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"explanation": "Tramadol should only be considered in cases where acute relief is needed. Therefore, it would not be appropriate in this case at this time",
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"comment": "Give them the loud pack rt ",
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"explanation": "# Summary \n\nShingles is a reactivation of the varicella zoster virus which can lie dormant in nerve ganglia following primary infection (chickenpox). It commonly occurs in the elderly and shingles in young adults should prompt investigation for an underlying immune condition. Management normally includes oral antivirals, but intravenous antiviral medications can be used if severe or if the patient is immunocompromised.\n\n# Signs & Symptoms\n\nShingles can manifest first as a tingling feeling in a dermatomal distribution. Progresses to erythematous papules occurring along one or more dermatomes within a few days, which develop into fluid-filled vesicles which then crust over and heal. May be associated with viral symptoms e.g. fever, headache, malaise.\n\n[lightgallery]\n\n[lightgallery1]\n\n**Herpes zoster ophthalmicus (HZO)** presents with symptoms including a painful red eye, fever, malaise, and headache, followed by an erythematous vesicular rash over the trigeminal division of the ophthalmic nerve. A lesion on the nose, known as **Hutchinson's sign,** may suggest ocular involvement.\n\n\n\n# Management\n\n- Oral antiviral (e.g. valaciclovir 1g three times per day for 7 days) within 72h of rash onset if immunocompromised (and infection is not severe) or moderate/severe rash or moderate/severe pain, or non-truncal involvement.\n- Admit to hospital for IV antivirals if severe disease or immunocompromise, ophthalmic symptoms or suspicion of meningitis/encaphalitis/myelitis\n- Advise avoiding contact with pregnant women, babies and those who are immunocompromised until the lesions are fully crusted over, as transmission can occur via skin contact\n- Pain can be managed with NSAIDs (e.g. ibuprofen). If unsuccessful, consider offering amitriptyline (off-label use), duloxetine (off-label use), gabapentin, or pregabalin\n\n# Shingles vaccine\n\nThere is a one-off vaccine available for shingles that is typically advised for those in their 70s.\n\n# Complications\n\n- Secondary bacterial infection of skin lesions\n- Corneal ulcers, scarring and blindness if eye involved\n- Post-herpetic neuralgia\n - Pain occurring at site of healed shingles infection\n - Can cause neuropathic type pain (burning, pins and needles)\n - Can cause allodynia (perception of pain from a normally non-painful stimulus e.g. light touch)\n\n# NICE Guidelines\n\n[NICE Clinical Knowledge Summary (CKS): Shingles](https://cks.nice.org.uk/topics/shingles/)\n\n[NICE Treatment Summary: Varicella-zoster vaccine](https://bnf.nice.org.uk/treatment-summary/varicella-zoster-vaccine-2.html)",
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"question": "A 57-year-old woman attends GP due to moderate pain. The pain is localised over the same area of skin where she had shingles three months ago. She now experiences pain whenever that area becomes cold or whenever it is touched lightly.\n\nThe GP diagnoses post-herpetic neuralgia and advises the patient to wear cotton clothes over the affected area; to wrap the area in clingfilm, and advised her how to improve her sleep.\n\nWhat pharmacological treatment could also be considered in the first instance?",
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"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",
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"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",
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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",
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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",
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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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"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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"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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"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",
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"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",
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"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)",
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"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",
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"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",
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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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"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",
"id": "32823",
"label": "a",
"name": "Ménière's disease",
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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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"label": "e",
"name": "Otitis media",
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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",
"id": "32825",
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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",
"id": "32826",
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"name": "Labyrinthitis",
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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",
"id": "32824",
"label": "b",
"name": "Benign paroxysmal positional vertigo (BPPV)",
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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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"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",
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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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"label": "d",
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"id": "32829",
"label": "b",
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"votes": 546
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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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"picture": null,
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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",
"picture": null,
"votes": 161
}
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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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"answer": false,
"explanation": "There is no evidence to support the use of antihistamines in acute otitis media",
"id": "32836",
"label": "d",
"name": "Regular analgesia and an antihistamine",
"picture": null,
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"__typename": "QuestionChoice",
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"explanation": "Antibiotics are advised for those who are suspected to have acute otitis media and a systemic infection. Also, those with otorrhoea or those aged less than 2 with a bilateral infection may benefit from a short course of antibiotics, usually amoxicillin. Acute otitis media will normally improve within 3 days without the need for antibiotic treatment so they should not be used in this case",
"id": "32837",
"label": "e",
"name": "Regular analgesia and a short course of antibiotics",
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"__typename": "QuestionChoice",
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"id": "32833",
"label": "a",
"name": "Regular analgesia",
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},
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"answer": false,
"explanation": "There is no evidence to support the use of decongestants or antihistamines in acute otitis media",
"id": "32835",
"label": "c",
"name": "Regular analgesia, a decongestant and an antihistamine",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "There is no evidence to support the use of decongestants in acute otitis media",
"id": "32834",
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"comment": "@Quesmed some general obs results would be nice as we don't want to just assume patients are otherwise systemically well",
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"comment": "weird hangup to have\n",
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"explanation": "# Summary\n\nOtitis media is inflammation of the middle ear often resulting from an infection. Key signs and symptoms include rapid-onset pain, fever, irritability, anorexia, vomiting, and impaired hearing. Diagnosis is based on history and physical examination, notably the appearance of the tympanic membrane. Management mainly consists of treating pain and fever. Antibiotics are reserved for children who are systemically unwell or at high risk of complications. Complications, although rare, can be life-threatening and include both intracranial and extracranial complications.\n\n# Definition\n\nOtitis media is an infection-induced inflammation of the middle ear, frequently occurring after a viral upper respiratory tract infection.\n\n# Epidemiology\n\nOtitis media is a common condition, predominantly affecting young children. \n\n# Aetiology\n\nThe primary cause of otitis media is bacterial infection, particularly common in young children, often following a viral upper respiratory tract infection. \n\n# Signs and Symptoms\n\nAcute otitis media is characterised by:\n\n- Rapid onset of deep-seated ear pain\n- Fever\n- Irritability\n- Anorexia\n- Vomiting\n- Impaired hearing\n- Systemic illness\n- Aural fullness followed by discharge when the tympanic membrane perforates, leading to relief of pain\n- Injection of blood vessels and diffuse erythema of the tympanic membrane\n\n[lightgallery1]\n\nChronic otitis media can present as:\n\n- Benign chronic otitis media: a dry tympanic membrane perforation without chronic infection\n- Chronic secretory otitis media or \"glue ear\": persistent pain lasting weeks after the initial episode with an abnormal-looking drum and reduced membrane mobility\n- Chronic suppurative otitis media: persistent purulent drainage through the perforated tympanic membrane\n\n[lightgallery]\n\n# Differential Diagnosis\n\nThe main differentials for otitis media include:\n\n- Otitis externa: characterised by pain exacerbated by tugging of the auricle, accompanied by otorrhoea and possible hearing loss\n- Mastoiditis: presenting with postauricular pain, erythema, and swelling, as well as protrusion of the ear\n- Temporomandibular joint disorder: characterized by jaw pain, difficulty in opening the mouth, and clicking or popping sounds during jaw movement\n\n# Investigations\n\nDiagnosis of otitis media is primarily clinical, based on history and physical examination, notably the appearance of the tympanic membrane.\n\nIf however there are concerns of **mastoiditis**, such as if there is continued systemic upset despite antibiotic treatment, a CT head should be arranged in the first instance. Mastoiditis is primarily managed with IV antibiotics although surgical intervention is sometimes needed.\n\n# Management\n\nIn managing otitis media:\n \n- Admit any children under 3 months with a temperature of 38 degrees Celsius or more, or children with suspected acute complications of otitis media such as meningitis, mastoiditis, or facial nerve palsy.\n- Consider admitting any children who are very systemically unwell.\n- Otherwise, treat pain and fever with paracetamol or ibuprofen.\n- Most children will not require antibiotics. A delayed antibiotic prescribing strategy can also be appropriate. This involves asking patients/parents to start taking antibiotics if symptoms don't improve within four days.\n- Offer an immediate antibiotic prescription to children who are systemically unwell (but don't require admission) or those at high risk of complications (e.g., immunocompromised patients).\n\n# Complications\n\nComplications of otitis media can be divided into intracranial and extra-cranial complications. They are potentially life-threatening and require immediate assessment and treatment.\n\nExtra-cranial complications include:\n\n- Facial nerve palsy\n- Mastoiditis\n- Petrositis\n- Labrynthtitis\n\nIntra-cranial complications include:\n\n- Meningitis\n- Sigmoid sinus thrombosis\n- Brain abscess\n\n# References\n\n[Click here for NICE CKS on otitis media - acute](https://cks.nice.org.uk/topics/otitis-media-acute/)",
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"question": "A 16-year-old woman attends her GP due to otalgia in her right ear. She has had the pain for the last 2 days. On otoscopic examination the GP identifies a cloudy and slightly bulging tympanic membrane.\n\nWhat is the correct management?",
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"comment": "how did people even know it was SIADH ?",
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"comment": "SIAD always presents with euvolemic hyponatraemia",
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"comment": "From the high urine sodium and osmolality we can tell that his urine is very concentrated, which is what ADH does. This would also be seen in dehydration, as the body is trying to hold on to water by releasing ADH, but in this case he is euvolaemic, so he is inappropriately concentrating his urine due to SIADH.",
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"explanation": "# Summary\n\nSyndrome of Inappropriate ADH secretion (SIADH) refers to excessive antidiuretic hormone (ADH) release, causing water to be retained resulting in a euvolemic hyponatraemia. There are a wide range of causes including medications, malignancy, central nervous system (CNS) disorders and infections. Patients may be asymptomatic and detected through an incidental finding of a low serum sodium, or may present with features of severe hyponatraemia (e.g. confusion, seizures) and/or the underlying cause of SIADH. Key investigations include U&Es for sodium, cortisol and thyroid function to rule out other causes of hyponatraemia and urinary sodium and osmolality (which will be greater than 30 mmol/L and 100 mOsm/kg respectively). First-line management is with fluid restriction to 500-1000 ml/day, as well as treating the underlying cause (e.g. stopping causative medications). Severe cases may require hypertonic saline, and resistant cases may be treated with tolvaptan (an vasopressin V2-receptor antagonist).\n\n# Definition\n\nSyndrome of Inappropriate ADH secretion (SIADH) is an important cause of hyponatraemia that occurs when there is inappropriate release of antidiuretic hormone (ADH) outside of normal homeostatic mechanisms, which leads to reduced urine output. The increase in total body water effectively dilutes serum sodium, leading to hyponatraemia. \n\nNormally, ADH (also referred to as vasopressin) is produced in the hypothalamus and released from the posterior pituitary when serum osmolality is high. It acts to normalise osmolality by acting on the distal convoluted tubules and collecting ducts of the kidney to stimulate increased water reabsorption. \n\nSIADH may involve excessive release of ADH from the pituitary gland or production of ADH by an abnormal non-pituitary source (e.g. a tumour).\n\n# Aetiology\n\nSIADH has a wide range of causes - these are some examples:\n\n- Pulmonary causes:\n\t- Pneumonia\n\t- Chronic Obstructive Pulmonary Disease (COPD)\n\t- Tuberculosis (TB)\n- Central Nervous System (CNS) disorders:\n\t- Meningitis\n\t- Stroke\n\t- Subarachnoid haemorrhage\n\t- Traumatic brain injury\n\t- Psychosis\n- Malignancies:\n\t- Small cell lung cancer\n\t- Pancreatic cancer\n\t- Lymphoma\n\t- Mesothelioma\n\t- Thymoma\n\t- Nasopharyngeal cancer\n- Medications:\n\t- Carbamazepine\n\t- Selective Serotonin Reuptake Inhibitors (SSRIs)\n\t- Opiates\n\t- Anti-psychotics\n\t- Cyclophosphamide\n- Other: \n\t- HIV\n\t- Surgery\n\t- Acute intermittent porphyria\n\t- Idiopathic\n\n# Signs and Symptoms\n\nSIADH presents with a euvolaemic hyponatraemia, and so patients may be asymptomatic or present with features of the underlying cause (e.g. pneumonia).\n\nSigns and symptoms of hyponatraemia are more likely to develop in severe cases and where sodium has fallen rapidly:\n\n- Lethargy\n- Anorexia\n- Headache\n- Nausea and vomiting\n- Muscle cramps\n- Drowsiness\n- Confusion\n- Seizures\n\n# Differential Diagnosis\n\nSee the Hyponatraemia chapter for a full list of differentials - other causes of a euvolaemic hyponatraemia include:\n\n- **Beer potomania** is a cause of hyponatraemia in the context of alcohol excess combined with low solute intake due to a poor diet\n- **Primary polydipsia** occurs when people drink excessive amounts of water, leading to polyuria with dilute urine (as opposed to the smaller volume of concentrated urine seen in SIADH)\n- **Hypothyroidism** may cause hyponatraemia in severe cases; patients will usually have other symptoms such as fatigue, cold intolerance and constipation\n- **Adrenal insufficiency** causes hyponatraemia with hyperkalaemia; other features include hypotension, abdominal pain and weakness\n- **Exercise-induced hyponatraemia** occurs during or in the 24 hours following prolonged exercise (e.g. running a marathon), usually due to excess intake of hypotonic fluids\n- **Hypotonic intravenous fluids** such as 5% dextrose or 0.45% saline may lead to iatrogenic hyponatraemia\n\n# Investigations\n\n**Bedside:**\n\n- **Venous blood gas** to confirm hyponatraemia - if there is a significant discrepancy between the sodium on the gas and the U&Es, suspect pseudohyponatremia (see Hyponatraemia chapter for details) \n- **Urine osmolality** will be high (> 100 mOsm/kg)\n- **Urine sodium** will be high (> 30 mmol/L)\n- NB urine osmolality and sodium cannot be interpreted in patients taking diuretics and so these need to be stopped prior to investigations\n\n**Blood tests:**\n\n- **U&Es** to confirm hyponatraemia; urea will also likely be low due to dilution\n- **Serum osmolality** will be low (< 280 mOsm/kg)\n- **Thyroid function tests** to exclude hypothyroidism as a cause of hyponatraemia\n- **9am serum cortisol** to exclude adrenal insufficiency as a cause of hyponatraemia\n\n**Imaging:**\n\n- **Chest X-ray** if there is no obvious cause of SIADH as an initial screen for malignancy and pulmonary disease (e.g. tuberculosis, pneumonia)\n- **CT chest, abdomen and pelvis** and **MRI head** may be considered to exclude occult malignancy if there is no identified cause\n\n# Management\n\n**Conservative:**\n\n- Identify and treat the underlying cause (e.g. stopping causative medications where possible)\n- Patients with suspected SIADH in primary care should be referred to endocrinology to confirm the diagnosis and advise on treatment\n- Closely monitor sodium levels and ensure these are corrected no faster than 8-10 mmol/L per 24 hours \n- Fluid restriction is the first-line management in most cases, usually to 500-1000 ml/day \n\n**Medical:**\n\n- Severe hyponatraemia should be treated with hypertonic saline, usually in the intensive care setting\n- In some cases (e.g. SIADH resistant to fluid restriction), tolvaptan may be considered - this is a vasopressin V2-receptor antagonist\n\n# Complications\n\n- **Cerebral oedema** may complicate severe and/or acute hyponatraemia and may be life-threatening - patients develop raised intracranial pressure with symptoms of vomiting, headache, seizures and coma\n- **Central pontine myelinolysis** is a complication of rapid correction of hyponatraemia - patients may present with confusion, ataxia, spastic quadriparesis and pseudobulbar palsy with dysphagia and dysarthria\n- Chronic hyponatraemia, especially in the elderly, increases the risk of **falls** as well as **cognitive impairment**\n\n# NICE Guidelines\n\n[NICE CKS - Hyponatraemia](https://cks.nice.org.uk/topics/hyponatraemia/)\n\n# References\n\n[Life in the Fast Lane - Hyponatraemia](https://litfl.com/hyponatraemia/)\n\n[Life in the Fast Lane - SIADH](https://litfl.com/siadh-syndrome-of-inappropriate-adh-secretion/)\n\n[Whittington Hospital Hyponatraemia Guideline](https://www.whittington.nhs.uk/document.ashx?id=6089)",
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"question": "A 79-year-old male was admitted to hospital with nausea and increased tiredness. His investigation results are as follows:\n\n\n||||\n|---------------------------|:-------:|--------------------|\n|Sodium|125 mmol/L|135 - 145|\n|Potassium|3.9 mmol/L|3.5 - 5.3|\n|Urea|5.6 mmol/L|2.5 - 7.8|\n|Creatinine|64 µmol/L|60 - 120|\n|Urinary Sodium (random)|60 mmol|20|\n|Urine Osmolality|145 mOsmol/kg|50 - 1200|\n\n\nThe patient is euvolaemic.\n\n\nWhich of the following is the next best step in the management of this patient?",
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"explanation": "# Summary\n\nAnaphylaxis is a medical emergency which often occurs due to a type 1 IgE mediated hypersensitivity reaction to an allergen. It is characterised by the rapid onset of life-threatening airway swelling, bronchospasm and/or circulatory dysfunction. In most cases skin or mucosal changes are also present. Triggers include medications (such as penicillins), foods (such as peanuts) and insect stings. Diagnosis is clinical, with repeated mast cell tryptase levels a useful way to confirm the diagnosis in retrospect. Management strategies include removing the trigger, ABCDE assessment, oxygen administration, and adrenaline administration, amongst other interventions. \n \n# Definition\n \nAnaphylaxis is a rapid onset syndrome of life-threatening airway, breathing or circulatory dysfunction. An immunological reaction occurs when patients are exposed to allergens such as medications, foods (such as peanuts or eggs) and bee or other insect stings. Many cases of anaphylaxis however are idiopathic with no known trigger, or may be mediated by other mechanisms other than the classical type 1 IgE-mediated pathway. \n\n# Epidemiology\n \nApproximately 1 in 1333 people in England have had an episode of anaphylaxis. There are approximately 20-30 deaths per year in the UK, with around half of these being iatrogenic (e.g. due to penicillin).\n \n\n# Aetiology\n \nCommon precipitants of IgE-mediated allergic anaphylaxis include:\n\n- Insect stings\n- Nuts\n- Other foods such as eggs or milk\n- Latex\n- Antibiotics (e.g. penicillins)\n- Intravenous contrast agents\n- Other medications (such as NSAIDs)\n \n\n# Signs and Symptoms\n\nSigns and symptoms are sudden in onset and progress rapidly. To be classed as anaphylaxis, patients need to have life-threatening problems affecting the:\n\n- **Airway** (pharyngeal or laryngeal oedema)\n - Symptoms include difficulty swallowing and breathing, feeling that the throat is closing\n - Signs include stridor, hoarse voice and swelling of the tongue and lips\n- **Breathing** (bronchospasm)\n - Symptoms include difficulty breathing, wheeze and cough\n - Signs include increased work of breathing and respiratory distress, hypoxaemia may cause confusion and cyanosis\n - Patients may fatigue leading to respiratory arrest\n- **Circulation** (anaphylactic shock)\n - Symptoms include dizziness\n - Signs include pallor, clamminess, tachycardia and hypotension\n - Patients may develop arrhythmias and anaphylaxis can lead to cardiac arrest\n\nContinuing with an A to E approach, the following signs and symptoms are often also seen:\n\n- **Disability** (altered neurological state)\n - Symptoms include anxiety and a \"sense of impending doom\"\n - Signs include confusion, agitation and loss of consciousness\n- **Exposure** (skin and mucosal changes)\n - These range from mild erythematous patches to florid generalised rashes\n - Often occur prior to the onset of other symptoms\n - Urticaria (hives) are itchy and can occur anywhere on the skin\n - Angioedema involves swelling of the eyelids and lips (as well as the tongue and throat causing airway obstruction)\n\n**Gastrointestinal** manifestations including abdominal pain, incontinence and vomiting are also commonly seen in cases of anaphylaxis.\n \n[lightgallery]\n\n# Differential Diagnosis\n\n- **Life-threatening asthma exacerbation** \n - Several overlapping features e.g. bronchospasm, tachycardia, reduced levels of consciousness\n - May cause raised mast cell tryptase also \n - Triggers can be similar to anaphylaxis triggers\n - Would not have features of upper airway obstruction e.g. stridor or mucosal/skin changes e.g. urticaria\n- **Other causes of angioedema** \n - e.g. hereditary angioedema, induced by medications e.g. ACE inhibitors\n - Both involve histamine and/or bradykinin mediators\n - No circulatory dysfunction and shock unlike in anaphylaxis\n- **Panic attack** \n - May have tachycardia and tachypnoea accompanied by anxiety and feelings of doom, skin flushing may also occur\n - No signs of airway obstruction or circulatory collapse and symptoms often resolve with reassurance\n- **Vasovagal episode** \n - May occur after triggers e.g. vaccination\n - Mimic features of pallor and loss of consciousness\n - No airway or breathing symptoms unlike in anaphylaxis\n \n# Investigations\n \nAnaphylaxis should be diagnosed clinically based on the above features.\n\nThe following investigations should be carried out in the emergency setting:\n\n- **ECG** - to look for myocardial ischaemia and arrhythmias which may be caused by anaphylaxis\n- **Arterial blood gas** should be considered in hypoxic patients, may show metabolic acidosis due to shock\n- **Bloods for mast cell tryptase** - the first sample should be taken as soon as possible after starting emergency treatment, with a second sample taken within 1 to 2 hours (no later than 4 hours from symptom onset) and a third sample taken after complete recovery (as a baseline)\n\nAn elevated serum tryptase from baseline is a useful confirmatory test for anaphylaxis especially where there is diagnostic uncertainty, although a normal level does not exclude anaphylaxis. \n \n\n# Management\n\n**Emergency management:**\n \n- Early recognition is key - call for help (put out a medical emergency call if in hospital)\n- Remove any ongoing trigger e.g. stop causative medication, remove insect stinger\n- Lie patient flat and elevate legs if hypotensive, or help to a seated position to aid breathing\n- Give intramuscular adrenaline - 0.5ml of 1:1000 (500mcg) in adults, usually into the anterolateral thigh\n- Secure the airway\n- Administer high flow oxygen and ensure monitoring in place (oxygen saturations, blood pressure and ECG)\n- Consider inhaled bronchodilators (salbutamol or ipratropium) for wheeze\n- Give an IV fluid bolus in patients with hypotension or shock, or who do not respond to the initial adrenaline dose\n- IM adrenaline can be repeated after 5 minutes if no response\n- In the case of a cardiac arrest, start CPR and give further adrenaline via the IV or IO route (as intramuscular administration is unreliable in this scenario)\n\n**Once stabilised:**\n\n- Give an non-sedating oral antihistamine (e.g. 10-20mg cetirizine) - if not able to swallow can give IV or IM chlorphenamine \n - This helps to treat cutaneous symptoms of anaphylaxis but is not a first-line treatment as they do not treat life-threatening features\n- Steroids are no longer routinely advised but may be considered in patients with an asthma exacerbation/anaphylaxis overlap or in cases of ongoing shock\n- Observe patients for a **biphasic reaction** (when symptoms of anaphylaxis reoccur without further exposure to a trigger)\n - This occurs in around 5% of patients\n - Patients with severe initial presentations, those who require multiple adrenaline doses or who had a delay in treatment are at increased risk\n - Patients should be risk stratified - those at the lowest risk can be discharged after 2 hours of observation, those at intermediate risk should be observed for at least 6 hours and those at the highest risk for at least 12 hours\n- Prior to discharge, patients and families should be educated about anaphylaxis, what actions to take and the risk of a biphasic reaction\n - Give two adrenaline auto-injectors (e.g. an EpiPen) and demonstrate how to use these\n - Advise on trigger avoidance\n- Refer for follow up in a specialist allergy service\n\n# NICE Guidelines\n\n[NICE - Anaphylaxis: assessment and referral after emergency treatment](Anaphylaxis: assessment and referral after emergency treatment)\n\n[NICE CKS - Angio-oedema and Anaphylaxis](https://cks.nice.org.uk/topics/angio-oedema-anaphylaxis/)\n\n# References\n \n[UK Resuscitation Council Anaphylaxis Guidelines](https://www.resus.org.uk/library/additional-guidance/guidance-anaphylaxis/emergency-treatment)",
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"question": "A 44-year-old female attends A&E after developing sudden onset breathing difficulties. Her lips are swollen and she has developed a widespread pruritic rash.\n\nWhich is the correct prescription?",
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"explanation": "This is the correct total score, but incorrect in the constituent parts. The patient's eyes only open to pain, therefore, this scores a 2. She is able to articulate words, rather than mumbling so scores at least a 3. However, because she is not able to form sentences, confused or otherwise, she only scores a 3. Motor of 2 would be decerebrate rather than decorticate. Decorticate means abnormal flexion in response to pain, which is therefore, a 3. Decerebrate means abnormal extension in response to pain and would therefore, score a 2",
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"explanation": "This is the correct answer. The patient's eyes only open to pain, therefore, this scores a 2. She is able to articulate words, rather than mumbling so scores at least a 3. However, because she is not able to form sentences, confused or otherwise, she only scores a 3. Decorticate means abnormal flexion in response to pain, which is therefore, a 3",
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"explanation": "This is incorrect. The patient's eyes only open to pain, therefore, this scores a 2. She is able to articulate single words only and therefore, scores a 3 for verbal. Motor of 2 would be decerebrate rather than decorticate. Decorticate means abnormal flexion in response to pain, which is therefore, a 3. Decerebrate means abnormal extension in response to pain and would therefore, score a 2",
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"explanation": "This is incorrect. The patient's eyes only open to pain, therefore, this scores a 2. She is able to articulate words, rather than mumbling so scores at least a 3. However, because she is not able to form sentences, confused or otherwise, she only scores a 3. Decorticate means abnormal flexion in response to pain, which is therefore, a 3",
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"explanation": "This is incorrect. The patient's eyes only open to pain, therefore, this scores a 2. She is able to articulate words, rather than mumbling so scores at least a 3. However, because she is not able to form sentences, confused or otherwise, she only scores a 3. Motor of 2 would be decerebrate rather than decorticate. Decorticate means abnormal flexion in response to pain, which is therefore, a 3. Decerebrate means abnormal extension in response to pain and would therefore, score a 2",
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"comment": "A bit unfair to those of us who didn't know what decorticate meant",
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"comment": "Easy to mix up decorticate and decerebrate at the best of times ",
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"comment": "decErebrate = Extension :) ",
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"comment": "please just say abnormal flexion...",
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"comment": "even taking english lit at a-level didnt prepare me for tht word",
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"explanation": "# Summary\n\nThe Glasgow Coma Scale (GCS) is a universal score used to standardise assessment of a patient's level of consciousness. The maximum score (normal level of consciousness) is 15 and the minimum score is 3 (comatose or dead patients). There are three components to the score: eye opening, verbal response and motor response. The score is presented as each of the three components and the total score, for example GCS 15 (E4 M6 V5). There are a wide variety of causes for a decreased GCS, and investigations should be targeted based on the clinical presentation e.g. a CT head in suspected head injury. Management again depends on the underlying cause, but supportive measures may be required, most importantly airway protection for patients with a GCS of 8 or below.\n\n# Definition\n \nThe Glasgow Coma Scale (GCS) is a standardised way of assessing and communicating a patient's level of consciousness. Scores range from 3 (a comatose or dead patient who is unresponsive) to 15 (an oriented and fully conscious patient). \n \n# Classification\n\nGCS is calculated as follows:\n\n**Eye Opening Response:**\n\n4 - Spontaneous\n \n3 - To speech\n\n2 - To pain\n\n1 - No response\n \n \n**Verbal Response:**\n\n5 - Oriented\n\n4 - Confused\n\n3 - Inappropriate speech \n\n2 - Incomprehensible speech or sounds\n\n1 - No response\n \n**Motor Response:**\n\n6 - Obeys commands\n\n5 - Localises pain\n\n4 - Withdraws from painful stimulus\n \n3 - Abnormal flexion to pain (decorticate posture)\n \n2 - Abnormal extension to pain (decerebrate posture)\n \n1 - No response\n \n**Note -** Appropriate painful stimuli are:\n\n- Applying pressure to a fingertip\n- Trapezius squeeze\n- Supraorbital pressure\n\n# Differential Diagnosis\n\nCauses of a reduced GCS include:\n\n- **Cerebral causes:** head injury, intracranial bleeding, space-occupying lesions, epilepsy\n- **Respiratory causes:** hypoxia, hypercapnia, carbon monoxide poisoning\n- **Cardiac causes:** arrhythmias, shock (leading to inadequate cerebral perfusion)\n- **Toxic causes:** medications, illicit drugs, alcohol intoxication, overdoses\n- **Metabolic causes:** hypo or hyperglycaemia, uraemia, hepatic encephalopathy\n- **Infective causes:** encephalitis, sepsis, meningitis, cerebral malaria\n\n# Investigations\n\nOne key consideration is what the patient's baseline GCS is - for example in a patient with dementia a normal GCS for them may be 14 due to confusion.\n\nAn A to E approach should be taken in most cases (especially if GCS is significantly reduced) and investigations targeted to suspected underlying causes.\n\nCommon investigations include:\n\n**Bedside tests:**\n\n- **Capillary blood glucose** for hypo or hyperglycaemia\n- **Arterial blood gas** looking for hypoxia, hypercapnia and metabolic disturbances\n- **Urinalysis** e.g. in suspected infection (urinary tract infections are a common cause of confusion)\n- **ECG** for arrhythmia\n\n**Blood tests:**\n\n- **FBC** and **CRP** for inflammatory markers\n- **U&Es** for uraemia and electrolyte imbalance\n- **Bone profile** for hypercalcaemia\n- **LFTs** for liver dysfunction that may precipitate hepatic encephalopathy\n- **Ammonia** if hepatic encephalopathy is suspected\n- **Blood cultures** if infection is suspected\n\n**Imaging:**\n\n- **Chest X-ray** as part of a septic screen if infection is suspected\n- **CT head** or other intracranial imaging if the cause of reduced GCS is unclear or an intracranial cause is suspected\n\n**Special tests:**\n\n- **Lumbar puncture** e.g. in suspected meningitis or subarachnoid haemorrhage\n- **EEG** in suspected encephalitis or non-convulsive status epilepticus\n\n# Management\n \nManagement involves treating the cause of reduced GCS, e.g. giving dextrose in hypoglycaemia, giving naloxone in opiate overdose.\n\nThe patient's medications should be reviewed and contributing medications may need to be held (e.g. opiates).\n\nSupportive management is also important especially if the cause is not immediately treatable - the priority is airway protection.\n\nPatients with a GCS of 8 or below are generally thought to require airway protection (e.g. intubation and ventilation) - immediate assistance from anaesthetics should be sought.\n \n# References\n\n[MDCalc - GCS Calculator](https://www.mdcalc.com/calc/64/glasgow-coma-scale-score-gcs)\n\n[Student BMJ - GCS explained](https://www.bmj.com/content/365/bmj.l1296)\n\n[Life in the Fast Lane - GCS](https://litfl.com/glasgow-coma-scale-gcs/)\n\n[Life in the Fast Lane - Examination of the Unconscious Patient](https://litfl.com/examination-of-the-unconscious-patient/)",
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"question": "A 56-year-old woman is brought in to A&E after a motorcycle accident. On examination her eyes open after administering a trapezius squeeze; she is able to say words but no clear sentences; her movement is described a \"decorticate\".\n\nWhat is her Glasgow Coma Scale score?",
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"explanation": "CSF examination in Mycobacterium Tuberculosis will most likely have a cloudy appearance; elevated protein; low glucose; white cell count of roughly 20 cells/ mL; and an elevated opening pressure. However, it will lead to a negative India ink stain",
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"explanation": "Streptococcus pneumonia and Neisseria meningitidis are the two most common causes of meningitis in children and adults. They are both bacterial infections, so will typically show on CSF a cloudy appearance; elevated protein; low glucose; white cell count above 200 cells/mL mostly made up of neutrophils; and an elevated opening pressure. They will lead to a negative India ink stain",
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"explanation": "This is a typical fungal meningitis. Fungal meningitis is most common in immunosuppressed patients, particularly patients who are HIV positive. India ink staining is used to detect cryptococcal fungi, which are most associated with HIV patients",
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"explanation": "Neisseria meningitidis and streptococcus pneumonia are the two most common causes of meningitis in children and adults. They are both bacterial infections, so will typically show a cloudy CSF appearance, with elevated protein, low glucose, a white cell count above 200 cells/mL mostly made up of neutrophils, and an elevated opening pressure. They will lead to a negative India ink stain",
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"explanation": "Viral meningitis tends to be milder clinically. On CSF examination, a viral infection typically produces CSF with a clear appearance; normal or mildly elevated protein; normal glucose; a raised white cell count up to 200 cells/mL with predominantly lymphocytes; and a slightly elevated opening pressure. Viral meningitis will lead to a negative India ink stain",
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"explanation": "# Summary\n \nMeningitis refers to inflammation of the meninges which line the brain and spinal cord. The most common cause is infection, with bacterial meningitis being an important emergency presentation that may be life-threatening. The commonest causative bacteria are Neisseria meningitidis, Streptococcus pneumoniae and Haemophilus influenza type b. Key investigations include a throat swab for meningococcal culture, blood testing including PCR for meningococcal and pneumococcal bacteria and a lumbar puncture. Management is with IV antibiotics, with ceftriaxone the recommended first line option until the cause is identified. \n \n# Definition\n \nMeningitis occurs when there is inflammation of the pia mater and arachnoid mater, the two innermost linings of the brain and spinal cord. This can occur for a variety of causes, including malignancy, autoimmune disorders and medications as well as infection. This chapter will focus on bacterial meningitis as the key emergency presentation, however other infections can cause meningitis including viral and fungal causes. \n \n# Epidemiology\n \nRisk factors for bacterial meningitis include:\n\n- Young age (especially under 2 year olds)\n- Older age (over 65 year olds)\n- Winter season\n- Immunocompromise e.g. HIV, chemotherapy\n- Incomplete immunisations against meningococcal, haemophilus influenza b and pneumococcal bacteria\n- Comorbidities e.g. splenic dysfunction, renal disease, sickle cell disease\n- Overcrowding or close living with other e.g. dormitories\n- Cochlear implants\n- Local infection e.g. otitis media, sinusitis\n \n# Aetiology\n\nThe commonest causative bacteria are:\n\n- Streptococcus pneumoniae (pneumococcus) - the commonest cause in adults\n- Neisseria meningitidis (meningococcus)\n- Haemophilus influenza type b (Hib)\n\nOther causes include Listeria monocytogenes, Escherichia coli and Streptococcus agalactiae.\n\n# Signs and Symptoms\n\n- Headache\n- Photophobia\n- Neck stiffness\n- Fever\n- Confusion or altered level of consciousness\n- Seizures\n- Nausea and vomiting\n- Kernig's sign (unable to fully extend the knee when the hip is flexed to 90 degrees due to pain)\n- Brudzinski's sign (when the neck is actively flexed, the knees and hips spontaneously flex)\n\nSigns of systemic infection or sepsis may be present e.g. tachypnoea, tachycardia and hypotension. \n\nPresence of a non-blanching rash is suggestive of meningococcal disease.\n\n# Differential Diagnosis\n\nCSF interpretation can be used to differentiate bacterial from other causes of meningitis, for example viral, fungal or tuberculous: \n\n| | **Bacterial meningitis** | **Viral meningitis** | **Fungal meningitis** | **Tuberculous meningitis** |\n|-----------------------|-----------------------------------------|----------------------------------------|------------------------------------------|------------------------------------------|\n| **Opening pressure** | Elevated | Normal or mildly elevated | Elevated | Elevated |\n| **Appearance** | Turbid | Clear | Fibrin web | Cloudy |\n| **White cells** | Elevated neutrophils | Elevated lymphocytes| Elevated lymphocytes | Elevated lymphocytes|\n| **Protein** | Elevated | Normal or mildly elevated | Elevated | Elevated |\n| **Glucose** | Decreased | Normal | Decreased | Decreased |\n| **Additional tests** | Gram stain and culture | PCR for viral DNA/RNA | Fungal staining, antigen tests or culture | Acid-fast bacilli staining, TB PCR |\n\n**Other differential diagnoses include:**\n\n- **Drug-induced meningitis** with causes including NSAIDs, co-trimoxazole and amoxicillin)\n- **Encephalitis** which shares features of fevers, headache and altered mental status however other neurological findings are present (e.g. dysphasia, motor abnormalities)\n- **Subarachnoid haemorrhage** which also causes meningism and altered mental status, however headache is usually \"thunderclap\" in nature followed by progressive worsening of other symptoms\n\n# Investigations \n \n**Bedside tests:**\n\n- **Lumbar puncture** is the key diagnostic test that should ideally be done before starting antibiotics (or as soon as possible after) - cerebrospinal fluid (CSF) should be sent for:\n - Cell count\n - Total protein\n - Glucose\n - Microscopy, culture and sensitivities\n - Bacterial PCR\n- **Throat swab** for meningococcal culture to identify meningococcal meningitis\n- **Capillary blood glucose** immediately before lumbar puncture to compare with CSF glucose levels\n\n**Blood tests:**\n\n- **Blood cultures** to identify a causative bacteria\n- **FBC** and **CRP** for inflammatory markers which should be raised\n- **HIV test** for all adults with bacterial meningitis\n- **Meningococcal and pneumococcal PCR** to identify the cause of meningitis\n- **U&Es**, **LFTs** and **coagulation screen** as a baseline, may be deranged due to infection\n\n**Imaging:**\n\n- **CT head** should be done prior to lumbar puncture in patients who have any of:\n - Risk factors for a space-occupying lesion\n - New focal neurological signs\n - Abnormal pupillary reactions\n - GCS < 10 or rapid decline in consciousness\n \n# Management\n\n- If there is a strong suspicion of bacterial meningitis, treatment may be started outside of hospital with IM or IV ceftriaxone or benzylpenicillin\n- Otherwise, antibiotics should be started within an hour of arrival in A&E\n- Ideally, a lumbar puncture and blood tests would be done prior to antibiotic administration however these should not delay treatment\n- IV ceftriaxone is first-line; amoxicillin should be given too in patients with risk factors for Listeria meningitis (e.g. neonates, elderly or immunocompromised patients)\n- Chloramphenicol is second line in patients with severe penicillin allergy\n- IV dexamethasone should be given to all over the age of 3 months with strongly suspected or confirmed bacterial meningitis - this is particularly important in pneumococcal meningitis to reduce neurological complications\n- Bacterial meningitis is a notifiable disease; ensure the local health protection unit is informed and antibiotic prophylaxis or vaccination may be required for close contacts\n \n# Complications\n\n- Hearing loss\n- Seizures\n- Cerebral infarction leading to focal neurological deficits including motor deficits and visual impairment\n- Cognitive impairment\n- Obstructive hydrocephalus\n- Death (bacterial meningitis has a mortality rate of 25% in adults) \n\n# NICE Guidelines\n\n[NICE - Meningitis (bacterial) and meningococcal disease](https://www.nice.org.uk/guidance/ng240/)\n\n[NICE CKS - Meningitis](https://cks.nice.org.uk/topics/meningitis-bacterial-meningitis-meningococcal-disease)\n\n# References\n \n[UK joint specialist societies guideline on the diagnosis and management of acute meningitis](https://www.journalofinfection.com/article/S0163-4453(16)00024-4/fulltext)\n\n[Public Health England - Guidance for public health management of meningococcal disease](https://assets.publishing.service.gov.uk/media/5d6fa400e5274a0989ca9aed/PHE_meningo_disease_guideline.pdf)",
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"question": "A 35-year-old male is brought to A&E by his girlfriend. He has been complaining of a progressive, severe headache for the last two hours. He has become increasingly violent in the waiting area. He has a past medical history of HIV and intravenous drug use (IVDU). On examination, he has neck stiffness and reduced visual acuity. A lumbar puncture is done urgently due to suspected meningitis.\n\nCerebrospinal fluid (CSF) results:\n\n- Appearance - Cloudy\n- Protein - Elevated\n- Glucose - Low\n- White Cell Count - 25 cells/mL\n- Opening pressure - Very high\n- India ink stain - Positive\n\nWhat is the likely cause of these symptoms?",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Lung function tests are unlikely to be useful in this acute scenario",
"id": "32861",
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"name": "Lung function tests",
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"__typename": "QuestionChoice",
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"explanation": "A chest x-ray would be a reasonable investigation to perform in this case. However, based on the history, although delirium secondary to pneumonia is a differential, it is not the most likely",
"id": "32860",
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"name": "Chest x-ray",
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"__typename": "QuestionChoice",
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"explanation": "A urine dipstick would be a reasonable investigation to perform in this case. However, based on the history, although delirium secondary to a urinary tract infection is a differential, it is not the most likely and would be unlikely to lead to headache or nausea",
"id": "32859",
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"explanation": "Alcohol intoxication is a common differential of carbon monoxide poisoning, and the two can occur concomitantly. However, the patient is unlikely to complain of vertigo, and there is no mention of alcohol use in the history",
"id": "32862",
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"name": "Blood ethanol levels",
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"explanation": "Carboxyhaemaglobin levels can be taken when there is a clinical suspicion of carbon monoxide poisoning. This patient is displaying classic signs and symptoms. Other classic signs are cherry red lips and peripheral cyanosis, which are more common in textbooks than in practice",
"id": "32858",
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"name": "Carboxyhaemaglobin levels",
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"explanation": "# Summary\n\nCarbon monoxide is a tasteless, odourless and invisible gas that may be produced by fires, faulty gas appliances and fuel-burning heaters. Signs and symptoms include confusion, nausea, vomiting, hypotension and dizziness. Pulse oximetry typically shows close to 100% oxygen saturations as monitors cannot differentiate between haemoglobin bound to oxygen or carbon monoxide. A blood gas will show high levels of carboxyhaemoglobin, and breath tests can be used to measure exhaled carbon monoxide. High-flow oxygen is the mainstay of treatment, with hyperbaric oxygen considered for certain high risk patients. \n \n\n# Definition\n \nCarbon monoxide poisoning is a serious and potentially fatal condition caused by acute or chronic inhalation of carbon monoxide gas. This gas is colourless and odourless, and can only be detected by equipment such as carbon monoxide alarms. It is produced by the incomplete combustion of fuel (when insufficient oxygen is present), for example in faulty heaters or cooking equipment.\n \n# Epidemiology\n \nIn England, there are approximately 4000 A&E attendances per year with carbon monoxide poisoning and approximately 40 deaths. Around half of cases are due to accidental exposure and around 40% are due to self-harm (e.g. from intentional inhalation of exhaust fumes in an enclosed space). \n\nPoisoning is more common in winter when heating equipment is more likely to be used, and is more common in groups affected by socio-economic deprivation.\n\nSome patient groups are more sensitive to the effects of carbon monoxide poisoning, including:\n\n- The elderly\n- Young children\n- Pregnant women \n- People with anaemia\n- People with cardiovascular disease\n\n# Aetiology\n\nInhaled carbon monoxide binds to haemoglobin with a much greater affinity than oxygen, forming carboxyhaemoglobin. This causes tissue hypoxia, especially affecting organ systems with a high oxygen demand such as the central nervous system and the cardiovascular system.\n\n**Prevention of carbon monoxide poisoning:**\n\n- Carbon monoxide alarms should be fitted in the home\n- Gas appliances should be correctly installed and be regularly serviced\n- Vulnerable patients (e.g. disabled or elderly patients) may be entitled to free annual gas safety checks\n- Landlords have a legal duty to ensure gas appliances are checked at least yearly\n- Do not burn charcoal indoors for cooking or heating\n- Do not use gas appliances if you suspect they may be faulty\n\n# Signs and Symptoms\n\n- Headache\n- Dizziness\n- Lethargy\n- Flushing\n- Myalgia and weakness\n- Confusion\n- Nausea and vomiting\n- Cherry red skin (rare)\n- Tachycardia and hypotension\n- Seizures\n\n# Differential Diagnosis\n \n- **Migraine:** headache is the predominant symptom of many cases of carbon monoxide poisoning; migraine is more likely to be associated with aura, photophobia and phonophobia\n- **Viral infections:** cause overlapping symptoms of headache and myalgia, may have other symptoms such as cough or fever not seen in carbon monoxide poisoning\n- **Diabetic ketoacidosis:** may have similar symptoms of nausea and vomiting, lethargy and weakness; blood glucose will be high with raised ketones\n \n# Investigations\n\n**Bedside tests:**\n\n- **Pulse oximetry** is likely to show close to 100% oxygen saturations; this is artifactual as the devices cannot differentiate carboxyhaemoglobin and oxyhaemoglobin.\n- A **blood gas** (either venous or arterial) should be taken to confirm the diagnosis by measuring carboxyhaemoglobin\n - The normal level in non-smokers is 1–2%\n - In smokers 5-10% is normal (heavy smokers can tolerate up to 15%)\n - Carboxyhaemoglobin of 10% or more is usually indicative of carbon monoxide poisoning\n - Toxicity usually manifests at levels of 15-20%\n - Carboxyhaemoglobin of 20% or higher is usually associated with severe cerebral or cardiac ischaemia\n- An **ECG** should be done to look for ischaemic changes\n- **Capillary blood glucose** to rule out hypoglycaemia or hyperglycaemia as a cause for lethargy and confusion\n\n**Blood tests:** \n\n- **FBC** for anaemia\n- **U&Es** for renal impairment\n- **CK** for rhabdomyolysis\n- **Troponin** for myocardial ischaemia\n- **Lactate** - may indicate concurrent cyanide exposure if high in the context of smoke exposure\n\n# Management\n \n- Take an **A to E approach** and ensure the airway is protected in the first instance\n- Administer **100% oxygen** via a tight-fitting face mask (if high-flow nasal cannulae available these can be used to administer up to 60L/min oxygen)\n- Continue high-flow oxygen until any symptoms have resolved and carboxyhaemoglobin levels are 2% or lower in non-smokers or 10% or lower in smokers\n- Correct hypotension with **IV fluids**\n- Contact the **National Poisons Information Service** (NPIS) if advice required\n- In certain severe cases (e.g. carboxyhaemoglobin > 25%) **hyperbaric oxygen therapy** may be considered however its use is currently not recommended by the NPIS\n- **Inform the local Health Protection Team** who will coordinate services to address the source of carbon monoxide poisoning\n\n# Complications\n\nMost patients will recover fully from carbon monoxide poisoning, although in a minority of people (generally those who have had severe or prolonged exposure) neuropsychiatric complications may develop, including:\n\n- Emotional lability and personality change\n- Difficulty concentrating\n- Insomnia\n- Lethargy\n- Movement disorders such as chorea and Parkinsonism\n- Memory impairment and dementia\n- Psychosis\n- Neuropathy\n\n# NICE Guidelines\n\n[NICE CKS - Carbon Monoxide Poisoning](https://cks.nice.org.uk/topics/carbon-monoxide-poisoning/)\n\n# References\n \n[RCEM Learning - Carbon Monoxide Poisoning](https://www.rcemlearning.co.uk/reference/carbon-monoxide-poisoning/)\n\n[London Fire Brigade - Carbon Monoxide Safety](https://www.london-fire.gov.uk/safety/the-home/carbon-monoxide-safety/)",
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"question": "An 89-year-old woman attends A&E. She moved into a new ground-floor flat two weeks ago and calls her daughter as she says her heating appears to have broken. Her daughter finds her confused, and she is complaining of a headache, nausea, vertigo, and dizziness.\n\nWhich of these investigations is most likely to lead to the correct diagnosis?",
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"explanation": "Linagliptin is a dipeptidylpeptidase-4 inhibitor. Liver damage is not a known side effect",
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"explanation": "This patient is displaying symptoms and signs of hepatocellular necrosis secondary to a staggered overdose of paracetamol. The patient's weight is only 44kg. Any patient less than 50kg is at increased risk of developing liver toxicity secondary to paracetamol overdose. Therefore, prescribing 500mg up to 4 times a day instead of 1000mg is advised. Early features of paracetamol poisoning can present initially and then improve within the first 24 hours. Recurrence of these features usually indicates the onset of hepatocellular necrosis",
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"explanation": "Liver damage is not a known side effect of levothyroxine. Caution should be taken when prescribing levothyroxine, even at this small dose, with diabetic medications as the dose of antidiabetic drugs may need to be increased",
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"name": "Levothyroxine, 25 micrograms, oral, once a day",
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"explanation": "A rare side effect of metformin is hepatitis. However, this is the lowest possible dose, and the clinical picture suggests hepatocellular necrosis. It would be important in this patient to consider withholding the metformin prescription because paracetamol poisoning can lead to renal necrosis, which may increase the likelihood of lactic acidosis secondary to the metformin. Lactic acidosis is not usually a concern unless the eGFR drops below 30 mL/minute/1.73 m2",
