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"explanation": "As the patient lacks capacity, decisions should be made in their best interests, involving the MDT and next of kin. It is important to remember that fluids and artifical nutrition are medical treatments and should be prescribed only when clinically indicated and when they are likely to help. Nausea and loss of appetite are common symptoms in the last days of life, which may warrant symptomatic management.",
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"name": "Discuss in the MDT as to whether fluids and nasogastric tube insertion are in her best interests",
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"explanation": "If the lack of eating is due to a possible swallowing difficulty, this will undoubtedly be useful, but there is no suggestion of that at present.",
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"explanation": "This is inappropriate. A more detailed discussion needs to be had to ascertain if these interventions are likely to be helpful and in the patient's best interests, as well as what the goals of treatment are.",
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"label": "c",
"name": "Advise IV fluids and NG tube will not be helpful at this stage",
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"explanation": "This may be helpful but it does not address the daughter's concerns about artificial nutrition and hydration.",
"id": "10017249",
"label": "d",
"name": "Encourage oral food and water",
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"votes": 80
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"explanation": "At this stage, we do not have enough information as to whether these treatments are indicated or were previously by the patient, see above answer for MDT discussion for further information.",
"id": "10017247",
"label": "b",
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"explanation": "# Summary\n\n\nWHO Performance status classification categorises patients into different groups dependent on their physical fitness, measured by their ability to perform activities of daily living. It is used to assess their suitability for chemotherapy, and has some prognostic significance. \n\n\nChemotherapy as a treatment is not without its side effects, which can limit quality of life and have negative impacts on other comorbidities. Treatment decisions involve a risk-benefit analysis, and as such a patients' performance status has a significant bearing on what treatment options are most appropriate.\n\n\n# Classification\n\n\nThe WHO performance status classification categorises patients as:\n\n\n- 0: able to carry out all normal activity without restriction\n- 1: restricted in strenuous activity but ambulatory and able to carry out light work\n- 2: ambulatory and capable of all self-care but unable to carry out any work activities; up and about more than 50% of waking hours\n- 3: symptomatic and in a chair or in bed for greater than 50% of the day but not bedridden\n- 4: completely disabled; cannot carry out any self-care; totally confined to bed or chair.\n\n\n# References\n\n[NICE Appendix C: WHO performance status classification](https://www.nice.org.uk/guidance/ta121/chapter/appendix-c-who-performance-status-classification#:~:text=The%20WHO%20performance%20status%20classification,to%20carry%20out%20light%20work)\n\n[JAMA Oncology: Performance status in patients with cancer](https://jamanetwork.com/journals/jamaoncology/fullarticle/2432463)",
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"question": "An 88 year old woman has stage 4 breast cancer with metastases in the brain, liver and lungs. It is felt she may be nearing the end of her life, and is currently bedbound with a WHO performance status of 4. She is unable to demonstrate capacity to make treatment decisions. Her daughter requests her mother is given intravenous fluids and is NG tube fed as she has not been eating and drinking for the last few days. There is no formal lasting power of attorney in place.\n\nWhat is the most appropriate course of action?",
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"explanation": "This may well be done, however, initiating a benzodiazepine should be done in the first instance by the medical team.",
"id": "10017254",
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"name": "Refer to liasion psychiatry team",
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"explanation": "This is correct. This is a case of alcohol withdrawal and delirium tremens with common symptoms including formication (feeling like insects are crawling on your skin), visual hallucinations (possibly of the insects), diaphoresis, confusion and a coarse tremor.",
"id": "10017251",
"label": "a",
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"explanation": "Lithium toxicity may well cause a similar coarse tremor, confusion and diaphoresis however is unlikely to cause visual hallucinations and formication. In any case, lithium levels would be required before stopping or withholding lithium.",
"id": "10017252",
"label": "b",
"name": "Discontinue lithium",
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"votes": 459
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"explanation": "This has no role in the acute treatment of alcohol withdrawal and delirium tremens which typically includes benzodiazepines and B vitamins in the first instance. Disulfiram may help with a later stage to quit drinking due to its role in aversion therapy.",
"id": "10017255",
"label": "e",
"name": "Initiate disulfiram",
"picture": null,
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"explanation": "Lithium toxicity may well cause a similar coarse tremor, confusion and diaphoresis however is unlikely to cause visual hallucinations and formication. In any case, lithium levels would be required before stopping or withholding lithium. Haemodialysis may used to treat severe cases of lithium toxicity.",
"id": "10017253",
"label": "c",
"name": "Initiate haemodialysis",
"picture": null,
"votes": 270
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"comment": "can this also be lithium toxicity?",
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"explanation": "# Summary\n\nHarmful alcohol consumption is very common in the UK, and prolonged periods of alcohol excess can lead to dependence. An important complication of alcohol dependence is acute withdrawal, when patients abruptly stop drinking or significantly reduce their alcohol consumption. Key signs and symptoms of withdrawal include agitation, tremor, nausea and vomiting, sweating and hallucinations. Seizures can occur, usually 24-48 hours after stopping drinking. Delirium tremens describes severe alcohol withdrawal characterised by delirium, haemodynamic instability and autonomic instability. Management strategies involve monitoring for symptoms of alcohol withdrawal using the CIWA scoring tool, giving a reducing course of benzodiazepines (usually chlordiazepoxide) and giving Pabrinex to prevent Wernicke-Korsakoff syndrome.\n \n\n# Definition\n \nAlcohol withdrawal is a syndrome that occurs when a patient who is alcohol dependent suddenly stops or drastically reduces their alcohol consumption. There are several stages of alcohol withdrawal that occur over the days following stopping drinking, and severity of withdrawal symptoms ranges from mild symptoms of tremor and insomnia to life-threatening manifestations such as delirium tremens or withdrawal seizures. \n \n# Epidemiology\n \n- Alcohol misuse is very common in the UK, with an estimated 24% of adults drinking in a harmful or hazardous way.\n- Around 600,000 adults in England are thought to be dependent on alcohol and so at risk of alcohol withdrawal.\n- Only 18% of these people with alcohol dependence are receiving treatment.\n- In England, there are approximately 1 million alcohol related hospital admissions per year (although alcohol withdrawal represents only a proportion of these)\n\n# Aetiology\n \nChronic alcohol excess causes tolerance to its effects, with reduced GABA and increased glutamate activity in the brain. The patient then relies on alcohol to balance this, and so when they stop drinking the imbalance manifests leading to excess glutamate and over-stimulation of the central nervous system. \n\nPatients often develop alcohol withdrawal after hospital admission as they are unable to maintain their normal intake whilst an inpatient.\n\nOther cases may occur when a patient decides to go \"cold turkey\" and stop drinking - patients should be advised to seek help to cut down on their alcohol intake safely.\n\n# Signs and Symptoms\n \nFrom 6 to 12 hours after the last drink, mild withdrawal symptoms may occur:\n\n- Insomnia\n- Tremors\n- Anxiety\n- Agitation\n- Nausea and vomiting\n- Sweating\n- Palpitations\n\nAt 12-24 hours, alcohol hallucinosis may begin:\n\n- Visual hallucinations\n- Auditory hallucinations\n- Tactile disturbances e.g. sensations of crawling bugs on the skin\n\nAlcohol withdrawal seizures are most likely to occur at 24-48 hours - these are usually generalised and tonic-clonic in nature.\n\nAt 48-72 hours, delirium tremens may occur:\n \n- Delirium and agitation\n- Hallucinations and delusions\n- Tachycardia\n- Hypertension\n- Hyperthermia\n- Diaphoresis\n- Coarse tremor\n \n# Differential Diagnosis\n\n- **Benzodiazepine withdrawal**: shares symptoms of insomnia, anxiety, tremor, sweating and nausea, and can also cause seizures; may coexist with alcohol withdrawal and is managed similarly with tapering doses of benzodiazepines. \n- **Sepsis**: can cause delirium and agitation, tachycardia and diaphoresis; hypotension is more common than the hypertension seen in severe alcohol withdrawal and patients may have focal signs of infection.\n- **Hepatic encephalopathy**: may occur in patients with decompensated cirrhosis secondary to alcohol, and has similar symptoms of tremor and confusion; ammonia will be elevated and there is often a background of chronic liver disease.\n- **Psychosis**: e.g. secondary to schizophrenia may cause similar symptoms of hallucinations, delusions and agitation.\n- **Hypoglycaemia**: causes similar symptoms of anxiety, agitation, tremor and diaphoresis; increased risk in patients who drink alcohol.\n\n# Investigations\n \n**Bedside tests:**\n\n- **ECG** - arrhythmias and other abnormalities (e.g. QT prolongation) may be seen in severe alcohol withdrawal\n- **Capillary blood glucose** for hypoglycaemia \n\n**Blood tests:**\n\n- **FBC** and **CRP** for inflammatory markers\n- **LFTs** for alcoholic liver disease\n- **U&Es** for baseline renal function and electrolytes\n- **Bone profile** and **magnesium** to monitor electrolytes for refeeding syndrome\n- **Blood cultures** if there are signs of infection\n\n**Imaging:**\n\n- **Chest X-ray** if there are signs of aspiration, especially if the patient has had a seizure or has a low GCS\n- **CT head** if evidence of head injury or ongoing seizures\n\n# Management\n \n- Patients presenting with or at risk of seizures or delirium tremens, or those who are vulnerable, frail or with significant comorbidities should be admitted for medical treatment of alcohol withdrawal\n- This involves use of the CIWA (Clinical Institute Withdrawal Assessment of Alcohol) scoring system, which is a standardised way of assessing severity of alcohol withdrawal symptoms in the following domains:\n - Nausea and vomiting\n - Tremor\n - Sweating\n - Anxiety\n - Agitation\n - Tactile disturbances\n - Auditory disturbances\n - Visual disturbances\n - Headache\n - Orientation\n- Each domain is scored from 0-7 other than orientation which is 0-4\n- A total score of 0-9 represents mild or no withdrawal, 10-19 is moderate withdrawal and > 20 is severe withdrawal\n- Higher scores warrant more frequent monitoring of symptoms\n- The CIWA score is used to guide prescription of benzodiazepines, which may be given PRN to manage withdrawal symptoms or regularly in a fixed-dose reducing regime over several days (plus PRNs when required)\n- Chlordiazepoxide is the first line benzodiazepine used, with oxazepam or lorazepam (shorter-acting benzodiazepines) being used for patients with liver disease\n- Alcohol withdrawal seizures should be treated with short acting benzodiazepines (e.g. IV lorazepam) in the first instance\n- Delirium tremens is also treated with oral lorazepam, with parenteral lorazepam or haloperidol being second line options\n- Pabrinex (1 pair of ampoules once daily) should be given to prevent Wernicke's encephalopathy - if there are signs or symptoms such as ataxia or nystagmus, give treatment dose (two pairs of ampoules TDS)\n- Monitor bloods for refeeding syndrome in malnourished patients\n- Ensure patients are followed up on discharge and referred to community support services\n\n# NICE Guidelines\n\n[NICE - Alcohol-use disorders: diagnosis and management of physical complications](https://www.nice.org.uk/guidance/cg100/)\n \n[NICE CKS - Alcohol Withdrawal](https://cks.nice.org.uk/topics/alcohol-problem-drinking/management/alcohol-misuse/)\n \n# References\n\n[BNF - Alcohol Dependence](https://bnf.nice.org.uk/treatment-summaries/alcohol-dependence/) \n\n[RCEM Learning - Acute Alcohol Withdrawal](https://www.rcemlearning.co.uk/reference/acute-alcohol-withdrawal/)\n\n[Patient UK - Acute alcohol withdrawal and delirium tremens](https://patient.info/doctor/acute-alcohol-withdrawal-and-delirium-tremens)",
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"question": "A 58 year old man is brought to A&E by police under section 136. They report he was screaming in the library about seeing and feeling insects crawling all over his skin. His past psychiatric history includes bipolar disorder and alcohol dependence. On inspection, he appears sweaty and confused and a coarse tremor is noted.\n\nWhich of the following is the most appropriate treatment?",
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"explanation": "This is the correct answer. It is important to counsel patients on the sexual side effects as they can negatively impact quality of life and persist, even after stopping them.",
"id": "10017256",
"label": "a",
"name": "SSRIs may cause sexual dysfunction",
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"explanation": "The recommendation is they should not be stopped until 6 months after symptomatic relief.",
"id": "10017259",
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"name": "SSRIs may be discontinued 3 months following symptomatic relief",
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"explanation": "This is incorrect. Sudden withdrawal can cause SSRI discontinuation syndrome which is characterised by flu like symptoms, insomnia, nausea, dizziness and sensory disturbances.",
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"name": "SSRIs may be stopped immediately with little side effects",
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"explanation": "SSRIs typically start working within 4-6 weeks of initiation. If no improvement in symptoms has been noted by then, switching to an alternative agent may be considered.",
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"explanation": "In young adults (often local guidelines may quote under 30 years of age), SSRIs may cause an initial increase in suicidal ideation within the first 2 weeks and there is, therefore, a recommendation to inform patients about this and review them at 1 week point following initiation.",
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"comment": "I think I disliked just cause I had an SSRI before and dont wanna feel insecure ",
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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 26 year old man comes to the GP with low mood, fatigue, anhedonia, as well as feelings of worthlessness and guilt. You decide to start him on a selectrive serotonin reuptake inhibitor.\n\nWhich of the following should you advise him?",
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"explanation": "This is typically used in the treatment of normal pressure hydrocephalus.",
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"explanation": "Decompressive craniectomy is where a bone flap is permanently removed from the skull and is used to treat traumatic brain injuries, chiari malformationss, stroke and other conditions causing a raised ICP. This may become required in the future if cerebral oedema develops, however it is not currently the most appropriate management.",
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"explanation": "This is correct. The history and imaging suggests a case of subarachnoid haemmorhage. The immediate priority is to treat vasospasm using nimodipine and optimise blood pressure control (140-160mmHg) to prevent rebleeding.",
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"explanation": "Craniotomy is where a bone flap is temporarily removed from the skull and replaced. It is useful in the treatment of space occupying lesions, blood clots, traumatic brain injury (TBI), and can also facilitate implantation of deep brain stimulators for Parkinson's disease.",
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"explanation": "This is typically used in the treatment of subdural and extradural haematomas, to reduce pressure on the brain.",
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"comment": "This is the final question i will ever see (hopefully) on this platform. My medical finals are on Monday. I hope that other people see this comment and realise that although the road is long, the journey is beautiful. I ponder if the greatest achievement of my life isn't making it through these last 6 years, but realising that the greatest achievement is those we meet along the way. Go well into the night future people who read this. Know that the road you walk was made by the people before you. Go out and do well unto the world. Namastè",
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"comment": "lies i saw you on quesmed yesterday ",
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"explanation": "## Summary\n\nSubarachnoid Haemorrhage (SAH) is a **surgical emergency** that involves bleeding into the subarachnoid space, often due to a ruptured aneurysm. It typically presents with a **sudden, severe \"thunderclap\" headache** that reaches maximum intensity within 5 minutes and is sometimes described as feeling like \"being hit on the back of the head,\" often with occipital localization. Other symptoms include reduced consciousness, seizures, and localizing neurological signs such as abducens nerve palsy. The initial diagnostic strategy includes a CT head scan followed by a lumbar puncture if indicated. Management includes medical, radiological, and surgical interventions, with **nimodipine** given to prevent vasospasm and **endovascular coiling** as the preferred treatment. SAH carries a significant mortality risk, but prognosis improves with early intervention.\n\n## Definition\n\nA Subarachnoid Haemorrhage (SAH) occurs when blood accumulates in the subarachnoid space, typically due to the rupture of an aneurysm or trauma.\n\n## Epidemiology\n\n- Incidence: SAH occurs in approximately 6-9 per 100,000 people annually. \n- Prevalence: The majority of non-traumatic SAH cases (~80%) are caused by **berry aneurysms**, most commonly on the **posterior communicating artery**.\n\n## Aetiology\n\nSAH can be classified as **traumatic** or **non-traumatic**.\n\n- **Non-traumatic SAH**: \n - The most common cause is a **ruptured berry aneurysm**. \n - Other causes include:\n \t\t- Arteriovenous malformations (AVMs)\n \t\t- Arterial dissection\n \t\t- Cerebral amyloid angiopathy.\n - Risk factors include **hypertension (HTN)**, **smoking**, **excessive alcohol consumption**, and **adult polycystic kidney disease (ADPCKD)**, with the latter being a risk factor due to the formation of berry aneurysms.\n\n- **Traumatic SAH**: \n - Typically caused by head injuries, where blood leaks into the subarachnoid space following trauma.\n\n## Signs and Symptoms\n\n- **Thunderclap headache**: A sudden, severe headache that reaches maximum intensity in less than 5 minutes.\n\t- Often described as \"being hit on the back of the head,\" commonly with **occipital headache** localization.\n- **Seizures**\n- **Reduced consciousness** or **loss of consciousness**.\n- **Meningism**: Neck stiffness and photophobia.\n- Neurological signs: Falsely localizing signs such as **abducens nerve palsy**, due to increased intracranial pressure affecting the longest cranial nerve.\n- Vomiting\n- Signs of raised intracranial pressure\n\n## Investigations\n\n- **CT head**: The first-line investigation, especially within the first 6 hours of symptom onset, is highly sensitive in detecting SAH. \n- **Lumbar puncture**: Used to assess for xanthochromia, a yellow discoloration in the cerebrospinal fluid indicating the breakdown of red blood cells.\n\t- Recent NICE guidelines state that if the **CT head is done within 6 hours** of headache onset and shows no SAH, alternative diagnoses should be considered. \n\t- If a CT Head is performed more than 6 hours after symptom onset and the result is negative, then a lumbar puncture can be considered at least **12 hours** after symptom onset\n- **CT angiography**: To detect any aneurysms or vascular malformations if SAH is confirmed or suspected.\n\n[lightgallery]\n[lightgallery1]\n\n## Management\n\nManagement can be medical, radiological, or surgical:\n\n- **Medical**: \n - **Nimodipine** is used to prevent delayed cerebral ischemia caused by vasospasm, which can occur after SAH.\n - Blood pressure management: Hypertension is not aggressively treated unless necessary to reduce the risk of rebleeding.\n\n- **Radiological/Surgical**: \n - **Endovascular coiling** is often preferred over surgical clipping due to better outcomes, but the choice depends on the aneurysm's location and characteristics. \n - **Clipping** may still be performed, particularly for aneurysms that are unsuitable for coiling.\n\n## Prognosis\n\n- Mortality is around **50%** overall, though many of these deaths occur before patients reach the hospital.\n- Among patients with a **Glasgow Coma Scale (GCS)** score of >14 on admission, the survival rate is greater than 90%, with low morbidity.\n\n\n## References\n\n[NICE Guidance](https://www.nice.org.uk/guidance/ng228)",
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"question": "A 65 year old man is brought to the emergency department by ambulance following reports of a severe headache and subsequent loss of consiousness. His GCS is 7. He is intubated and admitted to the ICU.\n\nA CT head shows\n\n[lightgallery]\n\nWhat is the most appropriate next step in the management of this patient?",
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"explanation": "The patient’s presentation suggests a case of drug-induced lupus. Common causes of drug induced lupus include isoniazid (used for TB), procainamide, hydralazine, minocycline and phenytoin.",
"id": "10017266",
"label": "a",
"name": "Active pulmonary tuberculosis",
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"explanation": "Trigeminal neuralgia is typically treated with carbamazapine, which can rarely cause drug-induced lupus but not as commonly as isoniazid.",
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"label": "c",
"name": "Trigeminal neuralgia",
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"explanation": "The anti-histone antibodies and joint pain point towards drug-induced lupus.",
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"label": "e",
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"explanation": "The anti-histone antibodies and joint pain are suggestive of drug-induced lupus.",
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"explanation": "Atrial fibrillation can be treated in a variety of ways, none of which are likely to cause drug-induced lupus.",
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"comment": "good question, shame I shat the bed on it ",
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"comment": "Gutted not to take all 3 points on this one",
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"explanation": "# Summary\n\nSystemic lupus erythematosus (SLE) is a multi-system autoimmune disease that may cause a wide variety of symptoms and affect major organs. It is more common in women and people of Afro-Caribbean heritage. Common signs and symptoms include rashes, hair loss, mouth ulcers, arthralgia and fatigue. Renal, cardiac and central nervous system involvement is common. Initial investigations include urinalysis, full blood count and auto-antibodies (e.g. anti-nuclear, anti-DNA and anti-Smith antibodies). First-line medical management is commonly with hydroxychloroquine, which may be escalated to immunosuppressants such as prednisolone, methotrexate, or biologic agents (e.g. rituximab). Patients should be regularly monitored to assess disease activity and organ involvement, as well as side effects of treatment and comorbidities.\n\n# Definition\n\nSystemic lupus erythematosus (SLE) is a complex autoimmune disease that may affect a wide variety of organs. The clinical course is commonly a relapsing-remitting one, with intermittent flares of disease activity.\n\n# Epidemiology\n\n- Prevalence in the UK is approximately 1 in 1000\n- SLE is nine times more common in women than men\n- It is most common in people of Afro-Caribbean and South Asian descent\n- Mean age at diagnosis is 49 years\n\n# Aetiology\n\n- The pathogenesis of SLE is complex, involving multiple autoantibodies leading to immune complex formation and deposition\n- There is a genetic contribution with many genetic risk factors identified \n- Proposed environmental risk factors include:\n- Smoking\n- Ultraviolet light\n- Silica exposure\n- Epstein-Barr virus\n- Flares of SLE may be triggered by:\n- Oestrogen exposure (e.g. pregnancy, the combined oral contraceptive pill)\n- Infections\n- Emotional stress\n- Physical stress e.g. surgery, injury\n- Excessive ultraviolet light exposure\n\n# Classification\n\nThe 2019 EULAR/ACR classification is used for diagnosis - patients need to have positive antinuclear antibodies (ANA) and score 10 or more with at least one clinical criterion:\n\n\n| **Clinical Domain** | **Criteria** | **Points** |\n|-------------------------|---------------------------------------------------|---------- | \n| Constitutional | Fever > 38 degrees | 2 |\n| Haematologic | Leukopenia | 3 |\n| | Thrombocytopenia | 4 |\n| | Autoimmune haemolysis | 4 |\n| Neuropsychiatric | Delirium | 2 |\n| | Psychosis | 3 |\n| | Seizure (generalised or focal) | 5 |\n| Mucocutaneous | Non-scarring alopecia | 2 |\n| | Oral ulcers | 2 |\n| | Subacute cutaneous or discoid lupus | 4 |\n| | Acute cutaneous lupus | 6 |\n| Serosal | Pleural or pericardial effusion | 5 |\n| | Acute pericarditis | 6 |\n| Musculoskeletal | Joint involvement (at least 2) | 6 |\n| Renal | Proteinuria > 0.5 g/24 hours | 4 |\n| | Class II or V lupus nephritis on biopsy | 8 |\n| | Class III or IV lupus nephritis on biopsy | 10 |\n| **Immunological Domain**| | |\n| Antiphospholipid antibodies | Anti-cardiolipin, _2 glycoprotein I, or lupus anticoagulant | 2 |\n| Complement proteins | Low C3 *or* low C4 | 3 |\n| | Low C3 *and* low C4 | 4 |\n| SLE-specific antibodies | Anti-dsDNA or anti_Smith | 6 |\n\n\n# Signs and Symptoms\n\n## Systemic manifestations\n\n- Fevers\n- Fatigue\n- Weight loss\n- Myalgia\n- Malaise\n\n## Dermatological manifestations\n\n[lightgallery] [lightgallery1] \n\n- 80% of patients have skin involvement\n- Photosensitivity is common\n- The classic malar rash appears as butterfly-shaped erythema across the cheeks, sparing the naso-labial folds\n- A discoid rash consists of indurated hyperpigmented plaques in sun-exposed areas, that may occur without systemic features\n- Livedo reticularis\n- A variety of other rashes may occur e.g. maculopapular, bullous, annular, urticarial or hypertrophic rashes\n- Nonscarring diffuse alopecia\n- Raynaud's phenomenon\n- Cutaneous vasculitis may manifest as splinter haemorrhages and/or purpura\n\n## Musculoskeletal manifestations\n\n- Generalised arthralgia, often with early morning stiffness, is common\n- A non-erosive symmetrical polyarthritis often affects the knees, wrists, shoulders and hands\n- A minority of patients develop a non-erosive arthropathy (**Jaccoud's arthropathy**) that may mimic rheumatoid arthritis deformities\n- Complications of chronic steroid treatment may be seen, including osteonecrosis, insufficiency fractures and tendinopathies\n\n## Renal manifestations\n\n- The majority of patients develop renal disease, with approximately 4% progressing to end-stage renal disease\n- Lupus nephritis varies in severity and may be asymptomatic, or present with nephritic or nephrotic syndrome\n- Presenting features include hypertension, frothy urine and peripheral oedema\n- Renal involvement is classified based on histology as below:\n\n| Class | Classification | Description |\n|-----------|-----------------------------------|-----------------------------------------------------------------------------------------------|\n| I | Minimal Mesangial Glomerulonephritis | Normal appearance under light microscopy; mesangial deposits on electron microscopy or immunofluorescence|\n| II | Mesangial Proliferative Lupus Nephritis | Mesangial hypercellularity and immune deposits on light microscopy |\n| III | Focal Lupus Nephritis | Involvement of less than 50% of glomeruli with thickened capillary loops and subendothelial immune complexes |\n| IV | Diffuse Lupus Nephritis | Involvement of more than 50% of glomeruli, rapidly progressive glomerulonephritis may be present |\n| V | Membranous Nephritis | Diffuse basement membrane thickening with proteinuria; nephrotic syndrome may develop |\n| VI | Advanced Sclerosing Lupus Nephritis | > 90% of glomeruli are sclerotic; usually progresses to end-stage renal disease |\n\n\n## Cardiovascular manifestations\n\n- Pericarditis is the most common cardiac feature of SLE, presenting with chest pain, dyspnoea, tachycardia and a pericardial rub may be heard on auscultation\n- Pericardial effusions are also common although the risk of tamponade is low\n- Myocarditis is rare and may present with arrhythmias and heart failure\n- Libman-Sacks endocarditis refers to the formation of non-infective vegetations that usually form on the mitral and aortic valves\n- There is a significantly increased risk of adverse cardiovascular events such as myocardial infarction \n\n## Respiratory manifestations\n\n- Pleurisy is very common (where there is inflammation of the pleura, typically presenting with sharp chest pain exacerbated by vigorous inhalation or expiration)\n- Pleural effusion\n- Patients with antiphospholipid antibodies are at increased risk of pulmonary emboli\n- Rarer pulmonary manifestations include:\n- Acute lupus pneumonitis\n- Pulmonary hypertension\n- Chronic interstitial pneumonitis\n- Obliterative bronchiolitis\n- Pulmonary vasculitis\n- Alveolar haemorrhage\n- Patients on immunosuppressive treatments are at increased risk of opportunistic infections\n\n## Neurological manifestations\n\n- Up to 80% of patients develop neuropsychiatric involvement \n- Seizures are the most common features (either generalised or local)\n- There is a significantly increased risk of stroke, which is contributed to by:\n- Antiphospholipid syndrome\n- Hypertension\n- Accelerated atherosclerosis\n- Embolisms from Libman-Sacks endocarditis\n- Thrombocytopaenia\n- Cerebral vasculitis\n- Psychosis \n- Delirium\n- Cognitive impairment (although usually not severe enough to result in dementia)\n- Increased rates of depression and anxiety\n- Headaches\n- Peripheral neuropathy (most commonly a sensorimotor polyneuropathy)\n\n## Haematological manifestations\n\n- Anaemia may occur due to chronic disease, medications or haemolysis\n- Leukopaenia and thrombocytopaenia are also common \n- Reactive lymphadenopathy and splenomegaly may be present, particularly in active disease\n- Antiphospholipid syndrome occurs in around 20% of patients (although higher numbers have antibodies without complications)\n\n## Gastrointestinal (GI) manifestations\n\n- Mouth ulcers are common and may be painful\n- A protein-losing enteropathy may be seen\n- Ascites may occur secondary to peritonitis or hypoalbuminaemia due to enteropathy or nephrotic syndrome\n- Pancreatitis\n- Splenic infarction\n- Hypoadrenalism\n- Hepatomegaly, hepatitis or cirrhosis may be seen\n- Vasculitis affecting the GI tract may cause colitis, mucosal ulceration, mesenteric ischaemia or oesophageal dysmotility\n- Antiphospholipid syndrome may cause Budd-Chiari syndrome or thrombosis of intestinal vessels\n\n# Differential Diagnosis\n\n- **Drug-induced lupus** presents similarly to SLE, commonly with systemic upset, a non-erosive arthritis and serositis\n- It occurs due to chronic use of triggering medications\n- These include procainamide, hydralazine, isoniazid, quinidine and methyldopa\n- Symptoms improve after withdrawal of the causative drug\n- Rashes, renal disease and neurological involvement are rare\n- Anti-histone antibodies are positive but anti-dsDNA and anti-Sm are negative\n- **Subacute cutaneous lupus** may be associated with SLE but is often seen in isolation or in association with other diseases such as Sjogren's syndrome or rheumatoid arthritis\n- Patients present with a widespread non-scarring papulosquamous rash\n- There are annular plaques which coalesce\n- It is photosensitive and typically affects the neck, upper trunk and arms\n- There may be associated features of alopecia, livedo reticularis and mouth ulcers\n- It may also be drug induced (e.g. due to thiazides, terbinafine or calcium channel blockers)\n- Patients are often anti-Ro positive\n- **Discoid lupus** also only affects the skin and is the commonest form of cutaneous lupus\n- Patients develop scaly plaques on the face and scalp which may become generalised in a minority of cases\n- It may be asymptomatic or itchy/sore\n- Atrophic scarring of the skin and scarring alopecia is common\n- ANA is usually negative unlike in SLE\n- **Rheumatoid arthritis** may present with similar features of systemic symptoms, cardiac and pulmonary involvement\n- However the polyarthritis seen in rheumatoid arthritis is typically erosive and deforming\n- Mouth ulcers, rashes and alopecia are suggestive of SLE\n- **Sarcoidosis** also shares systemic features such as fevers, weight loss and fatigue\n- Rashes include erythema nodosum and lupus pernio (red/purple plaques and nodules on the face)\n- Neurological, pulmonary, cardiac and GI involvement is also seen\n- **Rosacea** may mimic the classic malar rash of SLE and is also photosensitive\n- However pustules are common which are not seen in SLE\n- Systemic involvement is not seen\n\n# Investigations\n\n**Bedside tests:**\n\n- **Blood pressure** to monitor for hypertension \n- **Urine dip** for proteinuria or haematuria\n- **Urinary protein:creatinine ratio** may be useful to quantify proteinuria\n- **Urine microscopy** looking for casts\n- **ECG** in suspected cardiac involvement\n\n**Blood tests:**\n\n- **Full blood count** looking for anaemia, leukopenia and thrombocytopaenia\n- **U&Es** to screen for renal impairment due to lupus nephritis\n- **Liver function tests** are usually normal; hypoalbuminaemia may be seen due to GI or renal involvement\n- **ESR** is usually high; **CRP** may be normal or mildly raised\n- **Clotting screen** may show paradoxical prolongation of the APTT if there are anti-phospholipid antibodies present\n- **Complement** (**C3** and **C4**) may be low in active disease\n- **Antinuclear antibody (ANA)** is almost always positive \n- Results may be given as a titre (i.e.how much serum can be diluted and still test positive)\n- A titre of 1:160 or higher is considered positive\n- The pattern of staining may also be described - classically this is **speckled** in SLE\n- **Anti-double stranded DNA (anti-dsDNA) antibodies** are highly specific for SLE\n- T hey correlate with disease activity, especially lupus nephritis\n- **Anti-Smith (anti-Sm) antibodies** are found in fewer patients but are also highly specific\n- **Antiphospholipid antibodies** should be tested for in all patients\n- **Anti-histone antibodies** are found in both SLE and drug-induced lupus and so should be sent in patients on causative medications\n- **Anti-Ro** and **anti-La antibodies** are not specific to SLE but may be positive\n- They are associated with neonatal lupus syndrome in babies born to mothers with these antibodies\n- **Anti-RNP antibodies** may be positive in SLE but are non-specific; if found alone positivity suggests mixed connective tissue disease\n- **Creatine kinase** to screen for associated myositis\n- **Vitamin D** as patients avoiding sun exposure are at increased risk of deficiency\n- **Thyroid function** as thyroid disease often coexists with SLE and symptoms may overlap (e.g. fatigue)\n- **Immunoglobulins** prior to starting immunosuppressive medications that may lead to immunoglobulin deficiency \n- **Direct Coombs' test** to screen for autoimmune haemolytic anaemia\n\n**Imaging:**\n\n- **Chest X-ray** in all patients as a baseline and to screen for pulmonary involvement\n- **CT chest** may be required for more detailed assessment of lung involvement; **CT pulmonary angiography** is required in suspected pulmonary embolism\n- **Ultrasound of the kidney, ureters and bladder (KUB)** to exclude other causes of renal impairment e.g. obstruction\n- **X-rays of affected joints** looking for arthritis and fractures \n- Joint space narrowing is uncommon\n- Soft tissue swelling and periarticular osteoporosis may be seen\n- **Ultrasound of affected joints** may show signs of inflammation e.g. tenosynovitis\n- **CT** or (preferably) **MRI** brain if cerebral lupus is suspected\n- **Echocardiogram** may show pericarditis, heart failure, pericardial effusion or pulmonary hypertension\n\n**Special tests:**\n\n- **Renal biopsy** is the key diagnostic test for lupus nephritis and is important for classification\n- **Skin biopsy** may be useful for the diagnosis of dermatological manifestations\n- **Pulmonary function tests** if there \n- **Pleural tap** if there is an effusion present - the majority of cases are exudative\n- **Neurophysiology testing** in suspected peripheral neuropathy\n\n# Management\n\n**Conservative management:**\n\n- Patients with suspected SLE should all be referred to specialist services for confirmation of the diagnosis and ongoing management\n- All patients require regular follow up\n- 1-3 monthly follow up is appropriate for patients with active disease\n- Stable patients can be followed up every 6-12 months\n- Patient counselling and education, with signposting to resources and support\n- Advise on sun protection e.g. using sunscreen, limiting exposure and covering skin\n- Avoid triggers such as oestrogen-containing contraceptives\n- Optimise cardiovascular health with regular exercise, smoking cessation and a balanced diet\n- Ensure patients are up to date with vaccinations\n\n**Medical management:**\n\n- All patients should be treated with hydroxychloroquine\n- Steroids are also commonly used e.g. oral prednisolone; high-dose IV methylprednisolone is often required for acute severe disease (e.g. renal or neuropsychiatric lupus)\n- Use of steroid-sparing agents is very important to minimise the long-term effects of prolonged steroid use - options include methotrexate and azathioprine\n- Patients with severe or refractory disease may be considered for biologic agents such as belimumab or rituximab\n- Topical agents may be used in addition to systemic treatment for skin disease e.g. topical glucocorticoids or calcineurin inhibitors\n- Mycophenolate mofetil (MMF) and cyclophosphamide are commonly used for lupus nephritis, with most patients continuing on either MMF or azathioprine\n- If anti-phospholipid syndrome is present, this may require additional management (see separate chapter)\n- Cardiovascular risk factors such as hypertension and hyperlipidaemia may require medical treatment\n- Vitamin D supplementation may be required as well as bone protection in patients on long-term steroids\n\n# Complications\n\n- **Medication side effects** are common\n- Retinal toxicity is the main issue with hydroxychloroquine and all patients should undergo regular eye screening\n- Patients on immunosuppressive treatments are at increased risk of opportunistic infections\n- Reactivation of latent infections (e.g. tuberculosis, hepatitis) is also a risk and so these should be screened for prior to initiating treatment\n- Other DMARDs (e.g. methotrexate) have their own extensive side effect profiles\n- **End-stage renal failure** develops in approximately 20% of patients with lupus nephritis\n- This may require renal replacement therapy either with dialysis or transplant\n- **Accelerated atherosclerosis** leads to an increased risk of myocardial infarction, ischaemic stroke and peripheral vascular disease\n- **Overlap syndromes** may develop in patients with SLE (where the criteria for multiple rheumatological diseases are met), for example\n- Sjogren's syndrome\n- Antiphospholipid syndrome\n- Mixed connective tissue disease\n- **Neonatal lupus** is a complication that arises in babies born to mothers with anti-Ro and/or anti-La antibodies\n- These antibodies cross the placenta and cause a transient autoimmune syndrome \n- Manifestations include a red rash on the scalp and around the eyes, complete heart block, deranged liver function and cytopaenias\n- **Other pregnancy complications** include recurrent miscarriage, pre-eclampsia, intrauterine growth restriction and preterm delivery\n\n# Prognosis\n\n- Patients with SLE have a 2.6x increased mortality compared to the general population \n- Although death from active lupus is rare in the UK, life expectancy is shortened to an average of 54 years\n- A third of patients develop lupus nephritis and this is associated with a poorer prognosis, with a mean age of death of 40 years\n- Other poor prognostic factors include:\n- Black ethnicity\n- Male sex\n- Antiphospholipid antibodies\n- Central nervous system involvement\n\n# References\n\n[Patient UK - systemic lupus erythematosus](https://patient.info/doctor/systemic-lupus-erythematosus-pro)\n\n[2019 EULAR/ACR Classification Criteria for Systemic Lupus Erythematosus](https://pmc.ncbi.nlm.nih.gov/articles/PMC6827566/)\n\n[EULAR recommendations for the management of systemic lupus erythematosus](https://ard.bmj.com/content/78/6/736)\n\n[Management of systemic lupus erythematosus: British Society for Rheumatology guideline scope](https://academic.oup.com/rheumap/article/7/3/rkad093/7458323)\n\n[Radiopaedia - systemic lupus erythematosus](https://radiopaedia.org/articles/systemic-lupus-erythematosus?lang=gb)\n\n[DermNet - Systemic Lupus Erythematosus](https://dermnetnz.org/topics/systemic-lupus-erythematosus)",
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"explanation": "This would be inappropriate as extensive investigation are unlikely to ultimately affect treatment decisions. NICE guidelines CG104 recommend not routinely investigating to find the primary cancer, which a PET scan may be used to do. The man's age and comorbidities mean he will likely not be a candidate for active treatment.",
