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"explanation": "Daktacort is hydrocortisone with miconazole and is used mostly in mildly inflamed skin disorders with associated infection. It is not appropriate in this case due to the history being suggestive of leprosy",
"id": "32814",
"label": "b",
"name": "Daktacort (daily)",
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"explanation": "Rifampin, isoniazid, pyrazinamide, ethambutol are the regimen for the treatment of tuberculosis. Cutaneous tuberculosis is rare and is due to direct inoculation with tubercle bacilli into the skin. It does not generally lead to paraesthesia. Other types of mycobacterial skin infections include leprosy, which is what the patient is suffering from in this case",
"id": "32817",
"label": "e",
"name": "Rifampin, isoniazid, pyrazinamide, ethambutol (all daily)",
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"answer": false,
"explanation": "Betnovate is a potent topical corticosteroid. It is often prescribed in severe inflammatory conditions. It is not appropriate in this case due to the history being suggestive of leprosy",
"id": "32815",
"label": "c",
"name": "Betnovate (as required)",
"picture": null,
"votes": 312
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"explanation": "Metformin is the first line treatment of type II diabetes mellitus. The patient is displaying unilateral paraesthesia symptoms, which are less likely to be due to a peripheral nephropathy secondary to diabetes. The muscle wasting is a sign of peripheral nerve thickening, which suggests leprosy",
"id": "32816",
"label": "d",
"name": "Metformin (daily)",
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"explanation": "This patient has presented with features of leprosy. Therefore, the best management would be for multidrug therapy. The gold standard for diagnosis would be to await a skin swab which showed Mycobacterium leprae. A positive swab plus hypopigmented skin lesions with reduced sensations and peripheral nerve thickening are the three features required to make a leprosy diagnosis. This patient is displaying signs of left ulnar nerve thickening",
"id": "32813",
"label": "a",
"name": "Rifampicin (monthly), dapsone (daily)",
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"comment": "How do you know what left ulnar thickening is?\n",
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"comment": "spend more time on the wards :/",
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"explanation": "# Summary\n \n \nLeprosy is a disease endemic in many developing countries. The disease can manifest in various ways depending on host immunology and bacterial virulence. The two main forms are multibacillary (lepromatous) and paucibacillary (tuberculoid) leprosy. Differential diagnoses to consider include inherited diseases, endocrine disorders, and other conditions such as AL amyloidosis. Diagnosis is primarily based on clinical assessment and the presence of acid-fast bacilli in biopsies or smears. Management involves the use of medications such as dapsone, rifampicin, and clofazimine, with close monitoring for potential side effects and immunological complications. \n \n \n# Definition\n \n \nLeprosy is a mycobacterial disease caused by *Mycobacterium leprae* which typically presents with dermatological and neurological manifestations.\n \n# Epidemiology\n \nLeprosy is endemic in a number of developing countries across the world. Most new cases occur in Southeast Asia.\n \nIt is associated with severe morbidity, reduced psychosocial functioning and stigmatisation. While difficult to transmit, it is thought to be spread by the respiratory route via nasal discharge.\n \n# Aetiology\n \n - Leprosy is spread through droplets from the respiratory tract. Prolonged close contact (over months) is required to transmit the disease.\n - Leprosy manifests in a number of different ways owing to a range of factors, the most important being host immunology and bacterial virulence/initial infectious load\n - *M. leprae* grows best at 27–33° so it prefers to grow at **cooler** areas of the body (eg. skin, nerves close to the skin, mucous membranes)\n - There are five types, but broadly it can be classified as lepromatous and tuberculoid leprosy\n - In disseminated lepromatous/multibacillary leprosy, bacteria become widely disseminated due to poor Th1 cell-mediated responses. This causes symmetrical peripheral nerve damage through demyelination of peripheral nerves, as well as classical skin changes.\n - In tuberculoid/paucibacillary leprosy, there is a robust Th1 cell-mediated response, leading to better control by the immune system and milder clinical manifestations.\n \n# Symptoms & Signs\n \nThe clinical features of leprosy exist on a spectrum. At one end is **disseminated lepromatous/multibacillary leprosy**:\n \n - Coppery or hypopigmented anaesthetic patches; ≥5\n - Classic facial changes include nose destruction and ear swellings – leonine faces\n - Nerve thickening may be felt on palpation, with the most commonly affected nerves being the ulnar, median, radial cutaneous, greater auricular, common peroneal and posterior tibial nerves to control of the infection\n \nClinical features of **tuberculoid/paucibacillary leprosy** include a milder form of nerve damage and dermatological manifestations (<5 lesions)\n \nNerve damage in all forms can lead to contractures, ulceration and deformity in the long term\n \n# Differential diagnosis\n \n \nThe differential diagnosis for other causes of thickened peripheral nerves include:\n \n - **Inherited diseases** – Charcot–Marie–Tooth disease, Refsum's disease and neurofibromatosis. These can also cause peripheral neuropathies and cutaneous manifestations alongside a family history.\n - **Acromegaly** - coarsening features & nerve compression (especially carpal tunnel syndrome). Symptoms are more generalised and complications such as diabetes mellitus can develop.\n - **AL amyloidosis** - may be associated with symptoms of multiple myeloma (hypercalcaemia, renal dysfunction, anaemia, bone pain).\n - **Peripheral neuropathy** secondary to diabetes mellitus, alcohol use or, more acutely, Guillain-Barré syndrome. This is usually preceded by poorly controlled diabetes or alcoholism, or by a recent infection (precipitating GBS)\n \n \n# Diagnosis\n \nLeprosy is diagnosed with one or more of the following clinical features and laboratory tests:\n \n - Loss of sensation in a hypopigmented or reddened skin patch\n - Thickened peripheral nerve and sensory loss/weakness in the area supplied by the nerve\n - Slit-skin smear demonstrating acid-fast bacilli with a special stain\n \n \n# Treatment\n \nEarly diagnosis and treatment can reduce illness severity and long-term sequelae.\n \n - Treatment of multibacillary leprosy involves the use of dapsone, rifampicin and clofazimine (an immunosuppressive agent) for at least 12–24 months\n - Patients commenced on medications need to be monitored closely throughout the course of their treatment for immunological complications known as type I and II (erythema nodosum lepromum) reactions, which require hospital inpatient treatment. Treatment should continue with the addition of prednisolone, aspirin or thalidomide under specialist guidance.\n - Side effects of dapsone include methaemoglobinaemia, agranulocytosis, Stevens–Johnson Syndrome and the DRESS syndrome; it can also trigger a haemolytic crisis in G6PD deficiency\n - Clofozamine can cause abnormal skin pigmentation\n - Rifampicin can cause orange secretions and is a cytochrome P450 inducer, hence has several drug interactions\n - Treatment of paucibacillary leprosy involves rifampicin and dapsone for 6 months\n \n \n# References \n \n [BNF: Leprosy treatment summary](https://bnf.nice.org.uk/treatment-summaries/leprosy/#:~:text=Paucibacillary%20leprosy%20should%20be%20treated,is%20sufficient%20to%20treat%20tuberculosis.)\n \n [Click here for the WHO page on leprosy](https://www.who.int/news-room/fact-sheets/detail/leprosy)\n \n \n [Leprosy: review of the epidemiological, clinical, and etiopathogenic aspects - Part 1 - PMC (nih.gov)](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4008049/)",
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"learningPoint": "Leprosy is treated with a combination of antibiotics, typically including rifampicin (monthly) and dapsone (daily), as part of multidrug therapy to effectively reduce the bacterial load and prevent transmission.",
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"question": "A 42-year-old woman attends GP due to reduced sensation over a hypopigmented patch of skin. The symptoms have been getting worse for several months. The area of skin affected is a large plaque around 5cm by 6cm over the left upper arm. After taking a careful history, the GP finds out that the patient lived in Colombia before moving to the United Kingdom 5 years ago. On examination, the GP notes wasting of the hypothenar muscles of the left hand and reduced sensation over the lateral half of the 4th digit and the whole of the 5th digit.\n\nWhich of these would be the most appropriate management?",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "The causative organism of shingles is the reaction of varicella zoster rather than herpes simplex. Herpes simplex can also present with localised blistering, so it is a common differential of shingles",
"id": "32821",
"label": "d",
"name": "Swab for herpes simplex polymerase chain reaction (PCR)",
"picture": null,
"votes": 1074
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "There are different types of skin biopsies which are used to both investigate skin lesions. A punch biopsy would not be appropriate in this case because the diagnosis is shingles, which can be identified via PCR",
"id": "32820",
"label": "c",
"name": "Punch skin biopsy",
"picture": null,
"votes": 340
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"answer": true,
"explanation": "The image shows the early onset of shingles. This is caused by the reactivation of the varicella zoster virus. The initial infection of the varicella virus would have caused chickenpox. The diagnosis is usually clinical, as often the virus is difficult to recover from swabs. The likelihood of developing shingles increased by up to 40% in patients diagnosed with cancer",
"id": "32818",
"label": "a",
"name": "Swab for varicella zoster polymerase chain reaction (PCR)",
"picture": null,
"votes": 3053
},
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"answer": false,
"explanation": "The image shows the early onset of shingles. This is caused by the reactivation of the varicella zoster virus. The initial infection of the varicella virus would have caused chickenpox. There are no signs of an overlying bacterial infection",
"id": "32819",
"label": "b",
"name": "Bacterial swab",
"picture": null,
"votes": 122
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Ink burrow testing is performed to diagnose scabies. This is more commonly associated with fine, silvery lines usually seen in the interdigital spaces",
"id": "32822",
"label": "e",
"name": "Ink burrow test",
"picture": null,
"votes": 120
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"explanation": "# Summary \n\nShingles is a reactivation of the varicella zoster virus which can lie dormant in nerve ganglia following primary infection (chickenpox). It commonly occurs in the elderly and shingles in young adults should prompt investigation for an underlying immune condition. Management normally includes oral antivirals, but intravenous antiviral medications can be used if severe or if the patient is immunocompromised.\n\n# Signs & Symptoms\n\nShingles can manifest first as a tingling feeling in a dermatomal distribution. Progresses to erythematous papules occurring along one or more dermatomes within a few days, which develop into fluid-filled vesicles which then crust over and heal. May be associated with viral symptoms e.g. fever, headache, malaise.\n\n[lightgallery]\n\n[lightgallery1]\n\n**Herpes zoster ophthalmicus (HZO)** presents with symptoms including a painful red eye, fever, malaise, and headache, followed by an erythematous vesicular rash over the trigeminal division of the ophthalmic nerve. A lesion on the nose, known as **Hutchinson's sign,** may suggest ocular involvement.\n\n\n\n# Management\n\n- Oral antiviral (e.g. valaciclovir 1g three times per day for 7 days) within 72h of rash onset if immunocompromised (and infection is not severe) or moderate/severe rash or moderate/severe pain, or non-truncal involvement.\n- Admit to hospital for IV antivirals if severe disease or immunocompromise, ophthalmic symptoms or suspicion of meningitis/encaphalitis/myelitis\n- Advise avoiding contact with pregnant women, babies and those who are immunocompromised until the lesions are fully crusted over, as transmission can occur via skin contact\n- Pain can be managed with NSAIDs (e.g. ibuprofen). If unsuccessful, consider offering amitriptyline (off-label use), duloxetine (off-label use), gabapentin, or pregabalin\n\n# Shingles vaccine\n\nThere is a one-off vaccine available for shingles that is typically advised for those in their 70s.\n\n# Complications\n\n- Secondary bacterial infection of skin lesions\n- Corneal ulcers, scarring and blindness if eye involved\n- Post-herpetic neuralgia\n - Pain occurring at site of healed shingles infection\n - Can cause neuropathic type pain (burning, pins and needles)\n - Can cause allodynia (perception of pain from a normally non-painful stimulus e.g. light touch)\n\n# NICE Guidelines\n\n[NICE Clinical Knowledge Summary (CKS): Shingles](https://cks.nice.org.uk/topics/shingles/)\n\n[NICE Treatment Summary: Varicella-zoster vaccine](https://bnf.nice.org.uk/treatment-summary/varicella-zoster-vaccine-2.html)",
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"question": "A 23-year-old woman presents to her GP with a rash. She has just undergone chemotherapy for acute lymphoblastic leukaemia.\n\n[lightgallery]\n\nWhat investigation would give a definitive diagnosis?",
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"explanation": "Propylthiouracil is usually only prescribed by a specialist for hyperthyroidism. Propylthiouracil can lead to pancytopenia as well as hepatic disorders and hypersensitivity reactions. It is not first line because of the slightly increased likelihood of severe liver damage. Therefore, it is unlikely to have been prescribed to this patient",
"id": "32875",
"label": "c",
"name": "Propylthiouracil",
"picture": null,
"votes": 569
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Beta-blockers can lead to thrombocytopenia; however, pancytopenia is less common. Other side effects include fatigue, cold extremities and bronchospasm",
"id": "32876",
"label": "d",
"name": "Metoprolol",
"picture": null,
"votes": 23
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This patient has pancytopenia on their blood film and is displaying signs and symptoms of bone marrow depression. Bone marrow depression occurs in roughly 1 in 1000 patients who take carbimazole. The suppression is usually temporary and should improve within weeks if the carbimazole is stopped. More common side effects include headache, nausea and rashes",
"id": "32873",
"label": "a",
"name": "Carbimazole",
"picture": null,
"votes": 4878
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Beta-blockers can lead to thrombocytopenia; however, pancytopenia is less common. Other side effects include fatigue, cold extremities and bronchospasm",
"id": "32874",
"label": "b",
"name": "Propranolol",
"picture": null,
"votes": 97
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"explanation": "Beta-blockers can lead to thrombocytopenia; however, pancytopenia is less common. Other side effects include fatigue, cold extremities and bronchospasm",
"id": "32877",
"label": "e",
"name": "Nadolol",
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"comment": "It was really a 50/50 chance of getting this one right lol",
"createdAt": 1646267296,
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"comment": "Umm actually this should be a 100% chance of getting this right. You just need to spend more time on wards",
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"comment": "+1\n",
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"explanation": "# Summary\n \n\nHyperthyroidism is a condition resulting from an overactivity of the thyroid gland leading to an excess of thyroid hormones in the body. The syndrome caused by this excess is termed thyrotoxicosis. The common primary causes include Grave's disease, toxic adenoma, toxic multinodular goitre, certain medications, and thyroiditis. Key signs of hyperthyroidism encompass increased basal metabolic rate, heat intolerance, tachycardia, weight loss, and sleep disturbances. Management strategies comprise medications, radio-iodine therapy, surgery, and symptomatic relief with beta-blockers.\n \n\n# Definition\n - **Hyperthyroidism**: A condition in which the thyroid gland is overactive, leading to the production of excess thyroid hormones.\n \n - **Thyrotoxicosis**: The syndrome resulting from the presence of excessive thyroid hormones in the body, not always due to thyroid gland overactivity.\n \n\n# Epidemiology\nHyperthyroidism predominantly affects women and the elderly, with an estimated prevalence of 1-2% in the general population. Grave's disease is the predominant cause.\n \n\n# Aetiology\nPrimary causes of hyperthyroidism originate from the thyroid gland itself and include:\n - **Grave's disease**: Resulting from autoimmune stimulation of the thyroid gland by TSH receptor auto-antibodies.\n - **Toxic adenoma**: Adenoma that produces thyroid hormones.\n - **Toxic multinodular goitre**: Multiple thyroid nodules that produce thyroid hormones, leading to goitre.\n - **Medications**: Such as amiodarone.\n - **Thyroiditis**: Inflammation of the thyroid gland, e.g., de Quervain's thyroiditis.\n - Radiation exposure\n \n\nSecondary causes of hyperthyroidism, or those not caused by thyroid dysfunction, include:\n \n\n - Amiodarone\n - Lithium\n - TSH producing pituitary adenoma\n - Choriocarcinoma (beta-hCG can activate TSH receptors)\n - Gestational hyperthyroidism\n - Pituitary resistance to thyroxine (i.e., failure of negative feedback)\n - Struma ovarii (ectopic thyroid tissue in ovarian tumours)\n \n\n# Signs and Symptoms\nGeneral manifestations of hyperthyroidism include:\n \n\n - ↑ Basal metabolic rate\n - Heat intolerance\n - Tachycardia and arrhythmias\n - Weight loss\n - Diarrhoea\n - Sweaty skin\n - Insomnia and sleep disturbances\n - Restlessness and tremors\n - Goitre (depending on cause)\n \n\n [lightgallery1]\n \n\nBoth hyper- and hypothyroidism may result in:\n - Mood changes, depression, and anxiety\n - Menstrual disturbances\n \n\nSpecific features of **Grave's disease** are:\n \n\n - Exophthalmos/proptosis: Bulging eyes\n - Thyroid acropachy: Soft tissue swelling in extremities, nail clubbing, and periosteal new bone growth.\n - Pretibial myxoedema: Mucopolysaccharide deposition in the dermis leading to oedema and skin thickening, predominantly in the shins.\n \n\n [lightgallery]\n \n\n# Differential Diagnosis\n - **Anxiety Disorder**: While hyperthyroidism can cause anxiety-like symptoms, it's essential to consider anxiety disorders as a separate diagnosis.\n - **Pheochromocytoma**: This rare adrenal gland tumor can produce excessive catecholamines, leading to symptoms such as palpitations, sweating, and high blood pressure. Careful evaluation, including urine and blood tests, is necessary to differentiate it from hyperthyroidism.\n - **Other Thyroid Disorders**: Hypothyroidism or other thyroid conditions can sometimes present with symptoms that overlap with hyperthyroidism. Thyroid function tests (TFTs) help distinguish between these thyroid disorders.\n \n\n# Investigations\n \n\nWhen evaluating a patient suspected of having hyperthyroidism, the following investigations are commonly performed:\n \n\n 1. **Thyroid Function Tests (TFTs)**:\n - Elevated levels of free thyroxine (FT4) and free triiodothyronine (FT3) with suppressed thyroid-stimulating hormone (TSH) are indicative of hyperthyroidism.\n \n\n 2. **Blood Tests for Thyroid Antibodies**:\n - Detecting thyroid antibodies, such as thyroid-stimulating immunoglobulins (TSIAb) or thyrotropin receptor antibodies (TRAb), can help diagnose the underlying cause, particularly in Grave's disease.\n \n\n 3. **Ultrasound of the Thyroid**:\n - Ultrasonography is used to visualise the thyroid gland and assess its size, structure, and any nodules.\n \n\n 4. **Radioiodine Uptake Test**:\n - This test measures the thyroid's ability to take up radioactive iodine. It helps determine the cause of hyperthyroidism (e.g., diffuse uptake in Grave's disease or focal uptake in a toxic nodule).\n \n\n# Management\n \n\n 1. **Antithyroid drugs (ATDs)**:\n - First-line treatment for most patients.\n - Carbimazole or propylthiouracil (PTU) is used, with carbimazole being preferred due to fewer side effects.\n - Carbimazole can cause agranulocytosis, a severe and potentially life-threatening condition characterized by a significant decrease in white blood cells (neutrophils). Patients should be advised to seek immediate medical attention if they experience symptoms like fever, sore throat, mouth ulcers, or other signs of infection while taking Carbimazole.\n - In pregnant women or those planning pregnancy, PTU is preferred in the first trimester.\n \n\n 2. **Beta-blockers**:\n - Propranolol can be used for symptomatic relief, especially for symptoms associated with increased sympathetic activity.\n \n\n 3. **Radio-iodine**:\n - Considered for definitive treatment, especially for relapsed disease or when ATDs are not suitable.\n - Not typically used in patients under age 40 due to potential increased cancer risk.\n - Radioiodine is a radioactive form of iodine that selectively concentrates in the thyroid gland. It damages the thyroid tissue, reducing its hormone-producing ability. \n - Post-radioiodine therapy, patients often become hypothyroid, and they may require lifelong thyroid hormone replacement therapy.\n \n\n 4. **Surgery (Thyroidectomy)**:\n - An option for those with large goiters causing compression, suspicion of malignancy, or when other treatments are contraindicated or refused.\n - Requires preparation with ATDs to achieve euthyroid state before surgery to minimize risks.\n \n\n **Regular monitoring** is crucial, including thyroid function tests, to ensure appropriate dosing of medications and to detect early signs of remission or relapse.\n \n\n \n\n \n\n# Thyroid Storm\n \n\nThyroid storm is a rare but life-threatening medical emergency caused by untreated or inadequately managed hyperthyroidism. It is often precipitated by stressors like surgery, trauma, or infection. Key features of thyroid storm include:\n \n\n - Restlessness and agitation\n - High-output heart failure\n - Profound tachycardia\n - Fever\n - Delirium and altered mental status\n \n\nManagement of thyroid storm involves several principles:\n \n\n 1. **Counteract Peripheral Action of Thyroid Hormone**:\n - Intravenous propranolol and digoxin help control heart rate and manage cardiac symptoms.\n \n\n 2. **Inhibit Thyroid Synthesis**:\n - Propylthiouracil (PTU) through a nasogastric tube and Lugol's iodine are administered to reduce thyroid hormone production.\n \n\n 3. **Corticosteroids**:\n - Steroids like prednisolone or hydrocortisone are given to inhibit peripheral conversion of T4 to the more active T3 form.\n \n\n 4. **Supportive Care**:\n - Supportive measures include intravenous fluids, cooling measures for fever, and addressing any precipitating factors (e.g. infection).\n \n\n# Complications of Hyperthyroidism\n \n\nHyperthyroidism can lead to various complications, including:\n \n\n - **Thyroid Eye Disease (TED)**:(see separate page in Ophthalmology section for more detail)\n - Smoking is the most important risk factor for development and increased severity of TED in patients with Grave's disease, so it is important to counsel patients on the importance of smoking cessation\n - Sight-threatening complications include: exposure keratopathy, compressive optic neuropathy and diplopia. \n - Early medical management of TED has the potential to stabilise, slow or even reverse the disease process. Good control of thyrotoxicosis is essential and other medical therapies, such as steroids or other immunosuppressants, may be used\n - In sight-threatening TED, urgent surgical orbital decompression may be required, followed by intravenous corticosteroids\n - **Atrial Fibrillation**: Due to the increased strain on the heart, hyperthyroidism can lead to atrial fibrillation, a type of irregular heartbeat.\n - **High-Output Heart Failure**: The heart may become overworked, resulting in high-output heart failure.\n - **Osteopenia/Osteoporosis**: Hyperthyroidism can lead to bone loss and increase the risk of fractures.\n - **Upper Airway Obstruction**: Large goitres may cause upper airway obstruction, requiring intervention.\n - **Thyroid Cancer**: In some cases, hyperthyroidism may be associated with thyroid cancer, although it's not a common complication.\n - **Thyroid storm** - see above\n \n\n# NICE Guidelines\n [NICE CKS on Hyperthyroidism](https://cks.nice.org.uk/hyperthyroidism)",
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"explanation": "# Hypoglycaemia\n\n# Summary\n\nHypoglycaemia, defined as a blood glucose level below 3.5 mmol/L (NICE CKS), presents with symptoms like trembling, sweating, palpitations, hunger, headache, double vision, difficulty concentrating, slurred speech, confusion, and coma. Common causes include various drugs (e.g., insulin, sulphonylureas, GLP-1 analogues), acute liver failure, sepsis, adrenal insufficiency, insulinoma, and glycogen storage disease. The investigation plan typically includes a medication history review, serum insulin, C-peptide and proinsulin levels, a 72-hour fast test, 8am cortisol and/or synACTHen testing, and imaging for insulinoma. Management depends on the severity of the condition and can range from intake of fast-acting carbohydrates for mild cases to intravenous dextrose or intramuscular glucagon for severe cases.\n\n# Definition\nHypoglycaemia is a metabolic condition characterized by an abnormally low blood glucose level, typically defined as less than 3.5 mmol/L.\n\n# Epidemiology\nHypoglycaemia is common in patients with diabetes, especially those on insulin or sulphonylurea therapies. The prevalence increases with the duration of diabetes and the intensity of glucose-lowering treatment.\n\n# Aetiology\nCauses of hypoglycaemia include:\n\n- **Drugs:** Insulin, Sulphonylureas, GLP-1 analogues, DPP-4 inhibitors, Beta-blockers\n- **Alcohol**\n- **Acute liver failure**\n- **Sepsis**\n- **Adrenal insufficiency**\n- **Insulinoma**\n- **Glycogen storage disease**\n\n# Signs and Symptoms\n**Adrenergic Symptoms (Blood glucose concentrations <3.3 mmol/L):**\n\n- Trembling\n- Sweating\n- Palpitations\n- Hunger\n- Headache\n\n**Neuroglycopenic Symptoms (Blood glucose concentrations below <2.8 mmol/L):**\n\n- Double vision\n- Difficulty concentrating\n- Slurred speech\n- Confusion\n- Coma\n\n\n\n# Differential Diagnosis\nConditions to consider:\n\n- **Diabetic ketoacidosis:** May cause hypoglycaemia due to insulin treatment. Symptoms include polydipsia, polyuria, fatigue, and abdominal pain.\n- **Adrenal insufficiency:** Lack of cortisol may lead to hypoglycaemia. Features include fatigue, weight loss, hyperpigmentation, and hypotension.\n- **Insulinoma:** Insulin-secreting tumor resulting in hypoglycaemia. Symptoms mimic hypoglycaemia but can occur after meals.\n- **Alcohol intoxication:** Alcohol can inhibit hepatic gluconeogenesis, leading to hypoglycaemia. Symptoms include confusion, ataxia, slurred speech, and coma.\n\n#Investigations\n\nWhipple's triad:\n\n* Plasma hypoglycaemia\n* Symptoms attributable to a low blood sugar level\n* Resolution of symptoms with correction of the hypoglycaemia\n\nThe diagnostic approach for hypoglycaemia may involve the following:\n\n- Review medication history for potential drug-induced causes.\n- Measure serum insulin, C-peptide, and proinsulin levels to differentiate between exogenous and endogenous insulin sources.\n\t- High insulin AND high C-peptide and proinsulin imply endogenous production e.g. insulinoma\n\t- High insulin AND low C-peptide and proinsulin suggest exogenous administration.\n- Perform a 72-hour fast test to demonstrate episodic hypoglycaemia.\n- Conduct 8am cortisol and/or synACTHen testing for adrenal insufficiency.\n- Consider abdominal imaging (CT/MRI/PET) to locate an insulinoma.\n\n# Management\n**Mild Hypoglycaemia (Patient is conscious):**\n\n- ABCDE approach\n- Consume 15-20g of fast-acting carbohydrate (e.g., glucose tablets, non-diet soda, sweets, fruit juice).\n- Avoid chocolate due to slower absorption.\n- Follow up with slower-acting carbohydrates (e.g., toast).\n\n**Severe Hypoglycaemia (e.g. Seizures, Unconsciousness):**\n\n- ABCDE approach\n- Administer 200ml 10% dextrose IV (alternatively dextrose 20% can be administered via a large vein). \n- Administer 1mg glucagon IM if no IV access (Note: this won't work if alcohol ingestion is the cause due to its action blocking gluconeogenesis).\n- Manage prolonged or repeated seizures.\n\n**Aftercare:**\n\n- Consider medication changes.\n- Investigate non-drug causes if necessary.\n\n# DVLA Guidance on Hypoglycaemia\nThe DVLA has specific regulations for patients with hypoglycaemia who are driving. Requirements depend on the severity and frequency of episodes, type of driving license, and specific medication regimen.\n\n# NICE Guidelines\n\n[NICE CKS - hypoglycaemia management](https://cks.nice.org.uk/topics/insulin-therapy-in-type-2-diabetes/management/insulin-therapy-type-2-diabetes/#hypoglycaemia)\n\n\n# References\n [Patient.info on Hypoglycaemia](https://www.patient.info/doctor/hypoglycaemia)\n \n [DVLA Guidance on Hypoglycaemia and Driving](https://www.gov.uk/hypoglycaemia-and-driving)\n",
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"explanation": "The fluid moving coming out of the chest drain is lymph. The patient has a chylothorax which needs to drain from the chest cavity. Drainage may reduce pressure on the lungs and improve the patient's breathing. Nutritional support is important to remember in these patients, although they may require additional IV fluids",
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"name": "Clamp the chest drain and prescribe IV fluids",
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"explanation": "The fluid moving coming out of the chest drain is lymph. The patient has a chylothorax which needs to drain from the chest cavity. Drainage may reduce pressure on the lungs and improve the patient's breathing. It may be necessary to call the intensive care unit depending on the vital signs of the patient",
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"explanation": "Readmission to ITU is the most appropriate initial management. This patient has developed a chyle leak and needs to be managed in ITU given the serious nature of the complication. The chylothorax will need to be drained from the chest cavity. Drainage may reduce pressure on the lungs and improve the patient's breathing.",
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"explanation": "The fluid moving coming out of the chest drain is lymph. The patient has a chylothorax which needs to drain from the chest cavity. Drainage may reduce pressure on the lungs and improve the patient's breathing. IV furosemide is not require",
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"explanation": "This is a difficult question. This patient has developed chylothorax, which is leaking through his chest drain. Traumatic chylothoraces are the most common type, and they can occur in up to 4% of oesophagectomies. Lymph leaks from the thoracic duct into the chest cavity. In large leaks, the most effective initial management is to allow the lymph to drain and to support the patient with adequate nutritional support",
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"comment": "they've developed a what now ",
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"comment": "icu team come quick pls ",
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"comment": "Got it right for the wrong reasons. I assumed they put an NG in the lung…..",
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"comment": "confused why readmit isn't the right answer then?",
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"comment": "It says \"readmit to UTI is the most appropriate initial management\" so why is that answer wrong ??? ",
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"explanation": "# Summary\n\nOesophageal carcinoma, primarily categorised as adenocarcinoma or squamous cell carcinoma, is a malignancy impacting the oesophagus. Adenocarcinoma is most prevalent in the Western world, typically located in the lower third of the oesophagus and linked to gastro-oesophageal reflux disease. Squamous cell carcinoma is prevalent globally and typically seen in the upper two-thirds of the oesophagus. Smoking is a significant risk factor for both types. Key signs and symptoms include progressive dysphagia, weight loss, and possible hoarseness. The primary investigation method is upper GI endoscopy, with further assessments for staging including CT scans, MRI, endoscopic ultrasound, FDG-PET scan, and occasionally laparoscopy. Management approaches depend on the staging of the disease, but include surgical, endoscopic, and non-surgical options such as radiotherapy and chemotherapy.\n\n# Definition\n\nOesophageal carcinoma is a type of cancer that originates from the epithelial cells lining the oesophagus, primarily categorised into adenocarcinoma or squamous cell carcinoma.\n\n# Epidemiology\n\nSquamous cell carcinoma of the oesophagus is the most prevalent type globally, often seen in the upper two-thirds of the oesophagus. Conversely, adenocarcinoma has become the most common cause of oesophageal carcinoma in the Western world, owing to the increasing prevalence of GORD, and is often seen in the lower one-third of the oeseophagus.\n\n# Aetiology\n\nRisk factors for oesophageal carcinoma include:\n\n- **Smoking**: The most significant risk factor for both adenocarcinoma and squamous cell carcinoma.\n- High alcohol intake\n- Obesity and gastro-oesophageal reflux disease: Linked specifically to adenocarcinoma, as recurrent reflux leads to metaplastic formations of mucin-producing glandular tissue known as Barrett's oesophagus, which can further develop into neoplasia.\n- Achalasia\n- Zenker diverticulum\n- Oesophageal web\n- High intake of hot beverages\n- Dietary intake of:\n - Increased dietary nitrosamines\n - Areca or betel nuts\n\n# Signs and Symptoms\n\nPatients with oesophageal carcinoma often present with the following symptoms:\n\n- Progressive dysphagia: Initially for solids, and later for liquids. Dysphagia typically occurs when there is obstruction of more than two-thirds of the lumen.\n- Weight loss: This symptom, the second most common, results from a combination of anorexia and dysphagia.\n- Odynophagia: Pain on swallowing can occur.\n- Hoarseness: Can develop if there is local invasion of the recurrent laryngeal nerve.\n\n# Differential Diagnosis\n\n- Gastro-oesophageal reflux disease (GORD): GORD also presents with dysphagia and odynophagia, but is often associated with heartburn, regurgitation, and chest pain.\n- Achalasia: Achalasia is characterised by dysphagia for solids and liquids from the start, regurgitation of undigested food, and chest pain.\n- Peptic stricture: Presents with intermittent dysphagia for solid foods, heartburn, and acid regurgitation.\n- Zenker diverticulum: Presents with dysphagia, regurgitation of undigested food, halitosis, and possible aspiration pneumonia.\n- Neurological causes of dysphagia such as motor neuron disease, mysaesthenia gravis\n- Oesophagitis - often due to candidiasis and presents with odynophagia more than dysphagia. May be underlying immunosuppression e.g. HIV.\n\n# Investigations\n\n### NICE 2-week-wait criteria:\n\n- Offer urgent direct access upper gastrointestinal endoscopy (to be performed within 2 weeks) to assess for oesophageal cancer in people with **dysphagia** or those aged 55 years and over with weight loss and any of the following: upper abdominal pain, reflux, or dyspepsia.\n- Consider non-urgent direct access upper gastrointestinal endoscopy to assess for oesophageal cancer in people with haematemesis.\n\nInvestigations for oesophageal carcinoma encompass:\n\n\n\n- Initial investigation: Upper GI endoscopy is performed to visualise and grade the tumour via biopsy.\n- Staging:\n - CT chest, abdomen and pelvis: Assesses the size of the tumour, local and lymph node spread, and any visceral metastases.\n - MRI: Identifies metastatic spread to the liver and advanced local disease.\n - Endoscopic ultrasound: Assesses whether a tumour is amenable for resection.\n - FDG-PET scan: Identifies distant and nodal metastases.\n - Laparoscopy: Used to identify intra-abdominal metastases if all other imaging has been negative.\n\n# Management\n\nManagement of oesophageal carcinoma is based on the stage of the disease and may include:\n\n- Surgical resection: The primary choice for localised disease.\n- Endoscopic therapies: Such as endoscopic mucosal resection or endoscopic submucosal dissection for early-stage disease.\n- Non-surgical options: Such as radiotherapy, chemotherapy or chemoradiotherapy for advanced disease, or as neoadjuvant or adjuvant therapy with surgery.\n\n# NICE Guidelines\n\n[Click here to see the NICE guidelines on oesophageal cancer](https://www.nice.org.uk/guidance/conditions-and-diseases/cancer/oesophageal-cancer)",
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"question": "A 78-year-old male patient is on the surgical wards after an oesophagectomy. Several hours postoperatively, he develops shortness of breath. He has a chest drain in-situ, which has started to leak large amounts of milky fluid.\n\nWhich of these would be the most appropriate initial management?",
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"explanation": "It is important to restore circulatory volume first by giving fast fluids. Once circulatory volume has been restored, IV insulin can be commenced",
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"comment": "In a previous question it literally said to give the fluid slowly to prevent fluid overload and cerebral oedema?",
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"comment": "F them kids -Michael Jordan",
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"comment": "I think they assume 500ml stat is a safe enough dose for an \"assumably\" otherwise fit and healthy child since this is the usual volume used in A&E resus situations.",
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"comment": "1L 0.9% over an hour if their SBP is >90 and not vomiting and not confused. You then do 1L over 2 hours etc. If their SBP is <90, they're vomiting or confused, you bolus them first - this is why you give 500ml bolus in this scenario (Due to BP)",
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"comment": "This has been picked out from the Adult JBDS guidelines, he's only 15 so should be using the BSPED \"All children and young people with mild, moderate or severe DKA who are not shocked and are felt to require IV fluids should receive a 10 ml/kg 0.9% sodium chloride bolus over 30 minutes\"",
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"comment": "but he is shocked...",
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"explanation": "# Summary\n \nDiabetic ketoacidosis (DKA) is a life-threatening medical emergency characterised by hyperglycemia, acidosis and ketosis. DKA may be triggered by infection, dehydration or fasting, or may be the initial presentation of Type 1 diabetes. Symptoms include a 'fruity' breath odour, vomiting, dehydration, abdominal pain and altered mental state. Key investigations include blood glucose and ketones, urea and electrolytes and a venous blood gas to check pH. Management involves IV fluids and a fixed rate insulin infusion, with close monitoring both clinically and biochemically. Important complications that should be monitored for include cerebral oedema, hypoglycaemia and hypokalaemia. \n\n# Definition\n \nDiabetic ketoacidosis (DKA) is a medical emergency characterised by the triad of:\n \n - Hyperglycemia (blood glucose >11 mmol/L)\n - Ketosis (blood ketones >3 mmol/L or urinary ketones ++ or higher)\n - Acidosis (pH <7.3 or bicarbonate <15 mmol/L)\n - Note: patients on SGLT-2 inhibitors may present with euglycemic DKA (where glucose is normal)\n \n\n# Epidemiology\n \nDKA is most common in individuals with Type 1 diabetes (T1DM) but around a third of cases occur in patients with Type 2 diabetes. The incidence of DKA is highest in young people aged 18-24. \n\nDKA is the leading cause of death in people aged under 58 years old with T1DM, with cerebral oedema the most common cause of mortality. However, mortality in the UK is still <1%.\n \n\n# Aetiology \n\n- DKA occurs due to insulin deficiency (absolute or relative) leading to hyperglycaemia\n- Ketones, including acetone, 3-beta-hydroxybutyrate, and acetoacetate, are produced from ketogenesis, whereby fatty acids are metabolised as an alternative energy source\n- These ketones are responsible for the acidosis seen\n- Hyperglycaemia causes an osmotic diuresis that contributes to severe dehydration as well as electrolyte imbalance\n- Vomiting and decreased fluid intake secondary to altered mental state also exacerbate dehydration\n\n**10-20% of presentations of DKA represent a first presentation of Type 1 Diabetes**\n\n**Common triggers for DKA include:**\n\n- Infections\n- Dehydration and fasting\n- Missing doses of insulin\n- Medications e.g. steroid treatment or diuretics\n- Surgery\n- Stroke or myocardial infarction\n- Alcohol excess or illicit drug use\n- Pancreatitis\n\n# Classification\n\nPatients with at least one of the following may be classified as having **severe DKA**, which should prompt consideration of referral for higher dependency care:\n\n- Blood ketones > 6mmol/L\n- Bicarbonate < 5mmol/L\n- Blood pH < 7\n- Anion gap above 16\n- Hypokalaemia on admission\n- GCS less than 12\n- Oxygen saturations < 92% in air\n- Systolic BP < 90mmHg\n- Brady or tachycardia (heart rate < 60 or > 100bpm)\n\n\n# Signs and Symptoms\n \n**Symptoms:**\n\n- Nausea and vomiting\n- Abdominal pain\n- Polyuria\n- Polydipsia\n- Weakness\n\n**Signs:**\n\n- Dry mucous membranes\n- Hypotension\n- Tachycardia\n- Altered mental state (drowsiness, confusion, coma)\n- Kussmaul's breathing (deep, sighing breathing to compensate for metabolic acidosis by blowing off carbon dioxide)\n- Fruit-like smelling breath (due to ketosis)\n\n# Investigations\n \n**Bedside tests:**\n \n - Capillary blood glucose\n - Blood or urinary ketones\n - Urine dip +/- MSU (looking for evidence of a urinary tract infection which may precipitate DKA)\n - ECG (for ischaemic changes which may precipitate DKA, or changes secondary to electrolyte imbalance e.g. hypokalaemia)\n\n**Blood tests:**\n\n- Venous blood gas (for acid-base balance)\n- Urea and electrolytes (for electrolyte imbalance and AKI)\n- Full blood count and CRP (for infection markers) \n- Blood cultures (if infection is suspected)\n- HbA1c (to assess diabetic control over recent months)\n\n**Imaging:**\n\n- Consider chest X-ray as part of septic screen (if signs of infection as a trigger for DKA)\n\n# Management\n\n**Initial management:** \n\n- Initial **A to E assessment**\n - Drowsy patients may require airway protection and an **NG tube** to prevent aspiration\n - Ensure adequate IV access\n - If hypotensive give up to 1L in **fluid boluses** then seek urgent senior input if not resolved\n - Consider urinary catheterisation and monitor fluid balance\n- **IV fluid replacement with normal saline**\n - A regimen of large volumes of IV fluid replacement given relatively quickly initially then over longer durations should be followed\n - Slower infusion rates should be considered in young adults, the elderly, those with heart or kidney failure or other serious comorbidities\n - An example in a healthy adult would be 1L over 1 hour, then 2x 1L over 2 hours, then 2x 1L over 4 hours, then 1L over 6 hours\n - **Potassium replacement** should be added after the first bag, depending on serum potassium levels, bearing in mind potassium can be infused at a maximum of 10mmol/h:\n\n| Potassium level (mmol/L) | Potassium replacement mmol/L of next infusion | \n| :---------------: | :----------------: \n| > 5.5 | Nil | \n| 3.5 - 5.5 | 40 mmol/L | \n| < 3.5 | senior review – additional potassium required | \n \n \n- After IV fluids have started, a **fixed rate insulin infusion** should be set up \n- This is provided as an infusion of 50 units of Actrapid in 50ml of 0.9% NaCl, at a rate of 0.1 units/kg/hour\n- Continue long-acting insulin if the patient is already on this \n- Investigation and management of any underlying triggers (e.g. septic screen and start antibiotics if evidence of infection)\n- Ensure **VTE prophylaxis** with low molecular weight heparin is prescribed as patients are at high risk of developing clots due to dehydration\n\n**Ongoing emergency management:**\n\n- Patients should be closely monitored with hourly blood glucose and ketones\n - The aim is for ketones to fall by > 0.5mmol/L/hour\n - Blood glucose should fall by 3 mmol/L/hour\n - If these targets are not met, the rate of insulin infusion should be continued\n- Once blood glucose is below 14, a **10% glucose infusion** should be started alongside ongoing saline and insulin\n- Regular venous blood gases should also be done to monitor potassium, bicarbonate and pH\n- DKA is considered resolved once ketones are less than 0.6 mmol/L and pH is over 7.3 \n - If at this point they are able to eat and drink, a subcutaneous regimen of insulin should be started (usually with the input of a specialist diabetes team)\n - The insulin infusion should be stopped half an hour after the first dose of subcutaneous short acting insulin has been given \n\n# References\n \n[ABCD Guidelines: The Management of Diabetic\nKetoacidosis in Adults](https://abcd.care/sites/default/files/site_uploads/JBDS_Guidelines_Current/JBDS_02_DKA_Guideline_with_QR_code_March_2023.pdf)\n\n[RCEM - Diabetic Ketoacidosis](https://www.rcemlearning.co.uk/reference/diabetic-ketoacidosis/#1635853037528-05d8fa0f-621f)\n\n[Patient UK - Diabetic ketoacidosis](https://patient.info/doctor/diabetic-ketoacidosis#presentation)",
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"question": "A 17-year-old male patient attends A&E due to decreasing responsiveness. On examination, his breath smells like pear drops, and he has developed deep, rapid inspiration.\n\nHis observations are as follows:\n\nPulse 90bpm\nBlood pressure 85/55mmHg\nRespiratory rate 30bpm\nSpO2 98% on air\nTemperature 36.7°C\nWhat is the initial management?",
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"explanation": "The history, combined with the ascitic tap results, point towards a diagnosis of spontaneous bacterial peritonitis. Ascitic fluid is likely to appear cloudy in spontaneous bacterial peritonitis, with a high neutrophil and protein count. Spontaneous bacterial peritonitis is most commonly seen in patients with end-stage liver disease",
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"explanation": "Hepatocellular carcinoma may lead to feverish symptoms with abdominal pain. However, hepatocellular carcinoma is more likely to lead to a milky or bloody ascitic tap with mildly elevated red cell count and reduced glucose levels",
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"explanation": "Tuberculosis can lead to ascites, especially when granulomas spread to the peritoneum. However, tuberculosis is more likely to lead to a milky coloured ascitic tap along with raised protein levels. It is much rarer than spontaneous bacterial peritonitis",
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"explanation": "Pancreatic carcinoma may lead to feverish symptoms, but they classically present without pain. Those that do have abdominal pain are more likely to experience epigastric rather than generalised pain. It is more likely to lead to a milky or bloody ascitic tap with mildly elevated red cell count and reduced glucose levels",
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"explanation": "Liver cirrhosis is unlikely to be the sole cause of these symptoms; for example, cirrhotic patients will not become feverish without a secondary cause. Patients with liver cirrhosis are more likely to have clear or sometimes straw-coloured ascitic taps. They would also normally have a normal absolute neutrophil count",
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"explanation": "# Summary\n\nPeritonitis refers to the inflammation of the peritoneum, typically caused by perforation of a hollow viscus or an infection. The primary signs and symptoms include abdominal rigidity, rebound tenderness, fever, vomiting, tachycardia, and hypotension. Key investigations often involve imaging studies and peritoneal fluid analysis. Management strategies primarily focus on addressing the underlying cause and may involve surgical intervention, antibiotics, and supportive care. Peritonitis can be life-threatening if not treated early and carries a high mortality.\n\n# Definition\n\nPeritonitis is defined as inflammation of the peritoneum, which is the serous membrane lining the cavity of the abdomen and covering the abdominal organs.\n\n# Epidemiology\n\nEpidemiological data regarding peritonitis is somewhat variable, as it often presents secondary to other diseases or conditions. However, it is more commonly encountered in scenarios where there is a risk of abdominal infection or injury, such as abdominal surgeries, long-term peritoneal dialysis, or blunt abdominal trauma.\n\n# Aetiology\n\n\n- **Perforation of a hollow viscus:** This can be from a perforated oesophagus (Boerhaave syndrome), a perforated duodenal or gastric ulcer, a perforated intestine (secondary to conditions such as appendicitis, diverticulitis, intestinal infarction, colorectal cancer, or inflammatory bowel disease). Perforation may also occur due to trauma, such as the ingestion of a foreign body. Perforation can lead to **diffuse** or faeculent peritonitis.\n \n- **Infection:** Infections leading to peritonitis include spontaneous bacterial peritonitis and peritoneal infection secondary to peritoneal dialysis. Uncomplicated appendicities can cause **local** peritonitis due to inflammation of the surrounding peritoneum.\n \n\nRemember, sterile fluids can also leak into and irritate the peritoneum. This can occur with leakage of blood (e.g. in blunt abdominal trauma), bile (e.g. in liver biopsy), and pancreatic fluids (e.g. in acute pancreatitis).\n\n# Signs and Symptoms\n\n- Severe abdominal pain. Patients will often be lying completely still so as to not trigger/exacerbate pain\n- Systemic signs of illness such as fever, haemodynamic instability, tachycardia\n- Nausea and vomiting\n- **Abdominal rigidity/Involuntary abdominal guarding:** Involuntary tensing of the abdominal wall muscles in response to pressure on the abdomen (to protect inflamed abdominal organs).\n- **Rebound tenderness:** Pressing on the abdomen elicits **less** pain than releasing the hand (as the peritoneum bounces back into place).\n- Percussion tenderness\n\n# Differential Diagnosis\n\n- **Gastroenteritis:** Presents with nausea, vomiting, abdominal cramping, and diarrhea.\n- **Pancreatitis:** Characterized by severe upper abdominal pain, often radiating to the back, nausea, vomiting, and fever.\n- **Cholecystitis:** Signs and symptoms include right upper quadrant abdominal pain, nausea, vomiting, and fever.\n- **Appendicitis:** Symptoms include right lower quadrant pain, nausea, vomiting, and low-grade fever.\n- **Diverticulitis:** Usually presents with left lower quadrant pain, fever, and changes in bowel movements.\n\n# Investigations\n\n- Patients presenting with peritonitis can be very systemically unwell and the SEPSIS 6 should be initiated in these situation.\n- **Laboratory tests:** Blood tests to assess for elevated white blood cell count and markers of inflammation (e.g. C-reactive protein), kidney function, and liver function.\n- **Imaging:** Abdominal x-ray, ultrasound, or CT scan to identify fluid collections or perforations (looking for free gas - pneumoperitoneum, rigler’s sign and football sign).\n- **Peritoneal fluid analysis:** If feasible, an analysis of peritoneal fluid obtained by paracentesis can help identify the causative organism and guide treatment.\n\n# Management\n\nManagement of peritonitis is guided by the underlying cause but may include:\n\n- **Surgical intervention:** For conditions such as a perforated viscus, appendicitis, or diverticulitis, surgical intervention is often required to control the source of infection or inflammation.\n- **Antibiotics:** Empirical antibiotic therapy should be initiated as soon as possible and then tailored according to culture results.\n- **Supportive care:** Fluid resuscitation, pain management, and monitoring of vital signs are crucial in the management of peritonitis.\n\n# References\n\n[NHS UK - Peritonitis](https://www.nhs.uk/conditions/peritonitis/)",
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"question": "A 54-year-old woman presents to A&E with abdominal pain. The pain is generalised across the abdomen, which appears distended. She feels feverish and has been experiencing diarrhoea and vomiting. She has known liver cirrhosis.\n\n\nAn ascitic tap is performed:\n\n\n - Appearance cloudy\n\n\n||||\n|---------------------------------|:-------------------------:|-------|\n|RBC|80|none|\n|WBC|550 /mm<sup>3</sup>|< 300|\n|Albumin|5.2 g/L|< 40|\n|Glucose|4.5 mmol/L|3.5 - 5.5|\n|Amylase|350 U/L|< 100|\n\n\nWhat is the most likely diagnosis?",
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"explanation": "Anxiety may present with abdominal pain, which is sometimes described as \"churning\". However, it will not lead to the histological findings seen in this patient",
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"explanation": "Coeliac disease is likely to show subtotal villus atrophy on histology rather than serositis and granulomas. Serological testing whilst the patient is having gluten in their diet is usually done before biopsies",
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"explanation": "Serositis is absent in most ulcerative colitis histology, except in fulminant colitis and granulomas are absent, except in the case of ruptured crypts. Ulcerative colitis is more likely to present with bloody diarrhoea and colicky abdominal pain, urgency and tenesmus",
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"explanation": "The histology is highly specific for Crohn's disease. Serositis and granulomas are often present in Crohn's, whereas they are absent in ulcerative colitis. Crohn's disease can present with variable symptoms, including diarrhoea, which may or may not contain blood, as well as generalised abdominal pain",
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"explanation": "Irritable bowel syndrome may present with similar symptoms, which can become worse in periods of stress. However, the histology findings point towards an inflammatory cause",
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"explanation": "# Summary\n\nCrohn's disease (CD) is a chronic, relapsing inflammatory bowel disease (IBD) characterized by transmural granulomatous inflammation. Key signs and symptoms include gastrointestinal and systemic symptoms, such as crampy abdominal pain, diarrhoea, weight loss, and fever. The disease is diagnosed primarily through blood tests and endoscopy with imaging. Management strategies include monotherapy with glucocorticoids, azathioprine, mercaptopurine, and biological agents for severe cases. Surgical management is rarely curative and should be maximally conservative.\n\n# Definition\n\nCrohn's disease (CD) is a chronic relapsing inflammatory bowel disease (IBD). It is characterised by transmural granulomatous inflammation which can affect any part of the gastrointestinal tract ('from mouth to anus', most commonly the terminal ileum, leading to fistula formation or stricturing.\n\n# Aetiology\n\nThe exact cause is unknown, but it is thought to be an inappropriate reaction to gut flora in a susceptible person. Important risk factors include:\n\n- Family history - 10-25% of patients have a first-degree relative who also suffers from Crohn's disease\n- **Smoking** - x3 increased risk\n- Diets high in refined carbohydrates and fats have been implicated\n\n# Epidemiology\n\nIn Europe the incidence of Crohn's disease is 5.6 per 100, 000 at ages 15-64. The disease is more common in northern climates and developed countries. In the last 60 years the incidence of Crohn's disease has increased in Europe and North America, and is now approximately equal to that of ulcerative colitis.\n\nCrohn's disease has a bimodal age of onset: the most common age of onset is between 15 and 40 years old, but there is a smaller secondary peak between 60-80 years.\n\nCrohn's disease is more common in Caucasian people than in Asian and black people. Ashkenazi Jews have a 2-4 fold higher risk of Crohn's disease.\n\n\n# Signs and Symptoms\n\nSymptoms: \n\n- Gastrointestinal symptoms (crampy abdominal pain and non-bloody diarrhoea)\n- Up to 50% have perianal disease\n- Systemic symptoms (weight loss and fever)\n\nSigns: \n\n- General appearance: cachectic and pale (secondary to anaemia), clubbing.\n- Abdominal examination: aphthous ulcers in the mouth, right lower quadrant tenderness and a right iliac fossa mass.\n- PR examination to check for perianal skin tags, fistulae, or perianal abscess.\n\n[lightgallery] \n\n**Extra-gastrointestinal manifestations include:**\n\nDermatological manifestations:\n\n- Erythema nodosum (painful erythematous nodules/plaques on the shins)\n- Pyoderma gangrenosum (a well-defined ulcer with a purple overhanging edge)\n\n[lightgallery1] [lightgallery2]\n\nOcular manifestations:\n\n- Anterior uveitis (painful red eye with blurred vision and photophobia)\n- Episcleritis (painless red eye).\n\nMusculoskeletal manifestation:\n\n- Enteropathic arthropathy (symmetrical, non-deforming)\n- Axial spondyloarthropathy (sacro-iliitis), \n\nHepatobiliary manifestations:\n\n- Gallstones (these are more common in Crohn's disease than in ulcerative colitis) - reduced bile acid reabsorption and increased calcium loss predisposes to gallstones\n\nHaematological and renal manifestations:\n\n- AA amyloidosis (secondary to chronic inflammation) and renal stones (more common in Crohn's disease than in ulcerative colitis)\n\n# Investigations \n\n- Bedside:\n\t- Stool culture is necessary to exclude infection (MC&S and ovas/cysts/parasite).\n\t- **Faecal calprotectin** (an antigen produced by neutrophils) will be raised (this helps distinguish inflammatory bowel disease from irritable bowel syndrome).\n\n- Blood tests:\n - Raised white cell count\n - Raised ESR/CRP\n - Thrombocytosis\n - Anaemia (secondary to chronic inflammation)\n - Low albumin (secondary to malabsorption)\n - Haematinics and iron studies including (B12, folate) due to terminal ileum involvement\n\n\n- Imaging:\n\t- Endoscopy with imaging is required for diagnosis. Small bowel video capsule endoscopy can be used for proximal disease\n\t- MRI can be used for suspected small bowel disease.\n\t- Upper GI series may show the 'string sign of Kantour'. This is used to describe the string-like appearance of contrast-filled narrowed terminal ileum, and is suggestive of Crohn's disease.\n\t- Colonoscopy with biopsy will reveal:\n\t\t- Intermittent inflammation **('skip lesions')**\n\t\t- Cobblestone mucosa (due to ulceration and mural oedema)\n\t\t- Rose-thorn ulcers (due to transmural inflammation), ± fistulae or abscesses.\n\t\t- Non-caseating granulomas\n\n# Management\n\n- As a general management point, it is paramount to advise patients with Crohn's who are smokers to **stop smoking** as this is known to strongly impact disease activity\n\n## Inducing remission\n\n- The first step of treatment is inducing remission in patients having a flare\n- Patients should be offered monotherapy with glucocorticoids (oral prednisolone, or IV hydrocortisone if first presentation is severe flare necessitating admission).\n- There is an increasing role for biologics for acute management of severe flares\n\n## Maintaining remission\n\n- Azathioprine or mercaptopurine may be added on to induce remission if there are 2 or more exacerbations in a 12-month period or the glucocorticoid cannot be tapered.\n\n - It is important to assess for thiopurine methyltransferase (TPMT) activity before offering azathioprine or mercaptopurine. If there is underactivity, this greatly increases the risk of profound bone marrow suppression if the above medications are given\n\n- Methotrexate may be considered in patients who are intolerant/have a contraindication to azathioprine or mercaptopurine or who do not respond to azathioprine or mercaptopurine monotherapy.\n- Biological agents (such as infliximab or adalimumab) are recommended in patients with severe Crohn's disease who fail to respond to the above.\n\t- These patients should have a CXR before treatment initiation due to the risk of re-activation of latent TB\n\n\n## Surgical management\n\nSurgical management is rarely curative in Crohn's disease (unlike in ulcerative colitis) because disease can occur anywhere along the GI tract, however 50-80% of Crohn’s patients end up requiring surgery at some point.\n\nSurgical options will depend on the part of the GI tract that is affected, and is indicated in those who have failed medical therapy or in those with severe stricturing or fistulating disease:\n\r\n-\tControl fistulae \r\n-\tResection of strictures\r\n-\tRest/defunctioning of the bowel\r\n\n\n### Management of peri-anal fistulae\n\n- Drainage seton is the management of choice for high (trans-sphincteric) fistulae. A seton is a thread passed through the fistula tract, forming a ring between the internal and external openings. It is used in the management of high trans-sphincteric fistulae, to prevent division of the anal sphincter muscles and incontinence. Closure of the fistula occurs by the formation of granulation tissue.\n- Fistulotomy is the management of choice for low (submucosal) fistulae. Fistulotomy involves dissecting the superficial tissue and opening the fistula tract. This is not a treatment option for high fistulae due to the risk of incontinence.\n- 'Sphincter saving' methods include fibrin glue and fistula plug - these are still under investigation and have not yet been approved in mainstream management.\n\n### Management of peri-anal abscess\n\n- The patient should be started on intravenous antibiotics e.g. ceftriaxone + metronidazole.\n- Patients typically require examination under anaesthetic and incision and drainage. An incision is made in the affected region, the pus is broken up, the infected tissue material is excised, and anti-septic soaked packs are inserted. Healing occurs by secondary intention.\n\n# Complications\n\n- **Fistulas:**\n - Formation of abnormal connections between different parts of the digestive tract or between the digestive tract and other organs.\n - Commonly involves the small intestine and other structures like the bladder or skin.\n\n- **Strictures:**\n - Narrowing or tightening of the intestinal walls.\n - Can lead to bowel obstruction and difficulties with the passage of stool.\n\n- **Abscesses:**\n - Collection of pus within the abdomen, often near areas of inflammation.\n - Presents with localized pain, swelling, and may require drainage.\n\n- **Malabsorption:**\n - Impaired absorption of nutrients due to inflammation and damage to the intestinal lining.\n - Can lead to nutritional deficiencies and weight loss.\n\n- **Perforation:**\n - Formation of a hole or tear in the intestinal wall.\n - Can result in peritonitis, a serious and potentially life-threatening condition.\n\n- **Nutritional Deficiencies:**\n - Chronic inflammation can affect nutrient absorption.\n - Common deficiencies include vitamin B12, vitamin D, and iron.\n\n- **Increased Risk of Colon Cancer:**\n - Prolonged inflammation may elevate the risk of developing colorectal cancer, particularly in long-standing disease involving the colon.\n\n- **Osteoporosis:**\n - Reduced bone density due to chronic inflammation and corticosteroid use.\n - Increases the risk of fractures.\n\n- **Intestinal Obstruction andToxic Megacolon:**\n - Severe inflammation can lead to the dilation of the colon.\n - Presents as abdominal distension, fever, and can be a medical emergency.\n\n\n# Comparison with Ulcerative Colitis\n\nPlease see below a summary table comparing Crohn's disease and Ulcerative colitis:\n\n| Characteristic | Crohn's Disease | Ulcerative Colitis |\n|------------------------------------|---------------------------------------|-------------------------------------|\n| **Location** | Any part of the digestive tract, from the mouth to the anus (most commonly affects the terminal ileum and colon) | Limited to the colon and rectum |\n| **Inflammation Pattern** | Patchy, skip lesions | Continuous, involves the entire colon|\n| **Depth of Inflammation** | Full thickness (transmural) | Limited to the inner lining (mucosa and submucosa)|\n| **Symptoms** | Abdominal pain, non-bloody diarrhoea, weight loss | Bloody diarrhoea, abdominal cramps |\n| **Complications** | Fistulas, strictures, abscesses | Toxic megacolon, colon cancer risk |\n| **Extraintestinal Manifestations** | Joint pain, skin problems, eye inflammation | Joint pain, skin problems, eye inflammation |\n| **Endoscopy Findings** | Cobblestone appearance, deep ulcers | Continuous colonic inflammation, ulcers |\n| **Diagnostic Imaging** | Transmural inflammation visible on imaging (e.g, MRI) | Limited to the colonic mucosa and submucosa, visible on colonoscopy |\n| **Treatment Approach** | Individualised, may involve medications (e.g. steroids, immunosuppressants) and surgery | Medications (e.g. aminosalicylates, steroids, immunosuppressants), surgery (in severe cases) |\n| **Prognosis** | Variable, chronic condition with periods of remission and exacerbation | Variable, can be chronic with periods of remission, may require surgery in some cases |\n\n\n# NICE Guidelines\n\n[Click here to see information on NICE CKS on Crohn's disease](https://cks.nice.org.uk/topics/crohns-disease/)\n\n",
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"question": "A 21-year-old female presents to her GP because she has been feeling increasingly anxious. She has recently moved house and broken up with her partner. She has also been experiencing intermittent diarrhoea and diffuse abdominal pain. Her GP decides to send her for an ileocolonoscopy where biopsies are taken. These biopsies show granulomas and inflammation of the serous membrane.\n\nWhat is the most likely diagnosis?",
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"explanation": "Crohn's disease can present with bloody diarrhoea, however, the histology would be unlikely to show pseudopolyps. Increased thickness of the bowel wall would also be likely as well as more diffuse inflammation",
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"explanation": "Irritable bowel syndrome is common in younger adults. However, it is unlikely to present with bloody diarrhoea, and would not show inflammation on biopsy",
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"explanation": "Giardiasis is associated with foreign travel. It can lead to prolonged diarrhoea for more than one week. However, it is unlikely to lead to bloody diarrhoea. Plus, the biopsy results suggest chronic inflammation due to the irregular, dilated crypts seen. This makes giardiasis less likely",
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"explanation": "Shigellosis is associated with foreign travel. It usually leads to watery diarrhoea, however, blood and mucus can also be seen in the stool. It is a self-limiting disease that usually improves over a few days. It is less likely in this case because the biopsy results suggest chronic inflammation due to the irregular, dilated crypts seen",
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"explanation": "Bloody diarrhoea is the cardinal symptom of ulcerative colitis. Although the initial history suggests a short time-line, the biopsy results suggest chronic bowel inflammation due to the irregular, dilated crypts. Therefore, ulcerative colitis is the most likely diagnosis. An ulcerative colitis history may mimic that of a gastrointestinal infection. Therefore, attention should be given to the biopsy results",
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"comment": "naughty quesmed with the travel history\n",
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"explanation": "# Summary\n\nUlcerative colitis (UC) is a chronic inflammatory disease that affects the large bowel. Symptoms include diarrhoea, urgency, tenesmus, weight loss, and fever. The disease can present with extra-intestinal features such as dermatological (erythema nodosum), ocular (anterior uveitis), musculoskeletal (finger clubbing), and hepatobiliary manifestations (jaundice due to primary sclerosing cirrhosis). Investigations include blood tests, microbiological investigations, endoscopic investigations, and imaging. The management of UC is based on severity and involves inducing and maintaining remission using medications like aminosalicylates, steroids, and biologics. Surgery may be required in severe cases or when medical treatment is unsuccessful. Long-term complications include colorectal cancer, cholangiocarcinoma and colonic strictures.\n\n# Definition\n\nUlcerative colitis (UC) is a chronic relapsing-remitting inflammatory disease that primarily affects the large bowel. It usually affects the rectum first, then can extend to the part of the colon (left-hand-side colitis) or the entire colon (pancolitis). It does not spread beyond the ileocaecal valve or to the small bowel, except where backwash ileitis can occur.\n\n# Epidemiology\n\nUC is the most commonly diagnosed inflammatory bowel disease. It has an annual incidence rate of 10 per 100,000 people and a prevalence rate of 243 per 100,000. Although UC can develop at any age, it most frequently occurs in two peak age groups: 15 to 25 years and 55 to 65 years.\n\n# Aetiology\n\nThe exact cause of UC is unknown, but it is believed to result from a combination of genetic predisposition, environmental factors, and dysregulation of the immune system. There is also a higher incidence of UC among non-smokers and ex-smokers.\n\n# Signs and Symptoms\n\nThe main symptoms of UC are gastrointestinal and systemic. \n\nGastrointestinal symptoms include:\n\n- Diarrhoea often containing blood and/or mucus\n- Tenesmus or urgency\n- Generalised crampy abdominal pain in the left iliac fossa\n\nSystemic symptoms include:\n\n- Weight loss\n- Fever\n- Malaise\n- Anorexia\n\nPhysical examination may reveal general signs such as pallor due to anaemia and clubbing. Abdominal examination may reveal distension or tenderness, and a PR examination may show tenderness, and blood/mucus. \n\n\nExtra-intestinal signs occur in 10-20% of patients and include:\n\n- Dermatological manifestations: erythema nodosum, pyoderma gangrenosum\n- Ocular manifestations: anterior uveitis, episcleritis, conjunctivitis\n- Musculoskeletal manifestations: clubbing, non-deforming asymmetrical arthritis, sacroiliitis\n- Hepatobiliary manifestations: jaundice due to primary sclerosing cholangitis (PSC). 80% of those with PSC have ulcerative colitis.\n- Other features include AA amyloidosis\n\n\n\n\n# Differential Diagnosis\n\nThe differential diagnoses for UC include Crohn's disease, infectious colitis, and ischemic colitis. Key signs and symptoms to differentiate these conditions include:\n\n- Crohn's disease: Abdominal pain, weight loss, diarrhea, oral ulcers, anal fissures, and perianal fistulas.\n- Infectious colitis: Acute onset of diarrhea, fever, and abdominal pain. May be associated with recent antibiotic use, travel, or consumption of contaminated food or water.\n- Ischemic colitis: Sudden onset of abdominal pain, blood in stools, and a history of vascular disease or risk factors.\n\n# Investigations\n\n**Bedside:**\n\n- Microbiological investigations: Stool microscopy (for ova/cysts/parasites), culture and sensitivity, and stool C. difficile toxin to exclude infective colitis\n- Faecal calprotectin: Distinguishes between inflammatory bowel syndrome (normal) and inflammatory bowel disease (raised)\n\n**Bloods:**\n\n- Blood tests: FBC (anaemia and a raised white cell count), ESR/CRP is typically raised, LFTs may show a low albumin\n\n**Imaging/Invasive:**\n\n- Radiological investigations: Abdominal X-ray and erect chest x-ray in acute settings to exclude toxic megacolon and perforation.\n\t- Long-standing UC will show 'lead-pipe' colon on AXR \n- Endoscopic investigations: Colonoscopy, barium enema, and biopsy are used to confirm the diagnosis.\n - Colonoscopy will reveal shows continuous inflammation starting at the rectum that does not go beyond the submucosa with an erythematous mucosa, loss of haustral markings, and pseudopolyps.\n - Biopsy: loss of goblet cells, crypt abscess, and inflammatory cells (predominantly lymphocytes)\n - Barium enema will reveal lead-piping inflammation (secondary to loss of haustral markings), thumb-printing (a marker of bowel wall inflammation), and pseudopolyps (due to areas of ulcerating mucosa adjacent to areas of regenerating mucosa). This is less commonly used nowadays due to the increasing availability of endoscopic investigations\n\n# Truelove and Witt's Criteria for Severity\n\nAn acute exacerbation of ulcerative colitis should be assessed using the Truelove and Witt's severity index.\n\n| | **Mild** | **Moderate** | **Severe** |\n| --------------------------------------------- | ----------------------------------- | ----------------------- | ------------------------------------------------------------------------------------ |\n| **Bowel movements (no. per day)** | Fewer than 4 | 4-6 | 6 or more plus at least one of the features of systemic upset (marked with \\* below) |\n| **Blood in stools** | No more than small amounts of blood | Between mild and severe | Visible blood |\n| **Pyrexia (temperature greater than 37.8°C)** | No | No | Yes |\n| **Pulse rate greater than 90 bpm** | No | No | Yes |\n| **Anaemia (< 10g/100mL)** | No | No | Yes |\n| **Erythrocyte sedimentation rate (mm/hour)** | 30 or below | 30 or below | above 30 |\n\n\n# Management\n\n\n## Mild-moderate disease\n\nThe aim of step 1 treatment is to induce remission. If this does not work after 4 weeks, or symptoms worsen, move to step 2.\n\nThe first step in management for a moderate first presentation is to offer a topical aminosalicylate as first-line treatment. If remission is not achieved within 4 weeks, consider adding an oral aminosalicylate. In acute moderate disease if all other measures haven't worked then a trial of Etrasimod (also known as Velsipity). This is a selective sphingosine 1-phosphate (S1P) receptor modulator.\n\n- **Proctitis and proctosigmoiditis:**\n - Step 1: Topical ASA or oral ASA.\n - Step 2: Consider adding oral prednisolone. If this does not help after 2-4 weeks or symptoms worsen, consider adding oral tacrolimus.\n- **Left sided or extensive disease**\n - Step 1: High dose oral ASA.\n - Step 2: Consider adding oral prednisolone. If this does not help after 2-4 weeks or symptoms worsen, consider adding oral tacrolimus.\n\n## Acute severe disease\n\n- Step 1: IV corticosteroids (if contraindicated or not tolerated, use IV ciclosporin).\n- Step 2: If no improvement in 72 hours or worsening symptoms, add IV ciclosporin or consider surgery (if IV ciclosporin contraindicated or not tolerated, consider infliximab).\n- Step 3: A trial of Etrasimod (also known as Velsipity). This is a selective sphingosine 1-phosphate (S1P) receptor modulator.\n- Indications for emergency surgery:\n - Surgery should be considered in patients with:\n - Acute fulminant ulcerative colitis\n - Toxic megacolon who have little improvement after 48-72 hours of intravenous steroids\n - Symptoms worsening despite intravenous steroids\n\n_Note that an alternative is to initiate rescue therapy (with ciclosporin or infliximab) if the patient has a sub-optimal response to intravenous steroids but is stable enough to delay surgery. Surgery should be considered if patients fail to respond to rescue therapy within 3 days._\n\n## Surgical options\n\n- Panproctocolectomy with permanent end ilesotomy\n- Colectomy with temporary end ileostomy (approximately 3 months later the ileostomy can be reversed by forming an ileorectal anastomosis, an alternative option is completion proctectomy with a permanent end ileostomy or ileal pouch anal anastomosis (IPAA)).\n\n## Indications for elective surgery\n\n- This can be considered in patients in which there is failure to induce remission by medical means.\n- Surgical options include: panproctocolectomy with permanent end ileostomy or IPAA. An alternative is a total colectomy with ileorectal anastomosis (i.e. no stoma).\n\n# Complications\n\n## Short-term/acute complications\n\n- Toxic megacolon: this describes a severe form of colitis, and is seen in around 15% of ulcerative colitis patients.\n- Massive lower gastrointestinal haemorrhage: this occurs in up to 3% of patients.\n\n## Long-term complications\n\n- Colorectal cancer: this occurs in 3-5% of patients. There is a higher risk with disease duration, severity and extent of colitis, and concomitant primary sclerosing cholangitis (PSC).\n\n_NICE guidance suggests offering colonoscopy surveillance to high risk patients._\n\n- Cholangiocarcinoma: ulcerative colitis approximately doubles the risk of cholangiocarcinoma.\n- Colonic strictures: these can cause large bowel obstruction.\n\n## Variable-term complications\n\n- Primary Sclerosing Cholangitis: this is characterised by inflammation and fibrosis of the extra- and intra-hepatic biliary tree and affects 3-7% of patients with ulcerative colitis. LFTs should be monitored yearly to check for the presence of PSC.\n- Inflammatory pseudopolyps: these are areas of normal mucosa between areas of ulceration and regeneration.\n- Increased risk of VTE - as with any inflammatory disease, but in the acute and chronic context, patients have an increased risk of developing blood clots, especially during flares\n\n# References\n\n[Click here for more information on NICE CKS about ulcerative colitis](https://cks.nice.org.uk/topics/ulcerative-colitis/)",