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"label": "c",
"name": "Metformin modified release, 500mg, oral, once a day",
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"explanation": "The patient is displaying signs of hepatocellular necrosis. Liver disorders are a potential rare side effect of ibuprofen orally; however, there is little evidence that this can occur via the topical route",
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"name": "Ibuprofen 5% gel, topical, to be taken as required, up to 3 times a day",
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"comment": "poor. this could be pancreatitis",
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"comment": "Could be, unfortunately not one of the options. The questions asks for the most likely cause of the ones offered. It is trying to assess knowledge of reducing doses for low body weights, one of the most essential things to know as a safe prescriber. I think it's a good question",
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"comment": "^ DPP40- inhibitors cause pancreatitis ",
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"explanation": "# Summary\n \nParacetamol overdose accounts for 44% of all adult self-poisoning cases in the UK and results in approximately 150,000 hospital admissions annually. Some patients may be asymptomatic, or present with nausea, vomiting, abdominal pain, jaundice or altered mental state. Investigations should include baseline bloods including a clotting and a blood gas, as well as a paracetamol level. Management depends on the dose taken, timing of ingestion and the patient's clinical condition, with N-acetylcysteine being the mainstay of treatment. The decision to treat is often guided by a nomogram although in certain situations N-acetylcysteine should be started immediately.\n \n# Definition \n \nParacetamol overdose refers to when a potentially toxic dose of paracetamol is taken, either accidentally or in the context of a self-harm or suicide attempt. \n \n# Epidemiology \n \nParacetamol is the most common agent ingested in the context of intentional self-harm in the UK. Paracetamol overdose accounts for 44% of all adult self-poisoning cases in the UK, with approximately 150,000 people admitted to hospital each year due to poisoning.\n \n\n# Aetiology\n \n- The pathophysiology of paracetamol toxicity involves the build-up of its toxic metabolite NAPQI (N-acetyl-p-benzoquinone-imine). \n- Normally, NAPQI is inactivated by glutathione in the blood, but in a paracetamol overdose, glutathione stores are rapidly depleted. \n- NAPQI therefore accumulates, unmetabolised, and binds to cellular proteins, causing cell death.\n- This causes both severe hepatotoxicity and nephrotoxicity that can lead to liver and kidney failure. \n\n# Classification\n \n - **Acute overdose** - excessive paracetamol taken in less than 1 hour, usually in the context of self-harm\n - **Staggered overdose** - excessive paracetamol ingested over longer than 1 hour, usually in the context of self harm\n - **Therapeutic excess** - excessive paracetamol taken with the intent to treat pain or fever and without self-harm intent, ingested at a dose greater than 75mg/kg/24 hours.\n\n\n# Signs and Symptoms\n \n- These depend on how long has passed since the overdose was taken\n- In the first 24 hours patients may be asymptomatic or have nausea and vomiting\n- After this, up to around 72 hours, right upper quadrant pain and hypotension may develop\n- From 72 to 96 hours patients may develop liver and renal failure with resulting metabolic acidosis, encephalopathy and coagulopathy, with symptoms of:\n - Confusion\n - Drowsiness\n - Reduced urine output\n - Loin pain\n - Jaundice\n - Bleeding diathesis\n\n# Differential Diagnosis \n\n - **Acute gastroenteritis:** has similar symptoms of nausea, vomiting and abdominal pain; may have diarrhoea and history of unwell contacts\n - **Renal colic:** may also present with haematuria, nausea and vomiting; pain more likely to be \"loin to groin\" rather than right upper quadrant\n - **Decompensation of chronic liver disease:** can present with jaundice, abdominal pain and encephalopathy\n - **Sepsis:** can lead to a lactic acidosis and acute kidney injury; patients are often febrile and may have localising signs or symptoms of infection\n \n# Investigations\n \nBlood tests for paracetamol levels should be taken at least 4 hours after ingestion, as this is when plasma paracetamol concentration peaks so an earlier blood test may underestimate levels\n\nOther important blood tests include:\n \n - Full Blood Count (FBC)\n - Urea and Electrolytes\n - Clotting Screen\n - Liver Function Tests\n - Venous Blood Gas (may show metabolic acidosis)\n - Blood glucose (could also do a bedside capillary blood glucose)\n - Salicylate levels (to look for a mixed overdose with aspirin)\n\n# Management\n \n**Conservative:**\n\n- Weigh patient (important for determining dose of paracetamol taken per kg and to calculate N-acetylcysteine dosing)\n- Consider if any other substances may have been taken with paracetamol\n- If overdose was intentional, refer to liaison psychiatry for a mental health assessment\n - Consider if 1:1 observations are required for high-risk patients\n - Assess risk to self and ongoing suicidal ideation\n - Discharge planning and assess need for ongoing psychiatric input\n- Treat any other self-harm\n\n**Medical:**\n\nDecisions on medical treatment are guided by a nomogram which plots paracetamol levels against time from ingestion. \n\nThe management of paracetamol overdose is dependent on the timing of ingestion, the dose taken, and the patient's clinical condition:\n \n - **Ingestion less than 1 hour ago + dose >150mg/kg**: Administer activated charcoal\n - **Ingestion 1-4 hours ago**: Wait until 4 hours to take a level and treat with N-acetylcysteine (NAC) based on level\n - **Ingestion within 4-8 hours + dose >150mg/kg**: Start NAC immediately if there is going to be a delay of ≥8 hours in obtaining the paracetamol level, otherwise wait for level and treat if level high (above the treatment line on the nomogram)\n - **Ingestion within 8-24 hours + dose >150mg/kg**: Start NAC immediately\n - **Ingestion >24 hours ago**: Start NAC immediately if the patient has jaundice, right upper quadrant tenderness, elevated ALT, INR >1.3 or if the paracetamol concentration is detectable\n - **Staggered overdose**: Start NAC immediately\n \nNAC is given as an IV medication - it acts by increasing glutathione levels thereby preventing toxicity. \n\nThere are two ways to give NAC:\n\n- Standard regimen of 3 consecutive infusions totalling 21 hours in duration \n- The newer SNAP protocol (now recommended by Royal College of Emergency Medicine as standard) where the same dose of NAC is given over 12 hours in two infusions\n- If after either of these are completed, bloods show deranged LFTs, clotting or renal function NAC infusions should be continued and the patient discussed with local liver transplant services\n- Anaphylactoid reactions are a common side effect of NAC, characterised by urticaria, angioedema, nausea and vomiting, tachycardia and bronchospasm but rarely shock\n- These are managed by suspending treatment and giving chlorphenamine and salbutamol nebulisers before restarting (possibly at a slower rate)\n \n**Surgical:**\n\nPatients who develop acute liver failure may require an urgent liver transplant as a life-saving measure - the following groups of patients should be transferred to a liver transplant centre:\n\n- INR > 3 at 48 hours or > 4.5 at any time\n- Oliguric or creatinine > 200\n- pH < 7.3 despite fluid resuscitation\n- Hypotension (systolic blood pressure < 80mmHg)\n- Severe thrombocytopenia\n- Encephalopathy\n \nThe King's College Criteria is used to predict mortality from paracetamol overdose and to identify those patients who would potentially benefit from liver transplantation. It advises consideration of liver transplantation if:\n \n- Blood pH < 7.3\n \n\nOr **all** of:\n \n- Serum creatinine > 300 µmol/L\n- INR > 6.5 (Prothrombin time > 100s)\n- Grade III or IV hepatic encephalopathy\n\n# NICE Guidelines\n\n[NICE CKS - Poisoning or overdose](https://cks.nice.org.uk/topics/poisoning-or-overdose/)\n\n# References\n\n[BNF - Poisoning](https://bnf.nice.org.uk/treatment-summary/poisoning-emergency-treatment.html)\n\n[MHRA - Treating paracetamol overdose with intravenous acetylcysteine](https://www.gov.uk/drug-safety-update/treating-paracetamol-overdose-with-intravenous-acetylcysteine-new-guidance)\n\n[RCEM - SNAP Protocol Position Statement](https://rcem.ac.uk/wp-content/uploads/2021/11/Use_of_SNAP_for_Treatment_of_Paracetamol_Toxicity_Nov_2021.pdf)\n\n[Life in the Fast Lane - liver transplanation for paracetamol toxicity](https://litfl.com/liver-transplantation-for-paracetamol-toxicity/)",
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"question": "A 90-year-old woman attends A&E due to nausea and vomiting. She had visited her GP about it two days before, but she had thought it had settled. It has now become significantly worse. On examination, she has severe right subcostal tenderness and is visibly jaundiced. Her past medical history includes diabetes type 2 mellitus, hypothyroidism and osteoarthritis.\n\nHer current medications are as follows:\n\n- Paracetamol, 1000mg, oral, 4 times a day\n- Ibuprofen 5% gel, topical, to be taken as required, up to 3 times a day\n- Metformin modified release, 500mg, oral, once a day\n- Linagliptin, 5mg, oral, once a day\n- Levothyroxine, 25 micrograms, oral, once a day\n\nHer eGFR is 60 mL/minute/1.73 m2 and her weight is 44kg.\n\nWhich of these medications is most likely the cause of her symptoms?",
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"explanation": "This patient has presented with signs and symptoms of hypothermia. J waves can be seen in hypothermic patients, often at a temperature of less than 30 degrees. The height of the J wave is thought to be approximate to the degree of hypothermia. They are positive deflections between the QRS and the ST segment",
"id": "32868",
"label": "a",
"name": "J waves",
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"__typename": "QuestionChoice",
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"explanation": "Pathological Q waves usually indicate ongoing or historic myocardial infarction. Q waves are considered pathological if they are wider or deeper than normal",
"id": "32869",
"label": "b",
"name": "Pathological Q waves",
"picture": null,
"votes": 608
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"__typename": "QuestionChoice",
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"explanation": "These occur when sinus and ventricular rhythms coincide. They can help differentiate between Ventricular Tachycardia (VT) and Supraventricular Tachycardia (SVT) with aberrancy rhythms as they are more likely to occur in VT",
"id": "32870",
"label": "c",
"name": "Fusion beats",
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"__typename": "QuestionChoice",
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"explanation": "Brugada syndrome is due to an abnormality in a cardiac sodium channel which can lead to sudden death. Brugada sign is potentially diagnostic but does not necessarily lead to Brugada syndrome. There is ST elevation in more than one lead, followed by a negative T wave",
"id": "32871",
"label": "d",
"name": "Brugada sign",
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"explanation": "Capture beats occur when the sinoatrial node \"captures\" current from the ventricles during atrioventricular dissociation. This produces a normal QRS complex during ventricular tachycardia. They can help differentiate between VT and supraventricular tachycardia (SVT) with aberrancy rhythms as they are more likely to occur in VT",
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"comment": "thought it was RBBB :(\n",
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"explanation": "# Summary\n\nHypothermia refers to an abnormally low body temperature (usually defined as under 35°C). It can occur due to exposure to cold surroundings or because of another illness or event such as infection or trauma. Symptoms and signs include shivering, reduced level of consciousness, tachycardia and tachypnoea and arrhythmias. Investigations should include an ECG (with J waves being a key finding), blood tests and a chest X-ray looking for complications of aspiration pneumonia and pulmonary oedema. Management involves rewarming via a number of strategies, monitoring for and treating both causative factors and complications, and fluid resuscitation. Cardiac arrest may occur in severe hypothermia and in this case resuscitation should not be stopped until the patient has been rewarmed. \n\n# Definition\n\nHypothermia refers to a core body temperature below 35°C - it is a pathological state which has significant adverse effects on many body systems and can lead to death.\n\n# Classification\n\nHypothermia may be classified as **primary** or **secondary**:\n\n- **Primary hypothermia** is environmental, occurring for example after immersion in cold water or prolonged exposure to cold weather conditions\n- **Secondary hypothermia** occurs secondary to an insult or illness such as infection, alcohol excess, hypothyroidism or major trauma\n\nIt can also be classified by core body temperature as follows:\n\n- Mild - 32 to 35°C\n- Moderate - 28 to 32°C\n- Severe - 20 to 28°C\n- Profound - < 20°C\n\n# Signs and Symptoms \n\nSymptoms include:\n\n- Shivering\n- Hunger \n- Dizziness\n- Chills\n- Slurred speech\n- Paradoxical undressing\n\nSigns include:\n\n- Tachycardia initially; bradycardias may occur if severe with arrhythmias\n- Tachypnoea; respiratory depression followed by apnoeas if severe\n- Cool peripheries secondary to vasoconstriction\n- Hypotension\n- Ataxia\n- Reduced level of consciousness\n- Pupils may be fixed and dilated if severe\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urine toxicology screen** if drug intoxication is suspected (e.g. patient found unconscious outside \n- **Arterial blood gas** may show an initial respiratory alkalosis, followed by respiratory acidosis as hypothermia worsens\n- **ECG** may show:\n - Prolonged PR, QRS and QT intervals\n - Osborn (or J) waves - positive deflections where the QRS complex joins the ST segment\n - Bradyarrhythmias e.g. sinus bradycardia, atrial fibrillation with a slow ventricular response, slow junctional rhythms and AV block\n - Shivering artefact\n - Ventricular ectopics\n - Cardiac arrest (ventricular tachycardia, ventricular fibrillation or asystole)\n \n\n [lightgallery]\n\n\n**Blood tests:**\n\n- **FBC** and **CRP** for inflammatory markers\n- **U&Es** looking for renal complications of hypothermia and electrolyte derangement\n- **Coagulation screen** as hypothermia can cause a coagulopathy\n- **Creatinine kinase** as hypothermia can cause muscle damage and rhabdomyolysis\n- **Amylase** as pancreatitis can result from hypothermia\n- **Bone profile** and **magnesium** so that any electrolyte disturbance can be corrected\n- **Blood cultures** if sepsis is suspected as a driver of hypothermia\n\n**Imaging:**\n\n- **Chest X-ray** as aspiration pneumonia and pulmonary oedema may complicate hypothermia\n- **CT head** may be indicated e.g. elderly patients who become hypothermic after a fall and long lie\n\n# Management\n\n**Conservative management involves:**\n\n- Take an A to E approach; patients may require escalation to intensive care for intubation and ventilation e.g. if reduced levels of consciousness\n- Rewarming, which may be:\n - Passive rewarming - e.g. removing cold or wet clothes, cover with a blanket and cover head to reduce heat loss (useful in mild hypothermia)\n - Active external rewarming - usually using forced air systems such as a Bair Hugger\n - Active core rewarming - e.g. warmed intravenous fluids and warmed humidified oxygen\n- Core temperature monitoring may be required in more severe cases, with either a rectal or (if intubated) an oesophageal probe\n- Cardiac monitoring\n\n\n**Medical management involves:**\n\n- Fluid resuscitation as patients are usually dehydrated - careful fluid balance monitoring is needed due to the risk of fluid overload\n- Monitoring for and treating complications of hypothermia (see below) \n- Antiarrhythmic medication is rarely required for cardiac complications, with rewarming being the mainstay of treatment\n- Consider thiamine for malnourished or critically unwell patients, or those with suspected alcohol excess\n- Investigating for and treating causes of hypothermia (e.g. infection)\n- In the case of a cardiac arrest secondary to severe hypothermia, Resuscitation Council guidelines should be followed (e.g. defibrillation for VF arrests) and resuscitation should be continued at least until the patient has been rewarmed\n\n**Invasive management:**\n\n- In severely hypothermic patients with life-threatening complications who are not responding to other treatments, options include cavity lavage using warm fluids and extracorporeal blood rewarming (e.g. cardiopulmonary bypass)\n\n# Complications\n\n- Frostbite, which in severe cases may warrant amputation of non-viable tissues\n- Arrhythmias\n- Hypotension (especially on rewarming due to vasodilation)\n- Aspiration pneumonia\n- Pulmonary oedema\n- Pancreatitis\n- Acute tubular necrosis\n- Cardiac arrest and death\n\n# References\n\n[RCEM Learning - Hypothermia](https://www.rcemlearning.co.uk/reference/hypothermia/)\n \n[RCEM Learning - Severe Hypothermia](https://www.rcemlearning.co.uk/reference/severe-hypothermia/)\n\n[Patient UK - Hypothermia](https://patient.info/doctor/hypothermia-pro)\n \n[Life In The Fast Lane: ECG Changes in Hypothermia](https://litfl.com/hypothermia-ecg-library/)",
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"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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"question": "A 56-year-old woman visits her GP due to the development of new mouth ulcers. She also complains about a sore throat. On examination, she is warm to the touch. She has started a new medication due to a recent diagnosis of hyperthyroidism.\n\n\nHer bloods are as follows:\n\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|101 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|2.2x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|90x10<sup>9</sup>/L|150 - 400|\n\n\nWhich of these medications is most likely to be the cause?",
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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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"question": "A 62-year-old male patient presents to A&E due to a history of intermittent confusion, sweating and dizziness. These often improved towards the end of the day. His bloods are as follows:\n\n\n - Fasting glucose 1.2 (normal range 3.5-5.5 mmol/L)\n - Proinsulin raised\n - C-peptide raised\n\n\nA diagnosis of insulinoma is made. What is the most appropriate initial management?",
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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",
"id": "32883",
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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",
"id": "32884",
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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.",
"id": "32887",
"label": "e",
"name": "Readmit to ITU as soon as possible",
"picture": null,
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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",
"id": "32886",
"label": "d",
"name": "Clamp the chest drain and prescribe IV furosemide",
"picture": null,
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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",
"id": "32885",
"label": "c",
"name": "Clamp the chest drain and call the intensive care unit",
"picture": null,
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"__typename": "QuestionComment",
"comment": "they've developed a what now ",
"createdAt": 1646391119,
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"comment": "icu team come quick pls ",
"createdAt": 1682448217,
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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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"learningPoint": "A chylothorax is a condition where lymph leaks from the thoracic duct into the chest cavity, often occurring after trauma like oesophagectomy, and is typically managed by draining the lymph and ensuring adequate nutritional support.",
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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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"__typename": "QuestionSBA",
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"explanation": "It is important to first restore circulatory volume and start a fixed-rate IV insulin infusion",
"id": "32891",
"label": "d",
"name": "IV IV 0.9% sodium chloride 1L with potassium chloride over 2 hours",
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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",
"id": "32889",
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"name": "IV insulin with 0.9% sodium chloride at a concentration of 1 unit/mL; infused at a fixed rate of 0.1 units/kg/hour",
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"explanation": "The patient is hypotensive and requires fluid resuscitation with an IV bolus",
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"explanation": "Whilst ongoing fluid and potassium replacement is important, the priority here is to restore circulatory volume with an IV fluid bolus",
"id": "32892",
"label": "e",
"name": "1L IV 0.9% sodium chloride with 40 mmol KCl over 6 hours",
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"explanation": "The patient has presented with signs of diabetic ketoacidosis and is hypotensive. The correct initial management is to restore circulatory volume by giving a rapid bolus of IV fluid",
"id": "32888",
"label": "a",
"name": "500 mL IV sodium chloride 0.9% over 10–15 minutes",
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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": "This is a poor choice, even if the doctor has mitigated the scenario slightly by looking up the details of the surgery. This consent requires a complex understanding of the operation that only someone who has performed the surgery will have",
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"explanation": "This is the second best choice. You should not practice outside your boundaries of competence. (Even consultants need to ask others for help occasionally). However, explaining why they have refused would be best",
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"explanation": "This is a poor choice as the doctor is also involving a second underqualified doctor. It is up to interpretation whether this option is worse the consenting the patient after looking up the details first. Ultimately, both should not happen",
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"comment": "can't wait to be in that scenario myself and get demoted back to medical student",
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"comment": "I got this wrong because i chose 'refuse to consent the patient'. I see why it was explain that you are unable to consent, however i think the reasoning is incorrect. You can't consent the patient because you are not doing the procedure, not because you don't have enough experience (perhaps a secondary reason). ",
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"explanation": "# Consent \n\nConsent must be obtained from a patient before undertaking a treatment or procedure. If it is not, then this could constitute the offence of **battery** (\"touching in a harmful or offensive manner without consent or lawful justification\") - even if there was no hostile intent or harm caused.\n\n# Conditions for valid consent\n\nUnder the **Mental Capacity Act**, there are a number of conditions that have to be met for valid consent to be obtained from a patient:\n\n1. The patient must have **capacity**. For this, the individual must be able to: understand information, retain information, weigh the information and reach a conclusion, and communicate the decision they have reached.\n\n2. The consent must be **freely given** (i.e. uncoerced) and the patient must be **suitably informed** (i.e. have been given a suitable level of detail of the procedure, and expected outcomes and risks).\n\n# Assumed Capacity \n\nFor an adult, capacity is assumed unless there is reason to doubt; for example the patient has learning difficulties which impacts on their ability to understand and process new information.\n\n# How Is Consent Taken?\n\nValid consent can be received in writing, verbally or tacitly (where it is implied or indicated). A signed consent form does not - by itself - equal 'consent', it is purely _related evidence_.\n\n# Who Can Obtain Consent?\n\nThe person who should obtain the consent from a patient should be the professional undertaking the procedure, or someone familiar with it, who is able to explain all the necessary information and answer any questions the patient may have.",
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"explanation": "The first part of this choice is correct: the patient's capacity should be assessed in keeping with Principle 1 of the Mental Capacity Act (2005). However, there is nothing in the stem to suggest that giving the patient the flu jab would be against their best interests",
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"explanation": "This is incorrect. The patient's capacity needs to be assessed before making a decision here. The presence of a DNAR form only means that, in the event of a cardiac arrest, the patient should not have cardiopulmonary resuscitation. It does not mean the patient cannot have other treatments. This is a common misconception amongst patients",
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"name": "Do not assess whether the patient has capacity for this decision because they have a DNAR. Do not give the vaccination because the patient has a DNAR",
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"comment": "cant really assume that the vaccine is his best interest? ",
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"explanation": "# What are Best Interests? \n\nIf someone lacks capacity to make a specific decision, a decision may have to be made in their _best interests_. This means that a decision will be made on their behalf, having been considered from their point of view. The decision should be one that health and social care professionals believe is the right decision for _that individual patient themselves_ (and not the decision that the professionals desire without taking the patients interests into account).\n\n# Best Interests Criteria\n\nWhen making a best interests decision on behalf of someone who lacks capacity, five factors must be considered:\n\n1. Equal consideration and non-discrimination\n2. All relevant circumstances\n3. Regaining Capcity\n4. Participation\n5. Wishes, Feelings, Beliefs and Values\n\n# What are Equal Consideration and Non-discrimination? \n\nThe person making the decision about what is in the patient's best interests must not make assumptions based on _age, appearance, condition or behaviour_.\n\n# What are All Relevant Circumstances? \n\nIn order to determine what is in the patient's best interests, all the things that the patient would take into account if they were making the decision themselves should be identified .\n\n# Regaining Capacity \n\nIt must be considered whether the patient is likely to regain capacity. If so, the professional(s) need to consider whether or not the decision can be delayed until then.\n\n# Participation \n\nAll practicable steps should be taken in order to encourage and enable participation by the patient in the decision making process.\n\n# Wishes, Feelings, Beliefs and Values \n\nThe wishes, feelings, beliefs and values of the patient should be found out and taken into consideration. This includes views they have expressed in the past, religious or moral opinions, or other factors that might influence the decision they would make themselves.",
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"question": "A 75-year-old male patient is brought into his GP practice by his wife. He had received an invitation by the practice to come in for his annual flu vaccination. He has a history of Parkinson's dementia, type 2 diabetes mellitus and obesity. He requires carers four times a day, and on his last visit to the GP he scored 5 out of 30 on an MMSE (mini-mental state examination). He has a Do Not Attempt Resuscitation (DNAR) form but does not have an advanced directive.\n\nHis wife asks the GP whether he can have his flu vaccination, which of the following is the best next step?",
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"explanation": "Although the mother is upset about the lack of information that she has received it is still not acceptable to break patient-doctor confidentiality",
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"name": "Tell the daughter that her mother does have a DNAR form and update her about her current care",
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"answer": false,
"explanation": "Just because the daughter is the next of kin does not automatically mean that you can break patient-doctor confidentiality",
"id": "32904",
"label": "b",
"name": "Tell the daughter that her mother does have a DNAR form as she is the next of kin",
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"votes": 71
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"__typename": "QuestionChoice",
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"explanation": "You should not break patient-doctor confidentiality by disclosing this information without the patient's permission. Instead you must ask the mother whether it is acceptable to relay this information to her daughter. Whilst a DNACPR is a medical decision, this antagonistic response is likely to create further tension",
"id": "32906",
"label": "d",
"name": "Tell the daughter that their mother does have a DNAR form and explain that this is a medical decision and that her opinion will not change anything",
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"votes": 57
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is the correct answer. The patient had capacity to make the decision about resuscitation, therefore, it is likely that she will have capacity to make the decision about whether to communicate this decision to her daughter. If you did not ask permission, you would be breaking patient-doctor confidentiality",
"id": "32903",
"label": "a",
"name": "Check with the patient whether you can share this information with their daughter",
"picture": null,
"votes": 3665
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is the next best answer, as you cannot tell the daughter any information about her mother without her mother's consent",
"id": "32905",
"label": "c",
"name": "Refuse to tell the daughter anything",
"picture": null,
"votes": 43
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"comment": "Loving the passive aggressive options",
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"explanation": "# Overview\n\nA Do Not Attempt CPR (DNACPR) decision can also be known as Do Not Attempt Resuscitation (DNAR)\n\nA DNACPR decision provides information to healthcare professionals present on the best action to take if an individual suffers a cardiac arrest. A DNACPR is recorded, normally on a CPR Decision form, but is not in itself legally binding. This means that a doctor can overrule an existing DNACPR if they believe the circumstances do mean CPR would be in the patient's best interests.\n\nA DNACPR can be made if cardiac or respiratory arrest is an expected part of the dying process, and either CPR will not be successful, or if CPR may be successful but the clinical outcomes (e.g. trauma and prognosis) mean it is not clinically appropriate. A patient with capacity may also refuse CPR.\n\n# Best Interests \n\nDoctors can ultimately make the decision to put a DNACPR in place if it is in the patient's _best interests_, even if the patient themselves or their family disagrees. However, following a legal case in 2014, doctors must engage the patient and those close to them on the decision to make a DNACPR, and inform them if the decision to make a DNACPR order has occurred.\n\n# R (Tracey) v Cambridge University Hospitals NHS Foundation Trust, 2014 \n\nJanet Tracey died in Addenbrooke's Hospital in March 2011. She had been diagnosed with terminal lung cancer and had subsequently been involved in a car crash, in which she sustained a spinal injury. She required ventilation in the Intensive Care Unit (ICU), and after attempts to remove her from the ventilator were unsuccessful, a DNACPR notice was placed in her medical notes. Neither Janet Tracey nor her family were consulted about or informed of this decision.\n\nThe legal case concluded in favour of Tracey, finding that her Human Rights had been breached. The case acknowledged that the decision to put a DNACPR in place is ultimately a medical decision, and patients cannot demand treatment. But, the case did result in changes to DNACPR guidance:\n\nFirstly, the decision to not tell a patient about a DNACPR notice can no longer be based on the fact that telling them would cause “distress”. Only if discussing a DNACPR order would cause the patient “physical or psychological harm”, can doctors justify not discussing it. In other circumstances, doctors are legally obliged to discuss a DNACPR order that has been made.\n\nSecondly, it used to be the case that doctors were not obliged to discuss a DNACPR decision if the clinical decision has been made that CPR would be futile. This case amended this, making it a legal obligation for doctors to inform the patient that a DNACPR decision has been made, regardless of whether or not CPR could ever be successful (i.e. futility of CPR is justification for doctors making a best interests decision to make a DNACPR order - even if the patient wants CPR, but doctors are still legally obliged to inform the patient that a DNACPR order has been made).\n\nA DNACPR decision relates only to CPR, and is not a refusal of any other treatment.",
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"question": "A 95-year-old female is an inpatient on the acute medical unit. She has been treated for a urinary tract infection with antibiotics and is due to be discharged home. Before discharge, the patient agreed with the consultant to complete a Do Not Attempt Resuscitation (DNAR) form. The patient had capacity to make this decision. The patient's daughter (her next of kin) visits the ward and demands to know whether or not her mother has a DNAR form. She is very upset because she says it has been so difficult to contact the ward to find out how her mother has been doing.\n\nWhich is the best next step for you, as the ward resident doctor, to take?",
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"explanation": "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",
"id": "32913",
"label": "a",
"name": "Spontaneous bacterial peritonitis",
"picture": null,
"votes": 4638
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"__typename": "QuestionChoice",
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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",
"id": "32915",
"label": "c",
"name": "Tuberculosis",
"picture": null,
"votes": 39
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"__typename": "QuestionChoice",
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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",
"id": "32917",
"label": "e",
"name": "Pancreatic carcinoma",
"picture": null,
"votes": 67
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"__typename": "QuestionChoice",
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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",
"id": "32914",
"label": "b",
"name": "Cirrhosis",
"picture": null,
"votes": 150
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"__typename": "QuestionChoice",
"answer": false,
"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",
"id": "32916",
"label": "d",
"name": "Hepatocellular carcinoma",
"picture": null,
"votes": 165
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"comment": "is there a mistake in neutrophil count reference range?",
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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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"__typename": "QuestionChoice",
"answer": false,
"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",
"id": "32920",
"label": "c",
"name": "Irritable bowel syndrome",
"picture": null,
"votes": 462
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"__typename": "QuestionChoice",
"answer": false,
"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",
"id": "32919",
"label": "b",
"name": "Ulcerative colitis",
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"__typename": "QuestionChoice",
"answer": false,
"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",
"id": "32921",
"label": "d",
"name": "Anxiety",
"picture": null,
"votes": 32
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"__typename": "QuestionChoice",
"answer": false,
"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",
"id": "32922",
"label": "e",
"name": "Coeliac disease",
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"__typename": "QuestionChoice",
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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",
"id": "32918",
"label": "a",
"name": "Crohn's disease",
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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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"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. 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"learningPoint": "Bloody diarrhea is the cardinal symptom of ulcerative colitis, an inflammatory bowel disease that causes chronic inflammation and ulcers in the colon and rectum, often accompanied by abdominal pain, urgency, and weight loss.",
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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": "Pancreatic cancer classically presents as painless jaundice. There can be some accompanying generalised, nonspecific signs of epigastric or back pain. Painless obstructive jaundice is more likely to occur in tumours of the head of the pancreas. Risk factors for pancreatic cancer include smoking and high alcohol intake, as well as poor diet, diabetes and family history",
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"label": "a",
"name": "Pancreatic cancer",
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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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"name": "Liver cirrhosis",
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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",
"id": "32931",
"label": "d",
"name": "Primary biliary cholangitis",
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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",
"id": "32930",
"label": "c",
"name": "Nonspecific lower back pain",
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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",
"id": "32932",
"label": "e",
"name": "Hepatocellular carcinoma",
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"__typename": "QuestionComment",
"comment": "Why tanned skin?",
"createdAt": 1655378303,
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"comment": "Tanned and Jaundice are not the same.",
"createdAt": 1673019380,
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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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"comment": "yeah was expecting it to be haemachromatosis or something",
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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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"question": "A 56-year-old woman presents to her GP because her friends tell her that she looks tanned but hasn't been on holiday recently. On further questioning, she admits to some mild back pain, on and off for the last few months, which she has put down to her new exercise regime. She smokes 20-a-day and drinks alcohol \"at weekends\". On examination, she has scleral icterus and appears to be tanned.\n\nWhat is the most likely diagnosis?",
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"explanation": "Anticentromere antibodies are found to be positive in approximately 80% of patients with CREST syndrome. (CREST syndrome stands for calcinosis, Raynaud's phenomenon, (o)esophageal dysfunction, sclerodactyly and telangiectasia). This patient is displaying symptoms, signs and risk factors of primary biliary cholangitis, therefore, anticentromere antibodies are unlikely to be positive. However, CREST syndrome is a common risk factor for developing primary biliary cholangitis",
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"explanation": "Roughly 35% of primary biliary cholangitis patients will be positive for antinuclear antibodies, however these are less specific than antimitochondrial antibodies",
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"explanation": "This patient is presenting with symptoms, signs and risk factors of primary biliary cholangitis. This is an autoimmune disease that can lead to primary biliary cirrhosis (which primary biliary cholangitis used to be called but is now only used in the late stages). It is often found incidentally, as it is often asymptomatic in the early phases. Approximately 90% of affected individuals will be positive for antimitochondrial antibodies",
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"explanation": "Anti-Jo antibodies are most likely to be positive in polymyositis and dermatomyositis. These both lead to problems predominantly of the connective tissues. Therefore, anti-Jo antibodies are unlikely to be positive in this case",
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"explanation": "Anti-Ro antibodies are most likely to be positive in Sjogren's syndrome, or less commonly Systemic Lupus Erythematosus (SLE). Sjogren's syndrome is a common feature of the history of individuals who present with primary biliary cholangitis. However, in this case, the patient has fatigue, pruritus and hepatomegaly, which all suggest primary biliary cholangitis rather than Sjogren's syndrome",
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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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"question": "A 66-year-old woman presents to her GP with increasing fatigue and pruritus. On examination, hepatomegaly is present. She has a past medical history of obesity, hyperthyroidism and coeliac disease. \n\nYou suspect a diagnosis of Primary Biliary Cholangitis. Which of the following blood tests will be most specific to this condition?",
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"explanation": "Opiates should be avoided in migraine headache",
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"name": "Co-codamol 30/500mg",
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"__typename": "QuestionChoice",
"answer": true,
"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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"name": "Ibuprofen 400mg",
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"__typename": "QuestionChoice",
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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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"name": "Prochlorperazine 3mg",
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"explanation": "Propranolol is used for migraine prophylaxis, with a target dose of 80mg twice daily",
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"name": "Propranolol 80mg",
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"__typename": "QuestionChoice",
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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",
"id": "32940",
"label": "c",
"name": "Aspirin 300mg",
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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": "# 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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"explanation": "Ovarian cancer comes under category 1 in the UK Medical Eligibility criteria (UKMEC), therefore, they recommend unrestricted use",
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"comment": "According to Quesbook:\n\nAdvantages of a contraceptive outweigh the disadvantages (UKMEC 2)\nInitiation after current or past history of MI or stroke, multiple risk factors for arterial cardiovascular disease\n\nalso, cancer is said to be in UKMEC4 (absolute contraindications)",
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"explanation": "# Summary\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive containing synthetic oestrogen and progestogen. It works by inhibiting ovulation, thickening cervical mucus, and altering the endometrium to prevent fertilisation and implantation. Indications for COCP use include contraception, menstrual cycle regulation, and treatment of dysmenorrhea, menorrhagia, acne, and hirsutism. Contraindications are categorised by UKMEC criteria, detailed in this chapter. \n \n# Definition\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive. It contains synthetic versions of the female hormones oestrogen and progestogen. \n \n\n# Mechanism of Action\n \n\n* **Inhibition of Ovulation:** The COCP contains synthetic versions of the hormones oestrogen and progestogen. These hormones together suppress the release of gonadotrophins (LH and FSH) from the pituitary gland, preventing the maturation and release of an egg from the ovaries.\n \n\n* **Thickening of Cervical Mucus:** The progestogen component of the COCP increases the viscosity of cervical mucus, making it more difficult for sperm to enter the uterus and fertilise an egg.\n \n\n * **Alteration of the Endometrium:** The COCP induces changes in the lining of the uterus (endometrium), making it less suitable for the implantation of a fertilised egg.\n \n\n# Indications\n \n\nThere are a range of reasons for women to be recommended the oral combined contraceptive pill. For example:\n \n\n* **Contraception:** The COCP works as a long-term contraception. It is taken orally once a day, at around the same time each day. \n * **Menstrual Cycle Regulation:** The COCP can help regulate irregular menstrual cycles. \n * **Dysmenorrhea:** The COCP may be used to reduce menstrual cramps. \n * **Menorrhagia:** The COCP can decrease heavy menstrual bleeding.\n * **Acne and Hirsutism:** The COCP helps in the treatment of acne and excessive hirsutism in women, which may happen in conditions such as polycystic ovary syndrome (PCOS) or other androgen excess conditions.\n * **Premenstrual Syndrome (PMHS**: The COCP can alleviate symptoms of PMS, such as mood swings, bloating, and irritability.\n \n# Contraindications \n \nThere are numerous contra-indications to the Combined Oral Contraceptive Pill. These can be divided into absolute contraindications, known as ''UKMEC 4'', a situation where the disadvantages outweigh the advantages (UKMEC 3), a situation where the advantages outweigh the disadvantages (UKMEC 2), and a situation whereby there is no limit on that choice of contraception (UKMEC 1).\n \n\n## Absolute Contraindications to Contraception (UKMEC 4)\n \n \n * Known or suspected pregnancy\n * Hypertension with SBP ≥160 mmHg or DBP ≥100 mmHg\n * Smoker over the age of 35 who smokes >15 cigarettes a day \n * Current and history of ischaemic heart disease\n * History of stroke (including TIA) \n * Vascular disease\n * History or current VTE\n * Major surgery with prolonged immobilisation\n * Breastfeeding <6 weeks postpartum\n * Not breastfeeding and <3 weeks postpartum with other risk factors for VTE\n * Known thrombogenic mutations \n * Complicated valvular and congenital heart disease\n * Cardiomyopathy with impaired cardiac function\n * Atrial fibrillation \n * Migraine with aura (any age)\n * Current breast cancer \n * Severe (decompensated) cirrhosis \n * Hepatocellular adenoma and hepatocellular carcinoma\n * Positive antiphospholipid antibodies \n \n \n \n## Disadvantages of a contraceptive outweigh the advantages (UKMEC 3)\n \n * Obesity (BMI ≥35 kg/m2)\n * Multiple risk factors for cardiovascular disease (e.g. smoking, diabetes mellitus, hypertension, obesity, dyslipidaemia) \n * Well controlled hypertension, and hypertension with SBP >140-159 mmHg or DBP <90-99 mmHg\n * Smoker over age of 35 who smokes <15 cigarettes a day, or anyone over age of 35 who stopped smoking <1 year ago\n * Family history of thrombosis before 45 years old\n * Not breastfeeding and <3 weeks postpartum without other risk factors for VTE\n * Not breastfeeding and between 3-6 weeks postpartum with other risk factors for VTE\n * Organ transplant with complications (e.g. graft failure, rejection) \n * Immobility (unrelated to surgery)\n * Migraine without aura (any age) [applies to *continuation* of COCP]\n * History (≥5 years ago) of migraine\nwith aura (any age) \n * Undiagnosed breast mass or symptoms [applies to *initiation* of COCP] \n * Carriers of known gene mutations associated with breast cancer\n * Past breat cancer \n * Diabetes mellitus with nephropathy, retinopathy, neuropathy or other vascular complications \n * Symptomatic gall bladder disease treated medically or currently active \n * Past COCP associated cholestasis \n * Acute viral hepatitis [applies to *initiation* of COCP]\n \n \n \n## Advantages of a contraceptive outweigh the disadvantages (UKMEC 2)\n \n * Smokers under the age of 35, and people aged over 35 who stopped smoking over 1 year ago \n * Obesity (BMI ≥30–34 kg/m2) \n * Family history of VTE in first-degree relative aged ≥45 years\n * History of raised blood pressure in pregnancy \n * Breast feeding between 6 weeks-6 months postpartum\n * Not breastfeeding and between 3-6 weeks postpartum without other risk factors for VTE\n * Uncomplicated organ transplant \n * Known dyslipidaemia \n * Major surgery without prolonged immobilisation \n * Superficial venous thrombosis \n * Uncomplicated valvular and congenital heart disease\n * Cardiomyopathy with normal cardiac function \n * Long QT syndrome \n * Non-migrainous headaches [applies to *continuation* of COCP]\n * Migraine without aura [applies to *initiation* of COCP] \n * Idiopathic intracranial hypertension \n * Unexplained vaginal bleeding\n * Cervical cancer \n * Undiagnosed breast mass or symptoms [applies to *continuation* of COCP]\n * Insulin-dependent diabetes mellitus without vascular disease \n * Symptomatic gall bladder disease treated through cholecystectomy, or asymptomatic gall bladder disease, or history of pregnancy-related cholestasis \n * Acute viral hepatitis [applies to *continuation* of COCP]\n * Inflammatory bowel disease \n * Sickle cell disease \n * Rheumatoid arthritis\n * SLE without antiphospholipid antibodies \n \n\n \n\n# Side-effects and Complications\n \n**Common Side-Effects:**\n \n\n * Breast tenderness \n * Abdominal discomfort, nausea diarrhoea \n * Headaches\n * Mood changes\n * Reduced libido \n \n\n**Rare but Serious Side-Effects:**\n \n\n * Embolism or thrombus, including: DVT and PE, stroke, myocardial infarction\n * Increased risk of breast cancer\n * Increased risk of cervical cancer \n \n\n \n\n# Follow-up\n\nArrange follow up 3 months following initial prescription of a COCP, and annually thereafter.\n \n\nAt follow-up, ensure to: \n \n\n * Check blood pressure and BMI. \n * Ask about headaches (including migraine). \n * Check for risk factors that may be contraindicators to COCP (as per UKMEC criteria). \n * Enquire about side-effects. \n * Enquire about how woman is taking the COCP (i.e. adherence). \n \n\n \n\n# Missed Pill Rules\n \n\n**Missed One Pill:**\n \n\n* Advise patient to take the pill as soon as possible, even if it means taking two pills in one day.\n* * Continue taking the rest of the pack as usual.\nNo additional contraception needed if this is the only pill missed in the pack.\n \n\n**Missed Two or More Pills in Week 1 (Days 1-7):**\n \n\n * Advise patient to take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * Use additional contraception for the next 7 days.\n * If they had unprotected sex during this week, seek emergency contraception.\n \n\n**Missed Two or More Pills in Week 2 (Days 8-14):**\n \n\n * Take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n\n**Missed Two or More Pills in Week 3 (Days 15-21):**\n \n\n* Finish the active pills in the current pack, then start a new pack immediately without taking the usual 7-day break.\n* No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n# NICE Guidelines \n \n\n[Click here to view NICE Guidelines on COCP](https://cks.nice.org.uk/topics/contraception-combined-hormonal-methods/management/combined-oral-contraceptive/)\n \n \n# References\n \n[Click here to see the UKMEC summary sheet on contraception](https://www.fsrh.org/standards-and-guidance/documents/ukmec-2016-summary-sheets/)",
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"question": "A 19-year-old patient visits her GP to talk about different types of contraception. She is keen to start the combined oral contraceptive pill (COCP).\n\nWhich of these would be a contraindication for this patient to start the COCP?",
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"explanation": "This is the correct answer. Guidelines for progesterone only pills differ, depending on the pill. For the traditional POP you are not protected against pregnancy if it is more than 3 hours late, and with the desogestrel pill if you are more than 12 hours late. Therefore, whichever pill the patient was on in this scenario the advice remains the same. Take the missed pill as soon as possible, take that day's pill at the normal time, and use additional contraception for 48 hours",
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"label": "a",
"name": "Take the missed pill as soon as possible and then continue taking the rest of the pills as normal. They should advise the patient to use additional contraception, such as condoms, for the next 48 hours",
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"explanation": "The advice is not to skip the missed pill but to take it as soon as possible. Only take one pill as soon as possible - if more than 1 pill was missed do not take multiple. Additional contraception is advised for the next 48 hours because this is the time it takes for the cervical mucus to re-thicken",
"id": "32955",
"label": "c",
"name": "Skip out the missed pill but continue to take the rest of the pills as normal. They should advise the patient to use additional contraception, such as condoms, for the next week",
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"explanation": "Additional contraception is advised for the next 48 hours because this is the time it takes for the cervical mucus to re-thicken",
"id": "32956",
"label": "d",
"name": "Take the missed pill as soon as possible and then continue taking the rest of the pills as normal. They should advise the patient to use additional contraception, such as condoms, for the next week",
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"votes": 651
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"__typename": "QuestionChoice",
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"explanation": "The advice is not to skip the missed pill but to take it as soon as possible. Only take one pill as soon as possible - if more than 1 pill was missed do not take multiple",
"id": "32954",
"label": "b",
"name": "Skip out the missed pill but continue to take the rest of the pills as normal. They should advise the patient to use additional contraception, such as condoms, for the next 48 hours",
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"__typename": "QuestionChoice",
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"explanation": "The advice is not to skip the missed pill but to take it as soon as possible. Only take one pill as soon as possible - if more than 1 pill was missed do not take multiple. The patient will need additional contraception for the next 48 hours to allow time for the cervical mucus to re-thicken",
"id": "32957",
"label": "e",
