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"explanation": "Transoesophageal echocardiogram is superior to CTCA for detection of vegetations. CTCA is useful for coronary imaging in patients who require surgical intervention, or to detect paravalvular infection, abscess or pseudoaneurysms",
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"explanation": "This is likely to be of low yield as TOE has already been done. TOE has a higher sensitivity than TTE for the diagnosis of endocarditis and should be performed in the absence of contraindications",
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"explanation": "This may be useful to evaluate for stroke, however the patient is likely to have experienced a transient ischaemic attack and the scan would most likely be unremarkable in the absence of any lasting neurological deficits. Cerebral infarcts may be one of the complications of infective endocarditis, but this investigation would not help in confirming the underlying diagnosis",
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"comment": "Lord have mercy",
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"comment": "11% correct ",
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"comment": "This is total BS, if he has a prosthetic valve one can assume that he is on anticogulants and thus a TIA needs to be investigated with a CT to exclude hemorrhage.. ",
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"comment": "Wrong. PET looks at cellular activity. Please spend more time on the wards.",
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"comment": "JAK Gastro unfortunately the qs asks for the best investigation for underlying diagnosis, no for complications eg. stroke / tia ",
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"comment": "Can someone explain why you would do a trans-oesophageal echo in this patient as opposed to the normal transthoracic echo?",
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"comment": "trans-oesophageal is more sensitive for diagnosing endocarditis",
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"explanation": "# Summary\r\n\r\nInfective endocarditis (IE) is a rare infection of the inner surface of the heart (endocardium), usually the valves. Various risk factors contribute to its development, including age, sex, intravenous drug use, poor dentition, valvular disease, congenital heart disease, prosthetic valves, and certain medical conditions like HIV. Symptoms can be diverse and non-specific including fevers, night sweats, weight loss, and myalgia. Diagnosis is based on the modified Duke Criteria, which include major and minor criteria. Treatment involves prolonged courses of intravenous antibiotics, and surgical intervention may be necessary in certain cases. Complications can be severe, and without appropriate treatment, IE can lead to heart failure and death. Prevention through antibiotic prophylaxis is no longer recommended.\r\n\r\n# Definition \r\n\r\nInfective endocarditis (IE) is the infection of the inner surface of the heart (endocardium), usually the valves. \r\n\r\n# Epidemiology \r\n\r\nInfective endocarditis is a rare disease, impacting approximately 2-6 per 100,000 people every year. There are many risk factors implicated in the development of IE. \r\n\r\nRisk factors for IE: \r\n\r\n* Age >60 years\r\n* Male sex\r\n* IVDU: predisposition to _Staph. aureus_ infection and right-sided valve disease e.g. tricuspid endocarditis.\r\n* Poor dentition and dental infections\r\n* Valvular disease: rheumatic heart disease, mitral valve prolapse, aortic valve disease and any other valvular pathology. \r\n* Congenital heart disease: bicuspid aortic valve, pulmonary stenosis, and ventricular septal defects.\r\n* Prosthetic valves\r\n* Previous history of infective endocarditis\r\n* Intravascular devices: central catheters and shunts.\r\n* Haemodialysis\r\n* HIV infection\r\n\nAntibiotics have previously been prescribed to at-risk patients undergoing interventional procedures, frequently in dentistry, with the rationale that resultant bacteraemia could threaten to cause infective endocarditis. However, the evidence for this is inconclusive, and **NICE therefore do not advise antibiotic prophylaxis for IE.**\r\n\r\n# Pathophysiology\r\n\r\nA damaged endocardium can contribute to the development of IE. When part of the endocardium is damaged, the heart valve forms a local blood clot known as non-bacterial thrombotic endocarditis (NBTE). The platelets and fibrin deposits that form as part of the clotting process allows bacteria to stick to the endocardium leading to the formation of vegetations. The valves do not have a dedicated blood supply and so the body is unable to launch an appropriate immune response to the vegetations. The combination of damaged endocardium, vegetation development, and lack of an appropriate immune response results in infective endocarditis. \r\n\r\n# Classification \r\n\r\nIE can be considered according to different classification systems. \r\n\r\n## Acute vs. Subacute vs. Chronic IE \r\n\r\nIE can be considered according to duration of symptoms. \r\n\r\n* *Acute IE*: patient has signs or symptoms for days up to 6 weeks. Theoretically, a fulminant illness with rapid progression and so is most likely due to *S.aureus* infection. \r\n* *Subacute IE*: patients has signs or symptoms for 6 weeks up to 3 months. \r\n* *Chronic IE*: patients has signs or symptoms that persist for longer than 3 months. \r\n\r\n## Valve Type \r\n\r\nIE can be considered according to the type of valve involved. \r\n\r\n- *Native-valve endocarditis*: patient without prosthetic valve implant. \r\n- *Prosthetic-valve endocarditis*: \r\n\t- Early prosthetic valve endocarditis occurs within 1 year of surgery. This is usually due to intra-operative contamination or post-operative nosocomial contamination. \r\n\t- Late prosthetic valve endocarditis occurs beyond 1 year of surgery. This is usually due to community-acquired infections. \r\n\r\n# Common organisms \r\n\r\nThe most common organisms involved in infective endocarditis (in order of incidence) are:\r\n\r\n* _Staph. aureus_: now the most common cause of IE. Coagulase positive.\r\n* _Strep. viridans_: used to be the most common cause of IE. Implicated in patients with poor dental hygiene. \r\n* Enterococci\r\n* Coagulase negative _staphylococci_ e.g. _staph. epidermidis_: common culprit of prosthetic valve endocarditis. \r\n* _Strep. bovis_: important link with colorectal cancer. Need to consider colonoscopy and biopsy in these patients.\r\n* Fungal \r\n* HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella): culture negative causes of IE. \r\n* Non-infective: marantic endocarditis (malignancy - pancreatic cancer), Libman-Sacks endocarditis (SLE). \r\n\r\n# Symptoms\r\n\r\nClinical features of IE are diverse and variable. It may present acutely with a rapid deterioration or it can present subacutely/chronically with non-specific symptoms. \r\n\r\n* Common presenting symptoms: \r\n\t* Fever: most common symptom. \r\n\t* Night sweats \r\n\t* Anorexia \r\n\t* Weight loss \r\n\t* Myalgia\r\n\r\n* Others: \r\n\t* Headache \r\n\t* Arthalgia\r\n\t* Abdominal Pain \r\n\t* Cough \r\n\t* Pleuritic pain \r\n\r\n# Signs\r\n\r\n**Systemic signs**: \r\n\r\n* Febrile \r\n* Cachectic \r\n* Clubbing\r\n* Splenomegaly \r\n\r\n**Cardiac**: \r\n\r\n* Murmur: fever + new murmur is infective endocarditis until proven otherwise. \r\n* Bradycardia: aortic root abscess tracks down to the AVN causing heart block. \r\n\r\n**Vascular phenomena**: \r\n\r\n* Septic emboli: abdominal pain due to splenic infarct/abscess, focal neurology due to stroke, gangrenous fingers. \r\n* Janeway lesions: painless haemorrhagic cutaneous lesions in the palms and soles. \n* Splinter haemorrhages\r\n\r\n**Immunological phenomena**: due to immune-complex deposition. \r\n\r\n* Osler's nodes: painful pulp infarcts on end of fingers. \r\n* Roth spots: boat-shaped retinal haemorrhages with pale centres seen on fundoscopy. \r\n* Glomerulonephritis: identified on urine dip. \r\n\r\n# Differential Diagnoses\r\n\r\n* Non-infectious endocarditis/Nonbacterial thrombotic endocarditis (NBTE)\r\n\t* Similarities: both present with new murmurs and both may have constitutional symptoms including fevers and weight loss. \r\n\t* Differences: blood cultures will likely be positive in infective endocarditis and may identify microorganisms that are commonly associated with IE. NBTE is often associated with advanced malignancy (pancreatic cancer and marantic endocarditis), SLE (Libman Sacks endocarditis) or hypercoagulable states and will not have positive blood cultures. \r\n\r\n* Rheumatic Fever\r\n\t* Similarities: may both present with similar symptoms including fever, heart murmur and joint pain. \r\n\t* Differences: rheumatic fever is an autoimmune response triggered by a Group A strep infection and ASOT titres may be high. In comparison, infective endocarditis will likely have positive blood cultures that identify a particular micro-organism. \r\n\r\n\r\n# Modified Duke Criteria \r\n\r\nFor the diagnosis of IE, the modified Duke Criteria needs to be followed. \r\n\r\nA useful mnemonic to remember the criteria is **'BE FIVE PM'**:\r\n\r\n* Major Criteria: \r\n\t* **B**lood Cultures\r\n\t* **E**vidence of Endocardial Involvement: **E**cho\r\n\r\n* Minor Criteria: \r\n\t* **F**ever\r\n\t* **I**mmunological phenomena\r\n\t* **V**ascular phenomena\r\n\t* **E**chocardiogram minor criteria\r\n\t* **P**redisposing features\r\n\t* **M**icrobiological evidence that does not meet major criteria. \r\n\r\nFor a definitive diagnosis of IE two major criteria, or one major and three minor criteria, or all five minor criteria must be present. \r\n\r\n## Major Criteria \r\n\r\n**Blood culture positive for IE**\r\n\r\n* 2x separate positive blood cultures showing typical microorganisms consistent with IE (S viridans, S bovis, HACEK organisms, enterococcus). \r\n* Persistent bacteraemia with 2x blood cultures >12 hours apart or =>3 positive blood cultures with less specific microorganisms (S.aureus or S. epidermidis). \r\n* Single positive blood culture for Coxiella burnetti or positive antibody titre\r\n\r\n**Evidence of endocardial involvement with imaging positive for IE**\r\n\r\n* Echocardiogram (1st line TTE, then TOE) demonstrating vegetation, abscess, partial dehiscence of prosthetic valve or new valvular regurgitation. \r\n* Abnormal activity around site of prosthetic valve implantation on PET-CT\r\n* Paravalvular lesions on cardiac CT\r\n\r\n## Minor Criteria \r\n\r\n* **Fever**: >38.0 degrees celsius. \r\n* **Immunological phenomena**: Roth spots, Olser's nodes, immune complex-mediated glomerulonephritis, positive rheumatoid factor.\r\n* **Vascular phenomena**: Evidence of septic embolis (splenic infarct/abscess), Janeway lesions, conjunctival haemorrhages, mycotic aneurysm, intracranial haemorrhage. \r\n* **Echocardiogram minor criteria**: not meeting above criteria. \r\n* **Predisposing features**: known valvular disease, IVDU, prosthetic valves etc. \r\n* **Microbiological evidence that does not meet major criteria**: blood culture not meeting major criteria, or serological evidence of active infection with organism consistent with IE\r\n\r\n# Investigations\r\n\r\nBedside:\r\n\r\n- **ECG**: increasing prolongation of PR interval suggests development and worsening of aortic root abscess. \n- **Urine dip**: look for haematuria which may suggest development of glomerulonephritis. \r\n\r\nBlood tests:\r\n\r\n- **Routine bloods**: significant elevation of inflammatory markers and acute phase response is in line with infective endocarditis. If subacute/chronic process there may be a normocytic anaemia. \r\n- **Blood cultures**: required as per the modified Duke criteria. At least 3 sets of blood cultures taken at different times and sites. \r\n\r\nImaging:\r\n\r\n- **Echocardiogram**: \r\n\t* **1st line**: transthoracic echocardiogram \r\n\t* **2nd line**: transoesophageal echocardiogram; more invasive, but better view of mitral valve lesions and aortic root abscesses. It is the most sensitive diagnostic test. \r\n- **PET CT**: used to look for evidence of septic emboli. \r\n\r\n# Management\r\n\r\n## Medical \r\n\r\nMainstay of treatment for infective endocarditis is a prolonged course of IV antibiotics (approximately 6/52). Patients commonly require midline insertion to enable administration of IV antibiotics long-term. \r\n\r\nExamples of antibiotic choice demonstrated below: \r\n\r\n**Blind Therapy** when the organism and sensitivities are not yet known: \r\n\r\n* Native valve: amoxicillin (+/- gentamicin) \r\n* Pen-allergy/MRSA: vancomycin (+/- gentamicin) \r\n* Prosthetic valve: vancomycin + rifampicin + gentamicin \r\n\r\n**Native Valve S. aureus IE**\r\n\r\n* 1st line: flucloxacillin \r\n* 2nd line: vancomycin + rifampicin \r\n\r\n**Prosthetic Valve S. aureus IE**\r\n\r\n* 1st line: flucloxacillin + rifampicin + gentamicin \r\n\r\n\r\n**Strep viridans IE**\r\n\r\n* 1st line: benzylpenicillin \r\n* 2nd line: vancomycin + gentamicin \r\n\r\n**HACEK IE**: 1st line: ceftriaxone \r\n\r\n## Surgical \r\n\r\nDespite the main-stay of treatment for IE being medical management. The following scenarios are indications for surgical intervention: \r\n\r\n* Haemodynamic instability\r\n* Severe heart failure\r\n* Severe sepsis despite antibiotics/failed medical therapy\r\n* Valvular obstruction\r\n* Infected prosthetic valve\r\n* Persistent bacteraemia\r\n* Repeated emboli\r\n* Aortic root abscess\r\n\r\n**Common exam question**: PR interval prolongation in a patient with Infective Endocarditis is an indication for surgery as it can be secondary to aortic root abscess\r\n\r\n# Complications\r\n\r\nComplications of infective endocarditis can also be the initial presenting complaint\r\n\r\n* Acute valvular insufficiency causing heart failure\r\n* Neurologic complications e.g. stroke, abscess, haemorrhage (mycotic aneurysm)\r\n* Embolic complications causing infarction of kidneys, spleen or lung\r\n* Infection e.g. osteomyelitis, septic arthritis\r\n\r\n\r\nWithout timely and appropriate treatment, IE can rapidly lead to heart failure and death. The mortality rate within the first 30 days has been estimated at approximately 20%. Long-term survival for IE has been estimated at 50% at 10 years. The mortality in IE remains high. \r\n\r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines on Prophylactic Antibiotics in IE](https://www.nice.org.uk/guidance/cg64/ifp/chapter/infective-endocarditis)\r\n\r\n# References \r\n\n[American Heart Association Summary on Heart Valves and Endocarditis](<https://www.heart.org/en/health-topics/heart-valve-problems-and-disease/heart-valve-problems-and-causes/heart-valves-and-infective-endocarditis#:~:text=What%20is%20infective%20endocarditis%3F,greater%20risk%20of%20developing%20it.>)",
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"question": "A 75 year old male presents with a 2 week history of fatigue and night sweats. On admission, he had a transient episode of word finding difficulty which resolved within an hour. On auscultation of the chest, an opening click at S1 and an ejection systolic murmur is heard loudest at the apex. There are no residual neurological deficits. He has a past medical history of rheumatic heart disease and a prosthetic mitral valve replacement one year ago.\n\nSerial blood cultures have been negative so far. Transoesophageal echocardiogram (TOE) showed no vegetations and a functional prosthetic mitral valve with no leaks or stenoses. He has been started on IV antibiotics for 2 weeks with persistently raised inflammatory markers. Which is the next best investigation to evaluate the underlying cause?",
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"explanation": "This would be indicated for the management of essential hypertension in patients >55 years old or in Afro-Caribbeans. However, ACE inhibitors are specifically indicated for albuminuria in diabetes",
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"comment": "NICE says you only get ramipril if diabetic AND CKD or ACR >30\nthis does not fall under this",
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"comment": "you start ACEi if ACR >3 ",
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"comment": ">30mg/g OR >3mg/mmol - check your units",
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"comment": "HE DOES NOT HAVE HYPERTENSION!!!!",
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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 60 year old male is admitted to the general medical ward with a 2 day history of atypical chest pain. Serial troponin levels are normal and ECG shows no dynamic changes. He is a current smoker and has a past medical history of childhood asthma.\n\nHis observations are as follows:\n\n- Pulse 70\n- BP 125/80\n- SpO<sub>2</sub> 100%\n- Temperature 36.5°C\n\nBloods are sent off for cardiovascular risk factor screening and are as follows:\n\n- HbA1c 7.2%\n- Fasting glucose 7.8\n- Lipid panel unremarkable\n\nUrine albumin creatinine ratio shows microalbuminuria.\n\nHe is started on metformin by the consultant on the ward round. Which other medication should be started?",
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"explanation": "This is most likely to cause diabetic glomerulosclerosis, which shows Kimmelsteil-Wilson nodules (nodules of hyaline material) on biopsy",
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"explanation": "This woman has nephrotic syndrome, characterised by oedema, proteinuria and hypoalbuminaemia. The thickened glomerular basement membrane with subepithelial deposits is characteristic of membranous nephropathy as a cause of her nephrotic syndrome. Causes of membranous nephropathy include autoimmune disease and infection such as hepatitis B and hepatitis C. A renal biopsy would show a spike and dome pattern on a silver stain",
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"explanation": "This is most likely to cause mesangiocapillary glomerulonephritis, which may lead to nephrotic or nephritic syndrome. This would appear as double contouring of the capillary walls or a \"tram track\" appearance on electron microscopy",
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"comment": "19% seriously?? jesus you guys need to spend more time on the wards",
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"comment": "Ok Tom ",
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"comment": "I got this right but I though HIV could also cause membranous nephropathy?",
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"comment": "more often it causes focal segmental glomerulosclerosis?",
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"explanation": "# Summary\n\nNephrotic syndrome refers to the clinical triad of proteinuria, hypoalbuminemia and peripheral oedema. It occurs due to increased permeability of the glomerular basement membrane, which occurs either due to a variety of both primary (idiopathic) or secondary diseases. Renal biopsy is the key investigation to differentiate between causes and should be considered in all adults. Other investigations include a urine dip and protein:creatinine ratio, LFTs for albumin and investigations for an underlying cause such as myeloma or diabetes. First-line management is usually with steroids; other immunosuppressants may need to be added. Management options for oedema include lifestyle changes (low salt diet, fluid restriction) and/or diuretics.\n\n# Definition\n\nNephrotic syndrome occurs when there is excessive loss of protein in the urine, leading to hypoalbuminemia and peripheral oedema. Other resulting features include hyperlipidaemia, abnormal coagulation and immunodeficiency. \n\n# Aetiology\n\nThe common underlying pathology leading to nephrotic syndrome is damage to the glomerular basement membrane leading to excessive leakage of protein into the urine.\n\nThere are a wide variety of conditions that may lead to nephrotic syndrome which may be classified as either primary (idiopathic) or secondary (due to another underlying disease) - these include:\n\n- **Minimal change disease** causes the majority of cases of nephrotic syndrome in young children\n- It is usually idiopathic but may rarely be associated with lymphoma or NSAID use\n- Glomeruli are normal under light microscopy\n- Electron microscopy shows diffuse effacement of the podocyte food processes\n- Steroid responsiveness is characteristic\n- **Focal segmental glomerulosclerosis** may be primary or secondary to conditions including HIV, extensive nephron loss or drugs (e.g. heroin)\n- Biopsy shows sclerosis of segments of the glomerular tuft, only affecting some glomeruli\n- **Membranous nephropathy** is the leading cause of nephrotic syndrome in older people\n- Biopsy shows thickening of the glomerular basement membrane without cellular proliferation\n- A classic \"spike and dome\" appearance is described where subepithelial immune deposits are interspersed with new basement membrane growth\n- Most cases are primary; usually associated with PLA2R antibodies\n- Others may be secondary to malignancy, infections, autoimmune disease or drugs\n- **Membranoproliferative glomerulonephritis** is also referred to as membranoproliferative glomerulonephritis\n- It can present with nephrotic or nephritic syndrome\n- It may be idiopathic or secondary to infections such as hepatitis C or systemic lupus erythematosus\n- **Diabetic nephropathy** may affect patients with longstanding type 1 or 2 diabetes\n- It tends to be a progression from microalbuminuria, especially if untreated\n- Patients are at risk of end-stage renal disease\n- Biopsy shows thickening of the glomerular basement membrane, mesangial expansion and Kimmelstiel-Wilson nodules\n- **Amyloidosis**, especially AA amyloid due to chronic inflammation\n- AL amyloid (due to light chain deposition) and hereditary amyloidosis can also cause nephropathy\n- On biopsy, amyloid deposits stain with Congo red and display apple green birefringence under polarized light\n- **Multiple myeloma** can present with a variety of renal manifestations, with proteinuria and renal insufficiency the most common\n- Nephrotic syndrome occurs in a minority of cases and may be due to a number of underlying mechanisms\n- **Lupus nephritis** i.e. renal involvement due to systemic lupus erythematosus\n- Class V (membranous lupus nephritis) is the most likely to cause nephrotic syndrome\n- This is characterised histologically by subepithelial immune complex deposition\n- **Medications** are a rarer cause of nephrotic syndrome, including:\n- Bisphosphonates\n- NSAIDs\n- D-penicillamine\n- Probenecid\n- Tolbutamide\n\n# Classification\n\nThe diagnosis of nephrotic syndrome requires the presence of all of:\n\n- Proteinuria > 3.5 grams/24 hours\n- Serum albumin < 30 grams/litre\n- Peripheral oedema\n\n# Signs and Symptoms\n\n**Symptoms include:**\n\n- Frothy urine due to proteinuria\n- Swelling of the face and body\n- Weight gain due to fluid retention\n- Fatigue\n- Lethargy\n- Anorexia\n\n**Signs include:**\n\n- Oedema - typically peripheral and periorbital\n- Muehrcke's lines refers to paired white transverse lines across the nails that may occur secondary to hypoalbuminemia\n- Signs of hyperlipidaemia such as xanthelasma (yellow plaques over the eyelids)\n- Signs of pleural effusion e.g. dull bases to percussion with decreased air entry\n\nPatients may also present with signs and symptoms of complications e.g. infection, thrombosis.\n\n# Differential Diagnosis\n\n- **Heart failure** is a common cause of peripheral oedema; typically however patients cannot lie flat due to breathlessness and so facial oedema is unusual; proteinuria is not a feature\n- **Cirrhosis** is commonly complicated by fluid accumulation, usually in the form of ascites; although ascites may occur in nephrotic syndrome it is less common than fluid accumulation in the peripheries and face; proteinuria is not a feature\n- **Chronic kidney disease** may present with fluid retention, especially in patients with end-stage renal disease - it may coexist with nephrotic syndrome however renal function is often preserved\n- **Medications** may cause peripheral oedema including calcium channel blockers, NSAIDs and corticosteroids\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urine dipstick** looking for proteinuria; glycosuria may be present in diabetes but haematuria is not usually seen\n- **Urine protein:creatinine ratio** should be over 2 or **24 hour urine collection** should show proteinuria >3.5g/day\n\n**Blood tests:**\n\n- **LFTs** to confirm hypoalbuminemia\n- **U&Es** for renal function (significant impairment is unusual)\n- **FBC** may show anaemia in persistent nephrotic syndrome\n- **Vitamin D** may be low as this is lost in urine\n- **Bone profile** may show hypocalcemia secondary to decreased calcium absorption due to vitamin D deficiency\n- **Coagulation screen** is usually normal although there is a hypercoagulable state wiht increased risk of thromboembolism\n- **HbA1c** or **fasting glucose** for diabetes\n- **Lipid profile** often shows dyslipidemia\n- **CRP** and **ESR** may be raised due to an underlying inflammatory, malignant or infectious process\n- **Myeloma screen** i.e. immunoglobulins and serum protein electrophoresis if myeloma is suspected\n- **Autoimmune screen** e.g. for suspected systemic lupus erythematosus (antinuclear antibody, complement levels etc.)\n- **Infection screen** i.e. hepatitis B and C serology, HIV testing\n\n**Imaging tests:**\n\n- **Chest X-ray** if there are clinical signs of pleural effusion\n- **US KUB** (kidneys, ureters and bladder) if there is renal impairment to assess for obstruction and any structural abnormalities of the kidneys\n- Imaging may be required to diagnose complications, such as a **CT pulmonary angiogram** for suspected pulmonary embolism or **doppler ultrasound** of the limbs for suspected deep vein thrombosis\n\n**Special tests:**\n\n- **Renal biopsy** is the key investigation to diagnose the cause of nephrotic syndrome - this is important both for prognosis and to guide management \n- Biopsy is usually indicated in adults, however in children there are specific indications e.g. if not responsive to steroids\n\n# Management\n\n**Conservative:**\n\n- Restrict salt intake to <2g/day\n- Fluid restriction to <1.5L/day \n- Weight should be monitored, with a target of 1-2 kg weight loss per day until the patient reaches their predicted \"dry weight\" (i.e. weight when not oedematous)\n- Dietary changes (e.g. avoiding a high protein diet, limiting fat intake) may be advised and dietician input may be indicated\n- Mechanical thromboprophylaxis (TEDS) to reduce risk of venous thromboembolism\n\n**Medical:**\n\n- **Corticosteroids** are usually first-line for management of nephrotic syndrome - these should be weaned after remission is achieved\n- Other immunosuppressive drugs (e.g. ciclosporin, cyclophosphamide, mycophenolate mofetil or rituximab) may be added as steroid sparing agents or for severe or refractory cases\n- Diuretics are used to treat significant peripheral oedema, usually furosemide but potassium sparing and thiazide diuretics may be added as adjuncts\n- Risk of thromboembolism should be assessed and prophylactic anticoagulation considered\n- Antihypertensives may be required to maintain a normal blood pressure; ACE inhibitors and angiotensin II receptor blockers may also help to reduce proteinuria\n- Ensure patients are up to date with vaccinations (however live vaccines should not be given to patients who are immunocompromised)\n- In some cases hyperlipidaemia may require treatment with statins \n- Patients taking steroids may require co-administration of proton pump inhibitors for gastric protection and consideration of bone protection\n\n**Surgical:**\n\n- If nephrotic syndrome results in end-stage renal failure, renal replacement therapy may be required either with dialysis or renal transplantation\n\n# Complications\n\n- **Increased risk of infection** as immunoglobulins are lost in urine\n- **Venous thromboembolism** due to urinary loss of anti-thrombotic proteins such as antithrombin III\n- **Hyperlipidaemia** due to increased hepatic production of lipoproteins to compensate for hypoalbuminemia - this may also present with lipiduria (which may cause urine to appear milky) \n- **Acute kidney injury** may occur due to excessive diuresis or renal vein thrombosis\n- **Chronic kidney disease** may occur secondary to the underlying cause of nephrotic syndrome (e.g. diabetes, amyloidosis)\n- **Medication side-effects** especially with chronic steroid use (e.g. osteoporosis, psychiatric effects)\n- **Hypothyroidism** due to urinary losses of T4 and T3 with their binding proteins\n- **Vitamin D deficiency** as this is also lost in urine\n- **Anaemia** may result from persistent nephrotic syndrome as iron bound to transferrin and erythropoietin are lost in urine\n\n# Prognosis\n\nPrognosis varies between subtypes, for example minimal change disease rarely progresses to end-stage renal failure (1% of cases), whereas 50% of patients with FSGS will do over 5-10 years.\n\nMortality has been greatly reduced with the use of steroids and immunosuppression.\n\nRelapses are common and may require repeated courses of steroids or escalation to other immunosuppressive medications.\n\n# References\n\n[KDIGO Guidelines on Glomerular Diseases](https://kdigo.org/guidelines/gd/)\n\n[Patient UK - Nephrotic syndrome](https://patient.info/doctor/nephrotic-syndrome-pro)\n\n[Radiopaedia - Nephrotic syndrome](https://radiopaedia.org/articles/nephrotic-syndrome?lang=gb)",
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"question": "A 53 year old lady is admitted with a 2 week history of bilateral lower limb swelling. Albumin is 21g/L (normal range 35-50 g/L) and she has proteinuria of 6.5g/24h. She is referred to the nephrologist who decides to get a renal biopsy. This reveals a diffusely thickened glomerular basement membrane with IgG and C3 subepithelial deposits.\n\nWhich of the following is the most likely underlying cause of her condition?",
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"explanation": "This is a possible differential, as this may cause a bilateral facial palsy. However the progression of muscle weakness in myasthenia gravis is typically descending from the extraocular muscles to the face and limb girdle. Deep tendon reflexes are not affected. The clinical course is also longer in myasthenia gravis and may occur over months to years",
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"explanation": "Guillain-Barré Syndrome (GBS) typically presents with a symmetrical ascending flaccid paralysis of the lower limbs that later spreads to the trunk and may later affect the respiratory muscles. Areflexia may also be present. Bilateral facial nerve palsy can occur in Guillian Barre Syndrome. Miller Fisher syndrome is a valid differential. However, it should be remembered that Miller Fisher syndrome is extremely rare and it is still much more likely to encounter patients with GBS who have atypical features",
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"explanation": "This is a possible differential here and may also present with respiratory dysfunction. However, this tends to follow a more acute onset compared to GBS, and focal neurological symptoms such as weakness are not typically symmetrical. Stroke, as an upper motor neurone pathology, is also unlikely to cause hyporeflexia",
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"explanation": "Miller Fisher syndrome (MFS) presents as a triad of ataxia, areflexia and ophthalmoplegia. In this case, the predominant symptoms are of symmetrical ascending weakness, which has now likely extended to involve the chest muscles. You might also expect evidence of opthalmoplegia which is absent in this case. Bilateral facial nerve palsy can occur in Guillian Barre Syndrome. Miller Fisher syndrome is a valid differential. However, it should be remembered that Miller Fisher syndrome is extremely rare and it is still much more likely to encounter patients with GBS who have atypical features",
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"explanation": "This is an unlikely differential here, as it typically presents with confusion, ataxia and ophthalmoplegia (nystagmus is a common finding). This patient does not present with altered mental status and does not appear to have risk factors for thiamine deficiency, e.g. chronic alcoholism, malnutrition, malabsorption or gastrointestinal disease",
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"comment": "The question implies that the weakness started in the face and progressed to arms and then legs which is the opposite of GBS and was very confusing",
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"comment": "Agreed",
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"comment": "exactly!",
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"comment": "yes, it's atypical GBS, but it does happen and more commonly than miller fisher",
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"comment": "if it was atypical GBS, why didn't they give an explanation that mentions that it is atypical? Literally says here that GBS presents with a symmetrical ascending flaccid paralysis of the lower limbs, with 0 mention of any atypical presentations",
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"explanation": "## Summary\n\nGuillain-Barré Syndrome (GBS) is an acute inflammatory demyelinating polyneuropathy characterised by a rapid, progressive, ascending symmetrical weakness, often preceded by infection. Diagnosis is largely clinical but supported by specific investigations such as lumbar puncture and nerve conduction studies. Treatment is mainly supportive, with options for disease-modifying treatments like intravenous immunoglobulins (IVIG) or plasmapheresis in severe cases.\n\n## Definition\n\nGBS is an ascending inflammatory demyelinating polyneuropathy, typified by an acute onset of bilateral and roughly symmetric limb weakness. \n\n## Epidemiology\n\nThe prevalence of GBS is approximately 1-2 cases per 100,000 worldwide.\n\n## Aetiology\n\nGBS typically occurs 1-3 weeks following an infection, with common culprits being Campylobacter, mycoplasma, and Epstein-Barr Virus (EBV). \n\n40% of cases, however, are idiopathic. \n\nOther potential triggers include infections such as CMV, HIV, Hepatitis A, or following certain vaccinations such as for tetanus, rabies, or swine flu.\n\n## Signs and symptoms\n\nNeurological decline often progresses over days to weeks.\n\nClinical features of GBS include:\n\n- Progressive ascending symmetrical limb weakness (usually starting with the lower limbs)\n- Lower back pain due to radiculopathy\n- Paraesthesia, often preceding motor symptoms\n- Potential respiratory muscle involvement in severe cases\n- Potential cranial nerve involvement leading to diplopia, facial droop\n- **Lower motor neurone** signs in the lower limbs: hypotonia, flaccid paralysis, areflexia\n- Cranial nerve signs: ophthalmoplegia, lower motor neurone facial nerve palsy, bulbar palsy\n- Potential autonomic dysfunction (e.g., arrhythmia, labile blood pressure)\n\n## Variants\n\nSeveral variants of GBS exist, each presenting with unique characteristics:\n\n- Paraparetic variant\n - Primarily affects the lower limbs\n\n- Miller-Fisher syndrome\n - Presents with ataxia, ophthalmoplegia, and areflexia\n - Associated with **anti-GQ1B antibodies**\n\n- Pure motor variant\n - Ascending weakness without sensory involvement\n\n- Bilateral facial palsy with paraesthesias\n - Affects the cranial nerves\n\n- Pharyngeal-brachial-cervical weakness\n - Results in weakness of the upper limbs\n - Associated with **anti- GT1a antibodies**\n- Bickerstaff's Brainstem Encephalitis\n - Presents with encephalitis, ophthalmoplegia, and ataxia\n\nIt's worth noting that these variants rarely present purely as described, and there's often overlap in clinical presentation.\n\n\n## Differential diagnosis\n\n- Vascular: occasionally, brainstem strokes may present similarly\n- Infective/Inflammatory: \n - Polio: asymmetrical weakness from myelitis\n - Lyme disease\n - CMV\n - HIV\n - TB\n - Transverse myelitis \n - Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) \n - Myasthenia gravis\n- Traumatic/Structural:\n - Spinal cord compression\n- Metabolic:\n - Porphyrias: may result in an acute neuropathy\n - Electrolyte derangements: hypokalaemia, hypophosphataemia, hypermagnesaemia\n\t\n\n## Investigations\n\nInvestigations for GBS include:\n\n- Monitoring of forced vital capacity (FVC) for respiratory muscle involvement\n- Cardiac monitoring for autonomic instability\n- Blood tests, including arterial blood gas (ABG)\n- Serological tests: Anti-ganglioside antibodies\n- Lumbar puncture: may show **albuminocytological dissociation** \n\t- Increased level of protein (albumin) without a corresponding increase in white blood cells (cytology)\n- Nerve conduction studies\n\t- May show prolongation or loss of the F wave\n- Identification of the underlying cause: stool cultures, serology, CSF virology\n\n## Management\n\nManagement of GBS is primarily supportive and includes:\n\n- Regular monitoring of FVC\n\t- Early involvement of intensive care is essential if any reduction in FVC as deterioration may be rapid\n- Venous thromboembolism (VTE) prophylaxis: TEDS + LMWH\n- Analgesia: NSAIDs or opiates for radiculopathy-related back pain\n- Management of cardiac arrhythmias as per ALS guidelines\n- Careful use of antihypertensives due to potential autonomic dysfunction\n- Consideration of enteral feeding in those with unsafe swallow\n\nSpecific medical management for those with significant disability (e.g., inability to walk) include:\n\n- Intravenous immunoglobulin (IVIG) over a 5-day course\n- Plasmapheresis, which has similar efficacy to IVIG but is associated with more side effects.\n\n## Prognosis\n\nWhile GBS can be life-threatening, particularly when respiratory muscles are affected or in the presence of autonomic dysfunction, the majority of patients experience full recovery. \n\nHowever, residual fatigue and weakness can persist in some patients. Certain variants of GBS, like Miller-Fisher syndrome, generally have a good prognosis with full recovery being the norm. \n\nPrognostic indicators include speed of onset, severity at nadir, age and the presence of preceding diarrhoeal illness.\n\n## References\n\n1. Van den Berg, B., Walgaard, C., Drenthen, J., Fokke, C., Jacobs, B. C., & Van Doorn, P. A. (2014). Guillain–Barré syndrome: pathogenesis, diagnosis, treatment and prognosis. Nature Reviews Neurology, 10(8), 469-482.\n\n2. Yuki, N., & Hartung, H. P. (2012). Guillain–Barré syndrome. New England Journal of Medicine, 366(24), 2294-2304.\n\n3. Hughes, R. A., & Cornblath, D. R. (2005). Guillain-Barré syndrome. The Lancet, 366(9497), 1653-1666.\n\n4. Willison, H. J., Jacobs, B. C., & Van Doorn, P. A. (2016). Guillain-Barré syndrome. The Lancet, 388(10045), 717-727.\n",
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"question": "A 20-year-old male presents to Accident & Emergency with a one-week history of bilateral facial weakness and progressively weak arms and legs. Prior to this, he had an acute diarrhoeal illness which has since settled. He has no other past medical history.\n\nHis Glasgow coma scale (GCS) score is 15. On examination, he has a bilateral facial palsy, bilateral symmetrical lower and upper limb weakness and reduced tendon reflexes.\n\nHe has a sudden onset desaturation whilst on the general medical ward and is transferred to the intensive care unit for intubation and ventilation.\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "NICE recommend commencing anticoagulant in secondary care for people with ischaemic stroke or TIA and paroxysmal, persistent, or permanent atrial fibrillation or atrial flutter. The choice of anticoagulant is a DOAC in non-valvular AF. ",
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"explanation": "The patient has suffered a transient ischaemic attack (TIA) on a background of non-valvular atrial fibrillation (AF). In this case, as AF is likely the underlying cause of the TIA, anticoagulation (rivaroxaban) is superior to aspirin in stroke prevention. Therefore, aspirin would not be the best choice in this scenario.",
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"explanation": "The main priority is to initiate antiplatelet treatment with aspirin. The blood pressure is not dangerously high at this point and she does not have any serious concomitant medical issues requiring strict BP control (e.g. hypertensive encephalopathy, nephropathy or cardiac failure). In patients with a TIA who have recovered to their neurologic baseline and have no other evidence of infarction, anti-hypertensive treatment may be reinitiated",
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"explanation": "This is only recommended in acute ischaemic stroke within 4.5 hours of onset, where intracranial haemorrhage has been excluded on brain imaging. In this case, the patient has a transient ischaemic attack which would not warrant this",
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"explanation": "While this patient does have a history of gastroesophageal reflux, the priority is to start her on an antiplatelet therapy (i.e. aspirin). She may require a H2 receptor antagonist such as ranitidine as an adjunct",
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"comment": "How can the neuro exam be fine if he's had a stroke then?",
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"comment": "TIA",
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"comment": "ONLY after a CT scan has been done!!! this is wrong. he cannot be given aspirin until haemorrhagic ruled out",
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"comment": "you don't CT for TIA",
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"comment": "Yeah as above TIA can only be caused by a thrombus, a bleed cannot appear then disappear in the same way",
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"comment": "So if someone comes in with a suspected TIA you will immediately give Aspirin 300mg + refer to TIA clinic where they will get either an urgent carotid doppler or a weighted MRI (preferred) to determine the territory of ischaemia",
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"comment": "If a patient with a transient ischemic attack (TIA) has atrial fibrillation (AF), immediate CT head imaging is recommended to rule out hemorrhage before starting anticoagulation therapy. This is because AF increases the risk of stroke, and anticoagulation is often necessary to prevent further events. However, it's crucial to ensure there is no bleeding before initiating anticoagulation",
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"comment": "During the exam, if I too can't find a word for 15 mins I'll go to A&E",
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"comment": "i put rivarox but the aspirin answer doesnt really explain why aspirin is wrong",
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"comment": "I believe it is due to the presense of AF in this patient, if the patient were not in AF i think 300mg aspirin would be the correct answer, hope this helps\n",
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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 65-year-old woman presents to the emergency department with temporary word finding difficulty that lasted for 15 minutes, occurring approximately 2 hours ago. Past medical history includes hypertension and gastroesophageal reflux disease.\n\nObservations on triage were:\n\n- Temperature 36.5°C\n- Pulse 90\n- Blood pressure (BP) 170/85\n- SpO2 98% on room air\n\nAn electrocardiogram shows non-valvular atrial fibrillation. On examination, she has no neurological deficits.\n\nWhich of the following is the next best step in initial management?",
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"explanation": "While B12 deficiency can lead to neurological signs, it would not lead to abnormal findings on MRI, nor would symptoms resolve as spontaneously and rapidly",
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"explanation": "Whilst fundoscopy should be considered in any patient with a new visual deficit, it would be unlikely to lead to a definitive diagnosis in the context of a history suggesting MS, with an abnormal MRI. Fundoscopy is likely to be normal in MS",
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"explanation": "This patient has a history suggestive of multiple sclerosis, clinically isolated neurological deficits separated in time. The MRI confirmed several hyperintensities in the periventricular white matter. The next investigation is CSF examination, looking for the typical finding of oligoclonal bands, the presence of which gives a definitive diagnosis of MS",
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"explanation": "This patient has already undergone an MRI which has demonstrated white matter lesions separated in space. A CT head is not likely to provide further information, nor a definitive diagnosis",
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"explanation": "# Summary\n\nMultiple Sclerosis (MS) is a chronic, inflammatory, autoimmune disease of the central nervous system, characterised by the demyelination and axonal loss of neurons. Key symptoms include sensory disturbance, optic neuritis, internuclear ophthalmoplegia, cerebellar ataxia, and spastic paraparesis. Diagnosis largely involves the use of clinical history, MRI findings, and CSF analysis, aligning with the McDonald criteria. Management of MS involves both acute and chronic strategies, with glucocorticoids commonly used for acute attacks, and a combination of disease-modifying therapies (DMTs) and symptomatic treatments used in the long-term.\n\n# Definition\n\nMultiple sclerosis is a chronic autoimmune disease, primarily involving the central nervous system, which is marked by the degeneration of the insulating covers of nerve cells in the brain and spinal cord, leading to demyelination and eventual axonal loss.\n\n# Epidemiology\n\nMS predominantly affects females with a current ratio of 2.3:1 and a mean onset age of 30 years.\n\n# Aetiology\n\nThe exact cause of multiple sclerosis remains unknown. However, a combination of genetic and environmental factors, including potential viral pathogens, are believed to be contributing factors. \n\nPathologically, CD4-mediated destruction of oligodendroglial cells and a humoral response to myelin binding protein are key features of the disease.\n\n# Signs and Symptoms\n\nMultiple sclerosis can cause a wide range of symptoms depending on the affected area of the brain or spinal cord, but common presentations include:\n\n- Sensory disturbance, marked by patchy paraesthesia\n- Optic neuritis, characterised by loss of central vision, loss of red desaturation and painful eye movements\n- Internuclear ophthalmoplegia, a lesion in the medial longitudinal fasciculus of the brainstem\n- Subacute cerebellar ataxia\n- Spastic paraparesis, as seen in transverse myelitis, including Lhermitte's sign.\n- Bladder and bowel disturbance\n\n\n# Classification\n\nMultiple sclerosis may be divided into two groups:\n\n- Relapsing-remitting (which may become secondarily progressive)\n- Primary progressive.\n\nRelapsing remitting MS makes up 80% of disease at presentation, compared with primary progressive which is <10%.\n\nThe remaining 10% fall into a difficult to classify intermediate group of progressive-relapsing disease.\n\n# Differential Diagnosis\n\nDiseases that should be considered in differential diagnosis include:\n\n- **Neuromyelitis optica (Devic's disease)**: Characterised by optic neuritis and transverse myelitis.\n- **Systemic lupus erythematosus (SLE)**: Presents with multisystem involvement, including the CNS. Symptoms may include fatigue, joint pain, rash, and fever.\n- **Lyme Disease**: Early signs and symptoms include fever, chills, headache, fatigue, muscle and joint aches, and swollen lymph nodes. Later signs and symptoms may involve the nervous system.\n- **Neurosarcoidosis**: Symptoms include seizures, hearing loss, facial palsy, and psychiatric symptoms.\n- **Vitamin B12 Deficiency**: Presents with weakness, tiredness, or lightheadedness, heart palpitations and shortness of breath, pale skin, constipation, loss of appetite, nerve problems like numbness or tingling, and mental problems like depression, memory loss, or behavioral changes.\n\n\n# Investigations\n\nThe diagnosis of multiple sclerosis is based on at least two of:\n\n- Clinical history/examination\n- Imaging findings\n - Typically these are periventricular white matter lesions seen on MRI **disseminated in time and space**\n\n[lightgallery]\n\n- Oligoclonal bands in the CSF\n - These reflect various immunoglobulins seen on CSF electrophoresis and indicate the presence of an auto-immune process in the CNS.\n - They are very sensitive for multiple sclerosis although they can also be found in other auto-immune and infectious conditions including Lyme disease, SLE and neurosarcoid.\n - Visual evoked potential can help further characterise the diagnosis in patients presenting with optic neuropathy\n\n## McDonald criteria for Diagnosis\n\nThe McDonald criteria (last revised in 2017) is the generally accepted standard for diagnosis:\n\n| Clinical Presentation | Additional Data Needed |\n| ------------------------------------------------------------ | ------------------------------------------------------------ |\n| 2 or more attacks (relapses) <br />2 or more objective clinical lesions | None; clinical evidence will suffice (additional evidence desirable but must be consistent with MS) |\n| 2 or more attacks<br />1 objective clinical lesion | Dissemination in space, demonstrated by:<br /> MRI _or_ <br />A positive (cerebrospinal fluid) CSF and 2 or more MRI lesions consistent with MS _or_ <br />Further clinical attack involving different site |\n| 1 attack <br />2 or more objective clinical lesions | Dissemination in time, demonstrated by: <br />MRI _or_ <br />Second clinical attack |\n| 1 attack<br />1 objective clinical lesion (monosymptomatic presentation) | Dissemination in space demonstrated by: MRI or positive CSF and 2 or more MRI lesions consistent with MS **and** <br />Dissemination in time demonstrated by: MRI or second clinical attack |\n| Insidious neurological progression suggestive of MS (primary progressive MS) | One year of disease progression (retrospectively or prospectively determined) and TWO of the following: <br />a. Positive brain MRI (nine T2 lesions or four or more T2 lesions with positive visual evoked potentials [VEP) <br />b. Positive spinal cord MRI (two focal T2 lesions) <br />c. Positive CSF |\n\n# Acute management\n\n- An acute attack of multiple sclerosis should be treated with glucocorticoids involving local neurology services\n- 1g of intravenous methylprednisolone every 24 hours for 3 days is a typical regimen\n- Infections must first be excluded\n\t- \tAlways ensure to check routine bloods and urine dip to rule out any intercurrent infection.\n\t- While these interventions does not appear to affect long term outcome, it does appear to reduce the duration and severity of individual attacks.\n\n\n# Chronic management\n\nManagement of patients with multiple sclerosis should be led by a multidisciplinary team approach of neurologists, physiotherapists, occupational therapists, psychologists and many other allied healthcare professionals.\n\nThere are two groups of drugs used in the long term management of _relapsing remitting multiple sclerosis_: disease modifying therapies (DMTs) and symptomatic therapies.\n\nThe former group may be divided into three:\n\n- First-line injectables such as beta-interferon and glatiramer\n- New oral agents such as dimethyl fumarate, teriflunomide and fingolimod\n- Biologics such as natalizumab and alemtuzumab.\n\nAs a general rule, increasingly effective treatments are associated with increasingly significant side effects.\n\nThe extent to which long-term use of DMTs reduces risk of secondary progressive MS is not yet clearly established.\n\nSymptomatic therapies include:\n\n- Physiotherapy\n- Baclofen and Botox for spasticity\n- Modafinil and exercise therapy for fatigue\n- Anticholinergics for bladder dysfunction\n- SSRIs for depression\n- Sildenafil for erectile dysfunction\n- Clonazepam for tremor\n\n# Prognosis\n\nThe prognosis of multiple sclerosis (MS) can vary widely among individuals, and several risk factors have been identified that are associated with a worse prognosis. These risk factors may include:\n\n1. **Age at onset**: Onset of MS at an older age, typically over 40, is associated with a worse prognosis.\n2. **Male gender**: Men with MS often experience a more severe and rapidly progressing form of the disease compared to women.\n3. **Primary Progressive MS**: This form of MS is characterised by a steady and continuous worsening of symptoms without distinct relapses and remissions. It tends to have a worse prognosis compared to relapsing forms of the disease.\n4. **High relapse rate**: Frequent relapses and a higher relapse rate can indicate a more aggressive form of the disease, which may lead to greater disability over time.\n5. **Rapid accumulation of disability**: A quick accumulation of physical disability in the early stages of the disease is associated with a less favorable prognosis.\n7. **High lesion load**: A higher burden of lesions (plaques) in the brain and spinal cord on MRI scans is associated with a worse prognosis.\n8. **Cognitive impairment**: Cognitive dysfunction, such as memory problems and difficulties with thinking and processing information, can indicate a worse prognosis.\n10. **Comorbid conditions**: The presence of other medical conditions, such as depression or cardiovascular disease, can complicate the management of MS and lead to a worse prognosis.\n11. **Smoking**: Smoking has been associated with an increased risk of developing MS and may also contribute to a worse prognosis.\n\n\nIt's important to note that while these risk factors are associated with a worse prognosis, the course of MS is highly variable, and individual experiences can differ significantly. Early diagnosis, appropriate treatment, lifestyle modifications, and a strong support system can help improve the prognosis and quality of life for people living with MS. \n\n# NICE Guidelines\n\n[NICE Guidelines for Multiple Sclerosis](https://www.nice.org.uk/guidance/ng220)\n\n[NICE CKS for Multiple Sclerosis](https://cks.nice.org.uk/topics/multiple-sclerosis/)",
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"question": "A 29 year old female presents to the GP with a 5-day history of clouding of vision and difficulty differentiating colours. She has a past history of a 2-week period of left upper limb weakness that spontaneously resolved without intervention.\n\nAn MRI reveals several hyperintensities in the periventricular white matter at various regions.\n\nWhat investigation is most likely to give a definitive diagnosis?",
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"explanation": "This would suggest an S1 radiculopathy, which would involve loss of plantarflexion, weakness of leg extension and knee flexion and loss of the ankle jerk reflex. Sensation would be reduced on the posterior aspect of the leg and the lateral edge of the foot",
"id": "32097",
"label": "e",
"name": "Loss of sensation on the lateral edge of the foot",
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"explanation": "This would be present in a common peroneal nerve or L5 level lesion. The patient has suffered a common peroneal nerve lesion, the most common aetiologies of which are compression and trauma. Patients present with a loss of eversion and dorsiflexion (supplied by the common peroneal nerve), with intact inversion and plantarflexion (supplied by the tibial nerve). The common peroneal nerve also provides sensation to the anterolateral surface of the leg and dorsal aspect of the foot. Both the common peroneal and tibial nerve branches arise from the sciatic nerve",
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"name": "Loss of sensation on the dorsum of the foot",
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"explanation": "This would suggest an L5 radiculopathy or anterior horn cell dysfunction, which would also present with loss of dorsiflexion and eversion, but would also affect foot inversion, internal rotation and abduction of the hip. Patients typically present with back pain radiating down the lateral aspect of the leg",
"id": "32096",
"label": "d",
"name": "Inability to internally rotate the hip",
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"explanation": "This would suggest a saphenous nerve lesion or L4 level lesion. The saphenous nerve is the largest branch of the femoral nerve, and entrapment may result in deep thigh ache, knee pain and paraesthesia of the anteromedial aspect of the leg",
"id": "32095",
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"name": "Loss of sensation on the medial aspect of the leg",
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"explanation": "This would suggest a sciatic nerve lesion or S1 level lesion. Peripheral neuropathy and cauda equina syndrome may also result in a loss of the ankle jerk reflex; however, this is more likely to present with bilateral foot drop. In common peroneal nerve lesions, the ankle deep tendon reflex is intact",
"id": "32094",
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"explanation": "# Summary\n\nFoot drop is a condition characterized by weakness or paralysis of the foot dorsiflexion and eversion. It can associated with systemic conditions, trauma, or focal neurological lesions. \n\n# Definition\n\nFoot drop, also known as drop foot, is a gait abnormality characterized by the inability or difficulty in lifting the front part of the foot, resulting in dragging of the foot or a high-stepping gait. This condition is typically a symptom of an underlying neurological, muscular, or anatomical pathology.\n\n# Aetiology\n\nFoot drop may be caused by several factors:\n\n- Common peroneal nerve lesions: The most common cause of foot drop is disease or trauma affecting the common peroneal nerve, particularly where it loops over the fibula's head on the knee joint's lateral aspect.\n- L5 root lesion (radiculopathy): Foot drop can be a symptom of this condition, characterized by loss of **inversion** and sensory loss over the L5 dermatome. Lumbosacral disc herniation is the most common cause of this type of foot drop.\n- Distal motor neuropathy: This condition is often associated with foot drop, accompanied by glove and stocking sensory disturbance and loss of all movements of the foot.\n- Small cortical lesions: Foot drop can be associated with small cortical lesions, often presenting with other upper motor neuron features.\n- Other causes: Intrinsic cord disease, partial sciatic nerve disease, and myopathy may also mimic foot drop, although these are less common.\n\n# Signs and Symptoms\n\nKey motor findings in foot drop include:\n\n- Weakness or paralysis of dorsiflexion and eversion of the foot\n- Difficulty in lifting the front part of the foot\n- A high-stepping gait or foot dragging\n\nIn specific aetiologies, additional symptoms may be present:\n\n- In L5 root lesions, loss of **inversion** (a tibial nerve function not lost in common peroneal nerve lesions), sensory loss over the L5 dermatome, and sciatica-type shooting leg pain.\n- In distal motor neuropathy, glove and stocking sensory disturbance, and loss of all foot movements.\n\n\n# Investigations\n\nInvestigations for foot drop typically involve:\n\n- Neurological examination: To assess the strength, sensation, and reflexes in the lower limbs.\n- Electromyography (EMG) and Nerve Conduction Studies (NCS): To evaluate the electrical activity in the muscles and nerves.\n- Imaging studies: MRI or CT scans of the spine or brain may be ordered to identify potential causes such as disc herniations, spinal cord injuries, or small cortical lesions.\n- Blood tests: To identify potential underlying conditions such as diabetes or other systemic diseases.\n\n# Management\n\nIn most cases of common peroneal nerve palsy, the condition resolves spontaneously with lifestyle modifications avoiding the underlying cause of pressure or damage to the nerve.\n\nOther menaagement options include:\n\n- Physiotherapy: To strengthen the foot and leg muscles and improve gait.\n- Orthotic devices: Such as braces or ankle-foot orthoses (AFOs) to support the foot and ankle.\n- Medication: For underlying conditions that may cause foot drop such as diabetes\n- Surgery: In some cases, decompression surgery or nerve grafts may be necessary.",
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"question": "A 25-year-old football player presents to Accident & Emergency with a sudden onset right-sided foot drop. X-rays of the right lower limb do not show any fractures. On examination, he cannot dorsiflex or evert his foot, but can plantarflex and invert his foot.\n\nIn view of the underlying diagnosis, which of the following examination findings will most likely be present in his right leg?",
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"explanation": "Evidence suggests that low molecular weight heparin results in better outcomes than unfractionated heparin (UFH) for initial anticoagulation in cerebral venous sinus thrombosis. UFH may be considered in patients with renal impairment or those requiring very rapid reversal of anticoagulation, e.g. imminent surgical intervention",
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"explanation": "Direct oral anticoagulants can be considered for longer-term prophylaxis of venous thromboembolism",
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"explanation": "In cerebral venous sinus thrombosis, recurrent seizures are more likely to develop in those who present with seizures and in those with supratentorial brain lesions on imaging. This would not be appropriate in the initial management, but may be considered later on for seizure prophylaxis",
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"explanation": "This patient has presented with cerebral venous sinus thrombosis, for which the initial management would be subcutaneous low molecular weight heparin",
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"explanation": "This may be considered after the acute stage for longer-term prophylaxis of further cerebral and extracerebral venous thrombosis (i.e. deep vein thrombosis, pulmonary embolism). It would not be appropriate to start warfarin acutely as it has prothrombotic activity on initiation",
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"explanation": "# Summary\n\nCentral Venous Sinus Thrombosis (CVST) is a rare but serious condition involving the occlusion of cerebral venous sinuses. It primarily affects younger individuals, with women at higher risk, particularly those of childbearing age. Risk factors include hormonal influences, prothrombotic conditions, systemic diseases, and local factors like trauma or infection. Symptoms are variable but often include headaches, neurological deficits, and seizures. Diagnosis is typically confirmed with imaging, such as CT venogram. Management involves anticoagulation therapy, usually starting with low molecular weight heparin and possibly transitioning to Warfarin, along with addressing underlying causes.\n\n# Definition\n\nCentral Venous Sinus Thrombosis (CVST) refers to occlusion of venous vessels in sinuses of the cerebral veins\n\n# Epidemiology\n\nCVST has an incidence of approximately 3-4 cases per million people per year. Representing 0.5%-3% of all the types of stroke, affecting predominantly younger people. Women are affected more than men and mostly between the ages of 20 and 35. This is hypothesised to be due to pregnancy and the use of the COCP.\n\n# Risk factors\n\nRisk factors are similar to those for venous thromboembolism and include: \n\n- Hormonal factors (the pill, pregnancy, and the peri-partum period)\n- Prothrombotic haematological conditions or malignancy\n- Systemic disease (such as dehydration or sepsis)\n- Local factors (skull abnormalities, trauma, or local infection\n-\n\n# Presentation\n\n- Presentation is variable but common symptoms include headache, confusion/drowsiness, impaired vision, and nausea/vomiting.\n\n- Other signs include seizures, reduced consciousness, focal neurological deficits, cranial nerve palsies, and papilloedema.\n\n# Investigations\n\n- Non-contrast CT reveals a hyperdensity in the affected sinus.\n\n- CT venogram is used to look for a filling defect ('the empty delta sign').\n\nThe most common form of dural venous thrombosis affects the superior sagittal sinus.\n\nCavernous sinus thrombosis is less common. It is typically caused by spreading sinus infection and presents with chemosis, exophthalmos, and peri-orbital swelling.\n\n# Management\n\nThe mainstay of treatment is with low molecular weight heparin (LMWH) and addressing any underlying risk factors that may increase risk of clotting e.g. cancer, autoimmune disease.\n\nFollowing initial therapy with LMWH, this can be further bridged to a vitamin K antagonist such as Warfarin. \n\n# References\n\n[Click here for more info on intracranial venous thrombosis](https://patient.info/doctor/intracranial-venous-thrombosis)",
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"question": "A 45-year-old woman develops a persistent headache of 4 days duration, not resolving with over the counter painkillers. She presented to Accident & Emergency with bilateral eye pain and blurred vision. At triage, she suffers a generalised tonic-clonic seizure which is terminated with one dose of IV lorazepam. Computed tomography (CT) brain was done immediately, which showed a large clot in the cavernous sinus.\n\nWhich is the next best step in acute management?",
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"explanation": "The most likely drug to be used here is acetazolamide, a carbonic anhydrase inhibitor. The patient has idiopathic intracranial hypertension, with the typical features of raised intracranial pressure (headache, tinnitus, papilloedema, visual loss). The treatment involves carbonic anhydrase inhibitors to decrease the rate of cerebrospinal fluid production",
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"explanation": "This is the mechanism of action of prednisolone. Steroids are not recommended for use in idiopathic intracranial hypertension as their withdrawal can cause severe rebound intracranial hypertension with visual loss, and may worsen weight gain, which is a risk factor for the condition. It may, however, be useful as a temporary measure prior to surgery in the setting of acute visual loss",
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"explanation": "This is the mechanism of action of ibuprofen, a nonsteroidal inflammatory drug that may be used for pain relief of migraines but would not be the treatment in this case",
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"name": "Reversible inhibitor of cyclooxygenase-1 and 2 (COX-1 and 2) enzymes",
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"explanation": "This is the mechanism of action of sumatriptan, which may be used in the treatment of acute migraine. However, this would not be effective here as the headache is secondary to idiopathic intracranial hypertension",
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"explanation": "This is the mechanism of action of furosemide, which may be considered as an adjunct to acetazolamide",
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"explanation": "## Summary\n \n\nIdiopathic Intracranial Hypertension (IIH), also known formerly as benign intracranial hypertension or pseudotumor cerebri, is a condition characterised by increased intracranial pressure in the absence of a detectable cause. It predominantly affects young, overweight women and can lead to serious consequences such as permanent visual loss if left untreated. The mainstay of management includes weight loss, acetazolamide and symptomatic management of headaches. Severe cases may require surgical intervention, particularly if there is evidence of progressive visual loss.\n \n\n## Definition\n \nIIH is a disorder of unidentified cause which leads to increased intracranial pressure, typically with an opening pressure above 25 cmH2O on lumbar puncture. \n \nIt has been previously referred to as benign intracranial hypertension, though it is not benign, and pseudotumor cerebri, which can cause confusion as it is not related to an identifiable structural lesion.\n \n## Epidemiology\n \n\nThis condition most frequently occurs in young and obese women, with a sex ratio of approximately 9:1 favoring women. \n \n## Aetiology\n \n\nThe aetiology of IIH remains uncertain. There are some reported associations with several drugs, including:\n \n\n - Oral contraceptive pill\n - Steroids\n - Tetracycline\n - Vitamin A\n - Lithium\n \n\n\n## Signs and Symptoms\n \n\nClassic symptoms of IIH include:\n \n\n - Non-pulsatile, bilateral headaches, typically worse in the morning or after bending forwards. Some patients may also experience morning vomiting.\n - Visual disturbances, such as transient visual darkening or loss, likely due to optic nerve ischaemia. \n - Bilateral papilloedema seen on fundoscopy, indicating increased intracranial pressure.\n - 6th nerve palsy: horizontal diplopia\n \n\nIf untreated, permanent visual damage may result, with 1-3% of patients experiencing vision loss within a year of onset. \n \n\n## Differential Diagnosis\n \n\nDifferential diagnoses for IIH mainly include other causes of increased intracranial pressure or morning headaches, such as:\n \n\n - Brain tumour: Symptoms include new onset or change in pattern of headaches, headaches that gradually become more frequent and more severe, unexplained nausea or vomiting, vision problems, such as blurred vision, double vision or loss of peripheral vision, gradual loss of sensation or movement in an arm or a leg, difficulty with balance, speech difficulties, confusion in everyday matters, personality or behaviour changes, and seizures, especially in someone who doesn't have a history of seizures.\n - Venous sinus thrombosis: Presents with a headache, seizures, abnormal vision, and various neurological symptoms such as weakness, loss of sensation, and decreased level of consciousness. \n - Sleep apnoea: Characterized by excessive daytime sleepiness, loud snoring, observed episodes of stopped breathing during sleep, abrupt awakenings accompanied by gasping or choking, awakening with a dry mouth or sore throat, morning headache, difficulty concentrating during the day, experiencing mood changes, such as depression or irritability, high blood pressure, and nighttime sweating.\n - Migraines: Characterised by nausea, vomitting, phonophobia and photophobia. Usually without visual loss or postural headache.\n \n\n## Investigations\n \n\nSeveral investigations are used to diagnose IIH and rule out other causes of raised intracranial pressure:\n \n\n - Ophthalmoscopy, which typically shows bilateral papilloedema. A referral to ophthalmology for a detailed visual field assessment may be warranted.\n - Imaging studies such as CT and MRI of the head may show signs of increased intracranial pressure. An MRI Venogram may be performed to rule out secondary causes, particularly venous sinus thrombosis.\n - Lumbar puncture is a key diagnostic tool, typically revealing an opening pressure above 20 cmH2O. An abnormal CSF profile may suggest a different diagnosis.\n \n\n## Management\n \n\nManaging IIH effectively includes:\n \n\n - Encouraging weight loss as the first-line and best-supported intervention for managing IIH.\n - Carbonic anhydrase inhibitors such as acetazolamide can be used, but are often poorly tolerated due to side effects like peripheral paraesthesia.\n - Topiramate and candesartan are also commonly used alternatives.\n - More invasive procedures such as therapeutic lumbar punctures, surgical CSF shunting or optic nerve sheath fenestration may be necessary for resistant cases to prevent progressive visual loss.\n \n\n## Prognosis\n \n\nThe prognosis of Idiopathic Intracranial Hypertension (IIH) varies among patients. \n \n\nMost patients have a benign course, but a small proportion may develop severe visual impairment or blindness. \n \n\nVisual outcome can often be favourable if the disease is diagnosed and treated early. The visual morbidity mainly results from the delay in diagnosis or inadequate treatment which can lead to irreversible damage.\n \n\nWeight loss has been associated with remission and can potentially result in a better prognosis. Even a modest weight loss can lead to a significant reduction in intracranial pressure. In some patients, weight gain has been linked with worsening symptoms and increased intracranial pressure.\n \n\n## References\n \n\n 1. Friedman, D. I., Liu, G. T., & Digre, K. B. (2014). Revised diagnostic criteria for the pseudotumor cerebri syndrome in adults and children. Neurology, 81(13), 1159–1165. [Link](https://doi.org/10.1212/WNL.0b013e31824e9821)\n 2. Mollan, S. P., Davies, B., Silver, N. C., Shaw, S., Mallucci, C. L., Wakerley, B. R., Krishnan, A., Chavda, S. V., Ramalingam, S., Edwards, J., Hemmings, K., Williamson, M., Burdon, M. A., Hassan-Smith, G., Digre, K., Liu, G. T., Jensen, R. H., & Sinclair, A. J. (2018). Idiopathic intracranial hypertension: consensus guidelines on management. Journal of Neurology, Neurosurgery & Psychiatry, 89(10), 1088–1100. [Link](https://doi.org/10.1136/jnnp-2017-317440)\n 3. Wall, M. (2010). Idiopathic Intracranial Hypertension. Neurologic Clinics, 28(3), 593–617. [Link](https://doi.org/10.1016/j.ncl.2010.03.003)",
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"question": "A 45-year-old woman presents to Accident & Emergency with a one-week history of persistent headache. She was worried as she started experiencing bilateral blurring of vision in the past day. She also reports hearing the sound of 'rushing water' in both ears. Fundoscopy reveals bilateral swelling of the optic discs.\n\nThe consultant reviews her and decides to start her on medication. What is the mechanism of action of the most likely drug used?",
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"explanation": "This may be done to investigate ankylosing spondylitis. This may cause anterior uveitis, which leads to acute-onset painful vision loss with photophobia, red eye and a constricted pupil. Slit lamp may reveal a hypopyon in the anterior chamber and white precipitates on the cornea. This is not the case here, as the visual loss is painless with no red eye",
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"explanation": "The patient has sudden onset painless monocular vision loss with a fundoscopy finding suggestive of central retinal artery occlusion. This is usually due to thromboembolism, obstructing blood flow to the retinal artery. Workup for cardiovascular risk factors and a possible thromboembolic cause should be done, including investigations for stroke. The patient is hypertensive and a current smoker, both of which are contributing risk factors as well",
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"explanation": "This may be done if suspecting multiple sclerosis, which is the top cause of optic neuritis. Patients usually have painless monocular vision loss over hours to days with colour desaturation. Fundoscopy may show a swollen, blurred optic disc. Lumbar puncture would demonstrate oligoclonal bands in the cerebrospinal fluid",
"id": "32120",
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"explanation": "HIV is one of the systemic causes of eye disease, including HIV retinopathy, cytomegalovirus (CMV) retinitis, herpes simplex virus (HSV) keratitis or retinitis and toxoplasmosis. CMV retinitis tends to be the most common HIV-related eye condition, causing loss of central vision, blind spots, floaters or flashing lights. Fundoscopy typically shows a \"pizza pie\" appearance due to haemorrhagic retinal necrosis",
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"explanation": "This would be appropriate if suspecting acute anterior ischaemic optic neuropathy, which may occur due to giant cell arteritis (arteritic) or atherosclerosis (non-arteritic). Presenting symptoms include a sudden onset painless monocular vision loss with deterioration of colour vision, and fundoscopy reveals unilateral optic disc oedema with flame-shaped haemorrhages. In giant cell arteritis, erythrocyte sedimentation rate (ESR) would be raised, and temporal artery biopsy is the gold standard investigation",
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"comment": "GCA is also a possible cause of central retinal artery occlusion??",
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"comment": "In hindsight, I think the lack of Hx pointing towards GCA + the risk factors of cardioembolic cause would suggest an ECHO is the most correct answer -sucks to suck though because I also got this wrong!",
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"explanation": "# Summary\n\nCentral Retinal Artery Occlusion (CRAO) is an ocular condition marked by sudden, painless vision loss that typically occurs within seconds. The condition is less common than retinal vein occlusion and results in faster deterioration of vision. Key signs and symptoms include a pale retina with a cherry red spot at the macula, carotid bruits, hypertension, atrial fibrillation, diabetes mellitus, smoking, or hyperlipidaemia. Key investigations include fundoscopy and patient history and examination. Management involves treating the primary cause and may include anticoagulant therapy or ocular massage.\n\n# Definition\n\nCentral Retinal Artery Occlusion (CRAO) is a serious ocular condition characterized by a sudden, painless loss of vision. This abrupt vision loss typically occurs over seconds and is due to the occlusion of the central retinal artery.\n\n\n# Epidemiology\n\nCRAO is less common than retinal vein occlusion. However, it is associated with a faster rate of vision deterioration.\n\n\n# Pathophysiology\n\nThe retina receives its blood supply from two sources:\n\n1. Central retinal artery: \n\n - The internal carotid artery's first branch is the ophthalmic artery, which subsequently branches to the central retinal artery\n\n - The central retinal artery enters the eye at the optic disc, then branches into the superior and inferior retinal arteries, before branching into temporal and nasal subdivisions, which each supply a quadrant of the retina\n\n\n2. Choriocapillaries:\n - The peripheral retina receives its blood supply from the capillaries of the choroid, which are branches of the ciliary artery\n\n\nTherefore, the more proximal an occlusion is, the worse the effect on vision:\n\n- Occlusion of the retinal artery before branching is termed **central retinal artery occlusion** (CRAO)\n- Occlusion after branching is termed **branch retinal artery occlusion** (BRAO)\n\nPatients often present with the 'cherry red spot' finding on fundoscopy (see below) and this refers to the fact that the macula/fovea (responsible for central vision) are spared in CRAO. This is because the macula is supplied by the cilioertinal artery which is usually not affected in CRAO.\n\n# Aetiology\n\nCRAO is essentially a stroke that affects the eye, so it has similar risk factors and pathophysiology.\n\nOften the specific aetiology of a CRAO remains unclear, but the most common causes are:\n\n- Atherosclerosis – roughly 80% of cases\n- Embolism – carotid, cardiac or aortic\n- Inflammatory (e.g. GCA, SLE)\n- Thrombophilia (e.g. protein S or C deficiency, antiphospholipid syndrome)\n\n\n# Signs and Symptoms \n\n- In CRAO, patients present with sudden-onset painless loss of vision that typically occurs over seconds – in almost all cases, vision is reduced to counting fingers. \n- Patients may also report a history of amaurosis fugax.\n\nThe classic examination finding is a pale retina with a 'cherry red spot' at the macula. Patients may also have a relative afferent pupillary defect.\n\n[lightgallery]\n\nPatients should also be examined/investigated for risk factors for CRAO including: \n\n- Carotid bruits\n- Hypertension\n- Atrial fibrillation\n- Diabetes mellitus\n- Smoking\n- Hyperlipidaemia\n\n# Differential Diagnosis\n\nDifferential diagnoses for CRAO should include other conditions that can cause sudden vision loss. These may include:\n\n- Retinal Vein Occlusion: Characterised by sudden, painless vision loss, floaters, and decreased peripheral vision.\n- Retinal Detachment: Presenting with flashing lights, floaters, or a shadow in the peripheral vision.\n- Optic Neuritis: Symptoms may include pain, vision loss, and abnormalities in colour vision.\n- Ischemic Optic Neuropathy: Characterised by sudden, painless vision loss and a pale, swollen optic disc.\n\n# Investigations\n\n- Primary investigations for CRAO involve fundoscopy and a thorough patient history and examination. \n- Imaging techniques such as optical coherence tomography (OCT) and fluorescein angiography may also be utilized.\n\n# Management \n\nThe reversibility of damage to the retina decreases with time. Therefore, the window of time in which treatment is likely to be beneficial is short. Evidence to date suggests that, beyond 90–100 minutes, vision is unlikely to improve with treatment.\n\nThe aim of treatment in the acute setting is to reperfuse the ischaemic retina as quickly as possible. Some centres will advocate the following methods, but there is no proven benefit in the literature:\n\n- Ocular massage – aiming to dislodge the embolus\n- Vasodilation with isosorbide dinitrate\n- Anterior chamber paracentesis – aiming to reduce IOP to help dislodge the embolus\n\nLong-term management consists of secondary prevention of further ischaemic end-organ damage.\n\n# Prognosis \n\nThe visual prognosis is unfortunately very poor with CRAO as the neural layer of the retina atrophies swiftly without a blood supply. Only 30% of patients will have any improvement in vision after presentation.\n\n# Branch Retinal Artery Occlusion\n\nBRAO presents similarly to CRAO, but only some of the visual field is lost because only some of the retinal blood supply is occluded.\n\nManagement is the same as for CRAO and mainly consists of long-term secondary prevention.\n\n# References\n\nDenniston AK, Murray PI. Oxford Handbook of Ophthalmology. Fourth Edition. Oxford University Press. 2018.\n\n[Further information on Patient.co.uk](https://patient.info/doctor/retinal-artery-occlusions)\n",
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"question": "A 75-year-old male presents to the Emergency Department with sudden vision loss in his right eye. His past medical history includes hypertension, and he is a smoker.\n\nHis right eye is painless, and there is no conjunctival redness. Fundoscopy reveals a red spot at the macula.\n\nWhich of the following tests are most appropriate in investigating the underlying cause?",
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"explanation": "This is a beta-blocker that would be contraindicated in patients with asthma, COPD, heart block and severe heart failure, to name a few conditions. It may cause bronchoconstriction in a patient with asthma",
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"explanation": "This is an alpha agonist that reduces aqueous secretion and increases outflow through the trabecular meshwork. It is contraindicated in patients taking monoamine oxidase inhibitors (selegiline in this case) due to the risk of hypertensive crisis",
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"explanation": "This is a cycloplegic that dilates the pupil and is used in anterior uveitis to prevent the formation of posterior synechiae. It would worsen glaucoma as it exacerbates angle closure",
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"explanation": "This is a carbonic anhydrase inhibitor, which is contraindicated in those with sickle cell disease, as it may precipitate a vaso-occlusive crisis by exacerbating sickling of cells. In the absence of contraindications, IV acetazolamide may be given in acute glaucoma to lower intraocular pressure",
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"explanation": "This patient is presenting with acute angle closure. The immediate management of this includes pilocarpine eye drops, acetazolamide (contraindicated in this case), analgesia and an anti-emetic if needed.",
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"comment": "I'm flabbergasted ",
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"comment": "This case sounds like acute angle closure in which case they use pilocarpine first line. \nI’m pretty sure they sure latanoprost for open angle closure glaucoma instead. ",
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"comment": "why would acetazolamide be contraindicated in this case ??",
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"comment": "Acetazolamide is not advised for patients with sickle cell disease as it can cause metabolic acidosis, increasing the likelihood of red blood cell sickling and may trigger a vaso-occlusive crisis. Additionally, its diuretic effect can lead to dehydration, further heightening the risk of sickling episodes.",
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"explanation": "# Summary\n\nPrimary angle closure glaucoma (PACG) is a severe ocular condition primarily affecting older individuals, particularly those of Asian ethnicity or with hypermetropia. Key signs and symptoms include systemic discomfort, nausea, headaches, ocular pain, blurred vision, and a fixed-dilated pupil. Immediate referral to ophthalmology is necessary to prevent progression of visual loss. Key investigations include intraocular pressure measurement and ophthalmological examination. Management includes the prompt reduction of intraocular pressure via a combination of pharmaceutical interventions, and potentially a peripheral iridectomy.\n\n# Definition\n\nPrimary Angle Closure Glaucoma (PACG) is a type of glaucoma characterized by the blockage or narrowing of the drainage angle formed by the cornea and the iris, resulting in a sudden increase in intraocular pressure. \n\n# Pathophysiology\n\nIn health, aqueous humour, which is produced by the ciliary body, flows through the pupil and leaves the eye via the trabecular meshwork.\n\nThe trabecular meshwork is a circular structure that lies in the anterior chamber angle, which is where the cornea meets the iris.\n\nPprimary angle-closure glaucoma occurs when the iris blocks the drainage angle, which causes a rise in IOP and subsequent damage to the optic nerve. **Primary angle closure** is the term used to describe when the iris blocks the drainage angle but there is no evidence of optic nerve damage.\n\n# Epidemiology\n\nPACG predominantly affects older individuals, with an incidence rate of approximately 0.4% in individuals over 40 years of age in the UK.\n\n# Risk Factors\n\n* Hyperopia (long-sightedness) and short axial length of the eyeball\n* Age – the lens grows with age and can push the iris forwards into the angle\n* Ethnicity – Asian or Inuit populations\n* Pupillary dilatation – either iatrogenically (eg. topical mydriatics or systemic alpha-adrenergic agonists) or owing to the patient being in a dimly lit environment (eg. watching television in a dark room) \n\n\n# Signs and Symptoms\n\n## Symptoms\n\n- **Pain** – an extremely painful eye that develops rapidly, with pain spreading throughout the orbit\n- **Blurred vision** – can progress to vision loss\n- **Haloes** – patients will often describe coloured haloes around lights\n- **Systemically unwell** – nausea and vomiting are very common presenting symptoms\n\n\n## Signs\n\n- **Red eye** – ciliary flush with a hazy cornea\n- **Mid-dilated or fixed pupil** \n- **Closed iridocorneal angles** on gonioscopy\n- **Corneal oedema**\n- **Raised IOP** (defined as >21 mmHg) – the globe may feel hard on palpation\n\n\n# Differential Diagnosis\n\nThe main differential diagnoses for PACG include other types of glaucoma, such as open-angle glaucoma, as well as other ocular emergencies like acute anterior uveitis and retinal detachment. The key presenting signs and symptoms of these conditions are:\n\n- Open-angle glaucoma: Gradual loss of peripheral vision, usually in both eyes, and tunnel vision in the advanced stages.\n- Acute anterior uveitis: Red, painful eye, blurred vision, photophobia, and a small, irregular pupil.\n- Retinal detachment: Sudden appearance of floaters, flashes of light in the periphery, and a shadow or curtain over a portion of the visual field.\n\n# Investigations\n\nIn cases of suspected PACG, the following investigations are typically performed:\n\n- Gonioscopy - assessing angle between iris and cornea \n- Tonometry - measurement of intraocular pressure\n- Ophthalmological examination\n\n# Management\n\nAcute angle-closure glaucoma is an emergency and requires urgent admission and referral to ophthalmology.\n\n## Medical management\n\nThe intra-ocular pressure (IOP) must be reduced as soon as possible to prevent further damage to the optic nerve and preserve vision. Medical management consists of:\n\n- IOP-lowering agents e.g. a combination of beta blockers, pilocarpine, and IV acetazolamide.\n- Rarely intravenous hyperosmotics (eg. mannitol) may be added if there is no improvement in IOP\n- Analgesia and antiemetics\n\nThe aim of medical management is to stabilise or reduce the IOP while awaiting formal ophthalmological assessment and definitive surgical intervention.\n\n## **Surgical management**\n\n- **Peripheral iridotomy** – a laser is used to make a hole in the peripheral iris to allow free flow of aqueous – the contralateral eye is treated prophylactically as it is predisposed to PACG\n- **Surgical iridectomy** – rarely used nowadays, but still carried out when a laser iridectomy is not possible\n\n\n# NICE Guidelines\n\n[Click here for NICE CKS on glaucoma](https://cks.nice.org.uk/topics/glaucoma/)\n\n\n\n",
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"question": "A 50-year-old woman presents to the Emergency Department with sudden onset severe pain in her right eye. Her past medical history includes severe asthma, sickle cell disease and depression. She only takes selegiline. She has nausea and vomited once on the way to the hospital. On inspection, she has right conjunctival redness, and her right pupil reacts poorly to light.\n\nWhich of the following medications should be started?",
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"explanation": "This woman has presented with acute pancreatitis secondary to valproate, which is a rare cause of pancreatitis. Lipase is more sensitive in patients with pancreatitis as it has a longer half-life than amylase; thus, lipase levels may remain elevated even after amylase levels have normalised",
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"comment": "Drugs causing pancreatitis: FAT SHEEP.\n\nFurosemide\nAzathioprine / Asparaginase\nTetracyclines / Thiazides\n\nSulfa drugs, Sodium Valproate, Statins\nHydrochlorothiazides\nEthanol\nEstrogen\nProtease inhibitors.",
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"explanation": "# Summary\n \nAcute pancreatitis refers to inflammation of the pancreas; there are a wide variety of causes and severity ranges from mild and self-resolving pancreatitis to life-threatening multi-organ failure. The main symptom is acute-onset epigastric pain which radiates to the back, which may be accompanied by nausea and vomiting. Diagnosis is primarily with bloods showing an elevated amylase or lipase. Abdominal ultrasound is another important investigation to look for gallstones (the commonest cause of acute pancreatitis). General management includes aggressive fluid resuscitation, analgesia, antiemetics and nutritional support. \n\n# Definition\n\nAcute pancreatitis refers to an inflammatory process affecting the pancreas as well as local or distant tissues and organs in some cases.\n \n\n# Epidemiology\n \n- Acute pancreatitis has an incidence of approximately 30 cases per 100,000 people per year\n- There are many causes as detailed below\n- Half of cases are caused by gallstones, and around a quarter of cases by alcohol\n- 10% of cases are idiopathic\n- The majority of cases (around 80%) are mild and self-limiting, with low mortality rates (1-3%)\n- The 20% of patients with moderate or severe disease have a higher risk of death (estimated at 13-35%)\n\n# Aetiology\n\nCauses of acute pancreatitis can be remembered using the mnemonic GET SMASHED:\n \n - Gallstones \n - Ethanol (alcohol)\n - Trauma\n - Steroids\n - Mumps\n - Autoimmune disease (e.g. systemic lupus erythematosus, Sjogren's syndrome)\n - Scorpion stings\n - Hypercalcaemia, hypertriglyceridemia, hypothermia\n - ERCP\n - Drugs (e.g. thiazides, azathioprine, sulphonamides)\n\nOther causes include blunt abdominal trauma or local surgery, microlithiasis (tiny gallstones and biliary sludge), pancreatic tumours and cholangiocarcinomas and congenital abnormalities such as pancreas divisum. \n\n# Classification\n\nSeverity of pancreatitis is stratified using the Glasgow Score - each of the following scores 1 point and a score of **3 or more** predicts severe pancreatitis:\n\n- PaO2 < 8kPa\n- Age > 55 years\n- Neutrophils > 15\n- Calcium < 2\n- Renal i.e. Urea > 16 \n- Enzymes i.e. LDH > 600 or AST > 200\n- Albumin < 32\n- Sugar i.e. Glucose > 10\n\nThis should be calculated on admission and at 48 hours.\n \n# Signs and Symptoms\n\n- The main symptom of acute pancreatitis is epigastric pain which may radiate to the back\n- Nausea and vomiting are also common symptoms\n- Diarrhoea can occur\n \nOn examination, signs may include:\n\n- Abdominal tenderness\n- Peritonism, rebound tenderness and guarding may be seen\n- Abdominal distension \n- Fevers (which may be due to inflammation or superadded infection)\n- Tachycardia and hypotension if shocked\n- Haemorrhagic pancreatitis may present with Grey-Turner's sign (bruising in the flank area), Cullen's sign (bruising around the umbilicus) or Fox's sign (bruising over the inguinal ligament)\n\n[lightgallery]\n \n[lightgallery1]\n \n# Differential Diagnosis\n \n- **Acute Coronary Syndrome** may present atypically with epigastric rather than chest pain with nausea and vomiting - an ECG should be done to look for ischaemic changes.\n- **Perforated Peptic Ulcer** may present with sudden onset severe abdominal pain with nausea and vomiting and signs of peritonitis; amylase may be raised and a chest X-ray may show air under the diaphragm.\n- **Ruptured Abdominal Aortic Aneurysm** shares features of abdominal pain radiating to the back; patients are typically very unwell with haemodynamic instability. A bedside ultrasound can be done for rapid diagnosis.\n- **Bowel Obstruction** causes abdominal pain and distension with nausea and vomiting, constipation is seen rather than diarrhoea and pain is usually colicky in nature.\n- **Cholecystitis** typically presents with right upper quadrant pain and fever with a positive Murphy's sign on examination, also commonly related to gallstones \n\n# Investigations\n \n**Bedside tests:**\n\n- **ABG** if low oxygen saturations to help with risk stratification (the pO2 is needed for the Glasgow criteria)\n- **ECG** to rule out acute coronary syndrome as a cause of pain\n- **Pregnancy test** in women of child-bearing age to rule out causes of abdominal pain such as ectopic pregnancy\n- **Capillary blood glucose** as hyperglycaemia indicates severe pancreatitis\n\n**Blood tests:**\n\n- **FBC** and **CRP** for inflammatory markers\n- **U&Es** to look for kidney injury; urea is part of the Glasgow criteria\n- **LFTs** are often deranged; a low albumin and high AST indicate severe pancreatitis\n- **Amylase** is the key diagnostic test, with levels over 3x the upper limit of normal indicating acute pancreatitis\n- **Lipase** is not usually measured but can also be used to diagnose pancreatitis - it is more sensitive and specific than amylase\n- **LDH** and a **bone profile** for calcium are also required for the Glasgow criteria with hypocalcaemia being a poor prognostic factor\n- **Blood cultures** in patients with fevers or other signs of infection \n- **Coagulation screen** as a baseline - may be deranged in severe illness\n- **Lipid profile** if hypertriglyceridaemia is suspected as a cause of pancreatitis\n- **Autoimmune markers** if the cause of pancreatitis is unclear\n \n**Imaging:**\n \n- **Abdominal ultrasound** looking for gallstones and duct dilation\n- **Chest X-ray** for complications such as pleural effusions or acute respiratory distress syndrome\n- **CT pancreas with contrast** should be done in patients who are deteriorating or have signs of sepsis or organ failure after 6-10 days - may detect complications such as pseudocysts or necrotising pancreatitis\n- **Magnetic Resonance Cholangiopancreatography (MRCP)** may be required in cases of pancreatitis secondary to gallstones \n \n# Management\n\n**Conservative:**\n\n- Ensure patients with severe pancreatitis (e.g. Glasgow score 3+, hypotension, oliguria, respiratory distress) are referred for intensive care assessment and input\n- Catheterise and monitor input-output\n- Insert an NG tube if significant vomiting\n- If the patient can eat, encourage oral intake as tolerated - they should not be made nil by mouth unless there is another reason for this\n- Enteral nutrition should be started within 72 hours of presentation (e.g. NG feeding) - if this fails parenteral nutrition should be considered\n\n**Medical:**\n\n- IV fluid resuscitation is the mainstay of treatment - crystalloids should be used and should be titrated to achieve an adequate urine output\n- Ensure adequate analgesia is given - opioids may be required\n- Antiemetics for nausea and vomiting\n- Antibiotics should not be given routinely - in some cases (e.g. confirmed pancreatic necrosis) broad-spectrum antibiotics should be given\n- Monitor for and treat any complications\n- For alcohol-related pancreatitis, alcohol withdrawal treatment may be required (i.e. benzodiazepines and pabrinex)\n\n**Surgical:**\n\n- The underlying cause of pancreatitis should be treated; an ERCP may be required for gallstones in cases of jaundice, cholangitis or a dilated common bile duct on imaging\n- Laparoscopic cholecystectomy for gallstone pancreatitis should ideally be done in the same admission unless the patient is not fit for surgery\n- Surgical or interventional management may be required for complications e.g. drainage of large pancreatic pseudocysts or debridement of pancreatic necrosis\n\n# Complications\n\n**Local complications include:**\n\n- A **pancreatic pseudocyst** is a fluid-filled sac that lacks a true epithelial lining (the wall is vascular and fibrotic); typically these form weeks after an episode of acute pancreatitis and can become infected, rupture, haemorrhage or cause compression of surrounding structures\n- **Pancreatic necrosis** occurs due to ischaemia of the pancreas and may become infected causing systemic inflammation and multi-organ failure\n- **Peripancreatic fluid collections** may occur, which can get infected leading to abscess formation\n- **Haemorrhage** from local vessels (e.g. pancreatic or splenic arteries or veins) can occur due to inflammation and enzyme release\n- **Pancreatic fistulae** may form due to pancreatic duct disruption, causing these to communicate with for example the skin, the abdominal cavity or the pleural space\n \n**Systemic complications include:**\n\n- **Acute Respiratory Distress Syndrome (ARDS)** which is a severe lung injury with non-cardiogenic pulmonary oedema and respiratory failure\n- **Acute kidney injury** is a common complication which may require renal replacement therapy; often secondary to intravascular volume depletion due to third spacing \n- **Disseminated intravascular coagulation** \n- **Sepsis** for example secondary to infected pancreatic necrosis\n- **Multi-organ failure** which may lead to death\n- **Hypocalcaemia** occurs due to free fatty acids reacting with serum calcium to form salts, a process called saponification; this can cause tetany if severe\n- **Hyperglycaemia** due to disruptions in insulin production due to pancreatic destruction as well as systemic inflammation\n \n# NICE Guidelines\n\n[NICE CKS - Acute Pancreatitis](https://cks.nice.org.uk/topics/pancreatitis-acute/)\n\n[NICE - Pancreatitis](https://www.nice.org.uk/guidance/ng104/)\n \n# References\n\n[UK guidelines for the management of acute pancreatitis](https://gut.bmj.com/content/54/suppl_3/iii1)\n\n[British Society of Gastroenterology - Practical Guide to Acute Pancreatitis](https://www.bsg.org.uk/clinical-resource/practical-guide-to-the-acute-pancreatitis)",
