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"explanation": "Methotrexate is utilised for medical management of ectopic pregnancy under specific circumstances where the patient is haemodynamically stable. This patient is unstable and would therefore not be suitable for medical management",
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"explanation": "Ectopic pregnancy may result in hypovolaemia secondary to blood loss. A blood transfusion may be considered if there is a large volume of blood loss with a significant drop in haemoglobin. Bloods should be sent off for group and save, and 2-4 units crossmatched. However, in the acute setting, the patient should be resuscitated with IV fluids first",
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"explanation": "This patient is currently haemodynamically unstable and requires fluid resuscitation prior to the consideration of any surgery. Laparoscopy is usually the first-line diagnostic and therapeutic operation for ectopic pregnancy as it is less invasive and harbours a shorter recovery time than laparotomy. Emergency laparotomy would be indicated if the patient had an acute abdomen, or if other pathology e.g. bowel was suspected",
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"explanation": "There is high suspicion for an ectopic pregnancy in a young sexually active female with signs of tachycardia and hypotension suggesting blood loss. Up to half of transvaginal US scans may be inconclusive. As she is haemodynamically unstable, she should be resuscitated with IV fluids as a first priority",
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"comment": "surely give blood in preference to crystalloids (replace like for like) - your explanation says could transfuse if there is significant blood loss which this patient (SBP of 75) obviously has! I get in reality fluids more available but best theoretical answer is surely give O neg",
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"comment": "laparoscopy no more definitive its tvus",
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"comment": "I understand that we still do fluid first, but how do we know that this isn't ruptured?",
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"comment": "Group and save and crossmatch takes timme, followed by setting up transfusion. fluids are faster. (though in reality both would be done in clinical practice) ",
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"explanation": "# Summary\n \n \nEctopic pregnancy is a gynaecological emergency, referring to a fertilised ovum that has implanted anywhere outside the endometrial cavity. This may present with pelvic pain, shoulder tip pain, abnormal vaginal bleeding, and haemodynamic instability if ruptured. Diagnosis is confirmed by positive pregnancy test and a transvaginal ultrasound that has located the pregnancy outside the uterine cavity. Management strategies include conservative management, medical management with methotrexate, and surgical management, the choice of which depends on the patient's presentation and level of risk.\n \n \n \n# Definition\n \nAn ectopic pregnancy refers to a fertilised ovum that has implanted outside the endometrial cavity, usually in the fallopian tubes. This is a gynaecological emergency. \n \n \n \n \n# Epidemiology\n\n \nThe estimated incidence of ectopic pregnancies in the UK is 1.1%. The risk is higher in women with a history of pelvic inflammatory disease, genital infection, pelvic surgery, an intrauterine device in situ, assisted reproduction, previous ectopic pregnancy, or endometriosis.\n \n \n \n \n# Aetiology \n \n \nEctopic pregnancy usually presents in the 6-8th week of pregnancy, but can occur earlier or later. They can occur anywhere outside the endometrial cavity, but most commonly in the fallopian tube. \n\nRisk of an ectopic increases with conditions that impair the passage of a fertilised egg into the uterine cavity, or with conditions that cause the fertilised egg to implant prematurely. However, most ectopics are not associated with any risk factor. \n \nSpecific risk factors include: \n \n - Pelvic inflammatory disease and previous STIs\n - Pelvic surgery\n - Having an intrauterine device e.g. copper coil or Levonorgestrel-releasing intrauterine system (e.g. Mirena) in situ\n - Assisted reproduction e.g. IVF\n - Previous ectopic pregnancy\n - Endometriosis\n \n \n \n# Signs and Symptoms\n \nClinical features of ectopic pregnancy may include:\n \n \n - Pelvic pain, which may be unilateral to the side of the ectopic\n - Shoulder tip pain - If the ectopic pregnancy bleeds, the blood can irritate the diaphragm causing shoulder tip pain\n - Abnormal vaginal bleeding e.g. missed period or intermenstrual bleeding\n - Haemodynamic instability caused by blood loss if the ectopic ruptures, resulting in syncope/fainting\n - Abdominal examination may reveal unilateral tenderness\n - Cervical tenderness (chandelier sign) on bimanual examination\n \n \n# Differential Diagnosis\n\n1. **Miscarriage:** will also present with bleeding following a positive pregnancy test. However, less likely to have shoulder tip pain, beta-hCG levels will not be as high as in an ectopic (and will fall), and TV USS may show intrauterine pregnancy (if not yet completely expelled). \n\n\n2. **Pelvic inflammatory disease:** presents with abdominal pain and cervical tenderness, and may have bloody vaginal discharge. However, pregnancy test will be negative and inflammatory markers raised. Can be confirmed with positive swab. \n\n\n3. **Ovarian torsion:** also presents with abdominal pain, usually unilateral. Less likely to present with vaginal bleeding and will have negative pregnancy test. \n\n# Investigations\n \nThe investigations for ectopic pregnancy include:\n\n**Bedside**\n\n- Pregnancy test (to confirm pregnancy) \n\n \n**Bloods**\n\n* FBC (check for anaemia)\n* Serum beta-hCG (will help guide management)\n\n**Imaging**\n\n - Transvaginal ultrasound (to locate the pregnancy)\n \n \n# Management\n \n \nThere are three management options for ectopic pregnancy:\n \n \n **Conservative:**\n \n \n - This is an option for a small number of women with an ectopic pregnancy who have minimal or no symptoms, who are considered low risk (usually because there is a plateau or drop in beta-hCG levels indicating self-resolution of the ectopic). \n - These patients require close follow-up with serial repeat b-hCG tests. If the levels do not decrease at a satisfactory rate, medical/surgical management is recommended.\n \n \n**Medical:**\n \n \n - Involves administration of a one-off dose of methotrexate\n - Criteria for methotrexate treatment include: \n - No significant pain\n - Low hCG level (below 1500 IU/L)\n - Unruptured ectopic pregnancy measuring below 35mm and with no visible heartbeat\n - Ability to attend follow-up\n - Adherence to avoiding pregnancy for a period following treatment\n - No intrauterine pregnancy (confirmed on an ultrasound scan). \n - If the initial dose of methotrexate fails to treat the ectopic pregnancy, a second dose of methotrexate or surgical management may be indicated\n \n\n**Surgical:**\n \n - Recommended as first-line option if: \n - Patient is unable to attend follow-up\n - Serum hCG level of 5000 IU/L or higher \n - Adnexal mass of 35mm or greater\n - Foetal heartbeat is visible on ultrasound scan\n - Patient is in significant pain\n - Patient is haemodynamically unstable\n - Also offered second line in cases where medical manamgement has failed \n - The preferred surgical management is a **salpingectomy**, where the fallopian tube containing the ectopic pregnancy is removed. For patients with only one patent fallopian tube (e.g. due to previous PID or ectopic, or past removal of a fallopian tube), a **salpingotomy** may be performed instead, where only the ectopic pregnancy is removed and the ends of the fallopian tube are re-attached. \n - There is a risk with salpingotomy that not all the tissue may have been removed, and so serial serum b-hCG measurements are performed to exclude any remaining trophoblastic tissue within the fallopian tube\n - Offer **anti-D immunoglobulin** to all rhesus-negative women who have had surgical management of ectopic pregnancy. \n \n\n**Borderline Cases: Choosing Between Medical and Surgical Management**\n\n* There are some women who may be offered a choice of either methotrexate or surgical management as first-line.\n* This applies to women who: \n * Have a serum hCG level between 1500 IU/L and 5000 IU/L\n * Are able to return for follow up\n * Have no significant pain\n * Have an unruptured ectopic pregnancy with an adnexal mass smaller than 35 mm with no visible heartbeat.\n * Have no intrauterine pregnancy (confirmed on an ultrasound scan). \n \n\n# NICE Guidelines \n \n [Click here for NICE CKS on ectopic pregnancy ](https://cks.nice.org.uk/topics/ectopic-pregnancy/) \n \n# References\n\n\n[NHS UK - Ectopic pregnancy](https://www.nhs.uk/conditions/ectopic-pregnancy/)\n \n[Patient Info - Ectopic pregnancy](https://patient.info/doctor/ectopic-pregnancy-pro)",
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"question": "A 20 year old female has been brought into A&E by her partner with sudden onset right lower abdominal pain and vomiting for the past day. She had also briefly fainted just prior to arrival. In triage, she was afebrile, BP 75/50, HR 115, SpO<sub>2</sub> 98%. A urine pregnancy test was positive but transvaginal ultrasound scan (US) showed an empty uterus.\n\nWhat is the next most appropriate course of action?",
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"explanation": "# Summary\n \n \nPremature ovarian insufficiency (POI) is a condition characterised by menopause in women aged below 40 years. The key signs and symptoms include vasomotor disturbances such as hot flushes and night sweats, sexual dysfunction, and psychological issues. The diagnosis is confirmed by elevated FSH levels, which should be repeated to rule out anomalous results. The main management approach is hormone replacement therapy (HRT) until the age of normal menopause, unless contraindicated.\n \n \n# Definition\n \n \nPremature ovarian insufficiency (POI) is a medical condition characterised by the onset of menopause (ovarian insufficiency) in a woman aged below 40 years. \n \n \n# Epidemiology\n \n \nThe exact prevalence of POI is not known, but it's estimated to affect approximately 1% of women under the age of 40.\n \n \n# Aetiology\n \n \nThe aetiology of POI can be idiopathic or iatrogenic. Iatrogenic causes include invasive procedures or treatments such as ovarian surgery, radiotherapy, or chemotherapy that directly impact the ovaries.\n \n \n# Signs and symptoms\n \nWomen with POI typically develop the same symptoms as those undergoing natural menopause:\n \n \n - Vasomotor symptoms: hot flushes, night sweats\n - Sexual dysfunction: vaginal dryness, reduced libido, problems with orgasm, dyspareunia\n - Amenorrhoea: infrequent or no periods \n - Psychological symptoms: depression, anxiety, mood swings, lethargy, reduced concentration\n \n \n# Differential diagnosis\n \n \nWhen evaluating for POI, it is essential to rule out other conditions that could present with similar symptoms and cause amenorrhea:\n \n \n1. **Hypothyroidism:** presents with fatigue, weight gain, cold intolerance, depression, hair loss. \n2. **Hyperprolactinemia:** irregular menstrual cycles, infertility, breast milk production not related to childbirth or nursing. \n3. **Polycystic Ovary Syndrome (PCOS):** irregular periods, hirsutism, obesity, infertility. Will have raised LH:FSH ratio. \n \n \n# Investigations\n\n**Bedside:**\n \n* Pregnancy test (to rule out pregnancy as cause of amenorrhea)\n\n**Bloods:** \n\n* FSH levels: two samples taken 4-6 weeks apart, showing raised FSH levels is required for diagnosis\n* anti-Mullerian Hormone (AMH) level: may be low, but not required for diagnosis \n* LH level: may be raised, but not required for diagnosis \n\nOther blood tests to rule out alternative causes:\n\n* Prolactin \n* TFTs\n\n\n**Imaging:**\n\nNo imaging is required for diagnosis. However transvaginal ultrasound scan may show small ovaries and poor perfusion. \n \n\n \n# Management\n \n \n - The primary management strategy for women with POI is to offer hormone replacement therapy (HRT) until at least the expected age of menopause, unless the risks of HRT treatment outweigh the benefits. \n - Additionally, psychological support should be provided due to the potential mental health impacts of early menopause.\n - Vaginal oestrogen can also be provided for women experiencing vaginal dryness and subsequent dyspareunia. \n \n \n# Complications \n\n* Osteoporosis: Declines in oestrogen leads to loss of bone mineral density due to disruption in bone remodelling. \n* Cardiovascular disease: Oestrogen has cardioprotective effects, its decline leads to alternations in lipid profiles, inflammatory changes and endothelial dysfunction. \n* Infertility: Ovarian insufficiency leads to impaired development of ovarian follicles and ovulation, leading to infertility. \n \n \n# NICE Guidelines\n \n \n [Click here for the NICE guidelines on the menopause](https://www.nice.org.uk/guidance/ng23)\n \n# References\n\n[British Menopause Society](https://thebms.org.uk/publications/consensus-statements/premature-ovarian-insufficiency/)",
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"explanation": "This would be indicated in any serious or life-threatening bleeding requiring immediate reversal, regardless of the INR",
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"explanation": "# Summary\n\nThe International Normalised Ratio (INR) is a measure of blood coagulation, typically monitored in patients on anticoagulant therapy. High INR can result from an overdose of anticoagulant medication, drug interactions, dietary changes, and medical conditions such as liver failure or infection. The assessment of high INR includes a thorough patient history, complete blood count, and clotting screen. Management strategies are determined by the presence of active bleeding and the INR level, with a general focus on withholding anticoagulants and administering vitamin K. Re-evaluation of patient compliance and understanding of dosage regimens is also crucial.\n\n# Definition\n\nInternational normalised ratio (INR) is a measure of blood coagulation and is commonly monitored in patients on warfarin at high risk of thromboembolic events (e.g. those with prosthetic heart valves, atrial fibrillation, or those being treated for a thromboembolic event (e.g. DVT or PE).\n\n# Causes \n\n- Overdose of anticoagulant medication\n- Drug interaction (e.g. antibiotics, antifungals, Aspirin, Amiodarone)\n- Herbal products\n- Increase in alcohol consumption\n- Decrease in consumption of foods containing vitamin K\n- Liver failure\n- Infection\n\n# Assessment\n\n- History\n - Dosing history of anticoagulant\n - Concurrent illness\n - Change in medications\n - Change in diet/lifestyle (including alcohol and tobacco use)\n - History of any falls/injuries\n - History of blood loss\n - Haemoptysis\n - Haematemesis\n - Melaena\n - Bleeding from the gums\n- Examination\n \t- Evidence of bleeding\n - Overt blood loss\n - Bruising\n- Bloods\n - Full blood count to check for concurrent anaemia, signs of infection\n - Clotting screen to check for other clotting abnormalities\n\n\n# Management of high INR\n\nManagement depends on the presence of active bleeding and INR level.\n\nIf concerned regarding head injury and intracranial haemorrhage, consider CT head.\n\n- Major bleeding\n - Stop anticoagulants\n - Administer IV vitamin K\n - Administer prothrombin complex (preferred to FFP)\n- Minor bleeding\n - Stop anticoagulants\n - Administer IV vitamin K\n - Repeat INR after 24 hours, may need further vitamin K\n- No bleeding with INR > 8\n - Stop anticoagulants\n - Administer IV or oral vitamin K\n - Repeat INR after 24 hours\n- No bleeding with INR > 5\n - Withhold 1-2 doses of anticoagulant\n - Review maintenance dose of anticoagulant\n\nIt is important to also assess compliance and ensure the patient understands their dosing regime.\n\n# NICE Guidelines\n\n- [NICE Treatment Summary: Oral anticoagulants](https://bnf.nice.org.uk/treatment-summary/oral-anticoagulants.html)\n- [NICE British National Formulary (BNF): Warfarin Sodium](https://bnf.nice.org.uk/drug/warfarin-sodium.html)\n",
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"question": "An 80 year old woman is admitted to the ward with a one week history of confusion, dysuria and urinary incontinence. She lives alone with a carer coming in once weekly, who brought her into hospital upon realising she was \"slightly muddled\". She has a past medical history of ischaemic heart disease, atrial fibrillation and dementia and she currently takes warfarin. Her international normalised ratio (INR) is 6.5 on admission.\n\nA CT head no evidence of acute intracranial abnormality.\n\nWhich of the following is the most appropriate management?",
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"explanation": "The iron panel is not suggestive of iron deficiency anaemia",
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"explanation": "This is a rare cause of anaemia in rheumatoid arthritis. This is unlikely as reticulocyte count is not raised",
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"explanation": "# Summary \n\nMacrocytic anaemia is a type of anaemia characterized by the presence of larger-than-normal red blood cells (RBCs). It can be classified into megaloblastic and non-megaloblastic types. Megaloblastic anemia is primarily associated with impaired DNA synthesis, often due to deficiencies in vitamin B12 or folate, leading to the enlargement of RBC precursors and hypersegmented neutrophils on blood film. Non-megaloblastic macrocytic anaemia can be caused by various factors, and sometimes a patient may present with non-megaloblastic macrocytosis, without anaemia such as in pregnancy. Key investigations include FBC, blood film and measurement of specific vitamins such as folate and B12, and management centres on the underlying cause of the anaemia. For example, vitamin supplementation in B12/folate deficiency.\n\n\r\n# Definition\n\nMacrocytic anaemia refers to a condition in which red blood cells are larger than normal. It can be further classified into two main categories: megaloblastic and non-megaloblastic. Megaloblastic macrocytic anaemia is characterized by slow or impaired DNA synthesis, leading to delayed maturation of RBCs and, notably, hypersegmented neutrophils on blood film. Non-megaloblastic macrocytic anaemia may manifest as macrocytosis without the presence of anaemia.\n\n\n\r\n# Epidemiology \n\nThe epidemiology of macrocytic anaemia varies depending on the underlying cause. Megaloblastic macrocytic anaemia is often associated with vitamin B12 or folate deficiencies and is more prevalent in older adults. Non-megaloblastic macrocytic anaemia, on the other hand, can occur at any age and may be linked to factors such as alcohol consumption or pregnancy.\n\n\r\n# Classification\n\nMorphologically, macrocytic anaemia is usually typified by large RBCs due to abnormal RBC development, giant metamyelocytes and hypersegmented neutrophils (in the peripheral circulation). Macrocytic anaemia may be megaloblastic or non-megaloblastic.\n\n## Causes of megaloblastic anaemia \n\n* **B<sub>12</sub> deficiency** \n * reduced intake (eg. dietary) \n * reduced absorption (eg. pernicious anaemia, inflammatory bowel disease, gastrectomy)\n* **Folate deficiency**\n* Drugs\n * hydroxycarbamide (previously called hydroxyurea)\n * azathioprine\n * cytosine arabinoside\n * azidothymidine\n\n\n## Causes of non-megaloblastic/normoblastic macrocytic anaemia\n\n* Liver disease\n* Alcohol \n* Hypothyroidism\n* Myelodysplastic syndrome\n* Hypothyroidism\n* Pregnancy (usually a mild macrocytosis)\n\n\r\n# Signs and Symptoms \n\n- Fatigue and Weakness\n- Pallor\n- Shortness of Breath\n- **Glossitis and \"Beefy Tongue\":** A distinctive sign of megaloblastic anaemia, glossitis, is the inflammation of the tongue, giving it a swollen and reddened appearance, often referred to as a \"beefy tongue.\"\n- **Neurological Symptoms:** Severe vitamin B12 deficiency can affect the nervous system, leading to neurological symptoms such as paresthesias (tingling and numbness), ataxia (impaired coordination), and cognitive impairment.\n- Symptoms of associated conditions:\n\t- **Autoimmune Conditions:** Megaloblastic anemia, particularly pernicious anemia, is associated with autoimmune conditions such as autoimmune thyroid disease, type 1 diabetes, and autoimmune gastritis. Therefore, patients may present with features of these conditions.\n\t- **Hypothyroidism Symptoms:** In cases where megaloblastic anaemia is secondary to hypothyroidism, patients may exhibit classic hypothyroidism symptoms like fatigue, weight gain, cold intolerance, and changes in skin and hair.\n\n# Differential Diagnosis\n\n\n- **Megaloblastic Anaemia (Vitamin B12 or Folate Deficiency):** The primary differential diagnosis within the realm of macrocytic anaemia is megaloblastic anaemia, specifically caused by vitamin B12 or folate deficiency. Careful evaluation of vitamin levels, clinical symptoms, and peripheral blood smears can aid in the distinction.\n\n- **Non-Megaloblastic Macrocytic Anaemia:** Macrocytosis, without the typical features of megaloblastic anemia, may result from various non-megaloblastic causes, including alcohol consumption, liver disease, or pregnancy. These cases may present as isolated macrocytosis without the broader clinical picture of anaemia.\n\n- **Haemolysis:** Haemolytic anaemias, both inherited and acquired, can lead to an increase in reticulocyte count and macrocytosis, albeit for different reasons. Evaluating markers of haemolysis, such as elevated bilirubin levels or increased lactate dehydrogenase, can assist in distinguishing haemolytic anaemias from megaloblastic anaemias.\n\n- **Liver Disease:** Patients with liver disease, particularly alcohol-related liver disease, can exhibit macrocytosis. Evaluation of liver function tests and consideration of underlying liver pathology is necessary in such cases.\n\n- **Medications:** Certain medications, such as antiretroviral drugs and chemotherapy agents, can cause macrocytosis. A thorough medication history is important in identifying potential drug-induced macrocytosis.\n\n- **Bone Marrow Disorders:** In rare cases, macrocytic anaemia can be associated with underlying bone marrow disorders, including myelodysplastic syndromes (MDS) and myeloproliferative neoplasms (MPNs). A bone marrow biopsy may be warranted to evaluate these conditions.\n\n\r\n\r\n# Investigations \n\n* Investigations all patients should have include:\n\t* Full Blood Count (FBC): This reveals anaemia and macrocytosis. The presence of hypersegmented neutrophils in the blood film is characteristic of megaloblastic anemia.\n\t* Haematinics: Serum vitamin B12 and folate levels should be assessed to identify deficiencies.\n\t* Blood Film: A peripheral blood smear can show macrocytosis and the presence of hypersegmented neutrophils.\n* Specific tests to investigate for underlying causes include:\n\t* TFTs to look for hypothyroidism\n\t* LFTs to assess liver function\n\t* Antibodies to intrinsic factor +/- gastric parietal cells, seen in pernicious anaemia\n\t* Markers of haemolysis - bilirubin, DAT testing, LDH\n\n# Management\n\n* **Megaloblastic Anaemia:** In pernicious anemia, intramuscular hydroxocobalamin is typically administered to replace vitamin B12. \n* It is important to address vitamin B12 deficiency before folate replacement (if both are deficient) to avoid exacerbating neurological symptoms and precipitating subacute degeneration of the spinal cord (SACD). \n* In cases of folate deficiency, oral folate supplements are provided.\n* **Non-Megaloblastic Anaemia:** The management of non-megaloblastic macrocytic anemia depends on the underlying cause, such as addressing alcohol consumption or providing support during pregnancy.\n\n# NICE Guidelines\n\n[NICE CKS - B12/Folate-deficiency anaemia](https://cks.nice.org.uk/topics/anaemia-b12-folate-deficiency/)\r\n\r\n\n\n",
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"question": "A 70 year old lady is admitted with an acute polyarthritic flare of her hands and knees. She has a past medical history of rheumatoid arthritis and migraines. Her regular medications include methotrexate, prednisolone and ibuprofen.\n\n\nBloods on admission are as follows:\n\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|101 g/L|(M) 130 - 170, (F) 115 - 155|\n|Platelets|400x10<sup>9</sup>/L|150 - 400|\n|Mean Cell Volume (MCV)|108 fL|80 - 96|\n|Ferritin|170 μg/L|12 - 200|\n|Iron|20 μmol/L|(M) 14 - 31, (F) 11 - 30|\n|Transferrin saturation|28 %|(M) 16 - 50 (F) 16 - 40|\n\n\n - White cell count and neutrophils normal\n - Reticulocyte count normal\n\n\nWhat is the most likely cause of her anaemia?",
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"explanation": "This would be indicated in severe hypoxaemia, progression of the crisis despite simple transfusion, multi-lobar disease or a previous history of severe chest crisis",
"id": "32030",
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"name": "Exchange transfusion",
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"explanation": "This may be considered later down the line if the patient is failing to maintain oxygen saturations on increasing levels of oxygen. Frequent oxygen monitoring, incentive spirometry and arterial blood gases should be done to monitor progression in such patients",
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"explanation": "This patient has a productive cough and acute chest crisis in the context of sickle cell anaemia. Recommended treatment in acute chest crises would be intravenous broad spectrum empiric coverage with a third generation cephalosporin for bacterial coverage and a macrolide for atypical organism cover",
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"name": "Start oral amoxicillin",
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"explanation": "Effective pain control is key in the management of acute chest crises. Opioid analgesia can be started and titrated according to the pain ladder",
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"explanation": "This would be useful in long-term management to prevent future acute chest crises",
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"comment": "Typical exam question, where every option seems right...",
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"comment": "stem doesn't exclude infections cause does it ? \n",
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"comment": "no, it doesn't. You would definitely give an abx, but not oral as the last answer suggests - IV.",
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"explanation": "# Summary\n\nSickle cell anaemia (SCA) is an autosomal recessive condition in which a point mutation in the beta chain on chromosome 11 leads to the production of HbS (rather than HbA). HbS polymerises when deoxygenated leading to sickled red blood cells. These cells are fragile and sticky, causing vaso-occlusive crises leading to pain and ischaemia of vital organs. The most common acute presentation is painful vaso-occlusive crises, while the most dangerous is acute chest crises. Diagnosis is typically made postnatally in the UK via a national screening programme but otherwise presents with progressive anaemia in early life. Investigations may reveal microcytic anaemia with variable degrees of haemolysis, and a definitive diagnosis is achieved with haemoglobin electrophoresis +/- genetic testing. Management strategies include high-flow oxygen, IV fluids and analgesia for acute crises, hydroxycarbamide, regular exchange transfusions, vaccinations and antibiotics for chronic disease management.\n\n# Definition\n\nSickle cell anaemia (SCA) is a genetic condition where normal haemoglobin (where variable HbS is present) tends to form abnormal haemoglobin molecules (HbS) upon deoxygenation leading to distortion of RBCs.\n\n# Epidemiology\n\nSickle cell disease is common among individuals of Central and West African descent, where having the carrier (trait) status confers some protection against malaria. \n\n# Pathophysiology \n\n- HbS is produced when the glutamic acid at the 6th position of the β chain is replaced by valine \n- In its deoxygenated state, HbS undergoes polymerisation, forming crystals that cause polymers to form, which in turn leads to the development of RBCs with a sickle shape \n- The abnormal shape of the RBCs causes clotting in the microvasculature, which precipitates vaso-occlusive crises, leading to ischaemia of vital organs and pain\n- Deformation of the RBCs leads to chronic haemolysis, which decreases the body's nitric oxide – typically needed for vasoregulation – and this leads to chronic complications such as pulmonary hypertension and leg ulcers\n\n## Inheritance \n\n- Sickle cell anaemia (HbSS) is an autosomal recessive condition. The most predominant and most severe form, homozygous HbS, represents just one of the sickle cell disease syndromes.\n- Other forms of sickle cell disease involve the coinheritance of HbS with other haemoglobin variants.\n - Most commonly HbC or β-thalassaemia, leading to the HbSC or HbS-βthal forms of sickle cell disease.\n\n## Mechanism of hyposplenism\n\nIn addition, sickled red cells commonly sequester in the spleen, where they undergo phagocytosis by the reticular endothelial system, leading to extravascular haemolysis\n\n- Initially, this leads to splenic congestion and splenomegaly\n- This is followed by splenic infarction, leading to hyposplenism\n- Because of splenic compromise, there is reduced immune function \n - Individuals with sickle cell disease are prone to bacteraemia – the spleen is necessary for phagocytosis of encapsulated bacteria. This means there is vulnerability to encapsulated organisms such as Haemophilus influenzae type B.\n - Affected individuals should have up to date vaccinations for S. pneumoniae, H. influenzae B and N. meningitidis.\n\n\n# Signs and Symptoms\n\n## Vaso-occlusive crises\n\nPainful vaso-occlusive crises are the most common acute presentation of sickle cell anaemia\n\n- Primarily caused by microvascular obstruction due to RBC sickling and inflammation\n- May be triggered by local hypoxia (eg. in cold weather)\n\n## Acute chest crisis\n\nAcute chest crises are the most dangerous acute presentation\n\n- 3% mortality rate, causing 25% of sickle cell-related deaths \n- The cause is often unknown (maybe infectious)\n- Patients present with tachypnoea, wheeze, and cough, with hypoxia and pulmonary infiltrates on chest X-ray\n\n## Other complications \n\n- Splenic infarction and subsequent immunocompromise\n- Sequestration crisis\n- Osteomyelitis\n- Stroke\n- Dactylitis\n- Poor growth\n- Chronic renal disease\n- Gallstones\n- Retinal disorders\n- Priapism\n- Pulmonary fibrosis and pulmonary hypertension\n- Iron overload from repeated blood transfusions\n- Red cell aplasia (due to parvovirus B19 infection in the presence of chronic haemolytic anaemia)\n\n**Clinical severity** is highly variable: some patients have few symptoms; others have severe and frequent crises, haemolytic anaemia and end-organ damage\n\n- This is due to a range of factors such as the amount of HbF (foetal haemoglobin) – higher levels of HbF reduce the severity of clinical complications\n- Patients with Hb SC disease have milder anaemia and suffer fewer crises than people with Hb SS disease \n- Patients with Hb SC disease are however more prone to sickle cell retinopathy \n - Ophthalmological review is needed annually for all patients with Hb SC disease\n\n# Investigations\n\n- Bedside - peak flow, which is essential for monitoring patients with chest crisis\n- **FBC** may show microcytic anaemia with variable degrees of haemolysis \n - Reticulocytosis and unconjugated hyperbilirubinemia may be noted\n\n- Typical **blood film** findings include: \n - characteristic sickle cells\n - target cells\n - reticulocytosis with polychromasia \n - features of functional hyposplenism (Howell–Jolly bodies, nucleated red cells)\n\nDefinitive diagnosis is with **haemoglobin electrophoresis** +/– genetic testing. However, many labs use high-performance liquid chromatography (HPLC) and/or isoelectric focusing (IEF) instead of HB electrophoresis. \n\n[lightgallery]\n\n## Screening for sickle cell disease\n\n- Sickle cell disease in the UK is typically diagnosed postnatally (by the national screening programme)\n- Additionally, all patients of African or Caribbean descent should have a sickle cell test prior to surgery \n- Otherwise, it can present with progressive anaemia in early life when levels of foetal haemoglobin (which contains γ-chains) fall and are replaced by HbS (containing the variant β-globin)\n\n# Management \n\n## Acute sickle cell crisis\n\nTreatments include: \n\n- High-flow oxygen \n- IV fluids and analgesia\n- Top-up transfusions – required in some severe cases\n\nNote: ABO-compatible red cells matched for Rhesus and Kell antigens should be given as this will inhibit the development of antibodies that can otherwise complicate future transfusions.\n\n\n## Chronic sickle cell disease\n\n* **Hydroxycarbamide** if frequent crises occur\n * Increases foetal haemoglobin concentrations – needs to be balanced with risks of marrow suppression, reduced fertility and risk of teratogenicity\n\n* Alternatively regular exchange transfusions may be required for frequent sickle cell crises, acute chest syndrome, priapism and stroke prevention \n* **Vaccinations** and **antibiotic prophylaxis** – in view of hyposplenism and subsequent immunocompromise\n* Newer therapies include: \n * crizaniluzumab (p-selectin inhibitor) for treatment of pain crises \n * voxelotor (haemoglobin oxygen-affinity modulator) for haemolytic complications\n\n* Bone marrow transplant and gene-editing techniques are now becoming possible curative options for some patients\n\n# NICE Guidelines\n\n[Click here to see information on NICE CKS on sickle cell](https://cks.nice.org.uk/topics/sickle-cell-disease/)",
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"question": "A 19 year old male is admitted with a 1 day history of sudden onset severe chest pain and productive cough. He has a known history of sickle cell disease.\n\nVitals on admission:\n\n- T 38.5°C\n- BP 100/60\n- Pulse 105\n- Respiratory rate 25\n- SpO<sub>2</sub> 98% on 4L oxygen\n\nCXR reveals bilateral lower zone shadowing. What is the next best step?",
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"explanation": "Based on the evidence given, the sensitivity of PSA testing is only 20%, which is not high. This means that some men with low PSA levels might still have prostate cancer. However, lowering the PSA cutoff level may worsen specificity and result in overdiagnosis",
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"explanation": "There aree 100 true positives and 300 false positives = 400 total.The proportion of those men who actually have prostate cancer is 100 out of that 400 total, or 25%, which is the positive predictive value.\r\n",
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"explanation": "The specificity is defined as the proportion of people who test negative among all those who actually do not have the disease. It is calculated as (True negatives)/ (True negatives + False positives) = 1200/ (1200 + 300) = 80%.\n\nThe value of 20% is referring to the sensitivity of the test",
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"explanation": "The PPV is calculated as (True positives)/(True positives + False positives) = 100/ (100 + 300) = 25%. The value of 75% is referring to the negative predictive value",
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"explanation": "# Overview \n\nSeveral key parameters can be calculated to help describe how effective a certain test is at diagnosing a condition.\n\n| | Patients with colon cancer | No cancer |\n| ------------------ | :------------------------: | --------: |\n| Biomarker positive | a | b |\n| Biomarker negative | c | d |\n\n# Sensitivity\n\nSensitivity is the proportion of people with the condition who will have a positive result. If, for example, the sensitivity of a test is 80%, out of a hundred people with the condition, only 80 will have a positive test result.\n\nSensitivity = a/(a+c)\n\n# Specificity\n\nSpecificity describes the proportion of people without the disease who will have a negative test. A specificity of 90% can be interpreted as, out of 100 people without the disease, 90 will have a negative test result.\n\nSpecificity = d/(b+d)\n\n# Positive Predictive Value\n\nPositive predictive value (PPV) is the proportion of people with a positive test who actually have the disease. PPV varies with prevalence of disease in a population. The lower the prevalence, the lower the positive predictive value. A PPV of 78% will mean that if 100 people tested positive, 78 people will have the disease.\n\nPPV = a/(a+b)\n\n# Negative Predictive Value\n\nNegative predictive value (NPV) is the proportion of people with a negative test who truly do not have the disease.\n\nNPV varies with prevalence of disease in a population. The lower the prevalence, the higher the negative predictive value. An NPV of 97% will mean that if 100 people tested negative, 97 people will not have the disease.\n\nNPV = d/(c+d)\n\n# False positive rate\n\nThe false positive rate is the proportion of those without the condition who will test positive.\n\nFalse positive rate = 1 - specificity\n\nFalse negative rate = 1 - d/(b+d)\n\n# False negative rate\n\nThe false negative rate is the proportion of those with the condition who will test negative.\n\nFalse negative rate = 1 - sensitivity\n\nFalse negative rate = 1 - a/(a+c)\n",
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"question": "A 70-year-old retired statistician attends his General Practitioner's surgery for a routine medical checkup. He has done some reading online and would like to ask for advice on the utility of prostate specific antigen (PSA) testing to determine his likelihood of prostate cancer.\n\nHe has found a study in a population of 2000 males above 60 years old evaluating the prostate cancer detection rate using a PSA cut off of 4.0ng/mL. The data are as follows:\n\n| | Disease present | Disease absent |\n| ------------- | --------------- | -------------- |\n| Positive test | 100 | 300 |\n| Negative test | 400 | 1200 |\n\nWhich of the following is true based on the evidence above?",
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"explanation": "The NNT is calculated by taking the reciprocal of the absolute risk reduction. In this case, it would be 1/(22.4% - 14%) = 1/(8.4%) = 12",
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"explanation": "The relative risk reduction is calculated by taking the difference between the absolute risk in the control and therapeutic groups and dividing it by the absolute risk of the control group. In this case, it would be (22.4 - 14) / 22.4 = 37.5%",
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"explanation": "Confidence interval (CI) is a measure of how confident the study's authors are that the true population value lies within a particular range, and it is usually 95%. If the confidence interval does not include the null hypothesis value (for relative risk, this value is 1), we can say a statistically significant difference exists. In this case, as the CI is from 0.75 - 1.10 and includes 1, there is no significant reduction in death from all causes",
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"explanation": "# Definition\n\nRisk in medical statistics refers to the probability of an outcome (either good or bad) occurring within a studied population. There are several different types of risk that are often used in medical studies.\n\n# What is Risk/Prevalence?\n\nThis is simply the probability of an event occurring within a defined population.\n\n# What is Risk Ratio (RR)?\n\nThe risk ratio (also known as relative risk) is the probability of an event occurring in an exposed group compared to the probability occurring in a non-exposed group.\n\nThe risk ratio is calculated by finding the ratio of incidence of a disease amongst the exposed population and the incidence amongst the non-exposed population.\n\nRisk ratios are used in cohort studies and in interventional studies in which the experimenter intervenes at some point during the study, such as in randomised controlled trials and pre-post studies.\n\nHowever, in cross-sectional studies and case-control studies, the incidence of the disease in the exposed and unexposed populations cannot be found, since the data only provides the cases and controls.\n\nConsequently,the risk ratio cannot be calculated for case-control studies and cross-sectional studies. Instead, an odds ratio must be found.\n\n# What is Absolute Risk Reduction (ARR)?\n\nThe absolute risk reduction is the absolute difference in the risk between the control group and the experimental group. It tells you in absolute terms how much an intervention changes an outcome of interest.\n\n# Calculation of Absolute Risk Reduction\n\nIt is calculated as follows:\n\n_ARR = Risk(control group) - Risk(experimental group)_\n\nA given ARR is generally considered significant if the 95% confidence interval does not cross 0.\n\nARR can then be used to calculate the number needed to treat (NNT).\n\n# What is Relative Risk Reduction (RRR)?\n\nThe relative risk reduction can be thought of as the proportional reduction in risk bestowed by the intervention compared to the control situation. It is more useful in helping you understand the efficacy of an intervention when the absolute risk of outcomes are rare (for example when considering the benefits of a statin for reducing MI in a given population).\n\n# Calculating RRR\n\nIt is calculated as follows:\n\n_RRR = 1 - [Risk(Experimental group) / Risk(Control group)]_\n\nA given RRR is generally considered significant if the 95% confidence interval does not cross 1.",
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"question": "A 50-year-old gentleman is admitted to the Cardiology ward having suffered a myocardial infarction. He is started on numerous medications for secondary prevention and has done some reading up whilst recuperating on the ward. In particular, he some questions regarding rosuvastatin as he has heard that it is a highly effective drug.\n\n\nHe would like to discuss a study he read in a journal. The data is as follows:\n\n\n|Outcome|Rosuvastatin group<br />(N=2500)|Placebo group<br />(N=2500)|Relative Risk <br />(95% CI)|\n|---------------------------------------|--------------------------------|---------------------------|----------------------------|\n|Cardiovascular events (including death)|350 (14%)|560 (22.4%)|0.63 (0.59 - 0.72)|\n|Death from non- cardiovascular causes|110 (4.4%)|125 (5.0%)|0.88 (0.80 - 1.05)|\n|Death from any cause|270 (10.8%)|325 (13.0%)|0.83 (0.75 - 1.10)|\n\n\n _N (Total number of people in the group), CI (Confidence Interval)_\n\n\nWhich of the following is true based on the data above?",
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"explanation": "The diamond shows the pooled result of all the studies. The vertical line indicates the line of no effect, i.e. the point at which there is statistically no significant difference between the control and intervention group. The width of the diamond illustrates the length of the confidence interval. Therefore, if the diamond touches the vertical line, it means that the overall result is **not** statistically significant",
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"question": "Forest plots are often used to summarise the results of meta-analyses in a graphical form. An example is shown below:\n\n[lightgallery]\n\nWhich of the following statements is true of a forest plot?",
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"explanation": "This is a case report, which involves an in-depth study of one to a few individuals with the disease. It is typically used to analyse unusual presentations of disease or unexpected responses to treatment, and is useful with respect to rare or emerging diseases. However, as the sample size is very limited, it would not provide as much data on the various causes of the disease compared to a case-control study",
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"name": "A study involving a patient diagnosed with Castleman disease in the university hospital, and an in-depth investigation into his possible predisposing factors to the disease",
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"explanation": "This describes a case-control study, which is a retrospective observational study. It is best suited to study rare diseases for which the population size is very small, and would be able to look at a wide range of exposure factors from the patients' histories",
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"name": "A study involving two groups of patients, one with and one without Castleman disease. The groups are then compared to examine their exposure to possible causal factors such as human immunodeficiency virus (HIV) and human herpesvirus 8 (HHV-8)",
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"explanation": "This is a cross-sectional study that provides a snapshot of the disease prevalence and its risk factors in a specific population at one point in time. It would not be suitable in investigating rare diseases as it would be difficult to find a large enough sample size. In addition, it would only be able to identify a potential association between HHV-8 and Castleman disease, but would not be able to define a direct cause and effect relationship",
"id": "32060",
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"name": "A study looking at the prevalence of Castleman disease in all males aged 20-50 years old in London and finding out whether they have been exposed to human herpesvirus 8 (HHV-8)",
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"explanation": "This describes a prospective cohort study, a longitudinal study that observes participants over a period of time to see whether they develop the outcome in question. This would not be suitable in this case as the disease is very rare, and the time taken to develop the condition may be very long",
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"name": "A study involving two groups of patients, one infected with human immunodeficiency virus (HIV) and the other without. The groups are then followed up over a period of 5 years to determine whether or not they develop Castleman disease",
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"explanation": "This is a retrospective cohort study, which is useful for tracking the development of a disease with a long latency period. It is different from a prospective cohort study in that study groups are not followed up in the future. It would not be suitable in this case as the disease is very rare",
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"comment": "I thought that causality couldn't be inferred from case-control studies? Also, the requirement to know that Castleman disease is rare seems like an unnecessary knowledge requirement in a Q that is testing study design",
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"explanation": "**Observational Study**\n\nA type of study in which participants in two or more groups are observed without the addition of an intervention. This is in contrast to randomised controlled trials where researchers look at the effects of a specific intervention in the study groups.\n\n**Cohort studies**\n\nCohort studies are one type of observational study. This study design involves examining groups of people over a period of time, where one group is exposed to a certain risk factor and the other group is not in order to establish links between exposure and a health related outcome such as the development of disease.\n\nThese designs are usually prospective in nature however, can be conducted retrospectively by looking back at data already collected, such as hospital records. These studies are useful to measure incidence and risk however, they are prone to confounding factors and are often costly.\n\n**Case-control studies**\n\nCase-control studies examine an association between an outcome and exposure to a risk factor. The studies recruit participants based on the presence of an outcome from the outset of the study. Once cases are recruited, suitable controls are identified and selected for the study. Controls are participants without the outcome of interest. Data of exposure to a risk factor is recorded retrospectively for each of the participants and then compared between cases and controls.\n\nThese studies are more suited to investigate rare conditions as individuals with the outcome of interest are identified at the outset. Other advantages of case-control studies are that they are much quicker to carry out relative to cohort studies and are relatively inexpensive.\n\n**Bradford-Hill Criteria**\n\nThe Bradford-Hill criteria include 9 established viewpoints to help determine if observed epidemiologic associations are causal.\nHill advised that his following viewpoints of an association be considered in attempting to distinguish casual from non-casual associations: strength, consistency, specificity, temporality, biologic gradient, plausibility, coherence, experimental evidence and analogy.\n\n**Strength** - strong associations are more likely to be casual than weak associations (which may be explained by other factors or be affected by undetected biases.)\n\n**Consistency** - refers to the repeated observation of an association in different populations under different circumstances. Lack of consistency does not rule out a casual association, because some effects are produced by causes only under unusual circumstances.\n\n**Specificity** - The criterion of specificity requires that a cause leads to a single effect, not multiple effects. Hill's discussion of this criterion is with reservation, and many authors regard this criterion as useless and misleading on the basis that many outcomes can happen from one variable (e.g. smoking may cause lung cancer, COPD, other forms of cancer, interstitial lung disease..)\n\n**Temporality** - Temporality refers to the necessity that the cause precede the effect in time.\n\n**Biologic gradient** - Biologic gradient refers to the presence of a mono-tone (unidirectional) dose responsive curve. However, like specificity, the acknowledgement that disease frequency may be caused by different exposures shows that the existence of a monotonic association is neither necessary nor sufficient for a causal relation.\n\n**Plausibility** - Plausibility refers to the biologic plausibility of the hypothesis, an important concern but one that is far from objective or absolute.\n\n**Coherence** - implies that a cause and effect interpretation for an association does not conflict with what is known of the natural history and biology of the disease. On the other hand, presence of conflicting information may indeed undermine a hypothesis, but one must always remember that the conflicting information may be mistaken or misinterpreted.\n\n**Experimental evidence** - it is not clear what was meant by this criterion, however, it may have referred to errors when collecting data.\n\n**Analogy** - Analogy provides scientists with a source of more elaborate hypotheses about the associations under study; absence of such analogies only reflects lack of imagination or experience, not falsity of the hypothesis.\n\n[Source: https://www.rtihs.org/sites/default/files/26902%20Rothman%201998%20The%20encyclopedia%20of%20biostatistics.pdf]",
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"explanation": "This usually occurs after 20 weeks gestation and would involve hypertension with proteinuria. Symptoms may include headache, visual disturbances, epigastric pain and marked oedema. Proteinuria 1+ in this scenario may suggest preexisting renal disease as she is at an early gestational stage",
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"explanation": "This is the more severe end of the spectrum of nausea and vomiting in pregnancy, which usually occurs in the first trimester and resolves by 20 weeks. While there are no clear cut clinical criteria for this condition, it is typically based on the following factors - persistent vomiting, weight loss >5% of pre-pregnancy body weight and ketonuria",
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"explanation": "Nausea and vomiting is a common symptom that affects women mostly in the 1st trimester. The aetiology is multifactorial and may be due to a combination of hormonal changes, abnormal gastrointestinal motility and genetic factors. It is also important to consider other differentials for nausea and vomiting that may occur due to conditions unrelated to pregnancy",
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"explanation": "This usually occurs after 20 weeks gestation and would involve hypertension with proteinuria. Symptoms may include headache, visual disturbances, epigastric pain and marked oedema. Proteinuria 1+ in this scenario may suggest preexisting renal disease as she is at an early gestational stage",
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"explanation": "This usually occurs in the 3rd trimester, and patients may have abdominal pain, pruritus and features of cholestasis (pale stools, dark urine, steatorrhoea). In pregnancy, ALP levels are usually raised by about 1.5 to 2 times the normal level, as is the case in this question",
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"comment": "Does anyone know why she has an elevated ALP?\n",
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"comment": "Can be raised in normal pregnancy apaz ",
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"comment": "My understanding is that ALP is produced by the placenta so levels can go up during pregnancy",
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"comment": "Why does she have low platelets?",
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"explanation": "# Summary\n\nHyperemesis gravidarum is a severe form of nausea and vomiting that occurs before 20 weeks of gestation, often requiring hospital admission. Key signs and symptoms include relentless vomiting, dehydration, and metabolic disturbances. It is typically diagnosed through exclusion. Differential diagnoses involve various infections, gastrointestinal issues, metabolic conditions, drug toxicity, and molar pregnancy. Investigations may include urine tests, blood tests, and ultrasound. Management strategies encompass fluid and electrolyte replacement, anti-emetic medications, thiamine and folic acid supplementation, antacids, and venous thromboembolism prophylaxis.\n\n\n# Definition\n\n\nHyperemesis gravidarum is a condition characterized by severe nausea and vomiting, commencing before the 20th week of gestation. It is intense enough to necessitate hospital admission and is diagnosed through the process of exclusion.\n\n\n# Differential Diagnosis\n\n\n\nDifferential diagnoses for severe vomiting during pregnancy include:\n\n- Infections: Gastroenteritis, urinary tract infection, hepatitis, and meningitis\n- Gastrointestinal problems: Appendicitis, cholecystitis, bowel obstruction\n- Metabolic conditions: Diabetic ketoacidosis, thyrotoxicosis\n- Drug toxicity\n- Molar pregnancy: Characterized by abnormally high levels of beta-hCG due to gestational trophoblastic disease, which can cause severe nausea and vomiting\n\n\n# Management\n\n\nManagement of hyperemesis gravidarum primarily includes supportive care, such as:\n\n- Fluid replacement therapy to correct dehydration\n- Potassium chloride to address hypokalaemia resulting from excessive vomiting\n- Anti-emetic medications, including cyclizine (first line), or prochlorperazine. In severe cases, ondansetron (2nd line), metoclopramide (2nd line) or domperidone may be utilized.\n- Thiamine and folic acid supplementation to prevent the onset of Wernicke's encephalopathy\n- Antacids to alleviate epigastric discomfort\n- Thromboembolic (TED) stockings and low molecular weight heparin to mitigate the increased risk of venous thromboembolism due to a combination of pregnancy, immobility, and dehydration.\n\n# Complications\n\nPotential complications of hyperemesis gravidarum include:\n\n- Gastrointestinal problems: Mallory-Weiss tears, malnutrition, and anorexia\n- Dehydration leading to ketosis and venous thromboembolism\n- Metabolic disturbances, such as hyponatraemia, Wernicke's encephalopathy, kidney failure, and hypoglycaemia\n- Psychological sequelae, including depression, PTSD, and resentment towards the pregnancy\n- Severe conditions may impact the foetus due to maternal metabolic disturbance, leading to low birth weight, intrauterine growth restriction, and premature labour.\n",
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"question": "A 30-year-old primigravida at seven weeks gestation presents with a ten-day history of morning nausea and vomiting, often unable to tolerate breakfast but managing a light lunch.\n\n\nObservations: Temperature 37.0°C, pulse 90, blood pressure 140/90, respiratory rate 20, SpO2 99% on room air\n\n\n\nLiver function tests:\n\n\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)|210 IU/L|25 - 115|\n|Bilirubin|7 µmol/L|< 17|\n|Gamma Glutamyl Transferase (GGT)|20 U/L|9 - 40|\n\n\n\n\nFull blood count:\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|121 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|6.5x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|110x10<sup>9</sup>/L|150 - 400|\n\n\nUrine dip:\n\n\n\n - protein negative\n - blood negative\n - nitrites negative\n - leucocytes negative\n - ketones negative\n\n\n\nClinical examination reveals a soft and non-tender pregnant abdomen appropriate for gestational age.\n\n\n\nWhich of the following is the most likely differential?",
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"explanation": "This is a normal physiologic finding in pregnancy. In HELLP syndrome, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are typically elevated ≥2 times the upper limit of normal",
"id": "32109",
"label": "b",
"name": "Elevated ALP 2 times the upper limit of normal",
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"explanation": "In HELLP syndrome, LDH is typically elevated ≥600 IU/L, a non-specific marker associated with severe haemolysis or acute hepatocellular injury",
"id": "32112",
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"name": "Normal lactate dehydrogenase (LDH)",
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"explanation": "In HELLP syndrome, the PT, APTT and coagulation screen are normal. If prolonged, this may suggest disseminated intravascular coagulation, which is one complication of HELLP syndrome",
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"name": "Prolonged prothrombin time (PT)/activated partial thromboplastin clotting time (APTT)",
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"explanation": "Haptoglobin level is a specific marker of haemolysis, and a level of ≤25mg/dL would suggest haemolysis which occurs in HELLP syndrome",
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"name": "Low serum haptoglobin",
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"explanation": "This is typical of glucose-6-phosphate dehydrogenase (G6PD) deficiency. In HELLP syndrome, the usual finding is schistocytes and burr cells, which are fragmented red blood cells indicating microangiopathic haemolytic anaemia",
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"name": "Peripheral blood film showing blister and bite cells",
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"comment": "RBC is broken down into LDH and Hb\nHb is carried in the blood by haptoglobin\nLow levels of haptoglobin imply it's saturated by Hb\n\nAlso, haptoglobin is reduced in haemochromatosis\nIt is an acute phase reactant (like ferritin), and will be raised in states of inflammation and infection",
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"comment": "To make it simple:\nIn HELLP you get haemolysis.\nHaemolysis --> More free Haemoglobin --> More Haptoglobin binds to Haemoglobin to prevent toxic effects --> Less serum haptoglobin available",
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"explanation": "# Summary\n\nHELLP syndrome is a severe pregnancy complication characterized by hemolysis (H), elevated liver enzymes (EL), and low platelets (LP). It typically manifests during the third trimester and is part of a spectrum of hypertensive disorders of pregnancy, including preeclampsia. Key signs and symptoms include headache, nausea/vomiting, epigastric pain, right upper quadrant abdominal pain, blurred vision, and peripheral edema. Investigations may include blood tests and ultrasound scans. The definitive treatment is usually the delivery of the baby, with some mothers also requiring blood transfusions or steroids during pregnancy.\n\n\n# Definition\n\n\nHELLP syndrome is a complication of pregnancy characterized by the presence of hemolysis (H), elevated liver enzymes (EL), and low platelets (LP). It often manifests during the third trimester and is considered part of a spectrum of hypertensive disorders of pregnancy, which also includes preeclampsia.\n\n\n# Epidemiology\n\n\n\nHELLP syndrome is relatively rare, affecting approximately 0.5-0.9% of all pregnancies. However, it is a significant cause of maternal and perinatal morbidity and mortality.\n\n\n# Aetiology\n\n\n\nThe exact cause of HELLP syndrome is unknown. However, it is believed to be related to abnormal placentation, endothelial cell injury, and a generalized inflammatory response. Genetic predisposition and immune maladaptation may also play roles.\n\n\n# Signs and Symptoms\n\n\n\nPatients with HELLP syndrome may present with:\n\n- Headache\n- Nausea and/or vomiting\n- Epigastric pain\n- Right upper quadrant abdominal pain due to liver distension\n- Blurred vision\n- Peripheral edema\n\n\n# Differential Diagnosis\n\n\n\nThe differential diagnoses for HELLP syndrome include acute fatty liver of pregnancy, idiopathic thrombocytopenic purpura, and thrombotic thrombocytopenic purpura. These conditions can also present with similar signs and symptoms such as thrombocytopenia, liver dysfunction, and neurological symptoms.\n\n# Complications\n\nMaternal complications include:\n\n- Organ failure\n- Placental abruption\n- Disseminated intravascular coagulopathy (DIC).\n\nFoetal complications include:\n\n- Intrauterine growth restriction\n- Preterm delivery\n- Neonatal hypoxia\n\n\n# Investigations\n\n\nInvestigations for HELLP syndrome may include:\n\n- Full blood count to assess for low platelet count and evidence of hemolysis\n- Liver function tests to assess for elevated liver enzymes\n- Coagulation studies to evaluate for disseminated intravascular coagulation\n- Ultrasound scans to assess for liver abnormalities and placental abruption\n\n# Management\n\n\nThe definitive treatment for HELLP syndrome is usually the delivery of the baby. In some cases, mothers may also require blood transfusions to manage anemia and thrombocytopenia or steroids to accelerate lung maturation in the fetus prior to delivery. After delivery, supportive care and close monitoring are essential.",
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"question": "A 38 year old pregnant female at 32 weeks gestation presents to Maternity Triage with mild upper abdominal pain, vomiting and blurred vision. Her observations are normal, and cardiotocograph reveals no abnormalities with the foetus. Urinalysis is normal.\n\nWhich one of the following laboratory findings is most likely in HELLP (haemolysis, elevated liver enzymes, and low platelets) syndrome?",
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"explanation": "This is most likely to be affected in tennis elbow, which results from lateral epicondylitis as the radial nerve travels anterior to the lateral epicondyle to enter the forearm. Pain is exacerbated in resisted wrist extension or supination. It may lead to radial nerve entrapment syndrome, causing wrist drop, loss of sensation to the anatomical snuff box and radial 3.5 digits on the dorsum of the hand",
"id": "32129",
"label": "b",
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"explanation": "This is golfer's elbow, which results from medial epicondylitis. The ulnar nerve may be compressed as it passes through the ulnar groove, which lies posterior and lateral to the medial epicondyle, resulting in numbness and/or tingling in the 4th and 5th fingers",
"id": "32128",
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"explanation": "If median nerve injury occurs more proximally at the elbow (most commonly due to a supracondylar fracture of the humerus), this may result in a hand of benediction (inability to flex the 2nd and 3rd fingers when making a fist) and paralysis of the flexors and pronators of the forearm. Sensation to the palmar aspect of the lateral 3.5 fingers may also be affected",
"id": "32130",
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"explanation": "Isolated musculocutaneous nerve lesions are rare. This would result in weakness of elbow flexion and forearm supination, weak biceps tendon reflex and sensory loss over the lateral surface of the forearm",
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"explanation": "This is most commonly damaged by direct trauma to the shoulder or proximal humerus, such as in fracture of the surgical neck of the humerus or shoulder dislocation. It would result in regimental badge numbness (over the inferior portion of the deltoid) and inability to abduct the affected shoulder due to deltoid and teres minor muscle weakness",
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"explanation": "# Summary\n\nMedial epicondylitis, also known as 'golfer's elbow', is a condition resulting from tendinopathy of the wrist flexor tendons attaching to the medial epicondyle of the distal humerus. Patients typically present with gradual-onset medial elbow pain, which is exacerbated by activity, especially wrist flexion, and may also report wrist flexion weakness. The diagnosis is primarily clinical. Key investigations may include physical examination, MRI, and ultrasound. Management strategies predominantly involve conservative measures such as rest and guided rehabilitation, with surgical debridement as a potential course of action for cases unresponsive to six months of non-surgical treatment.\n\n# Definition\n\nMedial epicondylitis, or 'golfer's elbow', is a condition that arises due to tendinopathy of the wrist flexor tendons, which attach to the medial epicondyle of the distal humerus. The primary tendons involved include the flexor carpi radialis, pronator teres, palmaris longus, flexor digitorum superficialis, and flexor carpi ulnaris.\n\n# Epidemiology\n\nMedial epicondylitis most commonly affects individuals between 20 and 50 years of age. The condition is more prevalent in athletes or those involved in repetitive activities that stress the involved tendons. Despite its moniker \"golfer's elbow,\" it can affect individuals from various occupations and recreational backgrounds.\n\n# Aetiology\n\nMedial epicondylitis typically results from overuse and strain of the muscles and tendons involved in wrist flexion and forearm pronation. It often occurs due to repetitive strain, especially in sports like golf, but it can also arise from occupational activities that involve repetitive wrist flexion or twisting motions.\n\n# Signs and Symptoms\n\nPatients generally report a gradual onset of medial elbow pain that worsens with activity, particularly during wrist flexion. Additional symptoms may include weakness of wrist flexion and a decreased range of motion in the affected arm.\n\n# Differential Diagnosis\n\nThe main conditions to consider in the differential diagnosis include:\n\n- **Lateral Epicondylitis ('Tennis Elbow')**: Characterised by pain and tenderness over the lateral aspect of the elbow, exacerbated by wrist extension.\n- **Olecranon Bursitis**: Presents with swelling and pain at the back of the elbow.\n- **Cubital Tunnel Syndrome**: Marked by numbness or tingling in the ring and little fingers, weakness in the hand, and pain on the inside of the elbow.\n- **Ulnar Neuropathy**: Symptoms can include numbness and tingling in the fourth and fifth fingers, elbow pain, and weakness of the hand.\n\n# Investigations\n\nThe diagnosis of medial epicondylitis is primarily clinical. Physical examination can reveal pain and tenderness at the medial epicondyle, exacerbated by resisted wrist flexion and forearm pronation. If the clinical presentation is unclear, imaging modalities such as MRI or ultrasound may be utilized to confirm the diagnosis and assess the extent of the lesion.\n\n# Management\n\nMedial epicondylitis is generally managed conservatively with rest and guided rehabilitation, which can include physical therapy, pain management with NSAIDs, and corticosteroid injections. Surgical debridement of damaged tissue may be indicated in cases which do not respond to six months of non-surgical management.\n\n# External links\n\n- [Physiopedia: Medial Epicondyle Tendinopathy](https://www.physio-pedia.com/Medial_Epicondyle_Tendinopathy)\n- [Ortho Bullets: Medial Epicondylitis (Golfer's Elbow)](https://www.orthobullets.com/shoulder-and-elbow/3083/medial-epicondylitis-golfers-elbow)",
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"question": "A 30-year-old male presents to his GP with a two-month history of persistent right elbow pain. He describes a tingling sensation in the 4th and 5th fingers. On examination, the pain is aggravated by wrist flexion and pronation of the arm.\n\nWhich single nerve is involved?",
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"explanation": "This is an early finding in compartment syndrome",
"id": "32136",
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"explanation": "The patient has developed compartment syndrome due to significant trauma causing bleeding and raised intracompartmental pressure within the limb. Late findings may also include the absence of distal pulses, and hypoesthesia. The patient would require an urgent fasciotomy to relieve the pressure within the compartment. It is important to remember always to have a high index of suspicion for compartment syndrome as clinical signs may be varied, and consider urgent referral for any patient with a tense, painful muscle compartment",
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"explanation": "Tingling sensations in the limb are an early finding in compartment syndrome and would suggest ischaemic nerve dysfunction. Sensory deficits would typically precede motor deficits, i.e. weakness of the limb",
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"explanation": "# Summary\n \nCompartment syndrome occurs when an increase in pressure in a closed anatomical compartment causes local tissue ischaemia. Typically the increase in pressure is secondary to inflammation caused by a traumatic injury, usually a fracture. Key signs and symptoms include severe pain out of keeping with the associated injury, particularly during passive stretching, pallor, limb paralysis, pulselessness, and paraesthesia. Rapid diagnosis is crucial to prevent complications of limb loss, loss of function and rhabdomyolysis causing renal failure. Diagnosis is clinical however compartment pressures may be measured at the bedside or during surgery. Definitive management is urgent fasciotomy, with IV fluids and analgesia both important. \n\n# Definition\n \nCompartment syndrome refers to the condition that results when inflammation of injured muscle causes an increase in pressure within a fascial compartment. As the pressure rises, circulation is cut off leading to tissue ischaemia and necrosis. \n \n# Aetiology\n\nThe majority of cases of compartment syndrome occur secondary to fractures, with tibial, forearm and wrist fractures carrying the highest risk. \n\nOther causes include:\n\n- Crush injuries\n- Excessive exercise\n- Constrictive dressings or plaster casts\n- Prolonged immobilisation\n- Reperfusion of ischaemic limbs\n\n# Signs and Symptoms\n\nThe classic symptom of compartment syndrome is severe pain that is typically out of proportion to the initial injury. On examination, passive stretching of the affected muscles exacerbates the pain.\n\nOther signs and symptoms occur sequentially as the increasing pressure initially compresses veins, followed by nerves then arteries:\n\n- Paraesthesia\n- Pallor \n- Pulselessness\n- Paralysis\n- Coolness of the affected limb\n- The area may feel tense on palpation\n\n\n# Differential Diagnosis\n \n- **Deep vein thrombosis** also causes pain and may be associated with immobility and inflammation after injury, however the affected area is usually warm, erythematous and swollen\n- **Cellulitis** also causes localised pain and may be associated with injury; the patient may also be systemically unwell, however skin is erythematous and warm to touch \n- **Acute limb ischaemia** can both result from compartment syndrome and may also lead to compartment syndrome after reperfusion, however they are not always associated and are managed differently. Symptoms and signs of pain, paraesthesia, pallor, pulselessness, paralysis and \"perishing\" coldness of the limb are classic but the significant pain of compartment syndrome and a preceding injury may not be seen.\n\n# Investigations\n\nCompartment syndrome is a clinical diagnosis, however it is possible to measure intra-compartmental pressures directly (for example in atypical presentations). Normal compartment pressures are 0-8mmHg; in compartment syndrome these are often above 40mmHg. A difference between the patient's diastolic blood pressure and the compartment pressure of under 30mmHg is suggestive of compartment syndrome.\n\nOther useful tests include:\n\n- **CK** is often elevated due to ischaemic muscle damage\n- **U&Es** may be deranged secondary to rhabdomyolysis\n- **FBC**, **LFTs**, **clotting** and **group and saves** should be done in preparation for surgery\n- An **ECG** should also be done in preparation for surgery; arrhythmias may occur secondary to rhabdomyolysis\n\n# Management\n\n- Urgent surgical referral for immediate fasciotomies is the key management - surgery should occur within an hour of deciding to operate\n- This involves making surgical incisions through the fascia to relieve the pressure in the affected compartment\n- These incisions are left open and further operations may be required to debride necrotic tissues - a re-exploration should be performed at 24-48 hours\n- Remove any circumferential dressings or casts\n- Elevate the limb to the level of the heart to maximise perfusion\n- Resuscitate with IV fluids and supplementary oxygen to maintain perfusion and oxygenation\n- Ensure adequate analgesia is given (usually IV opioids); avoid regional anaesthesia as this may mask symptoms\n- Close monitoring including the neurovascular status of the limb is crucial\n- Ensure other injuries are addressed; intensive care input may be required especially if serious complications arise (e.g. renal failure secondary to rhabdomyolysis)\n\n# Complications\n \n- **Rhabdomyolysis** due to ischaemia of muscles, which may lead to renal failure and arrhythmias as well as death\n- **Limb amputation** may be required if there is extensive necrosis of tissues\n- **Volkmann contracture** refers to an ischaemic contracture which causes a flexion deformity of a limb due to ischaemic injury of its deep tissues\n\n# References\n\n[British Orthopaedic Assocation - Diagnosis and Management of Compartment Syndrome of the Limbs](https://www.boa.ac.uk/static/0d37694f-1cad-40d5-b4c1032eef7486ff/de4cfbe1-6ef3-443d-a7f2a0ee491d2229/diagnosis%20and%20management%20of%20compartment%20syndrome%20of%20the%20limbs.pdf) \n\n[Life in the Fast Lane - Compartment Syndrome](https://litfl.com/compartment-syndrome-ccc/)\n\n[Radiopaedia - Acute Compartment Syndrome](https://radiopaedia.org/articles/acute-compartment-syndrome?lang=gb)\n\n[Patient UK - Compartment Syndrome](https://patient.info/doctor/compartment-syndrome-pro)",
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"question": "A 40-year-old motorcyclist is involved in a road collision accident and sustains a displaced tibial shaft fracture. He undergoes closed reduction, and his leg is immobilised in a long cast. A few hours after the procedure, he complains of severe pain in the affected limb that seems disproportionate to clinical findings.\n\nGiven the most likely complication that has occurred, which of the following is considered a late finding in his condition?",
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"explanation": "This patient has presented with diabetic ketoacidosis, meeting the criteria of hyperglycaemia, acidosis and ketonaemia. A resuscitation fluid bolus of maximum 10-20ml/kg 0.9% normal saline should be given initially. It should not exceed this amount due to the increased risk of cerebral oedema. Subsequently, the maintenance fluid volumes should be calculated, and the volume deficit gradually replaced over the next 48 hours. The initial resuscitation fluid bolus should be subtracted from the maintenance fluid volume if the patient is not in shock",
"id": "32138",
"label": "a",
"name": "400 ml bolus of 0.9% normal saline over 30 minutes",
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"explanation": "This would be one of the treatments for hyperkalaemia. However, this should not be given as a fixed rate insulin infusion would be started for the initial management of diabetic ketoacidosis, which would drive potassium into cells and cause the K levels to fall. Potassium replacement should be added to bags of maintenance fluid unless the patient has K levels above the upper limit of normal",
"id": "32141",
"label": "d",
"name": "Oral calcium resonium",
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"explanation": "This would be a suitable maintenance fluid regimen. Maintenance fluid volumes for children in DKA can be calculated as reccommended by the BPSED DKA guideline as: 100ml/kg/day for the first 10kg of bodyweight, 50ml/kg/day for weight between 10-20kg and then 20ml/kg/day for each additional kg above 20kg. For a 40kg boy, it would be (100ml x 10kg) + (50ml x 10kg) + (20ml x 20kg) = 1000ml + 500ml + 400ml = 1900ml over 24 hours",
"id": "32139",
"label": "b",
"name": "1900 ml of 0.9% normal saline over 24 hours",
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"explanation": "This **should not** be given to children and young people with diabetic ketoacidosis. It should only be reserved for special situations in which the patient has compromised cardiac contractility caused by life-threatening hyperkalaemia or severe acidosis, and only after discussion with a senior. The initial metabolic acidosis should resolve upon treatment with intravenous fluids and an insulin infusion",
"id": "32142",
"label": "e",
"name": "Intravenous sodium bicarbonate",
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"explanation": "This is reserved for symptomatic hyponatraemia with a depressed level of consciousness and a high risk of cerebral oedema, which may occur if fluid administration is given too rapidly. **This should not be given without discussing with a senior first!** In diabetic ketoacidosis, the sodium levels should always be corrected for hyperglycaemia",
"id": "32140",
"label": "c",
"name": "100 ml of 2.7% hypertonic sodium chloride over 15 minutes",
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"comment": "explanation sounds like 1900ml over 24 hours is correct?\n",
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"comment": "think its describing that as an appropriate maintenance dose, but that this patient requires a bolus first as they are significantly dehydrated",
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"comment": "how do you work out they are significantly dehydrated?",
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"comment": "@relapse sclerosis electrolyte imbalances, urea, and just general clinical presentation",
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"comment": "40kg at 5 years old? Dude must be a giant. ",
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"comment": "i think explanation is wrong, rapid correction of hyponatremia causes central pontine myelinolysis, not cerebral oedema. the latter is if you correct hypernatraemia too quickly which this patient is not at risk of",
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"comment": "that is what I thought initially but apparently it is pseudohyponatraemia. Hyponatremia in DKA is often pseudohyponatremia, meaning the sodium level appears low on lab tests but is not truly low in the body. This occurs due to:\n\nHyperglycemia: High blood glucose levels cause water to shift out of cells and into the bloodstream (osmotic effect), diluting the sodium concentration. For every 100 mg/dL increase in blood glucose above normal, serum sodium decreases by approximately 1.6–2.4 mEq/L.\nCorrected Sodium Calculation: To determine the true sodium level, you can use the following formula:\nCorrected Sodium\n=\nMeasured Sodium\n+\n0.016\n×\n(\nGlucose\n−\n100\n)\nCorrected Sodium=Measured Sodium+0.016×(Glucose−100)\nThis adjustment accounts for the dilutional effect of hyperglycemia.",
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"comment": "Cerebral oedema is a well-recognised and potentially fatal complication of diabetic ketoacidosis (DKA) in children. Its mechanism is not fully understood, but it is thought to arise from rapid fluid shifts caused by a sudden decrease in serum osmolality during treatment.",
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"explanation": "# Summary\n \n\nDiabetic ketoacidosis (DKA) is a serious complication often associated with type 1 diabetes, characterised by hyperglycaemia, ketonaemia, and acidosis. Key signs and symptoms include fruity-smelling breath, vomiting, dehydration, abdominal pain, hyperventilation, and altered mental status. Investigations include blood glucose and ketone measurements, blood gas analysis, urea and electrolytes, and possibly blood cultures if infection is suspected. Management strategies largely depend on the patient's condition, including hydration and insulin administration via various routes and in various volumes based on severity. The major complication is cerebral oedema, a rare but potentially fatal condition that might be caused by rapid correction of dehydration with IV fluids.\n \n\n# Definition\n \n\nDiabetic ketoacidosis (DKA) is a severe and life-threatening medical complication characterised by hyperglycaemia, acidosis and ketonaemia.\n\nIt is defined by acidosis (bicarbonate < 15 mmol/l or pH <7.3) and ketones >3.0 mmol/L. \n \n\n# Epidemiology\n \n\nDKA is most commonly seen in individuals with type 1 diabetes. However, it can occur in those with type 2 diabetes under extreme stress or illness. The condition can be the first presentation of diabetes, especially type 1 diabetes in children and young adults.\n\nIt is more common in children under 5. \n \n\n# Aetiology\n \n\nDKA can be precipitated by several factors, including infection, dehydration, stress, burns, fasting, or untreated type 1 diabetes. It is important to note that fever is not a typical part of DKA presentation. A raised temperature could indicate an underlying infection that may have triggered the DKA.\n\nRisk factors include:\n\n- Previous episodes of DKA \n- Peripubertal and adolescent girls \n- Comorbidities including psychiatric disorders\n- Difficult home life\n- Insulin pump therapy \n\n\n# Classification\n\n- Mild: pH 7.1-7.29 or bicarbonate < 15 mmol/L. Dehydration 5%\n- Moderate: pH 7.1-7.19 or bicarbonate < 10 mmol/L. Dehydration 5%\n- Severe: pH <7.1 or bicarbonate < 5 mmol/L\n \n\n# Signs and Symptoms\n \n\nPatients with DKA may present with:\n \n\n - Fruity-smelling breath (due to the presence of acetone)\n - Vomiting\n - Dehydration secondary to polydipsia and polyuria \n - Abdominal pain\n - Deep, sighing respiration (Kussmaul respiration)\n - Signs of hypovolaemic shock\n - Altered mental status, including drowsiness or coma\n \n\n# Differential Diagnosis\n \n\nThe main differential diagnoses for DKA in children include:\n \n - **Lactic Acidosis**: This may present with rapid breathing, abdominal pain, and altered mental status. The patient may have a history of severe illness or sepsis, hepatic failure or metformin use.\n - **Starvation Ketosis**: This usually presents with weight loss, nausea, and clear mental status. The condition is mild, with low-level ketonaemia.\n - **Inborn errors of metabolism**: Tend to present earlier in life with metabolic disturbances or failure to thrive. \n - **Sepsis**: The child will be generally unwell, with a high or low temperature, hypotension and tachycardia. \n \n\n# Investigations\n \n\nDiagnosis of DKA involves assessment of clinical features along with:\n \n\n - Blood glucose (>11.1mmol/L)\n - Blood ketones (>3mmol/L)\n - Urea and electrolytes\n - Blood gas analysis\n - Urinary glucose and ketones\n - Blood cultures (if evidence of infection)\n - Cardiac monitoring/ECG (for any ischaemic changes or changes secondary to hypokalaemia)\n \n\nNote that hyperglycaemia may not always be present in DKA.\n \n\n# Management\n \n\nManagement of DKA should be based on the A to E approach followed by the following treatments: \n\n - IV fluids (initial bolus of 10ml/kg 0.9% NaCl, even if the patient is shocked) given over 15 minutes.\n - Repeat as needed to restore circulation\n - At 40 ml/kg then discuss with a senior for consideration for inotropes \n - Insulin infusion at 0.1 units/kg/hour 1 hour after starting IV fluids\n\n\nFluids:\n\n- Further fluids, following initial boluses should contain 40 mmol/l potassium chloride to protect against hypokalaemia. \n- Total fluid required = deficit + maintenance\n- Hourly rate = [(Deficit - initial bolus) / 48 hours ] + maintenance per hour \n- Deficit \n - A 5% fluid deficit is assumed for children with mild or moderate DKA\n - A 10% fluid deficit is assumed for children with severe DKA\n - Deficit should be replaced over 48 hours alongside maintenance fluids \n- Maintenance \n - Calculated by Holliday-Segar formula: 100 ml/kg/day for the first 10 kg, 50 ml/kg/day for the next 10 kg, and 20 ml/kg/day for each additional kg over 20 kgs. \n \nImportant points to consider: \n\n- Monitoring should include hourly blood glucose and ketones, neurological observations and fluid balance. \n- Investigations should be done to determine the cause of the DKA. \n- Many patients will require HDU-level care. \n- Intravenous insulin infusion should not be stopped until 1 hour after subcutaneous insulin has been given.\n- Long-acting insulin should continue to be given.\n\n\n# Resolving DKA\n\nIVF can be stopped once ketosis is resolving and oral fluids are tolerated without nausea or vomiting. \n\nSubcutaneous insulin can be started once ketosis is resolving and should be started at least 30 minutes before stopping intravenous insulin. \n\nDischarge can be considered once a child is eating and drinking, and stabilised on their subcutaneous insulin regime. \n \n\n# Complications\n\n\nImportant complications to monitor for include:\n\n- Cerebral oedema:\n - Can occur several hours after the onset of DKA due to rapid correction of dehydration with IV fluids. \n - Due to the potential risk, fluid deficit correction is recommended to be performed slowly, over 48 hours. \n - Though rare, this complication is fatal in 1 in 4 children. \n - Risk factors include younger age and longer duration of symptoms. \n - Management includes hypertonic (2.7%) sodium chloride and restriction of IV fluids. \n- Hypokalaemia \n- Aspiration pneumonia \n- Venous thromboembolism \n - Thromboembolic prophylaxis is not recommended in children < 16 years \n- Inadequate resuscitation \n- Hypoglycaemia\n - Blood glucose levels can fall rapidly with intravenous insulin, and if blood glucose falls below 14 mmol/L, IV fluids should include glucose. \n\n# Prognosis\n\nEarly detection and treatment results in good outcomes for patients with DKA, with many children discharged within a few days of DKA. Poorer outcomes are associated with delays in treatment and the development of cerebral oedema. \n\n\n# NICE Guidelines\n\n[BNFC Treatment Summaries: Diabetic hyperglycaemic emergencies](https://bnfc.nice.org.uk/treatment-summaries/diabetic-hyperglycaemic-emergencies/) \n \n\n# References\n \n[BSPED Guidelines for Management of DKA in Children](https://www.bsped.org.uk/media/1959/dka-guidelines.pdf)\n \n[Patient Info: Childhood ketoacidosis](https://patient.info/doctor/childhood-ketoacidosis#ref-2)",
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"question": "A 5-year-old boy presents to Accident & Emergency with a one-day history of abdominal pain and vomiting. He weighs 40 kg and has no past medical history of note.\n\n\nObservations on triage: Temperature 36.5°C, pulse 90, blood pressure 100/70, SpO2 98% on room air.\n\n\nOn examination, his abdomen is soft with mild generalised tenderness, and bowel sounds are present.\n\n\nInitial investigations are as follows:\n\n||||\n|---------------------------|:-------:|--------------------|\n|Sodium|124 mmol/L|135 - 145|\n|Potassium|5.5 mmol/L|3.5 - 5.3|\n|Chloride|85 mmol/L|95 - 106|\n|Urea|8 mmol/L|2.5 - 7.8|\n|Creatinine|100 µmol/L|60 - 120|\n|Non-fasting Glucose|30.5 mmol/L|< 6.1|\n|Ketones (Serum)|4 mmol/L|< 0.6|\n\n\nArterial blood gas:\n\n||||\n|--------------|:-------:|------------------|\n|pH|7.15|7.35 - 7.45|\n|PaO₂|12 kPa|11 - 15|\n|PaCO₂|4 kPa|4.6 - 6.4|\n|Bicarbonate|14 mmol/L|22 - 30|\n\n\nWhich is the next most appropriate prescription to administer?",
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"explanation": "This would only be considered in patients with life-threatening haemorrhage, persistent bleeding refractory to treatment or those requiring surgery. The patient is stable; hence this would not be required",
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"label": "c",
"name": "Intravenous immunoglobulin",
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"explanation": "Platelet transfusions are generally reserved for patients with active life-threatening haemorrhage, persistent bleeding refractory to treatment or those requiring surgery. The patient is stable, and hence this would not be required",
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"label": "d",
"name": "Oral vitamin K",
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"explanation": "Glucocorticoids may be given to raise the platelet count if it needs to be raised acutely. However, in the absence of any clinically significant bleeding, there is no need for this",
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"explanation": "The patient has immune thrombocytopenic purpura (ITP). Patients usually present with an isolated low platelet count with normal coagulation profile, peripheral blood film and reticulocyte count. The negative DAT rules out autoimmune haemolytic anaemia, which may occur in conjunction with ITP (Evans syndrome). The general approach in stable patients without clinically significant bleeding would be to wait and observe, with safety net advice given to avoid contact sports, blood-thinning medications and to monitor for signs of worsening bleeding",
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"__typename": "QuestionComment",
"comment": "How do you distinguish this from HSP?",
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"comment": "Dat scan is negative so no haemolytic anemia and in HSP, features include haemolytic anemia, aki and thrombocytopenia i thinkinggg ?",
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"comment": "HSP is an IgA mediated small vessel vasculitis whereas ITP is destruction of platelets. Therefore HSP would present with a palpable rash (ITP would not), as well as more systemic sx e.g. abdominal pain, arthralgia and haematuria. Platelets should not be low in ITP. ",