"name": "Skip out the missed pill but continue to take the rest of the pills as normal. The patient does not need to take additional contraception",
"picture": null,
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"comment": "attatched quesbook is for cocp",
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"explanation": "# Management of missed combined oral contraception pills\n\n\nIf patients are sick (vomit) within 3 hours of taking a combined pill, or within 2 hours of taking a progestogen-only pill, it probably will not have been absorbed by their body. Patients should take another pill straight away.\nAs long as they're not sick again, they will still be protected against pregnancy.\nPatient should be advised to take their next pill as usual.\n\n\nThe pill free week is the 7 days between taking packets of pills. There is occasionally a breakthrough bleed, a small bleed similar to a period, however the absence of a breakthrough bleed does not indicate pregnancy.\n\n\nMissed pill rules:\n\n\n- If pills are missed in week 1: use emergency contraception if she had UPSI in pill free interval for 1 week\n\n\n- If pills are missed in week 2: no need for emergency contraception\n\n\n- If pills are missed in week 3: Take the last pill that was missed, finish the current pack and start the next pack immediately after.\n\n\n# References\n\n\n[Click here to see information on NICE about missed pills](https://cks.nice.org.uk/topics/contraception-combined-hormonal-methods/management/combined-oral-contraceptive/#missed-coc-pills-except-qlaira-zoely)",
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"question": "An 18-year-old woman attends a GP appointment; she is worried because she missed the time for her progesterone only pill (POP) and she is now 22 hours late. She has not had sex in the meantime.\n\nWhat should the GP advise?",
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"explanation": "Guttate psoriasis also presents with salmon pink plaques, most commonly on the torso. It is usually preceded by a respiratory infection 2-3 weeks previously. However, there is not usually a herald patch associated with guttate psoriasis",
"id": "32959",
"label": "b",
"name": "Guttate psoriasis",
"picture": null,
"votes": 657
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"explanation": "Pityriasis rosea typically presents with a \"herald patch\". This can be preceded by prodromal symptoms such as fever or malaise. After 1-2 weeks, the secondary rash will appear, which is usually on the trunk and arms. This is symmetrical and classically described to be in the shape of a Christmas tree. Pityriasis rosea is usually self-limiting, is non-contagious and generally improves within 6 weeks. However, patients may require symptomatic treatment",
"id": "32958",
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"name": "Pityriasis rosea",
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"explanation": "Erythema multiforme is a hypersensitivity reaction, usually to an infection or drugs. The rash starts peripherally and moves centrally, therefore, is unlikely in this case. The rash is made up of \"target lesions\", which are made up of concentric rings",
"id": "32960",
"label": "c",
"name": "Erythema multiforme",
"picture": null,
"votes": 379
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"explanation": "Lichen planus is a skin disease with an unknown origin. It comprises pruritic, papular eruptions, most commonly on the genitals, flexor surfaces or mucous membranes. Therefore, it is unlikely in this patient",
"id": "32962",
"label": "e",
"name": "Lichen planus",
"picture": null,
"votes": 106
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"explanation": "Tinea corporis is a dermatophytosis (tinea) infection that affects the trunk and arms. Dermatophytes are a group of fungi causing lesions that are usually annular, scaly and have a raised edge. Herald patches are not associated with tinea corporis",
"id": "32961",
"label": "d",
"name": "Tinea corporis",
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"votes": 171
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"explanation": "# Summary\n\nPityriasis rosea is a common rash that is characterized by a preceding **herald patch** - a single, large, discoid (coin-shaped), erythematous patch. This patch classically has a 'collarette' of scale just inside the edge of the lesion. A few days later a widespread rash appears across the trunk consisting of multiple small, erythematous, scaly patches (similar but smaller than the herald patch). These lesions are classically distributed across the trunk in a **'christmas tree' pattern**. There are associations with viral infections and drugs. The condition is self-limiting and resolves without any treatment.\n\n# Definition\n\nA self-limiting rash that resolves after 10 weeks characterised by a herald patch and subsequent fir-tree pattern eruption\n\n# Pathophysiology\n\nTriggers of pityriasis rosea:\n\n- Viruses: such as HHV6/7, COVID-19, and Flu\n- Drugs: such as gold, ACEi, penicillamine, and biologics. \n- Many vaccines: BCG, hepatitis B, and pneumococcal. \n\t\n# Clinical Features\n\n- Usually, a few days after a viral infection e.g. an URTI, the patient presents with a 'herald patch.'\n- This is a red-pink oval/discoid plaque with a peripheral colarette of scale on the trunk or upper arm/thigh. It may be misdiagnosed as ringworm.\n- 1-20 days later, a similar widespread eruption (but the individual lesions may be smaller) occurs on the body that follows a fir tree (Christmas tree) pattern appears, with the long axis of the lesions sweeping from back to front as if following Langer's lines.\n- In most cases, there are virtually no symptoms except for the rash.\n\n[lightgallery]\n[lightgallery1]\n[lightgallery2]\n\n\n# Treatment\n\n- 25% patients may have intense pruritus. Antihistamines, emollients, and topical steroids may be of use in these patients. It is self-limiting and will resolve on its own. \n\n# NICE Guidelines\n\n[Click here for NICE CKS on pityriasis rosea](https://cks.nice.org.uk/topics/pityriasis-rosea/)",
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"question": "An 18-year-old female sees her GP with an itchy rash. Two weeks previously the patient had a fever and noticed a 5cm diameter, oval, salmon pink patch near her umbilicus. On examination, the rash now covers the majority of her torso. It is made up of multiple millimetre to centimetre wide, salmon pink patches.\n\nWhat is the most likely diagnosis?",
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"explanation": "Although there are signs of consolidation on the chest X-ray, there is concern that this could be due to an underlying malignancy rather than a persistent infection, therefore, the patient should be urgently referred",
"id": "32965",
"label": "c",
"name": "Admittance to A&E for intravenous antibiotics",
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"explanation": "The patient is at risk of developing chronic obstructive pulmonary disease (COPD). Therefore, salbutamol may be an appropriate treatment. However, there is concern that there is an underlying malignancy causing the patient's symptoms in this case. Therefore, the 2-week wait is the most appropriate next step at this stage",
"id": "32967",
"label": "e",
"name": "Salbutamol prescription",
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"explanation": "The British Thoracic Society advise that all patients who have continuing symptoms of pneumonia or are at risk of an underlying malignancy should have a follow up chest X-ray after 6 weeks. In up to 10% of pneumonias, there is an underlying malignancy. If therefore, the consolidation has not cleared on chest X-ray after 6 weeks, the patient should be referred to respiratory via the 2 week wait pathway",
"id": "32963",
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"name": "2 week-wait referral to respiratory",
"picture": null,
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"explanation": "Although there are signs of consolidation on the chest X-ray, there is concern that this could be due to an underlying malignancy rather than a persistent infection; therefore, the patient should be urgently referred",
"id": "32964",
"label": "b",
"name": "A further course of oral antibiotics",
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"__typename": "QuestionChoice",
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"explanation": "The patient is at risk of developing chronic obstructive pulmonary disease (COPD). Therefore, spirometry testing would be an appropriate investigation. However, in this case, there is concern that there is an underlying malignancy causing the patient's symptoms. Therefore, the 2-week wait is the most appropriate next step at this stage",
"id": "32966",
"label": "d",
"name": "Spirometry testing",
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"explanation": "# Summary\n\nLung cancers are divided into two main subtypes: small cell and non-small cell, with small cell lung cancers being more aggressive and incurable. Types of non-small cell lung cancer include squamous cell and adenocarcinomas, with several rarer subtypes. Most cases of lung cancer are linked to smoking. Lung cancers may present with chest symptoms such as cough, breathlessness or haemoptysis, systemic symptoms of weight loss and anorexia or symptoms of metastatic disease such as bone pain or seizures. Chest X-ray is the initial investigation of choice, followed by CT chest and a biopsy. Staging scans are done after diagnosis to help plan treatment. Management can be curative or palliative depending on the stage of the cancer, the subtype and the patient’s overall health. It may include chemotherapy, radiotherapy, immunotherapy, targeted therapies to specific mutations and surgery. \n\n\n# Definition\n\nLung cancer refers to a primary malignancy arising from the lung parenchyma or the bronchi. Cancers are classified as small cell (SCLC) or non-small cell (NSCLC), with 80% being non-small cell. The main histological subtypes of NSCLC are squamous cell cancers and adenocarcinomas.\n\n# Epidemiology\n\nLung cancer makes up the largest proportion of cancer deaths of any tumour type, with nearly 35,000 deaths per year in the UK (21% of all cancer deaths). It is the second most common cancer in both males and females (after prostate and breast respectively). \n\nIncidence is strongly related to age, with the highest rates in people aged over 75 years old. Although non-smokers can also get lung cancer, 86% of cases are linked to smoking and so the majority of cases are felt to be preventable.\n\n# Aetiology\n\nRisk factors for lung cancer include:\n\n- Tobacco smoking (e.g. cigarettes, pipes, cigars)\n- Passive smoke exposure\n- Occupational exposures (e.g. beryllium, cadmium, arsenic, asbestos, silica)\n- Radon exposure\n- Family history of lung cancer\n- Radiation to the chest (e.g. in lymphoma treatment)\n- Air pollution\n- Immunosuppression (e.g. HIV, medications)\n- Increasing age\n\n# Classification\n\nLung cancers are classified by the cell of origin of the malignancy. Small cell cancers come from neuroendocrine cells of the lung. Non-small cell cancers are split into adenocarcinomas (coming from alveolar type 2 epithelial cells), squamous cell carcinomas (coming from basal epithelial cells) and large cell carcinomas (which come from a variety of epithelial cells). There are also rarer subtypes of lung cancer such as sarcomatoid or salivary gland-type lung cancers which come under the NSCLC umbrella.\n\nStaging is also an important way to classify lung cancers depending on how advanced they are. TNM (tumour, node, metastasis) staging is used to describe how large the tumour is and where it has spread to. This can then be used to classify lung cancers into stage 1 to 4, where stage 1 is localised and small (under 4cm), stages 2 and 3 are locally advanced and stage 4 is metastatic. \n\n# Signs and symptoms\n\n**Symptoms include:**\n\n- Persistent cough\n- Haemoptysis\n- Dyspnoea especially on exertion\n- Chest pain\n- Weight loss\n- Recurrent chest infections, or infections resistant to treatment\n- Anorexia\n\n**Signs include:**\n\n- Cachexia\n- Finger clubbing\n- Lymphadenopathy (supraclavicular or persistent cervical)\n- If there is lung collapse due to an obstructing tumour - absent breath sounds, trachea deviated towards side of collapse\n- If there is a malignant pleural effusion - stony dull on percussion, decreased breath sounds over affected area\n\n**Other signs and symptoms related to paraneoplastic presentations of lung cancer:**\n\n- **Cushing syndrome** - usually SCLC producing ectopic ACTH, presents with dorsal cervical fat pads, truncal obesity, hypertension, striae and proximal muscle weakness\n- **Syndrome of inappropriate ADH secretion (SIADH)** - usually SCLC, present with symptoms of hyponatraemia e.g. fatigue, nausea, weakness, confusion or seizures\n- **Lambert-Eaton myasthenic syndrome (LEMS)** - usually SCLC, due to autoantibodies to presynaptic calcium channels at the neuromuscular junction develop proximal muscle weakness that improves with repeated movement, as well as autonomic effects such as dry mouth, lightheadedness, constipation, urinary symptoms and erectile dysfunction\n- **Humoral hypercalcaemia of malignancy** - usually squamous cell carcinomas (SCC) that release parathyroid hormone-related protein (PTHrP) that mimics PTH and causes hypercalcaemia, leading to symptoms of bone pain, constipation, anorexia, abdominal pain, excessive thirst and confusion\n- **Hypertrophic pulmonary osteoarthropathy** - usually adenocarcinomas which cause a periosteal reaction of bones, resulting in clubbing and arthritis especially affecting wrists and ankles\n\n# Differential diagnosis\n\n- Lung metastases from another primary cancer (e.g. breast or colorectal cancer)\n- Mesothelioma (cancer of the pleura, strongly related to asbestos exposure)\n- Tuberculosis \n- Bronchiectasis\n\n# Investigations\n\nIn primary care, patients should be referred on a 2 week wait pathway in the following situations:\n\n- Aged 40+ with unexplained haemoptysis\n- Chest X-ray findings suspicious for lung cancer\n\nUrgent chest X-rays (to be done within 2 weeks) should be done for patients aged 40+ who have one of these symptoms and have ever smoked (or two symptoms if they are never smokers):\n\n- Cough\n- Fatigue\n- Shortness of breath\n- Chest pain\n- Weight loss\n- Anorexia\n\nAn urgent chest X-ray should be considered in patients aged 40+ with any of:\n\n- Persistent/recurrent chest infection\n- Finger clubbing\n- Supraclavicular or persistent cervical lymphadenopathy\n- Thrombocytosis\n- Chest signs consistent with lung cancer (e.g. reduced breath sounds, dullness to percussion)\n\nChest X-ray findings include:\n\n- Lung mass (may be rounded or spiculated, squamous cell carcinomas may cavitate)\n- Consolidation (where there is infection downstream of the tumour obstructing an airway)\n- Bulky hilum (especially squamous cell carcinomas which often arise centrally)\n- Lobar collapse (due to bronchial obstruction, especially squamous cell carcinomas)\n- Pleural effusion\n\n[lightgallery]\n\nOther initial investigations include:\n\n- **Sputum cytology** - low sensitivity but may be of use in patients who decline or cannot have a biopsy\n- **Diagnostic thoracocentesis** - i.e. a pleural tap; if a pleural effusion is present this should be done and the fluid sent for cytology as well as cell count, microscopy, culture, glucose, LDG and protein (to determine whether it is a transudate or exudate)\n- **Blood tests** - including FBC for anaemia and thrombocytosis, U&Es for hyponatraemia and baseline renal function, LFTs for baseline liver function (may be deranged in liver metastases), bone profile for hypercalcaemia, CRP for superadded infection, clotting if interventions planned\n- **CT chest with contrast** - should be done after chest X-ray to better characterise any lesion seen and investigate for local spread\n- **Biopsy** - to confirm the diagnosis and subtype of cancer, may be done percutaneously for peripheral tumours or via bronchoscopy for central masses\n\nOnce a lung cancer is diagnosed, further investigations may include:\n\n- **Spirometry** - to assess lung function to determine if a patient is suitable for surgical intervention\n- **CT chest abdomen and pelvis** - to stage the cancer (determine if there are any metastases)\n- **PET-CT scan** - a more sensitive way to stage the cancer and look for local or distant spread\n- **CT or MRI head** - may be done as part of staging investigations if curative treatment is planned, or if there are symptoms suspicious of intracranial metastases \n\n# Management \n\n**Conservative:**\n\n- **Holistic support** and an **MDT approach** (e.g. clinical nurse specialist involvement, palliative care input for troubling symptoms or end of life care, signpost to support e.g. Macmillan groups)\n- **Smoking cessation**\n- Discussions around **advance care planning** where appropriate\n\n**Medical**\n\n- **Chemotherapy** is first line in most cases of small cell lung cancer and stage 3 or 4 non-small cell lung cancer - this is with palliative intent (i.e. not aiming to cure the disease but to prolong life and improve symptoms). It is also offered to some patients prior to (neoadjuvant) or after (adjuvant) curative surgery.\n- **Immunotherapy** is also used especially in advanced non-small cell lung cancer; this includes medications such as pembrolizumab or atezolizumab (again with palliative intent).\n- Other **targeted therapies** exist for patients with specific mutations, e.g. erlotinib for patients with advanced non-small cell lung cancers with EGFR-TK mutations.\n- **Radiotherapy** may be curative (for example in early non-small cell lung cancer) or palliative - it is often combined with chemotherapy or other treatment modalities.\n- **Supportive therapies** include analgesia, oxygen if hypoxic and opioid treatment for breathlessness.\n\n**Surgical**\n\n- **Lobectomy** is the standard curative therapy for early stage lung cancers (which can be open or thoracoscopic in approach).\n- Some small tumours can be removed with a **wedge resection.**\n- More extensive surgery such as a **pneumonectomy** (removal of a lung) may be required depending on the size and location of the tumour, however patients need to have adequate FEV1 on pre-operative spirometry to be appropriate for surgery (over 2L for a pneumonectomy).\n- All patients undergoing surgery should also have **mediastinal and hilar lymph nodes sampled** (to look for metastases) or **resected** (removed) to reduce the chances of recurrence.\n\n# Complications\n\n**Common sites of metastatic spread include:**\n\n- Lymph nodes\n- Liver - this can cause significant pain due to stretching of the liver capsule\n- Brain - may cause nausea and vomiting, headaches, seizures, personality changes, sensory or motor symptoms, dysphasia or cerebellar symptoms, depending on where in the brain is affected\n- Bones - mostly osteolytic metastases, can cause bony pain and pathological fractures; there is a risk of metastatic spinal cord compression with vertebral metastases\n- Adrenal glands - may cause flank pain and adrenal insufficiency\n- The contralateral lung or elsewhere in the ipsilateral lung\n\n**Local complications include:**\n\n- Horner’s syndrome - due to an apical (Pancoast) tumour, causes ipsilateral anhidrosis, miosis and partial ptosis\n- Superior vena cava obstruction (SCVO) - lung cancer is the commonest cause of SCVO, causing symptoms of breathlessness, dizziness, headache and swelling of the face, neck and arms. This is a medical emergency due to the risk of airway obstruction.\n- Malignant pleural effusion\n- Hoarse voice - secondary to invasion of left recurrent laryngeal nerve\n- Persistent lower respiratory tract infection due to obstructing tumour\n- Raised hemidiaphragm secondary to invasion of phrenic nerve\n- Brachial plexus injury secondary to tumour invasion from a Pancoast tumour\n\n# Prognosis\n\nOverall prognosis is poor, with an average 5 year survival rate of 17%. This is lower for small cell lung cancer and for metastatic cancers, both of which have around a 5% 5 year survival. Small cell lung cancers are aggressive and are usually metastatic at the time of presentation, hence curative treatment is not possible\n\nIn early stage cancers survival is better, with 70% of patients with stage 1 NSCLC undergoing curative surgery surviving 5 years from diagnosis.\n\n# NICE Guidelines\n\n[Lung cancer: diagnosis and management](https://www.nice.org.uk/guidance/ng122)\n\n[NICE CKS - recognition and referral of lung and pleural cancers](https://cks.nice.org.uk/topics/lung-pleural-cancers-recognition-referral/)\n\n# References\n\n[Radiopaedia - lung cancer](https://radiopaedia.org/articles/lung-cancer-3?lang=gb)\n\n[Patient UK - lung cancer](https://patient.info/doctor/lung-cancer-pro)\n\n[Cancer Research UK - lung cancer statistics](https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/lung-cancer)",
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"question": "A 65-year-old woman attends her GP due to a persistent cough. As well as coughing up green sputum, she has been having difficulty with breathlessness on exertion. She has a past medical history of type 2 diabetes mellitus, hypertension and hypercholesterolaemia. She was treated for community acquired pneumonia 6 weeks ago with oral antibiotics. She drinks approximately 8 units of alcohol per week and smokes 10-a-day. On examination, there are crackles on the lower right zone. The GP requests a repeat chest X-ray which shows persistent areas of consolidation, in line with a previous chest X-ray 6 weeks earlier.\n\nWhat is the correct next step?",
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"explanation": "Proctalgia fugax leads to intermittent severe pain localised to the rectum. It will usually completely resolve within seconds to minutes. The cause is unknown. Proctalgia fugax would not lead to spots of bright red blood on wiping",
"id": "32971",
"label": "d",
"name": "Proctalgia fugax",
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"votes": 18
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"explanation": "Internal haemorrhoids would be a differential in this case. The bright red blood on wiping and the constipation risk factor could suggest internal haemorrhoids. However, internal haemorrhoids are not severely painful, which makes anal fissure the more likely diagnosis",
"id": "32969",
"label": "b",
"name": "Internal haemorrhoids",
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"explanation": "Ulcerative colitis would be a differential for this patient due to the bright red blood on wiping. However, the pain profile is usually different. For example, abdominal pain is much more common than pain on defecation, which is a classic feature of anal fissures",
"id": "32970",
"label": "c",
"name": "Ulcerative colitis",
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"explanation": "Anal fissures are usually very painful when defecating and are classically described as like passing glass. This pain may persist for hours afterwards. Constipation is a risk factor for anal fissures. On examination, they are linear and have clear edges. Most will heal after a few weeks of conservative management; however, some will require surgical intervention",
"id": "32968",
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"explanation": "Crohn's disease would be a differential for this patient. However, the pain profile is usually different. Abdominal pain is much more common than pain on defecation, which is a classic feature of anal fissures",
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"explanation": "# Summary\n\nAnal fissures are commonly experienced by patients as severe anal pain or a tearing sensation while passing stools, persisting for hours afterward. Typical signs and symptoms include anal spasms and per rectum (PR) bleeding. Key risk factors are constipation and pregnancy. The initial management is typically conservative, including treatment of constipation and use of topical analgesics and vasodilators. For resistant cases, topical calcium channel blockers or oral medications can be used. Referral to a gastroenterologist is recommended for atypical cases or those suspected of Crohn's disease.\n\n# Definition\n\nAnal fissures are linear tears or cracks in the distal anal canal, often causing severe pain and bleeding during or after bowel movements.\n\n# Epidemiology\n\nAnal fissures are a common condition in the general population. However, they are more frequently encountered in certain groups such as those suffering from chronic constipation and pregnant women, particularly during the third trimester or post-delivery.\n\n# Aetiology\n\nAnal fissures occur due to various causes, most notably:\n\n- Constipation: Hard stools can cause tearing in the distal anal canal.\n- Pregnancy: Increased risk during the third trimester and post-delivery.\n\n# Signs and Symptoms\n\nPatients with anal fissures typically present with the following symptoms:\n\n- Severe anal pain or a tearing sensation during bowel movements, lasting for hours afterward.\n- Anal spasms reported by about 70% of patients.\n- Bright red PR bleeding typically noticed on the stool or the toilet paper.\n- Over 90% of fissures are in the posterior midline, visible on parting the buttocks.\n- In chronic cases, a sentinel pile (skin tag) may be visible.\n- In severe cases, digital rectal examination may not be possible due to pain.\n\n[lightgallery]\n\n# Differential Diagnosis\n\nThe differential diagnosis for anal fissures includes other conditions causing anal pain or bleeding, such as:\n\n- Hemorrhoids: Painful, swollen veins in the lower portion of the rectum or anus. Signs include painless bleeding during bowel movements, itching or irritation in the anal region, discomfort, swelling around the anus, and a lump near the anus.\n- Anal abscess or fistula: Symptoms include anal pain, rectal discharge, bleeding, irritation, and fever.\n- Anal cancer: Symptoms can include anal bleeding, anal itching, a lump or mass at the anal opening, pain or feeling of fullness in the anal area.\n- Inflammatory bowel disease (Crohn's disease or ulcerative colitis): Symptoms include diarrhea, rectal bleeding, abdominal cramps and pain, an urgent need to move the bowels, and weight loss.\n\n# Investigations\n\nInvestigation of anal fissures primarily involves a physical examination, including inspection of the anal area and potentially a digital rectal examination (if tolerable by the patient). Further investigations may be warranted in atypical cases or in those with potential signs of systemic disease like Crohn's disease.\n\n# Management\n\nThe management of anal fissures involves both conservative and pharmacologic strategies:\n\n- Treatment of constipation with the use of laxatives and dietary fiber.\n- Use of topical analgesics, such as lidocaine cream or jelly.\n- Application of topical vasodilators like nifedipine or nitroglycerine.\n- Second-line treatments include topical calcium channel blockers (diltiazem), or oral nifedipine / diltiazem.\n- Patients with atypical anal fissures or symptoms/signs suggestive of Crohn's disease should be referred to a gastroenterologist.\n\n# NICE Guidelines\n\n[NICE CKS - anal fissures](https://cks.nice.org.uk/topics/anal-fissure/)\n\n# References\n\n[NHS - anal fissures](https://www.nhs.uk/conditions/anal-fissure/)",
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"question": "A 31-year-old woman attends her GP due to severe pain on defecation. She describes the pain as like passing hard shards of glass. After opening her bowels, she occasionally sees bright red blood when wiping. She opens her bowels once every 2 or 3 days.\n\nWhat is the most likely diagnosis?",
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"answer": false,
"explanation": "IV gentamicin is commonly used for perioperative prophylaxis in urological surgeries",
"id": "32976",
"label": "d",
"name": "IV gentamicin",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Oral antibiotics are less appropriate than the intravenous route as antibiotic prophylaxis before a major operation",
"id": "32974",
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"name": "Oral co-amoxiclav",
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"explanation": "Intravenous antibiotic therpay is important for surgical prophylaxis in many major surgeries. Different health care systems may recommend different antibiotics for different surgeries however IV co-amoxiclav is a common regime for abdominal surgery",
"id": "32973",
"label": "a",
"name": "Intravenous co-amoxiclav",
"picture": null,
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"__typename": "QuestionChoice",
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"explanation": "Nasal mupirocin 2% (Bactroban Nasal®) is often used for MRSA eradication prior to hospital admission",
"id": "32977",
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"name": "IV mupirocin",
"picture": null,
"votes": 50
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"explanation": "This is the usual regime for suspected intra-abdominal sepsis",
"id": "32975",
"label": "c",
"name": "Intravenous amoxicillin, metronidazole and gentamicin",
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"explanation": "# Summary\n\nPeri-operative antibiotics are utilized to prevent postoperative wound infections in numerous surgical procedures, including those involving implantation of prostheses, contaminated or dirty procedures, thoracic procedures, most gastrointestinal, hepatobiliary, urological, open fracture repairs, and vascular surgeries. They are typically administered intravenously within 1 hour prior to the incision. The specifics regarding when and which antibiotics should be used are outlined in the SIGN Guideline 104.\n\n# Definition\n\nPeri-operative antibiotics are prophylactic antimicrobial agents administered during the perioperative period, specifically within 1 hour prior to the surgical incision, with the primary goal of reducing the risk of postoperative wound infections.\n\n# Aetiology\n\nThe need for peri-operative antibiotics arises from the risk of bacterial contamination during surgery, potentially leading to postoperative wound infections. This risk is exacerbated in procedures involving foreign bodies such as prosthetics, or in surgeries that involve opening body cavities, like the thorax or abdomen, which may expose the surgical field to the natural bacterial flora of these sites.\n\n# Signs and Symptoms\n\nWhile the use of peri-operative antibiotics is a preventative measure and not symptom-based, the signs and symptoms of a failed prophylaxis (i.e., a postoperative wound infection) may include:\n\n- Redness and swelling at the surgical site\n- Increased local temperature\n- Purulent discharge\n- Pain at the surgical site\n- Fever\n- Other systemic signs of infection\n\n# Differential Diagnosis\n\nDifferential diagnoses for postoperative wound infection may include:\n\n- Seroma: Fluid accumulation, typically presenting as a fluid-filled swelling at the surgical site with no signs of infection.\n- Hematoma: Accumulation of blood, presenting with a swelling or mass-like effect at the surgical site, often painful but without signs of infection.\n- Suture reaction: Localized inflammation due to the body's immune response to suture materials, often presenting with redness and swelling, but no purulent discharge or systemic signs of infection.\n\n# Investigations\n\nInvestigations related to the use and effectiveness of peri-operative antibiotics primarily focus on identifying postoperative wound infections. They may include:\n\n- Physical examination of the surgical site\n- Culture and sensitivity of wound discharge\n- Blood investigations, such as Full blood count (FBC) and inflammatory markers (CRP, ESR)\n\n# Management\n\nManagement strategies of peri-operative antibiotics focus on:\n\n- Administration of antibiotics within 1 hour before incision\n- Selection of appropriate antibiotic, taking into account the likely contaminating organisms and patient allergies\n- Review of the need for ongoing prophylaxis beyond the initial doses\n- Monitoring for signs of postoperative wound infection\n- Management of identified infections, including culture-guided antibiotic therapy\n\n# References\n\n[Click here for a summary of SIGN guideline 104 on the use of peri-operative antibiotics](https://www.nhstaysideadtc.scot.nhs.uk/Antibiotic%20site/pdf%20docs/Antibiotic%20prophylaxis%20in%20gen%20surgery.pdf)",
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"question": "A 62-year-old man is about to undergo a pancreatectomy.\n\nWhich antibiotic regime should be considered before the surgery?",
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"explanation": "NICE guidelines states that any patient with suspected acute cholecystitis should be urgently admitted to hospital. This patient has signs and symptoms highly suspicious of acute cholecystitis. They have a positive Murphy's sign (the patient stops in their inspiration due to tenderness over the right upper quadrant when palpated by the GP)",
"id": "32978",
"label": "a",
"name": "Urgent admission",
"picture": null,
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"__typename": "QuestionChoice",
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"explanation": "Liver Function Tests may be useful in aiding the diagnosis. However, there is high clinical suspicion of acute cholecystitis. Therefore, the patient requires urgent admission as they may need an urgent cholecystectomy",
"id": "32981",
"label": "d",
"name": "Urgent Liver Function Tests",
"picture": null,
"votes": 52
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"explanation": "This patient has signs and symptoms highly suspicious of acute cholecystitis. They have a positive Murphy's sign (the patient stops in their inspiration due to tenderness over the right upper quadrant when palpated by the GP). Although abdominal ultrasound is highly sensitive and specific for gallstones, the patient requires urgent admission for possible surgical treatment",
"id": "32979",
"label": "b",
"name": "Urgent outpatient abdominal ultrasound",
"picture": null,
"votes": 133
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"__typename": "QuestionChoice",
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"explanation": "This patient has signs and symptoms highly suspicious of acute cholecystitis. Although they do require antibiotic therapy and analgesia, the antibiotics will need to be intravenous and accompanied by intravenous fluids. The patient may also require urgent surgery. Therefore, this cannot be treated in the outpatient environment",
"id": "32982",
"label": "e",
"name": "Oral antibiotics, analgesia and urgent outpatient abdominal ultrasound",
"picture": null,
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"__typename": "QuestionChoice",
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"explanation": "This patient has signs and symptoms highly suspicious of acute cholecystitis. Although they do require antibiotic therapy and analgesia, the antibiotics will need to be intravenous and accompanied by intravenous fluids. The patient may also require urgent surgery. Therefore, they require urgent admission",
"id": "32980",
"label": "c",
"name": "Oral antibiotics and analgesia",
"picture": null,
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"comment": "Take the green thing out too!!",
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"explanation": "# Summary\n\nCholecystitis is the inflammation of the gallbladder, typically caused by cholelithiasis, and can present as acute or chronic. The characteristic symptoms are right upper quadrant or epigastric pain, fever, nausea, vomiting, and right upper quadrant tenderness. Murphy's sign is commonly positive. Diagnosis is primarily made with an abdominal ultrasound. Management strategies depend on the severity of the condition, with supportive care and early laparoscopic surgery being the definitive treatment. More severe cases may require intensive treatment unit (ITU) admission and urgent cholecystostomy.\n\n# Definition\n\nCholecystitis refers to the acute or chronic inflammation of the gallbladder, which is commonly precipitated by cholelithiasis, or gallstones. \nCholecystitis can be categorised into acute or chronic forms based on the duration and progression of inflammation, and into calculous or acalculous types based on the presence or absence of gallstones. \n\n# Epidemiology\n\nCholecystitis is a common gastrointestinal disease and one of the major causes of hospital admissions related to gastrointestinal disorders worldwide. It affects women more than men, with an estimated ratio of 2:1. Age is a significant risk factor, with incidence rising in individuals over 40 years of age. Other risk factors include obesity, ethnicity (higher prevalence in Hispanic and Native American populations), rapid weight loss, diabetes, pregnancy, and a family history of gallstones.\n\n# Pathophysiology\n\nCholecystitis predominantly results from the obstruction of the cystic duct by gallstones. This obstruction can lead to an infection in the gallbladder caused by organisms including:\n\n- E.coli (most common)\n- Klebsiella\n- Enterococcus\n\n# Classification\n\nCholecystitis can be classified into two main categories: acute and chronic. Additionally, cholecystitis can be further categorised based on the presence or absence of gallstones.\n\n1. **Acute Cholecystitis:** This is characterised by the sudden onset of inflammation in the gallbladder. It is often associated with the presence of gallstones, particularly when one of these stones obstructs the cystic duct, leading to a buildup of bile and subsequent inflammation. \n\n2. **Chronic Cholecystitis:** This is a long-term, smoldering inflammation of the gallbladder, usually caused by the repeated irritation of gallstones. Over time, chronic cholecystitis can lead to thickening of the gallbladder wall and a decrease in its overall function. Unlike acute cholecystitis, chronic cholecystitis may have milder and more intermittent symptoms, including recurrent abdominal discomfort after meals.\n\n3. **Calculous Cholecystitis:** This type of cholecystitis occurs when gallstones are present in the gallbladder. These stones can obstruct the cystic duct, impair bile flow, and trigger an inflammatory response. Calculous cholecystitis is the most common form of cholecystitis.\n\n4. **Acalculous Cholecystitis:** In contrast, acalculous cholecystitis develops without the presence of gallstones. It is often associated with other underlying medical conditions, such as critical illness, severe trauma, or prolonged fasting, which can lead to gallbladder stasis or ischaemia. Acalculous cholecystitis is less common but can be more severe and challenging to diagnose, as it may not present with the typical gallstone-related symptoms.\n\n\n# Signs and Symptoms\n\nPatients with acute cholecystitis present with:\n\n- Right upper quadrant/epigastric pain, which can radiate to the right shoulder tip if the diaphragm is irritated\n- Fever\n- Nausea and vomiting\n- Right upper quadrant tenderness\n- Positive Murphy's sign\n\nIn cases with associated biliary obstruction, patients may exhibit jaundice, dark urine, and pale stools. However, these are not key features of cholecystitis.\n\n# Differential Diagnosis\n\nThe differential diagnoses for cholecystitis primarily include other conditions that cause right upper quadrant pain. The key signs and symptoms for these conditions are:\n\n- **Acute pancreatitis**: Epigastric pain radiating to the back, nausea and vomiting, tenderness of the abdomen.\n- **Peptic ulcer disease**: Epigastric pain that may be relieved by eating, dark stool (melena), nausea and vomiting.\n- **Hepatitis**: Jaundice, fatigue, pale stools, dark urine, and flu-like symptoms.\n- **Right lower lobe pneumonia**: Cough, fever, shortness of breath, and right-sided abdominal pain.\n\n# Investigations\n\n* The first line investigation for suspected cholecystitis is an ultrasound examination of the abdomen, which can identify gallstones, gallbladder wall thickening, and pericholecystic fluid. \n* Alongside this, blood tests including FBC, U+Es, CRP and LFTs will help reveal if there is an underlying infection/evidence of sepsis, as well as any cholestasis\n* CT abdomen-pelvis (rarely MRI) is helpful to look for complications e.g. perforation, collections\n\n# Management\n\nThe management of cholecystitis varies depending on its subtype and the clinical circumstances. Here's a summary of management for each subtype of cholecystitis:\n\n**Acute Calculous Cholecystitis:**\n\n- **Conservative Management:** In mild cases, patients may be managed conservatively with bowel rest, fasting, and intravenous fluids to relieve symptoms.\n- **Antibiotics:** Antibiotics, often covering common pathogens like Escherichia coli and Klebsiella pneumoniae, are typically prescribed.\n- **Cholecystectomy:** The definitive treatment for acute calculous cholecystitis is laparoscopic cholecystectomy, which is recommended during the same hospital admission or within a week.\n\n**Acalculous Cholecystitis:**\n\n- **Prompt Surgery:** Acalculous cholecystitis is considered a surgical emergency, and prompt cholecystectomy is typically recommended.\n\n**Chronic Cholecystitis:**\n\n- **Elective Cholecystectomy:** For patients with chronic cholecystitis, an elective laparoscopic cholecystectomy may be performed to prevent recurrent episodes and complications.\n- **Symptomatic Management:** In some cases, patients may initially receive symptomatic management and dietary modifications, but surgery is eventually recommended.\n\nFurther research now focuses on timing of intervention, resulting in what is now known as 'hot' vs 'cold' laparoscopic cholecstectomies:\n\n**Hot Elective Cholecystectomy:**\n\n- In cases of acute cholecystitis where the patient's condition has improved with conservative management, but the inflammation is still present, an elective (\"hot\") laparoscopic cholecystectomy should be performed within 6 weeks of the acute episode.\n- This approach balances the need to address the underlying cause with allowing the patient's condition to stabilise.\n\n**Cold Elective Cholecystectomy:**\n\n- In cases of chronic cholecystitis or asymptomatic gallstones, where there is no acute inflammation or infection, an elective (\"cold\") laparoscopic cholecystectomy can be scheduled based on the patient's convenience and availability.\n- This approach avoids the urgency associated with acute inflammation.\n\nIn summary, the management of cholecystitis includes conservative measures, antibiotics, and surgical intervention, depending on the subtype and clinical circumstances. Elective laparoscopic cholecystectomy is recommended for both acute calculous cholecystitis (after symptom resolution) and chronic cholecystitis. The timing of surgery may vary, with \"hot\" cholecystectomy addressing acute inflammation and \"cold\" cholecystectomy focusing on non-urgent cases.\n\n### Complications of Laparoscopic Cholecystectomies\n\nWhile the exact prevalence can vary, complications occur in a small but significant proportion of patients undergoing cholecystectomy. Post-cholecystectomy syndrome is seen in approximately 10-15% of patients.\n\n- **Haemorrhage:** Rapid hypotension or development of a retroperitoneal haematoma. May require surgical intervention if severe.\n- **Post-cholecystectomy syndrome:** Symptoms include colicky abdominal pain, diarrhea, vague abdominal pain, and jaundice. Management is symptomatic with e.g. anti-spasmodics for pain and nausea.\n- **Bile duct injury:** Presents with dark-colored urine and stools, potentially progressing to chemical peritonitis, causing abdominal pain and distension. Sometimes this requires surgical intervention.\n- **Pneumoperitoneum:** Trapped air in the subcutaneous space can lead to subcutaneous emphysema, pneumothorax, or air embolism.\n\n# Complications\n\n\n1. **Empyema:** This occurs when the gallbladder becomes filled with pus due to a severe infection. It can lead to systemic infection and sepsis if not treated promptly.\n\n2. **Gangrenous Cholecystitis:** In severe cases of cholecystitis, the gallbladder tissue may become necrotic (dead) due to impaired blood flow. This condition is known as gangrenous cholecystitis and can lead to tissue perforation, abscess formation, or peritonitis.\n\n3. **Perforation:** Prolonged inflammation can cause the gallbladder to rupture or perforate, leading to bile leakage into the abdominal cavity. This is a life-threatening emergency requiring immediate surgery.\n\n4. **Abscess Formation:** A collection of pus can develop within or around the gallbladder, leading to an abscess. Abscesses may require drainage and antibiotic therapy.\n\n5. **Bile Duct Obstruction:** Inflammation or gallstones can cause blockage of the common bile duct, leading to jaundice, pancreatitis, or cholangitis (bile duct infection).\n\n6. **Chronic Cholecystitis Complications:** Long-term inflammation of the gallbladder may lead to scarring, thickening of the gallbladder walls, and impaired gallbladder function. This can result in chronic abdominal pain and discomfort.\n\n\n# NICE Guidelines\n\n[Click here to see the NICE guidelines on cholecystitis](https://cks.nice.org.uk/topics/cholecystitis-acute/)",
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"question": "A 55-year-old female attends her GP due to right upper quadrant pain. She has been vomiting and feels feverish. She has a past medical history of gallstones, hyperlipidaemia and obesity. On examination there is rebound tenderness over the right upper quadrant. Furthermore, when the GP rests two fingers over the right upper quadrant and asks the patient to inspire, this leads to acute tenderness and patient stopping her inspiration.\n\nWhat is the most appropriate management?",
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"explanation": "# COPD\n\nPatients with COPD are at higher risk of post-op complications than other patients because of their impaired respiratory function. It is therefore advisable to arrange the following tests before surgery:\n\n- Lung function tests\n- Chest x-ray\n- Arterial blood gas (if the patient is known to retain carbon dioxide)\n\nFurthermore, it is prudent to encourage patients to give up smoking before the operation and to start chest physio early after the operation.\n\n# Drugs to stop\n\n- **Cardiovascular drugs:** Clopidogrel should be stopped 7 days before surgery, warfarin should be (generally) stopped 5 days before surgery and instead patients should be on low molecular weight heparin until the night before, ACE inhibitors should be stopped the day before surgery.\n- **Combined oral contraceptive pill** should be stopped 4-6 weeks before surgery, and re-started at least 2 weeks after surgery (when the patient is mobile). This reduces the risk of DVT.\n\n# Patients taking steroids\nWhen the body experiences acute stress (e.g. illness, trauma, surgery), the steroid demand increases. \n\nPatients on long term steroids cannot respond to this demand because their adrenal function is suppressed.\n\nTherefore, patients who are on long term steroids usually need more steroids than usual during periods of physiological stress e.g. surgery or acute illness.\n\n\n## Management\n\nPeri-operative management is as follows:\n\n1. Switch oral steroids to 50-100mg IV hydrocortisone.\n2. If there is associated hypotension then fludrocortisone can be added.\n3. For minor operations oral prednisolone can be restarted immediately post-operatively. If the surgery is major then they may require IV hydrocortisone for up to 72 hours post-op.\n\n# Diabetes\nPeri-operative management of diabetes, both non-insulin-dependent (type 2 diabetes) and insulin-dependent (type 1 diabetes), involves careful monitoring and adjustment of medication regimens to mitigate the risk of peri-operative complications. The need for specific peri-operative management in diabetics arises due to physiological changes in response to stress (such as surgery), combined with the patient's underlying metabolic disorder. Surgical stress can induce hyperglycemia, and alterations in medication timing or dosage may be necessary due to fasting or changes in renal function.\n\n## Potential complications\n\n- **Hyperglycemia**: Characterised by blood glucose levels >180 mg/dL, symptoms include polyuria, polydipsia, and unexplained weight loss.\n- **Hypoglycemia**: Characterised by blood glucose levels <70 mg/dL, symptoms include palpitations, tremor, sweating, anxiety, and confusion.\n- **Diabetic Ketoacidosis (DKA)**: Common in type 1 diabetics, symptoms include polyuria, polydipsia, nausea, vomiting, abdominal pain, and fruity-smelling breath.\n- **Lactic Acidosis**: A potential complication of metformin use, especially in renal impairment. Symptoms include abdominal discomfort, nausea, vomiting, muscle pain, and rapid breathing.\n\n\n## Management\n\n\n| Drug | Plan |\n| ---------------------------- | ---------------------------------------------- |\n| Metformin (taken once daily) | Take during the morning of surgery |\n| DDP-IV inhibitors | Take during the morning of surgery |\n| GLP-1 analogues | Take during the morning of surgery |\n| SGLT-2 inhibitors | Omit the day of surgery due to the risk of DKA |\n\nFor insulin-dependent diabetics, key principles are:\n\n1. Schedule the patient as early on the theatre list as possible, minimising the amount of time the patient is nil by mouth.\n2. If on long-acting insulin, this should be continued but reduced by 20%.\n3. Stop any other insulin and begin sliding scale insulin infusion from when the patient is placed nil by mouth.\n4. Continue infusion until the patient is able to eat post-operatively.\n5. Switch to the normal insulin regimen around their first meal.\n\n*For some operations (particularly those that do not require contrast media) metformin does not need to be stopped, but one should always consider the risk of lactic acidosis.\n\nAfter surgery, all oral medications should generally be restarted the morning following surgery.\n\n\n\n# NICE Guidelines\n\n[NICE Guidelines on Diabetes management during the Peri-operative period](https://bnf.nice.org.uk/treatment-summaries/diabetes-surgery-and-medical-illness/)",
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"question": "An 48-year-old female was admitted to hospital due to central umbilical pain, which then moved to the right iliac fossa. She underwent an appendectomy. She has a past medical history of obesity, hypertension and type 2 diabetes mellitus. After the operation, she is started on an insulin-glucose infusion.\n\nWhen should she re-start her usual insulin medication?",
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"explanation": "Whilst many patients are treated with decompression via sigmoidoscopy, the first priority is to ensure the patient is nil by mouth and is given appropriate IV fluid replacement",
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"explanation": "If there was signs of sepsis, or if perforation was suspected, IV antibiotics may be indicated. This is suggested in the history, so the most appropriate immediate step is to administer IV fluids",
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"explanation": "Metoclopramide is a pro-kinetic antiemetic drug which may be used in the management of symptomatic partial small bowel obstruction. This patient has a large bowel obstruction",
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"explanation": "This x-ray shows the \"coffee bean\" sign indicating a sigmoid volvulus. This is typically managed using the \"drip and suck\" approach, whereby the patient is placed as nil by mouth, given IV fluids, and a nasogastric tube inserted to drain any stomach contents.",
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"comment": "Most patients with sigmoid volvulus are treated conservatively initially with decompression by sigmoidoscope and insertion of a flatus tube. I appreciate that IV fluid resus may be most appropriate management, but explanation for answer is wrong. ",
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"comment": "How is IV fluids a treatment option? You would treat with drip and suck not with the fluids so this is a daft question",
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"comment": "wait till you find out what \"drip\" means in drip and suck...",
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"comment": "Her observations are satisfactory, so fluids isn't the most appropriate option. Decompression of the volvulus would be the MOST appropriate. Poorly written and justified question ",
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"comment": "Common mistake here. You don't give fluids to resuscitate her in drip and suck, you give the fluids because you making the patient nil by mouth. Therefore, even patients with normal observations will require IV fluids",
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"explanation": "# Summary \n\nSmall bowel obstruction is a mechanical impediment in the small bowel leading to clinical symptoms such as bilious or faeculent vomiting, abdominal pain, and distension. Key causes include adhesions, intra-abdominal hernias, Crohn's disease, malignancy, and foreign body ingestion, among others. Noteworthy signs and symptoms include abdominal pain with distension, vomiting, failure to pass flatus or stool, and possible fever. Primary investigations include blood tests, abdominal and chest X-ray, CT abdomen and pelvis, and possibly a diagnostic laparotomy/laparoscopy. The management involves initial resuscitation, fluid and electrolyte correction, NG tube aspiration for decompression, potential gastrografin administration, and surgery if conservative measures fail.\n\n# Definition\n\nSmall bowel obstruction (SBO) is a mechanical disruption in the small bowel, leading to significant clinical symptoms such as bilious or faeculent vomiting, abdominal pain and distension, and complete constipation.\n\n# Epidemiology\n\nSBO is a common clinical issue seen in emergency departments worldwide. Adhesions following abdominal surgery are the leading cause, responsible for approximately 60-70% of all cases in adults. Intra-abdominal hernias, Crohn's disease, malignancy, and foreign body ingestion are other common causes. In children, intussusception, volvulus, and intestinal atresia are more common causes of SBO. The incidence of SBO tends to increase with age due to increasing rates of surgery, malignancies, and other predisposing conditions.\n\n# Aetiology\n\n## Factors outside the bowel\n\n- Adhesions\n \n - Most common cause in the Western world\n - Prior intra-abdominal surgeries increase the risk of adhesion development. The larger the operation, the higher the likelihood of adhesion formation.\n- Intra-abdominal hernia\n \n - Incarcerated hernias can precipitate acute obstruction\n\n## Factors relating to the bowel wall\n\n- Crohn's disease - stricturing (rather than fistulating) disease is what specifically causes SBO\n- Appendicitis\n\n## Factors relating to inside the bowel\n\n- Malignancy\n- Foreign body ingestion\n- Gallstone ileus\n\n## Diseases causing small bowel obstruction in children\n\n- Intussusception\n- Volvulus\n- Intestinal atresia\n- Appendicitis\n\n# Signs and Symptoms\n\nSBO typically presents with the following:\n\n- Abdominal pain with distension (Initially colicky pain that becomes continuous)\n- Bloating and vomiting (often bilious)\n- Failure to pass flatus or stool\n- History of abdominal/gynaecological surgery or hernia\n- Tympanic, high-pitched bowel sounds on examination\n- An empty rectum on examination in complete bowel obstruction\n\nPatients may also present with fever and significant fluid depletion. Peritonitis indicates severe bowel obstruction with developing complications (e.g. perforation, especially in closed-loop obstructions), necessitating urgent surgical intervention.\n\nSimple or partial SBO may still result in passing some flatus/stool and present with a mild temperature.\n\nIf untreated, SBO can progress to ischaemic or necrotic bowel, leading to perforation.\n\n\n# Differential Diagnosis\n\n- **Adhesions**: Pain, distention, bilious vomiting, constipation, history of previous surgeries.\n- **Intra-abdominal hernia**: Pain, distention, inability to pass flatus or stool, a palpable mass in the abdomen.\n- **Crohn's Disease**: Abdominal pain, diarrhea, weight loss, fatigue, fever.\n- **Malignancy**: Abdominal pain, weight loss, altered bowel habits, possible presence of blood in the stool.\n- **Foreign body ingestion**: Abdominal pain, possible history of foreign body ingestion, altered bowel habits.\n- **Gallstone ileus**: Abdominal pain, distention, bilious vomiting, history of gallstones or cholecystitis.\n- **Paralytic ileus**: Abdominal pain, distension and absent bowel sounds, often a post-operative complication\n\n# Investigations\n\n\nIn a patient presenting with potential intestinal obstruction, peritonitis is a worrisome sign and the consideration to transfer to theatre must be considered.\n\nBasic investigations include:\n\n- Basic blood tests including FBC, U+Es, and lactate\n - FBC (To identify leukocytosis or anaemia)\n - U+Es (To detect organ dysfunction or signs of hypovolaemia)\n - Lactate (To establish if there is bowel ischaemia or necrosis, though it can be falsely low due to liver metabolism)\n - Amylase (To rule out acute abdomen conditions)\n- Abdominal and chest X-ray\n - Performed in an upright position to detect pneumoperitoneum\n - Absence of air in the rectum can indicate complete obstruction\n\n \n| Feature | Small Bowel Obstruction (SBO) | Large Bowel Obstruction (LBO) |\n|--------------------------------|-------------------------------|------------------------------|\n| **Bowel Wall Thickness** | May be mildly thickened | Often markedly thickened |\n| **Valvulae Conniventes** | May be seen (small intestine) | Not typically seen (large intestine) |\n| **Gas Patterns** | Central or diffuse gas pattern | Peripheral or haustral pattern |\n| **Luminal Air Fluid Levels** | Commonly seen | Less frequently seen |\n| **Stool in Colon** | Minimal or absent | Often present |\n| **\"Bird's Beak\" Sign** | Absent | May be seen in LBO (sigmoid volvulus) |\n| **Peritoneal Fluid** | May be seen due to irritation | Less common unless perforation occurs |\n\n\n[lightgallery]\n\n[lightgallery1]\n\nIn the absence of peritonitis and given the patient's stable condition, the following investigations may be performed:\n\n- CT abdomen and pelvis\n - Best diagnostic test for identifying the underlying cause, the site of obstruction, and whether it's a partial vs. complete obstruction\n- Small bowel contrast study using gastrograffin\n - Used as a therapeutic measure in partial SBO\n - Presence of contrast in rectum 24 hours after ingestion signifies a resolving partial SBO, reducing the need for surgery\n- MRI abdomen\n - Comparable to CT scan, it is useful in young patients to avoid exposure to ionising radiation\n- US abdomen\n - Not as reliable as CT, but can be used in children to avoid ionising radiation exposure\n- Diagnostic laparotomy/laparoscopy\n - Used to distinguish between partial and complete obstruction if imaging doesn't provide clear evidence\n\n# Management\n\n- Begin with resuscitation protocols (ABCDE)\n- Correct fluid and electrolyte imbalances to reduce operative risk before surgery for obstruction\n- Fluid resuscitation and NG tube to aspirate content for decompression ('Drip and suck')\n- Gastrografin can be administered as both a diagnostic and therapeutic measure in cases of partial obstruction. The presence of gastrografin in the rectum 24 hours post-administration indicates a resolving partial SBO, reducing the need for surgical intervention.\n- If conservative measures fail, consider surgery. The type of surgery depends on the cause and may include:\n - Adhesionolysis\n - Bowel resection\n - Closure of hernias\n - Tumour resection\n",