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"question": "A 60-year-old lady is admitted with a three-day history of sudden onset epigastric pain, nausea and two episodes of vomiting.\n\n\nOn examination, her abdomen is soft and diffusely tender. There is no rigidity or guarding.\n\n\nObservations: temperature 37.0°C, HR 110 bpm, BP 90/60 mmHg, RR 20 bpm, SpO2 99% on room air.\n\n\nHer bloods show:\n\n||||\n|---------------------------|:-------:|--------------------|\n|Albumin|40 g/L|35 - 50|\n|Alanine Aminotransferase (ALT)|21 IU/L|10 - 50|\n|Aspartate Aminotransferase (AST)|32 IU/L|10 - 40|\n|Alkaline Phosphatase (ALP)|110 IU/L|25 - 115|\n|Bilirubin|7 µmol/L|< 17|\n|Gamma Glutamyl Transferase (GGT)|20 U/L|9 - 40|\n|Lipase|432 IU/L|< 101|\n|Amylase|289 U/L|< 220|\n\n\nShe was recently started on a new medication. Which of the following is the most likely cause of her current presentation?",
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"explanation": "# Summary \n\nHaematuria, the presence of blood in the urine, can be divided into macroscopic haematuria, visible to the naked eye, and microscopic haematuria, detectable only through urinalysis. Key causes include conditions affecting the kidney, ureters, and urethra, as well as certain medications and dietary items. Clinically significant signs and symptoms vary based on the underlying cause. Key investigations include urinalysis, urine culture, and urine microscopy, as well as blood tests and imaging of the renal tract. Management strategies depend on the identified cause.\n\n# Definitions\n\n- Macroscopic haematuria: Blood in the urine, visible to the naked eye.\n- Microscopic haematuria: Blood in the urine, detectable only on urinalysis.\n\n\n# Epidemiology\n\nThe prevalence of haematuria varies depending on population characteristics such as age and sex, and the criteria used to define haematuria. In general, haematuria is more common in older individuals and in males. In clinical settings, haematuria is a common finding on urinalysis.\n\n# Aetiology\n\n## Kidney-related causes\n\n- Glomerular: IgA nephropathy, Alport's syndrome, Glomerulonephritis.\n- Non-glomerular: Tumours (Renal cell carcinoma, Wilm's tumour), Nephrolithiasis, Infection, Polycystic kidneys, Trauma, Urethral stricture, Vascular conditions (infarction, renal vein thrombosis), Sickle cell disease, Certain drugs.\n\n## Ureter or Bladder-related causes\n\n- Stones\n- Tumours, particularly **Bladder Cancer**\n- Strictures\n- Infection\n\n## Urethral causes\n\n- Benign prostatic hypertrophy\n- Prostate cancer\n- Prostatitis\n- Trauma\n\n## Other causes\n\n- Menstruation\n- Post-coital\n- Certain medications\n- Viral illness\n\nNB: Anticoagulants doesn’t in itself cause haematuria, it makes any bleeding worse. E.g. renal cancer may present with NVH, but if the patient was taking anticoagulation, this would potentiates the bleeding leading to VH. \n\n# Signs and Symptoms\n\nSigns and symptoms of haematuria are largely dependent on the underlying cause and may include flank pain, abdominal pain, dysuria, frequency, urgency, and systemic symptoms such as fever or weight loss. In cases of macroscopic haematuria, patients may report pink, red, or brown urine.\n\n# Differential Diagnosis\n\nThe differential diagnosis of haematuria includes a broad range of conditions, and the main signs and symptoms of each can help to distinguish between them:\n\n- Glomerular diseases (e.g. IgA nephropathy, Alport's syndrome): Proteinuria, hypertension, oedema.\n- Non-glomerular kidney diseases (e.g. tumours like renal cell carcinoma, Wilm's tumour): Flank pain, mass, haematuria, weight loss.\n- Ureteral stones: Flank pain, haematuria, possibly signs of infection (fever, dysuria).\n- Urethral conditions (e.g. benign prostatic hypertrophy, prostate cancer): Lower urinary tract symptoms (e.g. difficulty urinating, frequency), possibly haematuria.\n- Pseudohaematuria: History of specific drug use or dietary intake. If there is any doubt over the legitimacy of haematuria, a lab sample should be sought. Causes of pseudohaematuria include:\n\t- Medications such as Rifampicin, Chlorzoxazone, Phenazopyridine, Phenothiazine, Doxorubicin, Phensuximide, Phenytoin, Daunomycin\n\t- Dietary items such as berries, beets, rhubarb\n\t- Myoglobin\n\t- Menstruation\n- Haemoglobinuria: Occurs due to haemolysis of red blood cells.\n- Myoglobinuria: Occurs due to muscle breakdown.\n\n# Investigations\n\n- Bedside - urinalysis.\n- Urine culture.\n- Urine microscopy - the type of blood cells seen may indicate the cause; dysmorphic red blood cells suggest glomerular origin, if red cell casts visible this suggests renal origin (precipitate with protein made in renal tubules)\n- Blood tests: Full Blood Count (FBC), Urea and Electrolytes (U+E), Prostate-Specific Antigen (PSA) for men, and coagulation studies.\n- Imaging: Renal tract ultrasound, Computed Tomography of kidneys, ureters, bladder (CT KUB).\n- Cystoscopy.\n- Renal biopsy.\n\n## 2 week wait referral criteria\n\n\n| Bladder cancer | Renal cancer | \n| ------------- |-------------| \n| If they are aged 45 years and over and have: 1) Unexplained visible haematuria without urinary tract infection, or 2) Visible haematuria that persists or recurs after successful treatment of urinary tract infection.| If they are aged 45 years and over and have: 1) Unexplained visible haematuria without urinary tract infection, or 2) Visible haematuria that persists or recurs after successful treatment of urinary tract infection.\r\nIf they are aged 60 years and over and have unexplained non-visible haematuria and either dysuria or a raised white cell count on a blood test. | |\nConsider non-urgent referral for bladder cancer in people aged 60 years and over with recurrent or persistent unexplained urinary tract infection.| | right-aligned |\n\n# Management\n\nManagement strategies are tailored based on the identified cause. They may include medical management for infections, surgical intervention for stones or tumours, lifestyle modification for certain causes of pseudohaematuria, or further specialist management for complex cases.\n\n# References\n\n[BMJ Best Practice: Assessment of visible haematuria](https://bestpractice.bmj.com/topics/en-gb/316)\n\n[British Association of Urological Surgeons: Haematuria](https://www.baus.org.uk/patients/conditions/2/blood_in_the_urine_haematuria)\n\n[Oxford Medical Education: Haematuria](https://www.oxfordmedicaleducation.com/wp-content/uploads/2015/04/Haematuria.protected.pdf)",
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"question": "A 65 year old gentleman presents to Accident & Emergency with a 5 day history of persistent haematuria. He has a background of atrial fibrillation and is on warfarin.\n\n\nBlood tests are as follows:\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|115 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|9.1x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|210x10<sup>9</sup>/L|150 - 400|\n|Neutrophils|5.5 x10<sup>9</sup>/L|2.0 - 7.5|\n|Sodium|137 mmol/L|135 - 145|\n|Potassium|4 mmol/L|3.5 - 5.3|\n|Chloride|102 mmol/L|95 - 106|\n|Urea|8 mmol/L|2.5 - 7.8|\n|Creatinine|95 µmol/L|60 - 120|\n|eGFR|85 mL/min/1.73m<sup>2</sup>|> 60|\n|International Normalised Ratio (INR)|2.1|1.0|\n\n\nUrinalysis showed red blood cells with no evidence of leucocytes or nitrites. Computed tomography (CT) of kidneys, ureters and bladder showed no stones.\n\n\nWhich is the next most appropriate investigation?",
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"explanation": "This may be useful in investigating voiding dysfunction in patients with lower urinary tract symptoms that point towards chronic bladder outflow obstruction. However, it would not be useful in a patient which has a high clinical likelihood of prostate cancer",
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"explanation": "This would be most appropriate in patients with suspected prostate cancer after taking into account relevant risk factors including age, prostate specific antigen level, DRE findings and comorbidities. However, this method is invasive and may risk missing the cancer depending on the area biopsied",
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"name": "Magnetic resonance imaging (MRI) scan of the prostate",
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"explanation": "This would be useful in investigating causes of obstructive uropathy. However, as prostate cancer is the most likely cause in this scenario given the DRE findings, it is better to proceed with an MRI prostate first",
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"explanation": "This would be useful in watchful waiting for asymptomatic patients in whom hormonal therapy is being deferred or as a staging scan for bone metastases. However, it is not the most useful in making a diagnosis of prostate cancer",
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"explanation": "# Summary\n\nProstate cancer is a common malignancy affecting males, particularly in Western societies. It is characterised by abnormal growth of cells in the prostate gland and can be asymptomatic in early stages. Advanced disease may manifest as urinary issues, pelvic discomfort, bone pain, and erectile dysfunction. The primary investigations are digital rectal examination and a urine dip, with PSA (Prostate Specific Antigen) testing, which carries issues of sensitivity and specificity. MRI is a key tool for assessment, alongside a Gleason score for grading biopsy samples. Management ranges from active surveillance for low-grade disease to hormonal therapy and surgery for more advanced cases.\n\n# Definition\n\nProstate cancer is a malignant tumour that arises from the cells of the prostate, a small walnut-sized gland that produces seminal fluid in men. This condition varies greatly in its presentation, with some cases growing slowly and requiring minimal treatment, while others are aggressive and can spread quickly.\n\nThe majority of prostate cancers are adenocarcinomas, and they usually primarily affect the peripheral prostate. They spread lymphatically first via the obturator nodes.\n\n\n# Epidemiology\n\nProstate cancer is responsible for approximately 48,000 new diagnoses each year in the UK, accounting for 13% of all cancer cases. It is the second most prevalent cancer among men globally, preceded only by lung cancer.\n\n\n# Aetiology\n\n### Non-modifiable risk factors\n\n- African ethnicity\n- BRCA gene mutations\n- Family history of prostate cancer\n- Age (risk increases with advancing age)\n\n### Modifiable risk factors\n\nResearch into modifiable risk factors is ongoing. Some potential factors are:\n\n- Obesity\n- Smoking\n- Diet rich in animal fats and dairy products\n\n# Signs and Symptoms\n\nIn its early stages, prostate cancer often produces no symptoms as it affects the peripheral prostate. However, as the disease progresses with local advancement (which can cause compression of the urethra), symptoms may include:\n\n- Urinary symptoms, including difficulty initiating or stopping urination\n- Poor urine stream\n- Haematospermia (blood in semen)\n- Pelvic discomfort\n- Bone pain, potentially indicating metastatic disease\n- Erectile dysfunction\n\n# Differential Diagnosis\n\nSeveral conditions can mimic the symptoms of prostate cancer and should be considered during evaluation:\n\n- Benign Prostatic Hyperplasia (BPH): Characterised by difficulty in urination, increased frequency of urination, nocturia, and potentially, haematuria.\n- Prostatitis: Acute or chronic inflammation of the prostate that can cause pelvic pain, urinary symptoms, and potentially, systemic symptoms such as fever and malaise.\n- Urinary Tract Infection (UTI): Can cause dysuria, urinary frequency, urgency, and potentially, systemic signs of infection.\n- Bladder cancer: May present with haematuria, dysuria, and urinary frequency.\n\n# Investigations\n\n* Initial examination should include a digital rectal examination and a urine dip.\n\t* An asymmetrical hard/craggy/nodular prostate with loss median sulcus is suspicious for malignancy.\n* A PSA blood test may be considered, despite its lack of sensitivity and specificity. This necessitates patient counselling about the potential for over-investigation and over-treatment. Causes of a falsely raised PSA include:\n\t* An active urinary infection or within previous 6 weeks.\n\t* Ejaculation in previous 48 hours.\n\t* Vigorous exercise, for example cycling, in the previous 48 hours.\n\t* Urological intervention such as prostate biopsy in previous 6 weeks.\n\nInterpretation of PSA results:\n\n| Age (years) | Prostate-specific antigen threshold (micrograms/L) |\n|-------------|--------------------------------------------------|\n| Below 40 | Use clinical judgement |\n| 40–49 | More than 2.5 |\n| 50–59 | More than 3.5 |\n| 60–69 | More than 4.5 |\n| 70–79 | More than 6.5 |\n| Above 79 | Use clinical judgement |\n\n\n* **Multi-parametric MRI** is the gold standard radiological investigation, and can show specific areas which can be targetted for biopsy. If metastatic disease is suspected, additional imaging such as CT scans (can show e.g. sclerotic bony lesions) and bone isotope scans may be required.\n* The Gleason grading system is used to assess prostate cancer severity on initial biopsy. It involves analysing the morphological features of prostatic tissue and assigning a score from 1 (normal tissue) to 5 (very poorly differentiated cells). The sum of the two most common scores represents the Gleason score, which has prognostic value.\n\n### 2 week wait referral criteria\n\n- Refer if their prostate feels malignant on DRE.\n- Consider referring a person with possible symptoms of prostate cancer using a suspected cancer pathway referral (for an appointment within 2 weeks) if their PSA level is above the threshold for their age (see above)\n\n# Classification\n\nThe TNM staging system for prostate cancer provides a standardised way to describe the extent of the disease based on three key parameters: tumour size and extent (T), involvement of regional lymph nodes (N), and the presence of distant metastasis (M).\n\n- **T (Tumour):**\n - **T1:** The tumour is not palpable or visible by imaging.\n - T1a: Tumour found incidentally in less than 5% of tissue removed.\n - T1b: Tumour found incidentally in more than 5% of tissue removed.\n - T1c: Identified by needle biopsy due to elevated PSA (prostate-specific antigen) levels.\n - **T2:** The tumour is confined to the prostate.\n - T2a: Tumour involves half or less of one side of the prostate.\n - T2b: Tumour involves more than half of one side but not both sides.\n - T2c: Tumour involves both sides.\n - **T3:** The tumour extends beyond the prostate.\n - T3a: Tumour extends through the prostate capsule.\n - T3b: Tumor invades seminal vesicle(s).\n - **T4:** The tumour invades adjacent structures other than seminal vesicles (e.g., bladder, rectum).\n\n- **N (Lymph Nodes):**\n - **N0:** No regional lymph node involvement.\n - **N1:** Regional lymph node involvement.\n\n- **M (Metastasis):**\n - **M0:** No distant metastasis.\n - **M1:** Distant metastasis present.\n - M1a: Non-regional lymph nodes.\n - M1b: Bones.\n - M1c: Other sites or multiple sites.\n\n\n# Management\n\nHere is a summary table demonstrating management approaches according to TNM staging:\n\n| TNM Stage | Management Options |\n|--------------------------|--------------------------------------------------------|\n| T1 (T1a, T1b, T1c) | Active surveillance (for low-risk cases) |\n| | Watchful waiting |\n| | Radical prostatectomy (for selected cases) |\n| T2 (T2a, T2b, T2c) | Radical prostatectomy (standard treatment) |\n| | External beam radiation therapy |\n| | Brachytherapy (seed implantation) |\n| | Active surveillance (for low-risk cases) |\n| T3 (T3a, T3b) | Hormonal therapy (to delay progression) |\n| | Radical prostatectomy (selected cases) |\n| | External beam radiation therapy |\n| T4 | Hormonal therapy (palliative, delays progression) |\n| | Radiation therapy (palliative) |\n| | Symptomatic management |\n| Not Fit for Radical Prostatectomy | Hormonal therapy (palliative) |\n| Metastatic (M1) | Hormonal therapy (androgen deprivation) |\n| | Chemotherapy (docetaxel, cabazitaxel) |\n| | Targeted therapy (abiraterone, enzalutamide) |\n| | Immunotherapy (sipuleucel-T) |\n\n\n## Active Surveillance\n\nThis approach is suitable for patients with low-grade prostate cancer and involves repeating investigations periodically to monitor disease progression.\n\n## Radiotherapy\n\nRadiotherapy can be used either as a curative measure or for palliation to reduce tumour bulk and associated pain.\n\n## Surgical Management\n\nSurgical removal of the prostate and any affected organs is an option for patients without metastatic disease. Minimally invasive techniques such as robotically assisted laparoscopic prostatectomy (RALP) are becoming more common.\n\n## Hormonal Management\n\nHormonal therapies aim to reduce testosterone levels, slowing the progression of metastatic prostate cancer. This can be achieved with GnRH analogues, androgen antagonists, or GnRH antagonists. \n\nHormonal therapies may cause sexual side effects, including decreased libido, impotence, infertility, and gynecomastia. Metabolic side effects include weight gain, osteoporosis, diabetes, and ischemic heart disease. Haematological side effects include anaemia.\n\n# NICE Guidelines\n\n[Click here for the NICE Guidelines](https://www.nice.org.uk/guidance/ng131)",
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"question": "A 85 year old male is admitted with acute urinary retention. Over the past year, he has been having urinary hesitancy and poor stream with nocturia up to 5-6 times a night. He had an objective 3kg loss of weight in the last year.\n\nDigital rectal examination (DRE) reveals a hard, asymmetrically enlarged prostate. Prostate specific antigen is elevated at 15ng/mL.\n\nWhich of the following is the next most appropriate investigation?",
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"explanation": "This has the highest association with smoking amongst the lung cancers. It typically presents with centrally located lung masses and tends to be associated with Cushing's syndrome due to ectopic production of adrenocorticotropic hormone. It is not likely here as it is very rare in patients who have never smoked",
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"name": "Large cell carcinoma",
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"explanation": "This has the highest association with smoking amongst the lung cancers. It typically presents with centrally located lung masses and tends to be associated with Cushing's syndrome due to ectopic production of adrenocorticotropic hormone. It is not likely here as it is very rare in patients who have never smoked",
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"name": "Small cell lung carcinoma",
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"explanation": "This is the second most common type of lung cancer and has a strong association with smoking compared to other non-small cell lung carcinomas. It is usually centrally located and originates in the bronchi. Associated paraneoplastic phenomena usually includes hypercalcaemia secondary to secretion of parathyroid hormone related peptide",
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"name": "Squamous cell carcinoma",
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"explanation": "This is the most common type of lung cancer, especially in females and non-smokers. This patient has presented with hypertrophic osteoarthropathy, with clubbing and a painful arthropathy that can be quite similar to inflammatory arthritis. It is most frequently associated with adenocarcinoma",
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"label": "a",
"name": "Adenocarcinoma",
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"explanation": "This is most commonly associated with asbestos exposure and would typically present with bilateral pleural thickening and plaques. This is not likely given her lack of occupational exposure",
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"comment": "I thought both adenocarcinoma and squamous cause hypertrophic pulmonary osteoarthropathy. Also hes a lifelong smoker so doesnt it make squamous more likely?",
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"comment": "she's a lifelong non-smoker - got confused by this as well and put squamous too. ",
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"comment": "Isn't HPOA most strongly associated with squamous cell lung cancer",
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"comment": "Radiopaedia says it's associated with non-small cell cancer generally, but \"particularly squamous cell carcinoma\". So I guess this question is trying to point out that as a non-smoker, adeno is more likely? Looked this up after I got it wrong!",
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"comment": "I literally read that as smoker lol, I am so tried ",
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"comment": "who says lifelong non-smoker? either she's a lifelong smoker or she's never smoked :(",
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"comment": "same I read the question wrong",
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"explanation": "# Summary\n\nLung cancers are divided into two main subtypes: small cell and non-small cell, with small cell lung cancers being more aggressive and incurable. Types of non-small cell lung cancer include squamous cell and adenocarcinomas, with several rarer subtypes. Most cases of lung cancer are linked to smoking. Lung cancers may present with chest symptoms such as cough, breathlessness or haemoptysis, systemic symptoms of weight loss and anorexia or symptoms of metastatic disease such as bone pain or seizures. Chest X-ray is the initial investigation of choice, followed by CT chest and a biopsy. Staging scans are done after diagnosis to help plan treatment. Management can be curative or palliative depending on the stage of the cancer, the subtype and the patient’s overall health. It may include chemotherapy, radiotherapy, immunotherapy, targeted therapies to specific mutations and surgery. \n\n\n# Definition\n\nLung cancer refers to a primary malignancy arising from the lung parenchyma or the bronchi. Cancers are classified as small cell (SCLC) or non-small cell (NSCLC), with 80% being non-small cell. The main histological subtypes of NSCLC are squamous cell cancers and adenocarcinomas.\n\n# Epidemiology\n\nLung cancer makes up the largest proportion of cancer deaths of any tumour type, with nearly 35,000 deaths per year in the UK (21% of all cancer deaths). It is the second most common cancer in both males and females (after prostate and breast respectively). \n\nIncidence is strongly related to age, with the highest rates in people aged over 75 years old. Although non-smokers can also get lung cancer, 86% of cases are linked to smoking and so the majority of cases are felt to be preventable.\n\n# Aetiology\n\nRisk factors for lung cancer include:\n\n- Tobacco smoking (e.g. cigarettes, pipes, cigars)\n- Passive smoke exposure\n- Occupational exposures (e.g. beryllium, cadmium, arsenic, asbestos, silica)\n- Radon exposure\n- Family history of lung cancer\n- Radiation to the chest (e.g. in lymphoma treatment)\n- Air pollution\n- Immunosuppression (e.g. HIV, medications)\n- Increasing age\n\n# Classification\n\nLung cancers are classified by the cell of origin of the malignancy. Small cell cancers come from neuroendocrine cells of the lung. Non-small cell cancers are split into adenocarcinomas (coming from alveolar type 2 epithelial cells), squamous cell carcinomas (coming from basal epithelial cells) and large cell carcinomas (which come from a variety of epithelial cells). There are also rarer subtypes of lung cancer such as sarcomatoid or salivary gland-type lung cancers which come under the NSCLC umbrella.\n\nStaging is also an important way to classify lung cancers depending on how advanced they are. TNM (tumour, node, metastasis) staging is used to describe how large the tumour is and where it has spread to. This can then be used to classify lung cancers into stage 1 to 4, where stage 1 is localised and small (under 4cm), stages 2 and 3 are locally advanced and stage 4 is metastatic. \n\n# Signs and symptoms\n\n**Symptoms include:**\n\n- Persistent cough\n- Haemoptysis\n- Dyspnoea especially on exertion\n- Chest pain\n- Weight loss\n- Recurrent chest infections, or infections resistant to treatment\n- Anorexia\n\n**Signs include:**\n\n- Cachexia\n- Finger clubbing\n- Lymphadenopathy (supraclavicular or persistent cervical)\n- If there is lung collapse due to an obstructing tumour - absent breath sounds, trachea deviated towards side of collapse\n- If there is a malignant pleural effusion - stony dull on percussion, decreased breath sounds over affected area\n\n**Other signs and symptoms related to paraneoplastic presentations of lung cancer:**\n\n- **Cushing syndrome** - usually SCLC producing ectopic ACTH, presents with dorsal cervical fat pads, truncal obesity, hypertension, striae and proximal muscle weakness\n- **Syndrome of inappropriate ADH secretion (SIADH)** - usually SCLC, present with symptoms of hyponatraemia e.g. fatigue, nausea, weakness, confusion or seizures\n- **Lambert-Eaton myasthenic syndrome (LEMS)** - usually SCLC, due to autoantibodies to presynaptic calcium channels at the neuromuscular junction develop proximal muscle weakness that improves with repeated movement, as well as autonomic effects such as dry mouth, lightheadedness, constipation, urinary symptoms and erectile dysfunction\n- **Humoral hypercalcaemia of malignancy** - usually squamous cell carcinomas (SCC) that release parathyroid hormone-related protein (PTHrP) that mimics PTH and causes hypercalcaemia, leading to symptoms of bone pain, constipation, anorexia, abdominal pain, excessive thirst and confusion\n- **Hypertrophic pulmonary osteoarthropathy** - usually adenocarcinomas which cause a periosteal reaction of bones, resulting in clubbing and arthritis especially affecting wrists and ankles\n\n# Differential diagnosis\n\n- Lung metastases from another primary cancer (e.g. breast or colorectal cancer)\n- Mesothelioma (cancer of the pleura, strongly related to asbestos exposure)\n- Tuberculosis \n- Bronchiectasis\n\n# Investigations\n\nIn primary care, patients should be referred on a 2 week wait pathway in the following situations:\n\n- Aged 40+ with unexplained haemoptysis\n- Chest X-ray findings suspicious for lung cancer\n\nUrgent chest X-rays (to be done within 2 weeks) should be done for patients aged 40+ who have one of these symptoms and have ever smoked (or two symptoms if they are never smokers):\n\n- Cough\n- Fatigue\n- Shortness of breath\n- Chest pain\n- Weight loss\n- Anorexia\n\nAn urgent chest X-ray should be considered in patients aged 40+ with any of:\n\n- Persistent/recurrent chest infection\n- Finger clubbing\n- Supraclavicular or persistent cervical lymphadenopathy\n- Thrombocytosis\n- Chest signs consistent with lung cancer (e.g. reduced breath sounds, dullness to percussion)\n\nChest X-ray findings include:\n\n- Lung mass (may be rounded or spiculated, squamous cell carcinomas may cavitate)\n- Consolidation (where there is infection downstream of the tumour obstructing an airway)\n- Bulky hilum (especially squamous cell carcinomas which often arise centrally)\n- Lobar collapse (due to bronchial obstruction, especially squamous cell carcinomas)\n- Pleural effusion\n\n[lightgallery]\n\nOther initial investigations include:\n\n- **Sputum cytology** - low sensitivity but may be of use in patients who decline or cannot have a biopsy\n- **Diagnostic thoracocentesis** - i.e. a pleural tap; if a pleural effusion is present this should be done and the fluid sent for cytology as well as cell count, microscopy, culture, glucose, LDG and protein (to determine whether it is a transudate or exudate)\n- **Blood tests** - including FBC for anaemia and thrombocytosis, U&Es for hyponatraemia and baseline renal function, LFTs for baseline liver function (may be deranged in liver metastases), bone profile for hypercalcaemia, CRP for superadded infection, clotting if interventions planned\n- **CT chest with contrast** - should be done after chest X-ray to better characterise any lesion seen and investigate for local spread\n- **Biopsy** - to confirm the diagnosis and subtype of cancer, may be done percutaneously for peripheral tumours or via bronchoscopy for central masses\n\nOnce a lung cancer is diagnosed, further investigations may include:\n\n- **Spirometry** - to assess lung function to determine if a patient is suitable for surgical intervention\n- **CT chest abdomen and pelvis** - to stage the cancer (determine if there are any metastases)\n- **PET-CT scan** - a more sensitive way to stage the cancer and look for local or distant spread\n- **CT or MRI head** - may be done as part of staging investigations if curative treatment is planned, or if there are symptoms suspicious of intracranial metastases \n\n# Management \n\n**Conservative:**\n\n- **Holistic support** and an **MDT approach** (e.g. clinical nurse specialist involvement, palliative care input for troubling symptoms or end of life care, signpost to support e.g. Macmillan groups)\n- **Smoking cessation**\n- Discussions around **advance care planning** where appropriate\n\n**Medical**\n\n- **Chemotherapy** is first line in most cases of small cell lung cancer and stage 3 or 4 non-small cell lung cancer - this is with palliative intent (i.e. not aiming to cure the disease but to prolong life and improve symptoms). It is also offered to some patients prior to (neoadjuvant) or after (adjuvant) curative surgery.\n- **Immunotherapy** is also used especially in advanced non-small cell lung cancer; this includes medications such as pembrolizumab or atezolizumab (again with palliative intent).\n- Other **targeted therapies** exist for patients with specific mutations, e.g. erlotinib for patients with advanced non-small cell lung cancers with EGFR-TK mutations.\n- **Radiotherapy** may be curative (for example in early non-small cell lung cancer) or palliative - it is often combined with chemotherapy or other treatment modalities.\n- **Supportive therapies** include analgesia, oxygen if hypoxic and opioid treatment for breathlessness.\n\n**Surgical**\n\n- **Lobectomy** is the standard curative therapy for early stage lung cancers (which can be open or thoracoscopic in approach).\n- Some small tumours can be removed with a **wedge resection.**\n- More extensive surgery such as a **pneumonectomy** (removal of a lung) may be required depending on the size and location of the tumour, however patients need to have adequate FEV1 on pre-operative spirometry to be appropriate for surgery (over 2L for a pneumonectomy).\n- All patients undergoing surgery should also have **mediastinal and hilar lymph nodes sampled** (to look for metastases) or **resected** (removed) to reduce the chances of recurrence.\n\n# Complications\n\n**Common sites of metastatic spread include:**\n\n- Lymph nodes\n- Liver - this can cause significant pain due to stretching of the liver capsule\n- Brain - may cause nausea and vomiting, headaches, seizures, personality changes, sensory or motor symptoms, dysphasia or cerebellar symptoms, depending on where in the brain is affected\n- Bones - mostly osteolytic metastases, can cause bony pain and pathological fractures; there is a risk of metastatic spinal cord compression with vertebral metastases\n- Adrenal glands - may cause flank pain and adrenal insufficiency\n- The contralateral lung or elsewhere in the ipsilateral lung\n\n**Local complications include:**\n\n- Horner’s syndrome - due to an apical (Pancoast) tumour, causes ipsilateral anhidrosis, miosis and partial ptosis\n- Superior vena cava obstruction (SCVO) - lung cancer is the commonest cause of SCVO, causing symptoms of breathlessness, dizziness, headache and swelling of the face, neck and arms. This is a medical emergency due to the risk of airway obstruction.\n- Malignant pleural effusion\n- Hoarse voice - secondary to invasion of left recurrent laryngeal nerve\n- Persistent lower respiratory tract infection due to obstructing tumour\n- Raised hemidiaphragm secondary to invasion of phrenic nerve\n- Brachial plexus injury secondary to tumour invasion from a Pancoast tumour\n\n# Prognosis\n\nOverall prognosis is poor, with an average 5 year survival rate of 17%. This is lower for small cell lung cancer and for metastatic cancers, both of which have around a 5% 5 year survival. Small cell lung cancers are aggressive and are usually metastatic at the time of presentation, hence curative treatment is not possible\n\nIn early stage cancers survival is better, with 70% of patients with stage 1 NSCLC undergoing curative surgery surviving 5 years from diagnosis.\n\n# NICE Guidelines\n\n[Lung cancer: diagnosis and management](https://www.nice.org.uk/guidance/ng122)\n\n[NICE CKS - recognition and referral of lung and pleural cancers](https://cks.nice.org.uk/topics/lung-pleural-cancers-recognition-referral/)\n\n# References\n\n[Radiopaedia - lung cancer](https://radiopaedia.org/articles/lung-cancer-3?lang=gb)\n\n[Patient UK - lung cancer](https://patient.info/doctor/lung-cancer-pro)\n\n[Cancer Research UK - lung cancer statistics](https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/lung-cancer)",
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"question": "A 75-year-old woman presents with worsening joint pain and swelling in her hands, wrists, and knees, along with deep bone aches that disrupt her sleep. She has lost 5kg over the past year with poor appetite. She has no significant medical history, occupational exposure, or smoking history.\n\n\nOn examination, she has clubbing bilaterally. She has symmetrical polyarthritis of the wrists, metacarpal joints and knees; with pain, swelling and reduced range of motion of the affected joints.\n\n\nX-rays of her tibia and fibula are suggestive of periosteal bone formation.\n\n\nChest X-ray shows a left lower lobe mass. The medical team decides to arrange an interventional radiology guided biopsy of the mass lesion.\n\n\nWhich of the following histology findings are most likely?",
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"explanation": "# Summary\r\n\r\nAcute pericarditis is the inflammation of the pericardium, the sac surrounding the heart. It is commonly seen in patients with chest pain following a viral infection, with pain typically relieved by leaning forward. The condition can be caused by various factors including infections (viral, bacterial), malignancies, cardiac causes, radiation, drugs/toxins, and rheumatological diseases. Diagnosis is based on clinical evaluation, ECG findings (ST elevation, PR depression), and imaging such as echocardiogram. Treatment options include NSAIDs, colchicine, and corticosteroids depending on the underlying cause. Complications are rare, and the prognosis is generally excellent with a low risk of long-term sequelae. \r\n\r\n# Definition \r\n\r\nAcute pericarditis is inflammation of the pericardium, the fibroelastic sac that surrounds the heart. Inflammation can also extend to the myocardium (heart muscle), in which case the condition is referred to as perimyocarditis or myopericarditis depending on which is predominant. \r\n\r\n# Epidemiology \r\n\r\nAcute pericarditis is one of the most common causes of pericardial disease and is estimated to occur in approximately 27.7 per 100,000 people annually. \r\n\r\n# Pathophysiology\r\n\r\nThe pathophysiology of pericarditis depends on the cause. The causes of pericarditis are discussed below. \r\n\r\n# Causes\r\n\r\nThe classification of pericarditis can be considered according to cause of the pericarditis. \r\n\r\n* Idiopathic\r\n\r\n* Infective causes\r\n\r\n * Viruses - viruses which cause pericarditis are **coxsackie B viruses**, echovirus, CMV, herpesvirus, HIV among other rarer causes.\r\n * Bacteria - staphylococcus, pneumococcus, streptococcus (rheumatic carditis), haemophilus and M. tuberculosis.\r\n * Fungi and parasites (rare)\r\n\r\n* Malignant causes\r\n\r\n * Lung cancer\r\n * Breast cancer\r\n * Hodgkin's lymphoma\r\n\r\n* Cardiac causes\r\n\r\n * Heart failure may cause pericarditis\r\n * Post-cardiac injury syndrome (Dressler's syndrome) including post-traumatic\r\n\r\n* Radiation - often secondary to therapy for other malignancies\r\n\r\n* Drugs and toxin causes\r\n\r\n * Anthracycline chemotherapy (Doxorubicin)\r\n * Hydralazine\r\n * Isoniazid\r\n * Methyldopa\r\n * Phenytoin\r\n * Penicillins (hypersensitivity)\r\n\r\n* Rheumatological disease\r\n\r\n * Systemic lupus erythematous (SLE)\r\n * Rheumatoid arthritis\r\n * Sarcoidosis\r\n * Vasculitides (Takayasu's, Behcet's)\r\n\r\n* Other causes\r\n * Renal failure (uraemia) - indication for emergency dialysis. \r\n * Hypothyroidism\r\n * Inflammatory bowel disease\r\n * Ovarian hyperstimulation\r\n \r\n# Symptoms\r\n\r\n* Pleuritic chest pain: central, worse on inspiration. \r\n* Postural chest pain: worse on lying flat and relieved on leaning forward.\r\n* Fever\r\n\r\n# Signs\r\n\r\n* Pericardial friction rub - high-pitched scratching noise, best heard over the left sternal border during expiration. Pathogonomonic of pericarditis. \r\n* Pericarditis can lead to the development of a pericardial effusion and cardiac tamponade in which case signs such as hypotension, raised JVP and muffled heart sounds (Beck's Triad) may be present. \r\n\r\n# Differential Diagnoses \r\n\r\n* **Acute Coronary Syndrome** \r\n\t* **Similarities**: both present with chest pain. \r\n\t* **Differences**: pericarditic chest pain is often described as sharp, pleuritic in nature, and relieved on sitting forward. In ACS, the chest pain is often described as a squeezing pressure that is not positional. \r\n\r\n\r\n* **Pleuritic Chest Pain e.g. Pulmonary Embolism or Pneumonia** \r\n\t* **Similarities**: both present with pleuritic chest pain. \r\n\t* **Differences**: PE and pneumonia will often present with very different histories and clinical features. Patients with pneumonia will describe a productive cough and fevers, whereas patients who have a pulmonary embolism will describe acute-onset pleuritic chest pain and will likely have risk factors for VTE. \r\n\r\n* **Musculoskeletal Chest Pain** \r\n\t* **Similarities**: various MSK conditions including costochondritis or muscle strains can cause chest pain that resembles pericarditis. These pains may also be positional. \r\n\t* **Differences**: MSK pain is reproducible with palpation or certain movements. \r\n\r\n\r\n* **Gastro-oesophageal Reflux Disease (GORD)** \r\n\t* **Similarities**: chest pain seen in GORD may be similar to that seen in pericarditis. Those with GORD may describe that symptoms are worse on lying flat, similar to pericarditis. \r\n\t* **Differences**: pericarditic pain is often described as sharp, whereas GORD discomfort may be described as a burning sensation that is worse with certain foods and bending over. \r\n\r\n\r\n# Investigations\r\n\r\nThe diagnosis of pericarditis is often clinical, but the following investigations can help aid diagnosis. \r\n\r\n## Bedside\r\n\r\n**1st line** = ECG \r\n\r\nECG features include: \r\n\r\n* Widespread saddle ST elevation (not following vascular territories) and PR depression. \r\n\r\nECG changes can sometimes evolve over weeks:\r\n\r\n* 1-3 weeks: normalisation of ST changes, T wave flattening\r\n* 3-8 weeks: flattened T waves become inverted\r\n* 8+ weeks: ECG returns to normal\r\n\r\n[lightgallery]\r\n\r\n## Bloods \r\n\r\n* Serial troponins: tend not to peak as in an MI, but tend to stay consistently elevated in the acute phase. \r\n* Inflammatory markers: raised inflammatory markers (WCC, CRP and ESR) are in keeping with an acute pericarditis. \r\n* Viral serology: may help to identify cause of the acute pericarditis. \r\n\r\n## Imaging\r\n\r\n* Echocardiogram - used to assess for pericardial effusion and distinguish between pericarditis and MI (e.g. looking for the absence of regional wall motion abnormalities). \r\n* Angiogram - shows normal coronary arteries (which excludes MI).\r\n* Cardiac MRI - in atypical cases, cardiac MRI can be used to visualise inflammation of the pericardium. \r\n\r\n# Management\r\n\r\n## Idiopathic or Viral Pericarditis \r\n\r\n**1st line**: exercise restriction, NSAIDS (+ PPI) for 1-2 weeks and colchicine for 3 months\r\n\r\n**2nd line**: colchicine (SE: diarrhoea, use in caution in those with renal or hepatic impairment). \r\n\r\n**3rd line**: corticosteroids (for those who cannot tolerate or refractory to NSAIDS). \r\n\r\n## Bacterial Pericarditis \r\n\r\n**1st line**: IV antibiotics +/- pericardiocentesis if purulent exudate present. \r\n\r\nRare cases - pericardectomy may be performed if adhesions or recurrent tamponade occurs. \r\n\r\n## Non-Infective Pericarditis \r\n\r\n**1st line**: corticosteroids (due to the risk of reactivation and if infection has been ruled out). \r\n\r\n# Complications\r\n\r\nComplications are rare but include cardiac tamponade and pericardial effusion requiring pericardiocentesis. In the long term patients occasionally develop constrictive pericarditis.\r\n\r\n# Prognosis \r\n\r\nAcute pericarditis has an excellent prognosis with less than 0.5% going on to develop long-term sequelae (e.g. constrictive pericarditis). \r\n\r\n# NICE Guidelines\r\n\r\n[NICE Guidelines on Cardiac Causes of Chest Pain](<https://cks.nice.org.uk/topics/chest-pain/diagnosis/cardiac-causes/>)\r\n\r\n# References\r\n\r\n[UptoDate Article on Acute Pericarditis: Treatment and Prognosis](<https://www.uptodate.com/contents/acute-pericarditis-treatment-and-prognosis>)",
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"question": "A 32-year-old man presents to his General Practitioner (GP) with a 3-day history of sharp, constant central chest pain. He reports the pain to be worse on inspiration and relieved by sitting forward. On questioning, he reveals a 1-week history of coryzal symptoms and myalgia, which are now improving. He denies cough, shortness of breath or palpitations.\n\nHe has no significant past medical history and examination and all observations are unremarkable.\n\nAn ECG shows widespread PR depression and concave ST elevation.\n\nGiven the likely diagnosis, which of the following is the first-line management?",
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"explanation": "A heart transplant would be reserved for patients with severe heart failure or coronary artery disease that is refractory to all medical and surgical management options. A CABG would be considered first for a patient with triple-vessel disease",
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"comment": "if there was only one or two vessels would stents be the best option? or would CABG still be preferred?",
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"comment": "Why not a PCI?",
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"comment": "AFAIK the choice to perform PCI vs CABG depends on many factors and may be influenced by the surgeon themselves as they may have a preference in terms of expertise. Generally in \"multivessel\" disease, CABG is the preferred option but there are instances where PCI could be used you are correct.\n\nI believe the highest yield takeaway from the question is that the patient is diabetic. Diabetic patients have far more extensive and complex disease of their coronary arteries compared to non diabetic patients. If multi-vessel disease occurs in a diabetic then CABG is strongly preferred over PCI.",
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"comment": "but would you attempt it in an acute setting though? i thought cabg would be done in a subacute setting",
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"explanation": "# Summary\r\n\r\nA coronary artery bypass graft (CABG) is a revascularisation technique used to treat coronary artery disease. It uses harvested blood vessels from other parts of the body to bypass narrowed coronary arteries thus improving blood flow to the heart. It should be considered in those whose symptoms are not controlled by optimal medical management and in those who have complex 3 vessel disease. CABG has an excellent prognosis, with a 5-year survival estimated at 92%. \r\n\r\n# Definition \r\n\r\nA coronary artery bypass graft (CABG) is a revascularisation technique used to treat coronary artery disease. A surgeon uses a healthy blood vessel, usually veins taken from the leg or chest, and attaches it to the heart so blood can get round the narrowed coronary artery. \r\n\r\n# Indication \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\nPCI may be more cost-effective than CABG. However, CABG confers a mortality benefit in patients who are >65 years old, have diabetes, or who have complex 3 vessel disease (with or without left main stem stenosis). \r\n\r\n# Procedure\r\n\r\nWith the patient under general anaesthetic, a midline sternotomy incision is made and the chest is opened. The heart may be placed 'on-pump' or the surgery may be'off-pump'. Blood vessels are usually either harvested from the legs (long saphenous vein) or from the chest (internal mammary artery). These blood vessels are then attached to the heart to bypass narrowed coronary arteries. The procedure often takes between 3-6 hours. Most people make a full requires within 12 weeks. \r\n\r\n# Identifying CABG patients \r\n\r\nCommon signs include: \r\n\r\n* Midline sternotomy scar\r\n* Harvest scars - longitudinal graft scar on either leg. \r\n* No 'click' that you would expect with metallic valve replacement. \r\n\r\n# Complications\r\n\r\nCommon post-operative complications include post-operative bleeding, arrhythmias (most commonly atrial fibrillation), low output cardiac syndrome (requiring inotropes), and midline sternotomy wound infection. \r\n\r\nLong-term complications include narrowing of grafted vessels that require further treatment.\r\n\r\n# Prognosis \r\n\r\nOverall survival at 5 years is estimated at 92%. \r\n\r\n# NICE Guidelines\r\n\n[NICE Guidance for CABG](<https://www.nice.org.uk/guidance/IPG377>)\n\r\n[NICE Guidance on Stable Angina](<https://www.nice.org.uk/guidance/cg126>)\r\n\r\n# References\r\n\r\n[2020 Article on the Role of Revascularisation in Stable Angina](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7305572/)",
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"question": "A 61-year-old man with a background of type 1 diabetes and hypertension presents with a 30-minute history of chest pain radiating to the left jaw, which is unrelieved by rest or glyceryl trinitrate (GTN). He has anterolateral ST elevation on his ECG and is sent for urgent coronary angiography.\n\nCoronary angiography shows significant stenosis of the left anterior descending, left circumflex and right coronary artery.\n\nWhich of the following is the best step in management?",
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"explanation": "Inotropes act to increase myocardial contractility and thereby increase cardiac output. They may be considered, but definitive management with pericardiocentesis should not be delayed",
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"explanation": "This patient has obstructive shock due to pericardial fluid that is reducing ventricular filling and thereby causing reduced cardiac output. Fluid challenges are more useful in the initial management of hypovolaemic (e.g. blood loss) and distributive shock (e.g. sepsis) but would not be as useful in this context",
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"explanation": "Cardiac tamponade is a medical emergency caused by the accumulation of fluid in the pericardial space, leading to reduced ventricular filling and haemodynamic compromise. Management is with pericardiocentesis which aims to remove the pericardial fluid",
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"explanation": "Thoracocentesis is a procedure that aims to remove fluid or air from the pleural space. An emergency thoracocentesis is used for urgent decompression of a tension pneumothorax",
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"explanation": "Although the patient has a raised JVP, they are not in congestive cardiac failure or pulmonary oedema. The raised JVP indicates increased right atrial pressure due to the pericardial fluid causing strain on the heart. As the patient is not fluid overloaded, there would be no benefit of giving diuretics. In this case, it would likely drop the patient's blood pressure further",
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"comment": "Good question but the wording isn’t clear - surely it should be best next step in management as pericardiocentesis is not necessarily definitive (fluid can reaccumulate in the pericardium if inflammation doesn’t clear up)",
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"comment": "This definitive thing got me all kinds of confused.",
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"explanation": "# Summary\n \nCardiac tamponade is a life-threatening emergency that occurs when fluid (or occasionally gas or malignant tissue) accumulates in the pericardial sac, compressing the heart and impairing cardiac filling. It is often caused by trauma leading to bleeding into the pericardial sac, but may also result from pericarditis or malignancy. Beck's triad refers to the classical findings of a raised jugular venous pressure (JVP), hypotension and muffled heart sounds. Diagnosis can be reached rapidly with an echocardiogram. Pericardiocentesis is the usual emergency treatment. \n\n# Definition\n \nCardiac tamponade refers to the compression of the heart by fluid accumulation (often blood, occasionally gas or malignant tissue) in the pericardial sac. This compression impairs cardiac filling during diastole, compromising cardiac output and rapidly leading to cardiac arrest if untreated. \n \n# Aetiology\n \nThe commonest cause of acute cardiac tamponade is trauma, especially penetrating injuries. These may occur in road traffic accidents.\n\nIatrogenic causes (e.g. cardiothoracic surgery) can also lead to blood tamponading the heart. \n\nOther causes include:\n\n- Pericarditis, which may be secondary to:\n - Malignancies\n - Myocardial infarction\n - Infections e.g. HIV, tuberculosis\n - Connective tissue diseases\n - Radiation\n - Chronic kidney disease\n- Aortic dissection\n- Medications (e.g. minoxidil, hydralazine)\n- Cardiac perforation during diagnostic procedures\n- Pneumopericardium (e.g. secondary to a gastropericardial fistula)\n\n# Signs and Symptoms\n\nThe presentation of cardiac tamponade varies depending on the underlying cause and on how acutely it has developed. \n\nSymptoms include:\n\n- Fatigue\n- Dyspnoea\n- Cold and clammy peripheries due to hypoperfusion\n- Confusion due to reduced cardiac output\n\nSigns include:\n\n- Beck's triad (raised jugular venous pressure, hypotension and muffled heart sounds)\n- Pulsus paradoxus (a decrease in systolic blood pressure by more than 10 mmHg during inspiration)\n- Tachycardia\n- Tachypnoea\n- Altered mental state\n- Hepatomegaly\n- Pericardial friction rub\n- Cyanosis\n- JVP shows an absent Y descent (due to reduced diastolic filling of the ventricles)\n\n# Differential Diagnosis\n\n- **Acute heart failure** - overlapping features of dyspnoea and peripheral oedema, pulmonary oedema can occur in tamponade. Can be distinguished with echocardiography (showing ventricular dysfunction in heart failure).\n- **Constrictive pericarditis** occurs when the pericardium is rigid or thickened (rather than fluid in the pericardial sac). It is usually chronic rather than acute, pericardial calcification may be seen on chest X-ray and Kussmaul's sign may be seen (when venous distention and pressure paradoxically increase in inspiration - rare in tamponade).\n- **Pulmonary embolism** also causes sudden onset dyspnoea, associated with pleuritic chest pain and may have haemoptysis. Can also lead to cardiac arrest if massive; distinguished with echocardiography in the emergency setting and CTPA if stable enough for CT.\n- **Tension pneumothorax** can also result from trauma and lead to rapid cardiac arrest, also causes acute dyspnoea but can be distinguished with examination findings of unilateral hyperresonance and reduced breath sounds, tracheal deviation to the contralateral side. \n \n\n# Investigations\n\n**Bedside tests:**\n\n- **ECG** may show electrical alternans, where the height of QRS complexes alternate due to movement of the heart in the pericardial space \n\n**Blood tests:**\n\n- **Full blood count and CRP** looking for raised inflammatory markers in infective or inflammatory causes of tamponade\n- **U&Es** as uraemia may cause pericarditis leading to tamponade\n- **Coagulation screen** is important if attempting interventions such as pericardiocentesis\n- **HIV testing** if this is a suspected cause of pericarditis\n- **Group and Save** especially if bleeding is the cause of tamponade\n- **Troponin** may be elevated in cardiac trauma or myocardial infarction\n\n**Imaging:**\n\n- An **echocardiogram** is the usual diagnostic test, looking for a pericardial effusion and evidence of impaired cardiac function\n- **Chest X-ray** may show cardiomegaly; the epicardial fat pad sign may be seen (suggestive of pericardial effusion)\n- **CT** sometimes detects evidence of tamponade (e.g. in the context of trauma)\n\n**Other tests:**\n\n- If the cause of tamponade is not clear, fluid drained from a pericardial effusion should be sent for culture and cytology\n\n# Management\n\n- Call for help - alert cardiology and intensive care\n- Supportive therapies e.g. oxygen, IV fluids and inotropes\n- Avoid positive-pressure ventilation as this may decrease venous return, worsening cardiac output\n- Perform **pericardiocentesis** (aspirating pericardial fluid, usually at the bedside under echocardiography guidance)\n- Open surgical drainage may be required in some cases e.g. ongoing intrapericardial bleeding\n- Options for recurrent tamponade include percutaneous balloon pericardiotomy, pericardiodesis or pericardiectomy\n- Treat the underlying cause e.g. infection, repair of traumatic injuries\n \n# References\n\n[Radiopaedia - Cardiac Tamponade](https://radiopaedia.org/articles/cardiac-tamponade)\n\n[Patient UK - Cardiac Tamponade](https://patient.info/doctor/cardiac-tamponade)\n\n[European Society of Cardiology - Cardiac Tamponade](https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-15/Cardiac-tamponade-a-clinical-challenge)",
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"question": "A 45-year-old man with a diagnosis of myocarditis is assessed following an episode of hypotension on the ward. On assessment, he is tachycardic and tachypnoeic with a blood pressure of 90/50 mmHg. He has a raised jugular venous pressure (JVP) and his heart sounds are difficult to auscultate.\n\nAn urgent bedside ECHO shows cardiac tamponade.\n\nWhich of the following is the best definitive step in management?",
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"explanation": "MRSA indicates that the staphylococcus aureus species are resistant to flucloxacillin. IV flucloxacillin for 4-6 weeks would be the treatment of methicillin-susceptible Staphylococcus aureus in a patient with native valve (i.e. no prosthetic valves) endocarditis",
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"explanation": "This would be a treatment option for a patient with native valve streptococcal endocarditis. Benzylpenicillin would not work for staphylococcal species",
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"explanation": "MRSA indicates that the staphylococcus aureus species are resistant to β-lactam antibiotics. In this case, for a patient with confirmed MRSA and without any prosthetic heart valves, the BNF advises treatment with vancomycin and rifampicin for 4 weeks",
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"explanation": "This is the empirical treatment for native valve endocarditis. As MRSA has been cultured, this regime needs to be escalated to vancomycin (and gentamicin) as amoxicillin will not cover MRSA",
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"comment": "was gonna be one or the other",
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"explanation": "# Summary\r\n\r\nInfective endocarditis (IE) is a rare infection of the inner surface of the heart (endocardium), usually the valves. Various risk factors contribute to its development, including age, sex, intravenous drug use, poor dentition, valvular disease, congenital heart disease, prosthetic valves, and certain medical conditions like HIV. Symptoms can be diverse and non-specific including fevers, night sweats, weight loss, and myalgia. Diagnosis is based on the modified Duke Criteria, which include major and minor criteria. Treatment involves prolonged courses of intravenous antibiotics, and surgical intervention may be necessary in certain cases. Complications can be severe, and without appropriate treatment, IE can lead to heart failure and death. Prevention through antibiotic prophylaxis is no longer recommended.\r\n\r\n# Definition \r\n\r\nInfective endocarditis (IE) is the infection of the inner surface of the heart (endocardium), usually the valves. \r\n\r\n# Epidemiology \r\n\r\nInfective endocarditis is a rare disease, impacting approximately 2-6 per 100,000 people every year. There are many risk factors implicated in the development of IE. \r\n\r\nRisk factors for IE: \r\n\r\n* Age >60 years\r\n* Male sex\r\n* IVDU: predisposition to _Staph. aureus_ infection and right-sided valve disease e.g. tricuspid endocarditis.\r\n* Poor dentition and dental infections\r\n* Valvular disease: rheumatic heart disease, mitral valve prolapse, aortic valve disease and any other valvular pathology. \r\n* Congenital heart disease: bicuspid aortic valve, pulmonary stenosis, and ventricular septal defects.\r\n* Prosthetic valves\r\n* Previous history of infective endocarditis\r\n* Intravascular devices: central catheters and shunts.\r\n* Haemodialysis\r\n* HIV infection\r\n\nAntibiotics have previously been prescribed to at-risk patients undergoing interventional procedures, frequently in dentistry, with the rationale that resultant bacteraemia could threaten to cause infective endocarditis. However, the evidence for this is inconclusive, and **NICE therefore do not advise antibiotic prophylaxis for IE.**\r\n\r\n# Pathophysiology\r\n\r\nA damaged endocardium can contribute to the development of IE. When part of the endocardium is damaged, the heart valve forms a local blood clot known as non-bacterial thrombotic endocarditis (NBTE). The platelets and fibrin deposits that form as part of the clotting process allows bacteria to stick to the endocardium leading to the formation of vegetations. The valves do not have a dedicated blood supply and so the body is unable to launch an appropriate immune response to the vegetations. The combination of damaged endocardium, vegetation development, and lack of an appropriate immune response results in infective endocarditis. \r\n\r\n# Classification \r\n\r\nIE can be considered according to different classification systems. \r\n\r\n## Acute vs. Subacute vs. Chronic IE \r\n\r\nIE can be considered according to duration of symptoms. \r\n\r\n* *Acute IE*: patient has signs or symptoms for days up to 6 weeks. Theoretically, a fulminant illness with rapid progression and so is most likely due to *S.aureus* infection. \r\n* *Subacute IE*: patients has signs or symptoms for 6 weeks up to 3 months. \r\n* *Chronic IE*: patients has signs or symptoms that persist for longer than 3 months. \r\n\r\n## Valve Type \r\n\r\nIE can be considered according to the type of valve involved. \r\n\r\n- *Native-valve endocarditis*: patient without prosthetic valve implant. \r\n- *Prosthetic-valve endocarditis*: \r\n\t- Early prosthetic valve endocarditis occurs within 1 year of surgery. This is usually due to intra-operative contamination or post-operative nosocomial contamination. \r\n\t- Late prosthetic valve endocarditis occurs beyond 1 year of surgery. This is usually due to community-acquired infections. \r\n\r\n# Common organisms \r\n\r\nThe most common organisms involved in infective endocarditis (in order of incidence) are:\r\n\r\n* _Staph. aureus_: now the most common cause of IE. Coagulase positive.\r\n* _Strep. viridans_: used to be the most common cause of IE. Implicated in patients with poor dental hygiene. \r\n* Enterococci\r\n* Coagulase negative _staphylococci_ e.g. _staph. epidermidis_: common culprit of prosthetic valve endocarditis. \r\n* _Strep. bovis_: important link with colorectal cancer. Need to consider colonoscopy and biopsy in these patients.\r\n* Fungal \r\n* HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella): culture negative causes of IE. \r\n* Non-infective: marantic endocarditis (malignancy - pancreatic cancer), Libman-Sacks endocarditis (SLE). \r\n\r\n# Symptoms\r\n\r\nClinical features of IE are diverse and variable. It may present acutely with a rapid deterioration or it can present subacutely/chronically with non-specific symptoms. \r\n\r\n* Common presenting symptoms: \r\n\t* Fever: most common symptom. \r\n\t* Night sweats \r\n\t* Anorexia \r\n\t* Weight loss \r\n\t* Myalgia\r\n\r\n* Others: \r\n\t* Headache \r\n\t* Arthalgia\r\n\t* Abdominal Pain \r\n\t* Cough \r\n\t* Pleuritic pain \r\n\r\n# Signs\r\n\r\n**Systemic signs**: \r\n\r\n* Febrile \r\n* Cachectic \r\n* Clubbing\r\n* Splenomegaly \r\n\r\n**Cardiac**: \r\n\r\n* Murmur: fever + new murmur is infective endocarditis until proven otherwise. \r\n* Bradycardia: aortic root abscess tracks down to the AVN causing heart block. \r\n\r\n**Vascular phenomena**: \r\n\r\n* Septic emboli: abdominal pain due to splenic infarct/abscess, focal neurology due to stroke, gangrenous fingers. \r\n* Janeway lesions: painless haemorrhagic cutaneous lesions in the palms and soles. \n* Splinter haemorrhages\r\n\r\n**Immunological phenomena**: due to immune-complex deposition. \r\n\r\n* Osler's nodes: painful pulp infarcts on end of fingers. \r\n* Roth spots: boat-shaped retinal haemorrhages with pale centres seen on fundoscopy. \r\n* Glomerulonephritis: identified on urine dip. \r\n\r\n# Differential Diagnoses\r\n\r\n* Non-infectious endocarditis/Nonbacterial thrombotic endocarditis (NBTE)\r\n\t* Similarities: both present with new murmurs and both may have constitutional symptoms including fevers and weight loss. \r\n\t* Differences: blood cultures will likely be positive in infective endocarditis and may identify microorganisms that are commonly associated with IE. NBTE is often associated with advanced malignancy (pancreatic cancer and marantic endocarditis), SLE (Libman Sacks endocarditis) or hypercoagulable states and will not have positive blood cultures. \r\n\r\n* Rheumatic Fever\r\n\t* Similarities: may both present with similar symptoms including fever, heart murmur and joint pain. \r\n\t* Differences: rheumatic fever is an autoimmune response triggered by a Group A strep infection and ASOT titres may be high. In comparison, infective endocarditis will likely have positive blood cultures that identify a particular micro-organism. \r\n\r\n\r\n# Modified Duke Criteria \r\n\r\nFor the diagnosis of IE, the modified Duke Criteria needs to be followed. \r\n\r\nA useful mnemonic to remember the criteria is **'BE FIVE PM'**:\r\n\r\n* Major Criteria: \r\n\t* **B**lood Cultures\r\n\t* **E**vidence of Endocardial Involvement: **E**cho\r\n\r\n* Minor Criteria: \r\n\t* **F**ever\r\n\t* **I**mmunological phenomena\r\n\t* **V**ascular phenomena\r\n\t* **E**chocardiogram minor criteria\r\n\t* **P**redisposing features\r\n\t* **M**icrobiological evidence that does not meet major criteria. \r\n\r\nFor a definitive diagnosis of IE two major criteria, or one major and three minor criteria, or all five minor criteria must be present. \r\n\r\n## Major Criteria \r\n\r\n**Blood culture positive for IE**\r\n\r\n* 2x separate positive blood cultures showing typical microorganisms consistent with IE (S viridans, S bovis, HACEK organisms, enterococcus). \r\n* Persistent bacteraemia with 2x blood cultures >12 hours apart or =>3 positive blood cultures with less specific microorganisms (S.aureus or S. epidermidis). \r\n* Single positive blood culture for Coxiella burnetti or positive antibody titre\r\n\r\n**Evidence of endocardial involvement with imaging positive for IE**\r\n\r\n* Echocardiogram (1st line TTE, then TOE) demonstrating vegetation, abscess, partial dehiscence of prosthetic valve or new valvular regurgitation. \r\n* Abnormal activity around site of prosthetic valve implantation on PET-CT\r\n* Paravalvular lesions on cardiac CT\r\n\r\n## Minor Criteria \r\n\r\n* **Fever**: >38.0 degrees celsius. \r\n* **Immunological phenomena**: Roth spots, Olser's nodes, immune complex-mediated glomerulonephritis, positive rheumatoid factor.\r\n* **Vascular phenomena**: Evidence of septic embolis (splenic infarct/abscess), Janeway lesions, conjunctival haemorrhages, mycotic aneurysm, intracranial haemorrhage. \r\n* **Echocardiogram minor criteria**: not meeting above criteria. \r\n* **Predisposing features**: known valvular disease, IVDU, prosthetic valves etc. \r\n* **Microbiological evidence that does not meet major criteria**: blood culture not meeting major criteria, or serological evidence of active infection with organism consistent with IE\r\n\r\n# Investigations\r\n\r\nBedside:\r\n\r\n- **ECG**: increasing prolongation of PR interval suggests development and worsening of aortic root abscess. \n- **Urine dip**: look for haematuria which may suggest development of glomerulonephritis. \r\n\r\nBlood tests:\r\n\r\n- **Routine bloods**: significant elevation of inflammatory markers and acute phase response is in line with infective endocarditis. If subacute/chronic process there may be a normocytic anaemia. \r\n- **Blood cultures**: required as per the modified Duke criteria. At least 3 sets of blood cultures taken at different times and sites. \r\n\r\nImaging:\r\n\r\n- **Echocardiogram**: \r\n\t* **1st line**: transthoracic echocardiogram \r\n\t* **2nd line**: transoesophageal echocardiogram; more invasive, but better view of mitral valve lesions and aortic root abscesses. It is the most sensitive diagnostic test. \r\n- **PET CT**: used to look for evidence of septic emboli. \r\n\r\n# Management\r\n\r\n## Medical \r\n\r\nMainstay of treatment for infective endocarditis is a prolonged course of IV antibiotics (approximately 6/52). Patients commonly require midline insertion to enable administration of IV antibiotics long-term. \r\n\r\nExamples of antibiotic choice demonstrated below: \r\n\r\n**Blind Therapy** when the organism and sensitivities are not yet known: \r\n\r\n* Native valve: amoxicillin (+/- gentamicin) \r\n* Pen-allergy/MRSA: vancomycin (+/- gentamicin) \r\n* Prosthetic valve: vancomycin + rifampicin + gentamicin \r\n\r\n**Native Valve S. aureus IE**\r\n\r\n* 1st line: flucloxacillin \r\n* 2nd line: vancomycin + rifampicin \r\n\r\n**Prosthetic Valve S. aureus IE**\r\n\r\n* 1st line: flucloxacillin + rifampicin + gentamicin \r\n\r\n\r\n**Strep viridans IE**\r\n\r\n* 1st line: benzylpenicillin \r\n* 2nd line: vancomycin + gentamicin \r\n\r\n**HACEK IE**: 1st line: ceftriaxone \r\n\r\n## Surgical \r\n\r\nDespite the main-stay of treatment for IE being medical management. The following scenarios are indications for surgical intervention: \r\n\r\n* Haemodynamic instability\r\n* Severe heart failure\r\n* Severe sepsis despite antibiotics/failed medical therapy\r\n* Valvular obstruction\r\n* Infected prosthetic valve\r\n* Persistent bacteraemia\r\n* Repeated emboli\r\n* Aortic root abscess\r\n\r\n**Common exam question**: PR interval prolongation in a patient with Infective Endocarditis is an indication for surgery as it can be secondary to aortic root abscess\r\n\r\n# Complications\r\n\r\nComplications of infective endocarditis can also be the initial presenting complaint\r\n\r\n* Acute valvular insufficiency causing heart failure\r\n* Neurologic complications e.g. stroke, abscess, haemorrhage (mycotic aneurysm)\r\n* Embolic complications causing infarction of kidneys, spleen or lung\r\n* Infection e.g. osteomyelitis, septic arthritis\r\n\r\n\r\nWithout timely and appropriate treatment, IE can rapidly lead to heart failure and death. The mortality rate within the first 30 days has been estimated at approximately 20%. Long-term survival for IE has been estimated at 50% at 10 years. The mortality in IE remains high. \r\n\r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines on Prophylactic Antibiotics in IE](https://www.nice.org.uk/guidance/cg64/ifp/chapter/infective-endocarditis)\r\n\r\n# References \r\n\n[American Heart Association Summary on Heart Valves and Endocarditis](<https://www.heart.org/en/health-topics/heart-valve-problems-and-disease/heart-valve-problems-and-causes/heart-valves-and-infective-endocarditis#:~:text=What%20is%20infective%20endocarditis%3F,greater%20risk%20of%20developing%20it.>)",
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"question": "A 35-year-old man with no previous past medical history presents with a 3-week history of intermittent fevers and night sweats. There are no localising symptoms of infection.\n\nOn examination, he is tachycardic and febrile with an early diastolic murmur noted over the left sternal edge.\n\nHe is treated empirically for infective endocarditis. Blood cultures subsequently grow methicillin-resistant staphylococcus aureus (MRSA).\n\nWhich of the following is the best antimicrobial regime?",
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"explanation": "# Summary\r\n\r\nWolff-Parkinson-White (WPW) syndrome is a congenital pre-excitation syndrome characterised by the presence of an abnormal accessory electrical pathway between the atria and ventricles. This pathway predisposes individuals to arrhythmias, including supraventricular tachycardias (SVTs) that can potentially lead to ventricular fibrillation. Diagnosis is based on electrocardiogram (ECG) findings such as delta waves, short PR interval, and broadened QRS complex. Management options include conservative monitoring, medical treatment with anti-arrhythmics, and definitive treatment through radiofrequency ablation of the accessory pathway. Emergency management of tachyarrhythmias in WPW syndrome varies based on patient stability and the specific rhythm present. Successful ablation has a high cure rate of 95%.\r\n\r\n# Definition \r\n\r\nWPW syndrome is a congenital pre-excitation syndrome that occurs due to the presence of an accessory electrical pathway between the atria and ventricles. It predisposes patients to supraventricular tachycardias, specifically an AVRT. \r\n\r\n# Epidemiology \r\n\r\nThe prevalence of WPW syndrome is approximately 100-300 per 100,000 people. Men are more commonly affected than women, with the ratio being approximately 2 to 1. \r\n\r\n# Classification \r\n\r\nWPW syndrome can be classified as Type A or Type B dependent on where the aberrant pathway is. \r\n\r\nType A \r\n\r\n* Pathway between the left atrium and ventricle. \r\n\r\nType B \r\n\r\n* Pathway between the right atrium and ventricle. \r\n\r\n\r\n# Symptoms and Signs\r\n\r\nPatients may present with:\r\n\r\n* No symptoms - WPW is often asymptomatic\r\n* Palpitations\r\n* Dizziness\r\n* Syncope\r\n\r\nThere are often no signs on examination unless the patient is currently experiencing a paroxysmal episode of SVT. \r\n\r\n# Investigations\r\n\r\n## Bedside\r\n\r\n**1st line = ECG** \r\n\r\n* Delta waves (slurred upstroke in the QRS) \r\n* Short PR interval (<120ms) \r\n* Broadened QRS complex \r\n* If a re-entrant circuit has developed the ECG will show a narrow complex tachycardia. \r\n\r\n[lightgallery]\r\n\r\nIf a patient is experiencing paroxysmal symptoms a 24 hour tape may be used for continuous monitoring. \r\n\r\n## Bloods \r\n\r\nRoutine bloods including TFTs should be completed to investigate non-cardiac causes of tachycardia. \r\n\r\n## Imaging\r\n\r\n* Echocardiogram: to assess for structural cardiac disease and to assess ventricular function. \r\n* Cardiac catheterisation - electrophysiological studies can help map the location of the accessory pathway and identify a focus for ablation. \r\n\r\n# Long-Term Management\r\n\r\n## Conservative \r\n\r\nWPW syndrome may just be monitored if asymptomatic. The majority of patients identified with ECG findings of pre-excitation do not develop tachyarrhythmias. \r\n\r\n## Medical \r\n\r\nAnti-arrhythmics may be used if a patient is having paroxysmal SVT. Medications include amiodarone and sotalol. These are contraindicated in structural heart disease. \r\n\r\n**Contraindications in WPW**: medications that block the AVN are contraindicated in WPW. If you block the AVN, more electrical activity is conducted down the accessory pathway prediposing to dangerous arrhythmias. Digoxin, adenosine, and non-dihydropyridine calcium-channel blockers (verapamil and diltiazem) are therefore contraindicated. \r\n\r\n## Interventional and Surgical \r\n\r\nDefinitive management of WPW syndrome is radiofrequency ablation of the accessory pathway. Rarely, surgical (open heart) ablation can be performed in complex cases. \r\n\r\n# Emergency Management\r\n\r\n**If a patient with WPW presents with a tachyarrhythmia manage as follows:** \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**\r\n\r\n*If the patient is stable they are managed according to the rhythm:*\r\n\r\n* In WPW patients with a narrow complex tachycardia with a short PR interval management is as per SVT management guidelines. \r\n\t* **1st line = vagal manouevres:** Valsalva manouevre or carotid sinus massage. \r\n\t* **2nd line = adenosine**\r\n\r\n* In WPW patients with a broad complex tachycardia, atrial fibrillation, or atrial flutter\r\n\t* **1st line = IV anti-arrhythmics:** procainamide or fleicanide as they help prevent rapid conduction through the accessory pathway. \r\n\t* **2nd line = DC cardioversion**\r\n\r\n# Complications\r\n\r\nDue to the accessory pathway in WPW, if a patient develops atrial fibrillation this can pass to ventricles, bypassing the AVN, and causing ventricular fibrillation and cardiac arrest. \r\n\r\n# Prognosis \r\n\r\nIt is estimated that there is a 95% success rate if WPW syndrome is treated with ablation. If radiofrequency ablation is successful, the WPW is considered cured. \r\n\r\n# NICE Guidelines\r\n\n[NICE Guidance on Palpitations](<https://cks.nice.org.uk/topics/palpitations/diagnosis/assessment/#:~:text=Wolff%2DParkinson%2DWhite%20(WPW)%20syndrome.&text=Slight%20widening%20of%20the%20QRS,syndrome%20can%20cause%20paroxysmal%20tachycardia.>)\r\n\r\n# References \r\n\n[Patient UK Information on WPW Syndrome](<https://patient.info/doctor/wolff-parkinson-white-syndrome-pro>)",
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"question": "A 23-year-old man presents to his General Practitioner (GP) with two brief episodes of syncope that were preceded by palpitations. He was admitted the previous year with palpitations which were found to be due to supraventricular tachycardia (SVT) that responded to initial management with vagal manoeuvres.\n\nClinical examination is unremarkable and his observations are normal. An ECG shows a short PR interval and a widespread slurred upstroke on the QRS complexes.\n\nWhich of the following is the best step in management?",
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"explanation": "Ranolazine is a potassium channel activator. NICE guidelines suggest adding ranolazine only after considering the use of both a calcium channel blocker and beta-blocker",
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"explanation": "NICE guidelines suggest that the first-line management for patients with angina is either a beta-blocker (e.g. bisoprolol) or a calcium-channel blocker (e.g. amlodipine). The initial drug should be up-titrated before switching to the other option or using a combination of the two",
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"comment": "I thought you SHOULD give a non-dihydropyridine as it acts on the heart directly, compared to non-rate limiting CCBs which would cause widespread vasodilation and so induce tachycardia as a reflex...which would worsen the angina? no?",
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"comment": "on research, is this correct to assume then:\n- give a non-dihydro. as first line if BB contraindicated\n- give a dihydro. if must be given with a BB as second line, due to risk of heart block (if non-dihydro. given in conjunction with a BB)\n...is this correct? any help would be great cheers",
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"comment": "Yep - you've got it",
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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 56-year-old man with a history of angina presents to his GP with central chest pain on exercise that is now occurring more frequently. The pain usually lasts a few minutes and is relieved by sublingual glyceryl trinitrate (GTN) spray. He denies any pain at rest, and an ECG shows no ischaemic changes.\n\nHis only current medications anti-anginal medication is bisoprolol which has been up-titrated to the maximum tolerated dose.\n\nWhich of the following is the next step in management?",
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"explanation": "# Summary\n\nErythema nodosum is a panniculitis subtype characterised by tender, red, raised nodules typically affecting the shins. The cause is often idiopathic, although associations with certain medications and diseases like sarcoidosis and inflammatory bowel disease are known. Diagnosis is clinical, with the disease usually resolving spontaneously. Management primarily focuses on treating the underlying cause, if identified, and providing symptomatic relief.\n\n# Definition\n\nErythema nodosum represents a form of panniculitis, or inflammation of the subcutaneous fat, which manifests as tender, raised, erythematous nodules predominantly affecting the shin area.\n\n# Epidemiology\n\nErythema nodosum affects a broad range of individuals and is more common in women than men. Although it can occur at any age, it typically affects individuals between 20-30 years of age.\n\n# Aetiology\n\nThe aetiology of erythema nodosum is often idiopathic, accounting for up to 50% of cases. Other identifiable causes, conveniently remembered by the acronym **NODOSUM**, include:\n\n- **NO** cause (Idiopathic)\n- **D**rugs, particularly sulfonamides and dapsone\n- **O**ral contraceptive pill (OCP)\n- **S**arcoidosis\n- **U**lcerative colitis and Crohn's disease\n- **M**icroorganisms: Tuberculosis, Streptococcus, Toxoplasmosis\n\n# Signs and Symptoms\n\nClinically, erythema nodosum presents as:\n\n- Tender, raised, red or violet nodules, usually located on the anterior surface of the legs.\n- Accompanied by systemic symptoms such as fever, malaise, and arthralgia in some cases.\n\n[lightgallery]\n\n[lightgallery1]\n\n# Differential Diagnosis\n\nThe differential diagnoses for erythema nodosum and their key signs and symptoms include:\n\n- **Cellulitis**: Characterised by local warmth, redness, swelling and tenderness, fever, and possibly lymphadenopathy.\n- **Deep vein thrombosis (DVT)**: Presents with pain, swelling, and redness of the affected limb; Homan's sign might be present.\n- **Necrobiosis lipoidica**: Typically presents as shiny, reddish-brown patches which slowly grow into larger plaques with a yellowish centre.\n- **Vasculitis**: Manifests with palpable purpura, ulcers, or digital infarcts.\n\n# Investigations\n\nWhile erythema nodosum is primarily diagnosed clinically, additional investigations may be performed to rule out underlying causes. These can include:\n\n- Full Blood Count (FBC)\n- Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)\n- Throat culture for streptococci\n- Chest x-ray (to rule out sarcoidosis or tuberculosis)\n- Tests for inflammatory bowel disease if suspected (e.g. colonoscopy)\n\n\n# Management\n\nThe management of erythema nodosum primarily involves treating the underlying cause, if identified. Additional strategies include:\n\n- Nonsteroidal anti-inflammatory drugs (NSAIDs) to alleviate pain and inflammation\n- Rest and leg elevation\n- Potassium iodide or colchicine may be used in severe cases\n- Corticosteroids are used sparingly and typically reserved for severe, refractory cases\n\n# References\n\n[Erythema Nodosum - DermNet NZ](https://dermnetnz.org/topics/erythema-nodosum)",
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"comment": "nothing in the quesbook about a rash in this condition ",
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"comment": "vascultis diseases tend to present with purpuric rash",
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"comment": "Features\nupper respiratory tract: epistaxis, sinusitis, nasal crusting\nlower respiratory tract: dyspnoea, haemoptysis\nrapidly progressive glomerulonephritis ('pauci-immune', 80% of patients)\nsaddle-shape nose deformity\nalso: vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions",
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"explanation": "# Summary\n\nGranulomatosis with polyangiitis (GPA), previously known as Wegener's granulomatosis, is an ANCA associated vasculitis affecting small and medium sized vessels. The classic triad of manifestations is of upper respiratory tract involvement, lower respiratory tract involvement, and pauci-immune glomerulonephritis. Additional organs may be involved, including the skin, the eyes and the peripheral nerves. Key investigations are blood tests including ANCA (c-ANCA is usually positive), chest X-ray or CT showing nodules +/- cavitation and biopsy (showing necrotising granulomas with associated vasculitis). Acute management is usually with steroids with another immunosuppressive agent, the choice of which is dependent on the severity of disease. Steroids should be tapered once remission is achieved whilst another immunosuppressant is continued.\n\n# Definition\n\nGranulomatosis with polyangiitis (GPA), formerly known as Wegener's granulomatosis, is a chronic granulomatous ANCA-associated vasculitis that primarily involves the upper and lower respiratory tracts and the kidneys. \n\n# Epidemiology\n\n- GPA is a rare disease with an annual incidence of 8.4 per million\n- Men are slightly more likely to be affected\n- Onset peaks between the ages of 35 to 55\n- There is a higher incidence of cases seen in the winter, suggesting that environmental exposures such as infections may trigger GPA\n- There is also a slightly increased risk in first degree relatives of people with GPA, indicating a genetic predisposition\n\n# Signs and Symptoms\n\nThe classic triad involved in GPA is as follows:\n\n- **Upper respiratory tract** \n- Chronic sinusitis with nasal obstruction and facial pain\n- Rhinorrhoea which is often bloody\n- Epistaxis\n- Ulceration and crusting in and around the nose\n- Destruction of nasal cartilage leading to a saddle-nose deformity \n- Subglottis stenosis may present with hoarseness, stridor or airway obstruction\n- Otitis media causing ear pain and fullness\n- Hearing loss\n- **Lower respiratory tract**\n- Cough\n- Haemoptysis due to pulmonary haemorrhage\n- Dyspnoea\n- Pleuritic chest pain\n- Wheeze\n- **Necrotising glomerulonephritis**\n- Haematuria\n- Frothy urine due to proteinuria\n- Oliguria\n\n**Systemic signs and symptoms** are common:\n\n- Fatigue\n- Malaise\n- Fevers\n- Night sweats\n- Anorexia\n- Weight loss\n- Arthralgia or arthritis\n\nOther organs may also be affected, for example:\n\n- **Skin**\n- Palpable purpura\n- Nodular, papular or vesicular rashes\n- Ulcers\n- **Eyes**\n- Granulomatous disease may cause an inflammatory mass in the orbit leading to proptosis \n- The optic nerve may also be compressed\n- Vasculitis may cause conjunctivitis, episcleritis, scleritis, uveitis, retinitis or optic neuritis\n- Eye pain, redness and visual loss may occur\n- **Peripheral nerves**\n- Mononeuritis multiple is the usual pattern seen\n- Sensory and motor deficits are seen in the distribution of particular peripheral nerves\n- Pain and paraesthesias of affected areas are common\n- **Central nervous system**\n- Granulomatous lesions\n- Vasculitis causing infarction\n- Intracranial haemorrhage\n- Symptoms include headaches, cranial nerve lesions, seizures, focal neurological deficits and altered consciousness\n- **Gastrointestinal (GI) tract**\n- Mouth ulcers\n- Strawberry gums (hyperplastic gingival lesions)\n- Ulceration elsewhere in the GI tract leading to bleeding or perforation\n- Ischaemic bowel disease\n- Symptoms include abdominal pain, vomiting and diarrhoea\n- **Heart**\n- Pericarditis or myocarditis\n- Coronary arteritis\n- Valvular disease\n- Conduction deficits\n- Symptoms include chest pain, dyspnoea, palpitations and dizziness\n\n# Differential Diagnosis\n\n- **Eosinophilic granulomatosis with polyangiitis** is another ANCA-associated systemic vasculitis which may share features of sinusitis, lung and renal involvement however almost all patients have asthma and eosinophilia\n- **Microscopic polyangiitis** is also an ANCA-associated systemic vasculitis which classically involves the lungs and kidneys, as well as the eyes, peripheral nerves, GI tract and skin, however features of sinusitis are not present\n- **Anti-GBM disease** (also known as Goodpasture's syndrome) causes diffuse pulmonary alveolar haemorrhage and rapidly progressive glomerulonephritis; antibodies against the glomerular basement membrane (GBM) are the key differentiating investigation; ANCA may also be positive\n- **Polyarteritis nodosa** also causes systemic symptoms and commonly involves the kidneys, however pulmonary involvement is very rare unlike in GPA\n- **IgA vasculitis** is an immune complex-mediated small vessel vasculitis that typically affects children; palpable purpura on the legs, abdominal pain and renal involvement are all shared features\n- **Infective endocarditis** causes similar systemic symptoms (e.g. fevers, malaise, weight loss) and septic emboli can affect the lungs and kidneys as well as the central nervous system\n- **Malignancy** may cause similar systemic symptoms of weight loss, fatigue, malaise and low-grade fevers, and specific malignancies may cause symptoms that mimic GPA (e.g. haemoptysis due to lung cancer, haematuria due to urological malignancies)\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urine dip** for blood and protein\n- **Urinary protein:creatine ratio** if proteinuria present on urinalysis\n- **Urine microscopy** may show red blood cell casts\n\n**Blood tests:**\n\n- **Full blood count** which may show a normocytic anaemia and thrombocytosis due to chronic inflammation, or a microcytic anaemia due to alveolar haemorrhage or GI bleeding\n- **U&Es** looking for renal impairment due to glomerulonephritis\n- **LFTs** may show hypoalbuminemia due to inflammation or proteinuria\n- **CRP** and **ESR** are raised due to systemic inflammation\n- **Bone profile** is typically normal, hypercalcaemia should raise suspicion of malignancy as an important differential\n- **ANCA** is usually positive - anti-PR3 or c-ANCA is most commonly seen but a small proportion of people are anti-MPO or p-ANCA positive\n\n**Imaging tests:**\n\n- **Chest X-ray**\n- The most common finding is multiple nodules of various sizes throughout both lung fields\n- These may cavitate\n- Pulmonary haemorrhage may also be seen with patchy or diffuse opacification\n- Focal areas of alveolar consolidation may occur and can also cavitate\n- Pleural effusions may be seen secondary to cardiac or renal GPA\n- **CT chest** is more sensitive for the above findings and may also show:\n- Micronodules due to bronchial wall involvement or retained blood in the distal airways\n- Mild bronchiectasis\n- Ground glass changes secondary to haemorrhage\n- Tracheobronchial wall thickening\n- **CT of the sinuses** may show:\n- Mucosal thickening\n- Soft tissues nodules\n- Erosions +/- perforation of the cartilage and bones\n- Sclerosis and calcification may also be present\n- **CT** or **MRI** of the head and orbits may show central nervous system involvement or granulomatous disease of the orbits\n- **CT** of the kidneys typically shows a hypovascular mass\n- **FDG-PET CT** can be used to identify occult sites of disease and investigate for differentials such as chronic infection or malignancy\n\n**Special tests include:**\n\n- **Renal biopsy** shows crescentic and necrotising glomerular lesions with no or few immune deposits (pauci-immune)\n- Other affected sites may also be amenable to biopsy, including skin, nasal mucosa and lung tissues \n- **Flexible nasendoscopy** may be done to look for features such as ulceration, septal perforation, crusting and subglottic stenosis\n- **Lung function testing** with **flow-volume loops** may show evidence of fixed upper airway obstruction in subglottic stenosis\n- **Nerve conduction studies** and **electromyography** may be useful in the investigation of mononeuritis multiplex\n- **Endoscopy** may be required in GPA associated with gastrointestinal bleeding\n- **Bronchoalveolar lavage** may be indicated in evaluating pulmonary infiltrates e.g. alveolar haemorrhage\n\n# Management\n\n- Organ or life-threatening GPA should be treated with high dose steroids (usually 1mg/kg prednisolone or equivalent) with either rituximab or cyclophosphamide\n- Avacopan (an oral C5a-receptor antagonist) may be substituted for steroids in severe GPA\n- Plasma exchange is another option that may be used for salvage therapy, especially in severe renal impairment due to rapidly progressive glomerulonephritis\n- Patients may require supportive treatment e.g. intensive care admission with intubation and ventilation and/or renal replacement therapy\n- If GPA is not organ or life-threatening, steroids and rituximab (in some cases methotrexate or mycophenolate mofetil may be used instead of rituximab) are recommended\n- Prednisolone should be tapered over several months\n- Options for maintenance treatment once remission is achieved include rituximab, azathioprine or methotrexate \n- Maintenance immunosuppressive treatment is usually continued for 2 to 4 years (longer in relapsing disease)\n- Patients should be counselled on the risks of immunosuppressive treatments, and prophylactic co-trimoxazole given to patients on rituximab, cyclophosphamide or high-dose steroids\n- In some cases, surgical treatment is required e.g. reconstructive surgery for nasal deformities or for subglottic stenosis\n- Long-term renal replacement therapy (haemodialysis or transplant) may be required for patients who develop end-stage renal disease\n\n# Complications\n\n- Renal failure due to rapidly progressive glomerulonephritis \n- Respiratory failure due to diffuse pulmonary haemorrhage\n- Hearing loss\n- Vision loss\n- Septal perforation or saddle nose deformity\n- Increased cardiovascular risk due to chronic inflammation\n- Increased risk of bladder cancer in patients treatment with cyclophosphamide - patients should have regular urinalysis as part of follow up\n- Side effects of immunosuppression e.g. osteoporosis, diabetes, peptic ulceration with prolonged steroid courses\n- Psychological distress and negative impacts on quality of life due to the burden of disease and its treatments\n\n# Prognosis\n\n- Without treatment, GPA is usually fatal\n- Patients with both renal and respiratory tract involvement have an increased risk of early death\n- Mortality with effective treatment is 14% at 1 year\n- The majority of patients respond to treatment although relapses are frequent (50% at 8 years)\n\n# References\n\n[EULAR recommendations for the management of ANCA-associated vasculitis](https://ard.bmj.com/content/83/1/30)\n\n[Radiopaedia - Granulomatosis with polyangiitis](https://radiopaedia.org/articles/granulomatosis-with-polyangiitis?lang=gb)\n\n[Patient UK - Granulomatosis with polyangiitis](https://patient.info/doctor/granulomatosis-with-polyangiitis-wegeners-granulomatosis-pro)\n\n[DermNet - Granulomatosis with polyangiitis](https://dermnetnz.org/topics/granulomatosis-with-polyangiitis)\n\n[StatPearls - Granulomatosis with polyangiitis](https://www.ncbi.nlm.nih.gov/books/NBK557827/)",
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"question": "A 34-year-old man presents with a two-week history of a purple coloured rash on his lower limbs. He also reports approximately 5kg weight loss in the last two months. He is otherwise well, and his only significant past medical history is of recurrent episodes of sinusitis in the past year.\n\nOn examination, there is a widespread palpable purpuric rash on the anterior aspects of both legs. Examination and observations are otherwise normal.\n\nWhich of the following is the next best step in management?",
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"explanation": "Around 30% of cases of erythroderma are idiopathic. Most cases of erythroderma are associated with a pre-existing skin condition",
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"explanation": "The rash is highly suggestive of erythroderma. Erythroderma is a dermatological emergency where there is widespread erythema affecting >90% of the skin surface. The increased urea level suggests dehydration, an important complication of erythroderma, and highlights the importance of the skin's function in fluid balance.\n\nThe most common cause of erythroderma is a pre-existing skin condition such as eczema or psoriasis",
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"explanation": "Haematological malignancies can cause erythroderma; however, the lack of systemic symptoms, largely normal blood tests and absence of lymphadenopathy would go against this",
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"explanation": "Drug reactions can cause erythroderma; however, this is less likely than a pre-existing skin condition preceding erythroderma.",
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"comment": "nah",
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"comment": "dean's list student question lmao",
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"comment": "Could just say she has a history of eczema. How are you supposed to deduce anything from such a short stem?",
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"comment": "there's literally nothing in the stem to suggest pre-existing skin condition but apparently that's the reason why drug-reaction is wrong",
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"comment": "I dont think that's the reason. I think it's simply much more commonly caused by pre-existing skin conditions. Since there was nothing to point you towards any particular cause, the most likely one is the most common one",
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"explanation": "# Summary\n\nErythroderma, a serious dermatological emergency, is characterised by widespread erythema affecting over 90% of the skin surface. Its primary signs and symptoms include significant skin redness and potential systemic symptoms due to heat and fluid loss. A broad range of conditions, such as dermatitis and psoriasis, or external triggers like drug allergies, can provoke erythroderma. Investigations mainly involve skin biopsy and blood tests. Management primarily focuses on supportive care, including fluid replacement and emollients, alongside treatment of the underlying cause, usually under the guidance of a dermatology specialist.\n\n# Definition\n\nErythroderma, also referred to as exfoliative dermatitis, is a severe and potentially life-threatening dermatological condition where there is widespread erythema covering more than 90% of the body's skin surface. This condition can lead to significant heat and fluid loss, which can further induce systemic symptoms, including hypothermia.\n\n# Aetiology\n\nThe most common cause of erythroderma is the exacerbation of a pre-existing skin condition. These include:\n\n- Dermatitis: Atopic dermatitis, seborrhoeic dermatitis, contact dermatitis\n- Psoriasis\n- Pityriasis rubra pilaris\n\nOther causative factors include:\n\n- Drug allergies\n- Idiopathic triggers\n- Sezary syndrome, a type of cutaneous T-cell lymphoma, which leads to erythroderma, lymphadenopathy, and hepatosplenomegaly. It is defined by the presence of Sezary cells, which are atypical T cells, in the peripheral blood circulation.\n\n# Signs and Symptoms\n\n[lightgallery]\n\nThe main sign of erythroderma is extensive redness (erythema) affecting over 90% of the skin surface. Other associated symptoms can include:\n\n- Skin scaling or shedding\n- Pruritus (itching)\n- Fever and chills due to systemic involvement\n- Swelling of the limbs (edema)\n- Increase in heart rate (tachycardia)\n\n# Differential Diagnosis\n\nWhen assessing a patient with suspected erythroderma, other conditions that could cause similar symptoms need to be considered:\n\n- Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome: Symptoms include skin rash, fever, lymphadenopathy, and involvement of internal organs.\n- Toxic epidermal necrolysis (TEN) and Stevens-Johnson Syndrome (SJS): Key signs are extensive skin detachment, mucosal involvement, and systemic symptoms.\n- Staphylococcal scalded skin syndrome (SSSS): Characterised by extensive skin blistering and sloughing, often accompanied by systemic symptoms.\n\n# Investigations\n\nAlthough the mainstay of diagnosis is clinical observation, further investigations may include:\n\n- Full blood count (FBC), C-Reactive Protein (CRP) and other blood tests to assess systemic involvement and rule out infection.\n- Skin biopsy to confirm diagnosis and identify underlying cause.\n- Other tests depending on the suspected underlying cause, such as allergy testing or immunophenotyping for Sezary syndrome.\n\n# Management\n\n* The management of erythroderma should involve supportive care, including referral/admission under dermatology, fluid replacement to prevent dehydration and the use of emollients to soothe the skin\n* Additionally, the underlying disease causing the erythroderma should be identified and treated, for instance, by administering steroids for an exacerbation of atopic dermatitis\n* Hospitalisation may be necessary for severe cases due to the risk of life-threatening complications\n\n# References\n[Erythroderma - DermNet NZ](https://dermnetnz.org/topics/erythroderma)\n",
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"question": "A 32-year-old woman presents with a three-day history of a worsening rash across her body.\n\nOn examination, there is an erythematous rash covering the majority of the patient's skin, both anteriorly and posteriorly. The skin is hot to touch, and there is associated scaling. Systemic examination is otherwise normal.\n\nBlood tests reveal increased urea to creatinine ratio but no other significant findings.\n\nWhich of the following is the most likely cause of the rash described?",