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"question": "A 25-year-old woman presents to her GP with bloody diarrhoea. This has been going on for the last week. She has also been experiencing fevers and malaise. She states that she has recently visited India to see her family.\n\nHer GP requests a colonoscopy where biopsies are taken. The biopsies show inflammation of the mucosa and the superficial submucosa. Neutrophilic infiltrates were seen, along with irregular, dilated crypts, pseudopolyps and lamina propria fibrosis.\n\nWhat is the most likely diagnosis?",
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"explanation": "Nonspecific lower back pain can only be diagnosed when no other cause of the back pain can be found. Therefore, it is a diagnosis of exclusion. Nonspecific lower back pain would not lead to jaundice",
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"name": "Nonspecific lower back pain",
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"explanation": "Liver cirrhosis occurs when the liver tissue because nodules surrounded by widespread fibrosis. This usually occurs over a number of years rather than months. Jaundice is a symptom of liver cirrhosis, but it is often accompanied by ascites and muscle wasting",
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"explanation": "Hepatocellular carcinoma is the most common cancer of the liver. Patients with cirrhosis are at high risk of developing hepatocellular carcinoma. It usually presents with pruritis, jaundice, abdominal distension and right upper quadrant pain",
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"explanation": "Primary biliary cholangitis is often found incidentally. It is an autoimmune disease of the biliary system which eventually leads to scarring, fibrosis and cirrhosis over years or decades. (In its late stages, it can also be called primary biliary cirrhosis). The first symptoms are often fatigue, pruritis and right upper quadrant pain",
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"comment": "Why tanned skin?",
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"comment": "Tanned and Jaundice are not the same.",
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"comment": "not sure why this can't be PBC? \n",
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"comment": "PBC presents with itching, extreme fatigue etc none of which are mentioned in her symptoms",
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"comment": "Tanned skin really threw me off",
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"explanation": "# Summary\n\nPancreatic cancer, primarily adenocarcinomas, is the fifth leading cause of cancer in the UK with approximately 9,000 new diagnoses annually. Early symptoms such as malaise, abdominal pain, nausea, or weight loss are often non-specific, leading to a late diagnosis. Advanced disease may exhibit complications such as obstructive jaundice, newly diagnosed diabetes in older patients, unexplained pancreatitis, paraneoplastic syndromes, and others. Diagnostic investigations includes ultrasound, CT scan, MRI, MRCP, and endoscopic ultrasound, with biopsy if necessary. Management strategies depend on the stage of the disease; surgical resection, specifically pancreaticoduodenectomy, is the only potentially curative approach for localized disease, while palliative therapies are used for advanced cases.\n\n# Definition\n\nPancreatic cancer is a malignant neoplasm originating from the pancreatic tissue. The pancreas is a glandular organ involved in both the digestive and endocrine systems of vertebrates. The most prevalent type of pancreatic cancer is pancreatic adenocarcinoma, which usually originates from the head of the pancreas.\n\n# Epidemiology\n\n- Pancreatic cancer ranks as the fifth most common cancer in the UK.\n- Adenocarcinomas make up the majority of these cancers, with a poor 5-year survival rate (<5%).\n- Each year in the UK, nearly 9,000 new pancreatic cancer cases are diagnosed.\n- On average, a full-time GP will diagnose approximately one person with pancreatic cancer every 3-5 years.\n\n# Aetiology\n\nThe exact cause of pancreatic cancer remains unknown. However, it is associated with several risk factors:\n\n- Age: Pancreatic cancer is more prevalent in elderly individuals.\n- Smoking: The risk significantly increases with tobacco use.\n- Obesity: Overweight and obese individuals have a higher risk.\n- Diabetes: Long-standing diabetes may increase risk.\n- Chronic pancreatitis: Chronic inflammation of the pancreas can lead to cancer.\n- Family history: Having a first-degree relative with pancreatic cancer increases the risk.\n- Certain genetic syndromes: Genetic mutations linked to pancreatic cancer include BRCA2, Lynch syndrome, and familial atypical mole and melanoma (FAMMM) syndrome.\n\n# Signs and Symptoms\n\nEarly-stage pancreatic cancer often presents with non-specific symptoms:\n\n- Malaise\n- Abdominal pain\n- Nausea\n- Weight loss\n- Painless jaundice\n- Courvoisier's sign - painless jaundice with a palpable gallbladder is usually indicative of a pancreatic or gallbladder malignancy (and less likely due to e.g. gallstones)\n\nAdvanced disease can present with complications including:\n\n- Obstructive jaundice, often due to blockage of the common bile duct by a tumour in the pancreatic head. It may present with Courvoisier's sign.\n- Diabetes mellitus, typically in an elderly patient with newly diagnosed diabetes and weight loss, may suggest a tumour in the body/tail of the pancreas.\n- Pancreatic infiltration can lead to unexplained pancreatitis and pancreatic exocrine dysfunction with steatorrhoea.\n- Paraneoplastic syndromes, such as Trousseau's syndrome (migratory thrombophlebitis), or marantic endocarditis.\n- Disseminated intravascular coagulation (DIC)\n\nPancreatic cancer often metastasises early to the lung, liver, and bowel.\n\n# Differential Diagnosis\n\nConditions with similar presentation to pancreatic cancer include:\n\n- Chronic pancreatitis: Chronic abdominal pain, steatorrhoea, diabetes mellitus.\n- Cholangiocarcinoma: Painless jaundice, weight loss, abdominal pain.\n- Gastric cancer: Dyspepsia, weight loss, anorexia, nausea and vomiting.\n- Hepatocellular carcinoma: Abdominal pain, weight loss, jaundice, hepatomegaly.\n\n# Investigations\n\n### NICE 2-week-wait criteria:\n\n* Refer people using a suspected cancer pathway referral (for an appointment within 2 weeks) for pancreatic cancer if they are aged 40 years and over and have jaundice.\n* Consider an urgent CT scan (to be performed within 2 weeks), or an urgent ultrasound scan if CT is not available, to assess for pancreatic cancer in people aged 60 years and over with weight loss and any of the following: diarrhoea, back pain, abdominal pain, nausea, vomiting, constipation, or new-onset diabetes.\n\nInvestigations for pancreatic cancer include:\n\n- Initial assessment with abdominal ultrasound to detect tumours (>2cm), potential liver metastases and any dilation of the common bile duct.\n- CT abdomen/pelvis for patients with a high clinical suspicion. This can predict surgical resectability and enables disease staging.\n- Magnetic resonance cholangiopancreatography (MRCP) for details about the biliary ducts.\n- Endoscopic ultrasound to detect small lesions (2-3mm) and for biopsy if needed.\n- PET-FDG and MRI as adjuncts.\n\n# Management\n\nThe only potentially curative treatment for pancreatic cancer is surgical resection. However, due to late presentation, only 15-20% of patients present with resectable disease.\n\nCriteria for resection include:\n\n- No evidence of superior mesenteric artery (SMA) or coeliac arteries involvement.\n- No evidence of distant metastases.\n\nThe common surgical procedure for tumours in the head of the pancreas is the Kausch-Whipple procedure (radical pancreaticoduodenectomy). Adjuvant chemotherapy is offered post-surgery to patients who have recovered well.\n\nIn cases of locally advanced or metastatic disease, palliative therapy is the only option. This includes:\n\n- Endoscopic stent insertion into the common bile duct.\n- Palliative surgery if endoscopic stent insertion fails.\n- Chemotherapy.\n- Radiotherapy (only for localised advanced disease).\n\nIt is crucial to refer these patients to palliative care services for pain management and psychological support.\n\n# NICE Guidelines\n\n[Click here to see the NICE guidelines on pancreatic cancer](https://www.nice.org.uk/guidance/ng85)",
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"explanation": "# Summary\n\nPrimary biliary cholangitis (PBC) is an autoimmune condition that causes granulomatous inflammation of primarily the intrahepatic bile ducts, resulting in scarring and eventually leading to liver cirrhosis. It primarily affects women under 40 years of age, with men making up about 10% of cases. Patients typically present with fatigue, itching, dry skin, dry eyes, and jaundice. They also have a higher risk of developing hepatocellular carcinoma. Diagnosis is typically through abnormal liver function tests, positive anti-mitochondrial antibodies in over 90% of individuals, abdominal ultrasound, and liver biopsy. Management is primarily supportive, including the use of ursodeoxycholic acid, cholestyramine, vitamin supplements, and liver transplantation, although the disease may recur after transplantation.\n\n# Definition\n\nPrimary biliary cholangitis (PBC), formerly known as primary biliary cirrhosis, is an autoimmune disease that results in scarring and inflammation of the bile ducts, leading to eventual liver cirrhosis.\n\n# Epidemiology\n\nPBC predominantly affects women, with approximately 25% of patients being women under 40 years of age. Men comprise about 10% of patients.\n\n# Aetiology\n\nThe exact cause of PBC is unknown, but it is thought to be due to a combination of genetic predisposition and environmental factors. The disease results from an autoimmune response that targets the small bile ducts within the liver. Risk factors include:\n\n- Previous family history of PBC\n- Female\n- Smoking\n- Predisposition to other autoimmune conditions (80% have Sjogren’s)\n\n# Signs and Symptoms\n\nPBC can initially be asymptomatic and only suspected due to incidental cholestatic LFTs.\n\n- Extreme fatigue\n- Pruritus (itching)\n- Xerosis (dry skin)\n- Sicca syndrome (dry eyes)\n- RUQ pain\n- Xanthelasma\n- Clubbing\n- Jaundice\n- Late signs include sequalae of chronic liver disease\n\nPatients with PBC also have an increased risk of developing hepatocellular carcinoma, and if this occurs, the prognosis is generally poor.\n\n# Differential Diagnosis\n\nOther conditions that may present with similar symptoms as PBC include:\n\n- Autoimmune hepatitis: Presents with fatigue, jaundice, hepatomegaly, or splenomegaly.\n- Chronic viral hepatitis: Symptoms include fatigue, mild right upper quadrant discomfort, and jaundice.\n- Primary sclerosing cholangitis: Presents with pruritus, fatigue, and jaundice.\n- Alcoholic liver disease: Presents with jaundice, hepatomegaly, and signs of chronic liver disease.\n\n# Investigations\n\nBloods:\n\n- Abnormal liver function tests with a cholestatic picture. If late stage with chronic liver disease there may also be an impact on synthetic function of the liver (deranged clotting, low albumin)\n- Positive **Anti-mitochondrial antibodies (AMAs)** in >90% of individuals\n- Raised serum IgM\n\nImaging:\n\n- Abdominal ultrasound to visualise the liver is a first line investigation to rule out extrahepatic biliary obstruction\n- MRCP is the gold standard for visualising the liver and bile ducts\n\nInvasive:\n\n- Liver biopsy is the gold standard for diagnosis, showing inflammation and scarring and granulomas around the bile duct\n\n# Management\n\nThe management of PBC is largely supportive and includes the following:\n\n- Ursodeoxycholic acid to slow disease progression by promoting bile flow\n- Cholestyramine for relief of pruritus\n- Vitamin supplements to manage deficiencies\n- Liver transplantation in advanced cases, often once bilirubin is >100 this is considered (Note: PBC may recur after transplantation) \n\n# Complications\n\n- Chronic liver disease eventually leads to cirrhosis, which can result in complications such as portal hypertension, deranged clotting (with increased risk of GI bleeding) and ascites\n- Osteomalacia is an important consideration (as bile salts are needed to emulsify fats to absorb fat-soluble vitamins like vitamin D) considering many affected patients are middle-aged/postmenopausal females who are already at risk of osteomalacia\n\n# References\n\n[Click here to see more information on PBC on rarediseases.org](https://rarediseases.org/rare-diseases/primary-biliary-cholangitis/)",
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"explanation": "Aspirin is an option in migraine but the dose is usually 900mg. Please don't despair and worry that you have to memorise drug doses! This choice was left in to teach you that an option for migraine is 900mg Aspirin which is one of the rare instances where a larger dose than 300mg is used",
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"explanation": "Whilst nausea is common with migraine, and prochlorperazine is a correct treatment, this will not directly relieve the migraine",
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"explanation": "This is the correct answer. First line treatment for migraines include: 1. Simple analgesia. 2. An anti-emetic if required. 3. Triptans (usually prescribed if moderate to severe symptoms)",
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"comment": "question was not clear if asking for acute management or prophylaxis",
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"comment": "also GP is unlikely to prescribe ibuprofen - would recommend buying over the counter ",
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"comment": "It says pain relief during acute episodes",
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"comment": "i thought exercise was a trigger for migraines?",
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"comment": "I agree, if it is worse when she doesn't do exercise in my opinion that exlcudes migraine as a diagnosis ",
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"comment": "Why not asprin?",
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"comment": "GPs would not prescribe ibruprofen, so I went up the pain ladder to a medication they may prescribe to relieve pain: FML ",
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"explanation": "# Summary\r\n\r\nMigraine is a common neurological disorder characterised by recurrent, unilateral, throbbing headaches often preceded by an aura such as visual or sensory symptoms. Migraines can last between 4-72 hours and often result in photophobia and phonophobia. Key signs and symptoms include a unilateral headache, a pulsating character, impairment or worsened by daily activities, and presence of nausea, vomiting or photophobia. Diagnosis is often based on clinical history, focusing on the presence of an aura. Management strategies include avoidance of triggers, prophylaxis with medications such as Propranolol, Topiramate or Amitriptyline, and managing acute attacks with oral triptans alongside Paracetamol or an NSAID.\r\n\r\n# Definition\r\n\r\nMigraine is a primary headache disorder characterised by intense episodes of debilitating headaches, usually unilateral and pulsating in nature. Symptoms may be preceded by an 'aura' which manifests as visual disturbances or sensory changes. The pain usually lasts from 4-72 hours and can be accompanied by nausea, vomiting, photophobia, and phonophobia.\r\n\r\n# Epidemiology\r\n\r\nMigraines are one of the most prevalent neurological disorders worldwide, affecting roughly 12% of the global population. It is more common in women, with a male to female ratio of approximately 1:3, likely related to hormonal influences. The peak incidence occurs between the ages of 30-39.\r\n\r\n# Aetiology\r\n\r\nThe exact cause of migraines is not fully understood, but it is likely a combination of genetic and environmental factors. \n\nThe triggering factors are variable and can include certain foods, changes in weather, stress, hormonal changes, and certain medications such as oral contraceptives.\r\n\r\n# Signs and Symptoms\r\n\r\n- Aura (usually visual or sensory symptoms preceding the headache)\r\n- Unilateral throbbing headache\r\n- Photophobia and phonophobia\r\n- Nausea and/or vomiting\r\n\r\nThe International Headache Society criteria for migraine without aura:\r\n\r\n| Criteria | Description |\r\n| -------- | ------------------------------------------------------------ |\r\n| A | At least five attacks fulfilling criteria B-D |\r\n| B | Headache attacks lasting 4-72 hours (untreated or unsuccessfully treated) |\r\n| C | Headache has at least two of the following four characteristics: <br>1. Unilateral location <br>2. Pulsating quality <br>3. Moderate to severe pain intensity <br>4. Aggravation by or causing avoidance of routine physical activity |\r\n| D | During headache, at least one of the following: <br>1. Nausea and/or vomiting <br>2. Photophobia and phonophobia |\r\n| E | Not better accounted for by another ICHD-3 diagnosis |\r\n\r\n# Differential Diagnosis\r\n\r\nMigraines must be differentiated from other conditions that present with severe headache. Some of these include:\r\n\r\n- Tension-type headache: Bilateral, band-like pressure or tightness, not worsened with physical activity, no associated nausea or vomiting.\r\n- Cluster headache: Severe, unilateral, orbital, supraorbital and/or temporal pain lasting 15-180 minutes, occurring up to 8 times a day, associated with autonomic symptoms like ptosis, miosis, lacrimation.\r\n- Subarachnoid hemorrhage: Sudden-onset severe headache, often described as \"the worst headache of my life\", associated with nausea, vomiting, and possible loss of consciousness.\r\n- Giant cell arteritis: New headache in a person over 50 years, scalp tenderness, jaw claudication, visual disturbances, elevated ESR and CRP.\r\n\r\n# Investigations\r\n\r\nDiagnosis is primarily clinical, based on the history and examination. \n\nA headache diary is important to help identify triggers and response to treatment.\n\nIf secondary causes of headaches are suspected, further investigations may be warranted, such as neuroimaging (MRI or CT) or blood tests (ESR, CRP for giant cell arteritis).\r\n\r\n# Acute Management\r\n\n- **Avoidance of triggers**: \n - Identify and avoid potential triggers like certain foods, stress, and poor sleep.\n- **Medications for acute attacks**: \n - **Triptans** (e.g., Sumatriptan) – avoid in patients with ischaemic heart disease.\n - **Paracetamol** or an **NSAID** (e.g., Ibuprofen) can be used in combination with triptans.\n - **Anti-emetics** (e.g., Metoclopramide)\n- **Special considerations**:\n - Female patients with migraine with aura should avoid the **combined oral contraceptive pill** due to increased risk of ischaemic stroke.\n\n# Prophylaxis\n\n- Medications:\n - **Propranolol** (contraindicated in asthma).\n - **Topiramate**.\n - **Amitriptyline**.\n - **Candesartan**.\n- Injections:\n\t- Greater Occipital Nerve Block\n\t- Botulinum Toxin Injection \n- **Newer treatments**:\n - **Rimegepant** (per NICE guidance, May 2023):\n - Used for preventing episodic migraine.\n - Suitable when at least 3 preventive treatments have failed.\n - Indicated for adults with 4-15 migraine attacks per month.\n\nRegular use of acute migraine medications (e.g., triptans, NSAIDs) more than 10-15 days per month can lead to **medication overuse headache (MOH)**.\n\nPatients should be counseled on limiting the use of acute treatments to prevent MOH.\n\n## References\r\n\r\n[Click here for NICE Clinical Knowledge Summaries on Migraines](https://cks.nice.org.uk/topics/migraine/)",
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"question": "A 23-year-old woman visits her GP due to headaches. They are unilateral, severe (8/10), last several hours and are associated with nausea. She has noticed that they are worst when she does not do any exercise.\n\nWhat medication should the GP prescribe for pain relief during acute episodes?",
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"explanation": "Tamsulosin is an alpha-blocker, usually used first line in treating BPH. However, here the patient has postural hypotension and so a 5-alpha reductase inhibitor would be preferable",
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"explanation": "Finasteride is a 5-alpha reductase inhibitor. Usually these are prescribed 2nd-line after alpha-blockers. However, in this case the patient has postural hypotension and therefore, alpha-blockers are relatively contraindicated because of their potential adverse effects on the patients blood pressure",
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"explanation": "# Summary\n\nLower Urinary Tract Symptoms (LUTS) encompass a wide range of symptoms related to issues with voiding, storage, and post-micturition. These symptoms are often the result of underlying pathologies affecting the bladder, prostate, or urethra, or due to neurological causes. Key signs and symptoms are categorised under voiding and storage symptoms. Investigations often include urinalysis, DRE, bladder diary, and urodynamics. Management strategies vary depending on the cause and often involve a combination of medical and surgical interventions.\n\n# Definition\n\nLower Urinary Tract Symptoms (LUTS) refer to a group of symptoms that occur as a result of abnormal storage, voiding, or post-micturition function of the bladder, prostate (in men), or urethra.\n\n# Aetiology\n\nThe commonest cause of LUTS are UTIs, which result in storage symptoms (below), and dysuria, haematuria and sometimes systemic upset.\n\nLUTS can be due to:\n\n- **Neurological causes**: Lesions at the higher functional centres or tracts that control micturition and continence\n- **Bladder causes**: Bladder underactivity or detrusor underactivity, where the bladder cannot generate sufficient pressures to overcome resistance downstream.\n- **Prostate causes**: An increase in prostate size, due to benign prostatic hyperplasia (BPH) or prostate cancer, can narrow the prostatic urethra and increase the resistance in the lumen.\n- **Other mass effect causes**: Including ovarian masses in women, which could be malignant or non-malignant (e.g. fibroids).\n- **Urethral causes**: Urethral strictures, which are the narrowing of the urethra due to congenital or traumatic causes.\n\n\n# Signs and Symptoms\n\n**Voiding Symptoms**\n\n- Weak or intermittent urinary stream\n- Straining\n- Hesitancy\n- Terminal dribbling\n- Incomplete emptying\n\n**Storage Symptoms**\n\n- Urgency\n- Frequency\n- Urgency incontinence\n- Nocturia\n\n# Differential Diagnosis\n\nThe key differentials for LUTS include:\n\n- **Bladder outlet obstruction**: Characterised by weak or intermittent urinary stream, straining, hesitancy, terminal dribbling, incomplete emptying, and sometimes urgency and frequency.\n- **Overactive bladder syndrome**: Typically presents with urgency, increased daytime frequency, nocturia, and may also include urgency incontinence.\n- **Prostatitis**: Symptoms can include voiding and storage symptoms, but often accompanied by discomfort or pain in the pelvic region.\n- **Bladder cancer**: Hematuria is the most common symptom but it may also present with LUTS.\n- **Urethral stricture**: Symptoms can include diminished force of the urinary stream, straining, spraying of urine, and incomplete emptying.\n\n# Investigations\n\nKey investigations for LUTS include:\n\n- Urinalysis\n- Digital Rectal Examination (DRE)\n- Bladder diary\n- Urodynamics\n\nThe most definitive tests available to determine the aetiology of both voiding dysfunction and LUTS are urodynamic studies which comprise a filling and storage phase, and a voiding phase.\n\n# Management\n\nManagement of LUTS depends on the underlying cause, which can be deduced from the investigations above. See dedicated sections on UTI, BPH, urinary incontinence and bladder cancer for more information.\n\n# NICE Guidelines\n\n[NICE CKS - Lower Urinary Tract Conditions](https://www.nice.org.uk/guidance/conditions-and-diseases/urological-conditions/lower-urinary-tract-symptoms)",
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"question": "A 65-year-old man presents to his GP with increased frequency. He has noticed that he has been getting up during the night to urinate more often. He reports having a poor stream, and having to try and force urine out because he often has a feeling of incomplete voiding. He has a past medical history of type 2 diabetes mellitus, obesity and postural hypotension. On digital rectal examination, the prostate was noted to be enlarged and smooth. A diagnosis of benign prostatic hypertrophy was made.\n\nWhich medication should the GP start this patient on?",
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"explanation": "Splenectomy causes an increased risk of infection from encapsulated organisms with a 10-20 times greater risk of acquiring sepsis. P. jirovecii is a yeast-like fungus, and it does not have a capsule",
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"name": "Pneumocystis jirovecii",
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"explanation": "Splenectomy causes an increased risk of infection from encapsulated organisms with a 10-20 times greater risk of acquiring sepsis. M. catarrhalis is not an encapsulated bacterium",
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"explanation": "Splenectomy causes an increased risk of infection from encapsulated organisms with a 10-20 times greater risk of acquiring sepsis. Mycoplasma pneumoniae is not an encapsulated bacterium",
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"explanation": "Splenectomy causes an increased risk of infection from encapsulated organisms with a 10-20 times greater risk of acquiring sepsis. The most common encapsulated bacteria are Haemophilus influenzae, Streptococcus pneumoniae, and Neisseria meningitidis. For this reason, patients are offered the pneumococcal vaccine, Hib vaccine, and the meningococcal vaccine post-operatively. Patients should also be offered annual flu vaccination and lifelong antibiotic prophylaxis",
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"explanation": "Splenectomy causes an increased risk of infection from encapsulated organisms with a 10-20 times greater risk of acquiring sepsis. C. psittaci is not an encapsulated bacterium",
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"explanation": "# Summary \n \nPneumonia is a radiological diagnosis, often due to a lower respiratory tract infection causing inflammation of the alveoli and terminal bronchioles, leading to consolidation of bronchopulmonary segment or lobe. Key signs and symptoms include rapid onset of high fever and productive cough for typical bacterial causes. Key investigations include blood tests, sputum culture, urinary antigen tests, and chest x-ray. Management strategies involve use of antibiotics, assessment of severity using CURB-65 score and inpatient treatment for severe cases.\n \n \n# Definition\n \n- Lower Respiratory Tract Infection/ Pneumonia is caused by infection and subsequent inflammation of the alveoli and terminal bronchioles.\n- This leads to an entire bronchopulmonary segment or lobe becoming consolidated, which means that tissue is filled with inflammatory cells and oedema.\n \n \n# Community Acquired Pneumonia (CAP)\n \n \n## Bacterial Causes\n \n \n- Typicals - so called because of the classical rapid onset of symptoms, including high fever and productive cough;\n- Streptococcus pneumoniae (gram +ve cocci found in pairs, also known as 'Pneumococcus')\n- Staphylococcus aureus\n- Haemophilus influenzae (gram -ve rod, potent beta-lactamase producer)\n- Moraxella catarrhalis (gram -coccus, potent beta-lactamase producer)\n- Atypicals: so called because of the more gradual onset of symptoms, which may be non-specific initially (fever, myalgia, dry cough). The organisms are also intracellular;\n- Mycoplasma pneumoniae\n- Chlamydia pneumoniae\n- Legionella pneumophila\n- Coxiella burnettii\n- Chlamydia psittaci\n \n \n## Viral Causes \n \n- Most commonly Influenza A, which can predispose to superadded Staph aureus (or strep pneumoniae) pneumonia.\n- Others: CMV, HSV, VZV\n \n## Fungal Causes\n \nCan be seen after silver staining and microscopy:\n \n- Candida - dimorphic yeast\n- Aspergillus - fungus with hyphae\n- Cryptococcus - encapsulated yeast\n \n \n## Specific Causes \n \nCOPD: \n \n- Pneumococcus still most common\n- Haemophilus influenzae\n- Morexella catarrhalis\n \nCystic Fibrosis:\n \n \n- Staph aureus\n- Pseudomonas aeruginosa\n- Burkholderia cepacia\n \nCauses in Homeless people: malnourished, alcohol or drug dependent, immunosuppressed:\n \n \n- Mycobacterium tuberculosis\n- Aspiration pneumonia (infection with normal flora of mouth and anaerobes, also consider in any patient with an unsafe swallow or with depressed consciousness)\n- Klebsiella pneumoniae (causes 'red-current jelly' sputum, and commonly causes lung abscess formation and empyema)\n \n \nOccupational/travel situations:\n \n- Aerosols from humidifiers and airconditioning (e.g. at holiday resorts) - Legionella pneumophila.\n- Patients can present with diarrhoea and vomiting, develop hepatorenal syndrome and have a low sodium. Severe pneumonia develops, with other rare complications such as:\n- Pancreatitis\n- Peritonitis\n- Myocarditis, endocarditis, pericarditis\n- Glomerulonephritis\n \n \nClosed populations e.g. schools, offices\n \n- Mycoplasma pneumoniae\n- Extra respiratory symptoms:\n- Erythema multiforme, erythema nodosum\n- Guillain-Barre Syndrome (and rarely other neurological complications e.g. aseptic meningitis, cerebellar disease, transverse myelitis).\n- Cold agglutinin production with haemolytic anaemia\n- Chlamydia pneumoniae\n \n \nZoonotic Causes: \n \n- In Abattoir worker, farmer, vets\n- Coxiella burnettii\n- Brucella spp.\n \n- Animal hide importers/sorters\n- Bacillus anthracis\n- Coxiella burnettii\n \n \n- Following exposure to birds\n- Chlamydia psittaci (causes psittacosis)\n- Exposure to bats/bat droppings\n- Histoplasma capsulatum (a fungus, classically affects cave-explorers)\n \n \n## Investigations\n \n \n- Bloods: including FBC, U+Es, CRP, WCC and blood cultures\n- Sputum culture\n- Urinary antigen tests for Legionella and pneumococcus\n- Chest X-Ray\n- Could assess pleural fluid aspirate in patients with pleural effusion\n \n \n## CURB-65 \n \n \n- Use the CURB-65 score to aid in deciding the severity of pneumonia and further management based on this\n- Components (1 point for each if present):\n- Confusion +/-\n- Urea >7\n- Respiratory Rate >30\n- Blood pressure: systolic < 90 or diastolic <60\n- More than 65 years old\n \n \nCURB-65 mortality by score:\n \n- 0 or 1 - 1.5%\n- 2 - about 10%\n- 3 or more - 10% or more \n \n \n \n \n## Management\n \nIf a patient is very unwell, adopt an A-E approach, initiate the sepsis six and seek early senior input.\n \n- Management based on CURB-65 score:\n- 0/1: home-based care, give oral amoxicillin for 5 days (macrolide e.g. clarithromycin, doxycycline or tetracycline if penicillin allergic).\n- 2: hospital-based care, 7-10 day course of dual antibiotic therapy with amoxicillin (IV or oral) and a macrolide\n- 3: Hospital/ITU-based care, 7-10 day course of dual antibiotic therapy with IV co-amoxiclav/ceftriaxone/tazocin and a macrolide.\n \n \n- Atypical and typical community-acquired pneumonia are both managed in the same way initially.\n- Liaise with microbiology to guide targeted antibiotics following culture results e.g. flucloxacillin for staph aureus pneumonia.\n- A repeat chest x-ray is required after 6 weeks to assess for underlying pathology.\n \n \n## Complications\n \n \n- Pleural effusion\n- Empyema (suspect if persistent, swinging fever with leucocytosis found after antibiotic therapy)\n- Abscess (can be caused by S. pneumoniae, Klebsiella, staph aureus). Can develop pyopneumothorax.\n- Pneumothorax\n- Septicemia\n- Atrial fibrillation\n- Post-infective bronchiectasis\n \n \n \n \n# Hospital Acquired Pneumonia\n \n \n## Definition\n \n \nLower respiratory tract infection that develops more than 48 hours after admission to hospital\n \n \n## Risk Factors\n \n \n- Poor hand hygiene and hospital infection control\n- Intubation and ventilation\n \n \n## Causative Organisms\n \n \n- Pseudomonas aeruginosa\n- E. coli\n- Klebsiella pneumoniae\n- Acinetobacter species (can acquire high potency beta-lactamases, known as ESBLs)\n- Serratia species (can acquire high potency beta-lactamases, known as ESBLs)\n \n \n## Investigations\n \nMay include:\n \n- Bloods: including FBC, U+Es, CRP, WCC and blood cultures\n- Sputum culture\n- Urinary antigen tests for Legionella and pneumococcus\n- Chest X-Ray\n- Could assess pleural fluid aspirate in patients with pleural effusion\n \n \n## Management \n \nIf a patient is very unwell, adopt an A-E approach, initiate the sepsis six and seek early senior input and discussion with microbiology. Empirical antibiotics are guided by severity and likelihood of resistant organisms:\n \n- HAP within 5 days of admission: co-amoxiclav is usually first line for non-severe symptoms\n- HAP more than 5 days after admission (associated with higher risk of resistance) or severe symptoms: tazocin or cephalosporin (e.g. ceftazidime) or quinolone first-line.\n- If MRSA is suspected, add vancomycin\n \n \n# Aspiration Pneumonia \n \n \n- Caused by any cause of depressed consciousness or impairment of the swallowing mechanism\n- Infection caused by mixed aerobic and anaerobic mouth flora, which can cause cavitary pneumonia or empyema\n- Same empirical therapy as for non-aspiration pneumonia, but later antibiotic choice made by pathogen and sensitivities. Metronidazole often added in to cover for anaerobic organisms. Local guidance should be sought.\n \n \n# NICE Guidelines\n \n \n[Click here for NICE CKS on chest infections](https://cks.nice.org.uk/topics/chest-infections-adult/)\n \n[Click here for NICE guidance on antimicrobial prescribing in hospital-acqui",
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"question": "A 32-year-old man presents to the emergency department with 3 days of shortness of breath, productive cough with green sputum, and pyrexia. 5 years ago, he underwent an emergency splenectomy following a road traffic collision.\n\nWhich of the following organisms is he at greater risk of infection?",
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"explanation": "This would present with positive anti-HBs and negative for HBsAg, anti-HBc, and IgM anti-HBc",
"id": "33040",
"label": "c",
"name": "Immune due to hepatitis B vaccination",
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"explanation": "This would present as positive anti-HBc and anti-HBs but negative HBsAg and IgM anti-HBc",
"id": "33041",
"label": "d",
"name": "Immune to hepatitis B due to natural infection",
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"explanation": "This would present with positive anti-HBc but negative HBsAg, anti-HBs, and IgM anti-HBc. These results could also indicate \"low-level\" chronic infection or resolved infection",
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"explanation": "This would present with positive HBsAg, anti-HBc, and IgM anti-HBc",
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"explanation": "HBsAg is a protein on the surface of the hepatitis B virus. It can be detected during acute or chronic hepatitis B infection and indicates the person is infectious. Anti-HBs indicates recovery and immunity from hepatitis B infection and also appears in those who have been successfully vaccinated. Anti-HBc indicates previous or ongoing infection in an undefined timeframe. It appears at the onset of symptoms in acute hepatitis B and persists for life. IgM anti-HBc indicates recent acute infection within the last 6 months. In this case, positive HBsAg and anti-HBc indicate the patient is infectious of hepatitis B with previous/ongoing infection. Negative IgM anti-HBc shows the infection is chronic",
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"explanation": "### Summary\n\nHepatitis means inflammation of the liver and may be caused by a range of infectious and non-infectious aetiologies.\n\nAll infectious hepatitis cases are notifiable diseases in the UK.\n\nThe most common causes of viral hepatitis in the UK are hepatitis A, B and C viruses. These can all cause acute disease, but HBV and HCV can also cause chronic infection. The latter can lead to liver fibrosis and hepatocellular carcinoma.\n\nOther causes of viral hepatitis include:\n\n- Hepatitis D Virus (can cause chronic hepatitis)\n- Hepatitis E Virus\n- CMV\n- EBV\n- Adenovirus\n\nClinical Features:\n\n- Malaise and fatigue\n* Nausea and vomiting\n* Right upper quadrant pain\n* diarrhoea (may have pale stools and dark urine)\n* Jaundice\n* Hepatomegaly\n* Splenomegaly and lymphadenopathy\n* Liver failure: characterised by hepatic encephalopathy, jaundice, ascites and abnormal clotting.\n* Other causes of acute hepatitis include drugs, toxins, alcohol, EBV, CMV, hepatitis E, leptospirosis, and malaria.\n\n### Hepatitis A\n\n- Virus type and transmission route\n\t* RNA picornavirus, transmitted by the faecal-oral route (occasionally through food sources or through anal sex)\n- Epidemiology of Hepatitis A\n\t- Prevalence is high in developing countries.\n\t- Increasing age is the only fundamental determinant of disease severity, with the most significant morbidity and mortality in those over 50 years old.\n\t- Travelers and those at risk can be offered immunisation\n- Presentation of Hepatitis A\n* Flu-like symptoms followed by jaundice, pale stools (in some), dark urine and abdominal pain.\n* Incubation period of 2-6 weeks\n* Complete recovery can take up to 6 months.\n- Investigations of Hepatitis A:\n\t- IgM and IgG antibodies to HAV.\n- Management of Hepatitis A\n\t- Management is largely supportive\n\n### Hepatitis B\n\n- Virus type\n\t- dsDNA virus of the Hepadnaviridae family\n- Hepatitis B Virus Epidemiology\n\t- The most common cause of hepatitis globally\n\t- High prevalence regions include sub-Saharan Africa, Asia and the Pacific Islands.\n\t- The disease is declining in children and adolescents in the UK due to routine vaccination\n- The incubation period is usually 60-90 days.\n- Hepatitis B Virus transmission\n\t* Transmission is via infected blood or body fluids\n\t* Vaginal/anal intercourse\n\t* Transfusion\n\t* Vertical transmission (in 90% of pregnancies where the mother is HBeAg positive, and 10% where this is negative).\n\t* In developing countries, infection is mostly in childhood through vertical or horizontal transmission. In areas of low endemicity (such as the UK), infections are mostly acquired in adulthood.\n* Hepatitis B Infection features\n\t* Only 5% of children have jaundice and severe symptoms, but the majority cannot clear the infection and develop chronic disease.\n\t- 30-50% of adults experience jaundice, fever, malaise, darkening of urine and lightening of stool. Some develop fulminant liver failure with decompensation (ascites, encephalopathy etc.). The risk of developing chronic disease is low (<5%).\n- Serology of Hepatitis B (**See detailed section below**)\n\t- HBsAg is detected 3-5 weeks after infection. If present for >6 months, this defines carrier status (5-10% of infections).\n\t- In carriers, HBeAg-positive patients are the most infectious.\n\t- If HBeAg-negative (and anti-HBe-antibody positive), they have lower infectivity.\n\t- Antibodies to HBsAg (anti-HBs) indicate previous vaccination\n\t- Antibodies to hep B core antigen (anti-HBc) indicate past infection.\n\t- Patients with chronic infection who are HBeAg -ve may have an immune escape phase when the virus mutates despite anti-HBe antibodies being present. These patients are the main pool for the spread in the UK, so all chronically infectious patients need yearly screens to identify this.\n\t- Patients with acute infection have raised IgM to HBcAg, which is negative in chronic infection.\n- Management of Hepatitis B\n\t- Only adults who are HBsAg-positive, have compensated liver disease, are pregnant or are of a young age may be referred for treatment\n\t- Peginterferon alfa-2a is the first line, with tenofovir and entecavir as second-line alternatives.\n\n### Hepatitis B Serology Interpretation\n\t\n\n#### I. Hepatitis B Surface Antigen (HBsAg)\n\nThis is the first detectable viral antigen in the course of infection and is a marker of active infection.\n\n| Result | Interpretation |\n| ------- | -------------- |\n| Positive | Possible acute or chronic Hepatitis B infection |\n| Negative | No active Hepatitis B infection |\n\n#### II. Hepatitis B Surface Antibody (anti-HBs)\n\nThis is an antibody produced by the immune system in response to the Hepatitis B surface antigen. It confers immunity against HBV.\n\n| Result | Interpretation |\n| ------- | -------------- |\n| Positive | Immunity to Hepatitis B (due to past infection or vaccination) |\n| Negative | No immunity to Hepatitis B |\n\n#### III. Hepatitis B Core Antigen (HBcAg)\n\nThis antigen is not detectable in the blood but triggers the production of core antibodies.\n\n#### IV. Hepatitis B Core Antibody (anti-HBc)\n\nIt can be present in both acute and chronic infection. IgM anti-HBc appears early in the infection and indicates a recent infection. IgG anti-HBc remains indefinitely and indicates past exposure.\n\n| Result | Interpretation |\n| ------- | -------------- |\n| IgM Positive | Acute or recent Hepatitis B infection |\n| IgG Positive | Past Hepatitis B infection or chronic infection |\n\n#### V. Hepatitis B e Antigen (HBeAg)\n\nThis is a marker of high replicative activity, indicating a high degree of infectivity.\n\n| Result | Interpretation |\n| ------- | -------------- |\n| Positive | High level of Hepatitis B replication; high infectivity |\n| Negative | Lower levels of Hepatitis B replication; lower infectivity |\n\n#### VI. Hepatitis B e Antibody (anti-HBe)\n\nIt appears after the clearance of HBeAg and indicates lower infectivity.\n\n| Result | Interpretation |\n| ------- | -------------- |\n| Positive | Lower level of Hepatitis B replication; lower infectivity |\n| Negative | Higher levels of Hepatitis B replication; higher infectivity |\n\n#### VII. Hepatitis B DNA (HBV DNA)\n\nThis test measures the amount of Hepatitis B viral load in the blood.\n\n| Result | Interpretation |\n| ------- | -------------- |\n| Positive | Active Hepatitis B replication |\n| Negative | No active Hepatitis B replication |\n\n#### VII. Hepatitis B DNA (HBV DNA)\n\nThis test measures the amount of Hepatitis B viral load in the blood.\n\n| Result | Interpretation |\n| ------- | -------------- |\n| Positive | Active Hepatitis B replication |\n| Negative | No active Hepatitis B replication |\n\n#### Summary\n\nBelow is a table summarizing the serological patterns associated with different stages of Hepatitis B infection:\n\n\n| Status/Marker | HBsAg | anti-HBs | IgM anti-HBc | IgG anti-HBc | HBeAg | anti-HBe | HBV DNA |\n| ------------- | ------- | --------- | ------------ | ------------ | ------- | --------- | ------- |\n| Acute HBV Infection with Immunity | Positive | Negative | Positive | Positive | Positive | Negative | Positive |\n| Chronic HBV Infection | Positive | Negative | Negative | Positive | Positive/Negative | Positive/Negative | Positive/Negative |\n| Immune due to Natural Infection | Negative | Positive | Negative | Positive | Negative | Positive | Negative |\n| Immune due to Hepatitis B Vaccination | Negative | Positive | Negative | Negative | Negative | Negative | Negative |\n\n\n\n\n### Hepatitis C\n\n- Virus type\n\t- RNA virus of the Flaviviridae family, with six major genetic types (genotypes 1 and 3 are most common in the UK, and genotype one is associated with more prolonged treatment and worse prognosis).\n- Hepatitis C Virus transmission\n\t- Transmitted via exchange of blood (the vast majority) and bodily fluids:\n\t* Intravenous drug use\n\t* Blood transfusion\n\t* Haemodialysis (rare in the UK)\n\t* Sexual transmission (less than 1% per year of relationship, but rate higher if co-infected with HIV)\n\t* Needlestick injuries in healthcare facilities - 3% risk of transmission.\n\t* Perinatal infection from infected mother.\n* Incubation period of 6-9 weeks.\n* Natural history of Hepatitis C:\n\t- Most infections are asymptomatic\n\t- Only 15-25% clear the virus; 75% go on to develop chronic infection\n\t- Patients with chronic infection have persistently high LFTs\n\t- Cirrhosis develops in 20-30%.\n\t- 1-4% of patients with cirrhosis develop hepatocellular carcinoma, and 2-5% develop liver failure.\n- Investigations of Hepatitis C\n\t- Anti-HCV serology - 90% are positive three months after infection, but it may take many months to become positive for some.\n\t- HCV RNA - if positive for more than two months, it needs to be treated.\n- Management of Hepatitis C\n\t- Symptomatic treatment in the early stages of the disease\n\t- Drug therapy should be considered for all patients and depends on the genotype of the virus. Nucleoside analogues are generally preferred, e.g. Sofosbuvir, and often lead to undetectable viral loads\n\t- Antivirals have a proven benefit in basically every patient, irrespective of the amount of cirrhosis and fibrosis\n\t- Manage any underlying cirrhosis\n\n### Hepatitis D\n\n- Virus type:\n\t- RNA virus\n- Hepatitis D viral transmission:\n\t- Infected blood products\n\t- Intravenous drug use\n\t- Sexual intercourse\n- Hepatitis D only occurs as a superinfection in patients with concurrent hepatitis B infection; consider this as a differential in a patient with established hepatitis B who has a sudden deterioration in hepatic function/decompensated liver disease.\n- Investigation in Hepatitis D:\n\t- Hepatitis D (IgM, IgG) antibody test\n- Management:\n\t- Pegylated interferon-alpha (low success rates)\n- Prevention:\n\t- No hepatitis D vaccination is available\n\t- Hepatitis B vaccination may be preventative (the patient needs to develop hepatitis B first to then develop hepatitis D).\n\n### Hepatitis E\n\n- Virus type:\n\t- Single-stranded RNA virus\n- Hepatitis E viral transmission:\n\t- faecal-oral transmission\n\t- Contaminated food\n\t\t- Classically transmitted through undercooked pork and seafood\n\t- Vertical transmission\n- Incubation period of 2-9 weeks\n- Endemic regions include Asia, the Middle East, Africa, and Central America\n- Pregnant women are at risk of severe disease; may develop fulminant hepatitis.",
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"question": "A 45-year-old Vietnamese man has presented to the emergency department with jaundice. A full liver screen is sent with the following results:\n\n| Serum | Result |\n| ------------------------------------------------------- | -------- |\n| Hepatitis B surface antigen (HBsAg) | positive |\n| Hepatitis B surface antibody (anti-HBs) | negative |\n| Total hepatitis B core antibody (anti-HBc) | positive |\n| IgM antibody to hepatitis B core antigen (IgM anti-HBc) | negative |",
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"explanation": "Hyperventilation from anxiety would result in hypocarbia (low paCO2) but would not affect serum bicarbonate levels",
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"comment": "He is in metabolic acidosis with low bicarb. How can we discern that it isn't T2RTA from this presentation?",
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"comment": "we wouldn’t necessarily be able to differentiate here; the question asks which diagnosis is most likely, and ckd mediated acidosis is more common than t2rta. ",
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"comment": "I also thought it would be t2rta but this explanation is helpful - thank you!",
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"comment": "Also if you look at the patients history he is known to have ESRF and no Risk factors for T2 Renal acidosis have been mentioned! ",
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"explanation": "# Summary\n\nChronic Kidney Disease (CKD) is a condition characterised by abnormal kidney function for over three months, with a decrease in glomerular filtration rate (GFR) and/or markers of kidney damage such as proteinuria. Classification is based on the cause of CKD, GFR and heaviness of proteinuria. Common causes include diabetes, hypertension and age-related decline. Most patients are asymptomatic in the early stages; signs and symptoms that may develop include lethargy, breathlessness, anorexia and oliguria. First-line investigations include blood tests for U&Es to determine serum creatinine and estimated GFR (eGFR), urine albumin:creatinine ratio and investigations to screen for a cause (e.g. renal tract ultrasound to look for structural abnormalities or obstruction). Management involves regular monitoring for complications (such as anaemia or bone disease), optimising risk factors such as blood pressure and diabetic control, and considering options for renal replacement therapy (RRT) in patients who have end-stage renal disease.\n\n# Definition\n\nCKD is defined by KDIGO as abnormal kidney function or structure for over 3 months, with implications for health. \n\nGlomerular filtration rate (GFR) refers to the volume of fluid filtered by the kidney's nephrons per minute. This can be estimated (eGFR) from serum creatinine although this may be less reliable in patients with extremes of muscle mass.\n\nA GFR below 60 ml/min/1.73m<sup>2</sup> is considered significantly abnormal kidney function.\n\nExamples of abnormal kidney structure include:\n\n- Urinary albumin:creatinine ratio > 3 mg/mmol\n- Urinary sediment abnormalities e.g. haematuria, pyuria or casts\n- Biochemical abnormalities (e.g. acidosis, electrolyte disturbance) due to tubular disorders\n- Histological abnormalities e.g. glomerulosclerosis, tubular atrophy\n- Structural abnormalities e.g. polycystic kidneys or reflux nephropathy\n- Previous renal transplant\n\n# Epidemiology\n\n- CKD is very common, with an estimated global prevalence of 9%\n- Diabetes is the commonest cause, accounting for up to 50% of cases\n- As the early stages of CKD are often asymptomatic, many cases are likely undiagnosed\n- Prevalence is rising due to the ageing population and increased prevalence of chronic diseases such as diabetes and hypertension\n- 50% of people over the age of 75 have CKD\n- Risk factors include:\n\t- Family history of CKD\n\t- Black or Hispanic ethnicity\n\t- History of acute kidney injury (AKI)\n\t- Older age\n\n# Aetiology\n\n- Diseases causing intrinsic kidney damage:\n\t- Diabetes\n\t- Hypertension\n\t- Glomerulonephritis, which may be primary or secondary\n\t- Conditions causing urinary tract obstruction:\n\t- Recurrent urolithiasis\n\t- Structural abnormalities (e.g. ureteropelvic junction obstruction)\n\t- External compression (e.g. from a pelvic mass)\n\t- Bladder voiding problems (e.g. benign prostatic hyperplasia, neurogenic bladder)\n- Iatrogenic causes:\n\t- Radiotherapy\n\t- Nephrotoxic drugs, e.g. aminoglycosides, lithium, NSAIDs\n- Renal involvement secondary to multisystem diseases:\n\t- HIV\n\t- Myeloma\n\t- Vasculitis\n\t- Systemic lupus erythematosus (lupus nephritis)\n\t- Amyloidosis\n\t- Genetic kidney diseases\n\t- Autosomal dominant polycystic kidney disease (ADPKD)\n\t- Alport's syndrome\n\t- Tuberous sclerosis\n\t- Cystinosis\n\t- Recurrent urinary tract infections\n\t- Often secondary to vesico-ureteric reflux or other anatomical defects\n\t- Leads to chronic pyelonephritis which may lead to end-stage renal disease\n\n# Classification\n\nThe KDIGO classification is used to stratify patients by risk of adverse outcomes from CKD based on their GFR and urinary albumin:creatinine ratio (ACR).\n\n||A1 - normal to mildly increased ACR (< 3 mg/mmol)|A2 - moderately increased ACR (3 to 30 mg/mmol)|A3 - severely increased ACR (over 30 mg/mmol)|\n|---------------|-----------|---------------|-----------|\n|**G1 - normal or high GFR (> 90 ml/min/1.73m<sup>2</sup>)**|Low risk/not CKD if no other markers of kidney damage|Moderate risk|High risk|\n|**G2 - mild reduction in GFR (60 - 89 ml/min/1.73m<sup>2</sup>)**|Low risk/not CKD if no other markers of kidney damage|Moderate risk|High risk|\n|**G3a - mild to moderate reduction in GFR (45 - 59 ml/min/1.73m<sup>2</sup>)**|Moderate risk|High risk|Very high risk|\n|**G3b - moderate to severe reduction in GFR (30-44 ml/min/1.73m<sup>2</sup>)**|Moderate risk|High risk|Very high risk|\n|**G4 - severe reduction in GFR (15 - 29 ml/min/1.73m<sup>2</sup>)**|High risk|Very high risk|Very high risk|\n|**G5 - renal failure (< 15 ml/min/1.73m<sup>2</sup>)**|Very high risk|Very high risk|Very high risk|\n\n\n# Signs and Symptoms\n\nCKD is often asymptomatic, however especially in later stages patients may have non-specific symptoms such as:\n\n- Lethargy\n- Anorexia\n- Headaches\n- Weight loss (or gain due to fluid overload)\n- Nausea and vomiting\n- Itching (uraemic pruritus)\n- Shortness of breath (due to anaemia, pulmonary oedema, pleural effusion or acidosis)\n- Muscle cramps, especially at night\n- Bone pain (due to renal osteodystrophy)\n- Taste changes\n- Cognitive impairment\n- Urinary symptoms: \n- Polyuria or oliguria may occur\n- Nocturia\n- Frothy urine (due to proteinuria)\n\nExamination findings may include:\n\n- Hypertension\n- Pallor (due to anaemia)\n- Abnormal fluid status\n- Fluid overload with peripheral and/or pulmonary oedema\n- Dehydration\n- Cachexia\n- Ammonia-like smelling breath due to uraemia\n- Tachypnoea (due to anaemia, pulmonary oedema, pleural effusion or acidosis \n- Flank mass(es) may be palpable due to malignancy or renal cysts (e.g. in ADPKD)\n- Patients on renal replacement therapy may have additional signs such as:\n- Arteriovenous fistula (AVF)\n- Peritoneal dialysis catheter\n- Renal transplant scar (usually right iliac fossa)\n- Parathyroidectomy scar may be present in patients requiring surgical management of secondary or tertiary hyperparathyroidism\n\n# Differential Diagnosis\n\n- **Acute kidney injury (AKI)** is the main differential \n\t- It may be difficult to differentiate AKI from CKD based on investigations showing renal impairment at a single point in time \n\t- To diagnose CKD markers of kidney damage or an eGFR of < 60mL/min/1.73m_ need to be present on two occasions at least 3 months apart\n\t- Abnormal kidneys on imaging (atrophy e.g. in chronic pyelonephritis, or enlarged kidneys e.g. in ADPKD) are indicative of CKD rather than AKI\n\t- Complications of CKD such as anaemia or secondary hyperparathyroidism may also be useful in differentiating the two\n\t- The two may co-exist if there is an acute insult causing AKI in a patient with pre-existing CKD (whether this is diagnosed or not)\n- **False-positive low eGFR results** may occur due to high serum creatinine results, for example in patients with high muscle mass, or after consumption of meat\n- **Urinary ACR** may also be high due to menstruation, strenuous exercise, orthostatic proteinuria or UTI\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urine dipstick** to screen for haematuria and proteinuria\n- Urine positive for haematuria should be sent for **MC&S** to screen for infection\n- Malignancy should also be considered in patients with persistent unexplained haematuria\n- **Early morning albumin:creatinine ratio** should be done in all patients \n- If this is between 3 and 70 mg/mmol it should be repeated within 3 months for confirmation\n\n**Blood tests:**\n\n- **U&Es** for creatinine, eGFR, urea and electrolytes\n- Patients should be advised not to eat meat 12 hours prior to the test\n- If eGFR is < 60 mL/min/1.73m_, this should be repeated within 2 weeks\n- If it remains low with no evidence of ongoing AKI, U&Es should be repeated in 3 months to diagnose CKD\n- **Full blood count** looking for anaemia secondary to CKD, which is usually normochromic and normocytic\n- **LFTs** may show a raised ALP due to bone disease; albumin may be low due to malnourishment or nephrotic syndrome\n- **Bone profile** may show an abnormal calcium; phosphate is usually high\n- **HbA1c** to screen for diabetes as a cause of CKD\n- **Bicarbonate** may be low due to metabolic acidosis\n- **Lipid profile** as dyslipidemia is common in CKD and is a modifiable risk factor for cardiovascular disease\n- **Clotting screen** in case renal biopsy is required\n- **Parathyroid hormone** often rises as renal function declines (secondary or tertiary hyperparathyroidism)\n- **HIV and hepatitis B and C serology** especially in patients for whom renal replacement therapy is being considered\n- **An autoimmune screen** may be sent if an underlying autoimmune condition is suspected\n\t- Antinuclear antibodies\n\t- ANCA antibodies\n\t- dsDNA antibodies\n\t- Anti-GBM antibodies\n\t- Serum complement \n- **Myeloma screen** i.e. immunoglobulins, protein electrophoresis and serum free light chains if this is suspected\n\n**Imaging:**\n\n- **Renal tract ultrasound** is not required in all patients, but should be offered to the following patients:\n- Accelerated progression of CKD (sustained decrease in GFR of 15 ml/min/1.73m_ per year **or** 25% or more **and** a change in GFR category within 12 months)\n- GFR < 30ml/min/1.73m_\n- Patients planned for renal biopsy\n- Suspected urinary tract obstruction\n- Persistent or visible haematuria\n- Family history of polycystic kidney disease\n- Kidneys are usually atrophic in advanced CKD\n- Large kidneys are seen in polycystic kidney disease and in the initial stages of diabetic nephropathy\n- **CT KUB** is the most sensitive imaging modality if renal stones are suspected\n- **CT or MRI angiography** may be indicated for suspected renal artery stenosis - **radionuclide scanning** is also an option\n\n**Special tests:**\n\n- **Renal biopsy** is not required in every case of CKD but may be indicated after initial investigations have been completed, for example if the cause of renal impairment is unclear, where there is rapid progression of CKD or where glomerulonephritis is suspected\n- Important contraindications include active pyelonephritis, uncontrolled hypertension or coagulopathy; biopsying a patient with a single kidney should be avoided where possible due to the (very rare) risk that a nephrectomy may be required to treat complications\n\n# Management\n\n**Conservative management:**\n\n- Patients with CKD are often managed in primary care, however the following should prompt referral to secondary care renal services:\n\t- End-stage renal disease\n\t- Rare or genetic cause for CKD known or suspected (e.g. ADPKD)\n\t- Suspected renal artery stenosis\n\t- Diagnostic uncertainty\n\t- Complications of CKD e.g. malnutrition, hyperkalaemia, anaemia, mineral and bone disorder, acidosis\n\t- Uncontrolled hypertension despite four antihypertensives\n\t- 5-year risk of needing RRT > 5% (see references for calculator)\n\t- Accelerated progression of CKD\n\t- Urinary ACR > 70 mg/mmol (or > 30 mg/mmol with persistent haematuria)\n\t- Patient with obstructive causes of CKD should be referred to urology\n\t- Individualised education on CKD including safety netting regarding complications and risk of AKI\n- Some patients may require additional counselling e.g. genetic counselling and advice regarding screening family members in ADPKD\n- Lifestyle advice should be provided, including:\n\t- Smoking cessation\n\t- Moderating alcohol intake\n\t- Maintaining a healthy weight with regular exercise\n\t- Maintaining a healthy diet\n\t- Avoid over-the-counter nephrotoxics e.g. NSAIDs, dietary supplements and herbal remedies\n- Dietician input may be required for end-stage renal disease (e.g. reducing phosphate, salt and potassium intake)\n- Regular monitoring of eGFR, urinary ACR and for any complications should be undertaken, more frequently in patients with more advanced CKD\n- Patients may benefit from education and/or support groups \n- In the later stages, psychological support and/or access to specialist nurse input may be helpful\n- Many patients with end-stage renal disease may not want or not be suitable for RRT - in these cases - conservative management is an important alternative (also referred to as \"supportive care\")\n\n**Medical management:**\n\n- Treat the underlying cause of CKD e.g. optimise diabetic control; specialist input for immunosuppressive treatments in autoimmune conditions\n- Review medications and consider reducing or stopping nephrotoxic drugs (e.g. NSAIDs, diuretics)\n- Treat hypertension with up to four antihypertensives \n- Aim for a target blood pressure of <140/90 if ACR is < 70 mg/mmol\n- Aim for < 130/80 if ACR is > 70 mg/mmol\n- Patients over 80 with type 1 diabetes should aim for < 150/90\n- An ACE-inhibitor or angiotensin-receptor blocker (ARB) should be first line if ACR is > 30 mg/mmol (if less then manage as per usual hypertension guidelines)\n- ACE-inhibitors or ARBs may be initiated in patients with diabetes and ACR > 3 mg/mmol in the absence of hypertension\n- However these should be avoided in patients with a potassium of > 5 mmol/L \n- They should be stopped if potassium rises to > 6 mmol/L on treatment\n- Consider starting a statin (usually atorvastatin 20mg) in all patients with CKD - the dose should be uptitrated to achieve effect lipid-lowering\n- Consider an antiplatelet (e.g. aspirin) for secondary prevention of cardiovascular disease (balanced against bleeding risk)\n- Sodium-glucose cotransporter-2 (SGLT-2) inhibitors may be considered in some patients on maximal ACE-inhibitor or ARB treatment who meet certain criteria (based on presence of type 2 diabetes, ACR and eGFR)\n- Ensure patients are up to date with vaccinations:\n- Annual influenza vaccine\n- 5-yearly pneumococcal vaccine (PPV23)\n- Covid vaccination as per national guidance\n- Medical management is often required for complications of CKD - see \"Complications\" section for more details\n\n**Surgical/interventional management:**\n\n- Renal replacement therapy is covered in detail in another chapter\n- Options include haemodialysis, peritoneal dialysis (which may be automated and mainly done overnight, or continuous and ambulatory) and renal transplant\n- Patients should be referred for consideration of RRT ideally at least a year before this is anticipated to be required\n- Indications include:\n- eGFR approximately 5-7 ml/min/1.73m_\n- Symptomatic uraemia affecting quality of life\n- Refractory fluid overload\n- Refractory biochemical abnormalities\n- Various options exist for dialysis access which may require surgical formation (e.g. an arteriovenous fistula)\n- Other surgical interventions may be required to treat complications of CKD, for example parathyroidectomy may be indicated in some patients with refractory hyperparathyroidism\n\n# Complications\n\n- **Anaemia** is often multifactorial, due to reduced erythropoietin production, iron deficiency and reduced red blood cell survival\n\t- Other contributing factors include B12 and folate deficiency, haemolysis due to dialysis and the underlying cause of CKD (e.g. myeloma, sickle cell disease)\n\t- Typically anaemia is normocytic and normochromic\n\t- Patients should be investigated if haemoglobin (Hb) is < 110 g/L or if symptomatic\n\t- If eGFR is > 60 ml/min/1.73m_, anaemia is unlikely to be due to CKD\n\t- Other investigations may be required to rule out other causes of anaemia (e.g. gastrointestinal bleeding, B12/folate deficiency)\n\t- All patients should be investigated for iron deficiency with percentage of hypochromic red blood cells being first-line (> 6% indicates functional iron deficiency)\n\t- Ferritin < 100 mcg/L is also indicative of iron deficiency\n\t- Iron supplementation may be either oral or IV (with IV usually preferred for patients on haemodialysis)\n\t- Ferritin should be monitored and iron supplements stopped before ferritin increases over 800 mcg/L\n\t- Once iron stores are replete, erythropoiesis-stimulating agent (ESA) treatment should be considered\n\t- These are usually given subcutaneously, with examples of ESAs including epoetin or darbepoetin\n\t- Roxadustat is a new oral alternative to ESAs which also acts to stimulate erythropoiesis (it is a hypoxia-inducible factor prolyl hydroxylase inhibitor)\n\t- Blood transfusion should be avoided, especially in patients who may require a renal transplant (due to the risk of allosensitization)\n\t- Target Hb is 100-120 g/L\n- **Mineral and bone disorder (MBD)** occurs due to abnormal metabolism of phosphate, vitamin D, calcium and parathyroid hormone\n\t- There is a spectrum of disease that involves abnormal bone turnover and mineralisation as well as vascular and soft tissue calcification\n\t- Risk of CKD-MBD increases once eGFR is < 60 mL/min/1.73m_\n\t- Phosphate retention occurs due to renal dysfunction -> calcitriol (active form of vitamin D) is downregulated, and is also decreased due to reduced renal activation of vitamin D -> calcium falls -> PTH rises (secondary hyperparathyroidism) -> calcium is released from bone\n\t- Tertiary hyperparathyroidism may also occur if there is longstanding secondary hyperparathyroidism (both may be treated with parathyroidectomy)\n\t- \"Renal osteodystrophy\" refers to a range of bone abnormalities seen in CKD including bone resorption, osteosclerosis and osteopenia\n\t- There is an increased risk of fracture - bone density assessment (e.g. DEXA scanning) and bone protection should be considered\n\t- Patients with at least stage 3a CKD should be regularly monitored with serum calcium, phosphate and PTH levels \n\t- Management involves normalising serum phosphate via dietary restriction of phosphate and phosphate binders (e.g. calcium carbonate, sevelamer)\n\t- Severe hyperparathyroidism may be treated with calcitriol and cinacalcet (a calcimimetic)\n\t- Vitamin D supplementation with ergocalciferol or cholecalciferol may be considered\n\t- Dialysis settings can be adjusted to remove excess phosphate and calcium\n- **Cardiovascular risk** is significantly increased, including myocardial infarction, stroke, peripheral arterial disease and heart failure\n\t- There is a high prevalence of comorbid conditions increasing cardiovascular risk (e.g. hypertension, hypercholesterolaemia, diabetes)\n\t- Patients also have additional CKD-related risk factors, including vascular calcification due to CKD-MBD, uraemia, oxidative stress and anaemia\n\t- Dialysis further increases the risk of cardiovascular disease, including ischaemic heart disease, valvular disease and hypertensive cardiomyopathy\n- **Uraemia** typically becomes symptomatic in patients with end-stage renal disease\n\t- Symptoms include nausea, vomiting, anorexia, taste disturbance, confusion, muscle cramps, pruritus and restless legs\n\t- Complications include pericarditis, neuropathy and encephalopathy\n\t- Symptomatic uraemia is an indication for renal replacement therapy\n- **Hyperkalaemia** is a common issue in CKD due to impaired potassium excretion\n\t- Medications such as ACE-inhibitors and ARBs also contribute to hyperkalemia\n\t- Dietary intake of potassium should be limited\n\t- Medical treatment with potassium binders may be required (e.g. sodium zirconium cyclosilicate (Lokelma), calcium resonium or patiromer)\n\t- Treatments such as sodium bicarbonate (for metabolic acidosis) and diuretics (for fluid overload) may also help to reduce serum potassium\n- **Metabolic acidosis** is common due to reduced renal acid excretion once eGFR < 50 ml/min/1.73m_\n\t- Chronic metabolic acidosis further increases kidney injury and fibrosis, bone demineralisation and muscle wasting and risk of cardiovascular events\n\t- Oral sodium bicarbonate should be considered for patients with an eGFR < 30 ml/min/1.73m_, or if serum bicarbonate is < 20 mmol/litre\n- **Fluid overload** with both pulmonary and peripheral oedema may occur in the later stages of CKD\n\t- Fluid restriction may be advised\n\t- Diuretics may also be used, with loop diuretics (e.g. furosemide) being first-line in most cases\n- **Malnutrition** is common, especially as CKD progresses\n\t- Uraemia may cause anorexia and taste disturbance\n\t- Low mood may also contribute to poor oral intake\n\t- Protein catabolism is promoted by acidosis and chronic inflammation\n\t- Patients should be regularly screened for malnutrition\n\t- Specialist renal dietician input should be offered for patients at risk of malnutrition\n\t- Oral nutritional supplements may be indicated in some cases (or less commonly enteral tube feeding or parenteral nutritional support) \n- **Acute kidney injury** - patients with CKD are at increased risk of AKI\n\t- Risk increases in patients with an eGFR of < 60 mL/min/1.73m_\n\t- There is also a risk of increased CKD progression with episodes of AKI\n\t- Triggers include intercurrent illness, especially with diarrhoea and vomiting, medications e.g. NSAIDs, antibiotics and urinary tract obstruction\n- **Increased risk of malignancy** especially of renal and thyroid cancers\n\t- Immunosuppressive medications further increase malignancy risk (e.g. after renal transplant)\n\t- Chronic uraemia is also a contributing factor\n- **Hypertension** both contributes to the development of CKD and is caused by CKD\n\t- Mechanisms include sodium dysregulation, upregulation of the renin angiotensin aldosterone system, and sympathetic nervous system hyperactivity\n\t- Regular monitoring of blood pressure and effective treatment is therefore key to minimising progression of CKD as well as other adverse cardiovascular events\n- **Reduced quality of life**, especially in patients with more severe CKD\n\t- As with any chronic disease, depression and anxiety are common\n\n# Prognosis\n\n- Prognosis is dependent on the underlying cause of CKD, for example ADPKD tends to progress more rapidly than other diseases\n- CKD is typically a progressive disease, although most patients die before reaching end-stage renal disease\n- Approximately 2% of patients with CKD develop end-stage renal disease\n- Progression can be slowed through modification of risk factors such as hypertension and proteinuria\n- The leading cause of death in CKD is cardiovascular disease\n\n# NICE Guidelines\n\n[NICE CKS - Chronic Kidney Disease](https://cks.nice.org.uk/topics/chronic-kidney-disease/)\n\n[NICE - Chronic kidney disease: assessment and management](https://www.nice.org.uk/guidance/ng203)\n\n[NICE - Renal replacement therapy and conservative management](https://www.nice.org.uk/guidance/ng107)\n\n[NICE technology appraisal - Roxadustat for treating symptomatic anaemia in chronic kidney disease](https://www.nice.org.uk/guidance/ta807/)\n\n# References\n\n[Patient UK - Chronic kidney disease](https://patient.info/doctor/chronic-kidney-disease-pro)\n\n[Patient UK - Anaemia in chronic kidney disease](https://patient.info/doctor/anaemia-in-chronic-kidney-disease)\n\n[UK Kidney Association eCKD guide](https://ukkidney.org/health-professionals/information-resources/uk-eckd-guide) \n\n[Kidney Failure Risk Equation]( https://www.kidneyfailurerisk.co.uk/)\n\n[KDIGO CKD Evaluation and Management](https://kdigo.org/guidelines/ckd-evaluation-and-management/)\n\n[KDIGO CKD Mineral and Bone Disorder guideline](https://kdigo.org/guidelines/ckd-mbd/)\n\n[Radiopaedia - Renal osteodystrophy](https://radiopaedia.org/articles/renal-osteodystrophy?lang=gb)\n\n[The Renal Association - Undernutrition in Chronic Kidney Disease Guideline](https://ukkidney.org/sites/renal.org/files/FINAL-Nutrition-guideline-June-2019-RNG-endorsed.pdf)\n\n[NHS Kidney Care - Chronic Kidney\nDisease in England: The Human and Financial Cost](https://www.england.nhs.uk/improvement-hub/wp-content/uploads/sites/44/2017/11/Chronic-Kidney-Disease-in-England-The-Human-and-Financial-Cost.pdf)",