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"explanation": "# Summary\n \n\nLung-related illnesses in HIV patients are multifaceted with numerous differential diagnoses including bacterial infections, bronchitis, pneumonia, Pneumocystis pneumonia (PCP), and various fungal infections like Cryptococcal, Histoplasmosis, and Aspergillus. Key signs and symptoms can include upper respiratory tract infection symptoms, COPD-like exacerbations, fever, weight loss, and nonspecific presentations. Investigations primarily include clinical examination and chest radiographs, which may often be atypical. Management strategies typically encompass the use of antimicrobials, including antibacterials and antifungals, adjusted according to the specific pathogen involved.\n \n\n# Definition\n \n\nLung-related illnesses in HIV patients are a group of diseases that affect the lungs of individuals with the Human Immunodeficiency Virus (HIV). These illnesses are frequently the result of the compromised immune system in these patients, leading to an increased susceptibility to infections. \n \n\n \n\n# Aetiology\n \n\nThe aetiology of lung-related illnesses in HIV patients is multifactorial, typically including bacterial, viral, and fungal pathogens that take advantage of the weakened immune system. Other factors such as smoking, drug abuse, and co-infections with other diseases like tuberculosis can increase the risk of lung-related illnesses.\n \n\n# Differential diagnosis\n \n\n| | Clinical features | Key investigations | CD4 count (cells/microlitre) |\n|---|---|---|---|\n|**Bronchitis** |Cough, wheeze, shortness of breath |Chest X-ray shows no focal consolidation; sputum culture | |\n| **Pneumonia** | Productive cough, chest pain, shortness of breath | Chest X-ray showing focal consolidation; sputum culture | |\n| **Pneumocystis pneumonia** | Fever, dry cough, shortness of breath, fatigue, desaturation on exertion | Chest X-ray showing ground-glass opacity in a perihilar distribution (can also be normal); CT showing more detailed changes; induced sputum culture | <350 |\n| **Cryptococcal infection** | Asymptomatic in some cases, otherwise presenting with fever, cough, shortness of breath | Variable chest X-ray features; sputum cultures | <200 |\n| **Histoplasmosis** | Fever, weight loss, shortness of breath | Chest X-ray: widespread nodules; sputum culture | <200 |\n| **Aspergillus** | Nonspecific including fever, cough, chest pain, haemoptysis | Chest X-ray, HRCT showing nodules, consolidation and infiltrates; sputum culture |\n| **Mycobacterium tuberculosis** | Cough, shortness of breath, haemoptysis and systemic symptoms of infection. Disseminated infection may cause meningitis or adrenal suppression | Chest X-ray showing fibronodular opacities in upper lobes; sputum acid-fast bacilli smear & culture; NAAT | <400 |\n \n\n# Investigations\n \nAssessment should follow a structured approach, including:\n\n- Full history including symptoms and past medical history\n- Physical examination including respiratory examination\n- Bedside tests including observations and pulse oximetry after walking short distances\n- Laboratory tests: blood tests (FBC, U&E, CRP, viral load, CD4 count), sputum cultures\n- Imaging: chest X-ray first line, may be followed by CT chest\n- Invasive tests may be indicated including bronchoscopy or lung biopsy \n\n# Management\n \n\nManagement of lung-related illnesses in HIV patients involves treating the specific pathogen causing the illness. This can include antibacterials for bacterial infections, antifungals for fungal infections (fluconazole for cryptococcal infections, liposomal amphotericin for histoplasmosis and aspergillosis), and co-trimoxazole for pneumocystis pneumonia. Supportive care, including oxygen therapy and respiratory support, may be required. \n \n\nLong-term management also involves optimising the patient's antiretroviral therapy to improve immune function.\n \n# References\n\n[European Respiratory Journal: Pulmonary infections in HIV-infected patients: an update in the 21st century](https://publications.ersnet.org/content/erj/39/3/730)\n\n[Radiopaedia: HIV/AIDS (pulmonary and thoracic manifestations)](https://radiopaedia.org/articles/hivaids-pulmonary-and-thoracic-manifestations-1?lang=gb#:~:text=Pulmonary%20and%20thoracic%20manifestations%20of,also%20play%20a%20significant%20role.)\n\n[Radiology of HIV/AIDS: HIV/AIDS related respiratory diseases](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7121050/)\n\n[BMJ Best Practice: Pulmonary tuberculosis](https://bestpractice.bmj.com/topics/en-gb/165?q=Pulmonary%20tuberculosis&c=suggested)\n\n[BMJ Best Practice: Cryptococcosis](https://bestpractice.bmj.com/topics/en-gb/917)\n\n[BMJ Best Practice: Pneumocystis jirovecii pneumonia](https://bestpractice.bmj.com/topics/en-gb/19?q=Pneumocystis%20jirovecii%20pneumonia&c=suggested)\n\n[BMJ Best Practice: Histoplasmosis](https://bestpractice.bmj.com/topics/en-gb/918)\n\n[BMJ Best Practice: Aspergillosis](https://bestpractice.bmj.com/topics/en-gb/425)",
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"explanation": "# Summary\n \n \nGonorrhoea is a sexually transmitted infection caused by the bacterium Neisseria gonorrhoeae. Key symptoms include genital discharge, dysuria, and sometimes, tenderness of inguinal nodes in men and abnormal bleeding in women. Diagnosis is primarily made through nucleic acid amplification tests (NAAT) and culture, and confirmed by the presence of monomorphic Gram-negative diplococci within polymorphonuclear leukocytes. The recommended first-line treatment is Ceftriaxone, with a test of cure needed to evaluate disease clearance and treatment effectiveness. Untreated, gonorrhoea can lead to complications such as pelvic inflammatory disease, epididymitis, systemic infection, and increased risk of HIV/AIDS.\n \n \n# Definition\n \n \nGonorrhoea is a sexually transmitted infection (STI) caused by the gram-negative diplococcus, Neisseria gonorrhoeae.\n \n \n# Epidemiology\n \n \nGonorrhoea is the most common bacterial sexually transmitted infection worldwide. It is most prevalent among young adults, specifically those aged 15–24 years.\n \n \n# Aetiology\n \n \nThe aetiology of gonorrhoea is exclusively the bacterium Neisseria gonorrhoeae, which is a gram-negative diplococcus.\n \nRisk factors for gonorrhoea infection include:\n \n- Young adults\n- New sexual contacts\n- Inconsistent barrier contraception\n- Men who have sex with men\n- Previous STI\n- Deprivation\n \n \n# Signs and Symptoms\n \n \nClinical manifestations of gonorrhoea can vary between genders:\n \n \n- Symptoms in men: often asymptomatic, discharge, dysuria, tender inguinal nodes\n- Symptoms in women: discharge, dysuria, abnormal bleeding\n \n \nUpon examination in women, discharge from the cervical os, Skene's gland or Bartholin's gland may be observed. Gonorrhoea may also present with extragenital complications including pharyngitis, conjunctivitis, rectal pain and discharge, septic arthritis and disseminated infection.\n \n \n# Differential Diagnosis\n \n \nConditions to consider in differential diagnosis include:\n \n \n- **Chlamydia trachomatis infection**: Presents with similar symptoms such as discharge and dysuria, often co-infected with gonorrhoea.\n- **Trichomonas vaginalis infection**: May present with pruritus, dysuria, and malodorous discharge.\n- **Bacterial vaginosis**: Characterised by a fishy-smelling discharge, increased vaginal pH and positive 'whiff' test.\n- **Candidiasis**: Symptoms include pruritus, burning sensation and thick, white, 'cottage cheese' like discharge.\n \n \n# Investigations\n \n \nDiagnostic modalities for gonorrhoea include:\n \n \n- Self-taken vulvovaginal swab in women or self-obtained first pass urine in men; self-obtained rectal swab; or clinician-obtained endocervical or penile swab\n- Microscopy revealing monomorphic Gram-negative diplococci within polymorphonuclear leukocytes\n- Nucleic acid amplification tests (NAAT)\n- Culture & sensitivities\n \n \n# Management\n \nAll patients should be referred to a genito-urinary medicine clinic or local specialist services for treatment, partner notification and screening for other STI's.\n \n- People who are systemically unwell should be admitted, and those with complications should be referred to the appropriate specialty.\n- The mainstay of treatment for gonorrhoea is antibiotics. Ideally antibiotics should be prescribed after culture results but sometimes this is not practicable. \n- Current guidelines recommend Ceftriaxone as the first-line treatment. This is given as a single intramuscular injection. \n- Alternative treatments include intramuscular gentamicin or oral cefixime, both with azithromycin orally. \n- Ciprofloxacin should only be considered when sensitivities are known and there are no suitable alternative antibiotics.\n \nFor pregnant or breastfeeding women, a single dose of intramuscular ceftriaxone or oral azithromycin should be used.\n \nFor all patients following treatment, a test of cure is essential to monitor disease clearance and assess the effectiveness of the chosen antibiotic regimen.\n \n \n# Complications\n \n \nIf untreated, gonorrhoea can lead to serious complications, including:\n \n \n- Infertility in women due to pelvic inflammatory disease (PID), which may result in scarring of the tubes and an increased risk of pregnancy complications\n- Infertility in men due to epididymitis caused by the spread of gonorrhoea to the epididymis\n- Disseminated infection that may affect joints and other areas of the body, leading to fever, rash, skin sores, joint pain, swelling and stiffness\n- Increased susceptibility to human immunodeficiency virus (HIV) infection, potentially leading to AIDS, and enhanced transmission of both diseases to partners\n \n \n# NICE guidelines\n \n[Click here to see information on NICE about gonorrhoea](https://cks.nice.org.uk/topics/gonorrhoea/)\n \n# References \n \n[Click here for BASHH guidelines on Neisseria gonorrhoeae](https://www.bashhguidelines.org/media/1238/gc-2018.pdf)",
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"question": "A 19-year-old man visits his GP due to urethral discharge and dysuria. This has been ongoing for the last week. He states that he had unprotected vaginal sex with two female partners and unprotected insertive anal sex with one male partner with over the last month.\n\nHis GP arranges for microscopy of the discharge. This showed gram-negative diplococci.\n\nWhat is the diagnosis?",
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"explanation": "Any woman (especially if 50 or over) presenting with persistent abdominal distention (or \"bloating\"), early satiety/loss of appetite, pelvic/abdominal pain, or increased urinary urgency/frequency should warrant investigation for ovarian malignancy. Unfortunately most women with ovarian cancer present late with advanced disease and so a low grade of suspicion is required to pick up on subtle symptoms. Beware of the diagnosis of IBS in middle-age and elderly patients; it rarely presents for the first time in people in these age groups and is a diagnosis of exclusion. Serum CA-125 is a tumour marker for ovarian cancer and is the _first_ test you would order in this scenario, as well as routine bloods. If CA-125 is raised, an ultrasound of the abdomen and pelvis should be arranged. If the ultrasound shows suspected ovarian malignancy, a risk of malignancy index (RMI Score) should be calculated. If RMI score is 250 or greater, they should be referred to a specialist multidisciplinary team.\n\nIn women under 40 with suspected ovarian cancer, you should also measure levels of alpha fetoprotein (AFP) and beta human chorionic gonadotrophin (beta-hCG) to screen for germ cell ovarian tumours",
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"explanation": "This is another sensible option as it is a good screening tool for abdominal and thoracic malignancies. Again, this patient's symptoms would warrant initial investigations with bloods, tumour markers, and likely subsequent ultrasound abdomen pelvis prior to full cross-sectional imaging. The question asks for the most appropriate _next_ investigation and we must start with simple investigations before exposing this patient to potentially unnecessary radiation. If the patient's CA-125 were raised and the ultrasound showed signs of malignancy, staging CT chest abdomen pelvis will likely be required to assess for metastases and guide management",
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"explanation": "This would be part of the investigations for a patient presenting with symptoms concerning of urological malignancy, particularly of urethral/bladder origin. This patient has a negative urine dip without haematuria and the history does not suggest any additional urological history. The history is more suggestive of other intraabdominal malignancy, particularly ovarian, and so other investigations would be conducted first",
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"explanation": "# Summary\n \n \nOvarian cancer is a major cause of gynaecological cancer-related mortality in the UK, due primarily to the non-specific nature of symptoms in early stages. The most common type is epithelial ovarian tumours, though germ cell tumours and sex cord stromal tumours also occur. Risk factors include older age, smoking, numerous ovulations, obesity, HRT, and BRCA genes. Parity, breastfeeding, early menopause, and COCP use can be protective. Symptoms typically include abdominal discomfort, bloating, early satiety, and urinary changes, with ascites signifying advanced disease. Differentials include IBS, fibroids, ovarian cysts, and other cancers. Initial investigations include CA-125 and pelvic and abdominal ultrasound. Management depends on disease stage and patient fitness, but can include surgery and chemotherapy.\n \n \n# Definition\n \n \nOvarian cancer is a malignancy originating from various cell types found within the ovary. \n \n \n# Aetiology\n \n \nThe causes of ovarian cancer can be divided into risk factors and protective factors. \n \n \nRisk factors include:\n \n \n - Advanced age\n - Smoking\n - Increased number of ovulations (early menarche, late menopause)\n - Obesity\n - Hormone replacement therapy (HRT)\n - Genetic predisposition (BRCA 1 and 2 genes)\n\nProtective factors include:\n\n - Childbearing (parity)\n - Breastfeeding\n - Early menopause\n - Use of combined oral contraceptive pill (COCP)\n\n\n# Classification\n \n \nThe types of ovarian cancers can be classified according to the cell type from which the cancer originates. The types include:\n \n \n**Epithelial ovarian tumours**\n \n \n - Originate from the epithelium which lines the fimbria of the fallopian tubes or the ovaries\n - Epithelial tumours are partially cystic, and the cysts can contain fluid. \n - The initial metastatic spread typically involves the peritoneal cavity, with seeding particularly affecting the bladder, paracolic gutters and the diaphragm. \n - Around 90% of ovarian cancers are epithelial ovarian tumours.\n \n \n**Germ cell tumours features**\n \n \n - Originate from the germ cells in the embryonic gonad. \n - These tumours typically grow rapidly and spread predominantly via the lymphatic route\n - Germ cell tumours most commonly arise in young women, which is atypical for most cases of ovarian cancer. \n - Tumour markers include alpha-fetoprotein and sometimes beta human chorionic gonadotrophin (B-HCG).\n \n \n**Sex cord stromal tumours**\n \n \n - Originate from connective tissue. \n - They are rare, making up less than 5% of all ovarian tumours. They are malignant tumours, but are much less aggressive than epithelial tumours. \n - Additionally, ovarian cancer can be secondary to another cancer elsewhere, which has metastasised to the ovary. A Krukenberg tumour refers to a \"signet ring\" sub-type of stromal tumour, typically gastrointestinal in origin, which has metastasised to the ovary. \n \n \n \n# Signs and Symptoms\n \n \nThe clinical features of ovarian cancer typically present late in the disease progression and include:\n \n \n - Abdominal discomfort\n - Bloating\n - Early satiety\n - Urinary frequency or change in bowel habits\n \n \nIn later stages, the disease may cause:\n \n \n - Ascites (due to vascular growth factors increasing vessel permeability)\n - Pelvic, back and abdominal pain\n - Palpable abdominal or pelvic mass\n \n \n# Differential diagnosis\n \n \nDifferential diagnoses for ovarian cancer include:\n \n \n- Gastrointestinal conditions (e.g., irritable bowel syndrome): characterised by abdominal pain, bloating, and changes in bowel habits. \n2. Fibroids: may cause heavy menstrual bleeding, pelvic pressure or pain, frequent urination, and constipation. \n3. Ovarian cysts: can cause pelvic pain, fullness or heaviness in the abdomen, and bloating.\n4. Other cancers (e.g., bladder, endometrial): may present with symptoms such as abnormal bleeding, pelvic pain, and urinary symptoms.\n \n \n# Investigations\n \n \nInvestigations for suspected ovarian cancer include:\n \n**Bedside:**\n \n * Abdominal examination: tenderness, abdominal mass\n * Bimanual examination: adnexal mass\n\n \n**Bloods:**\n \n* CA-125 levels\n * Measure CA125 in women (especially those aged over 50) with frequent or persistent symptoms of ovarian cancer (i.e. 12 or more times per month)\n * Consider this measurement in women with non-specific symptoms of malignancy, such as unexplained weight loss, fatigue or changes in bowel habit \n* AFP and beta-hCG levels (for younger women who may have germ cell cancers)\n\n \n**Imaging:**\n\n* Pelvic and abdominal ultrasound scan\n * May be helpful to rule out or identify malignancy where CA125 is 35 IU/ml or higher \n* CT chest/abdomen/pelvis (for staging)\n\n**Invasive:**\n \nFurther investigations may include:\n \n* Tissue biopsy \n \n \n**Risk of Malignancy Index** \n\nThese results can be used to calculate the Risk of Malignancy Index (RMI), which stratifies the likelihood of cancer: \n \n\n**RMI = U x M x CA125**\n\n\n* U = ultrasound result (between 0-3)\n* M = menopausal status (1 = premenopausal, 3 = postmenopausal) \n* Serum CA-125 is measured in IU/ml\n\n- NICE advise referring all women with an RMI I score of 250 or greater to a specialist multidisciplinary team\n\n\n**2 Week Wait (2WW) Referral Criteria:**\n\n* Physical examination showing ascites and/or a pelvic abdominal mass (that is not due to uterine fibroids) \n* Ultrasound findings suggestive of ovarian malignancy\n\n\n\n# Staging\n \n \nStage I (limited to the ovaries):\n \n - Stage IA: limited to one ovary, the capsule is intact\n - Stage IB: limited to both ovaries, capsules intact.\n - Stage IC: tumour limited to one or both ovaries with any of the following: capsule ruptured, tumour on ovarian surface, malignant cells in ascites or peritoneal washings.\n \n \nStage II (involving one or both ovaries with pelvic extension and/or implants):\n \n - Stage IIA: extension and/or implants on the uterus and/or Fallopian tubes. No malignant cells in ascites or peritoneal washings\n - Stage IIB: extension to and/or implants on other pelvic tissues. No malignant cells in ascites or peritoneal washings\n - Stage IIC: pelvic extension and/or implants (Stage IIA or Stage IIB) with malignant cells in ascites or peritoneal washings.\n \n \nStage III (involving one or both ovaries with microscopically confirmed peritoneal implants outside the pelvis):\n \n - Stage IIIA: microscopic peritoneal metastasis beyond pelvis (no macroscopic tumour)\n - Stage IIIB: macroscopic peritoneal metastasis beyond pelvis <2 cm\n - Stage IIIC: peritoneal metastasis beyond pelvis >2 cm and/or regional lymph node metastasis.\n \n \nStage IV: tumour involving one or both ovaries with distant metastasis.\n \n \n\n# Management\n \n \nManagement depends on the stage of the cancer and the patient's fitness for treatment.\n\nSurgery: \n\n* If early disease surgery can include removal of the uterus, ovaries, fallopian tubes and omentectomy\n* In advanced disease further debulking surgery can be performed.\n\n \nChemotherapy:\n\n* Adjuvant chemotherapy in combination with surgery\n* Intraperitoneal chemotherapy may be performed at the time of operation\n\nBiological therapies are being trialled \n \n \n# Complications\n\n* Bowel obstruction/constipation\n* Ascites\n* Chemotherapy complications: alopecia, intraperitoneal toxicity, neutropenia, peripheral neuropathy\n* Immunotherapy complications: bowel perforation or fistula, hypertension, poor wound healing \n* Surgical complications: thromboembolism, infection, haemorrhage, death\n* Death\n\n# Prognosis \n\n5-year survival:\n\n* 75% for women younger than 50\n* > 35% for women over 65\n* > 90% for women with localised disease on diagnosis\n* 30% for women with distant disease on diagnosis \n\n# NICE Guidelines\n \n \n [Click here to read NICE CKS on Ovarian cancer](https://cks.nice.org.uk/topics/ovarian-cancer/)\n \n \n# References \n\n[Patient Info](https://patient.info/doctor/ovarian-cancer-pro)",
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"question": "A 66-year-old woman presents to the GP with six months of increased urinary frequency, ongoing lower abdominal discomfort, early satiety, and persistent mild abdominal distention. She was diagnosed with irritable bowel syndrome (IBS) six months ago after an unremarkable colonoscopy to investigate alternating constipation/diarrhoea\n\nShe is otherwise fit and well and her full blood count, renal profile, and liver function tests are normal.\n\nAbdominal examination reveals a soft and non-tender abdomen, mildly distended, with no palpable masses. PR exam reveals soft stool in the rectum and no palpable masses.\n\nUrine dip is clear\n\nWhat is the most appropriate next investigation for this patient?",
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"explanation": "This may help in confirming the aetiology of the anaemia, although the clinical information provides enough information to reasonably assume the anaemia was caused either by menorrhagia or from malignancy. The patient has presented with an abdominal mass which must be investigated first",
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"explanation": "This patient most likely has uterine fibroids which has resulted in her menorrhagia, subfertility, and anaemia. She has a smooth benign-feeling suprapubic mass; however this still needs to be formally assessed sonographically to be characterised and assessed for malignancy",
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"explanation": "This may help in confirming the aetiology of the anaemia, although the clinical information provides enough information to reasonably assume the anaemia was caused either by menorrhagia or from malignancy. The patient has presented with an abdominal mass which must be investigated first",
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"explanation": "These would be reasonable suggestions to investigate subfertility/infertility if the patient did not present with an abdominal mass and ultrasound scans were unremarkable",
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"explanation": "MRI Pelvis provides excellent anatomic delineation of gynaecological structures. It is the most _accurate_ modality for detecting, localising, and characterising uterine fibroids. It is, however, not generally required for diagnosis and would not be the _first_ investigation of choice",
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"explanation": "# Summary\n \n \nFibroids are benign tumours of the myometrium of the uterus, common in women above 30, with peak incidence in perimenopausal years. Fibroids often present with menstrual dysfunction, such as menorrhagia and dysmenorrhoea, and can interfere with fertility if large enough. They are usually diagnosed following a transvaginal ultrasound scan. Management strategies depend on the symptoms and size of the fibroids, ranging from NSAIDs and contraceptive methods to surgical options including myomectomy, ablation, uterine artery embolisation, and hysterectomy.\n \n \n# Definition\n \n \nFibroids, or uterine leiomyomas, are benign smooth muscle tumours originating from the myometrium of the uterus.\n \n \n# Epidemiology\n \n \nUterine fibroids are the most prevalent benign uterine tumours in women and are the leading cause for hysterectomy. The incidence of fibroids increases with age until menopause. \n\nSymptomatic fibroids are less prevalent in women younger than 30 years of age, occurring in 20–50% of women older than 30 years. The peak incidence is observed in women in their 40s, with a crude incidence of 22.5 per 1000 woman-years.\n \n \n# Aetiology\n \n \nThe exact cause of fibroids is unknown but they are thought to be influenced by genetic, hormonal, and environmental factors. Oestrogen and progesterone, the hormones that stimulate the development of the uterine lining during each menstrual cycle in preparation for pregnancy, appear to promote the growth of fibroids. Fibroids contain more oestrogen and progesterone receptors than normal uterine muscle cells.\n \n \n# Signs and Symptoms\n \n \nFibroids can often be asymptomatic, especially when they are small. However, when symptoms do occur, they usually present as:\n \n \n - Menstrual dysfunction, such as menorrhagia and dysmenorrhoea\n - Sub/Infertility, if the fibroid is large enough to distort the uterine cavity\n - Palpable mass on abdominal or pelvic examination if the fibroid is large\n - Abdominal pain, worse during menstruation\n - Urinary frequency if large enough and putting pressure on the bladder\n \n \n# Differential Diagnosis\n \n \nThe main differentials for fibroids include other causes of menorrhagia and dysmenorrhoea. These include:\n \n \n1. **Endometrial polyps:** Present with irregular menstrual bleeding and spotting\n2. **Endometriosis:** Characterised by dysmenorrhoea, deep dyspareunia, chronic pelvic pain, and infertility\n \n \n# Investigations\n \n \n \n**Bedside:**\n\n* Bimanual examination: may feel enlarged uterus \n \n**Bloods**\n\n* Consider FBC if worried about anaemia \n \n**Imaging:**\n \n * Trans-vaginal ultrasound: Used to assess the size and location of the fibroids\n * MRI: Used if ultrasound does not provide enough detail to assess the fibroid for surgery\n \n**Invasive:**\n\n* Biopsy: May be taken if there is any doubt over the diagnosis to differentiate the fibroid from other conditions such as endometrial cancer\n\n\n \n# Management\n \nManagement of fibroids depends on the symptoms and size of the fibroids. It includes:\n \n - Non-surgical management for fibroids causing abnormal bleeding and under 3cm in size with no uterine distortion. This includes NSAIDs, anti-fibrinolytics (tranexamic acid), GnRH analogues, combined hormonal contraception, and Levonorgestrel-releasing intrauterine system (Mirena).\n - Surgical management for fibroids causing symptoms due to their mass effect. This includes myomectomy, ablation, uterine artery embolisation, and hysterectomy.\n\n# Complications\n\n* Recurrence \n* Haemorrhage and anaemia\n* Degeneration, especially during pregnancy (red degeneration)\n* Infertility (especially if large)\n* Torsion\n* Pressure effects (e.g. urinary retention, constipation)\n* Delivery complications (e.g. breech presentation, bleeding) and pregnancy complications, including miscarriage \n\n \n# NICE Guidelines\n \n \n[Click here for NICE CKS on fibroids](https://cks.nice.org.uk/topics/fibroids/)\n \n# References\n\n[Patient Info](https://patient.info/womens-health/periods-and-period-problems/fibroids)",
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"question": "A 32-year-old woman presents with 12 months of infertility despite regular unprotected intercourse. She reports regular periods, though increasingly heavy in recent years. She had normal childhood development and menarche at age 11, with up-to-date negative cervical smears for HPV, and has no past medical history. She is in a monogamous relationship with a negative sexually transmitted infection screen 6 months ago.\n\n\nOn examination, she has a firm, palpable painless 10cm smooth mass in the suprapubic region. Abdomen is otherwise soft non-tender with no shifting dullness or fluid thrill.\n\n\nRoutine bloods reveal microcytic iron deficiency anaemia but are otherwise unremarkable.\n\n\nUrine dip and beta HCG are negative.\n\n\nWhat is the most appropriate next investigation?",
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"explanation": "This patient is rightly concerned about her risk of endometrial cancer - having PCOS and having two family members who developed endometrial cancer places her at high risk. It would be reasonable to refer to genetic screening to determine if she, or her family, was genetically predisposed to endometrial cancer e.g. Lynch syndrome (mutation in MLH1 mismatch repair gene) or Cowden Syndrome (Mutations in PTEN tumour suppressor gene). The priority at this stage, however, is to investigate and manage her secondary amenorrhoea, and to reassure her there are no signs of malignancy",
"id": "33017",
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"explanation": "This would be a reasonable option to help regulate this patient's menstrual cycle and additionally provide hormonal contraception (although this patient did not state contraception was her main priority). It would be useful for this patient to have an ultrasound scan after a withdrawal bleed to assess the endometrium and so a short daily course of oral medroxyprogesterone would be used to achieve this. The three-monthly depo injection is less likely to induce a withdrawal bleed as quickly as a two week course of oral medroxyprogesterone because the progestogen dose is spread over a longer period of time. If the patient's ultrasound scan showed an endometrium of normal thickness and morphology, then a three-monthly progesterone injection would be an option - although the patient would not benefit from the anti-androgen effects of oestrogen within the COCP",
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"explanation": "This patient does require a TVUS to assess endometrial thickness and morphology, although a withdrawal bleed would need to be induced prior to scanning to accurately measure the endometrial thickness. For this the patient should be provided with oral medroxyprogesterone (Provera) for 14 days to induce a withdrawal bleed",
"id": "33015",
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"explanation": "This would be a reasonable option to help regulate this patient's menstrual cycle and additionally provide hormonal contraception (although this patient did not state contraception was her main priority). It would be useful for this patient to have an ultrasound scan after a withdrawal bleed to assess the endometrium and so a short daily course of oral medroxyprogesterone would be used to achieve this. The three-monthly depo injection is less likely to induce a withdrawal bleed as quickly as a two week course of oral medroxyprogesterone because the progestogen dose is spread over a longer period of time. If the patient's ultrasound scan showed an endometrium of normal thickness and morphology, then a three-monthly progesterone injection would be an option - although the patient would not benefit from the anti-androgen effects of oestrogen within the COCP",
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"name": "Insertion of levonorgestrel-releasing intrauterine system (e.g. Mirena®)",
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"explanation": "The most likely cause for this patient's secondary amenorrhoea (less that one period every three months) is her PCOS. Her LH:FSH Ratio is 3.5 and so makes PCOS more likely than premature ovarian failure (elevated FSH and LH), hypothalamic/hypopituitary amenorrhoea (low FSH, LH, testosterone, and prolactin), Hypothyroidism (low or high TSH), or androgen-secreting tumour/late onset congenital adrenal hyperplasia (raised testosterone). There is nothing in the question pointing to her amenorrhoea being weight, exercise, or stress-related.\n \n\n She is rightly concerned about her increased risk of endometrial cancer with PCOS and amenorrhoea. This is due to prolonged exposure of the endometrium to unopposed oestrogen. She will need referral for a transvaginal ultrasound (TVUS) to assess for endometrial thickness, although prior to this she will need to induce a withdrawal bleed to correctly interpret the ultrasound findings as her endometrium will be thickened given she has not menstruated for two months. To induce a withdrawal bleed in this patient, an oral cyclical progestogen such as medroxyprogesterone is given for 14 consecutive days. Following this, a TVUS should be conducted.\n \n\n If endometrial thickening is present (greater than 10mm) or the endometrium has an abnormal appearance, then she will need referral for endometrial sampling to exclude endometrial hyperplasia or cancer (unlikely in this patient's case). If the endometrium is of normal thickness and appearance, then the options to reduce risk of endometrial cancer are either:\n \n\n - An oral cyclical progestogen e.g. medroxyprogesterone for 14 days every 1-3 months\n - Low-dose combined oral contraceptive pill (COCP)\n - Levonorgestrel-releasing intrauterine system (e.g. Mirena®)\n \n\n If the patient is unwilling to take these, then they would likely need regular ultrasound scans every 6-12 months to assess the endometrium",
"id": "33013",
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"comment": "bruh",
"createdAt": 1649759733,
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"comment": "actually a pretty clever question! its so easy to forget about the fact that you have to induce the withdrawal bleed!! ",
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"comment": "shut up man",
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"comment": "LOOOL",
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"comment": "actually a hard question, props to the author",
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"comment": "YOU NEED TO SAY CYCLICAL IN THE ANSWER - IT MAKES IT LOOK LIKE IT'S JUST A ONE-OFF 14 DAY COURSE OF PROGESTERONE\n",
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"comment": "It's meant to be a one off in this case as they're doing it is in prep for a TVUS to assess the endometrium reliably for any hyperplasia. In the future, yes she may need cyclical progesterone to reduce her future risk of cancer. ",
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"comment": "m8 it is a one off...",
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"comment": "excellent question + excellent explanations",
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"comment": "do they still need to take it if they have post-menopausal bleeding?\n",
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"explanation": "# Summary\n \n \nPolycystic ovary syndrome (PCOS) is a disorder characterised by hyperandrogenism, ovulation disorders, and polycystic ovarian morphology. It is common among women of child-bearing age. Key signs and symptoms include oligomenorrhoea, hirsutism, acne, and subfertility among others. Investigations such as hormonal assays and imaging techniques are used in diagnosis. Management strategies encompass lifestyle modifications and a range of pharmacological treatments tailored to patient preferences, such as conception.\n \n \n# Definition\n \n \nPolycystic ovary syndrome (PCOS) is a disorder characterised by hyperandrogenism (manifesting as oligomenorrhoea, hirsutism, and acne), ovulation disorders, and polycystic ovarian morphology.\n \n \n# Epidemiology\n \n \nPolycystic ovary syndrome is a common endocrine condition, affecting up to a quarter of women during their reproductive years.\n \n \n# Aetiology\n \n \nThe precise aetiology of PCOS remains undetermined. However, potential hormonal imbalances implicated in this syndrome include hyperandrogenism, insulin resistance, elevated levels of luteinizing hormone (LH) and raised oestrogen levels.\n \n \n# Signs and Symptoms\n \n \nThe clinical presentation of PCOS is largely attributed to the hormonal imbalances, with symptoms including:\n \n \n - Oligomenorrhoea\n - Subfertility\n - Acne\n - Hirsuitism\n - Obesity\n - Mood changes including depression and anxiety\n - Male pattern baldness\n - Acanthosis nigricans (secondary to insulin resistance)\n \n \n# Differential Diagnosis\n \n \nFor accurate diagnosis, other endocrine disorders presenting similar clinical features must be excluded. These include:\n \n \n - Menopause: Characterised by cessation of menstruation, hot flashes, vaginal dryness, mood changes, and sleep problems.\n - Congenital adrenal hyperplasia (CAH): Presenting with signs of androgen excess like hirsutism, acne, and irregular periods. Presents earlier on and can lead to ambiguous genitalia (for affected females). \n - Hyperprolactinaemia: Symptoms include irregular periods, galactorrhoea, and infertility.\n - Androgen-secreting tumours: May cause virilisation, amenorrhoea, and hirsutism.\n - Cushing's syndrome: Characterised by weight gain, purple stretch marks, and easy bruising.\n \n \n# Investigations\n \n \nBiochemical assays and imaging techniques play a pivotal role in the diagnosis of PCOS:\n \n**Bedside:**\n\n- Clinical examination to identify features of hyperandrogenism (e.g. hirsutism) or features of insulin resistance (e.g. acanthosis nigricans, raised BMI)\n\n**Bloods:**\n\n- LH:FSH ratio: An increase (>2) aids in differentiating from menopause where the ratio is normal.\n- Total testosterone: May be normal or slightly elevated.\n- Fasting and oral glucose tolerance tests: Used to diagnose insulin resistance.\n- Other tests may include TFTs (for thyroid dysfunction), 17-hydroxyprogesterone levels (for CAH), prolactin (for hyperprolactinaemia), DHEA-S and free androgen index (for androgen-secreting tumours), and 24-hour urinary cortisol (for Cushing's syndrome).\n\n**Imaging:**\n\n- Transabdominal and transvaginal ultrasound: Reveals increased ovarian volume and multiple cysts. May be important for fulfilling Rotterdam Diagnostic Criteria (See below) \n\n\nNo **invasive tests** are required for diagnosis. \n\n \n **Rotterdam Diagnostic Criteria:**\n \n \nUpon exclusion of other causes, PCOS can be diagnosed if at least two of the following criteria are met:\n \n \n - Polycystic ovaries (defined as a follicle number per ovary of 20 or more in at least one ovary)\n - Oligo-/anovulation\n - Clinical or biochemical features of hyperandrogenism\n \n \n# Management\n \n \nThe management of PCOS primarily focuses on symptom control and prevention of complications, with endometrial cancer risk reduction achieved through regular menstruation.\n \n \n**Conservative:**\n \n \n - Encouragement of weight loss and exercise\n - Education on increased risks of cardiovascular disease, diabetes, and endometrial cancer\n \n \n**Medical, for women not planning pregnancy:**\n \n \n - Co-cyprindrol: Reduces hirsutism and promotes regular menstruation.\n - Combined oral contraceptive pill (COCP): Decreases irregular bleeding and offers protection against endometrial cancer.\n - Metformin: Aids in regularising menstruation, reducing hirsutism, and acne.\n \n \n**Medical, for women wishing to conceive:**\n \n \n - Clomiphene: Induces ovulation and enhances conception rates.\n - Metformin: Can be used alone or in combination with clomiphene to improve chances of pregnancy.\n - Gonadotrophins: Utilised to induce ovulation if clomiphene and metformin prove ineffective.\n\n**Surgical, for women wishing to conceive:**\n\n - Ovarian drilling: A second-line laparoscopic surgical procedure that damages the hormone-producing cells of the ovary. \n \n# Complications\n\n\n- Infertility: Caused by impaired or dysregulated ovulation.\n- Metabolic syndrome and dyslipidaemia: PCOS leads to raised triglycerides and LDL and fall in HDL. \n- Type 2 diabetes: PCOS increases risk of T2DM by approximately two fold as a result of insulin resistance \n- Cardiovascular disease: This is likely a consequence of metabolic complications of PCOS and hormonal alterations. \n- Hypertension: Greater risk of hypertension seen in premenopausal as opposed to postmenopausal women. \n- Obstructive sleep apnoea: This occurs as a result of obesity (usually secondary insulin resistance and metabolic changes). \n\n# NICE Guidelines\n\n[Click here for NICE guidelines on PCOS](https://cks.nice.org.uk/topics/polycystic-ovary-syndrome/)\n\n# References \n\n[BMJ Best Practice](https://bestpractice.bmj.com/topics/en-gb/141)\n\n[RCOG page](https://www.rcog.org.uk/for-the-public/browse-our-patient-information/polycystic-ovary-syndrome-pcos-what-it-means-for-your-long-term-health/)",
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"question": "A 25-year-old woman presents with prolonged amenorrhoea, having had only three periods in the last year, with the most recent two months ago. She has a history of irregular periods since menarche and was diagnosed with polycystic ovary syndrome (PCOS) as a teenager. She has a family history of endometrial cancer in her mother and maternal aunt.\n\n\nShe denies abdominal pain, bloating, fatigue, early satiety, or intermenstrual bleeding. Her medical history is unremarkable, and her BMI is 21.\n\n\n\n\nUrine dip is clear with negative beta-hCG.\n\n||||\n|---------------------------|:-------:|------------------------------|\n|Thyroid Stimulating Hormone|2.1 mU/L|0.3 - 4.2|\n|Luteinising Hormone|10.85 IU/L|1 - 11 (Luteal)|\n|Follicle Stimulating Hormone|3.1 IU/L|2 - 8 (Luteal)|\n|Testosterone|2.6 nmol/L|(M) 9.9 - 27.8, (F) 0.2 - 2.9|\n|Prolactin|450 IU/L|(M) 90 - 320, (F) 100 - 500||\n\n\n\nWhat is the best next management step for this patient?",
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"explanation": "Acute hepatitis would present with grossly deranged liver enzymes and raised bilirubin. A raised bilirubin with anaemia and normal liver enzymes is more typical for haemolytic anaemia",
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"explanation": "This patient likely has acute haemolytic anaemia from glucose-6-phosphate dehydrogenase deficiency following ingestion of fava beans. Direct antiglobulin test (direct Coombs test) is used to determine whether the patient has immune-mediated haemolytic anaemia",
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"comment": "lmfao think everyone took an L here",
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"comment": "na g allow it",
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"comment": "best bit is the 3% who did get it right, most likely just got the diagnosis wrong ",
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"comment": "you are just doing the most now",
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"comment": "don't lie everyone read fava beans and ran to G6PD, we're all guilty here",
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"comment": "Got sent to the cleaners\n",
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"explanation": "# Summary\n\nHaemolytic anaemia is a condition characterised by the premature destruction of red blood cells (RBCs), resulting in a reduced RBC lifespan. It can be categorised into hereditary and acquired forms, and further divided into intravascular or extravascular and autoimmune or non-autoimmune subtypes. The epidemiology varies depending on the specific type. Diagnosing haemolytic anaemia requires a comprehensive set of investigations, including a complete blood count (FBC), split bilirubin, haptoglobin, lactate dehydrogenase (LDH), reticulocytosis, and blood film analysis. Additional tests may be needed, such as direct antiglobulin test (DAT), electrophoresis, and further blood film examination. Management involves addressing the underlying cause and may include blood transfusions, immunosuppressive therapy, or splenectomy. Complications can include severe anaemia, gallstones, and organ damage.\n\n# Definition\n\nHaemolytic anaemia is a condition characterised by the premature destruction of red blood cells (RBCs), leading to a decrease in their lifespan. This condition can be classified into hereditary and acquired forms, with further subdivisions based on the site of haemolysis, either intravascular or extravascular, and the underlying cause, autoimmune or non-autoimmune.\n\n\n# Epidemiology\n\nThe prevalence and distribution of haemolytic anaemia vary significantly based on the specific subtype and its underlying causes:\n\n- Sickle cell disease predominantly affects individuals of African descent, and is most prevalent in sub-Saharan Africa.\n- Thalassemias: The distribution of thalassemias is linked to regions with a high prevalence of consanguineous marriages, notably in Mediterranean countries.\n- The prevalence of autoimmune haemolytic anaemia varies, but it is often associated with autoimmune diseases like systemic lupus erythematosus. It can affect individuals of any age and ethnicity. \n- The incidence of intravascular haemolysis may be higher in conditions involving mechanical trauma, such as prosthetic heart valves or microangiopathic disorders. \n- Extravascular haemolysis is often observed in hereditary conditions like hereditary spherocytosis and can affect individuals worldwide.\n\n# Classification\n\n### Hereditary Haemolytic Anaemia\nIncludes conditions like sickle cell disease, thalassemias, and hereditary spherocytosis, often caused by genetic mutations affecting RBC structure or function.\n\n### Acquired Haemolytic Anaemia\n\nCan result from autoimmune disorders, infections (e.g., malaria), medication reactions, or mechanical trauma.\n### Intravascular Haemolysis\n\nOccurs within the bloodstream, leading to the release of free haemoglobin into the circulation and the excess of haemoglobin is dealt with in many ways: \n\n- Combination with haptoglobin\n- Combination with albumin (**methaemalbuminaemia**)\n- Loss in the urine (**haemoglobinuria**)\n- Storage in tubular epithelial cells as **haemosiderin** \n- Shedding into the urine (haemosiderinuria)\n\t\nCauses of intravascular haemolytic anaemia include:\n\n- Intrinsic cellular injury (eg. G6PD deficiency)\n- Intravascular complement-mediated lysis (some autoimmune haemolytic anaemias)\n- Paroxysmal nocturnal haemoglobinuria and acute transfusion reactions\n- Mechanical injury – microangiopathic haemolytic anaemia and cardiac valves\n- Autoimmune haemolytic anaemia (AIHA)\n\n### Extravascular Haemolysis\n\n- Takes place outside the bloodstream, primarily in the spleen and liver, where RBCs are phagocytosed. It is not associated with dramatic release of free haemoglobin into the circulation. \n- Splenomegaly and hepatomegaly are typical.\n\nCauses include:\n\n- Abnormal red cells (e.g. sickle cell anaemia and hereditary spherocytosis)\n- Normal cells having been marked by antibodies for splenic phagocytosis\n\n### Autoimmune Haemolytic Anaemia\n\nRBC destruction is triggered by autoantibodies that target the body's own RBCs.\n\nTwo major causes include:\n\n1. Warm AIHA:\n\t- An **IgG-mediated extravascular** haemolytic disease, in which the spleen tags cells for splenic phagocytosis. \n\t- Causes: **SLE,** idiopathic, lymphoproliferative neoplasms (eg. chronic lymphocytic leukaemia and lymphoma), drugs (methyldopa)\n\t- Managed with prednisolone or immunosupression (e.g. AZT) and transfusions if severe \n2. Cold AIHA:\t\n\t- **IgM-mediated** haemolytic disease, in which IgM fixes **complement** causing **direct intravascular haemolysis**. It includes cold agglutinin disease\n\t- The IgM agglutinates also cause the hands and feet to become blue in cold conditions (**acrocyanosis**)\n\t- Causes: post-infectious (usually after **Mycoplasma** or EBV), idiopathic, lymphoproliferative disorders\n\t- Treatment is mostly supportive, warmed blood is transfused if required and resistant cases may trial rituximab\n\n### Non-Autoimmune Haemolytic Anaemia\n\nCaused by factors other than autoantibodies, such as infections or mechanical stress:\n\n- Microangiopathic haemolytic anaemia\n- Paroxysmal nocturnal haemoglobinuria (PNH)\n- Physical lysis of red cells (e.g. malaria, patients with mechanical heart valves)\n- Haemolytic uraemic syndrome (HUS) – often caused by *E. coli* 0157:H7\n- Infectious causes of disseminated intravascular coagulation (DIC) such as fulminant meningococcaemia\n\n# Signs and Symptoms\n\n**Haemolytic Anaemia - General:**\n\nHaemolytic anaemia, regardless of its underlying cause, often presents with a constellation of symptoms related to the accelerated breakdown of red blood cells and the body's response to anaemia. Common signs and symptoms include:\n\n- Fatigue \n- Pallor\n- Jaundice - Haemolysis releases bilirubin into the bloodstream, causing yellowing of the skin and sclera \n- Splenomegaly - The spleen becomes enlarged as it works to remove and destroy the damaged red blood cells.\n- Dark Urine\n- Gallstones - Excess bilirubin can accumulate in the gallbladder, increasing the risk of gallstone formation.\n- Leg Ulcers - In severe cases, reduced blood flow and oxygen supply can lead to painful leg ulcers.\n- Shortness of Breath\n- Heart Palpitations\n\n**Specific Causes and Their Signs and Symptoms:**\n\n- **Sickle Cell Disease:** Vaso-occlusive pain, acute chest syndrome, and strokes.\n- **Thalassemias:** Profound anaemia, skeletal deformities, and organ enlargement.\n- **Hereditary Spherocytosis:** Splenomegaly and fatigue due to haemolysis.\n- **Autoimmune Haemolytic Anaemia:** Variable symptoms linked to haemolysis extent and underlying autoimmune conditions.\n- **Infections (e.g., Malaria):** Fever, fatigue, and organ dysfunction.\n- **Medication-Induced:** Variable symptoms, jaundice, and specific drug-related effects.\n\n# Investigations\n\n1. First Identify Haemolytic Anaemia:\n\n\t* Full Blood Count (FBC): Reveals low haemoglobin levels, elevated reticulocytes, and alterations in RBC indices.\n\t* Reticulocytosis: Increased levels of reticulocytes indicate active RBC production.\n\t* Blood Film Analysis: reveals characteristic changes in RBC morphology depending on underlying cause.\n\t* LFTs may reveal raised bilirubin\n\t* Raised LDH indicative of high cell turnover\n\t* Raised urinary urobillinogen\n\n2. Identify the Cause:\n\n\t* Direct Antiglobulin Test (DAT): Detects the presence of autoantibodies on the RBC surface in autoimmune haemolytic anaemia.\n\t* Electrophoresis: Helps diagnose haemoglobinopathies like thalassemias and sickle cell disease.\n\t* Blood Film Examination: Further evaluates RBC morphology and inclusions.\n\n# Management\n\nTreatment aims to address the underlying cause and alleviate symptoms. General management principles include:\n\n* **Supportive Care:** Blood transfusions to manage severe anaemia however this won't be curative as there will be ongoing haemolysis if the underlying cause is not managed.\n* **Immunosuppressive Therapy:** In autoimmune haemolytic anaemia, medications like corticosteroids can reduce antibody production.\n* **Splenectomy:** May be considered in certain cases, particularly hereditary spherocytosis.\n* Specific management strategies depend on the type of haemolytic anaemia.\n\n\n# References\n\n[Patient.info - Haemolytic Anaemia](https://patient.info/doctor/haemolytic-anaemia)",