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"explanation": "In patients with a likely malignancy of unknown primary, in whom extensive investigation is unlikely to ultimately affect treatment decisions, NICE guidelines CG104 recommend not routinely investigating to find the primary. The man's age and comorbidities mean he will likely not be a candidate for active treatment.",
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"explanation": "While prostate cancer is a likely diagnosis, Ffurther investigations to identify the primary cancer are unlikely to be helpful in this case. In patients with a likely malignancy of unknown primary, in whom extensive investigation is unlikely to ultimately affect treatment decisions, NICE guidelines CG104 recommend not routinely investigating to find the primary. The man's age and comorbidities mean he will likely not be a candidate for active treatment.",
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"label": "e",
"name": "Multiparametric MRI of the prostate",
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"explanation": "Bone scans are used to assess the spread of cancer to bones. In this case, the presence of a lytic lesion demonstrates that bony metastases are already present. Further scanning to locate other lesions is unlikely to be helpful, as this patient is unlikely to be a candidate for active treatment.",
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"__typename": "QuestionComment",
"comment": "bro what",
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"comment": "bro even if u do ct and find cancer somwhere what u gonna do with a guy with CKD stage 4, pulmonary fibrosis, Alzheimer’s disease, heart failure, macular degeneration and osteoporosis ",
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"comment": "personally, id talk to the MDT",
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"comment": "does the patient get no choice in this decision? would you not offer to find out how far along his cancer is?",
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"comment": "Not sure abt the pt.'s choice in this, but in regards to how far along his cancer is, it really wouldn't matter with the results you get; you're not gonna do anything regardless of the results. Low grade cancer? -> He's unfit for surgery (this guy's probably an ASA 3 or 4). High grade cancer? -> Probably inoperable anyway.\n\nHope this helps :)",
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"explanation": "# Summary\n\n\nWHO Performance status classification categorises patients into different groups dependent on their physical fitness, measured by their ability to perform activities of daily living. It is used to assess their suitability for chemotherapy, and has some prognostic significance. \n\n\nChemotherapy as a treatment is not without its side effects, which can limit quality of life and have negative impacts on other comorbidities. Treatment decisions involve a risk-benefit analysis, and as such a patients' performance status has a significant bearing on what treatment options are most appropriate.\n\n\n# Classification\n\n\nThe WHO performance status classification categorises patients as:\n\n\n- 0: able to carry out all normal activity without restriction\n- 1: restricted in strenuous activity but ambulatory and able to carry out light work\n- 2: ambulatory and capable of all self-care but unable to carry out any work activities; up and about more than 50% of waking hours\n- 3: symptomatic and in a chair or in bed for greater than 50% of the day but not bedridden\n- 4: completely disabled; cannot carry out any self-care; totally confined to bed or chair.\n\n\n# References\n\n[NICE Appendix C: WHO performance status classification](https://www.nice.org.uk/guidance/ta121/chapter/appendix-c-who-performance-status-classification#:~:text=The%20WHO%20performance%20status%20classification,to%20carry%20out%20light%20work)\n\n[JAMA Oncology: Performance status in patients with cancer](https://jamanetwork.com/journals/jamaoncology/fullarticle/2432463)",
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"explanation": "This advice is usually given to parents of children suffering febrile convulsions.",
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"name": "If the episodes last for more than 5 minutes, call an ambulance",
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"explanation": "The presentation is consistent with Tetralogy of Fallot, which causes periods of cyanosis and may cause syncope commonly presenting a few months after birth. This manoeuvre compresses the femoral arteries and increases peripheral vascular resistance, reducing the magnitude of the shunt.",
"id": "10017276",
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"name": "During the episode, pick the child up and bring his knees towards the chest",
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"explanation": "This advice is usually given to parents of children who suffer breath holding attacks or reflex anoxic seixures.",
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"__typename": "QuestionComment",
"comment": "Surely surgery? \n",
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"comment": "ah yes tell the parents to cut the heart open",
"createdAt": 1709408186,
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"comment": "I thought this was breath holding...",
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"comment": "same here. tetralogy of fallot did not pop into my brain once :') ",
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"comment": "I think breath holding spells tend to happen a bit later on in life, toddler age onwards esp when they are upset/cry ",
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"comment": "surely you lay the child on their back rather than pick them up?",
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"explanation": "# Summary\n \n\nTetralogy of Fallot is a cyanotic congenital heart defect characterised by a ventricular septal defect, overriding aorta, right ventricular outflow tract obstruction, and right ventricular hypertrophy. It typically presents antenatally or in infancy, with signs such as cyanosis and 'tet spells' (acute episodes of deepened cyanosis). Key investigations include echocardiography and cardiac catheterisation. Management is primarily surgical, involving the correction of the right ventricular outflow tract obstruction and closure of the ventricular septal defect.\n \n\n# Definition\n \n\nTetralogy of Fallot (ToF) is a rare, cyanotic congenital cardiac condition. It consists of four key anatomical abnormalities:\n \n\n - Ventricular septal defect (VSD)\n - Overriding aorta: An aorta that is positioned over the right and left ventricles due to the presence of the VSD\n - Right ventricular outflow tract obstruction (RVOTO): The primary **determinant of the severity of cyanosis**\n - Right ventricular hypertrophy\n \n\n# Epidemiology\n \n\nAlthough relatively rare, affecting 1 in 3,600 infants, Tetralogy of Fallot is one of the most common congenital heart diseases, accounting for approximately 10% of all cases. It affects males and females equally. It may also occur alongside other chromosomal abnormalities such as Down syndrome or DiGeorge syndrome.\n \n\n# Aetiology\n \n\nThe aetiology of the Tetralogy of Fallot remains largely unknown. However, genetic factors, maternal use of alcohol or drugs during pregnancy, diabetes mellitus, and maternal age over 40 years have been implicated. Individuals with congenital heart disease are at an increased risk of having children with congenital heart disease.\n \nIt is associated with many conditions:\n \n - 22Q11 microdeletion syndrome\n - Down's Syndrome\n - DiGeorge Syndrome\n - Foetal Alcohol Spectrum Disorder \n \n\n# Signs and Symptoms\n \nToF is commonly diagnosed due to:\n\n- Abnormal foetal ultrasound scans\n- Hypoxia at birth \n- Heart murmur on newborn exam \n\nThis means many are diagnosed without the classical symptoms of Tetralogy of Fallot which include: \n\n- Cyanosis, which may be mild or severe depending on the degree of right ventricular outflow tract obstruction\n- Detection of a heart murmur in the first few months of life\n- Acute episodes of deepened cyanosis, known as 'tet spells', where there is a reversal of the shunt across the VSD, leading to a right-to-left shunt and exacerbated cyanosis\n- Poor feeding and growth \n \n\n# Differential Diagnosis\n \n\nWhen presented with a cyanotic infant, differentials may include:\n \n\n - **Transposition of the Great Arteries**: Characterised by a loud, single second heart sound and absence of murmurs.\n - **Tricuspid Atresia**: Features include cyanosis and a systolic murmur due to the associated ventricular septal defect or pulmonary stenosis.\n - **Persistent Pulmonary Hypertension of the Newborn (PPHN)**: Symptoms are severe respiratory distress and cyanosis within *hours* of birth.\n \n\n# Investigations\n \nToF may be diagnosed prenatally using foetal ultrasound and echocardiography. \n\nKey investigations for suspected Tetralogy of Fallot are:\n\n- Oxygen saturation at birth \n- Echocardiography: The first-line investigation to confirm diagnosis and define anatomy\n- Chest x-ray: May reveal a \"boot-shaped\" heart \n\nFurther tests may include: \n\n- Hyper-oxygenation test: \n - The neonate is given 100% FiO2 and then PaO2 is checked after 10 minutes. An increase of >25 mmHg and to a level of >100 mmHg would indicate a pulmonary cause, rather than. a cardiac cause, where the oxygen levels would not substantially increase. \n- Cardiac catheterisation: May be required to delineate the coronary artery anatomy and assess the degree of pulmonary vascular disease\n \n\n# Management\n\nManagement depends on the severity of the cyanosis in addition to the severity of the defects. \n\nIn neonates with severe hypoxia:\n\n- Resuscitation following the neonatal resuscitation guideline should be followed. This would likely be supplemented by IV prostaglandin E1 to keep ductus arteriosus open. It can also be kept open through the insertion of a metal stent. \n- Some infants may need a synthetic shunt to be made connecting the aorta to the pulmonary artery. This is a temporary measure until full surgical correction can be achieved. \n- Definitive treatment is corrective surgery at age 3-6 months. This may include: \n - Correction of the right ventricular outflow tract obstruction with widening of the pulmonary valve \n - Closure of the ventricular septal defect using a patch \n - Surgical correction before 3 months is associated with increased post-operative complications and poorer outcomes. Repairing later than 12 months enables prolonged exposure to hypoxia and increased right ventricular hypertrophy, with an associated increased morbidity. \n\n \nIn neonates with minimal symptoms: \n\n- Advice for the management of hypercyanotic \"tet\" spells is given to parents.\n- Definitive management is surgical repair of VSD and correction of right ventricular outflow tract obstruction at age 3-6 months, as for symptomatic neonates. \n- A transcatheter stent with a balloon may be used to dilate the stenosed pulmonary artery. \n\n\n \nManagement of hypercyanotic \"tet\" spells:\n\n- Initial measures include positioning the infant on their back and flexing their knees. \n- Oxygen should be administered in hospitals. \n- Prophylactic use of propranolol is practised in some centres.\n \n \n# Complications\n \nFollowing the intervention, patients may still face complications from ToF such as:\n \n - Delayed neurodevelopment\n - Reduced exercise tolerance\n - Sustained ventricular tachycardia \n - Aortic root dilatation \n - Pulmonary valve regurgitation \n - This may require subsequent surgical correction \n \n# Prognosis \n \nWithout surgical intervention, the prognosis of ToF is poor with a less than 5% survival rate at 40 years. However, following surgical correction, survival rates at 30 years have increased up to an estimated 90%. \n \n\n# References\n \n [Information from Great Ormond Street Hospital](https://www.gosh.nhs.uk/conditions-and-treatments/conditions-we-treat/tetralogy-fallot)\n \n\n [Information from the British Heart Foundation](https://www.bhf.org.uk/informationsupport/publications/children-and-young-people/understanding-your-childs-heart---tetralogy-of-fallot)\n \n [Patient Info Fallot's Tetralogy](https://patient.info/doctor/fallots-tetralogy)",
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"explanation": "# Summary\n\nThalassaemia is an inherited disorder characterized by abnormal haemoglobin production, with alpha and beta thalassaemia caused by defects in the alpha and beta globin genes, respectively. Key signs and symptoms include jaundice, fatigue, facial bone deformities, and severe anaemia. Diagnosis is made primarily through genetic testing and a full blood count. Management strategies include blood transfusions, stem cell transplantation, and splenectomy for alpha thalassaemia, and blood transfusions and iron chelating agents for beta thalassaemia.\n\n\n# Definition\n\nThalassaemia is a group of inherited disorders characterised by abnormal haemoglobin production. \n\nDefects in the four genes for α-globin result in α-thalassaemia in the two genes for β-globin result in β-thalassaemia\n\nThe absence/abnormality of the α- or β-globin genes leads to quantitative abnormality in globin chain production and an imbalance of the globin-chain synthesis\n\nThe clinical severity of the syndrome is proportional to the number of absent or abnormal genes\n\n[lightgallery]\n\n# Epidemiology\n\nGeographically, thalassaemias are prevalent in populations originating from Mediterranean Europe, Central Africa, the Middle East, the Indian subcontinent and Southeast Asia – having thalassaemia trait is believed to confer some protection against falciparum malaria.\n\n# Alpha-thalassaemia \n\n## Inheritance \n\n- Autosomal recessive inheritance\n\n\n## Pathophysiology \n\nα-thalassemia describes the spectrum of diseases caused by nonfunctioning copies of the four α-globin genes on chromosome 16.\n\nSymptomatic disease results when two or more copies of the gene are lost\n\n- Patients with **two** defective copies have a mild asymptomatic anaemia – so-called **α-thalassaemia trait** \n- Those with **three** defective copies have symptomatic **haemoglobin H disease** \n - Microcytic anaemia (Hb approximately 70 g/l)\n - Haemolysis \n - Splenomegaly\n - Normal survival is to be expected \n\n- inheritance of **four** defective copies (**hydrops fetalis**) is incompatible with life \n\n - The lack of α-globin chains results in excess γ-chains (creating Hb Barts), which are poor carriers of oxygen owing to their high affinity for oxygen\n\n - It may affect the fetus in utero\n\n\n## Signs and Symptoms \n\n- Jaundice\n- Fatigue\n- Facial bone deformities\n\n## Investigations \n\n- FBC will reveal a microcytic anaemia.\n- Hb electrophoresis – can be normal, so DNA analysis is required to make the diagnosis\n\n\n## Management \n\nCurrent treatment options for symptomatic thalassaemia include:\n\n- Blood transfusions \n- Stem cell transplantation\n\nA splenectomy is an option, particularly in patients with HbH disease.\n\nRegular folic acid can also be given, especially in those who are pregnant.\n\n# Beta-thalassaemia \n\n## Inheritance\n\n- Autosomal recessive inheritance\n\n\n## Pathophysiology \n\nβ-thalassemia describes the spectrum of diseases caused by nonfunctioning copies of the two β-globin genes\n\n- The mildest variant of β-thalassaemia is **β-thalassaemia minor** (also known as **thalassaemia trait**)\n - Patients typically have one functioning and one dysfunctional copy of the β-globin gene\n\n- The most severe form of β-thalassaemia (known as **β-thalassaemia major**) is caused by a complete absence of β-globin synthesis (null mutations in both copies of the β-globin gene)\n\n\n## Signs and Symptoms\n\n- **β-thalassaemia minor** - patients are typically asymptomatic\n- **β-thalassaemia major:**\n\t- **Severe symptomatic anaemia** at 3–9 months of age \n - Becomes evident when levels of HbF, which does not contain β-globin, fall and should be replaced by HbA (made up of two α- and two β-globin chains), which is lacking in β-thalassaemia major\n- Ineffective haematopoiesis results in extramedullary haematopoesis, which results in\n\t- Frontal bossing (hair-on-end appearance on Skull XR)\n\t- Maxillary overgrowth and prominent frontal/parietal bones (hypertrophy of ineffective marrow) - \"Chipmunk facies\"\n\t- Hepatosplenomegaly\n- Failure to thrive in infancy\n\n\n## Investigations \n\n**β-thalassaemia minor**\n\n- **Isolated microcytosis** (MCV approximately 63–77 fl) and mild anaemia (Hb typically not <100 g/l)\n - The degree of anaemia is often less severe than would be expected for the degree of microcytosis\n\n- Blood film - target cells and basophilic stippling \n- Increased red cell count\n- Hb electrophoresis (diagnostic) shows raised HbA<sub>2</sub> (>3.5%) – can be lowered by the presence of iron deficiency\n- Can be confused with iron deficiency – ferritin in β-thalassaemia minor is usually normal or high\n\n\n**β-thalassaemia major**\n\n- **Profound microcytic anaemia**; reduced MCV and reduced MCHC\n- Increased reticulocytes\n- Blood film – marked anisopoikilocytosis, target cells and nucleated RBCs. Teardrop cells from extramedullary haematopoeisis may also be present\n- Methyl blue stains – RBC inclusions with precipitated α-globin\n- High-performance liquid chromatography (HPLC) or electrophoresis (diagnostic) – mainly shows HbF\n- HbA<sub>2</sub> may be normal or mildly elevated\n- Haemolysis\n\n\n\n\n## Management of β-thalassaemia major\n\n- Treatment is with **regular blood transfusions**\n\n- The most important long-term consideration in these patients is to reduce the risk of iron overload toxicity \n\n - A condition which primarily affects the heart, joints, liver and endocrine glands\n - Half of patients with β-thalassaemia major die before the age of 35 years, usually from cardiac failure secondary to iron overload\n\n - Iron overload can be prevented with **iron chelating agents** (eg. desferrioxamine/deferiprone/deferasirox) \n\n- **Hydroxycarbamide** (previously known as hydroxyurea) can also be used to boost HbF levels\n\n- **Allogeneic bone marrow transplantation** (BMT) from a sibling or matched unrelated donor \n\n - A potentially curative option \n - Should be done before significant organ damage has occurred due to iron overload\n - Risks of transplant include graft rejection, graft vs. host disease, infection and transplant-related mortality \n\n - These risks must balanced against the long-term benefits of transfusion independence and 'cure'\n\n\n**Iron chelation**\n\n- **Desferrioxamine** \n\n - Used for decompensated organ dysfunction \n\n - Given via subcutaneous pump over 2–5 days each week \n\n - Compliance may be an issue\n\n- **Deferiprone** \n\n - Oral, given in three divided doses\n\n - Particularly good for cardiac iron overload\n\n - **side effects** include: \n - Nausea\n - Arthralgia\n - Agranulocytosis – weekly FBC needed \n - LFT disturbance \n - Zinc deficiency\n\n- **Deferasirox** \n\n - A newer oral iron chelator \n\n - Removes iron in the bile and faeces\n\n - Once daily suspension with similar efficacy to desferrioxamine\n\n - **Side effects** include: \n - Gastrointestinal upset\n - Cytopenias \n - Increased creatinine\n\n- **Monitoring required**\n - Ferritin 3 monthly\n - Annual assessment of: \n - Cardiac/liver T2* MRI\n - Endocrine tests\n - Audiology and ophthalmology \n\n \n## Complications of β-thalassaemia\n\n- Cardiomyopathy/cardiac arrhythmia/cardiac failure\n\t- Older patients are prone to atrial fibrillation \n\t- Urgent cardiac investigations (eg. ECG, echocardiogram, cardiac monitoring and chest X-ray) may be needed\n- Acute sepsis – bacterial sepsis (risk is further increased after splenectomy)\n\t- Consider central venous catheter infection (particularly with *Klebsiella*, *Yersinia enterocolitica* and encapsulated organisms \n\t- Give broad-spectrum antibiotics, and consider high-dependency unit input\n- Liver cirrhosis, portal hypertension and acute decompensation\n\t- Early liver unit input and careful fluid balance are required\n- Endocrine dysfunction \n - Hypocalcaemia with tetany due to hypoparathyroidism\n - Needs cardiac monitoring and IV calcium \n - Diabetes\n- **Iron overload** due to repeated blood transfusions. Presents similarly to Hereditary Haemochromatosis\n- Death is usually due to heart failure if it goes undiagnosed.\n\n\n# Screening\n\nHomozygous and compound heterozygous forms of thalassaemia can have huge clinical significance for which genetic counselling and prenatal testing should be offered.\n\nIf a patient proves to have thalassaemia, it is strongly recommended to test their partner too.\n\nThe **UK screening programme** uses a combination of the pregnant mothers' family of origin questionnaire (FOQ) and FBC, and if required the FOQ and FBC of the baby's father, to detect significant haemoglobinopathies antenatally\n\n- If the maternal MCH is <27 pg, iron studies and HPLC are performed\n\n\n- If these tests are negative, DNA studies/analyses are performed to look for α-thalassaemia if the pregnant woman and the baby's father are both from 'at risk' parts of the world\n\n\nDuring pregnancy, intrauterine diagnosis of thalassaemia major, ideally by chorionic villous sampling, can allow the option of therapeutic abortion of an affected fetus.\n\n# References\n\n[Patient.info - Thalassaemia](https://patient.info/doctor/thalassaemia-pro)",
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"question": "A 50 year old man with type 2 diabetes comes to the GP with scleral icterus. He describes severe pain in his knees and breathlessness on minimal exertion, over the last month. His past medical history is remarkable for beta thalassemia major.\n\nWhat is the most likely aetiology of his condition?",
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"explanation": "This is the correct course of action. Septal haematomas must be evacuated to preserve blood supply to the nasal cartilage, as the septal cartilage relies on nutrient and oxygen delivery from the perichondrium. Untreated, the septum may collapse, causing a saddle-nose deformity.",
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"comment": "septal haematomas also need Abx cover to prevent serious infections.",
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"explanation": "# Summary\n\nSeptal haematoma is a medical condition caused by bleeding under the perichondrium lining of the septal cartilage, typically due to nasal trauma. Key signs and symptoms include bilateral cherry-red swelling arising from the nasal septum, discernible through anterior rhinoscopy. Immediate referral to an ENT specialist for emergency incision and drainage is critical to prevent life-threatening infections and severe cosmetic nasal deformities.\n\n# Definition\n\nSeptal haematoma is a condition characterized by an accumulation of blood in the septal space due to bleeding under the perichondrium lining the septal cartilage. This is often a consequence of nasal trauma.\n\n\n# Aetiology\n\nThe primary cause of septal haematoma is bleeding under the perichondrium lining the septal cartilage, typically resulting from nasal trauma. The septal cartilage, which receives blood supply from the overlying mucosa, can be disrupted by the haematoma. If untreated, this damage can progress to irreversible septal perforation and necrosis within 24 hours, culminating in a saddle-nose deformity.\n\n# Signs and symptoms\n\nThe primary sign of a septal haematoma is a bilateral cherry-red swelling visible on the nasal septum. \n\nThis condition must be suspected and investigated whenever nasal trauma has occurred.\n\n# Differential diagnosis\n\nInclude:\n- Nasal fracture\n- Nasal abscess\n- Foreign body in the nose. \n\nEach of these conditions can present with similar symptoms such as nasal obstruction, pain, and swelling. However, they differ in their presentation and management.\n\n# Investigations\n\nAnterior rhinoscopy is the primary tool for investigating suspected septal haematoma. It reveals a bilateral **cherry-red swelling** arising from the nasal septum. It is critical to inspect the nasal septum following any nasal trauma.\n\n# Management\n\nPrompt referral to an Ear, Nose, and Throat (ENT) specialist for emergency incision and drainage is the standard management strategy for septal haematomas. \n\nThis intervention is essential for preventing life-threatening infectious complications and severe cosmetic nasal deformities.\n",
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"question": "A 15-year-old boy comes to the ED after getting hit in the face by the ball. On inspection of the nose, a bilateral red swelling can be observed.\n\nGiven the likely diagnosis, which of the following is the definitive management plan?",
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"explanation": "This is not routinely used in the assessment of IBS or colorectal cancer (another differential). It may be used in ovarian cancer, along with a transvaginal ultrasound, however it is not currently the most important investigation.",
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"explanation": "While this is a useful test to request, it is not the most important investigation in this case. The patient's age and symptomos are concerning for ovarian cancer.",
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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 59 year old woman has intermittent abdominal pain, accompanied by bloating and occasional diarrhoea. No other symptoms are present, and a diagnosis of irritable bowel syndrome is suspected. Her medical history is otherwise unremarkable.\n\nWhich is the most important investigation to request?",
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"explanation": "Tocolytic agents (such as nifedipine) are used in pre-term labour in order to buy time so that steroids can be administered to encourage foetal lung maturation. The patient is not in labour as evidenced by the CTG showing no contractions, meaning tocolysis is not indicated.",
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"explanation": "There are no current indications for an elective caesarean, such as malpresentation or placenta praevia. Elective caesarean sections often are planned at 39 weeks. An emergency caesarean section may be indicated if there are features of foetal distress.",
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"explanation": "IV benzylpenicillin may be used if the woman is in established labour and is febrile (material sepsis), or during delivery if there is a history of group B streptococcus colonisation. While antibiotics are required, oral erythromycin is the first choice for PPROM.",
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"explanation": "This is not appropriate. There are no features of foetal distress. Inducing labour this early poses risks to the foetus.",
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"explanation": "This patient has experienced a pre-term premature rupture of membranes. RCOG guidelines suggest antibiotics (preferably erythromycin) should be given for 10 days or until the woman is in established labour (whichever is sooner). They also recommend steroids are given until 33 weeks' 6 days' gestation.",
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"explanation": "\n# Summary\n\nPrelabour rupture of membranes at term (PROM at term) is a condition where the amniotic membranes rupture prior to the onset of labour after 37 weeks of gestation. Key signs and symptoms include foul-smelling or greenish amniotic fluid, maternal fever, and reduced foetal movements. Investigations should focus on assessing signs of infection and foetal distress. The primary management strategy is to induce labour if it does not commence spontaneously within 24 hours of PROM. If signs of infection or foetal compromise are evident, immediate induction of labour or a caesarean section may be necessary under specialist guidance. Following delivery, mother and baby should be closely monitored for 12 hours.\n\n\n# Definition\n\n\n\nPrelabour rupture of membranes at term (PROM at term) is a condition characterized by the rupture of the amniotic membranes before the onset of labour after 37 weeks gestation. This condition is associated with increased risks of chorioamnionitis and neonatal infection.\n\n\n# Epidemiology\n\n\n\nPROM at term is a common obstetric complication, affecting approximately 8% to 10% of pregnancies. Most women with PROM at term will start spontaneous labour within the subsequent 24 hours.\n\n\n# Aetiology\n\n\n\nThe exact cause of PROM is not well understood; however, it is believed to be due to a combination of factors including infection, inflammation, stress, and mechanical forces.\n\n\n# Signs and Symptoms\n\n\n\nWomen with PROM at term may experience the following signs and symptoms:\n\n- Foul-smelling or greenish amniotic fluid\n- Maternal fever\n- Reduced foetal movements\n\nDigital vaginal examination should be avoided in the absence of labour. The foetal heart should be monitored.\n\n\n# Differential Diagnosis\n\n\n\nThe main differentials for PROM include:\n\n- Urinary incontinence: This can be distinguished by the absence of amniotic fluid and the presence of urinary symptoms.\n- Vaginal discharge or infection: This can be ruled out by the absence of foul-smelling or greenish discharge and the absence of other infection symptoms.\n\n# Investigations\n\n\nInvestigations for PROM should focus on assessing signs of infection and foetal distress, including:\n\n- Monitoring maternal temperature\n- Assessing foetal movements\n- Monitoring foetal heart rate\n- Observing vaginal discharge\n\n# Management\n\n\nManagement of PROM at term involves the following steps:\n\n- If labour does not commence within 24 hours, induction of labour should be offered.\n- If there are any signs of infection, immediate induction of labour should be commenced under consultant guidance and a broad spectrum antibiotic should be given.\n- If there are any signs of foetal compromise, senior review is required to make a decision about whether immediate caesarean section is required.\n- Following delivery, even if both baby and mother are asymptomatic, they should be closely observed in hospital for 12 hours post-birth.\n\n# Complications\n\nPROM at term can lead to several complications, including:\n\n- Chorioamnionitis due to ascending infection\n- Preterm birth and the associated complications such as respiratory distress syndrome, necrotising enterocolitis, and foetal death\n- Developmental problems such as pulmonary hypoplasia, facial and limb deformities due to compression in the uterus, and cord prolapse due to low levels of amniotic fluid.",
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"explanation": "This is an important investigation as part of a septic screen, but results take 48 hours. A FBC is more important at this stage.",
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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": "A 24-year-old man with a long history of treatment-refractory psychosis is commenced on clozapine. He is poorly-compliant with monitoring. He presents to hospital with a fever and general malaise.\n\nWhich is the next most important investigation?",
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"explanation": "The MMR vaccine protects against measles, mumps, and rubella. Congenital rubella syndrome is a good differential as this can cause sensorineural deafness. However, there is no mention of the other features of CRS such as cataracts, a blueberry muffin rash, or heart defects (typically pulmonary stenosis).",
"id": "10017307",
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"explanation": "Ganciclovir or aciclovir may be used in maternal HSV infection.",
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"explanation": "This is used in the treatment of toxoplasmosis in pregnancy. Toxoplasmosis causes chorioretinitis, intracranial calcifications, and hydrocephalus. Treatment for toxoplasmosis in neonates includes sulfadiazine, pyrimethamine, and folate.",
"id": "10017309",
"label": "d",
"name": "Spiramycin treatment",
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"explanation": "The diagnosis is congenital syphilis, presenting with sensorineural deafness and a desquamating rash. Other features include Hutchinson's teeth, interstitial keratitis, and ostrochondritis visible on x-ray.",
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"name": "Benzathine benzylpenicillin",
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"explanation": "This is advice prevent neonatal listeriosis, as listeria can be present in raw (unpausturised) milk. The main presentations are neonatal sepsis and meningitis.",
"id": "10017308",
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"__typename": "QuestionComment",
"comment": "I swear I knew more in 3rd year than now 3 days out of my y5 finals",
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"comment": "you got this! these questions r just shit xx",
"createdAt": 1704888195,
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"comment": "Why can't this be congenital varicella ",
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"comment": "yes this is what I thought too!",
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"comment": "palmoplantar rash",
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"comment": "a point gained rather than 2 dropped on this one for me\n",
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"explanation": "# Summary\n \n \nSyphilis is a sexually transmitted infection that occurs in three distinct stages: primary, secondary, and tertiary. The primary stage presents with painless solitary lesions often located in the genital or perianal region. Secondary syphilis typically features a symmetrical maculopapular rash, and lymphadenopathy. Tertiary syphilis, occurring in about a third of untreated patients, may present with gummatous disease, cardiovascular complications, and neurological implications. Diagnosis often involves serological testing, and management primarily includes penicillin-based therapy.\n \n \n# Definition\n \n \nSyphilis is a sexually transmitted infection caused by the spirochete bacterium Treponema pallidum. It is primarily transmitted through direct contact with syphilis sores or rash during vaginal, anal, or oral sex. \n \n \n# Epidemiology\n \n \nSyphilis has a global prevalence with varied incidence based on geographical regions and specific population subsets. High-risk populations include men who have sex with men, sex workers, and individuals with multiple sexual partners.\n \n \n# Aetiology\n \n \nSyphilis is caused by the bacterium *Treponema pallidum*, which is transmitted through direct contact with syphilis sores during sexual activity. It can also be transmitted from an infected mother to her unborn child, resulting in congenital syphilis.\n \n \n# Signs and Symptoms\n \n \n- Primary syphilis: Characterised by the appearance of a single painless lesion, known as a chancre, typically at the site of inoculation. The lesion is round, with an indurated base, and heals spontaneously within 3-8 weeks. Painless regional lymphadenopathy may also be present.\n \n- Secondary syphilis: Manifests 4-10 weeks post-primary infection with a symmetrical maculopapular rash, often involving the palms, soles, and face. Mucosal ulcers and lymphadenopathy are common, and some patients may experience malaise, fever, hepatitis, glomerulonephritis and neurological complications.\n \n- Tertiary syphilis: This stage may occur 20-40 years after the primary infection in untreated patients. It presents with gummatous disease, cardiovascular complications (aortitis, arteritis, aortic valve regurgitation), and neurological complications (meningovascular syphilis, paresis, dementia, tabes dorsalis, Argyll-Robertson pupil).\n \n- Congenital syphilis: Resulting from the transmission of the Treponema pallidum bacterium from an infected mother to her fetus during pregnancy, presents shortly after birth or later in infancy with a rash on the palms/soles of feet, mucous patches/lesions in the mouth/nose/genitals, fever, hepatosplenomegaly, anaemia, bone developmental abnormalities ('saber shins'), neurological sequalae (seizures, developmental delay).\n \n# Differential diagnosis\n \nDifferential diagnoses for **primary syphilis** include:\n \n- Chancre (initial lesion): genital herpes, lymphogranuloma venereum, malignancy, Behcet's syndrome\n- lymphadenopathy: infection, systemic diseases, malignancy\n \nDifferential diagnoses for **secondary syphilis** include:\n \n- Rash: primary HIV infection, viral exanthem, drug eruptions\n- Lesions on oral mucosa: malignancy, infectious mononucleosis, aphthous ulcers\n \nDifferential diagnosis for **tertiary syphilis**:\n \n- Dementia\n- Psychiatric conditions\n- Diseases affecting mobility\n- Chronic granulomatous lesions\n \n# Investigations\n \n**Dark field microscopy** is used to directly observe *T. pallidum* in samples from primary lesions or secondary rash. However, it should not be used for oral lesions due to the presence of commensal treponemes which may cause a false positive result.\n \n**PCR** testing is used for oral lesions. This detects genetic material, so can differentiate between *T. pallidum* and other commensals.\n \n**Serological tests** can be used for screening, diagnosis confirmation and treatment monitoring.\n \n- **Treponemal** tests such as enzyme immunoassays (EIA) and chemiluminescent assays (CLIA) detect treponemal IgG and IgM. It is most sensitive for secondary, early latent and late latent stages, and are the recommended **screening tests**. These tests **remain positive even after treatment** so cannot be used for monitoring or re-infection.\n \n- **Non-treponemal tests** such as Venereal Diseases Research Laboratory (VDRL) also have higher sensitivity for secondary and early latent stages of syphilis, but is less sensitive in late stage disease. Titres decline with effective treatment, so it is useful for **monitoring treatment efficacy**.\n \n \n- **False negatives** may occur early in the disease, and non-treponemal tests may be negative in late-stage disease, or with HIV co-infection.\n \n- **False positives** can occur with non-treponemal tests due to viral infections, malignancy, autoimmunity, older age, IVDU and pregnancy.\n \nTo diagnose syphilis from screening serology, a repeat test must be performed using a different method.\n \nAdditional investigations to consider are:\n \n- **Virology** swabs of lesions to exclude HSV\n \n- Screening for other **STI's**\n \n- **CSF** examination: Should be considered in tertiary syphilis to evaluate for CNS involvement.\n \n \n# Management\n \n \nSyphilis is primarily managed with antibiotics:\n \n \n- Primary, secondary, and early latent syphilis: A single dose of intramuscular penicillin G (benzathine benzylpenicillin) is the first-line therapy.\n \n- Tertiary and late latent syphilis or syphilis of unknown duration: Requires a longer course of intramuscular penicillin G for 2-3 weeks.\n \n- Neurosyphilis: Treated with intravenous penicillin G for 10-14 days.\nPatients allergic to penicillin may be given doxycycline or tetracycline.\n \nA Jarisch-Herxheimer reaction may occur on treatment initiation. This is an acute febrile illness which is self-resolving within 24 hours. Generally, patients can be reassured and given antipyretics for the fever. In late syphilis or during pregnancy, specialist advice should be sought.\n \nPatients should be referred to a GUM clinic for partner notification and screening for other STIs.\n \n \n\n# NICE guidelines\n \n[NICE CKS guidelines on syphilis](https://cks.nice.org.uk/topics/syphilis/)\n \n# References\n \n[Patient.info: Syphilis](https://patient.info/doctor/syphilis-pro#syphilis-treatment-and-management)",
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"question": "A neonate is found to have a hearing impairment after being referred for an auditory brainstem response test. There is a desquamating rash on the feet and palms.\n\nWhich intervention would have prevented the vertical transmission of the infective agent causing these symptoms?",
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"a"
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173,464,682 | false | 32 | null | 6,495,162 | null | false | [] | null | 16,006 | {
"__typename": "QuestionSBA",
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{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Mastalgia can be caused by hormonal changes, such as those experienced in pregnancy or menstruation. The initial step in management should be a pregnancy test to investigate this.",
"id": "10017311",
"label": "a",
"name": "Urine beta-HCG",
"picture": null,
"votes": 1942
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Mammography is less useful in younger women, as they have dense breast tissue. If imaging is required (e.g. due to a palpable mass on examination), ultrasound would be a better modality of imaging.",
"id": "10017313",
"label": "c",
"name": "Mammography",
"picture": null,
"votes": 538
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "The COCP is not indicated in the management of cyclical mastalgia.",
"id": "10017315",
"label": "e",
"name": "Combined oral contraceptive pill",
"picture": null,
"votes": 115
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Danazol is used in mastalgia refractory to breast pain not responding to simple analgesia for at least 3 months. As this patient does not fit these criteria, danazol should not be prescribed.",
"id": "10017314",
"label": "d",
"name": "Danazol",
"picture": null,
"votes": 55
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This may be indicated if a lump is felt, or other investigations do not yield a cause of the pain.",
"id": "10017312",
"label": "b",
"name": "Ultrasound breast",
"picture": null,