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"question": "A 32-year-old man with HIV-associated nephropathy (HIVAN) and end-stage kidney disease (ESKD) presents to the emergency department with an oozing arteriovenous (AV) fistula following dialysis earlier that afternoon. He is referred to the vascular surgeons for ultrasound, review, and for consideration of surgical exploration.\n\n\nBloods are taken at the time with a venous blood gas, revealing the following:\n\n\n||||\n|--------------|:-------:|------------------|\n|pH|7.32|7.35 - 7.45|\n|PaO₂|14.3 kPa|11 - 15|\n|PaCO₂|3.6 kPa|4.6 - 6.4|\n|Bicarbonate|16 mmol/L|22 - 30|\n|Base Excess|-4 mmol/L|-2 to +2|\n|Lactate|1.1 mmol/L|0.6 - 1.4|\n\n\nWhich of the following is the most likely cause for the patient's low bicarbonate level?",
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"explanation": "Pre-renal uraemia is a very common cause of acute kidney injury in hospitals. The creatinine and urea can rise to these levels if the kidneys are very poorly perfused, either from shock or severe dehydration, although the kidneys would hold on to electrolytes with very concentrated urine. Urinary sodium would be <10mmol/L in this case, and so makes this a less likely cause for this patient's symptoms",
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"explanation": "Post-infectious glomerulonephritis can occur after almost any infection, but typically occurs 1-4 weeks following infection. Classically it presents following pharyngeal infection with Streptococcus pyogenes. While it can present with acute kidney injury and frank haematuria/dark brown urine, it would usually also present with generalised oedema and hypertension due to salt retention",
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"explanation": "This patient has had an infection followed by 5 days of intravenous gentamicin - a nephrotoxic medication. Worsening renal function with dark brown urine should raise suspicion of acute tubular necrosis. This is confirmed with a raised urinary sodium, implying less tubular modification of the glomerular filtrate with increased urinary electrolyte losses",
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"explanation": "Renal vein thrombosis can rarely occur following deep vein thrombosis in the legs - a common complication following knee surgery. It would unlikely present in an otherwise well adult unless there were severe dehydration or increased hypercoagulable state. If it were to cause such a severe acute kidney injury, it would present with haematuria and flank pain - opposed to dark brown urine with raised urinary sodium",
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"explanation": "# Summary\n\nAcute Tubular Necrosis (ATN) is the most prevalent cause of intrinsic acute kidney injury (AKI), characterised by parenchymal damage that may be caused by an ischaemic, nephrotoxic or inflammatory insult. Signs and symptoms are not specific to ATN as a cause of AKI, and include oliguria, fatigue and nausea. Evidence of an underlying cause should be sought, for example hypovolaemia (e.g. severe diarrhoea and vomiting, burns), exposure to nephrotoxic drugs, rhabdomyolysis or sepsis. Investigations include urinalysis, urinary sodium, urinary osmolality and U&Es. Management is supportive and involves correcting the underlying cause, \noptimising volume status with IV fluids and considering dialysis in severe cases.\n\n# Definition\n\nAcute Tubular Necrosis (ATN) is a common cause of acute kidney injury (AKI), where renal tubular epithelial cells are damaged either due to a nephrotoxic agent or ischaemic insult. Despite the name, necrosis is not seen in the majority of cases - as such, ATN is sometimes referred to as \"acute tubular injury\".\n\nIn ischaemic ATN, injury to renal tubular endothelial cells is followed by epithelial cell injury, whereas nephrotoxic agents directly damage epithelial cells. Tubular cells apoptose and slough off to form casts that obstruct the tubular lumen, causing renal impairment and oliguria.\n\n# Epidemiology\n\n- ATN is the leading cause of intrinsic AKI\n- It is often seen in acutely unwell inpatients and is a poor prognostic factor\n- It is responsible for the majority of cases of AKI in patients admitted to intensive care\n- The majority of cases are due to ischaemia\n- Risk factors include:\n- Hypovolaemia\n- Older age\n- Chronic kidney disease\n- Recent use of nephrotoxic drugs\n\n# Aetiology \n\n**Ischaemic causes** - usually due to prolonged hypotension\n\n- Hypovolaemia\n- Diarrhoea and/or vomiting\n- Haemorrhage\n- Dehydration\n- Burns\n- Renal losses (diuretics, osmotic diuresis)\n- Third-spacing (e.g. severe pancreatitis)\n- Systemic vasodilation\n- Anaphylaxis\n- Septic shock (also has toxic effects on the kidneys)\n- Surgery, due to a combination of:\n- Fluid losses\n- Haemodynamic changes under anaesthesia\n- Interruption of renal perfusion e.g. supra-aortic clamping in abdominal aortic aneurysm surgery\n\n**Nephrotoxic causes**\n\n- Medications, for example:\n- Aminoglycoside antibiotics (e.g. gentamicin)\n- Antifungals (e.g. amphotericin)\n- Chemotherapy agents (e.g. cisplatin)\n- Antivirals (e.g. tenofovir)\n- Nonsteroidal anti-inflammatory drugs (NSAIDs)\n- Contrast agents\n- Myoglobin (rhabdomyolysis)\n- Haemoglobin (intravascular haemolysis, e.g. transfusion reactions, autoimmune haemolytic anaemia)\n\n# Signs and Symptoms\n\nThere may be signs and symptoms of the cause of ATN (e.g. dehydration, nausea and vomiting)\n\nNon-specific presenting features of AKI may be present, including:\n\n- Lethargy and malaise\n- Nausea and vomiting\n- Oliguria or anuria (polyuria may be seen in the recovery phase)\n- Confusion\n- Drowsiness\n- Peripheral oedema\n\n# Differential Diagnosis\n\n- **Pre-renal AKI** occurs when reduced renal perfusion and/or hypotension cause renal impairment; patients are often dehydrated but improve rapidly with treatment (unlike in ATN)\n- **Acute interstitial nephritis** often occurs as a hypersensitivity reaction to a medication (but may also be triggered by autoimmune disease or infections); the classic triad is of a rash, fever and eosinophilia\n- **Post-renal AKI** occurs due to urinary tract obstruction, for example renal stones, prostatic enlargement or a blocked catheter; symptoms of obstruction such as pain are often present and there may be hydronephrosis on imaging\n\n# Investigations\n\n**Bedside:**\n\n- **Urine microscopy** shows muddy brown granular casts and renal tubular epithelial cells \n- **Urinary sodium** is key to differentiating pre-renal AKI from ATN - sodium is low in pre-renal AKI and high in ATN (usually > 40 mmol/L)\n- **Urine osmolality** is low as urine concentrating capacity is impaired (< 450 mOsmol/kg)\n- **Urine dip** may be falsely positive for blood if there is myoglobinuria or haemoglobinuria\n- **Blood gas** to assess for acidosis and hyperkalaemia that may complicate AKI\n- **ECG** looking for hyperkalaemic changes\n\n**Bloods:**\n\n- **U&Es** to confirm renal impairment and assess electrolytes\n- **Urea:creatinine ratio** is low in ATN as water, sodium and urea are not retained unlike in pre-renal AKI\n- **Full blood count** may show anaemia in some causes of ATN (e.g. haemorrhage, haemolysis); there may be a leukocytosis in sepsis\n- **Creatine kinase** if rhabdomyolysis is suspected\n- **Liver function tests** may show a concurrent ischaemic liver injury \n- **Bone profile** may be abnormal e.g. hypercalcaemia causing dehydration\n- **CRP** may be raised in some causes of ATN e.g. sepsis\n- **Blood cultures** should be sent in suspected sepsis\n- **Coagulation screen** may show a prolonged aPTT due to platelet dysfunction secondary to uraemia\n\n**Imaging:**\n\n- **Ultrasound KUB (kidneys, ureters and bladder)** to rule out obstructive causes and assess renal size and structure - usually normal in ATN\n\n**Special tests:**\n\n- **Renal biopsy** is not required unless there is suspicion of a primary renal disease - in ATN histology shows loss of tubular epithelial cells with exposed areas of basement membrane\n\n# Management\n\n**Conservative:**\n\n- Identify and treat the underlying cause (e.g. haemorrhage)\n- Avoid giving further nephrotoxic medications (e.g. NSAIDs, ACE-inhibitors)\n- Fluid balance monitoring and consider catheterisation\n\n**Medical:**\n\n- IV fluids to correct hypovolaemia and/or hypotension\n- Blood products are preferred in haemorrhage\n- Medical management may be required for the underlying cause (e.g. antibiotics in sepsis)\n- Vasopressors may be used with fluids in patients with shock\n\n**Interventional:**\n\n- Consider dialysis in AKI with complications (e.g. refractory fluid overload or uraemia)\n\n# Prognosis\n\n- ATN is a poor prognostic factor, with a mortality of approximately 50%\n- Patients who are septic or require dialysis have mortality rates of up to 80%\n- Survivors tend to have favourable outcomes, with around 5% going on to require renal replacement therapy \n- Complications are those of any AKI (see Acute Kidney Injury chapter for details)\n\n# NICE Guidelines\n\n[NICE CKS - Acute Kidney Injury](https://cks.nice.org.uk/topics/acute-kidney-injury/)\n\n# References \n\n[StatPearls - Acute Renal Tubular Necrosis](https://www.ncbi.nlm.nih.gov/books/NBK507815/)\n\n[Pathology Outlines - Acute tubular necrosis](https://www.pathologyoutlines.com/topic/kidneyatn.html)\n\n[International Journal of Nephrology - Long-Term Outcome of Patients Followed by Nephrologists after an Acute Tubular Necrosis Episode](https://onlinelibrary.wiley.com/doi/10.1155/2012/361528)",
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"learningPoint": "Acute tubular necrosis can occur following the use of nephrotoxic medications such as certain antibiotics, contrast agents, or chemotherapy drugs, leading to impaired kidney function, elevated creatinine levels, and dark brown urine due to the presence of damaged tubular cells and myoglobin.",
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"question": "A 71-year-old man has been admitted for an elective right total knee replacement. He suffers from a post-operative urinary tract infection and is given 5 days of gentamicin.\n\n\nFollowing this, his condition deteriorates with worsening acute kidney injury and dark brown urine. His blood tests show:\n\n||||\n|---------------------------|:-------:|--------------------|\n|Urea|14.1 mmol/L|2.5 - 7.8|\n|Creatinine|678 µmol/L|60 - 120|\n|Urinary Sodium (24hr)|350 mmol/24hrs|75 - 300|\n\n\nWhich of the following is the most likely cause of this patient's acute kidney injury?",
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"explanation": "Cinacalcet is a treatment used to treat secondary hyperparathyroidism, although it is reserved for patients on dialysis. It mimics the action of calcium on the tissues (calcimimetic) and increases the sensitivity of calcium receptors on parathyroid cells to reduce PTH",
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"label": "d",
"name": "Cinacalcet",
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"explanation": "Calcitriol is the active form of vitamin D - 1,25-dihydroxycholecalciferol. It increases calcium uptake in the gastrointestinal tract, increases renal absorption of calcium, and stimulates osteoclastic activity. This then sequentially suppresses parathyroid hormone, helping to prevent progression from secondary hyperparathyroidism into tertiary hyperparathyroidism",
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"label": "a",
"name": "Calcitriol",
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"explanation": "Calcitonin can occasionally be used in the treatment of hypercalcaemia by inhibiting osteoclast activity in bones and inhibiting renal reabsorption of calcium and phosphate. This patient is hypocalcaemic, and so this would reduce serum calcium levels further",
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"label": "c",
"name": "Calcitonin",
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"explanation": "Colecalciferol (vitamin D3) is the major form of vitamin D that provides nutritional supplementation. It should not be used to reduce PTH in those with normal vitamin D as an attempt to reduce the risk of progression into tertiary hyperparathyroidism. It can worsen hyperphosphataemia and lead to hypercalcaemia which can worsen cardiovascular morbidity",
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"name": "Colecalciferol",
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"explanation": "Colecalciferol should not be used to reduce PTH in those with normal vitamin D as an attempt to reduce the risk of progression into tertiary hyperparathyroidism. It can worsen hyperphosphataemia and lead to hypercalcaemia which can worsen cardiovascular morbidity. This would be exacerbated by additional calcium carbonate supplementation and would not improve survival benefit",
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"label": "e",
"name": "Colecalciferol with calcium carbonate",
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"comment": "Explanation for this question doesn't make sense: it says you should not use cholecalciferol as it can increase phosphate levels and worsen hypocalcaemia; but calcitriol will do the exact same thing!",
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"comment": "why is his calcium low?\n",
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"comment": "most likely secondary hyperparathyroidism",
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"explanation": "# Summary\n\nChronic Kidney Disease (CKD) is a condition characterised by abnormal kidney function for over three months, with a decrease in glomerular filtration rate (GFR) and/or markers of kidney damage such as proteinuria. Classification is based on the cause of CKD, GFR and heaviness of proteinuria. Common causes include diabetes, hypertension and age-related decline. Most patients are asymptomatic in the early stages; signs and symptoms that may develop include lethargy, breathlessness, anorexia and oliguria. First-line investigations include blood tests for U&Es to determine serum creatinine and estimated GFR (eGFR), urine albumin:creatinine ratio and investigations to screen for a cause (e.g. renal tract ultrasound to look for structural abnormalities or obstruction). Management involves regular monitoring for complications (such as anaemia or bone disease), optimising risk factors such as blood pressure and diabetic control, and considering options for renal replacement therapy (RRT) in patients who have end-stage renal disease.\n\n# Definition\n\nCKD is defined by KDIGO as abnormal kidney function or structure for over 3 months, with implications for health. \n\nGlomerular filtration rate (GFR) refers to the volume of fluid filtered by the kidney's nephrons per minute. This can be estimated (eGFR) from serum creatinine although this may be less reliable in patients with extremes of muscle mass.\n\nA GFR below 60 ml/min/1.73m<sup>2</sup> is considered significantly abnormal kidney function.\n\nExamples of abnormal kidney structure include:\n\n- Urinary albumin:creatinine ratio > 3 mg/mmol\n- Urinary sediment abnormalities e.g. haematuria, pyuria or casts\n- Biochemical abnormalities (e.g. acidosis, electrolyte disturbance) due to tubular disorders\n- Histological abnormalities e.g. glomerulosclerosis, tubular atrophy\n- Structural abnormalities e.g. polycystic kidneys or reflux nephropathy\n- Previous renal transplant\n\n# Epidemiology\n\n- CKD is very common, with an estimated global prevalence of 9%\n- Diabetes is the commonest cause, accounting for up to 50% of cases\n- As the early stages of CKD are often asymptomatic, many cases are likely undiagnosed\n- Prevalence is rising due to the ageing population and increased prevalence of chronic diseases such as diabetes and hypertension\n- 50% of people over the age of 75 have CKD\n- Risk factors include:\n\t- Family history of CKD\n\t- Black or Hispanic ethnicity\n\t- History of acute kidney injury (AKI)\n\t- Older age\n\n# Aetiology\n\n- Diseases causing intrinsic kidney damage:\n\t- Diabetes\n\t- Hypertension\n\t- Glomerulonephritis, which may be primary or secondary\n\t- Conditions causing urinary tract obstruction:\n\t- Recurrent urolithiasis\n\t- Structural abnormalities (e.g. ureteropelvic junction obstruction)\n\t- External compression (e.g. from a pelvic mass)\n\t- Bladder voiding problems (e.g. benign prostatic hyperplasia, neurogenic bladder)\n- Iatrogenic causes:\n\t- Radiotherapy\n\t- Nephrotoxic drugs, e.g. aminoglycosides, lithium, NSAIDs\n- Renal involvement secondary to multisystem diseases:\n\t- HIV\n\t- Myeloma\n\t- Vasculitis\n\t- Systemic lupus erythematosus (lupus nephritis)\n\t- Amyloidosis\n\t- Genetic kidney diseases\n\t- Autosomal dominant polycystic kidney disease (ADPKD)\n\t- Alport's syndrome\n\t- Tuberous sclerosis\n\t- Cystinosis\n\t- Recurrent urinary tract infections\n\t- Often secondary to vesico-ureteric reflux or other anatomical defects\n\t- Leads to chronic pyelonephritis which may lead to end-stage renal disease\n\n# Classification\n\nThe KDIGO classification is used to stratify patients by risk of adverse outcomes from CKD based on their GFR and urinary albumin:creatinine ratio (ACR).\n\n||A1 - normal to mildly increased ACR (< 3 mg/mmol)|A2 - moderately increased ACR (3 to 30 mg/mmol)|A3 - severely increased ACR (over 30 mg/mmol)|\n|---------------|-----------|---------------|-----------|\n|**G1 - normal or high GFR (> 90 ml/min/1.73m<sup>2</sup>)**|Low risk/not CKD if no other markers of kidney damage|Moderate risk|High risk|\n|**G2 - mild reduction in GFR (60 - 89 ml/min/1.73m<sup>2</sup>)**|Low risk/not CKD if no other markers of kidney damage|Moderate risk|High risk|\n|**G3a - mild to moderate reduction in GFR (45 - 59 ml/min/1.73m<sup>2</sup>)**|Moderate risk|High risk|Very high risk|\n|**G3b - moderate to severe reduction in GFR (30-44 ml/min/1.73m<sup>2</sup>)**|Moderate risk|High risk|Very high risk|\n|**G4 - severe reduction in GFR (15 - 29 ml/min/1.73m<sup>2</sup>)**|High risk|Very high risk|Very high risk|\n|**G5 - renal failure (< 15 ml/min/1.73m<sup>2</sup>)**|Very high risk|Very high risk|Very high risk|\n\n\n# Signs and Symptoms\n\nCKD is often asymptomatic, however especially in later stages patients may have non-specific symptoms such as:\n\n- Lethargy\n- Anorexia\n- Headaches\n- Weight loss (or gain due to fluid overload)\n- Nausea and vomiting\n- Itching (uraemic pruritus)\n- Shortness of breath (due to anaemia, pulmonary oedema, pleural effusion or acidosis)\n- Muscle cramps, especially at night\n- Bone pain (due to renal osteodystrophy)\n- Taste changes\n- Cognitive impairment\n- Urinary symptoms: \n- Polyuria or oliguria may occur\n- Nocturia\n- Frothy urine (due to proteinuria)\n\nExamination findings may include:\n\n- Hypertension\n- Pallor (due to anaemia)\n- Abnormal fluid status\n- Fluid overload with peripheral and/or pulmonary oedema\n- Dehydration\n- Cachexia\n- Ammonia-like smelling breath due to uraemia\n- Tachypnoea (due to anaemia, pulmonary oedema, pleural effusion or acidosis \n- Flank mass(es) may be palpable due to malignancy or renal cysts (e.g. in ADPKD)\n- Patients on renal replacement therapy may have additional signs such as:\n- Arteriovenous fistula (AVF)\n- Peritoneal dialysis catheter\n- Renal transplant scar (usually right iliac fossa)\n- Parathyroidectomy scar may be present in patients requiring surgical management of secondary or tertiary hyperparathyroidism\n\n# Differential Diagnosis\n\n- **Acute kidney injury (AKI)** is the main differential \n\t- It may be difficult to differentiate AKI from CKD based on investigations showing renal impairment at a single point in time \n\t- To diagnose CKD markers of kidney damage or an eGFR of < 60mL/min/1.73m_ need to be present on two occasions at least 3 months apart\n\t- Abnormal kidneys on imaging (atrophy e.g. in chronic pyelonephritis, or enlarged kidneys e.g. in ADPKD) are indicative of CKD rather than AKI\n\t- Complications of CKD such as anaemia or secondary hyperparathyroidism may also be useful in differentiating the two\n\t- The two may co-exist if there is an acute insult causing AKI in a patient with pre-existing CKD (whether this is diagnosed or not)\n- **False-positive low eGFR results** may occur due to high serum creatinine results, for example in patients with high muscle mass, or after consumption of meat\n- **Urinary ACR** may also be high due to menstruation, strenuous exercise, orthostatic proteinuria or UTI\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urine dipstick** to screen for haematuria and proteinuria\n- Urine positive for haematuria should be sent for **MC&S** to screen for infection\n- Malignancy should also be considered in patients with persistent unexplained haematuria\n- **Early morning albumin:creatinine ratio** should be done in all patients \n- If this is between 3 and 70 mg/mmol it should be repeated within 3 months for confirmation\n\n**Blood tests:**\n\n- **U&Es** for creatinine, eGFR, urea and electrolytes\n- Patients should be advised not to eat meat 12 hours prior to the test\n- If eGFR is < 60 mL/min/1.73m_, this should be repeated within 2 weeks\n- If it remains low with no evidence of ongoing AKI, U&Es should be repeated in 3 months to diagnose CKD\n- **Full blood count** looking for anaemia secondary to CKD, which is usually normochromic and normocytic\n- **LFTs** may show a raised ALP due to bone disease; albumin may be low due to malnourishment or nephrotic syndrome\n- **Bone profile** may show an abnormal calcium; phosphate is usually high\n- **HbA1c** to screen for diabetes as a cause of CKD\n- **Bicarbonate** may be low due to metabolic acidosis\n- **Lipid profile** as dyslipidemia is common in CKD and is a modifiable risk factor for cardiovascular disease\n- **Clotting screen** in case renal biopsy is required\n- **Parathyroid hormone** often rises as renal function declines (secondary or tertiary hyperparathyroidism)\n- **HIV and hepatitis B and C serology** especially in patients for whom renal replacement therapy is being considered\n- **An autoimmune screen** may be sent if an underlying autoimmune condition is suspected\n\t- Antinuclear antibodies\n\t- ANCA antibodies\n\t- dsDNA antibodies\n\t- Anti-GBM antibodies\n\t- Serum complement \n- **Myeloma screen** i.e. immunoglobulins, protein electrophoresis and serum free light chains if this is suspected\n\n**Imaging:**\n\n- **Renal tract ultrasound** is not required in all patients, but should be offered to the following patients:\n- Accelerated progression of CKD (sustained decrease in GFR of 15 ml/min/1.73m_ per year **or** 25% or more **and** a change in GFR category within 12 months)\n- GFR < 30ml/min/1.73m_\n- Patients planned for renal biopsy\n- Suspected urinary tract obstruction\n- Persistent or visible haematuria\n- Family history of polycystic kidney disease\n- Kidneys are usually atrophic in advanced CKD\n- Large kidneys are seen in polycystic kidney disease and in the initial stages of diabetic nephropathy\n- **CT KUB** is the most sensitive imaging modality if renal stones are suspected\n- **CT or MRI angiography** may be indicated for suspected renal artery stenosis - **radionuclide scanning** is also an option\n\n**Special tests:**\n\n- **Renal biopsy** is not required in every case of CKD but may be indicated after initial investigations have been completed, for example if the cause of renal impairment is unclear, where there is rapid progression of CKD or where glomerulonephritis is suspected\n- Important contraindications include active pyelonephritis, uncontrolled hypertension or coagulopathy; biopsying a patient with a single kidney should be avoided where possible due to the (very rare) risk that a nephrectomy may be required to treat complications\n\n# Management\n\n**Conservative management:**\n\n- Patients with CKD are often managed in primary care, however the following should prompt referral to secondary care renal services:\n\t- End-stage renal disease\n\t- Rare or genetic cause for CKD known or suspected (e.g. ADPKD)\n\t- Suspected renal artery stenosis\n\t- Diagnostic uncertainty\n\t- Complications of CKD e.g. malnutrition, hyperkalaemia, anaemia, mineral and bone disorder, acidosis\n\t- Uncontrolled hypertension despite four antihypertensives\n\t- 5-year risk of needing RRT > 5% (see references for calculator)\n\t- Accelerated progression of CKD\n\t- Urinary ACR > 70 mg/mmol (or > 30 mg/mmol with persistent haematuria)\n\t- Patient with obstructive causes of CKD should be referred to urology\n\t- Individualised education on CKD including safety netting regarding complications and risk of AKI\n- Some patients may require additional counselling e.g. genetic counselling and advice regarding screening family members in ADPKD\n- Lifestyle advice should be provided, including:\n\t- Smoking cessation\n\t- Moderating alcohol intake\n\t- Maintaining a healthy weight with regular exercise\n\t- Maintaining a healthy diet\n\t- Avoid over-the-counter nephrotoxics e.g. NSAIDs, dietary supplements and herbal remedies\n- Dietician input may be required for end-stage renal disease (e.g. reducing phosphate, salt and potassium intake)\n- Regular monitoring of eGFR, urinary ACR and for any complications should be undertaken, more frequently in patients with more advanced CKD\n- Patients may benefit from education and/or support groups \n- In the later stages, psychological support and/or access to specialist nurse input may be helpful\n- Many patients with end-stage renal disease may not want or not be suitable for RRT - in these cases - conservative management is an important alternative (also referred to as \"supportive care\")\n\n**Medical management:**\n\n- Treat the underlying cause of CKD e.g. optimise diabetic control; specialist input for immunosuppressive treatments in autoimmune conditions\n- Review medications and consider reducing or stopping nephrotoxic drugs (e.g. NSAIDs, diuretics)\n- Treat hypertension with up to four antihypertensives \n- Aim for a target blood pressure of <140/90 if ACR is < 70 mg/mmol\n- Aim for < 130/80 if ACR is > 70 mg/mmol\n- Patients over 80 with type 1 diabetes should aim for < 150/90\n- An ACE-inhibitor or angiotensin-receptor blocker (ARB) should be first line if ACR is > 30 mg/mmol (if less then manage as per usual hypertension guidelines)\n- ACE-inhibitors or ARBs may be initiated in patients with diabetes and ACR > 3 mg/mmol in the absence of hypertension\n- However these should be avoided in patients with a potassium of > 5 mmol/L \n- They should be stopped if potassium rises to > 6 mmol/L on treatment\n- Consider starting a statin (usually atorvastatin 20mg) in all patients with CKD - the dose should be uptitrated to achieve effect lipid-lowering\n- Consider an antiplatelet (e.g. aspirin) for secondary prevention of cardiovascular disease (balanced against bleeding risk)\n- Sodium-glucose cotransporter-2 (SGLT-2) inhibitors may be considered in some patients on maximal ACE-inhibitor or ARB treatment who meet certain criteria (based on presence of type 2 diabetes, ACR and eGFR)\n- Ensure patients are up to date with vaccinations:\n- Annual influenza vaccine\n- 5-yearly pneumococcal vaccine (PPV23)\n- Covid vaccination as per national guidance\n- Medical management is often required for complications of CKD - see \"Complications\" section for more details\n\n**Surgical/interventional management:**\n\n- Renal replacement therapy is covered in detail in another chapter\n- Options include haemodialysis, peritoneal dialysis (which may be automated and mainly done overnight, or continuous and ambulatory) and renal transplant\n- Patients should be referred for consideration of RRT ideally at least a year before this is anticipated to be required\n- Indications include:\n- eGFR approximately 5-7 ml/min/1.73m_\n- Symptomatic uraemia affecting quality of life\n- Refractory fluid overload\n- Refractory biochemical abnormalities\n- Various options exist for dialysis access which may require surgical formation (e.g. an arteriovenous fistula)\n- Other surgical interventions may be required to treat complications of CKD, for example parathyroidectomy may be indicated in some patients with refractory hyperparathyroidism\n\n# Complications\n\n- **Anaemia** is often multifactorial, due to reduced erythropoietin production, iron deficiency and reduced red blood cell survival\n\t- Other contributing factors include B12 and folate deficiency, haemolysis due to dialysis and the underlying cause of CKD (e.g. myeloma, sickle cell disease)\n\t- Typically anaemia is normocytic and normochromic\n\t- Patients should be investigated if haemoglobin (Hb) is < 110 g/L or if symptomatic\n\t- If eGFR is > 60 ml/min/1.73m_, anaemia is unlikely to be due to CKD\n\t- Other investigations may be required to rule out other causes of anaemia (e.g. gastrointestinal bleeding, B12/folate deficiency)\n\t- All patients should be investigated for iron deficiency with percentage of hypochromic red blood cells being first-line (> 6% indicates functional iron deficiency)\n\t- Ferritin < 100 mcg/L is also indicative of iron deficiency\n\t- Iron supplementation may be either oral or IV (with IV usually preferred for patients on haemodialysis)\n\t- Ferritin should be monitored and iron supplements stopped before ferritin increases over 800 mcg/L\n\t- Once iron stores are replete, erythropoiesis-stimulating agent (ESA) treatment should be considered\n\t- These are usually given subcutaneously, with examples of ESAs including epoetin or darbepoetin\n\t- Roxadustat is a new oral alternative to ESAs which also acts to stimulate erythropoiesis (it is a hypoxia-inducible factor prolyl hydroxylase inhibitor)\n\t- Blood transfusion should be avoided, especially in patients who may require a renal transplant (due to the risk of allosensitization)\n\t- Target Hb is 100-120 g/L\n- **Mineral and bone disorder (MBD)** occurs due to abnormal metabolism of phosphate, vitamin D, calcium and parathyroid hormone\n\t- There is a spectrum of disease that involves abnormal bone turnover and mineralisation as well as vascular and soft tissue calcification\n\t- Risk of CKD-MBD increases once eGFR is < 60 mL/min/1.73m_\n\t- Phosphate retention occurs due to renal dysfunction -> calcitriol (active form of vitamin D) is downregulated, and is also decreased due to reduced renal activation of vitamin D -> calcium falls -> PTH rises (secondary hyperparathyroidism) -> calcium is released from bone\n\t- Tertiary hyperparathyroidism may also occur if there is longstanding secondary hyperparathyroidism (both may be treated with parathyroidectomy)\n\t- \"Renal osteodystrophy\" refers to a range of bone abnormalities seen in CKD including bone resorption, osteosclerosis and osteopenia\n\t- There is an increased risk of fracture - bone density assessment (e.g. DEXA scanning) and bone protection should be considered\n\t- Patients with at least stage 3a CKD should be regularly monitored with serum calcium, phosphate and PTH levels \n\t- Management involves normalising serum phosphate via dietary restriction of phosphate and phosphate binders (e.g. calcium carbonate, sevelamer)\n\t- Severe hyperparathyroidism may be treated with calcitriol and cinacalcet (a calcimimetic)\n\t- Vitamin D supplementation with ergocalciferol or cholecalciferol may be considered\n\t- Dialysis settings can be adjusted to remove excess phosphate and calcium\n- **Cardiovascular risk** is significantly increased, including myocardial infarction, stroke, peripheral arterial disease and heart failure\n\t- There is a high prevalence of comorbid conditions increasing cardiovascular risk (e.g. hypertension, hypercholesterolaemia, diabetes)\n\t- Patients also have additional CKD-related risk factors, including vascular calcification due to CKD-MBD, uraemia, oxidative stress and anaemia\n\t- Dialysis further increases the risk of cardiovascular disease, including ischaemic heart disease, valvular disease and hypertensive cardiomyopathy\n- **Uraemia** typically becomes symptomatic in patients with end-stage renal disease\n\t- Symptoms include nausea, vomiting, anorexia, taste disturbance, confusion, muscle cramps, pruritus and restless legs\n\t- Complications include pericarditis, neuropathy and encephalopathy\n\t- Symptomatic uraemia is an indication for renal replacement therapy\n- **Hyperkalaemia** is a common issue in CKD due to impaired potassium excretion\n\t- Medications such as ACE-inhibitors and ARBs also contribute to hyperkalemia\n\t- Dietary intake of potassium should be limited\n\t- Medical treatment with potassium binders may be required (e.g. sodium zirconium cyclosilicate (Lokelma), calcium resonium or patiromer)\n\t- Treatments such as sodium bicarbonate (for metabolic acidosis) and diuretics (for fluid overload) may also help to reduce serum potassium\n- **Metabolic acidosis** is common due to reduced renal acid excretion once eGFR < 50 ml/min/1.73m_\n\t- Chronic metabolic acidosis further increases kidney injury and fibrosis, bone demineralisation and muscle wasting and risk of cardiovascular events\n\t- Oral sodium bicarbonate should be considered for patients with an eGFR < 30 ml/min/1.73m_, or if serum bicarbonate is < 20 mmol/litre\n- **Fluid overload** with both pulmonary and peripheral oedema may occur in the later stages of CKD\n\t- Fluid restriction may be advised\n\t- Diuretics may also be used, with loop diuretics (e.g. furosemide) being first-line in most cases\n- **Malnutrition** is common, especially as CKD progresses\n\t- Uraemia may cause anorexia and taste disturbance\n\t- Low mood may also contribute to poor oral intake\n\t- Protein catabolism is promoted by acidosis and chronic inflammation\n\t- Patients should be regularly screened for malnutrition\n\t- Specialist renal dietician input should be offered for patients at risk of malnutrition\n\t- Oral nutritional supplements may be indicated in some cases (or less commonly enteral tube feeding or parenteral nutritional support) \n- **Acute kidney injury** - patients with CKD are at increased risk of AKI\n\t- Risk increases in patients with an eGFR of < 60 mL/min/1.73m_\n\t- There is also a risk of increased CKD progression with episodes of AKI\n\t- Triggers include intercurrent illness, especially with diarrhoea and vomiting, medications e.g. NSAIDs, antibiotics and urinary tract obstruction\n- **Increased risk of malignancy** especially of renal and thyroid cancers\n\t- Immunosuppressive medications further increase malignancy risk (e.g. after renal transplant)\n\t- Chronic uraemia is also a contributing factor\n- **Hypertension** both contributes to the development of CKD and is caused by CKD\n\t- Mechanisms include sodium dysregulation, upregulation of the renin angiotensin aldosterone system, and sympathetic nervous system hyperactivity\n\t- Regular monitoring of blood pressure and effective treatment is therefore key to minimising progression of CKD as well as other adverse cardiovascular events\n- **Reduced quality of life**, especially in patients with more severe CKD\n\t- As with any chronic disease, depression and anxiety are common\n\n# Prognosis\n\n- Prognosis is dependent on the underlying cause of CKD, for example ADPKD tends to progress more rapidly than other diseases\n- CKD is typically a progressive disease, although most patients die before reaching end-stage renal disease\n- Approximately 2% of patients with CKD develop end-stage renal disease\n- Progression can be slowed through modification of risk factors such as hypertension and proteinuria\n- The leading cause of death in CKD is cardiovascular disease\n\n# NICE Guidelines\n\n[NICE CKS - Chronic Kidney Disease](https://cks.nice.org.uk/topics/chronic-kidney-disease/)\n\n[NICE - Chronic kidney disease: assessment and management](https://www.nice.org.uk/guidance/ng203)\n\n[NICE - Renal replacement therapy and conservative management](https://www.nice.org.uk/guidance/ng107)\n\n[NICE technology appraisal - Roxadustat for treating symptomatic anaemia in chronic kidney disease](https://www.nice.org.uk/guidance/ta807/)\n\n# References\n\n[Patient UK - Chronic kidney disease](https://patient.info/doctor/chronic-kidney-disease-pro)\n\n[Patient UK - Anaemia in chronic kidney disease](https://patient.info/doctor/anaemia-in-chronic-kidney-disease)\n\n[UK Kidney Association eCKD guide](https://ukkidney.org/health-professionals/information-resources/uk-eckd-guide) \n\n[Kidney Failure Risk Equation]( https://www.kidneyfailurerisk.co.uk/)\n\n[KDIGO CKD Evaluation and Management](https://kdigo.org/guidelines/ckd-evaluation-and-management/)\n\n[KDIGO CKD Mineral and Bone Disorder guideline](https://kdigo.org/guidelines/ckd-mbd/)\n\n[Radiopaedia - Renal osteodystrophy](https://radiopaedia.org/articles/renal-osteodystrophy?lang=gb)\n\n[The Renal Association - Undernutrition in Chronic Kidney Disease Guideline](https://ukkidney.org/sites/renal.org/files/FINAL-Nutrition-guideline-June-2019-RNG-endorsed.pdf)\n\n[NHS Kidney Care - Chronic Kidney\nDisease in England: The Human and Financial Cost](https://www.england.nhs.uk/improvement-hub/wp-content/uploads/sites/44/2017/11/Chronic-Kidney-Disease-in-England-The-Human-and-Financial-Cost.pdf)",
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"comment": "Isn’t it more common in older people, also why is cranial nerve exam normal?",
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"explanation": "# Summary\n\nTrigeminal neuralgia is a chronic neurological disorder characterised by severe shooting or stabbing pain in the distribution of one or more divisions of the trigeminal nerve. Pain can be triggered by light touch, eating, or wind blowing on the patient's face. Aetiology can be either primary or secondary (secondary to an underlying intracranial lesion). Diagnostic investigations primarily revolve around excluding other possible causes of facial pain. Management strategies include both medical (carbamazepine as the first-line drug) and surgical treatments.\n\n# Definition\n\nTrigeminal neuralgia is a chronic pain condition characterized by severe, sudden, and brief bouts of shooting or stabbing pain that follow the distribution of one or more divisions of the trigeminal nerve, affecting the patient's facial region.\n\n# Epidemiology\n\nTrigeminal neuralgia typically affects adults over the age of 50, with a higher prevalence in women. The incidence of trigeminal neuralgia is approximately 4-5 per 100,000 people annually.\n\n# Aetiology\n\nTrigeminal neuralgia can be classified as either primary (idiopathic) or secondary, with the latter being associated with identifiable etiological factors. Known causes include:\n\n- Malignancy: can lead to nerve compression or infiltration, resulting in pain\n- Arteriovenous malformation: abnormal, tangled blood vessels can compress the trigeminal nerve\n- Multiple sclerosis: demyelination in this condition can affect the trigeminal nerve\n- Sarcoidosis: granulomatous lesions can affect the trigeminal nerve\n- Lyme disease: infection and subsequent inflammation can affect the trigeminal nerve\n\n# Signs and Symptoms\n\n- Unilateral facial pain that is sudden, severe, and brief. \n- The pain is often described as shooting or stabbing,\n- Triggered by lightly touching the affected side of the face, eating, or wind blowing on the face.\n\nNeurological examination in these patients is typically normal.\n\n# Differential Diagnosis\n\nDifferential diagnoses of trigeminal neuralgia include:\n\n- Post-herpetic neuralgia: presents with persistent pain following the resolution of a shingles rash. The pain is typically continuous, aching, burning, or throbbing.\n- Temporomandibular joint disorders: presents with pain in the jaw joint and muscles controlling jaw movement. Other symptoms include difficulty chewing and joint locking.\n- Giant cell arteritis: presents with headache, scalp tenderness, jaw pain, and visual symptoms. Other symptoms include fatigue, loss of appetite, and fever.\n- Cluster headache: presents with severe, unilateral headaches occurring in clusters. Other symptoms include eye watering, nasal congestion, and ptosis on the affected side.\n- Trigeminal autonomic cephalalgias (TACS):a group of primary headache disorders characterised by intense unilateral pain with autonomic symptoms. Usually spontaneous and not triggered by touch\n\n# Investigations\n\nTrigeminal neuralgia is largely a clinical diagnosis, but investigations may be performed to rule out other causes of facial pain. \n\nNeuroimaging such as MRI can be used to exclude secondary causes, including tumours or vascular compression. \n\n# Management\n\nManagement of trigeminal neuralgia can be both medical and surgical. \n\n- Medical management typically includes;\n - **Carbamazepine** (first-line treatment)\n - Phenytoin\n - Lamotrigine\n - Gabapentin\n- Surgical management includes;\n - Microvascular decompression: a procedure to remove or relocate blood vessels that are in contact with the trigeminal root\n - Treatment of the underlying cause: such as removing a tumour or addressing an arteriovenous malformation\n - Alcohol or glycerol injections: used to damage the trigeminal nerve and reduce pain signals\n\n# References\n\n[Click here for NICE CKS on trigeminal neuralgia](https://cks.nice.org.uk/topics/trigeminal-neuralgia/)\n",
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"question": "A 26-year-old woman presents to the GP with paroxysmal allodynia and shock-like pains of the right side of her face. Cranial nerve examination and otoscopy are unremarkable.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "# Summary\n\nMyasthenia gravis is an autoimmune disease characterised by the production of antibodies against the postsynaptic nicotinic acetylcholine receptors at the neuromuscular junction, leading to muscle weakness. Primary symptoms include fatigable muscle weakness, bilateral ptosis, and bulbar features. Key investigations include blood tests for serum acetylcholine receptor antibody, imaging investigations like CT of the chest, and nerve conduction studies with repetitive nerve stimulation. Management strategies involve a multi-disciplinary approach, medical management with immunosuppressive therapy and anticholinesterase inhibitors, and surgical management with thymectomy in select cases.\n\n# Definition\n\nMyasthenia gravis is an autoimmune disease marked by the production of antibodies that target tthe postsynaptic nicotinic acetylcholine receptors at the neuromuscular junction. This immune-mediated interference reduces the ability of acetylcholine to trigger muscle contraction, resulting in muscle weakness.\n\n# Epidemiology\n\nMyasthenia Gravis affects both genders and all age groups, but there is a bimodal distribution with a higher incidence in women under 40 and men over 60.\n\n\n# Signs and symptoms\n\nThe key feature of weakness in patients with myasthenia gravis is **fatigability**.\n\nPatients with myasthenia gravis commonly present with:\n\n- **Fatiguable** limb muscle weakness\n- Ptosis\n- Diplopia\n- Facial palsy\n- Bulbar weakness e.g. dysphagia, dysphonia\n- Proximal muscle weakness\n\nThese signs and typically worsen with prolonged movement or by the end of the day.\n\nA number of drugs can exacerbate Myasthenia Gravis, including:\n\n- Beta blockers\n- Lithium\n- Penicillamine\n- Gentamicin\n- Quinolones\n- Phenytoin\n\n\n# Differential Diagnosis\n\nThe following conditions may present with similar symptoms and should be considered in the differential diagnosis:\n\n- Lambert-Eaton syndrome is a fluctuating weakness that improves with exercise, differentiating it from MG. This is usually due to underlying malignancy, most commonly small-cell lung cancer. It affects voltage-gated calcium channels in the presynaptic membrane.\n- Multiple sclerosis can present with any neurological sign that may fluctuate or persist over hours to days to weeks secondary to demyelination in the central nervous system. \n- Botulism presents with ptosis, double vision, progressive weakness, and pupillary abnormalities accompanied by systemic symptoms. Ingestion of honey or contaminated foods may be elicited in the patient's history.\n- Polymyositis and dermatomyositis cause proximal muscle weakness and is usually associated with pain. The pathology is the inflammation of the muscle itself.\n- Graves ophthalmopathy presents with eyelid retraction and widened palpebral fissure. These are caused by autoantibodies targeted toward the structures of the eye.\n\n# Investigations\n\nKey investigations in the diagnosis of myasthenia gravis include:\n\n- Bedside tests: Ice-pack test\n\t- Eye is placed over the eye for 2-5 minutes to assess for improvements in ptosis\n- Blood tests: Testing for serum acetylcholine receptor (anti-AChR) antibody and muscle-specific tyrosine kinase (anti-MusK) antibodies and (rarely) anti-LRP4 antibodies\n- Imaging investigations: CT scan of the chest to identify thymic hyperplasia or thymoma\n\t- Approximately 10% of patients with MG have a thymoma, and it is implicated in the production of autoantibodies\n- Nerve Conduction Studies/EMG: Repetitive nerve stimulation testing\n\nIn a myasthenic crisis, serial pulmonary function tests (spirometry) are performed. \n\nIf the forced vital capacity is 15 mL/kg or less, the patient should be considered for mechanical ventilation.\n\n# Management\n\nThe management of myasthenia gravis involves:\n\n- Regular review in neurology outpatients\n- Multidisciplinary team involvement as required (including occupational therapist, physiotherapist, speech and language therapist)\n- Medical management with immunosuppressive therapy (such as **steroids**) and anticholinesterase inhibitors (such as **pyridostigmine** or neostigmine). \n- Acute cases may require intravenous immunoglobulin (IVIG) or plasmapheresis in severe, steroid-refractory, cases.\n- Surgical management with thymectomy is indicated in patients with evidence of thymoma AND in patients with non-thymomatous antibody positive n-AChR MG\n\n# References\n\n1. Gilhus, N. E., & Verschuuren, J. J. (2015). Myasthenia gravis: subgroup classification and therapeutic strategies. The Lancet Neurology, 14(10), 1023-1036.\n2. Meriggioli, M. N., & Sanders, D. B. (2009). Autoimmune myasthenia gravis: emerging clinical and biological heterogeneity. The Lancet Neurology, 8(5), 475-490.\n3. Sanders, D. B., & Wolfe, G. I. (2021). Myasthenia Gravis and Lambert-Eaton Myasthenic Syndrome. In Harrison's Principles of Internal Medicine (21st edition). McGraw-Hill Education.\n",
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"explanation": "Excessive nitrous oxide inhalation oxidises the cobalt ion of vitamin B12, interfering with its bioavailability as a co-enzyme. Patients can then develop clinical symptoms of B12 deficiency, particularly subacute combined degeneration of the cord. This affects the posterior and lateral columns of the spinal cord, presenting with gradual upper and lower limb weakness, peripheral paraesthesia, and upper lower motor neurone signs, particularly with loss of vibration and touch sense",
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"comment": "TIL. Good question",
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"comment": "ahh its the bristol special ",
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"explanation": "# Summary\n\nSub-acute combined degeneration of the cord (SCDC) is a neurological disorder stemming from vitamin B12 deficiency, characterised by the degeneration of the dorsal columns and corticospinal tracts. Key signs and symptoms include symmetrical distal sensory symptoms, diminished vibration sense and proprioception in the legs, and mixed upper and lower motor neuron signs. Investigations primarily involve B12, folate levels, and homocysteine levels, in addition to MRI of the spine and nerve conduction studies. The primary management strategy involves B12 replacement therapy.\n\n# Definition\n\nSub-acute combined degeneration of the cord (SCDC) is a neurological complication associated with vitamin B12 deficiency. It is characterised by degeneration of both the dorsal columns and corticospinal tracts, whilst preserving pain and temperature sensations. It typically manifests as symmetrical sensory symptoms starting distally and progressing proximally, along with varying degrees of ataxia.\n\n# Aetiology\n\nThe underlying cause of SCDC is vitamin B12 deficiency, which can result from various factors including pernicious anemia, malabsorption syndromes, dietary deficiencies, and misuse of nitrous oxide (this causes a **functional** rather than a true B12 deficiency) .\n\n# Signs and Symptoms\n\n- Symmetrical distal sensory symptoms, typically beginning in the feet and progressing to the hands\n- Varying degrees of ataxia\n- Diminished vibration sense and proprioception in the legs\n- Mixed upper and lower motor neuron signs, which may present as exaggerated, diminished, or absent limb reflexes\n- Autonomic bladder or bowel symptoms\n- SCDC may manifest in both the presence and absence of haematological manifestations.\n\n# Investigations\n\nDiagnostic workup for SCDC should include:\n\n- Assessment of B12 and folate levels\n- Homocysteine level analysis; a raised level despite normal B12 could indicate a functional B12 deficiency\n- MRI of the spine to exclude cervical myelopathy\n- Nerve conduction studies, which will primarily show axonal neuropathy\n\n# Management\n\nThe mainstay of treatment for SCDC is:\n\n- Urgent Vitamin B12 replacement, typically using hydroxocobalamin 1 mg IM on alternate days until there is no further improvement, followed by maintenance treatment with hydroxocobalamin 1 mg IM every two months, as per [NICE guidelines](https://cks.nice.org.uk/topics/anaemia-b12-folate-deficiency/).",
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"explanation": "Motor neurone disease presents with gradual progression of upper and lower motor neurone signs. It would not present with the sensory deficit and would not present as rapidly as this",
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"explanation": "Multiple sclerosis typically presents with temporary visual or sensory loss with gradual progression. It can cause spastic weakness, ataxia, and tremor, but wouldn't present with sudden neurological deficit",
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"votes": 2664
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"explanation": "This patient is experiencing symptoms of mononeuritis multiplex, sporadically developing peripheral neuropathies most commonly from nerve ischaemia secondary to primary or secondary vasculitis. There are multiple causes for this, broadly classifying them into ischaemic (e.g. diabetes mellitus & peripheral nerve vasculitis), inflammatory (e.g. sarcoidosis, rheumatoid arthritis, and Guillain-Barré Syndrome), infectious (e.g. Lyme disease and cytomegalovirus), drug-induced (sulfonamides and hydralazine), genetic, malignant, or primary vasculitides (e.g. giant cell arteritis, granulomatosis with polyangiitis, or polyarteritis nodosa)",
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"explanation": "B12 deficiency presents with gradually progressive peripheral paraesthesia. It would not present with such sudden onset with a seemingly random distribution of the peripheral nerves",
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"comment": "FML",
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"comment": "I both second and third this",
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"comment": "4th, 5th and 6th ",
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"comment": "lmao what\n",
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"comment": "just say mononeuritis multiplex :(",
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"comment": "In finals, most exams will have 2 step qs such as this. Step 1 is identifying this is mononeuritis multiplex, step 2 is knowing what conditions cause that.",
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"comment": "ooof\n",
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"comment": "If i speak I am in big trouble, in big trouble",
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"comment": "Any one else know it was mononeuritis multiplex but BLANK on the causes FML \n",
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"explanation": "# Summary\n\nMononeuritis multiplex is a form of peripheral neuropathy that affects multiple individual nerves in different parts of the body. It typically begins asymmetrically, but as more nerves become involved, the condition can mimic polyneuropathy. It commonly presents with both motor and sensory deficits and can cause significant pain. Early recognition is crucial for distinguishing it from other neuropathies and for targeting appropriate management.\n\n# Definition\n\nMononeuritis multiplex refers to the involvement of two or more non-contiguous peripheral nerves. Initially, the pattern is asymmetrical, with different nerves affected either sequentially or simultaneously. As the disease progresses, the deficits can become more confluent and symmetrical, making it harder to differentiate from polyneuropathy. The condition typically presents with a sudden or subacute loss of sensory and motor function in the affected nerves.\n\n\n# Aetiology \n\nMononeuritis multiplex can be caused or associated with various systemic conditions, including:\n\n- **Diabetes mellitus** – one of the most common causes, often presenting as painful neuropathy in lower limbs.\n- **Vasculitis** – including polyarteritis nodosa, granulomatosis with polyangiitis (Wegener's), and eosinophilic granulomatosis with polyangiitis (Churg-Strauss). It can also occur secondary to **Rheumatoid Arthritis**\n- **Autoimmune disorders** – such as rheumatoid arthritis and systemic lupus erythematosus.\n- **Infectious causes** – including leprosy, Lyme disease, HIV, and Parvovirus B19.\n- **Sarcoidosis** – a granulomatous disease affecting multiple systems.\n- **Cryoglobulinaemia** – immune-complex-related vasculitis.\n- **Exposure to toxins** – such as trichloroethylene or drugs like dapsone.\n- **Rare causes** – such as reactions following stings from jellyfish like the sea nettle.\n\n# Clinical Features\n\nThe hallmark feature of mononeuritis multiplex is **asymmetry** in sensory and motor disturbances:\n\n- **Pattern of involvement**: Patients often experience asymmetric weakness or sensory deficits, particularly affecting the distribution of specific nerves.\n- **Nerve involvement**: \n - **Peroneal nerve involvement** is common in up to 75% of cases, leading to foot drop.\n - Other frequently affected nerves include the **tibial**, **ulnar**, **radial**, and **median** nerves.\n- **Pain**: Often deep and aching, worse at night, and typically in the lower back, hips, or legs.\n- **Diabetic mononeuritis multiplex**: Commonly presents with acute, severe, unilateral thigh pain followed by weakness in the quadriceps and loss of the knee reflex.\n\nAs the disease advances, the sensory and motor deficits may become more symmetrical, which can obscure the diagnosis.\n\n# Management \n\nThe treatment of mononeuritis multiplex involves both addressing the underlying condition and managing the neuropathic symptoms:\n\n1. **Conservative management**:\n - **Physical therapy (PT)** to maintain function in affected limbs.\n - **Orthotics** (such as foot braces) to support foot drop and other motor impairments.\n \n2. **Medical management**:\n - **Optimising underlying conditions** such as controlling blood sugar levels in diabetes, or using immunosuppressive therapy in autoimmune or vasculitic cases.\n - **Pain management**: Neuropathic pain can be managed using medications such as:\n - **Anticonvulsants** (e.g., gabapentin or pregabalin).\n - **Antidepressants** (e.g., amitriptyline or duloxetine).\n - **Analgesics** or **opioids** in severe cases.\n - **IVIG** (Intravenous Immunoglobulin): In some cases, especially those related to immune-mediated causes, IVIG may be used as part of the treatment plan to modulate the immune response.\n\n\n",
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"question": "A 52-year-old woman presents to the GP with acute right foot drop and loss of sensation on the dorsum of the foot. One month ago, she developed ulnar nerve palsy in her left hand, and six months ago, she had developed isolated 4th nerve palsy.\n\nWhich of the following conditions is associated with this disorder?",
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"explanation": "Vertebrobasilar insufficiency may present in this way, although symptoms are transient, similar to a posterior circulation TIA. They are often triggered by causes of transient reduced cerebral perfusion, such as orthostatic hypotension, which can accentuate previously unknown symptoms",
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"explanation": "Pontine infarcts can present with a range of signs from ipsilateral cranial nerve palsy (CN V, VI, VII, and VIII) with contralateral motor/sensory impairment to locked-in syndrome. A similar condition to PICA syndrome - lateral pontine syndrome - would likely produce similar symptoms with the addition of ipsilateral facial nerve palsy due to involvement of the facial nucleus",
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"explanation": "Weber syndrome presents as ipsilateral oculomotor nerve palsy and contralateral weakness",
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"explanation": "Lacunary infarcts present with relatively distinct symptoms based on the location within the internal capsule. 1) contralateral hemiparesis with dysarthria and dysphagia 2) ipsilateral cerebellar symptoms 3) hemiparesis with contralateral sensory impairment 4) Pure hemisensory loss. It would unlikely present with Horner's syndrome",
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"explanation": "Sudden onset vertigo, nystagmus, and ipsilateral dysphagia, reduced facial sensation, and Horner's syndrome suggests a central cause, particularly dysfunction of the lateral part of the medulla. This is commonly caused by a posterior inferior cerebellar artery or vertebral artery ischaemia. The sensation of vertigo and nystagmus arises from disruption of the lateral vestibular nucleus; dysphagia due to damage to cranial nerves IX & X; reduced facial sensation from the trigeminal nerve root; and Horner's syndrome from the hypothalamospinal fibres where sympathetic fibres run",
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"comment": "Could someone please explain the examination findings?🙏",
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"comment": "You can break Posterior Inferior Cerebellar Artery Syndrome into two sets of symptoms by area since the posterior inferior cerebellar artery supplies the inferior cerebellum and the lateral parts of the medulla (which is why it's also called lateral medullary syndrome)\n\n1 - cerebellum (damage is to the vestibulo-floccular connections)\n- dysarthria\n- ipsilateral limb ataxia\n- vertigo\n- Nystagmus\n\n2 - Brain Stem (Medulla)\n- ipsilateral Horner's syndrome (descending sympathetic nerve tract in lateral medulla)\n- ipsilateral sensory loss (CNV tract in lateral medulla)\n- ipsilateral pharyngeal and laryngeal paralysis (CNX exits on the lateral medulla)\n- C/L sensory loss (Spinothalmic tract in lateral medulla)\n\nIt really helps to look at an axial section of the medulla and go through the structures in the most lateral part and see what will be damaged by infarct.",
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"explanation": "# Summary\n\nAn ischaemic stroke is a medical emergency characterised by a sudden onset of focal neurological deficit secondary ischaemia. Depending on the affected cerebral area, symptoms can range from contralateral motor and sensory deficits, homonymous hemianopia, to higher cerebral dysfunction (such as aphasia and neglect). Initial management of suspected stroke necessitates urgent neuroimaging, primarily via non-contrast CT scan, to differentiate between ischaemic and haemorrhagic types. Further investigations such as carotid ultrasound, CT/MR angiography, echocardiogram, and various blood tests (e.g., serum glucose and lipids) help define the cause of stroke and quantify vascular risk factors. Acute management of ischaemic stroke involves thrombolysis in selected patients (usually within 4.5 hours of symptom onset), provided there are no contraindications, or mechanical thrombectomy for eligible patients. Long term management usually involves antiplatelet therapy, risk factor optimisation and multidisciplinary rehabilitation.\n\n\n# Definition\n\nAn ischaemic stroke describes a sudden onset focal neurological deficit secondary to focal brain ischaemia, with symptoms lasting >24 hours (or with evidence of infarction on imaging).\n\n# Aetiology\n\n85% of strokes are ischaemic while 15% are haemorrhagic.\n\nIschaemic stroke occurs when blood supply in a cerebral vascular territory is reduced secondary to stenosis or complete occlusion of a cerebral artery.\n\nThe ischaemic penumbra describes the cerebral area surrounding the ischaemic event where there is ischaemia without necrosis. This area is amenable to recovery with thrombolysis.\n\nIn terms of underlying aetiology of ischaemic stroke: \n\n- 25% are caused by intracranial small vessel atherosclerosis.\n- 50% are caused by large vessel atherosclerosis e.g. carotid artery stenosis.\n\t- Typically results from thrombus formation on the atherosclerotic plaque, and subsequent embolism of the thrombus to a smaller cerebral artery.\n- 20% of ischaemic strokes are cardio-embolic \n\t- e.g. in atrial fibrillation there is stasis of blood flow in the left atrium, predisposing to thrombus formation in the left atrium, and subsequent embolisation to the brain.\n\t- Rare causes of ischaemic stroke include primary vascular causes (such as vasculitis and arterial dissection) and haematological causes (prothrombotic states).\n\n\n\n# Stroke risk factors\n\n- Age\n- Male Sex\n- Family History\n- Hypertension\n- Smoking\n- Diabetes \n- Atrial fibrillation\n- High cholesterol\n- Obesity\n- Migraine \n\n# Stroke classification \n\nThe **Bamford/Oxford Stroke Classification System** is the most common classification system for ischaemic stroke. Although it is not used frequently in clinical practice, it is a helpful aide memoire to remember the localisation of common stroke syndromes.\n\nA total anterior circulation infarct (TACI) is defined by:\n\n- Contralateral hemiplegia or hemiparesis, AND\n- Contralateral homonymous hemianopia, AND\n- Higher cerebral dysfunction (e.g. aphasia, neglect)\nA TACI involves the anterior AND middle cerebral arteries on the affected side.\n\nA partial anterior circulation infarct (PACI) is defined by:\n\n- 2 of the above, OR\n- Higher cerebral dysfunction alone.\n- A PACI involves the anterior OR middle cerebral artery on the affected side.\n\nA lacunar infarct (LACI) is defined by: a pure motor stroke, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis or dysarthria-clumsy hand syndrome.\nA LACI affects small deep perforating arteries, typically supplying internal capsule or thalamus.\n\nA posterior circulation infarct (POCI) is defined by:\n\n- Cerebellar dysfunction, OR\n- Conjugate eye movement disorder, OR\n- Bilateral motor/sensory deficit, OR\n- Ipsilateral cranial nerve palsy with contralateral motor/sensory deficit, OR\n- Cortical blindness/isolated hemianopia.\n\nA POCI involves the vertebrobasilar arteries and associated branches (supplying the cerebellum, brainstem, and occipital lobe).\n\n[lightgallery]\n\n# Posterior Stroke Syndromes\n\nThere are a number of different posterior stroke syndromes that you should be aware of:\n\n- Basilar artery occlusion is more likely to present with locked in syndrome (quadriparesis with preserved consciousness and ocular movements), loss of consciousness, or sudden death.\n\n- Anterior inferior cerebellar artery results in lateral pontine syndrome, a condition similar to the lateral medullary syndrome but with additional involvement of pontine cranial nerve nuclei. It leads to cerebellar ataxia, vertigo, hearing loss as well as ipsilateral facial weakness\n- Wallenberg's syndrome (lateral medullary syndrome) causes ipsilateral Horner's syndrome, ipsilateral loss of pain and temperature sensation on the face, and contralateral loss of pain and temperature sensation over the contralateral body.\n- Weber's syndrome/medial midbrain syndrome (paramedian branches of the upper basilar and proximal posterior cerebral arteries): causes an ipsilateral oculomotor nerve palsy and contralateral hemiparesis.\n\n# Acute management of ischaemic stroke\n\n\n- Patients should be approached in the DR ABCDE manner.\n- CT Head should be perfomed on arrival to the emergency department to distinguish ischaemic from haemorrhagic stroke. \n- If no evidence of ischaemic stroke, a CT Angiogram and CT perfusion (in select patients) should be performed to assess for evidence of large vessel occlusion and a salvageable ischaemic penumbra\n- Thrombolysis with Alteplase (tissue plasminogen activator) is considered if:\n\t- The patient presents within 4.5 hours of symptom onset (Up to 9 hours in select patients with good baseline and favourable perfusion imaging) \n\t- No contraindications such as:\n\t\t- Recent head trauma\n\t\t- Recent surgery\n\t\t- Systolic lood Pressure above 185 \n\t\t- Currently taking oral anticoagulation\n\t\t- Raised INR (local guidelines vary)\n- Mechanical Thrombectomy is usually considered in patients with:\n\t- Anterior Circulation Stroke (evidence base is poorer for posterior circulation stroke)\n\t- Evidence of large vessel occlusion (ideally proximal up to distal M1)\n\t- Good functional baseline\n\t- Favourable perfusion criteria indicating salvageable tissue\n\t- Presenting within 6 hours (Up to 24 hours in select patients with good baseline and favourable perfusion imaging)\n\nIf hyper-acute treatments are not offered, patients are started on an antiplatelet agent such as Aspirin or Clopidogrel (local guidelines vary).\n\nIf hyper-acute treatments are offered, antiplatelets are usually started 24 hours after the treatment following a repeat CT Head that excludes any haemorrhagic transformation.\n\n# Stroke investigations (Post-acute)\n\nMRI Head with Diffusion Weighted Imaging (DWI) is the gold standard test to confirm the presence of an acute ischaemic stroke, which can be present within a few minutes of stroke onset. Due to logistical challenges of acute MRI scanning, this is normally performed within 24 hours following initial hyperacute treatment.\n\nInvestigations in the post-hyperacute phase aim to further define the cause of the stroke and to quantify vascular risk factors.\n\nThese include:\n\n- Carotid ultrasound (to identify critical carotid artery stenosis)\n- 24 to 72 hour cardiac monitoring to assess for evidence of atrial fibrillation\n- CT/MR angiography (to identify intracranial and extracranial stenosis)\n- Echocardiogram (if a cardio-embolic source is suspected). \n- In young patients further investigation e.g. a vasculitis screen or thrombophilia screen may be necessary.\n- HbA1c and Serum Lipids to optimise other cardiovascular risk factors \n\n\n# Stroke management (Chronic)\n\nRehabilitation and supportive management will include an **MDT approach** with involvement of physiotherapy, occupational therapy, speech and language therapy, and neurorehabiliation.\n\n\nThe key steps in secondary stroke prevention can be remembered by the mnemonic HALTSS:\n\n- Hypertension: \n\t- Studies show there is no benefit in lowering the blood pressure acutely (as this may impair cerebral perfusion) unless there is malignant hypertension (systolic blood pressure >180 mmHg). Anti-hypertensive therapy should, however, be initiated 2 weeks post-stroke.\n- Antiplatelet therapy:\n\t- Patients should be administered Clopidogrel 75 mg once daily for long-term antiplatelet therapy. In patients with ischaemic stroke secondary to atrial fibrillation, however, warfarin (target INR 2-3. or a direct oral anticoagulant (such as Rivaroxaban or Apixiban) is initiated 2 weeks post-stroke.\n- Lipid-lowering therapy:\n\t- Patients should be prescribed high dose atorvastatin 20-80 mg once nightly (irrespective of cholesterol level this lowers the risk of repeat stroke).\n- Tobacco\n\t- Offer smoking cessation support.\n- Sugar:\n\t- Patients should be screened for diabetes and managed appropriately.\n- Surgery:\n\t- Patients with ipsilateral carotid artery stenosis more than 50% should be referred for carotid endarterectomy. Patients with over 70% stenosis have the most benefit from endarterectomy\n\n\n\n# References\n\n[Click here for NICE Clinical Knowledge Summaries](https://cks.nice.org.uk/topics/stroke-tia/)\r\n\r\n[Click here for Radiopedia](https://radiopaedia.org/articles/lacunar-stroke-syndrome?lang=gb)",
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"explanation": "# Summary\n\nCentral retinal vein occlusion (CRVO) and Branch retinal vein occlusion (BRVO) are conditions that occur when the central retinal vein or its branches are occluded by a thrombus, respectively. They present with sudden, painless loss of vision or visual field defects. Classic signs include numerous flame haemorrhages, dot and blot haemorrhages, cotton wool spots, retinal oedema, and dilated or tortuous retinal veins. Investigations aim to identify the underlying aetiology and may include a full blood count, ESR, CRP, and renal, liver and lipid profiles. Management is generally conservative, though some situations may require laser photocoagulation or intravitreal anti-VEGF injections.\n\n# Definition\n\nCentral retinal vein occlusion (CRVO) and Branch retinal vein occlusion (BRVO) are distinct conditions in which the central retinal vein or one of its branches, respectively, is occluded by a thrombus.\n\n# Epidemiology\n\nCRVO and BRVO are more common than central retinal artery occlusion. Risk factors for these conditions are divided into atherosclerotic and haematological categories. \n\n\n| Atherosclerotic | Haematological |\n|-----------|------|\n| Age| Protein S, protein C or antithrombin deficiency |\n| Smoking | Factor V Leiden|\n| Obesity | Multiple myeloma |\n| Hypertension| Glaucoma |\n|Diabetes | Antiphospholipid syndrome |\n\n\n\n# Signs and symptoms\n\nCRVO typically presents with sudden, painless loss of vision or visual field defects. In BRVO, loss of vision may only be noticeable by patients if it affects the macula. \n\nIschaemic CRVO usually causes much worse reduced visual acuity (6/60 or worse).\n\nThe classic fundoscopy description of CRVO is a 'stormy sunset', with findings that include:\n\n- Numerous flame haemorrhages\n- Dot and blot haemorrhages\n- Cotton wool spots\n- Retinal oedema\n- Dilated or tortuous retinal veins\n- Visual field defects, depending on the site of the occlusion\n\nNote: For BRVO, these signs are present but only in the affected segment of the retina.\n\n# Differential diagnosis\n\n* **Diabetic Retinopathy:** Diabetic retinopathy, particularly the macular edema subtype, can lead to visual impairment and retinal swelling similar to CRVO. Distinguishing between the two conditions is crucial for appropriate management.\n* **Hypertensive Retinopathy:** Hypertensive retinopathy, resulting from long-standing high blood pressure, may manifest as retinal hemorrhages and cotton-wool spots. A detailed medical history and blood pressure evaluation can help differentiate hypertensive retinopathy from CRVO.\n* **Ocular Ischemic Syndrome (Carotid Artery Disease):** Ocular ischemic syndrome can present with similar retinal findings due to compromised blood flow to the eye. It often results from carotid artery disease, which can be detected through carotid artery imaging.\n* **Retinal Artery Occlusion:** Retinal artery occlusion, such as central retinal artery occlusion (CRAO), can cause sudden vision loss and retinal pallor, similar to CRVO. However, arterial occlusions typically have a more abrupt and severe onset.\n* **Retinal Detachment:** Retinal detachment may cause visual disturbances and can sometimes be mistaken for CRVO. Examination findings, including retinal detachment features like a detached retina, are crucial for differentiation.\n* **Macular Hole or Pucker:** Macular hole or epiretinal membrane (macular pucker) can result in distorted or decreased vision, resembling CRVO symptoms. Optical coherence tomography (OCT) can help distinguish these conditions.\n* **Optic Neuropathy:** Optic neuropathies, such as non-arteritic anterior ischemic optic neuropathy (NAION) or arteritic anterior ischemic optic neuropathy (AAION), can lead to sudden vision loss. \n\n# Investigations\n\nDuring bedside examination, fundoscopy findings (more so for ischaemic CRVO) include: macular oedema, optic nerve head oedema, **flame-haemorrhages,** venous tortuosity and cotton wool spots. Additionally, patients will have reduced visual acuity so assessing this with a Snellen chart will help aid diagnosis. In advanced disease, a relative afferent pupillary defect may also be present.\n\nInvestigations aim to identify the aetiology of the occlusion and may include:\n\n- Full blood count\n- Erythrocyte sedimentation rate (ESR) \n- C-reactive protein (CRP)\n- Renal, liver and lipid profiles\n- Clotting screen\n\nFurther screening tests for thrombophilia should be carried out if the patient has a family history of clotting disorders.\n\n[lightgallery]\n\n# Management\n\nMost patients with CRVO or BRVO are managed conservatively, as there is no evidence to support the use of anticoagulation or haemodilution in the acute setting. Specific treatments may be necessary in some situations:\n\n- Retinal neovascularisation is managed with laser photocoagulation\n- Macular oedema is treated with intravitreal anti-VEGF injections. If anti-VEGF is contraindicated (e.g., stroke or MI within 3 months, pregnancy), corticosteroids are administered\n\n# Complications\n\n- Neovascularisation – ischaemia in the retina promotes the production of vascular endothelial growth factor (VEGF), which stimulates new vessel growth\n- Vitreous haemorrhage – new vessels are fragile and can bleed, leading to vitreous haemorrhage\n- Hyphaema – neovascularisation in the iris can lead to bleeding in the anterior chamber (hyphaema); bleeding can obstruct the outflow of aqueous leading to neovascular (rubeotic) glaucoma\n\n# References\n\nDenniston AK, Murray PI. Oxford Handbook of Ophthalmology. Fourth Edition. Oxford University Press. 2018.\n\n[See Patient UK for a comprehensive review of CRVO](https://patient.info/doctor/retinal-vein-occlusions)",