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"explanation": "# Summary\n\nAntiphospholipid syndrome (APS) is a systemic autoimmune disease that occurs in patients with antiphospholipid antibodies, causing thrombosis of veins, arteries and small vessels. It may occur alone or in association with another condition such as systemic lupus erythematosus. Common manifestations include thrombosis of peripheral arteries or veins, adverse pregnancy outcomes including recurrent miscarriage and intrauterine growth restriction, pulmonary embolism, stroke, retinal thrombosis and valvular disease. Key investigations include a full blood count, clotting screen (aPTT is typically paradoxically raised) and testing for anti-cardiolipin, anti-beta2-glycoprotein I and lupus anticoagulant antibodies. Management involves treating thrombotic episodes with anticoagulation, with warfarin being the preferred option. Asymptomatic APS does not require treatment. Pregnant women with recurrent pregnancy loss require low molecular weight heparin and aspirin throughout pregnancy.\n\n# Definition\n\nAntiphospholipid syndrome (APS) is an autoimmune condition characterised by the presence of antiphospholipid antibodies with clinical manifestations of venous or arterial thrombosis and adverse pregnancy outcomes. \n\n# Epidemiology\n\n- Prevalence of APS in the UK is 50 per 100,000 in women and 9.8 per 100,000 in men\n- Onset is typically between the ages of 20 and 50\n- Antiphospholipid antibodies are found in 1-5% of the healthy population, and in 30% of people with systemic lupus erythematosus\n- Approximately 1 in 6 people under the age of 50 with strokes, deep vein thrombosis, myocardial infarct or recurrent miscarriages have APS \n\n# Aetiology\n\nAPS occurs due to antiphospholipid antibodies which cross-react with cell membrane phospholipids, leading to a hypercoagulable state that predisposes patients to vascular thrombosis.\n\nAPS can occur in isolation (primary APS), or in association with another autoimmune disease such as:\n\n- Systemic lupus erythematosus (SLE)\n- Rheumatoid arthritis\n- Sjogren's syndrome\n- Systemic sclerosis\n- Dermatomyositis\n\nMore rarely, cases may be associated with malignancies (e.g. lymphoma) or infections (e.g. HIV).\n\n# Diagnostic Criteria\n\nAPS is diagnosed using the **revised Sapporo criteria** - patients need at least one clinical and one laboratory criteria.\n\n**Clinical criteria:**\n\n- Vascular thrombosis \n- At least 1 episode of venous/arterial/small vessel thrombosis\n- Not including superficial thrombophlebitis\n- This should be unprovoked or provoked by a minor risk factor only\n- Pregnancy morbidity with any of:\n- 3 miscarriages < 10 weeks\n- 1 miscarriage _<_10 weeks\n- Premature birth < 34 weeks\n\n**Laboratory criteria:**\n\n- On at least 2 occasions at least 12 weeks apart, any of the following are positive:\n- Anticardiolipin antibodies\n- Anti-beta2-glycoprotein I antibodies\n- Lupus anticoagulant\n\n# Signs and Symptoms\n\nClinical manifestations are due to thrombosis of arteries, veins or small vessels which may affect a variety of organ systems:\n\n- Cerebral involvement e.g. ischaemic stroke, central venous sinus thrombosis (signs and symptoms include focal neurology such as weakness, sensory changes, dysphasia)\n- Rashes e.g. livedo reticularis, skin ulceration\n- Lung involvement e.g. pulmonary embolism, pulmonary hypertension (shortness of breath, haemoptysis, presyncope, tachycardia may occur)\n- Cardiac involvement e.g. myocardial infarction, valvular disease (mitral regurgitation is most common), may have chest pain, peripheral oedema, shortness of breath\n- Thrombosis of peripheral arteries leading to acute limb ischaemia (affected area will be cool; pallor, pulselessness, paraesthesia, paralysis and pain may be seen)\n- Deep vein thrombosis, causing swelling, erythema and pain of the affected limb\n- Obstetric complications including recurrent miscarriage, stillbirth, pre-eclampsia and intrauterine growth restriction\n- Retinal thrombosis (either arterial or venous) leading to blurred vision and painless visual loss in one eye\n- Adrenal infarction which may cause flank pain, as well as hypotension, fatigue and confusion\n- Budd-Chiari syndrome (due to hepatic vein thrombosis) causing abdominal pain, ascites and hepatomegaly\n- Mesenteric ischaemia causing abdominal pain, diarrhoea, nausea and vomiting\n- Avascular necrosis of bone leading to localised severe pain\n- Nephropathy which may present with nephrotic syndrome (e.g. oedema), hypertension or with flank pain and haematuria\n\n[lightgallery] \n\n# Differential Diagnosis\n\n- **Factor V Leiden** which is the commonest genetic thrombophilia and increases the risk of venous but not arterial thrombosis\n- **Protein C or S deficiency** are also genetic conditions that increase the risk of venous thrombosis (and possibly arterial thrombosis to a small extent)\n- **Antithrombin III deficiency** may be inherited or acquired (e.g. due to liver dysfunction, disseminated intravascular coagulation or nephrotic syndrome), causes venous thrombosis (and may also increase the risk of arterial thrombosis)\n- **Malignancy** is a prothrombotic state for a multitude of reasons, including tumour cells activating the coagulation system, cancer treatments causing immobility and venous stasis and disrupting the endothelium (e.g. indwelling lines); risk of both arterial and venous thrombosis is increased \n- **Polycythaemia** may be primary (polycythaemia vera) or secondary (usually due to chronic hypoxia, e.g. in chronic obstructive pulmonary disease); causes an increase in blood viscosity that is associated with both arterial and venous thrombosis\n- **Other causes of recurrent miscarriage** e.g. chromosomal abnormalities, uterine anomalies, cervical incompetence\n- **Multiple sclerosis** may cause similar symptoms to repeated cerebral infarctions in APS, e.g. decline in mobility, visual loss, dysphasia and cognitive impairment\n\n# Investigations\n\n**Bedside tests:**\n\n- Urine dip for proteinuria (which may occur in renal involvement, or indicate nephrotic syndrome as a differential)\n\n**Blood tests:**\n\n- Patients need to have at least one of the following antiphospholipid antibodies present on testing on two occasions at least 12 weeks apart:\n- Lupus anticoagulant\n- Anticardiolipin antibody\n- Anti-beta2-glycoprotein I antibody\n- Full blood count - may show thrombocytopenia and/or haemolytic anaemia\n- Clotting screen - may show paradoxical prolongation of the aPTT\n- U&Es looking for renal involvement\n- Testing for SLE if secondary APS is suspected (e.g. antinuclear, anti-double-stranded DNA and anti-smith antibodies)\n- Testing for other hypercoagulable states (e.g. factor V Leiden, protein C and S or antithrombin III deficiency) to rule out differentials\n\n**Imaging tests:**\n\n- Doppler ultrasound for suspected deep vein thrombosis\n- CT or MRI of the brain for suspected stroke\n- CT abdomen for suspected Budd-Chiari syndrome\n- CT pulmonary angiography for suspected pulmonary embolism\n- Transthoracic echocardiography for valvular disease and vegetations (Libman-Sacks endocarditis in SLE), and for pulmonary hypertension\n\n# Management \n\n**Conservative management:**\n\n- Asymptomatic APS does not require any specific treatment\n- All patients should be advised on measures to reduce risk of cardiovascular disease\n- Smoking cessation\n- Regular exercise\n- Maintaining a healthy diet and weight\n- Avoiding alcohol excess\n- Effective management of comorbid hypertension, diabetes and dyslipidemia\n- Patients should avoid oestrogen-containing contraceptive and hormone replacement therapy as this further increases thrombosis risk \n- Joint management with other services (e.g. stroke, cardiology) is important after stroke, myocardial infarction etc.\n\n**Medical management:**\n\n- Anticoagulation is the mainstay of treatment for patients after a thrombotic event, which is usually given lifelong\n- Warfarin is the anticoagulant of choice, with a target INR of 2-3 \n- DOACs are not recommended\n- A higher target INR should be considered in patients with recurrent thrombosis on warfarin (e.g. 3-4)\n- If thrombotic episodes continue, immunomodulatory treatments (e.g. hydroxychloroquine) can be considered\n- Adding an antiplatelet (e.g. aspirin) to warfarin treatment should be considered in patients after a stroke if they have additional vascular risk factors\n- All patients with stroke should be started on statins\n- Miscarriage prevention in APS is with low-dose aspirin and low molecular weight heparin (LMWH)\n- Pregnant patients with APS should take 75-150 mg aspirin daily from 12 weeks gestation until delivery\n- Warfarin is teratogenic and so should be switched to treatment dose LMWH during pregnancy; it is safe in breastfeeding and so can be switched back after birth\n\n# Complications\n\n- Catastrophic antiphospholipid syndrome is characterised by rapid-onset widespread small vessel thrombosis\n- It causes multiorgan dysfunction, often with a systemic inflammatory response syndrome\n- There may be an identifiable trigger, e.g. infection, surgery, pregnancy or subtherapeutic anticoagulation\n- Unregulated complement activation occurs and reduced C3 and C4 levels are often seen\n- Management involves triple therapy with treatment dose heparin, high-dose steroids and either IVIG or plasma exchange\n- Recurrent cerebral infarction can cause cognitive impairment, seizures and vascular dementia\n- Retinal artery or vein occlusion can lead to visual loss\n- Chronic pulmonary emboli or thrombosis may lead to pulmonary hypertension\n- Renal failure due to thrombosis may occur\n- Cardiac valvular disease may be severe enough to require replacement\n\n# Prognosis\n\n- Prognosis of APS varies widely\n- Overall survival is good - approximately 90-94% over 10 years\n- However, significant disability may result from complications such as stroke and pulmonary hypertension\n- With treatment, pregnant women have an 80% chance of a successful birth\n- Catastrophic APS occurs in only 1% of patients, however mortality is approximately 50%\n\n# References\n\n[British Society of Haematology Guidelines](https://b-s-h.org.uk/guidelines/guidelines/guidelines-on-the-investigation-and-management-of-antiphospholipid-syndrome)\n\n[Patient UK - Antiphospholipid syndrome](https://patient.info/doctor/antiphospholipid-syndrome-pro)\n\n[Radiopaedia - Antiphospholipid syndrome](https://radiopaedia.org/articles/antiphospholipid-syndrome)\n\n[StatPearls - Antiphospholipid syndrome](https://www.ncbi.nlm.nih.gov/books/NBK430980)",
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"learningPoint": "Lupus anticoagulant, anticardiolipin antibody, and anti-β2-glycoprotein I antibody are autoantibodies linked to antiphospholipid syndrome, which increases the risk of blood clots and pregnancy complications, indicating a higher risk of thrombotic events.",
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"question": "A 32-year-old woman has presented to the GP for advice about fertility. She has had four miscarriages prior to 20 weeks gestation, following which tests revealed no anatomical, hormonal, or chromosomal precipitating causes. She is otherwise well. Tests are requested to screen for thrombophilia with the results shown below:\n\n| Serum | Result | Result at 12 weeks |\n| ------------------------------- | -------- | ------------------ |\n| Lupus anticoagulant (LA) | positive | positive |\n| Anticardiolipin (aCL) antibody | positive | positive |\n| Anti-b2-glycoprotein I antibody | negative | negative |\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "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. C. psittaci 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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"name": "Haemophilus influenzae",
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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": "# 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-HBc but negative HBsAg, anti-HBs, and IgM anti-HBc. These results could also indicate \"low-level\" chronic infection or resolved infection",
"id": "33042",
"label": "e",
"name": "Resolved hepatitis B infection",
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"explanation": "This would present with positive HBsAg, anti-HBc, and IgM anti-HBc",
"id": "33039",
"label": "b",
"name": "Acute hepatitis B",
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"explanation": "This would present as positive anti-HBc and anti-HBs but negative HBsAg and IgM anti-HBc",
"id": "33041",
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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": "This would present with positive anti-HBs and negative for HBsAg, anti-HBc, and IgM anti-HBc",
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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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"explanation": "Splitting the table up into true positive (280), false positive (70), false negative (10), and true negative (640) can make answering these tables easier to understand. The specificity is the proportion of patients without the condition with a negative test result. This is calculated as the true negative/(true negative + false positive) = 640/(640+70) = 90.1%",
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"comment": "relative risk usually but can use relative risk reduction for interpretation in papers etc",
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"explanation": "# Definition\n\nRisk in medical statistics refers to the probability of an outcome (either good or bad) occurring within a studied population. There are several different types of risk that are often used in medical studies.\n\n# What is Risk/Prevalence?\n\nThis is simply the probability of an event occurring within a defined population.\n\n# What is Risk Ratio (RR)?\n\nThe risk ratio (also known as relative risk) is the probability of an event occurring in an exposed group compared to the probability occurring in a non-exposed group.\n\nThe risk ratio is calculated by finding the ratio of incidence of a disease amongst the exposed population and the incidence amongst the non-exposed population.\n\nRisk ratios are used in cohort studies and in interventional studies in which the experimenter intervenes at some point during the study, such as in randomised controlled trials and pre-post studies.\n\nHowever, in cross-sectional studies and case-control studies, the incidence of the disease in the exposed and unexposed populations cannot be found, since the data only provides the cases and controls.\n\nConsequently,the risk ratio cannot be calculated for case-control studies and cross-sectional studies. Instead, an odds ratio must be found.\n\n# What is Absolute Risk Reduction (ARR)?\n\nThe absolute risk reduction is the absolute difference in the risk between the control group and the experimental group. It tells you in absolute terms how much an intervention changes an outcome of interest.\n\n# Calculation of Absolute Risk Reduction\n\nIt is calculated as follows:\n\n_ARR = Risk(control group) - Risk(experimental group)_\n\nA given ARR is generally considered significant if the 95% confidence interval does not cross 0.\n\nARR can then be used to calculate the number needed to treat (NNT).\n\n# What is Relative Risk Reduction (RRR)?\n\nThe relative risk reduction can be thought of as the proportional reduction in risk bestowed by the intervention compared to the control situation. It is more useful in helping you understand the efficacy of an intervention when the absolute risk of outcomes are rare (for example when considering the benefits of a statin for reducing MI in a given population).\n\n# Calculating RRR\n\nIt is calculated as follows:\n\n_RRR = 1 - [Risk(Experimental group) / Risk(Control group)]_\n\nA given RRR is generally considered significant if the 95% confidence interval does not cross 1.",
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"question": "A new treatment has been developed for ulcerative colitis. In a large randomised controlled trial, 20% of participants in the placebo arm had an acute flare within the next year. In the treatment arm, 12% of participants developed an acute flare within the next year.\n\nWhat is the relative risk reduction of the new treatment?",
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"explanation": "The 95% confidence intervals, represented as the horizontal edges of the summary measure diamond, do not overlap with the odds ratio of 1 and therefore, there is a significant effect of corticosteroids on neonatal mortality (mean odds ratio 0.53)",
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"name": "There is no significant effect of corticosteroids on neonatal mortality",
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"explanation": "The heterogeneity, or I squared, is often used in forest plots, but it is not shown in the data set here. Heterogeneity is the degree to which data from multiple studies displaying the same effect overlap each other. The more heterogeneous the studies are within the met-analysis, the less conclusive the data is",
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"explanation": "The area of the squares correspond to the proportional study's weight in the meta-analysis and is unrelated to the p-value",
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"name": "The area of the square corresponds inversely to the study's p-value",
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"explanation": "The forest plot will include all studies investigated, regardless of their outcomes, analysed to determine the standardised mean difference, represented as the diamond in the bottom right of the image",
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"name": "Only the Auckland study showed significance, and so the other studies' results can be discounted",
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"explanation": "# Definition\n\nA meta-analysis is a study which combines the results of multiple studies to increase the statistical power of the results.\n\nMeta-analyses are often conducted as part of a systematic review.\n\n# Advantages\n\nMeta-analyses offer several advantages, such as increasing the statistical power and increasing the precision/reliability of the data.\n\n# Disadvantages\n\nMeta-analyses do have the problem that they cannot control for bias or experimental error if these are present in the included studies.",
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"question": "The following diagram is a forest plot from a systematic review by Crowley et al. showing the results of seven studies looking at the effect of corticosteroids on hastening neonatal lung development when given to women about to give birth prematurely.\n\n[lightgallery]\n\nWhich of the following statements is correct?",
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"explanation": "Positive predictive value is the chance that the patient has the condition if the test is positive. This corresponds to true positive/(true positive + false positive) = 600/(600+60) = 90.9%",
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"explanation": "This value corresponds to the specificity - the proportion of patients without the condition with a negative test result. This is calculated as the true negative/(true negative + false positive) = 290 / (290+60) =82.9%",
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"explanation": "Splitting the table up into true positive (600), false positive (60), false negative (50), and true negative (290) can make answering these tables easier to understand. Positive predictive value is the chance that the patient has the condition if the test is positive. This corresponds to true positive/(true positive + false positive) = 600/(600+60) = 90.9%",
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"explanation": "This value corresponds to the negative predictive value - the chance that the patient does not have the condition if the test is negative. This is calculated as the true negative/(true negative + false negative) = 290/(290+50) = 85.3%",
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"explanation": "This value corresponds to sensitivity - the proportion of patients with the condition who have a positive test result. This is calculated as the true positive/(true positive + false negative) = 600/(600+50) = 92.3%",
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"explanation": "# Overview \n\nSeveral key parameters can be calculated to help describe how effective a certain test is at diagnosing a condition.\n\n| | Patients with colon cancer | No cancer |\n| ------------------ | :------------------------: | --------: |\n| Biomarker positive | a | b |\n| Biomarker negative | c | d |\n\n# Sensitivity\n\nSensitivity is the proportion of people with the condition who will have a positive result. If, for example, the sensitivity of a test is 80%, out of a hundred people with the condition, only 80 will have a positive test result.\n\nSensitivity = a/(a+c)\n\n# Specificity\n\nSpecificity describes the proportion of people without the disease who will have a negative test. A specificity of 90% can be interpreted as, out of 100 people without the disease, 90 will have a negative test result.\n\nSpecificity = d/(b+d)\n\n# Positive Predictive Value\n\nPositive predictive value (PPV) is the proportion of people with a positive test who actually have the disease. PPV varies with prevalence of disease in a population. The lower the prevalence, the lower the positive predictive value. A PPV of 78% will mean that if 100 people tested positive, 78 people will have the disease.\n\nPPV = a/(a+b)\n\n# Negative Predictive Value\n\nNegative predictive value (NPV) is the proportion of people with a negative test who truly do not have the disease.\n\nNPV varies with prevalence of disease in a population. The lower the prevalence, the higher the negative predictive value. An NPV of 97% will mean that if 100 people tested negative, 97 people will not have the disease.\n\nNPV = d/(c+d)\n\n# False positive rate\n\nThe false positive rate is the proportion of those without the condition who will test positive.\n\nFalse positive rate = 1 - specificity\n\nFalse negative rate = 1 - d/(b+d)\n\n# False negative rate\n\nThe false negative rate is the proportion of those with the condition who will test negative.\n\nFalse negative rate = 1 - sensitivity\n\nFalse negative rate = 1 - a/(a+c)\n",
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"question": "A new blood test to help diagnose acute myocardial infarction (MI) has been developed. It is tested on 1000 individuals with suspected myocardial infarction in the emergency department :\n\n| | MI present | MI absent |\n| ----------------- | ---------- | --------- |\n| **Test positive** | 600 | 60 |\n| **Test negative** | 50 | 290 |\n\nWhat is the positive predictive value of the new test?",
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"explanation": "As functioning nephrons decline in CKD, acid secretion is initially compensated by ammonium excretion (up to 40-50mL/min glomerular filtration rate). Beyond this, CKD leads to the retention of hydrogen ions which is buffered by bicarbonate in the extracellular tissue. As the patient approaches ESKD, the plasma bicarbonate stabilises between 12 and 20 mmol/L, and can be partially compensated by increased respiratory rate and hypocarbia",
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"explanation": "Severe hypovolaemia can result in reduced renal perfusion and acute kidney injury, resulting in increased bicarbonate buffering of retained hydrogen ions by damaged nephrons and thus a decreased serum bicarbonate. This patient is not experiencing other signs of hypovolaemia and has not described any large volume haemorrhage from his fistula site",
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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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"explanation": "Type 2 renal tubular acidosis (RTA) is a failure of proximal tubular cells to reabsorb bicarbonate from the urine. It would result in a metabolic acidosis and reduced serum bicarbonate. Type 2 RTA is primarily a complication of genetic disorders such as Fanconi syndrome, cystinosis, and Lowe syndrome. It can be acquired in amyloidosis, multiple myeloma, and with HAART medication, but it is not linked directly to HIV or ESKD",
"id": "33066",
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"name": "Type 2 renal tubular acidosis",
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"explanation": "This patient is experiencing metabolic acidosis (low pH and low bicarbonate) with partial respiratory compensation (hypocarbia from increased respiratory rate) as a result of chronic kidney disease",
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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": "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": "Acute interstitial nephritis (AIN) is most commonly caused by medications (70-75% of cases), predominantly beta-lactam antibiotics, NSAIDs, rifampicin, ciprofloxacin, and diuretics. Classically patients with drug-induced AIN present with rash, pyrexia, and eosinophilia. They would also unlikely present with dark brown urine and more often present with urinary sediment of white cells, red cells, and white cell casts. Gross haematuria would also be distinctly unusual in AIN",
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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": "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": "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": "# 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": "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",
"id": "33077",
"label": "e",
"name": "Colecalciferol with calcium carbonate",
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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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"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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"label": "b",
"name": "Colecalciferol",
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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": "Syringomyelia presents with a bilateral loss of sensation to pain and temperature, but with sparing of light touch, vibration, and proprioception. It typically affects the neck, shoulders, and arms when a syrinx is present in the cervical spine",
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"comment": "TIL. Good question",
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"comment": "ahh its the bristol special ",
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"comment": "can see these sort of niche questions coming up \n",
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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": "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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"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": "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": "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": "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": "# Overview\n\nThe D antigen is found on red blood cells and is an important antigen in the rhesus factor system.\n\nRhesus isoimmunisation can occur when a rhesus negative mother has a baby which is rhesus positive. If any foetal red blood cells enter the maternal circulation, the mother will form anti-D antibodies against them.\n\nThe maternal anti-D antibodies can cross the placenta in subsequent pregnancies and cause Rhesus haemolytic disease if the future baby is rhesus positive.\n\n# Sensitisation events\n\n“Sensitisation” events are events which cause foetal blood to cross the placenta into the maternal circulation and thus these are indications for anti-D prophylaxis.\n\nExamples of sensitisation events include:\n\n- Antepartum haemorrhage\n- Placental abruption\n- Abdominal trauma\n- External cephalic version\n- Invasive uterine procedures such as amniocentesis and chorionic villus sampling\n- Rhesus positive blood transfusion to a rhesus negative woman\n- Intrauterine death, miscarriage or termination\n- Ectopic pregnancy\n- Delivery (normal, instrumental or caesarean section)\n\n# Testing\n\nAll mothers should be tested for rhesus status and anti-D antibodies at booking\n\n# Management of the Rh-D negative mother\n\nPresence of anti-D antibodies can result in incompatibility and haemolysis in future pregnancies. To attenuate this risk, anti-D antibodies are given to patients who have experienced a sensitising event. Anti-D is also given to all non-sensitised Rhesus negative mothers at 28 weeks. Note that anti-D has no effect once sensitisation has already occurred (it is prophylactic only).",
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"explanation": "# Summary\n\nPostpartum haemorrhage (PPH) is defined as the loss of at least 500ml of blood within the first 24 hours of delivery. The primary causes are uterine atony, birth canal injury or tear, retained placental or foetal tissue, and coagulopathies. Risk factors include a previous PPH, high BMI, multiple pregnancies, advanced maternal age, and more. Initial management involves resuscitation with an ABCDE approach and potentially activating a major haemorrhage protocol. Further management strategies may include rubbing the uterus, medication, or surgical treatment. Secondary PPH refers to bleeding from 24 hours to 12 weeks postpartum, typically caused by retained products of conception or endometritis. \n\n\n# Definition\n\n\n\nPostpartum haemorrhage (PPH) is defined as the loss of at least 500ml of blood within the first 24 hours of delivery.\n\n\n# Aetiology\n\n\nThe aetiology of postpartum haemorrhage (PPH) can be remembered using the mnemonic of the 4 'T's: \n\n- Tone: The most common cause of PPH is uterine atony, which is the failure of the uterus to contract after delivery.\n\n- Trauma: PPH can result from a birth canal injury or tear, with risk increased in instrumented deliveries.\n\n- Tissue: Retained placental or foetal tissue can cause continued bleeding.\n\n- Thrombin: Coagulopathies can lead to continued bleeding due to a failure of clotting.\n\n# Risk Factors\n\nRisk factors for postpartum haemorrhage (PPH) include:\n\n- PPH in previous pregnancy\n- BMI >35\n- Multiple pregnancy\n- Parity >4\n- Conditions such as placenta praevia or accreta, placental abruption, pre-eclampsia, gestational hypertension or anaemia\n- Delivery via Caesarean section\n- Induction of labour\n- Instrumented delivery (forceps or ventouse) and episiotomy\n- Prolonged labour (greater than 12 hours)\n- Macrosomia (>4kg baby)\n- Advanced maternal age\n\n\n# Investigations\n\n\nInvestigations for PPH include blood tests for Group/Save and Crossmatch, and consideration of fresh frozen plasma if clotting abnormalities are present. In cases of secondary PPH, ultrasound looking for retained products and endocervical/high vaginal swabs looking for infection are recommended.\n\n# Management\n\n\nInitial management of PPH involves:\n\n- Resuscitation with an ABCDE approach\n- Consideration of activation of a major haemorrhage protocol\n- Laying the woman flat \n- Inserting two large bore cannulas\n- Providing oxygen\n- Considering fresh frozen plasma if clotting abnormalities are present\n\nFurther management strategies may include:\n\n- Mechanical methods such as rubbing the uterus and catheterisation\n- Medical treatments including oxytocin, syntocinon, ergometrine, carboprost, misoprostol, and tranexamic acid\n- Surgical treatments such as intrauterine balloon tamponade, B-lynch suture around the uterus, uterine artery ligation, or hysterectomy \n\nFor secondary PPH, management depends on the cause and can include surgical evacuation for retained products of conception or antibiotics for infection.\n",
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"question": "A 29-year-old primigravida woman has delivered a healthy baby via vaginal delivery. The placenta was intact on delivery, and there were no initial complications. Unfortunately, the mother continues to bleed following delivery and has now lost 1.1L. Bimanual uterine compression is conducted and the mother is catheterised to empty the bladder. Despite this, she continues to haemorrhage and you begin transfusing blood.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "Tympanosclerosis is a cause of bilateral conductive hearing loss, and usually shows signs of scarring of the tympanic membrane with whitish discolouration",
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"explanation": "Chronic suppurative otitis media would typically present with chronic inflammation of the middle ear and mastoid cavity with recurrent otorrhoea through a tympanic membrane. It produces a bilateral conductive hearing loss, although otoscopy would show an oedematous auditory canal, discharge, and granulation tissue in the medial canal with possible perforation of the tympanic membrane",
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"name": "Chronic suppurative otitis media",
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"explanation": "Presbycusis is the leading cause of bilateral sensorineural hearing loss and is characterised by age-related loss of hearing acuity, predominantly at high frequencies. The examination would be Rinne's positive bilaterally in this case with non-localisation in Weber's test",
"id": "33116",
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"explanation": "Multiple sclerosis can rarely present with hearing loss, although it would unlikely produce bilateral hearing loss. It would produce sensorineural hearing loss and so would the patient would be Rinne's positive in one or both ears",
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"explanation": "This patient has presented with history and examination findings consistent with bilateral conductive hearing loss and tinnitus. The most common cause of this in young patients is ear wax, although otosclerosis is an important cause, particularly when otoscopy is unremarkable. It is treated with hearing aids and consideration of stapedectomy",
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"comment": "why is this in the ophthal section....",
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"comment": "Because you didn't see it coming!",
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"explanation": "# Summary\n\nOtosclerosis is a common cause of progressive deafness among young adults, typically manifesting as a conductive hearing loss due to abnormal bone growth around the stapes bone in the middle ear. It is an autosomal dominant condition often with significant family histories. Key signs and symptoms include progressive hearing loss, tinnitus and sometimes vertigo. Diagnosis is usually based on the patient's history, audiometric testing and sometimes CT scan. Initial management may involve hearing amplification through hearing aids or surgical intervention via a stapedectomy.\n\n# Definition\n\nOtosclerosis is a pathological condition of the ear where abnormal bone growth occurs around the stapes bone in the middle ear, impeding its function as a piston onto the cochlea. This can result in progressive conductive hearing loss.\n\n# Epidemiology\n\nOtosclerosis is the most common cause of progressive deafness in young adults. \n\n# Aetiology\n\nOtosclerosis is an autosomal dominant condition, meaning that the majority of patients have significant family histories of the disease.\n\n# Signs and symptoms\n\nPatients with otosclerosis typically present with the following symptoms:\n\n- Progressive hearing loss, often starting unilaterally and then affecting both ears\n- Tinnitus, often associated with the hearing loss\n- Sometimes vertigo, although this is less common\n\n# Differential diagnosis\n\nThe major differentials for otosclerosis include:\n\n- Presbycusis: The most common type of sensorineural hearing loss caused by natural aging of the auditory system. Key symptoms include gradual hearing loss in both ears, difficulty hearing in noisy environments, and trouble distinguishing high-pitched sounds.\n- Meniere's disease: A disorder of the inner ear causing severe dizziness (vertigo), tinnitus, hearing loss, and a feeling of fullness or congestion in the ear. \n- Acoustic neuroma: A slow-growing tumour of the nerve that connects the ear to the brain. Main symptoms are hearing loss, tinnitus, and imbalance.\n\n# Investigations\n\nDiagnosis of otosclerosis typically involves:\n\n- History taking, which often reveals a gradual onset of hearing loss\n- Audiometric testing, which usually shows a conductive hearing loss\n- CT scan may be used in some cases to confirm the diagnosis and evaluate the extent of the disease.\n\n# Management\n\nInitial treatment for otosclerosis may involve:\n\n- Hearing amplification through hearing aids, which can be beneficial in managing the hearing loss associated with otosclerosis\n- Surgical replacement of the stapes bone through a stapedectomy, which can restore hearing in many cases.\n\n# References\n\n[Click here for NICE CKS on hearing loss in adults](https://cks.nice.org.uk/topics/hearing-loss-in-adults/)",
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"question": "A 38-year old pregnant woman presents with gradual-onset bilateral painless hearing loss with tinnitus. Otoscopy is unremarkable with a normal tympanic membrane. Weber's test shows no localisation and she is Rinne's negative bilaterally.\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "Vertebral artery dissection presents as a severe occipital headache as well as posterior fossa ischaemic symptoms manifesting as ataxia, dysarthria, lateral medullary syndrome, and visual symptoms. It would not present with monocular vision loss or with the fundoscopy findings above",
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"explanation": "Optic neuritis is a gradual worsening of vision due to inflammation of the optic nerve, such as in multiple sclerosis. It would not present with sudden monocular vision loss and would not produce intra-retinal haemorrhages on fundoscopy",
"id": "33121",
"label": "d",
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"votes": 485
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"explanation": "Retinal detachment typically presents with amaurosis fugax, floaters, and flashing lights. If the retinal detachment were so severe that it would cause full monocular blindness, then it would be visible on fundoscopy. Given the patient's history of antiphospholipid syndrome with a hypercoagulable state, thromboembolic disease is more likely such as central retinal artery/vein occlusion",
"id": "33120",
"label": "c",
"name": "Retinal detachment",
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"votes": 232
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"explanation": "Usually, CRVO presents in older patients with cardiovascular history, diabetes, or hyperlipidaemia. This patient has antiphospholipid syndrome, a condition known to cause a hypercoagulable state, and so puts them at increased risk of thromboembolic disease. Sudden onset monocular vision loss with relative afferent pupillary defect (RAPD) implies a lesion of the optic nerve. As the retinal artery and veins are the sole source of blood supply to the retina, occlusion of either causes severe damage, blindness, and macular oedema",
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"name": "Central retinal vein occlusion (CRVO)",
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"explanation": "Ocular migraines can present with transient monocular blindness or flashing lights. They would not produce the fundoscopy findings shown above",
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"label": "b",
"name": "Ocular migraine",
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"comment": "CRVO - 'stormy sunset' ",
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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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"question": "A 28-year-old man with antiphospholipid syndrome presents with sudden painless monocular vision loss while driving. Fundoscopy shows macular oedema and multiple intra-retinal haemorrhages in each quadrant in the right eye. There is also a relative afferent pupillary defect.\n\nWhich of the following is the most likely diagnosis?",
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"__typename": "QuestionChoice",
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"explanation": "Thermal laser photocoagulation used to be the first-line treatment for wet AMD with extrafoveal choroidal neovascular membranes, although this has now largely been replaced by anti-VEGF treatment as treatment of subfoveal and juxtafoveal lesions often resulted in a dense scotoma with high recurrence rates",
"id": "33127",
"label": "e",
"name": "Thermal laser photocoagulation",
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"explanation": "Anti-VEGF injections are the mainstay of management of wet AMD, reducing or eliminating macular oedema and reduce neovascularisation, which can reduce disease progression and reverse visual loss",
"id": "33123",
"label": "a",
"name": "Intravitreal injection with vascular endothelial growth factor inhibitors (anti-VEGF)",
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"explanation": "This patient has progressed to advanced wet AMD with significant deterioration in vision. Wet AMD can be treated initially with anti-VEGF intravitreal injections and so this should be trialled first, providing there are no contraindications",
"id": "33124",
"label": "b",
"name": "Observation",
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"__typename": "QuestionChoice",
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"explanation": "Photodynamic therapy (PDT) is frequently used in wet AMD, although only as an adjunct as second-line treatment with anti-VEGF after anti-VEGF has already been tried",
"id": "33125",
"label": "c",
"name": "Photodynamic Therapy",
"picture": null,
"votes": 106
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Intravitreal corticosteroids can be given for macular oedema in diabetes, uveitis, and retinal vein occlusion. It is not currently recommended as a treatment for wet AMD",
"id": "33126",
"label": "d",
"name": "Intravitreal corticosteroids",
"picture": null,
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"__typename": "QuestionComment",
"comment": "is the patient male or female???",
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"comment": "\"She no has subretinal haemorrhages...\" what does that mean? Please fix the vignette ",
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"comment": "I thought anti-VEGF medications must be started within 3 months to be beneficial? \n",
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"explanation": "# Summary\n\nAge-related macular degeneration (ARMD) is the most prevalent cause of blindness in the UK, characterized by the degeneration of photoreceptors in the central retina leading to drusen formation. There are two types: dry (most common, characterised by drusen deposition), and wet (exudative, caused by neovascularisation and carries worse prognosis). Key symptoms include subacute loss of and/or distortion of the central visual field, reduced visual acuity, night blindness, and photopsia. The primary investigation methods include slit-lamp biomicroscopy, colour fundus photography, fluorescein angiography, and ocular coherence tomography (OCT). Management generally involves smoking cessation, and depending on the type of ARMD, zinc and antioxidant supplements (dry ARMD) or anti-vascular endothelial growth factor (anti-VEGF) injections (wet ARMD).\n\n# Definition\n\nAge-related macular degeneration (ARMD) is the leading cause of blindness in the UK. Patients present with subacute loss of and/or distortion of the central visual field.\n\nARMD describes degeneration of photoreceptors in the central retina (macula) that leads to the formation of drusen, which are visible on slit-lamp biomicroscopy.\n\n# Risk factors\n\n- Age – the biggest risk factor for developing ARMD\n- Male sex\n- Smoking (doubles the likelihood of ARMD-related vision loss) – a smoking history should always be taken in patients with ARMD\n- Family history \n- Cardiovascular risk factors: hypertension, diabetes mellitus, coagulopathy, dyslipidaemia\n\n# Dry vs Wet ARMD\n\n| | Dry ARMD | Wet ARMD |\n| ------------- |:-------------:| :-----:|\n| **Prevalence** | 85–90% of cases | 10–15% of cases|\n| **Features** |Drusen, macular thinning (geographic atrophy) | Neovascularisation, bleeding, leakage of fluid|\n| **Prognosis**| Slow progression over decades | Rapid progression over months, with poor prognosis |\n\n# Signs and Symptoms\n\n**Symptoms**:\n\n* Reduced visual acuity, worse for near vision and central vision (patients may say they struggle seeing faces)\n* Variability in visual disturbance from day to day is characteristic\n* Poor vision at night\n* Photopsia – perceived flickering of lights\n* Glare\n\n**Signs**:\n\n* Visual distortion – particularly line perception when tested with Amsler grids. This is known as metamorphopsia.\n* **Dr**usen in **dr**y ARMD – yellow pigmented spots on the retina that are collected around the macula\n* Subretinal or intraretinal haemorrhages in wet ARMD – seen as red patches on the retina around the macula\n\n[lightgallery]\n\n# Differential Diagnosis\n\n\n2. **Diabetic Macular Oedema (DME):**\n - **Diabetic Retinopathy:** Patients with diabetic retinopathy can experience macular oedema, which may lead to similar symptoms as neovascular AMD, such as visual distortion or blurred central vision.\n\n3. **Retinal Vein Occlusion (RVO):**\n - **Central or Branch RVO:** A blockage of retinal veins can lead to macular oedema, haemorrhages, and vision changes similar to those in neovascular AMD.\n\n4. **Central Serous Chorioretinopathy (CSC):**\n - **CSC:** This condition often presents with central serous retinal detachment, leading to vision disturbances. It can mimic wet AMD, but CSC is characterised by serous fluid accumulation rather than CNV.\n\n\nA comprehensive eye examination, including optical coherence tomography (OCT), fluorescein angiography, and fundus photography, is often necessary to differentiate AMD from these conditions and guide appropriate management and treatment decisions.\n\n# Investigations\n\n\n| Technique | Notes |\n|-----------|------|\n| **Slit-lamp biomicroscopy**| Allows identification of exudative, pigmentary or haemorrhagic changes in the retina to allow diagnosis of ARMD |\n| **Colour fundus photography** | Done at each assessment to monitor progression|\n| **Fluorescein angiography** | Used to identify neovascular ARMD to guide anti-VEGF therapy |\n| **Ocular coherence tomography (OCT)** | Allows assessment of all layers of the retina and identification of disease not visible by slit-lamp biomicroscopy |\n\n# Management\n\nSmoking cessation is important for all patients with ARMD.\n\n## Dry ARMD\n\nZinc and antioxidant vitamin A, C and E supplements have been shown to reduce progression by up to 30%.\n\n## Wet ARMD\n\nAnti-vascular endothelial growth factor (anti-VEGF) injections limit progression and can even reverse vision loss – typically administered in monthly injections.\n\n# NICE Guidelines\n\n[Click here for NICE CKS on ARMD](https://cks.nice.org.uk/topics/macular-degeneration-age-related/)\n\n# References\n\n[Click here for more detailed Eye Wiki notes on ARMD](https://eyewiki.aao.org/Age-Related_Macular_Degeneration#Management)",
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"question": "An 81-year-old male with wet age-related macular degeneration (AMD) is reviewed in clinic. Twelve months ago, she had early-stage disease, initially managed with risk factor modification, although her vision has now deteriorated from 6/24 to 6/60 vision in both eyes. On fundoscopy, she has subretinal haemorrhages, lipid exudates, and fibrovascular scarring - corresponding to advanced-stage disease.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "The x-ray shows reduced joint space, osteophytes at the joint margin, and subchondral sclerosis. There is severe joint narrowing at the superior aspect of the acetabulum, although there is no fracture present on the x-ray. Patient's with acetabular fractures would unlikely be able to fully weight bear or straight leg raise and so is less likely based on the clinical history",
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"explanation": "The x-ray shows reduced joint space, osteophytes at the joint margin, and subchondral sclerosis. The joint space is severely narrowed, and the bones are osteopenic, although there is no fracture demonstrated in the image. The patient can fully weight bear and perform straight leg raise, so hip fracture is unlikely",
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"explanation": "Septic arthritis may present similarly in the history, although the examination findings would likely be different. In septic arthritis, the joint is warm, swollen, and very tender. The patient would unlikely be able to weight bear or perform straight leg raise and may present as more clinically unwell",
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"explanation": "Slipped upper femoral epiphysis is a relatively common condition, although it presents in adolescents due to widening of the growth plate during limb growth. It would therefore be unlikely in a fully grown adult. The x-ray findings show an intact femoral epiphysis",
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"explanation": "# Summary\n\nOsteoarthritis (OA) is a chronic, degenerative joint disease characterised by loss of articular cartilage, remodelling of bone with osteophyte formation and mild synovitis. The main risk factor is older age, although obesity, joint injury and genetics also contribute. Presentation is with gradual onset pain that is worse with activity, with associated functional limitations. The most commonly affected joints are the knees, hips and small joints of the hands. Diagnosis is clinical, and severity of disease on X-ray does not correlate well with severity of symptoms. Management should be individualised, with important components being exercise, simple analgesia and optimisation of risk factors (such as maintaining a healthy weight). Where there is ongoing pain and disability, options include intra-articular steroid injections and surgical intervention (such as joint replacement).\n\n# Definition\n\nOsteoarthritis (OA) is the commonest form of arthritis, which is characterised by degenerative changes affecting the entirety of joints affected. Cartilage is lost, the subchondral bone becomes sclerosed with formation of osteophytes and subchondral cysts and there is inflammation of the synovial membrane lining the joint capsule (synovitis). \n\n# Epidemiology\n\n- Approximately 10 million people in the UK have osteoarthritis\n- More women than men are affected\n- Average age of onset is 55 \n- The commonest joint affected is the knee, followed by the hip then the hand\n\n# Aetiology\n\nOsteoarthritis develops due to a combination of factors, with important contributors including:\n\n- Older age\n- Female sex\n- Overweight or obesity\n- Family history of OA\n- Previous joint injury\n- Joint damage due to inflammation (e.g. in patients with inflammatory arthritis)\n- Physical inactivity and reduced muscle strength\n- Low bone density \n- Deformities such as development dysplasia of the hip or leg length discrepancy\n- Stresses on joints due to occupational factors (e.g. repetitive squatting or kneeling) or exercise\n\n# Signs and Symptoms\n\nKey symptoms include:\n\n- Pain in the affected joint exacerbated by use\n- Pain may radiate e.g to the thigh, knee and ankle in hip OA, or to the wrist in hand OA\n- Joints may feel stiff (although prolonged morning stiffness is suggestive of inflammatory arthritis)\n- Functional limitations such as difficulty opening jars (hand OA) or mobilising (knee or hip OA)\n- Locking or giving way of the knee\n\nExamination findings include:\n\n- Restricted and painful range of motion (e.g. in hip OA internal rotation with the hip flexed is particularly painful)\n- Crepitus (friction between bone and cartilage) \n- Affected joints may appear swollen or enlarged\n- A small effusion may form, especially when the knee is affected\n- Synovitis may present with mild soft tissue swelling, tenderness and warmth\n- Muscle wasting and weakness can result from disuse atrophy\n- Joint instability\n- An antalgic gait (\"limping\") in knee OA\n- Trendelenburg gait in hip OA (due to weak abductors patients lurch towards the affected hip)\n- Deformities, including:\n- Heberden's nodes (bony nodules over the distal interphalangeal joints) \n- Bouchard's nodes (bony nodules over the proximal interphalangeal joints) \n- Fixed flexion of the first carpometacarpal joint with hyperextension of the distal joints\n- This may lead to squaring of the joint with subluxation and remodelling\n- Ulnar or radial deviation of joints in the hand may occur\n- In severe hip OA the leg may be shortened due to fixed flexion and external rotation\n- Varus (most commonly) or valgus deformities of the knees \n\n# Differential Diagnosis\n\n- **Inflammatory arthritis** such as rheumatoid arthritis, ankylosing spondylitis; pain that improves with activity and morning stiffness lasting over 30 minutes are differentiating factors, systemic symptoms such as malaise and weight loss may be present\n- **Septic arthritis** is an important differential for all patients presenting with an acutely painful swollen joint (which may occur in an acute flare of osteoarthritis); patients may be systemically unwell with fevers\n- **Fracture** e.g. of the tibial plateau may mimic OA symptoms of pain and limited mobility; usually the patient is unable to weight bear with swelling of the affected area; a history of trauma should be elicited\n- **Malignancy** including bone metastases, multiple myeloma or sarcoma may cause mechanical pain leading to functional limitations; red flags include weight loss, night sweats, persistent pain not relieved by rest and night pain\n- **Greater trochanteric pain syndrome** most commonly occurs in middle-aged women and causes lateral hip pain and tenderness worsened by activity; it may also radiate to the lateral knee\n- **Iliotibial band syndrome** presents with lateral knee pain worse with activity, which is often accompanied by clicking or clunking sounds when the knee is moved; occurs most commonly due to repetitive knee flexion e.g. cyclists or runners \n- **Meniscal tear** may occur after an injury involving a twisting or pivoting movement; similar symptoms of pain, swelling, locking and giving way of the knee and range of motion may be limited on examination\n- **Trigger thumb** may mimic OA of the hand with pain, clicking and catching when the thumb is flexed; a nodule may be palpable in the tendon\n- **Ganglion cysts** occur more commonly in people with OA and present as soft tissue swellings e.g. at the base of the thumb; often asymptomatic but may cause pain and limit movement of the joint\n\n# Investigations\n\nDiagnosis of OA is clinical and can be made without any investigations in a patient of 45 or older if there are no features suggesting another underlying cause of symptoms.\n\nIf there is diagnostic uncertainty or a rapid deterioration in symptoms, **X-rays** of affected joints may be of use. Typical findings can be remembered with the mnemonic \"LOSS\":\n\n- **L**oss or narrowing of joint space due to thinning of cartilage\n- **O**steophytes i.e. formation of new bony spurs at the joint margins\n- **S**ubchondral sclerosis i.e. increased bone density beneath the cartilage\n- **S**ubchondral cysts which are fluid-filled sacs in the subchondral bone\n\n[lightgallery]\n\nHowever, severity of OA features on X-ray may not correlate well with severity of clinical disease.\n\nOther investigations if the diagnosis is in doubt should be targeted to the differential suspected, and may include:\n\n- Further imaging such as MRI to look for ligament or cartilage damage (e.g. a meniscal tear)\n- Joint aspiration with synovial fluid analysis to exclude septic arthritis or crystal arthritis\n- Blood tests for inflammatory markers, rheumatoid factor and anti-CCP (for example) if rheumatoid arthritis is suspected\n\nBaseline bloods for renal function and full blood count should be considered in all patients starting NSAID treatment, especially older patients who are at higher risk of adverse effects.\n\n# Management\n\n**Conservative management:**\n\n- Patient education and advice on self-care e.g. appropriate footwear\n- Weight loss advice and signposting to services in patients with excess body weight\n- Exercise has many benefits including strengthening muscles, improving fitness, reducing pain and improving function\n- Options include online fitness programmes designed for people with arthritis, physiotherapy and supervised exercise sessions\n- Physiotherapy services may also be able to offer manual therapies and joint supports such as braces or splints to reduce load and improve instability\n- Occupational health input may be needed in patients with functional impairment to assess their working environment and suggest adaptations\n- Patients should be asked about psychosocial stressors and support offered e.g. for associated depression and anxiety\n- Occupational therapy input may be helpful to advise on aids and devices to assist with activities of daily living (e.g. walking sticks, sock aids, grab rails, tap turners)\n- Podiatry input may be useful to assess the biomechanics of joint pain and advise on orthotic devices such as insoles\n- Referral to a pain management service may be appropriate for patients who have not responded to maximal medical (and if appropriate, surgical) management of OA\n- Assess falls risk and consider referral to specialist services for patients at risk (e.g. those with abnormal gait or balance, or who have had a fall in the last year)\n\n**Medical management:**\n\n- First-line analgesia is with topical NSAIDs (such as ibuprofen gel) - patients should be made aware that some systemic absorption may occur\n- If this is ineffective or unsuitable, oral NSAIDs should be considered (with a PPI for gastroprotection if there are risk factors for gastrointestinal side effects)\n- Paracetamol or weak opioids (e.g. codeine) may also be used in the short-term\n- Topical capsaicin is another option, especially for knee OA\n- Intra-articular steroid injections may be considered if other treatments are not effective, and/or to enable therapeutic exercise\n\n**Surgical management:**\n\n- Patients with OA of the hip, knee or shoulder who have symptoms significantly impacting quality of life despite optimal medical management should be considered for orthopaedic referral\n- The usual operation offered is an arthroplasty (joint replacement)\n- Rehabilitation before and after surgery is key to optimising outcomes\n\n# Complications\n\n- Joint deformities (as above)\n- Increased risk of falls\n- Functional limitations, e.g. hand OA may making writing, turning keys or fasting buttons challenging\n- Reduced mobility \n- Sleep difficulties\n- Low mood and anxiety\n- Chronic pain\n\n# Prognosis\n\n- Not all cases of OA are progressive and the disease course is variable\n- OA of the hands generally has a good prognosis, especially interphalangeal joint involvement\n- Hip OA has a poorer prognosis with many patients requiring arthroplasty\n- Knee arthroplasties for OA are also common however many patients' symptoms improve or remain stable with time \n- Intermittent flares of OA may occur, where symptoms increase in intensity suddenly\n- Flares tend to last for a few days before improving\n\n# NICE Guidelines\n\n[NICE CKS - Osteoarthritis](https://cks.nice.org.uk/topics/osteoarthritis)\n\n[NICE - Osteoarthritis in over 16s: diagnosis and management](https://www.nice.org.uk/guidance/ng226/)\n\n# References\n\n[WHO fact sheet - Osteoarthritis](https://www.who.int/news-room/fact-sheets/detail/osteoarthritis)\n\n[BNF Treatment Summaries - Osteoarthritis](https://bnf.nice.org.uk/treatment-summaries/osteoarthritis/)\n\n[Patient UK - Osteoarthritis](https://patient.info/doctor/osteoarthritis-pro)",