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"explanation": "Dapagliflozin is a sodium-glucose co-transporter 2 (SGLT2) inhibitor. There is no evidence to support its use in the management of steroid-induced diabetes",
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"explanation": "Insulin can be used for steroid-induced diabetes; however, NovoRapid is a fast-acting insulin and would not help maintain normal glucose levels throughout the day. Intermediate-acting human insulins such as Humulin I would be a better option and may be started as an alternative to gliclazide at a dose of around 10 Units in the morning",
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"comment": "not bad lol ",
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"comment": "Just until it goes down again?",
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"explanation": "# Summary\n\nSecondary causes of type 2 diabetes mellitus (T2DM) encompass a variety of conditions and factors that can induce or exacerbate hyperglycemia. These range from pancreatic and endocrine disorders to specific medications and glycogen storage diseases. It's important to consider these in patients with new-onset diabetes that presents atypically or doesn't respond to typical management.\n\n# Definition\n\nSecondary diabetes refers to forms of the disease where there is a clear causative factor aside from the typical insulin resistance or pancreatic β-cell failure associated with T2DM.\n\n# Epidemiology\n\nThe prevalence of secondary diabetes varies based on the causative condition. While some causes such as pancreatic cancer are relatively common, others, like glycogen storage disorders, are quite rare.\n\n# Aetiology\n\nSecondary causes of T2DM include:\n\n**Pancreatic Causes**\n\n- Cystic fibrosis: An autosomal recessive disorder leading to mucus accumulation in various organs including the pancreas, resulting in fibrosis and loss of exocrine and endocrine function.\n- Chronic pancreatitis: Long-standing inflammation of the pancreas can result in damage to islet cells, leading to diabetes.\n- Haemochromatosis: Iron overload can lead to deposition in various organs including the pancreas, leading to diabetes.\n- Cancer: Pancreatic neoplasms can destroy the islet cells, leading to diabetes.\n\n**Endocrine Causes**\n\n- Cushing's syndrome/disease: Elevated cortisol levels increase insulin resistance.\n- Acromegaly: Excess growth hormone leads to insulin resistance.\n- Pheochromocytoma: These rare adrenal tumors can induce diabetes through chronic catecholamine-induced glucose intolerance.\n- Thyrotoxicosis: Thyroid hormone excess can enhance hepatic gluconeogenesis and glycogenolysis and impair insulin secretion.\n\n**Drug Causes**\n\n- Steroids: Chronic use can lead to glucose intolerance and diabetes due to increased insulin resistance.\n- Atypical neuroleptics: These medications can lead to weight gain and increased insulin resistance.\n- Thiazides: These diuretics may impair glucose tolerance, possibly by reducing insulin secretion.\n- Beta-blockers: They can impair glycemic control through inhibition of insulin secretion and promoting insulin resistance.\n\n**Glycogen Storage Disorders**\n\n- Glycogen Storage Disease Type 1 (von Gierke's disease): The inability to perform gluconeogenesis can lead to hypoglycemia and secondary hyperglycemia.\n- Glycogen Storage Disease Type 2 (Pompe disease): It affects the heart and skeletal muscles more than it causes diabetes, but can present with variable symptoms.\n\n# Management\n\nManagement primarily involves addressing the underlying condition responsible for secondary diabetes. In cases where this is difficult/not possible, for example, pancreatic cancer, patients may require insulin therapy to manage hyperglycemia.\n\n\n\n# NICE Guidelines\n\n[NICE CKS on type 2 diabetes](https://cks.nice.org.uk/topics/diabetes-type-2/)",
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"comment": "so he's gone through the hyperthyroid phase, and the hypothyroid phase... and he didn't have any symptoms?",
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"comment": "Although correct, a low-dose dexamethasone test is now used more often in place of the 24h urinary free cortisol.",
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"comment": "Spend more time at GP because you cannot do low dose dex test at GP that is usually done by endocrine specialist ",
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"comment": "why not 9 am cortisol? ",
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"comment": "in cushings cortisol will be elevated. at 9 am is when your cortisol is naturally highest due to its diurnal variation. so if a 9 am cortisol comes back elevated, it doesn't really tell you if someone has cushings. ",
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"comment": "\nThe two most commonly used tests are:\novernight dexamethasone suppression test\nthis is the most sensitive test and is now used first-line to test for Cushing's syndrome\npatients with Cushing's syndrome do not have their morning cortisol spike suppressed\n24 hr urinary free cortisol",
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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. 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"question": "A 45-year-old woman presents to her General Practitioner (GP) with weakness in her shoulders and hips. She also reports an unintentional weight gain of 5kg over the last three months and associated easy bruising.\n\nOn examination, she is hypertensive, with central adiposity and violaceous striae are present on her abdomen.\n\nShe is subsequently referred to an endocrinologist.\n\nWhich of the following is the best initial investigation given the likely underlying diagnosis?",
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"explanation": "Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) and is not particularly useful for treating neuropathic pain. It would also not be appropriate in this case, given the history of a duodenal ulcer, as NSAIDs are a major cause of gastric and duodenal ulceration",
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"explanation": "This patient has signs and symptoms of diabetic neuropathy. Other symptoms of neuropathic pain include tingling, sensitivity to touch and electric-like sensations. NICE guidelines suggest using amitriptyline, duloxetine, pregabalin or gabapentin as the first-line treatment for neuropathic pain",
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"explanation": "Regular paracetamol would not be particularly useful for the treatment of neuropathic pain",
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"explanation": "Neuropathic pain may be responsive to treatment with opioids such as morphine. However, it should be reserved for persistent symptoms refractory to treatment with anti-depressants (e.g. amitriptyline or duloxetine) and anti-epileptics (pregabalin or gabapentin)",
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"name": "Start modified-release morphine sulphate",
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"explanation": "Low strength capsaicin cream can be used for the treatment of localised neuropathic pain. This patient's pain is more widespread and so topical treatment is unlikely to be beneficial. A patch containing 8% capsaicin is an option for peripheral neuropathic pain and could be considered under specialist supervision",
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"name": "Start 0.075% capsaicin cream",
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"__typename": "QuestionComment",
"comment": "All Diabetics Get Peripheral (Neuropathy) -->\nAmitriptyline, Duloxetine, Gabapentin, Pregabalin",
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"comment": "duloxetine increases bleeding risk (like NSAID) so would potentially not give in Hx of peptic ulcer disease ",
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"explanation": "# Summary\n\nDiabetic peripheral neuropathy (DPN) refers to a variety of peripheral nerve disorders as a result of diabetes. The primary causative factor is chronic hyperglycaemia, which leads to several distinct types of DPN, including Distal Symmetrical Sensory Neuropathy, Small-fibre Predominant Neuropathy, Diabetic Amyotrophy, Mononeuritis Multiplex, Autonomic Neuropathy and Charcot Arthropathy. Symptoms vary according to the subtype of DPN but usually involve sensory loss and/or pain in a glove and stocking distribution or proximal weakness. Key investigations focus on assessing the extent of neuropathy and rule out other potential causes of neuropathy. Management is primarily symptomatic and emphasises good glycaemic control. This section covers DPN broadly, with a later focus on Charcot arthropathy.\n\n# Definition\n\nDiabetic peripheral neuropathy (DPN) represents a spectrum of peripheral nerve disorders stemming from diabetes. The central driver behind their development is believed to be chronic hyperglycaemia.\n\n# Epidemiology\n\nDPN is a common complication of both type 1 and type 2 diabetes, with approximately 50% of long-term diabetic patients developing the condition. The risk increases with the duration of diabetes and poor glycemic control.\n\n# Aetiology\n\nChronic hyperglycaemia in diabetes is the primary cause of DPN, leading to damage to peripheral nerves through various mechanisms, including accumulation of advanced glycation end products, oxidative stress, and inflammatory pathways.\n\n# Clinical Features\n\nDPN can be categorised into several types, each presenting with distinct clinical features:\n\n## Distal Symmetrical Sensory Neuropathy\n\n- Most common form of DPN.\n- Resulting from loss of large sensory fibres.\n- Presents with sensory loss in a 'glove and stocking' distribution, typically affecting touch, vibration and proprioception.\n\n## Small-fibre Predominant Neuropathy\n\n- Due to the loss of small sensory fibres.\n- Manifests as deficits in pain and temperature sensation in a 'glove and stocking' distribution, often accompanied by episodes of burning pain.\n\n## Diabetic Amyotrophy\n\n- Originates from inflammation of the lumbosacral plexus or cervical plexus.\n- Characterised by severe pain around the thighs and hips, along with proximal weakness.\n\n## Mononeuritis Multiplex\n\n- Typically painful.\n- Defined as neuropathies involving two or more distinct peripheral nerves.\n\n## Autonomic Neuropathy\n\n- Presents with postural hypotension, gastroparesis, constipation, urinary retention, arrhythmias, and erectile dysfunction.\n\n# Differential Diagnosis\n\nThe differential diagnosis for DPN includes:\n\n- **Vitamin B12 deficiency**: Can present with peripheral neuropathy, typically in a glove and stocking distribution. May also feature megaloblastic anemia and glossitis.\n- **Alcohol-induced peripheral neuropathy**: Presents similarly to DPN but may also have accompanying signs of chronic alcohol misuse.\n- **Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)**: Often presents with both sensory loss and motor weakness, typically in a proximal and distal distribution.\n- **Hypothyroidism**: Can present with neuropathy, usually accompanied by other symptoms such as fatigue, weight gain, and cold intolerance.\n\n# Investigations\n\n- **Neurological examination**: To assess the extent of sensory and motor deficits.\n- **Nerve conduction studies**: To evaluate the nature and extent of neuropathy.\n- **Blood tests**: Including glucose levels, HbA1c, B12 levels, thyroid function tests, and liver function tests, to identify potential differential diagnoses or contributory conditions.\n\n# Complications\n\nIf uncontrolled, DPN can lead to serious complications such as foot ulcers due to loss of sensation, and autonomic neuropathy can lead to various cardiac, gastrointestinal, and genitourinary disturbances.\n\n# Management\n\nManagement strategies for DPN primarily revolve around the control of blood glucose levels to slow the progression of the disease. Symptomatic management may include pain control with medications such as gabapentin or pregabalin, as well as management of complications (e.g., treatment of foot ulcers, management of autonomic disturbances).\n\n# Charcot Arthopathy\n\n## Summary\n\nCharcot arthropathy is a chronic, progressive condition characterised by destructive changes in the bones and joints of patients with neuropathy, most commonly from diabetes. It presents with the '6Ds': Destruction, Deformity, Degeneration, Dense bones, Debris, and Dislocation. Diagnosis often involves imaging, typically with radiographs, and distinguishing it from osteomyelitis. Management focuses on immobilisation, orthotics, medication to manage pain and bone loss, and surgical interventions in advanced or refractory cases.\n\n## Definition\n\nCharcot arthropathy, also known as Charcot joint or neuropathic arthropathy, is a chronic, progressive condition characterised by painful or painless bone and joint destruction in the limbs that have lost sensory innervation. The condition primarily affects patients with peripheral neuropathy.\n\n## Epidemiology\n\nCharcot arthropathy is most commonly seen in patients with long-standing diabetes mellitus, with the prevalence being estimated to be around 0.1-0.9% in this group. It can occur at any age but is more frequently observed in the middle-aged and elderly population.\n\n## Aetiology\n\nThe underlying aetiology of Charcot arthropathy is primarily neuropathy. The most common cause of this is diabetes mellitus, which leads to microvascular disease, autonomic neuropathy, and peripheral neuropathy, resulting in cumulative damage to the joints. Other, rarer causes include conditions that cause neuropathy, such as syringomyelia, chronic alcohol abuse, and syphilis.\n\n## Signs and Symptoms\n\nCharcot arthropathy often presents with the '6Ds'(some of which are imaging features):\n\n- Destruction of bone and joint\n- Deformity\n- Degeneration\n- Dense bones\n- Debris of bone fragments\n- Dislocation\n\nIt classically affects the tarsometatarsal joints, but it can involve any joint in a limb that has lost sensation due to neuropathy.\n\n## Differential Diagnosis\n\nThe main differential diagnosis to rule out in the context of Charcot arthropathy is osteomyelitis, which also causes bone destruction but is typically associated with systemic symptoms like fever, increased inflammatory markers, and often a preceding or concurrent soft tissue infection.\n\n## Investigations\n\nThe diagnosis of Charcot arthropathy is primarily clinical but often involves imaging to assess the extent of the bone and joint involvement:\n\n- X-rays are usually the first-line imaging study. They can demonstrate bone destruction, debris, sclerosis (dense bones), and dislocation.\n- MRI can provide more detailed imaging, particularly in early disease or when osteomyelitis is suspected.\n- Bone scans may be used in complex cases or when other imaging is inconclusive.\n\n## Management\n\nThe management of Charcot arthropathy involves conservative and surgical strategies:\n\nConservative:\n- Prolonged off-loading, often involving special footwear or plaster casts, to allow healing and prevent further damage.\n- Use of orthotics for long-term management and prevention of recurrences.\n\nMedications:\n- Bisphosphonates can help slow down the process of bone destruction.\n- Neuropathic pain agents, such as gabapentin or pregabalin, for pain management.\n- Topical anesthetics can also be used to manage pain.\n\nSurgical:\n- Resection of bony prominences to prevent ulcers or improve fitting of footwear.\n- Correction of severe deformities, usually after the acute phase has settled.\n- Amputation may be required in severe cases or when there is a concurrent uncontrolled infection.\n\n\n# NICE Guidelines\n\n[Click here for NICE CKS on diabetes - type 2](https://cks.nice.org.uk/topics/diabetes-type-2/)\n",
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"question": "A 56-year-old man presents to his GP with a history of burning and numbness in his feet and lower legs for the last two months. His past medical history is significant for poorly controlled Type 1 diabetes and a previous duodenal ulcer.\n\nOn neurological examination, there is reduced sensation to pin-prick and fine-touch bilaterally from the feet to the knees.\n\nGiven the likely diagnosis, which of the following is the next best step in management?",
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173,468,822 | false | 49 | null | 6,495,278 | null | false | [] | null | 6,483 | {
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"explanation": "Haemochromatosis is a disorder of iron overload and can either be primary (an autosomal recessive disorder that results in an inability to regulate iron absorption) or secondary (due to frequent blood transfusions in conditions such as thalassaemia major). Haemochromatosis can cause liver disease and diabetes; however, the strong metabolic risk factors make NAFLD more likely in this case",
"id": "32415",
"label": "c",
"name": "Haemochromatosis",
"picture": null,
"votes": 165
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"__typename": "QuestionChoice",
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"explanation": "This patient has diabetes, hypertension and obesity, which are three major risk factors for NAFLD. NAFLD is the most common cause of liver disease worldwide and is characterised by fatty infiltration of hepatocytes without a secondary cause. It is strongly linked to metabolic syndrome, and the most typical liver enzyme abnormality is a raised ALT and/or GGT",
"id": "32413",
"label": "a",
"name": "Non-alcoholic fatty liver disease (NAFLD)",
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"explanation": "Although this patient drinks regular alcohol, his consumption is not excessive. It is, therefore, unlikely that he has alcoholic liver disease",
"id": "32414",
"label": "b",
"name": "Alcoholic liver disease",
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"votes": 1432
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"__typename": "QuestionChoice",
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"explanation": "Autoimmune hepatitis is a rare cause of chronic liver disease that is more common in women and those with a background of other autoimmune diseases (e.g. type 1 diabetes, autoimmune thyroid disease, ulcerative colitis). NAFLD is more likely in this case",
"id": "32417",
"label": "e",
"name": "Autoimmune hepatitis",
"picture": null,
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"explanation": "Viral hepatitis is less likely as the patient has no risk factors (e.g. recent travel, history of intravenous drug use, recent tattoos/piercings, blood transfusion etc.) or symptoms. Viral hepatitis would also usually present with a more significant rise in transaminases (i.e. ALT and AST). It should, however be excluded by conducting a full viral screen",
"id": "32416",
"label": "d",
"name": "Viral hepatitis",
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"comment": "Is there a way to differentiate with blood results?",
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"comment": "Only if you have AST and ALT. I think here the point is that he drinks within the limit, therefore not alcohol induced",
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"comment": "I was just out here thinking he was just lying about his intake",
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"explanation": "\n# Summary\n\nNon-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease globally. It encompasses a spectrum of liver conditions ranging from simple steatosis (fat accumulation) to non-alcoholic steatohepatitis (NASH), which can progress to fibrosis and ultimately cirrhosis. NAFLD is closely associated with metabolic syndrome, including obesity, type 2 diabetes, and hyperlipidaemia. Diagnosis often occurs incidentally through imaging or abnormal liver function tests. Management focuses on lifestyle modifications, managing comorbidities, and regular monitoring for liver complications. Early identification and intervention are crucial to prevent disease progression.\n\n# Definition\n\nNon-alcoholic fatty liver disease (NAFLD) refers to a range of liver conditions characterised by excessive fat accumulation in the liver in the absence of significant alcohol consumption. It includes simple steatosis, non-alcoholic steatohepatitis (NASH), and can progress to fibrosis and cirrhosis.\n\n# Epidemiology\nNAFLD is the leading cause of chronic liver disease worldwide, affecting approximately 25-30% of adults in developed countries. In the UK, the prevalence is similar, reflecting the high rates of obesity and type 2 diabetes, both of which are part of metabolic syndrome. NAFLD is increasingly recognised in children and adolescents, paralleling the rise in paediatric obesity.\n\n# Aetiology\nNAFLD is primarily associated with metabolic syndrome and its components:\n\n- **Obesity**\n- **Type 2 diabetes mellitus**\n- **Hyperlipidaemia (high triglycerides and low HDL)**\n- **Hypertension**\n\nOther risk factors include:\n\n- Jejunal bypass surgery\n- Rapid weight loss or prolonged starvation\n- Polycystic ovary syndrome (PCOS)\n- Hypothyroidism\n- Obstructive sleep apnoea\n\n# Pathophysiology\n\nNAFLD progresses through a continuum:\n\n- **Steatosis:** Simple fatty liver with fat accumulation in hepatocytes, usually asymptomatic and reversible with lifestyle changes.\n- **Non-Alcoholic Steatohepatitis (NASH):** Inflammation and hepatocellular injury in addition to fat accumulation, leading to fibrosis.\n- **Fibrosis and Cirrhosis:** Progressive scarring of the liver tissue, which can ultimately lead to liver failure and increased risk of hepatocellular carcinoma.\n\n# Signs and Symptoms\n\nNAFLD is often asymptomatic but can present with:\n\n- Fatigue\n- Right upper quadrant discomfort\n- Hepatomegaly\n\nAs the disease progresses to cirrhosis, symptoms may include:\n\n- Jaundice\n- Ascites\n- Peripheral oedema\n- Hepatic encephalopathy\n\n# Differential Diagnosis\n\n- **Alcoholic Liver Disease (ALD):** Similar histological features, but differentiated by history of significant alcohol intake.\n- **Chronic Hepatitis B and C:** Viral serologies positive; may have similar liver biopsy findings.\n- **Autoimmune Hepatitis:** Positive autoantibodies and elevated immunoglobulins.\n- **Wilson's Disease:** Low caeruloplasmin levels and elevated urinary copper.\n- **Haemochromatosis:** Elevated serum iron, ferritin, and transferrin saturation.\n- **Drug-Induced Liver Injury (DILI):** History of hepatotoxic drug use.\n\n# Investigations\n- **Bedside:**\n - Detailed history including alcohol consumption, medication use, and risk factors for liver disease.\n - Physical examination for signs of chronic liver disease.\n\n- **Bloods:**\n - Liver function tests (ALT, AST, GGT, ALP, bilirubin).\n - Full blood count.\n - Fasting glucose and lipid profile.\n - Tests to exclude other causes of liver disease: viral serologies (Hepatitis B and C), autoantibodies, serum iron studies, caeruloplasmin.\n\n- **Imaging:**\n - **Ultrasound:** Often the first test that shows fatty infiltration of the liver.\n - **Elastography (FibroScan):** Measures liver stiffness to assess fibrosis.\n - **Enhanced Liver Fibrosis (ELF) test:** Blood test assessing markers of fibrosis.\n\n- **Invasive:**\n - **Liver biopsy:** Considered the **gold standard** for diagnosing NASH and staging fibrosis, although often reserved for cases where non-invasive tests are inconclusive.\n\n# Management\n- **Conservative:**\n - Lifestyle modifications including weight loss if obese, exercise, and dietary changes.\n - Abstinence from alcohol.\n - Vaccination against hepatitis A and B.\n - Avoid hepatotoxic drugs where possible\n\n- **Medical:**\n - **Metabolic management:** Control of diabetes, hyperlipidaemia, and hypertension.\n - **Medications:** No specific drugs have been approved for NAFLD, but some off-label use of vitamin E (in non-diabetic patients) and pioglitazone in NASH.\n \t- These medications should only be prescribed in secondary care, and when consenting patients they should be made aware of the possible increase of 2-4% body weight (within 3 years of treatment) and the increased risk of bladder cancer and osteoporosis (in women). \n\n- **Monitoring and Screening:**\n - Regular follow-up with liver function tests and imaging.\n - Screening for hepatocellular carcinoma in patients with advanced fibrosis or cirrhosis.\n\n# Complications\n- **Reversible:**\n - Early steatosis with lifestyle changes.\n \n- **Irreversible:**\n - Progression to cirrhosis.\n - Liver failure.\n - Hepatocellular carcinoma.\n - Cardiovascular disease due to associated metabolic syndrome.\n\n# Prognosis\n\nThe prognosis of NAFLD varies widely. Simple steatosis generally has a good prognosis with lifestyle modifications. However, NASH can progress to fibrosis and cirrhosis, which are associated with significant morbidity and mortality. Early identification and management of risk factors are crucial in preventing disease progression.\n\n# NICE Guidelines\n\n[NICE CKS - Non-alcoholic fatty liver disease (NAFLD)\n](https://cks.nice.org.uk/topics/non-alcoholic-fatty-liver-disease-nafld/)",
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"question": "A 56-year-old man with a background of type 2 diabetes and hypertension presents to his GP for a routine set of blood tests.\n\n\nHe reports regularly drinking approximately 14 Units of alcohol per week. His body mass index (BMI) is 30, and a set of routine observations are unremarkable.\n\n\nThe blood tests reveal an alanine transaminase (ALT) of 195 U/L (7-56 U/L) and a gamma-glutamyl transferase (GGT) level of 85 U/L (<10 U/L). Glycosylated haemoglobin levels (HBA1C) are noted to be 52 mmol/l (42-47 mmol/l).\n\n\nWhich of the following is the most likely explanation for the deranged liver function tests?",
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"explanation": "This patient has symptoms suggestive of severe colitis, which has the potential to deteriorate significantly. He should be admitted to hospital for investigation and management",
"id": "32422",
"label": "e",
"name": "Monitor symptoms and review in three days",
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"explanation": "This patient has a history suggestive of inflammatory bowel disease (IBD). The significant rectal bleeding and tenesmus (urge to constantly open his bowels) are more suggestive of ulcerative colitis (UC) than Crohn's disease. Using the Truelove and Witts scoring system for UC, this patient has severe UC due to the number of bowel motions per day and anaemia. Hospital admission is recommended for patients with features suggestive of severe disease",
"id": "32418",
"label": "a",
"name": "Urgent hospital admission",
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"__typename": "QuestionChoice",
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"explanation": "# Summary\n\nUlcerative colitis (UC) is a chronic inflammatory disease that affects the large bowel. Symptoms include diarrhoea, urgency, tenesmus, weight loss, and fever. The disease can present with extra-intestinal features such as dermatological (erythema nodosum), ocular (anterior uveitis), musculoskeletal (finger clubbing), and hepatobiliary manifestations (jaundice due to primary sclerosing cirrhosis). Investigations include blood tests, microbiological investigations, endoscopic investigations, and imaging. The management of UC is based on severity and involves inducing and maintaining remission using medications like aminosalicylates, steroids, and biologics. Surgery may be required in severe cases or when medical treatment is unsuccessful. Long-term complications include colorectal cancer, cholangiocarcinoma and colonic strictures.\n\n# Definition\n\nUlcerative colitis (UC) is a chronic relapsing-remitting inflammatory disease that primarily affects the large bowel. It usually affects the rectum first, then can extend to the part of the colon (left-hand-side colitis) or the entire colon (pancolitis). It does not spread beyond the ileocaecal valve or to the small bowel, except where backwash ileitis can occur.\n\n# Epidemiology\n\nUC is the most commonly diagnosed inflammatory bowel disease. It has an annual incidence rate of 10 per 100,000 people and a prevalence rate of 243 per 100,000. Although UC can develop at any age, it most frequently occurs in two peak age groups: 15 to 25 years and 55 to 65 years.\n\n# Aetiology\n\nThe exact cause of UC is unknown, but it is believed to result from a combination of genetic predisposition, environmental factors, and dysregulation of the immune system. There is also a higher incidence of UC among non-smokers and ex-smokers.\n\n# Signs and Symptoms\n\nThe main symptoms of UC are gastrointestinal and systemic. \n\nGastrointestinal symptoms include:\n\n- Diarrhoea often containing blood and/or mucus\n- Tenesmus or urgency\n- Generalised crampy abdominal pain in the left iliac fossa\n\nSystemic symptoms include:\n\n- Weight loss\n- Fever\n- Malaise\n- Anorexia\n\nPhysical examination may reveal general signs such as pallor due to anaemia and clubbing. Abdominal examination may reveal distension or tenderness, and a PR examination may show tenderness, and blood/mucus. \n\n\nExtra-intestinal signs occur in 10-20% of patients and include:\n\n- Dermatological manifestations: erythema nodosum, pyoderma gangrenosum\n- Ocular manifestations: anterior uveitis, episcleritis, conjunctivitis\n- Musculoskeletal manifestations: clubbing, non-deforming asymmetrical arthritis, sacroiliitis\n- Hepatobiliary manifestations: jaundice due to primary sclerosing cholangitis (PSC). 80% of those with PSC have ulcerative colitis.\n- Other features include AA amyloidosis\n\n\n\n\n# Differential Diagnosis\n\nThe differential diagnoses for UC include Crohn's disease, infectious colitis, and ischemic colitis. Key signs and symptoms to differentiate these conditions include:\n\n- Crohn's disease: Abdominal pain, weight loss, diarrhea, oral ulcers, anal fissures, and perianal fistulas.\n- Infectious colitis: Acute onset of diarrhea, fever, and abdominal pain. May be associated with recent antibiotic use, travel, or consumption of contaminated food or water.\n- Ischemic colitis: Sudden onset of abdominal pain, blood in stools, and a history of vascular disease or risk factors.\n\n# Investigations\n\n**Bedside:**\n\n- Microbiological investigations: Stool microscopy (for ova/cysts/parasites), culture and sensitivity, and stool C. difficile toxin to exclude infective colitis\n- Faecal calprotectin: Distinguishes between inflammatory bowel syndrome (normal) and inflammatory bowel disease (raised)\n\n**Bloods:**\n\n- Blood tests: FBC (anaemia and a raised white cell count), ESR/CRP is typically raised, LFTs may show a low albumin\n\n**Imaging/Invasive:**\n\n- Radiological investigations: Abdominal X-ray and erect chest x-ray in acute settings to exclude toxic megacolon and perforation.\n\t- Long-standing UC will show 'lead-pipe' colon on AXR \n- Endoscopic investigations: Colonoscopy, barium enema, and biopsy are used to confirm the diagnosis.\n - Colonoscopy will reveal shows continuous inflammation starting at the rectum that does not go beyond the submucosa with an erythematous mucosa, loss of haustral markings, and pseudopolyps.\n - Biopsy: loss of goblet cells, crypt abscess, and inflammatory cells (predominantly lymphocytes)\n - Barium enema will reveal lead-piping inflammation (secondary to loss of haustral markings), thumb-printing (a marker of bowel wall inflammation), and pseudopolyps (due to areas of ulcerating mucosa adjacent to areas of regenerating mucosa). This is less commonly used nowadays due to the increasing availability of endoscopic investigations\n\n# Truelove and Witt's Criteria for Severity\n\nAn acute exacerbation of ulcerative colitis should be assessed using the Truelove and Witt's severity index.\n\n| | **Mild** | **Moderate** | **Severe** |\n| --------------------------------------------- | ----------------------------------- | ----------------------- | ------------------------------------------------------------------------------------ |\n| **Bowel movements (no. per day)** | Fewer than 4 | 4-6 | 6 or more plus at least one of the features of systemic upset (marked with \\* below) |\n| **Blood in stools** | No more than small amounts of blood | Between mild and severe | Visible blood |\n| **Pyrexia (temperature greater than 37.8°C)** | No | No | Yes |\n| **Pulse rate greater than 90 bpm** | No | No | Yes |\n| **Anaemia (< 10g/100mL)** | No | No | Yes |\n| **Erythrocyte sedimentation rate (mm/hour)** | 30 or below | 30 or below | above 30 |\n\n\n# Management\n\n\n## Mild-moderate disease\n\nThe aim of step 1 treatment is to induce remission. If this does not work after 4 weeks, or symptoms worsen, move to step 2.\n\nThe first step in management for a moderate first presentation is to offer a topical aminosalicylate as first-line treatment. If remission is not achieved within 4 weeks, consider adding an oral aminosalicylate. In acute moderate disease if all other measures haven't worked then a trial of Etrasimod (also known as Velsipity). This is a selective sphingosine 1-phosphate (S1P) receptor modulator.\n\n- **Proctitis and proctosigmoiditis:**\n - Step 1: Topical ASA or oral ASA.\n - Step 2: Consider adding oral prednisolone. If this does not help after 2-4 weeks or symptoms worsen, consider adding oral tacrolimus.\n- **Left sided or extensive disease**\n - Step 1: High dose oral ASA.\n - Step 2: Consider adding oral prednisolone. If this does not help after 2-4 weeks or symptoms worsen, consider adding oral tacrolimus.\n\n## Acute severe disease\n\n- Step 1: IV corticosteroids (if contraindicated or not tolerated, use IV ciclosporin).\n- Step 2: If no improvement in 72 hours or worsening symptoms, add IV ciclosporin or consider surgery (if IV ciclosporin contraindicated or not tolerated, consider infliximab).\n- Step 3: A trial of Etrasimod (also known as Velsipity). This is a selective sphingosine 1-phosphate (S1P) receptor modulator.\n- Indications for emergency surgery:\n - Surgery should be considered in patients with:\n - Acute fulminant ulcerative colitis\n - Toxic megacolon who have little improvement after 48-72 hours of intravenous steroids\n - Symptoms worsening despite intravenous steroids\n\n_Note that an alternative is to initiate rescue therapy (with ciclosporin or infliximab) if the patient has a sub-optimal response to intravenous steroids but is stable enough to delay surgery. Surgery should be considered if patients fail to respond to rescue therapy within 3 days._\n\n## Surgical options\n\n- Panproctocolectomy with permanent end ilesotomy\n- Colectomy with temporary end ileostomy (approximately 3 months later the ileostomy can be reversed by forming an ileorectal anastomosis, an alternative option is completion proctectomy with a permanent end ileostomy or ileal pouch anal anastomosis (IPAA)).\n\n## Indications for elective surgery\n\n- This can be considered in patients in which there is failure to induce remission by medical means.\n- Surgical options include: panproctocolectomy with permanent end ileostomy or IPAA. An alternative is a total colectomy with ileorectal anastomosis (i.e. no stoma).\n\n# Complications\n\n## Short-term/acute complications\n\n- Toxic megacolon: this describes a severe form of colitis, and is seen in around 15% of ulcerative colitis patients.\n- Massive lower gastrointestinal haemorrhage: this occurs in up to 3% of patients.\n\n## Long-term complications\n\n- Colorectal cancer: this occurs in 3-5% of patients. There is a higher risk with disease duration, severity and extent of colitis, and concomitant primary sclerosing cholangitis (PSC).\n\n_NICE guidance suggests offering colonoscopy surveillance to high risk patients._\n\n- Cholangiocarcinoma: ulcerative colitis approximately doubles the risk of cholangiocarcinoma.\n- Colonic strictures: these can cause large bowel obstruction.\n\n## Variable-term complications\n\n- Primary Sclerosing Cholangitis: this is characterised by inflammation and fibrosis of the extra- and intra-hepatic biliary tree and affects 3-7% of patients with ulcerative colitis. LFTs should be monitored yearly to check for the presence of PSC.\n- Inflammatory pseudopolyps: these are areas of normal mucosa between areas of ulceration and regeneration.\n- Increased risk of VTE - as with any inflammatory disease, but in the acute and chronic context, patients have an increased risk of developing blood clots, especially during flares\n\n# References\n\n[Click here for more information on NICE CKS about ulcerative colitis](https://cks.nice.org.uk/topics/ulcerative-colitis/)",
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"explanation": "# Summary\n\nAge-related macular degeneration (ARMD) is the most prevalent cause of blindness in the UK, characterized by the degeneration of photoreceptors in the central retina leading to drusen formation. There are two types: dry (most common, characterised by drusen deposition), and wet (exudative, caused by neovascularisation and carries worse prognosis). Key symptoms include subacute loss of and/or distortion of the central visual field, reduced visual acuity, night blindness, and photopsia. The primary investigation methods include slit-lamp biomicroscopy, colour fundus photography, fluorescein angiography, and ocular coherence tomography (OCT). Management generally involves smoking cessation, and depending on the type of ARMD, zinc and antioxidant supplements (dry ARMD) or anti-vascular endothelial growth factor (anti-VEGF) injections (wet ARMD).\n\n# Definition\n\nAge-related macular degeneration (ARMD) is the leading cause of blindness in the UK. Patients present with subacute loss of and/or distortion of the central visual field.\n\nARMD describes degeneration of photoreceptors in the central retina (macula) that leads to the formation of drusen, which are visible on slit-lamp biomicroscopy.\n\n# Risk factors\n\n- Age – the biggest risk factor for developing ARMD\n- Male sex\n- Smoking (doubles the likelihood of ARMD-related vision loss) – a smoking history should always be taken in patients with ARMD\n- Family history \n- Cardiovascular risk factors: hypertension, diabetes mellitus, coagulopathy, dyslipidaemia\n\n# Dry vs Wet ARMD\n\n| | Dry ARMD | Wet ARMD |\n| ------------- |:-------------:| :-----:|\n| **Prevalence** | 85–90% of cases | 10–15% of cases|\n| **Features** |Drusen, macular thinning (geographic atrophy) | Neovascularisation, bleeding, leakage of fluid|\n| **Prognosis**| Slow progression over decades | Rapid progression over months, with poor prognosis |\n\n# Signs and Symptoms\n\n**Symptoms**:\n\n* Reduced visual acuity, worse for near vision and central vision (patients may say they struggle seeing faces)\n* Variability in visual disturbance from day to day is characteristic\n* Poor vision at night\n* Photopsia – perceived flickering of lights\n* Glare\n\n**Signs**:\n\n* Visual distortion – particularly line perception when tested with Amsler grids. This is known as metamorphopsia.\n* **Dr**usen in **dr**y ARMD – yellow pigmented spots on the retina that are collected around the macula\n* Subretinal or intraretinal haemorrhages in wet ARMD – seen as red patches on the retina around the macula\n\n[lightgallery]\n\n# Differential Diagnosis\n\n\n2. **Diabetic Macular Oedema (DME):**\n - **Diabetic Retinopathy:** Patients with diabetic retinopathy can experience macular oedema, which may lead to similar symptoms as neovascular AMD, such as visual distortion or blurred central vision.\n\n3. **Retinal Vein Occlusion (RVO):**\n - **Central or Branch RVO:** A blockage of retinal veins can lead to macular oedema, haemorrhages, and vision changes similar to those in neovascular AMD.\n\n4. **Central Serous Chorioretinopathy (CSC):**\n - **CSC:** This condition often presents with central serous retinal detachment, leading to vision disturbances. It can mimic wet AMD, but CSC is characterised by serous fluid accumulation rather than CNV.\n\n\nA comprehensive eye examination, including optical coherence tomography (OCT), fluorescein angiography, and fundus photography, is often necessary to differentiate AMD from these conditions and guide appropriate management and treatment decisions.\n\n# Investigations\n\n\n| Technique | Notes |\n|-----------|------|\n| **Slit-lamp biomicroscopy**| Allows identification of exudative, pigmentary or haemorrhagic changes in the retina to allow diagnosis of ARMD |\n| **Colour fundus photography** | Done at each assessment to monitor progression|\n| **Fluorescein angiography** | Used to identify neovascular ARMD to guide anti-VEGF therapy |\n| **Ocular coherence tomography (OCT)** | Allows assessment of all layers of the retina and identification of disease not visible by slit-lamp biomicroscopy |\n\n# Management\n\nSmoking cessation is important for all patients with ARMD.\n\n## Dry ARMD\n\nZinc and antioxidant vitamin A, C and E supplements have been shown to reduce progression by up to 30%.\n\n## Wet ARMD\n\nAnti-vascular endothelial growth factor (anti-VEGF) injections limit progression and can even reverse vision loss – typically administered in monthly injections.\n\n# NICE Guidelines\n\n[Click here for NICE CKS on ARMD](https://cks.nice.org.uk/topics/macular-degeneration-age-related/)\n\n# References\n\n[Click here for more detailed Eye Wiki notes on ARMD](https://eyewiki.aao.org/Age-Related_Macular_Degeneration#Management)",
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"question": "An 81-year-old male with wet age-related macular degeneration (AMD) is reviewed in clinic. Twelve months ago, she had early-stage disease, initially managed with risk factor modification, although her vision has now deteriorated from 6/24 to 6/60 vision in both eyes. On fundoscopy, she has subretinal haemorrhages, lipid exudates, and fibrovascular scarring - corresponding to advanced-stage disease.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "This will almost certainly be done while an inpatient to determine the progression of this patient's prostate cancer. However given this patient's new neurology findings, he requires urgent therapy to relieve his spinal cord compression to prevent permanent neurological damage",
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"explanation": "Given this patient's new neurology findings he should have urgent radiotherapy within 24hrs to prevent permanent neurological damage. While dexamethasone is a crucial part of management of MSCC and cauda equina syndrome, we should not wait for a trial of dexamethasone as there is a risk of permanent neurological damage if the cord is not decompressed",
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"explanation": "Given this patient's new neurology findings he should have urgent radiotherapy within 24hrs to prevent permanent neurological damage. While dexamethasone is a crucial part of management of MSCC and cauda equina syndrome, we should not wait for a trial of dexamethasone as there is a risk of permanent neurological damage if the cord is not decompressed",
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"explanation": "This patient has metastatic spinal cord compression (MSCC) and cauda equina syndrome secondary to a metastatic deposit in the lumbar spine which is impinging on the spinal cord. High dose dexamethasone is given to reduce inflammation around the tumour. Given this patient's new neurology findings, however, he should have urgent radiotherapy within 24hrs to prevent permanent neurological damage. Radiotherapy to the tumour can reduce pressure on the cord through tumour shrinkage and can achieve local tumour control",
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"explanation": "# Summary\n\nSpinal cord compression (SCC) is a medical emergency that can lead to permanent neurological disability. It causes symptoms of weakness and sensory disturbance below the level of the compression, back pain deep and bladder and bowel involvement (incontinence, constipation or retention). Upper motor neurone signs are seen. Causes include trauma, malignancy (especially metastatic spinal cord compression), disc prolapse or compression by an abscess or epidural haematoma. An MRI of the whole spine is the key investigation. Management depends on the underlying cause; high dose steroids and referral to neurosurgery for consideration of decompression are key. \n\n\n# Definition\n\nSpinal cord compression (SCC) is a form of myelopathy caused by pressure on the cord by a variety of causes. It causes an upper motor neurone lesion, unlike the lower motor neurone signs seen in cauda equina syndrome, where compression is below the level of L1. \n\n\n# Epidemiology\n\n- Spinal cord injury affects approximately 15.4 million people globally\n- Trauma causes the most cases worldwide, with falls, road traffic accidents and violence being the most common precipitants\n- In the UK, there are around 4400 new cases of spinal cord injury per year\n- Metastatic spinal cord compression (MSCC) is the leading cause in the UK \n- In around a quarter of patients, MSCC is their first presentation of malignancy \n\n\n# Aetiology\n\n- **Trauma** - typically due to vertebral fractures or dislocation of facet joints; the cord may be severed in significant trauma\n- **Malignancy i.e. MSCC** - either due to pathological collapse of vertebrae or compression by growing tumours\n- **Infection** including abscess formation and chronic infections such as tuberculosis \n- **Epidural haematoma** where blood accumulates in the epidural space, compressing the cord\n- **Intervertebral disc prolapse** although this is much more rare than lumbar disc prolapses causing cauda equina syndrome\n\n\n\n\n# Signs and Symptoms\n\n**Symptoms include:**\n\n\n- Back pain, which is typically:\n- Severe\n- Progressive\n- Aggravated by straining e.g. coughing\n- Difficulty walking\n- Weakness below the level compressed (typically bilateral and symmetrical)\n- Numbness below the level compressed\n- Urinary or faecal incontinence\n- Urinary retention\n- Constipation\n\n\n**Signs seen (below the level of the lesion):**\n\n\n- Hypertonia\n- Hyperreflexia (although reflexes may be absent at the level compressed)\n- Clonus\n- Upgoing plantars\n- Sensory loss (a \"sensory level\")\n\n\nSymptoms and signs of an underlying cause may also be present, e.g. weight loss and fatigue in a patient with MSCC, fevers in a patient with tuberculosis. \n\n\n# Differential Diagnosis\n\n- **Transverse Myelitis** causes inflammation of the cord that presents similarly to SCC; it may be seen in the context of chronic demyelinating diseases such as Multiple Sclerosis or Neuromyelitis Optica (where other manifestations e.g. optic neuritis may be present)\n- **Cauda Equina Syndrome** is usually caused by herniation of a lumbar disc compressing the cauda equina; bowel and bladder disturbances may be present but signs are lower motor neurone (e.g. flaccid rather than spastic paralysis)\n- **Peripheral Neuropathy** also causes symptoms of weakness and sensory loss, signs are lower motor neurone rather than upper and distribution differs depending on aetiology (e.g. symptoms often unilateral in compression neuropathies)\n- **Spinal metastases** and other causes of back pain (e.g. musculoskeletal), especially if the predominant symptom is pain with minimal neurological symptoms and signs\n- **Sciatica** refers to pain in the lower back, buttocks and posterior legs caused by nerve root compression usually secondary to disc herniation in the lumbar spine; weakness can also occur but MRI will differentiate this from SCC\n\n\n# Investigations\n\nAn **MRI whole spine** is the key investigation\n\n\n- The whole spine should be imaged as there may be compression at multiple levels\n- In cases of suspected MSCC, this should be done within 24 hours as per NICE guidelines\n- Patients with suspected spinal metastases (e.g. back pain) with no neurological signs or symptoms suggestive of MSCC should have their MRI within 1 week\n\n\nIn some cases other imaging modalities may be used, e.g. **whole-body CT** in the context of major trauma. CT may also be used in patients for whom MRI is contraindicated.\n\n\nOther investigations indicated depend on the presentation and suspected aetiology:\n\n\n- Do a **bladder scan** if suspected urinary retention \n- An **ECG** and **baseline blood tests** should be done in anticipation of possible emergency surgical decompression (including a **group and save** and **clotting**)\n- In cases where MSCC is the first presentation of malignancy, further investigations are required to determine where the primary cancer is (guided by history and examination)\n- This may include further imaging e.g. a CT of the chest, abdomen and pelvis\n- Bloods may be done for tumour markers e.g. PSA in men\n- Biopsy is usually required to confirm the diagnosis\n\n# Management\n\n- Management depends on the underlying cause as well as the patient's background \n- Patients with traumatic spinal cord injuries should be transferred to a major trauma centre\n- General principles include:\n- Immobilise the patient and nurse with spinal precautions (e.g. log-rolling)\n- Regular repositioning to prevent pressure ulceration in immobile patients\n- Analgesia for pain\n- VTE prophylaxis \n- Catheterise if in urinary retention\n- Counselling and rehabilitation is key, with multidisciplinary input (e.g. physiotherapy) \n\n**Using MSCC as an example:**\n\n- Start high-dose steroids (usually 16mg dexamethasone initially) in patients with suspected MSCC - this reduces oedema helping to relieve compression\n- A proton pump inhibitor (PPI) should also be given to prevent peptic ulceration caused by steroids\n- Blood glucose should be monitored for hyperglycaemia secondary to steroids\n- Refer to neurosurgery urgently for consideration of surgical decompression (other options include vertebroplasty or kyphoplasty)\n- Patients unsuitable for surgery may have radiotherapy for spinal metastases - this can also be used as an adjuvant after surgery\n- Spinal braces may be used in patients not suitable for surgery to help with pain management and spinal stability\n- Oncology input is key both for diagnosis in patients without a known malignancy and for ongoing management (e.g. chemotherapy)\n\n\n# NICE Guidelines\n\n\n[NICE - Spinal injury: assessment and initial management](https://www.nice.org.uk/guidance/ng41/)\n\n\n[NICE - Spinal metastases and metastatic spinal cord compression](https://www.nice.org.uk/guidance/ng234)\n\n\n# References\n\n[Patient UK - Spinal Cord Compression](https://patient.info/doctor/spinal-cord-compression)\n\n\n[World Health Organisation - Spinal Cord Injury](https://www.who.int/news-room/fact-sheets/detail/spinal-cord-injury)",
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"question": "A 72-year-old man with prostate cancer and spinal metastases presents to the emergency department with 12 hours of painful urinary retention, 3 days of worsening lower limb weakness, and a flare of his chronic back pain. \nA urinary catheter is inserted, which drains 1200mL of clear urine.\n\n\nNeurological exam shows normal tone, reduced power (4/5) in both legs, reduced knee and ankle reflexes, upgoing plantars, and normal coordination. He has saddle anaesthesia and decreased anal tone on rectal examination.\n\nMRI spine shows severe metastatic spinal cord compression from L1 to L3.\n\nThe neurosurgery team opts for conservative management, and 16mg dexamethasone is prescribed.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "The midbrain may be damaged as a consequence of head injury; however, the nuclei of CN IX and X are found in the medulla, not the midbrain. The midbrain contains the nuclei of CN III and IV. These are not involved in the gag reflex.",
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"explanation": "The gag reflex is an evolutionary reflex with the primary role being to prevent foreign body inhalation. This reflex is made up of the glossopharyngeal nerve (CN IX) as the afferent limb and the vagus nerve (CN X) as the efferent. These two nerves have their nuclei in the brainstem medulla, alongside CN XI and XII. Compression may be as a result of raised intracranial pressure secondary to injury, given that no focal abnormalities were noted on his head scan.",
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"comment": "Stolen from another question:\n\nMidbrain CN 1,2,3,4\nPons CN 5,6,7,8\nMedulla CN 9,10,11,12",
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"explanation": "# Summary\n\nRaised intracranial pressure (ICP) can result from various underlying causes and presents with a range of symptoms. Concerning features include **headaches**, particularly those worse in the morning or with bending over, **visual disturbances**, **nausea and vomiting**, and **focal neurological deficits**. Additional worrying signs related to the underlying cause include **weight loss** and **night sweats**. Prompt recognition and management are essential to prevent serious complications like **seizures**, **reduced Glasgow Coma Scale (GCS)**, and potentially fatal outcomes such as **brain herniation (coning)** and death.\n\n# Definition\n\nRaised ICP refers to increased pressure within the skull, which can lead to brain damage and death if left untreated. The **Monro-Kellie Doctrine** explains that the skull is a fixed volume, and any increase in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) must be compensated for by a decrease in another component to maintain normal pressure. Failure to compensate leads to elevated ICP, increasing the risk of **coning** (herniation of brain tissue) and **brainstem death**.\n\n# Aetiology\n\nThe causes of raised ICP are varied and can be classified using the **VITAMIN C DEF** mnemonic:\n\n- **V**ascular: Stroke, intracranial hemorrhage (subdural, epidural, subarachnoid).\n- **I**nfective: Meningitis, encephalitis, brain abscess.\n- **T**rauma: Traumatic brain injury.\n- **A**utoimmune: Vasculitis.\n- **M**etabolic: Hepatic encephalopathy, hypercapnia.\n- **I**atrogenic: Post-surgical or procedural complications.\n- **N**eoplastic: Primary or metastatic brain tumors.\n- **C**ongenital: Hydrocephalus.\n- **D**egenerative: Normal pressure hydrocephalus (in elderly patients).\n- **E**ndocrine: Pituitary adenoma, hypothyroidism (myxedema coma).\n- **F**unctional: Idiopathic intracranial hypertension (IIH).\n\n# Symptoms and Signs\n\n## Symptoms\n\n- **Headaches**: Worse in the morning, with coughing, straining, or bending over.\n- **Nausea and vomiting**: Often early signs of raised ICP.\n- **Visual disturbances**: Blurred vision, diplopia, or papilledema (swelling of the optic disc).\n- **Seizures**: May occur as ICP rises.\n- **Focal neurological deficits**: Varies depending on the underlying cause (e.g., weakness, sensory changes).\n\n## Signs\n\n- **Cranial nerve involvement**: \n - **Abducens nerve (CN VI)** is most vulnerable due to its long course, leading to **lateral gaze palsy**.\n - **Third cranial nerve palsy** (uncal herniation): Ptosis, fixed dilated pupil, and eye deviation.\n- **Cushing’s triad**: A late sign of impending brain herniation, includes:\n - **Bradycardia**.\n - **Hypertension**.\n - **Irregular breathing**.\n\n# Investigations\n\n## Clinical assessment\n\n- **History and examination**: Look for signs of raised ICP and focal neurological deficits.\n- **Observations**: Watch for **Cushing’s triad** as a sign of impending coning.\n\n## Blood tests\n\n- Focus on identifying the underlying cause (e.g., infection, metabolic derangements).\n\n## Neuroimaging\n\n- **CT head (CTH)**: First-line imaging to assess for mass lesions, hemorrhage, or hydrocephalus.\n- **MRI**: May be used for further characterization of lesions or if clinical suspicion remains despite normal CT findings.\n\n# Management\n\n## Initial Assessment\nManagement begins with a standardized **ABCDE approach**:\n\n- **Airway, Breathing, Circulation**: Ensure airway patency and adequate oxygenation.\n- **Disability**: Assess using the **Glasgow Coma Scale (GCS)**.\n- **Exposure**: Check for signs of trauma, infection, or other causes of raised ICP.\n\n# Medical Management\n\n1. **Seizure management**: Detect and treat seizures with **anticonvulsants** as per the **status epilepticus protocol**.\n2. **Positioning**: Elevate the bed to **30-40 degrees** to facilitate venous drainage and reduce ICP.\n3. **Sedation and airway protection**: If **GCS < 8**, consult an **anesthetist** for airway management.\n4. **Hyperosmolar therapy**: \n - **Hypertonic saline** is preferred for reducing ICP through osmotic effects.\n - **Mannitol** may also be used, but carries risks such as **unpredictable pharmacokinetics** and potential **anaphylaxis**.\n5. **Control of underlying cause**: Treat infection (e.g., antibiotics for meningitis), control metabolic derangements, or manage systemic conditions contributing to raised ICP.\n\n# Surgical Management\n\n1. **Neurosurgical referral**: If the cause is a mass lesion, intracranial hemorrhage, or hydrocephalus, neurosurgical input is required.\n2. **Definitive interventions**: These may include:\n - **Decompressive craniectomy** to relieve pressure.\n - **Ventriculostomy** or **ventriculoperitoneal (VP) shunt** for drainage of CSF in cases of hydrocephalus.\n\n# Monitoring and Follow-Up\n\n- Continuous monitoring of **GCS** and **ICP** is critical.\n- Regular neuroimaging may be required to assess the progression of the underlying cause and response to treatment.\n\n",
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"question": "A 32-year-old man is brought in by ambulance to A&E after a road traffic collision. On examination, he has a large wound at the back of his head. His Glasgow Coma Score is 3. A CT scan of the head shows no abnormalities. A rapid sequence induction of anaesthetic is performed to secure his airway. A week into his admission, extubation is attempted on the Intensive Care Unit but this is unsuccessful. A gag reflex is documented as being absent in his medical notes.\n\nWhere is the lesion causing his clinical presentation?",
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"explanation": "There should be suspicion of a previously unwitnessed fall due to the presence of bruising along the patient's arm and reported low staffing levels by the carer. Unwitnessed falls can lead to head injury. The elderly are at higher risk of subdural haematomas after head injury due to brain atrophy stretching the bridging veins within the subdural space. Therefore, this presentation likely represents a subdural haematoma. A CT head can be used to confirm the diagnosis; the patient will have a crescent-shaped mass.",
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"explanation": "Extradural haematomas typically present after a head injury with a blow to the temples resulting in rupture of the middle meningeal artery. There is typically an initial loss of consciousness, followed by a period of lucidity then rapid decline in conscious level. There are no clinical features to suggest an extradural haematoma. The CT head would show a convex-shaped mass.",
"id": "52864",
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"explanation": "A subarachnoid haemorrhage would typically present with sudden-onset thunderclap headache and rapid clinical deterioration. Given the suspicion of a fall and the subacute presentation, a subdural haematoma is more likely in this age group due to brain atrophy and bridging vein tethering.",
"id": "52865",
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"explanation": "Urinary tract infections (UTIs) can cause acute confusional states (delirium). This patient is presenting acutely confused; therefore, it is a diagnosis worth considering. However, there are no clinical features of UTI in either the history (such as dysuria, frequency or urgency), or examination (such as fever or suprapubic pain). This makes a UTI unlikely.",
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"explanation": "Normal pressure hydrocephalus is a possible differential for the falling and confused patient. These patients are typically described as 'wet, wobbly and weird', relating to urinary incontinence, ataxia and confusion respectively. However, there is an absence of these features in the clinical history and a subdural haematoma is a diagnosis to exclude first.",
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"explanation": "\n### Summary\n\nA subdural haematoma (SDH) is a neurological condition characterized by the accumulation of venous blood between the dura mater and arachnoid mater, often following minor trauma in elderly patients. It can present with a reduced Glasgow Coma Scale (GCS), and is commonly seen in patients with fluctuating GCS. Diagnosis is typically established through a CT scan, with the appearance of the clot varying based on its age. Management strategies largely depend on the stage of the haematoma, with craniotomy indicated for acute haemorrhages, and burr holes recommended for chronic haemorrhages.\n\n### Definition\n\nA subdural haematoma is characterised by the accumulation of venous blood in the potential space between the dura mater and arachnoid mater of the brain.\n\n### Epidemiology\n\nSubdural haematomas typically occur in elderly individuals, particularly those over 65 years of age. It is often a consequence of minor trauma, leading to shearing forces that tear bridging veins between the cortex and dura mater. Risk factors include:\n\n- Advancing age (>65 years old)\n- Bleeding disorders or anticoagulant therapy\n- Chronic alcohol use\n- Trauma.\n\n### Aetiology\n\nThe haematoma results from shearing forces that tear the bridging veins between the cortex and dura mater. These forces commonly arise from minor head traumas but can also occur spontaneously in patients with bleeding disorders, anticoagulant therapy, or chronic alcohol use.\n\n### Signs and Symptoms\n\nClinical presentation of a subdural haematoma varies but may include:\n\n- Headache\n- Nausea or vomiting\n- Confusion\n- Fluctuating GCS\n- Behavioural change.\n\n\n### Differential Diagnosis\n\nDifferential diagnoses for subdural haematoma include:\n\n- Epidural haematoma: Characterized by a brief loss of consciousness, followed by a \"lucid interval\" and then rapid neurological deterioration.\n- Traumatic brain injury: Symptoms may include headache, confusion, lightheadedness, dizziness, blurred vision, or tired eyes.\n- Stroke: Presents with sudden numbness or weakness, especially on one side of the body, confusion, trouble speaking or understanding, trouble seeing in one or both eyes, and trouble walking, dizziness, or loss of balance or coordination.\n- Dementia: Gradual cognitive decline without fluctuating GCS.\n- Migraine: Recurrent headaches that might be accompanied by nausea, vomiting, and sensitivity to light and sound.\n\n### Investigations\n\nDiagnosis of a subdural haematoma is primarily established through a CT scan. \n\nThe appearance of the clot varies based on its age:\n\n- Hyperacute phase (<1 hour): The clot may appear isodense, with underlying cerebral oedema.\n- Acute phase (<3 days): The clot appears as a crescent-shaped hyperdense extra-axial collection over the affected hemisphere.\n- Sub-acute phase (3 days to 3 weeks): The clot appears more isodense compared to the adjacent cortex, making identification more difficult. Contrast-enhanced CT or MRI can aid identification. There may be associated mass effect causing midline shift and sulcal effacement.\n- Chronic phase (>3 weeks): The haematoma appears hypodense relative to the adjacent cortex.\n\n[lightgallery]\n\n[lightgallery1]\n\nFurther investigations may include:\n\n- Routine blood tests including FBC, Renal Profile, Liver Function Tests\n- Clotting profile (to assess for coagulopathy)\n\n### Management\n\nManagement of a subdural haematoma depends on the stage, patient’s premorbid baseline, and functional status. Many cases are managed conservatively, especially if there is no midline shift or cerebral oedema. However, for more severe cases, neurosurgical referral is required.\n\n- **Conservative management**: If no significant midline shift or cerebral oedema.\n\t- For patients taking the DOAC dabigatran, Idarucizumab is a licensed NICE-approval reversal agent which can be given.\n- **Surgical management**: In cases where intervention is necessary, options include:\n - **Craniotomy**: Typically for acute haemorrhages.\n - **Burr holes**: Typically for chronic haemorrhages.\n",
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"question": "An 83-year-old man with mild vascular dementia is brought to A&E by one of his carers. They report that he has not been himself for the past few weeks. He was previously independent with his activities of daily living but is now unable to feed or dress himself due to increasing confusion. This morning he was found to be very drowsy and withdrawn during breakfast. The carer admits that over the past few weeks they have been understaffed due to staff sickness. On examination, there is fading bruising along his left arm and shoulder. \n\nWhat is the most likely explanation for his presentation?",
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"explanation": "Relative afferent pupillary defects are present when there are issues with the afferent pathway of the pupillary reflex, that is, retinal or optic nerve pathology. Neither are involved in cavernous sinus syndrome.",
"id": "52869",
"label": "c",
"name": "Relative afferent pupillary defect",
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"answer": false,
"explanation": "Sensorineural deafness occurs due to disorders of the vestibulocochlear (VIII) nerve. This nerve does not run through the cavernous sinus.",
"id": "52870",
"label": "d",
"name": "Sensorineural deafness on the left",
"picture": null,
"votes": 292
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"explanation": "The facial nerve does not run through the cavernous sinus; therefore, this option is incorrect.",
"id": "52868",
"label": "b",
"name": "Facial nerve palsy",
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"votes": 666
},
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"explanation": "This patient has a cavernous sinus syndrome, probably due to a thrombus secondary to cavernous sinus infection. She is at higher risk of infection due to her poorly controlled diabetes and her recent paranasal sinus surgery. The cavernous sinus houses cranial nerves III, IV, VI, Va and Vb, and the internal carotid artery. The changes are ipsilateral to the side of the lesion. There is also an issue with venous drainage from the facial vein leading to chemosis, periorbital oedema, orbital pain and proptosis. Associated complications include seizures, septic emboli, Horner syndrome and intracranial hypertension.",
"id": "52867",
"label": "a",
"name": "Abducens nerve palsy",
"picture": null,
"votes": 880
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Sensation to the skin overlying the chin is provided by Vc (the mandibular branch of the trigeminal nerve). This does not run through the cavernous sinus.",
"id": "52871",
"label": "e",
"name": "Loss of sensation over the chin",
"picture": null,
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"comment": "A very good question- tests anatomy and clinical knowledge x",
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"comment": "allow being a sweat. \n",
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"explanation": "# Summary\n\nCentral Venous Sinus Thrombosis (CVST) is a rare but serious condition involving the occlusion of cerebral venous sinuses. It primarily affects younger individuals, with women at higher risk, particularly those of childbearing age. Risk factors include hormonal influences, prothrombotic conditions, systemic diseases, and local factors like trauma or infection. Symptoms are variable but often include headaches, neurological deficits, and seizures. Diagnosis is typically confirmed with imaging, such as CT venogram. Management involves anticoagulation therapy, usually starting with low molecular weight heparin and possibly transitioning to Warfarin, along with addressing underlying causes.\n\n# Definition\n\nCentral Venous Sinus Thrombosis (CVST) refers to occlusion of venous vessels in sinuses of the cerebral veins\n\n# Epidemiology\n\nCVST has an incidence of approximately 3-4 cases per million people per year. Representing 0.5%-3% of all the types of stroke, affecting predominantly younger people. Women are affected more than men and mostly between the ages of 20 and 35. This is hypothesised to be due to pregnancy and the use of the COCP.\n\n# Risk factors\n\nRisk factors are similar to those for venous thromboembolism and include: \n\n- Hormonal factors (the pill, pregnancy, and the peri-partum period)\n- Prothrombotic haematological conditions or malignancy\n- Systemic disease (such as dehydration or sepsis)\n- Local factors (skull abnormalities, trauma, or local infection\n-\n\n# Presentation\n\n- Presentation is variable but common symptoms include headache, confusion/drowsiness, impaired vision, and nausea/vomiting.\n\n- Other signs include seizures, reduced consciousness, focal neurological deficits, cranial nerve palsies, and papilloedema.\n\n# Investigations\n\n- Non-contrast CT reveals a hyperdensity in the affected sinus.\n\n- CT venogram is used to look for a filling defect ('the empty delta sign').\n\nThe most common form of dural venous thrombosis affects the superior sagittal sinus.\n\nCavernous sinus thrombosis is less common. It is typically caused by spreading sinus infection and presents with chemosis, exophthalmos, and peri-orbital swelling.\n\n# Management\n\nThe mainstay of treatment is with low molecular weight heparin (LMWH) and addressing any underlying risk factors that may increase risk of clotting e.g. cancer, autoimmune disease.\n\nFollowing initial therapy with LMWH, this can be further bridged to a vitamin K antagonist such as Warfarin. \n\n# References\n\n[Click here for more info on intracranial venous thrombosis](https://patient.info/doctor/intracranial-venous-thrombosis)",
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"question": "A 42-year-old woman presents with a 2-d history of reduced sensation to the left side of her face. She also has double vision and is struggling with pain in her left eye. She has a past medical history of poorly controlled type 2 diabetes and underwent paranasal sinus surgery 4 d ago. On examination, there is extensive left-sided periorbital oedema and proptosis. Her temperature is 38.4 °C.\n\nWhat additional finding might be present on physical examination?",
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"explanation": "An MRI is rarely done because a CT orbit is quicker to carry out and most often confirms the diagnosis. On T1, a low signal will be observed.",
"id": "52875",
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"explanation": "This patient likely has orbital cellulitis, as indicated by the presence of erythema and swelling surrounding the left eye, fever, diplopia (due to extraocular eye muscle involvement) and pain. The diplopia occurs due to complex ophthalmoplegia, which is when eye signs cannot be attributed to a single cranial nerve. The orbit is made up of seven bones, including the zygomatic, palatine and maxillary bones. Fractures of any of these bones are a risk factor for developing orbital cellulitis. This is a potentially sight-threatening emergency and can be further complicated by infective extension into the cavernous sinus. The best test is a CT orbit for this condition.",
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"explanation": "This is a highly sensitive imaging modality for evaluating thromboses within the venous sinuses, not for identifying orbital cellulitis.",
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"explanation": "This is a reasonable option and a CT of the head is often performed alongside a dedicated scan of the orbit. However, a dedicated scan of the orbit is still required, so this is not the best investigation.",
"id": "52873",
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"name": "CT head with contrast",
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"explanation": "An MRI is rarely done because a CT orbit is quicker to carry out and most often confirms the diagnosis. On T2, a high signal will be observed.",
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"comment": "ct a child?",
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"comment": "seeing T1 and T2 scared me ",
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"explanation": "# Summary\n\nOrbital cellulitis is a serious infection of the structures behind the orbital septum, presenting a sight- and life-threatening emergency. Key signs and symptoms include periocular pain and swelling, fever, malaise, erythematous, swollen and tender eyelid, chemosis, proptosis and restricted eye movements. The gold standard investigation for orbital cellulitis is a CT orbit. Management involves hospital admission for IV antibiotics and close monitoring. Preseptal cellulitis is a less severe infection of the tissue anterior to the orbital septum, which can progress to orbital cellulitis if not properly managed. \n\n# Definition\n\n**Orbital cellulitis** is a sight- and life-threatening emergency. It describes infection of the structures behind the orbital septum.\n\nThe orbital septum is a membranous sheet that forms the anterior border of the orbit, extending from the orbital rims (superior and inferior) and into the eyelids. \n\n**Preseptal cellulitis** refers to infection of tissue anterior to the orbital septum. It is much more common than orbital cellulitis and 80% of cases occur in children under the age of 10 years. It is less severe than orbital cellulitis, unless it spreads past the septum (which is not fully developed) and becomes orbital cellulitis.\n\n# Epidemiology\n\nOrbital cellulitis is less common than preseptal cellulitis, with the latter accounting for 80% of cases, mostly occurring in children under the age of 10.\n\n\n# Risk factors \n\n* Trauma\n* Surgical – ocular, adnexal or sinus\n* Sinus disease – ethmoidal sinusitis is the most common site of infection that spreads to the orbit\n* Other facial infections – preseptal, dental abscess or dacryocystitis\n\n# Signs and Symptoms\n\nOrbital cellulitis:\n\n* Periocular pain and swelling\n* Fever\n* Malaise\n* Erythematous, swollen and tender eyelid\n* Chemosis\n* Proptosis\n* Restricted eye movements +/– diplopia\n\nThe typical patient with **preseptal cellulitis** is a *child with an erythematous swollen eyelid, mild fever and erythema surrounding the orbit.*\n\n[lightgallery]\n\nImportant findings that suggest preseptal cellulitis, rather than orbital cellulitis, are:\n\n* No proptosis\n* Normal eye movements\n* No chemosis\n* Normal optic nerve function\n\n\n# Investigations\n\n- Blood tests: FBC, CRP to screen for raised inflammatory markers\n- Swabs sent for microscopy, culture and sensitivity\n- **CT orbit** is the gold standard investigation to distinguish orbital cellulitis from preseptal cellulitis\n\n# Management\n\n- Patients with orbital cellulitis require admission for IV antibiotics and close monitoring with input from the ophthalmology, ear, nose and throat and medical teams.\n- Preseptal cellulitis - Young or systemically unwell children should be admitted for IV antibiotics.\nOtherwise, treatment is with oral antibiotics and daily outpatient review.\n\n\n# References\n\nDenniston AK, Murray PI. Oxford Handbook of Ophthalmology. Fourth Edition. Oxford University Press. 2018.",
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"question": "A 14-year-old adolescent is brought to A&E after a week-long history of painful left eye movements and diplopia. One week ago, she was struck in the face with a hockey stick and sustained an undisplaced fracture of the zygomatic bone. She was sent home with analgesia and clinic follow-up with ophthalmology. On examination, you note swelling and erythema around the left eye. She has a complex ophthalmoplegia but the remainder of her cranial nerve examination is unremarkable. Her temperature is 38.7 °C.\n\nWhich of the following is the next best investigation?",
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"explanation": "Huntington's disease is an autosomal dominant disorder with observed genetic anticipation through spermatogenesis. It is caused by expansion of the triplet repeat, CAG encoding glutamine, in the huntingtin gene (*HTT*) on chromosome 4. Around 37+ CAG repeats are needed to develop the disease. In the earliest stages, the symptoms and signs are nonspecific, including low mood, difficulties with concentrating, coordination problems and irritability. As the disease progresses, chorea (involuntary jerking or dancing movements) and dementia occur. Anticipation is the process whereby expansion of a pathological repeat sequence, in this case CAG repeats, are observed after each generation. In the case of Huntington's disease, this is more notable with paternal inheritance. The longer the repeat sequence, the earlier the onset of the disorder. In this case, there has likely been inheritance from the paternal side due to earlier onset of the disorder being illustrated in the son and father's past medical history.",
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"explanation": "In Huntington's disease, there are pathological expansions in CAG repeats, with paternal inheritance being associated with higher genetic instability and therefore expansion. CTG repeats are the underlying cause for myotonic dystrophy type I, which is also autosomal dominant and exhibits anticipation. The other notable group of diseases that have pathological CAG repeats are the spinocerebellar ataxias (SCAs).",
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"explanation": "In Huntington's disease, there are pathological expansions in CAG repeats, with paternal inheritance being associated with higher genetic instability and anticipation. CCTG repeat is the pathological basis behind myotonic dystrophy type II.",
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"explanation": "CAG repeat expansions and anticipation are the cause of the early presentation of this patient's Huntington's disease. However, anticipation in Huntington's is observed through spermatogenesis and paternal transmission and not oogenesis/maternal transmission.",
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"explanation": "In Huntington's disease, there are pathological expansions in CAG repeats, with paternal inheritance being associated with higher genetic instability and therefore expansion. CTG repeats are the underlying cause for myotonic dystrophy type I, which is also autosomal dominant and exhibits anticipation. The other notable group of diseases that have pathological CAG repeats are SCAs.",
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"explanation": "# Summary\n\nHuntington's disease is an autosomal dominant neurodegenerative disorder characterized by choreoathetosis and dementia. Diagnosis is confirmed by genetic testing, and management involves a multidisciplinary approach to symptomatic relief and patient support. The disease progression is inevitable and usually leads to mortality due to complications from physical decline or suicide.\n\n# Definition\n\nHuntington's disease is a genetic disorder that causes progressive breakdown of nerve cells in the brain. It is characterised by motor, cognitive, and psychiatric abnormalities.\n\n# Epidemiology\n\nAs the most common hereditary neurodegenerative disorder, the prevalence of Huntington's disease is estimated to be between 1 in 10,000 and 1 in 20,000 individuals.\n\n# Aetiology\n\nHuntington’s disease is caused by an autosomal dominant mutation involving an excessive repetition of the CAG trinucleotide (>38 repeats) in the huntingtin gene, which encodes the huntingtin protein. \n\nThe number of CAG repeats is directly correlated with disease severity and age of onset, with **anticipation** observed in families—meaning that symptoms often present earlier in successive generations due to an increase in the number of repeats.\n\nThe pathogenesis is closely related to the gradual degeneration of specific brain regions, particularly the **caudate nucleus and putamen**, which are key components of the basal ganglia. This degeneration leads to the characteristic motor, cognitive, and psychiatric symptoms of the disease.\n\n# Signs and Symptoms\n\nHuntington's disease presents with a characteristic triad of symptoms:\n\n- Choreoathetosis: Unpredictable, flowing, and writhing movements\n- Cognitive impairment: Dementia, often marked by problems with judgment, memory, and other cognitive functions\n- Psychiatric abnormalities: Depression, irritability, apathy, and sometimes psychosis\n\n# Differential Diagnosis\n\nHuntington's disease should be differentiated from other disorders presenting with similar symptoms, such as:\n\n- **Parkinson's disease**: Characterized by bradykinesia, resting tremor, rigidity, and postural instability\n- **Wilson's disease**: Presents with liver disease, Kayser-Fleischer rings in the eye, and neurological symptoms such as dystonia, tremor, and dysarthria\n- **Huntington's disease-like disorders (HDL1, HDL2, HDL3, and HDL4)**: Present with a similar clinical picture but have different genetic backgrounds\n- **Neuroacanthocytosis syndromes**: Characterized by movement disorders and spiculated red blood cells (acanthocytes)\n\n# Investigations\n\nInvestigations in Huntington's disease include:\n\n- **Neuroimaging**: MRI and CT scans may show loss of striatal volume and an enlarged frontal horn of the lateral ventricles in moderate to severe disease stages\n- **Genetic testing**: Confirmatory, and also allows for predictive testing in at-risk family members with pre-test genetic counseling \n\n# Management\n\nAlthough no treatments can halt disease progression, management strategies aim at symptomatic relief and supporting the patient and their family:\n\n- **Chorea management**: Medications such as tetrabenazine are commonly used, with the most evidence base\n- **Depression management**: Selective serotonin reuptake inhibitors (SSRIs) are typically the first-line treatment\n- **Psychosis management**: Antipsychotics, preferably newer atypical agents, are used due to lower rates of extrapyramidal side effects\n- **Supportive care**: This includes a significant amount of physical and emotional support from a multidisciplinary team\n\n# Prognosis\n\nThe prognosis for Huntington's disease is poor, with an invariable decline in physical and cognitive abilities. Death usually occurs due to complications related to physical decline such as pneumonia, while suicide is the second most common cause of death.\n\n# References\n\n[Click here for more on Huntington's Disease](https://patient.info/doctor/huntingtons-disease-pro#nav-0)",
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"question": "A 27-year-old man presents to the Neurology Clinic with a 1-year history of progressive difficulty with concentrating, issues with coordination and irritability. Six months ago, he was admitted after a suicide attempt. He does not know his biological parents because he was adopted at a young age but he has been told that one of his biological parents had previously tried to kill themselves and are currently being reviewed by the memory clinic aged 45.\n\nWhat is the genetic basis of his underlying diagnosis?",
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"explanation": "Olanzapine is an atypical antipsychotic that can be used for the management of delirium. However, in this case, it would be most appropriate to trial nonpharmacological treatments first. In the elderly, olanzapine has also been associated with increased episodes of venous thromboembolism and may also worsen delirium. Like haloperidol, it should not be used in patients with Parkinson's disease or Lewy body dementia, due to its antidopaminergic effects and subsequent risk of precipitating rigidity.",
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"explanation": "Haloperidol is a recognised treatment for delirium. However, nonpharmacological interventions should be trialled in the first instance in this case. On occasion, pharmacological interventions may be tried as first-line treatment if necessary and proportionate, that is, if the patient poses an immediate risk to themselves or others. There is no evidence in this case that the patient is currently posing an immediate risk to herself or anyone around her. Haloperidol is a butyrophenone antipsychotic and antagonises the dopamine (D2) receptor. Therefore, it is avoided in patients with Parkinson's disease or Lewy body dementia, due to the risk of precipitating rigidity. The QTc should be checked before providing haloperidol wherever possible due to the risk of causing prolongation. Haloperidol may also worsen delirium in some patients.",
"id": "52888",
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"explanation": "This is a likely case of delirium precipitated by recent orthopaedic surgery. Despite the previous injury to staff earlier in the day, it would be most appropriate for you to try and de-escalate the situation using verbal reassurance and orientation before you consider pharmacological management. This is since it recognised that some of the drugs to treat delirium, for example, benzodiazepines, can worsen it and nonpharmacological measures if used appropriately can be quite effective. Interventions, such as reducing noise by nursing in a side room if safe, using familiar nurses, orientating with a clock and calendar, using photographs and inviting in the family, can often have a positive effect on these patients in their transient delirium.",
"id": "52887",
"label": "a",
"name": "Verbal reassurance and orientation",
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"explanation": "Lorazepam is a benzodiazepine given intravenously or orally. It can be used in the treatment of delirium alongside other types of benzodiazepines. However, it should not be used before nonpharmacological interventions in this case. Side effects include drowsiness and worsening of delirium. It is a suitable alternative to haloperidol in patients with Parkinson's disease or Lewy body dementia.",
"id": "52889",
"label": "c",
"name": "Lorazepam",
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"explanation": "Risperidone is an atypical antipsychotic that can be used for the management of delirium. However, in this case, it would be most appropriate to trial nonpharmacological interventions first. Like haloperidol, it should not be used in patients with Parkinson's disease or Lewy body dementia, due to its antidopaminergic effects and subsequent risk of precipitating rigidity. It can also cause worsening of delirium in some patients.",
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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 82-year-old woman is agitated after a total knee replacement 1d ago. The nurse in the bay has asked for help from the on call team as the patient is trying to leave her bed unattended and is shouting out non-specifically. The nurse reports that the patient settles if asked to remain in bed. The patient is often sleeping during the day but awake and eating throughout the night. She pushed over one of the physiotherapists earlier in the morning but there have been no further instances of aggression. The patient has no significant past medical or social history.\n\nWhat is the first step in the management of this patient?",
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"explanation": "This patient is presenting with acute dystonia in the form of torticollis (cervical dystonia) and an oculogyric crisis. Metoclopramide is primarily a D2 receptor antagonist and acts on the receptors in the chemoreceptor trigger zone in the central nervous system. It is also a prokinetic agent via its muscarinic activity. Due to antagonism at the D2 receptor, it may also cause blockade in the extrapyramidal circuits, leading to side effects including acute dystonia (such as oculogyric crises and cervical dystonias), and, with chronic use, tardive dyskinesias. The risk of acute dystonic reactions is increased with higher doses and younger patients.",
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"explanation": "This patient is presenting with acute dystonia, in the form of torticollis (cervical dystonia) and an oculogyric crisis. Cyclizine is a histamine H1 receptor antagonist. Side effects may include urinary retention but extrapyramidal side effects are not reported.",
"id": "52898",
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"explanation": "This patient is presenting with acute dystonia in the form of torticollis (cervical dystonia) and an oculogyric crisis. Ondansteron is an antiemetic particularly used in the case of nausea and vomiting caused by chemotherapy. It is a serotonin 5 HT3 receptor antagonist. It does not have any effect on the D2 receptors; therefore, acute dystonias are not a recognised side effect.",
"id": "52901",
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"explanation": "This patient is presenting with acute dystonia in the form of torticollis (cervical dystonia) and an oculogyric crisis. Promethazine is a first-generation antihistamine, antagonising the H1 receptor, and is generally used for its sedative effects, as opposed to its antiemetic effects. It has some antidopaminergic effects, which may lead to tardive dyskinesia, dystonias and akathisia but these are uncommon.",
"id": "52900",
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"explanation": "This patient is presenting with acute dystonia in the form of torticollis (cervical dystonia) and an oculogyric crisis. Chlopromazine is an antipsychotic that antagonises the D2 receptor and would not ordinarily be used to treat nausea and vomiting. Less commonly, it causes acute dystonias but it is known to cause tardive dyskinesia and akathisia, which are more likely at higher doses.",
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"comment": "does this hurt the fish",
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"comment": "This is an unfair question, chlopromazine is one of the anti-nausea medications recommended for treating N&V in pregnancy. It is also a typical antipsychotic- hence may also lead to acute dystonias in the same way as metoclopromide ",
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"comment": "Metoclopramide is a second line anti-emetic in N&V in pregnancy. Chlorpromazine is first line and can also cause extra-pyramidal side effects.... ",
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"explanation": "# Definition\n\nDystonias refer to a spectrum of movement disorders, characterised by involuntary muscle contractions leading to abnormal, often repetitive, movements and postures. These contractions can be prolonged and are often painful.\n\n# Epidemiology\n\nDystonias are considered the third most common movement disorder, following tremor and Parkinson's disease. It can occur at any age, but the timing and type of dystonia may vary based on whether it's primary or secondary.\n\n# Aetiology\n\n* **Primary dystonias** are idiopathic in nature, often genetic, and can be generalised or focal. A known example is the autosomal dominant generalised dystonia, also known as Flatau-Sterling syndrome. This usually starts in childhood and commences in the lower limbs before spreading to the rest of the body. Focal dystonia is limited to one part of the body, such as musician's cramp or spasmodic torticollis (cervical dystonias).\n* **Secondary dystonias** are usually attributable to specific causes or conditions, often related to drug use or neurological diseases. Common culprits include anti-dopaminergic drugs such as antipsychotics or anti-emetics (typically metoclopramide).\n\n# Signs and symptoms\n\nCommon signs and symptoms of dystonia include:\n\n* Prolonged muscle contractions\n* Abnormal postures\n* Repetitive movements\n* Cramping or pain in the affected muscles\n* Specific examples include: \n * Oculogyric crisis - upward deviation of the eyes\n \t\t* Commonly associated with starting a neuroleptic agent \n * Torticollis or cervical dystonia - abnormal, often painful, neck positioning\n * Trismus or lockjaw - difficulty opening the mouth due to muscle spasm\n\n# Differential diagnosis\n\nDystonias should be differentiated from other movement disorders and conditions that present with similar symptoms. Major differentials include:\n\n* **Parkinson's disease**: Characterized by bradykinesia, rigidity, rest tremor, and postural instability.\n* **Essential tremor**: Mainly causes action tremors, typically affecting the hands, head, or voice.\n* **Tardive dyskinesia**: Typically caused by long-term use of neuroleptic drugs, it manifests as involuntary, repetitive body movements such as grimacing, sticking out the tongue, or smacking the lips.\n* **Myoclonus**: Characterized by sudden, brief, involuntary muscle jerks.\n\n# Investigations\n\nInvestigation of dystonia often includes:\n\n* Detailed medical history\n* Neurological examination\n* Neuroimaging (e.g., MRI Head +- Spine)to assess for any structural cause\n* Genetic testing, especially in suspected primary dystonias\n* Evaluation of response to pharmacologic interventions\n\n\nplease can you re-group Mx section into primary and secondary dystonias. It’s a mid muddled here. Mainstay in secondary dystonia is stopping the offending drug e.g. neuroleptic/metoclopramide and managing the acute, painful dystonic reaction (with anticholinergics).\n\n# Management\n\nManagement of dystonia depends on whether it is primary (genetic or idiopathic) or secondary (due to an external factor such as medication or another condition):\n\n### Primary Dystonias\nFor primary dystonias (those that are genetic or idiopathic), the following treatments are often used:\n\n* **Botulinum toxin injections**: Particularly effective for focal dystonias.\n* **Oral medications**: These can include anticholinergics, benzodiazepines, and dopamine agonists to help manage symptoms.\n* **Physical therapy**: Helps to manage muscle function and reduce disability.\n* **Deep brain stimulation (DBS)**: Used for refractory cases that do not respond to other treatments.\n* **Genetic counseling**: Recommended for patients and their families to understand hereditary aspects.\n\n### Secondary Dystonias\nIn secondary dystonias (those caused by an identifiable external factor, such as medication):\n\n* **Withdrawal of offending agents**: Stopping the neuroleptic or metoclopramide that triggered the dystonia is essential.\n* **Management of acute dystonic reactions**: This often involves the use of anticholinergic medications to relieve painful muscle spasms.\n* **Further pharmacological therapies**: Botulinum toxin injections and oral medications (e.g., anticholinergics, benzodiazepines) may still be useful in ongoing management.\n* **Physical therapy**: Can aid in recovery and functional improvement.\n\n# References\n\nJankovic J. Treatment of dystonia. Lancet Neurology. 2006;5(10):864-872. doi:10.1016/S1474-4422(06)70572-1\n\nAlbanese A, Bhatia K, Bressman SB, et al. Phenomenology and classification of dystonia: a consensus update. Movement Disorders. 2013;28(7):863-873. doi:10.1002/mds.25475\n\nCloud LJ, Jinnah HA. Treatment strategies for dystonia. Neurotherapeutics. 2011;8(4):722-730. doi:10.1007/s13311-011-0074-7\n\n",
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"question": "A 33-year-old pregnant woman presents with persistent nausea and vomiting in the first trimester. She reports that she cannot keep any food down, and this has been the case for 5 d. She has managed small sips of water. On examination, she is tachycardic at 110 bpm, blood pressure 115/70 mmHg, respiratory rate 18 and is afebrile. A diagnosis of hyperemesis gravidarum is made by the admitting team and she is prescribed antiemetics and fluids. Two hours later the patient's head has rotated to one side and her eyes are periodically deviating upwards.\n\nWhat is the most likely antiemetic to have caused this side effect?",
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"explanation": "The recreational drug Ecstasy (3,4-methylenedioxy-methamphetamine) directly triggers ADH release, producing a syndrome of inappropriate antidiuretic hormone secretion. The drug also stimulates thirst, which can worsen the hyponatraemia by drinking. There is no suggestion of recreational drug use in the clinical history and the symptoms indicate the more likely diagnosis of AVP resistance (nephrogenic diabetes insipidus) secondary to lithium therapy. Sodium is also raised in this case.",
"id": "52905",
"label": "d",
"name": "Urine toxicology screen",
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"explanation": "This patient has presented with polyuria and polydipsia in the context of recent initiation of lithium therapy. The patient should be investigated for AVP resistance (nephrogenic diabetes insipidus), with the first investigation being paired serum and urine osmolalities. There would be a lack of response to desmopressin administration after water deprivation, due to resistance to desmopressin in the renal collecting ducts. In AVP deficiency (central diabetes insipidus), there is a deficiency of ADH; therefore, there should be a marked response to desmopressin administration, with over a 50% increase in urine osmolality. The desmopressin challenge may be useful further down the line during a water deprivation test line but not in the first instance.",
"id": "52906",
"label": "e",
"name": "Desmopressin challenge",
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"explanation": "This patient has presented with polyuria and polydipsia in the context of recent initiation of lithium therapy. The patient should be investigated for AVP resistance (nephrogenic diabetes insipidus) and in the first instance a paired serum and urine osmolality should be used. Water deprivation is a confirmatory test done further down the line since it is more time-consuming. During the water deprivation test, patients with AVP deficiency or resistance will develop an increasing osmolality of their serum as they become dehydrated. However, the urine remains dilute since they are unable to concentrate their urine in response to dehydration. A desmopressin challenge can be provided to distinguish between deficiency or resistance during this test. A response to desmopressin (ie. concentration of urine) would indicate a central cause. In AVP resistance there is little to no response to a desmopressin challenge.",
"id": "52904",
"label": "c",
"name": "Water deprivation test",
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"explanation": "This patient has been recently started on lithium, which is associated with AVP-resistance (nephrogenic diabetes insipidus). In AVP-R, the collecting ducts are insensitive to the effects of antidiuretic hormone (ADH) and aquaporins cannot be mounted. This results in an inability to concentrate urine and excessive free water loss. Patients typically present with polydipsia and polyuria and are at risk of dehydration if they do not maintain a good volume of oral fluid intake. The serum sodium may be raised or at the upper limit of normal due to dehydration. The best investigation for AVP deficiency or resistance in the first instance is paired urine and sodium osmolalities. Serum osmolality should be greater than 300 mOsm/kg and urine osmolality less than 750 mOsm/kg in this condition.",
"id": "52902",
"label": "a",
"name": "Urine and serum osmolality",
