypoxia\n- Cor pulmonale\n\n# Pathophysiology\n\nChronic Bronchitis:\n\n- As a protective reaction to smoke or other pollutants, goblet cells hypersecrete mucus in the bronchi and bronchioles of the lungs.\nCilia are not able to remove the excess mucus and so it obstructs the small airways.\nOngoing inflammation causes remodelling and thickening of the airway walls that also contributes to obstruction.\n\nEmphysema:\n\n- Inflammation in the lungs is usually countered by antiproteases such as alpha-1 antitrypsin, however the activity of these is reduced by smoke and other pollutants. \n- Without sufficient antiprotease activity, proteolytic enzymes produced by inflammatory cells break down the walls of the alveoli.\n- This causes enlargement of the terminal airspaces and reduces the surface area available for gas exchange.\n\n# Classification\n\nThe Global Initiative for Chronic Obstructive Lung Disease (GOLD) classifies COPD severity using airflow limitation (as measured by FEV1), severity of symptoms and frequency of exacerbations. \n\n| GOLD Grade | Severity | Post-Bronchodilator FEV₁ (% Predicted) |\n|------------|--------------------------|----------------------------------------|\n| 1 | Mild | ≥ 80% |\n| 2 | Moderate | 50-79% |\n| 3 | Severe | 30-49% |\n| 4 | Very Severe | < 30% |\n\n\nThe two measures used to quantify symptom severity are the CAT (COPD Assessment Test) and the mMRC (modified Medical Research Council) dyspnoea scale which is given below:\n\n| Grade | Description |\n|-------|----------------------------------------------------------------------------------------------------|\n| 0 | I only get breathless with strenuous exercise. |\n| 1 | I get short of breath when hurrying on level ground or walking up a slight hill. |\n| 2 | On level ground, I walk slower than people of the same age because of breathlessness, or I have to stop for breath when walking at my own pace. |\n| 3 | I stop for breath after walking about 100 yards or after a few minutes on level ground. |\n| 4 | I am too breathless to leave the house, or I am breathless when dressing or undressing. |\n\n# Signs and symptoms\n\n- Shortness of breath that worsens with exertion\n- Reduced exercise tolerance\n- Chronic productive cough\n- Recurrent lower respiratory tract infections\n- Wheeze\n- In more advanced cases, systemic symptoms such as weight loss and fatigue may be present\n\nExamination may be normal, though signs may include:\n\n- Wheeze or crackles on auscultation\n- Accessory muscle usage\n- Pursed lip breathing (this creates a small amount of positive end expiratory pressure to prevent the alveoli from collapsing)\n- Cyanosis \n- Hyperinflation of the chest\n- Cachexia\n- Raised JVP and peripheral oedema (indicating cor pulmonale has developed)\n\n# Investigations\n\n- **Spirometry** - the diagnostic investigation for COPD and key to classification of severity, may be used to monitor progression of the disease. A FEV1/FVC ratio <0.7 confirms obstruction.\n\n- **Bloods** - Full blood count looking for polycythaemia (resulting from chronic hypoxaemia) or anaemia (usually anaemia of chronic disease), consider BNP to assess for heart failure (with an **echocardiogram** if suspected, alpha-1 antitrypsin in young patients/minimal smoking history/strong family history\n- **ECG** - the following ECG changes are often seen in advanced COPD with features of e.g. cor pulmonale, and include:\n\t- Right axis deviation\n\t- Prominent P waves in inferior leads\n\t- Inverted P waves in high lateral leads (I, aVL)\n\t- Low voltage QRS\n\t- Delayed R/S transition in leads V1-V6\n\t- P pulmonale\n\t- Right ventricular strain pattern\n\t- RBBB\n\t- Multifocal atrial tachycardia\n\n- **Chest X-ray** - used to rule out other causes of symptoms (e.g. lung cancer, bronchiectasis), may show features of COPD including hyperinflation of the chest with flattening of the hemidiaphragms and bullae.\n\n[lightgallery1]\n\n- **Sputum culture** - during exacerbations to target antibiotic therapy\n\n# Differential diagnosis\n\n- **Asthma:** may coexist with COPD, suspect if onset of symptoms <35, history of atopy, non-smoker, variable or nocturnal symptoms.\n- **Bronchiectasis:** copious secretions and coarse crepitations on examination, triggering factors include severe childhood respiratory tract infections.\n- **Heart Failure:** suspect in patients with ischaemic heart disease, may have orthopnoea and paroxysmal nocturnal dyspnoea.\n- **Interstitial Lung Disease:** dry rather than a productive cough, fine crackles on examination.\n- **Lung cancer:** patients with COPD are usually at higher risk due to smoking history, need to investigate for malignancy in cases with a persistent cough/haemoptysis/weight loss.\n- **Tuberculosis:** similar symptoms, systemic manifestations include fevers and weight loss, consider in at-risk groups.\n\n# Management of Chronic COPD\n\n**Conservative:**\n\n- Patient education, ensure all patients have a personalised self-management plan\n- Smoking cessation support\n- Nutritional support and dietician referral if malnourished\n- Annual influenza and one-off pneumococcal vaccination\n- Pulmonary rehabilitation (refer if grade 3 and above on mMRC dyspnoea scale or a recent admission for an acute exacerbation)\n- Consider referral for respiratory physiotherapy to help with sputum clearance and breathing techniques\n\n**Medical:**\n\n\n- For patients whose activities are limited by breathlessness, start a short-acting beta-2 agonist (SABA, e.g. salbutamol) or short-acting muscarinic antagonist (SAMA, e.g. ipratropium) inhaler\n- The next step depends on if they have features of asthma or steroid responsiveness: if these are present then add a long-acting beta-2 agonist (LABA, e.g. formoterol) and an inhaled corticosteroid (ICS, e.g. beclomethasone). If these are not present then add a LABA and a long-acting muscarinic antagonist (LAMA, e.g. tiotropium). \n- If patients do not respond adequately to this, the third inhaler can then be trialled (i.e. all patients would be on a SABA/SAMA + LABA + LAMA + ICS).\n\nPatients who require further therapy should be referred to a specialist for ongoing management which may include oral steroids, oral theophylline or oral phosphodiesterase-4 inhibitors (e.g. roflumilast).\n\nManagement of stable COPD is can be tailored according to the patient’s clinical phenotype. The following groups are defined according to 2024 NICE guidance:\n\n**Group A**\n \n- **Definition**: Patients with minimal symptoms (mMRC grade 0–1 or CAT score <10) and no history of exacerbations requiring hospitalisation or oral corticosteroids in the last year. \n- **Management**:\n - Start with a **short-acting bronchodilator (SABA or SAMA)** as needed for symptom relief.\n - If symptoms are not controlled, consider switching to a long-acting bronchodilator: \n - **LAMA** or **LABA**, depending on individual tolerance and symptom profile. \n\n**Group B**\n \n- **Definition**: Patients with significant symptoms (mMRC grade ≥2 or CAT score ≥10) but no exacerbations requiring hospitalisation or oral corticosteroids in the last year. \n- **Management**: \n - Initiate treatment with a **LAMA** or **LABA** as maintenance therapy. \n - If symptoms persist despite monotherapy, escalate to **dual therapy (LABA + LAMA)**. \n\n**Group E**\n \n- **Definition**: Patients with frequent exacerbations (≥2 per year or ≥1 requiring hospitalisation) regardless of symptom burden. \n- **Management**: \n - First-line therapy is **LAMA** for exacerbation prevention. \n - If exacerbations persist, escalate to: \n\t - **Dual therapy (LABA + LAMA)**. \n\t - If asthmatic features or steroid responsiveness are present (e.g., eosinophilia or a history of asthma), consider **LABA + ICS**. \n - For patients who continue to experience exacerbations despite dual therapy, switch to **triple therapy (LABA + LAMA + ICS)**. \n\n\n\n| **Group** | **Phenotype** | **Initial Therapy** | **Escalation Therapy** | \n|-------------|--------------------------------|------------------------------|------------------------------------| \n| **Group A** | 0 or 1 moderate exacerbation not leading to hospitalisation | SABA or SAMA as needed | LAMA or LABA | \n| **Group B** | 0 or 1 moderate exacerbation not leading to hospitalisation| LAMA or LABA | LABA + LAMA | \n| **Group E** | 2 or more moderate exacerbations or 1 or more exacerbations leading to hospitalisation\t | LAMA | LABA + LAMA or LABA + LAMA + ICS | \n\n\nOther medical treatments that may be considered include:\n\n- Oral mucolytic therapy - for patients with a chronic cough productive of sputum.\n- Prophylactic antibiotics - in cases of frequent infective exacerbations, should be discussed with a specialist, a common choice would be azithromycin 3x per week.\n- Nebuliser therapy - for patients with disabling breathlessness despite optimised use of inhalers.\n- Long-term oxygen therapy (LTOT) - see below for more details\n\n\n**Surgical:**\n\n- In certain cases of severe COPD when patients have not responded to maximal medical therapies, surgical intervention may be considered. \n- Both the NICE recommended options involve lung volume reduction (which involves removing emphysematous areas of the lung so that the healthy lung can expand) - this can be done either by surgical resection or using bronchoscopy to site a one-way valve in one of the larger airways to collapse the diseased lung. \n\n### Long term oxygen therapy (LTOT)\n\n**The following patients should be referred for assessment for LTOT:**\n\n- Oxygen saturations <92% in air or cyanosis\n- FEV1 <30% predicted (consider referring if <49%)\n- Polycythaemia\n- Peripheral oedema or raised jugular venous pressure (suggesting cor pulmonale)\n\nThis assessment involves ensuring that patients are medically optimised and their COPD is stable (i.e. they’re not recovering from a recent exacerbation). Patients who are current smokers cannot be offered LTOT because of the risk of burns and fires. \n\nPatients then have two ABGs in air at least 3 weeks apart and the following patients should be offered LTOT (with the advice to use the oxygen for at least 15 hours per day):\n\n- PaO2 below 7.3kPa\n- PaO2 7.3-8kPa with any of secondary polycythaemia, peripheral oedema or pulmonary hypertension\n\n# Complications\n\n## Acute exacerbations\n\n- These present with worsening breathlessness, productive cough and wheeze, and patients may be febrile, tachycardic and tachypnoeic. \n- Patients who are clinically well may be treated at home with an increase in their usual inhalers, a short course of oral steroids (usually 30mg prednisolone for 5 days) and oral antibiotics if bacterial infection is suspected. \n- Those who have frequent exacerbations may be given a “rescue pack” of steroids and antibiotics to keep at home and start using in case of an exacerbation (alongside seeking medical help).\n\n- Patients requiring hospital admission should also receive steroids and antibiotics if indicated. \n- They may require nebulised bronchodilators, supplementary oxygen and in case of deterioration respiratory support with non-invasive ventilation may be required. \n- Advanced care planning and ensuring that escalation status is discussed with patients is therefore key, so that if they deteriorate to the point of needing intensive care support it is established whether or not this is appropriate and in line with their wishes.\n\n## Polycythaemia\n\n- Chronic tissue hypoxia as seen in COPD leads to a compensatory overproduction of erythropoietin, which leads to increased red blood cell production (i.e. secondary polycythaemia). \n- This causes an increase in blood viscosity that in turns increases risk of both arterial and venous thrombosis. \n\n\n## Cor Pulmonale\n\nCor pulmonale refers to right ventricular dilation or hypertrophy in response to pulmonary hypertension caused by chronic lung disease - COPD is not the only cause of this but it is the most common.\n\nThe pathophysiology is as follows:\n\n- Changes in the lungs and chronic hypoxaemia cause the walls of the pulmonary arteries to thicken.\n- This increases vascular resistance in the lungs.\n- The right ventricle then has to pump against greater resistance, which causes it to either dilate or hypertrophy.\n- Ultimately this leads to right heart failure, with resulting peripheral oedema, hepatomegaly and elevated jugular venous pressure (JVP).\n\nPeripheral oedema may be treated symptomatically with diuretics and long-term oxygen therapy has been shown to reduce morbidity and mortality. All patients with suspected cor pulmonale should be referred to secondary care.\n\n## Pneumothorax\n\n- COPD is a common cause of secondary pneumothoraces (i.e. a pneumothorax secondary to underlying lung disease). These occur when a bulla ruptures, releasing air into the pleural cavity. \n- Investigations and treatment are as per the BTS guidelines (see Pneumothorax chapter for more details).\n\n## Depression and anxiety\n- Over 1 in 3 people with COPD report symptoms of depression and anxiety so screening for this is important during patient reviews. \n- The COPD Assessment Test (CAT) can be used to assess the impact of COPD on everyday life. \n- Referral to psychological services for support may be appropriate, as well as holistic assessment and management.\n\n# NICE Guidelines\n\n[Click here for the NICE Guidelines](https://www.nice.org.uk/guidance/ng115)\n\n[NICE CKS - COPD](https://cks.nice.org.uk/topics/chronic-obstructive-pulmonary-disease/)\n\n# References\n\n[Patient UK - COPD](https://patient.info/doctor/chronic-obstructive-pulmonary-disease-pro)\n\n[GOLD report 2023](https://goldcopd.org/2023-gold-report-2/)\n\n[Radiopaedia - COPD](https://radiopaedia.org/articles/chronic-obstructive-pulmonary-disease-1?lang=gb)\n\n[Patient UK - Cor Pulmonale](https://patient.info/doctor/cor-pulmonale)",
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"question": "A 66 year old female attends the GP with a 6 month history of exertional breathlessness. On further questioning, she notes that she brings up a significant amount of sputum in the morning. Her weight is stable and she has not noted any blood in the sputum. Her past medical history includes myocardial infarction 1 year ago and she is a current smoker with a 40 pack year smoking history.\n\nWhat is the most likely diagnosis?",
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"explanation": "Myocardial infarction does present with chest pain, however it is characteristically a crushing chest pain radiating to the left arm and jaw. In this case the pain is more pleuritic, which is more in keeping with a pulmonary cause. There may or may not be signs on physical examination, ECG or chest x-ray in myocardial infarction however this patient has significant risk factors for pulmonary embolism rather than myocardial infarction, therefore in the context of the clinical history pulmonary embolism is more likely",
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"explanation": "Pericarditis typically presents with pleuritic chest pain as in this case. However, this typically has characteristic ECG signs (PR depression and widespread saddle shaped ST elevation), which were not present in this case. In the presence of sudden onset chest pain with significant risk factors for PE and an ECG showing tachycardia, a pulmonary embolism is the more likely diagnosis",
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"explanation": "Pneumonia can present with pleuritic chest pain, as described in this case. However, this is less likely to be of sudden onset and will probably be associated with other features including fever and a productive cough of green/rust coloured sputum. Most significantly, the chest x-ray is normal for this patient. In pneumonia, there are usually radiological features on the chest x-ray",
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"explanation": "Anxiety is a good differential in this case. It can present with chest pain and sinus tachycardia and should be considered if investigations are normal. However, pulmonary embolism can also present with the same physical examination and investigation results and the fact that this is sudden onset and in the presence of a significant risk factor increases the suspicion that this presentation is due to a pulmonary embolism. Therefore, pulmonary embolism should be considered above anxiety, until pulmonary embolism has either been confirmed or adequately ruled out",
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"explanation": "There are several features in this case that suggest a diagnosis of pulmonary embolism. Pleuritic chest pain is a typical feature of pulmonary diseases, including pulmonary embolism. In addition, the symptoms of a pulmonary embolism are typically described as being sudden onset. Tachycardia is another typical feature. Pulmonary embolism often has no signs on physical examination or chest x-ray. This patient has a significant risk factor of recent surgery and as they are on no current medications they may not have been prescribed any thromboprophylaxis (e.g. low molecular weight heparin). Notably, there are several typical features absent from this presentation including no haemoptysis and no clinically obvious deep vein thrombosis (DVT). The absence of these features, does not rule out a pulmonary embolism",
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"explanation": "# Definition\n\nA pulmonary embolism (PE) is when a blood clot in the pulmonary arterial vasculature develops, usually from an underlying deep vein thrombosis (DVT) of the lower limbs.\n\n# Epidemiology of pulmonary embolism (PE)\n\n2300 people died as a result of a pulmonary embolism in the UK in 2012, representing 2% of all deaths from lung diseases.\n\n# Presentation of a PE\n\n**Symptoms**\n\n- Sudden-onset shortness of breath, pleuritic chest pain, and haemoptysis (this is the 'typical' triad, although note that all three features are rarely present).\n\n- A massive pulmonary embolism may present with the above and syncope/shock.\n\n- A small pulmonary embolism may be asymptomatic.\n\n**Signs**\n\n- Classically tachypnoea, tachycardia and hypoxia is present. There may be low-grade pyrexia. Tachycardia may be the only presenting sign.\n\n- Note that a small pulmonary embolism may result in a normal examination.\n\n- A massive pulmonary embolism may present with hypotension, cyanosis, and signs of right heart strain (such as a raised JVP, parasternal heave, and loud P2).\n\nIt is important to look for signs of a concomitant deep vein thrombosis (a unilaterally swollen, tender calf).\n\n# ECG findings\n\nECG: Normal or sinus tachycardia. In a massive PE there may be evidence of right-heart strain (with P pulmonale, right axis deviation, right bundle branch block, and non-specific ST/T wave changes). The classic S1Q3T3 (deep S waves in lead I, pathological Q waves in lead III, and inverted T waves in lead III) is relatively uncommon (<20% of patients).\n\n# Blood tests in PE\n\nABG: This may be normal or show a type 1 respiratory failure (hypoxia without hypercapnia) and/or a respiratory alkalosis (due to hyperventilation secondary to hypoxia).\n\nRemember the baseline tests such as FBC (the patient may be anaemic if the PE has caused haemoptysis), CRP may be raised, U&E (to assess renal function before CTPA), clotting function (important if the patient is to be started on LMWH/Warfarin).\n\nSpecial tests include D-dimer (this is highly non-specific but has a 95% negative predictive value i.e. it is useful in ruling out a PE if negative).\n\n# Imaging Investigations in PE\n\nChest x-ray: this is typically normal in PE but possible findings include _Fleischner sign_ (an enlarged pulmonary artery), _Hampton's hump_ (a peripheral wedge shaped opacity), and _Westermark's sign_ (regional oligaemia). The chest x-ray is helpful in ruling out differentials (e.g. pneumonia, pneumothorax).\n\nCT pulmonary angiogram (CTPA): this is the diagnostic test of choice for a PE and will show a filling defect in the pulmonary vasculature. Note that a V/Q scan is preferred if the patient has renal impairment, contrast allergy or is pregnant.\n\nLower limb Duplex: helpful if a DVT is thought to be the cause of the PE (note this investigation is first-line - before a CTPA - in pregnancy).\n\nBedside echocardiogram: this is used if the patient is thought to have a massive PE (signs of right heart strain/hypotension), in order to assess suitability for thrombolysis.\n\n# Well's scoring system\n\nThe Well's score is a useful tool for risk stratifying patients with a suspected PE.\n\nPoints are allocated as follows:\n\n- 3 points:\n - Clinical signs and symptoms of a deep vein thrombosis (DVT)\n - If no alternative diagnosis is more likely than a PE\n- 1.5 points:\n - Tachycardia (heart rate >100 beats/minute)\n - If the patient has been immobile for more than 3 days or has had major surgery within the last month\n - If the patient has had a previous PE or DVT\n- 1 point:\n - If the patient presents with haemoptysis\n - If there is an active malignancy\n\nIf the Well's score is 4 or less the D-dimer should be measured. The D-dimer has a high negative predictive value but a low specificity so is only useful if the clinical suspicion of a PE is low.\n\nA low D-dimer excludes a PE. A raised D-dimer is an indication for diagnostic imaging (by CTPA or V/Q scan).\n\nIf the Well's score is more than 4 further diagnostic imaging is required. Low-molecular weight heparin is typically administered in the interim if the clinical suspicion of a PE is high (and should certainly be administered if there is delay in performing the CTPA).\n\n# Acute management of a PE\n\nIn the emergency department the patient should be assessed using the DR ABCDE approach:\n\n- Airway: likely to be patent.\n- Breathing: the patient may be tachypnoeic and hypoxic. Oxygen should be administered.\n- Circulation: the patient may be tachycardic. Signs of right heart strain are suggestive of a sub-massive PE. Hypotension is suggestive of a massive PE. Consider intravenous fluids if the systolic blood pressure is <90 mmHg.\n- Disability: likely to be unremarkable.\n- Exposure: the patient may have a low grade pyrexia. It is important to check for signs of a deep vein thrombosis (DVT). Consider analgesia at this stage if required.\n\nThrombolysis (an intravenous bolus of Alteplase) is indicated in a massive PE (features of haemodynamic instability). There is debate over whether it should be administered in a sub-massive PE.\n\n# Medical management of a PE\n\nAnticoagulation should be administered.\n\nIn the outpatient setting, direct oral anticoagulants such as apixaban or rivaroxaban should be started.\n\nIf neither of the above are suitable, dabigatran, edoxaban or warfarin can be considered. Low molecular weight heparin should be continued for at least 5 days and until 48 hours of therapeutic INR (>2) has been achieved if using warfarin. If using dabigatran or edoxaban then LMWH should be used for 5 day prior.\n\nThe duration of anticoagulation treatment depends on the aetiology of the PE. A provoked PE (identifiable risk factors e.g. surgery, peri-partum) should be treated for 3 months. An unprovoked PE should be treated for 6 months. If there is an ongoing cause (e.g. a thrombophilia) the patient should be treated for life.\n\nRecurrence of a VTE in a patient already on warfarin requires an increase in the target INR (to 3-4).\n\nIn the inpatient/emergency setting, low molecular weight heparin is usually started instead as it is shorter acting.\n\n# Interventional management of a PE\n\nEmbolectomy may be considered in patients with a massive PE when thrombolysis is contraindicated.\n\nAn inferior vena cava filter may be considered in patients with recurrent DVTs on Warfarin or patients in which anticoagulation is contraindicated.\n\n# References\n\n[Click for the NICE Guidelines](https://www.nice.org.uk/guidance/ng158)",
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"question": "A 54 year old man presents to the emergency department with a 2 hour history of chest pain. The chest pain is a sudden onset, stabbing pain on the right side of his chest, that gets worse when he breathes in. On examination, he has a heart rate of 107/min, respiratory rate of 22/min and is apyrexial. No abnormalities are noted on examination, his chest x-ray is normal, and an ECG shows sinus tachycardia. He has recently been discharged after a bilateral hip replacement surgery 1 week ago and is currently on no medications.\n\nWhat is the most likely diagnosis?",
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"explanation": "Primary pneumothoracies are more common in tall, thin, young men and scuba diving is a significant risk factor due rapid expansion of the lungs when ascending from a dive. Examination findings are also much in keeping with a pneumothorax, with hyper-resonance and reduced breath sounds on the affected side. This represents air in the pleural space that is more resonant than the surrounding lung tissue and a reduction in functioning lung tissue, which that is being compressed by surrounding free air. This patient will likely be managed by needle aspiration, as they are symptomatic with breathlessness. They will also likely be advised to avoid scuba diving in future",
"id": "33563",
"label": "a",
"name": "Pneumothorax",
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"explanation": "Pulmonary embolism characteristically presents with sudden onset pleuritic chest pain. However, pneumothoracies can also present with sudden onset pleuritic pain. When considering the risk factors and examination findings in this case, pneumothorax is the most likely diagnosis as pulmonary embolism does not present with these examination findings",
"id": "33564",
"label": "b",
"name": "Pulmonary embolism",
"picture": null,
"votes": 21
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"__typename": "QuestionChoice",
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"explanation": "Tension pneumothorax is a life-threatening condition that should always be considered in anyone with suspected pneumothorax. However in this case this patient has a normal heart rate and blood pressure and their trachea is central. In the presence of a well patient with normal observations and a central trachea, it is very unlikely to be a tension pneumothorax, therefore a pneumothorax is a more appropriate single best answer",
"id": "33565",
"label": "c",
"name": "Tension pneumothorax",
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"votes": 190
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"__typename": "QuestionChoice",
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"explanation": "Pleural effusion is fluid in the pleural space, in contrast to pneumothorax which is air in the pleural space. Therefore examination findings are slightly different. They may also present with reduced breath sounds on the affected side, but on percussion they would present with a \"stony\" dullness, when compared to the other side. This is because the fluid in the pleural space is denser than the surrounding lung tissue. The examination findings are more in keeping with a pneumothorax in this case. In addition, this case does not suggest a clear causative factor for a pleural effusion e.g. pneumonia, heart failure, inflammatory disease, whereas there is a clear causative factor for a pneumothorax",
"id": "33566",
"label": "d",
"name": "Pleural effusion",
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"votes": 25
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"__typename": "QuestionChoice",
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"explanation": "Bullous lung disease is a good differential for pneumothorax, especially in a patient with co-existing chronic obstructive pulmonary disease (the most common cause of bullous disease). However, in a 23 year old patient, it is a very unlikely that this patient will have COPD or any bullous disease. Therefore a primary pneumothorax in previous healthy lung tissue is the most likely diagnosis",
"id": "33567",
"label": "e",
"name": "Bullous lung disease",
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"explanation": "# Summary\n \nA pneumothorax is characterised by the abnormal presence of air in the pleural cavity, which may be spontaneous or traumatic in origin. Key signs and symptoms include sudden-onset shortness of breath, pleuritic chest pain, reduced chest expansion and reduced or absent breath sounds on the affected side. Chest X-ray is the key diagnostic investigation (although in cases of tension pneumothorax the diagnosis should be clinical). Management decisions depend on the size of the pneumothorax, the patient's clinical condition and their wishes. Options include conservative management, needle aspiration, chest drain insertion or an ambulatory device. In cases of tension pneumothorax needle decompression is the initial emergency management.\n \n# Definition\n \nA pneumothorax refers to a collection of air in the pleural cavity which may cause collapse of the underlying lung parenchyma. \n\n# Classification\n\n- They may be **spontaneous** or **traumatic** (including iatrogenic causes).\n\n- Spontaneous pneumothoraces can be further divided into **primary** pneumothoraces (in patients without an underlying lung disease) and **secondary** (in patients with underlying lung diseases such as COPD or asthma).\n\n- Patients aged over 50 years old with a significant smoking history who present with a spontaneous pneumothorax are generally considered to have a secondary pneumothorax. \n\n- A **tension pneumothorax** occurs when the defect in the pleura that has led to the pneumothorax creates a one-way valve effect whereby air can enter the pneumothorax but not leave it.\n - This causes the pneumothorax to progressively expand, putting pressure on the heart and great vessels and causing **mediastinal shift**\n - This is a medical emergency that rapidly leads to cardiac arrest if untreated\n \n\n# Signs and Symptoms\n \nThere may be no signs or symptoms (small pneumothoraces may be detected incidentally on imaging) however in an emergency presentation these may include:\n\n- Sudden onset shortness of breath\n- Pleuritic chest pain\n- Dry cough\n- Tachypnoea and increased work of breathing\n\nThe following signs will be found on the affected side of the chest:\n\n- Unilateral reduced expansion\n- Unilateral hyper-resonance to percussion\n- Reduced or absent breath sounds\n- Reduced vocal resonance or tactile vocal fremitus\n \nPatients with a tension pneumothorax may also have:\n\n- Tracheal deviation to the contralateral side\n- Tachycardia\n- Hypotension\n- Distended neck veins\n\n# Investigations\n \nPatients with a suspected tension pneumothorax should be diagnosed and treated with needle decompression based on the clinical picture, with no delay for investigations.\n\nFor other patients, an **erect PA chest X-ray** is diagnostic. \n\n [lightgallery]\n \n\n [lightgallery1]\n \n**CT chest** should be used in high-risk patients where it is not clear from the chest X-ray whether it is safe to place a chest drain.\n\n**Arterial blood gases** are not usually indicated however they may be of use in certain situations e.g. titrating oxygen in a patient with COPD and low saturations.\n\n# Management \n\n**Tension Pneumothoraces:** \n\n- If a tension pneumothorax is suspected, emergency management is to decompress this by inserting a large-bore cannula into the second intercostal space on the affected side, mid-clavicular line, or fifth intercostal space, mid-axillary line if a traumatic cause is suspected, as per ATLS guidelines.\n\n\n- If this fails, open thoracostomy should be done immediately\n- After initial emergency decompression, a chest drain should be inserted\n\nFor **primary or secondary spontaneous pneumothoraces**, management is guided by the 2023 BTS Guidelines as summarised below:\n\n [lightgallery2]\n \n- **Conservative management** involves no intervention for the pneumothorax, and patients are monitored to ensure they do not deteriorate and any symptoms resolve\n- **Ambulatory devices** (e.g. pleural vents) are one-way valves which allow air to leave the pneumothorax but not re-enter it\n - They can be inserted in a simple procedure under local anaesthetic\n - Patients can then be followed up as outpatients\n- Symptomatic patients with larger pneumothoraces (usually 2cm or larger on CXR - CT may be used if unclear) or those with high-risk features (significant hypoxia, bilateral pneumothoraces, underlying lung disease, 50 or older with a significant smoking history, haemopneumothorax) require a **chest drain** and admission for monitoring\n- In symptomatic patients without high-risk features but with pneumothoraces large enough for treatment (2cm or larger), management depends on their priorities\n - Conservative management allows avoidance of any procedure\n - Both needle aspiration and ambulatory devices offer more rapid symptomatic relief (ambulatory device insertion may not be available in all hospitals) \n\n\n**Follow up:**\n\n- All patients should be reviewed in an outpatient clinic 2–4 weeks after presenting with a pneumothorax (with repeat chest imaging)\n- Patients should be advised on smoking cessation if relevant\n - Advise patients not to fly until 7 days after chest imaging has confirmed resolution of the pneumothorax\n - Advise patients they should not take part in underwater diving for life (except in rare cases where they have been treated with bilateral open surgical pleurectomy)\n \n# References\n \n[British Thoracic Society Guidelines](https://thorax.bmj.com/content/thoraxjnl/78/11/1143.full.pdf)\n\n[Royal College of Emergency Medicine - Spontaneous Pneumothorax](https://www.rcemlearning.co.uk/reference/spontaneous-pneumothorax/)\n\n[Radiopaedia - Tension Pneumothorax](https://radiopaedia.org/articles/tension-pneumothorax)\n\n[Pleural Vent Ambulatory Devices](https://www.nth.nhs.uk/resources/pleural-vent-ambulatory-device/)",
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"question": "A 23 year old male presents to the emergency department with sudden onset breathlessness and right sided chest pain that occurred while he was scuba diving. On general inspection, he is noted to 6'4\" tall. His heart rate and blood pressure is normal, trachea is central, the right side of the chest is very resonant to percussion. There are reduced breath sounds on the right side of his chest on auscultation.\n\nWhat is the most likely diagnosis?",
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"__typename": "QuestionChoice",
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"explanation": "Pneumothorax can present with pleuritic chest pain and shortness of breath. However, they would not present with a productive cough or pyrexia due to a pneumothorax. In addition, they would have hyperresonance to percussion and decreased vocal resonance on auscultation",
"id": "33569",
"label": "b",
"name": "Pneumothorax",
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"votes": 56
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"__typename": "QuestionChoice",
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"explanation": "Pericarditis is caused by inflammation of the pericardial lining, typically due to a viral infection. Typical symptoms include pleuritic chest pain (typically worse on laying down and relieved on leaning forward) and fever. A pericardial rub may be heard on auscultation. In this case, this patient has a productive cough, and their pain does not change with posture, making a diagnosis of pneumonia more likely. Their examination findings would also not be present in pericarditis and are better explained by the diagnosis of pneumonia",
"id": "33572",
"label": "e",
"name": "Pericarditis",
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"explanation": "Pneumonia typically presents with an acute history of productive cough, breathlessness, chest pain and fever. Other typical features include haemoptysis, septic shock, atrial fibrillation and confusion in the elderly. Rust coloured sputum suggests a _Streptococcus pneumoniae_ infection, which is the most common cause of pneumonia. Dullness to percussion, reduced breath sounds and increased vocal resonance are all typical examination features of pneumonia. The next step in the management of this patient is a CRB-65 score to determine the prognosis and management of this patient. Pneumonia is a radiological diagnosis, so for confirmation of this diagnosis, a patient must have a chest x-ray showing signs of consolidation",
"id": "33568",
"label": "a",
"name": "Pneumonia",
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"explanation": "Pulmonary embolism can present with breathlessness, sudden onset pleuritic chest pain, haemoptysis and the presence of deep vein thrombosis, usually in a patient with other risk factors for pulmonary embolism. It may also present with pyrexia (which is usually mild). Physical examination of the chest is typically normal. As this patient has a history of productive cough, gradual onset pleuritic chest pain, high fever and physical examination suggestive of pneumonia, pneumonia is the more likely diagnosis",
"id": "33571",
"label": "d",
"name": "Pulmonary embolism",
"picture": null,
"votes": 72
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Empyema is a collection of pus within the pleural cavity. This can be a complication following pneumonia, so it can initially present with symptoms of pneumonia. Specific symptoms indicating empyema include fever, chest pain, and breathlessness refractory to antibiotic treatment for pneumonia. Examination findings are similar to pleural effusion, including reduced breath sounds, dullness to percussion and reduced vocal resonance. The presence of productive cough and increased vocal resonance makes a diagnosis of pneumonia more likely",
"id": "33570",
"label": "c",
"name": "Empyema",
"picture": null,
"votes": 463
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"explanation": "# Summary \n \nPneumonia is a radiological diagnosis, often due to a lower respiratory tract infection causing inflammation of the alveoli and terminal bronchioles, leading to consolidation of bronchopulmonary segment or lobe. Key signs and symptoms include rapid onset of high fever and productive cough for typical bacterial causes. Key investigations include blood tests, sputum culture, urinary antigen tests, and chest x-ray. Management strategies involve use of antibiotics, assessment of severity using CURB-65 score and inpatient treatment for severe cases.\n \n \n# Definition\n \n- Lower Respiratory Tract Infection/ Pneumonia is caused by infection and subsequent inflammation of the alveoli and terminal bronchioles.\n- This leads to an entire bronchopulmonary segment or lobe becoming consolidated, which means that tissue is filled with inflammatory cells and oedema.\n \n \n# Community Acquired Pneumonia (CAP)\n \n \n## Bacterial Causes\n \n \n- Typicals - so called because of the classical rapid onset of symptoms, including high fever and productive cough;\n- Streptococcus pneumoniae (gram +ve cocci found in pairs, also known as 'Pneumococcus')\n- Staphylococcus aureus\n- Haemophilus influenzae (gram -ve rod, potent beta-lactamase producer)\n- Moraxella catarrhalis (gram -coccus, potent beta-lactamase producer)\n- Atypicals: so called because of the more gradual onset of symptoms, which may be non-specific initially (fever, myalgia, dry cough). The organisms are also intracellular;\n- Mycoplasma pneumoniae\n- Chlamydia pneumoniae\n- Legionella pneumophila\n- Coxiella burnettii\n- Chlamydia psittaci\n \n \n## Viral Causes \n \n- Most commonly Influenza A, which can predispose to superadded Staph aureus (or strep pneumoniae) pneumonia.\n- Others: CMV, HSV, VZV\n \n## Fungal Causes\n \nCan be seen after silver staining and microscopy:\n \n- Candida - dimorphic yeast\n- Aspergillus - fungus with hyphae\n- Cryptococcus - encapsulated yeast\n \n \n## Specific Causes \n \nCOPD: \n \n- Pneumococcus still most common\n- Haemophilus influenzae\n- Morexella catarrhalis\n \nCystic Fibrosis:\n \n \n- Staph aureus\n- Pseudomonas aeruginosa\n- Burkholderia cepacia\n \nCauses in Homeless people: malnourished, alcohol or drug dependent, immunosuppressed:\n \n \n- Mycobacterium tuberculosis\n- Aspiration pneumonia (infection with normal flora of mouth and anaerobes, also consider in any patient with an unsafe swallow or with depressed consciousness)\n- Klebsiella pneumoniae (causes 'red-current jelly' sputum, and commonly causes lung abscess formation and empyema)\n \n \nOccupational/travel situations:\n \n- Aerosols from humidifiers and airconditioning (e.g. at holiday resorts) - Legionella pneumophila.\n- Patients can present with diarrhoea and vomiting, develop hepatorenal syndrome and have a low sodium. Severe pneumonia develops, with other rare complications such as:\n- Pancreatitis\n- Peritonitis\n- Myocarditis, endocarditis, pericarditis\n- Glomerulonephritis\n \n \nClosed populations e.g. schools, offices\n \n- Mycoplasma pneumoniae\n- Extra respiratory symptoms:\n- Erythema multiforme, erythema nodosum\n- Guillain-Barre Syndrome (and rarely other neurological complications e.g. aseptic meningitis, cerebellar disease, transverse myelitis).\n- Cold agglutinin production with haemolytic anaemia\n- Chlamydia pneumoniae\n \n \nZoonotic Causes: \n \n- In Abattoir worker, farmer, vets\n- Coxiella burnettii\n- Brucella spp.\n \n- Animal hide importers/sorters\n- Bacillus anthracis\n- Coxiella burnettii\n \n \n- Following exposure to birds\n- Chlamydia psittaci (causes psittacosis)\n- Exposure to bats/bat droppings\n- Histoplasma capsulatum (a fungus, classically affects cave-explorers)\n \n \n## Investigations\n \n \n- Bloods: including FBC, U+Es, CRP, WCC and blood cultures\n- Sputum culture\n- Urinary antigen tests for Legionella and pneumococcus\n- Chest X-Ray\n- Could assess pleural fluid aspirate in patients with pleural effusion\n \n \n## CURB-65 \n \n \n- Use the CURB-65 score to aid in deciding the severity of pneumonia and further management based on this\n- Components (1 point for each if present):\n- Confusion +/-\n- Urea >7\n- Respiratory Rate >30\n- Blood pressure: systolic < 90 or diastolic <60\n- More than 65 years old\n \n \nCURB-65 mortality by score:\n \n- 0 or 1 - 1.5%\n- 2 - about 10%\n- 3 or more - 10% or more \n \n \n \n \n## Management\n \nIf a patient is very unwell, adopt an A-E approach, initiate the sepsis six and seek early senior input.\n \n- Management based on CURB-65 score:\n- 0/1: home-based care, give oral amoxicillin for 5 days (macrolide e.g. clarithromycin, doxycycline or tetracycline if penicillin allergic).\n- 2: hospital-based care, 7-10 day course of dual antibiotic therapy with amoxicillin (IV or oral) and a macrolide\n- 3: Hospital/ITU-based care, 7-10 day course of dual antibiotic therapy with IV co-amoxiclav/ceftriaxone/tazocin and a macrolide.\n \n \n- Atypical and typical community-acquired pneumonia are both managed in the same way initially.\n- Liaise with microbiology to guide targeted antibiotics following culture results e.g. flucloxacillin for staph aureus pneumonia.\n- A repeat chest x-ray is required after 6 weeks to assess for underlying pathology.\n \n \n## Complications\n \n \n- Pleural effusion\n- Empyema (suspect if persistent, swinging fever with leucocytosis found after antibiotic therapy)\n- Abscess (can be caused by S. pneumoniae, Klebsiella, staph aureus). Can develop pyopneumothorax.\n- Pneumothorax\n- Septicemia\n- Atrial fibrillation\n- Post-infective bronchiectasis\n \n \n \n \n# Hospital Acquired Pneumonia\n \n \n## Definition\n \n \nLower respiratory tract infection that develops more than 48 hours after admission to hospital\n \n \n## Risk Factors\n \n \n- Poor hand hygiene and hospital infection control\n- Intubation and ventilation\n \n \n## Causative Organisms\n \n \n- Pseudomonas aeruginosa\n- E. coli\n- Klebsiella pneumoniae\n- Acinetobacter species (can acquire high potency beta-lactamases, known as ESBLs)\n- Serratia species (can acquire high potency beta-lactamases, known as ESBLs)\n \n \n## Investigations\n \nMay include:\n \n- Bloods: including FBC, U+Es, CRP, WCC and blood cultures\n- Sputum culture\n- Urinary antigen tests for Legionella and pneumococcus\n- Chest X-Ray\n- Could assess pleural fluid aspirate in patients with pleural effusion\n \n \n## Management \n \nIf a patient is very unwell, adopt an A-E approach, initiate the sepsis six and seek early senior input and discussion with microbiology. Empirical antibiotics are guided by severity and likelihood of resistant organisms:\n \n- HAP within 5 days of admission: co-amoxiclav is usually first line for non-severe symptoms\n- HAP more than 5 days after admission (associated with higher risk of resistance) or severe symptoms: tazocin or cephalosporin (e.g. ceftazidime) or quinolone first-line.\n- If MRSA is suspected, add vancomycin\n \n \n# Aspiration Pneumonia \n \n \n- Caused by any cause of depressed consciousness or impairment of the swallowing mechanism\n- Infection caused by mixed aerobic and anaerobic mouth flora, which can cause cavitary pneumonia or empyema\n- Same empirical therapy as for non-aspiration pneumonia, but later antibiotic choice made by pathogen and sensitivities. Metronidazole often added in to cover for anaerobic organisms. Local guidance should be sought.\n \n \n# NICE Guidelines\n \n \n[Click here for NICE CKS on chest infections](https://cks.nice.org.uk/topics/chest-infections-adult/)\n \n[Click here for NICE guidance on antimicrobial prescribing in hospital-acqui",
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"question": "A 67-year-old female presents to her GP with a four-day history of worsening shortness of breath. This is associated with a cough productive of rust coloured sputum and gradual onset right-sided sharp chest pain that worsens with inspiration. She has a heart rate of 81/min, a respiratory rate of 22/min, a blood pressure of 111/78 and a temperature of 38.3ºC. On examination, there is dullness to percussion, reduced breath sounds and increased vocal resonance on the right side of the chest.\n\nWhat is the most likely diagnosis?",
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"__typename": "QuestionChoice",
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"explanation": "Infective exacerbation of COPD would be a likely differential for this patient's initial clinical presentation. However, the history of new-onset drowsiness and this man's ABG findings in the context of COPD and the initiation of oxygen therapy is more suggestive of acute on chronic retention of CO2",
"id": "33575",
"label": "c",
"name": "Infective exacerbation of COPD",
"picture": null,
"votes": 912
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Pulmonary embolism would typically present with type 1 respiratory failure. This would mean they have a low oxygen and a low to normal CO2 on an ABG. As this patient has a high CO2, they are in type 2 respiratory failure, not type 1",
"id": "33576",
"label": "d",
"name": "Pulmonary embolism",
"picture": null,
"votes": 92
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Pneumonia would be a likely differential for this patient's initial clinical presentation (differentiated based on chest x-ray findings). However, the history of new-onset drowsiness and this man's ABG findings in the context of COPD and the initiation of oxygen therapy is more suggestive of acute on chronic retention of CO2",
"id": "33574",
"label": "b",
"name": "Pneumonia",
"picture": null,
"votes": 111
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"__typename": "QuestionChoice",
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"explanation": "Myasthenia gravis can present with type 2 respiratory failure, and the typical age of onset in men is between 60 and 70 years old. However, it usually presents with diplopia, swallowing difficulties and arm weakness that worsens with repeated usage. Given this patient's history, acute on chronic retention of CO2 on a background of COPD and high flow oxygen administration is the more likely diagnosis",
"id": "33577",
"label": "e",
"name": "Myasthenia gravis",
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This patient is presenting with type 2 respiratory failure secondary to oxygen therapy. Patients with COPD can develop a reduction in hypercapnic drive due to increased carbon dioxide content in the blood. This means they are reliant on hypoxic drive. Therefore, when given high flow oxygen therapy, they lose hypoxic drive, which means they have a lower respiratory effort and retain CO2. This presents clinically as drowsiness. This patient may also have an element of chronic hypercapnoea, as they have a raised bicarbonate. This is a typical ABG of someone in type 2 respiratory failure: a low pH and high CO2 indicating respiratory acidosis and high bicarbonate, suggesting this is an acute on chronic retention of carbon dioxide. Of note, if a patient is presenting with severe hypoxia and a history of COPD, they should still be commenced on high flow oxygen as their hypoxia is immediately threatening to life. However, in this case (patient with COPD who is a known retainer), it is more appropriate to keep them on a Venturi mask and aim for saturations of 88-92%",
"id": "33573",
"label": "a",
"name": "High flow oxygen therapy",
"picture": null,
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"explanation": "### Mean pressures in pulmonary circulation \n\n- Pulmonary artery 12-15mmHg\n- Left atrium 5mmHg\n- Pressure gradient 7-10mmHg\n\n### Ventilation perfusion ratio\n\nV/Q ratio - the ratio of alveolar ventilation (V) to alveolar blood perfusion (Q).\n\n- To attain efficient gaseous exchange, ventilation and perfusion must be matching.\n- The normal V/Q ratio is 0.8, which means that alveolar ventilation has to be at least 80% of pulmonary blood flow.\n\t- 4L/min of air enters the alvoeli\n\t- 5L/min of blood flows through the lungs\n\nV/Q ratio is different across different lung zones:\n\n- Zone 1 (upper zones, lung apices) has the lowest ventilation and perfusion;\n- Zone 3 (lower zone, lung bases) has the highest ventilation and perfusion due to gravity.\n- However, the regional differences in ventilation are less marked than perfusion, resulting in a higher V/Q ratio in zone 1 (3.3 apically) and lower in zone 3 (0.63 basally).\n\nThe significance of the V/Q ratio lies in its influence on the partial pressure of oxygen (PO2) and the partial pressure of carbon dioxide (PCO2).\n\n- At a high V/Q ratio, the gaseous exchange is more efficient, so PO2 is higher and PCO2 is lower, and vice versa.\n- Normal PO2 in arterial blood is 100mmHg, while normal PCO2 in arterial blood is 40mmHg when the V/Q ratio is at its optimum value, which is 0.8.\n\n### Right-to-left shunt \n\nWhen there is a right-to-left shunt or airway obstruction, where there is no ventilation to a well-perfused alveolus, V/Q = 0; hence, gaseous exchange does not occur. PO2 and PCO2 in the arterial blood remain the same as that in the venous blood, which are 40mmHg and 46mmHg, respectively.\n\n### Dead space \n\nWhen there are alveoli which are well-ventilated but not perfused, this is termed a physiological dead space. V/Q = ∞; hence, gaseous exchange does not occur. An example of this is a pulmonary embolism. PO2 and PCO2 in the alveoli remain the same as that in the inspired air, which are 150mmHg and 0mmHg, respectively.",
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"question": "A 66-year-old man presents to the emergency department with breathlessness, productive cough and fever. He is admitted and commenced on 15L high flow oxygen as his oxygen saturation is 89% and his respiratory rate is 22/min. He has a past medical history of COPD.\n\nThirty minutes later, he is drowsy and has a respiratory rate of 13/min. His ABG is shown below:\n\npH: 7.29 [7.35-7.45]\n\nPaO2: 10 [9.5-14]\n\nPaCO2: 7.1 [4.6-6]\n\nHCO3-: 33 [22-30]\n\nWhat is the most likely cause of this patient's new symptoms?",
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"explanation": "HIV-associated nephropathy is a disease of the kidneys caused by infection with HIV. It presents with a nephrotic syndrome picture; however, this would not explain this patient's jaundice or palmar erythema. This patient is also currently taking antiretroviral treatment, which is protective against developing HIV-associated nephropathy",
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"explanation": "Chronic and excessive use of alcohol can damage hepatic tissue and lead to hepatitis and eventually cirrhosis. However, in this case, the patient is adamant that they do not drink alcohol. Patients are of course not always honest about their intake of alcohol. However, this patient has a history of intravenous drug use with a co-diagnosis of HIV. These are risk factors for hepatitis C, and therefore at this stage, this is the most likely diagnosis",
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"explanation": "This patient is presenting clinically with chronic liver disease, most likely cirrhosis. This is indicated primarily by their examination findings. They have ascites and peripheral oedema, with excessive water retention likely causing them to gain weight. Heart failure, renal failure, and liver failure can all present with peripheral oedema and ascites; however, only liver failure would present with jaundice and palmar erythema. This patient doesn't report drinking alcohol, they have evidence of intravenous drug use, and it is likely they are not using clean needles as they also have a diagnosis of HIV (although it is possible this is not related to their IV drug use). This supports the diagnosis of viral hepatitis. Acute hepatitis B infection leads to chronicity in about 5% of adults, whereas acute hepatitis C infection leads to chronicity in 75% of adults. Hepatitis C is also the most common viral hepatitis found in the UK. This makes hepatitis C infection the most likely diagnosis",
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"explanation": "Heart failure can present with ascites, peripheral oedema and hepatomegaly (a consequence of congestion of the systemic vasculature due to right heart failure). However, this would not explain why this patient is jaundiced and has palmar erythema. In combination with clear risk factors for hepatitis C infection, this makes hepatitis C the most likely diagnosis",
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"comment": "tough q tbs",
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"explanation": "# Summary\n\nCirrhosis refers to chronic liver disease where there is irreversible scarring of the liver with loss of normal hepatic architecture. The key signs and symptoms vary based on if the cirrhosis is compensated or decompensated, ranging from fatigue and anergia to ascites and jaundice. Investigations include blood tests and imaging or invasive procedures, with the Child-Pugh score used to estimate the severity of cirrhosis. Management strategies involve nutritional guidance, medication, and possibly a liver transplant for severe cases.\n\n# Definition\n\nCirrhosis refers to **irreversible** scarring of the liver with loss of normal hepatic architecture.\n\n# Epidemiology\n\nThe prevalence and incidence of cirrhosis are dependent on the underlying aetiological factors prevalent in the population. Alcohol and viral hepatitis, particularly Hepatitis B and C, are major contributors globally. Non-alcoholic fatty liver disease is increasingly becoming a significant cause due to rising obesity rates.\n\n# Aetiology\n\n\n- Commonest causes:\n - **Alcohol**\n - **Hepatitis B and C**\n - **Non-alcoholic fatty liver disease (NAFLD)**\n- Less common causes:\n - Autoimmune:\n - Autoimmune hepatitis\n - Primary biliary cirrhosis\n - Primary sclerosis cholangitis\n - Sarcoid\n - Genetic:\n - Haemochromatosis\n - Wilson's disease\n - Alpha-1-antitrypsin deficiency\n - Drugs:\n - Methotrexate\n - Amiodarone\n - Isoniazid\n - Others:\n - Budd-Chiari Syndrome\n - Heart failure\n - Tertiary syphilis\n\n# Signs and Symptoms\n\nClinical features of cirrhosis can be divided based on whether the cirrhosis is compensated or decompensated.\n\n## Compensated Cirrhosis\n\n- Fatigue and anergia\n- Anorexia and cachexia\n- Nausea or abdominal pain\n- Spider naevi\n- Gynaecomastia\n- Finger clubbing\n- Leuconychia\n- Dupuytren's contracture\n- Caput medusae\n- Splenomegaly\n\n[lightgallery]\n\n## Decompensated Cirrhosis\n\nIn addition to the symptoms of compensated cirrhosis:\n\n- Ascites and oedema\n- Jaundice\n- Pruritus\n- Palmar erythema\n- Gynaecomastia and testicular atrophy\n- Easy bruising\n- Encephalopathy/confusion\n- Liver 'flap'\n\n[lightgallery1][lightgallery2]\n\n# Differential Diagnosis\n\n- Hepatic steatosis: Characterised by the accumulation of fat in the liver, leading to hepatomegaly, mildly elevated serum aminotransferases, and possible right upper quadrant pain. If managed early these changes are reversible, however if not managed there will be progression to cirrhosis.\n- Chronic hepatitis: Presents with fatigue, malaise, low-grade fever, and hepatomegaly.\n- Congestive heart failure: Symptoms include dyspnoea, fatigue, fluid retention, and peripheral oedema.\n\n\n# Investigations\n\nInitial blood tests for cirrhosis should include:\n\n- Liver Function Tests: AST, ALT, ALP, GGT, Albumin, and Bilirubin\n- Full blood count to look for leucocytosis, thrombocytopaenia, and anaemia \n- Urea and electrolytes to establish baseline renal function and look for hepato-renal syndrome or any electrolyte abnormalities \n- INR to look for coagulopathy\n- A low platelet count, elevated aspartate aminotransferase (AST): alanine transaminase (ALT) ratio, high bilirubin, low albumin, or increased prothrombin time or international normalized ratio (INR) can suggest impaired liver function. Patients can however also present with normal blood tests which is why clinical examination findings are equally important.\n- Specific tests to determine the potential cause such as Hepatitis serology, cytomegalovirus serology, iron studies, α-1 anti-trypsin, caeruloplasmin level, and auto-antibodies\n\nImaging and invasive investigations may include:\n\n- Peritoneal tap for microscopy and culture if ascites is present\n- Doppler ultrasound to identify Budd-Chiari syndrome\n- Transient elastography (fibroscan) or acoustic radiation force impulse imaging should be done for patient groups at risk of cirrhosis: those with hepatitis C infection, increased alcohol intake (men who drink >50 units of alcohol/week, women who drink >35 units of alcohol/week), and those with known alcohol-related disease\n\t- If cirrhosis is not diagnosed on initial testing, these patients should have retesting for cirrhosis every 2 years\n- Liver biopsy for confirmation of diagnosis if in doubt\n\n### Child-Pugh Score\n\nThe severity of liver cirrhosis can be estimated by calculating the Child-Pugh score. This scoring system is shown in the table below:\n\n| Score | 1 | 2 | 3 |\n| ------------------------------------ | ---- | ----- | ------ |\n| Bilirubin (umol/l) | <34 | 34-51 | >51 |\n| Albumin (g/l) | >35 | 28-35 | <28 |\n| Prothrombin time (seconds prolonged) | <4 | 4-6 | >6 |\n| Encephalopathy | none | mild | marked |\n| Ascites | none | mild | marked |\n\nThe scores are added and the degree of cirrhosis is classified as Child-Pugh A (<7 points), B (7-9 points) or C (>9 points). The score can be used as a predictor of mortality, and may also be used to predict the need for a liver transplant.\n\n### MELD Score\n\n- The Model for End-Stage Liver Disease (MELD) score evaluates the severity of liver disease based on bilirubin, creatinine, and INR levels. \n- Higher scores indicate a greater risk of mortality within a three-month period. MELD scores are used to prioritise patients for liver transplantation. \n- In liver cirrhosis, MELD scores ≥15 typically indicate significant disease severity, with increased mortality rates and the need for liver transplantation consideration.\n\n\n|MELD Score|Interpretation|\n|---|---|\n|6-9|Low risk of mortality; Class I (less than 10%)|\n|10-19|Intermediate risk of mortality; Class II (19%)|\n|20-29|High risk of mortality; Class III (52%)|\n|30-39|Severe risk of mortality; Class IV (71%)|\n|≥40|Very severe risk of mortality; Class V (95%)|\n\n# Management\n\nConservative: \n\n- Ensuring good nutrition and total alcohol abstinence\n- Avoiding non-steroidal anti-inflammatory drugs, sedatives, and opiates\n- 6 monthly ultrasound scans and serum α-fetoprotein tests for hepatocellular carcinoma detection\n- Upper gastrointestinal endoscopy surveillance for oesophageal varices may be needed at diagnosis (one-off) and every 3 years, unless the person is taking carvedilol or propranolol non-selective beta-blocker therapy for primary prevention of decompensation, or for primary prevention of bleeding from medium or large varices\n\nMedical: \n\n- Using cholestyramine for pruritus\n- Managing ascites with fluid restriction, low-salt diet, pharmacological management with spironolactone; furosemide, therapeutic paracentesis, and albumin infusions in severe cases\n- Reducing recurrent episodes of encephalopathy through prophylactic lactulose and rifaximin\n- Using prophylactic antibiotics in patients at high-risk of spontaneous bacterial peritonitis \n\nSurgical:\n\n- Liver transplantation is the only definitive management for liver cirrhosis, and different scoring criteria are used to assess severity and suitability for transplanation\n- If there is acute liver failure, the King's criteria is used (below):\n\nParacetamol Toxicity:\n\n- **pH** - < 7.3 at any time or < 7.30 - 7.35 after fluid resuscitation\n- **Prothrombin time (INR)** - > 100 seconds or > 6.5\n- **Grade 3 or 4 encephalopathy**\n\nNon-Paracetamol-Induced Fulminant Hepatic Failure:\n\n- **INR** - > 50 seconds or > 3.5 despite Vitamin K treatment\n- **Serum Creatinine** - > 300 µmol/L\n- **Grade 3 or 4 encephalopathy**\n\n\n- If there is chronic liver failure leading to advanced cirrhosis, UK End-stage Liver Disease (UKELD) score is used to predict disease severity and is based on the MELD score but also includes sodium\n\n\n# Complications\n\n## Ascites\n\nThis results from portal hypertension and hypoalbuminaemia. It gives rise to other complications such as spontaneous bacterial peritonitis.\n\n## Spontaneous bacterial peritonitis (SBP)\n\nSudden peritonitis can occur in patients with ascites. It may present atypically (often with no abdominal tenderness or guarding) and should be suspected in patients who deteriorate suddenly with no other obvious cause. An ascitic tap with neutrophils >250mm³ indicates SBP. Patients with a low ascitic albumin are especially at risk and should be treated with prophylactic antibiotics.\n\n## Liver failure\n\nWith its sequelae of hepatic encephalopathy, jaundice and coagulopathy. The former can result in cerebral oedema progressing to raised intracranial pressure and death, and the latter can contribute to life-threatening bleeds in those with a source of bleeding due to thrombocytopaenia.\n\n## Hepatocellular carcinoma\n\nPatients with cirrhosis are at significantly increased risk, especially those with Hepatitis B and C.\n\n## Oesophageal varices ± haemorrhage\n\nThe development of portal hypertension in cirrhosis leads to dilatation of oesophageal veins. These are liable to rupture and this can be fatal, especially in patients with coagulopathy. There can also be gastric varices, and caput medusae (dilatation of umbilical veins) – these are due to portosystemic collaterals trying to get around the cirrhotic liver.\n\n## Renal failure\n\nCirrhosis and ascites with renal failure is known as hepatorenal syndrome if other causes of acute kidney injury have been ruled out. Abnormal haemodynamics in liver disease cause renal vasoconstriction which makes the kidneys more susceptible to injury. It has a very poor prognosis.\n\n\n\n\n# NICE Guidelines\n\n[Click here to see information on NICE CKS about cirrhosis](https://cks.nice.org.uk/topics/cirrhosis/)",