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"explanation": "# Summary\n \n\nCyclical mastalgia, or cyclic breast pain, is a condition characterised by breast tenderness that fluctuates in intensity with the menstrual cycle. It is often associated with premenstrual syndrome and may begin a few days before the onset of menstruation, subsiding by the end of the period. This condition is thought to be linked to hormonal changes during the menstrual cycle and may also be associated with fibrocystic changes in the breast or duct ectasia. Cyclical mastalgia is more prevalent in peri- and premenopausal women. Key investigations include physical examination, mammography, and ultrasound, and the primary management strategies involve lifestyle modifications and pharmacological therapy.\n \n\n# Definition\n \n\nCyclical mastalgia is a clinical condition that involves breast tenderness, which fluctuates in relation to the monthly menstrual cycle.\n \n\n# Epidemiology\n \n\nCyclical mastalgia is predominantly experienced by peri- and premenopausal women, with a notable decrease in incidence among postmenopausal women.\n \n\n# Aetiology\n \n\nThe aetiology of cyclical mastalgia is believed to be linked to variations in hormone levels during the menstrual cycle, particularly oestrogen and progesterone. It may also be associated with fibrocystic changes in the breast, presenting as breast \"lumpiness\", or with duct ectasia.\n \n\n# Signs and Symptoms\n \n\n- Breast tenderness\n- Pain usually beginning a few days before the onset of menstruation and subsiding by the end of the period\n- Possible breast \"lumpiness\" associated with fibrocystic changes\n- Potential presentation of duct ectasia\n \n\n# Differential Diagnosis\n \n\n- **Fibrocystic breast changes**: These can present with breast pain, lumpiness, and sometimes nipple discharge.\n- **Breast abscess**: Characterised by localised pain, redness, swelling, and warmth of the affected area, often accompanied by fever.\n- **Mastitis**: Similar to a breast abscess, mastitis presents with breast pain, redness, swelling, and warmth but is usually associated with breastfeeding.\n- **Breast cancer**: Though pain is not a common symptom, breast cancer can present with a painless lump, skin dimpling, nipple inversion, or nipple discharge.\n \n\n# Investigations\n \n\n- Clinical breast examination: to assess for any palpable masses, skin changes, or nipple discharge\n- Mammography or ultrasound: especially for women over 40, or those with significant risk factors\n- Hormone profile: for suspected hormonal imbalances\n \n\n# Management\n \n\n- **Lifestyle modifications**: Including regular exercise, a healthy diet, and limiting caffeine and salt intake\n- **Pharmacological therapy**: Non-prescription pain relief such as paracetamol or non-steroidal anti-inflammatory drugs (NSAIDs); hormone-modulating medications like oral contraceptives or danazol may be used in severe cases\n- **Follow-up and surveillance**: Regular follow-ups to monitor symptoms and evaluate the effectiveness of management strategies\n \n\n# NICE Guidelines\n \n\n[Click here for NICE CKS on breast pain - cyclical](https://cks.nice.org.uk/topics/breast-pain-cyclical/#:~:text=pain%20%2D%20cyclical%3A%20Summary-,Cyclical%20breast%20pain%20is%20related%20to%20the%20menstrual%20cycle%20and,moderate%2Dto%2Dsevere%20pain.)",
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"learningPoint": "Mastalgia, which can be caused by hormonal changes like those in pregnancy or menstruation, should initially be evaluated with a pregnancy test.",
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"question": "A 31-year-old patient visits her GP as she is experiencing bilateral breast pain. Her mother had a mastectomy for breast cancer at the age of 58, and she is anxious that she may have breast cancer.\n\nWhat is the most appropriate initial management step?",
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"a"
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"answer": false,
"explanation": "This may be ordered as part of a thrombophilia screen, however the history and examination findings are concerning for antiphospholipid syndrome, rather than hyperhomocystinaemia.",
"id": "10017318",
"label": "c",
"name": "Homocysteine levels",
"picture": null,
"votes": 193
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Serum triglyceride levels are unlikely to be helpful at this point.",
"id": "10017320",
"label": "e",
"name": "Triglycerides",
"picture": null,
"votes": 134
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would be required if the patient suffered an ischaemic stroke. Patients with antiphospholipid syndrome are susceptible to both venous and arterial thrombosis.",
"id": "10017317",
"label": "b",
"name": "Carotid doppler",
"picture": null,
"votes": 88
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "The history of an unprovoked pulmonary embolus, along with the finding of livedo reticularis (often described as a lace-like rash), is suspicious for a diagnosis of antiphospholipid syndrome. Lupus anticoagulant should be tested for as part of a screen for the syndrome, along with anti-cardiolipin antibodies and beta-2 glycoprotein antibodies.",
"id": "10017316",
"label": "a",
"name": "Lupus anticoagulant",
"picture": null,
"votes": 2927
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This may be ordered as part of a screen to investigate excessive bleeding, rather than a thrombophilia screen. It is not to be mistaken with the test for Factor V Leiden (an activated protein C test), which may be undertaken in this case.",
"id": "10017319",
"label": "d",
"name": "Factor V activity",
"picture": null,
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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 30-year old woman has a massive pulmonary embolus requiring thrombolysis. She has a lace-like rash on her shins.\n\nWhich investigation is most likely to reveal the underlying diagnosis?",
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"explanation": "This is the agent used to confer passive immunity to respiratory syncytial virus, the pathogen causing bronchiolitis, which this patient's cousin likely has. It should be administered to children at risk of severe illness if infected with RSV, once a month, during RSV season.",
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"comment": "had no idea you could vaccinate against rsv",
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"comment": "were we meant to know the cousin had bronchiolitis simply because of 'wheeze'?",
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"comment": "wheeze and hospital admission for a kid under 2 usually is bronchiolitis",
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"comment": "Is bronchiolitis not LRTI rather than URTI??",
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"comment": "Yes it is according to quesmed notes and google",
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"comment": "As of 1 September 2024, the RSV vaccine is offered to pregnant women from 28 weeks gestation onwards to protect infants from RSV bronchiolitis during the first 6 months of life.\n\n(It's also offered to adults aged 75-79).",
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"comment": "i was thinking pavilizumab, but it doesn't technically \"Prevent you from contracting the condition\" in my understanding it just reduces your chances of having severe illness by giving preexisting antibodies - or am i understanding this wrong?",
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"explanation": "# Summary\n \nBronchiolitis is a prevalent chest infection that primarily affects infants aged 1-12 months. This infection is typically caused by the Respiratory Syncytial Virus (RSV) and is characterised by symptoms such as a cough, laboured breathing, wheezing, tachypnoea, intercostal recession, grunting, and nasal flaring. Diagnosis is typically made through clinical presentation and possibly chest X-rays. Management includes prophylactic measures in high-risk patients, supportive care, and oxygen therapy, which may escalate to mechanical ventilation. Ribavirin may be used in severe cases. The key complications of bronchiolitis include bronchiolitis obliterans, also known as popcorn lung, which may result from the overactive cellular repair process. \n \n\n# Definition\n \n\nBronchiolitis is a widespread chest infection, predominantly affecting infants aged 1-12 months. This lower respiratory tract disease targets the bronchioles, causing inflammation and congestion.\n \n\n# Epidemiology\n\nBronchiolitis is very common, affecting around 1 in 3 infants. Bronchiolitis mainly affects children under the age of 1, with approximately 90% of affected children being aged between 1-9 months. It is rare beyond the age of 1 year. \n\nBronchiolitis epidemics are typically observed during winter months from October to March. \n \n\n# Aetiology\n \n\nThe majority of bronchiolitis cases (around 80%) are attributable to the Respiratory Syncytial Virus (RSV). The virus infects epithelial cells of bronchioles. This causes inflammation, mucous production and the epithelial cells to slough off, obstructing the airways. This obstruction results in hypoxia and breathlessness. \n\nRisk factors for developing bronchiolitis include:\n\n- Nursery attendance or having older siblings\n- Passive smoking in the household\n- Overcrowding \n- Exclusive formula-feeding \n\nMore severe bronchiolitis is seen in infants with the following risk factors:\n\n- Prematurity or low birth weight \n- Age < 12 weeks\n- History of mechanical ventilation, chronic lung disease, congenital heart disease or neurological disease\n- Immunocompromise\n- Congenital defects of the airway\n- Down's Syndrome \n \n\n# Signs and Symptoms\n \n\nA diagnosis of bronchiolitis should be considered in an infant with the following:\n \n- Preceding coryzal symptoms for 1-3 days \n- Cough\n- Either tachypnoea or chest recession \n- Either wheeze or crackles on auscultation\n\nOther symptoms they may present with:\n\n- Fever (typically < 39C) \n- Reduced oral intake \n- Apnoea \n\n\n# Differential Diagnosis\n \n\nThe differential diagnoses for bronchiolitis primarily include the following:\n \n\n - **Asthma**: Characterised by recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. This is typically seen in older children than those affected by bronchiolitis. \n - **Pneumonia**: Symptoms include cough with phlegm or pus, high fever (>39C) and persistently focal crackles. \n - **Viral Induced Wheeze**: Seen in children with persistent wheeze and a family history of atopy, more commonly seen in children over the age of 1. \n - **Foreign body aspiration**: This condition may present with sudden onset of respiratory distress, choking, gagging, wheezing, or coughing.\n \n\n# Investigations\n \n\nDiagnosis of bronchiolitis is primarily clinical based on the characteristic symptoms. \n\nFurther investigations may include:\n\n- Pulse oximetry to monitor oxygen saturation\n- Throat swab for respiratory viruses \n- Chest X-rays if focal chest signs or deterioration is seen \n \n\n# Management\n \nThe majority of patients can be managed at home, but admission may be indicated for children with:\n \n - Tachypnoea (>60 breaths/min)\n - Reduced oral intake (< 50% normal) \n - Clinical dehydration\n - Oxygen saturation less than 92% \n - Cyanosis \n - Apnoea \n - Respiratory distress (grunting, intercostal or subcostal recession, tracheal tugging) \n\n\nManagement of bronchiolitis involves:\n \n- Supportive Care:\n - Adequate hydration and nutrition\n - If not tolerating oral intake, an NG tube can be used to provide fluids. \n - If fever is causing distress to the infant, paracetamol may be used. \n- Oxygen Therapy: \n - For oxygen saturations less than 90% for children over 6 weeks.\n - This may be escalated to CPAP in severe cases with threatened respiratory failure.\n- Antiviral Therapy: Ribavirin may be used in severe cases.\n\nAntibiotics, steroids and salbutamol are not used in the management of bronchiolitis. \n \nPrevention may include the administration of Palivizumab (a monoclonal antibody) in high-risk patients (i.e. with haemodynamically significant congenital heart disease). This reduces the risk of RSV-related hospital and PICU admission.\n\n# Complications\n\nBronchiolitis may result in the following complications:\n\n- Respiratory failure requiring intubation \n- Dehydration \n- Cough lasting weeks following bronchiolitis \n- Bronchiolitis obliterans \n \n\nBronchiolitis obliterans:\n\n- A rare, chronic complication of bronchiolitis, colloquially known as popcorn lung. \n- The bronchioles are injured due to infection (usually adenovirus) or inhalation of a harmful substance, leading to an overactive cellular repair process and subsequent build-up of scar tissue. The scar tissue obstructs the bronchioles, impairing oxygen absorption in the body. The scarring and narrowing of the bronchioles may continue to worsen over time, potentially leading to respiratory failure. \n- Lung transplant recipients are at particular risk of developing bronchiolitis obliterans syndrome, with about 50% developing the condition within five years of transplant due to organ rejection.\n\n\n# Prognosis \n\nFortunately for many infants, bronchiolitis can be managed at home and the illness lasts for up to 7 days. The cough may take up to 3 weeks to resolve. \n\n2-3% of infants, however, require hospitalisation. Risk factors for more severe bronchiolitis include chronic lung disease, immunodeficiency, age under 3 months, prematurity, congenital heart disease and neuromuscular disorders. In these high-risk infants, the mortality rate is roughly 3%. \n\n# NICE Guidelines \n\n[NICE Guidelines on Bronchiolitis](https://www.nice.org.uk/guidance/ng9) \n \n\n# References\n\n[NHS Information on Bronchiolitis](https://www.nhs.uk/conditions/bronchiolitis/) \n\n[Great Ormond Street Hospital Bronchiolitis Information](https://media.gosh.nhs.uk/documents/Bronchiolitis_F1533_A5_col_FINAL_Mar16.pdf)\n\n[Patient Info Bronchiolitis](https://patient.info/doctor/bronchiolitis-pro)",
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"question": "The parents of a 9-month old boy who has undergone cardiac surgery are concerned about his contact with his 1 year old cousin who has been admitted to hospital with a wheeze following a recent upper respiratory tract infection.\n\nWhich of the following is useful in preventing the child contracting this condition?",
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"comment": "I read this question 10 times and still did not get it right :(",
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"comment": "thanks, son's crying",
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"comment": "This question was basically Liverpool (A)",
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"explanation": "# Uses\n\nRandomised controlled trials are useful to determine whether a cause-effect relationship exists between treatment and outcome. They can also be used to assess the cost-effectiveness of a treatment.\n\n# Important features of randomised controlled trials\n\n- Random allocation to intervention groups\n- Patients and trialists should remain unaware of which treatment was given until the study is completed-although such **double blind** studies are not always feasible or appropriate\n- All intervention groups are treated identically except for the experimental treatment\n- Patients are normally analysed within the group to which they were allocated, irrespective of whether they experienced the intended intervention (intention to treat analysis)\n- The analysis is focused on estimating the size of the difference in predefined outcomes between intervention groups.\n\n# Improving RCT value \n\n**Increasing the strength of RCTs using meta-analyses**\n\nTo strengthen the evidence further, a meta-analysis of RCTs investigating the same intervention can be conducted.\n\nMeta-analyses enable the combining of data from multiple studies to derive conclusions based on the application of objective formulas to the combined data.\n\nIn this way, meta-analyses increase the statistical power and enable a more accurate assessment of the validity of a hypothesis than can be achieved by a single study.",
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"question": "A medication is being studied for the treatment of lung cancer. An ethics committee does not approve a randomised controlled trial of the medication, as they do not believe there is genuine uncertainty about whether the current standard of care is better or worse than this new medication.\n\nWhat best describes the ethical concept the investigators are referring to?",
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"explanation": "This would be an appropriate strategy to manage shingles. There is no suggestion of a rash present in a dermatomal distribution, or any vesicles. The unilateral nipple findings are concerning for Paget's disease of the nipple.",
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"explanation": "While the red, scaly rash may look eczematous, it is important to recognise that this is possibly Paget's disease of the nipple, associated with an underlying cancer. The patient requires triple assessment on a 2-week pathway.",
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"explanation": "The patient's symptoms and examination findings suggest Paget's disease of the nipple, a condition that is frequently associated with ductal carcinoma of the breast. This should not be mistaken for eczema or an infection. NICE recommend a 2-week referral for women aged over 50 with unilateral nipple changes that are concerning. A triple assessment will involve imaging (likely a mammogram), examination, and biopsy.",
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"explanation": "# Summary\n \n\nPaget's disease of the nipple is a rare form of breast cancer that initially presents with eczema-like changes to the nipple and areola. Main signs and symptoms include a crusty, inflamed rash on the nipple and areola, bloody nipple discharge, pain, and nipple retraction or inversion. On occasions, a palpable breast lump or unhealing skin ulcer may also be present. Key investigations involve a physical examination, mammography, ultrasound, and biopsy to confirm the diagnosis. Management primarily involves surgical interventions such as mastectomy, along with radiation and hormonal therapies depending on the underlying cancer's nature.\n \n\n# Definition\n \n\nPaget's disease of the nipple, also known as Paget's disease of the breast, is a rare condition characterised by the presence of cancer cells in the skin of the nipple. This disease often suggests an underlying ductal carcinoma in situ (DCIS) or invasive breast cancer.\n \n\n# Epidemiology\n \n\nPaget's disease of the nipple is a rare disorder, accounting for less than 5% of all breast cancer cases. It is most commonly seen in postmenopausal women, but it can occur in men and women of any age.\n \n\n# Aetiology\n \n\nThe exact cause of Paget's disease of the nipple is not fully understood. There are two main theories: the epidermotropic theory, which suggests that cancer cells from an underlying breast tumour migrate to the nipple; and the intraepidermal origin theory, which proposes the disease originates in the nipple itself.\n \n\n# Signs and Symptoms\n \n\nCommon clinical features of Paget's disease of the nipple include:\n \n\n- Eczema-like rash on the skin of the nipple and areola that is often itchy, red, crusty, and inflamed\n- Bloody nipple discharge\n- Burning sensation, increased sensitivity, or pain in the nipple\n- Changes to the nipple, such as retraction or inversion\n- Palpable breast lump (in some cases)\n- Non-healing skin ulcer (in some cases)\n \n\n[lightgallery]\n \n\n# Differential Diagnosis\n \n\nWhen assessing Paget's disease of the nipple, the main differential diagnoses include:\n \n\n- **Atopic dermatitis (eczema)**: characterised by itchy, red, and inflamed skin, usually occurring in patches\n- **Contact dermatitis**: caused by irritants or allergens, presents with a red rash, itching, and possibly blisters\n- **Intraductal papilloma**: produces bloody nipple discharge but typically does not involve skin changes\n- **Mastitis or breast abscess**: presents with breast redness, swelling, pain, and possible fever; often related to breastfeeding\n- **Psoriasis**: presents with silvery scales on red, raised patches, often with itching or burning\n \n\n# Investigations\n \n\nTo diagnose Paget's disease of the nipple, the following investigations are typically carried out:\n \n\n- Physical examination of the breasts and lymph nodes\n- Mammography or breast ultrasound\n- Biopsy of the affected skin and nipple discharge cytology\n- MRI may be used in certain circumstances to better assess the extent of disease\n \n\n# Management\n \n\nManagement of Paget's disease of the nipple primarily involves surgical intervention and is guided by the presence and extent of underlying breast cancer. Approaches can include:\n \n\n- Simple mastectomy: Removal of the entire breast, including the nipple and areola\n- Modified radical mastectomy: Removal of the entire breast along with some of the axillary (underarm) lymph nodes\n- Breast-conserving surgery (lumpectomy): If the underlying cancer is small and limited\n \n\nAdditionally, adjunctive treatments such as radiation therapy, chemotherapy, or hormonal therapy may be used depending on the characteristics of the underlying breast cancer.",
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"question": "A 54 year old woman attends her GP with an itchy nipple. On examination, she has a raised, scaly, red rash extending to the areola. There is no nipple inversion or discharge. Examination of both breasts is otherwise normal.\n\nWhat is the most appropriate next step?",
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"explanation": "Hypothyroidism can result in an unconjugated hyperbilirubinaemia, however heel-prick testing would detect congenital hypothyroidism. Further TFTs may be undertaken, but this is not the most important next step given that the baby is febrile.",
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"explanation": "IVIG is considered for babies undergoing phototherapy in cases of ABO or rhesus haemolytic disease, when bilirubin levels rise by more than 8.5 micromol/litre/hour. This is not the case.",
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"explanation": "# Summary\n \n\nNeonatal jaundice, a common condition characterized by a yellowing of the skin and eyes due to bilirubin accumulation, typically presents as physiological but may also indicate serious underlying pathologies. Key signs and symptoms include yellow discoloration of the skin and eyes, poor feeding, lethargy, and in severe cases, kernicterus. Important investigations involve bilirubin levels, gestational age assessment, and potential additional tests for underlying causes. Management strategies can range from watchful waiting to phototherapy and exchange transfusion.\n \n\n# Definition\n \n\nNeonatal jaundice is a clinical condition that presents as a yellowing of a newborn's skin and eyes. It results from the accumulation of bilirubin, a by-product of the breakdown of red blood cells, in the body.\n \n\n# Epidemiology\n \n\nNeonatal jaundice is a common condition affecting a significant proportion of newborns. While most cases are physiological and self-limiting, a subset may be pathological, representing serious conditions requiring prompt identification and management.\n\nNeonatal jaundice is more commonly seen in male and East Asian infants. \n \n\n# Aetiology\n \n\nThe causes of neonatal jaundice can be classified based on the age of onset:\n \n\n **Causes <24 hours**\n \n\n - Haemolytic disorders (Rhesus incompatibility, ABO incompatibility, G6PD deficiency, spherocytosis)\n - Congenital infections (TORCH screen indicated)\n - Sepsis\n \n\n**Causes 24 hours - 14 days**\n \n\n - Physiological jaundice\n - Breast milk jaundice\n - Dehydration\n - Infection, including sepsis\n - Haemolysis\n - Bruising\n - Polycythaemia\n - Crigler-Najjar Syndrome\n \n\n**Causes >14 days (>21 if preterm)**\n \n\n - Physiologic jaundice\n - Breast milk jaundice\n - Infection\n - Hypothyroidism\n - Biliary obstruction (including biliary atresia)\n - Neonatal hepatitis\n \n# Classification\n\nPhysiological jaundice is largely attributable to:\n \n\n - Relative polycythaemia in newborns\n - Shorter red blood cell lifespan compared to adults\n - Less efficient hepatic bilirubin metabolism in the first few days of life\n\nBreast milk jaundice is seen in an otherwise well baby (and can suggest mild, but not clinical dehydration) and usually resolves within 6 weeks. \n \n\n# Signs and Symptoms\n \n\n - Yellowing of the skin and eyes\n - Poor feeding\n - Lethargy\n - In severe cases, kernicterus, a rare but serious complication of untreated jaundice, can occur. This results from excess bilirubin damaging the brain, particularly the basal ganglia.\n - Symptoms include irritability, vomiting, hypotonia followed by hypertonia) \n\nIf the neonatal jaundice is due to hepatitis or biliary atresia, there will be pale stools and dark urine seen. \n\n# Investigations\n \n\nInvestigations should include:\n \n\n - Measuring transcutaneous bilirubin levels. If elevated, confirm with serum bilirubin level, and plot on the nomograms produced by BNF/NICE, taking into account the patient's gestation and age.\n - Serum bilirubin should always be used if jaundice occurs in the first 24 hours of life or if the neonate is less than 35 weeks gestational age. \n- Depending on the clinical history, further investigations may also be warranted to elucidate a cause.\n - Consider FBC, blood film, Coombs' test, LFTs, G6PD levels\n - Ultrasound or liver biopsy may be required to investigate for hepatitis and biliary atresia \n \n\n# Management\n \n - Admit to neonatal or paediatric unit urgently if < 24 hours old, >7 days old, if the neonate is unwell, gestational age < 35 weeks. \n - If the neonate is well, the cause is likely physiological or breastmilk jaundice, and the bilirubin is below the treatment threshold, no treatment is indicated. Parents should be educated to monitor the jaundice and to return if the neonate becomes unwell or if the jaundice is not resolving. \n - Increase fluid intake (ideally orally, but IV may be required) \n - If intervention is required due to elevated bilirubin levels, patients may need:\n - Phototherapy \n - Ensure adequate fluid intake and eye care \n - An exchange transfusion\n- Monitoring of bilirubin levels:\n - Patients with bilirubin levels nearing the phototherapy line should have a repeat measurement in 24 hours.\n - Further management based on clinical history may also be necessary to uncover the underlying cause.\n\n# Complications\n \nThe complications of neonatal jaundice depend on the underlying cause. Complications are rare for breastmilk or physiological jaundice.\n \nComplications may include:\n \n - Related to phototherapy\n - Loose stools and dehydration\n - Kernicterus \n - Prolonged exposure to excess bilirubin causes neurologic damage\n\n# Prognosis \n\nNeonatal jaundice is usually short-lived and benign. Breastfeeding can continue during the jaundice. For more serious causes (ie biliary atresia, sepsis), the prognosis will depend on how quickly treatment is initiated and the underlying cause. \n \n\n# NICE Guidelines\n \n [NICE Clinical Knowledge Summary on Neonatal Jaundice](https://cks.nice.org.uk/topics/jaundice-in-the-newborn/)\n \n# References \n\n [NHS page about Jaundice in Newborns](https://www.nhs.uk/conditions/jaundice-newborn/)\n \n [Patient Info - Neonatal Jaundice](https://patient.info/doctor/neonatal-jaundice-pro#)",
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"question": "A 10-day-old baby is referred to the paediatric emergency department by her GP as her skin and sclerae look yellow. She was born at full term. There were no complications during pregnancy or birth. She is exclusively breastfed. Her parents report that she is feeding slightly less than normal and has a runny nose, but is wetting nappies as usual.\n\n\nBlood results show:\n\n\n * Total bilirubin 120 micromoles/litre (refer to image of treatment graph)\n\n\nObservations:\n\n\n * Heart rate 152 beats/minute (normal 140-160 beats/minute)\n\n\n * Blood pressure 63/42 mmHg (normal 50-70 / 25-45 mmHg)\n\n\n * Respiratory rate 72 breaths/minute (normal <60 breaths/minute)\n\n\n * Temperature 38.0 degrees Celcius\n\n\nJaundice treatment graphs:\n\n\n [lightgallery]\n\n\nWhich of the following is the most important next step?",
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"explanation": "This is an option for patients for a short period of time, to induce a 'pseudo-menopause' and shrink the size of the fibroids. This is not appropriate in somebody who would like to become pregnant.",
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"explanation": "This is likely to alleviate some of the symptoms, but perhaps not her menorrhagia. Further, this does not address the element of subfertility that may be caused by the fibroids.",
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"name": "Symptomatic relief with NSAIDs",
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"explanation": "This is clearly contraindicated as pregnancy is desired.",
"id": "10017345",
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"explanation": "This is an option for patients who have no contraindications to hormonal contraceptives, and who do not want to become pregnant.",
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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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"explanation": "The most likely diagnois is pelvic inflammatory disease (PID), as evidenced by dyspareunia, discharge, and right upper quadrant pain (Fitz-Hugh-Curtis syndrome). This should be treated empirically to limit the infection and reduce the risk of complications.",
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"comment": "Yeah it's one off. Pretty sure the doxy is just for 7 days as well, not sure about metro",
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"explanation": "# Summary\n\n\nPelvic Inflammatory Disease (PID) is a sexually transmitted infection that spreads from the vagina into the cervix and upper genital tract. The primary pathogens are Chlamydia trachomatis and Neisseria gonorrhoeae, though often, no pathogen can be isolated. Patients typically present with generalised abdominal pain, discharge, postcoital bleeding, adnexal tenderness, cervical motion tenderness, and sometimes right upper quadrant pain due to Fitz-Hugh-Curtis syndrome. The diagnostic approach includes pelvic examination, pregnancy test, swabs for gonorrhoea and chlamydia, blood tests, and transvaginal ultrasound. Management typically consists of a combination of antibiotics, usually administered in an outpatient setting, and analgesia as required.\n\n\n# Definition\n\n\nPelvic inflammatory disease (PID) is a condition that arises when an infection spreads from the vagina to the cervix, and subsequently to the upper genital tract.\n\n\n# Aetiology\n\n\nWhile Gonorrhoea and Chlamydia contribute to approximately 20% of PID cases, various anaerobic bacteria are also implicated. In certain instances, no pathogen can be isolated. PID is predominantly spread via sexual contact.\n\n\n# Signs and Symptoms\n\n\nPID is typically diagnosed based on clinical symptoms and signs. These include:\n\n\n- Bilateral abdominal pain\n- Vaginal discharge\n- Post-coital bleeding\n- Adnexal tenderness\n- Cervical motion tenderness upon bi-manual examination\n- Fever\n\n\nApproximately 10% of patients present with right upper quadrant pain, secondary to inflammation of the liver capsule. This condition is referred to as Fitz-Hugh-Curtis syndrome (see below).\n\n\n# Differential Diagnosis\n\n\nSeveral conditions may present similarly to PID and should be considered in the differential diagnosis:\n\n\n- **Appendicitis:** Presents with right lower quadrant abdominal pain, fever, nausea, and vomiting.\n- **Ectopic Pregnancy:** Symptoms may include unilateral lower abdominal pain and vaginal bleeding. A positive pregnancy test is a key distinguishing factor.\n- **Endometriosis:** Chronic pelvic pain, dysmenorrhea, and dyspareunia are common. Pain typically worsens during menstruation.\n- **Ovarian Cyst:** Symptoms can include unilateral lower abdominal pain, bloating, and a palpable mass on examination.\n- **Urinary Tract Infection:** Symptoms usually include dysuria, frequency, urgency, suprapubic pain, and possible fever.\n\n\n# Investigations\n\n\nThe following investigations are usually carried out to diagnose PID:\n\n\n**Bedside:**\n\n\n- Bimanual examination, which may show cervical motion tenderness\n- Pregnancy test\n- Swabs for gonorrhoea and chlamydia, or urinary NAAT testing \n\n\n**Bloods:**\n\n\n- FBC, including WCC \n- CRP \n\n\n**Imaging:** \n\n- Transvaginal ultrasound\n\n\n# Management\n\n\nTreatment of PID is **medical** involves a combination of antibiotics, the first-line being:\n\n- Ceftriaxone (given intramuscularly) + doxycycline + metronidazole\n\n\nIf the infection is mild/moderate, these antibiotics are given orally (except ceftriaxone which is intramuscularly) and in an outpatient setting. \nIf the infection is severe, all three antibiotics are given intravenously (and may later be converted to oral) in an inpatient setting.\n\n\n\n\nIn addition, it is important to avoid unprotected intercourse whilst PID is untreated to prevent spread of infection to sexual partners.\n\n\n# Complications\n\n\nThe potential complications associated with PID are:\n\n\n- Chronic pelvic pain: This is likely a result of tubal damage, secondary to inflammation. \n- Infertility: Occurs as a result of tubal damage, impairing passage of an ovum and/or sperm for fertilisation to occur. \n- Ectopic pregnancy: Occurs as a result of tubal damage and scarring causing impaired passage of a fertilised ovum through to the endometrium. \n- Fitz-Hugh-Curtis Syndrome (see below). \n\n# Fitz-Hugh-Curtis Syndrome\n\n\nFitz-Hugh-Curtis syndrome occurs when adhesions form between the anterior liver capsule and the anterior abdominal wall or diaphragm in the context of PID. Despite this, liver function tests are usually normal. An abdominal ultrasound should be performed to rule out the presence of stones. A definitive diagnosis and treatment typically require laparoscopy and administration of antibiotics.\n\n\n# NICE Guidelines\n\n[Click here to see information on NICE about PID](https://cks.nice.org.uk/topics/pelvic-inflammatory-disease/)\n\n# References\n\n\n[Patient Info](https://patient.info/womens-health/pelvic-pain-in-women/pelvic-inflammatory-disease)",
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"question": "A 23-year-old woman with a history of recurrent sexually transmitted infections visits a genitourinary medicine clinic with increasing vaginal discharge. She also has right upper quadrant pain and deep dyspareunia.\n\nObservations are stable and a urine pregnancy test is negative. There is minimal tenderness to palpation of the abdomen.\n\nHigh vaginal swabs and a urine NAAT for chlamydia, gonorrhoea, and mycoplasma are sent.\n\nWhat is the most appropriate course of management?",
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"explanation": "Amiodarone is not yet indicated. This may be administered after the third shock.",
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"explanation": "# Summary \n\nVentricular Tachycardia (VT) is a regular broad complex tachycardia that originates from the ventricles of the heart. The patient may have a pulse or not - if VT is pulseless it is one of the shockable cardiac arrest rhythms. Emergency management involves identification of VT on an ECG or heart monitor, then treating patients with a pulse and no adverse features with IV amiodarone. Patients who do not respond to this or have adverse features should be treated with synchronised DC cardioversion. Patients in cardiac arrest with VT should be treated as per the Advanced Life Support (ALS) algorithm with cardiopulmonary resuscitation (CPR), adrenaline and amiodarone as well as unsynchronised shocks. \n\n# Definition\n \nVentricular Tachycardia (VT) is a type of broad complex tachycardia characterised by a heart rate of more than 100 bpm and a QRS width of more than 120ms. Other types of broad complex tachycardias include Torsades de Pointes (which is a type of ventricular tachycardia described as polymorphic, where there are multiple ventricular foci) and Supraventricular Tachycardia with aberrant conduction.\n \n[lightgallery]\n \n\n# Aetiology\n \nFactors that increase the risk of VT include:\n \n- Electrolyte abnormalities such as hypokalaemia and hypomagnesaemia\n- Structural heart disease including previous myocardial infarction and cardiomyopathies\n- Drugs that cause QT prolongation e.g. clarithromycin, erythromycin (for Torsades de Pointes) \n- Inherited channelopathies e.g. Romano-Ward syndrome (for Torsades de Pointes)\n\n# Management\n \n**Pulseless VT:**\n\nPulseless VT is one of the four cardiac arrest rhythms, as so is managed as per Advanced Life Support guidelines:\n\n- CPR will be in progress\n- 120-360 J unsynchronised shock should be administered as early as possible, then every 2 minutes\n- IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock\n- Adrenaline should be administered every 3-5 minutes thereafter\n- A further dose of amiodarone 150 mg IV should be given after 5 shocks\n\n**Pulsed VT with adverse features:**\n\nIf a patient has a pulse, management is determined by whether they have any of the following adverse features:\n\n - Heart failure\n - Myocardial ischaemia (chest pain)\n - Shock\n - Syncope\n\nIf one or more of these are present, attempt to cardiovert the patient using synchronised DC shocks (up to 3 attempts). If the patient is conscious this will require sedation or anaesthesia.\n\nIf this is not effective, an amiodarone infusion would be the next step under expert guidance (300mg IV over 10-20 minutes followed by 900mg infusion over 24 hours).\n\n**Pulsed VT with no adverse features:**\n\nFirst line treatment is amiodarone 300mg IV over 10-60 minutes.\n\nIf this is ineffective then attempt to cardiovert using synchronised DC shocks (up to 3 attempts) with sedation or anaesthesia.\n\n**Torsades de Pointes:**\n\nThis is a special situation which is managed differently to monomorphic VT - Torsades de Pointes often self-terminates but the risk is that it deteriorates into ventricular fibrillation (causing cardiac arrest).\n\nIV Magnesium is the mainstay of treatment, along with treatment of any underlying cause identified (e.g. correcting electrolyte imbalance, stopping QT-prolonging medications).\n\n# References\n \n[Resuscitation Council UK - Adult advanced life support Guidelines](https://www.resus.org.uk/library/2021-resuscitation-guidelines/adult-advanced-life-support-guidelines)\n\n[Resuscitation Council UK - Adult Tachycardia Algorithm](https://www.resus.org.uk/sites/default/files/2021-04/Tachycardia%20Algorithm%202021.pdf)\n\n[Patient UK - Torsades de Pointes](https://patient.info/doctor/torsades-de-pointes)",
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"question": "A patient admitted to the resuscitation room of the emergency department is being examined when the cardiac monitor alarms. The trace monitor shows new ventricular tachycardia (previously sinus rhythm). There is no pulse present.\n\nWhat is the most appropriate action to take?",
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"explanation": "This likely will be requested to detect any signs of a head injury given the lack of a history, however it is not the most important next step.",
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"explanation": "This may be necessary as he is twitching which may represent seizure activity, but hypoglycaemia must be excluded first.",
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"explanation": "# Summary\n \nStatus epilepticus is defined as either continuous or recurrent seizure activity that lasts for more than 5 minutes. It can be convulsive or non-convulsive, with the latter form being more difficult to recognise. It is a medical emergency that can be fatal or lead to permanent neurological damage. Management follows an algorithm which involves early administration of anticonvulsants starting with benzodiazepines. Looking for reversible causes (e.g. hypoglycaemia) and ensuring that the seizure is timed to allow prompt drug administration are both important aspects of management. \n \n\n# Definition\n \nStatus epilepticus (SE) refers to a prolonged period of seizure activity of any time (i.e. convulsive or non-convulsive). **Established** SE is used to describe seizures lasting for 30 minutes or longer (without any episodes of complete recovery in between seizures), whereas in clinical practice any seizure activity which has not terminated within 5 minutes is considered SE.\n\n# Aetiology\n\nIn one third of patients, SE is the first presentation of chronic epilepsy. \n\nOne third of patients presenting with SE already have a known background of epilepsy - the following may trigger prolonged seizures:\n\n- A withdrawal or change in antiepileptic medications\n- Non-compliance with antiepileptic medications\n- Seizure threshold-lowering medications (e.g. tramadol) \n- Intercurrent illness\n- Metabolic abnormalities (e.g. hyponatraemia)\n\nAnother third of patients do not have epilepsy - the following may be factors causing seizures:\n\n- Infection (e.g. cerebral abscess or encephalitis)\n- Brain injury (e.g. trauma, stroke, subarachnoid haemorrhage)\n- Withdrawal from drugs such as alcohol or benzodiazepines\n\n# Signs and Symptoms\n\n**Convulsive status epilepticus:**\n\n- Abrupt generalised muscle stiffening (tonic phase) followed by rhythmic jerking of the muscles (clonic phase)\n- Loss of consciousness\n- Tongue biting - typically lateral tongue\n- Urinary or faecal incontinence\n- Clenched jaw\n- Erratic eye movements\n- Drooling\n- Cyanosis\n\n**Non-convulsive SE:**\n\n- Reduced levels of consciousness\n- Catatonia\n- Behavioural changes/psychosis\n- Subtle motor signs e.g. myoclonus, eye deviation or twitching\n- Autonomic dysfunction\n- Speech disturbance e.g. aphasia or perseveration\n\n# Differential Diagnosis\n\nThe main differential for convulsive SE is **non-epileptic seizures** - these can be difficult to differentiate and may co-exist in patients with known epilepsy. Non-epileptic seizures typically last longer than epileptic seizures but often have the following features that would be atypical in a true seizure:\n\n- Eyes closed\n- Emotional vocalisations e.g. crying or screaming \n- Limbs moving in phase with each other\n- Head and trunk moving side to side\n- Pelvic thrusting\n- React to external stimuli e.g. noises\n- Incontinence and tongue biting rare\n\n**Rigors** and **acute dystonic reactions** may also share some features of abnormal movements however they are usually distinguishable by the quality of the movements and the duration.\n\nNon-convulsive SE has many differentials and EEG is often required to help with diagnostics - the following are some examples:\n\n- Encephalitis \n- Hypoglycaemia\n- Psychogenic pseudocoma\n- Alcohol or benzodiazepine withdrawal\n- Transient global amnesia\n- Stroke\n\n# Investigations\n \n**Bedside tests:**\n\n- **Capillary blood glucose** for hypoglycaemia\n- **Blood gas** for electrolytes, lactate and acid-base status\n- **Urine toxicology screen** if illicit drug use is suspected (may also test blood for this)\n- **Pregnancy test** if woman of childbearing age as many antiepileptic medications are teratogenic\n- **ECG** as some medications used require cardiac monitoring (e.g. phenytoin), may see other signs of triggers such as electrolyte imbalance or subarachnoid haemorrhage\n\n**Blood tests:**\n\n- **Full blood count and CRP** for inflammatory markers\n- **U&Es, bone profile and magnesium** for electrolyte derangement\n- **LFTs** as a baseline prior to starting anticonvulsant medications\n**Clotting screen** as intracranial haemorrhage may be a trigger\n- **Serum anticonvulsant levels** if on antiepileptic medications\n- **Blood cultures** if febrile or other signs of septicaemia\n\n**Imaging:**\n\n- **CT head** may be done once patient stabilised if an intracranial cause is supected\n- **Chest X-ray** once seizure terminated if signs or symptoms of aspiration\n\n**Other tests:**\n\n- **EEG** is not usually required acutely but can be useful e.g. in the diagnosis of suspected non-convulsive SE\n- **Lumbar puncture** may be done after the patient is stabilised and seizures have terminated e.g. in suspected meningitis or subarachnoid haemorrhage\n\n# Management\n \n- As soon as a seizure is recognised, start a timer to time the seizure (crucial to ensure that medications are given on time and the patient is escalated appropriately)\n- Ensure the patient is in a safe place and the head is protected (e.g. by putting padding around them)\n- Insert an airway adjunct (e.g. nasopharyngeal airway) if safe to do so \n- Give high-flow oxygen via a non-rebreather mask\n- Check glucose and correct hypoglycaemia if present (give Pabrinex first if any suspicion of alcohol excess or malnutrition)\n- In cases of known epilepsy, check if the patient has a personalised emergency management plan - in most cases follow the below algorithm:\n\t- At **5 minutes** give 4 mg IV lorazepam (or rectal diazepam/buccal midazolam if no IV access)\n\t- At **10 minutes** repeat benzodiazepine as above\n\t- At **15 minutes** give an IV infusion of one of levetiracetam, phenytoin or valproate (if still no IV access gain intraosseous access)\n\t- If this is unsuccessful consider one of the other second-line treatments; phenobarbital is also an option\n\t- At **30 minutes** ongoing seizures are considered **refractory SE** which is treated with induction and maintenance of general anaesthesia (usually with propofol and/or midazolam)\n\nOnce the seizure has terminated:\n\n- Reassess the patient to identify any complications (e.g. aspiration)\n- Treat any identified underlying cause (e.g. intercurrent infection or electrolyte imbalance)\n- Ensure appropriate antiepileptic medications are prescribed - neurology advice may be required \n\n**Note** - non-convulsive SE is treated with similar medications (e.g. benzodiazepines and anticonvulsants) but may be difficult to diagnose and so treatment is often delayed - see below references for further details.\n\n# NICE Guidelines\n\n[NICE - Treating Status Epilepticus](https://www.nice.org.uk/guidance/ng217/chapter/7-Treating-status-epilepticus-repeated-or-cluster-seizures-and-prolonged-seizures)\n\n[NICE CKS - Epilepsy](https://cks.nice.org.uk/topics/epilepsy/)\n\n# References\n \n[RCEM Learning - Status Epilepticus](https://www.rcemlearning.co.uk/reference/status-epilepticus/)\n\n[Patient UK - Status Epilepticus Management](https://patient.info/doctor/status-epilepticus-management)\n\n[Life in the Fast Lane - Differential Diagnosis of Seizures](https://litfl.com/seizures-ddx/)\n\n[Life in the Fast Lane - Non-convulsive Status Epilepticus](https://litfl.com/non-convulsive-status-epilepticus-ncse/)",