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"explanation": "This patient is presenting with polyuria and polydipsia, after recent commencement on lithium therapy for bipolar disorder. A diagnosis of AVP resistance (nephrogenic diabetes insipidus should be suspected). Diabetes insipidus is split into AVP deficiency (cranial DI) and AVP resistance. AVP deficiency is a deficiency of ADH, which is released from the posterior pituitary gland, whereas in AVP resistance, ADH is present but there is a failure of response in the renal collecting ducts. An MRI head would be indicated to evaluate for a central cause. In this case, given the initiation of lithium therapy and the absence of any neurological history or signs, AVP resistance is more likely. In any case, the diagnosis is still best initially made using paired serum and urine osmolalities.",
"id": "52903",
"label": "b",
"name": "MRI head with contrast",
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"explanation": "# Summary\n\nArginine vasopressin disorder, formerly known as Diabetes Insipidus, is a condition characterised by the reduced production or response to arginine vasopressin (AVP), also called antidiuretic hormone (ADH), resulting in excessive urination and thirst. The aetiology of DI varies with deficiency of AVP (AVP-D, more common) and AVP resistance (AVP-R) causes, such as head trauma, drug reactions, and genetic factors. Key clinical features include the production of large volumes of dilute urine, nocturia, and excessive thirst. Diagnostic investigations include urea and electrolyte tests, blood glucose tests, and measurement of paired serum and urine osmolality. Management depends on the underlying cause, and can include desmopressin, correction of metabolic abnormalities, and, in the case of AVP-R, potentially the use of a thiazide diuretic and a non-steroidal anti-inflammatory drug.\n\n# Definition\n\nArginine vasopressin disorder (formally diabetes insipidus) is an endocrine condition characterised by either an inadequate production (AVP-D) or an insufficient renal response (AVP-R) to arginine vasopressin (AVP), also called antidiuretic hormone (ADH).\n\n# Epidemiology\n\nIt is a rare condition, with AVP-D more common than AVP-R. The prevalence is approximately 1 in 25,000 individuals.\n\n# Aetiology\n\n**Causes of AVP Deficiency (Cranial DI)**\n\n- Head trauma\n- Inflammatory conditions (e.g., sarcoidosis)\n- Cranial infections such as meningitis\n- Vascular conditions such as sickle cell disease\n- Rare genetic causes\n\n**Causes of AVP Resistance (Nephrogenic DI)**\n\n\n- Drugs (e.g., lithium)\n- Metabolic disturbances (e.g., hypercalcaemia, hypokalaemia, hyperglycaemia)\n- Chronic renal disease\n- Rare genetic causes (e.g., Wolfram's syndrome)\n\n# Signs and Symptoms\n\n- Large volumes of dilute urine (>3 litres in 24 hours and a urine osmolality of <300 mOsm/kg)\n- Nocturia\n- Excessive thirst\n\nIn children, additional symptoms may include:\n\n- Failure to thrive\n- Enuresis\n\n# Differential Diagnosis\n\n- Diabetes mellitus: Polyuria, polydipsia, and weight loss\n- Primary polydipsia (compulsive water drinking): Large urine output, thirst\n- Chronic kidney disease: Fatigue, anemia, pruritus, electrolyte imbalances\n\n# Investigations\n\n- Urea and electrolytes (sodium may be raised)\n- Blood glucose (to rule out diabetes mellitus)\n- Urine dip\n- Paired serum and urine osmolality measurements\n\nArginine vasopressin disorder is present when the serum osmolality is raised (>295 mOsm/kg) with inappropriately dilute urine (urine osmolality < 300 mOsm/kg).\n\nIf the diagnosis remains uncertain, a **water deprivation test** can be performed:\n\n* This should only be done if there is evidence of hypovolaemia or hypernatraemia\n* The patient is deprived of fluids while monitored for urine osmolality and body weight changes\n* In AVP-D, urine osmolality increases with ADH administration\n* In AVP-R, urine osmolality remains low/unchanged despite ADH administration\n\n### Interpretation of water deprivation test\n\n| | AVP-D | AVP-R | Normal Results |\n|-----------------------------------|--------------------------|-------------------------|----------------------|\n| **Initial Urine Osmolality (Uosm)** | Reduced (<300 mOsm/kg) | Reduced (<300 mOsm/kg) | Elevated (>300 mOsm/kg) |\n| **Initial Serum Osmolality (Sosm)** | Elevated (>300 mOsm/kg) | Elevated (>300 mOsm/kg) | Stable (~280-300 mOsm/kg) |\n| **Urine Osmolality after ADH (Uosm)** | Rapidly increases | Remains low | Rapidly increases |\n| **Interpretation** | Partial response to ADH | No response to ADH | Adequate response to ADH |\n\nNB: The deprivation test also distinguishes arginine vasopressin disorder from primary polydipsia which is a condition characterised by similar symptoms of polydipsia and polyuria. The latter condition is usually due to a psychological cause of excessive drinking. Upon testing, urine osmolality is normal both after fluid deprivation and after desmopressin is given.\n\n# Management\n\n**Management of AVP-D (Cranial DI)**\n\n- AVP-D can be managed with desmopressin, a medication which mimics the action of endogenous ADH.\n- Sodium levels should be monitored routinely due to the risk of hyponatraemia.\n\n**Management of AVP-R (Nephrogenic DI)**\n\n- AVP-R is managed by correcting any underlying metabolic abnormalities and discontinuing any offending drugs.\n- High dose desmopressin has been used with variable results.\n- Other potential treatments include using a thiazide diuretic (counter-intuitive, we know) and a non-steroidal anti-inflammatory drug to reduce urine volume.\n\n# References\n\n[Patient.info - Diabetes insipidus](https://patient.info/doctor/diabetes-insipidus-pro)\n\n[NHS UK - DI](https://www.nhs.uk/conditions/diabetes-insipidus/causes/)",
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"learningPoint": "Lithium can cause nephrogenic diabetes insipidus, a condition where the kidneys become resistant to antidiuretic hormone (ADH), leading to the production of large volumes of dilute urine, decreased urine osmolality, and an elevated serum osmolality due to the body’s inability to concentrate urine properly.",
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"question": "A 34-year-old woman is referred to A&E from an inpatient psychiatric unit with a 3-d history of polyuria. She also reports being excessively thirsty despite drinking lots of water. Four weeks ago, she was diagnosed with epilepsy and bipolar disorder and was commenced on lithium and carbamazepine with good effect. Routine bloods performed by the psychiatry team are unremarkable, except for a sodium of 146.\n\nWhich of the following is the next best investigation?",
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"explanation": "An abdominal aortic aneurysm rupture may present with shock due to bleeding and subsequent reduced consciousness. Headache is not a typical component of the presentation and there is no evidence of haemodynamic instability here. Abdominal aortic aneurysms are also more likely in older male patients.",
"id": "52909",
"label": "c",
"name": "Abdominal aortic aneurysm rupture",
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"explanation": "A myocardial infarction (MI) typically presents with chest pain, breathlessness or syncope. Patients are typically older with cardiovascular risk factors. Younger patients may present with MIs, especially if there are strong risk factors such as use of cocaine or hereditary hypercholesterolaemia. ADPKD does not typically increase the risk of MI until there is a significant degree of renal impairment. The most likely cause of this presentation is a berry aneurysm rupture.",
"id": "52910",
"label": "d",
"name": "Myocardial infarction",
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"explanation": "Meningitis can cause headache and reduced consciousness. However, the natural history in this case is hyperacute, and therefore a haemorrhage is more likely since meningitis tends to have a more insidious onset. There are also no clinical features of infection, such as fever, or other features of meningism, such as neck stiffness. Furthermore, in this case the presence of bilateral flank masses should also raise suspicion of autosomal dominant polycystic kidney disease and the presence of a ruptured berry aneurysm.",
"id": "52908",
"label": "b",
"name": "Meningitis",
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"explanation": "Berry aneurysms are a recognised feature of autosomal dominant polycystic kidney disease (ADPCKD), which is an inherited cause of end-stage renal failure. The palpable bilateral flank masses should raise suspicion of underlying ADPCKD. Berry aneurysms have a propensity to rupture leading to a subarachnoid haemorrhage, presenting with a traditional sudden-onset 'thunderclap' headache and rapid neurological deterioration.",
"id": "52907",
"label": "a",
"name": "Subarachnoid haemorrhage",
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"explanation": "An extradural haematoma typically presents after a traumatic head injury with a brief loss of consciousness followed by recovery (lucid interval) and subsequent rapid deterioration in conscious level. It occurs typically due to a blow to the temples and rupture of the middle meningeal branch of the maxillary artery (a branch of the external carotid). There is no history of trauma in this patient and the clinical features of a lucid interval are not present.",
"id": "52911",
"label": "e",
"name": "Extradural haematoma",
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"comment": "\"Complained of a headache\" is underselling SAH pain a little",
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"explanation": "# Summary\n\nAutosomal Dominant Polycystic Kidney Disease (ADPKD) is the commonest inherited renal disease. It arises due to mutations in the PKD1 and PKD2 genes. PKD1 mutations are more common and tend to cause more severe disease. The disease is characterised by cyst formation both in the kidneys and in other organs, such as the liver, ovaries, spleen, pancreas and seminal vesicles. Patients may be detected on screening if family members are affected, or present with symptoms of loin pain, haematuria or abdominal masses. Patients may also present with complications such as hypertension and renal impairment. Other complications include cyst haemorrhage or infection, renal stones and an increased risk of cerebral berry aneurysms which may rupture, causing subarachnoid haemorrhage. Ultrasound is the first-line diagnostic investigation to identify renal cysts; genetic testing is not usually required but may be considered in some cases (e.g. atypical renal imaging). Management is primarily supportive, including lifestyle changes, regular monitoring and genetic counselling. Tolvaptan is used in some patients with rapidly progressive chronic kidney disease to slow the growth of renal cysts and renal impairment. Renal replacement therapy may be required if patients develop end-stage kidney disease.\n\n# Definition\n\nAutosomal Dominant Polycystic Kidney Disease (ADPKD) is an inherited renal disorder characterised by continuous formation and growth of cysts in the kidneys. This leads to progressive renal impairment due to destruction of nephrons and may cause end-stage kidney disease (ESKD). \n\nADPKD also has several extrarenal manifestations, including cyst formation in the liver and other organs and intracranial aneurysms.\n\n# Epidemiology\n \n- ADPKD is the most common genetic kidney disorder in adults\n- Prevalence is approximately 1:1000\n- Men and women are affected equally, and it occurs in patients of all ethnicities\n- It is responsible for up to 10% of end-stage renal disease\n- Approximately 85% of patients have PKD1 mutations and 15% have PKD2 mutations\n- Around 15% of patients with ADPKD have no family history of the condition (for example due to de novo mutations)\n \n# Aetiology\n\n- The PKD genes cause mutations in polycystin 1 and 2, which lead to cyst formation and expansion\n- PKD1 is located on chromosome 16, and PKD2 is located on chromosome 4\n- Disease is typically more severe with PKD1 mutations\n- A large number of causative mutations have been identified\n- Inheritance is autosomal dominant\n\n# Signs and Symptoms\n \nPatients may present with symptoms of:\n \n- Flank pain \n - May be acute, secondary to cyst haemorrhage, infection or urinary tract stones\n - Chronic pain is common and may be severe\n- Haematuria (often due to cyst rupture)\n- Fever and systemic illness due to infection i.e. malaise, nausea and vomiting\n - May present with recurrent urinary tract infections\n- Polyuria and nocturia\n- Chronic kidney disease e.g. lethargy, peripheral oedema, pruritus\n\nExamination findings include:\n\n- Bilateral large masses in the flanks (palpable enlarged kidneys)\n- Hepatomegaly (up to 70% have liver cysts)\n- Hypertension\n- Splenomegaly is rarer (5% have splenic cysts)\n\n# Differential Diagnosis\n\n- **Simple renal cysts** are very common and incidence increases with age\n - Patients have normal sized kidneys and renal function is not affected\n - Symptoms are rare\n - They are often an incidental finding on imaging or autopsy\n- **Acquired cystic kidney disease** is common in patients with chronic kidney disease\n - Patients on dialysis are particularly affected\n - Multiple bilateral small cysts are seen\n - Kidneys are often small in size\n - Cysts are usually asymptomatic\n- **Autosomal recessive polycystic kidney disease** is much rarer than ADPKD and manifests in infancy\n - It occurs when two copies of a mutated PKHD1 gene are inherited\n - Patients may be diagnosed in utero and pulmonary hypoplasia may be fatal in neonates\n - Biliary dysgenesis causes cholangitis and portal hypertension\n- **Tuberous sclerosis** is an autosomal dominant neurocutaneous disorder that usually occurs due to spontaneous mutations of tumour suppressor genes TSC1 or TSC2\n - Renal cysts are common as well as angiomyolipomas (benign renal tumours)\n - Seizures, learning difficulties and cardiac rhabdomyomas are common features\n - Cutaneous lesions include hypopigmented macules (ash leaf spots), facial angiofibromas (adenoma sebaceum) and shagreen patches\n- **Von Hippel-Lindau disease** is a rare autosomal dominant condition that leads to cysts and tumours developing in various organs\n - It is caused by a VHL gene mutation\n - Renal cysts are usually benign and asymptomatic\n - Renal cell carcinoma is more common and patients require surveillance for this\n - Retinal angiomas, haemangioblastomas of the cerebellum or spinal cord, pancreatic neuroendocrine tumours and phaeochromocytomas are other features not seen in ADPKD\n- **Medullary cystic kidney disease** is a rare autosomal dominant disease\n - Multiple small medullary cysts are seen\n - Kidneys are small or normal in size\n - Chronic tubulointerstitial nephritis leads to end stage renal disease\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urine dip** for haematuria and proteinuria (microalbuminuria may be seen but heavy proteinuria is rare)\n- **Urinary albumin:creatinine ratio** to grade CKD\n- **Urine MC&S** if infection is suspected\n\n**Blood tests:**\n\n- **FBC** may show polycythaemia (as polycystic kidneys may produce excessive erythropoietin); leukocytosis may be seen in infection\n- **U&Es** to monitor renal function\n- **Bone profile** is important in patients with chronic kidney disease to look for electrolyte derangement such as hyperphosphatemia\n- **LFTs** are usually normal despite hepatic cysts; rarely large cysts or biliary cystic lesions may cause obstructive jaundice\n\n**Imaging tests:**\n\n- **Ultrasound of the kidneys** is the key diagnostic test and is used for screening adult family members \n - 3+ renal cysts in total if aged 15-39 is sufficient to diagnose ADPKD\n - 2+ cysts in each kidney if aged 40-59 is sufficient to diagnose ADPKD\n - No cysts if aged 40+ is sufficient to exclude ADPKD\n- **CT** or **MRI** of the kidneys is more sensitive and so may be used in specific circumstances e.g. living donor evaluations\n- **MRI head** is indicated for screening of patients with a family history of intracranial aneurysms or subarachnoid haemorrhage\n- **Abdominal ultrasound** may also detect hepatic or splenic cysts\n- **Echocardiogram** if there is suspected valvular disease or hypertensive heart disease\n\n**Special tests:**\n\n- **Genetic testing** is challenging due to the heterogeneity of mutations seen\n - Up to 15% of patients with suspected ADPKD have no identifiable mutation\n - The majority of patients do not require genetic testing\n - It may be useful in atypical cases (e.g. significant asymmetry of cystic disease, no family history) or severe disease\n- **Renal biopsy** may be considered in specific cases, for example in patients with nephrotic-range proteinuria to rule out another renal pathology\n \n# Management\n \n**Conservative management:**\n\n- All patients should be referred to specialist services for diagnosis and management\n- Patient education, including providing information regarding implications for family members\n- Screening of at-risk adult relatives should be offered - children at risk should have regular blood pressure monitoring\n- Advise patients to avoid contact sports which may cause abdominal trauma and cyst rupture\n- Lifestyle advice on how to reduce cardiovascular risk should be provided (smoking cessation, healthy diet and regular exercise)\n- Avoid nephrotoxic drugs and oestrogens (promote hepatic cyst growth)\n- Patients require regular monitoring including serial ultrasounds to monitor renal volume\n\n**Medical management:**\n\n- Tolvaptan is an option for patients with stage 2 or 3 CKD with rapidly progressive disease, to slow cyst growth and renal impairment\n- Antihypertensives may be required to maintain a blood pressure of < 130/80\n - ACE inhibitors or angiotensin-II receptor antagonists are first-line\n- Analgesia is an important component of pain management, which may be acute or chronic\n- Antibiotics may be required for urinary tract infections, including cyst infections\n\n**Surgical management:**\n\n- Drainage of painful or infected renal cysts may be done percutaneously, laparoscopically or via a laparotomy\n- Nephrectomy may be required in some cases e.g. very large cysts, uncontrolled haemorrhage, symptomatic mass effect\n- For patients with ESRD requiring renal replacement therapy, renal transplant is preferred \n - Patients often have few comorbidities and so are good candidates\n - In some cases, removal of the native kidney may be required prior to transplantation to make space\n - Rarely, combined liver/kidney transplants are required if there is concurrent severe hepatic cyst disease\n- Symptomatic liver cysts may also require drainage or resection\n- Intracranial aneurysms detected on screening may be treated prophylactically (e.g. clipping or coiling) - observation is also an option \n\n# Complications\n\n- **Cyst haemorrhage** and **haematuria** are usually self-limiting\n - Rarely persistent or severe bleeding may cause subcapsular or retroperitoneal haematomas\n - Tranexamic acid may be used to treat bleeding\n - Investigating for malignancy may be appropriate e.g. in older patients or persistent haematuria\n- **Cyst infection** usually presents with fever, abdominal pain and raised inflammatory markers\n - Prolonged courses of IV antibiotics may be required\n - Infected cysts may be drained percutaneously or surgically\n- **Recurrent urinary tract infections** including pyelonephritis may be seen\n- **Renal stones** are common due to increased urinary static and metabolic abnormalities\n - CT is used for diagnosis\n - Treatment is the same as for patients without ADPKD\n- **Liver cysts** are the commonest extrarenal manifestation \n - 80% of patients have liver cysts by the age of 30\n - These increase with age, especially in women\n - 20% of patients will develop symptoms\n - These include abdominal and back pain, abdominal distension, early satiety and gastro-oesophageal reflux\n - Liver cysts may also rupture, bleed or become infected\n - Treatment options include aspiration and sclerotherapy or fenestration of cysts\n - In some cases liver resection is indicated for symptomatic relief\n- **Pancreatic cysts** are seen in around 10% of ADPKD patients\n - They usually cause no symptoms\n - If they compress the pancreatic duct, chronic pancreatitis may result\n- **Seminal vesicle cysts** are seen in 40% of male ADPKD patients\n - These are usually asymptomatic\n - There is no clear association with infertility\n- **Arachnoid membrane cysts** are typically asymptomatic and are found in 8-12% of ADPKD patients\n - However they may increase the risk of subdural haematoma\n- **Intracranial aneurysms** may lead to **subarachnoid haemorrhage** if they rupture\n - Decision making around whether to intervene if an unruptured aneurysm is detected is complex\n - Morbidity and mortality from aneurysm rupture are high\n - The majority of aneurysms are in the anterior circulation\n- **Aneurysm** may occur elsewhere and lead to arterial dissection\n - The aortic, popliteal, coronary and splenic arteries may be affected\n- **Cardiac valvular disease** including mitral valve prolapse and aortic insufficiency with aortic root dilatation\n - These may be progressive but rarely require valve replacement\n- **Chronic pain** especially in the flanks is common in ADPKD\n - It may develop after an acutely painful episode\n - Pain may be severe and disabling, with impacts on sleep, activities and mood\n - Treatment involves both medical management with analgesia, and considering interventional options\n - If cyst aspiration relieves pain, more permanent approaches such as cyst scleroisis or fenestration may be considered\n- **End stage renal disease** occurs in the majority of patients\n - Renal replacement therapy should be considered early as in all cases of CKD\n\n# Prognosis\n\n- Approximately 50% of patients reach ESRD by the age of 60; this rises to 75% by age 70\n- Poor prognostic factors include:\n - PKD1 genotype\n - Younger age of onset\n - Larger kidneys\n - Hypertension\n - Male sex\n\n# NICE Guidelines\n\n[NICE Technology Appraisal - Tolvaptan for treating autosomal dominant polycystic kidney disease](https://www.nice.org.uk/guidance/ta358/)\n\n# References\n\n[KDIGO - Autosomal Dominant Polycystic Kidney Disease](https://kdigo.org/wp-content/uploads/2017/02/KDIGO-ADPKD-Supplemental-Full-Report-FINAL.pdf)\n\n[Patient UK: Polycystic kidney disease](https://patient.info/doctor/autosomal-dominant-polycystic-kidney-disease)\n\n[Genomics Education - Polycystic kidney disease](https://www.genomicseducation.hee.nhs.uk/blog/polycystic-kidney-disease-and-genomic-testing/)\n\n[Radiopaedia - Autosomal dominant polycystic kidney disease](https://radiopaedia.org/articles/autosomal-dominant-polycystic-kidney-disease-1?lang=gb)",
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"question": "A 38-year-old woman is brought in by ambulance to A&E. She was having lunch with a friend when she complained of a headache and lost consciousness soon after. On examination, she has a Glasgow Coma Scale score of 3 and bilateral flank masses palpable on her abdomen. Her observations are otherwise within normal parameters.\n\nWhat is the cause of her neurological presentation?",
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"explanation": "This is the treatment for preproliferative/proliferative diabetic retinopathy. Photocoagulation is also done for maculopathy but more locally. Alternatives include intravitreal antivascular endothelial growth factor treatment. This patient has only got background changes on her retinal imaging. The treatment for this is good glycaemic control and maintaining a healthy and active lifestyle. This patient should be advised to stop smoking.",
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"explanation": "This is a patient with type 2 diabetes with background changes (also known as mild preproliferative retinopathy) on her retinal photography (dot/blot/flame haemorrhages, microaneurysms, hard exudates.) There is no evidence of preproliferative change (soft exudates, also known as cotton wool spots, or venous changes) or proliferative changes (new vessels and frank haemorrhage). There are no changes at the macula or within one optic disc space of the macula, which would indicate a diagnosis of maculopathy. The optic disc is normally vertically oval in shape and the central depression is otherwise known as the optic cup. The normal cup:disc ratio is 0.3. For background changes, the mainstay of treatment is lifestyle modifications, such as weight loss, smoking cessation and healthy diet. Glycaemic control is good in this case and it is important to note that rapid tightening of glycaemic control can make retinopathy acutely worse; long-term, gradual control is important for improving long-term outcomes.",
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"explanation": "This is one of the first-line pharmacological treatments for acute angle closure glaucoma (AACG). Diabetic patients have a higher risk of AACG; however, this patient has no symptoms consistent with this, such as pain, loss of vision or vomiting. The patient also has normal optic discs; in glaucoma there is a raised cup:disc ratio. The retinal findings are consistent with background diabetic retinopathy; therefore, first-line treatment is lifestyle advice and good glycaemic control.",
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"explanation": "This is the definitive management for AACG. This patient has no features of glaucoma on clinical presentation or on her retinal photographs. The retinal photography findings describe the normal appearance of the optic discs and of background diabetic retinopathy, the first-line treatment for which is lifestyle advice.",
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"explanation": "The retinal image findings are consistent with background diabetic retinopathy; therefore, the first-line treatment is lifestyle advice and good glycaemic control. This patient continues to smoke and has a high BMI. Advice to lose weight and quit smoking can improve her long-term outcomes, both in terms of microvascular disease but also macrovascular disease.",
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"explanation": "# Summary\n\nDiabetic retinopathy is a serious complication of diabetes mellitus characterised by vascular occlusion and leakage in the retinal capillaries, leading to potential sight loss if unmanaged. Key signs on fundoscopy include 'dots' (microaneurysms), hard exudates, 'blots' (haemorrhages), engorged tortuous veins, and cotton wool spots. Diagnosis is primarily through fundoscopy, with advanced stages confirmed by fluorescein angiography. Management involves optimal blood glucose control, with advanced cases requiring laser photocoagulation, vitrectomy or intravitreal injections of anti-vascular endothelial growth factor agents.\n\n# Definition\n\nDiabetic retinopathy is a sight-threatening complication of diabetes mellitus, resulting from poor glycaemic control. This leads to vascular occlusion and leakage from the capillaries that supply the retina, causing retinal ischaemia, neovascularisation and, if left untreated, potential loss of sight.\n\nDiabetic retinopathy is a broad term encompassing two primary stages: non-proliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR). NPDR presents in three severity levels:\n\n- **Mild NPDR:** Microaneurysms and dot haemorrhages on fundoscopy.\n- **Moderate NPDR:** Microaneurysms, dot and blot haemorrhages, cotton-wool spots, and hard exudates.\n- **Severe NPDR:** Beaded veins, intraretinal microvascular abnormalities (IRMA), and extensive retinal hemorrhages.\n\nPDR involves neovascularisation and fibrous proliferation on the retina or vitreous, posing a higher risk of severe vision loss.\n\n\n\n# Epidemiology\n\nDiabetes is the leading cause of severe visual impairment among working-age individuals in England, Wales, and Scotland. The risk of diabetic retinopathy increases with the duration of diabetes and poor glycaemic control.\n\n# Pathophysiology\n\nChronic hyperglycaemia in diabetes mellitus causes structural changes to the retinal capillaries, including thickening of the basement membrane and loss of pericytes. This results in capillary occlusion and leakage, leading to retinal ischaemia and formation of new, fragile vessels.\n\n# Signs and symptoms\n\nEarly stages of diabetic retinopathy may be asymptomatic. As the disease progresses, symptoms can include:\n\n- Floaters or dark spots in the vision\n- Blurred or distorted vision\n- Difficulty seeing at night\n- Sudden loss of vision\n\n# Differential diagnosis\n\nOther conditions that can cause similar symptoms include:\n\n- Age-related macular degeneration: Mainly affects central vision. Symptoms include distorted vision and difficulty recognising faces.\n- Retinal vein occlusion: Sudden painless loss of vision in one eye, often associated with a history of hypertension, hyperlipidaemia or glaucoma.\n- Hypertensive retinopathy: Characterised by arteriolar narrowing, copper or silver wiring, flame haemorrhages, and cotton wool spots.\n\n# Investigations\n\n- Fundoscopy: \n\t- Signs of milder disease include:\n\t\t- Microaneurysms\n\t\t- Hard exudates\n\t\t- Blot haemorrhages \n\t- Severe disease presents with:\n\t\t- Engorged tortuous veins\n\t\t- Large blot haemorrhages. \n\t- In proliferative diabetic retinopathy (PDR), neovascularisation can be observed on the retina or optic disc.\n- Optical Coherence Tomography (OCT): Can be used to detect macular oedema.\n- Fluorescein angiography: Used in advanced cases to evaluate the extent of neovascularisation and guide treatment.\n\n[lightgallery]\n\n[lightgallery1]\n\n[lightgallery3]\n\n\n\n# Management\n\nManagement strategies include:\n\n- Optimisation of blood glucose control to slow the progression of retinopathy.\n- Laser photocoagulation for proliferative diabetic retinopathy and clinically significant macular oedema.\n- Intravitreal injections of anti-vascular endothelial growth factor (anti-VEGF) agents for diabetic macular oedema.\n- Vitrectomy surgery for advanced cases with complications such as vitreous haemorrhage or retinal detachment.\n\n[lightgallery2]\n\n# Complications\n\n* **Vitreous Hemorrhage:** Can cause sudden vision loss.\n* **Tractional Retinal Detachment:** May lead to blindness.\n* **Macular Oedema:** Causes central vision loss.\n* **Neovascular Glaucoma:** Can result in severe pain and vision loss.\n* **Blindness:** The ultimate complication in untreated or advanced cases.\n\n# References\n\n[Click here for more information on diabetic retinopathy](https://patient.info/doctor/diabetic-retinopathy-and-diabetic-eye-problems)\n",
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"question": "A 45-year-old woman with type 2 diabetes mellitus presents for her routine eye screening appointment. She is on metformin monotherapy and her last HbA1c was 44. She is a current smoker. On examination, she has a body mass index (BMI) of 30. Retinal photography reveals dot and blot haemorrhages and hard exudates. There is no evidence of microvascular growth. The optic discs are vertically oval in shape with a central depression, which has a ratio compared with the disc of 0.3.\n\nWhat is the most appropriate management for this patient?",
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"explanation": "The presence of voiding lower urinary tract symptoms and microscopic haematuria and the patient's age and occupational history (factory work, with potential exposure to dyes and rubber) should raise suspicion of bladder cancer. Prostate cancer may also present in a similar way. Patients in the one-stop Haematuria Clinic are thoroughly evaluated for a malignant cause of their symptoms, including flexible cystoscopy to evaluate the bladder and prostate, CT or ultrasound scanning of the urinary tree, bloods (such as for the prostate-specific antigen) and urine dipstick testing.",
"id": "52917",
"label": "a",
"name": "Refer to one-stop Haematuria Clinic",
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"explanation": "This patient has a mildly raised PSA and has been diagnosed with BPH. This does not rule out prostate cancer; however, the patient's symptoms can certainly be explained by the presence of a prostatic malignancy but this is less likely given the presence of microscopic haematuria and the history of factory work. Referral to a one-stop haematuria service is the first step in the management of this presentation due to the presence of haematuria, which requires a dedicated set of investigations. An MRI prostate may be requested further down the line if there is concern that there is prostate cancer if no explanation for his symptoms are identified during the one-stop service or as a first-line investigation for suspected prostate cancer.",
"id": "52920",
"label": "d",
"name": "MRI prostate",
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"explanation": "Prostate-specific antigen (PSA) has high sensitivity but low specificity for prostate cancer. It can be raised in other conditions, such as benign prostatic hypertrophy; thus, alone it cannot be used to diagnose prostate cancer. Furthermore, a negative PSA does not rule out malignancy of the prostate or elsewhere in the urinary tract. Given the continuation of this patient's urinary symptoms after pharmacological management and the presence of haematuria, malignancy should be ruled out in a dedicated one-stop Haematuria Clinic.",
"id": "52919",
"label": "c",
"name": "Repeat prostate-specific antigen",
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"explanation": "This would be the investigation of choice if evaluating for metastatic spread of confirmed cancer. It is done further down the line once a malignancy is diagnosed. In the first instance, the patient needs to be reviewed in the one-stop haematuria service, where biopsies may be taken if a lesion is identified to clinch the diagnosis.",
"id": "52921",
"label": "e",
"name": "CT chest, abdomen and pelvis",
"picture": null,
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"explanation": "This patient has haematuria with voiding lower urinary tract symptoms. He should therefore be investigated for malignancy in a dedicated one-stop clinic in the first instance. Transurethral resection of the prostate is performed for benign prostatic hypertrophy (BPH) with symptoms recalcitrant to optimum medical therapy (usually a combination of finasteride and tamsulosin). Therefore, it is not appropriate to refer the patient for this at this stage, where the diagnosis remains uncertain, and the BPH treatment is not yet optimised.",
"id": "52918",
"label": "b",
"name": "Refer for transurethral resection of the prostate",
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"explanation": "# Summary\n\nBladder cancer, primarily characterised by transitional cell carcinoma, is the 11th most common cancer in the UK. Key risk factors vary by subtype and include smoking, exposure to aromatic amines, schistosomiasis infection, long-term catheterisation, and the presence of other types of bladder cancer. The hallmark sign is visible haematuria, along with potential systemic symptoms like weight loss and night sweats, and local symptoms such as UTIs and hydronephrosis. The disease primarily metastasises to the lungs, liver, and bone. Diagnosis involves various investigations including urine dip, CT urogram, flexible cystoscopy, and other imaging studies. Management strategies differ based on whether the cancer is muscle invasive or non-muscle invasive, and can include surgery, chemotherapy, immunotherapy, and radiotherapy.\n\n# Definition\n\nBladder cancer is a malignant growth within the urinary bladder. The most common histological subtype in developed countries is transitional cell carcinoma, accounting for 90% of all bladder cancers, followed by squamous cell carcinoma and other types.\n\n# Epidemiology\n\nBladder cancer is the 11th most common cancer in the UK. In developed countries, 90% of bladder cancers are transitional cell carcinomas, while the remainder are primarily squamous cell carcinomas.\n\n# Aetiology\n\nRisk factors vary depending on the histological subtype of the cancer:\n\n## Risk factors for Transitional Cell Carcinoma\n\n- Smoking\n- Exposure to aromatic amines (employed in rubber, dyes, and chemical industry)\n- Use of Cyclophosphamide\n\n## Risk factors for Squamous Cell Carcinoma\n\n- Schistosomiasis infection\n- Long-term catheterisation (10+ years)\n\n## Risk factors for Adenocarcinoma\n\n- Presence of other types of bladder cancer\n- Local bowel cancer\n\n## Risk factors for Small Cell Bladder Cancer\n\n- Association with other types of bladder cancer\n\n# Signs and Symptoms\n\nThe cardinal sign of bladder cancer is **painless visible haematuria.** Clinical features can be grouped into local and systemic categories, with the severity depending on the advancement of the disease.\n\nLocal features:\n- Painless haematuria\n- Recurrent UTIs\n- Hydronephrosis\n\nBladder cancer can also invade adjacent structures such as the obturator nerve, resulting in neuropathic pain on the medial thigh.\n\nSystemic features:\n- Unintended weight loss\n- Night sweats\n\n# Differential Diagnosis\n\nBladder cancer should be differentiated from other conditions presenting with similar symptoms:\n\n- Urinary tract infection: Characterised by dysuria, frequency, urgency, lower abdominal pain and potentially haematuria.\n- Kidney stones: Present with colicky flank pain, haematuria, and potentially UTI symptoms.\n- Benign prostatic hyperplasia: Symptoms include nocturia, urinary hesitancy, and a weak stream. There may be microscopic haematuria but typically no gross haematuria.\n- Interstitial cystitis: Characterised by chronic pelvic pain, urinary frequency, and urgency in the absence of an identifiable cause.\n\n# Investigations\n\nInitial bedside investigations include a urine dipstick test to identify haematuria. If there's doubt over the presence of true haematuria, a lab sample can be sent (urine MCS) to confirm the presence of red blood cells, as well as casts (if there are dysmorphic red blood cells it suggests bleeding is glomerular in nature and not from lower urinary tract).\n\nImaging investigations are crucial for diagnosis and staging:\n\n- CT Urogram: Contrast is injected into a vein, filtered by the kidney, and excreted into the urinary collecting system. A CT scan then visualises the urinary tract to identify filling defects indicating a tumour.\n\n- Flexible cystoscopy: Allows for visualisation of any defects in the bladder and the morphology of any suspicious lesions. If a lesion is identified, a biopsy can be taken.\n\nFurther staging investigations may include radiographs, CT scans, MRI scans, and bone isotope scans.\n\n## 2 week wait referral criteria\n\nRefer people using a suspected cancer pathway referral (for an appointment within 2 weeks) for bladder cancer:\n\n- If they are aged 45 years and over and have:\r\n\t- Unexplained visible haematuria without urinary tract infection, or\r\n\t- Visible haematuria that persists or recurs after successful treatment of urinary tract infection.\r\n- If they are aged 60 years and over and have unexplained non-visible haematuria and either dysuria or a raised white cell count on a blood test.\r\n- Consider non-urgent referral for bladder cancer in people aged 60 years and over with recurrent or persistent unexplained urinary tract infection.\r\n\n\n# Classification\n\nBladder cancer can be classified according to stage and grade, utilising the WHO TNM system. The staging system is based on localised tumour invasion (T), presence of lymph nodes (N), and distant disease (M). Both imaging modalities and pathological specimens are used for staging, with a key objective being differentiation between muscle invasive and non-muscle invasive bladder cancer.\n\nThe grade of cancerous cells can be histologically graded from 1-3, with 1 being the least aggressive and 3 the most aggressive.\n\nWhen it comes to classification and staging the most important aspect is whether the tumour is non-invasive or muscle-invasive as this determines treatment:\n\n-\tNon-muscle invasive: Tis (non-invasive, in situ), Ta – non-invasive, T1 – tumour invades inner lining and connective tissues. \r\n-\tMuscle invasive: T2 (tumour invades muscle), T3 (invades perivesical fat and LN), T4 (metastatic spread). \r\n\n\n# Management\n\nThe management of bladder cancer is categorised based on whether the cancer is muscle invasive or non-muscle invasive.\n\n## Non-muscle invasive bladder cancer\n\nThis includes stages CIS, Ta, and T1 and is managed with:\n- Surgery: Transurethral resection of the bladder tumour (TURBT) is the gold standard.\n- Chemotherapy: The bladder can be instilled with chemotherapeutic agents such as Mitomycin C (single dose if low risk, 6 week course if intermediate risk).\n- Immunotherapy: BCG immunotherapy can be instilled into the bladders of patients with high-risk non-muscle invasive cancers or carcinoma in situ (CIS).\n- If there is high-risk muscle non-muscle invasive cancer/CIS a radical cystectomy may still be considered.\n\n## Muscle invasive bladder cancer\n\nThis includes any stage from T2 and above. The gold standard treatment is a radical cystectomy with urinary diversion, with options including an ileal conduit, neo-bladder, or Mitrofanoff procedure. Non-surgical treatment options include radiotherapy and chemotherapy, which can be used in both curative and palliative capacities.\n\n# NICE Guidelines\n\n[Click here for the NICE Guidelines](https://www.nice.org.uk/guidance/ng2)\n\n[NICE CKS - Urological cancers - recognition and referral\n](https://cks.nice.org.uk/topics/urological-cancers-recognition-referral/)",
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"question": "A 73-year-old man is referred to the Urology Clinic with a 3-month history of voiding symptoms. He finds he has intermittent poor stream and hesitancy when passing urine. He denies any weight loss, fatigue or night sweats and any other urinary symptoms. He is a retired factory worker. His GP had detected an enlarged prostate and a mildly raised prostate-specific antigen 3 months ago and diagnosed him with benign prostatic hypertrophy. He has been taking tamsulosin since but his symptoms are unchanged. His urine dipstick in clinic today is positive for blood.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "Co-cyprindiol is an oral contraceptive pill with antiandrogenic effects. It contains cyproterone acetate (antiandrogenic) and ethinyloestradiol. NICE guidelines recommend this medication in patients with polycystic ovary syndrome and acne not responding to conventional first-line topical and oral antibiotic therapies. Therefore, this patient does not qualify for this treatment and would be contraindicated anyway due to the presence of previous DVT.",
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"explanation": "This could be a service to offer this patient in conjunction with acne treatment if her mental health were significantly affected: symptoms of depression, anxiety, body dysmorphia, suicidal ideation or self-harm. This is not the case here. Furthermore, it would not treat her condition alone since psychological support would not address the root cause (ie. the acne) of any mood disorder if present.",
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"explanation": "Short courses of prednisolone can be used to treat some severe acne flares, such as acne fulminans. It has no place in the routine or long-term management of most acne presentations.",
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"explanation": "This patient has moderate acne indicated by the presence of many inflammatory lesions (pustules and inflammatory papules). Mild acne is defined by the presence of mostly comedones with few inflammatory lesions. There are no markers of severe acne (nodules, cysts and scars). She has not responded to topical agents, so as per National Institute for Health and Care Excellence (NICE) guidelines oral antibiotics are indicated. This is usually doxycycline or lymecycline but alternatives include clarithromycin or trimethoprim. Topical agents should be continued while on oral antibiotics. Combined oral contraceptives with antiandrogenic effects (such as co-cyprindiol) could be considered in some patients but this would not be an option in the context of previous deep vein thrombosis.",
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"comment": "All this moderate?",
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"comment": "You would refer to derm cuz of scarring no?\n",
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"explanation": "# Summary\n\nAcne vulgaris is a common chronic disorder of the pilo-sebaceous unit, resulting in blockage of the follicle, formation of comedones and inflammation. Key signs and symptoms include open/closed comedones, inflammatory papules and pustules, and in severe cases, nodules and cysts. The disorder predominantly affects the face, neck, chest, and back, and has a significant psychological impact due to altered physical appearance. Acne is primarily diagnosed clinically, with further investigations necessary only in uncertain cases or prior to commencing certain treatments like isotretinoin. Treatment is guided by severity and may involve topical or systemic therapy based on the NICE guidelines. Potential complications include post-inflammatory hyperpigmentation, hypopigmentation, erythema, psycho/social/sexual dysfunction, and scarring.\n\n\n# Definition\n\n- A a chronic disorder of the skin affecting the pilo-sebaceous unit, in which there is blockage of the follicle leading to comedones and inflammation. \n- Vulgaris translates as \"common\", which is true as this condition affects over 80% of adolescents.\n\n# Epidemiology\n\n* It is one of the most common dermatological conditions globally, affecting individuals of all ethnicities and ages.\n* Prevalence is highest in adolescents and young adults, with up to 80% of individuals experiencing some degree of acne during their lifetime.\n* While most common in adolescents, adult-onset acne can occur, affecting people well into their 30s and beyond.\n* Acne affects both males and females, but the prevalence and severity may vary between genders.\n* The psychological impact of acne can be significant, affecting self-esteem and overall quality of life.\n\n# Risk Factors\n\nSeveral factors contribute to the development and exacerbation of acne, including:\n\n* Hormonal changes (e.g. during puberty, menstrual cycle, polycystic ovary syndrome)\n* Increased sebum (oil) production\n* Blockage of hair follicles and sebaceous glands by keratin and sebum\n* Bacterial colonization (Propionibacterium acnes)\n* Family history of acne\n* Certain medications (e.g. corticosteroids, hormonal treatments)\n\n# Pathophysiology\n\n- In normal skin, skin cells in the stratum corneum of the epidermis (corneocytes) desquamate successfully without blocking pilo-sebaceous units.\n- In acne, the corneocytes are excessively cohesive. They do not detach successfully.\n- Because of this, the keratin rich corneocytes accumulate and block off hair follicles causing follicular hyperkeratinisation.\n- Sebum is trapped in the hair follicle since it cannot be drained away. Androgens may also contribute to this causing sebaceous gland hyperplasia and increased sebum production. \n- This combination of sebum and keratin forms micro-comedones - the earliest feature of acne vulgaris. This is only visible under a microscope.\n- Gradually, the follicle becomes more distended with keratin and sebum, and the micro-comedone enlarges to become a comedone. \n- Initially, these are closed comedones, referred to as whiteheads. The contents are not exposed to the skin surface or oxygen, and therefore appear as fleshy/white papules. \n- Eventually, closed comedones become open comedones. As their contents become exposed to oxygen, they oxidise which causes black discolouration. Open comedones are therefore referred to as blackheads.\n- Comedones are then colonised with a gram positive bacillus called Propionibacterium (Cutibacterium) acnes. This is a commensal organism (part of the normal skin flora) but leads to an inflammatory response in the right conditions of the comedone, in a predisposed patient. \n- The comedone is subsequently transformed into an inflammatory papule, which is now associated with erythema. A papule is a solid, raised lesion less than 0.5cm in diameter. \n- As things progress and more neutrophils accumulate, the inflammatory papule becomes a pustule; this is a lesion less than 0.5cm in diameter that contains pus. \n- Eventually, the inflammatory papule or pustule becomes so distended that it ruptures into the dermis, triggering a marked and deep seated inflammatory response. \n- This leads to the formation of nodules/cysts, which are painful and red. A nodule is a solid lesion larger than 0.5cm, and cysts are walled off fluid containing structures. \n\n[lightgallery]\n\n# Classification\n\n- Non-inflammatory: blackheads and whiteheads.\n- Inflammatory: inflammatory papules, pustules, and nodules (cysts.)\n- Mild acne: predominantly non-inflammatory lesions. \n- Moderate acne: predominantly inflammatory papules and pustules. \n- Severe acne: nodules (cysts), scarring, acne fulminans, and acne conglobata. \n\n# Clinical Features\n\n- Open/closed Comedones, inflammatory papules and pustules, nodules, and cysts may be present.\n- The face is most often affected. The neck, chest and back may also be affected.\n- Psychological dysfunction due to changes physical appearance\n- Scarring: associated with inflammatory acne. Hypertrophic and keloid scars are more common in darker skin tones. \n\t- Atrophic: flat or indented, such as ice-pick, box-car, or rolling scars.\n\t- Hypertrophic: raised scars.\n\t- Keloid: raised scars that extend beyond the initial boundaries of the injury. \n- Post-inflammatory hyperpigmentation and hypopigmentation: associated with inflammatory acne. \n- Post inflammatory erythema: associated with inflammatory acne.\n- Acne fulminans: an uncommon but severe, serious acne presentation. \n\t- Inflammatory nodules/cysts that are painful, ulcerating, and haemorrhagic appear, with associated systemic upset (raised white cell count, joint pain, fever, fatigue.) \n\t- These patients should be reviewed urgently within 24 hours. It usually affects teenage male patients.\n- Acne conglobata: another uncommon presentation of severe nodular/cystic acne with interconnecting sinus tracts and extensive scaring. \n\n[lightgallery1]\n\n[lightgallery2]\n\n# Investigations\n\n- Acne is a clinical diagnosis and investigations are not usually needed. \n- Swabs may be indicated if the diagnosis is uncertain (e.g. if ruling out infectious pustules.)\n- Investigations will be required prior to commencing isotretinoin if indicated.\n- In some particular presentations where an endocrine cause is suspected, there may be endocrinological investigations (hyperandrogenic states such as PCOS or androgen secreting tumours.)\n\n# Treatment\n\nManagement of acne is multifaceted including education, topical/oral treatments and lifestyle modifications. \n\n- Each treatment combination is given as a 12 week course. \n- Combination therapies help reduce antimicrobial resistance. \n- Antibiotics are used predominantly since they have anti-inflammatory effects, rather than for their antimicrobial effects.\n- **Mild-moderate acne** is treated with any 2 of the following in combination:\n\t- Topical benzoyl peroxide.\n\t- Topical antibiotics (clindamycin)\n\t- Topical retinoids (tretinoin/adapalene)\n- **Moderate-severe acne** is treated with a 12-week coures of the following first line options:\n\t- Topical retinoids (tretinoin/adapelene) + topical benzoyl peroxide.\n\t- Topical retinoids + topical antibiotics (clindamycin)\n\t- Topical benzoyl peroxide + topical retinoid (tretinoin/adapelene) + oral antibiotic (lymecycline/doxycycline.) \n\t- Topical azelaic acid + oral antibiotic (lymecycline/doxycycline) \n\t- Second line oral antibiotics: trimethoprim and erythromycin e.g. in pregnant/breast-feeding women where tetracyclines are contra-indicated. \n\t- Combined oral contraceptives (COCPs) (if not contraindicated) in combination with topical agents can be considered as an alternative to systemic antibiotics in women\n\nNB: topical retinoids and oral tetracyclines are contraindicated during pregnancy and when planning a pregnancy, and so women of childbearing potential will need to use effective contraception, or choose an alternative treatment to these options.\n\t\n- As per NICE guidelines, referral to specialist Dermatology is indicated in the case of:\n\t- Acne fulminans.\n\t- Mild-moderate acne not responding to two 12 week courses of treatment as above.\n\t- Moderate-severe acne not responding to one 12 week course of treatment as above, including an oral antibiotic.\n\t- Psychological distress/mental health disorder contributed to by acne.\n\t- Acne with persistent pigmentary changes.\n\t- Acne with scarring.\n- Other available agents:\n\t- Co-cyprindiol: anti-androgenic contraceptive agent - may be trialled in primary care on female patients, but usually second line COCP due to increased risk of venous thromboembolism, and can only be given for 3 months. \n\t- Spironolactone: anti-androgenic - not often used. Not for male patients. \n\t- **Isotretinoin (oral retinoid):** the usual next step if the standard treatment fails and is prescribed by a dermatologist. \n\t\t* Notable adverse effects: dry skin/mouth/eyes/lips (most common), teratogenecity, photosensitivity, low mood, nose bleeds, hair thinning, raised triglycerides, intracranial hypertension \n\t\t* Isotretinoin is a well established teratogen that results in miscarriages and severe birth defects. As a result, the manufacturer recommends that all female patients taking isotretinoin are also using two forms of contraception from one month before until one month after use. For this reason a pregnancy test should also be done before initiating treatment\n\t\t* There is a controversial association between isotretinoin and depression/suicide. Recent research has shown that concerns about links between isotretinoin and depression or suicide are not established. This has now been included into the NICE guidelines. However it is still important to screen for depression/suicidal ideation before prescribing and during treatment.\n\t\n\t\n# Complications\n\n- Post-inflammatory erythema\n- Post-inflammatory hyper- and hypo- pigmentation\n- Psycho/social/sexual dysfunction \n- Scars (atrophic, hypertrophic, keloid)\n\t- Keloid scars: over-proliferating scar tissue/collagen extending beyond the boundaries of the lesion. Takes 3-4 weeks typically to develop after injury. They can cause itch and pain. It is fleshy, smooth, firm, and does not regress with time. The original injury may be minor, for example piercing or insect bite. Treatment is usually with intralesional steroids (triamcinolone). Cryotherapy and laser may also be used. Surgical resection is unlikely to be successful due to further scarring. Risk factors include:\n\t\t- Darker skin/Chinese/Hispanic origin \n\t\t- Less than 30 years of age\n\t\t- Previous keloid scarring \n\t- These are distinct from hypetrophic scars, which are thick and raised but remain within the injured boundary and tend to improve over time. \n\n# NICE Guidelines\n\n[NICE CKS for Acne Vulgaris](https://cks.nice.org.uk/topics/acne-vulgaris/)",
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"question": "A 20-year-old female presents to general practice with questions regarding her ongoing acne. She has extensive pustules and erythematous papules across her face and upper back. She is embarrassed of her skin but denies any low mood. She has previously tried combinations of topical Differin, topical benzoylperoxide and topical clindamycin with no improvement. She has had a previous deep vein thrombosis (DVT) after surgery. She takes no regular medications currently and has no drug allergies.\n\nWhat is the most appropriate next step in management?",
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"explanation": "Since this patient has only one kidney, they are at risk of end-stage renal disease and may, eventually, require a renal transplant. Kidney transplants are reserved for patients with established end-stage renal failure (which this patient does not have). It can take several years for an appropriate donor match to be identified, so it is not an acute form of renal replacement therapy; if this patient went on to sustain a severe acute kidney injury, haemofiltration may be required. If they did not recover from the acute injury, then they would need long-term dialysis as a bridge to transplant.",
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"explanation": "This would be the treatment of choice for removal of stones less than 20 mm in size. This breaks the stone up and allows the patient to pass the pieces through the urine. This is not the best approach in acute obstructions with hydronephrosis and would not be appropriate for this patient where the stone is 30 mm in size.",
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"explanation": "Haemofiltration may be required if this patient presents with certain features of severe kidney injury, such as treatment-resistant fluid overload, hyperkalaemia, acidosis or uraemia. This patient is at risk of acute kidney injury and may require filtration further down the line if the obstruction is not rapidly relieved. There is no indication that this is an issue at present, with his blood tests within normal parameters.",
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"explanation": "There is radiographic evidence of renal obstruction with an associated large stone in the context of a single kidney. This patient is at significant risk of deterioration from sepsis due to the obstruction. Prompt action is also required due to the presence of a single kidney to protect his long-term kidney health but also due to the absence of a second kidney to compensate in terms of providing adequate renal function in the acute setting. In the first instance, decompression with a nephrostomy is required. The stone is likely to require subsequent surgical removal due to its large size (> 10 mm).",
"id": "52932",
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"explanation": "This is a large stone with radiological evidence of obstruction and hydronephrosis in the context of a single kidney. Therefore, it would be inappropriate to manage this expectantly since the stone is unlikely to be spontaneously passed and more urgent treatment is required due to susceptibility to acute kidney injury, long-term sequelae for his solitary kidney and risk of urosepsis.",
"id": "52933",
"label": "b",
"name": "Expectant management with regular diclofenac",
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"explanation": "\"# Summary\n\nUrolithiasis refers to stones that may form anywhere in the urinary tract (usually in the kidneys). They are often asymptomatic but may cause pain +/- obstruction of the flow of urine. Stones usually form due to supersaturation of urine, with the main types including calcium oxalate, calcium phosphate, uric acid, struvite and cystine stones. A common presentation is with renal or ureteric colic, where there is severe spasmodic pain that classically moves from loin to groin. Other symptoms include nausea, vomiting and haematuria; patients who develop an infected obstructed urinary system may be systemically unwell and febrile. Investigations include a urine dip and culture, blood tests for renal function and inflammation markers and a non-contrast CT KUB. Ultrasound is an alternative for young people and pregnant women. Management depends on how likely stones are to pass spontaneously based on location and size as well as symptom severity, presence of complications (e.g. infection, obstruction) and the patient's background. Options include watchful waiting with analgesia, medical expulsive therapy, percutaneous nephrolithotomy, ureteroscopy, shock wave lithotripsy, or (rarely) open surgery. Thought should be given to whether an underlying condition (such as hyperparathyroidism) may be driving stone formation and patients should be advised on how to reduce the risk of recurrence. Preventative medical treatment may be indicated in some cases of recurrent stones.\n\n# Definition\n\nUrolithiasis refers to urinary calculi (stones) anywhere in the urinary tract. They form due to supersaturation of urine causing crystal formation, which then aggregate into larger stones.\n \n# Epidemiology\n \n- Urinary tract stones are common, with a lifetime prevalence of 12% in men and 7% in women\n- Peak incidence is between 35-45 years of age\n- Modifiable risk factors include:\n - Obesity\n - Chronic dehydration\n - High ambient temperatures\n - Diet high in oxalate, urate, sodium and animal protein\n- Non-modifiable risk factors include:\n - White ethnicity\n - Family history of stone formation\n - Structurally abnormal renal tract (e.g. vesicoureteric reflux, horseshoe kidney)\n - Comorbidities including diabetes, gout, hyperparathyroidism, Crohn's disease, cystinuria \n \n# Aetiology\n\n- **Calcium oxalate stones**\n - Majority (approximately 70%) of stones\n - Radiopaque\n - Can form in any urine pH\n - Associated with low urine volume and hypercalciuria\n- **Calcium phosphate stones**\n - Approximately 10% of stones\n - Radiopaque\n - Tend to form in alkaline urine\n - Associated with renal tubular acidosis types 1 and 3\n - Associated with primary hyperparathyroidism\n- **Uric acid stones**\n - Approximately 10% of stones\n - Radiolucent\n - Only form in acidic urine (pH < 5.5)\n - Associated with diabetes, obesity and gout\n - May occur due to malignancy (due to high cell turnover, especially due to chemotherapy)\n- **Struvite stones**\n - Approximately 5% of stones\n - Radiopaque\n - Composed of magnesium, ammonium and phosphate\n - Often occur due to urease-producing bacterial infection (e.g. Proteus, Enterobacter, Klebsiella)\n - Associated with alkaline urine\n - May form staghorn calculi (which involve the renal pelvis and extend into mulitple calyces)\n- **Cystine stones**\n - 1% of stones\n - Faintly radiopaque\n - Occur due to cystinuria (an autosomal recessive condition affecting renal reabsorption of amino acids)\n - More likely to form in alkaline urine\n - Often occur in young patients\n- **Medication-induced stones**\n - 1% of stones\n - Occur due to crystallisation of medications or their compounds\n - e.g. indinavid, ceftriaxone, allopurinol, zonisamide\n \n# Signs and Symptoms\n \n- Stones are often asymptomatic, especially if small, and may be detected incidentally on imaging\n- The classic presentation is with renal or ureteric colic\n - There is severe, spasmodic pain that often starts in one flank (or \"\"loin\"\")\n - It may then radiate to the groin (i.e. \"\"loin to groin\"\" pain)\n - It may also radiate to the scrotum, labia or anterior thigh\n - Onset is usually sudden\n - Patients may be restless and pace or writhe around due to severe pain\n- Renal angle tenderness may be present on examination\n- Visible haematuria (or may be microscopic and detected on dipstick only)\n- Dysuria, urinary frequency and having to strain to pass urine may occur (due to detrusor muscle irritation)\n- Nausea and vomiting\n- Fever, diaphoresis, rigors and hypotension may be present if there is concurrent infection\n- There may be urinary hesitancy or an intermittent stream if there is obstruction\n \n# Differential Diagnosis\n \n- **Pyelonephritis** presents with fever, flank pain, nausea and vomiting and urinary symptoms such as frequency, urgency and dysuria - it may complicate obstruction due to urinary stones but often occurs in the absence of stones (often due to an ascending lower urinary tract infection)\n- **Appendicitis** presents with periumbilical pain migrating to the right lower quadrant (rather than flank pain), nausea, vomiting and fever are common and patients may have classic examination findings (e.g. maximal tenderness at McBurney's point, Rovsing's sign)\n- **Diverticulitis** presents with intermittent left lower quadrant pain and tenderness, fever is common as well as altered bowel habit (often with the passage of blood and/or mucus) \n- **Ovarian torsion** presents with acute severe pelvic or lower abdominal pain (which may be intermittent and radiate to the flank), nausea and vomiting; there may be a palpable mass on examination\n- **Ectopic pregnancy** presents with lower abdominal or pelvic pain and vaginal bleeding, often in women with a history of a recent missed period; if there is tubal rupture patients may develop vomiting, tachycardia, hypotension and shock \n- **Rupture or dissection of an abdominal aortic aneurysm** may mimic renal colic, especially in older men presenting with flank and groin pain and haemodynamic instability\n\n# Investigations\n\n**Bedside:**\n\n- **Urinalysis** for haematuria; nitrites and leukocytes may be present in infection (leucocytes may also be present in urine due to ureteral irritation) - urine pH may also guide the likely cause of stones\n- **Urine MC&S** looking for any bacteria that may be causing a complicating infection or struvite stones\n- **24 hour urine collection** in recurrent stone formers to assess urine volume, calcium, oxalate, uric acid, citrate, sodium and creatinine\n\n**Bloods:**\n\n- **Full blood count** may show raised white cell count due to infection\n- **U&Es** may show deranged renal function e.g. if there is obstruction\n- **CRP** which may be significantly raised in infection\n- **Bone profile** looking for hypercalcaemia\n- **Serum urate** if raised may increase suspicion of uric acid stones\n- **Venous blood gas** may show acidosis and low bicarbonate if there is underlying renal tubular acidosis; lactate may be raised in patients systemically unwell with infection\n- **Coagulation screen** to check for a bleeding diathesis prior to intervention \n- **Blood cultures** in patients with suspected infection\n\n**Imaging:**\n \n- **Non-contrast CT KUB** should be done urgently in patients with suspected renal colic\n- **Ultrasound KUB** is an alternative that should be offered to pregnant women and under 16 year olds\n- **Abdominal X-ray** also has a role e.g. to follow up radio-opaque stones that are being managed conservatively\n\n**Special tests:**\n\n- **Stone analysis** to identify their composition and guide prophylactic management - sieving urine may be advised to retrieve fragments especially if there is recurrent stone formation\n \n# Management \n \n**Conservative:**\n\n- Patients should be educated on urinary tract stones and safety-netted regarding risks (e.g. infection, obstruction)\n- As stones often pass spontaneously, watchful waiting may be appropriate for asymptomatic stones < 5mm with no complications (this may also be trialled in larger stones if patients have been counselled regarding risks and benefits)\n- Dietary and lifestyle advice should be provided on how to reduce recurrence risk\n - Drink 2.5-3 litres of water per day\n - Avoid carbonated drinks (may acidify urine)\n - Add fresh lemon juice to water (contains citrate which reduces stone formation)\n - Eat a balanced diet and maintain a healthy weight\n - Reduce salt intake\n - Do not restrict dietary calcium intake \n\n**Medical:**\n\n- Analgesia should be provided promptly\n - Non-steroidal anti-inflammatory drugs (NSAIDs) are first-line\n - Alternatives to the oral route (e.g. PR or IM diclofenac) may be required if patients are vomiting\n - IV paracetamol may be given if NSAIDs are contraindicated or insufficient\n - Opioid analgesia is the next step if neither of these are sufficient\n- Medical expulsive therapy can be considered for patients with distal ureteric stones < 10mm \n - This involves using an alpha-blocker (e.g. tamsulosin) to relax smooth muscle and promote passage of stones\n- Patients with suspected infection secondary to renal stones should be treated urgently with IV antibiotics (e.g. gentamicin, co-amoxiclav)\n- IV fluids may be required for patients dehydrated due to vomiting, decreased oral intake or infection\n- Antiemetics may be required for vomiting\n- Medical prophylaxis may be considered for recurrent stone formation\n - Potassium citrate is used for recurrent calcium oxalate stones\n - Thiazide diuretics may also be used for recurrent calcium oxalate stones \n\n**Surgical:**\n\n- Patients with obstruction and hydronephrosis require urgent decompression with nephrostomy insertion\n- Stenting is another option for ureteric obstruction\n- Extracorporeal shockwave lithotripsy (ESWL) refers to using high-energy shock waves to fragment a stone under fluoroscopic guidance\n - It can be used for stones < 2 cm in size and is first-line if < 1cm\n - It is contraindicated in pregnancy, coagulopathy and infection\n- Ureteroscopy refers to retrieving stones endoscopically\n - First-line for ureteric stones 1-2 cm in size\n - Stenting may be offered in patients after retrieval of larger stones\n- Percutaneous nephrolithotomy is used for renal stones > 2cm including complex stones such as staghorn calculi\n - It may also be used in smaller stones when other treatment approaches have failed\n- Open stone surgery is rarely required but may be needed in complex cases or when other options have failed\n\n# Complications\n\n- **Obstruction** of the urinary tract by a stone leads to acute kidney injury and may cause irreversible renal impairment if not urgently decompressed\n- **Infection** of an obstructed urinary system may be severe and life-threatening - pyelonephritis (upper urinary tract infection) and pyonephrosis (a buildup of pus in the kidney) may occur and there is a risk of sepsis\n- **Ureteric strictures** may form if ureteric stones are not passed within a couple of weeks\n- **Increased risk of renal cancers** (both renal cell carcinomas and upper tract urothelial carcinomas) is seen in patients with renal stones\n- **Renal calyx rupture** is a rare complication and may lead to a urinoma (collection of urine in the abdomen)\n\n# Prognosis\n\n- 95% of stones < 5mm will pass spontaneously within 40 days\n- 70% of distal ureteric stones (of all sizes) will pass spontaneously\n- Rates of spontaneous passage are lower for more proximal stones (25% of proximal ureteric stones pass spontaneously)\n- Recurrence rates are high - 80% at 10 years - although 50% of these people will only have one recurrence\n- Frequent recurrence is seen in approximately 10% of patients\n \n# NICE Guidelines\n\n[NICE CKS - Renal or ureteric colic](https://cks.nice.org.uk/topics/renal-or-ureteric-colic-acute/)\n\n[NICE - Renal and ureteric stones: assessment and management](https://www.nice.org.uk/guidance/ng118/)\n \n# References\n\n[Radiopaedia - Ureteric calculi](https://radiopaedia.org/articles/ureteric-calculi?lang=gb)\n\n[Patient UK - Urinary tract stones](https://patient.info/doctor/urinary-tract-stones-urolithiasis)\n\n[RCEM Learning - Renal colic](https://www.rcemlearning.co.uk/reference/renal-colic/)\n\"",
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"question": "A 43-year-old man presents with left-sided loin-to-groin pain. He has vomited twice. On examination, he appears to be in significant discomfort but his vital signs are within normal parameters. He is given a dose of diclofenac and a CT kidneys, ureters and bladder is performed. The CT scan reveals a left single kidney with a 30mm stone at the pelvico-ureteric junction and evidence of associated hydronephrosis. His blood tests are unremarkable.\n\nWhat is the next best step in management?",
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"explanation": "Acting out dreams can indicate a REM disorder. This can be an early feature of Parkinson's disease, where a DaTscan can illustrate loss of dopaminergic neurones in the basal ganglia. However, given the patient demographics and the absence of any parkinsonian features, the more likely underlying cause of the REM sleep disorder is OSA. The first-line investigation would be polysomnography.",
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"explanation": "Waking in the middle of the night can occur in the context of heart failure, where the patient reports waking up breathless and coughing pink, frothy sputum (paroxysmal nocturnal dyspnoea (PND)). In this case, there are no reported heart failure symptoms, such as shortness of breath, PND, orthopnoea or ankle swelling. The clinical presentation is more in keeping with OSA.",
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"explanation": "The history of snoring and daytime somnolence in a patient who is obese points towards a diagnosis of obstructive sleep apnoea (OSA). Acting out dreams can be a rapid eye movement (REM) disorder, which can also be seen in a small number of these patients. The first-line investigation for OSA would be polysomnography.",
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"explanation": "Enlarged tonsils, adenoids or a narrowed airway can be risk factors for OSA. A laryngoscopy could be used to evaluate any structural abnormalities narrowing the airway. However, this is not first line and is generally reserved for patients undergoing potential surgical treatment, where standard medical therapy such as continuous positive airway pressure has failed or not been tolerated.",
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"explanation": "A sleep diary is unlikely to yield much additional information since the patient and his wife have already given detailed accounts of his sleep patterns. Their accounts point towards a diagnosis of OSA; therefore, he should be referred for polysomnography.",
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"explanation": "# Summary\n\nObstructive sleep apnoea (OSA) is caused by intermittent obstruction of the upper airways during sleep when there is loss of oropharyngeal muscle tone. Patients predisposed to this include those with obesity, large neck circumferences, anatomically smaller airways and decreased muscle tone due to alcohol or drugs (amongst other risk factors). The intermittent airway obstruction and resulting hypoxaemia leads to frequent awakening from sleep and so symptoms include excessive daytime sleepiness, morning headaches and poor concentration. The diagnostic investigation is polysomnography (a sleep study) to determine how many apnoeic or hypopnoeic episodes a patient is experiencing. Treatment includes modifying risk factors such as excess body weight and sleeping position, and continuous positive airway pressure (CPAP) devices to prevent airway obstruction overnight. \n\n# Definition\n\nObstructive sleep apnoea (OSA) is a condition where the upper airway becomes completely or partially obstructed during sleep, causing apnoeas (where breathing temporarily stops) or hypopnoeic episodes (decreased airflow during breathing). These episodes cause oxygen desaturations which cause brief arousals from sleep which can be hundreds of times per night. This leads to poor sleep quality which causes symptoms of daytime drowsiness, morning headaches and impaired concentration.\n\n# Epidemiology\n\nOSA is common, affecting an estimated 1.5 million adults in the UK, however around 85% of these are undiagnosed. Around half of people affected are overweight or obese, with 40% of obese people and 77% of morbidly obese people having OSA.\n\nOSA is strongly linked with cardiovascular disease and the metabolic syndrome, and is a significant risk factor for coronary artery disease, type 2 diabetes and stroke.\n\nDaytime sleepiness is an important consideration, especially in patients who drive or whose jobs require vigilance. Patients who drive for work and so are on the road for long periods of time and may be driving large vehicles are of particular concern due to the increased risk of injury to themselves and other road users.\n\n# Aetiology\n\nDuring sleep there is a normal loss of muscle tone in the oropharynx. In most people, there is still sufficient airway patency during sleep so that it does not become obstructed. Patients with OSA, however, require the muscle tone when awake to counteract additional pressures on their airway and so are unable to maintain patency when asleep.\n\nRisk factors for OSA include:\n\n- Obesity\n- Male sex\n- Older age\n- Decreased muscle tone - e.g. alcohol excess, sedative medications, muscular dystrophy or other neuromuscular disorders\n- Anatomical defects - e.g. retrognathia, macroglossia\n- Large neck circumference\n- Adenotonsillar hypertrophy (particularly in children)\n- Sleeping supine\n- Down’s syndrome\n\n# Signs and symptoms\n\n- Unrefreshing sleep, or frequent waking at night\n- Daytime sleepiness\n- Others may witness snoring, apnoeas, gasping or choking during sleep\n- Difficulty concentrating\n- Morning headaches\n- Behavioural problems and hyperactivity in children\n\nOn examination, patients may be drowsy and may have some of the risk factors above such as:\n\n- Obesity (check BMI)\n- Large neck circumference (can measure or ask collar size) \n- Jaw abnormalities (retrognathia or micrognathia)\n- Mouth breathing or nasal speech (due to nasopharyngeal obstruction, e.g. due to adenotonsillar enlargement)\n\nAlso look for signs and symptoms of complications of OSA such as hypertension or arrhythmias. \n\n# Differential Diagnosis\n\n- **Insomnia** - defined as difficulty falling asleep, staying asleep or poor sleep quality that leads to daytime impairment, commonly associated with other mental and physical health conditions\n- **Sleep disturbance** - for example due to shift work\n- **Restless legs syndrome** - patients get irresistible urges to move their legs accompanied by unpleasant sensations, often at night disturbing sleep\n- **Narcolepsy** - excessive daytime sleepiness, sudden attacks of sleep, excessive dreaming are common, may be associated with cataplexy (sudden loss of muscle tone, often triggered by strong emotions)\n- **Hypothyroidism** - also a risk factor for OSA, causes fatigue, poor concentration, weight gain and depression among other symptoms\n- **Depression** - associated with OSA, overlapping symptoms include low energy levels, poor concentration and low mood\n- **Medications** - SSRIs, antiepileptic medications and benzodiazepines can cause symptoms of daytime sleepiness and disturbed sleep\n- **Gastro-oesophageal reflux disease** - mimics nocturnal symptoms of choking and gasping, can disturb sleep\n\n# Investigations\n\nInitial screening for OSA symptoms and severity should be done using a questionnaire - the two recommended are STOP-Bang and the Epworth sleepiness scale.\n\n**STOP-Bang** asks about snoring, sleepiness, apnoeas, hypertension, obesity, neck circumference, age and sex and gives a low, medium or high risk of OSA.\n\nThe **Epworth sleepiness scale** focuses on daytime sleepiness and asks how likely the patient would be to fall asleep in a variety of situations (e.g. when watching TV). This gives a result of either normal daytime sleepiness or mild, moderate or severe excessive daytime sleepiness.\n\nThe definitive investigation is **polysomnography** (also called a sleep study) which would usually be arranged by a specialist clinic.\n\nPatients should be referred for this urgently (to be seen within 4 weeks) if:\n\n- Excessive sleepiness is impacting on their safety to work (e.g. professional driver)\n- They have a related comorbid condition such as treatment resistant hypertension or COPD\n- They have upcoming major surgery \n- They are pregnant\n\nPatients who do not fall into the above categories but have moderate or severe OSA or mild OSA which is impacting quality of life should be referred routinely to a sleep clinic for consideration of polysomnography.\n\nUsually polysomnography is done as an outpatient and patients can do the study at home overnight. In some situations an overnight admission may be required.\n\nThe study looks at how many episodes of apnoeas or hypopnoeas lasting 10 seconds or more patients have per hour of sleep (referred to as the apnoea-hypopnoea index or AHI). Five or more is diagnostic of OSA and severity is classified as below:\n\n- Mild OSA: AHI 5-14 per hour\n- Moderate OSA: AHI 15-30 per hour\n- Severe OSA: AHI over 30 per hour\n\nThe number of episodes of oxygen desaturation per hour is also measured, with more episodes of desaturation predictive of poorer cardiovascular outcomes.\n\n# Management\n\n**Conservative management includes:**\n\n- Patient education, especially concerning driving (see section on driving advice)\n- Advise to sleep on their side rather than supine where possible (aids such as repositioning pillows may be of help)\n- Weight loss advice and support (including diet, exercise, medications and surgery)\n- Reduction in alcohol intake\n- Smoking cessation\n\n**Medical management includes:**\n\n- Continuous Positive Airway Pressure (CPAP) therapy - this is first line in symptomatic OSA and is a long-term treatment. \n- A mask over the nose or face is used to deliver additional airway pressure that splints open the airways and prevents the collapse seen in OSA. \n- Education and support are key as tolerance can be a problem and masks need to fit well to be effective.\n- If patients do not tolerate or respond to CPAP, an intra-oral mandibular advancement device is another option. \n- These devices pull the mandible forward, opening the airway and preventing obstruction. \n- Management of comorbidities including hypertension, diabetes and depression is also important.\n\n**Surgical management includes:**\n\n- In cases where there is oropharyngeal obstruction e.g. due to adenotonsillar enlargement, surgery may be considered to relieve this for example a tonsillectomy.\n\n# Driving advice\n\nAll patients with daytime sleepiness due to OSA should be advised as follows:\n\n- If OSA is suspected or mild, advise patients not to drive until symptoms are controlled. If this is not achieved within 3 months, they should inform the DVLA.\n- If OSA is moderate or severe, patients should inform the DVLA immediately and not drive; this will be reviewed by the DVLA and they may be allowed to drive once symptoms are controlled.\n\nThis is the same for group 1 drivers (cars and motorbikes) and group 2 (lorries, buses and coaches), however group 2 drivers returning to driving after symptom control is achieved require annual reviews of this (rather than 3 yearly for group 1 drivers).\n\n# Complications\n\nComplications related to daytime sleepiness include:\n\n- Road traffic collisions - patients with OSA have a 2.5x increased risk compared to those without the condition\n- Accidents at home or at work\n- Deterioration in mental health, including irritability and depression\n\nCardiovascular and metabolic complications include:\n\n- Stroke\n- Coronary artery disease\n- Hypertension that may be treatment resistant\n- Congestive heart failure\n- Type 2 diabetes\n\n# NICE Guidelines\n\n[NICE CKS - Obstructive sleep apnoea syndrome](https://cks.nice.org.uk/topics/obstructive-sleep-apnoea-syndrome/)\n\n# References\n\n[Patient UK - Obstructive sleep apnoea](https://patient.info/doctor/obstructive-sleep-apnoea-syndrome-pro) \n\n[British Lung Foundation - OSA Toolkit](https://www.asthmaandlung.org.uk/sites/default/files/OSA_Toolkit_2015_BLF_0.pdf) \n\n[DVLA - Tiredness can kill: advice for drivers](https://www.gov.uk/government/publications/tiredness-can-kill-advice-for-drivers)",
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"learningPoint": "Polysomnography is the gold standard investigation for diagnosing obstructive sleep apnoea, it simultaneously records brain activity, eye movement, muscle activity, heart rate, respiratory effort, airflow, and oxygen saturation during sleep to identify apneic episodes and assess their severity.",
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"question": "A 42-year-old man attends his GP after a 6-month history of difficulty sleeping. He reports waking up multiple times a night gasping for breath and then napping more regularly in the day. His wife has also noticed that he tends to act out his dreams while asleep and snores heavily. On examination, his body mass index is 35 and otherwise unremarkable.\n\nWhat is the best next investigation for his poor sleep?",
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"explanation": "Aldosterone is also produced by the adrenal glands, alongside cortisol. It can also be deficient in Addison's disease and fludrocortisone replacement may be required alongside hydrocortisone in these cases. However, the first step in suspected Addison's disease is to evaluate the cortisol insufficiency since this is the most classical feature. A short syncathen test evaluates cortisol levels in response to exogenous ACTH administration and is the definitive initial test. In the case of Addison's disease (primary adrenal insufficiency), there will not be a rise in cortisol levels after ACTH administration.",
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"explanation": "Cortisol levels fluctuate during the course of the day and with stress, such as that induced by surgery. Although the levels of a random cortisol may be within a normal range, it is still possible that the patient could have a diagnosis of adrenal insufficiency since even apparently normal values may be insufficient for that patient at that particular moment in time. Therefore, a random cortisol will not provide adequate definitive diagnostic information.",
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"explanation": "Assessment of adrenal size and architecture can be useful for the evaluation of adrenal insufficiency, especially if there is concern that there may be an underlying cause, such as malignancy or infection. This is unlikely in this patient since there is no suggestion of there being an underlying cause; it is most likely that this patient has autoimmune Addison's disease, especially given the history of vitiligo.",
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"explanation": "Secondary adrenal insufficiency is caused by insufficient production of adrenocorticotropic hormone (ACTH) from the pituitary gland. Assessment of the size and architecture of the pituitary gland could be useful if this was suspected. This usually comes to light during a short synacthen test, where the baseline ACTH is evaluated, which would be low in the case of secondary adrenal insufficiency. Secondary adrenal insufficiency responds normally to short synacthen with a rise in cortisol; however, prolonged secondary adrenal insufficiency may result in underactive adrenal glands that do not respond well to short synacthen; in this case, a long synacthen test will be needed to stimulate cortisol release.",
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"explanation": "This patient is presenting with an addisonian crisis postsurgery, as evidenced by refractory hypotension, hyperkalaemia, low-normal sodium and the past medical history of autoimmune disease. A 9 a.m. cortisol < 50 is usually sufficient to make the diagnosis and > 550 to rule out the diagnosis. In between, further testing is required. For primary adrenal insufficiency (Addison's disease), this test will be a short synacthen test.",
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"explanation": "# Summary\n\nAdrenal insufficiency is a condition where destruction of the adrenal cortex leads to reduced glucocorticoid production. It can be classified as primary (Addison's disease) or secondary, each with different causes. Key signs and symptoms include hypotension, fatigue, weakness, gastrointestinal symptoms, and increased pigmentation. Initial investigations should focus on levels of sodium, potassium, glucose, cortisol, ACTH, renin, and aldosterone, while further tests should be used to establish the underlying cause. Management includes patient education on 'sick day' rules, glucocorticoid and mineralocorticoid replacement, and regular screening for complications like adrenal crisis and osteoporosis.\n\n# Definition\n\nAdrenal insufficiency is a clinical syndrome that arises due to the insufficient production of glucocorticoids and mineralocorticoids from the adrenal cortex. \n\nIt can be categorized as primary, commonly known as Addison's disease, where the cause lies within the adrenal glands themselves, or secondary, where inadequate stimulation of the adrenal glands by the pituitary or hypothalamus is the culprit.\n\n\n# Epidemiology\n\nAdrenal insufficiency is a relatively rare disease. Primary adrenal insufficiency (Addison's disease) affects approximately 100-140 people per million in developed countries. Secondary adrenal insufficiency is considered more common but accurate prevalence rates are difficult to determine.\n\n# Pathophysiology\n\nAdrenal insufficiency can result from damage to the adrenal cortex or disruptions in the hypothalamus-pituitary-adrenal (HPA) axis. The HPA axis regulates adrenal hormone production. In primary adrenal insufficiency (Addison's disease), the adrenal glands are damaged, while secondary adrenal insufficiency is due to dysfunction in the hypothalamus or pituitary. The lack of cortisol then disrupts feedback mechanisms, leading to elevated adrenocorticotropic hormone (ACTH) levels.\n\n\nPrimary adrenal insufficiency (Addison's disease) can be caused by:\n\n- Auto-immune destruction (most common)\n- Surgical removal of the adrenal glands\n- Trauma to the adrenal glands\n- Infectious diseases, such as tuberculosis (more common in developing countries)\n- Haemorrhage (e.g., Waterhouse-Friderichsen syndrome)\n- Infarction\n- Less commonly, neoplasms, sarcoidosis, or amyloidosis\n\nSecondary adrenal insufficiency can occur due to:\n\n- Congenital disorders\n- Fracture of the base of the skull\n- Pituitary or hypothalamic surgery or Neoplasms in the pituitary or hypothalamus\n- Infiltration or infection of the brain\n- Deficiency of corticotropin-releasing hormone (CRH)\n\n# Signs and Symptoms \n\nClinical features of adrenal insufficiency include:\n\n- Hypotension\n- Fatigue and weakness\n- Gastrointestinal symptoms\n- Syncope\n- Skin pigmentation due to increased ACTH which stimulates production of alpha melanocyte stimulating hormone (MSH).\n\n[lightgallery]\n\nIn the case of auto-immune Addison's disease, approximately 60% of patients may also have vitiligo or other autoimmune endocrinopathies.\n\n[lightgallery1]\n\n# Differential Diagnosis\n\nAdrenal insufficiency can be misdiagnosed as several other conditions, including:\n\n- Chronic fatigue syndrome: Presents with persistent fatigue, cognitive difficulties, and other non-specific symptoms\n- Dehydration or septic shock: Hypotension and tachycardia can mimic adrenal insufficiency\n- Primary psychiatric illnesses: Depression or other psychiatric illnesses may present with fatigue, decreased appetite, and weight loss.\n\n# Investigations\n\n* First line investigations are U+E and serum cortisol, where you may find:\n\t* Hyponatraemia (low sodium)\n\t* Hyperkalaemia (high potassium)\n\t* Low serum cortisol\n- Glucose (typically low)\n- Therefore in a patient with Addison's who is acutely unwell, you would expect a blood gas to show a **hyperkalaemic, hyponatraemic, hypoglycaemic metabolic acidosis**\n- ACTH: High in primary insufficiency, low or low-normal in secondary insufficiency\n- Renin (high in Addison's disease)\n- Aldosterone (low in Addison's disease)\n\nAn ACTH (Short Synacthen) test is the gold standard investigation to confirm the diagnosis.\n\nFurther investigations to establish the cause can include:\n\n- Testing for adrenal auto-antibodies\n- Chest X-ray\n- CT scan of the adrenal glands\n- MRI of the brain\n\n# Management\n\n**Management of adrenal insufficiency involves:**\n\n- Patient education on 'sick day' rules, carrying a steroid card, and wearing a medical alert bracelet\n- Doubling the regular steroid medication dose during any intercurrent illness\n- Replacement of both glucocorticoids (typically with hydrocortisone) and mineralocorticoids (typically with fludrocortisone)\n- Regular screening for complications including an adrenal crisis and osteoporosis\n\n**Management of Addisonian Crisis**\n\nAn Addisonian crisis, a life-threatening condition characterized by severe hypotension and electrolyte imbalances, should be managed with:\n\n- Aggressive fluid resuscitation\n- Administration of intravenous/IM (if no access) steroids STAT\n- Glucose administration if hypoglycaemia is present\n\n# Complications\n* Addisonian crisis (life-threatening adrenal crisis)\n* Severe electrolyte imbalances\n* Cardiovascular collapse\n* Hypoglycemia\n* Side effects of long term corticosteroid use e.g. osteoporosis\n\n# NICE Guidelines\n\n[Click here for NICE CKS on Addison's disease](https://cks.nice.org.uk/topics/addisons-disease/)\n",
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"question": "A 58-year-old man has been referred to intensive care by the anaesthetic registrar in orthopaedic theatre. He has had a knee replacement but has developed a persistent vasopressor requirement despite extensive intravenous fluids. His past medical history is significant for type 2 diabetes, hypertension, osteoarthritis and vitiligo. His blood gases reveal the following: \n\n\n||||\n|---------------------------|:-------:|--------------------|\n|Sodium|137 mmol/L|135 - 145|\n|Potassium|6.2 mmol/L|3.5 - 5.3|\n|Fasting Glucose|3.9 mmol/L|3.5 - 5.5|\n\n\nWhat is the definitive investigation for his underlying disease?",
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"explanation": "This patient is in DKA. The initial management is fluid resuscitation, followed by an insulin infusion of 0.1 U/kg/h. Patients with DKA are profoundly dehydrated due to the osmotic effects of hyperglycaemia; therefore, fluid resuscitation is the first action to take, followed by insulin administration to enable ketone clearance.",
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"explanation": "This patient is in DKA. The initial management is fluid resuscitation, followed by an insulin infusion of 0.1 U/kg/h. This patient's potassium is within the normal range at present, but will fall once the insulin infusion is running since this will drive potassium intracellularly. Therefore, potassium replacement is usually given in subsequent bags of normal saline; however, the first bag of normal saline, which is given rapidly over an hour, should not contain any potassium.",
"id": "52961",
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"name": "1 litre 0.9% NaCl with 40 mmol KCl over 4 h",
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"explanation": "This patient is in DKA. The initial management is fluid resuscitation, followed by an insulin infusion of 0.1 U/kg/h. Patients with DKA are profoundly dehydrated due to the osmotic effects of hyperglycaemia; therefore, fluid resuscitation is the first action to take, followed by insulin administration to enable ketone clearance.",
"id": "52958",
"label": "b",
"name": "0.1 U/kg/h of Actrapid in 50 ml 0.9% NaCl",
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"explanation": "This patient is in DKA. The initial management is fluid resuscitation, followed by an insulin infusion of 0.1 U/kg/h. 0.05 U/kg/h is the treatment of choice for hyperosmolar hyperglycaemic state if there is inadequate response to fluid therapy. Patients with DKA are profoundly dehydrated due to the osmotic effects of hyperglycaemia; therefore, fluid resuscitation is the first action to take, followed by insulin administration to enable ketone clearance.",
"id": "52959",
"label": "c",
"name": "0.05 U/kg/h Actrapid in 50 ml 0.9% NaCl",
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"explanation": "This patient is in diabetic ketoacidosis (DKA). The initial management is fluid resuscitation, followed by an insulin infusion of 0.1 U/kg/h. The key elements of the history supporting the diagnosis include polyuria, confusion and recent illness in someone who is a known diabetic. When patients become unwell and eat less, they can omit insulin doses due to concerns over hypoglycaemia, pushing themselves instead into DKA. This is the likely situation for this patient.",
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"comment": "shouldnt fluid therapy in this case be a bolus stat (15mins)?",
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"comment": "His BP ain't the worst of worst",
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"comment": "no bc its >90 SBP",
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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 A&E with a 3 day history of drowsiness, polyuria, vomiting and confusion. His mother reports he has recently been eating less due to an episode of food poisoning a week ago. He denies any recreational drug use. He has type 1 diabetes and uses a combination of short- and long-acting insulin. His heart rate is 110 bpm, blood pressure 100/75 mmHg, temperature 37.2 °C and oxygen saturation of 98% on air.\n\n\n\nArterial blood gases (ABGs) on room air:\n\n\n||||\n|--------------|:-------:|------------------|\n|pH|7.28|7.35 - 7.45|\n|PaO₂|8.9 kPa|11 - 15|\n|PaCO₂|3.6 kPa|4.6 - 6.4|\n|Bicarbonate|12 mmol/L|22 - 30|\n|Sodium|136 mmol/L|135 - 145|\n|Potassium|4.2 mmol/L|3.5 - 5.3|\n|Fasting Glucose|22 mmol/L|3.5 - 5.5|\n\n\n\n\nA urine dipstick is positive for ketones (++++) and glucose (+++).\n\n\n\nWhat is the next step in his management?",
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"explanation": "This patient is likely vitamin D-deficient due to parathyroid gland removal during total thyroidectomy surgery. Correcting the hypocalcaemia is the first port of call due to her having had a seizure. Vitamin D replacement is important for long-term management.",
"id": "52969",
"label": "c",
"name": "Oral high-dose vitamin D",
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"explanation": "This would be the treatment of choice for mild hypocalcaemia. This patient likely has profound hypocalcaemia due parathyroid gland removal during total thyroidectomy surgery. This patient has had serious complication of hypocalcaemia, including a seizure, and therefore IV calcium gluconate is the most appropriate initial treatment.",
"id": "52968",
"label": "b",
"name": "Oral calcium carbonate",
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"explanation": "This patient has had a seizure, terminated by one dose of lorazepam. Phenytoin is given after multiple unsuccessful doses of lorazepam 10 min apart. The likely cause of the seizure is hypocalcaemia and therefore it is best to treat the underlying cause to prevent further seizures.",
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"explanation": "This patient likely has hypocalcaemia, secondary to parathyroid gland removal during total thyroidectomy. The sign elicited on examination is Chvostek sign, one of the two signs for hypocalcaemia, the other being Trousseau's. Trousseau's sign is carpopedal spasm when a blood pressure cuff is applied and inflated on the arm. The patient has also presented with a seizure, suggesting profound hypocalcaemia. An ECG would also be an important investigation due to these patients being at risk of prolonged QTc and subsequent torsades de pointes.",
"id": "52967",
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"name": "IV calcium gluconate",
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"explanation": "This patient has had a seizure, which has terminated with one dose of lorazepam. If she had another seizure then another dose may be given as part of the emergency management. However, given that there are no current seizures, treating the underlying cause to prevent further episodes is the best next step. Therefore, calcium gluconate is the best answer.",
"id": "52971",
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"comment": "Great question author",