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"question": "A 52-year-old woman presents to her GP as she has gained weight over the last eight months. On examination, she has yellow sclera, track marks in the antecubital fossae, reddened palms, abdominal distension with shifting dullness, hepatomegaly and bilateral ankle oedema. Auscultation of the chest is normal. She has a past medical history of HIV diagnosed ten years ago, for which she takes antiretroviral therapy. She regularly uses heroin, but she does not drink.\n\nWhat is the most likely diagnosis?",
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"explanation": "Boerhaave's syndrome is caused by perforation of the oesophagus. It can also be caused by vomiting and retching; however the patient would be much more unwell as this is a life-threatening condition. Pain, dysphagia, massive haematemesis, haemodynamic instability and surgical emphysema are much more typical features of Boerhaave's syndrome. Given how well this patient is, Mallory-Weiss tear is a much more likely diagnosis",
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"explanation": "One of the complications of peptic ulcer disease is an upper GI bleed. Peptic ulcer disease can present in young adults, with causes including alcohol, H. pylori infection and regular NSAID use. However, given that vomiting and straining are typical causes of a Mallory-Weiss tear, this patient is more likely to be presenting with a Mallory-Weiss tear",
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"explanation": "One of the complications of oesophageal cancer is an upper GI bleed. However, it is exceedingly rare for a 22-year-old to develop oesophageal cancer, especially in the absence of any specific risk factors in the history",
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"explanation": "A Mallory-Weiss tear is caused by tears in the oesophageal mucosa. This is typically caused by vomiting and retching, increasing the pressure at the gastro-oesophageal junction. This typically presents with haematemesis or blood-stained vomitus in the presence of vomiting or retching. In this case, this is on a background of acute alcohol intoxication leading to excessive vomiting. These patients will typically have a normal examination/examination in keeping with the cause of vomiting, although there can be haemodynamic instability if a significant amount of blood is lost. The majority of patient resolve spontaneously with no complications. All patients with an upper GI bleed should receive oesophagogastroduodenoscopy, with urgency based on clinical presentation and Glasgow-Blatchford score",
"id": "33588",
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"explanation": "Oesophageal varices are enlarged veins that develop due to portal hypertension. These can rupture, leading to life-threatening upper GI bleeds and are generally associated with cirrhosis. This patient is relatively young, so is unlikely to have developed cirrhosis at the age of 22. They also have no features of chronic liver disease on examination. Although alcohol is a common cause of cirrhosis, there is no evidence this patient has chronic harmful alcohol use or alcohol dependency. It is more likely that this patient was acutely intoxicated with alcohol",
"id": "33589",
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"explanation": "# Summary\n \nAn upper gastrointestinal bleed (UGIB) is a common emergency presentation, with the main symptoms being haematemesis, coffee-ground vomiting and melaena. Haemorrhage can be anywhere in the oesophagus, stomach or duodenum and common causes include peptic ulcer disease, variceal bleeding, Mallory-Weiss tears and angiodysplasia. Management involves resuscitation with IV fluids and blood products, and identification of the likely cause which may be treatable via an endoscopic approach. \n \n# Definition\n \nAn UGIB is defined as any haemorrhage of the gastrointestinal tract between the oesophagus and the duodenum at the ligament of Treitz (the anatomical landmark that differentiates upper from lower GI bleeds).\n \n# Epidemiology\n \n- Acute UGIB is a common medical emergency, accounting for 50,000-70,000 admissions to hospital in the UK per year\n- In hospital mortality is approximately 10%\n- Older patients and those with comorbidities are more likely to experience higher morbidity and mortality than young fit patients with more physiological reserve\n- Men are more affected than women\n- The most common cause identified is peptic ulcer disease\n \n# Aetiology\n\n**Bleeding from the oesophagus:**\n\n- **Oesophageal varices:** usually secondary to portal hypertension due to hepatic cirrhosis\n- **Oesophagitis:** inflammation may be due to gastro-oesophageal reflux, infections (especially in immunocompromised patients), or medications such as bisphosphonates\n- **Mallory-Weiss tear:** longitudinal mucosal lacerations that occur after severe vomiting or retching\n- **Oesophageal cancer:** friable blood vessels in the tumour may cause chronic or acute bleeds\n \n\n**Bleeding from the stomach:**\n\n- **Peptic ulceration:** usually secondary to Helicobacter pylori infection or chronic NSAID use\n- **Gastric varices:**: also associated with portal hypertension\n- **Gastritis:** may be due to H. pylori infection, NSAIDs, alcohol or stress-related mucosal inflammation\n- **Gastric cancer:** tumours may ulcerate or erode blood vessels\n- **Vascular malformations:** a Dieulafoy lesion is a dilated submucosal artery that erodes the gastrointestinal mucosa resulting in massive bleeding\n \n**Bleeding from the duodenum:**\n\n- **Peptic ulceration:** as per ulceration in the stomach\n- **Aortoenteric fistula:** a rare but life-threatening condition where an abnormal connection forms between the aorta and the gastrointestinal tract, usually following abdominal aortic aneurysm repair\n\n# Classification\n\nThere are two main scoring systems used to classify patients as high or lower risk:\n\n- The Glasgow-Blatchford score is used as an initial assessment to determine how urgently endoscopy is indicated\n - It takes into account haemoglobin, urea, systolic blood pressure, tachycardia, melaena, syncope, heart failure and liver disease\n - Patients scoring 0 are considered to be low-risk and may be discharged for an outpatient OGD \n- The Rockall score can be calculated both pre and post-endoscopy but NICE recommends using it post-endoscopy to help with risk stratification\n - The following table shows how this is calculated (with only the first three parameters used in the pre-endoscopy scoring)\n \n\n | | 0 points | 1 point | 2 points | 3 points |\n | ----------------------------------------- | ------------------------- | ------------------- | ---------------------------------------------------------- | ------------------------------------------ |\n | Age (years) | <60 | 60-79 | >80 | |\n | Systolic blood pressure/pulse rate (mmHg) | SBP>100, HR<100 | SBP>100, HR>100 | SBP<100 | |\n | Comorbidities | None | | Ischaemic heart disease or cardiac failure | Liver failure, renal failure or metastatic cancer |\n | Post endoscopy diagnosis | Mallory-Weiss tear | All other diagnoses | Upper GI malignancy | |\n | Signs at endoscopy | No blood or dark red spot | | Blood in upper GI tract, spurting vessel or adherent clot |\n \n\n# Signs & Symptoms\n\nThe most common symptoms are **haematemesis** (vomiting blood) which is seen in 50% of patients, and **melaena** (black, sticky and tarry stool) which is seen in 70%.\n\nOther symptoms include:\n\n- \"Coffee-ground\" vomiting (dark digested blood)\n- Lightheadedness\n- Syncope\n- Abdominal pain\n- Symptoms of anaemia in subacute or chronic bleeds\n - Fatigue\n - Shortness of breath\n - Decreased exercise tolerance\n - Palpitations\n \nSigns include:\n\n- Tachycardia\n- Hypotension\n- Prolonged capillary refill time\n- Altered mental state\n- Abdominal tenderness\n- Melaena or haematochezia (fresh red blood) on rectal examination\n- Stigmata of chronic liver disease in patients with cirrhosis, e.g.\n - Spider naevi\n - Gynaecomastia\n - Palmar erythema\n - Caput medusae\n\n# Investigations\n \n**Bedside tests:**\n\n- **Venous blood gas** to obtain urgent haemoglobin, lactate may be raised if shocked\n- **ECG** as cardiac ischaemia may complicate haemorrhage (type 2 myocardial infarction), screen for arrhythmias if tachycardic\n\n**Blood tests:**\n\n- **Full blood count** for haemoglobin (note that there may be a delay in this falling due to haemoconcentration so do not be falsely reassured if normal)\n- **U&Es** - classically urea is disproportionately raised due to digestion of blood\n- **LFTs** to screen for liver cirrhosis (increased risk of variceal bleeding)\n- **Coagulation screen** so that abnormalities might be corrected to reduce bleeding\n- **Group and save** in case blood transfusion is required\n- **Cross-match** so that matched blood can be given when needed\n\n\n**Imaging/special tests:**\n\n- **Oesophago-gastroduodenoscopy** (OGD) \n - Also referred to as an upper GI endoscopy\n - Usually the definitive diagnostic test to look for a cause of bleeding\n - Allows risk stratification with the Rockall score\n - Facilitates endoscopic treatment (see Management section)\n- **Chest X-ray** to look for evidence of aspiration or perforation (e.g. pneumomediastinum or free air under the diaphragm)\n\n\n# Management\n \n**Resuscitation:**\n\n- Take an A to E approach as in any medical emergency and activate the **major haemorrhage protocol** for any significant bleed\n- Consider if **airway support** required (e.g. in an unconscious patient) and position to reduce aspiration risk if ongoing vomiting\n- Ensure adequate **IV access** (2x wide bore cannulae in the antecubital fossae ideally) and take urgent bloods including a blood gas\n- **Resuscitation** with IV fluids and/or blood \n - Give a **fluid bolus** if unstable\n - In a massive bleed follow local transfusion protocols\n - **Transfuse red blood cells** if Hb < 70, targeting a Hb of 70-100\n - Consider transfusion at a higher Hb in patients who are unstable or have ischaemic heart disease\n - **Transfuse platelets** if these are below 50 \n- **Correct any coagulopathy** or **anticoagulant** medication (may require haematology input)\n- In suspected variceal bleeds, give **terlipressin** and **prophylactic antibiotics**\n- **Immediate endoscopy** is required in severe UGIB; all other patients should have an endoscopy within 24 hours of admission\n - Non-variceal bleeds can be treated mechanically (e.g. **clipping**), with **thermal coagulation** or with **fibrin or thrombin** (plus adrenaline)\n - Oesophageal variceal bleeds should be treated with **band ligation**\n - Gastric variceal bleeds should be treated with N-butyl-2-cyanoacrylate injections (**sclerotherapy**)\n- **Proton pump inhibitors** (PPIs) should **not** be given prior to endoscopy - if the OGD shows a non-variceal UGIB with stigmata of recent haemorrhage (e.g. a peptic ulcer) high-dose IV or PPIs should be started\n- **Review medications** with associated bleeding risks\n - Hold DOACs\n - Hold warfarin\n - Hold P2Y12 inhibitors (e.g. clopidogrel, ticagrelor) - discuss with cardiology if the patient has coronary artery stents \n - Aspirin can be continued\n \n \n# Complications\n\n- **Rebleeding** is a major complication which can occur after endoscopic therapy\n - Repeat endoscopy should be offered +/- endoscopic treatment\n - Patients may require additional treatment to stop bleeding which may be via an interventional radiology or a surgical approach \n - Options for varices that continue to bleed include Sengstaken-Blakemore tube insertion (a bridging therapy) or a transjugular intrahepatic portosystemic shunt (a definitive treatment to reduce portal pressure in appropriate patients)\n- **Aspiration** of haematemesis or coffee-ground vomit may cause aspiration pneumonia or pneumonitis - risk is increased in patients with reduced levels of consciousness\n- **Complications of endoscopy** e.g. perforation\n- **Death** occurs in 10% of patients admitted with an UGIB; mortality is especially high in those who rebleed and require salvage surgery\n\n# NICE Guidelines\n\n[NICE - Acute upper gastrointestinal bleeding in over 16s](https://www.nice.org.uk/guidance/cg141/)\n\n# References\n \n[British Society of Gastroenterology - Acute upper GI bleed care bundle](https://www.bsg.org.uk/clinical-resource/bsge-acute-upper-gi-bleed-care-bundle)\n\n[RCEM Learning - Upper Gastrointestinal Haemorrhage](https://www.rcemlearning.co.uk/reference/upper-gastrointestinal-haemorrhage/)\n\n[Patient UK - Upper Gastrointestinal Bleeding](https://patient.info/doctor/upper-gastrointestinal-bleeding-includes-rockall-score)",
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"question": "A 23-year-old man presents to the emergency department complaining of vomiting blood. He started vomiting last night at a house party, followed by forceful retching a few hours later. Physical examination shows no abnormalities, and he is haemodynamically stable.\n\nWhat is the most likely diagnosis?",
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"explanation": "GORD can present with dyspepsia, but it more typically presents with retrosternal pain and a bitter, acidic taste in the mouth. Pain associated with GORD typically gets worse, not better, after meals",
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"explanation": "Duodenal ulcers are the most common type of peptic ulcer. 90% of them are related to H. pylori infection. They are typically improved by eating and worsened a few hours after meals or when the patient is hungry. They may present with epigastric tenderness on examination. All suspected ulcers should be investigated for _H. pylori_, the positive urea breath test, in this case, indicating _H. pylori_ as the primary cause. Other common causes include NSAIDs and corticosteroids. First-line treatment of _H. pylori_ associated duodenal ulcers is eradication therapy using a one week course of amoxicillin, clarithromycin and a PPI, e.g. omeprazole. They should be tested 4-8 weeks later to ensure eradication",
"id": "33598",
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"explanation": "Gastric ulcers are peptic ulcers in the gastric mucosa. Gastric ulcers and duodenal ulcers have very similar risk factors, including H. pylori. Gastric ulcers are typically exacerbated upon eating, whereas in this case, eating relieves these symptoms. These symptoms are more typical of a duodenal ulcer; therefore this is the most likely diagnosis",
"id": "33599",
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"name": "Gastric ulcer",
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"explanation": "Gastric cancer can present with dyspepsia. However, it is an exceedingly rare diagnosis in a 24-year-old and would usually have red flag symptoms such as weight loss, vomiting or loss of appetite. Of note, mucosa-associated lymphoid tissue (MALT) lymphoma is a rare non-Hodgkin's lymphoma associated with H. pylori infection. However, given the typical temporal relation of symptoms to eating and the rarity of MALT lymphoma, duodenal ulcers are the most likely diagnosis",
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"explanation": "Biliary colic typically occurs after a heavy, fatty meal. This patient also isn't in the typical demographics, with biliary colic typically affecting middle-aged women with a high BMI. As eating makes this pain better, and this patient has _H. pylori_, a diagnosis of duodenal ulcer is more likely",
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"comment": "difference between CLO test and urea breath test? and also why is stool antigen test not done for H Pylori at all?",
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"explanation": "# Summary\n\nPeptic ulcer disease, encompassing both duodenal and gastric ulcers, is a condition where the stomach lining's self-protection mechanisms fail, often due to the presence of external factors like H. Pylori. Key signs and symptoms include pain, nausea, vomiting and loss of appetite. The primary investigation tool is endoscopy, which allows for a direct visual inspection of the ulcers. Management strategies include both pharmaceutical interventions, such as PPI treatment, and lifestyle changes, like cessation of smoking and dietary adjustments.\n\n# Definition\n\nPeptic ulcer disease refers to painful sores or ulcers in the lining of the stomach or the first part of the small intestine, known as the duodenum. The frequency of duodenal ulcers is four times higher than that of gastric ulcers. It is an endoscopic diagnosis (NB: dyspepsia is a clinical diagnosis). Peptic ulcer disease can be uncomplicated, or complicated (perforation, bleeding).\n\n# Epidemiology\n\nPeptic ulcer disease is a common condition, with the prevalence of duodenal ulcers being four times that of gastric ulcers. It's noteworthy that approximately 90% of duodenal ulcers are caused by H. Pylori infection.\n\n# Aetiology\n\nThe primary cause of duodenal ulcers is the infection by H. Pylori. Other factors contributing to the development of these ulcers include:\n\n- NSAIDs\n- Chronic use of steroids\n- SSRIs\n- Increased secretion of gastric acid\n- Smoking\n- Blood group O\n- Accelerated gastric emptying \n\nFor gastric ulcers, the risk factors include:\n\n- NSAIDs\n- H. Pylori infection\n- Smoking\n- Delayed gastric emptying\n- Severe stress\n\n# Signs and Symptoms\n\nPatients with peptic ulcer disease may present with:\n\n- Abdominal pain\n- Nausea\n- Vomiting\n- Loss of appetite\n- Unexplained weight loss\n- Patients with complicated peptic ulcer disease may present with coffee ground vomiting (bleeding), and can be haemodynamically unstable due to perforation\n\nDuodenal ulcers typically present with epigastric pain typically relieved on eating (closure of pyloric sphincter, less acid irritating ulcerated surface). Symptoms of gastric ulcers on the other hand are often worsened by eating - stomach increases acid production in response to food and irritates ulcerated surface.\n\n# Differential Diagnosis\n\nThe symptoms of peptic ulcer disease can mimic those of other conditions, including:\n\n- Gastritis: inflammation of the stomach lining, presenting with nausea, vomiting, and abdominal discomfort.\n- Gastro-oesophageal reflux disease (GORD): chronic acid reflux, characterized by heartburn, regurgitation, and swallowing difficulties.\n- Stomach cancer: may cause similar symptoms, but often accompanied by significant weight loss, loss of appetite, and anemia.\n\n# Investigations\n\n- Patients >55 with weight loss and dyspepsia should be referred for an urgent OGD (within 2 weeks) to investigate for oesophageal and gastric cancer\n- Patients should be investigated for H.pylori infection with C-13 urea breath test (ensure the person has not taken a PPI in the past 2 weeks, or antibiotics in the past 4 weeks)\n- Investigation tools for peptic ulcer disease primarily include endoscopy, which allows a direct visual inspection of the ulcers. Biopsies may be taken to rule out malignancy.\n\n# Management\n\nManagement of H. Pylori-negative peptic ulcer disease involves a 4-8 week course of full-dose PPI treatment in conjunction with lifestyle advice, such as:\n\n- Smoking cessation\n- Reducing alcohol intake\n- Regular, small meals and avoiding eating 4 hours before bedtime\n- Avoidance of acidic, fatty or spicy foods, and coffee\n- Weight loss if overweight \n- Stress management\n- Avoidance of NSAIDs, steroids, bisphosphonates, potassium supplements, SSRIs, and crack cocaine\n- Over-the-counter antacids\n\n\n- If the patient is H.pylori positive with a proven gastric/duodenal ulcer which is:\n\t- Associated with NSAID use: 8 week PPI therapy followed by first-line eradication therapy - PPI (omeprazole/lansoperazole) + amoxicillin + clarithromycin/metronidazole for 7 days\n\t\t- If penicillin allergic, offer: PPI + clarithromycin + metronidazole for 7 days \n\t- Not associated with NSAID use: eradication therapy with PPI (omeprazole/lansoperazole) + amoxicillin + clarithromycin/metronidazole for 7 days\n\t- If the person is allergic to pencillin and has had previous exposure to clarithromycin, offer a 7-day quadruple therapy regimen of:\nPPI + metronidazole + tetracycline hydrochloride + bismuth subsalicylate\n\n- For patients with gastric ulcers, a repeat endoscopy 6-8 weeks following the start of PPI treatment is recommended to ensure ulcer healing and rule out malignancy, as well as H.pylori re-testing (C-13 urea breath test first-line, stool antigen test second line) if appropriate.\n- Complicated peptic ulcer disease requires urgent surgical intervention with OGD for underunning of ulcers and haemostasis\n\t- Perforated peptic ulcers present initially with localised epigastric pain which later becomes generalised and peritonitic. These patients require an AXR and erect CXR to look for pneumoperitoneum. \n\n# NICE Guidelines\n\n[Click here to see more information NICE CKS on peptic ulcer disease](https://cks.nice.org.uk/topics/dyspepsia-proven-peptic-ulcer/management/management-proven-peptic-ulcer/)",
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"question": "A 24-year-old male presents to the GP with a one-month history of epigastric pain. This gets better after he eats a meal but is at its worst again a few hours later. On examination, the abdomen is soft with tenderness in the epigastrium. A urea breath test is performed, which is positive.\n\nWhat is the most likely diagnosis?",
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"explanation": "Irritable bowel syndrome causes diarrhoea/constipation, bloating and abdominal pain. Although it can be very distressing for some patients, it is not typically associated with any weight loss and does not cause any malabsorption or mouth ulcers. A colonoscopy would be normal in a patient with irritable bowel syndrome. Therefore, it is important to do the less invasive investigations first (e.g. blood tests, faecal calprotectin) to avoid performing any unnecessary procedures",
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"explanation": "Gastroenteritis typically has a shorter time course, not usually more than a few weeks. As this is a six-week history, in the absence of any foreign travel that may suggest an atypical cause like _Giardia lamblia_, most causes of gastroenteritis should have resolved by now. This would also not explain the mouth ulcers, weight loss or colonoscopy findings",
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"explanation": "Ulcerative colitis is another type of inflammatory bowel disease; however, there are some key differences that distinguish it from Crohn's disease. Firstly, these patients are more likely to present with rectal bleeding as the area of mucosa affected almost always starts in the rectum. Smoking also characteristically relieves symptoms of ulcerative colitis, whereas they are worsened in this case. Finally, on colonoscopy, ulcerative colitis creates a continuous lesion without any cobblestoning, with typical features of ulcerative colitis including pseudopolyps and crypt abscesses. These differences make Crohn's disease the more likely diagnosis",
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"explanation": "Colorectal cancer should always be considered in a patient over the age of 60 years old presenting with a new change in bowel habit according to NICE guidelines. However, this patient is also presenting with mouth ulcers, a previous episode of similar symptoms and pain on palpation of the right iliac fossa, which would not fit with the diagnosis of colorectal cancer. In addition, the colonoscopy findings are typical of Crohn's disease, and there was no indication of a mass that would suggest a diagnosis of colorectal cancer",
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"explanation": "Crohn's disease is a type of inflammatory bowel disease that can affect any area of the GI tract. It has a bimodal distribution, with a peak between 15-40 years old and 60-80 years old. Typical symptoms include abdominal pain, diarrhoea, weight loss, fever, malabsorption, mouth ulcers, perianal disease and systemic features (including dermatological, ophthalmic and rheumatological symptoms). Although it can affect any area of the GI tract, the ileocaecal junction is the most commonly affected area, which corresponds with the examination findings in this case. Although haematochezia may be seen in Crohn's disease, it is much more common in ulcerative colitis as the part of the GI tract affected in ulcerative colitis is usually more distal. Smoking exacerbates symptoms of Crohn's disease. Diagnosis involves blood tests (including ESR and CRP), faecal calprotectin and colonoscopy to confirm the diagnosis. Typical features on colonoscopy include skip lesions, cobblestone mucosa and non-caseating granulomas",
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"explanation": "# Summary\n\nCrohn's disease (CD) is a chronic, relapsing inflammatory bowel disease (IBD) characterized by transmural granulomatous inflammation. Key signs and symptoms include gastrointestinal and systemic symptoms, such as crampy abdominal pain, diarrhoea, weight loss, and fever. The disease is diagnosed primarily through blood tests and endoscopy with imaging. Management strategies include monotherapy with glucocorticoids, azathioprine, mercaptopurine, and biological agents for severe cases. Surgical management is rarely curative and should be maximally conservative.\n\n# Definition\n\nCrohn's disease (CD) is a chronic relapsing inflammatory bowel disease (IBD). It is characterised by transmural granulomatous inflammation which can affect any part of the gastrointestinal tract ('from mouth to anus', most commonly the terminal ileum, leading to fistula formation or stricturing.\n\n# Aetiology\n\nThe exact cause is unknown, but it is thought to be an inappropriate reaction to gut flora in a susceptible person. Important risk factors include:\n\n- Family history - 10-25% of patients have a first-degree relative who also suffers from Crohn's disease\n- **Smoking** - x3 increased risk\n- Diets high in refined carbohydrates and fats have been implicated\n\n# Epidemiology\n\nIn Europe the incidence of Crohn's disease is 5.6 per 100, 000 at ages 15-64. The disease is more common in northern climates and developed countries. In the last 60 years the incidence of Crohn's disease has increased in Europe and North America, and is now approximately equal to that of ulcerative colitis.\n\nCrohn's disease has a bimodal age of onset: the most common age of onset is between 15 and 40 years old, but there is a smaller secondary peak between 60-80 years.\n\nCrohn's disease is more common in Caucasian people than in Asian and black people. Ashkenazi Jews have a 2-4 fold higher risk of Crohn's disease.\n\n\n# Signs and Symptoms\n\nSymptoms: \n\n- Gastrointestinal symptoms (crampy abdominal pain and non-bloody diarrhoea)\n- Up to 50% have perianal disease\n- Systemic symptoms (weight loss and fever)\n\nSigns: \n\n- General appearance: cachectic and pale (secondary to anaemia), clubbing.\n- Abdominal examination: aphthous ulcers in the mouth, right lower quadrant tenderness and a right iliac fossa mass.\n- PR examination to check for perianal skin tags, fistulae, or perianal abscess.\n\n[lightgallery] \n\n**Extra-gastrointestinal manifestations include:**\n\nDermatological manifestations:\n\n- Erythema nodosum (painful erythematous nodules/plaques on the shins)\n- Pyoderma gangrenosum (a well-defined ulcer with a purple overhanging edge)\n\n[lightgallery1] [lightgallery2]\n\nOcular manifestations:\n\n- Anterior uveitis (painful red eye with blurred vision and photophobia)\n- Episcleritis (painless red eye).\n\nMusculoskeletal manifestation:\n\n- Enteropathic arthropathy (symmetrical, non-deforming)\n- Axial spondyloarthropathy (sacro-iliitis), \n\nHepatobiliary manifestations:\n\n- Gallstones (these are more common in Crohn's disease than in ulcerative colitis) - reduced bile acid reabsorption and increased calcium loss predisposes to gallstones\n\nHaematological and renal manifestations:\n\n- AA amyloidosis (secondary to chronic inflammation) and renal stones (more common in Crohn's disease than in ulcerative colitis)\n\n# Investigations \n\n- Bedside:\n\t- Stool culture is necessary to exclude infection (MC&S and ovas/cysts/parasite).\n\t- **Faecal calprotectin** (an antigen produced by neutrophils) will be raised (this helps distinguish inflammatory bowel disease from irritable bowel syndrome).\n\n- Blood tests:\n - Raised white cell count\n - Raised ESR/CRP\n - Thrombocytosis\n - Anaemia (secondary to chronic inflammation)\n - Low albumin (secondary to malabsorption)\n - Haematinics and iron studies including (B12, folate) due to terminal ileum involvement\n\n\n- Imaging:\n\t- Endoscopy with imaging is required for diagnosis. Small bowel video capsule endoscopy can be used for proximal disease\n\t- MRI can be used for suspected small bowel disease.\n\t- Upper GI series may show the 'string sign of Kantour'. This is used to describe the string-like appearance of contrast-filled narrowed terminal ileum, and is suggestive of Crohn's disease.\n\t- Colonoscopy with biopsy will reveal:\n\t\t- Intermittent inflammation **('skip lesions')**\n\t\t- Cobblestone mucosa (due to ulceration and mural oedema)\n\t\t- Rose-thorn ulcers (due to transmural inflammation), ± fistulae or abscesses.\n\t\t- Non-caseating granulomas\n\n# Management\n\n- As a general management point, it is paramount to advise patients with Crohn's who are smokers to **stop smoking** as this is known to strongly impact disease activity\n\n## Inducing remission\n\n- The first step of treatment is inducing remission in patients having a flare\n- Patients should be offered monotherapy with glucocorticoids (oral prednisolone, or IV hydrocortisone if first presentation is severe flare necessitating admission).\n- There is an increasing role for biologics for acute management of severe flares\n\n## Maintaining remission\n\n- Azathioprine or mercaptopurine may be added on to induce remission if there are 2 or more exacerbations in a 12-month period or the glucocorticoid cannot be tapered.\n\n - It is important to assess for thiopurine methyltransferase (TPMT) activity before offering azathioprine or mercaptopurine. If there is underactivity, this greatly increases the risk of profound bone marrow suppression if the above medications are given\n\n- Methotrexate may be considered in patients who are intolerant/have a contraindication to azathioprine or mercaptopurine or who do not respond to azathioprine or mercaptopurine monotherapy.\n- Biological agents (such as infliximab or adalimumab) are recommended in patients with severe Crohn's disease who fail to respond to the above.\n\t- These patients should have a CXR before treatment initiation due to the risk of re-activation of latent TB\n\n\n## Surgical management\n\nSurgical management is rarely curative in Crohn's disease (unlike in ulcerative colitis) because disease can occur anywhere along the GI tract, however 50-80% of Crohn’s patients end up requiring surgery at some point.\n\nSurgical options will depend on the part of the GI tract that is affected, and is indicated in those who have failed medical therapy or in those with severe stricturing or fistulating disease:\n\r\n-\tControl fistulae \r\n-\tResection of strictures\r\n-\tRest/defunctioning of the bowel\r\n\n\n### Management of peri-anal fistulae\n\n- Drainage seton is the management of choice for high (trans-sphincteric) fistulae. A seton is a thread passed through the fistula tract, forming a ring between the internal and external openings. It is used in the management of high trans-sphincteric fistulae, to prevent division of the anal sphincter muscles and incontinence. Closure of the fistula occurs by the formation of granulation tissue.\n- Fistulotomy is the management of choice for low (submucosal) fistulae. Fistulotomy involves dissecting the superficial tissue and opening the fistula tract. This is not a treatment option for high fistulae due to the risk of incontinence.\n- 'Sphincter saving' methods include fibrin glue and fistula plug - these are still under investigation and have not yet been approved in mainstream management.\n\n### Management of peri-anal abscess\n\n- The patient should be started on intravenous antibiotics e.g. ceftriaxone + metronidazole.\n- Patients typically require examination under anaesthetic and incision and drainage. An incision is made in the affected region, the pus is broken up, the infected tissue material is excised, and anti-septic soaked packs are inserted. Healing occurs by secondary intention.\n\n# Complications\n\n- **Fistulas:**\n - Formation of abnormal connections between different parts of the digestive tract or between the digestive tract and other organs.\n - Commonly involves the small intestine and other structures like the bladder or skin.\n\n- **Strictures:**\n - Narrowing or tightening of the intestinal walls.\n - Can lead to bowel obstruction and difficulties with the passage of stool.\n\n- **Abscesses:**\n - Collection of pus within the abdomen, often near areas of inflammation.\n - Presents with localized pain, swelling, and may require drainage.\n\n- **Malabsorption:**\n - Impaired absorption of nutrients due to inflammation and damage to the intestinal lining.\n - Can lead to nutritional deficiencies and weight loss.\n\n- **Perforation:**\n - Formation of a hole or tear in the intestinal wall.\n - Can result in peritonitis, a serious and potentially life-threatening condition.\n\n- **Nutritional Deficiencies:**\n - Chronic inflammation can affect nutrient absorption.\n - Common deficiencies include vitamin B12, vitamin D, and iron.\n\n- **Increased Risk of Colon Cancer:**\n - Prolonged inflammation may elevate the risk of developing colorectal cancer, particularly in long-standing disease involving the colon.\n\n- **Osteoporosis:**\n - Reduced bone density due to chronic inflammation and corticosteroid use.\n - Increases the risk of fractures.\n\n- **Intestinal Obstruction andToxic Megacolon:**\n - Severe inflammation can lead to the dilation of the colon.\n - Presents as abdominal distension, fever, and can be a medical emergency.\n\n\n# Comparison with Ulcerative Colitis\n\nPlease see below a summary table comparing Crohn's disease and Ulcerative colitis:\n\n| Characteristic | Crohn's Disease | Ulcerative Colitis |\n|------------------------------------|---------------------------------------|-------------------------------------|\n| **Location** | Any part of the digestive tract, from the mouth to the anus (most commonly affects the terminal ileum and colon) | Limited to the colon and rectum |\n| **Inflammation Pattern** | Patchy, skip lesions | Continuous, involves the entire colon|\n| **Depth of Inflammation** | Full thickness (transmural) | Limited to the inner lining (mucosa and submucosa)|\n| **Symptoms** | Abdominal pain, non-bloody diarrhoea, weight loss | Bloody diarrhoea, abdominal cramps |\n| **Complications** | Fistulas, strictures, abscesses | Toxic megacolon, colon cancer risk |\n| **Extraintestinal Manifestations** | Joint pain, skin problems, eye inflammation | Joint pain, skin problems, eye inflammation |\n| **Endoscopy Findings** | Cobblestone appearance, deep ulcers | Continuous colonic inflammation, ulcers |\n| **Diagnostic Imaging** | Transmural inflammation visible on imaging (e.g, MRI) | Limited to the colonic mucosa and submucosa, visible on colonoscopy |\n| **Treatment Approach** | Individualised, may involve medications (e.g. steroids, immunosuppressants) and surgery | Medications (e.g. aminosalicylates, steroids, immunosuppressants), surgery (in severe cases) |\n| **Prognosis** | Variable, chronic condition with periods of remission and exacerbation | Variable, can be chronic with periods of remission, may require surgery in some cases |\n\n\n# NICE Guidelines\n\n[Click here to see information on NICE CKS on Crohn's disease](https://cks.nice.org.uk/topics/crohns-disease/)\n\n",
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"question": "A 62-year-old man presents to the GP with a history of diarrhoea. This has been occurring over the last six weeks, and he is now passing at least six stools a day. He has also lost around 7kg in weight. He had similar symptoms in his 20s, which worsened with smoking. On examination, he has multiple painful ulcers in his mouth and a soft abdomen with tenderness in the right iliac fossa. He is later seen in gastroenterology, where a colonoscopy is performed, showing areas of cobblestone mucosa separated by areas of normal mucosa.\n\nWhat is the most likely diagnosis?",
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"explanation": "Hypercalcaemia has a broad range of features, including renal stones, bone pain, constipation, nausea, abdominal pain, confusion, polydipsia, polyuria, depression and psychosis. Over 90% of cases of hypercalcaemia are due to either primary hyperparathyroidism or malignancy, with other causes including sarcoidosis and Paget's disease of the bone. Although hypercalcaemia can cause polyuria and polydipsia (due to nephrogenic diabetes insipidus), diffuse abdominal pain and nausea, this does not explain the presence of Kussmaul breathing or hyperglycaemia. Therefore diabetic ketoacidosis is the most likely diagnosis",
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"explanation": "Diabetes insipidus is a rare condition affecting either the production of antidiuretic hormone (cranial) or the kidney's sensitivity to antidiuretic hormone (nephrogenic). These patients present with very severe dehydration, polydipsia and polyuria. However, they would not present with Kussmaul breathing or hyperglycaemia, making diabetic ketoacidosis the more likely diagnosis",
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"explanation": "Hyperglycaemic hyperosmolar state (HHS) is a rare condition associated with type 2 diabetes. As a 19-year-old patient, in the absence of obesity, this patient is very unlikely to have type 2 diabetes. In addition, they have Kussmaul breathing suggesting metabolic acidosis. Metabolic acidosis is not a feature of HHS",
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"explanation": "Appendicitis will typically have a shorter history over a few hours. They will typically have more localised abdominal pain, with nausea and low-grade fever. Kussmaul breathing, polydipsia, dehydration and hyperglycaemia are not typical features of appendicitis",
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"explanation": "This is a typical presentation of diabetic ketoacidosis (DKA). This patient presents with a prodrome of type 1 diabetes symptoms (including polydipsia and weight loss) which have now worsened. They have deep, laboured breathing in keeping with Kussmaul breathing, a sign of metabolic acidosis. They are also dehydrated, which is common in DKA. Their capillary glucose is 26, which is >11 mmol/L (part of the diagnostic criteria for DKA). Other diagnostic criteria include blood ketones ≥3 mmol/L and metabolic acidosis (pH <7.3 or bicarbonate <15). Management of this patient would include IV 0.9% NaCl (initially 1L over 1 hour), a fixed rate insulin infusion (0.1 units/kg/hour). Potassium is added to further bags of 0.9% NaCl (as insulin can cause hypokalaemia), and the underlying cause of their DKA should be considered (e.g. sepsis, non-compliance, myocardial infarction)",
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"explanation": "# Summary\n \nDiabetic ketoacidosis (DKA) is a life-threatening medical emergency characterised by hyperglycemia, acidosis and ketosis. DKA may be triggered by infection, dehydration or fasting, or may be the initial presentation of Type 1 diabetes. Symptoms include a 'fruity' breath odour, vomiting, dehydration, abdominal pain and altered mental state. Key investigations include blood glucose and ketones, urea and electrolytes and a venous blood gas to check pH. Management involves IV fluids and a fixed rate insulin infusion, with close monitoring both clinically and biochemically. Important complications that should be monitored for include cerebral oedema, hypoglycaemia and hypokalaemia. \n\n# Definition\n \nDiabetic ketoacidosis (DKA) is a medical emergency characterised by the triad of:\n \n - Hyperglycemia (blood glucose >11 mmol/L)\n - Ketosis (blood ketones >3 mmol/L or urinary ketones ++ or higher)\n - Acidosis (pH <7.3 or bicarbonate <15 mmol/L)\n - Note: patients on SGLT-2 inhibitors may present with euglycemic DKA (where glucose is normal)\n \n\n# Epidemiology\n \nDKA is most common in individuals with Type 1 diabetes (T1DM) but around a third of cases occur in patients with Type 2 diabetes. The incidence of DKA is highest in young people aged 18-24. \n\nDKA is the leading cause of death in people aged under 58 years old with T1DM, with cerebral oedema the most common cause of mortality. However, mortality in the UK is still <1%.\n \n\n# Aetiology \n\n- DKA occurs due to insulin deficiency (absolute or relative) leading to hyperglycaemia\n- Ketones, including acetone, 3-beta-hydroxybutyrate, and acetoacetate, are produced from ketogenesis, whereby fatty acids are metabolised as an alternative energy source\n- These ketones are responsible for the acidosis seen\n- Hyperglycaemia causes an osmotic diuresis that contributes to severe dehydration as well as electrolyte imbalance\n- Vomiting and decreased fluid intake secondary to altered mental state also exacerbate dehydration\n\n**10-20% of presentations of DKA represent a first presentation of Type 1 Diabetes**\n\n**Common triggers for DKA include:**\n\n- Infections\n- Dehydration and fasting\n- Missing doses of insulin\n- Medications e.g. steroid treatment or diuretics\n- Surgery\n- Stroke or myocardial infarction\n- Alcohol excess or illicit drug use\n- Pancreatitis\n\n# Classification\n\nPatients with at least one of the following may be classified as having **severe DKA**, which should prompt consideration of referral for higher dependency care:\n\n- Blood ketones > 6mmol/L\n- Bicarbonate < 5mmol/L\n- Blood pH < 7\n- Anion gap above 16\n- Hypokalaemia on admission\n- GCS less than 12\n- Oxygen saturations < 92% in air\n- Systolic BP < 90mmHg\n- Brady or tachycardia (heart rate < 60 or > 100bpm)\n\n\n# Signs and Symptoms\n \n**Symptoms:**\n\n- Nausea and vomiting\n- Abdominal pain\n- Polyuria\n- Polydipsia\n- Weakness\n\n**Signs:**\n\n- Dry mucous membranes\n- Hypotension\n- Tachycardia\n- Altered mental state (drowsiness, confusion, coma)\n- Kussmaul's breathing (deep, sighing breathing to compensate for metabolic acidosis by blowing off carbon dioxide)\n- Fruit-like smelling breath (due to ketosis)\n\n# Investigations\n \n**Bedside tests:**\n \n - Capillary blood glucose\n - Blood or urinary ketones\n - Urine dip +/- MSU (looking for evidence of a urinary tract infection which may precipitate DKA)\n - ECG (for ischaemic changes which may precipitate DKA, or changes secondary to electrolyte imbalance e.g. hypokalaemia)\n\n**Blood tests:**\n\n- Venous blood gas (for acid-base balance)\n- Urea and electrolytes (for electrolyte imbalance and AKI)\n- Full blood count and CRP (for infection markers) \n- Blood cultures (if infection is suspected)\n- HbA1c (to assess diabetic control over recent months)\n\n**Imaging:**\n\n- Consider chest X-ray as part of septic screen (if signs of infection as a trigger for DKA)\n\n# Management\n\n**Initial management:** \n\n- Initial **A to E assessment**\n - Drowsy patients may require airway protection and an **NG tube** to prevent aspiration\n - Ensure adequate IV access\n - If hypotensive give up to 1L in **fluid boluses** then seek urgent senior input if not resolved\n - Consider urinary catheterisation and monitor fluid balance\n- **IV fluid replacement with normal saline**\n - A regimen of large volumes of IV fluid replacement given relatively quickly initially then over longer durations should be followed\n - Slower infusion rates should be considered in young adults, the elderly, those with heart or kidney failure or other serious comorbidities\n - An example in a healthy adult would be 1L over 1 hour, then 2x 1L over 2 hours, then 2x 1L over 4 hours, then 1L over 6 hours\n - **Potassium replacement** should be added after the first bag, depending on serum potassium levels, bearing in mind potassium can be infused at a maximum of 10mmol/h:\n\n| Potassium level (mmol/L) | Potassium replacement mmol/L of next infusion | \n| :---------------: | :----------------: \n| > 5.5 | Nil | \n| 3.5 - 5.5 | 40 mmol/L | \n| < 3.5 | senior review – additional potassium required | \n \n \n- After IV fluids have started, a **fixed rate insulin infusion** should be set up \n- This is provided as an infusion of 50 units of Actrapid in 50ml of 0.9% NaCl, at a rate of 0.1 units/kg/hour\n- Continue long-acting insulin if the patient is already on this \n- Investigation and management of any underlying triggers (e.g. septic screen and start antibiotics if evidence of infection)\n- Ensure **VTE prophylaxis** with low molecular weight heparin is prescribed as patients are at high risk of developing clots due to dehydration\n\n**Ongoing emergency management:**\n\n- Patients should be closely monitored with hourly blood glucose and ketones\n - The aim is for ketones to fall by > 0.5mmol/L/hour\n - Blood glucose should fall by 3 mmol/L/hour\n - If these targets are not met, the rate of insulin infusion should be continued\n- Once blood glucose is below 14, a **10% glucose infusion** should be started alongside ongoing saline and insulin\n- Regular venous blood gases should also be done to monitor potassium, bicarbonate and pH\n- DKA is considered resolved once ketones are less than 0.6 mmol/L and pH is over 7.3 \n - If at this point they are able to eat and drink, a subcutaneous regimen of insulin should be started (usually with the input of a specialist diabetes team)\n - The insulin infusion should be stopped half an hour after the first dose of subcutaneous short acting insulin has been given \n\n# References\n \n[ABCD Guidelines: The Management of Diabetic\nKetoacidosis in Adults](https://abcd.care/sites/default/files/site_uploads/JBDS_Guidelines_Current/JBDS_02_DKA_Guideline_with_QR_code_March_2023.pdf)\n\n[RCEM - Diabetic Ketoacidosis](https://www.rcemlearning.co.uk/reference/diabetic-ketoacidosis/#1635853037528-05d8fa0f-621f)\n\n[Patient UK - Diabetic ketoacidosis](https://patient.info/doctor/diabetic-ketoacidosis#presentation)",
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"question": "A 19-year-old man presents to the emergency department with diffuse abdominal pain and nausea. He has been feeling very thirsty for the past two weeks and lost some weight over that time period. On examination, he has dry mucous membranes, is tachypnoeic and breathing deeply. His capillary blood glucose level is 26.\n\nWhat is the most likely diagnosis?",
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"explanation": "In asymptomatic patients, two separate readings are required for diagnosis. As this patient has only had one reading, they cannot be diagnosed with type 2 diabetes at this point, but they should have a follow-up reading to confirm the diagnosis",
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"explanation": "The diagnosis of type 2 diabetes depends on whether the patient is symptomatic or asymptomatic. For symptomatic patients, only one positive HbA1c, fasting glucose or random glucose is used for diagnosis. In asymptomatic patients, two separate readings are required for diagnosis. As this patient has only had one reading, they cannot be diagnosed with type 2 diabetes at this point, but they should have a follow-up reading to confirm the diagnosis",
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"explanation": "In asymptomatic patients, two separate readings are required for diagnosis. NICE CKS recommends the same modality that was used for the original test is used, meaning HbA1c is the most appropriate answer, as this is the test that was originally used",
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"explanation": "# Summary\n\nType 2 Diabetes Mellitus is a chronic metabolic disorder characterised by pancreatic beta-cell insufficiency and insulin resistance. The resulting hyperglycaemia leads to symptoms such as polyuria, polydipsia and if chronic can have microvascular and macrovascular complications. Key investigations include random and fasting blood glucose, 2-hour glucose tolerance, and HbA1C tests, and diagnosis is based on the results of these +/- symptoms. Management of type 2 diabetes primarily revolves around lifestyle modifications, hypoglycaemic agents, and insulin therapy when necessary, as well as reducing risks for serious complications such as cardiovascular and cerebrovascular disease. Other complications from chronic hyperglycaemia involve the gastrointestinal system, nervous system, peripheral arteries, foot infections, sexual dysfunction, and cardiac system. \n\n# Definition\n\nType 2 Diabetes Mellitus (T2DM) is a chronic metabolic condition characterized by inadequate insulin production from pancreatic beta cells, resulting in insulin resistance. This leads to an elevation in blood glucose levels, causing hyperglycaemia.\n\n# Epidemiology\n\nT2DM generally manifests in adults, and it is often associated with a strong familial predisposition. It accounts for approximately 90-95% of all diagnosed cases of diabetes.\n\n# Aetiology\n\nT2DM results from a combination of genetic and environmental factors. Known contributors include:\n\n- Poor dietary habits\n- Lack of physical activity\n- Obesity\n\n# Signs and symptoms\n\nIndividuals with T2DM may initially be asymptomatic, but over time, they may develop:\n\n- Polyuria\n- Polydipsia\n- Unexplained weight loss\n- Blurry vision\n- Fatigue\n\n# Differential diagnosis\n\nThe primary differentials for T2DM include Type 1 Diabetes Mellitus, Maturity Onset Diabetes of the Young (MODY), and Secondary Diabetes Mellitus. The main distinguishing features of these differentials are:\n\n- Type 1 Diabetes Mellitus: Early onset (typically in childhood or adolescence), often presents with ketoacidosis, and requires insulin therapy from diagnosis.\n- MODY (Maturity Onset Diabetes of the Young):\n\t- MODY 3 is the commonest cause, occurring due to a mutation in HNF1A. It is characterised by a very high blood sugar (10-20), and is very sensitive to sulphonylureas (e.g. gliclazide.) Insulin is the next line of treatment if it doesn't respond.\n\t- MODY 2 is the second commonest cause, occurring due to a glucokinase mutation. Blood sugars rarely rise above 7-8, over many years. Patients are generally well with few complications and the diabetes often responds to diet alone.\n\t- MODY 5 is associated with HNF1 beta mutation, and is associated with pancreatic atrophy, renal cycsts (causing palpable kidneys), epidydymal cysts, a bicornuate uterus, and abnormal LFTs\n- Secondary Diabetes Mellitus: Often presents with other signs of pancreatic disease (e.g., pancreatitis, cystic fibrosis), or due to certain medications (e.g., glucocorticoids, antipsychotics).\n\n# Investigations\n\nIf symptomatic, one of the following results is sufficient for diagnosis:\n\n- Random blood glucose ≥ 11.1mmol/l\n- Fasting plasma glucose ≥ 7mmol/l\n- 2-hour glucose tolerance ≥ 11.1mmol/l\n- HbA1C ≥ 48mmol/mol (6.5%)\n\nIf the patient is asymptomatic, two results are required from different days.\n\n# Management\n\nManagement of T2DM involves patient education, lifestyle modifications, pharmacological interventions, and close monitoring of glucose levels:\n\n- Lifestyle modifications: Advice on diet, regular physical activity, and smoking cessation\n- Pharmacological interventions: \n\t- Initial drug treatment is usually metformin, with consideration of other agents like Pioglitazone, DPP‑4 inhibitors, sulphonylureas, or SGLT-2 inhibitors for those who cannot take metformin.\n\t- If on monotherapy HbA1c >58mmol/mol consider dual therapy with metformin, pioglitazone, a DPP‑4 inhibitor or a sulphonylurea (such as gliclizide).\n\t- If dual therapy has not controlled drug glucose, triple therapy using the above medications can be considered. Otherwise, starting insulin may be necessary.\n- Close Monitoring: Measure HbA1c levels at 3-6 month intervals. If the patient is on insulin or is at risk of hypoglycaemia, self-monitoring of glucose at home is necessary.\n\n\n**Insulin Therapy**\n\nNICE guidance recommends basal insulin therapy with isophane (NPH) insulin as the first type to be used as it is most cost effective eg. Insulatard. Quick acting insulin analogues eg. Humalog, Novorapid, may be added in with meals if there is a big post meal glucose excursion.\n\nLong acting insulin analogues include Levemir, Lantus, Insulin Degludec and Abasaglar (a biosimilar insulin).\n\nMixed insulin combination which contain varying proportions of short and intermediate acting insulin such as Novomix 30 (30% short acting, 70% intermediate acting insulin) are more convenient because of fewer injections per day but may not be as successful.\n\n**Blood Pressure targets in Diabetes**\n\n- Blood pressure control needs to be strict in diabetes because these patients are at higher risk of macro- and microvascular complications.\n- NICE Hypertension Guidance [CG136] sets the same blood pressure targets as those who do not have diabetes, however in diabetics with HTN, ACE-inhibitors are first line as they are reno-protective\n\n# Complications\n\nComplications of diabetes are diverse, affecting multiple systems:\n\n### Macrovascular:\n\n* **Cardiac Complications** - diabetes significantly increases the risk of cardiovascular disease, contributing to major morbidity and mortality.\n* **Peripheral Arterial Disease (PAD)** - patients present with foot discolouration, gangrene, intermittent claudication, rest pain, night pain and absent peripheral pulses (confirmed on doppler).\n* **Cerebrovascular disease** - patients with diabetes are at significantly increased risk of TIAs and stroke and as such it is paramount to address the main risk factors (lipids, BP, smoking, obesity) for these as a broader part of management\n\n\n### Microvascular:\n\n* **Diabetic retinopathy** - characterised by vascular occlusion and leakage in the retinal capillaries, leading to potential sight loss if unmanaged, it is the leading cause of visual loss in adults. See separate section.\n* **Diabetic nephropathy** - a leading cause of chronic kidney disease, it is characterised by proteinuria. Prevention of this complication is achieved with ACE inhibitors/ARBs (by managing blood pressure) and SGLT-2 inhibitors.\n\t* Histological changes include Kimmelstiel-Wilson nodules which are the spherical, eosinophilic, sclerotic nodules characteristic of nodular diabetic glomerulosclerosis \n* **Diabetic neuropathy** - the primary causative factor is chronic hyperglycaemia, which leads to several distinct types neuropathy. See separate section.\n\t* **Autonomic Neuropathy** - may lead to postural hypotension and associated symptoms like dizziness, falls, and loss of consciousness.\n\t* **Gastrointestinal Complications: Gastroparesis** - a result of poor glycaemic control leading to nerve damage of the autonomic nervous system. Characterized by delayed gastric emptying, early satiety, abnormal stomach wall movements, and morning nausea.\n\t* **Foot Complications: Diabetic Foot Infections** - patients with vascular and neuropathic complications are at high risk for diabetic foot ulceration and subsequent infection.\n* **Sexual Dysfunction** - caused by a combination of factors including poor glycaemic control, neuropathy, microvascular complications, obesity, hypertension, depression, medication side effects, etc.\n\n# 'Sick day' rules\n\n1. **Temporary Medication Adjustments**: During acute illness, consider temporarily stopping certain medications until the person is eating and drinking normally for 24–48 hours. \n\t- **Angiotensin-Converting Enzyme Inhibitors (ACEIs), Diuretics, and NSAIDs**: Stop treatment if there is a risk of dehydration to reduce the likelihood of acute kidney injury (AKI).\n\n3. **Metformin**: Stop treatment if there is a risk of dehydration to lower the risk of lactic acidosis.\n\n4. **Sulfonylureas**: Be cautious, as they may increase the risk of hypoglycemia, especially if dietary intake is reduced.\n\n5. **SGLT-2 Inhibitors**: Check for ketones and stop treatment if acutely unwell and/or at risk of dehydration due to the risk of euglycemic diabetic ketoacidosis (DKA).\n\n6. **GLP-1 Receptor Agonists**: Stop treatment if there is a risk of dehydration to reduce the risk of AKI.\n\n7. **Insulin Therapy**: Do not stop insulin treatment; instead, consider adjusting the dose with guidance from the specialist diabetes team.\n\n8. **Blood Glucose Monitoring (if indicated)**: \n - Increase monitoring frequency to at least every 3–4 hours, including overnight.\n - Adjust insulin doses based on results.\n - Continue careful monitoring until blood glucose levels return to baseline.\n - Seek urgent medical advice if blood glucose remains uncontrolled.\n\n9. **Ketone Monitoring (Blood or Urinary)**: \n - Check ketone levels regularly (at least every 3–4 hours, including overnight).\n - Seek immediate medical advice if urine ketone level is greater than 2+ or blood ketone level is greater than 3 mmol/L.\n\n10. **Maintain Normal Meal Pattern**: Encourage maintaining regular meals and fluids, including carbohydrates, if appetite is reduced.\n\n11. **Fluid and Carbohydrate Replacement**:\n - If unable to eat or vomiting, replace meals with carbohydrate-containing drinks (e.g. fruit juices, sugary drinks).\n - Adjust fluid intake based on blood glucose levels (sugar-free fluids for high levels, sugary fluids for low levels).\n\n\n\n# NICE Guidelines\n\n[Click here for NICE CKS on T2DM](https://cks.nice.org.uk/topics/diabetes-type-2/)\n",