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"question": "A homeless man with no identification is conveyed to the emergency department by ambulance after suffering mutliple seizures. He has been given a dose of buccal midazolam and intravenous lorazepam with the ambulance service. He smells of alcohol and is intermittently twitching.\n\nWhat is the most important next step?",
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"explanation": "There is little high quality evidence for therapeutic hypothermia, and some evidence of harm. Normothermia should be promoted.",
"id": "10017365",
"label": "e",
"name": "Cool the head (therapeutic hypothermia)",
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"explanation": "A higher blood pressure should be maintained to ensure the brain is adequately perfused.",
"id": "10017364",
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"explanation": "Patients with brain injuries should be deeply sedated to reduce metabolic demands and reduce distress, which helps lower intracranial pressure and thus the risk of brain herniation.",
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"explanation": "This is the correct answer. This position helps to reduce intracranial pressure, and thus the risk of brain herniation.",
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"explanation": "A lower PaCO2 is usually achieved through hyperventilation. A lower PaCO2 causes vasoconstriction in the cerebral arterioles, moderately reducing cerebral perfusion, and thus ICP.",
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"name": "Aim for a PaCO2 of 6 mmHg",
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"comment": "Can someone explain why is the first one not correct if controlled hyperventilation can lower ICP please? ",
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"comment": "the PaCO2 is 6 here which is at the upper end of normal; to produce the cerebral vasoconstriction you would have to aim for a pCO2 at the lower end of normal :)",
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"explanation": "# Summary\n \nHead injury is a common emergency presentation that ranges in severity from mild trauma with no brain injury to life-threatening intracranial bleeds. NICE has clear criteria for who should be assessed in hospital and what scenarios warrant a CT head. The guidance states in what circumstances this should be done within an hour (e.g. Glasgow Coma Scale 12 or less on initial assessment) and when this should be done within 8 hours (e.g. anyone aged 65 or over with a head injury). Management depends on the severity of injury identified and may be conservative (e.g. observation alone), medical (e.g. management of raised intracranial pressure) and/or surgical (e.g. evacuation of an intracranial haemorrhage).\n\n# Epidemiology\n \nHead injury is the commonest cause of death and disability in people aged 1 to 40 years old in the UK. However, 90% of head injuries that present to A&E are minor, with 0.2% of patients dying as a result of the injury (most of whom have low Glasgow Coma Scale (GCS) scores).\n\n# Aetiology\n \nMany forms of trauma can lead to a head injury, including:\n\n- Road traffic accidents\n- Falls (considered a dangerous mechanism of injury if height greater than 1 metre or 5 steps) \n- Assault (including non-accidental injury in babies and children)\n- Sports injuries\n- Accidents at work\n\n# Classification\n\nNot all head injuries lead to **traumatic brain injury** (when neurological function is impacted by the injury).\n\nTraumatic brain injuries can be categorised as mild (also known as concussion), moderate and severe depending on the patient's GCS as follows:\n\n- Mild - GCS 14-15\n- Moderate - GCS 9-13\n- Severe - GCS 3-8\n \n# Signs and Symptoms\n\nSymptoms of head injury include:\n\n- Pain in the head or neck\n- Loss of consciousness or drowsiness\n- Confusion or amnesia\n- Seizures\n- Vomiting\n- Changes to vision or hearing\n- Neurological symptoms such as weakness, sensory changes, ataxia or difficulty speaking\n\nSigns include:\n\n- External injuries e.g. scalp lacerations or haematoma\n- Retinal haemorrhages or papilloedema on fundoscopy\n- Unequal or unreactive pupils \n- Cranial nerve palsies (e.g. down and out pupil deviation in a oculomotor nerve palsy)\n- Signs of **basal skull fracture:**\n - Haemotympanum (blood behind the eardrum)\n - Periorbital haematomas\n - Cerebrospinal fluid otorrhea or rhinorrhea\n - Battle's sign (bruising over the mastoid process)\n- Cushing's triad of raised intracranial pressure:\n - Hypertension\n - Bradycardia\n - Irregular breathing\n- Decreased GCS\n- Cognitive impairment\n- Focal neurological signs\n \n\n# Differential Diagnosis\n \nThere is a wide range of injuries that can occur after head trauma:\n\n- **Concussion** i.e. mild traumatic brain injury which causes transient disturbance in brain functioning with symptoms of headache, dizziness, difficulty concentrating and confusion\n- **Intracranial haemorrhage** which can take multiple forms including extradural, subdural, subarachnoid or intracerebral haemorrhages (see separate chapters for details)\n- **Skull fracture:** which may be displaced or non-displaced, and may be detected clinically if there is obvious deformity or other signs (e.g. of basal skull fracture) or on imaging\n- **Vascular injuries** e.g. arterial dissection secondary to skull base fracture, traumatic fistula formation or venous thrombosis\n- **Brain contusion** i.e. a bruise of the brain caused by its collision against the inner surface of the skull, causing haemorrhage, oedema and inflammation\n- **Secondary brain injuries** which is indirect injury to the parenchyma following the initial insult e.g. cerebral oedema or hypoxia\n\n \n# Investigations\n\n## CT Head Guidelines\n\nThe key investigation in head injury is a CT head - this is not required in every case but there are clear NICE guidelines on who requires imaging of what urgency as follows:\n\n**CT head should be done within 1 hour of presentation:**\n\n- GCS of 12 or less on initial assessment in the Emergency Department\n- GCS less than 15 2 hours after injury\n- Suspected open or depressed skull fracture\n- Signs of basal skull fracture as above\n- New focal neurology\n- More than 1 episode of vomiting\n- Post-traumatic seizure\n \n\n**CT head should be done within 8 hours of the injury (or within 1 hour if presenting later than this) in patients with any loss of consciousness or amnesia and one of:**\n \n- Aged 65 or older\n- Bleeding or clotting disorder\n- Dangerous mechanism of injury (e.g. hit by a car, fall down more than 5 steps)\n- More than 30 minutes of amnesia for events prior to the injury\n\n**Consider** a CT head within 8 hours of the injury in patients without any of the above but who are on anticoagulant or antiplatelet medications (except if taking aspirin alone).\n\n**Note - these guidelines apply to patients aged 16 and over; see references below for full NICE guidance including in paediatric patients**\n\n## Other Investigations\n\n**Bedside tests:**\n\n- **Capillary blood glucose** to rule out hypoglycaemia as a cause of reduced GCS\n- **Blood gas** especially if other traumatic injuries to look at haemoglobin and lactate\n- **ECG** as some intracranial injuries (e.g. subarachnoid haemorrhage) can cause cardiac abnormalities\n- **Toxicology screen** if drug intoxication is suspected\n\n**Blood tests:**\n\n- **Full blood count** for anaemia\n- **U&Es and LFTs** as a baseline prior to treatment\n- **Coagulation screen** to look for any bleeding diathesis\n- **Group and save** +/- crossmatch in case a blood transfusion is required\n\n**Imaging:**\n\n- Other imaging may be warranted for suspected injuries (e.g. a chest X-ray if suspecting traumatic pneumothorax)\n- **MRI head** is sometimes used after CT or in subacute presentations of head injury (e.g. if normal CT but ongoing clinical suspicions of traumatic brain injury)\n\n# Management\n \n**Conservative Management:**\n\n- Patients with mild head injuries who are GCS 15 with no concerning symptoms, signs or risk factors can be managed in the community with observation by a responsible adult for 24 hours and careful safety-netting regarding when to seek medical advice\n- Follow trauma algorithms (see ATLS chapter for more details) and ensure other injuries are assessed and managed appropriately\n- Intubation and ventilation may be required e.g. in patients with a GCS of 8 or less or irregular breathing \n- Assess for cervical spine injury and immobilise if needed (see spinal injury chapter for more details) \n- Consider safeguarding e.g. in suspected abuse or neglect and refer to appropriate teams\n- Regular neurological observations (half-hourly until GCS is 15)\n- Patients with significant injuries may need to be transferred to a specialist neurosurgical centre\n- In the longer term, multidisciplinary neurorehabilitation and social support are crucial for patients with ongoing disability as a result of traumatic brain injury\n\n**Medical Management:**\n\n- Resuscitation with IV fluids if hypotensive, oxygen if low saturations\n- Analgesia is crucial and helps with raised intracranial pressure \n- Consider tranexamic acid (2 grams IV bolus) in patients with a head injury and a GCS of 12 or less\n- Consider reversal of anticoagulation e.g. in intracranial haemorrhage (with haematology input as needed)\n- Medical treatment of seizures may be required (e.g. benzodiazepines)\n- Maintain normoglycaemia with insulin or dextrose\n- Monitor intracranial pressure and treat with hypertonic saline or mannitol, nurse with head elevated at 30 degrees\n\n**Surgical Management:**\n\n- Discuss the following patients with neurosurgery:\n - Significant injuries identified on CT head\n - GCS less than 8 despite resuscitation\n - Deterioration in GCS as an inpatient\n - Progressive focal neurology\n - Seizure without full recovery\n - Penetrating injury (e.g. a knife or gun wound)\n - Cerebrospinal fluid leak\n - Unexplained confusion for over 4 hours\n- Neurosurgical management depends on the nature of the injury identified (e.g. a craniectomy or craniotomy to facilitate evacuation of a large extradural or subdural haematoma)\n\n \n# Complications\n\n- **Herniation** occurs due to raised intracranial pressure and mass effect e.g. from a large intracranial bleed.\n - \"Coning\" is used to describe herniation of the cerebellar tonsils through the foramen magnum; this puts pressure on the brainstem causing respiratory arrest and death\n - The uncus of the temporal lobe can herniate through the tentorial notch - this causes compression of the oculomotor nerve leading to a unilateral \"blown pupil\"\n- **Hypopituitarism** occurs in 33-50% of people with traumatic brain injuries, especially moderate and severe injuries. This can present months after the initial injury and should be suspected in patients with hypotension or hyponatraemia.\n- **Post-traumatic seizures** are common especially after moderate or severe traumatic brain injury\n- **Permanent neurological deficits** include weakness, spasticity, contractures, dysarthria and dysphasia\n- **Mental health problems** including depression, anxiety and post-traumatic stress disorder are very common after traumatic brain injuries and can occur even if there is amnesia regarding the event.\n- **Cognitive impairment** is also common and ranges in severity; difficulties may be seen with memory, concentration, language, planning and challenging behaviours such as disinhibition.\n \n# NICE Guidelines\n\n[NICE - Head injury: assessment and early management](https://www.nice.org.uk/guidance/ng232)\n\n[NICE CKS - Head Injury](https://cks.nice.org.uk/topics/head-injury/)\n\n# References\n \n[Radiopaedia - Traumatic Brain Injury](https://radiopaedia.org/articles/traumatic-brain-injury?lang=gb)\n\n[Headway - The Brain Injury Association](https://www.headway.org.uk/)",
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"question": "A patient who has sustained a traumatic brain injury is intubated and ventilated on the intensive care unit, awaiting a neurosurgical opinion.\n\nWhat is the most appropriate management?",
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"explanation": "The most likely diagnosis is a tension pneumothorax causing respiratory and circulatory compromise. Immediate needle decompression should be undertaken.",
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"explanation": "Cardiac tamponade is a differential, however the absence of air entry over the right hemithorax and the desaturation makes this less likely. If a focussed echocardiogram demonstrates a tamponade, thoracotomy may be used to drain the blood.",
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"explanation": "Cardiac tamponade is a differential, however the absence of air entry over the right hemithorax and the desaturation makes this less likely. A focussed echocardiogram would be useful after the patient is stabilised. In trauma, a thoracotomy is preferred to pericardiocentesis, as the tamponade will re-accumulate.",
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"explanation": "Although the patient is hypotensive and tachycardic, this patient is likely in obstructive shock due to a tension pneumothorax. A fluid bolus will likely also be administered, but needle decompression is the priority.",
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"comment": "This is incorrect. New BTS guidelines suggest emergency thoracotomy into the triangle of safety is superior to needle decompression.",
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"comment": "especially in a major trauma centre, expertise should be available ",
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"comment": "thoracostomy is not the same as thoracotomy",
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"comment": "Why can't this be a hameothorax\n",
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"comment": "dangerously incorrect, may i add to 10 Jan 24 comment\n\n",
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"explanation": "# Summary\n \nA pneumothorax is characterised by the abnormal presence of air in the pleural cavity, which may be spontaneous or traumatic in origin. Key signs and symptoms include sudden-onset shortness of breath, pleuritic chest pain, reduced chest expansion and reduced or absent breath sounds on the affected side. Chest X-ray is the key diagnostic investigation (although in cases of tension pneumothorax the diagnosis should be clinical). Management decisions depend on the size of the pneumothorax, the patient's clinical condition and their wishes. Options include conservative management, needle aspiration, chest drain insertion or an ambulatory device. In cases of tension pneumothorax needle decompression is the initial emergency management.\n \n# Definition\n \nA pneumothorax refers to a collection of air in the pleural cavity which may cause collapse of the underlying lung parenchyma. \n\n# Classification\n\n- They may be **spontaneous** or **traumatic** (including iatrogenic causes).\n\n- Spontaneous pneumothoraces can be further divided into **primary** pneumothoraces (in patients without an underlying lung disease) and **secondary** (in patients with underlying lung diseases such as COPD or asthma).\n\n- Patients aged over 50 years old with a significant smoking history who present with a spontaneous pneumothorax are generally considered to have a secondary pneumothorax. \n\n- A **tension pneumothorax** occurs when the defect in the pleura that has led to the pneumothorax creates a one-way valve effect whereby air can enter the pneumothorax but not leave it.\n - This causes the pneumothorax to progressively expand, putting pressure on the heart and great vessels and causing **mediastinal shift**\n - This is a medical emergency that rapidly leads to cardiac arrest if untreated\n \n\n# Signs and Symptoms\n \nThere may be no signs or symptoms (small pneumothoraces may be detected incidentally on imaging) however in an emergency presentation these may include:\n\n- Sudden onset shortness of breath\n- Pleuritic chest pain\n- Dry cough\n- Tachypnoea and increased work of breathing\n\nThe following signs will be found on the affected side of the chest:\n\n- Unilateral reduced expansion\n- Unilateral hyper-resonance to percussion\n- Reduced or absent breath sounds\n- Reduced vocal resonance or tactile vocal fremitus\n \nPatients with a tension pneumothorax may also have:\n\n- Tracheal deviation to the contralateral side\n- Tachycardia\n- Hypotension\n- Distended neck veins\n\n# Investigations\n \nPatients with a suspected tension pneumothorax should be diagnosed and treated with needle decompression based on the clinical picture, with no delay for investigations.\n\nFor other patients, an **erect PA chest X-ray** is diagnostic. \n\n [lightgallery]\n \n\n [lightgallery1]\n \n**CT chest** should be used in high-risk patients where it is not clear from the chest X-ray whether it is safe to place a chest drain.\n\n**Arterial blood gases** are not usually indicated however they may be of use in certain situations e.g. titrating oxygen in a patient with COPD and low saturations.\n\n# Management \n\n**Tension Pneumothoraces:** \n\n- If a tension pneumothorax is suspected, emergency management is to decompress this by inserting a large-bore cannula into the second intercostal space on the affected side, mid-clavicular line, or fifth intercostal space, mid-axillary line if a traumatic cause is suspected, as per ATLS guidelines.\n\n\n- If this fails, open thoracostomy should be done immediately\n- After initial emergency decompression, a chest drain should be inserted\n\nFor **primary or secondary spontaneous pneumothoraces**, management is guided by the 2023 BTS Guidelines as summarised below:\n\n [lightgallery2]\n \n- **Conservative management** involves no intervention for the pneumothorax, and patients are monitored to ensure they do not deteriorate and any symptoms resolve\n- **Ambulatory devices** (e.g. pleural vents) are one-way valves which allow air to leave the pneumothorax but not re-enter it\n - They can be inserted in a simple procedure under local anaesthetic\n - Patients can then be followed up as outpatients\n- Symptomatic patients with larger pneumothoraces (usually 2cm or larger on CXR - CT may be used if unclear) or those with high-risk features (significant hypoxia, bilateral pneumothoraces, underlying lung disease, 50 or older with a significant smoking history, haemopneumothorax) require a **chest drain** and admission for monitoring\n- In symptomatic patients without high-risk features but with pneumothoraces large enough for treatment (2cm or larger), management depends on their priorities\n - Conservative management allows avoidance of any procedure\n - Both needle aspiration and ambulatory devices offer more rapid symptomatic relief (ambulatory device insertion may not be available in all hospitals) \n\n\n**Follow up:**\n\n- All patients should be reviewed in an outpatient clinic 2–4 weeks after presenting with a pneumothorax (with repeat chest imaging)\n- Patients should be advised on smoking cessation if relevant\n - Advise patients not to fly until 7 days after chest imaging has confirmed resolution of the pneumothorax\n - Advise patients they should not take part in underwater diving for life (except in rare cases where they have been treated with bilateral open surgical pleurectomy)\n \n# References\n \n[British Thoracic Society Guidelines](https://thorax.bmj.com/content/thoraxjnl/78/11/1143.full.pdf)\n\n[Royal College of Emergency Medicine - Spontaneous Pneumothorax](https://www.rcemlearning.co.uk/reference/spontaneous-pneumothorax/)\n\n[Radiopaedia - Tension Pneumothorax](https://radiopaedia.org/articles/tension-pneumothorax)\n\n[Pleural Vent Ambulatory Devices](https://www.nth.nhs.uk/resources/pleural-vent-ambulatory-device/)",
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"question": "A 29-year-old man is taken to a major trauma centre after a high-speed car accident. They are having a CT scan of the entire body, when they deteriorate.\n\nObservations show:\n\n* Heart rate 113 beats/minute\n\n* Blood pressure 90/59 mmHg\n\n* Respiratory rate 32 breaths/minute\n\n* Oxygen saturations 88% on 15 litres/minute oxygen (non-rebreather mask)\n\nOn examination, he is cyanosed. There is absent air entry across the right side of the thorax.\n\nWhat is the most appropriate next step to take?",
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"explanation": "Fever in a patient undergoing chemotherapy should be taken seriously. This patient is at high risk for neutropenic sepsis, which suually presents 7-10 days after chemotherapy, when neutrophils are at their lowest. He requires urgent inpatient investigation and intravenous antibiotics through an emergency admission to hospital.",
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"name": "Reassure this is likely a viral infection and discharge with safety-netting",
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"explanation": "While an urgent full blood count will be required to check the neutrophil count, this should not be undertaken in the GP surgery. The priority should be admitting the patient to hospital for IV antibiotics. The GP is unlikely to be able to receive the results of blood tests in time to act on them in an emergency situation.",
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"explanation": "Fever in a patient undergoing chemotherapy should be taken seriously. This patient is at high risk for neutropenic sepsis, which suually presents 7-10 days after chemotherapy, when neutrophils are at their lowest. He requires urgent inpatient investigation and intravenous antibiotics. Local guidelines vary, but the antibiotic of choice is usually IV piparicillin/tazobactam (in patients without a penicillin allergy).",
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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 patient presents to his GP feeling generally unwell. He has a background of Burkitt's lymphoma, for which he received chemotherapy 8 days ago. Observations show:\n\n* Heart rate 83 beats/minute\n\n* Blood pressure 132/83 mmHg\n\n* Respiratory rate 13 breaths/minute\n\n* Temperature 38.2 degrees Celcius\n\nOn examination, he looks tired but has no other signs of note.\n\nWhat is the most appropriate next step in management?",
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"explanation": "The patient's presentation is suggestive of hypercalcaemia caused by malignancy, which is likely leading to abdominal pain. There are no specific examination findings (e.g. right upper quadrant pain) mentioned that immediately warrant an ultrasound scan.",
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"explanation": "While brain metastases may account for the confusion and these may be seen on CT, the next best investigation would be a bone profile to check whether the symptoms are due to hypercalcaemia. A simple blood test is both quicker and easier than performing imaging.",
"id": "10017378",
"label": "c",
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"explanation": "While brain metastases may account for the confusion and these may be seen on MRI, the next best investigation would be a bone profile to check whether the symptoms are due to hypercalcaemia.",
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"comment": "I mean kidney stone is a sign of hypercalcaemia and severe abdominal pain (when we aren't told where in the abdomen) could be an indication of a colicky picture so CT KUB sounds plausible here",
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"comment": "and if my grandma had wheels, she'd be a bike",
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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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"learningPoint": "In metastatic breast cancer, a bone profile, including calcium, phosphate, alkaline phosphatase (ALP), and albumin, is performed to assess bone involvement and detect complications such as bone metastases, hypercalcemia, or changes in bone density.",
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"question": "A 55-year-old woman with a background of metastatic breast cancer is admitted to hospital due to severe abdominal pain. She is being treated with hormonal therapy (letrozole) and her disease has been stable for the past few years.\n\nShe becomes increasingly confused and agitated on the ward. Her family also notice she has become more thirsty.\n\nWhich of the following is the next best investigation to perform?",
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"explanation": "NICE recommend lifestyle modification measures in the first instance for patients who have a QRISK score of over 10%. If these are ineffective in lowering cholesterol, a statin should be offered.",
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"explanation": "This is inappropriate as her QRISK score (which is a measure of the risk of a cardiovascular event) is over 10%. She should be encouraged to engage in lifestyle modification measures. If these are ineffective, a statin may be offered.",
"id": "10017388",
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"explanation": "This is inappropriate. Aspirin has no role in the primary prevention of strokes.",
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"explanation": "This may well be required if lifestyle modification does not lower her cholesterol, however NICE recommend lifestyle measures in the first instance. Statins may be offered if the QRISK is above 10% and lifestyle modification is inappropriate/ineffective.",
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"comment": "https://cks.nice.org.uk/topics/cvd-risk-assessment-management/management/cvd-risk-10percent-or-more/\n --> Discuss the benefit of lifestyle modifications and optimize the management of all other modifiable CVD risk factors, including any relevant comorbidities that may not be optimally treated.\nOffer the opportunity to reassess CVD risk again after they have tried to change their lifestyle. \nRecognise that some people may need support to change their lifestyle — to help, refer them to programmes such as exercise referral schemes or smoking cessation services.\n-->Offer statin treatment after risk assessment if lifestyle modification is ineffective or inappropriate.",
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"explanation": "# Definition\n\nHypercholesterolaemia is the term used to denote raised serum levels of one or more of total cholesterol.\n\n# Causes\n\nCauses can primary or secondary.\n\nSecondary causes include:\n\n- Familial dyslipidaemias\n- Familial hypercholesterolaemia\n- Apoprotein disorders\n- Medical conditions\n\t- Hypothyroidism\n\t- Obstructive jaundice\n\t- Cushings syndrome\n\t- Nephrotic syndrome\n\t- Chronic Kidney Disease\n- Drugs e.g. thiazide diuretics, glucocorticoids, ciclosporin\n- Pregnancy\n- Obesity \n- Alcohol abuse\n\n\n# Physicial signs\n\nDiagnosis is usually biochemical. \n\nThere are two key physical signs which may indicate familial hypercholesterolaemia\n\n - Premature arcus senilis\n - Tendon xanthomata\n\n# Investigations\n\n- Lipid profile \n- Fasting blood glucose\n- Renal function\n- Liver function tests\n- Thyroid function tests\n\n# Management\n\n\n## Statins\n\n- Statins are the first line treatment of high cholesterol. \n- They are HMG-CoA reductase inhibitors. \n- This enzyme plays a key role in the production of cholesterol, so inhibiting it reduces the cholesterol in the body.\n- In patients with high cholesterol, the QRISK score is used to see if they would benefit from statins as primary prevention against cardiovascular disease. \n- If an adult is under 80 years old and their QRISK is greater than 10% then a statin should be offered. \n- For primary prevention of CVD aim for a greater than 40% reduction in non-HDL cholesterol\n- For secondary prevention of CVD, aim for low-density lipoprotein (LDL) cholesterol levels of 2.0 mmol per litre or less, or non-HDL cholesterol levels of 2.6 mmol per litre or less.\n\n## Doses\n\n- Atorvastatin 20mg is the usual starting dose for primary prevention.\n- For patients who need a statin as secondary prevention, e.g following a stroke, heart attack, peripheral arterial disease or angina, atorvastatin at 80mg starting dose should be used.\n\n## Side effects of statins\n\n\nCommon side effects of statins include muscle pain, abdominal pain, constipation and headache.\n\nIf a patient is struggling with significant myalgia, this may indeed indicate a myositis. Creatinine Kinase can be measured and if it is 5-10 times the upper limit of normal, the statin should be stopped. \n\nStatins can also cause abnormal liver function so this should be monitored with a repeat blood test in 4-6 weeks time. If the transaminases (ALT, AST) are 3 times the upper limit the statin should be stopped.\n\nOffer ezetimibe instead of a statin to people for whom statins are contraindicated/cause abnormal blood test results.\n\n# NICE Guidelines\n\n[NICE Guidelines - Cardiovascular disease: risk assessment and reduction, including lipid modification ](https://www.nice.org.uk/guidance/ng238/chapter/Recommendations)",
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"question": "A 68-year-old woman visits her GP as she is concerned about her risk of having a stroke, as her brother has just suffered a transient ischaemic attack.\n\nShe currently takes no medication, and her QRISK 3 score is calculated as 13%. Blood tests show a mildly raised total cholesterol level, with a normal HbA1c and liver function tests.\n\nWhat is the most appropriate next step to take?",
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"explanation": "This is inappropriate as the diagnosis of hypertension (and need for treatment) should be established first. A thiazide-like diuretic would not be the first-line medication to prescribe in this case, if drug treatment is required.",
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"explanation": "This is inappropriate as the diagnosis of hypertension (and need for treatment) should be established first. A calcium channel blocker would not be the first-line medication to prescribe in this case, as the patient is under 55 and is not of black AFrican/African Caribbean family origin.",
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"explanation": "This is inappropriate as the diagnosis of hypertension (and its stage) should be established first. Secondary causes should be considered if there are signs/symptoms of an underlying condition, the patient is young (<40 years old), hypertension is severe, or if it fails to respond to drug therapy.",
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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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"id": "10035735",
"label": "d",
"name": "150 micrograms IM adrenaline",
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"answer": false,
"explanation": "Bronchoconstriction can cause respiratory distress in infants, however a wheeze rather than stridor would be found on examintation. The history and examination is more consistent with an inhaled foreign body.",
"id": "10035733",
"label": "b",
"name": "Nebulised salbutamol",
"picture": null,
"votes": 722
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{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The history and examination is consistent with an inhaled foreign body. The immediate management is a rigid bronchoscopy to remove it. Foreign body inhalations are often unwitnessed in children and it is an important differential for anyone presenting with stridor and respiratory distress. Although not common practice, this question has appeared in previous writers' MLA AKT exams so we have included it in our bank.",
"id": "10035732",
"label": "a",
"name": "Rigid bronchoscopy",
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"comment": "Would CXR be indicated at all?",
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"comment": "If it's already suspected that the kiddy has eaten the forbidden plastic chocolate brick then you are already there with the grabber to remove it with a bronchoscopy. A CXR would only confirm the diagnosis but exposure them to extra radiation and you would still need to go in with the scope. Hope this helps / makes sense :D ",
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"comment": "thanks uncs",
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"explanation": "# Summary\n\nForeign Body Ingestion (FBI) refers to the swallowing of objects that are not intended to be ingested. Clinical manifestations vary from being asymptomatic to significant morbidity, including esophageal obstruction or perforation, depending on the type and location of the foreign body. Most instances can be managed conservatively, but high-risk objects may necessitate invasive interventions such as endoscopy or open surgery. High-risk objects include batteries, large objects, absorbent materials, magnets swallowed with metal objects, lead-based objects, and objects containing toxins.\n\n# Definition\n\nForeign Body Ingestion is a common pediatric complaint and involves the swallowing of objects not intended for ingestion. While most foreign bodies pass harmlessly through the gastrointestinal tract, some can cause significant complications.\n\n# Epidemiology\n\nForeign Body Ingestion is a prevalent issue among children, particularly those between the ages of six months to three years. This high incidence is attributed to their oral exploratory behavior. Most ingested objects pass spontaneously without causing complications, but a subset may pose a significant health risk.\n\n# Aetiology\n\nObjects often ingested include coins, toys, jewelry, batteries, and food items. The list of potentially ingestible items is virtually limitless but varies based on cultural, environmental, and individual factors. High-risk objects include batteries, large objects that may become trapped at the pylorus, absorbent materials that may cause obstruction, magnets swallowed with metal objects, lead-based objects, and objects containing toxins.\n\n# Signs and Symptoms\n\nThe clinical presentation can range from asymptomatic to significant morbidity. Symptoms include, but are not limited to:\n\n- Drooling\n- Difficulty swallowing or painful swallowing\n- Refusal to eat\n- Chest, throat, or abdominal pain\n- Vomiting\n- Blood in the stool\n\nThe onset and type of symptoms can be influenced by the size, shape, location, and nature of the foreign body.\n\n# Differential Diagnosis\n\nConsider the following conditions in a patient presenting with symptoms suggestive of foreign body ingestion:\n\n- Gastroenteritis: Characterized by nausea, vomiting, diarrhea, abdominal pain.\n- Esophagitis or Gastritis: These could present with similar symptoms of painful swallowing, refusal to eat, and abdominal pain.\n- Appendicitis: Presents with abdominal pain, loss of appetite, nausea, and vomiting.\n- Esophageal stricture or tumor: Can present with difficulty swallowing, chest pain, weight loss, and regurgitation of food or fluids.\n\n# Investigations\n\nInvestigations are unnecessary in an asymptomatic child with a low-risk ingestion. In symptomatic patients or those who have ingested high-risk objects, investigations may include:\n\n- Plain radiography: Most commonly used and can detect radio-opaque objects.\n- Computed Tomography (CT): Offers better sensitivity and specificity for detecting radiolucent foreign bodies.\n- Direct visualization with endoscopy: Useful when there is a high index of suspicion, even if radiological studies are negative.\n\n# Management\n\nThe majority of foreign bodies that are swallowed can be managed conservatively, including observation and symptomatic treatment. High-risk objects such as batteries, sharp objects, or large objects may require endoscopic or surgical removal. Clinicians should provide clear discharge instructions regarding potential complications and when to seek immediate medical attention.\n\n# References\n\n[BMJ Best Practice: Foreign Body Ingestion](https://bestpractice.bmj.com/topics/en-gb/1050)",
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"question": "A 10-month old girl is rushed into the Emergency Department with sudden onset cough, respiratory distress, and noisy breathing. This started 20 minutes ago whilst at a playdate, and she had previously been well. On examination she is making a high-pitched inspiratory sound whilst breathing and is coughing ineffectively. There is no wheeze, rash, or angioedema. Her respiratory rate is elevated at 48 (30-40) and she is tachycardic at 152 bpm (80-140), her other vital signs are normal.\n\nWhat is the most appropriate management?",
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"explanation": "This is only indicated in tonsillitis that is very severe and impairs the patient's ability to swallow which is not the case here.",
"id": "10035811",
"label": "e",
"name": "IV maintenance fluids",
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"explanation": "This patient is presenting with features of tonsillitis. As his Centor score is only 2 (tonsillar exudate and absence of a cough) antibiotics are not warranted currently. Antibiotics are only given if the Centor score is 3 or above. Therefore, this patient requires analgesia and appropriate safety netting to return in case the symptoms do not resolve. \n\n[NICE guidelines](https://www.nice.org.uk/guidance/ng84/chapter/Recommendations) currently advise using the **original** Centor scoring criteria, which **does not include age.** The modified/McIsaac Centor score, which is available via MDCalc however, does include age, which is why some users may have calculated this patient's score as 3.\n",
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"explanation": "This patient has a Centor score of 2 and therefore, they do not warrant antibiotics. Oral clarithromycin would be an option if they had a Centor score of 3 or more and a penicillin allergy.",
"id": "10035810",
"label": "d",
"name": "Oral clarithromycin",
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"votes": 234
},
{
"__typename": "QuestionChoice",
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"explanation": "This patient has a Centor score of 2. Therefore, antibiotics are not warranted. IV antibiotics would be used if the patient were septic or had severe consequences from the tonsillitis that impaired their ability to swallow safely.",
"id": "10035808",
"label": "b",
"name": "IV co-amoxiclav",
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"votes": 68
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"answer": false,
"explanation": "This patient has a Centor score of 2 and therefore, does not warrant antibiotics. Oral penicillin V would be used if they had a Centor score of 3 or more.",
"id": "10035809",
"label": "c",
"name": "Oral penicillin V",
"picture": null,
"votes": 4641
}
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{
"__typename": "QuestionComment",
"comment": "the one thing medicine gave me was teaching me how to finesse the system with a telephone call to get abx for my recurrent tonsillitis",
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"comment": "Isnt the centor score 3 because of the age as well??? \n+1 age between 3-14, +1 exudate, +1 no cough",
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"comment": "Only modified Centor includes age which NICE doesn't use :(",
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"comment": "If you use FEVERPAIN score then is score = 4...consider abx",
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"comment": "Exactly :’)",
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"comment": "Need to spend more time in GP",
"createdAt": 1718976723,
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"comment": "its just 3 (purulent tonsils, inflamed tonsils, no cough) 2-3 is apparently a delayed abx prescription so giving PenV now is wrong i guess?",
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"comment": "I work in OOH...",
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"comment": "fever, tonsilar exudate, no cough - I count 3..",
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"comment": "Temp is 37.4 so not considered a fever",