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"comment": "I would like half a mark for realising its hypocalcaemia",
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"explanation": "# Summary\n\nHypocalcaemia refers to an abnormally low serum calcium, adjusted for serum albumin concentration. A calcium of below 2.2 mmol/L is generally considered low although laboratory reference ranges may vary slightly. Causes include vitamin D deficiency, hypoparathyroidism, acute pancreatitis, chronic kidney disease and hypomagnesaemia. Symptoms usually occur when adjusted calcium falls below 1.9 mmol/L, and include muscle cramps, spasms and paraesthesias (classically perioral). Signs include carpopedal spasm and tetany. Investigations include an ECG, bone profile, parathyroid hormone (PTH) level, magnesium, U&Es and a vitamin D. Management involves treating the underlying cause and giving calcium supplementation - oral if mild (e.g. Calcichew tablets) and intravenous (e.g. calcium gluconate) if severe or symptomatic. Vitamin D and/or magnesium supplementation should be given if required. \n\n# Definition\n\nThe normal range for serum calcium is approximately 2.2-2.6 mmol/L. This is adjusted for serum albumin levels, which is important as approximately 40% of serum calcium is bound to albumin and so when albumin levels are low, serum calcium will be underestimated. \n\n99% of the body's calcium is stored in the skeleton and is crucial for the mineralisation of bone. It has many other roles in important functions such as muscle contraction, cardiac pacemaker activity, clotting, cell membrane stability and permeability.\n\nHypocalcaemia refers to an adjusted serum calcium of 2.2 mmol/L or lower.\n\n# Aetiology\n\n- Hypoparathyroidism\n - Iatrogenic due to parathyroid or thyroid surgery or radiotherapy\n - Autoimmune (may be part of a polyglandular syndrome)\n - Infiltration e.g. malignancy, thalassaemia, amyloidosis, Wilson's disease, haemochromatosis\n - Congenital e.g. DiGeorge syndrome (cleft palate, thymic aplasia, facial dysmorphism, cardiac defects and parathyroid agenesis)\n- Hypomagnesaemia (causes reversible functional hypoparathyroidism)\n- Vitamin D deficiency\n - Lack of sun exposure\n - Malnutrition\n - Malabsorption (e.g. due to pancreatic insufficiency)\n - Abnormal metabolism due to chronic kidney or liver disease\n- Medications \n - Calcimimetics (e.g. cinacalcet)\n - Bisphosphonates\n - Loop diuretics\n - Cisplatin\n - Foscarnet\n - Phenytoin\n - Ketoconazole\n- Genetic conditions such as autosomal dominant hypocalcaemia (due to a gain-of-function mutation in the calcium-sensing receptor (CaSR) gene) \n- Pseudohypoparathyroidism\n - PTH resistance due to genetic mutations in its signalling pathway\n - Manifests with hypocalcaemia, hyperphosphataemia and elevated PTH\n - May be associated with Albright hereditary osteodystrophy, where patients have a short stature, obesity, brachymetacarpals (especially the 4th and 5th digits), developmental delay and subcutaneous ossifications\n- Alkalosis causes a fall in ionised calcium (the metabolically active form) due to increased binding to albumin \n - This may be a respiratory alkalosis e.g. due to a panic attack or tachypnoea due to pneumonia or pulmonary embolism\n - Metabolic alkalosis may occur due to prolonged vomiting or excessive bicarbonate administration\n- Massive blood transfusion (as the citrate added to products to prevent clotting chelates calcium)\n - The same mechanism leads to hypocalcaemia in plasmapheresis (plasma contains citrate)\n- Renal replacement therapy with citrate used as an anticoagulant also causes chelation of calcium\n - Any form of continuous renal replacement therapy causes ongoing magnesium and calcium loss\n- Acute pancreatitis (due to saponification of calcium)\n- Hungry bone syndrome\n - Usually occurs after parathyroidectomy\n - There is prolonged PTH exposure with net bone resorption which suddenly shifts towards osteoblastic activity once PTH falls\n - There is a resulting influx of minerals into bone leading to hypocalcaemia and hypophosphataemia\n- Hyperphosphataemia (as phosphate binds with calcium), e.g. due to:\n - Chronic kidney disease\n - Tumour lysis syndrome\n - Rhabdomyolysis\n- Sepsis may lead to hypocalcaemia - this is multifactorial due to the effects of systemic inflammation on calcium homeostasis\n\n# Signs and Symptoms\n\nMild cases of hypocalcaemia (calcium > 2 mmol/L) are usually asymptomatic - once calcium falls below 2 the following symptoms may occur:\n\n- Paraesthesias (typically periorally and affecting the digits)\n- Muscle cramps\n- Muscle spasms\n- Anxiety and depression\n- Confusion\n- Weakness and fatigue\n- Myalgia\n- Dry skin\n- Coarse hair \n- Brittle nails \n\nSigns include:\n\n- Hyperreflexia\n- Muscle fasciculations\n- Chvostek's sign - tapping the facial nerve where it passes in front of the ear provokes muscular spasm of the face \n- This indicates neuromuscular hyperexcitability\n- Trousseau's sign of latent tetany - inflating a blood pressure cuff above the patient's systolic level and keeping this on for up to three minutes causes spasm of the forearm and hand muscles\n- The wrist and metacarpophalangeal joints flex, the fingers adduct and the distal and proximal interphalangeal joints extend\n- Hypotension (rarely)\n- Bradycardia\n- Decreased consciousness\n- Delirium\n- Papilloedema \n- Skin changes e.g. eczema, dermatitis, hyperpigmentation\n- Patchy alopecia\n- Transverse grooving of nails\n\n# Differential Diagnosis\n\n- **Pseudohypocalcaemia** occurs due to hypoalbuminaemia - total calcium will be low in these patients (hence the importance of correcting serum calcium for albumin levels)\n- **Contamination of blood bottles** with EDTA or citrate will lead to artefactual hypocalcaemia - hyperkalaemia will also be seen with EDTA and hypernatraemia with sodium citrate\n\n# Investigations\n\n**Bedside:**\n\n- **ECG** may show a prolonged QTc or rarely arrhythmias (e.g. atrial fibrillation)\n- **Blood gas** to rapidly confirm hypocalcaemia (NB blood gas machines measure ionised calcium only so the reference ranges are significantly lower)\n- **Urine dip** may be positive for protein in CKD or falsely positive for blood due to myoglobinuria in rhabdomyolysis\n\n**Blood tests:**\n\n- **Bone profile** to confirm hypocalcaemia and check phosphate levels\n- **PTH levels** are helpful to help identify a cause - they will be low in hypoparathyroidism and high for example in vitamin D deficiency or pseudohypoparathyroidism\n- **Full blood count** may show anaemia related to chronic disease (e.g. chronic kidney disease) or leukocytosis in sepsis\n- **U&Es** to look for chronic kidney disease\n- **CRP** to screen for inflammation for example in sepsis\n- **Magnesium** to check for hypomagnesaemia\n- **LFTs** to check albumin; liver function may be deranged in some causes e.g. metastatic malignancy \n- **Vitamin D level** to look for deficiency\n- **Amylase** if pancreatitis is suspected\n- **Creatine kinase** if rhabdomyolysis is suspected\n\n**Special tests:**\n\n- **Genetic testing** may be offered to patients with a suspected genetic mutation e.g. autosomal dominant hypocalcaemia\n\n# Management \n\n**Conservative:**\n\n- Identification and management of the underlying cause is key e.g. stopping causative medications where possible\n- Ensure oral intake of calcium is adequate (700 mg/day is recommended for most adults; patients with osteoporosis should have double this)\n- Patients with ECG changes require cardiac monitoring as well as urgent intravenous calcium replacement (see below)\n- Some patients with mild asymptomatic hypocalcaemia e.g. due to critical illness do not require treatment and should be monitored\n\n**Medical:**\n\n- Mild hypocalcaemia (calcium 1.9 mmol/L or higher) can be treated with oral replacement e.g. Calcichew 2 tablets twice a day\n- Severe hypocalcaemia (calcium < 1.9 mmol/L or symptomatic) should be treated urgently with intravenous calcium replacement \n- For example, 10-20 ml of calcium gluconate 10% in 5% glucose over 10 minutes\n- This can be repeated if necessary or followed by a calcium gluconate infusion\n- Vitamin D supplementation should be provided if low - colecalciferol (vitamin D3) is the usual supplement prescribed however other compounds may be required e.g. alfacalcidol (1α-hydroxycholecalciferol) in CKD\n- Replace magnesium if low (see hypomagnesaemia chapter for details) - hypocalcaemia is unlikely to resolve if magnesium is still low\n\n# Complications\n\n**Complications of acute hypocalcaemia:**\n\n- Seizures - may be generalised motor or absence seizures, or focal\n- Arrhythmias - e.g. torsades de pointes due to QTc prolongation\n- Laryngospasm - common in infancy but rarer in adults\n- Bronchospasm - also uncommon in adults, may mimic an asthma exacerbation\n\n**Complications of chronic hypocalcaemia:**\n\n- Cataracts - typically bilateral, not reversible with correction of hypocalcaemia\n- Dental disease - e.g. enamel hypoplasia, increased risk of caries\n- Basal ganglia calcification - may be asymptomatic or lead to movement disorders, parkinsonism or dementia\n\n# References\n\n[Patient UK - Hypocalcaemia](https://patient.info/doctor/hypocalcaemia)\n\n[BNF - Calcium imbalance](https://bnf.nice.org.uk/treatment-summaries/calcium-imbalance/)\n\n[GGC Medicines UK - Management of Hypocalcaemia](https://handbook.ggcmedicines.org.uk/guidelines/electrolyte-disturbances/management-of-hypocalcaemia/)\n\n[The Internet Book of Critical Care - Hypocalcaemia](https://emcrit.org/ibcc/hypocalcemia/)\n\n[Life in the Fast Lane - Hypocalcaemia ECG library](https://litfl.com/hypocalcaemia-ecg-library/)",
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"question": "A 32-year-old woman is brought to A&E by ambulance accompanied by her mother. She was discharged from hospital 3 d ago after a total thyroidectomy for papillary thyroid cancer. Today, her mother witnessed her having a tonic-clonic seizure, which terminated after a single dose of lorazepam provided by paramedics. There have been no further seizures. On examination, gentle tapping over the facial nerve produces spasm of her face ipsilaterally.\n\nWhat is the first-line initial treatment for her diagnosis?",
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"explanation": "This woman gives a typical history of stress incontinence. She passes small amounts of urine involuntarily when her abdominal pressure is increased, such as when coughing or after eating a large meal. She has risk factors for stress incontinence such as being female, overweight, smoking and drinking coffee. She would be advised to limit her alcohol and coffee intake and be offered help to lose weight and quit smoking. She would also be referred for pelvic floor exercises.",
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"explanation": "This is a beta 3 agonist used for the management of urge (overactive bladder) incontinence. The history here is not consistent with urge incontinence.",
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"comment": "man why did I think pelvic floor exercises were part of lifestyle advice, now i'm part of the 5% that chose duloxetine :(",
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"explanation": "# Summary\n\nUrinary incontinence refers to the involuntary loss of urine and can be categorised into stress, urge, overflow, functional, and mixed types. Key signs and symptoms vary, ranging from involuntary urine leakage when intra-abdominal pressure is raised in stress incontinence, to an abrupt and uncontrollable urge to urinate in urge incontinence. Essential investigations encompass physical examination, questionnaires, bladder diaries, urinalysis, and occasionally cystometry or cystograms. Management strategies depend on the type and severity of incontinence, encompassing conservative methods (like lifestyle modifications), medical treatment (such as Duloxetine, anticholinergics), and surgical options (for example, incontinence pessaries, mid-urethral slings). Generally, stress incontinence is managed with pelvic floor exercises, whereas urge incontinence is initially managed with bladder re-training exercises.\n\n# Types \n\nUrinary incontinence can be categorised into:\n\n1. Stress incontinence\n2. Urge incontinence\n3. Overflow incontinence\n3. Functional incontinence\n4. Mixed incontinence \n\nReversible causes of urinary incontinence can be remembered using the mneumonic **'DIAPPERS':**\n\nD - Delirium\n\nI - Infection\n\nA - Atrophic vaginitis or urethritis\n\nP - Pharmaceutical (medications)\n\nP - Psychiatric disorders\n\nE - Endocrine disorders (e.g. diabetes)\n\nR - Restricted mobility\n\nS - Stool impaction\n\n\n# Approach to Incontinence\n\nOne of the keys is to rule out reversible causes and then try to work out which type of urinary incontinence is. A framework or approach to this is below:\n\n- Physical examination\n\n - An examination will identify features of pelvic organ prolapse as well as the ability to contract pelvic floor muscles.\n\n- Questionnaires\n\n - These are recommended in order to quantify the symptoms and assess the severity on patients quality of life which may help when deciding if a patient would benefit from more invasive treatment\n\n- Bladder diary\n\n - These are also useful for quantifying symptoms and documenting the number and type of episodes of incontinence. They may potentially show a relationship between causes and symptoms.\n\n- Urinalysis\n\n - This will help to rule out infection as an acute cause\n\n- Cystometry\n\n - This is an investigation which measures bladder pressure whilst voiding. It is not recommended in patients with clear histories where the diagnosis is clear.\n\n- Cystogram\n\n - If a fistula is suspected, contrast is instilled into the bladder and a radiological image is obtained in order to see if the contrast travels anywhere else.\n\n\n# Stress incontinence\n\nThis involves leaking of urine when intra-abdominal pressure is raised, putting pressure on the bladder. The pressure of the urine overcomes the mechanisms designed to maintain continence.\n\n## Risk factors \n\n- Childbirth (especially vaginal).This may be due to a combination of injury to the pelvic floor musculature and connective tissue (for example leading to prolapse), as well as nerve damage as a result of pregnancy and labor.\n- Hysterectomy\n\n\n## Triggers\n\nActs such as coughing, laughing, sneezing or exercising can increase abdominal pressure sufficiently.\n\n## Causes\n\nAny abnormality in the anatomy of the bladder, sphincters and urethra can result in stress incontinence.\n\n\n## Conservative management\n\nGeneral lifestyle advice such as avoiding caffeine, fizzy and sugary drinks, as well as avoiding excessive fluid intake, can go far in helping incontinence.\n\nPelvic floor exercises when done with good technique and consistently strengthen the muscles of the pelvic floor. It can help both stress and urge incontinence and can be more effective than drug treatment.\n\n## Medical management\n\nDuloxetine can help with stress incontinence, but it's only recommended if conservative measures fail and the patient is not a surgical candidate.\n\n## Surgical management \n\n- Incontinence pessaries are placed transvaginally and apply pressure to the anterior vaginal wall. This helps to support the urethra and sphincters. However, the evidence for them is poor in individuals without prolapse and isn't recommended by NICE. It would be worth trying if there was a clinical prolapse.\n- Bulking agents are injectable materials placed at the bladder neck to improve continence. This procedure is typically reserved for patients who are poor surgical candidates and isn't as efficacious as other methods\n- Colposuspension and fascial slings involve suspending the anterior vaginal wall to the iliopectineal ligament of Cooper.\n- Mid-urethral slings are the gold standard surgical treatment of stress incontinence. It compresses the urethra against a supportive layer and assists in the closure of the urethra during increased intra-abdominal pressures. It's minimally invasive and can be performed in the outpatient setting.\n\n\n# Urge incontinence\n\n## Definition \n\nThis involves the sudden and involuntary loss of urine associated with urgency.\n\n## Risk factors \n\nRisk factors for urgency include:\n\n- Recurrent urinary tract infections\n- High BMI\n- Advancing age\n- Smoking\n- Caffeine\n\n\n## Conservative management \n\nGeneral lifestyle advice such as avoiding caffeine, fizzy and sugary drinks as well as avoiding excessive fluid intake can go far in helping incontinence. Chemicals contained in these drinks can irritate the bladder, contributing to urge symptoms.\n\nPelvic floor exercises when done with good technique and consistently, strengthen the muscles of the pelvic floor. It can help both stress and urge incontinence and can be more effective than drug treatment. In urge incontinence, contraction of the pelvic floor relaxes the detrusor. Bladder training is also helpful.\n\n## Medical/surgical management\n\n- Pharmacological management\n\t- Anticholinergic medications can help reduce the symptoms of urge and overactive bladder by inhibiting the parasympathetic action on the detrusor muscle.\n\t\t- Examples include: **Oxybutynin, Tolterodine, Fesoterodine, Solifenacin**. If one agent has limited impact, it can be combined with another. Use with caution in elderly however due to increased risk of delirium (side-effect).\n\t- Mirabegron (beta-3 receptor agonist) can be used in older people, but should be used with caution in patients with hypertension.\n\n- Bladder instillation\n\n - Intravesical injection of Botox can be used to paralyse the detrusor muscle and reduce the symptoms of urge and overactive bladder.\n\n- Sacral neuromodulation\n\n - Sacral nerve stimulation has been shown to control symptoms of an overactive bladder. This is only done in tertiary centres for patient who have failed or are unsuitable for all other treatments.\n\n\n# Functional incontinence\n\n## Definition \n\nThis involves an individual having the urge to pass urine, but for whatever reason they're unable to access the necessary facilities and as a result are incontinent.\n\n## Causes \n\nFunctional incontinence associated with:\n\n- Sedating medications\n- Alcohol\n- Dementias\n\n# Overflow incontinence\n\n## Definition \n\nThis occurs when small amounts of urine leak without warning. When the pressure within the bladder overcomes the pressures of the outlet structures urine leaks.\n\n## Causes \n\nThis occurs either due to underactivity of the detrusor muscle such as from neurological damage, or if the urinary outlet pressures are too high, as in constipation or prostatism.\n\n\n\n# NICE Guidelines\n\n[NICE Guidance - Urinary incontinence and pelvic organ prolapse in women: management](https://www.nice.org.uk/guidance/ng123)",
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"question": "A 42-year-old woman presents to her GP with frequent leaking of small volumes of urine. This is worse when she drinks coffee, coughs or eats a large meal. She denies urinary urgency or any other urinary symptoms. She is a current smoker and on examination her body mass index is 30.\n\nApart from lifestyle advice, what is the next best step in management?",
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"explanation": "This patient denies any symptoms of leakage following raised abdominal pressure, for example, with coughing or sneezing. Urine leakage is consistent throughout the day, which is most in keeping with a vesicovaginal fistula, especially in the context of recent radiotherapy to the pelvis.",
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"explanation": "A rectovaginal fistula would cause the passage of faeces through the vagina, with an increased risk of urinary tract infections. This patient describes a continuous urine leakage throughout the day, with recent pelvic radiotherapy, making a vesicovaginal fistula the most likely diagnosis.",
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"explanation": "Chronic cystitis would more typically give a history of dysuria, pelvic pain, urinary urgency and frequency. This patient describes urinary leakage throughout the day with no mention of pain in the history. The most likely diagnosis is a vesicovaginal fistula given the painless continuous leakage of urine plus recent pelvic radiotherapy.",
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"explanation": "# Summary\n\nUrinary incontinence refers to the involuntary loss of urine and can be categorised into stress, urge, overflow, functional, and mixed types. Key signs and symptoms vary, ranging from involuntary urine leakage when intra-abdominal pressure is raised in stress incontinence, to an abrupt and uncontrollable urge to urinate in urge incontinence. Essential investigations encompass physical examination, questionnaires, bladder diaries, urinalysis, and occasionally cystometry or cystograms. Management strategies depend on the type and severity of incontinence, encompassing conservative methods (like lifestyle modifications), medical treatment (such as Duloxetine, anticholinergics), and surgical options (for example, incontinence pessaries, mid-urethral slings). Generally, stress incontinence is managed with pelvic floor exercises, whereas urge incontinence is initially managed with bladder re-training exercises.\n\n# Types \n\nUrinary incontinence can be categorised into:\n\n1. Stress incontinence\n2. Urge incontinence\n3. Overflow incontinence\n3. Functional incontinence\n4. Mixed incontinence \n\nReversible causes of urinary incontinence can be remembered using the mneumonic **'DIAPPERS':**\n\nD - Delirium\n\nI - Infection\n\nA - Atrophic vaginitis or urethritis\n\nP - Pharmaceutical (medications)\n\nP - Psychiatric disorders\n\nE - Endocrine disorders (e.g. diabetes)\n\nR - Restricted mobility\n\nS - Stool impaction\n\n\n# Approach to Incontinence\n\nOne of the keys is to rule out reversible causes and then try to work out which type of urinary incontinence is. A framework or approach to this is below:\n\n- Physical examination\n\n - An examination will identify features of pelvic organ prolapse as well as the ability to contract pelvic floor muscles.\n\n- Questionnaires\n\n - These are recommended in order to quantify the symptoms and assess the severity on patients quality of life which may help when deciding if a patient would benefit from more invasive treatment\n\n- Bladder diary\n\n - These are also useful for quantifying symptoms and documenting the number and type of episodes of incontinence. They may potentially show a relationship between causes and symptoms.\n\n- Urinalysis\n\n - This will help to rule out infection as an acute cause\n\n- Cystometry\n\n - This is an investigation which measures bladder pressure whilst voiding. It is not recommended in patients with clear histories where the diagnosis is clear.\n\n- Cystogram\n\n - If a fistula is suspected, contrast is instilled into the bladder and a radiological image is obtained in order to see if the contrast travels anywhere else.\n\n\n# Stress incontinence\n\nThis involves leaking of urine when intra-abdominal pressure is raised, putting pressure on the bladder. The pressure of the urine overcomes the mechanisms designed to maintain continence.\n\n## Risk factors \n\n- Childbirth (especially vaginal).This may be due to a combination of injury to the pelvic floor musculature and connective tissue (for example leading to prolapse), as well as nerve damage as a result of pregnancy and labor.\n- Hysterectomy\n\n\n## Triggers\n\nActs such as coughing, laughing, sneezing or exercising can increase abdominal pressure sufficiently.\n\n## Causes\n\nAny abnormality in the anatomy of the bladder, sphincters and urethra can result in stress incontinence.\n\n\n## Conservative management\n\nGeneral lifestyle advice such as avoiding caffeine, fizzy and sugary drinks, as well as avoiding excessive fluid intake, can go far in helping incontinence.\n\nPelvic floor exercises when done with good technique and consistently strengthen the muscles of the pelvic floor. It can help both stress and urge incontinence and can be more effective than drug treatment.\n\n## Medical management\n\nDuloxetine can help with stress incontinence, but it's only recommended if conservative measures fail and the patient is not a surgical candidate.\n\n## Surgical management \n\n- Incontinence pessaries are placed transvaginally and apply pressure to the anterior vaginal wall. This helps to support the urethra and sphincters. However, the evidence for them is poor in individuals without prolapse and isn't recommended by NICE. It would be worth trying if there was a clinical prolapse.\n- Bulking agents are injectable materials placed at the bladder neck to improve continence. This procedure is typically reserved for patients who are poor surgical candidates and isn't as efficacious as other methods\n- Colposuspension and fascial slings involve suspending the anterior vaginal wall to the iliopectineal ligament of Cooper.\n- Mid-urethral slings are the gold standard surgical treatment of stress incontinence. It compresses the urethra against a supportive layer and assists in the closure of the urethra during increased intra-abdominal pressures. It's minimally invasive and can be performed in the outpatient setting.\n\n\n# Urge incontinence\n\n## Definition \n\nThis involves the sudden and involuntary loss of urine associated with urgency.\n\n## Risk factors \n\nRisk factors for urgency include:\n\n- Recurrent urinary tract infections\n- High BMI\n- Advancing age\n- Smoking\n- Caffeine\n\n\n## Conservative management \n\nGeneral lifestyle advice such as avoiding caffeine, fizzy and sugary drinks as well as avoiding excessive fluid intake can go far in helping incontinence. Chemicals contained in these drinks can irritate the bladder, contributing to urge symptoms.\n\nPelvic floor exercises when done with good technique and consistently, strengthen the muscles of the pelvic floor. It can help both stress and urge incontinence and can be more effective than drug treatment. In urge incontinence, contraction of the pelvic floor relaxes the detrusor. Bladder training is also helpful.\n\n## Medical/surgical management\n\n- Pharmacological management\n\t- Anticholinergic medications can help reduce the symptoms of urge and overactive bladder by inhibiting the parasympathetic action on the detrusor muscle.\n\t\t- Examples include: **Oxybutynin, Tolterodine, Fesoterodine, Solifenacin**. If one agent has limited impact, it can be combined with another. Use with caution in elderly however due to increased risk of delirium (side-effect).\n\t- Mirabegron (beta-3 receptor agonist) can be used in older people, but should be used with caution in patients with hypertension.\n\n- Bladder instillation\n\n - Intravesical injection of Botox can be used to paralyse the detrusor muscle and reduce the symptoms of urge and overactive bladder.\n\n- Sacral neuromodulation\n\n - Sacral nerve stimulation has been shown to control symptoms of an overactive bladder. This is only done in tertiary centres for patient who have failed or are unsuitable for all other treatments.\n\n\n# Functional incontinence\n\n## Definition \n\nThis involves an individual having the urge to pass urine, but for whatever reason they're unable to access the necessary facilities and as a result are incontinent.\n\n## Causes \n\nFunctional incontinence associated with:\n\n- Sedating medications\n- Alcohol\n- Dementias\n\n# Overflow incontinence\n\n## Definition \n\nThis occurs when small amounts of urine leak without warning. When the pressure within the bladder overcomes the pressures of the outlet structures urine leaks.\n\n## Causes \n\nThis occurs either due to underactivity of the detrusor muscle such as from neurological damage, or if the urinary outlet pressures are too high, as in constipation or prostatism.\n\n\n\n# NICE Guidelines\n\n[NICE Guidance - Urinary incontinence and pelvic organ prolapse in women: management](https://www.nice.org.uk/guidance/ng123)",
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"question": "A 72-year-old female presents to her GP with leakage of urine. She says that urine leaks continuously throughout the day and is affecting her ability to leave the house since she frequently has to change her underwear. She does not report her symptoms worsening with alcohol, caffeine, straining or coughing. She does not report any urinary urgency or any other urinary symptoms. She underwent radiotherapy after resection of a rectal tumour 4 months ago. There has been no signs of recurrence from her most recent follow-up. She is otherwise well, has never smoked and has a body mass index of 25. She had one child via caesarian section 40 years ago.\n\nWhat is the most likely diagnosis?",
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"explanation": "This will be raised in hepatitis but it is not a measure of synthetic liver function or a good prognosticator for fulminant hepatic failure.",
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"explanation": "This will be raised in hepatitis but it is not a measure of synthetic liver function or a good prognosticator for fulminant hepatic failure.",
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"explanation": "The international normalised ratio is the best prognostic indicator for patients who have sustained hepatic injury due to paracetamol overdose. This is because it represents the synthetic function of the liver.",
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"explanation": "The liver produces albumin, the main component of the blood-maintaining oncotic pressure. When albumin levels drop, fluid moves from the intravascular space to the interstitial space, causing peripheral oedema and ascites. The half-life of albumin is 3 weeks; therefore, it is not a good measure of liver function in the acute setting.",
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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 28-year-old man presents to A&E after an overdose of paracetamol. He said he took 40 tablets over a 6-h period yesterday evening. It is now 11 a.m.\n\nWhich of the following tests provides the best prognostic indicator?",
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"explanation": "This patient has positive IgG antibodies to the core antigen of hepatitis B virus and positive surface antigen antibodies. This is in keeping with previous exposure to hepatitis B virus with recovery and the presence of current antibodies.",
"id": "53002",
"label": "a",
"name": "Previous exposure and recovery to hepatitis B",
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"explanation": "This patient has positive IgG antibodies to the core antigen of the hepatitis B virus and positive surface antigen antibodies. Previous vaccination would mean only antibodies for the surface antigen would be present since there is no core antigen present in the vaccine. This patient has antibodies to both, indicating previous infection with immunity.",
"id": "53005",
"label": "d",
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"explanation": "This patient has positive IgG antibodies to the core antigen of hepatitis B virus and positive surface antigen antibodies. Early acute infection would have a positive surface antigen present, without presence of antibodies. The first type of antibody to appear would then be IgM.",
"id": "53006",
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"explanation": "This patient has positive IgG antibodies to the core antigen of hepatitis B virus and positive surface antigen antibodies. If the infection were chronic, we would expect a positive surface antigen to be present due to ongoing virus particle production. The surface antigen is currently negative, indicating recovery from the infection.",
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"explanation": "### Summary\n\nHepatitis is an inflammation of the liver caused by a variety of infectious and non-infectious factors. The most prevalent causes of viral hepatitis in the UK are hepatitis A, B, and C viruses. Hepatitis can present with symptoms such as fatigue, nausea, vomiting, and jaundice. The different hepatitis viruses can cause different spectra of disease, with some more likely to cause an acute hepatitis, and others a chronic hepatitic picture. The differential diagnosis includes conditions such as drugs, toxins, alcohol, EBV, CMV, leptospirosis, and malaria. Key investigations include serology for specific hepatitis types. The management of hepatitis is largely supportive, with some patients requiring antiviral treatment depending on the type of hepatitis.\n\n### Definition\n\nHepatitis refers to the inflammation of the liver. It is typically caused by viral infection but can also result from non-infectious aetiologies such as toxins and alcohol. \n\nHepatitis A and Hepatitis E can lead to acute liver failure, whereas Hepatitis B and Hepatitis C tend to lead to chronic liver failure. Hepatitis D only occurs in individuals who are infected with Hepatitis B. \n\n### Epidemiology\n\nViral hepatitis is common in the UK with the primary causes being hepatitis A, B, and C viruses. These can cause acute disease, but hepatitis B and C can also lead to chronic infection, liver fibrosis, and hepatocellular carcinoma. The prevalence of Hepatitis A is higher in developing countries, while Hepatitis B is the most common cause of hepatitis globally.\n\nOther causes of acute hepatitis include drugs, toxins, alcohol, EBV, CMV, hepatitis E, leptospirosis, and malaria.\n\nNB: All infectious hepatitis cases are notifiable diseases in the UK.\n\n### Signs and Symptoms\n\n#### Acute liver failure\n\n- Predominantly caused by Hepatitis A and E\n- Prodromal viral illness:\n\u0001- Fever\n\u0001- Malaise\n\u0001- Anorexia\n\u0001- Nausea and vomiting\n\n#### Acute hepatitis\n\n- Right upper quadrant pain\n- Jaundice\n- Tender hepatosplenomegaly (due to swelling of the liver capsule)\n\n#### Chronic liver failure\n\n- Hepatic encephalopathy\n- Jaundice\n- Ascites\n- Coagulopathy due to abnormal clotting\n\n\n### Hepatitis A\n\n- RNA picornavirus, transmitted by faecal-oral route (occasionally through food sources or through anal sex)\n\n#### Epidemiology \n\n- Prevalence is high in developing countries.\n- Increasing age is the only real determinant of disease severity, with the greatest morbidity and mortality in those over 50 years old.\n- Travellers and those at risk can be offered immunisation\n- It is transmitted via the faecal-oral route (commonly through shellfish)\n\n#### Presentation \n\n- Flu-like symptoms followed by jaundice, pale stools (in some), dark urine and abdominal pain\n- Incubation period of 2-6 weeks, presents only as an **acute** hepatitis with no chronic phase\n- Complete recovery can take up to 6 months.\n\n#### Investigations \n\n- Hepatitic LFTs, with ALT/AST as high as in the 1000s\n- IgM and IgG antibodies to HAV\n\n#### Management \n\n- Management is largely supportive\n\n#### Hepatitis E\n- Similarly spread via faecal-oral route (commonly undercooked pork)\n- It is **e**xtremely dangerous in pregnancy, with a mortality rate up to 20%\n- Similar to Hepatitis A with only an acute presentation and no chronic phase, with management also supportive in nature\n\n### Hepatitis B \n\n- dsDNA virus of Hepadnaviridae family\n- Primarily causes an acute hepatitis, with the main and most severe complication being progression to chronic hepatitis infection\n\n#### Epidemiology\n\n- Most common cause of hepatitis globally\n- High prevalence regions include sub-Saharan Africa, Asia and the Pacific Islands.\n- Decline of disease in children and adolescents in the UK is due to **routine vaccination**\n- Incubation period usually 60-90 days.\n\n#### Transmission\n\n- Transmission is via infected blood or body fluids\n - Vaginal/anal intercourse\n - Transfusion\n - Vertical transmission (in 90% of pregnancies where the mother is HBeAg positive, and 10% where this is negative).\n - In developing countries, infection is mostly in childhood through vertical or horizontal transmission. In areas of low endemicity (such as the UK), infections are mostly acquired in adulthood.\n\n#### Presentation\n\n- Children - Only 5% of children have jaundice and severe symptoms i.e. it is mostly an asymptomatic primary infection, but the majority (90%) develop chronic disease with only 10% able to clear the virus\n- Adults - more likely to have an acute hepatitis picture with jaundice, fever, malaise, viral prodrome and occasionally darkening of urine and lightening of stool. Some develop fulminant liver failure with decompensation (ascites, encephalopathy etc.). 90% clear the infection, with only around 10% developing chronic disease\n- Chronic features occur when the virus has been unable to be cleared for more than 6 months - development of cirrhosis, decompensated liver failure, and increased risk for **hepatocellular carcinoma**\n- Rarer features of hepatitis B infection include glomerulonephritis, cryoglobulinaemia and polyarteritis nodosa\n\n#### Investigations\n\n- HBsAg is detected 3-5 weeks after infection. If present for >6 months, this defines carrier status (5-10% of infections).\n- In carriers, HBeAg-positive patients are the most infectious. If HBeAg-negative (and anti-HBe-antibody positive), they have lower infectivity.\n- Patients with chronic infection who are HBeAg -ve may get immune escape phase when the virus mutates despite anti-HBe antibodies being present. These patients are the main pool for the spread in the UK, and so all chronically infectious patients need yearly screens to identify this.\n\nA summary table of the serology in Hepatitis B is below:\n\n\n| Marker | Description |\n|-----------------------------|-------------------------------------------------|\n| HBsAg (Hepatitis B Surface Antigen) | Indicates current infection; persists >6 months |\n| Anti-HBs (Hepatitis B Surface Antibody) | Indicates immunity from past infection or vaccination |\n| HBeAg (Hepatitis B e Antigen) | Indicates active viral replication; higher infectivity |\n| Anti-HBe (Hepatitis B e Antibody) | Indicates lower infectivity; seroconversion is associated with reduced viral replication |\n| HBcAb (Hepatitis B Core Antibody) | IgM indicates acute infection; IgG indicates past infection or vaccination |\n| HBV DNA (Hepatitis B Virus DNA) | Quantifies viral load; used to monitor response to treatment |\n\n- Biopsy of the liver in chronic hepatitis B infection will reveal 'ground-glass' hepatocytes on light microscopy\n\n#### Management \n\n- There is no **cure** for chronic hepatitis B, but there is a *functional* cure as you can prevent liver disease with pegylated interferon\n- Indications for antiviral treatment\n\u0001- Adults aged 30 years and older who have HBV DNA greater than 2000 IU/ml and abnormal ALT on 2 consecutive tests conducted 3 months apart\n\u0001- Adults who have HBV DNA greater than 20,000 IU/ml and abnormal ALT on 2 consecutive tests conducted 3 months apart regardless of age or the extent of liver disease\n\u0001- Adults with cirrhosis and detectable HBV DNA, regardless of HBeAg status, HBV DNA and ALT levels\n- Pegylated interferon alfa-2a is the first line, with tenofovir and entecavir as second-line alternatives\n\u0001- Pegylated interferon can lead to viral suppression which leads to ALT normalisation and improved liver histology\n\nIf a patient with hepatitis B becomes suddenly very unwell with a worsening hepatitic picture, consider if they are now suffering co-infection with **Hepatitis D**\n\n### Hepatitis C \n\n- RNA virus of the Flaviviridae family, with 6 major genetic types (genotypes 1 and 3 are most common in the UK, and genotype 1 is associated with longer treatment and worse prognosis)\n- There is no vaccination for Hepatitis C, currently\n\n#### Transmission\n\n- Transmitted via exchange of blood and bodily fluids:\n - Intravenous drug use\n - Blood transfusion\n - Haemodialysis (rare in the UK)\n - Sexual transmission (less than 1% per year of relationship, but rate higher if co-infected with HIV)\n - Needlestick injuries in healthcare facilities - 3% risk of transmission.\n - Perinatal infection from infected mother.\n- Incubation period of 6-9 weeks.\n\n#### Presentation\n\n- Most infections are asymptomatic, and only 15-25% clear the virus. 75% go on to develop chronic infection\n- Patients with chronic infection have persistently high LFTs, and cirrhosis develops in 20-30%\n- 1-4% of patients with cirrhosis develop hepatocellular carcinoma, and 2-5% develop liver failure\n- Additional features – arthralgia/arthritis, Sjogren’s syndrome, cryoglobulinaemia, porphyria cutanea tarda, membranoproliferative glomerulonephritis\n\n#### Investigations \n\n- Anti-HCV serology - 90% are positive 3 months after infection but it may take many months to become positive for some\n- Even if the virus has been cleared, HCV antibodies can remain positive for months afterwards\n- HCV RNA - if positive for more than two months then need to be treated.\n\n#### Management \n\n- Symptomatic treatment in the early stages of the disease\n- There is a **c**ure (Hepatitis **C** for **C**ure), unlike in Hepatitis B\n- Drug therapy should be considered for all patients and depends on the genotype of the virus. Nucleoside analogs are generally preferred e.g. Sofosbuvir and often lead to undetectable viral loads\n- Sofosbuvir and daclatsavir may be used as combination therapy\n- Antivirals of proven benefit in basically every patient irrespective of the amount of cirrhosis and fibrosis\n- Manage any underlying cirrhosis\n\n### NICE Guidelines\n\n[Click here for NICE CKS on hepatitis A](https://cks.nice.org.uk/topics/hepatitis-a/)\n\n[Click here for NICE CKS on hepatitis B](https://cks.nice.org.uk/topics/hepatitis-b/#!references)\n\n[Click here for NICE CKS on hepatitis C]([https://cks.nice.org.uk/topics/hepatitis-c/)",
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"question": "A 42-year-old man has some blood tests conducted by his hepatology team in the outpatient department. The results are shown below:\n\nHepatitis B surface antigen - negative\nAnti-hepatitis B surface antibody - positive\nIgM anti-HBc - negative\nIgG anti-HBc - positive\n\nWhich of the following is the most likely explanation for these results?",
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"explanation": "Duloxetine is a serotonin-noradrenaline reuptake inhibitor, which works by increasing urethral tone and reducing urinary leaks. It is indicated as a second-line option to surgery where surgery is not a possible treatment (ie. if the patient is not fit for, or does not want to have, surgery, as in this case). Common side effects include gastrointestinal disturbance and drowsiness. It is used with caution in the elderly and may reduce the seizure threshold.",
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"__typename": "QuestionChoice",
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"explanation": "An oestrogen pessary can improve vaginal dryness in postmenopausal women. It will not help in the case of an overactive bladder.",
"id": "53084",
"label": "c",
"name": "Oestrogen pessary",
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"explanation": "This patient does not want surgical management. Colposuspension is a surgical treatment for stress urinary incontinence, which involves securing the bladder neck with stitches, so that it does not drop down and cause urinary leakage.",
"id": "53086",
"label": "e",
"name": "Referral for colposuspension",
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"explanation": "This patient has committed to pelvic floor exercises for 6 months without improvement of her symptoms. National Institute for Health and Care Excellence guidelines state that at least 3 months of pelvic floor exercises should be trialled and further treatments considered if this fails. Therefore, it would be inappropriate to ask her to complete another 6 months of pelvic floor exercises and she should now be considered for pharmacological or surgical management.",
"id": "53083",
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"explanation": "Mirabegron is a beta 3 agonist approved for use in overactive bladder, otherwise known as urge incontinence. It has been shown to have equal efficacy to tolterodine and solifenacin for urge incontinence. Its side effects include raised blood pressure and increased risk of urinary tract infection. This would not be a treatment for stress incontinence.",
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"explanation": "# Summary\n\nUrinary incontinence refers to the involuntary loss of urine and can be categorised into stress, urge, overflow, functional, and mixed types. Key signs and symptoms vary, ranging from involuntary urine leakage when intra-abdominal pressure is raised in stress incontinence, to an abrupt and uncontrollable urge to urinate in urge incontinence. Essential investigations encompass physical examination, questionnaires, bladder diaries, urinalysis, and occasionally cystometry or cystograms. Management strategies depend on the type and severity of incontinence, encompassing conservative methods (like lifestyle modifications), medical treatment (such as Duloxetine, anticholinergics), and surgical options (for example, incontinence pessaries, mid-urethral slings). Generally, stress incontinence is managed with pelvic floor exercises, whereas urge incontinence is initially managed with bladder re-training exercises.\n\n# Types \n\nUrinary incontinence can be categorised into:\n\n1. Stress incontinence\n2. Urge incontinence\n3. Overflow incontinence\n3. Functional incontinence\n4. Mixed incontinence \n\nReversible causes of urinary incontinence can be remembered using the mneumonic **'DIAPPERS':**\n\nD - Delirium\n\nI - Infection\n\nA - Atrophic vaginitis or urethritis\n\nP - Pharmaceutical (medications)\n\nP - Psychiatric disorders\n\nE - Endocrine disorders (e.g. diabetes)\n\nR - Restricted mobility\n\nS - Stool impaction\n\n\n# Approach to Incontinence\n\nOne of the keys is to rule out reversible causes and then try to work out which type of urinary incontinence is. A framework or approach to this is below:\n\n- Physical examination\n\n - An examination will identify features of pelvic organ prolapse as well as the ability to contract pelvic floor muscles.\n\n- Questionnaires\n\n - These are recommended in order to quantify the symptoms and assess the severity on patients quality of life which may help when deciding if a patient would benefit from more invasive treatment\n\n- Bladder diary\n\n - These are also useful for quantifying symptoms and documenting the number and type of episodes of incontinence. They may potentially show a relationship between causes and symptoms.\n\n- Urinalysis\n\n - This will help to rule out infection as an acute cause\n\n- Cystometry\n\n - This is an investigation which measures bladder pressure whilst voiding. It is not recommended in patients with clear histories where the diagnosis is clear.\n\n- Cystogram\n\n - If a fistula is suspected, contrast is instilled into the bladder and a radiological image is obtained in order to see if the contrast travels anywhere else.\n\n\n# Stress incontinence\n\nThis involves leaking of urine when intra-abdominal pressure is raised, putting pressure on the bladder. The pressure of the urine overcomes the mechanisms designed to maintain continence.\n\n## Risk factors \n\n- Childbirth (especially vaginal).This may be due to a combination of injury to the pelvic floor musculature and connective tissue (for example leading to prolapse), as well as nerve damage as a result of pregnancy and labor.\n- Hysterectomy\n\n\n## Triggers\n\nActs such as coughing, laughing, sneezing or exercising can increase abdominal pressure sufficiently.\n\n## Causes\n\nAny abnormality in the anatomy of the bladder, sphincters and urethra can result in stress incontinence.\n\n\n## Conservative management\n\nGeneral lifestyle advice such as avoiding caffeine, fizzy and sugary drinks, as well as avoiding excessive fluid intake, can go far in helping incontinence.\n\nPelvic floor exercises when done with good technique and consistently strengthen the muscles of the pelvic floor. It can help both stress and urge incontinence and can be more effective than drug treatment.\n\n## Medical management\n\nDuloxetine can help with stress incontinence, but it's only recommended if conservative measures fail and the patient is not a surgical candidate.\n\n## Surgical management \n\n- Incontinence pessaries are placed transvaginally and apply pressure to the anterior vaginal wall. This helps to support the urethra and sphincters. However, the evidence for them is poor in individuals without prolapse and isn't recommended by NICE. It would be worth trying if there was a clinical prolapse.\n- Bulking agents are injectable materials placed at the bladder neck to improve continence. This procedure is typically reserved for patients who are poor surgical candidates and isn't as efficacious as other methods\n- Colposuspension and fascial slings involve suspending the anterior vaginal wall to the iliopectineal ligament of Cooper.\n- Mid-urethral slings are the gold standard surgical treatment of stress incontinence. It compresses the urethra against a supportive layer and assists in the closure of the urethra during increased intra-abdominal pressures. It's minimally invasive and can be performed in the outpatient setting.\n\n\n# Urge incontinence\n\n## Definition \n\nThis involves the sudden and involuntary loss of urine associated with urgency.\n\n## Risk factors \n\nRisk factors for urgency include:\n\n- Recurrent urinary tract infections\n- High BMI\n- Advancing age\n- Smoking\n- Caffeine\n\n\n## Conservative management \n\nGeneral lifestyle advice such as avoiding caffeine, fizzy and sugary drinks as well as avoiding excessive fluid intake can go far in helping incontinence. Chemicals contained in these drinks can irritate the bladder, contributing to urge symptoms.\n\nPelvic floor exercises when done with good technique and consistently, strengthen the muscles of the pelvic floor. It can help both stress and urge incontinence and can be more effective than drug treatment. In urge incontinence, contraction of the pelvic floor relaxes the detrusor. Bladder training is also helpful.\n\n## Medical/surgical management\n\n- Pharmacological management\n\t- Anticholinergic medications can help reduce the symptoms of urge and overactive bladder by inhibiting the parasympathetic action on the detrusor muscle.\n\t\t- Examples include: **Oxybutynin, Tolterodine, Fesoterodine, Solifenacin**. If one agent has limited impact, it can be combined with another. Use with caution in elderly however due to increased risk of delirium (side-effect).\n\t- Mirabegron (beta-3 receptor agonist) can be used in older people, but should be used with caution in patients with hypertension.\n\n- Bladder instillation\n\n - Intravesical injection of Botox can be used to paralyse the detrusor muscle and reduce the symptoms of urge and overactive bladder.\n\n- Sacral neuromodulation\n\n - Sacral nerve stimulation has been shown to control symptoms of an overactive bladder. This is only done in tertiary centres for patient who have failed or are unsuitable for all other treatments.\n\n\n# Functional incontinence\n\n## Definition \n\nThis involves an individual having the urge to pass urine, but for whatever reason they're unable to access the necessary facilities and as a result are incontinent.\n\n## Causes \n\nFunctional incontinence associated with:\n\n- Sedating medications\n- Alcohol\n- Dementias\n\n# Overflow incontinence\n\n## Definition \n\nThis occurs when small amounts of urine leak without warning. When the pressure within the bladder overcomes the pressures of the outlet structures urine leaks.\n\n## Causes \n\nThis occurs either due to underactivity of the detrusor muscle such as from neurological damage, or if the urinary outlet pressures are too high, as in constipation or prostatism.\n\n\n\n# NICE Guidelines\n\n[NICE Guidance - Urinary incontinence and pelvic organ prolapse in women: management](https://www.nice.org.uk/guidance/ng123)",
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"question": "A 65-year-old woman with known stress incontinence presents to her GP after having completed 6 months of pelvic floor exercises and lifestyle changes without significant improvement of her incontinence. She reports good compliance with her pelvic floor exercises. She has no significant past medical history or drug allergies. She does not want any surgical treatment at this stage.\n\nWhat is the next most appropriate management to offer her?",
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"explanation": "This patient has evidence of corticospinal tract involvement since there is evidence of motor dysfunction with associated hand clawing. However, this would not explain his sensory symptoms, which is the question being asked.",
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"label": "b",
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"explanation": "The dorsal columns are responsible for fine touch, vibration and proprioception. The patient has no issues with these sensory modalities and so this is not responsible for his symptoms. Progression of the syrinx can, over time, impinge on the dorsal columns and cause deficiencies within these sensory modalities.",
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"explanation": "The description of loss of pain and temperature over the neck and back (in a cape-like distribution) and predominant upper-limb dysfunction with bilateral hand clawing fits with a diagnosis of syringomyelia. Syringomyelia is a fluid-filled cyst (syrinx) that forms within the centre of the spinal cord, initially compressing the decussation of the spinothalamic tract and leading to localised loss of pain and temperature sensation. Over time, it gets larger and can expand to multiple levels of the cord as well as other structures, such as the anterolateral corticospinal tracts, which this patient has evidence of due to the presence of motor symptoms, and the dorsal columns.",
"id": "53097",
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"name": "Spinothalamic tract",
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"explanation": "The motor cortex is a cerebral structure within the frontal lobe. A lesion in the motor cortex causes upper motor neurone pathology and spasticity (hyperreflexia, pyramidal distribution of weakness and a velocity-dependent increase in tone). Sensory involvement is spared. A lesion in the motor cortex will therefore not explain this patient's symptoms.",
"id": "53100",
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"explanation": "The somatosensory cortex is a cerebral structure within the parietal lobe. Depending on the precise location of the lesion in the somatosensory cortex, any sensory modality may be lost in the distribution as dictated by the sensory homunculus. However, sensory loss with cerebral lesions do not have such a defined pattern of presentation, with dorsal column sparing and a cape-like distribution. Loss of sensation in this pattern should raise clinical suspicion of a spinal lesion.",
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"comment": "Spain = (s)pain = Spinothalamic ",
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"explanation": "# Summary\n\nSyringomyelia is a neurological condition characterised by a fluid-filled cavity, known as a syrinx, that forms within the spinal cord. This condition typically manifests with distinct neurologic symptoms such as pain and temperature loss in a 'shawl-like distribution' across the upper body, tactile sensory loss, muscle weakness, and autonomic dysfunction including bladder, bowel, and sexual dysfunction. Diagnosis is typically confirmed via imaging techniques, primarily MRI of the spinal cord and CT of the bony spinal canal. Management approaches are generally tailored to the individual, ranging from physiotherapy and rehabilitation to surgical intervention when symptomatology and the nature of the lesion warrant such.\n\n# Definition\n\nSyringomyelia is a neurological disorder characterised by the formation of a fluid-filled cavity or cyst, known as a syrinx, within the spinal cord. This syrinx often expands and elongates over time, exerting pressure on the spinal cord and damaging nerve fibres.\n\n# Epidemiology\n\nSyringomyelia is a relatively rare condition, with the prevalence reported as approximately 8.4 per 100,000 individuals, with a slight male predominance. The condition is typically diagnosed in adulthood, most often between the ages of 20 and 40.\n\n# Aetiology\n\nThe formation of a syrinx in syringomyelia can be attributed to a variety of causes:\n\n* Cerebrospinal Fluid (CSF) blockage or disruption, often secondary to conditions such as arachnoiditis or presence of space-occupying lesions.\n* Spina Bifida\n* Post-traumatic syringomyelia following spinal cord injury.\n* Spinal cord tumours, which may create a blockage of CSF flow.\n* Idiopathic syringomyelia, where no specific cause can be identified.\n* Familial predisposition has also been noted in some cases.\n\n# Signs and Symptoms\n\nThe clinical manifestations of syringomyelia can be diverse and primarily revolve around damage to various neural pathways:\n\n* Pain and temperature loss, typically presenting in a 'shawl-like distribution' over the arms, shoulders, and upper body due to damage to the spinothalamic tract.\n* Impaired light touch, vibration and position senses as the syrinx enlarges and further compromises the spinal cord.\n* Muscle weakness and atrophy may ensue as the syrinx extends and damages the anterior horn cells and their lower motor neurons.\n* Autonomic dysfunction leading to bladder, bowel, and sexual dysfunction may also occur.\n\n# Differential Diagnosis\n\nThe clinical presentation of syringomyelia can mimic other neurological disorders, warranting consideration for the following differential diagnoses:\n\n* Multiple Sclerosis: Characterised by episodic neurologic deficits that change over time and space, including optic neuritis, limb weakness, and ataxia.\n* Amyotrophic Lateral Sclerosis (ALS): Characterised by progressive muscle weakness, atrophy, and fasciculations due to a combination of upper and lower motor neuron damage.\n* Spinal cord tumour: May present with back pain, sensory changes, motor weakness, and bladder/bowel dysfunction similar to syringomyelia.\n* Cervical Spondylotic Myelopathy: Presents with neck pain, hand clumsiness, gait imbalance, and sometimes bladder symptoms.\n\n# Investigations\n\nThe diagnosis of syringomyelia is typically confirmed through imaging studies:\n\n* MRI of the spinal cord: This is the gold standard diagnostic modality, providing detailed visualisation of the syrinx and surrounding spinal cord structures.\n* CT of the bony spinal canal: May provide supplementary information regarding any bony abnormalities or spinal cord compression.\n\n# Management\n\nThe management of syringomyelia is patient-specific and depends on the severity of the symptoms and the underlying cause of the syrinx:\n\n* Physiotherapy and Rehabilitation: Helps to manage symptoms such as muscle weakness and improve overall functional capacity.\n* Surgery: May be recommended in cases where there are severe or worsening symptoms, or where the nature of the lesion (such as a tumour or significant CSF blockage) necessitates surgical intervention.\n",
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"question": "A 32-year-old man presents to the Neurology Clinic with impaired sensation over his neck and upper back. He says he cannot feel pain over this region when he pinches the skin, as well as weakness in his hands. On examination, he has a loss of pain and temperature sensation over his neck, back and upper shoulders. There is some clawing of his hands bilaterally with atrophy of the muscles of the forearm. Fine touch, proprioception and vibration are spared. There are no sensory or motor abnormalities of the lower limbs.\n\nWhere is the lesion responsible for his sensory symptoms?",
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"explanation": "CRP can be raised in any infection or conditions that cause inflammation in the body. It is a non-specific marker which would not be helpful in determining the cause of this patient's symptoms, since it may be raised in conditions such as sarcoidosis, but also other inflammatory conditions, including pneumonia.",
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"explanation": "This scan can be requested later on by a specialist within the hospital setting. A CT chest is useful to further characterise how the sarcoidosis has affected the patient's lungs. This would be requested after a CXR, since starting with simple, least invasive/harmful investigations is most appropriate in the first instance.",
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"explanation": "This is a specialist investigation which would not be requested by the GP. This investigation can be diagnostic for sarcoidosis, but it does not represent the next best investigation. Typically, you would find non-caseating granulomas on a biopsy.",
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"explanation": "This patient has sarcoidosis which explains her long-term symptoms. In the early stages, a CXR may show evidence of bilateral hilar lymphadenopathy and fibrosis in the later stages. It can also rule out other causes of shortness of breath and crepitations, such as pneumonia.",
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"explanation": "Serum ACE levels are raised in sarcoidosis, however it would not be the next best investigation since ACE is neither specific to, nor diagnostic of, sarcoidosis.",
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"name": "Angiotensin-converting enzyme (ACE) levels",
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"comment": "If patient is in GP would they not do a blood test first? Agree CXR is the 'better' investigation, but 'next' would be a blood test?",
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"comment": "ngl i thought it was TB with spinal infection :/",
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"comment": "what is causing the tingling down her legs?",
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"comment": "It can cause neuro Sx such as peripheral neuropathy, ( meningitis, bilateral Bell’s palsy)",
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"explanation": "# Summary\n\nSarcoidosis is an inflammatory disease characterised by granuloma formation in various organs, with the most commonly affected being the lungs. Symptoms include fever, polyarthralgia, erythema nodosum, dry cough, dyspnoea, fatigue and weight loss. Investigations include blood tests (with calcium and serum ACE being important), chest X-ray and biopsy of a granuloma. Management depends on the severity of disease and may include NSAIDs, corticosteroids and other immunosuppressants.\n\n# Definition\n\nSarcoidosis is a multi-system disease that is characterised by the formation of non-caseating granulomas around the body. This leads to inflammation and scarring in the organs affected, most commonly the lungs and skin. Other organs affected include the nerves, the brain, the heart, the liver and the eyes.\n\n# Epidemiology\n\nIn the UK, there are approximately 4,500 new diagnoses of sarcoidosis each year, with a prevalence around 1 in 10,000 people. Prevalence varies significantly depending on region, with the highest rates seen in Northern Europe (e.g. Sweden, Finland and Denmark). Some ethnicities are more at risk than others, with people of African descent being affected more often and with more severe disease.\n\nPeak onset is in adults aged between 30 and 55 years old, and it is slightly more common in women than men.\n\n# Aetiology\n\nThe cause of sarcoidosis is not known, with the main theories being that it is an inflammatory response to a yet unidentified environmental exposure or infection, or that is is caused by autoimmunity.\n\nA small percentage of cases are familial and the wide variation in prevalence across different populations suggests that genetic factors are likely to contribute to its development.\n\n# Signs and Symptoms\n\n**Pulmonary manifestations**\n\n- Dry cough\n- Dyspnoea\n- Reduced exercise tolerance\n- Chest pain\n- Clubbing\n- Fine crackles on auscultation\n\n**Dermatological manifestations**\n\n- Erythema nodosum (inflammation of subcutaneous fat leading to tender nodules especially on the shins)\n- Lupus pernio (red/purple plaques and nodules on the face)\n- Hyper or hypopigmentation of the skin\n\n**Neurological manifestations**\n\n- Meningitis\n- Peripheral neuropathy\n- Facial nerve palsy (may be bilateral)\n- Headache\n- Seizures/encephalopathy\n\n**Ocular manifestations**\n\n- Uveitis\n- Keratoconjunctivitis sicca\n- Glaucoma\n\n**Cardiac manifestations**\n\n- Arrhythmias\n- Restrictive cardiomyopathy\n- Syncope\n\n**Abdominal manifestations**\n\n- Hepatomegaly\n- Splenomegaly\n- Renal stones\n\n**Systemic manifestations**\n\n- Fatigue\n- Weight loss\n- Arthralgia\n- Low-grade fevers\n- Lymphadenopathy\n- Enlarged parotid glands\n\n**Lofgren's syndrome** refers to the acute onset of:\n\n- Fever\n- Polyarthralgia\n- Erythema nodosum\n- Bilateral hilar lymphadenopathy (seen on chest X-ray)\n\n**Heerfordt's syndrome** refers to the combination of:\n\n- Fever\n- Uveitis\n- Parotid swelling\n- Facial nerve palsy\n\n# Differential Diagnosis\n\n- **Tuberculosis:** may present very similarly with chronic cough, night sweats, weight loss, bilateral hilar lymphadenopathy so important to rule out (see investigations).\n- **Lymphoma:** also may present with unexplained weight loss, fever, night sweats and lymphadenopathy, pulmonary symptoms less predominant, can be distinguished on biopsy.\n- **Other causes of interstitial lung disease:** similar pulmonary features of dyspnoea, cough and chest pain, and may have weight loss and malaise. Extrapulmonary features (e.g. rashes and hypercalcaemia) seen in sarcoidosis help to differentiate.\n\n# Investigations\n\n**Bedside investigations include:**\n\n- **ECG** looking for arrhythmias or changes related to hypercalcaemia (e.g. QT shortening)\n- **Mantoux test** looking for evidence of exposure to tuberculosis (an important differential)\n- **Lung function testing** - if pulmonary sarcoidosis suspected\n- **Ophthalmological examination** if ocular sarcoidosis suspected\n\n**Blood tests include:**\n\n- **FBC** may show lymphopenia, anaemia or raised white cells\n- **LFTs** for liver disease\n- **Renal function** for renal impairment (not common in sarcoidosis)\n- **Bone profile** for hypercalcaemia\n- **ESR** may be raised due to chronic inflammation\n- **Serum ACE** is elevated in around 60% and normalises if the disease resolves (with or without treatment)\n\n**Imaging studies include:**\n\n- **Chest X-ray** can be used to stage sarcoidosis as below:\n\t- Stage 1 - Bilateral hilar lymphadenopathy (BHL)\n\t- Stage 2 - BHL with peripheral infiltrates\n\t- Stage 3 - Peripheral infiltrates alone\n\t- Stage 4 - Pulmonary fibrosis\n- **High-resolution CT chest** should be done if sarcoidosis suspected on chest X-ray to further assess for pulmonary fibrosis \n- **PET scanning** may be used if there is ongoing diagnostic uncertainty\n- **Echocardiogram** if cardiac disease is suspected\n\n**Other investigations include:**\n\n- **Biopsy** is required to confirm the diagnosis in most cases (with a classic presentation of chronic pulmonary disease or a clear case of Lofgren's syndrome being exceptions) - this is looking for the classic finding of noncaseating granulomas\n- **Bronchoalveolar lavage** may also be done in suspected pulmonary sarcoidosis, with classic findings of raised lymphocytes and an elevated CD4/CD8 ratio\n\n[lightgallery]\n\n# Management\n\n**Conservative treatment includes:**\n\n- Patient education and support\n- Smoking cessation\n- **No active treatment is needed in many cases of sarcoidosis** \n\n**Medical treatment includes:**\n\n- Steroids e.g. oral prednisolone with a higher dose at induction which is then reduced to a lower maintenance dose\n- Second line immunosuppressants (e.g. if steroids contraindicated or not effective) include methotrexate, mycophenolate or azathioprine\n- Third line treatment is usually with biologics (e.g. infliximab)\n\n**Note - Medical treatment should be started only if sarcoidosis symptoms are affecting quality of life or there is significant risk of morbidity or mortality from sarcoidosis**\n\n**Surgical treatment includes:**\n\n- Rarely in severe cases of pulmonary sarcoidosis a lung transplant may be considered\n- In cases of pulmonary sarcoidosis complicated by aspergilloma, surgical management of haemoptysis is sometimes required\n\n# Complications\n\n- Pulmonary fibrosis (stage IV pulmonary sarcoidosis\n- Cor pulmonale\n- Pulmonary hypertension\n- Aspergillomas can form in cavities left by granulomatous pulmonary disease\n- Arrhythmias and sudden death in cardiac sarcoidosis\n- Low mood and anxiety\n- Complications of long-term steroid use (e.g. osteoporosis, hyperglycaemia)\n\n# Prognosis\n\n- In general prognosis is good, with two-thirds of people experiencing disease remission within 2-5 years (usually with no treatment required).\n- Around 20% of people develop chronic disease requiring treatment\n- Remission is more common in earlier stages of sarcoidosis\n- Only 6-8% of people with sarcoidosis have a reduced life expectancy, with the commonest cause of death being pulmonary disease (interstitial lung disease and pulmonary hypertension)\n\n# NICE Guidelines\n\n[NICE CKS - Sarcoidosis](https://cks.nice.org.uk/topics/sarcoidosis/)\n\n# References\n\n[Patient UK - Sarcoidosis](https://patient.info/doctor/sarcoidosis-pro)\n\n[Radiopaedia - Sarcoidosis](https://radiopaedia.org/articles/sarcoidosis-1?lang=gb)",
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"question": "A 35-year-old female presents to the GP with a 6-month history of fatigue. During this time, she also describes feeling short of breath when running for the bus and recurrent episodes of tingling down her leg. On examination, she has swollen lymph nodes and crepitations on chest auscultation. She has a temperature of 37.7.\n\nWhich of the following is the next best investigation?",
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"explanation": "This is because an abdominal aorta diameter of 3.3cm is considered to be small and so he would be offered annual ultrasound scans in this case. Note that all men in the UK are offered a one-off ultrasound scan at the age of 65 which determines the frequency of scanning if needed. Patients are usually asymptomatic unless the aneurysm has ruptured. Operative management is offered 5.5cm+. AAA's measuring 3-4.4cm are scanned every 12 months, and every 3 months between 4.5-5.4cm.",
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"explanation": "This would be indicated if the patient presented with a ruptured aneurysm, or as an elective procedure to repair large or rapidly expanding AAAs where anatomical considerations make EVAR's unsuitable. A ruptured AAA presents with shock and abdominal pain radiating to the back/back pain. This patient has no features of a ruptured AAA and he does not require repair at this stage due to the small size of the AAA. Open repair surgery is much more invasive than EVAR procedures, and some patients may not be fit enough for this procedure.",
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"explanation": "# Summary\n\n\nAn abdominal aortic aneurysm (AAA) is a common, potentially life-threatening condition characterised by an abdominal aorta diameter greater than 3cm. It's most frequently located between the renal and inferior mesenteric arteries. Key signs and symptoms include a typically asymptomatic presentation, occasionally manifesting as a pulsatile, expansile abdominal mass. Diagnosis primarily relies on abdominal ultrasound screening, with follow-up frequency varying based on the aneurysm size. Management strategies focus on surgical repair, with indications being a size >5.5cm or rapid expansion, encompassing open repair or Endovascular Aneurysm Repair (EVAR).\n\n\n# Definition\n\n\nAbdominal aortic aneurysm (AAA) is a prevalent, potentially lethal condition characterised by an enlargement of the abdominal aorta exceeding a diameter of 3cm. This dilatation affects all three layers of the arterial wall. Many individuals with AAA are asymptomatic and do not cause any problems to the individual. In the absence of repair, a ruptured AAA is generally fatal.\n\n\n# Epidemiology\n\n\nAbdominal aortic aneurysm (AAA) predominantly affects older adults, especially those over 65 years of age. At the time of screening at age 95, 0.92% of men undergoing screening are found to have an abdominal aortic aneurysm. It is approximately 4-6 times more prevalent among men than women. An estimated 4-8% of men and 1-2% of women aged over 65 years are affected, but due to the asymptomatic nature of the condition, the actual prevalence may be higher. \n\nThere is a significant geographic and ethnic variation, with higher prevalence reported in Western countries. Lifestyle factors such as smoking and a history of cardiovascular disease increase the risk. \n\nAAA morbidity and mortality are reducing in the UK due to increasing elective repair of AAA and a reduction in smoking rates. \n\n\n# Aetiology\n\n\nThe precise aetiology of AAA is complex and multifactorial, typically involving a combination of genetic, environmental, and lifestyle factors.\n\n\nRisk factors include:\n\n- Being male\n- Age 65 or over\n- Smoking \n- Hypertension\n- Hypercholesterolaemia \n- Family history of AAA\n- Personal history of peripheral arterial disease or myocardial infarction\n- COPD\n- Connective tissue disorders (i.e. Marfan's) \n\n\n\n# Signs and Symptoms\n\n\nMost AAAs remain asymptomatic for a long time and are often detected incidentally during radiological investigations for other abdominal or pelvic conditions. \n\nWhen symptomatic, the clinical presentation can vary:\n\n\n- Pulsatile abdominal mass: \n- The most classical finding on physical examination is a pulsatile, expansile abdominal mass. This is typically non-tender unless rupture is imminent.\n- Approximately 3 in 5 AAA over 3 cm are palpable.\n- This may also be associated with abdominal bruit.\n\n- Abdominal or back pain: \n- Pain is usually a late manifestation, suggesting rapid expansion or impending rupture of the aneurysm. \n- It is typically severe, constant, and localised in the abdomen or lower back, often radiating to the flank or groin.\n- There can also be testicular pain if the blood supply to this area is compromised by rupture\n- 90% of aortic aneurysms are infrarenal (originating below the renal arteries) \n\n\nIn advanced cases, a large aneurysm may cause symptoms due to compression or displacement of adjacent structures, resulting in early satiety, nausea, weight loss, altered bowel habits, or deep venous thrombosis (due to compression of the inferior vena cava).\n\n\n# Differential Diagnosis\n\n\nDifferential diagnoses for AAA include, but are not limited to:\n\n\n- **Renal colic**: Typically presents with severe, sudden onset flank pain that can radiate to the groin, accompanied by haematuria and urinary urgency.\n- **Pancreatitis**: Characterised by persistent, severe epigastric pain radiating to the back, often associated with nausea, vomiting, and elevated pancreatic enzymes.\n- **Peptic ulcer disease**: Often presents with burning epigastric pain that is relieved by eating, weight loss, and potential signs of bleeding like melaena or hematemesis.\n- **Diverticulitis**: Usually presents with left lower quadrant pain, fever, and changes in bowel habits.\n\n\n\n# Investigations\n\nNHS AAA screening programme: \n\n- Offered to men at age 65\n- Consists of an abdominal ultrasound\n- Follow-up screening depends on the size of the aneurysm:\n\n- Small AAA (3-4.4cm): Yearly repeat ultrasound is offered.\n- Medium AAA (4.5-5.4cm): Repeat ultrasound every 3 months is offered.\n- Large AAA (>5.5cm): Surgical intervention is generally recommended.\n\nOnce an abdominal aortic aneurysm has been detected, further investigations may be required, including: \n\n- **Computed Tomography (CT) Angiography:** \n- CT angiography is the imaging modality of choice for preoperative evaluation, determining the size, shape, and extent of the AAA, and planning the surgical approach. \n- It provides detailed information about the aneurysm's relationship to branch arteries and the potential presence of thrombus or calcification within the aneurysm. \n- It is also the preferred imaging modality in suspected rupture cases due to its rapid acquisition time and high sensitivity and specificity.\n\n- **Magnetic Resonance Angiography (MRA):** MRA is an alternative to CT angiography for patients who cannot be exposed to ionizing radiation or iodinated contrast medium. MRA can provide high-resolution images of the AAA and surrounding structures but is less readily available and takes more time than CT.\n\n- **Blood tests:** While there is no specific blood test to diagnose AAA, complete blood count, coagulation profile, renal function tests, and electrolyte levels are typically evaluated prior to surgery.\n\n\n\nFinally, regular surveillance of known AAAs is critical. The frequency of surveillance depends on the size of the aneurysm, with smaller aneurysms monitored less frequently and larger ones requiring closer observation.\n\n\n# Management\n\n### Conservative \n\nManagement of abdominal aortic aneurysms may be through conservative measures such as: \n\n- Surveillance:\n- This is typically offered for smaller aneurysms with a lower risk of rupture. It is very rare for smaller AAA to rupture. \n- Small AAA (3-4.4cm): Yearly repeat ultrasound is offered.\n- Medium AAA (4.5-5.4cm): Repeat ultrasound every 3 months is offered.\n- Large AAA (>5.5cm) require referral to vascular surgery to be seen within 2 weeks of diagnosis. \n- Measures to reduce the risk of rupture:\n- Referral to a stop-smoking service\n- Management of hypertension \n\n\n### Surgical \n\n\nElective repair of AAA may be considered for individuals with AAA who meet the following criteria:\n\n- They are symptomatic \n- Their AAA has grown by more than 1 cm in 1 year and is larger than 4 cm\n- Their AAA is 5.5 cm or larger \n\n\nTwo primary surgical options are available for managing AAA: \n\n- Open surgical repair\n- Typically best for men under age 70. \n- However, it can be contraindicated by anaesthetic risks, medical comorbidities or anatomic difficulties (i.e. horseshoe kidney, stoma, numerous previous surgeries resulting in significant adhesions)\n- Endovascular Aneurysm Repair (EVAR)\n- A stent graft is inserted through the femoral arteries into the aorta, where it channels blood flow into the iliac arteries. The surrounding aneurysm then becomes thrombosed around the graft. \n- EVAR has reduced perioperative deaths and is associated with shorter hospital stays. However, it has an overall higher long-term morbidity and mortality than open repair. \n\n\n# Complications\n\n\n### Rupture\n\nAAA rupture is a surgical emergency. Abdominal aortic aneurysms are more likely to rupture in women than men but are more common in men and such account for more presentations in men. \n\nAAA tend to enlarge over time and with increasing size, the risk of rupture increases. \n\n\n### Embolization\n\nRarely distal embolisation from mural thrombus can lead to symptoms related to ischemia, most commonly affecting the distal extremities, such as blue toe syndrome.\n\n### Open Repair-Related Complications\n\nThose undergoing open surgical repair of an AAA have risks including:\n\n- Spinal cord ischaemia \n- Anastomotic pseudoaneurysm \n- Graft infection \n- Death (mortality during elective repair is reported to be 5% of men and 7% of women)\n\n### EVAR-Related Complications\n\nPatients who have undergone EVAR may require surveillance for EVAR-related complications. \n\n- Endoleak\n- Defined as the presence of blood flow within the aneurysm sac but outside the EVAR graft\n- Contrast-enhanced CT angiography, or contrast-enhanced ultrasound if CT is contraindicated, is used to assess for endoleak. \n- They can be repaired using open, endovascular or percutaneous intervention for endoleak \n- Post-implantation syndrome \n- Cytokine release due to EVAR can cause fever, back pain and feeling generally unwell following EVAR.\n\n# Prognosis \n\nAbdominal aortic aneurysms will continue to increase in diameter, with the ultimate outcome being rupture. 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"explanation": "This is incorrect because this describes the finding in normal pressure hydrocephalus. The classic symptoms for this condition can be remembered by wet, weird and wobbly: urinary incontinence, dementia, and recurrent falls. Note that this is a type of reversible dementia.",
"id": "53121",
"label": "e",
"name": "Enlarged ventricles",
"picture": null,
"votes": 98
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Alpha-synuclein inclusions are found within the substantia nigra in Parkinson's disease and Lewy Body Dementia. These conditions are characterised by a typical triad of bradykinesia, rigidity and a resting tremor, which this patient does not have. Lewy Body Dementia is also classically associated with visual hallucinations, typically of Lilliputian bodies.",
"id": "53118",
"label": "b",
"name": "Alpha-synuclein",
"picture": null,
"votes": 169
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect because this describes the finding in vascular dementia. Patients typically have a step-wise decline in function following a cerebrovascular event. They usually have cardiovascular risk factors such as hypertension, hypercholesterolaemia or diabetes.",
"id": "53120",
"label": "d",
"name": "Multiple infarcts with white matter damage",
"picture": null,
"votes": 32
},
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This patient has Alzheimer's disease. Histopathology would demonstrate beta amyloid plaques and neurofibrillary tangles made of tau protein.",
"id": "53117",
"label": "a",
"name": "Amyloid plaques",
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"explanation": "# Summary\n\nAlzheimer's disease, the most common form of dementia, is a progressive neurodegenerative disorder that leads to cognitive decline, memory impairment, and a range of behavioural and psychological symptoms. Its impact extends beyond the individual, affecting families and healthcare systems worldwide. This comprehensive guide explores the key aspects of Alzheimer's disease, from its definition and pathophysiology to clinical features, diagnostic considerations, management approaches, and prognosis. Adherence to NICE guidelines ensures evidence-based care for patients with this challenging condition.\n\n# Definition\n\nAlzheimer's disease is a chronic, neurodegenerative disorder characterized by the progressive accumulation of abnormal protein deposits, primarily amyloid plaques and tau tangles, in the brain. This leads to the deterioration of cognitive function, memory loss, and various behavioural and psychological symptoms.\n\n\n# Epidemiology\n\nAlzheimer's disease is a global health concern, with an increasing prevalence as the population ages. It is estimated that millions of individuals worldwide are affected, with higher incidence rates in older age groups. Women are more commonly affected than men, and several genetic and environmental factors influence disease risk.\n\n\n# Pathophysiology\n\n\nAlzheimer's disease is a complex and progressive neurodegenerative disorder characterized by distinct pathophysiological hallmarks. These hallmarks are responsible for the gradual decline in cognitive function and the characteristic clinical features observed in affected individuals.\n\n1. **Amyloid Plaques:** The accumulation of beta-amyloid protein fragments outside nerve cells in the form of plaques is a hallmark feature. These abnormal protein deposits are believed to disrupt neuronal communication, trigger inflammation, and ultimately lead to cell death.\n\n2. **Tau Tangles:** Inside nerve cells, abnormal tau protein accumulates, forming neurofibrillary tangles. These tangles interfere with the transport of essential nutrients within neurons, contributing to their dysfunction and eventual demise.\n\n3. **Neuronal Loss and Brain Atrophy:** As the disease progresses, significant neuronal loss occurs, particularly in brain regions responsible for memory and cognitive function, such as the hippocampus and the cerebral cortex. This loss is associated with brain atrophy, visible on imaging studies.\n\n4. **Neurotransmitter Imbalance:** Alzheimer's disease disrupts the balance of neurotransmitters, particularly acetylcholine, which plays a crucial role in memory and learning. Reduced acetylcholine levels further contribute to cognitive decline.\n\n5. **Inflammatory Response:** Chronic neuroinflammation, characterized by the activation of microglia and astrocytes, is a prominent feature in Alzheimer's disease. Inflammation may exacerbate neuronal damage and contribute to the progression of the disease.\n\n# Risk Factors\n\nSeveral factors influence an individual's risk of developing Alzheimer's disease. These include:\n\n- **Age:** Advanced age is the most significant risk factor, with the incidence of Alzheimer's disease increasing exponentially after the age of 65.\n\n- **Genetic Predisposition:** Mutations in specific genes, such as the apolipoprotein E (APOE) gene, increase the risk of developing Alzheimer's disease. Additionally, individuals with Down's syndrome are at a higher risk due to a triplication of chromosome 21, which carries the amyloid precursor protein (APP) gene.\n\n- **Family History:** Having a first-degree relative with Alzheimer's disease can increase one's susceptibility.\n\n- **Cardiovascular Risk Factors:** Conditions like hypertension, diabetes, obesity, and hypercholesterolemia have been associated with an elevated risk of Alzheimer's disease.\n\n- **Lifestyle Factors:** Physical inactivity, smoking, and a diet high in saturated fats may contribute to increased risk.\n\n- **Traumatic Brain Injury:** A history of head injuries, particularly repeated concussions, has been linked to a higher risk of developing Alzheimer's disease.\n\n- **Low Educational Attainment:** Lower levels of education may be associated with an increased risk.\n\nUnderstanding these risk factors and their relationship to the disease's pathophysiology is crucial for early identification, prevention, and management of Alzheimer's disease.\n\n# Clinical Features\n\nAlzheimer's disease is characterized by a constellation of cognitive and behavioural symptoms, which may include:\n\n* **Memory Impairment:** Early in the disease, individuals often experience difficulties in recalling recent events and conversations.\n* **Language Impairment:** This may manifest as difficulty finding words, struggling to express oneself, and, in later stages, aphasia.\n* **Executive Dysfunction:** Impaired ability to plan, organize, and carry out tasks, leading to difficulties in activities of daily living.\n* **Behavioural Changes:** Individuals may exhibit agitation, aggression, or apathy, sometimes accompanied by mood swings and irritability.\n* **Psychological Symptoms:** Hallucinations, delusions, and paranoia can occur, particularly in later stages of the disease.\n* **Disorientation:** Affected individuals may become disoriented in familiar surroundings, unable to recognize places or people.\n* **Loss of Motor Skills:** In advanced stages, motor skills decline, leading to difficulties with mobility and self-care.\n\n# Differential Diagnosis\n\n\n1. **Vascular Dementia:** Cognitive impairment in vascular dementia often presents suddenly and is associated with a history of cerebrovascular events.\n\n2. **Lewy Body Dementia:** Visual hallucinations and fluctuating cognitive impairment are more common in Lewy body dementia.\n\n3. **Frontotemporal Dementia:** This condition typically presents with profound behavioural and personality changes, often affecting social conduct.\n\n4. **Mild Cognitive Impairment (MCI):** MCI is a transitional state between normal cognitive aging and dementia. Unlike Alzheimer's, MCI may not significantly impact daily functioning.\n\n5. **Normal Age-Related Cognitive Decline:** Age-related cognitive changes are common but do not interfere significantly with daily activities.\n\n# Investigations\n\nDiagnosing Alzheimer's disease may involve a series of assessments, including:\n\n- **History** - including a functional history, which may be informed using a structured instrument such as the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) or the Functional Activities Questionnaire (FAQ). A collateral history may be necessary, and a risk assessment should also be taken.\n- Assess cognitive decline using an approved scoring tool such as MMSE, MOCA, 10-point Cognitive Screener (10-CS), 6-item Cognitive Impairment Test (6-CIT), 6-item Screener, Memory Impairment Screen (MIS), Mini-Cog, Test Your Memory (TYM) \n- **Examination** - physical examination including a full neurological examination looking for abnormaliities in coordination, gait, sensation and motor signs.\n- **Blood tests** - to rule out reversible causes, this is known as a confusion screen and is often done in primary care. It includes FBC, U&E, LFTs, CRP/ESR, Ca2+, TFTs, B12, folate, syphilis, HIV. If there is an acute onset of symptoms delirium should be considered as this is a different pathway.\n- Once reversible causes are ruled out and a diagnosis of dementia is still suspected, refer to a specialist dementia diagnostic service (such as a memory clinic or community old age psychiatry service. Here, a full functional assessment is carried out and the patient will be referred for **neuroimaging**, such as CT or MRI.\n\t- **Brain Imaging:** Magnetic resonance imaging (MRI) and positron emission tomography (PET) scans can reveal brain atrophy and the presence of amyloid plaques.\n\t- **Cerebrospinal Fluid Analysis:** May be used to detect specific biomarkers associated with Alzheimer's disease.\n\n# Management\n\n- **Non-Pharmacological Approaches:** Psychological interventions, cognitive stimulation therapy, and occupational therapy can help manage behavioural and psychological symptoms.\n\n- **Support for Caregivers:** Education and support for family members and caregivers are vital to help them navigate the challenges of providing care.\n\n- **Patient-Centered Care:** Tailoring interventions to the individual's needs and preferences, while ensuring their safety and well-being.\n- **Pharmacological Intervention:** Medications, such as cholinesterase inhibitors (e.g. donepezil) and N-methyl-D-aspartate (NMDA) receptor antagonists (e.g. memantine), may be prescribed to manage cognitive symptoms.\n\t- Pharmacological treatments may have modest benefits, and include the cholinesterase inhibitors rivastigamine, galantamine, and donpezil in mild-moderate dementia, and the NMDA inhibitor memantine in severe dementia (as classified using the MMSE score: severe: <10; moderate: 10-20; mild: 21-26/30. \n\t- If there is evidence of behavioral and psychological symptoms of dementia (BPSD), low-dose risperidone may be started\n\n\n# NICE Guidelines\n\n[NICE CKS - Dementia](https://cks.nice.org.uk/topics/dementia/)\n\n# References\n\n[NHS UK - Alzheimer's Disease](https://www.nhs.uk/conditions/alzheimers-disease/)\n\n[Alzheimer's Association](https://www.alz.org/alzheimers-dementia/what-is-alzheimers)\n\n\n\n\n\n",
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"question": "A 74-year-old female presents to the memory clinic after referral by her GP. Her family report that her memory for recent events is worsening, and she is struggling to manage her finances, remember words, and recognise objects. Her childhood memories remain relatively preserved.\n\nGiven the most likely diagnosis, which of the following is the most likely pathological finding?",
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is correct because this patient has severe acne vulgaris which is evident by the presence of widespread inflammatory lesions and scarring. This would be the best next step in management. Topical adapelene with topical benzoyl peroxide should be prescribed with an oral antibiotic such as lymecycline to prevent antibiotic resistance. Tetracyclines have anti-inflammatory effects, but note that these are contraindicated in pregnancy or breast-feeding which does not apply to this case.",
"id": "53122",
"label": "a",
"name": "Topical adapelene with topical benzoyl peroxide and oral lymecycline",
"picture": null,
"votes": 2504
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"__typename": "QuestionChoice",
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"explanation": "This is incorrect because oral isotretinoin is prescribed for patients with severe acne vulgaris resistant to traditional topical and systemic antibiotic therapies. This patient has not tried topical medication or antibiotics yet. Although this patient wants stronger medication, isotretinoin is not prescribed within primary care due to its side effect profile. Some of these include deranged liver function, increased risk of suicide and depression, and teratogenicity.",
"id": "53126",
"label": "e",
"name": "Oral isotretinoin",
"picture": null,
"votes": 430
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"__typename": "QuestionChoice",
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"explanation": "This is incorrect because this is the treatment for mild acne rosacea. In acne rosacea, patients typically present with papules, pustules and flushing of the nose, cheeks and forehead. It usually affects an older patient demographic and can present with telangiectasia. Topical metronidazole is not used for acne vulgaris.",
"id": "53123",
"label": "b",
"name": "Topical metronidazole",
"picture": null,
"votes": 91
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect because this is the treatment for impetigo which is an infection typically caused by Staphylococcus aureus and usually affects infants. It presents with golden crusted lesions which this patient does not have. Impetigo is usually managed in primary care with oral antibiotics and topical fusidic acid.",
"id": "53124",
"label": "c",
"name": "Oral flucloxacillin and topical fusidic acid",
"picture": null,
"votes": 183
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect because spironolactone is rarely used as a first-line treatment for acne vulgaris. It is also important to avoid prescribing this drug in males because it is an anti-androgen medication which works by reducing testosterone levels and can cause feminising side effects.",
"id": "53125",
"label": "d",
"name": "Spironolactone",
"picture": null,
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"__typename": "QuestionComment",
"comment": "Is this not severe enough for isotretinoin?????",
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"comment": "innit scarring is usually an indication for isotretinoin????",
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"comment": "I think the GP has to try the initial management methods, before referring him to derm for isotretinoin.",
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"comment": "GPs dont prescribe oral isotretinoin",
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"comment": "why refer to dermatology for actual treatment when you can just let a 15 year old get extensive scarring first (clowns)",
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"comment": "Once scarring has started any GP in their right mind should be turning to accutane, that's what mine said at least. ",
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"comment": "no GP should be prescribing accutane mate",
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"comment": "If there's scarring he should be referred to dermatology for isotretinoin. ",