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"comment": "platelets shouldn't be low in ITP? do you mean HSP?",
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"comment": "thought palpable rash was is HSP not ITP?",
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"comment": "can't agree",
"createdAt": 1737302821,
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"comment": "how is 3 days of nosebleeds not clinically significant :((",
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"explanation": "# Summary \n \n\nImmune thrombocytopenic purpura (ITP) is an autoimmune disease characterised by a reduction in circulating platelets. In children, it usually follows a viral infection and is self-limiting. Primary investigation includes Full Blood Count (FBC), blood film and exclusion of differential diagnoses. Management generally involves a 'watch and wait' approach due to the high rate of spontaneous remission. In persistent cases, steroids are employed, and splenectomy may be considered in refractory cases. \n \n\n# Definition\n \n\nImmune thrombocytopenia purpura (ITP) is an autoimmune condition, characterised by a reduction in the number of circulating platelets. It is a type II hypersensitivity reaction whereby the spleen produces antibodies directed against the glycoprotein IIb/IIIa or Ib-V-IX complex.\n \n\n# Epidemiology\n \n\nIn children, ITP often presents as a self-limiting disease following a viral infection in approximately 60% of cases. It affects 4 in 100,000 children per year, with more girls affected than boys and with an average age at onset of 5.7 years. \n \n\n# Aetiology\n \n\nITP in children is often triggered by a viral infection or following immunisation. \n\nSecondary ITP is rare in children but it can be due to:\n\n- Autoimmune conditions (i.e. systemic lupus erythematosus)\n- Infections (i.e. H pylori and CMV)\n- Medications\n- Lymphoproliferative disorders \n \n\n# Signs and Symptoms\n \n\nITP typically presents with:\n \n\n - Easy or excessive bruising (purpura)\n - Superficial bleeding into the skin that appears as a rash of pinpoint-sized reddish-purple spots (petechiae), usually on the lower legs\n - Prolonged bleeding from cuts\n - Spontaneous bleeding from the gums or nose - ITP presents with mucocutaneous bleeding (rather than e.g. haemarthrosis which is often associated with defects in the coagulation cascade like in haemophilia)\n - Blood in urine or stools\n - Unusually heavy menstrual flow in females \n \n\n# Differential Diagnosis\n \n\nDifferential diagnoses for ITP include aplastic anaemia, leukaemia, and thrombotic thrombocytopenic purpura. These diagnoses can be differentiated by their unique signs and symptoms:\n \n\n - **Aplastic anaemia**: Children would show symptoms of anaemia - including shortness of breath, rapid or irregular heart rate and pallor. They will also have increased bleeding and frequent or prolonged infections.\n - **Leukaemia**: Children will generally be more unwell with fatigue, frequent infections, lymphadenopathy, easy bleeding or bruising and weight loss. \n - **Thrombotic thrombocytopenic purpura**: This is a more severe condition, with purpura, fatigue, fever, thrombocytopenia, haemolytic anaemia, and neurological abnormalities.\n\nIn neonates, hereditary thrombocytopenia or ITP in the mother should be considered. \n \n\n# Investigations\n \nThe primary investigations for ITP include:\n \n\n - Full Blood Count (FBC)\n - Blood film\n - Inflammatory markers to check for active infection\n\nFurther tests may be done to exclude other differential diagnoses:\n\n - Bone marrow examination (biopsy), which is only required if the case appears atypical or there is suspicion of malignancy\n \n\n [lightgallery]\n \n\n# Management\n \n\n * The management of ITP is generally conservative, with a watch-and-wait approach typically adopted due to the high rate of spontaneous remission. \n * Tranexamic acid (TXA) may be used to help blood clot, particularly used for menorrhagia. \n * For persistent cases, steroids (immunosuppressant) can be used for 4-7 days. \n * IVIG can also be used as it is immunomodulatory, reducing antibody production. \n * In cases that prove refractory for 12-24 months, splenectomy may be considered.\n * Platelet transfusions should be avoided unless there is life-threatening bleeding. This is because giving more platelets will increase the rate of platelet destruction.\n\nIbuprofen should be avoided in children with ITP. \n \n \n# Complications\n\nITP is generally mild in children. Serious complications are rare but can include:\n\n- Significant bleeds (affecting 3% of children with ITP)\n- Intracranial haemorrhage in 1 in 300 children with ITP\n\nThese complications typically occur when platelet counts are less than 20, and occur in patients with pre-existing vascular abnormalities. \n\n# Prognosis \n\nITP is generally self-resolving within weeks to months without intervention. However, up to 1 in 5 children will follow a chronic course. If recovery is not achieved by 6 months, a differential diagnosis should be considered, and a bone marrow aspirate may be needed. For some children, ITP can become chronic. \n\nITP is typically an isolated event in children, with only 5% having a recurrence. \n\n \n# NICE Guidelines\n\n[NICE Guidelines on Platelets - abnormal counts and cancer](https://cks.nice.org.uk/topics/platelets-abnormal-counts-cancer/) \n \n\n# References\n\n[ITP Support Association - ITP in children](https://itpsupport.org.uk/itp-in-children/#:~:text=How%20common%20is%20ITP%20and,common%20in%20girls%20than%20boys.)\n\n[Patient Info Immune Thrombocytopenic Purpura](https://patient.info/doctor/immune-thrombocytopenia-pro)",
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"question": "A 10-year-old boy presents to A&E with a 3-day history of nosebleeds and palpable, non-blanching red spots on his arms and legs. (refer to image provided).\n\n\n\n [lightgallery]\n\n\n\nHe has no past medical history of note. He has otherwise been well apart from a recent cold two weeks ago. His mother says that he has not had any recent trauma and does not play any contact sports.\n\n\n\nInvestigations are as follows:\n\n\n\nFull blood count:\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|140 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|9x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|55x10<sup>9</sup>/L|150 - 400|\n|Reticulocytes|1 %|0.2 - 2|\n\n\n\n\nCoagulation screen:\n\n\n||||\n|---------------|:-------:|------------------------|\n|Activated Partial Thromboplastin Time (APTT)|30 seconds|22 - 41|\n|Prothrombin Time (PT)|12 seconds|10 - 12|\n|Fibrinogen|0.4 g/dL|1.5 - 4.0|\n\n\n\n\n\nPeripheral blood film:\n\n\n\n - Normal sized platelets, no clumping seen\n\n\n\nDirect antiglobulin test (DAT): Negative\n\n\n\nWhich is the most appropriate management of his condition?",
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"explanation": "This is the dose that should be given in anaphylaxis in adults or children >12 years old",
"id": "32149",
"label": "b",
"name": "IM Adrenaline (1:1000) 500 micrograms",
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"explanation": "This may be considered in cases of anaphylaxis with severe or persistent bronchospasm. However, adrenaline takes priority in this situation",
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"name": "Salbutamol nebulisers",
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"explanation": "This is the dose that should be given in a cardiac arrest as part of the paediatric advanced life support algorithm",
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"label": "c",
"name": "IV Adrenaline (1:10,000) 10 micrograms per kg",
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"explanation": "The patient has developed anaphylaxis, most likely to amoxicillin. Warning signs in this scenario include stridor, wheeze, hypotension and desaturation. The single most important medication to administer is adrenaline, which should be done as soon as possible. This is the dose that should be given in children 6-12 years old. IV adrenaline for anaphylaxis should only be given by experienced specialists in an appropriate setting",
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"explanation": "This may be given if the patient has hypotension due to anaphylactic shock. However, adrenaline takes priority in this situation",
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"comment": "i forgot its a child",
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"explanation": "# Summary\n \n\nAnaphylaxis is an acute, life-threatening allergic reaction characterised by multi-system involvement, typically involving the skin, respiratory, cardiovascular, and gastrointestinal systems. Triggered primarily by allergens such as certain foods, medications, and insect stings, anaphylaxis requires immediate management with adrenaline and patient monitoring for any rebound symptoms. Investigations commonly involve the measurement of serum mast cell tryptase levels. Upon discharge, patients newly diagnosed with anaphylaxis should be provided with two adrenaline auto-injectors and proper counselling on how to use them.\n \n\n# Definition\n \n\nAnaphylaxis is an acute and severe type 1 hypersensitivity reaction. It is a systemic, potentially life-threatening condition that involves multiple organ systems due to the release of mediators from mast cells and basophils.\n \n\n# Epidemiology\n \n\nAnaphylaxis is relatively uncommon, affecting 1-3 per 10,000 annually. Its incidence appears to be rising, particularly in Western countries. It affects people of all ages and both sexes, though certain groups, such as those with a history of asthma or atopy, are at higher risk.\n \n\n# Aetiology\n \nAs a type 1 hypersensitivity reaction, an allergen reacts with specific IgE antibodies causing a rapid release of histamine and other vasoactive substances. This increases capillary permeability, causing oedema and shock. \n\nCommon triggers of anaphylaxis include:\n \n\n - Animals: Insect stings, animal dander\n - Foods: Nuts, peanuts, shellfish, fish, eggs, milk\n - Medications: Antibiotics, IV contrast media, NSAIDs\n \n\n# Signs and Symptoms\n \n\nThe clinical manifestations of anaphylaxis can vary greatly but are best assessed following the ABCDE approach. \n \n\n - **A**irway: Hoarse voice, lip swelling, stridor indicative of upper airway obstruction and laryngeal oedema \n - **B**reathing: Wheezing, shortness of breath, fatigue, SpO2 < 94%\n - **C**irculation: Tachycardia, hypotension/shock, angioedema, confusion\n - **D**isability: Confusion\n - **E**verything else: \n - Gastrointestinal: Abdominal pain, diarrhoea, vomiting\n - Urticaria \n \n\n [lightgallery]\n \n\n# Differential Diagnosis\n \n\nThe differential diagnoses for anaphylaxis may include:\n \n -**Anaphylactoid Reaction**: These are similar reactions which cause similar mast cell activation but are not due to IgE. \n - **Vasovagal reaction**: Characterised by hypotension, bradycardia, pallor, diaphoresis, and nausea.\n - **Panic attack**: Shortness of breath, tachycardia, sweating, tremors, and feeling of impending doom, but lacks skin involvement.\n - **Asthma exacerbation**: Primarily respiratory symptoms such as wheezing, cough, and breathlessness, without systemic involvement.\n - **Carcinoid syndrome**: Flushing, diarrhoea, abdominal pain, and wheezing due to serotonin release but generally has a more chronic course.\n \n\n# Investigations\n \n\nThe primary investigation in anaphylaxis is the measurement of serum levels of mast cell tryptase, which rises within an hour of onset and can confirm the diagnosis. **However, this should not delay management**\n \nDuring the A to E assessment, investigations may include:\n\n- Pulse oximetry to detect hypoxia\n- Bloods to include:\n\t- Mast cell tryptase: These levels peak 1 hour following anaphylaxis, but remain elevated for up to 6 hours. In children, mast cell tryptase is only indicated if the trigger is believed to be idiopathic or related to venom or drugs. \n\n\n# Management\n \n\nPrompt management of anaphylaxis is crucial and includes:\n \n\n - Immediate administration of adrenaline (1:1000, IM):\n - Child > 12 years: 500 micrograms IM (0.5 mL)\n - Child 6-12 years: 300 micrograms IM (0.3 mL)\n - Child 6 months - 6 years: 150 micrograms IM (0.15 mL)\n - Child < 6 months: 100-150 micrograms IM (0.1-0.15 mL) \n - Removing the trigger if possible\n - Early call for help\n - Placing the patient in a supine position and raising their legs\n - Managing the airway and administering high-flow oxygen when skills and equipment are available\n - Administering IV fluids (10 mL/kg bolus) if patient \n - Attaching the patient to monitoring equipment\n - If no response 5 minutes after IM adrenaline: \n \t- Repeat adrenaline \n - If no improvement despite 2 doses of IM adrenaline \n - Follow refractory anaphylaxis guidelines\n \n\nPost-crisis, patients should be monitored for 6-12 hours after the initial presentation in case of a rebound episode. Children are admitted to hospital under the care of the paediatric medical team. Upon discharge, newly diagnosed patients (and their carers) should receive:\n \n\n - Counselling on the use of adrenaline auto-injectors\n - A supply of two auto-injectors\n - Written advice\n - A referral to the local allergy service for follow-up\n \n# References\n \n\n[UK Resuscitation Council Guidelines](https://www.resus.org.uk/sites/default/files/2020-06/EmergencyTreatmentOfAnaphylacticReactions%20%281%29.pdf)\n\n [A simple summary of managing anaphylaxis in all groups](https://www.resus.org.uk/EasySiteWeb/GatewayLink.aspx??alId=793)\n \n [RCPCH Anaphylaxis Care Pathway](https://www.rcpch.ac.uk/resources/allergy-care-pathway-anaphylaxis)\n \n [Patient Info Anaphylaxis and its treatment](https://patient.info/doctor/anaphylaxis-and-its-treatment)",
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"question": "A 10-year-old boy collapses in the Emergency Department after being administered a dose of amoxicillin for otitis media. He has no other past medical history of note.\n\nHe develops a sudden onset wheeze and shortness of breath.\n\nObservations:\n\n- Temperature 37.5°C\n- pulse 150\n- BP 80/60\n- SpO<sub>2</sub> 88% room air\n\nWhat is the next most important medication to administer?",
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"explanation": "Antibiotics have no role in the routine management of uncomplicated croup, as most cases are caused by viruses. They should only be used to treat cases of bacterial superinfection, such as pneumonia or bacterial tracheitis",
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"explanation": "Salbutamol does not play a role in the management of croup. It would be useful as a bronchodilator in asthma",
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"explanation": "Nebulised adrenaline may be used in acute symptom relief of croup by reducing stridor and work of breathing, as it works by decreasing airway oedema and relieving airway obstruction. However, it would not alter the natural clinical course of croup",
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"comment": "what does the xray show?",
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"comment": "steeple sign",
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"comment": "what does the xray show?",
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"comment": "Subglottic narrowing - also known as Steeple Sign",
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"comment": "how do you tell this from epiglottitis? thank you! ",
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"comment": "thumbprint sign on x-ray",
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"comment": "whoops I thought steeple sign = epiglottitis",
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"comment": "Can be present in both",
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"explanation": "# Summary\n \n\nCroup (also known as acute laryngotracheobronchitis) is a common childhood infection characterised by a harsh barking cough and inspiratory stridor. It is usually mild and self-limiting, however, some cases may cause severe respiratory distress requiring hospitalisation and supportive treatment. Parainfluenza viruses are the commonest causes, but the diagnosis is a clinical one and as symptoms such as stridor can worsen if the child is distressed, investigations should only be done if necessary. Oral steroids should be given to all children; in moderate to severe cases nebulised adrenaline, supplementary oxygen and airway support may be indicated.\n \n\n# Definition\n \n\nCroup, or acute laryngotracheobronchitis, is an upper respiratory tract infection that in most cases has a viral aetiology. Key symptoms include a barking cough, hoarse voice and inspiratory stridor. \n\n# Epidemiology\n \n\nCroup commonly affects children aged from 6 months old to 3 years old, with the peak incidence at 2 years. It is uncommon after the age of 6.\n\nSimilar to other viral infections, it is commonest in the autumn and winter months and is linked to parainfluenza epidemics. \n\n# Aetiology\n \nThe commonest cause is the parainfluenza virus. Other viral causes include adenovirus, respiratory syncytial virus (RSV), rhinovirus and influenza.\nRarely, bacteria can cause croup (e.g. Mycoplasma pneumoniae).\n\nThe pathophysiology involves infection and resulting inflammation of the subglottic and laryngeal mucosa which causes partial obstruction of the airways leading to respiratory distress and stridor.\n\n# Signs and Symptoms\n\n- The prodromal phase of coryzal symptoms, fever and a non-specific cough usually lasts 12-72 hours.\n- Characteristic symptoms of croup such as the harsh barking cough, hoarse voice or cry and inspiratory stridor then develop - these tend to be worse at night.\n- In severe cases, children may become drowsy and lethargic, or conversely more agitated.\n- The usual course of disease is resolution of symptoms within 48 hours (up to a week at most).\n\nOn examination, look for the following red flags that may indicate impending respiratory failure:\n\n- Signs of respiratory distress e.g. intercostal recessions, accessory muscle usage, tachypnoea\n- Cyanosis\n- Decreased level of consciousness\n- Stridor may decrease due to worsening airway obstruction\n- Decreased air entry on auscultation of the chest\n- Tachycardia\n\n# Differential Diagnosis\n \n\n- **Epiglottitis**: Sudden onset high fever, drooling, and dysphagia are seen without the barking cough of croup. Usually secondary to Haemophilus influenzae B and so significantly rarer since routine immunisation against this.\n- **Bacterial tracheitis**: Suspect if acute deterioration following initial viral symptoms, with high fevers, stridor and respiratory distress.\n- **Foreign body aspiration**: No prodrome or fever, usually sudden onset of choking, cough or wheeze after eating or playing with small objects.\n- **Anaphylaxis**: Rapid onset stridor, possible urticarial rash and facial swelling; suspect if history of previous episodes with allergens or family history of atopy.\n \n\n# Investigations\n \nDiagnosis is clinical, and investigations need to be carefully considered as distressing the child may lead to worsening of symptoms due to agitation.\n\nFurther investigation may include: \n\n- Pulse oximetry should be done to determine if supplementary oxygen is required.\n- Chest X-ray may be of use if a differential diagnosis such as an inhaled foreign body is suspected. \n - In croup, an X-ray may show a steeple sign, where the upper trachea is seen to taper.\n \n\n# Management\n\nClassifying the severity of croup is key to determining appropriate management:\n\n| Severity | Description |\n|------------------------------|---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|\n| Mild | Seal-like barking cough but no stridor or sternal/intercostal recession at rest. |\n| Moderate | Seal-like barking cough with stridor and sternal recession at rest; no (or little) agitation or lethargy. |\n| Severe | Seal-like barking cough with stridor and sternal/intercostal recession associated with agitation or lethargy. |\n| Impending respiratory failure | Minimal barking cough, stridor may become harder to hear. Increasing upper airway obstruction, sternal/intercostal recession, asynchronous chest wall and abdominal movement, fatigue, pallor or cyanosis, decreased level of consciousness or tachycardia. The degree of chest wall recession may diminish with the onset of respiratory failure as the child tires. A respiratory rate of over 70 breaths/minute is also indicative of severe respiratory distress. |\n\nMild cases with no stridor or chest wall recessions at rest may be treated at home with a single dose of oral dexamethasone (0.15mg/kg). In children treated at home, families should be safety-netted on signs of deterioration and advised to check on the child regularly and encourage fluids. Paracetamol or ibuprofen can be used for fever and pain.\n\nChildren with any of the following should be considered for hospital admission:\n\n* Stridor and/or sternal recession at rest\n* High fever\n* Respiratory rate > 60\n* Cyanosis\n* Lethargy or agitation\n* Fluid intake < 75% of normal or no wet nappies for 12 hours\n* Aged under 3 months\n* Chronic conditions such as immunodeficiency, chronic lung disease or neuromuscular disorders\n\nManagement is supportive as there is no treatment indicated for the usual causative viruses, and may include:\n\n- Supplementary oxygen if low saturations - consider how best to deliver this so as not to distress the child (e.g. a parent holding an oxygen mask to the face)\n- Steroids for all - if unable to swallow oral dexamethasone or prednisolone can give nebulised budesonide\n- Nebulised adrenaline for temporary symptom relief\n- Anaesthetics +/- ENT input if concerns regarding airway or respiratory failure\n\n# Complications\n\n- Dehydration secondary to poor fluid intake during illness\n- Pneumonia due to secondary bacterial infection \n- Respiratory failure \n- Death is very rare (1 in every 30,000 cases)\n\n# Prognosis\n\nUsually, symptoms resolve within 48 hours but may last longer. Occasionally, severe upper airway obstruction can occur, causing respiratory failure and arrest.\n\n# NICE Guidelines\n\n[NICE CKS: Croup](https://cks.nice.org.uk/topics/croup/)\n\n# References\n \n[BNF Treatment summaries: Croup](https://bnf.nice.org.uk/treatment-summaries/croup/)\n\n[Patient.info: Croup](https://patient.info/doctor/croup-pro)",
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"question": "A 12-month-old girl is brought in by her worried parents to the children's Accident & Emergency department with a three-day history of persistent cough, hoarse voice and shortness of breath.\n\nObservations:\n\n- Temperature 38.5°C\n- pulse 150\n- BP 80/60\n- respiratory rate 40\n- SpO<sub>2</sub> 95% room air\n\nA posterior-anterior chest X-ray is done and is shown below.\n\n[lightgallery]\n\nGiven her most likely diagnosis, which single therapy has been shown to improve disease outcomes?",
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"explanation": "This would be an initial surgical procedure done in Tetralogy of Fallot to create a pathway between the subclavian and pulmonary arteries, thus relieving cyanosis whilst awaiting definitive corrective surgery",
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"explanation": "This is a surgical procedure done to stabilise patients with severe hypoxaemia due to inadequate mixing between the two parallel circuits in transposition of the great arteries (TGA). A balloon is placed across the atrial septum and used to enlarge the foramen ovale or existing atrial septal defect. However, it is only a temporary measure before corrective surgery for TGA",
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"explanation": "This would be part of initial management to maintain patency of the ductus arteriosus, allowing blood to travel from the left to the right side of the heart. However, in this case, the presence of a ventricular septal defect would already allow for left to right shunting of blood",
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"explanation": "This neonate has transposition of the great arteries (TGA) and has presented in heart failure. He has not developed rapid cyanosis on day 2 of birth (with closure of the ductus arteriosus) but has presented later at a few weeks of age, as the presence of a ventricular septal defect (VSD) has allowed for improved inter-circulatory mixing. The classical finding on CXR would be an \"egg on string\" appearance. The definitive treatment would be an operation to translocate both the great arteries to the opposite root, establishing ventriculoarterial concordance",
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"explanation": "This is a prostaglandin antagonist that is used in the treatment of patent ductus arteriosus. Anatomical closure would likely already have occurred at this age. Furthermore, it should not be used in cyanotic heart disease as it would worsen hypoxaemia by closing off the left to right shunt",
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"comment": "Sounded like Tet spells to me",
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"comment": "How can you tell he has both TGA and a VSD and not TOF?",
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"comment": "TOF would be ejection systolic murmur at left upper edge- pulmonary stenosis.",
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"comment": "it honestly sounds like TOF >> TGA with a VSD? the only thing is that a BT shunt is a temp procedure so sure that's not 'definitive' treatment but the stem should really be changed to look more like TGA maybe? the only indication for this to be a tga for me was mom having diabetes but. idk. ",
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"comment": "I still dont 100% agree that this is great description of TGA BUT after doing this paper again, I suppose one can argue and say that in TOF, the murmur is usually of pulmonary stenosis rather than the VSD and the CXR findings of a narrow mediastinum + large heart are also more likely to be TGA because \n\nThe heart appears globular due to an abnormal convexity of the right atrial border and left atrial enlargement and therefore appears like an egg.\n\nThe superior mediastinum appears narrow due to stress-induced thymic atrophy and hyperinflated lungs which give the picture of an egg suspended by a string on a chest radiograph, hence the name egg-on-a-string.",
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"comment": "can wait to perform my first blalock-taussig shunt as an F1",
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"comment": "Anyone not think of ebsteins anamoly, pan-systolic murmur heard at lower left sternal border with signs of right sided heart failure. Any help would be appreciated ",
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"comment": "This is exactly what I thought",
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"explanation": "# Summary\n \nCongenital cardiac disease refers to a variety of heart abnormalities present at birth, often influenced by maternal risk factors such as infectious disease during pregnancy (e.g. rubella), exposure to teratogenic drugs (e.g. thalidomide, isotretinoin, lithium), substance misuse (e.g., alcohol), and poorly controlled type 1 or 2 diabetes. Identification primarily relies on signs and symptoms observed in newborns, with murmurs often being present, with/without cyanosis, and confirmatory investigations such as echocardiography. Management is typically multidisciplinary and can involve medical therapy, interventional procedures, or surgery, depending on the severity and type of heart defect.\n \n \n# Definition\n \n\nCongenital cardiac disease is a general term referring to abnormalities in the heart's structure that arise before birth. These defects can involve the heart walls, heart valves, or the arteries and veins near the heart.\n \n\n# Epidemiology\n \n\nThe global incidence of congenital heart disease is estimated to be around 1% of live births, making it the most common type of congenital disorder. \n \n\n# Aetiology\n \n\nSeveral factors can contribute to the development of congenital heart disease:\n \n\n- Infectious causes: \n - Maternal rubella infection during pregnancy\n- Teratogenic drugs: \n - Exposure to certain medications during pregnancy, such as thalidomide, isotretinoin, and lithium, increases the likelihood of developing congenital heart disease.\n- Substance misuse: \n - Maternal misuse of substances such as alcohol can also lead to this condition.\n- Maternal diabetes: \n - Poorly controlled type 1 and type 2 diabetes during pregnancy\n - Maternal gestational diabetes is not a known risk factor \n- Family history of congenital heart disease\n - Risk is also increased in consanguineous couples \n\n \n# Classification\n\nCongenital heart disease can be divided into cyanotic or acynotic heart disease.\n\nCyanotic Heart Disease:\n\n- Transposition of the great arteries (TGA)\n- Pulmonary and tricuspid atresias\n- Tetralogy of Fallot (ToF)\n- Total anomalous pulmonary venous return \n- Persistent truncus arteriosus\n- Hypoplastic left heart\n\nAcyanotic Heart Disease:\n\n- Ventricular septal defect (VSD)\n- Atrial septal defect (ASD)\n- Patent ductus arteriosus (PDA)\n- Aortic stenosis \n- Pulmonic stenosis \n- Coarctation of the aorta \n- Endocardial fibroelastosis \n \n\n# Signs and Symptoms\n \n\nNewborns with congenital cardiac disease may present with a variety of signs and symptoms, including:\n \n\n - Cyanosis\n - Fast or troubled breathing\n - Fatigue\n - Poor feeding\n - Delayed growth\n - Heart murmur on auscultation\n \n\nThese symptoms can vary widely depending on the type and severity of the heart defect.\n \n\n# Differential Diagnosis\n \n\nIn an infant presenting with the signs and symptoms of congenital heart disease, several conditions should be considered:\n \n\n - **Respiratory distress syndrome**: This condition can cause fast, troubled breathing, and fatigue. However, it is typically associated with prematurity.\n - **Pneumonia**: Can also lead to breathing difficulties and fatigue, but it is often accompanied by fever and abnormal lung sounds on auscultation.\n - **Gastrointestinal disorders**: These can cause poor feeding and delayed growth but are typically accompanied by vomiting, diarrhoea, or abdominal distension.\n \n\n# Investigations\n \n\nWhilst some cases are detected during prenatal scans, many cases are detected after birth. The following investigations are key to diagnosing congenital heart disease:\n \n\n - Pulse oximetry: To detect low oxygen levels in the blood. This should be measured both pre and post-ductal, with > 3% difference being significant. \n - Chest X-ray: Can reveal an enlarged heart or abnormal heart shape.\n - Electrocardiogram (ECG): Can detect abnormal heart rhythms.\n - Echocardiogram: The gold standard in diagnosing congenital heart disease, providing a detailed image of the heart's structure and function.\n \n\n# Management\n \n\nThe management of congenital heart disease is complex and depends on the type and severity of the heart defect.\n\nRed flag features require more urgent management. These features include:\n\n- Lower limb saturations < 96%\n- More than 3% pre/post ductal difference \n- Signs of heart failure or shock\n\n\nIt typically involves a multidisciplinary team and can include:\n\n- Conservative management:\n - For certain defects (i.e. mild atrial septal defects, a watch-and-wait approach may be adopted as many will close by age 1)\n\n- Medical management:\n - Some patients will require medications including diuretics and ACE inhibitors depending on the type of congenital heart disease. \n- Interventional procedures: Catheter-based procedures to repair certain types of heart defects.\n \n- Surgical intervention: For more complex or severe heart defects, surgery may be necessary.\n\n# Complications\n\nDepending on the type and severity of congenital heart disease, potential complications include:\n\n- Learning difficulties\n- Pneumonia \n- Infective Endocarditis \n- Pulmonary hypertension \n- Heart failure \n\nSudden cardiac death is very rare. \n\n# Prognosis\n\nSurgically corrected congenital heart disease, particularly when isolated, has a good prognosis, however, there is still a reduced life expectancy when compared to the general population. \n\n# NICE Guidelines\n\n[NICE Guidelines on Structural Heart Defects](https://www.nice.org.uk/guidance/conditions-and-diseases/cardiovascular-conditions/structural-heart-defects) \n\n \n# References\n \n [NHS Congenital Heart Disease](https://www.nhs.uk/conditions/congenital-heart-disease/#:~:text=Congenital%20heart%20disease%20is%20a,babies%20born%20in%20the%20UK.) \n \n [British Heart Foundation Congenital Heart Disease](https://www.bhf.org.uk/informationsupport/conditions/congenital-heart-disease) \n \n [Patient Info Congenital Heart Disease in Children](https://patient.info/doctor/congenital-heart-disease-in-children) ",
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"learningPoint": "The arterial switch operation is the standard surgical treatment for transposition of the great arteries (TGA), a congenital heart defect where the aorta and pulmonary artery are swapped. This procedure involves switching the positions of the aorta and pulmonary artery, reattaching the coronary arteries to the new aorta, and correcting the alignment to restore normal circulation.",
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"question": "A 21-day old baby boy is brought into the Emergency Department by his worried mother as he has been having shortness of breath and irritability during feeds. His weight is on the 5th percentile for his age.\n\nHis mother has diabetes mellitus, but otherwise had an uncomplicated pregnancy and spontaneous vaginal delivery at 38 weeks.\n\nHe is tachypnoeic with accessory muscle use. On examination, there is a pansystolic murmur at the lower left sternal border and hepatomegaly.\n\nAn electrocardiogram shows right axis deviation. Chest X-ray (CXR) reveals a narrow mediastinum and an enlarged heart.\n\nWhich is the most definitive management of his condition?",
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"explanation": "This would only be indicated in an acute asthma attack, which is not the case here.",
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"comment": "The answers for this are muddled? If he's not doing great on salmeterol and beclometasone (LABA + ICS) surely go for a MART. If the salmeterol is a typo and they mean salbutamol then you'd go for a LTRA like montelukast?",
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"comment": "I thought the same but the stem says \"salButamol\" and the answer is montelukast, just unlike the step up from a LABA you dont have to discontinue a SABA.",
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"comment": "all wales national guidelines say to Step 2 of persistent asthma include management with MART or LABA/ICS , so seeing as he has trailed the latter and it hasn't worked, it is reasonable to move to step 3 and commence trail of montelukast for 6 weeks, 10mg nocte ,",
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"explanation": "# Summary\n\nAsthma is the commonest chronic condition in children in the UK, affecting 1 in 11 children. Diagnosis and management, although there are similarities with the adult pathways, have some important differences and vary between young children aged under 5 and those aged above 5. Under 5s are diagnosed clinically, whereas older children the first investigation to offer is FeNO testing. Management is holistic and involves regular reviews, reducing exposure to triggers and ensuring families have a personalised asthma plan with education on how to manage exacerbations. Pharmacological treatment involves a ladder of escalating inhaled medications, as well as considering leukotriene receptor antagonists (an oral medication) in some cases.\n\n# Definition\n\nAsthma is a common condition in children and young people which usually presents with a triad of wheeze, cough and shortness of breath. Symptoms are intermittent and occur in response to triggers, such as dust mites, viral respiratory infections, smoke or exercise. \n\n# Epidemiology\n\nAsthma is the commonest chronic condition in childhood in the UK and affects 1 in 11 children. Unfortunately outcomes in the UK are some of the worst in Europe, with approximately 25-30 children per year dying of asthma. 90% of these deaths are thought to be preventable with better care and tackling the deprivation that contributes to poor outcomes. \n\n# Aetiology \n\nThe characteristic intermittent bronchoconstriction that causes shortness of breath and wheezing can be caused by a variety of triggers, including:\n\n- Air pollution\n- Dust mites\n- Viral respiratory tract infections\n- Exercise\n- Cold air\n- Strong emotions \n- Medications (e.g. NSAIDs)\n \nChildren who have asthma often have other conditions caused by atopy (the tendency to produce an exaggerated IgE mediated response to benign triggers) including allergic rhinitis, eczema or food allergies. There may also be a family history of these conditions. \n\nOther risk factors for paediatric asthma include preterm birth, low birth weight and obesity in childhood. Environmental contributors to the development of asthma include air pollution, exposure to damp or mould in the home and exposure to secondhand smoke. \n\n# Signs and Symptoms\n\nExamination may be normal in between exacerbations, or the following may be found:\n\n- Widespread wheeze on auscultation\n- Chest hyperinflation\n- Signs of respiratory distress during an exacerbation, e.g. tachypnoea, accessory muscle usage\n\n# Differential Diagnosis\n\n- **Respiratory tract infection** - may present with wheeze, cough and difficulty breathing, often accompanied by fever, malaise and coryzal symptoms.\n- **Cystic fibrosis** - lifelong symptoms, as well as respiratory manifestations would have gastrointestinal symptoms and failure to thrive.\n- **Bronchopulmonary dysplasia** - chronic lung disease caused by prematurity, usually presents in babies who required ventilation for respiratory distress syndrome. Presents with respiratory distress and low oxygen saturations in infants, asthma-like symptoms can develop in childhood.\n- **Bronchiectasis** - often follows severe lower respiratory tract infection, persistent productive cough with copious sputum.\n- **Gastro-oesophageal reflux or aspiration** - can present with cough and wheeze due to irritation from gastric contents, may have vomiting and failure to thrive.\n- **Foreign body inhalation** - may mimic asthma symptoms, acute onset and focal wheeze.\n- **Bronchiolitis** - common infection in the under 2s caused by RSV, causes coryzal symptoms, fevers, cough, shortness of breath and wheeze.\n\n# Investigations\n\nChildren under 5:\n\n- In the under 5s, after a detailed history and examination a provisional diagnosis of asthma can be made and treatment initiated based on clinical judgement.\n- This should be reviewed regularly and the diagnosis reconsidered if response to treatment is not as expected.\n\nChildren aged 5 and above:\n\n- At the age of 5, investigations should be offered to aid in diagnosis. If children are unable to perform the tests, these should be offered every 6-12 months with treatment based on clinical impression in the meantime.\n- The first investigation to offer is **FeNO testing** (fractional exhaled nitric oxide) which quantifies eosinophilic inflammation in the airways - if this is 35 parts per billion or more this is diagnostic of asthma.\n- If this is not raised or FeNO testing is not available, offer **spirometry with bronchodilator reversibility** - if this finds reversible obstruction (FEV1 increase of 12% or more from baseline, or an increase 10% or more of the predicted normal FEV1) this is sufficient to diagnose asthma.\n- If spirometry is delayed or not available, advise patients/families to measure peak flow twice daily for 2 weeks - variability over 20% is diagnostic of asthma.\n- If all of FeNO, bronchodilator reversibility and peak flow variability are negative but asthma is still suspected, either take bloods for eosinophil count and total IgE level, or do skin prick testing to the house dust mite:\n - Negative skin prick testing or a normal total IgE level can be used to rule out asthma.\n - A raised IgE and eosinophil count or evidence of sensitisation on skin prick testing are diagnostic of asthma.\n- Children in whom there is ongoing diagnostic uncertainty should be referred to specialist services for further investigations (e.g. a bronchial challenge test).\n\n# Management\n\n- All children and young people should have regular reviews in primary care (at least annually), with monitoring of asthma control using symptoms, peak flow or spirometry.\n- Inhaler technique should be checked and all patients should have an up-to-date personalised asthma action plan with details of current treatments and instructions on what to do in case of an acute asthma exacerbation.\n- Education of both children and caregivers on modifiable risk factors (such as smoke exposure, household chemicals and obesity) is also key.\n\n## Under 5 years old\n\n- For children with suspected asthma and either a history of severe asthma exacerbations or interval symptoms, consider a trial of a twice-daily paediatric low-dose inhaled corticosteroid (ICS) as maintenance therapy with a short-acting beta-2 agonist (SABA) reliever inhaler.\n- If symptoms do not resolve, check adherence and inhaler technique, look for environmental triggers such as mould or smoke exposure, and review the diagnosis of asthma.\n- Refer children who do not respond to treatment and where there is no clear explanation for this to specialist asthma services.\n- If symptoms resolve with treatment, consider stopping inhalers after 8-12 weeks with a planned review of symptoms in 3 months time.\n- If children respond to initial treatment but symptoms recur or they have a significant exacerbation (requiring hospital admission or oral steroids), restart treatment with an ICS and SABA.\n- The ICS may be titrated up to a paediatric moderate dose if required.\n- If this is not sufficient to control symptoms, the next step is a trial of a leukotriene receptor antagonist (LTRA) e.g. montelukast - this should be stopped if ineffective after 8-12 weeks.\n- If asthma is still uncontrolled, children should then be referred to secondary care for further assessment.\n\n## 5 to 11 years old\n\n- As in the under 5s, a twice-daily paediatric low-dose inhaled corticosteroid (ICS) as maintenance therapy with a short-acting beta-2 agonist (SABA) reliever inhaler is the first step in management.\n- If this does not control symptoms, there are two options to step up treatment:\n - A single maintenance and reliever therapy (MART) inhaler may be started, which contains both a paediatric low-dose ICS and a fast-acting long-acting beta-2 agonist (LABA).\n - If the child isn't able to manage a MART regimen, the alternative is adding a LTRA and assessing response to this after 8-12 weeks.\n- The next steps after this are respectively: - Increasing the low-dose ICS in the MART to a moderate-dose ICS\n - Switching the low-dose ICS to a combination inhaler with a low-dose ICS with a LABA, as well as continuing the SABA +/- the LTRA if this was effective \n- For patients on a low-dose ICS//LABA inhaler + SABA +/- LTRA, this could then be increased to a moderate dose ICS if needed\n- If asthma is not controlled at this stage, patients should be referred to specialist services - options include switching to a high dose ICS or adding another medication e.g. theophylline.\n\n## 12 years or older\n\n- Young people from the age of 12 should be managed as per the adult guidelines - please see the separate Asthma chapter for details\n\n# NICE Guidelines\n\n[Click here for the NICE Guidelines](https://www.nice.org.uk/guidance/ng245/)\n\n# References\n\n[RCPCH - State of Child Health](https://stateofchildhealth.rcpch.ac.uk/evidence/long-term-conditions/asthma)\n\n[Asthma and Lung UK](https://www.asthmaandlung.org.uk/conditions/asthma/child)\n\n\n\n\n\n",
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"learningPoint": "In children aged 5-11 whose asthma is uncontrolled while on salbutamol and low-dose ICS, if they are unable to tolerate MART therapy, montelukast (LTRA) should be trialled.",
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"question": "A 7-year-old boy attends his General Practitioner for a routine asthma review. His regular inhalers include salbutamol and beclometasone 200 micrograms (mcg) daily. He was previously unable to tolerate a MART regimen. He has been compliant with his inhalers but has been using his salbutamol inhaler every other day for the past two months due to wheezing. He is an active boy at school and plays sports; however his symptoms limit his exercise tolerance. \n\nWhich of the following is the next best management for his asthma?",
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"comment": "i know its not an option, but surely check TFTs etc?",
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"comment": "she lost her job cos of her symptoms - this would be enough to start meds",
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"comment": "Surely this stem can't be enough to diagnose her with anxiety?? What if she has idiopathic tension headaches and then suffered with the poor sleep and concentration as a consequence?",
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"explanation": "# Summary \n\nAnxiety disorders constitute a range of psychiatric conditions, including generalized anxiety disorder (GAD), specific phobias, panic disorder, obsessive-compulsive disorder (OCD), and post-traumatic stress disorder (PTSD). These disorders are typified by excessive fear, worry, and physical symptoms such as insomnia, restlessness, and gastrointestinal symptoms. Key diagnostic steps include history-taking, clinical examination, and the utilization of rating scales like the Beck Anxiety Inventory and the Hospital Anxiety and Depression Scale. Management strategies encompass counseling, cognitive behavioral therapy (CBT), and pharmacotherapy with SSRIs, SNRIs, and benzodiazepines. \n\n\n# Generalised Anxiety Disorder (GAD)\n\nGeneralized Anxiety Disorder (GAD) constitutes a chronic and pervasive condition characterized by excessive, uncontrollable worry extending across various life domains. GAD encompasses physical symptoms such as restlessness, muscle tension, and fatigue, accompanied by cognitive manifestations like difficulty concentrating and disrupted sleep patterns. Prevalent in middle age, affecting 3-5% of the population, GAD's aetiology involves a complex interplay of biological, psychological, and environmental factors. D. Cognitive-Behavioral Therapy and pharmacotherapy, particularly with SSRIs, form integral components of its multifaceted management.\n\n\r\n## Definition\n\n**ICD-11 Criteria:**\n\n- Excessive worry and apprehension.\n- Difficulty controlling worry.\n- Associated symptoms: Restlessness, muscle tension, fatigue.\n- Duration: At least 6 months.\n\n**DSM-V Criteria:**\n\n- Excessive anxiety and worry about various domains.\n- Difficulty controlling worry.\n- Associated symptoms: Restlessness, muscle tension, fatigue, irritability.\n- Duration: At least 6 months.\n\n\r\n## Epidemiology \n\n* Predominantly affects females.\n* Affects up to 10% of the general population.\n* Commonly comorbid with depression, substance misuse, and personality disorder.\n* An onset beyond the age of 35-40 years is more likely indicative of depressive disorder or organic disease.\n* Associated risk factors include lower socioeconomic status, unemployment, divorce, renting rather than owning a home, lack of educational qualifications, and urban living.\n\r\n## Clinical Features\n\n- Psychological: Fears, worries, poor concentration, irritability, depersonalization, derealization, insomnia, night terrors\n- Motor symptoms: Restlessness, fidgeting, a feeling of being on edge\n- Neuromuscular: Tremor, tension headache, muscle ache, dizziness, tinnitus\n- Gastrointestinal: Dry mouth, dysphagia, nausea, indigestion, \"butterflies\" in the stomach, flatulence, frequent or loose bowel movements\n- Cardiovascular: Chest discomfort, palpitations\n- Respiratory: Dyspnea, tight/constricted chest\n- Genitourinary: Urinary frequency, erectile dysfunction, amenorrhea\n\n\r\n## Differential Diagnosis \n\n- Hyperthyroidism - look for goiter, tremor, tachycardia, weight loss, arrhythmia, exophthalmos\n- Cardiac causes - palpitations/arrythmias can either be part of GAD or seperate diagnoses in and of themselves\n- Medication-induced anxiety - e.g. overuse of SABA inhalers/nebulisers such as salbutamol\n- Substance misuse - intoxication – amphetamines; withdrawal – benzodiazepines, alcohol\n- Excessive caffeine intake\n- Depression: anxiety is a common feature of depression and vice versa. Identifying which condition appeared first and which is currently more prominent provides useful diagnostic cues. If both conditions are present, a diagnosis of mixed anxiety and depressive disorder is made.\n- Anxious (avoidant) personality disorder: the patient describes themselves as an anxious person without a recent significant increase in anxiety levels. (Note, this disorder can predispose the individual to anxiety disorders.)\n- Early-stage dementia\n- Early-stage schizophrenia\n\n\r\n## Management \n\n- The majority of patients can be treated in a primary care setting\n- Advice and reassurance can help prevent early or mild problems from worsening (psycho-education)\n- Counselling alone may be highly effective – it addresses patients' worries and provides reassurance about somatic symptoms\n- First line - low-intensity psychological interventions:\n\t- Individual non-facilitated self-help - written/electronic materials that the patient can work through over a period of around 6 weeks, with occasional but minimal therapist contact.\n\t- Individual guided self-help - written/electronic materials that a patient works through with 5–7 weekly or fortnightly face-to-face or telephone sessions (30 minutes each) with a trained practitioner.\n\t- Psychoeducational groups - interactive CBT-guided group sessions consisting of 6 weekly 2-hour sessions\n- Second line: for people with GAD and marked functional impairment, or with GAD that has not improved following the above:\n\t- High-intensity psychological intervention such as CBT or applied relaxation\n\t- Medical management - SSRIs are preferred i.e. sertraline, and if one does not work an alternative can be trialled e.g. escitalopram, paroxetine, or an SNRI (venlafaxine or duloxetine) can be used\n\t\t- In the first week of treatment there may be increased anxiety, agitation, and sleeping problems, and in people aged under 30 years that in a minority of people aged under 30 years, SSRIs and SNRIs are associated with an increased risk of suicidal thinking and self-harm. \n\t\t- **Patients under 30 should therefore have a follow-up appointment within 1 week to monitor progress.**\n\t\t- Symptomatic management with propranolol for palpitations can also be used.\n\n# Panic Disorder\n\nPanic Disorder, a prevalent anxiety disorder, is characterized by the occurrence of recurrent, unexpected panic attacks, each marked by intense fear or discomfort. These episodes prompt persistent worry about future attacks and may lead to avoidance behaviors, altering one's lifestyle to prevent potential episodes. Onset typically arises in adolescence or early adulthood, and the disorder exhibits a lifetime prevalence of 2-5%. Biological, psychological, and environmental factors contribute to its development. Differential diagnosis involves distinguishing panic disorder from other anxiety and medical conditions with overlapping symptoms. Cognitive-Behavioral Therapy, pharmacotherapy (especially with SSRIs), and lifestyle modifications are essential components of its comprehensive management.\n\n## Definition\n\n**ICD-11 Criteria:**\n\n- Recurrent, unexpected panic attacks.\n- At least one attack followed by a month of persistent concern.\n- Avoidance behaviors related to attacks.\n\n**DSM-V Criteria:**\n\n- Recurrent, unexpected panic attacks.\n- Persistent concern about future attacks.\n- Behavioral changes: Avoidance of situations associated with attacks.\n\r\n## Epidemiology \n\n- Prevalence of 1-2% in the general population.\n- 2-3 times more prevalent in females.\n- Bimodal incidence, peaking at ages 20 and 50.\n- Agoraphobia is concurrent in 30-50% of cases.\n- Increased risk of attempted suicide with comorbid depression, alcohol misuse, or substance misuse.\n\r\n## Clinical Features\n\n- Difficulties in breathing.\n- Chest discomfort.\n- Palpitations.\n- Hyperventilation, leading to tingling or numbness in the hands, feet, or around the mouth due to hypocalcemia resulting from increased blood pH and calcium binding to albumin. If extreme, carpopedal spasm (curling of fingers and toes) can occur.\n- Shaking, sweating, dizziness.\n- Depersonalization/derealization.\n- May result in fear of situations where panic attacks occur or lead to agoraphobia.\n- Development of a conditioned fear-of-fear pattern.\n\r\n## Differential Diagnosis \n\n- Other anxiety disorders, such as Generalized Anxiety Disorder (GAD) and agoraphobia.\n- Depression (takes precedence if it predates panic disorder or fulfills diagnostic criteria).\n- Alcohol or drug withdrawal.\n- Organic causes like cardiovascular or respiratory diseases, hypoglycemia, hyperthyroidism. Rarely, pheochromocytoma.\n\n\r\n## Management \n\n- Cognitive Behavioral Therapy (CBT) effective in 80-100% of cases and is the first-line treatment.\n\t- Initial education about the nature of panic attacks and fear-of-fear cycles.\n\t- Cognitive restructuring and detection of logical flaws.\n\t- Interoceptive exposure techniques such as controlled exposure to somatic symptoms (breathing in CO2 and physical exercise).\n\t- Treatment of secondary agoraphobic avoidance through situational exposure and anxiety management techniques.\n- Selective Serotonin Reuptake Inhibitors (SSRIs) are the first-line drug treatment (second-line to CBT).\n- Clomipramine, a tricyclic with a similar action on serotonin, is also effective, and propranolol can be used as needed for symptomatic management.\n\n# Phobias\n\nPhobias, encompassing specific phobia, social anxiety disorder (SAD), and agoraphobia, represent a cluster of anxiety disorders characterized by excessive and irrational fears. Specific phobia involves intense anxiety triggered by a specific object or situation, leading to avoidance behavior. Social anxiety disorder revolves around a marked fear of social scrutiny and performance situations, impeding daily functioning. Agoraphobia entails anxiety about situations where escape might be difficult or help unavailable. These conditions, distinct in their triggering stimuli, share common features of avoidance and significant impairment in daily life. Cognitive-Behavioral Therapy, exposure therapy, and pharmacotherapy, in alignment with NICE guidelines, form the cornerstone of their comprehensive management.\n\n\n## Definition\n\n **ICD-11 criteria:** \n- Restricted to highly specific situations such as proximity to particular animals, heights, thunder, flying, exposure to blood, etc.\n\r\n\r\n## Clinical Features\n\nGeneral features of phobias include:\n\n- Usually apparent in early adulthood.\n- Leads to avoidance behavior.\n- Phobias of blood and bodily injury can result in bradycardia and hypotension upon exposure.\n- Severity is dependent on the effect on quality of life (e.g., pilots afraid of flying).\n- Always rule out comorbid depression.\n\n\n\n## Specific Phobias\n\n### Agoraphobia\n\n- **ICD-11 criteria:** Fear of open spaces and associated factors like the presence of crowds or the perceived difficulty of immediate easy escape to a safe place, usually home (may occur with or without panic disorder).\n- Typically begins in 20s or mid-thirties.\n- Onset may be gradual or precipitated by a sudden panic attack.\n- Comorbid depression is common (beware of reliance on drugs and alcohol for coping).\n\n\r\n### Social Phobia/Social Anxiety Disorder (SAD)\n\n- Most common anxiety disorder.\n- **ICD-11 criteria:** Fear of scrutiny by others in relatively small groups (as opposed to crowds), resulting in the avoidance of social situations.\n- Relatively small groups generally consist of around 5-6 people (usually 1-2 is tolerable).\n- May be specific (public speaking) or generalized (any social setting).\n- Physical symptoms include blushing, fear of vomiting.\n- Symptoms include blushing (characteristic), palpitations, trembling, sweating.\n- Can be precipitated by stressful or humiliating experiences, parental death, separation, chronic stress.\n- Genetic predisposition is possible.\n- May lead to alcohol or drug abuse (perpetuating the problem).\n- Mental state examination: may appear relaxed as the phobic object or situation is not present.\r\n\r\n## Management \n\n- CBT is first-line management for all phobias:\n\t- Exposure techniques are the most widely used, aiming for systematic desensitization (using a graded hierarchy approach, for example).\n\t- Flooding (exposing someone with a fear of heights to a tower),\n\t- Modelling (individual observes therapist interacting with phobic stimulus).\n- If ineffective/severe functional impairment, SSRIs are first-line medical management. Propranolol can be used if somatic symptoms predominate.\n\n\r\n# NICE guidelines \n\n[NICE CKS - GAD](https://cks.nice.org.uk/topics/generalized-anxiety-disorder/)\n\r\n# References \n\n3. The British Psychological Society. (2011). Good Practice Guidelines on the use of psychological formulation.\n4. Royal College of Psychiatrists. (2011). Anxiety, panic and phobias.\n5. Mental Health Foundation. (2021). How to manage and reduce stress.\n6. UK Psychological Trauma Society (UKPTS). (2012). Post-traumatic stress disorder.\r\n",
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"explanation": "# Summary\n\n\n\n# Typical antipsychotics\n\n- Also known as 'first-generation' antipsychotics, these not only act as antagonists to D2 receptors but also on cholinergic, adrenergic and histaminergic receptors. The most commonly used medication in this class is **Haloperidol**, though other examples include Chlorpromazine and flupentixol. \n- Side effects can therefore be grouped according to receptor blockade (see below).\n\n### Dopamine D2 Receptor Blockade:\n\n1. **Extrapyramidal Symptoms (EPS):**\n - **Acute Dystonia:** Involuntary muscle contractions causing spasms.\n - **Akathisia:** Restlessness and an inability to sit still.\n - **Parkinsonism:** Tremors, rigidity, and bradykinesia (slowed movements).\n - **Tardive Dyskinesia:** Involuntary, repetitive movements, especially of the face.\n\n2. **Hyperprolactinemia:**\n - Elevated levels of prolactin, leading to:\n - Menstrual irregularities in women.\n - Gynecomastia (breast enlargement) in men.\n - Sexual dysfunction in both genders.\n\n### Other Receptors:\n\n1. **Histamine H1 Receptor Blockade:**\n - **Sedation:** Drowsiness and sleepiness.\n\n2. **Alpha-1 Adrenergic Receptor Blockade:**\n - **Orthostatic Hypotension:** A sudden drop in blood pressure upon standing, leading to dizziness or fainting.\n\n3. **Muscarinic Receptor Blockade:**\n - **Anticholinergic Effects:**\n - Dry mouth.\n - Constipation.\n - Blurred vision.\n - Urinary retention.\n\n\n# Atypical antipsychotics\n\n- Also known as 'second-generation' antipsychotics, these are D2, D3 and 5-HT2A antagonists, with less overspill into other receptors. \n- As effective as typical antipsychotics (even slightly better at negative symptoms), and have a more favourable side effect profile with reduced extrapyramidal effects, but increased metabolic side-effects. \n- They are 1st line for new-onset psychosis. Examples include risperidone, quetiapine, olanzapine, aripiprazole and clozapine (see below). \n\n### Dopamine Receptor Blockade:\n\n1. **D2 Receptor Blockade:**\n - **EPS (Extrapyramidal Symptoms):**\n - Atypicals generally have a lower risk of causing EPS compared to typicals.\n - Lower risk of tardive dyskinesia.\n\n### Serotonin Receptor Blockade:\n\n1. **5-HT2A Receptor Blockade:**\n - **Lower Risk of EPS:** Atypicals have a reduced risk of causing EPS due to serotonin receptor blockade.\n\n### Other Receptors:\n\n1. **Histamine H1 Receptor Blockade:**\n - **Sedation:** Although less common than with typicals, some atypicals can cause drowsiness.\n\n2. **Alpha-1 Adrenergic Receptor Blockade:**\n - **Orthostatic Hypotension:** Some atypicals may cause a drop in blood pressure upon standing.\n\n3. **Muscarinic Receptor Blockade:**\n - **Anticholinergic Effects:**\n - Generally less pronounced compared to typicals.\n - Mild dry mouth, constipation, or blurred vision.\n\n### Metabolic Effects:\n\n1. **Weight Gain:**\n - **Common Side Effect:** Atypical antipsychotics, in general, have a higher risk of causing weight gain compared to typicals.\n - **Varying Degrees:** The degree of weight gain can vary among different atypicals.\n\n2. **Dyslipidemia and Glucose Metabolism:**\n - **Increased Risk:** Some atypicals are associated with an increased risk of dyslipidemia and impaired glucose metabolism.\n\n3. **Prolactin Elevation:**\n - **Variable:** Some atypicals may elevate prolactin levels, leading to menstrual irregularities and sexual dysfunction.\n\n### Other side effects:\n\n1. **Seizures:**\n - **Low Risk:** Generally, atypicals have a lower risk of lowering the seizure threshold compared to typicals.\n\n2. **QT Prolongation:**\n - **Potential Risk:** Some atypicals may have a mild effect on the QT interval, but the clinical significance varies.\n\n3. **Increased risk of VTE and stroke in elderly**\n\n### Monitoring\n\n* Weight should be measured at the start of therapy, then weekly for the first 6 weeks, then at 12 weeks, at 1 year, and then yearly.\n* Fasting blood glucose, HbA1c, and blood lipid concentrations should be measured at baseline, at 12 weeks, at 1 year, and then yearly. \n* Prolactin concentrations should also be measured at baseline.\n* Before initiating antipsychotic drugs, an ECG may be required, particularly if there are cardiovascular risk factors (e.g. high blood pressure), if there is a personal history of cardiovascular disease, or if the patient is being admitted as an inpatient.\n* Blood pressure monitoring before starting therapy, at 12 weeks, at 1 year and then yearly during treatment and dose titration of antipsychotic drugs.\n\n# Clozapine\n\n- Clozapine is an atypical antipsychotic that is indicated if there is failure of treatment of 2 other antipsychotic medication, known as treatment-resistant schizophrenia.\n- Treats both positive and negative symptoms, slightly more effective than other antipsychotics.\n- Important side effects include: **agranulocytosis**, neutropenia, reduced seizure threshold, myocarditis, slurred speech (due to hypersalivation), constipation (most common cause of mortality when related to clozapine use).\n\n### Monitoring\n\n- Due to its unique and potentially serious side effect profile, monitoring while on clozapine is very important.\n- Patients should have weekly FBC (to look at white cell counts) for the first 18 weeks of treatment then fortnightly for up to one year, and then monthly.\n- Blood lipids and weight should be measured at baseline, every 3 months for the first year, and then yearly.\n- Fasting blood glucose should be tested at baseline, after one months’ treatment, then every 4–6 months.\n\n\n# Neuroleptic Malignant Syndrome\n\nNeuroleptic Malignant Syndrome (NMS) is a rare, but potentially life-threatening, idiosyncratic reaction to antipsychotic medications, particularly those that block dopamine receptors. It typically occurs as a response to the introduction or an increase in the dosage of neuroleptic medications.\n\n### Clinical Features\n\n1. **Hyperthermia:**\n - Profound elevation of body temperature is a hallmark feature.\n \n2. **Altered Mental Status:**\n - Fluctuating levels of consciousness, ranging from confusion to catatonia.\n\n3. **Autonomic Dysregulation:**\n - Dysautonomia characterized by fluctuations in blood pressure, tachycardia, and diaphoresis.\n\n4. **Rigidity:**\n - Generalized muscle stiffness, often described as \"lead-pipe\" rigidity.\n\n### Differential Diagnosis\n\n- **Malignant Hyperthermia** - a rare, genetic condition triggered by certain medications, often during anaesthesia.\n\n- **Serotonin Syndrome** similar to NMS but associated with serotoninergic medications. Presents with hyperthermia, autonomic dysregulation, and altered mental status.\n\n### Investigations \n\n- Bloods:\n\t- FBC - Monitoring for potential leukocytosis or signs of infection.\n - **Creatine Kinase (CK) Levels:** Markedly elevated CK levels are often observed due to muscle breakdown.\n - Renal and Liver Function Tests: monitoring organ function due to the potential systemic effects.\n \n### Management\n\n1. **Discontinuation of Causative Agent:**\n - Immediate cessation of the implicated neuroleptic medication.\n\n2. **Supportive Care:**\n - Aggressive cooling measures to address hyperthermia, including cooling blankets and IV fluids to prevent renal failure.\n\n3. **Benzodiazepines:**\n - Administering benzodiazepines to manage agitation and muscle rigidity.\n\n4. **Dantrolene:**\n - Consideration of dantrolene, a skeletal muscle relaxant, in severe cases.\n\n5. **Intensive Monitoring:**\n - Continuous monitoring of vital signs, fluid balance, and laboratory parameters.",
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"question": "An 80-year-old gentleman with a background of mixed dementia is admitted to the care of the elderly ward with a urinary tract infection. He has challenging behaviour on the ward, being aggressive to nursing staff and refusing to take his medications. Collateral history from his family reveals that he has also displayed such behaviour at home.\n\nHe is diagnosed as having behavioural and psychological symptoms of dementia and is started on quetiapine.\n\nWhich is the following potential side effects is he at increased risk of with this new medication?",
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"explanation": "This would not be appropriate in a patient with chronic kidney disease as it may worsen renal function. Creatinine clearance should be calculated first. Proton pump inhibitor therapy should also be considered if initiating treatment with non-steroidal anti-inflammatory drugs",
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"explanation": "This would be a second-line agent for urate lowering therapy if allopurinol is contraindicated, not tolerated or unable to achieve target serum uric acid",
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"explanation": "This patient likely has an acute attack of crystal arthropathy. Septic arthritis should be ruled out, especially in a diabetic patient who may be immunocompromised. Joint aspiration should be considered for diagnosis. Colchicine would be suitable in a patient with chronic kidney disease, and renal adjustment considered if eGFR 10-50, below which it would be contraindicated",
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"comment": "As this patient has a high temperature, wouldn't you be concerned about septic arthritis?",
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"comment": "Surely this question should be about next step in management i.e. performing joint aspiration to rule out septic arthritis rather than going straight to gout treatment?",
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"comment": "Why is the WCC raised\n",
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"comment": "crystals are DAMPS -> activates innate immune response",
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"explanation": "# Summary\n\nGout is a type of arthritis caused by the accumulation of monosodium urate crystals in and around the joints. It presents acutely with rapid onset of severe pain, swelling and redness of affected joints, with the first metatarsophalangeal joints the most commonly affected. Chronic untreated gout may lead to tophi which are hard nodules made up of monosodium urate crystals that deposit in soft tissues. Gout may be diagnosed clinically, with supportive investigations including a serum urate and synovial fluid analysis looking for monosodium urate crystals. Management of acute gout is with NSAIDs, colchicine or a short course of oral steroids. Urate-lowering therapy with allopurinol or febuxostat should be considered to reduce the risk of further gout flares. \n\n# Definition\n\nGout is a form of arthritis that occurs when monosodium urate crystals deposit in joints. This causes both acute inflammation (gout flares) and in the longer-term, a chronic gouty arthritis with tophi (hard deposits of monosodium urate crystals in soft tissues).\n\n# Epidemiology\n\n- Gout is the most common inflammatory arthritis and prevalence is increasing with time (currently 2.5%)\n- Hyperuricaemia (high urate) is the main risk factor (although most patients with a high urate do not develop gout, and some patients develop gout with a normal urate)\n- Factors that contribute to this include:\n- Older age - typically patients are above the age of 40\n- Male sex (post-menopausal women are also at increased risk)\n- Comorbidities including chronic kidney disease (CKD), diabetes, osteoarthritis, hypertension\n- Excess alcohol consumption\n- Dietary excess of meat, seafood and sugary drinks\n- Overweight or obesity\n- Medications such as thiazide diuretics and ciclosporin\n- Family history of hyperuricaemia and gout\n- Genetic disorders associated with hyperuricaemia such as Lesch-Nyhan or glycogen storage disorders\n- Organ transplant recipients\n- Acute attacks may be triggered by stressors including:\n- Trauma and surgery\n- Intercurrent illness\n- Alcohol excess\n- Sudden excess of protein in the diet\n- Chemotherapy (due to cell breakdown)\n- Urate-lowering medications can cause a flare (as crystals are shed into the joint space)\n\n# Signs and Symptoms\n\nOverlapping clinical syndromes are caused by the deposition of monosodium urate crystals in different tissues:\n\n**Acute gout** \n\n- Commonly presents with a monoarthritis\n- Pain is severe and rapid in onset, reaching a peak within 24 hours \n- Affected joints become swollen, erythematous and tender\n- The first metatarsophalangeal (MTP) joint is the most commonly affected (70% of first attacks)\n- Other common sites include the knees, ankles, midtarsal joints, wrists, elbows and small joints of the hands\n- Systemic features such as fever and malaise may be seen\n- Patients may be tachycardic due to pain\n\n**Tophaceous gout**\n\n- Patients will usually have a history of longstanding recurrent acute gout\n- However in atypical cases patients may present with tophi without previous flares\n- Tophi are firm white nodules of sodium monosulphate crystals under the skin\n- They commonly occur on extensor surfaces of joints such as knees or elbows, the Achilles tendons, backs of hands and feet and on the helices of the ears\n- Usually they are painless however they can become infected, inflamed or ulcerated\n- They may discharge white material onto the skin surface\n- Chronic gouty arthritis may present with tender and stiff joints with reduced range of motion\n\n# Differential Diagnosis\n\n- **Septic arthritis** must be ruled out in patients who are systemically unwell with an acute monoarthritis - urgent synovial fluid analysis is needed if this is suspected\n- **Pseudogout** typically affects the knee and wrists rather than the MTP joint; synovial fluid analysis shows calcium pyrophosphate crystals\n- **Cellulitis** causes erythema, pain and swelling of the skin rather than the joint - patients may be systemically unwell\n- **Trauma** should be asked about in the history as this may cause similar symptoms of pain, difficulty mobilising and swelling\n- **Other inflammatory arthritides** such as rheumatoid arthritis may mimic chronic gouty arthritis\n\n# Investigations\n\n**Bedside tests:**\n\n- **Joint aspiration** is the gold standard diagnostic investigation \n- Needle-shaped monosodium urate crystals with negative birefringence are seen in gout\n- Synovial fluid should also be sent for gram stain and culture to rule out septic arthritis\n- Tophi can be biopsied to look for these crystals\n\n**Blood tests:**\n\n- **Serum uric acid** should be measured in all patients with suspected gout\n- A serum urate of 360 micromol/L or more confirms the diagnosis\n- Levels may be falsely low in an acute attack and so should be repeated 2-4 weeks after the flare has resolved\n- Levels are used to guide urate-lowering therapy if this is initiated as prophylaxis\n- **Screening for risk factors** should be considered:\n- Fasting glucose or HbA1c for diabetes\n- Renal function and urine albumin:creatinine ratio for CKD\n- Lipids for hypercholesterolaemia\n- **Inflammatory markers** with FBC and CRP should be checked if septic arthritis is suspected\n- **Liver function tests** are needed prior to starting febuxostat\n- Patients from Han Chinese, Thai and Korean backgrounds should be screened for **HLA-B5801** prior to starting allopurinol (as this increases the risk of severe cutaneous adverse reactions if present)\n\n**Imaging tests:**\n\n- These may be useful to assess chronic disease or where the diagnosis of acute gout is uncertain\n- X-rays in chronic disease show punched-out periarticular erosions, areas of sclerosis and tophi\n- Ultrasound may show joint effusions, tophi, synovial thickening and erosions\n\n# Management \n\n**Acute gout flares** \n\nThere are three first-line options for treatment of a gout flare:\n\n- NSAIDs e.g. naproxen\n- Give at maximum dose\n- Continue until 1-2 days after resolution of symptoms\n- Consider giving with a PPI for gastric protection\n- Avoid in heart failure, patients at high risk of gastrointestinal bleeding and severe renal failure\n- Colchicine\n- Dosing is 500 mcg 2-4 times per day\n- Continue until pain resolves\n- Dose-dependent side effects include diarrhoea, nausea and vomiting\n- Oral corticosteroids\n- e.g. prednisolone 30mg once a day for 3-5 days\n- Useful in patients with contraindications to both NSAIDs and colchicine\n- An injection of intramuscular, intravenous or intra-articular steroids can also be considered\n- Alongside this, consider other analgesia (e.g. paracetamol) and other non-pharmacological pain relief such as ice packs\n- A combination of the above may be tried if a single agent is ineffective\n- Patients should be advised to keep the affected joint cool and exposed and to rest and elevate the affected limb\n- Patients already on urate lowering treatment should continue this throughout the acute flare\n\n## Prevention\n\nPatients should be followed up 4-6 weeks after an acute episode of gout to think about preventative strategies and assess for risk factors (also see Investigations). \n\nOptimisation of risk factors may include:\n\n- Reducing alcohol consumption\n- Maintaining a balanced diet and healthy weight\n- Investigate and treat for comorbidities such as hypertension or CKD\n- Review medications and consider switching medications such as thiazides that cause hyperuricaemia\n- Where possible, switch antihypertensive medications to losartan or amlodipine, which have modest urate-lowering effects \n- Initiating urate-lowering therapy (see below)\n\nMost patients can be managed in primary care, however the following should prompt referral to or discussion with specialist services:\n\n- Patients with complications of gout\n- Atypical presentations (e.g. aged under 30) or uncertain diagnosis\n- Pregnant patients\n- Stage 3b to 5 CKD\n- Organ transplant recipients\n- Those at risk of adverse effects with standard medical treatment, or if treatment is ineffective or not tolerated\n\nIndications for **urate-lowering therapy** include:\n\n- Multiple or troublesome gout flares\n- Chronic gouty arthritis or tophi\n- Patients taking diuretics\n- CKD stage 3 to 5\n\n**Starting and monitoring urate-lowering therapy (ULT):**\n\n- ULT should be started at least 2-4 weeks after an acute flare if possible as medications can precipitate further attacks\n- Colchicine should be given whilst starting ULT to reduce the risk of a flare (NSAIDs or steroids are second-line)\n- Doses should be uptitrated with monthly monitoring of serum urate levels, aiming for a target of 360 micromol/L\n- A target urate level of 300 micromol/L may be helpful in patients with tophi or chronic arthritis due to gout, or those who continue to have flares despite ULT\n- First-line options are either allopurinol or febuxostat which are both xanthine oxidase inhibitors (so reduce uric acid production)\n- Allopurinol is preferred in patients with significant cardiovascular disease\n- Second line options include uricosuric medications (e.g. probenecid) - these can promote stone formation so should be avoided if there is nephrolithiasis\n\n# Complications\n\n- Chronic gouty arthritis and permanent joint damage\n- Tophi, which may become inflamed or infected\n- Nephrolithiasis due to uric acid precipitation - these are responsible for 8% of renal calculi and are radiolucent\n- Chronic urate nephropathy - urate deposition in the renal interstitium causes inflammation and fibrosis\n- Both allopurinol and febuxostat can cause rashes, which in rare cases may be severe (e.g. Stevens Johnson syndrome or toxic epidermal necrolysis)\n- Increased risk of cardiovascular disease and mortality\n\n# NICE Guidelines\n\n[NICE CKS - Gout](https://cks.nice.org.uk/topics/gout/)\n\n[NICE - Gout: diagnosis and management](https://www.nice.org.uk/guidance/ng219/)\n\n# References\n\n[Patient UK - Gout](https://patient.info/doctor/gout-pro)\n\n[Radiopaedia - Gout](https://radiopaedia.org/articles/gout?lang=gb)",
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"question": "A 70-year-old man is admitted with sudden onset right ankle pain and swelling for 1 day, the third episode this year. His medical history includes type 2 diabetes and chronic kidney disease, likely from diabetic nephropathy.\n\n\nOn examination, his right ankle is erythematous, warm, and tender, with full range of movement.\n\n\n\n\nObservations: Temperature 38.1°C, pulse 90, BP 110/70, respiratory rate 18, SpO<sub>2</sub> 100% on room air\n\n\n\nInitial blood tests are as follows:\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|142 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|16.1x10<sup>9</sup>/L|3.0 - 10.0|\n|Neutrophils|5.5x10<sup>9</sup>/L|2.0 - 7.5|\n|Platelets|210x10<sup>9</sup>/L|150 - 400|\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|151 µmol/L|60 - 120|\n|eGFR|60 mL/min/1.73m<sup>2</sup>|> 60|\n\n\n\n\n\nX-ray of the right ankle showed no acute fractures or bony erosions.\n\n\n\nWhich of the following is the next most appropriate treatment?",
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"explanation": "This would appear as Gram-positive diplococci in clusters. This is seen as purple staining cocci that appear similar to \"bunches of grapes\". S. aureus is a common cause of septic arthritis in otherwise healthy adults and may be associated with prosthetic joint infections",
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"explanation": "# Summary\n\nSeptic arthritis is an infection of the joint characterized by acute inflammation and swelling. It is caused by a bacterial or viral pathogen that infects the synovial fluid. The most commonly implicated organism is Staphylococcus aureus. Noteworthy clinical signs include a tender, swollen joint with reduced mobility, often accompanied by systemic illness. Key investigations include joint aspiration for Microscopy Culture and Sensitivity, along with blood tests showing increased white blood cell count and elevated ESR/CRP. Management typically involves IV antibiotics, joint washout under general anaesthesia, and physiotherapy once the acute infection has resolved.\n\n# Definition\n\nSeptic arthritis is an infection of the joint, specifically the synovial fluid. It is typically caused by a bacterial or viral pathogen and necessitates prompt medical intervention due to the high risk of joint damage and other severe complications.\n\n# Epidemiology\n\nSeptic arthritis has an annual incidence of 4-10 cases per 100,000 patients in Western Europe. It can affect individuals of any age, though certain populations are at a higher risk due to underlying conditions.\n\n# Aetiology\n\nThe most prevalent organism implicated in septic arthritis is Staphylococcus aureus. Other responsible organisms include:\n\n- Gonococcus: primarily in sexually active individuals\n- Streptococcus spp.\n- Gram-negative bacilli\n\nRisk factors contributing to septic arthritis include:\n\n- Pre-existing joint diseases such as rheumatoid arthritis\n- Chronic kidney disease\n- Immunosuppressive states\n- Presence of prosthetic joints\n\n# Signs and Symptoms\n\nThe clinical presentation of septic arthritis usually involves:\n\n- Acute onset of tender, swollen joint\n- Reduced range of joint movement\n- Systemic symptoms such as fever, malaise, or chills\n\n# Differential Diagnosis\n\nDifferential diagnoses for septic arthritis include:\n\n- Gout and pseudogout: characterized by intense joint pain, redness, and swelling, often in the big toe or knee.\n- Osteoarthritis: presents with joint pain, stiffness, and sometimes swelling, generally improving with movement.\n- Rheumatoid arthritis: marked by joint pain, swelling, and stiffness, often symmetrical and worse after rest.\n- Lyme disease: may show erythema migrans rash, flu-like symptoms, and possibly migratory joint pains.\n\n# Investigations\n\nDiagnostic investigations for septic arthritis include:\n\n- Joint aspiration for Microscopy, Culture, and Sensitivity: The aspirate usually appears turbid and yellow, resembling pus.\n- Blood tests: elevated white cell count, high ESR/CRP\n- Blood cultures: to identify causative organisms\n- Imaging: X-ray of the joint may be performed to evaluate for osteomyelitis or other complications.\n\n# Management\n\nThe treatment of septic arthritis involves:\n\n- IV antibiotics guided by local antibiograms and susceptibilities\n- Consideration of joint washout under general anaesthesia to remove infected material\n- Physiotherapy following the resolution of acute infection to restore joint function\n\nComplications of septic arthritis can include:\n\n- Osteomyelitis: infection of the bone\n- Chronic arthritis: persistent joint inflammation\n- Ankylosis: joint fusion resulting in immobility\n\n# References\n\n[Click here for the BNF Treatment Summary for Musculoskeletal infections](https://bnf.nice.org.uk/treatment-summary/musculoskeletal-system-infections-antibacterial-therapy.html)\n\n[Click here for the BMJ Best Practice Summary of Septic Arthritis](https://bestpractice.bmj.com/topics/en-us/486)",
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"question": "A 40 year old gentleman is admitted to the acute medical unit with a 1 day history of sudden onset right ankle pain and swelling. He has no other past medical history.\n\n\n\nOn examination, his right ankle is erythematous, warm and tender on palpation. There is limited active and passive range of movement in the ankle joint due to pain.\n\n\n\nObservations:\n\n\n\n - Temperature 38.5°C\n - pulse 90\n - BP 110/70\n - respiratory rate 18\n - SpO<sub>2</sub> 100% on room air\n\n\n\nInitial blood tests are as follows:\n\n\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|142 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|16.1x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|210x10<sup>9</sup>/L|150 - 400|\n|Neutrophils|13x10<sup>9</sup>/L|2.0 - 7.5|\n\n\n\nJoint aspiration is done which shows a cloudy yellow fluid with a predominance of neutrophils. The following is seen on Gram stain:\n\n\n\n [lightgallery]\n\n\n\nWhich is the most likely causative organism?",
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"explanation": "This is classically found in ankylosing spondylitis, which may present with neck or back pain with morning stiffness that improves on exercise. However, this is more likely associated with anterior uveitis, which would cause painful visual loss",
"id": "32220",
"label": "c",
"name": "Inflammation of the sacroiliac joints",
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"explanation": "This is highly specific for rheumatoid arthritis (RA), which is an inflammatory arthritis that may also present with pain and morning stiffness in joints. However, RA is more likely to have peripheral joint involvement, as opposed to axial involvement in polymyalgia rheumatica",
"id": "32222",
"label": "e",
"name": "Anticyclic citrullinated peptide (anti-CCP) antibody positivity",
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"explanation": "This may be found in transient ischaemic attack (TIA) due to carotid thromboembolism, which may result in transient monocular visual loss or amaurosis fugax. A TIA would not explain the frontal headache and joint stiffness",
"id": "32219",
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"explanation": "This patient has giant cell arteritis and polymyalgia rheumatica, which are closely associated. Raised ESR is a characteristic finding. Sudden onset vision loss is a red flag and requires urgent steroid treatment to avoid permanent vision loss",
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"name": "Raised erythrocyte sedimentation rate (ESR)",
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"explanation": "Headache may be a symptom of raised intracranial pressure. This may occur due to a wide range of aetiologies, including intracranial haemorrhage, neoplasm, stroke, infections, hydrocephalus. However, the patient does not have any neurological abnormalities so this would be less likely. Idiopathic intracranial hypertension may present with headache and vision loss but this is less likely to be unilateral",
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"explanation": "# Summary\n\nGiant cell arteritis (GCA) is a form of vasculitis which affects medium and large arteries. It classically affects the branches of the external carotid artery and the ophthalmic artery, which is often referred to as temporal arteritis. Key signs and symptoms include a temporal headache, jaw claudication, amaurosis fugax, thickening and tenderness of the temporal artery, and scalp tenderness. Systemic symptoms and features of polymyalgia rheumatica are common. The diagnosis is clinical in the first instance, and patients with visual symptoms should be treated immediately with high-dose steroids, however supportive investigations include full blood count, CRP and ESR. Confirmation of the diagnosis is with vascular ultrasound and temporal artery biopsy. Management is with high-dose steroids, with steroid sparing agents considered in patients who relapse when steroids are weaned.\n\n# Definition\n\nGiant cell arteritis (GCA) is a large vessel vasculitis which commonly affects the extracranial external carotid artery branches. Involvement of other vessels may occur, with patients presenting atypically with systemic symptoms and aortic involvement rather than temporal arteritis.\n\n# Epidemiology\n\n- GCA is the most common primary vasculitis \n- Age is an important risk factor - GCA is rare in the under 50s, with cases peaking in those aged 70-79\n- Women are 2-3x more likely to be affected than men\n- Northern European descent is also a risk factor\n\n# Signs and Symptoms\n\n**Symptoms include:**\n\n- Headache - usually temporal but may be generalised, occipital or parietal; present in 2/3 of people with GCA\n- Jaw or tongue claudication (pain on chewing food)\n- Amaurosis fugax (transient monocular blindness, often described as a dark curtain descending vertically)\n- Diplopia\n- Changes to colour vision\n- Fatigue\n- Anorexia and weight loss\n- Depression\n- Features of polymyalgia rheumatica e.g. pain and stiffness of shoulders and pelvic girdle\n\n**Signs include:**\n\n- Tenderness, thickening or nodularity of the temporal artery\n- Pulsation of the temporal artery may be reduced or absent\n- Scalp tenderness or necrosis\n- Visual field defect\n- Low-grade fever\n- On fundoscopy: pallor and oedema of the optic disc, \"cotton-wool\" patches and retinal haemorrhages\n- Involvement of extracranial vessels may be associated with arterial bruits, difference in blood pressure between arms and decreased arterial pulses\n\n# Differential Diagnosis\n\n- **Other causes of headaches** e.g. tension headaches, migraines - lack associated features e.g. jaw claudication, less likely to be new in an older patient\n- **Acute angle closure glaucoma** leads to visual loss and headaches, eye will be painful and red and feel hard on palpation\n- **Shingles** leads to pain and systemic features may be present, however a rash typically appears over the affected area within a few days\n- **Transient ischaemic attack** can cause amaurosis fugax, other features such as headache are not usually present\n\n\n# Investigations\n\n**Bedside tests:**\n\n- Urgent ophthalmological assessment for patients with visual symptoms \n\n**Blood tests:**\n\n- **ESR** and **CRP** - raised in GCA\n- **Full blood count** often shows an elevated platelet count and a normochromic normocytic anaemia\n- Baseline bloods for liver and renal function (**LFTs** and **U&Es**) and a **bone profile** for calcium should be considered to screen for alternative diagnoses e.g. other vasculitides\n- Bloods to screen for increased risk of complications with steroids (such as diabetes or osteoporosis) include an **HbA1c**, **vitamin D** and **thyroid function tests** \n\n**Imaging tests:**\n\n- **Doppler ultrasonography** of the temporal and axillary arteries can be used as a confirmatory diagnostic test\n- **Halo sign** refers to hypoechoic wall thickening of the artery imaged\n- This disappears with steroid treatment\n- Stenosis of the vessel may also be visualised\n- **MRI brain** with vessel wall imaging is an alternative\n- GCA is supported by findings of mural inflammation in the superficial temporal arteries\n- MRI can also be used to look for complications such as ischaemic stroke as well as involvement of other arteries\n- **FDG-PET scanning** can be useful to rule out differential such as malignancy or infection\n- In GCA there will be uptake in affected arteries\n- It can be particularly useful to demonstrate involvement of other arteries e.g. the aorta\n- A **DEXA** scan for baseline bone density should be done for patients starting long-term steroids (due to the risk of osteoporosis)\n\n**Invasive tests:**\n\n- **Temporal artery biopsy**\n- This is the definitive investigation for GCA\n- Typical histological features include granulomatous inflammation of arteries with inflammatory cells including multinucleated giant cells\n- Inflammation is often segmental with \"skip lesions\" i.e. normal parts of the artery in between areas of inflammation, and so false negative biopsies can occur\n- Biopsies may remain positive for several weeks after starting steroids\n\n# Management\n\n- Patients with visual loss usually require **IV steroid treatment** e.g. pulsed methylprednisolone\n- All other patients should be treated with **high dose oral steroids**, usually 40-60 mg prednisolone once a day\n- **Safety netting** patients to seek urgent medical attention if they develop visual symptoms or a relapse on steroids is key\n- Patients seen in primary care should be **referred urgently to rheumatology** for confirmation of the diagnosis and ongoing management\n- **Steroids are tapered** gradually once symptoms and raised inflammatory markers have resolved\n- **Steroid sparing agents** such as methotrexate or tocilizumab (an anti-IL6 biologic) may be added to help with steroid tapering e.g. in patients with recurrent relapses or at increased risk of side effects with steroids\n- All patients should be assessed for risk of steroid side effects:\n- Consider gastric protection with a proton pump inhibitor\n- Consider bone protection e.g. vitamin D and calcium supplementation, bisphosphonates\n- Monitor for steroid-induced diabetes, hypertension and glaucoma\n- Advise on immunosuppression e.g. avoiding contact with patients with diseases such as chickenpox if not immune\n- Give patients a blue steroid card and advise them not to suddenly stop steroids due to the risk of adrenal crisis\n- Aspirin is currently **not** recommended for adjunctive treatment of GCA \n\n# Complications\n\n- Loss of vision - may occur in up to 30% of people with GCA (either total or partial)\n- Scalp necrosis\n- Ischaemic stroke\n- Aortic aneurysms - in 10-20% of people with GCA, most commonly in the thoracic aorta\n- Aortic dissection and aortic regurgitation are less common than aneurysms\n- Stenosis of large arteries\n- Increased risk of cardiovascular disease including stroke, myocardial infarction and peripheral arterial disease\n- Side-effects from long-term steroids e.g. osteoporosis and fragility fracture, weight gain, diabetes, gastric ulcers\n\n# Prognosis\n\n- Most patients respond rapidly to steroids - failure to respond should prompt investigations for an alternative diagnosis\n- Up to 50% of people will experience relapsing disease however\n- Most patients require at least 1-2 years of steroid treatment, with an increased risk of relapse if steroids are stopped within a year of diagnosis\n\n# NICE Guidelines\n\n[NICE CKS - Giant Cell Arteritis](https://cks.nice.org.uk/topics/giant-cell-arteritis/)\n\n# References\n\n[British Society for Rheumatology guideline on diagnosis and treatment of giant cell arteritis](https://academic.oup.com/rheumatology/article/59/3/e1/5714024)\n\n[Radiopaedia - Giant Cell Arteritis](https://radiopaedia.org/articles/giant-cell-arteritis?lang=gb)\n\n[Patient UK - Giant Cell Arteritis](https://patient.info/doctor/giant-cell-arteritis-pro)",