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"explanation": "# Summary\n \nTonsillitis is an acute inflammation of the tonsils, often with a purulent exudate in bacterial cases. The most common cause of tonsillitis are viruses, however, the most common bacterium causing tonsillitis is Streptococcus pyogenes (group A streptococcus). The CENTOR criteria can be used to determine the likelihood of a bacterial infection, and management of bacterial tonsillitis often involves antibiotic treatment. Key signs and symptoms can include tonsillar exudate, tender anterior cervical lymphadenopathy, fever over 38 degrees Celsius, and absence of a cough. \n \n# Definition\n \n\nTonsillitis is a form of pharyngitis characterised by acute inflammation of the tonsils, often with a purulent exudate present in bacterial tonsillitis.\n \n\n# Epidemiology\n \n\nIn the UK, tonsillitis is a common condition that predominantly affects children and adolescents, with an estimated 7.4% of GP consultations for children under 15 years involving a sore throat or tonsillitis as the primary reason for the visit.\n \n\n# Aetiology\n \n\nThe most common causative organism of tonsillitis is Streptococcus pyogenes (group A streptococcus). Epstein-Barr virus (EBV) is another common cause.\n \nRisk factors for tonsillitis include:\n \n - Age 5-15 years\n - Immunodeficiency \n - Family history of tonsillitis \n - Close contact with an infected individual \n \n\n# Signs and Symptoms \n \n - Sore throat \n - The child may also complain of referred pain in the ears or a headache \n - Changes to the sound of the child's voice or cry \n - Purulent and inflamed tonsils\n - Lymphadenopathy \n \n\n# Differential Diagnosis\n \n\nDifferential diagnoses for tonsillitis include the following:\n \n\n - **Bacterial Tonsillitis**: Main signs and symptoms include cervical lymphadenopathy, tonsillar exudate, and fever.\n - **Viral Tonsillitis**: Symptoms are often milder, and accompanied by coryzal symptoms (i.e. cough, rhinorrhoea). \n - **Infectious Mononucleosis**: Also known as glandular fever, this is more common in teenagers. This presents with enlarged tonsils, fatigue and occasionally with splenomegaly. \n - **Hand, foot and mouth disease**: This is caused by the Coxsackie virus, and will feature blisters on the tonsils and roof of the child's mouth. Blisters may also be found on the feet and hands.\n \n\n# Investigations\n \n\nThe CENTOR criteria can be used to indicate the likelihood of a sore throat being due to a bacterial infection. The criteria are as follows:\n \n\n 1. Tonsillar exudate\n 2. Tender anterior cervical lymphadenopathy\n 3. Fever over 38 degrees Celsius\n 4. Absence of a cough\n \n\n [lightgallery]\n \n\nEach of the CENTOR criteria scores 1 point, with a maximum score of 4. A score of 0, 1 or 2 is thought to be associated with a 3 to 17% likelihood of isolating Streptococcus. A score of 3 or 4 is thought to be associated with a 32 to 56% likelihood of isolating Streptococcus.\n\nAlternatively, the FeverPAIN score can be used. The criteria for this include:\n\n- **Fever**\n- **P**us on tonsils\n- **A**ttended within 3 days of symptom onset\n- **I**nflamed tonsils\n- **N**o cough or coryza \n\nDiagnosis is usually clinical, however, in some cases, further investigations may include:\n\n- Throat swab for microscopy and culture\n- Monospot (heterophile antibody) test for glandular fever \n \n\n# Management\n \n\nBacterial tonsillitis with a CENTOR criteria score of 3/4, FeverPAIN score of 4 or 5, or evidence of systemic upset/immunosuppression warrants prescribing antibiotics:\n \n\n- 1st line: Penicillin V PO QDS for 5-10 days\n - Dose is dependent on age, see BNFc for dosing \n- Alternative in penicillin allergy: Clarithromycin/Erythromycin PO BD for 5 days\n - Dose is dependent on age, see BNFc for dosing \n\nFor patients with a CENTOR score of 0-2 or FeverPAIN score of 0 or 1:\n\n- Advise that antibiotics are not needed as they do not tend to alter how long symptoms last and may cause side effects such as diarrhoea and nausea.\n- Conservative management including paracetamol for analgesia and ensuring adequate fluid intake. \n\nIf the child is systemically very unwell or has severe complications, consider referring the child to the hospital. \n\n# Complications\n\n- Quinsy (peritonsillar abscess)\n- Acute otitis media \n- If tonsillitis is due to Group A beta haemolytic step:\n - Rheumatic fever\n - Syndenham's chorea \n - Glomerulonephritis \n - Scarlet fever \n\n# Prognosis \n\nTonsillitis is usually self-resolving within 3-4 days. Some children will have recurrent tonsillitis, and this recurrence may be reduced by smoking cessation for the parents or through tonsillectomy. \n\nTonsillectomy may be indicated for severe recurrent tonsillitis (more than 7 episodes/year for one year, more than 5 episodes/year for two years and more than 3 episodes per year for 3 years). This may be done via diathermy or coblation. \n\n\n# NICE Guidelines\n\n[NICE Guidelines Sore Throat (acute)](https://www.nice.org.uk/guidance/ng84) \n\n[NICE Flowsheet on Antimicrobial Prescribing](https://www.nice.org.uk/guidance/ng84/resources/sore-throat-acute-in-adults-antimicrobial-prescribing-visual-summary-pdf-11315864557) \n \n\n# References\n \n[NHS Information on Tonsillitis](https://www.nhs.uk/conditions/tonsillitis/)\n\n[Patient Info Tonsillitis](https://patient.info/doctor/tonsillitis-pro) \n\n[Great Ormond Street Hospital Tonsillectomy](https://www.gosh.nhs.uk/conditions-and-treatments/procedures-and-treatments/your-child-having-his-or-her-tonsils-andor-adenoids-removed/)",
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"question": "A 13-year-old boy presents to General Practice complaining of a sore throat for the last four days with no cough. He is able to eat and drink. He has no past medical history, is not taking any medications and has no allergies. Examination reveals no lymphadenopathy but there is swelling of the tonsils bilaterally with exudate. His observations are:\n\n- Temperature 37.4 degrees Celsius\n- Pulse 78 bpm\n- Respiratory rate 15\n- Oxygen saturation 98% on room air.\n\nWhat is most appropriate management plan?",
"sbaAnswer": [
"a"
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Systemic corticosteroids are not recommended for mild, uncomplicated pityriasis rosea. Their use is generally reserved for severe or refractory cases and would be prescribed by a Dermatologist, rather than in primary care.",
"id": "10052657",
"label": "d",
"name": "Prescribe oral prednisolone",
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"explanation": "Topical antifungal agents like clotrimoxazole are not appropriate as pityriasis rosea is not a fungal infection. The scaly plaques may mimic tinea corporis, but the clinical presentation (herald patch, secondary rash, history of viral illness) is inconsistent with a fungal cause.",
"id": "10052658",
"label": "e",
"name": "Prescribe topical clotrimoxazole",
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"explanation": "This is the correct answer. The patient's presentation of a herald patch followed by smaller secondary lesions distributed in a \"Christmas tree\" pattern on the trunk is classic for pityriasis rosea. Common triggers for the rash include viral illnesses such as influenza. Although the condition is self-limiting and usually resolves in 6-12 weeks, the pruritus can significantly impact quality of life. NICE guidelines recommend topical corticosteroids for symptomatic relief of itching.",
"id": "10052654",
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"explanation": "While pityriasis rosea is a self-limiting condition, the itching is causing functional impairment for the patient, so management should address her symptoms. Simply reassuring her without treatment would not address the impact on her job.",
"id": "10052655",
"label": "b",
"name": "Reassure and advise the rash will resolve on its own",
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"explanation": "Antihistamines like chlorphenamine can reduce itching, but oral sedating antihistamines are not first-line treatment, particularly when the patient reports that the rash is interfering with her ability to work. Non-sedating alternatives or topical treatment are preferable. This would have been an appropriate option if the patient complained that the itch was interfering with her sleep.",
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"name": "Prescribe oral chlorphenamine",
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"question": "A 29 year old woman presents to the GP with a new rash that has developed over the past week. It started as a single patch on her thigh but over the past 48 hours the rash is now all over her back and abdomen. Other than suffering influenza 2 weeks ago, she has no other past medical history. On examination, there is a red, discoid plaque with a scaly periphery on her right thigh, with multiple smaller lesions over her abdomen and back. The rash is very itchy and it is starting to interfere with her job as a nail technician.\n\nGiven the most likely diagnosis, what is the most appropriate management?",
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"explanation": "This occurs in a normal cell cycle during the M phase. This will not be seen in this patient as they are experiencing necrosis.",
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"explanation": "This is the proposed mechanism of systemic lupus erythematosus (SLE) in which small autoantibody complexes attach to small blood vessels. Phagocytes then try to clear these complexes leading to inflammation.",
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"explanation": "This man has urosepsis, so the main priority is to rapidly perform the sepsis 6 protocol. Prescribing pain relief may be part of the treatment plan, but it will not be the first priority in the management of this patient.",
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"explanation": "As this is only local disease, the best treatment option is to surgically remove the cancer, as well as a margin of normal tissue to ensure that all of the cancer has been removed. Most centres also advise radiotherapy after surgery to prevent the breast cancer from coming back in the future.",
"id": "10023495",
"label": "a",
"name": "Surgical removal of tumour and radiotherapy",
"picture": null,
"votes": 17
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This malignancy is only carcinoma in-situ which means that surgical excision with preventative radiotherapy will be sufficient for this patient. The side effects of chemotherapy outweigh the benefits of giving her this treatment.",
"id": "10023496",
"label": "b",
"name": "Surgical removal of tumour and chemotherapy",
"picture": null,
"votes": 12
}
],
"comments": [],
"concept": {
"__typename": "Concept",
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"__typename": "Chapter",
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"id": "2693",
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"typeId": 7
},
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"demo": null,
"entitlement": null,
"id": "4315",
"name": "Molecular basis of cancer",
"status": null,
"topic": {
"__typename": "Topic",
"id": "182",
"name": "Cancer Biology",
"typeId": 7
},
"topicId": 182,
"totalCards": null,
"typeId": null,
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"userNote": null,
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"qaAnswer": null,
"question": "A 74-year-old woman has a biopsy taken to investigate a breast cancer diagnosis. The pathologist's report states 'severe cell differentiation indicative of malignancy contained within the basement membrane'.\n\nWhat is the best treatment for this malignancy?",
"sbaAnswer": [
"a"
],
"totalVotes": 50,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,847 | false | 7 | null | 6,495,166 | null | false | [] | null | 17,098 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect as the patient has an autosomal recessive condition, so a child can never be a 100% carrier of the condition.",
"id": "10023504",
"label": "e",
"name": "100%",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "As the mother has an autosomal recessive trait and the partner does not have the trait, the child has a 50% chance of being a carrier of cystic fibrosis. The child will not inherit the disease.",
"id": "10023500",
"label": "a",
"name": "50%",
"picture": null,
"votes": 26
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "As the mother has the disease trait, there will always be a 50% chance that the child is a carrier and a 50% chance of the child being homozygous normal (i.e. not having any cystic fibrosis trait at all).",
"id": "10023501",
"label": "b",
"name": "0%",
"picture": null,
"votes": 11
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would be the likelihood of a child having cystic fibrosis if one parent was a carrier and the other parent had the disease.",
"id": "10023503",
"label": "d",
"name": "75%",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would be the likelihood of a child having cystic fibrosis if both patients were carriers.",
"id": "10023502",
"label": "c",
"name": "25%",
"picture": null,
"votes": 15
}
],
"comments": [],
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},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "4451",
"name": "Autosomal recessive conditions",
"status": null,
"topic": {
"__typename": "Topic",
"id": "156",
"name": "Medical Genetics",
"typeId": 7
},
"topicId": 156,
"totalCards": null,
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"question": "A 26-year-old woman becomes pregnant and is screened for hereditary conditions. It is found that she is a carrier for cystic fibrosis which is an autosomal recessive condition. Her partner is screened for cystic fibrosis and is found to not have the trait or be a carrier.\n\nWhat is the likelihood of the child being a carrier for cystic fibrosis?",
"sbaAnswer": [
"a"
],
"totalVotes": 54,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,848 | false | 8 | null | 6,495,166 | null | false | [] | null | 17,099 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect as the kidney plays no part in the absorption of vitamin B12, the molecule that intrinsic factor binds to. This complex is absorbed in the terminal ileum.",
"id": "10023508",
"label": "d",
"name": "Kidney",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The molecule that intrinsic factor binds to is vitamin B12. Vitamin B12 needs intrinsic factor to bind to it so it can be absorbed in the terminal ileum.",
"id": "10023505",
"label": "a",
"name": "Terminal ileum",
"picture": null,
"votes": 48
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is where gastric parietal cells secrete intrinsic factor, not where vitamin B12 (which binds to intrinsic factor) is absorbed in the body.",
"id": "10023506",
"label": "b",
"name": "Stomach",
"picture": null,
"votes": 3
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Vitamin B12 is the molecule that is bound to intrinsic factor and is absorbed in the terminal ileum. The liver plays no role in the absorption of vitamin B12.",
"id": "10023507",
"label": "c",
"name": "Liver",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect as the jejunum absorbs vitamins A, D, E, and K. It does not absorb vitamin B12 which is what intrinsic factor binds to. Vitamin B12 is absorbed in the terminal ileum.",
"id": "10023509",
"label": "e",
"name": "Jejunum",
"picture": null,
"votes": 4
}
],
"comments": [],
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"id": "2693",
"pictures": [],
"typeId": 7
},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "5682",
"name": "Intrinsic factor",
"status": null,
"topic": {
"__typename": "Topic",
"id": "149",
"name": "Gastro-intestinal physiology",
"typeId": 7
},
"topicId": 149,
"totalCards": null,
"typeId": null,
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"userNote": null,
"videos": []
},
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"difficulty": 1,
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"question": "A 48-year-old woman presents to her GP with lethargy. After ruling out lack of sleep, the GP decides to do some blood tests. The results show that she has autoantibodies against intrinsic factor.\n\nWhere in the body is the molecule that intrinsic factor binds to absorbed?",
"sbaAnswer": [
"a"
],
"totalVotes": 56,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,849 | false | 9 | null | 6,495,166 | null | false | [] | null | 17,100 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Myosin light chain kinase needs to be phosphatised into myosin light chain phosphatase before it can activate myosin. This has no role in unblocking the binding sites of actin.",
"id": "10023513",
"label": "d",
"name": "Myosin light chain kinase",
"picture": null,
"votes": 14
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Protein kinase C can independently activate myosin light chain kinase, without the need for the calcified calmodulin. Myosin light chain kinase needs to be phosphatised into myosin light chain phosphatase before it can activate myosin.",
"id": "10023514",
"label": "e",
"name": "Protein Kinase C",
"picture": null,
"votes": 10
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Myosin light chain phosphatase causes the activation of myosin which binds to actin causing smooth muscle contraction.",
"id": "10023511",
"label": "b",
"name": "Myosin light chain phosphatase",
"picture": null,
"votes": 5
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is the correct answer as calcified calmodulin binds to calponin to unblock actin-binding sites and myosin light chain phosphatase to activate myosin. The binding of myosin to actin causes smooth muscle contraction.",
"id": "10023510",
"label": "a",
"name": "Calponin",
"picture": null,
"votes": 5
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Calmodulin is the molecule that once calcified, activates both calponin and myosin light chain phosphatase, which in turn causes smooth muscle contraction.",
"id": "10023512",
"label": "c",
"name": "Calmodulin",
"picture": null,
"votes": 18
}
],
"comments": [],
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},
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"demo": null,
"entitlement": null,
"id": "5683",
"name": "Gastric structure and function",
"status": null,
"topic": {
"__typename": "Topic",
"id": "149",
"name": "Gastro-intestinal physiology",
"typeId": 7
},
"topicId": 149,
"totalCards": null,
"typeId": null,
"userChapter": null,
"userNote": null,
"videos": []
},
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"conditions": [],
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"dislikes": 0,
"explanation": null,
"highlights": [],
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"question": "A 53-year-old male comes into the clinic expressing pains in his stomach. He describes it as waves of squeezing pains. The doctor explains that it is his intestines undergoing peristalsis which is where the smooth muscle in the intestines contract in waves.\n\nWith regards to calcium-dependent smooth muscle contraction, what molecule unblocks the binding sites of actin?",
"sbaAnswer": [
"a"
],
"totalVotes": 52,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,850 | false | 10 | null | 6,495,166 | null | false | [] | null | 17,101 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect as the Th1 response is due to gliadin antigens, not gluten antigens. Tissue transglutaminases break down gluten into gliadin which then leads to the autoimmune response.",
"id": "10023518",
"label": "d",
"name": "Th1 response happens in response to gluten antigens",
"picture": null,
"votes": 11
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is the pathogenesis of *Clostridium difficile* infection: an opportunistic infection in which antibiotics prescribed for another infection allow *C. difficile* bacteria into the gut and cause a diarrhoeal infection.",
"id": "10023519",
"label": "e",
"name": "Antibiotics kill off colonised bacteria allowing harmful bacteria to enter the gut",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect as it is a Th1 response that occurs due to gliadin antigens. This Th1 response causes antibodies to be released by B cells.",
"id": "10023517",
"label": "c",
"name": "Th2 response happens in response to gliadin antigens",
"picture": null,
"votes": 9
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is the correct answer as the first step for coeliac disease to occur is the breakdown of gluten into gliadin. This then leads to dendritic cells taking up the antigens and presenting them to Th1 cells, resulting in antibody production.",
"id": "10023515",
"label": "a",
"name": "Tissue transglutaminases break gluten down into gliadin",
"picture": null,
"votes": 24
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is the incorrect answer as it is the gluten that is being broken down into gliadin, not the other way around.",
"id": "10023516",
"label": "b",
"name": "Tissue transglutaminases break down gliadin into gluten",
"picture": null,
"votes": 3
}
],
"comments": [],
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"__typename": "Chapter",
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"typeId": 7
},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "4236",
"name": "Coeliac disease",
"status": null,
"topic": {
"__typename": "Topic",
"id": "136",
"name": "Gastroenterology",
"typeId": 7
},
"topicId": 136,
"totalCards": null,
"typeId": null,
"userChapter": null,
"userNote": null,
"videos": []
},
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"conditions": [],
"difficulty": 1,
"dislikes": 0,
"explanation": null,
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"question": "A 26-year-old female attends the GP surgery following laboratory tests which indicate she has coeliac disease. The doctor has thought about the mechanism by which this diagnosis has occurred.\n\nWhich of the following is a step in the pathogenesis of coeliac disease?",
"sbaAnswer": [
"a"
],
"totalVotes": 48,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,851 | false | 11 | null | 6,495,166 | null | false | [] | null | 17,102 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "G cells in the duodenum secrete gastrin in response to amino acids and peptides in the stomach. The gastrin stimulates digestive enzyme secretion by acinar cells. Remember **G** cells as secreting **G**astrin.",
"id": "10023520",
"label": "a",
"name": "G cells secrete gastrin",
"picture": null,
"votes": 25
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "S cells secrete secretin, not cholecystokinin (CCK). Cholecystokinin (CCK) is produced by I cells in the duodenum.",
"id": "10023524",
"label": "e",
"name": "S cells secrete cholecystokinin (CCK)",
"picture": null,
"votes": 3
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "S cells secrete secretin when chyme enters the duodenum and the pH is less than 4.5. Secretin has several roles including stimulating the secretion of bicarbonate-rich pancreatic fluid.",
"id": "10023521",
"label": "b",
"name": "S cells secrete secretin",
"picture": null,
"votes": 12
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect as G cells secrete gastrin, not secretin. Gastrin is produced in response to amino acids and peptides in the stomach. Secretin is produced by S cells.",
"id": "10023523",
"label": "d",
"name": "G cells secrete secretin",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is the response to fatty acids, not amino acids and peptides. Cholecystokinin (CCK) causes contraction of the gallbladder and relaxation of the sphincter of Oddi.",
"id": "10023522",
"label": "c",
"name": "I cells secrete cholecystokinin (CCK)",
"picture": null,
"votes": 12
}
],
"comments": [],
"concept": {
"__typename": "Concept",
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"__typename": "Chapter",
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"pictures": [],
"typeId": 7
},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "4515",
"name": "Amino acid and small peptide absorption",
"status": null,
"topic": {
"__typename": "Topic",
"id": "149",
"name": "Gastro-intestinal physiology",
"typeId": 7
},
"topicId": 149,
"totalCards": null,
"typeId": null,
"userChapter": null,
"userNote": null,
"videos": []
},
"conceptId": 4515,
"conditions": [],
"difficulty": 1,
"dislikes": 0,
"explanation": null,
"highlights": [],
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"multiAnswer": null,
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"psaSectionId": null,
"qaAnswer": null,
"question": "A 38-year-old male with special dietary requirements due to progressive Crohn's disease is on the ward speaking to a dietician. They are wondering how their food gets into their body now that they have had many surgeries on their intestines.\n\nWhich cell and corresponding hormone are involved in amino acid and small peptide breakdown?",
"sbaAnswer": [
"a"
],
"totalVotes": 52,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,852 | false | 12 | null | 6,495,166 | null | false | [] | null | 17,103 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The afferent arteriole vasoconstricts in high blood pressure due to the influx of calcium via stretch-mediated calcium channels. This results in decreased renin secretion.",
"id": "10023527",
"label": "c",
"name": "Afferent arteriole vasodilates and decreases renin secretion",
"picture": null,
"votes": 16
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Even though the afferent arteriole vasoconstricts in high blood pressure, there is decreased renin secretion which reduces the effects of the renin-angiotensin-aldosterone (RAAS) system and subsequently reduces blood pressure.",
"id": "10023526",
"label": "b",
"name": "Afferent arteriole vasoconstricts and increases renin secretion",
"picture": null,
"votes": 6
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The increased blood pressure activates Ca2+ stretch-sensitive channels, causing an influx of calcium and leading to smooth muscle contraction in the afferent arteriole. This vasoconstriction causes renin secretion to be reduced.",
"id": "10023525",
"label": "a",
"name": "Afferent arteriole vasoconstricts and reduces renin secretion",
"picture": null,
"votes": 22
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The afferent arteriole vasoconstricts in high blood pressure due to the influx of calcium via stretch-mediated calcium channels. This results in decreased renin secretion, not increased renin secretion. This is because the RAAS system will further increase the blood pressure, which is not what the patient needs if his blood pressure is already high.",
"id": "10023528",
"label": "d",
"name": "Afferent arteriole vasodilates and increases renin secretion",
"picture": null,
"votes": 6
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Even though the afferent arteriole does vasoconstrict, there is a decrease in renin secretion. As this patient's blood pressure is high, the RAAS system needs to be reduced. This is because when the RAAS system is activated it causes an increase in blood pressure.",
"id": "10023529",
"label": "e",
"name": "Afferent arteriole vasoconstricts and there is no change in renin",
"picture": null,
"votes": 0
}
],
"comments": [],
"concept": {
"__typename": "Concept",
"chapter": {
"__typename": "Chapter",
"explanation": null,
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"id": "2693",
"pictures": [],
"typeId": 7
},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "3952",
"name": "Endocrine function of the kidney",
"status": null,
"topic": {
"__typename": "Topic",
"id": "168",
"name": "Renal Physiology",
"typeId": 7
},
"topicId": 168,
"totalCards": null,
"typeId": null,
"userChapter": null,
"userNote": null,
"videos": []
},
"conceptId": 3952,
"conditions": [],
"difficulty": 1,
"dislikes": 0,
"explanation": null,
"highlights": [],
"id": "17103",
"isLikedByMe": null,
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"likes": 0,
"multiAnswer": null,
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"psaSectionId": null,
"qaAnswer": null,
"question": "A 66-year-old male comes to see the GP about his high blood pressure. The GP measures his blood pressure and it is 174/118mmHg. The GP is worried about this patient's kidney function due to his high blood pressure.\n\nWhat happens to the afferent arteriole and renin secretion when blood pressure is high?",
"sbaAnswer": [
"a"
],
"totalVotes": 50,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,853 | false | 13 | null | 6,495,166 | null | false | [] | null | 17,104 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect as the question asks about bowel control after the injury, not urine control.",
"id": "10023534",
"label": "e",
"name": "Loss of voiding urine control",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "As the lesion is above T12, the enteric nervous system and afferent spinal pathways are intact. These pathways allow the defecation reflex to occur even though the patient will have lost sensation in the bowel, meaning they will not know when their rectum is full.",
"id": "10023530",
"label": "a",
"name": "The defecation reflex remains intact",
"picture": null,
"votes": 20
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "In lesions above and below T12, there is a loss of descending control of the bowel, meaning that bowel sensation and the voluntary control to defecate are lost.",
"id": "10023531",
"label": "b",
"name": "Bowel sensation remains intact",
"picture": null,
"votes": 8
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This only occurs when the spinal injury is below T12. This is because, below the T12 level, there is a loss of afferent neurons from the bowel to the brain, meaning that the defecation reflex and tone of the anal sphincters are lost.",
"id": "10023532",
"label": "c",
"name": "Loss of reflex tone of anal sphincters",
"picture": null,
"votes": 12
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This only occurs when the spinal injury is below T12. This is because, below the T12 level, there is a loss of afferent neurons from the bowel to the brain, meaning that the defecation reflex and tone of the anal sphincters are lost.",
"id": "10023533",
"label": "d",
"name": "Loss of defecation reflex",
"picture": null,
"votes": 8
}
],
"comments": [],
"concept": {
"__typename": "Concept",
"chapter": {
"__typename": "Chapter",
"explanation": null,
"files": null,
"highlights": [],
"id": "2693",
"pictures": [],
"typeId": 7
},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "4234",
"name": "Structure and innervation of the GI tract",
"status": null,
"topic": {
"__typename": "Topic",
"id": "149",
"name": "Gastro-intestinal physiology",
"typeId": 7
},
"topicId": 149,
"totalCards": null,
"typeId": null,
"userChapter": null,
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"question": "A 39-year-old male is brought to the emergency department following a car accident. They have a full-body trauma CT which shows a spinal cord injury at T11.\n\nWhat is the correct statement regarding this patient's bowel control with this injury?",
"sbaAnswer": [
"a"
],
"totalVotes": 52,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,854 | false | 14 | null | 6,495,166 | null | false | [] | null | 17,105 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is the response during dehydration as the body tries to absorb more water by increasing aquaporin channels in the collecting ducts. This results in more concentrated urine.",
"id": "10023539",
"label": "e",
"name": "Increases production of aquaporin II channels",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Type II Na+/Pi transporters are important in modulating the uptake of the phosphate to maintain homoeostasis.",
"id": "10023537",
"label": "c",
"name": "Increases type II Na+/Pi transporters",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Hypoxia prevents the hydroxylation of the transcription factor HIF-2α, encouraging EPO production in the kidneys. This leads to an increase in red blood cells and by extension, an increase in the capacity to carry oxygen.",
"id": "10023535",
"label": "a",
"name": "Increases erythropoietin (EPO) production",
"picture": null,
"votes": 43
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Hypoxia increases the production of EPO, stimulating the production of more red blood cells and allowing for a greater capacity for the body to carry oxygen.",
"id": "10023536",
"label": "b",
"name": "Decreases EPO production",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is the response when there is an increase in blood pressure.",
"id": "10023538",
"label": "d",
"name": "The afferent arteriole vasoconstricts",
"picture": null,
"votes": 3
}
],
"comments": [],
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"demo": null,
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"id": "4222",
"name": "Renal erythropoietin secretion",
"status": null,
"topic": {
"__typename": "Topic",
"id": "193",
"name": "Haematological Science",
"typeId": 7
},
"topicId": 193,
"totalCards": null,
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},
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"question": "A 28-year-old female is hiking up Mount Everest and requires oxygen due to the low oxygen levels at the high altitude. The doctor travelling with them explains to her how the kidneys work to help blood get more oxygen.\n\nHow does the kidney respond to hypoxia?",
"sbaAnswer": [
"a"
],
"totalVotes": 48,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,855 | false | 15 | null | 6,495,166 | null | false | [] | null | 17,106 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This muscle acts to depress the hyoid bone, not the thyroid cartilage. It arises from the thyroid cartilage and ascends to attach to the hyoid bone.",
"id": "10023543",
"label": "d",
"name": "Thyrohyoid muscle",
"picture": null,
"votes": 15
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is the only muscle that depresses the thyroid cartilage. It is found in the deep plane of the cervical fascia in the neck. It arises from the manubrium of the sternum and attaches to the thyroid cartilage.",
"id": "10023540",
"label": "a",
"name": "Sternothyroid muscle",
"picture": null,
"votes": 22
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This muscle acts to depress the hyoid bone, not the thyroid cartilage. It originates from the sternum and sternoclavicular joint and then ascends and inserts onto the hyoid bone.",
"id": "10023542",
"label": "c",
"name": "Sternohyoid muscle",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This muscle acts to depress the hyoid bone, not the thyroid cartilage, and has 2 muscle bellies, connected by a muscular tendon.",
"id": "10023541",
"label": "b",
"name": "Omohyoid muscle",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This muscle performs lateral flexion, rotation, and extension for the neck. It is innervated by the accessory nerve (cranial nerve XI).",
"id": "10023544",
"label": "e",
"name": "Sternocleidomastoid muscle",
"picture": null,
"votes": 4
}
],
"comments": [],
"concept": {
"__typename": "Concept",
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"__typename": "Chapter",
"explanation": null,
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},
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"demo": null,
"entitlement": null,
"id": "3765",
"name": "Hypothyroidism",
"status": null,
"topic": {
"__typename": "Topic",
"id": "133",
"name": "Endocrinology",
"typeId": 5
},
"topicId": 133,
"totalCards": null,
"typeId": null,
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"userNote": null,
"videos": []
},
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"highlights": [],
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"question": "A 93-year-old female on a ward is having difficulty swallowing. The speech and language therapists (SALT) come to review her and realise that the thyroid cartilage does not move when she swallows.\n\nWhich muscle acts to depress the thyroid cartilage?",
"sbaAnswer": [
"a"
],
"totalVotes": 47,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,856 | false | 16 | null | 6,495,166 | null | false | [] | null | 17,107 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would suggest a diagnosis of Hashimoto's thyroiditis. This is also an autoimmune thyroid disease like Grave's disease, but this causes hypothyroidism, not hyperthyroidism.",
"id": "10023549",
"label": "e",
"name": "TPO antibodies",
"picture": null,
"votes": 9
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would most likely suggest post-partum thyroiditis. This is because the beta chain of hCG is very similar to the beta chain of TSH, therefore it can mimic TSH and activate the thyroid gland to produce fT3 and fT4. The typical clinical progression of post-partum thyroiditis is hyperthyroidism, followed by hypothyroidism, before returning to euthyroidism.",
"id": "10023548",
"label": "d",
"name": "The discovery that the patient gave birth 3 months ago",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would most likely suggest a toxic adenoma due to there only being a single nodule on the thyroid gland. Even though there are signs of hyperthyroidism in the blood tests, the only way to confirm that this is Grave's disease is to look for the presence of TSH antibodies.",
"id": "10023547",
"label": "c",
"name": "A single nodule on thyroid ultrasound",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would most likely indicate a toxic multinodular goitre. Even though there are signs of hyperthyroidism in the blood tests, the only way to confirm that this is Grave's disease is to look for the presence of TSH antibodies.",
"id": "10023546",
"label": "b",
"name": "Multiple nodules during the neck examination",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Grave's disease is an autoimmune condition in which there is an overproduction of antibodies that stimulate the TSH receptor. This causes an increase in fT3 and fT4, leading to symptoms of hyperthyroidism.",
"id": "10023545",
"label": "a",
"name": "TSH antibodies",
"picture": null,
"votes": 37
}
],
"comments": [],
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"__typename": "Chapter",
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"id": "2693",
"pictures": [],
"typeId": 7
},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "3959",
"name": "Hyperthyroidism",
"status": null,
"topic": {
"__typename": "Topic",
"id": "133",
"name": "Endocrinology",
"typeId": 5
},
"topicId": 133,
"totalCards": null,
"typeId": null,
"userChapter": null,
"userNote": null,
"videos": []
},
"conceptId": 3959,
"conditions": [],
"difficulty": 1,
"dislikes": 0,
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"highlights": [],
"id": "17107",
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"likes": 0,
"multiAnswer": null,
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"qaAnswer": null,
"question": "A 26-year-old male presents to the GP with tremors, visual disturbances, and constant sweating. The GP examines the patient and finds a swelling in the neck.\n\nThe GP performs blood tests that show: TSH <0.01 (low), fT3 - 16 (high), and fT4 - 41 (high).\n\nWhat is the finding that will confirm that this is Grave's disease?",
"sbaAnswer": [
"a"
],
"totalVotes": 47,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,857 | false | 17 | null | 6,495,166 | null | false | [] | null | 17,108 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The left gastric artery supplies the oesophagus and lesser curvature of the stomach. It is a branch of the coeliac trunk. The structure affected in this patient is the gallbladder, which is supplied by the cystic artery.",
"id": "10023553",
"label": "d",
"name": "Left gastric artery",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The middle adrenal artery supplies the adrenal glands. The structure affected in this patient is the gallbladder, which is supplied by the cystic artery.",
"id": "10023552",
"label": "c",
"name": "Middle adrenal artery",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The cystic artery supplies the gallbladder which is the source of biliary colic pain. The cystic artery is a branch of the right hepatic artery.",
"id": "10023550",
"label": "a",
"name": "Cystic artery",
"picture": null,
"votes": 44
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The splenic artery supplies the spleen and pancreas. The structure affected in this patient is the gallbladder, which is supplied by the cystic artery.",
"id": "10023551",
"label": "b",
"name": "Splenic artery",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The right subclavian artery supplies the right upper limb, not the abdomen. It is a branch of the brachiocephalic trunk. The structure affected in this patient is the gallbladder, which is supplied by the cystic artery.",
"id": "10023554",
"label": "e",
"name": "Right subclavian artery",
"picture": null,
"votes": 0
}
],
"comments": [],
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"__typename": "Concept",
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"__typename": "Chapter",
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"pictures": [],
"typeId": 7
},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "5684",
"name": "Right upper quadrant pain",
"status": null,
"topic": {
"__typename": "Topic",
"id": "135",
"name": "General surgery",
"typeId": 7
},
"topicId": 135,
"totalCards": null,
"typeId": null,
"userChapter": null,
"userNote": null,
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},
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"question": "A 43-year-old female presents to the ED with right upper quadrant abdominal pain which is worse after eating fatty meals. The pain can stop suddenly without any explanation.\n\nOn examination, the patient is slightly pyrexic and is tender in the right upper quadrant. The doctor thinks this could be biliary colic.\n\nWhat is the blood supply to the structure affected in this patient?",
"sbaAnswer": [
"a"
],
"totalVotes": 49,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,858 | false | 18 | null | 6,495,166 | null | false | [] | null | 17,109 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Vancomycin is used for MRSA-associated infections. As this patient is MRSA-negative, there is no need to use this drug as it has more severe side effects than co-amoxiclav.",
"id": "10023557",
"label": "c",
"name": "Vancomycin",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Doxycycline is used to treat hospital-acquired pneumonia if a patient is allergic to penicillin. This patient has no allergies so co-amoxiclav is the first choice.",
"id": "10023558",
"label": "d",
"name": "Doxycycline",
"picture": null,
"votes": 6
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "This patient has developed hospital-acquired pneumonia from being on the wards for 3 days. The first-line treatment for hospital-acquired pneumonia as per NICE is co-amoxiclav.",
"id": "10023555",
"label": "a",
"name": "Co-amoxiclav",
"picture": null,
"votes": 27
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Co-trimoxazole is typically used to treat ventilator-associated pneumonia. As this patient has not been ventilated, there is no need to use this drug to treat their hospital-acquired pneumonia. Co-trimoxazole contains trimethoprim and sulfamethoxazole. It can be used to treat hospital-acquired pneumonia if a patient is penicillin allergic or if there is a high resistance to penicillin in the local population.",
"id": "10023556",
"label": "b",
"name": "Co-trimoxazole",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Nitrofurantoin is used to treat urinary tract infections, not pneumonia.",
"id": "10023559",
"label": "e",
"name": "Nitrofurantoin",
"picture": null,
"votes": 15
}
],
"comments": [],
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"__typename": "Concept",
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"__typename": "Chapter",
"explanation": null,
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"id": "2693",
"pictures": [],
"typeId": 7
},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "3709",
"name": "Pneumonia",
"status": null,
"topic": {
"__typename": "Topic",
"id": "132",
"name": "Respiratory",
"typeId": 7
},
"topicId": 132,