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"explanation": "# Summary\n\nAcne vulgaris is a common chronic disorder of the pilo-sebaceous unit, resulting in blockage of the follicle, formation of comedones and inflammation. Key signs and symptoms include open/closed comedones, inflammatory papules and pustules, and in severe cases, nodules and cysts. The disorder predominantly affects the face, neck, chest, and back, and has a significant psychological impact due to altered physical appearance. Acne is primarily diagnosed clinically, with further investigations necessary only in uncertain cases or prior to commencing certain treatments like isotretinoin. Treatment is guided by severity and may involve topical or systemic therapy based on the NICE guidelines. Potential complications include post-inflammatory hyperpigmentation, hypopigmentation, erythema, psycho/social/sexual dysfunction, and scarring.\n\n\n# Definition\n\n- A a chronic disorder of the skin affecting the pilo-sebaceous unit, in which there is blockage of the follicle leading to comedones and inflammation. \n- Vulgaris translates as \"common\", which is true as this condition affects over 80% of adolescents.\n\n# Epidemiology\n\n* It is one of the most common dermatological conditions globally, affecting individuals of all ethnicities and ages.\n* Prevalence is highest in adolescents and young adults, with up to 80% of individuals experiencing some degree of acne during their lifetime.\n* While most common in adolescents, adult-onset acne can occur, affecting people well into their 30s and beyond.\n* Acne affects both males and females, but the prevalence and severity may vary between genders.\n* The psychological impact of acne can be significant, affecting self-esteem and overall quality of life.\n\n# Risk Factors\n\nSeveral factors contribute to the development and exacerbation of acne, including:\n\n* Hormonal changes (e.g. during puberty, menstrual cycle, polycystic ovary syndrome)\n* Increased sebum (oil) production\n* Blockage of hair follicles and sebaceous glands by keratin and sebum\n* Bacterial colonization (Propionibacterium acnes)\n* Family history of acne\n* Certain medications (e.g. corticosteroids, hormonal treatments)\n\n# Pathophysiology\n\n- In normal skin, skin cells in the stratum corneum of the epidermis (corneocytes) desquamate successfully without blocking pilo-sebaceous units.\n- In acne, the corneocytes are excessively cohesive. They do not detach successfully.\n- Because of this, the keratin rich corneocytes accumulate and block off hair follicles causing follicular hyperkeratinisation.\n- Sebum is trapped in the hair follicle since it cannot be drained away. Androgens may also contribute to this causing sebaceous gland hyperplasia and increased sebum production. \n- This combination of sebum and keratin forms micro-comedones - the earliest feature of acne vulgaris. This is only visible under a microscope.\n- Gradually, the follicle becomes more distended with keratin and sebum, and the micro-comedone enlarges to become a comedone. \n- Initially, these are closed comedones, referred to as whiteheads. The contents are not exposed to the skin surface or oxygen, and therefore appear as fleshy/white papules. \n- Eventually, closed comedones become open comedones. As their contents become exposed to oxygen, they oxidise which causes black discolouration. Open comedones are therefore referred to as blackheads.\n- Comedones are then colonised with a gram positive bacillus called Propionibacterium (Cutibacterium) acnes. This is a commensal organism (part of the normal skin flora) but leads to an inflammatory response in the right conditions of the comedone, in a predisposed patient. \n- The comedone is subsequently transformed into an inflammatory papule, which is now associated with erythema. A papule is a solid, raised lesion less than 0.5cm in diameter. \n- As things progress and more neutrophils accumulate, the inflammatory papule becomes a pustule; this is a lesion less than 0.5cm in diameter that contains pus. \n- Eventually, the inflammatory papule or pustule becomes so distended that it ruptures into the dermis, triggering a marked and deep seated inflammatory response. \n- This leads to the formation of nodules/cysts, which are painful and red. A nodule is a solid lesion larger than 0.5cm, and cysts are walled off fluid containing structures. \n\n[lightgallery]\n\n# Classification\n\n- Non-inflammatory: blackheads and whiteheads.\n- Inflammatory: inflammatory papules, pustules, and nodules (cysts.)\n- Mild acne: predominantly non-inflammatory lesions. \n- Moderate acne: predominantly inflammatory papules and pustules. \n- Severe acne: nodules (cysts), scarring, acne fulminans, and acne conglobata. \n\n# Clinical Features\n\n- Open/closed Comedones, inflammatory papules and pustules, nodules, and cysts may be present.\n- The face is most often affected. The neck, chest and back may also be affected.\n- Psychological dysfunction due to changes physical appearance\n- Scarring: associated with inflammatory acne. Hypertrophic and keloid scars are more common in darker skin tones. \n\t- Atrophic: flat or indented, such as ice-pick, box-car, or rolling scars.\n\t- Hypertrophic: raised scars.\n\t- Keloid: raised scars that extend beyond the initial boundaries of the injury. \n- Post-inflammatory hyperpigmentation and hypopigmentation: associated with inflammatory acne. \n- Post inflammatory erythema: associated with inflammatory acne.\n- Acne fulminans: an uncommon but severe, serious acne presentation. \n\t- Inflammatory nodules/cysts that are painful, ulcerating, and haemorrhagic appear, with associated systemic upset (raised white cell count, joint pain, fever, fatigue.) \n\t- These patients should be reviewed urgently within 24 hours. It usually affects teenage male patients.\n- Acne conglobata: another uncommon presentation of severe nodular/cystic acne with interconnecting sinus tracts and extensive scaring. \n\n[lightgallery1]\n\n[lightgallery2]\n\n# Investigations\n\n- Acne is a clinical diagnosis and investigations are not usually needed. \n- Swabs may be indicated if the diagnosis is uncertain (e.g. if ruling out infectious pustules.)\n- Investigations will be required prior to commencing isotretinoin if indicated.\n- In some particular presentations where an endocrine cause is suspected, there may be endocrinological investigations (hyperandrogenic states such as PCOS or androgen secreting tumours.)\n\n# Treatment\n\nManagement of acne is multifaceted including education, topical/oral treatments and lifestyle modifications. \n\n- Each treatment combination is given as a 12 week course. \n- Combination therapies help reduce antimicrobial resistance. \n- Antibiotics are used predominantly since they have anti-inflammatory effects, rather than for their antimicrobial effects.\n- **Mild-moderate acne** is treated with any 2 of the following in combination:\n\t- Topical benzoyl peroxide.\n\t- Topical antibiotics (clindamycin)\n\t- Topical retinoids (tretinoin/adapalene)\n- **Moderate-severe acne** is treated with a 12-week coures of the following first line options:\n\t- Topical retinoids (tretinoin/adapelene) + topical benzoyl peroxide.\n\t- Topical retinoids + topical antibiotics (clindamycin)\n\t- Topical benzoyl peroxide + topical retinoid (tretinoin/adapelene) + oral antibiotic (lymecycline/doxycycline.) \n\t- Topical azelaic acid + oral antibiotic (lymecycline/doxycycline) \n\t- Second line oral antibiotics: trimethoprim and erythromycin e.g. in pregnant/breast-feeding women where tetracyclines are contra-indicated. \n\t- Combined oral contraceptives (COCPs) (if not contraindicated) in combination with topical agents can be considered as an alternative to systemic antibiotics in women\n\nNB: topical retinoids and oral tetracyclines are contraindicated during pregnancy and when planning a pregnancy, and so women of childbearing potential will need to use effective contraception, or choose an alternative treatment to these options.\n\t\n- As per NICE guidelines, referral to specialist Dermatology is indicated in the case of:\n\t- Acne fulminans.\n\t- Mild-moderate acne not responding to two 12 week courses of treatment as above.\n\t- Moderate-severe acne not responding to one 12 week course of treatment as above, including an oral antibiotic.\n\t- Psychological distress/mental health disorder contributed to by acne.\n\t- Acne with persistent pigmentary changes.\n\t- Acne with scarring.\n- Other available agents:\n\t- Co-cyprindiol: anti-androgenic contraceptive agent - may be trialled in primary care on female patients, but usually second line COCP due to increased risk of venous thromboembolism, and can only be given for 3 months. \n\t- Spironolactone: anti-androgenic - not often used. Not for male patients. \n\t- **Isotretinoin (oral retinoid):** the usual next step if the standard treatment fails and is prescribed by a dermatologist. \n\t\t* Notable adverse effects: dry skin/mouth/eyes/lips (most common), teratogenecity, photosensitivity, low mood, nose bleeds, hair thinning, raised triglycerides, intracranial hypertension \n\t\t* Isotretinoin is a well established teratogen that results in miscarriages and severe birth defects. As a result, the manufacturer recommends that all female patients taking isotretinoin are also using two forms of contraception from one month before until one month after use. For this reason a pregnancy test should also be done before initiating treatment\n\t\t* There is a controversial association between isotretinoin and depression/suicide. Recent research has shown that concerns about links between isotretinoin and depression or suicide are not established. This has now been included into the NICE guidelines. However it is still important to screen for depression/suicidal ideation before prescribing and during treatment.\n\t\n\t\n# Complications\n\n- Post-inflammatory erythema\n- Post-inflammatory hyper- and hypo- pigmentation\n- Psycho/social/sexual dysfunction \n- Scars (atrophic, hypertrophic, keloid)\n\t- Keloid scars: over-proliferating scar tissue/collagen extending beyond the boundaries of the lesion. Takes 3-4 weeks typically to develop after injury. They can cause itch and pain. It is fleshy, smooth, firm, and does not regress with time. The original injury may be minor, for example piercing or insect bite. Treatment is usually with intralesional steroids (triamcinolone). Cryotherapy and laser may also be used. Surgical resection is unlikely to be successful due to further scarring. Risk factors include:\n\t\t- Darker skin/Chinese/Hispanic origin \n\t\t- Less than 30 years of age\n\t\t- Previous keloid scarring \n\t- These are distinct from hypetrophic scars, which are thick and raised but remain within the injured boundary and tend to improve over time. \n\n# NICE Guidelines\n\n[NICE CKS for Acne Vulgaris](https://cks.nice.org.uk/topics/acne-vulgaris/)",
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"caption": "*A mixture of papules, pustules and comedones seen on the anterior aspect of the chest.*",
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"caption": "*Ice pick scarring seen on the cheeks following severe acne.*",
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"question": "A 15-year-old male presents to the GP with concerns regarding changes to his skin. He says this has occurred over the past year and he has used several over-the-counter facial washes which have not helped. On examination, there are widespread inflammatory papules and pustules, nodules, and scars on his face, neck, and shoulders. He is adamant that he wants to try a stronger medication.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "Leptospirosis is caused by Leptospira interrogans which can be transmitted by rats. Occupational exposure may occur through working in sewers. The key symptoms here are headache, fever, red eyes, deranged liver function tests, acute kidney injury, and reduced platelets. Note that patients with leptospirosis can also get diarrhoea, abdominal pain, and a rash. Liver and kidney failure may complicate its course.",
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"explanation": "This is incorrect because asbestosis presents with gradually worsening shortness of breath. Occupational exposure may occur in those who work in construction or on boilers.",
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"explanation": "This is incorrect because Bartonella henselae causes a condition known as Cat Scratch disease. This presents with painful local lymphadenopathy and fever. There is no mention of a cat scratch in this case.",
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"explanation": "This is incorrect because lead poisoning would present with abdominal pain, mood changes, motor neuropathy and memory loss. Lead poisoning can also cause a microcytic anaemia and Burton's lines in the gums which appear blue. This is a good differential as lead poisoning can also present with headaches and may relate to this patient's occupation. However, the presence of conjunctivitis, his deranged blood results, acute presentation, and occupation should point towards leptospirosis.",
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"explanation": "This is incorrect because Cryptosporidium parvum typically presents with chronic watery, green diarrhoea in patients who are immunosuppressed (typically, those patients with HIV.)",
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"comment": "I may not know the featurs of lepto but I sure do know you get it in the sewers",
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"explanation": "# Summary\n \n \nLeptospirosis is a zoonotic infection caused by a spirochete found in the urine of multiple animal species. It is typically misdiagnosed as malaria due to its similar presenting features. The disease is characterised by a biphasic illness, with an acute febrile phase followed by a phase marked by fever and potential complications such as liver failure and meningitis. Diagnosis is primarily achieved through serology, blood culture, and urine culture, while PCR of blood for *Leptospira* may also be used. Treatment is dependent on the severity of the disease and generally includes antibiotics such as doxycycline alongside supportive measures.\n \n \n# Definition\n \n \nLeptospirosis is a spirochete that represents a zoonotic infection found in the urine of multiple animal species. Typical animal hosts include **rodents** (main host), cattle, pigs, dogs, sheep and goats. Infection can be misdiagnosed as malaria.\n \n \n# Epidemiology\n \n \n - Approximately 1 million cases per year \n - Human infections occur from exposure to infected animals who excrete the organism in their urine, although it can also occur through cuts\n - Found widely in tropical regions \n - Occupational exposure – increased risk in farmers, sewage and abattoir workers, as well as those from lower socioeconomic groups\n \n \n# Signs and Symptoms\n \n \n - Spectrum of clinical features from self-limiting mild symptoms to life-threatening fatal disease\n - Classically a **biphasic illness**: first phase – acute febrile disease (2–9 days); second phase – fever and complications (eg. liver failure, meningitis etc.)\n - First phase presents with **abrupt fever**, **rigors**, **myalgia** and **headache** (75–100% of cases)\n - Classically conjunctival redness (can easily be missed)\n - Second phase can cause hepatosplenomegaly and skin rash as well as:\n - **Weil's disease** – presence of jaundice and renal failure (which can require dialysis)\n - **Life-threatening complications**– acute respiratory distress syndrome, pulmonary haemorrhage, myocarditis\n - **Aseptic meningitis**\n \n \n \n \n# Investigations\n \n \n - **FBC** (may show thrombocytopenia), **U&E's** (low sodium & altered renal function), **raised CK**\n - **Serology** is the most frequently used test for diagnosis – can be delayed, becoming positive only on day 5–7 of the illness (**note:** if in an endemic area, it may be positive due to previous and not acute infection)<\n - **Blood culture** (gold standard) and **urine culture** can be used to confirm leptospirosis (during the first and second weeks of illness, respectively)\n - **PCR** of blood for *Leptospira* (if available)\n - **Chest X-ray**\n \n \n# Management\n \n \n - Most cases are self-limiting and as such do not require treatment\n - There is a risk of **Jarisch–Herxheimer reaction** on administering antibiotics\n - For mild disease – doxycycline 7 days (if pregnant azithromycin)\n - For severe disease (eg. Weil's disease) – ceftriaxone \n - ICU may be indicated for severe disease\n \n \n### Prevention\n \n \nAvoiding potential sources of infection (eg. stagnant water, rodent control and avoidance of food contamination)\n \n \n# References\n \n \n 1. [Costa F et al. Global Morbidity and Mortality of Leptospirosis: A systematic review. *PLoS Negl Trop Dis*.2015;9(9)](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4574773/)\n 2. [Guerrier G, D'Ortenzio E. The Jarisch-Herxheimer reaction in leptospirosis: a systematic review. *PLoS One*.2013;8(3):]([https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3608636/)\n 3. [Click here for further information about Leptospirosis](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8813018/pdf/clinmed-22-1-14.pdf)\n 4. [Patient.info: Leptospirosis](https://patient.info/doctor/leptospirosis-weils-disease)",
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"question": "A 40-year-old man presents to A&E with a headache and itchy, red eyes for the past 8 days. He works as a water engineer and spends a lot of time in the sewers. He has no significant past medical history. On examination, his eyes are red and his liver edge is palpable. He has a low-grade fever of 37.7. Blood tests show a mildly raised AST and ALT, low platelets, and a high urea and creatinine.\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "This is incorrect because Hepatitis C would present with fever, malaise, and jaundice, with other risk factors in the history such as transmission through blood, birth, or sexual intercourse. Note that Hepatitis C would also cause deranged LFTs, but CMV infection is more likely in this patient following a renal transplant.",
"id": "53136",
"label": "e",
"name": "Hepatitis C",
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"explanation": "This is incorrect because VZV can cause shingles in the later years of life when a patient is immunosuppressed. This would present as a painful, vesicular, dermatomal rash which this patient does not have. VZV is also screened for prior to a renal transplant.",
"id": "53135",
"label": "d",
"name": "Varicella Zoster Virus",
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"votes": 39
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"explanation": "This is incorrect because Hepatitis B would present with fever, malaise, and potentially jaundice, with other risk factors in the history such as transmission through blood, birth, or sexual intercourse. Note that acute Hepatitis B would also cause deranged LFTs with the AST and ALT possibly in the 1000s. However, CMV infection is more common in this patient following a renal transplant.",
"id": "53134",
"label": "c",
"name": "Hepatitis B",
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"explanation": "This is correct because this patient has recently undergone a renal transplant. These patients are at risk of reactivation of latent CMV from within donor tissue within the first 6 weeks after a transplant secondary to immunosuppression. Note that a fever and deranged LFTs are key features for identifying CMV infection. It is managed with ganciclovir.",
"id": "53132",
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"name": "Cytomegalovirus",
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"explanation": "This is incorrect because EBV would present with fever, lymphadenopathy and a sore throat. Hepatosplenomegaly may also be found on palpation. EBV infection in transplant patients typically occurs due to reactivation of latent EBV from donor tissue. It generally takes longer to present (6 months+), and is often associated with post transplant lymphoproliferative disorder. As such, this case is too early post transplant to raise suspicion of an EBV mediated pathology.",
"id": "53133",
"label": "b",
"name": "Epstein-Barr Virus",
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"comment": "thank you renal placement xxx",
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"explanation": "# Summary\n\nRenal transplantation is a form of renal replacement therapy (RRT) that may be offered to patients with end-stage renal disease (ESRD). Transplant is not suitable for all patients however long-term outcomes are better than other forms of RRT and quality of life is significantly improved. Donors are either living or deceased, with deceased donors being classified as either donation after circulatory death (DCD) or donation after brainstem death (DBD) donors. Thorough assessment and work-up is required prior to listing for transplant, with the patient's preferences and shared decision making central to the process. Lifelong immunosuppression is required following transplantation, which carries its own complications. Despite immunosuppression, transplants may be rejected in either the hyperacute, acute or chronic setting. Other complications include infection, thrombosis of the renal vein or artery and ureteric injury. \n\n# Definition\n\nRenal transplantation refers to the surgical implantation of a healthy kidney from a donor (either living or deceased) into a patient with end-stage renal failure or progressive chronic kidney disease. It is one form of **renal replacement therapy**, with the other main type being dialysis. \n\n# Epidemiology\n\n- Renal transplant is the most common solid organ transplant in the UK\n- From 2023-2024 there were 3094 adult kidney only transplants performed in the UK\n- 1142 were from DBD donors, 1115 from DCD donors and 837 from living donors\n- There were 5779 adults on the active UK transplant waiting list on 31st March 2024\n- There are significant inequalities in access to renal transplant\n- People from South Asian and Black backgrounds typically wait 168-262 days longer than white patients to receive a transplant\n- This is in part due to a shortage of donors from these communities\n- The average age of a renal transplant recipient is 51 years\n- More men than women receive renal transplants (reflecting the greater incidence of end-stage renal disease in men)\n\n# Aetiology\n\nRenal transplantation should be considered in patients with end-stage renal failure or chronic kidney disease (CKD) stage 4 with progressive disease - causes of these include:\n\n- Diseases causing intrinsic kidney damage:\n- Diabetes\n- Hypertension\n- Glomerulonephritis, which may be primary or secondary\n- Conditions causing urinary tract obstruction:\n- Recurrent urolithiasis\n- Structural abnormalities (e.g. ureteropelvic junction obstruction)\n- External compression (e.g. from a pelvic mass)\n- Bladder voiding problems (e.g. benign prostatic hyperplasia, neurogenic bladder)\n- Iatrogenic causes:\n- Radiotherapy\n- Nephrotoxic drugs, e.g. aminoglycosides, lithium, NSAIDs\n- Renal involvement secondary to multisystem diseases\n- HIV\n- Myeloma\n- Vasculitis\n- Systemic lupus erythematosus (lupus nephritis)\n- Amyloidosis\n- Genetic kidney diseases\n- Autosomal dominant polycystic kidney disease (ADPKD)\n- Alport's syndrome\n- Tuberous sclerosis\n- Cystinosis\n- Recurrent urinary tract infections\n- Often secondary to vesico-ureteric reflux or other anatomical defects\n- Leads to chronic pyelonephritis which may lead to end-stage renal disease\n\nNB important **absolute contraindications** to renal transplantation include:\n\n- Untreated malignancy\n- Active infection (including untreated HIV)\n- Active systemic vasculitis\n- Life expectancy < 2 years for any reason\n- Current IV drug abuse\n\n# Classification\n\nRenal transplants are categorised based on from whom the kidney has come from (i.e. the donor):\n\n- **Live donors**\n- May be related or unrelated, including non-directed altruistic donors (who do not know the recipient)\n- Patients need to have compatible blood groups and HLA matching with the donor\n- Donor-recipient pairs who are incompatible and so cannot directly donate are registered in the UK Living Kidney Sharing Scheme\n- This allows either paired donation between two donor-recipient pairs, or a pooled donation where more than two pairs are involved\n- Outcomes are best from live donors\n- **Deceased donors**\n- There are two main types - donors after brain death (DBD) and donors after circulatory death (DCD)\n- Kidneys are retrieved from DBD patients whilst the heart is still beating, and after the heart has stopped in DCD patients\n- The majority of DCD patients have had planned withdrawal of care (for example in intensive care)\n- Long term outcomes are similar between DBD and DCD kidneys however delayed graft function is more common with DCD\n\n# Investigations\n\nPrior to being listed for a renal transplant, potential recipients need to undergo assessment of their fitness:\n\n- Blood type (ABO) and tissue typing for HLA\n- Crossmatch with donor to look for antibodies\n- Baseline blood tests to ensure patients are optimised for surgery and to screen for undiagnosed comorbidities\n- FBC, U&Es, LFTs, bone profile, clotting, lipids, HbA1c, parathyroid hormone\n- Group and saves as for any surgery\n- Assessment of cardiovascular risk\n- All patients require a chest X-ray and ECG\n- Higher risk patients (e.g. diabetes, older age) should also have an echocardiogram and cardiac stress test +/- angiography\n- Testing for viral infections\n- Cytomegalovirus (CMV)\n- Epstein-Barr virus (EBV)\n- Varicella zoster virus (VZV)\n- Hepatitis B and C\n- HIV \n- Risk assess for tuberculosis \n- High risk patients (e.g. born in an endemic area) should be tested with an interferon gamma release assay (IGRA)\n- Malignancy screening\n- Ensure patients are up to date with national cancer screening (mammograms, cervical smear tests)\n- Men over the age of 50 may be offered a PSA test (not part of a national screening programme)\n- Patients with a heavy smoking history should be offered a CT chest to screen for occult lung cancer\n- Cystoscopy should be considered for patients at high risk of bladder cancer (e.g. high-level cyclophosphamide exposure)\n- Psychosocial assessment for all candidates \n- Specialist input (e.g. psychiatry, social work) may be required for patients at higher risk of poor outcomes, for example:\n- Difficulties understanding the treatment process\n- Lack of social support\n- Neurocognitive difficulties\n- Severe or poorly controlled mental illness\n- Substance misuse or dependence\n- Dental assessment to screen for dental and periodontal disease that may be an infection risk\n- Patients with respiratory disease or symptoms should have lung function tests\n\n# Management\n\n**Conservative:**\n\n- Ensure patients are well informed regarding their options for renal replacement therapy, including the option of conservative management\n- Ensure patients have regular opportunities to re-discuss decision making around renal replacement therapy and their concerns and preferences\n- After transplant, renal transplant recipients require lifelong follow-up with multidisciplinary team input\n- Monitoring adherence to immunosuppressive treatment is crucial\n\n**Medical:**\n\n- All renal transplant recipients (apart from some transplants between identical twins) require lifelong immunosuppressive treatment\n- Patients receive induction therapy for up to 2 weeks around the time of transplant - this is a more intensive immunosuppressive regimen\n- For example, tacrolimus + mycophenolate mofetil (MMF) + steroids + basiliximab (an interleukin-2 receptor antagonist)\n- Following this, lifelong maintenance therapy is commenced\n- Triple therapy is standard, e.g. tacrolimus + MMF + low-dose steroids\n\n**Surgical:**\n\n- Offer a pre-emptive living donor transplant if available or listing for deceased donor transplantation\n- During the transplant operation, a ureteric stent is usually placed to support the anastomosis of the bladder and ureter - this is removed around 6 weeks later\n- In most cases the graft (donor kidney) is placed extraperitoneally in the right iliac fossa\n- In most cases, the native kidneys are left in place \n- Nephrectomy of native kidneys (either before, during or after transplant) may be indicated e.g. in cases of recurrent pyelonephritis, or in autosomal dominant polycystic kidney disease if huge kidney size is a hindrance surgically\n\n# Complications\n\n## Immediate complications\n\n- **Hyperacute rejection** may occur immediately after perfusion of the allograft intraoperatively, or in the following minutes to hours\n- It is antibody mediated, e.g. due to ABO or HLA incompatibility\n- The transplanted kidney will not function and needs to be removed\n- Very rare in the UK due to pre-transplant cross-matching\n- **Haemorrhage** which may be massive e.g. due to dissection of the renal artery anastomosis \n- **Ureteric injury** may require repeat surgical intervention - the ureteric-bladder anastomosis may also break down also causing intra-abdominal leakage of urine\n\n## Early complications\n\n- **Delayed graft function** is defined as a requirement for dialysis in the first week after transplant \n- It is a risk factor for graft rejection and decreased longevity of the graft\n- Grafts with prolonged warm and/or cold ischaemia times are at increased risk \n- Warm ischaemia time refers to the time between the kidney being perfused by the donor to when it is perfused with preservation solution\n- Cold ischaemia time refers to the time between the kidney being perfused with preservation solution to when it is re-perfused by the recipient's blood\n- **Renal vein thrombosis** is a serious complication that leads to loss of the kidney in the majority of patients\n- Patients present with refractory pain, reduced urine output, haematuria and deteriorating renal function\n- Renal doppler ultrasound is first-line to confirm the diagnosis\n- **Renal artery thrombosis** is rarer than renal vein thrombosis but also usually leads to graft loss\n- Risk factors include hypercoagulable states, prolonged cold ischaemia time and hypovolaemia\n- Patients present with sudden onset oliguria with pain and tenderness over the graft\n- **Wound infection** is common especially as patients are on immunosuppressive treatment\n- Other risk factors include diabetes, wound haematomas and urinary fistulas\n- **Wound dehiscence** is not uncommon; patients are at increased risk due to poor wound healing because of prolonged uraemia and anaemia \n- Early, eg. bleeding, thrombosis, infection, urinary leak, lymphocele\n- Late, eg. RAS, ureteric stenosis, bladder dysfunction\n- **Acute graft rejection** usually occurs in the first few weeks or months after transplant\n- Typically there is a T-cell mediated immune response against the graft\n- A biopsy of the graft may be required for diagnosis\n- IV methylprednisolone is usually first-line treatment, followed by escalation of immunosuppression\n\n## Late complications\n\n- **Chronic graft rejection** usually occurs at least a year after transplant\n- It is characterised by a gradual deterioration in graft function, with interstitial fibrosis and tubular atrophy on biopsy\n- **Infection** may mimic graft rejection, with patients at risk of opportunistic infections due to immunosuppression\n- There is an increased risk of urinary tract infection in particular\n- Patients may be given prophylactic antibiotics (e.g. co-trimoxazole for pneumocystis jirovecii) and antivirals (e.g. valganciclovir for cytomegalovirus)\n- Cytomegalovirus (CMV) is the commonest opportunistic infection and manifests in a variety of ways including with fevers, cytopenias and gastrointestinal symptoms such as abdominal pain and diarrhoea\n- Epstein-Barr virus (EBV) may reactivate, which may cause a glandular fever-like syndrome or posttransplant lymphoproliferative disorder\n- BK virus is a type of polyomavirus that may reactivate due to immunosuppression and cause a nephropathy that can mimic acute rejection\n- **Side effects of immunosuppressive medications**, for example:\n- Corticosteroids: insomnia, weight gain, diabetes, hypertension, osteoporosis, Cushing syndrome, avascular necrosis of the hip\n- Tacrolimus: impaired glucose tolerance, nephrotoxicity, peripheral neuropathy, alopecia, tremor\n- Ciclosporin: nephrotoxicity, hirsutism, gingival hypertrophy, dyslipidemia\n- Mycophenolate mofetil: gastrointestinal upset, leukopenia, photosensitivity\n- Azathioprine: myelosuppression, pancreatitis, nausea\n- **Malignancy** affects transplant recipients at higher rates than the general population\n- Non-melanoma skin cancers are very common\n- Other malignancies (e.g. renal cell carcinoma, lymphomas) are also seen more frequently\n- Patients should undergo skin surveillance as well as national screening for cervical, breast and colorectal cancer\n\n# Prognosis\n\n- A kidney transplant from a deceased donor lasts on average 15-20 years\n- A transplant from a living donor lasts 20-25 years\n- However these are very variable, and 30-40% of grafts fail in the first 10 years after transplant\n- Approximately 3% of grafts fail annually, with these patients having to go back on dialysis (and possibly be listed for another transplant)\n- There is a significant survival benefit compared to dialysis \n- Good prognostic factors are younger age, shorter pre-transplant dialysis duration and absence of cardiovascular disease\n- Poor prognostic factors include acute rejection, post-transplant infections and delayed graft function\n\n# NICE Guidelines\n\n[NICE - Renal replacement therapy and conservative management](https://www.nice.org.uk/guidance/ng107)\n\n[NICE Technology Appraisal - Immunosuppressive therapy for kidney transplant in adults](https://www.nice.org.uk/guidance/ta481)\n\n# References\n\n[NHS Blood and Transplant - Annual Report on Kidney Transplantation 2023/2024](https://nhsbtdbe.blob.core.windows.net/umbraco-assets-corp/34295/nhsbt-kidney-transplantation-report-2324.pdf)\n\n[Kidney Research UK - Kidney Health Inequalities](https://kidneyresearchuk.org/wp-content/uploads/2019/09/Health_Inequalities_lay_report_FINAL_WEB_20190311.pdf)\n\n[Patient UK - Renal Replacement Therapy and Transplantation](https://patient.info/doctor/renal-replacement-therapy-and-transplantation)\n\n[Royal Free Hospital Kidney Transplants - Types of donors](https://www.royalfree.nhs.uk/services/kidney-services/kidney-transplants/types-donors)\n\n[KDIGO Guideline on the Evaluation of Candidates for Kidney Transplantation](https://kdigo.org/wp-content/uploads/2018/08/KDIGO-Txp-Candidate-GL-FINAL.pdf)\n\n[Chronic Kidney Disease, Dialysis, and Transplantation - Infection in Renal Transplant Recipients](https://pmc.ncbi.nlm.nih.gov/articles/PMC7152484/)\n\n[British Transplantation Society - Post-Operative Care in the Kidney Transplant Recipient](https://ukkidney.org/sites/renal.org/files/FINAL-Post-Operative-Care-Guideline-1.pdf)",
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"question": "A 49-year-old man presents to A&E with fever and myalgia. He denies any recent unwell contacts or coryzal symptoms. His past medical history includes chronic kidney disease stage 5, hypertension and a kidney transplant 6 weeks ago. On examination, he appears pale. He has a temperature of 38.5. His blood tests reveal deranged liver function.\n\nWhich of the following is the most likely causative organism?",
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"explanation": "This is incorrect because FFP contains clotting factors which is used in the context of bleeding disorders or massive haemorrhage. This is not indicated in this patient because this would not help increase the haemoglobin level and there is no evidence of coagulopathy.",
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"explanation": "This is incorrect because this is the management for pericarditis. Pericarditis presents as pleuritic chest pain which improves on leaning forward and worsens on lying flat. Classical ECG findings are PR depression and widespread saddle-shaped ST elevation. It has many causes including viral infections. The first line treatment is usually an NSAID, and alternative treatments include colchicine.",
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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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"comment": "Inferior radiation does superior vision ",
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"comment": "and the numbers 12-3 are where on a clock",
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"explanation": "# Summary\n\nVisual field loss encompasses a range of distinct patterns, each indicative of underlying pathologies affecting different segments of the visual pathway. Monocular vision loss often results from retinal, optic nerve, or corneal disorders in one eye. Bitemporal hemianopia, characteristic of pituitary tumours and craniopharyngiomas, involves the loss of outer visual fields in both eyes. Contralateral homonymous hemianopia points to stroke or occipital lobe lesions, with loss of half the visual field in both eyes on the same side. Quadrantanopias may stem from stroke or trauma, leading to the loss of a quarter of the visual field. In occipital lobe lesions, macular sparing preserves central vision despite peripheral field loss. Recognizing these patterns and their differentials is crucial for accurate diagnosis and tailored management.\n\n\n# Pathologies seen at different parts of the optic pathway\n\nDifferent parts of the optic pathway present as various forms of visual deficits when disrupted.\n\n\n| **Visual Field Loss Pattern** | **Optic Pathway** | **Differential Diagnoses** |\n|----------------------------------------|-------------------------|----------------------------------------------------|\n| Monocular Vision Loss | Optic Nerve | - Retinal disorders, optic nerve disorders, corneal disorders |\n| Bitemporal Hemianopia | Optic Chiasm | - Pituitary tumours |\n| Contralateral Homonymous Hemianopia | Optic Radiation | - Stroke affecting optic radiation, occipital lobe lesions |\n| Quadrantanopias | Optic Radiation | - Stroke affecting specific pathways in the optic radiation, trauma, craniopharyngioma |\n| Macular Sparing in Occipital Lobe Lesions | Occipital Lobe | - Occipital infarcts or haemorrhages |\n\n\n[lightgallery]\n\n[lightgallery1]\n\n# Further Details \n\nConsidering that the fibres of each optic radiation that correspond to the lower retina (which receives stimulation by the upper half of the visual field) pass through the temporal lobe while the fibres that carry visual stimuli from the upper retina (representing the lower half of the visual fields) pass through the parietal lobe, it is clear that:\n\n- A lesion in the temporal lobe would cause contralateral homonymous superior (upper) quadrantanopia\n\n[lightgallery2]\n\n- A lesion in the parietal lobe would cause contralateral homonymous inferior (lower) quadrantanopia\n\t- A mneumonic for remembering this is **PITS** - P - parietal I - inferior; T - temporal S - superior\n- Parietal lobe damage also manifests as a defect of attention in the contralateral visual field, astereognosis, constructional apraxia (non-dominant), dressing apraxia (non-dominant) and ideomotor apraxia (dominant). Right hemisphere (i.e. non-dominant) parietal lesions are particularly prone to producing visual neglect. \n- A lesion in the occipital lobe would cause contralateral homonymous hemianopia\n\t- When an occipital lobe lesion occurs, it may damage a specific area of the visual cortex, resulting in visual field loss. However, the central representation of the macula has a larger cortical area dedicated to it, making it less vulnerable to damage. As a result, the central vision remains intact, creating a spared or preserved area of vision even in the presence of peripheral visual field loss.\n\n# References\n\n1. [Neuro-Ophthalmology Review Manual](https://www.thieme.com/books-main/ophthalmology/product/1040-neuro-ophthalmology-review-manual)\n2. [NICE Guidelines: Stroke and Transient Ischaemic Attack](https://www.nice.org.uk/guidance/cg68)\n3. [Visual Field Defects Overview on MedlinePlus](https://medlineplus.gov/ency/article/003879.htm)",
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"question": "A 54-year-old woman presents to A&E with sudden, painless loss of vision. This has not happened to her before. There was no obvious trigger, since she was sitting at home when this happened. She has a past medical history of severe left temporal lobe epilepsy and recently underwent surgery for this. When asked to point out the numbers on a clock face, she is only able to see from number 4 to 11 in both eyes. Fundoscopic examination is unremarkable.\n\nWhat is responsible for this patient's visual field defect?",
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"explanation": "Vasopressin, also known as anti-diuretic hormone, is essential for enabling the reabsorption of free water from the collecting duct in the nephron through aquaporin channels. Excess vasopressin results in excessive free water reabsorption, and a classical euvolaemic hyponatraemia as seen in SIADH. Low sodium results in non-specific symptoms, such as confusion and lethargy, and, if very low, seizures. This patient's bloods are normal, and there are no clinical features suggestive of low sodium.",
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"explanation": "Thyrotoxicosis can result in sweating, palpitations, anxiety, and hypertension. However, this patient has normal thyroid function tests, and no clinical features of hyperthyroidism, such as tremor, diarrhoea, or a goitre.",
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"explanation": "Excess growth hormone, usually from a pituitary adenoma, results in acromegaly. Pituitary tumours can cause headaches, and excessive growth hormone may result in hypertension, as seen in this case. However, acromegalous features are absent in this patient, such macroglossia, prognathism, changes in physical appearance, and growing hands/feet.",
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"explanation": "Excess cortisol leads to Cushing's syndrome, which is associated with hypertension. However, other features of Cushing's syndrome are notably absent, such as proximal weakness, striae, central adiposity, and thinning/bruising of the skin. Cushing's disease refers to Cushing's syndrome secondary to a pituitary tumour, whilst Cushing's syndrome is excess cortisol of any cause, including secondary to exogenous steroid use.",
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"explanation": "This patient has likely got a pheochromocytoma which is a catecholamine-secreting tumour in the adrenal medulla. Excess of circulating catecholamines result in hypertension, headaches, flushing, palpitations, and anxiety.",
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"comment": "i think it should be more clear that these symptoms are episodic - phaeo wouldn't typically have constant headaches, hypertension and sweating",
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"explanation": "# Summary\n \n\nA pheochromocytoma is a catecholamine-secreting tumour originating in the chromaffin cells of the adrenal medulla, while a paraganglioma arises in sympathetic nerve tissue elsewhere in the body. These tumours commonly manifest between the 3rd and 5th decades of life, with an incidence of 0.5 to 2 in 1,000 hypertension patients. They may present with episodic hypertension, anxiety, weight loss, palpitations, among other signs and symptoms. Symptoms can be precipitated by stress, exercise, and certain medications. Diagnostic investigations focus on confirming catecholamine excess with plasma and urinary metanephrines tests. CT and MRI scans are also performed to locate the tumour. Management includes surgical resection, preceded by alpha blockade with phenoxybenzamine to prevent hypertensive crises.\n \n\n# Definition\n \n\nA pheochromocytoma is a catecholamine-secreting tumour that originates in the adrenal medulla. When a similar tumour arises in sympathetic nerve tissue elsewhere in the body, it is termed a paraganglioma.\n \n\n# Epidemiology\n \n\nPheochromocytomas and paragangliomas occur in between 0.5 and 2 in 1,000 patients diagnosed with hypertension. The condition most commonly manifests between the 3rd and 5th decades of life.\n \n\n# Aetiology\n \n\nThe aetiology of pheochromocytoma and paraganglioma is multifactorial and can be sporadic or hereditary. Multiple genes are implicated in familial cases, such as RET, VHL, NF1, and SDH.\n \n\n# Signs and Symptoms\n \n\nThe clinical presentation can vary, with the following symptoms commonly reported:\n \n\n - Episodic hypertension\n - Anxiety\n - Weight loss\n - Fatigue\n - Palpitations\n - Excessive sweating\n - Headaches\n - Flushing\n - Fever\n - Difficulty breathing (dyspnea)\n - Abdominal pain\n \n\nPhysical examination may reveal:\n \n\n - Hypertension\n - Postural hypotension\n - Tremor\n - Hypertensive retinopathy\n \n\nSymptoms can be precipitated by stress, exercise, surgery, straining, and certain medications like beta blockers, anaesthetic agents, and opiates.\n \n\n# Differential Diagnosis\n \n\nThe differential diagnosis for pheochromocytoma includes:\n \n\n - **Anxiety disorders:** Manifest with anxiety, palpitations, sweating, but lack the characteristic episodic hypertension of pheochromocytoma.\n - **Hyperthyroidism:** Features weight loss, tremor, palpitations, but typically includes symptoms like heat intolerance and changes in hair and skin texture.\n - **Essential hypertension:** Chronic high blood pressure without an identifiable secondary cause. It lacks the episodic nature of pheochromocytoma.\n \n\n# Investigations\n \n\nThe evaluation of suspected pheochromocytoma involves confirming catecholamine excess and identifying the tumour's location. This includes:\n \n\n - Plasma metanephrines testing followed by urinary metanephrines.\n - Adrenal imaging should be pursued only after biochemical confirmation. CT of the chest, abdomen, and pelvis is the modality of choice, followed by MRI if needed.\n - Extra-adrenal pheochromocytomas can be identified using specific imaging studies such as iodine-labeled metaiodobenzylguanidine (MIBG) scans or PET scans.\n \n\n# Management\n \n\nThe definitive treatment for pheochromocytoma and paraganglioma is surgical resection of the tumour. Preoperative management includes:\n \n\n - Alpha blockade with phenoxybenzamine is initiated first to prevent intraoperative hypertensive crises.\n - Beta blockade can be added subsequently if necessary, to manage tachycardia or arrhythmias after adequate alpha blockade is achieved.\n \n\n# References\n \n\n [Patient.info - Phaeochromocytoma](https://patient.info/doctor/phaeochromocytoma-pro)",
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"question": "A 52-year-old woman presents to her GP with a headache for a month. She has also been waking in the middle of the night feeling sweaty which is unusual for her, and has been feeling more anxious. She has reported no change to her physical appearance. On examination, her blood pressure is 167/98mmHg, and the remainder of her physical assessment is unremarkable. Blood tests show a normal white cell count, normal urea and electrolytes, and normal thyroid function.\n\nWhich of the following hormones is the most likely cause of this patient's presentation?",
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"explanation": "This is incorrect because this woman has a CRB65 score of 1 and there is clinical evidence of a community-acquired pneumonia on examination. NICE guidelines clearly state that an antibiotic must be offered for people with community-acquired pneumonia.",
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"label": "b",
"name": "No treatment",
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"explanation": "This is correct because this woman has a CRB65 score of 1. She scores 1 point for her age as she is above 65 years old. Note that the CRB65 scoring system is used in the GP setting for pneumonia because the urea is not immediately available. A 5-day course of oral amoxicillin 500mg three times daily (since she has no known allergies) is suitable for this patient as she has a CRB65 score of 1.",
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"explanation": "This is incorrect because this woman's CRB65 score of 1 does not currently warrant hospital admission. If her CRB65 score were 2 or above, hospital admission would be considered as intravenous antibiotics would be needed.",
"id": "53205",
"label": "d",
"name": "Admit to hospital",
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"explanation": "This is incorrect because steroids are not used in the routine management of community-acquired pneumonia, unless they are complicating an exacerbation of an obstructive airways disease. This patient has no wheeze or past medical history of obstructive airway pathology, and as such steroids will not be required in her management.",
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"explanation": "Doxycycline is used instead of amoxicillin for patients with a penicillin allergy, which this patient does not have, in the management of community acquired pneumonia. An alternative medication is oral clarithromycin which is also taken for 5 days.",
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"label": "e",
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"comment": "Does AMTS score of 9/10 not indicate confusion?",
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"comment": "confusion = abbreviated mental test score 8 or below\n",
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"comment": "It's normally 8 or less",
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"explanation": "# Summary\n\n\nPneumocystis Pneumonia (PCP) is a fungal infection caused by _Pneumocystis Jirovecii_ that affects immunocompromised patients. Key symptoms include fever, a dry cough, and exertional breathlessness. Desaturation on exertion is characteristic of PCP pneumonia. Chest X-ray may be normal or show bilateral infiltrates, and a definitive diagnosis is reached with either sputum samples or bronchoscopy with bronchoalveolar lavage. Management involves antibiotics, usually co-trimoxazole as the first line treatment, with steroids added for more severe cases.\n\n\n# Definition\n\n\nPneumocystis Pneumonia (PCP) is an infection caused by the fungus _Pneumocystis Jirovecii_. It usually affects patients who are immunocompromised, for example patients with late-stage HIV or those on immunosuppressant medications after an organ transplant.\n\n\n# Epidemiology\n\n\nIn the UK, rates of PCP are falling in patients with HIV due to improvements in antiretroviral therapies. However, there has been an increase in PCP in patients immunosuppressed for other reasons (such as transplant or haematological malignancies). Currently around half of patients with PCP have HIV and half do not.\n\n\nPatients at risk of PCP should be treated with prophylaxis (usually oral co-trimoxazole) - this includes all patients with HIV with a CD4 count of below 200. \n\n\n# Aetiology\n\n\nPCP is caused by _Pneumocystis Jirovecii_, a fungus that causes pulmonary infections. Patients at risk of PCP are those who are immunocompromised (it is classed as an opportunistic infection, and an AIDS-defining illness in those with HIV). \n\n\nRisk factors include:\n\n\n- HIV with a CD4 count below 200\n- Steroids or other immunosuppressive medications\n- Previous organ transplant\n- Congenital immunodeficiencies (e.g. hypogammaglobulinaemia)\n- Severe malnutrition\n- Comorbid lung disease\n- Haematological malignancies\n\n\n# Signs and Symptoms\n\n\n- Fever\n- Dry cough\n- Exertional breathlessness\n- Chest pain\n\n\nOn examination, the chest may be clear, or end-inspiratory crackles and wheeze may be present.\n\n\n# Differential Diagnosis\n\n\n- Bacterial or viral pneumonia: similar symptoms, more likely to have a productive cough.\n- Tuberculosis: chronic cough, haemoptysis, weight loss, night sweats and fever. \n- Pulmonary embolism: less likely to have fevers, dry cough and shortness of breath on exertion typical, may have haemoptysis.\n\n\n# Investigations\n\n\n**Bedside tests include:**\n\n\n- Oxygen saturations on exertion \n- Arterial blood gas for hypoxia, important to grade severity and determine if steroids are indicated\n- Sputum samples (may need to be induced e.g with saline nebulisers): **silver staining** is used to confirm the diagnosis of PCP (shows a characteristic Mexican hat appearance), also send sputum for routine and mycobacterial culture (to rule out TB or other infections)\n\n\n**Blood tests include:**\n\n\n- Routine bloods for FBC and CRP (looking for infection markers) and baseline liver and renal function prior to starting antibiotics\n- HIV testing\n- CD4 count if HIV positive\n\n\n**Imaging includes:**\n\n\n- Chest X-ray: often shows bilateral hilar interstitial infiltrates, however 10% have a normal chest X-ray.\n- High-resolution CT scan: if chest X-ray is normal and PCP is suspected, a high-resolution CT is more sensitive.\n\n\n**Other investigations:**\n\n\n- Bronchoscopy with bronchoalveolar lavage: if sputum samples are negative, this is the definitive investigation to gain a respiratory sample for staining. \n\n\n[lightgallery]\n\n\n# Management\n\n\n- Supportive treatment with analgesia, oxygen if hypoxic, consider holding immunosuppressant treatment (with liaison with specialist teams as needed)\n- Patients with mild disease (only mild changes on CXR, normal oxygen saturations) can be treated as outpatients; moderate and severe cases should be admitted\n- High dose co-trimoxazole is the primary treatment\n- Alternative therapies if co-trimoxazole is contraindicated or not tolerate include: atovaquone, dapsone with trimethoprim or pentamidine. \n- Steroids should be given in all patients with moderate or severe PCP (i.e.PaO2<11kPa) - either oral prednisolone or IV hydrocortisone. \n\n\n# NICE Guidelines\n\n\n[NICE CKS - HIV infection and AIDS](https://cks.nice.org.uk/topics/hiv-infection-aids/)\n\n\n# References\n\n\n[Patient UK - Pneumocystis Jirovecii Pneumonia](https://patient.info/doctor/pneumocystis-jirovecii-pneumonia)\n\n\n[BNF treatment summary - Pneumocystis Pneumonia](https://bnf.nice.org.uk/treatment-summary/pneumocystis-pneumonia.html)",
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"question": "A 68-year-old woman presents to the GP with a 3-day history of a cough productive of green phlegm, as well as exertional dyspnoea. She has no past medical history, takes no regular medications, and has no drug allergies. Her vital signs are: HR 89bpm, RR 14 breaths per minute, O2 saturation 99% on room air, BP 145/78mmHg. Her AMTS is 9/10. On examination, there are crepitations in the left lower zone of her chest.\n\nWhich of the following is the next best step in the management of this patient?",
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"explanation": "Escherichia coli can present in a similar way to C. Jejuni with bloody diarrhoea, fever, and abdominal pain in the context of food poisoning. It is important to remember the 0157: H7 strain which can trigger haemolytic uraemic syndrome. However, E. Coli is a gram negative rod, as opposed to spiral/comma shaped.",
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"explanation": "Bacillus cereus is a gram positive rod presenting with rapid onset, toxin mediated food poisoning (within hours.) It is classically associated with takeaways or reheating rice. It is not associated with bloody diarrhoea. The incubation period in this case, findings on stool culture, and bloody diarrhoea point against Bacillus cereus.",
"id": "53211",
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"explanation": "C. jejuni is a spiral or comma-shaped gram negative organism, which commonly presents with a flu-like prodrome, crampy abdominal pain, and bloody diarrhoea. It is a common cause of food poisoning and has a long incubation period of around 5 days. It is associated with Guillain Barre syndrome, which presents with ascending, bilateral weakness in the lower limbs; this child is complaining of lower limb weakness, so this should raise clinical suspicion of this complication.",
"id": "53207",
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"explanation": "Entamoeba histolytica causes amoebic dysentery. It is associated with foreign travel and stool microscopy would show trophozoites.",
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"explanation": "Salmonella enteritidis can present in a similar way to C. Jejuni with bloody diarrhoea, fever, and abdominal pain in the context of food poisoning. However, it presents earlier than C. jejuni as the incubation period is shorter (around 12-48 hours.) Furthermore, Salmonella is a gram-negative rod rather than a spiral-shaped/comma-shaped organism.",
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"comment": "don't know my rods from my spirals\n",
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"explanation": "# Summary\n \nGastroenteritis is an enteric infection causing acute-onset diarrhoea, sometimes with additional symptoms. Food poisoning results from consuming contaminated substances, while acute diarrhoea involves three or more liquid or semi-liquid stools in 24 hours, lasting less than 14 days. Prolonged diarrhoea lasts over 14 days, and dysentery is acute infectious diarrhoea with blood and mucus. Infectious diarrhoea is commonly spread via the faeco-oral route and often caused by viruses like norovirus, rotavirus, and adenovirus. Bacterial causes include Campylobacter, E. coli, Salmonella, Cholera, Shigella, and Yersinia. Parasites like Cryptosporidium, Entamoeba histolytica, and Giardia can also cause prolonged diarrhoea. Symptoms include sudden-onset diarrhoea, nausea, vomiting, fever, and abdominal pain. Diagnosis often involves assessing hydration status and may require stool cultures or blood tests. Treatment includes rehydration and, in some cases, antimicrobials. Preventative measures include proper food hygiene and handwashing. Certain infections must be reported to health authorities. High-risk groups include young children, the elderly, immunocompromised individuals, and pregnant women, who may face complications such as dehydration, haemorrhagic colitis, and sepsis.\n \n# Definition\n \n **Gastroenteritis:** an enteric infection causing acute-onset diarrhoea, with or without associated symptoms\n \n **Food poisoning:** illness caused by eating or drinking substances contaminated with disease-causing pathogens, toxins or chemicals.\n \n **Acute diarrhoea:** 3+ episodes liquid/semi-liquid stools in in a 24h period, lasting less than 14 days\n \n **Prolonged diarrhoea:** acute-onset diarrhoea lasting over 14 days\n \n **Dysentery:** is acute infectious diarrhoea with blood & mucus, often with associated symptoms\n \n# Aetiology\n \nMost cases of infectious diarrhoea are spread by the faeco-oral route and are caused by viruses. These include:\n \n - **Norovirus:** **most common** cause in the population, and often causes outbreaks. Typically causes projectile vomiting and non-bloody diarrhoea.\n - **Rotavirus:** the most common cause of gastroenteritis in children.\n - **Adenovirus:** typically causes respiratory tract infections but may cause gastrointestinal symptoms in children.\n \nBacteria causing infectious diarrhoea include:\n \n - **Campylobacter**: often associated with contaminated food & drink (in exams: a recent barbeque!), this is the most common cause of bacterial gastroenteritis in the UK. On microscopy, gram-negative rods are seen with characteristic 'seagull' shape, which release enterotoxin in the gut and invade the mucosa. Incubation period is 1 - 5 days and may cause bloody diarrhoea, though vomiting is rare.\n - **E. coli**: the most common cause of traveller's diarrhoea. In the UK, O157:H7 is the most common type and may cause bloody diarrhoea. Sources include improperly cooked meat. Associated complications include haemolytic uraemic syndrome, which typically affects the very young are old and can be fatal.\n - **Salmonella** is associated with consumption of contaminated foods, particularly poultry, eggs and milk. These are gram negative bacteria with an incubation of 16-48 hours. *Salmonella* can cause bloody diarrhoea and is associated with complications such as sepsis, endocarditis, mycotic aneurysm and osteomyelitis.\n - **Cholera** is associated with contaminated water supplies and causes very watery diarrhoea associated with dehydration.\n - **Shigella** and *Yersinia* tend to occur in children. The former can cause severe, bloody diarrhoea.\n - **Bacillus cereus** are gram-positive rods that produce two toxins causing diarrhoea and vomiting within hours of eating contaminated food (in exams, this is usually reheated rice).\n - **Staphylococcus aureus** produces a heat-stable enterotoxin that causes profuse vomiting with mild diarrhoea and abdominal pain. The incubation period is short (under 6 hours) after eating contaminated foods. The bacteria are usually introduced from the skin of the person preparing the food. Foods which do not require cooking carry greater risk.\n \nParasites can be spread by ingestion of contaminated food/drink or from person to person, and often associated with recent travel.\n \n - **Cryptosporidium**: a protozoal infection which may cause prolonged symptoms\n - **Entamoeba histolytica**: most cases are mild but severe cases cause dysentery\n - **Giardia**: causing diarrhoea, constitutional symptoms and bloating which may be prolonged\n \n# Signs and Symptoms\n \nSymptoms include:\n \n - Sudden-onset diarrhoea, with or without blood\n - Faecal urgency\n - Nausea & vomiting\n - Fever, malaise\n - Abdominal pain\n - Associated symptoms specific to the cause\n \n \n# Differential Diagnosis\n \n - ***Clostridium difficile*** infection, causing antibiotic-associated (in particular, cephalosporins) diarrhoea. Patients usually have predisposing risk factors such as recent antibiotics, immunocompromise or PPI use. Typically causes foul-smelling diarrhoea and can cause severe systemic upset and GI complications.\n - Other causes of **diarrhoea**, including irritable bowel syndrome, inflammatory bowel disease, malignancy, endocrine conditions such as thyrotoxicosis. These usually have a more prolonged history and may be associated with other systemic symptoms (except IBS).\n - Other causes of **abdominal pain**, such as appendicitis, intestinal obstruction, diverticulitis, pancreatitis. These are associated with other symptoms such as absolute constipation and vomiting (obstruction) or pain relieved on leaning forward (pancreatitis). Often, there is also more systemic upset and deranged blood tests.\n \n# Investigations\n \n - Often, infectious diarrhoea is a clinical diagnosis and, providing the patient is not systemically unwell, may not need further investigation. \n - It is important to assess hydration status and consider whether the person can tolerate oral fluids.\n - A stool culture may be needed if there are any higher risk features. These include if the person is systemically unwell, is immunocompromised, presents with dysentery or prolonged diarrhoea, there is increased risk of transmission, food poisoning is suspected or symptoms are associated with recent travel.\n - If a person is unwell presenting to secondary care, consider performing blood tests to include FBC, U&Es, CRP, LFTs and TFTs. \n - Consider a VBG, blood cultures and monitoring urine output if they appear septic.\n \n \n# Management\n \n - If a person is systemically unwell, or severely dehydrated, adopt an A-E approach and consider initiating the sepsis six. Admit the patient and seek senior help early. They may need IV fluids, antiemetics or antibiotics.\n - Conservative: advise regular fluids, with or without rehydration salts, and safetynet for signs of dehydration. Antidiarrhoeal drugs are not routinely used, and should be avoided if the patient has symptoms of dysentery or suspected *E. coli 0157*.\n - Medical: antimicrobials are not routinely indicated, but clinical suspicion or positive cultures of the following may prompt initiation of antibiotics:\n \n - *Campylobacter*: macrolide e.g. clarithromycin\n - *Amoeba, Giardia*: anti-protozoal e.g. metronidazole\n - *Cholera*: tetracycline\n \n - If a patient is systemically unwell, immunosuppressed or elderly, consider empirical antibiotics following local pathways and microbiology advice.\n \n - Infectious diarrhoea can be prevented by avoiding foods that are undercooked or prepared in unsanitary conditions, and handwashing at appropriate times and hygiene measures. \n - Enhanced precautions such as isolation and barrier nursing along with handwashing can prevent spread in clinical settings. People should not return to work until 48 hours after their symptoms have resolved.\n \nThe following are notifiable diseases, and should be reported to the local health protection scheme:\n \n - Food poisoning\n - Haemolytic uraemic syndrome\n - Dysentery\n - Enteric fever\n - Cholera\n \n# Complications\n \nYoung children, elderly, people with comorbidities or immunocompromised and pregnant women are at highest risk of complications. These include:\n \n - Dehydration, electrolyte disturbance, acute kidney injury\n - Haemorrhagic colitis, haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura\n - Reactive arthritis\n - Toxic megacolon\n - Sepsis\n \nLonger-term complications include: faltering growth, irritable bowel syndrome and lactose intolerance.\n \nSpecific complications may occur depending on the causative organism.\n \n# NICE Guidelines\n [NICE CKS: Gastroenteritis](https://cks.nice.org.uk/topics/gastroenteritis/)",
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"question": "A 14-year-old boy presents to A&E with his dad complaining of abdominal pain. He describes it as crampy, which paracetamol has not relieved. Over the last 2 days, he is complaining of leg weakness, fever, and bloody diarrhoea. His dad is concerned that he may have ulcerative colitis. There is no travel history of note. They went to a barbecue 5 days ago where they ate chicken. On examination, the patient has a temperature of 39.8. A faecal sample is taken which shows a spiral shaped organism.\n\nWhich of the following organisms is the most likely cause?",
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"explanation": "Zollinger-Ellison syndrome presents with recurrent ulcers in the stomach and duodenum secondary to excessive gastrin levels released from gastrinomas, which are malignant. Gastrin stimulates mucosal growth of the stomach and the release of acid from gastric parietal cells. These patients also present with diarrhoea due to excessive gastric acid leading to inactivation of lipase and subsequent fat malabsorption. Endoscopy would reveal multiple ulcers, as well as thickened gastric folds. This condition is commonly associated with multiple endocrine neoplasia 1 (MEN1.) Treatment is with high dose PPI or somatostatin analogues.",
"id": "53219",
"label": "c",
"name": "Zollinger-Ellison syndrome",
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"explanation": "Oesophageal cancer typically presents with progressive dysphagia, initially for solids and eventually for liquids, as well as hoarseness of the voice if there is compression of the recurrent laryngeal nerve which runs close to the oesophagus in the thorax. Risk factors include smoking, acid reflux (due to Barrett's oesophagus), and high levels of alcohol intake. Helicobacter pylori causes achlorhydria chronically, and as such is actually protective against oesophageal adenocarcinoma. Weight loss and anorexia may also occur. This patient's endoscopy reveals no oesphageal lesion, with the only finding in the stomach, and reports no dysphagia. Therefore, oesophageal malignancy is unlikely.",
"id": "53221",
"label": "e",
"name": "Oesophageal cancer",
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"explanation": "Crohn's disease is an inflammatory bowel disorder, which can present with abdominal pain and weight loss. Additional clinical features usually include diarrhoea, which is absent in this case. Inflammation can be present throughout the entire GI tract, from mouth to anus, and additional clinical features, such as mouth ulcers, may be present. The history of abdominal pain worse on eating, relieved by antacids, and the appearances on endoscopy, are not consistent with a diagnosis of Crohn's disease.",
"id": "53220",
"label": "d",
"name": "Crohn's disease",
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"explanation": "Gastric cancer may also present with epigastric pain, weight loss, and anorexia. Patients may also have iron deficiency anaemia. Risk factors for gastric cancer are similar to peptic ulcer disease, and include smoking as well as Helicobacter pylori infection. The endoscopic appearances here are in keeping with an ulcer, however, as opposed to gastric cancer, and the clinical feature of pain worsening on eating should also raise suspicion of an ulcer.",
"id": "53218",
"label": "b",
"name": "Gastric adenocarcinoma",
"picture": null,
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This patient's endoscopy findings are in keeping with a peptic ulcer. His symptoms of epigastric pain, worsened on eating, typically indicate a gastric ulcer (with pain from duodenal ulcers relieved by eating.) This patient has rheumatoid arthritis, and it is possible he may use NSAIDs frequently; this, alongside his smoking history, places him at higher risk of peptic ulcer disease. Another key risk factor is Helicobacter pylori infection, which this patient will be tested for during endoscopy. It is important to note that this patient was referred for endoscopy appropriately under the 2-week-wait pathway as he fit the criteria for urgent investigation due to his age over 55, weight loss, and abdominal pain, in line with NICE guidance.",
"id": "53217",
"label": "a",
"name": "Peptic ulcer disease",
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"comment": "man said unintenional weight loss and smoking history. WHAT YOU PLAYING AT QUESMED?",
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"comment": "I think it's because unintentional weight loss and smoking history can be suggestive of cancer, and that's why he'd qualify for an endoscopy. But the endoscopy findings are not consistent with gastric carcinoma ",
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"comment": "and the weight loss could have been eluded to the fact that he may not be eating as much",
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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 57-year-old male presents to the GP with a 7-month history of epigastric pain which gets worse after eating. Over the same time period, he has lost his appetite and 1.5kg unintentionally. He has a past medical history of rheumatoid arthritis and a smoking history of 31 pack years. He admits that he often uses over-the-counter antacids, which help occasionally. He is referred for a two-week wait upper gastrointestinal endoscopy, which reveals granulation tissue with a necrotic layer.\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "Recombinant factor VIII is used in the management of Haemophilia A, which is an X linked recessive disorder characterised by factor VIII deficiency. Haemophilia A is the most common inherited bleeding disorder which presents with recurrent haemarthroses and bruising. Blood tests reveal a prolonged APTT.",
"id": "53224",
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"name": "Recombinant clotting factor VIII",
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"explanation": "Recombinant factor IX is used in the management of Haemophilia B, which is an X linked recessive disorder characterised by factor IX deficiency. Haeomophilia B is also known as Christmas disease.. Blood tests reveal a prolonged APTT.",
"id": "53225",
"label": "d",
"name": "Recombinant clotting factor IX",
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"explanation": "Cryoprecipitate, which contains high levels of von Willebrand Factor and fibrinogen, may be required during massive haemorrhage, but it is not routinely provided, unlike packed red cells, platelets, and FFP. The decision to provide cryoprecipitate depends on close monitoring of bloods during the resuscitation efforts, and is usually required when the fibrinogen levels are less than 1. Treatment of massive haemorrhage should utilise the expertise of a haematologist since coagulopathy and complications can be extreme.",
"id": "53223",
"label": "b",
"name": "Cryoprecipitate",
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"explanation": "This patient is presenting with a ruptured abdominal aortic aneurysm. He will need transfusing according to a major haemorrhage protocol, which involves providing platelets, fresh frozen plasma, and packed red cells in a 1:1:1 ratio. It will be incorrect to transfuse him packed red cells only since this will not correct/worsen any coagulopathy sustained because of the massive haemorrhage.",
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"explanation": "This patient is presenting with a ruptured abdominal aortic aneurysm. He will need transfusing according to a major haemorrhage protocol, which involves providing platelets, fresh frozen plasma, and packed red cells in a 1:1:1 ratio. Once stabilised, he will be able to go to theatre for either endovascular or open abdominal aortic aneurysm repair.",
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"explanation": "# Summary\n\n\nAn abdominal aortic aneurysm (AAA) is a common, potentially life-threatening condition characterised by an abdominal aorta diameter greater than 3cm. It's most frequently located between the renal and inferior mesenteric arteries. Key signs and symptoms include a typically asymptomatic presentation, occasionally manifesting as a pulsatile, expansile abdominal mass. Diagnosis primarily relies on abdominal ultrasound screening, with follow-up frequency varying based on the aneurysm size. Management strategies focus on surgical repair, with indications being a size >5.5cm or rapid expansion, encompassing open repair or Endovascular Aneurysm Repair (EVAR).\n\n\n# Definition\n\n\nAbdominal aortic aneurysm (AAA) is a prevalent, potentially lethal condition characterised by an enlargement of the abdominal aorta exceeding a diameter of 3cm. This dilatation affects all three layers of the arterial wall. Many individuals with AAA are asymptomatic and do not cause any problems to the individual. In the absence of repair, a ruptured AAA is generally fatal.\n\n\n# Epidemiology\n\n\nAbdominal aortic aneurysm (AAA) predominantly affects older adults, especially those over 65 years of age. At the time of screening at age 95, 0.92% of men undergoing screening are found to have an abdominal aortic aneurysm. It is approximately 4-6 times more prevalent among men than women. An estimated 4-8% of men and 1-2% of women aged over 65 years are affected, but due to the asymptomatic nature of the condition, the actual prevalence may be higher. \n\nThere is a significant geographic and ethnic variation, with higher prevalence reported in Western countries. Lifestyle factors such as smoking and a history of cardiovascular disease increase the risk. \n\nAAA morbidity and mortality are reducing in the UK due to increasing elective repair of AAA and a reduction in smoking rates. \n\n\n# Aetiology\n\n\nThe precise aetiology of AAA is complex and multifactorial, typically involving a combination of genetic, environmental, and lifestyle factors.\n\n\nRisk factors include:\n\n- Being male\n- Age 65 or over\n- Smoking \n- Hypertension\n- Hypercholesterolaemia \n- Family history of AAA\n- Personal history of peripheral arterial disease or myocardial infarction\n- COPD\n- Connective tissue disorders (i.e. Marfan's) \n\n\n\n# Signs and Symptoms\n\n\nMost AAAs remain asymptomatic for a long time and are often detected incidentally during radiological investigations for other abdominal or pelvic conditions. \n\nWhen symptomatic, the clinical presentation can vary:\n\n\n- Pulsatile abdominal mass: \n- The most classical finding on physical examination is a pulsatile, expansile abdominal mass. This is typically non-tender unless rupture is imminent.\n- Approximately 3 in 5 AAA over 3 cm are palpable.\n- This may also be associated with abdominal bruit.\n\n- Abdominal or back pain: \n- Pain is usually a late manifestation, suggesting rapid expansion or impending rupture of the aneurysm. \n- It is typically severe, constant, and localised in the abdomen or lower back, often radiating to the flank or groin.\n- There can also be testicular pain if the blood supply to this area is compromised by rupture\n- 90% of aortic aneurysms are infrarenal (originating below the renal arteries) \n\n\nIn advanced cases, a large aneurysm may cause symptoms due to compression or displacement of adjacent structures, resulting in early satiety, nausea, weight loss, altered bowel habits, or deep venous thrombosis (due to compression of the inferior vena cava).\n\n\n# Differential Diagnosis\n\n\nDifferential diagnoses for AAA include, but are not limited to:\n\n\n- **Renal colic**: Typically presents with severe, sudden onset flank pain that can radiate to the groin, accompanied by haematuria and urinary urgency.\n- **Pancreatitis**: Characterised by persistent, severe epigastric pain radiating to the back, often associated with nausea, vomiting, and elevated pancreatic enzymes.\n- **Peptic ulcer disease**: Often presents with burning epigastric pain that is relieved by eating, weight loss, and potential signs of bleeding like melaena or hematemesis.\n- **Diverticulitis**: Usually presents with left lower quadrant pain, fever, and changes in bowel habits.\n\n\n\n# Investigations\n\nNHS AAA screening programme: \n\n- Offered to men at age 65\n- Consists of an abdominal ultrasound\n- Follow-up screening depends on the size of the aneurysm:\n\n- Small AAA (3-4.4cm): Yearly repeat ultrasound is offered.\n- Medium AAA (4.5-5.4cm): Repeat ultrasound every 3 months is offered.\n- Large AAA (>5.5cm): Surgical intervention is generally recommended.\n\nOnce an abdominal aortic aneurysm has been detected, further investigations may be required, including: \n\n- **Computed Tomography (CT) Angiography:** \n- CT angiography is the imaging modality of choice for preoperative evaluation, determining the size, shape, and extent of the AAA, and planning the surgical approach. \n- It provides detailed information about the aneurysm's relationship to branch arteries and the potential presence of thrombus or calcification within the aneurysm. \n- It is also the preferred imaging modality in suspected rupture cases due to its rapid acquisition time and high sensitivity and specificity.\n\n- **Magnetic Resonance Angiography (MRA):** MRA is an alternative to CT angiography for patients who cannot be exposed to ionizing radiation or iodinated contrast medium. MRA can provide high-resolution images of the AAA and surrounding structures but is less readily available and takes more time than CT.\n\n- **Blood tests:** While there is no specific blood test to diagnose AAA, complete blood count, coagulation profile, renal function tests, and electrolyte levels are typically evaluated prior to surgery.\n\n\n\nFinally, regular surveillance of known AAAs is critical. The frequency of surveillance depends on the size of the aneurysm, with smaller aneurysms monitored less frequently and larger ones requiring closer observation.\n\n\n# Management\n\n### Conservative \n\nManagement of abdominal aortic aneurysms may be through conservative measures such as: \n\n- Surveillance:\n- This is typically offered for smaller aneurysms with a lower risk of rupture. It is very rare for smaller AAA to rupture. \n- Small AAA (3-4.4cm): Yearly repeat ultrasound is offered.\n- Medium AAA (4.5-5.4cm): Repeat ultrasound every 3 months is offered.\n- Large AAA (>5.5cm) require referral to vascular surgery to be seen within 2 weeks of diagnosis. \n- Measures to reduce the risk of rupture:\n- Referral to a stop-smoking service\n- Management of hypertension \n\n\n### Surgical \n\n\nElective repair of AAA may be considered for individuals with AAA who meet the following criteria:\n\n- They are symptomatic \n- Their AAA has grown by more than 1 cm in 1 year and is larger than 4 cm\n- Their AAA is 5.5 cm or larger \n\n\nTwo primary surgical options are available for managing AAA: \n\n- Open surgical repair\n- Typically best for men under age 70. \n- However, it can be contraindicated by anaesthetic risks, medical comorbidities or anatomic difficulties (i.e. horseshoe kidney, stoma, numerous previous surgeries resulting in significant adhesions)\n- Endovascular Aneurysm Repair (EVAR)\n- A stent graft is inserted through the femoral arteries into the aorta, where it channels blood flow into the iliac arteries. The surrounding aneurysm then becomes thrombosed around the graft. \n- EVAR has reduced perioperative deaths and is associated with shorter hospital stays. However, it has an overall higher long-term morbidity and mortality than open repair. \n\n\n# Complications\n\n\n### Rupture\n\nAAA rupture is a surgical emergency. Abdominal aortic aneurysms are more likely to rupture in women than men but are more common in men and such account for more presentations in men. \n\nAAA tend to enlarge over time and with increasing size, the risk of rupture increases. \n\n\n### Embolization\n\nRarely distal embolisation from mural thrombus can lead to symptoms related to ischemia, most commonly affecting the distal extremities, such as blue toe syndrome.\n\n### Open Repair-Related Complications\n\nThose undergoing open surgical repair of an AAA have risks including:\n\n- Spinal cord ischaemia \n- Anastomotic pseudoaneurysm \n- Graft infection \n- Death (mortality during elective repair is reported to be 5% of men and 7% of women)\n\n### EVAR-Related Complications\n\nPatients who have undergone EVAR may require surveillance for EVAR-related complications. \n\n- Endoleak\n- Defined as the presence of blood flow within the aneurysm sac but outside the EVAR graft\n- Contrast-enhanced CT angiography, or contrast-enhanced ultrasound if CT is contraindicated, is used to assess for endoleak. \n- They can be repaired using open, endovascular or percutaneous intervention for endoleak \n- Post-implantation syndrome \n- Cytokine release due to EVAR can cause fever, back pain and feeling generally unwell following EVAR.\n\n# Prognosis \n\nAbdominal aortic aneurysms will continue to increase in diameter, with the ultimate outcome being rupture. However, many individuals with AAA do not rupture during their lifetimes. The rupture of AAA is fatal for many individuals. \n\nFor those who have had their AAA electively repaired before rupture, those who have had an open surgical repair tend to fare better with reduced complications and overall improved survival. \n\n\n# NICE Guidelines\n\n[NICE guidelines: Abdominal Aortic Aneurysm](https://www.nice.org.uk/guidance/ng156)\n\n\n# References\n\n[NHS Abdominal Aortic Aneurysm](https://www.nhs.uk/conditions/abdominal-aortic-aneurysm/) \n\n[NHS Inform Abdominal Aortic Aneurysm](https://www.nhsinform.scot/illnesses-and-conditions/a-to-z/abdominal-aortic-aneurysm/) \n\n[Patient Info Abdominal Aortic Aneurysms](https://patient.info/doctor/abdominal-aortic-aneurysms)",
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"question": "A 68-year-old male presents to A&E feeling generally unwell. He is unable to give a history as he is feeling light-headed. On examination, his abdomen is tender, and there is a pulsatile, expansile abdominal mass. Observations: HR 130bpm, RR 19 breaths per min, O2 saturations 98% on room air, BP 98/60mmHg, temperature 36.7. Blood tests show: \n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|121 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|1.9x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|38x10<sup>9</sup>/L|150 - 400|\n\nA CT scan is requested and he is prepared for immediate surgery.\n\n\nGiven the most likely diagnosis, which of the following will he require during his resuscitation?",
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"explanation": "Acamprosate is a medication prescribed to patients who have already successfully achieved abstinence, to prevent relapse through reducing cravings. This patient has not reached that stage yet.",
"id": "53236",
"label": "e",
"name": "Prescribe acamprosate",
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"__typename": "QuestionChoice",
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"explanation": "Patients must first be assessed by community drug and alcohol services, who will try to aid abstinence in the community. If community support fails, referral may be made for intensive rehabilitation, and so this is not the next step.",
"id": "53234",
"label": "c",
"name": "Refer to intensive rehabilitation",
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is correct because this patient is willing to quit alcohol and she needs further advice on how to do so. A GP can either refer patients to local drug and alcohol services or offer treatment at the practice. Patients who are not comfortable approaching the GP also have the option to self-refer to the local drug and alcohol service. Patient activation measures assess the knowledge, skills and confidence of patients to manage their health and has been consistently used as an outcome measure of health interventions. In this case, level 3 suggests that this patient is willing to take action, that she has good self-management skills, and feels that she is part of the healthcare team.",
"id": "53232",
"label": "a",
"name": "Referral to local community drug and alcohol services",
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"explanation": "This patient may require cognitive behavioural therapy if she has problems with her mental health in terms of mood and anxiety. However, this is not her current priority, and she seems to be managing her mental health well. Cognitive behavioural therapy referral at this stage will not directly assist her desire to overcome her addiction to alcohol, and as such does not represent the best next step.",
"id": "53235",
"label": "d",
"name": "Refer for cognitive behavioural therapy",
"picture": null,
"votes": 199
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"__typename": "QuestionChoice",
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"explanation": "Chlordiazepoxide is a short acting benzodiazepine drug used to aid alcohol detoxification since it ameliorates the side-effects of alcohol withdrawal and protects against life threatening delirium tremens. Detoxification programmes using chlordiazepoxide need careful planning with the support of local drug and alcohol services and as such the patient needs to be referred to see them first before this is commenced. Detox is usually done as an inpatient, but community detoxification programmes are being increasingly undertaken.",
"id": "53233",
"label": "b",
"name": "Prescribe chlordiazepoxide",
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"explanation": "# Summary\n\nHarmful alcohol consumption is very common in the UK, and prolonged periods of alcohol excess can lead to dependence. An important complication of alcohol dependence is acute withdrawal, when patients abruptly stop drinking or significantly reduce their alcohol consumption. Key signs and symptoms of withdrawal include agitation, tremor, nausea and vomiting, sweating and hallucinations. Seizures can occur, usually 24-48 hours after stopping drinking. Delirium tremens describes severe alcohol withdrawal characterised by delirium, haemodynamic instability and autonomic instability. Management strategies involve monitoring for symptoms of alcohol withdrawal using the CIWA scoring tool, giving a reducing course of benzodiazepines (usually chlordiazepoxide) and giving Pabrinex to prevent Wernicke-Korsakoff syndrome.\n \n\n# Definition\n \nAlcohol withdrawal is a syndrome that occurs when a patient who is alcohol dependent suddenly stops or drastically reduces their alcohol consumption. There are several stages of alcohol withdrawal that occur over the days following stopping drinking, and severity of withdrawal symptoms ranges from mild symptoms of tremor and insomnia to life-threatening manifestations such as delirium tremens or withdrawal seizures. \n \n# Epidemiology\n \n- Alcohol misuse is very common in the UK, with an estimated 24% of adults drinking in a harmful or hazardous way.\n- Around 600,000 adults in England are thought to be dependent on alcohol and so at risk of alcohol withdrawal.\n- Only 18% of these people with alcohol dependence are receiving treatment.\n- In England, there are approximately 1 million alcohol related hospital admissions per year (although alcohol withdrawal represents only a proportion of these)\n\n# Aetiology\n \nChronic alcohol excess causes tolerance to its effects, with reduced GABA and increased glutamate activity in the brain. The patient then relies on alcohol to balance this, and so when they stop drinking the imbalance manifests leading to excess glutamate and over-stimulation of the central nervous system. \n\nPatients often develop alcohol withdrawal after hospital admission as they are unable to maintain their normal intake whilst an inpatient.\n\nOther cases may occur when a patient decides to go \"cold turkey\" and stop drinking - patients should be advised to seek help to cut down on their alcohol intake safely.\n\n# Signs and Symptoms\n \nFrom 6 to 12 hours after the last drink, mild withdrawal symptoms may occur:\n\n- Insomnia\n- Tremors\n- Anxiety\n- Agitation\n- Nausea and vomiting\n- Sweating\n- Palpitations\n\nAt 12-24 hours, alcohol hallucinosis may begin:\n\n- Visual hallucinations\n- Auditory hallucinations\n- Tactile disturbances e.g. sensations of crawling bugs on the skin\n\nAlcohol withdrawal seizures are most likely to occur at 24-48 hours - these are usually generalised and tonic-clonic in nature.\n\nAt 48-72 hours, delirium tremens may occur:\n \n- Delirium and agitation\n- Hallucinations and delusions\n- Tachycardia\n- Hypertension\n- Hyperthermia\n- Diaphoresis\n- Coarse tremor\n \n# Differential Diagnosis\n\n- **Benzodiazepine withdrawal**: shares symptoms of insomnia, anxiety, tremor, sweating and nausea, and can also cause seizures; may coexist with alcohol withdrawal and is managed similarly with tapering doses of benzodiazepines. \n- **Sepsis**: can cause delirium and agitation, tachycardia and diaphoresis; hypotension is more common than the hypertension seen in severe alcohol withdrawal and patients may have focal signs of infection.\n- **Hepatic encephalopathy**: may occur in patients with decompensated cirrhosis secondary to alcohol, and has similar symptoms of tremor and confusion; ammonia will be elevated and there is often a background of chronic liver disease.\n- **Psychosis**: e.g. secondary to schizophrenia may cause similar symptoms of hallucinations, delusions and agitation.\n- **Hypoglycaemia**: causes similar symptoms of anxiety, agitation, tremor and diaphoresis; increased risk in patients who drink alcohol.\n\n# Investigations\n \n**Bedside tests:**\n\n- **ECG** - arrhythmias and other abnormalities (e.g. QT prolongation) may be seen in severe alcohol withdrawal\n- **Capillary blood glucose** for hypoglycaemia \n\n**Blood tests:**\n\n- **FBC** and **CRP** for inflammatory markers\n- **LFTs** for alcoholic liver disease\n- **U&Es** for baseline renal function and electrolytes\n- **Bone profile** and **magnesium** to monitor electrolytes for refeeding syndrome\n- **Blood cultures** if there are signs of infection\n\n**Imaging:**\n\n- **Chest X-ray** if there are signs of aspiration, especially if the patient has had a seizure or has a low GCS\n- **CT head** if evidence of head injury or ongoing seizures\n\n# Management\n \n- Patients presenting with or at risk of seizures or delirium tremens, or those who are vulnerable, frail or with significant comorbidities should be admitted for medical treatment of alcohol withdrawal\n- This involves use of the CIWA (Clinical Institute Withdrawal Assessment of Alcohol) scoring system, which is a standardised way of assessing severity of alcohol withdrawal symptoms in the following domains:\n - Nausea and vomiting\n - Tremor\n - Sweating\n - Anxiety\n - Agitation\n - Tactile disturbances\n - Auditory disturbances\n - Visual disturbances\n - Headache\n - Orientation\n- Each domain is scored from 0-7 other than orientation which is 0-4\n- A total score of 0-9 represents mild or no withdrawal, 10-19 is moderate withdrawal and > 20 is severe withdrawal\n- Higher scores warrant more frequent monitoring of symptoms\n- The CIWA score is used to guide prescription of benzodiazepines, which may be given PRN to manage withdrawal symptoms or regularly in a fixed-dose reducing regime over several days (plus PRNs when required)\n- Chlordiazepoxide is the first line benzodiazepine used, with oxazepam or lorazepam (shorter-acting benzodiazepines) being used for patients with liver disease\n- Alcohol withdrawal seizures should be treated with short acting benzodiazepines (e.g. IV lorazepam) in the first instance\n- Delirium tremens is also treated with oral lorazepam, with parenteral lorazepam or haloperidol being second line options\n- Pabrinex (1 pair of ampoules once daily) should be given to prevent Wernicke's encephalopathy - if there are signs or symptoms such as ataxia or nystagmus, give treatment dose (two pairs of ampoules TDS)\n- Monitor bloods for refeeding syndrome in malnourished patients\n- Ensure patients are followed up on discharge and referred to community support services\n\n# NICE Guidelines\n\n[NICE - Alcohol-use disorders: diagnosis and management of physical complications](https://www.nice.org.uk/guidance/cg100/)\n \n[NICE CKS - Alcohol Withdrawal](https://cks.nice.org.uk/topics/alcohol-problem-drinking/management/alcohol-misuse/)\n \n# References\n\n[BNF - Alcohol Dependence](https://bnf.nice.org.uk/treatment-summaries/alcohol-dependence/) \n\n[RCEM Learning - Acute Alcohol Withdrawal](https://www.rcemlearning.co.uk/reference/acute-alcohol-withdrawal/)\n\n[Patient UK - Acute alcohol withdrawal and delirium tremens](https://patient.info/doctor/acute-alcohol-withdrawal-and-delirium-tremens)",
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"question": "A 37-year-old female presents to the GP concerned about her recent diagnosis of liver cirrhosis secondary to chronic alcoholism. Her past medical history includes moderate depression and chronic fatigue syndrome. She is managing both conditions well. However, she does not have any support at home or at work and she lives alone. Her GP conducts a motivational interview and concludes that she is keen to quit alcohol but she is unsure about how to do this. Her GP measures her patient activation level as 3.\n\nWhich of the following is the next best step in the management of this patient?",
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"explanation": "Annual l follow-up is required if the testes descend after 3 months but remain retractile since there is a risk of the testes ascending over time. This baby needs follow up at 3 months to see if the testicles have descended or not; by then, the child will be 4-5 months of age, and if the testicle hasn't persisted, will warrant referral to a urologist for review, as per NICE guidelines.",
"id": "53270",
"label": "d",
"name": "Annual follow-up",
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"explanation": "Urological surgery may be warranted if the testis remains undescended by 6 months. Unilateral undescended testis is common and usually resolves spontaneously within the first 3-6 months of life. Therefore, urological review is not required at this stage or urgently. This baby needs follow up at 3 months to see if the testicles have descended or not; by then, the child will be 4-5 months of age, and if the testicle hasn't persisted, will warrant referral to a urologist for review, as per NICE guidelines.",
"id": "53271",
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"name": "Refer to urology routinely",
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"__typename": "QuestionChoice",
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"explanation": "Urological surgery may be warranted if the testis remains undescended by 6 months. Unilateral undescended testis is common and usually resolves spontaneously within the first 3-6 months of life. Therefore, urological review is not required at this stage or urgently.",
"id": "53269",
"label": "c",
"name": "Refer urgently to a senior urologist within 2 weeks",
"picture": null,
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"__typename": "QuestionChoice",
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"explanation": "Bilateral undescended testes may represent a serious underlying endocrinological or developmental abnormality, such as congenital adrenal hyperplasia, and as such the NICE guidelines suggest urgent review within 2 weeks by a paediatrician.",
"id": "53268",
"label": "b",
"name": "Refer urgently to a senior paediatrician within 2 weeks",
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"explanation": "This newborn has a unilateral undescended testicle which has been noted on the 8-week baby check up. This is a common presentation at the baby check with around 1/25 boys being born with undescended testicles. In most instances, these will descend naturally during the first 3-6 months of life, and no treatment will be required. Therefore, at this stage, follow up in 3 months is all that is required. If undescended by 6 months, then it is unlikely they will descend spontaneously, and as such surgery is warranted, ideally before the child reaches 12 months of age. Referral is usually done around 4-5 months of age if the testicles are undescended, in order to minimise delays. Note that by the first year of life, 2/3 of undescended testes resolve spontaneously. Note that undescended testes are a big risk factor for testicular tumours which are identified as an inguinal lump later on in life.",
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"explanation": "# Summary\n\nUndescended testes, or cryptorchidism, is a condition present at birth where one or both of the male testes have not descended into the scrotum prior to birth. It occurs in about 1-4.5% of term and 30-45% of premature newborns, with around two-thirds spontaneously descending by the first year of life. Key symptoms include the absence of one or both testes in the scrotum. Orchidopexy is a common treatment, and management strategies depend on whether the condition is unilateral or bilateral. Management of this condition is important as undescended testes are a risk factor for testicular cancer.\n\n# Definition\n\nCryptorchidism, or undescended testes, is a congenital condition in which one or both of the testes fail to descend into the scrotum before birth.\n\n# Epidemiology\n\nCryptorchidism is present in approximately 1-4.5% of term newborns and about 30-45% of premature newborns. By the first year of life, around two-thirds of these cases will have spontaneously descended.\n\n# Aetiology\n\nThe exact cause of cryptorchidism is unknown, but it is thought to be multifactorial, with genetic, maternal, and environmental factors potentially playing roles. Maternal factors may include alcohol consumption, smoking, and exposure to certain medications during pregnancy. Cryptorchidism is also more common in premature and low birth weight infants.\n\n# Signs and Symptoms\n\nThe primary sign of cryptorchidism is the absence of one or both testes in the scrotum. This can often be identified during a physical examination.\n\n# Differential Diagnosis\n\nWhen considering cryptorchidism, other conditions that may present with similar symptoms include:\n\n- **Retractile testes:** The testes may be in the scrotum at times but can retract into the inguinal canal when the cremaster muscle contracts. Key signs include the ability to manipulate the testes into the scrotum and staying in place at least temporarily.\n- **Inguinal hernias:** These present with a palpable mass in the inguinal region which can increase in size with crying or straining. They are often associated with discomfort or pain.\n- **Ectopic testes:** This condition is characterized by testes that have deviated from the normal path of descent and are located in abnormal positions, such as the perineum or femoral region.\n\n# Investigations\n\nThe initial investigation of cryptorchidism involves a thorough physical examination. In some cases, further investigations like ultrasound or MRI may be considered, especially in cases of non-palpable testes. Hormonal testing may also be needed in certain cases.\n\n# Management\n\nThe primary management of cryptorchidism is surgical, with the most common procedure being orchidopexy, a surgery designed to bring the undescended testes into the scrotum.\n\nManagement strategies vary depending on whether the condition is unilateral or bilateral:\n\n- For undescended testes that are **bilateral** at birth, an urgent referral to a senior paediatrician within 24 hours is needed for potential endocrine or genetic investigation (e.g. congenital adrenal hyperplasia, or CAH). If these conditions are ruled out and the testes remain undescended by 3 months, the child should be referred to surgeons by 6 months of age.\n- For undescended testes that are **unilateral** at birth, arrange a review at 6-8 weeks of age. If the testis remains undescended at the 3-month review, re-examine at 4-5 months\n- At 4–5 months (corrected for gestational age), if the testis remains undescended, arrange referral to paediatric surgery or urology for specialist management depending on local referral pathways, to be seen by 6 months of age\n- The British Association of Paediatric Surgeons (BAPS) recommends that if orchidopexy is indicated, it should be performed around 12 months of age\n\n\n# NICE Guidelines\n\n[NICE CKS - Undescended Testes](https://cks.nice.org.uk/topics/undescended-testes/)\n",
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"question": "An 8-week-old baby boy presents to the GP with his father for his baby check. He is currently feeding well, opening his bowels and passing urine. There are no concerns regarding his growth and development as he is following the centiles adequately. On examination, he is fixing and following objects and smiling at his dad. The GP notices that he has a right unilateral undescended testicle.\n\nWhich of the following is the next best step in the management of this patient?",
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"explanation": "This is incorrect because she has a CURB-65 score of 2. Patients with a score of 0 or 1 can be discharged for management within the community with oral antibiotics, such as amoxicillin (or doxycycline/clarithromycin if there is a penicillin allergy.) This patient also requires intravenous fluids due to the hypotension.",
"id": "53283",
"label": "b",
"name": "Discharge with a 5 day course of oral antibiotics",
"picture": null,
"votes": 204