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"explanation": "# Summary\n\nBarrett's oesophagus is a condition seen in patients with long standing gastro-oesophageal reflux disease (GORD). It describes when chronic acid exposure leads to a _change in the distal oesophagus from the usual squamous epithelium to metaplastic columnar epithelium_, known as metaplasia, and this usually occurs in the distal third of the oesophagus. This condition increases risk of oesophageal adenocarcinoma 100-fold which is why monitoring and prompt management is vital.\n\n# Definition\n\nBarrett's oesophagus is defined as an oesophagus in which any part of the distal squamous epithelial lining has been replaced by metaplastic columnar epithelium, visible endoscopically (≥1 cm) above the gastro-oesophageal junction and confirmed histopathologically (e.g. from a biopsy). It is classified according to the degree of dysplasia.\n\n\n# Epidemiology\n\nPrimarily affecting males over 50 with longstanding GORD, the condition has become increasingly prevalent in the UK due to several factors including rising obesity rates and the ageing population. It is thought that about 1 in 20 people who have recurring acid reflux eventually develops Barrett's oesophagus. The risk is mainly in people who have had severe acid reflux for many years.\n\n\n# Aetiology\n\nThe main risk factor for developing Barrett's oesophagus is longstanding **GORD**, however, other risk factors include:\n\n* Obesity\n* Smoking\n* Hiatus hernia \n* Increasing age (peak incidence 50-70 years)\n\n# Signs and Symptoms\n\nThese are the same as those in GORD:\n\n* Pain in the upper abdomen and chest\r\n* Heartburn \r\n* Acid taste in the mouth\r\n* Bloating\r\n* Belching\r\n\nPresence of 'ALARM' signs and symptoms (anaemia, loss of weight, anorexia, recent onset/progressive symptoms, melaena) may suggest progression to adenocarcinoma.\n\n# Investigations\n- OGD is the gold-standard for diagnosing and classifying Barret's oesophagus\n\n### 2-week-wait referral criteria\n\n- If there is dysphagia or, in those aged 55 years and over with weight loss and any of the following: upper abdominal pain, reflux, or dyspepsia.\n- Consider non-urgent direct access upper gastrointestinal endoscopy to assess for oesophageal cancer in people with haematemesis.\n\n# Management\n\nSymptoms should be managed as per GORD management. Further management of Barrett's oesophagus specifically can be categorised into either surveillance or ablation, depending on the classification.\n\n- If there is short-segment (less than 3 cm) Barrett's oesophagus without intestinal metaplasia then no further surveillance is required\n\n## Endoscopic surveillance\n\n- In long-segment (3 cm or longer) Barrett's oesophagus, there should be a repeat OGD every 2 to 3 years \n- In short-segment (less than 3 cm) Barrett's oesophagus with intestinal metaplasia this should be done every 3 to 5 years\n- Patients with indefinite dysplasia should have surveillance every 6 months\n\n## Ablation\n\nPatients with **dysplasia** are eligible for ablation therapy, of which there are two techniques of equal efficacy: endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD).\n\n- First-line management of patients with visible high-grade dysplasia is endoscopic ablation of visualised lesions\n- These patients should be followed up with endoscopic surveillance, with endoscopic ablation of any residual Barrett's oesophagus offered \n\n\n# Complications\n\nIt is an important condition to identify as it carries a risk of progression to **oesophageal adenocarcinoma**.\n\nThe risk of developing Barrett's oesophagus increases with the length and severity of reflux symptoms.\n\n# NICE Guidelines\n\n[Barrett's oesophagus and stage 1 oesophageal adenocarcinoma: monitoring and management](https://www.nice.org.uk/guidance/ng231/chapter/Recommendations)\n",
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"question": "A 60-year-old man is referred for an outpatient gastroscopy following worsening reflux symptoms over the last six months.\n\nGastrosopcy shows a red, velvety appearance of the oesophageal mucosa and biopsies from this region show \"metaplastic columnar epithelium replacing the oesophageal squamous epithelium\". There are no areas of dysplasia identified.\n\nWhich of the following is the best step in management?",
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"explanation": "This is less likely to be the case here as the movements described are not typical of a tonic-clonic seizure where the movements are more synchronous jerking of the limbs, with the head often remaining still. Tongue biting in epileptic seizure is more commonly a lateral bite, and incontinence is frequently reported",
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"explanation": "This is a relatively typical description of non-epileptic attack disorder. The more informal term for this condition is a pseudoseizure. The movements described in terms of back arching and pelvic thrusting are less in keeping with a tonic-clonic seizure. The eyes tend to remain open, and making noise is less likely in true epileptic seizures. Tongue biting may occur in both true seizures and non-epileptic attacks; however in epileptic seizures, it is usually the sides of the tongue that are bitten as opposed to the tip. Other signs that would point towards non-epileptic attacks are if they always occur in the company of others or if stressful or highly emotional situations induce them",
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"explanation": "Whilst vasovagal syncope is common in young females, the description above is more in keeping with a non-epileptic attack than a vasovagal syncope as syncopal episodes usually only last 30 seconds to 2 minutes, and any movements are also short-lived. Tongue biting is also rare in syncope, and the patient usually reports more prodromal symptoms such as disturbed vision, palpitations and feeling warm",
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"explanation": "Absence seizures are a form of epilepsy most common in children and are commonly associated with being very still, fluttering of the eyelids and suddenly stopping activity. They can occur with muscle jerking and shaking, though this is less common than with other forms of epileptic seizure",
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"explanation": "There is no evidence in the case vignette that this episode is related to low blood sugar, and the blood tests are reported to be normal. It is always good to bear in mind hypoglycaemia in young women and, in particular, in diabetic patients on insulin or sulfonylureas such as gliclazide.\nSymptoms of low blood sugars include sweating, dizziness, tingling lips and can cause unusual behaviour, seizures and collapse if untreated",
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"comment": "😀😀😀",
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"comment": "hip thrusting is usually specific to NEAD...",
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"explanation": "# Summary\n \nSyncope means a transient loss of consciousness and is a common emergency presentation. There are many causes with important differentials being reflex syncope, orthostatic hypotension and cardiac syncope. The term \"blackouts\" is commonly used to refer to a loss of consciousness, and includes differentials such as seizures. A thorough history (including a collateral if available) is important to help to differentiate the above, followed by examination including a lying-standing blood pressure. Initial investigations include an ECG, a blood glucose and consideration of a basic set of bloods to screen for abnormalities such as hyponatraemia that could trigger seizures. Emergency management encompasses ruling out serious causes, treating any injuries sustained during the episode and referral on for specialist investigations and management as appropriate.\n\n# Definition \n\nBlackouts refer to episodes of transient loss of consciousness, which occur for a variety of reasons. Syncope refers to a transient loss of consciousness secondary to cerebral hypoperfusion, with syncopal presentations making up the majority of cases of blackouts.\n \n# Epidemiology \n \nBlackouts are common, with an estimated 50% of the population experiencing at least one in their lifetime. 3% of emergency department presentations and 1% of hospital admissions in the UK are due to blackouts.\n \n# Aetiology\n \n**Causes of cardiac syncope:**\n\n- Structural\n - Acute myocardial infarction \n - Aortic stenosis \n - Ischaemic cardiomyopathy\n - Hypertrophic obstructive cardiomyopathy\n - Cardiac tamponade\n- Electrical \n - Tachyarrhythmias e.g. superventricular tachycarcia (SVT), ventricular tachycardia (VT), ventricular fibrillation (VF)\n - Bradyarrhythmias e.g. sick sinus syndrome, heart block\n - Inherited channelopathies e.g. Brugada syndrome\n\n**Causes of reflex syncope:**\n \n - Vasovagal syncope (\"fainting\")\n - Situational syncope e.g. following defecation, post-exercise, or straining to pass urine\n - Carotid sinus syndrome - occurs due to hypersensitivity of the carotid sinus baroreceptor\n\n**Other causes of syncope:**\n \n - Orthostatic hypotension\n - Pulmonary embolism\n - Occult haemorrhage e.g. subarachnoid haemorrhage, GI bleeding, ruptured aortic aneurysm\n - Head trauma\n - Hypoglycaemia\n\n **Non-syncopal causes of blackouts:**\n \n - Seizures\n - Psychogenic pseudosyncope\n - Psychogenic non-epileptic seizures\n\n# Symptoms and Signs\n \nWhen taking a history and examining a patient after a blackout, there are several additional symptoms and signs to elicit that can help identify the likely cause. If the blackout was witnessed, take a collateral history also. \n\n**Questions to ask about before the blackout:**\n\n- What were they doing/any triggers?\n - Exertional syncope (cardiac)\n - After exercise (vasovagal/orthostatic hypotension)\n - Head movements/pressure on neck (carotid sinus syndrome)\n - Prolonged standing (orthostatic hypotension)\n - Pain (vasovagal)\n - Repeated episodes after defecation/micturition/swallowing/coughing (situational syncope)\n - After a meal (vasovagal or orthostatic hypotension)\n- Prodromal symptoms?\n - Feeling warm/hot, sweating, nausea (vasovagal)\n - Déjà vu or jamais vu (epilepsy)\n- Intercurrent illness?\n - e.g. diarrhoea and vomiting leading to dehydration and hypotension\n- Associated symptoms?\n - Palpitations/chest pain/shortness of breath (cardiac/PE)\n - Headache (subarachnoid haemorrhage)\n - Visual disturbance (if worse on standing may be orthostatic hypotension/vasovagal)\n - Lightheadedness (orthostatic hypotension/vasovagal)\n \n**Questions to ask about during the blackout:**\n \n- Any protective measures taken?\n - e.g. hands outstretched to break fall \n - It can be difficult to ascertain whether the patient lost consciousness\n - If protective measures were observed may be a fall rather than a blackout\n - Patients having a vasovagal may lower themselves to the floor\n- Tongue biting?\n - Lateral tongue typical in epilepsy\n - Tip of tongue typical in vasovagal\n- Incontinence of bowels or bladder? (epilepsy)\n- Duration of loss of consciousness\n - Less than 30 seconds (suggests syncope)\n - Over 1 minute (suggests epilepsy)\n - Over 5 minutes (psychogenic causes more likely)\n- Seizure activity observed?\n - Myoclonic jerks are common in vasovagal syncope\n - Prolonged limb jerking and abnormal posturing suggests a seizure\n- Appearance during blackout e.g. pallor, eyes closed or open? \n \n\n**Questions to ask about after the blackout:**\n\n- Any injuries sustained during the blackout?\n - Ask about site and severity\n- Confusion or amnesia after conciousness regained?\n - If lasts minutes may indicate post-ictal state after a seizure\n- Focal neurological signs (e.g. weakness down one side)\n\n**Other important questions:**\n\n- Any previous blackouts/similar events?\n- Past medical history e.g. any heart disease?\n- Medications (may contribute to orthostatic hypotension)\n- Family history including sudden cardiac or unexplained death in young relatives\n- Recreational drug and alcohol use (alcohol may exacerbate orthostatic hypotension)\n\n**On examination:**\n\n- Do a full set of observations including a lying standing blood pressure to assess for a postural drop\n - A fall in systolic blood pressure by 20mmHg or more or diastolic by 10mmHg or more, or a fall in the systolic to <90mmHg with symptoms indicates orthostatic hypotension\n- Full systems examination focusing on the heart (e.g. any murmurs or abnormalities of the pulse?)\n- Neurological examination including cognitive function (may be abnormal in the post-ictal state)\n \n# Investigations\n \nInitial investigations as follows should be carried out in the emergency setting; patients should also be referred for further specialist investigations (e.g. EEG for epilepsy, Holter monitoring for suspected arrhythmias) as appropriate.\n\n- **Blood glucose** for hypoglycaemia\n- **ECG** looking for arrhythmias, ischaemic changes or evidence of structural abnormalities (e.g. left ventricular hypertrophy in severe aortic stenosis)\n- **Blood tests** looking for electrolyte abnormalities that could trigger seizures or arrhythmias, anaemia in haemorrhage, raised inflammatory markers in intercurrent illness, AKI in dehydration\n- **Transthoracic Echocardiography** should be done in suspected structural heart disease (e.g. aortic stenosis)\n- **24 hour ambulatory blood pressure monitoring** with an activity diary may be useful to assess for e.g. post-prandial hypotension\n \n# Management\n \n- Specific emergency management may be required for any serious cause identified (e.g. head injury, ruptured aortic aneurysm).\n- Investigate for and treat any injuries resulting from the collapse and provide analgesia.\n- Some patients can be discharged with reassurance and advice e.g. uncomplicated vasovagal episode, situational syncope.\n- Patients with suspected epilepsy should be referred to a first fit clinic.\n- Patients with suspected psychogenic causes of blackouts should also be referred for neurology assessment as these can be difficult to differentiate from epilepsy\n- Patients with suspected cardiac syncope (e.g. abnormal ECG, exercise-induced syncope, heart murmur, heart failure, new/unexplained breathlessness or family history of sudden cardiac death in the young/inherited cardiac condition) should be referred for specialist review within 24 hours.\n- Consider urgent referral for cardiovascular review in all patients over 65 with syncope and no prodromal symptoms.\n- All patients with syncope of unclear cause should be referred for specialist cardiovascular review (with urgency based on the clinical picture)\n\n **Driving advice for patients with syncope:**\n\n- Patients with unexplained syncope must inform the DVLA and their licence will be revoked for 6 months (12 months if Group 2) \n- Patients with a vasovagal whilst standing can drive and need not inform the DVLA if they are Group 1 drivers (Group 2 drivers must not drive and should inform the DVLA)\n- Patients with cardiac syncope must not drive and should inform the DVLA - group 1 drivers may be allowed to drive after 4 weeks if a cause is identified and treated\n- Full guidance including for seizures can be found in the references section\n \n# NICE Guidelines\n \n[NICE CKS Guidance on Blackouts](https://cks.nice.org.uk/topics/blackouts/)\n\n[NICE: Transient loss of consciousness ('blackouts') in over 16s](https://www.nice.org.uk/guidance/cg109)\n \n# References \n \n[DVLA guidance on transient loss of consciousness](https://www.gov.uk/guidance/neurological-disorders-assessing-fitness-to-drive#transient-loss-of-consciousness-blackouts--or-lostaltered-awareness)",
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"question": "A 16-year-old female presents to the emergency department after an episode of loss of consciousness witnessed by her mother. Her mother reports that her daughter fell to the floor without warning then started shaking and making grunting noises. Her eyes were closed throughout, and her main movements were back arching and pelvic thrusting. She reports that she has bitten the tip of her tongue but retained continence. The episode lasted about 5-10 minutes in total.\nBlood tests, urinalysis and examination findings are all normal.\nWhat is the most likely diagnosis?",
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"explanation": "An arterial blood may be normal in Guillain-Barré Syndrome, with hypoxia or hypercapnoea being a late sign of impending neuromuscular respiratory failure. Spirometry is recommended as a more accurate reflection of a patients requirement for respiratory support",
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"explanation": "In the absence of signs and symptoms of pulmonary embolism, CTPA is unlikely to be of value in this case. A normal CTPA does not preclude the need for intubation in Guillain-Barré Syndrome",
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"explanation": "Whilst a chest x-ray would rule out other causes of breathlessness, this patient is presumed to have Guillain-Barré Syndrome, and a chest x-ray is likely to be normal, and would not help to predict the need for intubation",
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"explanation": "A lumbar puncture in Guillain-Barré Syndrome typically shows an elevated cerebrospinal fluid (CSF) protein with a normal cell count. LP findings do not correlate with severity of illness or need for intubation",
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"explanation": "This patient has Guillain-Barré Syndrome (GBS), characterised by the preceding gastrointestinal illness and the pattern of bilateral ascending weakness. Bedside spirometry, particularly forced vital capacity (FVC) has a significant correlation with the risk of respiratory failure and need for intubation. If the FVC < 20mL/Kg, the patient likely needs intensive care, and if <15mL/Kg, likely requires intubation",
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"comment": "My dude you feel like shit? Here blow into the plastic tube for me.",
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"comment": "See I knew that but I didn't know that",
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"explanation": "## Summary\n\nGuillain-Barré Syndrome (GBS) is an acute inflammatory demyelinating polyneuropathy characterised by a rapid, progressive, ascending symmetrical weakness, often preceded by infection. Diagnosis is largely clinical but supported by specific investigations such as lumbar puncture and nerve conduction studies. Treatment is mainly supportive, with options for disease-modifying treatments like intravenous immunoglobulins (IVIG) or plasmapheresis in severe cases.\n\n## Definition\n\nGBS is an ascending inflammatory demyelinating polyneuropathy, typified by an acute onset of bilateral and roughly symmetric limb weakness. \n\n## Epidemiology\n\nThe prevalence of GBS is approximately 1-2 cases per 100,000 worldwide.\n\n## Aetiology\n\nGBS typically occurs 1-3 weeks following an infection, with common culprits being Campylobacter, mycoplasma, and Epstein-Barr Virus (EBV). \n\n40% of cases, however, are idiopathic. \n\nOther potential triggers include infections such as CMV, HIV, Hepatitis A, or following certain vaccinations such as for tetanus, rabies, or swine flu.\n\n## Signs and symptoms\n\nNeurological decline often progresses over days to weeks.\n\nClinical features of GBS include:\n\n- Progressive ascending symmetrical limb weakness (usually starting with the lower limbs)\n- Lower back pain due to radiculopathy\n- Paraesthesia, often preceding motor symptoms\n- Potential respiratory muscle involvement in severe cases\n- Potential cranial nerve involvement leading to diplopia, facial droop\n- **Lower motor neurone** signs in the lower limbs: hypotonia, flaccid paralysis, areflexia\n- Cranial nerve signs: ophthalmoplegia, lower motor neurone facial nerve palsy, bulbar palsy\n- Potential autonomic dysfunction (e.g., arrhythmia, labile blood pressure)\n\n## Variants\n\nSeveral variants of GBS exist, each presenting with unique characteristics:\n\n- Paraparetic variant\n - Primarily affects the lower limbs\n\n- Miller-Fisher syndrome\n - Presents with ataxia, ophthalmoplegia, and areflexia\n - Associated with **anti-GQ1B antibodies**\n\n- Pure motor variant\n - Ascending weakness without sensory involvement\n\n- Bilateral facial palsy with paraesthesias\n - Affects the cranial nerves\n\n- Pharyngeal-brachial-cervical weakness\n - Results in weakness of the upper limbs\n - Associated with **anti- GT1a antibodies**\n- Bickerstaff's Brainstem Encephalitis\n - Presents with encephalitis, ophthalmoplegia, and ataxia\n\nIt's worth noting that these variants rarely present purely as described, and there's often overlap in clinical presentation.\n\n\n## Differential diagnosis\n\n- Vascular: occasionally, brainstem strokes may present similarly\n- Infective/Inflammatory: \n - Polio: asymmetrical weakness from myelitis\n - Lyme disease\n - CMV\n - HIV\n - TB\n - Transverse myelitis \n - Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) \n - Myasthenia gravis\n- Traumatic/Structural:\n - Spinal cord compression\n- Metabolic:\n - Porphyrias: may result in an acute neuropathy\n - Electrolyte derangements: hypokalaemia, hypophosphataemia, hypermagnesaemia\n\t\n\n## Investigations\n\nInvestigations for GBS include:\n\n- Monitoring of forced vital capacity (FVC) for respiratory muscle involvement\n- Cardiac monitoring for autonomic instability\n- Blood tests, including arterial blood gas (ABG)\n- Serological tests: Anti-ganglioside antibodies\n- Lumbar puncture: may show **albuminocytological dissociation** \n\t- Increased level of protein (albumin) without a corresponding increase in white blood cells (cytology)\n- Nerve conduction studies\n\t- May show prolongation or loss of the F wave\n- Identification of the underlying cause: stool cultures, serology, CSF virology\n\n## Management\n\nManagement of GBS is primarily supportive and includes:\n\n- Regular monitoring of FVC\n\t- Early involvement of intensive care is essential if any reduction in FVC as deterioration may be rapid\n- Venous thromboembolism (VTE) prophylaxis: TEDS + LMWH\n- Analgesia: NSAIDs or opiates for radiculopathy-related back pain\n- Management of cardiac arrhythmias as per ALS guidelines\n- Careful use of antihypertensives due to potential autonomic dysfunction\n- Consideration of enteral feeding in those with unsafe swallow\n\nSpecific medical management for those with significant disability (e.g., inability to walk) include:\n\n- Intravenous immunoglobulin (IVIG) over a 5-day course\n- Plasmapheresis, which has similar efficacy to IVIG but is associated with more side effects.\n\n## Prognosis\n\nWhile GBS can be life-threatening, particularly when respiratory muscles are affected or in the presence of autonomic dysfunction, the majority of patients experience full recovery. \n\nHowever, residual fatigue and weakness can persist in some patients. Certain variants of GBS, like Miller-Fisher syndrome, generally have a good prognosis with full recovery being the norm. \n\nPrognostic indicators include speed of onset, severity at nadir, age and the presence of preceding diarrhoeal illness.\n\n## References\n\n1. Van den Berg, B., Walgaard, C., Drenthen, J., Fokke, C., Jacobs, B. C., & Van Doorn, P. A. (2014). Guillain–Barré syndrome: pathogenesis, diagnosis, treatment and prognosis. Nature Reviews Neurology, 10(8), 469-482.\n\n2. Yuki, N., & Hartung, H. P. (2012). Guillain–Barré syndrome. New England Journal of Medicine, 366(24), 2294-2304.\n\n3. Hughes, R. A., & Cornblath, D. R. (2005). Guillain-Barré syndrome. The Lancet, 366(9497), 1653-1666.\n\n4. Willison, H. J., Jacobs, B. C., & Van Doorn, P. A. (2016). Guillain-Barré syndrome. The Lancet, 388(10045), 717-727.\n",
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"question": "A 65-year-old male attends the Emergency Department complaining of progressive numbness and weakness that started in his legs and moved slowly up his body. He has recently had an episode of diarrhoea and vomiting after eating a \"dodgy takeaway\".\n\nHe has been transferred to the hospital's adjoining tertiary neurology centre with a presumed diagnosis of Guillain-Barré Syndrome (GBS). On arrival in the neurology ward, he appears breathless.\n\nWhat is the most appropriate investigation to help predict the need for intubation?",
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"explanation": "We know that this patient has postural hypotension, and therefore lying and standing blood pressure measurements would prove this to be true. However, there are many causes for postural hypotension in the elderly, and therefore this would not prove a Parkinson's plus syndrome",
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"explanation": "Parkinson's disease is closely linked to Lewy Body Dementia, and therefore in all patients with Parkinson's disease, it is important to assess cognitive function. However, this would not account for the recurrent falls and would not be likely to aid further diagnosis here.",
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"explanation": "This history is not suggestive of syncopal episodes as a cause for his falls. Whilst an ECG should always be performed in patients with recurrent falls to look for arrhythmias; a stand-alone ECG is unlikely to pick up a cause for falls. 24 hour Halter monitoring is more sensitive and would be a reasonable investigation if there were concerns about a cardiac cause for his falls",
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"explanation": "The two main differential diagnoses in this scenario are Progressive Supranuclear Palsy (PSP) and Multiple system atrophy (MSA). This patient likely has a Parkinson's plus syndrome as he has symptoms of autonomic instability (urinary incontinence, postural hypotension and recurrent chest infections, which raises a concern about poor swallow), and the co-benyldopa does not seem to have had much effect. It's important to test for vertical gaze palsy to help you narrow down your differential diagnosis. ",
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"explanation": "# Summary\n\nParkinsonism refers to a group of neurological conditions that share the core motor features of Parkinson’s disease—bradykinesia, rigidity, resting tremor, and postural instability. While Parkinson’s disease is the most common cause of parkinsonism, several other important neurodegenerative conditions can present with a similar signs and symptoms. These conditions are collectively known as **Parkinson-plus syndromes**. These include **progressive supranuclear palsy (PSP)**, **multiple system atrophy (MSA)**, **Lewy body dementia (LBD)**, and **corticobasal degeneration (CBD)**. \n\n## Progressive Supranuclear Palsy (PSP)\n\n- Also known as **Steele-Richardson-Olszewski syndrome**\n- Early postural instability and frequent falls.\n- **Impairment of vertical gaze** (particularly downgaze).\n- Stiff, broad-based gait.\n- Parkinsonism (bradykinesia, rigidity).\n- An MRI of the brain may show a **hummingbird sign**, a characteristic shape of midbrain atrophy seen in PSP.\n\n\n\n## Multiple System Atrophy (MSA)\n\n- Presents with parkinsonism and early **autonomic dysfunction**. \n- It is divided into two types based on the predominant symptoms:\n\t1. **MSA-P** (Parkinsonian type): Similar to Parkinson's disease but with early autonomic issues.\n\t2. **MSA-C** (Cerebellar type, also known as Shy-Drager syndrome): Presents with **cerebellar ataxia**, alongside parkinsonism. Early signs include **postural hypotension**, **urinary incontinence**, and **erectile dysfunction** (an early prominent feature in men).\n- Generally exhibits poor response to levodopa therapy\n\n\n## Lewy Body Dementia (LBD)\n\n- Characterised by **dementia and parkinsonism**, often occurring within one year of each other. \n- The hypothesised pathophysiology involves the early death of dopaminergic neurons in the **cerebrum**, which then extends to the basal ganglia, leading to motor symptoms.\n- Unlike Alzheimer’s, LBD affects **attention and executive function** early on, with less involvement of memory (hippocampus). \n- **Visual hallucinations** are a prominent feature and tend to occur early in the disease.\n\n## Corticobasal Degeneration (CBD)\n\n### Key Clinical Features:\n- Unilateral parkinsonism, typically affecting one limb.\n- **Alien limb phenomenon**.(patients feel that their limbs move involuntarily outside of their control\n- **Cortical sensory loss** (patients cannot recognise objects by touch despite normal sensory input).\n- **Apraxia** (difficulty with purposeful movement despite intact motor function).\n\n\n## Other Conditions Mimicking Parkinsonism\n\n### Vascular Parkinsonism\n\n- Often affects the **lower limbs** and is seen in patients with a history of **vascular disease** (e.g., strokes). \n- Patients develop gait issues with rigidity and bradykinesia predominantly in the lower extremities.\n\n### Dementia Pugilistica\n\n- Also known as **chronic traumatic encephalopathy** (CTE), this condition arises from **repetitive head trauma**, commonly seen in **boxers**. \n- It presents with parkinsonism and cognitive decline.\n\n### Drug-Induced Parkinsonism\n\n- Caused by medications such as **antipsychotics** (e.g., haloperidol, risperidone), **metoclopramide**, and **prochlorperazine**.\n- Onset is typically **rapid** and **bilateral**.\n- Management involves stopping the offending drug and, in some cases, using **procyclidine** to manage symptoms.\n- Can lead to **neuroleptic malignant syndrome** (a life-threatening condition characterized by fever, rigidity, and altered mental status).\n",
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"question": "A 74-year-old male is referred to the falls clinic after he suffers three mechanical falls at home within two months. He has a past medical history that includes postural hypotension, urinary incontinence, recurrent chest infections and six months ago was diagnosed with Parkinson's disease. He currently takes, co-benyldopa and has just finished a course of amoxicillin. On examination, you note that he has hypomimia, rigidity and bradykinesia with a very mild tremor.\n\nYou suspect a Parkinson's Plus Syndrome. Which of the following would you perform next?",
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"explanation": "Cerumen (ear wax) in the ear canal is one of the most common causes of conductive hearing loss. It would not lead to a change in the appearance of the tympanic membrane",
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"explanation": "Tympanosclerosis refers to calcification of the middle ear and tympanic membrane. The aetiology is not fully understood, but the major risk factors are middle ear infections and grommet insertion. The condition is characterised by chalky white patches on the tympanic membrane and a conductive pattern of hearing loss",
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"comment": "Probably important to note here that negative Rinne's = BC>AC (referring to a true negative Rinne's) as I've only really seen it written out in full",
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"explanation": "# Summary\n\nTympanosclerosis is a condition characterised by chronic inflammation and scarring of the tympanic membrane, leading to its subsequent calcification. Patients typically present with significant hearing loss and chalky-white patches on the tympanic membrane. Key investigations include an otoscopic examination and audiometric testing. Management strategies include the use of hearing aids and, in refractory cases, surgical excision of the sclerotic areas and repair of the ossicular chain.\n\n# Definition\n\nTympanosclerosis is a chronic disease that involves inflammation, fibrosis, and calcification of the tympanic membrane and other structures within the middle ear.\n\n# Epidemiology\n\nThe epidemiology of tympanosclerosis is not well understood due to the paucity of data. However, it is known to be associated with certain risk factors such as a history of chronic otitis media and tympanostomy tube insertion.\n\n# Aetiology\n\nThe exact cause of tympanosclerosis remains unclear, but it is believed to be associated with chronic otitis media and the insertion of tympanostomy tubes, also known as grommets. Other potential contributing factors may include trauma, ototoxic drugs, and genetic predisposition.\n\n# Signs and Symptoms\n\nThe primary symptom of tympanosclerosis is significant hearing loss. Upon physical examination, the tympanic membrane will often display chalky white patches due to the calcification process.\n\n[lightgallery]\n\n# Differential Diagnosis\n\nThe differential diagnosis for tympanosclerosis includes:\n- Chronic otitis media: Characterised by recurrent ear infections, persistent ear discharge, fullness or pressure in the ear, and hearing loss.\n- Otosclerosis: Presents with progressive conductive hearing loss, tinnitus, and occasionally vertigo.\n- Cholesteatoma: Symptoms include hearing loss, ear discharge, and a sensation of fullness or pressure in the ear.\n\n# Investigations\n\nThe diagnosis of tympanosclerosis typically involves a comprehensive otoscopic examination and audiometric testing to assess the degree of hearing impairment.\n\n# Management\n\nManagement of tympanosclerosis primarily involves addressing the hearing loss. Common strategies include:\n- The use of hearing aids to improve auditory function.\n- In cases that are refractory to hearing aids, surgical intervention may be considered. This involves the excision of the sclerotic areas and repair of the ossicular chain.",
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"question": "A 40-year-old man with a history of recurrent right-sided otitis media presents with a one-month history of gradually worsening hearing loss in his right ear. He denies any other symptoms, and his past medical history is otherwise unremarkable.\n\nOn examination, otoscopy reveals chalky white patches on the tympanic membrane. Rinne's test is negative on the right, and Weber's test lateralises to the right ear.\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "A subarachnoid haemorrhage is an important differential in this context, given the history of severe headache and reduced GCS. However, he is not in the right age range for a subarachnoid haemorrhage. In any case, you will likely get a CT Head for this patient but this is not the single best answer",
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"comment": "wouldnt his wife have it too usually",
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"comment": "Would the oxygen saturations be wrongly high at 100%?\n",
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"comment": "O2 sats are supposedly falsely high in CO poisoning as the sats probe detects 'bound' haemoglobin, which is the case of CO it strongly binds.",
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"comment": "So much wrong. Similarly an Arterial ABG would also show MetHB - wtf\n",
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"comment": "for the love of all that is fuck, WHY does he have a severe headache?????????????????",
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"explanation": "# Summary\n\nCarbon monoxide is a tasteless, odourless and invisible gas that may be produced by fires, faulty gas appliances and fuel-burning heaters. Signs and symptoms include confusion, nausea, vomiting, hypotension and dizziness. Pulse oximetry typically shows close to 100% oxygen saturations as monitors cannot differentiate between haemoglobin bound to oxygen or carbon monoxide. A blood gas will show high levels of carboxyhaemoglobin, and breath tests can be used to measure exhaled carbon monoxide. High-flow oxygen is the mainstay of treatment, with hyperbaric oxygen considered for certain high risk patients. \n \n\n# Definition\n \nCarbon monoxide poisoning is a serious and potentially fatal condition caused by acute or chronic inhalation of carbon monoxide gas. This gas is colourless and odourless, and can only be detected by equipment such as carbon monoxide alarms. It is produced by the incomplete combustion of fuel (when insufficient oxygen is present), for example in faulty heaters or cooking equipment.\n \n# Epidemiology\n \nIn England, there are approximately 4000 A&E attendances per year with carbon monoxide poisoning and approximately 40 deaths. Around half of cases are due to accidental exposure and around 40% are due to self-harm (e.g. from intentional inhalation of exhaust fumes in an enclosed space). \n\nPoisoning is more common in winter when heating equipment is more likely to be used, and is more common in groups affected by socio-economic deprivation.\n\nSome patient groups are more sensitive to the effects of carbon monoxide poisoning, including:\n\n- The elderly\n- Young children\n- Pregnant women \n- People with anaemia\n- People with cardiovascular disease\n\n# Aetiology\n\nInhaled carbon monoxide binds to haemoglobin with a much greater affinity than oxygen, forming carboxyhaemoglobin. This causes tissue hypoxia, especially affecting organ systems with a high oxygen demand such as the central nervous system and the cardiovascular system.\n\n**Prevention of carbon monoxide poisoning:**\n\n- Carbon monoxide alarms should be fitted in the home\n- Gas appliances should be correctly installed and be regularly serviced\n- Vulnerable patients (e.g. disabled or elderly patients) may be entitled to free annual gas safety checks\n- Landlords have a legal duty to ensure gas appliances are checked at least yearly\n- Do not burn charcoal indoors for cooking or heating\n- Do not use gas appliances if you suspect they may be faulty\n\n# Signs and Symptoms\n\n- Headache\n- Dizziness\n- Lethargy\n- Flushing\n- Myalgia and weakness\n- Confusion\n- Nausea and vomiting\n- Cherry red skin (rare)\n- Tachycardia and hypotension\n- Seizures\n\n# Differential Diagnosis\n \n- **Migraine:** headache is the predominant symptom of many cases of carbon monoxide poisoning; migraine is more likely to be associated with aura, photophobia and phonophobia\n- **Viral infections:** cause overlapping symptoms of headache and myalgia, may have other symptoms such as cough or fever not seen in carbon monoxide poisoning\n- **Diabetic ketoacidosis:** may have similar symptoms of nausea and vomiting, lethargy and weakness; blood glucose will be high with raised ketones\n \n# Investigations\n\n**Bedside tests:**\n\n- **Pulse oximetry** is likely to show close to 100% oxygen saturations; this is artifactual as the devices cannot differentiate carboxyhaemoglobin and oxyhaemoglobin.\n- A **blood gas** (either venous or arterial) should be taken to confirm the diagnosis by measuring carboxyhaemoglobin\n - The normal level in non-smokers is 1–2%\n - In smokers 5-10% is normal (heavy smokers can tolerate up to 15%)\n - Carboxyhaemoglobin of 10% or more is usually indicative of carbon monoxide poisoning\n - Toxicity usually manifests at levels of 15-20%\n - Carboxyhaemoglobin of 20% or higher is usually associated with severe cerebral or cardiac ischaemia\n- An **ECG** should be done to look for ischaemic changes\n- **Capillary blood glucose** to rule out hypoglycaemia or hyperglycaemia as a cause for lethargy and confusion\n\n**Blood tests:** \n\n- **FBC** for anaemia\n- **U&Es** for renal impairment\n- **CK** for rhabdomyolysis\n- **Troponin** for myocardial ischaemia\n- **Lactate** - may indicate concurrent cyanide exposure if high in the context of smoke exposure\n\n# Management\n \n- Take an **A to E approach** and ensure the airway is protected in the first instance\n- Administer **100% oxygen** via a tight-fitting face mask (if high-flow nasal cannulae available these can be used to administer up to 60L/min oxygen)\n- Continue high-flow oxygen until any symptoms have resolved and carboxyhaemoglobin levels are 2% or lower in non-smokers or 10% or lower in smokers\n- Correct hypotension with **IV fluids**\n- Contact the **National Poisons Information Service** (NPIS) if advice required\n- In certain severe cases (e.g. carboxyhaemoglobin > 25%) **hyperbaric oxygen therapy** may be considered however its use is currently not recommended by the NPIS\n- **Inform the local Health Protection Team** who will coordinate services to address the source of carbon monoxide poisoning\n\n# Complications\n\nMost patients will recover fully from carbon monoxide poisoning, although in a minority of people (generally those who have had severe or prolonged exposure) neuropsychiatric complications may develop, including:\n\n- Emotional lability and personality change\n- Difficulty concentrating\n- Insomnia\n- Lethargy\n- Movement disorders such as chorea and Parkinsonism\n- Memory impairment and dementia\n- Psychosis\n- Neuropathy\n\n# NICE Guidelines\n\n[NICE CKS - Carbon Monoxide Poisoning](https://cks.nice.org.uk/topics/carbon-monoxide-poisoning/)\n\n# References\n \n[RCEM Learning - Carbon Monoxide Poisoning](https://www.rcemlearning.co.uk/reference/carbon-monoxide-poisoning/)\n\n[London Fire Brigade - Carbon Monoxide Safety](https://www.london-fire.gov.uk/safety/the-home/carbon-monoxide-safety/)",
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"question": "A 75-year-old man presents to the Emergency Department (ED), having been found collapsed at his home by his wife. His wife tells you that they recently moved to a new house and had been moving things into the basement.\n\nOn assessment, he reports a severe headache and has a GCS of 14. On examination, there is significant accessory muscle usage, tachypnoea and vesicular breath sounds are heard throughout both lung fields. Oxygen saturations are 96% on room air. An arterial blood gas (ABG) shows a PaO<sub>2</sub> of 11.5kPa (>11kPa) and a PCO<sub>2</sub> of 5.1kPa (4.5-6kPa).\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "Given his underlying COPD and age, this patient has high risk characteristics associated with his pneumothorax. As it is greater than 2cm (i.e. amenable to drainage), guidelines suggest that chest drain insertion is the best management",
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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 65-year-old patient with a background of chronic obstructive pulmonary disease (COPD) presents with acute onset chest pain and shortness of breath.\n\nOn assessment, he has decreased chest expansion in the left upper zones with associated hyper-resonance and reduced air entry. A chest x-ray confirms a 2.5 cm left sided apical pneumothorax.\n\nWhich of the following is the next best step in management.",
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"explanation": "300mg of amiodarone is used in cardiac arrest secondary to VF or VT. However, it is only given after the 3rd shock",
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"comment": "The question needs to make it clear whether he does or does not have a pulse at this point - this would determine whether or not we follow the ALS algorithm. ",
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"comment": "Exactly!",
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"comment": "I don't think you need to know he has a pulse at this stage, from the stem you know he's in VT and receiving CPR - whether or not he has a pulse he's going to need a shock. Although I do agree the stem should probably make it clearer he's in VT and not another rhythm. ",
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"comment": "if he has no pulse, you'd do shock. if he does have a pulse, it becomes VT so you wont do ALS.",
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"comment": "“A man has a cardiac arrest in hospital” means no pulse chief, VT with pulse is not a cardiac arrest ",
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"comment": "tachycardia outpatient out here doing CPR on people with pulses...",
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"comment": "The stem says he's in cardiac arrest, i.e. pulseless... It could be clearer but that's absolutely clear enough to me. Also the option of synchronised cardioversion (treatment of choice for VT with a pulse with haemodynamic compromise - like collapse in this patient) is not an option. You're really missing the point of the question if you got this wrong guys",
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"comment": "VT needs a synchronised shock not unsycn",
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"comment": "That's VT WITH a pulse, the case is describing WITHOUT a pulse as he has \"had a cardiac arrest\" and is \"receiving CPR\". Unsynchronised cardioversion is another way of saying defibrillation",
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"comment": "Questioning why they couldn't have just labelled this as \"requires shock\", in a real life situation I'm not going to state he needs unsynchronised cardioversion at 200j ",
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"explanation": "# Summary\n\nAdvanced Life Support (ALS) describes an algorithmic approach to the management of a cardiac arrest by those trained in delivering it. It involves early recognition, taking steps to secure the airway and initiate high quality chest compressions and obtaining intravenous or intraosseous access promptly. Cardiac monitoring should be applied to identify if the rhythm is shockable or non-shockable, which determines what treatment is given. Shockable rhythms require defibrillation, with adrenaline and amiodarone given later on; non-shockable rhythms are treated with adrenaline. \n\n# Definition\n\nAdvanced Life Support is a guideline-based approach to treating patients who have had a cardiac arrest to improve the chances of successful resuscitation and survival. \n\n# Epidemiology\n\nCardiac arrests can be categorised into those that occur out of hospital and those that occur in hospitals. Most out of hospital cardiac arrests occur at home (72%) and 8 out of 10 are due to a cardiac cause. In 7 out of 10 cases resuscitation is attempted, however only 9% of these patients survive to hospital discharge.\n\nIn hospital cardiac arrests tend to occur in older patients (average age 70), with return of spontaneous circulation (ROSC) achieved in 53% of patients. However, only 24% of patients survive to hospital discharge. \n\n# Aetiology\n\nCauses of cardiac arrest can be remembered using the 4Hs and 4Ts mnemonic:\n\n- Hypoxia\n- Hypovolaemia\n- Hypo/hyperkalaemia (and other electrolyte abnormalities)\n- Hypo/hyperthermia\n- Thromboembolism (pulmonary embolism or coronary artery thrombosis)\n- Tamponade\n- Tension pneumothorax\n- Toxins \n\n# Classification\n\nCardiac arrests are managed differently depending on whether the rhythm is **shockable** or **non-shockable**.\n\n**Shockable** rhythms are:\n\n- **Pulseless Ventricular Tachycardia (pVT)** - regular broad complex tachycardia\n- **Ventricular Fibrillation (VF)** - chaotic irregular deflections of varying amplitude\n\n**Non-shockable** rhythms are:\n\n- **Pulseless Electrical Activity (PEA)** - electrical activity that should produce a pulse, but doesn't due to absent or insufficient cardiac output \n- **Asystole** - no detectable electrical activity \n\n# Management\n\n## Management for all cardiac arrests\n\n- **Rapid recognition** of cardiac arrest (ineffective breathing or absent central pulse) is key \n- The first responder should start **cardiopulmonary resuscitation (CPR)** immediately and **call for help**, for example by asking for a cardiac arrest call (2222) to be put out\n- Every two minutes CPR should be stopped for a **rhythm check**\n- Secure the **airway**\n - Oropharyngeal or nasopharyngeal airways may be used initially with a bag valve mask for ventilation\n - Either a supraglottic airway (laryngeal mask airway or i-gel) or an endotracheal tube should be inserted\n - Tracheal intubation should only be attempted by those with a high success rate\n - Confirm the position of the endotracheal tube with waveform capnography (measuring end-tidal carbon dioxide)\n- Give **high-flow oxygen**\n- Gain IV access - if not possible the intraosseous (IO) route can be used\n- Consider reversible causes (as above) and treat as appropriate\n - IV or IO fluids if secondary to hypovolaemia\n - Thrombolysis if secondary to pulmonary embolism\n - Point of care ultrasound (POCUS) may be used to investigate for cardiac tamponade and pneumothorax\n \n## Management of shockable rhythms\n\n- **Defibrillation** should be delivered as early as possible\n - Remove oxygen (ventilator circuits can remain attached)\n - Ensure no one is touching the patient before the shock is delivered\n - No specific energy is specified in guidelines; anything from 120 to 360 joules is suitable\n- Immediately resume CPR after the shock is delivered for two minutes\n- After 3 shocks, give 300mg amiodarone and 1mg adrenaline IV or IO\n- Give repeat doses of adrenaline every 3-5 minutes (i.e. every other cycle)\n- After 5 shocks, give a further dose of amiodarone 150mg\n\n## Management of non-shockable rhythms \n\n- Give adrenaline 1mg IV or IO as soon as possible\n- Give repeat doses of adrenaline every 3-5 minutes (as per shockable rhythms)\n- Defibrillation and amiodarone are not used unless the rhythm changes to a shockable one\n\n# NICE Guidelines\n\n[NICE CKS - Advanced Life Support](https://cks.nice.org.uk/topics/cardiac-arrest-out-of-hospital-care/management/advanced-life-support-adult/)\n\n# References\n\n[Resuscitation Council UK - Adult Advanced Life Support Guidelines](https://www.resus.org.uk/library/2021-resuscitation-guidelines/adult-advanced-life-support-guidelines)\n \n[Resuscitation Council UK - Epidemiology of Cardiac Arrest](https://www.resus.org.uk/library/2021-resuscitation-guidelines/epidemiology-cardiac-arrest-guidelines)\n\n[BNF Treatment Summaries - Cardiopulmonary Resuscitation](https://bnf.nice.org.uk/treatment-summaries/cardiopulmonary-resuscitation/)",
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"explanation": "# Summary\n\n\nDisseminated intravascular coagulation (DIC) is a haematological emergency, characterized initially by the inappropriate activation of the clotting cascades, leading to thrombus formation (in microvasculature) and depletion of clotting factors and platelets, which then results in bleeding. Key signs and symptoms include excessive bleeding (such as epistaxis, gingival bleeding, haematuria, and bleeding from cannula sites), fever, confusion, and potential coma. The physical signs include petechiae, bruising, confusion, and hypotension. Key investigations include testing for thrombocytopenia, increased prothrombin time, increased fibrin degradation products (such as D-dimer), and decreased fibrinogen. Management strategies revolve around treating the underlying cause and supportive care.\n\n\n# Definition\n\n\nDisseminated intravascular coagulation (DIC) is a complex condition that describes the inappropriate activation of the clotting cascades, resulting in thrombus formation and subsequently leading to the depletion of clotting factors and platelets.\n\n\n# Epidemiology\n\n\nDIC often occurs in the context of severe systemic disease (see aetiology below). DIC is often encountered in a hospital setting, particularly in intensive care units, surgical wards, and obstetric units due to the high prevalence of associated risk factors. It is associated with a high mortality rate, with the outcome is largely dependent on the prompt diagnosis and treatment of the underlying cause.\n\n\n# Aetiology\n\n\n- Major trauma or burns\n- Multi-organ failure\n- Severe sepsis or infection\n- Severe obstetric complications\n- Solid tumours or haematological malignancies \n- **Acute promyelocytic leukaemia (APL)** is an uncommon subtype of AML that is associated with DIC \n- **Note**: This comes up frequently in written exams\n\n\n# Signs and Symptoms\n\n\nPatients with DIC commonly present with:\n\n\n- Excessive bleeding e.g. epistaxis, gingival bleeding, haematuria, bleeding/oozing from cannula sites\n- Fever\n- Confusion\n- Potential coma\n\n\nPhysical signs include:\n\n\n- Petechiae\n- Bruising\n- Confusion\n- Hypotension\n\n\n# Differential Diagnosis\n\n\nThe differential diagnosis for DIC includes conditions that cause similar symptoms such as:\n\n\n- Other coagulopathies, which may also present with excessive bleeding and bruising\n- Sepsis, which can cause fever, confusion, and hypotension\n- Multi-organ failure, which can cause a similar range of systemic symptoms including confusion and hypotension\n\n\n# Investigations\n\n\n- Blood tests, including:\n- FBC (thrombocytopenia)\n- Blood film may show schistocytes due to microangiopathic haemolytic anaemia (MAHA)\n- Raised d-dimer (a fibrin degradation product)\n- Clotting profile - increased prothrombin time (due to consumption of clotting factors), increased APTT, decreased fibrinogen (consumed due to microvascular thrombi)\n\n\n# Management\n\n\nManagement of DIC is primarily focused on treating the underlying cause. Supportive care is also essential to manage symptoms and prevent complications. This may include transfusions of platelets or clotting factors, and in some cases, anticoagulation therapy may be necessary.",
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"comment": "I thought this could be hypoglycaemia..... happened to me when i was in DKA ",
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"explanation": "# Summary\n \nDiabetic ketoacidosis (DKA) is a life-threatening medical emergency characterised by hyperglycemia, acidosis and ketosis. DKA may be triggered by infection, dehydration or fasting, or may be the initial presentation of Type 1 diabetes. Symptoms include a 'fruity' breath odour, vomiting, dehydration, abdominal pain and altered mental state. Key investigations include blood glucose and ketones, urea and electrolytes and a venous blood gas to check pH. Management involves IV fluids and a fixed rate insulin infusion, with close monitoring both clinically and biochemically. Important complications that should be monitored for include cerebral oedema, hypoglycaemia and hypokalaemia. \n\n# Definition\n \nDiabetic ketoacidosis (DKA) is a medical emergency characterised by the triad of:\n \n - Hyperglycemia (blood glucose >11 mmol/L)\n - Ketosis (blood ketones >3 mmol/L or urinary ketones ++ or higher)\n - Acidosis (pH <7.3 or bicarbonate <15 mmol/L)\n - Note: patients on SGLT-2 inhibitors may present with euglycemic DKA (where glucose is normal)\n \n\n# Epidemiology\n \nDKA is most common in individuals with Type 1 diabetes (T1DM) but around a third of cases occur in patients with Type 2 diabetes. The incidence of DKA is highest in young people aged 18-24. \n\nDKA is the leading cause of death in people aged under 58 years old with T1DM, with cerebral oedema the most common cause of mortality. However, mortality in the UK is still <1%.\n \n\n# Aetiology \n\n- DKA occurs due to insulin deficiency (absolute or relative) leading to hyperglycaemia\n- Ketones, including acetone, 3-beta-hydroxybutyrate, and acetoacetate, are produced from ketogenesis, whereby fatty acids are metabolised as an alternative energy source\n- These ketones are responsible for the acidosis seen\n- Hyperglycaemia causes an osmotic diuresis that contributes to severe dehydration as well as electrolyte imbalance\n- Vomiting and decreased fluid intake secondary to altered mental state also exacerbate dehydration\n\n**10-20% of presentations of DKA represent a first presentation of Type 1 Diabetes**\n\n**Common triggers for DKA include:**\n\n- Infections\n- Dehydration and fasting\n- Missing doses of insulin\n- Medications e.g. steroid treatment or diuretics\n- Surgery\n- Stroke or myocardial infarction\n- Alcohol excess or illicit drug use\n- Pancreatitis\n\n# Classification\n\nPatients with at least one of the following may be classified as having **severe DKA**, which should prompt consideration of referral for higher dependency care:\n\n- Blood ketones > 6mmol/L\n- Bicarbonate < 5mmol/L\n- Blood pH < 7\n- Anion gap above 16\n- Hypokalaemia on admission\n- GCS less than 12\n- Oxygen saturations < 92% in air\n- Systolic BP < 90mmHg\n- Brady or tachycardia (heart rate < 60 or > 100bpm)\n\n\n# Signs and Symptoms\n \n**Symptoms:**\n\n- Nausea and vomiting\n- Abdominal pain\n- Polyuria\n- Polydipsia\n- Weakness\n\n**Signs:**\n\n- Dry mucous membranes\n- Hypotension\n- Tachycardia\n- Altered mental state (drowsiness, confusion, coma)\n- Kussmaul's breathing (deep, sighing breathing to compensate for metabolic acidosis by blowing off carbon dioxide)\n- Fruit-like smelling breath (due to ketosis)\n\n# Investigations\n \n**Bedside tests:**\n \n - Capillary blood glucose\n - Blood or urinary ketones\n - Urine dip +/- MSU (looking for evidence of a urinary tract infection which may precipitate DKA)\n - ECG (for ischaemic changes which may precipitate DKA, or changes secondary to electrolyte imbalance e.g. hypokalaemia)\n\n**Blood tests:**\n\n- Venous blood gas (for acid-base balance)\n- Urea and electrolytes (for electrolyte imbalance and AKI)\n- Full blood count and CRP (for infection markers) \n- Blood cultures (if infection is suspected)\n- HbA1c (to assess diabetic control over recent months)\n\n**Imaging:**\n\n- Consider chest X-ray as part of septic screen (if signs of infection as a trigger for DKA)\n\n# Management\n\n**Initial management:** \n\n- Initial **A to E assessment**\n - Drowsy patients may require airway protection and an **NG tube** to prevent aspiration\n - Ensure adequate IV access\n - If hypotensive give up to 1L in **fluid boluses** then seek urgent senior input if not resolved\n - Consider urinary catheterisation and monitor fluid balance\n- **IV fluid replacement with normal saline**\n - A regimen of large volumes of IV fluid replacement given relatively quickly initially then over longer durations should be followed\n - Slower infusion rates should be considered in young adults, the elderly, those with heart or kidney failure or other serious comorbidities\n - An example in a healthy adult would be 1L over 1 hour, then 2x 1L over 2 hours, then 2x 1L over 4 hours, then 1L over 6 hours\n - **Potassium replacement** should be added after the first bag, depending on serum potassium levels, bearing in mind potassium can be infused at a maximum of 10mmol/h:\n\n| Potassium level (mmol/L) | Potassium replacement mmol/L of next infusion | \n| :---------------: | :----------------: \n| > 5.5 | Nil | \n| 3.5 - 5.5 | 40 mmol/L | \n| < 3.5 | senior review – additional potassium required | \n \n \n- After IV fluids have started, a **fixed rate insulin infusion** should be set up \n- This is provided as an infusion of 50 units of Actrapid in 50ml of 0.9% NaCl, at a rate of 0.1 units/kg/hour\n- Continue long-acting insulin if the patient is already on this \n- Investigation and management of any underlying triggers (e.g. septic screen and start antibiotics if evidence of infection)\n- Ensure **VTE prophylaxis** with low molecular weight heparin is prescribed as patients are at high risk of developing clots due to dehydration\n\n**Ongoing emergency management:**\n\n- Patients should be closely monitored with hourly blood glucose and ketones\n - The aim is for ketones to fall by > 0.5mmol/L/hour\n - Blood glucose should fall by 3 mmol/L/hour\n - If these targets are not met, the rate of insulin infusion should be continued\n- Once blood glucose is below 14, a **10% glucose infusion** should be started alongside ongoing saline and insulin\n- Regular venous blood gases should also be done to monitor potassium, bicarbonate and pH\n- DKA is considered resolved once ketones are less than 0.6 mmol/L and pH is over 7.3 \n - If at this point they are able to eat and drink, a subcutaneous regimen of insulin should be started (usually with the input of a specialist diabetes team)\n - The insulin infusion should be stopped half an hour after the first dose of subcutaneous short acting insulin has been given \n\n# References\n \n[ABCD Guidelines: The Management of Diabetic\nKetoacidosis in Adults](https://abcd.care/sites/default/files/site_uploads/JBDS_Guidelines_Current/JBDS_02_DKA_Guideline_with_QR_code_March_2023.pdf)\n\n[RCEM - Diabetic Ketoacidosis](https://www.rcemlearning.co.uk/reference/diabetic-ketoacidosis/#1635853037528-05d8fa0f-621f)\n\n[Patient UK - Diabetic ketoacidosis](https://patient.info/doctor/diabetic-ketoacidosis#presentation)",
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"explanation": "# Summary\n\nA haemorrhagic stroke results from the rupture of a cerebral vessel, leading to intracranial bleeding. Signs include severe headache, altered consciousness, meningism and focal neurological deficits. CT Head is the first-line investigation to quickly identify haemorrhage. MRI scans may be used to provide more detailed images and help identify an underlying cause. Management should be in a specialist unit (either a stroke unit or neurocritical care) with a focus on optimal blood pressure control, particularly in the early phase. Any anticoagulation treatment should be reversed and blood pressure control is key to optimising outcomes. In select cases, surgical decompression may be considered.\n\n# Definition\n\nHaemorrhagic stroke is a cerebrovascular event that occurs when there is bleeding into the brain parenchyma, ventricles or subarachnoid space. This may lead to haematoma formation with raised intracranial pressure, as well as neuronal damage.\n \n# Epidemiology\n\n- Haemorrhagic strokes contribute to 10% to 20% of strokes annually\n- Incidence is around 12 to 15% per 1,000,000 per year \n- Incidence is more common in men and increases with age\n- The case fatality rate is 25 to 30% \n\n\n# Aetiology\n \nRisk factors for haemorrhagic stroke include:\n\n - Older age \n - Male sex\n - Family history of haemorrhagic stroke\n - Haemophilia and other bleeding disorders\n - Cerebral amyloid angiopathy (CAA)\n - **Hypertension**\n - Anticoagulation therapy\n - Recreational drugs such as cocaine and amphetamines\n - Arteriovenous malformations (particularly in younger patients)\n\n# Signs and Symptoms\n \n- Severe headache\n- Altered consciousness, ranging from drowsiness to coma\n- Vomiting\n- Nuchal rigidity\n- Focal neurologic signs e.g. weakness, visual loss, sensory changes\n- Aphasia\n- Seizures\n- Hypertension\n \n# Differential Diagnosis\n \n- **Ischaemic stroke:** Both present with sudden onset neurological defict. Headache is more likely in haemorrhagic stroke. CT is required to rule out haemorrhage before treating for ischaemic stroke\n- **Space-occupying lesion:** e.g. a brain tumour can cause similar symptoms of headache, focal neurological deficits and altered consciousness however these are usually chronic and progressive rather than acute in onset\n- **Meningitis:** also causes headache, meningism and altered mental status; more likely to have features of infection e.g. fevers, tachycardia \n- **Hypertensive encephalopathy:** also presents with acute onset of headache, confusion, visual disturbances and seizures associated with hypertension; may have other complications e.g. myocardial ischaemia, renal dysfunction, differentiated from stroke with a CT head\n \n# Investigations\n \n**Bedside tests:**\n\n- **Capillary blood glucose** as maintaining normoglycaemia improves outcomes \n- **Blood pressure** is important to monitor as a potential cause and during the management blood pressure control is key\n- **ECG** as there may be cardiac complications of haemorrhagic stroke e.g. arrhythmias\n- **Urine toxicology screen** if illicit drug use is suspected\n\n**Blood tests:**\n\n- **FBC** and **CRP** for inflammatory markers \n- **Coagulation screen** to identify any bleeding diathesis\n- **U&Es** to identify any renal impairment that may be associated with hypertension\n- **LFTs** as a baseline\n\n**Imaging**\n\n- **Non Contrast CT head** is the key investigation to identify haemorrhagic stroke\n- **MRI head** may be done in some cases to give more detail, identify an underlying cause and plan treatment\n- **MR angiography** or **digital subtraction angiography** can help identify any vascular abnormalities that may have caused the haemorrhage\n\n# Management\n \n- Emergency management of a haemorrhagic stroke should involve urgently contacting the stroke team +/- critical care (for example in cases with reduced consciousness)\n- Urgent neurosurgical referral may be required e.g. for haematoma evacuation\n- Reverse any anticoagulation treatment or clotting disorders\n- Rapid blood pressure lowering should be initiated in patients with a systolic blood pressure of 150-220 mmHg \n - This is usually with IV antihypertensives such as GTN or labetalol\n - Aim for a systolic blood pressure of below 140 mmHg, but without a fall of > 60 mmHg in the first hour of treatment\n - This excludes patients with an underlying structural cause (e.g. an aneurysm), a GCS below 6 and those who are going for early neurosurgery\n- Make patients nil by mouth until they have had a swallowing assessment\n- Assess hydration and give fluids if dry\n- Management of subarachnoid haemorrhage and raised intracranial pressure is addressed in a separate chapter\n\n# Complications\n\n- Decreased mobility e.g. hemiparesis or hemiplegia\n- Seizures\n- Delirium\n- Hydrocephalus due to bleeding into the ventricles\n- Cardiac complications e.g. arrhythmias\n- Recurrence of haemorrhagic stroke\n- Increased risk of infection e.g. aspiration pneumonia\n- Increased risk of falls in the longer-term\n- Incontinence\n- Neuropathic or musculoskeletal pain\n- Fatigue\n- Cognitive decline\n\n# Prognosis\n\n- Mortality is significantly higher than in ischaemic stroke - approximately 30% at 30 days\n- There is also a higher risk of recurrence; 3.2 per 100 patient years in haemorrhagic stroke\n- Morbidity is also high - at 3-6 months after a haemorrhagic stroke only 20-30% of patients are able to live independently\n- Poor prognostic factors include larger volume haemorrhages, old age, intraventricular bleeding and impaired consciousness at presentation\n\n# NICE Guidelines\n\n[NICE - Stroke and transient ischaemic attack in over 16s](https://www.nice.org.uk/guidance/ng128)\n\n[NICE CKS - Stroke and TIA](https://cks.nice.org.uk/topics/stroke-tia/)\n\n# References\n\n[RCEM Learning - Stroke in the ED](https://www.rcemlearning.co.uk/reference/stroke-in-the-ed/)\n\n[National Clinical Guideline for Stroke for the UK and Ireland](https://www.strokeguideline.org/)\n \n[Patient UK - Cerebrovascular Events](https://patient.info/doctor/cerebrovascular-events)",
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"explanation": "# Criteria used when assessing capacity in adults\n\nThere are **four criteria** used when assessing capacity in adults.\n\n1. The individual must be able to understand the information relating to the decision\n2. The individual must be able to retain that information\n3. The individual must be able to weigh up the information and reach a conclusion\n4. The individual must be able to communicate the decision they have made.\n\n# Ways to Meet the Criteria \n\nHelp and support can be provided in order to enable an individual to meet the above assessment criteria. For example, using simple language in order to explain the information, or allowing someone to communicate their decision in a number of ways (in writing, verbally, in sign-language, or their normal form of communication, etc.)\n\n# Mental Capacity Act \n\nIf an individual is not able to do any of the above four criteria, then the Mental Capacity Act (MCA) will assess them and therefore treat them as lacking capacity for that specific decision in question.\n\n# Fluctuating Capacity \n\nIt is important to note here that capacity is not absolute. Sometimes, an individual's capacity can fluctuate (e.g. someone with dementia). Or in other circumstances, someone will have the capacity to make a decision on something simple but not something more complex. It is therefore always important to assess whether individuals have the capacity to make a _specific_ decision at that time.",
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"question": "A 56-year-old man with progressive motor neurone disease is assessed by the speech and language team due to concerns about his swallowing.\n\nFollowing the assessment, the recommendation is that he would benefit from a pureed diet to reduce the risk of aspiration.\n\nHaving explained the recommendation and the risks associated with continuing with a normal diet, the patient refuses and states that he wishes to continue with a normal diet. He can understand, retain and weigh up the decision but only able to communicate in writing.\n\nWhich of the following is the next best step in management?",
"sbaAnswer": [
"a"
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173,469,888 | false | 9 | null | 6,495,312 | null | false | [] | null | 6,480 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Drivers have a legal duty to inform the Driver and Vehicle Licensing Agency (DVLA) if they have a condition that impairs their ability to drive. A doctor should inform the patient of this duty and make every reasonable effort to make sure they do this. However, if a patient continues not to disclose the information, doctors have a **_professional duty_** to break confidentiality in the public's best interests",
"id": "32399",
"label": "b",
"name": "Conditions that impair the ability to drive",
"picture": null,
"votes": 2292
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "In these cases, the doctor should first try and convince the patient to make the disclosure themselves. If this is not possible, a doctor should disclose the necessary information only and try and avoid identifying the patient where possible. This would be considered a case where a doctor may have a **legal defence** for breaching confidentiality in the public's best interests",
"id": "32402",
"label": "e",
"name": "Disclosing personal information to a sexual partner",
"picture": null,
"votes": 64
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Identification of patients who are suspected of committing a road traffic offence is one of the specific statutory requirements where doctors have a legal duty to break confidentiality",
"id": "32398",
"label": "a",
"name": "Identification of a patient who committed a road traffic offence",
"picture": null,
"votes": 705
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "General Medical Council (GMC) guidance in 2017 has highlighted that there is no duty to inform the police in the case of serious crime. However, a doctor may still break confidentiality if they believe that it is in the public's best interests. In these cases, there may be a **legal defence** for breaching confidentiality",
"id": "32401",
"label": "d",
"name": "Gunshot/knife wounds",
"picture": null,
"votes": 1293
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "If the harm is only to the patient, a doctor should accept a competent adult's refusal to disclose information. However, if there are any children involved, a referral to social services is mandated",
"id": "32400",
"label": "c",
"name": "Domestic violence involving a young couple",
"picture": null,
"votes": 374
}
],
"comments": [
{
"__typename": "QuestionComment",
"comment": "The world is f***ed. a road traffic offense > terrible shit",
"createdAt": 1647371001,
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"comment": "quesnitch",
"createdAt": 1675014673,
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"comment": "surely this is wrong?",
"createdAt": 1677067237,
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"comment": "say mums ",
"createdAt": 1683080904,
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"comment": "Do docs have to report you sell crack?",
"createdAt": 1694612059,