"totalCards": null,
"typeId": null,
"userChapter": null,
"userNote": null,
"videos": []
},
"conceptId": 3709,
"conditions": [],
"difficulty": 1,
"dislikes": 0,
"explanation": null,
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"id": "17109",
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"likes": 0,
"multiAnswer": null,
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"question": "An 84-year-old woman comes into the hospital with a UTI and is treated on the wards. 3 days in, the patient develops a cough with purulent sputum. She is MRSA-negative and has no allergies. The doctor prescribes antibiotics for this patient.\n\nAs per NICE, which antibiotics would be given to this patient, given their new presentation?",
"sbaAnswer": [
"a"
],
"totalVotes": 51,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,859 | false | 19 | null | 6,495,166 | null | false | [] | null | 17,110 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The spinothalamic tracts are affected due to this patient having impaired pain and thermal sensation. However, the cyst has to be on the left-hand side as the spinothalamic tract decussates within the spinal cord. If the cyst was on the right-hand side, there would be symptoms on the left-hand side.",
"id": "10023561",
"label": "b",
"name": "The spinothalamic tract on the right-hand side",
"picture": null,
"votes": 11
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The spinothalamic tracts are affected due to this patient having impaired pain and thermal sensation. It is on the left-hand side because the spinothalamic tract decussates within the spinal cord, meaning that the cyst will have to be on the left-hand side to cause right-hand symptoms.",
"id": "10023560",
"label": "a",
"name": "The spinothalamic tract on the left-hand side",
"picture": null,
"votes": 33
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The dorsal column is responsible for vibration and proprioception. This patient has intact vibration sense so the tract affected is the spinothalamic tract. The cyst affects the left-hand side as the symptoms affect the right-hand side: the spinothalamic tracts decussated within the spinal cord, meaning the side affected is opposite to the side of the lesion.",
"id": "10023562",
"label": "c",
"name": "The dorsal column on the left-hand side",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The corticospinal tract is responsible for voluntary movements of the body. As this patient has normal limb movement, we can assume that this tract isn't affected. As the patient has reduced temperature and pain sensation, this indicates that the spinothalamic tract has been affected.",
"id": "10023564",
"label": "e",
"name": "The corticospinal tract on the left-hand side",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The dorsal column is responsible for vibration and proprioception. This patient has intact vibration sense so the tract affected is the spinothalamic tract. The cyst affects the left-hand side as the symptoms affect the right-hand side: the spinothalamic tracts decussated within the spinal cord, meaning the side affected is opposite to the side of the lesion. If the cyst was on the right-hand side, there would be symptoms on the left-hand side.",
"id": "10023563",
"label": "d",
"name": "The dorsal column on the right-hand side",
"picture": null,
"votes": 1
}
],
"comments": [],
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"__typename": "Concept",
"chapter": {
"__typename": "Chapter",
"explanation": null,
"files": null,
"highlights": [],
"id": "2693",
"pictures": [],
"typeId": 7
},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "5685",
"name": "Syringomyelia",
"status": null,
"topic": {
"__typename": "Topic",
"id": "141",
"name": "Neurology",
"typeId": 7
},
"topicId": 141,
"totalCards": null,
"typeId": null,
"userChapter": null,
"userNote": null,
"videos": []
},
"conceptId": 5685,
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"difficulty": 1,
"dislikes": 0,
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"question": "A patient is referred to the neurology clinic after burning her right hand in hot water without realising it.\n\nOn examination, the patient has impaired pain and thermal sensation, but position and vibration sensation are both intact.\n\nThe neurologist suspects syringomyelia.\n\nWhat tract is affected and which side of the spine has the cyst formed?",
"sbaAnswer": [
"a"
],
"totalVotes": 49,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,860 | false | 20 | null | 6,495,166 | null | false | [] | null | 17,111 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "There is no indication of malignancy of the bone or osteoporosis in this question, and there are no signs of these conditions on the x-ray. Hence, it is unlikely this patient has a pathological fracture. The patient has a comminuted fracture as there are multiple fragments of bone on the x-ray.",
"id": "10023569",
"label": "e",
"name": "Comminuted, pathological fracture",
"picture": null,
"votes": 6
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "A simple fracture is where there is a clean break of the bone, leading to 2 segments, not multiple segments. This patient likely has a transverse fracture as the impact from the fall would have been a direct blow to the leg.",
"id": "10023566",
"label": "b",
"name": "Simple, transverse fracture",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "There is no indication of malignancy of the bone or osteoporosis in this question, and there are no signs of these conditions on the x-ray. Hence, it is unlikely this patient has a pathological fracture. Indeed, she has a comminuted fracture as there are multiple fragments of bone shown on the x-ray. The fracture is likely transverse as the impact from the fall would have been a direct blow to the leg.",
"id": "10023567",
"label": "c",
"name": "Transverse, pathological fracture",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is correct as the patient fell off a horse, so the impact would have been a direct blow to the leg. Since there are multiple fragments of bone on the x-ray, the fracture is comminuted.",
"id": "10023565",
"label": "a",
"name": "Transverse, comminuted fracture",
"picture": null,
"votes": 15
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "There was no pulling force from a tendon or muscle that caused this fracture; it was due to a fall from a horse. The patient has a comminuted fracture as there are multiple fragments of bone on the X-ray.",
"id": "10023568",
"label": "d",
"name": "Comminuted, avulsion fracture",
"picture": null,
"votes": 23
}
],
"comments": [],
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"__typename": "Concept",
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"__typename": "Chapter",
"explanation": null,
"files": null,
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"id": "2693",
"pictures": [],
"typeId": 7
},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "5686",
"name": "Fracture types",
"status": null,
"topic": {
"__typename": "Topic",
"id": "154",
"name": "Musculoskeletal physiology and disease",
"typeId": 7
},
"topicId": 154,
"totalCards": null,
"typeId": null,
"userChapter": null,
"userNote": null,
"videos": []
},
"conceptId": 5686,
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"question": "A 24-year-old female comes into the ED via ambulance with a tibia fracture after falling off a horse while horse riding. The doctor requests an x-ray which shows that there are multiple fragments of bone resulting from the fracture.\n\nWhat kind of fracture does this patient likely have?",
"sbaAnswer": [
"a"
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173,464,861 | false | 21 | null | 6,495,166 | null | false | [] | null | 17,112 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "GABA-alpha antagonists are used in benzodiazepine overdoses and have no neuropathic pain-relieving properties.",
"id": "10023574",
"label": "e",
"name": "GABA-alpha antagonists",
"picture": null,
"votes": 15
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "These drugs, such as baclofen, act on GABA-beta receptors to decrease spasticity in conditions such as cerebral palsy.",
"id": "10023571",
"label": "b",
"name": "GABA-beta agonists",
"picture": null,
"votes": 10
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Selective serotonin reuptake inhibitors (SSRI) stop the reuptake of serotonin in the brain, resulting in increased concentrations of serotonin within synapses. SSRIs such as sertraline and fluoxetine are mainly used to treat depression and anxiety.",
"id": "10023572",
"label": "c",
"name": "Selective serotonin reuptake inhibitor",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Serotonin and noradrenaline reuptake inhibitors (SNRI) stop the reuptake of serotonin and noradrenaline, resulting in increased concentrations of these neurotransmitters within synapses. SNRIs such as duloxetine are used as second-line treatment for depression and anxiety, as well as for neuropathic pain.",
"id": "10023573",
"label": "d",
"name": "Serotonin and noradrenaline reuptake inhibitor",
"picture": null,
"votes": 5
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Gabapentin acts to bind and inhibit pre-synaptic voltage-gated calcium channels, therefore reducing the density of these channels that are available for neurotransmission. This results in reduced excitatory neurotransmitter release which, in turn, reduces pain perception.",
"id": "10023570",
"label": "a",
"name": "Binds to pre-synaptic voltage-gated calcium channels",
"picture": null,
"votes": 14
}
],
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"id": "3825",
"name": "Pain sensation",
"status": null,
"topic": {
"__typename": "Topic",
"id": "152",
"name": "Neuroscience",
"typeId": 7
},
"topicId": 152,
"totalCards": null,
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"question": "A 58-year-old male with a background of previous disc herniation presents to the GP with sharp shooting pains going down his left arm. He says that the pain is constant and is stopping him from performing daily tasks. He also reports that sometimes his arm and hand go numb and tingly. He has tried paracetamol and amitriptyline which both have not helped the pain. The GP decides to prescribe him gabapentin.\n\nWhat is the mechanism of action of this drug?",
"sbaAnswer": [
"a"
],
"totalVotes": 46,
"typeId": 1,
"userPoint": null
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173,464,862 | false | 22 | null | 6,495,166 | null | false | [] | null | 17,113 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This nerve innervates all the muscles of the posterior forearm, but not any structures of the leg and ankle. It has nerve roots from C5-T1.",
"id": "10023578",
"label": "d",
"name": "Deep branch of the radial nerve",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The tibial nerve innervates the muscles within the superficial and deep layers of the posterior compartment of the leg, not the lateral compartment of the leg. The tibial nerve is a continuation of the sciatic nerve once it passes through the popliteal fossa.",
"id": "10023579",
"label": "e",
"name": "Tibial nerve",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The sural nerve only provides sensation to the cutaneous part of the posteolateral leg. It does not innervate any muscles of the leg.",
"id": "10023577",
"label": "c",
"name": "Sural nerve",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The muscles of the lateral compartment of the leg (fibularis longus and brevis) are innervated by the superficial fibular nerve which has roots from L4-S1.",
"id": "10023575",
"label": "a",
"name": "Superficial fibular nerve",
"picture": null,
"votes": 34
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The deep fibular nerve innervates the anterior compartment muscles of the leg.",
"id": "10023576",
"label": "b",
"name": "Deep fibular nerve",
"picture": null,
"votes": 10
}
],
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"id": "3773",
"name": "Common peroneal nerve injury",
"status": null,
"topic": {
"__typename": "Topic",
"id": "145",
"name": "Orthopaedics",
"typeId": 7
},
"topicId": 145,
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"question": "An 18-year-old male presents to the walk-in clinic after twisting his ankle during a football game.\n\nThe doctor examines his ankle and asks him to perform some movements. There is pain upon eversion and plantarflexion of the foot. The doctor thinks that the fibularis longus muscle has been damaged.\n\nWhat is the innervation to the fibularis longus muscle?",
"sbaAnswer": [
"a"
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"totalVotes": 47,
"typeId": 1,
"userPoint": null
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173,464,863 | false | 23 | null | 6,495,166 | null | false | [] | null | 17,114 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "RF does have a high affinity for the IgG antibody but it is specifically the Fc region, not the Fab region.",
"id": "10023581",
"label": "b",
"name": "Fab region of IgG antibody",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is not an antibody but a cytokine which is produced in rheumatoid arthritis and recruits monocytes, lymphocytes, basophils and eosinophils into the synovial joint.",
"id": "10023584",
"label": "e",
"name": "CCL3",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "RF has a high affinity for the Fc region of IgG antibodies, not the Fab region of IgE antibodies.",
"id": "10023583",
"label": "d",
"name": "Fab region of IgE antibody",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "RF has a high affinity for the Fc region of IgG antibodies, not the Fc region of IgM antibodies. RF itself can be an IgM, IgG, IgA or IgE class antibody.",
"id": "10023582",
"label": "c",
"name": "Fc region of IgM antibody",
"picture": null,
"votes": 6
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "RF has a high affinity for the Fc region of the IgG antibody.",
"id": "10023580",
"label": "a",
"name": "Fc region of IgG antibody",
"picture": null,
"votes": 36
}
],
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"id": "5687",
"name": "Antibodies in rheumatological disease",
"status": null,
"topic": {
"__typename": "Topic",
"id": "146",
"name": "Rheumatology",
"typeId": 7
},
"topicId": 146,
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"question": "A 64-year-old woman attends the rheumatology clinic to discuss her recent blood results. She is found to be rheumatoid factor (RF) positive. The rheumatologist explains to the patient what this means.\n\nWhich antibody does rheumatoid factor (RF) have a high affinity for?",
"sbaAnswer": [
"a"
],
"totalVotes": 46,
"typeId": 1,
"userPoint": null
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173,464,864 | false | 24 | null | 6,495,166 | null | false | [] | null | 17,115 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "This patient has symptoms typical of rheumatoid arthritis, including swollen joints in the hands, and pain and stiffness that is worst in the morning but improves after roughly an hour. The pain in the morning is what differentiates this from osteoarthritis, as in osteoarthritis, the pain will be longer than 1 hour and might get worse throughout the day.",
"id": "10023585",
"label": "a",
"name": "Rheumatoid arthritis",
"picture": null,
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{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "As this patient has reported no fevers or recent infections, it is more likely that she has rheumatoid or osteoarthritis. Septic arthritis typically causes a single hot swollen joint, rather than multiple swollen cool joints.",
"id": "10023587",
"label": "c",
"name": "Septic arthritis",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Fracturing all of the left proximal interphalangeal joints is very unlikely and would result in an inability to move one's hands and fingers. There has been no history of trauma in this patient as well.",
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"label": "e",
"name": "Proximal interphalangeal joint fractures",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Gout usually affects the first metatarsophalangeal joint (big toe joint) and is usually very sudden in onset. This patient's pain has been over months so it is unlikely to be gout. Gout is caused by the crystallisation of uric acid within the synovial space.",
"id": "10023588",
"label": "d",
"name": "Gout",
"picture": null,
"votes": 5
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Osteoarthritis has similar symptoms such as swollen hands, but the morning stiffness usually lasts for longer than an hour. The joints usually affected are the distal interphalangeal joints, not the proximal interphalangeal joints.",
"id": "10023586",
"label": "b",
"name": "Osteoarthritis",
"picture": null,
"votes": 9
}
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"name": "Rheumatoid Arthritis",
"status": null,
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"question": "A 53-year-old female presents to the GP with a 3-month history of swelling in her left hand and legs. She says that the pain and stiffness last for an hour in the morning and that she also has difficulty opening jars. She reports no fevers or recent infections. There has been no trauma to those areas either.\n\nOn examination, the proximal interphalangeal joints on her left hand are swollen but they are not hot to touch.\n\nWhat is the cause of this patient's swollen hands?",
"sbaAnswer": [
"a"
],
"totalVotes": 47,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,865 | false | 25 | null | 6,495,166 | null | false | [] | null | 17,116 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "There is no indication of septic arthritis in this patient as the joint is not swollen and the pain is not acute-onset; the pain has been present for the last 2 months. This case is a classical presentation of lateral epicondylitis (tennis elbow).",
"id": "10023592",
"label": "c",
"name": "Septic arthritis",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Lateral epicondylitis occurs when the muscles of the posterior compartment of the forearm are used repetitively, causing strain on those muscles, and subsequent pain. The classic presentation of tennis elbow is pain on wrist extension at the elbow.",
"id": "10023590",
"label": "a",
"name": "Lateral epicondylitis (tennis elbow)",
"picture": null,
"votes": 23
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is where the ulnar nerve is compressed in the cubital fossa, leading to numbness and tingling in the ring and little finger. As this patient describes no numbness or tingling, this diagnosis is unlikely.",
"id": "10023594",
"label": "e",
"name": "Cubital tunnel syndrome",
"picture": null,
"votes": 3
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Medial epicondylitis (golfer's elbow) occurs when the muscles of the anterior compartment of the forearm are used repetitively, leading to pain. This typically presents as elbow pain worse on wrist flexion, not extension.",
"id": "10023591",
"label": "b",
"name": "Medial epicondylitis (golfer's elbow)",
"picture": null,
"votes": 17
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would present with pain in the whole arm, not just the elbow joint. There would also be numbness and tingling.",
"id": "10023593",
"label": "d",
"name": "Brachial plexus injury",
"picture": null,
"votes": 4
}
],
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"id": "5688",
"name": "Lateral epicondylitis",
"status": null,
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"__typename": "Topic",
"id": "145",
"name": "Orthopaedics",
"typeId": 7
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"topicId": 145,
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"question": "A 28-year-old male presents to the GP with pain in his left elbow, which has been present for 2 months. He finds that it is worse when his arm is outstretched and he extends his wrist.\n\nThere is no numbness or tingling in his left arm and his radial pulses are strong. There is no swelling of the elbow joint.\n\nHe is a keen sportsman, playing a variety of sports including tennis and golf.\n\nWhat is the cause of his elbow pain?",
"sbaAnswer": [
"a"
],
"totalVotes": 47,
"typeId": 1,
"userPoint": null
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173,464,866 | false | 26 | null | 6,495,166 | null | false | [] | null | 17,117 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The supraspinous ligament extends from the sacrum to C7 where it merges with the nuchal ligament. Its role is to limit flexion of the spine.",
"id": "10023598",
"label": "d",
"name": "Supraspinous ligament",
"picture": null,
"votes": 5
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The interspinous ligament extends from the C1 axis to S1. Anteriorly, it connects with ligamentum flavum and posteriorly, it connects to the supraspinous ligament. Its role is to limit flexion of the spine.",
"id": "10023599",
"label": "e",
"name": "Interspinous ligament",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The posterior longitudinal ligament extends from the C2 axis vertebra to the sacrum along the vertebral canal on the posterior aspect of the vertebral bodies. The function of this ligament is to help prevent posterior disc herniations along with weakly resisting vertebral hyperflexion.",
"id": "10023595",
"label": "a",
"name": "Posterior longitudinal ligament",
"picture": null,
"votes": 34
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The anterior longitudinal ligament extends from the pelvic surface of the sacrum to the anterior tubercle of vertebra C1 and the occipital bone. It covers and connects the anterolateral aspects of the vertebral bodies and intervertebral discs. It prevents hyperflexion and limits extension of the spine.",
"id": "10023596",
"label": "b",
"name": "Anterior longitudinal ligament",
"picture": null,
"votes": 5
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The intertransverse ligament is found between a superior transverse process and the transverse process of the vertebra below it. Its role is to limit lateral flexion of the spine.",
"id": "10023597",
"label": "c",
"name": "Intertransverse ligament",
"picture": null,
"votes": 1
}
],
"comments": [],
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"__typename": "Concept",
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"__typename": "Chapter",
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"typeId": 7
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"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "4660",
"name": "Spinal Cord Compression",
"status": null,
"topic": {
"__typename": "Topic",
"id": "141",
"name": "Neurology",
"typeId": 7
},
"topicId": 141,
"totalCards": null,
"typeId": null,
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},
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"question": "A 42-year-old male presents with neuropathic back pain. It does not radiate anywhere and is sharp in nature. The doctor orders an MRI which shows that there is a posterior disc herniation at T9.\n\nWhich ligament is affected in this patient to allow a posterior disc herniation?",
"sbaAnswer": [
"a"
],
"totalVotes": 49,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,867 | false | 27 | null | 6,495,166 | null | false | [] | null | 17,118 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Metabolic hyperaemia causes **vasodilation** of blood vessels during exercise, not vasoconstriction. The increase in waste products such as lactic acid and CO2 decreases the pH of the extracellular fluid. This causes localised vasodilation of blood vessels, to help flush out the waste products and allow more oxygen to get there to meet the demand of the muscles. The increased blood flow leads to an increase in venous return, leading to a greater cardiac output.",
"id": "10023603",
"label": "d",
"name": "Metabolic hyperaemia causes vasoconstriction of blood vessels",
"picture": null,
"votes": 10
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Sympathetic venoconstriction decreases venous volume so increases mean systemic filling pressure. This increases the pressure gradient between veins and the heart so increases venous return to the heart, leading to a greater cardiac output.",
"id": "10023600",
"label": "a",
"name": "Sympathetic venoconstriction",
"picture": null,
"votes": 16
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Inactive skeletal muscles **vasoconstrict**, not vasodilate during exercise. If the vessels vasodilated during exercise, the total peripheral resistance would drop, resulting in reduced blood pressure.",
"id": "10023604",
"label": "e",
"name": "Vasodilation of inactive skeletal muscles",
"picture": null,
"votes": 7
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Muscle contraction leads to the **compression** of veins and therefore increases blood pressure. This increase in blood pressure leads to an increase in venous return, leading to a greater cardiac output.",
"id": "10023601",
"label": "b",
"name": "Muscle contraction causing the expansion of veins",
"picture": null,
"votes": 12
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Pulmonary artery pressure **increases** during exercise. This leads to a decrease in pulmonary vascular resistance, causing alveolar vessels to open up and distend more. This respiratory muscle pump allows for an increase in venous return, leading to a greater cardiac output.",
"id": "10023602",
"label": "c",
"name": "Pulmonary artery pressure decreases",
"picture": null,
"votes": 2
}
],
"comments": [],
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"__typename": "Concept",
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"__typename": "Chapter",
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"id": "2693",
"pictures": [],
"typeId": 7
},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "4231",
"name": "Blood flow through the heart",
"status": null,
"topic": {
"__typename": "Topic",
"id": "159",
"name": "Cardiovascular physiology",
"typeId": 7
},
"topicId": 159,
"totalCards": null,
"typeId": null,
"userChapter": null,
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"videos": []
},
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"question": "A 23-year-old female attends a sports and exercise medicine clinic. The doctor monitors her cardiac output as she is performing different exercises.\n\nWhich of the following causes an increase in cardiac output?",
"sbaAnswer": [
"a"
],
"totalVotes": 47,
"typeId": 1,
"userPoint": null
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173,464,868 | false | 28 | null | 6,495,166 | null | false | [] | null | 17,119 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "ARBs, such as losartan, work by binding to the angiotensin II receptor, preventing endogenous angiotensin II from binding to them. This results in vasodilation which reduces blood pressure. Ramipril is an ACE inhibitor, not an angiotensin receptor blocker.",
"id": "10023606",
"label": "b",
"name": "Angiotensin receptor blocker (ARB)",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Beta-blockers, such as propranolol, work by blocking beta-2 adrenoreceptors in blood vessels. This results in less cAMP formation, which leads to vasodilation. Ramipril is an ACE inhibitor, not a beta blocker.",
"id": "10023609",
"label": "e",
"name": "Beta-blocker",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Ramipril is an ACE inhibitor, therefore it inhibits the formation of angiotensin-II. It also increases bradykinin levels in the blood, causing vasodilation which leads to reduced blood pressure.",
"id": "10023605",
"label": "a",
"name": "ACE inhibitor",
"picture": null,
"votes": 43
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Thiazide-like diuretics, such as indapamide, work by inhibiting sodium reabsorption, and by extension, decreasing fluid reabsorption via osmotic gradients. This, in turn, reduces blood pressure. Ramipril is an ACE inhibitor, not a thiazide-like diuretic.",
"id": "10023608",
"label": "d",
"name": "Thiazide-like diuretic",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "CCBs, such as amlodipine, work by blocking voltage-dependent L-type calcium channels, therefore inhibiting the influx of calcium and causing smooth muscle relaxation and vasodilation. This decreases blood pressure. Ramipril is an ACE inhibitor, not a calcium channel blocker.",
"id": "10023607",
"label": "c",
"name": "Calcium channel blocker (CCB)",
"picture": null,
"votes": 0
}
],
"comments": [],
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"id": "4215",
"name": "ACE inhibitors",
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"id": "169",
"name": "Cardiovascular pharmacology",
"typeId": 7
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"question": "A 56-year-old male presents to the GP for his annual check-up. The GP records his blood pressure as 153/102mmHg and decides to prescribe him ramipril to help control his blood pressure.\n\nWhat is the mechanism of action of this drug?",
"sbaAnswer": [
"a"
],
"totalVotes": 48,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,869 | false | 29 | null | 6,495,166 | null | false | [] | null | 17,120 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "In haemophilia A, there is a deficiency of factor VIII, not VII. Factor VII combines with tissue factor in the extrinsic pathway to initiate the coagulation cascade via factor X.",
"id": "10023612",
"label": "c",
"name": "Clotting factor VII which affects the extrinsic pathway",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Haemophilia A occurs due to a deficiency in clotting factor VIII. Factor VIII is part of the intrinsic pathway and has many downstream effects, including increasing the conversion of factor XIII to factor XIIIa, and increasing the conversion of fibrin into a fibrin clot.",
"id": "10023610",
"label": "a",
"name": "Clotting factor VIII which affects the intrinsic pathway",
"picture": null,
"votes": 27
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "In haemophilia A, there is a deficiency of factor VIII, not II. Factor II (thrombin) activates fibrinogen to form fibrin in the intrinsic pathway, which helps with the formation of a clot.",
"id": "10023613",
"label": "d",
"name": "Clotting factor II which affects the the intrinsic pathway",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "In haemophilia A, there is a deficiency in factor VIII, not XI. Factor XI deficiency is called haemophilia C. Both haemophilia A and C play a role in the intrinsic pathway.",
"id": "10023614",
"label": "e",
"name": "Clotting factor XI which affects the intrinsic pathway",
"picture": null,
"votes": 3
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "There is indeed a deficiency in clotting factor VIII in haemophilia A, but it is the intrinsic coagulation pathway that is affected, not the extrinsic pathway.",
"id": "10023611",
"label": "b",
"name": "Clotting factor VIII which affects the extrinsic pathway",
"picture": null,
"votes": 4
}
],
"comments": [],
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"id": "5689",
"name": "Coagulation Cascade",
"status": null,
"topic": {
"__typename": "Topic",
"id": "193",
"name": "Haematological Science",
"typeId": 7
},
"topicId": 193,
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"question": "A 24-year-old female presents to the ED with prolonged bleeding after a small cut on her leg. She has tried to put pressure on the wound but it has not helped. She is not on any anticoagulant medications.\n\nIt is found that she has haemophilia A.\n\nWhich molecule is depleted in haemophilia A and which pathway of the coagulation cascade does this affect?",
"sbaAnswer": [
"a"
],
"totalVotes": 40,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,870 | false | 30 | null | 6,495,166 | null | false | [] | null | 17,121 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is an angiotensin receptor blocker, which like ACE inhibitors is associated with hyperkalaemia, not hypokalaemia.",
"id": "10023618",
"label": "d",
"name": "Candesartan",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is an ACE inhibitor which causes hyperkalaemia, not hypokalaemia.",
"id": "10023616",
"label": "b",
"name": "Ramipril",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Digoxin causes delayed after-depolarisations (DADs), not early after-depolarisations. It causes DADs by inhibiting Na+/K+ ATPase which leads to an increased intracellular Na+ conc (usually pumps Na+ out and K+ in) as well as reduced Ca2+ efflux via NCX. This results in high concentrations of Ca2+ inside the myocyte. When the Ca2+ content in the sarcoplasmic reticulum is too high, RyR receptors spontaneously open during diastole which releases Ca2+ without an action potential stimulus. This increases Ca2+ efflux via NCX (increasing the intracellular Na+ concentration) and causes depolarisation leading to a delayed after depolarisation. If this depolarisation reaches the threshold to open voltage-gated Na+ channels, it causes an action potential to be formed.",
"id": "10023619",
"label": "e",
"name": "Digoxin",
"picture": null,
"votes": 15
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is a loop diuretic which can cause hypokalaemia. Hypokalaemia reduces the activity of K+ channels and the Na/K pump. This prolongs the plateau phase of the cardiac action potential, leading to increased Ca2+ influx via L-type Ca2+ channels. This results in an increase in the cytosolic Ca2+ concentration, so more Ca2+ leaves the cell via NCX (sodium-calcium-exchangers) and more Na+ is brought into the cell. This can cause depolarisation and action potentials before a cell has a chance to repolarise, leading to EADs.",
"id": "10023615",
"label": "a",
"name": "Furosemide",
"picture": null,
"votes": 17
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is a potassium-sparing diuretic which can cause hyperkalemia, not hypokalaemia.",
"id": "10023617",
"label": "c",
"name": "Spironolactone",
"picture": null,
"votes": 8
}
],
"comments": [],
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"__typename": "Concept",
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"__typename": "Chapter",
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"entitlement": null,
"id": "5690",
"name": "Conduction pathways through the heart",
"status": null,
"topic": {
"__typename": "Topic",
"id": "159",
"name": "Cardiovascular physiology",
"typeId": 7
},
"topicId": 159,
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"question": "A 74-year-old male is experiencing palpitations and comes to the ED. An ECG is performed which shows prolonged early after-depolarisations (EADs). The patient is on a variety of medications which the doctor thinks could be contributing to his EADs.\n\nWhich of the following medications can cause EADs?",
"sbaAnswer": [
"a"
],
"totalVotes": 42,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,871 | false | 31 | null | 6,495,166 | null | false | [] | null | 17,122 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "C-type natriuretic peptide (CNP) is released from the vascular endothelium, not the ventricles. These peptides cause vasodilatation and natriuresis (which is an increase in sodium excretion) in an attempt to decrease fluid overload.",
"id": "10023623",
"label": "d",
"name": "C-type natriuretic peptide (CNP) from the ventricles",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "BNP is released from the ventricles in response to cardiac strain. BNP, along with atrial natriuretic peptide and C-type peptide cause vasodilatation and natriuresis (which is an increase in sodium excretion) in an attempt to decrease fluid overload.",
"id": "10023620",
"label": "a",
"name": "Brain natriuretic peptide (BNP) from the ventricles",
"picture": null,
"votes": 33
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Atrial natriuretic peptide (ANP) is released from the atria, not the vascular endothelium. These peptides cause vasodilatation and natriuresis (which is an increase in sodium excretion) in an attempt to decrease fluid overload.",
"id": "10023624",
"label": "e",
"name": "Atrial natriuretic peptide (ANP) from the vascular endothelium",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Atrial natriuretic peptide (ANP) is secreted from the atria, not the ventricles. These peptides cause vasodilatation and natriuresis (which is an increase in sodium excretion) in an attempt to decrease fluid overload.",
"id": "10023622",
"label": "c",
"name": "Atrial natriuretic peptide (ANP) from the ventricles",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Even though the name might suggest this, BNP is secreted from the ventricles, not the brain. These peptides cause vasodilatation and natriuresis (which is an increase in sodium excretion) in an attempt to decrease fluid overload.",
"id": "10023621",
"label": "b",
"name": "Brain natriuretic peptide (BNP) from the brain",
"picture": null,
"votes": 2
}
],
"comments": [],
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"chapterId": 2693,
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"id": "4582",
"name": "Heart failure",
"status": null,
"topic": {
"__typename": "Topic",
"id": "159",
"name": "Cardiovascular physiology",
"typeId": 7
},
"topicId": 159,
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"question": "A 68-year-old male presents to the GP with shortness of breath and swelling of his legs which have gradually gotten worse over the last 5 months. He has noticed that he cannot walk to the shops without getting out of breath and that his shoes are getting tighter around his ankles. The GP suspects he has heart failure and orders a specific blood test to help confirm the diagnosis.\n\nGiven the diagnosis, what molecule is this blood test measuring and where is it released from?",
"sbaAnswer": [
"a"
],
"totalVotes": 42,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,872 | false | 32 | null | 6,495,166 | null | false | [] | null | 17,123 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This artery supplies the posterior parts of the right and left ventricles, as well as the posterior interventricular septum.",
"id": "10023626",
"label": "b",
"name": "Posterior interventricular artery",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This artery supplies the right ventricle and the apex of the heart.",
"id": "10023627",
"label": "c",
"name": "Right marginal artery",
"picture": null,
"votes": 7
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This artery supplies the left atrium and ventricle.",
"id": "10023629",
"label": "e",
"name": "Left circumflex artery",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This artery supplies the anterior parts of the right and left ventricles, as well as the anterior interventricular septum.",
"id": "10023628",
"label": "d",
"name": "Left anterior descending artery",
"picture": null,
"votes": 3
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The right coronary artery supplies the right atrium and SA node. It arises from the right aortic sinus within the aorta.",
"id": "10023625",
"label": "a",
"name": "Right coronary artery",
"picture": null,
"votes": 34
}
],
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"id": "3792",
"name": "Coronary blood flow",
"status": null,
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"__typename": "Topic",
"id": "159",
"name": "Cardiovascular physiology",
"typeId": 7
},
"topicId": 159,
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"question": "A 55-year-old male comes into the ED via ambulance after experiencing palpitations. His ECG shows an ST elevation myocardial infarction. Treatment is commenced and he is admitted to the hospital. The doctors want to know the underlying cause of this presentation so arrange for the cardiology team to investigate. They find that the patient has a reduced blood supply to the sino-atrial (SA) node upon completion of an angiogram.\n\nWhat is the blood supply to the SA node?",
"sbaAnswer": [
"a"
],
"totalVotes": 46,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,873 | false | 33 | null | 6,495,166 | null | false | [] | null | 17,124 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is correct as this patient has a pupil that will not constrict, meaning that it is permanently dilated. The nerve that causes constriction of the pupil is the oculomotor nerve.",
"id": "10023630",
"label": "a",
"name": "Oculomotor nerve",
"picture": null,
"votes": 44
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This nerve provides sensation to the upper lip, nose and lower eyelid, along with parasympathetic innervation to the lacrimal gland.",
"id": "10023631",
"label": "b",
"name": "Maxillary branch of the trigeminal nerve",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The vestibulocochlear nerve's function is hearing (cochlear portion) and balance (vestibular portion). It plays no role in eye movement or pupil size.",
"id": "10023632",
"label": "c",
"name": "Vestibulocochlear nerve",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The glossopharyngeal nerve provides parasympathetic innervation to the parotid, submandibular and sublingual glands. It also provides sensation to the middle ear cavity via the tympanic plexus within the middle ear cavity.",
"id": "10023633",
"label": "d",
"name": "Glossopharyngeal nerve",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The facial nerve supplies taste to the posterior 1/3rd of the tongue, motor function to muscles of facial expression, and sensory function to a small area of the skin around the external ear.",
"id": "10023634",
"label": "e",
"name": "Facial nerve",
"picture": null,
"votes": 1
}
],
"comments": [],
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"entitlement": null,
"id": "4305",
"name": "Autonomic nervous system",
"status": null,
"topic": {
"__typename": "Topic",
"id": "152",
"name": "Neuroscience",
"typeId": 7
},
"topicId": 152,
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"question": "A 25-year-old male presents to the GP as his parents have noticed that his right eye is looking different. The patient has experienced no new symptoms. The GP looks into the patient's eye and finds that his right pupil is dilated, even when a torch is shone on it.\n\nGiven the diagnosis, what nerve is affected?",
"sbaAnswer": [
"a"
],
"totalVotes": 47,
"typeId": 1,
"userPoint": null
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173,464,874 | false | 34 | null | 6,495,166 | null | false | [] | null | 17,125 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Ondansetron is an anti-emetic. It works by blocking 5HT-3 receptors in the gastrointestinal tract and the CNS. It does not affect gout.",
"id": "10023638",
"label": "d",
"name": "Ondansetron",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Losartan is an angiotensin II receptor blocker which affects the RAAS system and blood pressure. It decreases the risk of gout as it causes a decrease in uric acid levels within the blood.",
"id": "10023636",
"label": "b",
"name": "Losartan",
"picture": null,
"votes": 7
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Tazocin is an antibiotic comprising of piperacillin and tazobactam. It has no role in gout, only in treating bacterial infections.",
"id": "10023639",
"label": "e",
"name": "Tazocin",
"picture": null,
"votes": 3
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Bendroflumethiazide is a thiazide diuretic that can also directly increase uric acid re-absorption in the proximal renal tubules, which can cause hyperuricaemia. As gout is due to a build-up of urate crystals in a joint, having a higher concentration of uric acid in the blood will increase the likelihood of a flare-up.",