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"question": "A 50 year old woman presents with an episode of sudden painless visual loss in her right eye this morning. She also complains of a 2 week history of persistent frontal headache and morning stiffness of the shoulders and hips worse in the past year.\n\nPhysical examination is otherwise unremarkable.\n\nComputed tomography (CT) brain showed no acute intracranial abnormalities.\n\nWhich of the following findings is most likely associated with her condition?",
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"explanation": "This breakthrough dose would be too high for his current pain requirements. The conversion ratio from oral to subcutaneous morphine is 2:1",
"id": "32250",
"label": "c",
"name": "10mg hourly as required",
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"explanation": "Both the regular and breakthrough doses of oral morphine should be added together to obtain the total daily dose of oral morphine required. Furthermore, a shorter dosing interval between breakthrough doses would be required to allow for adequate pain relief",
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"label": "d",
"name": "5mg 6-8 hourly",
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"explanation": "A shorter dosing interval between breakthrough doses would be required to allow for adequate pain relief",
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"name": "2mg 6-8 hourly",
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"explanation": "Both the regular and breakthrough doses of oral morphine should be added together to obtain the total daily dose of oral morphine required",
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"explanation": "Syringe drivers are given as continuous subcutaneous infusions over 24 hours. The oral morphine dose needs to be halved for subcutaneous (SC) administration via the syringe driver. The total daily oral morphine dose is (10mg x 3) + (2mg x 3) = 36mg. This would be SC morphine 18mg. As breakthrough doses should be one-sixth to one-tenth of the total daily dose, you should therefore prescribe him 2-3mg every hourly as required. The lower limit of the dose range may be prescribed to avoid concerns of toxicity. If more than 6 doses are required in 24 hours, consider seeking senior advice or review",
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"comment": "1/6 of 36 = 6?",
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"comment": "that would be 24 hr ORAL dose, you need to halve it for SC dose ",
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"comment": "1/6 of 18 is 3??",
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"comment": "which would be the max with possible concerns for toxicity its 1/10 TO 1/6 (eg. 1.8-3), take lower dose to start",
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"comment": "Why is the patient only on 2mg of oral morphine for breakthrough at the start? Shouldn't the patient's breakthrough dose be between 3.6 - 6mg? I think it's a little confusing that after conversion from oral to SC, the breakthrough dose remained at 2mg",
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"comment": "1/6 of 18 after conversion to subcut = 3 so highest you should give is 3 hourly > process of elimination",
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"explanation": "# Summary\n\nMedications in end-of-life care focus on alleviating distressing symptoms in patients nearing death. A holistic approach is vital, considering physical, emotional, and social aspects of symptoms, often involving a multidisciplinary team. For pain management, the WHO pain ladder guides pharmacological strategies, with morphine as the primary strong opioid. Specific treatments for other symptoms depend on the underlying cause and it is important to consider reversible causes and non-pharmacological measures.\n\n\n\n# Definition\n\nMedications used in end of life care aim to relieve distressing symptoms which may appear in the last days, weeks, or months of life. They are commonly prescribed as 'anticipatory' or 'just in case' medications for a patient known to be nearing the end of life.\n\n\nThey can be administered:\n\n\n- Orally - if the patient is safely able to swallow\n- Subcutaneously - via single dose or continuous syringe pump\n- Transdermally - especially for stable symptoms and if available\n- Intramuscularly - less common\n- Intravenously - less common, but may be helpful if a patient already has access\n\n## A note on holistic care\n\nIn palliative care, and in medicine, it is important to consider all symptoms in context. There are many different aspects to symptoms. These include the physical cause, the patient's beliefs about their illness and symptoms, social contributors and impacts, their emotional and behavioural responses. Holistic assessment and management are crucial, which is why the multidisciplinary team is so important. \n\nFor example, a patient may have been prescribed very effective analgesia but is unable to administer medicines themselves. They may also have a very strong emotional response to pain or believe that they deserve their symptoms. They may benefit from a package of care or financial support for terminal illness which a social worker could help with, or an occupational therapist to help with activities of daily living. Counselling may give the patient a space to explore their feelings around their symptoms and their illness, while spiritual support could alleviate some existential distress. These additional interventions work alongside pharmacological therapy to optimise a person's quality of life through their illness.\n\nThis chapter focuses on medications for symptoms towards the end of life, but it is crucial to remember that each patient has a different combination of needs which requires an individual assessment and management plan, often with input from a range of health and social care professionals.\n\n# Pain\n\n\nInitial pharmacological management of pain should follow the WHO pain ladder. Once patients have reached the top of this ladder (requiring regular strong opioids), careful optimisation is necessary to ensure the right level of pain relief while minimising side effects.\n\n- Morphine is the first-line strong opioid analgesic. This can be given as a modified release or immediate release form. \n- Generally, patients would have a regular 'background' dose based on their 24-hour requirements, plus a PRN dose available for **breakthrough pain.** PRN doses are usually 1/6-1/10 of the 24 hour dose. Analgesia requirements should be reviewed regularly, for example every 24 hours.\n- Alternatives to morphine may be necessary for patients with poor renal function. These include oxycodone, alfentanyl or buprenorphine.\n- When prescribing opioid analgesia consider co-prescribing a regular laxative and an as-required anti-emetic. Monitor for signs of opioid toxicity (respiratory depression, sedation, myoclonus) and switch to alternatives or dose reduce as necessary.\n\nWhen switching analgesia, it is helpful to convert the dose first to oral morphine before converting to the desired medication. Please note that different routes also have different equivalent doses, so it is always safest to check guidelines.\n\n\nThe following table shows dose equivalents of 10mg oral morphine\n\n\n| Analgesic/Route | Dose | Conversion Factor |\n| ----------------------------- | ------- | ----------------- |\n| Codeine/tramadol/dihydrocodeine oral | 100mg | x10 |\n| Diamorphine IM/IV/Subcut | 3mg | x3.3 |\n| Morphine IM/IV/Subcut | 5mg | x2 |\n| Oxycodone oral\\* | 5mg\\* | x2\\* |\n| Oxycodone Subcut\\* | 2.5mg\\* | x4\\* |\n| Alfentanil Subcut | 0.3mg | x30 |\n\n\n*NB - oral oxycodone potency is between 1.3-2x that of oral morphine. Different trusts will adopt different guidance on which you should use. If in doubt, always opt for the lower dose and titrate up.\n\n\n# Breathlessness\n\nConsider non-pharmacological measures for breathlessness first. For example, sitting the patient up, opening a window or setting up a fan can all help.\n\nPharmacological management may involve low-dose opioids, benzodiazepines or therapeutic oxygen, and should be tailored to the patient.\n\n\n# Nausea and vomiting\n\nIt is important to consider the likely cause of nausea and vomiting, as medications target different parts of the vomiting pathway. Perform a full assessment to determine the likely cause of the nausea and vomiting. Consider parenteral routes of administration - patients may have severe gastrointestinal disturbance or at least may not be able to keep down oral antiemetics long enough to be effective.\n\nThe following table shows the primary site of activity and side effects of commonly used antiemetics:\n\n| Antiemetic | Receptor activity | Side effects & cautions | Useful for |\n|---|---|---|---|\n| Metoclopramide | Dopamine antagonist | Extrapyramidal symptoms, drowsiness, restlessness, diarrhoea. Do not give with antimuscarinics or in mechanical bowel obstruction | Gastric stasis, functional bowel obstruction |\n| Cyclizine | Histamine, acetylcholine antagonist | Drowsiness, antimuscarinic | Raised intracranial pressure, vestibular dysfunction |\n| Hyoscine | Acetylcholine antagonist | Antimuscarinic | Motion sickness |\n| Haloperidol | Dopamine antagonist | Less common in palliative care doses | Chemical |\n| Levomepromazine | Dopamine, histamine, acetylcholine, 5HT2 antagonist | Sedation, postural hypotension, antimuscarinic |Broad range |\n| Ondansetron | 5HT3 antagonist | Constipation, arrhythmias, movement disorder | Cytotoxic-related |\n\n- For chemically-mediated symptoms (for example medications, metabolic derangemenet), aim to treat the underlying cause. Antiemetics that may be helpful include haloperidol, metoclopramide or levomepromazine.\n- For nausea and vomiting due to raised intracranial pressure, cyclizine is usually used first-line. Dexamethasone or radiotherapy may be helpful to reduce the pressure-associated symptoms.\n- For patients with vestibular disturbance (for example symptoms associated with movement), cyclizine usually used first-line. Alternatives include hyoscine hydrobromide.\n- For patients with bowel obstruction, seek specialist advice. If due to peristaltic failure, review medications and consider starting metoclopramide (providing there is no colic). Likewise for gastric stasis, consider metoclopramide. For patients with mechanical obstruction and/or colic, do not give metoclopramide. Exclude constipation, give cyclizine for nausea and treat colic with hyoscine butylbromide.\n- If nausea and vomiting is due to compression from an abdominal or pelvic tumour, cyclizine should be used first-line.\n- For anxiety-related nausea and vomiting, begin with non-pharmacological measures for anxiety, such as CBT. A benzodiazepine or levomepromazine would be first-line pharmacological options.\n\n# Agitation\n\nAs with other symptoms, aim to manage reversible causes of agitation and possible delirium first. Consider non-pharmacological measures such as environmental modification. For patients in their last days of life, haloperidol or low-dose midazolam may be prescribed. Often, this is done as part of anticipatory prescribing.\n\n\n# Respiratory tract secretions\n\nRespiratory tract secretions often occur in the last days of life as a person becomes less able to clear their airways. They are rarely a cause of distress to the patient, but may be upsetting for family members or those close to the patient. An antimuscarinic such as hyoscine butylbromide or glycopyrronium bromide may be prescribed for noisy respiratory secretions.\n\n\n# NICE guidelines\n\n\n[NICE Guidance: Care of dying adults in the last days of life](https://www.nice.org.uk/guidance/ng31)\n\n[NICE CKS: Palliative care - general issues](https://cks.nice.org.uk/topics/palliative-care-general-issues/)\n\n[NICE CKS: Palliative care - dyspnoea](https://cks.nice.org.uk/topics/palliative-care-dyspnoea/)\n\n[NICE CKS: Palliative care - nausea and vomiting](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative care - secretions](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative cancer care - pain](https://cks.nice.org.uk/topics/)\n\n# References\n\n[Pallcare.info](https://www.pallcare.info/book.php)\n\n[BNF: Ondansetron](https://bnf.nice.org.uk/drugs/ondansetron/#drug-action)\n\n[BNF: Nausea and labyrinth disorders](https://bnf.nice.org.uk/treatment-summaries/nausea-and-labyrinth-disorders/)\n\n[BNF: Prescribing in palliative care](https://bnf.nice.org.uk/medicines-guidance/prescribing-in-palliative-care/)",
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"question": "A 90 year old gentleman is admitted to the medical ward with an infected sacral sore. He has a background of advanced dementia and previous stroke. During his stay, he develops aspiration pneumonia and his condition begins to deteriorate.\n\nHe is reviewed by the Palliative team who plan to start him on end of life medications via a syringe driver. He is currently on oral morphine 10mg TDS and has required three breakthrough doses of oral morphine 2mg in the past day. What is the most appropriate subcutaneous breakthrough dose he should be prescribed?",
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"explanation": "# Summary\n \n\nBenign breast diseases are a variety of non-cancerous conditions that cause breast symptoms such as lumps, pain, and nipple discharge. They include fibroadenoma, breast cysts, mastitis, intraductal papilloma, radial scar, fat necrosis, fibrocystic breast disease, and mammary duct ectasia. Clinical examination, mammography, ultrasound, and biopsy are the key investigative tools, while management includes reassurance, medication, and sometimes surgical interventions.\n \n\n# Definition\n \n\nBenign breast diseases are a group of non-cancerous conditions affecting the breast, which often manifest as breast lumps, nipple discharge, or other abnormalities.\n \n\n# Epidemiology\n \n\nThe majority of patients referred for breast symptoms are diagnosed with benign breast disease, making it a highly common condition. Women of various age groups can be affected, with some conditions like fibroadenoma being more common in younger women and others like breast cysts or fibrocystic breast disease being more prevalent from age 35 until menopause.\n \n\n# Aetiology\n \n\n - **Fibroadenomas** arise from the breast lobule stroma.\n - **Breast cysts** occur due to the overgrowth of glandular and connective tissue, leading to blocked breast ducts and subsequent fluid accumulation.\n - **Mastitis** is typically caused by bacterial infections, often related to breaks in the skin around the nipple.\n - **Intraductal papilloma** is a benign tumour of the breast ducts.\n - **Radial scar** is a benign sclerosing breast lesion.\n - **Fat necrosis** is a response to adipose tissue damage.\n - **Fibrocystic breast disease** is due to an exaggerated hormonal response causing inflammation, fibrosis, cyst formation, or adenosis.\n - **Mammary duct ectasia** is due to inflammation and dilation of the large breast ducts.\n \n\n# Signs and Symptoms\n \nIn general, features that suggest a breast mass is benign include being round, mobile, well-demarcated and smooth. This contrasts features that suggest a breast mass is malignant such as being hard or firm, having irregular borders and being fixed to the underlying structures (i.e. muscles or ribs). \n\n - **Fibroadenoma**: Highly mobile, encapsulated breast masses.\n - **Breast cysts**: Presence of breast lumps, potentially with distension.\n - **Mastitis**: Breast redness, mastalgia, malaise, and fever.\n - **Intraductal papilloma**: Bloody discharge from the nipple which can present with/without a palpable mass. Breast tenderness may also be present.\n - **Radial scar**: Presents on the mammogram as a stellate pattern of central scarring surrounded by proliferating glandular tissue.\n - **Fat necrosis**: Painless breast mass, skin thickening, or radiographic changes on mammography.\n - **Fibrocystic breast disease**: Breast lumps, pain, and tenderness.\n - **Mammary duct ectasia**: Palpable peri-areolar breast mass, thick nipple discharge, and potential mammographic similarities to cancer.\n \n\n# Differential Diagnosis\n \n\n - **Breast cancer**: Characterised by hard, immobile lumps, nipple retraction, skin changes (like peau d'orange), or bloody nipple discharge.\n - **Gynecomastia**: Enlargement of male breast tissue, which may be tender or painful.\n - **Abscess**: A collection of pus in the breast tissue, often painful and associated with redness, warmth, and fever.\n - **Lipoma**: Soft, mobile, non-tender fatty lumps beneath the skin.\n - **Pregnancy**: During pregnancy and breastfeeding, women may experience an increase in the size of their breasts, darkening of the nipple and areola, and discharge of colostrum from the nipple. \n \n\n# Investigations\n \nNICE Guidelines recommend referral under two-week wait protocols for:\n\n- Women over 30 years with an unexplained breast lump\n- Women over 50 with changes to the nipple (i.e. discharge, retraction, skin changes)\n- A referral should also be considered in women with skin changes suggestive of breast cancer or for women aged over 30 years with an unexplained lump in the axilla.\n\nTwo-week wait clinic will consist of a triple assessment of: \n\n - Clinical breast examination: To identify any palpable abnormalities.\n - Mammography and ultrasound: To visualise the internal structures and evaluate any identified lumps or abnormalities.\n - Fine-needle aspiration or biopsy: To confirm the diagnosis of identified lumps or suspicious areas.\n\n\nIn cases of diagnostic uncertainty or when there is a more acute presentation, blood tests may be required to identify signs of infection or hormonal imbalances in certain cases.\n \n\n# Management\n \n\n - Reassurance: Often, benign breast diseases require only monitoring and reassurance, especially when symptoms are minimal and there is no sign of complications.\n - Conservative measures such as ensuring a well-fitting bra and warm compresses may offer some symptomatic relief. \n - Antibiotics: Used in case of infections such as mastitis.\n - Analgesics: To manage pain or discomfort associated with various conditions.\n - Surgical intervention: In some cases, like large fibroadenomas, persistent cysts, or symptomatic intraductal papillomas.\n - Hormonal therapy: May be considered in cases of fibrocystic breast disease.\n\n \n# Prognosis \n \nBenign breast disease can vary in prognosis from non-proliferative disorders with no associated increased breast cancer risk, to atypical hyperplasias with a significantly increased breast cancer risk. \n\n \n# NICE Guidelines \n\n[NICE Guidelines Breast Cancer Recognition and Referral](https://cks.nice.org.uk/topics/breast-cancer-recognition-referral/) \n \n \n# References\n\n[Patient Info Benign Breast Disease](https://patient.info/doctor/benign-breast-disease#types-of-benign-breast-diseases) \n\n[BMJ Best Practice Assessment of Breast Mass](https://bestpractice.bmj.com/topics/en-gb/1179/differentials)",
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"question": "A 32-year-old woman presents to her General Practitioner (GP) with a right-sided breast lump. She first noticed it one week ago and denies any other symptoms including breast pain, discharge, skin or nipple changes. She has no personal or family history of any cancers.\n\nOn examination, there is a smooth 1cm lump in the upper inner quadrant of the left breast. The borders are well defined, and the lump moves under the skin on palpation. There is no associated lymphadenopathy.\n\nWhich of the following is the best step in management?",
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"comment": "I thought if patient was ER+ve they would go on aromatase inhibitors which could cause osteoporosis, so you would wanna do DEXA scan",
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"comment": "Do we start on both treatments simultanously or ER is the first-line then HER-2 therapy??",
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"comment": "stupid q why make her positive for both its clearly reasonable to do a DEXA before starting anastrozole so we didnt know which one to pick",
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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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"explanation": "# Summary\n\nHoarseness, an inability to produce sound with altered voice pitch or quality, is a common complaint often indicative of underlying conditions such as laryngeal cancer, chronic laryngitis, acute laryngitis, or Reinke's Oedema. Hoarseness lasting more than three weeks necessitates an investigation due to its potential association with laryngeal cancer. Key signs and symptoms, investigations, and management strategies for each condition are detailed in the following sections.\n\n# Definition\n\nHoarseness is characterized by the inability to produce sound or a change in voice pitch or quality. It is often a symptom of an underlying condition and not a disease in itself.\n\n# Epidemiology\n\nHoarseness is a common presenting complaint in primary care and ENT clinics. While the exact prevalence is not known, it is frequently associated with a range of conditions from benign vocal cord lesions to more serious laryngeal cancers.\n\n# Aetiology\n\nThe primary causes of hoarseness include:\n\n**Laryngeal cancer**\n\n- Hoarseness lasting more than 3 weeks.\n- Significant smoking history is a common feature in the patient's history.\n\n**Chronic Laryngitis**\n\n- Associated with gastroesophageal reflux disease.\n- Often presents as worse in the morning.\n\n**Acute Laryngitis**\n\n- A common cause of hoarseness, typically viral and self-limiting.\n- May be secondary to gastroesophageal reflux disease (GORD) or autoimmune disease.\n\n**Reinke's Oedema**\n\n- Enlargement of the vocal cords associated with hypothyroidism, leading to persistent hoarseness.\n\n# Signs and symptoms\n\nThe primary symptom of these conditions is hoarseness. However, each condition has unique features:\n\n**Laryngeal cancer**\n\n- Hoarseness lasting more than 3 weeks.\n- A history of significant smoking.\n\n**Chronic Laryngitis**\n\n- Hoarseness, particularly severe in the morning.\n- Potential history of gastroesophageal reflux disease.\n\n**Acute Laryngitis**\n\n- Hoarseness, typically viral and self-limiting.\n- Can be secondary to GORD or autoimmune disease.\n\n**Reinke's Oedema**\n\n- Prolonged and persistent hoarseness.\n- Potential history of hypothyroidism.\n\n# Differential diagnosis\n\nThe differential diagnosis for hoarseness includes:\n\n- Laryngeal cancer: Characterized by hoarseness lasting more than 3 weeks and a history of significant smoking.\n- Chronic laryngitis: Hoarseness that is worse in the morning and potentially associated with gastroesophageal reflux disease.\n- Acute laryngitis: Hoarseness that is typically viral and self-limiting, and could be secondary to GORD or autoimmune disease.\n- Reinke's Oedema: Persistent hoarseness due to enlargement of the vocal cords, associated with hypothyroidism.\n\n# Investigations\n\nInvestigations for hoarseness primarily involve referral to an ENT specialist for further evaluation, which may include laryngoscopy, imaging studies, and potentially biopsy in cases where malignancy is suspected.\n\n# Management\n\nManagement strategies for hoarseness depend on the underlying cause:\n\n- Laryngeal cancer: Urgent referral to ENT specialists under a 2-week wait rule.\n- Chronic laryngitis: Management of underlying gastroesophageal reflux disease.\n- Acute laryngitis: Typically self-limiting and supportive care is often sufficient.\n- Reinke's Oedema: Treatment of underlying hypothyroidism and voice therapy.\n\n# References\n\n[Click here for NICE CKS on head and neck cancers - recognition and referral](https://cks.nice.org.uk/topics/head-neck-cancers-recognition-referral/)",
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"explanation": "# Summary\n\nOtitis media is inflammation of the middle ear often resulting from an infection. Key signs and symptoms include rapid-onset pain, fever, irritability, anorexia, vomiting, and impaired hearing. Diagnosis is based on history and physical examination, notably the appearance of the tympanic membrane. Management mainly consists of treating pain and fever. Antibiotics are reserved for children who are systemically unwell or at high risk of complications. Complications, although rare, can be life-threatening and include both intracranial and extracranial complications.\n\n# Definition\n\nOtitis media is an infection-induced inflammation of the middle ear, frequently occurring after a viral upper respiratory tract infection.\n\n# Epidemiology\n\nOtitis media is a common condition, predominantly affecting young children. \n\n# Aetiology\n\nThe primary cause of otitis media is bacterial infection, particularly common in young children, often following a viral upper respiratory tract infection. \n\n# Signs and Symptoms\n\nAcute otitis media is characterised by:\n\n- Rapid onset of deep-seated ear pain\n- Fever\n- Irritability\n- Anorexia\n- Vomiting\n- Impaired hearing\n- Systemic illness\n- Aural fullness followed by discharge when the tympanic membrane perforates, leading to relief of pain\n- Injection of blood vessels and diffuse erythema of the tympanic membrane\n\n[lightgallery1]\n\nChronic otitis media can present as:\n\n- Benign chronic otitis media: a dry tympanic membrane perforation without chronic infection\n- Chronic secretory otitis media or \"glue ear\": persistent pain lasting weeks after the initial episode with an abnormal-looking drum and reduced membrane mobility\n- Chronic suppurative otitis media: persistent purulent drainage through the perforated tympanic membrane\n\n[lightgallery]\n\n# Differential Diagnosis\n\nThe main differentials for otitis media include:\n\n- Otitis externa: characterised by pain exacerbated by tugging of the auricle, accompanied by otorrhoea and possible hearing loss\n- Mastoiditis: presenting with postauricular pain, erythema, and swelling, as well as protrusion of the ear\n- Temporomandibular joint disorder: characterized by jaw pain, difficulty in opening the mouth, and clicking or popping sounds during jaw movement\n\n# Investigations\n\nDiagnosis of otitis media is primarily clinical, based on history and physical examination, notably the appearance of the tympanic membrane.\n\nIf however there are concerns of **mastoiditis**, such as if there is continued systemic upset despite antibiotic treatment, a CT head should be arranged in the first instance. Mastoiditis is primarily managed with IV antibiotics although surgical intervention is sometimes needed.\n\n# Management\n\nIn managing otitis media:\n \n- Admit any children under 3 months with a temperature of 38 degrees Celsius or more, or children with suspected acute complications of otitis media such as meningitis, mastoiditis, or facial nerve palsy.\n- Consider admitting any children who are very systemically unwell.\n- Otherwise, treat pain and fever with paracetamol or ibuprofen.\n- Most children will not require antibiotics. A delayed antibiotic prescribing strategy can also be appropriate. This involves asking patients/parents to start taking antibiotics if symptoms don't improve within four days.\n- Offer an immediate antibiotic prescription to children who are systemically unwell (but don't require admission) or those at high risk of complications (e.g., immunocompromised patients).\n\n# Complications\n\nComplications of otitis media can be divided into intracranial and extra-cranial complications. They are potentially life-threatening and require immediate assessment and treatment.\n\nExtra-cranial complications include:\n\n- Facial nerve palsy\n- Mastoiditis\n- Petrositis\n- Labrynthtitis\n\nIntra-cranial complications include:\n\n- Meningitis\n- Sigmoid sinus thrombosis\n- Brain abscess\n\n# References\n\n[Click here for NICE CKS on otitis media - acute](https://cks.nice.org.uk/topics/otitis-media-acute/)",
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"question": "A 16-year-old woman attends her GP due to otalgia in her right ear. She has had the pain for the last 2 days. On otoscopic examination the GP identifies a cloudy and slightly bulging tympanic membrane.\n\nWhat is the correct management?",
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"explanation": "IV adrenaline is not given during anaphylaxis unless it is performed by a specialist. This will usually require continuous monitoring",
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"explanation": "This is the correct answer. The patient is experiencing anaphylaxis and therefore, requires IM adrenaline urgently. Note that the correct concentration for IM adrenaline is (1:1000) compared to IV adrenaline (1:10000) which is used during a cardiac arrest. The more concentrated form is therefore, the form that is injected into muscles whereas it would be inadvisable to inject such a dose directly into the vasculature",
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"explanation": "# Summary\n\nAnaphylaxis is a medical emergency which often occurs due to a type 1 IgE mediated hypersensitivity reaction to an allergen. It is characterised by the rapid onset of life-threatening airway swelling, bronchospasm and/or circulatory dysfunction. In most cases skin or mucosal changes are also present. Triggers include medications (such as penicillins), foods (such as peanuts) and insect stings. Diagnosis is clinical, with repeated mast cell tryptase levels a useful way to confirm the diagnosis in retrospect. Management strategies include removing the trigger, ABCDE assessment, oxygen administration, and adrenaline administration, amongst other interventions. \n \n# Definition\n \nAnaphylaxis is a rapid onset syndrome of life-threatening airway, breathing or circulatory dysfunction. An immunological reaction occurs when patients are exposed to allergens such as medications, foods (such as peanuts or eggs) and bee or other insect stings. Many cases of anaphylaxis however are idiopathic with no known trigger, or may be mediated by other mechanisms other than the classical type 1 IgE-mediated pathway. \n\n# Epidemiology\n \nApproximately 1 in 1333 people in England have had an episode of anaphylaxis. There are approximately 20-30 deaths per year in the UK, with around half of these being iatrogenic (e.g. due to penicillin).\n \n\n# Aetiology\n \nCommon precipitants of IgE-mediated allergic anaphylaxis include:\n\n- Insect stings\n- Nuts\n- Other foods such as eggs or milk\n- Latex\n- Antibiotics (e.g. penicillins)\n- Intravenous contrast agents\n- Other medications (such as NSAIDs)\n \n\n# Signs and Symptoms\n\nSigns and symptoms are sudden in onset and progress rapidly. To be classed as anaphylaxis, patients need to have life-threatening problems affecting the:\n\n- **Airway** (pharyngeal or laryngeal oedema)\n - Symptoms include difficulty swallowing and breathing, feeling that the throat is closing\n - Signs include stridor, hoarse voice and swelling of the tongue and lips\n- **Breathing** (bronchospasm)\n - Symptoms include difficulty breathing, wheeze and cough\n - Signs include increased work of breathing and respiratory distress, hypoxaemia may cause confusion and cyanosis\n - Patients may fatigue leading to respiratory arrest\n- **Circulation** (anaphylactic shock)\n - Symptoms include dizziness\n - Signs include pallor, clamminess, tachycardia and hypotension\n - Patients may develop arrhythmias and anaphylaxis can lead to cardiac arrest\n\nContinuing with an A to E approach, the following signs and symptoms are often also seen:\n\n- **Disability** (altered neurological state)\n - Symptoms include anxiety and a \"sense of impending doom\"\n - Signs include confusion, agitation and loss of consciousness\n- **Exposure** (skin and mucosal changes)\n - These range from mild erythematous patches to florid generalised rashes\n - Often occur prior to the onset of other symptoms\n - Urticaria (hives) are itchy and can occur anywhere on the skin\n - Angioedema involves swelling of the eyelids and lips (as well as the tongue and throat causing airway obstruction)\n\n**Gastrointestinal** manifestations including abdominal pain, incontinence and vomiting are also commonly seen in cases of anaphylaxis.\n \n[lightgallery]\n\n# Differential Diagnosis\n\n- **Life-threatening asthma exacerbation** \n - Several overlapping features e.g. bronchospasm, tachycardia, reduced levels of consciousness\n - May cause raised mast cell tryptase also \n - Triggers can be similar to anaphylaxis triggers\n - Would not have features of upper airway obstruction e.g. stridor or mucosal/skin changes e.g. urticaria\n- **Other causes of angioedema** \n - e.g. hereditary angioedema, induced by medications e.g. ACE inhibitors\n - Both involve histamine and/or bradykinin mediators\n - No circulatory dysfunction and shock unlike in anaphylaxis\n- **Panic attack** \n - May have tachycardia and tachypnoea accompanied by anxiety and feelings of doom, skin flushing may also occur\n - No signs of airway obstruction or circulatory collapse and symptoms often resolve with reassurance\n- **Vasovagal episode** \n - May occur after triggers e.g. vaccination\n - Mimic features of pallor and loss of consciousness\n - No airway or breathing symptoms unlike in anaphylaxis\n \n# Investigations\n \nAnaphylaxis should be diagnosed clinically based on the above features.\n\nThe following investigations should be carried out in the emergency setting:\n\n- **ECG** - to look for myocardial ischaemia and arrhythmias which may be caused by anaphylaxis\n- **Arterial blood gas** should be considered in hypoxic patients, may show metabolic acidosis due to shock\n- **Bloods for mast cell tryptase** - the first sample should be taken as soon as possible after starting emergency treatment, with a second sample taken within 1 to 2 hours (no later than 4 hours from symptom onset) and a third sample taken after complete recovery (as a baseline)\n\nAn elevated serum tryptase from baseline is a useful confirmatory test for anaphylaxis especially where there is diagnostic uncertainty, although a normal level does not exclude anaphylaxis. \n \n\n# Management\n\n**Emergency management:**\n \n- Early recognition is key - call for help (put out a medical emergency call if in hospital)\n- Remove any ongoing trigger e.g. stop causative medication, remove insect stinger\n- Lie patient flat and elevate legs if hypotensive, or help to a seated position to aid breathing\n- Give intramuscular adrenaline - 0.5ml of 1:1000 (500mcg) in adults, usually into the anterolateral thigh\n- Secure the airway\n- Administer high flow oxygen and ensure monitoring in place (oxygen saturations, blood pressure and ECG)\n- Consider inhaled bronchodilators (salbutamol or ipratropium) for wheeze\n- Give an IV fluid bolus in patients with hypotension or shock, or who do not respond to the initial adrenaline dose\n- IM adrenaline can be repeated after 5 minutes if no response\n- In the case of a cardiac arrest, start CPR and give further adrenaline via the IV or IO route (as intramuscular administration is unreliable in this scenario)\n\n**Once stabilised:**\n\n- Give an non-sedating oral antihistamine (e.g. 10-20mg cetirizine) - if not able to swallow can give IV or IM chlorphenamine \n - This helps to treat cutaneous symptoms of anaphylaxis but is not a first-line treatment as they do not treat life-threatening features\n- Steroids are no longer routinely advised but may be considered in patients with an asthma exacerbation/anaphylaxis overlap or in cases of ongoing shock\n- Observe patients for a **biphasic reaction** (when symptoms of anaphylaxis reoccur without further exposure to a trigger)\n - This occurs in around 5% of patients\n - Patients with severe initial presentations, those who require multiple adrenaline doses or who had a delay in treatment are at increased risk\n - Patients should be risk stratified - those at the lowest risk can be discharged after 2 hours of observation, those at intermediate risk should be observed for at least 6 hours and those at the highest risk for at least 12 hours\n- Prior to discharge, patients and families should be educated about anaphylaxis, what actions to take and the risk of a biphasic reaction\n - Give two adrenaline auto-injectors (e.g. an EpiPen) and demonstrate how to use these\n - Advise on trigger avoidance\n- Refer for follow up in a specialist allergy service\n\n# NICE Guidelines\n\n[NICE - Anaphylaxis: assessment and referral after emergency treatment](Anaphylaxis: assessment and referral after emergency treatment)\n\n[NICE CKS - Angio-oedema and Anaphylaxis](https://cks.nice.org.uk/topics/angio-oedema-anaphylaxis/)\n\n# References\n \n[UK Resuscitation Council Anaphylaxis Guidelines](https://www.resus.org.uk/library/additional-guidance/guidance-anaphylaxis/emergency-treatment)",
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"question": "A 44-year-old female attends A&E after developing sudden onset breathing difficulties. Her lips are swollen and she has developed a widespread pruritic rash.\n\nWhich is the correct prescription?",
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"explanation": "This is incorrect. The patient's eyes only open to pain, therefore, this scores a 2. She is able to articulate single words only and therefore, scores a 3 for verbal. Motor of 2 would be decerebrate rather than decorticate. Decorticate means abnormal flexion in response to pain, which is therefore, a 3. Decerebrate means abnormal extension in response to pain and would therefore, score a 2",
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"explanation": "This is incorrect. The patient's eyes only open to pain, therefore, this scores a 2. She is able to articulate words, rather than mumbling so scores at least a 3. However, because she is not able to form sentences, confused or otherwise, she only scores a 3. Motor of 2 would be decerebrate rather than decorticate. Decorticate means abnormal flexion in response to pain, which is therefore, a 3. Decerebrate means abnormal extension in response to pain and would therefore, score a 2",
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"explanation": "This is the correct total score, but incorrect in the constituent parts. The patient's eyes only open to pain, therefore, this scores a 2. She is able to articulate words, rather than mumbling so scores at least a 3. However, because she is not able to form sentences, confused or otherwise, she only scores a 3. Motor of 2 would be decerebrate rather than decorticate. Decorticate means abnormal flexion in response to pain, which is therefore, a 3. Decerebrate means abnormal extension in response to pain and would therefore, score a 2",
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"explanation": "This is incorrect. The patient's eyes only open to pain, therefore, this scores a 2. She is able to articulate words, rather than mumbling so scores at least a 3. However, because she is not able to form sentences, confused or otherwise, she only scores a 3. Decorticate means abnormal flexion in response to pain, which is therefore, a 3",
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"label": "c",
"name": "9 - Eyes 2, Verbal 4, Motor 3",
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"explanation": "This is the correct answer. The patient's eyes only open to pain, therefore, this scores a 2. She is able to articulate words, rather than mumbling so scores at least a 3. However, because she is not able to form sentences, confused or otherwise, she only scores a 3. Decorticate means abnormal flexion in response to pain, which is therefore, a 3",
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"comment": "A bit unfair to those of us who didn't know what decorticate meant",
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"comment": "Easy to mix up decorticate and decerebrate at the best of times ",
"createdAt": 1671970143,
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"comment": "decErebrate = Extension :) ",
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"comment": "please just say abnormal flexion...",
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"comment": "even taking english lit at a-level didnt prepare me for tht word",
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"explanation": "# Summary\n\nThe Glasgow Coma Scale (GCS) is a universal score used to standardise assessment of a patient's level of consciousness. The maximum score (normal level of consciousness) is 15 and the minimum score is 3 (comatose or dead patients). There are three components to the score: eye opening, verbal response and motor response. The score is presented as each of the three components and the total score, for example GCS 15 (E4 M6 V5). There are a wide variety of causes for a decreased GCS, and investigations should be targeted based on the clinical presentation e.g. a CT head in suspected head injury. Management again depends on the underlying cause, but supportive measures may be required, most importantly airway protection for patients with a GCS of 8 or below.\n\n# Definition\n \nThe Glasgow Coma Scale (GCS) is a standardised way of assessing and communicating a patient's level of consciousness. Scores range from 3 (a comatose or dead patient who is unresponsive) to 15 (an oriented and fully conscious patient). \n \n# Classification\n\nGCS is calculated as follows:\n\n**Eye Opening Response:**\n\n4 - Spontaneous\n \n3 - To speech\n\n2 - To pain\n\n1 - No response\n \n \n**Verbal Response:**\n\n5 - Oriented\n\n4 - Confused\n\n3 - Inappropriate speech \n\n2 - Incomprehensible speech or sounds\n\n1 - No response\n \n**Motor Response:**\n\n6 - Obeys commands\n\n5 - Localises pain\n\n4 - Withdraws from painful stimulus\n \n3 - Abnormal flexion to pain (decorticate posture)\n \n2 - Abnormal extension to pain (decerebrate posture)\n \n1 - No response\n \n**Note -** Appropriate painful stimuli are:\n\n- Applying pressure to a fingertip\n- Trapezius squeeze\n- Supraorbital pressure\n\n# Differential Diagnosis\n\nCauses of a reduced GCS include:\n\n- **Cerebral causes:** head injury, intracranial bleeding, space-occupying lesions, epilepsy\n- **Respiratory causes:** hypoxia, hypercapnia, carbon monoxide poisoning\n- **Cardiac causes:** arrhythmias, shock (leading to inadequate cerebral perfusion)\n- **Toxic causes:** medications, illicit drugs, alcohol intoxication, overdoses\n- **Metabolic causes:** hypo or hyperglycaemia, uraemia, hepatic encephalopathy\n- **Infective causes:** encephalitis, sepsis, meningitis, cerebral malaria\n\n# Investigations\n\nOne key consideration is what the patient's baseline GCS is - for example in a patient with dementia a normal GCS for them may be 14 due to confusion.\n\nAn A to E approach should be taken in most cases (especially if GCS is significantly reduced) and investigations targeted to suspected underlying causes.\n\nCommon investigations include:\n\n**Bedside tests:**\n\n- **Capillary blood glucose** for hypo or hyperglycaemia\n- **Arterial blood gas** looking for hypoxia, hypercapnia and metabolic disturbances\n- **Urinalysis** e.g. in suspected infection (urinary tract infections are a common cause of confusion)\n- **ECG** for arrhythmia\n\n**Blood tests:**\n\n- **FBC** and **CRP** for inflammatory markers\n- **U&Es** for uraemia and electrolyte imbalance\n- **Bone profile** for hypercalcaemia\n- **LFTs** for liver dysfunction that may precipitate hepatic encephalopathy\n- **Ammonia** if hepatic encephalopathy is suspected\n- **Blood cultures** if infection is suspected\n\n**Imaging:**\n\n- **Chest X-ray** as part of a septic screen if infection is suspected\n- **CT head** or other intracranial imaging if the cause of reduced GCS is unclear or an intracranial cause is suspected\n\n**Special tests:**\n\n- **Lumbar puncture** e.g. in suspected meningitis or subarachnoid haemorrhage\n- **EEG** in suspected encephalitis or non-convulsive status epilepticus\n\n# Management\n \nManagement involves treating the cause of reduced GCS, e.g. giving dextrose in hypoglycaemia, giving naloxone in opiate overdose.\n\nThe patient's medications should be reviewed and contributing medications may need to be held (e.g. opiates).\n\nSupportive management is also important especially if the cause is not immediately treatable - the priority is airway protection.\n\nPatients with a GCS of 8 or below are generally thought to require airway protection (e.g. intubation and ventilation) - immediate assistance from anaesthetics should be sought.\n \n# References\n\n[MDCalc - GCS Calculator](https://www.mdcalc.com/calc/64/glasgow-coma-scale-score-gcs)\n\n[Student BMJ - GCS explained](https://www.bmj.com/content/365/bmj.l1296)\n\n[Life in the Fast Lane - GCS](https://litfl.com/glasgow-coma-scale-gcs/)\n\n[Life in the Fast Lane - Examination of the Unconscious Patient](https://litfl.com/examination-of-the-unconscious-patient/)",
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"explanation": "Streptococcus pneumonia and Neisseria meningitidis are the two most common causes of meningitis in children and adults. They are both bacterial infections, so will typically show on CSF a cloudy appearance; elevated protein; low glucose; white cell count above 200 cells/mL mostly made up of neutrophils; and an elevated opening pressure. They will lead to a negative India ink stain",
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"explanation": "Viral meningitis tends to be milder clinically. On CSF examination, a viral infection typically produces CSF with a clear appearance; normal or mildly elevated protein; normal glucose; a raised white cell count up to 200 cells/mL with predominantly lymphocytes; and a slightly elevated opening pressure. Viral meningitis will lead to a negative India ink stain",
"id": "32854",
"label": "b",
"name": "Herpes simplex virus",
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"explanation": "Neisseria meningitidis and streptococcus pneumonia are the two most common causes of meningitis in children and adults. They are both bacterial infections, so will typically show a cloudy CSF appearance, with elevated protein, low glucose, a white cell count above 200 cells/mL mostly made up of neutrophils, and an elevated opening pressure. They will lead to a negative India ink stain",
"id": "32856",
"label": "d",
"name": "Neisseria Meningitidis",
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is a typical fungal meningitis. Fungal meningitis is most common in immunosuppressed patients, particularly patients who are HIV positive. India ink staining is used to detect cryptococcal fungi, which are most associated with HIV patients",
"id": "32853",
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"explanation": "# Summary\n \nMeningitis refers to inflammation of the meninges which line the brain and spinal cord. The most common cause is infection, with bacterial meningitis being an important emergency presentation that may be life-threatening. The commonest causative bacteria are Neisseria meningitidis, Streptococcus pneumoniae and Haemophilus influenza type b. Key investigations include a throat swab for meningococcal culture, blood testing including PCR for meningococcal and pneumococcal bacteria and a lumbar puncture. Management is with IV antibiotics, with ceftriaxone the recommended first line option until the cause is identified. \n \n# Definition\n \nMeningitis occurs when there is inflammation of the pia mater and arachnoid mater, the two innermost linings of the brain and spinal cord. This can occur for a variety of causes, including malignancy, autoimmune disorders and medications as well as infection. This chapter will focus on bacterial meningitis as the key emergency presentation, however other infections can cause meningitis including viral and fungal causes. \n \n# Epidemiology\n \nRisk factors for bacterial meningitis include:\n\n- Young age (especially under 2 year olds)\n- Older age (over 65 year olds)\n- Winter season\n- Immunocompromise e.g. HIV, chemotherapy\n- Incomplete immunisations against meningococcal, haemophilus influenza b and pneumococcal bacteria\n- Comorbidities e.g. splenic dysfunction, renal disease, sickle cell disease\n- Overcrowding or close living with other e.g. dormitories\n- Cochlear implants\n- Local infection e.g. otitis media, sinusitis\n \n# Aetiology\n\nThe commonest causative bacteria are:\n\n- Streptococcus pneumoniae (pneumococcus) - the commonest cause in adults\n- Neisseria meningitidis (meningococcus)\n- Haemophilus influenza type b (Hib)\n\nOther causes include Listeria monocytogenes, Escherichia coli and Streptococcus agalactiae.\n\n# Signs and Symptoms\n\n- Headache\n- Photophobia\n- Neck stiffness\n- Fever\n- Confusion or altered level of consciousness\n- Seizures\n- Nausea and vomiting\n- Kernig's sign (unable to fully extend the knee when the hip is flexed to 90 degrees due to pain)\n- Brudzinski's sign (when the neck is actively flexed, the knees and hips spontaneously flex)\n\nSigns of systemic infection or sepsis may be present e.g. tachypnoea, tachycardia and hypotension. \n\nPresence of a non-blanching rash is suggestive of meningococcal disease.\n\n# Differential Diagnosis\n\nCSF interpretation can be used to differentiate bacterial from other causes of meningitis, for example viral, fungal or tuberculous: \n\n| | **Bacterial meningitis** | **Viral meningitis** | **Fungal meningitis** | **Tuberculous meningitis** |\n|-----------------------|-----------------------------------------|----------------------------------------|------------------------------------------|------------------------------------------|\n| **Opening pressure** | Elevated | Normal or mildly elevated | Elevated | Elevated |\n| **Appearance** | Turbid | Clear | Fibrin web | Cloudy |\n| **White cells** | Elevated neutrophils | Elevated lymphocytes| Elevated lymphocytes | Elevated lymphocytes|\n| **Protein** | Elevated | Normal or mildly elevated | Elevated | Elevated |\n| **Glucose** | Decreased | Normal | Decreased | Decreased |\n| **Additional tests** | Gram stain and culture | PCR for viral DNA/RNA | Fungal staining, antigen tests or culture | Acid-fast bacilli staining, TB PCR |\n\n**Other differential diagnoses include:**\n\n- **Drug-induced meningitis** with causes including NSAIDs, co-trimoxazole and amoxicillin)\n- **Encephalitis** which shares features of fevers, headache and altered mental status however other neurological findings are present (e.g. dysphasia, motor abnormalities)\n- **Subarachnoid haemorrhage** which also causes meningism and altered mental status, however headache is usually \"thunderclap\" in nature followed by progressive worsening of other symptoms\n\n# Investigations \n \n**Bedside tests:**\n\n- **Lumbar puncture** is the key diagnostic test that should ideally be done before starting antibiotics (or as soon as possible after) - cerebrospinal fluid (CSF) should be sent for:\n - Cell count\n - Total protein\n - Glucose\n - Microscopy, culture and sensitivities\n - Bacterial PCR\n- **Throat swab** for meningococcal culture to identify meningococcal meningitis\n- **Capillary blood glucose** immediately before lumbar puncture to compare with CSF glucose levels\n\n**Blood tests:**\n\n- **Blood cultures** to identify a causative bacteria\n- **FBC** and **CRP** for inflammatory markers which should be raised\n- **HIV test** for all adults with bacterial meningitis\n- **Meningococcal and pneumococcal PCR** to identify the cause of meningitis\n- **U&Es**, **LFTs** and **coagulation screen** as a baseline, may be deranged due to infection\n\n**Imaging:**\n\n- **CT head** should be done prior to lumbar puncture in patients who have any of:\n - Risk factors for a space-occupying lesion\n - New focal neurological signs\n - Abnormal pupillary reactions\n - GCS < 10 or rapid decline in consciousness\n \n# Management\n\n- If there is a strong suspicion of bacterial meningitis, treatment may be started outside of hospital with IM or IV ceftriaxone or benzylpenicillin\n- Otherwise, antibiotics should be started within an hour of arrival in A&E\n- Ideally, a lumbar puncture and blood tests would be done prior to antibiotic administration however these should not delay treatment\n- IV ceftriaxone is first-line; amoxicillin should be given too in patients with risk factors for Listeria meningitis (e.g. neonates, elderly or immunocompromised patients)\n- Chloramphenicol is second line in patients with severe penicillin allergy\n- IV dexamethasone should be given to all over the age of 3 months with strongly suspected or confirmed bacterial meningitis - this is particularly important in pneumococcal meningitis to reduce neurological complications\n- Bacterial meningitis is a notifiable disease; ensure the local health protection unit is informed and antibiotic prophylaxis or vaccination may be required for close contacts\n \n# Complications\n\n- Hearing loss\n- Seizures\n- Cerebral infarction leading to focal neurological deficits including motor deficits and visual impairment\n- Cognitive impairment\n- Obstructive hydrocephalus\n- Death (bacterial meningitis has a mortality rate of 25% in adults) \n\n# NICE Guidelines\n\n[NICE - Meningitis (bacterial) and meningococcal disease](https://www.nice.org.uk/guidance/ng240/)\n\n[NICE CKS - Meningitis](https://cks.nice.org.uk/topics/meningitis-bacterial-meningitis-meningococcal-disease)\n\n# References\n \n[UK joint specialist societies guideline on the diagnosis and management of acute meningitis](https://www.journalofinfection.com/article/S0163-4453(16)00024-4/fulltext)\n\n[Public Health England - Guidance for public health management of meningococcal disease](https://assets.publishing.service.gov.uk/media/5d6fa400e5274a0989ca9aed/PHE_meningo_disease_guideline.pdf)",
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"question": "A 35-year-old male is brought to A&E by his girlfriend. He has been complaining of a progressive, severe headache for the last two hours. He has become increasingly violent in the waiting area. He has a past medical history of HIV and intravenous drug use (IVDU). On examination, he has neck stiffness and reduced visual acuity. A lumbar puncture is done urgently due to suspected meningitis.\n\nCerebrospinal fluid (CSF) results:\n\n- Appearance - Cloudy\n- Protein - Elevated\n- Glucose - Low\n- White Cell Count - 25 cells/mL\n- Opening pressure - Very high\n- India ink stain - Positive\n\nWhat is the likely cause of these symptoms?",
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"explanation": "Lung function tests are unlikely to be useful in this acute scenario",
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"explanation": "Alcohol intoxication is a common differential of carbon monoxide poisoning, and the two can occur concomitantly. However, the patient is unlikely to complain of vertigo, and there is no mention of alcohol use in the history",
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"explanation": "A urine dipstick would be a reasonable investigation to perform in this case. However, based on the history, although delirium secondary to a urinary tract infection is a differential, it is not the most likely and would be unlikely to lead to headache or nausea",
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"explanation": "A chest x-ray would be a reasonable investigation to perform in this case. However, based on the history, although delirium secondary to pneumonia is a differential, it is not the most likely",
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"explanation": "Carboxyhaemaglobin levels can be taken when there is a clinical suspicion of carbon monoxide poisoning. This patient is displaying classic signs and symptoms. Other classic signs are cherry red lips and peripheral cyanosis, which are more common in textbooks than in practice",
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"explanation": "# Summary\n\nCarbon monoxide is a tasteless, odourless and invisible gas that may be produced by fires, faulty gas appliances and fuel-burning heaters. Signs and symptoms include confusion, nausea, vomiting, hypotension and dizziness. Pulse oximetry typically shows close to 100% oxygen saturations as monitors cannot differentiate between haemoglobin bound to oxygen or carbon monoxide. A blood gas will show high levels of carboxyhaemoglobin, and breath tests can be used to measure exhaled carbon monoxide. High-flow oxygen is the mainstay of treatment, with hyperbaric oxygen considered for certain high risk patients. \n \n\n# Definition\n \nCarbon monoxide poisoning is a serious and potentially fatal condition caused by acute or chronic inhalation of carbon monoxide gas. This gas is colourless and odourless, and can only be detected by equipment such as carbon monoxide alarms. It is produced by the incomplete combustion of fuel (when insufficient oxygen is present), for example in faulty heaters or cooking equipment.\n \n# Epidemiology\n \nIn England, there are approximately 4000 A&E attendances per year with carbon monoxide poisoning and approximately 40 deaths. Around half of cases are due to accidental exposure and around 40% are due to self-harm (e.g. from intentional inhalation of exhaust fumes in an enclosed space). \n\nPoisoning is more common in winter when heating equipment is more likely to be used, and is more common in groups affected by socio-economic deprivation.\n\nSome patient groups are more sensitive to the effects of carbon monoxide poisoning, including:\n\n- The elderly\n- Young children\n- Pregnant women \n- People with anaemia\n- People with cardiovascular disease\n\n# Aetiology\n\nInhaled carbon monoxide binds to haemoglobin with a much greater affinity than oxygen, forming carboxyhaemoglobin. This causes tissue hypoxia, especially affecting organ systems with a high oxygen demand such as the central nervous system and the cardiovascular system.\n\n**Prevention of carbon monoxide poisoning:**\n\n- Carbon monoxide alarms should be fitted in the home\n- Gas appliances should be correctly installed and be regularly serviced\n- Vulnerable patients (e.g. disabled or elderly patients) may be entitled to free annual gas safety checks\n- Landlords have a legal duty to ensure gas appliances are checked at least yearly\n- Do not burn charcoal indoors for cooking or heating\n- Do not use gas appliances if you suspect they may be faulty\n\n# Signs and Symptoms\n\n- Headache\n- Dizziness\n- Lethargy\n- Flushing\n- Myalgia and weakness\n- Confusion\n- Nausea and vomiting\n- Cherry red skin (rare)\n- Tachycardia and hypotension\n- Seizures\n\n# Differential Diagnosis\n \n- **Migraine:** headache is the predominant symptom of many cases of carbon monoxide poisoning; migraine is more likely to be associated with aura, photophobia and phonophobia\n- **Viral infections:** cause overlapping symptoms of headache and myalgia, may have other symptoms such as cough or fever not seen in carbon monoxide poisoning\n- **Diabetic ketoacidosis:** may have similar symptoms of nausea and vomiting, lethargy and weakness; blood glucose will be high with raised ketones\n \n# Investigations\n\n**Bedside tests:**\n\n- **Pulse oximetry** is likely to show close to 100% oxygen saturations; this is artifactual as the devices cannot differentiate carboxyhaemoglobin and oxyhaemoglobin.\n- A **blood gas** (either venous or arterial) should be taken to confirm the diagnosis by measuring carboxyhaemoglobin\n - The normal level in non-smokers is 1–2%\n - In smokers 5-10% is normal (heavy smokers can tolerate up to 15%)\n - Carboxyhaemoglobin of 10% or more is usually indicative of carbon monoxide poisoning\n - Toxicity usually manifests at levels of 15-20%\n - Carboxyhaemoglobin of 20% or higher is usually associated with severe cerebral or cardiac ischaemia\n- An **ECG** should be done to look for ischaemic changes\n- **Capillary blood glucose** to rule out hypoglycaemia or hyperglycaemia as a cause for lethargy and confusion\n\n**Blood tests:** \n\n- **FBC** for anaemia\n- **U&Es** for renal impairment\n- **CK** for rhabdomyolysis\n- **Troponin** for myocardial ischaemia\n- **Lactate** - may indicate concurrent cyanide exposure if high in the context of smoke exposure\n\n# Management\n \n- Take an **A to E approach** and ensure the airway is protected in the first instance\n- Administer **100% oxygen** via a tight-fitting face mask (if high-flow nasal cannulae available these can be used to administer up to 60L/min oxygen)\n- Continue high-flow oxygen until any symptoms have resolved and carboxyhaemoglobin levels are 2% or lower in non-smokers or 10% or lower in smokers\n- Correct hypotension with **IV fluids**\n- Contact the **National Poisons Information Service** (NPIS) if advice required\n- In certain severe cases (e.g. carboxyhaemoglobin > 25%) **hyperbaric oxygen therapy** may be considered however its use is currently not recommended by the NPIS\n- **Inform the local Health Protection Team** who will coordinate services to address the source of carbon monoxide poisoning\n\n# Complications\n\nMost patients will recover fully from carbon monoxide poisoning, although in a minority of people (generally those who have had severe or prolonged exposure) neuropsychiatric complications may develop, including:\n\n- Emotional lability and personality change\n- Difficulty concentrating\n- Insomnia\n- Lethargy\n- Movement disorders such as chorea and Parkinsonism\n- Memory impairment and dementia\n- Psychosis\n- Neuropathy\n\n# NICE Guidelines\n\n[NICE CKS - Carbon Monoxide Poisoning](https://cks.nice.org.uk/topics/carbon-monoxide-poisoning/)\n\n# References\n \n[RCEM Learning - Carbon Monoxide Poisoning](https://www.rcemlearning.co.uk/reference/carbon-monoxide-poisoning/)\n\n[London Fire Brigade - Carbon Monoxide Safety](https://www.london-fire.gov.uk/safety/the-home/carbon-monoxide-safety/)",
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"question": "An 89-year-old woman attends A&E. She moved into a new ground-floor flat two weeks ago and calls her daughter as she says her heating appears to have broken. Her daughter finds her confused, and she is complaining of a headache, nausea, vertigo, and dizziness.\n\nWhich of these investigations is most likely to lead to the correct diagnosis?",
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"explanation": "Linagliptin is a dipeptidylpeptidase-4 inhibitor. Liver damage is not a known side effect",
"id": "32866",
"label": "d",
"name": "Linagliptin, 5mg, oral, once a day",
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"explanation": "This patient is displaying symptoms and signs of hepatocellular necrosis secondary to a staggered overdose of paracetamol. The patient's weight is only 44kg. Any patient less than 50kg is at increased risk of developing liver toxicity secondary to paracetamol overdose. Therefore, prescribing 500mg up to 4 times a day instead of 1000mg is advised. Early features of paracetamol poisoning can present initially and then improve within the first 24 hours. Recurrence of these features usually indicates the onset of hepatocellular necrosis",
"id": "32863",
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"name": "Paracetamol, 1000mg, oral, 4 times a day",
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"explanation": "The patient is displaying signs of hepatocellular necrosis. Liver disorders are a potential rare side effect of ibuprofen orally; however, there is little evidence that this can occur via the topical route",
"id": "32864",
"label": "b",
"name": "Ibuprofen 5% gel, topical, to be taken as required, up to 3 times a day",
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"__typename": "QuestionChoice",
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"explanation": "A rare side effect of metformin is hepatitis. However, this is the lowest possible dose, and the clinical picture suggests hepatocellular necrosis. It would be important in this patient to consider withholding the metformin prescription because paracetamol poisoning can lead to renal necrosis, which may increase the likelihood of lactic acidosis secondary to the metformin. Lactic acidosis is not usually a concern unless the eGFR drops below 30 mL/minute/1.73 m2",
"id": "32865",
"label": "c",
"name": "Metformin modified release, 500mg, oral, once a day",
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"explanation": "Liver damage is not a known side effect of levothyroxine. Caution should be taken when prescribing levothyroxine, even at this small dose, with diabetic medications as the dose of antidiabetic drugs may need to be increased",
"id": "32867",
"label": "e",
"name": "Levothyroxine, 25 micrograms, oral, once a day",
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"comment": "poor. this could be pancreatitis",
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"comment": "Could be, unfortunately not one of the options. The questions asks for the most likely cause of the ones offered. It is trying to assess knowledge of reducing doses for low body weights, one of the most essential things to know as a safe prescriber. I think it's a good question",
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"comment": "^ DPP40- inhibitors cause pancreatitis ",
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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 90-year-old woman attends A&E due to nausea and vomiting. She had visited her GP about it two days before, but she had thought it had settled. It has now become significantly worse. On examination, she has severe right subcostal tenderness and is visibly jaundiced. Her past medical history includes diabetes type 2 mellitus, hypothyroidism and osteoarthritis.\n\nHer current medications are as follows:\n\n- Paracetamol, 1000mg, oral, 4 times a day\n- Ibuprofen 5% gel, topical, to be taken as required, up to 3 times a day\n- Metformin modified release, 500mg, oral, once a day\n- Linagliptin, 5mg, oral, once a day\n- Levothyroxine, 25 micrograms, oral, once a day\n\nHer eGFR is 60 mL/minute/1.73 m2 and her weight is 44kg.\n\nWhich of these medications is most likely the cause of her symptoms?",
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"explanation": "This patient has presented with signs and symptoms of hypothermia. J waves can be seen in hypothermic patients, often at a temperature of less than 30 degrees. The height of the J wave is thought to be approximate to the degree of hypothermia. They are positive deflections between the QRS and the ST segment",
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"explanation": "# Summary\n\nHypothermia refers to an abnormally low body temperature (usually defined as under 35°C). It can occur due to exposure to cold surroundings or because of another illness or event such as infection or trauma. Symptoms and signs include shivering, reduced level of consciousness, tachycardia and tachypnoea and arrhythmias. Investigations should include an ECG (with J waves being a key finding), blood tests and a chest X-ray looking for complications of aspiration pneumonia and pulmonary oedema. Management involves rewarming via a number of strategies, monitoring for and treating both causative factors and complications, and fluid resuscitation. Cardiac arrest may occur in severe hypothermia and in this case resuscitation should not be stopped until the patient has been rewarmed. \n\n# Definition\n\nHypothermia refers to a core body temperature below 35°C - it is a pathological state which has significant adverse effects on many body systems and can lead to death.\n\n# Classification\n\nHypothermia may be classified as **primary** or **secondary**:\n\n- **Primary hypothermia** is environmental, occurring for example after immersion in cold water or prolonged exposure to cold weather conditions\n- **Secondary hypothermia** occurs secondary to an insult or illness such as infection, alcohol excess, hypothyroidism or major trauma\n\nIt can also be classified by core body temperature as follows:\n\n- Mild - 32 to 35°C\n- Moderate - 28 to 32°C\n- Severe - 20 to 28°C\n- Profound - < 20°C\n\n# Signs and Symptoms \n\nSymptoms include:\n\n- Shivering\n- Hunger \n- Dizziness\n- Chills\n- Slurred speech\n- Paradoxical undressing\n\nSigns include:\n\n- Tachycardia initially; bradycardias may occur if severe with arrhythmias\n- Tachypnoea; respiratory depression followed by apnoeas if severe\n- Cool peripheries secondary to vasoconstriction\n- Hypotension\n- Ataxia\n- Reduced level of consciousness\n- Pupils may be fixed and dilated if severe\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urine toxicology screen** if drug intoxication is suspected (e.g. patient found unconscious outside \n- **Arterial blood gas** may show an initial respiratory alkalosis, followed by respiratory acidosis as hypothermia worsens\n- **ECG** may show:\n - Prolonged PR, QRS and QT intervals\n - Osborn (or J) waves - positive deflections where the QRS complex joins the ST segment\n - Bradyarrhythmias e.g. sinus bradycardia, atrial fibrillation with a slow ventricular response, slow junctional rhythms and AV block\n - Shivering artefact\n - Ventricular ectopics\n - Cardiac arrest (ventricular tachycardia, ventricular fibrillation or asystole)\n \n\n [lightgallery]\n\n\n**Blood tests:**\n\n- **FBC** and **CRP** for inflammatory markers\n- **U&Es** looking for renal complications of hypothermia and electrolyte derangement\n- **Coagulation screen** as hypothermia can cause a coagulopathy\n- **Creatinine kinase** as hypothermia can cause muscle damage and rhabdomyolysis\n- **Amylase** as pancreatitis can result from hypothermia\n- **Bone profile** and **magnesium** so that any electrolyte disturbance can be corrected\n- **Blood cultures** if sepsis is suspected as a driver of hypothermia\n\n**Imaging:**\n\n- **Chest X-ray** as aspiration pneumonia and pulmonary oedema may complicate hypothermia\n- **CT head** may be indicated e.g. elderly patients who become hypothermic after a fall and long lie\n\n# Management\n\n**Conservative management involves:**\n\n- Take an A to E approach; patients may require escalation to intensive care for intubation and ventilation e.g. if reduced levels of consciousness\n- Rewarming, which may be:\n - Passive rewarming - e.g. removing cold or wet clothes, cover with a blanket and cover head to reduce heat loss (useful in mild hypothermia)\n - Active external rewarming - usually using forced air systems such as a Bair Hugger\n - Active core rewarming - e.g. warmed intravenous fluids and warmed humidified oxygen\n- Core temperature monitoring may be required in more severe cases, with either a rectal or (if intubated) an oesophageal probe\n- Cardiac monitoring\n\n\n**Medical management involves:**\n\n- Fluid resuscitation as patients are usually dehydrated - careful fluid balance monitoring is needed due to the risk of fluid overload\n- Monitoring for and treating complications of hypothermia (see below) \n- Antiarrhythmic medication is rarely required for cardiac complications, with rewarming being the mainstay of treatment\n- Consider thiamine for malnourished or critically unwell patients, or those with suspected alcohol excess\n- Investigating for and treating causes of hypothermia (e.g. infection)\n- In the case of a cardiac arrest secondary to severe hypothermia, Resuscitation Council guidelines should be followed (e.g. defibrillation for VF arrests) and resuscitation should be continued at least until the patient has been rewarmed\n\n**Invasive management:**\n\n- In severely hypothermic patients with life-threatening complications who are not responding to other treatments, options include cavity lavage using warm fluids and extracorporeal blood rewarming (e.g. cardiopulmonary bypass)\n\n# Complications\n\n- Frostbite, which in severe cases may warrant amputation of non-viable tissues\n- Arrhythmias\n- Hypotension (especially on rewarming due to vasodilation)\n- Aspiration pneumonia\n- Pulmonary oedema\n- Pancreatitis\n- Acute tubular necrosis\n- Cardiac arrest and death\n\n# References\n\n[RCEM Learning - Hypothermia](https://www.rcemlearning.co.uk/reference/hypothermia/)\n \n[RCEM Learning - Severe Hypothermia](https://www.rcemlearning.co.uk/reference/severe-hypothermia/)\n\n[Patient UK - Hypothermia](https://patient.info/doctor/hypothermia-pro)\n \n[Life In The Fast Lane: ECG Changes in Hypothermia](https://litfl.com/hypothermia-ecg-library/)",
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"question": "An 86-year-old woman attends A&E after her carers found her with slurred speech and pale skin. This is her ECG:\n\n[lightgallery]\n\nAtrial fibrillation is noted. What other abnormality can be seen on the ECG?",
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"explanation": "This is the second best choice. You should not practice outside your boundaries of competence. (Even consultants need to ask others for help occasionally). However, explaining why they have refused would be best",
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"explanation": "This is a poor choice, even if the doctor has mitigated the scenario slightly by looking up the details of the surgery. This consent requires a complex understanding of the operation that only someone who has performed the surgery will have",
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"name": "Consent the patient after looking up the details of the surgery in more detail",
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"explanation": "This is a poor choice as the doctor is also involving a second underqualified doctor. It is up to interpretation whether this option is worse the consenting the patient after looking up the details first. Ultimately, both should not happen",
"id": "32896",
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"name": "Ask another Foundation Year 1 doctor, who has seen the surgery performed before, to consent the patient",
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"explanation": "This is the best answer. As a Foundation Year 1 doctor, they should not be consenting a patient for a procedure which is unknown to them as they would be unable to sufficiently explain the risks and benefits for the surgery to the patient. They would also be unlikely to answer any further questions from the patient. A good general rule that can be used is: if you can do the procedure yourself then you can ascertain consent. If you cannot, then it may not be appropriate to be obtaining consent",
"id": "32893",
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"name": "Explain to the consultant that they are unable to consent the patient as they do not have enough experience",
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"explanation": "This is the worst choice as the doctor is unlikely to be able to provide clear guidance, and the patient would have reasonable grounds to complain as it would negatively affect their care",
"id": "32894",
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"comment": "can't wait to be in that scenario myself and get demoted back to medical student",
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"comment": "I got this wrong because i chose 'refuse to consent the patient'. I see why it was explain that you are unable to consent, however i think the reasoning is incorrect. You can't consent the patient because you are not doing the procedure, not because you don't have enough experience (perhaps a secondary reason). ",
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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 Foundation Year 1 doctor is on their first rotation in urology. They are asked by the urology consultant to consent a 67-year-old male patient for a trans urethral resection of a bladder tumour. The patient is due to go to theatre that afternoon. The Foundation Year 1 doctor has never seen this surgery performed before and does not have a clear idea about what it entails.\n\nWhich of the following is the most appropriate action for the Foundation Year 1 doctor?",
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"explanation": "This is best answer. The Mental Capacity Act (2005) states that all patients should be assumed to have capacity unless proven otherwise (Principle 1). Therefore, it is important to assess this patient's capacity, even though you know their condition and previous MMSE scores make it unlikely that they do have capacity. If an individual does not have capacity for a particular decision then the doctor must make a decision that both, acts in the patient's best interests (Principle 4), and is the least restrictive option (Principle 5). In this case, the information in the stem suggests that having the vaccination would be in the patient's best interests: he is at risk, and there is no evidence that it would have been against his wishes when he did have capacity",
"id": "32898",
"label": "a",
"name": "Assess whether the patient has capacity for this decision. If the patient does not have capacity, then give the flu vaccination because it is in the patient's best interests",
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"__typename": "QuestionChoice",
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"explanation": "The first part of this choice is correct: the patient's capacity should be assessed in keeping with Principle 1 of the Mental Capacity Act (2005). However, there is nothing in the stem to suggest that giving the patient the flu jab would be against their best interests",
"id": "32900",
"label": "c",
"name": "Assess whether the patient has capacity for this decision. If the patient does not have capacity, then do not give the flu vaccination because it is not in the patient's best interests",
"picture": null,
"votes": 62
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "The first part of this choice is correct: the patient's capacity should be assessed in keeping with Principle 1 of the Mental Capacity Act (2005). However, if there is no advanced directive then the doctor will have to act in the patient's best interests (Principle 4). An advanced directive is a helpful tool for a patient to create (when they have capacity). Not having one though, should not preclude treatment if they are deemed not to have capacity",
"id": "32901",
"label": "d",
"name": "Assess whether the patient has capacity for this decision. If the patient does not have capacity, then do not give the flu vaccination because the patient does not have an advanced directive",
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"explanation": "The first part of this choice is correct: the patient's capacity should be assessed in keeping with Principle 1 of the Mental Capacity Act (2005). However, if the patient does not have capacity, the GP should think about what is in the patient's best interests (Principle 4). In this case, that is done by giving the vaccination",
"id": "32899",
"label": "b",
"name": "Assess whether the patient has capacity for this decision. If the patient does not have capacity, then the GP cannot give the flu vaccination",
"picture": null,
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"explanation": "This is incorrect. The patient's capacity needs to be assessed before making a decision here. The presence of a DNAR form only means that, in the event of a cardiac arrest, the patient should not have cardiopulmonary resuscitation. It does not mean the patient cannot have other treatments. This is a common misconception amongst patients",
"id": "32902",
"label": "e",
"name": "Do not assess whether the patient has capacity for this decision because they have a DNAR. Do not give the vaccination because the patient has a DNAR",
"picture": null,
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"comment": "cant really assume that the vaccine is his best interest? ",
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"explanation": "# What are Best Interests? \n\nIf someone lacks capacity to make a specific decision, a decision may have to be made in their _best interests_. This means that a decision will be made on their behalf, having been considered from their point of view. The decision should be one that health and social care professionals believe is the right decision for _that individual patient themselves_ (and not the decision that the professionals desire without taking the patients interests into account).\n\n# Best Interests Criteria\n\nWhen making a best interests decision on behalf of someone who lacks capacity, five factors must be considered:\n\n1. Equal consideration and non-discrimination\n2. All relevant circumstances\n3. Regaining Capcity\n4. Participation\n5. Wishes, Feelings, Beliefs and Values\n\n# What are Equal Consideration and Non-discrimination? \n\nThe person making the decision about what is in the patient's best interests must not make assumptions based on _age, appearance, condition or behaviour_.\n\n# What are All Relevant Circumstances? \n\nIn order to determine what is in the patient's best interests, all the things that the patient would take into account if they were making the decision themselves should be identified .\n\n# Regaining Capacity \n\nIt must be considered whether the patient is likely to regain capacity. If so, the professional(s) need to consider whether or not the decision can be delayed until then.\n\n# Participation \n\nAll practicable steps should be taken in order to encourage and enable participation by the patient in the decision making process.\n\n# Wishes, Feelings, Beliefs and Values \n\nThe wishes, feelings, beliefs and values of the patient should be found out and taken into consideration. This includes views they have expressed in the past, religious or moral opinions, or other factors that might influence the decision they would make themselves.",
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"question": "A 75-year-old male patient is brought into his GP practice by his wife. He had received an invitation by the practice to come in for his annual flu vaccination. He has a history of Parkinson's dementia, type 2 diabetes mellitus and obesity. He requires carers four times a day, and on his last visit to the GP he scored 5 out of 30 on an MMSE (mini-mental state examination). He has a Do Not Attempt Resuscitation (DNAR) form but does not have an advanced directive.\n\nHis wife asks the GP whether he can have his flu vaccination, which of the following is the best next step?",
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"explanation": "Although the mother is upset about the lack of information that she has received it is still not acceptable to break patient-doctor confidentiality",
"id": "32907",
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"name": "Tell the daughter that her mother does have a DNAR form and update her about her current care",
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"explanation": "You should not break patient-doctor confidentiality by disclosing this information without the patient's permission. Instead you must ask the mother whether it is acceptable to relay this information to her daughter. Whilst a DNACPR is a medical decision, this antagonistic response is likely to create further tension",
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"name": "Tell the daughter that their mother does have a DNAR form and explain that this is a medical decision and that her opinion will not change anything",
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"id": "32904",
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"name": "Tell the daughter that her mother does have a DNAR form as she is the next of kin",
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"explanation": "This is the correct answer. The patient had capacity to make the decision about resuscitation, therefore, it is likely that she will have capacity to make the decision about whether to communicate this decision to her daughter. If you did not ask permission, you would be breaking patient-doctor confidentiality",
"id": "32903",
"label": "a",
"name": "Check with the patient whether you can share this information with their daughter",
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"comment": "Loving the passive aggressive options",
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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 95-year-old female is an inpatient on the acute medical unit. She has been treated for a urinary tract infection with antibiotics and is due to be discharged home. Before discharge, the patient agreed with the consultant to complete a Do Not Attempt Resuscitation (DNAR) form. The patient had capacity to make this decision. The patient's daughter (her next of kin) visits the ward and demands to know whether or not her mother has a DNAR form. She is very upset because she says it has been so difficult to contact the ward to find out how her mother has been doing.\n\nWhich is the best next step for you, as the ward resident doctor, to take?",
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"explanation": "Although paracetamol may be helpful as an antipyretic and analgesia, it would not help treat the underlying infective cause",
"id": "32997",
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"name": "Paracetamol",
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"explanation": "The patient is suffering from a pneumocystis jirovecii infection. This is a fungus that can cause pneumonia in at-risk patients. It is an acquired immune deficiency syndrome (AIDs)-defining infection in individuals who are HIV positive. The most appropriate treatment is high dose co-trimoxazole (trimethoprim and sulfamethoxazole)",
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"explanation": "The patient has a non-productive cough and has been short of breath, which may suggest an asthma diagnosis. However, the fever and widespread scattered crackles point to an infective cause",
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"name": "Salbutamol",
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"explanation": "The patient is showing signs of an infection, therefore, prednisolone is not appropriate at this stage",
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"explanation": "This may be appropriate for a bacterial pneumonia. However, the patient is HIV positive and has signs of oral thrush. These greatly increase the risk of an atypical infection. Pneumoncystis jirovecci is a common cause of pneumonia in immunocompromised patients",
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"explanation": "# Summary\n \n\nLung-related illnesses in HIV patients are multifaceted with numerous differential diagnoses including bacterial infections, bronchitis, pneumonia, Pneumocystis pneumonia (PCP), and various fungal infections like Cryptococcal, Histoplasmosis, and Aspergillus. Key signs and symptoms can include upper respiratory tract infection symptoms, COPD-like exacerbations, fever, weight loss, and nonspecific presentations. Investigations primarily include clinical examination and chest radiographs, which may often be atypical. Management strategies typically encompass the use of antimicrobials, including antibacterials and antifungals, adjusted according to the specific pathogen involved.\n \n\n# Definition\n \n\nLung-related illnesses in HIV patients are a group of diseases that affect the lungs of individuals with the Human Immunodeficiency Virus (HIV). These illnesses are frequently the result of the compromised immune system in these patients, leading to an increased susceptibility to infections. \n \n\n \n\n# Aetiology\n \n\nThe aetiology of lung-related illnesses in HIV patients is multifactorial, typically including bacterial, viral, and fungal pathogens that take advantage of the weakened immune system. Other factors such as smoking, drug abuse, and co-infections with other diseases like tuberculosis can increase the risk of lung-related illnesses.\n \n\n# Differential diagnosis\n \n\n| | Clinical features | Key investigations | CD4 count (cells/microlitre) |\n|---|---|---|---|\n|**Bronchitis** |Cough, wheeze, shortness of breath |Chest X-ray shows no focal consolidation; sputum culture | |\n| **Pneumonia** | Productive cough, chest pain, shortness of breath | Chest X-ray showing focal consolidation; sputum culture | |\n| **Pneumocystis pneumonia** | Fever, dry cough, shortness of breath, fatigue, desaturation on exertion | Chest X-ray showing ground-glass opacity in a perihilar distribution (can also be normal); CT showing more detailed changes; induced sputum culture | <350 |\n| **Cryptococcal infection** | Asymptomatic in some cases, otherwise presenting with fever, cough, shortness of breath | Variable chest X-ray features; sputum cultures | <200 |\n| **Histoplasmosis** | Fever, weight loss, shortness of breath | Chest X-ray: widespread nodules; sputum culture | <200 |\n| **Aspergillus** | Nonspecific including fever, cough, chest pain, haemoptysis | Chest X-ray, HRCT showing nodules, consolidation and infiltrates; sputum culture |\n| **Mycobacterium tuberculosis** | Cough, shortness of breath, haemoptysis and systemic symptoms of infection. Disseminated infection may cause meningitis or adrenal suppression | Chest X-ray showing fibronodular opacities in upper lobes; sputum acid-fast bacilli smear & culture; NAAT | <400 |\n \n\n# Investigations\n \nAssessment should follow a structured approach, including:\n\n- Full history including symptoms and past medical history\n- Physical examination including respiratory examination\n- Bedside tests including observations and pulse oximetry after walking short distances\n- Laboratory tests: blood tests (FBC, U&E, CRP, viral load, CD4 count), sputum cultures\n- Imaging: chest X-ray first line, may be followed by CT chest\n- Invasive tests may be indicated including bronchoscopy or lung biopsy \n\n# Management\n \n\nManagement of lung-related illnesses in HIV patients involves treating the specific pathogen causing the illness. This can include antibacterials for bacterial infections, antifungals for fungal infections (fluconazole for cryptococcal infections, liposomal amphotericin for histoplasmosis and aspergillosis), and co-trimoxazole for pneumocystis pneumonia. Supportive care, including oxygen therapy and respiratory support, may be required. \n \n\nLong-term management also involves optimising the patient's antiretroviral therapy to improve immune function.\n \n# References\n\n[European Respiratory Journal: Pulmonary infections in HIV-infected patients: an update in the 21st century](https://publications.ersnet.org/content/erj/39/3/730)\n\n[Radiopaedia: HIV/AIDS (pulmonary and thoracic manifestations)](https://radiopaedia.org/articles/hivaids-pulmonary-and-thoracic-manifestations-1?lang=gb#:~:text=Pulmonary%20and%20thoracic%20manifestations%20of,also%20play%20a%20significant%20role.)\n\n[Radiology of HIV/AIDS: HIV/AIDS related respiratory diseases](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7121050/)\n\n[BMJ Best Practice: Pulmonary tuberculosis](https://bestpractice.bmj.com/topics/en-gb/165?q=Pulmonary%20tuberculosis&c=suggested)\n\n[BMJ Best Practice: Cryptococcosis](https://bestpractice.bmj.com/topics/en-gb/917)\n\n[BMJ Best Practice: Pneumocystis jirovecii pneumonia](https://bestpractice.bmj.com/topics/en-gb/19?q=Pneumocystis%20jirovecii%20pneumonia&c=suggested)\n\n[BMJ Best Practice: Histoplasmosis](https://bestpractice.bmj.com/topics/en-gb/918)\n\n[BMJ Best Practice: Aspergillosis](https://bestpractice.bmj.com/topics/en-gb/425)",