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"question": "A 55-year-old man presents to the general practice after being invited for their 5-yearly NHS health check. They are currently asymptomatic with no past medical history. Their examination and blood results are normal, besides a BMI of 32 and a HbA1c of 53 mmol/mol.\n\nWhich of the following investigations is most likely to confirm the diagnosis?",
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"explanation": "Denosumab is a monoclonal antibody therapy that is used for the treatment of osteoporosis. Denosumab is used second line for osteoporosis, so would only be initiated if bisphosphonates were not tolerated or are contraindicated",
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"explanation": "The FRAX® score is used to risk stratify a patient for the probability of a major osteoporotic fracture over the next ten years.\nAs this patient has intermediate risk, the next most appropriate step is to get a DEXA scan",
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"explanation": "The FRAX® score is used to risk stratify a patient for the probability of a major osteoporotic fracture over the next ten years.\n\nAs this patient has intermediate risk, the next most appropriate step is to get a DEXA scan. They may need to start bisphosphonate therapy based on the result of the DEXA scan, but a DEXA scan should be performed first",
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"name": "Start oral bisphosphonate therapy",
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"explanation": "Dental checkups are recommended before and during bisphosphonate therapy. This is because of the risk of osteonecrosis of the jaw while taking bisphosphonate therapy. As this patient is intermediate risk, they should have a DEXA scan before bisphosphonates are considered. Therefore, a dental checkup is not the next best step in management as they may not need to start bisphosphonate therapy",
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"explanation": "The FRAX® score is used to risk stratify a patient for the probability of a major osteoporotic fracture over the next ten years. In accordance with National Osteoporosis Guideline Group (NOGG) 2017 guidelines, they are stratified into:\n\n- Low risk - give reassurance and lifestyle advice, reassess within the next five years.\n- Intermediate risk - perform a DEXA scan to guide management.\n- High risk - start bisphosphonate therapy; no need to perform a DEXA scan first.\n\nA DEXA scan is used to measure bone mineral density. A T score of <-2.5 is diagnostic for osteoporosis.\nAs this patient has intermediate risk, the next most appropriate step is to get a DEXA scan",
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"explanation": "# Summary \r\n\r\nOsteoporosis is a chronic condition characterised by low bone density and increased propensity to sustain fragility fractures. It is diagnosed with a dual-energy X-ray absorptiometry (DEXA) scan if a patient's T-score is less than -2.5. It is very common in older patients, especially post-menopausal women, with other risk factors including long-term corticosteroid use, low body weight and immobility. Other key investigations include checking calcium and vitamin D levels as these may require supplementation if low. Treatment is with bone-sparing treatment, with bisphosphonates being the first-line option in the majority of patients. Lifestyle changes such as smoking cessation, taking regular exercise and maintaining a healthy diet are important. Falls risk assessment is also key to reducing the risk of fragility fractures, especially in older patients. \r\n\r\n# Definition\r\n\r\nOsteoporosis refers to a state of low bone density with structural deterioration of bones. This causes bones to weaken, increasing the risk of fragility fractures (defined as a fracture sustained due to a fall from standing or without any trauma). \r\n\r\nPatients are defined as having osteoporosis if their bone mineral density (BMD) is at least 2.5 standard deviations below the mean peak mass of young healthy adults. This is measured with a dual-energy X-ray absorptiometry (DEXA) scan which gives BMD for the lumbar vertebrae and the femur. \r\n\r\n# Epidemiology\r\n\r\n- In the UK, around 2 million people are estimated to have osteoporosis\r\n- Post-menopausal women are particularly at risk due to accelerated bone loss secondary to decreased oestrogen production\r\n- Prevalence also increases significantly with age\r\n- Almost 50% of 80 year old women have osteoporosis\r\n- White ethnicity is also a risk factor\r\n- There are approximately 300,000 fragility fractures per year in the UK, with osteoporosis often being undiagnosed at the time of presentation\r\n\r\n# Aetiology\r\n\r\nRisk of fragility fractures increases as bone density declined, however there are many other factors that increase fracture risk:\r\n\r\n| Risk factors reducing bone density | Risk factors that do not reduce bone density |\r\n|----------|----------|\r\n| Low body weight | Older age |\r\n| Menopause | Inflammatory arthritis (e.g. rheumatoid arthritis) |\r\n| Immobility | Prolonged use of oral corticosteroids |\r\n| Chronic disease e.g. chronic kidney disease, chronic obstructive pulmonary disease, chronic liver disease | Smoking |\r\n| Malabsorption e.g. coeliac disease, inflammatory bowel disease, pancreatic insufficiency | Alcohol excess |\r\n| Endocrine disease e.g. hyperparathyroidism, hyperthyroidism | History of fragility fracture |\r\n| Certain medications (proton pump inhibitors, selective serotonin reuptake inhibitors, carbamazepine) - mixed evidence | Parental hip fracture |\r\n\r\n# Signs and Symptoms\r\n\r\nOsteoporosis itself is asymptomatic and so is usually diagnosed either with screening of people at high risk (e.g. those on long-term corticosteroids) or when someone presents with a fragility fracture.\r\n\r\nThe most common fragility fractures seen are:\r\n\r\n- Vertebral body\r\n- Neck of femur (hip)\r\n- Distal radius\r\n- Proximal humerus\r\n- Pelvis\r\n\r\nSome osteoporotic fractures (e.g. vertebral fractures) may also be asymptomatic acutely. Loss of height and kyphosis may occur due to multiple vertebral fractures, with severe kyphosis leading to reduced mobility and function.\r\n\r\nOther common symptoms of fragility fractures include acute severe pain, difficulty weight-bearing (e.g. for a hip fracture) and mobilising. \r\n\r\nSigns include deformities, such as a shortened and externally rotated leg due to a hip fracture or a \"dinner fork\" deformity in a Colles' wrist fracture.\r\n\r\nThe area around the fracture may be bruised, swollen and tender to touch. \r\n\r\n# Differential Diagnosis\r\n\r\n- **Bone metastases** may lead to pathological fractures, either in patients with known malignancies or as a first presentation of cancer (especially lung, prostate, breast, kidney and thyroid)\r\n- **Osteomalacia** usually occurs secondary to severe vitamin D deficiency and increases fracture risk due to bone weakening; other symptoms include bone pain, muscle pain and proximal weakness with a waddling gait\r\n- **Multiple myeloma** also is associated with pathological fractures, as well as hypercalcaemia, renal impairment, anaemia and bone pain\r\n- **Paget's disease** increases the risk of fracture due to abnormal bone remodelling, leading to features of bone pain and bowing of the long bones\r\n- **Osteogenesis imperfecta** is a genetic condition that commonly presents in childhood with fragility fractures, bowing of the long bones, short stature and blue sclera\r\n- **Avascular necrosis** may mimic a spontaneous fracture with severe pain after no or minimal trauma, commonly affecting the femoral head\r\n\r\n# Investigations\r\n\r\n- The diagnostic investigation for osteoporosis is a **dual-energy X-ray absorptiometry scan (DEXA)**\r\n- This measures **bone mineral density (BMD)**\r\n- A T-score of -2.5 or less is considered diagnostic of osteoporosis\r\n- If the T-score is between -1 and -2.5 this is referred to as osteopenia\r\n- Z-score is also reported (this compares bone density to a age, sex and ethnicity matched population rather than healthy young adults) - below -2 is low for their age\r\n- The following patients should be offered a DEXA scan as the initial step in assessment\r\n- Aged over 50 presenting with a fragility fracture\r\n- Aged under 40 with a major risk factor for fragility fracture (e.g. long-term steroids) \r\n- Those about to start treatment that will rapidly decrease bone density (e.g. hormone deprivation in breast cancer) - consider\r\n- All other patients with risk factors should have their fracture risk assessed as the initial step\r\n- **QFracture** and **FRAX** are the two online assessment tools used\r\n- These both predict a patient's 10-year risk of hip and major osteoporotic fractures\r\n- QFracture is interpreted based on whether the risk score is greater or less than 10%\r\n- FRAX plots fracture risk versus age on a graph that stratifies people into low/intermediate/high risk\r\n- With QFracture, those at approximately 10% risk or more at 10 years should have a DEXA scan \r\n- With FRAX, patients at intermediate or high risk of fracture should have a DEXA\r\n- In women over the age of 75 with a history of fragility fractures, a clinical diagnosis of osteoporosis may be appropriate (if a DEXA is unfeasible)\r\n\r\nOther investigations required in all patients include:\r\n\r\n- **Vitamin D** to check for deficiency; this is needed prior to starting bisphosphonate treatment\r\n- **Bone profile** to check serum calcium as this may also require supplementation\r\n- **X-rays** or other imaging modalities (e.g. CT or MRI) may be required to diagnose and assess fragility fractures\r\n\r\nIf an underlying cause is suspected, the following investigations may be appropriate:\r\n\r\n- **Full blood count** which may show anaemia in malabsorption or malignancy, and leukocytosis in malignancy or inflammatory disease\r\n- **Liver function tests** for chronic liver disease\r\n- **U&Es** for chronic kidney disease\r\n- **ESR** or **CRP** which may be raised in inflammatory disease or malignancy\r\n- **Thyroid function tests** if hyperthyroidism is suspected\r\n- **Testosterone** and **sex hormone-binding globulin** if hypogonadism is suspected in men\r\n- **Anti-TTG antibodies** for coeliac disease if there is evidence of malabsorption\r\n\r\n# Management\r\n\r\n**Conservative management:**\r\n\r\n- Identification and treatment of any underlying condition contributing to osteoporosis\r\n- Optimisation of risk factors e.g. smoking cessation, alcohol reduction\r\n- Advise patients to take regular weight-bearing exercise to improve muscle strength, including walking, strength training and balance and flexibility training\r\n- Advise patients to eat a balanced diet and assess their calcium intake\r\n- Assess falls risk and consider measures to reduce this, including referral to multidisciplinary falls teams \r\n- Referral to specialist services for patients with very high fracture risk (e.g. T score less than -3.5, multiple vertebral fractures)\r\n\r\n**Medical management:**\r\n\r\n- Prescribing vitamin D supplementation for patients not exposed to adequate sunlight\r\n- Prescribing calcium supplements to patients with an inadequate dietary calcium intake\r\n- For patients at high risk of fragility fracture, prescribe bone-sparing treatment\r\n- Treatment should be started promptly after a fragility fracture to reduce the risk of another fracture\r\n- Oral bisphosphonates are the first-line treatment in the majority of patients \r\n- Options include alendronate and risedronate, which can be given either daily or weekly\r\n\t- These must be taken on an empty stomach, at least 30 minutes before food or other medications\r\n\t- Tablets need to be swallowed whole with a glass of water whilst the patient is upright; they should stay upright for at least 30 minutes after this\r\n\t- Common side effects include nausea, dyspepsia, gastritis, abdominal pain and musculoskeletal pains\r\n\t- Rarer side effects include oesophagitis or ulceration, stricturing or erosions, osteonecrosis of the jaw or external auditory canal and atypical stress fractures\r\n\t- To minimise risk of osteonecrosis of the jaw, patients with poor dentition or malignancy should have a dental check-up (and any work required performed) before starting bisphosphonates\r\n\t- They should also continue to have routine dental checks and maintain good oral hygiene during treatment \r\n\t- Contraindications include severe chronic kidney disease, hypocalcaemia or vitamin D deficiency, and oesophageal abnormalities such as stricture or achalasia \r\n\t- Patients with recent peptic ulceration, upper gastrointestinal bleeding or surgery, dysphagia, gastritis or duodenitis should be prescribed bisphosphonates with caution\r\n- If oral bisphosphonates are not tolerated or unsuitable, options for bone-sparing treatment include:\r\n\t- Parenteral bisphosphonates (e.g. zoledronate)\r\n\t- Denosumab\r\n\t- Raloxifene hydrochloride\r\n\t- Strontium ranelate\r\n\t- Hormone replacement therapy should be considered for younger women experiencing menopausal symptoms as this will also reduce their fragility fracture risk\r\n\t- Teriparatide and romosozumab are other bone-sparing treatments that may be recommended first-line in women with severe osteoporosis - these are then followed by bisphosphonate treatment\r\n\r\n**Surgical management:**\r\n\r\n- Fragility fractures may require surgical fixation or joint replacement (e.g. hip arthroplasty for a fractured neck of femur)\r\n\r\n# Complications\r\n\r\n- Hip fractures are high-consequence injuries and lead to permanent disability in 50% and death in 20% of patients \r\n- Vertebral fractures may lead to disabling and painful kyphosis which may in turn cause difficulty breathing and gastrointestinal problems such as dyspepsia\r\n- Wrist fractures can significantly affect independence and functional ability\r\n- Many patients experience a \"fracture cascade\" where further fractures occur in the years following the initial one\r\n- Pain from fractures can lead to poor sleep, low mood and reduced quality of life\r\n- Complications of treatment may be significant (e.g. osteonecrosis of the jaw or oesophageal ulceration with bisphosphonates)\r\n\r\n# Prognosis\r\n\r\n- There is no cure for osteoporosis\r\n- In general however, prognosis is good with effective treatment\r\n- Bisphosphonate treatment should be reviewed after 3-5 years\r\n- If patients remain at high risk of fracture it may be continued for up to 7-10 years\r\n- Patients with previous hip or vertebral fractures, those aged 70 or older or those who sustain another fragility fracture whilst on bone protection often require longer durations of treatment\r\n- Repeat DEXA may be appropriate to aid decision making\r\n- If bone protection is stopped, fracture risk should be reassessed 18 months to 3 years later\r\n\r\n# NICE Guidelines\r\n\r\n[NICE CKS: Osteoporosis - prevention of fragility fractures](https://cks.nice.org.uk/topics/osteoporosis-prevention-of-fragility-fractures/)\r\n\r\n[NICE - Osteoporosis: assessing the risk of fragility fracture](https://www.nice.org.uk/guidance/cg146)\r\n\r\n# References\r\n\r\n[National Osteoporosis Guideline Group - Prevention and Treatment of Osteoporosis](https://www.nogg.org.uk/full-guideline)\r\n\r\n[BNF Treatment Summary - Osteoporosis](https://bnf.nice.org.uk/treatment-summaries/osteoporosis/)\r\n\r\n[Radiopaedia - Dual-energy x-ray absorptiometry](https://radiopaedia.org/articles/dual-energy-x-ray-absorptiometry-1?lang=gb)\r\n\r\n[WHO - Fragility fractures](https://www.who.int/news-room/fact-sheets/detail/fragility-fractures)\r\n\r\n[International Longevity Centre UK report on Osteoporosis](https://ilcuk.org.uk/wp-content/uploads/2018/10/OsteoporosisUK.pdf)\r\n\r\n\r\n",
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"question": "A 73-year-old woman presents to the general practice to ask about 'weak bones', as her mother fractured her hip around her age. She has not had a previous hip fracture, and her BMI is 26.7. A FRAX® score is performed, which stratifies this patient as intermediate risk for a major fracture in the next ten years.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "Acute interstitial nephritis is a hypersensitivity reaction causing inflammation of the interstitium of the kidneys. This presents with a delayed presentation of fever, rash and acute kidney injury. It is typically a drug reaction with common causes including penicillin antibiotics, NSAIDs and proton pump inhibitors. The urine dipstick results typically found in acute interstitial nephritis include pyuria, but not haematuria. As this patient has presented with a dipstick positive for blood in the context of a long lie, rhabdomyolysis is the more likely diagnosis",
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"explanation": "Dehydration can be a cause of pre-renal acute kidney injury, particularly in those who are elderly or have other risk factors such as dementia. In this case, this patient presents with myalgia, a urine dipstick positive for blood and changes to the colour of their urine. These are not features of dehydration and suggest a different cause. Therefore, rhabdomyolysis is the more likely differential",
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"explanation": "Glomerulonephritis is a diverse group of conditions that can be separated broadly into nephrotic syndrome and nephritic syndrome. Nephrotic presents differently to this case, typically with a triad of oedema, hypercholesterolaemia and hypoalbuminaemia. It is diagnosed based on a high protein level in the urine. Nephritic syndrome causes blood in the urine; however, like the vast majority of glomerular disorders, it will also cause proteinuria. This is because glomerular damage causes a leak of protein and blood. As this patient did not have a urine dipstick positive for protein, glomerulonephritis is unlikely to be the cause of this presentation",
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"explanation": "Rhabdomyolysis is a condition characterised by skeletal muscle breakdown. There are several typical features of rhabdomyolysis in this question. This is an elderly patient presenting after a long lie, which is a typical cause of rhabdomyolysis. The patient is complaining of soreness in their arms and legs, which may be myalgia associated with rhabdomyolysis (the breakdown of muscle tissue). Breakdown of skeletal muscle tissue releases myoglobin into the systemic circulation, which is associated with renal complications, including acute kidney injury. This explains the colour of this patient's urine, with urine in rhabdomyolysis typically described as being \"cola coloured\". The 3+ blood is actually a false positive reading for haemoglobin, as it is actually myoglobin responsible for this result",
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"explanation": "Stones can present with a dipstick positive for blood. However, they will also probably present with colicky abdominal pain, whereas this patient presents with generalised pain affecting their arms and legs. These features, in combination with a long lie, make a diagnosis of rhabdomyolysis more likely",
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"explanation": "# Summary\n\nRhabdomyolysis refers to the breakdown of skeletal muscle, causing release of intracellular contents (including electrolytes and myoglobin) into the circulation and extracellular space. It often occurs after trauma or a long lie; other causes include excessive exertion, status epilepticus, compartment syndrome and medications such as statins. Presentation is classically with myalgia, weakness and brown urine (due to myoglobinuria). It is diagnosed by confirming that serum creatine kinase (CK) is 5 times the upper limit of normal. Myoglobin causes significant nephrotoxicity leading to acute kidney injury in many cases. Management is supportive, with aggressive IV fluids, correction of hyperkalaemia and treatment of any underlying cause.\n\n# Definition\n\nRhabdomyolysis is a potentially life-threatening condition that occurs when there is rapid breakdown of skeletal muscle. Intracellular contents of muscle cells are released, including creatine kinase, myoglobin and potassium.\n\n# Aetiology\n\nThere are a wide variety of causes of rhabdomyolysis, including:\n\n- Prolonged immobilisation (e.g. a long lie in elderly patients who have fallen) \n- Crush injuries\n- Severe burns\n- High-voltage electrical injury\n- Prolonged seizures\n- Compartment syndrome\n- Excessive physical exertion\n- Medications (e.g. statins, fibrates, neuroleptic malignant syndrome)\n- Recreational drugs (e.g. ecstasy, cocaine)\n- Toxins (e.g. snake venom)\n- Heatstroke \n- Myositis (e.g. viral or autoimmune) \n- Delirium tremens (alcohol withdrawal)\n- Ischaemic injuries\n- Metabolic or genetic disorders (e.g. glycogen storage diseases, muscular dystrophies)\n- Diabetic ketoacidosis\n- Thyroid storm\n\n# Signs and Symptoms\n\nSymptoms include:\n\n- Muscle pain\n- Weakness\n- Tea-coloured urine\n- Malaise\n- Fevers\n- Anorexia\n- Nausea and vomiting\n\nSigns on examination include:\n\n- Tender and swollen muscles (often disproportionate to the injury sustained)\n- Altered mental state - agitation, delirium\n- Oliguria or anuria\n\n# Differential Diagnosis\n\n- **Compartment syndrome** may cause or complicate rhabdomyolysis or occur alone\n- Often occurs after injury, or due to a deep vein thrombosis or tight cast or splint\n- Presents with severe pain in the affected limb disproportion to the injury\n- Other features of acute limb ischaemia may develop, e.g. paralysis, paraesthesia, pulselessness and pallor\n- **Acute kidney injury (AKI)** may occur in the absence of rhabdomyolysis\n- For example a patient admitted after a long lie may develop a pre-renal AKI due to dehydration but without rhabdomyolysis \n- Presenting features may include oliguria or anuria, malaise and confusion\n- **Myositis** may be complicated by rhabdomyolysis but this is rare\n- Typically patients present with a more chronic onset of symptoms of myalgia, diffuse weakness and fatigue\n- Pain and muscular tenderness are variable\n- There is a wide range of causes, including autoimmune, infective and malignancy-associated myositis\n- **Deep vein thrombosis** presents with swelling, pain, tenderness and erythema of the affected limb (rather than widespread muscle involvement)\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urine dipstick** is falsely positive for blood due to myoglobinuria\n- **Urine microscopy** shows no red cells in the urine\n- **Venous blood gas** to rapidly obtain serum potassium; may show a metabolic acidosis\n- **ECG** may show changes due to hyperkalaemia or hypocalcaemia\n\n**Blood tests:**\n\n- **Creatine kinase** is the key diagnostic test - a CK > 5x the upper limit of normal is expected\n- **U&Es** looking for renal impairment and hyperkalaemia; creatinine is raised out of proportion to urea\n- **Full blood count** as a baseline; white cells may be raised if inflammation or infection is driving rhabdomyolysis\n- **Coagulation screen** to monitor for disseminated intravascular coagulation\n- **Bone profile** may show hypocalcaemia initially as calcium deposits in necrotic muscle tissue; this may later be released causing hypercalcaemia; phosphate may be high\n- **Liver function tests** may show a liver injury; AST and ALT will be raised due to muscle damage\n- **Urate**, **lactate dehydrogenase** and **aldolase** are raised (these are non-specific)\n\n**Imaging:**\n\n- Imaging is not routinely required\n- **MRI** is the imaging modality of choice, and will show oedematous muscles with features of myonecrosis in severe cases\n\n**Special tests:**\n\n- In cases of diagnostic uncertainty, further investigations may be required to look for an underlying cause\n- Examples include **acetyl carnitine profile**, **urine organic acids**, **HIV serology** and an **autoimmune screen**\n- **Muscle biopsy** may also be considered; this should be delayed for at least a month after an acute episode of rhabdomyolysis\n\n# Management\n\n**Conservative management:**\n\n- Close input-output monitoring is required, especially for patients at increased risk of fluid overload (e.g. frail elderly patients)\n- Catheterisation should be considered \n- Stop any medications that may be possible triggers (e.g. statins)\n- Identify the underlying cause and initiate treatment (e.g. cooling measures for hyperthermia)\n- Renal function and acid-base status should be closely monitored\n- Early referral for intensive care and renal input is advised in severe rhabdomyolysis\n\n**Medical management:**\n\n- IV fluid rehydration - large volumes may be required to meet a target urine output of 200-300ml/hour (or 3 ml/kg/hour) until CK normalises\n- Hyperkalaemia should be managed as per usual emergency guidelines, with calcium gluconate for myocardial protection and iV insulin/dextrose\n- In some cases, IV sodium bicarbonate may be considered to correct acidosis (although this may exacerbate hypocalcaemia and so is not routinely used)\n- Complications may require additional medical treatment e.g. correction of disseminated intravascular coagulation\n\n**Interventional management:**\n\n- Intensive care admission for renal replacement therapy may be required in severe rhabdomyolysis e.g. in cases of refractory hyperkalaemia or metabolic acidosis\n- Some causes of rhabdomyolysis may require surgical intervention e.g. fasciotomies for compartment syndrome\n\n# Complications\n\n- **Acute kidney injury** is the major complication, which may lead to acute renal failure; it occurs due to a combination of hypovolaemia leading to renal ischaemia, tubular obstruction with heme pigment casts and direct tubular injury\n- **Arrhythmias** including cardiac arrest may occur due to hyperkalaemia and hypocalcaemia\n- **Metabolic acidosis** is common, often with an increased anion gap\n- **Disseminated intravascular coagulation** is a rare complication that may occur due to release of prothrombotic substances from damaged muscle\n- **Compartment syndrome** may occur secondary to inflammation and oedema of damaged muscles, especially after fluid resuscitation\n- **Hypercalcaemia** occurs after initial hypocalcaemia due to release of calcium from injured muscle\n- **Liver injury** is seen in up to 25% of patients - this is typically reversible \n\n# Prognosis\n\n- Prognosis varies significantly depending on the severity of rhabdomyolysis\n- Some patients may be asymptomatic, whereas in others the condition is life-threatening\n- Up to 65% of patients with rhabdomyolysis develop acute kidney injury (AKI) as a result\n- Mortality in severe rhabdomyolysis is 20% \n- Some residual muscle weakness in those who recover is common\n\n# References\n\n[Patient UK - Rhabdomyolysis and myoglobinuria](https://patient.info/doctor/rhabdomyolysis-and-other-causes-of-myoglobinuria)\n\n[RCEM Learning - Acute Rhabdomyolysis](https://www.rcemlearning.co.uk/reference/acute-rhabdomyolysis/)\n\n[Faculty of Intensive Care Medicine - Rhabdomyolysis](https://www.ficm.ac.uk/documents/case-of-the-month-27-rhabdomyolysis/)\n\n[National Genomics Education Programme - Rhabdomyolysis](https://www.genomicseducation.hee.nhs.uk/genotes/in-the-clinic/presentation-adult-with-rhabdomyolysis/)\n\n[Radiopaedia - Rhabdomyolysis](https://radiopaedia.org/articles/rhabdomyolysis)",
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"question": "A 77-year-old female presents to the emergency department after their daughter found them on the floor in their home. The patient is unsure how long she was on the floor, but she said her arms and legs feel sore. A urine dipstick is performed, which shows 3+ blood. Her urine is also dark brown in colour.\n\nWhat is the most likely diagnosis?",
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"explanation": "Chronic kidney disease can only be diagnosed in someone with an eGFR ≤59 or in those with structural kidney disease. This patient has an eGFR of 61, a normal urine dipstick and no other evidence of any structural kidney disease. Therefore, they do not have chronic kidney disease",
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"name": "Chronic kidney disease stage 3b",
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"explanation": "Chronic kidney disease (CKD) is diagnosed with a combination of estimated glomerular filtration rate (eGFR) readings and urine dipstick findings. eGFR is an estimation of the rate at which the kidneys filter the blood and is an approximation of how well the kidneys are functioning. The eGFR that determines chronic kidney disease depends on whether there is evidence of other structural damage, e.g. haematuria, proteinuria, imaging abnormalities or histological abnormalities. If there is structural damage present, CKD can be diagnosed at any eGFR, even in those greater than 90. If there is no structural damage, the eGFR must be ≤59 to diagnose a patient with CKD. In this patient, their eGFR was 61; they have a normal urine dipstick and no evidence of structural kidney disease. Therefore they do not have chronic kidney disease",
"id": "33633",
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"name": "No chronic kidney disease",
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"explanation": "Chronic kidney disease can only be diagnosed in someone with an eGFR ≤59 or in those with structural kidney disease. This patient has an eGFR of 61, a normal urine dipstick and no other evidence of any structural kidney disease. Therefore, they do not have chronic kidney disease",
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"name": "Chronic kidney disease stage 3a",
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"explanation": "Chronic kidney disease can only be diagnosed in someone with an eGFR ≤59 or in those with structural kidney disease. This patient has an eGFR of 61, a normal urine dipstick and no other evidence of any structural kidney disease. Therefore, they do not have chronic kidney disease",
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"explanation": "Chronic kidney disease can only be diagnosed in someone with an eGFR ≤59 or in those with structural kidney disease. This patient has an eGFR of 61, a normal urine dipstick and no other evidence of any structural kidney disease. Therefore, they do not have chronic kidney disease",
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"comment": "the old double bluff",
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"comment": "For stages 1 and 2, renal damage clues 🕵️♀️ ",
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"comment": "With 2 low eGFRs surely it's more 'likely' you'd find histological changes if you actually did a biopsy?",
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"explanation": "# Summary\n\nChronic Kidney Disease (CKD) is a condition characterised by abnormal kidney function for over three months, with a decrease in glomerular filtration rate (GFR) and/or markers of kidney damage such as proteinuria. Classification is based on the cause of CKD, GFR and heaviness of proteinuria. Common causes include diabetes, hypertension and age-related decline. Most patients are asymptomatic in the early stages; signs and symptoms that may develop include lethargy, breathlessness, anorexia and oliguria. First-line investigations include blood tests for U&Es to determine serum creatinine and estimated GFR (eGFR), urine albumin:creatinine ratio and investigations to screen for a cause (e.g. renal tract ultrasound to look for structural abnormalities or obstruction). Management involves regular monitoring for complications (such as anaemia or bone disease), optimising risk factors such as blood pressure and diabetic control, and considering options for renal replacement therapy (RRT) in patients who have end-stage renal disease.\n\n# Definition\n\nCKD is defined by KDIGO as abnormal kidney function or structure for over 3 months, with implications for health. \n\nGlomerular filtration rate (GFR) refers to the volume of fluid filtered by the kidney's nephrons per minute. This can be estimated (eGFR) from serum creatinine although this may be less reliable in patients with extremes of muscle mass.\n\nA GFR below 60 ml/min/1.73m<sup>2</sup> is considered significantly abnormal kidney function.\n\nExamples of abnormal kidney structure include:\n\n- Urinary albumin:creatinine ratio > 3 mg/mmol\n- Urinary sediment abnormalities e.g. haematuria, pyuria or casts\n- Biochemical abnormalities (e.g. acidosis, electrolyte disturbance) due to tubular disorders\n- Histological abnormalities e.g. glomerulosclerosis, tubular atrophy\n- Structural abnormalities e.g. polycystic kidneys or reflux nephropathy\n- Previous renal transplant\n\n# Epidemiology\n\n- CKD is very common, with an estimated global prevalence of 9%\n- Diabetes is the commonest cause, accounting for up to 50% of cases\n- As the early stages of CKD are often asymptomatic, many cases are likely undiagnosed\n- Prevalence is rising due to the ageing population and increased prevalence of chronic diseases such as diabetes and hypertension\n- 50% of people over the age of 75 have CKD\n- Risk factors include:\n\t- Family history of CKD\n\t- Black or Hispanic ethnicity\n\t- History of acute kidney injury (AKI)\n\t- Older age\n\n# Aetiology\n\n- Diseases causing intrinsic kidney damage:\n\t- Diabetes\n\t- Hypertension\n\t- Glomerulonephritis, which may be primary or secondary\n\t- Conditions causing urinary tract obstruction:\n\t- Recurrent urolithiasis\n\t- Structural abnormalities (e.g. ureteropelvic junction obstruction)\n\t- External compression (e.g. from a pelvic mass)\n\t- Bladder voiding problems (e.g. benign prostatic hyperplasia, neurogenic bladder)\n- Iatrogenic causes:\n\t- Radiotherapy\n\t- Nephrotoxic drugs, e.g. aminoglycosides, lithium, NSAIDs\n- Renal involvement secondary to multisystem diseases:\n\t- HIV\n\t- Myeloma\n\t- Vasculitis\n\t- Systemic lupus erythematosus (lupus nephritis)\n\t- Amyloidosis\n\t- Genetic kidney diseases\n\t- Autosomal dominant polycystic kidney disease (ADPKD)\n\t- Alport's syndrome\n\t- Tuberous sclerosis\n\t- Cystinosis\n\t- Recurrent urinary tract infections\n\t- Often secondary to vesico-ureteric reflux or other anatomical defects\n\t- Leads to chronic pyelonephritis which may lead to end-stage renal disease\n\n# Classification\n\nThe KDIGO classification is used to stratify patients by risk of adverse outcomes from CKD based on their GFR and urinary albumin:creatinine ratio (ACR).\n\n||A1 - normal to mildly increased ACR (< 3 mg/mmol)|A2 - moderately increased ACR (3 to 30 mg/mmol)|A3 - severely increased ACR (over 30 mg/mmol)|\n|---------------|-----------|---------------|-----------|\n|**G1 - normal or high GFR (> 90 ml/min/1.73m<sup>2</sup>)**|Low risk/not CKD if no other markers of kidney damage|Moderate risk|High risk|\n|**G2 - mild reduction in GFR (60 - 89 ml/min/1.73m<sup>2</sup>)**|Low risk/not CKD if no other markers of kidney damage|Moderate risk|High risk|\n|**G3a - mild to moderate reduction in GFR (45 - 59 ml/min/1.73m<sup>2</sup>)**|Moderate risk|High risk|Very high risk|\n|**G3b - moderate to severe reduction in GFR (30-44 ml/min/1.73m<sup>2</sup>)**|Moderate risk|High risk|Very high risk|\n|**G4 - severe reduction in GFR (15 - 29 ml/min/1.73m<sup>2</sup>)**|High risk|Very high risk|Very high risk|\n|**G5 - renal failure (< 15 ml/min/1.73m<sup>2</sup>)**|Very high risk|Very high risk|Very high risk|\n\n\n# Signs and Symptoms\n\nCKD is often asymptomatic, however especially in later stages patients may have non-specific symptoms such as:\n\n- Lethargy\n- Anorexia\n- Headaches\n- Weight loss (or gain due to fluid overload)\n- Nausea and vomiting\n- Itching (uraemic pruritus)\n- Shortness of breath (due to anaemia, pulmonary oedema, pleural effusion or acidosis)\n- Muscle cramps, especially at night\n- Bone pain (due to renal osteodystrophy)\n- Taste changes\n- Cognitive impairment\n- Urinary symptoms: \n- Polyuria or oliguria may occur\n- Nocturia\n- Frothy urine (due to proteinuria)\n\nExamination findings may include:\n\n- Hypertension\n- Pallor (due to anaemia)\n- Abnormal fluid status\n- Fluid overload with peripheral and/or pulmonary oedema\n- Dehydration\n- Cachexia\n- Ammonia-like smelling breath due to uraemia\n- Tachypnoea (due to anaemia, pulmonary oedema, pleural effusion or acidosis \n- Flank mass(es) may be palpable due to malignancy or renal cysts (e.g. in ADPKD)\n- Patients on renal replacement therapy may have additional signs such as:\n- Arteriovenous fistula (AVF)\n- Peritoneal dialysis catheter\n- Renal transplant scar (usually right iliac fossa)\n- Parathyroidectomy scar may be present in patients requiring surgical management of secondary or tertiary hyperparathyroidism\n\n# Differential Diagnosis\n\n- **Acute kidney injury (AKI)** is the main differential \n\t- It may be difficult to differentiate AKI from CKD based on investigations showing renal impairment at a single point in time \n\t- To diagnose CKD markers of kidney damage or an eGFR of < 60mL/min/1.73m_ need to be present on two occasions at least 3 months apart\n\t- Abnormal kidneys on imaging (atrophy e.g. in chronic pyelonephritis, or enlarged kidneys e.g. in ADPKD) are indicative of CKD rather than AKI\n\t- Complications of CKD such as anaemia or secondary hyperparathyroidism may also be useful in differentiating the two\n\t- The two may co-exist if there is an acute insult causing AKI in a patient with pre-existing CKD (whether this is diagnosed or not)\n- **False-positive low eGFR results** may occur due to high serum creatinine results, for example in patients with high muscle mass, or after consumption of meat\n- **Urinary ACR** may also be high due to menstruation, strenuous exercise, orthostatic proteinuria or UTI\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urine dipstick** to screen for haematuria and proteinuria\n- Urine positive for haematuria should be sent for **MC&S** to screen for infection\n- Malignancy should also be considered in patients with persistent unexplained haematuria\n- **Early morning albumin:creatinine ratio** should be done in all patients \n- If this is between 3 and 70 mg/mmol it should be repeated within 3 months for confirmation\n\n**Blood tests:**\n\n- **U&Es** for creatinine, eGFR, urea and electrolytes\n- Patients should be advised not to eat meat 12 hours prior to the test\n- If eGFR is < 60 mL/min/1.73m_, this should be repeated within 2 weeks\n- If it remains low with no evidence of ongoing AKI, U&Es should be repeated in 3 months to diagnose CKD\n- **Full blood count** looking for anaemia secondary to CKD, which is usually normochromic and normocytic\n- **LFTs** may show a raised ALP due to bone disease; albumin may be low due to malnourishment or nephrotic syndrome\n- **Bone profile** may show an abnormal calcium; phosphate is usually high\n- **HbA1c** to screen for diabetes as a cause of CKD\n- **Bicarbonate** may be low due to metabolic acidosis\n- **Lipid profile** as dyslipidemia is common in CKD and is a modifiable risk factor for cardiovascular disease\n- **Clotting screen** in case renal biopsy is required\n- **Parathyroid hormone** often rises as renal function declines (secondary or tertiary hyperparathyroidism)\n- **HIV and hepatitis B and C serology** especially in patients for whom renal replacement therapy is being considered\n- **An autoimmune screen** may be sent if an underlying autoimmune condition is suspected\n\t- Antinuclear antibodies\n\t- ANCA antibodies\n\t- dsDNA antibodies\n\t- Anti-GBM antibodies\n\t- Serum complement \n- **Myeloma screen** i.e. immunoglobulins, protein electrophoresis and serum free light chains if this is suspected\n\n**Imaging:**\n\n- **Renal tract ultrasound** is not required in all patients, but should be offered to the following patients:\n- Accelerated progression of CKD (sustained decrease in GFR of 15 ml/min/1.73m_ per year **or** 25% or more **and** a change in GFR category within 12 months)\n- GFR < 30ml/min/1.73m_\n- Patients planned for renal biopsy\n- Suspected urinary tract obstruction\n- Persistent or visible haematuria\n- Family history of polycystic kidney disease\n- Kidneys are usually atrophic in advanced CKD\n- Large kidneys are seen in polycystic kidney disease and in the initial stages of diabetic nephropathy\n- **CT KUB** is the most sensitive imaging modality if renal stones are suspected\n- **CT or MRI angiography** may be indicated for suspected renal artery stenosis - **radionuclide scanning** is also an option\n\n**Special tests:**\n\n- **Renal biopsy** is not required in every case of CKD but may be indicated after initial investigations have been completed, for example if the cause of renal impairment is unclear, where there is rapid progression of CKD or where glomerulonephritis is suspected\n- Important contraindications include active pyelonephritis, uncontrolled hypertension or coagulopathy; biopsying a patient with a single kidney should be avoided where possible due to the (very rare) risk that a nephrectomy may be required to treat complications\n\n# Management\n\n**Conservative management:**\n\n- Patients with CKD are often managed in primary care, however the following should prompt referral to secondary care renal services:\n\t- End-stage renal disease\n\t- Rare or genetic cause for CKD known or suspected (e.g. ADPKD)\n\t- Suspected renal artery stenosis\n\t- Diagnostic uncertainty\n\t- Complications of CKD e.g. malnutrition, hyperkalaemia, anaemia, mineral and bone disorder, acidosis\n\t- Uncontrolled hypertension despite four antihypertensives\n\t- 5-year risk of needing RRT > 5% (see references for calculator)\n\t- Accelerated progression of CKD\n\t- Urinary ACR > 70 mg/mmol (or > 30 mg/mmol with persistent haematuria)\n\t- Patient with obstructive causes of CKD should be referred to urology\n\t- Individualised education on CKD including safety netting regarding complications and risk of AKI\n- Some patients may require additional counselling e.g. genetic counselling and advice regarding screening family members in ADPKD\n- Lifestyle advice should be provided, including:\n\t- Smoking cessation\n\t- Moderating alcohol intake\n\t- Maintaining a healthy weight with regular exercise\n\t- Maintaining a healthy diet\n\t- Avoid over-the-counter nephrotoxics e.g. NSAIDs, dietary supplements and herbal remedies\n- Dietician input may be required for end-stage renal disease (e.g. reducing phosphate, salt and potassium intake)\n- Regular monitoring of eGFR, urinary ACR and for any complications should be undertaken, more frequently in patients with more advanced CKD\n- Patients may benefit from education and/or support groups \n- In the later stages, psychological support and/or access to specialist nurse input may be helpful\n- Many patients with end-stage renal disease may not want or not be suitable for RRT - in these cases - conservative management is an important alternative (also referred to as \"supportive care\")\n\n**Medical management:**\n\n- Treat the underlying cause of CKD e.g. optimise diabetic control; specialist input for immunosuppressive treatments in autoimmune conditions\n- Review medications and consider reducing or stopping nephrotoxic drugs (e.g. NSAIDs, diuretics)\n- Treat hypertension with up to four antihypertensives \n- Aim for a target blood pressure of <140/90 if ACR is < 70 mg/mmol\n- Aim for < 130/80 if ACR is > 70 mg/mmol\n- Patients over 80 with type 1 diabetes should aim for < 150/90\n- An ACE-inhibitor or angiotensin-receptor blocker (ARB) should be first line if ACR is > 30 mg/mmol (if less then manage as per usual hypertension guidelines)\n- ACE-inhibitors or ARBs may be initiated in patients with diabetes and ACR > 3 mg/mmol in the absence of hypertension\n- However these should be avoided in patients with a potassium of > 5 mmol/L \n- They should be stopped if potassium rises to > 6 mmol/L on treatment\n- Consider starting a statin (usually atorvastatin 20mg) in all patients with CKD - the dose should be uptitrated to achieve effect lipid-lowering\n- Consider an antiplatelet (e.g. aspirin) for secondary prevention of cardiovascular disease (balanced against bleeding risk)\n- Sodium-glucose cotransporter-2 (SGLT-2) inhibitors may be considered in some patients on maximal ACE-inhibitor or ARB treatment who meet certain criteria (based on presence of type 2 diabetes, ACR and eGFR)\n- Ensure patients are up to date with vaccinations:\n- Annual influenza vaccine\n- 5-yearly pneumococcal vaccine (PPV23)\n- Covid vaccination as per national guidance\n- Medical management is often required for complications of CKD - see \"Complications\" section for more details\n\n**Surgical/interventional management:**\n\n- Renal replacement therapy is covered in detail in another chapter\n- Options include haemodialysis, peritoneal dialysis (which may be automated and mainly done overnight, or continuous and ambulatory) and renal transplant\n- Patients should be referred for consideration of RRT ideally at least a year before this is anticipated to be required\n- Indications include:\n- eGFR approximately 5-7 ml/min/1.73m_\n- Symptomatic uraemia affecting quality of life\n- Refractory fluid overload\n- Refractory biochemical abnormalities\n- Various options exist for dialysis access which may require surgical formation (e.g. an arteriovenous fistula)\n- Other surgical interventions may be required to treat complications of CKD, for example parathyroidectomy may be indicated in some patients with refractory hyperparathyroidism\n\n# Complications\n\n- **Anaemia** is often multifactorial, due to reduced erythropoietin production, iron deficiency and reduced red blood cell survival\n\t- Other contributing factors include B12 and folate deficiency, haemolysis due to dialysis and the underlying cause of CKD (e.g. myeloma, sickle cell disease)\n\t- Typically anaemia is normocytic and normochromic\n\t- Patients should be investigated if haemoglobin (Hb) is < 110 g/L or if symptomatic\n\t- If eGFR is > 60 ml/min/1.73m_, anaemia is unlikely to be due to CKD\n\t- Other investigations may be required to rule out other causes of anaemia (e.g. gastrointestinal bleeding, B12/folate deficiency)\n\t- All patients should be investigated for iron deficiency with percentage of hypochromic red blood cells being first-line (> 6% indicates functional iron deficiency)\n\t- Ferritin < 100 mcg/L is also indicative of iron deficiency\n\t- Iron supplementation may be either oral or IV (with IV usually preferred for patients on haemodialysis)\n\t- Ferritin should be monitored and iron supplements stopped before ferritin increases over 800 mcg/L\n\t- Once iron stores are replete, erythropoiesis-stimulating agent (ESA) treatment should be considered\n\t- These are usually given subcutaneously, with examples of ESAs including epoetin or darbepoetin\n\t- Roxadustat is a new oral alternative to ESAs which also acts to stimulate erythropoiesis (it is a hypoxia-inducible factor prolyl hydroxylase inhibitor)\n\t- Blood transfusion should be avoided, especially in patients who may require a renal transplant (due to the risk of allosensitization)\n\t- Target Hb is 100-120 g/L\n- **Mineral and bone disorder (MBD)** occurs due to abnormal metabolism of phosphate, vitamin D, calcium and parathyroid hormone\n\t- There is a spectrum of disease that involves abnormal bone turnover and mineralisation as well as vascular and soft tissue calcification\n\t- Risk of CKD-MBD increases once eGFR is < 60 mL/min/1.73m_\n\t- Phosphate retention occurs due to renal dysfunction -> calcitriol (active form of vitamin D) is downregulated, and is also decreased due to reduced renal activation of vitamin D -> calcium falls -> PTH rises (secondary hyperparathyroidism) -> calcium is released from bone\n\t- Tertiary hyperparathyroidism may also occur if there is longstanding secondary hyperparathyroidism (both may be treated with parathyroidectomy)\n\t- \"Renal osteodystrophy\" refers to a range of bone abnormalities seen in CKD including bone resorption, osteosclerosis and osteopenia\n\t- There is an increased risk of fracture - bone density assessment (e.g. DEXA scanning) and bone protection should be considered\n\t- Patients with at least stage 3a CKD should be regularly monitored with serum calcium, phosphate and PTH levels \n\t- Management involves normalising serum phosphate via dietary restriction of phosphate and phosphate binders (e.g. calcium carbonate, sevelamer)\n\t- Severe hyperparathyroidism may be treated with calcitriol and cinacalcet (a calcimimetic)\n\t- Vitamin D supplementation with ergocalciferol or cholecalciferol may be considered\n\t- Dialysis settings can be adjusted to remove excess phosphate and calcium\n- **Cardiovascular risk** is significantly increased, including myocardial infarction, stroke, peripheral arterial disease and heart failure\n\t- There is a high prevalence of comorbid conditions increasing cardiovascular risk (e.g. hypertension, hypercholesterolaemia, diabetes)\n\t- Patients also have additional CKD-related risk factors, including vascular calcification due to CKD-MBD, uraemia, oxidative stress and anaemia\n\t- Dialysis further increases the risk of cardiovascular disease, including ischaemic heart disease, valvular disease and hypertensive cardiomyopathy\n- **Uraemia** typically becomes symptomatic in patients with end-stage renal disease\n\t- Symptoms include nausea, vomiting, anorexia, taste disturbance, confusion, muscle cramps, pruritus and restless legs\n\t- Complications include pericarditis, neuropathy and encephalopathy\n\t- Symptomatic uraemia is an indication for renal replacement therapy\n- **Hyperkalaemia** is a common issue in CKD due to impaired potassium excretion\n\t- Medications such as ACE-inhibitors and ARBs also contribute to hyperkalemia\n\t- Dietary intake of potassium should be limited\n\t- Medical treatment with potassium binders may be required (e.g. sodium zirconium cyclosilicate (Lokelma), calcium resonium or patiromer)\n\t- Treatments such as sodium bicarbonate (for metabolic acidosis) and diuretics (for fluid overload) may also help to reduce serum potassium\n- **Metabolic acidosis** is common due to reduced renal acid excretion once eGFR < 50 ml/min/1.73m_\n\t- Chronic metabolic acidosis further increases kidney injury and fibrosis, bone demineralisation and muscle wasting and risk of cardiovascular events\n\t- Oral sodium bicarbonate should be considered for patients with an eGFR < 30 ml/min/1.73m_, or if serum bicarbonate is < 20 mmol/litre\n- **Fluid overload** with both pulmonary and peripheral oedema may occur in the later stages of CKD\n\t- Fluid restriction may be advised\n\t- Diuretics may also be used, with loop diuretics (e.g. furosemide) being first-line in most cases\n- **Malnutrition** is common, especially as CKD progresses\n\t- Uraemia may cause anorexia and taste disturbance\n\t- Low mood may also contribute to poor oral intake\n\t- Protein catabolism is promoted by acidosis and chronic inflammation\n\t- Patients should be regularly screened for malnutrition\n\t- Specialist renal dietician input should be offered for patients at risk of malnutrition\n\t- Oral nutritional supplements may be indicated in some cases (or less commonly enteral tube feeding or parenteral nutritional support) \n- **Acute kidney injury** - patients with CKD are at increased risk of AKI\n\t- Risk increases in patients with an eGFR of < 60 mL/min/1.73m_\n\t- There is also a risk of increased CKD progression with episodes of AKI\n\t- Triggers include intercurrent illness, especially with diarrhoea and vomiting, medications e.g. NSAIDs, antibiotics and urinary tract obstruction\n- **Increased risk of malignancy** especially of renal and thyroid cancers\n\t- Immunosuppressive medications further increase malignancy risk (e.g. after renal transplant)\n\t- Chronic uraemia is also a contributing factor\n- **Hypertension** both contributes to the development of CKD and is caused by CKD\n\t- Mechanisms include sodium dysregulation, upregulation of the renin angiotensin aldosterone system, and sympathetic nervous system hyperactivity\n\t- Regular monitoring of blood pressure and effective treatment is therefore key to minimising progression of CKD as well as other adverse cardiovascular events\n- **Reduced quality of life**, especially in patients with more severe CKD\n\t- As with any chronic disease, depression and anxiety are common\n\n# Prognosis\n\n- Prognosis is dependent on the underlying cause of CKD, for example ADPKD tends to progress more rapidly than other diseases\n- CKD is typically a progressive disease, although most patients die before reaching end-stage renal disease\n- Approximately 2% of patients with CKD develop end-stage renal disease\n- Progression can be slowed through modification of risk factors such as hypertension and proteinuria\n- The leading cause of death in CKD is cardiovascular disease\n\n# NICE Guidelines\n\n[NICE CKS - Chronic Kidney Disease](https://cks.nice.org.uk/topics/chronic-kidney-disease/)\n\n[NICE - Chronic kidney disease: assessment and management](https://www.nice.org.uk/guidance/ng203)\n\n[NICE - Renal replacement therapy and conservative management](https://www.nice.org.uk/guidance/ng107)\n\n[NICE technology appraisal - Roxadustat for treating symptomatic anaemia in chronic kidney disease](https://www.nice.org.uk/guidance/ta807/)\n\n# References\n\n[Patient UK - Chronic kidney disease](https://patient.info/doctor/chronic-kidney-disease-pro)\n\n[Patient UK - Anaemia in chronic kidney disease](https://patient.info/doctor/anaemia-in-chronic-kidney-disease)\n\n[UK Kidney Association eCKD guide](https://ukkidney.org/health-professionals/information-resources/uk-eckd-guide) \n\n[Kidney Failure Risk Equation]( https://www.kidneyfailurerisk.co.uk/)\n\n[KDIGO CKD Evaluation and Management](https://kdigo.org/guidelines/ckd-evaluation-and-management/)\n\n[KDIGO CKD Mineral and Bone Disorder guideline](https://kdigo.org/guidelines/ckd-mbd/)\n\n[Radiopaedia - Renal osteodystrophy](https://radiopaedia.org/articles/renal-osteodystrophy?lang=gb)\n\n[The Renal Association - Undernutrition in Chronic Kidney Disease Guideline](https://ukkidney.org/sites/renal.org/files/FINAL-Nutrition-guideline-June-2019-RNG-endorsed.pdf)\n\n[NHS Kidney Care - Chronic Kidney\nDisease in England: The Human and Financial Cost](https://www.england.nhs.uk/improvement-hub/wp-content/uploads/sites/44/2017/11/Chronic-Kidney-Disease-in-England-The-Human-and-Financial-Cost.pdf)",
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"question": "A 55-year-old patient comes to the GP to discuss his recent blood tests. His latest eGFR was 61 ml/min/1.73m2, with his previous eGFR two years prior being 68 ml/min/1.73m<sup>2</sup>. His urine dipstick is normal.\n\nWhat is the most likely diagnosis?",
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"explanation": "Bladder cancer most typically presents as painless haematuria. An acute presentation of dysuria, haematuria and frequency is much more likely to be a urinary tract infection than bladder cancer. However, as there is microscopic haematuria in this woman, she should have a repeat urine dipstick after her symptoms have resolved to check for persistent haematuria. If there is still blood in the urine, alternative diagnoses should be considered, including bladder cancer",
"id": "33640",
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"name": "Bladder cancer",
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"explanation": "Nephritic syndrome is a group of conditions characterised by glomerular destruction. The presentation can vary based on the cause, but symptoms can include haematuria, hypertension and symptoms of nephrotic syndrome if protein loss through the kidneys is also high. Urine dipstick findings include proteinuria and haematuria. As this patient has no proteinuria, in addition to frequency and dysuria, which are primarily symptoms of the lower urinary tract, this makes a diagnosis of urinary tract infection more likely",
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"label": "d",
"name": "Nephritic syndrome",
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"explanation": "This is a typical history of a urinary tract infection. It is more common in women than men, as women have a shorter urethra. Typical presenting symptoms include urinary frequency, dysuria and visible or non-visible haematuria. Urinary tract infections are typically positive for nitrite and leukocyte esterase. This because E. coli (the most common cause) produces nitrites, but whether nitrites are positive or not also depends on the bacterial cause. Management for this patient would be with a three day course of antibiotics (first-line antibiotics include nitrofurantoin and trimethoprim). This patient should also be brought back after completing antibiotics for a repeat urine dipstick to ensure the haematuria has resolved",
"id": "33638",
"label": "a",
"name": "Urinary tract infection",
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"explanation": "Chlamydia is the most common bacterial sexually transmitted infection in the UK. It can present similarly; with dysuria, and may have other features, including vaginal discharge. However, the majority of cases are asymptomatic (up to 70% in women). In this case, this woman presents with typical symptoms of a urinary tract infection and has a positive urine dip. Chlamydia infection would not cause an abnormal urinalysis",
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"name": "Chlamydia",