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"question": "A 67-year-old woman has presented to the GP with worsening left hip pain after a fall from standing height 2 days earlier after tripping on the carpet. Prior to this, she has been experiencing 12 months of worsening bilateral groin pain. The pain is worse later in the day and on prolonged exertion.\n\nOn examination, she has a painful straight leg raise bilaterally but a full range of motion. She can walk unaided but with an antalgic gait on her left side.\n\nAn X-ray of her left hip is shown below.\n\n[lightgallery]\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "This patient has presented with an acute, hot, tender, swollen joint with suspicion of septic arthritis. This can destroy joints quickly with irreversible loss of joint function, and so knee aspiration and intravenous antibiotics should be started",
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"explanation": "This patient may benefit from intravenous fluids as he is pyrexial and tachycardic with likely septic arthritis, although it is not the immediate priority. A joint aspiration followed by intravenous antibiotics must be given first",
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"explanation": "This patient will require admission and intravenous flucloxacillin, although ideally a knee aspiration should be done prior to starting antibiotics if possible, to provide the best chance of growth of any pathogens",
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"comment": "how do we know he isn't septic?",
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"comment": "surely since this guy has a history of trauma, although fracture etc is unlikely, you would want an X-ray before sticking a needle in the joint?",
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"explanation": "# Summary\n\nSeptic arthritis is an infection of the joint characterized by acute inflammation and swelling. It is caused by a bacterial or viral pathogen that infects the synovial fluid. The most commonly implicated organism is Staphylococcus aureus. Noteworthy clinical signs include a tender, swollen joint with reduced mobility, often accompanied by systemic illness. Key investigations include joint aspiration for Microscopy Culture and Sensitivity, along with blood tests showing increased white blood cell count and elevated ESR/CRP. Management typically involves IV antibiotics, joint washout under general anaesthesia, and physiotherapy once the acute infection has resolved.\n\n# Definition\n\nSeptic arthritis is an infection of the joint, specifically the synovial fluid. It is typically caused by a bacterial or viral pathogen and necessitates prompt medical intervention due to the high risk of joint damage and other severe complications.\n\n# Epidemiology\n\nSeptic arthritis has an annual incidence of 4-10 cases per 100,000 patients in Western Europe. It can affect individuals of any age, though certain populations are at a higher risk due to underlying conditions.\n\n# Aetiology\n\nThe most prevalent organism implicated in septic arthritis is Staphylococcus aureus. Other responsible organisms include:\n\n- Gonococcus: primarily in sexually active individuals\n- Streptococcus spp.\n- Gram-negative bacilli\n\nRisk factors contributing to septic arthritis include:\n\n- Pre-existing joint diseases such as rheumatoid arthritis\n- Chronic kidney disease\n- Immunosuppressive states\n- Presence of prosthetic joints\n\n# Signs and Symptoms\n\nThe clinical presentation of septic arthritis usually involves:\n\n- Acute onset of tender, swollen joint\n- Reduced range of joint movement\n- Systemic symptoms such as fever, malaise, or chills\n\n# Differential Diagnosis\n\nDifferential diagnoses for septic arthritis include:\n\n- Gout and pseudogout: characterized by intense joint pain, redness, and swelling, often in the big toe or knee.\n- Osteoarthritis: presents with joint pain, stiffness, and sometimes swelling, generally improving with movement.\n- Rheumatoid arthritis: marked by joint pain, swelling, and stiffness, often symmetrical and worse after rest.\n- Lyme disease: may show erythema migrans rash, flu-like symptoms, and possibly migratory joint pains.\n\n# Investigations\n\nDiagnostic investigations for septic arthritis include:\n\n- Joint aspiration for Microscopy, Culture, and Sensitivity: The aspirate usually appears turbid and yellow, resembling pus.\n- Blood tests: elevated white cell count, high ESR/CRP\n- Blood cultures: to identify causative organisms\n- Imaging: X-ray of the joint may be performed to evaluate for osteomyelitis or other complications.\n\n# Management\n\nThe treatment of septic arthritis involves:\n\n- IV antibiotics guided by local antibiograms and susceptibilities\n- Consideration of joint washout under general anaesthesia to remove infected material\n- Physiotherapy following the resolution of acute infection to restore joint function\n\nComplications of septic arthritis can include:\n\n- Osteomyelitis: infection of the bone\n- Chronic arthritis: persistent joint inflammation\n- Ankylosis: joint fusion resulting in immobility\n\n# References\n\n[Click here for the BNF Treatment Summary for Musculoskeletal infections](https://bnf.nice.org.uk/treatment-summary/musculoskeletal-system-infections-antibacterial-therapy.html)\n\n[Click here for the BMJ Best Practice Summary of Septic Arthritis](https://bestpractice.bmj.com/topics/en-us/486)",
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"question": "A 65-year-old man has presented with 24 hours of worsening painful swelling of his right knee. He recently fell onto his right side while cycling 3 days earlier, sustaining some grazes on his right leg but no other acute injuries. He has type 2 diabetes but no other medical problems.\n\nOn examination, he is pyrexial and tachycardic. His right knee is hot to touch, erythematous, and markedly swollen. There is a reduced range of motion and he is not able to weight bear.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "Due to the association of aspirin with Reye's syndrome in children, it is very rarely given",
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"explanation": "Nebulised adrenaline can be given for temporary improvement of symptoms with upper airway obstruction in croup, although it is not the _next_ best management option. Oral steroids should be given first here unless the child is critically unwell",
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"explanation": "Nebulised salbutamol can be given in acute stridor, although in croup it would unlikely reverse the upper airway narrowing as it does not contain smooth muscle",
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"comment": "Just a random q: Why is it not IV steroids I know it's a GP setting, but wouldn't the IV in a hospital have a faster onset and therefore be more effective?",
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"explanation": "# Summary\n \n\nCroup (also known as acute laryngotracheobronchitis) is a common childhood infection characterised by a harsh barking cough and inspiratory stridor. It is usually mild and self-limiting, however, some cases may cause severe respiratory distress requiring hospitalisation and supportive treatment. Parainfluenza viruses are the commonest causes, but the diagnosis is a clinical one and as symptoms such as stridor can worsen if the child is distressed, investigations should only be done if necessary. Oral steroids should be given to all children; in moderate to severe cases nebulised adrenaline, supplementary oxygen and airway support may be indicated.\n \n\n# Definition\n \n\nCroup, or acute laryngotracheobronchitis, is an upper respiratory tract infection that in most cases has a viral aetiology. Key symptoms include a barking cough, hoarse voice and inspiratory stridor. \n\n# Epidemiology\n \n\nCroup commonly affects children aged from 6 months old to 3 years old, with the peak incidence at 2 years. It is uncommon after the age of 6.\n\nSimilar to other viral infections, it is commonest in the autumn and winter months and is linked to parainfluenza epidemics. \n\n# Aetiology\n \nThe commonest cause is the parainfluenza virus. Other viral causes include adenovirus, respiratory syncytial virus (RSV), rhinovirus and influenza.\nRarely, bacteria can cause croup (e.g. Mycoplasma pneumoniae).\n\nThe pathophysiology involves infection and resulting inflammation of the subglottic and laryngeal mucosa which causes partial obstruction of the airways leading to respiratory distress and stridor.\n\n# Signs and Symptoms\n\n- The prodromal phase of coryzal symptoms, fever and a non-specific cough usually lasts 12-72 hours.\n- Characteristic symptoms of croup such as the harsh barking cough, hoarse voice or cry and inspiratory stridor then develop - these tend to be worse at night.\n- In severe cases, children may become drowsy and lethargic, or conversely more agitated.\n- The usual course of disease is resolution of symptoms within 48 hours (up to a week at most).\n\nOn examination, look for the following red flags that may indicate impending respiratory failure:\n\n- Signs of respiratory distress e.g. intercostal recessions, accessory muscle usage, tachypnoea\n- Cyanosis\n- Decreased level of consciousness\n- Stridor may decrease due to worsening airway obstruction\n- Decreased air entry on auscultation of the chest\n- Tachycardia\n\n# Differential Diagnosis\n \n\n- **Epiglottitis**: Sudden onset high fever, drooling, and dysphagia are seen without the barking cough of croup. Usually secondary to Haemophilus influenzae B and so significantly rarer since routine immunisation against this.\n- **Bacterial tracheitis**: Suspect if acute deterioration following initial viral symptoms, with high fevers, stridor and respiratory distress.\n- **Foreign body aspiration**: No prodrome or fever, usually sudden onset of choking, cough or wheeze after eating or playing with small objects.\n- **Anaphylaxis**: Rapid onset stridor, possible urticarial rash and facial swelling; suspect if history of previous episodes with allergens or family history of atopy.\n \n\n# Investigations\n \nDiagnosis is clinical, and investigations need to be carefully considered as distressing the child may lead to worsening of symptoms due to agitation.\n\nFurther investigation may include: \n\n- Pulse oximetry should be done to determine if supplementary oxygen is required.\n- Chest X-ray may be of use if a differential diagnosis such as an inhaled foreign body is suspected. \n - In croup, an X-ray may show a steeple sign, where the upper trachea is seen to taper.\n \n\n# Management\n\nClassifying the severity of croup is key to determining appropriate management:\n\n| Severity | Description |\n|------------------------------|---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|\n| Mild | Seal-like barking cough but no stridor or sternal/intercostal recession at rest. |\n| Moderate | Seal-like barking cough with stridor and sternal recession at rest; no (or little) agitation or lethargy. |\n| Severe | Seal-like barking cough with stridor and sternal/intercostal recession associated with agitation or lethargy. |\n| Impending respiratory failure | Minimal barking cough, stridor may become harder to hear. Increasing upper airway obstruction, sternal/intercostal recession, asynchronous chest wall and abdominal movement, fatigue, pallor or cyanosis, decreased level of consciousness or tachycardia. The degree of chest wall recession may diminish with the onset of respiratory failure as the child tires. A respiratory rate of over 70 breaths/minute is also indicative of severe respiratory distress. |\n\nMild cases with no stridor or chest wall recessions at rest may be treated at home with a single dose of oral dexamethasone (0.15mg/kg). In children treated at home, families should be safety-netted on signs of deterioration and advised to check on the child regularly and encourage fluids. Paracetamol or ibuprofen can be used for fever and pain.\n\nChildren with any of the following should be considered for hospital admission:\n\n* Stridor and/or sternal recession at rest\n* High fever\n* Respiratory rate > 60\n* Cyanosis\n* Lethargy or agitation\n* Fluid intake < 75% of normal or no wet nappies for 12 hours\n* Aged under 3 months\n* Chronic conditions such as immunodeficiency, chronic lung disease or neuromuscular disorders\n\nManagement is supportive as there is no treatment indicated for the usual causative viruses, and may include:\n\n- Supplementary oxygen if low saturations - consider how best to deliver this so as not to distress the child (e.g. a parent holding an oxygen mask to the face)\n- Steroids for all - if unable to swallow oral dexamethasone or prednisolone can give nebulised budesonide\n- Nebulised adrenaline for temporary symptom relief\n- Anaesthetics +/- ENT input if concerns regarding airway or respiratory failure\n\n# Complications\n\n- Dehydration secondary to poor fluid intake during illness\n- Pneumonia due to secondary bacterial infection \n- Respiratory failure \n- Death is very rare (1 in every 30,000 cases)\n\n# Prognosis\n\nUsually, symptoms resolve within 48 hours but may last longer. Occasionally, severe upper airway obstruction can occur, causing respiratory failure and arrest.\n\n# NICE Guidelines\n\n[NICE CKS: Croup](https://cks.nice.org.uk/topics/croup/)\n\n# References\n \n[BNF Treatment summaries: Croup](https://bnf.nice.org.uk/treatment-summaries/croup/)\n\n[Patient.info: Croup](https://patient.info/doctor/croup-pro)",
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"question": "A 9-month-old child is brought to the GP with two days of pyrexia and worsening barking cough, worse at night time. She has prominent inspiratory high-pitched wheeze with mild intercostal recession at rest. There is no sialorrhoea and her oral mucosa is unremarkable.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "This child has acute otitis media, which would be managed with reassurance and analgesia in the well child. As they are on immunosuppressants, they should be prescribed oral antibiotics unless unwell, where it can be escalated to intravenous antibiotics and admission",
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"explanation": "Back-up antibiotics can be given to children whose signs of infection do not resolve within 3 days or worsen significantly or rapidly at any time. As this child is on immunosuppressants, they should receive antibiotics immediately",
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"label": "d",
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"explanation": "This child has presented with acute otitis media. It is very common in children and is often managed conservatively without antibiotics. Antibiotics should be prescribed if the symptoms last >4 days, they are systemically unwell, are immunocompromised, or have evidence of tympanic perforation. This child is well but on immunosuppression and so oral antibiotics should suffice with good safety netting",
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"label": "a",
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"explanation": "While this patient is on immunosuppressants, they are systemically well with acute otitis media. This will require oral antibiotics at present, but should have a low threshold for admission and intravenous antibiotics if not resolving in the community",
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"label": "b",
"name": "Admit for intravenous antibiotics",
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"explanation": "This child is on immunosuppressants but is systemically well at present with only one previous episode of acute otitis media. A child should be referred to the local emergency department if unwell or have systemic complications of acute otitis media such as meningitis, mastoiditis, intracranial abscess sinus thrombosis, or facial nerve paralysis. A child can be referred to ENT if they have recurrent unexplained episodes or they have a craniofacial abnormality. In this case, she can be managed with oral antibiotics alone",
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"comment": "Also because the child is 2 years old right?",
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"comment": "I thought this was malignant otitis externa ",
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"comment": "Bulging of the tympanic membrane is better explained by otitis media. Typical signs of otitis external are not present eg. swollen eczematous canal etc ",
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"explanation": "# Summary\n \n\nAcute otitis media is a common infection resulting in inflammation of the middle ear. It typically presents with rapid onset of symptoms such as ear pain, fever, irritability, and vomiting. Key investigations include physical examination of the tympanic membrane and assessing systemic illness. Management primarily consists of pain and fever relief, with antibiotics reserved for severe cases or those at high risk of complications. Possible complications can be intracranial or extracranial and may be life-threatening.\n \n\n# Definition\n \n\nAcute otitis media (AOM) is inflammation of the middle ear with an associated effusion. It can be due to bacterial or viral infections. \n \n\n# Epidemiology\n \n\nAcute otitis media is a common condition, particularly among young children, often occurring after a viral upper respiratory tract infection. It affects 70% of children before the age of 2 years, peaking between ages 6-15 months before reducing as the child grows older. It affects boys slightly more than girls. \n \n\n# Aetiology\n\nAcute otitis media is common in children because the less acute angle between the Eustachian tube and the wall of the pharynx enables organisms in the nasopharynx to enter the ear. \n\nThe primary cause of otitis media is bacterial infection, especially prevalent in young children. The most common causative pathogens include: \n\n- Streptococcus pneumoniae \n- Haemophilus influenzae\n- Moraxella catarrhalis \n\nViral causes are less common but normally precede AOM (i.e. respiratory syncytial virus, adenovirus, enterovirus)\n\nRisk factors include:\n\n- Age below 2 years\n- Male sex\n- Parental smoking\n- Immunodeficiency \n- Formula feeding \n- Attendance at nursery or daycare\n- Structural abnormalities (i.e. associated with Down's syndrome, presence of cochlear implants) \n\nRecurrence is more common in children with GORD or those who use dummies. \n \n\n# Signs and Symptoms\n \n\nAcute otitis media typically presents with a rapid onset of symptoms such as:\n \n\n - Earache \n - Ear tugging in younger children\n - Pain\n - Fever\n - Irritability\n - Anorexia\n - Vomiting\n \nOtoscopy may reveal:\n\n- Erythema of tympanic membrane \n- Presence of an effusion in the middle ear: air-fluid levels, bulging tympanic membrane\n- Evidence of perforation: tear in tympanic membrane or discharge \n \n\n [lightgallery]\n \nRed Flag symptoms to screen for (which may indicate intracranial spread):\n \n- Changes to vision \n- Photophobia or headache\n- Nystagmus \n- Post auricular swelling \n- Facial paralysis \n \n\n# Differential Diagnosis\n \n\nThe key signs and symptoms of the differential diagnoses of otitis media include:\n \n - **Chronic Benign Otitis Media**: Characterised by a dry tympanic membrane perforation without chronic infection.\n - **Otitis media with effusion (Glue Ear)**: Persistent presence of middle ear effusion without acute infective symptoms. \n - **Chronic Suppurative Otitis Media**: Persistent purulent drainage through the perforated tympanic membrane.\n - **Upper respiratory tract infection**: Symptoms include a runny nose, cough, and sore throat.\n - **Mastoiditis**: Symptoms include postauricular swelling, ear pain, fever, and irritability.\n - **Otitis externa**: Presents with ear pain, itching, discharge, and hearing loss. Associated with sloughy discharge within the ear canal.\n \n\n# Investigations\n \n\nInvestigations for otitis media primarily involve a physical examination of the tympanic membrane, assessing the presence of systemic illness, and evaluating the patient's symptoms.\n\nFurther investigations may include:\n\n- Culture of discharge in chronic or recurrent AOM\n- CT or MRI if concerns of mastoiditis or intracranial spread\n- Audiometry, following resolution of infection if chronic hearing loss secondary to AOM is suspected\n \n\n# Management\n \nAdmission should be considered for:\n \n - Children under 3 months with a temperature of 38 or more.\n - Children with suspected acute complications of otitis media such as meningitis, mastoiditis, or facial nerve palsy.\n - Children who are severely systemically unwell.\n\nImmediate antibiotics should be given if the child is systemically unwell, or at high risk of complications (e.g. immunocompromised patients). It may be considered if the child has otorrhoea or is aged < 2 years and has bilateral AOM.\n\n\n- Amoxicillin for 5-7 days is typically given as first line. \n - Clarithromycin is used if penicillin allergic. \n- If symptoms do not improve after 2-3 days of antibiotic, then co-amoxiclav may be considered.AOM\n\n\nIf immediate antibiotics are not required:\n \n - Maximise pain relief using paracetamol or ibuprofen.\n - A warm compress over the ear may help to relieve pain.\n - Eardrops containing an anaesthetic and analgesic (phenazone 40 mg/g with lidocaine 10 mg/g) may also be used if antibiotics are not given and there are no signs of eardrum perforation. \n - Parental/caregiver education:\n - Antibiotics make little difference to the duration of symptoms or complication rates associated with AOM.\n - Most children will not require antibiotics. \n - Antibiotics may also cause side effects of diarrhoea and nausea. \n- Consider a delayed antibiotic prescription to be taken if symptoms don't improve within 3 days.\n - Can be considered if the child has otorrhoea or is age <2 years and bilateral AOM.\n \nChildren can return to school once no longer febrile. \n \n\n# Complications of Otitis Media \n \n\nWhilst the majority of children recover without any acute or chronic complications, otitis media can lead to a wide range of complications, many of which are potentially life-threatening. These can be divided into intracranial and extra-cranial complications.\n \n\n**Extra-cranial Complications of Otitis Media**:\n \n - **Facial nerve palsy**: Acute otitis media can lead to a lower motor neuron lesion of the VII cranial nerve. Patients usually recover well with treatment of the otitis media.\n - **Mastoiditis**: Infection can spread from the middle ear to form an abscess in the mastoid air spaces of the temporal bone, leading to postauricular swelling and mastoid tenderness.\n - **Petrositis**: Infection spreading to the apex of the petrous temporal bone, leading to Gradenigo syndrome: otorrhoea, deep ear and eye pain, and ipsilateral VI nerve palsy.\n - **Labyrinthitis**: Inflammation of the middle ear can lead to inflammation of the semi-circular canals, leading to symptoms of vertigo, nausea, vomiting, and imbalance.\n \n\n**Intra-cranial Complications of Otitis Media**:\n \n - **Meningitis**: An important and life-threatening complication presenting with sepsis, headache, vomiting, photophobia, and phonophobia.\n - **Sigmoid sinus thrombosis**: Patients present with sepsis, swinging pyrexia, and meningitis.\n - **Brain abscess**: A patient will present with sepsis and neurological signs due to compression of cranial nerves.\n\n**Chronic complications may include**:\n\n- Hearing loss \n- Otitis media with effusions (\"glue ear\"):\n - If children are under the age of 3, a \"watch and wait\" approach can be taken initially.\n - If children are over the age of 3, or have developed associated language or behavioural problems, then referral to ENT for consideration of grommets would be appropriate. \n- Chronic suppurative otitis media\n - A persistent tympanic membrane perforation results in re-infection and chronic inflammation. It is often associated with conductive hearing loss. It is not commonly seen in the UK and is more common in the developing world.\n\n# Prognosis\n \nThe majority of children will not have severe complications from acute otitis media. 60% of children will have symptom resolution within 24 hours, with most symptom-free by 1 week. \n\n## Recurrent Acute Otitis Media\n\nChildren are considered to have recurrent otitis media if they have had more than 3 episodes of AOM in 6 months or more than 4 episodes in one year. This should prompt consideration of reducing risk factors (i.e. parental smoking, avoiding supine feeding and reducing use of dummies). These children may be referred to ENT for consideration of grommets or prophylactic antibiotics. \n\n# NICE Guidelines\n \n[NICE CKS on otitis media - acute](https://cks.nice.org.uk/topics/otitis-media-acute/)\n \n# References \n \n[NHS Inform Middle Ear Infections](https://www.nhsinform.scot/illnesses-and-conditions/ears-nose-and-throat/middle-ear-infection-otitis-media/) \n \n[Microbial Etiologies of Acute Otitis Media](https://www.clinicalmicrobiologyandinfection.com/article/S1198-743X(14)64948-X/fulltext)\n\n[Patient Info Acute Otitis Media in Children](https://patient.info/doctor/acute-otitis-media-in-children) \n\n[Patient Info Otitis Media with Effusion](https://patient.info/doctor/otitis-media-with-effusion)",
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"question": "A 2-year-old child presents with 2 days of right-sided otalgia and pyrexia. She is otherwise well and had a similar problem two weeks ago which initially self-resolved. She is currently taking immunosuppressants for a liver transplant she had as a neonate for extrahepatic biliary atresia. On otoscopy there is bulging of the tympanic membrane with surrounding erythema.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "Physiological jaundice presents at day 2 or 3 of age, begins to disappear towards the end of the first week, and has usually resolved by day 10. Jaundice lasting longer than 14 days (prolonged jaundice) always warrants further investigation for more sinister pathology",
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"name": "Physiological jaundice",
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"explanation": "Congenital rubella is a cause of early neonatal jaundice, with onset within less than 24 hrs, due to hepatic dysfunction by the rubella virus. This baby has presented with late jaundice and so this is less is unlikely",
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"name": "Congenital rubella",
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"explanation": "G6PD is a cause of early neonatal jaundice, with onset within less than 24 hrs, due to haemolytic anaemia. This baby has presented with late jaundice and so G6PD is unlikely",
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"name": "Glucose-6-phosphate dehydrogenase deficiency (G6PD)",
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"explanation": "Biliary atresia is the obliteration or blockage of the extrahepatic biliary system. It presents as prolonged jaundice in the neonate, lasting longer than 14 days in infants and 21 days in preterm infants. It is characterised by jaundice >14 days, dark urine, pale stools, and poor appetite",
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"explanation": "Crigler-Najjar syndrome is a cause of early neonatal jaundice, with onset within less than 24 hrs, due to inborn errors in bilirubin metabolism. This baby has presented with late jaundice and so this is less is unlikely",
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"comment": "What's the mechanism for the hepatosplenomegaly?",
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"comment": "i think it's bc bile cannot flow out, so the 'traffic jam' results in hepatocellular damage. the congestion may result in increased resistance causing splenomegaly too (similar mechanism to how portal htn can cause splenomegaly?)",
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"comment": "but the jaundice has only been present 3 days??",
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"explanation": "# Summary\n \nBiliary atresia is a severe liver disorder in which the bile ducts of a newborn are progressively fibrosed and destroyed, leading to conjugated hyperbilirubinaemia, liver failure, and death if left untreated. Its key signs and symptoms include prolonged jaundice and indications of biliary obstruction, such as dark urine and chalky white stool. Diagnosis primarily involves a suite of tests, including blood work, hepatic scintigraphy, abdominal ultrasound, and cholangiography. The main treatment strategy is surgical intervention, namely, hepatoportoenterostomy or the Kasai procedure.\n \n\n# Definition\n \n \nBiliary atresia is a rare but serious condition where the bile ducts in a newborn's liver undergo progressive fibrosis and destruction. This leads to conjugated hyperbilirubinaemia, liver failure, and if not treated promptly, death.\n \n\n# Epidemiology\n \n\nThis condition predominantly affects newborns and is the most common cause of neonatal cholestasis. In the UK, it is estimated to affect 1 in 8,000-18,000 live births. Globally, it is the most common reason for paediatric liver transplants. \n \n\n# Aetiology\n \n\nThe cause of biliary atresia is unknown. It's believed to be likely due to a combination of genetic and environmental factors, potentially including an aberrant immune response to a viral infection affecting the bile ducts of the newborn.\n\n20% of affected patients have co-existing congenital anomalies. \n \n\n# Signs and Symptoms\n \n\nPatients with biliary atresia typically present with the following symptoms:\n \n\n - Prolonged jaundice (i.e. jaundice persisting beyond 14 days of life or 21 days if preterm)\n - Signs of biliary obstruction such as dark urine and pale or chalky white stool\n \n\n# Differential Diagnosis\n \n\nWhen examining a neonate with jaundice and symptoms suggestive of biliary obstruction, the differential diagnosis includes:\n \n\n - **Alagille syndrome**: Presents with neonatal jaundice, peripheral pulmonary artery stenosis, and characteristic facial features.\n - **Choledochal cyst**: Presents with the classic triad of abdominal pain, jaundice, and an abdominal mass.\n - **Neonatal hepatitis**: This condition also presents with jaundice, along with hepatomegaly and elevated liver enzymes.\n - **Inborn errors of metabolism**: Conditions such as galactosemia and tyrosinemia can present with jaundice, poor feeding, and developmental delay.\n \n\n# Investigations\n \n\nInvestigations for biliary atresia include:\n\n- Blood tests: These will typically show raised conjugated bilirubin and deranged liver function tests.\n - GGT is typically higher in biliary atresia than other causes of neonatal cholestasis\n- Hepatic scintigraphy (Technetium-99m scan): The liver will take up the isotope but there will be poor excretion into the bowel, indicating destroyed bile ducts.\n- Abdominal ultrasound: This may reveal echogenic fibrosis.\n- Cholangiography: This is the definitive diagnostic test, which will fail to show the normal architecture of the biliary tree, confirming biliary atresia.\n\nLiver histology by percutaneous biopsy is the gold standard. \n\nCurrently screening in the UK is not recommended for biliary atresia. \n \n\n# Management\n\n\nThe main management strategy for biliary atresia is surgical intervention:\n \n\n - Hepatoportoenterostomy (Kasai procedure): This surgery creates a new pathway from the liver to the gut to bypass the fibrosed bile ducts.\n - In severe cases where liver failure is advanced, transplantation may be required. \n\n# Complications\n \nComplications of biliary atresia include:\n \n - Ascending cholangitis following surgery \n - Cirrhosis, portal hypertension and liver failure \n - Osteomalacia or biliary rickets \n\n \n# Prognosis \n\nBiliary atresia prognosis is dependent on the levels of fibrosis and management given. Survival of the native liver is poor - with only 10% of adults having their native liver 30 years after the Kasai procedure, highlighting the role of liver transplant. \n \n\n# NICE Guidelines\n\n[NICE Clinical Knowledge Summary of Jaundice in the Newborn](https://cks.nice.org.uk/topics/jaundice-in-the-newborn/)\n \n# References\n\n[Patient Info Biliary atresia](https://patient.info/doctor/biliary-atresia) \n\n[UK.GOC Health Screening Biliary Atresia](https://view-health-screening-recommendations.service.gov.uk/biliary-atresia/)",
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"question": "A 19-day-old baby is brought to accident and emergency by her parents with jaundice and poor feeding for the last three days. On further questioning, they report she has been passing pale stools and dark urine over the last week. On examination, the baby is visibly jaundiced and has a distended abdomen with hepatosplenomegaly.\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "This would be a reasonable option for a child who has developed constipation and subsequent anal tear/fissure, which is deemed unlikely caused by non-accidental injury. In this case, the more pressing issue is the inconsistency of the story and the child's injury, raising suspicion of possible sexual abuse. In this case, referral to the safeguarding lead is more pressing",
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"explanation": "In this scenario, the child's injuries are not consistent with the father's explanation of events. His symptoms fit with an anal fissure/laceration. This can occur commonly with constipation in children, although a low threshold to suspect sexual abuse is required in a child who has an anal laceration where constipation, Crohn's disease, and passing hard stool have been excluded as the cause. He states he is passing stools normally and regularly, but with fresh red PR bleeding and so an anal fissure is the most likely cause and constipation less likely",
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"explanation": "Topical glyceryl trinitrate (GTN) is given to treat chronic anal fissures in adults, but not children, as it is unlicensed. It is used to relieve pain caused by the fissure and help the external anal sphincter relax, allowing more blood flow to the mucosa, which may further aid the healing process. In children, anal fissures are initially managed by reducing constipation with high-fibre diets, considering use of laxatives, warm baths, and encouragement of drinking plenty of fluids. In this case, the more pressing issue is the inconsistency of the story and the child's injury, raising suspicion of possible sexual abuse. In this case, referral to the safeguarding lead is more pressing",
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"explanation": "Constipation may be the first sign of Crohn's disease, where the child is opening their bowels less than three times per week. Constipation can cause anal fissures in children, resulting in the symptoms this child is experiencing. Often in Crohn's disease, however, there are other signs such as bloating, diarrhoea (sometimes with blood and mucus), reduced appetite, weight loss, fatigue, and slow growth. If inflammatory bowel disease is suspected, then a faecal calprotectin would be appropriate. The history, however, does not suggest this child is constipated or has any other systemic issues. In this case, the more pressing issue is the inconsistency of the story and the child's injury, raising suspicion of possible sexual abuse, and raising concern of a sinister cause for his anal fissure. In this case, referral to the safeguarding lead is more pressing",
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"explanation": "This would be a reasonable option for a child who has developed constipation and subsequent anal tear/fissure, which is deemed unlikely caused by non-accidental injury. Usually a trial of high fibre diet would be trialled first, followed by laxatives if unsuccessful. In this case, the more pressing issue is the inconsistency of the story and the child's injury, raising suspicion of possible sexual abuse. In this case, referral to the safeguarding lead is more pressing",
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"comment": "This is beyond dark",
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"comment": "I honestly would rather not make assumptions about what is truly going on….",
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"comment": "Better to be safe than sorry tho just incase ",
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"comment": "if you don't make assumptions that kid is gonna keep getting abused",
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"comment": "Welcome to the real world...",
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"comment": "it's not about what you would rather do though, you are obligated by law to raise this with the safeguarding team (or by professional duty if it was an adult)",
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"comment": "this kind of question makes it very real. I got goosebumps. ",
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"comment": "Refer to safe guarding and give the dad a slap?",
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"explanation": "# Summary\n \n\nNon-accidental injury refers to any intentional injury inflicted upon a child or harm that occurs due to caregiver neglect. Common signs and symptoms include delayed presentation, inconsistent caregiver narratives, injuries of varying ages, and specific findings such as subconjunctival or retinal haemorrhage. Key investigations include a full skeletal radiographic survey and blood tests to exclude organic causes of presentations. Management involves immediate senior and safeguarding lead notification, admission for safeguarding, treatment of injuries, thorough documentation, and liaison with social care.\n \n\n# Definition\n \n\nNon-accidental injury is a term used to describe any physical harm in a child that is deliberately inflicted or results from the failure of a caregiver to prevent such harm.\n \n\n# Epidemiology\n\nNon-accidental injury predominantly affects children under the age of 2 years. Precise epidemiological data can be challenging to establish due to underreporting and differing definitions of abuse.\n\nThe Crime Survey for England and Wales estimates that 7.6% of adults aged 18-74 had experienced physical abuse before the age of 16. Unfortunately, over 100,000 incidents of physical abuse to children were recorded in 2019. In approximately 80% of cases the abuser is the parent or carer. \n \n\n# Aetiology\n\nNon-accidental injury results from deliberate harm inflicted by a caregiver or due to a caregiver's failure to prevent harm.\n \nRisk factors may include:\n\n- Previous child maltreatment or domestic violence in the family \n- Caregiver substance abuse or mental health issues\n- History of the caregiver being abused\n- Emotional volatility \n- Poverty and poor housing\n- Children in the care system \n\nChildren and young people with disabilities are more likely to be the victim of abuse. \n \n\n# Signs and symptoms\n \n\nIn non-accidental injury, key clinical manifestations may include:\n \n\n - History\n \n - Predominantly occurs in children under 2 years old\n - Often delayed presentation following injury\n - Inconsistencies in the caregiver's narrative, including:\n - Changing stories\n - Severity/type of injury not corresponding to the narrative\n - Injuries in a child not yet independently mobile \n - Unwitnessed injuries\n - Evidence of drug or alcohol use in the household\n - Physical Examination Findings\n \n - Injuries of varying ages\n - Presence of burns or scalds\n - Bruises:\n - To any part of the body in an infant\n - Bruises on the head and face most common sites of abusive bruising\n - Consistent with gripping\n - Subconjunctival haemorrhage\n - Retinal haemorrhage\n - Human bite marks\n - Immersion scalds: most commonly on lower limbs. This may spare the buttocks if they were pressed against the bottom of the bath. \n - Torn frenum: Associated with head injuries or force-feeding of an infant.\n - Cigarette burns \n - Female genital mutilation (see below)\n\n \nWith investigation, other sites of non-accidental injury may include:\n\n- Subdural haemorrhage \n- Long bone fractures in a child not yet independently mobile \n- Fractures of different ages \n- Rib fractures without a history of major trauma \n \n\n# Differential diagnosis\n \n\nDifferential diagnoses can include accidental injury, bleeding disorders, and certain types of malignancies. Each presents with specific signs and symptoms:\n \n\n - **Accidental injury**: Injuries correspond to the history provided and are developmentally appropriate. \n - **Bleeding disorders**: May present with easy bruising, nosebleeds, heavy or prolonged menstrual bleeding, and excessive bleeding from minor cuts or after surgery or dental work.\n - **Haematological malignancy**: May present with fatigue, shortness of breath, recurrent infections, easy bruising or bleeding, and unexplained weight loss.\n\nOther forms of child abuse to consider are:\n \n - **Physical Abuse**: This may include NAI, but also includes female genital mutilation, which is illegal in the UK.\n - **Emotional Abuse**: The psychological ill-treatment or neglect of a child's emotional needs. This may include bullying, corruption, making the child scared or preventing the child from enjoying normal social activity.\n - **Sexual Abuse**: Forcing a child to engage in sexual behaviours ranging from viewing pornography to engaging in sexual activity. \n - **Neglect**: This is when a child's basic needs are not met. The child may not have adequate food, provision of medical care or housing. \n \n\n# Investigations\n \n - It is important to record a detailed history and complete a body map. \n - Radiology: A comprehensive skeletal survey may be necessary to identify:\n \n - Rib fractures\n - Skull fractures or intracranial bleeds\n - Metaphyseal corner fractures (caused by a twisting or pulling motion on a limb)\n - Finger fractures\n - Clavicle fractures\n - Laboratory testing: Blood tests are important to rule out organic causes such as clotting disorders or haematological malignancies.\n - Medical photography may also be used. \n \n\n# Management\n \n\n - Report suspicions: Always inform a senior or a named safeguarding lead if non-accidental injury is suspected.\n - Safeguarding measures: Admit the child for safeguarding while investigations continue. Ensure the safety of other children in the home.\n - Treatment: Administer appropriate medical management for injuries.\n - Documentation: Maintain clear and thorough documentation.\n - Social care liaison: Contact social care to investigate if the child or caregiver is already known to them.\n\n# Complications\n\n- Recurrence or escalation of the NAI\n- Psychological distress \n- Poor health outcomes \n- Substance misuse and employment difficulties later in life\n\n\n# Female Genital Mutilation \n\nFemale Genital Mutilation (FGM) is a term for intentional injuries, cuts and alterations of female genitals without a medical indication. It is illegal in the UK and is considered to be child abuse. It most commonly affects girls between the ages of 0 and 15. It can have serious complications to the physical and mental health of the individual including chronic pain, infection, fertility problems, PTSD and depression. \n\nIt is illegal to perform FGM, assist an individual to perform FGM or fail to protect a girl for whom you're responsible from FGM. \n\nIf you see a patient and are concerned about a patient being at risk of FGM, it is important to contact 999 if the risk is imminent, or if not imminent, to inform the police on 101 and NSPCC on 0800 028 3550. \n\n \n# Prognosis \n \nNon-accidental injury is important for any healthcare worker to be aware of. In 2017/2018, almost 100 children were the victim of a homicide and almost 60 died due to assault. Furthermore, there were over 15,000 cases of neglect and over 50,000 sexual offences against children reported to the police. \n \n\n# NICE Guidelines\n \n[NICE Guidance: Child maltreatment: when to suspect maltreatment in under 18s](https://www.nice.org.uk/guidance/cg89)\n\n[NICE Guidance: Child abuse and neglect](https://www.nice.org.uk/guidance/ng76/resources/child-abuse-and-neglect-pdf-1837637587141) \n\n# References \n \n[Office for National Statistics Child Physical Abuse](https://www.ons.gov.uk/peoplepopulationandcommunity/crimeandjustice/articles/childphysicalabuseinenglandandwales/yearendingmarch2019) \n\n[Patient Info Safeguarding Children](https://patient.info/doctor/safeguarding-children-referral-and-management-of-an-abused-or-at-risk-child) \n\n[BMJ Best Practice Child Abuse](https://bestpractice.bmj.com/topics/en-gb/846/epidemiology)\n\n[NHS Female Genital Mutilation](https://www.nhs.uk/conditions/female-genital-mutilation-fgm/)",
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"question": "An 8-year-old boy is brought to the GP by his father for 3 days of painful bowel motions. He has recently switched GPs and in previous records, he has not been brought in to any of his routine appointments. The child is quiet and withdrawn, but states he has been opening his bowels once per day, with no change in frequency or consistency. His father states it started when he fell down onto one of his toys while playing with his sister. On further questioning, he states there has been some fresh red blood on the toilet paper on wiping. He explains he has been afraid to open his bowels as, for the last three days, he has found it very painful to go, but still has managed without straining. He denies abdominal pain, recent change in diet, or loss of appetite.\n\nOn examination, observations are unremarkable and his abdomen is soft and non-tender. An attempt at PR exam is abandoned as he finds it incredibly painful.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "Listeria monocytogenes accounts for approximately 5% of early-onset neonatal sepsis in premature neonates, although it is rare in those >35 weeks gestation. It is commonly transmitted by aspiration or swallowing of amniotic fluid or vaginal secretions from the mother, although can also be transmitted transplacentally. Pregnant women typically acquire listeria infection from contaminated foods such as contaminated meats, poultry, dairy products, and vegetables",
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"explanation": "GBS is harboured asymptomatically in various sites, including the genital tract. Early-onset neonatal sepsis (<72 hours from birth) is most commonly caused by transmission of pathogens from the mother's genital tract during delivery. Risk factors for neonatal sepsis include prolonged prelabour rupture of membranes, intrapartum fever and suspected or confirmed bacterial infection. The most common pathogen in early-onset neonatal sepsis is GBS, causing 38-43% of all cases",
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"comment": "I don’t get why the mother would have a temperature in labour? Since GBS is harmless for her? ",
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"explanation": "# Summary\n \n\nNeonatal sepsis, a severe infection occurring in infants younger than 90 days of age, is classified into early onset (within 72 hours of life) and late-onset (after 72 hours). Key causes of early onset sepsis include Group B Streptococcus and other microbes ascending from the cervix, and pathogens like Listeria, Toxoplasma, Rubella, and CMV via the placenta. Late-onset sepsis is predominantly caused by Staphylococcus aureus, Staphylococcus epidermidis, E. coli, Pseudomonas, and Klebsiella. Risk factors comprise of premature birth, multiple pregnancies, prolonged rupture of membranes, and maternal intrapartum fever. Initial investigations include FBC, CRP, and blood culture, supplemented by lumbar puncture or chest X-ray based on symptoms. Management typically begins with empirical treatment using benzylpenicillin and gentamicin, followed by adjustments according to culture results and clinical progress.\n \n\n# Definition\n \nNeonatal sepsis is a severe systemic infection occurring in infants less than 90 days old, classified into early onset (within 72 hours of life) and late-onset (after 72 hours of life).\n\nEarly onset neonatal sepsis is often caused by ascending infections from the maternal genital tract or transplacental infections. Late-onset neonatal sepsis usually results from organisms present in the hospital environment or the infant's intestinal flora.\n \n\n# Epidemiology\n \nAround 2 in every 1,000 live births are affected by serious acute infections. The incidence rises to 26 per every 1,000 live births in infants weighing less than 1,000 grams. The majority of cases present in the first 24 hours of life. \n\n# Aetiology\n \n\nEarly onset neonatal sepsis (<72 hours of life) is commonly caused by:\n \n\n - Ascending microorganisms from the cervix:\n \n - E. coli. and Group B streptococcus (GBS) (most common) \n - Typically colonises the genital tract\n - Can cause asymptomatic bacteriuria or UTI in the mother\n - There is no routine screening for GBS in the UK\n - IV benzylpenicillin is the recommended treatment during childbirth if risk factors are present\n \n - Transplacental infections:\n \n - Listeria\n - Toxoplasma\n - Rubella\n - CMV\n \n\nLate-onset sepsis (>72 hours of life) is frequently caused by:\n \n\n - Staphylococcus aureus (most common)\n - Staphylococcus epidermidis\n - E. coli\n - Pseudomonas\n - Klebsiella\n \n\nThe following risk factors significantly increase the likelihood of early-onset neonatal sepsis:\n \n\n - Multiple pregnancies with a sibling who has suspected or confirmed infection\n - Evidence of GBS in a previous baby or current pregnancy\n - Premature birth\n - Rupture of membranes >18 hours for pre-term babies, or >24 hours for term babies\n - Maternal intrapartum temperature >38C\n - Suspected or confirmed maternal sepsis\n - Chorioamnionitis\n \n\n# Signs and Symptoms\n \n\nClinical presentations of neonatal sepsis can vary:\n\n- Nonspecific symptoms \n - Feeding problems\n - Temperature instability\n - Reduced levels of consciousness \n- Respiratory distress\n- Jaundice \n- Shock and multi-organ failure \n \nThere may be signs specific to the site of infection:\n \n - Purulent discharge from the eyes may indicate infection with chlamydia or gonococcus\n - Periumbilical cellulitis \n - Signs of meningitis: bulging fontanelle, seizures \n \n\n# Differential Diagnosis\n \n\nThe clinical picture of neonatal sepsis can mimic a variety of other conditions including:\n \n\n - **Metabolic and endocrine disorders**: Presents with lethargy, poor feeding, and seizures. Hypoglycaemia, hypocalcaemia, and congenital adrenal hyperplasia are common examples.\n - **Cardiovascular disorders**: Manifestations include cyanosis, pallor, and tachypnoea. Examples include congenital heart disease and persistent pulmonary hypertension of the newborn.\n - **Respiratory disorders**: Conditions like transient tachypnoea of the newborn, neonatal pneumonia, and respiratory distress syndrome present with respiratory distress and cyanosis.\n - **Neurological disorders**: Conditions like intraventricular haemorrhage and hypoxic-ischemic encephalopathy present with altered levels of consciousness, seizures, and abnormal tone.\n \n\n# Investigations\n \n\nThe key investigations for diagnosing neonatal sepsis include:\n \n - Temperature is assessed in the axilla \n - Full blood count (FBC), C-reactive protein (CRP), and blood culture. A blood culture should be taken **before** the first dose of antibiotics\n - Consider lumbar puncture (LP) in the presence of neurological symptoms or strong clinical suspicion. LP is essential if neonatal meningitis is suspected as neonates do not often have clear signs of meningitis. \n - Chest X-rays are advised only if there is a strong suspicion of a chest source. NICE advises against a urine culture in early-onset neonatal sepsis\n - CRP should be repeated 24-36 hours after the initial dose of antibiotics\n - If late-onset neonatal sepsis, a urine sample should be sent for microscopy and culture. \n\nIf there are localising signs of infection (ie purulent discharge from the eye or umbilicus) then swabs can be sent for microbiology. \n \n\n# Management\n \n\nFor early-onset neonatal sepsis: \n \n - NICE recommends empirical treatment with IV benzylpenicillin and IV gentamicin \n - The treatment regimen is adjusted based on culture results and the clinical picture\n - Monitoring of gentamicin levels is required due to its narrow therapeutic index and potential for toxicity\n - Antibiotics are typically given for 7 days \n\nFor late-onset neonatal sepsis:\n \n - NICE recommends narrow-spectrum antibiotics (IV flucloxacillin and IV gentamicin) \n\n\nOther special considerations:\n \n - If concerned about bacterial meningitis, IV cefotaxime and IV gentamicin should be used \n - If necrotising enterocolitis is suspected, add metronidazole to cover for anaerobic bacteria \n - In a septic infant born to a febrile mother with chorioamnionitis, to cover for Listeria bacteria, IV amoxicillin and IV gentamicin will be used\n - IV aciclovir may be used if there are signs of potential Herpes Simplex Virus (HSV) infection (i.e. thrombocytopaenia, hepatomegaly, encephalitis, vesicular rash)\n - IV Ganciclovir may be used for suspected congenital cytomegalovirus (CMV) in infants with \"blueberry muffin\" purpuric rash, colitis, thrombocytopenia or hepatic dysfunction. \n - IV ambisome may be used if a fungal cause is suspected (i.e. thrombocytopenia, very low birth weight infants and infants not responding to broad-spectrum antibiotics) \n\n \n# Prevention \n\nThe risk of neonatal sepsis is reduced by:\n\n- Prophylactic antibiotics during labour for women who have evidence of GBS colonisation, are in pre-term labour or have chorioamnionitis. \n\nFor early-onset neonatal sepsis, if the blood cultures in the neonate are positive, obstetrics should be notified to consider antibiotic treatment for the mother. \n\n# Complications\n\n- Sepsis can cause multi-system organ failure and is potentially fatal.\n- Seizures may occur.\n- Chronic complications may include bronchopulmonary dysplasia, intraventricular haemorrhage and necrotising enterocolitis. \n\n\n# Prognosis\n\nNeonatal sepsis has a 2-4% mortality rate in the UK. Early identification and treatment of neonatal sepsis offers the best prognosis. \n \n\n# NICE Guidelines\n \n[NICE Guidelines: Neonatal infection: antibiotics for prevention and treatment](https://www.nice.org.uk/guidance/ng195/resources/neonatal-infection-antibiotics-for-prevention-and-treatment-pdf-66142083827653)\n\n# References\n\n[RCOG Green-top guideline: Group B streptococcal Disease, Early-onset](https://obgyn.onlinelibrary.wiley.com/doi/full/10.1111/1471-0528.14821) \n\n[NHSGGC Paediatrics for Health Professionals Early-onset sepsis in the neonate: prevention and treatment](https://www.clinicalguidelines.scot.nhs.uk/nhsggc-guidelines/nhsggc-guidelines/neonatology/early-onset-sepsis-in-the-neonate-prevention-and-treatment/)\n\n[Patient Info Congenital, Perinatal and Neonatal Infections](https://patient.info/doctor/congenital-perinatal-and-neonatal-infections) \n\n[NHSGGC Paediatric for Health Professionals](https://www.clinicalguidelines.scot.nhs.uk/nhsggc-guidelines/nhsggc-guidelines/neonatology/antibiotic-guidelines-for-the-neonatal-unit/)",