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"question": "A 46-year-old woman presents to her GP. She has been experiencing a non-productive cough for the last week. She has become short of breath of exercise and has felt intermittently feverish. On examination you notice oral thrush, a raised heart rate and widespread, scattered crackles. She is human immunodeficiency virus (HIV) positive.\n\nWhat is the most appropriate management?",
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"explanation": "Syphilis does not usually present in this way. Instead, there will most often be an initial chancre, a small painless ulcer, found on the glans of the penis",
"id": "33000",
"label": "c",
"name": "Syphilis",
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"votes": 42
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Penile discharge is common in trichomoniasis. However, it is caused by a protozoan rather than a bacterium",
"id": "33001",
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"name": "Trichomoniasis",
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"votes": 20
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"__typename": "QuestionChoice",
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"explanation": "Zoon's balanitis is an inflammation around the head of the penis and the foreskin. It leads to well-defined, itchy, red patches. Histology shows increased plasma cells on skin samples",
"id": "33002",
"label": "e",
"name": "Zoon's balanitis",
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"__typename": "QuestionChoice",
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"explanation": "Chlamydia is likely to present with similar symptoms to gonorrhoea however is a rod-shaped gram-negative bacteria",
"id": "32999",
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"votes": 320
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "Urethral discharge is a common symptom in males with gonorrhoea. Gonorrhoea is a gram-negative diplococcus",
"id": "32998",
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"name": "Gonorrhoea",
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"explanation": "# Summary\n \n \nGonorrhoea is a sexually transmitted infection caused by the bacterium Neisseria gonorrhoeae. Key symptoms include genital discharge, dysuria, and sometimes, tenderness of inguinal nodes in men and abnormal bleeding in women. Diagnosis is primarily made through nucleic acid amplification tests (NAAT) and culture, and confirmed by the presence of monomorphic Gram-negative diplococci within polymorphonuclear leukocytes. The recommended first-line treatment is Ceftriaxone, with a test of cure needed to evaluate disease clearance and treatment effectiveness. Untreated, gonorrhoea can lead to complications such as pelvic inflammatory disease, epididymitis, systemic infection, and increased risk of HIV/AIDS.\n \n \n# Definition\n \n \nGonorrhoea is a sexually transmitted infection (STI) caused by the gram-negative diplococcus, Neisseria gonorrhoeae.\n \n \n# Epidemiology\n \n \nGonorrhoea is the most common bacterial sexually transmitted infection worldwide. It is most prevalent among young adults, specifically those aged 15–24 years.\n \n \n# Aetiology\n \n \nThe aetiology of gonorrhoea is exclusively the bacterium Neisseria gonorrhoeae, which is a gram-negative diplococcus.\n \nRisk factors for gonorrhoea infection include:\n \n- Young adults\n- New sexual contacts\n- Inconsistent barrier contraception\n- Men who have sex with men\n- Previous STI\n- Deprivation\n \n \n# Signs and Symptoms\n \n \nClinical manifestations of gonorrhoea can vary between genders:\n \n \n- Symptoms in men: often asymptomatic, discharge, dysuria, tender inguinal nodes\n- Symptoms in women: discharge, dysuria, abnormal bleeding\n \n \nUpon examination in women, discharge from the cervical os, Skene's gland or Bartholin's gland may be observed. Gonorrhoea may also present with extragenital complications including pharyngitis, conjunctivitis, rectal pain and discharge, septic arthritis and disseminated infection.\n \n \n# Differential Diagnosis\n \n \nConditions to consider in differential diagnosis include:\n \n \n- **Chlamydia trachomatis infection**: Presents with similar symptoms such as discharge and dysuria, often co-infected with gonorrhoea.\n- **Trichomonas vaginalis infection**: May present with pruritus, dysuria, and malodorous discharge.\n- **Bacterial vaginosis**: Characterised by a fishy-smelling discharge, increased vaginal pH and positive 'whiff' test.\n- **Candidiasis**: Symptoms include pruritus, burning sensation and thick, white, 'cottage cheese' like discharge.\n \n \n# Investigations\n \n \nDiagnostic modalities for gonorrhoea include:\n \n \n- Self-taken vulvovaginal swab in women or self-obtained first pass urine in men; self-obtained rectal swab; or clinician-obtained endocervical or penile swab\n- Microscopy revealing monomorphic Gram-negative diplococci within polymorphonuclear leukocytes\n- Nucleic acid amplification tests (NAAT)\n- Culture & sensitivities\n \n \n# Management\n \nAll patients should be referred to a genito-urinary medicine clinic or local specialist services for treatment, partner notification and screening for other STI's.\n \n- People who are systemically unwell should be admitted, and those with complications should be referred to the appropriate specialty.\n- The mainstay of treatment for gonorrhoea is antibiotics. Ideally antibiotics should be prescribed after culture results but sometimes this is not practicable. \n- Current guidelines recommend Ceftriaxone as the first-line treatment. This is given as a single intramuscular injection. \n- Alternative treatments include intramuscular gentamicin or oral cefixime, both with azithromycin orally. \n- Ciprofloxacin should only be considered when sensitivities are known and there are no suitable alternative antibiotics.\n \nFor pregnant or breastfeeding women, a single dose of intramuscular ceftriaxone or oral azithromycin should be used.\n \nFor all patients following treatment, a test of cure is essential to monitor disease clearance and assess the effectiveness of the chosen antibiotic regimen.\n \n \n# Complications\n \n \nIf untreated, gonorrhoea can lead to serious complications, including:\n \n \n- Infertility in women due to pelvic inflammatory disease (PID), which may result in scarring of the tubes and an increased risk of pregnancy complications\n- Infertility in men due to epididymitis caused by the spread of gonorrhoea to the epididymis\n- Disseminated infection that may affect joints and other areas of the body, leading to fever, rash, skin sores, joint pain, swelling and stiffness\n- Increased susceptibility to human immunodeficiency virus (HIV) infection, potentially leading to AIDS, and enhanced transmission of both diseases to partners\n \n \n# NICE guidelines\n \n[Click here to see information on NICE about gonorrhoea](https://cks.nice.org.uk/topics/gonorrhoea/)\n \n# References \n \n[Click here for BASHH guidelines on Neisseria gonorrhoeae](https://www.bashhguidelines.org/media/1238/gc-2018.pdf)",
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"question": "A 19-year-old man visits his GP due to urethral discharge and dysuria. This has been ongoing for the last week. He states that he had unprotected vaginal sex with two female partners and unprotected insertive anal sex with one male partner with over the last month.\n\nHis GP arranges for microscopy of the discharge. This showed gram-negative diplococci.\n\nWhat is the diagnosis?",
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"explanation": "An ultrasound abdomen and pelvis will form a crucial part of the diagnosis of ovarian malignancy, although the question asks for the most appropriate _next_ investigation. If CA-125 was negative, you may consider alternative investigations such as CT chest abdomen pelvis for possible intra-abdominal malignancy, CT Urogram for urological malignancy, or ordering further tumour markers and bloods for more rare causes of this patient's symptoms",
"id": "33004",
"label": "b",
"name": "Ultrasound abdomen and pelvis",
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"explanation": "Any woman (especially if 50 or over) presenting with persistent abdominal distention (or \"bloating\"), early satiety/loss of appetite, pelvic/abdominal pain, or increased urinary urgency/frequency should warrant investigation for ovarian malignancy. Unfortunately most women with ovarian cancer present late with advanced disease and so a low grade of suspicion is required to pick up on subtle symptoms. Beware of the diagnosis of IBS in middle-age and elderly patients; it rarely presents for the first time in people in these age groups and is a diagnosis of exclusion. Serum CA-125 is a tumour marker for ovarian cancer and is the _first_ test you would order in this scenario, as well as routine bloods. If CA-125 is raised, an ultrasound of the abdomen and pelvis should be arranged. If the ultrasound shows suspected ovarian malignancy, a risk of malignancy index (RMI Score) should be calculated. If RMI score is 250 or greater, they should be referred to a specialist multidisciplinary team.\n\nIn women under 40 with suspected ovarian cancer, you should also measure levels of alpha fetoprotein (AFP) and beta human chorionic gonadotrophin (beta-hCG) to screen for germ cell ovarian tumours",
"id": "33003",
"label": "a",
"name": "CA-125",
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"__typename": "QuestionChoice",
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"explanation": "Bloods and tumour markers would be the _next_ most appropriate investigation followed by abdominal ultrasound. TVUS is more sensitive than transabdominal ultrasound for characterising gynaecological malignancies",
"id": "33007",
"label": "e",
"name": "Transvaginal ultrasound (TVUS)",
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"explanation": "This is another sensible option as it is a good screening tool for abdominal and thoracic malignancies. Again, this patient's symptoms would warrant initial investigations with bloods, tumour markers, and likely subsequent ultrasound abdomen pelvis prior to full cross-sectional imaging. The question asks for the most appropriate _next_ investigation and we must start with simple investigations before exposing this patient to potentially unnecessary radiation. If the patient's CA-125 were raised and the ultrasound showed signs of malignancy, staging CT chest abdomen pelvis will likely be required to assess for metastases and guide management",
"id": "33005",
"label": "c",
"name": "CT chest abdomen pelvis",
"picture": null,
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"__typename": "QuestionChoice",
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"explanation": "This would be part of the investigations for a patient presenting with symptoms concerning of urological malignancy, particularly of urethral/bladder origin. This patient has a negative urine dip without haematuria and the history does not suggest any additional urological history. The history is more suggestive of other intraabdominal malignancy, particularly ovarian, and so other investigations would be conducted first",
"id": "33006",
"label": "d",
"name": "Flexible cystoscopy",
"picture": null,
"votes": 99
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"explanation": "# Summary\n \n \nOvarian cancer is a major cause of gynaecological cancer-related mortality in the UK, due primarily to the non-specific nature of symptoms in early stages. The most common type is epithelial ovarian tumours, though germ cell tumours and sex cord stromal tumours also occur. Risk factors include older age, smoking, numerous ovulations, obesity, HRT, and BRCA genes. Parity, breastfeeding, early menopause, and COCP use can be protective. Symptoms typically include abdominal discomfort, bloating, early satiety, and urinary changes, with ascites signifying advanced disease. Differentials include IBS, fibroids, ovarian cysts, and other cancers. Initial investigations include CA-125 and pelvic and abdominal ultrasound. Management depends on disease stage and patient fitness, but can include surgery and chemotherapy.\n \n \n# Definition\n \n \nOvarian cancer is a malignancy originating from various cell types found within the ovary. \n \n \n# Aetiology\n \n \nThe causes of ovarian cancer can be divided into risk factors and protective factors. \n \n \nRisk factors include:\n \n \n - Advanced age\n - Smoking\n - Increased number of ovulations (early menarche, late menopause)\n - Obesity\n - Hormone replacement therapy (HRT)\n - Genetic predisposition (BRCA 1 and 2 genes)\n\nProtective factors include:\n\n - Childbearing (parity)\n - Breastfeeding\n - Early menopause\n - Use of combined oral contraceptive pill (COCP)\n\n\n# Classification\n \n \nThe types of ovarian cancers can be classified according to the cell type from which the cancer originates. The types include:\n \n \n**Epithelial ovarian tumours**\n \n \n - Originate from the epithelium which lines the fimbria of the fallopian tubes or the ovaries\n - Epithelial tumours are partially cystic, and the cysts can contain fluid. \n - The initial metastatic spread typically involves the peritoneal cavity, with seeding particularly affecting the bladder, paracolic gutters and the diaphragm. \n - Around 90% of ovarian cancers are epithelial ovarian tumours.\n \n \n**Germ cell tumours features**\n \n \n - Originate from the germ cells in the embryonic gonad. \n - These tumours typically grow rapidly and spread predominantly via the lymphatic route\n - Germ cell tumours most commonly arise in young women, which is atypical for most cases of ovarian cancer. \n - Tumour markers include alpha-fetoprotein and sometimes beta human chorionic gonadotrophin (B-HCG).\n \n \n**Sex cord stromal tumours**\n \n \n - Originate from connective tissue. \n - They are rare, making up less than 5% of all ovarian tumours. They are malignant tumours, but are much less aggressive than epithelial tumours. \n - Additionally, ovarian cancer can be secondary to another cancer elsewhere, which has metastasised to the ovary. A Krukenberg tumour refers to a \"signet ring\" sub-type of stromal tumour, typically gastrointestinal in origin, which has metastasised to the ovary. \n \n \n \n# Signs and Symptoms\n \n \nThe clinical features of ovarian cancer typically present late in the disease progression and include:\n \n \n - Abdominal discomfort\n - Bloating\n - Early satiety\n - Urinary frequency or change in bowel habits\n \n \nIn later stages, the disease may cause:\n \n \n - Ascites (due to vascular growth factors increasing vessel permeability)\n - Pelvic, back and abdominal pain\n - Palpable abdominal or pelvic mass\n \n \n# Differential diagnosis\n \n \nDifferential diagnoses for ovarian cancer include:\n \n \n- Gastrointestinal conditions (e.g., irritable bowel syndrome): characterised by abdominal pain, bloating, and changes in bowel habits. \n2. Fibroids: may cause heavy menstrual bleeding, pelvic pressure or pain, frequent urination, and constipation. \n3. Ovarian cysts: can cause pelvic pain, fullness or heaviness in the abdomen, and bloating.\n4. Other cancers (e.g., bladder, endometrial): may present with symptoms such as abnormal bleeding, pelvic pain, and urinary symptoms.\n \n \n# Investigations\n \n \nInvestigations for suspected ovarian cancer include:\n \n**Bedside:**\n \n * Abdominal examination: tenderness, abdominal mass\n * Bimanual examination: adnexal mass\n\n \n**Bloods:**\n \n* CA-125 levels\n * Measure CA125 in women (especially those aged over 50) with frequent or persistent symptoms of ovarian cancer (i.e. 12 or more times per month)\n * Consider this measurement in women with non-specific symptoms of malignancy, such as unexplained weight loss, fatigue or changes in bowel habit \n* AFP and beta-hCG levels (for younger women who may have germ cell cancers)\n\n \n**Imaging:**\n\n* Pelvic and abdominal ultrasound scan\n * May be helpful to rule out or identify malignancy where CA125 is 35 IU/ml or higher \n* CT chest/abdomen/pelvis (for staging)\n\n**Invasive:**\n \nFurther investigations may include:\n \n* Tissue biopsy \n \n \n**Risk of Malignancy Index** \n\nThese results can be used to calculate the Risk of Malignancy Index (RMI), which stratifies the likelihood of cancer: \n \n\n**RMI = U x M x CA125**\n\n\n* U = ultrasound result (between 0-3)\n* M = menopausal status (1 = premenopausal, 3 = postmenopausal) \n* Serum CA-125 is measured in IU/ml\n\n- NICE advise referring all women with an RMI I score of 250 or greater to a specialist multidisciplinary team\n\n\n**2 Week Wait (2WW) Referral Criteria:**\n\n* Physical examination showing ascites and/or a pelvic abdominal mass (that is not due to uterine fibroids) \n* Ultrasound findings suggestive of ovarian malignancy\n\n\n\n# Staging\n \n \nStage I (limited to the ovaries):\n \n - Stage IA: limited to one ovary, the capsule is intact\n - Stage IB: limited to both ovaries, capsules intact.\n - Stage IC: tumour limited to one or both ovaries with any of the following: capsule ruptured, tumour on ovarian surface, malignant cells in ascites or peritoneal washings.\n \n \nStage II (involving one or both ovaries with pelvic extension and/or implants):\n \n - Stage IIA: extension and/or implants on the uterus and/or Fallopian tubes. No malignant cells in ascites or peritoneal washings\n - Stage IIB: extension to and/or implants on other pelvic tissues. No malignant cells in ascites or peritoneal washings\n - Stage IIC: pelvic extension and/or implants (Stage IIA or Stage IIB) with malignant cells in ascites or peritoneal washings.\n \n \nStage III (involving one or both ovaries with microscopically confirmed peritoneal implants outside the pelvis):\n \n - Stage IIIA: microscopic peritoneal metastasis beyond pelvis (no macroscopic tumour)\n - Stage IIIB: macroscopic peritoneal metastasis beyond pelvis <2 cm\n - Stage IIIC: peritoneal metastasis beyond pelvis >2 cm and/or regional lymph node metastasis.\n \n \nStage IV: tumour involving one or both ovaries with distant metastasis.\n \n \n\n# Management\n \n \nManagement depends on the stage of the cancer and the patient's fitness for treatment.\n\nSurgery: \n\n* If early disease surgery can include removal of the uterus, ovaries, fallopian tubes and omentectomy\n* In advanced disease further debulking surgery can be performed.\n\n \nChemotherapy:\n\n* Adjuvant chemotherapy in combination with surgery\n* Intraperitoneal chemotherapy may be performed at the time of operation\n\nBiological therapies are being trialled \n \n \n# Complications\n\n* Bowel obstruction/constipation\n* Ascites\n* Chemotherapy complications: alopecia, intraperitoneal toxicity, neutropenia, peripheral neuropathy\n* Immunotherapy complications: bowel perforation or fistula, hypertension, poor wound healing \n* Surgical complications: thromboembolism, infection, haemorrhage, death\n* Death\n\n# Prognosis \n\n5-year survival:\n\n* 75% for women younger than 50\n* > 35% for women over 65\n* > 90% for women with localised disease on diagnosis\n* 30% for women with distant disease on diagnosis \n\n# NICE Guidelines\n \n \n [Click here to read NICE CKS on Ovarian cancer](https://cks.nice.org.uk/topics/ovarian-cancer/)\n \n \n# References \n\n[Patient Info](https://patient.info/doctor/ovarian-cancer-pro)",
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"question": "A 66-year-old woman presents to the GP with six months of increased urinary frequency, ongoing lower abdominal discomfort, early satiety, and persistent mild abdominal distention. She was diagnosed with irritable bowel syndrome (IBS) six months ago after an unremarkable colonoscopy to investigate alternating constipation/diarrhoea\n\nShe is otherwise fit and well and her full blood count, renal profile, and liver function tests are normal.\n\nAbdominal examination reveals a soft and non-tender abdomen, mildly distended, with no palpable masses. PR exam reveals soft stool in the rectum and no palpable masses.\n\nUrine dip is clear\n\nWhat is the most appropriate next investigation for this patient?",
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"explanation": "These would be reasonable suggestions to investigate subfertility/infertility if the patient did not present with an abdominal mass and ultrasound scans were unremarkable",
"id": "33010",
"label": "c",
"name": "Mid luteal phase progesterone",
"picture": null,
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"__typename": "QuestionChoice",
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"explanation": "MRI Pelvis provides excellent anatomic delineation of gynaecological structures. It is the most _accurate_ modality for detecting, localising, and characterising uterine fibroids. It is, however, not generally required for diagnosis and would not be the _first_ investigation of choice",
"id": "33012",
"label": "e",
"name": "MRI Pelvis",
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"__typename": "QuestionChoice",
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"explanation": "This may help in confirming the aetiology of the anaemia, although the clinical information provides enough information to reasonably assume the anaemia was caused either by menorrhagia or from malignancy. The patient has presented with an abdominal mass which must be investigated first",
"id": "33011",
"label": "d",
"name": "Low vaginal swab for chlamydia and gonorrhoea",
"picture": null,
"votes": 35
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This patient most likely has uterine fibroids which has resulted in her menorrhagia, subfertility, and anaemia. She has a smooth benign-feeling suprapubic mass; however this still needs to be formally assessed sonographically to be characterised and assessed for malignancy",
"id": "33008",
"label": "a",
"name": "Transvaginal ultrasound scan",
"picture": null,
"votes": 4172
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This may help in confirming the aetiology of the anaemia, although the clinical information provides enough information to reasonably assume the anaemia was caused either by menorrhagia or from malignancy. The patient has presented with an abdominal mass which must be investigated first",
"id": "33009",
"label": "b",
"name": "Blood film",
"picture": null,
"votes": 15
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"explanation": "# Summary\n \n \nFibroids are benign tumours of the myometrium of the uterus, common in women above 30, with peak incidence in perimenopausal years. Fibroids often present with menstrual dysfunction, such as menorrhagia and dysmenorrhoea, and can interfere with fertility if large enough. They are usually diagnosed following a transvaginal ultrasound scan. Management strategies depend on the symptoms and size of the fibroids, ranging from NSAIDs and contraceptive methods to surgical options including myomectomy, ablation, uterine artery embolisation, and hysterectomy.\n \n \n# Definition\n \n \nFibroids, or uterine leiomyomas, are benign smooth muscle tumours originating from the myometrium of the uterus.\n \n \n# Epidemiology\n \n \nUterine fibroids are the most prevalent benign uterine tumours in women and are the leading cause for hysterectomy. The incidence of fibroids increases with age until menopause. \n\nSymptomatic fibroids are less prevalent in women younger than 30 years of age, occurring in 20–50% of women older than 30 years. The peak incidence is observed in women in their 40s, with a crude incidence of 22.5 per 1000 woman-years.\n \n \n# Aetiology\n \n \nThe exact cause of fibroids is unknown but they are thought to be influenced by genetic, hormonal, and environmental factors. Oestrogen and progesterone, the hormones that stimulate the development of the uterine lining during each menstrual cycle in preparation for pregnancy, appear to promote the growth of fibroids. Fibroids contain more oestrogen and progesterone receptors than normal uterine muscle cells.\n \n \n# Signs and Symptoms\n \n \nFibroids can often be asymptomatic, especially when they are small. However, when symptoms do occur, they usually present as:\n \n \n - Menstrual dysfunction, such as menorrhagia and dysmenorrhoea\n - Sub/Infertility, if the fibroid is large enough to distort the uterine cavity\n - Palpable mass on abdominal or pelvic examination if the fibroid is large\n - Abdominal pain, worse during menstruation\n - Urinary frequency if large enough and putting pressure on the bladder\n \n \n# Differential Diagnosis\n \n \nThe main differentials for fibroids include other causes of menorrhagia and dysmenorrhoea. These include:\n \n \n1. **Endometrial polyps:** Present with irregular menstrual bleeding and spotting\n2. **Endometriosis:** Characterised by dysmenorrhoea, deep dyspareunia, chronic pelvic pain, and infertility\n \n \n# Investigations\n \n \n \n**Bedside:**\n\n* Bimanual examination: may feel enlarged uterus \n \n**Bloods**\n\n* Consider FBC if worried about anaemia \n \n**Imaging:**\n \n * Trans-vaginal ultrasound: Used to assess the size and location of the fibroids\n * MRI: Used if ultrasound does not provide enough detail to assess the fibroid for surgery\n \n**Invasive:**\n\n* Biopsy: May be taken if there is any doubt over the diagnosis to differentiate the fibroid from other conditions such as endometrial cancer\n\n\n \n# Management\n \nManagement of fibroids depends on the symptoms and size of the fibroids. It includes:\n \n - Non-surgical management for fibroids causing abnormal bleeding and under 3cm in size with no uterine distortion. This includes NSAIDs, anti-fibrinolytics (tranexamic acid), GnRH analogues, combined hormonal contraception, and Levonorgestrel-releasing intrauterine system (Mirena).\n - Surgical management for fibroids causing symptoms due to their mass effect. This includes myomectomy, ablation, uterine artery embolisation, and hysterectomy.\n\n# Complications\n\n* Recurrence \n* Haemorrhage and anaemia\n* Degeneration, especially during pregnancy (red degeneration)\n* Infertility (especially if large)\n* Torsion\n* Pressure effects (e.g. urinary retention, constipation)\n* Delivery complications (e.g. breech presentation, bleeding) and pregnancy complications, including miscarriage \n\n \n# NICE Guidelines\n \n \n[Click here for NICE CKS on fibroids](https://cks.nice.org.uk/topics/fibroids/)\n \n# References\n\n[Patient Info](https://patient.info/womens-health/periods-and-period-problems/fibroids)",
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"question": "A 32-year-old woman presents with 12 months of infertility despite regular unprotected intercourse. She reports regular periods, though increasingly heavy in recent years. She had normal childhood development and menarche at age 11, with up-to-date negative cervical smears for HPV, and has no past medical history. She is in a monogamous relationship with a negative sexually transmitted infection screen 6 months ago.\n\n\nOn examination, she has a firm, palpable painless 10cm smooth mass in the suprapubic region. Abdomen is otherwise soft non-tender with no shifting dullness or fluid thrill.\n\n\nRoutine bloods reveal microcytic iron deficiency anaemia but are otherwise unremarkable.\n\n\nUrine dip and beta HCG are negative.\n\n\nWhat is the most appropriate next investigation?",
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"explanation": "This would be a reasonable option to help regulate this patient's menstrual cycle and additionally provide hormonal contraception (although this patient did not state contraception was her main priority). It would be useful for this patient to have an ultrasound scan after a withdrawal bleed to assess the endometrium and so a short daily course of oral medroxyprogesterone would be used to achieve this. The three-monthly depo injection is less likely to induce a withdrawal bleed as quickly as a two week course of oral medroxyprogesterone because the progestogen dose is spread over a longer period of time. If the patient's ultrasound scan showed an endometrium of normal thickness and morphology, then a three-monthly progesterone injection would be an option - although the patient would not benefit from the anti-androgen effects of oestrogen within the COCP",
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"explanation": "This patient does require a TVUS to assess endometrial thickness and morphology, although a withdrawal bleed would need to be induced prior to scanning to accurately measure the endometrial thickness. For this the patient should be provided with oral medroxyprogesterone (Provera) for 14 days to induce a withdrawal bleed",
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"explanation": "This patient is rightly concerned about her risk of endometrial cancer - having PCOS and having two family members who developed endometrial cancer places her at high risk. It would be reasonable to refer to genetic screening to determine if she, or her family, was genetically predisposed to endometrial cancer e.g. Lynch syndrome (mutation in MLH1 mismatch repair gene) or Cowden Syndrome (Mutations in PTEN tumour suppressor gene). The priority at this stage, however, is to investigate and manage her secondary amenorrhoea, and to reassure her there are no signs of malignancy",
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"explanation": "The most likely cause for this patient's secondary amenorrhoea (less that one period every three months) is her PCOS. Her LH:FSH Ratio is 3.5 and so makes PCOS more likely than premature ovarian failure (elevated FSH and LH), hypothalamic/hypopituitary amenorrhoea (low FSH, LH, testosterone, and prolactin), Hypothyroidism (low or high TSH), or androgen-secreting tumour/late onset congenital adrenal hyperplasia (raised testosterone). There is nothing in the question pointing to her amenorrhoea being weight, exercise, or stress-related.\n \n\n She is rightly concerned about her increased risk of endometrial cancer with PCOS and amenorrhoea. This is due to prolonged exposure of the endometrium to unopposed oestrogen. She will need referral for a transvaginal ultrasound (TVUS) to assess for endometrial thickness, although prior to this she will need to induce a withdrawal bleed to correctly interpret the ultrasound findings as her endometrium will be thickened given she has not menstruated for two months. To induce a withdrawal bleed in this patient, an oral cyclical progestogen such as medroxyprogesterone is given for 14 consecutive days. Following this, a TVUS should be conducted.\n \n\n If endometrial thickening is present (greater than 10mm) or the endometrium has an abnormal appearance, then she will need referral for endometrial sampling to exclude endometrial hyperplasia or cancer (unlikely in this patient's case). If the endometrium is of normal thickness and appearance, then the options to reduce risk of endometrial cancer are either:\n \n\n - An oral cyclical progestogen e.g. medroxyprogesterone for 14 days every 1-3 months\n - Low-dose combined oral contraceptive pill (COCP)\n - Levonorgestrel-releasing intrauterine system (e.g. Mirena®)\n \n\n If the patient is unwilling to take these, then they would likely need regular ultrasound scans every 6-12 months to assess the endometrium",
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"explanation": "This would be a reasonable option to help regulate this patient's menstrual cycle and additionally provide hormonal contraception (although this patient did not state contraception was her main priority). It would be useful for this patient to have an ultrasound scan after a withdrawal bleed to assess the endometrium and so a short daily course of oral medroxyprogesterone would be used to achieve this. The three-monthly depo injection is less likely to induce a withdrawal bleed as quickly as a two week course of oral medroxyprogesterone because the progestogen dose is spread over a longer period of time. If the patient's ultrasound scan showed an endometrium of normal thickness and morphology, then a three-monthly progesterone injection would be an option - although the patient would not benefit from the anti-androgen effects of oestrogen within the COCP",
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"comment": "bruh",
"createdAt": 1649759733,
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"comment": "actually a pretty clever question! its so easy to forget about the fact that you have to induce the withdrawal bleed!! ",
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"comment": "shut up man",
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"comment": "LOOOL",
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"comment": "actually a hard question, props to the author",
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"comment": "YOU NEED TO SAY CYCLICAL IN THE ANSWER - IT MAKES IT LOOK LIKE IT'S JUST A ONE-OFF 14 DAY COURSE OF PROGESTERONE\n",
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"comment": "It's meant to be a one off in this case as they're doing it is in prep for a TVUS to assess the endometrium reliably for any hyperplasia. In the future, yes she may need cyclical progesterone to reduce her future risk of cancer. ",
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"comment": "m8 it is a one off...",
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"comment": "excellent question + excellent explanations",
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"comment": "do they still need to take it if they have post-menopausal bleeding?\n",
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"explanation": "# Summary\n \n \nPolycystic ovary syndrome (PCOS) is a disorder characterised by hyperandrogenism, ovulation disorders, and polycystic ovarian morphology. It is common among women of child-bearing age. Key signs and symptoms include oligomenorrhoea, hirsutism, acne, and subfertility among others. Investigations such as hormonal assays and imaging techniques are used in diagnosis. Management strategies encompass lifestyle modifications and a range of pharmacological treatments tailored to patient preferences, such as conception.\n \n \n# Definition\n \n \nPolycystic ovary syndrome (PCOS) is a disorder characterised by hyperandrogenism (manifesting as oligomenorrhoea, hirsutism, and acne), ovulation disorders, and polycystic ovarian morphology.\n \n \n# Epidemiology\n \n \nPolycystic ovary syndrome is a common endocrine condition, affecting up to a quarter of women during their reproductive years.\n \n \n# Aetiology\n \n \nThe precise aetiology of PCOS remains undetermined. However, potential hormonal imbalances implicated in this syndrome include hyperandrogenism, insulin resistance, elevated levels of luteinizing hormone (LH) and raised oestrogen levels.\n \n \n# Signs and Symptoms\n \n \nThe clinical presentation of PCOS is largely attributed to the hormonal imbalances, with symptoms including:\n \n \n - Oligomenorrhoea\n - Subfertility\n - Acne\n - Hirsuitism\n - Obesity\n - Mood changes including depression and anxiety\n - Male pattern baldness\n - Acanthosis nigricans (secondary to insulin resistance)\n \n \n# Differential Diagnosis\n \n \nFor accurate diagnosis, other endocrine disorders presenting similar clinical features must be excluded. These include:\n \n \n - Menopause: Characterised by cessation of menstruation, hot flashes, vaginal dryness, mood changes, and sleep problems.\n - Congenital adrenal hyperplasia (CAH): Presenting with signs of androgen excess like hirsutism, acne, and irregular periods. Presents earlier on and can lead to ambiguous genitalia (for affected females). \n - Hyperprolactinaemia: Symptoms include irregular periods, galactorrhoea, and infertility.\n - Androgen-secreting tumours: May cause virilisation, amenorrhoea, and hirsutism.\n - Cushing's syndrome: Characterised by weight gain, purple stretch marks, and easy bruising.\n \n \n# Investigations\n \n \nBiochemical assays and imaging techniques play a pivotal role in the diagnosis of PCOS:\n \n**Bedside:**\n\n- Clinical examination to identify features of hyperandrogenism (e.g. hirsutism) or features of insulin resistance (e.g. acanthosis nigricans, raised BMI)\n\n**Bloods:**\n\n- LH:FSH ratio: An increase (>2) aids in differentiating from menopause where the ratio is normal.\n- Total testosterone: May be normal or slightly elevated.\n- Fasting and oral glucose tolerance tests: Used to diagnose insulin resistance.\n- Other tests may include TFTs (for thyroid dysfunction), 17-hydroxyprogesterone levels (for CAH), prolactin (for hyperprolactinaemia), DHEA-S and free androgen index (for androgen-secreting tumours), and 24-hour urinary cortisol (for Cushing's syndrome).\n\n**Imaging:**\n\n- Transabdominal and transvaginal ultrasound: Reveals increased ovarian volume and multiple cysts. May be important for fulfilling Rotterdam Diagnostic Criteria (See below) \n\n\nNo **invasive tests** are required for diagnosis. \n\n \n **Rotterdam Diagnostic Criteria:**\n \n \nUpon exclusion of other causes, PCOS can be diagnosed if at least two of the following criteria are met:\n \n \n - Polycystic ovaries (defined as a follicle number per ovary of 20 or more in at least one ovary)\n - Oligo-/anovulation\n - Clinical or biochemical features of hyperandrogenism\n \n \n# Management\n \n \nThe management of PCOS primarily focuses on symptom control and prevention of complications, with endometrial cancer risk reduction achieved through regular menstruation.\n \n \n**Conservative:**\n \n \n - Encouragement of weight loss and exercise\n - Education on increased risks of cardiovascular disease, diabetes, and endometrial cancer\n \n \n**Medical, for women not planning pregnancy:**\n \n \n - Co-cyprindrol: Reduces hirsutism and promotes regular menstruation.\n - Combined oral contraceptive pill (COCP): Decreases irregular bleeding and offers protection against endometrial cancer.\n - Metformin: Aids in regularising menstruation, reducing hirsutism, and acne.\n \n \n**Medical, for women wishing to conceive:**\n \n \n - Clomiphene: Induces ovulation and enhances conception rates.\n - Metformin: Can be used alone or in combination with clomiphene to improve chances of pregnancy.\n - Gonadotrophins: Utilised to induce ovulation if clomiphene and metformin prove ineffective.\n\n**Surgical, for women wishing to conceive:**\n\n - Ovarian drilling: A second-line laparoscopic surgical procedure that damages the hormone-producing cells of the ovary. \n \n# Complications\n\n\n- Infertility: Caused by impaired or dysregulated ovulation.\n- Metabolic syndrome and dyslipidaemia: PCOS leads to raised triglycerides and LDL and fall in HDL. \n- Type 2 diabetes: PCOS increases risk of T2DM by approximately two fold as a result of insulin resistance \n- Cardiovascular disease: This is likely a consequence of metabolic complications of PCOS and hormonal alterations. \n- Hypertension: Greater risk of hypertension seen in premenopausal as opposed to postmenopausal women. \n- Obstructive sleep apnoea: This occurs as a result of obesity (usually secondary insulin resistance and metabolic changes). \n\n# NICE Guidelines\n\n[Click here for NICE guidelines on PCOS](https://cks.nice.org.uk/topics/polycystic-ovary-syndrome/)\n\n# References \n\n[BMJ Best Practice](https://bestpractice.bmj.com/topics/en-gb/141)\n\n[RCOG page](https://www.rcog.org.uk/for-the-public/browse-our-patient-information/polycystic-ovary-syndrome-pcos-what-it-means-for-your-long-term-health/)",
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"question": "A 25-year-old woman presents with prolonged amenorrhoea, having had only three periods in the last year, with the most recent two months ago. She has a history of irregular periods since menarche and was diagnosed with polycystic ovary syndrome (PCOS) as a teenager. She has a family history of endometrial cancer in her mother and maternal aunt.\n\n\nShe denies abdominal pain, bloating, fatigue, early satiety, or intermenstrual bleeding. Her medical history is unremarkable, and her BMI is 21.\n\n\n\n\nUrine dip is clear with negative beta-hCG.\n\n||||\n|---------------------------|:-------:|------------------------------|\n|Thyroid Stimulating Hormone|2.1 mU/L|0.3 - 4.2|\n|Luteinising Hormone|10.85 IU/L|1 - 11 (Luteal)|\n|Follicle Stimulating Hormone|3.1 IU/L|2 - 8 (Luteal)|\n|Testosterone|2.6 nmol/L|(M) 9.9 - 27.8, (F) 0.2 - 2.9|\n|Prolactin|450 IU/L|(M) 90 - 320, (F) 100 - 500||\n\n\n\nWhat is the best next management step for this patient?",
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"explanation": "This patient likely has acute haemolytic anaemia from glucose-6-phosphate dehydrogenase deficiency following ingestion of fava beans. Direct antiglobulin test (direct Coombs test) is used to determine whether the patient has immune-mediated haemolytic anaemia",
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"comment": "lmfao think everyone took an L here",
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"comment": "best bit is the 3% who did get it right, most likely just got the diagnosis wrong ",
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"comment": "you are just doing the most now",
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"comment": "don't lie everyone read fava beans and ran to G6PD, we're all guilty here",
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"explanation": "# Summary\n\nHaemolytic anaemia is a condition characterised by the premature destruction of red blood cells (RBCs), resulting in a reduced RBC lifespan. It can be categorised into hereditary and acquired forms, and further divided into intravascular or extravascular and autoimmune or non-autoimmune subtypes. The epidemiology varies depending on the specific type. Diagnosing haemolytic anaemia requires a comprehensive set of investigations, including a complete blood count (FBC), split bilirubin, haptoglobin, lactate dehydrogenase (LDH), reticulocytosis, and blood film analysis. Additional tests may be needed, such as direct antiglobulin test (DAT), electrophoresis, and further blood film examination. Management involves addressing the underlying cause and may include blood transfusions, immunosuppressive therapy, or splenectomy. Complications can include severe anaemia, gallstones, and organ damage.\n\n# Definition\n\nHaemolytic anaemia is a condition characterised by the premature destruction of red blood cells (RBCs), leading to a decrease in their lifespan. This condition can be classified into hereditary and acquired forms, with further subdivisions based on the site of haemolysis, either intravascular or extravascular, and the underlying cause, autoimmune or non-autoimmune.\n\n\n# Epidemiology\n\nThe prevalence and distribution of haemolytic anaemia vary significantly based on the specific subtype and its underlying causes:\n\n- Sickle cell disease predominantly affects individuals of African descent, and is most prevalent in sub-Saharan Africa.\n- Thalassemias: The distribution of thalassemias is linked to regions with a high prevalence of consanguineous marriages, notably in Mediterranean countries.\n- The prevalence of autoimmune haemolytic anaemia varies, but it is often associated with autoimmune diseases like systemic lupus erythematosus. It can affect individuals of any age and ethnicity. \n- The incidence of intravascular haemolysis may be higher in conditions involving mechanical trauma, such as prosthetic heart valves or microangiopathic disorders. \n- Extravascular haemolysis is often observed in hereditary conditions like hereditary spherocytosis and can affect individuals worldwide.\n\n# Classification\n\n### Hereditary Haemolytic Anaemia\nIncludes conditions like sickle cell disease, thalassemias, and hereditary spherocytosis, often caused by genetic mutations affecting RBC structure or function.\n\n### Acquired Haemolytic Anaemia\n\nCan result from autoimmune disorders, infections (e.g., malaria), medication reactions, or mechanical trauma.\n### Intravascular Haemolysis\n\nOccurs within the bloodstream, leading to the release of free haemoglobin into the circulation and the excess of haemoglobin is dealt with in many ways: \n\n- Combination with haptoglobin\n- Combination with albumin (**methaemalbuminaemia**)\n- Loss in the urine (**haemoglobinuria**)\n- Storage in tubular epithelial cells as **haemosiderin** \n- Shedding into the urine (haemosiderinuria)\n\t\nCauses of intravascular haemolytic anaemia include:\n\n- Intrinsic cellular injury (eg. G6PD deficiency)\n- Intravascular complement-mediated lysis (some autoimmune haemolytic anaemias)\n- Paroxysmal nocturnal haemoglobinuria and acute transfusion reactions\n- Mechanical injury – microangiopathic haemolytic anaemia and cardiac valves\n- Autoimmune haemolytic anaemia (AIHA)\n\n### Extravascular Haemolysis\n\n- Takes place outside the bloodstream, primarily in the spleen and liver, where RBCs are phagocytosed. It is not associated with dramatic release of free haemoglobin into the circulation. \n- Splenomegaly and hepatomegaly are typical.\n\nCauses include:\n\n- Abnormal red cells (e.g. sickle cell anaemia and hereditary spherocytosis)\n- Normal cells having been marked by antibodies for splenic phagocytosis\n\n### Autoimmune Haemolytic Anaemia\n\nRBC destruction is triggered by autoantibodies that target the body's own RBCs.\n\nTwo major causes include:\n\n1. Warm AIHA:\n\t- An **IgG-mediated extravascular** haemolytic disease, in which the spleen tags cells for splenic phagocytosis. \n\t- Causes: **SLE,** idiopathic, lymphoproliferative neoplasms (eg. chronic lymphocytic leukaemia and lymphoma), drugs (methyldopa)\n\t- Managed with prednisolone or immunosupression (e.g. AZT) and transfusions if severe \n2. Cold AIHA:\t\n\t- **IgM-mediated** haemolytic disease, in which IgM fixes **complement** causing **direct intravascular haemolysis**. It includes cold agglutinin disease\n\t- The IgM agglutinates also cause the hands and feet to become blue in cold conditions (**acrocyanosis**)\n\t- Causes: post-infectious (usually after **Mycoplasma** or EBV), idiopathic, lymphoproliferative disorders\n\t- Treatment is mostly supportive, warmed blood is transfused if required and resistant cases may trial rituximab\n\n### Non-Autoimmune Haemolytic Anaemia\n\nCaused by factors other than autoantibodies, such as infections or mechanical stress:\n\n- Microangiopathic haemolytic anaemia\n- Paroxysmal nocturnal haemoglobinuria (PNH)\n- Physical lysis of red cells (e.g. malaria, patients with mechanical heart valves)\n- Haemolytic uraemic syndrome (HUS) – often caused by *E. coli* 0157:H7\n- Infectious causes of disseminated intravascular coagulation (DIC) such as fulminant meningococcaemia\n\n# Signs and Symptoms\n\n**Haemolytic Anaemia - General:**\n\nHaemolytic anaemia, regardless of its underlying cause, often presents with a constellation of symptoms related to the accelerated breakdown of red blood cells and the body's response to anaemia. Common signs and symptoms include:\n\n- Fatigue \n- Pallor\n- Jaundice - Haemolysis releases bilirubin into the bloodstream, causing yellowing of the skin and sclera \n- Splenomegaly - The spleen becomes enlarged as it works to remove and destroy the damaged red blood cells.\n- Dark Urine\n- Gallstones - Excess bilirubin can accumulate in the gallbladder, increasing the risk of gallstone formation.\n- Leg Ulcers - In severe cases, reduced blood flow and oxygen supply can lead to painful leg ulcers.\n- Shortness of Breath\n- Heart Palpitations\n\n**Specific Causes and Their Signs and Symptoms:**\n\n- **Sickle Cell Disease:** Vaso-occlusive pain, acute chest syndrome, and strokes.\n- **Thalassemias:** Profound anaemia, skeletal deformities, and organ enlargement.\n- **Hereditary Spherocytosis:** Splenomegaly and fatigue due to haemolysis.\n- **Autoimmune Haemolytic Anaemia:** Variable symptoms linked to haemolysis extent and underlying autoimmune conditions.\n- **Infections (e.g., Malaria):** Fever, fatigue, and organ dysfunction.\n- **Medication-Induced:** Variable symptoms, jaundice, and specific drug-related effects.\n\n# Investigations\n\n1. First Identify Haemolytic Anaemia:\n\n\t* Full Blood Count (FBC): Reveals low haemoglobin levels, elevated reticulocytes, and alterations in RBC indices.\n\t* Reticulocytosis: Increased levels of reticulocytes indicate active RBC production.\n\t* Blood Film Analysis: reveals characteristic changes in RBC morphology depending on underlying cause.\n\t* LFTs may reveal raised bilirubin\n\t* Raised LDH indicative of high cell turnover\n\t* Raised urinary urobillinogen\n\n2. Identify the Cause:\n\n\t* Direct Antiglobulin Test (DAT): Detects the presence of autoantibodies on the RBC surface in autoimmune haemolytic anaemia.\n\t* Electrophoresis: Helps diagnose haemoglobinopathies like thalassemias and sickle cell disease.\n\t* Blood Film Examination: Further evaluates RBC morphology and inclusions.\n\n# Management\n\nTreatment aims to address the underlying cause and alleviate symptoms. General management principles include:\n\n* **Supportive Care:** Blood transfusions to manage severe anaemia however this won't be curative as there will be ongoing haemolysis if the underlying cause is not managed.\n* **Immunosuppressive Therapy:** In autoimmune haemolytic anaemia, medications like corticosteroids can reduce antibody production.\n* **Splenectomy:** May be considered in certain cases, particularly hereditary spherocytosis.\n* Specific management strategies depend on the type of haemolytic anaemia.\n\n\n# References\n\n[Patient.info - Haemolytic Anaemia](https://patient.info/doctor/haemolytic-anaemia)",
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"explanation": "# Summary\n\nChronic Lymphocytic Leukaemia (CLL) is a mature B-cell neoplasm characterized by the accumulation of monoclonal B lymphocytes in the blood, bone marrow, and lymphoid tissues. The CLL cells accumulate because they survive for a very long time, rather than because they divide at an accelerated rate. It is therefore an indolent disease of deregulated programmed cell death. It primarily affects older adults and often progresses slowly. CLL may be asymptomatic, but common symptoms include fatigue, lymphadenopathy, and hepatosplenomegaly. Diagnosis is confirmed through blood counts, flow cytometry, and genetic tests. Treatment is typically indicated for symptomatic or progressive disease and may involve chemotherapy, targeted therapy, and stem cell transplantation.\n\n# Definition\n\nChronic Lymphocytic Leukaemia (CLL) is a haematologic malignancy characterized by the accumulation of mature monoclonal B lymphocytes in the blood, bone marrow, and lymphoid tissues. These abnormal B cells are often slow-growing and crowd out healthy blood cells.\n\n\n# Epidemiology\n\nCLL is most common in men over the age of 60 years – incidence is 50 per 100,000 individuals after the age of 70 years and it is the most common leukaemia in Western countries\n\n# Aetiology\n\nThe precise cause of CLL is not well-defined, but genetic and environmental factors may contribute to its development. A family history of CLL or exposure to certain chemicals may be associated with an increased risk.\n\n\n# Signs and Symptoms \n\nCLL typically presents asymptomatically, but patients may present with:\n\n- Non-tender symmetrical lymphadenopathy\n- Hepatosplenomegaly\n- B symptoms – weight loss, night sweats and fever \n\nFeatures of marrow failure (infection, anaemia and bleeding) are less common than in acute leukaemias.\n\n# Differential Diagnosis\n\n- **Hairy Cell Leukaemia (HCL):** HCL is another mature B-cell leukaemia and may share some clinical features with CLL. However, the distinct hairy appearance of leukaemic cells in HCL helps differentiate the two.\n- **Small Lymphocytic Lymphoma (SLL):** SLL is closely related to CLL and is considered the tissue-based counterpart. Differentiating between CLL and SLL depends on whether the predominant site of involvement is in the blood or lymph nodes.\n- **Infections:** Some infectious diseases, such as infectious mononucleosis, can mimic lymphadenopathy and other symptoms of CLL.\n\n# Investigations \n\n- The most common initial blood result is an **incidental lymphocytosis** (80% of cases)\n- **Blood film** shows smudge cells – cells damaged as the film is made because they lack a cytoskeletal protein\n- **Immunophenotype** of the cells is CD5 and CD23 positive, FMC negative, CD22 and surface immunoglobulin weak\n- Chromosomal abnormalities are found in approximately 50% of patients \n- Direct antiglobulin test can be positive – AIHA can complicate CLL\n- Hypogammaglobulinaemia is common in advanced disease\n\n[lightgallery]\n\n- Other tests include bone marrow biopsy, which will show lymphocytic infiltration of mature lymphocytes, with some smear cells\n\nNICE advise considering an urgent FBC (within 48h) to assess for leukaemia in adults with any of the following:\n\n* Pallor\n* Persistent fatigue\n* Unexplained fever\n* Unexplained persistent or recurrent infection\n* Generalized lymphadenopathy\n* Unexplained bruising\n* Unexplained bleeding\n* Unexplained petechiae\n* Hepatosplenomegaly\n\n# Staging\n\nThe disease is often staged using Binet's system based on lymphoid tissue enlargement, haemoglobin and platelets.\n\n# Management \n\n- Treatment depends on the stage and activity of the disease i.e. rapidly progressive, bulky, with disabling systemic symptoms or there is associated cytopenias or shortened lymphocyte doubling time. \n- There is no evidence that intervening with treatment at an earlier, asymptomatic phase is beneficial. So often, watchful monitoring is often useful at this stage.\n- Traditionally, intensive chemotherapy including rituximab was first-line therapy. This has now changed in the world of targeted pathway inhibitors superseding chemotherapy. \n- In a patient with no co-morbidities and TP53 intact, +/- mutated IGHV mutated status, we can now start with Venetoclax (selective inhibitor of B-cell lymphoma-2, BCL-2)-Obinutuzumab (anti-CD20 monoclonal antibody) (Ven-O) upfront. \n- In fit patients with TP53 mutational disruption or any IGHV mutated status, first-line therapy is with Acalabrutinib (bruton tyrosine kinase inhibitor) +/- Obinutuzumab or upfront Ibrutinib (tyrosine kinase inhibitor, TKI) monotherapy. \n- Allogeneic stem cell transplant should be considered in those fit patients who have failed at least 2 of : chemoimmunotherapy, BTKi, BCL2i or have Richter’s transformation (sudden transformation into a significantly more aggressive form of large cell lymphoma). \n- If they are high-risk patients (TP53 disrupted), then an allogenic transplant can be considered after the failure of these therapies.\n- Steroids and monoclonal antibody treatments (eg. rituximab) may be useful in autoimmune haemolytic disease. \n- Prevention or treatment of infection with antibiotics or immunoglobulins is also part of the management. \n\n# Complications\n\n* **Infections:** Patients with CLL are at an increased risk of infections due to compromised immune function.\n* **Transformation to Diffuse Large B-Cell Lymphoma (Richter Transformation):** A small percentage of CLL patients may experience aggressive transformation to a high-grade lymphoma, which has a poor prognosis.\n* **Autoimmune Haemolytic Anaemia:** Some CLL patients may develop autoimmune complications, such as heamolytic anaemia or immune thrombocytopenia.\n\n# Prognosis \n\nCLL is a very variable disease: 1/3 of cases don't progress, 1/3 of cases progress slowly, and 1/3 of cases progress actively. \n\nFactors that affect prognosis are: \n\n- Disease stage \n- Atypical lymphocyte morphology\n- Lymphocyte doubling time <12 months\n- Bone marrow trephine showing diffuse involvement\n- Chromosomal/genetic abnormalities, in particular TP53\n- Unmutated immunoglobulin VH (IGVH) gene status\n- Male sex\n- High expression CD38\n\nGiven the improvement in the CLL therapeutic landscape, CLL prognosis now has a median 5-year survival at 87%.\n\nA small proportion of patients with CLL will progress to a more aggressive type with:\n\n- Refractoriness to treatment\n- Increase in systemic symptoms and disease bulk, plus a change in morphological features, specifically 'high-grade lymphomatous (Richter's) transformation'. \n\n\n\n# NICE Guidelines \n\n[NICE 2ww for Haematological Cancers](https://cks.nice.org.uk/topics/haematological-cancers-recognition-referral/management/referral-for-haematological-cancer/#refer-an-adult-for-suspected-leukaemia)",
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"question": "A 72-year-old man presents to the GP with 3 months of general fatigue, malaise, and night sweats.\n\n\nBloods reveal the following:\n\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|78 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|16.3x10<sup>9</sup>/L|3.0 - 10.0|\n|Neutrophils|3.1x10<sup>9</sup>/L|2.0 - 7.5|\n|Lymphocytes|8.2x10<sup>9</sup>/L|1.5 - 4.0|\n\n\nPeripheral blood film shows smudge cells and small mature lymphocytes with round nuclei and clumped chromatin.\n\n\nGiven the likely diagnosis, which of the following is the next best investigation?",
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"explanation": "While aCL antibodies can be found in Behçet's syndrome, there would likely also be a history of recurrent aphthous ulcers and uveitis. With positive LA antibodies, this points to antiphospholipid syndrome",
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"explanation": "The name lupus anticoagulant is a misnomer and has only a weak association with SLE. It is a prothrombotic antibody where most patients with positive antibodies do not have SLE, and only a small proportion proceeds to develop the disease. The patient is otherwise well with no other systemic features and so makes the diagnosis of SLE unlikely",
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"explanation": "Protein C deficiency is a rare cause of thrombosis, which can present with recurrent miscarriages. It is not, however, associated with LA, aCL, or anti-b2-glycoprotein I antibodies",
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"explanation": "# Summary\n\nAntiphospholipid syndrome (APS) is a systemic autoimmune disease that occurs in patients with antiphospholipid antibodies, causing thrombosis of veins, arteries and small vessels. It may occur alone or in association with another condition such as systemic lupus erythematosus. Common manifestations include thrombosis of peripheral arteries or veins, adverse pregnancy outcomes including recurrent miscarriage and intrauterine growth restriction, pulmonary embolism, stroke, retinal thrombosis and valvular disease. Key investigations include a full blood count, clotting screen (aPTT is typically paradoxically raised) and testing for anti-cardiolipin, anti-beta2-glycoprotein I and lupus anticoagulant antibodies. Management involves treating thrombotic episodes with anticoagulation, with warfarin being the preferred option. Asymptomatic APS does not require treatment. Pregnant women with recurrent pregnancy loss require low molecular weight heparin and aspirin throughout pregnancy.\n\n# Definition\n\nAntiphospholipid syndrome (APS) is an autoimmune condition characterised by the presence of antiphospholipid antibodies with clinical manifestations of venous or arterial thrombosis and adverse pregnancy outcomes. \n\n# Epidemiology\n\n- Prevalence of APS in the UK is 50 per 100,000 in women and 9.8 per 100,000 in men\n- Onset is typically between the ages of 20 and 50\n- Antiphospholipid antibodies are found in 1-5% of the healthy population, and in 30% of people with systemic lupus erythematosus\n- Approximately 1 in 6 people under the age of 50 with strokes, deep vein thrombosis, myocardial infarct or recurrent miscarriages have APS \n\n# Aetiology\n\nAPS occurs due to antiphospholipid antibodies which cross-react with cell membrane phospholipids, leading to a hypercoagulable state that predisposes patients to vascular thrombosis.\n\nAPS can occur in isolation (primary APS), or in association with another autoimmune disease such as:\n\n- Systemic lupus erythematosus (SLE)\n- Rheumatoid arthritis\n- Sjogren's syndrome\n- Systemic sclerosis\n- Dermatomyositis\n\nMore rarely, cases may be associated with malignancies (e.g. lymphoma) or infections (e.g. HIV).\n\n# Diagnostic Criteria\n\nAPS is diagnosed using the **revised Sapporo criteria** - patients need at least one clinical and one laboratory criteria.\n\n**Clinical criteria:**\n\n- Vascular thrombosis \n- At least 1 episode of venous/arterial/small vessel thrombosis\n- Not including superficial thrombophlebitis\n- This should be unprovoked or provoked by a minor risk factor only\n- Pregnancy morbidity with any of:\n- 3 miscarriages < 10 weeks\n- 1 miscarriage _<_10 weeks\n- Premature birth < 34 weeks\n\n**Laboratory criteria:**\n\n- On at least 2 occasions at least 12 weeks apart, any of the following are positive:\n- Anticardiolipin antibodies\n- Anti-beta2-glycoprotein I antibodies\n- Lupus anticoagulant\n\n# Signs and Symptoms\n\nClinical manifestations are due to thrombosis of arteries, veins or small vessels which may affect a variety of organ systems:\n\n- Cerebral involvement e.g. ischaemic stroke, central venous sinus thrombosis (signs and symptoms include focal neurology such as weakness, sensory changes, dysphasia)\n- Rashes e.g. livedo reticularis, skin ulceration\n- Lung involvement e.g. pulmonary embolism, pulmonary hypertension (shortness of breath, haemoptysis, presyncope, tachycardia may occur)\n- Cardiac involvement e.g. myocardial infarction, valvular disease (mitral regurgitation is most common), may have chest pain, peripheral oedema, shortness of breath\n- Thrombosis of peripheral arteries leading to acute limb ischaemia (affected area will be cool; pallor, pulselessness, paraesthesia, paralysis and pain may be seen)\n- Deep vein thrombosis, causing swelling, erythema and pain of the affected limb\n- Obstetric complications including recurrent miscarriage, stillbirth, pre-eclampsia and intrauterine growth restriction\n- Retinal thrombosis (either arterial or venous) leading to blurred vision and painless visual loss in one eye\n- Adrenal infarction which may cause flank pain, as well as hypotension, fatigue and confusion\n- Budd-Chiari syndrome (due to hepatic vein thrombosis) causing abdominal pain, ascites and hepatomegaly\n- Mesenteric ischaemia causing abdominal pain, diarrhoea, nausea and vomiting\n- Avascular necrosis of bone leading to localised severe pain\n- Nephropathy which may present with nephrotic syndrome (e.g. oedema), hypertension or with flank pain and haematuria\n\n[lightgallery] \n\n# Differential Diagnosis\n\n- **Factor V Leiden** which is the commonest genetic thrombophilia and increases the risk of venous but not arterial thrombosis\n- **Protein C or S deficiency** are also genetic conditions that increase the risk of venous thrombosis (and possibly arterial thrombosis to a small extent)\n- **Antithrombin III deficiency** may be inherited or acquired (e.g. due to liver dysfunction, disseminated intravascular coagulation or nephrotic syndrome), causes venous thrombosis (and may also increase the risk of arterial thrombosis)\n- **Malignancy** is a prothrombotic state for a multitude of reasons, including tumour cells activating the coagulation system, cancer treatments causing immobility and venous stasis and disrupting the endothelium (e.g. indwelling lines); risk of both arterial and venous thrombosis is increased \n- **Polycythaemia** may be primary (polycythaemia vera) or secondary (usually due to chronic hypoxia, e.g. in chronic obstructive pulmonary disease); causes an increase in blood viscosity that is associated with both arterial and venous thrombosis\n- **Other causes of recurrent miscarriage** e.g. chromosomal abnormalities, uterine anomalies, cervical incompetence\n- **Multiple sclerosis** may cause similar symptoms to repeated cerebral infarctions in APS, e.g. decline in mobility, visual loss, dysphasia and cognitive impairment\n\n# Investigations\n\n**Bedside tests:**\n\n- Urine dip for proteinuria (which may occur in renal involvement, or indicate nephrotic syndrome as a differential)\n\n**Blood tests:**\n\n- Patients need to have at least one of the following antiphospholipid antibodies present on testing on two occasions at least 12 weeks apart:\n- Lupus anticoagulant\n- Anticardiolipin antibody\n- Anti-beta2-glycoprotein I antibody\n- Full blood count - may show thrombocytopenia and/or haemolytic anaemia\n- Clotting screen - may show paradoxical prolongation of the aPTT\n- U&Es looking for renal involvement\n- Testing for SLE if secondary APS is suspected (e.g. antinuclear, anti-double-stranded DNA and anti-smith antibodies)\n- Testing for other hypercoagulable states (e.g. factor V Leiden, protein C and S or antithrombin III deficiency) to rule out differentials\n\n**Imaging tests:**\n\n- Doppler ultrasound for suspected deep vein thrombosis\n- CT or MRI of the brain for suspected stroke\n- CT abdomen for suspected Budd-Chiari syndrome\n- CT pulmonary angiography for suspected pulmonary embolism\n- Transthoracic echocardiography for valvular disease and vegetations (Libman-Sacks endocarditis in SLE), and for pulmonary hypertension\n\n# Management \n\n**Conservative management:**\n\n- Asymptomatic APS does not require any specific treatment\n- All patients should be advised on measures to reduce risk of cardiovascular disease\n- Smoking cessation\n- Regular exercise\n- Maintaining a healthy diet and weight\n- Avoiding alcohol excess\n- Effective management of comorbid hypertension, diabetes and dyslipidemia\n- Patients should avoid oestrogen-containing contraceptive and hormone replacement therapy as this further increases thrombosis risk \n- Joint management with other services (e.g. stroke, cardiology) is important after stroke, myocardial infarction etc.\n\n**Medical management:**\n\n- Anticoagulation is the mainstay of treatment for patients after a thrombotic event, which is usually given lifelong\n- Warfarin is the anticoagulant of choice, with a target INR of 2-3 \n- DOACs are not recommended\n- A higher target INR should be considered in patients with recurrent thrombosis on warfarin (e.g. 3-4)\n- If thrombotic episodes continue, immunomodulatory treatments (e.g. hydroxychloroquine) can be considered\n- Adding an antiplatelet (e.g. aspirin) to warfarin treatment should be considered in patients after a stroke if they have additional vascular risk factors\n- All patients with stroke should be started on statins\n- Miscarriage prevention in APS is with low-dose aspirin and low molecular weight heparin (LMWH)\n- Pregnant patients with APS should take 75-150 mg aspirin daily from 12 weeks gestation until delivery\n- Warfarin is teratogenic and so should be switched to treatment dose LMWH during pregnancy; it is safe in breastfeeding and so can be switched back after birth\n\n# Complications\n\n- Catastrophic antiphospholipid syndrome is characterised by rapid-onset widespread small vessel thrombosis\n- It causes multiorgan dysfunction, often with a systemic inflammatory response syndrome\n- There may be an identifiable trigger, e.g. infection, surgery, pregnancy or subtherapeutic anticoagulation\n- Unregulated complement activation occurs and reduced C3 and C4 levels are often seen\n- Management involves triple therapy with treatment dose heparin, high-dose steroids and either IVIG or plasma exchange\n- Recurrent cerebral infarction can cause cognitive impairment, seizures and vascular dementia\n- Retinal artery or vein occlusion can lead to visual loss\n- Chronic pulmonary emboli or thrombosis may lead to pulmonary hypertension\n- Renal failure due to thrombosis may occur\n- Cardiac valvular disease may be severe enough to require replacement\n\n# Prognosis\n\n- Prognosis of APS varies widely\n- Overall survival is good - approximately 90-94% over 10 years\n- However, significant disability may result from complications such as stroke and pulmonary hypertension\n- With treatment, pregnant women have an 80% chance of a successful birth\n- Catastrophic APS occurs in only 1% of patients, however mortality is approximately 50%\n\n# References\n\n[British Society of Haematology Guidelines](https://b-s-h.org.uk/guidelines/guidelines/guidelines-on-the-investigation-and-management-of-antiphospholipid-syndrome)\n\n[Patient UK - Antiphospholipid syndrome](https://patient.info/doctor/antiphospholipid-syndrome-pro)\n\n[Radiopaedia - Antiphospholipid syndrome](https://radiopaedia.org/articles/antiphospholipid-syndrome)\n\n[StatPearls - Antiphospholipid syndrome](https://www.ncbi.nlm.nih.gov/books/NBK430980)",
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"question": "A 32-year-old woman has presented to the GP for advice about fertility. She has had four miscarriages prior to 20 weeks gestation, following which tests revealed no anatomical, hormonal, or chromosomal precipitating causes. She is otherwise well. Tests are requested to screen for thrombophilia with the results shown below:\n\n| Serum | Result | Result at 12 weeks |\n| ------------------------------- | -------- | ------------------ |\n| Lupus anticoagulant (LA) | positive | positive |\n| Anticardiolipin (aCL) antibody | positive | positive |\n| Anti-b2-glycoprotein I antibody | negative | negative |\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "This value corresponds to the negative predictive value - the chance that the patient does not have the condition if the test is negative. This is calculated as the true negative/(true negative + false negative) = 640/(640+10) = 98.5%",
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"explanation": "This value is the positive predictive value. Positive predictive value is the chance that the patient has the condition if the test is positive. This corresponds to true positive/(true positive + false positive) = 280/(280+70) = 80%",
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"explanation": "The specificity is the proportion of patients without the condition with a negative test result. This is calculated as the true negative/(true negative + false positive) = 640/(640+70) = 90.1%",
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"explanation": "Splitting the table up into true positive (280), false positive (70), false negative (10), and true negative (640) can make answering these tables easier to understand. The specificity is the proportion of patients without the condition with a negative test result. This is calculated as the true negative/(true negative + false positive) = 640/(640+70) = 90.1%",
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"explanation": "This value is the sensitivity. The sensitivity is the proportion of patients with the condition who have a positive test result. This is calculated as the true positive/(true positive + false negative) = 280/(280+10) = 96.6%",
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"explanation": "# Overview \n\nSeveral key parameters can be calculated to help describe how effective a certain test is at diagnosing a condition.\n\n| | Patients with colon cancer | No cancer |\n| ------------------ | :------------------------: | --------: |\n| Biomarker positive | a | b |\n| Biomarker negative | c | d |\n\n# Sensitivity\n\nSensitivity is the proportion of people with the condition who will have a positive result. If, for example, the sensitivity of a test is 80%, out of a hundred people with the condition, only 80 will have a positive test result.\n\nSensitivity = a/(a+c)\n\n# Specificity\n\nSpecificity describes the proportion of people without the disease who will have a negative test. A specificity of 90% can be interpreted as, out of 100 people without the disease, 90 will have a negative test result.\n\nSpecificity = d/(b+d)\n\n# Positive Predictive Value\n\nPositive predictive value (PPV) is the proportion of people with a positive test who actually have the disease. PPV varies with prevalence of disease in a population. The lower the prevalence, the lower the positive predictive value. A PPV of 78% will mean that if 100 people tested positive, 78 people will have the disease.\n\nPPV = a/(a+b)\n\n# Negative Predictive Value\n\nNegative predictive value (NPV) is the proportion of people with a negative test who truly do not have the disease.\n\nNPV varies with prevalence of disease in a population. The lower the prevalence, the higher the negative predictive value. An NPV of 97% will mean that if 100 people tested negative, 97 people will not have the disease.\n\nNPV = d/(c+d)\n\n# False positive rate\n\nThe false positive rate is the proportion of those without the condition who will test positive.\n\nFalse positive rate = 1 - specificity\n\nFalse negative rate = 1 - d/(b+d)\n\n# False negative rate\n\nThe false negative rate is the proportion of those with the condition who will test negative.\n\nFalse negative rate = 1 - sensitivity\n\nFalse negative rate = 1 - a/(a+c)\n",
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"question": "A novel screening test has been developed to detect breast cancer early in high-risk individuals. It is tested on 1000 individuals with risk factors for breast cancer:\n\n| | Breast cancer present | Breast cancer absent |\n| ----------------- | --------------------- | -------------------- |\n| **Test positive** | 280 | 70 |\n| **Test negative** | 10 | 640 |\n\nWhat is the specificity of the new test?",
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173,469,539 | false | 20 | null | 6,495,304 | null | false | [] | null | 6,610 | {
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"explanation": "Relative risk reduction shows how much the treatment has reduced the risk of bad outcomes relative to the control. The risk reduction is (20-12%)/20% = 0.4 or 40%, i.e. a patient is 40% less likely to develop a colitic flair within the next year by taking the drug vs taking a placebo",
"id": "33048",
"label": "a",
"name": "40%",
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"votes": 1521
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"answer": false,
"explanation": "If the treatment causes an increased risk of bad outcome, then it is termed the \"relative risk increase\". 66.7% would be the relative risk increase if the treatment arm resulted in 20% of colitic flares within 1 year and the placebo arm resulted in 12%",
"id": "33050",
"label": "c",
"name": "66.7%",
"picture": null,
"votes": 261
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "8% corresponds to the absolute relative risk, calculated as 20%-12%. This means that if you treated 100 people with this drug, 8 would be prevented from having a colitic flare in the next year. The number needed to treat (NNT) is calculated from this figure as 100/8 = 12.5, i.e. 12.5 people would need to be treated with this drug to prevent one episode",
"id": "33049",
"label": "b",
"name": "8%",
"picture": null,
"votes": 778
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "60% is the value of the relative risk (in percentage form). Relative risk is a proportional measure to determine the size of effect of a treatment compared to other interventions or a control. It is the proportion of bad outcomes in the intervention group divided by the proportion of bad outcomes in the control group. In this case 12%/20% = 0.6",
"id": "33051",
"label": "d",
"name": "60%",
"picture": null,
"votes": 870
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "140% relative risk reduction cannot exist as the maximum reduction of any bad outcome is 100%",
"id": "33052",
"label": "e",
"name": "140%",
"picture": null,
"votes": 19
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],
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"comment": "Do you usually measure relative risk or relative risk reduction in RCTs? ",
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"comment": "relative risk usually but can use relative risk reduction for interpretation in papers etc",
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"explanation": "# Definition\n\nRisk in medical statistics refers to the probability of an outcome (either good or bad) occurring within a studied population. There are several different types of risk that are often used in medical studies.\n\n# What is Risk/Prevalence?\n\nThis is simply the probability of an event occurring within a defined population.\n\n# What is Risk Ratio (RR)?\n\nThe risk ratio (also known as relative risk) is the probability of an event occurring in an exposed group compared to the probability occurring in a non-exposed group.\n\nThe risk ratio is calculated by finding the ratio of incidence of a disease amongst the exposed population and the incidence amongst the non-exposed population.\n\nRisk ratios are used in cohort studies and in interventional studies in which the experimenter intervenes at some point during the study, such as in randomised controlled trials and pre-post studies.\n\nHowever, in cross-sectional studies and case-control studies, the incidence of the disease in the exposed and unexposed populations cannot be found, since the data only provides the cases and controls.\n\nConsequently,the risk ratio cannot be calculated for case-control studies and cross-sectional studies. Instead, an odds ratio must be found.\n\n# What is Absolute Risk Reduction (ARR)?\n\nThe absolute risk reduction is the absolute difference in the risk between the control group and the experimental group. It tells you in absolute terms how much an intervention changes an outcome of interest.\n\n# Calculation of Absolute Risk Reduction\n\nIt is calculated as follows:\n\n_ARR = Risk(control group) - Risk(experimental group)_\n\nA given ARR is generally considered significant if the 95% confidence interval does not cross 0.\n\nARR can then be used to calculate the number needed to treat (NNT).\n\n# What is Relative Risk Reduction (RRR)?\n\nThe relative risk reduction can be thought of as the proportional reduction in risk bestowed by the intervention compared to the control situation. It is more useful in helping you understand the efficacy of an intervention when the absolute risk of outcomes are rare (for example when considering the benefits of a statin for reducing MI in a given population).\n\n# Calculating RRR\n\nIt is calculated as follows:\n\n_RRR = 1 - [Risk(Experimental group) / Risk(Control group)]_\n\nA given RRR is generally considered significant if the 95% confidence interval does not cross 1.",
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"question": "A new treatment has been developed for ulcerative colitis. In a large randomised controlled trial, 20% of participants in the placebo arm had an acute flare within the next year. In the treatment arm, 12% of participants developed an acute flare within the next year.\n\nWhat is the relative risk reduction of the new treatment?",
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173,469,540 | false | 21 | null | 6,495,304 | null | false | [] | null | 6,611 | {
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "The forest plot will include all studies investigated, regardless of their outcomes, analysed to determine the standardised mean difference, represented as the diamond in the bottom right of the image",
"id": "33057",
"label": "e",
"name": "Only the Auckland study showed significance, and so the other studies' results can be discounted",
"picture": null,
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"answer": false,
"explanation": "The 95% confidence intervals, represented as the horizontal edges of the summary measure diamond, do not overlap with the odds ratio of 1 and therefore, there is a significant effect of corticosteroids on neonatal mortality (mean odds ratio 0.53)",
"id": "33054",
"label": "b",
"name": "There is no significant effect of corticosteroids on neonatal mortality",
"picture": null,
"votes": 408
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"explanation": "The heterogeneity, or I squared, is often used in forest plots, but it is not shown in the data set here. Heterogeneity is the degree to which data from multiple studies displaying the same effect overlap each other. The more heterogeneous the studies are within the met-analysis, the less conclusive the data is",
"id": "33056",
"label": "d",
"name": "The heterogeneity of the study is 0.53",
"picture": null,
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"explanation": "The summary measure of the meta-analysis is portrayed as a diamond, with the vertical points lying on the mean effect and the horizontal points measuring the confidence intervals",
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"name": "The width of the diamond corresponds to the 95% confidence interval of the summary measure",
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"explanation": "The area of the squares correspond to the proportional study's weight in the meta-analysis and is unrelated to the p-value",
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"name": "The area of the square corresponds inversely to the study's p-value",
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"question": "The following diagram is a forest plot from a systematic review by Crowley et al. showing the results of seven studies looking at the effect of corticosteroids on hastening neonatal lung development when given to women about to give birth prematurely.\n\n[lightgallery]\n\nWhich of the following statements is correct?",
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173,469,541 | false | 22 | null | 6,495,304 | null | false | [] | null | 6,612 | {
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"explanation": "Positive predictive value is the chance that the patient has the condition if the test is positive. This corresponds to true positive/(true positive + false positive) = 600/(600+60) = 90.9%",
"id": "33062",
"label": "e",
"name": "67.4%",
"picture": null,
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"explanation": "This value corresponds to sensitivity - the proportion of patients with the condition who have a positive test result. This is calculated as the true positive/(true positive + false negative) = 600/(600+50) = 92.3%",
"id": "33059",
"label": "b",
"name": "92.3%",
"picture": null,
"votes": 628
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"answer": false,
"explanation": "This value corresponds to the specificity - the proportion of patients without the condition with a negative test result. This is calculated as the true negative/(true negative + false positive) = 290 / (290+60) =82.9%",
"id": "33060",
"label": "c",
"name": "82.9%",
"picture": null,
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"explanation": "Splitting the table up into true positive (600), false positive (60), false negative (50), and true negative (290) can make answering these tables easier to understand. Positive predictive value is the chance that the patient has the condition if the test is positive. This corresponds to true positive/(true positive + false positive) = 600/(600+60) = 90.9%",
"id": "33058",
"label": "a",
"name": "90.9%",
"picture": null,
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"__typename": "QuestionChoice",
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"explanation": "This value corresponds to the negative predictive value - the chance that the patient does not have the condition if the test is negative. This is calculated as the true negative/(true negative + false negative) = 290/(290+50) = 85.3%",
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"label": "d",
"name": "85.3%",
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"explanation": "# Overview \n\nSeveral key parameters can be calculated to help describe how effective a certain test is at diagnosing a condition.\n\n| | Patients with colon cancer | No cancer |\n| ------------------ | :------------------------: | --------: |\n| Biomarker positive | a | b |\n| Biomarker negative | c | d |\n\n# Sensitivity\n\nSensitivity is the proportion of people with the condition who will have a positive result. If, for example, the sensitivity of a test is 80%, out of a hundred people with the condition, only 80 will have a positive test result.\n\nSensitivity = a/(a+c)\n\n# Specificity\n\nSpecificity describes the proportion of people without the disease who will have a negative test. A specificity of 90% can be interpreted as, out of 100 people without the disease, 90 will have a negative test result.\n\nSpecificity = d/(b+d)\n\n# Positive Predictive Value\n\nPositive predictive value (PPV) is the proportion of people with a positive test who actually have the disease. PPV varies with prevalence of disease in a population. The lower the prevalence, the lower the positive predictive value. A PPV of 78% will mean that if 100 people tested positive, 78 people will have the disease.\n\nPPV = a/(a+b)\n\n# Negative Predictive Value\n\nNegative predictive value (NPV) is the proportion of people with a negative test who truly do not have the disease.\n\nNPV varies with prevalence of disease in a population. The lower the prevalence, the higher the negative predictive value. An NPV of 97% will mean that if 100 people tested negative, 97 people will not have the disease.\n\nNPV = d/(c+d)\n\n# False positive rate\n\nThe false positive rate is the proportion of those without the condition who will test positive.\n\nFalse positive rate = 1 - specificity\n\nFalse negative rate = 1 - d/(b+d)\n\n# False negative rate\n\nThe false negative rate is the proportion of those with the condition who will test negative.\n\nFalse negative rate = 1 - sensitivity\n\nFalse negative rate = 1 - a/(a+c)\n",
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"question": "A new blood test to help diagnose acute myocardial infarction (MI) has been developed. It is tested on 1000 individuals with suspected myocardial infarction in the emergency department :\n\n| | MI present | MI absent |\n| ----------------- | ---------- | --------- |\n| **Test positive** | 600 | 60 |\n| **Test negative** | 50 | 290 |\n\nWhat is the positive predictive value of the new test?",
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"explanation": "An indirect Coombs test can be used to determine whether there are antibodies to the Rhesus factor in the mother's blood and therefore whether she has been \"sensitised\". A positive Coombs test indicates whether a Rh-positive foetus has the possibility of being harmed from rhesus D alloimmunisation. In this case, a sensitisation event has occurred in a miscarriage >12 weeks, and so anti-D must be given regardless",
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"explanation": "A Kleihauer test measures the amount of foetal haemoglobin transferred from a foetus to a mother's bloodstream following exposure to a sensitising event from a RhD positive baby. It is conducted on all RhD negative women who have delivered a RhD positive baby, in pregnant women who have had a potentially sensitising event at >20 weeks gestation, and on all pregnant women who have had an invasive procedure. The test helps with dosing Anti-D immunoglobulin. In this case, however, a sensitisation event has occurred in a miscarriage >12 weeks, and so anti-D must be given regardless",
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"explanation": "Anti-D is given regardless of the biological father's rhesus status",
"id": "33105",
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"name": "Anti-D only required if the biological father is rhesus positive",
"picture": null,
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"explanation": "In pregnancies between 12 and 20 weeks gestation, anti-D immunoglobulin should be given in any sensitising event such as miscarriage, even if managed medically. No tests are required prior to administration",
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"name": "Give anti-D immunoglobulin within 72hrs",
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"id": "33104",
"label": "b",
"name": "No need for anti-D immunoglobulin",
"picture": null,
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"explanation": "# Overview\n\nThe D antigen is found on red blood cells and is an important antigen in the rhesus factor system.\n\nRhesus isoimmunisation can occur when a rhesus negative mother has a baby which is rhesus positive. If any foetal red blood cells enter the maternal circulation, the mother will form anti-D antibodies against them.\n\nThe maternal anti-D antibodies can cross the placenta in subsequent pregnancies and cause Rhesus haemolytic disease if the future baby is rhesus positive.\n\n# Sensitisation events\n\n“Sensitisation” events are events which cause foetal blood to cross the placenta into the maternal circulation and thus these are indications for anti-D prophylaxis.\n\nExamples of sensitisation events include:\n\n- Antepartum haemorrhage\n- Placental abruption\n- Abdominal trauma\n- External cephalic version\n- Invasive uterine procedures such as amniocentesis and chorionic villus sampling\n- Rhesus positive blood transfusion to a rhesus negative woman\n- Intrauterine death, miscarriage or termination\n- Ectopic pregnancy\n- Delivery (normal, instrumental or caesarean section)\n\n# Testing\n\nAll mothers should be tested for rhesus status and anti-D antibodies at booking\n\n# Management of the Rh-D negative mother\n\nPresence of anti-D antibodies can result in incompatibility and haemolysis in future pregnancies. To attenuate this risk, anti-D antibodies are given to patients who have experienced a sensitising event. Anti-D is also given to all non-sensitised Rhesus negative mothers at 28 weeks. Note that anti-D has no effect once sensitisation has already occurred (it is prophylactic only).",
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"explanation": "Following basic resuscitation measures, IV or IM ergometrine is given 2nd line for postpartum haemorrhage if IV syntocinon is unsuccessful or contraindicated",
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"explanation": "This woman is experiencing significant postpartum haemorrhage, most likely due to uterine atony. After standard resuscitation measures and bimanual uterine compression, the next step is to give IV syntocinon (oxytocin) to induce uterine contractions",
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"explanation": "Selective arterial embolisation is reserved for uncontrolled postpartum haemorrhage despite physical and pharmacological measures. Embolising the artery under radiological guidance reduces the blood supply to the uterus and, therefore capacity to bleed. Conservative measures such as IV syntocinon should be imitated first in this case",