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"explanation": "# Summary \n\nLower urinary tract infections (LUTIs), often manifesting as cystitis, typically involve the infection of the bladder. Primarily caused by transurethral ascent of colonic commensals like E. coli, symptoms include urinary frequency, dysuria, urgency, foul-smelling urine, and suprapubic pain. Investigations are generally limited to a urine dipstick test for leucocytes and nitrites, while management involves oral nitrofurantoin or trimethoprim, and conservative measures. A key differential diagnosis is pyelonephritis, a urinary tract infection affecting the kidneys. Pyelonephritis exhibits more severe symptoms like fever, malaise, loin pain, and vomiting, and requires hospital admission and intravenous antibiotics.\n\n# Definition \n\nA lower urinary tract infection (LUTI) is generally defined as an infection of the bladder, often manifesting as cystitis.\n\n# Aetiology \n\nLUTIs are caused by the transurethral ascent of colonic commensals, most commonly **E. coli**.\n\n# Signs and symptoms\n\nPatients with LUTIs generally present with:\n\n- Urinary frequency\n- Dysuria\n- Urgency\n- Foul-smelling urine\n- Suprapubic pain\n- Clinical examination may be normal or reveal suprapubic tenderness.\n\nRed flag symptoms such as haematuria, loin pain, rigors, nausea, vomiting, and altered mental state may indicate more serious infection, and these patients may have/are at risk of developing pyelonephritis (see below) and likely need referral to A&E.\n\n\n# Investigations\n\nFor LUTIs:\n\n- Urine dipstick is positive for leucocytes and nitrites in most cases.\n- In uncomplicated cases, no further investigations are required.\n- In children, men, and pregnant women a mid-stream urine sample should be sent.\n\nNB: Urine dipstick is unreliable in women aged older than 65 years and those who are catheterised.\n\nIf being managed in secondary care due to red flag symptoms consider:\n\n- If there are signs of systemic upset consider routine blood tests such as FBC, U+E, and CRP.\n- For uncomplicated UTIs, imaging is rarely required, but if there are concerns over antecedents/complications such as urinary retention/obstruction, an USS bladder/kidney scan would be the first port of call.\n\n# Management \n\n[lightgallery]\n\n[lightgallery1]\n\nFor LUTIs:\n\n- First line management is with oral nitrofurantoin or trimethoprim. Antibiotic duration can vary (see below) however in women the standard course length is 3 days.\n- The patient should be advised on conservative measures to reduce the risk of further infection e.g. regular fluid intake, post-coital voiding.\n\n## Specific situations\n\n**UTI in Men:**\n\n- Empirical antibiotic drug treatment (if no cultures with sensitivities) with trimethoprim or nitrofurantoin for **7 days.**\n- Refer to urology if there are ongoing symptoms despite treatment, if there is an underlying risk factor for UTIs (e.g. urinary calculi, suspected obstruction, previous GU surgery), or if there are recurrent episodes of UTI.\n\n**UTI during Pregnancy (with no haematuria):**\n\n- First-line antibiotics are nitrofurantoin (but *avoid at term),* for **7 days.**\n- If nitrofurantoin is not suitable due to e.g. renal function, or there is no improvement in symptoms, consider second-choice antibiotics such as amoxicillin/cefalexin for 7 days.\n\n\n# NICE Guidelines\n\n[Click here for NICE CKS on urinary tract infection (lower) - women](https://cks.nice.org.uk/topics/urinary-tract-infection-lower-women/)\n\n[Click here for NICE CKS on pyelonephritis - acute](https://cks.nice.org.uk/topics/pyelonephritis-acute/)\n",
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"question": "A 52-year-old patient presents to the GP with a three-day history of urinary frequency and dysuria. Her husband is her only sexual partner. A urine dipstick is performed, showing blood +1 and is positive for leukocyte esterase and nitrites.\n\nWhat is the most likely diagnosis?",
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"explanation": "Renal calculi can present with back pain, which is typically \"loin to groin\". However, this patient has a fever, features of lower urinary tract infection (dysuria, frequency) and typical urine dipstick findings for urinary tract infection (leukocyte esterase and nitrites), which are not found in simple renal calculi. These features make an ascending urinary tract infection (pyelonephritis) more likely than renal calculus",
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"explanation": "Polycystic kidney disease is an autosomal dominant genetic disease leading to cyst formation on the kidneys, liver and pancreas. This can present with cyst rupture, which can cause back pain. However, this would usually be accompanied by haematuria. In addition, this would not explain the positive urine dipstick for nitrites and leukocyte esterase",
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"explanation": "There are some typical features of lower urinary tract infection in this question, including dysuria and urinary frequency. However, flank pain and fever are features that point towards a diagnosis of upper urinary tract infection, over a simple lower urinary tract infection",
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"explanation": "Renal cell carcinoma is an adenocarcinoma of the kidneys. Typical presenting features include haematuria, pain or mass in the flank and manifestations of metastatic disease. It is unlikely that a patient with renal cell carcinoma would develop symptoms this rapidly, combined with a clinical urinary tract infection",
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"explanation": "# Summary \n\nLower urinary tract infections (LUTIs), often manifesting as cystitis, typically involve the infection of the bladder. Primarily caused by transurethral ascent of colonic commensals like E. coli, symptoms include urinary frequency, dysuria, urgency, foul-smelling urine, and suprapubic pain. Investigations are generally limited to a urine dipstick test for leucocytes and nitrites, while management involves oral nitrofurantoin or trimethoprim, and conservative measures. A key differential diagnosis is pyelonephritis, a urinary tract infection affecting the kidneys. Pyelonephritis exhibits more severe symptoms like fever, malaise, loin pain, and vomiting, and requires hospital admission and intravenous antibiotics.\n\n# Definition \n\nA lower urinary tract infection (LUTI) is generally defined as an infection of the bladder, often manifesting as cystitis.\n\n# Aetiology \n\nLUTIs are caused by the transurethral ascent of colonic commensals, most commonly **E. coli**.\n\n# Signs and symptoms\n\nPatients with LUTIs generally present with:\n\n- Urinary frequency\n- Dysuria\n- Urgency\n- Foul-smelling urine\n- Suprapubic pain\n- Clinical examination may be normal or reveal suprapubic tenderness.\n\nRed flag symptoms such as haematuria, loin pain, rigors, nausea, vomiting, and altered mental state may indicate more serious infection, and these patients may have/are at risk of developing pyelonephritis (see below) and likely need referral to A&E.\n\n\n# Investigations\n\nFor LUTIs:\n\n- Urine dipstick is positive for leucocytes and nitrites in most cases.\n- In uncomplicated cases, no further investigations are required.\n- In children, men, and pregnant women a mid-stream urine sample should be sent.\n\nNB: Urine dipstick is unreliable in women aged older than 65 years and those who are catheterised.\n\nIf being managed in secondary care due to red flag symptoms consider:\n\n- If there are signs of systemic upset consider routine blood tests such as FBC, U+E, and CRP.\n- For uncomplicated UTIs, imaging is rarely required, but if there are concerns over antecedents/complications such as urinary retention/obstruction, an USS bladder/kidney scan would be the first port of call.\n\n# Management \n\n[lightgallery]\n\n[lightgallery1]\n\nFor LUTIs:\n\n- First line management is with oral nitrofurantoin or trimethoprim. Antibiotic duration can vary (see below) however in women the standard course length is 3 days.\n- The patient should be advised on conservative measures to reduce the risk of further infection e.g. regular fluid intake, post-coital voiding.\n\n## Specific situations\n\n**UTI in Men:**\n\n- Empirical antibiotic drug treatment (if no cultures with sensitivities) with trimethoprim or nitrofurantoin for **7 days.**\n- Refer to urology if there are ongoing symptoms despite treatment, if there is an underlying risk factor for UTIs (e.g. urinary calculi, suspected obstruction, previous GU surgery), or if there are recurrent episodes of UTI.\n\n**UTI during Pregnancy (with no haematuria):**\n\n- First-line antibiotics are nitrofurantoin (but *avoid at term),* for **7 days.**\n- If nitrofurantoin is not suitable due to e.g. renal function, or there is no improvement in symptoms, consider second-choice antibiotics such as amoxicillin/cefalexin for 7 days.\n\n\n# NICE Guidelines\n\n[Click here for NICE CKS on urinary tract infection (lower) - women](https://cks.nice.org.uk/topics/urinary-tract-infection-lower-women/)\n\n[Click here for NICE CKS on pyelonephritis - acute](https://cks.nice.org.uk/topics/pyelonephritis-acute/)\n",
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"question": "A 33-year-old female presents to their GP with a one-day history of left-sided back pain. This was preceded by a five-day history of dysuria and urinary frequency. On examination, her temperature is 38.7ºC, and there is suprapubic and renal-angle tenderness. Urine dipstick is positive for leukocyte esterase and nitrites.\n\nWhat is the most likely diagnosis?",
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"explanation": "Polymyositis is a type of idiopathic inflammatory myopathy caused by autoimmune damage to the muscle. This typically presents as bilateral, proximal muscle weakness. Polymyositis is a key differential for polymyalgia rheumatica, however as this patient has normal muscle power on examination, a diagnosis of polymyalgia rheumatica is more likely",
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"explanation": "Polymyositis is a type of idiopathic inflammatory myopathy caused by autoimmune damage to the muscle. This typically presents with bilateral, proximal muscle weakness with associated skin rashes (including heliotrope rash, Gouttron's papules and mechanic's hands). Dermatomyositis is a key differential for polymyalgia rheumatica, however as this patient has normal muscle power on examination, which makes a diagnosis of polymyalgia rheumatica more likely. They also do not have any skin disease, making a diagnosis of dermatomyositis less likely",
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"explanation": "Giant cell arteritis is an inflammatory large vessel vasculitis affecting the temporal arteries. Typical symptoms include temporal headache, jaw claudication (pain upon repeated movement of the jaw, e.g. chewing), scalp tenderness (e.g. while brushing hair) and ocular complications (e.g. blindness, amaurosis fugax). This typically affects patients >50 years old and can be associated with polymyalgia rheumatica. As this patient has not had any of these symptoms, it is more likely this is simply a diagnosis of polymyalgia rheumatica. It is important to safety net this patient for these symptoms, as they should be started on prednisolone at presentation of suspected giant cell arteritis, instead of once the diagnosis has been confirmed in polymyalgia rheumatica",
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"comment": "No mention of muscle pain in the question... \"The most characteristic symptoms include shoulder and hip girdle stiffness AND pain\"",
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"comment": "-myalgia, pain is literally in the name ugh I hated this question",
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"comment": "does anyone know why in PMR they experience weakness but their power is normal on examination ???",
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"comment": "The weakness experienced by individuals with PMR is not due to muscle damage or neurological problems but is rather a consequence of the inflammation and pain associated with the condition. The inflammation affects the muscles and surrounding tissues, leading to pain, stiffness, and limited range of motion. These symptoms can make it difficult for individuals to exert their full strength, resulting in a subjective feeling of weakness.\n\nDuring a physical examination, muscle strength is assessed by asking the patient to perform specific movements or resist against force. While the patient may perceive weakness due to pain and stiffness, the actual muscle strength may be intact. This can be attributed to the fact that PMR primarily affects the large muscles around the shoulders and hips, which are responsible for movements like lifting or pushing. In contrast, the small muscles responsible for fine motor skills may be less affected, leading to normal strength on examination.",
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"explanation": "# Summary\n\nPolymyalgia rheumatica is a systemic inflammatory condition characterised by pain and stiffness of the neck, shoulders and pelvis. It is primarily a disease of older age, and particularly affects people of Northern European descent. Systemic symptoms include weight loss, low-grade fevers, fatigue and anorexia. Diagnosis is essentially clinical and is supported by responsiveness of steroid treatment, however patients should all have baseline bloods and a urine dipstick to rule out differentials. Most patients can be managed in primary care with oral prednisolone, however those with atypical features or a poor response to steroids should be referred to rheumatology for further assessment. \n\n# Definition\n\nPolymyalgia rheumatica (PMR) is a chronic inflammatory condition which presents with stiffness and pain of the proximal large joints. \n\n# Epidemiology\n\n- PMR has a prevalence of approximately 1% in the UK\n- Incidence increases with age, peaking in those aged 70-80 years old\n- PMR is very rare in the under 50s\n- Women make up the majority of cases\n- Incidence is significantly higher in patients with Northern European ancestry \n- Approximately 15-20% of patients with PMR develop giant cell arteritis (see separate topic), and PMR affects up to 60% of patients with giant cell arteritis\n\n# Signs and Symptoms\n\n- The key symptom is bilateral shoulder, neck and pelvic girdle pain \n- Joints feel stiff, especially after rest or sleep, and movement worsens pain\n- Pain may radiate to the elbows or knees\n- Systemic symptoms are common, including:\n- Low-grade fevers\n- Loss of appetite \n- Weight loss\n- Malaise\n- Depression\n- On examination, muscle power is usually preserved (unless there is disuse atrophy from prolonged symptoms)\n- Active range of motion may be limited by pain and stiffness\n- Some patients may have associated swelling and pain in peripheral joints (e.g. wrists and ankles) - this is usually asymmetrical \n- Hands and feet may be swollen with pitting oedema\n- Carpal tunnel syndrome may be present\n\n# Differential Diagnosis\n\n- **Myositis** is often painless but associated with prominent muscle weakness on examination; skin changes are seen in dermatomyositis and CK will be significantly increased\n- **Rheumatoid arthritis** causes joint deformities, primarily affecting the small joints of the hands and feet rather than the larger proximal joints affected in PMR\n- **Malignancy** can cause similar systemic features of weight loss and low-grade fevers; an apical lung cancer may cause shoulder pain (Pancoast tumour) and bone pain is seen in myeloma\n- **Osteoarthritis** also causes joint pain and stiffness, more likely to involve hands, knees, hips and spine\n- **Frozen shoulder** may sometimes be bilateral and causes pain and stiffness with limited range of motion\n- **Chronic infections** such as tuberculosis or infective endocarditis cause similar systemic features and may present non-specifically\n- **Hypothyroidism** also causes fatigue and myalgia; other symptoms include weight gain and constipation\n- **Osteomalacia** causes bone pain and proximal muscle weakness due to vitamin D deficiency\n\n# Investigations \n\nPMR is fundamentally a clinical diagnosis which is supported by resolution of symptoms with steroid treatment.\n\nHowever, given the wide variety of differentials, basic investigations should be undertaken in all patients as follows:\n\n- **Urine dipstick** may be positive for blood due to myoglobin released in myositis\n- **ESR** and/or **CRP** are usually moderately raised in PMR\n- **FBC** - raised white cells may indicate infection, anaemia may be seen in malignancy or due to chronic disease\n- **U&Es** may show renal impairment in myeloma or infection\n- **LFTs** may be deranged e.g. due to metastatic cancer or a high ALP in osteomalacia\n- **Bone profile** may show high calcium in myeloma, or low calcium in osteomalacia\n- **Creatine kinase** will be raised in myositis \n- **Thyroid function tests** for hypo or hyperthyroidism\n- **Protein electrophoresis** to screen for myeloma; **urine Bence Jones protein** should be considered\n- **Rheumatoid factor** as a screen for rheumatoid arthritis, **ANA** and **anti-CCP** antibodies should also be sent if there is clinical suspicion\n- **HbA1c** prior to starting steroids due to their impact on blood glucose control\n- **Chest X-ray** may be indicated if there is suspicion of tuberculosis or lung cancer\n\n# Management\n\n- Patients with core symptoms of PMR, no atypical features and no suspicion of differentials after initial investigations should be started on steroids in primary care\n- 15mg of oral prednisolone once a day is the usual regimen\n- Patients should be reassessed after a week to assess treatment response, and ESR/CRP should be rechecked at 3-4 weeks\n- Consider weaning steroids at 3 weeks - this should be done slowly with close monitoring \n- Usually patients require steroids for 1-2 years\n- Safety-net patients for the risk of giant cell arteritis and advise them to seek urgent medical attention if symptoms develop\n\nImportant management considerations when starting long-term steroids include:\n\n- Give patients a steroid card\n- Advise never to stop steroids suddenly due to the risk of adrenal insufficiency\n- If they are unable to take tablets (e.g. due to vomiting) they need to seek urgent medical advice\n- Explain the risk of immunosuppression and check vaccination status - advise seeking urgent medical advice in patients not immunised if they are exposed to chickenpox, shingles or measles\n- Consider starting bone protection with bisphosphonates +/- vitamin D and calcium supplementation; this should be continued for the duration of steroid treatment before reassessing fragility fracture risk\n- Assess the risk of peptic ulceration and consider starting a proton pump inhibitor for gastric protection\n- Monitor blood pressure and glucose (as hypertension and hyperglycaemia are common side effects)\n\nThe following patients should be referred to rheumatology:\n\n- Atypical clinical features:\n- Aged under 60\n- No shoulder/pelvic girdle pain\n- No stiffness lasting > 45 minutes on waking/after rest\n- Chronic onset of symptoms\n- Red flag signs or symptoms e.g. weight loss or night pain\n- Atypical inflammatory markers i.e. normal or very high (ESR > 100 mm/hour)\n- Limited or no response to steroid treatment\n- Steroids required for over 2 years\n- Unable to wean steroids without relapses\n- Significant adverse effects (or high risk of these) with steroids\n- Suspected giant cell arteritis (ideally requires same day assessment with same day ophthalmology assessment also if there is visual loss)\n\nSecondary care management options for PMR include methotrexate and azathioprine, and physiotherapy may also be of benefit.\n\n# Prognosis\n\n- Generally prognosis is good, with most patients rapidly responding to steroids\n- However relapse is common when steroids are weaned\n- Usually patients require 1-2 years of steroids \n- Some may need many years or even lifelong steroid treatment\n\n# NICE Guidelines\n\n[NICE CKS - Polymyalgia Rheumatica](https://cks.nice.org.uk/topics/polymyalgia-rheumatica/)\n\n# References\n\n[Patient UK - Polymyalgia Rheumatica](https://patient.info/doctor/polymyalgia-rheumatica-pro)\n\n[British Society for Rheumatology - Treatment of polymyalgia rheumatica](https://academic.oup.com/rheumap/article/8/1/rkae002/7606885)",
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"question": "A 65-year-old woman presents to the GP complaining of fatigue and weakness over the last four months. She says she feels stiff, especially around her shoulders and hips. On examination, all movements are 5/5 power using the Medical Research Council (MRC) muscle scale. She does not report any headaches and has no skin rashes.\n\nWhat is the most likely diagnosis?",
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"explanation": "Osteoarthritis is a degenerative arthritis caused by wearing of the articular cartilage. Risk factors include old age and obesity. It typically presents with a long gradual onset of pain and stiffness in affected joints. Distribution can be asymmetrical or symmetrical. Examination findings include reduced range of motion, swelling and crepitus. In the hip, internal rotation is often the first movement to become painful. According to NICE, the diagnosis is confirmed in a patient with all of the following:\n\n- ≥45 years old\n- Activity related joint pain\n- No morning stiffness / <30 minutes of morning stiffness\n\nThis patient meets these criteria and, as such, can be diagnosed with osteoarthritis. Initial management for osteoarthritis includes conservative (weight loss, exercise) and medical (first line: paracetamol) measures, with surgery considered later in disease (arthroplasty)",
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"explanation": "Ankylosing spondylitis is a HLA-B27 associated inflammatory arthritis. It presents with inflammatory joint pain and >30 minutes of morning stiffness. Symptoms are improved by exercise and worsened by rest. In addition, it is an axial spondyloarthropathy. This means it typically affects the spine, with other features including sacroiliac pain. In this case, there is no back pain. This makes ankylosing spondylitis much less likely",
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"explanation": "Rheumatoid arthritis is an inflammatory arthritis. It presents with inflammatory joint pain, with >30 minutes of morning stiffness. Pain and stiffness tend to be improved by exercise and worsened by rest. In addition, although rheumatoid arthritis can affect the hip, it is a less likely site to be affected. More typical sites for early rheumatoid arthritis include the hands, feet and wrists",
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"explanation": "Septic arthritis describes an infection of a joint, which can be life-threatening. Septic arthritis typically presents with pain and swelling over hours to days. There are also no other systemic features like fever or sepsis, which may be present with septic arthritis (although their absence does not rule out septic arthritis)",
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"explanation": "Systemic lupus erythematosus (SLE) is a connective tissue disease that presents with inflammatory arthritis. It presents with inflammatory joint pain, >30 minutes of morning stiffness and pain and stiffness is improved by exercise and worsened by rest. In addition, there are often other extra-articular features in SLE, including fatigue, fever, weight loss, alopecia, malar rash, pericarditis, pleural effusion, blood abnormalities, and neurological involvement. There is also an association with antiphospholipid syndrome. None of these features are present in this case, making a diagnosis of SLE less likely",
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"explanation": "# Summary\n\nOsteoarthritis (OA) is a chronic, degenerative joint disease characterised by loss of articular cartilage, remodelling of bone with osteophyte formation and mild synovitis. The main risk factor is older age, although obesity, joint injury and genetics also contribute. Presentation is with gradual onset pain that is worse with activity, with associated functional limitations. The most commonly affected joints are the knees, hips and small joints of the hands. Diagnosis is clinical, and severity of disease on X-ray does not correlate well with severity of symptoms. Management should be individualised, with important components being exercise, simple analgesia and optimisation of risk factors (such as maintaining a healthy weight). Where there is ongoing pain and disability, options include intra-articular steroid injections and surgical intervention (such as joint replacement).\n\n# Definition\n\nOsteoarthritis (OA) is the commonest form of arthritis, which is characterised by degenerative changes affecting the entirety of joints affected. Cartilage is lost, the subchondral bone becomes sclerosed with formation of osteophytes and subchondral cysts and there is inflammation of the synovial membrane lining the joint capsule (synovitis). \n\n# Epidemiology\n\n- Approximately 10 million people in the UK have osteoarthritis\n- More women than men are affected\n- Average age of onset is 55 \n- The commonest joint affected is the knee, followed by the hip then the hand\n\n# Aetiology\n\nOsteoarthritis develops due to a combination of factors, with important contributors including:\n\n- Older age\n- Female sex\n- Overweight or obesity\n- Family history of OA\n- Previous joint injury\n- Joint damage due to inflammation (e.g. in patients with inflammatory arthritis)\n- Physical inactivity and reduced muscle strength\n- Low bone density \n- Deformities such as development dysplasia of the hip or leg length discrepancy\n- Stresses on joints due to occupational factors (e.g. repetitive squatting or kneeling) or exercise\n\n# Signs and Symptoms\n\nKey symptoms include:\n\n- Pain in the affected joint exacerbated by use\n- Pain may radiate e.g to the thigh, knee and ankle in hip OA, or to the wrist in hand OA\n- Joints may feel stiff (although prolonged morning stiffness is suggestive of inflammatory arthritis)\n- Functional limitations such as difficulty opening jars (hand OA) or mobilising (knee or hip OA)\n- Locking or giving way of the knee\n\nExamination findings include:\n\n- Restricted and painful range of motion (e.g. in hip OA internal rotation with the hip flexed is particularly painful)\n- Crepitus (friction between bone and cartilage) \n- Affected joints may appear swollen or enlarged\n- A small effusion may form, especially when the knee is affected\n- Synovitis may present with mild soft tissue swelling, tenderness and warmth\n- Muscle wasting and weakness can result from disuse atrophy\n- Joint instability\n- An antalgic gait (\"limping\") in knee OA\n- Trendelenburg gait in hip OA (due to weak abductors patients lurch towards the affected hip)\n- Deformities, including:\n- Heberden's nodes (bony nodules over the distal interphalangeal joints) \n- Bouchard's nodes (bony nodules over the proximal interphalangeal joints) \n- Fixed flexion of the first carpometacarpal joint with hyperextension of the distal joints\n- This may lead to squaring of the joint with subluxation and remodelling\n- Ulnar or radial deviation of joints in the hand may occur\n- In severe hip OA the leg may be shortened due to fixed flexion and external rotation\n- Varus (most commonly) or valgus deformities of the knees \n\n# Differential Diagnosis\n\n- **Inflammatory arthritis** such as rheumatoid arthritis, ankylosing spondylitis; pain that improves with activity and morning stiffness lasting over 30 minutes are differentiating factors, systemic symptoms such as malaise and weight loss may be present\n- **Septic arthritis** is an important differential for all patients presenting with an acutely painful swollen joint (which may occur in an acute flare of osteoarthritis); patients may be systemically unwell with fevers\n- **Fracture** e.g. of the tibial plateau may mimic OA symptoms of pain and limited mobility; usually the patient is unable to weight bear with swelling of the affected area; a history of trauma should be elicited\n- **Malignancy** including bone metastases, multiple myeloma or sarcoma may cause mechanical pain leading to functional limitations; red flags include weight loss, night sweats, persistent pain not relieved by rest and night pain\n- **Greater trochanteric pain syndrome** most commonly occurs in middle-aged women and causes lateral hip pain and tenderness worsened by activity; it may also radiate to the lateral knee\n- **Iliotibial band syndrome** presents with lateral knee pain worse with activity, which is often accompanied by clicking or clunking sounds when the knee is moved; occurs most commonly due to repetitive knee flexion e.g. cyclists or runners \n- **Meniscal tear** may occur after an injury involving a twisting or pivoting movement; similar symptoms of pain, swelling, locking and giving way of the knee and range of motion may be limited on examination\n- **Trigger thumb** may mimic OA of the hand with pain, clicking and catching when the thumb is flexed; a nodule may be palpable in the tendon\n- **Ganglion cysts** occur more commonly in people with OA and present as soft tissue swellings e.g. at the base of the thumb; often asymptomatic but may cause pain and limit movement of the joint\n\n# Investigations\n\nDiagnosis of OA is clinical and can be made without any investigations in a patient of 45 or older if there are no features suggesting another underlying cause of symptoms.\n\nIf there is diagnostic uncertainty or a rapid deterioration in symptoms, **X-rays** of affected joints may be of use. Typical findings can be remembered with the mnemonic \"LOSS\":\n\n- **L**oss or narrowing of joint space due to thinning of cartilage\n- **O**steophytes i.e. formation of new bony spurs at the joint margins\n- **S**ubchondral sclerosis i.e. increased bone density beneath the cartilage\n- **S**ubchondral cysts which are fluid-filled sacs in the subchondral bone\n\n[lightgallery]\n\nHowever, severity of OA features on X-ray may not correlate well with severity of clinical disease.\n\nOther investigations if the diagnosis is in doubt should be targeted to the differential suspected, and may include:\n\n- Further imaging such as MRI to look for ligament or cartilage damage (e.g. a meniscal tear)\n- Joint aspiration with synovial fluid analysis to exclude septic arthritis or crystal arthritis\n- Blood tests for inflammatory markers, rheumatoid factor and anti-CCP (for example) if rheumatoid arthritis is suspected\n\nBaseline bloods for renal function and full blood count should be considered in all patients starting NSAID treatment, especially older patients who are at higher risk of adverse effects.\n\n# Management\n\n**Conservative management:**\n\n- Patient education and advice on self-care e.g. appropriate footwear\n- Weight loss advice and signposting to services in patients with excess body weight\n- Exercise has many benefits including strengthening muscles, improving fitness, reducing pain and improving function\n- Options include online fitness programmes designed for people with arthritis, physiotherapy and supervised exercise sessions\n- Physiotherapy services may also be able to offer manual therapies and joint supports such as braces or splints to reduce load and improve instability\n- Occupational health input may be needed in patients with functional impairment to assess their working environment and suggest adaptations\n- Patients should be asked about psychosocial stressors and support offered e.g. for associated depression and anxiety\n- Occupational therapy input may be helpful to advise on aids and devices to assist with activities of daily living (e.g. walking sticks, sock aids, grab rails, tap turners)\n- Podiatry input may be useful to assess the biomechanics of joint pain and advise on orthotic devices such as insoles\n- Referral to a pain management service may be appropriate for patients who have not responded to maximal medical (and if appropriate, surgical) management of OA\n- Assess falls risk and consider referral to specialist services for patients at risk (e.g. those with abnormal gait or balance, or who have had a fall in the last year)\n\n**Medical management:**\n\n- First-line analgesia is with topical NSAIDs (such as ibuprofen gel) - patients should be made aware that some systemic absorption may occur\n- If this is ineffective or unsuitable, oral NSAIDs should be considered (with a PPI for gastroprotection if there are risk factors for gastrointestinal side effects)\n- Paracetamol or weak opioids (e.g. codeine) may also be used in the short-term\n- Topical capsaicin is another option, especially for knee OA\n- Intra-articular steroid injections may be considered if other treatments are not effective, and/or to enable therapeutic exercise\n\n**Surgical management:**\n\n- Patients with OA of the hip, knee or shoulder who have symptoms significantly impacting quality of life despite optimal medical management should be considered for orthopaedic referral\n- The usual operation offered is an arthroplasty (joint replacement)\n- Rehabilitation before and after surgery is key to optimising outcomes\n\n# Complications\n\n- Joint deformities (as above)\n- Increased risk of falls\n- Functional limitations, e.g. hand OA may making writing, turning keys or fasting buttons challenging\n- Reduced mobility \n- Sleep difficulties\n- Low mood and anxiety\n- Chronic pain\n\n# Prognosis\n\n- Not all cases of OA are progressive and the disease course is variable\n- OA of the hands generally has a good prognosis, especially interphalangeal joint involvement\n- Hip OA has a poorer prognosis with many patients requiring arthroplasty\n- Knee arthroplasties for OA are also common however many patients' symptoms improve or remain stable with time \n- Intermittent flares of OA may occur, where symptoms increase in intensity suddenly\n- Flares tend to last for a few days before improving\n\n# NICE Guidelines\n\n[NICE CKS - Osteoarthritis](https://cks.nice.org.uk/topics/osteoarthritis)\n\n[NICE - Osteoarthritis in over 16s: diagnosis and management](https://www.nice.org.uk/guidance/ng226/)\n\n# References\n\n[WHO fact sheet - Osteoarthritis](https://www.who.int/news-room/fact-sheets/detail/osteoarthritis)\n\n[BNF Treatment Summaries - Osteoarthritis](https://bnf.nice.org.uk/treatment-summaries/osteoarthritis/)\n\n[Patient UK - Osteoarthritis](https://patient.info/doctor/osteoarthritis-pro)",
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"question": "A 77-year-old man presents to his GP complaining of right hip pain. This has been gradually getting worse over the last two years is worsened by movement. He is stiff for around 20 minutes in the morning. On examination, he has a large body habitus and has pain upon internal rotation of the right hip.\n\nWhat is the most likely diagnosis?",
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"explanation": "Osteoarthritis is a non-inflammatory \"wear and tear\" arthritis. It presents with degenerative joint pain. This means there will not be any morning stiffness (or <30 minutes), and the pain gets worse on exercise. In addition, osteoarthritis typically affects those over 45 years old and has a longer, more gradual onset (typically over years). Although osteoarthritis can affect the hands, it is unlikely to affect so many joints in the hand symmetrically",
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"explanation": "Enteric arthropathy is a spondyloarthropathy that is often associated with inflammatory bowel disease. The joints affected include the spine and large peripheral joints. The absence of inflammatory bowel disease and the distribution of joint disease makes enteric arthropathy a less likely diagnosis",
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"explanation": "Psoriatic arthritis is also an inflammatory arthritis. Symmetrical polyarthritis is a subtype of psoriatic arthritis that can present in the same distribution shown in the question. However, it tends to be associated with skin psoriasis, so many patients will also present with psoriatic plaques or psoriatic nail changes (although some patients will still not present with skin psoriasis). In addition, psoriatic arthritis also tends to affect the distal interphalangeal joints (DIPJ), unlike rheumatoid arthritis. The absence of DIPJ involvement and skin psoriasis makes a diagnosis of rheumatoid arthritis more likely",
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"explanation": "Rheumatoid arthritis is an inflammatory arthritis that can present at any age but typically presents in middle-aged females and smokers. It typically comes on over a few months, with pain and stiffness improved with exercise and worsened by rest, along with prolonged morning stiffness. The typical distribution in early rheumatoid arthritis is the metacarpophalangeal joints and proximal interphalangeal joints in the hands and the small joints of the feet and wrists. The distal interphalangeal joints are characteristically not affected in rheumatoid arthritis. This patient should have some blood tests, hand x-rays and a referral to rheumatology for consideration of a disease-modifying anti-rheumatic drug (DMARD)",
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"explanation": "Systemic lupus erythematosus (SLE) is a connective tissue disease that presents with inflammatory arthritis. However, there are often other extra-articular features in SLE, including fatigue, fever, weight loss, alopecia, malar rash, pericarditis, pleural effusion, blood abnormalities, neurological involvement, and there is an association with antiphospholipid syndrome. None of these features are present in this case, making a diagnosis of SLE less likely",
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"explanation": "# Side effects of corticosteroids\n\n**Corticosteroids** (think CORTICOSTEROIDS):\n\n- Cushing's syndrome\n- Osteoporosis\n- Retardation of growth\n- Thin skin, easy bruising\n- Immunosuppression\n- Cataracts and glaucoma\n- Oedema\n- Suppression of HPA axis\n- Teratogenic\n- Emotional disturbance (including psychosis\n- Rise in BP\n- Obesity (truncal)\n- Increased hair growth (hirsutism)\n- Diabetes mellitus\n- Striae\n\n# Side effects of NSAIDs\n\n- Indigestion\n- Peptic ulcer disease,\n- Increased risk of venous thrombo-embolus\n- Peripheral oedema\n- Slightly increased risk of stroke and heart attack\n\n# Side effects of Methotrexate\n\n- Gastro-intestinal disturbance\n- Folate deficiency - anaemia\n- Immunosuppression\n- Pulmonary fibrosis\n- Liver toxicity\n- Interstitial pneumonitis\n- Rash\n- Teratogenicity - Methotrexate is contraindicated during conception and pregnancy. The recommendation is a washout of a few months (at least 3 months) before conception. In the event of a disease flare, low-dose steroids are thought to be relatively safe. Note that high doses are associated with a small increased risk of the child having a cleft palate.\n\n# Side effects of Sulfasalazine\n\n- Myelosuppression\n- Nausea\n- Rash\n- Oral ulcers\n- Decreased sperm count\n\n# Side effects of Hydroxychloroquine\n\n- Retinopathy\n- Rash\n\n# Side effects of Biologic therapy (e.g. etanercept, infliximab, adalimumab)\n\n- Immunosuppression\n- Reactivation of TB\n- Allergic reaction, reaction at infusion site\n\n# Side effects of Gold\n\n- Myelosuppression\n- Renal toxicity (Nephrotic syndrome)\n- Mouth ulcers\n- Photosensitivity\n- Chrysiasis (skin discolouration)",
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"question": "A 31-year-old female medical secretary presents to her GP with a two-month history of painful and stiff hands. The pain gets better throughout the day, but she has to get up 3 hours before work to have time for the stiffness to subside. On examination, there is swelling over all metacarpophalangeal joints and proximal interphalangeal joints on both hands.\n\nWhat is the most likely diagnosis?",
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"explanation": "This patient does have cellulitis. They have a red, swollen leg after a history of penetrating trauma (that introduced infection to the leg). However, this is not the whole picture. Cellulitis is unlikely to cause such a high heart rate without being accompanied by sepsis. A heart rate above 130/min is a red flag symptom of sepsis. According to NICE guidelines, any patient with one red flag feature of sepsis should have an urgent senior review and be managed as sepsis until proven otherwise",
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"explanation": "Deep vein thrombosis (DVT) also presents with a red, hot, swollen leg. However, this patient has no risk factors for DVT – no surgery, long haul travel, malignancy, personal history of thrombosis or family history of thrombosis (which could suggest hereditary thrombophilia). A diagnosis of DVT would not explain why this patient developed these symptoms after a penetrating leg injury (unless this history clearly stated prolonged immobility after this injury). Pulmonary embolism (associated with deep vein thrombosis) can present with tachycardia; however, this patient has pyrexia of 38.6ºC, whereas DVT and PE typically present with a no fever or a low-grade fever",
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"explanation": "A ruptured Baker's cyst can present similarly to a DVT and cellulitis, with redness, swelling and pain. However, a ruptured Baker's cyst does not explain the presence of a fever and tachycardia. Symptoms of a ruptured Baker's cyst are usually only confined to the leg, without any systemic symptoms",
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"explanation": "Necrotising fasciitis is a life-threatening infection of the skin. It can present after a penetrating injury, typically as an area of erythema with a necrotic centre. This necrosis can spread, leading to sepsis and death. What differentiates this case from necrotising fasciitis is the time course. Necrotising fasciitis is rapidly progressive, so it is unlikely this patient will have a slow progression over a couple of days. There is also likely to be signs of necrosis on limb examination",
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"explanation": "Sepsis is a dysregulated immune response to infection, most often associated with a bacterial infection. In this case, this patient likely has cellulitis of their leg, which has progressed to sepsis. The examination findings suggest sepsis is the most likely diagnosis. He has a heart rate of 136/min, a red flag feature of sepsis (>130/min). They are also presenting with a high fever, which supports the diagnosis of cellulitis and sepsis. Heart rate can be raised for other reasons, including pain and anxiety. However, in the case of someone presenting with red flag features of sepsis in the clinical context of infection, they should be treated as sepsis until proven otherwise. If they have a high heart rate from anxiety or pain, they would probably also have high blood pressure as well. According to NICE guidelines, any patient with one red flag feature of sepsis should have an urgent senior review and be managed as sepsis until proven otherwise. In addition to a senior review, they should have the \"sepsis 6\" within 1 hour (including blood culture, blood lactate, urine output measurements, IV antibiotics, IV fluids and oxygen). This patient is quite well considering the likely diagnosis of sepsis. However, as they are a 27-year-old man, they probably have an excellent physiological reserve and compensate well. This patient should still be treated promptly to prevent rapid deterioration",
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"comment": "Bruh :'(",
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"comment": "Right but the overall diagnosis is cellulitis?",
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"comment": "It’s asking for an explanation for the obs which show he is systemically unwell",
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"comment": "why does this shit website want to catch you out all the time",
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"comment": "This gave me AIDS",
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"comment": "like bruh... were all trying to pass finals you dont have to catch us out 24/7",
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"comment": "it says in the explanation he's 27 but in the vignette its saying 72?",
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"explanation": "# Summary\n \nSepsis is a syndrome characterised by life-threatening organ dysfunction that occurs due to a dysregulated response to infection. Key signs and symptoms include fever, altered mental state, tachycardia, hypotension and dehydration, as well as localising signs of infection. The \"Sepsis Six\" bundle is used to guide care in the first hour following recognition of sepsis; this involves taking blood tests including cultures, a blood gas to measure lactate and monitoring urine output, and giving oxygen, IV broad-spectrum antibiotics and IV fluids.\n \n# Definition\n\nThe terminology used to describe sepsis has changed, with terms like \"severe sepsis\" and SIRS (systemic inflammatory response syndrome) no longer in use.\n\n**Sepsis** is defined as a syndrome of life-threatening organ dysfunction due to a dysregulated host response to infection.\n\n**Septic shock** is another term used to describe some patients with sepsis who are at greater risk of death. To be classified as having septic shock, patients need to be persistently hypotensive, requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more **and** have a lactate of over 2 mmol/L despite adequate fluid resuscitation. \n\n# Epidemiology\n\n- Due to variations in coding and definitions, statistics related to admissions to hospital with sepsis tend to be inconsistent\n- Approximately 200,000 people are admitted to hospital with sepsis per year\n- Approximately 20% of these (40,000 per year) require intensive care admission\n- Mortality is also approximately 20%, with deaths estimated at up to 48,000 per year in the UK\n- Men are more commonly affected than women\n- Patients at the extremes of age (infants under a year and people aged over 75) are more at risk\n\n# Aetiology\n\n- The commonest sources of infection are respiratory, genitourinary, renal and gastrointestinal \n- Most causative pathogens are bacteria, although fungal, parasitic and viral infections can also lead to sepsis\n- The commonest organisms identified are Staphylococcus aureus, Escherichia coli and Pseudomonas species\n- In 50% of sepsis cases, no causative pathogen is identified \n\n**Risk factors** for sepsis include:\n\n- Pregnancy\n- Recent miscarriage or abortion\n- Frailty\n- Immunocompromise due to chronic comorbidities e.g. HIV, diabetes, sickle cell disease\n- Immunosuppression secondary to medications e.g. chemotherapy, steroids\n- Recent surgery or trauma\n- Skin breaks or infections\n- Drug or alcohol misuse\n- Indwelling lines or catheters\n\n# Signs and Symptoms\n\nSymptoms include:\n\n- General malaise\n- Fevers, sweats or chills\n- Localising signs of infection e.g. rashes, dysuria\n- Decreased urine output\n- Confusion\n- Breathlessness\n- Nausea and vomiting\n- Myalgia\n \nOn examination, signs include:\n \n- Tachycardia\n- Hypotension\n- Pyrexia or hypothermia\n- Dehydration e.g. dry mucous membranes\n- Altered mental state including delirium\n- Irritability\n- Respiratory distress e.g. tachypnoea, accessory muscle usage\n- Cyanosis and hypoxia\n- Delayed capillary refill time\n- Cool extremities\n- Skin appears mottled or ashen\n\n# Differential Diagnosis\n\n- **Acute alcohol withdrawal** causes altered mental state, tachycardia and sweating; patients are usually tremulous and may have withdrawal seizures if severe\n- **Acute haemorrhage** may cause hypovolaemic shock with signs of shock including tachycardia, hypotension, delayed capillary refill and cool extremities; differentiated by signs of bleeding which may be overt or more subtle (e.g. abdominal pain)\n- **Diabetic ketoacidosis** causes malaise, tachypnoea (with Kussmaul breathing), dehydration and confusion; metabolic acidosis may be seen in both but in diabetic ketoacidosis glucose will be very high\n- **Pulmonary embolism** may cause tachycardia, hypotension, respiratory distress and a low-grade fever; may have haemoptysis and pleuritic chest pain (which could also be seen in sepsis secondary to pneumonia) - CTPA can be used to differentiate if unclear\n- **Thyrotoxicosis** produces similar symptoms of confusion and fevers and signs of tachycardia; thyroid function testing shows high T4 and suppressed TSH\n- **Drug reactions** e.g. neuroleptic malignant syndrome - shares features of fever, confusion, labile blood pressure and sweating; differentiated by a recent history of antipsychotic use, no localising signs of infection\n\n# Investigations \n\nThe **Sepsis Six** involves taking three key measures (as well as giving three key treatments):\n\n- **Blood cultures** ideally prior to antibiotic administration\n- **Lactate** (i.e. a blood gas - venous or arterial)\n- **Urine output** (which may involve inserting a urinary catheter)\n\nOther **bedside tests** should include:\n\n- **Capillary blood glucose** as hypo or hyperglycaemia may contribute to confusion\n- **Urine pregnancy test** in women of childbearing age\n- **Urine dip** and send for **MC&S** looking for evidence of urinary tract infection\n- **ECG** as in any acutely unwell patient, looking for arrhythmias and ischaemic changes\n\n**Blood tests** should include:\n\n- **FBC** and **CRP** for inflammatory markers\n- **U&Es** looking for evidence of acute kidney injury\n- **LFTs** as a baseline prior to giving antibiotics, may be deranged in sepsis\n- **Coagulation screen** as this may be deranged in sepsis\n\n**Imaging** should include:\n\n- **Chest X-ray** as part of a septic screen\n\nOther investigations should be targeted at a suspected underlying cause, e.g. respiratory or wound swabs, other imaging e.g. a CT abdomen or echocardiogram or special tests e.g. lumbar puncture when stable.\n\n# Management \n \nThe three things that should be given as part of the **Sepsis Six** are:\n\n- IV fluid resuscitation (usually a 500ml bolus over 15 minutes initially)\n- Supplementary oxygen to target saturations of 94-98% (88-92% if at risk of type 2 respiratory failure)\n- Broad-spectrum IV antibiotics (as per local guidelines)\n\nOther **conservative** management considerations involve:\n\n- Close monitoring of observations, fluid balance, clinical condition and bloods including serial lactate measurement\n- Early escalation for senior review and inform intensive care as may require interventions such as inotropes or vasopressors\n\nOther **medical** management involves:\n\n- Modify antibiotic therapy if a source of infection is identified or microbiological results become available\n- Further IV fluids may be required however this should be done with careful fluid balance monitoring\n\n**Surgical** management involves:\n\n- Source control, e.g. draining abscesses or debriding infected tissue\n- Infected devices may need to be removed\n \n# Complications\n\n- **Multi-organ failure** including renal failure, heart failure, acute respiratory distress syndrome and cholestasis\n- **Coagulopathy** including disseminated intravascular coagulation\n- **Delirium** which may be associated with long-term cognitive impairment e.g. difficulty concentrating and memory loss\n- **Mental health impacts** including anxiety, depression and post-traumatic stress disorder\n- **Secondary infections** which are often hospital-acquired\n- **Polyneuropathy** i.e. critical illness polyneuropathy, characterised by generalised weakness and sensory loss\n- **Death**\n\n# Prognosis\n\n- Overall mortality has been estimated at around 20-30%\n- This increases to 64% in patients aged over 85 years\n- Patients with septic shock also have higher mortality (40-60%) \n- Risk of death in survivors remains raised after recovery (15% of sepsis survivors die within a year of discharge, with 6-8% more dying each year for the following 5 years) \n\n# NICE Guidelines\n\n[NICE - Sepsis: recognition, diagnosis and early management](https://www.nice.org.uk/guidance/ng51)\n\n[NICE CKS - Sepsis](https://cks.nice.org.uk/topics/sepsis/)\n\n# References \n \n[UK Sepsis Trust](https://sepsistrust.org/)\n\n[Patient UK - Sepsis](https://patient.info/doctor/sepsis-septicaemia-pro)",
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"question": "A 72-year-old man presents to the emergency department with a two-day history of a painful, red, swollen left leg. \n\nHis past medical history includes type 2 diabetes, hypercholesterolaemia and hypertension.\n\nOn examination, his respiratory rate is 18/min, heart rate is 136/min, blood pressure is 108/72 and temperature 38.6ºC. The left lower leg is erythematous and hot to touch. There are no discernible areas of necrosis. The left leg is 3.1cm larger than the right. The right leg is normal in appearance and temperature.\r\n\r\nWhat is the most likely diagnosis?",
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"explanation": "This patient presents with a typical history of deep vein thrombosis (DVT): a red, hot, swollen calf in the presence of risk factors for venous thrombosis (in this case, long haul flight). The next thing to do in the evaluation of this patient would be a Wells' 2-level DVT score. This patient's Wells' score is 3 points, scoring for: calf swelling >3cm, localised tenderness along the deep venous system and pitting oedema confined to the symptomatic leg. A Wells' score of ≥2 means the patient should have a doppler ultrasound scan of the entire leg to identify any thrombi or emboli in the venous system to confirm the diagnosis. As this patient has a Wells' score of 3, this should be the first investigation",
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"explanation": "Echocardiograms can be used to look for right heart strain associated with a pulmonary embolism, especially in massive pulmonary embolism. However, this patient does not have any signs of pulmonary embolism, so does not need an echocardiogram",
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"explanation": "V/Q scan is used to diagnose PE in patients with symptoms of PE who are unable to have a CTPA. This patient has no features of PE",
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"explanation": "This patient presents with a history typical of deep vein thrombosis, and their Wells' score is 3. In patients with a Wells' score of ≥2, a doppler ultrasound should be performed first line. If their Wells' score was ≤1, then a d-dimer should be performed. D-dimer has a high sensitivity but low specificity for DVT. This makes it a good rule-out test, but it cannot confirm a DVT. A raised d-dimer can have many causes, including malignancy, infection, pregnancy and stroke",
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"explanation": "Deep vein thrombosis (DVT) is associated with pulmonary embolism, as the original clot in the leg can embolise and travel through the systemic vasculature, through the heart and into the pulmonary arteries. However, there are no features suggestive of pulmonary embolism in this case, including no history of breathlessness, chest pain or haemoptysis. A percentage of patients with DVT will have a silent PE, but asymptomatic patients should not receive a CT pulmonary angiography scan to diagnose a silent pulmonary embolism",
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"explanation": "# Summary\n\nDeep Vein Thrombosis (DVT) refers to intra-luminal occlusion of a deep vein with a blood clot, obstructing blood flow. Commonly these occur in the legs although other veins may be affected. DVTs are categorised as \"provoked\" if a transient risk factor such as pregnancy or surgery is identifiable, and \"unprovoked\" if not. Key signs and symptoms include leg pain, unilateral erythema, warmth and swelling and distention of superficial veins. The Wells score is commonly used to assess how likely a DVT is based on clinical findings and risk factors; this guides whether a D-dimer blood test or a Doppler ultrasound should be offered first-line. Management is usually with anticoagulation; in rare cases other strategies such as mechanical thrombectomy and IVC filters may be required.\n \n# Definition\n \nA deep vein thrombosis (DVT) is a blood clot or thrombus that blocks a deep vein, commonly in the legs or pelvis. \n \n# Epidemiology\n \n- Venous thromboembolism (which includes both DVT and pulmonary embolism) is common, affecting 1-2 per 1000 people per year\n- Two-thirds of cases are DVTs and one-third are pulmonary emboli (PE), with DVT being the main risk factor for PE\n- It is particularly common in unwell patients in hospital, with an incidence of up to 37% in critically ill patients\n\n# Aetiology\n \nRisk factors for DVT can be remembered with the mnemonic **THROMBOSIS:**\n \n\n * **T**hrombophilia\n * **H**ormonal (COCP, pregnancy and the postpartum period, HRT)\n * **R**elatives (family history of VTE)\n * **O**lder age (>60)\n * **M**alignancy\n * **B**one fractures\n * **O**besity\n * **S**moking\n * **I**mmobilisation (long-distance travel, recent surgery or trauma)\n * **S**ickness (e.g. acute infection, dehydration)\n\n# Signs and Symptoms\n \n- Unilateral erythema, warmth, swelling and pain in the affected area\n- Pain on palpation of deep veins\n- Distention of superficial veins\n- Difference in calf circumference if the leg is affected\n - This should be measured 10cm below the tibial tuberosity\n - > 3cm difference between the legs is significant\n\n# Differential Diagnosis\n\n- **Cellulitis** also causes erythema, warmth, swelling and pain and often affects the legs, patients may have other signs of infection e.g. fevers and there may be an obvious wound or discharge\n- **Calf muscle tear** also causes swelling, erythema and pain; there will usually be a history of trauma immediately preceding the development of symptoms\n- **Superficial thrombophlebitis** often occurs in the lower limbs in association with varicose veins, however pain is localised to a thrombosed vein rather than there being generalised pain and swelling of the limb\n- **Compartment syndrome** can be differentiated by severe pain out of proportion to clinical signs, often preceded by traumatic injury\n\n# Investigations\n \nThe two-level DVT Wells score is used to risk-stratify patients into patients likely or unlikely to have a DVT as follows:\n\n**Add one point** for each of:\n\n- Active cancer (treatment within the last 6 months or palliative)\n- Paralysis, paresis, or recent plaster immobilisation of the legs\n- Recently bedridden for 3 days or more, or major surgery within the last 12 weeks\n- Localised tenderness along the distribution of the deep venous system\n- Entire leg is swollen.\n- Calf swelling at least 3 cm larger than asymptomatic side\n- Pitting oedema confined to the symptomatic leg\n- Collateral superficial veins\n- Personal history of DVT\n\n**Minus 2 points** if an alternative cause is considered at least as likely as a DVT.\n\nIf the score is **2 or more**:\n \n- DVT is **likely** and an ultrasound doppler of the proximal leg veins should be done within 4 hours\n- If this isn't possible within 4 hours, do a D-dimer test, start interim anticoagulation and arrange the doppler to happen within 24 hours\n \nIf the score is **1 or less**:\n \n- DVT is **unlikely** and a D-dimer should be sent\n- If the results cannot be obtained within 4 hours, offer interim anticoagulation whilst awaiting results\n- If the D-dimer is positive, do an ultrasound doppler of the proximal leg veins \n- If it is negative, anticoagulation should be stopped if it was started and an alternative diagnosis considered\n\n[lightgallery] \n\nD-dimer is not a specific test and is often raised in infection, trauma, malignancy, post-surgery or haemorrhage. \n\nNote that separate guidelines exist for pregnant and postpartum women - linked below in references.\n\n**Baseline blood tests** should be taken when anticoagulation is started, including a FBC, U&Es, LFTs and a coagulation screen. \n\n# Management\n \n- First-line anticoagulant medications are **DOACs** (e.g. apixaban, rivaroxaban)\n- If these are not suitable, second-line options include low molecular weight heparin (LMWH) for at least 5 days followed by dabigatran or edoxaban, or LMWH bridging with warfarin (with a target INR of 2.5)\n- Treatment duration should be at least 3 months for all patients, and 3-6 months for people with active cancer\n- At this point the risk of VTE recurrence should be weighed against the risks of continuing anticoagulation to make a decision about whether to continue\n- In cases of provoked DVTs (where a major transient risk factor is identifiable e.g. surgery), anticoagulation would usually be stopped at 3 months\n- In cases of unprovoked DVTs, consider testing for thrombophilia with antiphospholipid antibodies in patients who are stopping anticoagulation\n- Patients with unprovoked DVTs should be reviewed with baseline blood tests and an examination to investigate the possibility of an undiagnosed cancer - further investigations should be guided by the patient's signs or symptoms\n\n[lightgallery1]\n \n# Complications\n\n- Pulmonary embolism\n- Post-thrombotic syndrome (chronic venous hypertension post-DVT that may cause significant morbidity)\n- Complications of anticoagulation e.g. gastrointestinal bleeding\n\n \n# NICE Guidelines\n \n[NICE CKS - DVT](https://cks.nice.org.uk/topics/deep-vein-thrombosis/)\n\n[NICE - Venous thromboembolic diseases](https://www.nice.org.uk/guidance/ng158/)\n \n# References\n\n[RCEM Learning - Deep Vein Thrombosis](https://www.rcemlearning.co.uk/reference/deep-vein-thrombosis)\n\n[RCOG - Thromboembolic Disease in Pregnancy and the Puerperium](https://www.rcog.org.uk/media/wj2lpco5/gtg-37b-1.pdf)",