"id": "10023635",
"label": "a",
"name": "Bendroflumethiazide",
"picture": null,
"votes": 23
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Allopurinol is a gout treatment, so would not cause a flare-up of this patient's gout. Allopurinol blocks the effects of xanthine oxidase - the protein that converts hypoxanthine to uric acid - reducing the level of uric acid within the body.",
"id": "10023637",
"label": "c",
"name": "Allopurinol",
"picture": null,
"votes": 10
}
],
"comments": [],
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"__typename": "Concept",
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"pictures": [],
"typeId": 7
},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "3815",
"name": "Thiazide diuretics",
"status": null,
"topic": {
"__typename": "Topic",
"id": "169",
"name": "Cardiovascular pharmacology",
"typeId": 7
},
"topicId": 169,
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},
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"question": "A 63-year-old male with a history of gout presents to the GP with a hot, swollen first metatarsophalangeal joint (big toe joint). The GP suspects another flare-up of gout and thinks it may be due to some of his medications.\n\nWhich of the following medications could precipitate his gout?",
"sbaAnswer": [
"a"
],
"totalVotes": 44,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,875 | false | 35 | null | 6,495,166 | null | false | [] | null | 17,126 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "3rd generation cephalosporins such as ceftriaxone are useful against TEM-1 bacteria, however, are ineffective against ESBL A&B-producing bacteria. This means that these drugs will not be effective at treating mecA plasmid bacteria.",
"id": "10023641",
"label": "b",
"name": "Ceftriaxone",
"picture": null,
"votes": 8
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Macrolides such as doxycycline are ineffective as the mecA plasmid usually has genes that encode proteins that make all macrolides ineffective. This means that doxycycline is not the correct antibiotic of choice for this patient.",
"id": "10023643",
"label": "d",
"name": "Doxycycline",
"picture": null,
"votes": 5
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Aminoglycosides such as gentamicin are ineffective as the mecA plasmid usually has genes that encode proteins that make all aminoglycosides ineffective.",
"id": "10023644",
"label": "e",
"name": "Gentamicin",
"picture": null,
"votes": 12
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The only class of drugs that counter mecA plasmid bacteria are glycopeptides. Vancomycin is a glycopeptide so can be used in this patient to help treat her infection.",
"id": "10023640",
"label": "a",
"name": "Vancomycin",
"picture": null,
"votes": 18
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Aminopenicillins such as amoxicillin are ineffective as the mecA plasmid bacteria produce PBP2a (which the mecA plasmid gene encodes), which cannot be effectively inhibited by any beta-lactam. Therefore, this class of antibiotics are ineffective at treating mecA plasmid bacteria.",
"id": "10023642",
"label": "c",
"name": "Amoxicillin",
"picture": null,
"votes": 3
}
],
"comments": [],
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"id": "5691",
"name": "Mechanisms of anti-microbial resistance",
"status": null,
"topic": {
"__typename": "Topic",
"id": "148",
"name": "Microbiology",
"typeId": 7
},
"topicId": 148,
"totalCards": null,
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"question": "A 93-year-old female is being treated for a UTI with broad-spectrum antibiotics. She is not feeling any better so urine cultures are sent to microbiology, who call back saying that there are bacteria present that have a mecA plasmid resistance.\n\nWhat antibiotic would be best to treat this kind of bacteria?",
"sbaAnswer": [
"a"
],
"totalVotes": 46,
"typeId": 1,
"userPoint": null
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173,464,876 | false | 36 | null | 6,495,166 | null | false | [] | null | 17,127 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Hydrocortisone IV is given if oral prednisolone cannot be given. Both hydrocortisone and prednisolone are corticosteroid drugs, so hydrocortisone has the same side effect profile as prednisolone and does not cause a tremor.",
"id": "10023647",
"label": "c",
"name": "Hydrocortisone",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Omeprazole is a proton pump inhibitor (PPI) and plays no role in treating asthma exacerbations. It also does not cause a tremor.",
"id": "10023649",
"label": "e",
"name": "Omeprazole",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Prednisolone is used in acute exacerbations of asthma, however, it does not cause a tremor. The main side effects of prednisolone are GI discomfort, and increased risk of peptic ulcer and osteoporosis if used long-term.",
"id": "10023646",
"label": "b",
"name": "Prednisolone",
"picture": null,
"votes": 8
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Co-amoxiclav is an antibiotic used if there is a suspected infective cause of the asthma exacerbation. It does not cause a tremor, but a serious side effect can be anaphylaxis if the patient is allergic to penicillin, so remember to check the patient's allergies before giving it.",
"id": "10023648",
"label": "d",
"name": "Co-amoxiclav",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The exact mechanism by which salbutamol causes tremor is still unknown, but the leading theory is that salbutamol acts on beta-2 adrenoreceptors in muscles, leading to incomplete muscle relaxation and contraction, leading to tremors. There is also an alternative theory that suggests that salbutamol causes hypokalaemia which subsequently causes the tremor.",
"id": "10023645",
"label": "a",
"name": "Salbutamol",
"picture": null,
"votes": 33
}
],
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"id": "4197",
"name": "Side effects of asthma medications",
"status": null,
"topic": {
"__typename": "Topic",
"id": "189",
"name": "Respiratory Pharmacology",
"typeId": 7
},
"topicId": 189,
"totalCards": null,
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"question": "A 23-year-old female is being treated for an asthma exacerbation in the ED. She has been given a variety of drugs but now complains of having a tremor in her hands, making it difficult for her to eat and drink. She would like to know what is the cause of this tremor.\n\nWhat medication is causing this patient's tremor?",
"sbaAnswer": [
"a"
],
"totalVotes": 45,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,877 | false | 37 | null | 6,495,166 | null | false | [] | null | 17,128 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "This patient has most likely been given the wrong type of blood, which causes IgG antibodies to be produced towards the incompatible blood type, leading to the agglutination of these cells and inflammation.",
"id": "10023650",
"label": "a",
"name": "Type II hypersensitivity reaction",
"picture": null,
"votes": 18
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "There is no type V hypersensitivity reaction, so this option is incorrect.",
"id": "10023654",
"label": "e",
"name": "Type V hypersensitivity reaction",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is when an antigen-antibody complex is deposited into the small vasculature, causing an immune response which leads to inflammation. This can cause autoimmunity; an example of a type III hypersensitivity reaction is rheumatoid arthritis.",
"id": "10023652",
"label": "c",
"name": "Type III hypersensitivity reaction",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "An example of this is contact dermatitis. The reactive molecule binds as a hapten to an endogenous protein which is recognised and taken up by Langerhans cells. This causes T helper cells to secrete IFN-γ and cause a pro-inflammatory state within the tissue. This patient is not experiencing this type of reaction.",
"id": "10023653",
"label": "d",
"name": "Type IV hypersensitivity reaction",
"picture": null,
"votes": 11
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is when an allergen is picked up by dendritic cells which activate B cells and produce IgE antibodies. These IgE antibodies attach to mast cells and cause them to degranulate, releasing histamine. This patient has experienced a type II, not type I hypersensitivity reaction.",
"id": "10023651",
"label": "b",
"name": "Type I hypersensitivity reaction",
"picture": null,
"votes": 10
}
],
"comments": [],
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},
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"id": "4091",
"name": "Hypersensitivity reactions",
"status": null,
"topic": {
"__typename": "Topic",
"id": "158",
"name": "Immunology",
"typeId": 7
},
"topicId": 158,
"totalCards": null,
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},
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"question": "A 53-year-old male comes into the hospital as he is feeling tired all the time and experiencing occasional dizziness. The doctor performs some blood tests and finds that he has a haemoglobin of 58g/dl. The doctor organises a blood transfusion for this patient as his haemoglobin is low.\n\nHowever, during the blood transfusion, the patient starts to develop a fever. The doctor on-call thinks this is due to a hypersensitivity reaction.\n\nWhich type of hypersensitivity reaction has this patient experienced?",
"sbaAnswer": [
"a"
],
"totalVotes": 42,
"typeId": 1,
"userPoint": null
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173,464,878 | false | 38 | null | 6,495,166 | null | false | [] | null | 17,129 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is where the trachea bifurcates and splits into the left and right primary (main) bronchi. It is located at the level of the sternal angle.",
"id": "10023658",
"label": "d",
"name": "Carina",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "These cells are found in the walls of the alveoli and they form the squamous epithelium. This allows for a very small barrier for gaseous exchange, therefore increasing the concentration of oxygen getting into the capillaries and carbon dioxide leaving the capillaries.",
"id": "10023656",
"label": "b",
"name": "Type 1 pneumocytes",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "These cells are found in the walls of alveoli and their main role is to produce surfactant. Surfactant is produced to prevent the collapse of the alveoli when there is positive pressure in the lungs (during expiration).",
"id": "10023655",
"label": "a",
"name": "Type 2 pneumocytes",
"picture": null,
"votes": 43
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Bronchioles have ciliated columnar epithelium with very few goblet cells. They do not contain cartilage or submucosal glands as the walls are mostly smooth muscle. Bronchioles do not secrete surfactant or mucus.",
"id": "10023657",
"label": "c",
"name": "Bronchioles",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The visceral pleura covers the lungs and is adherent to all its surfaces. It contains a small volume of serous fluid, which has 2 major functions:\n\n* Lubricates the surface of the pleurae, allowing them to slide over each other\n* Produces surface tension, pulling the parietal and visceral pleura together – this ensures that when the thorax expands, the lungs also expand, allowing it to be filled up with air.\n\nThe visceral pleura does not secrete surfactant.",
"id": "10023659",
"label": "e",
"name": "Visceral pleura",
"picture": null,
"votes": 0
}
],
"comments": [],
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"__typename": "Concept",
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"__typename": "Chapter",
"explanation": null,
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"pictures": [],
"typeId": 7
},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "4199",
"name": "Surfactant",
"status": null,
"topic": {
"__typename": "Topic",
"id": "150",
"name": "Respiratory physiology",
"typeId": 7
},
"topicId": 150,
"totalCards": null,
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},
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"question": "A 34-week-old premature neonate is being treated for respiratory distress. The neonatal consultant suspects that they are deficient in surfactant.\n\nWhat is responsible for producing surfactant in the lungs?",
"sbaAnswer": [
"a"
],
"totalVotes": 47,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,879 | false | 39 | null | 6,495,166 | null | false | [] | null | 17,130 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The Mantoux test is used to test for latent disease (when there are no symptoms), either before receiving the BCG vaccine or if there has been recent contact with a person with tuberculosis. This patient has an active tuberculosis infection so the best way to confirm the diagnosis is with a sputum culture.",
"id": "10023661",
"label": "b",
"name": "Mantoux test",
"picture": null,
"votes": 9
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "An ECG will not help detect or confirm tuberculosis, but it might help detect any cardiac abnormalities.",
"id": "10023664",
"label": "e",
"name": "ECG",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "A chest x-ray might show that there is shadowing within the lung fields, however, it will not give a definite diagnosis of tuberculosis infection. There is usually lung cavitation and hilar lymph node shadowing on a chest x-ray during a tuberculosis infection.",
"id": "10023662",
"label": "c",
"name": "Chest x-ray",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is the correct answer as this patient has an active tuberculosis infection, therefore obtaining a sputum culture to look for acid-fast bacilli is the best way to confirm the diagnosis.",
"id": "10023660",
"label": "a",
"name": "Sputum culture",
"picture": null,
"votes": 25
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is used to test for latent disease, not active tuberculosis. It is a lot more sensitive and specific than Mantoux so allows for detection in immunosuppressed patients. It works because memory T cells release IFN-gamma upon detection of *M. tuberculosis* antigens which can be detected by a machine.",
"id": "10023663",
"label": "d",
"name": "IFN-gamma release assay",
"picture": null,
"votes": 6
}
],
"comments": [],
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"__typename": "Concept",
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"__typename": "Chapter",
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"typeId": 7
},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "4331",
"name": "Tuberculosis",
"status": null,
"topic": {
"__typename": "Topic",
"id": "194",
"name": "Infectious Diseases",
"typeId": 7
},
"topicId": 194,
"totalCards": null,
"typeId": null,
"userChapter": null,
"userNote": null,
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},
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"dislikes": 0,
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"question": "A 34-year-old male presents to the GP with blood-streaked sputum. He has recently returned from Nigeria. The medical team suspect tuberculosis.\n\nWhich investigation should be used to confirm the diagnosis of tuberculosis?",
"sbaAnswer": [
"a"
],
"totalVotes": 42,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,880 | false | 40 | null | 6,495,166 | null | false | [] | null | 17,131 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Residual volume is the volume of air remaining in the lungs after maximum forceful expiration. This air cannot be expelled from the lungs; otherwise, the alveoli would collapse.",
"id": "10023667",
"label": "c",
"name": "Residual volume",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Vital capacity is the maximal volume of air that can be exhaled following maximum inspiration. It is usually measured from the highest peak to the lowest trough on the graph.",
"id": "10023665",
"label": "a",
"name": "Vital capacity",
"picture": null,
"votes": 36
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Inspiratory capacity is the amount of air that can be inhaled after the end of a normal expiration. It can be worked out by combining the tidal volume and the inspiratory reserve volume.",
"id": "10023668",
"label": "d",
"name": "Inspiratory capacity",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Tidal volume is the amount of air that moves in or out of the lungs with each respiratory cycle and is usually around 500ml.",
"id": "10023666",
"label": "b",
"name": "Tidal volume",
"picture": null,
"votes": 6
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Expiratory reserve volume is the reserve amount of air that can be exhaled forcefully after passive exhalation.",
"id": "10023669",
"label": "e",
"name": "Expiratory reserve volume",
"picture": null,
"votes": 4
}
],
"comments": [],
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"__typename": "Concept",
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"__typename": "Chapter",
"explanation": null,
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"typeId": 7
},
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"demo": null,
"entitlement": null,
"id": "3726",
"name": "Spirometry",
"status": null,
"topic": {
"__typename": "Topic",
"id": "132",
"name": "Respiratory",
"typeId": 7
},
"topicId": 132,
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"question": "A 24-year-old female is undergoing spirometry for her asthma to assess how well-controlled it is. The doctor explains to the patient what each of the lines on the graph means.\n\nAs part of the test, the doctor asks the patient to take in the deepest breath that she can and then blow out as much air as she can.\n\nWhat is the name given to this volume of air on the spirometry graph?",
"sbaAnswer": [
"a"
],
"totalVotes": 47,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,881 | false | 41 | null | 6,495,166 | null | false | [] | null | 17,132 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The sternocleidomastoid muscle attaches to the manubrium and clavicle and helps elevate the sternum during inspiration. This increases the length of the thoracic cavity, allowing for greater expansion of the lungs, and increasing gaseous exchange.",
"id": "10023670",
"label": "a",
"name": "Sternocleidomastoid muscle",
"picture": null,
"votes": 20
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The posterior scalene muscle attaches to the inner border of the second rib, elevating it during inspiration. The sternocleidomastoid muscle elevates the sternum during inspiration.",
"id": "10023672",
"label": "c",
"name": "Posterior scalene muscle",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The diaphragm is located at the bottom of the ribcage, not connecting to the sternum at any point, and is dome-shaped. During inspiration, the dome descends, thus increasing the vertical dimension of the thoracic cavity.",
"id": "10023674",
"label": "e",
"name": "Diaphragm",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The external intercostal muscles elevate the ribs during inspiration, causing an increase in thoracic cavity width. The sternocleidomastoid muscle elevates the sternum during inspiration.",
"id": "10023673",
"label": "d",
"name": "External intercostal muscles",
"picture": null,
"votes": 16
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The anterior scalene muscle attaches to the inner border of the first rib and elevates it during inspiration. The sternocleidomastoid muscle elevates the sternum during inspiration.",
"id": "10023671",
"label": "b",
"name": "Anterior scalene muscle",
"picture": null,
"votes": 9
}
],
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"__typename": "Concept",
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"demo": null,
"entitlement": null,
"id": "3778",
"name": "The role of chest muscles in breathing",
"status": null,
"topic": {
"__typename": "Topic",
"id": "150",
"name": "Respiratory physiology",
"typeId": 7
},
"topicId": 150,
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"question": "An 86-year-old male is being observed breathing by the medical team on the respiratory ward. It is noted that he is using his accessory muscles to breathe, which is concerning the medical team.\n\nWhat accessory muscle elevates the sternum during inspiration?",
"sbaAnswer": [
"a"
],
"totalVotes": 47,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,882 | false | 42 | null | 6,495,166 | null | false | [] | null | 17,133 | {
"__typename": "QuestionSBA",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "C6-T1 nerve roots form the majority of the brachial plexus. These nerves innervate the shoulder, arm and hand on each side of the body. These nerves do not innervate the diaphragm.",
"id": "10023678",
"label": "d",
"name": "C6-T1",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "C1,2 and 3 all innervate the head and neck, allowing for control of forward, backwards and sideways movement of the head and neck. They do not control the diaphragm.",
"id": "10023676",
"label": "b",
"name": "C1-C3",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "T1 and T2 are thoracic nerves and run between the ribs, with each thoracic nerve being named after the vertebra above it. These nerves innervate the intercostal muscles, not the diaphragm.",
"id": "10023677",
"label": "c",
"name": "T1-T2",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "C3,4 and 5 all innervate the diaphragm, causing it to flatten during inspiration and return to a dome shape during expiration. Remember the phrase 'C3,4,5 keeps the diaphragm alive'.",
"id": "10023675",
"label": "a",
"name": "C3-C5",
"picture": null,
"votes": 44
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "L4-S3 nerve roots form the sacral plexus, which forms the sciatic nerve. This nerve runs down from the lumbar region of the spinal cord, into the leg.",
"id": "10023679",
"label": "e",
"name": "L4-S3",
"picture": null,
"votes": 0
}
],
"comments": [],
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"demo": null,
"entitlement": null,
"id": "4514",
"name": "Innervation of the respiratory system",
"status": null,
"topic": {
"__typename": "Topic",
"id": "150",
"name": "Respiratory physiology",
"typeId": 7
},
"topicId": 150,
"totalCards": null,
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"question": "A 19-year-old male is on a ventilator after being involved in a severe car crash. The ventilator is taking over his breathing, replacing the function of the diaphragm.\n\nWhich nerve roots innervate the diaphragm?",
"sbaAnswer": [
"a"
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173,464,883 | false | 43 | null | 6,495,166 | null | false | [] | null | 17,134 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Wilson's disease is a build-up of copper in the body due to an inability to excrete excess copper. If there were Kayser–Fleischer rings present (golden-brown eye discolouration), then it would be appropriate to screen for Wilson's disease.",
"id": "10023682",
"label": "c",
"name": "Wilson's disease",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Scleritis is inflammation of the sclera and causes symptoms such as pain on eye movement. This does not need to be screened for when a patient presents with optic neuritis.",
"id": "10023681",
"label": "b",
"name": "Scleritis",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would be reasonable if the patient had xanthelasma around the eye and eyelid; however, this patient has presented with optic neuritis which can be the first sign of multiple sclerosis.",
"id": "10023684",
"label": "e",
"name": "High cholesterol",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Thyroid eye disease would present with bulging, dry, irritated eyes. If this was the presentation, then it would be reasonable to do blood tests to check for hyperthyroidism and antibodies.",
"id": "10023683",
"label": "d",
"name": "Graves' disease",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Optic neuritis is a very common first presentation for multiple sclerosis (MS). MS is screened for using MRI scans which have to show 2 separate lesions on 2 separate MRIs (McDonald criteria - an individual must have symptoms/radiological signs which are disseminated in both space and time to be diagnosed with MS).",
"id": "10023680",
"label": "a",
"name": "Multiple sclerosis",
"picture": null,
"votes": 30
}
],
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"id": "5692",
"name": "Optic neuritis",
"status": null,
"topic": {
"__typename": "Topic",
"id": "140",
"name": "Ophthalmology",
"typeId": 7
},
"topicId": 140,
"totalCards": null,
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"question": "A 26-year-old female presents to the GP with a 2-day history of pain behind the eye. She also describes a bit of blurriness and some changes to her red colour vision. The GP suspects this is optic neuritis and manages it accordingly.\n\nWhat other pathology should be screened for in this woman?",
"sbaAnswer": [
"a"
],
"totalVotes": 41,
"typeId": 1,
"userPoint": null
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173,464,884 | false | 44 | null | 6,495,166 | null | false | [] | null | 17,135 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Na+ channels in rod cells close in response to light as rhodopsin is activated. This leads to hyperpolarisation of the cell and a subsequent decrease in synaptic glutamate release due to the closure of voltage-gated calcium channels.",
"id": "10023686",
"label": "b",
"name": "Na+ channels in rod cells",
"picture": null,
"votes": 9
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Rod cells in the eye contain rhodopsin which is activated when light is shone onto it. This molecule closes Na+ channels, hyperpolarising the cell. This leads to a decrease in synaptic glutamate release due to the closure of voltage-gated calcium channels.",
"id": "10023685",
"label": "a",
"name": "Rhodopsin",
"picture": null,
"votes": 17
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Drusen are yellow fat/protein deposits in the macular which cause photoreceptor loss, leading to dry age-related macular degeneration. This is pathological and is not usually found in healthy people, so has no role in normal visual pathways.",
"id": "10023689",
"label": "e",
"name": "Drusen",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Vitreous humour is the jelly-like substance in the posterior chamber of the eye that helps maintain the eye's shape and acts as a shock absorber. It is not involved in the phototransduction pathway.",
"id": "10023687",
"label": "c",
"name": "Vitreous humour",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Cone cells are activated by coloured lights. There are 3 types of cones: green cones, red cones and blue cones; all dedicated to detecting different wavelengths of light.",
"id": "10023688",
"label": "d",
"name": "Cone cells",
"picture": null,
"votes": 11
}
],
"comments": [],
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"demo": null,
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"id": "4508",
"name": "Anatomy of visual pathways",
"status": null,
"topic": {
"__typename": "Topic",
"id": "152",
"name": "Neuroscience",
"typeId": 7
},
"topicId": 152,
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},
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"question": "A 64-year-old diabetic presents to the eye clinic complaining of some vision loss. The ophthalmologist shines a light into the patient's eye and diagnoses a cataract. The patient asks what is the cause of his inability to see specific parts of his visual field.\n\nWhat is activated in the phototransduction pathway when white light is shone onto it?",
"sbaAnswer": [
"a"
],
"totalVotes": 37,
"typeId": 1,
"userPoint": null
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173,464,885 | false | 45 | null | 6,495,166 | null | false | [] | null | 17,136 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "According to NICE, a patient with otitis media with effusion without hearing loss should be monitored for 3 months, with regular examinations and audiology assessments if needed.",
"id": "10023690",
"label": "a",
"name": "Watch and wait for a month",
"picture": null,
"votes": 7
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "NICE advises to not prescribe corticosteroids for otitis media with effusion as there is no evidence that they change the outcome or the course of the disease. This patient needs to be monitored for another month as her symptoms should resolve spontaneously.",
"id": "10023694",
"label": "e",
"name": "Prescribe prednisolone",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "As this patient has no fever or systemic upset, antibiotics are not needed. Otitis media with effusion usually resolves spontaneously without any treatment. Giving antibiotics unnecessarily might incur antimicrobial resistance.",
"id": "10023691",
"label": "b",
"name": "Prescribe a 7-day course of amoxicillin",
"picture": null,
"votes": 21
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "These may be offered to children with persistent bilateral otitis media with effusion and hearing loss instead of surgery. This patient does not have hearing loss and this is the first time she has experienced these symptoms, so it is not appropriate to give her hearing aids.",
"id": "10023693",
"label": "d",
"name": "Hearing aids",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "NICE has certain criteria for referring a patient to ENT with otitis media: hearing loss or persistent foul-smelling discharge indicative of cholesteatoma. As this patient has none of these, there is no indication to refer to ENT.",
"id": "10023692",
"label": "c",
"name": "Referral to ENT",
"picture": null,
"votes": 7
}
],
"comments": [],
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"__typename": "Concept",
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"__typename": "Chapter",
"explanation": null,
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"typeId": 7
},
"chapterId": 2693,
"demo": null,
"entitlement": null,
"id": "5693",
"name": "Otits Media",
"status": null,
"topic": {
"__typename": "Topic",
"id": "138",
"name": "Ear, Nose & Throat",
"typeId": 7
},
"topicId": 138,
"totalCards": null,
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},
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"question": "An 8-year-old female is brought to the GP by her parents as she is repeatedly tugging on her left ear. She also complains of pain coming from that ear. There has been no fever or hearing loss and this is the first time she has been experiencing these symptoms. The symptoms have been going on for 2 months.\n\nThe GP performs otoscopy and sees a bulging tympanic membrane, indicating otitis media with effusion.\n\nWhat is the management of this patient?",
"sbaAnswer": [
"a"
],
"totalVotes": 37,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,886 | false | 46 | null | 6,495,166 | null | false | [] | null | 17,137 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The stapedius muscle attaches to the stapes and is innervated by the facial nerve. This question asks about which muscle pulls on the malleus, not the stapes.",
"id": "10023696",
"label": "b",
"name": "Stapedius",
"picture": null,
"votes": 13
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The tensor tympani pulls the handle of the malleus medially when contracting during the acoustic reflex. It is innervated by the tensor tympani nerve, which is a branch of the mandibular nerve. The acoustic reflex is when the muscles of the inner ear contract in response to loud noise, inhibiting the vibrations of the auditory ossicles and reducing the transmission of sound to the inner ear.",
"id": "10023695",
"label": "a",
"name": "Tensor tympani",
"picture": null,
"votes": 18
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The membranous labyrinth lies within the bony labyrinth of the inner ear. It consists of the cochlear duct, semi-circular ducts, utricle and saccule. The cochlear duct is an organ of hearing and the semi-circular ducts, utricle and saccule are organs of balance. They play no role in the acoustic reflex.",
"id": "10023699",
"label": "e",
"name": "Membranous labyrinth",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The pars tensa is part of the tympanic membrane but is not a muscle. It may play some role in the acoustic reflex but it does not contract (as it is not a muscle) to pull the malleus medially.",
"id": "10023697",
"label": "c",
"name": "Pars tensa",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The tragus is located anterior to the beginning of the external acoustic meatus. It is an elevation of cartilaginous tissue and plays no part in the acoustic reflex.",
"id": "10023698",
"label": "d",
"name": "Tragus",
"picture": null,
"votes": 3
}
],
"comments": [],
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"__typename": "Concept",
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"demo": null,
"entitlement": null,
"id": "4112",
"name": "Middle ear anatomy",
"status": null,
"topic": {
"__typename": "Topic",
"id": "138",
"name": "Ear, Nose & Throat",
"typeId": 7
},
"topicId": 138,
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"question": "A 37-year-old male is at a football game when his team scores a goal. The noise level increases dramatically as everyone celebrates. The man's acoustic reflex helps protect his ears from the damage of the loud noises surrounding him.\n\nIn the acoustic reflex, which muscle contracts and pulls the malleus medially?",
"sbaAnswer": [
"a"
],
"totalVotes": 36,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,887 | false | 47 | null | 6,495,166 | null | false | [] | null | 17,138 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "In essential tremor, the tremor persists and the handwriting stays the same size, unlike in this patient where his handwriting gets smaller and his tremor disappears. This, along with the bradykinesia, suggests a diagnosis of Parkinson's disease over essential tremor.",
"id": "10023701",
"label": "b",
"name": "Essential tremor",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "In functional tremor, there is uncontrollable shaking of a part of the body. This is due to the nervous system not working properly, not due to an underlying neurological disease.",
"id": "10023704",
"label": "e",
"name": "Functional tremor",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "An intention tremor happens during deliberate, voluntary movements. It happens as the consequence of cerebellar dysfunction, particularly on the same side as the tremor. As this tremor is present at rest, an intentional tremor is unlikely.",
"id": "10023703",
"label": "d",
"name": "Intention tremor",
"picture": null,
"votes": 3
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This patient has no medical conditions which makes the diagnosis of hyperthyroidism unlikely. The handwriting getting smaller and the tremor disappearing are also suggestive of Parkinson's disease.",
"id": "10023702",
"label": "c",
"name": "Hyperthyroidism",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The symptoms of resting tremor and bradykinesia (slow, little steps) suggest a diagnosis of Parkinson's disease. The handwriting getting smaller and the tremor disappearing suggests PD over essential tremor as in essential tremor, the tremor persists and the handwriting remains the same size.",
"id": "10023700",
"label": "a",
"name": "Parkinson's disease (PD)",
"picture": null,
"votes": 27
}
],
"comments": [],
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"id": "3747",
"name": "Parkinson's Disease",
"status": null,
"topic": {
"__typename": "Topic",
"id": "141",
"name": "Neurology",
"typeId": 7
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"topicId": 141,
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"question": "A 72-year-old male presents to the GP with a tremor that is present at rest. The GP also notices that the patient takes slow, little steps when walking. The patient has no other medical conditions.\n\nThe GP asks the patient to write some words on a bit of paper and notices that his handwriting gets smaller and the tremor disappears while doing this.\n\nWhat is the most likely diagnosis?",
"sbaAnswer": [
"a"
],
"totalVotes": 38,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,888 | false | 48 | null | 6,495,166 | null | false | [] | null | 17,139 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "HER2 is a proto-oncogene that, when activated, leads to the increased production of downstream proteins and signalling molecules that promote cell growth and differentiation.",
"id": "10023707",
"label": "c",
"name": "HER2",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Telomeres are the structures at the end of chromosomes that control how many replications a cell can undergo. As DNA is replicated, the very end of the strand is lost. As a healthy cell divides, the telomeres shorten and once there are no telomeres, the cell undergoes apoptosis. Cancer cells can evade this apoptosis by making more telomerase enzymes which prevent the telomeres from getting shorter.",
"id": "10023705",
"label": "a",
"name": "Telomeres",
"picture": null,
"votes": 41
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "TNF-alpha is a pro-inflammatory chemokine that is produced by white blood cells during inflammation and leads to the necrosis or apoptosis of cells.",
"id": "10023709",
"label": "e",
"name": "TNF-alpha",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "p53 is a tumour suppressor gene which repairs DNA damage if detected. It is often inactivated in breast cancer, hence disrupting the cell cycle and allowing the cancerous cells to keep dividing.",
"id": "10023706",
"label": "b",
"name": "p53",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "BRCA1 encodes a protein that recognises and repairs ds-DNA breaks. Therefore, cells that lack BRCA proteins have a reduced ability to detect and repair damaged DNA, leading to a significant increase in the risk of that cell progressing through the cell cycle without being destroyed. This means that there is a higher chance of the cells becoming cancerous.",
"id": "10023708",
"label": "d",
"name": "BRCA1",
"picture": null,
"votes": 3
}
],
"comments": [],
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},
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"demo": null,
"entitlement": null,
"id": "4362",
"name": "Genetic concepts",
"status": null,
"topic": {
"__typename": "Topic",
"id": "156",
"name": "Medical Genetics",
"typeId": 7
},
"topicId": 156,
"totalCards": null,
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},
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"question": "A 66-year-old female has just been diagnosed with breast cancer and asks what has caused the cancer to grow as fast as it has done, as she only noticed the lump on her breast a few weeks ago. The doctor explains that there are regions at the end of DNA strands that protect them from damage, and every time a cell divides they get shorter. When they get too short, the cell they are in usually dies. However, some cancer cells can evade this death by making these regions longer, allowing them to continue proliferating.\n\nWhat structure is the doctor referring to?",
"sbaAnswer": [
"a"
],
"totalVotes": 46,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,889 | false | 49 | null | 6,495,166 | null | false | [] | null | 17,140 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "A stye is an infection of a hair follicle within the eyelid. It can present as a little bump on the eyelid and is usually painful. The most common organism that causes styes is *S. aureus*. Usually, no treatment is needed, but a warm compress can be used to help relieve symptoms.",
"id": "10023710",
"label": "a",
"name": "Stye",
"picture": null,
"votes": 19
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Entropion is where the eyelid is turned inwards, leading to the eyelashes scraping the cornea. As there is no mention of the eyelid being turned inwards in this question, this answer choice is unlikely.",
"id": "10023714",
"label": "e",
"name": "Entropion",
"picture": null,
"votes": 3
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Herpes simplex keratitis (HSK) is inflammation of the cornea, not the eyelid. The symptoms are typically a painful, gritty sensation in the eye, along with decreased visual acuity.",
"id": "10023712",
"label": "c",
"name": "Herpes simplex keratitis",
"picture": null,
"votes": 5
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Ectropion is where the eyelid is turned outwards, leading to a watery, inflamed eye. It is almost always the lower eyelid, so is unlikely to happen in this patient as their swelling is on the upper eyelid. The treatment for ectropion is surgical correction of the eyelid.",
"id": "10023713",
"label": "d",
"name": "Ectropion",
"picture": null,
"votes": 6
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "A chalazion is a swelling of the eyelid due to a blocked Meibomian gland (which contributes to creating tears) and is usually firmer than a stye. It can be differentiated from a stye as a chalazion is not usually painful, whereas a stye usually is.",
"id": "10023711",
"label": "b",
"name": "Chalazion",
"picture": null,
"votes": 6
}
],
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"id": "4637",
"name": "Styes and chalazions",
"status": null,
"topic": {
"__typename": "Topic",
"id": "140",
"name": "Ophthalmology",
"typeId": 7
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"question": "A 35-year-old female presents to the GP with pain around her eye and swelling around the upper eyelid. There is no change to her vision.\n\nOn closer examination, the GP notices that there is a swollen infected hair follicle.\n\nWhat is the most likely diagnosis?",
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"a"
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173,464,890 | false | 50 | null | 6,495,166 | null | false | [] | null | 17,141 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The glossopharyngeal nerve provides sensation to the oropharynx, carotid body and sinus, posterior 1/3 of the tongue, middle ear cavity and Eustachian tube. It provides motor function to the stylopharyngeus muscle in the pharynx, provides taste sensation to the posterior 1/3 of the tongue and provides parasympathetic innervation to the parotid gland.",
"id": "10023717",
"label": "c",
"name": "Glossopharyngeal nerve",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The zygomatic branch of the facial nerve provides motor function to the orbicularis oculi muscle, which closes the eyelid.",
"id": "10023719",
"label": "e",
"name": "Zygomatic branch of the facial nerve",
"picture": null,
"votes": 9
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The maxillary branch of the trigeminal nerve provides sensation to the upper lip, mucosa of the nose and upper teeth. It also has some parasympathetic fibres that go to the lacrimal, nasal and palatine glands.",
"id": "10023715",
"label": "a",
"name": "Maxillary branch of the trigeminal nerve",
"picture": null,
"votes": 26
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The mandibular branch of the trigeminal nerve provides motor function to the muscles of mastication and sensation to the lower part of the face and chin and anterior 2/3rds of the tongue.",