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"explanation": "# Overview\n\nPatients have a legal right to confidentiality (under both Common Law and Human Rights Law), and doctors have the corresponding legal duty to provide this right to confidentiality.\n\nHowever, this right to confidentiality is not absolute. There are a number of situations in which the law obliges doctors to breach confidentiality, i.e. there is a legal duty to breach confidentiality. There are also some situations where a doctor has a legal defence to breach confidentiality.\n\n# Legal Duties to Breach Confidentiality\n\n1. If ordered to by a court or judge\n2. To satisfy statutory requirements\n\n _e.g. to inform the local authority about notifiable diseases under the Public Health Act 1984_\n\n _e.g. under the Road Traffic Act, must provide identifying information to the police on request_\n\n _e.g. under the Terrorism Act 2000, must report any suspicions of terrorism_",
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"question": "A junior medical student has learnt that all patients have a legal right to confidentiality. However, he is unsure of the circumstances in which confidentiality can be breached.\n\nIn which of the following situations does a doctor have a legal duty to breach confidentiality?",
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"a"
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173,469,889 | false | 10 | null | 6,495,312 | null | false | [] | null | 6,481 | {
"__typename": "QuestionSBA",
"choices": [
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "It is good practice to discuss patients' wishes regarding CPR even in cases such as this where it is unlikely to be successful. This is important to maintain an honest and transparent patient-doctor relationship",
"id": "32403",
"label": "a",
"name": "Explore the patient's wishes regarding CPR",
"picture": null,
"votes": 3322
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Although CPR is unlikely to be successful, it would be inappropriate to complete a DNACPR form without a discussion regarding the matter with the patient",
"id": "32405",
"label": "c",
"name": "Complete a do not attempt cardiopulmonary resuscitation (DNACPR) as CPR is not likely to be successful",
"picture": null,
"votes": 133
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "CPR should be discussed with the patient prior to making a decision on whether they should be for it or not.",
"id": "32407",
"label": "e",
"name": "Proceed with full treatment and keep the patient for CPR",
"picture": null,
"votes": 1195
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "It would not be appropriate to ask the patient's family for their opinion without the patient's prior consent unless this was done in the patient's best interest. There are no signs to suggest that the patient lacks capacity in this case so it would be worth speaking to the patient first",
"id": "32406",
"label": "d",
"name": "Ask the patient's family about their thoughts on CPR",
"picture": null,
"votes": 11
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Although CPR is unlikely to be successful, there is no reason why active treatment for the patient's stroke and cancer should not continue",
"id": "32404",
"label": "b",
"name": "Explain to the patient why active treatment will not be offered",
"picture": null,
"votes": 94
}
],
"comments": [
{
"__typename": "QuestionComment",
"comment": "Very good question. Finally some real quesmed stuff",
"createdAt": 1709051181,
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"comment": "but CPR is a medical decision? If the pt's decision was to be resuscitated it would probably be overriden anyway? \"exploring the pt's wishes\" sounds like the decision is being made by the patient",
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"__typename": "QuestionComment",
"comment": "Guess it's about making the patient feel heard before telling them anyway",
"createdAt": 1736727565,
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"concept": {
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"explanation": "# Overview\n\nA Do Not Attempt CPR (DNACPR) decision can also be known as Do Not Attempt Resuscitation (DNAR)\n\nA DNACPR decision provides information to healthcare professionals present on the best action to take if an individual suffers a cardiac arrest. A DNACPR is recorded, normally on a CPR Decision form, but is not in itself legally binding. This means that a doctor can overrule an existing DNACPR if they believe the circumstances do mean CPR would be in the patient's best interests.\n\nA DNACPR can be made if cardiac or respiratory arrest is an expected part of the dying process, and either CPR will not be successful, or if CPR may be successful but the clinical outcomes (e.g. trauma and prognosis) mean it is not clinically appropriate. A patient with capacity may also refuse CPR.\n\n# Best Interests \n\nDoctors can ultimately make the decision to put a DNACPR in place if it is in the patient's _best interests_, even if the patient themselves or their family disagrees. However, following a legal case in 2014, doctors must engage the patient and those close to them on the decision to make a DNACPR, and inform them if the decision to make a DNACPR order has occurred.\n\n# R (Tracey) v Cambridge University Hospitals NHS Foundation Trust, 2014 \n\nJanet Tracey died in Addenbrooke's Hospital in March 2011. She had been diagnosed with terminal lung cancer and had subsequently been involved in a car crash, in which she sustained a spinal injury. She required ventilation in the Intensive Care Unit (ICU), and after attempts to remove her from the ventilator were unsuccessful, a DNACPR notice was placed in her medical notes. Neither Janet Tracey nor her family were consulted about or informed of this decision.\n\nThe legal case concluded in favour of Tracey, finding that her Human Rights had been breached. The case acknowledged that the decision to put a DNACPR in place is ultimately a medical decision, and patients cannot demand treatment. But, the case did result in changes to DNACPR guidance:\n\nFirstly, the decision to not tell a patient about a DNACPR notice can no longer be based on the fact that telling them would cause “distress”. Only if discussing a DNACPR order would cause the patient “physical or psychological harm”, can doctors justify not discussing it. In other circumstances, doctors are legally obliged to discuss a DNACPR order that has been made.\n\nSecondly, it used to be the case that doctors were not obliged to discuss a DNACPR decision if the clinical decision has been made that CPR would be futile. This case amended this, making it a legal obligation for doctors to inform the patient that a DNACPR decision has been made, regardless of whether or not CPR could ever be successful (i.e. futility of CPR is justification for doctors making a best interests decision to make a DNACPR order - even if the patient wants CPR, but doctors are still legally obliged to inform the patient that a DNACPR order has been made).\n\nA DNACPR decision relates only to CPR, and is not a refusal of any other treatment.",
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"learningPoint": "In advanced care planning, it is essential to discuss patients' wishes regarding CPR, regardless of their prognosis.",
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"question": "An 85-year-old man with a background of metastatic prostate cancer is admitted to hospital with a stroke. On examination, he has significant left-sided weakness and sensory loss but no disturbance in cognition or speech.\n\nWhich of the following is the most appropriate next step in regards to advanced care planning?",
"sbaAnswer": [
"a"
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} | MarksheetMark |
173,469,890 | false | 11 | null | 6,495,312 | null | false | [] | null | 6,482 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Duty of candour states that \"all healthcare professionals should be open and honest with patients when treatment or care causes, or has the potential to cause, harm or distress\". In this situation, the doctor should contact the patient as soon as possible and inform them of the error. They should also report the incident so it can be investigated internally to reduce similar occurrences in the future",
"id": "32408",
"label": "a",
"name": "Professional duty of candour",
"picture": null,
"votes": 3949
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Confidentiality is a legal right that all patients have. Although the doctor has inadvertently breached confidentiality by informing the patient of another patients test results, duty of candour is more pertinent given that a patient is likely to undergo an unnecessary operation",
"id": "32409",
"label": "b",
"name": "Confidentiality",
"picture": null,
"votes": 548
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The doctrine of double effect states that if the primary intervention was in a patient's best interests, then an unintended adverse effect is not necessarily unlawful. It does not apply in this case",
"id": "32410",
"label": "c",
"name": "The doctrine of double effect",
"picture": null,
"votes": 182
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Informed consent relies on the principles of the patient being fully informed, having mental capacity and not being coerced into a decision. It is not applicable in this case as the patient has consented to a surgery based on the wrong information",
"id": "32411",
"label": "d",
"name": "Informed consent",
"picture": null,
"votes": 78
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Shared decision refers to a process where both the doctor and the patient contribute towards making a personalised decision on management",
"id": "32412",
"label": "e",
"name": "Shared decision making",
"picture": null,
"votes": 31
}
],
"comments": [
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"__typename": "QuestionComment",
"comment": "We thank you for your candour!",
"createdAt": 1685953534,
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"__typename": "QuestionComment",
"comment": "are all dr's griffindor?",
"createdAt": 1704405614,
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"explanation": "# Overview\n\nAccording to guidance from the General Medical Council, it is important to respond constructively when things go wrong. It is important to establish _open and honest_ communication, and do the following:\n\n- Apologise (**this is not an admission of liability**)\n- Explain what has happened\n- Notify a senior clinician\n- Direct the patient and their family to the Patient Advice and Liaison Service, and advise them on the complaints procedure\n- Explain to them what investigations will be carried out",
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"question": "A 32-year-old woman attends an appointment in the emergency surgery clinic due to persistent abdominal pain.\n\nThe patient is seen by a doctor and listed for an outpatient cholecystectomy following a review of the imaging she had the previous day.\n\nHowever, it transpires that the doctor has mistakenly reviewed the imaging of a patient with the same name, having failed to check the patient's age and hospital number.\n\nWhich of the following principles is most pertinent following identification of this error?",
"sbaAnswer": [
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173,469,891 | false | 12 | null | 6,495,312 | null | false | [] | null | 6,488 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Croup (acute laryngotracheobronchitis) is an upper airways disease that is most common in children aged between 6 months to 3 years. It usually presents with difficulty in breathing, fever, stridor and a seal or dog-like barking-cough on the background of a coryzal illness. Parainfluenza virus is the most common causative organism",
"id": "32438",
"label": "a",
"name": "Parainfluenza",
"picture": null,
"votes": 2947
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Bordetella is the causative agent in pertussis (whooping cough). This is a bacterial infection that is rarer than croup due to effective vaccination. Pertussis can present with an inspiratory gasp; however, the high-pitching rasping sound described in the question is more suggestive of stridor",
"id": "32441",
"label": "d",
"name": "Bordetella pertussis",
"picture": null,
"votes": 558
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Rhinovirus is a well-recognised cause of croup; however, it is less common than parainfluenza",
"id": "32442",
"label": "e",
"name": "Rhinovirus",
"picture": null,
"votes": 93
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "RSV can cause croup; however, parainfluenza is more common. RSV is the most common causative organism in bronchiolitis",
"id": "32439",
"label": "b",
"name": "Respiratory syncytial virus (RSV)",
"picture": null,
"votes": 1680
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Mycoplasma is a rare cause of croup",
"id": "32440",
"label": "c",
"name": "Mycoplasma pneumoniae",
"picture": null,
"votes": 45
}
],
"comments": [
{
"__typename": "QuestionComment",
"comment": "Is the only reason this isn't bronchiolitis is that he has a high pitched rasping sound on inspiration?",
"createdAt": 1684171756,
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{
"__typename": "QuestionComment",
"comment": "Also somewhat out of the peak age bracket for it? I know things aren't that exact in real life but this is quesmed",
"createdAt": 1684494198,
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"explanation": "# Summary\n \n\nCroup (also known as acute laryngotracheobronchitis) is a common childhood infection characterised by a harsh barking cough and inspiratory stridor. It is usually mild and self-limiting, however, some cases may cause severe respiratory distress requiring hospitalisation and supportive treatment. Parainfluenza viruses are the commonest causes, but the diagnosis is a clinical one and as symptoms such as stridor can worsen if the child is distressed, investigations should only be done if necessary. Oral steroids should be given to all children; in moderate to severe cases nebulised adrenaline, supplementary oxygen and airway support may be indicated.\n \n\n# Definition\n \n\nCroup, or acute laryngotracheobronchitis, is an upper respiratory tract infection that in most cases has a viral aetiology. Key symptoms include a barking cough, hoarse voice and inspiratory stridor. \n\n# Epidemiology\n \n\nCroup commonly affects children aged from 6 months old to 3 years old, with the peak incidence at 2 years. It is uncommon after the age of 6.\n\nSimilar to other viral infections, it is commonest in the autumn and winter months and is linked to parainfluenza epidemics. \n\n# Aetiology\n \nThe commonest cause is the parainfluenza virus. Other viral causes include adenovirus, respiratory syncytial virus (RSV), rhinovirus and influenza.\nRarely, bacteria can cause croup (e.g. Mycoplasma pneumoniae).\n\nThe pathophysiology involves infection and resulting inflammation of the subglottic and laryngeal mucosa which causes partial obstruction of the airways leading to respiratory distress and stridor.\n\n# Signs and Symptoms\n\n- The prodromal phase of coryzal symptoms, fever and a non-specific cough usually lasts 12-72 hours.\n- Characteristic symptoms of croup such as the harsh barking cough, hoarse voice or cry and inspiratory stridor then develop - these tend to be worse at night.\n- In severe cases, children may become drowsy and lethargic, or conversely more agitated.\n- The usual course of disease is resolution of symptoms within 48 hours (up to a week at most).\n\nOn examination, look for the following red flags that may indicate impending respiratory failure:\n\n- Signs of respiratory distress e.g. intercostal recessions, accessory muscle usage, tachypnoea\n- Cyanosis\n- Decreased level of consciousness\n- Stridor may decrease due to worsening airway obstruction\n- Decreased air entry on auscultation of the chest\n- Tachycardia\n\n# Differential Diagnosis\n \n\n- **Epiglottitis**: Sudden onset high fever, drooling, and dysphagia are seen without the barking cough of croup. Usually secondary to Haemophilus influenzae B and so significantly rarer since routine immunisation against this.\n- **Bacterial tracheitis**: Suspect if acute deterioration following initial viral symptoms, with high fevers, stridor and respiratory distress.\n- **Foreign body aspiration**: No prodrome or fever, usually sudden onset of choking, cough or wheeze after eating or playing with small objects.\n- **Anaphylaxis**: Rapid onset stridor, possible urticarial rash and facial swelling; suspect if history of previous episodes with allergens or family history of atopy.\n \n\n# Investigations\n \nDiagnosis is clinical, and investigations need to be carefully considered as distressing the child may lead to worsening of symptoms due to agitation.\n\nFurther investigation may include: \n\n- Pulse oximetry should be done to determine if supplementary oxygen is required.\n- Chest X-ray may be of use if a differential diagnosis such as an inhaled foreign body is suspected. \n - In croup, an X-ray may show a steeple sign, where the upper trachea is seen to taper.\n \n\n# Management\n\nClassifying the severity of croup is key to determining appropriate management:\n\n| Severity | Description |\n|------------------------------|---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|\n| Mild | Seal-like barking cough but no stridor or sternal/intercostal recession at rest. |\n| Moderate | Seal-like barking cough with stridor and sternal recession at rest; no (or little) agitation or lethargy. |\n| Severe | Seal-like barking cough with stridor and sternal/intercostal recession associated with agitation or lethargy. |\n| Impending respiratory failure | Minimal barking cough, stridor may become harder to hear. Increasing upper airway obstruction, sternal/intercostal recession, asynchronous chest wall and abdominal movement, fatigue, pallor or cyanosis, decreased level of consciousness or tachycardia. The degree of chest wall recession may diminish with the onset of respiratory failure as the child tires. A respiratory rate of over 70 breaths/minute is also indicative of severe respiratory distress. |\n\nMild cases with no stridor or chest wall recessions at rest may be treated at home with a single dose of oral dexamethasone (0.15mg/kg). In children treated at home, families should be safety-netted on signs of deterioration and advised to check on the child regularly and encourage fluids. Paracetamol or ibuprofen can be used for fever and pain.\n\nChildren with any of the following should be considered for hospital admission:\n\n* Stridor and/or sternal recession at rest\n* High fever\n* Respiratory rate > 60\n* Cyanosis\n* Lethargy or agitation\n* Fluid intake < 75% of normal or no wet nappies for 12 hours\n* Aged under 3 months\n* Chronic conditions such as immunodeficiency, chronic lung disease or neuromuscular disorders\n\nManagement is supportive as there is no treatment indicated for the usual causative viruses, and may include:\n\n- Supplementary oxygen if low saturations - consider how best to deliver this so as not to distress the child (e.g. a parent holding an oxygen mask to the face)\n- Steroids for all - if unable to swallow oral dexamethasone or prednisolone can give nebulised budesonide\n- Nebulised adrenaline for temporary symptom relief\n- Anaesthetics +/- ENT input if concerns regarding airway or respiratory failure\n\n# Complications\n\n- Dehydration secondary to poor fluid intake during illness\n- Pneumonia due to secondary bacterial infection \n- Respiratory failure \n- Death is very rare (1 in every 30,000 cases)\n\n# Prognosis\n\nUsually, symptoms resolve within 48 hours but may last longer. Occasionally, severe upper airway obstruction can occur, causing respiratory failure and arrest.\n\n# NICE Guidelines\n\n[NICE CKS: Croup](https://cks.nice.org.uk/topics/croup/)\n\n# References\n \n[BNF Treatment summaries: Croup](https://bnf.nice.org.uk/treatment-summaries/croup/)\n\n[Patient.info: Croup](https://patient.info/doctor/croup-pro)",
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"question": "A 2-year-old boy presents to the paediatric emergency department (ED) after his parents noted that he was struggling with his breathing. They note that for the last three days, he has had a dry cough and runny nose with mild temperature spikes.\n\nOn examination, the boy is tachypnoeic and using his accessory muscles. His temperature is 38°C, and there is a high-pitched rasping sound audible during inspiration.\n\nGiven the likely diagnosis, which of the following is the most likely causative organism?",
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"explanation": "The most likely diagnosis is lymphogranuloma venerum (LGV). This is a sexually transmitted infection that is caused by specific serovars of Chlamydia trachomatis. The primary infection of infection is characterised by painless genital ulceration. The secondary stage follows weeks later with painful, inguinal and/or femoral lymphadenopathy (buboes). The first-line treatment option is with a three-week course of doxycycline",
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"explanation": "This is the first-line treatment for syphilis. Although primary syphilis presents with a painless genital ulcer, secondary syphilis would present differently with features such as a maculopapular rash, generalised lymphadenopathy and constitutional symptoms",
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"explanation": "Aciclovir can be used for recurrent cases of genital herpes which is caused by Herpes simplex virus. Genital herpes would present with painful genital ulceration and it is not associated with buboes",
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"explanation": "Conservative management would be the first-line treatment for genital herpes. Genital herpes would present with painful genital ulceration and it is not associated with buboes",
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"explanation": "Ceftriaxone is the first-line treatment for uncomplicated, anogenital gonorrhoea. The clinical vignette is suggestive of LGV which is caused by Chlamydia species",
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"comment": "Would have been nice if stem mentioned whether lymphadenopathy is tender or not",
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"comment": "Doesn't mention painful lymphadenopathy at all. This could be syphilis? ",
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"comment": "stem did not mention pain. pain = LGV, painless = syphilis ",
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"comment": "painless ulcer but painful lymphadenopathy in LGV*",
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"comment": "My thoughts are if the majority of people get the answer wrong it's probably a vague question that would be taken out of the exam anyway so I am not gonna sweat it ",
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"comment": "Is LGV bilateral a reason for it being answer ",
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"comment": "I thought LGV would usually be unilateral?",
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"comment": "Is the ans LGV because picture is showing 'groove sign'? ",
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"comment": "This question came up on full screen whilst I was sat in a coffee shop. Can't imagine what the other people must've thought",
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"explanation": "# Summary\n\n\nLymphogranuloma venereum (LGV) is a sexually transmitted infection caused by specific serovars (L1, L2, or L3) of *Chlamydia trachomatis*. Characterised by painless genital ulcers and inguinal lymphadenopathy, LGV is more common in men who have sex with men. Its diagnosis is mainly based on molecular techniques, like PCR, to detect *C. trachomatis* from a swab of the ulcer. Management involves a 21-day course of antibiotics, including doxycycline, tetracycline, or erythromycin. \n\n\n# Definition\n\n\nLymphogranuloma venereum (LGV) is a sexually transmitted infection (STI) predominantly caused by the L1, L2, or L3 serovars of *Chlamydia trachomatis*.\n\n\n# Epidemiology\n\n\nLGV is more frequently observed in men who have sex with men (MSM). HIV infection is also a risk factor.\n\n\n# Aetiology\n\n\nThe aetiology of LGV involves infection with the L1, L2, or L3 serovars of *Chlamydia trachomatis*, typically through sexual contact.\n\n\n# Signs and Symptoms\n\n\n- Painless genital ulcer\n- Typically appears 3-12 days after infection\n- It might go unnoticed, particularly if it occurs inside the vagina\n- Inguinal lymphadenopathy, often noticeable\n- Proctitis, associated with rectal pain and discharge (in case of rectal infections)\n- Systemic symptoms can include fever and malaise\n\n\n# Differential Diagnosis \n\n\n- **Primary syphilis**: Presents with a solitary, painless genital ulcer (chancre) and regional lymphadenopathy.\n- **Herpes simplex virus infection**: Characterised by multiple painful vesicles or ulcers, systemic symptoms, and occasional inguinal lymphadenopathy.\n- **Chancroid**: Caused by *Haemophilus ducreyi*, it presents with painful genital ulcers and painful inguinal lymphadenopathy.\n\n\n# Investigations\n\n\nMolecular diagnostic techniques, such as polymerase chain reaction (PCR), are used to detect *C. trachomatis* from a swab of the genital ulcer.\n\nIt is also important to screen for other sexually transmitted infections and blood-borne infections such as HIV.\n\n\n# Management\n\n\nThe standard treatment for LGV involves antibiotics. Common regimes include:\n\n\n- Oral doxycycline: 100 mg administered twice daily for 21 days\n- Oral tetracycline: 2 g administered daily for 21 days\n- Oral erythromycin: 500 mg given four times daily for 21 days\n\n\n# References\n\n\n[BASHH guidelines: Lymphogranuloma venereum](https://www.bashhguidelines.org/media/1054/2013-lgv-guideline.pdf)",
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"question": "A 24-year-old homosexual male presents with a two-week history of enlarging lumps in both sides of his groin. He reports noticing a painless penile ulcer around three weeks ago that resolved spontaneously.\n\nHe denies any other symptoms on questioning but reports having had multiple sexual partners over the last three months.\n\nExamination of his groin is significant for the findings shown in the image below.\n\n[lightgallery]\n\nGiven the likely diagnosis, which of the following is the most appropriate treatment option?",
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"explanation": "This is a reasonable next step test if you are concerned that this is secondary amenorrhoea due to a hypothalamic or pituitary cause. In this case it's more likely to be due to intensive exercise",
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"name": "Serum FSH and LH measurement",
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"explanation": "TVUS is an invasive examination and would therefore not be the initial investigation of choice. A TVUS may be indicated where the pregnancy test is negative and polycystic ovary syndrome is a possible cause of her amenorrhoea",
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"explanation": "A high testosterone might indicate an androgen secreting tumour or polycystic ovary syndrome which is less likely in this example",
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"explanation": "Whilst the most likely cause is exercise induced amenorrhoea, a urinary pregnancy test is indicated in this patient in the first instance",
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"comment": "why all the thumbs down? good question as reminds you to always remember pregnancy",
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"explanation": "# Summary\n \n \nSecondary amenorrhoea is characterised by the absence of menstruation for six months or more in a woman who previously had regular menstrual cycles. The most common cause is pregnancy, but other factors such as breastfeeding, menopause, intrauterine adhesions, PCOS, drug-induced amenorrhoea, physical stress, pituitary gland pathology, and thyroid issues can also be responsible. Key signs and symptoms include absence of menstruation, and depending on the underlying cause, symptoms of pregnancy, menopause, or other related conditions. Investigations typically involve pregnancy tests, hormone level checks, and imaging studies. Management strategies depend on the underlying cause and can range from lifestyle changes and medication to surgery in severe cases.\n \n \n# Definition\n \n \nSecondary amenorrhoea is defined as the absence of menstruation for six months or longer in a woman who has previously had regular menstrual cycles.\n \n \n# Epidemiology\n \n \nSecondary amenorrhoea is a common condition affecting approximately 4-5% of women of reproductive age. It is most frequently observed in women aged 20-39 years.\n \n \n# Aetiology\n \n \nThe potential causes of secondary amenorrhoea include:\n \n \n - Pregnancy (most common cause)\n - Breastfeeding\n - Menopause\n - Intrauterine adhesions leading to outflow tract obstruction (Asherman's syndrome)\n - Polycystic ovary syndrome (PCOS)\n - Drug-induced amenorrhoea (e.g. contraceptive use)\n - Physical stress, excess exercise, and weight loss\n - Pituitary gland pathology, such as Sheehan syndrome or hyperprolactinaemia\n - Hypothyroidism or hyperthyroidism\n \n \n# Signs and Symptoms\n \n \nThe primary symptom of secondary amenorrhoea is the absence of menstrual periods for six months or longer. Additional symptoms, depending on the underlying cause, may include:\n \n \n - Pregnancy signs: nausea, breast tenderness, increased urination, food cravings or aversions\n - Menopause symptoms: hot flashes, night sweats, sleep problems, mood changes\n - Symptoms of PCOS: acne, weight gain, hirsutism (excessive body hair), thinning hair\n - Symptoms of pituitary gland pathology: headaches, vision problems, unexplained weight gain or loss\n \n \n# Differential Diagnosis\n \n \nThe differential diagnosis for secondary amenorrhoea includes:\n \n \n - **Pregnancy:** confirmed by a positive pregnancy test, ultrasound, and physical examination\n - **Menopause:** diagnosed based on age, symptoms such as hot flashes and night sweats, and elevated FSH levels\n - **PCOS:** diagnosed based on irregular periods, signs of high testosterone levels (acne, hirsutism), and presence of numerous small cysts on the ovaries\n - **Asherman's Syndrome:** diagnosed based on history of uterine surgery and confirmed by hysteroscopy\n \n \n# Investigations\n \n **Bedside:**\n \n - Pregnancy test\n\n **Bloods:**\n \n - Hormone level checks, including FSH, LH, TSH, prolactin, and testosterone\n\n**Imaging:**\n\n - Ultrasound to identify potential structural abnormalities. Other imaging (e.g. MRI) may also be appropriate, but TVUSS is usually the first line option. \n\n**Invasive:**\n\n - Hysteroscopy, in cases where intrauterine adhesions are suspected\n \n \n# Management\n \n \nThe management of secondary amenorrhoea is largely determined by the underlying cause:\n \n \n - For pregnancy: regular prenatal care\n - For menopause: hormone replacement therapy (HRT) if symptoms are troublesome\n - For PCOS: lifestyle changes, hormonal contraceptives, and potentially metformin\n - For Asherman's syndrome: surgical removal of adhesions and hormone therapy\n - For drug-induced amenorrhoea: discontinuing the offending drug if possible and safe to do so\n - For conditions related to physical stress, weight loss, or excessive exercise: lifestyle modifications and nutritional counselling.\n \n\n# NICE Guidelines\n[Click here to read NICE guidelines](https://cks.nice.org.uk/topics/amenorrhoea/)\n\n# References \n\n[Patient info](https://patient.info/doctor/amenorrhoea)",
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"question": "A 17 year old competitive triathlete presents to her GP concerned that her periods have stopped. She tells you she has been stressed recently as she is training intensively for an upcoming national competition.\n\nWhich is the most appropriate initial investigation?",
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"explanation": "This is unlikely in this case as there is nothing in the history to suggest that this patient has heart failure and she has no other features of heart failure (e.g. peripheral oedema, raised JVP). Heart failure may cause _bilateral_ reduced air entry",
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"explanation": "This patient has a known benign solid ovarian tumour and the case vignette points towards Meigs' syndrome. Meigs' syndrome is defined as the triad of benign ovarian tumour (most commonly a fibroma), pleural effusion and ascites",
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"comment": "Meigs BAPS\n\nBenign Ovarian Tumour\nAscites\nPleural effusion ",
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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": "An 56 year old female with a known ovarian fibroma presents to accident and emergency with breathlessness and abdominal distension. On examination, she is breathless at rest with reduced air entry at the right base. Her abdomen is soft, non tender and distended with evidence of shifting dullness on percussion.\n\nWhat is the most likely cause of her breathlessness?",
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"explanation": "A knee x-ray may be helpful in showing a large effusion but the history is not suggestive of a bony injury therefore x-ray will not give you a definitive diagnosis in this case",
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"explanation": "Whilst blood cultures should always be taken in patients who present with sepsis, a positive blood culture would not necessarily tell you the focus of the infection. As the knee is the presumed focus, an aspirate directly from the joint will likely yield the definitive diagnosis",
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"comment": "You'd definitely Sepsis 6 him before aspirating his knee though?",
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"explanation": "# Summary\n\nSickle cell anaemia (SCA) is an autosomal recessive condition in which a point mutation in the beta chain on chromosome 11 leads to the production of HbS (rather than HbA). HbS polymerises when deoxygenated leading to sickled red blood cells. These cells are fragile and sticky, causing vaso-occlusive crises leading to pain and ischaemia of vital organs. The most common acute presentation is painful vaso-occlusive crises, while the most dangerous is acute chest crises. Diagnosis is typically made postnatally in the UK via a national screening programme but otherwise presents with progressive anaemia in early life. Investigations may reveal microcytic anaemia with variable degrees of haemolysis, and a definitive diagnosis is achieved with haemoglobin electrophoresis +/- genetic testing. Management strategies include high-flow oxygen, IV fluids and analgesia for acute crises, hydroxycarbamide, regular exchange transfusions, vaccinations and antibiotics for chronic disease management.\n\n# Definition\n\nSickle cell anaemia (SCA) is a genetic condition where normal haemoglobin (where variable HbS is present) tends to form abnormal haemoglobin molecules (HbS) upon deoxygenation leading to distortion of RBCs.\n\n# Epidemiology\n\nSickle cell disease is common among individuals of Central and West African descent, where having the carrier (trait) status confers some protection against malaria. \n\n# Pathophysiology \n\n- HbS is produced when the glutamic acid at the 6th position of the β chain is replaced by valine \n- In its deoxygenated state, HbS undergoes polymerisation, forming crystals that cause polymers to form, which in turn leads to the development of RBCs with a sickle shape \n- The abnormal shape of the RBCs causes clotting in the microvasculature, which precipitates vaso-occlusive crises, leading to ischaemia of vital organs and pain\n- Deformation of the RBCs leads to chronic haemolysis, which decreases the body's nitric oxide – typically needed for vasoregulation – and this leads to chronic complications such as pulmonary hypertension and leg ulcers\n\n## Inheritance \n\n- Sickle cell anaemia (HbSS) is an autosomal recessive condition. The most predominant and most severe form, homozygous HbS, represents just one of the sickle cell disease syndromes.\n- Other forms of sickle cell disease involve the coinheritance of HbS with other haemoglobin variants.\n - Most commonly HbC or β-thalassaemia, leading to the HbSC or HbS-βthal forms of sickle cell disease.\n\n## Mechanism of hyposplenism\n\nIn addition, sickled red cells commonly sequester in the spleen, where they undergo phagocytosis by the reticular endothelial system, leading to extravascular haemolysis\n\n- Initially, this leads to splenic congestion and splenomegaly\n- This is followed by splenic infarction, leading to hyposplenism\n- Because of splenic compromise, there is reduced immune function \n - Individuals with sickle cell disease are prone to bacteraemia – the spleen is necessary for phagocytosis of encapsulated bacteria. This means there is vulnerability to encapsulated organisms such as Haemophilus influenzae type B.\n - Affected individuals should have up to date vaccinations for S. pneumoniae, H. influenzae B and N. meningitidis.\n\n\n# Signs and Symptoms\n\n## Vaso-occlusive crises\n\nPainful vaso-occlusive crises are the most common acute presentation of sickle cell anaemia\n\n- Primarily caused by microvascular obstruction due to RBC sickling and inflammation\n- May be triggered by local hypoxia (eg. in cold weather)\n\n## Acute chest crisis\n\nAcute chest crises are the most dangerous acute presentation\n\n- 3% mortality rate, causing 25% of sickle cell-related deaths \n- The cause is often unknown (maybe infectious)\n- Patients present with tachypnoea, wheeze, and cough, with hypoxia and pulmonary infiltrates on chest X-ray\n\n## Other complications \n\n- Splenic infarction and subsequent immunocompromise\n- Sequestration crisis\n- Osteomyelitis\n- Stroke\n- Dactylitis\n- Poor growth\n- Chronic renal disease\n- Gallstones\n- Retinal disorders\n- Priapism\n- Pulmonary fibrosis and pulmonary hypertension\n- Iron overload from repeated blood transfusions\n- Red cell aplasia (due to parvovirus B19 infection in the presence of chronic haemolytic anaemia)\n\n**Clinical severity** is highly variable: some patients have few symptoms; others have severe and frequent crises, haemolytic anaemia and end-organ damage\n\n- This is due to a range of factors such as the amount of HbF (foetal haemoglobin) – higher levels of HbF reduce the severity of clinical complications\n- Patients with Hb SC disease have milder anaemia and suffer fewer crises than people with Hb SS disease \n- Patients with Hb SC disease are however more prone to sickle cell retinopathy \n - Ophthalmological review is needed annually for all patients with Hb SC disease\n\n# Investigations\n\n- Bedside - peak flow, which is essential for monitoring patients with chest crisis\n- **FBC** may show microcytic anaemia with variable degrees of haemolysis \n - Reticulocytosis and unconjugated hyperbilirubinemia may be noted\n\n- Typical **blood film** findings include: \n - characteristic sickle cells\n - target cells\n - reticulocytosis with polychromasia \n - features of functional hyposplenism (Howell–Jolly bodies, nucleated red cells)\n\nDefinitive diagnosis is with **haemoglobin electrophoresis** +/– genetic testing. However, many labs use high-performance liquid chromatography (HPLC) and/or isoelectric focusing (IEF) instead of HB electrophoresis. \n\n[lightgallery]\n\n## Screening for sickle cell disease\n\n- Sickle cell disease in the UK is typically diagnosed postnatally (by the national screening programme)\n- Additionally, all patients of African or Caribbean descent should have a sickle cell test prior to surgery \n- Otherwise, it can present with progressive anaemia in early life when levels of foetal haemoglobin (which contains γ-chains) fall and are replaced by HbS (containing the variant β-globin)\n\n# Management \n\n## Acute sickle cell crisis\n\nTreatments include: \n\n- High-flow oxygen \n- IV fluids and analgesia\n- Top-up transfusions – required in some severe cases\n\nNote: ABO-compatible red cells matched for Rhesus and Kell antigens should be given as this will inhibit the development of antibodies that can otherwise complicate future transfusions.\n\n\n## Chronic sickle cell disease\n\n* **Hydroxycarbamide** if frequent crises occur\n * Increases foetal haemoglobin concentrations – needs to be balanced with risks of marrow suppression, reduced fertility and risk of teratogenicity\n\n* Alternatively regular exchange transfusions may be required for frequent sickle cell crises, acute chest syndrome, priapism and stroke prevention \n* **Vaccinations** and **antibiotic prophylaxis** – in view of hyposplenism and subsequent immunocompromise\n* Newer therapies include: \n * crizaniluzumab (p-selectin inhibitor) for treatment of pain crises \n * voxelotor (haemoglobin oxygen-affinity modulator) for haemolytic complications\n\n* Bone marrow transplant and gene-editing techniques are now becoming possible curative options for some patients\n\n# NICE Guidelines\n\n[Click here to see information on NICE CKS on sickle cell](https://cks.nice.org.uk/topics/sickle-cell-disease/)",
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"question": "A 27 year old male with known sickle cell disease presents to his local accident and emergency department with an eight hour history of a painful right knee. His triage observations are as follows: SpO<sub>2</sub> 97% on air, respiratory rate 18, pulse 108 (regular), blood pressure 90/60 mmHg, temperature 39.2°C.\n\nHis knee is erythematous and hot to the touch and he has very minimal active movement.\n\nWhat test will give you the definitive diagnosis?",
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"explanation": "Apixaban is a factor Xa inhibitor, the same as rivaroxaban. This patient has already failed this therapy and therefore an anticoagulant with a different mechanism of action is indicated here",
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"explanation": "Inferior vena cava filters are only indicated in patients who cannot take blood thinning medications. Changing to a different oral anticoagulant is the preferred option here",
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"explanation": "Venesection is a recognised treatment for some haematological conditions such as hereditary haemochromatosis and polycythaemia (both of which can increase the risk of DVT) however this woman has been investigated for these conditions previously, therefore this treatment is not indicated",
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"explanation": "20mg once a day is already the maximum dose for rivaroxaban and therefore a dose increase should only be undertaken in complex cases under the advice of a haematologist. The better option here is to change to a difference mode of anticoagulation",
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"explanation": "# Summary\n\nDeep Vein Thrombosis (DVT) refers to intra-luminal occlusion of a deep vein with a blood clot, obstructing blood flow. Commonly these occur in the legs although other veins may be affected. DVTs are categorised as \"provoked\" if a transient risk factor such as pregnancy or surgery is identifiable, and \"unprovoked\" if not. Key signs and symptoms include leg pain, unilateral erythema, warmth and swelling and distention of superficial veins. The Wells score is commonly used to assess how likely a DVT is based on clinical findings and risk factors; this guides whether a D-dimer blood test or a Doppler ultrasound should be offered first-line. Management is usually with anticoagulation; in rare cases other strategies such as mechanical thrombectomy and IVC filters may be required.\n \n# Definition\n \nA deep vein thrombosis (DVT) is a blood clot or thrombus that blocks a deep vein, commonly in the legs or pelvis. \n \n# Epidemiology\n \n- Venous thromboembolism (which includes both DVT and pulmonary embolism) is common, affecting 1-2 per 1000 people per year\n- Two-thirds of cases are DVTs and one-third are pulmonary emboli (PE), with DVT being the main risk factor for PE\n- It is particularly common in unwell patients in hospital, with an incidence of up to 37% in critically ill patients\n\n# Aetiology\n \nRisk factors for DVT can be remembered with the mnemonic **THROMBOSIS:**\n \n\n * **T**hrombophilia\n * **H**ormonal (COCP, pregnancy and the postpartum period, HRT)\n * **R**elatives (family history of VTE)\n * **O**lder age (>60)\n * **M**alignancy\n * **B**one fractures\n * **O**besity\n * **S**moking\n * **I**mmobilisation (long-distance travel, recent surgery or trauma)\n * **S**ickness (e.g. acute infection, dehydration)\n\n# Signs and Symptoms\n \n- Unilateral erythema, warmth, swelling and pain in the affected area\n- Pain on palpation of deep veins\n- Distention of superficial veins\n- Difference in calf circumference if the leg is affected\n - This should be measured 10cm below the tibial tuberosity\n - > 3cm difference between the legs is significant\n\n# Differential Diagnosis\n\n- **Cellulitis** also causes erythema, warmth, swelling and pain and often affects the legs, patients may have other signs of infection e.g. fevers and there may be an obvious wound or discharge\n- **Calf muscle tear** also causes swelling, erythema and pain; there will usually be a history of trauma immediately preceding the development of symptoms\n- **Superficial thrombophlebitis** often occurs in the lower limbs in association with varicose veins, however pain is localised to a thrombosed vein rather than there being generalised pain and swelling of the limb\n- **Compartment syndrome** can be differentiated by severe pain out of proportion to clinical signs, often preceded by traumatic injury\n\n# Investigations\n \nThe two-level DVT Wells score is used to risk-stratify patients into patients likely or unlikely to have a DVT as follows:\n\n**Add one point** for each of:\n\n- Active cancer (treatment within the last 6 months or palliative)\n- Paralysis, paresis, or recent plaster immobilisation of the legs\n- Recently bedridden for 3 days or more, or major surgery within the last 12 weeks\n- Localised tenderness along the distribution of the deep venous system\n- Entire leg is swollen.\n- Calf swelling at least 3 cm larger than asymptomatic side\n- Pitting oedema confined to the symptomatic leg\n- Collateral superficial veins\n- Personal history of DVT\n\n**Minus 2 points** if an alternative cause is considered at least as likely as a DVT.\n\nIf the score is **2 or more**:\n \n- DVT is **likely** and an ultrasound doppler of the proximal leg veins should be done within 4 hours\n- If this isn't possible within 4 hours, do a D-dimer test, start interim anticoagulation and arrange the doppler to happen within 24 hours\n \nIf the score is **1 or less**:\n \n- DVT is **unlikely** and a D-dimer should be sent\n- If the results cannot be obtained within 4 hours, offer interim anticoagulation whilst awaiting results\n- If the D-dimer is positive, do an ultrasound doppler of the proximal leg veins \n- If it is negative, anticoagulation should be stopped if it was started and an alternative diagnosis considered\n\n[lightgallery] \n\nD-dimer is not a specific test and is often raised in infection, trauma, malignancy, post-surgery or haemorrhage. \n\nNote that separate guidelines exist for pregnant and postpartum women - linked below in references.\n\n**Baseline blood tests** should be taken when anticoagulation is started, including a FBC, U&Es, LFTs and a coagulation screen. \n\n# Management\n \n- First-line anticoagulant medications are **DOACs** (e.g. apixaban, rivaroxaban)\n- If these are not suitable, second-line options include low molecular weight heparin (LMWH) for at least 5 days followed by dabigatran or edoxaban, or LMWH bridging with warfarin (with a target INR of 2.5)\n- Treatment duration should be at least 3 months for all patients, and 3-6 months for people with active cancer\n- At this point the risk of VTE recurrence should be weighed against the risks of continuing anticoagulation to make a decision about whether to continue\n- In cases of provoked DVTs (where a major transient risk factor is identifiable e.g. surgery), anticoagulation would usually be stopped at 3 months\n- In cases of unprovoked DVTs, consider testing for thrombophilia with antiphospholipid antibodies in patients who are stopping anticoagulation\n- Patients with unprovoked DVTs should be reviewed with baseline blood tests and an examination to investigate the possibility of an undiagnosed cancer - further investigations should be guided by the patient's signs or symptoms\n\n[lightgallery1]\n \n# Complications\n\n- Pulmonary embolism\n- Post-thrombotic syndrome (chronic venous hypertension post-DVT that may cause significant morbidity)\n- Complications of anticoagulation e.g. gastrointestinal bleeding\n\n \n# NICE Guidelines\n \n[NICE CKS - DVT](https://cks.nice.org.uk/topics/deep-vein-thrombosis/)\n\n[NICE - Venous thromboembolic diseases](https://www.nice.org.uk/guidance/ng158/)\n \n# References\n\n[RCEM Learning - Deep Vein Thrombosis](https://www.rcemlearning.co.uk/reference/deep-vein-thrombosis)\n\n[RCOG - Thromboembolic Disease in Pregnancy and the Puerperium](https://www.rcog.org.uk/media/wj2lpco5/gtg-37b-1.pdf)",
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"question": "A 62 year old female has recurrent deep vein thromboses (DVT) for which she takes rivaroxaban 20mg once a day. Unfortunately she develops a new unilateral leg swelling and ultrasound investigation confirms a further deep vein thrombosis. She has been investigated previously for underlying hypercoagulable conditions and all the tests have been negative.\n\nHow should you treat this patient?",
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"explanation": "A parapharyngeal abscess is another recognised complication of under-treated bacterial throat infections. It may present with a neck swelling and can lead to Lemierre's syndrome, but not all parapharyngeal abscesses have an associated thrombus, therefore this is not the correct answer. It can be life threatening as it may lead to airway compromise and thus must be surgically drained under general anaesthetic",
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"explanation": "A quinsey is another term for a peritonsillar abscess. This is a more common complication of under-treated bacterial throat infections and often requires incision and drainage. A quinsey can develop into a parapharyngeal abscess if left untreated, but as with parapharyngeal abscess it does not always have an associated thrombosis and therefore is not the correct answer here",
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"explanation": "This is a combination of symptoms that arise from damage to the sympathetic trunk. The classical signs are of miosis (constricted pupil), partial ptosis (weak droopy eyelid) and anhydrosis (reduced sweating). This presentation is more in keeping with an acute inflammatory/infective process as opposed to disruption of nerve signals",
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"explanation": "Reye's syndrome is acute encephalopathy and liver failure after a febrile viral illness such as influenza and upper respiratory tract infections. It does not present with neck swelling and liver failure is more commonly associated with bleeding as opposed to thrombosis. This is therefore not the correct answer",
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"explanation": "# Summary\n \n \nTonsillitis is a condition characterised by the inflammation of the tonsils due to infection. The main signs and symptoms include sore throat, headache, fever, and lymphadenopathy. Investigation methods such as throat swabs are not routinely performed, and blood tests are reserved for patients with immunodeficiency. Management strategies primarily include treatment with paracetamol and ibuprofen, with antibiotics prescribed in certain cases.\n \n \n# Definition\n \n \nTonsillitis is a medical condition that is characterised by the inflammation of the tonsils, which are the masses of lymphoid tissue located at the back of the throat. This inflammation is primarily due to an infection.\n \n \n# Epidemiology\n \n \nSore throat is a very common presenting complaint. Cases are highest in children during the winter months.\n \n# Aetiology\n \n \nThe aetiology of tonsillitis is usually due to a viral or bacterial infection. 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A key difference is the presence of severe fatigue and splenomegaly.\n \n \n# Investigations\n \n \nInvestigations for tonsillitis typically involve clinical examination and patient history. Additional tests such as throat swabs are only used when an alternative bacterial cause is suspected. Blood tests are primarily reserved for those with suspected immunodeficiency.\n \n## Scoring systems to predict the need of antibiotic treatment:\n \n \n### Centor Criteria\n \n \nThe Centor Criteria is a set of clinical predictors used to identify patients with Group A streptococcal pharyngitis:\n \n \n - History of fever\n - Presence of tonsillar exudates\n - Absence of cough\n - Tender anterior cervical lymphadenopathy\n \n \nPatients presenting with three or four of these criteria should be considered for antibiotic treatment.\n \nFeverPAIN criteria:\n \n - Fever\n - Purulence (exudate)\n - Attended within 3 days of symptom onset\n - Inflamed tonsils\n - No cough or coryza (suggests viral origin)\n \nA score of four or five indicates a high probability of streptococcal infection and hence the need for antibiotics.\n \n \n# Management\n \n \nManagement strategies for tonsillitis include:\n \n \n - Symptomatic treatment with paracetamol and ibuprofen\n - Antibiotic therapy in cases featuring (phenoxymethylpenicillin is first-line):\n - Marked systemic upset\n - Three or more Centor criteria, or four or more FeverPAIN criteria\n - Underlying immunodeficiency\n - Increased risk of complications \n - Clarithromycin can be used if there is penicillin allergy \n - In some cases a delayed antibiotic prescription may be indicated\n \nIf a patient appears severely unwell, dehydrated or presents with complications, refer urgently to hospital or for specialist assessment.\n \nPatients may be referred to ENT for tonsillitis if they have recurrent episodes of tonsillitis. The criteria for this is:\n \n - 7+ episodes in one year\n - 5+ episodes per year for two years\n - 3+ episodes per year for three years\n \n# Complications\n \n \nPotential complications of tonsillitis include:\n \n \n - Recurrent Tonsillitis: This is the most common complication. The evidence base for tonsillectomies as a treatment is poor, leading to stricter referral criteria.\n - Retropharyngeal Abscess: A rare complication characterised by soft tissue swelling, more common in young children. Symptoms include a stiff and extended neck and refusal to eat or drink.\n - Peritonsillar Abscess (Quinsy): Presents with sore throat, difficulty swallowing, peritonsillar bulge, uvular deviation, trismus, and muffled voice. Treatment has shifted from surgical drainage to antibiotics and aspiration.\n - Lemierre's Syndrome: In this rare complication, inflammation leads to pharyngotonsilitis, inflammation within the internal jugular vein, and septic emboli. 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"learningPoint": "Lemierre's syndrome is a serious condition arising from untreated bacterial throat infections, leading to jugular vein thrombosis.",
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"question": "An 18 year old female with recurrent tonsillitis presents to her local accident and emergency with a four day history of sore throat, fever and inability to swallow her own saliva. She has a tender swelling over the lateral aspect of her neck and targetted ultrasound reveals a thrombus in her jugular vein.\n\nWhat is the name of the likely condition?",
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"explanation": "Sensitivity of a test is the ability of a test to correctly identify those with a disease.\n\nSensitivity = true positives / (true positives + false negatives)\n\nSo in this case 80/(80+15) = 84.2%",
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"explanation": "This is the specificity of the test, not the sensitivity. Specificity of a test is the ability of the test to correctly identify those without a disease.\n\nSpecificity = true negatives / (true negatives + false positives).\nIn this case = 920/(920+3) = 99.7%",
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"explanation": "This is the number of true negatives expressed as a percentage, not the sensitivity",
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"explanation": "This is the number of true negatives expressed as a percentage, not the sensitivity",
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"explanation": "This is the number of true positives expressed as a percentage, not the sensitivity",
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"explanation": "# Overview \n\nSeveral key parameters can be calculated to help describe how effective a certain test is at diagnosing a condition.\n\n| | Patients with colon cancer | No cancer |\n| ------------------ | :------------------------: | --------: |\n| Biomarker positive | a | b |\n| Biomarker negative | c | d |\n\n# Sensitivity\n\nSensitivity is the proportion of people with the condition who will have a positive result. If, for example, the sensitivity of a test is 80%, out of a hundred people with the condition, only 80 will have a positive test result.\n\nSensitivity = a/(a+c)\n\n# Specificity\n\nSpecificity describes the proportion of people without the disease who will have a negative test. A specificity of 90% can be interpreted as, out of 100 people without the disease, 90 will have a negative test result.\n\nSpecificity = d/(b+d)\n\n# Positive Predictive Value\n\nPositive predictive value (PPV) is the proportion of people with a positive test who actually have the disease. PPV varies with prevalence of disease in a population. The lower the prevalence, the lower the positive predictive value. A PPV of 78% will mean that if 100 people tested positive, 78 people will have the disease.\n\nPPV = a/(a+b)\n\n# Negative Predictive Value\n\nNegative predictive value (NPV) is the proportion of people with a negative test who truly do not have the disease.\n\nNPV varies with prevalence of disease in a population. The lower the prevalence, the higher the negative predictive value. An NPV of 97% will mean that if 100 people tested negative, 97 people will not have the disease.\n\nNPV = d/(c+d)\n\n# False positive rate\n\nThe false positive rate is the proportion of those without the condition who will test positive.\n\nFalse positive rate = 1 - specificity\n\nFalse negative rate = 1 - d/(b+d)\n\n# False negative rate\n\nThe false negative rate is the proportion of those with the condition who will test negative.\n\nFalse negative rate = 1 - sensitivity\n\nFalse negative rate = 1 - a/(a+c)\n",
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"question": "A company develops a new coronavirus test. They trial it on 1000 people and have 83 positive tests, of which 80 were later confirmed to be positive through alternative means of testing. Of those who tested negative, 15 were later confirmed positive through alternative testing.\n\nWhat is the sensitivity of the new test?",
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"explanation": "This is incorrect as this is the risk of developing diabetes in the placebo group",
"id": "32551",
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"name": "0.72",
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"answer": false,
"explanation": "This is incorrect as this is the risk of developing diabetes in the group given the drug",
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"explanation": "The relative risk or risk ratio is the probability of an outcome occurring in a patient group exposed to a change (in this case, a new drug). Of those given the drug, 50% went on to develop diabetes compared to 72% in the placebo group.\n\nRelative risk = risk in the group exposed to drug/risk in those not exposed to the drug.\n\n50/72 = 0.69",
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"answer": false,
"explanation": "This is incorrect as the group that has been exposed to the change is those given the drug",
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"picture": null,
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"answer": false,
"explanation": "This is incorrect as this is the risk of not developing diabetes in the placebo group",
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"explanation": "# Definition\n\nRisk in medical statistics refers to the probability of an outcome (either good or bad) occurring within a studied population. There are several different types of risk that are often used in medical studies.\n\n# What is Risk/Prevalence?\n\nThis is simply the probability of an event occurring within a defined population.\n\n# What is Risk Ratio (RR)?\n\nThe risk ratio (also known as relative risk) is the probability of an event occurring in an exposed group compared to the probability occurring in a non-exposed group.\n\nThe risk ratio is calculated by finding the ratio of incidence of a disease amongst the exposed population and the incidence amongst the non-exposed population.\n\nRisk ratios are used in cohort studies and in interventional studies in which the experimenter intervenes at some point during the study, such as in randomised controlled trials and pre-post studies.\n\nHowever, in cross-sectional studies and case-control studies, the incidence of the disease in the exposed and unexposed populations cannot be found, since the data only provides the cases and controls.\n\nConsequently,the risk ratio cannot be calculated for case-control studies and cross-sectional studies. Instead, an odds ratio must be found.\n\n# What is Absolute Risk Reduction (ARR)?\n\nThe absolute risk reduction is the absolute difference in the risk between the control group and the experimental group. It tells you in absolute terms how much an intervention changes an outcome of interest.\n\n# Calculation of Absolute Risk Reduction\n\nIt is calculated as follows:\n\n_ARR = Risk(control group) - Risk(experimental group)_\n\nA given ARR is generally considered significant if the 95% confidence interval does not cross 0.\n\nARR can then be used to calculate the number needed to treat (NNT).\n\n# What is Relative Risk Reduction (RRR)?\n\nThe relative risk reduction can be thought of as the proportional reduction in risk bestowed by the intervention compared to the control situation. It is more useful in helping you understand the efficacy of an intervention when the absolute risk of outcomes are rare (for example when considering the benefits of a statin for reducing MI in a given population).\n\n# Calculating RRR\n\nIt is calculated as follows:\n\n_RRR = 1 - [Risk(Experimental group) / Risk(Control group)]_\n\nA given RRR is generally considered significant if the 95% confidence interval does not cross 1.",
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"question": "A new drug is developed that claims to prevent diabetes mellitus in patients with impaired glucose tolerance. A randomised control trial is undertaken in 100 patients with HbA1c of 42-47, where half the participants are given the new drug, and the other half are given a placebo.\n\nIn those who were given the new drug, 25 patients developed diabetes within five years; in the group who were not given the drug, 36 patients developed diabetes within five years.\n\nWhat is the relative risk of developing diabetes if treated with the new drug?",
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"explanation": "This is incorrect as the ratio here is very close to 1, indicating that the risk of recurrence from her technique is very similar to the risk of recurrence from other techniques",
"id": "32555",
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"name": "Edwards et al. show the biggest difference in the risks of hernia recurrence between her technique and other techniques",
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"explanation": "This is false as all of the forest plot lines are above 1. In risk ratios or relative risk, if the ratio is >1, then this means that the intervention has a less favourable risk than in the group not subject to the intervention, i.e. greater risk of hernia recurrance.",
"id": "32557",
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"name": "All the studies suggest that her method has a lower risk of hernia recurrence",
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"explanation": "This is incorrect as the horizontal line is a representation of the confidence intervals. A wide confidence interval is more likely to be representative of a smaller data set",
"id": "32556",
"label": "d",
"name": "James et al. likely had the most participants in their study",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect as the horizontal line on a forest plot indicates the confidence intervals as opposed to the range of the data sets. A wide confidence interval indicates instability of results, for example, due to a very small data set",
"id": "32554",
"label": "b",
"name": "James et al. have the largest range of results",
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"explanation": "This is true as all of the forest plot lines are at or above 1. In risk ratios or relative risk, if the ratio is >1, then this means that the intervention has a less favourable risk than in the group not subject to the intervention, i.e. greater risk of hernia recurrance.",
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"name": "None of the studies suggest that her method has a lower risk of hernia recurrence",
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"comment": "No because Edwards et al has a range from below 1 to above 2",
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"comment": "also shade on the colleague",
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"explanation": "# Definition \n\nA type of clinical study in which participants are assigned to groups that receive one or more intervention/treatment (or no intervention) so that researchers can evaluate the effects of the interventions on biomedical or health-related outcomes.\n\n# Types of interventional trials \n\nA randomized control trial is the strongest type of interventional trial, but other forms include non-randomised controlled trials, pre-post studies and quasi experiments.\n\nA pre-post study is a study in which occurrence of an outcome is measured both before and after an intervention is administered; it is in this way that the effect of the intervention can be properly assessed. If the occurrence of the outcome was only measured after the intervention; the exact effect of the intervention cannot be determined.\n\nAnother form of trial is a crossover randomized control trial. A crossover RCT is a type of interventional study design where study participants intentionally “crossover” to the other treatment arm.\n\n# Uses \n\nInterventional studies are used to answer study questions relating to either therapeutic agents, and evaluating the efficacy of therapeutic agents, or are used to assess mechanisms of preventing potential causes of damage.",
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"question": "Your colleague has a particular way of performing inguinal hernia repairs that is less commonly used. She wants to know whether her technique has a higher or lower rate of recurrence. She finds five studies that use her method compared to the routine method and plots them in a forest plot (x-axis represents the relative risk of recurrence in your colleague's method compared to the routine method).\n\n[lightgallery]\n\nWhich of these statements about her findings is true?",
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"explanation": "A liver ultrasound would be useful in diagnosing biliary atresia, serious but rare cause of neonatal jaundice. However, biliary atresia usually develops around three weeks after birth. This history is more in keeping with an acute haemolytic cause for jaundice than a structural issue",
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"explanation": "This history suggests rhesus haemolytic disease of the newborn, as this is a woman in her second pregnancy, and the jaundice is apparent in the first 24 hours after birth. You would therefore expect a positive direct Coombs test. A direct Coombs test is used to test for autoimmune haemolytic anaemia where the immune system breaks down red blood cells, leading to anaemia. The direct Coombs test is used to detect antibodies or complement proteins attached to the surface of red blood cells",
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"explanation": "An indirect Coombs test looks at antibodies floating freely in the blood and, therefore, can be used in prenatal testing for pregnant women or in testing prior to blood transfusion. A positive indirect Coombs would not diagnose the cause for haemolysis in this case",
"id": "32604",
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"explanation": "Breastfeeding is a common cause for prolonged jaundice in newborns; however, it would not develop in the first few hours of life. Visible jaundice in the first 24 hours of life is always abnormal",
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"label": "e",
"name": "Withdrawal of breastfeeding",
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"explanation": "Whilst liver function tests would help confirm whether this was true jaundice, they would not help diagnose the underlying cause",
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"comment": "I'm confused - are we testing the mum or the baby?\nIndirect Coombs test would be positive in the baby due to the alloimmune destruction wouldn't it? ",
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"comment": "good question\n",
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"explanation": "# Summary\n\nHaemolytic Disease of the Newborn (HDN) is an immunological disorder that occurs when a rhesus negative mother becomes sensitised to her baby's rhesus positive blood cells in utero. Key signs and symptoms include hydrops foetalis, yellow amniotic fluid, neonatal jaundice, kernicterus, foetal anaemia, hepatomegaly or splenomegaly, and severe oedema if hydrops foetalis was present in utero. It is vital to identify and manage HDN to prevent complications including neurodevelopmental issues and foetal death. Key investigations include Direct Antiglobulin Test (DAT), Ultrasound, and LFTs. Management strategies include intrauterine transfusions, early delivery, and postnatal management with phototherapy or exchange transfusion.\n\n\n# Definition\n\n\n\nHaemolytic Disease of the Newborn (HDN) is an immunological condition that arises when a rhesus negative mother becomes sensitised to the rhesus positive blood cells of her baby while in utero.\n\n\n# Epidemiology\n\n\n\nHDN is relatively rare, but it can have serious consequences if not properly managed. It is most common in pregnancies where there is blood group incompatibility between the mother and the foetus. \n\n\n# Aetiology\n\n\n\nHDN occurs due to immune response following rhesus or ABO blood group incompatibility between the mother and foetus. The sensitisation events are responsible for enabling foetal blood to cross the placenta into the maternal circulation. These events include antepartum haemorrhage, placental abruption, abdominal trauma, external cephalic version, invasive uterine procedures such as amniocentesis and chorionic villus sampling, rhesus positive blood transfusion to a rhesus negative woman, intrauterine death, miscarriage or termination, ectopic pregnancy, and delivery.\n\n\n# Signs and Symptoms\n\n\nThe features of haemolytic disease of the newborn include:\n\n- Hydrops foetalis appearing as foetal oedema in at least two compartments, seen on antenatal ultrasound\n- Yellow coloured amniotic fluid due to excess bilirubin\n- Neonatal jaundice and kernicterus\n- Foetal anaemia causing skin pallor\n- Hepatomegaly or splenomegaly\n- Severe oedema if hydrops foetalis was present in utero\n\n\n# Differential Diagnosis\n\n\nIt is important to differentiate HDN from other conditions that can present with similar symptoms, including:\n\n- Spherocytosis: Characterised by haemolytic anaemia, jaundice, and splenomegaly\n- G6PD deficiency: Causes episodic haemolysis, jaundice and pallor\n- Thalassemia: Presents with anaemia, hepatosplenomegaly, and jaundice\n\n# Investigations\n\n\nInvestigations for HDN include:\n\n- Direct Antiglobulin Test (DAT)\n- Ultrasound to detect foetal oedema\n- Liver function tests (LFTs) to check for complications\n\n# Management\n\n\nManagement of HDN includes:\n\n- Intrauterine transfusions if severe anaemia is detected in the foetus\n- Early delivery if the condition is severe\n- Postnatal management with phototherapy or exchange transfusion to manage high bilirubin levels\n- Immunoglobulin administration to the newborn to prevent further haemolysis\n- Regular follow-up to assess for any developmental issues",
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"learningPoint": "Rhesus haemolytic disease of the newborn typically presents with jaundice within 24 hours of birth and is confirmed by a positive direct Coombs test.",
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"question": "A 28-year-old female gives birth to her second child at full term following an uneventful pregnancy. You check on the baby three hours after delivery, and you notice that the neonate is jaundiced. Observations are otherwise normal.\n\nWhat test would confirm your diagnosis?",
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"explanation": "This is a concerning blood sample indicating that the foetus is acidotic, implying hypoxia and therefore needs urgent delivery",
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"explanation": "Asking the mother to lie in the left lateral position can shift weight off the maternal vessels and correct cord compression, however as the foetal blood sampling is abnormal, the foetus needs to be delivered. Therefore, this is not the right answer",