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"question": "A 45-year-old presents to the emergency department with a red, hot and swollen left leg. They have recently travelled back to the UK from Australia. On examination, their pulse is 88/min, and they are apyrexial. Their left lower leg is erythematous to the knee, there is pain on palpation of the leg, pitting oedema, and the left leg is 3.4cm larger than the right.\n\nWhich of the following is the next best investigation?",
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"explanation": "This patient is presenting with a paracetamol overdose. However, they took the first dose 6 hours ago. Activated charcoal binds to paracetamol in the GI tract, preventing its absorption. As this patient is not presenting within 1 hour of their overdose, the paracetamol has already absorbed, so activated charcoal will not be effective",
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"explanation": "IV sodium bicarbonate can be used to manage salicylic (aspirin) overdose and tricyclic antidepressant overdose. It does not play a role in the management of paracetamol overdose",
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"explanation": "Paracetamol overdose can be life-threatening and associated with hepatocellular necrosis, renal tubular necrosis, hepatic encephalopathy and death. The most common symptoms of paracetamol overdose are nausea and vomiting. Some patients may also be asymptomatic. The toxic dose of paracetamol is generally >150mg/kg, which this patient would be above, presuming they are 60-100kg. The management of paracetamol overdose depends on certain clinical factors:\n\n- Give immediate n-acetylcysteine — if ingested >15 hours ago or a staggered overdose (taking above recommended dose of paracetamol spaced over more than 1 hour)\n- Give activated charcoal — if ingested within the last hour\n- Wait until 4 hours after ingestion to take paracetamol level — if presenting with ingestion less than 4 hours ago\n- Take a paracetamol level — if presenting 4 hours after ingestion\n\nWhen taking a paracetamol level before treatment, use a nomogram to determine whether nN-acetylcysteine should be given, based on the plasma concentration of paracetamol at that time. N-acetylcysteine also should be given immediately to those at increased risk of toxicity, including those on enzyme inducers, those with pre-existing liver disease or regular alcohol use and those with glutathione depletion (e.g. eating disorders, malnutrition).\n\nThis patient has presented with a staggered overdose of paracetamol, and they have a history of anorexia nervosa that may put them in a glutathione depleted state. These are both indications to start immediate N-acetylcysteine, so this should be the next step in managing this patient",
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"explanation": "As this overdose has been staggered, a plasma paracetamol concentration will not be accurate enough to guide management. It is, therefore, more appropriate to commence treatment with N-acetylcysteine without a paracetamol level",
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"explanation": "This patient is presenting with a paracetamol overdose. However, this a staggered overdose. As the overdose has been taken over a considerable period, a plasma paracetamol concentration will not be accurate enough to guide management. It is, therefore, more appropriate to commence treatment with N-acetylcysteine without a paracetamol level",
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"explanation": "# Summary\n \nParacetamol overdose accounts for 44% of all adult self-poisoning cases in the UK and results in approximately 150,000 hospital admissions annually. Some patients may be asymptomatic, or present with nausea, vomiting, abdominal pain, jaundice or altered mental state. Investigations should include baseline bloods including a clotting and a blood gas, as well as a paracetamol level. Management depends on the dose taken, timing of ingestion and the patient's clinical condition, with N-acetylcysteine being the mainstay of treatment. The decision to treat is often guided by a nomogram although in certain situations N-acetylcysteine should be started immediately.\n \n# Definition \n \nParacetamol overdose refers to when a potentially toxic dose of paracetamol is taken, either accidentally or in the context of a self-harm or suicide attempt. \n \n# Epidemiology \n \nParacetamol is the most common agent ingested in the context of intentional self-harm in the UK. Paracetamol overdose accounts for 44% of all adult self-poisoning cases in the UK, with approximately 150,000 people admitted to hospital each year due to poisoning.\n \n\n# Aetiology\n \n- The pathophysiology of paracetamol toxicity involves the build-up of its toxic metabolite NAPQI (N-acetyl-p-benzoquinone-imine). \n- Normally, NAPQI is inactivated by glutathione in the blood, but in a paracetamol overdose, glutathione stores are rapidly depleted. \n- NAPQI therefore accumulates, unmetabolised, and binds to cellular proteins, causing cell death.\n- This causes both severe hepatotoxicity and nephrotoxicity that can lead to liver and kidney failure. \n\n# Classification\n \n - **Acute overdose** - excessive paracetamol taken in less than 1 hour, usually in the context of self-harm\n - **Staggered overdose** - excessive paracetamol ingested over longer than 1 hour, usually in the context of self harm\n - **Therapeutic excess** - excessive paracetamol taken with the intent to treat pain or fever and without self-harm intent, ingested at a dose greater than 75mg/kg/24 hours.\n\n\n# Signs and Symptoms\n \n- These depend on how long has passed since the overdose was taken\n- In the first 24 hours patients may be asymptomatic or have nausea and vomiting\n- After this, up to around 72 hours, right upper quadrant pain and hypotension may develop\n- From 72 to 96 hours patients may develop liver and renal failure with resulting metabolic acidosis, encephalopathy and coagulopathy, with symptoms of:\n - Confusion\n - Drowsiness\n - Reduced urine output\n - Loin pain\n - Jaundice\n - Bleeding diathesis\n\n# Differential Diagnosis \n\n - **Acute gastroenteritis:** has similar symptoms of nausea, vomiting and abdominal pain; may have diarrhoea and history of unwell contacts\n - **Renal colic:** may also present with haematuria, nausea and vomiting; pain more likely to be \"loin to groin\" rather than right upper quadrant\n - **Decompensation of chronic liver disease:** can present with jaundice, abdominal pain and encephalopathy\n - **Sepsis:** can lead to a lactic acidosis and acute kidney injury; patients are often febrile and may have localising signs or symptoms of infection\n \n# Investigations\n \nBlood tests for paracetamol levels should be taken at least 4 hours after ingestion, as this is when plasma paracetamol concentration peaks so an earlier blood test may underestimate levels\n\nOther important blood tests include:\n \n - Full Blood Count (FBC)\n - Urea and Electrolytes\n - Clotting Screen\n - Liver Function Tests\n - Venous Blood Gas (may show metabolic acidosis)\n - Blood glucose (could also do a bedside capillary blood glucose)\n - Salicylate levels (to look for a mixed overdose with aspirin)\n\n# Management\n \n**Conservative:**\n\n- Weigh patient (important for determining dose of paracetamol taken per kg and to calculate N-acetylcysteine dosing)\n- Consider if any other substances may have been taken with paracetamol\n- If overdose was intentional, refer to liaison psychiatry for a mental health assessment\n - Consider if 1:1 observations are required for high-risk patients\n - Assess risk to self and ongoing suicidal ideation\n - Discharge planning and assess need for ongoing psychiatric input\n- Treat any other self-harm\n\n**Medical:**\n\nDecisions on medical treatment are guided by a nomogram which plots paracetamol levels against time from ingestion. \n\nThe management of paracetamol overdose is dependent on the timing of ingestion, the dose taken, and the patient's clinical condition:\n \n - **Ingestion less than 1 hour ago + dose >150mg/kg**: Administer activated charcoal\n - **Ingestion 1-4 hours ago**: Wait until 4 hours to take a level and treat with N-acetylcysteine (NAC) based on level\n - **Ingestion within 4-8 hours + dose >150mg/kg**: Start NAC immediately if there is going to be a delay of ≥8 hours in obtaining the paracetamol level, otherwise wait for level and treat if level high (above the treatment line on the nomogram)\n - **Ingestion within 8-24 hours + dose >150mg/kg**: Start NAC immediately\n - **Ingestion >24 hours ago**: Start NAC immediately if the patient has jaundice, right upper quadrant tenderness, elevated ALT, INR >1.3 or if the paracetamol concentration is detectable\n - **Staggered overdose**: Start NAC immediately\n \nNAC is given as an IV medication - it acts by increasing glutathione levels thereby preventing toxicity. \n\nThere are two ways to give NAC:\n\n- Standard regimen of 3 consecutive infusions totalling 21 hours in duration \n- The newer SNAP protocol (now recommended by Royal College of Emergency Medicine as standard) where the same dose of NAC is given over 12 hours in two infusions\n- If after either of these are completed, bloods show deranged LFTs, clotting or renal function NAC infusions should be continued and the patient discussed with local liver transplant services\n- Anaphylactoid reactions are a common side effect of NAC, characterised by urticaria, angioedema, nausea and vomiting, tachycardia and bronchospasm but rarely shock\n- These are managed by suspending treatment and giving chlorphenamine and salbutamol nebulisers before restarting (possibly at a slower rate)\n \n**Surgical:**\n\nPatients who develop acute liver failure may require an urgent liver transplant as a life-saving measure - the following groups of patients should be transferred to a liver transplant centre:\n\n- INR > 3 at 48 hours or > 4.5 at any time\n- Oliguric or creatinine > 200\n- pH < 7.3 despite fluid resuscitation\n- Hypotension (systolic blood pressure < 80mmHg)\n- Severe thrombocytopenia\n- Encephalopathy\n \nThe King's College Criteria is used to predict mortality from paracetamol overdose and to identify those patients who would potentially benefit from liver transplantation. It advises consideration of liver transplantation if:\n \n- Blood pH < 7.3\n \n\nOr **all** of:\n \n- Serum creatinine > 300 µmol/L\n- INR > 6.5 (Prothrombin time > 100s)\n- Grade III or IV hepatic encephalopathy\n\n# NICE Guidelines\n\n[NICE CKS - Poisoning or overdose](https://cks.nice.org.uk/topics/poisoning-or-overdose/)\n\n# References\n\n[BNF - Poisoning](https://bnf.nice.org.uk/treatment-summary/poisoning-emergency-treatment.html)\n\n[MHRA - Treating paracetamol overdose with intravenous acetylcysteine](https://www.gov.uk/drug-safety-update/treating-paracetamol-overdose-with-intravenous-acetylcysteine-new-guidance)\n\n[RCEM - SNAP Protocol Position Statement](https://rcem.ac.uk/wp-content/uploads/2021/11/Use_of_SNAP_for_Treatment_of_Paracetamol_Toxicity_Nov_2021.pdf)\n\n[Life in the Fast Lane - liver transplanation for paracetamol toxicity](https://litfl.com/liver-transplantation-for-paracetamol-toxicity/)",
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"question": "A 25-year-old female presents to the emergency department after taking 30 tablets of paracetamol l. They took the first tablet 6 hours ago and took the rest over the course of 5 hours. They feel very nauseous and have vomited, but are otherwise well. Their past medical history includes anorexia nervosa and borderline personality disorder.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "Alcohol abuse can cause a macrocytosis. This patient is drinking above the recommended weekly limit for alcohol consumption; however, he presents with a microcytic anaemia, making alcohol an unlikely cause for his anaemia",
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"label": "e",
"name": "Alcoholism",
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"explanation": "This patient is presenting with a microcytic anaemia. The most common cause of microcytic anaemia is iron-deficiency anaemia. In any patient >60 years old presenting with iron deficiency anaemia, they must be referred as an urgent 2-week wait referral for colonoscopy for colorectal cancer, unless their history suggests an alternative, more likely diagnosis. This patient may have a falsely normal ferritin, as ferritin is an acute phase reactant, elevated in inflammatory states such as infection or malignancy",
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"label": "a",
"name": "Colorectal cancer",
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"explanation": "Thalassaemia is a haemoglobinopathy related to faulty production of haemoglobin. This becomes apparent a few months after birth when the body stops producing foetal haemoglobin (HbF). This can present as a microcytic anaemia; however, this patient has previously had a normal full blood count, making thalassaemia highly unlikely",
"id": "33679",
"label": "b",
"name": "Thalassaemia",
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"explanation": "Megaloblastic anaemia is a macrocytic anaemia caused by folate or vitamin B12 deficiency. This patient is presenting with microcytic anaemia, making megaloblastic anaemia unlikely",
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"label": "d",
"name": "Megaloblastic anaemia",
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"explanation": "Autoimmune haemolytic anaemia (AIHA) usually presents as a normocytic or macrocytic anaemia. This patient is presenting with a microcytic anaemia, making AIHA unlikely",
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"label": "c",
"name": "Autoimmune haemolytic anaemia",
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"explanation": "# Summary\n\nIron deficiency anaemia (IDA) is a common haematological disorder characterized by a shortage of iron in the body, leading to diminished red blood cell production and subsequent oxygen transport. Typical symptoms include fatigue, paleness, shortness of breath, and cognitive impairment. In older adults, it is imperative to consider the possibility of colorectal malignancy, as IDA may result from gastrointestinal bleeding. Thorough investigations, including endoscopic procedures, are often necessary. Management involves iron supplementation, dietary adjustments, and addressing underlying causes. \n\n# Definition\n\nIron deficiency anaemia is a haematological disorder stemming from an insufficient supply of iron, which is vital for the synthesis of haemoglobin—a crucial component of red blood cells. Without adequate iron, the body struggles to produce a sufficient quantity of healthy red blood cells, leading to a reduction in oxygen-carrying capacity and subsequent symptoms of anaemia.\n\n# Epidemiology\n\nIron deficiency anaemia is a global health concern, affecting individuals of all age groups. The prevalence is particularly high among young children, women of childbearing age, and elderly individuals. Geographical variations in prevalence exist, with a higher burden in regions with limited access to diverse diets and iron-rich foods.\n\n\n# Aetiology \n\nThe causes of iron deficiency anaemia are multifactorial and can be attributed to several factors:\n\n- **Dietary Insufficiency:** Inadequate iron intake, especially in individuals with restrictive diets or limited access to iron-rich foods.\n- **Chronic Blood Loss:** Gastrointestinal bleeding, heavy menstrual periods, and other sources of chronic blood loss (e.g. angiodysplasia) can deplete iron stores.\n- **Malabsorption Disorders:** Conditions like coeliac disease, inflammatory bowel disease and atrophic gastritis can hinder iron absorption in the gut. Hookworms are a more prominent cause in tropical setting.\n- **Increased Demand:** During pregnancy and rapid growth phases, the body's iron requirements can surpass the available supply. This can also occur if there is chronic haemolysis\n\n# Signs and Symptoms\n\nThe symptoms of iron deficiency anaemia include: \n\n- Tiredness\n- Lethargy\n- Weakness\n- Palpitations: An increased heart rate may be noticeable, especially when at rest.\n- Cognitive Impairment: Some patients may exhibit difficulty concentrating or memory issues.\n- Cold Intolerance\n- Headaches and dizziness\n- Brittle Nails: Changes in the nails, such as brittleness and spoon-shaped deformities **(koilonychia)**, can be observed.\n- Angular stomatitis\n- Atrophic glossitis\n- Pica: Iron-deficiency anaemia may manifest as pica, with cravings for non-food substances like ice (pagophagia) or clay (geophagia). This is more common in children.\n\n\n# Differential Diagnosis\n\nDistinguishing IDA from other forms of anaemia (such as anaemia of chronic disease) and underlying conditions is crucial. \n\n- **Colorectal Malignancy:** In older adults, it is imperative to rule out colorectal malignancies, especially when IDA is detected. Gastrointestinal bleeding, often occult, can be a sign of an underlying tumour.\n- **Thalassaemias:** Thalasasemias, a group of genetic disorders affecting haemoglobin production, may present with microcytic anaemia. Hemoglobin electrophoresis can help differentiate thalassaemias from IDA.\n- **Chronic Inflammatory Conditions:** Chronic diseases like rheumatoid arthritis or inflammatory bowel disease can lead to anaemia of chronic disease, which must be considered in the evaluation.\n\n# Investigations\n\nTogether with classical symptoms, full blood count (FBC) and blood film will show the presence of: \n\n- **Hypochromic, microcytic red cells** \n- Additional **pencil cells** \n- Occasional **target cells**\n\nReticulocyte counts will be low for the degree of anaemia; red cell count will also be low.\n\n**Further tests** may be performed to confirm the diagnosis of iron deficiency anaemia including:\n\n- **Total iron binding capacity** (TIBC) – Will typically be high as the body mobilises available iron stores owing to the iron deficiency\n\n- **Ferritin** – will be low as available iron stores in the body are mobilised to counteract the iron deficiency\n\n - Note: Ferritin should be measured alongside B<sub>12</sub> and folate to assess possible coexisting haematinic deficiency\n\n - A low ferritin is diagnostic of iron deficiency; however, a normal or high ferritin does not exclude iron deficiency\n\n - Ferritin is an acute phase protein so levels can be masked/influenced by other conditions, particularly inflammation \n – It is good to check a C-reactive protein (CRP) at the same time\n\nIron deficiency anaemia in patients >60y should prompt suspicion **colonic malignancy until proven otherwise** and prompt FIT testing and subsequent 2 week wait referral if indicated according to NICE guidelines. \n\n# Management\n\n* **Iron Supplementation:** Oral or intravenous iron supplements are administered to correct iron deficiency. Intravenous iron is preferred in cases of severe deficiency or malabsorption. Important considerations of oral iron supplementation (usually a 3 month course) include:\n\t* Side effects - diarrhoea, constipation, black stools, abdominal pain, nausea\n\t* If it is not tolerated due to SEs, reduce the dose to one tablet on alternate days, or consider alternative oral preparations.\n\t* Iron supplements should be taken on an empty stomach (preferably one hour before a meal) with a drink containing vitamin C, such as a glass of orange juice or another juice drink with added vitamin C. This aids absorption.\n\t* Oral iron decreases the absorption of oral Levothyroxine. Therefore if both are prescribed, advise patients to take at least 4 hours apart.\n\t* Monitoring - recheck FBC within 4 weeks of starting treatment (haemoglobin concentration should rise by about 20 g/L over 3–4 weeks). Then check the FBC again at 2–4 months to ensure that the haemoglobin level has returned to normal. Once Hb is normal can continue supplementation for 3 further months, and then monitor at 3/6/12-monthly intervals.\n* **Dietary Modifications:** Encouraging a diet rich in iron sources, such as red meat, leafy greens, and fortified cereals, can help maintain iron levels.\n* **Treatment of Contributing Conditions:** If the cause of IDA is chronic blood loss or malabsorption, addressing the underlying condition is essential.\n* **Endoscopic Procedures:** In cases where gastrointestinal bleeding is suspected, endoscopy and colonoscopy may be necessary to locate and treat the bleeding source.\n\n\n# NICE Guidelines\n\n[NICE CKS - Iron-deficiency anaemia](https://cks.nice.org.uk/topics/anaemia-iron-deficiency/)",
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"question": "A 67 year old man presents to the GP complaining of tiredness. Physical examination shows no abnormalities. He drinks 40 units of alcohol per week. He has some blood tests, which are shown below:\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|115 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|4.5x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|200x10<sup>9</sup>/L|150 - 400|\n|Mean Cell Volume (MCV)|66 fL|80 - 96|\n|Ferritin|56 μg/L|12 - 200|\n|Serum Vitamin B12|800 ng/L|160 - 925|\n|Serum Folate|8 μg/L|(3 - 15|\n\n\nHe had no abnormalities on his previous full blood count and haematinics, which were taken two years ago.\n\n\nWhich of the following is the most likely cause of this patient's blood results?",
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"explanation": "Alcoholism is a cause of macrocytosis. It can also be associated with alcoholic neuropathy. However, this patient reports only drinking four units a week, which is within the recommended weekly intake for alcohol. Patients are not always honest about their alcohol intake, but given their history of autoimmune disease and current neurological signs, vitamin B12 deficiency secondary to pernicious anaemia is the more likely diagnosis",
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"explanation": "Hypothyroidism can cause macrocytosis. This patient has hypothyroidism; however, their thyroid function tests are normal. As their thyroid disease is well controlled, it is unlikely that this is causing their macrocytosis. In addition, autoimmune hypothyroidism (the most common cause of hypothyroidism in the UK) is associated with other autoimmune diseases, including pernicious anaemia. Hypothyroidism is unlikely to cause this patient's neurological signs",
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"explanation": "Pernicious anaemia is an autoimmune condition with antibodies targeting intrinsic factor and/or gastric parietal cells. Intrinsic factor is a cofactor produced by gastric parietal cells essential for the absorption of vitamin B12 in the terminal ileum. Therefore, pernicious anaemia can cause a vitamin B12 deficiency. This presents as a macrocytic anaemia with other signs of anaemia, including tiredness and pallor. In addition, B12 deficiency can cause neurological symptoms including paraesthesia, weakness and acute degeneration of the cord in severe cases. As pernicious anaemia is an autoimmune condition, it is associated with other autoimmune disorders, including type 1 diabetes and autoimmune thyroid disorders",
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"explanation": "Type 1 diabetes is associated with diabetic neuropathy and can cause tiredness when the patient is hyperglycemic. However, this patient's type 1 diabetes is well controlled (HbA1c <48 mmol/mol), and this would not explain the macrocytosis in his blood results. Therefore, vitamin B12 deficiency secondary to pernicious anaemia is the more likely diagnosis",
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"explanation": "Iron deficiency anaemia presents with a microcytic anaemia. This patient has a macrocytic anaemia, making iron deficiency anaemia less likely",
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"explanation": "# Summary\n\nPernicious anaemia is a type of megaloblastic anaemia primarily caused by the inability to absorb vitamin B12, essential for red blood cell production, due to autoimmune destruction of the gastric parietal cells. This disorder can lead to a variety of symptoms, including fatigue, pallor, and neurological deficits. Diagnosis often involves blood tests revealing abnormal red blood cells and low levels of vitamin B12. Management primarily involves life-long replacement treatment with cobalamin as well as monitoring for potential complications such as gastric cancer and carcinoids.\n\n# Definition\n\nPernicious anaemia is a deficiency in RBCs caused by lack of vitamin B<sub>12</sub> in the blood\n\nIn the strictest sense, it is caused by autoimmune impairment of intrinsic factor production\n\nThe term is also widely used to describe B<sub>12</sub> deficiency-related anaemia secondary to other causes as well.\n\n# Pathophysiology\n\nThe pathophysiology of pernicious anaemia primarily revolves around the autoimmune destruction of gastric parietal cells, which play a central role in the absorption of vitamin B12. This complex process involves several key factors:\n\n1. **Autoimmune Attack:** In pernicious anaemia, the body's immune system mistakenly targets and destroys gastric parietal cells. These cells are responsible for producing intrinsic factor, a protein necessary for vitamin B12 absorption.\n\n2. **Intrinsic Factor Deficiency:** As a result of autoimmune destruction, intrinsic factor levels decrease, leading to impaired vitamin B12 absorption in the ileum, the final part of the small intestine.\n\n3. **Vitamin B12 Deficiency:** Reduced absorption of vitamin B12 results in a deficiency of this essential nutrient. Vitamin B12 is crucial for erythropoiesis (the formation of red blood cells) and the maintenance of the nervous system.\n\n4. **Megaloblastic Changes:** Vitamin B12 deficiency leads to impaired DNA synthesis in developing blood cells. This results in megaloblastic changes, causing larger, structurally abnormal red blood cells (megaloblasts) in the bone marrow. These larger cells are less effective at carrying oxygen, leading to anaemia.\n\n\n6. **Haemolysis:** Pernicious anaemia can lead to haemolysis (the breakdown of red blood cells) due to their structural abnormalities. .\n\n\n# Epidemiology\n\nPernicious anaemia is more common in individuals of Northern European, Scandinavian, and African descent, typically affecting adults aged 60 or older. It is often associated with other autoimmune conditions, such as autoimmune thyroid diseases and type 1 diabetes. The prevalence of pernicious anaemia may be underestimated due to underdiagnosis.\n\n# Aetiology\n\nPernicious anaemia is primarily autoimmune in nature, with the destruction of gastric parietal cells leading to a lack of intrinsic factor. Contributing factors may include genetics, as pernicious anaemia can run in families. Other autoimmune conditions are often comorbid with this disorder.\n\n# Signs and Symptoms\n\n* Fatigue\n* Pallor\n* Glossitis - inflammation of the tongue, leading to a smooth, beefy-red appearance.\n* Neurological Symptoms and subacute combined degeneration of the cord: Pernicious anaemia may cause neuropathy, affecting balance, sensation, and coordination.\n* Jaundice - due to haemolysis\n* Cognitive Impairment - memory problems, confusion, and mood changes may occur\n\n# Differential Diagnosis\n\n* **Iron-Deficiency Anaemia (IDA):** Both conditions can lead to anaemia, but IDA is characterised by low ferritin levels and microcytic RBCs, whereas pernicious anaemia causes megaloblastic changes.\n* **Folate Deficiency Anaemia:** Like pernicious anaemia, folate deficiency leads to megaloblastic anaemia, but serum levels of vitamin B12 and folate help differentiate the two.\n* **Myelodysplastic Syndromes (MDS):** MDS can mimic the clinical and laboratory findings of pernicious anaemia but often occurs in older adults and involves specific bone marrow abnormalities.\n\n\n# Investigations\n\n* Full Blood Count (FBC): Reveals macrocytic anaemia and may show hypersegmented neutrophils.\n\t- Low haemoglobin level\n\t- High MCV\n\t- High mean corpuscular haemoglobin (MCH)\n\t- Normal mean corpuscular haemoglobin concentration (MCHC)\n\t- Low reticulocyte count\n- Blood smear - abnormally large and oval-shaped RBCs \n* Vitamin B12 Assays: Measure serum vitamin B12 levels, which are typically low in pernicious anaemia.\n* Intrinsic Factor Antibodies: These antibodies help confirm the autoimmune nature of the condition. This test is highly specific.\n* Parietal cell Antibodies: This test is highly sensitive.\n* Bone Marrow Aspiration and Biopsy: May show megaloblastic changes in erythropoiesis.\n\n\nPernicious anaemia is associated with atrophic body gastritis – diagnostic criteria are based on histologic evidence of gastric body atrophy associated with hypochlorhydria.\n\n**Note**: 'active' vitamin B<sub>12</sub> or holotranscobalamin is a more sensitive measure of vitamin B<sub>12</sub> deficiency – total vitamin B<sub>12</sub> is mostly bound to carrier proteins.\n\n\n# Management\n\nManagement of patients with pernicious anaemia is **lifelong replacement** by **quarterly treatment with hydroxycobalamin** and close monitoring to ensure early diagnosis of any subsequently unmasked iron deficiency. Folate replacement is also often necessary.\n\n\n# Complications\n\nPatients should be advised about possible long-term gastrointestinal consequences, such as gastric cancer and carcinoid.\n\nVitamin B<sub>12</sub> is required for the nervous system so, in vitamin B<sub>12</sub> deficiency, always consider: \n\n- Peripheral neuropathy\n- Subacute combined degeneration of the cord\n- Optic atrophy \n- Dementia\n\nVitamin B<sub>12</sub> deficiency can be associated with other autoimmune disorders such as hypothyroidism and vitiligo.\n\n# NICE Guidelines\n\n[NICE CKS - B12/Folate deficiency anaemia summmary](https://cks.nice.org.uk/topics/anaemia-b12-folate-deficiency/)\n\n",
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"question": "A 33 year old patient presents to the GP with a four-month history tiredness and a one-month history of pins and needles in their legs. They have a past medical history of type 1 diabetes and hypothyroidism. They drink 6 units of alcohol per week. Their blood results are shown below:\n\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|105 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|7x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|303x10<sup>9</sup>/L|150 - 400|\n|Mean Cell Volume (MCV)|105 fL|80 - 96|\n|HbA1c (Glycated Haemoglobin)|47 mmol/mol|20 - 42 or 4-6%|\n|Thyroid Stimulating Hormone|3.6 mU/L|0.3 - 4.2|\n|Free T4|14 pmol/L|9 - 25|\n\n\nWhich of the following is the most likely cause of this patient's blood results?",
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"explanation": "Acute chest syndrome is a severe complication of sickle cell disease. It is caused by infarction of lung tissue as the sickled red blood cells occlude pulmonary vasculature. Typical presenting features include fever, cough, chest pain and shortness of breath. Their physical examination can be normal, or findings such as crepitations and reduced air entry on auscultation can be found. Anaemia and thrombocytopenia are also typical features. However, this would not explain the white cell count. The main differentiating biochemical feature is this patient's reticulocyte count. There will be a high reticulocyte count in acute chest syndrome as the body is trying to produce red blood cells to replace those lost in haemolysis. A low reticulocyte count indicates a failure of bone marrow. This makes aplastic crisis secondary to parvovirus B19 infection the most likely diagnosis",
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"explanation": "Autoimmune haemolytic anaemia can present as a normocytic (or macrocytic) anaemia. However, this would not typically cause a low white cell or platelet count. Reticulocyte count is also characteristically high in autoimmune haemolytic anaemia as the body is trying to compensate and produce more red blood cells",
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"explanation": "B12 deficiency anaemia presents with a macrocytic anaemia. In this case, this patient presented with a normocytic anaemia. This would also not explain the leukopenia and thrombocytopenia in this patient's blood tests. Of note, a combination of iron deficiency anaemia and megaloblastic anaemia can present as a normocytic anaemia, as the macrocytic and microcytic cells create a normocytic mean cell volume. This could be further investigated with a red cell distribution width. However, this is more common in conditions like coeliac disease. Given this patient's clear history of sickle cell disease and the presence of leukopenia, thrombocytopenia and a low reticulocyte count, aplastic crisis secondary to parvovirus B19 infection is the most likely diagnosis",
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"explanation": "An aplastic crisis is a sickle cell crisis associated with the bone marrow not producing any cells. The most common cause is infection with parvovirus B19. Parvovirus B19 causes fifth's disease (also known as slapped cheek syndrome or erythema infectiosum), usually a benign, self-resolving childhood illness. In children with sickle cell disease, their red blood cells have a much shorter survivability meaning that cessation of new blood cell production, which can be associated with parvovirus B19 infection, can lead to pancytopenia over days. Features that point to this diagnosis include a history of sickle cell disease, acute onset of pallor and breathlessness over a few days, normal auscultation and pancytopenia with normocytic anaemia. Reticulocyte count is another key feature in this question. In haemolytic anaemias, reticulocyte count is high as the body tries to make red blood cells to compensate for the haemolysis. Low reticulocyte count suggests red cell production failure, making aplastic crisis secondary to parvovirus B19 infection the most likely diagnosis. Of note, although chest auscultation is often normal in anaemia, a flow murmur may be heard in severe anaemia",
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"explanation": "Acute lymphoblastic leukaemia (ALL) can also present with pancytopenia, although it typically affects children under 6. Lymphadenopathy and hepatosplenomegaly are characteristic features of leukaemia, although their absence does not rule out leukaemia. Although patients with ALL can present with low haemoglobin and low platelets, the white cell count is characteristically high. This is because the bone marrow produces an excessive amount of lymphoblasts (lymphocyte precursors), which reduces the proportion of bone marrow able to produce other cells (leading to thrombocytopenia and anaemia). The low white cell count makes acute lymphoblastic leukaemia unlikely in this patient",
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"explanation": "# Summary\n \n\nFifth disease, also known as \" slapped cheek syndrome\" or erythema infectiosum, is a viral illness caused by Parvovirus B19. It typically presents in children with a prodrome of fever, coryza, and diarrhoea, followed by a distinctive 'lace-like' rash across the body and bright red cheeks. Diagnosis is typically clinical, with management being largely supportive. Complications can include red cell aplasia, severe anaemia in vulnerable populations, and severe foetal anaemia in pregnant women, which can lead to hydrops foetalis and miscarriage. \n \n\n# Definition\n \n\nFifth disease, or erythema infectiosum, is a viral illness caused by Parvovirus B19 most commonly occurring in children.\n \n\n# Epidemiology\n \n\nThis illness is widespread and can occur in outbreaks, particularly in school settings. It is most common in late winter and early spring. \n\nIt is most common in children aged 6-10 years but can affect individuals of any age. 50% of children aged 15 years and almost 90% of older people have evidence of previous parvovirus B19 infection. \n \n\n# Aetiology\n \n\nFifth disease is caused by Parvovirus B19, a virus that specifically targets erythroid progenitor cells, hence its particular association with certain haematological complications. It is spread through droplet transmission with an incubation period of 14-21 days. \n \n\n# Signs and Symptoms\n \n\n- Prodrome of fever, coryza, abdominal pain, headache\n- This is followed 1-2 weeks later by \n - Characteristic bright red rash on the cheeks, giving rise to the name \" slapped cheek syndrome\"\n - A few days later - a diffuse 'lace-like' rash develops across the body, this may last 1-3 weeks \n\nMany people are asymptomatic with the virus. \n\n[lightgallery]\n \n\n# Differential Diagnosis\n \n\n - **Rubella**: presents with a similar rash, but also includes lymphadenopathy and conjunctivitis\n - **Scarlet fever**: presents with a similar rash, but also includes a sore throat and a 'strawberry' tongue\n - **Roseola infantum**: presents with a high fever followed by a rash, but the rash is typically non-pruritic and pink in colour\n \n\n# Investigations\n \n\nDiagnoses are typically made clinically based on presentation. In atypical cases or when complications are suspected, serological testing for Parvovirus B19 can be performed. FBC may reveal low reticulocyte count.\n \n\n# Management\n \n\n- Management is largely supportive, including rest, hydration, and over-the-counter remedies for fever and itching\n- In cases with severe complications such as aplastic crisis, hospitalisation and transfusions may be required.\n\nThe rash means that the child is no longer infectious, so is able to attend school and nursery. The school, however, should be notified such that high-risk groups who have been in contact with the child should seek attention (i.e. pregnant women or immunocompromised). \n \n\n# Complications\n \n\n - Red cell aplasia: Parvovirus infection reduces erythropoiesis, which can precipitate severe anaemia and aplastic crisis in vulnerable groups such as those with conditions like sickle cell anaemia and hereditary spherocytosis.\n - Severe foetal anaemia: Infection in the first half of pregnancy can cause severe foetal anaemia that can precipitate hydrops foetalis and subsequent miscarriage.\n - Cardiomyopathy\n - Neurologic complications:\n - Encephalitis, meningitis, stroke, and peripheral neuropathy can all occur due to parvovirus B19 infection\n\n \n# Prognosis \n\nSlapped cheek syndrome is typically a mild, self-limiting viral syndrome but thereafter the individual is immune lifelong. \n\n \n# NICE Guidelines \n \n [NICE Guidelines Parvovirus B19 infection](https://cks.nice.org.uk/topics/parvovirus-b19-infection/) \n \n\n# References\n \n [NHS Information on Slapped cheek syndrome](https://www.nhs.uk/conditions/slapped-cheek-syndrome/) \n\n [Information on Parvovirus B19](https://www.arthritis.org/diseases/fifth-disease)\n \n [Patient Info Slapped cheek disease](https://patient.info/childrens-health/slapped-cheek-disease-leaflet)",
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"question": "An 8-year-old boy presents to the emergency department with shortness of breath, gradually getting worse over the last few days. He has a history of sickle cell disease. On examination, he has conjunctival pallor, normal auscultation of the chest and no hepatosplenomegaly. His blood results are shown below:\n\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|72 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|1.2x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|43x10<sup>9</sup>/L|150 - 400|\n|Mean Cell Volume (MCV)|88 fL|80 - 96|\n|Reticulocytes|1x10<sup>9</sup>/L|25 - 100|\n\n\nWhich of the following is the most likely cause of this patient's blood results?",
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"explanation": "Transfusion-associated circulatory overload presents with features of fluid overload, e.g. peripheral oedema, coarse inspiratory crackles on auscultation. This patient is well and not presenting with any examination or auscultation findings, so it is unlikely to be transfusion-related circulatory overload",
"id": "33697",
"label": "e",
"name": "Transfusion-associated circulatory overload",
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"explanation": "Anaphylaxis typically presents with angiooedema, urticaria, stridor, wheeze and hypotension. This patient is very well, so this is unlikely to be anaphylaxis",
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"label": "c",
"name": "Anaphylaxis",
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"explanation": "Transfusion-related acute lung injury typically presents with signs of pulmonary oedema, e.g. coarse inspiratory crackles on auscultation. This patient is well and not presenting with auscultation findings, so it is unlikely to be transfusion-related acute lung injury",
"id": "33696",
"label": "d",
"name": "Transfusion-related acute lung injury",
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"explanation": "Febrile non-haemolytic transfusion reaction typically presents with fever (with or without chills and rigors) only, with otherwise normal observations. This is the case with this patient. Typical management would be to stop transfusion, give paracetamol and reintroduce the transfusion at a slower rate",
"id": "33693",
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"explanation": "Acute haemolytic transfusion reaction typically presents with other symptoms, e.g. hypotension, back pain, disseminated intravascular coagulation. This typically occurs as a result of ABO incompatibility. This patient is very well, so this is unlikely to be an acute haemolytic transfusion reaction",
"id": "33694",
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"name": "Acute haemolytic transfusion reaction",
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"explanation": "# Summary\n\nBlood comprises two core components: cellular elements and plasma. Cellular components consist of white blood cells (neutrophils, eosinophils, basophils, monocytes, lymphocytes), red blood cells (RBCs or erythrocytes), and platelets (thrombocytes). Plasma encompasses clotting factors, albumin, and immunoglobulins. Blood groups, notably ABO and Rh, influence transfusion compatibility, with group O individuals universal donors. Acute and late transfusion reactions require vigilant monitoring and management. Iron overload can result from frequent transfusions, necessitating interventions to lower iron levels.\n\n# Blood Components\n\nBlood is made of two main components: cells and plasma\n\n- The cellular components of blood include: \n - white blood cells (neutrophils, eosinophils, basophils, monocytes, lymphocytes)\n - RBCs (erythrocytes) \n - platelets (thrombocytes)\n\n- Plasma consists of: \n - clotting factors\n - albumin \n - immunoglobulins\n\n## Lifespan of components\n\nThe normal lifespan of the following cellular components of blood is:\n\n- RBCs, 90–120 days\n- platelets, 10 days\n- neutrophils, 4 days\n\n## Products for transfusion\n\nFour products are readily transfusable:\n\n- **Red blood cells**\n - Generally **stored at 4 °C** for up to 35 days \n - In vivo, RBCs typically have a lifespan of about 120 days; however, it is important to note that transfused red cells last around 50–60 days\n\n\n- **Fresh frozen plasma** (FFP)\n - **Stored at –30 °C**, with a shelf life of a year\n - Used in patients with coagulopathy (impaired blood coagulation) to replace clotting factors\n - The type of FFP used depends on the patient's blood group\n\n\n- **Platelets**\n\n - **Stored at room temperature** for up to 7 days\n - Have a lifespan of 10 days before they are phagocytosed in the spleen and liver\n - 1 pool of platelets comes from 4 donors\n \n \n - Platelets are given if levels are <10 x 10<sup>9</sup>/l in patients with thrombocytopenia due to marrow failure from chemotherapy and radiotherapy – This threshold can be increased if there is sepsis or bleeding, or for a planned surgical procedure \n \n \n - Platelet transfusions should not be used in conditions where there is immune destruction of platelets (eg. immune thrombocytopenia unless there is a haemorrhagic emergency)\n \n \n - Platelet transfusion is also contraindicated in TTP or HUS as it can contribute to the microvascular occlusion in the brain and kidneys that is associated with these conditions\n \n\n\n- **Cryoprecipitate**\n\n - Cryoprecipitate is made by thawing FFP overnight at 4–8 °C\n - It has a shelf life of 1 year **stored at –30 °C**\n - It contains fibrinogen, factor VIII and von Willebrand factor\n - It is generally used in patients with massive bleeding and low fibrinogen\n\n# Blood Groups\n\n* Blood groups, defined as antigens on the surface of red blood cells, are critical in determining blood compatibility for transfusions. \n* There are over 400 blood groups but the ABO and Rh blood groups are the most important, each with distinct inheritance patterns. \n* The ABO antigens develop on red cells 16 weeks after birth, meaning neonates do not require blood cross-matching for transfusions. \n* Adults with group O red cells can universally donate due to the absence of A or B antigens, and group AB plasma can be universally donated due to the lack of anti-A or anti-B antibodies.\n* The A and B genes show co-dominant inheritance, whereas the O gene is recessive.\n\n# Antigens and Compatibility\n\n* **Rhesus antigen** - The Rh group includes 5 main antigens with Rhesus D being the most important. The Rhesus D antigen has an autosomal dominant mode of inheritance.\n- **ABO antigens** - not expressed on red cells until 16 weeks after birth. Therefore, in neonates, there is no need to cross-match for blood transfusions as antibodies are not yet made.\n\nPlease see the summary table below on blood group compatibility and donation:\n\n\n| Blood Type | Can Receive From | Can Donate To |\n|------------|-----------------|--------------|\n| A+ | A+, A-, O+, O- | A+, AB+ |\n| A- | A-, O- | A+, A-, AB+, AB- |\n| B+ | B+, B-, O+, O- | B+, AB+ |\n| B- | B-, O- | B+, B-, AB+, AB- |\n| AB+ | All Blood Types | AB+ |\n| AB- | AB-, A-, B-, O- | AB+, AB- |\n| O+ | O+, O- | A+, B+, AB+, O+ |\n| O- | O- | All Blood Types |\n\n# Acute Transfusion Reactions\n\n## Allergy \n\n- Presentation ranges from urticaria to angioedema and anaphylaxis\n- Management – stop the transfusion if concerns over anaphylaxis (if mild urticaria, can slow the transfusion and give antihistamine), give saline, adrenaline (in case of anaphylaxis), chlorphenamine, and hydrocortisone\n\n## Acute haemolytic transfusion reaction \n\n- Caused by giving an incompatible blood bag to a patient\n- Early signs include fever, abdominal pain, hypotension and anxiety\n- Late complications include generalised bleeding secondary to DIC\n- Management – stop the transfusion, give saline, treat DIC\n\n## Febrile non-haemolytic transfusion reaction \n\nBritish Society for Haematology guidelines recommend that: \n\n- In patients with a **mild** reaction:\n\n - A temperature rise of 1 - 2°C leading to pyrexia ≥38°C, but <39°C\n - And/or pruritus or a rash\n - WITHOUT other features\n\nThe transfusion can be continued with appropriate treatment (oral paracetamol 500 - 1000mg) and direct observation. If a rash/pruritis is also present, slow the transfusion)\n \n- In patients who develop **moderate** reactions:\n - Temperature ≥39°C OR a rise of ≥2°C from baseline\n - AND/OR systemic symptoms such as chills, rigors, myalgia, nausea or vomiting)\n\nSymptomatic treatment should be considered. If symptoms settle, the transfusion can be resumed. If symptoms are sustained, bacterial contamination or a haemolytic reaction should be considered.\n\n## Transfusion-related acute lung injury (TRALI)\n\n- Presents with pulmonary oedema and can cause acute respiratory distress syndrome (ARDS)\n\n- Management – stop the transfusion, give saline, treat ARDS and give supplementary oxygen as needed\n\n## Transfusion-associated circulatory overload (TACO)\n\n- Presents with fluid overload\n\n- Management – Slow the transfusion, give furosemide and supplementary oxygen as needed\n\n# Late Transfusion Reactions\n\n## Delayed haemolytic transfusion reaction \n\n- Caused by an exaggerated response to a foreign red cell antigen that the patient has been exposed to before\n- Patients present with jaundice, anaemia, and fever, usually on day 5 post-transfusion\n\n## Transfusion-associated graft-versus-host disease \n\n- Caused by donor blood lymphocytes attacking the recipient's body \n- Rare but carries a high risk of mortality\n\n## Iron Overload\n\n- Iron overload may be related to the pathophysiology of the condition (eg. haemochromatosis) or iatrogenic (eg. related to a blood transfusion or excess oral iron) \n - There is no secretion pathway for iron and approximately 1 mg of iron is lost via gut mucosal cells\n - Absorption of luminal iron is mediated by enterocytes, which respond to iron stores in the body\n - The enterocyte is modulated via its transferrin receptor, which regulates transferrin uptake from the plasma\n - In turn, the HFE protein modulates transferrin receptor activity\n- Iron overload usually becomes an issue after 20 units have been given or if serum ferritin rises above 1000 µg/l \n- Subcutaneous desferrioxamine is required regularly to lower iron levels\n\n# References\n\n[Click here to see more information on Patient UK about transfusion reactions](https://patient.info/doctor/blood-transfusion-reactions)\n\n[Click here to see more information on the British Society for Haematology guidelines on acute transfusion reactions](https://onlinelibrary.wiley.com/doi/full/10.1111/bjh.18789)",
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"question": "A 23-year-old female is receiving a blood transfusion in the respiratory ward. After 10 minutes, she reports that she feels cold. Her observations are as follows: heart rate 70/min, blood pressure 123/81 mmHg, respiratory rate 13/min, oxygen saturations 97% and temperature 38.6ºC.\n\nWhat is the most likely diagnosis?",
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"explanation": "Paranoid schizophrenia is a psychiatric disorder associated with paranoid delusions and auditory hallucinations. It is more common in patients between 20-30 years old (some female patients may also present in their 40s). This condition does not develop overnight, so there would likely be some mention of these symptoms when initially presenting to the emergency department. Although they have paranoid delusions, there is no evidence of any auditory hallucinations",
"id": "33702",
"label": "e",
"name": "Paranoid schizophrenia",
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"votes": 91
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"explanation": "Delirium tremens is a condition associated with acute withdrawal from alcohol in an alcohol-dependent person. This typically occurs 72 hours after alcohol cessation and presents with confusion, agitation, cravings, visual hallucinations and tremor. This patient is presenting too early for this (assuming their last drink would be just before admission), and they do not have any tremor or visual hallucinations",
"id": "33701",
"label": "d",
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"explanation": "Alzheimer's disease generally presents with a long history of cognitive decline. This patient presents with an acute onset of disorientation, behavioural change and delusions after a hip fracture. This is not typical for dementia, making delirium the more appropriate diagnosis. Dementia is, however, a risk factor for delirium and having delirium in the past increases a patient's risk of developing dementia",
"id": "33699",
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"name": "Alzheimer's disease",
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"explanation": "Delirium is an acute confusional state with a variety of causes. The two most significant risk factors are trauma/severe illness and being elderly, both present in this case. This woman is presenting with hypoactive delirium, as she is withdrawn. In addition, she is presenting with distractibility and disorientation, which are other characteristic features of delirium. Patients with delirium may also present with persecutory delusions, as in this case. This patient should be managed conservatively initially by reorientating them to the environment and addressing reversible causes, e.g. pain management, eating and drinking, urinary retention and constipation, managing infection and reviewing medications",
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"explanation": "Vascular dementia generally presents with a long history of stepwise cognitive decline. This patient presents with an acute onset of disorientation, behavioural change and delusions after a hip fracture. This is not typical for dementia, making delirium the more appropriate diagnosis. Dementia is, however, a risk factor for developing delirium",
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"explanation": "# Summary\n\nDelirium tremens (DT) is a severe form of alcohol withdrawal that presents with acute confusion, hallucinations, autonomic hyperactivity, and, in rare cases, seizures. Typically occurring around 72 hours after the cessation of alcohol intake, DT necessitates immediate medical attention and management. The first-line treatment is lorazepam, administered either orally or parenterally, followed by maintenance management strategies.\n\n# Definition\n\nDelirium tremens is a life-threatening condition characterized by a rapid onset of confusion often precipitated by alcohol withdrawal. It generally develops around 72 hours after the cessation of alcohol intake and can persist for several days. This condition is marked by extreme autonomic hyperactivity and neuropsychiatric symptoms.\n\n# Aetiology\n\nThe primary cause of delirium tremens is abrupt withdrawal or a significant reduction in alcohol intake in a person with prolonged, heavy alcohol use. Other factors that can precipitate DT include infection, trauma, or illness in a person with a history of chronic alcoholism.\n\n# Signs and Symptoms\n\nSymptoms typically peak between the 4th and 5th day post-withdrawal. The clinical features of delirium tremens include:\n\n- Confusion and disorientation\n- Hallucinations, which can be visual or tactile (e.g., formication – the sensation of crawling insects on or under the skin)\n- Autonomic hyperactivity, manifesting as sweating and hypertension\n- Rarely, seizures\n\n\n# Differential Diagnosis\n\nDelirium tremens must be distinguished from other conditions that can present with similar symptoms:\n\n- **Alcohol withdrawal syndrome:** Features include anxiety, insomnia, anorexia, tremor, and autonomic hyperactivity, but without the severe confusion or hallucinations seen in DT.\n- **Wernicke-Korsakoff syndrome:** This condition is characterized by ataxia, ophthalmoplegia, and confusion but lacks the autonomic instability of DT.\n- **Encephalitis:** Features include fever, headache, altered mental status, and focal neurological signs which are not typically observed in DT.\n- **Meningitis:** This presents with fever, neck stiffness, and altered mental status but without the characteristic hallucinations seen in DT.\n\n\n\n# Investigations\n\nInvestigations largely aim to rule out other conditions. These include:\n\n- Routine Blood panel including B12, Folate, Thyroid Function\n- Infection screen: Chest Xray, Urine dip, Blood Cultures\n- CT Head to assess for evidence of a structural brain lesion e.g. subdural haemorrhage in patients presenting with an unwitnessed fall while intoxicated\n- Lumbar Puncture if meningitis or encephalitis are suspected\n\n\n# Management\n\nNICE guidelines suggest offering oral lorazepam as the first-line treatment. \n\nIf symptoms persist, or oral medication is declined, offer parenteral lorazepam or haloperidol.\n\nFor maintenance management of alcohol withdrawal, the following steps are recommended:\n\n- Administer Chlordiazepoxide. Eventually this can be tapered according to **Clinical Institute Withdrawal Assessment for Alcohol (CIWA)** scoring\n- Ensure adequate hydration with fluids\n- Provide anti-emetics to manage nausea\n- Pabrinex to replenish vitamins\n- Refer the patient to local drug and alcohol liaison teams for further support and management\n\nWhen patients present with seizures, sometimes they remain in hospital for inpatient detoxification. This is however rare and the evidence shows that community detoxification is more effective.\n\n# NICE Guidelines\n\n[NICE CKS - Alcohol-use disorders](https://www.nice.org.uk/guidance/cg100/chapter/Recommendations)",
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"question": "An 88-year-old female presents to the emergency department, where she is diagnosed and treated for a neck of femur fracture and admitted to the orthopaedic ward. The next day, she does not engage with the medical staff and seems withdrawn and distractible. She does not know where she is and has not eaten her food as she thinks it has been poisoned.\n\nWhat is the most likely diagnosis?",
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"explanation": "Charles-Bonnet syndrome is a condition causing visual hallucinations (usually of people or animals) associated with severe visual impairment. There is nothing in this question to suggest this patient has any visual impairment; therefore, this is not the most likely diagnosis",
"id": "33705",
"label": "c",
"name": "Charles-Bonnet syndrome",
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"explanation": "This is a progressive neurological condition characterised by Lewy Body (alpha-synuclein) deposition in the brain. Key features demonstrated in this question include fluctuating symptoms (worse on some days) and visual hallucinations (he has a dog his wife can't see). The patient may also present with Parkinsonism, but cognitive symptoms must occur either before, or within 12 months of the onset of motor symptoms",
"id": "33703",
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"explanation": "Parkinson's dementia presents with dementia in the presence of Parkinson's disease. Parkinsonism (e.g. resting tremor, bradykinesia, resting tremor) must occur at least 12 months before the onset of cognitive symptoms. As this patient has developed cognitive symptoms before symptoms of Parkinsonism, dementia with Lewy Bodies is the more likely diagnosis",
"id": "33704",
"label": "b",
"name": "Parkinson's dementia",
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"votes": 24
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"explanation": "Alzheimer's disease typically presents with short term memory loss, word-finding difficulties and difficulty recognising objects and people. Alzheimer's does not typically present with visual hallucinations, making dementia with Lewy Bodies the more likely diagnosis",
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"explanation": "Vascular dementia is characterised by a stepwise cognitive decline due to either macrovascular (e.g. stroke) or microvascular events. Symptoms are largely dependent on the area affected; however, it would not present as a fluctuant dementia with visual hallucinations. Therefore, dementia with Lewy Bodies is the more likely diagnosis",