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"explanation": "# Summary\n\nPostpartum haemorrhage (PPH) is defined as the loss of at least 500ml of blood within the first 24 hours of delivery. The primary causes are uterine atony, birth canal injury or tear, retained placental or foetal tissue, and coagulopathies. Risk factors include a previous PPH, high BMI, multiple pregnancies, advanced maternal age, and more. Initial management involves resuscitation with an ABCDE approach and potentially activating a major haemorrhage protocol. Further management strategies may include rubbing the uterus, medication, or surgical treatment. Secondary PPH refers to bleeding from 24 hours to 12 weeks postpartum, typically caused by retained products of conception or endometritis. \n\n\n# Definition\n\n\n\nPostpartum haemorrhage (PPH) is defined as the loss of at least 500ml of blood within the first 24 hours of delivery.\n\n\n# Aetiology\n\n\nThe aetiology of postpartum haemorrhage (PPH) can be remembered using the mnemonic of the 4 'T's: \n\n- Tone: The most common cause of PPH is uterine atony, which is the failure of the uterus to contract after delivery.\n\n- Trauma: PPH can result from a birth canal injury or tear, with risk increased in instrumented deliveries.\n\n- Tissue: Retained placental or foetal tissue can cause continued bleeding.\n\n- Thrombin: Coagulopathies can lead to continued bleeding due to a failure of clotting.\n\n# Risk Factors\n\nRisk factors for postpartum haemorrhage (PPH) include:\n\n- PPH in previous pregnancy\n- BMI >35\n- Multiple pregnancy\n- Parity >4\n- Conditions such as placenta praevia or accreta, placental abruption, pre-eclampsia, gestational hypertension or anaemia\n- Delivery via Caesarean section\n- Induction of labour\n- Instrumented delivery (forceps or ventouse) and episiotomy\n- Prolonged labour (greater than 12 hours)\n- Macrosomia (>4kg baby)\n- Advanced maternal age\n\n\n# Investigations\n\n\nInvestigations for PPH include blood tests for Group/Save and Crossmatch, and consideration of fresh frozen plasma if clotting abnormalities are present. In cases of secondary PPH, ultrasound looking for retained products and endocervical/high vaginal swabs looking for infection are recommended.\n\n# Management\n\n\nInitial management of PPH involves:\n\n- Resuscitation with an ABCDE approach\n- Consideration of activation of a major haemorrhage protocol\n- Laying the woman flat \n- Inserting two large bore cannulas\n- Providing oxygen\n- Considering fresh frozen plasma if clotting abnormalities are present\n\nFurther management strategies may include:\n\n- Mechanical methods such as rubbing the uterus and catheterisation\n- Medical treatments including oxytocin, syntocinon, ergometrine, carboprost, misoprostol, and tranexamic acid\n- Surgical treatments such as intrauterine balloon tamponade, B-lynch suture around the uterus, uterine artery ligation, or hysterectomy \n\nFor secondary PPH, management depends on the cause and can include surgical evacuation for retained products of conception or antibiotics for infection.\n",
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"question": "A 29-year-old primigravida woman has delivered a healthy baby via vaginal delivery. The placenta was intact on delivery, and there were no initial complications. Unfortunately, the mother continues to bleed following delivery and has now lost 1.1L. Bimanual uterine compression is conducted and the mother is catheterised to empty the bladder. Despite this, she continues to haemorrhage and you begin transfusing blood.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "The x-ray shows reduced joint space, osteophytes at the joint margin, and subchondral sclerosis. The joint space is severely narrowed, and the bones are osteopenic, although there is no fracture demonstrated in the image. This makes osteoarthritis of the hip without associated fracture the most likely diagnosis. The patient can be reassured that the pain from the fall should subside with analgesia over the next 2-4 weeks. Given the severe osteoarthritis, however, this patient should be referred to orthopaedics if her pain continues to not be controlled by analgesia and self-management strategies",
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"explanation": "Slipped upper femoral epiphysis is a relatively common condition, although it presents in adolescents due to widening of the growth plate during limb growth. It would therefore be unlikely in a fully grown adult. The x-ray findings show an intact femoral epiphysis",
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"explanation": "The x-ray shows reduced joint space, osteophytes at the joint margin, and subchondral sclerosis. There is severe joint narrowing at the superior aspect of the acetabulum, although there is no fracture present on the x-ray. Patient's with acetabular fractures would unlikely be able to fully weight bear or straight leg raise and so is less likely based on the clinical history",
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"explanation": "Septic arthritis may present similarly in the history, although the examination findings would likely be different. In septic arthritis, the joint is warm, swollen, and very tender. The patient would unlikely be able to weight bear or perform straight leg raise and may present as more clinically unwell",
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"explanation": "The x-ray shows reduced joint space, osteophytes at the joint margin, and subchondral sclerosis. The joint space is severely narrowed, and the bones are osteopenic, although there is no fracture demonstrated in the image. The patient can fully weight bear and perform straight leg raise, so hip fracture is unlikely",
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"explanation": "# Summary\n\nOsteoarthritis (OA) is a chronic, degenerative joint disease characterised by loss of articular cartilage, remodelling of bone with osteophyte formation and mild synovitis. The main risk factor is older age, although obesity, joint injury and genetics also contribute. Presentation is with gradual onset pain that is worse with activity, with associated functional limitations. The most commonly affected joints are the knees, hips and small joints of the hands. Diagnosis is clinical, and severity of disease on X-ray does not correlate well with severity of symptoms. Management should be individualised, with important components being exercise, simple analgesia and optimisation of risk factors (such as maintaining a healthy weight). Where there is ongoing pain and disability, options include intra-articular steroid injections and surgical intervention (such as joint replacement).\n\n# Definition\n\nOsteoarthritis (OA) is the commonest form of arthritis, which is characterised by degenerative changes affecting the entirety of joints affected. Cartilage is lost, the subchondral bone becomes sclerosed with formation of osteophytes and subchondral cysts and there is inflammation of the synovial membrane lining the joint capsule (synovitis). \n\n# Epidemiology\n\n- Approximately 10 million people in the UK have osteoarthritis\n- More women than men are affected\n- Average age of onset is 55 \n- The commonest joint affected is the knee, followed by the hip then the hand\n\n# Aetiology\n\nOsteoarthritis develops due to a combination of factors, with important contributors including:\n\n- Older age\n- Female sex\n- Overweight or obesity\n- Family history of OA\n- Previous joint injury\n- Joint damage due to inflammation (e.g. in patients with inflammatory arthritis)\n- Physical inactivity and reduced muscle strength\n- Low bone density \n- Deformities such as development dysplasia of the hip or leg length discrepancy\n- Stresses on joints due to occupational factors (e.g. repetitive squatting or kneeling) or exercise\n\n# Signs and Symptoms\n\nKey symptoms include:\n\n- Pain in the affected joint exacerbated by use\n- Pain may radiate e.g to the thigh, knee and ankle in hip OA, or to the wrist in hand OA\n- Joints may feel stiff (although prolonged morning stiffness is suggestive of inflammatory arthritis)\n- Functional limitations such as difficulty opening jars (hand OA) or mobilising (knee or hip OA)\n- Locking or giving way of the knee\n\nExamination findings include:\n\n- Restricted and painful range of motion (e.g. in hip OA internal rotation with the hip flexed is particularly painful)\n- Crepitus (friction between bone and cartilage) \n- Affected joints may appear swollen or enlarged\n- A small effusion may form, especially when the knee is affected\n- Synovitis may present with mild soft tissue swelling, tenderness and warmth\n- Muscle wasting and weakness can result from disuse atrophy\n- Joint instability\n- An antalgic gait (\"limping\") in knee OA\n- Trendelenburg gait in hip OA (due to weak abductors patients lurch towards the affected hip)\n- Deformities, including:\n- Heberden's nodes (bony nodules over the distal interphalangeal joints) \n- Bouchard's nodes (bony nodules over the proximal interphalangeal joints) \n- Fixed flexion of the first carpometacarpal joint with hyperextension of the distal joints\n- This may lead to squaring of the joint with subluxation and remodelling\n- Ulnar or radial deviation of joints in the hand may occur\n- In severe hip OA the leg may be shortened due to fixed flexion and external rotation\n- Varus (most commonly) or valgus deformities of the knees \n\n# Differential Diagnosis\n\n- **Inflammatory arthritis** such as rheumatoid arthritis, ankylosing spondylitis; pain that improves with activity and morning stiffness lasting over 30 minutes are differentiating factors, systemic symptoms such as malaise and weight loss may be present\n- **Septic arthritis** is an important differential for all patients presenting with an acutely painful swollen joint (which may occur in an acute flare of osteoarthritis); patients may be systemically unwell with fevers\n- **Fracture** e.g. of the tibial plateau may mimic OA symptoms of pain and limited mobility; usually the patient is unable to weight bear with swelling of the affected area; a history of trauma should be elicited\n- **Malignancy** including bone metastases, multiple myeloma or sarcoma may cause mechanical pain leading to functional limitations; red flags include weight loss, night sweats, persistent pain not relieved by rest and night pain\n- **Greater trochanteric pain syndrome** most commonly occurs in middle-aged women and causes lateral hip pain and tenderness worsened by activity; it may also radiate to the lateral knee\n- **Iliotibial band syndrome** presents with lateral knee pain worse with activity, which is often accompanied by clicking or clunking sounds when the knee is moved; occurs most commonly due to repetitive knee flexion e.g. cyclists or runners \n- **Meniscal tear** may occur after an injury involving a twisting or pivoting movement; similar symptoms of pain, swelling, locking and giving way of the knee and range of motion may be limited on examination\n- **Trigger thumb** may mimic OA of the hand with pain, clicking and catching when the thumb is flexed; a nodule may be palpable in the tendon\n- **Ganglion cysts** occur more commonly in people with OA and present as soft tissue swellings e.g. at the base of the thumb; often asymptomatic but may cause pain and limit movement of the joint\n\n# Investigations\n\nDiagnosis of OA is clinical and can be made without any investigations in a patient of 45 or older if there are no features suggesting another underlying cause of symptoms.\n\nIf there is diagnostic uncertainty or a rapid deterioration in symptoms, **X-rays** of affected joints may be of use. Typical findings can be remembered with the mnemonic \"LOSS\":\n\n- **L**oss or narrowing of joint space due to thinning of cartilage\n- **O**steophytes i.e. formation of new bony spurs at the joint margins\n- **S**ubchondral sclerosis i.e. increased bone density beneath the cartilage\n- **S**ubchondral cysts which are fluid-filled sacs in the subchondral bone\n\n[lightgallery]\n\nHowever, severity of OA features on X-ray may not correlate well with severity of clinical disease.\n\nOther investigations if the diagnosis is in doubt should be targeted to the differential suspected, and may include:\n\n- Further imaging such as MRI to look for ligament or cartilage damage (e.g. a meniscal tear)\n- Joint aspiration with synovial fluid analysis to exclude septic arthritis or crystal arthritis\n- Blood tests for inflammatory markers, rheumatoid factor and anti-CCP (for example) if rheumatoid arthritis is suspected\n\nBaseline bloods for renal function and full blood count should be considered in all patients starting NSAID treatment, especially older patients who are at higher risk of adverse effects.\n\n# Management\n\n**Conservative management:**\n\n- Patient education and advice on self-care e.g. appropriate footwear\n- Weight loss advice and signposting to services in patients with excess body weight\n- Exercise has many benefits including strengthening muscles, improving fitness, reducing pain and improving function\n- Options include online fitness programmes designed for people with arthritis, physiotherapy and supervised exercise sessions\n- Physiotherapy services may also be able to offer manual therapies and joint supports such as braces or splints to reduce load and improve instability\n- Occupational health input may be needed in patients with functional impairment to assess their working environment and suggest adaptations\n- Patients should be asked about psychosocial stressors and support offered e.g. for associated depression and anxiety\n- Occupational therapy input may be helpful to advise on aids and devices to assist with activities of daily living (e.g. walking sticks, sock aids, grab rails, tap turners)\n- Podiatry input may be useful to assess the biomechanics of joint pain and advise on orthotic devices such as insoles\n- Referral to a pain management service may be appropriate for patients who have not responded to maximal medical (and if appropriate, surgical) management of OA\n- Assess falls risk and consider referral to specialist services for patients at risk (e.g. those with abnormal gait or balance, or who have had a fall in the last year)\n\n**Medical management:**\n\n- First-line analgesia is with topical NSAIDs (such as ibuprofen gel) - patients should be made aware that some systemic absorption may occur\n- If this is ineffective or unsuitable, oral NSAIDs should be considered (with a PPI for gastroprotection if there are risk factors for gastrointestinal side effects)\n- Paracetamol or weak opioids (e.g. codeine) may also be used in the short-term\n- Topical capsaicin is another option, especially for knee OA\n- Intra-articular steroid injections may be considered if other treatments are not effective, and/or to enable therapeutic exercise\n\n**Surgical management:**\n\n- Patients with OA of the hip, knee or shoulder who have symptoms significantly impacting quality of life despite optimal medical management should be considered for orthopaedic referral\n- The usual operation offered is an arthroplasty (joint replacement)\n- Rehabilitation before and after surgery is key to optimising outcomes\n\n# Complications\n\n- Joint deformities (as above)\n- Increased risk of falls\n- Functional limitations, e.g. hand OA may making writing, turning keys or fasting buttons challenging\n- Reduced mobility \n- Sleep difficulties\n- Low mood and anxiety\n- Chronic pain\n\n# Prognosis\n\n- Not all cases of OA are progressive and the disease course is variable\n- OA of the hands generally has a good prognosis, especially interphalangeal joint involvement\n- Hip OA has a poorer prognosis with many patients requiring arthroplasty\n- Knee arthroplasties for OA are also common however many patients' symptoms improve or remain stable with time \n- Intermittent flares of OA may occur, where symptoms increase in intensity suddenly\n- Flares tend to last for a few days before improving\n\n# NICE Guidelines\n\n[NICE CKS - Osteoarthritis](https://cks.nice.org.uk/topics/osteoarthritis)\n\n[NICE - Osteoarthritis in over 16s: diagnosis and management](https://www.nice.org.uk/guidance/ng226/)\n\n# References\n\n[WHO fact sheet - Osteoarthritis](https://www.who.int/news-room/fact-sheets/detail/osteoarthritis)\n\n[BNF Treatment Summaries - Osteoarthritis](https://bnf.nice.org.uk/treatment-summaries/osteoarthritis/)\n\n[Patient UK - Osteoarthritis](https://patient.info/doctor/osteoarthritis-pro)",
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"question": "A 67-year-old woman has presented to the GP with worsening left hip pain after a fall from standing height 2 days earlier after tripping on the carpet. Prior to this, she has been experiencing 12 months of worsening bilateral groin pain. The pain is worse later in the day and on prolonged exertion.\n\nOn examination, she has a painful straight leg raise bilaterally but a full range of motion. She can walk unaided but with an antalgic gait on her left side.\n\nAn X-ray of her left hip is shown below.\n\n[lightgallery]\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "This patient will require admission and intravenous flucloxacillin, although ideally a knee aspiration should be done prior to starting antibiotics if possible, to provide the best chance of growth of any pathogens",
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"explanation": "This patient would warrant a knee x-ray given the examination findings, although it is not the first priority. A joint aspiration followed by intravenous antibiotics must be given first for possible septic arthritis",
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"explanation": "This patient may benefit from intravenous fluids as he is pyrexial and tachycardic with likely septic arthritis, although it is not the immediate priority. A joint aspiration followed by intravenous antibiotics must be given first",
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"explanation": "This patient has presented with an acute, hot, tender, swollen joint after a previous soft tissue injury around the knee. This raises concerns for septic arthritis. An urgent knee aspiration must be conducted, ideally prior to starting antibiotics. If there is an unavoidable delay in performing a knee aspiration or the patient is septic, then antibiotics can be given first",
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"comment": "how do we know he isn't septic?",
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"comment": "It's never too late to quit med and start something else",
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"comment": "surely since this guy has a history of trauma, although fracture etc is unlikely, you would want an X-ray before sticking a needle in the joint?",
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"explanation": "# Summary\n\nSeptic arthritis is an infection of the joint characterized by acute inflammation and swelling. It is caused by a bacterial or viral pathogen that infects the synovial fluid. The most commonly implicated organism is Staphylococcus aureus. Noteworthy clinical signs include a tender, swollen joint with reduced mobility, often accompanied by systemic illness. Key investigations include joint aspiration for Microscopy Culture and Sensitivity, along with blood tests showing increased white blood cell count and elevated ESR/CRP. Management typically involves IV antibiotics, joint washout under general anaesthesia, and physiotherapy once the acute infection has resolved.\n\n# Definition\n\nSeptic arthritis is an infection of the joint, specifically the synovial fluid. It is typically caused by a bacterial or viral pathogen and necessitates prompt medical intervention due to the high risk of joint damage and other severe complications.\n\n# Epidemiology\n\nSeptic arthritis has an annual incidence of 4-10 cases per 100,000 patients in Western Europe. It can affect individuals of any age, though certain populations are at a higher risk due to underlying conditions.\n\n# Aetiology\n\nThe most prevalent organism implicated in septic arthritis is Staphylococcus aureus. Other responsible organisms include:\n\n- Gonococcus: primarily in sexually active individuals\n- Streptococcus spp.\n- Gram-negative bacilli\n\nRisk factors contributing to septic arthritis include:\n\n- Pre-existing joint diseases such as rheumatoid arthritis\n- Chronic kidney disease\n- Immunosuppressive states\n- Presence of prosthetic joints\n\n# Signs and Symptoms\n\nThe clinical presentation of septic arthritis usually involves:\n\n- Acute onset of tender, swollen joint\n- Reduced range of joint movement\n- Systemic symptoms such as fever, malaise, or chills\n\n# Differential Diagnosis\n\nDifferential diagnoses for septic arthritis include:\n\n- Gout and pseudogout: characterized by intense joint pain, redness, and swelling, often in the big toe or knee.\n- Osteoarthritis: presents with joint pain, stiffness, and sometimes swelling, generally improving with movement.\n- Rheumatoid arthritis: marked by joint pain, swelling, and stiffness, often symmetrical and worse after rest.\n- Lyme disease: may show erythema migrans rash, flu-like symptoms, and possibly migratory joint pains.\n\n# Investigations\n\nDiagnostic investigations for septic arthritis include:\n\n- Joint aspiration for Microscopy, Culture, and Sensitivity: The aspirate usually appears turbid and yellow, resembling pus.\n- Blood tests: elevated white cell count, high ESR/CRP\n- Blood cultures: to identify causative organisms\n- Imaging: X-ray of the joint may be performed to evaluate for osteomyelitis or other complications.\n\n# Management\n\nThe treatment of septic arthritis involves:\n\n- IV antibiotics guided by local antibiograms and susceptibilities\n- Consideration of joint washout under general anaesthesia to remove infected material\n- Physiotherapy following the resolution of acute infection to restore joint function\n\nComplications of septic arthritis can include:\n\n- Osteomyelitis: infection of the bone\n- Chronic arthritis: persistent joint inflammation\n- Ankylosis: joint fusion resulting in immobility\n\n# References\n\n[Click here for the BNF Treatment Summary for Musculoskeletal infections](https://bnf.nice.org.uk/treatment-summary/musculoskeletal-system-infections-antibacterial-therapy.html)\n\n[Click here for the BMJ Best Practice Summary of Septic Arthritis](https://bestpractice.bmj.com/topics/en-us/486)",
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"question": "A 65-year-old man has presented with 24 hours of worsening painful swelling of his right knee. He recently fell onto his right side while cycling 3 days earlier, sustaining some grazes on his right leg but no other acute injuries. He has type 2 diabetes but no other medical problems.\n\nOn examination, he is pyrexial and tachycardic. His right knee is hot to touch, erythematous, and markedly swollen. There is a reduced range of motion and he is not able to weight bear.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "A health and social care assessment assesses what help and support can be provided at home, such as disability equipment and adaptations to the home, organising respite, and arrangements for parenting classes. In this case, there is no information suggesting they require functional adaptations to their home. Parent training is usually focused on children younger than 11 years old and so would unlikely be suggested in this scenario",
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"explanation": "In parent training programmes, parenting skills are improved by using modelling, rehearsing, and feedback. Parent training is usually focused on children younger than 11 years old and so would unlikely be suggested in this scenario",
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"explanation": "This would be appropriate if the child had a co-existing mental health problem, a neurodevelopmental condition, or learning disability, or if there was any indication of underlying mental health disorder",
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"explanation": "Methylphenidate is not recommended in conduct disorder but is occasionally used in attention deficit hyperactive disorder (ADHD) to control challenging behaviour",
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"explanation": "This child is exhibiting behaviour typical of conduct disorder. Child-focused programmes are usually offered to children aged 9-14 with conduct disorder, involving group social and cognitive behavioural problem-solving exercises with rehearsal and feedback to improve behaviour",
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"comment": "Patient.info \"Community-based help\nIf the behavioural problems are severe and persistent or a conduct disorder is suspected, ask your GP for advice.\n\nAntisocial behaviours are commonly seen in specialist services. If specialist help is needed, the GP will make a referral to your local child and adolescent mental health service (CAMHS). This specialist team will work together with you, the school and other community groups to support you and your child.\"",
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"comment": "I'm also sure that a lot of oppositional defiant disorders (<18y/o) are co-morbid with mood/mental health disorders ",
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"explanation": "# Summary\n \nConduct disorder is a diagnosis characterised by persistent behaviour in patients under 18 that repeatedly violates the rights of others and demonstrates a disregard for societal norms. Key signs include demonstration of physical aggression, destructive behaviour, and stealing. Primary investigations into conduct disorder often involve psycho-social assessments and physical examinations to rule out potential differential diagnoses such as Oppositional Defiant Disorder (ODD) or Attention-Deficit/Hyperactivity Disorder (ADHD). Management strategies typically involve a combination of psychotherapy, family therapy, and in some cases, pharmacological treatments.\n \n\n# Definition\n \nConduct disorder is a psychological diagnosis given to patients under the age of 18 years old who consistently exhibit behaviours and attitudes that disrespect and violate the rights of others, often breaching societal norms and rules, and interfering with the patient's ability to live a normal life. \n \n\n# Epidemiology\n \nWhile the prevalence rates can vary, conduct disorder is found in 4.6% of 5-19-year-olds in England according to an NHS survey in 2017. Higher rates were observed in boys (5.8%) compared to girls (3.4%). It is most common in those ages 11-16 and is less common to onset after age 16. It is also more common amongst white British compared to Black/Black British or Asian/Asian British populations. \n\nThe disorder is more common in urban areas and among families with lower socioeconomic status. Looked after children in foster care or children's homes show higher rates of conduct disorder. \n\n\n# Aetiology\n \nThe aetiology of conduct disorder is multifactorial, involving a complex interplay of genetic, environmental, and psychological factors. These can include a family history of mental health disorders, childhood maltreatment or neglect, peer influence, and underlying neurological abnormalities. \n \n\n# Signs and Symptoms\n \n\nThe key clinical manifestations of conduct disorder are:\n \n\n - Persistent and serious violation of rules, societal norms, and the rights of others\n - Physical aggression directed towards people and animals\n - Destructive behaviour, such as arson or vandalism\n - Deceitfulness or theft\n - Serious violation of rules, such as truancy or running away from home\n \n\n# Differential Diagnosis\n \n\nIn evaluating conduct disorder, several other disorders should be considered, including:\n \n\n - **Oppositional Defiant Disorder (ODD)**: Presents with angry and irritable mood, argumentative and defiant behaviour, but usually lacks the severe aggression, violation of societal norms, and respect for the rights of others seen in conduct disorder.\n - **Attention-Deficit/Hyperactivity Disorder (ADHD)**: Characterised by a persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development. This can be distinguished from conduct disorder by the absence of consistent antisocial behaviours.\n - **Mood Disorders**: Depressive and bipolar disorders can sometimes be associated with disruptive behaviours. However, in these conditions, mood symptoms predominate and there is usually no persistent pattern of violation of the rights of others.\n \n\n# Investigations\n \n\nInvestigations for conduct disorder primarily involve psycho-social assessments by CAMHS, which include:\n \n\n - Interviews with the child and parents to gather a comprehensive developmental, familial, and social history\n - Observations of the child’s behaviour in various settings\n - Use of standardised assessment tools and questionnaires (Strengths and Difficulties Questionnaire) \n - Physical examination and other tests to rule out medical conditions that could contribute to the behaviour\n \n\n# Management\n \n\nManagement strategies for conduct disorder may include:\n \n\n - **Psychotherapy**: Cognitive-behavioral therapy (CBT) can be effective in helping the child to control their anger and improve their problem-solving skills.\n - **Family therapy**: This can help improve family interactions and communication, which in turn can reduce symptoms of conduct disorder. \n - **Parent training programmes**: Use modelling, rehearsal and feedback to improve parenting skills. \n - **Pharmacological treatments**: Not used first line, but in some cases medications may be used to manage comorbid conditions or specific problematic behaviours, such as impulsivity, aggression, or mood symptoms.\n - **School-based interventions**: These may also be beneficial in promoting positive behaviours and reducing disruptive behaviours.\n \n\n# Prognosis\n \n\nThe prognosis of conduct disorder is generally poor:\n \n\n - Around 50% of children with conduct disorder develop antisocial personality disorder\n - Around 50% develop substance misuse issues\n - Around 40% become recurring young offenders\n\nYounger age of behavioural problems increases the risk of the patient becoming involved with crime. \n \n \n# NICE Guidelines\n \n [NICE Guideline on Antisocial behaviour and Conduct Disorders in children and Young People: recognition and Management](https://www.nice.org.uk/guidance/cg158) \n \n\n# References\n \n[Royal College of Psychiatrists \" Behavioural problems and conduct disorder\"](https://www.rcpsych.ac.uk/mental-health/parents-and-young-people/information-for-parents-and-carers/behavioural-problems-and-conduct-disorder-for-parents)\n\n [Information on Conduct Disorder](https://patient.info/childrens-health/behavioural-problems-and-conduct-disorder)\n \n [WHO Conduct Disorder](https://applications.emro.who.int/docs/EMRPUB_leaflet_2019_mnh_217_en.pdf)",
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"question": "A 12-year-old boy is brought to the GP by his father for 12 months of recurrent vandalism, frequent theft of other children's property, repeated episodes of lying to his teachers, and has started smoking. His son does not feel his behaviour is problematic. He often becomes \"uncontrollable\" at home breaking dishes and furniture with no guilt or remorse in harming others.\n\nHe has no history of mental health problems and there is no indication of an underlying mental health disorder. He does not have any developmental disorders or learning disabilities.\n\nWhich of the following is the most appropriate next management step?",
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"explanation": "This child is experiencing symptoms of croup with stridor and signs of increased respiratory effort. This is managed with a single dose of oral dexamethasone 0.15mg/kg immediately with consideration of admission to hospital, depending on their risk factors",
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"explanation": "Nebulised salbutamol can be given in acute stridor, although in croup it would unlikely reverse the upper airway narrowing as it does not contain smooth muscle",
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"name": "Give nebulised salbutamol",
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"explanation": "Due to the association of aspirin with Reye's syndrome in children, it is very rarely given",
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"explanation": "Nebulised adrenaline can be given for temporary improvement of symptoms with upper airway obstruction in croup, although it is not the _next_ best management option. Oral steroids should be given first here unless the child is critically unwell",
"id": "33147",
"label": "e",
"name": "Give nebulised adrenaline",
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"explanation": "This child has symptoms of croup - a viral infection most commonly associated with parainfluenza virus. Antibiotics would therefore not be indicated unless there was suspicion of superadded bacterial pneumonia",
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"comment": "Just a random q: Why is it not IV steroids I know it's a GP setting, but wouldn't the IV in a hospital have a faster onset and therefore be more effective?",
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"comment": "Getting IV access in a 9 month old would realistically be a job for the paediatrician and even then, probably not faster than just giving an oral dose",
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"explanation": "# Summary\n \n\nCroup (also known as acute laryngotracheobronchitis) is a common childhood infection characterised by a harsh barking cough and inspiratory stridor. It is usually mild and self-limiting, however, some cases may cause severe respiratory distress requiring hospitalisation and supportive treatment. Parainfluenza viruses are the commonest causes, but the diagnosis is a clinical one and as symptoms such as stridor can worsen if the child is distressed, investigations should only be done if necessary. Oral steroids should be given to all children; in moderate to severe cases nebulised adrenaline, supplementary oxygen and airway support may be indicated.\n \n\n# Definition\n \n\nCroup, or acute laryngotracheobronchitis, is an upper respiratory tract infection that in most cases has a viral aetiology. Key symptoms include a barking cough, hoarse voice and inspiratory stridor. \n\n# Epidemiology\n \n\nCroup commonly affects children aged from 6 months old to 3 years old, with the peak incidence at 2 years. It is uncommon after the age of 6.\n\nSimilar to other viral infections, it is commonest in the autumn and winter months and is linked to parainfluenza epidemics. \n\n# Aetiology\n \nThe commonest cause is the parainfluenza virus. Other viral causes include adenovirus, respiratory syncytial virus (RSV), rhinovirus and influenza.\nRarely, bacteria can cause croup (e.g. Mycoplasma pneumoniae).\n\nThe pathophysiology involves infection and resulting inflammation of the subglottic and laryngeal mucosa which causes partial obstruction of the airways leading to respiratory distress and stridor.\n\n# Signs and Symptoms\n\n- The prodromal phase of coryzal symptoms, fever and a non-specific cough usually lasts 12-72 hours.\n- Characteristic symptoms of croup such as the harsh barking cough, hoarse voice or cry and inspiratory stridor then develop - these tend to be worse at night.\n- In severe cases, children may become drowsy and lethargic, or conversely more agitated.\n- The usual course of disease is resolution of symptoms within 48 hours (up to a week at most).\n\nOn examination, look for the following red flags that may indicate impending respiratory failure:\n\n- Signs of respiratory distress e.g. intercostal recessions, accessory muscle usage, tachypnoea\n- Cyanosis\n- Decreased level of consciousness\n- Stridor may decrease due to worsening airway obstruction\n- Decreased air entry on auscultation of the chest\n- Tachycardia\n\n# Differential Diagnosis\n \n\n- **Epiglottitis**: Sudden onset high fever, drooling, and dysphagia are seen without the barking cough of croup. Usually secondary to Haemophilus influenzae B and so significantly rarer since routine immunisation against this.\n- **Bacterial tracheitis**: Suspect if acute deterioration following initial viral symptoms, with high fevers, stridor and respiratory distress.\n- **Foreign body aspiration**: No prodrome or fever, usually sudden onset of choking, cough or wheeze after eating or playing with small objects.\n- **Anaphylaxis**: Rapid onset stridor, possible urticarial rash and facial swelling; suspect if history of previous episodes with allergens or family history of atopy.\n \n\n# Investigations\n \nDiagnosis is clinical, and investigations need to be carefully considered as distressing the child may lead to worsening of symptoms due to agitation.\n\nFurther investigation may include: \n\n- Pulse oximetry should be done to determine if supplementary oxygen is required.\n- Chest X-ray may be of use if a differential diagnosis such as an inhaled foreign body is suspected. \n - In croup, an X-ray may show a steeple sign, where the upper trachea is seen to taper.\n \n\n# Management\n\nClassifying the severity of croup is key to determining appropriate management:\n\n| Severity | Description |\n|------------------------------|---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|\n| Mild | Seal-like barking cough but no stridor or sternal/intercostal recession at rest. |\n| Moderate | Seal-like barking cough with stridor and sternal recession at rest; no (or little) agitation or lethargy. |\n| Severe | Seal-like barking cough with stridor and sternal/intercostal recession associated with agitation or lethargy. |\n| Impending respiratory failure | Minimal barking cough, stridor may become harder to hear. Increasing upper airway obstruction, sternal/intercostal recession, asynchronous chest wall and abdominal movement, fatigue, pallor or cyanosis, decreased level of consciousness or tachycardia. The degree of chest wall recession may diminish with the onset of respiratory failure as the child tires. A respiratory rate of over 70 breaths/minute is also indicative of severe respiratory distress. |\n\nMild cases with no stridor or chest wall recessions at rest may be treated at home with a single dose of oral dexamethasone (0.15mg/kg). In children treated at home, families should be safety-netted on signs of deterioration and advised to check on the child regularly and encourage fluids. Paracetamol or ibuprofen can be used for fever and pain.\n\nChildren with any of the following should be considered for hospital admission:\n\n* Stridor and/or sternal recession at rest\n* High fever\n* Respiratory rate > 60\n* Cyanosis\n* Lethargy or agitation\n* Fluid intake < 75% of normal or no wet nappies for 12 hours\n* Aged under 3 months\n* Chronic conditions such as immunodeficiency, chronic lung disease or neuromuscular disorders\n\nManagement is supportive as there is no treatment indicated for the usual causative viruses, and may include:\n\n- Supplementary oxygen if low saturations - consider how best to deliver this so as not to distress the child (e.g. a parent holding an oxygen mask to the face)\n- Steroids for all - if unable to swallow oral dexamethasone or prednisolone can give nebulised budesonide\n- Nebulised adrenaline for temporary symptom relief\n- Anaesthetics +/- ENT input if concerns regarding airway or respiratory failure\n\n# Complications\n\n- Dehydration secondary to poor fluid intake during illness\n- Pneumonia due to secondary bacterial infection \n- Respiratory failure \n- Death is very rare (1 in every 30,000 cases)\n\n# Prognosis\n\nUsually, symptoms resolve within 48 hours but may last longer. Occasionally, severe upper airway obstruction can occur, causing respiratory failure and arrest.\n\n# NICE Guidelines\n\n[NICE CKS: Croup](https://cks.nice.org.uk/topics/croup/)\n\n# References\n \n[BNF Treatment summaries: Croup](https://bnf.nice.org.uk/treatment-summaries/croup/)\n\n[Patient.info: Croup](https://patient.info/doctor/croup-pro)",
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"question": "A 9-month-old child is brought to the GP with two days of pyrexia and worsening barking cough, worse at night time. She has prominent inspiratory high-pitched wheeze with mild intercostal recession at rest. There is no sialorrhoea and her oral mucosa is unremarkable.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "This child has acute otitis media, which would be managed with reassurance and analgesia in the well child. As they are on immunosuppressants, they should be prescribed oral antibiotics unless unwell, where it can be escalated to intravenous antibiotics and admission",
"id": "33150",
"label": "c",
"name": "Analgesia and reassurance",
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"explanation": "This child is on immunosuppressants but is systemically well at present with only one previous episode of acute otitis media. A child should be referred to the local emergency department if unwell or have systemic complications of acute otitis media such as meningitis, mastoiditis, intracranial abscess sinus thrombosis, or facial nerve paralysis. A child can be referred to ENT if they have recurrent unexplained episodes or they have a craniofacial abnormality. In this case, she can be managed with oral antibiotics alone",
"id": "33152",
"label": "e",
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"explanation": "This child has presented with acute otitis media. It is very common in children and is often managed conservatively without antibiotics. Antibiotics should be prescribed if the symptoms last >4 days, they are systemically unwell, are immunocompromised, or have evidence of tympanic perforation. This child is well but on immunosuppression and so oral antibiotics should suffice with good safety netting",
"id": "33148",
"label": "a",
"name": "Oral antibiotics",
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"explanation": "Back-up antibiotics can be given to children whose signs of infection do not resolve within 3 days or worsen significantly or rapidly at any time. As this child is on immunosuppressants, they should receive antibiotics immediately",
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"label": "d",
"name": "Prescribe a back-up antibiotics prescription to take if not improving after three days",
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"__typename": "QuestionChoice",
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"explanation": "While this patient is on immunosuppressants, they are systemically well with acute otitis media. This will require oral antibiotics at present, but should have a low threshold for admission and intravenous antibiotics if not resolving in the community",
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"name": "Admit for intravenous antibiotics",
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"comment": "Also because the child is 2 years old right?",
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"comment": "I thought this was malignant otitis externa ",
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"comment": "Bulging of the tympanic membrane is better explained by otitis media. Typical signs of otitis external are not present eg. swollen eczematous canal etc ",
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"explanation": "# Summary\n \n\nAcute otitis media is a common infection resulting in inflammation of the middle ear. It typically presents with rapid onset of symptoms such as ear pain, fever, irritability, and vomiting. Key investigations include physical examination of the tympanic membrane and assessing systemic illness. Management primarily consists of pain and fever relief, with antibiotics reserved for severe cases or those at high risk of complications. Possible complications can be intracranial or extracranial and may be life-threatening.\n \n\n# Definition\n \n\nAcute otitis media (AOM) is inflammation of the middle ear with an associated effusion. It can be due to bacterial or viral infections. \n \n\n# Epidemiology\n \n\nAcute otitis media is a common condition, particularly among young children, often occurring after a viral upper respiratory tract infection. It affects 70% of children before the age of 2 years, peaking between ages 6-15 months before reducing as the child grows older. It affects boys slightly more than girls. \n \n\n# Aetiology\n\nAcute otitis media is common in children because the less acute angle between the Eustachian tube and the wall of the pharynx enables organisms in the nasopharynx to enter the ear. \n\nThe primary cause of otitis media is bacterial infection, especially prevalent in young children. The most common causative pathogens include: \n\n- Streptococcus pneumoniae \n- Haemophilus influenzae\n- Moraxella catarrhalis \n\nViral causes are less common but normally precede AOM (i.e. respiratory syncytial virus, adenovirus, enterovirus)\n\nRisk factors include:\n\n- Age below 2 years\n- Male sex\n- Parental smoking\n- Immunodeficiency \n- Formula feeding \n- Attendance at nursery or daycare\n- Structural abnormalities (i.e. associated with Down's syndrome, presence of cochlear implants) \n\nRecurrence is more common in children with GORD or those who use dummies. \n \n\n# Signs and Symptoms\n \n\nAcute otitis media typically presents with a rapid onset of symptoms such as:\n \n\n - Earache \n - Ear tugging in younger children\n - Pain\n - Fever\n - Irritability\n - Anorexia\n - Vomiting\n \nOtoscopy may reveal:\n\n- Erythema of tympanic membrane \n- Presence of an effusion in the middle ear: air-fluid levels, bulging tympanic membrane\n- Evidence of perforation: tear in tympanic membrane or discharge \n \n\n [lightgallery]\n \nRed Flag symptoms to screen for (which may indicate intracranial spread):\n \n- Changes to vision \n- Photophobia or headache\n- Nystagmus \n- Post auricular swelling \n- Facial paralysis \n \n\n# Differential Diagnosis\n \n\nThe key signs and symptoms of the differential diagnoses of otitis media include:\n \n - **Chronic Benign Otitis Media**: Characterised by a dry tympanic membrane perforation without chronic infection.\n - **Otitis media with effusion (Glue Ear)**: Persistent presence of middle ear effusion without acute infective symptoms. \n - **Chronic Suppurative Otitis Media**: Persistent purulent drainage through the perforated tympanic membrane.\n - **Upper respiratory tract infection**: Symptoms include a runny nose, cough, and sore throat.\n - **Mastoiditis**: Symptoms include postauricular swelling, ear pain, fever, and irritability.\n - **Otitis externa**: Presents with ear pain, itching, discharge, and hearing loss. Associated with sloughy discharge within the ear canal.\n \n\n# Investigations\n \n\nInvestigations for otitis media primarily involve a physical examination of the tympanic membrane, assessing the presence of systemic illness, and evaluating the patient's symptoms.\n\nFurther investigations may include:\n\n- Culture of discharge in chronic or recurrent AOM\n- CT or MRI if concerns of mastoiditis or intracranial spread\n- Audiometry, following resolution of infection if chronic hearing loss secondary to AOM is suspected\n \n\n# Management\n \nAdmission should be considered for:\n \n - Children under 3 months with a temperature of 38 or more.\n - Children with suspected acute complications of otitis media such as meningitis, mastoiditis, or facial nerve palsy.\n - Children who are severely systemically unwell.\n\nImmediate antibiotics should be given if the child is systemically unwell, or at high risk of complications (e.g. immunocompromised patients). It may be considered if the child has otorrhoea or is aged < 2 years and has bilateral AOM.\n\n\n- Amoxicillin for 5-7 days is typically given as first line. \n - Clarithromycin is used if penicillin allergic. \n- If symptoms do not improve after 2-3 days of antibiotic, then co-amoxiclav may be considered.AOM\n\n\nIf immediate antibiotics are not required:\n \n - Maximise pain relief using paracetamol or ibuprofen.\n - A warm compress over the ear may help to relieve pain.\n - Eardrops containing an anaesthetic and analgesic (phenazone 40 mg/g with lidocaine 10 mg/g) may also be used if antibiotics are not given and there are no signs of eardrum perforation. \n - Parental/caregiver education:\n - Antibiotics make little difference to the duration of symptoms or complication rates associated with AOM.\n - Most children will not require antibiotics. \n - Antibiotics may also cause side effects of diarrhoea and nausea. \n- Consider a delayed antibiotic prescription to be taken if symptoms don't improve within 3 days.\n - Can be considered if the child has otorrhoea or is age <2 years and bilateral AOM.\n \nChildren can return to school once no longer febrile. \n \n\n# Complications of Otitis Media \n \n\nWhilst the majority of children recover without any acute or chronic complications, otitis media can lead to a wide range of complications, many of which are potentially life-threatening. These can be divided into intracranial and extra-cranial complications.\n \n\n**Extra-cranial Complications of Otitis Media**:\n \n - **Facial nerve palsy**: Acute otitis media can lead to a lower motor neuron lesion of the VII cranial nerve. Patients usually recover well with treatment of the otitis media.\n - **Mastoiditis**: Infection can spread from the middle ear to form an abscess in the mastoid air spaces of the temporal bone, leading to postauricular swelling and mastoid tenderness.\n - **Petrositis**: Infection spreading to the apex of the petrous temporal bone, leading to Gradenigo syndrome: otorrhoea, deep ear and eye pain, and ipsilateral VI nerve palsy.\n - **Labyrinthitis**: Inflammation of the middle ear can lead to inflammation of the semi-circular canals, leading to symptoms of vertigo, nausea, vomiting, and imbalance.\n \n\n**Intra-cranial Complications of Otitis Media**:\n \n - **Meningitis**: An important and life-threatening complication presenting with sepsis, headache, vomiting, photophobia, and phonophobia.\n - **Sigmoid sinus thrombosis**: Patients present with sepsis, swinging pyrexia, and meningitis.\n - **Brain abscess**: A patient will present with sepsis and neurological signs due to compression of cranial nerves.\n\n**Chronic complications may include**:\n\n- Hearing loss \n- Otitis media with effusions (\"glue ear\"):\n - If children are under the age of 3, a \"watch and wait\" approach can be taken initially.\n - If children are over the age of 3, or have developed associated language or behavioural problems, then referral to ENT for consideration of grommets would be appropriate. \n- Chronic suppurative otitis media\n - A persistent tympanic membrane perforation results in re-infection and chronic inflammation. It is often associated with conductive hearing loss. It is not commonly seen in the UK and is more common in the developing world.\n\n# Prognosis\n \nThe majority of children will not have severe complications from acute otitis media. 60% of children will have symptom resolution within 24 hours, with most symptom-free by 1 week. \n\n## Recurrent Acute Otitis Media\n\nChildren are considered to have recurrent otitis media if they have had more than 3 episodes of AOM in 6 months or more than 4 episodes in one year. This should prompt consideration of reducing risk factors (i.e. parental smoking, avoiding supine feeding and reducing use of dummies). These children may be referred to ENT for consideration of grommets or prophylactic antibiotics. \n\n# NICE Guidelines\n \n[NICE CKS on otitis media - acute](https://cks.nice.org.uk/topics/otitis-media-acute/)\n \n# References \n \n[NHS Inform Middle Ear Infections](https://www.nhsinform.scot/illnesses-and-conditions/ears-nose-and-throat/middle-ear-infection-otitis-media/) \n \n[Microbial Etiologies of Acute Otitis Media](https://www.clinicalmicrobiologyandinfection.com/article/S1198-743X(14)64948-X/fulltext)\n\n[Patient Info Acute Otitis Media in Children](https://patient.info/doctor/acute-otitis-media-in-children) \n\n[Patient Info Otitis Media with Effusion](https://patient.info/doctor/otitis-media-with-effusion)",
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"question": "A 2-year-old child presents with 2 days of right-sided otalgia and pyrexia. She is otherwise well and had a similar problem two weeks ago which initially self-resolved. She is currently taking immunosuppressants for a liver transplant she had as a neonate for extrahepatic biliary atresia. On otoscopy there is bulging of the tympanic membrane with surrounding erythema.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "Congenital rubella is a cause of early neonatal jaundice, with onset within less than 24 hrs, due to hepatic dysfunction by the rubella virus. This baby has presented with late jaundice and so this is less is unlikely",
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"explanation": "Biliary atresia is the obliteration or blockage of the extrahepatic biliary system. It presents as prolonged jaundice in the neonate, lasting longer than 14 days in infants and 21 days in preterm infants. It is characterised by jaundice >14 days, dark urine, pale stools, and poor appetite",
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"explanation": "Crigler-Najjar syndrome is a cause of early neonatal jaundice, with onset within less than 24 hrs, due to inborn errors in bilirubin metabolism. This baby has presented with late jaundice and so this is less is unlikely",
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"explanation": "G6PD is a cause of early neonatal jaundice, with onset within less than 24 hrs, due to haemolytic anaemia. This baby has presented with late jaundice and so G6PD is unlikely",
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"comment": "What's the mechanism for the hepatosplenomegaly?",
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"comment": "i think it's bc bile cannot flow out, so the 'traffic jam' results in hepatocellular damage. the congestion may result in increased resistance causing splenomegaly too (similar mechanism to how portal htn can cause splenomegaly?)",
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"comment": "but the jaundice has only been present 3 days??",
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"explanation": "# Summary\n \nBiliary atresia is a severe liver disorder in which the bile ducts of a newborn are progressively fibrosed and destroyed, leading to conjugated hyperbilirubinaemia, liver failure, and death if left untreated. Its key signs and symptoms include prolonged jaundice and indications of biliary obstruction, such as dark urine and chalky white stool. Diagnosis primarily involves a suite of tests, including blood work, hepatic scintigraphy, abdominal ultrasound, and cholangiography. The main treatment strategy is surgical intervention, namely, hepatoportoenterostomy or the Kasai procedure.\n \n\n# Definition\n \n \nBiliary atresia is a rare but serious condition where the bile ducts in a newborn's liver undergo progressive fibrosis and destruction. This leads to conjugated hyperbilirubinaemia, liver failure, and if not treated promptly, death.\n \n\n# Epidemiology\n \n\nThis condition predominantly affects newborns and is the most common cause of neonatal cholestasis. In the UK, it is estimated to affect 1 in 8,000-18,000 live births. Globally, it is the most common reason for paediatric liver transplants. \n \n\n# Aetiology\n \n\nThe cause of biliary atresia is unknown. It's believed to be likely due to a combination of genetic and environmental factors, potentially including an aberrant immune response to a viral infection affecting the bile ducts of the newborn.\n\n20% of affected patients have co-existing congenital anomalies. \n \n\n# Signs and Symptoms\n \n\nPatients with biliary atresia typically present with the following symptoms:\n \n\n - Prolonged jaundice (i.e. jaundice persisting beyond 14 days of life or 21 days if preterm)\n - Signs of biliary obstruction such as dark urine and pale or chalky white stool\n \n\n# Differential Diagnosis\n \n\nWhen examining a neonate with jaundice and symptoms suggestive of biliary obstruction, the differential diagnosis includes:\n \n\n - **Alagille syndrome**: Presents with neonatal jaundice, peripheral pulmonary artery stenosis, and characteristic facial features.\n - **Choledochal cyst**: Presents with the classic triad of abdominal pain, jaundice, and an abdominal mass.\n - **Neonatal hepatitis**: This condition also presents with jaundice, along with hepatomegaly and elevated liver enzymes.\n - **Inborn errors of metabolism**: Conditions such as galactosemia and tyrosinemia can present with jaundice, poor feeding, and developmental delay.\n \n\n# Investigations\n \n\nInvestigations for biliary atresia include:\n\n- Blood tests: These will typically show raised conjugated bilirubin and deranged liver function tests.\n - GGT is typically higher in biliary atresia than other causes of neonatal cholestasis\n- Hepatic scintigraphy (Technetium-99m scan): The liver will take up the isotope but there will be poor excretion into the bowel, indicating destroyed bile ducts.\n- Abdominal ultrasound: This may reveal echogenic fibrosis.\n- Cholangiography: This is the definitive diagnostic test, which will fail to show the normal architecture of the biliary tree, confirming biliary atresia.\n\nLiver histology by percutaneous biopsy is the gold standard. \n\nCurrently screening in the UK is not recommended for biliary atresia. \n \n\n# Management\n\n\nThe main management strategy for biliary atresia is surgical intervention:\n \n\n - Hepatoportoenterostomy (Kasai procedure): This surgery creates a new pathway from the liver to the gut to bypass the fibrosed bile ducts.\n - In severe cases where liver failure is advanced, transplantation may be required. \n\n# Complications\n \nComplications of biliary atresia include:\n \n - Ascending cholangitis following surgery \n - Cirrhosis, portal hypertension and liver failure \n - Osteomalacia or biliary rickets \n\n \n# Prognosis \n\nBiliary atresia prognosis is dependent on the levels of fibrosis and management given. Survival of the native liver is poor - with only 10% of adults having their native liver 30 years after the Kasai procedure, highlighting the role of liver transplant. \n \n\n# NICE Guidelines\n\n[NICE Clinical Knowledge Summary of Jaundice in the Newborn](https://cks.nice.org.uk/topics/jaundice-in-the-newborn/)\n \n# References\n\n[Patient Info Biliary atresia](https://patient.info/doctor/biliary-atresia) \n\n[UK.GOC Health Screening Biliary Atresia](https://view-health-screening-recommendations.service.gov.uk/biliary-atresia/)",
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"question": "A 19-day-old baby is brought to accident and emergency by her parents with jaundice and poor feeding for the last three days. On further questioning, they report she has been passing pale stools and dark urine over the last week. On examination, the baby is visibly jaundiced and has a distended abdomen with hepatosplenomegaly.\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "Topical glyceryl trinitrate (GTN) is given to treat chronic anal fissures in adults, but not children, as it is unlicensed. It is used to relieve pain caused by the fissure and help the external anal sphincter relax, allowing more blood flow to the mucosa, which may further aid the healing process. In children, anal fissures are initially managed by reducing constipation with high-fibre diets, considering use of laxatives, warm baths, and encouragement of drinking plenty of fluids. In this case, the more pressing issue is the inconsistency of the story and the child's injury, raising suspicion of possible sexual abuse. In this case, referral to the safeguarding lead is more pressing",
"id": "33161",
"label": "d",
"name": "Topical glyceryl trinitrate per rectum",
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"explanation": "Constipation may be the first sign of Crohn's disease, where the child is opening their bowels less than three times per week. Constipation can cause anal fissures in children, resulting in the symptoms this child is experiencing. Often in Crohn's disease, however, there are other signs such as bloating, diarrhoea (sometimes with blood and mucus), reduced appetite, weight loss, fatigue, and slow growth. If inflammatory bowel disease is suspected, then a faecal calprotectin would be appropriate. The history, however, does not suggest this child is constipated or has any other systemic issues. In this case, the more pressing issue is the inconsistency of the story and the child's injury, raising suspicion of possible sexual abuse, and raising concern of a sinister cause for his anal fissure. In this case, referral to the safeguarding lead is more pressing",
"id": "33162",
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"name": "Send a faecal calprotectin",
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"explanation": "In this scenario, the child's injuries are not consistent with the father's explanation of events. His symptoms fit with an anal fissure/laceration. This can occur commonly with constipation in children, although a low threshold to suspect sexual abuse is required in a child who has an anal laceration where constipation, Crohn's disease, and passing hard stool have been excluded as the cause. He states he is passing stools normally and regularly, but with fresh red PR bleeding and so an anal fissure is the most likely cause and constipation less likely",
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"explanation": "This would be a reasonable option for a child who has developed constipation and subsequent anal tear/fissure, which is deemed unlikely caused by non-accidental injury. In this case, the more pressing issue is the inconsistency of the story and the child's injury, raising suspicion of possible sexual abuse. In this case, referral to the safeguarding lead is more pressing",
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"label": "c",
"name": "Recommend a high-fibre diet",
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"explanation": "This would be a reasonable option for a child who has developed constipation and subsequent anal tear/fissure, which is deemed unlikely caused by non-accidental injury. Usually a trial of high fibre diet would be trialled first, followed by laxatives if unsuccessful. In this case, the more pressing issue is the inconsistency of the story and the child's injury, raising suspicion of possible sexual abuse. In this case, referral to the safeguarding lead is more pressing",
"id": "33159",
"label": "b",
"name": "Prescribe 7 days of laxatives",
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"comment": "This is beyond dark",
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"comment": "I honestly would rather not make assumptions about what is truly going on….",
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"comment": "Better to be safe than sorry tho just incase ",
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"comment": "if you don't make assumptions that kid is gonna keep getting abused",
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"comment": "Welcome to the real world...",
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"comment": "it's not about what you would rather do though, you are obligated by law to raise this with the safeguarding team (or by professional duty if it was an adult)",
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"comment": "this kind of question makes it very real. I got goosebumps. ",
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"comment": "Refer to safe guarding and give the dad a slap?",
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"explanation": "# Summary\n \n\nNon-accidental injury refers to any intentional injury inflicted upon a child or harm that occurs due to caregiver neglect. Common signs and symptoms include delayed presentation, inconsistent caregiver narratives, injuries of varying ages, and specific findings such as subconjunctival or retinal haemorrhage. Key investigations include a full skeletal radiographic survey and blood tests to exclude organic causes of presentations. Management involves immediate senior and safeguarding lead notification, admission for safeguarding, treatment of injuries, thorough documentation, and liaison with social care.\n \n\n# Definition\n \n\nNon-accidental injury is a term used to describe any physical harm in a child that is deliberately inflicted or results from the failure of a caregiver to prevent such harm.\n \n\n# Epidemiology\n\nNon-accidental injury predominantly affects children under the age of 2 years. Precise epidemiological data can be challenging to establish due to underreporting and differing definitions of abuse.\n\nThe Crime Survey for England and Wales estimates that 7.6% of adults aged 18-74 had experienced physical abuse before the age of 16. Unfortunately, over 100,000 incidents of physical abuse to children were recorded in 2019. In approximately 80% of cases the abuser is the parent or carer. \n \n\n# Aetiology\n\nNon-accidental injury results from deliberate harm inflicted by a caregiver or due to a caregiver's failure to prevent harm.\n \nRisk factors may include:\n\n- Previous child maltreatment or domestic violence in the family \n- Caregiver substance abuse or mental health issues\n- History of the caregiver being abused\n- Emotional volatility \n- Poverty and poor housing\n- Children in the care system \n\nChildren and young people with disabilities are more likely to be the victim of abuse. \n \n\n# Signs and symptoms\n \n\nIn non-accidental injury, key clinical manifestations may include:\n \n\n - History\n \n - Predominantly occurs in children under 2 years old\n - Often delayed presentation following injury\n - Inconsistencies in the caregiver's narrative, including:\n - Changing stories\n - Severity/type of injury not corresponding to the narrative\n - Injuries in a child not yet independently mobile \n - Unwitnessed injuries\n - Evidence of drug or alcohol use in the household\n - Physical Examination Findings\n \n - Injuries of varying ages\n - Presence of burns or scalds\n - Bruises:\n - To any part of the body in an infant\n - Bruises on the head and face most common sites of abusive bruising\n - Consistent with gripping\n - Subconjunctival haemorrhage\n - Retinal haemorrhage\n - Human bite marks\n - Immersion scalds: most commonly on lower limbs. This may spare the buttocks if they were pressed against the bottom of the bath. \n - Torn frenum: Associated with head injuries or force-feeding of an infant.\n - Cigarette burns \n - Female genital mutilation (see below)\n\n \nWith investigation, other sites of non-accidental injury may include:\n\n- Subdural haemorrhage \n- Long bone fractures in a child not yet independently mobile \n- Fractures of different ages \n- Rib fractures without a history of major trauma \n \n\n# Differential diagnosis\n \n\nDifferential diagnoses can include accidental injury, bleeding disorders, and certain types of malignancies. Each presents with specific signs and symptoms:\n \n\n - **Accidental injury**: Injuries correspond to the history provided and are developmentally appropriate. \n - **Bleeding disorders**: May present with easy bruising, nosebleeds, heavy or prolonged menstrual bleeding, and excessive bleeding from minor cuts or after surgery or dental work.\n - **Haematological malignancy**: May present with fatigue, shortness of breath, recurrent infections, easy bruising or bleeding, and unexplained weight loss.\n\nOther forms of child abuse to consider are:\n \n - **Physical Abuse**: This may include NAI, but also includes female genital mutilation, which is illegal in the UK.\n - **Emotional Abuse**: The psychological ill-treatment or neglect of a child's emotional needs. This may include bullying, corruption, making the child scared or preventing the child from enjoying normal social activity.\n - **Sexual Abuse**: Forcing a child to engage in sexual behaviours ranging from viewing pornography to engaging in sexual activity. \n - **Neglect**: This is when a child's basic needs are not met. The child may not have adequate food, provision of medical care or housing. \n \n\n# Investigations\n \n - It is important to record a detailed history and complete a body map. \n - Radiology: A comprehensive skeletal survey may be necessary to identify:\n \n - Rib fractures\n - Skull fractures or intracranial bleeds\n - Metaphyseal corner fractures (caused by a twisting or pulling motion on a limb)\n - Finger fractures\n - Clavicle fractures\n - Laboratory testing: Blood tests are important to rule out organic causes such as clotting disorders or haematological malignancies.\n - Medical photography may also be used. \n \n\n# Management\n \n\n - Report suspicions: Always inform a senior or a named safeguarding lead if non-accidental injury is suspected.\n - Safeguarding measures: Admit the child for safeguarding while investigations continue. Ensure the safety of other children in the home.\n - Treatment: Administer appropriate medical management for injuries.\n - Documentation: Maintain clear and thorough documentation.\n - Social care liaison: Contact social care to investigate if the child or caregiver is already known to them.\n\n# Complications\n\n- Recurrence or escalation of the NAI\n- Psychological distress \n- Poor health outcomes \n- Substance misuse and employment difficulties later in life\n\n\n# Female Genital Mutilation \n\nFemale Genital Mutilation (FGM) is a term for intentional injuries, cuts and alterations of female genitals without a medical indication. It is illegal in the UK and is considered to be child abuse. It most commonly affects girls between the ages of 0 and 15. It can have serious complications to the physical and mental health of the individual including chronic pain, infection, fertility problems, PTSD and depression. \n\nIt is illegal to perform FGM, assist an individual to perform FGM or fail to protect a girl for whom you're responsible from FGM. \n\nIf you see a patient and are concerned about a patient being at risk of FGM, it is important to contact 999 if the risk is imminent, or if not imminent, to inform the police on 101 and NSPCC on 0800 028 3550. \n\n \n# Prognosis \n \nNon-accidental injury is important for any healthcare worker to be aware of. In 2017/2018, almost 100 children were the victim of a homicide and almost 60 died due to assault. Furthermore, there were over 15,000 cases of neglect and over 50,000 sexual offences against children reported to the police. \n \n\n# NICE Guidelines\n \n[NICE Guidance: Child maltreatment: when to suspect maltreatment in under 18s](https://www.nice.org.uk/guidance/cg89)\n\n[NICE Guidance: Child abuse and neglect](https://www.nice.org.uk/guidance/ng76/resources/child-abuse-and-neglect-pdf-1837637587141) \n\n# References \n \n[Office for National Statistics Child Physical Abuse](https://www.ons.gov.uk/peoplepopulationandcommunity/crimeandjustice/articles/childphysicalabuseinenglandandwales/yearendingmarch2019) \n\n[Patient Info Safeguarding Children](https://patient.info/doctor/safeguarding-children-referral-and-management-of-an-abused-or-at-risk-child) \n\n[BMJ Best Practice Child Abuse](https://bestpractice.bmj.com/topics/en-gb/846/epidemiology)\n\n[NHS Female Genital Mutilation](https://www.nhs.uk/conditions/female-genital-mutilation-fgm/)",
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"question": "An 8-year-old boy is brought to the GP by his father for 3 days of painful bowel motions. He has recently switched GPs and in previous records, he has not been brought in to any of his routine appointments. The child is quiet and withdrawn, but states he has been opening his bowels once per day, with no change in frequency or consistency. His father states it started when he fell down onto one of his toys while playing with his sister. On further questioning, he states there has been some fresh red blood on the toilet paper on wiping. He explains he has been afraid to open his bowels as, for the last three days, he has found it very painful to go, but still has managed without straining. He denies abdominal pain, recent change in diet, or loss of appetite.\n\nOn examination, observations are unremarkable and his abdomen is soft and non-tender. An attempt at PR exam is abandoned as he finds it incredibly painful.\n\nWhich of the following is the best next step in the management of this patient?",
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"comment": "I don’t get why the mother would have a temperature in labour? Since GBS is harmless for her? ",
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"explanation": "# Summary\n \n\nNeonatal sepsis, a severe infection occurring in infants younger than 90 days of age, is classified into early onset (within 72 hours of life) and late-onset (after 72 hours). Key causes of early onset sepsis include Group B Streptococcus and other microbes ascending from the cervix, and pathogens like Listeria, Toxoplasma, Rubella, and CMV via the placenta. Late-onset sepsis is predominantly caused by Staphylococcus aureus, Staphylococcus epidermidis, E. coli, Pseudomonas, and Klebsiella. Risk factors comprise of premature birth, multiple pregnancies, prolonged rupture of membranes, and maternal intrapartum fever. Initial investigations include FBC, CRP, and blood culture, supplemented by lumbar puncture or chest X-ray based on symptoms. Management typically begins with empirical treatment using benzylpenicillin and gentamicin, followed by adjustments according to culture results and clinical progress.\n \n\n# Definition\n \nNeonatal sepsis is a severe systemic infection occurring in infants less than 90 days old, classified into early onset (within 72 hours of life) and late-onset (after 72 hours of life).\n\nEarly onset neonatal sepsis is often caused by ascending infections from the maternal genital tract or transplacental infections. Late-onset neonatal sepsis usually results from organisms present in the hospital environment or the infant's intestinal flora.\n \n\n# Epidemiology\n \nAround 2 in every 1,000 live births are affected by serious acute infections. The incidence rises to 26 per every 1,000 live births in infants weighing less than 1,000 grams. The majority of cases present in the first 24 hours of life. \n\n# Aetiology\n \n\nEarly onset neonatal sepsis (<72 hours of life) is commonly caused by:\n \n\n - Ascending microorganisms from the cervix:\n \n - E. coli. and Group B streptococcus (GBS) (most common) \n - Typically colonises the genital tract\n - Can cause asymptomatic bacteriuria or UTI in the mother\n - There is no routine screening for GBS in the UK\n - IV benzylpenicillin is the recommended treatment during childbirth if risk factors are present\n \n - Transplacental infections:\n \n - Listeria\n - Toxoplasma\n - Rubella\n - CMV\n \n\nLate-onset sepsis (>72 hours of life) is frequently caused by:\n \n\n - Staphylococcus aureus (most common)\n - Staphylococcus epidermidis\n - E. coli\n - Pseudomonas\n - Klebsiella\n \n\nThe following risk factors significantly increase the likelihood of early-onset neonatal sepsis:\n \n\n - Multiple pregnancies with a sibling who has suspected or confirmed infection\n - Evidence of GBS in a previous baby or current pregnancy\n - Premature birth\n - Rupture of membranes >18 hours for pre-term babies, or >24 hours for term babies\n - Maternal intrapartum temperature >38C\n - Suspected or confirmed maternal sepsis\n - Chorioamnionitis\n \n\n# Signs and Symptoms\n \n\nClinical presentations of neonatal sepsis can vary:\n\n- Nonspecific symptoms \n - Feeding problems\n - Temperature instability\n - Reduced levels of consciousness \n- Respiratory distress\n- Jaundice \n- Shock and multi-organ failure \n \nThere may be signs specific to the site of infection:\n \n - Purulent discharge from the eyes may indicate infection with chlamydia or gonococcus\n - Periumbilical cellulitis \n - Signs of meningitis: bulging fontanelle, seizures \n \n\n# Differential Diagnosis\n \n\nThe clinical picture of neonatal sepsis can mimic a variety of other conditions including:\n \n\n - **Metabolic and endocrine disorders**: Presents with lethargy, poor feeding, and seizures. Hypoglycaemia, hypocalcaemia, and congenital adrenal hyperplasia are common examples.\n - **Cardiovascular disorders**: Manifestations include cyanosis, pallor, and tachypnoea. Examples include congenital heart disease and persistent pulmonary hypertension of the newborn.\n - **Respiratory disorders**: Conditions like transient tachypnoea of the newborn, neonatal pneumonia, and respiratory distress syndrome present with respiratory distress and cyanosis.\n - **Neurological disorders**: Conditions like intraventricular haemorrhage and hypoxic-ischemic encephalopathy present with altered levels of consciousness, seizures, and abnormal tone.\n \n\n# Investigations\n \n\nThe key investigations for diagnosing neonatal sepsis include:\n \n - Temperature is assessed in the axilla \n - Full blood count (FBC), C-reactive protein (CRP), and blood culture. A blood culture should be taken **before** the first dose of antibiotics\n - Consider lumbar puncture (LP) in the presence of neurological symptoms or strong clinical suspicion. LP is essential if neonatal meningitis is suspected as neonates do not often have clear signs of meningitis. \n - Chest X-rays are advised only if there is a strong suspicion of a chest source. NICE advises against a urine culture in early-onset neonatal sepsis\n - CRP should be repeated 24-36 hours after the initial dose of antibiotics\n - If late-onset neonatal sepsis, a urine sample should be sent for microscopy and culture. \n\nIf there are localising signs of infection (ie purulent discharge from the eye or umbilicus) then swabs can be sent for microbiology. \n \n\n# Management\n \n\nFor early-onset neonatal sepsis: \n \n - NICE recommends empirical treatment with IV benzylpenicillin and IV gentamicin \n - The treatment regimen is adjusted based on culture results and the clinical picture\n - Monitoring of gentamicin levels is required due to its narrow therapeutic index and potential for toxicity\n - Antibiotics are typically given for 7 days \n\nFor late-onset neonatal sepsis:\n \n - NICE recommends narrow-spectrum antibiotics (IV flucloxacillin and IV gentamicin) \n\n\nOther special considerations:\n \n - If concerned about bacterial meningitis, IV cefotaxime and IV gentamicin should be used \n - If necrotising enterocolitis is suspected, add metronidazole to cover for anaerobic bacteria \n - In a septic infant born to a febrile mother with chorioamnionitis, to cover for Listeria bacteria, IV amoxicillin and IV gentamicin will be used\n - IV aciclovir may be used if there are signs of potential Herpes Simplex Virus (HSV) infection (i.e. thrombocytopaenia, hepatomegaly, encephalitis, vesicular rash)\n - IV Ganciclovir may be used for suspected congenital cytomegalovirus (CMV) in infants with \"blueberry muffin\" purpuric rash, colitis, thrombocytopenia or hepatic dysfunction. \n - IV ambisome may be used if a fungal cause is suspected (i.e. thrombocytopenia, very low birth weight infants and infants not responding to broad-spectrum antibiotics) \n\n \n# Prevention \n\nThe risk of neonatal sepsis is reduced by:\n\n- Prophylactic antibiotics during labour for women who have evidence of GBS colonisation, are in pre-term labour or have chorioamnionitis. \n\nFor early-onset neonatal sepsis, if the blood cultures in the neonate are positive, obstetrics should be notified to consider antibiotic treatment for the mother. \n\n# Complications\n\n- Sepsis can cause multi-system organ failure and is potentially fatal.\n- Seizures may occur.\n- Chronic complications may include bronchopulmonary dysplasia, intraventricular haemorrhage and necrotising enterocolitis. \n\n\n# Prognosis\n\nNeonatal sepsis has a 2-4% mortality rate in the UK. Early identification and treatment of neonatal sepsis offers the best prognosis. \n \n\n# NICE Guidelines\n \n[NICE Guidelines: Neonatal infection: antibiotics for prevention and treatment](https://www.nice.org.uk/guidance/ng195/resources/neonatal-infection-antibiotics-for-prevention-and-treatment-pdf-66142083827653)\n\n# References\n\n[RCOG Green-top guideline: Group B streptococcal Disease, Early-onset](https://obgyn.onlinelibrary.wiley.com/doi/full/10.1111/1471-0528.14821) \n\n[NHSGGC Paediatrics for Health Professionals Early-onset sepsis in the neonate: prevention and treatment](https://www.clinicalguidelines.scot.nhs.uk/nhsggc-guidelines/nhsggc-guidelines/neonatology/early-onset-sepsis-in-the-neonate-prevention-and-treatment/)\n\n[Patient Info Congenital, Perinatal and Neonatal Infections](https://patient.info/doctor/congenital-perinatal-and-neonatal-infections) \n\n[NHSGGC Paediatric for Health Professionals](https://www.clinicalguidelines.scot.nhs.uk/nhsggc-guidelines/nhsggc-guidelines/neonatology/antibiotic-guidelines-for-the-neonatal-unit/)",
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"question": "A woman brings her newborn boy to A&E with signs of respiratory distress. He was born 36 hours ago at 39 weeks and is currently grunting, tachypnoeic, and pyrexial with nasal flaring and use of accessory muscles. You suspect he has neonatal sepsis.\n\nThe mother had not attended any of her pre-natal screening sessions and reports her waters breaking over 24 hours before she went into labour. She also had a temperature in labour\n\nWhich of the following is the most likely organism responsible for this early-onset neonatal sepsis?",
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"comment": "takes 4-6 weeks for SSRIs to work - whether to stop at 4 or 6 is clinical judgement + patient decision-making",
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"explanation": "# Summary\n\nDepression is a common mental health disorder typified by low mood, anhedonia, significant weight change, sleep and activity changes, fatigue, feelings of guilt or worthlessness, or poor concentration. It is defined by the DSM as the presence of 5 out of 8 symptoms for at least 2 weeks. It is more prevalent in females. Key investigations include FBC, TFT, U+E, LFT, Glucose, B12/folate, cortisol, toxicology screen, and CNS imaging to rule out organic causes. Management strategies encompass low to high intensity psychological interventions, pharmacotherapy including anti-depressants, and in severe cases, lithium or ECT.\n\n# Definition\n\nDepression is a mental health disorder characterised by:\n\n- **ICD-11 Criteria:**\n - Depressive Episode: Depressed mood, loss of interest (anhedonia), and reduced energy (fatigue) persisting for at least two weeks.\n\n- **DSM-V Criteria:**\n - Major Depressive Disorder (MDD): Presence of a major depressive episode lasting at least two weeks, with specific criteria regarding mood, cognitive, and physical symptoms.\n - Persistent Depressive Disorder (Dysthymia): A chronic form of depression lasting for at least two years. \n\nThis consists of the presence of at least five out of a possible eight defining symptoms, during the same two-week period, where at least one of the symptoms is depressed mood or loss of interest or pleasure\n\n**Severity:**\n\n- Mild: Few, if any, symptoms in excess of those required to make the diagnosis (associated symptoms, see below), and the symptoms result in minor functional impairment.\n- Moderate: Symptoms or functional impairment between \"mild\" and \"severe.\"\n- Severe: The number of symptoms, intensity, and impairment are all greatly increased.\n\n\n# Epidemiology\n\nDepression is a highly prevalent mental health disorder. It represents the third most common reason for consulting a general practitioner in the UK. Depression demonstrates a higher prevalence in females.\n\n# Aetiology\n\nThe aetiology of depression involves a complex interplay of genetic and environmental factors. History of previous mental health issues, physical illnesses, and social challenges like divorce, poverty, and unemployment can all contribute to its development.\n\n# Clinical Features\n\nDepression is defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM) as the presence of 5 out of the following 9 symptoms, occurring nearly every day for at least 2 weeks:\n\n1. **Depressed mood or irritability** for most of the day, indicated by either subjective report (feels sad or empty) or observation by others (appears tearful).\n2. **Anhedonia:** Decreased interest or pleasure in most activities, most of the day.\n3. Significant **weight change** (5%) or change in appetite.\n4. **Sleep alterations:** Insomnia or hypersomnia.\n5. **Activity changes:** Psychomotor agitation or retardation.\n6. **Fatigue** or loss of energy.\n7. **Guilt or feelings of worthlessness:** Excessive or inappropriate guilt or feelings of worthlessness.\n8. **Cognitive issues:** Diminished ability to think or concentrate, or increased indecisiveness.\n9. **Suicidality:** Thoughts of death or suicide, or formulation of a suicide plan.\n\n### Additional Features (Severe Depression)\n- **Psychotic Features:** Delusions (e.g. nihilistic delusions, Cotard's syndrome) and hallucinations.\n- **Depressive Stupor:** Profound immobility, mutism, and refusal to eat or drink, sometimes necessitating electroconvulsive therapy (ECT).\n\n# Differential Diagnosis\n\nThe main differentials and their key signs and symptoms include:\n\n- **Bipolar Disorder:** Characterised by periods of mania/hypomania (elevated mood, inflated self-esteem, decreased need for sleep, increased talkativeness, distractibility, increased goal-directed activity) alternating with depressive episodes.\n- **Anxiety Disorders:** Persistent and excessive worry, restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and sleep disturbance.\n- **Psychotic Disorders:** Hallucinations, delusions, disorganised speech, grossly disorganised or catatonic behaviour.\n- **Substance/Medication-Induced Mood Disorder:** Mood disturbance associated with intoxication or withdrawal from substances or side effects of medications.\n- **Adjustment Disorders:** Development of emotional or behavioural symptoms in response to identifiable stressors.\n\n\nVarious organic causes should be considered and ruled out through careful history-taking, physical examination, and relevant investigations. These include:\n\n- Neurological disorders such as Parkinson's disease, dementia, and multiple sclerosis.\n- Endocrine disorders, especially thyroid dysfunction and hypo/hyperadrenalism (e.g., Cushing's and Addison's disease).\n- Substance use or medication side effects (e.g., steroids, isotretinoin, alcohol, beta-blockers, benzodiazepines, and methyldopa).\n- Chronic conditions such as diabetes and obstructive sleep apnea.\n- Long-standing infections, such as mononucleosis.\n- Neoplasms and cancers - low mood can theoretically be a presenting complaint in any cancer, with pancreatic cancer being a notable example.\n\n\n# Investigations\n\n- Standard investigations for depression may include Full Blood Count (FBC), Thyroid Function Test (TFT), Urea and Electrolytes (U&E), Liver Function Test (LFT), Glucose, B12/folate levels, cortisol levels, toxicology screen, and imaging of the Central Nervous System (CNS).\n- These help rule out organic causes (listed above) such as endocrine disorders (e.g. thyroid disorders).\n- There are several questionnaires that can also be used to help assess depressive symptoms, such as the Hospital Anxiety and Depression (HAD) Scale and Patient Health Questionnaire (PHQ-9).\n\n# Management\n\nDepression is usually managed in primary care. GPs can refer to secondary care (Psychiatry) if there is a high-suicide risk, symptoms of bipolar disorder, symptoms of psychosis, or if there is evidence of severe depression unresponsive to initial treatment.\n\r\n**Persistent subthreshold depressive symptoms or mild-to-moderate depression:**\n\n- 1st line = Low-intensity psychological interventions (individual self-help, computerised CBT). \r\n- 2nd line = High-intensity psychological interventions (individual CBT, interpersonal therapy) \r\n- 3rd line = Consider antidepressants \r\n\r\n**Mild depression unresponsive to treatment and moderate-to-severe depression:**\n\n- 1st line = High-intensity psychological interventions + antidepressants (1st line = SSRI)\r\n- 2nd line (Treatment-resistant depression) – switch antidepressants and then use adjuncts \r\n\r\n**Severe depression and poor oral intake/psychosis/stupor:**\n\n- 1st line = ECT \n- Although the exact mechanism remains elusive, it is thought that the induced seizure, rather than the ECT procedure itself, has therapeutic benefits. Short-term side effects of ECT include headache, muscle aches, nausea, temporary memory loss, and confusion, while long-term side effects can include persistent memory loss. Due to the induced seizure, there is a risk of oral damage, and due to the general anaesthetic, a small risk of death.\r\n\n**Recurrent depression:** \n\n- Treated with antidepressant + lithium \r\n\n\nMedical management of depression - additional notes:\n\n- First-line pharmacological treatment typically involves a Selective Serotonin Reuptake Inhibitor (SSRI) such as sertraline. SNRIs such as venlafaxine can also be used first-line, but are less preferable due to the risk of damage from overdose, which is less likely with SSRIs.\n- In people aged 18-25 there is an increased risk of impulsivity and suicidal risk upon commencing antidepressant medication and so they should have a follow-up appointment arranged after one week to monitor progress. Initial reviews can otherwise be arranged 2-4 weeks after starting medication in patients >25.\n- Continuation of antidepressants for at least six months post-remission is recommended to mitigate relapse risk. Tapering should be done gradually over a four-week period when discontinuing antidepressants.\n\n\n\n# NICE Guidelines\n\n[NICE Guidance on the Management of Depression](https://www.nice.org.uk/guidance/cg90)",
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"question": "A 78-year-old woman has been seeing her GP for the last 4 months with symptoms of depression. She was started on sertraline a week ago and has presented for her 1 week follow-up appointment. She states she feels no different and would like to try another agent.\n\nFor how long should her treatment be continued before considering a switch to a different anti-depressant?",
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"explanation": "When a patient is detained under section 3 of the mental health act, they can be detained for up to 6 months with option of further renewal. This patient has only had a short assessment so far and so would need a longer period of detention. Usually the least restrictive method, and therefore the shortest time required, would be used and so detention under section 2 would be used initially to detain the patient for 28 days",
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"explanation": "A patient can be detained under section 5(4) of the mental health act by a nurse who has been qualified and trained to work with mental health problems or learning disabilities. It is a short term emergency section to detain a patient for up to 6 hours until they can be seen by a doctor. This patient has already been detained under section 5(2) and so detention under section with a longer time period would be required to provide further assessments and/or treatment. The most appropriate answer would therefore be section 2 to detain the patient for up to 28 days",
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"explanation": "Section 136 is slightly different to section 135. Both are carried out by police officers if they believe the patient has a mental disorder and in need of immediate care of control where they can detain a patient against their will to be taken to a place of safety until examined by a doctor. Section 135 is used when police require entry to a persons home, if need be by force, when they believe a person is at serious risk of harming themselves or others. Section 136 is used when police find the person in a public place and feel they need to bring the patient to a place of safety. A patient can be detained under section 135 and 136 for up to 24 hours",