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"name": "Ask the mother to lie in the left lateral position",
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"explanation": "This is an abnormal and very worrying result, and therefore time is of the essence. NICE guidance suggests that if pH < 7.20 or lactate is >4.9mmol/L, the foetus should be delivered immediately. If the pH were 7.21 - 7.24 or lactate were 4.2 -4.8mmol/L, it would be reasonable to retest in the first instance",
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"name": "Repeat the test in 30 minutes",
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"explanation": "This is an abnormal and very worrying result, and therefore, time is of the essence, and the baby needs to be delivered urgently. Whilst it is important to stay calm and keep the mother reassured, it is important not to give false reassurance at the gravity of the situation",
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"name": "Reassure the mother that everything is normal",
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"explanation": "The cardiotocograph will give you an accurate assessment of foetal heart rate (and, in this case, is showing abnormal decelerations). Auscultation would unlikely add anything in this scenario",
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"comment": "Notes below say prolonged deceleration is a contraindication to FBS. So why was it done?",
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"comment": "CAT1 C-Section \n",
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"explanation": "# Summary\n\n\nFoetal blood sampling (FBS) is a procedure used during labour to confirm whether foetal hypoxia is present in the cases of a suspicious cardiotocograph. The procedure involves a small transvaginal incision in the foetal scalp to collect blood for analysis of acidaemia. It is contraindicated in certain situations such as prolonged decelerations on cardiotocography, maternal infections, and prematurity. The interpretation of FBS results involves either pH or lactate measurements, with results guiding further management which may involve informing a senior obstetrician and the neonatal team, discussing the situation with the woman and her birth companion(s), and potentially expediting the birth.\n\n# Definition\n\n\nFoetal blood sampling (FBS) is a technique used during labour to assess the presence or absence of foetal hypoxia. \n\nThe need for FBS arises from situations where foetal hypoxia is suspected, often indicated by abnormal foetal heart rate patterns on cardiotocography.\n\n\n# Signs and Symptoms\n\n\nClinical scenarios that may prompt the use of FBS include:\n\n- Suspicious cardiotocograph\n- Lack of progress in labour\n- Abnormal pH or lactate measurements in previous samples\n\n\n# Differential Diagnosis\n\n\nThe main differential diagnoses for the findings that prompt FBS include:\n\n- Normal labour variation: Characterised by occasional decelerations in the foetal heart rate with good recovery and no other signs of foetal distress.\n- Foetal distress: Characterised by persistent decelerations in the foetal heart rate, poor variability, or late decelerations.\n- Maternal hypotension: Characterised by sudden prolonged decelerations in the foetal heart rate, often with a rapid recovery once the mother's blood pressure is corrected.\n\n# Interpretation of FBS\n\nUse either pH or lactate when interpreting foetal blood sample results.\n\nUse the following classifications for foetal blood sample results:\n\npH:\n\n- normal: 7.25 or above\n- borderline: 7.21 to 7.24\n- abnormal: 7.20 or below\n\nOR\n\nLactate:\n\n- Normal: 4.1 mmol/l or below\n- Borderline: 4.2 to 4.8 mmol/l\n- Abnormal: 4.9 mmol/l or above\n\nInterpret foetal blood sample results taking into account:\n\n- Any previous pH or lactate measurement\n- Clinical features of the woman and baby, such as rate of progress in labour and cardiotocography\n\nIf the foetal blood sample result is abnormal:\n\n- Inform a senior obstetrician and the neonatal team\n- Talk to the woman and her birth companion(s) about what is happening and take her preferences into account and\n- Expedite the birth\n\nIf the foetal blood sample result is borderline and there are no accelerations in response to foetal scalp stimulation, consider taking a second foetal blood sample no more than 30 minutes later.\n\nIf the foetal blood sample result is normal and there are no accelerations in response to foetal scalp stimulation, consider taking a second foetal blood sample no more than 1 hour later.\n\n# References\n\n[NICE guidelines](https://www.nice.org.uk/guidance/cg190/chapter/recommendations#fetal-blood-sampling)\n\n\n",
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"question": "A 37-year-old primigravida is established in the first stage of labour, and you notice some prolonged decelerations on the cardiotocograph. Foetal blood sampling is performed, and the results are as follows:\n\n\n||||\n|--------------|:-------:|------------------|\n|pH|7.14|7.35 - 7.45|\n|Lactate|5.3 mmol/L|0.6 - 1.4|\n\n\n\nWhat should you do?",
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"explanation": "Whilst it is important to obtain samples for microbiology to determine whether the knee is the source of infection and help guide antimicrobial therapy in a joint containing a prosthesis, this is best undertaken in the theatre environment. In suspected septic joints where there is no prosthesis involved, it would be reasonable to undertake aspiration in an aseptic manner in the ward or the Emergency Department prior to starting antibiotics",
"id": "32634",
"label": "b",
"name": "Aspiration of the joint on the ward",
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"explanation": "This patient remains unwell despite broad-spectrum antibiotics. As a prosthesis is involved, he will likely need a surgical washout of the joint in theatres and may even need removal of the prosthesis to control his sepsis. Samples should be taken intraoperatively for microbiology. Aspiration of a septic joint where there is a prosthesis should never be undertaken outside of the sterile theatre environment, as by performing the aspiration, you run the risk of introducing infection",
"id": "32633",
"label": "a",
"name": "Surgical washout",
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"explanation": "A PCA may be of benefit in helping this patient with his pain; however, it would not help treat the underlying cause of his illness and therefore is not the next step in the management of his sepsis",
"id": "32636",
"label": "d",
"name": "Start a patient controlled analgesia (PCA)",
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"explanation": "It may be worth speaking to the microbiologists and changing the antibiotics to a different combination; however, it would be difficult for them to provide advice without a causative organism or confirmed diagnosis. As this patient has been on broad-spectrum antibiotics for 48 hours and is not improving, it is important to get source control of his sepsis, and this is best done by a washout in theatres",
"id": "32635",
"label": "c",
"name": "Change antibiotics",
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"__typename": "QuestionChoice",
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"explanation": "A CT of the knee would be beneficial if you were trying to determine whether there was osteomyelitis or bone involvement which would be a more chronic infection. Also, as this patient has had a recent prosthesis made of metal, there would likely be a significant artefact from this. So imaging would unlikely move you forward in management",
"id": "32637",
"label": "e",
"name": "CT of the knee",
"picture": null,
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"comment": "Would you not give analgesia first then do the washout straight after?",
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"comment": "If you're taking them to be anaesthetised you probably wouldn't bother with analgesia before ",
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"explanation": "# Summary\n\nSeptic arthritis is an infection of the joint characterized by acute inflammation and swelling. It is caused by a bacterial or viral pathogen that infects the synovial fluid. The most commonly implicated organism is Staphylococcus aureus. Noteworthy clinical signs include a tender, swollen joint with reduced mobility, often accompanied by systemic illness. Key investigations include joint aspiration for Microscopy Culture and Sensitivity, along with blood tests showing increased white blood cell count and elevated ESR/CRP. Management typically involves IV antibiotics, joint washout under general anaesthesia, and physiotherapy once the acute infection has resolved.\n\n# Definition\n\nSeptic arthritis is an infection of the joint, specifically the synovial fluid. It is typically caused by a bacterial or viral pathogen and necessitates prompt medical intervention due to the high risk of joint damage and other severe complications.\n\n# Epidemiology\n\nSeptic arthritis has an annual incidence of 4-10 cases per 100,000 patients in Western Europe. It can affect individuals of any age, though certain populations are at a higher risk due to underlying conditions.\n\n# Aetiology\n\nThe most prevalent organism implicated in septic arthritis is Staphylococcus aureus. Other responsible organisms include:\n\n- Gonococcus: primarily in sexually active individuals\n- Streptococcus spp.\n- Gram-negative bacilli\n\nRisk factors contributing to septic arthritis include:\n\n- Pre-existing joint diseases such as rheumatoid arthritis\n- Chronic kidney disease\n- Immunosuppressive states\n- Presence of prosthetic joints\n\n# Signs and Symptoms\n\nThe clinical presentation of septic arthritis usually involves:\n\n- Acute onset of tender, swollen joint\n- Reduced range of joint movement\n- Systemic symptoms such as fever, malaise, or chills\n\n# Differential Diagnosis\n\nDifferential diagnoses for septic arthritis include:\n\n- Gout and pseudogout: characterized by intense joint pain, redness, and swelling, often in the big toe or knee.\n- Osteoarthritis: presents with joint pain, stiffness, and sometimes swelling, generally improving with movement.\n- Rheumatoid arthritis: marked by joint pain, swelling, and stiffness, often symmetrical and worse after rest.\n- Lyme disease: may show erythema migrans rash, flu-like symptoms, and possibly migratory joint pains.\n\n# Investigations\n\nDiagnostic investigations for septic arthritis include:\n\n- Joint aspiration for Microscopy, Culture, and Sensitivity: The aspirate usually appears turbid and yellow, resembling pus.\n- Blood tests: elevated white cell count, high ESR/CRP\n- Blood cultures: to identify causative organisms\n- Imaging: X-ray of the joint may be performed to evaluate for osteomyelitis or other complications.\n\n# Management\n\nThe treatment of septic arthritis involves:\n\n- IV antibiotics guided by local antibiograms and susceptibilities\n- Consideration of joint washout under general anaesthesia to remove infected material\n- Physiotherapy following the resolution of acute infection to restore joint function\n\nComplications of septic arthritis can include:\n\n- Osteomyelitis: infection of the bone\n- Chronic arthritis: persistent joint inflammation\n- Ankylosis: joint fusion resulting in immobility\n\n# References\n\n[Click here for the BNF Treatment Summary for Musculoskeletal infections](https://bnf.nice.org.uk/treatment-summary/musculoskeletal-system-infections-antibacterial-therapy.html)\n\n[Click here for the BMJ Best Practice Summary of Septic Arthritis](https://bestpractice.bmj.com/topics/en-us/486)",
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"question": "A 63-year-old male has been admitted to hospital with sepsis following a recent total knee replacement. His knee is red, hot and swollen, and so he is started on broad-spectrum antibiotics. After 48 hours, he is still pyrexial, in significant pain, and his inflammatory markers continue to rise.\n\nWhat is the next step in management?",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This blood gas demonstrates an alkalosis which may be caused by loss of electrolytes (commonly potassium) as seen in severe vomiting and diarrhoea. DKA cause an acidosis, demonstrated by a low pH",
"id": "32641",
"label": "d",
"name": "A pH of 7.49",
"picture": null,
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"__typename": "QuestionChoice",
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"explanation": "This patient has DKA, and you would therefore expect the blood gas to show hyperglycaemia. Patients can rarely have euglycaemic diabetic ketoacidosis but this is often associated with certain medications such as SGLT2 inhibitors",
"id": "32642",
"label": "e",
"name": "A glucose of 10.4mmol/L",
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"explanation": "This blood gas shows a hypercapnoea. This is common in acute respiratory presentations such as an acute asthma attack. In DKA the carbon dioxide tends to be low due to compensatory hyperventilation for the acidosis",
"id": "32640",
"label": "c",
"name": "A PaCO2 5.4kPa",
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"explanation": "Reduced conscious level in a young patient with high peripheral blood sugars should make you think of the first presentation of type 1 diabetes. This vignette is a classic example of a patient in diabetic ketoacidosis where she cannot utilise glucose for her energy needs and has therefore gone into a ketotic state. You would therefore expect her blood gas to show a metabolic acidosis. She has a high respiratory rate as she is trying to use hyperventilation to compensate for her acidosis by expelling her carbon dioxide",
"id": "32638",
"label": "a",
"name": "A pH of 7.20",
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"__typename": "QuestionChoice",
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"explanation": "This would indicate hypoxaemia, commonly seen respiratory failure in conditions such as chronic obstructive pulmonary disease (COPD). Hypoxaemia is not a common finding in DKA",
"id": "32639",
"label": "b",
"name": "A PaO2 of 7.1kPa",
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"comment": "I thought increased respiratory rate points towards hyperventilation --> respiratory alkalosis and hence a high pH (7.49)?",
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"comment": "I did the same thing ",
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"comment": "The raised RR is to compensate for the metabolic acidosis but it will only be partial.",
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"comment": "I need to go back to primary school at this rate",
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"explanation": "# Summary\n \n\nDiabetic ketoacidosis (DKA) is a serious complication often associated with type 1 diabetes, characterised by hyperglycaemia, ketonaemia, and acidosis. Key signs and symptoms include fruity-smelling breath, vomiting, dehydration, abdominal pain, hyperventilation, and altered mental status. Investigations include blood glucose and ketone measurements, blood gas analysis, urea and electrolytes, and possibly blood cultures if infection is suspected. Management strategies largely depend on the patient's condition, including hydration and insulin administration via various routes and in various volumes based on severity. The major complication is cerebral oedema, a rare but potentially fatal condition that might be caused by rapid correction of dehydration with IV fluids.\n \n\n# Definition\n \n\nDiabetic ketoacidosis (DKA) is a severe and life-threatening medical complication characterised by hyperglycaemia, acidosis and ketonaemia.\n\nIt is defined by acidosis (bicarbonate < 15 mmol/l or pH <7.3) and ketones >3.0 mmol/L. \n \n\n# Epidemiology\n \n\nDKA is most commonly seen in individuals with type 1 diabetes. However, it can occur in those with type 2 diabetes under extreme stress or illness. The condition can be the first presentation of diabetes, especially type 1 diabetes in children and young adults.\n\nIt is more common in children under 5. \n \n\n# Aetiology\n \n\nDKA can be precipitated by several factors, including infection, dehydration, stress, burns, fasting, or untreated type 1 diabetes. It is important to note that fever is not a typical part of DKA presentation. A raised temperature could indicate an underlying infection that may have triggered the DKA.\n\nRisk factors include:\n\n- Previous episodes of DKA \n- Peripubertal and adolescent girls \n- Comorbidities including psychiatric disorders\n- Difficult home life\n- Insulin pump therapy \n\n\n# Classification\n\n- Mild: pH 7.1-7.29 or bicarbonate < 15 mmol/L. Dehydration 5%\n- Moderate: pH 7.1-7.19 or bicarbonate < 10 mmol/L. Dehydration 5%\n- Severe: pH <7.1 or bicarbonate < 5 mmol/L\n \n\n# Signs and Symptoms\n \n\nPatients with DKA may present with:\n \n\n - Fruity-smelling breath (due to the presence of acetone)\n - Vomiting\n - Dehydration secondary to polydipsia and polyuria \n - Abdominal pain\n - Deep, sighing respiration (Kussmaul respiration)\n - Signs of hypovolaemic shock\n - Altered mental status, including drowsiness or coma\n \n\n# Differential Diagnosis\n \n\nThe main differential diagnoses for DKA in children include:\n \n - **Lactic Acidosis**: This may present with rapid breathing, abdominal pain, and altered mental status. The patient may have a history of severe illness or sepsis, hepatic failure or metformin use.\n - **Starvation Ketosis**: This usually presents with weight loss, nausea, and clear mental status. The condition is mild, with low-level ketonaemia.\n - **Inborn errors of metabolism**: Tend to present earlier in life with metabolic disturbances or failure to thrive. \n - **Sepsis**: The child will be generally unwell, with a high or low temperature, hypotension and tachycardia. \n \n\n# Investigations\n \n\nDiagnosis of DKA involves assessment of clinical features along with:\n \n\n - Blood glucose (>11.1mmol/L)\n - Blood ketones (>3mmol/L)\n - Urea and electrolytes\n - Blood gas analysis\n - Urinary glucose and ketones\n - Blood cultures (if evidence of infection)\n - Cardiac monitoring/ECG (for any ischaemic changes or changes secondary to hypokalaemia)\n \n\nNote that hyperglycaemia may not always be present in DKA.\n \n\n# Management\n \n\nManagement of DKA should be based on the A to E approach followed by the following treatments: \n\n - IV fluids (initial bolus of 10ml/kg 0.9% NaCl, even if the patient is shocked) given over 15 minutes.\n - Repeat as needed to restore circulation\n - At 40 ml/kg then discuss with a senior for consideration for inotropes \n - Insulin infusion at 0.1 units/kg/hour 1 hour after starting IV fluids\n\n\nFluids:\n\n- Further fluids, following initial boluses should contain 40 mmol/l potassium chloride to protect against hypokalaemia. \n- Total fluid required = deficit + maintenance\n- Hourly rate = [(Deficit - initial bolus) / 48 hours ] + maintenance per hour \n- Deficit \n - A 5% fluid deficit is assumed for children with mild or moderate DKA\n - A 10% fluid deficit is assumed for children with severe DKA\n - Deficit should be replaced over 48 hours alongside maintenance fluids \n- Maintenance \n - Calculated by Holliday-Segar formula: 100 ml/kg/day for the first 10 kg, 50 ml/kg/day for the next 10 kg, and 20 ml/kg/day for each additional kg over 20 kgs. \n \nImportant points to consider: \n\n- Monitoring should include hourly blood glucose and ketones, neurological observations and fluid balance. \n- Investigations should be done to determine the cause of the DKA. \n- Many patients will require HDU-level care. \n- Intravenous insulin infusion should not be stopped until 1 hour after subcutaneous insulin has been given.\n- Long-acting insulin should continue to be given.\n\n\n# Resolving DKA\n\nIVF can be stopped once ketosis is resolving and oral fluids are tolerated without nausea or vomiting. \n\nSubcutaneous insulin can be started once ketosis is resolving and should be started at least 30 minutes before stopping intravenous insulin. \n\nDischarge can be considered once a child is eating and drinking, and stabilised on their subcutaneous insulin regime. \n \n\n# Complications\n\n\nImportant complications to monitor for include:\n\n- Cerebral oedema:\n - Can occur several hours after the onset of DKA due to rapid correction of dehydration with IV fluids. \n - Due to the potential risk, fluid deficit correction is recommended to be performed slowly, over 48 hours. \n - Though rare, this complication is fatal in 1 in 4 children. \n - Risk factors include younger age and longer duration of symptoms. \n - Management includes hypertonic (2.7%) sodium chloride and restriction of IV fluids. \n- Hypokalaemia \n- Aspiration pneumonia \n- Venous thromboembolism \n - Thromboembolic prophylaxis is not recommended in children < 16 years \n- Inadequate resuscitation \n- Hypoglycaemia\n - Blood glucose levels can fall rapidly with intravenous insulin, and if blood glucose falls below 14 mmol/L, IV fluids should include glucose. \n\n# Prognosis\n\nEarly detection and treatment results in good outcomes for patients with DKA, with many children discharged within a few days of DKA. Poorer outcomes are associated with delays in treatment and the development of cerebral oedema. \n\n\n# NICE Guidelines\n\n[BNFC Treatment Summaries: Diabetic hyperglycaemic emergencies](https://bnfc.nice.org.uk/treatment-summaries/diabetic-hyperglycaemic-emergencies/) \n \n\n# References\n \n[BSPED Guidelines for Management of DKA in Children](https://www.bsped.org.uk/media/1959/dka-guidelines.pdf)\n \n[Patient Info: Childhood ketoacidosis](https://patient.info/doctor/childhood-ketoacidosis#ref-2)",
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"learningPoint": "In diabetic ketoacidosis (DKA), an arterial blood gas (ABG) typically shows metabolic acidosis with a low pH (usually <7.35), decreased bicarbonate (HCO3-) levels, and an anion gap that is often elevated due to the accumulation of ketoacids.",
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"question": "A 14-year-old female is brought into the Emergency Department by her parents due to a reduced consciousness level. On examination, she is thin and appears dehydrated and drowsy. Her observations are as follows:\n\n\n - Temperature 36.5°C\n - Blood pressure 110/65 mmHg\n - Heart rate 120 bpm\n - Respiratory rate 32 bpm\n - Oxygen saturations 99% (on air)\n - Peripheral blood glucose 25mmol/L (normal <6.1 mmol/L)\n\n\nWhich of the following findings are you most likely to find on an arterial blood gas?",
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"explanation": "This child may have had a first presentation of epilepsy and therefore needs to be followed up in a specialist clinic such as a first fit clinic",
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"explanation": "Levetiracetam is an antiepileptic medication that can be used in the treatment of childhood epilepsy. However, this child has only had one self-limiting episode and does not yet have a confirmed diagnosis of epilepsy; therefore, starting an antiepileptic medication is not indicated here",
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"explanation": "Paracetamol is one of the mainstays of treatment in febrile convulsions. This child is well, and no fever is reported; therefore, paracetamol is not currently indicated",
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"explanation": "Buccal midazolam is useful in the management of acute seizure and status epilepticus. This child is currently well and has recovered from the episode, so the use of benzodiazepines is not indicated here",
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"explanation": "This child may well be developing epilepsy and, therefore, should be followed up in a first fit clinic. The parents should be educated on what do to if it happens again and advised on when to present to the hospital (if seizures ongoing for an extended period of time or if having multiple seizures in quick succession). They should also be advised to try to record any further episodes",
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"comment": "Including that the child has been recently well without preceding viral illness would make the history a touch more complete for us",
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"comment": "I agree, but here's what I found online: Most febrile seizures occur between 6 months and 3 years of age with the peak incidence at 18 months. Approximately 6–15% occur after 4 years, and onset after 6 years is unusual.",
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"comment": "if he is still drowsy wouldnt this be status epilepticus \n",
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"explanation": "# Summary\n \n\nEpilepsy is a group of neurological disorders typified by chronic and recurrent unprovoked seizures, which result from abnormal electrical brain activity. Both focal and generalised seizures may occur, with symptoms corresponding to the affected brain areas. Diagnosis is primarily through EEG, and management involves a comprehensive approach, including optimising anti-epileptic medications, preparing emergency seizure plans, and providing support.\n \n \n# Definition\n \n\nEpilepsy refers to a spectrum of neurological disorders characterised by chronic and recurrent unprovoked seizures. This stems from abnormal brain electrical activity, which can be either synchronous or excessive, leading to focal (restricted to a single lobe) or generalised (involving both hemispheres) symptoms and signs.\n \nStatus epilepticus is defined as a seizure lasting 5 minutes or more, or two or more seizures without complete recovery between episodes. \n \n\n# Epidemiology\n \n\n - Epilepsy affects roughly 1% of the population in the UK.\n - One in every 220 children in the UK has epilepsy, with over 60,000 children and young people in the UK affected. \n - It occurs more commonly in children than adults. \n \n\n# Aetiology\n \n\nEpilepsy can be due to an idiopathic generalised epilepsy syndrome (see classification below), or can be caused by various factors including:\n\n- Genetic predispositions\n - Children of parents with epilepsy are more likely to have seizures, however, the overall risk is still low. \n- Head trauma\n- Tumours\n - More common in supratentorial tumours \n - Can be seen due to hamartomas in Tuberous Sclerosis \n- Infectious diseases\n - Meningitis and encephalitis \n- Prenatal injuries\n- Electrolyte disturbances \n - Hyper and hyponatraemia \n - Hypoglycaemia\n - Hypocalcaemia\n - Hypomagnesaemia\n- Developmental disorders\n- Metabolic disorders\n - Maple Syrup Urine Disease\n - MCAD deficiency \n\nIn children with established epilepsy, seizures can be triggered by:\n \n - Sleep deprivation \n - Playing video games or watching television \n\n\n## Febrile Convulsions \n\nAn important cause of seizures in children is fever. Febrile convulsions, or febrile seizures, are common in children between 6 months to 6 years, presenting as seizures that occur during a fever. The seizures are typically generalised tonic-clonic in nature and usually last less than 5 minutes. Approximately 1 in 20 children will have a febrile seizure. \n \nDiagnosis is generally made from history alone, and management involves treating the underlying fever cause and ensuring the child is safe whilst they are having the seizure. \n\n\n# Classification\n\nThere are many idiopathic epilepsy syndromes affecting children. These include: \n\n\n## Childhood Absence Epilepsy (CAE)\n\nAbsence seizures can occur up to 100 times per day, and many episodes may not be noticed. It is common in children aged 4-10 years and often does not persist into adulthood. Diagnosis is often based on clinical history and EEG showing spike and wave activity, stimulated by hyperventilation. \n\nCAE is typically responsive to anti-epileptics such as ethosuximide. CAE is associated with a good prognosis, as children often do not develop other types of seizures.\n\n\n## West Syndrome\n \n\nWest Syndrome, or infantile spasms, starts between 4-8 months of age. The primary symptom is myoclonic jerking, termed 'jack-knife' spasms, which usually occur in clusters. This syndrome is often associated with developmental regression and high morbidity. Diagnosis is typically made based on the distinctive form of seizure activity and characteristic EEG findings of hypsarrhythmia. Most children may have genetic abnormalities, metabolic conditions or brain injuries/malformations, however, 1 in 3 have no known cause for the seizures. \n\nManagement usually includes prednisolone, ACTH, and/or vigabatrin. Early treatment optimises the child's development, as most children will have intellectual disability later in life. Many children with West syndrome develop Lennox-Gastaut later in childhood.\n \n## Dravet's Syndrome\n \nSevere myoclonic epilepsy typically onsets in infancy in an otherwise healthy infant. Typically will present with convulsive status epilepticus during intercurrent illness or following a vaccination. It is typically refractory to anti-epileptic treatment. \n\nThe syndrome is also associated with loss of developmental milestones and Autism Spectrum Disorder. \n\nDiagnosis is achieved by genetic testing, and management includes multidisciplinary team engagement. Unfortunately, there is an estimated 15% mortality by age 20.\n\n## Lennox Gastaut Syndrome\n\nA syndrome of tonic, atonic and atypical absence seizures occurring in children aged 3-5 years. Absence seizures are considered atypical as they last longer and have a gradual onset when compared to typical absence seizures. EEG will show classic findings of generalised spike-and-wave discharges.\n\nIt is subdivided into idiopathic or symptomatic. In idiopathic Lennox Gastaut syndrome, the child has normal psychomotor development. In symptomatic Lennox Gastaut syndrome, there are associated neurological or neuroradiological abnormalities (i.e. tuberous sclerosis, brain malformations, birth injuries). \n\nIn addition to seizures, children often have motor, behavioural and language dysfunction. \n\nManagement is difficult, as seizures are commonly refractory to anti-epileptics. Sodium valproate is used first line, but other options include lamotrigine and clobazam. Surgical intervention including corpus callostomy and vagus nerve stimulation may be tried for refractory cases. \n\n## Juvenile Myoclonic Epilepsy \n\nMost commonly onset in adolescence and early adulthood, patients will have early morning myoclonic jerks of the upper limbs - with arms \"flinging\" in the air. After a few months, the myoclonic jerks commonly progress to generalised tonic-clonic seizures. Patients may also suffer from absence seizures, and children may have a history of childhood absence seizures. \n\nWhile many have a family history of JME in distant relatives, there is no genetic test specific for JME. Seizures are often triggered by lack of sleep, stress, flashing lights or alcohol intake. Management focuses on avoiding these triggers. It is typically well controlled using anti-epileptic medications, with sodium valproate and lamotrigine being the medications of choice. Most patients require lifelong treatment with anti-epileptic drugs. \n\n## Panayiotopoulos Syndrome\n\nFeatures autonomic seizures with ictal vomiting, pupil dilation and syncope lasting up to 30 minutes. Some children will have vision changes including flashing lights, blurring, and loss of vision. It onsets in childhood, around age 3-6 years. EEG will show characteristic multiple shifting foci predominantly in the occipital region. \n\nChildren have otherwise normal development; typically, seizures stop after 2-3 years. There is no associated increased risk of epilepsy later in life. \n\n## Benign Epilepsy with Centrotermporal Spikes (BECTS) \n\nThis condition, formerly known as Benign Rolandic Epilepsy, typically affects children aged 3-10 years and mostly occurs during sleep. Parents might notice the child experiencing a tonic seizure overnight or find the child on the floor or with disrupted bedding in the morning. The diagnosis is based on history and characteristic EEG findings during sleep of centro-temporal spikes.\n\nIt is the most common form of childhood epilepsy and is associated with an excellent prognosis, with resolution in most children by adolescence. \n \n\n# Signs and Symptoms\n \nEpilepsy may present with focal seizures, generalised seizures, or both. \n\nFocal seizures may produce symptoms specific to the involved lobe: \n\n- Occipital lobe seizures may cause visual phenomena \n- Temporal lobe seizures may cause the child to experience unusual smells \n\n\nGeneralised seizures may include:\n\n- Typical absence seizures:\n - Brief, sudden onset, episodes of unresponsiveness where the child may stop what they are doing and stare \n - The child may also flutter their eyelids or movements of their arms \n - They will not respond even to vigorous stimulation\n- Atypical Absence seizures:\n - Children will be unresponsive and commonly stare blankly, but these episodes occur more gradually and last longer than typical absence seizures. \n- Tonic: muscle stiffening\n- Tonic-clonic: muscle stiffening followed by rhythmic jerking\n- Myoclonic: brief jerking movements\n - Such as seen in infantile spasms or juvenile myoclonic epilepsy\n- Atonic: sudden falls, the child suddenly becomes limp \n - Can be seen in Lenox-Gastaut or Dravet syndrome \n\n \n\n# Differential Diagnosis\n \n\n - **Syncope**: A brief loss of consciousness, with rapid recovery. Often associated with prodromal symptoms of dizziness, nausea and changes to the vision. Associated with a history of prolonged standing, dehydration or heat. \n - **Non-epileptic attack**: Also referred to as dissociative seizures, the child or young person may have convulsive movements of their body/limbs, become incontinent or become unresponsive. These seizures tend to last longer than epileptic seizures and are not managed with benzodiazepines. \n - **Night terrors**: Episodes occur at night, when the child awakens inconsolably, crying and screaming. The child does not remember the episodes in the morning, and children outgrow these episodes by age 10. \n - **Day Dreaming**: A common differential for absence seizures. This typically onsets more gradually. It is able to be ended by others attempting to gain the child's attention. \n\n# Investigations\n \n\nRefer children urgently (less than 2 weeks) for assessment by a paediatrician with expertise in assessing first seizures. \n\n - Epilepsy is diagnosed based on history and examination\n - An EEG may be used to provide information about seizure type, but an EEG is not used to exclude a diagnosis of epilepsy. \n - Seizures can be provoked by hyperventilation, photic stimulation, or sleep deprivation.\n - Imaging modalities such as MRI or CT are usually performed to rule out structural brain abnormalities.\n - An ECG may be done to identify cardiac conditions which may mimic epilepsy. \n\nIf epilepsy onset is below age 2 or there are other features (i.e. learning disability, structural abnormality, autism spectrum disorder), then whole genome sequencing may be done. \n \n\n# Management\n\nWhen there is a known reversible cause for the seizure (i.e. electrolyte or metabolic disturbance), this should be managed appropriately (i.e. glucose for hypoglycaemia). \n\nFor idiopathic seizures or those associated with epilepsy syndromes, management necessitates a multidisciplinary approach to optimise the child's care. This may include: \n\n- Anti-epileptic medications\n- Some children will be recommended a ketogenic diet or low glycaemic diet \n- Surgery may be used in refractory cases or if the seizures are caused by tumours\n - This may include removal of a tumour, vagus nerve stimulation or corpus callosotomy \n- MDT support for comorbidities such as educational and psychological support \n- Emergency seizure plans for both home and school \n - Parents should be advised to ensure their child is safe whilst having a seizure, to call 999 and start a timer. Once the seizure has finished, they should place the child in the recovery position. \n\n# Complications\n\nThe rates of complications depend on the underlying cause of epilepsy, but may include:\n\n- Mood disorders\n- Status Epilepticus \n - Prolonged seizure activity lasting more than 5 minutes. \n- Sudden Unexpected Death in Epilepsy (SUDEP)\n - A rare complication of epilepsy in which an otherwise healthy individual with epilepsy dies unexpectedly. \n- Developmental delay or regression \n\n# Prognosis \n\nThe prognosis of epilepsy in childhood is dependent on the underlying cause. Childhood Absence seizures and Benign Rolandic Epilepsy both are associated with a good prognosis. \n\n# NICE Guidelines\n \n[NICE Guidelines on Epilepsies in Children, Young People and Adults](https://www.nice.org.uk/guidance/ng217) \n\n# References \n\n [NHS page on Febrile Seizures](https://www.nhs.uk/conditions/febrile-seizures/)\n \n [Resuscitation Council UK Paediatric Status Epilepticus Algorithm](https://www.resus.org.uk/sites/default/files/2022-03/RCUK%20Paediatric%20emergency%20algorithms%20and%20resources%20Mar%2022%20V1.pdf) \n \n [Non Epileptic Attack Disorder](https://www.mind.org.uk/information-support/types-of-mental-health-problems/dissociation-and-dissociative-disorders/nead/)\n \n [Patient Info Epilepsy in Children and Young People](https://patient.info/doctor/epilepsy-in-children-and-young-people) \n \n [Patient Info Lennox-Gastaut Syndrome](https://patient.info/doctor/lennox-gastaut-syndrome) \n \n [Epilepsy Society Children with Epilepsy](https://epilepsysociety.org.uk/children)\n \n [Epilepsy Action Childhood Absence Epilepsy](https://www.epilepsy.org.uk/info/syndromes/childhood-absence-epilepsy-cae)",
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"question": "A 5-year-old boy is brought to the Emergency Department after his parents witness a seizure at home. This has never happened before, and they are understandably very concerned. On review in the department, his observations are normal; he is well though slightly drowsy.\n\nWhat is your next step in management?",
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"explanation": "This patient fulfils the Fraser Guidelines and therefore should be prescribed contraception. The Fraser Guidelines are as follows:\n\n- They understand the doctor's advice\n- The young person cannot be persuaded to inform their parents that they are seeking contraceptive advice\n- They are likely to begin or continue having intercourse with or without the contraceptive treatment\n- Unless they receive the contraception, their physical or mental health is likely to suffer\n- It is in the young person's best interests to provide contraceptive advice and/or treatment without parental consent",
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"name": "Arrange for her to have the implant fitted",
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"explanation": "This would be a reasonable choice if you felt that she was being pressured into intercourse or if there was a suggestion that the intercourse was with someone older or otherwise inappropriate. She has attended her appointment with a partner who appears supportive, and there is no suggestion here that there is abuse in this case",
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"name": "Make a referral to safeguarding",
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"explanation": "This patient has clearly stated that she is already having intercourse with her boyfriend and is requesting contraception. Refusing to provide her with treatment is unsafe and not in her best interests",
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"name": "Refuse her request",
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"explanation": "This is a breach of confidentiality and would only be acceptable if you felt that she was putting herself or others at risk. It is important that you try to persuade her that involving her parents is a good idea however you cannot force her to tell them, nor can you tell them without her permission",
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"name": "Arrange a consultation with her and her parents",
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"explanation": "This patient has fulfilled the Fraser Guidelines to be provided with contraception and has requested the implant, not the contraceptive pill. It is worth exploring her choice to make sure she is fully informed; however, she has requested the implant, and therefore this should be what you provide",
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"comment": "Additionally to Frasier considerations (and her preference), Nexplanon is the contraceptive of choice in young people due to concerns about reliability of taking the pill and concerns about the effect of Depo on bone mineral density :)",
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"comment": "hope i read the question in the exam ",
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"explanation": "# Summary \n \n\nThe Fraser guidelines are a set of criteria that must be met for a health professional to advise a child <16 years old regarding contraception and sexual health without breaking confidentiality. \n \n\n# Guidelines\n \n\n 1. He/she has sufficient maturity and intelligence to understand the nature and implications of the proposed treatment\n 2. He/she cannot be persuaded to tell her parents or to allow the doctor to tell them\n 3. He/she is very likely to begin or continue having sexual intercourse with or without contraceptive treatment\n 4. His/her physical or mental health is likely to suffer unless he/she receives advice or treatment\n 5. The advice or treatment is in the young person's best interests.\n \n\nIf all of the above criteria are met, the child is deemed to be \"Fraser competent\" and can therefore receive advice without breaking confidentiality.\n \nIf the child does not meet these criteria, parental consent should be sought. \n \nThe Fraser criteria apply to England and Wales, while in Scotland it is a similar criteria called the Age of Legal Capacity Act 1991.\n \n\n# NICE Guidelines\n \n[NICE Clinical Knowledge Summary (CKS): Contraception](https://cks.nice.org.uk/topics/contraception-assessment/)\n\n# References\n\n[Gillick v West Norfolk and Wisbech Area Health Authority and Department of Health and Social Security 1985](https://swarb.co.uk/gillick-v-west-norfolk-and-wisbech-area-health-authority-and-department-of-health-and-social-security-hl-17-oct-1985/)\n\n[National Society for the Prevention of Cruelty to Children (NSPCC): Gillick competency and Fraser guidelines](https://learning.nspcc.org.uk/child-protection-system/gillick-competence-fraser-guidelines)",
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"question": "A 15-year-old female presents with her boyfriend, who is in the same year at school, to General Practice requesting the contraceptive implant. She and her boyfriend are already sleeping together, and she is adamant that she will not discuss this with her parents. She understands the risk of pregnancy and would like to discuss different types of contraception. She is able to weigh up the pros and cons of each.\r\n\r\nWhat should you do?",
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"explanation": "This newborn has a positive Ortolani and therefore investigation and prompt treatment are indicated",
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"explanation": "Ultrasound examination is indicated in this baby, however serial ultrasounds are not of benefit, particularly if developmental dysplasia is detected as it does not treat the problem.\nIn babies where there is no clinical suspicion of developmental dysplasia, Public Health England does not recommend routine ultrasound examination unless specific risk factors are present:\n\n1. There is a first-degree family history of hip problems in early life unless DDH was definitively excluded.\n2. There is a breech presentation:\n\n- At or after 36 completed weeks of pregnancy, irrespective of presentation at delivery or mode of delivery; or\n- At delivery if this is earlier than 36 weeks.\n- In the case of a multiple birth, if any of the babies fall into either of these categories, all babies in this pregnancy should have an ultrasound examination",
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"explanation": "This baby has a positive Ortolani's test and an ultrasound suggestive of developmental dysplasia of the hip. Risk factors include: breech presentation, female gender, family history of developmental dysplasia.\n\nEarly detection and management are key, with bracing as the first-line treatment. Surgery is reserved for those who do not respond to bracing or are diagnosed later (after six months of age) and where bracing is contraindicated (for example, if the hip is irreducible). Harness or splint treatment is much less successful if it is started after 6-8 weeks",
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"comment": "\"A newborn baby is examined as part of the routine 6-week baby check and the on gentle gentle forward pressure of the left there is movement palpable suggesting that the hip is dislocated or subluxed, but reducible.\"\n\nQuesmed please hire a proofreader, that is actually awful :/",
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"comment": "I have officially applied for the job, hopefully they have the sense to get back to me and hire me! Or anyone else haha, it's needed!",
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"comment": "im cnofused is the baby 6w old or 4w old?",
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"comment": "the on gentle gentle forward pressure of the left",
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"explanation": "# Summary\n \n\nDevelopmental Dysplasia of the Hip (DDH) is a congenital abnormality where the femoral head and the acetabulum do not articulate correctly. This condition can lead to easy dislocation and abnormal development of the joint. Key signs and symptoms include limited hip abduction, asymmetrical gluteal and thigh skinfolds, and limb length discrepancy. Barlow and Ortolani manoeuvres serve as primary screening tools. The condition's diagnosis mainly relies on hip ultrasonography. Management ranges from observation in mild cases to the use of a Pavlik harness or surgery in more severe cases.\n \n\n# Definition\n \n\nDevelopmental dysplasia of the hip (DDH) is a congenital abnormality of the hip joint in which the ball of the femur (femoral head) and the socket of the pelvis (acetabulum) do not articulate appropriately. This mal-alignment can result in the joint dislocating easily and continuing to develop abnormally.\n \n\n# Epidemiology\n \n\nThe incidence of DDH varies worldwide, ranging from 1 to 34 cases per 1000 births. The variability is due to differing diagnostic criteria and screening practices among countries. In the UK, it is estimated to affect 1-2% of newborns. \n\nIt is more common in the left hip than the right, but occurs bilaterally in 20% of cases. \n \n\n# Aetiology\n \n\nDDH is commonly associated with certain risk factors known as the 5 Fs:\n \n\n - Female: The condition is more prevalent in females in a 4:1 female-to-male ratio. \n - Firstborn: Firstborn children have a higher risk.\n - Family history: DDH often runs in families.\n - Frank breech presentation: Babies presenting buttocks or feet first in the womb have a 17-fold higher risk of DDH.\n - Fluid: Low amniotic fluid levels (oligohydramnios) can increase the risk.\n\nOther risk factors include:\n \n - Prematurity\n - Multiple pregnancy \n - Neuromuscular conditions (i.e. cerebral palsy)\n \n\n# Signs and Symptoms\n \n\nClinical presentation may vary based on age. In infants, key signs include:\n \n\n - Limited hip abduction, especially when the hip is flexed.\n - Asymmetry of gluteal and thigh skinfolds.\n - Apparent limb length discrepancy.\n \n\nIn older children, the following signs may be present:\n \n - Galeazzi sign: Unilateral femoral shortening is a positive result. This may suggest DDH but it can also be due to other causes of discrepency of limb length. \n - Walking difficulties or a limp.\n - Delayed walking.\n - Waddling gait in bilateral cases.\n\nIn cases of bilateral DDH:\n \n - Waddling gait with hyperlordosis.\n - Typically it is difficult to diagnose as there is often less pronounced limb length discrepency. \n \n\n# Differential Diagnosis\n \n\nDifferential diagnoses for DDH include:\n \n\n - **Transient synovitis**: Presents with acute onset of hip pain, refusal to bear weight, and fever.\n - **Septic arthritis**: Similar to transient synovitis but with a high fever and systemic symptoms. Prompt diagnosis is crucial to prevent joint damage.\n - **Legg-Calve-Perthes disease**: Typically presents in children aged 4-10 years with a gradual onset of limping, pain in the hip, thigh, or knee, and decreased range of motion.\n - **Slipped Upper Femoral Epiphysis (SUFE)**: Common in obese preteens and teenagers. Symptoms include hip pain, limping, and sometimes knee pain.\n \n\n# Investigations\n \n\nScreening Examination\n \n- Barlow (tests for posterior dislocation) and Ortolani (tests for relocation on hip abduction) manoeuvres are primary screening tools. \n- Both are used during the newborn physical screening examination and the infant screening examination at 6-8 weeks. \n\nFor infants with risk factors (i.e. family history of DDH, breech presentation), then a screening ultrasound should be done within the first 6 weeks of life. \n\nIf DDH is clinically suspected, hip ultrasonography should be ordered for confirmation, especially in infants less than 6 months of age. For older infants and children, pelvic radiography may be more suitable.\n \n\n# Management\n \n\nThe management approach is largely dependent on the severity and age at diagnosis:\n \n\n - In mild cases or those detected early, the condition may be self-limiting within the first few months of life.\n - A Pavlik harness may be used to maintain the hip in a flexed and abducted position for 6-12 weeks.\n - More severe cases, those diagnosed > 6 months of age, or those not responding to non-operative management, may necessitate surgical intervention for reduction and stabilization.\n \n# Complications\n\nDDH can result in degeneration of the hip joint and pain in the lower back and hip. It is responsible for approximately 1 in 3 hip replacements before the age of 60. \n\n# NICE Guidelines\n \n[NICE Guidelines for Childhood Limp](https://cks.nice.org.uk/topics/acute-childhood-limp/diagnosis/differential-diagnosis/) \n\n# References \n \n [NHS UK - DDH](https://www.nhs.uk/conditions/developmental-dysplasia-of-the-hip/)\n \n [Patient Info - Developmental dysplasia of the hip](https://patient.info/doctor/developmental-dysplasia-of-the-hip-pro)",
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"question": "A newborn baby is examined as part of the routine 6-week baby check and the on gentle gentle forward pressure of the left there is movement palpable suggesting that the hip is dislocated or subluxed, but reducible. Ultrasound examination is undertaken at 4 weeks of age which is suspicious of developmental dysplasia of the hip joint.\n\nWhat is the correct management?",
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"explanation": "The use of CPAP may be indicated in those children with impending respiratory failure, for example, due to bronchiolitis. However, this clinical presentation is more in keeping with a cardiac cause for cyanosis as opposed to a respiratory cause. Although there is minimal improvement with high flow oxygen, and there is a temptation to start a more intense form of respiratory support, it is unlikely to improve the neonate's clinical picture",
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"explanation": "A single dose of oral corticosteroid (such as prednisolone or dexamethasone) may be given in the initial treatment of croup. If the child is too unwell to take the steroid orally, it is reasonable to administer it intramuscular (such as dexamethasone) or nebulised (such as budesonide). However, croup is not the most likely diagnosis here as there is no cough, stridor or temperature",
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"explanation": "Antibiotics would be indicated if you felt that this was an acute infective respiratory diagnosis; however, at four days old and without any other signs of infection and no temperature, this is not the likely diagnosis here. If bronchiolitis was suspected, this would also not necessarily be an indication for antibiotics as bronchiolitis is usually viral in origin, with the management being mainly supportive",
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"explanation": "Nebulised bronchodilators such as salbutamol are used to treat reversible airway obstruction, such as acute asthma exacerbations. As this neonate is only four days old, the concern here is of a cyanotic congenital heart abnormality, and therefore salbutamol is not indicated",
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"explanation": "This baby is likely to have a cyanotic congenital heart abnormality such as transposition of great arteries or tetralogy of Fallot. There is not always a clinically audible murmur present. This typically presents as an increasingly cyanotic newborn in the first few days of life, as the previously patent ductus arteriosus closes and the newborn can no longer rely on it to allow oxygenated blood into the systemic circulation. These babies don't appear to work so hard to breathe compared with babies with lung disease. Another clue that this is less likely to be a respiratory condition is the minimal improvement with high flow oxygen. A prostaglandin infusion will help keep the ductus arteriosus open whilst awaiting specialist input",
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"comment": "when do you want to close the PDA vs keep it open?",
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"comment": "PDA open if its the only thing keeping them alive i.e. in cyanotic heart diseases like TOF. If they have a PDA that didn't close by itself and no other heart conditions, then you want to close it with indomethacin.",
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"comment": "If its PDA why was there no murmur heard when listening to heart sounds?",
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"comment": "oh come on, you can't just give us a condition and then give it to us in a rare presentation with no murmur. ffs.",
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"comment": "literally got thrown off becoz no murmur mentioned",
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"comment": "yeh sure lets just whack prostaglandins into a 4 day old baby when we're just guessing whats wrong with them",
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"comment": "get on the wards, mate!",
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"explanation": "# Summary\n \nCongenital cardiac disease refers to a variety of heart abnormalities present at birth, often influenced by maternal risk factors such as infectious disease during pregnancy (e.g. rubella), exposure to teratogenic drugs (e.g. thalidomide, isotretinoin, lithium), substance misuse (e.g., alcohol), and poorly controlled type 1 or 2 diabetes. Identification primarily relies on signs and symptoms observed in newborns, with murmurs often being present, with/without cyanosis, and confirmatory investigations such as echocardiography. Management is typically multidisciplinary and can involve medical therapy, interventional procedures, or surgery, depending on the severity and type of heart defect.\n \n \n# Definition\n \n\nCongenital cardiac disease is a general term referring to abnormalities in the heart's structure that arise before birth. These defects can involve the heart walls, heart valves, or the arteries and veins near the heart.\n \n\n# Epidemiology\n \n\nThe global incidence of congenital heart disease is estimated to be around 1% of live births, making it the most common type of congenital disorder. \n \n\n# Aetiology\n \n\nSeveral factors can contribute to the development of congenital heart disease:\n \n\n- Infectious causes: \n - Maternal rubella infection during pregnancy\n- Teratogenic drugs: \n - Exposure to certain medications during pregnancy, such as thalidomide, isotretinoin, and lithium, increases the likelihood of developing congenital heart disease.\n- Substance misuse: \n - Maternal misuse of substances such as alcohol can also lead to this condition.\n- Maternal diabetes: \n - Poorly controlled type 1 and type 2 diabetes during pregnancy\n - Maternal gestational diabetes is not a known risk factor \n- Family history of congenital heart disease\n - Risk is also increased in consanguineous couples \n\n \n# Classification\n\nCongenital heart disease can be divided into cyanotic or acynotic heart disease.\n\nCyanotic Heart Disease:\n\n- Transposition of the great arteries (TGA)\n- Pulmonary and tricuspid atresias\n- Tetralogy of Fallot (ToF)\n- Total anomalous pulmonary venous return \n- Persistent truncus arteriosus\n- Hypoplastic left heart\n\nAcyanotic Heart Disease:\n\n- Ventricular septal defect (VSD)\n- Atrial septal defect (ASD)\n- Patent ductus arteriosus (PDA)\n- Aortic stenosis \n- Pulmonic stenosis \n- Coarctation of the aorta \n- Endocardial fibroelastosis \n \n\n# Signs and Symptoms\n \n\nNewborns with congenital cardiac disease may present with a variety of signs and symptoms, including:\n \n\n - Cyanosis\n - Fast or troubled breathing\n - Fatigue\n - Poor feeding\n - Delayed growth\n - Heart murmur on auscultation\n \n\nThese symptoms can vary widely depending on the type and severity of the heart defect.\n \n\n# Differential Diagnosis\n \n\nIn an infant presenting with the signs and symptoms of congenital heart disease, several conditions should be considered:\n \n\n - **Respiratory distress syndrome**: This condition can cause fast, troubled breathing, and fatigue. However, it is typically associated with prematurity.\n - **Pneumonia**: Can also lead to breathing difficulties and fatigue, but it is often accompanied by fever and abnormal lung sounds on auscultation.\n - **Gastrointestinal disorders**: These can cause poor feeding and delayed growth but are typically accompanied by vomiting, diarrhoea, or abdominal distension.\n \n\n# Investigations\n \n\nWhilst some cases are detected during prenatal scans, many cases are detected after birth. The following investigations are key to diagnosing congenital heart disease:\n \n\n - Pulse oximetry: To detect low oxygen levels in the blood. This should be measured both pre and post-ductal, with > 3% difference being significant. \n - Chest X-ray: Can reveal an enlarged heart or abnormal heart shape.\n - Electrocardiogram (ECG): Can detect abnormal heart rhythms.\n - Echocardiogram: The gold standard in diagnosing congenital heart disease, providing a detailed image of the heart's structure and function.\n \n\n# Management\n \n\nThe management of congenital heart disease is complex and depends on the type and severity of the heart defect.\n\nRed flag features require more urgent management. These features include:\n\n- Lower limb saturations < 96%\n- More than 3% pre/post ductal difference \n- Signs of heart failure or shock\n\n\nIt typically involves a multidisciplinary team and can include:\n\n- Conservative management:\n - For certain defects (i.e. mild atrial septal defects, a watch-and-wait approach may be adopted as many will close by age 1)\n\n- Medical management:\n - Some patients will require medications including diuretics and ACE inhibitors depending on the type of congenital heart disease. \n- Interventional procedures: Catheter-based procedures to repair certain types of heart defects.\n \n- Surgical intervention: For more complex or severe heart defects, surgery may be necessary.\n\n# Complications\n\nDepending on the type and severity of congenital heart disease, potential complications include:\n\n- Learning difficulties\n- Pneumonia \n- Infective Endocarditis \n- Pulmonary hypertension \n- Heart failure \n\nSudden cardiac death is very rare. \n\n# Prognosis\n\nSurgically corrected congenital heart disease, particularly when isolated, has a good prognosis, however, there is still a reduced life expectancy when compared to the general population. \n\n# NICE Guidelines\n\n[NICE Guidelines on Structural Heart Defects](https://www.nice.org.uk/guidance/conditions-and-diseases/cardiovascular-conditions/structural-heart-defects) \n\n \n# References\n \n [NHS Congenital Heart Disease](https://www.nhs.uk/conditions/congenital-heart-disease/#:~:text=Congenital%20heart%20disease%20is%20a,babies%20born%20in%20the%20UK.) \n \n [British Heart Foundation Congenital Heart Disease](https://www.bhf.org.uk/informationsupport/conditions/congenital-heart-disease) \n \n [Patient Info Congenital Heart Disease in Children](https://patient.info/doctor/congenital-heart-disease-in-children) ",
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"question": "A new mother presents to the Emergency Department with her four-day-old child, concerned about his breathing and colour. Initial observations are as follows:\n\n- Temperature 36.8°C\n- Heart rate 200 bpm\n- Blood pressure 80/50 mmHg\n- Respiratory rate 80 bpm\n- Oxygen saturations 80% (on room air), which improves to 85% on 100% oxygen.\n\nThe neonate is a mottled blue colour, but lung fields are clear on auscultation, and heart sounds are normal. Alongside your initial A-E assessment, what other treatment is important to initiate in this case?",
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"explanation": "Parainfluenza virus can be a cause of bronchiolitis but is more commonly implicated in croup. Croup usually affects young children aged between six months and three years, with most cases occurring in one-year-olds and presents with a distinctive barking cough",
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"explanation": "Streptococcus pneumonia is a common cause for bacterial pneumonia and should be considered in the differential diagnosis; however, as this child had a preceding coryzal illness and the crackles are widespread, this leans more towards a viral diagnosis such as bronchiolitis. In bacterial pneumonia, crackles are more likely to be localised to one zone",
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"explanation": "Group B streptococcal infections are a potentially life-threatening cause of sepsis in neonates. One in four women carry group B streptococci vaginally, which can infect the amniotic fluid before delivery or infect the baby during delivery, causing sepsis, pneumonia, or meningitis. Early-onset infections usually occur in the first seven days of life, and late-onset infections are usually from seven to 90 days of life. Pneumonia is more commonly associated with early-onset infection, as the baby swallows infected amniotic fluid during the delivery. This case vignette is not likely to be due to Group B streptococcus",
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"explanation": "This is a case of bronchiolitis, the most common respiratory presentation in children under the age of two years old, peaking between the ages of three and six months. It is usually commonly viral in origin and most often due to RSV. Other viral causative agents include human metapneumovirus (hMPV), adenovirus, rhinovirus, and parainfluenza and influenza viruses",
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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": "A five-month-old baby is brought to the Emergency Department with laboured breathing and a raised temperature following a short coryzal illness. On examination, he has subcostal recession and audible, widespread crackles on chest auscultation.\n\nWhat is the likely causative organism for this presentation?",
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"explanation": "This patient is showing signs of lithium toxicity, for which intravenous fluids is the mainstay of treatment. Common causes of lithium toxicity include dehydration, alcohol intake and angiotensin-converting enzyme inhibitors (ACE-i) such as ramipril as they reduce glomerular filtration rate (GFR) and enhance the tubular reabsorption of lithium (thus increasing plasma concentrations of lithium). In addition, the patient has recently been through a time zone change and therefore may have taken his medications at different times to his usual; therefore, one should be alert to the possibility of lithium toxicity",
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"explanation": "This patient's presentation could be due to traveller's diarrhoea; however, it would not explain the tremor. If traveller's diarrhoea was the diagnosis, then management is mainly supportive (for example, with intravenous fluids). Antibiotics are generally not indicated in traveller's diarrhoea, however in some cases, they have been shown to improve symptoms, and a fluoroquinolone such as azithromycin may be a reasonable choice. Still, it would not be the basis of treatment",
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"explanation": "Benzodiazepines such as lorazepam are used in the treatment of serotonin syndrome, which occurs as a result of high levels of serotonin in the body. It is an uncommon but serious side effect of certain medications used to treat psychiatric conditions such as depression (for example, citalopram, fluoxetine, sertraline). This patient's symptoms could be explained by serotonin syndrome; however, he is not taking any medications that might induce this",
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"explanation": "Oral antibiotics from the tetracycline, fluoroquinolone or macrolide class would be a reasonable treatment if suspecting an atypical pneumonia such as legionnaires disease. Legionnaires disease is associated with water from ventilation systems. Most people become infected when they inhale microscopic water droplets containing legionella bacteria, e.g., the spray from a shower, faucet or whirlpool, or water from the ventilation systems. Whilst atypical pneumonia such as legionella may present with gastrointestinal symptoms, it would be uncommon to have no respiratory symptoms, and there is no history of a fever. It would also not account for the tremor that the patient has reported",
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"explanation": "# Summary\n\nLithium, commonly used in psychiatric disorders, may produce a range of side effects, which can be categorised into those seen at a therapeutic dose and those indicating toxicity. Therapeutic dose side effects may include fine tremor, dry mouth, GI disturbances, increased thirst and urination, drowsiness, and thyroid dysfunction. Signs of toxicity encompass coarse tremor, CNS disturbance (including seizures, impaired coordination, dysarthria), arrhythmias, and visual disturbance. Diagnosis relies on identifying these clinical features and serum lithium levels. Management involves supportive measures, electrolyte balance maintenance, renal function monitoring, seizure control, IV fluid therapy, and, in severe cases, haemodialysis.\n\n# Indications\n\nLithium is used primarily to treat bipolar disorder and mania, but can also be used in depression (especially if recurrent) and as mood stabiliser for aggressive/self-harming behaviour.\n\nIt is contraindicated in: Addison’s disease, cardiac disease associated with rhythm disorder, personal/family history of Brugada syndrome, low sodium diets and untreated hypothyroidism.\n\nIt should be avoided in severe renal impairment due to the risk of toxicity, as it has a very narrow therapeutic index.\n\n# Side Effects\n\nCan be remembered with the mneumonic LITHIuM:\n\n* **L**eucocytosis\n* **I**nsipidus\n* **T**remor (fine)\n* **H**ypothyroid\n* **I**ncreased weight\n* **U**\n* **M**etallic taste \n\nWomen of child bearing age should take contraception if commenced on lithium, which is generally avoided in pregnancy due to the high risk of development of cardiac malformations in the first trimester.\n\n# Monitoring\n\n- Before starting: renal (U+Es), cardiac (ECG), and thyroid function (TFTs). BMI and FBC should also be done beforehand.\n- Monitor body-weight or BMI, serum electrolytes, eGFR, and thyroid function every 6 months during treatment, and more often if there is evidence of impaired renal or thyroid function, or raised calcium levels\n\n\n# Lithium Toxicity\n\n## Signs and Symptoms\n\n### Clinical features at therapeutic dose \n\n- Fine tremor\n- Dry mouth\n- Gastrointestinal disturbance\n- Increased thirst\n- Increased urination\n- Drowsiness\n- Thyroid dysfunction\n\n### Clinical features in lithium toxicity\n\n- Coarse tremor\n- Central nervous system disturbance, which may include seizures, impaired coordination, and dysarthria\n- Cardiac arrhythmias\n- Visual disturbance\n\n\n\n\n## Differential Diagnosis\n\nLithium side effects and toxicity may be mistaken for several other conditions:\n\n- **Neurological conditions**: Given the tremors, dysarthria, and impaired coordination, conditions like Parkinson's disease or cerebellar disorders may be considered.\n- **Endocrine disorders**: Increased thirst and urination could point towards diabetes insipidus or diabetes mellitus.\n- **Cardiac conditions**: Arrhythmias might suggest primary cardiac disease.\n- **Substance intoxication or withdrawal**: Some symptoms overlap with those of alcohol or benzodiazepine withdrawal, or other substance intoxications.\n\n## Investigations\n\n- Serum lithium levels: This is the gold standard for diagnosing lithium toxicity.\n- Electrolyte levels: To assess for any electrolyte imbalance.\n- Thyroid function tests: Given the potential for thyroid dysfunction.\n- Renal function tests: Given lithium's potential to cause renal impairment.\n- ECG: To assess for arrhythmias.\n\n## Management\n\nManagement of lithium toxicity is largely supportive and often requires specialist input. Key strategies include:\n\n- Maintaining electrolyte balance\n- Monitoring renal function\n- Seizure control\n- IV fluid therapy and urine alkalisation, which enhance the excretion of the drug\n- Benzodiazepines may be used to treat agitation and seizures\n- Haemodialysis might be required if renal function is poor\n\n# References\n\n[Click here to see the BNF guidance on Lithium](https://bnf.nice.org.uk/drug/lithium-carbonate.html)",
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"question": "A 46-year-old man presents to the Emergency Department with abdominal pain, diarrhoea and vomiting. He feels weak and reports a new-onset tremor. He has just come back from a cruise in the Caribbean. His only past medical history is bipolar disorder, for which he takes lithium and newly diagnosed hypertension, for which his GP has recently started him on ramipril.\n\nWhat intervention should form the basis of your treatment?",
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"explanation": "Risperidone has a lower risk of producing extrapyramidal side effects than typical antipsychotics such as chlorpromazine and haloperidol; however, there is still a risk of drug-induced Parkinsonism, particularly at higher doses. It does not, however, cause Parkinson's Disease",
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"explanation": "There is a small increased risk of stroke when starting certain antipsychotic medications. The National Institute for Health and Care Excellence (NICE) quotes an absolute risk increase of 1.22% (an extra 12 strokes per 1000 people starting an antipsychotic)",
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"explanation": "Patients started on risperidone should be monitored for prolactin concentration at the start of therapy, at six months, and then yearly. Clozapine can cause agranulocytosis and therefore requires differential white blood cell monitoring weekly for 18 weeks, then fortnightly for up to one year, and then monthly. This is not the case for risperidone",
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"comment": "Damn got me on the wording, gotta remember PD =/= Parkinsonism",
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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 76-year-old female is diagnosed with Alzheimer's dementia. Over the last few years, her cognition has declined, and her behaviour has become less manageable. She is now becoming aggressive towards staff and other residents in her care home. Her GP is considering starting risperidone to help manage her aggression as behavioural measures are failing.\n\nWhich of the following is a recognised risk of risperidone?",
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"explanation": "This patient is showing some of the classic signs and symptoms of early opiate withdrawal. Treatment in the first instance should be supportive, and patients may require fluid resuscitation to replace fluids lost through sweating and diarrhoea. Should they wish it, the patient can have withdrawal management with either buprenorphine or methadone; however, this should be managed by an experienced professional",
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"explanation": "This patient may well be anxious as they have just been arrested, and anxiety can account for some of the symptoms described but would not account for the shivering or the dilated pupils",
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"explanation": "This is a reasonable differential as the signs and symptoms of alcohol and opiate withdrawal are very similar, however, dilated pupils are more commonly associated with opiate withdrawal than alcohol",
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"explanation": "Drug abuse can lead to drug-induced psychosis. However, this is not the clinical picture here",
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"explanation": "Drug and alcohol abuse (particularly cocaine use) can raise the risk of myocardial infarction; however, this is not the most likely diagnosis",