"id": "33707",
"label": "e",
"name": "Vascular dementia",
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"comment": "How do we know this is a visual hallucination?",
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"comment": "yeah should definitely be made clearer\n",
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"comment": "Yes this seemed to me like he still thought he had a dog - it's not clearly a hallucination since its not currently in room",
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"comment": "Isn't the dog thing more a memory problem than a hallucination?",
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"comment": "Needs to be made clearer that the dog is a hallucination, it sounds more like a memory problem",
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"comment": "plot twist",
"createdAt": 1684877262,
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"comment": "I don't think this sounds like a visual hallucination - mistakenly believing he has a dog doesn't mean he thinks he can see it",
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"comment": "As a dog I can confirm that I am not a hallucination",
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"explanation": "# Summary\n\nDementia with Lewy bodies (DLB) is a progressive, complex condition, accounting for approximately 10-15% of dementia cases. DLB is characterised by the presence of Lewy bodies, abnormal protein deposits, within brain cells, particularly in the substantia nigra, paralimbic, and neocortical areas. The clinical picture is often characterised by fluctuating cognition, Parkinsonism, and visual hallucinations. A diagnosis is primarily clinical, although dopamine uptake scanning can provide supplementary data. Patients with DLB are highly sensitive to neuroleptics, potentially exacerbating Parkinsonism. \n\n# Definition\n\nDementia with Lewy bodies (DLB) is a type of progressive dementia caused by deposits of an abnormal protein, alpha-synuclein, forming cytoplasmic inclusions known as Lewy bodies within brain cells. These aggregates disrupt normal cell functioning and eventually lead to neuronal death.\n\n# Epidemiology\n\nDLB is the third most common type of dementia, following Alzheimer's disease and vascular dementia. It represents around 10-15% of all dementia cases.\n\n# Aetiology\n\nThe primary pathological feature of DLB is the presence of Lewy bodies in the brain's substantia nigra, paralimbic, and neocortical areas. However, the exact cause of this accumulation remains unknown. An association with Parkinson's disease has been noted, with many patients exhibiting overlapping symptoms. \n\nNew research suggests that LBD and Parkinson’s disease have much more overlap than originally thought. Parkinson’s disease starts in the basal ganglia/brainstem and then progresses upwards towards cerebral cortex (hence dementia is late), whereas in LBD the process progresses downwards from the cerebral cortex.\n\n# Clinical Features\n\nThe clinical features of DLB include:\n\n- Fluctuating cognition: Changes in attention and alertness may occur\n- Parkinsonism: Rigidity, bradykinesia, and postural instability are common\n- Visual hallucinations: Patients often experience complex and recurrent visual hallucinations\n\t- Classically, patients complain of seeing small mammals around them \n- High sensitivity to neuroleptics: These drugs can induce or worsen parkinsonism\n\nA general rule of thumb that can help with distinguishing LBD form Parkinson's disease (PD) is if cognitive impairment and parkinsonism develop <1 year of each other, it is likely LBD. If diagnosed with PD and dementia develops >1 year later this is Parkinson’s disease.\n\n# Differential Diagnosis\n\nDifferential diagnoses for DLB include:\n\n- Alzheimer's disease: Characterised by gradual memory loss, difficulties with problem-solving, and changes in mood or behaviour. However, Alzheimer's patients do not typically exhibit the severe sensitivity to neuroleptics seen in DLB.\n- Parkinson's disease dementia: While it shares many symptoms with DLB, Parkinson's disease dementia typically starts with motor symptoms before cognitive decline. \n- Vascular dementia: This condition features stepwise cognitive decline and evidence of cerebrovascular disease. Parkinsonism and hallucinations are less common.\n\n# Investigations\n\nDiagnosis is primarily clinical, involving a careful medical history and physical examination. However, some additional investigations may be useful, such as:\n\n- Dopamine transporter (DaT) scan: This can help distinguish DLB from other types of dementia.\n- Neuropsychological testing: To assess cognitive functioning and fluctuations.\n- Electroencephalography (EEG): Although not diagnostic, a slowing background rhythm may be seen in DLB.\n\n\n# Management\n\nManagement of DLB includes should follow the biopsychosocial model - please see our Dementia section for holistic management principles.\n\n- Non-pharmacological interventions: These include cognitive stimulation, physical therapy, and occupational therapy.\n- Supportive care: As DLB is a progressive disorder, palliative and end-of-life care considerations are essential.\n- Medications: Cholinesterase inhibitors can help manage cognitive symptoms. However, caution is required with antipsychotic medications due to neuroleptic sensitivity.\n\n\n# NICE Guidelines\n\n[Click here to see information on NICE CKS on dementia](https://cks.nice.org.uk/topics/dementia/)",
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"question": "A 76-year-old man presents to the GP with his wife, who has noticed that his memory has worsened over the last 18 months. She thinks that his memory is worse on some days compared to others. The patient does not think he has a problem with his memory and is eager to leave as he left his dog tied up outside the GP surgery. His wife is confused as they do not own a dog. Neurological examination shows no abnormalities.\n\nWhat is the most likely diagnosis?",
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"explanation": "This is a typical description of a generalised tonic-clonic seizure. The onset of stiffness characterises the tonic part, which can cause a patient to fall. Rhythmic jerking motions characterise the clonic part. Incontinence and tongue biting are not unique to seizures but are also common features of seizure, with lateral tongue biting being more suggestive of seizure and tip tongue biting being more suggestive of syncope. Post-ictal state (drowsiness lasting up to 30 minutes post-seizure) is common after generalised tonic-clonic seizures",
"id": "33708",
"label": "a",
"name": "Generalised tonic-clonic seizure",
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"explanation": "Focal seizures originate in a single part of the brain, most often in the temporal lobe. Post-ictal state is common, and this seizure may progress to involve the whole brain (secondary generalisation). However, the seizure started as a generalised seizure, in this case, making a generalised tonic-clonic seizure more likely",
"id": "33709",
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"name": "Focal seizure with impairment of consciousness",
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"explanation": "Atonic seizures are characterised by the sudden loss of muscle tone (atonia) without the patient losing consciousness. As this patient lost consciousness and had stiffness, not atonia, a diagnosis of atonic seizure is unlikely",
"id": "33711",
"label": "d",
"name": "Atonic seizures",
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"explanation": "Vasovagal syncope usually occurs after prolonged standing or strong emotion (e.g. seeing blood). The patient may feel dizzy before the episode, will have a faint to the ground with or without some jerking of all four limbs, but will quickly recover within minutes. The presence of stiffness, lateral tongue biting, and a post-ictal state makes a vasovagal syncope diagnosis unlikely",
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"name": "Vasovagal syncope",
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"explanation": "Myoclonic seizures present with involuntary contraction of muscles leading to jerking. However, the patient remains conscious and don't have any post-ictal state, making this diagnosis unlikely",
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"label": "c",
"name": "Myoclonic seizure",
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"explanation": "# Summary\n\nEpilepsy is a neurological disorder characterised by an enduring predispotion to generate epileptic seizures. Affecting around 50 million people globally, it is one of the most common neurological conditions. Seizures can be either focal or generalised, with various triggers and symptoms. Differential diagnoses include syncope, transient ischemic attacks (TIA), migraines, panic disorder, and non-epileptic attack disorder (NEAD). Treatment primarily involves antiseizure medications (ASMs), tailored to the type of epilepsy, with surgery and psychological support as additional options in refractory cases. Complications include status epilepticus, psychiatric issues, and Sudden unexpected death in epilepsy (SUDEP).\n\n# Definition\n\nEpilepsy is a neurological disorder characterised by an enduring predisposition to generate epileptic seizures and the neurobiological, cognitive, psychological, and social consequences of this condition. \n\nSeizures are transient occurrences of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain. \n\n# Epidemiology\n\nEpilepsy affects approximately 50 million people worldwide, making it one of the most common neurological disorders.\n\nIt has a lifetime prevalence of 7.6 per 100 people. \n\nIncidence rates vary depending on age, with higher rates in the very young and the elderly. Both males and females are affected equally.\n\n# Aetiology\n\nThere is a strong debate amongst epileptologists regarding the classification of epilepsy syndromes by aetiology. \n\nBroadly, epilepsy syndromes can be classified into:\n\n1. Idiopathic Generalised Epilepsies (IGEs):\n\n- Childhood Absence Epilepsy\n- Juvenile Absence Epilepsy\n- Juvenile Mycolonic Epilspy\n- Generalised Tonic Clonic Seizures Alone\n\n2. Structural aetiology:\n\n- Acquired\n\t- Stroke\n\t- Trauma\n- Genetic\n\t- Malformations of cortical development \n\n3. Genetic aetiology\n4. Infectious aetiology\n4. Metabolic aetiology\n5. Immune aetiology\n6. Unknown aetiology\n\n\n# Signs and symptoms\n\nSigns and symptoms vary between focal and generalized seizures:\n\n- **Focal seizures**: \n - *With impaired consciousness ('complex')*: patients lose consciousness, usually post an aura or at seizure onset. Commonly originate from the temporal lobe, and post-ictal symptoms such as confusion are common.\n - *Without impaired consciousness ('simple')*: patients retain consciousness, experiencing only focal symptoms. Post-ictal symptoms are absent.\n - *Evolving to a bilateral, convulsive seizure ('secondary generalised')*: patients first experience a focal seizure that evolves into a generalized seizure, typically tonic-clonic.\n\n- **Generalized seizures**:\n - *Absence seizures*: brief pauses for less than 10 seconds.\n - *Tonic-clonic seizures*: characterized by loss of consciousness, stiffening (tonic), and jerking (clonic) of limbs. Post-ictal confusion is common.\n - *Myoclonic seizures*: sudden jerks of a limb, trunk, or face.\n - *Atonic seizures*: sudden loss of muscle tone, causing the patient to fall, with consciousness retained.\n\nSpecific epilepsy syndromes to note:\n\n- Temporal lobe epilepsy\n - Associated with complex partial seizures\n - Can present with initial sensory auras e.g. smelling burnt toast, feelings of deja vu or jamai vu (feeling unfamiliar in familiar surroundings), automatisms such as lip smacking\n - Patients often exhibit postictal confusion after each episode\n- Jacksonian March\n\t- A type of focal motor seizure that progressively 'marches' through adjacent areas of the brain\n\t- Typically starts in the hand or face then gradually spreads to other muscle groups following the smatotopic organisation of the motor cortex (starting from hand and spreading to arm, shoulder and face)\n\t- The seizure may progress into a generalised tonic clonic seizure\n\t- Often associated with structural brain lesions\n- Todd's Paresis\n\t- Refers to temporary postictal weakness or paralysis following a seizure\n\t- Usually lasts minutes to hours but can last up to 48 hours \n\t- Usually unilateral but can be bilateral\n\t- It is transient so the patient will reover following resolution of the postictal state\n\n\n\n# Differential diagnosis\n\nThe differential diagnosis for seizures includes:\n\n- **Syncope**: characterized by a sudden, transient loss of consciousness and postural tone followed by spontaneous recovery. Triggered by low blood flow to the brain.\n- **Transient Ischemic Attack (TIA)**: brief episodes of focal neurologic dysfunction caused by ischemia that does not cause lasting brain injury. Symptoms depend on the brain area affected.\n- **Migraines**: characterized by recurrent headaches often accompanied by a variety of symptoms such as visual disturbances (auras), nausea, vomiting, dizziness, extreme sensitivity to sound, light, touch and smell, and tingling or numbness in the extremities or face.\n- **Panic Disorder**: sudden periods of intense fear that may include palpitations, sweating, shaking, shortness of breath, numbness, or a feeling that something terrible is going to happen.\n- **Non-Epileptic Attach Disorder (NEAD)**: characterized by episodes that resemble epileptic seizures but occur without abnormal electrical activity in the brain. NEAD is often associated with psychological or emotional stress, and symptoms may include convulsions, loss of consciousness, or other seizure-like movements. Diagnosis is confirmed by video EEG monitoring, showing no seizure activity during an episode.\n\n# Investigations\n\nDiagnostic workup of epilepsy includes:\n\n- Detailed history and neurological examination\n- Collateral history and, if present, reviewing any videos of previous episodes (with the patient's consent)\n- Imaging such as CT or MRI\n- Electroencephalogram (EEG)\n\t- Video-EEG telemetry can also be considered in select cases\n- Other investigations can be considered to investigate contributory causes which include blood tests, lumbar puncture and more advanced imaging investigations.\n\n\n# Management\n\nThe goal of epilepsy treatment is to minimize seizures and optimise the patient's quality of life via a biopsychosocial model.\n\nAntiseizure medications (ASMs) remain the mainstay of treatment, with the specific drug chosen based on seizure type, patient age, comorbidities, potential side effects, and the patient's personal considerations. \n\nPrinciples of epilepsy ASM management include:\n\n- Aim for optimum quality of life through seizure control, balanced against potential side effects, particularly teratogenesis in women of childbearing age.\n- Initiation of medication may not always be appropriate after a \"provoked\" first seizure; discuss such cases with a specialist.\n- The choice of antiepileptic drugs involves complexity due to the lack of head-to-head trials comparing different medications.\n- Interactions with other medications, particularly with phenytoin and carbamazepine, should be considered.\n- Issues regarding teratogenicity, particularly with valproate, which carries a high risk of neural tube defects, should be considered. Lamotrigine is a better choice for women of childbearing age.\n\nSpecific ASMs:\n\n- According to [NICE Guidelines](https://bnf.nice.org.uk/treatment-summaries/epilepsy/#focal-seizures-with-or-without-secondary-generalisation), Lamotrigine or Levetiracetam should be considered as first-line for focal seizures. \n- Sodium valproate can be offered as first-line for myoclonic seizures in males.\n- Ethosuximide is the drug of choice for absence seizures.\n- Carbamazepine may worsen myoclonic seizures.\n\nSurgical intervention may be an option in cases where AEDs are ineffective. \n\nPsychological support is a vital part of comprehensive epilepsy management.\n\nSpecific guidance on patients presenting with a 'first fit':\n\n- Usual protocols will advise to refer to outpatient neurology following a patient's first seizure\n- Most neurologists would start an ASM after a second seizure, unless there is a specific structural cause or a second fit would be unacceptable to the patient. \n- Following a discussion regarding the risks and benefits of starting an ASM, patients are given information on reducing risks e.g. driving advice or taking showers rather than baths. \n- Patient education via leaflets or online websites are utilised heavily as part of the initial discussions and further follow up or advice is usually relayed via a dedicated epilepsy nurse\n\n# Complications\n\nComplications of epilepsy include:\n\n- **Status epilepticus**: Seizures lasting more than 5 minutes, necessitating immediate medical intervention OR more than 2 seizures within 5 minutes without returning to normal between each seizure.\n- **Psychiatric complications**: Increased risk of depression and suicide.\n- **Sudden unexpected death in epilepsy (SUDEP)**: Thought to occur due to excessive electrical activity inducing a cardiac arrhythmia and subsequent death.\n\n# Side Effects of Anti-Epileptic Drugs\n\nSide effects of common anti-epileptic drugs include:\n\n- **Topiramate**: Abdominal pain, cognitive impairment, confusion, mood changes, muscle spasm, nausea and vomiting, nephrolithiasis, tremor, weight loss.\n- **Lamotrigine**: Blurred vision, arthralgia, ataxia, diarrhoea, dizziness, headache, insomnia, rash, tremor.\n- **Carbamazepine**: Ataxia, blood disorders, blurring of vision, fatigue, hyponatraemia, skin problems.\n- **Sodium Valproate**: Ataxia, Anaemia, confusion, gastric irritation, haemorrhage, hyponatraemia, tremor, weight gain.\n- **Phenytoin**: Acne, anorexia, constipation, dizziness, gingival hypertrophy, hirsutism, insomnia, rash, tremor.\n\n# Driving Guidance\n\nThe DVLA has issued guidelines on driving with medical conditions, including epilepsy:\n\n- For car/motorbike licence: reapply after 6 months for a one-off seizure, or after 1 year for more than one seizure. After a seizure following a change in anti-epileptic medications, reapply to drive if the seizure was more than 6 months ago or you've been back on the previous medication for 6 months.\n- For bus/coach/lorry licence: reapply after 5 years for a one-off seizure if no anti-epileptic medications have been taken during this period. For more than one seizure, reapply after 10 seizure-free years during which no anti-epileptic medication has been taken.\n\nThe DVLA's complete guidelines for epilepsy and driving can be found [here](https://www.gov.uk/epilepsy-and-driving).\n\n# References\n\n[ILAE Guidelines](https://www.ilae.org/guidelines)\n\n[NICE Guidelines](https://www.nice.org.uk/guidance/ng217)\n\n[Driving Guidance on Gov.uk](https://www.gov.uk/epilepsy-and-driving)\n",
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"question": "A 25-year-old man presents to the emergency department after a transient loss of consciousness 15 minutes ago. His mother reports that he was getting ready for work when he suddenly went stiff, fell to the ground and then began shaking his limbs. He lost control of his bladder and bit both sides of his tongue. You attempt to gain a history from him, but he is drowsy.\n\nWhat is the most likely diagnosis?",
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"explanation": "IV phenytoin is given third-line for status epilepticus after the patient has received two doses of benzodiazepine (e.g. IV lorazepam), 10 minutes apart",
"id": "33717",
"label": "e",
"name": "Give IV Phenytoin 15mg/kg",
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"explanation": "PR diazepam (or buccal midazolam) is given first-line in status epilepticus in the community as these patients usually don't have IV access. As this patient is in hospital and has IV access, lorazepam is more appropriate",
"id": "33715",
"label": "c",
"name": "Give PR diazepam 10 mg",
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"explanation": "Rapid sequence induction is considered after seizure activity for 45 minutes, reserved for patients who cannot have their seizures terminated with benzodiazepines or other drugs like phenytoin",
"id": "33716",
"label": "d",
"name": "Rapid sequence induction with sodium thiopentone",
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"explanation": "50 ml of IV glucose 50% is given to patients in status epilepticus who have hypoglycaemia. This patient has a normal glucose, however, so this therapy is not appropriate",
"id": "33714",
"label": "b",
"name": "Give 50 ml of IV glucose 50%",
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"explanation": "This patient is in status epilepticus, as they have had a seizure lasting more than 5 minutes. As they are in status epilepticus, they should be treated with a seizure terminating medication. The first-line medication in status epilepticus in a hospital setting is IV lorazepam if the patient has IV access",
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"label": "a",
"name": "Give IV lorazepam 4mg",
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"explanation": "# Summary\n\nStatus Epilepticus is defined as a seizure lasting 5 minutes or more, or multiple seizures occurring within a 5-minute window without regaining full consciousness between episodes. It is a medical emergency, and treatment should begin promptly at the 5-minute mark. Initial management involves administering benzodiazepines, such as rectal diazepam, buccal midazolam, or intravenous lorazepam. If there is no response to two doses of benzodiazepines, second-line treatments include levetiracetam, phenytoin, or sodium valproate. Refractory cases may require general anesthesia with agents like propofol or midazolam. Investigations include blood tests, toxicology screen as well as neuroimaging and CSF analysis if the cause remains unclear\n\n# Definition\n\nStatus epilepticus is defined as a seizure lasting 5 minutes or more OR multiple seizures over 5 minutes without returning to a full level of consciosuness between episodes.\n\nIt should be assumed at 5 minutes and appropriate treatment and investigations initiated.\n\n# Acute management of status epilepticus\n\nEmergency AED therapy for convulsive status epilepticus [NICE guidelines](https://www.nice.org.uk/guidance/ng217/chapter/7-Treating-status-epilepticus-repeated-or-cluster-seizures-and-prolonged-seizures):\n\n\n\n\n**Premonitory stage (0-10 minutes)** \n\n- Diazepam 10−20 mg given rectally, repeated once 15 minutes later if status continues to threaten, or midazolam 10 mg given buccally. If seizures continue, treat as below.\n\n**Early status (0-30 minutes)** \n\n- If in the community:\n\t- Buccal Midazolam or Rectal Diazepam \n- If IV access is obtained and resuscitation facilities are available:\n\t- Lorazepam (intravenous) 0.1 mg/kg (usually a 4 mg bolus, repeated once after 10−20 minutes; rate not critical). \n\n**Established status (0-60 minutes)** \n\n- If not responding to 2 doses of benzodiazepine, give any of the following as second-line treatment\n\t- Levitiracetam\n\t- Phenytoin\n\t- Sodium Valproate\n\n**Refractory status (30-90 minutes)**\n\n- General anaesthesia, with one of:\n\n\t- Propofol (1–2 mg/kg bolus, then 2–10 mg/kg/hour) titrated to effect\n\t- Midazolam (0.1–0.2 mg/kg bolus, then 0.05–0.5 mg/kg/hour) titrated to effect\n\t- Thiopental sodium (3–5 mg/kg bolus, then 3–5 mg/kg/hour) titrated to effect; after 2–3 days infusion rate needs reduction as fat stores are saturated\n\t- Anaesthetic continued for 12−24 hours after the last clinical or electrographic seizure, then dose tapered.\n\n\n# Investigations\n\n- Arterial Blood Gas\n- Routine Blood tests including FBC, U&E, LFT, CRP, Clotting, Bone Profile \n- Toxicology screen (urine)\n- Anti-epileptic drug levels (if appropriate)\n- If the underlying cause is unclear, further investigations can include:\n\t- CT/MRI Brain Imaging\n\t- Lumbar Puncture \n\n\n# References\n\n[Click here for the NICE guidelines on managing status epilepticus](https://www.nice.org.uk/guidance/ng217/chapter/7-Treating-status-epilepticus-repeated-or-cluster-seizures-and-prolonged-seizures)",
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"question": "A 64-year-old man is brought to the emergency department with a stroke. Bloods are taken, and IV access is obtained. While in the emergency department, he begins to have a seizure. His oxygen saturations are 97%, and his blood glucose is 5.6 mmol/L (normal <6.1 mmol/L). Five minutes have now passed.\n\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "The headaches are having a significant impact on this patient’s quality of life so continuing to only manage the acute attacks with simple analgesia is not adequate treatment. Prophylaxis of future attacks should be offered for this patient.",
"id": "33719",
"label": "b",
"name": "Continue with paracetamol as required",
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"explanation": "Topiramate is contraindicated in pregnancy or in patients trying to conceive.",
"id": "33720",
"label": "c",
"name": "Topiramate",
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"explanation": "Verapamil is used as prophylaxis for cluster headaches. These presents as multiple short-lived headaches in a short period of time and usually involve tearing or redness of the eye on the affected side. The patient here has a clear history of migraines.",
"id": "33722",
"label": "e",
"name": "Verapamil",
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"explanation": "Carbamazepine is offered to patients with trigeminal neuralgia and not with migraines. Trigeminal neuralgia would presents with electric shock like painful episodes occurring across one cheek.",
"id": "33721",
"label": "d",
"name": "Carbamazepine",
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"explanation": "This patient is presenting with recurrent migraines. A migraine is a primary headache disorder that typically presents with a unilateral throbbing pain, worsened by light and noise. Patients will often describe needing to go to sleep or rest in a dark room to help the headache, which interferes with carrying out daily activities. Management includes trigger avoidance, and treatment of acute episodes with an oral triptan or simple analgesia like paracetamol/NSAIDs.\n\nIn patients where the headaches are having a significant impact on their daily function, as in this patient, prophylaxis should be offered. NICE recommends prophylaxis of attacks with propranolol, topiramate or amitriptyline. Topiramate is contraindicated in pregnancy or in those trying to conceive, so propranolol is the most appropriate option here.",
"id": "33718",
"label": "a",
"name": "Propranolol",
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"explanation": "# Summary\r\n\r\nMigraine is a common neurological disorder characterised by recurrent, unilateral, throbbing headaches often preceded by an aura such as visual or sensory symptoms. Migraines can last between 4-72 hours and often result in photophobia and phonophobia. Key signs and symptoms include a unilateral headache, a pulsating character, impairment or worsened by daily activities, and presence of nausea, vomiting or photophobia. Diagnosis is often based on clinical history, focusing on the presence of an aura. Management strategies include avoidance of triggers, prophylaxis with medications such as Propranolol, Topiramate or Amitriptyline, and managing acute attacks with oral triptans alongside Paracetamol or an NSAID.\r\n\r\n# Definition\r\n\r\nMigraine is a primary headache disorder characterised by intense episodes of debilitating headaches, usually unilateral and pulsating in nature. Symptoms may be preceded by an 'aura' which manifests as visual disturbances or sensory changes. The pain usually lasts from 4-72 hours and can be accompanied by nausea, vomiting, photophobia, and phonophobia.\r\n\r\n# Epidemiology\r\n\r\nMigraines are one of the most prevalent neurological disorders worldwide, affecting roughly 12% of the global population. It is more common in women, with a male to female ratio of approximately 1:3, likely related to hormonal influences. The peak incidence occurs between the ages of 30-39.\r\n\r\n# Aetiology\r\n\r\nThe exact cause of migraines is not fully understood, but it is likely a combination of genetic and environmental factors. \n\nThe triggering factors are variable and can include certain foods, changes in weather, stress, hormonal changes, and certain medications such as oral contraceptives.\r\n\r\n# Signs and Symptoms\r\n\r\n- Aura (usually visual or sensory symptoms preceding the headache)\r\n- Unilateral throbbing headache\r\n- Photophobia and phonophobia\r\n- Nausea and/or vomiting\r\n\r\nThe International Headache Society criteria for migraine without aura:\r\n\r\n| Criteria | Description |\r\n| -------- | ------------------------------------------------------------ |\r\n| A | At least five attacks fulfilling criteria B-D |\r\n| B | Headache attacks lasting 4-72 hours (untreated or unsuccessfully treated) |\r\n| C | Headache has at least two of the following four characteristics: <br>1. Unilateral location <br>2. Pulsating quality <br>3. Moderate to severe pain intensity <br>4. Aggravation by or causing avoidance of routine physical activity |\r\n| D | During headache, at least one of the following: <br>1. Nausea and/or vomiting <br>2. Photophobia and phonophobia |\r\n| E | Not better accounted for by another ICHD-3 diagnosis |\r\n\r\n# Differential Diagnosis\r\n\r\nMigraines must be differentiated from other conditions that present with severe headache. Some of these include:\r\n\r\n- Tension-type headache: Bilateral, band-like pressure or tightness, not worsened with physical activity, no associated nausea or vomiting.\r\n- Cluster headache: Severe, unilateral, orbital, supraorbital and/or temporal pain lasting 15-180 minutes, occurring up to 8 times a day, associated with autonomic symptoms like ptosis, miosis, lacrimation.\r\n- Subarachnoid hemorrhage: Sudden-onset severe headache, often described as \"the worst headache of my life\", associated with nausea, vomiting, and possible loss of consciousness.\r\n- Giant cell arteritis: New headache in a person over 50 years, scalp tenderness, jaw claudication, visual disturbances, elevated ESR and CRP.\r\n\r\n# Investigations\r\n\r\nDiagnosis is primarily clinical, based on the history and examination. \n\nA headache diary is important to help identify triggers and response to treatment.\n\nIf secondary causes of headaches are suspected, further investigations may be warranted, such as neuroimaging (MRI or CT) or blood tests (ESR, CRP for giant cell arteritis).\r\n\r\n# Acute Management\r\n\n- **Avoidance of triggers**: \n - Identify and avoid potential triggers like certain foods, stress, and poor sleep.\n- **Medications for acute attacks**: \n - **Triptans** (e.g., Sumatriptan) – avoid in patients with ischaemic heart disease.\n - **Paracetamol** or an **NSAID** (e.g., Ibuprofen) can be used in combination with triptans.\n - **Anti-emetics** (e.g., Metoclopramide)\n- **Special considerations**:\n - Female patients with migraine with aura should avoid the **combined oral contraceptive pill** due to increased risk of ischaemic stroke.\n\n# Prophylaxis\n\n- Medications:\n - **Propranolol** (contraindicated in asthma).\n - **Topiramate**.\n - **Amitriptyline**.\n - **Candesartan**.\n- Injections:\n\t- Greater Occipital Nerve Block\n\t- Botulinum Toxin Injection \n- **Newer treatments**:\n - **Rimegepant** (per NICE guidance, May 2023):\n - Used for preventing episodic migraine.\n - Suitable when at least 3 preventive treatments have failed.\n - Indicated for adults with 4-15 migraine attacks per month.\n\nRegular use of acute migraine medications (e.g., triptans, NSAIDs) more than 10-15 days per month can lead to **medication overuse headache (MOH)**.\n\nPatients should be counseled on limiting the use of acute treatments to prevent MOH.\n\n## References\r\n\r\n[Click here for NICE Clinical Knowledge Summaries on Migraines](https://cks.nice.org.uk/topics/migraine/)",
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"question": "A 21-year-old female patient presents to the GP with a three-month history of recurrent headaches. The headache starts as a throbbing pain on one side of her head and worsens with bright lights and noise. She typically takes paracetamol, lays down in a dark room, and sleeps, which helps the headaches. She does not notice any symptoms preceding the headache, and physical examination shows no abnormalities. The headaches have caused her to have several days off of university. She is currently trying to conceive.\n\nWhat is the most appropriate treatment for this patient?",
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"explanation": "Haemorrhagic stroke can present similarly; however, symptoms would not self resolve within 24 hours",
"id": "33725",
"label": "c",
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"explanation": "Transient ischaemic attack (TIA) is an ischaemic cerebrovascular event that self-resolves within 24 hours. Risk factors include age, pre-existing cardiovascular disease, hypertension, atrial fibrillation and smoking. This patient has a history of cardiovascular disease in the presence of symptoms suggestive of an ischaemic cerebrovascular event. As this has since resolved, this is most likely a TIA. This patient should be given 300mg of aspirin and referred to the TIA clinic (within 24 hours) to confirm the diagnosis",
"id": "33723",
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"name": "Transient ischaemic attack",
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"explanation": "Hypoglycaemia should be ruled out in every patient presenting with a TIA. However, there are no risk factors for hypoglycaemia like insulin therapy, sulphonylurea therapy, liver disease, malnutrition or insulinoma. There is also no mention of this patient's symptoms resolving upon eating sugar. Therefore TIA is the more likely diagnosis",
"id": "33726",
"label": "d",
"name": "Hypoglycaemia",
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"explanation": "Bell's palsy is an idiopathic lower motor neurone lesion of the facial nerve. It presents with ipsilateral weakness of the whole side of the face, with no sparing of the eyebrows. It does not present with arm weakness and will not resolve after one minute",
"id": "33727",
"label": "e",
"name": "Bell's palsy",
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"votes": 21
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"explanation": "Ischaemic stroke can present similarly; however, symptoms would not self resolve within 24 hours",
"id": "33724",
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"explanation": "# Summary\n\nA Transient Ischaemic Attack (TIA), colloquially known as a \"mini-stroke\", represents a sudden focal neurological deficit of vascular origin, characterised by symptom resolution typically within an hour. The absence of an acute infarct on imaging differentiates it from a stroke. Key signs and symptoms include speech difficulty, or arm/leg weakness or sensory changes. Important differential diagnoses include focal seizures, migraine, and intracranial bleeding. Investigations primarily involve neuroimaging, while management aims at reducing future stroke risk with lifestyle changes, control of vascular risk factors, and initiation of antiplatelet therapy. NICE guidelines recommend immediate referral for individuals with suspected TIA for assessment within 24 hours.\n\n# Definition\n\nA transient ischaemic attack (TIA) is a sudden-onset focal neurological deficit with a vascular aetiology, typically resolving symptoms within less than 1 hour. \n\n# Epidemiology\n\nTIA is a significant health concern worldwide due to its association with future stroke risk. \n\nThe incidence is 230 cases per 100000 person-years.\n\nRisk factors include:\n \n* Hypertension\n* Diabetes mellitus\n* High cholesterol\n* Atrial fibrillation\n* Carotid stenosis\n* Smoking\n* Family history of cardiovascular disease/stroke\n* History of cardio-embolic events\n\n# Signs and Symptoms\n\nPatients typically present with a sudden onset of focal neurological deficits which may include:\n\n- Speech difficulty (dysphasia)\n- Arm or leg weakness\n- Sensory changes \n- Ataxia, vertigo or loss of balance\n- Visual disturbance: Homonymous hemianopia, diplopia \n\nSymptoms of TIA are transient, with most resolving within 1 hour.\n\n# Differential Diagnosis\n\nIn assessing for a TIA, clinicians should consider the following differential diagnoses:\n\n- **Stroke**: Persistent symptoms with evidence of ischaemia on MRI imaging\n- **Focal motor seizures**: These might be suggested by positive symptoms preceding the weakness, such as shaking.\n- **Migraine with aura**: Characterized by a preceding aura which may present with visual disturbances, tingling, or numbness, followed by headache.\n\n\n# Investigations\n\nTo confirm the diagnosis and assess the extent of vascular disease, the following investigations are generally recommended:\n\n- Neuroimaging \n\t- The preferred modality is MRI to assess for any evidence of ischaemia, haemorrhage or consider alternative pathologies\n- Carotid ultrasound (looking for carotid stenosis\n- Echocardiogram (looking for cardiac thrombous)\n- 24 hour tape (looking for atrial fibrillation)\n- Blood tests (including glucose, lipid profile, clotting factors)\n\n\n# Management\n\nPatients who have had a suspected TIA should be referred for immediate assessment, ideally to be seen **within 24 hours** of onset of symptoms. The aim of management is to reduce the future risk of stroke and includes:\n\n- Lifestyle modifications (smoking cessation, regular exercise, healthy diet)\n- Control of vascular risk factors (hypertension, diabetes, dyslipidaemia)\n- Initiation of antiplatelet therapy (e.g., aspirin, clopidogrel) unless contraindicated\n- In selected cases, endarterectomy or stenting of the carotid artery might be indicated:\n\t- > 70% stenosis according European Carotid Surgery Trialists' Collaborative Group criteria (ECST) or\n\t- > 50% according to North American Symptomatic Carotid Endarterectomy Trial criteria (NASCT)\n\n# References\n\n[Click here for NICE Clinical Knowledge Summaries](https://cks.nice.org.uk/topics/stroke-tia/management/suspected-transient-ischaemic-attack/)",
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"question": "A 72-year-old man presents to the emergency department with right-sided arm and face weakness that occurred 40 minutes ago. These symptoms lasted for 1 minute and then resolved. He has a past medical history of two myocardial infarctions and peripheral vascular disease.\n\nWhat is the most likely diagnosis?",
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"explanation": "Features present in a posterior circulation stroke include either: cerebellar symptoms, bilateral motor/sensory symptoms, ipsilateral cranial nerve palsy + contralateral motor/sensory symptoms or bilateral anopia. This patient is not presenting with any of these symptoms, making this diagnosis unlikely",
"id": "33730",
"label": "c",
"name": "Posterior circulation infarct",
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"explanation": "A partial anterior circulation infarct is diagnosed when a patient presents with 2 of the 3 features used to define a total anterior circulation infarct. As this patient presents with all 3 of these features, she is presenting with a total anterior circulation infarct",
"id": "33729",
"label": "b",
"name": "Partial anterior circulation infarct",
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"explanation": "A total anterior circulation infarct is diagnosed when a patient has a combination of: contralateral hemiplegia/hemiparesis + contralateral homonymous hemianopia + higher cerebral dysfunction (aphasia). This patient is presenting with all these features, making this the most likely diagnosis",
"id": "33728",
"label": "a",
"name": "Total anterior circulation infarct",
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"explanation": "Lacunar infarcts (affecting vessels supplying internal capsule and thalamus) present affecting either: just motor function, just sensory function, just sensory and motor function or as an ataxic hemiparesis. This patient presents with a visual field defect and aphasia, so this cannot be a lacunar stroke",
"id": "33731",
"label": "d",
"name": "Lacunar infarct",
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"explanation": "Haemorrhagic stroke can cause these symptoms; however, 85% of strokes are ischaemic. This makes ischaemic stroke less likely than haemorrhagic stroke (in the absence of risk factors like malignant hypertension and anticoagulation)",
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"name": "Haemorrhagic stroke",
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"explanation": "# Summary\n\nAn ischaemic stroke is a medical emergency characterised by a sudden onset of focal neurological deficit secondary ischaemia. Depending on the affected cerebral area, symptoms can range from contralateral motor and sensory deficits, homonymous hemianopia, to higher cerebral dysfunction (such as aphasia and neglect). Initial management of suspected stroke necessitates urgent neuroimaging, primarily via non-contrast CT scan, to differentiate between ischaemic and haemorrhagic types. Further investigations such as carotid ultrasound, CT/MR angiography, echocardiogram, and various blood tests (e.g., serum glucose and lipids) help define the cause of stroke and quantify vascular risk factors. Acute management of ischaemic stroke involves thrombolysis in selected patients (usually within 4.5 hours of symptom onset), provided there are no contraindications, or mechanical thrombectomy for eligible patients. Long term management usually involves antiplatelet therapy, risk factor optimisation and multidisciplinary rehabilitation.\n\n\n# Definition\n\nAn ischaemic stroke describes a sudden onset focal neurological deficit secondary to focal brain ischaemia, with symptoms lasting >24 hours (or with evidence of infarction on imaging).\n\n# Aetiology\n\n85% of strokes are ischaemic while 15% are haemorrhagic.\n\nIschaemic stroke occurs when blood supply in a cerebral vascular territory is reduced secondary to stenosis or complete occlusion of a cerebral artery.\n\nThe ischaemic penumbra describes the cerebral area surrounding the ischaemic event where there is ischaemia without necrosis. This area is amenable to recovery with thrombolysis.\n\nIn terms of underlying aetiology of ischaemic stroke: \n\n- 25% are caused by intracranial small vessel atherosclerosis.\n- 50% are caused by large vessel atherosclerosis e.g. carotid artery stenosis.\n\t- Typically results from thrombus formation on the atherosclerotic plaque, and subsequent embolism of the thrombus to a smaller cerebral artery.\n- 20% of ischaemic strokes are cardio-embolic \n\t- e.g. in atrial fibrillation there is stasis of blood flow in the left atrium, predisposing to thrombus formation in the left atrium, and subsequent embolisation to the brain.\n\t- Rare causes of ischaemic stroke include primary vascular causes (such as vasculitis and arterial dissection) and haematological causes (prothrombotic states).\n\n\n\n# Stroke risk factors\n\n- Age\n- Male Sex\n- Family History\n- Hypertension\n- Smoking\n- Diabetes \n- Atrial fibrillation\n- High cholesterol\n- Obesity\n- Migraine \n\n# Stroke classification \n\nThe **Bamford/Oxford Stroke Classification System** is the most common classification system for ischaemic stroke. Although it is not used frequently in clinical practice, it is a helpful aide memoire to remember the localisation of common stroke syndromes.\n\nA total anterior circulation infarct (TACI) is defined by:\n\n- Contralateral hemiplegia or hemiparesis, AND\n- Contralateral homonymous hemianopia, AND\n- Higher cerebral dysfunction (e.g. aphasia, neglect)\nA TACI involves the anterior AND middle cerebral arteries on the affected side.\n\nA partial anterior circulation infarct (PACI) is defined by:\n\n- 2 of the above, OR\n- Higher cerebral dysfunction alone.\n- A PACI involves the anterior OR middle cerebral artery on the affected side.\n\nA lacunar infarct (LACI) is defined by: a pure motor stroke, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis or dysarthria-clumsy hand syndrome.\nA LACI affects small deep perforating arteries, typically supplying internal capsule or thalamus.\n\nA posterior circulation infarct (POCI) is defined by:\n\n- Cerebellar dysfunction, OR\n- Conjugate eye movement disorder, OR\n- Bilateral motor/sensory deficit, OR\n- Ipsilateral cranial nerve palsy with contralateral motor/sensory deficit, OR\n- Cortical blindness/isolated hemianopia.\n\nA POCI involves the vertebrobasilar arteries and associated branches (supplying the cerebellum, brainstem, and occipital lobe).\n\n[lightgallery]\n\n# Posterior Stroke Syndromes\n\nThere are a number of different posterior stroke syndromes that you should be aware of:\n\n- Basilar artery occlusion is more likely to present with locked in syndrome (quadriparesis with preserved consciousness and ocular movements), loss of consciousness, or sudden death.\n\n- Anterior inferior cerebellar artery results in lateral pontine syndrome, a condition similar to the lateral medullary syndrome but with additional involvement of pontine cranial nerve nuclei. It leads to cerebellar ataxia, vertigo, hearing loss as well as ipsilateral facial weakness\n- Wallenberg's syndrome (lateral medullary syndrome) causes ipsilateral Horner's syndrome, ipsilateral loss of pain and temperature sensation on the face, and contralateral loss of pain and temperature sensation over the contralateral body.\n- Weber's syndrome/medial midbrain syndrome (paramedian branches of the upper basilar and proximal posterior cerebral arteries): causes an ipsilateral oculomotor nerve palsy and contralateral hemiparesis.\n\n# Acute management of ischaemic stroke\n\n\n- Patients should be approached in the DR ABCDE manner.\n- CT Head should be perfomed on arrival to the emergency department to distinguish ischaemic from haemorrhagic stroke. \n- If no evidence of ischaemic stroke, a CT Angiogram and CT perfusion (in select patients) should be performed to assess for evidence of large vessel occlusion and a salvageable ischaemic penumbra\n- Thrombolysis with Alteplase (tissue plasminogen activator) is considered if:\n\t- The patient presents within 4.5 hours of symptom onset (Up to 9 hours in select patients with good baseline and favourable perfusion imaging) \n\t- No contraindications such as:\n\t\t- Recent head trauma\n\t\t- Recent surgery\n\t\t- Systolic lood Pressure above 185 \n\t\t- Currently taking oral anticoagulation\n\t\t- Raised INR (local guidelines vary)\n- Mechanical Thrombectomy is usually considered in patients with:\n\t- Anterior Circulation Stroke (evidence base is poorer for posterior circulation stroke)\n\t- Evidence of large vessel occlusion (ideally proximal up to distal M1)\n\t- Good functional baseline\n\t- Favourable perfusion criteria indicating salvageable tissue\n\t- Presenting within 6 hours (Up to 24 hours in select patients with good baseline and favourable perfusion imaging)\n\nIf hyper-acute treatments are not offered, patients are started on an antiplatelet agent such as Aspirin or Clopidogrel (local guidelines vary).\n\nIf hyper-acute treatments are offered, antiplatelets are usually started 24 hours after the treatment following a repeat CT Head that excludes any haemorrhagic transformation.\n\n# Stroke investigations (Post-acute)\n\nMRI Head with Diffusion Weighted Imaging (DWI) is the gold standard test to confirm the presence of an acute ischaemic stroke, which can be present within a few minutes of stroke onset. Due to logistical challenges of acute MRI scanning, this is normally performed within 24 hours following initial hyperacute treatment.\n\nInvestigations in the post-hyperacute phase aim to further define the cause of the stroke and to quantify vascular risk factors.\n\nThese include:\n\n- Carotid ultrasound (to identify critical carotid artery stenosis)\n- 24 to 72 hour cardiac monitoring to assess for evidence of atrial fibrillation\n- CT/MR angiography (to identify intracranial and extracranial stenosis)\n- Echocardiogram (if a cardio-embolic source is suspected). \n- In young patients further investigation e.g. a vasculitis screen or thrombophilia screen may be necessary.\n- HbA1c and Serum Lipids to optimise other cardiovascular risk factors \n\n\n# Stroke management (Chronic)\n\nRehabilitation and supportive management will include an **MDT approach** with involvement of physiotherapy, occupational therapy, speech and language therapy, and neurorehabiliation.\n\n\nThe key steps in secondary stroke prevention can be remembered by the mnemonic HALTSS:\n\n- Hypertension: \n\t- Studies show there is no benefit in lowering the blood pressure acutely (as this may impair cerebral perfusion) unless there is malignant hypertension (systolic blood pressure >180 mmHg). Anti-hypertensive therapy should, however, be initiated 2 weeks post-stroke.\n- Antiplatelet therapy:\n\t- Patients should be administered Clopidogrel 75 mg once daily for long-term antiplatelet therapy. In patients with ischaemic stroke secondary to atrial fibrillation, however, warfarin (target INR 2-3. or a direct oral anticoagulant (such as Rivaroxaban or Apixiban) is initiated 2 weeks post-stroke.\n- Lipid-lowering therapy:\n\t- Patients should be prescribed high dose atorvastatin 20-80 mg once nightly (irrespective of cholesterol level this lowers the risk of repeat stroke).\n- Tobacco\n\t- Offer smoking cessation support.\n- Sugar:\n\t- Patients should be screened for diabetes and managed appropriately.\n- Surgery:\n\t- Patients with ipsilateral carotid artery stenosis more than 50% should be referred for carotid endarterectomy. Patients with over 70% stenosis have the most benefit from endarterectomy\n\n\n\n# References\n\n[Click here for NICE Clinical Knowledge Summaries](https://cks.nice.org.uk/topics/stroke-tia/)\r\n\r\n[Click here for Radiopedia](https://radiopaedia.org/articles/lacunar-stroke-syndrome?lang=gb)",
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"question": "An 82-year-old female presents to the emergency department with sudden onset left-sided face and arm weakness. The patient cannot give a full history as she is unable to speak, but she gestures that the left side of her vision is missing on visual field testing.\n\nWhat is the most likely diagnosis?",
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"explanation": "Migraine typically presents with unilateral throbbing pain, worsened by light and noise. Although this patient has photophobia, the presence of neck stiffness and fever is more suggestive of a diagnosis of meningitis",
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"explanation": "Meningococcal septicaemia is caused by Neisseria meningitidis infecting the blood. This can present as a petechial rash (usually non-blanching) with or without haemodynamic compromise. This patient does not present with these features; therefore, this is less likely than meningitis",
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"explanation": "Subarachnoid haemorrhage presents as a \"thunderclap headache\" to the back of the head, which is very painful and may feel as though they have been hit in the back of the head. They may also have features of meningism (neck stiffness, photophobia) as blood irritates the meninges. The longer history and presence of fever, in this case, make meningitis more likely",
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"explanation": "Meningitis is caused by inflammation of the meninges lining the brain. Clinical presentation includes: a triad of headache, neck stiffness and photophobia; fever; focal neurology; seizure or features of meningococcal septicaemia. As this patient is presenting with features of meningism and fever, meningitis is the most likely diagnosis",
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"explanation": "Space occupying lesions typically present with red flag symptoms including: morning headache; headache on coughing, straining or lying down; vomiting; focal neurological signs; personal history of cancer. This patient is not presenting with any of these symptoms, and the history of meningism and fever make a diagnosis of meningitis more likely",
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"explanation": "# Summary\n \nMeningitis is a potentially life-threatening condition characterised by the inflammation of the meninges, the membranes enveloping the brain and spinal cord. Its causes span from infectious agents, such as bacteria, viruses, fungi, and parasites, to non-infective causes like malignancy and certain medications. Symptoms are often non-specific, necessitating accurate differential diagnoses and prompt investigations. Timely management, including empirical antibiotics and targeted therapy post-identification of causative agent, is crucial to mitigate complications and improve patient outcomes. \n \n \n# Definition\n \n \nMeningitis is an inflammation of the meninges, which are composed of three layers: the dura mater, arachnoid mater, and pia mater. This inflammation may arise from both infective and non-infective aetiologies. \n \n \n# Epidemiology\n \n \nBacterial meningitis, while not the most common form of meningitis, is particularly significant due to its high morbidity and mortality rates. \n \nViral meningitis, predominantly caused by enteroviruses, is more common but typically less severe. Fungal and parasitic causes are relatively rare, except in immunosuppressed individuals. \n \nIn the United States, the annual incidence of bacterial meningitis is approximately 1.38 cases/100,000 population with a case fatality rate of 14.3%.\n\n# Aetiology\n \n \nInfective causes of meningitis include:\n \n \n - Bacterial: **Streptococcus pneumoniae (most common bacterial cause),** Neisseria meningitidis, Haemophilus influenzae, Listeria monocytogenes, among others.\n - Viral: **Enteroviruses are overall most common** (Echoviruses, Coxsackie viruses A and B, poliovirus), herpes viruses (HSV2, HSV1), Paramyxovirus, measles and rubella viruses, Varicella Zoster Virus, Arboviruses, Rabies virus.\n - Fungal: Particularly Cryptococcus neoformans, mainly affecting the immunosuppressed population.\n - Parasitic: Amoeba (Acanthamoeba), Toxoplasma gondii.\n \n \nNon-infective causes of meningitis encompass:\n \n \n - Malignancies such as leukaemia, lymphoma, and other tumours\n - Chemical meningitis\n - Certain drugs, including NSAIDs and trimethoprim\n - Systemic inflammatory diseases such as sarcoidosis, systemic lupus erythematosus, Behcet's disease.\n \n \n# Signs and Symptoms\n \n \nThe cardinal features of meningitis include:\n \n \n- Headache\n- Fever\n- Neck stiffness\n- Photophobia\n- Nausea and vomiting\n- Focal neurology\n- Seizures\n- Reduced conscious level\n- Features of overwhelming sepsis, such as non-blanching petechial rash indicative of impending Disseminated Intravascular Coagulation (DIC). \n \nSpecific signs suggestive of meningeal irritation (and therefore not specific to meningitis) include:\n \n \n1. **Kernig's sign:** Kernig's sign is a test performed to evaluate the presence of meningeal irritation and stiffness in the hamstrings and lower back. To perform this test, the patient is positioned lying on their back with the hip and knee flexed at 90 degrees. The examiner then attempts to extend the patient's knee. If the patient experiences pain and resistance to knee extension, especially when attempting to straighten the leg, it is considered a positive Kernig's sign. This sign suggests meningeal irritation or inflammation.\n \n \n2. **Brudzinski's sign:** Brudzinski's sign is another manoeuvre used to assess for meningeal irritation. This test involves passive neck flexion, where the examiner gently flexes the patient's neck forward toward the chest while the patient is lying on their back. If the patient involuntarily flexes their hips and knees in response to neck flexion, it is considered a positive Brudzinski's sign. This involuntary movement indicates irritation of the meninges.\n \n \n \n \n# Differential Diagnosis\n \nThe key differentials for meningitis often present with overlapping symptoms. These include:\n \n \n- **Encephalitis**: Headache, fever, altered consciousness, seizures, focal neurological signs, behaviour changes.\n- **Subarachnoid hemorrhage**: Sudden severe headache, nausea and vomiting, neck stiffness, altered consciousness, seizures.\n- **Brain abscess**: Headache, fever, nausea and vomiting, focal neurological deficits, seizures, altered mental status.\n- **Sinusitis**: Headache, fever, facial pain, nasal congestion.\n- **Migraine**: Recurrent headaches, often unilateral and throbbing, accompanied by nausea/vomiting, photophobia, phonophobia.\n \n \n# Investigations\n \n \nDiagnostic investigations for suspected meningitis include:\n \n \n - Blood tests: Full Blood Count, Urea and Electrolytes, Clotting, Glucose, PCT\n - Arterial Blood Gas\n - Blood cultures\n - Bacterial throat swab for meningococcus\n - PCR for meningococcus & pneumococcus\n - HIV test\n - Imaging: CT Head if there are signs of raised intracranial pressure (ICP)\n - Lumbar puncture for Cerebrospinal Fluid (CSF) analysis, once confirmed there are no signs of raised ICP.\n \n \n## CSF Findings \n \n \nAnalysis of the cerebrospinal fluid in acute meningitis can provide important clues as to the underlying aetiology. Once establishing that it is safe to do so, a CSF sample should be taken via lumbar puncture and the opening pressure should be measured.\n \n \nThis can be examined macroscopically, and then sent for haematology, biochemistry, and microbiological microscopy, culture and sensitivities, as well as PCR.\n \n| | **Appearance** | **Predominant cell type** | **Culture** | **Protein** | **Glucose** |\n|---------------------------|-------------------------------------|---------------------------------------------------|--------------------------------------------------------|-------------|-------------|\n| **Bacterial meningitis** | Clear or turbid | **Polymorphonuclear** cells (i.e. neutrophils) | Positive | Raised | **Reduced** |\n| **Aseptic (viral) meningitis** | Clear or slightly turbid | **Lymphocytes** | Negative | Raised | **Normal** |\n| **Tuberculous meningitis** | Clear or slightly turbid ± fibrin web | **Lymphocytes** + polymorphonuclear cells | Negative gram stain; acid-fast bacilli positive (auramine staining) | Raised | **Reduced** |\n\n \nN.b. Cryptococcal meningitis may give any of the above results, so should be considered as a differential in any HIV or immunocompromised patient. Classically the opening pressure is very high, and this is a poor prognostic sign. If suspected, request cryptococcal antigen or India Ink staining.\n \n \n# Management\n \n \n- Empirical antibiotic therapy for suspected bacterial meningitis typically includes 2g of IV ceftriaxone twice daily to ensure CNS penetration, with IV amoxicillin added in patients at age extremes for listeria coverage.\n- In primary care, IM benzylpenicillin or ceftriaxone should be given while awaiting urgent transfer to hospital, especially if meningococcal disease is suspected.\n- Dexamethasone should be given if bacterial meningitis is strongly suspected in the absence of a rash\n\t- This has been shown to reduce neurological sequelae in bacterial meningitis but not meningococcal meningitis\n- In cases of suspected viral encephalitis, IV aciclovir should also be administered. For patients allergic to penicillin, alternatives such as chloramphenicol may be used. \n- It's important to note that any empirical antibiotic regimen should be adjusted based on culture results when available.\n \n **Additional notes**\n \nClose contacts of the patient should receive prophylactic antibiotics. This will be guided by specialists but may be a single dose of oral ciprofloxacin, or rifampicin.\n \nBacterial meningitis is a notifiable disease and any suspected cases should be reported to the local health protection team.\n \n \n# Complications\n \n \nMeningitis may lead to severe complications if not promptly treated, such as:\n \n - Septic shock\n - Disseminated Intravascular Coagulation\n - Coma\n - Subdural effusions\n - Syndrome of inappropriate antidiuretic hormone secretion\n - Seizures\n - Delayed complications: Hearing loss, cranial nerve dysfunction, hydrocephalus, intellectual deficits, ataxia, blindness\n - Death\n \n \n# NICE guidelines\n \n [NICE CKS: Meningitis - bacterial meningitis and meningococcal disease](https://cks.nice.org.uk/topics/meningitis-bacterial-meningitis-meningococcal-disease/)\n \n [NICE: meningitis (bacterial) and meningococcal disease: recognition, diagnosis and management](https://www.nice.org.uk/guidance/ng240/resources/meningitis-bacterial-and-meningococcal-disease-recognition-diagnosis-and-management-pdf-66143949881029)\n \n# References\n \n [BNF: Ciprofloxacin](https://bnf.nice.org.uk/drugs/ciprofloxacin/)",