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"explanation": "This patient has presented with an acute psychotic episode and is currently not safe to leave due to strong concerns that he is at risk of ending his life if he were to leave. He should therefore be detained under section 2 of the mental health act which allows detention for a period of 28 days. If the patient continues to require psychiatric treatment after the 28 days, then he could be considered to be detained under section 3 which would allow him to be detained for up to 6 months with option of further renewals. Section 2 can't normally be extended or renewed once expired",
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"comment": "Can i just point out for clarification, you can't use a 5(2) in A+E.",
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"comment": "As a med student not studying in England where the law is different, these questions make me so stressed",
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"comment": "also police can only enter patient's property under section 136 (NOT 135 as stated in the stem)",
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"comment": "136 is used in public to a place of safety\n135 is used to enter a house ",
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"explanation": "# Summary\n\nThe Mental Capacity Act (MCA) is a crucial legal framework that provides guidance on decision-making for individuals who may lack the capacity to make specific choices. Enacted in 2005, the MCA establishes the principles and procedures for assessing mental capacity and ensures that decisions made on behalf of individuals without capacity are made in their best interests. Capacity, as defined by the MCA, involves the ability to understand, retain, weigh, and communicate information relevant to a specific decision. It is time- and decision-specific. The Act empowers individuals to make choices whenever possible, respecting their autonomy, while also safeguarding those who lack capacity through a structured and person-centered decision-making process.\n\n# 5 Key Principles\n\nThe Mental Capacity Act (MCA) is used when a patient lacks capacity. It allows doctors (or less commonly, those with Lasting Power of Attorney) to make decisions in the best interests of their patient. There are 5 key principles:\n\n- A person is assumed to have capacity unless proven otherwise\n- Steps must be taken to help a person have capacity\n- An unwise decision does not mean a person lacks capacity\n- Any decisions made under the MCA must be in the person's best interests\n- Any decisions made should be the least restrictive to a person's rights and freedoms\n\n# Assessing capacity\n\nAssessing capacity is a two step process: \n\n1) Is there an impairment of, or disturbance in, the functioning of the mind or brain? \n\nIf yes, then step 2) For a person to lack capacity they must show an 'impairment of, or disturbance in, the functioning of the mind or brain' AND they are unable to undertake any of the following:\n\n- Understand relevant information\n- Retain the relevant information\n- Weigh up the relevant information\n- Communicate a decision\n\n**If they are unable to do one of these things then they do not have capacity.**\n\n### Next steps\n\n- If they do not have capacity, can we wait until they do before making a decision? Consider the (clinical) urgency of the decision that needs to be made\n- Do they have a Lasting Power of Attorney (LPA), Advanced Directive, or Advanced Statement?\n- Does a best interests meeting need to be had, including the MDT, and relatives/friends who know the patient well. If there is nobody who can advocate for the patient, an Independent Mental Capacity Advocate (IMCA) can represent them when making a best interests decision.\n\n# Deprivation of Liberty Safeguards (DOLS)\n\nThe Deprivation of Liberty Safeguards is the procedure in law used where it is necessary to deprive a patient or resident of their liberty as they lack capacity to consent to treatment or care to keep them safe from harm. It safeguards for those who lack capacity and do not want to be somewhere and are not free to leave. There are a series of checks to make sure that any care someone receives that restricts their freedom is appropriate and in their best interests. \n\nIf a patient lacks capacity to make decisions about ongoing care and are not free to leave, then an application for a DOLS may be made (proportionate and not excessively restrictive actions). This can be common in acute medical/geriatrics wards.\n\nThe following conditions must be met to allow a person to be deprived of their liberty under the safeguards:\n\n* The person must be 18 or over.\n* The person must be suffering from a mental disorder.\n* The person must be a patient in hospital or a resident in a care home.\n* The person lacks capacity to decide for themselves about the restrictions which are proposed so they can receive the necessary care and treatment.\n* The proposed restrictions would deprive the person of their liberty.\n* The proposed restrictions would be in the person's best interests.\n* Whether the person should instead be considered for detention under the Mental Health Act.\n* There is no valid advance decision to refuse treatment or support that would be overridden by any DoLS process.\n\n# References\n\n[Click here to see information on Legislation UK on the MHA](https://www.legislation.gov.uk/ukpga/1983/20/contents)\n\n[Click here to see information on Legislation UK on the MCA](https://www.legislation.gov.uk/ukpga/2005/9/contents)",
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"question": "A 28-year-old man was admitted under psychiatry for an acute psychotic episode after his colleague found plans to end his life and called the police. The police brought him to hospital under section 135. In A&E, he exhibited persecutory delusions and suicidal ideation, stating he has made several plans to end his life and would do so if discharged.\n\n\nHe has been held under section 5(2) while awaiting a full assessment and it has been decided that he is not safe to leave as he is a high risk to himself with serious concern that he would end his life if he were to leave.\n\n\nUnder which section of the mental health act (1983) should he be detained?",
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"explanation": "This patient has recently started clozapine for his schizophrenia and has now developed pyrexia, general malaise, and symptoms of pharyngitis. Clozapine is associated with a relatively high risk of agranulocytosis and neutropenia within the first few months of treatment. They are therefore at risk of neutropenic sepsis.\n \n\n Unfortunately we do not know this patients neutrophil count yet although, given his risk factors, he should be started on intravenous antibiotics within one hour of recognition of signs of sepsis. As patients with neutropenia cannot mount the normal immune response to infection that others can, they can look and feel completely well for some time, with relatively normal observations, before rapidly becoming unwell and deteriorating. It is therefore important to have a high index of suspicion and treat aggressively early",
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"explanation": "This patient has recently started clozapine and so is at risk of agranulocytosis and neutropenia (black box warning). We do not have his blood results back but, given he has developed new pyrexia with general malaise, he must be treated as suspected neutropenic sepsis",
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"explanation": "This patient has recently started clozapine and so is at risk of agranulocytosis and neutropenia (black box warning). We do not have his blood results back but, given he has developed new pyrexia with general malaise, he must be treated as suspected neutropenic sepsis",
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"explanation": "This patient is at risk of agranulocytosis and neutropenia and has signs and symptoms of possible sepsis so reassurance is not a safe option, and he requires urgent treatment",
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"explanation": "Nasendoscopy is an excellent way to assess pathology within the nasal passage, larynx, and vocal cords. If epiglottitis or supraglottitis were suspected in this patient, then urgent referral to ENT would be warranted with help from anaesthetics for airway support. This patient is not showing signs of airway obstruction e.g. drooling, stridor, hoarse voice, or respiratory distress and so epiglottitis is unlikely",
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"explanation": "# Summary\n\n\n\n# Typical antipsychotics\n\n- Also known as 'first-generation' antipsychotics, these not only act as antagonists to D2 receptors but also on cholinergic, adrenergic and histaminergic receptors. The most commonly used medication in this class is **Haloperidol**, though other examples include Chlorpromazine and flupentixol. \n- Side effects can therefore be grouped according to receptor blockade (see below).\n\n### Dopamine D2 Receptor Blockade:\n\n1. **Extrapyramidal Symptoms (EPS):**\n - **Acute Dystonia:** Involuntary muscle contractions causing spasms.\n - **Akathisia:** Restlessness and an inability to sit still.\n - **Parkinsonism:** Tremors, rigidity, and bradykinesia (slowed movements).\n - **Tardive Dyskinesia:** Involuntary, repetitive movements, especially of the face.\n\n2. **Hyperprolactinemia:**\n - Elevated levels of prolactin, leading to:\n - Menstrual irregularities in women.\n - Gynecomastia (breast enlargement) in men.\n - Sexual dysfunction in both genders.\n\n### Other Receptors:\n\n1. **Histamine H1 Receptor Blockade:**\n - **Sedation:** Drowsiness and sleepiness.\n\n2. **Alpha-1 Adrenergic Receptor Blockade:**\n - **Orthostatic Hypotension:** A sudden drop in blood pressure upon standing, leading to dizziness or fainting.\n\n3. **Muscarinic Receptor Blockade:**\n - **Anticholinergic Effects:**\n - Dry mouth.\n - Constipation.\n - Blurred vision.\n - Urinary retention.\n\n\n# Atypical antipsychotics\n\n- Also known as 'second-generation' antipsychotics, these are D2, D3 and 5-HT2A antagonists, with less overspill into other receptors. \n- As effective as typical antipsychotics (even slightly better at negative symptoms), and have a more favourable side effect profile with reduced extrapyramidal effects, but increased metabolic side-effects. \n- They are 1st line for new-onset psychosis. Examples include risperidone, quetiapine, olanzapine, aripiprazole and clozapine (see below). \n\n### Dopamine Receptor Blockade:\n\n1. **D2 Receptor Blockade:**\n - **EPS (Extrapyramidal Symptoms):**\n - Atypicals generally have a lower risk of causing EPS compared to typicals.\n - Lower risk of tardive dyskinesia.\n\n### Serotonin Receptor Blockade:\n\n1. **5-HT2A Receptor Blockade:**\n - **Lower Risk of EPS:** Atypicals have a reduced risk of causing EPS due to serotonin receptor blockade.\n\n### Other Receptors:\n\n1. **Histamine H1 Receptor Blockade:**\n - **Sedation:** Although less common than with typicals, some atypicals can cause drowsiness.\n\n2. **Alpha-1 Adrenergic Receptor Blockade:**\n - **Orthostatic Hypotension:** Some atypicals may cause a drop in blood pressure upon standing.\n\n3. **Muscarinic Receptor Blockade:**\n - **Anticholinergic Effects:**\n - Generally less pronounced compared to typicals.\n - Mild dry mouth, constipation, or blurred vision.\n\n### Metabolic Effects:\n\n1. **Weight Gain:**\n - **Common Side Effect:** Atypical antipsychotics, in general, have a higher risk of causing weight gain compared to typicals.\n - **Varying Degrees:** The degree of weight gain can vary among different atypicals.\n\n2. **Dyslipidemia and Glucose Metabolism:**\n - **Increased Risk:** Some atypicals are associated with an increased risk of dyslipidemia and impaired glucose metabolism.\n\n3. **Prolactin Elevation:**\n - **Variable:** Some atypicals may elevate prolactin levels, leading to menstrual irregularities and sexual dysfunction.\n\n### Other side effects:\n\n1. **Seizures:**\n - **Low Risk:** Generally, atypicals have a lower risk of lowering the seizure threshold compared to typicals.\n\n2. **QT Prolongation:**\n - **Potential Risk:** Some atypicals may have a mild effect on the QT interval, but the clinical significance varies.\n\n3. **Increased risk of VTE and stroke in elderly**\n\n### Monitoring\n\n* Weight should be measured at the start of therapy, then weekly for the first 6 weeks, then at 12 weeks, at 1 year, and then yearly.\n* Fasting blood glucose, HbA1c, and blood lipid concentrations should be measured at baseline, at 12 weeks, at 1 year, and then yearly. \n* Prolactin concentrations should also be measured at baseline.\n* Before initiating antipsychotic drugs, an ECG may be required, particularly if there are cardiovascular risk factors (e.g. high blood pressure), if there is a personal history of cardiovascular disease, or if the patient is being admitted as an inpatient.\n* Blood pressure monitoring before starting therapy, at 12 weeks, at 1 year and then yearly during treatment and dose titration of antipsychotic drugs.\n\n# Clozapine\n\n- Clozapine is an atypical antipsychotic that is indicated if there is failure of treatment of 2 other antipsychotic medication, known as treatment-resistant schizophrenia.\n- Treats both positive and negative symptoms, slightly more effective than other antipsychotics.\n- Important side effects include: **agranulocytosis**, neutropenia, reduced seizure threshold, myocarditis, slurred speech (due to hypersalivation), constipation (most common cause of mortality when related to clozapine use).\n\n### Monitoring\n\n- Due to its unique and potentially serious side effect profile, monitoring while on clozapine is very important.\n- Patients should have weekly FBC (to look at white cell counts) for the first 18 weeks of treatment then fortnightly for up to one year, and then monthly.\n- Blood lipids and weight should be measured at baseline, every 3 months for the first year, and then yearly.\n- Fasting blood glucose should be tested at baseline, after one months’ treatment, then every 4–6 months.\n\n\n# Neuroleptic Malignant Syndrome\n\nNeuroleptic Malignant Syndrome (NMS) is a rare, but potentially life-threatening, idiosyncratic reaction to antipsychotic medications, particularly those that block dopamine receptors. It typically occurs as a response to the introduction or an increase in the dosage of neuroleptic medications.\n\n### Clinical Features\n\n1. **Hyperthermia:**\n - Profound elevation of body temperature is a hallmark feature.\n \n2. **Altered Mental Status:**\n - Fluctuating levels of consciousness, ranging from confusion to catatonia.\n\n3. **Autonomic Dysregulation:**\n - Dysautonomia characterized by fluctuations in blood pressure, tachycardia, and diaphoresis.\n\n4. **Rigidity:**\n - Generalized muscle stiffness, often described as \"lead-pipe\" rigidity.\n\n### Differential Diagnosis\n\n- **Malignant Hyperthermia** - a rare, genetic condition triggered by certain medications, often during anaesthesia.\n\n- **Serotonin Syndrome** similar to NMS but associated with serotoninergic medications. Presents with hyperthermia, autonomic dysregulation, and altered mental status.\n\n### Investigations \n\n- Bloods:\n\t- FBC - Monitoring for potential leukocytosis or signs of infection.\n - **Creatine Kinase (CK) Levels:** Markedly elevated CK levels are often observed due to muscle breakdown.\n - Renal and Liver Function Tests: monitoring organ function due to the potential systemic effects.\n \n### Management\n\n1. **Discontinuation of Causative Agent:**\n - Immediate cessation of the implicated neuroleptic medication.\n\n2. **Supportive Care:**\n - Aggressive cooling measures to address hyperthermia, including cooling blankets and IV fluids to prevent renal failure.\n\n3. **Benzodiazepines:**\n - Administering benzodiazepines to manage agitation and muscle rigidity.\n\n4. **Dantrolene:**\n - Consideration of dantrolene, a skeletal muscle relaxant, in severe cases.\n\n5. **Intensive Monitoring:**\n - Continuous monitoring of vital signs, fluid balance, and laboratory parameters.",
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"explanation": "Start broad spectrum intravenous antibiotics",
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"learningPoint": "Clozapine treatment increases the risk of agranulocytosis which si treated with broad spectrum intravenous antibiotics.",
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"question": "A 35-year-old man is currently detained in a psychiatric unit under section 3 of the mental health act after an acute deterioration of his schizophrenia two months ago, for which he was started on clozapine. He complains of a two-day history of a sore throat and general malaise. On examination his respiratory rate is 16, oxygen saturations are 100% on room air, heart rate 95, blood pressure 118/65, temperature 38.0°C. He looks well, and has an erythematous oropharynx with no purulent discharge and no deviation of his uvula. \n\nRoutine bloods and blood cultures have been taken.\n\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "Sarcoidosis presents with pyrexia, night sweats, malaise, and lethargy. The lungs are the most common organ to be affected with a restrictive pattern seen from diffuse parenchymal disease. It can affect virtually any organ, but in the joints, it often causes soft-tissue swelling, dactylitis, and tenosynovitis. It is less likely to present with swan neck deformity the proximal interphalangeal and metacarpophalangeal joints - this is more typical of rheumatoid arthritis",
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"explanation": "Limited cutaneous systemic sclerosis, previously named CREST syndrome, causes calcinosis, Raynaud's disease, oesophageal dysmotility, sclerodactyly, and telangiectasia. It may produce hard and thickened skin with non-pitting oedema of the fingers and toes (sclerodactyly). While it may result in joint pain and swelling with pulmonary fibrosis, the characteristic tenderness, inflammation, and swan neck deformity in the proximal interphalangeal and metacarpophalangeal joints is more typical of rheumatoid arthritis",
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"explanation": "Reactive arthritis is an RF-seronegative, HLA-B27-linked inflammatory arthritis that develops in response to a recent infection. It usually develops following gastrointestinal infections such as _Salmonella_, _Shigella_, or _Campylobacter_ or genitourinary infections such as _Chlamydia trachomatis_. It is characterised by large joint asymmetric inflammatory oligoarthritis, conjunctivitis/uveitis, and urethritis/cervicitis (can't see, pee, or climb a tree). This patient does not complain of ocular symptoms, dysuria, or symptoms of urethritis and so reactive arthritis is less likely",
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"name": "Seronegative reactive arthritis",
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"explanation": "Systemic lupus erythematosus (SLE) is a multiorgan disease presenting with a wide range of signs and symptoms. The patients often have non-specific symptoms such as pyrexia, malaise, fatigue, lymphadenopathy, and arthralgia. Arthralgia can present as early morning stiffness in peripheral symmetrical joints along with SLE arthropathy with swan-neck deformity. It can less-commonly affect the lungs causing fibrosing alveolitis or obliterative bronchiolitis. While the patient is experiencing both of these issues, patients with SLE will usually display other constitutional symptoms. The characteristic tenderness, inflammation, and swan neck deformity in the proximal interphalangeal and metacarpophalangeal joints is more typical of rheumatoid arthritis",
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"explanation": "The history and examination findings are most consistent with rheumatoid arthritis (chronic pain and stiffness in the morning) with extra-articular pulmonary fibrosis (exertional dyspnoea with end-inspiratory crackles on examination). Rheumatoid factor (RF) is positive in 60-70% of patients with rheumatoid arthritis. Anti-CCP antibody positive in 80% of patients with rheumatoid arthritis. There are a subgroup of patients with rheumatoid arthritis with negative RF and anti-CCP antibodies - known as seronegative rheumatoid arthritis. In these cases, diagnosis is made by x-ray findings with history and examination",
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"comment": "Seronegative RA + rare complication pulmonary fibrosis, what an unlucky madam",
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"comment": "Did you just… assume their luck in life…",
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"explanation": "# Side effects of corticosteroids\n\n**Corticosteroids** (think CORTICOSTEROIDS):\n\n- Cushing's syndrome\n- Osteoporosis\n- Retardation of growth\n- Thin skin, easy bruising\n- Immunosuppression\n- Cataracts and glaucoma\n- Oedema\n- Suppression of HPA axis\n- Teratogenic\n- Emotional disturbance (including psychosis\n- Rise in BP\n- Obesity (truncal)\n- Increased hair growth (hirsutism)\n- Diabetes mellitus\n- Striae\n\n# Side effects of NSAIDs\n\n- Indigestion\n- Peptic ulcer disease,\n- Increased risk of venous thrombo-embolus\n- Peripheral oedema\n- Slightly increased risk of stroke and heart attack\n\n# Side effects of Methotrexate\n\n- Gastro-intestinal disturbance\n- Folate deficiency - anaemia\n- Immunosuppression\n- Pulmonary fibrosis\n- Liver toxicity\n- Interstitial pneumonitis\n- Rash\n- Teratogenicity - Methotrexate is contraindicated during conception and pregnancy. The recommendation is a washout of a few months (at least 3 months) before conception. In the event of a disease flare, low-dose steroids are thought to be relatively safe. Note that high doses are associated with a small increased risk of the child having a cleft palate.\n\n# Side effects of Sulfasalazine\n\n- Myelosuppression\n- Nausea\n- Rash\n- Oral ulcers\n- Decreased sperm count\n\n# Side effects of Hydroxychloroquine\n\n- Retinopathy\n- Rash\n\n# Side effects of Biologic therapy (e.g. etanercept, infliximab, adalimumab)\n\n- Immunosuppression\n- Reactivation of TB\n- Allergic reaction, reaction at infusion site\n\n# Side effects of Gold\n\n- Myelosuppression\n- Renal toxicity (Nephrotic syndrome)\n- Mouth ulcers\n- Photosensitivity\n- Chrysiasis (skin discolouration)",
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"learningPoint": "In patients with rheumatoid arthritis who test negative for rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies—referred to as seronegative rheumatoid arthritis—diagnosis is typically made based on clinical history, physical examination, and characteristic x-ray findings that show joint damage, erosions, and narrowing.",
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"question": "A 32-year-old woman presents the GP with six months of worsening pain and stiffness in her fingers bilaterally, particularly in the mornings. She works as a builder and is struggling to cope at work with the pain. She has become gradually more short of breath on exertion over recent months with a dry cough.\n\nOn examination there are fine bilateral inspiratory crackles in the chest, and bilateral swan neck deformity in the proximal interphalangeal and metacarpophalangeal joints.\n\nBloods are shown below\n\n| Serum | Result | Reference Range |\n| ------------------------------------------------ | ------ | --------------- |\n| Rheumatoid factor (RF) | 45 | <60 U/mL |\n| Anti-cyclic citrullinated peptide (CCP) antibody | 1 | <7 U/mL |\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "Septic arthritis should always be on your differentials with an acute hot and swollen joint. It is a medical emergency with 10% mortality and the most serious cause of monoarthritis. If not treated urgently, the patient may develop joint damage, functional impairment, and persistent pain. The most usual sites for septic arthritis are the knee in adults and the hip in children. The patient may be pyrexial and generally unwell, although systemic symptoms occur in fewer than 50% of cases of septic arthritis, so a low clinical suspicion is required. It uncommonly presents in the metatarsophalangeal joint (2% of joints). The patient in this question is systemically well with rapid onset of symptoms and inflammation presenting in the 1st metatarsophalangeal joint. The most likely diagnosis is therefore acute gout. In practice if there were any doubt, you would take a joint aspirate and start antibiotics while awaiting the fluid analysis, microscopy, culture, and sensitivity",
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"explanation": "Charcot can present with a hot, swollen, and erythematous joint. It is caused by neuropathy in the foot, most commonly as a result of poorly-controlled diabetes. The patient loses the protective sensation mechanisms which compensate for microtrauma within the feet which then leads to the destruction of the foot and ankle joints. Charcot feet are often not as painful as septic arthritis or gout, and are often painless. They don't present with raised inflammatory markers and the erythema will decrease with elevation. Septic arthritis often will present with raised inflammatory markers and the erythema will be unchanged on elevation. In this question, Charcot foot would unlikely present solely in the metatarsophalangeal joint and with such acute pain. Given the rest of the examination was unremarkable, it is unlikely that it is the cause of this patient's symptoms",
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"label": "c",
"name": "Charcot foot",
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"explanation": "Acute gout presents with a rapid-onset (<24hrs) hot, exquisitely tender, and swollen joint, caused by crystal inflammation from uric acid crystals depositing within the joint. 50% of all attacks and 70% of first attacks present in the first metatarsophalangeal joint. There may also be systemic upset and skin desquamation over the site. Risk factors for gout include male gender, alcohol excess, obesity, renal impairment, diabetes mellitus, and diuretics. Gout may be diagnosed without further investigations in someone with hyperuricaemia and podagra (classic acute arthritis in first metatarsophalangeal joint). If there is any doubt, then the gold standard is joint aspiration synovial fluid analysis. Diagnosis would be confirmed if monosodium urate crystals are seen on synovial fluid analysis - they show strong negative birefringence with needle-like morphology",
"id": "33213",
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"name": "Gout",
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"explanation": "Septic arthritis should always be on your differentials with an acute hot and swollen joint. It is a medical emergency with 10% mortality and the most serious cause of monoarthritis. If not treated urgently, the patient may develop joint damage, functional impairment, and persistent pain. The most usual sites for septic arthritis are the knee in adults and the hip in children. The patient may be pyrexial and generally unwell, although systemic symptoms occur in fewer than 50% of cases of septic arthritis, so a low clinical suspicion is required. It uncommonly presents in the metatarsophalangeal joint (2% of joints). The patient in this question is systemically well with rapid onset of symptoms and inflammation presenting in the 1st metatarsophalangeal joint. The most likely diagnosis is therefore acute gout. In practice if there were any doubt, you would take a joint aspirate and start antibiotics while awaiting the fluid analysis, microscopy, culture, and sensitivity",
"id": "33214",
"label": "b",
"name": "Septic arthritis",
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"explanation": "Acute pseudogout presents similarly to gout, but with less severe pain and less commonly in the 1st metatarsophalangeal joint. It most frequently presents in the knees and wrists with an acutely inflamed, warm, erythematous, painful joint. Patients may also be pyrexial with raised inflammatory markers. Diagnosis is often made after joint aspiration showing positively birefringent rhomboid-shaped crystals",
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"label": "e",
"name": "Acute pseudogout",
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"comment": "Taste not gout?",
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"comment": "What are the water tablets?",
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"comment": "Likely a thiazide diuretic as they're known to cause gout ",
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"comment": "loop diuretics can also cause gout",
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"explanation": "# Summary\n\nGout is a type of arthritis caused by the accumulation of monosodium urate crystals in and around the joints. It presents acutely with rapid onset of severe pain, swelling and redness of affected joints, with the first metatarsophalangeal joints the most commonly affected. Chronic untreated gout may lead to tophi which are hard nodules made up of monosodium urate crystals that deposit in soft tissues. Gout may be diagnosed clinically, with supportive investigations including a serum urate and synovial fluid analysis looking for monosodium urate crystals. Management of acute gout is with NSAIDs, colchicine or a short course of oral steroids. Urate-lowering therapy with allopurinol or febuxostat should be considered to reduce the risk of further gout flares. \n\n# Definition\n\nGout is a form of arthritis that occurs when monosodium urate crystals deposit in joints. This causes both acute inflammation (gout flares) and in the longer-term, a chronic gouty arthritis with tophi (hard deposits of monosodium urate crystals in soft tissues).\n\n# Epidemiology\n\n- Gout is the most common inflammatory arthritis and prevalence is increasing with time (currently 2.5%)\n- Hyperuricaemia (high urate) is the main risk factor (although most patients with a high urate do not develop gout, and some patients develop gout with a normal urate)\n- Factors that contribute to this include:\n- Older age - typically patients are above the age of 40\n- Male sex (post-menopausal women are also at increased risk)\n- Comorbidities including chronic kidney disease (CKD), diabetes, osteoarthritis, hypertension\n- Excess alcohol consumption\n- Dietary excess of meat, seafood and sugary drinks\n- Overweight or obesity\n- Medications such as thiazide diuretics and ciclosporin\n- Family history of hyperuricaemia and gout\n- Genetic disorders associated with hyperuricaemia such as Lesch-Nyhan or glycogen storage disorders\n- Organ transplant recipients\n- Acute attacks may be triggered by stressors including:\n- Trauma and surgery\n- Intercurrent illness\n- Alcohol excess\n- Sudden excess of protein in the diet\n- Chemotherapy (due to cell breakdown)\n- Urate-lowering medications can cause a flare (as crystals are shed into the joint space)\n\n# Signs and Symptoms\n\nOverlapping clinical syndromes are caused by the deposition of monosodium urate crystals in different tissues:\n\n**Acute gout** \n\n- Commonly presents with a monoarthritis\n- Pain is severe and rapid in onset, reaching a peak within 24 hours \n- Affected joints become swollen, erythematous and tender\n- The first metatarsophalangeal (MTP) joint is the most commonly affected (70% of first attacks)\n- Other common sites include the knees, ankles, midtarsal joints, wrists, elbows and small joints of the hands\n- Systemic features such as fever and malaise may be seen\n- Patients may be tachycardic due to pain\n\n**Tophaceous gout**\n\n- Patients will usually have a history of longstanding recurrent acute gout\n- However in atypical cases patients may present with tophi without previous flares\n- Tophi are firm white nodules of sodium monosulphate crystals under the skin\n- They commonly occur on extensor surfaces of joints such as knees or elbows, the Achilles tendons, backs of hands and feet and on the helices of the ears\n- Usually they are painless however they can become infected, inflamed or ulcerated\n- They may discharge white material onto the skin surface\n- Chronic gouty arthritis may present with tender and stiff joints with reduced range of motion\n\n# Differential Diagnosis\n\n- **Septic arthritis** must be ruled out in patients who are systemically unwell with an acute monoarthritis - urgent synovial fluid analysis is needed if this is suspected\n- **Pseudogout** typically affects the knee and wrists rather than the MTP joint; synovial fluid analysis shows calcium pyrophosphate crystals\n- **Cellulitis** causes erythema, pain and swelling of the skin rather than the joint - patients may be systemically unwell\n- **Trauma** should be asked about in the history as this may cause similar symptoms of pain, difficulty mobilising and swelling\n- **Other inflammatory arthritides** such as rheumatoid arthritis may mimic chronic gouty arthritis\n\n# Investigations\n\n**Bedside tests:**\n\n- **Joint aspiration** is the gold standard diagnostic investigation \n- Needle-shaped monosodium urate crystals with negative birefringence are seen in gout\n- Synovial fluid should also be sent for gram stain and culture to rule out septic arthritis\n- Tophi can be biopsied to look for these crystals\n\n**Blood tests:**\n\n- **Serum uric acid** should be measured in all patients with suspected gout\n- A serum urate of 360 micromol/L or more confirms the diagnosis\n- Levels may be falsely low in an acute attack and so should be repeated 2-4 weeks after the flare has resolved\n- Levels are used to guide urate-lowering therapy if this is initiated as prophylaxis\n- **Screening for risk factors** should be considered:\n- Fasting glucose or HbA1c for diabetes\n- Renal function and urine albumin:creatinine ratio for CKD\n- Lipids for hypercholesterolaemia\n- **Inflammatory markers** with FBC and CRP should be checked if septic arthritis is suspected\n- **Liver function tests** are needed prior to starting febuxostat\n- Patients from Han Chinese, Thai and Korean backgrounds should be screened for **HLA-B5801** prior to starting allopurinol (as this increases the risk of severe cutaneous adverse reactions if present)\n\n**Imaging tests:**\n\n- These may be useful to assess chronic disease or where the diagnosis of acute gout is uncertain\n- X-rays in chronic disease show punched-out periarticular erosions, areas of sclerosis and tophi\n- Ultrasound may show joint effusions, tophi, synovial thickening and erosions\n\n# Management \n\n**Acute gout flares** \n\nThere are three first-line options for treatment of a gout flare:\n\n- NSAIDs e.g. naproxen\n- Give at maximum dose\n- Continue until 1-2 days after resolution of symptoms\n- Consider giving with a PPI for gastric protection\n- Avoid in heart failure, patients at high risk of gastrointestinal bleeding and severe renal failure\n- Colchicine\n- Dosing is 500 mcg 2-4 times per day\n- Continue until pain resolves\n- Dose-dependent side effects include diarrhoea, nausea and vomiting\n- Oral corticosteroids\n- e.g. prednisolone 30mg once a day for 3-5 days\n- Useful in patients with contraindications to both NSAIDs and colchicine\n- An injection of intramuscular, intravenous or intra-articular steroids can also be considered\n- Alongside this, consider other analgesia (e.g. paracetamol) and other non-pharmacological pain relief such as ice packs\n- A combination of the above may be tried if a single agent is ineffective\n- Patients should be advised to keep the affected joint cool and exposed and to rest and elevate the affected limb\n- Patients already on urate lowering treatment should continue this throughout the acute flare\n\n## Prevention\n\nPatients should be followed up 4-6 weeks after an acute episode of gout to think about preventative strategies and assess for risk factors (also see Investigations). \n\nOptimisation of risk factors may include:\n\n- Reducing alcohol consumption\n- Maintaining a balanced diet and healthy weight\n- Investigate and treat for comorbidities such as hypertension or CKD\n- Review medications and consider switching medications such as thiazides that cause hyperuricaemia\n- Where possible, switch antihypertensive medications to losartan or amlodipine, which have modest urate-lowering effects \n- Initiating urate-lowering therapy (see below)\n\nMost patients can be managed in primary care, however the following should prompt referral to or discussion with specialist services:\n\n- Patients with complications of gout\n- Atypical presentations (e.g. aged under 30) or uncertain diagnosis\n- Pregnant patients\n- Stage 3b to 5 CKD\n- Organ transplant recipients\n- Those at risk of adverse effects with standard medical treatment, or if treatment is ineffective or not tolerated\n\nIndications for **urate-lowering therapy** include:\n\n- Multiple or troublesome gout flares\n- Chronic gouty arthritis or tophi\n- Patients taking diuretics\n- CKD stage 3 to 5\n\n**Starting and monitoring urate-lowering therapy (ULT):**\n\n- ULT should be started at least 2-4 weeks after an acute flare if possible as medications can precipitate further attacks\n- Colchicine should be given whilst starting ULT to reduce the risk of a flare (NSAIDs or steroids are second-line)\n- Doses should be uptitrated with monthly monitoring of serum urate levels, aiming for a target of 360 micromol/L\n- A target urate level of 300 micromol/L may be helpful in patients with tophi or chronic arthritis due to gout, or those who continue to have flares despite ULT\n- First-line options are either allopurinol or febuxostat which are both xanthine oxidase inhibitors (so reduce uric acid production)\n- Allopurinol is preferred in patients with significant cardiovascular disease\n- Second line options include uricosuric medications (e.g. probenecid) - these can promote stone formation so should be avoided if there is nephrolithiasis\n\n# Complications\n\n- Chronic gouty arthritis and permanent joint damage\n- Tophi, which may become inflamed or infected\n- Nephrolithiasis due to uric acid precipitation - these are responsible for 8% of renal calculi and are radiolucent\n- Chronic urate nephropathy - urate deposition in the renal interstitium causes inflammation and fibrosis\n- Both allopurinol and febuxostat can cause rashes, which in rare cases may be severe (e.g. Stevens Johnson syndrome or toxic epidermal necrolysis)\n- Increased risk of cardiovascular disease and mortality\n\n# NICE Guidelines\n\n[NICE CKS - Gout](https://cks.nice.org.uk/topics/gout/)\n\n[NICE - Gout: diagnosis and management](https://www.nice.org.uk/guidance/ng219/)\n\n# References\n\n[Patient UK - Gout](https://patient.info/doctor/gout-pro)\n\n[Radiopaedia - Gout](https://radiopaedia.org/articles/gout?lang=gb)",
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"question": "A 73-year-old man presents with 12 hours of worsening right foot pain (10/10 severity) and inability to weight-bear. He has no history of trauma.\n\n\nHe can never remember the names of his medical problems or his regular medications, but states he takes \"water tablets\" for his \"heart problems\".\n\n\nOn examination, observations are normal. The left foot and knee are non-tender, non-erythematous, with full range of motion. The right knee is unremarkable. The right foot has a large, tender, warm, erythematous mass on the 1st metatarsophalangeal joint, with the rest of the foot showing full range of motion and intact neurovascular function.\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "Reactive arthritis is an RF-seronegative, HLA-B27-linked inflammatory arthritis that develops in response to a recent infection. It usually develops following gastrointestinal infections such as _Salmonella_, _Shigella_, or _Campylobacter_ or genitourinary infections such as _Chlamydia trachomatis_. It also presents in ages 20-40 and predominantly in males but is characterised by large joint asymmetric inflammatory oligoarthritis, conjunctivitis/uveitis, and urethritis/cervicitis (can't see, pee, or climb a tree). This patient does not complain of dysuria or symptoms of urethritis and so Behçet's disease is more likely. While reactive arthritis can occasionally cause recurrent aphthous ulcers, on balance the patient's symptoms are more in keeping with Behçet's disease",
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"explanation": "HIV Seroconversion presents 3-12 weeks following initial infection. It presents with a mononucleosis-like illness with symptoms including fever, malaise, lethargy, myalgia, lymphadenopathy, pharyngitis, painful oral/genital ulcers, and/or non-pruritic maculopapular rash. It very rarely presents with anterior uveitis and would not present with on-and-off self-resolving ulcers over 12 months",
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"explanation": "Syphilis can present with a wide array of symptoms . Primary syphilis presents with a painless genital ulcer (chancre) and local non-tender lymphadenopathy. It can present with painless oral ulcers although this is less common. Secondary syphilis occurs 4-10 weeks after infection and manifests with a non-pruritic rough red/reddish-brown papular rash, typically on the trunk, and flu-like symptoms such as pyrexia, pharyngitis, malaise, arthalgia/myalgia, lymphadenopathy, and headache. There are a wide variety of rare manifestations, hence the nickname \"the great imitator\", including uveitis, hepatitis, meningitis, glomerulonephritis, periostitis, cranial nerve palsies, and patchy alopecia. The patient in this question does not have any flu-like symptoms or lymphadenopathy and his ulcers are painful, making secondary syphilis less likely",
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"explanation": "# Summary\n\nBehcet's disease is a chronic systemic inflammatory disease which mainly affects people from the Middle East, the Mediterranean and East Asia. The classic triad of manifestations is with oral and genital ulceration and ocular involvement (e.g. uveitis or retinal vasculitis). The gastrointestinal tract, central nervous system, skin and cardiovascular systems may also be affected. Investigations include blood tests showing raised inflammatory markers during acute attacks, testing for HLA-B51 (the most strongly associated genetic risk factor) and a pathergy test (where minor skin trauma leads to the formation of a skin lesion). Management may be local (e.g. topical steroids for orogenital ulceration) or systemic, which may include steroids or other immunosuppressive treatments such as azathioprine or cyclophosphamide. Complications include aneurysm rupture, ischaemia due to vessel thrombosis, permanent visual loss and cerebral vein thrombosis.\n\n# Definition\n\nBehcet's disease is a rare multisystem inflammatory disease that typically causes mouth and genital ulceration, skin lesions, uveitis and arthralgia. Severe complications may result from pulmonary, cardiovascular or central nervous system involvement (also referred to as neuro-Behcet's disease).\n\n# Epidemiology\n\n- The disease is most common in people from Turkey (approximately 80 to 370 cases per 100,000 people)\n- North Africa, the Middle East, South East Asia and other Mediterranean countries also have a relatively high prevalence of cases\n- Overall however it is a rare condition, and can affect people of all ethnicities\n- Men and women are equally likely to develop Behcet's disease, but men tend to be more severely affected\n- HLA-B51 is the most strongly associated genetic risk factor\n- Age of onset is usually in the 20s or 30s, although around 20% of cases present in childhood\n\n# Diagnostic Criteria\n\nThe **International Criteria for Behcet's Disease** are based on the presence of typical clinical features as follows - a score of 4 or more is indicative of a diagnosis of BehcBehcet'set's disease:\n\n| Clinical feature| Points |\n|----------|----------|\n| Ocular lesions | 2 |\n| Genital aphthosis (painful ulceration) | 2 |\n| Oral aphthosis | 2 |\n| Skin lesions | 1 |\n| Neurological manifestations | 1 |\n| Vascular manifestations | 1 |\n| Positive pathergy test (optional) | 1|\n\n\n# Signs and Symptoms\n\n**Systemic** symptoms include:\n\n- Fatigue\n- Malaise\n- Myalgia\n- Low-grade fevers\n- Headaches\n- Arthralgia (an inflammatory arthritis may also occur)\n\n**Mucocutaneous** signs and symptoms include:\n\n- Recurrent oral ulceration (the most common manifestation)\n- Mouth ulcers are usually painful\n- They may cause difficulty eating and drinking\n- Usually heal within 7-21 days\n- Recurrent genital ulceration\n- These are very painful\n- Usually occur on the scrotum in males, and the vulva and in the vagina in females\n- Skin lesions\n- Erythema nodosum (painful nodules usually on the legs)\n- Acne-like papulopustular or nodular lesions on the limbs\n- Pathergy (eruption of papulopustules at the site of minor skin trauma within 24-48 hours)\n- Superficial thrombophlebitis (tender subcutaneous nodules overlying the inflamed vein)\n\n**Ocular** manifestations include:\n\n- Uveitis (anterior or posterior)\n- The affected eye is red and painful\n- Vision is blurred with photophobia\n- Visual loss may occur\n- Retinal vasculitis may present with sudden visual loss\n\n**Pulmonary** involvement:\n\n- Seen in a minority of people\n- Pulmonary arterial aneurysms may form\n- These are usually multiple and bilateral\n- May be asymptomatic\n- May cause dyspnoea, chest pain and cough\n- Rupture can lead to haemoptysis, syncope, cardiogenic shock and sudden death \n- Small vessel vasculitis may occur\n- Ground glass appearances and/or alveolar haemorrhage may be seen on imaging\n- This can also cause haemoptysis, dyspnoea and chest pain\n- Pulmonary artery thrombosis may occur\n- This causes haemoptysis, dyspnoea and chest pain (i.e. similar to symptoms of a pulmonary embolism)\n\n**Central nervous system** manifestations include:\n\n- Headaches\n- Personality changes\n- Cerebellar signs\n- Dysarthria\n- Sensory changes\n- Memory loss\n- Meningoencephalitis\n- Cerebral vein thrombosis\n- Presents with headache, decreased consciousness, visual loss and nausea and vomiting\n- Signs include papilloedema, focal neurological deficits, seizures and cranial nerve palsies\n\n**Gastrointestinal** (GI) involvement may present with:\n\n- Ulceration causing GI bleeding or perforation\n- May cause nausea and vomiting, abdominal pain, anorexia and diarrhoea\n\n**Cardiovascular** involvement may include:\n\n- Deep vein thrombosis (with limb swelling, erythema and tenderness)\n- Pericarditis \n- Vasculitis may affect the aorta and superior vena cava\n- Coronary artery aneurysms may lead to acute coronary syndrome\n- Cardiomyopathy with subsequent heart failure\n\n[lightgallery]\n\n[lightgallery1]\n\n\n# Differential Diagnosis\n\n- **Herpes simplex virus** as a cause of recurrent painful genital and oral ulceration with associated systemic symptoms of malaise \n- **Sarcoidosis** causes similar features of erythema nodosum, arthritis and uveitis and may also affect the lungs and central nervous system, however genital ulcers are not a feature\n- **Reactive arthritis** may present with orogenital ulcers and uveitis, although the urethritis and sacroiliitis seen are not typical of Behcet's disease\n- **Crohn's disease** often causes oral ulceration, GI symptoms that may affect anywhere in the GI tract (as in Behcet's disease), and extraintestinal features of rashes, arthritis and uveitis may also occur; however genital ulcers and central nervous system features are not seen in Crohn's disease \n- **Systemic lupus erythematosus** shares many features including systemic symptoms, arthritis, central nervous system involvement and ulcers (common in the mouth but rare in the genital area); typical rashes differ from Behcet's disease (e.g. malar rash on the face) and blood tests may show antinuclear, anti-double stranded DNA and/or anti-Smith antibodies\n\n# Investigations\n\nThere is no specific diagnostic test for Behcet's disease - investigations may be to rule out differential diagnoses or identify specific organ complications.\n\n**Bedside tests:**\n\n- **Wound swabs** from oral or genital ulcers may be sent for microscopy and/or viral PCR to rule out infectious causes\n- **Urinalysis** should be done to look for blood and protein indicating renal involvement which may occur in differentials such as systemic lupus erythematosus\n\n**Blood tests:**\n\n- **FBC** often shows a high white cell count and a mild anaemia of chronic disease\n- **CRP** and **ESR** may be raised but can be normal even when disease is active\n- **HLA-B51** is not generally useful for diagnosis \n- **Rheumatoid factor**, **ANA** and **ANCA** are typically negative\n- **Syphilis serology** as another cause of oral and genital ulceration\n- Baseline **U&Es** and **LFTs** prior to starting treatment\n- Genetic testing with **next generation sequencing** is increasingly used to rule out monogenetic conditions that may mimic Behcets disease\n\n**Imaging:**\n\n- **MRI head** in neuro-Behcet disease may show parenchymal lesions, most commonly affecting the thalamus, midbrain and internal capsule\n- **MR venography** may be done if central venous sinus thrombosis is suspected\n- **Angiography** is used to identify and assess aneurysms\n- **High-resolution CT chest** may be done in patients with respiratory symptoms to identify pulmonary involvement\n\n**Special tests:**\n\n- A **pathergy test** is non-specific but may be used to support the diagnosis\n- A sterile needle is used to make a skin prick\n- The area is then reassessed after 24-48 hours \n- The test is positive if there a papule or pustule forms at that site\n- It is often positive in pyoderma gangrenosum and acute febrile neutrophilic dermatosis\n- It can also be positive in inflammatory bowel disease or in healthy people\n- **Lumbar puncture** may be indicated in neuro-Behcet disease \n- e.g. to rule out infective causes of meningoencephalitis\n- Elevated cerebrospinal fluid pressure may be seen\n- Raised protein, a pleocytosis and absent oligoclonal bands is typical\n- **Endoscopy** may be required for investigation of GI symptoms and to rule out inflammatory bowel disease \n- **Biopsy of skin lesions** may show leukocytoclastic vasculitis and panniculitis (inflammation of the subcutaneous fat)\n\n# Management\n\n**Conservative management:**\n\n- Patients should be managed in specialist services, with input from multiple specialities often required for different manifestations\n- Prompt management of ocular disease in particular is key to minimise the risk of sight loss\n- Physiotherapy, occupational therapy and/or podiatry input may be helpful for joint disease or functional impairment e.g. in neuro-Behcets\n- Patients should be educated on the disease and on self-management, for example for mouth ulcers:\n- Maintain good oral hygiene\n- Attend regular dental appointments\n- Use topic antiseptics e.g. chlorhexidine mouthwash\n- Avoid foods that cause irritation\n- Patients should be regularly assessed for both disease extent, overall disease activity and quality of life \n- Clinical psychology input is key for general emotional support and focused interventions to support self-management and address distress\n- Neuropsychology assessment should be carried out for all patients with neuro-Behcets\n\n**Medical management:**\n\n- Systemic steroids with a steroid-sparing agent (e.g. methotrexate or azathioprine) are first-line for ocular Behcets\n- Oral and genital ulcers may be treated with potent topical steroids (combined preparations with antibiotics and antifungals are also available)\n- Colchicine is a second-line option for mucocutaneous lesions, and the first-line treatment for arthritis and arthralgia\n- Second-line treatments for joint disease include intra-articular or oral steroids or NSAIDs\n- Gastrointestinal Behcets is managed with similar medications to inflammatory bowel disease, with 5-aminosalicylic acid, azathioprine and 6-mercaptopurine all first line options as well as steroids for flares\n- Neuro-Behcets should be treated with high-dose steroids +/- cyclophosphamide or anti-tumour necrosis factor (TNF) biologics\n- Patients with deep vein thrombosis should not be anticoagulated due to the risk of adverse effects - steroids and azathioprine or anti-TNF agents are first-line\n\n**Surgical and interventional management:**\n\n- Emergency surgery may be required for complications such as major GI bleeding or perforation\n- Stenting or surgery may be required for arterial involvement e.g. aneurysms\n\n# Complications\n\n- Visual loss\n- GI bleeding \n- GI perforation\n- Acute ischaemia of limbs or organs due to vasculitis or thrombosis\n- Acute coronary syndrome\n- Aneurysm rupture (e.g. in the lungs or the brain)\n- Seizures\n- Cognitive impairment is common especially in neuro-Behcets\n- Psychological distress including depression and anxiety\n\n# Prognosis\n\n- The typical disease course is with flares of disease with intervening periods of remission\n- The disease often becomes less active over time\n- Mortality is generally low but is higher in men and patients with an early age of onset\n- However death may occur due to neurological, GI or cardiovascular involvement\n- Immunosuppressive treatments are also associated with significant risks e.g. of infection \n\n# References\n\n[Behcets UK Factsheets](https://behcetsuk.org/behcets-medical-factsheets/)\n\n[British Association of Dermatologists and British Society for Rheumatology living guideline](https://academic.oup.com/rheumatology/advance-article/doi/10.1093/rheumatology/keae438/7753993)\n\n[The International Criteria for Behcets Disease](https://behcetsuk.org/wp-content/uploads/2018/06/ICBD-New-Criteria-2013.pdf)\n\n[Patient UK - Behcet's Disease](https://patient.info/doctor/behcets-disease-pro)\n\n[Radiopaedia - Behcet's Disease](https://radiopaedia.org/articles/behcet-disease-2?lang=gb)\n\n[DermNet NZ - Behcet's Disease](https://dermnetnz.org/topics/behcet-disease)",
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"question": "A 35-year-old Turkish man presents to accident and emergency with painful erythematous sclera and blurred vision of his right eye. He has had something similar in the past however it was not painful and resolved without treatment. \n\nHe also describes 3 episodes of self-terminating painful oral and genital ulcers in the past year and ongoing bilateral arthralgia in his proximal joints.\n\n\nObservations are normal. On examination, he has a globally erythematous right sclera. Vision is 6/12 in right, 6/6 in left (baseline 6/6 bilaterally). He has four well-circumscribed aphthous ulcers in his oral cavity and two further ulcers on the glans and shaft of his penis.\n\nWhat is the most likely diagnosis?",
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"explanation": "In primary hypoparathyroidism, PTH is low, calcium is low, and phosphate is high. This is because of reduced osteoclastic activity in bone and so reduced serum calcium produced from bone reabsorption. Low PTH would also result in reduced reabsorption of calcium in the distal tubules and collecting ducts (reduces serum calcium), and reduced inhibition of reabsorption of phosphate from tubular fluid (increases serum phosphate)",
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"explanation": "This patient does have iron-deficiency anaemia, although this is very common in patients with cancer. There is no evidence of acute haemorrhage to cause this patient's confusion and a mildly increased urea gives further evidence against having had an upper gastrointestinal haemorrhage. Patients often compensate very well with chronic anaemia and may have few or no symptoms. They may complain of general lethargy and shortness of breath on exertion with haemoglobin (Hb) in the 80s, but without signs of acute haemorrhage, this is unlikely to cause confusion",
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"explanation": "Tumour lysis syndrome (TLS) is a potentially fatal complication from chemotherapy. It is more likely seen in cancers with high cell turnover rates, particularly haematological malignancies, e.g. lymphomas and leukaemias, but other solid tumours have also been associated with TLS. It is caused by tumour cells being lysed during treatment and releasing their contents into the blood, producing similar electrolyte abnormalities as rhabdomyolysis. It results in hyperkalaemia, hyperphosphataemia, hypocalcaemia, and hyperuricaemia (high blood uric acid). The patient has presented with symptoms that could be consistent with TLS, although it has been four weeks since his last cycle of chemotherapy and so this is very unlikely. His blood markers are also not consistent with TLS, and so this would be an unlikely cause for this patient's symptoms",
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"explanation": "The patient's symptoms are most likely caused by his hypercalcaemia. It rarely presents with _all_ of \"stones, moans, groans, and psychic overtones\" and often presents solely as lethargy or confusion. Non-small cell lung cancers often can cause hypercalcaemia due to tumour secretion of parathyroid-related protein (PTHrP). This acts in the same way as parathyroid hormone (PTH), activating parathyroid hormone receptors in tissue which results in increased osteoclastic bone resorption (with or without bone metastases), increased renal tubular absorption of calcium, and decreased reabsorption of phosphate in the kidney. The body's normal homeostatic mechanisms are still intact, and so secretion of PTH from the parathyroid gland is reduced to combat the patient's hypercalcaemia. Alkaline phosphatase is increased because of increased osteoclastic bone resorption. This patient's palpitations and new ECG findings can also be explained by hypercalcaemia. ECG findings found in hypercalcaemia are short QT interval, prolonged PR-interval (1st degree heart block), and Osborn waves.\n \n\n This patient has likely also developed an acute kidney injury (AKI) secondary to dehydration from hypercalcaemia - driven by forced diuresis and reduced oral intake from nausea/confusion. NB: The patient may not volunteer polyuria unless asked directly. While the patient does have raised urea, likely from pre-renal AKI, this would not usually elicit cognitive dysfunction at this concentration.\n \n\n This patient does have iron-deficiency anaemia, although this is very common in patients with cancer. There is no evidence of acute haemorrhage to cause this patient's confusion and a mildly increased urea gives further evidence against having had an upper gastrointestinal haemorrhage",
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"explanation": "In primary hypoparathyroidism, PTH is low, calcium is low, and phosphate is high. This is because of reduced osteoclastic activity in bone and so reduced serum calcium produced from bone reabsorption. Low PTH would also result in reduced reabsorption of calcium in the distal tubules and collecting ducts (reduces serum calcium), and reduced inhibition of reabsorption of phosphate from tubular fluid (increases serum phosphate)",
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"comment": "A question longer than johnny sins",
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"comment": "why is PTH low if PTH is being secreted causing high calcium?",
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"comment": "The tumour secretes parathyroid-related protein not PTH. This causes a rise in calcium similar to if there was a rise in PTH. This results in negative feedback on the parathyroid and the body is like, 'hey I don't need to increase calcium' so PTH levels from the parathyroid fall to very low levels.",
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"comment": "PTHrP =! PTH-> suppressed PTH due to HHM.",
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"comment": "A very well-thought out Q testing lots of areas (tough, but not in the normal bull rote learning Quesmed way)",
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"explanation": "# Summary\n\nConfusion is a common issue in oncology, with diverse causes including metabolic disturbances, infections, and metastatic spread to the brain. It is crucial to identify and treat underlying factors, as confusion can distress patients and families. Delirious patients face higher risks of falls and complications, requiring careful management strategies.\n\n\n# Differentials of confusion in oncology\n\nConfusion is a common presenting complaint within general medicine and oncology. Confusion seen in the context of a cancer patient alters the likelihood of certain causes of confusion.\n\nThere are a diverse range of causes for confusion in oncology patients:\n\n- **Metabolic disturbance** (hypoglycaemia, hypercalcaemia): this may present acutely or subacutely. Patients often have concurrent symptoms such as feeling hungry or shaky for hypoglycaemia and very thirsty or GI upset for hypercalcaemia.\n- **Neutropenic sepsis**: this is an oncological emergency and may be difficult to spot, as many usual signs of infection may be absent. In any patient with known or suspected neutropenia presenting with confusion, neutropenic sepsis should be top of the differential list.\n- **Infection** (pneumonia, UTI): patients may have localising symptoms of infection. For example, a cough or dysuria. However patients may present atypically so always consider whether sepsis could be causing the confusion, even in the absence of typical signs.\n- **Metastatic spread to the brain**: typically, this is subacute onset and associated with headache, visual disturbances and/or focal neurology. The most common cancers to spread to the brain are lung, breast, colorectal, melanoma and renal cell carcinoma. Therefore have a low threshold for suspecting metastases especially in these cancers.\n- **Anaemia**: this may be difficult to diagnose clinically, as cancer and its treatment causes fatigue for most patients. A full blood count is a useful investigation to rule out anaemia and neutropenia.\n- Other causes of delirium, including **pain, constipation and medications**. It is important to rule out these reversible causes of confusion. This can be elicited in the history and medication review, and treatment can make a significant difference to the patient's mental status and quality of life.\n\n# Management\n\nIt is important to recognise and treat the underlying cause of confusion. This can be distressing for the patient and relatives alike.\n\nPatients with delirium (acute confusional state) are at increased risk of falls, increased mortality and morbidity. Environmental modifications can help reduce confusion, as well as optimising reversible factors and falls risk reduction measures. Pharmacological management is reserved for when non-pharmacological measures do not work or when a patient is agitated towards the end of life.\n\n# NICE guidelines\n\n[NICE CKS: Delirium](https://cks.nice.org.uk/topics/delirium/)\n\n# References\n\n[Marie Curie: Delirium in palliative care](https://www.mariecurie.org.uk/professionals/palliative-care-knowledge-zone/symptom-control/delirium)",
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"question": "A 65-year-old man is brought to A&E with progressive confusion over the past week, lethargy and sleepiness. He is disoriented and reports occasional palpitations. He has a 60-pack-year smoking history and was diagnosed with non-small cell lung cancer nine months ago, and has completed multiple cycles of chemotherapy and radiotherapy, with the last cycle four weeks ago.\n\n\nHe is tachycardic, apyrexial, and has dry mucous membranes. His chest is clear, abdomen is soft and non-tender, with no focal neurology. \n\n\nECG shows new 1st degree heart block; urine dip is clear. Chest X-ray shows a known left hilar mass.\n\n\n\nBloods tests:\n\n\n|Serum|Result|Reference Range|\n|---------------------------|------|-----------------------------|\n|Haemoglobin|82|130 - 170 mg/dL|\n|White Cell Count|4.1|3.0 - 10.0 x 10⁹ /L|\n|Platelets|180|150 - 400 x 10⁹/L|\n|Mean Cell Volume|71|80 - 96 fL|\n|Urea|10.1|2.5 - 7.8 mmol/L|\n|Creatinine|170|60 - 120 µmol/L|\n|eGFR|37|≥ 60 mL/min/1.73m<sup>2</sup>|\n|Iron|5.6|14 - 31 μmol/L|\n|Total Iron Binding Capacity|35|54 - 75 μmol/L|\n|Corrected Calcium|3.6|2.2 - 2.6 mmol/L|\n|Magnesium|0.65|0.7 - 1.0 mmol/L|\n|Phosphate|0.4|0.8 - 1.5|\n|Parathyroid Hormone|0.1|1.6 - 8.5 pmol/L|\n\n\nWhat is the most likely cause of this patient's symptoms?",
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"explanation": "The main concern in patients on chemotherapy with pyrexia is neutropenic sepsis. This is defined as a temperature of greater than 38.0°C, OR any symptoms and/or signs of sepsis, in a person with absolute neutrophil count of 0.5 x 10⁹/L or lower.\n \n\n These patients are severely immunosuppressed and cannot mount the normal immune response to infection that others can. They can look and feel completely well for some time, with relatively normal observations, before rapidly becoming unwell and deteriorating. Low threshold are needed to treat aggressively early and take cultures from any possible source to help guide choice of step-down antibiotics",
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"explanation": "This patient has neutropenic sepsis: a temperature of greater than 38.0°C, OR any symptoms and/or signs of sepsis, in a person with absolute neutrophil count of 0.5 x 10⁹/L or lower. They need cultures from possible infection sites and broad spectrum antibiotics as they are at high risk of deteriorating",
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"name": "Tranfuse one unit of packed red blood cells",
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"explanation": "This patient has neutropenic sepsis: a temperature of greater than 38.0°C, OR any symptoms and/or signs of sepsis, in a person with absolute neutrophil count of 0.5 x 10⁹/L or lower. They are at high risk of deteriorating and so should be admitted for cultures and broad spectrum antibiotics",
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"name": "Discharge the patient and provide extensive safety-netting advice to return if develops any signs of infection",
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"explanation": "This patient has neutropenic sepsis: a temperature of greater than 38.0°C, OR any symptoms and/or signs of sepsis, in a person with absolute neutrophil count of 0.5 x 10⁹/L or lower. They need cultures from possible infection sites and broad spectrum antibiotics as they are at high risk of deteriorating",
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"explanation": "This patient has neutropenic sepsis and are at high risk of deteriorating and so should be admitted for cultures and broad spectrum antibiotics. CT scans can be used to identify the source of the infection, particularly if there any underlying collections, although it is not the first line investigation for determining the source. Cultures should be taken first and cross-sectional imaging to be considered if the source is still not identified despite this and the patient is still symptomatic",
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"explanation": "# Summary\n\nNeutropenic sepsis is a serious infection that can occur in immunocompromised patients. According to NICE, in patients undergoing cancer treatment, it is identified by a temperature exceeding 38<sup>o</sup>C or any signs of infection, coupled with a neutrophil count below 0.5 x 10<sup>9</sup>/l. This condition is most prevalent among those receiving anticancer therapies and is considered an oncological emergency. Risk factors include severe or prolonged neutropenia, advanced malignancies, and certain medical comorbidities. Clinical presentation may be subtle, necessitating a high index of suspicion for any febrile immunocompromised patient. Prompt investigation and management, including the sepsis six protocol and early senior input, are crucial, as untreated neutropenic sepsis carries a significant risk of mortality and complications from treatment, such as multi-drug resistant infections.\n\n\n\n# Definition\n\nIn simple terms, neutropenic sepsis can be defined as the presence of both:\n\n- Neutropenia, a low number of neutrophils in the blood.\n- Sepsis, defined as a dysregulated response to infection causing life-threatening organ dysfunction.\n\nNICE define neutropenic sepsis in patients receiving anticancer treatment as a temperature **above 38<sup>o</sup>C or any other signs of infection and a neutrophil count of less than 0.5x10<sup>9</sup>/l**.\n\nIt most commonly occurs in people receiving anticancer therapy, and is an oncological emergency. It can also occur in immunocompromise due to other causes, for example immunosuppression, HIV infection or congenital immunodeficiency syndromes.\n\nNeutropenic fever is another commonly used term. It refers to a single temperature reading of above 38.3<sup>o</sup>C or two consecutive readings above above 38<sup>o</sup>C for two hours, along with a known or expected neutrophil count of less than 0.5x10<sup>9</sup>/l, and carries a greater risk of sepsis.\n\n***In practice, any fever in the context of known or suspected neutropenia is a medical emergency which can be life-threatening if not treated promptly.***\n\n# Aetiology\n\nRisk factors for neutropenic sepsis include:\n\n- Severe and/or prolonged neutropenia\n- Extremes of age\n- Previous febrile neutropenia\n- Haematological or advanced malignancy\n- Prolonged hospital admission or previous surgery\n- Medical comorbidities\n- Indwelling lines\n- Concurrent corticosteroids\n\nPathogens which can cause neutropenic sepsis include:\n\n- Gram-positive bacteria: Staphylococci sp. (including *S. aureus* & *S. epidermidis*), Enterococcus sp. and Streptococci sp.\n- Gram-negative bacteria: *Escherichia coli*, Klebsiella sp., Enterobacter sp. and *Pseudomonas aeruginosa*\n- Fungal infections with *Candida* or *Aspergillus* species\n- Viral infections\n\n# Signs and symptoms\n\nClinical features of neutropenic sepsis may be very difficult to distinguish, as neutropenic patients do not have a normal immune response. Therefore, you should have a low threshold for suspecting neutropenic sepsis in any immunocompromised person who becomes unwell. Clinical features may include:\n\n- Focal signs of infection, for example dysuria, productive cough, diarrhoea\n- Physiological derangement, including fever or hypothermia, elevated respiratory rate, tachycardia, hypotension, skin colour changes, altered mental state\n- Any concern from the patient or relative\n\n# Differential diagnosis\n\n- **Sepsis** causing neutropenia: the person will have presented with symptoms of sepsis first and had a normal or high white cell count, before subsequently developing a neutropenia due to the infection.\n- **Drug fever** can occur with many pharmacological agents. Patients may have associated eosinophilia, rash, hepatic or renal derangement. Tests for infection would be negative.\n- **Tumour fever**: this is a low-grade fever caused by progression of a malignancy causing inflammation. Tests for infection would be negative and tumour fevers do not respond to antibiotics.\n- **Venous thromboembolism**: patients would typically have concurrent symptoms of a deep vein thrombosis or pulmonary embolism (painful swollen leg, chest pain respectively). Definitive diagnosis would be via doppler ultrasound or the leg or CT angiogram of the chest.\n\n\n# Investigations\n\nIt is important to initiate investigations and management for neutropenic sepsis as soon as it is suspected. Initial investigations to request alongside an A-E assessment are:\n\n- Bedside: full set of observations, blood gas, glucose measurement, urine dip, ECG\n- Bloods: FBC, CRP, U&E's, LFT's, clotting, lactate\n- Cultures: blood cultures, urine, sputum, any indwelling lines or other potential sources of infection\n- Imaging: chest X-ray, and any further imaging related to the potential source of infection as appropriate\n\n# Management\n\n**For any patient with suspected neutropenic sepsis, adopt an A-E approach, initiate the sepsis six and seek early senior input.**\n\nThis will include:\n\n- Giving **oxygen** to maintain saturations above 94%\n- IV access to give **fluids** to maintain blood pressure, take bloods and give antibiotics\n- Giving IV broad-spectrum **antibiotics** according to local guidelines, to be given within an hour. 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"question": "A 44-year-old woman presents with a temperature of 38.1°C, 3 days after starting cycle 2 of chemotherapy for advanced colorectal cancer. She had T3a rectal cancer resected 8 weeks ago with an end colostomy.\n\nShe feels well, with normal observations. Examination shows moist, oral mucosa, a clear chest, a soft, non-tender abdomen, and a pink, warm colostomy producing type 5 stool. No focal neurological signs, meningism, rash, or cellulitis are present.\n\nInvestigations:\n\nUrine dip: Clear\nBeta-hCG: Negative\nChest X-ray: Unremarkable\n \n \n\n| Serum | Result | Reference Range |\n| ------------------------------------ | ------ | ------------------- |\n| Haemoglobin | 95 | 115-155 mg/dL |\n| White Cell Count | 2.1 | 3.0 - 10.0 x 10⁹ /L |\n| Platelets | 160 | 150 - 400 x 10⁹/L |\n| Neutrophils | 0.5 | 2.0 - 7.5 x 10⁹ /L |\n| Sodium | 135 | 135 - 146 mmol/L |\n| Potassium | 3.6 | 3.5 - 5.3 mmol/L |\n| Urea | 2.8 | 2.5 - 7.8 mmol/L |\n| Creatinine | 45 | 60 - 120 µmol/L |\n| eGFR | >90 | \\> 60 mL/min/1.73m2 |\n| C reactive protein | 25 | < 5 mg/L |\n| Lactate | 1.2 | 0.20-1.80 mmol/L |\n \n \n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "This would be too large of an increment of as required oral morphine to increase to for the current long-acting morphine dose. This increases the risk of needless opioid toxicity/overdose and of systemic side-effects",
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"explanation": "Breakthrough dose of morphine in adults with cancer is calculated by dividing the 24-hour dose of oral morphine by 6. Usually a range is required and so the range should be approximately 1/10th-1/6th of the 24-hour total morphine dose.\n \n\n The principal is the same for all opioids, although it is best practice to convert the full 24 hour dose of opioids to the corresponding _oral_ morphine dose, and then convert back to the desired drug and route. This is of use when the long-acting drug is different to the breakthrough drug e.g. oral oxycodone breakthrough with a buprenorphine patch.\n \n\n The total dose of oral morphine in this case is 180mg/24hrs. 1/6th of this is 30mg and 1/10th of this is 18mg. For practicality in administration, this has been rounded to 20-30mg",
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"comment": "i was always taught 1/6th of background makes up a breakthrough dose - so seeing 2 answers with 30 mg really isn't that helpful",
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"comment": "Max breakthrough dose is 1/6th of maintenance, so you really shouldn't be giving anything higher than 30mg",
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"explanation": "# Summary\n\nMedications in end-of-life care focus on alleviating distressing symptoms in patients nearing death. A holistic approach is vital, considering physical, emotional, and social aspects of symptoms, often involving a multidisciplinary team. For pain management, the WHO pain ladder guides pharmacological strategies, with morphine as the primary strong opioid. Specific treatments for other symptoms depend on the underlying cause and it is important to consider reversible causes and non-pharmacological measures.\n\n\n\n# Definition\n\nMedications used in end of life care aim to relieve distressing symptoms which may appear in the last days, weeks, or months of life. They are commonly prescribed as 'anticipatory' or 'just in case' medications for a patient known to be nearing the end of life.\n\n\nThey can be administered:\n\n\n- Orally - if the patient is safely able to swallow\n- Subcutaneously - via single dose or continuous syringe pump\n- Transdermally - especially for stable symptoms and if available\n- Intramuscularly - less common\n- Intravenously - less common, but may be helpful if a patient already has access\n\n## A note on holistic care\n\nIn palliative care, and in medicine, it is important to consider all symptoms in context. There are many different aspects to symptoms. These include the physical cause, the patient's beliefs about their illness and symptoms, social contributors and impacts, their emotional and behavioural responses. Holistic assessment and management are crucial, which is why the multidisciplinary team is so important. \n\nFor example, a patient may have been prescribed very effective analgesia but is unable to administer medicines themselves. They may also have a very strong emotional response to pain or believe that they deserve their symptoms. They may benefit from a package of care or financial support for terminal illness which a social worker could help with, or an occupational therapist to help with activities of daily living. Counselling may give the patient a space to explore their feelings around their symptoms and their illness, while spiritual support could alleviate some existential distress. These additional interventions work alongside pharmacological therapy to optimise a person's quality of life through their illness.\n\nThis chapter focuses on medications for symptoms towards the end of life, but it is crucial to remember that each patient has a different combination of needs which requires an individual assessment and management plan, often with input from a range of health and social care professionals.\n\n# Pain\n\n\nInitial pharmacological management of pain should follow the WHO pain ladder. Once patients have reached the top of this ladder (requiring regular strong opioids), careful optimisation is necessary to ensure the right level of pain relief while minimising side effects.\n\n- Morphine is the first-line strong opioid analgesic. This can be given as a modified release or immediate release form. \n- Generally, patients would have a regular 'background' dose based on their 24-hour requirements, plus a PRN dose available for **breakthrough pain.** PRN doses are usually 1/6-1/10 of the 24 hour dose. Analgesia requirements should be reviewed regularly, for example every 24 hours.\n- Alternatives to morphine may be necessary for patients with poor renal function. These include oxycodone, alfentanyl or buprenorphine.\n- When prescribing opioid analgesia consider co-prescribing a regular laxative and an as-required anti-emetic. Monitor for signs of opioid toxicity (respiratory depression, sedation, myoclonus) and switch to alternatives or dose reduce as necessary.\n\nWhen switching analgesia, it is helpful to convert the dose first to oral morphine before converting to the desired medication. Please note that different routes also have different equivalent doses, so it is always safest to check guidelines.\n\n\nThe following table shows dose equivalents of 10mg oral morphine\n\n\n| Analgesic/Route | Dose | Conversion Factor |\n| ----------------------------- | ------- | ----------------- |\n| Codeine/tramadol/dihydrocodeine oral | 100mg | x10 |\n| Diamorphine IM/IV/Subcut | 3mg | x3.3 |\n| Morphine IM/IV/Subcut | 5mg | x2 |\n| Oxycodone oral\\* | 5mg\\* | x2\\* |\n| Oxycodone Subcut\\* | 2.5mg\\* | x4\\* |\n| Alfentanil Subcut | 0.3mg | x30 |\n\n\n*NB - oral oxycodone potency is between 1.3-2x that of oral morphine. Different trusts will adopt different guidance on which you should use. If in doubt, always opt for the lower dose and titrate up.\n\n\n# Breathlessness\n\nConsider non-pharmacological measures for breathlessness first. For example, sitting the patient up, opening a window or setting up a fan can all help.\n\nPharmacological management may involve low-dose opioids, benzodiazepines or therapeutic oxygen, and should be tailored to the patient.\n\n\n# Nausea and vomiting\n\nIt is important to consider the likely cause of nausea and vomiting, as medications target different parts of the vomiting pathway. Perform a full assessment to determine the likely cause of the nausea and vomiting. Consider parenteral routes of administration - patients may have severe gastrointestinal disturbance or at least may not be able to keep down oral antiemetics long enough to be effective.\n\nThe following table shows the primary site of activity and side effects of commonly used antiemetics:\n\n| Antiemetic | Receptor activity | Side effects & cautions | Useful for |\n|---|---|---|---|\n| Metoclopramide | Dopamine antagonist | Extrapyramidal symptoms, drowsiness, restlessness, diarrhoea. Do not give with antimuscarinics or in mechanical bowel obstruction | Gastric stasis, functional bowel obstruction |\n| Cyclizine | Histamine, acetylcholine antagonist | Drowsiness, antimuscarinic | Raised intracranial pressure, vestibular dysfunction |\n| Hyoscine | Acetylcholine antagonist | Antimuscarinic | Motion sickness |\n| Haloperidol | Dopamine antagonist | Less common in palliative care doses | Chemical |\n| Levomepromazine | Dopamine, histamine, acetylcholine, 5HT2 antagonist | Sedation, postural hypotension, antimuscarinic |Broad range |\n| Ondansetron | 5HT3 antagonist | Constipation, arrhythmias, movement disorder | Cytotoxic-related |\n\n- For chemically-mediated symptoms (for example medications, metabolic derangemenet), aim to treat the underlying cause. Antiemetics that may be helpful include haloperidol, metoclopramide or levomepromazine.\n- For nausea and vomiting due to raised intracranial pressure, cyclizine is usually used first-line. Dexamethasone or radiotherapy may be helpful to reduce the pressure-associated symptoms.\n- For patients with vestibular disturbance (for example symptoms associated with movement), cyclizine usually used first-line. Alternatives include hyoscine hydrobromide.\n- For patients with bowel obstruction, seek specialist advice. If due to peristaltic failure, review medications and consider starting metoclopramide (providing there is no colic). Likewise for gastric stasis, consider metoclopramide. For patients with mechanical obstruction and/or colic, do not give metoclopramide. Exclude constipation, give cyclizine for nausea and treat colic with hyoscine butylbromide.\n- If nausea and vomiting is due to compression from an abdominal or pelvic tumour, cyclizine should be used first-line.\n- For anxiety-related nausea and vomiting, begin with non-pharmacological measures for anxiety, such as CBT. A benzodiazepine or levomepromazine would be first-line pharmacological options.\n\n# Agitation\n\nAs with other symptoms, aim to manage reversible causes of agitation and possible delirium first. Consider non-pharmacological measures such as environmental modification. For patients in their last days of life, haloperidol or low-dose midazolam may be prescribed. Often, this is done as part of anticipatory prescribing.\n\n\n# Respiratory tract secretions\n\nRespiratory tract secretions often occur in the last days of life as a person becomes less able to clear their airways. They are rarely a cause of distress to the patient, but may be upsetting for family members or those close to the patient. An antimuscarinic such as hyoscine butylbromide or glycopyrronium bromide may be prescribed for noisy respiratory secretions.\n\n\n# NICE guidelines\n\n\n[NICE Guidance: Care of dying adults in the last days of life](https://www.nice.org.uk/guidance/ng31)\n\n[NICE CKS: Palliative care - general issues](https://cks.nice.org.uk/topics/palliative-care-general-issues/)\n\n[NICE CKS: Palliative care - dyspnoea](https://cks.nice.org.uk/topics/palliative-care-dyspnoea/)\n\n[NICE CKS: Palliative care - nausea and vomiting](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative care - secretions](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative cancer care - pain](https://cks.nice.org.uk/topics/)\n\n# References\n\n[Pallcare.info](https://www.pallcare.info/book.php)\n\n[BNF: Ondansetron](https://bnf.nice.org.uk/drugs/ondansetron/#drug-action)\n\n[BNF: Nausea and labyrinth disorders](https://bnf.nice.org.uk/treatment-summaries/nausea-and-labyrinth-disorders/)\n\n[BNF: Prescribing in palliative care](https://bnf.nice.org.uk/medicines-guidance/prescribing-in-palliative-care/)",
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"question": "A 75-year-old woman with metastatic mesothelioma presents with progressive shortness of breath and uncontrolled pleuritic chest pain. Her eGFR is 85mL/min/1.73m<sup>2</sup> and her liver function tests are all within normal range.\n\n\nShe currently takes 900mg gabapentin TDS, 1g paracetamol QDS, 80mg modified standard release morphine sulfate (long acting) BD, and 75mg amitriptyline ON. S She is currently using all her prescribed as-needed oral morphine doses and frequently requests her next dose due to ongoing pain.\n\n\nYou decide to increase her modified standard release morphine sulfate dose to 90mg twice daily. Calculate the most appropriate breakthrough oral morphine sulfate immediate release dose for this new regime.",
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"explanation": "Morphine sulfate accumulates in renal failure with eGFR <45mL/min/1.73m2 and so the choice of opioid should be changed to one with less renal excretion. In those with eGFR 10-30mL/min/1.73m2, the most common choice is oxycodone. With eGFR <10mL/min/1.73m2, the most common choice is alfentanil.\n \n\n This would be the correct dosing of alfentanil, although paracetamol is not available as a subcutaneous injection and so must be given orally or IV",
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"explanation": "This patient is on 90mg twice daily of morphine sulfate modified release and has used 4 doses of 30mg morphine immediate release, equating to a total of 300mg oral morphine sulfate in24hrs.\n \n\n Morphine sulfate accumulates in renal failure with eGFR <45mL/min/1.73m2 and so the choice of opioid should be changed to one with less renal excretion.\n \n\n In patient such as this one, with eGFR 10-30mL/min/1.73m2, the most common choice is oxycodone.\n \n\n To convert between opioids, always convert to the 24hr dose of oral morphine from the current opioid regime and then convert to the new drug of choice.\n \n\n If you are unsure, always look up conversions online or in your local trust guidance. The following table shows dose equivalents of 10mg oral morphine\n \n\n| Analgesic/Route | Dose | Conversion Factor |\n| -------------- | ------- | ----------------- |\n| Codeine/tramadol/dihydrocodeine oral | 100mg | x10 |\n| Diamorphine IM/IV/Subcut | 3mg | ÷3.3 |\n| Morphine IM/IV/Subcut | 5mg | ÷2 |\n| Oxycodone oral\\* | 6.6mg\\* | ÷1.5\\* |\n| Oxycodone Subcut\\* | 5mg\\* | ÷2\\* |\n| Alfentanil Subcut | 0.3mg | ÷30 |\n \n\n \\*NB - oral oxycodone potency is between 1.3-2x that of oral morphine. Different trusts will adopt different guidance on which you should use. If in doubt, always opt for the lower dose and titrate up.\n \n\n This patient is on 300mg/24hrs oral morphine equating to 150mg subcutaneous oxycodone/24hrs. Breakthrough analgesia dose is calculated 1/10th-1/6th the 24hr dose. This equates to 15mg-25mg subcutaneous oxycodone as required.\n \n\n Paracetamol is not available as a subcutaneous injection and so must be given orally or IV. Often when patients approach the end of their life intravenous medications are stopped or converted to other routes to avoid repetitive cannulations",
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"explanation": " This patient is on 300mg/24hrs oral morphine equating to 150mg subcutaneous oxycodone/24hrs. Subcutaneous oxycodone is twice as potent as as oral morphine",