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"question": "A woman brings her newborn boy to A&E with signs of respiratory distress. He was born 36 hours ago at 39 weeks and is currently grunting, tachypnoeic, and pyrexial with nasal flaring and use of accessory muscles. You suspect he has neonatal sepsis.\n\nThe mother had not attended any of her pre-natal screening sessions and reports her waters breaking over 24 hours before she went into labour. She also had a temperature in labour\n\nWhich of the following is the most likely organism responsible for this early-onset neonatal sepsis?",
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"comment": "takes 4-6 weeks for SSRIs to work - whether to stop at 4 or 6 is clinical judgement + patient decision-making",
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"explanation": "# Summary\n\nDepression is a common mental health disorder typified by low mood, anhedonia, significant weight change, sleep and activity changes, fatigue, feelings of guilt or worthlessness, or poor concentration. It is defined by the DSM as the presence of 5 out of 8 symptoms for at least 2 weeks. It is more prevalent in females. Key investigations include FBC, TFT, U+E, LFT, Glucose, B12/folate, cortisol, toxicology screen, and CNS imaging to rule out organic causes. Management strategies encompass low to high intensity psychological interventions, pharmacotherapy including anti-depressants, and in severe cases, lithium or ECT.\n\n# Definition\n\nDepression is a mental health disorder characterised by:\n\n- **ICD-11 Criteria:**\n - Depressive Episode: Depressed mood, loss of interest (anhedonia), and reduced energy (fatigue) persisting for at least two weeks.\n\n- **DSM-V Criteria:**\n - Major Depressive Disorder (MDD): Presence of a major depressive episode lasting at least two weeks, with specific criteria regarding mood, cognitive, and physical symptoms.\n - Persistent Depressive Disorder (Dysthymia): A chronic form of depression lasting for at least two years. \n\nThis consists of the presence of at least five out of a possible eight defining symptoms, during the same two-week period, where at least one of the symptoms is depressed mood or loss of interest or pleasure\n\n**Severity:**\n\n- Mild: Few, if any, symptoms in excess of those required to make the diagnosis (associated symptoms, see below), and the symptoms result in minor functional impairment.\n- Moderate: Symptoms or functional impairment between \"mild\" and \"severe.\"\n- Severe: The number of symptoms, intensity, and impairment are all greatly increased.\n\n\n# Epidemiology\n\nDepression is a highly prevalent mental health disorder. It represents the third most common reason for consulting a general practitioner in the UK. Depression demonstrates a higher prevalence in females.\n\n# Aetiology\n\nThe aetiology of depression involves a complex interplay of genetic and environmental factors. History of previous mental health issues, physical illnesses, and social challenges like divorce, poverty, and unemployment can all contribute to its development.\n\n# Clinical Features\n\nDepression is defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM) as the presence of 5 out of the following 9 symptoms, occurring nearly every day for at least 2 weeks:\n\n1. **Depressed mood or irritability** for most of the day, indicated by either subjective report (feels sad or empty) or observation by others (appears tearful).\n2. **Anhedonia:** Decreased interest or pleasure in most activities, most of the day.\n3. Significant **weight change** (5%) or change in appetite.\n4. **Sleep alterations:** Insomnia or hypersomnia.\n5. **Activity changes:** Psychomotor agitation or retardation.\n6. **Fatigue** or loss of energy.\n7. **Guilt or feelings of worthlessness:** Excessive or inappropriate guilt or feelings of worthlessness.\n8. **Cognitive issues:** Diminished ability to think or concentrate, or increased indecisiveness.\n9. **Suicidality:** Thoughts of death or suicide, or formulation of a suicide plan.\n\n### Additional Features (Severe Depression)\n- **Psychotic Features:** Delusions (e.g. nihilistic delusions, Cotard's syndrome) and hallucinations.\n- **Depressive Stupor:** Profound immobility, mutism, and refusal to eat or drink, sometimes necessitating electroconvulsive therapy (ECT).\n\n# Differential Diagnosis\n\nThe main differentials and their key signs and symptoms include:\n\n- **Bipolar Disorder:** Characterised by periods of mania/hypomania (elevated mood, inflated self-esteem, decreased need for sleep, increased talkativeness, distractibility, increased goal-directed activity) alternating with depressive episodes.\n- **Anxiety Disorders:** Persistent and excessive worry, restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and sleep disturbance.\n- **Psychotic Disorders:** Hallucinations, delusions, disorganised speech, grossly disorganised or catatonic behaviour.\n- **Substance/Medication-Induced Mood Disorder:** Mood disturbance associated with intoxication or withdrawal from substances or side effects of medications.\n- **Adjustment Disorders:** Development of emotional or behavioural symptoms in response to identifiable stressors.\n\n\nVarious organic causes should be considered and ruled out through careful history-taking, physical examination, and relevant investigations. These include:\n\n- Neurological disorders such as Parkinson's disease, dementia, and multiple sclerosis.\n- Endocrine disorders, especially thyroid dysfunction and hypo/hyperadrenalism (e.g., Cushing's and Addison's disease).\n- Substance use or medication side effects (e.g., steroids, isotretinoin, alcohol, beta-blockers, benzodiazepines, and methyldopa).\n- Chronic conditions such as diabetes and obstructive sleep apnea.\n- Long-standing infections, such as mononucleosis.\n- Neoplasms and cancers - low mood can theoretically be a presenting complaint in any cancer, with pancreatic cancer being a notable example.\n\n\n# Investigations\n\n- Standard investigations for depression may include Full Blood Count (FBC), Thyroid Function Test (TFT), Urea and Electrolytes (U&E), Liver Function Test (LFT), Glucose, B12/folate levels, cortisol levels, toxicology screen, and imaging of the Central Nervous System (CNS).\n- These help rule out organic causes (listed above) such as endocrine disorders (e.g. thyroid disorders).\n- There are several questionnaires that can also be used to help assess depressive symptoms, such as the Hospital Anxiety and Depression (HAD) Scale and Patient Health Questionnaire (PHQ-9).\n\n# Management\n\nDepression is usually managed in primary care. GPs can refer to secondary care (Psychiatry) if there is a high-suicide risk, symptoms of bipolar disorder, symptoms of psychosis, or if there is evidence of severe depression unresponsive to initial treatment.\n\r\n**Persistent subthreshold depressive symptoms or mild-to-moderate depression:**\n\n- 1st line = Low-intensity psychological interventions (individual self-help, computerised CBT). \r\n- 2nd line = High-intensity psychological interventions (individual CBT, interpersonal therapy) \r\n- 3rd line = Consider antidepressants \r\n\r\n**Mild depression unresponsive to treatment and moderate-to-severe depression:**\n\n- 1st line = High-intensity psychological interventions + antidepressants (1st line = SSRI)\r\n- 2nd line (Treatment-resistant depression) – switch antidepressants and then use adjuncts \r\n\r\n**Severe depression and poor oral intake/psychosis/stupor:**\n\n- 1st line = ECT \n- Although the exact mechanism remains elusive, it is thought that the induced seizure, rather than the ECT procedure itself, has therapeutic benefits. Short-term side effects of ECT include headache, muscle aches, nausea, temporary memory loss, and confusion, while long-term side effects can include persistent memory loss. Due to the induced seizure, there is a risk of oral damage, and due to the general anaesthetic, a small risk of death.\r\n\n**Recurrent depression:** \n\n- Treated with antidepressant + lithium \r\n\n\nMedical management of depression - additional notes:\n\n- First-line pharmacological treatment typically involves a Selective Serotonin Reuptake Inhibitor (SSRI) such as sertraline. SNRIs such as venlafaxine can also be used first-line, but are less preferable due to the risk of damage from overdose, which is less likely with SSRIs.\n- In people aged 18-25 there is an increased risk of impulsivity and suicidal risk upon commencing antidepressant medication and so they should have a follow-up appointment arranged after one week to monitor progress. Initial reviews can otherwise be arranged 2-4 weeks after starting medication in patients >25.\n- Continuation of antidepressants for at least six months post-remission is recommended to mitigate relapse risk. Tapering should be done gradually over a four-week period when discontinuing antidepressants.\n\n\n\n# NICE Guidelines\n\n[NICE Guidance on the Management of Depression](https://www.nice.org.uk/guidance/cg90)",
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"question": "A 78-year-old woman has been seeing her GP for the last 4 months with symptoms of depression. She was started on sertraline a week ago and has presented for her 1 week follow-up appointment. She states she feels no different and would like to try another agent.\n\nFor how long should her treatment be continued before considering a switch to a different anti-depressant?",
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"explanation": "A patient can be detained under section 5(4) of the mental health act by a nurse who has been qualified and trained to work with mental health problems or learning disabilities. It is a short term emergency section to detain a patient for up to 6 hours until they can be seen by a doctor. This patient has already been detained under section 5(2) and so detention under section with a longer time period would be required to provide further assessments and/or treatment. The most appropriate answer would therefore be section 2 to detain the patient for up to 28 days",
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"explanation": "When a patient is detained under section 3 of the mental health act, they can be detained for up to 6 months with option of further renewal. This patient has only had a short assessment so far and so would need a longer period of detention. Usually the least restrictive method, and therefore the shortest time required, would be used and so detention under section 2 would be used initially to detain the patient for 28 days",
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"explanation": "Section 136 is slightly different to section 135. Both are carried out by police officers if they believe the patient has a mental disorder and in need of immediate care of control where they can detain a patient against their will to be taken to a place of safety until examined by a doctor. Section 135 is used when police require entry to a persons home, if need be by force, when they believe a person is at serious risk of harming themselves or others. Section 136 is used when police find the person in a public place and feel they need to bring the patient to a place of safety. A patient can be detained under section 135 and 136 for up to 24 hours",
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"comment": "Can i just point out for clarification, you can't use a 5(2) in A+E.",
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"comment": "As a med student not studying in England where the law is different, these questions make me so stressed",
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"comment": "also police can only enter patient's property under section 136 (NOT 135 as stated in the stem)",
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"comment": "136 is used in public to a place of safety\n135 is used to enter a house ",
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"explanation": "# Summary\n\nThe Mental Capacity Act (MCA) is a crucial legal framework that provides guidance on decision-making for individuals who may lack the capacity to make specific choices. Enacted in 2005, the MCA establishes the principles and procedures for assessing mental capacity and ensures that decisions made on behalf of individuals without capacity are made in their best interests. Capacity, as defined by the MCA, involves the ability to understand, retain, weigh, and communicate information relevant to a specific decision. It is time- and decision-specific. The Act empowers individuals to make choices whenever possible, respecting their autonomy, while also safeguarding those who lack capacity through a structured and person-centered decision-making process.\n\n# 5 Key Principles\n\nThe Mental Capacity Act (MCA) is used when a patient lacks capacity. It allows doctors (or less commonly, those with Lasting Power of Attorney) to make decisions in the best interests of their patient. There are 5 key principles:\n\n- A person is assumed to have capacity unless proven otherwise\n- Steps must be taken to help a person have capacity\n- An unwise decision does not mean a person lacks capacity\n- Any decisions made under the MCA must be in the person's best interests\n- Any decisions made should be the least restrictive to a person's rights and freedoms\n\n# Assessing capacity\n\nAssessing capacity is a two step process: \n\n1) Is there an impairment of, or disturbance in, the functioning of the mind or brain? \n\nIf yes, then step 2) For a person to lack capacity they must show an 'impairment of, or disturbance in, the functioning of the mind or brain' AND they are unable to undertake any of the following:\n\n- Understand relevant information\n- Retain the relevant information\n- Weigh up the relevant information\n- Communicate a decision\n\n**If they are unable to do one of these things then they do not have capacity.**\n\n### Next steps\n\n- If they do not have capacity, can we wait until they do before making a decision? Consider the (clinical) urgency of the decision that needs to be made\n- Do they have a Lasting Power of Attorney (LPA), Advanced Directive, or Advanced Statement?\n- Does a best interests meeting need to be had, including the MDT, and relatives/friends who know the patient well. If there is nobody who can advocate for the patient, an Independent Mental Capacity Advocate (IMCA) can represent them when making a best interests decision.\n\n# Deprivation of Liberty Safeguards (DOLS)\n\nThe Deprivation of Liberty Safeguards is the procedure in law used where it is necessary to deprive a patient or resident of their liberty as they lack capacity to consent to treatment or care to keep them safe from harm. It safeguards for those who lack capacity and do not want to be somewhere and are not free to leave. There are a series of checks to make sure that any care someone receives that restricts their freedom is appropriate and in their best interests. \n\nIf a patient lacks capacity to make decisions about ongoing care and are not free to leave, then an application for a DOLS may be made (proportionate and not excessively restrictive actions). This can be common in acute medical/geriatrics wards.\n\nThe following conditions must be met to allow a person to be deprived of their liberty under the safeguards:\n\n* The person must be 18 or over.\n* The person must be suffering from a mental disorder.\n* The person must be a patient in hospital or a resident in a care home.\n* The person lacks capacity to decide for themselves about the restrictions which are proposed so they can receive the necessary care and treatment.\n* The proposed restrictions would deprive the person of their liberty.\n* The proposed restrictions would be in the person's best interests.\n* Whether the person should instead be considered for detention under the Mental Health Act.\n* There is no valid advance decision to refuse treatment or support that would be overridden by any DoLS process.\n\n# References\n\n[Click here to see information on Legislation UK on the MHA](https://www.legislation.gov.uk/ukpga/1983/20/contents)\n\n[Click here to see information on Legislation UK on the MCA](https://www.legislation.gov.uk/ukpga/2005/9/contents)",
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"question": "A 28-year-old man was admitted under psychiatry for an acute psychotic episode after his colleague found plans to end his life and called the police. The police brought him to hospital under section 135. In A&E, he exhibited persecutory delusions and suicidal ideation, stating he has made several plans to end his life and would do so if discharged.\n\n\nHe has been held under section 5(2) while awaiting a full assessment and it has been decided that he is not safe to leave as he is a high risk to himself with serious concern that he would end his life if he were to leave.\n\n\nUnder which section of the mental health act (1983) should he be detained?",
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"explanation": "This patient has recently started clozapine for his schizophrenia and has now developed pyrexia, general malaise, and symptoms of pharyngitis. Clozapine is associated with a relatively high risk of agranulocytosis and neutropenia within the first few months of treatment. They are therefore at risk of neutropenic sepsis.\n \n\n Unfortunately we do not know this patients neutrophil count yet although, given his risk factors, he should be started on intravenous antibiotics within one hour of recognition of signs of sepsis. As patients with neutropenia cannot mount the normal immune response to infection that others can, they can look and feel completely well for some time, with relatively normal observations, before rapidly becoming unwell and deteriorating. It is therefore important to have a high index of suspicion and treat aggressively early",
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"explanation": "This patient has recently started clozapine and so is at risk of agranulocytosis and neutropenia (black box warning). We do not have his blood results back but, given he has developed new pyrexia with general malaise, he must be treated as suspected neutropenic sepsis",
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"explanation": "This patient is at risk of agranulocytosis and neutropenia and has signs and symptoms of possible sepsis so reassurance is not a safe option, and he requires urgent treatment",
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"explanation": "Nasendoscopy is an excellent way to assess pathology within the nasal passage, larynx, and vocal cords. If epiglottitis or supraglottitis were suspected in this patient, then urgent referral to ENT would be warranted with help from anaesthetics for airway support. This patient is not showing signs of airway obstruction e.g. drooling, stridor, hoarse voice, or respiratory distress and so epiglottitis is unlikely",
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"explanation": "This patient has recently started clozapine and so is at risk of agranulocytosis and neutropenia (black box warning). We do not have his blood results back but, given he has developed new pyrexia with general malaise, he must be treated as suspected neutropenic sepsis",
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"explanation": "# 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 35-year-old man is currently detained in a psychiatric unit under section 3 of the mental health act after an acute deterioration of his schizophrenia two months ago, for which he was started on clozapine. He complains of a two-day history of a sore throat and general malaise. On examination his respiratory rate is 16, oxygen saturations are 100% on room air, heart rate 95, blood pressure 118/65, temperature 38.0°C. He looks well, and has an erythematous oropharynx with no purulent discharge and no deviation of his uvula. \n\nRoutine bloods and blood cultures have been taken.\n\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "CURB-65 is made up of five components, all scoring either 0 or 1: confusion, urea >7mmol/L, respiratory rate ≥ 30, systolic BP < 90 mmHg or diastolic BP ≤ 60 mmHg , and age ≥ 65. This patient scores for all sections except respiratory rate, therefore she scores 4, putting her in the highest risk group with 27.8 30-day mortality",
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"explanation": "CURB-65 is made up of five components, all scoring either 0 or 1: confusion, urea >7mmol/L, respiratory rate ≥ 30, systolic BP < 90 mmHg or diastolic BP ≤ 60 mmHg , and age ≥ 65. It's purpose is to estimate mortality for community-acquired pneumonia to help determine whether they should be managed as an inpatient or outpatient i.e. whether to admit them. CURB-65 score 0-1 assigns them to a low risk group with 2.7% 30-day mortality where they can likely be managed as an outpatient. Score 2 assigns them to moderate risk group with 6.8% 30-day mortality where they should either be managed as an inpatient or as an outpatient with close follow-up. Score 3 assigns them to severe risk group with 14.0% 30-day mortality where they should be admitted with possible intensive care admission. Score 4-5 puts them in the highest risk group with 27.8% 30-day mortality where they should be admitted with possible intensive care admission. This patient scores for all sections except respiratory rate, therefore she scores 4, putting her in the highest risk group",
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"explanation": "CURB-65 is made up of five components, all scoring either 0 or 1: confusion, urea >7mmol/L, respiratory rate ≥ 30, systolic BP < 90 mmHg or diastolic BP ≤ 60 mmHg , and age ≥ 65. This patient scores for all sections except respiratory rate, therefore she scores 4, putting her in the highest risk group with 27.8 30-day mortality",
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"explanation": "CURB-65 is made up of five components, all scoring either 0 or 1: confusion, urea >7mmol/L, respiratory rate ≥ 30, systolic BP < 90 mmHg or diastolic BP ≤ 60 mmHg , and age ≥ 65. This patient scores for all sections except respiratory rate, therefore she scores 4, putting her in the highest risk group with 27.8 30-day mortality",
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"explanation": "CURB-65 is made up of five components, all scoring either 0 or 1: confusion, urea >7mmol/L, respiratory rate ≥ 30, systolic BP < 90 mmHg or diastolic BP ≤ 60 mmHg , and age ≥ 65. This patient scores for all sections except respiratory rate, therefore she scores 4, putting her in the highest risk group with 27.8 30-day mortality",
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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 72-year-old woman with advanced motor neurone disease presents to A&E with a 3-day history of worsening breathlessness, fever, and acute confusion.\nOn examination her respiratory rate is 28, peripheral oxygen saturations 95% on 2L nasal cannula, heart rate 107, blood pressure 104/58, temperature 38.2°C\n\nAuscultation reveals reduced air entry at both bases and coarse inspiratory crepitations in the left lower zone. GCS: 13 (E4V3M6). \n\nChest X-ray reveals bibasal atelectasis and left lower zone patchy consolidation\n\nBloods reveal the following\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|118 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|17.1x10<sup>9</sup>/L|3.0 - 10.0|\n|Urea|11.1 mmol/L|2.5 - 7.8|\n|Creatinine|170 µmol/L|60 - 120|\n|C Reactive Protein|135 mg/L|< 5|\n\n\nWhat of the following is the patient's calculated CURB-65 score?",
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"explanation": "Intramuscular adrenaline (1:1000) is part of the primary management of anaphylaxis. This patient is assumed to be having an acute severe exacerbation of asthma and so intramuscular adrenaline would not be indicated unless there were suspicion of anaphylaxis",
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"explanation": "This patient is experiencing an acute severe exacerbation of his asthma. The next step in their management would be intravenous magnesium sulfate. Intravenous aminophylline is rarely used in acute severe exacerbation of asthma, and would only be considered in life-threatening exacerbations of impending respiratory failure after discussion with senior colleagues",
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"explanation": "This patient is experiencing an acute severe exacerbation of his asthma. Life-threatening asthma would be characterised by PEFR <33% best or one of: oxygen saturations <92%, altered consciousness, exhaustion, cardiac arrhythmia, hypotension, cyanosis, poor respiratory effort, silent chest, or confusion.\n\nManagement for acute severe exacerbation of asthma is: Oxygen, inhaled short acting bronchodilator (beta-2 agonist) driven by wet oxygen nebs, and corticosteroids e.g. oral prednisolone or intravenous hydrocortisone (same efficacy) for minimum 5 days or until recovery. If requires further therapy, then nebulised ipratropium which can be given back-to-back with salbutamol if not improving after 15-30 minutes of treatment. If the patient is still not improving, then you could consider IV magnesium sulfate over 20 minutes.\n\nOther further management may include intravenous aminophylline and mechanical ventilation",
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"explanation": "This patient is experiencing an acute severe exacerbation of his asthma. He should be discussed with senior colleagues regarding next steps in management, where he will likely be given intravenous magnesium sulfate. If this were to fail, or the patient was more unwell and experiencing a life-threatening asthma exacerbation, then early consultation with critical care for consideration of mechanical ventilation is paramount. This is not required just yet as he is having an acute severe exacerbation with other treatment options available.\n\nKew KM, Kirtchuk L, Michell CI. Intravenous magnesium sulfate for treating adults with acute asthma in the emergency department. Cochrane Database of Systematic Reviews 2014, Issue 5. Art. No.: CD010909. DOI: 10.1002/14651858.CD010909.pub2",
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"explanation": "Intravenous salbutamol can be considered if inhaled beta-2 agonist therapy cannot be used reliably. This patient shows no issues of tolerating nebulised salbutamol and therefore intravenous salbutamol would not be indicated",
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"explanation": "# Summary\n\nAsthma is a common disease of the airways, involving reversible bronchoconstriction, hyperreactivity and chronic inflammation. When bronchoconstriction is triggered (an “asthma attack”), patients experience episodes of wheeze, dyspnoea, cough and chest tightness. Initial investigations for all adults with suspected asthma are fractional exhaled nitric oxide (FeNO) or a full blood count looking for eosinophilia. If neither of these are confirmatory, patients should be assessed with spirometry including bronchodilator reversibility. Management involves a stepwise approach to medications, starting with “reliever therapy” (usually short-acting beta-2 agonists such as salbutamol inhalers) in combination with “preventer therapy” medications including inhaled corticosteroids, leukotriene receptor antagonists and long-acting beta-2 agonist inhalers. Allergen avoidance, smoking cessation, regular peak flow monitoring and inhaler technique are all key to good asthma control.\n\n# Definition\n\nAsthma is a common disease in both adults and children, characterised by intermittent \"asthma attacks\" with wheeze, cough, shortness of breath and chest tightness. There are several underlying mechanisms that centre around reversible bronchoconstriction, hyperreactivity and chronic inflammation.\n\n# Epidemiology\n\nIn the UK, approximately 8 million people have been diagnosed with asthma, of which 5.4 million are on treatment. Onset is usually in childhood and some find symptoms remit with age, although relapse is possible after long periods of being well.\n\nOn average, three people die from an asthma attack each day in the UK. The majority of these deaths are preventable, with an estimated 7/10 people with asthma not receiving basic preventative care such as inhaler technique checks and a personalised asthma plan.\n\nPeople experiencing socioeconomic deprivation are more likely to have asthma and to have worse outcomes (e.g. higher rates of hospitalisation). This is multifactorial, with these groups more likely to be exposed to triggers such as smoking and air pollution, and to have lower health literacy and access to healthcare.\n\n# Pathophysiology\n\nAsthma is often associated with a personal and/or family history of atopy, including the atopic triad of asthma, allergic rhinitis, and eczema. In asthma, there is an exaggerated response to a wide range of triggers. These include:\n\n- Cold air and exercise\n- Pollution and cigarette smoke\n- Allergens such as animal dander, dust mites and pollen\n- Irritants such as perfumes, paints or air fresheners\n- Medications such as NSAIDs or beta-blockers\n\nThese trigger a type 1 hypersensitivity reaction which is mediated by IgE. T Helper 2 cells produce IL4, IL5 and IL13 cytokines which activate the humoral immune system, leading to the proliferation of eosinophils, mast cells and dendritic cells. These cells then produce more inflammatory mediators such as leukotrienes and histamine.\n\nThis inflammation contributes to airway hyperresponsiveness leading to bronchospasm, as well as mucus hypersecretion that also obstructs airways. Over time in severe asthma, airway remodelling mediated by fibroblasts causes chronic obstruction and thickening of smooth muscle.\n\n# Risk factors\n\n- Family history of asthma or atopy\n- Personal history of atopy (eczema, allergic rhinitis, allergic conjunctivitis)\n- Exposure to smoke, including maternal smoking in pregnancy\n- Respiratory infections in infancy\n- Prematurity and low birth weight\n- Obesity\n- Social deprivation\n- Occupational exposures (e.g. flour dust, isocyanates from paint)\n\n# Symptoms\n\n- Wheeze\n- Dyspnoea\n- Cough\n- Chest tightness\n\nThe above symptoms should be episodic and usually show **diurnal variation** (worse at night or in the early morning). The patient may be able to identify specific triggers as listed above.\n\n# Signs\n\nIn between asthma exacerbations, clinical examination may be normal. If asthma is poorly controlled or during an exacerbation, signs include:\n\n- Tachypnoea\n- Increased work of breathing\n- Hyperinflated chest\n- Expiratory polyphonic wheeze throughout the lung fields\n- Decreased air entry (if severe)\n\n\n# Differential diagnosis\n\n- **Bronchiectasis** - usually associated with a productive cough, patients get frequent chest infections and coarse crackles rather than wheeze predominate on examination.\n- **Vocal cord dysfunction** - shares many triggers with asthma, inspiration more difficult than expiration, may have stridor.\n- **Chronic obstructive pulmonary disease** - patients usually >35 years old with a significant smoking history, may overlap with asthma in some.\n- **Gastro-oesophageal reflux disease** - microaspiration of stomach acid due to reflux can cause episodes of cough and wheeze which mimic asthma (although these may coexist and reflux can trigger asthma exacerbations). Symptoms are often postural and related to eating.\n- **Eosinophilic Granulomatosis with Polyangiitis** (Churg-Strauss syndrome) - small vessel vasculitis associated with pANCA, aside from asthma symptoms include nasal polyps, sinusitis, purpuric rashes and peripheral neuropathy.\n\n# Investigations \n\n- **FeNO (fractional exhaled nitric oxide) testing:** offer this **or** blood eosinophil count to all adults to confirm eosinophilic airway inflammation, asthma can be diagnosed if this is >50 parts per billion.\n- **Full blood count** to check **eosinophil count:** offer this **or** FeNO first-line to all adults - asthma can be diagnosed if this is above the normal reference range.\n- If neither of these confirm asthma, **spirometry** with **bronchodilator reversibility** should be offered to confirm airway obstruction (i.e. FEV1/FVC<70%). A bronchodilator (e.g. salbutamol inhaler) is given and spirometry repeated to assess response to treatment. An improvement in FEV1 of 12% or more or 200ml is diagnostic of asthma.\n- If spirometry is delayed or not available, patients may be asked to monitor their peak flow twice a day for 2 weeks and keep a diary of the readings. This is then used to assess **peak flow variability** (the difference between the highest and lowest readings as a percentage of the average PEF). Variability >20% is a positive result.\n- If none of the above are confirmatory, patients may be referred to specialist services for a **direct bronchial challenge test**, where histamine or metacholine is inhaled to trigger bronchoconstriction. Airway hyperresponsiveness is assessed by looking at the concentration of the triggering medication required to cause a 20% decrease in FEV1 - 8mg/ml or less is a positive result.\n\nNote: All of the above tests may be falsely negative in patients treated with inhaled corticosteroids.\n\n# Management of Chronic asthma\n\nThe aim of chronic asthma management is to achieve complete control over symptoms, with no need for rescue medications and no restrictions on physical activity. All patients should have a personalised asthma action plan which should be reviewed at least annually. Components of management include:\n\n## Non-pharmacological\n\n- Teach good inhaler technique and review this regularly\n- Spacer devices can be used to optimise medication delivery\n- Regular peak flow monitoring\n- Smoking cessation\n- Advice on avoiding triggers where possible (e.g. allergens, certain medications)\n- Ensure vaccinations are up to date, including annual influenza vaccination\n- Assess for occupational asthma by asking if symptoms are better when the patient is away from work and arrange specialist referral if this is suspected\n\n## Pharmacological\n\n- Prescribe all patients a combination inhaler with a **long-acting beta-2 agonist** (LABA) i.e. formoterol and a low-dose **inhaled corticosteroid** (ICS) i.e. budesonide to use as a reliever inhaler (i.e. PRN) - this is referred to as anti-inflammatory reliever (AIR) therapy.\n- Patients who do not respond adequately to AIR therapy, who are highly symptomatic at presentation or who present with a severe asthma exacerbation should be started on a low-dose **maintenance and reliever therapy inhaler** (MART). MART is a combination inhaler with ICS and a fast-acting LABA (e.g. beclomethasone + formoterol which is also known as Fostair), which is used as both a reliever inhaler (PRN) and as maintenance treatment (usually twice daily).\n- The next step would be increasing the ICS dose from low to **moderate** in the MART inhaler.\n- At this stage if asthma is not controlled, check FeNO and blood eosinophil count and refer to specialist asthma services if either are raised.\n- If neither are raised, consider adding either a **leukotriene receptor antagonist** (LTRA) such as montelukast (this is a tablet taken every night) or a **long-acting muscarinic agonist** (LAMA) such as tiotropium.\n- One of these should be trialled for 8-12 weeks alongside the moderate-dose MART - if asthma is well-controlled it can be continued.\n- If there is some improvement in control but this is still inadequate, the other medication can be trialled in addition (i.e. moderate dose MART + LTRA + LAMA).\n- If control has not improved, stop the medication and try the other one - if this is not successful refer to specialist services.\n- Options in specialist clinics include therapies such as **biologics** (e.g. omalizumab, which targets IgE).\n\nOther than patients who are not responding to treatment, the following situations shold also prompt a secondary care referral:\n\n- Uncertainty regarding diagnosis\n- Suspected occupational asthma\n- Severe or life-threatening asthma requiring admission to hospital\n- Multiple exacerbations requiring oral steroid treatment per year\n\n# Acute asthma\n\nAcute asthma exacerbations are graded in severity as below:\n\n\n| Severity | Clinical Features |\n|-----------------------|-----------------------------------------------|\n| Moderate | PEFR > 50% of predicted or best |\n| | No features of severe/life-threatening asthma |\n| Severe | PEFR 33-50% of predicted or best |\n| | Heart rate > 110 |\n| | Respiratory rate > 25 |\n| | Unable to complete sentences in one breath. |\n| | Accessory muscle use |\n| Life-threatening | PEFR < 33% of predicted or best |\n| | Oxygen saturation < 92% or cyanosis |\n| | Altered conciousness/confusion |\n| | Exhaustion/poor respiratory effort |\n| | Cardiac arrhythmia |\n| | Hypotension |\n| | Silent chest |\n\n\n## Investigations \n\n- **Peak expiratory flow rate (PEFR)** to help assess severity as per the classification above and monitor response to treatment.\n- **Arterial blood gas** if the patient is hypoxic to assess oxygenation and ventilation in patients - CO2 is expected to be low due to hyperventilation and if this is raised this indicates the asthma attack is near fatal.\n- **Portable chest X-ray** if a trigger such as pneumonia or a complication such as pneumothorax is suspected clinically.\n\n## Management \n\n- Recognise that this may be a medical emergency, assess using an ABCDE approach and escalate early to senior colleagues/critical care if not responding to treatment\n- Titrate oxygen to maintain saturations of 94-98%\n- Nebulised salbutamol driven by oxygen (if out of hospital, give up to 10 puffs of inhaled salbutamol and call an ambulance if not responding)\n- If the attack is severe or life-threatening or if response to salbutamol has been poor, add nebulised ipratropium bromide\n- Give prednisolone 40-50mg orally, or IV hydrocortisone if the patient is unable to swallow\n- Can consider IV magnesium sulphate and/or aminophylline if the patient is not responding to nebulisers\n- If the patient continues to deteriorate despite maximal therapy, they may require intubation and ventilation in an intensive care setting (for example in cases of severe hypoxia or exhaustion)\n\nFollow up after an acute asthma attack is crucial, with NICE guidelines stating that patients should be reviewed within 2 days of discharge from hospital to assess their symptoms, inhaler technique and current management.\n\n# NICE Guidelines\n\n[NICE - Asthma: diagnosis, monitoring and chronic asthma management](https://www.nice.org.uk/guidance/ng245)\n\n# References\n\n[NICE CKS](https://cks.nice.org.uk/topics/asthma/)\n\n[Report on health inequalities and asthma](https://www.asthmaandlung.org.uk/sites/default/files/2023-03/auk-health-inequalities-final.pdf)\n\n[Guideline on severe asthma in primary care](https://www.pcrs-uk.org/sites/default/files/pcru/articles/2019-Autumn-Issue-18-SevereAsthmaReferral.pdf)\n\n\n\n",
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"question": "A 22-year-old man with asthma presents to accident and emergency acutely short of breath. He is unable to complete sentences in one breath and has bilateral expiratory wheeze on examination. Peak expiratory flow rate (PEFR) is 40% of his best. You suspect an acute exacerbation of asthma.\n\nHe has received oxygen-driven nebulised salbutamol back-to-back with nebulised ipratropium and 40mg oral prednisolone. Following this his PEFR is 45% best and he is still unable to complete sentences. He remains wheezy.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "Pancreatitis presents with acute central/epigastric abdominal pain, often radiating to the back. They will almost certainly have a tender abdomen, often with peritonism, and will rarely complain of back pain alone. Aside from long-term use of corticosteroids, this patient has no other risk factors for acute pancreatitis. There is no indication in the question that she is suffering from nausea, vomiting, or loose stools. This patient has numerous risk factors for osteoporosis and has pain on lateral rotation and forward flexion of her spine - this should raise concerns of an osteoporotic vertebral fracture",
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"explanation": "The patient does have sinus tachycardia and acute pain in her thorax, which would raise concern of a pulmonary embolism. She denies anterior chest pain or any new respiratory symptoms, however, and her pain is described as \"severe back pain\". This makes pulmonary embolism less likely. This patient has numerous risk factors for osteoporosis and has pain on lateral rotation and forward flexion of her spine - this should raise concerns of an osteoporotic vertebral fracture",
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"explanation": "This patient has presented with acute severe thoracic back pain. This should not be readily dismissed and is often a sign of acute pathology. She has a number of risk factors for osteoporosis: post-menopausal, female gender, low BMI, current smoker, and longstanding corticosteroid use. Patients with osteoporotic vertebral fractures often have mild or no history of trauma and they may present with acute worsening back pain with no trigger. Her tachycardia is likely primarily a result of her pain, but could also be compounded from likely small vessel disease from smoking. She has pain on lateral rotation and forward flexion of her spine, providing further evidence of possible vertebral fracture. Though she lacks severe tenderness on palpation of her spinous processes, this does not absolutely rule out vertebral fracture, particularly if the pathology is more anteriorly located",
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"explanation": "Patients with asthma are at higher risk of spontaneous pneumothorax although more commonly when they are receiving positive pressure ventilation as they require high pressures to open a narrow airway resulting in barotrauma and alveolar rupture. A patient with pneumothorax would typically present with acute shortness of breath and chest pain. There would likely be signs on examination such as absent air entry from the affected area and hyper-resonant percussion (although these can be easily missed in practice if the pneumothorax is small). This patient has numerous risk factors for osteoporosis and has pain on lateral rotation and forward flexion of her spine - this should raise concerns of an osteoporotic vertebral fracture and is a more likely diagnosis",
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"name": "Simple pneumothorax",
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"explanation": "Aortic dissection can often mimic other conditions - presenting typically as acute severe, often \"tearing\", back/chest pain, sweating, collapse, or lightheadedness. You must have a high index of suspicion as it can be easily missed, carrying a 50% (type A dissection) and 10% (type B dissection) mortality if not treated. While it should be in your differentials, as she has acute back (not chest) pain, a normal ECG, with pain on movement of the thoracic spine - aortic dissection is less likely than a thoracic vertebral fracture",
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"explanation": "# Summary\n\nAsthma is a common disease of the airways, involving reversible bronchoconstriction, hyperreactivity and chronic inflammation. When bronchoconstriction is triggered (an “asthma attack”), patients experience episodes of wheeze, dyspnoea, cough and chest tightness. Initial investigations for all adults with suspected asthma are fractional exhaled nitric oxide (FeNO) or a full blood count looking for eosinophilia. If neither of these are confirmatory, patients should be assessed with spirometry including bronchodilator reversibility. Management involves a stepwise approach to medications, starting with “reliever therapy” (usually short-acting beta-2 agonists such as salbutamol inhalers) in combination with “preventer therapy” medications including inhaled corticosteroids, leukotriene receptor antagonists and long-acting beta-2 agonist inhalers. Allergen avoidance, smoking cessation, regular peak flow monitoring and inhaler technique are all key to good asthma control.\n\n# Definition\n\nAsthma is a common disease in both adults and children, characterised by intermittent \"asthma attacks\" with wheeze, cough, shortness of breath and chest tightness. There are several underlying mechanisms that centre around reversible bronchoconstriction, hyperreactivity and chronic inflammation.\n\n# Epidemiology\n\nIn the UK, approximately 8 million people have been diagnosed with asthma, of which 5.4 million are on treatment. Onset is usually in childhood and some find symptoms remit with age, although relapse is possible after long periods of being well.\n\nOn average, three people die from an asthma attack each day in the UK. The majority of these deaths are preventable, with an estimated 7/10 people with asthma not receiving basic preventative care such as inhaler technique checks and a personalised asthma plan.\n\nPeople experiencing socioeconomic deprivation are more likely to have asthma and to have worse outcomes (e.g. higher rates of hospitalisation). This is multifactorial, with these groups more likely to be exposed to triggers such as smoking and air pollution, and to have lower health literacy and access to healthcare.\n\n# Pathophysiology\n\nAsthma is often associated with a personal and/or family history of atopy, including the atopic triad of asthma, allergic rhinitis, and eczema. In asthma, there is an exaggerated response to a wide range of triggers. These include:\n\n- Cold air and exercise\n- Pollution and cigarette smoke\n- Allergens such as animal dander, dust mites and pollen\n- Irritants such as perfumes, paints or air fresheners\n- Medications such as NSAIDs or beta-blockers\n\nThese trigger a type 1 hypersensitivity reaction which is mediated by IgE. T Helper 2 cells produce IL4, IL5 and IL13 cytokines which activate the humoral immune system, leading to the proliferation of eosinophils, mast cells and dendritic cells. These cells then produce more inflammatory mediators such as leukotrienes and histamine.\n\nThis inflammation contributes to airway hyperresponsiveness leading to bronchospasm, as well as mucus hypersecretion that also obstructs airways. Over time in severe asthma, airway remodelling mediated by fibroblasts causes chronic obstruction and thickening of smooth muscle.\n\n# Risk factors\n\n- Family history of asthma or atopy\n- Personal history of atopy (eczema, allergic rhinitis, allergic conjunctivitis)\n- Exposure to smoke, including maternal smoking in pregnancy\n- Respiratory infections in infancy\n- Prematurity and low birth weight\n- Obesity\n- Social deprivation\n- Occupational exposures (e.g. flour dust, isocyanates from paint)\n\n# Symptoms\n\n- Wheeze\n- Dyspnoea\n- Cough\n- Chest tightness\n\nThe above symptoms should be episodic and usually show **diurnal variation** (worse at night or in the early morning). The patient may be able to identify specific triggers as listed above.\n\n# Signs\n\nIn between asthma exacerbations, clinical examination may be normal. If asthma is poorly controlled or during an exacerbation, signs include:\n\n- Tachypnoea\n- Increased work of breathing\n- Hyperinflated chest\n- Expiratory polyphonic wheeze throughout the lung fields\n- Decreased air entry (if severe)\n\n\n# Differential diagnosis\n\n- **Bronchiectasis** - usually associated with a productive cough, patients get frequent chest infections and coarse crackles rather than wheeze predominate on examination.\n- **Vocal cord dysfunction** - shares many triggers with asthma, inspiration more difficult than expiration, may have stridor.\n- **Chronic obstructive pulmonary disease** - patients usually >35 years old with a significant smoking history, may overlap with asthma in some.\n- **Gastro-oesophageal reflux disease** - microaspiration of stomach acid due to reflux can cause episodes of cough and wheeze which mimic asthma (although these may coexist and reflux can trigger asthma exacerbations). Symptoms are often postural and related to eating.\n- **Eosinophilic Granulomatosis with Polyangiitis** (Churg-Strauss syndrome) - small vessel vasculitis associated with pANCA, aside from asthma symptoms include nasal polyps, sinusitis, purpuric rashes and peripheral neuropathy.\n\n# Investigations \n\n- **FeNO (fractional exhaled nitric oxide) testing:** offer this **or** blood eosinophil count to all adults to confirm eosinophilic airway inflammation, asthma can be diagnosed if this is >50 parts per billion.\n- **Full blood count** to check **eosinophil count:** offer this **or** FeNO first-line to all adults - asthma can be diagnosed if this is above the normal reference range.\n- If neither of these confirm asthma, **spirometry** with **bronchodilator reversibility** should be offered to confirm airway obstruction (i.e. FEV1/FVC<70%). A bronchodilator (e.g. salbutamol inhaler) is given and spirometry repeated to assess response to treatment. An improvement in FEV1 of 12% or more or 200ml is diagnostic of asthma.\n- If spirometry is delayed or not available, patients may be asked to monitor their peak flow twice a day for 2 weeks and keep a diary of the readings. This is then used to assess **peak flow variability** (the difference between the highest and lowest readings as a percentage of the average PEF). Variability >20% is a positive result.\n- If none of the above are confirmatory, patients may be referred to specialist services for a **direct bronchial challenge test**, where histamine or metacholine is inhaled to trigger bronchoconstriction. Airway hyperresponsiveness is assessed by looking at the concentration of the triggering medication required to cause a 20% decrease in FEV1 - 8mg/ml or less is a positive result.\n\nNote: All of the above tests may be falsely negative in patients treated with inhaled corticosteroids.\n\n# Management of Chronic asthma\n\nThe aim of chronic asthma management is to achieve complete control over symptoms, with no need for rescue medications and no restrictions on physical activity. All patients should have a personalised asthma action plan which should be reviewed at least annually. Components of management include:\n\n## Non-pharmacological\n\n- Teach good inhaler technique and review this regularly\n- Spacer devices can be used to optimise medication delivery\n- Regular peak flow monitoring\n- Smoking cessation\n- Advice on avoiding triggers where possible (e.g. allergens, certain medications)\n- Ensure vaccinations are up to date, including annual influenza vaccination\n- Assess for occupational asthma by asking if symptoms are better when the patient is away from work and arrange specialist referral if this is suspected\n\n## Pharmacological\n\n- Prescribe all patients a combination inhaler with a **long-acting beta-2 agonist** (LABA) i.e. formoterol and a low-dose **inhaled corticosteroid** (ICS) i.e. budesonide to use as a reliever inhaler (i.e. PRN) - this is referred to as anti-inflammatory reliever (AIR) therapy.\n- Patients who do not respond adequately to AIR therapy, who are highly symptomatic at presentation or who present with a severe asthma exacerbation should be started on a low-dose **maintenance and reliever therapy inhaler** (MART). MART is a combination inhaler with ICS and a fast-acting LABA (e.g. beclomethasone + formoterol which is also known as Fostair), which is used as both a reliever inhaler (PRN) and as maintenance treatment (usually twice daily).\n- The next step would be increasing the ICS dose from low to **moderate** in the MART inhaler.\n- At this stage if asthma is not controlled, check FeNO and blood eosinophil count and refer to specialist asthma services if either are raised.\n- If neither are raised, consider adding either a **leukotriene receptor antagonist** (LTRA) such as montelukast (this is a tablet taken every night) or a **long-acting muscarinic agonist** (LAMA) such as tiotropium.\n- One of these should be trialled for 8-12 weeks alongside the moderate-dose MART - if asthma is well-controlled it can be continued.\n- If there is some improvement in control but this is still inadequate, the other medication can be trialled in addition (i.e. moderate dose MART + LTRA + LAMA).\n- If control has not improved, stop the medication and try the other one - if this is not successful refer to specialist services.\n- Options in specialist clinics include therapies such as **biologics** (e.g. omalizumab, which targets IgE).\n\nOther than patients who are not responding to treatment, the following situations shold also prompt a secondary care referral:\n\n- Uncertainty regarding diagnosis\n- Suspected occupational asthma\n- Severe or life-threatening asthma requiring admission to hospital\n- Multiple exacerbations requiring oral steroid treatment per year\n\n# Acute asthma\n\nAcute asthma exacerbations are graded in severity as below:\n\n\n| Severity | Clinical Features |\n|-----------------------|-----------------------------------------------|\n| Moderate | PEFR > 50% of predicted or best |\n| | No features of severe/life-threatening asthma |\n| Severe | PEFR 33-50% of predicted or best |\n| | Heart rate > 110 |\n| | Respiratory rate > 25 |\n| | Unable to complete sentences in one breath. |\n| | Accessory muscle use |\n| Life-threatening | PEFR < 33% of predicted or best |\n| | Oxygen saturation < 92% or cyanosis |\n| | Altered conciousness/confusion |\n| | Exhaustion/poor respiratory effort |\n| | Cardiac arrhythmia |\n| | Hypotension |\n| | Silent chest |\n\n\n## Investigations \n\n- **Peak expiratory flow rate (PEFR)** to help assess severity as per the classification above and monitor response to treatment.\n- **Arterial blood gas** if the patient is hypoxic to assess oxygenation and ventilation in patients - CO2 is expected to be low due to hyperventilation and if this is raised this indicates the asthma attack is near fatal.\n- **Portable chest X-ray** if a trigger such as pneumonia or a complication such as pneumothorax is suspected clinically.\n\n## Management \n\n- Recognise that this may be a medical emergency, assess using an ABCDE approach and escalate early to senior colleagues/critical care if not responding to treatment\n- Titrate oxygen to maintain saturations of 94-98%\n- Nebulised salbutamol driven by oxygen (if out of hospital, give up to 10 puffs of inhaled salbutamol and call an ambulance if not responding)\n- If the attack is severe or life-threatening or if response to salbutamol has been poor, add nebulised ipratropium bromide\n- Give prednisolone 40-50mg orally, or IV hydrocortisone if the patient is unable to swallow\n- Can consider IV magnesium sulphate and/or aminophylline if the patient is not responding to nebulisers\n- If the patient continues to deteriorate despite maximal therapy, they may require intubation and ventilation in an intensive care setting (for example in cases of severe hypoxia or exhaustion)\n\nFollow up after an acute asthma attack is crucial, with NICE guidelines stating that patients should be reviewed within 2 days of discharge from hospital to assess their symptoms, inhaler technique and current management.\n\n# NICE Guidelines\n\n[NICE - Asthma: diagnosis, monitoring and chronic asthma management](https://www.nice.org.uk/guidance/ng245)\n\n# References\n\n[NICE CKS](https://cks.nice.org.uk/topics/asthma/)\n\n[Report on health inequalities and asthma](https://www.asthmaandlung.org.uk/sites/default/files/2023-03/auk-health-inequalities-final.pdf)\n\n[Guideline on severe asthma in primary care](https://www.pcrs-uk.org/sites/default/files/pcru/articles/2019-Autumn-Issue-18-SevereAsthmaReferral.pdf)\n\n\n\n",
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"question": "A 67-year-old woman presents to accident and emergency with acute severe back pain in the thoracic region. She does not recall any recent trauma or falls. She denies any chest pain, palpitations, or new respiratory symptoms.\n\nShe has chronic asthma on regular budesonide and salbutamol, is a heavy smoker, and has BMI 17.\n\nHer heart rate is 105 but her observation are otherwise unremarkable. On examination her chest is clear, good air entry bilaterally, with resonant percussion. Abdomen is soft, non-tender. She is not overly tender on palpation on any spinous processes. She has limited range of movement, due to pain, on lateral rotation and forward flexion of her spine. Full neurology exam is unremarkable.\n\nElectrocardiogram shows sinus tachycardia.\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "This patient has a provoked DVT from a long haul flight. NICE guidance states the patient should receive 3 months of anticoagulation with apixaban or rivaroxaban, unless contraindicated. 6 months is the course length for patients with provoked DVT who have underlying malignancy - this is due to the prothrombotic nature of various malignancies. NB - these patients are often kept on anticoagulants _ad infinitum_ if their cancer is incurable, due to the prothrombotic tendencies",