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"question": "A 20-year-old university student presents to the emergency department with a one-day history of headache. On examination, you notice he is wearing sunglasses. He is unable to touch his chin to his chest, but tone, power, and reflexes are all normal, and there are no rashes. His temperature is 38.7ºC, heart rate 88/min and his blood pressure is 120/80mmHg.\n\nWhat is the most likely diagnosis?",
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"explanation": "Femoral shaft fractures can occur from a fall from standing in patients with a history of osteoporosis; however, most femoral shaft fractures occur in road traffic accidents. Other causes include a fall from height and gunshot wounds. Patients can present similarly, with a shortened externally rotated leg. However, in an elderly patient presenting with a fall, a neck of femur fracture is the more common aetiology",
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"explanation": "Osteoarthritis is a degenerative arthritis that comes on over years and is worsened by movement. The rapid onset of pain and examination findings, in this case, make a diagnosis of neck of femur fracture more likely",
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"explanation": "Neck of femur fractures are a relatively common fracture, typically occurring in elderly patients. Neck of femur fractures typically occur after a minor fall and present with sudden onset pain, with a shortened and externally rotated leg on examination. This position is formed by several muscles (including iliopsoas and hip abductors) creating force, pulling up and externally rotating the leg. Smoking and low BMI are risk factors for osteoporosis. The diagnosis is confirmed by hip x-ray (AP and lateral view), and management varies on fracture classification, e.g. intracapsular/extracapsular, non-displaced/displaced",
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"name": "Left neck of femur fracture",
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"explanation": "Hip dislocation typically occurs after a road traffic accident. It usually presents with shortening of the leg, as in this case. However, the leg is internally rotated, not externally rotated. This is because most hip dislocations are posterior, meaning the femoral head travels posteriorly to the acetabulum",
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"explanation": "Septic arthritis is a life-threatening condition associated with infection in the joint. It presents with a history of red, hot, swollen joint that comes on over hours-days, which may be accompanied by fever and sepsis. The history of onset of pain after a fall and the examination findings make a diagnosis of neck of femur fracture more likely",
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"comment": "\"Out For Intense Disco\" - Outward = Fracture and Internal = Dislocation",
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"explanation": "# Summary\n\nA fracture of the neck of the femur is a break occurring in the upper part of the femur, just below the ball-and-socket hip joint. This fracture is common among the elderly population, particularly those with osteoporosis. Notable symptoms include severe hip or groin pain, an inability to bear weight on the affected leg, and external rotation and shortening of the affected leg. Diagnosis typically involves X-rays, though CT scans or MRI may be employed for more complex cases. Management is primarily surgical, with options including cannulated screw fixation, dynamic hip screw, hemiarthroplasty, and total hip arthroplasty, chosen based on factors such as the patient's age, health, and the type of fracture. Complications can include non-union, avascular necrosis, deep vein thrombosis, and pulmonary embolism.\n\n# Definition\n\nA fracture of the neck of the femur is a type of hip fracture that specifically involves the upper part of the femur, just below the ball of the hip's ball-and-socket joint.\n\n# Types of Neck of Femur Fracture\n\nFractures of the neck of the femur are generally classified into two types based on their location in relation to the hip joint capsule:\n\n- **Intracapsular Fractures**: These fractures occur within the joint capsule. They are further subdivided into displaced and non-displaced fractures. Displaced fractures carry a high risk of avascular necrosis due to possible disruption of the blood supply to the femoral head.\n \n- **Extracapsular Fractures**: These fractures occur outside the joint capsule and include intertrochanteric and subtrochanteric fractures. They have a better prognosis due to a lower risk of avascular necrosis.\n\n# Epidemiology\n\nFractures of the neck of the femur are a common injury, particularly in older individuals. This is largely attributed to the increased prevalence of osteoporosis in this population, which makes the bones more susceptible to fractures.\n\n# Aetiology\n\nThe main cause of a fracture to the neck of the femur is a fall, often in the elderly and those with weakened bones due to osteoporosis. Other potential causes can include high-energy trauma such as car accidents, especially in younger individuals.\n\n# Signs and Symptoms\n\nPatients with a fractured neck of femur commonly present with:\n\n- Severe pain in the hip or groin\n- Inability to bear weight on the affected leg\n- Shortening and external rotation of the affected leg\n- Swelling or bruising over the hip area\n\n# Differential Diagnosis\n\nThe differential diagnosis for a fractured neck of femur should include other injuries that could present with similar symptoms:\n\n- **Intertrochanteric Fracture**: Another type of hip fracture, characterised by pain in the hip or groin, inability to bear weight, and often shortening and external rotation of the affected leg.\n- **Pelvic Fracture**: Can be caused by falls or high-energy trauma. Symptoms can include severe pain in the hip or groin, inability to bear weight, and possible signs of internal bleeding.\n- **Hip Dislocation**: Usually a result of high-energy trauma, symptoms include severe hip pain, inability to move the leg, and a visibly deformed hip.\n\n# Investigations\n\nThe primary investigation for a suspected fractured neck of femur is a hip X-ray, which typically reveals the fracture and its severity. In cases where the fracture is not clear on X-ray, a CT scan or MRI may be necessary.\n\n[lightgallery]\n\n# Management\n\nManagement of a fractured neck of the femur is primarily surgical. The choice of surgical intervention depends on several factors, including the type of fracture, the patient's age, general health, and mobility prior to the injury.\n\n- **Cannulated Screw Fixation**: This is often used for non-displaced intracapsular fractures. The procedure involves the insertion of screws across the fracture line to stabilise it.\n \n- **Dynamic Hip Screw (DHS)**: This technique is usually used for stable, extracapsular fractures. It involves the insertion of a single large screw into the femoral head, combined with a side plate fixed to the femoral shaft.\n \n- **Hemiarthroplasty**: This involves replacing the femoral head and neck with a prosthesis. It is typically performed for displaced intracapsular fractures in older patients with lower activity levels, as these fractures have a high risk of non-union and avascular necrosis.\n \n- **Total Hip Arthroplasty (THA)**: This procedure involves the replacement of both the femoral head and the acetabulum with prosthetic components. It is typically used for displaced intracapsular fractures in younger, more active patients or older patients with pre-existing osteoarthritis.\n \n\n# Complications\n\nPotential complications from a fracture of the neck of the femur include:\n\n- Non-union of the fracture\n- Avascular necrosis due to interruption of blood supply to the femoral head\n- Deep vein thrombosis (DVT)\n- Pulmonary embolism (PE)\n- Infection\n- Dislocation of the hip prosthesis, in cases where arthroplasty has been performed\n\n# References\n\n[Click here to read more about fractures of the neck of femur](https://teachmesurgery.com/orthopaedic/hip/femoral-neck-fractures/)",
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"question": "A 78-year-old female presents to the emergency department with left hip pain that came on immediately following a fall. She is a current smoker and has a body mass index of 18.8. On examination, the left leg is shortened and externally rotated.\n\nWhat is the most likely diagnosis?",
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"explanation": "Hyperkalaemia is defined as a potassium level >5.5mmol/L. There are many causes; in this case, it is most likely due to the initiation of a potassium-sparing diuretic (especially as it is given in combination with an ACE inhibitor). This patient also presents with ECG features of hyperkalaemia, including tall tented T waves and flattened P waves. Other ECG features include broad QRS and a \"sine wave\" pattern. Management should include calcium gluconate (cardiac stabiliser), insulin and dextrose with or without salbutamol (to lower potassium level), and potentially reducing the dose of spironolactone",
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"explanation": "ECG signs associated with hypercalcaemia include PR shortening and J waves (if severe). Other systemic signs of hypercalcaemia include renal stones, bone pain, constipation, nausea, abdominal pain, confusion, polydipsia, polyuria, depression and psychosis. The features on this ECG are more in keeping with hyperkalaemia",
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"explanation": "ECG signs associated with hypokalaemia include QTc prolongation, PR prolongation and U waves. This ECG is more in keeping with an ECG showing hyperkalaemia. This patient is also unlikely to develop hypokalaemia now after initiation with a potassium-sparing diuretic",
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"explanation": "# Summary\n\nHyperkalaemia is a potentially life-threatening electrolyte abnormality, defined as a serum potassium concentration greater than 5.5mmol/L. A potassium of 6.0-6.5 mmol/L is classed as moderate hyperkalaemia, and > 6.5 mmol/L is classed as severe. Causes include acute or chronic renal impairment, medications such as ACE inhibitors, adrenal insufficiency and rhabdomyolysis. Pseudohyperkalaemia is also common and occurs when there is haemolysis of the blood collected that causes potassium to leak from cells. Key investigations include an ECG, a blood gas to confirm hyperkalaemia is true, and U&Es for renal function. Management depends on the severity of hyperkalaemia and may include calcium gluconate or calcium carbonate to stabilise the myocardium and insulin-dextrose infusion to drive potassium into the cells, as well as treating the cause of hyperkalaemia. Potassium binders such as sodium zirconium cyclosilicate (Lokelma) may also be used. The main complication is cardiac conduction abnormalities, with possible findings including tall tented T waves, flattened P waves, bradyarrhythmias and QRS widening with bizarre morphology. \n\n# Definition\n\nHyperkalaemia is a common electrolyte abnormality that is defined as an abnormally high serum potassium. The normal range is 3.5-5.0 mmol/L, with a level of > 5.5 mmol/L generally described as hyperkalaemia. It is seen in around 1-10% of hospital inpatients and is often asymptomatic.\n\n# Aetiology\n\n- Impaired excretion of potassium\n - Acute kidney injury\n - Chronic kidney disease\n - Medications (ACE inhibitors, potassium sparing diuretics, NSAIDs, heparin, trimethoprim, ciclosporin)\n - Type 4 renal tubular acidosis\n - Hypoadrenalism (e.g. Addison's disease)\n- Increased potassium intake\n - Oral intake (especially if combined with impaired excretion)\n - Excessive IV potassium\n- Increased cellular release \n - Metabolic acidosis\n - Hyperglycaemia\n - Rhabdomyolysis\n - Tumour lysis syndrome\n - Packed red blood cell transfusion\n - Digoxin toxicity\n - Beta blockers\n - Severe burns\n - Hyperkalaemic periodic paralysis\n\n# Classification\n\nThe European Resuscitation Guidelines stratify severity of hyperkalaemia as follows:\n\n||Serum potassium (mmol/L)|\n|--------------------------|------------------------------------|\n|**Mild**|5.5–5.9|\n|**Moderate**|6.0–6.4|\n|**Severe**|≥6.5|\n\n# Signs and Symptoms\n\nHyperkalaemia is often asymptomatic and only detected on blood tests - there may be symptoms or signs of the underlying cause however (e.g. dark urine in rhabdomyolysis)\n\n**Symptoms include:**\n\n- Palpitations\n- Fatigue\n- Chest pain\n- Shortness of breath\n- Paralysis\n\n**Signs include:**\n\n- Arrhythmias (e.g. bradycardia)\n- Reduced muscle power +/- flaccid paralysis\n- Hyporeflexia\n\n# Differential Diagnosis\n\n**Pseudohyperkalaemia** is common and refers to an artifactual increase in potassium in the sample tested - causes of this include:\n\n- Prolonged tourniquet time\n- Difficult venepuncture\n- Excessive fist clenching\n- Delayed specimen processing\n- Contamination with potassium EDTA anticoagulant in FBC bottles\n- Thrombocytosis\n- Leukocytosis\n\n# Investigations\n\n- **Blood gas** to confirm hyperkalaemia rapidly and check acid-base status and lactate\n- **ECG** to look for cardiac conduction abnormalities associated with hyperkalaemia. ECG changes include tall-tented T waves, PR prolongation, p wave flattening and QRS broadening.\n- **U&Es** to confirm hyperkalaemia, check sodium (may be an associated hyponatraemia e.g. in adrenal insufficiency) and renal function\n\n# Management \n\n**Conservative management:**\n\n- Stop any potassium-containing fluids\n- Address any underlying causes e.g. stop any contributing medications where possible, manage constipation\n- Consider advising the patient on a low potassium diet (e.g. in patients with chronic kidney disease) - dietician referral may be helpful\n- Patients with ECG changes may require cardiac monitoring\n- Mild-moderate cases of hyperkalaemia without ECG changes may be managed by addressing the underlying cause alone\n\n**Medical management:**\n\n- Patients with ECG changes or severe hyperkalaemia require treatment\n- Give 10 ml of IV 10% calcium carbonate or 30ml of IV 10% calcium gluconate immediately\n- This does not reduce serum potassium but acts to stabilise the myocardium and reduce the risk of arrhythmias\n- Further doses may be given if required\n- Give an insulin and glucose infusion (e.g. 10 units of Actrapid in 50 ml of 50% glucose over 15-30 minutes\n- This reduces serum potassium by shifting potassium into cells, however does not eliminate potassium from the body\n- Nebulised salbutamol may be given in addition which has the same effect\n- Potassium binders may be considered to eliminate potassium via the gut, especially in patients with chronic or refractory hyperkalaemia\n- Newer agents such as sodium zirconium cyclosilicate (Lokelma) are better tolerated than older resins (e.g. sodium polystyrene sulfonate)\n- Furosemide may also be useful to increase urinary potassium excretion especially in patients with fluid overload\n- Consider sodium bicarbonate for patients with acidosis and hyperkalaemia\n- Medical treatment may be required to correct the cause of hyperkalaemia (e.g. IV fluids for a pre-renal AKI or rhabdomyolysis)\n\n**Interventional management:**\n\n- Refractory hyperkalaemia despite medical therapy is an indication for emergency dialysis\n\n# Complications\n\nThe main complication of hyperkalaemia is cardiac conduction abnormalities and arrhythmias which in the most severe cases may cause cardiac arrest - changes in order of increasing severity are:\n\n1. Tall tented T-waves\n2. Flattened P-waves\n3. Prolonged PR interval\n4. Widened QRS complexes\n5. Idioventricular rhythms (bradycardia of ventricular origin)\n6. Sine wave pattern (pre-terminal rhythm)\n7. Ventricular fibrillation/asystole\n\n# References\n\n[BNF Treatment Summary - Hyperkalaemia](https://bnf.nice.org.uk/treatment-summaries/hyperkalaemia/)\n\n[The Renal Association - Treatment of Acute Hyperkalaemia in Adults](https://www.ukkidney.org/sites/default/files/RENAL%20ASSOCIATION%20HYPERKALAEMIA%20GUIDELINE%20-%20JULY%202022%20V2_0.pdf)\n\n[Patient UK - Hyperkalaemia in adults](https://patient.info/doctor/hyperkalaemia-in-adults)\n\n[Whittington Hospital Hyperkalaemia Guideline](https://www.whittington.nhs.uk/document.ashx?id=6250)\n\n[Life in the Fast Lane - Hyperkalaemia](https://litfl.com/hyperkalaemia-ecg-library/)",
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"question": "A 55-year-old patient is on the cardiology ward with an exacerbation of heart failure. They have been commenced on spironolactone and are currently taking bisoprolol and ramipril. They are complaining of palpitations, and their most recent ECG is shown below:\n\n[lightgallery]\n\nWhat is the most likely diagnosis?",
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"explanation": "Hyponatraemia is defined as a sodium level <135 mmol/L). There are many causes, but in this case, the most likely cause is syndrome of inappropriate antidiuretic hormone (SIADH) secondary to small cell lung cancer. Hyponatraemia presents with drowsiness, headache, seizures and coma.\n\nManagement depends on the severity of hyponatraemia and whether it is acute or chronic in onset. Rapid correction of chronic severe hyponatraemia is associated with central pontine myelinolysis, a severe neurological disorder associated with high morbidity and mortality. For this reason, severe hyponatraemia (<120 mmol/L) should only be raised by 12 mmol/L/day",
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"explanation": "Brain metastases can present with seizures. However, you would expect some other associated focal neurological deficit. This patient also had a normal CT scan, which did not show any metastatic brain lesions. This makes metastatic lung cancer very unlikely",
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"explanation": "Epilepsy is a disorder characterised by recurrent seizures. This patient has only had one seizure in the absence of a clear seizure syndrome. Other underlying causes have not yet been ruled out. Given his history of small cell lung cancer, hyponatraemia should be ruled out (along with other causes of seizures) before a diagnosis of epilepsy is made",
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"name": "Epilepsy",
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"explanation": "Migraine headaches can present with hemiparesis and other motor features; however, they do not present with transient loss of consciousness or features resembling a tonic-clonic seizure. There is also no history of migraines in this case. In a patient with seizures with a diagnosis of small cell lung cancer, syndrome of inappropriate antidiuretic hormone (SIADH) and associated hyponatraemia should be ruled out",
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"explanation": "Encephalitis is a condition (usually infective) where there is inflammation of the brain. Patients typically present with fever, headache, personality change, focal neurological signs and seizures. This patient is not presenting with fever, personality change or focal neurological signs making it not a specific presentation for encephalitis. In a patient presenting with a generalised presentation with a history of small cell lung cancer, hyponatraemia is the more likely diagnosis",
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"label": "d",
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"explanation": "# Summary\n\nHyponatraemia is defined as a serum sodium concentration of less than 135 mmol/L. It may develop acutely or chronically, and is often asymptomatic especially in mild cases. There are many causes which may be classified by whether the patient is hypovolaemic, euvolaemic or hypervolaemic. Symptoms are more likely in severe hyponatraemia and where serum sodium has fallen acutely, including headache, nausea and vomiting and confusion. Key investigations include U&Es for sodium, potassium and renal function, cortisol and thyroid function to rule out other causes of hyponatraemia and urinary sodium and osmolality. Management differs depending on the cause of hyponatraemia - what may improve hyponatraemia in some cases may worsen it in others. In severe cases where more rapid correction of sodium is required, hypertonic saline may be administered with close monitoring of sodium levels.\n\n# Definition\n\nNormal serum sodium is between 135-145 mmol/L, and so levels below 135 mmol/L are classified as hyponatraemia. This may be mild (130-135 mmol/L), moderate (125-129 mmol/L) or severe (< 125 mmol/L). Acute cases develop within 48 hours, with most cases considered to be chronic (i.e. over 48 hours duration) if the onset is unclear. \n\n# Epidemiology\n\n- Hyponatraemia is the commonest electrolyte disorder seen in clinical practice\n- Approximately 15-20% of hospital inpatients are hyponatraemia\n- Incidence increases with age and is particularly common in older people who are nursing home residents or in hospital\n- Other risk factors include:\n- Medications (e.g. diuretics, antidepressants)\n- Comorbidities (e.g. chronic kidney disease, heart failure)\n\n# Aetiology\n\n## Hypovolaemic hyponatraemia\n\nBoth sodium and water are lost (but more sodium than water)\n\n- Diarrhoea\n- Vomiting\n- Medications (e.g. thiazide diuretics)\n- Adrenal insufficiency\n- Burns\n- Excessive sweating\n- Cerebral salt-wasting (rare cause of hyponatraemia that occurs due to intracranial disease, e.g. subarachnoid haemorrhage or traumatic brain injury)\n- Salt-wasting nephropathy (e.g. Bartter syndrome)\n- Third space losses (e.g. sepsis, pancreatitis, bowel obstruction)\n\n## Euvolaemic hyponatraemia\n\nNo loss of sodium but total body water increases causing a dilutional effect\n\n- Syndrome of Inappropriate ADH release (SIADH)\n- Beer potomania (alcohol excess combined with low solute intake)\n- Primary polydipsia\n- Hypothyroidism\n- Secondary adrenal insufficiency\n- Exercise-induced hyponatraemia \n- Hypotonic intravenous fluids\n\n## Hypervolaemic hyponatraemia\n\nBoth total body water and sodium increase, with a greater increase in water resulting in oedema\n\n- Heart failure\n- Chronic liver disease\n- Renal disease (nephrotic syndrome, chronic kidney disease or acute kidney injury)\n\n# Signs and Symptoms\n\nMany patients, especially those with mild and/or chronic hyponatraemia are asymptomatic and detected incidentally.\n\nSymptoms and signs include:\n\n- Lethargy\n- Anorexia\n- Headache\n- Nausea and vomiting\n- Muscle cramps\n- Drowsiness\n- Confusion\n- Seizures\n\nPatients may also have features of either dehydration (in hypovolaemic hyponatraemia) or fluid overload (in hypervolaemic hypernatraemia - see separate chapters for details.\n\n# Differential Diagnosis\n\n- **Pseudohyponatraemia** refers to a falsely low serum sodium reading due to an increase in serum lipid or protein content\n- Serum osmolality will usually be normal or high (unlike in true hyponatraemia where it is low)\n- Causes include:\n- Hypertriglyceridemia\n- Hypercholesterolemia\n- Hyperglycaemia\n- Paraproteinaemia (e.g. in multiple myeloma)\n\n# Investigations\n\n**Bedside:**\n\n- **Venous blood gas** to confirm hyponatraemia - if there is a significant discrepancy between the sodium on the gas and the U&Es, suspect pseudohyponatraemia\n- **Urine osmolality** is used to assess ADH activity - it will be high (i.e. urine is concentrated) if ADH is acting, e.g. in SIADH, and low (i.e. urine is dilute) if ADH is not acting, e.g. in polydipsia\n- **Urine sodium** can be used to help determine the cause of hyponatraemia; in patients who are hypovolaemic:\n- If urine sodium is appropriately low, this indicates extrarenal salt loss - consider vomiting/diarrhoea/third spacing\n- If urine sodium is high (> 30 mmol/L), this indicates renal salt loss - consider diuretics, adrenal insufficiency or cerebral salt-wasting\n- NB urine osmolality and sodium cannot be interpreted in patients taking diuretics and so these may need to be stopped prior to investigations\n- **Urine dip** looking for blood and protein if renal disease is suspected\n\n**Blood tests:**\n\n- **U&Es** to confirm hyponatraemia and to check potassium and renal function\n- **Serum osmolality** should be low in true hyponatraemia - if this is normal or raised suspect pseudohyponatraemia (hypertonic fluids such as mannitol may cause a true hyponatraemia with a raised serum osmolality)\n- **Thyroid function tests** to exclude hypothyroidism as a cause of hyponatraemia\n- **9am serum cortisol** to exclude adrenal insufficiency as a cause of hyponatraemia\n- **NT-proBNP** if heart failure is suspected\n- **Liver function tests** if cirrhosis is suspected (e.g. in patients with ascites)\n\n# Management\n\n**Conservative:**\n\n- Identify and treat the underlying cause (e.g. stopping causative medications where possible)\n- Patients with hyponatraemia which is severe, acute or symptomatic should usually be admitted to hospital for treatment\n- Consider referral to the appropriate speciality for advice on management of the underlying cause of hyponatraemia (e.g. cardiology for heart failure, endocrinology for adrenal insufficiency)\n- Closely monitor sodium levels and ensure these are corrected no faster than 8-10 mmol/L per 24 hours \n- Fluid restriction is the first-line management for SIADH and may also be used in some cases of hypervolaemic hyponatraemia\n\n**Medical:**\n\n- Severe hyponatraemia should be treated with hypertonic saline, usually in the intensive care setting\n- Hypovolaemic hyponatraemia is treated with IV normal saline\n- In some cases of SIADH tolvaptan may be considered - this is a vasopressin V2-receptor antagonist\n- Correction of endocrine abnormalities may be required e.g. levothyroxine for hypothyroidism; corticosteroids for adrenal insufficiency\n\n# Complications\n\n- **Cerebral oedema** may complicate severe and/or acute hyponatraemia and may be life-threatening - patients develop raised intracranial pressure with symptoms of vomiting, headache, seizures and coma\n- **Central pontine myelinolysis** is a complication of rapid correction of hyponatraemia - patients may present with confusion, ataxia, spastic quadriparesis and pseudobulbar palsy with dysphagia and dysarthria\n- Chronic hyponatraemia, especially in the elderly, increases the risk of **falls** as well as **cognitive impairment**\n\n# NICE Guidelines\n\n[NICE CKS - Hyponatraemia](https://cks.nice.org.uk/topics/hyponatraemia/)\n\n# References\n\n[Life in the Fast Lane - Hyponatraemia](https://litfl.com/hyponatraemia/)\n\n[Whittington Hospital Hyponatraemia Guideline](https://www.whittington.nhs.uk/document.ashx?id=6089)",
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"comment": "Given the patient has difficulty sleeping, wouldn't you consider Mirtazapine as a first line choice?",
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"comment": "Sertraline is the safest because of the history of post-MI (has the most evidence base) for this past medical history. ",
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"comment": "This man has had a recent MI and Sertraline is known to prolong QTc. Given no ECG information has been given, wouldn't the safest drug be Fluoxetine (which does not prolong QTc)?",
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"explanation": "# Summary\n\nDepression is a common mental health disorder typified by low mood, anhedonia, significant weight change, sleep and activity changes, fatigue, feelings of guilt or worthlessness, or poor concentration. It is defined by the DSM as the presence of 5 out of 8 symptoms for at least 2 weeks. It is more prevalent in females. Key investigations include FBC, TFT, U+E, LFT, Glucose, B12/folate, cortisol, toxicology screen, and CNS imaging to rule out organic causes. Management strategies encompass low to high intensity psychological interventions, pharmacotherapy including anti-depressants, and in severe cases, lithium or ECT.\n\n# Definition\n\nDepression is a mental health disorder characterised by:\n\n- **ICD-11 Criteria:**\n - Depressive Episode: Depressed mood, loss of interest (anhedonia), and reduced energy (fatigue) persisting for at least two weeks.\n\n- **DSM-V Criteria:**\n - Major Depressive Disorder (MDD): Presence of a major depressive episode lasting at least two weeks, with specific criteria regarding mood, cognitive, and physical symptoms.\n - Persistent Depressive Disorder (Dysthymia): A chronic form of depression lasting for at least two years. \n\nThis consists of the presence of at least five out of a possible eight defining symptoms, during the same two-week period, where at least one of the symptoms is depressed mood or loss of interest or pleasure\n\n**Severity:**\n\n- Mild: Few, if any, symptoms in excess of those required to make the diagnosis (associated symptoms, see below), and the symptoms result in minor functional impairment.\n- Moderate: Symptoms or functional impairment between \"mild\" and \"severe.\"\n- Severe: The number of symptoms, intensity, and impairment are all greatly increased.\n\n\n# Epidemiology\n\nDepression is a highly prevalent mental health disorder. It represents the third most common reason for consulting a general practitioner in the UK. Depression demonstrates a higher prevalence in females.\n\n# Aetiology\n\nThe aetiology of depression involves a complex interplay of genetic and environmental factors. History of previous mental health issues, physical illnesses, and social challenges like divorce, poverty, and unemployment can all contribute to its development.\n\n# Clinical Features\n\nDepression is defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM) as the presence of 5 out of the following 9 symptoms, occurring nearly every day for at least 2 weeks:\n\n1. **Depressed mood or irritability** for most of the day, indicated by either subjective report (feels sad or empty) or observation by others (appears tearful).\n2. **Anhedonia:** Decreased interest or pleasure in most activities, most of the day.\n3. Significant **weight change** (5%) or change in appetite.\n4. **Sleep alterations:** Insomnia or hypersomnia.\n5. **Activity changes:** Psychomotor agitation or retardation.\n6. **Fatigue** or loss of energy.\n7. **Guilt or feelings of worthlessness:** Excessive or inappropriate guilt or feelings of worthlessness.\n8. **Cognitive issues:** Diminished ability to think or concentrate, or increased indecisiveness.\n9. **Suicidality:** Thoughts of death or suicide, or formulation of a suicide plan.\n\n### Additional Features (Severe Depression)\n- **Psychotic Features:** Delusions (e.g. nihilistic delusions, Cotard's syndrome) and hallucinations.\n- **Depressive Stupor:** Profound immobility, mutism, and refusal to eat or drink, sometimes necessitating electroconvulsive therapy (ECT).\n\n# Differential Diagnosis\n\nThe main differentials and their key signs and symptoms include:\n\n- **Bipolar Disorder:** Characterised by periods of mania/hypomania (elevated mood, inflated self-esteem, decreased need for sleep, increased talkativeness, distractibility, increased goal-directed activity) alternating with depressive episodes.\n- **Anxiety Disorders:** Persistent and excessive worry, restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and sleep disturbance.\n- **Psychotic Disorders:** Hallucinations, delusions, disorganised speech, grossly disorganised or catatonic behaviour.\n- **Substance/Medication-Induced Mood Disorder:** Mood disturbance associated with intoxication or withdrawal from substances or side effects of medications.\n- **Adjustment Disorders:** Development of emotional or behavioural symptoms in response to identifiable stressors.\n\n\nVarious organic causes should be considered and ruled out through careful history-taking, physical examination, and relevant investigations. These include:\n\n- Neurological disorders such as Parkinson's disease, dementia, and multiple sclerosis.\n- Endocrine disorders, especially thyroid dysfunction and hypo/hyperadrenalism (e.g., Cushing's and Addison's disease).\n- Substance use or medication side effects (e.g., steroids, isotretinoin, alcohol, beta-blockers, benzodiazepines, and methyldopa).\n- Chronic conditions such as diabetes and obstructive sleep apnea.\n- Long-standing infections, such as mononucleosis.\n- Neoplasms and cancers - low mood can theoretically be a presenting complaint in any cancer, with pancreatic cancer being a notable example.\n\n\n# Investigations\n\n- Standard investigations for depression may include Full Blood Count (FBC), Thyroid Function Test (TFT), Urea and Electrolytes (U&E), Liver Function Test (LFT), Glucose, B12/folate levels, cortisol levels, toxicology screen, and imaging of the Central Nervous System (CNS).\n- These help rule out organic causes (listed above) such as endocrine disorders (e.g. thyroid disorders).\n- There are several questionnaires that can also be used to help assess depressive symptoms, such as the Hospital Anxiety and Depression (HAD) Scale and Patient Health Questionnaire (PHQ-9).\n\n# Management\n\nDepression is usually managed in primary care. GPs can refer to secondary care (Psychiatry) if there is a high-suicide risk, symptoms of bipolar disorder, symptoms of psychosis, or if there is evidence of severe depression unresponsive to initial treatment.\n\r\n**Persistent subthreshold depressive symptoms or mild-to-moderate depression:**\n\n- 1st line = Low-intensity psychological interventions (individual self-help, computerised CBT). \r\n- 2nd line = High-intensity psychological interventions (individual CBT, interpersonal therapy) \r\n- 3rd line = Consider antidepressants \r\n\r\n**Mild depression unresponsive to treatment and moderate-to-severe depression:**\n\n- 1st line = High-intensity psychological interventions + antidepressants (1st line = SSRI)\r\n- 2nd line (Treatment-resistant depression) – switch antidepressants and then use adjuncts \r\n\r\n**Severe depression and poor oral intake/psychosis/stupor:**\n\n- 1st line = ECT \n- Although the exact mechanism remains elusive, it is thought that the induced seizure, rather than the ECT procedure itself, has therapeutic benefits. Short-term side effects of ECT include headache, muscle aches, nausea, temporary memory loss, and confusion, while long-term side effects can include persistent memory loss. Due to the induced seizure, there is a risk of oral damage, and due to the general anaesthetic, a small risk of death.\r\n\n**Recurrent depression:** \n\n- Treated with antidepressant + lithium \r\n\n\nMedical management of depression - additional notes:\n\n- First-line pharmacological treatment typically involves a Selective Serotonin Reuptake Inhibitor (SSRI) such as sertraline. SNRIs such as venlafaxine can also be used first-line, but are less preferable due to the risk of damage from overdose, which is less likely with SSRIs.\n- In people aged 18-25 there is an increased risk of impulsivity and suicidal risk upon commencing antidepressant medication and so they should have a follow-up appointment arranged after one week to monitor progress. 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"explanation": "# Drug choice feedback\n\nThis gentleman is suffering from moderate to severe major depressive disorder. Apart from recommending cognitive behavioural therapy, the first line pharmacological therapy is a selective serotonin reuptake inhibitor (SSRI). Given his recent myocardial infarct, sertraline is the optimal choice in light of its safety being studied in this group of patients and a lower propensity of interactions with other medications. All other SSRIs should be considered only if the patient is intolerant to sertraline or no significant clinical effect is seen.\n\n# Dose/Route/Frequency/Duration feedback\n\nThe initial dose is 50mg orally once-daily. This needs to be reviewed regularly.",
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"question": "Case Presentation: A 52-year-old gentleman sees his GP for low mood and energy with anhedonia. He has trouble sleeping and has low self-confidence. He does not report major problems with eating nor any suicidal thoughts.\n\n\n## PH\n\nHyperlipidaemia, Type 2 Diabetes Mellitus, Myocardial Infarct (3 months ago)\n\n## DH\n\nAtorvastatin 80mg PO OD, Enalapril maleate 10mg PO OD, Bisoprolol 2.5mg PO OD, Metformin 1g PO BD (NKDA)\n\n## On examination\n\nAppears low in mood, speech volume reduced. Slow spontaneous movement and reactivity noted.\n\nTemperature 36.2°C, HR 76, RR 14, BP 135/88, O<sub>2</sub> 99% RA, GCS 15, Weight 89kg\n\n## Investigations\n\nECG: Normal sinus rhythm\n\n# Prescribing Request\n\nWrite a prescription for one drug that is most appropriate for treating his condition.",
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"comment": "yeah I had the same question, just cause hes allergic to one PPI does that mean hes off all of them? like is this like amoxicillin no penicillin rule?",
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"comment": "all H2 receptor are on hold, no?\n",
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"comment": "No, only ranitidine is discontinued due to impurities in the product. Others like famotidine are still available",
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"comment": "Why is ranitidine wrong? its in the bnf as an option ",
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"comment": "says do not prescribe lower down but just remove it from the bnf innit!",
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"comment": "where on the bnf can you find a list of H2 antagonists?",
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"comment": "go to 'clinical knowledge summaries' (one of the tabs), type dyspepsia -> functional dyspepsia -> H2 receptor antagonists",
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"comment": "We aren't allowed to use CKS in the PSA :/\n",
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"explanation": "# Summary\n\nGastro-oesophageal reflux disease (GORD) is characterised by the reflux of gastric contents into the oesophagus due to a defective lower oesophageal sphincter. Key signs and symptoms include dyspepsia, sensation of acid regurgitation, and potentially more atypical symptoms such as epigastric pain and laryngitis. Alarm symptoms include weight loss and persistent vomiting. Key investigations include a trial of proton pump inhibitor therapy and oesophagogastroduodenoscopy (OGD) if certain symptoms are present. Management strategies include lifestyle interventions, proton pump inhibitor therapy, and in refractory cases, anti-reflux surgery.\n\n# Definition\n\nGastro-oesophageal reflux disease (GORD) is a clinical diagnosis based on the presence of typical symptoms (dyspepsia, \"\"heartburn\"\" or \"\"acid reflux\"\") resulting from the reflux of gastric contents into the oesophagus caused by a defective lower oesophageal sphincter.\n\n# Epidemiology\n\nIn the UK, about 10% of adults experience symptoms of GORD daily, with a higher prevalence observed in individuals over 50 years of age.\n\n# Aetiology\n\nGORD is caused by a defective lower oesophageal sphincter, which enables the reflux of gastric contents into the oesophagus.\n\nRisk factors contributing to the development of GORD include obesity, alcohol use, smoking, and intake of specific foods (e.g. coffee, citrus foods, spicy foods, fat).\n\n\n# Signs and symptoms\n\nTypical symptoms:\n\n- Dyspepsia (\"\"heartburn\"\")\n- Sensation of acid regurgitation \n\nAtypical symptoms:\n\n- Epigastric or chest pain\n- Nausea\n- Bloating\n- Belching\n- Globus\n- Laryngitis\n- Tooth erosion\n\nAlarm symptoms:\n\n- Weight loss\n- Anaemia\n- Dysphagia\n- Haematemesis\n- Melaena\n- Persistent vomiting\n\n# Differential Diagnosis\n\nConditions that may present similarly and should be considered in the differential diagnosis include:\n\n- Gastric ulcers: These may present with epigastric pain, nausea, vomiting, and weight loss.\n- Oesophageal cancer: This may present with dysphagia, weight loss, and potentially haematemesis.\n- Functional dyspepsia: This condition may present with similar gastrointestinal symptoms without a clear organic cause.\n- Hiatus hernia: Often coexists with GORD but can cause pain without significant reflux.\n\n\n# Investigations\n\n- Urea (13C) breath test, Stool Helicobacter Antigen Test (SAT), or laboratory-based serology **if** symptoms suggestive of H.pylori infection.\n- Oesophagogastroduodenoscopy (OGD) if alarm features or atypical, persistent or relapsing symptoms are present.\n- Oesophageal manometry\n\n**Referral criteria for urgent (within 2 weeks) OGD to investigate for oesophageal and gastric cancer:**\n\n- Aged 55 years and over with weight loss + dyspepsia/reflux\n\nReferral criteria for non-urgent OGD:\n\nAged 55 years and over plus\n\n- Treatment-resistant dyspepsia\n \nOR\n\n- Raised platelet count + dyspepsia/reflux\n- Nausea/vomiting + dyspepsia/reflux\n\n# Management\n\n- Lifestyle interventions - weight loss, dietary changes, elevation of the head of the bed at night, avoidance of late-night eating.\n- Proton pump inhibitor therapy. For patients <40 years old who present with typical symptoms and no red flags, commence treatment with a standard-dose PPI for 4 weeks in combination with lifestyle changes.\n\t- If the patient meets criteria for urgent OGD, they should only be commenced on PPI therapy after this has been done\n- Antacids for symptomatic relief.\n- Anti-reflux surgery for refractory cases.\n- Treatment for H.pylori infection if confirmed (PPI + antibiotics), with retesting using the urea breath test\n\t- It should not be performed within 2 weeks of treatment with a proton pump inhibitor or within 4 weeks of antibacterial treatment, as this can lead to false negatives.\n\n# Complications\n\nPotential complications of GORD include:\n\n- Oesophageal ulcer\n- Oesophageal stricture\n- Barrett's oesophagus\n- Adenocarcinoma of the oesophagus\n\n# NICE Guidelines \n\n- [NICE: Gastro-oesophageal reflux disease and dyspepsia in adults: investigation and management](https://www.nice.org.uk/guidance/cg184)\n\n# References\n\n- [BMJ Best Practice: Gastro-oesophageal reflux disease](https://bestpractice.bmj.com/topics/en-gb/82)\n- [European Association of Endoscopic Surgery: Recommendations for the management of gastroesophageal reflux disease](https://link.springer.com/article/10.1007/s00464-014-3431-z)",
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"explanation": "# Drug choice feedback\n\nThis gentleman has benign gastric ulceration. Whilst a proton-pump inhibitor is first line, his allergy is a contra-indication. Hence, H2-antagonists have to be used. The options licensed in the UK are as above. Antacids only provide short-term symptomatic relief but do not definitively treat benign gastric ulceration.\n\n# Dose/Route/Frequency/Duration feedback\n\nEach medication has its own optimal dose. All are orally taken and have varying dosing frequencies.",
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"question": "Case Presentation: A 57-year-old gentleman presents to his GP with dyspepsia. He does not report any weight loss, no vomiting, no changes to appetite.\n\n\n## PH\n\nObesity\n\n## DH\n\nNIL (Allergy to Omeprazole)\n\n## FHx\n\nNo upper gastrointestinal cancer\n\n## On examination\n\nAlert and oriented. Mild epigastric tenderness, otherwise abdomen soft and non-tender, no masses palpated.\n\nTemperature 36.8°C, HR 70, RR 13, BP 139/81, O<sub>2</sub> 98% RA, GCS 15, Weight 86kg\n\n## Investigations\n\nFBC: Hb 152, WCC 6.2, Plt 283\nUrgent OGD performed: \"Benign gastric ulceration noted, no oesophagitis, no masses seen.\"\n\nStool antigen test for _H. pylori_: negative\n\n# Prescribing Request\n\nWrite a prescription for one drug that is most appropriate for treating his condition.",
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"comment": "Why would Plasmalyte not be correct?",
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"comment": "i gave 250 ml saline over 15 mins, would this be wrong? i just thought due to his older age and slightly lower eGFR? :/",
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"comment": "250ml fluid challenge is usually given in patients with heart failure as you don't want to overload them with too much fluid - not sure if this info is on BNF ",
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"comment": "Why is 0.9% NaCl over 10m incorrect? Does it have to be 15m?",
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"comment": "in the actual PSA it has to be 10 because guidelines say <15m ",
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"explanation": "# Summary\n\nIntravenous (IV) fluid resuscitation describes when fluids are given to help restore the circulating volume and improve tissue perfusion. It is often required in patients who are hypovolaemic, for example due to infection, haemorrhage or other fluid losses e.g. severe vomiting and diarrhoea. Crystalloid fluids are first-line (e.g. 0.9% sodium chloride or Hartmann's) and NICE recommends giving an initial 500 ml bolus over less than 15 minutes. Regular reassessment is important, and although repeated fluid boluses can be given if the patient has signs of shock or has received over 2 litres of fluid expert help should be sought. Complications of IV fluid resuscitation include fluid overload and electrolyte imbalance. \n\n# Definition\n\nIV fluids are given in two main situations: maintenance fluids (where the patient's normal requirements are met plus replacement of abnormal fluid and electrolyte losses) and fluid resuscitation.\n\nNICE guidelines give an algorithm of how patients' fluid and electrolyte needs should be assessed and prescribed. \n\nIndicators that a patient may need fluid resuscitation include:\n\n- Systolic blood pressure < 100 mmHg\n- Heart rate > 90\n- Respiratory rate > 20\n- National Early Warning Score (NEWS) of 5 or more\n- Cold peripheries\n- Capillary refill time > 2 seconds\n\nNICE suggests doing a passive leg raise test to assess fluid responsiveness. This involves lying the patient flat with their legs raised to greater than 45 degrees for 30-90 seconds. If this leads to haemodynamic improvement (e.g. a rise in blood pressure), this indicates fluid responsiveness i.e. fluid resuscitation is likely to be of benefit. \n\n# Investigations\n\nPrior to prescribing fluid resuscitation, patients need an assessment of their fluid and electrolyte needs\n\nThis involves taking into account:\n\n- History (e.g. recent fluid intake, thirst, abnormal fluid losses and comorbidities)\n- Examination (observations, capillary refill, jugular venous pressure, signs of pulmonary or peripheral oedema, postural hypotension)\n- Fluid balance charts \n- Weight\n- Full blood count (e.g. to assess for anaemia due to bleeding)\n- U&Es for renal function and electrolytes\n- Lactate levels and/or pH\n- Serum chloride in patients receiving high chloride IV fluids (e.g. normal saline) \n\n# Management\n\n- Identifying and treating the cause of hypovolaemia is key (e.g. gastrointestinal bleeding, sepsis)\n- Patients should be prescribed a 500ml bolus of a crystalloid (e.g. normal saline or Hartmann's) over less than 15 minutes initially\n- In some cases (e.g. frail elderly patients) a smaller volume of fluid such as 250ml may be given\n- They should then be reassessed using an A-E approach and if required further 250-500ml boluses should be given, to a maximum of 2 litres \n- After 2 litres have been given, or if the patient has signs of shock, expert help should be sought (e.g. intensive care in case inotropic support is required)\n- NICE recommend that in patients with severe sepsis only, human albumin solution 4-5% may be considered for fluid resuscitation\n- In patients who are hypovolaemic due to haemorrhage, replacement with blood products is preferrable\n\n# Complications\n\n- Hyperchloremic acidosis due to excess administration of normal saline\n- Fluid overload with pulmonary and/or peripheral oedema\n- Electrolyte imbalance (e.g. hypokalaemia) if fluids are insufficiently tailored to the patient's requirements \n- Dilutional anaemia\n\n# References\n\n[NICE - Intravenous fluid therapy in adults in hospital](https://www.nice.org.uk/guidance/cg174/)\n\n[RCP Ten Top Tips for Intravenous Fluid Administration](https://www.bapen.org.uk/images/pdfs/rcp-ten-top-tips/intravenous-fluid-administration.pdf)",
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"explanation": "# Drug choice feedback\n\nThis patient requires urgent fluid resuscitation as part of the management for his wound sepsis. Crystalloid fluids such as 0.9% sodium chloride or Hartmann's solution are first-line in such cases.\n\n# Dose/Route/Frequency/Duration feedback\n\n500mL is the standard dose used for a fluid bolus ('fluid challenge') in resuscitation. Vital observations such as heart rate and blood pressure are monitored after each dose to see if a further bolus is required. Fluids can only be given intravenously; this route of administration also ensures the fastest response to be seen in the patient. A duration of 15 minutes or less for every 500mL is acceptable.",
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"question": "Case Presentation: A 68-year-old gentleman admitted to the general ward for observation after a right hemicolectomy 7 days ago is being treated for sepsis. He is found to be drowsy and confused.\n\n\n\n\n## PH\n\n\nColorectal cancer, Hyperlipidaemia, Gout\n\n\n## DH\n\n\nAtorvastatin 40mg PO ON, Allopurinol 300mg PO OD\n\n\n## On examination\n\n\nAppears delirious and not oriented to time and place. Peripheries warm, CRT 3s. HS I + II + 0, chest clear.\n\n\nTemperature 38.9°C, HR 96, RR 27, BP 95/65, O2 95% RA, GCS 13, Weight 75kg\n\n\n## Investigations\n\n\nFBC: Hb 148, WCC 15.5, Plts 420\n\n\nU&Es: Na<sup>+</sup> 141, K<sup>+</sup> 4.3, Cl<sup>-</sup> 98, Ur 9.2, Cr 110, eGFR 61mL/min/1.73m<sup>2</sup>\n\n\nBM: 6.7mmol/L (normal rnage 3.5-5.5 mmol/L)\n\n\n# Prescribing Request\n\n\nWrite a prescription for one fluid that is most appropriate for treating his current condition",
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"comment": "why not GTN to treat \"episodes of pain\"",
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"comment": "He’s already on it ",
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"comment": "Can anyone tell if I wouldn't score anything for this question if my medication choice was \"verapamil hydrochloride 40 mg tablets\" ?",
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"comment": "in the PSA you'll probably get 4/5 marks for that because it is technically correct, but you're giving two tablets instead of one, so it's less ideal than giving 80mg tablets",
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"explanation": "# Summary\r\n\r\nStable angina, characterised by chest pain triggered by myocardial ischemia, is most commonly caused by coronary artery disease. Typical anginal chest pain is described as an exertional chest discomfort that may radiate to the jaw/neck/arm and that is alleviated by rest (<5 minutes) or with GTN spray. Diagnosis involves investigations such as ECG, blood tests, and CT coronary angiogram. Management includes conservative measures to optimise cardiovascular risk factors, medical treatment with anti-anginal medications, and revascularisation options like coronary artery bypass graft or percutaneous coronary intervention in cases not controlled by medical therapy.\r\n\r\n# Definition \r\n\r\nTypical anginal chest pain is defined by the following 3 features:\r\n\r\n1. Constriction/heavy discomfort to chest that may radiate to the jaw/neck/arm.\r\n2. Brought on by exertion.\r\n3. Alleviated by rest (<5 minutes) or GTN spray. \r\n\r\n3/3 features = typical angina pain \r\n\r\n2/3 features = atypical angina pain\r\n\r\n0-1/3 features = non-anginal pain \r\n\r\n# Epidemiology \r\n\r\nA 2020 Health Survey for England estimated prevalence in all UK adults as 3%, increasing to a prevalence of 10–12% in women aged 65–84 years and 12–14% in similarly aged men. \r\n\r\n# Pathophysiology\r\n\r\nStable angina occurs as a result of a mismatch of myocardial oxygen supply and demand. Most commonly, stable angina is due to coronary artery disease. Coronary artery disease refers to the narrowing of coronary arteries by atherosclerosis and plaque formation. When demand for myocardial oxygen increases with exertion, narrowed coronary arteries cannot meet this increased demand leading to myocardial ischaemia and pain. \r\n\r\nOther rarer causes of stable angina include anaemia, aortic stenosis, or hypertrophic cardiomyopathy.\r\n \r\n# Classification \r\n \r\nStable angina pain can be considered by its limitations on day-to-day activity:\r\n\r\n* Class I: no angina with normal physical activity. Strenuous activity may cause symptoms. \r\n* Class II: angina pain causes slight limitation on normal physical activity. \r\n* Class III: angina causes marked limitation on normal physical activity. \r\n* Class IV: angina occurs with any physical activity and may occur at rest (see unstable angina). \r\n\r\n# Symptoms and Signs\r\n\r\n* Central, constricting chest pain that radiates to neck/jaw/arm. \r\n* Exertional chest pain that is relieved on rest/GTN. \r\n* Associated symptoms: nausea, vomiting, clamminess or sweating. \r\n\r\nStable angina may have no clinical signs on examination at rest.\r\n\r\n# Differential Diagnoses \r\n\r\n* **Acute Coronary Syndrome (ACS)** \r\n\t* **Similarities**: cardiac-sounding chest pain as a presenting complaint for both. Similar patient profile with significant risk factors for coronary artery disease. \r\n\t* **Differences**: stable angina only occurs on exertion and is alleviated by rest. ACS chest pain occurs at rest. \r\n\r\n* **Gastro-oesophageal reflux disease (GORD)** \r\n\t* **Similarities**: both may present with central chest discomfort/pain. \r\n\t* **Differences**: discomfort in stable angina commonly described as a squeezing or pressure-like pain brought on by exertion. GORD-related chest discomfort often described as a burning sensation that is triggered by certain foods, alcohol, or lying down. \r\n\r\n* **Costochondritis** \r\n\t* **Similarities**: both present with chest pain. \r\n\t* **Differences**: costochondritis refers to inflammation of the cartilage connecting ribs to the sternum. The pain is described as sharp and can be reproduced by pressing on the chest wall. \r\n\r\n* **Pleuritic Chest Pain e.g. Pulmonary Embolism, Pneumonia** \r\n\t* **Similarities**: both present with chest pain or discomfort. \r\n\t* **Differences**: pleuritic chest pain is often described as sharp and worse on inspiration. Pleuritic chest pain will also be accompanied by clinical features relating to the underlying cause e.g. productive cough, fevers, risk factors for VTE, or a hot swollen calf. \r\n\r\nOther differential diagnoses include anxiety, aortic dissection (radiates to the back), and other causes of musculoskeletal chest pain. \r\n\r\n# Investigations\r\n\r\nOnce atypical/typical anginal pain is suspected: \r\n\r\n**Routine investigations in primary care**: \r\n\r\n* ECG - to assess for ischaemic changes or previous MI. \r\n* Bloods - FBC and TFTs (to exclude anaemia and hyperthyroidism respectively which can exacerbate angina symptoms).\r\n* Consider cardivascular risk factors: hypertension, hypercholesterolaemia, diabetes mellitus, smoking. \r\n\r\n**1st line investigations**\r\n\r\n* CT coronary angiogram (CT CA)- indicated if typical/atypical angina pain or if ECG shows ischaemic changes in chest pain with <2 angina features.\r\n\r\n**2nd line investigations** \r\n\r\nIf CTCA is inconclusive the patient may undergo functional imaging: \r\n\r\n* Stress echocardiogram \r\n* Myocardial perfusion SPECT \r\n* Cardiac MRI\r\n\r\n**3rd line investigations**\r\n\r\nInvasive coronary angiography can be performed if there are inconclusive results from non-invasive testing.\r\n\r\n# Management\r\n\r\n## Conservative management\r\n\r\nConservative management involves the optimisation of cardiovascular risk factors to reduce the atherosclerotic process. \r\n\r\n* Smoking cessation\r\n* Glycaemic control\r\n* Hypertension\r\n* Hyperlipidaemia\r\n* Weight loss\r\n* Alcohol intake \r\n\r\n## Medical management \r\n\r\n* Secondary prevention: aspirin 75mg OD and statin 80mg ON. \r\n* GTN spray for symptom relief: inform patient of side-effects (headache, flushing, dizziness) and to repeat dose if pain not stopped after 5 minutes. \r\n\r\n*Emergency help should be sought if pain not subsided after 2 doses of GTN as this may indicate acute coronary syndrome.* \r\n\r\n**Anti-anginal medications**\r\n\r\n**1st line** = beta-blocker (bisoprolol) OR calcium channel blocker (verapamil or diltiazem). *Do not combine due to risk of heart block*. \n\nIf taking a beta-blocker and symptoms are uncontrolled, switch to, or add, a long-acting dihydropyridine calcium-channel blocker (CCB), such as amlodipine, modified-release nifedipine. If taking a non-dyhydropyridine calcium channel blocker already, switch to a beta blocker.\r\n\r\nIf neither can be tolerated, consider a long-acting nitrate (ISMN), ivabradine, nicorandil or ranolazine. \r\n\r\n**2nd line** = beta-blocker (bisoprolol) AND long-acting dihydropyridine calcium channel blocker (amlodipine or nifedipine)\r\n\r\n**3rd line** = beta-blocker (bisoprolol) AND long-acting dihydropyridine calcium channel blocker AND long-acting nitrate.\r\n\r\nA 3rd medication should only be added if the patient is symptomatic despite 2 anti-anginal drugs. At this stage, revascularisation with PCI or CABG must be considered. \r\n\r\n## Revascularisation\r\n\r\nRevascularisation with coronary artery bypass graft (CABG) or percutaneous coronary intervention (PCI) must be considered in patients with: \r\n\r\n* Symptoms which are not controlled by optimal medical management.\r\n* Complex 3 vessel disease and/or significant left main stem on CTCA. \r\n\r\n# NICE Guidelines\n\r\n[NICE Guidance on Cardiac-Sounding Chest Pain](<https://www.nice.org.uk/guidance/cg95/chapter/Recommendations>) \r\n\n[NICE Guidance on Stable Angina](<https://www.nice.org.uk/guidance/cg126/chapter/Guidance>) \r\n\r\n# References\r\n\r\n[Patient UK Information on Stable Angina](<https://patient.info/doctor/stable-angina-2>) ",
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"question": "Case Presentation: A 62-year-old gentleman has been admitted to the ward after being seen in the Emergency Department for episodes of chest pain on exertion which resolve when at rest.\n\n\n## PH\n\nHypertension, Type 2 Diabetes Mellitus, Asthma\n\n## DH\n\nRamipril 5mg PO OD, Metformin 500mg BD PO, Salbutamol metered dose inhaler 200 mcg/dose INH PRN, Beclometasone inhalation powder 200 mcg/dose INH BD. He was prescribed Glyceryl Trinitrate 400micrograms/dose aerosol sublingual spray, 1 spray PRN in the Emergency Department (Allergy to Clarithromycin)\n\n## On examination\n\nAppears well, oriented to time and place. HS I + II + 0, chest clear.\n\nTemperature 36.2°C, HR 76, RR 14, BP 135/88, O<sub>2</sub> 99% RA, GCS 15, Weight 89kg\n\n## Investigations\n\nCXR: Normal, no cardiomegaly\n\nECG: Normal sinus rhythm, no Q-waves or inverted T-waves\n\n# Prescribing Request\n\nWrite a prescription for one additional drug that is most appropriate for treating his episodes of chest pain.",