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"comment": "Pinpoint pupils = opiate misuse/overdose, withdrawal causes dilation. ",
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"explanation": "\n# Substance misuse\n\n### Definition\n- According to ICD-10, mental and behavioural disorders secondary to substance misuse may be categorised as follows: \n\t- Acute intoxication\n\t- Harmful use (damage to health, either physical or mental)\n\t- Dependence syndrome\n\t- Withdrawal state\n\t- Withdrawal state with delirium\n\t- Psychotic disorder\n\t- Amnesic syndrome\n\t- Residual and late-onset psychotic disorder\n \n# Opiate Intoxication and Withdrawal \n- This includes heroin, and they exert their effects through acting on the opioid receptors\n- Features are:\n\t- Drowsiness\n\t- Confusion\n\t- Decreased respiratory rate\n\t- Decreased heart rate\n\t- Constricted pupils\n\t- Track marks (needle marks) if the intravenous route has been used; abscesses at injection sites; veins thrombosed and damaged causing difficulties with intravenous access (causing difficulty in \n- Opiate withdrawal is a common issue that may be encountered within general medicine due to the prevalence of opiate abuse. Withdrawal from heroin can begin as early as 6 hours after the last dose, with symptoms peaking at 36-72 hours. Unlike alcohol withdrawal, it is unpleasant but not especially dangerous or life-threatening.\n- Features include: \n\t- Agitation\n\t- Anxiety and irritability \n\t- Muscle aches or cramps\n\t- Chills\n\t- Runny eyes\n\t- Runny nose\n\t- Sweating\n\t- Hypersalivation\n\t- Yawning\n\t- Insomnia\n\t- Gastrointestinal disturbance such as abdominal cramps, nausea, diarrhoea and vomiting\n\t- Dilated pupils\n\t- Piloerection \n\t- Increased heart rate and blood pressure\n- Drugs used in the management of opiate abuse include:\n\t- **During withdrawal** the following drugs may be used to help with symptoms:\n\t\t- Methadone: beware, may cause prolonged QTc\n\t\t- Lofexidine (alpha 2 receptor agonist)\n\t\t- Loperamide (for diarrhea) \n\t\t- Anti-emetics (for nausea)\n\t\t- Benzodiazepines (for agitation)\n\t\t--> NICE advises against prescribing opiates during opiate withdrawal, but prefers symptomatic management or use of lofexidine. \n\t- **Detox programmes** use methadone and buprenorphine (the latter is a partial agonist of the opiate receptor, so can trigger withdrawal) \n\t- **Relapse** can be prevented using neltrexone once detox is complete.\n\t- **Overdose** can be managed with naloxone \n\n# Alcohol Intoxication, Withdrawal, and Wernicke-Korsakoff Syndrome \n- Alcohol abuse is common. Features of intoxication include:\n\t- Ataxic gait\n\t- Nausea and vomiting\n\t- Reduced GCS\n\t- Dysarthria\n\t- Impaired judgement \n- Alcohol withdrawal is a potentially life-threatening syndrome with characteristic features. Onset is usually 12 hours after the last drink:\n\t- Nausea and vomiting\n\t- Tremor\n\t- Sweating\n\t- Anxiety\n\t- Agitation\n\t- Headache\n\t- Clouding of consciousness \n\t\t- These features are summarised by the 'CIWA' score - Clinical Institute Withdrawal Assessment for Alcohol - which could be used to monitor for signs of alcohol withdrawal, and to guide management.\n\t\t- Prevention and treatment of alcohol withdrawal is with short acting benzodiazepines such as chlordiazepoxide (Librium) and oxazepam (latter if there is evidence of liver injury.)\n\t\t- Supportive treatment includes fluids, anti-emetics, and Pabrinex (to prevent Wernicke-Korsakoff's syndrome.)\n\t\t- Referral to local drug and alcohol liaison teams should be offered.\n\t- Delirium tremens is a life threatening medical emergency, and usually occurs at day 3 of withdrawal, and lasts 3 days, characterised by paranoid delusions, visual/auditory and classically haptic (tactile) hallucinations (sensation of crawling e.g. formication), and seizures. Once delirium tremens starts, NICE recommends oral lorazepam as first line, and if the oral route cannot be used for whatever reason, parenteral lorazepam or haloperidol. \n- Wernicke-Korsakoff Syndrome:\n\t- A syndrome associated with chronic alcohol abuse that occurs due to B1 (thiamine) deficiency, resulting in mammillary body atrophy. It is not exclusive to alcohol abuse, however, with any individual with severe nutritional deficiency at risk. \n\t- It may be precipitated by a period of excess vomiting (which may reduce nutrition further) and giving a glucose load prior to provision of B vitamins in a hypoglycaemic, malnourished patient. \n\t- Wernicke's encephalopathy - a reversible presentation (treaed with high dose intravenous thiamine, e.g. Pabrinex), characterised by a classical tetrad of: \n\t\t- Confusion\n\t\t- Ataxia\n\t\t- Ophthalmoplegia: classically of the lacteral rectus, but can also be an internuclear ophthalmoplegia or upward-gaze defects \n\t\t- Nystagmus \n\t\t- Less classical features include urinary incontinence and hypothermia due to autonomic neuropathy, making normal pressure hydrocephalus a key differential. \n\t- Korsakoff's psychosis - this is an irreversible manifestation of untreated Wernicke's encephalopathy. It is characterised by:\n\t\t- Retrograde amnesia\n\t\t- Anterograde amnesia\n\t\t- Confabulation \n\n# Cannabis Intoxication\n- This includes marijuana, and they exert their effects through acting on the cannabinoid receptors\n- Features are:\n\t- Drowsiness\n\t- Impaired memory\n\t- Slowed reflexes \n\t- Slowed motor skills \n\t- Conjunctival injection \n\t- Increased appetite\n\t- Paranoia and psychotic symptoms (contrast with cannabinoid associated schizophrenia, which has a more insidious onset, over many years)\n\t- Tachycardia\n\t- Dry mouth \n\n# LSD (Lysergic Acid Dethylamide) Intoxication\n- LSD, a psychedelic drug, acts at the dopamine receptors primarily.\n- Features include: \n\t- Labile mood\n\t- Hallucinations\n\t- Increased blood pressure\n\t- Increased heart rate\n\t- Increased temperature\n\t- Sweating\n\t- Insomnia\n\t- Dry mouth\n\n# Stimulant Intoxication\n- These include cocaine, methamphetamine, or MDMA (ecstasy) \n\t- MDMA induces rapid serotonin and dopamine release, and directly binds to the 5HT2 receptor\n\t- Cocaine prevents reuptake of dopamine, noradrenaline, and seroton, resulting in increased levels of free serotonin and dopamine\n\t- Methamphetamine acts at the sigma receptors, which induces dopamine release \n\t- Stimulants such as cocaine or methamphetamine can, in low doses, produce a feeling of increased concentration and focus. Cocaine acts at dopamine receptors. Methamphetamine acts at TAAR1 (Trace Amine-Associated Receptor 1) receptors. Both increase the available amount of dopamine in the brain, producing the associated pleasurable effects of the drugs.\n- Features include:\n\t- Euphoria\n\t- Hypertensive crises\n\t- Increased heart rate\n\t- Dilated pupils\n\t- Increased temperature\n\t- Rhabdomyolysis \n\t- Seizures\n\t- Agitation \n\t- Arrythmias \n\t- Psychosis \n\t- Excessive thirst and SIADH, resulting in water overload and hyponatraemia, especially with MDMA, and associated complications from this.\n\t- Ischaemic events (cardiac, pulmonary, bowel, CNS) with cocaine due to vasospasm \n- Deaths can occur due to hyperpyrexia and hypertension, so cooling, use of antihypertensives such as nitroprusside or GTN, and benzodiazepines, is the mainstay of management. \n- Withdrawal syndromes are not a typical feature of stimulant abuse.\n\n\n",
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"question": "The police bring a 32-year-old male to the Emergency Department after being injured whilst resisting arrest for theft. On review, he has only minor injuries, but you notice that he is starting to shiver, sweat, retch and has a tremor. His pupils are dilated.\n\nWhat is the most likely diagnosis?",
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"explanation": "Apixaban is an anticoagulant (in the DOAC category) that is often used in the treatment of deep vein thrombosis and in patients who are pro-coagulant. It is not currently used in the treatment of Raynaud's phenomenon",
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"explanation": "This patient most likely has Raynaud's phenomenon as she is experiencing paroxysmal digital ischaemia when exposed to the cold. It is often associated with underlying rheumatological conditions, including systemic sclerosis, rheumatoid arthritis and systemic lupus erythematosus (SLE). Treatment is mostly trigger management - keeping fingers warm, smoking cessation and avoiding stress - however in some cases, nifedipine may help symptoms",
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"explanation": "Warfarin is an anticoagulant that is sometimes used in patients who are pro-coagulant or who have venous thrombosis, particularly if they have failed treatment with a direct oral anticoagulant (DOAC). It is also used in patients with metal heart valves. It is not of benefit in this patient's case",
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"name": "Warfarin",
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"explanation": "Epoprostenol is also known as prostaglandin I2 and is an effective vasodilator. It is sometimes used to treat severe attacks of Raynaud's, e.g. where there are concerns about digital gangrene or the development of digital necrosis. It is a rescue therapy and is not used routinely. Relapse is common after infusion, and some patients with severe disease require regular infusions, particularly in the winter months",
"id": "32712",
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"name": "Epoprostenol",
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"explanation": "Aspirin is an antiplatelet medication often used in peripheral vascular disease. While this patient has digital ischaemia, it is paroxysmal; therefore, aspirin is not the treatment of choice",
"id": "32709",
"label": "b",
"name": "Aspirin",
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"comment": "how does everyone know this lol",
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"explanation": "# Summary\n\nRaynaud's phenomenon refers to episodes of vasospasm of small arteries and arterioles, which leads to reduced blood flow to the extremities, usually the fingers and toes. This classically manifests with the digits going pale, then cyanosed, then erythematous (with this final stage often being uncomfortable). Triggers include cold exposure and emotional stress. The majority of cases are classified as primary, however around 10% of cases are associated with underlying disease such as systemic sclerosis or polycythaemia. Diagnosis is clinical; however underlying causes should be screened for with a full blood count, ESR and antinuclear antibodies. Other investigations should be carried out if an underlying cause is suspected. Management involves lifestyle changes such as wearing gloves and warm footwear, smoking cessation and reviewing medications that may exacerbate Raynaud's. If conservative measures are ineffective, medical treatment with nifedipine can be considered. Patients with suspected secondary Raynaud's phenomenon should be referred to rheumatology. \n\n# Definition\n\nRaynaud's phenomenon is a condition where arteries or arterioles constrict, decreasing blood flow to the affected areas. Attacks are usually triggered by cold exposure, with other triggers including emotional stress, vibration injury, smoking and medications (e.g. beta-blockers). The fingers and toes are the most commonly affected areas. \n\n# Epidemiology\n\n- Primary Raynaud's phenomenon is common and affects around 5% of people\n- It is more common in women and in people living in colder climates\n- Other risk factors include:\n- Family history\n- Smoking\n- Migraine\n- Secondary Raynaud's phenomenon is much less common, making up 10-20% of cases\n- Patients with secondary Raynaud's phenomenon tend to be older than patients with primary disease (suspect if symptoms start over the age of 30)\n\n# Classification\n\n**Primary Raynaud's phenomenon** (PRP, also known as \"idiopathic\" Raynaud's) is not associated with an underlying cause\n\n- It typically develops between the ages of 10 and 30\n- It is usually a benign condition which may improve with age\n- Although some patients may experience significant discomfort with severe primary Raynaud's, complications such as ischaemia or ulceration are not seen\n\n**Secondary Raynaud's phenomenon** (SRP) may be associated with a variety of pathologies including:\n\n- Rheumatological conditions e.g. systemic sclerosis, systemic lupus erythematosus, dermatomyositis, rheumatoid arthritis and Sjogren's syndrome\n- Haematological conditions e.g. polycythaemia, protein C/S/antithrombin III deficiency, paraproteinaemia, Factor V Leiden\n- Medications e.g. beta-blockers, methylphenidate, some chemotherapy agents and interferons\n- Recreational drugs e.g. cocaine, amphetamines\n- Occupational causes e.g. vinyl chloride exposure, hand-arm vibration syndrome (due to long-term use of tools such as chainsaws or grinders)\n- Extrinsic compression of vessels e.g. carpal tunnel syndrome\n- Endocrine conditions e.g. hypothyroidism, carcinoid syndrome and phaeochromocytoma\n\nSymptoms of secondary Raynaud's phenomenon are usually more severe than in PRP, especially in cases secondary to a connective tissue disorder.\n\nFeatures that should raise suspicion of SRP include:\n\n- Onset after age 30\n- Asymmetrical digit involvement\n- Intense and painful episodes\n- Digital ulcers, gangrene or ischaemia\n- Abnormal nail fold capillaroscopy\n- Clinical features suggestive of underlying disease (e.g. sclerodactyly)\n- Positive antinuclear antibodies\n\n# Signs and Symptoms \n\n- Typically the tips of the digits go pale - this may spread proximally and is clearly demarcated\n- They may then become blue and cyanosed\n- The affected digits may be numb or painful\n- This is often followed by a hyperaemic phase where the affected areas become erythematous with associated discomfort and paraesthesias\n- The thumb is usually spared\n- Other areas that may be affected include:\n- Tip of the nose\n- Ear lobes\n- Nipples\n- Tongue\n\n[lightgallery] \n\nEspecially in PRP, there may be no signs on examination unless the patient is currently experiencing an attack. \n\nSigns in SRP may include:\n\n- Abnormal nailfold capillaries (examine with a dermatoscope)\n- Asymmetrical peripheral pulses or blood pressure between arms\n- Ulceration, ischaemia or necrosis of digits\n- Scarring\n- Secondary infection\n\n# Differential Diagnosis\n\n- **Frostbite** - occurs when tissues are frozen, causing microvascular occlusion and ischaemia. Skin is cold and numb, and may be discoloured and purple with blistering and necrosis in more severe cases.\n- **Chilblains** - localised inflammatory lesions caused by cold exposure; itchy, red-purple swellings form that may blister and ulcerate.\n- **Acrocyanosis** - persistent painless cyanosis of the extremities that is exacerbated by cold exposure, usually associated with clamminess and hyperhidrosis\n- **Erythromelalgia** - vasodilatation of small vessels causes burning pain, warmth and erythema of the hands and feet which may be continuous or episodic; often triggered by heat or exercise\n- **Livedo reticularis** - red-blue mottling of the skin that in physiological cases is triggered by cold weather (in pathological cases the rash is persistent)\n- **Vascular occlusion** e.g. acute cholesterol embolism may cause blue discolouration of the toes however this is not episodic; there is often ischaemia of other organs and a systemic inflammatory response\n\n# Investigations\n\n- Patients should all have basic bloods for the following:\n- **Full blood count** - looking for polycythaemia, a thrombocytosis may be seen in inflammatory states\n- **Erythrocyte sedimentation rate** (ESR) - raised in inflammatory conditions\n- **Antinuclear antibodies** (ANA) - positive in around 10% of the general population, associated with some causes of SRP such as systemic lupus erythematosus and scleroderma \n\nOther investigations should be targeted if there are signs and symptoms of another underlying cause, e.g. thyroid function tests, testing for prothrombotic conditions, chest X-ray looking for a cervical rib\n\nPatients with suspected SRP should be referred for nailfold capillaroscopy to examine these for abnormalities (such as widened capillaries and microhaemorrhages in systemic sclerosis)\n\n# Management\n\n**Conservative:**\n\n- Lifestyle advice and education:\n- The whole body should be kept warm, with gloves and warm footwear worn in cold weather\n- Hand and foot warming devices may be useful\n- Regular exercise\n- Smoking cessation\n- Address emotional stress if this is a trigger\n- Review medications for triggers (such as beta-blockers) and consider stopping or switching to an alternative if possible\n- Occupational health referral for patients whose Raynaud's phenomenon may be work-related (e.g. secondary to vibrating tools)\n- Patients with suspected secondary Raynaud's phenomenon should be referred to rheumatology, as well as patients with severe or treatment-resistant primary Raynaud's\n- Patients with severe ischaemia of digits or other significant complications require emergency hospital admission\n\n**Medical:**\n\n- Nifedipine (a calcium channel blocker) as the first-line prophylactic treatment\n- If this is not tolerated (common side-effects being headaches, flushing, ankle swelling, palpitations and dizziness), an alternative is amlodipine\n- Patients may take this regularly or intermittently e.g. when the weather is cold or when doing outdoor activities\n- Secondary care options for patients with severe complications include intravenous prostaglandins (e.g. iloprost), sildenafil and bosentan (an endothelin receptor antagonist)\n\n**Interventional:**\n\n- Rarely, some patients with severe disease may be offered a sympathectomy, where sympathetic nerves that cause vasoconstriction are resected surgically\n- Botox injections to block the sympathetic nerves in the hands and/or feet are also an option\n\n# Prognosis\n\n- Primary Raynaud's syndrome is typically benign and may improve over time\n- Some patients enter a state of remission where they no longer experience episodes\n- However some patients who have severe symptoms may find their quality of life is affected by discomfort and functional impairment\n- Secondary Raynaud's syndrome is in general more severe and may lead to complications including:\n- Digital ischaemia, with pitting, ulceration or gangrene\n- Tissue loss and scarring\n- Poor wound healing and secondary infection\n- The prognosis for secondary Raynaud's syndrome is variable depending on the underlying cause and whether this is avoidable or treatable\n\n# NICE Guidelines\n\n[NICE CKS - Raynaud's Phenomenon](https://cks.nice.org.uk/topics/raynauds-phenomenon/)\n\n# References\n\n[Patient UK - Raynaud's Phenomenon](https://patient.info/doctor/raynauds-phenomenon-pro)",
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"question": "A 48-year-old female presents to General Practice complaining of cold, painful fingers. She reports that her fingers go blue after being outside (particularly if she forgets her gloves) but that they regain their colour when she comes inside. Her only past medical history is significant for rheumatoid arthritis, for which she takes methotrexate.\n\nWhat medication should you consider starting?",
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"explanation": "This patient has osteoarthritis. As she is morbidly obese and young, one of the first interventions should be lifestyle advice and weight loss, particularly as she also has diabetes and hypertension. Weight loss would reduce the stress on her load-bearing joints and also improve her health generally as well as her diabetes and hypertension",
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"comment": "i'm not sure you'd really tell this poor cleaner with pain to lose weight and not prescribe an NSAID? how long would weight loss take to have an effect?\n\n\n",
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"comment": "thats what threw me off too initial managment ?? what about their pain ",
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"explanation": "# Summary\n\nOsteoarthritis (OA) is a chronic, degenerative joint disease characterised by loss of articular cartilage, remodelling of bone with osteophyte formation and mild synovitis. The main risk factor is older age, although obesity, joint injury and genetics also contribute. Presentation is with gradual onset pain that is worse with activity, with associated functional limitations. The most commonly affected joints are the knees, hips and small joints of the hands. Diagnosis is clinical, and severity of disease on X-ray does not correlate well with severity of symptoms. Management should be individualised, with important components being exercise, simple analgesia and optimisation of risk factors (such as maintaining a healthy weight). Where there is ongoing pain and disability, options include intra-articular steroid injections and surgical intervention (such as joint replacement).\n\n# Definition\n\nOsteoarthritis (OA) is the commonest form of arthritis, which is characterised by degenerative changes affecting the entirety of joints affected. Cartilage is lost, the subchondral bone becomes sclerosed with formation of osteophytes and subchondral cysts and there is inflammation of the synovial membrane lining the joint capsule (synovitis). \n\n# Epidemiology\n\n- Approximately 10 million people in the UK have osteoarthritis\n- More women than men are affected\n- Average age of onset is 55 \n- The commonest joint affected is the knee, followed by the hip then the hand\n\n# Aetiology\n\nOsteoarthritis develops due to a combination of factors, with important contributors including:\n\n- Older age\n- Female sex\n- Overweight or obesity\n- Family history of OA\n- Previous joint injury\n- Joint damage due to inflammation (e.g. in patients with inflammatory arthritis)\n- Physical inactivity and reduced muscle strength\n- Low bone density \n- Deformities such as development dysplasia of the hip or leg length discrepancy\n- Stresses on joints due to occupational factors (e.g. repetitive squatting or kneeling) or exercise\n\n# Signs and Symptoms\n\nKey symptoms include:\n\n- Pain in the affected joint exacerbated by use\n- Pain may radiate e.g to the thigh, knee and ankle in hip OA, or to the wrist in hand OA\n- Joints may feel stiff (although prolonged morning stiffness is suggestive of inflammatory arthritis)\n- Functional limitations such as difficulty opening jars (hand OA) or mobilising (knee or hip OA)\n- Locking or giving way of the knee\n\nExamination findings include:\n\n- Restricted and painful range of motion (e.g. in hip OA internal rotation with the hip flexed is particularly painful)\n- Crepitus (friction between bone and cartilage) \n- Affected joints may appear swollen or enlarged\n- A small effusion may form, especially when the knee is affected\n- Synovitis may present with mild soft tissue swelling, tenderness and warmth\n- Muscle wasting and weakness can result from disuse atrophy\n- Joint instability\n- An antalgic gait (\"limping\") in knee OA\n- Trendelenburg gait in hip OA (due to weak abductors patients lurch towards the affected hip)\n- Deformities, including:\n- Heberden's nodes (bony nodules over the distal interphalangeal joints) \n- Bouchard's nodes (bony nodules over the proximal interphalangeal joints) \n- Fixed flexion of the first carpometacarpal joint with hyperextension of the distal joints\n- This may lead to squaring of the joint with subluxation and remodelling\n- Ulnar or radial deviation of joints in the hand may occur\n- In severe hip OA the leg may be shortened due to fixed flexion and external rotation\n- Varus (most commonly) or valgus deformities of the knees \n\n# Differential Diagnosis\n\n- **Inflammatory arthritis** such as rheumatoid arthritis, ankylosing spondylitis; pain that improves with activity and morning stiffness lasting over 30 minutes are differentiating factors, systemic symptoms such as malaise and weight loss may be present\n- **Septic arthritis** is an important differential for all patients presenting with an acutely painful swollen joint (which may occur in an acute flare of osteoarthritis); patients may be systemically unwell with fevers\n- **Fracture** e.g. of the tibial plateau may mimic OA symptoms of pain and limited mobility; usually the patient is unable to weight bear with swelling of the affected area; a history of trauma should be elicited\n- **Malignancy** including bone metastases, multiple myeloma or sarcoma may cause mechanical pain leading to functional limitations; red flags include weight loss, night sweats, persistent pain not relieved by rest and night pain\n- **Greater trochanteric pain syndrome** most commonly occurs in middle-aged women and causes lateral hip pain and tenderness worsened by activity; it may also radiate to the lateral knee\n- **Iliotibial band syndrome** presents with lateral knee pain worse with activity, which is often accompanied by clicking or clunking sounds when the knee is moved; occurs most commonly due to repetitive knee flexion e.g. cyclists or runners \n- **Meniscal tear** may occur after an injury involving a twisting or pivoting movement; similar symptoms of pain, swelling, locking and giving way of the knee and range of motion may be limited on examination\n- **Trigger thumb** may mimic OA of the hand with pain, clicking and catching when the thumb is flexed; a nodule may be palpable in the tendon\n- **Ganglion cysts** occur more commonly in people with OA and present as soft tissue swellings e.g. at the base of the thumb; often asymptomatic but may cause pain and limit movement of the joint\n\n# Investigations\n\nDiagnosis of OA is clinical and can be made without any investigations in a patient of 45 or older if there are no features suggesting another underlying cause of symptoms.\n\nIf there is diagnostic uncertainty or a rapid deterioration in symptoms, **X-rays** of affected joints may be of use. Typical findings can be remembered with the mnemonic \"LOSS\":\n\n- **L**oss or narrowing of joint space due to thinning of cartilage\n- **O**steophytes i.e. formation of new bony spurs at the joint margins\n- **S**ubchondral sclerosis i.e. increased bone density beneath the cartilage\n- **S**ubchondral cysts which are fluid-filled sacs in the subchondral bone\n\n[lightgallery]\n\nHowever, severity of OA features on X-ray may not correlate well with severity of clinical disease.\n\nOther investigations if the diagnosis is in doubt should be targeted to the differential suspected, and may include:\n\n- Further imaging such as MRI to look for ligament or cartilage damage (e.g. a meniscal tear)\n- Joint aspiration with synovial fluid analysis to exclude septic arthritis or crystal arthritis\n- Blood tests for inflammatory markers, rheumatoid factor and anti-CCP (for example) if rheumatoid arthritis is suspected\n\nBaseline bloods for renal function and full blood count should be considered in all patients starting NSAID treatment, especially older patients who are at higher risk of adverse effects.\n\n# Management\n\n**Conservative management:**\n\n- Patient education and advice on self-care e.g. appropriate footwear\n- Weight loss advice and signposting to services in patients with excess body weight\n- Exercise has many benefits including strengthening muscles, improving fitness, reducing pain and improving function\n- Options include online fitness programmes designed for people with arthritis, physiotherapy and supervised exercise sessions\n- Physiotherapy services may also be able to offer manual therapies and joint supports such as braces or splints to reduce load and improve instability\n- Occupational health input may be needed in patients with functional impairment to assess their working environment and suggest adaptations\n- Patients should be asked about psychosocial stressors and support offered e.g. for associated depression and anxiety\n- Occupational therapy input may be helpful to advise on aids and devices to assist with activities of daily living (e.g. walking sticks, sock aids, grab rails, tap turners)\n- Podiatry input may be useful to assess the biomechanics of joint pain and advise on orthotic devices such as insoles\n- Referral to a pain management service may be appropriate for patients who have not responded to maximal medical (and if appropriate, surgical) management of OA\n- Assess falls risk and consider referral to specialist services for patients at risk (e.g. those with abnormal gait or balance, or who have had a fall in the last year)\n\n**Medical management:**\n\n- First-line analgesia is with topical NSAIDs (such as ibuprofen gel) - patients should be made aware that some systemic absorption may occur\n- If this is ineffective or unsuitable, oral NSAIDs should be considered (with a PPI for gastroprotection if there are risk factors for gastrointestinal side effects)\n- Paracetamol or weak opioids (e.g. codeine) may also be used in the short-term\n- Topical capsaicin is another option, especially for knee OA\n- Intra-articular steroid injections may be considered if other treatments are not effective, and/or to enable therapeutic exercise\n\n**Surgical management:**\n\n- Patients with OA of the hip, knee or shoulder who have symptoms significantly impacting quality of life despite optimal medical management should be considered for orthopaedic referral\n- The usual operation offered is an arthroplasty (joint replacement)\n- Rehabilitation before and after surgery is key to optimising outcomes\n\n# Complications\n\n- Joint deformities (as above)\n- Increased risk of falls\n- Functional limitations, e.g. hand OA may making writing, turning keys or fasting buttons challenging\n- Reduced mobility \n- Sleep difficulties\n- Low mood and anxiety\n- Chronic pain\n\n# Prognosis\n\n- Not all cases of OA are progressive and the disease course is variable\n- OA of the hands generally has a good prognosis, especially interphalangeal joint involvement\n- Hip OA has a poorer prognosis with many patients requiring arthroplasty\n- Knee arthroplasties for OA are also common however many patients' symptoms improve or remain stable with time \n- Intermittent flares of OA may occur, where symptoms increase in intensity suddenly\n- Flares tend to last for a few days before improving\n\n# NICE Guidelines\n\n[NICE CKS - Osteoarthritis](https://cks.nice.org.uk/topics/osteoarthritis)\n\n[NICE - Osteoarthritis in over 16s: diagnosis and management](https://www.nice.org.uk/guidance/ng226/)\n\n# References\n\n[WHO fact sheet - Osteoarthritis](https://www.who.int/news-room/fact-sheets/detail/osteoarthritis)\n\n[BNF Treatment Summaries - Osteoarthritis](https://bnf.nice.org.uk/treatment-summaries/osteoarthritis/)\n\n[Patient UK - Osteoarthritis](https://patient.info/doctor/osteoarthritis-pro)",
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"question": "A 46-year-old female presents to General Practice with bilateral knee pain that has been present for six months. She currently works part-time as a cleaner. Her past medical history includes type two diabetes mellitus, hypertension, gastro-oesophageal reflux (GORD) and morbid obesity.\nKnee x-rays are requested and show loss of joint space with some subchondral sclerosis.\n\nWhat is your initial management?",
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"explanation": "Low dose amitriptyline may be used in neuropathic pain and migraine prophylaxis; however, whilst migraine can cause headache and visual loss/disturbance in some cases, it is unlikely for a patient to have a new diagnosis of migraine at the age of 63 and therefore other causes should be considered",
"id": "32720",
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"explanation": "300mg of aspirin would be the treatment of choice if this patient were suspected of having a transient ischaemic attack (TIA); however, whilst TIAs can present with blindness, they do not usually cause headache and would not explain the scalp or jaw pain",
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"explanation": "This history is suspicious for temporal arteritis, aka giant cell arteritis (GCA). As she has experienced vision loss, it is important to start high dose steroid treatment immediately; otherwise, she may have permanent loss. Symptoms of GCA include scalp tenderness, jaw claudication and headache. Patients usually require steroids for a two-year course then have complete remission, and steroids can be reduced once symptoms have resolved. The main cause of death and morbidity in GCA are related to long term steroid use, so risks and benefits of treatment should be considered carefully, and gastric and bone protection should be considered",
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"name": "Start high dose steroids",
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"explanation": "Thrombolysis with alteplase would be an appropriate treatment for an ischaemic stroke within 4.5 hours of the onset of symptoms. Whilst ischaemic stroke can cause blindness, it would not usually cause headaches and would not explain the scalp or jaw pain",
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"label": "e",
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"explanation": "Carbemazipine is the first line treatment for trigeminal neuralgia. This would be in the differential for unilateral facial pain; however, it would not account for the blindness, and the pain she describes does not sound neuropathic",
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"label": "d",
"name": "Start 100mg carbamazepine",
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"explanation": "# Summary\n\nGiant cell arteritis (GCA) is a form of vasculitis which affects medium and large arteries. It classically affects the branches of the external carotid artery and the ophthalmic artery, which is often referred to as temporal arteritis. Key signs and symptoms include a temporal headache, jaw claudication, amaurosis fugax, thickening and tenderness of the temporal artery, and scalp tenderness. Systemic symptoms and features of polymyalgia rheumatica are common. The diagnosis is clinical in the first instance, and patients with visual symptoms should be treated immediately with high-dose steroids, however supportive investigations include full blood count, CRP and ESR. Confirmation of the diagnosis is with vascular ultrasound and temporal artery biopsy. Management is with high-dose steroids, with steroid sparing agents considered in patients who relapse when steroids are weaned.\n\n# Definition\n\nGiant cell arteritis (GCA) is a large vessel vasculitis which commonly affects the extracranial external carotid artery branches. Involvement of other vessels may occur, with patients presenting atypically with systemic symptoms and aortic involvement rather than temporal arteritis.\n\n# Epidemiology\n\n- GCA is the most common primary vasculitis \n- Age is an important risk factor - GCA is rare in the under 50s, with cases peaking in those aged 70-79\n- Women are 2-3x more likely to be affected than men\n- Northern European descent is also a risk factor\n\n# Signs and Symptoms\n\n**Symptoms include:**\n\n- Headache - usually temporal but may be generalised, occipital or parietal; present in 2/3 of people with GCA\n- Jaw or tongue claudication (pain on chewing food)\n- Amaurosis fugax (transient monocular blindness, often described as a dark curtain descending vertically)\n- Diplopia\n- Changes to colour vision\n- Fatigue\n- Anorexia and weight loss\n- Depression\n- Features of polymyalgia rheumatica e.g. pain and stiffness of shoulders and pelvic girdle\n\n**Signs include:**\n\n- Tenderness, thickening or nodularity of the temporal artery\n- Pulsation of the temporal artery may be reduced or absent\n- Scalp tenderness or necrosis\n- Visual field defect\n- Low-grade fever\n- On fundoscopy: pallor and oedema of the optic disc, \"cotton-wool\" patches and retinal haemorrhages\n- Involvement of extracranial vessels may be associated with arterial bruits, difference in blood pressure between arms and decreased arterial pulses\n\n# Differential Diagnosis\n\n- **Other causes of headaches** e.g. tension headaches, migraines - lack associated features e.g. jaw claudication, less likely to be new in an older patient\n- **Acute angle closure glaucoma** leads to visual loss and headaches, eye will be painful and red and feel hard on palpation\n- **Shingles** leads to pain and systemic features may be present, however a rash typically appears over the affected area within a few days\n- **Transient ischaemic attack** can cause amaurosis fugax, other features such as headache are not usually present\n\n\n# Investigations\n\n**Bedside tests:**\n\n- Urgent ophthalmological assessment for patients with visual symptoms \n\n**Blood tests:**\n\n- **ESR** and **CRP** - raised in GCA\n- **Full blood count** often shows an elevated platelet count and a normochromic normocytic anaemia\n- Baseline bloods for liver and renal function (**LFTs** and **U&Es**) and a **bone profile** for calcium should be considered to screen for alternative diagnoses e.g. other vasculitides\n- Bloods to screen for increased risk of complications with steroids (such as diabetes or osteoporosis) include an **HbA1c**, **vitamin D** and **thyroid function tests** \n\n**Imaging tests:**\n\n- **Doppler ultrasonography** of the temporal and axillary arteries can be used as a confirmatory diagnostic test\n- **Halo sign** refers to hypoechoic wall thickening of the artery imaged\n- This disappears with steroid treatment\n- Stenosis of the vessel may also be visualised\n- **MRI brain** with vessel wall imaging is an alternative\n- GCA is supported by findings of mural inflammation in the superficial temporal arteries\n- MRI can also be used to look for complications such as ischaemic stroke as well as involvement of other arteries\n- **FDG-PET scanning** can be useful to rule out differential such as malignancy or infection\n- In GCA there will be uptake in affected arteries\n- It can be particularly useful to demonstrate involvement of other arteries e.g. the aorta\n- A **DEXA** scan for baseline bone density should be done for patients starting long-term steroids (due to the risk of osteoporosis)\n\n**Invasive tests:**\n\n- **Temporal artery biopsy**\n- This is the definitive investigation for GCA\n- Typical histological features include granulomatous inflammation of arteries with inflammatory cells including multinucleated giant cells\n- Inflammation is often segmental with \"skip lesions\" i.e. normal parts of the artery in between areas of inflammation, and so false negative biopsies can occur\n- Biopsies may remain positive for several weeks after starting steroids\n\n# Management\n\n- Patients with visual loss usually require **IV steroid treatment** e.g. pulsed methylprednisolone\n- All other patients should be treated with **high dose oral steroids**, usually 40-60 mg prednisolone once a day\n- **Safety netting** patients to seek urgent medical attention if they develop visual symptoms or a relapse on steroids is key\n- Patients seen in primary care should be **referred urgently to rheumatology** for confirmation of the diagnosis and ongoing management\n- **Steroids are tapered** gradually once symptoms and raised inflammatory markers have resolved\n- **Steroid sparing agents** such as methotrexate or tocilizumab (an anti-IL6 biologic) may be added to help with steroid tapering e.g. in patients with recurrent relapses or at increased risk of side effects with steroids\n- All patients should be assessed for risk of steroid side effects:\n- Consider gastric protection with a proton pump inhibitor\n- Consider bone protection e.g. vitamin D and calcium supplementation, bisphosphonates\n- Monitor for steroid-induced diabetes, hypertension and glaucoma\n- Advise on immunosuppression e.g. avoiding contact with patients with diseases such as chickenpox if not immune\n- Give patients a blue steroid card and advise them not to suddenly stop steroids due to the risk of adrenal crisis\n- Aspirin is currently **not** recommended for adjunctive treatment of GCA \n\n# Complications\n\n- Loss of vision - may occur in up to 30% of people with GCA (either total or partial)\n- Scalp necrosis\n- Ischaemic stroke\n- Aortic aneurysms - in 10-20% of people with GCA, most commonly in the thoracic aorta\n- Aortic dissection and aortic regurgitation are less common than aneurysms\n- Stenosis of large arteries\n- Increased risk of cardiovascular disease including stroke, myocardial infarction and peripheral arterial disease\n- Side-effects from long-term steroids e.g. osteoporosis and fragility fracture, weight gain, diabetes, gastric ulcers\n\n# Prognosis\n\n- Most patients respond rapidly to steroids - failure to respond should prompt investigations for an alternative diagnosis\n- Up to 50% of people will experience relapsing disease however\n- Most patients require at least 1-2 years of steroid treatment, with an increased risk of relapse if steroids are stopped within a year of diagnosis\n\n# NICE Guidelines\n\n[NICE CKS - Giant Cell Arteritis](https://cks.nice.org.uk/topics/giant-cell-arteritis/)\n\n# References\n\n[British Society for Rheumatology guideline on diagnosis and treatment of giant cell arteritis](https://academic.oup.com/rheumatology/article/59/3/e1/5714024)\n\n[Radiopaedia - Giant Cell Arteritis](https://radiopaedia.org/articles/giant-cell-arteritis?lang=gb)\n\n[Patient UK - Giant Cell Arteritis](https://patient.info/doctor/giant-cell-arteritis-pro)",
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"question": "A 63-year-old female presents to Accident and Emergency with sudden right-sided blindness associated with a headache. She has never had issues with headaches before. On further questioning, she reveals that she has tenderness on brushing her hair and has been to the dentist recently with toothache but did not need any dental work done.\n\nWhat should your initial management be?",
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"explanation": "Breakdown of cells includes the breakdown of their nucleic acid, which has a phosphate group, and therefore a high phosphate is expected in TLS. As phosphate leads to calcium chelation, patients will also have low calcium rather than high calcium. High calcium is associated with malignancy with boney metastasis, for example, lung cancer, breast cancer and renal cancer",
"id": "32735",
"label": "c",
"name": "Adjusted Calcium 3.70 mmol/L",
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"explanation": "Hyponatreamia can be a sign of paraneoplastic syndromes such as syndrome of inappropriate ADH. It is not in keeping with tumour lysis syndrome",
"id": "32736",
"label": "d",
"name": "Sodium 128 mmol/L",
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"__typename": "QuestionChoice",
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"explanation": "As rapid cell breakdown releases potassium, a low potassium would be unusual in TLS",
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"name": "Potassium 2.9 mmol/L",
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"explanation": "TLS is a severe metabolic disturbance caused by the abrupt release of cellular components following the rapid lysis of malignant cells upon initiation of treatment. Therefore high potassium, high urea, high phosphate and low calcium are expected.\n\nLactate, urate and LDH may also be increased and so should be monitored, but are not diagnostic.\n\nIt is usually within 1-5 days of starting chemotherapy and can cause seizures, cardiac arrhythmias, kidney injury and even death. Management is through prevention and careful monitoring and treatment of any complications should they occur",
"id": "32733",
"label": "a",
"name": "Urea 22 mmol/L",
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"explanation": "This is a normal potassium level. A high potassium level would be associated with TLS",
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"name": "Potassium 4.2 mmol/L",
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"__typename": "QuestionComment",
"comment": "I know in tumour lysis syndrome there is raised K, PO4 and uric acid with low Ca. But is urea the same as uric acid (ie urate)?",
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"comment": "innit? i was thinking the samee bc notes say high urate rather than urea idk if they are used interchangeablyyy",
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"comment": "They're not the same.",
"createdAt": 1683323089,
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"comment": "the urea is raised due to AKI due to the TLS",
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"comment": "Feel like this is a bit mean and also kind of teaching people that uric acid and urea are the same thing (they're not). The lab criteria of TLS is uric acid, calcium, phosphate and potassium.",
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"explanation": "# Summary\n\n\nTumour lysis syndrome is a potentially lethal condition caused by the rapid death of tumour cells often following chemotherapy or rapid progression of haematological malignancies, resulting in the massive release of intracellular contents. It is an oncological emergency. Patients commonly present with acute-onset dysuria/oliguria, abdominal pain, or weakness. Key investigations include measurements of U&E (showing raised potassium and phosphate), calcium (typically low), uric acid (raised), and ECG to detect metabolic abnormalities and life-threatening arrhythmias. Initial management involves the correction of electrolyte abnormalities and intravenous fluid administration.\n\n\n# Definition\n\n\nTumour lysis syndrome is a serious metabolic disorder caused by the rapid death of tumour cells in response to chemotherapy. This results in a massive release of intracellular contents into the bloodstream, leading to significant electrolyte imbalances.\n\n\nTumour lysis syndrome is most commonly associated with aggressive, rapidly proliferating tumours such as acute leukaemia and high-grade lymphomas, particularly after the initiation of cytotoxic therapy. \n\n\n# Aetiology\n\n\nThe syndrome occurs due to the rapid release of intracellular contents from dying tumour cells, often following chemotherapy. It can however also be caused by high-grade lymphomas and acute leukaemias. This leads to hyperuricaemia, hyperphosphatemia, hyperkalaemia, and hypocalcaemia. These metabolic abnormalities lead to the clinical manifestations including acute kidney injury and arrhythmias.\n\n\n# Signs and symptoms\n\n\nPatients may present with symptoms related to electrolyte abnormalities and hyperuricaemia, which include:\n\n\n* Dysuria or oliguria\n* Abdominal pain\n* Weakness\n* Nausea or vomiting\n* Muscle cramps\n* Seizures\n* Cardiac arrhythmias\n* Gout/joint swelling\n\n\n# Differential diagnosis\n\n\nDifferential diagnosis should consider other causes of similar symptoms and laboratory abnormalities, such as:\n\n\n* **Acute kidney injury**: while tumour lysis syndrome can cause AKI, other causes should be considered. For example, patients may have significant dehydration or have received nephrotoxic drugs contributing to AKI. Careful history-taking and the absence of other features of tumour lysis syndrome should raise suspicion of AKI due to other causes. It is important to note though, that AKI can cause significant electrolyte abnormalities, so careful monitoring is required.\n* **Isolated hyperkalaemia**: presents with muscle weakness, fatigue, palpitations, and potentially life-threatening cardiac arrhythmias. Patients may have a history of renal failure or taking potassium-sparing medications. Uric acid, phosphate and calcium levels would be normal.\n* **Isolated hyperphosphateamia**: presents with muscle cramps, itching, and perioral tingling or numbness. Uric acid and potassium would be normal.\n* **Isolated hypocalcaemia**: presents with numbness and tingling in the hands, feet, and around the mouth, muscle cramps, and seizures. Uric acid, potassium and phosphate would be normal\n\n\n# Investigations\n\n\nKey investigations for tumour lysis syndrome include:\n\n* Basic observations\n* U&E: Potassium and phosphate are usually raised, raised Cr suggestive of AKI/renal failure.\n* Calcium: Typically low in tumour lysis syndrome.\n* Uric acid: Usually elevated.\n* ECG: To assess risk of arrhythmias caused by electrolyte abnormalities.\n* Hyperkalaemia may cause tented T waves, broad QRS, flattened P-wave and a prolonged PR interval. \n* Hypocalcaemia may cause a prolonged QT interval.\n\n\n# Management\n\n\nManagement of tumour lysis syndrome primarily focuses on:\n\n\n* Correction of electrolyte imbalances & mitigation of arrhythmia risk.\n* For example in severe hyperkalaemia, calcium gluconate is given followed by an insulin-dextrose infusion or nebulised salbutamol. Further management may include calcium resonium to prevent further potassium absorption from the gut.\n* Severe hypocalcaemia may require parenteral replacement.\n* Dialysis may be required in severe cases.\n* Administration of intravenous fluids to help flush out the intracellular contents released by the dying tumour cells.\n* Medications: rasburicase (a recombinant form of the urate oxidase enzyme) transforms uric acid into allantoin. Allantoin is more soluble in urine than uric acid, and more easily eliminated by the kidney.\n\n\n### Prevention \n\n\n* Low/intermediate risk patients can be managed with a combination of adequate hydration and allopurinol. \n* Rasburicase (a recombinant form of the urate oxidase enzyme) can be used as a prophylactic agent in adults with hyperuricaemia that is inadequately managed by allopurinol or febuxostat.\n\n\n# References\n\n[British Society for Haemotology: Management of Tumour Lysis Syndrome in Adults and Children with Haematological Malignancies](https://b-s-h.org.uk/guidelines/guidelines/management-of-tumour-lysis-syndrome-in-adults-and-children-with-haematological-malignancies)\n\n[Patient.info: Oncological emergencies](https://patient.info/doctor/oncological-emergencies#tumour-lysis-syndrome)",
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"question": "A 24-year-old male is treated for Hodgkin's lymphoma with chemotherapy.\n\nAs he has a high tumour burden, he is deemed at high risk of tumour lysis syndrome (TLS); which of the following blood tests would suggest tumour lysis syndrome?",
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"explanation": "Asthma can cause breathlessness, but this is not usually progressive in nature. Auscultation of the chest would reveal polyphonic wheeze or, in a severe attack, may be silent",
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"explanation": "Pulmonary fibrosis is a recognised side effect of bleomycin, and fine crackles on auscultation should prompt this diagnosis. A chest x-ray should be performed, and the medication may need to be stopped",
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"explanation": "# Summary \n\n\nCytotoxic drugs, or chemotherapeutics, are medicines which are capable of destroying cells at particular stages of the cell cycle. Typically, they have more effect on rapidly dividing cells, such as cancer cells. The action of chemotherapeutic agents varies with different classes of medication available and each class will have specific side effect profiles.\n\n\n# Side effects\n\nCommon side effects of many cytotoxic drugs include:\n\n- Increased risk of infection\n- Anaemia\n- Easy bruising\n- Fatigue\n- Gastrointestinal upset\n- Appetite loss\n- Mucositis\n- Hair loss\n- Skin & nail changes\n- Emotional & cognitive changes\n- Increased risk of infertility\n\nBefore each cycle of chemotherapy, blood tests including FBC, U&Es & LFTs are carried out to assess for toxicity, and to check fitness for chemotherapy treatment.\n\n# Specific chemotherapy drugs\n\nSome chemotherapy drugs carry an increased risk of some side effects. It is important to be aware of these in exam settings and in clinical practice as a patient may present with long-term side effects of anticancer treatments.\n\n### Doxorubicin\n\nDoxorubicin is a member of the anthracycline family of **cytotoxic** antibiotics. It inhibits topoisomerase II, an enzyme which joins the DNA double helix, therefore halting the cell cycle. Doxorubicin also generates free radicals which damage the DNA and cell membrane structures. It is used to treat **haematological cancers** and solid tumours including **breast cancer**.\n\nDoxorubicin can cause **cardiomyopathy**, which presents up to 15 years after treatment. Doxorubicin's cardiotoxic effects range from isolated ECG changes to pericarditis and established cardiomyopathy. Before treatment begins cardiac function should be assessed with an ECG and/or echocardiogram.\n\n### Cisplatin\n\nCisplatin is a platinum-based agent which works by crosslinking with DNA purine bases, causing DNA damage and disrupting repair mechanisms. It is used to treat **testicular, ovarian, lung, bladder, cervical** and **head and neck** cancers.\n\nKey side effects of cisplatin use are **peripheral neuropathy** and **hearing loss**. It is also known for causing severe nausea and vomiting.\n\n### Cyclophosphamide\n\nCyclophosphamide is an alkylating agent which damages DNA, and is activated by the liver. It is used to treat a number of cancers including **haematological** cancers and **breast** cancer. It is also used as an immunosuppressant.\n\nCyclophosphamide can cause urothelial toxicity, specifically **haemorrhagic cystitis** and, in the longer term, transitional cell carcinoma of the bladder. Mesna is used with high dose cyclophosphamide to reduce the concentration of active metabolite in the urinary tract and reduce the risk of this occurring.\n\n### Bleomycin\n\nBleomycin is a cytotoxic antibiotic that works by inhibiting DNA synthesis. It is used to treat metastatic **germ cell** cancers, **head and neck** cancers and some **non-Hodgkin's lymphomas**.\n\nOne key side effect to be aware of is **lung fibrosis**. Respiratory side effects typically begin 1-6 months after treatment completion, although may occur sooner if a hypersensitivity reaction occurs.\n\n### Cytarabine\n\nCytarabine is an antimetabolite chemotherapeutic drug. It prevents the synthesis and repair of DNA. It is used to treat **haematological** cancers.\n\nCytarabine can cause **ataxia** due to an acute cerebellar syndrome, especially at higher doses. This may also cause **dysarthria.**\n\n### Methotrexate\n\nMethotrexate is an **antifolate** drug, commonly used as an immunosuppressant but is also used in treatment for a number of cancers including **haematological** cancers, **gestational trophoblastic** disease and **breast cancer**.\n\nSide effects to be aware of include **bone marrow suppression, gastrointestinal toxicity, photosensitivity, liver and pulmonary toxicity**. Folinic acid is typically given alongside and FBC should be monitored closely.\n\n\n# References\n\n[BNF: Cytotoxic drugs](https://bnf.nice.org.uk/treatment-summaries/cytotoxic-drugs/)\n\n[BNF: Cisplatin](https://bnf.nice.org.uk/drugs/cisplatin-specialist-drug/)\n\n[BNF: Bleomycin](https://bnf.nice.org.uk/drugs/bleomycin-specialist-drug/)\n\n[BNF: Cytarabine](https://bnf.nice.org.uk/drugs/cytarabine-specialist-drug/)\n\n[BNF: Methotrexate](https://bnf.nice.org.uk/drugs/methotrexate/)\n\n[NHS: Chemotherapy side effects](https://www.nhs.uk/conditions/chemotherapy/side-effects/)\n\n[Cancer research UK: Cytarabine](https://www.cancerresearchuk.org/about-cancer/treatment/drugs/cytarabine)\n\n[An overview of doxorubicin formulations in cancer therapy](https://journals.lww.com/cancerjournal/fulltext/2014/10040/an_overview_of_doxorubicin_formulations_in_cancer.9.aspx)\n\n[Doxorubicin-induced cardiomyopathy: from molecular mechanisms to therapeutic strategies](https://www.sciencedirect.com/science/article/pii/S0022282812001150)\n\n[Cancer research UK: doxorubicin](https://www.cancerresearchuk.org/about-cancer/treatment/drugs/doxorubicin)\n\n[StatPearls: Cyclophosphamide](https://www.ncbi.nlm.nih.gov/books/NBK553087/#:~:text=Cyclophosphamide%20is%20a%20medication%20primarily,anti%2Dneoplastic%20effects%20through%20alkylation.)\n\n[Drugbank.com: Bleomycin](https://go.drugbank.com/drugs/DB00290)\n\n[Chemotherapy agents with known pulmonary side effects and their anaesthetic and critical care implications](https://www.sciencedirect.com/science/article/abs/pii/S1053077015005698)\n\n[Cytarabine induced acute cerebellar syndrome during hyper-CVAD treatment for B-cell acute lymphoblastic leukaemia](https://pmc.ncbi.nlm.nih.gov/articles/PMC5437478/)\n\n[Drugbank.com: Methotrexate](https://go.drugbank.com/drugs/DB00563#)",
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"question": "A 74-year-old male diagnosed with Non-Hodgkin's lymphoma and started on bleomycin. He presents to General Practice complaining about progressive breathlessness. On auscultation of his chest, you notice bilateral fine crackles.\n\nWhat is the likely diagnosis?",
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"explanation": "Garde 1 would require her to be able to carry out light housework or work of a sedentary nature",
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"explanation": "She is ambulatory and capable of all self-care but unable to carry out any work activities. She is up and about more than 50% of the day",
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"comment": "we don't know about her waking hours why is the answer not grade 1?\n",
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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": "Glycopyrronium is a medication from the muscarinic anticholinergic group. It is often used for respiratory tract secretions in palliative care patients who can no longer manage their own secretions due to impaired cough reflex",
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"explanation": "Nebulised salbutamol is used in the treatment of airway inflammation. As this patient does not currently have symptoms of airway inflammation, this is not currently indicated, and the use of the nebuliser may be more distressing for the patient",
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"explanation": "Haloperidol is often used in the palliative care setting for agitation and delirium. It may well be beneficial in this case; however, as this patient is likely agitated from his secretions, glycopyrronium will be of more help",
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"explanation": "Pain in the palliative setting is important to bear in mind and manage as patients may not be able to communicate fully. Morphine will cause respiratory depression, which again may be of benefit in this patient; however will not help with the distressing secretions",
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"explanation": "High flow oxygen can be very uncomfortable and not well tolerated. This patient's issues are related to respiratory secretions, and oxygen will not assist with those secretions",
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"explanation": "# Summary\n\nMedications in end-of-life care focus on alleviating distressing symptoms in patients nearing death. A holistic approach is vital, considering physical, emotional, and social aspects of symptoms, often involving a multidisciplinary team. For pain management, the WHO pain ladder guides pharmacological strategies, with morphine as the primary strong opioid. Specific treatments for other symptoms depend on the underlying cause and it is important to consider reversible causes and non-pharmacological measures.\n\n\n\n# Definition\n\nMedications used in end of life care aim to relieve distressing symptoms which may appear in the last days, weeks, or months of life. They are commonly prescribed as 'anticipatory' or 'just in case' medications for a patient known to be nearing the end of life.\n\n\nThey can be administered:\n\n\n- Orally - if the patient is safely able to swallow\n- Subcutaneously - via single dose or continuous syringe pump\n- Transdermally - especially for stable symptoms and if available\n- Intramuscularly - less common\n- Intravenously - less common, but may be helpful if a patient already has access\n\n## A note on holistic care\n\nIn palliative care, and in medicine, it is important to consider all symptoms in context. There are many different aspects to symptoms. These include the physical cause, the patient's beliefs about their illness and symptoms, social contributors and impacts, their emotional and behavioural responses. Holistic assessment and management are crucial, which is why the multidisciplinary team is so important. \n\nFor example, a patient may have been prescribed very effective analgesia but is unable to administer medicines themselves. They may also have a very strong emotional response to pain or believe that they deserve their symptoms. They may benefit from a package of care or financial support for terminal illness which a social worker could help with, or an occupational therapist to help with activities of daily living. Counselling may give the patient a space to explore their feelings around their symptoms and their illness, while spiritual support could alleviate some existential distress. These additional interventions work alongside pharmacological therapy to optimise a person's quality of life through their illness.\n\nThis chapter focuses on medications for symptoms towards the end of life, but it is crucial to remember that each patient has a different combination of needs which requires an individual assessment and management plan, often with input from a range of health and social care professionals.\n\n# Pain\n\n\nInitial pharmacological management of pain should follow the WHO pain ladder. Once patients have reached the top of this ladder (requiring regular strong opioids), careful optimisation is necessary to ensure the right level of pain relief while minimising side effects.\n\n- Morphine is the first-line strong opioid analgesic. This can be given as a modified release or immediate release form. \n- Generally, patients would have a regular 'background' dose based on their 24-hour requirements, plus a PRN dose available for **breakthrough pain.** PRN doses are usually 1/6-1/10 of the 24 hour dose. Analgesia requirements should be reviewed regularly, for example every 24 hours.\n- Alternatives to morphine may be necessary for patients with poor renal function. These include oxycodone, alfentanyl or buprenorphine.\n- When prescribing opioid analgesia consider co-prescribing a regular laxative and an as-required anti-emetic. Monitor for signs of opioid toxicity (respiratory depression, sedation, myoclonus) and switch to alternatives or dose reduce as necessary.\n\nWhen switching analgesia, it is helpful to convert the dose first to oral morphine before converting to the desired medication. Please note that different routes also have different equivalent doses, so it is always safest to check guidelines.\n\n\nThe following table shows dose equivalents of 10mg oral morphine\n\n\n| Analgesic/Route | Dose | Conversion Factor |\n| ----------------------------- | ------- | ----------------- |\n| Codeine/tramadol/dihydrocodeine oral | 100mg | x10 |\n| Diamorphine IM/IV/Subcut | 3mg | x3.3 |\n| Morphine IM/IV/Subcut | 5mg | x2 |\n| Oxycodone oral\\* | 5mg\\* | x2\\* |\n| Oxycodone Subcut\\* | 2.5mg\\* | x4\\* |\n| Alfentanil Subcut | 0.3mg | x30 |\n\n\n*NB - oral oxycodone potency is between 1.3-2x that of oral morphine. Different trusts will adopt different guidance on which you should use. If in doubt, always opt for the lower dose and titrate up.\n\n\n# Breathlessness\n\nConsider non-pharmacological measures for breathlessness first. For example, sitting the patient up, opening a window or setting up a fan can all help.\n\nPharmacological management may involve low-dose opioids, benzodiazepines or therapeutic oxygen, and should be tailored to the patient.\n\n\n# Nausea and vomiting\n\nIt is important to consider the likely cause of nausea and vomiting, as medications target different parts of the vomiting pathway. Perform a full assessment to determine the likely cause of the nausea and vomiting. Consider parenteral routes of administration - patients may have severe gastrointestinal disturbance or at least may not be able to keep down oral antiemetics long enough to be effective.\n\nThe following table shows the primary site of activity and side effects of commonly used antiemetics:\n\n| Antiemetic | Receptor activity | Side effects & cautions | Useful for |\n|---|---|---|---|\n| Metoclopramide | Dopamine antagonist | Extrapyramidal symptoms, drowsiness, restlessness, diarrhoea. Do not give with antimuscarinics or in mechanical bowel obstruction | Gastric stasis, functional bowel obstruction |\n| Cyclizine | Histamine, acetylcholine antagonist | Drowsiness, antimuscarinic | Raised intracranial pressure, vestibular dysfunction |\n| Hyoscine | Acetylcholine antagonist | Antimuscarinic | Motion sickness |\n| Haloperidol | Dopamine antagonist | Less common in palliative care doses | Chemical |\n| Levomepromazine | Dopamine, histamine, acetylcholine, 5HT2 antagonist | Sedation, postural hypotension, antimuscarinic |Broad range |\n| Ondansetron | 5HT3 antagonist | Constipation, arrhythmias, movement disorder | Cytotoxic-related |\n\n- For chemically-mediated symptoms (for example medications, metabolic derangemenet), aim to treat the underlying cause. Antiemetics that may be helpful include haloperidol, metoclopramide or levomepromazine.\n- For nausea and vomiting due to raised intracranial pressure, cyclizine is usually used first-line. Dexamethasone or radiotherapy may be helpful to reduce the pressure-associated symptoms.\n- For patients with vestibular disturbance (for example symptoms associated with movement), cyclizine usually used first-line. Alternatives include hyoscine hydrobromide.\n- For patients with bowel obstruction, seek specialist advice. If due to peristaltic failure, review medications and consider starting metoclopramide (providing there is no colic). Likewise for gastric stasis, consider metoclopramide. For patients with mechanical obstruction and/or colic, do not give metoclopramide. Exclude constipation, give cyclizine for nausea and treat colic with hyoscine butylbromide.\n- If nausea and vomiting is due to compression from an abdominal or pelvic tumour, cyclizine should be used first-line.\n- For anxiety-related nausea and vomiting, begin with non-pharmacological measures for anxiety, such as CBT. A benzodiazepine or levomepromazine would be first-line pharmacological options.\n\n# Agitation\n\nAs with other symptoms, aim to manage reversible causes of agitation and possible delirium first. Consider non-pharmacological measures such as environmental modification. For patients in their last days of life, haloperidol or low-dose midazolam may be prescribed. Often, this is done as part of anticipatory prescribing.\n\n\n# Respiratory tract secretions\n\nRespiratory tract secretions often occur in the last days of life as a person becomes less able to clear their airways. They are rarely a cause of distress to the patient, but may be upsetting for family members or those close to the patient. An antimuscarinic such as hyoscine butylbromide or glycopyrronium bromide may be prescribed for noisy respiratory secretions.\n\n\n# NICE guidelines\n\n\n[NICE Guidance: Care of dying adults in the last days of life](https://www.nice.org.uk/guidance/ng31)\n\n[NICE CKS: Palliative care - general issues](https://cks.nice.org.uk/topics/palliative-care-general-issues/)\n\n[NICE CKS: Palliative care - dyspnoea](https://cks.nice.org.uk/topics/palliative-care-dyspnoea/)\n\n[NICE CKS: Palliative care - nausea and vomiting](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative care - secretions](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative cancer care - pain](https://cks.nice.org.uk/topics/)\n\n# References\n\n[Pallcare.info](https://www.pallcare.info/book.php)\n\n[BNF: Ondansetron](https://bnf.nice.org.uk/drugs/ondansetron/#drug-action)\n\n[BNF: Nausea and labyrinth disorders](https://bnf.nice.org.uk/treatment-summaries/nausea-and-labyrinth-disorders/)\n\n[BNF: Prescribing in palliative care](https://bnf.nice.org.uk/medicines-guidance/prescribing-in-palliative-care/)",