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect because ITU admission is considered for patients with a CURB-65 score of 3 and above. This is because they are likely to require close monitoring, inotropic, or vasopressor support. The outreach team in the hospital are useful points of contact for patients who are critically unwell. This patient doesn't currently display any need for ITU support; she is slightly hypotensive but a trial of intravenous fluids will be needed in the first instance, and her hypoxia is likely correctible with a small amount of oxygen therapy.",
"id": "53284",
"label": "c",
"name": "Contact the outreach team and consider ITU admission",
"picture": null,
"votes": 404
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"__typename": "QuestionChoice",
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"explanation": "This is incorrect because this patient should not be discharged home unless they are clinically well and have a CURB-65 score of 0 or 1. It is important to give all patients correct safety netting if they go home, however this patient needs IV antibiotics and fluids and has a confirmed source of infection, which needs treatment.",
"id": "53285",
"label": "d",
"name": "Discharge patient with safety netting advice",
"picture": null,
"votes": 7
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"__typename": "QuestionChoice",
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"explanation": "This is the correct answer because this patient has community-acquired pneumonia and a CURB-65 score of 2 for confusion and systolic blood pressure <90mmHg. The CURB-65 score is used to guide management and prognosticate in community acquired pneumonia. Pneumonia typically presents as shortness of breath, productive cough, pleuritic chest pain, and fever. On examination, you can hear focal coarse inspiratory crepitations. This patient should be admitted as she will need IV antibiotics and fluids, which she cannot have within the community.",
"id": "53282",
"label": "a",
"name": "Admit patient to the medical ward and start intravenous antibiotics",
"picture": null,
"votes": 2386
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect because DOACs are not the correct treatment for community-acquired pneumonia. DOACs are the correct treatment for a pulmonary embolism, which could present in a similar manner. However, given the chest X-ray findings, the clinical presentation is better explained by a pneumonia at this moment.",
"id": "53286",
"label": "e",
"name": "Admit patient to the medical ward and start a direct oral anti-coagulant (DOAC)",
"picture": null,
"votes": 30
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"__typename": "QuestionComment",
"comment": "Am I being thick why is here creatinine on the floor?",
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"comment": "Shush AD",
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"comment": "idk bro she seems septic to me..id still be checking in with ITU just in case",
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"explanation": "# Summary\n\n\nPneumocystis Pneumonia (PCP) is a fungal infection caused by _Pneumocystis Jirovecii_ that affects immunocompromised patients. Key symptoms include fever, a dry cough, and exertional breathlessness. Desaturation on exertion is characteristic of PCP pneumonia. Chest X-ray may be normal or show bilateral infiltrates, and a definitive diagnosis is reached with either sputum samples or bronchoscopy with bronchoalveolar lavage. Management involves antibiotics, usually co-trimoxazole as the first line treatment, with steroids added for more severe cases.\n\n\n# Definition\n\n\nPneumocystis Pneumonia (PCP) is an infection caused by the fungus _Pneumocystis Jirovecii_. It usually affects patients who are immunocompromised, for example patients with late-stage HIV or those on immunosuppressant medications after an organ transplant.\n\n\n# Epidemiology\n\n\nIn the UK, rates of PCP are falling in patients with HIV due to improvements in antiretroviral therapies. However, there has been an increase in PCP in patients immunosuppressed for other reasons (such as transplant or haematological malignancies). Currently around half of patients with PCP have HIV and half do not.\n\n\nPatients at risk of PCP should be treated with prophylaxis (usually oral co-trimoxazole) - this includes all patients with HIV with a CD4 count of below 200. \n\n\n# Aetiology\n\n\nPCP is caused by _Pneumocystis Jirovecii_, a fungus that causes pulmonary infections. Patients at risk of PCP are those who are immunocompromised (it is classed as an opportunistic infection, and an AIDS-defining illness in those with HIV). \n\n\nRisk factors include:\n\n\n- HIV with a CD4 count below 200\n- Steroids or other immunosuppressive medications\n- Previous organ transplant\n- Congenital immunodeficiencies (e.g. hypogammaglobulinaemia)\n- Severe malnutrition\n- Comorbid lung disease\n- Haematological malignancies\n\n\n# Signs and Symptoms\n\n\n- Fever\n- Dry cough\n- Exertional breathlessness\n- Chest pain\n\n\nOn examination, the chest may be clear, or end-inspiratory crackles and wheeze may be present.\n\n\n# Differential Diagnosis\n\n\n- Bacterial or viral pneumonia: similar symptoms, more likely to have a productive cough.\n- Tuberculosis: chronic cough, haemoptysis, weight loss, night sweats and fever. \n- Pulmonary embolism: less likely to have fevers, dry cough and shortness of breath on exertion typical, may have haemoptysis.\n\n\n# Investigations\n\n\n**Bedside tests include:**\n\n\n- Oxygen saturations on exertion \n- Arterial blood gas for hypoxia, important to grade severity and determine if steroids are indicated\n- Sputum samples (may need to be induced e.g with saline nebulisers): **silver staining** is used to confirm the diagnosis of PCP (shows a characteristic Mexican hat appearance), also send sputum for routine and mycobacterial culture (to rule out TB or other infections)\n\n\n**Blood tests include:**\n\n\n- Routine bloods for FBC and CRP (looking for infection markers) and baseline liver and renal function prior to starting antibiotics\n- HIV testing\n- CD4 count if HIV positive\n\n\n**Imaging includes:**\n\n\n- Chest X-ray: often shows bilateral hilar interstitial infiltrates, however 10% have a normal chest X-ray.\n- High-resolution CT scan: if chest X-ray is normal and PCP is suspected, a high-resolution CT is more sensitive.\n\n\n**Other investigations:**\n\n\n- Bronchoscopy with bronchoalveolar lavage: if sputum samples are negative, this is the definitive investigation to gain a respiratory sample for staining. \n\n\n[lightgallery]\n\n\n# Management\n\n\n- Supportive treatment with analgesia, oxygen if hypoxic, consider holding immunosuppressant treatment (with liaison with specialist teams as needed)\n- Patients with mild disease (only mild changes on CXR, normal oxygen saturations) can be treated as outpatients; moderate and severe cases should be admitted\n- High dose co-trimoxazole is the primary treatment\n- Alternative therapies if co-trimoxazole is contraindicated or not tolerate include: atovaquone, dapsone with trimethoprim or pentamidine. \n- Steroids should be given in all patients with moderate or severe PCP (i.e.PaO2<11kPa) - either oral prednisolone or IV hydrocortisone. \n\n\n# NICE Guidelines\n\n\n[NICE CKS - HIV infection and AIDS](https://cks.nice.org.uk/topics/hiv-infection-aids/)\n\n\n# References\n\n\n[Patient UK - Pneumocystis Jirovecii Pneumonia](https://patient.info/doctor/pneumocystis-jirovecii-pneumonia)\n\n\n[BNF treatment summary - Pneumocystis Pneumonia](https://bnf.nice.org.uk/treatment-summary/pneumocystis-pneumonia.html)",
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"learningPoint": "A CURB-65 score of 2 or higher indicates a moderate risk of mortality in pneumonia patients, suggesting that management should include hospital admission, and treatment with intravenous antibiotics and supportive care",
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"question": "A 52-year-old female presents to A&E with her partner as he has concerns regarding a recent change in behaviour. He reports she has been confused at home for the past 2 days. She is unable to give a history. Observations: HR 95bpm, RR 21, O2 saturation 93% on room air, BP 89/65mmHg, temperature 38.1. On examination, she has coarse inspiratory crackles at the right base. Her blood test results show the following:\n\n||||\n|-------|:-------:|-------|\n|Sodium|145 mmol/L|135 - 145|\n|Potassium|3.6 mmol/L|3.5 - 5.3|\n|Urea|6.5mmol/L|2.5 - 7.8|\n|Creatinine|21 µmol/L|60 - 120|\n\n\nA chest radiograph demonstrates right lower zone airspace opacification with air bronchograms.\n\n\nWhich of the following is the next best step in management?",
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"explanation": "This is incorrect because primary polycythaemia is due to the spontaneous proliferation of red blood cells in the bone marrow. This is less likely, though is an important differential, given the normal platelet and white cell count, which are also usually deranged in polycythaemia rubra vera, and an otherwise clear and logical explanation ie. chronic hypoxia in COPD. There is also no history of itching on hot baths, which is more likely in polycythaemia rubra vera.",
"id": "53288",
"label": "b",
"name": "Primary polycythaemia",
"picture": null,
"votes": 329
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"__typename": "QuestionChoice",
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"explanation": "Blood tests show a raised haemoglobin, which is suggestive of polycythaemia. This patient has got a disorder (COPD) leading to chronic hypoxia, and as a result has developed secondary polycythaemia. Primary polycythaemia, such as polycythaemia rubra vera, indicates a primary bone marrow disorder, and given the normal platelet and white cell count values, this is less likely, though an important differential. There is also no history of itching on hot baths, which is more likely in polycythaemia rubra vera. It is important to note that a pO2 of <7.3 is the usual criteria for LTOT, but between 7.3-8 he would qualify if he had complications related to chronic hypoxia, such as polycythaemia. He would now most likely fuflfil LTOT criteria, and referral back to the LTOT service will be indicated. Symptoms of polycythaemia include dizziness and fatigue.",
"id": "53287",
"label": "a",
"name": "Secondary polycythaemia",
"picture": null,
"votes": 2796
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Myelofibrosis presents with constitutional symptoms such as fatigue, weight loss, fever, and night sweats, alongside splenomegaly. Blood tests show potential pancytopenia due to bone marrow failure secondary to fibrosis, which usually results in dry taps during bone marrow aspiration. Blood film findings are tear-drop poikilocytes.",
"id": "53289",
"label": "c",
"name": "Myelofibrosis",
"picture": null,
"votes": 68
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"__typename": "QuestionChoice",
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"explanation": "Essential thrombocythaemia is a myeloproliferative disorder characterised by an increased number of platelets in the blood. This patient's platelet levels are within the normal range. It is associated with proliferation of megakaryocytes (platelet precursors.)",
"id": "53291",
"label": "e",
"name": "Essential thrombocythaemia",
"picture": null,
"votes": 89
},
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"__typename": "QuestionChoice",
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"explanation": "Patients with CLL are usually diagnosed incidentally after finding a raised white cell count, and specifically lymphocytes, on blood tests. The white cell count is normal in this patient. Patients with CLL may present with lymphadenopathy, hepatosplenomegaly, and constitutional symptoms. It is important to remember the blood film finding for CLL which can show smudge cells as they become damaged due to the lack of a cytoskeletal protein.",
"id": "53290",
"label": "d",
"name": "Chronic lymphocytic leukaemia",
"picture": null,
"votes": 54
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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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"comment": "Could the subcutaneous painless nodules not be Janeway lesions (i.e. supportive of endocarditis)?",
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"comment": "May be being pedantic but think the question may benefit from some rephrasing: \"Which clinical sign is most likely to be seen in this patient?\". \n\nThe question asks for the a specific sign for the diagnosis. The diagnosis is infective endocarditis, not aortic regurgitation (which has other causes).",
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"explanation": "# Summary\r\n\r\nInfective endocarditis (IE) is a rare infection of the inner surface of the heart (endocardium), usually the valves. Various risk factors contribute to its development, including age, sex, intravenous drug use, poor dentition, valvular disease, congenital heart disease, prosthetic valves, and certain medical conditions like HIV. Symptoms can be diverse and non-specific including fevers, night sweats, weight loss, and myalgia. Diagnosis is based on the modified Duke Criteria, which include major and minor criteria. Treatment involves prolonged courses of intravenous antibiotics, and surgical intervention may be necessary in certain cases. Complications can be severe, and without appropriate treatment, IE can lead to heart failure and death. Prevention through antibiotic prophylaxis is no longer recommended.\r\n\r\n# Definition \r\n\r\nInfective endocarditis (IE) is the infection of the inner surface of the heart (endocardium), usually the valves. \r\n\r\n# Epidemiology \r\n\r\nInfective endocarditis is a rare disease, impacting approximately 2-6 per 100,000 people every year. There are many risk factors implicated in the development of IE. \r\n\r\nRisk factors for IE: \r\n\r\n* Age >60 years\r\n* Male sex\r\n* IVDU: predisposition to _Staph. aureus_ infection and right-sided valve disease e.g. tricuspid endocarditis.\r\n* Poor dentition and dental infections\r\n* Valvular disease: rheumatic heart disease, mitral valve prolapse, aortic valve disease and any other valvular pathology. \r\n* Congenital heart disease: bicuspid aortic valve, pulmonary stenosis, and ventricular septal defects.\r\n* Prosthetic valves\r\n* Previous history of infective endocarditis\r\n* Intravascular devices: central catheters and shunts.\r\n* Haemodialysis\r\n* HIV infection\r\n\nAntibiotics have previously been prescribed to at-risk patients undergoing interventional procedures, frequently in dentistry, with the rationale that resultant bacteraemia could threaten to cause infective endocarditis. However, the evidence for this is inconclusive, and **NICE therefore do not advise antibiotic prophylaxis for IE.**\r\n\r\n# Pathophysiology\r\n\r\nA damaged endocardium can contribute to the development of IE. When part of the endocardium is damaged, the heart valve forms a local blood clot known as non-bacterial thrombotic endocarditis (NBTE). The platelets and fibrin deposits that form as part of the clotting process allows bacteria to stick to the endocardium leading to the formation of vegetations. The valves do not have a dedicated blood supply and so the body is unable to launch an appropriate immune response to the vegetations. The combination of damaged endocardium, vegetation development, and lack of an appropriate immune response results in infective endocarditis. \r\n\r\n# Classification \r\n\r\nIE can be considered according to different classification systems. \r\n\r\n## Acute vs. Subacute vs. Chronic IE \r\n\r\nIE can be considered according to duration of symptoms. \r\n\r\n* *Acute IE*: patient has signs or symptoms for days up to 6 weeks. Theoretically, a fulminant illness with rapid progression and so is most likely due to *S.aureus* infection. \r\n* *Subacute IE*: patients has signs or symptoms for 6 weeks up to 3 months. \r\n* *Chronic IE*: patients has signs or symptoms that persist for longer than 3 months. \r\n\r\n## Valve Type \r\n\r\nIE can be considered according to the type of valve involved. \r\n\r\n- *Native-valve endocarditis*: patient without prosthetic valve implant. \r\n- *Prosthetic-valve endocarditis*: \r\n\t- Early prosthetic valve endocarditis occurs within 1 year of surgery. This is usually due to intra-operative contamination or post-operative nosocomial contamination. \r\n\t- Late prosthetic valve endocarditis occurs beyond 1 year of surgery. This is usually due to community-acquired infections. \r\n\r\n# Common organisms \r\n\r\nThe most common organisms involved in infective endocarditis (in order of incidence) are:\r\n\r\n* _Staph. aureus_: now the most common cause of IE. Coagulase positive.\r\n* _Strep. viridans_: used to be the most common cause of IE. Implicated in patients with poor dental hygiene. \r\n* Enterococci\r\n* Coagulase negative _staphylococci_ e.g. _staph. epidermidis_: common culprit of prosthetic valve endocarditis. \r\n* _Strep. bovis_: important link with colorectal cancer. Need to consider colonoscopy and biopsy in these patients.\r\n* Fungal \r\n* HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella): culture negative causes of IE. \r\n* Non-infective: marantic endocarditis (malignancy - pancreatic cancer), Libman-Sacks endocarditis (SLE). \r\n\r\n# Symptoms\r\n\r\nClinical features of IE are diverse and variable. It may present acutely with a rapid deterioration or it can present subacutely/chronically with non-specific symptoms. \r\n\r\n* Common presenting symptoms: \r\n\t* Fever: most common symptom. \r\n\t* Night sweats \r\n\t* Anorexia \r\n\t* Weight loss \r\n\t* Myalgia\r\n\r\n* Others: \r\n\t* Headache \r\n\t* Arthalgia\r\n\t* Abdominal Pain \r\n\t* Cough \r\n\t* Pleuritic pain \r\n\r\n# Signs\r\n\r\n**Systemic signs**: \r\n\r\n* Febrile \r\n* Cachectic \r\n* Clubbing\r\n* Splenomegaly \r\n\r\n**Cardiac**: \r\n\r\n* Murmur: fever + new murmur is infective endocarditis until proven otherwise. \r\n* Bradycardia: aortic root abscess tracks down to the AVN causing heart block. \r\n\r\n**Vascular phenomena**: \r\n\r\n* Septic emboli: abdominal pain due to splenic infarct/abscess, focal neurology due to stroke, gangrenous fingers. \r\n* Janeway lesions: painless haemorrhagic cutaneous lesions in the palms and soles. \n* Splinter haemorrhages\r\n\r\n**Immunological phenomena**: due to immune-complex deposition. \r\n\r\n* Osler's nodes: painful pulp infarcts on end of fingers. \r\n* Roth spots: boat-shaped retinal haemorrhages with pale centres seen on fundoscopy. \r\n* Glomerulonephritis: identified on urine dip. \r\n\r\n# Differential Diagnoses\r\n\r\n* Non-infectious endocarditis/Nonbacterial thrombotic endocarditis (NBTE)\r\n\t* Similarities: both present with new murmurs and both may have constitutional symptoms including fevers and weight loss. \r\n\t* Differences: blood cultures will likely be positive in infective endocarditis and may identify microorganisms that are commonly associated with IE. NBTE is often associated with advanced malignancy (pancreatic cancer and marantic endocarditis), SLE (Libman Sacks endocarditis) or hypercoagulable states and will not have positive blood cultures. \r\n\r\n* Rheumatic Fever\r\n\t* Similarities: may both present with similar symptoms including fever, heart murmur and joint pain. \r\n\t* Differences: rheumatic fever is an autoimmune response triggered by a Group A strep infection and ASOT titres may be high. In comparison, infective endocarditis will likely have positive blood cultures that identify a particular micro-organism. \r\n\r\n\r\n# Modified Duke Criteria \r\n\r\nFor the diagnosis of IE, the modified Duke Criteria needs to be followed. \r\n\r\nA useful mnemonic to remember the criteria is **'BE FIVE PM'**:\r\n\r\n* Major Criteria: \r\n\t* **B**lood Cultures\r\n\t* **E**vidence of Endocardial Involvement: **E**cho\r\n\r\n* Minor Criteria: \r\n\t* **F**ever\r\n\t* **I**mmunological phenomena\r\n\t* **V**ascular phenomena\r\n\t* **E**chocardiogram minor criteria\r\n\t* **P**redisposing features\r\n\t* **M**icrobiological evidence that does not meet major criteria. \r\n\r\nFor a definitive diagnosis of IE two major criteria, or one major and three minor criteria, or all five minor criteria must be present. \r\n\r\n## Major Criteria \r\n\r\n**Blood culture positive for IE**\r\n\r\n* 2x separate positive blood cultures showing typical microorganisms consistent with IE (S viridans, S bovis, HACEK organisms, enterococcus). \r\n* Persistent bacteraemia with 2x blood cultures >12 hours apart or =>3 positive blood cultures with less specific microorganisms (S.aureus or S. epidermidis). \r\n* Single positive blood culture for Coxiella burnetti or positive antibody titre\r\n\r\n**Evidence of endocardial involvement with imaging positive for IE**\r\n\r\n* Echocardiogram (1st line TTE, then TOE) demonstrating vegetation, abscess, partial dehiscence of prosthetic valve or new valvular regurgitation. \r\n* Abnormal activity around site of prosthetic valve implantation on PET-CT\r\n* Paravalvular lesions on cardiac CT\r\n\r\n## Minor Criteria \r\n\r\n* **Fever**: >38.0 degrees celsius. \r\n* **Immunological phenomena**: Roth spots, Olser's nodes, immune complex-mediated glomerulonephritis, positive rheumatoid factor.\r\n* **Vascular phenomena**: Evidence of septic embolis (splenic infarct/abscess), Janeway lesions, conjunctival haemorrhages, mycotic aneurysm, intracranial haemorrhage. \r\n* **Echocardiogram minor criteria**: not meeting above criteria. \r\n* **Predisposing features**: known valvular disease, IVDU, prosthetic valves etc. \r\n* **Microbiological evidence that does not meet major criteria**: blood culture not meeting major criteria, or serological evidence of active infection with organism consistent with IE\r\n\r\n# Investigations\r\n\r\nBedside:\r\n\r\n- **ECG**: increasing prolongation of PR interval suggests development and worsening of aortic root abscess. \n- **Urine dip**: look for haematuria which may suggest development of glomerulonephritis. \r\n\r\nBlood tests:\r\n\r\n- **Routine bloods**: significant elevation of inflammatory markers and acute phase response is in line with infective endocarditis. If subacute/chronic process there may be a normocytic anaemia. \r\n- **Blood cultures**: required as per the modified Duke criteria. At least 3 sets of blood cultures taken at different times and sites. \r\n\r\nImaging:\r\n\r\n- **Echocardiogram**: \r\n\t* **1st line**: transthoracic echocardiogram \r\n\t* **2nd line**: transoesophageal echocardiogram; more invasive, but better view of mitral valve lesions and aortic root abscesses. It is the most sensitive diagnostic test. \r\n- **PET CT**: used to look for evidence of septic emboli. \r\n\r\n# Management\r\n\r\n## Medical \r\n\r\nMainstay of treatment for infective endocarditis is a prolonged course of IV antibiotics (approximately 6/52). Patients commonly require midline insertion to enable administration of IV antibiotics long-term. \r\n\r\nExamples of antibiotic choice demonstrated below: \r\n\r\n**Blind Therapy** when the organism and sensitivities are not yet known: \r\n\r\n* Native valve: amoxicillin (+/- gentamicin) \r\n* Pen-allergy/MRSA: vancomycin (+/- gentamicin) \r\n* Prosthetic valve: vancomycin + rifampicin + gentamicin \r\n\r\n**Native Valve S. aureus IE**\r\n\r\n* 1st line: flucloxacillin \r\n* 2nd line: vancomycin + rifampicin \r\n\r\n**Prosthetic Valve S. aureus IE**\r\n\r\n* 1st line: flucloxacillin + rifampicin + gentamicin \r\n\r\n\r\n**Strep viridans IE**\r\n\r\n* 1st line: benzylpenicillin \r\n* 2nd line: vancomycin + gentamicin \r\n\r\n**HACEK IE**: 1st line: ceftriaxone \r\n\r\n## Surgical \r\n\r\nDespite the main-stay of treatment for IE being medical management. The following scenarios are indications for surgical intervention: \r\n\r\n* Haemodynamic instability\r\n* Severe heart failure\r\n* Severe sepsis despite antibiotics/failed medical therapy\r\n* Valvular obstruction\r\n* Infected prosthetic valve\r\n* Persistent bacteraemia\r\n* Repeated emboli\r\n* Aortic root abscess\r\n\r\n**Common exam question**: PR interval prolongation in a patient with Infective Endocarditis is an indication for surgery as it can be secondary to aortic root abscess\r\n\r\n# Complications\r\n\r\nComplications of infective endocarditis can also be the initial presenting complaint\r\n\r\n* Acute valvular insufficiency causing heart failure\r\n* Neurologic complications e.g. stroke, abscess, haemorrhage (mycotic aneurysm)\r\n* Embolic complications causing infarction of kidneys, spleen or lung\r\n* Infection e.g. osteomyelitis, septic arthritis\r\n\r\n\r\nWithout timely and appropriate treatment, IE can rapidly lead to heart failure and death. The mortality rate within the first 30 days has been estimated at approximately 20%. Long-term survival for IE has been estimated at 50% at 10 years. The mortality in IE remains high. \r\n\r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines on Prophylactic Antibiotics in IE](https://www.nice.org.uk/guidance/cg64/ifp/chapter/infective-endocarditis)\r\n\r\n# References \r\n\n[American Heart Association Summary on Heart Valves and Endocarditis](<https://www.heart.org/en/health-topics/heart-valve-problems-and-disease/heart-valve-problems-and-causes/heart-valves-and-infective-endocarditis#:~:text=What%20is%20infective%20endocarditis%3F,greater%20risk%20of%20developing%20it.>)",
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"question": "A 34-year-old woman presents to A&E with a three day history of fevers and joint pains. She denies any unwell contacts. She has a history of intravenous drug use but no other past medical history. Her vital signs are: HR 101bpm, RR 17 breaths per minute, O2 saturations of 98% on air, BP 157/61mmHg, and temperature 39.5. On examination, there is an early diastolic murmur on auscultation of the aortic area.\n\nWhich of the following clinical signs is specific to his diagnosis?",
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"explanation": "This is incorrect because this patient's blood pressure is greater than his target, and so his antihypertensive management requires escalation. He is already on maximum dose amlodipine and continuing this is unlikely to achieve his target.",
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"explanation": "Beta-blockers are used in the management of hypertension after conventional therapies - ACEi, calcium channel blockers, and thiazide-like diuretics - have been considered. It is a 4th line agent, alongside spironolactone and alpha-blockers; spironolactone is used when the potassium is <4.5, and a beta-blocker/alpha-blocker >4.5. Side effects of atenolol include vivid dreams, erectile dysfunction, and fatigue.",
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"explanation": "Anti-hypertensives should only be discontinued if they produce unwanted side effects or if the patient refuses to take them, since adding additional agents is more likely to produce better control than substituting with novel agents. Indapamide is a thiazide-like diuretic which is used after calcium channel blockers and ACEi as a third step. Common side effects of indapamide include hyperuricaemia, postural hypotension, and hypokalaemia.",
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"explanation": "This is the correct answer because this patient is already taking amlodipine hence the next step in management is to add an ACE-inhibitor such as ramipril. Step 2 in the management of hypertension involves combining an ACE-inhibitor with a calcium channel blocker. The blood pressure target for this patient (an adult under 80) should be 140/90mmHg in clinic and 135/85mmHg at home. Remember common side effects of ACE-inhibitors such as a dry cough, delayed angioedema, and a dry mouth.",
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"explanation": "Nifedipine is another dihydropyridine calcium channel blocker like amlodipine. It is unlikely he will respond to this when he has not responded to amlodipine, and the two would not be prescribed together. The next step is therefore to add an ACEi.",
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"comment": "isn't add in an ACEi/ARB OR a thiazide-like duiretic on the flowchart?\n",
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"explanation": "# Summary\r\n\r\nPrimary hypertension, accounting for approximately 90-95% of cases of hypertension, is characterised by persistently elevated blood pressure due to age-related pathophysiological changes. It is a major risk factor for cardiovascular disease, cerebrovascular disease, chronic kidney disease, and peripheral vascular disease. Diagnosis is based on ambulatory blood pressure monitoring (ABPM) readings of 135/85mmHg or higher. Classification is determined by the severity of the hypertension. Management depends on the classification of the hypertension and involves lifestyle modifications and pharmacological anithypertensives according to NICE guidelines. Effective management, through lifestyle changes and medications, significantly reduces the associated risks and improves outcomes for individuals with hypertension.\r\n\r\n# Definition \r\n\r\nA 'normal' blood pressure ranges between 90/60mmHg to 140/90mmHg. The definition of hypertension is a 24h ambulatory blood pressure average reading (ABPM) that is more than or equal to 135/85mmHg. \r\n\r\n# Epidemiology\r\n\r\nIn 2015, it was reported that high blood pressure affected more than 1 in 4 adults in England (31% of men; 26% of women). In England, it is estimated that primary hypertension affects around 13.5 million people and contributed to 75,000 deaths.\r\n\r\n# Pathophysiology\r\n\r\nPrimary hypertension is as a result of a series of complex physiological changes as we age. Hypertension often occurs as a result of reduced elasticity of large arteries, age-related and atherosclerosis-related calcification, and degradation of arterial elastin. It may also be present in conditions associated with increased cardiac output, such as anaemia, hyperthyroidism and aortic regurgitation.\r\n\r\nAlthough the risk of cardiovascular disease increases progressively with increasing systolic and diastolic blood pressure, raised systolic pressure is more important than raised diastolic pressure as a risk factor for cardiovascular and renal disease.\r\n\r\n# Classification \r\n\r\nHypertension can be classified according to how high a patient's blood pressure is. \r\n\r\n* Stage 1: Clinic => 140/90mmHg; ABPM => 135/85mmHg \r\n* Stage 2: Clinic => 160/100mmHg; ABPM =>150/95mmHg \r\n* Stage 3: Clinic systolic BP (SBP) => 180 or diastolic BP (DBP) =>120mmHg\r\n\r\n\r\n# Symptoms and Signs\r\n\r\nHypertension, unless malignant, is asymptomatic and does not have any clinical signs. It is diagnosed with ABPM and further investigations should focus on diagnosing end-organ complications of hypertension. \r\n\r\n# Investigations\r\n\r\n[lightgallery]\r\n\r\n* Hypertensive patients are commonly first identified at GP appointments or during hospital admissions. Due to the prominence of 'white coat hypertension', ABPM is now required for the diagnosis of hypertension. \r\n* Hypertension should be suspected in a patient who has a clinic blood pressure of =>140/90mmHg. \r\n* **1st line: ABPM** or home blood pressure monitoring if ABPM is not tolerated or declined. \r\n* Alongside ABPM: assessment for end-organ damage and assessment of cardiovascular risk (QRISK2 scores). \r\n * Urine dip and albumin:creatinine level\r\n * Blood glucose, lipids and renal function\r\n * Fundoscopy for evidence of hypertensive retinopathy\r\n * ECG: look for evidence of LV hypertrophy\r\n\r\n\r\nN.B. if presentation is suspicious for secondary hypertension refer and investigate as appropriate (see section). \r\n\r\nN.B. Referral for same-day specialist assessment should be arranged for people with: \r\n\r\n* Clinic blood pressure of 180/120mmHg and higher with signs of retinal haemorrhage or papilloedema (accelerated hypertension) or life-threatening symptoms (e.g. new onset confusion, chest pain, heart failure signs or AKI). \r\n\r\n# Management\r\n\r\n## Principles of Management \r\n\r\n### Conservative Management \r\n\r\nControlling risk factors for cardiovascular disease:\r\n\r\n* Weight loss\r\n* Healthy diet (reduce salt and saturated fats)\r\n* Reduce alcohol and caffeine\r\n* Reduce stress\r\n* Stop smoking\r\n\r\n### Medical Management\r\n\r\nIndications to start pharmacological management of primary hypertension:\r\n\r\n* Stage 1 hypertensive patients who are <80 years old with end organ damage, CVS disease, renal disease, diabetes or 10-year CVS risk >10% OR\r\n* Anyone with stage 2 hypertension\r\n\r\n### 2019 NICE Guidelines for Pharmacological Management of Primary Hypertension \r\n\r\n[lightgallery1]\r\n\r\n* Step 1: \r\n\t* **ACE-inhibitor** (e.g. Ramipril) if <=55 years old\r\n\t* **DHP-Calcium Channel Blocker** (e.g. Amlodipine) if >55 years old OR African or Caribbean ethnicity\r\n\t* If unable to tolerate ACE-inhibitor then switch to _Angiotensin Receptor Blocker_ (e.g. Candesartan)\r\n* Step 2: \r\n\t* (If maximal dose of Step 1 has failed or not tolerated)\r\n\t* **Combine CCB and ACE-I/ARB**\r\n* Step 3:\r\n\t* (If maximal doses of Step 2 has failed or not tolerated)\r\n\t* **Add thiazide-like diuretic** (e.g. Indapamide)\r\n* Step 4: *Resistant Hypertension*\r\n\t* If blood potassium <4.5mmol/L then add **spironolactone**\r\n\t* If >4.5mmol/L **increase thiazide-like diuretic dose**\r\n\t* Other options at this point if the potassium is >4.5mmol/L include:\r\n\t\t* Alpha blocker (e.g. Doxazosin)\r\n\t\t* Beta blocker (e.g. Atenolol)\r\n\t\t* Referral to cardiology for further advice\r\n\r\n**ABPM Targets:**\r\n \r\n* Age <80 ABPM target <135/85\r\n* Age >80 ABPM target <145/85 (due to risk of postural drop and falls)\r\n* T1DM with end-organ damage <130/80\r\n\r\n# Complications\r\n\r\n* Increased risk of morbidity and mortality from all causes\r\n* Coronary artery disease\r\n* Heart failure\r\n* Renal failure\r\n* Stroke\r\n* Peripheral vascular disease\r\n\r\n# Prognosis \r\n\r\nHypertension remains one of the biggest risk factors for cardiovascular disease and its associated disabilities. Management of hypertension (with lifestyle modifications or pharmacological therapies) has been shown to reduce these risks significantly. \r\n\r\n# NICE Guidelines\r\n> <https://cks.nice.org.uk/topics/hypertension/> \r\n\r\n# References \r\n\r\n<https://patient.info/heart-health/high-blood-pressure-hypertension>\r\n<https://www.ahajournals.org/doi/full/10.1161/01.CIR.101.3.329> ",
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"question": "A 59-year-old male presents to the GP for a follow-up appointment after his hypertension annual review. He is currently asymptomatic and takes amlodipine 10mg once daily. His average blood pressure reading is 151/98mmHg.\n\nWhich of the following is the next best step in the management of this patient?",
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"explanation": "According to [NICE CKS guidelines](https://cks.nice.org.uk/topics/urinary-tract-infection-lower-women/management/acute-uti-no-visible-haematuria-not-pregnant-or-catheterized/), this is the second-line antibiotic regimen where nitrofurantoin and trimethoprim are contraindicated (see other explanations), or where there is no improvement in symptoms.",
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"explanation": "The BNF advises that ciprofloxacin be used with caution in patients with G6PD deficiency. Furthermore, this medication would be more appropriate for patients with acute pyelonephritis managed in the community. The lack of additional symptoms in this patient i.e. flank pain or features of sepsis makes acute pyelonephritis unlikely. ",
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"explanation": "Methotrexate is listed as a severe interaction with trimethoprim in the BNF, due to the increased risk of haematological side effects that can be fatal. This is a very important drug interaction to remember.",
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"explanation": "G6PD deficiency is listed as a contra-indication to nitrofurantoin in the BNF.",
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"explanation": "This would be appropriate for patients with suspected urosepsis. This patient does not present with any features of sepsis e.g. hypotension and therefore does not require a stat dose of gentamicin.",
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"comment": "So focussed on the G6PD stuff I didn't even see the methotrexate god",
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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 55-year-old woman presents to the GP clinic with pain on passing urine for the past three days. She is otherwise well in herself. She has a past medical history of G6PD deficiency and rheumatoid arthritis, for which she takes methotrexate. She does not take any other medication and has no known drug allergies.\n\nShe has a temperature of 36.5 degrees Celsius, pulse 65 bpm, BP 125/86 mmHg.\n\nUrine dipstick shows 2+ leukocytes and 3+ nitrites.\n\nThe GP decides to prescribe a course of antibiotics for this patient. Which is the most appropriate regimen to prescribe?",
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"explanation": "The presence of a productive cough and herpes labialis makes a bacterial cause of pneumonia more likely than viral. A virus PCR screen may be helpful in this scenario, but certainly not the test that would confirm the diagnosis. Depending on the hospital, a virus screen will usually include influenza A & B, parainfluenza viruses, RSV, adenovirus and rhinovirus.",
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"explanation": "This would be the confirmatory test for *Mycoplasma pneumoniae*. This is more commonly associated with a dry cough, erythema multiforme, and cold autoimmune haemolytic anaemia (AIHA).",
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"explanation": "This is the diagnostic test for *Streptococcus pneumonia*, which is the most likely cause of this patient's pneumonia. The key feature in this scenario are the cold sores, also known as herpes labialis. Other common characteristics include rust-coloured sputum and pleuritic chest pain.",
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"explanation": "These are also important investigations to send off, but will not confirm the most likely diagnosis of *Streptococcus pneumonia* in this patient. Gram-stain will be useful to confirm Staphylococcus and other Streptococcus species, while silver-stain is used for *Pneumocystis jirovecii* pneumonia.",
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"explanation": "A CXR will not be able to confirm the microbial cause of the pneumonia. It is however an important step in the management of pneumonia to look for any consolidation. A follow-up CXR 6 weeks later is also needed to rule out any underlying malignancies which may be hidden by the original consolidations.",
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"comment": "spend more time on the wards\n",
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"comment": "Rishi Sunak? ",
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"comment": "Thought this was going to be Klebsiella but I guess 20 units a week isn’t enough for that in a question? 🤷♀️",
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"comment": "damn I thought urinary antigen test was just for legionella ",
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"comment": "but… you can’t call it pneumonia without have a cxr as it’s a radiological diagnosis",
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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 62-year-old man presents to the Emergency Department with a 2-day history of fever, a productive cough and cold sores around his mouth. He has a past medical history of type 2 diabetes, hypertension and rheumatoid arthritis. He is a current smoker and drinks 20 units of alcohol per week on average. The doctor suspects a community-acquired pneumonia and sends off a series of investigations.\n\nWhich of the following would confirm the most likely cause of this patient's pneumonia?",
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"explanation": "This would be the appropriate management for blepharitis, which usually presents with dry eye. In allergic conjunctivitis, cold compresses (instead of hot) are advised to relieve symptoms of itchiness.",
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"name": "Advise gentle cleaning of the eyelid margins and hot compresses",
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"explanation": "This is an antibiotic eye drop used to treat bacterial conjunctivitis, which is more likely to present with purulent 'sticky' discharge. This patient's symptom of tearing suggests a more watery discharge. Even if bacterial conjunctivitis was suspected, most cases resolve spontaneously within 5-7 days without treatment. Antibiotic eye drops such as chloramphenicol are only indicated in severe cases or situations that require rapid resolution.",
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"explanation": "The most likely diagnosis in this scenario is allergic conjunctivitis given the patient's symptoms of red eye, watery discharge and itching. It is also commonly associated with other atopic conditions such as eczema, hay fever and asthma. According to [NICE guidelines](https://cks.nice.org.uk/topics/conjunctivitis-allergic/management/management-in-primary-care/#management-in-primary-care), the 1st line treatment is a topical mast cell stabilizer (sodium cromoglycate) and topical antihistamine (antazoline).",
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"explanation": "Given the most likely diagnosis of allergic conjunctivitis in this scenario, this can be managed in primary care in the first instance. There are no concerning symptoms or adverse features in the patient's history that would warrant an urgent same-day referral. NICE CKS provides some useful guidelines on [when to refer to secondary care in allergic conjunctivitis.](https://cks.nice.org.uk/topics/conjunctivitis-allergic/management/referral/)",
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"explanation": "Lubricating eye drops are used to relieve symptoms of dry eyes. It will not relieve the itchiness that this patient is presenting with.",
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"comment": "womp womp\n",
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"explanation": "# Summary\n \n \nConjunctivitis is an inflammation of the conjunctiva that can be either infectious or noninfectious. This condition is typically classified into allergic, viral, and bacterial types. Common symptoms include redness, pain, itchiness, and varying types of discharge from the eyes. The condition is diagnosed through physical examination and patient history. Management strategies largely depend on the underlying cause but may involve avoidance of allergens, use of artificial tears, or topical antibiotics in severe cases.\n \n \n# Definition\n \n \nConjunctivitis, also known as \"\"pink eye,\"\" is a common condition that involves inflammation or infection of the conjunctiva, the transparent membrane that lines the eyelid and covers the white part of the eye. This condition can be either infectious (caused by bacteria or viruses) or noninfectious (due to allergies or other irritants).\n \n \n# Epidemiology\n \n \nWhile specific epidemiological data varies, conjunctivitis is a widely prevalent condition that affects people of all ages and demographics. It is especially common in children and can spread rapidly in schools and daycare centers. Its prevalence can also vary seasonally, particularly for allergic conjunctivitis which is often exacerbated during allergy season.\n \n \n# Aetiology\n \n \nConjunctivitis can be caused by a variety of factors:\n \n \n - **Allergic conjunctivitis** is caused by a Type I hypersensitivity reaction to allergens in the environment. Common triggers include pollen, dust mites, and pet dander. This is the most common type of conjunctivitis, which tends to worsen at certain times of year or in particular environments.\n \n \n - **Viral conjunctivitis** is most often caused by adenoviruses but can also be caused by herpes simplex virus. It is highly contagious and often associated with upper respiratory tract infections or colds. This is the most common acute infectious cause.\n \n \n - **Bacterial conjunctivitis** is caused by bacterial infection. Common pathogens include Staphylococcus aureus, Staphylococcus epidermis, Streptococcus pneumoniae and Haemophilus influenzae. Sexually transmitted infections like gonorrhoea or chlamydia can also cause bacterial conjunctivitis, so it is important to take a sexual history if suspected.\n \n \n \n# Signs and symptoms\n \n \n [lightgallery]\n \n \nCommon signs and symptoms of conjunctivitis include:\n \n \n - Eye redness\n - Itching\n - Irritation \n - Excessive tearing\n - Discharge from the eyes, which can vary in consistency based on the cause. For example viral aetiologies produce a more watery discharge, wheres bacterial causes produce purulent discharge.\n - Photophobia, which suggests corneal involvement (keratoconjunctivitis) \n \nNotably, visual acuity should not be affected by conjunctivitis.\n \n **Red flags** for more serious causes of a red eye include:\n \n - Reduced visual acuity\n - Marked eye pain, headache, photophobia\n - Red sticky eye in a neonate\n - History of trauma or foreign body\n - Rapidly progressive discharge\n - Infection with herpes virus\n - Contact lens use\n - Pupil abnormalities or pain on constriction\n - Loss of red reflex\n - Blood or pus in the anterior chamber\n \n \n# Differential diagnosis\n \n \nThe differential diagnosis for conjunctivitis includes a variety of conditions, each with their own distinct signs and symptoms:\n \n \n - **Dry eyes** – presents with dryness, burning, a feeling of something in the eye\n - **Corneal abrasion** – severe pain, photophobia, watering of the eye\n - **Uveitis** – eye pain, blurred vision, photophobia, floaters, redness\n - **Glaucoma** – severe eye pain, nausea, vomiting, blurred vision, halos around lights\n \n \n# Investigations\n \n \nThe diagnosis of conjunctivitis is typically based on the patient's history and physical examination. In certain cases, conjunctival swabs for bacterial cultures may be taken, particularly if the patient does not respond to initial treatment, presents severe or unusual symptoms, or in cases of suspected gonococcal or chlamydial conjunctivitis.\n \n \n# Management\n \n \nThe management of conjunctivitis depends on its cause:\n \n \n - **Allergic conjunctivitis** – Patients are advised to avoid allergens when possible and may be prescribed artificial tears, topical antihistamines, or mast cell stabilisers such as topical sodium cromoglycate.\n \n \n - **Viral conjunctivitis** – As this form is self-limiting, treatment focuses on symptom relief and prevention of spread through good hygiene practices.\n \n \n - **Bacterial conjunctivitis** – This form is also generally self-limiting, but in severe cases, topical antibiotics like chloramphenicol and fusidic acid may be recommended.\n - Conjunctivitis associated with contact lense wear should be managed with an aminoglycoside (e.g. gentamycin) or a quinolone (e.g. levofloxacin or moxifloxacin), to cover for gram -ve organisms. Patients should immediately stop wearing contact lenses until symptom resolution and antibiotic course completion.\n \n \nIn all cases, patients should be advised to seek medical attention if their condition worsens or fails to improve after a week of treatment.\n \n - If there is evidence of any red flag signs (see above), patients should be referred urgently to ophthalmology.\n \n# NICE Guidelines\n \n \n [Click here for NICE CKS on allergic conjunctivitis](https://cks.nice.org.uk/topics/conjunctivitis-allergic/)\n \n [Click here for NICE CKS on infective conjunctivitis](https://cks.nice.org.uk/topics/conjunctivitis-infective/)\n \n [Click here for NICE CKS on red eye](https://cks.nice.org.uk/topics/red-eye/)",
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"question": "A 19-year-old man presents to the GP clinic with redness in both eyes that developed over the past week. He also complains of tearing and an itchy sensation around his eyes. He has never experienced these symptoms before. He has a past medical history of eczema as a child and takes over-the-counter antihistamines for hay fever. He is otherwise well in himself.\n\nGiven the most likely diagnosis, what is the most appropriate course of action?",
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"explanation": "Bibasal crackles on chest auscultation suggest pulmonary congestion due to heart failure. However, they are not the most significant prognostic factor. They indicate the severity of current symptoms but do not provide as much prognostic information as LVEF.",
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"explanation": "A history of hypertension is a significant risk factor for developing heart failure, but it is not the most critical prognostic factor once heart failure has been diagnosed. The degree of left ventricular dysfunction (measured by LVEF) has a greater impact on prognosis.",
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"explanation": "While the presence of peripheral oedema indicates volume overload and congestion, it is not the most significant prognostic factor in heart failure. Peripheral oedema is a symptom that can be managed with diuretics, but it does not directly correlate with mortality as strongly as LVEF.",
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"explanation": "Hyperlipidaemia is a risk factor for coronary artery disease and subsequent heart failure. However, it is not the most significant prognostic factor in patients already diagnosed with heart failure. Management of lipid levels is important, but LVEF provides more direct prognostic information.",
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"explanation": "From the list of options given here, left ventricular ejection fraction (LVEF) is the most significant prognostic factor in heart failure. A lower LVEF is associated with a worse prognosis, as it indicates more severe systolic dysfunction and a higher risk of morbidity and mortality. This patient should ideally be commenced on a beta-blocker and an ACE inhibitor, as these have been shown to reduce mortality overall.",
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"comment": "i thought symptomatic heart failure with pulmonary oedema was a really bad prognostic factor",
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"explanation": "# Summary\r\n\r\nHeart failure (HF) is a clinical syndrome characterised by the heart's inability to pump enough blood to meet the body's needs. It is a common condition primarily affecting the elderly population. HF can be classified based on various factors, such as the type of dysfunction (systolic or diastolic), the onset (acute or chronic), and the severity of symptoms (NYHA classification). The clinical features of HF differ depending on whether it primarily affects the left or right ventricle, but broadly include fatigue, shortness of breath, and peripheral oedema. Diagnosis involves evaluating symptoms, NT-pro-BNP levels, and echocardiography. Management includes lifestyle modifications, medical therapy, and, in some severe cases, cardiac resynchronisation therapy. The prognosis for HF varies, but approximately 50% of those diagnosed are alive at 5 years.\r\n\r\n# Definition \r\n\r\nHeart failure (HF), also known as congestive heart failure (CHF) and congestive cardiac failure (CCF), is defined as the failure of the heart to generate sufficient cardiac output to meet the metabolic demands of the body.\r\n\r\n# Epidemiology \r\n\r\n* HF is common: the prevalence in the UK is estimated at 1-2%.\r\n\r\n* HF primarily affects the elderly population: the average age of diagnosis is 75 years old. The incidence of HF has been increasing with the ageing population.\r\n\r\n* In Europe and North America the most common causes are coronary artery disease, hypertension, and valvular disease.\r\n\r\n* Although Chagas disease is a rare cause in Europe and North America, it is a significant cause of heart failure in Central/South America.\r\n\r\n# Pathophysiology\r\n\r\nThe pathophysiology for HF is diverse and depends on the aetiology of the HF. \r\n\r\n# Classification \r\n\r\nHF can be classified in different ways. It can be classified as being low output vs. high output HF, predominantly systolic or diastolic dysfunction, whether the process has been acute or chronic, or by the severity of symptoms (and consideration for predominantly left or right ventricle features). \r\n\r\n## Low-output HF vs. High-output HF \r\n\r\nLow-output HF is much more common than high-output HF. Low-output HF occurs when cardiac output is reduced due to a primary problem with the heart and the heart is unable to meet the body's needs. Conversely, high-output HF refers to a heart that has a normal cardiac output, but there is an increase in peripheral metabolic demands that the heart is unable to meet. \r\n\r\nThe common causes of low-output HF will be further discussed below. Common causes of high-output HF include: \r\n\r\n* Anaemia\r\n* Arteriovenous malformation\r\n* Paget's disease\r\n* Pregnancy\r\n* Thyrotoxicosis\r\n* Thiamine deficiency (wet Beri-Beri)\r\n\r\nThese can be remembered with the AAPPTT mnemonic. \r\n\r\n## Systolic vs. Diastolic HF\r\n\r\nSystolic dysfunction refers to an impairment of ventricular contraction. The ventricles are able to fill well, but the heart is unable to pump the blood sufficiently out of the ventricle due to impaired myocardial contraction during systole (reduced ejection fraction). Common causes include: ischaemic heart disease, dilated cardiomyopathy, myocarditis or infiltration (haemochromatosis or sarcoidosis). \r\n\r\nIn comparison, diastolic dysfunction refers to the inability of the ventricles to relax and fill normally, hence the heart is still able to pump well but pumps out less blood per contraction due to reduced diastolic filling (preserved ejection fraction). Common causes include: uncontrolled chronic hypertension (significant left ventricular hypertrophy reduces filling of the left ventricle), hypertrophic cardiomyopathy, cardiac tamponade, and constrictive pericarditis. \r\n\r\n## Acute vs. Chronic HF \r\n\r\nHF can also be classified according to the time of onset. Acute HF occurs with new-onset HF symptoms (acute mitral regurgitation following an MI) or an acute deterioration in a patient with known, chronic HF. In comparison, chronic HF progresses more slowly and may take many years to develop. \r\n\r\n## Severity of Symptoms\r\n\r\n**New York Heart Association (NYHA) Classification of HF**\r\n\r\nThe NYHA Classification system is used to classify HF through the severity of symptoms. It runs from Class I (no limitation) to Class IV (discomfort at rest). \r\n\r\n* Class I - no limitation in physical activity, and activity does not cause undue fatigue, palpitations or dyspnoea.\r\n* Class II - slight limitation of physical activity, and comfort at rest. Ordinary physical activity causes fatigue, palpitations and/or dyspnoea.\r\n* Class III - marked limitation in physical activity, but comfort at rest. Minimal physical activity causes fatigue (less than ordinary).\r\n* Class IV - inability to carry on any physical activity without discomfort, with symptoms occurring at rest. If any activity takes place, discomfort increases.\r\n\r\n# Symptoms and Signs\r\n\r\nThe clinical features of HF can be considered according to the ventricle most impacted. However, a common presenting complaint for all types of heart failure is **fatigue**. \r\n\r\n\r\n## Clinical features of left heart failure (LHF)\r\n\r\nLHF, or left ventricular failure (LVF), causes pulmonary congestion (pressure builds up in the LHS of the heart and there is backpressure to the lungs) and systemic hypoperfusion.\r\n\r\n### Symptoms \r\n\r\n* Shortness of breath on exertion\r\n* Orthopnoea\r\n* Paroxysmal nocturnal dyspnoea\r\n* Nocturnal cough (± pink frothy sputum)\r\n* **Fatigue**\r\n\r\n### Signs \r\n\r\n* Tachypnoea\r\n* Bibasal fine crackles on auscultation of the lungs\r\n* Cyanosis\r\n* Prolonged capillary refill time \r\n* Hypotension\r\n* Less common signs: pulsus alternans (alternating strong and weak pulse), S3 gallop rhythm (produced by large amounts of blood striking compliant left ventricle), features of functional mitral regurgitation. \r\n\r\n## Clinical features of right heart failure \r\n\r\nRight heart failure causes venous congestion (pressure builds up behind the right heart) and pulmonary hypoperfusion (reduced right heart output).\r\n\r\n### Symptoms \r\n\r\n* Ankle swelling \r\n* Weight gain \r\n* Abdominal swelling and discomfort \r\n* Anorexia and nausea \r\n\r\n### Signs\r\n\r\n* Raised JVP\r\n* Pitting peripheral oedema (ankle to thighs to sacrum)\r\n* Tender smooth hepatomegaly\r\n* Ascites\r\n* Transudative pleural effusions (typically bilaterally)\r\n\r\n*NB. Sometimes left-sided heart failure can lead to pulmonary congestion which in turn also pushes the right ventricle into failure. In these cases, signs and symptoms of both left and right-sided heart failure may be present. This is congestive cardiac failure.* \r\n\r\n# Differential Diagnoses\r\n\r\n* **Chronic Obstructive Pulmonary Disease (COPD)** \r\n\t* **Similarities**: both may present with dyspnoea (and significant respiratory distress) and fatigue. \r\n\t* **Differences**: in heart failure, the shortness of breath is typically worse on lying flat (orthopnoea) and may be accompanied by paroxysmal nocturnal dyspnoea and peripheral oedema. Shortness of breath in COPD tends to be worse with exertion and is likely accompanied by other symptoms including chronic productive cough, wheeze and a significant smoking history. \r\n\r\n* **Acute Respiratory Distress Syndrome** \r\n\t* **Similarities**: both may present with shortness of breath, tachypnoea and respiratory distress. Both lead to the accumulation of fluid in the lungs and impaired gaseous exchange leading to hypoxaemia. \r\n\t* **Differences**: the underlying pathology between the two is different. Heart failure is a result of raised pressures in pulmonary capillaries, whereas ARDS is usually due to increased pressures in pulmonary capillaries secondary to a large insult (e.g. pneumonia, aspiration, or trauma). They can be distinguished by taking pulmonary capillary wedge pressures. \r\n\r\n* **Renal Failure** \r\n\t* **Similarities**: fluid retention and peripheral overload. \r\n\t* **Differences**: other signs and symptoms will allow distinction between HF and renal failure. In the latter, you may find uraemic symptoms(nausea, anorexia, uraemic flap) and potentially signs of renal replacement therapy. \r\n\r\n* **Liver Failure** \r\n\t* **Similarities**: fluid retention and peripheral overload especially ascites. \r\n\t* **Differences**: liver failure patients will present with other signs and symptoms including jaundice, hepatic encephalopathy and chronic liver disease signs (gynaecomastia, spider naevi, and excoriations). \r\n\r\n\r\n# Investigations\r\n\r\nIf a stable patient is presenting to the GP with suspected chronic heart failure, investigations should be carried out as per NICE guidelines. \r\n\r\n**1st line = NT-pro-BNP level**\r\n\r\nNT-pro-BNP is released by the ventricles in response to myocardial stretch. It has a high negative predictive value.\r\n\r\nInterpret NT-pro-BNP results as follows: \r\n\r\n* >2000ng/L (236pmol/L): refer urgently for specialist assessment and TTE <2 weeks. \r\n* 400-2000ng/L (47-236pmol/L): refer for specialist assessment and TTE <6 weeks. \r\n* If <400ng/L: diagnosis of heart failure is less likely. \r\n\r\n**Arrange a 12-lead ECG in all patients** \r\n\r\nECG may be normal or hint at underlying aetiology (ischaemic changes or arrhythmias). \r\n\r\n**Transthoracic echocardiogram (TTE)**\r\n\r\nAn echocardiogram will confirm the presence and degree of ventricular dysfunction.\r\n\r\n* Ventricular dysfunction is normally measured by the ejection fraction (EF). \r\n * EF <40% = HF with reduced ejection fraction (HFrEF, systolic dysfunction). \r\n * EF >40% but with raised BNP = HF with preserved ejection fraction (HFpEF, diastolic dysfunction).\r\n * EF 50-70% with normal BNP = normal. \r\n\r\n**Other Investigations:** \r\n\r\n* **Bloods**: U&E (renal function for medication and hyponatraemia), LFTS (deranged LFTs suggest hepatic congestion), TFTs (hyperthyroidism and high-output HF), glucose and lipid profile (modifiable CV risk factors)\r\n\r\n* **CXR**: CXR findings in heart HF can be remembered by the ABCDEF mnemonic:\r\n * A: **Alveolar** oedema (with 'batwing' perihilar shadowing)\r\n * B: **Kerley B** lines (caused by interstitial oedema)\r\n * C: **Cardiomegaly** (cardiothoracic ratio >0.5)\r\n * D: upper lobe blood **diversion**\r\n * E: **Pleural effusions** (typically bilateral transudates)\r\n * F: **Fluid in the horizontal fissure**\r\n\r\n[lightgallery]\r\n\r\n[lightgallery1] \r\n\r\n# Management\r\n\r\n## Conservative management\r\n\r\n* Weight loss if BMI >30. \r\n* Smoking cessation \r\n* Salt and fluid restriction - improves mortality\r\n* Supervised exercise-based group rehabilitation programme for people with heart failure. \r\n\r\nOffer annual influenza and one-off pneumococcal vaccinations for patients diagnosed with heart failure. \r\n\r\n## Medical management\r\n\r\n**Symptom management**: \r\n\r\n* For fluid overload, prescribe loop diuretics (e.g. furosemide or bumetanide). These do not affect overall mortality from heart failure. \r\n\r\n\r\n**Management which improves mortality**:\r\n \r\n1st line = ACE-I and beta-blocker \r\n\r\n* Consider ARB if intolerant to ACE-I. \r\n* Consider hydralazine if intolerant to ACE-I/ARB. \r\n\r\nIf symptoms persist and NYHA Class 3 or 4 consider adding:\r\n\r\n* Aldosterone antagonists = spironolactone or eplerenone. \r\n* Hydralazine and a nitrate for Afro-Caribbean patients. \r\n* Ivabradine if in sinus rhythm and impaired EF. \r\n* Digoxin = useful in those with AF. This <u>worsens</u> mortality but improves morbidity.\r\n\r\nNICE also advices seeking specialist guidance for prescribing **SGLT2 inhibitors** (dapagliflozin or empagliflozin). These should be given in symptomatic chronic heart failure with preserved or reduced ejection fraction, or as an add-on for patients already optimised with ACE-i/ARB/sacubitril-valsartan (i.e. combination), beta-blockers and aldosterone antagonists.\r\n\r\n**BASH Mnemonic**\r\n\r\n* BASH medications demonstrate a mortality benefit in patients with HFrEF = Beta-blockers, ACE-inhibitors/ARB, Spironolactone and Hydralazine. \r\n* There are no medications that improve mortality in diastolic heart failure. \r\n\r\n[lightgallery2]\r\n\r\n# Surgical/Interventional management \r\n\r\n* Cardiac resynchronisation therapy\r\n* Implantable cardiac defibrillators (ICDs) are indicated if the following criteria are fulfilled: \r\n * QRS interval <120ms, high risk sudden cardiac death, NYHA class I-III\r\n * QRS interval 120-149ms without LBBB, NYHA class I-III\r\n * QRS interval 120-149ms with LBBB, NYHA class I\r\n\r\n## Adverse effects of heart failure medications\r\n\r\nThe common side-effects for different heart failure medications are listed below\r\n\r\n* **Beta blockers**: Bradycardia, hypotension, fatigue, dizziness\r\n* **ACE inhibitors**: Hyperkalaemia, renal impairment, dry cough, lightheadedness, fatigue, GI disturbances, angioedema\r\n* **Spironolactone**: Hyperkalaemia, renal impairment, gynaecomastia, breast tenderness/hair growth in women, changes in libido\r\n* **Furosemide**: Hypotension, hyponatraemia/kalaemia,\r\n* **Hydralazine/nitrates**: Headache, palpitations, flushing\r\n* **Digoxin**: Dizziness, blurred vision, GI disturbances\n* **SGLT-2 inhibitors:** Thrush, UTIs, DKA in patients with pre-existing diabetes\r\n\r\n# Prognosis \r\n\r\nIt is estimated that >50% of people diagnosed with HF will survive after 5 years. Approximately 35% will be alive in 10 years. \r\n\r\n# NICE Guidelines\r\n\r\n[NICE Guidelines on Acute Heart Failure](https://www.nice.org.uk/guidance/cg187/chapter/1-Recommendations)\n\n[NICE Guidelines on Chronic Heart Failure](https://cks.nice.org.uk/topics/heart-failure-chronic)\r\n\r\n# References \r\n\r\n[2022 Stat Pearls Summary of Congestive Heart Failure](https://www.ncbi.nlm.nih.gov/books/NBK430873)",
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"explanation": "Completing the death certificate with atrial fibrillation as the cause is incorrect because the primary cause of death was the intracranial haemorrhage resulting from the fall. This death needs to be referred to the coroner. A phrase along the lines of \"atrial fibrillation (treated)\" will be likely to ultimately go in part 2 of the certificate, reflecting that the anticoagulation contributed to the death but was not part of the direct sequence of events.",
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"explanation": "# Summary\n \nAn extradural haematoma is a type of intracranial haemorrhage where blood accumulates between the dura mater and the skull. The condition typically results from blunt trauma, usually leading to fracture of the pterion bone damaging the middle meningeal artery. The classic presentation of an extradural haematomas is a history of trauma or a fall, followed by a transient loss of consciousness, then a lucid interval with ongoing headache before subsequent deterioration of consciousness. A CT scan is the usual diagnostic investigation, looking for a biconvex hyperdense lesion with or without associated overlying skull fracture. Management may be conservative with monitoring and observation, or surgical with a craniotomy or Burr hole formation. This depends on the size of the haematoma, the patient's clinical condition and whether mass effect is present.\n \n# Definition\n \nAn extradural haematoma occurs when a collection of blood forms between the dura mater, the outermost meningeal layer, and the inner surface of the skull. This commonly results from a traumatic arterial bleed, with the middle meningeal artery implicated in the majority of cases.\n \n\n# Epidemiology\n\nApproximately 2% of head injuries presenting to emergency services are found to have caused extradural haematomas. Most of these are acute but subacute and chronic presentations also occur. \n\nThe most common age group affected is 20-30 year olds, with men making up the majority of cases (linked to high risk activities in this demographic such as contact sports and violence).\n\n# Aetiology\n \nExtradural haematomas are almost always secondary to traumatic head injury, most commonly with a fracture of the temporal or parietal bone which damages underlying vessels.\n\nThe most common vessel damaged is the middle meningeal artery, however extradural haematomas can also result from a venous bleed.\n \n# Signs and Symptoms\n \nThe classic clinical course seen in extradural haematomas is as follows:\n\n - Brief loss of consciousness following the initial traumatic head injury\n - A period of regained consciousness and apparent recovery (the lucid interval)\n \t- There may be ongoing headache during this time \n - Subsequent deterioration with worsening symptoms and signs\n\nSymptoms may include:\n\n- Headache\n- Nausea and vomiting\n- Seizures\n- Limb weakness, numbness or other neurological symptoms\n- Confusion\n \nSigns may include:\n\n- External injuries e.g. signs of skull fractures, haematomas or lacerations on the head\n- Reduced level of consciousness\n- Seizures\n- Cushings Triad: Bradycardia, hypertension and irregular breathing (sign of raised intracranial pressure)\n- 6th nerve palsy (a false localising sign secondary to raised intracranial pressure\n- Cerebrospinal fluid otorrhea or rhinorhoea (sign of dural tearing)\n- Unequal pupils\n- Focal neurological signs e.g. visual field defects, ataxia\n\n# Differential Diagnosis\n \n- **Subdural haematoma**: Presents with fluctuating levels of consciousness, memory impairment and headache. This often presents subacutely or chronically in older patients, often with a history of minor head trauma.\n- **Subarachnoid haemorrhage**: Characterised by a sudden, severe headache (often described as a 'thunderclap' headache), nausea, vomiting, and symptoms and signs of meningism such as neck stiffness.\n- **Intracerebral haemorrhage**: i.e. bleeding within the brain parenchyma. Presents with a sudden onset of neurological deficits, headache and decreased consciousness levels.\n- **Alcohol intoxication**: can present with overlapping symptoms of decreased levels of consciousness, ataxia, nausea and vomiting. May co-present with an extradural haematoma in patients who injure themselves whilst intoxicated.\n\n# Investigations\n \n**Bedside investigations:**\n\n- **ECG** in bradycardic patients to rule out other causes e.g. heart block\n- **Capillary blood glucose** to rule out hypoglycaemia as a cause of decreased consciousness\n\n**Blood tests:**\n\n- **Full blood count** looking for anaemia from blood loss (especially if other injuries)\n- **U&Es and LFTs** as a baseline in case a general anaesthetic is needed for surgical management\n- **Coagulation screen** looking for a bleeding diathesis\n- **Group and save** in preparation for possible surgery\n\n**Imaging:**\n\n- **Non-contrast CT Head** is the diagnostic investigation, looking for a lentiform or biconvex hyperdense extra-axial collection \n\n - Complications resulting from raised intracranial pressure such as midline shift or subfalcine/uncal herniation may necessitate urgent neurosurgical intervention\n \n\n [lightgallery]\n \n\n# Management\n\nManagement depends on the size of the haematoma, the patient's clinical condition and whether there is mass effect seen on imaging. \n\n**Urgent neurosurgical referral** is required in all patients presenting with suspected extradural haematoma.\n\n**Conservative management:**\n\n- Patients with small extradural haematomas may be admitted for neurological observations and monitoring with serial imaging\n- This may also be the treatment of choice in patients who are unfit for neurosurgery due to frailty or comorbidities\n- Patients undergoing medical or surgical management also require conservative management with neurorehabilitation, optimisation of nutrition and multidisciplinary team involvement\n\n**Medical management:**\n\n- Initial A to E assessment and resuscitation (e.g. patients with a GCS < 8 may require airway support)\n- Ensure other life-threatening injuries are addressed\n- Reverse any anticoagulant medication or coagulopathy (may require haematology input)\n- Anticonvulsants may be required for seizure prophylaxis\n- Prophylactic antibiotics may be started e.g. in cases of open skull fracture\n- Consider place of care - patients with raised intracranial pressure are often admitted to intensive care for intubation and ventilation\n- Intracranial pressure (ICP) can be monitored and **neuroprotective measures** put in place to help normalise this:\n - Ensure sedation and paralysis are adequate\n - Maintain oxygen and carbon dioxide levels in the normal range\n - Maintain a normal temperature\n - Consider raising head to 30 degrees (if appropriate in context of other injuries)\n - Hypertonic saline or mannitol may be used to reduce ICP\n\n**Surgical management:**\n\n- Burr hole craniotomy may be used to evacuate the haematoma\n- Trauma craniotomy is another emergency procedure that can relieve raised intracranial pressure and evacuate the haematoma \n- Vessels with ongoing bleeding should be ligated or cauterised\n\n# NICE Guidelines\n\n[NICE CKS - Head Injury](https://cks.nice.org.uk/topics/head-injury/)\n\n# References\n \n[Radiopaedia: Extradural haemorrhage](https://radiopaedia.org/articles/extradural-haemorrhage?lang=gb)\n\n[Patient UK: Extradural haematoma](https://patient.info/doctor/extradural-haematoma-pro)",
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"question": "An 85-year-old woman is admitted to the emergency department following a fall at home, resulting in a head injury. She has a past medical history of atrial fibrillation and is on apixaban. On examination, she is drowsy and confused. An urgent CT head scan shows an intracranial haemorrhage. The patient dies shortly afterwards.\n\nSelect the single most appropriate next step in management from the list below. Select one option only.",
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"explanation": "Although this patient does have signs of heart failure (an \"adverse feature\"), this is chronic and long standing and doesn't appear to be secondary to her arrhythmia. Therefore, cardioversion is not indicated in this instance",
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"explanation": "Flecainide can be used to treat VT, but is not as effective as amiodarone",
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"explanation": "Her heart failure is chronic and not secondary to her arrhythmia so this is not an indication for cardioversion. She has no other indications for cardioversion such as shock, syncope or myocardial ischaemia. If she did have any of these symptoms then up to 3 synchronised DC shocks can be given in attempt to cardiovert",
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"explanation": "According to NICE guidelines, amiodarone is the preferred drug to manage VT",
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"explanation": "IV furosemide would not treat this patient's ventricular tachycardia",
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"comment": "The question does not clarify whether the VT is mono- or polymorphic. Although IV mag sulph isn't an answer, it does make the question more confusing",
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"comment": "don't introduce what ifs. If the VT was polymorphic they would have to say so. ",
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"comment": "She has acute exacerbation of heart failure does this not mean DC cardioversion?",
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"comment": "however she is haemodynamically stable\n",
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"comment": "no because heat failure is a long standing problem that is not caused by the arrhythmia ",
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"explanation": "# Summary \n\nVentricular Tachycardia (VT) is a regular broad complex tachycardia that originates from the ventricles of the heart. The patient may have a pulse or not - if VT is pulseless it is one of the shockable cardiac arrest rhythms. Emergency management involves identification of VT on an ECG or heart monitor, then treating patients with a pulse and no adverse features with IV amiodarone. Patients who do not respond to this or have adverse features should be treated with synchronised DC cardioversion. Patients in cardiac arrest with VT should be treated as per the Advanced Life Support (ALS) algorithm with cardiopulmonary resuscitation (CPR), adrenaline and amiodarone as well as unsynchronised shocks. \n\n# Definition\n \nVentricular Tachycardia (VT) is a type of broad complex tachycardia characterised by a heart rate of more than 100 bpm and a QRS width of more than 120ms. Other types of broad complex tachycardias include Torsades de Pointes (which is a type of ventricular tachycardia described as polymorphic, where there are multiple ventricular foci) and Supraventricular Tachycardia with aberrant conduction.\n \n[lightgallery]\n \n\n# Aetiology\n \nFactors that increase the risk of VT include:\n \n- Electrolyte abnormalities such as hypokalaemia and hypomagnesaemia\n- Structural heart disease including previous myocardial infarction and cardiomyopathies\n- Drugs that cause QT prolongation e.g. clarithromycin, erythromycin (for Torsades de Pointes) \n- Inherited channelopathies e.g. Romano-Ward syndrome (for Torsades de Pointes)\n\n# Management\n \n**Pulseless VT:**\n\nPulseless VT is one of the four cardiac arrest rhythms, as so is managed as per Advanced Life Support guidelines:\n\n- CPR will be in progress\n- 120-360 J unsynchronised shock should be administered as early as possible, then every 2 minutes\n- IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock\n- Adrenaline should be administered every 3-5 minutes thereafter\n- A further dose of amiodarone 150 mg IV should be given after 5 shocks\n\n**Pulsed VT with adverse features:**\n\nIf a patient has a pulse, management is determined by whether they have any of the following adverse features:\n\n - Heart failure\n - Myocardial ischaemia (chest pain)\n - Shock\n - Syncope\n\nIf one or more of these are present, attempt to cardiovert the patient using synchronised DC shocks (up to 3 attempts). If the patient is conscious this will require sedation or anaesthesia.\n\nIf this is not effective, an amiodarone infusion would be the next step under expert guidance (300mg IV over 10-20 minutes followed by 900mg infusion over 24 hours).\n\n**Pulsed VT with no adverse features:**\n\nFirst line treatment is amiodarone 300mg IV over 10-60 minutes.\n\nIf this is ineffective then attempt to cardiovert using synchronised DC shocks (up to 3 attempts) with sedation or anaesthesia.\n\n**Torsades de Pointes:**\n\nThis is a special situation which is managed differently to monomorphic VT - Torsades de Pointes often self-terminates but the risk is that it deteriorates into ventricular fibrillation (causing cardiac arrest).\n\nIV Magnesium is the mainstay of treatment, along with treatment of any underlying cause identified (e.g. correcting electrolyte imbalance, stopping QT-prolonging medications).\n\n# References\n \n[Resuscitation Council UK - Adult advanced life support Guidelines](https://www.resus.org.uk/library/2021-resuscitation-guidelines/adult-advanced-life-support-guidelines)\n\n[Resuscitation Council UK - Adult Tachycardia Algorithm](https://www.resus.org.uk/sites/default/files/2021-04/Tachycardia%20Algorithm%202021.pdf)\n\n[Patient UK - Torsades de Pointes](https://patient.info/doctor/torsades-de-pointes)",
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"question": "A medical emergency call is put out for a 70-year-old female patient on a medical ward. Ventricular tachycardia (VT) is present on her ECG. She is haemodynamically stable. On examination, she is well perfused, has a GCS of 15, and has pitting oedema to her knees bilaterally.\n\nShe was admitted to hospital three days prior for an exacerbation of heart failure and was being treated with intravenous furosemide.\n\nWhich of the following treatments is most appropriate to manage VT in this patient?",
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"explanation": "This patient has a known penicillin allergy and therefore flucloxacillin is contraindicated",
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"explanation": "This patient has a known penicillin allergy and therefore co-amoxiclav is contraindicated",
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"explanation": "# Summary\n \n\nMastitis is an inflammation of the breast, often associated with lactation in postpartum women, referred to as puerperal mastitis. Key signs and symptoms include localised pain, tenderness, redness and heat in the breast, along with systemic symptoms such as fever, rigours, myalgia, fatigue, nausea and headache. Diagnosis is primarily clinical. Ultrasound may be used if a breast abscess is suspected. Management strategies focus on reassurance about continued breastfeeding, advice on milk removal, analgesia, antibiotics, and in severe cases, surgical intervention.\n \n\n# Definition\n \n\nMastitis is the inflammation of the breast tissue, which can be with or without an infection. When associated with lactation in postpartum women, the condition is specified as puerperal mastitis. Alternatively, mastitis can be seen in women who are not breastfeeding.\n \n\n# Epidemiology\n \n\nNon-lactational mastitis is significantly less common than lactational mastitis, and its most common in women with immunodeficiency and diabetes. \n \n\n# Aetiology\n \nMastitis unrelated to pregnancy and breastfeeding is typically due to obstruction of the ducts from cellular debris. This can result in a local inflammatory response in non-infectious mastitis. \n\nIn infectious mastitis, bacteria from the skin can then enter the ducts, causing inflammation and may progress to peri-areolar abscesses. The most common causative pathogen is Staphylococcus aureus. \n\nRisk factors for non-lactational mastitis include:\n\n- Cigarette smoking\n- Nipple rings \n- Diabetes mellitus\n- Immunocompromise \n \n\n# Signs and Symptoms\n \n\nMastitis diagnosis is primarily clinical, based on characteristic local and systemic symptoms.\n \n\n - Localised symptoms: Painful, tender, red, and hot breast.\n - Systemic symptoms: Fever, rigours, myalgia, fatigue, nausea, and headache.\n - Additional information: The condition is usually unilateral and tends to present within the first week postpartum.\n \n\nIn some cases, mastitis may develop into a breast abscess, manifesting as a fluctuant, tender mass with overlying erythema.\n \n\n# Differential Diagnosis\n \n\nThe differential diagnosis for mastitis should include other conditions that also cause breast pain and inflammation:\n \n\n - **Breast abscess**: Fluctuant mass, tenderness, overlying erythema, systemic signs of infection.\n - **Inflammatory breast cancer**: Swelling, skin changes resembling orange peel, nipple inversion, axillary lymphadenopathy.\n - **Breast engorgement**: Typically bilateral and associated with milk stasis, painful, and tense breasts.\n \n\n# Investigations\n \n\nWhile the diagnosis of mastitis is primarily clinical, further investigations may be necessary in certain circumstances.\n \n\n - Ultrasound: Utilised to identify a potential abscess, appearing as a collection of pus.\n - Additional information: Early referral to secondary care is vital if an abscess is suspected.\n \n\n# Management\n \n\nManaging mastitis involves multiple strategies:\n \n\n - Provide analgesia to manage symptoms (i.e. paracetamol, ibuprofen)\n\t - Warm and cold compresses may also help.\n - Antibiotics may be considered if acute pain, severe symptoms or symptoms lasting more than 12-24 hours, fever or positive cultures \n\t - Flucloxacillin or clindamycin for those with penicillin allergy\n\t - Treatment is indicated for 10-14 days.\n - In cases where the condition does not improve, consider intravenous antibiotics (i.e. vancomycin) or ultrasound to evaluate for the presence of a breast abscess.\n - Patients may also benefit from antifungal therapy (i.e. nystatin) for concomitant nipple candidiasis \n\n \n# Complications\n \nComplications of mastitis include:\n \n - Breast abscess\n - Recurrence:\n\t - More common if treatment is delayed or too short in duration \n \n\n# NICE Guidelines\n \n[NICE CKS on mastitis and breast abscess](https://cks.nice.org.uk/topics/mastitis-breast-abscess/)\n\n# References\n\n[BMJ Best Practice Mastitis and Breast Abscess](https://bestpractice.bmj.com/topics/en-gb/1084)\n\n[Patient Info Benign Breast Diseas](https://bestpractice.bmj.com/topics/en-gb/1084) \n\n[NHS Mastitis](https://www.nhs.uk/conditions/mastitis/)",
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"comment": "Unlikely but are we outright assuming she's post-menopause?",
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"comment": "At 70? That's not much of an assumption mate",
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"explanation": "# Summary\n\n\nBreast carcinoma is the most prevalent form of cancer among women and the second leading cause of cancer death in the UK. It manifests in various histological subtypes including ductal, lobular, medullary, and phyllodes tumours, each displaying distinct characteristics. Certain genetic mutations, especially BRCA1 and BRCA2, can increase the risk for breast carcinoma. Notable signs and symptoms include unexplained breast mass, nipple discharge, retraction, or skin changes suggestive of breast cancer. Key investigations comprise a triple assessment—clinical examination, radiological examination, and biopsy. Treatment strategies encompass surgical management (wide local excision or mastectomy), radiotherapy, chemotherapy, biological therapy, and hormonal therapy. Risk factors for breast cancer include increased hormone exposure, susceptibility gene mutations, advancing age, and lifestyle factors like obesity, physical inactivity, and alcohol and tobacco use.\n\n\n# Definition\n\n\nBreast carcinoma refers to a malignant tumour originating from the cells of the breast tissue. It exhibits different subtypes each with unique cellular properties and clinical implications. The carcinomas can be invasive, indicating they have broken through the basement membrane of the tissue of origin and have the potential to metastasize, or non-invasive (in situ), suggesting they are confined to the initial location.\n\n\n# Epidemiology\n\n\nBreast carcinoma is the most common type of cancer in women and accounts for approximately 15% of new cancer cases, representing 50,000 new cases annually. It is the second most common cause of cancer death in the UK.\n\n\n# Aetiology\n\nMost breast cancers are either ductal (arising from the epithelial lining of the ducts) or lobular (originating from epithelial cells in the terminal ducts of the lobules).\n\n\nRisk factors for breast carcinoma include:\n\n\n- Being female\n- 99% of breast cancer cases occur in women\n- Increased hormone exposure\n- Early menarche or late menopause\n- Nulliparity or late first pregnancy\n- Oral contraceptives or Hormonal Replacement Therapy\n- Susceptibility gene mutations\n- Most commonly BRCA mutations (BRCA1/BRCA2)\n- Advancing age\n- Caucasian ethnicity\n- Obesity and lack of physical activity\n- Alcohol and tobacco use\n- History of breast cancer\n- Previous radiotherapy treatment\n\n\n# Classification\n\n\nBreast cancer is not a single disease, but a collection of several subtypes, each with its unique characteristics, prognosis, and treatment options.It can be classified based on its origin cell type such as:\n\n\n- **Invasive ductal carcinoma (IDC)**: This is the most common type, accounting for about 80% of all breast cancers. It starts in a milk duct, breaks through the wall of the duct, and invades the fatty tissue of the breast.\n- **Invasive lobular carcinoma (ILC)**: This type begins in the milk-producing glands (lobules) and can spread to other parts of the body.\n- **Ductal carcinoma in situ (DCIS)**: This is a non-invasive or pre-invasive cancer where the cells are confined to the ducts in the breast and have not spread into the surrounding breast tissue.\n- **Lobular carcinoma in situ (LCIS)**: This is not a cancer but an area of abnormal cell growth that increases a person's risk of developing invasive breast cancer later.\n- **Paget's disease of breast**: Infiltrating carcinoma of nipple epithelium.\n\n\nIt can also be classified based on the hormone receptors present on the surface of the breast cancer:\n\n- **Inflammatory breast cancer (IBC)**: This is a rare but aggressive type of breast cancer that causes the lymph vessels in the skin of the breast to become blocked.\n\n- **Triple-negative breast cancer (TNBC)**: This type lacks estrogen receptors, progesterone receptors, and does not have an excess of the HER2 protein on the cancer cell surfaces. It tends to be more aggressive and has fewer targeted treatments available.\n\n- **HER2-positive breast cancer**: This is a cancer that tests positive for a protein called human epidermal growth factor receptor 2 (HER2), which promotes the growth of cancer cells. It tends to be more aggressive than other types of breast cancer, but it may respond well to targeted therapies that can block HER2.\n\n\n# Signs and Symptoms\n\n\nCommon clinical manifestations of breast carcinoma include:\n\n\n- Unexplained breast mass in patients aged 30 and above, with or without pain\n- In those aged 50 and older, nipple discharge, retraction/inversion, or other concerning symptoms\n- This can also include eczema-type changes surrounding the nipple as seen in Paget's disease of the breast\n- Skin changes suggestive of breast cancer\n- This includes skin retraction, peau d'orange appearance or ulceration of the skin above an underlying mass.\n- Unexplained axillary mass in those aged 30 and above\n\n\nApproximately 25% of cases are found in routine breast cancer screening (mammography).\n\n\n# Differential Diagnosis\n\n\nWhile an unexplained breast mass is a key indicator of breast carcinoma, it can also represent various other conditions, each characterized by distinct signs and symptoms:\n\n\n- **Fibroadenoma**: Typically presents as a solitary, painless, and well-circumscribed breast lump in young women\n- **Breast Cyst**: Characterized by a round or oval, well-defined, and movable mass. It may be painful and size may vary with the menstrual cycle.\n- **Mastitis**: Typically presents in breastfeeding women, characterized by a painful, warm, red breast often accompanied by systemic symptoms like fever.\n- **Lipoma**: Presents as a soft, mobile, and painless lump.\n\n\n# Breast Cancer Screening in the UK\n\n\nIn the United Kingdom, the NHS Breast Screening Programme provides free breast screening services for all women registered with a GP. The programme invites women between the ages of 50 and 70 for breast screening every three years, with the first invitation to screening usually sent to women before they turn 53.\n\n\nThis screening process involves a mammogram, which is an X-ray of the breasts that can help detect breast cancers early, often before they can be felt. The aim of breast cancer screening is to find cancer at an early stage when treatment is most effective.\n\n\nIn 2018, the age range for screening was extended as part of a trial, and some women were invited for screening from the age of 47 up to the age of 73. Women over 70 can still self-refer for screening every three years.\n\n\n# Investigations\n\nCriteria for 2-week wait:\n\n- Age 30 or more with unexplained breast lump (with or without pain)\n- Age 50 or more with nipple discharge, retraction or other changes\n- Consider a 2-week wait if a patient is 30 or over with skin changes suggestive of breast cancer or an unexplained lump in the axilla\n\nNB: a non-urgent referral should be considered for patients under the age of 30 with an unexplained breast lump.\n\n### Triple Assessment\n\nTriple assessment is used to investigate suspected breast carcinoma:\n\n\n1. Clinical examination: of the breast and surrounding lymph nodes\n2. Radiological examination:\n\t- Ultrasound is used for women under the age of 40 or those with higher breast density.\n\t- A mammogram is commonly used for women over 40 years.\n\t- If there are concerns of metastatic disease, a CT or PET scan may be done.\n3. Biopsy: often a core needle biopsy or fine needle aspirate (FNA)\n\t- Fine needle aspiration (FNA): Often combined with mammography, however, has a high rate of false negatives.\n\t- Core needle biopsy: method of choice, can be combined with imaging to aid accuracy.\n\t- DCIS biopsy will show cellular atypia and hyperchromatic nuclei involving the ducts, but not passing the basement membrane\n\t- In invasive breast cancer, these abnormal cells will pass the basement membrane\n\t- In lobular carcinoma, the abnormal cells will be found within the lobular acini\n\n### Further Investigations\n\nFollowing the triple assessment, further investigations will include:\n\n- Biopsies to determine\n- Oestrogen and progesterone receptor status\n- Epidermal growth factor receptor status\n- Routine blood tests (i.e. LFTs)\n- CXR\n- MRI is not routinely used. It is used for women with:\n- Discrepancy between the extent of disease between clinical examination and imaging\n- Dense breast tissue limiting mammography\n- Invasive lobular carcinoma to evaluate tumour size when planning breast-conserving surgery\n- BRCA1/2 testing is done for women < 50 years with triple-negative breast cancer regardless of family history\n\n\n### Staging\n\nStaging involves the TNM system considering the size of the tumour (T), the spread to the lymph nodes (N), and the presence of metastases (M). For locally invasive breast cancer, this can include:\n\n- Axilla ultrasound with needle sampling if abnormal lymph nodes are identified\n\nIf the cancer is deemed to be advanced, staging investigations should include:\n\n- CT, MRI or bone scintigraphy to determine the presence and extent of visceral and bony metastasis\n- PET CT is only used to diagnose metastasis\n\n\n# Management\n\n\nThe management strategy for breast carcinoma can vary based on several factors including the subtype of carcinoma, stage, hormonal receptor status, and the patient's overall health and preferences.\n\n\n- Surgical management: Wide local excision (WLE) or mastectomy, with sentinel node biopsies for invasive cancers and possible axillary node clearance for positive nodes. Breast reconstruction can be done concurrently or later.\n- Radiotherapy: Adjuvant radiotherapy is commonly offered following WLE to reduce recurrence. It may also be given to patients with higher-stage cancers post-mastectomy.\n\n**Chemotherapy:**\n\n- Suggested for hormone receptor-negative and HER2 over-expressing patients. Neoadjuvant chemotherapy may be given to downstage tumours before surgery. This commonly includes an anthracycline (i.e. doxorubicin) and a taxane (i.e. paclitaxel)\n- Biological Therapy:\n\t- Trastuzumab (Herceptin) should be given to HER2-positive patients with tumour size T1c and above in combination with surgery, chemotherapy and radiotherapy. Patients should have regular cardiac function assessments.\n\t- Abermaciclib (selective inhibitor of cyclin-dependent kinases 4 and 6) for HER2-negative, hormone receptor-positive breast cancer\n\t- Pembrolizumab for triple-negative breast cancer\n\t- Olaparib (PSTP inhibitor) for BRCA positive, HER2 negative high-risk early breast cancer\n- **Hormonal Therapy** for oestrogen-positive breast cancer:\n\t- Anastrozole (aromatase inhibitor) for postmenopausal women\n\t- Tamoxifen (oestrogen receptor antagonist) for premenopausal patients\n\t- Bisphosphonates: May be used for reducing occurrence in node-positive cancers.\n\t- Zoledronic acid has been shown to improve disease-free survival in postmenopausal women with node-positive invasive breast cancer.\n\t- Bisphosphonates are also advised for treatment-induced menopause in women treated with aromatase inhibitors\n\n\n# Complications\n\n### Complications of Breast Carcinoma\n\n- Fatigue\n- Bone metastases\n- Brain metastases\n- Psychological difficulties: Anxiety, depression and damage to the individual's self-esteem.\n- Recurrence:\n\t- Local: recurrence in the same breast as the original tumour\n\t- Regional: recurrence in the axillary or sub-clavicular lymph nodes draining the breast cancer\n\t- Distant: recurrence once already metastasized to other parts of the body (i.e. liver, lungs, brain, bone)\n\n\n### Side Effects of Medication Used to Treat Breast Cancer\n\n\nTreatment for breast cancer often involves medication, including chemotherapy, hormone therapy, and targeted drug therapy. Each of these can have different side effects.\n\n\n**Chemotherapy** drugs are powerful medications that aim to destroy rapidly dividing cells, such as cancer cells. However, they can also affect healthy cells, leading to a range of side effects, including fatigue, hair loss, easy bruising and bleeding, infection, anaemia, nausea and vomiting, appetite changes, peripheral neuropathy, and problems with concentration or memory.\n\nChemotherapy agents can have specific side effects such as:\n\n- Doxorubicin is associated with cardiac toxicity (e.g. cardiac arrhythmias, myopericarditis)\n- Paclitaxel is associated with lung fibrosis.\n\n\n**Hormone therapy** drugs, such as tamoxifen and aromatase inhibitors, are used to treat hormone receptor-positive breast cancers. Common side effects include hot flushes, vaginal dryness or discharge, menstrual changes, fatigue, mood changes, and osteoporosis. In rare cases, tamoxifen can increase the risk of serious conditions like endometrial cancer and blood clots.\n\n\n**Targeted drug therapies** such as trastuzumab (Herceptin), pertuzumab (Perjeta), and ado-trastuzumab emtansine (Kadcyla), are designed to interfere with specific proteins or processes that contribute to cancer growth.\n\nSide effects include:\n\n- Infections\n- Bruising and easy bleeding\n- Anaemia\n- Cardiac (i.e. arrhythmias)\n- Insomnia\n- GI side effects (i.e. diarrhoea, vomiting, constipation, appetite loss, weight loss)\n- Runny nose\n- Conjunctivitis\n- Hair loss\n- Nail changes\n- Hand foot syndrome: the palms and plantar surfaces become sore, peel, crack and blister.\n- Hepatotoxicity\n\n\n\n### Surgical Complications\n\nKey surgical complications include:\n\n- Venous thromboembolism\n- Lymphoedema\n- Pain\n\n\n### Breast Cancer in Pregnancy\n\nBreast cancer is the most common malignancy to occur during pregnancy. Radiotherapy and chemotherapy are most commonly delayed until completion of pregnancy, but surgical intervention can be considered.\n\n# Prognosis\n\nThe prognosis for individuals with breast cancer has vastly improved, almost doubling over the past 50 years. The ten-year survival for breast cancer in England is 75.9%\n\nA poorer prognosis is associated with:\n\n- Advancing age\n- Being male\n- Stage III or IV\n- Tumour size\n- Tumour grade\n- Hormone receptor-negative tumours (oestrogen or progesterone receptor-negative)\n- HER 2 positive tumours\n\n\n# NICE Guidelines\n\n[NICE Guidelines on Early and Locally Advanced Breast Cancer](https://www.nice.org.uk/guidance/ng101)\n\n[NICE Guidelines on Advanced Breast Cancer](https://www.nice.org.uk/guidance/cg81)\n\n# References\n\n[Patient Info Breast Cancer](https://www.nice.org.uk/guidance/cg81)\n\n[BMJ Best Practice Breast Cancer](https://bestpractice.bmj.com/topics/en-gb/718?q=Metastatic%20breast%20cancer&c=suggested)\n\n[NHS Breast Cancer in Women](https://www.nhs.uk/conditions/breast-cancer-in-women/)\n\n[Cancer Research UK Breast Cancer](https://www.cancerresearchuk.org/about-cancer/breast-cancer/survival)",
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"question": "A 70-year-old female is referred to the breast clinic with a left breast lump. A biopsy is obtained which shows a ductal carcinoma which is oestrogen receptor (ER) positive, HER2 negative, and progestogen receptor (PR) negative.\n\nWhich of the following medical therapies is indicated for the management of this patient's breast cancer?",
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"explanation": "This is age-related sensorineural hearing loss. We can be fairly certain that the hearing loss are from his bilateral vestibular schwannomas which are shown on the MRI. This would not explain why he has bilateral vestibular schwannomas",
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"explanation": "Neurofibromatosis type 2 is a genetic condition characterised by tumour formation within nervous tissue. It is associated with bilateral vestibular schwannomas. They normally present by this age, unlike unilateral vestibular schwannomas which tend to present in older people",
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"comment": "Vestibular Schwannomas on BOTH sides = NF is 2",