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"comment": "haematuria but otherwise normal dip - is peel not a concern?",
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"comment": "She's allergic to co-trimoxazole, which contains trimethoprim, so best to avoid it :)",
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"explanation": "# Summary\n\nVesicoureteral reflux (VUR) is a congenital condition where urine flows backwards from the bladder into the ureters and kidneys, increasing the risk of recurrent urinary tract infections (UTIs). Symptoms include recurrent UTIs, fevers, and abdominal pain, with severe cases leading to renal scarring and hypertension. Diagnosis can involve ultrasound, MCUG, MAG reflux test, and DMSA scan. Management includes prophylactic antibiotics, monitoring, and possibly surgery for severe cases. Complications include UTIs, pyelonephritis, and chronic kidney disease.\n\n# Definition\n\nVesicoureteral reflux (VUR) is a condition where urine flows backwards from the bladder into the ureters and potentially the kidneys, rather than the usual one-way flow from the kidneys to the ureters and then to the bladder. This condition is typically present from birth and can lead to recurrent UTIs, as the backward flow of urine can carry bacteria up into the kidneys, causing an infection. It is a significant risk factor for atypical UTIs and recurrent infections.\n \n\n# Epidemiology\n \n\nVUR affects around 1-3% of all children and can occur in all age groups. It is more commonly diagnosed in children with UTIs, especially if these UTIs are recurrent or atypical. A familial predisposition is often present.\n \n\n# Pathophysiology\n\nThe abnormal flow of urine in VUR can occur due to a variety of reasons, including a shortened intravesical ureter (the part of the ureter that passes through the bladder wall), an improperly functioning valve where the ureter joins the bladder, or a neurological disorder affecting the bladder.\n \n\n# Signs and Symptoms\n \nVUR is often asymptomatic and may only be detected when investigating recurrent or atypical UTIs. \n\nSymptoms can include:\n\n- Recurrent UTIs or persistent bacteriuria\n- Unexplained fevers\n- Abdominal or flank pain\n- In severe cases, renal scarring can occur leading to hypertension and chronic kidney disease\n \n\n# Investigations\n \n\nIn children with recurrent or atypical UTIs, investigations considering VUR include:\n \n- Ultrasound of the kidneys and bladder is often performed initially \n - Used to detect hydronephrosis, dilatation of renal pelvis or incomplete bladder voiding \n- Micturating Cystourethrogram (MCUG) \n - Contrast is passed into the bladder, and the patient passes urine whilst x-rays are taken.\n - This enables the refluxing of urine to be visualised \n- MAG (mercapto acetyl triglycine 3) reflux test \n - IV contrast recorded on x-ray whilst the child passes urine, to enable any reflux to be visualised \n- Dimercaptosuccinic acid (DMSA) scan\n - This can detect scarring or damage to the kidneys as a result of VUR\n \n\n# Management\n \n\nThe management of VUR can be conservative or surgical, depending on the severity of the condition, the age of the patient, and the risk of kidney damage. \n\n- Conservative management:\n - Prophylactic antibiotics to prevent UTIs\n - Regular monitoring of kidney function and growth\n - Treatment of constipation if present\n- Surgical treatment, such as ureteral reimplantation, may be considered in severe cases or when conservative management fails.\n \n\n# Complications\n\nPotential complications of VUR include:\n \n\n - Recurrent UTIs\n - Pyelonephritis\n - Renal scarring and Chronic Kidney Disease (CKD)\n - Hypertension\n \nThis highlights the importance of early detection and management of VUR, especially in children with recurrent or atypical UTIs.\n \n# NICE Guidelines \n\n[NICE Guideline Urinary tract infection in under 16s: diagnosis and management](https://www.nice.org.uk/guidance/ng224/chapter/Recommendations-for-research) \n \n# References\n\n[Kidney Research UK Vesicoureteral reflux](https://www.kidneyresearchuk.org/conditions-symptoms/vesico-uretal-reflux/)",
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"explanation": "# Drug choice feedback\n\nThis woman likely has a lower urinary tract infection with no overt complications. In cases whereby there is a low risk of resistance, the two possible first line agents for non-pregnant women include nitrofurantoin or trimethoprim. Given that she is allergic to co-trimoxazole which contains trimethoprim, only nitrofurantoin can be prescribed.\n\n# Dose/Route/Frequency/Duration feedback\n\nThe recommended dose is either 50mg or 100mg, and the frequency is QDS or BD, depending on whether the immediate- or modified-release form is prescribed respectively. It should be prescribed for 3 days. Women who are pregnant and all men who have a lower urinary tract infection require a longer prescription of 7 days.",
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"question": "Case Presentation: A 51-year-old woman attends the GP with urinary frequency, foul-smelling urine and dysuria. She mentions the symptoms are causing her distress. She does not report any loin-to-groin pain nor rigours.\n\n\n## PH\n\nBreast cyst diagnosed 23 years ago, surgically removed without recurrence or complications\n\n## DH\n\nNIL (Allergy to Co-trimoxazole)\n\n## On examination\n\nAlert and oriented. No loin tenderness.\n\nTemperature 36.5°C, HR 75, RR 12, BP 125/79, O<sub>2</sub> 98% RA, GCS 15, Weight 68kg\n\n## Investigations\n\nHaematuria 1+ on dipstick, otherwise normal\n\nUrinary MC&S not appropriate as of now as clinically low risk of resistance.\n\n# Prescribing Request\n\nWrite a prescription for one antibiotic that is most appropriate for treating her condition.",
"sbaAnswer": null,
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173,458,245 | false | 6 | null | 6,494,949 | null | false | [] | null | 6,794 | {
"__typename": "QuestionMultiA",
"choices": [
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"__typename": "QuestionChoice",
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"explanation": null,
"id": "33905",
"label": "d",
"name": "Dexamethasone;22.5mg;Oral (PO);Once only",
"picture": null,
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"id": "33904",
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"id": "33903",
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"picture": null,
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}
],
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"comment": "Are steroids not contraindicated in GORD?",
"createdAt": 1737573295,
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"explanation": "#### Monitoring\r\n\r\nThe BNF advises to monitor lung function (in patients with a history of obstructive airway disease).\r\n\r\n#### Overdoses\r\n\r\nOverdosages with beta-blockers may cause cardiac effects such as bradycardia, hypotension, syncope, conduction abnormalities, and heart failure. Bradycardia is the most common arrhythmia, but some beta-blockers may induce ventricular tachyarrhythmias secondary to prolongation of QT interval (e.g. sotalol) or QRS duration (e.g. propranolol).\r\nNon-cardiovascular effects include central nervous system effects (including drowsiness, confusion, convulsions, hallucinations, and in severe cases coma), respiratory depression, and bronchospasm.\r\n\r\nManagement\r\n - Airway protection \r\n - Activated charcoal within 1 hour\r\n - IV Fluids\r\n \r\nIV glucagon is the first-line management.\r\n \r\nFor symptomatic bradycardia, IV atropine may be used.\r\n",
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"explanation": "1. The dose of dexamethasone for croup is 150 micrograms/kg. The girl is 15kg in weight. Hence, the correct dose that should be prescribed is 2.25mg.\n2. Tetracycline is contra-indicated in children under 12 years. Tetracycline binds to calcium and gets deposited in growing bone and teeth. Use of tetracycline in children is associated with teeth staining and dental hypoplasia.",
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"question": "Case presentation: A 3-year-old girl is brought to the emergency department by her mother in the middle of night. The little girl has developed a fever and a sudden-onset seal-like “barking” cough. Her weight is 15kg PH: Constipation, Anaemia, Rosacea, GORD DH: Her current regular prescriptions are listed below\n\n\n**On examination**: Seal-like barking cough, hoarse cry and an inspiratory stridor when crying\n\n**Vital signs**: Temperature 37.8°C, HR 125, O2 Sat 99% (room air), RR 30\nCroup (acute laryngotracheobronchitis) is suspected and treatment is commenced.\n\nQuestion 1: Select the ONE prescription that contains a serious dosing error. (mark them with a tick in column A)\nQuestion 2: Select the ONE prescription that is contra-indicated. (mark it with a tick in column B)",
"sbaAnswer": null,
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} | MarksheetMark |
173,458,246 | false | 7 | null | 6,494,949 | null | false | [] | null | 6,792 | {
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"id": "33893",
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},
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},
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"id": "33891",
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"picture": null,
"votes": 0
},
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"id": "33889",
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"picture": null,
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},
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"label": "g",
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"picture": null,
"votes": 0
}
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"explanation": "#### Monitoring\r\n\r\nThe BNF advises to monitor lung function (in patients with a history of obstructive airway disease).\r\n\r\n#### Overdoses\r\n\r\nOverdosages with beta-blockers may cause cardiac effects such as bradycardia, hypotension, syncope, conduction abnormalities, and heart failure. Bradycardia is the most common arrhythmia, but some beta-blockers may induce ventricular tachyarrhythmias secondary to prolongation of QT interval (e.g. sotalol) or QRS duration (e.g. propranolol).\r\nNon-cardiovascular effects include central nervous system effects (including drowsiness, confusion, convulsions, hallucinations, and in severe cases coma), respiratory depression, and bronchospasm.\r\n\r\nManagement\r\n - Airway protection \r\n - Activated charcoal within 1 hour\r\n - IV Fluids\r\n \r\nIV glucagon is the first-line management.\r\n \r\nFor symptomatic bradycardia, IV atropine may be used.\r\n",
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"id": "2725",
"name": "Drugs causing drowsiness & constipation",
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"id": "74",
"name": "Elderly Care",
"typeId": 5
},
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"explanation": "1. Confusion is a common or very common side effect of a beta-adrenoceptor blocker such as carvedilol. Drowsiness is also listed as a common or very common side effect of amitriptyline. Promethazine is also known to cause drowsiness although the frequency of such side effect is unknown. Patients taking these medications should be reminded that their performance of skilled tasks like driving and operating heavy machinery could be affected.\n2. Constipation is a common or very common side effect of amlodipine, and can also be caused by amitriptyline due to its anticholinergic activity.",
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"question": "Case presentation: A 80-year old man is taken to A&E via ambulance after being found lying on the floor by his daughter. His daughter reports that his father has become increasingly drowsy and confused over the past few days. His father has also been complaining of constipation recently. **PH:** Atrial fibrillation, Congestive Cardiac Failure, Type 2 Diabetes Mellitus, Hayfever, Neuropathic pain, Otitis externa **DH:** His current regular prescriptions are listed below\n\n\n**On examination**: Abbreviated Mental Test Score 6/10. Chest is clear with no added lung sounds. Heart sounds I + II + 0. Abdomen soft and non tender. Bruises on left hip with no active bleeding. Pain on external rotation of left leg.\n**Vital signs**: BP 125/80, Temperature 36.8°C, HR 80, O2 Sat 99% (room air), RR 18\n\nQuestion 1: Select the THREE prescriptions that are most likely to be a cause of the drowsiness and confusion (mark them with a tick in column A)\nQuestion 2: Select the TWO prescriptions that are most likely to be a cause of his constipation (mark it with a tick in column B)",
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173,458,247 | false | 8 | null | 6,494,949 | null | false | [] | null | 6,795 | {
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"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
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"id": "33909",
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"picture": null,
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},
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"__typename": "QuestionChoice",
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"id": "33910",
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},
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"id": "33911",
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"picture": null,
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},
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"__typename": "QuestionChoice",
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"explanation": null,
"id": "33912",
"label": "e",
"name": "Dermacort hydrocortisone 0.1% cream;-;Topical;Daily",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
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"explanation": null,
"id": "33913",
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"name": "Chloroquine;225mg;Nebulised (NEB);Once weekly",
"picture": null,
"votes": 0
},
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"__typename": "QuestionChoice",
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"id": "33908",
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"picture": null,
"votes": 0
}
],
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"explanation": "#### Monitoring\r\n\r\nThe BNF advises to monitor lung function (in patients with a history of obstructive airway disease).\r\n\r\n#### Overdoses\r\n\r\nOverdosages with beta-blockers may cause cardiac effects such as bradycardia, hypotension, syncope, conduction abnormalities, and heart failure. Bradycardia is the most common arrhythmia, but some beta-blockers may induce ventricular tachyarrhythmias secondary to prolongation of QT interval (e.g. sotalol) or QRS duration (e.g. propranolol).\r\nNon-cardiovascular effects include central nervous system effects (including drowsiness, confusion, convulsions, hallucinations, and in severe cases coma), respiratory depression, and bronchospasm.\r\n\r\nManagement\r\n - Airway protection \r\n - Activated charcoal within 1 hour\r\n - IV Fluids\r\n \r\nIV glucagon is the first-line management.\r\n \r\nFor symptomatic bradycardia, IV atropine may be used.\r\n",
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"explanation": "1. Nitrofurantoin is an antibiotic that works by damaging bacterial DNA. Chloroquine is a medication used to prevent and treat malaria. Nitrofurantoin and chloroquine are contra-indicated in patients with G6PD-deficiency because are they known to cause severe haemolytic anaemia.\n2. Ibuprofen is known to cause bronchospasm in patients with asthma, especially those with a history of hypersensitivity to aspirin or any other NSAID. Ibuprofen inhibits the activity cyclooxygenase-1 (Cox-1). The inhibition leads to activation of lipoxygenase pathway that in turn increases the release of cysteinyl leukotrienes (Cys-LTs) that induces bronchospasm.",
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"question": "Case presentation: A 9-year old boy arrives at A&E with shortness of breath and wheeze. He presented to his GP two days ago with increased urinary frequency and dysuria. A diagnosis of lower urinary tract infection was made and antibiotic treatment was commenced. He has a past medical history of asthma which has so far been well controlled. His weight is 30kg. His mother who is accompanying him informs that the family has just come back from Nigeria and that they have been taking malaria prophylaxis. PH: Asthma, Allergic rhinitis, Eczema, Lower urinary tract infection, vesicoureteral reflux, Glucose-6-phosphate dehydrogenase (G6PD) deficiency DH: Her current regular prescriptions are listed below\n\n\n**On examination**: Breathing using accessory muscles, polyphonic expiratory wheeze\n\n**Vital signs**: Temperature 36.6°C, HR 90, O2 Sat 92% (room air), RR 26\n\nQuestion 1: Select the TWO prescriptions that are contra-indicated or should be used with caution in the context of G6PD deficiency (mark them with a tick in column A)\nQuestion 2: Select the ONE prescription that is most likely to have led to exacerbation of asthma symptoms (mark it with a tick in column B)",
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} | MarksheetMark |
173,458,248 | false | 9 | null | 6,494,949 | null | false | [] | null | 6,787 | {
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},
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},
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"label": "d",
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"picture": null,
"votes": 0
}
],
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{
"__typename": "QuestionComment",
"comment": "Prednisolone can lead to fluid retention for sure, but I don't know regarding angioedema.\n",
"createdAt": 1709372835,
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"comment": "why wouldnt amlodipine be correct - is it becuase it only causes peripheral oedema and not angioedema \n",
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"comment": "well duh",
"createdAt": 1737654904,
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"comment": "if in a question, theres a few cuases of oedema - how woudl you narrow it down ",
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"explanation": "#### Monitoring\r\n\r\nThe BNF advises to monitor lung function (in patients with a history of obstructive airway disease).\r\n\r\n#### Overdoses\r\n\r\nOverdosages with beta-blockers may cause cardiac effects such as bradycardia, hypotension, syncope, conduction abnormalities, and heart failure. Bradycardia is the most common arrhythmia, but some beta-blockers may induce ventricular tachyarrhythmias secondary to prolongation of QT interval (e.g. sotalol) or QRS duration (e.g. propranolol).\r\nNon-cardiovascular effects include central nervous system effects (including drowsiness, confusion, convulsions, hallucinations, and in severe cases coma), respiratory depression, and bronchospasm.\r\n\r\nManagement\r\n - Airway protection \r\n - Activated charcoal within 1 hour\r\n - IV Fluids\r\n \r\nIV glucagon is the first-line management.\r\n \r\nFor symptomatic bradycardia, IV atropine may be used.\r\n",
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"id": "2720",
"name": "Dosing error & angioedema",
"status": null,
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"id": "75",
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"typeId": 5
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"explanation": "1. ACEi (perindopril arginine) and tetracycline (oxytetracycline) commonly cause angioedema with the former more common in the Afro-Carribean population. Calcium channel blockers (amlodipine) also cause angioedema but are not common.\n2. Bisoprolol fumarate, given for the treatment of hypertension is given at 5-10mg daily with a maximum dose of 20mg daily. Hence, the correct prescription for 20mg should be daily instead of 12-hrly.",
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"question": "Case presentation: A 70-year-old Afro-Carribean gentleman presents to the GP for his annual flu vaccine. PH Infective exacerbation of COPD, for which he has been receiving treatment for the past 5 days, Hypertension. DH His current regular medicines are listed (below).\n\n\n**On Examination** Red swellings beneath the surface of his eyelid consistent with angioedema.\n\nQuestion 1: Select the ONE prescription that is most likely to be contributing to the angioedema (mark them with a tick in column A)\nQuestion 2: Select the ONE prescription that contains a serious dosing error (mark it with a tick in column B).",
"sbaAnswer": null,
"totalVotes": 0,
"typeId": 3,
"userPoint": null
} | MarksheetMark |
173,458,249 | false | 10 | null | 6,494,949 | null | false | [] | null | 6,788 | {
"__typename": "QuestionMultiA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": null,
"id": "33859",
"label": "f",
"name": "Bumetanide;1mg;Oral (PO);Daily",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
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"explanation": null,
"id": "33858",
"label": "e",
"name": "Simvastatin;40mg;Oral (PO);Daily",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": null,
"id": "33856",
"label": "c",
"name": "Chlortalidone;50mg;Oral (PO);Daily",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": null,
"id": "33857",
"label": "d",
"name": "Cetirizine hydrochloride;10mg;Oral (PO);Daily",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": null,
"id": "33860",
"label": "g",
"name": "Fluoxetine;100mg;Oral (PO);Daily",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": null,
"id": "33854",
"label": "a",
"name": "Amlodipine;5mg;Oral (PO);Daily",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": null,
"id": "33855",
"label": "b",
"name": "Losartan potassium;50mg;Oral (PO);Daily",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": null,
"id": "33861",
"label": "h",
"name": "Colecalciferol (Vit D3);800 units;Oral (PO);Daily",
"picture": null,
"votes": 0
}
],
"comments": [
{
"__typename": "QuestionComment",
"comment": "Hyponatremia is rare in fluoxetine and unknown in losartan. How do we know which one to put since supposedly we dont need much theory to be able to do the PSA",
"createdAt": 1654497389,
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"comment": "Do ARBs not cause hyponatraemia too",
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"explanation": "#### Monitoring\r\n\r\nThe BNF advises to monitor lung function (in patients with a history of obstructive airway disease).\r\n\r\n#### Overdoses\r\n\r\nOverdosages with beta-blockers may cause cardiac effects such as bradycardia, hypotension, syncope, conduction abnormalities, and heart failure. Bradycardia is the most common arrhythmia, but some beta-blockers may induce ventricular tachyarrhythmias secondary to prolongation of QT interval (e.g. sotalol) or QRS duration (e.g. propranolol).\r\nNon-cardiovascular effects include central nervous system effects (including drowsiness, confusion, convulsions, hallucinations, and in severe cases coma), respiratory depression, and bronchospasm.\r\n\r\nManagement\r\n - Airway protection \r\n - Activated charcoal within 1 hour\r\n - IV Fluids\r\n \r\nIV glucagon is the first-line management.\r\n \r\nFor symptomatic bradycardia, IV atropine may be used.\r\n",
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"id": "2721",
"name": "Dosing error & drugs causing hyponatremia",
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"__typename": "Topic",
"id": "92",
"name": "General Practice",
"typeId": 5
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"explanation": "1. Chlortalidone is a thiazide-like diuretic that inhibits the Na+/Cl- cotransporter at the distal convoluted tubule of nephron, leading to reduced Na+ reabsorption. Bumetanide is a loop diuretic that acts on the Na+-K+-2Cl− symporter (NKCC2) in the thick ascending limb of the loop of Henle to inhibit sodium, chloride and potassium reabsorption. Both chlortalidone and bumetanide are known to cause hyponatraemia. Hyponatraemia is also a recognised side effect of fluoxetine. BNF cautions against prescribing fluoxetine to elderly patients with significant hyponatraemia i.e. serum sodium less than 130 mmol/L due to risk of exacerbating or precipitating hyponatraemia.\n2. The maximum daily dose of fluoxetine is 60mg.",
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"question": "Case presentation: A 45-year old man attends his GP appointment complaining of nausea and tiredness. PH: Hypertension, Allergic rhinitis, Hypercholesterolaemia, Peripheral oedema, Vitamin D deficiency DH: His current regular prescriptions are listed below\n\n\n\n\n **On examination**: Chest is clear with no added lung sounds. Heart sounds I + II + 0. Abdomen soft and non-tender.\n\n\n **Vital signs**: BP 125/80, Temperature 36.5°C, HR 80, O2 Sat 99% (room air), RR 18\n\n\n **Investigations**:\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|130 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|5x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|300x10<sup>9</sup>/L|150 - 400|\n|Mean Cell Volume (MCV)|90 fL|80 - 96|\n|Neutrophils|5x10<sup>9</sup>/L|2.0 - 7.5|\n|Lymphocytes|2x10<sup>9</sup>/L|1.5 - 4.0|\n|Sodium|125 mmol/L|135 - 145|\n|Potassium|4 mmol/L|3.5 - 5.3|\n|Urea|7 mmol/L|2.5 - 7.8|\n|Creatinine|109 µmol/L|60 - 120|\n|Thyroid Stimulating Hormone|3.8 mU/L|0.3 - 4.2|\n|Free T4|17 pmol/L|9 - 25|\n\n\nQuestion 1: Select the THREE prescriptions that are most likely to be a cause of his hyponatraemia (mark them with a tick in column A)\nQuestion 2: Select the ONE prescription that contains a serious dosing error (mark it with a tick in column B)",
"sbaAnswer": null,
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173,458,250 | false | 11 | null | 6,494,949 | null | false | [] | null | 6,809 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Foscarnet is an antiviral drug with activity against some herpesviruses such as CMV. It has no role in the acute management of shingles",
"id": "33992",
"label": "c",
"name": "Foscarnet 40mg/kg IV TDS",
"picture": null,
"votes": 25
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "This patient is presenting with shingles. Oral acyclovir has been shown to reduce the duration and intensity of symptoms, but not to reduce the incidence of post-herpetic neuralgia",
"id": "33990",
"label": "a",
"name": "Aciclovir 800mg PO 5 times a day",
"picture": null,
"votes": 5577
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Gabapentin is used to treat neuropathic pain and some types of seizures. It has no role in the acute management of shingles but can be prescribed to treat post-herpetic neuralgia",
"id": "33993",
"label": "d",
"name": "Gabapentin 300mg PO OD",
"picture": null,
"votes": 132
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Paracetamol may provide some pain relief from symptoms but does not treat shingles itself",
"id": "33994",
"label": "e",
"name": "Paracetamol 1g PO QDS",
"picture": null,
"votes": 397
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Duloxetine is an SNRI used to treat neuropathic pain. It has no role in the acute management of shingles but can be prescribed to treat post-herpetic neuralgia",
"id": "33991",
"label": "b",
"name": "Duloxetine 60mg PO OD",
"picture": null,
"votes": 18
}
],
"comments": [
{
"__typename": "QuestionComment",
"comment": "I thought you could only give Acyclovir if within 72 hours, wouldn't a 3 day history potentially be over this?",
"createdAt": 1704930155,
"dislikes": 0,
"id": "38489",
"isLikedByMe": 0,
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"displayName": "Relapse Complement",
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"comment": "only treat is pain is moderate or severe or weakened immune system, pt reports neither of these?",
"createdAt": 1737391931,
"dislikes": 0,
"id": "61065",
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"comment": "'Consider oral antiviral treatment for patients aged over 50 years to reduce the risk of post-herpetic neuralgia.' under 'Herpesvirus infections' treatment summary",
"createdAt": 1737718714,
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"id": "61414",
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"explanation": "#### Monitoring\r\n\r\nThe BNF advises to monitor lung function (in patients with a history of obstructive airway disease).\r\n\r\n#### Overdoses\r\n\r\nOverdosages with beta-blockers may cause cardiac effects such as bradycardia, hypotension, syncope, conduction abnormalities, and heart failure. Bradycardia is the most common arrhythmia, but some beta-blockers may induce ventricular tachyarrhythmias secondary to prolongation of QT interval (e.g. sotalol) or QRS duration (e.g. propranolol).\r\nNon-cardiovascular effects include central nervous system effects (including drowsiness, confusion, convulsions, hallucinations, and in severe cases coma), respiratory depression, and bronchospasm.\r\n\r\nManagement\r\n - Airway protection \r\n - Activated charcoal within 1 hour\r\n - IV Fluids\r\n \r\nIV glucagon is the first-line management.\r\n \r\nFor symptomatic bradycardia, IV atropine may be used.\r\n",
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"demo": null,
"entitlement": null,
"id": "2742",
"name": "Shingles",
"status": null,
"topic": {
"__typename": "Topic",
"id": "74",
"name": "Elderly Care",
"typeId": 5
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"topicId": 74,
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"question": "Case Presentation: A 73 year old man attends his GP with a 3 day history of a painful rash. **PH** aortic abdominal aneurysm (<5.5cm), benign prostatic hypertrophy. **DH** tamsulosin hydrochloride 400 micrograms PO OD. NKDA\n\n\n**O/E**\n\nHR 70, RR 13, BP 132/65, O2 100% RA, Temperature 36.4°C. Erythematous vesicular rash on right side of abdomen in the distribution of T10 dermatome.\n\nQuestion: Select the most appropriate management at this stage.",
"sbaAnswer": [
"a"
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"totalVotes": 6149,
"typeId": 1,
"userPoint": null
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173,458,251 | false | 12 | null | 6,494,949 | null | false | [] | null | 6,807 | {
"__typename": "QuestionSBA",
"choices": [
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "The initial medical management of peripheral vascular disease generally involves a single antiplatelet with preference for clopidogrel over aspirin as supported by the best available evidence. In addition, a high-dose statin should be prescribed",
"id": "33980",
"label": "a",
"name": "Clopidogrel 75mg PO OD and atorvastatin 80mg PO OD",
"picture": null,
"votes": 3167
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Dual antiplatelet therapy may be eventually indicated in the medical management of peripheral vascular disease but is no longer recommended as an initial treatment option. In addition, a high-dose statin should be prescribed",
"id": "33982",
"label": "c",
"name": "Aspirin 75mg PO OD and clopidogrel 75mg PO OD",
"picture": null,
"votes": 733
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "While antiplatelet therapy is recommended for the medical management of peripheral vascular disease, the current evidence supports the use of clopidogrel over aspirin. Aspirin may still be prescribed if clopidogrel is not tolerated",
"id": "33981",
"label": "b",
"name": "Aspirin 75mg PO OD and atorvastatin 80mg PO O",
"picture": null,
"votes": 1075
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This patient should be prescribed lipid-lowering therapy on account of likely peripheral vascular disease. However a statin should be the first line agent of choice rather than a fibrate, which are prescribed as adjuncts to statins or if statins are not appropriate",
"id": "33983",
"label": "d",
"name": "Clopidogrel 75mg PO OD and fenofibrate 200mg PO OD",
"picture": null,
"votes": 120
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This patient is presenting with symptoms of intermittent claudication and risk factors suggesting he has peripheral vascular disease. As such he should be prescribed an antiplatelet drug such as clopidogrel and a high-dose statin. In this option the dosages are incorrect – the dose of clopidogrel is too high and the dose of atorvastatin is too low",
"id": "33984",
"label": "e",
"name": "Clopidogrel 300mg PO OD and atorvastatin 20mg PO OD",
"picture": null,
"votes": 366
}
],
"comments": [
{
"__typename": "QuestionComment",
"comment": "Where can you find this in the BNF?",
"createdAt": 1646844711,
"dislikes": 0,
"id": "8299",
"isLikedByMe": 0,
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"__typename": "QuestionComment",
"comment": "https://cks.nice.org.uk/topics/peripheral-arterial-disease/management/intermittent-claudication/#managing-cardiovascular-risk\nhttps://cks.nice.org.uk/topics/antiplatelet-treatment/\nhttps://bnf.nice.org.uk/drug/clopidogrel.html",
"createdAt": 1647104548,
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"displayName": "Tuberculosis222",
"id": 18252
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"__typename": "QuestionComment",
"comment": "we cant use CKS in the exam...where can we find this info via medicine's complete?",
"createdAt": 1675167657,
"dislikes": 1,
"id": "17485",
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"displayName": "Gas Haemophilus",
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"__typename": "QuestionComment",
"comment": "BMJ Best practice states \"Antiplatelet therapy with aspirin is recommended.[2] Clopidogrel is an effective alternative to aspirin.\" Would the option with aspirin and the statin not also be correct?",
"createdAt": 1672407284,
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"explanation": "#### Monitoring\r\n\r\nThe BNF advises to monitor lung function (in patients with a history of obstructive airway disease).\r\n\r\n#### Overdoses\r\n\r\nOverdosages with beta-blockers may cause cardiac effects such as bradycardia, hypotension, syncope, conduction abnormalities, and heart failure. Bradycardia is the most common arrhythmia, but some beta-blockers may induce ventricular tachyarrhythmias secondary to prolongation of QT interval (e.g. sotalol) or QRS duration (e.g. propranolol).\r\nNon-cardiovascular effects include central nervous system effects (including drowsiness, confusion, convulsions, hallucinations, and in severe cases coma), respiratory depression, and bronchospasm.\r\n\r\nManagement\r\n - Airway protection \r\n - Activated charcoal within 1 hour\r\n - IV Fluids\r\n \r\nIV glucagon is the first-line management.\r\n \r\nFor symptomatic bradycardia, IV atropine may be used.\r\n",
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"name": "Medical management of peripheral vascular disease",
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"__typename": "Topic",
"id": "13",
"name": "Neurosurgery",
"typeId": 5
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"question": "Case Presentation: A 68-year-old man has been having pain in his legs for six months. The pain typically comes on when he is climbing stairs or has been walking for longer than 30 minutes, and is concentrated in the backs of his calves. **PH** hypertension. **DH** amlodipine 10mg PO OD. **SH** current smoker 10-20 per day, total 45 pack year history. NKDA\n\n\n**O/E**\n\nHR 74 regular, RR 14, BP 134/85. No pain at rest. Lower limbs pale and cool to knee level. Weak dorsalis pedis and posterior tibial pulses bilaterally. Normal power and tone, reflexes and sensation preserved. Capillary refill at toes 3s.\n\n**Investigations**\n\nABPI: 0.7 bilaterally\n\nQuestion: Select the most appropriate management at this stage.",
"sbaAnswer": [
"a"
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"totalVotes": 5461,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,458,252 | false | 13 | null | 6,494,949 | null | false | [] | null | 6,812 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is a combination medication given topically to treat acute otitis externa, or acute otitis media with grommets present",
"id": "34007",
"label": "c",
"name": "Ciprofloxacin with dexamethasone topical ear drops BD",
"picture": null,
"votes": 198
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Clarithromycin is an acceptable option in treating acute otitis media where antibiotics are required",
"id": "34008",
"label": "d",
"name": "Clarithromycin 250mg PO BD",
"picture": null,
"votes": 32
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Amoxicillin may be given to treat acute otitis media that has not resolved after 3-4 days or if there is any evidence of complications",
"id": "34006",
"label": "b",
"name": "Amoxicillin 250mg PO TDS",
"picture": null,
"votes": 1323
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "While most cases of acute otitis media are self-limiting and resolve in a few days, the child is clearly in some pain and distress. At the very least, simple oral analgesia should be prescribed",
"id": "34009",
"label": "e",
"name": "No additional treatment is required",
"picture": null,
"votes": 1366
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Paracetamol is available as a flavoured syrup for young children who will not tolerate tablets or are adverse to the bitter taste",
"id": "34005",
"label": "a",
"name": "Paracetamol oral suspension 240mg PO QDS",
"picture": null,
"votes": 2503
}
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"explanation": "#### Monitoring\r\n\r\nThe BNF advises to monitor lung function (in patients with a history of obstructive airway disease).\r\n\r\n#### Overdoses\r\n\r\nOverdosages with beta-blockers may cause cardiac effects such as bradycardia, hypotension, syncope, conduction abnormalities, and heart failure. Bradycardia is the most common arrhythmia, but some beta-blockers may induce ventricular tachyarrhythmias secondary to prolongation of QT interval (e.g. sotalol) or QRS duration (e.g. propranolol).\r\nNon-cardiovascular effects include central nervous system effects (including drowsiness, confusion, convulsions, hallucinations, and in severe cases coma), respiratory depression, and bronchospasm.\r\n\r\nManagement\r\n - Airway protection \r\n - Activated charcoal within 1 hour\r\n - IV Fluids\r\n \r\nIV glucagon is the first-line management.\r\n \r\nFor symptomatic bradycardia, IV atropine may be used.\r\n",
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"question": "Case Presentation: A 4 year old girl is brought to GP by her parents as she has been unsettled and complaining of right-sided ear pain for the past 24 hours.\n\n\n**O/E**\n\nTemperature 37.0°C. HR 84, RR 15, O2 99% RA. Visibly restless and tugging at right pinna. Oropharynx pale pink with moist mucous membranes. Cervical lymph nodes not palpable. Otoscopy – left ear unremarkable, right ear hyperaemic tympanic membrane with loss of light reflex but no visible effusion.\n\nCardiovascular examination unremarkable. She has no known drug allergies.\n\nQuestion: Select the most appropriate management at this stage.",
"sbaAnswer": [
"a"
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173,458,253 | false | 14 | null | 6,494,949 | null | false | [] | null | 6,800 | {
"__typename": "QuestionSBA",
"choices": [
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "The patient has a CURB-65 score of 3 and has a higher risk of mortality. Meropenem is a broad-spectrum carbapenem antibiotic that would not be initiated without specialist input from microbiology",
"id": "33947",
"label": "c",
"name": "Admit with meropenem 1g IV TDS",
"picture": null,
"votes": 112
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would be a possible option with a CURB-65 of 0. However the patient scores 3 and warrants admission and more intensive treatment",
"id": "33948",
"label": "d",
"name": "Discharge with amoxicillin 500mg PO TDS",
"picture": null,
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"answer": true,
"explanation": "The patient has a CURB-65 score of 3 and has a higher risk of mortality, thus warranting intensive inpatient treatment with IV antibiotics",
"id": "33945",
"label": "a",
"name": "Admit with co-amoxiclav 1.2g IV TDS and clarithromycin 500mg IV BD",
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},
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"__typename": "QuestionChoice",
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"explanation": "This would be a possible option with a CURB-65 of 2. However the patient scores 3 and warrants more intensive treatment",
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"name": "Admit with amoxicillin 500mg PO TDS and clarithromycin 500mg PO BD",
"picture": null,
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"explanation": "Doxycycline is an acceptable alternative in patients who are penicillin-allergic. However a discharge is inappropriate as the patient has a CURB-65 of 3D",
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"name": "Discharge with doxycycline 200mg PO OD and clarithromycin 500mg PO BD",
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"__typename": "QuestionComment",
"comment": "why is the CURB score 3? i understand 1 point for their urea and resp rate but what's the last point?",
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"comment": "I imagine this is the drowsiness that the patient has presented with. Perhaps this has been interpreted as confusion.",
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"comment": "AMTS score 6/10",
"createdAt": 1710155512,
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"comment": "Not too sure how the CURB 65 is 3 so please do expand. I got a score of 2 on RR and Urea. BP was ok, No confusion and is under 65? ",
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"comment": "AMTS score was 6/10",
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"comment": "Confusion is aka AMTS<8 ",
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"explanation": "#### Monitoring\r\n\r\nThe BNF advises to monitor lung function (in patients with a history of obstructive airway disease).\r\n\r\n#### Overdoses\r\n\r\nOverdosages with beta-blockers may cause cardiac effects such as bradycardia, hypotension, syncope, conduction abnormalities, and heart failure. Bradycardia is the most common arrhythmia, but some beta-blockers may induce ventricular tachyarrhythmias secondary to prolongation of QT interval (e.g. sotalol) or QRS duration (e.g. propranolol).\r\nNon-cardiovascular effects include central nervous system effects (including drowsiness, confusion, convulsions, hallucinations, and in severe cases coma), respiratory depression, and bronchospasm.\r\n\r\nManagement\r\n - Airway protection \r\n - Activated charcoal within 1 hour\r\n - IV Fluids\r\n \r\nIV glucagon is the first-line management.\r\n \r\nFor symptomatic bradycardia, IV atropine may be used.\r\n",
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"id": "2733",
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"question": "Case Presentation: A 62 year old man is brought to A&E with fever, productive cough and shortness of breath. **PH** Parkinson’s disease, osteoarthritis. **DH** co-careldopa 25/250mg PO TDS, codeine phosphate 30mg PO PRN (max 6-hourly), senna 7.5mg PO BD. NKDA\n\n\n**O/E**\n\nDrowsy but able to answer in full sentences. Appears sweaty. Peripheries warm, CRT < 2s. Coarse creps L mid to lower zone.\n\nTemperature 38.4°C, HR 112, RR 32, BP 115/78, O2 94% RA, AMTS 6/10\n\n**Investigations**\n\nFBC: Hb 124, WCC 16.3, Plts 203 x 10^9, MCV 82\n\nU&Es: Na 133, K 4.6, Cl 100, Ur 8.1, Cr 117, eGFR 83mL/min/1.73m^2\n\nCRP 155\n\nQuestion: Select the most appropriate management at this stage.",
"sbaAnswer": [
"a"
],
"totalVotes": 6100,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,458,254 | false | 15 | null | 6,494,949 | null | false | [] | null | 6,820 | {
"__typename": "QuestionSBA",
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{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Clindamycin has activity against common Gram-positive bacteria responsible for skin and soft tissue infections, but would not be a first line option to treat uncomplicated lactational mastitis",
"id": "34047",
"label": "c",
"name": "Clindamycin 300mg PO TDS for 7 days",
"picture": null,
"votes": 36
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "flucloxacillin is recommended first line to treat lactational mastitis",
"id": "34045",
"label": "a",
"name": "Flucloxacillin 500mg PO QDS for 14 days",
"picture": null,
"votes": 5809
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "All tetracycline antibiotics are contraindicated in breastfeeding due to the risk of irreversible teeth discolouration in the infant",
"id": "34048",
"label": "d",
"name": "Doxycycline 200mg PO OD for 14 days",
"picture": null,
"votes": 15
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Ciprofloxacin is a fluoroquinolone antibiotic with a mid to broad spectrum of activity. It is not generally used to treat lactational mastitis",
"id": "34046",
"label": "b",
"name": "Ciprofloxacin 400mg PO BD for 7 days",
"picture": null,
"votes": 36
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Erythromycin is an acceptable second line agent to treat lactational mastitis",
"id": "34049",
"label": "e",
"name": "Erythromycin 500mg PO QDS for 14 days",
"picture": null,
"votes": 113
}
],
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"concept": {
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"explanation": "#### Monitoring\r\n\r\nThe BNF advises to monitor lung function (in patients with a history of obstructive airway disease).\r\n\r\n#### Overdoses\r\n\r\nOverdosages with beta-blockers may cause cardiac effects such as bradycardia, hypotension, syncope, conduction abnormalities, and heart failure. Bradycardia is the most common arrhythmia, but some beta-blockers may induce ventricular tachyarrhythmias secondary to prolongation of QT interval (e.g. sotalol) or QRS duration (e.g. propranolol).\r\nNon-cardiovascular effects include central nervous system effects (including drowsiness, confusion, convulsions, hallucinations, and in severe cases coma), respiratory depression, and bronchospasm.\r\n\r\nManagement\r\n - Airway protection \r\n - Activated charcoal within 1 hour\r\n - IV Fluids\r\n \r\nIV glucagon is the first-line management.\r\n \r\nFor symptomatic bradycardia, IV atropine may be used.\r\n",
"files": null,
"highlights": [],
"id": "2618",
"pictures": [],
"typeId": 2
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"chapterId": 2618,
"demo": null,
"entitlement": null,
"id": "2753",
"name": "Lactational mastitis",
"status": null,
"topic": {
"__typename": "Topic",
"id": "76",
"name": "Obstetrics and Gynaecology",
"typeId": 5
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"topicId": 76,
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"question": "Case Presentation: A 24 year old woman has had pain in her left breast for the last three days. She is currently 6 weeks post-partum, and while she has been taking simple oral analgesia and continuing to express milk at the advice of her health visitor, her symptoms remain unresolving. She has no known drug allergies.\n\n\n**O/E**\n\nRight breast grossly normal, no palpable lumps. Left breast area of erythema at 3 o’ clock position from the areola, measuring approximately 2 x 3 cm. Warm and very tender to touch, but no nipple fissuring or fluctuant lumps on palpation.\n\nTemperature 37.1°C. HR 70, RR 12.\n\nQuestion: Select the most appropriate management at this stage.",
"sbaAnswer": [
"a"
],
"totalVotes": 6009,
"typeId": 1,
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173,458,255 | false | 16 | null | 6,494,949 | null | false | [] | null | 6,847 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Metronidazole is associated with decrease in appetite",
"id": "34183",
"label": "d",
"name": "Metronidazole can lead to increased appetite and weight gain",
"picture": null,
"votes": 31
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "It is important to remind the patients not to consume any alcohol during the course of treatment and for 48 hours after the completion of therapy. Metronidazole can interact with alcohol to produce a disulfiram-like reaction that brings about side effects such as hot flushes, palpitation and headache",
"id": "34180",
"label": "a",
"name": "She should not drink alcohol during the course of treatment",
"picture": null,
"votes": 6528
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Metronidazole is an antibiotic that is highly effective against anaerobic bacteria and protozoa",
"id": "34181",
"label": "b",
"name": "Metronidazole is an antifungal medication",
"picture": null,
"votes": 171
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Patients should continue the full course of treatment even if they have felt better to in order to prevent the development of antibiotic resistance in the future",
"id": "34182",
"label": "c",
"name": "She should stop taking the medication once the discharge has gone to reduce the risk of side effects",
"picture": null,
"votes": 199
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Dark urine is a rare side effect of metronidazole",
"id": "34184",
"label": "e",
"name": "Dark urine is a common side effect of metronidazole",
"picture": null,
"votes": 493
}
],
"comments": [
{
"__typename": "QuestionComment",
"comment": "no mention of alcohol in BNF section...",
"createdAt": 1675176140,
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"likes": 14,
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"__typename": "QuestionComment",
"comment": "The interaction does appear under the interaction tab of the BNF ",
"createdAt": 1705068062,
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{
"__typename": "QuestionComment",
"comment": "from personal experience do NOT try to do this omfg",
"createdAt": 1738166981,
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"explanation": "#### Monitoring\r\n\r\nThe BNF advises to monitor lung function (in patients with a history of obstructive airway disease).\r\n\r\n#### Overdoses\r\n\r\nOverdosages with beta-blockers may cause cardiac effects such as bradycardia, hypotension, syncope, conduction abnormalities, and heart failure. Bradycardia is the most common arrhythmia, but some beta-blockers may induce ventricular tachyarrhythmias secondary to prolongation of QT interval (e.g. sotalol) or QRS duration (e.g. propranolol).\r\nNon-cardiovascular effects include central nervous system effects (including drowsiness, confusion, convulsions, hallucinations, and in severe cases coma), respiratory depression, and bronchospasm.\r\n\r\nManagement\r\n - Airway protection \r\n - Activated charcoal within 1 hour\r\n - IV Fluids\r\n \r\nIV glucagon is the first-line management.\r\n \r\nFor symptomatic bradycardia, IV atropine may be used.\r\n",
"files": null,
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"demo": null,
"entitlement": null,
"id": "3426",
"name": "Metronidazole and anaerobic cells",
"status": null,
"topic": {
"__typename": "Topic",
"id": "92",
"name": "General Practice",
"typeId": 5
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"question": "Case presentation: A 25-year-old woman attends her GP appointment with a one-week history of vaginal discharge. She describes the discharge as thin and white and has a fishy odour. A swab is performed and clue cells are seen under the microscope. \r\n\nThe patient is advised to commence treatment with metronidazole 400mg PO twice daily for 7 seven days.\n\nQuestion: Select the most appropriate information that should be provided for this patient.",
"sbaAnswer": [
"a"
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173,458,256 | false | 17 | null | 6,494,949 | null | false | [] | null | 6,842 | {
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{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Tamoxifen increases risk of thromboembolism. Hence, patients should seek medical attention straightaway if they suddenly experience breathlessness, chest pain and other signs that are suggestive of pulmonary embolus",
"id": "34155",
"label": "a",
"name": "She should immediately seek medical help if she experiences sudden onset breathlessness and chest pain",
"picture": null,
"votes": 7132
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Cataract is a common side effect while corneal changes are rarely caused by Tamoxifen",
"id": "34159",
"label": "e",
"name": "Tamoxifen more commonly causes corneal changes than cataract",
"picture": null,
"votes": 58
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Angioedema is a rare side effect of tamoxifen",
"id": "34158",
"label": "d",
"name": "Angioedema is a common side effect of tamoxifen",
"picture": null,
"votes": 40
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Tamoxifen is contraindicated during pregnancy due to its teratogenicity. Patients should use effective contraception during treatment and for 2 months after cessation of treatment",
"id": "34156",
"label": "b",
"name": "She could attempt to get pregnant during the course of treatment",
"picture": null,
"votes": 69
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Tamoxifen is associated with increased endometrial changes that can subsequently lead to hyperplasia, polyps and cancer",
"id": "34157",
"label": "c",
"name": "Tamoxifen reduces the risk of endometrial hyperplasia and polyps",
"picture": null,
"votes": 87
}
],
"comments": [],
"concept": {
"__typename": "Concept",
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"__typename": "Chapter",
"explanation": "#### Monitoring\r\n\r\nThe BNF advises to monitor lung function (in patients with a history of obstructive airway disease).\r\n\r\n#### Overdoses\r\n\r\nOverdosages with beta-blockers may cause cardiac effects such as bradycardia, hypotension, syncope, conduction abnormalities, and heart failure. Bradycardia is the most common arrhythmia, but some beta-blockers may induce ventricular tachyarrhythmias secondary to prolongation of QT interval (e.g. sotalol) or QRS duration (e.g. propranolol).\r\nNon-cardiovascular effects include central nervous system effects (including drowsiness, confusion, convulsions, hallucinations, and in severe cases coma), respiratory depression, and bronchospasm.\r\n\r\nManagement\r\n - Airway protection \r\n - Activated charcoal within 1 hour\r\n - IV Fluids\r\n \r\nIV glucagon is the first-line management.\r\n \r\nFor symptomatic bradycardia, IV atropine may be used.\r\n",
"files": null,
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"id": "2618",
"pictures": [],
"typeId": 2
},
"chapterId": 2618,
"demo": null,
"entitlement": null,
"id": "2774",
"name": "Tamoxifen",
"status": null,
"topic": {
"__typename": "Topic",
"id": "76",
"name": "Obstetrics and Gynaecology",
"typeId": 5
},
"topicId": 76,
"totalCards": null,
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"difficulty": 1,
"dislikes": 0,
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"psaSectionId": 4,
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"question": "Case presentation: A 35-year-old woman attends the breast clinic to discuss about hormonal therapy for her oestrogen-receptor positive breast cancer. \r\n\nPMH: Breast cancer, Hypertension\nDH: Amlodipine 5mg OD\nSH: Lives alone, smoker (10 pack-year history)\nShe is advised to commence treatment with Tamoxifen 20mg PO daily.\n\nQuestion: Select the most appropriate information that should be provided for this patient.",
"sbaAnswer": [
"a"
],
"totalVotes": 7386,
"typeId": 1,
"userPoint": null
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173,458,257 | false | 18 | null | 6,494,949 | null | false | [] | null | 6,827 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "When administering insulin, patients are advised to inject it at a different spot each time to prevent lipohypertrophy",
"id": "34081",
"label": "b",
"name": "She should inject insulin at the same spot each time",
"picture": null,
"votes": 10
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Insulin should be stored in the fridge and not the freezer because very low temperatures might damage the insulin",
"id": "34082",
"label": "c",
"name": "She should store the insulin in the freezer when not using",
"picture": null,
"votes": 75
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Insulin could cause hypoglycaemia, hence patients are encouraged to bring along a source of sugar with them at all times",
"id": "34084",
"label": "e",
"name": "Insulin is not known to cause hypoglycaemia",
"picture": null,
"votes": 9
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "During sickness, patients are advised to check blood glucose levels every 2 to 4 hours and adjust the insulin dose accordingly. It is common for patients to need an increased insulin dose during sickness to help keep the blood glucose level within control. There is a need for insulin dose to be increased because adrenaline and cortisol produced by the body to fight against infection may contribute to insulin resistance, ultimately leading to stress hyperglycaemia. Hence, patients are advised to never omit their insulin (especially basal long-acting insulin) even if there is a reduction in dietary intake",
"id": "34080",
"label": "a",
"name": "She should continue her long-acting insulin during sickness",
"picture": null,
"votes": 5112
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Insulin may lead to weight gain",
"id": "34083",
"label": "d",
"name": "Insulin may cause weight loss",
"picture": null,
"votes": 54
}
],
"comments": [],
"concept": {
"__typename": "Concept",
"chapter": {
"__typename": "Chapter",
"explanation": "#### Monitoring\r\n\r\nThe BNF advises to monitor lung function (in patients with a history of obstructive airway disease).\r\n\r\n#### Overdoses\r\n\r\nOverdosages with beta-blockers may cause cardiac effects such as bradycardia, hypotension, syncope, conduction abnormalities, and heart failure. Bradycardia is the most common arrhythmia, but some beta-blockers may induce ventricular tachyarrhythmias secondary to prolongation of QT interval (e.g. sotalol) or QRS duration (e.g. propranolol).\r\nNon-cardiovascular effects include central nervous system effects (including drowsiness, confusion, convulsions, hallucinations, and in severe cases coma), respiratory depression, and bronchospasm.\r\n\r\nManagement\r\n - Airway protection \r\n - Activated charcoal within 1 hour\r\n - IV Fluids\r\n \r\nIV glucagon is the first-line management.\r\n \r\nFor symptomatic bradycardia, IV atropine may be used.\r\n",
"files": null,
"highlights": [],
"id": "2618",
"pictures": [],
"typeId": 2
},
"chapterId": 2618,
"demo": null,
"entitlement": null,
"id": "2760",
"name": "Insulin sick day rules",
"status": null,
"topic": {
"__typename": "Topic",
"id": "92",
"name": "General Practice",
"typeId": 5
},
"topicId": 92,
"totalCards": null,
"typeId": null,
"userChapter": null,
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"conceptId": 2760,
"conditions": [],
"difficulty": 1,
"dislikes": 0,
"explanation": null,
"highlights": [],
"id": "6827",
"isLikedByMe": null,
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"likes": 0,
"multiAnswer": null,
"pictures": [],
"prescribeAnswer": null,
"presentations": [],
"psaSectionId": 4,
"qaAnswer": null,
"question": "Case presentation: A 30-year-old woman visits her GP complaining of weight loss, excessive thirst and frequent urination. \r\n\nPMH: Coeliac disease, Vitiligo\nFH: Type 1 Diabetes Mellitus\nInvestigation: HbA1c 63 mmol/mol (20-42)\nTreatment with insulin is to be initiated.\n\nQuestion: Select the most important information that should be provided for this patient.",
"sbaAnswer": [
"a"
],
"totalVotes": 5260,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
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