"id": "10023718",
"label": "d",
"name": "Mandibular branch of the trigeminal nerve",
"picture": null,
"votes": 10
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The vestibulocochlear nerve has the function of hearing (cochlear portion) and balance (vestibular portion).",
"id": "10023716",
"label": "b",
"name": "Vestibulocochlear nerve",
"picture": null,
"votes": 0
}
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"id": "5694",
"name": "Lower motor neuron lesions",
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"id": "152",
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"question": "A 45-year-old male presents to the neurology clinic after being referred by his GP. The patient describes a loss of sensation in his upper lip. He says that eating is now a strange feeling due to this.\n\nWhat cranial nerve is affected?",
"sbaAnswer": [
"a"
],
"totalVotes": 45,
"typeId": 1,
"userPoint": null
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173,464,929 | false | 1 | null | 6,495,169 | null | false | [] | null | 17,192 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is the process of the cytoplasm and cell membrane splitting into 2 daughter cells at the end of the cycle.",
"id": "10023972",
"label": "c",
"name": "Cytokinesis Phase",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The G1 phase is the longest phase of the cell cycle and the beginning of interphase. It occurs in between the M-phase and the S-phase. During this phase, cells are the most metabolically active. The duration of G1 varies thus determining the length of the cell cycle.",
"id": "10023970",
"label": "a",
"name": "G1 Phase",
"picture": null,
"votes": 35
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The G2 phase is also a growth phase but different to G1. The DNA has already been duplicated so during the G2 phase, the cell prepares for division and corrects any errors in chromosome number.",
"id": "10023971",
"label": "b",
"name": "G2 Phase",
"picture": null,
"votes": 8
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The M phase, or mitosis, is the phase of actual cell division. Whilst it's a critical part of the cell cycle, it doesn't determine the length of the entire cell cycle. The M phase is relatively short and follows the G2 phase.",
"id": "10023974",
"label": "e",
"name": "M Phase (Mitosis)",
"picture": null,
"votes": 8
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The S phase comes after G1 during interphase. Cellular DNA is replicated during this phase.",
"id": "10023973",
"label": "d",
"name": "S Phase",
"picture": null,
"votes": 22
}
],
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"id": "5709",
"name": "Phases of the Cell Cycle",
"status": null,
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"question": "Which of the following phases of the cell cycle is responsible for determining the length of the cell cycle?",
"sbaAnswer": [
"a"
],
"totalVotes": 74,
"typeId": 1,
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173,464,930 | false | 2 | null | 6,495,169 | null | false | [] | null | 17,193 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "During anaphase, chromosomes move towards opposite poles of the cell. There is no further introduction of genetic variation in this stage.",
"id": "10023978",
"label": "d",
"name": "Anaphase",
"picture": null,
"votes": 31
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The G2 phase occurs after DNA replication (S phase) and is mainly associated with further preparation for cell division (mitosis). It is not a phase where genetic variation is introduced but rather one where the cell ensures that it is ready for mitosis.",
"id": "10023979",
"label": "e",
"name": "G2 phase",
"picture": null,
"votes": 10
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Telophase is the fifth and final phase of mitosis, the process that separates the duplicated genetic material carried in the nucleus of a parent cell into two identical daughter cells. There is no introduction of genetic variation during this phase.",
"id": "10023976",
"label": "b",
"name": "Telophase",
"picture": null,
"votes": 12
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "During pachytene in prophase 1, genetic information is exchanged between homologous pairs of chromosomes at the chiasmata. This is an example of genetic variation being introduced as the chromosomes come from 2 genetically unique individuals.",
"id": "10023975",
"label": "a",
"name": "Pachytene",
"picture": null,
"votes": 9
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is the first phase of prophase during which the chromosomes just begin to condense. There is no \"crossing over\" yet and thus no introduction of genetic variation.",
"id": "10023977",
"label": "c",
"name": "Leptotene",
"picture": null,
"votes": 3
}
],
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"name": "Cell Cycle",
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"id": "278",
"name": "Cell Basics",
"typeId": 7
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"question": "During the cell cycle, genetic variation is introduced in specific phases.\n\nWhich of the following is a correct example of this?",
"sbaAnswer": [
"a"
],
"totalVotes": 65,
"typeId": 1,
"userPoint": null
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173,464,931 | false | 3 | null | 6,495,169 | null | false | [] | null | 17,194 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Iron is not absorbed in the stomach, but Fe3+ is converted to Fe2+ here. The proximal jejunum is where the absorption of iron occurs.",
"id": "10023981",
"label": "b",
"name": "Stomach & proximal jejunum",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is an incorrect choice as the stomach is not a site for iron absorption.",
"id": "10023983",
"label": "d",
"name": "Stomach & duodenum",
"picture": null,
"votes": 5
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "At physiological pH, iron exists in the oxidised, ferric (Fe3+) state. To be absorbed, iron must be in the ferrous (Fe2+) state or bound by a protein such as heme. It is absorbed in the duodenum and proximal jejunum.",
"id": "10023980",
"label": "a",
"name": "Duodenum & proximal jejunum",
"picture": null,
"votes": 37
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The colon is primarily responsible for water and electrolyte absorption, but it is not involved in the absorption of iron. The anus is the endpoint of the GI tract and is not involved in the absorption of nutrients.",
"id": "10023984",
"label": "e",
"name": "Colon & anus",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The distal jejunum is responsible for small absorption of B12, water and sodium. Larger amounts of these are absorbed in the ileum.",
"id": "10023982",
"label": "c",
"name": "Distal jejunum & ileum",
"picture": null,
"votes": 20
}
],
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"name": "Iron Metabolism",
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"name": "Biochemistry",
"typeId": 7
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"question": "With regards to the metabolism of iron, where is iron absorbed in the GI tract?",
"sbaAnswer": [
"a"
],
"totalVotes": 63,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,932 | false | 4 | null | 6,495,169 | null | false | [] | null | 17,195 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "In competitive inhibition, Vmax remains the same. Competitive inhibitors compete with the substrate for the active site of an enzyme but do not affect the maximum rate of the enzyme-catalysed reaction.",
"id": "10023986",
"label": "b",
"name": "Vmax is decreased",
"picture": null,
"votes": 14
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Vmax is unaffected because competitive inhibitors do not alter an enzyme's maximal catalytic capacity. Instead, they primarily affect the affinity of an enzyme for its substrate. This can easily be overcome by increasing the concentration of the substrate.",
"id": "10023985",
"label": "a",
"name": "Vmax is unaffected",
"picture": null,
"votes": 28
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Competitive inhibition does not lead to an increase in Vmax. It specifically affects the affinity of an enzyme for its substrate but not the maximum rate of the reaction.",
"id": "10023987",
"label": "c",
"name": "Vmax is increased",
"picture": null,
"votes": 3
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Competitive inhibition does not directly inhibit Vmax. Instead, it reduces the effectiveness of the enzyme-substrate interaction by competing with the substrate for the active site.",
"id": "10023988",
"label": "d",
"name": "Vmax is partially inhibited",
"picture": null,
"votes": 8
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is a general statement that applies to Michaelis-Menten kinetics, but it is not specific to competitive inhibition. Competitive inhibition primarily affects the Km (Michaelis constant), which is a measure of the affinity of an enzyme for its substrate, and not the Vmax.",
"id": "10023989",
"label": "e",
"name": "Vmax is inversely proportional to substrate concentration",
"picture": null,
"votes": 7
}
],
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"name": "Enzyme Kinetics",
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"typeId": 7
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"question": "What is the effect of a competitive inhibitor on the Vmax of an enzyme?",
"sbaAnswer": [
"a"
],
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"typeId": 1,
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} | MarksheetMark |
173,464,933 | false | 5 | null | 6,495,169 | null | false | [] | null | 17,196 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "EDS is not an immune system disorder. Immune system disorders are distinct from EDS.",
"id": "10023993",
"label": "d",
"name": "Immune system disorder",
"picture": null,
"votes": 3
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "EDS primarily affects the connective tissues and does not directly relate to respiratory disorders. However, EDS can lead to respiratory issues if it affects the structural integrity of the chest wall.",
"id": "10023992",
"label": "c",
"name": "Respiratory disorder",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "EDS can have neurological symptoms, but it is not primarily a neurological disorder. The neurological symptoms are often related to complications arising from structural weaknesses in connective tissues, such as Chiari malformations. EDS is fundamentally a connective tissue disorder.",
"id": "10023994",
"label": "e",
"name": "Neurological disorder",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "EDS is indeed an example of a connective tissue disorder. It is a group of inherited disorders that affect the connective tissues in the body, primarily due to defects in collagen production or structure. This leads to various physical and physiological manifestations, including joint hypermobility, skin hyperelasticity, and fragility of tissues, such as blood vessels and internal organs. It is said to be associated primarily with a Type 1 collagen defect.",
"id": "10023990",
"label": "a",
"name": "Connective tissue disorder",
"picture": null,
"votes": 48
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "EDS primarily affects connective tissues, leading to symptoms such as hypermobility of joints, skin hyperelasticity, and tissue fragility. Whilst cardiovascular issues can be associated with EDS due to its effects on blood vessels, EDS itself is not primarily a cardiovascular disorder.",
"id": "10023991",
"label": "b",
"name": "Cardiovascular disorder",
"picture": null,
"votes": 1
}
],
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"name": "Ehlers-Danlos",
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"name": "Tissues of the Body",
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"question": "Ehlers-Danlos syndrome (EDS) is an example of which of the following defects?",
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"a"
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} | MarksheetMark |
173,464,934 | false | 6 | null | 6,495,169 | null | false | [] | null | 17,197 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Blood vessels are lined with simple squamous epithelium, also known as endothelium, which is adapted for the exchange of substances between blood and tissues. It does not have the stretching properties of transitional epithelium.",
"id": "10023998",
"label": "d",
"name": "Blood vessels",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The oesophagus is lined with stratified squamous epithelium to withstand the mechanical stress of food passing through it. Transitional epithelium is not found in the oesophagus.",
"id": "10023999",
"label": "e",
"name": "Oesophagus",
"picture": null,
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},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The small intestine is primarily lined with simple columnar epithelium to aid in nutrient absorption, not transitional epithelium.",
"id": "10023996",
"label": "b",
"name": "Lining of the small intestine",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
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"explanation": "The trachea is lined with pseudostratified ciliated columnar epithelium to help trap and remove foreign particles from the respiratory tract. It does not require the stretching and contraction capabilities of transitional epithelium.",
"id": "10023997",
"label": "c",
"name": "Trachea",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Transitional epithelium is found in the urinary bladder and the urinary tract in general. It allows the bladder to stretch as it fills with urine and then contract when the urine is expelled. It is also found in the renal pelvis, the ureter and parts of the urethra.",
"id": "10023995",
"label": "a",
"name": "Urinary bladder",
"picture": null,
"votes": 51
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"id": "5714",
"name": "Types of Cells",
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"topic": {
"__typename": "Topic",
"id": "279",
"name": "Tissues of the Body",
"typeId": 7
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173,464,935 | false | 7 | null | 6,495,169 | null | false | [] | null | 17,198 | {
"__typename": "QuestionSBA",
"choices": [
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Inserting the needle directly into the spinal cord is not the correct procedure for a lumbar puncture and can be extremely dangerous or fatal.",
"id": "10024001",
"label": "b",
"name": "Spinal Cord",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The intervertebral foramen is a passageway for spinal nerves, and inserting the needle here is not the correct site for a lumbar puncture. This can cause permanent disability.",
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"label": "d",
"name": "Intervertebral Foramen",
"picture": null,
"votes": 2
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "The epidural space is located outside the dura mater and contains fat and blood vessels. A lumbar puncture is not performed in the epidural space.",
"id": "10024002",
"label": "c",
"name": "Epidural Space",
"picture": null,
"votes": 19
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "A lumbar puncture is performed by inserting a needle into the subarachnoid space, which is located between the arachnoid mater and the pia mater. This is where cerebrospinal fluid (CSF) is found and can be safely obtained for diagnostic purposes. This should be done at the L3-L4 or L4-L5 interspace as this is considered the safe zone away from the spinal cord which is prone to injury. Inserting the needle at the wrong site can cause lasting damage and is a never-event.",
"id": "10024000",
"label": "a",
"name": "Subarachnoid space",
"picture": null,
"votes": 33
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Inserting the needle between vertebral discs can risk damaging the spinal cord, nerves, and blood vessels. A lumbar puncture is typically performed in the subarachnoid space, not between the vertebral discs.",
"id": "10024004",
"label": "e",
"name": "Between the vertebral discs",
"picture": null,
"votes": 8
}
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"id": "5715",
"name": "Lumbar Puncture",
"status": null,
"topic": {
"__typename": "Topic",
"id": "280",
"name": "Nerves",
"typeId": 7
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"topicId": 280,
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"question": "An F2 doctor suspects meningitis in a 25-year-old man. As part of his investigations, he needs to perform a lumbar puncture.\n\nWhich of the following sites should the needle be inserted into?",
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"a"
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173,464,936 | false | 8 | null | 6,495,169 | null | false | [] | null | 17,199 | {
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"choices": [
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Calcium ions are not primarily responsible for the depolarisation phase of the action potential. They play a significant role in synaptic transmission and various cellular processes but are not the key ions involved in the rising phase of the action potential.",
"id": "10024008",
"label": "d",
"name": "Calcium (Ca2+)",
"picture": null,
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},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Magnesium ions are not involved in the depolarisation phase of the action potential. Magnesium primarily serves as a cofactor in enzymatic reactions and does not play a significant role in the ionic mechanism of action potentials.",
"id": "10024009",
"label": "e",
"name": "Magnesium (Mg2+)",
"picture": null,
"votes": 0
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{
"__typename": "QuestionChoice",
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"explanation": "In a typical neuron, the depolarisation phase of an action potential is primarily driven by the influx of sodium ions (Na+) through voltage-gated sodium channels. This influx of positive sodium ions into the cell leads to a rapid change in membrane potential, creating the rising phase of the action potential.",
"id": "10024005",
"label": "a",
"name": "Sodium (Na+)",
"picture": null,
"votes": 50
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{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Chloride ions do play a role in the action potential, but they are primarily responsible for the hyperpolarisation phase (falling phase) and the maintenance of the resting membrane potential. They are not responsible for the initial depolarisation.",
"id": "10024006",
"label": "b",
"name": "Chloride (Cl-)",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Potassium ions do play a role in the repolarisation and hyperpolarisation phases of the action potential. They are responsible for returning the membrane potential to its resting state and maintaining it. They are not the ions responsible for the initial depolarisation.",
"id": "10024007",
"label": "c",
"name": "Potassium (K+)",
"picture": null,
"votes": 8
}
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"name": "Ionic Mechanism of Action Potentials",
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173,464,937 | false | 9 | null | 6,495,169 | null | false | [] | null | 17,200 | {
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"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Nitric oxide is a signalling molecule with a single nitrogen atom. It is not used as a source of nitrogen for urea synthesis.",
"id": "10024012",
"label": "c",
"name": "Nitric oxide (NO)",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Urea synthesis involves the combination of ammonia (NH3) and carbon dioxide (CO2) in a series of enzymatic reactions. Two ammonia molecules contribute their nitrogen atoms to form the two nitrogen atoms found in the urea molecule. This process occurs in the liver and is a key part of the urea cycle, which helps eliminate excess nitrogen (ammonia) from the body. Aspartate also contributes to the requirement for nitrogen atoms.",
"id": "10024010",
"label": "a",
"name": "Ammonia (NH3)",
"picture": null,
"votes": 45
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{
"__typename": "QuestionChoice",
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"explanation": "Whilst nitrate contains nitrogen, it is not directly used in the synthesis of urea. Nitrate can be converted into nitrite and then into ammonia, which can then be incorporated into the urea cycle.",
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"label": "b",
"name": "Nitrate (NO3-)",
"picture": null,
"votes": 7
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Nitrogen gas (N2) is abundant in the atmosphere but is not a form of nitrogen that the human body can readily use for urea synthesis. It needs to be converted into ammonia before it can be incorporated into the urea cycle.",
"id": "10024013",
"label": "d",
"name": "Nitrogen gas (N2)",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Uric acid contains nitrogen, but it is not directly involved in the synthesis of urea. Uric acid is the end product of purine metabolism, and excess nitrogen in the form of uric acid is excreted in the urine. It is not a precursor for urea formation.",
"id": "10024014",
"label": "e",
"name": "Uric acid",
"picture": null,
"votes": 6
}
],
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"id": "5717",
"name": "Urea Cycle",
"status": null,
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"id": "281",
"name": "Muscles",
"typeId": 7
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173,464,938 | false | 10 | null | 6,495,169 | null | false | [] | null | 17,201 | {
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{
"__typename": "QuestionChoice",
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"explanation": "Calcium ions do not initiate the opening of sodium channels. Sodium channels are primarily regulated by changes in voltage potential, specifically by depolarisation which allows sodium ions to enter the cell and initiate action potentials.",
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"label": "c",
"name": "Calcium ions initiate the opening of sodium (Na+) channels",
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"explanation": "In smooth muscle cells, calcium ions play a crucial role in initiating contraction. When calcium ions enter a cell, they bind to and activate myosin light chain kinase, which, in turn, phosphorylates myosin. This phosphorylation is a key step in the initiation of smooth muscle contraction. The other answer choices do not accurately describe the primary role of calcium ions in smooth muscle action potentials.",
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"explanation": "Whilst calcium ions do play a role in neurotransmitter release in neurons, this question is about calcium movement during action potentials in smooth muscle cells, where their primary function is related to muscle contraction, not neurotransmitter release.",
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"label": "d",
"name": "Calcium ions trigger the release of neurotransmitters",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "The repolarisation phase of an action potential typically involves the efflux of potassium ions (K+), not calcium ions. Calcium ions primarily play a role in the initiation and maintenance of muscle contraction.",
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"label": "b",
"name": "Calcium ions are responsible for the repolarisation of the cell membrane",
"picture": null,
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{
"__typename": "QuestionChoice",
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"explanation": "Calcium ions promote, rather than inhibit, the contraction of smooth muscle. They activate myosin light chain kinase, which is a key step in the initiation of smooth muscle contraction.",
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"label": "e",
"name": "Calcium ions inhibit the contraction of smooth muscle",
"picture": null,
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}
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173,464,939 | false | 11 | null | 6,495,169 | null | false | [] | null | 17,202 | {
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"choices": [
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "The neural crest is involved in the development of various structures, including certain nerves and components of the face. It is not associated with liver development.",
"id": "10024024",
"label": "e",
"name": "Neural crest",
"picture": null,
"votes": 3
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The mesoderm is responsible for forming structures like muscle, bone, blood, and the urinary and reproductive systems. Whilst mesoderm contributes to many organs, it is not the primary germ layer from which the liver originates.",
"id": "10024022",
"label": "c",
"name": "Mesoderm",
"picture": null,
"votes": 20
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The trophoblast is a layer of cells in early embryonic development that primarily forms the placenta, which plays a crucial role in nutrient and waste exchange between the mother and the developing fetus. The trophoblast does not directly contribute to liver development.",
"id": "10024023",
"label": "d",
"name": "Trophoblast",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The ectoderm primarily gives rise to structures such as the skin, nervous system, and parts of the eyes and ears. It does not contribute to the development of the liver.",
"id": "10024021",
"label": "b",
"name": "Ectoderm",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The liver primarily originates from the endoderm germ layer during embryonic development. The endoderm gives rise to many of the body's internal organs, including the liver, pancreas, and gastrointestinal tract. The other answer choices represent different germ layers and do not contribute significantly to liver development.",
"id": "10024020",
"label": "a",
"name": "Endoderm",
"picture": null,
"votes": 34
}
],
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"id": "5719",
"name": "Germ Layers",
"status": null,
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"typeId": 7
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173,464,940 | false | 12 | null | 6,495,169 | null | false | [] | null | 17,203 | {
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"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Cri du chat syndrome results from a deletion of a part of chromosome 5, not from having an extra chromosome 18.",
"id": "10024029",
"label": "e",
"name": "Cri du chat syndrome",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Klinefelter syndrome is associated with having an extra X chromosome, resulting in a karyotype of 47, XXY. It does not involve an extra chromosome 18.",
"id": "10024028",
"label": "d",
"name": "Klinefelter syndrome",
"picture": null,
"votes": 4
},
{
"__typename": "QuestionChoice",
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"explanation": "Turner syndrome is characterised by having only one X chromosome, leading to a total of 45 chromosomes (45, X), not an extra chromosome 18.",
"id": "10024027",
"label": "c",
"name": "Turner syndrome",
"picture": null,
"votes": 21
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Edwards' syndrome, or Trisomy 18, is characterised by an extra copy of chromosome 18. Individuals with Edwards' syndrome typically have severe intellectual and physical disabilities, as well as multiple congenital anomalies. The other syndromes mentioned are caused by different chromosomal abnormalities, and none of them involve an extra chromosome 18.",
"id": "10024025",
"label": "a",
"name": "Edwards' syndrome",
"picture": null,
"votes": 33
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Down syndrome is caused by an extra copy of chromosome 21 (Trisomy 21), not chromosome 18.",
"id": "10024026",
"label": "b",
"name": "Down syndrome",
"picture": null,
"votes": 2
}
],
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"id": "5720",
"name": "Abnormalities of Chromosome Number",
"status": null,
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"name": "Genes/Embryology",
"typeId": 7
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"topicId": 283,
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"question": "Which of the following is an example of a chromosome number abnormality in which an individual has an extra chromosome 18?",
"sbaAnswer": [
"a"
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"totalVotes": 61,
"typeId": 1,
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173,464,941 | false | 13 | null | 6,495,169 | null | false | [] | null | 17,204 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Photosynthesis is an anabolic process. It involves the synthesis of complex organic molecules, such as glucose, from simpler substances (carbon dioxide and water) using energy from sunlight.",
"id": "10024031",
"label": "b",
"name": "Photosynthesis",
"picture": null,
"votes": 0
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "In the bone marrow, erythropoiesis is the process of creating new red blood cells from precursor cells. This is essential to maintain adequate oxygen-carrying capacity in the blood. This requires energy.",
"id": "10024033",
"label": "d",
"name": "Erythropoiesis",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Protein synthesis is an anabolic process. It involves the assembly of complex proteins from amino acids, and it requires energy input.",
"id": "10024032",
"label": "c",
"name": "Protein synthesis",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Glycogenesis is the process of forming glycogen from glucose molecules. This is a way for the body to store excess glucose for later use when energy demands are high, such as during physical activity or between meals. This is anabolic as a more complex molecule is formed from a comparatively simpler molecule using energy.",
"id": "10024034",
"label": "e",
"name": "Glycogenesis",
"picture": null,
"votes": 9
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is a catabolic process. ATP (adenosine triphosphate) is broken down to ADP (adenosine diphosphate) to release energy for various cellular processes. Anabolic processes, on the other hand, involve the synthesis of complex molecules from simpler ones, often requiring energy input.",
"id": "10024030",
"label": "a",
"name": "Conversion of ATP to ADP",
"picture": null,
"votes": 46
}
],
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"id": "5721",
"name": "Catabolic & Anabolic Processes",
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"__typename": "Topic",
"id": "284",
"name": "Metabolism",
"typeId": 7
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"topicId": 284,
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"question": "Which of the following is an example of a catabolic process?",
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"a"
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} | MarksheetMark |
173,464,942 | false | 14 | null | 6,495,169 | null | false | [] | null | 17,205 | {
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Glucokinase is an enzyme primarily involved in regulating glucose levels in the liver and pancreas. It phosphorylates glucose during its uptake and storage as glycogen but is not a key enzyme in glycogen degradation.",
"id": "10024036",
"label": "b",
"name": "Glucokinase",
"picture": null,
"votes": 6
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Amylase is an enzyme responsible for the hydrolysis of starches and glycogen into simpler sugars. Whilst it plays a role in the digestion of glycogen in the digestive system, it is not the primary enzyme for glycogen degradation within cells.",
"id": "10024038",
"label": "d",
"name": "Amylase",
"picture": null,
"votes": 10
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is a crucial enzyme in the breakdown of glycogen into glucose-1-phosphate, allowing for the release of glucose when needed. The other 2 primary enzymes are glycogen debranching enzyme & phosphoglucomutase.",
"id": "10024035",
"label": "a",
"name": "Glycogen phosphorylase",
"picture": null,
"votes": 32
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Phosphofructokinase is an enzyme involved in glycolysis, specifically in the conversion of fructose-6-phosphate to fructose-1,6-bisphosphate. It is not a primary enzyme in glycogen degradation.",
"id": "10024037",
"label": "c",
"name": "Phosphofructokinase",
"picture": null,
"votes": 7
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Hexokinase is an enzyme involved in the initial steps of glycolysis, where glucose is converted to glucose-6-phosphate. It is not directly involved in glycogen degradation.",
"id": "10024039",
"label": "e",
"name": "Hexokinase",
"picture": null,
"votes": 2
}
],
"comments": [],
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"id": "5722",
"name": "Glycogen Metabolism",
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"id": "284",
"name": "Metabolism",
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"sbaAnswer": [
"a"
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"typeId": 1,
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} | MarksheetMark |
173,464,943 | false | 15 | null | 6,495,169 | null | false | [] | null | 17,206 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "*Escherichia coli* is a rod-shaped bacterium that does not retain the crystal violet stain and takes up the red counterstain during the Gram staining procedure, classifying it as Gram-negative.",
"id": "10024040",
"label": "a",
"name": "Gram-negative bacilli",
"picture": null,
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{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Gram-positive bacilli are rod-shaped bacterial cells that retain the crystal violet stain during Gram staining. Examples include *Bacillus* and *Clostridium*.",
"id": "10024042",
"label": "c",
"name": "Gram-positive bacilli",
"picture": null,
"votes": 5
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{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Gram-positive cocci refer to spherical bacterial cells that retain the crystal violet stain during the Gram staining procedure. Examples include *Staphylococcus* and *Streptococcus*.",
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"label": "e",
"name": "Gram-positive cocci",
"picture": null,
"votes": 9
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Gram-negative cocci refer to spherical bacterial cells that do not retain the crystal violet stain and take up the red counterstain during the Gram staining procedure. *Neisseria gonorrhoeae* is an example of a Gram-negative cocci.",
"id": "10024043",
"label": "d",
"name": "Gram-negative cocci",
"picture": null,
"votes": 16
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Gram-negative spirilla are spiral-shaped bacterial cells, an example of which is *Helicobacter pylori*.",
"id": "10024041",
"label": "b",
"name": "Gram-negative spirilla",
"picture": null,
"votes": 1
}
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"name": "Bacterial Pathogens",
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"name": "Blood/ Immunity",
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"question": "With reference to the morphology of bacterial pathogens, *Escherichia coli* is an example of a:",
"sbaAnswer": [
"a"
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"totalVotes": 60,
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} | MarksheetMark |
173,464,944 | false | 16 | null | 6,495,169 | null | false | [] | null | 17,207 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Oxytocin is a hormone often used to induce or augment labour, but it is not administered to the mother after the delivery of her first child to prevent HDN. HDN is primarily related to Rh incompatibility.",
"id": "10024047",
"label": "c",
"name": "Oxytocin",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "The correct answer is \"anti-D immunoglobulin\" (Rh immunoglobulin), which is administered to the Rh-negative mother after the delivery of her first Rh-positive child to prevent sensitisation to the Rh antigen, which can lead to haemolytic disease of the newborn in subsequent pregnancies.",
"id": "10024045",
"label": "a",
"name": "Anti-D Immunoglobulin",
"picture": null,
"votes": 41
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "\"Anti-F immunoglobulin\" is not a recognised or standard term in the context of medical immunoglobulins or blood group antibodies.",
"id": "10024048",
"label": "d",
"name": "Anti-F immunoglobulin",
"picture": null,
"votes": 6
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The hepatitis B vaccine is recommended for infants shortly after birth to protect against hepatitis B infection, but it is not administered to the mother after the delivery of her first child to prevent HDN.",
"id": "10024046",
"label": "b",
"name": "Hepatitis B vaccine",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Vitamin K is administered to newborns to prevent bleeding disorders. It is not administered to the mother after the birth of her first child to prevent HDN.",
"id": "10024049",
"label": "e",
"name": "Vitamin K",
"picture": null,
"votes": 8
}
],
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"chapterId": 2693,
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"id": "5724",
"name": "Rhesus D",
"status": null,
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"__typename": "Topic",
"id": "285",
"name": "Blood/ Immunity",
"typeId": 7
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"topicId": 285,
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"question": "In order to prevent haemolytic disease of the newborn (HDN), which of the following should be administered to a Rhesus-negative mother after delivery of her first Rhesus-positive child?",
"sbaAnswer": [
"a"
],
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"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,945 | false | 17 | null | 6,495,169 | null | false | [] | null | 17,208 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Inhibiting leukotriene receptors is not the primary mechanism of action of NSAIDs. Leukotrienes are primarily targeted by leukotriene modifiers, a different class of anti-inflammatory drugs.",
"id": "10024054",
"label": "e",
"name": "Inhibition of leukotriene receptors",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is not the primary mechanism of action of NSAIDs. Inhibiting 5-lipoxygenase is associated with another class of anti-inflammatory drugs called leukotriene modifiers, not NSAIDs.",
"id": "10024051",
"label": "b",
"name": "Inhibition of 5-lipoxygenase",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is an effect of NSAIDs, but the primary mechanism is the inhibition of cyclooxygenases (COX). NSAIDs can inhibit the production of prostacyclin (a vasodilator and platelet aggregation inhibitor) as a result of COX inhibition.",
"id": "10024052",
"label": "c",
"name": "Inhibition of prostacyclin synthesis",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "NSAIDs do not activate COX-2; they inhibit it. COX-2 is an enzyme involved in the production of inflammatory prostaglandins. Inhibition of COX-2 is one of the key mechanisms of NSAIDs.",
"id": "10024053",
"label": "d",
"name": "Activation of COX-2",
"picture": null,
"votes": 6
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "NSAIDs work by inhibiting COX enzymes, particularly COX-1 and COX-2. This inhibition reduces the production of prostaglandins, which are involved in inflammation, pain, and fever.",
"id": "10024050",
"label": "a",
"name": "Inhibition of cyclooxygenases (COX)",
"picture": null,
"votes": 49
}
],
"comments": [],
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"entitlement": null,
"id": "5725",
"name": "Anti-Inflammatory Drugs",
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"topic": {
"__typename": "Topic",
"id": "286",
"name": "Infection/ Inflammation",
"typeId": 7
},
"topicId": 286,
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"typeId": null,
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},
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"question": "Which of the following describes the mechanism of action of an NSAID?",
"sbaAnswer": [
"a"
],
"totalVotes": 59,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
173,464,946 | false | 18 | null | 6,495,169 | null | false | [] | null | 17,209 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Growth factors, such as transforming growth factor-beta (TGF-beta) and platelet-derived growth factor (PDGF), play a role in tissue repair and regeneration, rather than tissue degradation. They stimulate cell proliferation and extracellular matrix production.",
"id": "10024056",
"label": "b",
"name": "Growth factors",
"picture": null,
"votes": 1
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Antioxidants, such as vitamins C and E, help protect cells from oxidative damage and support tissue healing but are not directly responsible for tissue degradation.",
"id": "10024057",
"label": "c",
"name": "Antioxidants",
"picture": null,
"votes": 3
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Whilst metalloproteinases, such as matrix metalloproteinases (MMPs), are involved in tissue remodelling and the degradation of damaged tissue, they are not produced by leukocytes and macrophages but by various cell types, including fibroblasts and endothelial cells. Leukocytes and macrophages release cytokines, such as IL-1, which can stimulate the production of metalloproteinases by other cells.",
"id": "10024059",
"label": "e",
"name": "Metalloproteinases",
"picture": null,
"votes": 12
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Fibroblasts are involved in the synthesis of collagen and other extracellular matrix components, contributing to tissue repair and remodelling. They are not primarily responsible for tissue degradation.",
"id": "10024058",
"label": "d",
"name": "Fibroblasts",
"picture": null,
"votes": 10
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "During the late phase of wound healing, activated leukocytes and macrophages produce various factors, including cytokines, that contribute to the degradation of damaged tissue by influencing various processes, including the production of metalloproteinases by other cells. The cytokine IL-1 is indeed one of these factors. TNF is also another factor of note.",
"id": "10024055",
"label": "a",
"name": "Cytokine IL1",
"picture": null,
"votes": 33
}
],
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},
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"id": "5726",
"name": "Wound Healing",
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"__typename": "Topic",
"id": "286",
"name": "Infection/ Inflammation",
"typeId": 7
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},
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"question": "During the late phase of wound healing, which of the following are produced by activated leukocytes and macrophages, and contribute to the degradation of damaged tissue?",
"sbaAnswer": [
"a"
],
"totalVotes": 59,
"typeId": 1,
"userPoint": null
} | MarksheetMark |
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