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"explanation": "# Summary\n\nMedications in end-of-life care focus on alleviating distressing symptoms in patients nearing death. A holistic approach is vital, considering physical, emotional, and social aspects of symptoms, often involving a multidisciplinary team. For pain management, the WHO pain ladder guides pharmacological strategies, with morphine as the primary strong opioid. Specific treatments for other symptoms depend on the underlying cause and it is important to consider reversible causes and non-pharmacological measures.\n\n\n\n# Definition\n\nMedications used in end of life care aim to relieve distressing symptoms which may appear in the last days, weeks, or months of life. They are commonly prescribed as 'anticipatory' or 'just in case' medications for a patient known to be nearing the end of life.\n\n\nThey can be administered:\n\n\n- Orally - if the patient is safely able to swallow\n- Subcutaneously - via single dose or continuous syringe pump\n- Transdermally - especially for stable symptoms and if available\n- Intramuscularly - less common\n- Intravenously - less common, but may be helpful if a patient already has access\n\n## A note on holistic care\n\nIn palliative care, and in medicine, it is important to consider all symptoms in context. There are many different aspects to symptoms. These include the physical cause, the patient's beliefs about their illness and symptoms, social contributors and impacts, their emotional and behavioural responses. Holistic assessment and management are crucial, which is why the multidisciplinary team is so important. \n\nFor example, a patient may have been prescribed very effective analgesia but is unable to administer medicines themselves. They may also have a very strong emotional response to pain or believe that they deserve their symptoms. They may benefit from a package of care or financial support for terminal illness which a social worker could help with, or an occupational therapist to help with activities of daily living. Counselling may give the patient a space to explore their feelings around their symptoms and their illness, while spiritual support could alleviate some existential distress. These additional interventions work alongside pharmacological therapy to optimise a person's quality of life through their illness.\n\nThis chapter focuses on medications for symptoms towards the end of life, but it is crucial to remember that each patient has a different combination of needs which requires an individual assessment and management plan, often with input from a range of health and social care professionals.\n\n# Pain\n\n\nInitial pharmacological management of pain should follow the WHO pain ladder. Once patients have reached the top of this ladder (requiring regular strong opioids), careful optimisation is necessary to ensure the right level of pain relief while minimising side effects.\n\n- Morphine is the first-line strong opioid analgesic. This can be given as a modified release or immediate release form. \n- Generally, patients would have a regular 'background' dose based on their 24-hour requirements, plus a PRN dose available for **breakthrough pain.** PRN doses are usually 1/6-1/10 of the 24 hour dose. Analgesia requirements should be reviewed regularly, for example every 24 hours.\n- Alternatives to morphine may be necessary for patients with poor renal function. These include oxycodone, alfentanyl or buprenorphine.\n- When prescribing opioid analgesia consider co-prescribing a regular laxative and an as-required anti-emetic. Monitor for signs of opioid toxicity (respiratory depression, sedation, myoclonus) and switch to alternatives or dose reduce as necessary.\n\nWhen switching analgesia, it is helpful to convert the dose first to oral morphine before converting to the desired medication. Please note that different routes also have different equivalent doses, so it is always safest to check guidelines.\n\n\nThe following table shows dose equivalents of 10mg oral morphine\n\n\n| Analgesic/Route | Dose | Conversion Factor |\n| ----------------------------- | ------- | ----------------- |\n| Codeine/tramadol/dihydrocodeine oral | 100mg | x10 |\n| Diamorphine IM/IV/Subcut | 3mg | x3.3 |\n| Morphine IM/IV/Subcut | 5mg | x2 |\n| Oxycodone oral\\* | 5mg\\* | x2\\* |\n| Oxycodone Subcut\\* | 2.5mg\\* | x4\\* |\n| Alfentanil Subcut | 0.3mg | x30 |\n\n\n*NB - oral oxycodone potency is between 1.3-2x that of oral morphine. Different trusts will adopt different guidance on which you should use. If in doubt, always opt for the lower dose and titrate up.\n\n\n# Breathlessness\n\nConsider non-pharmacological measures for breathlessness first. For example, sitting the patient up, opening a window or setting up a fan can all help.\n\nPharmacological management may involve low-dose opioids, benzodiazepines or therapeutic oxygen, and should be tailored to the patient.\n\n\n# Nausea and vomiting\n\nIt is important to consider the likely cause of nausea and vomiting, as medications target different parts of the vomiting pathway. Perform a full assessment to determine the likely cause of the nausea and vomiting. Consider parenteral routes of administration - patients may have severe gastrointestinal disturbance or at least may not be able to keep down oral antiemetics long enough to be effective.\n\nThe following table shows the primary site of activity and side effects of commonly used antiemetics:\n\n| Antiemetic | Receptor activity | Side effects & cautions | Useful for |\n|---|---|---|---|\n| Metoclopramide | Dopamine antagonist | Extrapyramidal symptoms, drowsiness, restlessness, diarrhoea. Do not give with antimuscarinics or in mechanical bowel obstruction | Gastric stasis, functional bowel obstruction |\n| Cyclizine | Histamine, acetylcholine antagonist | Drowsiness, antimuscarinic | Raised intracranial pressure, vestibular dysfunction |\n| Hyoscine | Acetylcholine antagonist | Antimuscarinic | Motion sickness |\n| Haloperidol | Dopamine antagonist | Less common in palliative care doses | Chemical |\n| Levomepromazine | Dopamine, histamine, acetylcholine, 5HT2 antagonist | Sedation, postural hypotension, antimuscarinic |Broad range |\n| Ondansetron | 5HT3 antagonist | Constipation, arrhythmias, movement disorder | Cytotoxic-related |\n\n- For chemically-mediated symptoms (for example medications, metabolic derangemenet), aim to treat the underlying cause. Antiemetics that may be helpful include haloperidol, metoclopramide or levomepromazine.\n- For nausea and vomiting due to raised intracranial pressure, cyclizine is usually used first-line. Dexamethasone or radiotherapy may be helpful to reduce the pressure-associated symptoms.\n- For patients with vestibular disturbance (for example symptoms associated with movement), cyclizine usually used first-line. Alternatives include hyoscine hydrobromide.\n- For patients with bowel obstruction, seek specialist advice. If due to peristaltic failure, review medications and consider starting metoclopramide (providing there is no colic). Likewise for gastric stasis, consider metoclopramide. For patients with mechanical obstruction and/or colic, do not give metoclopramide. Exclude constipation, give cyclizine for nausea and treat colic with hyoscine butylbromide.\n- If nausea and vomiting is due to compression from an abdominal or pelvic tumour, cyclizine should be used first-line.\n- For anxiety-related nausea and vomiting, begin with non-pharmacological measures for anxiety, such as CBT. A benzodiazepine or levomepromazine would be first-line pharmacological options.\n\n# Agitation\n\nAs with other symptoms, aim to manage reversible causes of agitation and possible delirium first. Consider non-pharmacological measures such as environmental modification. For patients in their last days of life, haloperidol or low-dose midazolam may be prescribed. Often, this is done as part of anticipatory prescribing.\n\n\n# Respiratory tract secretions\n\nRespiratory tract secretions often occur in the last days of life as a person becomes less able to clear their airways. They are rarely a cause of distress to the patient, but may be upsetting for family members or those close to the patient. An antimuscarinic such as hyoscine butylbromide or glycopyrronium bromide may be prescribed for noisy respiratory secretions.\n\n\n# NICE guidelines\n\n\n[NICE Guidance: Care of dying adults in the last days of life](https://www.nice.org.uk/guidance/ng31)\n\n[NICE CKS: Palliative care - general issues](https://cks.nice.org.uk/topics/palliative-care-general-issues/)\n\n[NICE CKS: Palliative care - dyspnoea](https://cks.nice.org.uk/topics/palliative-care-dyspnoea/)\n\n[NICE CKS: Palliative care - nausea and vomiting](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative care - secretions](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative cancer care - pain](https://cks.nice.org.uk/topics/)\n\n# References\n\n[Pallcare.info](https://www.pallcare.info/book.php)\n\n[BNF: Ondansetron](https://bnf.nice.org.uk/drugs/ondansetron/#drug-action)\n\n[BNF: Nausea and labyrinth disorders](https://bnf.nice.org.uk/treatment-summaries/nausea-and-labyrinth-disorders/)\n\n[BNF: Prescribing in palliative care](https://bnf.nice.org.uk/medicines-guidance/prescribing-in-palliative-care/)",
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"explanation": "75mg oxycodone/24hrs subcutaneously via a syringe driver with 7.5-12.5mg subcutaneous oxycodone as required 4-hourly for breakthrough pain",
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"question": "A 72-year-old man with metastatic colorectal cancer and chronic kidney disease is admitted with sepsis. After three days of treatment, he deteriorates. Following discussions, the decision is made to discontinue antibiotics and fluids, focusing on end-of-life care.\n\nHis current analgesia is paracetamol 1g QDS, morphine sulfate modified release (long-acting) 90mg BD, and morphine sulfate immediate release oral liquid (short acting) 30mg PRN, 4-hourly. He has used 4 doses of the PRN oral morphine in 24hrs.\n\n\nHis eGFR is 22 mL/min/1.73m². The patient asks if his oral medications can be reduced or converted to a syringe driver due to difficulty swallowing.\n\nWhich of the following prescriptions would be most suitable for this patient?",
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"explanation": "In the hand, the median nerve supplies the muscles of the thenar eminence (opponens pollicis, abductor pollicis brevis and flexor pollicis brevis), as well as the radial 2 lumbricals. Its motor supply can be remembered using the helpful mnemonic LOAF. It also supplies sensation to the thenar eminence and the radial 3 1/2 fingers on their palmar aspect. Finger abduction/adduction will not be affected since the interossei are innervated by the ulnar nerve. The most common site of compression of the median nerve is at the carpal tunnel.",
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"explanation": "The radial nerve supplies the BEST muscles: brachioradialis, extensors of the forearm, supinator and triceps. It also supplies sensation to the dorsal arm and forearm, and the dorsal aspect of the radial 3 1/2 fingers. Finger abduction/adduction will not be affected since the interossei are innervated by the ulnar nerve. The radial nerve can be damaged at multiple points, including the wrist (eg. tight handcuffs), which causes finger drop (loss of finger extension), proximal forearm or in the spiral groove (eg. a fracture of the humerus or prolonged tourniquet), which presents with wrist drop, or at the level of the brachial plexus (crutches or a honeymoon/Saturday night palsy), which causes loss of triceps as well wrist drop.",
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"explanation": "In the hand, the ulnar nerve provides motor innervation to the interossei muscles, which are responsible for finger abduction and adduction. It also supplies the third and fourth lumbricals, the adductor pollicis and sensation over the hypothenar eminence and ulnar 1 and 1/2 fingers. The ulnar nerve runs medially around the elbow, through the cubital tunnel and along the medial aspect of the forearm. The most likely area of impingement is around the elbow, where there is notable swelling on examination. Damage can either occur due to bony impingement in the context of a fracture or oedema compressing the ulnar nerve through its course in the cubital tunnel.",
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"explanation": "The musculocutaneous nerve supplies the coracobrachialis (which flexes and adducts the shoulder), biceps brachii (which flexes and supinates the forearm) and brachialis muscles (flexes the forearm). Injury to this nerve manifests with inability to flex and adduct the shoulder and flex the elbow. Finger abduction is conducted by the interossei muscles, which are innervated by the ulnar nerve. The musculocutaneous nerve does not supply any intrinsic hand muscles.",
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"explanation": "The axillary nerve supplies the deltoid and teres minor muscles. This manifests with inability to abduct the arm. It also supplies sensation to the regimental badge area. Finger abduction is conducted by the interossei muscles, which are innervated by the ulnar nerve. The axillary nerve does not supply any intrinsic hand muscles.",
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"comment": "Finger abduction- ulnar\nPincer grip strength between thumb and index finger- median\nWrist extension strength against resistance- radial",
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"explanation": "# Summary\n\nThe ulnar nerve, deriving from nerve roots C8-T1, is integral to motor and sensory functions in the arm. Motor functions include innervating most of the intrinsic hand muscles and two muscles in the forearm, while sensory functions encompass innervation to the skin of the medial 1.5 digits and associated palm area. Noteworthy anatomical landmarks include its passage in the cubital tunnel at the elbow and Guyon's canal in the wrist, and its bifurcation into deep and superficial branches.\n\n# Definition\n\nThe ulnar nerve is a peripheral nerve that arises from the medial cord of the brachial plexus, with its roots in the C8-T1 nerve roots. It serves both motor and sensory functions in the forearm and hand.\n\n# Epidemiology\n\nUlnar nerve injuries, often a result of elbow trauma or continuous pressure on the elbow, are relatively frequent. Individuals at high risk include those participating in physical activities, sports, or with specific medical conditions predisposing them to nerve compression or trauma.\n\n# Aetiology\n\nThe ulnar nerve can be injured through various mechanisms, including:\n\n- Direct trauma or injury to the nerve\n- Compression or entrapment (e.g., in conditions such as cubital tunnel syndrome or Guyon's canal syndrome)\n- Iatrogenic causes during surgical procedures\n- Systemic diseases that affect the peripheral nerves (e.g., diabetes mellitus)\n\n# Anatomical Course\n\n \n\nThe ulnar nerve comes off the medial cord of the brachial plexus, and passes through the axilla with the axillary artery on its lateral side and the axillary vein on its medial side. In the arm, the ulnar nerve travels alongside the brachial artery until half-way down, where it passes through the medial septal fascia to enter the posterior compartment of the arm. The ulnar nerve then passes posterior to the elbow through a small space between the medial epicondyle and olecranon called the ulnar tunnel.\n\n \n\nIn the forearm, the ulnar nerve pierces between the two heads of flexor carpi ulnaris, and travels deep to the muscle alongside the ulna. Three branches come off the ulnar nerve in the forearm:\n\n \n\n- Muscular branch = innervates muscles of the anterior compartment\n\n \n\n- Palmar cutaneous branch = innervates the medial half of the palm\n\n- Dorsal cutaneous branch = innervates the dorsal surface of the medial 1 1/2 digits and associated dorsal hand area\n\n \n\nThe ulnar nerve passes through the wrist superficial to the flexor retinaculum and medial to the ulnar artery, and enters the hand through the ulnar (or Guyon's) canal. It terminates into two branches:\n\n \n\n- Superficial = innervates the palmar surface of the medial 1 1/2 digits\n\n- Deep = intrinsic muscles of the hand (hypothenar muscles, medial two lumbricals, adductor pollicis, palmar and dorsal interossei, palmaris brevis)\n\n \n\n**\"LOAF\"**.\n\n \n\n*All the muscles in the hand are supplied by the ulnar nerve except LOAF which are supplied by the median nerve*\n\n \n\nL - lateral two lumbricals\n\n \n\nO - opponens pollicis\n\n \n\nA - abductor pollicis brevis\n\n \n\nF - flexor pollicis brevis\n\n \n\nThe majority of the intrinsic muscles of the hand are supplied by the deep branch of the ulnar nerve, except palmaris brevis which is supplied by the superficial branch of the ulnar nerve.\n\n**Summary table**\n\n \n\n| Nerve roots | C8-T1 |\n| --------------------- | ------------------------------------------------------------ |\n| **Motor functions** | Innervates flexor carpi ulnaris and the medial half of flexor digitorum profundus. Innervates the intrinsic muscles of the hand (except for the LOAF muscles*) |\n| **Sensory functions** | Innervates the medial 1 1/2 digits and the associated palm area |\n\n# Signs and Symptoms\n\nSigns and symptoms of ulnar nerve injury may include:\n\n- Weakness or paralysis of the muscles innervated by the ulnar nerve (e.g., most of the intrinsic hand muscles and two muscles in the forearm)\n- Numbness, tingling, or pain in the sensory distribution of the ulnar nerve (skin of the medial 1.5 digits and associated palm area)\n\n# Differential Diagnosis\n\nOther conditions that could present with similar symptoms include:\n\n- Brachial Plexopathy: Similar motor and sensory loss, but usually involves other nerves of the brachial plexus.\n- Carpal Tunnel Syndrome: Primarily causes sensory changes in the palmar aspect of the hand and motor weakness in the median nerve distribution.\n- Radial Neuropathy: Presents with sensory and motor deficits in the radial nerve distribution, including the dorsal surface of the lateral 3 1/2 digits.\n- Cervical Radiculopathy: Symptoms may overlap with ulnar nerve injury, but there may also be neck pain, and symptoms may be exacerbated by neck movements.\n\n# Investigations\n\nInvestigations for a suspected ulnar nerve injury may include:\n\n- Neurological examination: to assess sensory and motor deficits\n- Electromyography (EMG) and Nerve Conduction Studies (NCS): to evaluate nerve function\n- MRI or CT scan: to identify any anatomical causes of nerve injury such as a fracture or mass lesion\n\n# Management\n\nThe management of ulnar nerve injuries depends on the underlying cause:\n\n- Conservative measures: including rest, physical therapy, and use of splints to prevent muscle contractures in cases of mild nerve injury\n- Pharmacological interventions: such as analgesics for pain management\n- Surgical interventions: in cases of severe nerve injury or where the cause is a correctable lesion such as a tumor or fracture",
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"question": "A 43-year-old right-handed man presents to A&E after an accident at work. He was carrying a large glass window when he tripped and fell onto his left side. You note extensive bruising and swelling around his left elbow. An X-ray demonstrates a supracondylar fracture of the elbow. You assess his range of movement and find he is unable to abduct his fingers.\n\nWhich nerve has been damaged?",
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"explanation": "Inhaled corticosteroids will not provide immediate benefit to a patient presenting with an acute asthma flare-up. They have a role in long-term asthma control. They should be continued on the drug chart if a patient is admitted with an asthma flare-up and is already on them in the community; adding them in the acute setting will not provide significant rapid relief. Oral steroids are indicated in the management of acute asthma exacerbations. In the context of a raised PaCO<sub>2</sub>, this patient requires mechanical ventilation without delay.",
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"name": "Add high-dose inhaled corticosteroids",
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"explanation": "A nasopharyngeal airway is an airway adjunct that will help maintain an airway at risk of obstruction/obstructed at the nasopharyngeal level. It does not provide definitive airway support and will not enable mechanical ventilation, which this tiring patient with asthma with a near-fatal flare-up requires at this stage.",
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"name": "Insert a nasopharyngeal airway",
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"explanation": "This would be a sensible addition. However, this patient is tiring and so while magnesium may be provided, the next step should be summoning the intensive care team immediately with a view to intubation and ventilation before any further time is spent on medical management.",
"id": "52940",
"label": "d",
"name": "Start a magnesium sulphate infusion",
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"explanation": "This patient has already had ipratropium bromide at the correct dose. Ipratropium is not provided back to back because it does not provide additional benefit in this manner and has anticholinergic side effects. The next dose would be due in 6-h time (500 μg 4 times a day). Furthermore, no additional time should be spent on medical management as a next step since seeking intensive care review with a view to intubation and ventilation is most important at this stage.",
"id": "52941",
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"name": "Provide a further dose of nebulised ipratropium bromide",
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"explanation": "This patient has raised carbon dioxide levels, indicating that he is tiring. This represents a near-fatal asthma exacerbation. An intensive care review is now required since he will need intubation and ventilation. Practically, a 2222 call may need to be placed to summon the intensive care team immediately.",
"id": "52937",
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"name": "Immediate intensive care review",
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"explanation": "# Summary\n\nAsthma is a common disease of the airways, involving reversible bronchoconstriction, hyperreactivity and chronic inflammation. When bronchoconstriction is triggered (an “asthma attack” or exacerbation), patients experience episodes of wheeze, dyspnoea, cough and chest tightness. Initial investigations in an asthma exacerbation include doing a peak flow measurement, an arterial blood gas (ABG) if oxygen saturations are low or hypercapnia is suspected, and a chest X-ray in selected cases (e.g. where there are signs of pneumonia). Management involves supplementary oxygen, bronchodilators (either inhaled or nebulised) and steroids. Patients with severe or life-threatening asthma exacerbations may require additional treatments including escalation to intensive care for intubation and ventilation in some cases.\n\n# Definition\n\nAsthma is a common disease in both adults and children, characterised by intermittent []()exacerbations with wheeze, cough, shortness of breath and chest tightness. There are several underlying mechanisms that centre around reversible bronchoconstriction, hyperreactivity and chronic inflammation.\n\n# Epidemiology\n\nIn the UK, approximately 8 million people have been diagnosed with asthma, of which 5.4 million are on treatment. Onset is usually in childhood and some find symptoms remit with age, although relapse is possible after long periods of being well.\n\nAsthma exacerbations are the cause of 60,000 hospital admissions per year in the UK. Over 1000 people die of asthma per year, with two-thirds of these deaths thought to be preventable. An estimated 7/10 people with asthma do not receive basic preventative care such as inhaler technique checks and a personalised asthma plan.\n\nPeople experiencing socioeconomic deprivation are more likely to have asthma and to have worse outcomes (e.g. higher rates of hospitalisation). This is multifactorial, with these groups more likely to be exposed to triggers such as smoking and air pollution, and to have lower health literacy and access to healthcare.\n\n# Aetiology\n\nAsthma is often associated with a personal and/or family history of atopy, including the atopic triad of asthma, allergic rhinitis, and eczema. In asthma, there is an exaggerated response to a wide range of triggers. These include:\n\n- Cold air and exercise\n- Pollution and cigarette smoke\n- Allergens such as animal dander, dust mites and pollen\n- Irritants such as perfumes, paints or air fresheners\n- Medications such as NSAIDs or beta-blockers\n\nThese trigger a type 1 hypersensitivity reaction which is mediated by IgE. T Helper 2 cells produce IL4, IL5 and IL13 cytokines which activate the humoral immune system, leading to the proliferation of eosinophils, mast cells and dendritic cells. These cells then produce more inflammatory mediators such as leukotrienes and histamine.\n\nThis inflammation contributes to airway hyperresponsiveness leading to bronchospasm, as well as mucus hypersecretion that also obstructs airways. Over time in severe asthma, airway remodelling mediated by fibroblasts causes chronic obstruction and thickening of smooth muscle.\n\n# Classification\n\nAcute asthma exacerbations are graded in severity as below:\n\n\n| Severity | Clinical Features |\n|-----------------------|-----------------------------------------------|\n| Moderate | PEFR > 50% of predicted or best |\n| | No features of severe/life-threatening asthma |\n| Severe | PEFR 33-50% of predicted or best |\n| | Heart rate > 110 |\n| | Respiratory rate > 25 |\n| | Unable to complete sentences in one breath |\n| | Accessory muscle use |\n| Life-threatening | PEFR < 33% of predicted or best |\n| | Oxygen saturation < 92% or cyanosis |\n| | Altered conciousness/confusion |\n| | Exhaustion/poor respiratory effort |\n| | Cardiac arrhythmia |\n| | Hypotension |\n| | Silent chest |\n| Near fatal | Raised PaCO2 |\n| | Requiring mechanical ventilation with raised inflation pressures |\n\n\n# Signs and Symptoms\n\nPatients experiencing an asthma exacerbation present with progressive worsening of the following symptoms, usually over the course of several hours:\n\n- Wheeze\n- Difficulty breathing\n- Struggling to eat, speak or sleep due to breathlessness\n- Cough\n- Chest tightness\n- Dizziness\n\nOn examination, patients may have:\n\n- Tachypnoea\n- Increased work of breathing\n- Hyperinflated chest\n- Expiratory polyphonic wheeze throughout the lung fields\n- Decreased air entry \n- Cyanosis\n- Tachycardia\n- Altered mental state, e.g. drowsiness or confusion\n- Exhaustion\n- Hypotension\n\nThey may be able to identify a trigger and have signs and symptoms of this (e.g. fever and coryza in viral infection).\n\n\n# Differential diagnosis\n\n- **Pulmonary embolism** - associated with risk factors e.g. immobility, malignancy; shares features of shortness of breath and cough, may have haemoptysis and pleuritic chest pain.\n- **Vocal cord dysfunction** - shares many triggers with asthma, inspiration more difficult than expiration, may have stridor.\n- **Acute exacerbation of chronic obstructive pulmonary disease** - patients usually >35 years old with a significant smoking history, may overlap with asthma in some.\n- **Gastro-oesophageal reflux disease** - microaspiration of stomach acid due to reflux can cause episodes of cough and wheeze which mimic asthma (although these may coexist and reflux can trigger asthma exacerbations). Symptoms are often postural and related to eating.\n- **Anaphylaxis** - also may present with sudden-onset shortness of breath and wheeze, usually more rapid onset and may have skin and mucosal changes such as urticaria and lip swelling\n\n# Investigations \n\n**Bedside tests:**\n\n- **Peak expiratory flow rate (PEFR)** to help assess severity as per the classification above and monitor response to treatment.\n- **Arterial blood gas** if the patient is hypoxic to assess oxygenation and ventilation in patients - CO2 is expected to be low due to hyperventilation and if this is raised this indicates the asthma attack is near fatal.\n- **ECG** to look for arrhythmias especially if tachycardic.\n\n**Blood tests:**\n\n- **FBC** and **CRP** for inflammatory markers\n- **U&Es** and **LFTs** as a baseline - patients may develop acute kidney injury if too breathless to drink for prolonged periods\n- **Blood cultures** if bacterial infection suspected e.g. an unwell patient with fevers\n\n**Imaging:**\n\n- **Portable chest X-ray** if a trigger such as pneumonia or a complication such as pneumothorax is suspected clinically.\n\n# Management \n\n- Recognise that this may be a medical emergency, assess using an ABCDE approach and escalate early to senior colleagues/critical care if not responding to treatment\n- Titrate oxygen to maintain saturations of 94-98%\n- Nebulised salbutamol (5mg) driven by oxygen (if out of hospital, give up to 10 puffs of inhaled salbutamol and call an ambulance if not responding)\n- If the attack is severe or life-threatening or if response to salbutamol has been poor, add nebulised ipratropium bromide (500mcg 4-6 hourly)\n- Give prednisolone 40-50 mg OD orally, or 100mg IV hydrocortisone QDS if the patient is unable to swallow\n- Continue steroids for at least 5 days or until recovery (whichever is longer)\n- Can consider IV magnesium sulphate (1.2-2 grams over 20 minutes) and/or aminophylline if the patient is not responding to nebulisers\n- If the patient continues to deteriorate despite maximal therapy, they may require intubation and ventilation in an intensive care setting (for example in cases of severe hypoxia or exhaustion)\n- Antibiotics should not be given routinely, especially as many infectious triggers of asthma exacerbations are viral\n\nFollow up after an acute asthma attack is crucial, with NICE guidelines stating that patients should be reviewed within 2 days of discharge from hospital to assess their symptoms, inhaler technique and current management. Ensure all patients have an up-to-date personalised asthma action plan.\n\n# Complications\n\n- **Respiratory failure** which may be type 1 (hypoxaemia alone) or type 2 (hypoxaemia with hypercapnia)\n- **Pneumothorax** - airway obstruction during asthma exacerbations may cause barotrauma and alveolar rupture, causing pneumothoraces or pneumomediastinum\n- **Status asthmaticus** - repeated asthma attacks without recovery in between, or which do not respond to treatment\n- **Death** - patients with previous severe asthma attacks and those adverse psychosocial factors are more likely to die of asthma (e.g. drug or alcohol abuse, repeated failure to attend appointments and learning difficulties)\n\n# NICE Guidelines\n\n[NICE CKS - Asthma](https://cks.nice.org.uk/topics/asthma/)\n\n# References\n\n[British Thoracic Society Asthma Guidelines](https://www.brit-thoracic.org.uk/quality-improvement/guidelines/asthma/)\n\n[BNF - Acute Asthma](https://bnf.nice.org.uk/treatment-summaries/asthma-acute/)\n\n[Report on health inequalities and asthma](https://www.asthmaandlung.org.uk/sites/default/files/2023-03/auk-health-inequalities-final.pdf)",
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"explanation": "# Summary\n\nPre-eclampsia is a placental condition that often affects pregnant women from around 20 weeks of gestation, characterised by hypertension and proteinuria. Other symptoms include peripheral oedema, severe headache, drowsiness, visual disturbances, epigastric pain, nausea/vomiting and hyperreflexia. The exact aetiology is not entirely understood, but it may be due to dysfunctional trophoblast invasion of the spiral arterioles. Key investigations include blood pressure and urine protein measurements. Management strategies include anti-hypertensive treatment, with labetalol as the first-line agent. Magnesium sulphate is used to prevent and treat eclamptic seizures, but the ultimate curative treatment is delivery of the placenta.\n\n# Epidemiology\n\n\n\nPre-eclampsia affects a significant percentage of pregnancies worldwide, although the exact number varies significantly between different populations and healthcare settings. Risk factors include nulliparity, a previous history or family history of pre-eclampsia, increasing maternal age, pre-existing diseases such as hypertension, diabetes, renal disease, autoimmune disease, obesity, and multiple pregnancies.\n\n\n# Aetiology\n\n\n\nThe exact aetiology of pre-eclampsia remains unclear. However, it's believed to be related to dysfunctional trophoblast invasion of the spiral arterioles, which results in decreased uteroplacental blood flow and subsequent endothelial cell damage.\n\n\n# Signs and Symptoms\n\n\nPre-eclampsia is characterised by:\n\n- Hypertension\n- Proteinuria\n- Peripheral oedema\n- Severe headache\n- Drowsiness\n- Visual disturbances\n- Epigastric pain\n- Nausea/vomiting\n- Hyperreflexia\n\n# Maternal complications\n\n- Eclampsia (seizures due to cerebrovascular vasospasm)\n- Organ failure\n- Disseminated intravascular coagulation (DIC)\n- HELLP syndrome (the presence of haemolysis (H), elevated liver enzymes (EL) and low platelets (LP))\n\n# Foetal complications\n\n- Intrauterine growth restriction\n- Pre-term delivery\n- Placental abruption\n- Neonatal hypoxia\n\n\n# Differential Diagnosis\n\n\nThe differential diagnosis for pre-eclampsia includes other conditions that can present with hypertensive disorders in pregnancy, such as chronic hypertension, gestational hypertension, and HELLP syndrome. Key signs and symptoms for these conditions include persistent high blood pressure, proteinuria, and various combinations of haemolysis, elevated liver enzymes, and low platelet levels.\n\n# Investigations\n\n\nKey investigations for pre-eclampsia include:\n\n- Blood pressure measurement: To confirm hypertension.\n- Urinalysis: To confirm proteinuria.\n- Blood tests: To assess kidney function, liver function, and clotting status.\n\n# Management\n\nAspirin is used for prophylaxis against the development of pre-eclampsia. It is given from 12 weeks gestation until birth to women with one high risk factor or two (or more) moderate risk factors. \n\nManagement of pre-eclampsia primarily involves anti-hypertensive treatment, with labetalol being the recommended first-line agent. Other agents that can be used include Nifedipine, Methyldopa and hydralazine. \n\nMagnesium sulphate can be administered for the prevention and treatment of eclamptic seizures. \n\nThe only definitive curative treatment is the delivery of the placenta. It is also crucial to monitor the mother and foetus closely for complications.\n",
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"explanation": "Gout or pseudogout can present with an acutely hot and painful joint. However, it is not typical for the paediatric age range. Moreover, given the presentation, septic arthritis is the most important diagnosis to exclude; thus, an aspirate for microscopy, culture and sensitivity is the best first test.",
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"comment": "Septic arthritis has systemic upset\nTransient synovitis is just ouch hurt after viral infection",
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"explanation": "# Summary\n\nSeptic arthritis is an infection of the joint characterized by acute inflammation and swelling. It is caused by a bacterial or viral pathogen that infects the synovial fluid. The most commonly implicated organism is Staphylococcus aureus. Noteworthy clinical signs include a tender, swollen joint with reduced mobility, often accompanied by systemic illness. Key investigations include joint aspiration for Microscopy Culture and Sensitivity, along with blood tests showing increased white blood cell count and elevated ESR/CRP. Management typically involves IV antibiotics, joint washout under general anaesthesia, and physiotherapy once the acute infection has resolved.\n\n# Definition\n\nSeptic arthritis is an infection of the joint, specifically the synovial fluid. It is typically caused by a bacterial or viral pathogen and necessitates prompt medical intervention due to the high risk of joint damage and other severe complications.\n\n# Epidemiology\n\nSeptic arthritis has an annual incidence of 4-10 cases per 100,000 patients in Western Europe. It can affect individuals of any age, though certain populations are at a higher risk due to underlying conditions.\n\n# Aetiology\n\nThe most prevalent organism implicated in septic arthritis is Staphylococcus aureus. Other responsible organisms include:\n\n- Gonococcus: primarily in sexually active individuals\n- Streptococcus spp.\n- Gram-negative bacilli\n\nRisk factors contributing to septic arthritis include:\n\n- Pre-existing joint diseases such as rheumatoid arthritis\n- Chronic kidney disease\n- Immunosuppressive states\n- Presence of prosthetic joints\n\n# Signs and Symptoms\n\nThe clinical presentation of septic arthritis usually involves:\n\n- Acute onset of tender, swollen joint\n- Reduced range of joint movement\n- Systemic symptoms such as fever, malaise, or chills\n\n# Differential Diagnosis\n\nDifferential diagnoses for septic arthritis include:\n\n- Gout and pseudogout: characterized by intense joint pain, redness, and swelling, often in the big toe or knee.\n- Osteoarthritis: presents with joint pain, stiffness, and sometimes swelling, generally improving with movement.\n- Rheumatoid arthritis: marked by joint pain, swelling, and stiffness, often symmetrical and worse after rest.\n- Lyme disease: may show erythema migrans rash, flu-like symptoms, and possibly migratory joint pains.\n\n# Investigations\n\nDiagnostic investigations for septic arthritis include:\n\n- Joint aspiration for Microscopy, Culture, and Sensitivity: The aspirate usually appears turbid and yellow, resembling pus.\n- Blood tests: elevated white cell count, high ESR/CRP\n- Blood cultures: to identify causative organisms\n- Imaging: X-ray of the joint may be performed to evaluate for osteomyelitis or other complications.\n\n# Management\n\nThe treatment of septic arthritis involves:\n\n- IV antibiotics guided by local antibiograms and susceptibilities\n- Consideration of joint washout under general anaesthesia to remove infected material\n- Physiotherapy following the resolution of acute infection to restore joint function\n\nComplications of septic arthritis can include:\n\n- Osteomyelitis: infection of the bone\n- Chronic arthritis: persistent joint inflammation\n- Ankylosis: joint fusion resulting in immobility\n\n# References\n\n[Click here for the BNF Treatment Summary for Musculoskeletal infections](https://bnf.nice.org.uk/treatment-summary/musculoskeletal-system-infections-antibacterial-therapy.html)\n\n[Click here for the BMJ Best Practice Summary of Septic Arthritis](https://bestpractice.bmj.com/topics/en-us/486)",
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"question": "A 14-year-old adolescent presents with a red-hot swollen knee joint after a chest infection last week. He has been unable to walk due to the pain in his knee despite analgesia. He has a background history of type 1 diabetes managed with an insulin pump. On examination there is erythema overlying the joint and pain whenever the joint is moved in any direction. His temperature is 38.3 °C.\n\nWhat is the most important next step?",
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"explanation": "This patient is unlikely to tolerate a CT abdomen since she has already declined one because of claustrophobia. Furthermore, an ultrasound examination is usually preferred in young female patients in the first instance. Before any imaging, a pregnancy test will be a sensible next step to guide the diagnostic process.",
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"explanation": "Since this patient did not have a CT kidneys, ureters and bladder, a pregnancy test may have been missed by the assessing doctor, who may have otherwise been prompted to do one before exposing a woman of child-bearing age to radiation. In any woman of child-bearing age presenting with abdominal pain, a pregnancy test should always be done to rule out life-threatening causes of abdominal pain, such as ectopic pregnancy.",
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"explanation": "A urinary tract infection may cause abdominal pain and may complicate kidney stones. However, this patient has seen some improvement in her pain without antibiotics and a urine dipstick yesterday was negative for leukocytes and nitrites. The persistent pain is in the left iliac fossa and so gynaecological causes should be excluded. Therefore, the next best step is a pregnancy test.",
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"explanation": "This may be a useful investigation to evaluate for any free fluid in the pelvis or ovarian cysts, without exposing her to the radiation of a CT scan. It is likely she will have this test further down the line if the pain persists but a pregnancy test is a quick, noninvasive, appropriate immediate next step to further guide diagnosis.",
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"explanation": "Abdominal X-rays provide limited information in the context of acute abdominal pain. They can help diagnose bowel obstruction, mega-colon, chronic inflammatory bowel disease changes and radio-opaque kidney stones. She requires a pregnancy test in the first instance to guide the diagnostic process.",
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"comment": "guess that doctor didn't use Quesmed for his exams LOL!",
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"explanation": "# Summary\n \n \nEctopic pregnancy is a gynaecological emergency, referring to a fertilised ovum that has implanted anywhere outside the endometrial cavity. This may present with pelvic pain, shoulder tip pain, abnormal vaginal bleeding, and haemodynamic instability if ruptured. Diagnosis is confirmed by positive pregnancy test and a transvaginal ultrasound that has located the pregnancy outside the uterine cavity. Management strategies include conservative management, medical management with methotrexate, and surgical management, the choice of which depends on the patient's presentation and level of risk.\n \n \n \n# Definition\n \nAn ectopic pregnancy refers to a fertilised ovum that has implanted outside the endometrial cavity, usually in the fallopian tubes. This is a gynaecological emergency. \n \n \n \n \n# Epidemiology\n\n \nThe estimated incidence of ectopic pregnancies in the UK is 1.1%. The risk is higher in women with a history of pelvic inflammatory disease, genital infection, pelvic surgery, an intrauterine device in situ, assisted reproduction, previous ectopic pregnancy, or endometriosis.\n \n \n \n \n# Aetiology \n \n \nEctopic pregnancy usually presents in the 6-8th week of pregnancy, but can occur earlier or later. They can occur anywhere outside the endometrial cavity, but most commonly in the fallopian tube. \n\nRisk of an ectopic increases with conditions that impair the passage of a fertilised egg into the uterine cavity, or with conditions that cause the fertilised egg to implant prematurely. However, most ectopics are not associated with any risk factor. \n \nSpecific risk factors include: \n \n - Pelvic inflammatory disease and previous STIs\n - Pelvic surgery\n - Having an intrauterine device e.g. copper coil or Levonorgestrel-releasing intrauterine system (e.g. Mirena) in situ\n - Assisted reproduction e.g. IVF\n - Previous ectopic pregnancy\n - Endometriosis\n \n \n \n# Signs and Symptoms\n \nClinical features of ectopic pregnancy may include:\n \n \n - Pelvic pain, which may be unilateral to the side of the ectopic\n - Shoulder tip pain - If the ectopic pregnancy bleeds, the blood can irritate the diaphragm causing shoulder tip pain\n - Abnormal vaginal bleeding e.g. missed period or intermenstrual bleeding\n - Haemodynamic instability caused by blood loss if the ectopic ruptures, resulting in syncope/fainting\n - Abdominal examination may reveal unilateral tenderness\n - Cervical tenderness (chandelier sign) on bimanual examination\n \n \n# Differential Diagnosis\n\n1. **Miscarriage:** will also present with bleeding following a positive pregnancy test. However, less likely to have shoulder tip pain, beta-hCG levels will not be as high as in an ectopic (and will fall), and TV USS may show intrauterine pregnancy (if not yet completely expelled). \n\n\n2. **Pelvic inflammatory disease:** presents with abdominal pain and cervical tenderness, and may have bloody vaginal discharge. However, pregnancy test will be negative and inflammatory markers raised. Can be confirmed with positive swab. \n\n\n3. **Ovarian torsion:** also presents with abdominal pain, usually unilateral. Less likely to present with vaginal bleeding and will have negative pregnancy test. \n\n# Investigations\n \nThe investigations for ectopic pregnancy include:\n\n**Bedside**\n\n- Pregnancy test (to confirm pregnancy) \n\n \n**Bloods**\n\n* FBC (check for anaemia)\n* Serum beta-hCG (will help guide management)\n\n**Imaging**\n\n - Transvaginal ultrasound (to locate the pregnancy)\n \n \n# Management\n \n \nThere are three management options for ectopic pregnancy:\n \n \n **Conservative:**\n \n \n - This is an option for a small number of women with an ectopic pregnancy who have minimal or no symptoms, who are considered low risk (usually because there is a plateau or drop in beta-hCG levels indicating self-resolution of the ectopic). \n - These patients require close follow-up with serial repeat b-hCG tests. If the levels do not decrease at a satisfactory rate, medical/surgical management is recommended.\n \n \n**Medical:**\n \n \n - Involves administration of a one-off dose of methotrexate\n - Criteria for methotrexate treatment include: \n - No significant pain\n - Low hCG level (below 1500 IU/L)\n - Unruptured ectopic pregnancy measuring below 35mm and with no visible heartbeat\n - Ability to attend follow-up\n - Adherence to avoiding pregnancy for a period following treatment\n - No intrauterine pregnancy (confirmed on an ultrasound scan). \n - If the initial dose of methotrexate fails to treat the ectopic pregnancy, a second dose of methotrexate or surgical management may be indicated\n \n\n**Surgical:**\n \n - Recommended as first-line option if: \n - Patient is unable to attend follow-up\n - Serum hCG level of 5000 IU/L or higher \n - Adnexal mass of 35mm or greater\n - Foetal heartbeat is visible on ultrasound scan\n - Patient is in significant pain\n - Patient is haemodynamically unstable\n - Also offered second line in cases where medical manamgement has failed \n - The preferred surgical management is a **salpingectomy**, where the fallopian tube containing the ectopic pregnancy is removed. For patients with only one patent fallopian tube (e.g. due to previous PID or ectopic, or past removal of a fallopian tube), a **salpingotomy** may be performed instead, where only the ectopic pregnancy is removed and the ends of the fallopian tube are re-attached. \n - There is a risk with salpingotomy that not all the tissue may have been removed, and so serial serum b-hCG measurements are performed to exclude any remaining trophoblastic tissue within the fallopian tube\n - Offer **anti-D immunoglobulin** to all rhesus-negative women who have had surgical management of ectopic pregnancy. \n \n\n**Borderline Cases: Choosing Between Medical and Surgical Management**\n\n* There are some women who may be offered a choice of either methotrexate or surgical management as first-line.\n* This applies to women who: \n * Have a serum hCG level between 1500 IU/L and 5000 IU/L\n * Are able to return for follow up\n * Have no significant pain\n * Have an unruptured ectopic pregnancy with an adnexal mass smaller than 35 mm with no visible heartbeat.\n * Have no intrauterine pregnancy (confirmed on an ultrasound scan). \n \n\n# NICE Guidelines \n \n [Click here for NICE CKS on ectopic pregnancy ](https://cks.nice.org.uk/topics/ectopic-pregnancy/) \n \n# References\n\n\n[NHS UK - Ectopic pregnancy](https://www.nhs.uk/conditions/ectopic-pregnancy/)\n \n[Patient Info - Ectopic pregnancy](https://patient.info/doctor/ectopic-pregnancy-pro)",
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"question": "A 28-year-old woman was admitted to hospital overnight with severe left-sided loin-to-groin pain. A urine dipstick revealed blood, no nitrites or leukocytes. Due to claustrophobia, she declined a CT scan and she was subsequently diagnosed with kidney stones clinically and treated with analgesia. Today, she reports she no longer has any flank pain but has persistent pain in the left iliac fossa.\n\nWhat is the next most important test to conduct?",
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"explanation": "Sentinel lymph nodes are identified intraoperatively using radioactive blue dye. The surgeon injects the dye under the nipple and identifies the sentinel lymph node using radioactive readings and colour change.",
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"explanation": "For breast cancer, we know that the common sites of spread include the lungs, brain and bones. Histology, alongside other factors, may give us an idea of prognosis and the degree of aggression and therefore propensity to metastasise but it does not suggest where those sites will be.",
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"explanation": "Histology indicates which treatments would be effective for the cell types of breast cancer. Generally, positivity for the oestrogen receptor, progesterone receptor or HER2 allow specific therapies to be employed. However, the response to therapy is variable and other factors influence prognosis, most notably staging. The better and more direct answer is that histology helps guide treatment.",
"id": "53008",
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"explanation": "Histology is crucial for breast cancer management because cell type governs the chemotherapy or hormonal treatments offered. The main subtypes of clinical relevance include oestrogen receptor, progesterone receptor and human epidermal growth factor receptor 2 (HER2) status. For this patient, her breast cancer is oestrogen receptor-positive, meaning it could be susceptible to an aromatase inhibitor, such as anastrozole, or a selective oestrogen receptor modulator, such as tamoxifen. The other factors that influence the choice of chemotherapy or hormonal therapy include age, comorbidities and cancer stage.",
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"explanation": "Certain hereditary cancer syndromes, such as *BRCA1*/*BRCA2*, are associated with triple-negative breast cancers (negative for the oestrogen and progesterone receptors and the HER2 receptor). However, patients who do not possess these mutations can also be triple-negative; therefore, diagnosis of hereditary cancer syndromes cannot be made on histology alone.",
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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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"explanation": "This patient has presented with pruritus in the third trimester of pregnancy, which should raise the suspicion of intrahepatic cholestasis of pregnancy. The best test for this would be serum bile acids. There is a raised bilirubin in only a quarter of cases and raised bilirubin lacks specificity for this pathology.",
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"comment": "this is so dumb you're never going to order just one liver investigation.. and you need to see the other results to exclude other causes anyway",
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"explanation": "# Summary\n\n\nObstetric cholestasis is a pregnancy-related condition typically occurring after 24 weeks of gestation, characterised by the accumulation of bile acids. Key signs and symptoms include pruritus, fatigue, nausea, loss of appetite, occasional mild maternal jaundice, and right upper quadrant abdominal pain. Key investigations encompass liver function tests, bile acids measurement, and fetal monitoring. Management strategies include administration of chlorphenamine and vitamin K, early delivery planning, and off-license use of Ursodeoxycholic Acid (UDCA).\n\n\n# Definition\n\n\nObstetric cholestasis, also known as intra-hepatic cholestasis of pregnancy, is a pregnancy-related hepatobiliary disorder that typically manifests after the 24th week of gestation. The condition is characterised by impaired bile flow leading to the accumulation of bile acids.\n\n# Aetiology\n\n\nThe exact cause of obstetric cholestasis is not fully understood. However, it is believed to be influenced by hormonal and genetic factors, as well as environmental triggers.\n\n\n# Signs and Symptoms\n\nClinical manifestations of obstetric cholestasis include:\n\n- Pruritus: This is often severe and typically more intense on the hands and feet. It is not associated with a rash, although excoriation marks from scratching may be present.\n- General discomfort: Patients may experience fatigue or malaise.\n- Gastrointestinal symptoms: Nausea and loss of appetite are common.\n- Jaundice: Mild maternal jaundice characterised by dark urine and pale stools may occasionally occur.\n- Abdominal pain: Pain is typically localised in the right upper quadrant.\n\n\n# Differential Diagnosis\n\n\nThe differential diagnoses for obstetric cholestasis include:\n\n- Pruritic urticarial papules and plaques of pregnancy (PUPPP): Characterised by itchy, red bumps and large patches of hives.\n- Prurigo of pregnancy: Characterised by small, itchy bumps on the skin.\n- Pruritus gravidarum: Generalised itching during pregnancy with no apparent cause.\n- Other hepatobiliary disorders: These include viral hepatitis and gallstones, which can present with similar symptoms.\n\n# Investigations\n\nInvestigations for obstetric cholestasis focus on liver function tests and bile acids measurement. Fetal monitoring may be required due to the risk of spontaneous intrauterine death associated with the condition.\n\n# Management\n\nObstetric cholestasis is managed with the administration of chlorphenamine and emollients to alleviate itching, vitamin K to minimize the risk of bleeding, and early delivery planning to reduce the prolonged risk of spontaneous intrauterine death. Ursodeoxycholic Acid (UDCA) can be used on an off-license basis to reduce serum bile acids and relieve pruritus, but its routine use is no longer recommended by RCOG.\n\n# References\n\n[RCOG - Intrahepatic cholestasis of pregnancy (Green-top Guideline No. 43)](https://obgyn.onlinelibrary.wiley.com/doi/epdf/10.1111/1471-0528.17206)",
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"question": "A 34-year-old primigravida woman who is 35 weeks pregnant presents with itchy skin for 5 d to A&E. There has been no response to antihistamines or creams. The itching is particularly intense on her palms and soles and at night. Her pregnancy has been unremarkable so far and she has no prior health conditions. She reports that her mother had a similar problem during her pregnancies. On examination, she has extensive scratch marks to her arms and abdomen. The remainder of the examination is normal.\n\nWhich investigation is most specific for her underlying diagnosis?",
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"explanation": "This patient is a competent adult and there is no apparent immediate risk to others or legal obligation to break her confidentiality. Therefore, one should only offer to contact the police and respect her wishes if she chooses not to. It is advised that FGM, which is illegal, should be reported to the police but in an adult patient (over 18), this should be done with her consent. In a patient less than 18 years of age (ie. a child), it is a legal duty to contact the police via 101 to disclose this information and you are therefore allowed to break confidentiality in this case. As ever, if breaking confidentiality, it is important to inform the patient of this and the rationale, that is, a legal obligation.",
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"explanation": "This patient is a competent adult and there is no apparent immediate risk to others or legal obligation to break her confidentiality. Therefore, one should only offer to contact the police and respect her wishes if she chooses not to. It is advised that FGM, which is illegal, should be reported to the police; however, in an adult patient (over 18), this should be done with her consent. In a patient less than 18 years of age (ie. a child), it is a legal duty to contact the police via 101 to disclose this information and you are therefore allowed to break confidentiality in this case. As ever, if breaking confidentiality, it is important to inform the patient of this and the rationale, that is, a legal obligation.",
"id": "53017",
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"explanation": "The patient is not a child and there is no mention of a particular vulnerability or other relatives at risk. Therefore, it would be best to explore this with the patient and then notify if there were any concerns. It would be most suitable to discuss whether she would want any psychological support and refer to gynaecology if they have experienced any physical complications from FGM, for example, incontinence, painful menstruation and frequent urinary tract infections.",
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"explanation": "# Summary\n\n\nFemale Genital Mutilation (FGM), often referred to as \"\"cutting\"\" or \"\"female circumcision,\"\" involves the injury or cutting of the female genitalia without medical justification. It comes in four types, ranging from clitoridectomy to other non-medical procedures like piercing. Complications include major tearing during labour, urethral damage and increased pain. Management of FGM, which is illegal in the UK, includes making a child protection referral if FGM is suspected, and performing an anterior episiotomy under local anaesthetic or regional block during the second stage of labour.\n\n\n# Definition\n\n\nFemale Genital Mutilation (FGM) is the harmful practice of injuring or cutting the female genitalia for non-medical reasons, often referred to as \"\"cutting\"\" or \"\"female circumcision.\"\"\n\n# Classification\n\nFGM is classified into four types:\n\n- Type I – Clitoridectomy: Partial or total removal of the clitoris and/or the prepuce.\n- Type II – Excision: Partial or total removal of the clitoris and the inner labia, with or without excision of the outer labia.\n- Type III – Infibulation: The narrowing of the vaginal opening by repositioning the inner or outer labia, with or without removal of the clitoris.\n- Type IV – Other: All other harmful procedures to the female genitalia for non-medical purposes, such as piercing, incising, scraping, or cauterising.\n\nThese procedures can cause significant complications including major tearing during labour, urethral damage and increased pain.\n\n\n# Management\n\nFGM is illegal in the UK. If there's suspicion that a child may be at risk of FGM, an immediate child protection referral must be made. Current management recommendations include performing an anterior episiotomy during the second stage of labour under local anaesthetic or regional block. Deinfibulation should be performed by experienced healthcare professionals, with careful measures to protect the urethra.\n",
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"comment": "No fever?",
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"comment": "Only if it becomes infected - this is then an abscess so will have a fever ",
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"explanation": "# Summary\n\nChronic pancreatitis is a long-term condition characterised by progressive inflammation and fibrosis of the pancreas leading to irreversible destruction of the exocrine and endocrine functions of the pancreas. Common symptoms include epigastric pain, malabsorption, steatorrhoea, and symptoms of diabetes mellitus. Structural and functional investigations are key to diagnosing the condition, which may be caused by a variety of factors, the most common being chronic alcohol excess. Management strategies include lifestyle changes, medication, and in some cases, invasive interventions. \n\n# Definition\n\nChronic pancreatitis is a medical condition characterised by persistent inflammation and fibrosis of both the exocrine and endocrine components of the pancreas.\n\n# Epidemiology\n\nChronic pancreatitis is most commonly caused by chronic alcohol excess, accounting for approximately 80% of cases. Less common causes include genetic factors, obstructive factors, and metabolic factors, while up to 15% of cases are idiopathic.\n\n# Aetiology\n\nThe primary cause of chronic pancreatitis is chronic alcohol excess. Other less common causes include:\n\n- Genetic factors such as cystic fibrosis\n- Obstructive causes such as pancreatic cancer\n- Metabolic causes such as elevated triacylglycerides\n\n# Pathophysiology\n\nProgressive inflammation and the development of fibrotic tissue in the pancreas results in a loss of exocrine function (lipase, amylase) and endocrine function (insulin). This manifests as malabsorption and impaired impaired blood glucose control, respectively.\n\n# Signs and Symptoms\n\nPatients with chronic pancreatitis typically present with the following:\n\n- Epigastric pain which is typically exacerbated after eating fatty food and relieved by sitting forward\n\t- Usually 15-30 minutes after eating\n- Bloating\n- Weight loss \n- Symptoms of exocrine dysfunction, such as malabsorption and steatorrhoea\n\t- Specifically absorption of fat-soluble vitamins (A, D, E and K) is reduced/lost, resulting in vitamin deficiencies and their own complications\t\n- Symptoms of endocrine dysfunction, such as diabetes mellitus, with symptoms including thirst and polyuria\n- Physical examination may reveal epigastric tenderness and signs of chronic liver disease, which could suggest alcohol as a cause\n\n# Differential Diagnosis\n\nDifferential diagnoses for chronic pancreatitis include acute pancreatitis, pancreatic cancer, and peptic ulcer disease. The main signs and symptoms of these differentials include:\n\n- Acute pancreatitis: severe acute-onset epigastric pain radiating to the back, nausea, vomiting, and elevated serum amylase and lipase\n- Pancreatic cancer: weight loss, jaundice, and abdominal pain\n- Peptic ulcer disease: burning abdominal pain, bloating, and heartburn\n- Abdominal aortic aneurysm - abdominal/back pain, shock/hypotension, expansile and pulsatile mass palpable in the abdomen\n\n# Investigations\n\n- Bedside - blood glucose, and faecal elastase (low if there is exocrine insufficiency)\n- Blood tests - serum amylase and lipase are not typically raised in chronic pancreatitis, unlike in acute pancreatitis\n- Imaging - abdominal x-ray (to detect calcifications) and CT scan (to show pancreatic calcification), the latter being more sensitive at detecting calcification\n\n\n# Management\n\nManagement of chronic pancreatitis includes:\n\n- Conservative measures such as abstinence from alcohol and maintaining a healthy diet\n- Medical measures including pain control with analgesia, management of endocrine dysfunction with insulin, and management of exocrine dysfunction with pancreatic enzyme replacement therapy (Creon is a common brand name you may come across, containing mixtures of amylase, lipase, and protease).\n- Invasive interventions may be considered if the above measures fail, such as coeliac plexus block and pancreatectomy.\n\n# Complications\n\nComplications of chronic pancreatitis can be local (such as pseudocyst or pancreatic cancer) or systemic (endocrine dysfunction leading to diabetes mellitus, or exocrine dysfunction leading to malabsorption and steatorrhoea).\n\n# NICE Guidelines\n\n[Click here to see NICE CKS information on chronic pancreatitis](https://cks.nice.org.uk/topics/pancreatitis-chronic/)",
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"question": "A 35-year-old woman with a history of chronic pancreatitis presents with post-prandial vomiting and abdominal pain. She denies weight loss, fevers, pruritus and any family history of malignancy.\n\nHer blood tests are significant for a cholestatic pattern of liver function tests.\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "The history of autoimmune disease, symptoms and associated microcytic anaemia are suggestive of Coeliac disease. The most commonly used screening test for Coeliac disease is checking for the presence of auto-antibodies against tissue transglutaminase (TTG). This has a high specificity and sensitivity; however, false negatives may be found in patients with IgA deficiency. IgA deficiency is more common in patient's with coeliac disease, and therefore, all patients should have IgA levels measured alongside antibodies against TTG. The next step in patients with IgA deficiency would be to measure antibodies against TTG from the IgG class",
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"explanation": "Faecal calprotectin is a measure of intestinal inflammation. It may be raised in coeliac disease and conditions such as inflammatory bowel disease, colorectal cancer and infectious colitis. The main use of faecal calprotectin is to exclude inflammatory bowel disease (IBD), given that it has a high specificity in this context",
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"comment": "According to the answer \"if there is enough clinical suspicion\" to do a duodenal biopsy- does the history and blood results not give us a high enough level of clinical suspicion? ",
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"explanation": "# Summary\n\nCoeliac disease is a T cell-mediated autoimmune condition characterised by the body's inflammatory response to dietary gluten, leading to small bowel damage and malabsorption. Key signs and symptoms include gastrointestinal disturbances such as diarrhoea, abdominal pain, nausea, vomiting, and systemic symptoms like fatigue, weight loss or failure to thrive in children. Additionally, dermatitis herpetiformis may be observed. The gold standard for diagnosis involves an oesophago-gastroduodenoscopy (OGD) and duodenal/jejunal biopsy, supplemented by serological tests like anti-TTG IgA antibody measurement. The primary management strategy is a lifelong adherence to a gluten-free diet, alongside regular monitoring for complications. \n\n# Definition\n\nCoeliac disease is a T cell-mediated autoimmune disorder affecting the small intestine. The condition arises due to the production of an auto-antibody against gluten, specifically its component called prolamin, which results in inflammation and villous atrophy of the small bowel leading to malabsorption.\n\n# Epidemiology\n\nCoeliac disease is a prevalent chronic disorder, affecting roughly 0.5 to 1 percent of the general population worldwide. In areas such as Europe, the United States, and Australia, the prevalence varies, ranging from 1 in 80 to 1 in 300 children. The condition disproportionately affects females, with a female to male ratio of approximately 2:1. Coeliac disease exhibits a bimodal age of onset, presenting either in infancy or between the ages of 50-60. It is notably more prevalent in individuals of Irish descent.\n\n# Aetiology\n\nCoeliac disease is associated with a positive family history, the presence of the HLA-DQ2 allele, and other autoimmune diseases, including type 1 diabetes mellitus.\n\n# Signs and Symptoms\n\nGastrointestinal symptoms include:\n\n- Abdominal pain\n- Distension\n- Nausea and vomiting\n- Diarrhoea\n- **Steatorrhoea** (indication of severe disease)\n\nSystemic symptoms encompass:\n\n- Fatigue\n- **Weight loss or failure to thrive in children** (indication of severe disease)\n\nPhysical examination may reveal:\n\n- Pallor (secondary to anaemia)\n- **Short stature and wasted buttocks** (secondary to malnutrition)\n- Signs of vitamin deficiency due to malabsorption (e.g., bruising secondary to vitamin K deficiency)\n- Dermatological manifestations: **dermatitis herpetiformis** (pruritic papulovesicular lesions over the buttocks and extensor surfaces of the arms, legs, and trunk).\n- Abdominal distension\n\n[lightgallery]\n\n# Differential Diagnosis\n\nThe main differential diagnoses for coeliac disease include:\n\n- **Irritable bowel syndrome (IBS)**: Characterised by chronic abdominal pain, bloating, and altered bowel habits without any organic cause.\n- **Inflammatory bowel disease (IBD)**: Crohn's disease and ulcerative colitis are forms of IBD and may present with abdominal pain, diarrhoea, weight loss, and systemic signs of inflammation.\n- **Food intolerance/allergy**: Abdominal discomfort, bloating, and diarrhoea are common.\n- **Gastroenteritis**: Acute diarrhoea and vomiting, often with fever.\n- **Malabsorption syndromes (other than coeliac disease)**: Chronic diarrhoea, weight loss, and signs of specific nutrient deficiencies.\n\n# Investigations\n\nBedside:\n\n- Stool culture to exclude infectious causes. A faecal calprotectin may also be done as IBD is a differential.\n\nBloods:\n\n- Blood tests include FBC, U&E, bone profile, LFT, Iron, B12, and Folate levels.\n\t- It is important to screen for conditions related to malabsorption such as mixed anaemias, vitamin deficiencies.\n- First line serological tests such as anti-TTG IgA antibody and IgA level, followed by anti-TTG IgG, anti-endomyseal antibody, (anti-gliadin is not recommended by NICE.)\n\nImaging/Invasive:\n\n- Oesophago-gastroduodenoscopy (OGD) and duodenal/jejunal biopsy, is considered the gold standard for diagnosis.\n- Histology typically reveals sub-total villous atrophy, crypt hyperplasia, and intra-epithelial lymphocytes.\n\nNB: in the context of antibody blood tests and OGDs looking for changes, the patient needs to have been eating gluten for 6 weeks prior to the investigation.\n\n# Management\n\n- Primary management of coeliac disease is a lifelong commitment to a gluten-free diet. Patient education about food items containing gluten is crucial.\n- Common food items which contain gluten include bread, pasta, pastries and most beers.\n- Regular monitoring of the patient is necessary to ensure adherence to the diet and screen for potential complications. Serological tests can also be done to assess response to removing dietary gluten intake.\n- Dermatitis herpetiformis is managed with dapsone\n\n# Complications\n\n- Mixed anaemia\n- Hyposplenism (increasing susceptibility to encapsulated organisms). Patients with coeliac disease therefore require annual flu and one-off pneumovax vaccinations\n- Osteoporosis (a DEXA scan may be needed)\n- Enteropathy-associated T cell lymphoma (EATL; a rare type of non-Hodgkin lymphoma), the likelihood of which is proportional to the strength of adherence to a gluten-free diet.\n\n# NICE Guidelines\n\n[Click here to see information on NICE CKS about coeliac disease](https://cks.nice.org.uk/topics/coeliac-disease/)",
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"question": "A 32-year-old with type 1 diabetes presents to her GP with a 6-month history of diarrhoea, weight loss and bloating.\n\nExamination reveals conjunctival pallor and a soft, non-tender abdomen.\n\nHer blood tests show a microcytic anaemia, thrombocytopenia, normal anti-tissue transglutaminase (TTG) antibody levels and low serum immunoglobulin A (IgA).\n\nWhich of the following is the next best investigation given the likely diagnosis?",
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"explanation": "Nifedipine is a calcium-channel blocker. It would be indicated if this patient did not have co-existing type 2 diabetes",
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"name": "Start nifedipine",
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"explanation": "This patient has stage 1 hypertension and type 2 diabetes. Therefore, the recommended first-line management of hypertension is with an angiotensin-converting enzyme (ACE) inhibitor. ACE inhibitors are renoprotective in type 2 diabetes and are therefore recommended for the management of hypertension regardless of age or ethnicity",
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"explanation": "Bendroflumethiazide is not an initial treatment option for hypertension. It can be considered if the patient is intolerant to lisinopril or if blood pressure is not controlled after the dose has been up-titrated",
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"explanation": "Metformin would be the first-line management option for this patient's type 2 diabetes, but it would not be used for treating hypertension",
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"explanation": "Home blood pressure monitoring (HBPM) is an alternative to ambulatory blood pressure monitoring. HBPM is not indicated if a diagnosis of hypertension has been confirmed with ambulatory monitoring",
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"comment": "it is unclear whether the question is asking for treatment for the diabetes or hypertension \n",
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"comment": "No it isnt, literally says for his HTN",
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"comment": "oh no moron alert",
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"comment": "could someone explain why we don't need home blood pressure monitoring/more readings? The information below says \"Single reading >140/90 mmHg AND average ambulatory readings >135/85 mmHg\". Does this differ if there's a comorbidity like diabetes? Thanks!",
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"comment": "ambulatory means they have already done extended readings (eg, strapped on them or often multiple readings at home). We can therefore exclude white coat syndrome and start treatment.",
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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 65-year-old Caucasian patient registers with a GP in the UK, having emigrated from Italy.\n\n\nFollowing a set of initial investigations, it is found that his ambulatory blood pressure is 145/90 mmHg. He also has a glycosylated haemoglobin (HBA1C) level of 52 mmol/mol (normal range 20-42 mmol/mol) and a fasting blood glucose of 7.2 mmol/L (normal <6.1 mmol/L).\n\n\nHe notes that he was recently diagnosed with type 2 diabetes but has not started any treatment.\n\n\nWhich of the following is the most appropriate next step in the management of this patient's hypertension?",
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"explanation": "Warfarin is not used in acute limb ischaemia. Commencement of warfarin would delay any surgical intervention that may be necessary due to its long half-life",
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"explanation": "An unfractionated heparin infusion is preferable to treatment dose LMWH in the management of acute limb ischaemia. As unfractionated heparin has a shorter half-life than LMWH, patients can be taken to theatre more promptly with reduced bleeding risk",
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"explanation": "This patient has signs and symptoms consistent with acute limb ischaemia. The prominent popliteal pulsation suggests that the aetiology may be embolic disease from a popliteal aneurysm. Medical management of acute limb ischaemia is with high flow oxygen and initiation of an unfractionated heparin infusion. Surgical intervention may be necessary depending on classification using the Rutherford system",
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"explanation": "# Summary\n\n\nAcute limb ischaemia (ALI) is a severe, symptomatic hypoperfusion of a limb, typically presenting for less than 2 weeks. This condition is a surgical emergency demanding immediate intervention, ideally within 4-6 hours of presentation. The key signs and symptoms are summarised by the mnemonic \"6Ps\": pulseless, pain, pallor, paralysis, paraesthesia, and poikilothermia. Important investigations include complete blood count, U&E, group and save, clotting, and ECG. The management of ALI depends on the cause, with strategies varying for thrombotic and embolic causes. In some cases, limb amputation may be necessary.\n\n\n# Definition\n\n\nAcute limb ischaemia (ALI) is a severe, symptomatic hypoperfusion of a limb that has been occurring for less than 2 weeks. Although the definition specifies a 2-week period, this condition is considered a surgical emergency and demands urgent intervention, ideally within 4-6 hours, however, missed or delayed diagnosis is common. \n\n\n# Epidemiology\n\n\nIn the United Kingdom, acute limb ischaemia (ALI) is not uncommon and presents a significant clinical challenge. Although exact figures vary, incidence rates are estimated at approximately 14 cases per 100,000 persons annually. The condition is more prevalent in older populations, with the majority of cases occurring in individuals over the age of 60. Additionally, factors such as smoking, diabetes, and other forms of cardiovascular disease increase the risk of ALI.\n\n\n# Aetiology\n\n\nAcute limb ischaemia can be caused by:\n\n\n- Thrombosis (80-85%):\n- This often results from the rupture of atherosclerotic plaques.\n- Cardiac or aortic embolisation \n- This accounts for approximately 10-15% of cases. \n- Seen due to atrial fibrillation or mural thrombus formation post-myocardial infarction. \n- Aortic dissection\n- Hypercoagulable states \n- Thrombosis of a pre-existing graft \n- Vasospasm - such as observed in Raynaud's phenomenon.\n- External vascular compromise:\n- Trauma\n- Compartment syndrome\n\n\nAcute limb ischaemia secondary to thrombosis typically has a sub-acute onset and is associated with features of peripheral vascular disease in the contralateral limb. In contrast, ALI secondary to embolisation has a more acute onset and often results from atrial fibrillation.\n\nRisk factors for acute limb ischaemia are similar to those of general cardiovascular risk factors, such as:\n\n- Smoking\n- Diabetes mellitus\n- Obesity\n- Older age\n- Hypertension\n- Hypercholesterolaemia\n\nThe absence of risk factors for acute limb ischaemia should not exclude ALI from the differential diagnosis, as it can be seen in individuals in the absence of risk factors. \n\n\n# Classification \n\nThe Rutherford Classification system is commonly used to grade the severity of acute limb ischaemia.\n\n|**Rutherford Class**|**Sensory Impairment**|**Motor Impairment**|**Doppler Signals**|\n|----------------------------|--------------------------------------------------------|----------------------------|------------------------------------------|\n|**Class 1**|None|None|**Arterial:** Audible <br> **Venous:** Audible|\n|**Class 2a**|Minimal|None|**Arterial:** Audible <br> **Venous:** Audible|\n|**Class 2b**|Involves forefoot with possible rest pain|Mild to moderate|**Arterial:** Absent <br> **Venous:** Present|\n|**Class 3**|Insensate|Severe, rigorous|**Arterial:** Absent <br> **Venous:** Absent|\n\n\n\n# Signs and Symptoms\n\nAcute limb ischaemia most commonly occurs in the lower limbs, but can also occur elsewhere in the body, including the upper limb. \n\nThe signs and symptoms of ALI are represented by the mnemonic \"6Ps\":\n\n\n- **Pulseless**\n- Peripheral pulses may be difficult to palpate or impalpable.\n- **Painful**\n- The pain is described as constant and severe. It occurs at rest. \n- If it is worse on passive movement, this may be a sign of compartment syndrome, a severe complication of acute limb ischaemia. \n- **Pallour**\n- The limb may also have cyanosis or mottling. \n- **Poikilothermia**\n- This is also referred to as \"perishingly cold\" \n- **Paraesthaesia**\n- Loss of sensation occurs before loss of motor power due to the smaller diameter of sensory nerves compared to motor nerves. \n- **Paralysis**\n- Patients may have a reduction or complete loss of muscular power. \n\n\nIf a limb has already lost motor and sensory function, which are late signs seen in acute limb ischaemia, it is generally considered unsalvageable.\n\n### Distinguishing Signs and Symptoms based on Cause\n\nThe signs and symptoms of acute limb ischaemia vary slightly depending if the underlying cause is embolism or thrombosis.\n\n|**Characteristic**|**Thrombosis-Related ALI**|**Embolism-Related ALI**|\n|----------------------------------------|-------------------------------------------------------------------------------------------|------------------------------------------------------------------------------------|\n|**Onset**|Gradual onset. Chronic peripheral arterial disease stimulates collateral vessel development.|Acute onset symptoms.|\n|**Ischemia Border**|No clear border of ischemia due to the presence of chronic peripheral arterial disease.|Well-demarcated area of ischemia, may have a mottled appearance.|\n|**Appearance of Unaffected Limb**|Signs of peripheral arterial disease, such as ulcers and reduced pulses, likely present.|Vascular exam of the other leg is typically normal.|\n\n\n\n# Differential Diagnosis\n\n\nThe main differential diagnoses for acute limb ischaemia include:\n\n\n- **Critical Limb Ischaemia**: This is limb ischaemia which has been occurring for more than 2 weeks. It will also have reduced or absent pulses, but will have ulcers and signs or gangrene. These limbs may have a pink colouration due to collateral formation and compensatory vasodilation surrounding the stenosis. \n- **Compartment syndrome** - Symptoms typically include severe pain, pallor, paresthesia, pulselessness, and paralysis.\n- **Deep vein thrombosis (DVT)** - Symptoms can include unilateral leg swelling, pain, and redness.\n- **Raynaud's phenomenon** - Symptoms are episodic and include pallor, cyanosis, and rubor in response to cold or stress.\n\n\n\n\n# Investigations\n\n\nInitial investigations should include:\n\n- Handheld Doppler ultrasound to determine arterial flow of peripheral vessels\n- This can be used to calculate the ankle-brachial index (ABI). This is where blood pressure is calculated in the ankle and the arm, and then applied to the following equation to determine the ABI. \n- ABI = Highest ankle systolic pressure (dorsalis pedis or posterior tibial) / Highest brachial systolic pressure (left or right arm)\n- < 0.7 is indicative of poor prognosis \n- ECG\n- This is particularly useful to detect atrial fibrillation, suggesting an embolic cause for ALI.\n- Bloods to include:\n- Full blood count (FBC), urea and electrolytes (U&E), creatinine kinase, blood grouping and save, clotting profile\n\nImaging may include:\n\n- Digital subtraction angiogram (DSA)\n- This is considered the standard investigation as it allows determination of the cause of the ischaemia and management can be initiated at the same time. \n- Crescent-shaped occlusion, also referred to as the meniscus sign suggests embolic cause \n- Thrombotic ALI is associated with atherosclerosis of other vessels and the presence of collaterals\n- Duplex Doppler ultrasound\n- CT angiogram \n- Enables visualisation of arteries perfusing the lower limb, however, is contraindicated in those with poor renal function due to the use of dyes. \n- MR angiogram \n- This also uses a dye as during the arterial phase of a contrast bolus the arteries can be visualised. \n\n\n# Management\n\nAcute limb ischaemia is a medical emergency which requires urgent assessment by a vascular surgeon.\n\nIn all cases, all patients should be kept nil by mouth in preparation for potential surgical interventions. Whilst awaiting definitive management, the patient should have:\n\n- Intravenous heparin to prevent thrombus propagation (dependent on local protocols and based on surgeons' advice)\n- Oxygen \n- Analgesia\n- NSAIDs should typically be avoided as many patients are vasculopaths and NSAIDs have an associated risk of cardiovascular events.\n- Intravenous fluids \n- Patients are commonly dehydrated, and risk renal damage due to the release of intracellular components.\n\n### Definitive Management \n\nThe management of acute limb ischaemia varies based on the patient's comorbidities, underlying cause and severity and duration of symptoms. Management options include:\n\n- Endovascular techniques such as:\n- Percutaneous catheter-directed thrombolysis \n- Thrombolytic drugs (i.e. alteplase) are used to dissolve the thrombus. \n- Percutaneous mechanical thrombectomy \n- The thrombus is removed using endovascular tools. \n- Surgery may be indicated due to severity or if endovascular techniques have failed. Options include:\n- Surgical thromboembolectomy\n- Endarterectomy\n- Bypass surgery \n- The occluded vessel is bypassed using a graft to restore perfusion. \n- Fasciotomies\n- These are commonly performed prophylactically for severe ALI with a high risk of developing compartment syndrome. \n- Amputation \n- Used when the limb is considered to be non-viable or if other treatments have failed. \n\n\n### Use of Rutherford Classification\n\nAcute limb ischaemia can be further classified according to the Rutherford criteria, which can help stratify management:\n\n* Stage I: Viable limb. There is an arterial signal that can be picked up with Doppler.\n* Stage IIa: Mild sensory deficit and no motor deficit.\n* Stage IIb: Severe sensory deficit; usually more than just the toes. There may also be rest pain and a motor deficit. \n* Limb salvage depends on immediate treatment.\n* Fasciotomies are often required.\n* Stage III: Irreversibly non-viable limb.\n* Sometimes patients with stage III undergo amputation due to significant risk of complications such as reperfusion injuries and high mortality. \n* Very early treatment can rarely result in some degree of reversal.\n\n\n### Follow Up\n\nFollowing the immediate management of an acutely ischaemic limb, follow-up should include:\n\n- Smoking cessation advice\n- Management of diabetes if present\n- Diet and exercise advice for weight loss \n- Lipid-lowering therapy should be considered \n- Use of anti-platelet agents for those with peripheral arterial disease should be started long-term \n\n\n# Complications\n\nIndividuals with ALI risk having the following complications:\n\n- Reperfusion injury:\n- Ischaemia causes tissue death. When perfusion is restored to the limb, potassium and hydrogen ions can be released, resulting in hyperkalaemia and acidosis. \n- Hyperkalaemia can result in weakness and cardiac arrhythmias. \n- Damage to the muscle causes the release of myoglobin, which can cause acute kidney injury. \n- Compartment syndrome: \nReperfusion of previously ischaemic tissue can cause oedema. This increases the pressure within a restricted fascial compartment, resulting in compartment syndrome. \n- This is an emergency which requires urgent fasciectomy to treat and reduce the loss of muscle. \n- Peripheral nerve injury:\n- Prolonged ischaemia can result in long-term damage to the nerves, resulting in chronic pain pathology. \n- Amputation:\n- If not diagnosed and treated within a timely manner, the limb may require amputation. \n- This is more common in cases caused by thrombosis due to the underlying peripheral arterial disease.\n\n\n# Prognosis\n\nAcute limb ischaemia is associated with an up to 20% mortality rate, which is often the result of reperfusion injury. A poorer prognosis is associated with more severe arterial disease and prolonged time to perfusion. This is seen as prolonged ischaemia time is associated with higher rates of amputation, as a 24-hour delay between symptom onset and reperfusion is associated with a 20% amputation rate. \n\n# NICE Guidelines\n\n[NICE Guidelines Peripheral Arterial Disease](https://bestpractice.bmj.com/topics/en-gb/431?q=Peripheral%20arterial%20disease&c=recentlyviewed) \n\n\n# References\n\n[NHS Peripheral Arterial Disease](https://www.nhs.uk/conditions/peripheral-arterial-disease-pad/) \n\n[BMJ Best Practice Peripheral Arterial Disease](https://bestpractice.bmj.com/topics/en-gb/431?q=Peripheral%20arterial%20disease&c=recentlyviewed) \n\n[Royal College of Emergency Medicine: Acute Limb Ischaemia](https://www.rcemlearning.co.uk/reference/acute-limb-ischaemia/) \n\n[European Society for Vascular Surgery 2020 Guidelines](https://esvs.org/wp-content/uploads/2021/08/Acute-Limb-Ischaemia-Feb-2020.pdf) \n\n[Patient Info: Limb Embolism and Ischaemia](https://patient.info/doctor/limb-embolism-and-ischaemia)",
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"question": "A 56-year-old man with a background of type 2 diabetes, hypertension and ischaemic heart disease presents with a cold and painful left foot.\n\nHe reports that the symptoms came on suddenly around two hours ago. On examination, the left foot is pale and cold with absent dorsalis pedis and posterior tibial pulses; however, a prominent popliteal pulse is detected. Sensation and movement of the foot are preserved.\n\nWhich of the following is the most appropriate intervention whilst awaiting diagnostic imaging?",
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"explanation": "Steroids may be used as a supportive measure to reduce oedema that may be contributing to airway obstruction in this context; however, it is not the definitive step in management",
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"explanation": "This patient has acute airway obstruction secondary to a neck haematoma. Neck haematoma is a life-threatening complication of thyroid surgery and can present with signs of airway obstruction (e.g. stridor, respiratory distress), dysphagia, hoarseness and a painful neck mass. Definitive management is with an urgent return to theatre to open the stitches and evacuate the haematoma",
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"explanation": "# Summary\n\nThyroid cancer, although an uncommon malignancy, is the most prevalent cancer of the endocrine system. It encompasses several types, including papillary, follicular, medullary, anaplastic, and thyroid lymphoma. These types differ in frequency, age of presentation, metastatic patterns, associated conditions, and prognosis. Key diagnostic investigations include thyroid ultrasound, fine-needle aspiration, and measurement of serum thyroid-stimulating hormone (TSH) and calcitonin levels. Management strategies are largely determined by the type and stage of thyroid cancer, and generally involve surgery, radioactive iodine treatment, external beam radiation, targeted therapy, or chemotherapy.\n\n# Definition\n\nThyroid cancer is a malignant tumour that originates in the cells of the thyroid gland, a butterfly-shaped organ located at the base of the neck that produces hormones that regulate the body's metabolism.\n\n# Aetiology\n\nThyroid cancer results from genetic changes or mutations that allow cells to grow and multiply rapidly. The accumulation of these abnormal cells forms a tumour. The type of thyroid cancer is determined by the specific cell type within the thyroid that has become cancerous.\n\n# Types of Thyroid Cancer\n\n1. **Papillary Thyroid Cancer**: Constitutes around 70% of all cases (think **P**apillary = **P**opular). Generally presents between 30-40 years of age and can metastasise to bone and lung. Small tumours carry an excellent prognosis.\n \n2. **Follicular Thyroid Cancer**: This type is more common in areas with low iodine and among women, and typically presents between 30-60 years of age. It tends to metastasise to lung and bones rather than locally invade.\n \n3. **Medullary Thyroid Cancer**: Comprising around 5% of thyroid cancer cases, it originates from calcitonin-producing C-cells. It can present with hypocalcaemia and diarrhoea due to increased calcitonin. While 75% of cases are sporadic, it is associated with Multiple Endocrine Neoplasia (MEN) syndrome type 2A and 2B. Metastasis often occurs to lymph nodes, and the prognosis is worse than papillary and follicular carcinoma.\n \n4. **Anaplastic Thyroid Cancer**: The rarest form, it generally presents between 60-70 years old. Characterised by its aggressive nature, patients present with rapidly growing masses. The prognosis is extremely poor with a median survival rate of 8 months.\n \n5. **Thyroid Lymphoma**: Accounts for 10% of thyroid cancers and is typically Non-Hodgkins lymphoma. It is mainly seen between 50-80 years old and is strongly associated with Hashimoto's thyroiditis.\n \n\n# Signs and Symptoms\n\nWhile the symptoms vary depending on the type of thyroid cancer, some common signs and symptoms include a lump or swelling in the neck, voice changes, difficulty swallowing, pain in the neck and throat, and persistent cough.\n\n# Differential Diagnosis\n\nThe differential diagnosis for a patient presenting with a thyroid mass includes:\n\n1. **Benign thyroid nodules**: Often asymptomatic, may present with compressive symptoms like dysphagia and dyspnea.\n2. **Thyroiditis (Hashimoto's or De Quervain's)**: Pain and swelling of the thyroid gland, with Hashimoto's often presenting with hypothyroid symptoms.\n3. **Thyroid cyst**: A fluid-filled sac in the thyroid, often asymptomatic but may cause neck swelling.\n4. **Goitre**: Swelling in the neck due to enlarged thyroid gland, often accompanied by hypothyroid or hyperthyroid symptoms depending on the cause.\n\n# Investigations\n\nThyroid cancer investigations include thyroid ultrasound for imaging of the gland, fine-needle aspiration for cytology, and measurement of serum thyroid-stimulating hormone (TSH) and calcitonin levels to determine the function of the gland and the activity of medullary thyroid cancer, respectively.\n\n# Management\n\nManagement of thyroid cancer is dependent on the type and stage of the disease, but strategies typically involve:\n\n1. **Surgery**: Thyroidectomy or lobectomy, often followed by radioactive iodine treatment.\n2. **Radioactive Iodine (RAI) Treatment**: Used post-surgery to destroy remaining thyroid tissue and treat thyroid cancer cells throughout the body.\n3. **External Beam Radiation Therapy (EBRT)**: Employed in inoperable cases or to relieve symptoms in advanced disease.\n4. **Targeted Therapy**: Used for advanced or metastatic disease, including tyrosine kinase inhibitors.\n5. **Chemotherapy**: Used sparingly, often in combination with radiation for anaplastic thyroid cancer.\n\n## Complications of Thyroid Surgery\n- **Hypocalcaemia** may arise due to accidental injury or removal of the parathyroid glands during thyroid surgery. Symptoms include tingling in the hands and face, muscle spasms, and, at its most severe, ventricular arrhythmias.\n- **Hypothyroidism** is a guaranteed outcome of total thyroidectomy and may occur following a partial thyroidectomy. Patients will need to be on lifelong thyroxine replacement therapy post-surgery.\n- **Damage to the recurrent or superior laryngeal nerves** results from surgical interference with these nerves. This leads to hoarseness and dyspnoea. Management of laryngeal nerve damage may involve speech therapy or reconstructive surgery.\n- **Neck haematoma** arises from post-operative bleeding within the neck. Can be confirmed with USS or CT, but if threatens airway function requires immediate surgical intervention.\n- **Thyrotoxic storm** can occur due to the manipulation of the thyroid gland in a patient who is hyperthyroid. Management of thyrotoxic storm includes beta-blockers, antithyroid medications, and supportive care.\n",
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"question": "A 43-year-old woman is recovering following a total thyroidectomy the previous day. The surgical notes reveal an uncomplicated operation, and all observations post-operatively have been normal.\n\nThe on-call doctor is called to see the patient urgently as her oxygen saturations have dropped acutely to 90% on room air. On assessment, the patient can speak in short sentences only and is using her accessory muscles. Examination of the lung fields are unremarkable; however, there is an intermittent high pitched sound heard on inspiration and an erythematous neck swelling.\n\nWhich of the following is the most appropriate definitive step in management?",
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"explanation": "Arterial imaging would be of benefit if there was a concern about circulatory deficit preventing healing. The pathophysiology of diabetic foot ulcers is usually microvascular in nature and therefore arterial duplexes are not indicated",
"id": "32535",
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"name": "Arterial lower limb duplex",