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"explanation": "# Summary\n\nA vestibular schwannoma is a benign subarachnoid tumour that predominantly affects the VIII cranial nerve. Key signs and symptoms include unilateral hearing loss, progressive ipsilateral tinnitus, and in severe cases, signs of raised intracranial pressure due to mass effect. Key investigations primarily involve an MRI scan, especially in patients presenting with unilateral tinnitus and sensorineural deafness. The definitive management strategy is surgical intervention for tumours over 40mm, while those under 40mm are monitored with 6-monthly annual surveillance scans via MRI.\n\n# Definition\n\nA vestibular schwannoma is defined as a benign subarachnoid tumour that exerts local pressure effects on the VIII cranial nerve.\n\n# Epidemiology\n\nIn the UK, vestibular schwannomas, also known as acoustic neuromas, are relatively rare and are estimated to occur in about 1 in 100,000 people annually, most commonly presenting in adults between the ages of 40 and 60.\n\n# Aetiology\n\nVestibular schwannomas, are benign tumors that develop from the Schwann cells of the vestibulocochlear nerve, with the majority being sporadic cases, though a small percentage are associated with a genetic disorder called neurofibromatosis type II.\n\n# Signs and Symptoms\n\n- The most common symptoms reported are asymmetric or unilateral hearing loss and progressive ipsilateral tinnitus.\n- Larger tumours may cause a mass effect leading to signs of raised intracranial pressure and can result in focal neurology including compression of the fifth, seventh, and eighth cranial nerves.\n- Additional symptoms include: dizziness, headaches, and disequilibrium.\n\n# Differential Diagnosis\n\n\n* **Meniere's Disease:** Characterized by recurrent episodes of vertigo, hearing loss, and tinnitus. While both conditions may cause vertigo, Meniere's disease has a different clinical presentation and is not a tumor.\n* **Labyrinthitis:** An inflammation of the inner ear, often caused by viral or bacterial infections, resulting in symptoms similar to vestibular neuromas.\n* **Benign Paroxysmal Positional Vertigo (BPPV):** A common cause of recurrent vertigo, often triggered by head movements. BPPV is not associated with tumors but with dislodged otoliths in the inner ear.\n* **Migraine-Associated Vertigo:** Individuals with migraines may experience vestibular symptoms, which can sometimes be mistaken for vestibular neuromas.\n* **Other Intracranial Lesions:** While less common, intracranial lesions, such as brainstem or cerebellar tumors, can present with similar vestibular symptoms.\n* **Posterior Circulation Stroke:** Vertigo can be a symptom of a stroke, especially when associated with other neurological deficits.\n* **Autoimmune Inner Ear Disease:** An immune-mediated condition affecting the inner ear, causing hearing loss and vestibular symptoms.\n* **Otosclerosis:** An abnormal bone growth in the middle ear that can lead to hearing loss and sometimes imbalance.\n* **Superior Semicircular Canal Dehiscence (SSCD):** A rare condition where there is a hole in the bone covering the superior semicircular canal, leading to vertigo triggered by loud sounds or pressure changes.\n\n\n\n# Investigations\n\nIn patients presenting with unilateral tinnitus and sensorineural deafness, an MRI scan should be performed to exclude the evidence of malignancy.\n\n[lightgallery]\n\n# Management\n\nThe definitive management of vestibular schwannoma is surgery, specifically for tumours over 40mm in size. For tumours under 40mm in size, 6-monthly annual surveillance scans via MRI are recommended.\n\n# References\n\n[Click here for NICE CKS on hearing loss in adults](https://cks.nice.org.uk/topics/hearing-loss-in-adults/)\n\n[Click here for NICE CKS on tinnitus](https://cks.nice.org.uk/topics/tinnitus/)",
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"question": "A 30 year old man is referred to the outpatient ENT clinic with gradual onset bilateral sensorineural hearing loss and tinnitus.\n\nOn examination, he has absent corneal reflexes bilaterally.\n\nAn MRI cerebellopontine angle confirms bilateral vestibular schwannomas.\n\nWhat is the most likely underlying diagnosis?",
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"explanation": "NICE guidelines suggest that ENT referral is only warranted if the signs of symptoms are atypical or do not resolve in 4 weeks, or there have been at least 3 periods during which the patient has experienced episodes of vertigo",
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"explanation": "This is correct. This patient has benign paroxysmal positional vertigo (BPPV), as confirmed by the Dix-Hallpike manoeuvre. The patient can be taught Brandt-Daroff exercises to do at home. The patient should be advised to return after 4 weeks if her dizzy spells have not resolved",
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"explanation": "Symptomatic drug treatment is of limited value in managing BPPV",
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"explanation": "This is an anti-emetic to reduce vomiting.",
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"explanation": "Drug treatment is of limited value in the management of BPPV. Prochlorperazine may sometimes be used in viral labyrinthitis to manage dizziness",
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"comment": "Difference between Epley manoeuvre and \"Brandt-Daroff exercises\" ?",
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"comment": "\"There are alternative manoeuvres that can be used to treat BPPV, such as an Epley manoeuvre. Your specialist may perform an Epley manoeuvre with you in clinic and then recommend Brandt-Daroff exercises for you to use at home as these are easier to perform unsupervised.\"\n\nFrom a patient leaflet about the two... had never heard of it either! ",
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"comment": "Really...\n",
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"explanation": "# Summary\n\nBenign Paroxysmal Positional Vertigo (BPPV) is a condition characterised by sudden episodes of vertigo, typically following head movement. It is the most common cause of vertigo, particularly in the elderly due to calcium deposition within the semicircular canals. The key signs and symptoms include sudden attacks of rotational vertigo lasting for 30 seconds to 1 minute, triggered by changing head positions. There are no associated auditory symptoms. Diagnosis is made using the Dix-Hallpike manoeuvre, and management primarily involves the Epley manoeuvre. \n\n# Definition\n\nBenign Paroxysmal Positional Vertigo (BPPV) is a medical condition characterised by sudden, episodic attacks of vertigo induced by changes in head position. This condition is due to detachment of otoliths in the inner ear, which results in hair cell stimulation and subsequent vertigo symptoms.\n\n# Epidemiology\n\nBPPV is the leading cause of vertigo and is especially prevalent within the elderly population. This increased prevalence is largely attributed to the accumulation of calcium deposits, known as cholelithiasis, within the semicircular canals of the inner ear.\n\n# Aetiology\n\nBPPV arises due to a detachment of otoliths from the utricle of the inner ear. These detached particles can migrate into the semicircular canals, where they stimulate hair cells and lead to symptoms of vertigo.\n\n# Signs and Symptoms\n\nKey clinical features of BPPV include:\n\n- Vertigo attacks provoked by specific head movements, such as turning the head to one side while in bed or looking upwards\n- Episodes of rotational vertigo lasting between 30 seconds to 1 minute\n- Absence of auditory symptoms\n- Recurrent episodes, often resolving naturally over weeks to months\n\n# Differential Diagnosis\n\nDifferential diagnoses for BPPV include other conditions that can cause vertigo such as Meniere's disease, vestibular neuritis, and labyrinthitis. Key signs and symptoms for these conditions include:\n\n- Meniere's disease: episodic vertigo, tinnitus, hearing loss, and a sensation of fullness in the ear\n- Vestibular neuritis: sudden onset of severe vertigo, nausea, and imbalance lasting for several days\n- Labyrinthitis: vertigo, hearing loss, and tinnitus\n\n# Investigations\n\nThe primary diagnostic test for BPPV is the Dix-Hallpike manoeuvre. This test involves a series of specific head movements that provoke the characteristic vertigo and nystagmus associated with BPPV.\n\n[Click here for more information](https://www.thebsa.org.uk/wp-content/uploads/2014/04/HM.pdf)\n\n# Management\n\nThe mainstay of BPPV management is the Epley manoeuvre. This therapeutic manoeuvre aims to move the detached otoliths out of the semicircular canal and back to the utricle where they originate.\n\n[Click here for more information](https://www.racgp.org.au/download/Documents/AFP/2013/January/February/201301handi.pdf)\n\n# References\n\n[Click here for NICE CKS on benign paroxysmal positional vertigo](https://cks.nice.org.uk/topics/benign-paroxysmal-positional-vertigo/)",
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"question": "An 88 year old woman presents to her GP with recurrent episodes of dizziness and vertigo which she says is often brought on when rolling over in bed. The GP performs the Dix-Hallpike manoeuvre which is positive. She is keen for something to manage her symptoms.\n\nWhat is the next best step in managing this patient's dizziness?",
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"explanation": "This would be the next step if the bleeding stopped with first aid measures",
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"comment": "im sorry but no. you would pack and send to A+E for cauterising",
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"comment": "they're already in A&E",
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"comment": "im sorry but no, cautery goes ahead of nasal packing if an obvious bleeding site is seen and you are in the ED ",
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"comment": "You're not Dr brighton yet xx",
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"explanation": "# Summary\n \nEpistaxis refers to nosebleeds, which are a common condition ranging significantly in severity. Many are mild and self-limiting with simple first-aid, however larger bleeds may be life-threatening and require rapid intervention and resuscitation. Contributing factors include trauma (e.g. nose-picking), inflammation, drug use (e.g. cocaine), recent surgery, tumours and bleeding diatheses. Management of epistaxis involves a stepwise approach starting with direct pressure on the cartilaginous part of the nose, cautery, nasal packing, followed by interventions such as arterial embolisation or ligation if bleeding is refractory to other treatments. \n \n# Definition\n \nEpistaxis refers to bleeding from the nose - this usually originates from the anterior nasal septum (Little's area and Kiesselbach's plexus specifically) but around 10% of cases are posterior, originating from branches of the sphenopalatine artery. \n \n# Aetiology\n \nMost cases of epistaxis are mild and self-limiting, with no specific underlying cause identified. Factors that may contribute to epistaxis include:\n\n- Trauma (e.g. nose-picking, blunt trauma, septal perforations and foreign bodies in the nose)\n- Oxygen via nasal cannulae (causes drying and irritation of the nasal mucosa)\n- Recent ENT or maxillofacial surgery\n- Tumours, either malignant (e.g. squamous cell carcinomas) or benign (e.g. angiofibromas)\n- Inflammation (e.g. rhinosinusitis, nasal polyps)\n- Alcohol excess\n- Illicit drug use e.g. snorting cocaine \n- Medications such as nasal steroids\n- Vasculitides (e.g. granulomatosis with polyangiitis)\n- Bleeding diatheses (e.g. thrombocytopenia, Von Willebrand disease, haemophilia, antiplatelet or anticoagulant medications)\n- Environmental factors e.g. inhaled irritants, temperature and humidity\n\n# Signs and symptoms\n\nThe major symptom is nasal bleeding - other signs and symptoms may include:\n\n- Bleeding down the throat (which may present as haemoptysis or haematemesis) - may signify posterior epistaxis\n- Bleeding from both nostrils is another sign of possible posterior epistaxis\n- Signs and symptoms of haemodynamic instability if blood loss is significant (e.g. tachycardia, pallor, syncope)\n- Signs and symptoms of an underlying cause (e.g. nasal obstruction and rhinorrhoea may indicate a tumour or nasal polyps)\n\n# Investigations\n\nIn most cases of nosebleeds, no investigations are required.\n\nIf bleeding is significant, a **venous blood gas** and **FBC** should be done to look for anaemia and thrombocytopenia, a **clotting screen** looking for coagulopathy and a **group and save** or **crossmatch** if blood transfusion is required.\n\nInvestigations may also be required if an underlying serious cause is suspected, e.g. imaging or flexible nasendoscopy for a suspected tumour, or specific blood tests for bleeding disorders such as Von Willebrand disease.\n\n# Management\n\n- The first step in management is **direct compression**.\n- The patient should sit forward (minimising bleeding into the nasopharynx), breathing through their mouth, and pinch the cartilaginous part of the nose for 10-15 minutes. \n- Sucking ice cubes, cold drinks or placing an ice pack on the back of the neck can help to reduce bleeding.\n- This is sufficient to resolve the majority of anterior epistaxis.\n- A **topic antiseptic** (e.g. Naseptin or mupirocin) may be prescribed to reduce crusting and rebleeding.\n- If direct compression does not resolve the epistaxis and a bleeding point can be visualised, **cautery** may be performed. \n- This involves applying a local anaesthetic spray with a vasoconstrictor (e.g. lidocaine with phenylephrine) to temporarily halt bleeding, then apply silver nitrate (chemical cautery) or electrocautery to the area. \n- Only one side of the septum should be cauterised to avoid perforation.\n- If a bleeding point cannot be visualised or bleeding continues despite cautery, **nasal packing** may be used. \n- The most common devices used are nasal tampons (e.g. Merocel) or inflatable packs (e.g. Rapid-Rhino). \n- Both nostrils can be packed to increase pressure on the area of bleeding.\n- In cases of posterior epistaxis, **posterior packing** may be required which may involve insertion of a Foley catheter with the balloon inflated to compress the bleeding area.\n- Packing should be left in place for 24-48 hours to ensure bleeding has stopped.\n- If bleeding continues despite packing, a **surgical approach** may be required (e.g examination under anaesthesia with ligation of bleeding vessels) or interventional radiology may perform an **embolisation**.\n- **Tranexamic acid** should be given to all patients with severe bleeding.\n- Antiplatelets and anticoagulants should usually be held - may need speciality input (e.g. cardiology) in difficult cases such as patients with metallic heart valves.\n- Anticoagulation may need to be reversed with haematology input if needed.\n- Patients who are haemodynamically unstable may need resuscitation and blood transfusion.\n\n# Complications\n\n- Anaemia\n- Recurrent epistaxis\n- Hypovolaemia\n- Aspiration of blood and airway compromise\n- Nasal cautery may cause septal perforation\n- Nasal packing may lead to sinusitis, septal haematoma or pressure necrosis\n\n# NICE Guidelines\n\n[NICE CKS - Epistaxis](https://cks.nice.org.uk/topics/epistaxis-nosebleeds/)\n\n# References\n\n[ENT UK - Epistaxis Guideline](https://www.entuk.org/_userfiles/pages/files/guidelines/global%20ent%20guidelines/nosebleeds.pdf)\n \n[Life in the Fast Lane - Epistaxis](https://litfl.com/a-case-of-epistaxis/)\n\n[Patient UK - Epistaxis](https://patient.info/doctor/nosebleed-epistaxis-pro)",
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"question": "A 24 year old male presents to the Emergency Department with epistaxis which started 1 hour prior to being seen. The nurse practitioner has already applied nasal pressure for 15 minutes. On examination using a nasal speculum, there is an obvious bleeding site in the anterior aspect of the septum. The patient is haemodynamically stable.\n\nWhat is the next best step in management of this patient's epistaxis?",
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"explanation": "This patient has a pneumothorax with high-risk characteristics and so this patient requires admission and insertion of a chest drain",
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"explanation": "This is correct. As this man is over 50 and has a significant smoking history, and is known to have lung disease, this is a pneumothorax with high-risk characteristics. The pneumothorax is over 2cm in size and is therefore amenable to drainage, with chest drain the best option.",
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"explanation": "High flow oxygen is not indicated at this stage. He has normal saturations on room air and, in addition to this, it is not unreasonable to suspect that this patient might be oxygen sensitive given his background of COPD",
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"explanation": "This would be the case if the patient's pneumothorax was less than 1cm",
"id": "31845",
"label": "c",
"name": "Observe for 24h",
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"explanation": "This would be the case if the patient's pneumothorax was an acceptable size without high-risk characteristics",
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"comment": "With the new guidelines, even if there are high-risk characteristics such as existing lung disease would we not now just observe with regular x-ray and follow-up?\n",
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"comment": "in secondary pneumothorax, if pt is breathless or it's >2cm (of which this pt has both) you go with chest drain\nfor secondary, i think you only admit and observe if they'er asymptomatic and it's <1cm",
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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 55 year old presents to the emergency department with sudden onset of breathlessness. He is known to have chronic obstructive pulmonary disease (COPD) and has smoked 20 cigarettes per day for approximately 40 years. His chest x-ray shows a pneumothorax of approximately 3cm in size.\n\nHis observations are all normal and his saturations are 96% on air.\n\nWhat is the next step in this patient's management?",
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"explanation": "This patient has pulseless electrical activity (PEA), which is a non-shockable rhythm. The management should include immediate resumption of CPR, with a rhythm check in 2 minutes",
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"comment": "you would give Adrenaline as soon as possible- question is wrong",
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"comment": "That's not an option. Also, high quality BLS always takes priority over ALS",
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"comment": "However, it is the next step according to advanced life support guidelines as per question.",
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"comment": "Not true. After checking the rhythm, if it is non shockable, the next step is resume cpr. Giving adrenaline comes after cpr has been restarted and in practice would be done by another person to prevent interruption. Question is right.",
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"explanation": "# Summary\n\nAdvanced Life Support (ALS) describes an algorithmic approach to the management of a cardiac arrest by those trained in delivering it. It involves early recognition, taking steps to secure the airway and initiate high quality chest compressions and obtaining intravenous or intraosseous access promptly. Cardiac monitoring should be applied to identify if the rhythm is shockable or non-shockable, which determines what treatment is given. Shockable rhythms require defibrillation, with adrenaline and amiodarone given later on; non-shockable rhythms are treated with adrenaline. \n\n# Definition\n\nAdvanced Life Support is a guideline-based approach to treating patients who have had a cardiac arrest to improve the chances of successful resuscitation and survival. \n\n# Epidemiology\n\nCardiac arrests can be categorised into those that occur out of hospital and those that occur in hospitals. Most out of hospital cardiac arrests occur at home (72%) and 8 out of 10 are due to a cardiac cause. In 7 out of 10 cases resuscitation is attempted, however only 9% of these patients survive to hospital discharge.\n\nIn hospital cardiac arrests tend to occur in older patients (average age 70), with return of spontaneous circulation (ROSC) achieved in 53% of patients. However, only 24% of patients survive to hospital discharge. \n\n# Aetiology\n\nCauses of cardiac arrest can be remembered using the 4Hs and 4Ts mnemonic:\n\n- Hypoxia\n- Hypovolaemia\n- Hypo/hyperkalaemia (and other electrolyte abnormalities)\n- Hypo/hyperthermia\n- Thromboembolism (pulmonary embolism or coronary artery thrombosis)\n- Tamponade\n- Tension pneumothorax\n- Toxins \n\n# Classification\n\nCardiac arrests are managed differently depending on whether the rhythm is **shockable** or **non-shockable**.\n\n**Shockable** rhythms are:\n\n- **Pulseless Ventricular Tachycardia (pVT)** - regular broad complex tachycardia\n- **Ventricular Fibrillation (VF)** - chaotic irregular deflections of varying amplitude\n\n**Non-shockable** rhythms are:\n\n- **Pulseless Electrical Activity (PEA)** - electrical activity that should produce a pulse, but doesn't due to absent or insufficient cardiac output \n- **Asystole** - no detectable electrical activity \n\n# Management\n\n## Management for all cardiac arrests\n\n- **Rapid recognition** of cardiac arrest (ineffective breathing or absent central pulse) is key \n- The first responder should start **cardiopulmonary resuscitation (CPR)** immediately and **call for help**, for example by asking for a cardiac arrest call (2222) to be put out\n- Every two minutes CPR should be stopped for a **rhythm check**\n- Secure the **airway**\n - Oropharyngeal or nasopharyngeal airways may be used initially with a bag valve mask for ventilation\n - Either a supraglottic airway (laryngeal mask airway or i-gel) or an endotracheal tube should be inserted\n - Tracheal intubation should only be attempted by those with a high success rate\n - Confirm the position of the endotracheal tube with waveform capnography (measuring end-tidal carbon dioxide)\n- Give **high-flow oxygen**\n- Gain IV access - if not possible the intraosseous (IO) route can be used\n- Consider reversible causes (as above) and treat as appropriate\n - IV or IO fluids if secondary to hypovolaemia\n - Thrombolysis if secondary to pulmonary embolism\n - Point of care ultrasound (POCUS) may be used to investigate for cardiac tamponade and pneumothorax\n \n## Management of shockable rhythms\n\n- **Defibrillation** should be delivered as early as possible\n - Remove oxygen (ventilator circuits can remain attached)\n - Ensure no one is touching the patient before the shock is delivered\n - No specific energy is specified in guidelines; anything from 120 to 360 joules is suitable\n- Immediately resume CPR after the shock is delivered for two minutes\n- After 3 shocks, give 300mg amiodarone and 1mg adrenaline IV or IO\n- Give repeat doses of adrenaline every 3-5 minutes (i.e. every other cycle)\n- After 5 shocks, give a further dose of amiodarone 150mg\n\n## Management of non-shockable rhythms \n\n- Give adrenaline 1mg IV or IO as soon as possible\n- Give repeat doses of adrenaline every 3-5 minutes (as per shockable rhythms)\n- Defibrillation and amiodarone are not used unless the rhythm changes to a shockable one\n\n# NICE Guidelines\n\n[NICE CKS - Advanced Life Support](https://cks.nice.org.uk/topics/cardiac-arrest-out-of-hospital-care/management/advanced-life-support-adult/)\n\n# References\n\n[Resuscitation Council UK - Adult Advanced Life Support Guidelines](https://www.resus.org.uk/library/2021-resuscitation-guidelines/adult-advanced-life-support-guidelines)\n \n[Resuscitation Council UK - Epidemiology of Cardiac Arrest](https://www.resus.org.uk/library/2021-resuscitation-guidelines/epidemiology-cardiac-arrest-guidelines)\n\n[BNF Treatment Summaries - Cardiopulmonary Resuscitation](https://bnf.nice.org.uk/treatment-summaries/cardiopulmonary-resuscitation/)",
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"question": "A cardiac arrest is called to a medical ward. On arrival, the patient is unresponsive and not breathing. Nursing staff on the ward have already commenced cardiopulmonary resuscitation (CPR) at a rate of 30:2 and attached the defibrillator. An ECG shows normal sinus rhythm, but central pulses cannot be felt.\n\nAccording to the advanced life support (ALS) guidelines, what is the next step in this instance?",
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"__typename": "QuestionChoice",
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"explanation": "This is the management of hyponatraemia in a euvolaemic patient. This patient has a normal sodium level and has is noted to be clinically dehydrated. This patient likely has hyperosmolar hyperglycaemic state (HHS) which leads to severe dehydration which is managed with IV fluids (not restricting)",
"id": "31861",
"label": "d",
"name": "Fluid restriction to 1L per day",
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is the first line fluid for management of hyperosmolar hyperglycaemic state (HHS). Compared to the serum of a patient with HHS, 0.9% is relatively hypotonic so should restore serum osmolarity to a normal level",
"id": "31858",
"label": "a",
"name": "IV 0.9% NaCl",
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"explanation": "This patient has hyperosmolar hyperglycaemic state (HHS) which should be addressed and treated before consideration of adjusting their long term diabetic medication",
"id": "31862",
"label": "e",
"name": "Increase their metformin to 500mg twice daily",
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"explanation": "This is the management for hyperkalaemia. This patient has a normal potassium level and likely has hyperosmolar hyperglycaemic state (HHS). There is evidence to suggest that patients with HHS actually tend to have worse outcomes if they are treated with the diabetic ketoacidosis (DKA) protocol such as with an insulin infusion",
"id": "31860",
"label": "c",
"name": "Insulin and dextrose infusion",
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"explanation": "This is incorrect. This patient has hyperosmolar hyperglycaemic state (HHS) which should be treated with fluids. There is evidence to suggest that patients with HHS actually tend to have worse outcomes if they are treated with the diabetic ketoacidosis (DKA) protocol such as with an insulin infusion",
"id": "31859",
"label": "b",
"name": "Sliding scale insulin infusion",
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"explanation": "# Summary \n \nHyperosmolar Hyperglycaemic State (HHS) is a life-threatening complication of type 2 diabetes, where patients become severely hyperglycaemic and fluid deplete over several days. It tends to present with polyuria and polydipsia, confusion and nausea, and is often triggered by intercurrent infection. Key investigations include blood glucose, ketones and a blood gas to check pH (patients with HHS should not be acidotic or have significant ketonaemia - presence of these may suggest an overlapping syndrome with diabetic ketoacidosis). Bloods including U&Es should be done and serum osmolality calculated or measured. The mainstay of treatment is fluid resuscitation to normalise osmolality and blood glucose. Foot care and venous thromboembolism prophylaxis are also important to prevent complications.\n \n# Definition\n \nHyperosmolar Hyperglycaemic State (HHS) is a complication of type 2 diabetes that is usually seen in older patients with known diabetes (although it may represent a first presentation).\n\nThe key features of HHS are:\n\n- Blood glucose ≥ 30 mmol/L\n- Serum osmolality ≥ 320 mOsm/kg\n- Significant hypovolaemia \n- Blood ketones ≤ 3 mmol/L\n- pH ≥ 7.3 and bicarbonate ≥15.0 mmol/L\n\nPatients who otherwise meet the criteria for HHS but are acidotic or have high blood ketones may have a mixed picture of HHS and diabetic ketoacidosis (DKA) - these patients require an insulin infusion alongside fluid resuscitation in order to suppress ketosis. \n\n# Aetiology\n\nFactors that may precipitate HHS include:\n\n- Infection (commonly chest or urinary tract)\n- Recent trauma or surgery\n- Other acute events e.g. stroke or myocardial infarction\n- Medications e.g. steroids\n\n# Signs and symptoms\n \nSymptoms often develop over the course of several days to short weeks, including:\n \n - Polyuria\n - Polydipsia\n - Nausea\n - Lethargy\n - Weakness\n - Confusion\n - Drowsiness\n - Loss of consciousness\n \nSigns:\n\n- Tachycardia\n- Hypotension\n- Altered mental state\n- Sunken eyes\n- Dry mucous membranes\n\n# Investigations\n \n**Bedside tests:**\n\n- Capillary blood glucose - if 30 or higher indicates HHS\n- Venous blood gas - to check acid-base status\n- Capillary blood ketones - if > 3 suspect HHS/DKA overlap\n- ECG - to look for precipitating events or complications e.g. ischaemic changes\n- Urine dip and MSU - looking for urinary tract infection, will show glycosuria\n\n**Blood tests:**\n\n- Serum osmolality **(can calculate as (2xNa+) + glucose + urea)**\n- Serum glucose\n- U&Es - looking for AKI and electrolyte imbalances\n- FBC and CRP - inflammatory markers may be raised in intercurrent infection\n- LFTs - may be deranged in some triggering infections e.g. ascending cholangitis\n- Bone profile - looking for other causes of confusion e.g. hypercalcaemia\n- Blood cultures - if infection suspected\n\n**Imaging:**\n\n- Chest X-ray - as part of septic screen \n- Other imaging based on suspected triggers - e.g. CT head for suspected stroke, liver ultrasound if suspected biliary infection\n\n# Management\n \n- The key to emergency management of HHS is prompt initiation of fluid resuscitation\n - Start with 1L of 0.9% saline over 1 hour\n - Close monitoring is needed especially in elderly patients or those at risk of heart failure\n - Catheterisation may be required for close monitoring of fluid balance\n- An insulin infusion is **not** required initially unless there is a mixed picture of HHS and DKA\n- Potassium replacement:\n\t- if <3.5 or >6, senior review/ICU input required\n\t- 5.5-5.9 - nil potassium needed\n\t- 3.5-5.5 - add 40mmol/L to next bag of fluids\n- Patients should be assessed for an underlying cause of HHS (e.g. sepsis, stroke) and appropriate management instigated\n- Assess foot health and instigate foot care (offload heels, daily checks)\n- Intensive monitoring is required with hourly bloods to check glucose, ketones, U&Es and calculate serum osmolality for the first 6 hours\n - The target is for osmolality to fall by 3-8 mOsm/kg/hr\n - If this is not achieved with 0.9% saline and fluid balance is adequate, fluids may be switched to 0.45% saline\n - If glucose plateaus and fluid balance is adequate, consider starting an insulin infusion at 0.05 units/kg/hour\n- Ensure venous thromboembolism prophylaxis is prescribed (patients are high risk due to immobility and dehydration)\n- Refer to the inpatient diabetes team for assessment prior to discharge\n\n# Complications\n\n* Hypovolemic shock\n* Cerebral oedema\n* Thromboembolic events\n* Acute kidney injury\n* Cardiac arrhythmias\n* Respiratory failure\n* Long-term neurological sequelae\n\n# NICE Guidelines\n\n[NICE CKS - Type 2 Diabetes](https://cks.nice.org.uk/topics/diabetes-type-2/)\n\n# References\n \n[Association of British Clinical Diabetologists - Management of\nHyperosmolar Hyperglycaemic State in Adults](https://abcd.care/sites/default/files/site_uploads/JBDS_Guidelines_Current/JBDS_06_The_Management_of_Hyperosmolar_Hyperglycaemic_State_HHS_%20in_Adults_FINAL_0.pdf)\n\n[ABCD - HHS algorithm](https://abcd.care/sites/default/files/site_uploads/JBDS_Guidelines_Current/JBDS_06_HHS_care_pathway_in_adults_2022.pdf)",
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"explanation": "# Summary\n \nAspirin overdose (which is the most common type of salicylate poisoning) may occur accidentally or intentionally as a means of self-harm. Symptoms include nausea and vomiting, epigastric pain, tinnitus, lethargy and confusion. Signs include fever, diaphoresis, seizures and coma. Acid-base balance is complex, with respiratory alkalosis occurring secondary to hyperventilation as well as a metabolic acidosis secondary to the aspirin itself. Investigations include salicylate levels, a VBG to look at acid-base status and bloods for electrolyte levels. Management includes activated charcoal for recent ingestion, intravenous fluids with electrolyte replacement, and sodium bicarbonate which acts to enhance urinary excretion of salicylates. Haemodialysis may be required in severe cases where there are complications such as renal failure, severe metabolic acidosis or seizures.\n \n\n# Definition\n \nAspirin overdose occurs when an excessive amount of aspirin is ingested, either accidentally or intentionally. There is a spectrum of clinical manifestations, ranging from mild toxicity to severe and life-threatening complications.\n\n# Signs and symptoms\n\nSymptoms include:\n\n- Nausea and vomiting\n- Tinnitus\n- Epigastric pain \n- Confusion\n- Dizziness\n\nSigns include:\n\n- Hyperventilation\n- Tachycardia and a bounding pulse\n- Diaphoresis\n- Fevers\n- Pulmonary oedema\n- Seizures\n- Coma\n\n# Investigations\n \n**Bedside tests:**\n\n- **Venous blood gas** classically shows respiratory alkalosis initially due to hyperventilation, before progressing to a metabolic acidosis\n- **Capillary blood glucose** screening for hypo or hyperglycaemia causing altered mental state; aspirin overdose can cause hypoglycaemia\n- **ECG** - aspirin overdose can cause QRS widening, AV block or ventricular arrhythmias\n- **Urinary pH** may be measured to guide urinary alkalinisation \n\n**Blood tests:**\n\n- **Salicylate levels** at repeated intervals (e.g. 2 hourly) until levels stop rising (as absorption of aspirin may be slow), helps to assess severity of poisoning and guide need for haemodialysis if very high\n- **U&Es** to monitor electrolytes (hypokalaemia may occur) and for renal failure\n- **Paracetamol levels** to screen for a mixed overdose\n \n# Management\n \n- Give activated charcoal if aspirin ingestion occurred less than 1 hour ago\n- IV fluid resuscitation if volume-deplete\n- Correct hypokalaemia if present before giving bicarbonate\n- IV sodium bicarbonate is given to alkalinise the urine which enhances excretion of salicylates (can cause hypokalaemia so need to monitor potassium as well as urinary pH)\n- Manage complications e.g. cooling measures for hyperthermia, benzodiazepines for seizures\n- Haemodialysis may be required for severe poisoning, for example:\n - Salicylate levels > 700mg/kg\n - Severe metabolic acidosis \n - Seizures or coma\n- Once stabilised, psychological assessment for patients presenting with an intentional overdose\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 - Emergency Treatment of Poisoning](https://bnf.nice.org.uk/treatment-summary/poisoning-emergency-treatment.html)",
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"explanation": "# Summary\n\nTricyclic antidepressants (TCAs) e.g. amitriptyline, are primarily noradrenaline and serotonin reuptake inhibitors, which may be fatal in overdose. Key signs and symptoms include drowsiness, confusion, arrhythmias, seizures, vomiting, headache, dry mouth and dilated pupils. Investigations include a blood gas looking for acidosis, bloods for electrolyte disturbances (hypokalaemia may occur) and an ECG to check for arrhythmias. Management is supportive; activated charcoal can be given to patients presenting within an hour of the overdose and sodium bicarbonate is used to treat arrhythmias and acidosis. \n \n# Definition\n \nTricyclic antidepressants (TCAs) are a class of drugs that act as noradrenaline and serotonin reuptake inhibitors. Examples include amitriptyline, dosulepin and nortriptyline.\n\nThey are now less commonly prescribed than other antidepressant classes, but are often used for other indications such as neuropathic pain or migraine prophylaxis. \n\nTCA overdose can cause severe toxicity due to blockade of sodium channels and antimuscarinic effects. Neurological and cardiovascular toxicities predominate, although anticholinergic symptoms are wide-ranging.\n\n# Aetiology\n\nThe majority of cases of TCA overdose are intentional as a means of self-harm or a suicide attempt. Accidental ingestion may also occur, particularly in children.\n\nTCAs have a narrow therapeutic index and a dose of 10-20 mg/kg represents a potentially fatal overdose.\n \n# Signs and Symptoms\n \nSymptoms include:\n\n- Palpitations\n- Drowsiness\n- Dry mouth\n- Hot, dry skin\n- Confusion\n- Hallucinations\n- Headache\n- Nausea and vomiting\n\nSigns include:\n\n - Reduced level of consciousness\n - Seizures\n - Mydriasis\n - Urinary retention\n - Ileus\n - Hypotension\n - Tachycardia\n \n\n# Differential Diagnosis\n\n- **Sodium channel blocker overdose** e.g. antiarrhythmics such as flecainide or quinine; cause similar ECG findings with arrhythmias and QRS widening as well as seizures and coma\n- **Anticholinergic overdose** other medications such as carbamazepine, antipsychotics and antihistamines as well as plants (e.g. deadly nightshade) have similar manifestations in overdose with cardiovascular and neurological effects\n- **Alcohol intoxication** can cause overlapping symptoms of nausea and vomiting, drowsiness and reduced levels of consciousness but not the anticholinergic effects\n\n# Investigations\n\n**Bedside tests:**\n\n- **ECG** typically shows a widened QRS and prolonged QTc, may progress to life-threatening arrhythmias (QRS > 100ms is predictive of seizures; >160ms of ventricular arrhythmias)\n- **Venous blood gas** looking for acidosis (usually mixed respiratory and metabolic)\n- **Bladder scan** if urinary retention is suspected to confirm need for a catheter\n- **Capillary blood glucose** to rule out hypoglycaemia as a cause of symptoms\n\n**Blood tests:**\n\n- **Full blood count** as a baseline\n- **U&Es** looking for hypokalaemia that increases the risk of arrhythmias, and renal impairment that increases the risk of toxicity\n- **Bone profile and magnesium** looking for other electrolyte abnormalities that may contribute to arrhythmias\n- **LFTs** especially if concurrent paracetamol overdose is suspected\n- **Paracetamol and salicylate levels** to screen for other concurrent overdoses\n \n[lightgallery]\n \n# Management\n \n- A to E approach; ensure airway is secured if reduced level of consciousness or seizures\n- **Cardiac monitoring** if significant overdose or ECG changes\n- Give **activated charcoal** if within 1 hour of overdose (via an NG tube if needed)\n- Resuscitate with **IV fluids** +/- vasopressors if hypotensive\n- Give **IV sodium bicarbonate** if acidotic, QRS prolongation or arrhythmias \n- **Benzodiazepines** may be required for agitation or seizures\n- **Intensive care admission** may be required in significant overdose - hyperventilation can be used in intubated patients to treat acidosis\n- **Catheterise** if in urinary retention\n- **Psychiatry input** once recovered for patients who have taken an intentional overdose\n\n# NICE Guidelines\n\n[NICE CKS - Antidepressant toxicity in overdose](https://cks.nice.org.uk/topics/depression/prescribing-information/antidepressant-toxicity-in-overdose/)\n\n# References\n \n[Life in the Fast Lane - Tricyclic Overdose](https://litfl.com/tricyclic-overdose-sodium-channel-blocker-toxicity/)\n\n[Emergency Medical Minute - Tricyclic Overdose](https://emergencymedicalminute.org/tca-overdose/)",
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"explanation": "Section 5(4) allows a qualified nurse to detain a patient in hospital for up to 6 hours until a fully registered doctor can assess the need for further detention. It cannot be used to treat patients against their wishes",
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"comment": "Because they're in A&E do they not have to admitted under a 5(2) first? And then psych can come see them and put in place a section 2 for treatment? Thanks in advance:)",
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"comment": "sec 5(2) and 5(4) are is not valid for A and E",
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"comment": "Section 5 applies to patient's in the ward rather than ED",
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"comment": "In A and E surely they should be initially placed under a Section 4, then converted to a section 2?",
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"comment": "This is what I was thinking as well. During my Psych placement, the psychiatrist told me it can sometimes take 5 days to get a section 2!",
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"comment": "Section 2 can't be applied in an emergency department",
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"comment": "In some hospitals the ED counts as a public place so think it can?",
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"comment": "section 3 would be a better answer as she's already got a diagnosis and been assessed",
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"comment": "I'm pretty sure an explanation to a previous (similar) question said section 2 is specifically for 'assessment' and section 3 is specifically for 'treatment'",
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"comment": "yeah but you can still give treatment under section 2",
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"comment": "Section 2 is assessment/investigation, she already has a formal diagnosis so should be a section 4 then section 3 when appropriate",
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"explanation": "# Summary\n\nAnorexia nervosa is a severe psychiatric disorder characterized by extreme dietary restriction, an intense fear of gaining weight, and a distorted body image. This complex condition predominantly affects young individuals, particularly females, and poses significant health risks, including malnutrition, electrolyte imbalances, and potential life-threatening complications. It has the highest mortality rate of all psychiatric disorders.\n\n# Definition\n\nAnorexia nervosa is a serious mental health disorder characterized by self-imposed starvation and a relentless pursuit of extreme thinness. Individuals with anorexia nervosa have a distorted body image, viewing themselves as overweight even when they are dangerously underweight. There are two main subtypes:\n\n- **Restrictive Subtype:** Characterized by minimal food intake and excessive exercise.\n- **Bulimic Subtype:** Involves episodic binge eating followed by behaviors like laxative use or induced vomiting.\n\nIt is diagnosed based on specific criteria outlined in both the International Classification of Diseases, 11th Edition (ICD-11) and the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5):\n\n**ICD-11 Criteria:**\n\nTo meet the ICD-11 criteria for anorexia nervosa, individuals must exhibit the following:\n\n1. **Significantly Low Body Weight:** The individual's body weight is significantly below the normal or expected weight for their age and height.\n\n2. **Fear of Gaining Weight:** There is an intense fear of gaining weight, or becoming fat, even when underweight.\n\n3. **Distorted Body Image:** The individual has a distorted self-perception, with an overemphasis on their weight and shape.\n\n4. **Restrictive Eating:** There is persistent restrictive eating, often leading to malnutrition.\n\n**DSM-5 Criteria:**\n\nThe DSM-5 criteria for anorexia nervosa include the following:\n\n1. **Restriction of Energy Intake:** The individual persistently limits their food intake, leading to low body weight relative to their age, sex, developmental trajectory, and physical health.\n\n2. **Intense Fear of Gaining Weight:** A preoccupation with body weight or shape, as well as the fear of gaining weight, is a core feature.\n\n3. **Body Image Disturbance:** A distorted body image, where the individual perceives themselves as overweight despite being underweight, is present.\n\nThe specific criteria may vary between ICD-11 and DSM-5, but the essential elements of severe dietary restriction, weight and shape preoccupation, and distorted body image are central to the diagnosis. Note that BMI and amenorrhoea are no longer specifically mentioned in DSM-5 anymore.\n\n# Epidemiology\n\nAnorexia nervosa primarily affects adolescents and young adults, with a higher prevalence among females. However, it can occur in individuals of any age or gender. The condition is more common in industrialized countries and often co-occurs with other psychiatric disorders, such as depression and anxiety.\nThe incidence of anorexia nervosa is 6/100,000, with the highest incidence occurring between age 13-17. \n\n# Pathophysiology\n\n- Anorexia nervosa is not due to a single causative factor, with complex biopsychosocial factors at play:\n\t- Biological factors include the presence of family history and genetic influence\n\t- Psychological: Presence of comorbid mental health disorders, such as anxiety, depression, obsessive-compulsive disorders or obsessive/perfectionist personalities\n\t- Social: Maternal encouragement of weight loss or at risk professions such as models, dancers or sportspeople\n\n# Clinical features\n\n- History:\n\t- Preoccupation with food and calories\n\t- Starvation via restricting intake, purging (through induced emesis, diuretic or laxative abuse) or excessive exercise\n\t- Poor insight \n\t- Overvalued, intrusive obsession with weight, shape and fear of becoming fat\n\t- Weight/calorie goals in mind regardless of their impact on physical health \n- Examination:\n\t- BMI <17.5 kg/m<sup>2</sup> (contrast with bulimia nervosa, where there may be many similar features, but the BMI is normal‚ a key distinguishing feature)\n\t- Hypotension\n\t- Bradycardia\n\t- Enlarged salivary glands\n\t- Lanugo hair (fine hair covering the skin)\n\t- Amenorrhoea (hypogonadotropic hypogonadism)\n\t- Additional features in the 'bulimic' subtype may include hypokalaemic hypochloraemic metabolic alkalosis, pitted teeth, parotid swelling, and scarring of the dorsum of the hand (Russell’s sign).\n\n# Investigations\n\n- Blood results:\n\t- Deranged electrolytes - typically low calcium, magnesium, phosphate and potassium \n\t- Low sex hormone levels (FSH, LH, oestrogen and testosterone)\n\t- Leukopenia\n\t- Raised growth hormone and cortisol levels (stress hormones)\n\t- Hypercholesterolaemia\n\t- Metabolic alkalosis, either due to vomiting or use of diuretics \n\n# Management \n\nManagement approaches are multi-faceted and tailored to the patient's specific needs. In adults, interventions may include:\n\n- **Cognitive Behavioral Therapy for Eating Disorders (CBT-ED):** Focusing on changing thoughts and behaviors related to eating and body image.\n- **MANTRA (Maudsley Model of Anorexia Nervosa Treatment for Adults):** Targeting the core beliefs behind anorexia.\n- **Specialist Supportive Clinical Management (SSCM):** Providing a supportive framework for treatment.\n\nFor individuals under 18, AN-focused family therapy is often the first-line approach, with CBT-ED as a second-line option.\n\n- **Medical**\n\t- Selective serotonin release inhibitors (SSRIs) may be used‚ these have not been shown to be effective at treating the anorexia nervosa directly, but may be effective for comorbid mental health issues, commonly depression and anxiety\n- **Mental Health Act**\n\t- In some cases where the patient's life is considered at immediate risk, admission under the Mental Health Act with structured feeding (and in some cases nasogastric tube feeding) is warranted\n\t- Under the Mental Health Act, feeding is a treatment for anorexia nervosa and, as such, treatment can occur without patient consent under this framework\n\n**Inpatient Admission:**\n\nIndications for specialist inpatient programs may include severe or rapid weight loss, significant suicide risk, or inability to perform the SUSS test (sit-up, squat, and stand). Admission is also indicated if proximal muscle weakness suggests weak respiratory muscles.\n\nIf patients are very unwell the **MARSIPAN checklist** should be used to guide management.\n\n# Complications \n\n- Refeeding syndrome:\n\t- A potentially fatal disorder that occurs when nutritional intake is resumed too rapidly after a period of low caloric intake\n\t- symptoms may include oedema, confusion and tachycardia\n\t- \tRapidly increasing insulin levels lead to shifts of potassium, magnesium and phosphate from extracellular to intracellular spaces‚ these need to be replenished\n\t- Preventative measures include: \n\t - The provision of high-dose vitamins (eg. Pabrinex<sup></sup>) before feeding commences\n\t - Monitoring with daily bloods and replenishing electrolytes early \n\t - Building caloric intake gradually with the help of a dietitian‚ NICE recommends that refeeding is started at no more than 50% of calorie requirement in 'patients who have eaten little or nothing for more than 5 days'\n- Cardiac arrhythmias: \n\t- These patients are at higher risk of arrhythmias and an ECG should be performed periodically, especially if they are complaining of cardiac symptoms (eg. palpitations, fainting episodes or dizzy/light-headed spells)\n\t- Bradycardia and prolonged QTc are often seen\n- Osteoporosis‚ a long-term complication\n\n# Prognosis\n\n- Positive prognostic indicators include:\n\t- The presence of normal social‚ emotional milestones‚ this is important to form bonds with therapists during CBT\n- Negative prognostic indicators include:\n\t- Presentation after the age of 20 years‚ difficult to reverse fixed beliefs\n\t- BMI <16 kg/m<sup>2</sup>\n\t- Marked anxiety when eating in front of others, which indicates issues with socialisation \n\t- Binging/vomiting responds less well to CBT than starvation\n\n# NICE Guidelines \n\n[NICE Guidelines: Eating Disorders](https://www.nice.org.uk/guidance/ng69)",
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"question": "A 19-year-old female with a background of anorexia nervosa is brought to the emergency department by her mother, who is concerned about her physical health. Her mother reports that she hasn't eaten anything in 5 days. On examination, she appears cachectic, has a heart rate of 55 beats per minute, and a blood pressure of 85/50mmHg. The patient refuses to be admitted to hospital.\n\nThe multi-disciplinary team are all in agreement that this patient should be admitted for artificial feeding. Under which section of the Mental Health Act should this be done?",
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173,469,408 | false | 13 | null | 6,495,298 | null | false | [] | null | 6,380 | {
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"explanation": "This would be breaking patient confidentiality. The clinician should inform the DVLA but should not speak to a next of kin against the patient's wishes",
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"name": "Ring his next kin and insist they inform the DVLA on his behalf",
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"explanation": "If the clinician has concerns that the patient has not informed the DVLA that they shouldn't be driving, then they should inform the DVLA as soon as reasonably possible. By delaying this for a week, they would be putting the wider public at risk",
"id": "31902",
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"name": "Arrange a follow-up appointment for one week and ensure then that he has informed the DVLA",
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"explanation": "This is one of the few circumstances in which a doctor can break patient confidentiality. In this circumstance, the wider risk to the public is deemed more important than the patient's right to confidentiality and, if the patient refuses to inform the DVLA themselves, the clinician is obliged to notify the DVLA",
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"explanation": "There is no legal requirement to inform the police if patients are driving against advice",
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"name": "Report this to the police",
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"explanation": "This is correct. This is one of the few circumstances where the clinician is obliged to break confidentiality and inform the DVLA if the patient refuses to, as the risk to the general public is more important than the patient's right to confidentiality. It is best practice to inform the patient that you will notify the DVLA before you do so",
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"explanation": "# Overview\n\nPatients have a legal right to confidentiality (under both Common Law and Human Rights Law), and doctors have the corresponding legal duty to provide this right to confidentiality.\n\nHowever, this right to confidentiality is not absolute. There are a number of situations in which the law obliges doctors to breach confidentiality, i.e. there is a legal duty to breach confidentiality. There are also some situations where a doctor has a legal defence to breach confidentiality.\n\n# Legal Duties to Breach Confidentiality\n\n1. If ordered to by a court or judge\n2. To satisfy statutory requirements\n\n _e.g. to inform the local authority about notifiable diseases under the Public Health Act 1984_\n\n _e.g. under the Road Traffic Act, must provide identifying information to the police on request_\n\n _e.g. under the Terrorism Act 2000, must report any suspicions of terrorism_",
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"comment": "Is the documented discussion enough to retrospectively fill out a DNACPR form? ",
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"comment": "i thought that in-hospital DNACPR forms were only valid for that hospital admission and had to be reassessed and rewritten on each admission? If she'd changed her mind etc. wouldn't it be better to ask loved ones until she's able to communicate herself?",
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"comment": "Agreed, each DNACPR form can either be written for that specific hospital admission or with no-end date. NHS website says \"It's recommended that a DNACPR is reviewed each time your situation changes – for example, when you leave hospital.\"",
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"explanation": "# Overview\n\nA Do Not Attempt CPR (DNACPR) decision can also be known as Do Not Attempt Resuscitation (DNAR)\n\nA DNACPR decision provides information to healthcare professionals present on the best action to take if an individual suffers a cardiac arrest. A DNACPR is recorded, normally on a CPR Decision form, but is not in itself legally binding. This means that a doctor can overrule an existing DNACPR if they believe the circumstances do mean CPR would be in the patient's best interests.\n\nA DNACPR can be made if cardiac or respiratory arrest is an expected part of the dying process, and either CPR will not be successful, or if CPR may be successful but the clinical outcomes (e.g. trauma and prognosis) mean it is not clinically appropriate. A patient with capacity may also refuse CPR.\n\n# Best Interests \n\nDoctors can ultimately make the decision to put a DNACPR in place if it is in the patient's _best interests_, even if the patient themselves or their family disagrees. However, following a legal case in 2014, doctors must engage the patient and those close to them on the decision to make a DNACPR, and inform them if the decision to make a DNACPR order has occurred.\n\n# R (Tracey) v Cambridge University Hospitals NHS Foundation Trust, 2014 \n\nJanet Tracey died in Addenbrooke's Hospital in March 2011. She had been diagnosed with terminal lung cancer and had subsequently been involved in a car crash, in which she sustained a spinal injury. She required ventilation in the Intensive Care Unit (ICU), and after attempts to remove her from the ventilator were unsuccessful, a DNACPR notice was placed in her medical notes. Neither Janet Tracey nor her family were consulted about or informed of this decision.\n\nThe legal case concluded in favour of Tracey, finding that her Human Rights had been breached. The case acknowledged that the decision to put a DNACPR in place is ultimately a medical decision, and patients cannot demand treatment. But, the case did result in changes to DNACPR guidance:\n\nFirstly, the decision to not tell a patient about a DNACPR notice can no longer be based on the fact that telling them would cause “distress”. Only if discussing a DNACPR order would cause the patient “physical or psychological harm”, can doctors justify not discussing it. In other circumstances, doctors are legally obliged to discuss a DNACPR order that has been made.\n\nSecondly, it used to be the case that doctors were not obliged to discuss a DNACPR decision if the clinical decision has been made that CPR would be futile. This case amended this, making it a legal obligation for doctors to inform the patient that a DNACPR decision has been made, regardless of whether or not CPR could ever be successful (i.e. futility of CPR is justification for doctors making a best interests decision to make a DNACPR order - even if the patient wants CPR, but doctors are still legally obliged to inform the patient that a DNACPR order has been made).\n\nA DNACPR decision relates only to CPR, and is not a refusal of any other treatment.",
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"question": "A 90-year-old is admitted to hospital from a care home with a two day history of dysuria, urinary incontinence and increased confusion. She is pyrexial and extremely drowsy and is unable to hold a conversation. She has a background of congestive heart failure, hypertension, dementia and recurrent urinary tract infection. On her electronic patient record, there is a discussion documented from an admission with a fall three months ago where she states that she would not like to be resuscitated in the event of a cardiac arrest. It was documented by the team at the time that she had capacity. \n\nWhich of the following is the next best step?",
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"explanation": "Verbal consent is required for an intimate examination, and this should be documented formally",
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"name": "Verbal consent and document this in the notes",
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"explanation": "Consent in writing is not required for a rectal examination; verbal consent will suffice. A formal consent form with the patient's signature is required for surgical procedures",
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"comment": "fairs to the 2% who decided they dont need consent x",
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"explanation": "# Consent \n\nConsent must be obtained from a patient before undertaking a treatment or procedure. If it is not, then this could constitute the offence of **battery** (\"touching in a harmful or offensive manner without consent or lawful justification\") - even if there was no hostile intent or harm caused.\n\n# Conditions for valid consent\n\nUnder the **Mental Capacity Act**, there are a number of conditions that have to be met for valid consent to be obtained from a patient:\n\n1. The patient must have **capacity**. For this, the individual must be able to: understand information, retain information, weigh the information and reach a conclusion, and communicate the decision they have reached.\n\n2. The consent must be **freely given** (i.e. uncoerced) and the patient must be **suitably informed** (i.e. have been given a suitable level of detail of the procedure, and expected outcomes and risks).\n\n# Assumed Capacity \n\nFor an adult, capacity is assumed unless there is reason to doubt; for example the patient has learning difficulties which impacts on their ability to understand and process new information.\n\n# How Is Consent Taken?\n\nValid consent can be received in writing, verbally or tacitly (where it is implied or indicated). A signed consent form does not - by itself - equal 'consent', it is purely _related evidence_.\n\n# Who Can Obtain Consent?\n\nThe person who should obtain the consent from a patient should be the professional undertaking the procedure, or someone familiar with it, who is able to explain all the necessary information and answer any questions the patient may have.",
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"question": "A 60-year-old inpatient experiences rectal bleeding. A rectal examination is indicated, which is performed by a junior doctor at the bedside. There are no concerns about their capacity to make decisions.\n\nIn terms of consent, which of the following is required?",
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"explanation": "NICE recommend using either the FeverPAIN criteria or Centor criteria to identify which patients are more likely to benefit from antibiotics. This patient has a FeverPAIN score of 5 (for fever, purulence, attended rapidly, inflamed tonsils, and no cough or coryza) and a Centor score of 3 (tonsillar exudate, history of ever and s=absence of cough). Both of these mean that the patient should receive antibiotics. The first line for a patient not allergic or intolerant to penicillin is phenoxymethylpenicillin. In patients who are penicillin allergic or intolerant, alternative antibiotic choices include clarithromycin or erythromycin",
"id": "31938",
"label": "a",
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"explanation": "Doxycycline is not indicated for use in tonsillitis. Doxycycline is most commonly used in respiratory tract infections particularly in those who are penicillin allergic or intolerant",
"id": "31942",
"label": "e",
"name": "Prescribe doxycycline 200mg for 1 dose, then maintenance 100mg OD for 5 days total",
"picture": null,
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"explanation": "Antibiotic are indicated in this patient as he has a FeverPAIN score of 5 or a Centor score of 3",
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"name": "Reassure and explain that there is no indication for antibiotics at present",
"picture": null,
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Amoxicillin is not indicated for use in tonsillitis. Common indications for amoxicillin include respiratory tract and urinary tract infections",
"id": "31941",
"label": "d",
"name": "Prescribe amoxicillin 500mg TDS for 5 days",
"picture": null,
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"__typename": "QuestionChoice",
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"explanation": "There is no indication that this patient would not, at present, be able to manage at home. Indications for referral to hospital would include stridor, clinical suspicion of acute epiglottitis, dehydration, or signs of any complications. He does not appear to be systemically unwell from his observations. Immunosuppression is another indication to urgently refer to hospital, which we have no reason to think that this patient is",
"id": "31939",
"label": "b",
"name": "Refer urgently to hospital",
"picture": null,
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"comment": "doesnt centor criteria need fever of >38.5?",
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"comment": ">38 I believe",
"createdAt": 1683130593,
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"comment": "Swear the prescription is for 10 days and not 5 which is what threw me off",
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"explanation": "# Summary\n \nTonsillitis is an acute inflammation of the tonsils, often with a purulent exudate in bacterial cases. The most common cause of tonsillitis are viruses, however, the most common bacterium causing tonsillitis is Streptococcus pyogenes (group A streptococcus). The CENTOR criteria can be used to determine the likelihood of a bacterial infection, and management of bacterial tonsillitis often involves antibiotic treatment. Key signs and symptoms can include tonsillar exudate, tender anterior cervical lymphadenopathy, fever over 38 degrees Celsius, and absence of a cough. \n \n# Definition\n \n\nTonsillitis is a form of pharyngitis characterised by acute inflammation of the tonsils, often with a purulent exudate present in bacterial tonsillitis.\n \n\n# Epidemiology\n \n\nIn the UK, tonsillitis is a common condition that predominantly affects children and adolescents, with an estimated 7.4% of GP consultations for children under 15 years involving a sore throat or tonsillitis as the primary reason for the visit.\n \n\n# Aetiology\n \n\nThe most common causative organism of tonsillitis is Streptococcus pyogenes (group A streptococcus). Epstein-Barr virus (EBV) is another common cause.\n \nRisk factors for tonsillitis include:\n \n - Age 5-15 years\n - Immunodeficiency \n - Family history of tonsillitis \n - Close contact with an infected individual \n \n\n# Signs and Symptoms \n \n - Sore throat \n - The child may also complain of referred pain in the ears or a headache \n - Changes to the sound of the child's voice or cry \n - Purulent and inflamed tonsils\n - Lymphadenopathy \n \n\n# Differential Diagnosis\n \n\nDifferential diagnoses for tonsillitis include the following:\n \n\n - **Bacterial Tonsillitis**: Main signs and symptoms include cervical lymphadenopathy, tonsillar exudate, and fever.\n - **Viral Tonsillitis**: Symptoms are often milder, and accompanied by coryzal symptoms (i.e. cough, rhinorrhoea). \n - **Infectious Mononucleosis**: Also known as glandular fever, this is more common in teenagers. This presents with enlarged tonsils, fatigue and occasionally with splenomegaly. \n - **Hand, foot and mouth disease**: This is caused by the Coxsackie virus, and will feature blisters on the tonsils and roof of the child's mouth. Blisters may also be found on the feet and hands.\n \n\n# Investigations\n \n\nThe CENTOR criteria can be used to indicate the likelihood of a sore throat being due to a bacterial infection. The criteria are as follows:\n \n\n 1. Tonsillar exudate\n 2. Tender anterior cervical lymphadenopathy\n 3. Fever over 38 degrees Celsius\n 4. Absence of a cough\n \n\n [lightgallery]\n \n\nEach of the CENTOR criteria scores 1 point, with a maximum score of 4. A score of 0, 1 or 2 is thought to be associated with a 3 to 17% likelihood of isolating Streptococcus. A score of 3 or 4 is thought to be associated with a 32 to 56% likelihood of isolating Streptococcus.\n\nAlternatively, the FeverPAIN score can be used. The criteria for this include:\n\n- **Fever**\n- **P**us on tonsils\n- **A**ttended within 3 days of symptom onset\n- **I**nflamed tonsils\n- **N**o cough or coryza \n\nDiagnosis is usually clinical, however, in some cases, further investigations may include:\n\n- Throat swab for microscopy and culture\n- Monospot (heterophile antibody) test for glandular fever \n \n\n# Management\n \n\nBacterial tonsillitis with a CENTOR criteria score of 3/4, FeverPAIN score of 4 or 5, or evidence of systemic upset/immunosuppression warrants prescribing antibiotics:\n \n\n- 1st line: Penicillin V PO QDS for 5-10 days\n - Dose is dependent on age, see BNFc for dosing \n- Alternative in penicillin allergy: Clarithromycin/Erythromycin PO BD for 5 days\n - Dose is dependent on age, see BNFc for dosing \n\nFor patients with a CENTOR score of 0-2 or FeverPAIN score of 0 or 1:\n\n- Advise that antibiotics are not needed as they do not tend to alter how long symptoms last and may cause side effects such as diarrhoea and nausea.\n- Conservative management including paracetamol for analgesia and ensuring adequate fluid intake. \n\nIf the child is systemically very unwell or has severe complications, consider referring the child to the hospital. \n\n# Complications\n\n- Quinsy (peritonsillar abscess)\n- Acute otitis media \n- If tonsillitis is due to Group A beta haemolytic step:\n - Rheumatic fever\n - Syndenham's chorea \n - Glomerulonephritis \n - Scarlet fever \n\n# Prognosis \n\nTonsillitis is usually self-resolving within 3-4 days. Some children will have recurrent tonsillitis, and this recurrence may be reduced by smoking cessation for the parents or through tonsillectomy. \n\nTonsillectomy may be indicated for severe recurrent tonsillitis (more than 7 episodes/year for one year, more than 5 episodes/year for two years and more than 3 episodes per year for 3 years). This may be done via diathermy or coblation. \n\n\n# NICE Guidelines\n\n[NICE Guidelines Sore Throat (acute)](https://www.nice.org.uk/guidance/ng84) \n\n[NICE Flowsheet on Antimicrobial Prescribing](https://www.nice.org.uk/guidance/ng84/resources/sore-throat-acute-in-adults-antimicrobial-prescribing-visual-summary-pdf-11315864557) \n \n\n# References\n \n[NHS Information on Tonsillitis](https://www.nhs.uk/conditions/tonsillitis/)\n\n[Patient Info Tonsillitis](https://patient.info/doctor/tonsillitis-pro) \n\n[Great Ormond Street Hospital Tonsillectomy](https://www.gosh.nhs.uk/conditions-and-treatments/procedures-and-treatments/your-child-having-his-or-her-tonsils-andor-adenoids-removed/)",
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"question": "A 25 year old man presents to his general practice with a sore throat which started 2 days ago. He also reports feeling feverish and unwell and denies a cough or coryza. He is still able to eat and drink. He has no allergies and does not take any regular medications.\n\nHis observations are as follows:\n\n- Heart rate: 70 beats per minute\n- Blood pressure: 115/80mmHg\n- Respiratory rate: 14 breaths per minute\n- Saturations: 99% on room air\n- Temperature: 38.1 degrees Celsius\n\nOn examination, his tonsils are inflamed and purulent. He does not have any tender cervical lymphadenopathy.\n\nWhat is the next best step in the management of this patient?",
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"answer": true,
"explanation": "This is correct. All women aged 25 to 49 are invited for \"routine recall\" if a cervical sample is negative for high-risk HPV",
"id": "31948",
"label": "a",
"name": "Return for cervical screening in 3 years",
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"explanation": "The NHS employ a \"HPV first\" system whereby a the sample is first tested for high risk strains of HPV, and cytological examination is only performed if this is positive",
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"label": "e",
"name": "Cytological examination of the sample",
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"explanation": "All women aged 25 to 49 are invited for routine cervical screening every 3 years. Between the ages of 50 and 64 this becomes every 5 years",
"id": "31949",
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"explanation": "Colposcopy is only indicated if the cytology of the cells is abnormal, or there are two consecutive inadequate samples. In the current \"HPV first\" system in the NHS screening programme, the sample is only tested for cytology if it is positive for high risk strains of HPV. As this patient's sample was negative, it was not tested for cytology",
"id": "31951",
"label": "d",
"name": "Refer for colposcopy",
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"explanation": "All women aged 25 to 49 are invited for screening every 3 years, even if their previous screening was normal",
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"comment": "This has very recently been changed to 5 years instead of 3 (with quite a bit of controversy)",
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"comment": "its been changed in wales and scotland!",
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"comment": "For England and Northern Ireland – you get an invite every 3 years if you are aged 25 to 49. After that, you get an invite every 5 years until the age of 64.\n\nFor Wales and Scotland – you get an invite every 5 years if you are aged 25 to 64.\n",
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"comment": "Yes I agree, feel this needs to state which country the patient is in as this is varies across the UK \n",
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"comment": "Yeah as per previous comments, in Scotland this is 5 years",
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"explanation": "# Summary\n \n \nCervical cancer is the 3rd most common cancer worldwide and the 4th largest cause of cancer death. It is primarily caused by persistent human papillomavirus (HPV) infection and is commonly squamous cell carcinoma. The key clinical features include vaginal discharge, bleeding, discomfort, and changes in urinary or bowel habits. Investigations involve an urgent colposcopy and CT scans for staging. Management strategies depend on the stage of cancer and the patient's fertility desires, ranging from conisation and radical trachelectomy for early-stage cancers to radiotherapy and chemotherapy for more advanced cases.\n \n \n# Definition\n \n \nCervical cancer is a type of cancer that occurs in the cells of the cervix (the lower part of the uterus that connects to the vagina). The majority of cervical cancers are squamous cell carcinomas. \n \n \n# Epidemiology\n \n \nCervical cancer is the 4th most common cancer in women worldwide. In the UK, it is the 14th most common cancer amongst women.\nOver 90% of cervical cancer deaths and similarly higher prevalence is seen in low- and middle-income countries (LMICs), highlighting inequity in access to HPV-prevention (vaccination), cervical cancer screening and treatment options between LMICs and high-income countries. \n \n \n# Aetiology\n \nCervical cancer is strongly associated with persistent human papilloma virus (HPV) infection. The majority of cases are squamous cell carcinoma.\n \nRisk factors for cervical cancer include: \n \n - HPV 16 and 18 infection (accounts for 70% of cases)\n - Multiple sexual partners\n - Smoking\n - Immunosuppression (e.g. HIV or organ transplants)\n \n \n# Signs and symptoms\n \n \nMost cases of cervical cancer are picked up asymptomatically at cervical screening. Other clinical features include:\n \n - Vaginal discharge\n - Bleeding (e.g. postcoital or with micturition or defaecation)\n - Vaginal discomfort\n - Urinary or bowel habit change\n - Suprapubic pain\n - Abnormal white/red patches on the cervix.\n - Pelvic bulkiness on PV examination\n - Mass felt on PR examination\n \n \n# Differential diagnosis\n \n \nThe differential diagnosis for cervical cancer includes other causes of abnormal vaginal bleeding or discharge such as vaginitis, cervicitis, endometrial cancer, and cervical polyps. Key signs and symptoms of these differentials include:\n \n \n1. **Vaginitis:** itching, burning, pain, and abnormal discharge\n2. **Cervicitis:** abnormal discharge, pelvic pain, and postcoital bleeding\n3. **Endometrial cancer:** abnormal vaginal bleeding, pelvic pain, and unintentional weight loss\n4. **Cervical polyps:** abnormal vaginal bleeding, discharge, and pain during intercourse\n \n \n# Investigations\n\n**Bedside:**\n\n* Speculum examination (with sample for cytology and HPV testing) \n\n**Bloods:**\n\n* FBC (anaemia)\n* LFTs (liver involvement)\n* U&Es (renal involvement) \n\n**Imaging:**\n\n* CT chest/abdomen/pelvis (for staging)\n\n**Invasive:** \n\n* Colposcopy (urgent) and cervical biopsy \n \n\n# Management\n \n \nThe treatment for cervical cancer depends on the stage of the cancer, and also whether the woman wants to retain fertility.\n \n \n - For very small cancers in stage IA treatment options include conisation with free margins if aiming to spare fertility. Conisation is done using a scalpel (cold-knife conisation), laser, or electrosurgical loop, and is usually performed as an outpatient.\n - Radical trachelectomy can be done for slightly more advanced, yet still early-stage cancers when the aim is to spare fertility. This involves removal of the cervix, the upper vagina and pelvic lymph nodes.\n - Where maintaining fertility is not an aim a laparoscopic hysterectomy and lymphadenectomy is offered for women for early-stage cancer.\n - For invasive, infiltrating and early metastatic cancer a radical (Wertheim's) hysterectomy can be performed which involves removal of the uterus, primary tumour, pelvic lymph nodes, and sometimes the upper third of the vagina and uterovesical and uterosacral ligaments.\n - If the cancer has spread outside the cervix and uterus, then surgical management is often unlikely to be curative. These cancers are treated with radiotherapy and/or chemotherapy.\n \n# Complications \n\n* Surgical complications: bladder dysfunction, leg oedema (due to lymphadenectomy), preterm birth \n* Radiation complications: vaginal stenosis, vaginal atrophy, bladder dysfunction, urethral strictures\n\n# Prognosis \n\nCervical cancer is preventable through screening. Mortality has decreased significantly as a result of improved treatment and screening programmes. Overall 5-year survival is 67%. However, this varies based on stage of disease at diagnosis:\n\n* Stage I: >90%\n* Stage II-III: 50-70%\n* Stage IV: <20%\n\n# Cervical Screening\n \n \n - For all women and people with a cervix between the age of 25-64 years. \n - Cervical sample is taken and tested for high-risk HPV viruses. \n - From 24 to 49 women are called every three years, and afterwards every five years.\n- The idea behind the screening process is to identify dyskaryotic cells which are pre-cancerous allowing management before invasive cancer can develop.\n \n \n## Outcomes in screening\n \n \nOutcomes from screening can be as follows:\n \n \n - Anybody with a negative HPV test is returned to routine recall.\n - Anybody with a positive HPV test has cytological testing. \n - Patients who are HPV positive but have negative cytology results should have a repeat HPV test in 12 months and again at 24 months if still positive. If they remain positive at 24 months they should be referred to colposcopy.\n - In some cases the sample may be inadequate, in which case the smear should be repeated. If it still not adequate for the next two samples, then the woman should be referred for colposcopy.\n \n \n# HPV Vaccination\n \n \n - Girls and boys aged 12 to 13 years are offered the HPV vaccine as part of the NHS vaccination programme\n - The vaccine helps protect against cancers caused by HPV, including cervical cancer, some mouth and throat cancers and some cancers of the anal and genital areas. It also helps protect against genital warts\n - Gardasil is the vaccination used and protects against HPV types 6, 11, 16, 18, 31, 33, 45, 52 and 58\n \n# NICE Guidelines\n \n [Click here for NICE CKS on Cervical cancer](https://cks.nice.org.uk/topics/cervical-cancer-hpv/)\n \n \n [Click here for NICE CKS on Cervical cancer screening](https://cks.nice.org.uk/topics/cervical-screening/)\n \n \n# References\n \n[Cancer UK](https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/cervical-cancer) \n[NHS Page](https://www.nhs.uk/conditions/cervical-cancer/)",
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"question": "A 25 year old female presents to her general practice for her first routine cervical screening. She has no gynaecological symptoms.\n\nOn speculum examination, her cervix appears normal.\n\nThe sample returns as negative for human papillomavirus (HPV).\n\nWhat is the next best step?",
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"explanation": "This is a sensible differential in a trauma patient with haemodynamic instability, although it would not explain the petechial rash and is unlikely to cause such significant respiratory compromise and neurological disturbance",
"id": "31974",
"label": "b",
"name": "Internal haemorrhage",
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"explanation": "Although this may explain his respiratory compromise, it would not explain the petechial rash. It is unlikely to cause acute confusion and drowsiness in someone so young, and the normal temperature is also going against this diagnosis. Pneumonia would also typically cause unilateral crackles on auscultation",
"id": "31975",
"label": "c",
"name": "Hospital-acquired pneumonia",
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"votes": 217
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"__typename": "QuestionChoice",
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"explanation": "This may explain his acute respiratory distress but would not explain the petechial rash and is unlikely to cause such acute neurological disturbance",
"id": "31977",
"label": "e",
"name": "Acute respiratory distress syndrome (ARDS)",
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"votes": 1220
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would not explain his respiratory compromise or petechial rash. Although a subarachnoid haemorrhage is the most common type of brain haemorrhage secondary to trauma in the acute phase",
"id": "31976",
"label": "d",
"name": "Subarachnoid haemorrhage",
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"explanation": "Fat embolism classically presents with the triad of respiratory compromise, neurological disturbance and a petechial rash. It typically occurs 24-72 hours after a long bone injury or surgical procedure",
"id": "31973",
"label": "a",
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"__typename": "QuestionComment",
"comment": "Can someone explain the crackles?",
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"comment": "would it give you hypotension though",
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"explanation": "# Summary\n\nFat embolism refers to a medical condition characterized by the entry of fat fragments into the systemic circulation, subsequently lodging in the small vessels of the lungs or other tissues. This typically occurs due to fractures, especially long bone fractures. Clinical manifestations vary depending on the site of embolism, with breathlessness being a common symptom in pulmonary fat embolism. Investigations may include radiographic imaging and serum markers. The mainstay of management is supportive care, focused on oxygenation and symptomatic relief.\n\n# Definition\n\nFat embolism is a clinical syndrome resulting from the dissemination and subsequent lodgment of fat droplets or fat globules in the small vessels of the systemic and/or pulmonary circulation. This event typically follows trauma, particularly fractures of long bones or pelvic bones, but it can also occur after non-traumatic events such as orthopedic surgery or severe burns.\n\n# Epidemiology\n\nThe incidence of fat embolism varies and is largely dependent on the context. It is estimated to occur in 1-3% of all long bone fractures, but the incidence can be as high as 10-30% in patients with polytrauma or after major orthopedic surgeries. Fat embolism syndrome, a severe manifestation of fat embolism characterized by multisystem involvement, is estimated to occur in approximately 10% of all cases of fat embolism.\n\n# Aetiology\n\nThe aetiology of fat embolism generally involves:\n\n- Trauma, particularly long bone and pelvic fractures\n- Non-traumatic events such as orthopedic surgeries (hip or knee arthroplasty)\n- Severe burns\n- Liposuction\n- Prolonged corticosteroid therapy\n\n# Signs and Symptoms\n\nThe signs and symptoms of fat embolism are largely determined by the site of embolization:\n\n- Pulmonary: Breathlessness, hypoxia, tachycardia, tachypnea, and fever\n- Neurologic: Altered mental status, seizures, focal deficits, or coma\n- Dermatologic: Petechial rash predominantly on the upper body\n\n# Differential Diagnosis\n\nDifferential diagnosis for fat embolism includes conditions that present similarly such as:\n\n- Pulmonary embolism: Presents with sudden onset shortness of breath, chest pain, and hemoptysis.\n- Acute respiratory distress syndrome (ARDS): Presents with severe shortness of breath, rapid breathing, and bluish skin coloration (cyanosis).\n- Pneumonia: Presents with cough (often productive), fever, shortness of breath, and chest discomfort.\n- Sepsis: Presents with fever, increased heart rate, increased respiratory rate, and confusion.\n\n# Investigations\n\nThe diagnosis of fat embolism is typically clinical, supported by relevant investigations:\n\n- Imaging studies: Chest X-ray may reveal diffuse bilateral infiltrates; CT of the chest may show fat within the vessels.\n- Laboratory tests: Serum markers such as fat macroglobulinemia, increased serum lipase, and increased serum LDH.\n- Bronchoalveolar lavage: To identify fat droplets in macrophages.\n\n# Management\n\nManagement of fat embolism is primarily supportive and includes:\n\n- Oxygen therapy: To relieve hypoxia and dyspnea.\n- Fluid resuscitation: To maintain hydration and support circulatory function.\n- Pharmacological therapy: Prophylactic low-molecular-weight heparin may be considered to prevent thromboembolic events.\n- Fracture stabilization: Early immobilization of fractures can reduce the incidence of fat embolism.\n\n# References\n\n- [Ortho Bullets: Fat Embolism Syndrome](https://www.orthobullets.com/basic-science/9055/fat-embolism-syndrome)",
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"question": "A 40 year old man is admitted to hospital following a road traffic accident. He has a pelvic x-ray which shows a stable pelvic fracture which is managed conservatively.\n\nApproximately 48 hours later, he becomes acutely confused, drowsy and breathless.\n\nHis observations are as follows:\n\n- Respiratory rate: 25 breaths per minute\n- Saturations: 90% on room air\n- Heart rate: 90 beats per minute\n- Blood pressure: 95/65mmHg\n- Temperature: 36.5 degrees Celsius\n\nOn examination, auscultation of his chest reveals bibasal coarse crackles. There is also a petechial rash on the anterior aspect of his chest.\n\nWhat is the most likely diagnosis?",
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173,469,417 | false | 19 | null | 6,495,298 | null | false | [] | null | 6,399 | {
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "There is no link with hepatitis B and oesophageal candidiasis or dysphagia",
"id": "31996",
"label": "d",
"name": "Hepatitis B antigen",
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"votes": 199
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "The endoscopy image above shows a severe case of oesophageal candidiasis. The most common cause of this includes HIV and topical steroid treatment such as steroid inhalers",
"id": "31993",
"label": "a",
"name": "HIV testing",
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"votes": 5047
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"answer": false,
"explanation": "This would investigate for myasthenia gravis which may be a cause of dysphagia. However, the endoscopy image above shows oesophageal candidiasis",
"id": "31994",
"label": "b",
"name": "Antibodies against acetylcholine receptor (AChR)",
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"votes": 328
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would investigate systemic lupus erythematosus (SLE), which is a cause of dysphagia, but the endoscopy image above clearly shows oesophageal candidiasis, which would not be explained by SLE",
"id": "31997",
"label": "e",
"name": "Anti-dsDNA",
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"votes": 594
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would investigate systemic lupus erythematosus (SLE), which is a cause of dysphagia, but the endoscopy image above clearly shows oesophageal candidiasis, which would not be explained by SLE",
"id": "31995",
"label": "c",
"name": "Anti-nuclear antibodies (ANA)",
"picture": null,
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"comment": "My thought process: Esophageal dysmotility -> CREST syndrome -> Sclerosis -> Autoimmune -> ANA",
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"__typename": "QuestionComment",
"comment": "This is undergrad med bro ",
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"comment": "Same",
"createdAt": 1711467455,
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"comment": "For a second i thought this was IBD lmaoo",
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"explanation": "# Summary\n \n\nCertain diseases are considered clinical indicator diseases for adult HIV infection. Patients that present with these diseases are considered at risk of underlying HIV infection, and are thus routinely tested for HIV infection. Similarly, certain conditions can be complicated by HIV infection, for example pregnancy and TB, so HIV testing is commonplace in these situations. \n \n\n# Who should be offered a HIV test?\n \nAs per NICE & BASHH guidelines, the following groups of patients should be offered a HIV test:\n\n|Classification |Examples |\n|---|---|\n|Increased risk of exposure to HIV |Men who have sex with men; injected drug users; sex workers; people from a country with high seroprevalence; children of HIV-positive mothers; sexual partners of those with HIV |\n|Healthcare services |Sexual health; addiction & substance misuse; antenatal; termination of pregnancy; hepatitis, tuberculosis, lymphoma; chemotherapy & immunosuppression; areas with high HIV seroprevalence |\n| AIDS-defining conditions | Kaposi's sarcoma; Cryptosporidiosis diarrhoea; severe candidiasis; non-Hodgkin lymphoma; cervical cancer; cytomegalovirus; cerebral toxoplasmosis; progressive multifocal leukencephalopathy; pneumocystis pneumonia; mycobacterial diseases |\n|HIV indicator conditions |Oral hairy leukoplakia; exanthema; herpes zoster; seborrhoeic dermatitis; mononucleosis-like illness; anal & cervical dysplasias; viral hepatitis; sexually transmitted infections; pneumonias & invasive pneumococcal disease; chronic/unexplained lymphadenopathy, diarrhoea, renal impairment, neurological symptoms, weight loss |\n \nNB: Repeat tests may be indicated, taking into account the window period. The window period is the time between becoming infected and antibodies appearing - HIV antibodies usually appear 4-6 weeks after infection but can take up to 12 weeks.\n\n\n# NICE guidelines\n \n\n [Click here to see the NICE guidelines on HIV testing](https://cks.nice.org.uk/topics/hiv-infection-aids/diagnosis/asymptomatic-hiv-infection/)\n \n# References\n \n\n [Click here for the BIVA/BASHH guidelines on HIV testing ](https://www.bashhguidelines.org/current-guidelines/hiv/hiv-testing-guidelines-with-bhivabia-2020)",
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"learningPoint": "Oesophageal candidiasis often suggests underlying immunosuppression, such as HIV infection, and individuals presenting with this condition should be tested for HIV.",
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"question": "A 25 year old woman presents with pain in her throat on swallowing. She has no significant past medical history.\n\nShe has an endoscopy which shows the following:\n\n[lightgallery]\n\nWhich of the following blood tests is best to do next in this patient?",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "There is no indication for an ultrasound of the kidneys at present",
"id": "32000",
"label": "c",
"name": "Ultrasound of kidneys",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is only indicated if there is protein in the urine, which there is not",
"id": "32002",
"label": "e",
"name": "Send urine for PCR",
"picture": null,
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "There is no need to send this urine for culture if it is negative for nitrites and leukocytes, it is unlikely to be due to an infection",
"id": "32001",
"label": "d",
"name": "Urine culture",
"picture": null,
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is correct. This is a simple test to investigate the next most common cause of dysuria in a young female patient",
"id": "31998",
"label": "a",
"name": "Sexually transmitted disease (STD) screen",
"picture": null,
"votes": 5842
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Simpler investigations should first be carried out before referral for consideration of cystoscopy",
"id": "31999",
"label": "b",
"name": "Refer for cystoscopy",
"picture": null,
"votes": 269
}
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"explanation": "# Candidiasis \n\n\nThe most common cause of Candidiasis is Candida Albicans. This is the causative organism in 85-90% of cases. Candida infection is associated with pregnancy, antibiotic use and immunosuppression. The method of transmission is generally non-sexual.\n\n\n- Symptoms in women include: itching, white curdy discharge, sour milk odour, dysuria, superficial dyspareunia\n\n\n- Examination in women: redness, fissuring, swelling, intertrigo, thick white discharge\n\n\n- Symptoms in men: soreness, pruritis, redness\n\n\n- Examination in men: dry, dull, red glazed plaques and papules\n\n\n# Bacterial Vaginosis \n\n\nBacterial Vaginosis is a bacterial overgrowth, leading to vaginal discharge with an associated fishy odour. This is associated with UPSI and menstruation\n\n\nIn order to diagnose Bacterial Vaginosis, the Amstel criteria are used. Three out of four features are needed to confer a diagnosis:\n\n\n- Vaginal pH >4.5\n- Homogenous grey discharge\n- Whiff test - 10% potassium hydroxide produces fishy odour\n- Clue cells present on wet mount\n\n\nThe treatment of choice is Metronidazole or Clindamycin. The treatment used in pregnancy is Metronidazole.\n\n\n# Trichomoniasis \n\n\nTrichomonas infection is caused by Trichomonas Vaginalis, a flagellated protozoan. Transmission is usually sexual, with an incubation period of around 7 days.\n\n\n- Symptoms in women: can be asymptomatic, but classically profuse, frothy, yellow vaginal discharge. There can also be vulval irritation and dyspareunia present.\n\n\n- Symptoms in men: can cause non gonococcal urethritis, can be asymptomatic\n\n\n- On examination:commonly normal, strawberry cervix is a rare sign\n\n\n- Diagnosis: Direct microscopy and culture\n\n\n- Treatment: Metronidazole (PO state or BD for 7 days), follow up in one week, screen sexual contacts.\n\n\n# Chlamydia \n\n\nChlamydia trachomatis is an obligate intracellular bacterium, responsible for the infection of 1/10 women in the UK. Incubation is less than 4 weeks for men\n\n\n- Asymptomatic infections are common. The most common symptoms in men are urethral discharge and dysuria, with the main symptoms in women being dysuria, inter menstrual bleeding and vaginal discharge. Neonates can be affected with pneumonia and conjunctivitis.\n\n\n- Diagnosis is made by collecting endocervical swab and analysing using the NAAT test, the current investigation of choice. In males, urine and urethral swabs can be collected and analysed in a similar manner.\n\n\n- Treatment is either by using Doxycycline BD for 7 days or Azithromycin 1g single dose. There is no need for a test of cure.\n\n\n# Gonorrhoea \n\n\nNeisseria Gonorrhoeae is a gram-negative diplococcus.\n\n\n- Symptoms in men: asymptomatic, discharge, dysuria, tender inguinal nodes.\n\n\n- Symptoms in women: discharge, dysuria, abnormal bleeding.\n\n\n- Examination may show discharge from the os, Skene's gland or Bartholin's gland.\n\n\n- There can be extra-genital complications,including pharyngitis, rectal pain and discharge and disseminated infection.\n\n\n- Diagnosis is made by microscopy and successful culture.\n\n\n- The current guidance on treatment recommends treatment with both Ceftriaxone and Azithromycin to cover possible Chlamydia co-infection. A test of cure is recommended.",
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"question": "A 30 year old woman presents to her general practice with dysuria for the last 3 days. She denies blood in her urine, urinary frequency, or abdominal pain and her last period started 10 days ago, and has now finished.\n\nA urine dipstick test is performed:\n\n- Glucose: none\n- Bilirubin: none\n- Ketones: none\n- Specific gravity: 1.020 (1.002-1.035mOsm/kg)\n- pH 5 (4.5-8)\n- Blood: none\n- Protein: none\n- Nitrites: none\n- Leukocytes: none\n\nWhat is the next best step to investigate this patient's dysuria?",
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"explanation": "# Summary\n \n \nPostmenopausal bleeding is an important symptom that requires thorough investigation due to the potential for serious underlying pathology, such as endometrial cancer. The primary investigations include referral to gynaecology, transvaginal ultrasound, and biopsy of the endometrium. Management strategies will be determined based on the underlying cause of the bleeding. \n \n \n# Definition\n \nPostmenopausal bleeding is any vaginal bleeding that occurs after a patient has not experienced periods for 12 months or more, and who are not receiving hormone therapy. If a woman is receiving hormone replacement therapy (HRT), bleeding is considered postmenopausal if it occurs more than 6 months after menstruation has stopped.\n \n \n# Aetiology\n \nThe most common causes of postmenopausal bleeding include:\n\n* Endometrial atrophy\n* Vaginal atrophy\n* Endometrial polyps\n* Uterine fibroids\n* Endometrial cancer. \n\nOther less common causes include cervical cancer, ovarian tumours and certain medications, such as hormone replacement therapy (HRT) and anticoagulants.\n \n \n# Signs and symptoms\n \n \nFurther symptoms to postmenopausal bleeding will depend on the underlying cause, but may include pelvic pain, weight loss, and systemic symptoms of malignancy.\n \n \n# Differential Diagnosis\n \n \n - **Endometrial cancer:** Often the only symptom is postmenopausal bleeding.\n - **Vaginal atrophy:** Can also cause pruritus, dyspareunia, and vaginal discharge.\n - **Cyclical combined HRT:** Causes regular vaginal bleeding. With continuous HRT, it is common to experience breakthrough bleeding in the first 6 months.\n - **Bleeding disorders:** May be suggested if there is frequent bleeding elsewhere (e.g. recurrent epistaxis) or a family history of a bleeding disorder.\n \n \n# Investigations\n \nAll cases of postmenopausal bleeding should be referral to gynaecology under the 2-week wait pathway. \n\nThe gynaecologist will likely consider the following investigations: \n\n**Bedside:**\n\n- Bimanual and speculum examination\n\n**No blood tests** are required for diagnosis in the first instance, though if underlying bleeding/clotting disorders are suspected a clotting screen would be indicated. \n\n**Imaging:**\n\n - Transvaginal ultrasound to look for abnormal thickening of the endometrium\n - CT CAP: performed following diagnosis of endometrial cancer, for FIGO staging \n\n**Special tests:**\n\n - Biopsy of the endometrium, obtained via hysteroscopy or pipelle\n\n**2 Week Wait Criteria**\n\n- All cases of postmenopausal bleeding in women aged 55 or older should be referred to gynaecology under a 2-week wait. \n\n- In women aged under 55, a 2-week wait referral should also be considered.\n\n- For those not referred in the immediate instance who have a TV USS performed, refer under 2-week wait if endometrial thickness is >4mm, or if otherwise high clinical suspicion of endometrial cancer remains. \n\n \n# Management\n \n \nThe management of postmenopausal bleeding is guided by the underlying cause. This may include hormonal therapy for conditions such as endometrial atrophy, surgical interventions for polyps or cancers, or supportive care for symptoms related to vaginal atrophy. In all cases, ongoing monitoring is essential to ensure that treatment is effective and to detect any changes in the patient's condition.\n\n\n# NICE Guidelines\n\n[Click here for NICE guidelines on Gynaecological Cancers](https://cks.nice.org.uk/topics/gynaecological-cancers-recognition-referral/)\n\n# References\n\n[Patient Info: Postmenopausal bleeding](https://patient.info/doctor/postmenopausal-bleeding)",
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