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"explanation": "# Summary\n\n\nBreast carcinoma is the most prevalent form of cancer among women and the second leading cause of cancer death in the UK. It manifests in various histological subtypes including ductal, lobular, medullary, and phyllodes tumours, each displaying distinct characteristics. Certain genetic mutations, especially BRCA1 and BRCA2, can increase the risk for breast carcinoma. Notable signs and symptoms include unexplained breast mass, nipple discharge, retraction, or skin changes suggestive of breast cancer. Key investigations comprise a triple assessment—clinical examination, radiological examination, and biopsy. Treatment strategies encompass surgical management (wide local excision or mastectomy), radiotherapy, chemotherapy, biological therapy, and hormonal therapy. Risk factors for breast cancer include increased hormone exposure, susceptibility gene mutations, advancing age, and lifestyle factors like obesity, physical inactivity, and alcohol and tobacco use.\n\n\n# Definition\n\n\nBreast carcinoma refers to a malignant tumour originating from the cells of the breast tissue. It exhibits different subtypes each with unique cellular properties and clinical implications. The carcinomas can be invasive, indicating they have broken through the basement membrane of the tissue of origin and have the potential to metastasize, or non-invasive (in situ), suggesting they are confined to the initial location.\n\n\n# Epidemiology\n\n\nBreast carcinoma is the most common type of cancer in women and accounts for approximately 15% of new cancer cases, representing 50,000 new cases annually. It is the second most common cause of cancer death in the UK.\n\n\n# Aetiology\n\nMost breast cancers are either ductal (arising from the epithelial lining of the ducts) or lobular (originating from epithelial cells in the terminal ducts of the lobules).\n\n\nRisk factors for breast carcinoma include:\n\n\n- Being female\n- 99% of breast cancer cases occur in women\n- Increased hormone exposure\n- Early menarche or late menopause\n- Nulliparity or late first pregnancy\n- Oral contraceptives or Hormonal Replacement Therapy\n- Susceptibility gene mutations\n- Most commonly BRCA mutations (BRCA1/BRCA2)\n- Advancing age\n- Caucasian ethnicity\n- Obesity and lack of physical activity\n- Alcohol and tobacco use\n- History of breast cancer\n- Previous radiotherapy treatment\n\n\n# Classification\n\n\nBreast cancer is not a single disease, but a collection of several subtypes, each with its unique characteristics, prognosis, and treatment options.It can be classified based on its origin cell type such as:\n\n\n- **Invasive ductal carcinoma (IDC)**: This is the most common type, accounting for about 80% of all breast cancers. It starts in a milk duct, breaks through the wall of the duct, and invades the fatty tissue of the breast.\n- **Invasive lobular carcinoma (ILC)**: This type begins in the milk-producing glands (lobules) and can spread to other parts of the body.\n- **Ductal carcinoma in situ (DCIS)**: This is a non-invasive or pre-invasive cancer where the cells are confined to the ducts in the breast and have not spread into the surrounding breast tissue.\n- **Lobular carcinoma in situ (LCIS)**: This is not a cancer but an area of abnormal cell growth that increases a person's risk of developing invasive breast cancer later.\n- **Paget's disease of breast**: Infiltrating carcinoma of nipple epithelium.\n\n\nIt can also be classified based on the hormone receptors present on the surface of the breast cancer:\n\n- **Inflammatory breast cancer (IBC)**: This is a rare but aggressive type of breast cancer that causes the lymph vessels in the skin of the breast to become blocked.\n\n- **Triple-negative breast cancer (TNBC)**: This type lacks estrogen receptors, progesterone receptors, and does not have an excess of the HER2 protein on the cancer cell surfaces. It tends to be more aggressive and has fewer targeted treatments available.\n\n- **HER2-positive breast cancer**: This is a cancer that tests positive for a protein called human epidermal growth factor receptor 2 (HER2), which promotes the growth of cancer cells. It tends to be more aggressive than other types of breast cancer, but it may respond well to targeted therapies that can block HER2.\n\n\n# Signs and Symptoms\n\n\nCommon clinical manifestations of breast carcinoma include:\n\n\n- Unexplained breast mass in patients aged 30 and above, with or without pain\n- In those aged 50 and older, nipple discharge, retraction/inversion, or other concerning symptoms\n- This can also include eczema-type changes surrounding the nipple as seen in Paget's disease of the breast\n- Skin changes suggestive of breast cancer\n- This includes skin retraction, peau d'orange appearance or ulceration of the skin above an underlying mass.\n- Unexplained axillary mass in those aged 30 and above\n\n\nApproximately 25% of cases are found in routine breast cancer screening (mammography).\n\n\n# Differential Diagnosis\n\n\nWhile an unexplained breast mass is a key indicator of breast carcinoma, it can also represent various other conditions, each characterized by distinct signs and symptoms:\n\n\n- **Fibroadenoma**: Typically presents as a solitary, painless, and well-circumscribed breast lump in young women\n- **Breast Cyst**: Characterized by a round or oval, well-defined, and movable mass. It may be painful and size may vary with the menstrual cycle.\n- **Mastitis**: Typically presents in breastfeeding women, characterized by a painful, warm, red breast often accompanied by systemic symptoms like fever.\n- **Lipoma**: Presents as a soft, mobile, and painless lump.\n\n\n# Breast Cancer Screening in the UK\n\n\nIn the United Kingdom, the NHS Breast Screening Programme provides free breast screening services for all women registered with a GP. The programme invites women between the ages of 50 and 70 for breast screening every three years, with the first invitation to screening usually sent to women before they turn 53.\n\n\nThis screening process involves a mammogram, which is an X-ray of the breasts that can help detect breast cancers early, often before they can be felt. The aim of breast cancer screening is to find cancer at an early stage when treatment is most effective.\n\n\nIn 2018, the age range for screening was extended as part of a trial, and some women were invited for screening from the age of 47 up to the age of 73. Women over 70 can still self-refer for screening every three years.\n\n\n# Investigations\n\nCriteria for 2-week wait:\n\n- Age 30 or more with unexplained breast lump (with or without pain)\n- Age 50 or more with nipple discharge, retraction or other changes\n- Consider a 2-week wait if a patient is 30 or over with skin changes suggestive of breast cancer or an unexplained lump in the axilla\n\nNB: a non-urgent referral should be considered for patients under the age of 30 with an unexplained breast lump.\n\n### Triple Assessment\n\nTriple assessment is used to investigate suspected breast carcinoma:\n\n\n1. Clinical examination: of the breast and surrounding lymph nodes\n2. Radiological examination:\n\t- Ultrasound is used for women under the age of 40 or those with higher breast density.\n\t- A mammogram is commonly used for women over 40 years.\n\t- If there are concerns of metastatic disease, a CT or PET scan may be done.\n3. Biopsy: often a core needle biopsy or fine needle aspirate (FNA)\n\t- Fine needle aspiration (FNA): Often combined with mammography, however, has a high rate of false negatives.\n\t- Core needle biopsy: method of choice, can be combined with imaging to aid accuracy.\n\t- DCIS biopsy will show cellular atypia and hyperchromatic nuclei involving the ducts, but not passing the basement membrane\n\t- In invasive breast cancer, these abnormal cells will pass the basement membrane\n\t- In lobular carcinoma, the abnormal cells will be found within the lobular acini\n\n### Further Investigations\n\nFollowing the triple assessment, further investigations will include:\n\n- Biopsies to determine\n- Oestrogen and progesterone receptor status\n- Epidermal growth factor receptor status\n- Routine blood tests (i.e. LFTs)\n- CXR\n- MRI is not routinely used. It is used for women with:\n- Discrepancy between the extent of disease between clinical examination and imaging\n- Dense breast tissue limiting mammography\n- Invasive lobular carcinoma to evaluate tumour size when planning breast-conserving surgery\n- BRCA1/2 testing is done for women < 50 years with triple-negative breast cancer regardless of family history\n\n\n### Staging\n\nStaging involves the TNM system considering the size of the tumour (T), the spread to the lymph nodes (N), and the presence of metastases (M). For locally invasive breast cancer, this can include:\n\n- Axilla ultrasound with needle sampling if abnormal lymph nodes are identified\n\nIf the cancer is deemed to be advanced, staging investigations should include:\n\n- CT, MRI or bone scintigraphy to determine the presence and extent of visceral and bony metastasis\n- PET CT is only used to diagnose metastasis\n\n\n# Management\n\n\nThe management strategy for breast carcinoma can vary based on several factors including the subtype of carcinoma, stage, hormonal receptor status, and the patient's overall health and preferences.\n\n\n- Surgical management: Wide local excision (WLE) or mastectomy, with sentinel node biopsies for invasive cancers and possible axillary node clearance for positive nodes. Breast reconstruction can be done concurrently or later.\n- Radiotherapy: Adjuvant radiotherapy is commonly offered following WLE to reduce recurrence. It may also be given to patients with higher-stage cancers post-mastectomy.\n\n**Chemotherapy:**\n\n- Suggested for hormone receptor-negative and HER2 over-expressing patients. Neoadjuvant chemotherapy may be given to downstage tumours before surgery. This commonly includes an anthracycline (i.e. doxorubicin) and a taxane (i.e. paclitaxel)\n- Biological Therapy:\n\t- Trastuzumab (Herceptin) should be given to HER2-positive patients with tumour size T1c and above in combination with surgery, chemotherapy and radiotherapy. Patients should have regular cardiac function assessments.\n\t- Abermaciclib (selective inhibitor of cyclin-dependent kinases 4 and 6) for HER2-negative, hormone receptor-positive breast cancer\n\t- Pembrolizumab for triple-negative breast cancer\n\t- Olaparib (PSTP inhibitor) for BRCA positive, HER2 negative high-risk early breast cancer\n- **Hormonal Therapy** for oestrogen-positive breast cancer:\n\t- Anastrozole (aromatase inhibitor) for postmenopausal women\n\t- Tamoxifen (oestrogen receptor antagonist) for premenopausal patients\n\t- Bisphosphonates: May be used for reducing occurrence in node-positive cancers.\n\t- Zoledronic acid has been shown to improve disease-free survival in postmenopausal women with node-positive invasive breast cancer.\n\t- Bisphosphonates are also advised for treatment-induced menopause in women treated with aromatase inhibitors\n\n\n# Complications\n\n### Complications of Breast Carcinoma\n\n- Fatigue\n- Bone metastases\n- Brain metastases\n- Psychological difficulties: Anxiety, depression and damage to the individual's self-esteem.\n- Recurrence:\n\t- Local: recurrence in the same breast as the original tumour\n\t- Regional: recurrence in the axillary or sub-clavicular lymph nodes draining the breast cancer\n\t- Distant: recurrence once already metastasized to other parts of the body (i.e. liver, lungs, brain, bone)\n\n\n### Side Effects of Medication Used to Treat Breast Cancer\n\n\nTreatment for breast cancer often involves medication, including chemotherapy, hormone therapy, and targeted drug therapy. Each of these can have different side effects.\n\n\n**Chemotherapy** drugs are powerful medications that aim to destroy rapidly dividing cells, such as cancer cells. However, they can also affect healthy cells, leading to a range of side effects, including fatigue, hair loss, easy bruising and bleeding, infection, anaemia, nausea and vomiting, appetite changes, peripheral neuropathy, and problems with concentration or memory.\n\nChemotherapy agents can have specific side effects such as:\n\n- Doxorubicin is associated with cardiac toxicity (e.g. cardiac arrhythmias, myopericarditis)\n- Paclitaxel is associated with lung fibrosis.\n\n\n**Hormone therapy** drugs, such as tamoxifen and aromatase inhibitors, are used to treat hormone receptor-positive breast cancers. Common side effects include hot flushes, vaginal dryness or discharge, menstrual changes, fatigue, mood changes, and osteoporosis. In rare cases, tamoxifen can increase the risk of serious conditions like endometrial cancer and blood clots.\n\n\n**Targeted drug therapies** such as trastuzumab (Herceptin), pertuzumab (Perjeta), and ado-trastuzumab emtansine (Kadcyla), are designed to interfere with specific proteins or processes that contribute to cancer growth.\n\nSide effects include:\n\n- Infections\n- Bruising and easy bleeding\n- Anaemia\n- Cardiac (i.e. arrhythmias)\n- Insomnia\n- GI side effects (i.e. diarrhoea, vomiting, constipation, appetite loss, weight loss)\n- Runny nose\n- Conjunctivitis\n- Hair loss\n- Nail changes\n- Hand foot syndrome: the palms and plantar surfaces become sore, peel, crack and blister.\n- Hepatotoxicity\n\n\n\n### Surgical Complications\n\nKey surgical complications include:\n\n- Venous thromboembolism\n- Lymphoedema\n- Pain\n\n\n### Breast Cancer in Pregnancy\n\nBreast cancer is the most common malignancy to occur during pregnancy. Radiotherapy and chemotherapy are most commonly delayed until completion of pregnancy, but surgical intervention can be considered.\n\n# Prognosis\n\nThe prognosis for individuals with breast cancer has vastly improved, almost doubling over the past 50 years. The ten-year survival for breast cancer in England is 75.9%\n\nA poorer prognosis is associated with:\n\n- Advancing age\n- Being male\n- Stage III or IV\n- Tumour size\n- Tumour grade\n- Hormone receptor-negative tumours (oestrogen or progesterone receptor-negative)\n- HER 2 positive tumours\n\n\n# NICE Guidelines\n\n[NICE Guidelines on Early and Locally Advanced Breast Cancer](https://www.nice.org.uk/guidance/ng101)\n\n[NICE Guidelines on Advanced Breast Cancer](https://www.nice.org.uk/guidance/cg81)\n\n# References\n\n[Patient Info Breast Cancer](https://www.nice.org.uk/guidance/cg81)\n\n[BMJ Best Practice Breast Cancer](https://bestpractice.bmj.com/topics/en-gb/718?q=Metastatic%20breast%20cancer&c=suggested)\n\n[NHS Breast Cancer in Women](https://www.nhs.uk/conditions/breast-cancer-in-women/)\n\n[Cancer Research UK Breast Cancer](https://www.cancerresearchuk.org/about-cancer/breast-cancer/survival)",
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"question": "A 56-year-old woman presents to her GP with worsening shortness of breath which is worse on exertion. She also experiences breathlessness when lying flat and at night. She has a history of breast cancer, hyperthyroidism and type II diabetes mellitus. On examination, she has bilateral pitting oedema in her ankles. Her medications include tamoxifen, trastuzumab, carbimazole, metformin and linagliptin.\n\nWhich of her medications is most likely to be the cause of her symptoms?",
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"comment": "Would we ever consider not operating on it? If it is benign and the patient doesnt care much for it shouldnt it be fine?",
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"comment": "One third of phyllodes tumours convert to malignancy according to teach me surgery therefore they are excised to reduce risk ",
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"explanation": "# Summary\n\n\nBreast carcinoma is the most prevalent form of cancer among women and the second leading cause of cancer death in the UK. It manifests in various histological subtypes including ductal, lobular, medullary, and phyllodes tumours, each displaying distinct characteristics. Certain genetic mutations, especially BRCA1 and BRCA2, can increase the risk for breast carcinoma. Notable signs and symptoms include unexplained breast mass, nipple discharge, retraction, or skin changes suggestive of breast cancer. Key investigations comprise a triple assessment—clinical examination, radiological examination, and biopsy. Treatment strategies encompass surgical management (wide local excision or mastectomy), radiotherapy, chemotherapy, biological therapy, and hormonal therapy. Risk factors for breast cancer include increased hormone exposure, susceptibility gene mutations, advancing age, and lifestyle factors like obesity, physical inactivity, and alcohol and tobacco use.\n\n\n# Definition\n\n\nBreast carcinoma refers to a malignant tumour originating from the cells of the breast tissue. It exhibits different subtypes each with unique cellular properties and clinical implications. The carcinomas can be invasive, indicating they have broken through the basement membrane of the tissue of origin and have the potential to metastasize, or non-invasive (in situ), suggesting they are confined to the initial location.\n\n\n# Epidemiology\n\n\nBreast carcinoma is the most common type of cancer in women and accounts for approximately 15% of new cancer cases, representing 50,000 new cases annually. It is the second most common cause of cancer death in the UK.\n\n\n# Aetiology\n\nMost breast cancers are either ductal (arising from the epithelial lining of the ducts) or lobular (originating from epithelial cells in the terminal ducts of the lobules).\n\n\nRisk factors for breast carcinoma include:\n\n\n- Being female\n- 99% of breast cancer cases occur in women\n- Increased hormone exposure\n- Early menarche or late menopause\n- Nulliparity or late first pregnancy\n- Oral contraceptives or Hormonal Replacement Therapy\n- Susceptibility gene mutations\n- Most commonly BRCA mutations (BRCA1/BRCA2)\n- Advancing age\n- Caucasian ethnicity\n- Obesity and lack of physical activity\n- Alcohol and tobacco use\n- History of breast cancer\n- Previous radiotherapy treatment\n\n\n# Classification\n\n\nBreast cancer is not a single disease, but a collection of several subtypes, each with its unique characteristics, prognosis, and treatment options.It can be classified based on its origin cell type such as:\n\n\n- **Invasive ductal carcinoma (IDC)**: This is the most common type, accounting for about 80% of all breast cancers. It starts in a milk duct, breaks through the wall of the duct, and invades the fatty tissue of the breast.\n- **Invasive lobular carcinoma (ILC)**: This type begins in the milk-producing glands (lobules) and can spread to other parts of the body.\n- **Ductal carcinoma in situ (DCIS)**: This is a non-invasive or pre-invasive cancer where the cells are confined to the ducts in the breast and have not spread into the surrounding breast tissue.\n- **Lobular carcinoma in situ (LCIS)**: This is not a cancer but an area of abnormal cell growth that increases a person's risk of developing invasive breast cancer later.\n- **Paget's disease of breast**: Infiltrating carcinoma of nipple epithelium.\n\n\nIt can also be classified based on the hormone receptors present on the surface of the breast cancer:\n\n- **Inflammatory breast cancer (IBC)**: This is a rare but aggressive type of breast cancer that causes the lymph vessels in the skin of the breast to become blocked.\n\n- **Triple-negative breast cancer (TNBC)**: This type lacks estrogen receptors, progesterone receptors, and does not have an excess of the HER2 protein on the cancer cell surfaces. It tends to be more aggressive and has fewer targeted treatments available.\n\n- **HER2-positive breast cancer**: This is a cancer that tests positive for a protein called human epidermal growth factor receptor 2 (HER2), which promotes the growth of cancer cells. It tends to be more aggressive than other types of breast cancer, but it may respond well to targeted therapies that can block HER2.\n\n\n# Signs and Symptoms\n\n\nCommon clinical manifestations of breast carcinoma include:\n\n\n- Unexplained breast mass in patients aged 30 and above, with or without pain\n- In those aged 50 and older, nipple discharge, retraction/inversion, or other concerning symptoms\n- This can also include eczema-type changes surrounding the nipple as seen in Paget's disease of the breast\n- Skin changes suggestive of breast cancer\n- This includes skin retraction, peau d'orange appearance or ulceration of the skin above an underlying mass.\n- Unexplained axillary mass in those aged 30 and above\n\n\nApproximately 25% of cases are found in routine breast cancer screening (mammography).\n\n\n# Differential Diagnosis\n\n\nWhile an unexplained breast mass is a key indicator of breast carcinoma, it can also represent various other conditions, each characterized by distinct signs and symptoms:\n\n\n- **Fibroadenoma**: Typically presents as a solitary, painless, and well-circumscribed breast lump in young women\n- **Breast Cyst**: Characterized by a round or oval, well-defined, and movable mass. It may be painful and size may vary with the menstrual cycle.\n- **Mastitis**: Typically presents in breastfeeding women, characterized by a painful, warm, red breast often accompanied by systemic symptoms like fever.\n- **Lipoma**: Presents as a soft, mobile, and painless lump.\n\n\n# Breast Cancer Screening in the UK\n\n\nIn the United Kingdom, the NHS Breast Screening Programme provides free breast screening services for all women registered with a GP. The programme invites women between the ages of 50 and 70 for breast screening every three years, with the first invitation to screening usually sent to women before they turn 53.\n\n\nThis screening process involves a mammogram, which is an X-ray of the breasts that can help detect breast cancers early, often before they can be felt. The aim of breast cancer screening is to find cancer at an early stage when treatment is most effective.\n\n\nIn 2018, the age range for screening was extended as part of a trial, and some women were invited for screening from the age of 47 up to the age of 73. Women over 70 can still self-refer for screening every three years.\n\n\n# Investigations\n\nCriteria for 2-week wait:\n\n- Age 30 or more with unexplained breast lump (with or without pain)\n- Age 50 or more with nipple discharge, retraction or other changes\n- Consider a 2-week wait if a patient is 30 or over with skin changes suggestive of breast cancer or an unexplained lump in the axilla\n\nNB: a non-urgent referral should be considered for patients under the age of 30 with an unexplained breast lump.\n\n### Triple Assessment\n\nTriple assessment is used to investigate suspected breast carcinoma:\n\n\n1. Clinical examination: of the breast and surrounding lymph nodes\n2. Radiological examination:\n\t- Ultrasound is used for women under the age of 40 or those with higher breast density.\n\t- A mammogram is commonly used for women over 40 years.\n\t- If there are concerns of metastatic disease, a CT or PET scan may be done.\n3. Biopsy: often a core needle biopsy or fine needle aspirate (FNA)\n\t- Fine needle aspiration (FNA): Often combined with mammography, however, has a high rate of false negatives.\n\t- Core needle biopsy: method of choice, can be combined with imaging to aid accuracy.\n\t- DCIS biopsy will show cellular atypia and hyperchromatic nuclei involving the ducts, but not passing the basement membrane\n\t- In invasive breast cancer, these abnormal cells will pass the basement membrane\n\t- In lobular carcinoma, the abnormal cells will be found within the lobular acini\n\n### Further Investigations\n\nFollowing the triple assessment, further investigations will include:\n\n- Biopsies to determine\n- Oestrogen and progesterone receptor status\n- Epidermal growth factor receptor status\n- Routine blood tests (i.e. LFTs)\n- CXR\n- MRI is not routinely used. It is used for women with:\n- Discrepancy between the extent of disease between clinical examination and imaging\n- Dense breast tissue limiting mammography\n- Invasive lobular carcinoma to evaluate tumour size when planning breast-conserving surgery\n- BRCA1/2 testing is done for women < 50 years with triple-negative breast cancer regardless of family history\n\n\n### Staging\n\nStaging involves the TNM system considering the size of the tumour (T), the spread to the lymph nodes (N), and the presence of metastases (M). For locally invasive breast cancer, this can include:\n\n- Axilla ultrasound with needle sampling if abnormal lymph nodes are identified\n\nIf the cancer is deemed to be advanced, staging investigations should include:\n\n- CT, MRI or bone scintigraphy to determine the presence and extent of visceral and bony metastasis\n- PET CT is only used to diagnose metastasis\n\n\n# Management\n\n\nThe management strategy for breast carcinoma can vary based on several factors including the subtype of carcinoma, stage, hormonal receptor status, and the patient's overall health and preferences.\n\n\n- Surgical management: Wide local excision (WLE) or mastectomy, with sentinel node biopsies for invasive cancers and possible axillary node clearance for positive nodes. Breast reconstruction can be done concurrently or later.\n- Radiotherapy: Adjuvant radiotherapy is commonly offered following WLE to reduce recurrence. It may also be given to patients with higher-stage cancers post-mastectomy.\n\n**Chemotherapy:**\n\n- Suggested for hormone receptor-negative and HER2 over-expressing patients. Neoadjuvant chemotherapy may be given to downstage tumours before surgery. This commonly includes an anthracycline (i.e. doxorubicin) and a taxane (i.e. paclitaxel)\n- Biological Therapy:\n\t- Trastuzumab (Herceptin) should be given to HER2-positive patients with tumour size T1c and above in combination with surgery, chemotherapy and radiotherapy. Patients should have regular cardiac function assessments.\n\t- Abermaciclib (selective inhibitor of cyclin-dependent kinases 4 and 6) for HER2-negative, hormone receptor-positive breast cancer\n\t- Pembrolizumab for triple-negative breast cancer\n\t- Olaparib (PSTP inhibitor) for BRCA positive, HER2 negative high-risk early breast cancer\n- **Hormonal Therapy** for oestrogen-positive breast cancer:\n\t- Anastrozole (aromatase inhibitor) for postmenopausal women\n\t- Tamoxifen (oestrogen receptor antagonist) for premenopausal patients\n\t- Bisphosphonates: May be used for reducing occurrence in node-positive cancers.\n\t- Zoledronic acid has been shown to improve disease-free survival in postmenopausal women with node-positive invasive breast cancer.\n\t- Bisphosphonates are also advised for treatment-induced menopause in women treated with aromatase inhibitors\n\n\n# Complications\n\n### Complications of Breast Carcinoma\n\n- Fatigue\n- Bone metastases\n- Brain metastases\n- Psychological difficulties: Anxiety, depression and damage to the individual's self-esteem.\n- Recurrence:\n\t- Local: recurrence in the same breast as the original tumour\n\t- Regional: recurrence in the axillary or sub-clavicular lymph nodes draining the breast cancer\n\t- Distant: recurrence once already metastasized to other parts of the body (i.e. liver, lungs, brain, bone)\n\n\n### Side Effects of Medication Used to Treat Breast Cancer\n\n\nTreatment for breast cancer often involves medication, including chemotherapy, hormone therapy, and targeted drug therapy. Each of these can have different side effects.\n\n\n**Chemotherapy** drugs are powerful medications that aim to destroy rapidly dividing cells, such as cancer cells. However, they can also affect healthy cells, leading to a range of side effects, including fatigue, hair loss, easy bruising and bleeding, infection, anaemia, nausea and vomiting, appetite changes, peripheral neuropathy, and problems with concentration or memory.\n\nChemotherapy agents can have specific side effects such as:\n\n- Doxorubicin is associated with cardiac toxicity (e.g. cardiac arrhythmias, myopericarditis)\n- Paclitaxel is associated with lung fibrosis.\n\n\n**Hormone therapy** drugs, such as tamoxifen and aromatase inhibitors, are used to treat hormone receptor-positive breast cancers. Common side effects include hot flushes, vaginal dryness or discharge, menstrual changes, fatigue, mood changes, and osteoporosis. In rare cases, tamoxifen can increase the risk of serious conditions like endometrial cancer and blood clots.\n\n\n**Targeted drug therapies** such as trastuzumab (Herceptin), pertuzumab (Perjeta), and ado-trastuzumab emtansine (Kadcyla), are designed to interfere with specific proteins or processes that contribute to cancer growth.\n\nSide effects include:\n\n- Infections\n- Bruising and easy bleeding\n- Anaemia\n- Cardiac (i.e. arrhythmias)\n- Insomnia\n- GI side effects (i.e. diarrhoea, vomiting, constipation, appetite loss, weight loss)\n- Runny nose\n- Conjunctivitis\n- Hair loss\n- Nail changes\n- Hand foot syndrome: the palms and plantar surfaces become sore, peel, crack and blister.\n- Hepatotoxicity\n\n\n\n### Surgical Complications\n\nKey surgical complications include:\n\n- Venous thromboembolism\n- Lymphoedema\n- Pain\n\n\n### Breast Cancer in Pregnancy\n\nBreast cancer is the most common malignancy to occur during pregnancy. Radiotherapy and chemotherapy are most commonly delayed until completion of pregnancy, but surgical intervention can be considered.\n\n# Prognosis\n\nThe prognosis for individuals with breast cancer has vastly improved, almost doubling over the past 50 years. The ten-year survival for breast cancer in England is 75.9%\n\nA poorer prognosis is associated with:\n\n- Advancing age\n- Being male\n- Stage III or IV\n- Tumour size\n- Tumour grade\n- Hormone receptor-negative tumours (oestrogen or progesterone receptor-negative)\n- HER 2 positive tumours\n\n\n# NICE Guidelines\n\n[NICE Guidelines on Early and Locally Advanced Breast Cancer](https://www.nice.org.uk/guidance/ng101)\n\n[NICE Guidelines on Advanced Breast Cancer](https://www.nice.org.uk/guidance/cg81)\n\n# References\n\n[Patient Info Breast Cancer](https://www.nice.org.uk/guidance/cg81)\n\n[BMJ Best Practice Breast Cancer](https://bestpractice.bmj.com/topics/en-gb/718?q=Metastatic%20breast%20cancer&c=suggested)\n\n[NHS Breast Cancer in Women](https://www.nhs.uk/conditions/breast-cancer-in-women/)\n\n[Cancer Research UK Breast Cancer](https://www.cancerresearchuk.org/about-cancer/breast-cancer/survival)",
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"explanation": "Vertigo, tinnitus and fluctuating hearing loss are classic Ménière's disease symptoms. The hallmark of the disease is that these symptoms are episodic and fluctuating in nature",
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"explanation": "Otitis media in adults is most likely to present with otalgia. Otitis media can rarely cause vertigo or tinnitus; however it is unlikely to be intermittent or affect both ears simultaneously",
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"explanation": "BPPV is unlikely, as episodes of vertigo usually last for seconds to minutes and are related to head movement. Hearing loss and tinnitus are not typical features",
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"explanation": "Vestibular neuritis and labyrinthitis are sometimes used interchangeably. However, vestibular neuritis refers to inflammation of the vestibular nerve only, whereas labyrinthitis refers to inflammation of the vestibular nerve and the labyrinth. Vestibular neuritis leads to sudden severe vertigo, which is unlikely to be affected by head movement. There is no accompanying hearing loss or tinnitus",
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"explanation": "Labyrinthitis and vestibular neuritis are sometimes used interchangeably. However, labyrinthitis refers to inflammation of the vestibular nerve and the labyrinth, whereas vestibular neuritis refers to inflammation of the vestibular nerve only. Labyrinthitis can present with vertigo, hearing loss and tinnitus; however, it is more likely to present suddenly and does not follow a fluctuating course. Labyrinthitis is also more likely to be unilateral",
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"explanation": "# Summary\n\nMeniere's disease is a condition characterized by the dilation of the endolymphatic spaces of the membranous labyrinth, causing episodes of vertigo lasting for 12-24 hours. Key signs and symptoms include paroxysmal vertigo, associated deafness, and tinnitus. Diagnosis typically involves clinical evaluation and audiometric testing. Management primarily involves the prophylactic use of betahistine to reduce the frequency of attacks and the acute use of prochlorperazine. \n\n# Definition\n\nMeniere's disease is an inner ear disorder caused by increased fluid pressure in the endolymphatic spaces of the membranous labyrinth. This results in recurrent episodes of vertigo, hearing loss, and tinnitus.\n\n# Epidemiology\n\nMeniere's disease typically presents in individuals between the ages of 30 and 60 and predominantly affects only one ear. \n\n# Aetiology\n\nThe exact cause of Meniere's disease is unknown, but it is believed to be associated with the dilation of the endolymphatic spaces of the membranous labyrinth. This dilation leads to an increased fluid pressure within the inner ear, causing the characteristic symptoms of the disease.\n\n# Signs and Symptoms\n\n- Sudden attacks of paroxysmal vertigo\n- Associated deafness\n- Tinnitus\n- Attacks often occur in clusters, with periods of remission where function is recovered\n- The condition can be incredibly disabling, leaving patients bed-bound and suffering from nausea, vomiting, and fluctuating hearing.\n\n# Differential Diagnosis\n\nWhen diagnosing Meniere's disease, it's important to consider other conditions that may present with similar symptoms, such as:\n\n- Vestibular neuritis: Characterized by sudden onset vertigo, nausea, vomiting, and unsteadiness\n- Labyrinthitis: Presents with vertigo, hearing loss, and tinnitus\n- Benign paroxysmal positional vertigo (BPPV): Characterized by brief episodes of mild to intense dizziness triggered by specific changes in the position of the head\n\n# Investigations\n\nDiagnosis of Meniere's disease typically relies on clinical evaluation and audiometric testing. Additional imaging or laboratory tests may be needed to rule out other potential causes of the symptoms.\n\n# Management\n\n- Prophylactic use of betahistine to reduce the frequency of attacks\n- Acute use of prochlorperazine to manage symptoms during attacks\n- Diuretics can also be used to reduce endolymphatic fluid, however this is only prescribed by specialists (i.e. ENT clinics)\n- Surgical approaches are available, but currently lack a strong evidence base. \n- Low-salt diets can also help prevent attacks, by reducing the volume of endolymphatic fluid.\n\n# References\n\n[Click here for NICE CKS on Meniere's disease](https://cks.nice.org.uk/topics/menieres-disease/)\n\n[Patient.info - Meniere's Disease](https://patient.info/ears-nose-throat-mouth/tinnitus-leaflet/menieres-disease)",
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"question": "A 44-year-old woman visits her GP practice because of problems with intermittent, fluctuating hearing loss. She has accompanying symptoms of vertigo and tinnitus. These occurrences tend to last around an hour and have happened a few times in the last month. They were initially in her right ear, but she now experiences the same problems in both ears.\n\nWhat is the most likely diagnosis?",
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"explanation": "An oncocytoma is a type of tumour that is usually benign and develops from oncocytes. These are epithelial cells that have a high concentration of mitochondria. These most often present in the kidneys, salivary glands or thyroid",
"id": "32832",
"label": "e",
"name": "Oncocytoma",
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"explanation": "Pilocytic astrocytomas are brain tumours which most commonly occur in children or young adults. They most often occur in the cerebellum",
"id": "32830",
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"name": "Pilocytic astrocytoma",
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"explanation": "Pleomorphic adenoma is the most common tumour of the parotid gland. It is a benign tumour, but in a very small minority of cases can become malignant. Signs of malignant tumours in the parotids are: fast-growth, pain, facial palsy and fixation",
"id": "32828",
"label": "a",
"name": "Pleomorphic adenoma",
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"explanation": "This is the most common malignant tumour of the lacrimal gland. However, it is less common than pleomorphic adenomas and is more likely to present in younger adults. It is more likely to present as fast-growing, painful, with possible accompanying facial palsy and fixation",
"id": "32829",
"label": "b",
"name": "Adenoid cystic carcinoma",
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"explanation": "Warthin's tumours are painless and slow growing. However, they are the second most common type of benign tumour occurring in the salivary gland. The most common is a pleomorphic adenoma",
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"comment": "why does it say superior to TMJ when the parotid gland in inferior?\n",
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"explanation": "# Summary\n\nSalivary gland tumours are neoplasms that can affect the parotid gland, submandibular gland, and sublingual glands. The majority of salivary gland tumours, approximately 80%, occur in the parotid gland and most are benign. The most common benign tumour is the Pleomorphic adenoma, while malignant tumours commonly present with invasion of other structures, such as the facial nerve causing a VII nerve palsy. It is generally recommended that persistent salivary gland swellings without a clear cause should be removed.\n\n# Definition\n\nSalivary gland tumours are abnormal growths of cells in the glands that produce saliva. These tumours can be benign or malignant and can affect any of the salivary glands including the parotid, submandibular, and sublingual glands.\n\n# Epidemiology\n\n- Tumours of the salivary gland can affect the parotid gland, submandibular gland, and sublingual glands.\n- Approximately 80% of salivary gland tumours are located within the parotid gland, and 80% of these tumours are benign.\n\n# Aetiology\n\nThe precise cause of salivary gland tumours is unknown, but it is thought to involve a combination of genetic and environmental factors.\n\n# Signs and Symptoms\n\n- Salivary gland tumours typically present as a lump or swelling in the affected gland.\n- Malignant tumours often invade surrounding structures, leading to symptoms such as facial nerve palsy.\n\n# Differential Diagnosis\n\nConditions that can present similarly to salivary gland tumours include:\n\n- Sialadenitis: Inflammation of the salivary gland, usually caused by an infection. Symptoms include painful swelling of the gland, fever, and pus draining from the gland.\n- Sialolithiasis: Presence of salivary stones in the gland. Symptoms include painful swelling, especially during meals, and possible infection of the gland.\n- Sjogren's syndrome: An autoimmune disease that affects the salivary and tear glands. Symptoms include dry mouth and eyes, and swelling of the glands.\n\n# Investigations\n\nInvestigations for suspected salivary gland tumours include:\n\n- Biopsy: To determine the type of tumour and whether it is benign or malignant.\n- Imaging studies: Such as ultrasound, CT, or MRI to assess the size and location of the tumour.\n\n# Management\n\n- For salivary gland swellings that have been present for over 1 month with no clear underlying cause, removal is typically recommended.\n- Further management strategies depend on the type and stage of the tumour, and may include radiation therapy or chemotherapy for malignant tumours.\n\n# References\n\n[Click here for NICE CKS on neck lumps](https://cks.nice.org.uk/topics/neck-lump/)",
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"question": "A 75-year-old woman visits her GP because she has noticed a facial swelling. This has occurred on the right side of her face and has been slowly growing over the last few months. On examination, the GP feels a small, non-tender, non-fixed lump superior to her right temporomandibular joint. She also notices a slight eversion of the right ear lobe.\n\nWhat is the most likely cause of this lump?",
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"explanation": "Ribbon gauze can be used in severe otitis externa if there is significant inflammation of the ear canal that prevents ear drops from passing into the canal. There is only mild inflammation in this case, making topical antibiotics a better first-line option",
"id": "32331",
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"explanation": "Acetic acid can be used in the very early stages of infection. In this case, the inflammation, discharge and pain favour using a combination antibiotic/steroid ear drop",
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"name": "2% acetic acid ear drops",
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"explanation": "Oral antibiotics are usually not used in otitis externa due to poor penetration of the skin that lines the external ear canal. However, if there is spread beyond this (i.e. to bone or face), then oral antibiotics should be considered",
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"explanation": "# Summary\n\nOtitis externa, a common cause of otalgia, usually presents with minimal discharge, itch and pain due to acute inflammation of the skin of the external auditory meatus. The most common causative organisms are Pseudomonas species and Staphylococcus aureus. The condition is managed based on its severity, with systemic antibiotics reserved for patients with fever or lymphadenitis. Topical drops may be used for mild to moderate cases, while severe cases may require the use of a ribbon gauze known as “Pope” wicks for the application of topical antibiotics.\n\n# Definition\n\nOtitis externa is an inflammatory condition affecting the skin of the external auditory meatus, often resulting in otalgia. It is characterised by minimal discharge, itchiness and pain.\n\n# Epidemiology\n\nOtitis externa is a common condition, frequently seen in primary care and ENT practices. \n\n# Aetiology\n\nThe most common causative organisms of otitis externa are Pseudomonas species and Staphylococcus aureus.\n\n# Signs and Symptoms\n\nPatients with otitis externa typically present with the following symptoms:\n\n- Otalgia (ear pain)\n- Minimal discharge\n- Itchiness\n- Pain due to inflammation\n- Impaired hearing if the meatus becomes blocked by swelling or discharge\n\n[lightgallery]\n\n# Differential Diagnosis\n\nThe differential diagnosis for otitis externa includes:\n\n- Otitis media: Characterised by middle ear pain, fever, hearing loss and sometimes discharge.\n- Furunculosis: Presents with localised pain, swelling and redness, and occasionally fever.\n- Eczema: Features include itching, redness, and scaling of the skin.\n\n# Investigations\n\nThe diagnosis of otitis externa is primarily clinical. However, microbiological cultures may be useful in refractory or severe cases to determine the causative organism and guide antibiotic treatment.\n\n# Management\n\nThe management of otitis externa depends on the severity:\n\n- Mild to Moderate Otitis Externa: Can be treated with topical drops including combined antibiotic/steroid drops (e.g. Gentamix), acetic acid and other preparations. Patients should be advised to keep the ear dry for the next 7-10 days.\n- Severe Otitis Externa: Treated using a strip of ribbon gauze known as “Pope” wicks which can be used for the application of topical antibiotics (classically gentamicin) enabling deeper penetration.\n- Indications to Consider Oral Antibiotics: Cellulitis extending beyond the external ear canal, when the ear canal is occluded by swelling and debris and a wick cannot be inserted, and in people with diabetes or compromised immunity with severe infection or high risk of severe infection.\n\n# References\n\n[Click here for NICE CKS on otitis externa](https://cks.nice.org.uk/topics/otitis-externa/)",
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"question": "A 19-year-old woman presents to her general practitioner (GP) with pain and discharge from her right ear. She reports the symptoms began two days ago after returning from a beach holiday in Spain.\n\nShe has no significant past medical history, and her observations are all normal.\n\nOn examination, there is tenderness on gentle movement of the right ear. Otoscopy reveals a mildly inflamed and erythematous ear canal with scant white discharge. The tympanic membrane remains intact.\n\nWhich of the following is the next best step in management?",
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"explanation": "Synchronised DC cardioversion is used in cases of SVT where there are adverse features (myocardial ischaemic, heart failure, syncope or shock) present.\n\nIn synchronised cardioversion, the electrical shock is delivered during ventricular depolarisation in the cardiac cycle. This is important to reduce the risk of the rhythm changing into a life-threatening cardiac arrest rhythm (e.g. VF)",
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"explanation": "Adenosine is contraindicated in poorly controlled asthmatics as it can cause bronchospasm. Therefore verapamil is often preferred in this cohort of patients who present with SVT if vagal manoeuvres fail",
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"explanation": "# Summary\n\nSupraventricular Tachycardia (SVT) is an umbrella term for several arrhythmias originating above the ventricles, including AV re-entry tachycardia and AV nodal re-entry tachycardia. Atrial fibrillation, atrial flutter and sinus tachycardias are all technically SVTs but are usually considered separately. Emergency treatment of SVT if the patient is stable involves vagal manoeuvres then administering adenosine if these are not successful. If the patient is unstable, cardioversion should be attempted with a synchronised DC shock.\n\n# Definition\n \nA Supraventricular Tachycardia (SVT) is any rhythm with a fast heart rate (over 100bpm) that originates from anywhere in the heart above the level of the Bundle of His. Unless there is aberrant conduction (e.g. bundle branch block), these will be narrow complex (i.e. QRS width is less than 120ms).\n \nSinus tachycardia, Atrial Fibrillation, Atrial Flutter, AV Re-entry Tachycardia (AVRT) and AV Nodal Re-entry Tachycardia (AVNRT) are examples of SVTs. Sinus tachycardia, Atrial Fibrillation and Atrial Flutter are considered separately and have different emergency management.\n \n[lightgallery]\n \n# Management \n\n**Unstable patients**\n \nPatients with any of the following adverse features should be treated with a synchronised DC shock, which can be repeated if unsuccessful:\n\n- Shock\n- Syncope\n- Heart Failure\n- Myocardial Ischaemia (usually presenting as chest pain)\n\nPatients who are conscious require sedation or anaesthesia prior to attempting cardioversion.\n\n**Stable patients**\n\nPatients with no adverse features should be treated initially with vagal manoeuvres, e.g. carotid sinus massage or the Valsalva manoeuvre (get the patient to blow into a 10ml syringe for 15-20 seconds)\n\nIf this fails, the next step is giving IV Adenosine 6mg, following this with 12mg then 18mg boluses if the previous one is unsuccessful. \n\nThis should be done with continuous ECG monitoring.\n\nIf adenosine fails to terminate the SVT, verapamil or a beta-blocker could be tried, with DC cardioversion also an option if medical treatment is unsuccessful.\n\n**Further information on Adenosine**\n \n- Adenosine is a medication that works by temporarily blocking conduction through the AV node\n- It is given as a rapid IV bolus over 1-3 seconds \n- Prior to administration, patients should be warned that they may experience difficulty breathing, chest tightness and flushing\n- Because of the risk of bronchospasm, patients with asthma should not be given adenosine (verapamil should be used instead)\n- In patients with a central line, a reduced dose of 3mg should be given\n\n# References\n\n[UK Resuscitation Council Adult Tachycardia Algorithm](https://www.resus.org.uk/sites/default/files/2021-04/Tachycardia%20Algorithm%202021.pdf)\n\n[BNF Treatment Summary - Arrhythmias](https://bnf.nice.org.uk/treatment-summaries/arrhythmias/#paroxysmal-supraventricular-tachycardia)",
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"question": "A 22-year-old patient with a background of asthma is admitted with a four-hour history of palpitations.\n\nHis heart rate is 180bpm, blood pressure 110/68mmHg, respiratory rate 18, SpO2 98% on air\n\nHis ECG shows a heart rate of 183 bpm and a regular narrow complex tachycardia. The admission chest x-ray is clear, and troponin levels are normal.\n\nWhich of the following is the next best step in management?",
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"explanation": "Antibiotics should be prescribed in cases that are likely to be due to infectious mastitis. These include the presence of a nipple fissure, symptoms not improving with continuous milk removal for 12-24 hours and a positive breast milk culture",
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"comment": "why wedge shape?",
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"comment": "Possibly trying to confuse us with another question about non lactational mastitis, in which they also have a wedge but needed co amoxiclav instead",
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"comment": "What is the significance of the wedge shaped erythema ?",
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"comment": "She's got a fever, how is this not infective mastitis?",
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"comment": "it doesnt say how long she has had symptoms for which is what guides treatment !!",
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"explanation": "# Summary\n \n\nMastitis is an inflammation of the breast, often associated with lactation in postpartum women, referred to as puerperal mastitis. Key signs and symptoms include localised pain, tenderness, redness and heat in the breast, along with systemic symptoms such as fever, rigours, myalgia, fatigue, nausea and headache. Diagnosis is primarily clinical. Ultrasound may be used if a breast abscess is suspected. Management strategies focus on reassurance about continued breastfeeding, advice on milk removal, analgesia, antibiotics, and in severe cases, surgical intervention.\n \n\n# Definition\n \n\nMastitis is the inflammation of the breast tissue, which can be with or without an infection. When associated with lactation in postpartum women, the condition is specified as puerperal mastitis. Alternatively, mastitis can be seen in women who are not breastfeeding.\n \n\n# Epidemiology\n \n\nNon-lactational mastitis is significantly less common than \n \n\n# Aetiology\n \nMastitis unrelated to pregnancy and breastfeeding is typically due to obstruction of the ducts from cellular debris. This can result in a local inflammatory response in non-infectious mastitis. \n\nIn infectious mastitis, bacteria from the skin can then enter the ducts, causing inflammation and may progress to peri-areolar abscesses. The most common causative pathogen is Staphylococcus aureus. \n\nRisk factors for non-lactational mastitis include:\n\n- Cigarette smoking\n- Nipple rings \n- Diabetes mellitus\n- Immunocompromise \n \n\n# Signs and Symptoms\n \n\nMastitis diagnosis is primarily clinical, based on characteristic local and systemic symptoms.\n \n\n - Localised symptoms: Painful, tender, red, and hot breast.\n - Systemic symptoms: Fever, rigours, myalgia, fatigue, nausea, and headache.\n - Additional information: The condition is usually unilateral and tends to present within the first week postpartum.\n \n\nIn some cases, mastitis may develop into a breast abscess, manifesting as a fluctuant, tender mass with overlying erythema.\n \n\n# Differential Diagnosis\n \n\nThe differential diagnosis for mastitis should include other conditions that also cause breast pain and inflammation:\n \n\n - **Breast abscess**: Fluctuant mass, tenderness, overlying erythema, systemic signs of infection.\n - **Inflammatory breast cancer**: Swelling, skin changes resembling orange peel, nipple inversion, axillary lymphadenopathy.\n - **Breast engorgement**: Typically bilateral and associated with milk stasis, painful, and tense breasts.\n \n\n# Investigations\n \n\nWhile the diagnosis of mastitis is primarily clinical, further investigations may be necessary in certain circumstances.\n \n\n - Ultrasound: Utilised to identify a potential abscess, appearing as a collection of pus.\n - Additional information: Early referral to secondary care is vital if an abscess is suspected.\n \n\n# Management\n \n\nManaging mastitis involves multiple strategies:\n \n\n - Provide analgesia to manage symptoms (i.e. paracetamol, ibuprofen)\n\t - Warm and cold compresses may also help.\n - Antibiotics may be considered if acute pain, severe symptoms or symptoms lasting more than 12-24 hours, fever or positive cultures \n\t - Flucloxacillin or clindamycin for those with penicillin allergy\n\t - Treatment is indicated for 10-14 days.\n - In cases where the condition does not improve, consider intravenous antibiotics (i.e. vancomycin) or ultrasound to evaluate for the presence of a breast abscess.\n - Patients may also benefit from antifungal therapy (i.e. nystatin) for concomitant nipple candidiasis \n\n \n# Complications\n \nComplications of mastitis include:\n \n - Breast abscess\n - Recurrence:\n\t - More common if treatment is delayed or too short in duration \n \n\n# NICE Guidelines\n \n[NICE CKS on mastitis and breast abscess](https://cks.nice.org.uk/topics/mastitis-breast-abscess/)\n\n# References\n\n[BMJ Best Practice Mastitis and Breast Abscess](https://bestpractice.bmj.com/topics/en-gb/1084)\n\n[Patient Info Benign Breast Diseas](https://bestpractice.bmj.com/topics/en-gb/1084) \n\n[NHS Mastitis](https://www.nhs.uk/conditions/mastitis/)",
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"question": "A 25-year-old woman presents to her GP with an 8 hour history of a red and swollen left breast. She is ten weeks post-partum and has been regularly breastfeeding with no complications.\n\nOn examination, she has a temperature of 37.6°C and an erythematous and tender left breast. The erythema is noted to extend in a wedge-shaped distribution.\n\nWhich of the following is the next best step in management?",
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"explanation": "A CT head would be indicated if a central cause of vertigo (e.g. stroke) was suspected. Signs of central vertigo on a HINTS exam are a negative head impulse test, bidirectional nystagmus and an abnormal test of skew. The fact he is young and has no cardiac risk factors makes the diagnosis of stroke less likely",
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"explanation": "There is no indication for treatment with antibiotics. Vestibular neuronitis is often a sequelae of a viral upper respiratory tract infection",
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"explanation": "The likely diagnosis is vestibular neuronitis. This is a peripheral cause of vertigo, and the findings described on the HINTS (head impulse, nystagmus and test of skew) examination are suggestive of this. Vestibular neuronitis is characterised by inflammation of the vestibular nerve, often after a viral infection. Common symptoms include acute, spontaneous vertigo, nausea, vomiting and unsteadiness. Prochlorperazine is often used for symptomatic treatment",
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"explanation": "Aspirin would be indicated if an ischaemic stroke was suspected as the cause of vertigo following exclusion of haemorrhage on a CT head",
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"explanation": "# Summary\n\nVertigo is a sensory misperception or illusion of motion, often characterised as rotatory dizziness. The sensation can arise from various conditions such as Benign Positional Paroxysmal Vertigo (BPPV), Acute Labyrinthitis, Ménière's Disease, Acoustic Neuroma, Ramsay Hunt Syndrome, and Ototoxicity. Key investigations include the Hallpike manoeuvre for BPPV and hearing evaluation for conditions such as Acute Labyrinthitis and Acoustic Neuroma. Management strategies differ across conditions, and can include repositioning manoeuvres, use of sedatives, and antiviral therapy.\n\n# Definition\n\nVertigo is a sensory phenomenon where an individual perceives a false sensation of movement or spinning. This perceived motion frequently gives the impression of a tilting or spinning environment.\n\n# Epidemiology\n\nVertigo is a common presenting symptom in medical practice. The prevalence of vertigo increases with age and is more common in women than in men. The most common cause of vertigo is BPPV, followed by Ménière's disease and vestibular migraine. \n\n# Signs & Symptoms\n\nThe following table from NICE can help differentiate between central and peripheral causes:\n\n| **Clinical features** | **Peripheral** | **Central** |\n|--------------------------------------|---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|\n| **Postural stability** | Can walk, although may be unstable and may not wish to mobilise. | Inability to stand up or walk even with the eyes open. |\n| **Hearing loss or tinnitus** | Possible with some causes (for example Meniere's disease, labyrinthitis). | Uncommon but may occur (for example stroke or intracranial tumour). |\n| **Other neurological symptoms** | No. | Usually (for example cranial nerve dysfunction, visual disturbance, speech defects, dysarthria, weakness, sensory changes, memory loss, and gait ataxia). However, not all people with vertigo due to a stroke will have focal neurological signs. |\n| **Nystagmus** | Horizontal nystagmus with a torsional component that does not alter in direction when the gaze changes. Beats away from the affected side. Disappears with fixation of the gaze. Large amplitude nystagmus is usually only seen early in the course of Meniere's disease or vestibular neuronitis. | Direction-changing nystagmus on lateral gaze (right beating on right gaze, left beating on left gaze). Purely vertical or torsional. Not suppressed by visual fixation. Non-fatiguable. Commonly large amplitude nystagmus. |\n| **Head impulse test** | May be positive with acute unilateral vestibular loss. | Negative, indicating a normal vestibulo-ocular reflex. |\n| **Dix-Hallpike manoeuvre** | In BPPV: latency of symptoms and nystagmus with fatiguability and habituation; severe vertigo. | Abnormal response (for example vertical nystagmus without latency or fatiguability; direction not classical horizontal towards the downward ear). |\n| **Alternate cover test** | Normal. | Slight vertical correction (up on one side, down on the other) suggestive of a central lesion such as stroke. |\n\n\n\n# Differential Diagnosis\n\nThe differential diagnosis for vertigo includes:\n\n- BPPV: Characterised by vertigo with positional change and fatiguable nystagmus.\n- Acute Labyrinthitis: Presents with severe, acute vertigo, associated with nausea and vomiting. Hearing loss and tinnitus may be present.\n- Stroke: Sudden onset vertigo, tends to present with other focal neurology, usually with cardiovascular risk factors\n- Ménière's Disease: Features recurrent episodes of vertigo, sensorineural hearing loss, tinnitus, and a feeling of fullness in the ear.\n- Acoustic Neuroma: Usually presents with unilateral hearing loss and cranial nerve dysfunction.\n- Ramsay Hunt Syndrome: Characterized by facial nerve palsy, which may be accompanied by vertigo, tinnitus, and hearing loss.\n- Ototoxicity: Presents with hearing loss or vertigo following exposure to ototoxic drugs.\n\nOther causes include systemic causes such as:\n\n- Orthostatic Hypotension\n- Cardiac Arrhythmias\n- Medications (e.g., aminoglycoside antibiotics and loop diuretics).\n\n\n\n# Investigations\n\n\n- Dix-Hallpike Manouvre\n\t- This test is crucial for diagnosing BPPV. \n\t- The patient is seated with their head turned 45 degrees to one side, and then quickly laid back so the head hangs slightly off the edge of the bed. \n\t- The test is positive if vertigo and nystagmus are elicited, indicating a peripheral cause like BPPV.\n\t- Nystagmus typically lasts a few seconds and fatigues with repeated testing.\n\nOther investigations may include:\n\n- Audiometry: For suspected cases of Ménière's Disease or Acoustic Neuroma.\n- Imaging (MRI/CT): To rule out central causes such as cerebrovascular disease or tumours.\n- Vestibular function tests: To further characterise and monitor vestibular dysfunction \n\n# Management\n\n\nStemetil (Prochlorperazine) is commonly used for symptomatic relief of vertigo, particularly in the acute setting.\n\nIn terms of specific conditions: \n\n- BPPV: Treated effectively with repositioning manoeuvres such as the Epley or Brandt-Doroff exercises, which aim to move the displaced otoliths back into the utricle.\n- Acute Labyrinthitis/Vestibular Neuritis: Managed with vestibular suppressants (e.g., antihistamines like cinnarizine or meclizine) and possibly corticosteroids.\n- Ménière's Disease: Managed with a combination of diuretics, low-sodium diet, and vestibular suppressants. Intratympanic steroid injections or surgery may be required in refractory cases.\n- Ramsay Hunt Syndrome: Treated with antiviral agents (e.g., acyclovir) and corticosteroids.\n\nFor patients with chronic vestibular disorders, vestibular rehabilitation can be considered. This nvolves exercises that aim to improve balance and reduce dizziness.",
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"question": "A 35-year-old man with presents to the Emergency Department with persistent dizziness since waking up four hours ago. He reports the room spinning around him and associated nausea but no vomiting.\n\nFull systems review is otherwise unremarkable; however, the patient does reveal having some mild coryzal symptoms a few days ago. On examination, there is a positive head impulse test, unidirectional nystagmus and no abnormal test of skew.\n\nGiven the likely diagnosis, which of the following is the most appropriate management?",
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"explanation": "This patient's symptoms and examination findings are suggestive of bacterial vaginosis (BV). It is the most common cause of abnormal vaginal discharge in women of child-bearing age and is characterised by an overgrowth of anaerobic organisms in the vagina. In addition, there is an associated increase in vaginal pH to above 4.5. In most women with characteristic signs and symptoms, empirical treatment should be started without further investigations",
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"name": "Oral metronidazole",
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"explanation": "Doxycycline is the first-line treatment for Chlamydia. The white discharge and absence of any other genito-urinary symptoms make BV the most likely diagnosis",
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"explanation": "IM ceftriaxone is the first-line treatment for uncomplicated anogenital gonorrhoea infections in the community. The white discharge and absence of any other genito-urinary symptoms make BV the most likely diagnosis.\nDoxycycline",
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"explanation": "If measured, vaginal pH would be greater than 4.5 in BV. However, testing is not required if the history and examination findings suggest the diagnosis in non-pregnant women at low risk of having a sexually transmitted infection (STI)",
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"label": "c",
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"explanation": "Microscopy of vaginal secretions may reveal \"clue cells\" in BV. However, testing is not required if the history and examination findings suggest the diagnosis in non-pregnant women at low risk of having a sexually transmitted infection (STI)",
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"comment": "The Amsel criteria are often used to diagnose bacterial vaginosis. Three out of the four following features are needed to confer a diagnosis:\nVaginal pH >4.5\nHomogenous grey or milky discharge\nPositive whiff test (addition of 10% potassium hydroxide produces a fishy odour)\nClue cells present on wet mount\n\nSurely we don't start Abx yet?",
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"explanation": "# Summary \n \n \nBacterial Vaginosis (BV) is an imbalance in the vaginal microbiome characterised by an overgrowth of anaerobic bacteria and a loss of lactobacilli, leading to symptoms such as increased vaginal discharge with a characteristic \"fishy\" odour. It is the most common cause of abnormal vaginal discharge in women of childbearing age. Diagnosis is based on the Amsel criteria, which include elevated vaginal pH, homogeneous discharge, positive whiff test, and presence of clue cells on wet mount. Treatment involves the use of metronidazole or clindamycin, either orally or intravaginally. Pregnancy can increase the risk of BV and associated complications, although it generally does not cause issues in the majority of pregnancies.\n \n \n# Definition\n \n \nBacterial vaginosis is a bacterial imbalance of the vagina caused by an overgrowth of anaerobic bacteria, such as Gardnerella vaginalis, and a loss of lactobacilli, the dominant bacterial species responsible for maintaining an acidic vaginal pH.\n \n \n# Epidemiology\n \n \nBacterial vaginosis is the most common cause of abnormal vaginal discharge in women of childbearing age, with prevalence rates as high as 50% in some populations. It is more common in sexually active women, but it is not considered a sexually transmitted infection.\n \n \n# Aetiology\n \n \nThe precise cause of bacterial vaginosis is unknown, but it is associated with a change in the balance of the normal bacteria found in the vagina. Factors that may contribute to this imbalance include:\n \n \n- Having multiple sexual partners or a new sexual partner\n- Douching\n- Lack of consistent condom use\n- Hormonal changes, such as those that occur in pregnancy\n \n \n# Signs and Symptoms\n \n \n- Increased vaginal discharge\n- Grey-white watery discharge\n- Characteristic \"fishy\" smelling discharge, particularly after intercourse\n- Vaginal itching or irritation may be present but is less common\n \n \n# Differential Diagnosis\n \n \nWhen considering bacterial vaginosis, several other conditions can present with similar symptoms and should therefore be considered:\n \n \n- **Vulvovaginal Candidiasis**: Characterised by itching, burning, dyspareunia, and white, curd-like discharge.\n- **Trichomonas Vaginalis Infection**: Presents with purulent, frothy, greenish discharge, pruritus, dyspareunia, and dysuria.\n- **Chlamydia or Gonorrhoea infection**: May present with increased vaginal discharge and possibly lower abdominal pain, but are often asymptomatic.\n- **Atrophic Vaginitis**: Most commonly seen in postmenopausal women, presenting with dryness, burning, dyspareunia, and thin, watery discharge.\n \n \n# Investigations\n \n \nThe **Amsel criteria** are often used to diagnose bacterial vaginosis. Three out of the four following features are needed to confer a diagnosis:\n \n \n- Vaginal pH >4.5\n- Homogenous grey or milky discharge\n- Positive whiff test (addition of 10% potassium hydroxide produces a fishy odour)\n- Clue cells present on wet mount\n \n \n# Management\n \n \nThe treatment of choice for bacterial vaginosis is usually either Metronidazole or Clindamycin, which can be administered orally or intravaginally. Sexual partners do not typically require treatment. Recurrence is common and may require repeated or prolonged treatment. Avoidance of common triggers such as smoking, vaginal douching and bubble baths can help to prevent recurrence.\n \n \n# Pregnancy \n \n \nPregnant women are at increased risk of bacterial vaginosis due to hormonal changes. BV during pregnancy can increase the risk for premature birth and low birth weight, but in most cases, it causes no problems. If symptomatic, it can be managed with metronidazole (PO/PV). Regular antenatal care should include screening for BV and other infections to minimise potential risks.\n \n# NICE guidelines\n \n[Click here to see information on NICE about bacterial vaginosis](https://cks.nice.org.uk/topics/bacterial-vaginosis/)\n \n# References\n \n[WHO: Bacterial vaginosis](https://www.who.int/news-room/fact-sheets/detail/bacterial-vaginosis#",
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"explanation": "The common bile duct is formed by the union of the cystic duct and common hepatic duct. The common bile duct in turn joins the pancreatic duct which is labelled to form the ampulla of Vater. The ampulla of Vater allows for pancreatic juices and bile (required for the breakdown of food) to enter the duodenum.",
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173,469,954 | false | 6 | null | 6,495,314 | null | false | [] | null | 20,452 | {
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}
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"explanation": "Anatomically, the liver is composed of four lobes: the right, left, caudate and quadrate lobes. The quadrate and caudate lobe are often termed accessory lobes. The quadrate lobe is the smallest of the four and is located on the inferior surface of the right lobe between the gallbladder and a fossa produced by the ligamentum teres.",
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{
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"explanation": "Anatomically, the liver is composed of four lobes: the right, left, caudate and quadrate lobes. Here the quadrate lobe is labelled. The left and right lobes are divided anteriorly by the falciform ligament. The left triangular lobe attaches the left lobe of the liver to the diaphragm.",
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"explanation": "Anatomically, the liver is composed of four lobes: the right, left, caudate and quadrate lobes. Here the quadrate lobe is labelled. The right lobe is the largest of all four lobes. The right lobe is attached to the diaphragm by the right triangular ligament.",
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"explanation": "Anatomically, the liver is composed of four lobes: the right, left, caudate and quadrate lobes. Here, the quadrate lobe is labelled.",
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"name": "Middle lobe",
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"explanation": "Anatomically, the liver is composed of four lobes: the right, left, caudate and quadrate lobes. The quadrate and caudate lobe are often termed accessory lobes. Here, the quadrate lobe is labelled. The caudate lobe is located on the upper aspect of the visceral surface, located between the IVC and a fossa produced by the ligamentum venosum.",
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173,469,958 | false | 10 | null | 6,495,314 | null | false | [] | null | 20,456 | {
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"explanation": "The renal impression is labelled. This is a deep impression located posterior to the colic impression. It is formed by the right kidney and adrenal gland. The stomach is located in the epigastrium, it leaves a gastric impression on the inferior surface of the *left* lobe of the liver.",
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"explanation": "The renal impression is labelled. This is a deep impression located posterior to the colic impression. It is formed by the right kidney and adrenal gland. The duodenum leaves a small impression on the liver, medial to the renal impression.",
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"explanation": "The renal impression is labelled. This is a deep impression located posterior to the colic impression. It is formed by the right kidney and adrenal gland. The spleen does not leave an impression of the liver.",
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"explanation": "The renal impression is labelled. This is a deep impression located posterior to the colic impression. It is formed by the right kidney and adrenal gland.",
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"label": "a",
"name": "Right kidney",
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"explanation": "The renal impression is labelled. This is a deep impression located posterior to the colic impression. It is formed by the right kidney and adrenal gland. The left kidney does not leave an impression on the liver.",
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"explanation": "The fimbriae are labelled. They are finger like projections that capture the ovum that is released by the ovary.",
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"explanation": "This describes the ampulla of the fallopian tube.",
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"explanation": "This is an action of the overall fallopian tube rather than the specific structure labelled.",
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"explanation": "This answer describes the infundibulum. The infundibulum is the beginning of the fallopian tube located near to the ovary. The fimbriae are attached to the infundibulum.",
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"name": "A funnel shaped opening near the ovary where fimbriae attach.",
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"explanation": "This describes the isthmus which is the portion of tube that connects the uterus to the fallopian tubes.",
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"name": "The narrowest section of the fallopian tube which connects the ampulla to the uterine cavity.",
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173,469,960 | false | 12 | null | 6,495,314 | null | false | [] | null | 20,458 | {
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"explanation": "This describes the ovarian ligament which attaches the ovary to the uterus.",
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"name": "Attaches to the ovary inferiorly and lateral side of the uterus",
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"explanation": "The suspensory ligament of the ovary attaches the ovary to the lateral abdominal wall.",
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"explanation": "This describes the broad ligament which is labelled. The broad ligament contains 3 main parts - the mesometrium, mesovarium and mesosalpinx and is a flat sheet of peritoneum which supports the female reproductive system.",
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"explanation": "The cardinal ligament is a major ligament of the uterus that provides support and extends from the cervix to the lateral pelvic walls. The uterine artery and veins run within the cardinal ligament.",
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"name": "Situated along the inferior border of the broad ligament. Contains the uterine artery and veins and provides attachment to lateral pelvic wall.",
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"explanation": "This describes the round ligament of uterus, which develops from the female gubernaculum. The round ligament of the uterus is a robe like band of connective tissue that supports the uterus and attaches to the lower abdominal wall.",
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"name": "Originates from the female gubernaculum",
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173,469,961 | false | 13 | null | 6,495,314 | null | false | [] | null | 20,459 | {
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"explanation": "The lesser omentum is a double layer of peritoneum that extends from the inferior surface of the liver to the lesser curvature of the stomach and the first part of the duodenum. The portion of the lesser omentum that runs between the liver and stomach is also termed the hepatogastric ligament.",
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"explanation": "The pyloric sphincter lies between the pylorus and the duodenum. It is composed of a ring of smooth muscle and controls the passage of food from the stomach into the duodenum. Sympathetic innervation is provided via the celiac ganglion.",
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"explanation": "The greater curvature of the stomach forms the lateral border of the stomach. It receives its arterial supply from the short gastric arteries and the right and left gastroepiploic arteries.",
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173,469,962 | false | 14 | null | 6,495,314 | null | false | [] | null | 20,460 | {
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"explanation": "This describes the duodenum. The duodenum adds additional digestive enzyme to the stomach contents to aid digestion. The label points to the pylorus of the stomach.",
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"name": "Further digestion of chyme and stomach contents",
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"explanation": "This describes the fundus of the stomach, which is located at the proximal stomach. The fundus lies superior and to the left of the cardia. The label points to the pylorus of the stomach at the most inferior end.",
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"explanation": "This describes the cardiac sphincter of the stomach at the superior portion of the stomach. The label points to the pylorus of the stomach which is located at the distal portion of the stomach.",
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"name": "Prevents stomach contents from passing back into the oesophagus",
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"explanation": "This describes the function of the oesophagus. The label points to the pylorus of the stomach.",
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"explanation": "This answer describes the femoral nerve. The pudendal nerve is labelled. The pudendal nerve arises from the anterior divisions of the spinal nerves S2-S4.",
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"explanation": "The greater omentum is labelled. The greater omentum is essentially an apron of folded peritoneum that extends from the greater curvature of the stomach to the transverse colon. The greater omentum plays an important role in the defence against pathogens and injury.",
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173,469,966 | false | 18 | null | 6,495,314 | null | false | [] | null | 20,465 | {
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"explanation": "Whilst this answer is technically correct, it is not the **most** correct answer. In both males and females, the urethra is innervated by the vesical plexus, which in turn originates from the inferior hypogastric plexus.",
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"explanation": "The puborectalis allows for tonic contraction of the anal canal which contributes to faecal continence.",
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"explanation": "The inferior facet is labelled. The inferior facet of a lumbar vertebra forms part of a facet joint by articulating with the superior facet of the vertebra below it. These facet joints allow for controlled movements such as flexion, extension, and limited lateral bending in the lumbar spine, while providing stability.",
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"label": "a",
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"explanation": "Intervertebral discs are cushion-like structures between the vertebrae of the spine. They act as shock absorbers, reducing the impact of movements such as walking, running, and lifting. Each disc has a tough outer layer (annulus fibrosus) and a gel-like centre (nucleus pulposus), allowing flexibility and even distribution of pressure across the spine.",
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Subsets and Splits