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"explanation": "Venous doppler scanning is predominantly used to look for venous thrombosis. Whilst haemostasis in the legs due to poor drainage can cause venous ulceration the vignette here indicates this is a diabetic foot ulcer and therefore dopplers are not indicated",
"id": "32536",
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"name": "Lower limb venous doppler",
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"explanation": "Blood cultures would be indicated if this patient had presented acutely septic, however this is a chronic infection and therefore blood cultures are unlikely to be positive or helpful in this case",
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"name": "Blood cultures",
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"explanation": "Given the chronicity of this infection and the relative immunosuppression of a patient with poorly controlled diabetes, it is important to rule out osteomyelitis which would require extended intravenous antibiotic therapy. The best modality for this is MRI",
"id": "32533",
"label": "a",
"name": "Magnetic resonance imaging (MRI) of the foot",
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"explanation": "Serum HbA1C is useful in determining both the initial diagnosis and long term control of diabetes. Whilst in this case we know the patient has poorly controlled diabetes and tighter diabetic control will lead to better outcomes it does not deal with the acute issue at hand",
"id": "32537",
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"name": "Serum haemoglobin A1C (HbA1C) measurement",
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"explanation": "# 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",
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"question": "A 73 year old female with poorly controlled type two diabetes mellitus has had a chronically infected foot ulcer for six weeks and it is not improving with oral antibiotics. She's become increasingly unable to weight bear over the past week.\n\nWhich investigation will be most useful to guide your management?",
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"explanation": "Whilst a urine dip might be helpful in diagnosis if obstruction is not the cause, he has reported he has not passed urine for over 12 hours therefore obtaining a urine sample may not be possible without inserting a catheter",
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"explanation": "This is not an unreasonable investigation, as patients with metastatic disease may present with cauda equina, however the bladder scan is not suggestive of urinary retention at a spinal level and therefore less likely than external compression of a ureter for example",
"id": "32566",
"label": "d",
"name": "Magnetic resonance imaging (MRI) of the spine",
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"explanation": "Whilst a CT of his abdomen and pelvis would be useful in aiding diagnosis, at the moment his renal function is poor and contrast is best avoided",
"id": "32564",
"label": "b",
"name": "Computerised tomography (CT) of abdomen and pelvis with contrast",
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"explanation": "A FAST scan is used to detect free fluid in the abdomen in a trauma situation and therefore is not indicated in this case",
"id": "32567",
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"explanation": "This patient has a significant acute kidney injury, is anuric, and has a known intraabdominal malignancy. It is important to rule out a urological obstruction as cause for his presentation. The bladder scan does not show retention, however there may be an obstruction at the ureteric level",
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"explanation": "# Summary\n\nAcute kidney injury (AKI) refers to a sudden deterioration in kidney function which may lead to oliguria, electrolyte imbalance, and accumulation of urea and other waste products. It is characterised by increased serum creatinine levels and reduced urine output. Causes are typically categorised as pre-renal, renal and post-renal, with most cases being pre-renal. Initial investigations include a urine dip, U&Es and a bladder scan. If there is no obvious cause, common next steps involve an ultrasound of the kidneys, ureters and bladder to look for post-renal causes (i.e. obstruction) and bloods to look for renal causes. Management involves treating the underlying cause as well as addressing complications such as hyperkalaemia.\n\n# Definition\n\nAn acute kidney injury is characterised by a decline in renal function that happens rapidly (over hours to days). It is diagnosed based on the Kidney Disease: Improving Global Outcomes (KDIGO) criteria as below:\n\n- Increase in serum creatinine by >26.5 mmol/l within 48 h, or\n- Increase in serum creatinine > 1.5x the baseline within the last 7 days, or\n- Urine output < 0.5 ml/kg/h for 6 hours\n\nUnlike chronic kidney disease (CKD), AKI is typically reversible, at least in part. \n\n# Epidemiology\n\nAKI is common, affecting approximately 20% of patients admitted to hospital and up to 50% of critically unwell patients in intensive care.\n\nIt is a marker of severe illness, with a 90-day mortality rate of approximately 25%. \n\nPatients at increased risk of AKI include:\n\n- Patients with CKD\n- Elderly patients\n- Previous AKI \n- Malignancy\n- Medical conditions increasing risk of urinary obstruction (e.g. benign prostatic hyperplasia)\n- Cognitive impairment and disability (may be reliant on others for fluid intake) \n- Recent use of medications such as NSAIDs or ACE inhibitors\n- Recent administration of iodine-containing contrast media\n\n# Aetiology\n\nCauses AKI are categorised into pre-renal, renal, and post-renal causes:\n\n**Pre-renal causes** are the most common, and occur due to decreased renal perfusion e.g. due to:\n\n- Hypovolaemia (e.g. dehydration, haemorrhage, gastrointestinal losses, burns)\n- Renovascular disease (e.g. renal artery stenosis)\n- Medications reducing blood pressure or renal blood flow (e.g. NSAIDs, ACE inhibitors, ARBs, diuretics)\n- Hypotension due to reduced cardiac output (e.g. heart failure, sepsis)\n\n**Renal causes** occur due to structural damage to the kidneys, which may affect:\n\n- The glomeruli (e.g. acute glomerulonephritis, nephrotic syndrome)\n- The tubules (e.g. acute tubular necrosis due to ischaemia or toxins, rhabdomyolysis)\n- The interstitium (e.g. acute interstitial nephritis secondary to drugs)\n- The renal vessels (e.g. renal vein thrombosis, vasculitis)\n\n\n**Post-renal causes** involve obstructed to urinary flow anywhere along the urinary tract, which may be:\n\n- Luminal (e.g. ureteric stones or a blocked catheter) \n- Intramural (e.g. urethral or ureteric strictures, ureteric carcinomas) \n- Due to external compression (e.g. an abdominal or pelvic tumour, benign prostatic hyperplasia)\n\n# Classification\n\nAKIs are staged according to the KDIGO criteria as follows:\n\n**Stage 1 - any of:**\n\n- Creatinine rise of 26 micromol/L or more within 48 hours\n- Creatinine rise to 1.5-1.99x baseline within 7 days\n- Urine output < 0.5 mL/kg/hour for more than 6 hours\n\n**Stage 2 - any of:**\n\n- Creatinine rise to 2-2.99x baseline within 7 days \n- Urine output < than 0.5 mL/kg/hour for more than 12 hours\n\n**Stage 3 - any of:** \n\n- Creatinine rise to 3x baseline or higher within 7 days\n- Creatinine rise to 354 micromol/L or more with either\n- Acute rise of 26 micromol/L or more within 48 hours or\n- 50% or more rise within 7 days \n- Urine output < than 0.3 mL/kg/hour for 24 hours\n- Anuria for 12 hours\n\n# Signs and Symptoms\n\nAn AKI may be asymptomatic and be detected on blood tests only, or may be diagnosed due to a fall in urine output.\n\nSymptoms may be seen especially in severe cases where uraemia occurs, and include:\n\n- Nausea and vomiting \n- Fatigue\n- Confusion\n- Anorexia\n- Pruritus \n\nOn examination, look for:\n\n- Hypertension (a complication of AKI)\n- Bladder distension due to urinary retention\n- Hypotension and dehydration (in many pre-renal causes)\n- Signs of fluid overload (e.g. raised jugular venous pressure, pulmonary and peripheral oedema) as a complication of AKI\n- Signs related to the underlying cause (e.g., fevers in sepsis, rashes in vasculitis)\n- Pericardial rub (in uraemic pericarditis)\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urinalysis** - urine dip may show blood and protein in glomerular disease, increased white blood cells may suggest infection or interstitial nephritis\n- **ECG** to screen for complications of hyperkalaemia\n- **Blood gas** to look for acidosis as a complication of AKI, allows rapid potassium measurement\n\n**Blood tests:**\n\n- **U&Es** to get creatinine for diagnosis (compare to baseline if available) and check for hyperkalaemia\n- **Full blood count** may show anaemia in vasculitis or raised white cells in infection\n- **LFTs** may be deranged in severe hypotension causing ischaemic hepatitis \n- **Clotting** as a baseline in case a renal biopsy is later required (rare)\n- **Bone profile** to screen for hypercalcaemia (seen in myeloma which can cause renal AKI)\n- **Creatinine kinase** to look for rhabdomyolysis\n- **CRP** may be raised in infection or vasculitis\n\n**Imaging:**\n\n- **Bladder scan** if urinary retention is suspected\n- **Ultrasound KUB (kidneys, ureters and bladder)** if a post-renal cause is suspected, may show hydronephrosis. The next line of imaging would be a **CT KUB** as this is a more sensitive modality.\n\nIf initial investigations do not reveal a cause, bloods for an acute **renal screen** may be done, including:\n\n- ANA\n- Double-stranded DNA\n- Anti-nuclear cytoplasmic antibodies\n- Anti-GBM antibodies\n- Erythrocyte sedimentation rate\n- Serum immunoglobulins\n- Serum electrophoresis\n- Serum free light chains\n- Complement levels (C3 and C4)\n- HIV screening\n- Hepatitis B and C serology\n\nIf the diagnosis is still unclear and a renal cause is suspected, a **renal biopsy** may be indicated.\n\n# Management\n\n- The key to AKI management is identification and treatment of the underlying cause\n- The **most common cause of AKI is dehydration,** and so for many patients IV fluid resuscitation will be required \n- Careful assessment of fluid status is crucial though, as in certain cases where the patient is fluid overloaded diuretic treatment rather than fluids may be required\n- Fluid balance should be monitored closely with consideration of catheterisation to monitor urine output \n- A catheter may be the definitive treatment in some cases (e.g. post-renal AKI due to urethral obstruction)\n- Screen for complications of AKI (e.g. hyperkalaemia, acidosis, pulmonary oedema) and instigate treatment promptly\n- Involve the renal team early in severe or complicated AKIs, where the cause is unclear or where a renal cause is suspected\n- Review regular medications and **suspend any nephrotoxic drugs** (e.g. NSAIDs, aminoglycosides, ACE inhibitors, ARBs) and review those that may cause complications in cases of renal impairment (e.g. opiates, metformin)\n- Low-risk patients with an uncomplicated stage 1 or 2 AKI may be considered for discharge if there is an identifiable cause that can be managed in the community\n- The following should prompt referral for consideration of renal replacement therapy with dialysis or haemofiltration (remembered by the AEIOU mnemonic): \n\t- **A**cidosis (severe metabolic acidosis with pH of <7.20)\n\t- **E**lectrolyte imbalance (resistant hyperkalaemia)\n\t- **I**ntoxication (AKI secondary to certain drugs or poisons)\n\t- **O**edema (refractory pulmonary oedema)\n\t- **U**raemia (uraemic encephalopathy or pericarditis)\n\n# NICE Guidelines\n\n[NICE CKS - Acute Kidney Injury](https://cks.nice.org.uk/topics/acute-kidney-injury/) \n\n[NICE: Acute kidney injury: prevention, detection and management](https://www.nice.org.uk/guidance/ng148) \n\n# References\n\n[KDIGO - AKI guideline](https://kdigo.org/guidelines/acute-kidney-injury/) \n\n[Patient UK - Acute Kidney Injury](https://patient.info/doctor/acute-kidney-injury-pro)",
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"question": "An 83 year old male with metastatic colorectal cancer presents to the emergency department with abdominal pain. He reports not passing urine for the last 12 hours. On examination he has moist mucous membranes, his JVP is not raised and his abdomen is diffusely tender without being peritonitic. Bladder scan shows a volume of 20ml.\n\n\nHis admission bloods are as follows:\n\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|83 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|16.5x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|235x10<sup>9</sup>/L|150 - 400|\n|Sodium|134 mmol/L|135 - 145|\n|Potassium|5.4 mmol/L|3.5 - 5.3|\n|Urea|14 mmol/L|2.5 - 7.8|\n|Creatinine|300 µmol/L|60 - 120|\n|C Reactive Protein|15 mg/L|< 5|\n\n\nWhat is the most important next investigation?",
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"explanation": "Whilst hypertension requires aggressive treatment in IgA nephropathy, 5mg is a high starting dose as patients are usually started at 1.25-2.5mg and then gradually increased at two weekly intervals",
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"explanation": "The National Institute of Clinical Excellence (NICE) states that calcium channel blocker is first line antihypertensive medication for those over the age of 55 or of African or Afro-Caribbean family origin. As this patient is young an ACEi is therefore first line",
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"comment": "pretty sure ramipril is nephrotoxic?\n",
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"comment": "jAK spend time on the wards\n",
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"comment": "good for GN bad for CKD as i understand it bcs it lowers pressure in glomerulus",
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"comment": "In the acute setting stop, long term these are renoprotective",
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"comment": "bad for aki,good for ckd, ",
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"comment": "if someone's mad at me for not knowing this as an F1 then that's their f problem",
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"comment": "you'd know this as an F1 if you spent more time on the wards mate",
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"comment": "wish I could just download the BNF to my brain",
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"explanation": "# Summary\n\nIgA nephropathy, also known as Berger disease, is the most common primary glomerulonephritis. It occurs due to deposition of immune complexes made up of immunoglobulin A (IgA) in the mesangium, which trigger glomerular inflammation. Patients typically present with macroscopic haematuria in the days following development of an upper respiratory tract infection. A significant proportion are asymptomatic and are diagnosed following an incidental finding of microscopic haematuria and proteinuria. Initial investigations include a urine dip and microscopy, as well as bloods for renal function. The gold standard diagnostic test is a renal biopsy. Management involves supportive care with blood pressure control, consideration of sodium-glucose cotransporter 2 (SGLT2) inhibitors for patients with significant proteinuria, followed by consideration of immunosuppression (e.g. steroids or an alternative such as mycophenolate mofetil). For most patients IgA nephropathy is a benign disease however approximately 40% progress to chronic renal disease.\n\n# Definition\n\nIgA nephropathy is a type of glomerulonephritis that occurs due to deposition of IgA in the mesangium of the glomerulus. It may lead to progressive renal impairment and chronic kidney disease. \n\n# Epidemiology\n\n- IgA nephropathy is the commonest primary glomerulonephritis, with a worldwide incidence of 2.5 cases per 100,000 people per year\n- However, there is wide geographic variation in prevalence; it is rare in African countries with the highest rates seen in Eastern and Pacific Asian countries\n- Median age at diagnosis is approximately 40 years old\n- In European and American patients, men are more commonly affected (there is an even gender split in other countries)\n\n# Aetiology\n\n- There is excessive generation of IgA1, often triggered by mucosal infection (e.g. upper respiratory tract or gastrointestinal)\n- There is no evidence that there is a specific infectious agent responsible\n- The IgA forms immune complexes that deposit in the glomerular mesangium\n- This immune complexes trigger glomerular inflammation, with mesangial cell proliferation, complement activation and recruitment of macrophages, monocytes and T cells\n- A small percentage of cases have a familial form of IgA nephropathy; the majority of cases are sporadic\n\n# Signs and Symptoms\n\n- Many patients are asymptomatic and are identified due to an incidental finding of microscopic haematuria or proteinuria (usually mild)\n- Most commonly, patients present with visible haematuria\n- This usually occurs 12-72 hours after an upper respiratory tract or gastrointestinal infection\n- It is typically self-limiting within a few days\n- Haematuria typically recurs with subsequent infections\n- Loin pain (either unilateral or bilateral) may accompany episodes of haematuria\n\nSigns include:\n\n- Hypertension\n- Oedema and frothy urine in patients presenting with nephrotic syndrome (approximately 5% of cases)\n\n# Differential Diagnosis\n\n- **Secondary IgA nephropathy** may occur due to a variety of other diseases that can cause renal IgA deposition - this is important as treatment in these cases should be directed at the underlying cause rather than consideration of immunosuppression\n- Liver cirrhosis causes reduced clearance of IgA complexes\n- Coeliac disease is another association\n- HIV is associated with higher serum IgA levels\n- Other infections such as hepatitis B are also associated with IgA nephropathy\n- **Post-streptococcal glomerulonephritis** also presents with visible haematuria after an infection, specifically beta-haemolytic streptococci (e.g. tonsillitis secondary to Streptococcus pyogenes) - typically this is 1-3 weeks after the infection rather than a couple of days in IgA nephropathy\n- **Henoch Schonlein Purpura** is a disease related to IgA nephropathy that usually occurs in children, which presents with a purpuric rash, arthralgia, haematuria and renal involvement (also with glomerular IgA deposits)\n- **Lupus nephritis** may involve IgA mesangial deposition as well as other immunoglobulins and complement - this is referred to as a \"full house\" on renal biopsy when all of IgA, IgG, IgM, C3 and C1Q are positive\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urine dip** looking for blood and protein\n- **Urine microscopy and culture** to rule out infection and look for dysmorphic red blood cells and casts\n- **24 hour urinary protein** or a **protein:creatinine ratio** to quantify proteinuria - this is usually mild\n\n**Blood tests:**\n\n- **U&Es** to assess renal function\n- **Immunoglobulins** may show raised serum IgA1 levels in up to 50% of patients (however this does not correlate with disease severity)\n- **Complement** is usually normal\n- **Liver function tests** to rule out cirrhosis\n- **Full blood count** looking for anaemia and to check platelets prior to biopsy\n- **Clotting screen** to screen for coagulopathy prior to biopsy\n\n**Imaging tests:**\n\n- **Renal ultrasound** to check kidney size - this may be normal or kidneys may be small in chronic kidney disease\n\n**Special tests:**\n\n- **Renal biopsy** is the diagnostic test and shows diffuse mesangial IgA immune complex deposits\n\n# Management\n\n**Conservative management:**\n\n- All patients should be referred to secondary care services for confirmation of the diagnosis and ongoing management\n- Lifestyle changes including regular exercise, maintaining a healthy diet and weight and smoking cessation\n- Dietary salt should be restricted\n\n**Medical management:**\n\n- Control blood pressure with a target of < 120-130/80\n- ACE inhibitors or angiotensin II receptor blockers (ARBs) are first-line for hypertension and may also be used for proteinuria > 0.5 g/day\n- SGLT2 inhibitors can be added if patients with persistent haematuria despite an ACE inhibitor or ARB\n- Clinical trial enrollment should be considered for patients with high risk of progression\n- The next step is immunosuppression - options vary with patient ethnicity\n- Hydroxychloroquine and mycophenolate mofetil are options in Chinese patients\n- Systemic steroids may be required in some cases e.g. nephrotic syndrome or rapidly progressive glomerulonephritis\n\n**Surgical management:**\n\n- Patients with end-stage renal disease require renal replacement therapy with dialysis or transplant\n- However, IgA nephropathy often recurs after transplant (up to 30% of cases)\n\n# Prognosis\n\n- Disease severity varies significantly\n- Most patients experience persistent microscopic haematuria, although episodes of macroscopic haematuria typically become less frequent with time\n- Less than 10% of patients experience complete resolution of haematuria and proteinuria\n- Within 25 years of diagnosis, approximately 30% of patients progress to end-stage renal disease\n- Risk factors for renal failure include impaired renal function at diagnosis, significant proteinuria and hypertension\n\n# References\n\n[UK Kidney Association - IgA Nephropathy](https://ukkidney.org/rare-renal/clinician/iga-nephropathy)\n\n[Patient UK - IgA Nephropathy](https://patient.info/doctor/iga-nephropathy-bergers-disease-pro)\n\n[IgA nephropathy in adults - treatment standard](https://academic.oup.com/ndt/article/38/11/2464/7221084)\n\n[IgA Nephropathy: Core Curriculum in Nephrology](https://www.ajkd.org/article/S0272-6386(21)00598-9/fulltext)",
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"question": "A 31 year old male presents to the general practice with rose coloured urine and fatigue. He reports that he had a recent upper respiratory tract infection, but otherwise has no past medical history of note. He undergoes a renal biopsy and is diagnosed with IgA nephropathy. During his follow up he is found to have hypertension on serial blood pressure measurements.\n\nWhat single medication ought to be started in the first instance?",
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"explanation": "Chronic rejection is a possibility in this case and should be considered in clinical practice. However, the picture of declining renal function in chronic rejection is more gradual in nature and would not account for the changes in his liver function",
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"explanation": "Those who suffer from ADPKD can also develop liver cysts, which can alter liver function; however, it is unusual to develop new cysts in a transplanted kidney",
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"explanation": "Tremor and headache are two well-known symptoms of tacrolimus toxicity which is also both nephrotoxic and hepatotoxic. The fact that this patient might be mixing up his medications raises the concern that he may be overdosing his tacrolimus",
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"explanation": "Whilst vascular dementia may be the precipitating factor for his cognitive decline; it would not account for the changes in his blood tests",
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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 75-year-old male is seen in clinic and is noted to have renal and liver function off his usual baseline. His wife is concerned his memory isn't what it used to be, and he has been mixing up his medications of late. She has also noticed his hands are shaking. His past medical history includes autosomal dominant polycystic kidney (ADPKD) disease, for which he had a renal transplant ten years ago.\n\nWhat is the most likely cause for this clinical picture?",
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"explanation": "This would be a reasonable choice if the patient did not have IV access, but as we have secured access in this patient, IV lorazepam is a better option as it is faster acting and does not run the risk of whoever is administering it being accidentally bitten by the patient while they seize",
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"explanation": "# Summary\n\nStatus Epilepticus is defined as a seizure lasting 5 minutes or more, or multiple seizures occurring within a 5-minute window without regaining full consciousness between episodes. It is a medical emergency, and treatment should begin promptly at the 5-minute mark. Initial management involves administering benzodiazepines, such as rectal diazepam, buccal midazolam, or intravenous lorazepam. If there is no response to two doses of benzodiazepines, second-line treatments include levetiracetam, phenytoin, or sodium valproate. Refractory cases may require general anesthesia with agents like propofol or midazolam. Investigations include blood tests, toxicology screen as well as neuroimaging and CSF analysis if the cause remains unclear\n\n# Definition\n\nStatus epilepticus is defined as a seizure lasting 5 minutes or more OR multiple seizures over 5 minutes without returning to a full level of consciosuness between episodes.\n\nIt should be assumed at 5 minutes and appropriate treatment and investigations initiated.\n\n# Acute management of status epilepticus\n\nEmergency AED therapy for convulsive status epilepticus [NICE guidelines](https://www.nice.org.uk/guidance/ng217/chapter/7-Treating-status-epilepticus-repeated-or-cluster-seizures-and-prolonged-seizures):\n\n\n\n\n**Premonitory stage (0-10 minutes)** \n\n- Diazepam 10−20 mg given rectally, repeated once 15 minutes later if status continues to threaten, or midazolam 10 mg given buccally. If seizures continue, treat as below.\n\n**Early status (0-30 minutes)** \n\n- If in the community:\n\t- Buccal Midazolam or Rectal Diazepam \n- If IV access is obtained and resuscitation facilities are available:\n\t- Lorazepam (intravenous) 0.1 mg/kg (usually a 4 mg bolus, repeated once after 10−20 minutes; rate not critical). \n\n**Established status (0-60 minutes)** \n\n- If not responding to 2 doses of benzodiazepine, give any of the following as second-line treatment\n\t- Levitiracetam\n\t- Phenytoin\n\t- Sodium Valproate\n\n**Refractory status (30-90 minutes)**\n\n- General anaesthesia, with one of:\n\n\t- Propofol (1–2 mg/kg bolus, then 2–10 mg/kg/hour) titrated to effect\n\t- Midazolam (0.1–0.2 mg/kg bolus, then 0.05–0.5 mg/kg/hour) titrated to effect\n\t- Thiopental sodium (3–5 mg/kg bolus, then 3–5 mg/kg/hour) titrated to effect; after 2–3 days infusion rate needs reduction as fat stores are saturated\n\t- Anaesthetic continued for 12−24 hours after the last clinical or electrographic seizure, then dose tapered.\n\n\n# Investigations\n\n- Arterial Blood Gas\n- Routine Blood tests including FBC, U&E, LFT, CRP, Clotting, Bone Profile \n- Toxicology screen (urine)\n- Anti-epileptic drug levels (if appropriate)\n- If the underlying cause is unclear, further investigations can include:\n\t- CT/MRI Brain Imaging\n\t- Lumbar Puncture \n\n\n# References\n\n[Click here for the NICE guidelines on managing status epilepticus](https://www.nice.org.uk/guidance/ng217/chapter/7-Treating-status-epilepticus-repeated-or-cluster-seizures-and-prolonged-seizures)",
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"explanation": "# Summary\n\nDiplopia is commonly caused by third, fourth, and sixth nerve palsies which refer to paralysis of the oculomotor, trochlear, and abducens nerves respectively. Each nerve controls different sets of extraocular muscles, contributing to various distinct clinical presentations. \n\n# Epidemiology\n\nThese nerve palsies are relatively rare, with an estimated prevalence ranging from 1 in 1,000 to 1 in 10,000 depending on the specific nerve involved. They can occur in all age groups but tend to be more prevalent in older adults due to higher rates of vascular disease and diabetes which are common aetiological factors.\n\n# Aetiology\n\n- **Third nerve palsy**: This condition can result from surgical lesions (compressive) such as a posterior communicating artery aneurysm, or medical lesions (non-compressive), such as multiple sclerosis or vascular causes like diabetes.\n\t- Compressive lesions compresse parasympathetic fibres which are at the outermost of the nerve, leads to unopposed sympathetic action which leads to fixed pupil dilatation. This doesn’t happen in medical pathologies as no physical compression of those outermost parasympathetic fibres. Please see section on medical third nerve palsy for more information\n- **Fourth nerve palsy**: Common causes include ocular trauma and diabetes mellitus.\n- **Sixth nerve palsy**: Common causes are diabetic neuropathy, stroke, infection, multiple sclerosis and trauma. It's known for being a 'false localizing sign' due to the path of the sixth nerve within the brain, making it easily compromised in a state of raised intracranial pressure.\n\n# Signs and Symptoms\n\n- **Third nerve palsy**: The eye's classic resting position is looking 'down and out'. Other features include ptosis, proptosis, and a fixed pupil dilatation if the lesion is compressive rather than medical.\n\n[lightgallery]\n\n\n- **Fourth nerve palsy**: The presentation is a result of paralysis or partial paralysis of the superior oblique muscle. At rest, the eye points upwards and inwards, and the patient may present with a tilted head to compensate for the palsy. Patients present with double vision worse in the vertical plane, and potentially hypertropia.\n\n- **Sixth nerve palsy**: The eye fails to ABduct due to paralysis of the abducens nerve. It may be medially deviated at rest, and diplopia worsens when the patient is asked to look horizontally away from the midline on the side of the lesion.\n\n[lightgallery1]\n\n# Differential Diagnosis \n\nThe primary systemic differentials include:\n\n- **Myasthenia gravis**: Presents with weakness that is exacerbated by continued use of the muscle. Patients often have ocular symptoms of diplopia and ptosis that worsen throughout the day or while watching television.\n- **Strabismus**: Common cause of diplopia in children and occasionally in adults. Esotropia – a convergent squint – is the commonest type, where the malaligned eye diverges inwards towards the midline.\n- **Thyroid eye disease**: Exophthalmos in Graves' disease can cause double vision through compression of the extraocular muscles and lack of space for the eye to rotate.\n\n[lightgallery2]\n\n# Investigations\n\n- Typically, the workup includes a comprehensive ophthalmologic examination to evaluate eye movements, visual acuity, and pupillary function. \n- Neuro-imaging, such as MRI or CT scan, is often necessary, particularly for third nerve palsy, to identify any compressive lesions. \n- Additional tests depend on the suspected aetiology and may include blood tests, cerebrospinal fluid analysis (LP), and nerve conduction studies.\n\n# Management\n\n- Management strategies vary depending on the specific nerve involved, aetiology, and severity of symptoms. Initial management may include prismatic glasses to correct diplopia and use of occlusion for troublesome diplopia. \n- Definitive management may include strabismus surgery or treatment of the underlying cause (e.g. blood sugar control in diabetic neuropathy, immunosuppression in multiple sclerosis). \n- In some cases, spontaneous recovery can occur.\n\n# References\n\n1. Rucker JC. \"Cranial Neuropathies: Oculomotor, Trochlear, and Abducens Nerve Palsies.\" In: Brazis PW, Masdeu JC, Biller J, editors. Localization in Clinical Neurology. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2016. pp. 239-256.\n \n2. Brazis PW. \"Isolated palsies of cranial nerves III, IV, and VI.\" Semin Neurol. 2009;29(1):14-28. doi:10.1055/s-0028-1124022.\n\n3. Malik SRK, Gupta AK, Choudhry S. \"Strabismus and Ocular Paralysis.\" In: Clinical Ophthalmology: Modern Perspectives. New Delhi, India: Jaypee Brothers Medical Publishers; 2019. pp. 307-334.\n\n4. Bahn RS. \"Graves' ophthalmopathy.\" N Engl J Med. 2010;362(8):726-738. doi:10.1056/NEJMra0905750.\n\n",
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"question": "A 58-year-old female presents to the Emergency Department concerned she has had a stroke. Her past medical history includes hypertension, gout, recurrent urinary tract infections, chronic kidney disease (CKD) stage three, type two diabetes on insulin, and a previous N-STEMI. On examination, she is GCS 15/15 and talking in complete and coherent sentences. She has normal power, tone, sensation, reflexes and coordination in all four limbs. She has double vision and a mild ptosis. Her pupils are both symmetrical and equal.\n\nAn MRI Head is performed which is normal.\n\nWhich of the following is the most likely underlying cause of her presentation?",
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"explanation": "A cataract is an opacity of the lens of the eye and is usually a gradual age-related process. Presentation is usually with gradual blurring of the vision. Whilst diabetes is a risk factor for cataracts; this history is too acute",
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"explanation": "This is a classic history suggestive of retinal detachment. Risk factors for exudative retinal detachment include hypertension, vasculitis and macular degeneration, whereas myopia is a cause for tractional detachment. Other causes of detachment may be traumatic in nature, allowing fluid to pass from the vitreous space into the subretinal space",
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"comment": "I thought that retinal detachment typically caused progressive lateral vision loss, and vascular causes lead to top-down vision loss? confusing. ",
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"explanation": "# Summary\n\nRetinal detachment is a medical condition referring to the separation of the retina from the retinal pigment epithelium (RPE), commonly caused by trauma. Characterized by symptoms such as floaters, photopsia, reduced visual acuity and visual field impairment, this condition can cause irreparable sight loss if the detachment progresses to the macula. Diagnosis can be confirmed through a variety of examinations and tests, such as fundoscopy, ultrasound or optical coherence tomography. Management strategies include surgical and non-surgical treatments like laser therapy, cryotherapy, vitrectomy, scleral buckling and pneumatic retinopexy.\n\n# Definition\n\nRetinal detachment is a medical condition that refers to a separation of the retina from the retinal pigment epithelium (RPE). There are different types of retinal detachment, but the most common is rhegmatogenous retinal detachment, commonly caused by trauma.\n\n# Epidemiology\n\nEpidemiological data on retinal detachment varies, but it is generally agreed that the condition is more common in individuals over the age of 40 and in those with a history of severe myopia or previous eye surgery.\n\n# Aetiology \n\nRetinal detachment can occur due to a variety of causes, including:\n\n- Trauma, which can create tears or holes in the retina\n- Severe myopia, which can thin the retina and make it more prone to tears\n- Previous eye surgery, particularly cataract surgery\n- Certain diseases, such as diabetes or sickle cell disease\n- Age-related changes in the vitreous, which can pull the retina away from the back of the eye\n\n# Signs and Symptoms\n\nPatients with retinal detachment may present with the following symptoms:\n\n- Floaters\n- Photopsia (flashes of light)\n- Progressive and rapidly reduced visual acuity and visual field loss\n- Painlessly in most cases\n\nThe danger is that if the detachment progresses to the macula, sight may be irreparably lost.\n\n# Differential Diagnosis\n\nThe main differentials for retinal detachment include:\n\n- Posterior vitreous detachment: Characterized by floaters, light flashes, and a \"\"cobweb\"\" effect in vision\n- Age-related macular degeneration: Symptoms include blurred or reduced central vision, distorted vision, and difficulty reading or recognizing faces\n- Vitreous hemorrhage: Presents with sudden loss of vision, floaters or shadows in the field of vision\n\n# Investigations \n\nTo diagnose retinal detachment, a variety of examinations and tests may be used, such as:\n\n- Fundoscopy: To visually inspect the back of the eye \n\t- One of the key findings to note in retinal detachments is if the macula is attached **(macula-on)** or macula-detached **(macula-off).** It is the status of the macula that defines the urgency with which surgical repair should be undertaken\n- Ultrasound: To get a detailed image of the eye\n- Optical coherence tomography: To provide cross-sectional images of the retina\n\n# Management\n\nThere are various surgical and non-surgical treatments available for retinal detachment, depending on the extent of the condition. If the macula remains attached, there should be greater urgency to act faster as any vision-loss may still be salavagable, with poorer outcomes for macula-off RD. These include:\n\n- Laser therapy or cryotherapy: To seal retinal tears or holes\n- Vitrectomy: To remove the vitreous and replace it with a gas bubble or silicone oil\n- Scleral buckling: To push the sclera toward the retinal tear\n- Pneumatic retinopexy: To push the retina back into place using a gas bubble.",
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"question": "A 58-year-old male presents to the Emergency Department with painless visual loss that he describes as a curtain coming down over his vision. He has never had this happen before. His only past medical history is well-controlled diabetes, and he is short-sighted.\n\nWhat is the most likely diagnosis?",
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"explanation": "Eye taping at night is beneficial if unable to close the eyelid to help prevent drying and abrasions whilst sleeping. Some patients with severe thyroid eye disease and very protuberant eyes may need assistance with lid closure; however, this intervention would not address the patient's visual loss",
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"comment": "So the GP can sUrGiCalLy dEcoMpReSs the optic nerve???????",
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"comment": "qs doen't imply this, it simply asks for the intervention likely needed. not the next best step",
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"explanation": "# Summary\n\nThyroid Eye Disease, also known as Graves' Ophthalmopathy, is a complex autoimmune condition closely associated with hyperthyroidism. It manifests with a range of ocular symptoms, including eyelid retraction, proptosis, double vision, and ocular discomfort. The disease primarily affects the orbital tissues and extraocular muscles due to an immune response targeting the thyroid gland and surrounding structures. Diagnosis relies on clinical evaluation, imaging, and thyroid function tests. Management encompasses medical therapy, supportive care, and in severe cases, surgical interventions to address disfiguring or vision-threatening complications. \n\n# Definition\n\nThyroid eye disease (TED) is a complication of Grave's disease, which is an autoimmune hyperthyroidism. An inflammatory process results in swelling of the extraocular muscles and orbital fat, which leads to multiple ocular complications.\n\n# Pathophysiology\n\nAn idiopathic autoimmune inflammatory process is responsible for TED, the exact mechanism of which remains unclear. Evidence suggests that an autoimmune reaction to TSH receptors results in lymphocyte infiltration into orbital tissues, which initiates an inflammatory process.\n\nThe **inflammatory phase** of TED typically lasts 6–24 months and results in the swelling of extraocular muscles and orbital fat – it is only during this initial inflammatory phase that TED is responsive to medical management.\n\nAfter the inflammatory phase, there is an **inactive fibrotic phase**, which is nonresponsive to medical therapy.\n\nHyperthyroidism and TED usually present within 18 months of each other, but each can be present in isolation.\n\n# Epidemiology\n\n- Roughly half of patients with Grave's disease develop TED\n- 80% of cases of TED are due to Grave's disease\n\n# Risk factors\n\n- **Smoking** – the most important risk factor for development and increased severity of TED in patients with Grave's disease, so it is important to counsel patients on the importance of smoking cessation\n- Family history of Grave's disease and other autoimmune disease\n- Female sex\n- Poor thyroid control\n\n\n# Signs and Symptoms\n\n- Ocular pain – often worse on movement\n- Dry, red eyes\n- 'Bulging eyes'\n- Painful eyelids\n- Proptosis/exophthalmos\n- Lid retraction and lid lag\n- Chemosis\n- Orbital fat prolapse\n- Exposure keratopathy\n\n[lightgallery] \n\n\n\n# Management \n\nEarly medical management of TED has the potential to stabilise, slow or even reverse the disease process. Good control of thyrotoxicosis is essential and other medical therapies, such as steroids or other immunosuppressants, may be used.\n\nIn sight-threatening TED, urgent surgical orbital decompression may be required, followed by intravenous corticosteroids.\n\nConservative therapy consists of artificial tears, ointments and prisms to help with the symptoms of dry eye and diplopia.\n\n# Complications\n\nSight-threatening complications include:\n\n- **Exposure keratopathy** – where corneal damage and infection occur as the patient is unable to close their eyes\n\n- **Compressive optic neuropathy** – occurs when the retro-orbital swelling begins to compress on the optic nerve \n - suspect this when signs of optic nerve involvement occur – reduced visual fields, reduced colour vision, reduced visual acuity, relative afferent pupillary defect\n\n- **Diplopia** – due to fibrosis of the extraocular muscles limiting gaze in various directions\n\n# References\n\nDenniston AK, Murray PI. Oxford Handbook of Ophthalmology. Fourth Edition. Oxford University Press. 2018.\n\n[Click here for an in-depth review of TED on the Patient UK website](https://patient.info/doctor/thyroid-eye-disease-pro)\n",
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"explanation": "A foreign body may cause irritation and lead to inflammation of the eye; however, this history does not suggest trauma to the eye",
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"label": "d",
"name": "Foreign body",
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"explanation": "Scleritis is a generalised inflammation of the sclera itself and is strongly associated with systemic disease, commonly vasculitis and rheumatoid arthritis. Ocular movements are painful, and often headache and photophobia are present. As the vessels of the sclera are deeper, they will not blanch on probing. Management is guided by underlying cause and ranges from steroids and topical NSAIDs to immunosuppressive therapy such as cyclophosphamide and rituximab",
"id": "32623",
"label": "a",
"name": "Scleritis",
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"votes": 4222
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"explanation": "Episcleritis is inflammation below the conjunctiva and often associated with an inflammatory nodule. As these vessels are more superficial, they will move and blanch on probing with a phenylephrine soaked cotton bud",
"id": "32624",
"label": "b",
"name": "Episcleritis",
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"votes": 196
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Patients with acute closed angle glaucoma usually present with nausea and vomiting. However, they rarely have visual complaints, and only about 25% will have a headache and a painful red eye",
"id": "32627",
"label": "e",
"name": "Acute closed angle glaucoma",
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"votes": 594
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is harmless bleeding of blood behind the conjunctiva and is often associated with the use of anticoagulants. It is usually more alarming than anything else and would not normally cause pain and therefore is not the most likely diagnosis here",
"id": "32625",
"label": "c",
"name": "Subconjunctival haemorrhage",
"picture": null,
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"explanation": "# Summary\n\nScleritis and episcleritis are ocular conditions characterized by inflammation of the sclera and the episclera respectively. Both conditions present with red eye. However, scleritis is associated with severe pain, pain on ocular movement and nonblanching vessels, and may be associated with systemic illnesses such as rheumatoid arthritis. Episcleritis, on the other hand, has milder symptoms and often resolves without intervention. Key investigations for scleritis include urine dipstick, FBC, CRP, U&Es, LFT and autoimmune serology. Management strategies include NSAIDs for mild scleritis and corticosteroids for severe or necrotising scleritis.\n\n# Definition\n\nScleritis is a severe inflammation of the sclera, and episcleritis is an inflammation of the episclera, the layer underneath the conjunctiva.\n\n\n# Aetiology\n\nScleritis may be associated with systemic illnesses such as rheumatoid arthritis or granulomatosis with polyangiitis.\n\n# Signs and Symptoms\n\n[lightgallery]\n[lightgallery1]\n\n## Scleritis\n\n- Red eye\n- Severe pain in the orbit\n- Pain on eye movement\n- Bluish tinge to the white of the eye in severe or necrotising scleritis\n- Systemic symptoms in ~50% of patients\n\n## Episcleritis\n\n- Sectoral redness\n- Tenderness over the inflamed area\n- Milder pain compared to scleritis\n- Episcleral vessels move or blanch when pressed with a cotton bud\n\n\n\n# Investigations\n\n## For Scleritis:\n\n- Urine dipstick to identify renal disease\n- FBC, CRP, U&Es, LFT to identify anaemia of chronic disease, neutrophilia, renal function\n- Autoimmune serology\n- Phenylephrine eye drops - these blanch the conjunctival and episcleral vessels but not the scleral vessels. So if there is no blanching this is suggestive of scleritis\n\n# Management\n\nManagement of episcleritis is mostly supportive with the majority of cases self-resolving within weeks. Artifical tears may be used for symptomatic relief.\n\n## For Scleritis:\n\n- NSAIDs such as fluriprofen PO 100 mg TDS for mild cases\n- Corticosteroids such as oral prednisolone or pulsed IV methylprednisolone for severe or necrotising cases\n- Steroid-sparing therapies for long-term treatment\n\n# Prognosis\n\nLess than 5% of patients lose useful vision long-term; however, vision deteriorates in 25% of patients in the years following scleritis and some patients develop cataracts.\n\n# References\n\n- [Scleritis](https://eyewiki.aao.org/Scleritis)\n- [EpiScleritis](https://eyewiki.aao.org/Episcleritis)",
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"question": "A 56-year-old man presents to the Emergency Department with headache, photophobia and a very painful, red eye that has gradually worsened over the past two days. He reports no noticeable discharge from the eye. His past medical history includes diabetes, high cholesterol and rheumatoid arthritis. On examination, the entire sclera is bright red, and there is discomfort on eye movements. On probing with a phenylephrine soaked cotton bud, the redness does not change.\n\nWhat is the most likely diagnosis?",
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "A varicocele is caused by dilated veins of the pampiniform plexus and often may only be present on standing. 90% occur on the left. They are associated with subfertility, but surgical repair appears to have little effect on subsequent pregnancy rates. Treatment is with scrotal support or surgery (varicocelectomy)/embolisation",
"id": "32723",
"label": "a",
"name": "Varicocoele",
"picture": null,
"votes": 1936
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is infection/inflammation of the testis and epididymis. It is often caused by sexually transmitted infections such as chlamydia but also caused by viral causes such as mumps. Patients report a tender generalised swelling and may have other associated features of infection (temperature, dysuria, penile discharge). Treatment is with antibiotics depending on the likely source (NB if sexually transmitted infection deemed likely source then contact tracing and treatment of partners should be initiated)",
"id": "32725",
"label": "c",
"name": "Epididimo-orchitis",
"picture": null,
"votes": 122
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would be in the differential and are caused by fluid within the tunica vaginalis; however, the description and the lack of transillumination make varicocoele more likely",
"id": "32724",
"label": "b",
"name": "Hydrocoele",
"picture": null,
"votes": 176
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is unlikely but should be carefully considered in the differential as testicular tumours are the commonest malignancy in this age demographic. They usually present as a painless, firm lump in the testes found after trauma/infection and may have a secondary hydrocoele",
"id": "32726",
"label": "d",
"name": "Testicular tumour",
"picture": null,
"votes": 466
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This presents as a painless nodule at the head of the epididymis adjacent to the inferior pole of the testis and will transilluminate. They may contain clear or milky (spermatocele) fluid",
"id": "32727",
"label": "e",
"name": "Epididymal cyst",
"picture": null,
"votes": 1834
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"__typename": "QuestionComment",
"comment": "how dare you not say bag of worms",
"createdAt": 1683139753,
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"comment": "WHERE BAG OF WORMS ",
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"comment": "\"lump\" is not a good description of a varicocele...",
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"explanation": "# Summary\n\nVaricocele is defined as an enlargement of the scrotal veins, often asymptomatic but may cause a sense of aching or heaviness within the scrotum. They can also contribute to male infertility, accounting for 25-40% of such cases. Diagnostic investigations include physical examination, Doppler ultrasound, and possibly hormonal assays. Management is dependent on symptom severity and includes options such as watchful waiting, embolization, and surgery.\n\n# Definition\n\nVaricocele is a condition characterized by an enlargement of the veins within the scrotum, similar in nature to varicose veins that can occur elsewhere in the body.\n\n# Epidemiology\n\nWhile varicocele is relatively common, affecting around 15-20% of all men, its prevalence significantly increases in the infertile population, reaching up to 40%. It typically develops in adolescence and early adulthood.\n\n# Aetiology\n\nVaricoceles develop due to faulty valves within the spermatic cord veins, causing blood to pool and enlarge these veins. Although the exact mechanism that leads to male infertility is unclear, it's hypothesized that increased testicular temperature and oxidative stress may play a role. In a minority of cases, left-sided varicoceles can be caused by compression of the gonadal vein, such as from a renal cell carcinoma.\n\n# Signs and Symptoms\n\nWhile many varicoceles are asymptomatic, when symptoms do present, they may include:\n\n- Aching or heavy feeling in the scrotum\n- Visibly enlarged or twisted veins in the scrotum, often described as a \"bag of worms\"\n- Testicular atrophy\n- Impaired fertility\n\n# Differential Diagnosis\n\nThe primary conditions to consider when diagnosing varicocele include:\n\n- Epididymitis: Key signs and symptoms include scrotal pain and swelling, potentially with fever and urinary symptoms.\n- Testicular torsion: This presents with sudden severe testicular pain, swelling, nausea, and vomiting.\n- Inguinal hernia: Symptoms typically include a visible bulge in the groin region or scrotum, pain, and possible bowel or bladder symptoms.\n- Hydrocele: This condition usually causes painless scrotal swelling.\n\n# Investigations\n\nThe following investigations can aid in diagnosing varicocele:\n\n- Physical examination: Varicoceles can often be identified by palpation of the scrotum, especially while standing or during a Valsalva maneuver.\n- Doppler ultrasound: This imaging modality can identify the enlarged veins and assess for retrograde blood flow, confirming the diagnosis.\n- Hormonal assays: In cases where infertility is suspected, evaluation of testosterone, FSH, LH, and semen analysis can be useful.\n\n# Management\n\nThe management strategy for a varicocele depends largely on the symptom severity and patient’s fertility desires. Options include:\n\n- Watchful waiting: For asymptomatic varicoceles or those not causing fertility problems.\n- Embolization: This minimally invasive procedure involves blocking the blood flow to the enlarged veins.\n- Surgery: Varicocele repair surgery can be performed through open surgery, laparoscopically, or with robotic assistance.",
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"learningPoint": "A varicocele, often present only when standing and typically occurring on the left, is caused by dilated veins of the pampiniform plexus, associated with subfertility, and treated with scrotal support or surgery/embolization.",
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"question": "A 34-year-old male presents to the sexual health clinic concerned about a lump he has found in his left testicle. He is sexually active but does not complain of any penile discharge or any urinary symptoms. On examination, there is a soft fleshy lump that is separate from the spermatic cord. It is only palpable when the patient is standing and not when lying down. It does not transilluminate.\n\nWhat is the most likely diagnosis?",
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"a"
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"__typename": "QuestionSBA",
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{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This patient has an infected obstructed system which requires urgent intervention. She is also septic, and therefore treatment with oral antibiotics is unlikely to be sufficient",
"id": "32729",
"label": "b",
"name": "Oral antibiotics",
"picture": null,
"votes": 151
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "If medical expulsion therapy does not work in stable patients with stones >5mm, then ESWL is a reasonable choice. This patient is septic and therefore requires urgent decompression with a nephrostomy or ureteric stenting",
"id": "32731",
"label": "d",
"name": "Extracorporeal shockwave lithotripsy (ESWL)",
"picture": null,
"votes": 738
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This patient has an obstructed infected urinary system that needs urgent decompression. As her stone is 6mm and in the upper part of the urethra, decompression with a nephrostomy is indicated. She should also be managed in accordance with sepsis six and started on antibiotics",
"id": "32728",
"label": "a",
"name": "Urgent right nephrostomy",
"picture": null,
"votes": 4028
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{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Analgesia is indicated in this patient's case; however, it will not treat her underlying condition",
"id": "32732",
"label": "e",
"name": "Analgesia",
"picture": null,
"votes": 211
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Whilst the stone is 6mm and therefore unlikely to pass spontaneously, the main issue here is the infected obstructed system that requires urgent intervention. If she was not septic, then medical expulsive therapy with tamsulosin would be a reasonable choice",
"id": "32730",
"label": "c",
"name": "Tamsulosin",
"picture": null,
"votes": 49
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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 25-year-old female presents to the Emergency Department with right-sided loin to groin pain that she describes as coming in waves and is associated with nausea but no vomiting. Her observations at triage show she is pyrexial at 38.8, tachycardic and hypotensive. Her urine dip is positive for blood and nitrites and negative for pregnancy, and her blood tests reveal raised inflammatory markers.\nA CT of kidneys, ureters and bladder (KUB) is performed, demonstrating a right-sided 6mm obstructing calculus associated with hydroureter and hydronephrosis.\n\nWhat treatment is urgently required?",
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"comment": "Causes of Third Degree Heart Block:\n\nMyocardial infarction (especially inferior)\nDrugs acting at the AV node (beta blockers, calcium channel blockers)\nIdiopathic fibrosis.\n\nok... ",
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"explanation": "# Summary\r\n\r\nHeart block refers to an obstruction in the electrical conduction system of the heart. This obstruction can occur at various points in the conduction system, including the sinoatrial node, atrioventricular node, Bundle of His, or bundle branches. Atrioventricular heart block specifically affects the conduction between the atria and ventricles. The severity of heart block can range from first degree, which is generally benign, to second degree (Mobitz Type I and II), to complete (third degree) heart block, which requires immediate management with a permanent pacemaker due to the risk of asystole. The underlying causes and management strategies differ for each type of heart block.\r\n\r\n# Definition \r\n\r\nHeart block occurs due to an obstruction in the electrical conduction system of the heart. It can occur anywhere along the conduction system of the heart from the sinoatrial node to the atrioventricular node to the Bundle of His or within the bundle branches themselves. \r\n\r\nSinoatrial node block rarely leads to symptoms as the atrioventricular node acts as a secondary pacemaker. Bundle branch blocks are a form of heart block but they are discussed in a separate section. The rest of this section will discuss atrioventricular block in more detail. \r\n\r\nPatients with atrioventricular heart block may be asymptomatic or may present with fatigue, lightheadeness, syncope, shortness of breath and most seriously in cardiac arrest or with sudden death. \r\n\r\n# First Degree Heart Block\r\n\r\n## Definition\r\n\r\nThis is caused by prolonged conduction of electrical activity through the AV node. It can be identified on ECG by finding a PR interval >200ms.\r\n\r\n[lightgallery]\r\n\r\n## Causes\r\n\r\n* High vagal tone: e.g. athletes\r\n* Acute inferior MI\r\n* Electrolyte abnormalities: e.g. hyperkalaemia\r\n* Drugs: e.g. NHP-CCBs, beta-blockers, digoxin, cholinesterase inhibitors\r\n\r\n## Management\r\n\r\nFirst degree heart block itself is benign and does not need treating. However, any pathological underlying cause should be reversed.\r\n\r\n# Second Degree Heart Block \r\n\r\nSecond degree heart block is split into Mobitz Type I and Mobitz Type II heart block. \r\n\r\n# Mobitz Type I\r\n\r\n## Definition\r\n\r\nWenckebach phenomenon or Mobitz type I is a type of second degree heart block that is usually due to reversible conduction block at the AV node. It is characterised by progressive lengthening of the PR interval which results in a P wave that fails to conduct a QRS.\r\n\r\n[lightgallery1]\r\n\r\n## Causes\r\n\r\n* MI (mainly inferior)\r\n* Drugs such as beta/calcium channel blockers, digoxin\r\n* Professional athletes due to high vagal tone\r\n* Myocarditis\r\n* Cardiac surgery\r\n\r\n## Management\r\n\r\nIt is generally asymptomatic and does not require any specific management as the risk of high AV block/complete heart block is low. If symptoms do arise, ECG monitoring may be required, precipitating drugs must be stopped and if they are bradycardic with adverse features they should be treated with atropine.\r\n\r\n# Mobitz Type II\r\n\r\n## Definition\r\n\r\nMobitz type II block is a type of second degree AV block where there are intermittent non-conducted P waves. The _PR interval is constant_ (may be normal or prolonged) and there may no pattern or fixed ratios such as 2:1 or 3:1 block. It is usually caused by conduction system failure, especially at the His-Purkinje system.\r\n\r\nIn most cases there is a broad QRS indicating a distal block in the His-Purkinje system and many patients have pre-existing left bundle branch block/bifascicular block.\r\n\r\n[lightgallery2]\r\n\r\n## Causes\r\n\r\n* Infarction: particularly anterior MI which damages the bundle branches\r\n* Surgery: mitral valve repair or septal ablation\r\n* Inflammatory/autoimmune: rheumatic heart disease, SLE, systemic sclerosis, myocarditis\r\n* Fibrosis: Lenegre's disease\r\n* Infiltration: sarcoidosis, haemochromatosis, amyloidosis\r\n* Medication: beta-blockers, calcium channel blockers, Digoxin, amiodarone\r\n\r\n## Management\r\n\r\nDefinitive management is with a permanent pacemaker as these <u>_patients are at risk of complete heart block_</u> and at risk of becoming haemodynamically unstable.\r\n\r\n# Complete (Third degree) Heart Block\r\n\r\n## Definition\r\n\r\nComplete heart block occurs when atrial impulses fail to be conducted to the ventricles. Sufficient cardiac output may be secondary to a ventricular or junctional escape rhythm.\r\n\r\nECG shows severe bradycardia and complete dissociation between the P waves and the QRS complexes. These patients are at high risk of asystole, ventricular tachycardia and cardiac arrest. \r\n\r\n[lightgallery3]\r\n\r\n## Causes\r\n\r\n* Myocardial infarction: especially inferior\r\n* Drugs acting at the AVN: beta blockers, dihydropyridine calcium channel blockers, or adenosine\r\n* Idiopathic fibrosis\r\n\r\n## Management\r\n\r\nManagement of complete (third degree) heart block is via the acute bradycardia guideline (see below). Permanent pacemaker insertion is eventually required due to the risk of sudden death.\n\nAcute management:\n\nFor emergencies, always follow an A-E structure. Identify reversible causes (dyselectrolytaemias, drugs, cardiac causes etc.) \r\n\r\n*If there are adverse signs (e.g. shock, syncope, heart failure, myocardial ischaemia):* \r\n\r\n* **1st line** = **500 micrograms atropine IV**\r\n * Atropine blocks the vagal nerve which increases firing rate of the SAN. \r\n* **2nd line** = if the first dose of atropine is not working can consider giving additional doses of atropine 500mcg up to 3mg until response. Alternatively, **transcutaenous pacing** or **isoprenaline** or **adrenaline** or **alternative drugs** including aminophylline, adrenaline, glucagon (in beta-blocker or calcium channel blocker overdose). \r\n\r\n*If there are no adverse signs but a risk of asystole, or a satisfactory response to 500mcg atropine:*\r\n\r\n* Risk of asystole: recent asystole, mobitz type II block, complete heart block + broad QRS, ventricular pauses >3s. \r\n* **1st line** = administer **500 micrograms atropine IV**. Alternatively, **transcutaenous pacing** or **isoprenaline** or **adrenaline** or **alternative drugs** including aminophylline, adrenaline, glucagon (in beta-blocker or calcium channel blocker overdose). \r\n\r\n*If there are no adverse signs and there is no risk of asystole*\r\n\r\n* Observe\r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines on Pacing](<https://www.nice.org.uk/guidance/ta88/chapter/2-clinical-need-and-practice>) \r\n\r\n# References\r\n\r\n[Life in the Fast Lane Heart Block ECG Summary](https://litfl.com/heart-block-and-conduction-abnormalities/)\r\n\r\n[Resuscitation Council Adult Bradycardia Algorithm](<https://www.resus.org.uk/sites/default/files/2020-05/G2015_Adult_bradycardia.pdf>)",
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"question": "A 90-year-old woman is brought to A&E because she has been complaining of chest pain. She is a poor historian because of known Alzheimer's dementia. She also has a past medical history of Parkinson's and a previous suspected transient ischaemic attack. On examination, she is visibly short of breath.\n\nOn her ECG, there is complete dissociation of the P waves and QRS complexes.\n\nHer current medication is as follows: donepezil, ropinirole, amlodipine, atorvastatin, aspirin. Which of these medications is most likely to have caused this problem?",
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"explanation": "Hypotension and raised jugular venous pressure may occur in pneumothorax, especially a tension pneumothorax. However, this is likely to be accompanied by sudden onset pleuritic chest pain, making it less likely. Therefore, a needle thoracostomy would not be appropriate",
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"explanation": "This would be appropriate in acute heart failure. The patient does display some signs and symptoms in keeping with acute heart failure, such as dyspnoea, raised jugular venous pressure, and bibasal crepitations. However, this wouldn't explain the muffled heart sounds",
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"explanation": "The patient cannot talk in full sentences, which is one of the features of an acute severe asthma attack. However, this is less likely when considering the raised jugular venous pressure and bibasal crepitations without wheeze. Therefore, nebulised salbutamol would not be appropriate",
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"explanation": "The patient is displaying all the three hallmarks of Beck's triad. These are distended neck veins, hypotension and muffled heart sounds. When presenting acutely, the first presentation may be anxiety and fatigue. Dyspnoea, tachycardia and tachypnoea are also seen. Therefore, the definitive treatment is pericardiocentesis, where a needle is inserted into the pericardium to drain fluid",
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"comment": "i believe it should say \"Beck's triad\" rather than Back's",
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"comment": " (systolic blood pressure 111-219 mmHg) ???",
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"comment": "maybe it's trying to hint at pulsus parodoxus with a rising and falling systolic BP, but those numbers (the cut-off is a variability of 10 mmhg) and the way it's written make absolutely no sense",
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"comment": "I think it's because on NEWS2 you don't score for hypertension until it's 220 systolic so the 'normal' values are indicating what is a NEWS2 of 0. Even though I probably wouldn't be chilled if someone had a systolic of 219. ",
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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 67-year-old woman attends A&E with anxiety and fatigue. She has been experiencing worsening shortness of breath and is unable to talk in full sentences. On examination, she has raised jugular venous pressure and bibasal crepitations, and it is difficult to hear heart sounds. Her observations are as follows:\n\n- Temperature - 37.1 (36 - 38 degrees centigrade)\n- Respiratory rate - 25 (12-20 breaths per minute)\n- Heart rate - 110 (50-90 beats per minute)\n- Blood pressure - 87/64 (systolic blood pressure 111-219 mmHg)\n- Oxygen saturations - 92 (>96%)\n\nWhat is the definitive treatment?",
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"explanation": "Blockage of the diagonal branch of the left coronary artery leads to lateral STEMI. Therefore, the leads that are most likely to be affected are the so-called lateral leads. These are leads I, aVL, V5 and V6",
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"explanation": "The left anterior descending artery supplies the anterior section of the heart. An anterior STEMI would usually show ST elevation in V1, V2, V3 and V4. Anterior infarcts have the poorest outcomes",
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"explanation": "Occlusion of the circumflex branch of the left coronary artery can lead to inferior STEMI. However, this would be more likely if there was ST elevation higher in lead II compared to lead III, without any reciprocal changes in lead I",
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"explanation": "There is marked ST elevation present in leads II, III and aVF. There is reciprocal ST depression in aVL. This pattern of ST elevation suggests an inferior ST-elevation myocardial infarction (STEMI). Therefore, this is most likely due to blockage of either the right coronary artery or the circumflex branch of the left coronary artery. In this case, it is the right coronary artery as the ST elevation is most significant in lead III compared to II, and there are reciprocal changes in lead I, plus mildly elevated ST waves in V1 and V2. These findings point towards right ventricular damage",
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"explanation": "The sinoatrial artery supplies the atrial node. Therefore, it operates in the superior part of the heart. It is a branch of the right coronary artery which means that some acute inferior STEMIs may also have concurrent problems with the area supplied by the sinoatrial artery. This occurs if the occlusion to the right coronary artery is proximal to the branch of the sinoatrial artery. However, the ECG of this patient shows ischaemia in the inferior leads II, III and aVF. Occlusion to only the sinoatrial artery could not lead to these changes",
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"explanation": "# Summary\r\n\r\nAcute coronary syndrome (ACS) refers to a set of symptoms and signs that occur due to reduced blood flow to the heart at rest. It encompasses 3 distinct diagnoses: unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). In the case of infarction, this is a medical emergency requiring urgent treatment. ACS is most commonly caused by the rupture of atherosclerotic plaques in coronary arteries leading to further narrowing, and potentially complete occlusion, of these critical blood vessels. Diagnosis involves clinical evaluation, ECGs, and troponin levels. Treatment strategies differ for STEMI and NSTEMI/unstable angina but include oxygen therapy if hypoxic, antiplatelet medication, glyceryl trinitrates, morphine, and percutaneous coronary intervention (PCI). Post-MI management includes aspirin, dual antiplatelet therapy, beta-blockers, ACE inhibitors, high-dose statins, and cardiac rehabilitation. There are many complications to be aware of post-ACS and these include arrhythmias, heart failure, and cardiac tamponade, and others.\r\n\r\n# Definition \r\n\r\nAcute coronary syndrome is a set of symptoms and signs that occur due to decreased blood flow to the heart at rest. It broadly refers to three distinct diagnoses: unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI). \r\n\r\n# Epidemiology \r\n\r\nIn the UK, there are over 80,000 hospital admissions due to ACS every year. Coronary artery disease remains the largest cause of death in the UK. \r\n\r\n# Pathophysiology\r\n\r\nCoronary artery disease refers to the narrowing of coronary arteries by atherosclerosis and plaque formation. In stable angina, when the demand for myocardial oxygen increases with exertion, narrowed coronary arteries cannot meet this increased demand leading to myocardial ischaemia and pain. Conversely, in ACS, the symptoms occur at rest. This is because there is sudden plaque rupture and clot formation in the narrowed coronary arteries. If there is partial occlusion of the coronary artery this leads to ischaemia and chest pain at rest (unstable angina). If the coronary artery becomes more occluded or fully occluded this leads to significant hypoperfusion of the myocardium and ultimately leads to infarction (death) of the myocardial tissue (NSTEMI or STEMI). \r\n\r\n# Risk Factors\r\n\r\nCoronary artery disease and the development of plaques can be attributed to non-modifiable and modifiable risk factors. Modifiable risk factors must be addressed in the management of IHD. \r\n\r\n* Non-modifiable:\r\n * Age\r\n * Male sex\r\n * Family history\r\n * Ethnicity (particularly South Asians)\r\n* Modifiable:\r\n * Smoking\r\n * Hypertension\r\n * Hyperlipidaemia\r\n * Hypercholesterolaemia\r\n * Obesity\r\n * Diabetes\r\n * Stress\r\n * High fat diets\r\n * Physical inactivity\r\n\r\n# Classification \r\n\r\nAcute coronary syndrome can be split up into three distinct diagnoses: \r\n\r\n1. **Unstable angina**: caused by partial occlusion of a coronary artery. Troponin negative chest pain with normal/abnormal ECG signs. \r\n2. **Non-ST Elevation Myocardial Infarction**: caused by severe but incomplete occlusion of a coronary artery. Troponin positive chest pain without ST elevation. \r\n3. **ST-Elevation Myocardial Infarction**: caused by complete occlusion of a coronary artery. Troponin positive chest pain with ST elevation on ECG. \r\n\r\n*Myocardial Ischaemia vs. Myocardial Infarction and the Release of Troponin*\r\n\r\nIt is important at this stage to distinguish between angina (stable angina is on exertion and unstable angina is at rest) and myocardial infarction. Angina refers to myocardial ischaemia that causes chest pain but does not lead to the death of myocardial tissue and does not lead to a troponin rise. In myocardial infarction, the hypoperfusion of the myocardium is so profound that it leads to the death of myocardial tissue. It is when there is myocardial tissue death that troponin is released into the bloodstream and a troponin rise is found on blood tests.\r\n\r\n*Type 2 Myocardial Infarction* \r\n\r\nIt is also important to mention that some patient may have myocardial infarctions due to cardiac hypoperfusion for other reasons (e.g. severe sepsis, hypotension, hypovolaemia or coronary artery spasm). These are usually termed type 2 myocardial infarctions and may not require the conventional treatment outlined below. \r\n\r\n# Symptoms and Signs\r\n\r\n* Chest pain - the classical presentation can be considered in terms of the SOCRATES mnemonic:\r\n * Site - Central/left sided\r\n * Onset - Sudden\r\n * Character - Crushing ('like someone is sitting on your chest')\r\n * Radiation - Left arm, neck and jaw\r\n * Associated symptoms - Nausea, sweating, clamminess, shortness of breath, sometimes vomiting or syncope\r\n * Timing - Constant\r\n * Exacerbating/relieving factors - Worsened by exercise/exertion and may be improved by GTN\r\n * Severity - Often extremely severe\r\n* Atypical presentations may include:\r\n * Epigastric pain\r\n * No pain (more common in elderly and **patients with diabetes**):\r\n * Acute breathlessness\r\n * Palpitations\r\n * Acute confusion\r\n * Diabetic hyperglycaemic crises\r\n * Syncope\r\n\r\n# Differential Diagnoses\r\n\r\nIt is important to remember that there are non-MI causes of chest pain and these should be considered when making a diagnosis:\r\n\r\n* Cardiac\r\n * Myocarditis\r\n * Pericarditis\r\n * Cardiomyopathy\r\n * Valvular disease\r\n * Cardiac trauma\r\n* Pulmonary\r\n * PE\r\n * Pneumonia\r\n * Pneumothorax\r\n* Vascular\r\n * Aortic dissection\r\n* GI\r\n * Oesophageal spasm\r\n * Oesophagitis\r\n * Peptic ulcer\r\n * Pancreatitis\r\n * Cholecystitis\r\n* MSK\r\n * Rib fracture\r\n * Costochondritis\r\n * Muscle injury\r\n * Herpes zoster\r\n\r\n# Diagnosis of ACS \r\n\r\nDiagnosis depends on a combination of clinical, ECG and biochemical findings which helps distinguish between the various types of ACS.\r\n\r\n* Unstable angina - cardiac chest pain at rest + abnormal/normal ECG + **normal troponin**.\r\n* NSTEMI - cardiac chest pain at rest + abnormal/normal ECG (but not ST-elevation) + **raised troponin**\r\n* STEMI - cardiac chest pain at rest + **persistent ST-elevation/new LBBB** (note that there is no need for a troponin in this case).\r\n\r\n## Diagnosis of STEMI\r\n\r\n* ST segment elevation **>2mm** in adjacent chest leads\r\n* ST segment elevation **>1mm** in adjacent limb leads\r\n* New left bundle branch block (LBBB) with chest pain or suspicion of MI\r\n\r\n## Diagnosis of NSTEMI\r\n\r\nDiagnosis of NSTEMI requires two of the following:\r\n\r\n* Cardiac chest pain\r\n* Newly abnormal ECG which does not demonstrate ST-elevation e.g. ST depression, T wave inversion or non-specific changes. \r\n* Raised troponin (with no other reasonable explanation)\r\n\r\n# Investigations\r\n\r\n## Bedside \r\n\r\n* ECG \r\n\t* Looking for ST-elevation, LBBB or other ST abnormalities\r\n\t* This is the most important investigation and should not be delayed for other investigations (e.g. bloods) because this will define immediate management.\r\n\t* If an ECG shows STEMI then troponin is essentially irrelevant and the patient requires immediate treatment.\r\n\r\n## Bloods \r\n\r\n* Troponin: performed **at least 3 hours** after pain starts. It will also need to be repeated (usually 6 hours after the first level) in order to demonstrate a dynamic troponin rise. \r\n* Renal function: good renal function is required for coronary angiogram +/- PCI due to the use of contrast. \r\n* HbA1c and lipid profile: looking for modifiable risk factors for coronary artery disease. \r\n* FBC and CRP - rule out infectious causes of chest pain\r\n* D-dimer - may be used in _appropriate_ patients to rule out PE. *Be very careful about who you do a D-dimer on!*\r\n\r\n## Imaging \r\n\r\n* CXR: should be completed in all those presenting with a chest symptoms. It will help to rule out other causes of chest pain (e.g. pneumothorax) and look for complications of a large MI (e.g. pulmonary oedema in acute heart failure). \r\n\r\n# ECG Interpretation - Cardiac Territories and Affected Vessels\r\n\r\nThe importance of a 12-lead ECG is that it allows one to view electrical activity of the heart from different \"views\". In MI (particularly STEMI) this allows you to understand which territory (and therefore which vessel) is being affected.\r\n\r\n| Location of ST elevation | Area of myocardium | Coronary artery |\r\n| -------------------------- | ------------------ | -------------------- |\r\n| II, III, aVF | Inferior | RCA |\r\n| V1-2 | Septal | Proximal LAD |\r\n| V3-4 | Anterior | LAD |\r\n| V5-6 | Apex | Distal LAD/ LCx/ RCA |\r\n| I, aVL | Lateral | Lcx |\r\n| V7-V9 (ST depression V1-3) | Posterolateral | RCA/ LCx |\r\n\r\n\r\nRCA: right coronary artery, LAD: left anterior descending, LCx: Left circumflex\r\n\r\n[lightgallery]\r\n\r\n[lightgallery2]\r\n\r\n[lightgallery3]\r\n\r\n[lightgallery4]\r\n\r\n\r\nNSTEMIs may also show T wave abnormalities (such as ST depression and T wave inversions) in vascular territories as above. However, changes can also often not include all the specific leads of that territory in an NSTEMI.\r\n\r\n# Troponin Interpretation\r\n\r\nTroponin is a myocardial protein that is released into the bloodstream when cardiac myocytes are damaged. Serum levels typically rise **3 hours** after myocardial infarction begins.\r\n\r\nDifferent hospitals have differing guidelines (and assays) for interpretations of results. In general there are three groups of troponin levels:\r\n\r\n* Low - definitely no myocardial cell death. The patient is not having an MI although they may be experiencing unstable angina.\r\n* Mildly raised - This is an equivocal result and may be due to other non-MI related factors (see below). These patients usually need a <u>6-12 hour repeat test</u>.\r\n * If repeat troponin is raised on the repeat they are having an MI.\r\n * If repeat troponin is stable or falling then they are unlikely to be having an MI.\r\n* Definitely raised with sequential dynamic troponin rises - MI confirmed (be aware of the possibility of a Type 2 MI)\r\n\r\n## Non-ACS causes of a raised troponin\r\n\r\nAlthough troponin is often used diagnose myocardial infarction, there are in fact many causes of a raised troponin:\r\n\r\n* Myocardial infarction\r\n* Pericarditis\r\n* Myocarditis\r\n* Arrythmias\r\n* Defibrillation\r\n* Acute heart failure\r\n* Pulmonary embolus\r\n* Type A aortic dissection\r\n* Chronic kidney disease\r\n* Prolonged strenuous exercise\r\n* Sepsis\r\n\r\nIt is therefore critical to have good clinical grounds to test a troponin in order to avoid unnecessary treatments and investigations.\r\n\r\n# Management\r\n\r\nAcute management depends on the type of acute coronary syndrome. It is broadly split into the management of STEMI and the management of NSTEMI/unstable angina. \r\n\r\n# Management of STEMI\r\n\r\n[lightgallery5]\r\n\r\nFor emergencies, always follow A-E structure. \r\n\r\n1. Targeted oxygen therapy (aiming for sats >90%)\r\n2. Loading dose of **PO aspirin 300mg**\r\n - Note that some hospital protocols will also call for a loading dose of a second anti-platelet agent such as clopidogrel (300mg) or ticagrelor (180mg)\r\n - For those going on to have PCI, NICE guidance suggests adding prasugrel (if not on anti-coagulation) or clopidogrel (if on anti-coagulation)\r\n3. **Sublingual GTN spray** - for symptom relief\r\n4. **IV morphine/diamorphine** - in addition this causes vasodilation reducing preload on the heart\r\n5. Primary percutaneous coronary intervention (PPCI) for those who:\r\n - Present **within 12 hours of onset of pain** AND\r\n - Are **<2 hours** since <u>first medical contact</u>\r\n\r\nRemember that (particularly in STEMI) _time is heart_ therefore urgent treatment, escalation, and delivery of PPCI is critical to good outcomes.\r\n\r\n# Management of NSTEMI/Unstable Angina\r\n\r\n[lightgallery6]\r\n\r\nFor emergencies, always follow A-E structure. \r\n\r\n1. Targeted oxygen therapy (aiming for sats >90%)\r\n2. Loading dose of **PO aspirin 300mg** and fondaparinux\r\n * Patients should have their 6 month mortality score (often the GRACE score) calculated as early as possible - all those who are anything other than lowest risk should also be given **prasugrel or ticagrelor** unless they have a high risk of bleeding where **PO clopidogrel 300mg** is more appropriate.\r\n3. **Sublingual GTN spray** - for symptom relief\r\n4. **IV morphine/diamorphine** - in addition this causes vasodilation reducing preload on the heart\r\n5. Start antithrombin therapy such as **treatment dose low molecular weight heparin** or **fondaparinux** if they are for an immediate angiogram\r\n6. Patients with <u>high 6 month risk of mortality</u> should be offered an angiogram within 96 hours of symptom onset.\r\n\r\nNote that management of unstable angina is similar to that of NSTEMI with aspirin for all patients and fondaparinux and early angiography for those at high risk.\r\n\r\n# Post-MI management\r\n\r\n[lightgallery7]\r\n\r\n* ALL patients post-MI patients should be started on the following 5 drugs:\r\n 1. **Aspirin 75mg OM** + second anti-platelet (**clopidogrel 75mg OD** or **ticagrelor 90mg OD**)\r\n 2. **Beta blocker (normally bisoprolol)**\r\n 3. **ACE-inhibitor (normally ramipril)**\r\n 4. **High dose statin (e.g. Atorvastatin 80mg ON)**\r\n* All patients should have an **ECHO** performed to assess systolic function and any evidence of heart failure should be treated.\r\n* All patients should be referred to **cardiac rehabilitation**.\r\n* Patients who have been treated without angiography should be considered for ischaemia testing to assess for inducible ischaemia. \r\n\r\n# Complications\r\n\r\n* Ventricular arrhythmia\r\n* Recurrent ischaemia/infarction/angina\r\n* Acute mitral regurgitation\r\n* Congestive heart failure\r\n* 2nd, 3rd degree heart block\r\n* Cardiogenic shock\r\n* Cardiac tamponade\r\n* Ventricular septal defects\r\n* Left ventricular thrombus/aneurysm\r\n* Left/right ventricular free wall rupture\r\n* Dressler's Syndrome\r\n* Acute pericarditis\r\n\r\n## Ventricular Arrhythmias\r\n\r\n* Ventricular arrhythmias can occur as a consequence of MI, during cardiac catheterisation, or after reperfusion.\r\n* Most post-MI ventricular arrhythmias are short lived and self-resolve.\r\n* However if sustained VT or VF occurs they should be treated as per the Advanced Life Support protocols.\r\n\r\n## Recurrent Ischaemia/Infarction/Angina\r\n\r\n* Occasionally inserted stents can thrombose requiring reintervention.\r\n* New infarcts can occur in different vascular territories - this is less likely in the age of PCI where all territory are imaged during the procedure.\r\n* Angina and chest pain can continue for some time after an MI and is more common in NSTEMI patients.\r\n\r\n## Congestive Heart Failure\r\n\r\n* Heart failure can occur as a consequence of impairment heart muscle function secondary to ischaemia.\r\n* It should be treated as any other acute heart failure.\r\n* Ventricular function may improve over months as the heart muscle recovers.\r\n\r\n## Heart Block\r\n\r\n* Various levels of heart block are common - particularly following **inferior** infarcts (because the right coronary artery supplies the SAN).\r\n* These may be treated with:\r\n * Simple observation (as many will revert back to sinus rhythm)\r\n * Transcutaneous/venous pacing (if symptomatic)\r\n * Permanent pacing (if failing to resolve)\r\n\r\n## Left Ventricular Thrombus/Aneurysm\r\n\r\n* Aneurysm can occur following an anterior MI where the myocardium can be susceptible to wall stress leading to an aneurysm.\r\n* It may be silent, cause arrhythmias or embolic events.\r\n* It is definitely diagnosed on ECHO but ECG may show persisting ST elevation.\r\n* Thrombus can form either within an above described aneurysm or around hypokinetic regions of the myocardium.\r\n* Thrombi can embolise causing complications such as stroke, acute limb ischaemia and mesenteric ischaemia.\r\n\r\n## Left/Right Ventricular Free Wall Rupture\r\n\r\n* Necrosis of the free walls of either ventricle can lead to rupture allowing blood into the pericardial space.\r\n* This leads to a rapid tamponade and normally leads to cardiac arrest/death within seconds.\r\n* Treatment includes pericardiocentesis and surgery but prognosis is extremely poor.\r\n\r\n## Acute Mitral Regurgitation\r\n\r\n* This can occur because of papillary muscle rupture and carries a poor prognosis. Occurs commonly due to infero-osterior MI. \r\n* This presents with:\r\n * Pansystolic murmur heard best at the apex\r\n * Severe and sudden heart failure\r\n* It is diagnosed on echocardiogram and may require surgical correction.\r\n\r\n## Ventricular Septal Defect\r\n\r\n* Interventricular septal rupture is a short-term complications of myocardial infarction.\r\n* Rupture caused by an anterior infarct is generally apical and simple.\r\n* Rupture caused by an inferior infarct is generally basal and more complex.\r\n* Without reperfusion, septal rupture typically occurs within the first week after the infarction.\r\n* Features of septal rupture include:\r\n * Shortness of breath\r\n * Chest pain\r\n * Heart failure\r\n * Hypotension\r\n * Harsh, loud pan-systolic murmur along the left sternal border.\r\n * Palpable parasternal thrill.\r\n* Diagnosis is with echocardiogram.\r\n* Patients are managed with emergency cardiac surgery.\r\n\r\n## Dressler's syndrome\r\n\r\n* Dressler's syndrome or post-infarction pericarditis typically presents with persistent fever and pleuritic chest pain **2-3 weeks** or up to a few months after an MI.\r\n* Note that patients can get pericarditis immediately following MI which is NOT considered Dressler's syndrome.\r\n* Symptoms usually resolve after several days.\r\n* Occasionally it can also present with features of pericardial effusion and has become relatively uncommon since the introduction of PCI.\r\n* Management: **high dose aspirin**\r\n\r\n# Prognosis \r\n\r\nDue to the development of PPCI and post-MI care (cardiac rehabilitation) the mortality rates following myocardial infarction continue to decline. Those patients who go on to develop heart failure after myocardial infarction have a significantly worse prognosis than those who do not. \r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines for Unstable Angina and NSTEMI](https://www.nice.org.uk/guidance/cg94)\r\n\n[NICE Guidelines for STEMI](https://www.nice.org.uk/guidance/cg167)\r\n\r\n# References\r\n\r\n[Patient UK Information on Acute Coronary Syndrome](<https://patient.info/doctor/acute-coronary-syndrome-pro>)",
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"explanation": "# 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. 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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 60-year-old male patient attends GP due to hypertension. He is currently taking four different medications to try and control it:\n\n\nAmlodipine, ramipril, indapamide, spironolactone.\n\n\nHis most recent bloods are as follows:\n\n\n||||\n|---------------------------|:-------:|--------------------|\n|Sodium|135 mmol/L|135 - 145|\n|Potassium|5.7 mmol/L|3.5 - 5.3|\n|Urea|3.6 mmol/L|2.5 - 7.8|\n|Creatinine|74 µmol/L|60 - 120|\n|eGFR|85 mL/min/1.73m<sup>2</sup>|> 60|\n\n\n\nHis blood pressure in the GP was 145/95.\n\n\nWhat is the most likely cause of his hyperkalaemia?",
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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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"explanation": "# Summary \n\nShingles is a reactivation of the varicella zoster virus which can lie dormant in nerve ganglia following primary infection (chickenpox). It commonly occurs in the elderly and shingles in young adults should prompt investigation for an underlying immune condition. Management normally includes oral antivirals, but intravenous antiviral medications can be used if severe or if the patient is immunocompromised.\n\n# Signs & Symptoms\n\nShingles can manifest first as a tingling feeling in a dermatomal distribution. Progresses to erythematous papules occurring along one or more dermatomes within a few days, which develop into fluid-filled vesicles which then crust over and heal. May be associated with viral symptoms e.g. fever, headache, malaise.\n\n[lightgallery]\n\n[lightgallery1]\n\n**Herpes zoster ophthalmicus (HZO)** presents with symptoms including a painful red eye, fever, malaise, and headache, followed by an erythematous vesicular rash over the trigeminal division of the ophthalmic nerve. A lesion on the nose, known as **Hutchinson's sign,** may suggest ocular involvement.\n\n\n\n# Management\n\n- Oral antiviral (e.g. valaciclovir 1g three times per day for 7 days) within 72h of rash onset if immunocompromised (and infection is not severe) or moderate/severe rash or moderate/severe pain, or non-truncal involvement.\n- Admit to hospital for IV antivirals if severe disease or immunocompromise, ophthalmic symptoms or suspicion of meningitis/encaphalitis/myelitis\n- Advise avoiding contact with pregnant women, babies and those who are immunocompromised until the lesions are fully crusted over, as transmission can occur via skin contact\n- Pain can be managed with NSAIDs (e.g. ibuprofen). If unsuccessful, consider offering amitriptyline (off-label use), duloxetine (off-label use), gabapentin, or pregabalin\n\n# Shingles vaccine\n\nThere is a one-off vaccine available for shingles that is typically advised for those in their 70s.\n\n# Complications\n\n- Secondary bacterial infection of skin lesions\n- Corneal ulcers, scarring and blindness if eye involved\n- Post-herpetic neuralgia\n - Pain occurring at site of healed shingles infection\n - Can cause neuropathic type pain (burning, pins and needles)\n - Can cause allodynia (perception of pain from a normally non-painful stimulus e.g. light touch)\n\n# NICE Guidelines\n\n[NICE Clinical Knowledge Summary (CKS): Shingles](https://cks.nice.org.uk/topics/shingles/)\n\n[NICE Treatment Summary: Varicella-zoster vaccine](https://bnf.nice.org.uk/treatment-summary/varicella-zoster-vaccine-2.html)",
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"question": "A 57-year-old woman attends GP due to moderate pain. The pain is localised over the same area of skin where she had shingles three months ago. She now experiences pain whenever that area becomes cold or whenever it is touched lightly.\n\nThe GP diagnoses post-herpetic neuralgia and advises the patient to wear cotton clothes over the affected area; to wrap the area in clingfilm, and advised her how to improve her sleep.\n\nWhat pharmacological treatment could also be considered in the first instance?",
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