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"explanation": "For a provoked deep vein thrombosis (DVT) or pulmonary embolism (PE) with no other risk factors, such as cancer or coagulation disorder, the NICE recommendation is to complete 3 months of anticoagulation (apixaban/rivaroxaban). From then, if the provoking factor is no longer present (in this case a long-haul flight) and the clinical course has been uncomplicated, then you can consider stopping anticoagulation. If the patient has cancer with a provoked DVT, then the anticoagulation treatment should last 3-6 months. For patients with unprovoked DVTs, then further investigation needs to be conducted while on anticoagulation to determine the cause of the DVT such as antiphospholipid syndrome, previously unknown underlying malignancy, or hereditary thrombophilia, among others",
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"explanation": "This patient has a provoked DVT from a long haul flight. NICE guidance states the patient should receive 3 months of anticoagulation with apixaban or rivaroxaban, unless contraindicated. There is no specific guidance for a course to be one year. Course lengths are 3 months for provoked DVT without malignancy, 6 months in those with malignancy, and continued lifelong in those with unprovoked DVT unless a cause is found and treated appropriately. Those on anticoagulation should be reviewed at least once a year by the GP for ongoing bleeding/clotting risks",
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"explanation": "This patient has a provoked DVT from a long haul flight. NICE guidance states the patient should receive 3 months of anticoagulation with apixaban or rivaroxaban, unless contraindicated. 4 weeks is the post-operative course length of prophylactic low molecular weight heparin after major operations within the abdomen (28 days) or the spine (30 days). This is to protect against DVTs from reduced mobility",
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"explanation": "This patient has a provoked DVT from a long haul flight. NICE guidance states the patient should receive 3 months of anticoagulation with apixaban or rivaroxaban, unless contraindicated. A patient would be kept on lifelong treatment if they developed an unprovoked DVT and the cause, such as antiphospholipid syndrome or incurable malignancy, were irreversible. The patient may also be kept on lifelong anticoagulation if the cause of their unprovoked DVT has not been found, but the risk of venous thromboembolism outweighed the bleeding risk",
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"comment": "Got the right answer as assumed quested would define this as provoked but this doesn't seem to align with the definition of provoked pe from any clinical resources.",
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"comment": "Questionable whether this is a 'provoked' PE - reconsider this question",
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"comment": "a 36 year old man should not have a PE from a flight unless he has an underlying condition ",
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"explanation": "# Definition\n\nA pulmonary embolism (PE) is when a blood clot in the pulmonary arterial vasculature develops, usually from an underlying deep vein thrombosis (DVT) of the lower limbs.\n\n# Epidemiology of pulmonary embolism (PE)\n\n2300 people died as a result of a pulmonary embolism in the UK in 2012, representing 2% of all deaths from lung diseases.\n\n# Presentation of a PE\n\n**Symptoms**\n\n- Sudden-onset shortness of breath, pleuritic chest pain, and haemoptysis (this is the 'typical' triad, although note that all three features are rarely present).\n\n- A massive pulmonary embolism may present with the above and syncope/shock.\n\n- A small pulmonary embolism may be asymptomatic.\n\n**Signs**\n\n- Classically tachypnoea, tachycardia and hypoxia is present. There may be low-grade pyrexia. Tachycardia may be the only presenting sign.\n\n- Note that a small pulmonary embolism may result in a normal examination.\n\n- A massive pulmonary embolism may present with hypotension, cyanosis, and signs of right heart strain (such as a raised JVP, parasternal heave, and loud P2).\n\nIt is important to look for signs of a concomitant deep vein thrombosis (a unilaterally swollen, tender calf).\n\n# ECG findings\n\nECG: Normal or sinus tachycardia. In a massive PE there may be evidence of right-heart strain (with P pulmonale, right axis deviation, right bundle branch block, and non-specific ST/T wave changes). The classic S1Q3T3 (deep S waves in lead I, pathological Q waves in lead III, and inverted T waves in lead III) is relatively uncommon (<20% of patients).\n\n# Blood tests in PE\n\nABG: This may be normal or show a type 1 respiratory failure (hypoxia without hypercapnia) and/or a respiratory alkalosis (due to hyperventilation secondary to hypoxia).\n\nRemember the baseline tests such as FBC (the patient may be anaemic if the PE has caused haemoptysis), CRP may be raised, U&E (to assess renal function before CTPA), clotting function (important if the patient is to be started on LMWH/Warfarin).\n\nSpecial tests include D-dimer (this is highly non-specific but has a 95% negative predictive value i.e. it is useful in ruling out a PE if negative).\n\n# Imaging Investigations in PE\n\nChest x-ray: this is typically normal in PE but possible findings include _Fleischner sign_ (an enlarged pulmonary artery), _Hampton's hump_ (a peripheral wedge shaped opacity), and _Westermark's sign_ (regional oligaemia). The chest x-ray is helpful in ruling out differentials (e.g. pneumonia, pneumothorax).\n\nCT pulmonary angiogram (CTPA): this is the diagnostic test of choice for a PE and will show a filling defect in the pulmonary vasculature. Note that a V/Q scan is preferred if the patient has renal impairment, contrast allergy or is pregnant.\n\nLower limb Duplex: helpful if a DVT is thought to be the cause of the PE (note this investigation is first-line - before a CTPA - in pregnancy).\n\nBedside echocardiogram: this is used if the patient is thought to have a massive PE (signs of right heart strain/hypotension), in order to assess suitability for thrombolysis.\n\n# Well's scoring system\n\nThe Well's score is a useful tool for risk stratifying patients with a suspected PE.\n\nPoints are allocated as follows:\n\n- 3 points:\n - Clinical signs and symptoms of a deep vein thrombosis (DVT)\n - If no alternative diagnosis is more likely than a PE\n- 1.5 points:\n - Tachycardia (heart rate >100 beats/minute)\n - If the patient has been immobile for more than 3 days or has had major surgery within the last month\n - If the patient has had a previous PE or DVT\n- 1 point:\n - If the patient presents with haemoptysis\n - If there is an active malignancy\n\nIf the Well's score is 4 or less the D-dimer should be measured. The D-dimer has a high negative predictive value but a low specificity so is only useful if the clinical suspicion of a PE is low.\n\nA low D-dimer excludes a PE. A raised D-dimer is an indication for diagnostic imaging (by CTPA or V/Q scan).\n\nIf the Well's score is more than 4 further diagnostic imaging is required. Low-molecular weight heparin is typically administered in the interim if the clinical suspicion of a PE is high (and should certainly be administered if there is delay in performing the CTPA).\n\n# Acute management of a PE\n\nIn the emergency department the patient should be assessed using the DR ABCDE approach:\n\n- Airway: likely to be patent.\n- Breathing: the patient may be tachypnoeic and hypoxic. Oxygen should be administered.\n- Circulation: the patient may be tachycardic. Signs of right heart strain are suggestive of a sub-massive PE. Hypotension is suggestive of a massive PE. Consider intravenous fluids if the systolic blood pressure is <90 mmHg.\n- Disability: likely to be unremarkable.\n- Exposure: the patient may have a low grade pyrexia. It is important to check for signs of a deep vein thrombosis (DVT). Consider analgesia at this stage if required.\n\nThrombolysis (an intravenous bolus of Alteplase) is indicated in a massive PE (features of haemodynamic instability). There is debate over whether it should be administered in a sub-massive PE.\n\n# Medical management of a PE\n\nAnticoagulation should be administered.\n\nIn the outpatient setting, direct oral anticoagulants such as apixaban or rivaroxaban should be started.\n\nIf neither of the above are suitable, dabigatran, edoxaban or warfarin can be considered. Low molecular weight heparin should be continued for at least 5 days and until 48 hours of therapeutic INR (>2) has been achieved if using warfarin. If using dabigatran or edoxaban then LMWH should be used for 5 day prior.\n\nThe duration of anticoagulation treatment depends on the aetiology of the PE. A provoked PE (identifiable risk factors e.g. surgery, peri-partum) should be treated for 3 months. An unprovoked PE should be treated for 6 months. If there is an ongoing cause (e.g. a thrombophilia) the patient should be treated for life.\n\nRecurrence of a VTE in a patient already on warfarin requires an increase in the target INR (to 3-4).\n\nIn the inpatient/emergency setting, low molecular weight heparin is usually started instead as it is shorter acting.\n\n# Interventional management of a PE\n\nEmbolectomy may be considered in patients with a massive PE when thrombolysis is contraindicated.\n\nAn inferior vena cava filter may be considered in patients with recurrent DVTs on Warfarin or patients in which anticoagulation is contraindicated.\n\n# References\n\n[Click for the NICE Guidelines](https://www.nice.org.uk/guidance/ng158)",
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"question": "A 32-year-old man presents to accident and emergency with acute right-sided pleuritic chest pain and haemoptysis. He flew to the UK from South Africa yesterday and since then has had persistent pleuritic chest pain. He has also noticed new swelling of his right calf over the same period.\n\nHe has no known past medical history and is otherwise fit and well.\n\nElectrocardiogram shows sinus tachycardia. He is haemodynamically stable.\n\nCT pulmonary angiogram (CTPA) reveals a right lower lobe segmental pulmonary embolism (PE). Ultrasound doppler of his right calf reveals deep vein thrombosis (DVT) in his right popliteal vein.\n\nYou decide to start him on apixaban.\n\nWhich of the following is the most appropriate anticoagulation course length?",
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"explanation": "Severe pneumonia can present within 48hrs and can be precipitated by poor inspiratory effort from abdominal pain, resulting in mucous plugging, atelectasis, and poor clearing of secretions. Often to develop into fulminant chest sepsis, the patient either has an acute precipitant e.g. aspiration, is immunosuppressed, or has poor residual lung function. This patient does not have evidence of these from the information above and so pneumonia would be a less likely cause of rapid respiratory deterioration in a patient with pancreatitis. The patient's chest x-ray shows interstitial fluid from pulmonary oedema and small bilateral pleural effusions, providing further evidence of acute respiratory distress syndrome over pneumonia",
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"name": "Severe bilateral lobar pneumonia",
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"explanation": "The patient has signs and symptoms of acute pulmonary oedema. Differentiating between cardiogenic and non-cardiogenic pulmonary oedema can be challenging, although the patient's history, cardiac history, fluid balance, and echocardiography signs can provide useful information. This patient has no cardiac history and has only been resuscitated with 2L intravenous fluid per day for two days with only mild pedal oedema on examination. It is unlikely that the pulmonary oedema is cardiogenic based on this information, and given the history of acute pancreatitis, acute respiratory distress syndrome is more likely",
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"explanation": "The patient has signs and symptoms of acute pulmonary oedema. Differentiating between cardiogenic and non-cardiogenic pulmonary oedema can be challenging, although the patient's history, cardiac history, fluid balance, and echocardiography signs can provide useful information. This patient has no cardiac history and has only been resuscitated with 2L intravenous fluid per day for two days with only mild pedal oedema on examination. It is unlikely that the pulmonary oedema is cardiogenic based on this information, and given the history of acute pancreatitis, acute respiratory distress syndrome is more likely",
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"explanation": "Acute interstitial pneumonitis (AIP) presents as acute respiratory distress and is the only acute form of idiopathic interstitial pneumonitis. It has a similar presentation and chest x-ray appearance as ARDS due to extensive diffuse alveolar damage. It usually occurs following a prodromal viral upper respiratory tract infection and then 1-2 weeks later rapidly progresses into respiratory failure. It is a very rare disease, not associated with pancreatitis, and is therefore a less likely cause of this patient's deterioration than ARDS",
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"explanation": "This patient has presented with an acute respiratory deterioration on a background of acute pancreatitis. Examination findings and chest x-ray point to pulmonary oedema as the likely cause. The patient has no cardiac history and has been resuscitated with 2L intravenous fluid per day. It is unlikely that the pulmonary oedema is cardiogenic based on this (although is common as patients with pancreatitis are often given aggressive fluid resuscitation). The most likely cause of this patients rapid deterioration and new florid pulmonary oedema is acute respiratory distress syndrome (ARDS) secondary to acute pancreatitis. The patient will likely be in the initial exudative phase of ARDS, characterised by diffuse alveolar damage, microvascular injury, type I pneumocyte necrosis, and influx of inflammatory cells. The mechanism of this is likely a consequence of systemic inflammatory response with increased endothelial and epithelial barrier permeability, resulting in leakage of protein-rich substances into the alveolar space and interstitial tissues. Increased cytokines and chemokines result in increased pulmonary infiltration of neutrophils into the interstitial tissue where they cause breakdown of pulmonary parenchyma",
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"comment": "why does ards cause leg oedema",
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"explanation": "# Summary\n\nAcute respiratory distress syndrome (ARDS) is a syndrome of non-cardiogenic pulmonary oedema and diffuse lung inflammation, which may be secondary to a lung injury or systemic illness. Key signs and symptoms include acute onset respiratory failure, severe dyspnoea, tachypnoea, confusion, and presyncope (crucially, not explained by heart failure or volume overload). Key investigations include chest X-ray and CT showing bilateral alveolar infiltrates, and ABG to assess oxygenation. Management involves treating the underlying cause, and supportive management usually in an intensive care setting. This may involve intubation and ventilation, maintaining cardiac output with haemodynamic support, DVT prophylaxis, nutritional support and regular repositioning to prevent pressure ulcers.\n\n# Definition\n\nAcute respiratory distress syndrome (ARDS) is defined as acute lung damage leading to non-cardiogenic pulmonary oedema, with a wide variety of potential causes. The pathophysiology involves diffuse alveolar damage with hyaline membrane formation. Mortality is around 50%, with many survivors developing fibrotic lung disease.\n\n**Criteria:**\n\nThe Berlin criteria are used to determine if a patient has ARDS - they need to have all of the following:\n\n* Acute onset (< 1 week)\n* Chest X-ray shows bilateral opacities\n* Decreased ratio of arterial to inspired oxygen concentrations (PaO₂/FiO₂) ≤300\n\n\n# Pathophysiology\n\nARDS is an acute form of respiratory failure occurring within one week of a trigger. It involves diffuse bilateral alveolar injury, with endothelial disruption and leakage of fluid into the alveoli from pulmonary capillaries. There is also a decrease in surfactant production, although it is important to differentiate ARDS from neonatal respiratory distress syndrome which is caused by insufficient lung surfactant production due to prematurity.\n\n# Aetiology\n\nCommon causes of ARDS include:\n\n- Sepsis\n- Pneumonia\n- Aspiration\n- Pancreatitis\n- Major trauma\n\nOther causes include:\n\n- Fat embolism\n- Drowning\n- Burns\n- Transfusion reactions (transfusion-related acute lung injury)\n- Drug overdose\n- Disseminated Intravascular Coagulation (DIC)\n\n# Signs and Symptoms\n\nPatients with ARDS present with acute onset respiratory failure which progressively worsens, often with an identifiable trigger such as trauma or critical illness.\n\nSymptoms include:\n\n- Severe dyspnoea\n- Tachypnoea\n- Confusion and presyncope (secondary to hypoxia)\n\nPatients are critically unwell, often with multiorgan failure, and appear in respiratory distress. Commonly there will be diffuse crepitations on auscultation of the chest.\n\n\n# Differential Diagnosis\n\nThe differential diagnosis of ARDS includes other causes of acute respiratory failure in an unwell patient:\n\n- **Cardiogenic pulmonary oedema** (i.e. acute heart failure): suspect this in patients with a history of cardiac disease or acute myocardial infarction, chest X-ray may show cardiomegaly, BNP levels will be raised and an echocardiogram can help to differentiate this from ARDS.\n- **COVID-19**: many patients with severe pneumonia secondary to COVID-19 may meet the criteria for ARDS and they present similarly with no difference in imaging findings.\n- **Bilateral pneumonia**: patients may have the same signs and symptoms as in ARDS with severe pneumonia but may not meet the criterion for severe hypoxaemia (low oxygen levels in the blood).\n- **Diffuse alveolar haemorrhage**: patients can bleed into the airways for a range of reasons, including vasculitis, mitral stenosis, lupus and medications. This can be differentiated from ARDS as bronchoalveolar lavage will be bloody.\n\n\n# Investigations\n\n- Respiratory viral swab: looking for COVID-19, Influenza and other possible viral triggers.\n- Sputum, blood and urine cultures: septic screen for any triggering infection.\n- Arterial blood gases: important to determine severity of hypoxaemia.\n- Serum amylase: screening for pancreatitis (common cause of ARDS)\n- Chest X-ray: bilateral alveolar infiltrates without other features of heart failure (such as cardiomegaly and Kerley B lines).\n\n[lightgallery]\n\n- CT chest: can further characterise changes found on X-rays and may show evidence of an underlying pulmonary disease causing the ARDS (e.g. pneumonia).\n\n# Management\n\nIdentification and treatment of the underlying cause is key, for example antibiotics if sepsis is suspected. Patients are usually treated in an intensive care setting, as most require intubation and ventilation.\n\n**Key points to consider in management are:**\n\n- Ventilatory support using a “protective strategy” - for example, using low tidal volumes to limit trauma to damaged lungs, consider proning to improve oxygenation.\n- Haemodynamic support - aim for a mean arterial pressure (MAP) > 60mmHg, transfuse if haemoglobin < 70 to maintain oxygen delivery.\n- Nutritional support - the enteral route is preferred e.g. via an NG tube.\n- Regular repositioning to help prevent pressure ulcers.\n- DVT prophylaxis whilst immobile.\n- PPI cover to prevent gastric ulceration (common in critically unwell patients).\n\n\n# References\n[Patient UK - ARDS](https://patient.info/doctor/acute-adult-respiratory-distress-syndrome)\n\n[Radiopaedia - ARDS](https://radiopaedia.org/articles/acute-respiratory-distress-syndrome-1?lang=gb)",
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"question": "A 54-year-old woman with severe gallstone pancreatitis is reviewed after 2 days of worsening condition, now requiring oxygen. She received 4L IV fluids over 48 hours for nausea and vomiting, with examination findings showing intravascular depletion of fluid.\n\n\nShe has no known cardiac history\n\n\nOn examination her respiratory rate is 35, peripheral oxygen saturations 94% on 10L (40%) Venturi mask, heart rate 115, blood pressure 105/58, temperature 35.6°C.\n\nRespiratory exam reveals diffuse bilateral coarse crepitations and reduced bibasal air entry. Mild pedal oedema extends to the knees. Abdominal exam shows epigastric guarding with mild distension; her abdomen is otherwise soft and non-tender.\n\nPortable chest x-ray is shown below\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "Limited cutaneous systemic sclerosis, previously named CREST syndrome, causes calcinosis, Raynaud's disease, oesophageal dysmotility, sclerodactyly, and telangiectasia. It may produce hard and thickened skin with non-pitting oedema of the fingers and toes (sclerodactyly). While it may result in joint pain and swelling with pulmonary fibrosis, the characteristic tenderness, inflammation, and swan neck deformity in the proximal interphalangeal and metacarpophalangeal joints is more typical of rheumatoid arthritis",
"id": "33211",
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"explanation": "The history and examination findings are most consistent with rheumatoid arthritis (chronic pain and stiffness in the morning) with extra-articular pulmonary fibrosis (exertional dyspnoea with end-inspiratory crackles on examination). Rheumatoid factor (RF) is positive in 60-70% of patients with rheumatoid arthritis. Anti-CCP antibody positive in 80% of patients with rheumatoid arthritis. There are a subgroup of patients with rheumatoid arthritis with negative RF and anti-CCP antibodies - known as seronegative rheumatoid arthritis. In these cases, diagnosis is made by x-ray findings with history and examination",
"id": "33208",
"label": "a",
"name": "Rheumatoid arthritis",
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"explanation": "Sarcoidosis presents with pyrexia, night sweats, malaise, and lethargy. The lungs are the most common organ to be affected with a restrictive pattern seen from diffuse parenchymal disease. It can affect virtually any organ, but in the joints, it often causes soft-tissue swelling, dactylitis, and tenosynovitis. It is less likely to present with swan neck deformity the proximal interphalangeal and metacarpophalangeal joints - this is more typical of rheumatoid arthritis",
"id": "33209",
"label": "b",
"name": "Sarcoidosis",
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"explanation": "Systemic lupus erythematosus (SLE) is a multiorgan disease presenting with a wide range of signs and symptoms. The patients often have non-specific symptoms such as pyrexia, malaise, fatigue, lymphadenopathy, and arthralgia. Arthralgia can present as early morning stiffness in peripheral symmetrical joints along with SLE arthropathy with swan-neck deformity. It can less-commonly affect the lungs causing fibrosing alveolitis or obliterative bronchiolitis. While the patient is experiencing both of these issues, patients with SLE will usually display other constitutional symptoms. The characteristic tenderness, inflammation, and swan neck deformity in the proximal interphalangeal and metacarpophalangeal joints is more typical of rheumatoid arthritis",
"id": "33210",
"label": "c",
"name": "Systemic lupus erythematosus",
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"explanation": "Reactive arthritis is an RF-seronegative, HLA-B27-linked inflammatory arthritis that develops in response to a recent infection. It usually develops following gastrointestinal infections such as _Salmonella_, _Shigella_, or _Campylobacter_ or genitourinary infections such as _Chlamydia trachomatis_. It is characterised by large joint asymmetric inflammatory oligoarthritis, conjunctivitis/uveitis, and urethritis/cervicitis (can't see, pee, or climb a tree). This patient does not complain of ocular symptoms, dysuria, or symptoms of urethritis and so reactive arthritis is less likely",
"id": "33212",
"label": "e",
"name": "Seronegative reactive arthritis",
"picture": null,
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"__typename": "QuestionComment",
"comment": "Seronegative RA + rare complication pulmonary fibrosis, what an unlucky madam",
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"comment": "Did you just… assume their luck in life…",
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"explanation": "# Side effects of corticosteroids\n\n**Corticosteroids** (think CORTICOSTEROIDS):\n\n- Cushing's syndrome\n- Osteoporosis\n- Retardation of growth\n- Thin skin, easy bruising\n- Immunosuppression\n- Cataracts and glaucoma\n- Oedema\n- Suppression of HPA axis\n- Teratogenic\n- Emotional disturbance (including psychosis\n- Rise in BP\n- Obesity (truncal)\n- Increased hair growth (hirsutism)\n- Diabetes mellitus\n- Striae\n\n# Side effects of NSAIDs\n\n- Indigestion\n- Peptic ulcer disease,\n- Increased risk of venous thrombo-embolus\n- Peripheral oedema\n- Slightly increased risk of stroke and heart attack\n\n# Side effects of Methotrexate\n\n- Gastro-intestinal disturbance\n- Folate deficiency - anaemia\n- Immunosuppression\n- Pulmonary fibrosis\n- Liver toxicity\n- Interstitial pneumonitis\n- Rash\n- Teratogenicity - Methotrexate is contraindicated during conception and pregnancy. The recommendation is a washout of a few months (at least 3 months) before conception. In the event of a disease flare, low-dose steroids are thought to be relatively safe. Note that high doses are associated with a small increased risk of the child having a cleft palate.\n\n# Side effects of Sulfasalazine\n\n- Myelosuppression\n- Nausea\n- Rash\n- Oral ulcers\n- Decreased sperm count\n\n# Side effects of Hydroxychloroquine\n\n- Retinopathy\n- Rash\n\n# Side effects of Biologic therapy (e.g. etanercept, infliximab, adalimumab)\n\n- Immunosuppression\n- Reactivation of TB\n- Allergic reaction, reaction at infusion site\n\n# Side effects of Gold\n\n- Myelosuppression\n- Renal toxicity (Nephrotic syndrome)\n- Mouth ulcers\n- Photosensitivity\n- Chrysiasis (skin discolouration)",
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"learningPoint": "In patients with rheumatoid arthritis who test negative for rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies—referred to as seronegative rheumatoid arthritis—diagnosis is typically made based on clinical history, physical examination, and characteristic x-ray findings that show joint damage, erosions, and narrowing.",
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"question": "A 32-year-old woman presents the GP with six months of worsening pain and stiffness in her fingers bilaterally, particularly in the mornings. She works as a builder and is struggling to cope at work with the pain. She has become gradually more short of breath on exertion over recent months with a dry cough.\n\nOn examination there are fine bilateral inspiratory crackles in the chest, and bilateral swan neck deformity in the proximal interphalangeal and metacarpophalangeal joints.\n\nBloods are shown below\n\n| Serum | Result | Reference Range |\n| ------------------------------------------------ | ------ | --------------- |\n| Rheumatoid factor (RF) | 45 | <60 U/mL |\n| Anti-cyclic citrullinated peptide (CCP) antibody | 1 | <7 U/mL |\n\nWhich of the following is the most likely diagnosis?",
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"__typename": "QuestionChoice",
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"explanation": "Acute gout presents with a rapid-onset (<24hrs) hot, exquisitely tender, and swollen joint, caused by crystal inflammation from uric acid crystals depositing within the joint. 50% of all attacks and 70% of first attacks present in the first metatarsophalangeal joint. There may also be systemic upset and skin desquamation over the site. Risk factors for gout include male gender, alcohol excess, obesity, renal impairment, diabetes mellitus, and diuretics. Gout may be diagnosed without further investigations in someone with hyperuricaemia and podagra (classic acute arthritis in first metatarsophalangeal joint). If there is any doubt, then the gold standard is joint aspiration synovial fluid analysis. Diagnosis would be confirmed if monosodium urate crystals are seen on synovial fluid analysis - they show strong negative birefringence with needle-like morphology",
"id": "33213",
"label": "a",
"name": "Gout",
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"__typename": "QuestionChoice",
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"explanation": "Septic arthritis should always be on your differentials with an acute hot and swollen joint. It is a medical emergency with 10% mortality and the most serious cause of monoarthritis. If not treated urgently, the patient may develop joint damage, functional impairment, and persistent pain. The most usual sites for septic arthritis are the knee in adults and the hip in children. The patient may be pyrexial and generally unwell, although systemic symptoms occur in fewer than 50% of cases of septic arthritis, so a low clinical suspicion is required. It uncommonly presents in the metatarsophalangeal joint (2% of joints). The patient in this question is systemically well with rapid onset of symptoms and inflammation presenting in the 1st metatarsophalangeal joint. The most likely diagnosis is therefore acute gout. In practice if there were any doubt, you would take a joint aspirate and start antibiotics while awaiting the fluid analysis, microscopy, culture, and sensitivity",
"id": "33214",
"label": "b",
"name": "Septic arthritis",
"picture": null,
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"__typename": "QuestionChoice",
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"explanation": "Charcot can present with a hot, swollen, and erythematous joint. It is caused by neuropathy in the foot, most commonly as a result of poorly-controlled diabetes. The patient loses the protective sensation mechanisms which compensate for microtrauma within the feet which then leads to the destruction of the foot and ankle joints. Charcot feet are often not as painful as septic arthritis or gout, and are often painless. They don't present with raised inflammatory markers and the erythema will decrease with elevation. Septic arthritis often will present with raised inflammatory markers and the erythema will be unchanged on elevation. In this question, Charcot foot would unlikely present solely in the metatarsophalangeal joint and with such acute pain. Given the rest of the examination was unremarkable, it is unlikely that it is the cause of this patient's symptoms",
"id": "33215",
"label": "c",
"name": "Charcot foot",
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"explanation": "Septic arthritis should always be on your differentials with an acute hot and swollen joint. It is a medical emergency with 10% mortality and the most serious cause of monoarthritis. If not treated urgently, the patient may develop joint damage, functional impairment, and persistent pain. The most usual sites for septic arthritis are the knee in adults and the hip in children. The patient may be pyrexial and generally unwell, although systemic symptoms occur in fewer than 50% of cases of septic arthritis, so a low clinical suspicion is required. It uncommonly presents in the metatarsophalangeal joint (2% of joints). The patient in this question is systemically well with rapid onset of symptoms and inflammation presenting in the 1st metatarsophalangeal joint. The most likely diagnosis is therefore acute gout. In practice if there were any doubt, you would take a joint aspirate and start antibiotics while awaiting the fluid analysis, microscopy, culture, and sensitivity",
"id": "33216",
"label": "d",
"name": "Hallux valgus",
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"__typename": "QuestionChoice",
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"explanation": "Acute pseudogout presents similarly to gout, but with less severe pain and less commonly in the 1st metatarsophalangeal joint. It most frequently presents in the knees and wrists with an acutely inflamed, warm, erythematous, painful joint. Patients may also be pyrexial with raised inflammatory markers. Diagnosis is often made after joint aspiration showing positively birefringent rhomboid-shaped crystals",
"id": "33217",
"label": "e",
"name": "Acute pseudogout",
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"comment": "Taste not gout?",
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"comment": "What are the water tablets?",
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"comment": "Likely a thiazide diuretic as they're known to cause gout ",
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"comment": "loop diuretics can also cause gout",
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"explanation": "# Summary\n\nGout is a type of arthritis caused by the accumulation of monosodium urate crystals in and around the joints. It presents acutely with rapid onset of severe pain, swelling and redness of affected joints, with the first metatarsophalangeal joints the most commonly affected. Chronic untreated gout may lead to tophi which are hard nodules made up of monosodium urate crystals that deposit in soft tissues. Gout may be diagnosed clinically, with supportive investigations including a serum urate and synovial fluid analysis looking for monosodium urate crystals. Management of acute gout is with NSAIDs, colchicine or a short course of oral steroids. Urate-lowering therapy with allopurinol or febuxostat should be considered to reduce the risk of further gout flares. \n\n# Definition\n\nGout is a form of arthritis that occurs when monosodium urate crystals deposit in joints. This causes both acute inflammation (gout flares) and in the longer-term, a chronic gouty arthritis with tophi (hard deposits of monosodium urate crystals in soft tissues).\n\n# Epidemiology\n\n- Gout is the most common inflammatory arthritis and prevalence is increasing with time (currently 2.5%)\n- Hyperuricaemia (high urate) is the main risk factor (although most patients with a high urate do not develop gout, and some patients develop gout with a normal urate)\n- Factors that contribute to this include:\n- Older age - typically patients are above the age of 40\n- Male sex (post-menopausal women are also at increased risk)\n- Comorbidities including chronic kidney disease (CKD), diabetes, osteoarthritis, hypertension\n- Excess alcohol consumption\n- Dietary excess of meat, seafood and sugary drinks\n- Overweight or obesity\n- Medications such as thiazide diuretics and ciclosporin\n- Family history of hyperuricaemia and gout\n- Genetic disorders associated with hyperuricaemia such as Lesch-Nyhan or glycogen storage disorders\n- Organ transplant recipients\n- Acute attacks may be triggered by stressors including:\n- Trauma and surgery\n- Intercurrent illness\n- Alcohol excess\n- Sudden excess of protein in the diet\n- Chemotherapy (due to cell breakdown)\n- Urate-lowering medications can cause a flare (as crystals are shed into the joint space)\n\n# Signs and Symptoms\n\nOverlapping clinical syndromes are caused by the deposition of monosodium urate crystals in different tissues:\n\n**Acute gout** \n\n- Commonly presents with a monoarthritis\n- Pain is severe and rapid in onset, reaching a peak within 24 hours \n- Affected joints become swollen, erythematous and tender\n- The first metatarsophalangeal (MTP) joint is the most commonly affected (70% of first attacks)\n- Other common sites include the knees, ankles, midtarsal joints, wrists, elbows and small joints of the hands\n- Systemic features such as fever and malaise may be seen\n- Patients may be tachycardic due to pain\n\n**Tophaceous gout**\n\n- Patients will usually have a history of longstanding recurrent acute gout\n- However in atypical cases patients may present with tophi without previous flares\n- Tophi are firm white nodules of sodium monosulphate crystals under the skin\n- They commonly occur on extensor surfaces of joints such as knees or elbows, the Achilles tendons, backs of hands and feet and on the helices of the ears\n- Usually they are painless however they can become infected, inflamed or ulcerated\n- They may discharge white material onto the skin surface\n- Chronic gouty arthritis may present with tender and stiff joints with reduced range of motion\n\n# Differential Diagnosis\n\n- **Septic arthritis** must be ruled out in patients who are systemically unwell with an acute monoarthritis - urgent synovial fluid analysis is needed if this is suspected\n- **Pseudogout** typically affects the knee and wrists rather than the MTP joint; synovial fluid analysis shows calcium pyrophosphate crystals\n- **Cellulitis** causes erythema, pain and swelling of the skin rather than the joint - patients may be systemically unwell\n- **Trauma** should be asked about in the history as this may cause similar symptoms of pain, difficulty mobilising and swelling\n- **Other inflammatory arthritides** such as rheumatoid arthritis may mimic chronic gouty arthritis\n\n# Investigations\n\n**Bedside tests:**\n\n- **Joint aspiration** is the gold standard diagnostic investigation \n- Needle-shaped monosodium urate crystals with negative birefringence are seen in gout\n- Synovial fluid should also be sent for gram stain and culture to rule out septic arthritis\n- Tophi can be biopsied to look for these crystals\n\n**Blood tests:**\n\n- **Serum uric acid** should be measured in all patients with suspected gout\n- A serum urate of 360 micromol/L or more confirms the diagnosis\n- Levels may be falsely low in an acute attack and so should be repeated 2-4 weeks after the flare has resolved\n- Levels are used to guide urate-lowering therapy if this is initiated as prophylaxis\n- **Screening for risk factors** should be considered:\n- Fasting glucose or HbA1c for diabetes\n- Renal function and urine albumin:creatinine ratio for CKD\n- Lipids for hypercholesterolaemia\n- **Inflammatory markers** with FBC and CRP should be checked if septic arthritis is suspected\n- **Liver function tests** are needed prior to starting febuxostat\n- Patients from Han Chinese, Thai and Korean backgrounds should be screened for **HLA-B5801** prior to starting allopurinol (as this increases the risk of severe cutaneous adverse reactions if present)\n\n**Imaging tests:**\n\n- These may be useful to assess chronic disease or where the diagnosis of acute gout is uncertain\n- X-rays in chronic disease show punched-out periarticular erosions, areas of sclerosis and tophi\n- Ultrasound may show joint effusions, tophi, synovial thickening and erosions\n\n# Management \n\n**Acute gout flares** \n\nThere are three first-line options for treatment of a gout flare:\n\n- NSAIDs e.g. naproxen\n- Give at maximum dose\n- Continue until 1-2 days after resolution of symptoms\n- Consider giving with a PPI for gastric protection\n- Avoid in heart failure, patients at high risk of gastrointestinal bleeding and severe renal failure\n- Colchicine\n- Dosing is 500 mcg 2-4 times per day\n- Continue until pain resolves\n- Dose-dependent side effects include diarrhoea, nausea and vomiting\n- Oral corticosteroids\n- e.g. prednisolone 30mg once a day for 3-5 days\n- Useful in patients with contraindications to both NSAIDs and colchicine\n- An injection of intramuscular, intravenous or intra-articular steroids can also be considered\n- Alongside this, consider other analgesia (e.g. paracetamol) and other non-pharmacological pain relief such as ice packs\n- A combination of the above may be tried if a single agent is ineffective\n- Patients should be advised to keep the affected joint cool and exposed and to rest and elevate the affected limb\n- Patients already on urate lowering treatment should continue this throughout the acute flare\n\n## Prevention\n\nPatients should be followed up 4-6 weeks after an acute episode of gout to think about preventative strategies and assess for risk factors (also see Investigations). \n\nOptimisation of risk factors may include:\n\n- Reducing alcohol consumption\n- Maintaining a balanced diet and healthy weight\n- Investigate and treat for comorbidities such as hypertension or CKD\n- Review medications and consider switching medications such as thiazides that cause hyperuricaemia\n- Where possible, switch antihypertensive medications to losartan or amlodipine, which have modest urate-lowering effects \n- Initiating urate-lowering therapy (see below)\n\nMost patients can be managed in primary care, however the following should prompt referral to or discussion with specialist services:\n\n- Patients with complications of gout\n- Atypical presentations (e.g. aged under 30) or uncertain diagnosis\n- Pregnant patients\n- Stage 3b to 5 CKD\n- Organ transplant recipients\n- Those at risk of adverse effects with standard medical treatment, or if treatment is ineffective or not tolerated\n\nIndications for **urate-lowering therapy** include:\n\n- Multiple or troublesome gout flares\n- Chronic gouty arthritis or tophi\n- Patients taking diuretics\n- CKD stage 3 to 5\n\n**Starting and monitoring urate-lowering therapy (ULT):**\n\n- ULT should be started at least 2-4 weeks after an acute flare if possible as medications can precipitate further attacks\n- Colchicine should be given whilst starting ULT to reduce the risk of a flare (NSAIDs or steroids are second-line)\n- Doses should be uptitrated with monthly monitoring of serum urate levels, aiming for a target of 360 micromol/L\n- A target urate level of 300 micromol/L may be helpful in patients with tophi or chronic arthritis due to gout, or those who continue to have flares despite ULT\n- First-line options are either allopurinol or febuxostat which are both xanthine oxidase inhibitors (so reduce uric acid production)\n- Allopurinol is preferred in patients with significant cardiovascular disease\n- Second line options include uricosuric medications (e.g. probenecid) - these can promote stone formation so should be avoided if there is nephrolithiasis\n\n# Complications\n\n- Chronic gouty arthritis and permanent joint damage\n- Tophi, which may become inflamed or infected\n- Nephrolithiasis due to uric acid precipitation - these are responsible for 8% of renal calculi and are radiolucent\n- Chronic urate nephropathy - urate deposition in the renal interstitium causes inflammation and fibrosis\n- Both allopurinol and febuxostat can cause rashes, which in rare cases may be severe (e.g. Stevens Johnson syndrome or toxic epidermal necrolysis)\n- Increased risk of cardiovascular disease and mortality\n\n# NICE Guidelines\n\n[NICE CKS - Gout](https://cks.nice.org.uk/topics/gout/)\n\n[NICE - Gout: diagnosis and management](https://www.nice.org.uk/guidance/ng219/)\n\n# References\n\n[Patient UK - Gout](https://patient.info/doctor/gout-pro)\n\n[Radiopaedia - Gout](https://radiopaedia.org/articles/gout?lang=gb)",
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"question": "A 73-year-old man presents with 12 hours of worsening right foot pain (10/10 severity) and inability to weight-bear. He has no history of trauma.\n\n\nHe can never remember the names of his medical problems or his regular medications, but states he takes \"water tablets\" for his \"heart problems\".\n\n\nOn examination, observations are normal. The left foot and knee are non-tender, non-erythematous, with full range of motion. The right knee is unremarkable. The right foot has a large, tender, warm, erythematous mass on the 1st metatarsophalangeal joint, with the rest of the foot showing full range of motion and intact neurovascular function.\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "Syphilis can present with a wide array of symptoms . Primary syphilis presents with a painless genital ulcer (chancre) and local non-tender lymphadenopathy. It can present with painless oral ulcers although this is less common. Secondary syphilis occurs 4-10 weeks after infection and manifests with a non-pruritic rough red/reddish-brown papular rash, typically on the trunk, and flu-like symptoms such as pyrexia, pharyngitis, malaise, arthalgia/myalgia, lymphadenopathy, and headache. There are a wide variety of rare manifestations, hence the nickname \"the great imitator\", including uveitis, hepatitis, meningitis, glomerulonephritis, periostitis, cranial nerve palsies, and patchy alopecia. The patient in this question does not have any flu-like symptoms or lymphadenopathy and his ulcers are painful, making secondary syphilis less likely",
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"explanation": "Behçet's disease is a systemic disorder of recurrent acute inflammation. It affects multiple organs, although is primarily characterised by oral ulcers, recurrent genital ulcers (which disappear and recur spontaneously), and anterior uveitis. It can also effect other organ systemic including skin, pulmonary, vascular, gastrointestinal, musculoskeletal, and central nervous systems. It is most common in ages 20-40, predominantly in males, and has greatest prevalence in Eastern Asia and the Mediterranean. There are no specific tests for Behçet's disease although HLA-B51 is the most strongly associated known genetic factor. In this question the patient is describing anterior uveitis, oral and genital ulcers, and arthralgia and so Behçet's disease is the most likely diagnosis",
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"explanation": "Reactive arthritis is an RF-seronegative, HLA-B27-linked inflammatory arthritis that develops in response to a recent infection. It usually develops following gastrointestinal infections such as _Salmonella_, _Shigella_, or _Campylobacter_ or genitourinary infections such as _Chlamydia trachomatis_. It also presents in ages 20-40 and predominantly in males but is characterised by large joint asymmetric inflammatory oligoarthritis, conjunctivitis/uveitis, and urethritis/cervicitis (can't see, pee, or climb a tree). This patient does not complain of dysuria or symptoms of urethritis and so Behçet's disease is more likely. While reactive arthritis can occasionally cause recurrent aphthous ulcers, on balance the patient's symptoms are more in keeping with Behçet's disease",
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"explanation": "Reactive arthritis is an RF-seronegative, HLA-B27-linked inflammatory arthritis that develops in response to a recent infection. It usually develops following gastrointestinal infections such as _Salmonella_, _Shigella_, or _Campylobacter_ or genitourinary infections such as _Chlamydia trachomatis_. It also presents in ages 20-40 and predominantly in males but is characterised by large joint asymmetric inflammatory oligoarthritis, conjunctivitis/uveitis, and urethritis/cervicitis (can't see, pee, or climb a tree). This patient does not complain of dysuria or symptoms of urethritis and so Behçet's disease is more likely. While reactive arthritis can occasionally cause recurrent aphthous ulcers, on balance the patient's symptoms are more in keeping with Behçet's disease",
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"comment": "Turkish man with Behçet's. Nice.",
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"explanation": "# Summary\n\nBehcet's disease is a chronic systemic inflammatory disease which mainly affects people from the Middle East, the Mediterranean and East Asia. The classic triad of manifestations is with oral and genital ulceration and ocular involvement (e.g. uveitis or retinal vasculitis). The gastrointestinal tract, central nervous system, skin and cardiovascular systems may also be affected. Investigations include blood tests showing raised inflammatory markers during acute attacks, testing for HLA-B51 (the most strongly associated genetic risk factor) and a pathergy test (where minor skin trauma leads to the formation of a skin lesion). Management may be local (e.g. topical steroids for orogenital ulceration) or systemic, which may include steroids or other immunosuppressive treatments such as azathioprine or cyclophosphamide. Complications include aneurysm rupture, ischaemia due to vessel thrombosis, permanent visual loss and cerebral vein thrombosis.\n\n# Definition\n\nBehcet's disease is a rare multisystem inflammatory disease that typically causes mouth and genital ulceration, skin lesions, uveitis and arthralgia. Severe complications may result from pulmonary, cardiovascular or central nervous system involvement (also referred to as neuro-Behcet's disease).\n\n# Epidemiology\n\n- The disease is most common in people from Turkey (approximately 80 to 370 cases per 100,000 people)\n- North Africa, the Middle East, South East Asia and other Mediterranean countries also have a relatively high prevalence of cases\n- Overall however it is a rare condition, and can affect people of all ethnicities\n- Men and women are equally likely to develop Behcet's disease, but men tend to be more severely affected\n- HLA-B51 is the most strongly associated genetic risk factor\n- Age of onset is usually in the 20s or 30s, although around 20% of cases present in childhood\n\n# Diagnostic Criteria\n\nThe **International Criteria for Behcet's Disease** are based on the presence of typical clinical features as follows - a score of 4 or more is indicative of a diagnosis of BehcBehcet'set's disease:\n\n| Clinical feature| Points |\n|----------|----------|\n| Ocular lesions | 2 |\n| Genital aphthosis (painful ulceration) | 2 |\n| Oral aphthosis | 2 |\n| Skin lesions | 1 |\n| Neurological manifestations | 1 |\n| Vascular manifestations | 1 |\n| Positive pathergy test (optional) | 1|\n\n\n# Signs and Symptoms\n\n**Systemic** symptoms include:\n\n- Fatigue\n- Malaise\n- Myalgia\n- Low-grade fevers\n- Headaches\n- Arthralgia (an inflammatory arthritis may also occur)\n\n**Mucocutaneous** signs and symptoms include:\n\n- Recurrent oral ulceration (the most common manifestation)\n- Mouth ulcers are usually painful\n- They may cause difficulty eating and drinking\n- Usually heal within 7-21 days\n- Recurrent genital ulceration\n- These are very painful\n- Usually occur on the scrotum in males, and the vulva and in the vagina in females\n- Skin lesions\n- Erythema nodosum (painful nodules usually on the legs)\n- Acne-like papulopustular or nodular lesions on the limbs\n- Pathergy (eruption of papulopustules at the site of minor skin trauma within 24-48 hours)\n- Superficial thrombophlebitis (tender subcutaneous nodules overlying the inflamed vein)\n\n**Ocular** manifestations include:\n\n- Uveitis (anterior or posterior)\n- The affected eye is red and painful\n- Vision is blurred with photophobia\n- Visual loss may occur\n- Retinal vasculitis may present with sudden visual loss\n\n**Pulmonary** involvement:\n\n- Seen in a minority of people\n- Pulmonary arterial aneurysms may form\n- These are usually multiple and bilateral\n- May be asymptomatic\n- May cause dyspnoea, chest pain and cough\n- Rupture can lead to haemoptysis, syncope, cardiogenic shock and sudden death \n- Small vessel vasculitis may occur\n- Ground glass appearances and/or alveolar haemorrhage may be seen on imaging\n- This can also cause haemoptysis, dyspnoea and chest pain\n- Pulmonary artery thrombosis may occur\n- This causes haemoptysis, dyspnoea and chest pain (i.e. similar to symptoms of a pulmonary embolism)\n\n**Central nervous system** manifestations include:\n\n- Headaches\n- Personality changes\n- Cerebellar signs\n- Dysarthria\n- Sensory changes\n- Memory loss\n- Meningoencephalitis\n- Cerebral vein thrombosis\n- Presents with headache, decreased consciousness, visual loss and nausea and vomiting\n- Signs include papilloedema, focal neurological deficits, seizures and cranial nerve palsies\n\n**Gastrointestinal** (GI) involvement may present with:\n\n- Ulceration causing GI bleeding or perforation\n- May cause nausea and vomiting, abdominal pain, anorexia and diarrhoea\n\n**Cardiovascular** involvement may include:\n\n- Deep vein thrombosis (with limb swelling, erythema and tenderness)\n- Pericarditis \n- Vasculitis may affect the aorta and superior vena cava\n- Coronary artery aneurysms may lead to acute coronary syndrome\n- Cardiomyopathy with subsequent heart failure\n\n[lightgallery]\n\n[lightgallery1]\n\n\n# Differential Diagnosis\n\n- **Herpes simplex virus** as a cause of recurrent painful genital and oral ulceration with associated systemic symptoms of malaise \n- **Sarcoidosis** causes similar features of erythema nodosum, arthritis and uveitis and may also affect the lungs and central nervous system, however genital ulcers are not a feature\n- **Reactive arthritis** may present with orogenital ulcers and uveitis, although the urethritis and sacroiliitis seen are not typical of Behcet's disease\n- **Crohn's disease** often causes oral ulceration, GI symptoms that may affect anywhere in the GI tract (as in Behcet's disease), and extraintestinal features of rashes, arthritis and uveitis may also occur; however genital ulcers and central nervous system features are not seen in Crohn's disease \n- **Systemic lupus erythematosus** shares many features including systemic symptoms, arthritis, central nervous system involvement and ulcers (common in the mouth but rare in the genital area); typical rashes differ from Behcet's disease (e.g. malar rash on the face) and blood tests may show antinuclear, anti-double stranded DNA and/or anti-Smith antibodies\n\n# Investigations\n\nThere is no specific diagnostic test for Behcet's disease - investigations may be to rule out differential diagnoses or identify specific organ complications.\n\n**Bedside tests:**\n\n- **Wound swabs** from oral or genital ulcers may be sent for microscopy and/or viral PCR to rule out infectious causes\n- **Urinalysis** should be done to look for blood and protein indicating renal involvement which may occur in differentials such as systemic lupus erythematosus\n\n**Blood tests:**\n\n- **FBC** often shows a high white cell count and a mild anaemia of chronic disease\n- **CRP** and **ESR** may be raised but can be normal even when disease is active\n- **HLA-B51** is not generally useful for diagnosis \n- **Rheumatoid factor**, **ANA** and **ANCA** are typically negative\n- **Syphilis serology** as another cause of oral and genital ulceration\n- Baseline **U&Es** and **LFTs** prior to starting treatment\n- Genetic testing with **next generation sequencing** is increasingly used to rule out monogenetic conditions that may mimic Behcets disease\n\n**Imaging:**\n\n- **MRI head** in neuro-Behcet disease may show parenchymal lesions, most commonly affecting the thalamus, midbrain and internal capsule\n- **MR venography** may be done if central venous sinus thrombosis is suspected\n- **Angiography** is used to identify and assess aneurysms\n- **High-resolution CT chest** may be done in patients with respiratory symptoms to identify pulmonary involvement\n\n**Special tests:**\n\n- A **pathergy test** is non-specific but may be used to support the diagnosis\n- A sterile needle is used to make a skin prick\n- The area is then reassessed after 24-48 hours \n- The test is positive if there a papule or pustule forms at that site\n- It is often positive in pyoderma gangrenosum and acute febrile neutrophilic dermatosis\n- It can also be positive in inflammatory bowel disease or in healthy people\n- **Lumbar puncture** may be indicated in neuro-Behcet disease \n- e.g. to rule out infective causes of meningoencephalitis\n- Elevated cerebrospinal fluid pressure may be seen\n- Raised protein, a pleocytosis and absent oligoclonal bands is typical\n- **Endoscopy** may be required for investigation of GI symptoms and to rule out inflammatory bowel disease \n- **Biopsy of skin lesions** may show leukocytoclastic vasculitis and panniculitis (inflammation of the subcutaneous fat)\n\n# Management\n\n**Conservative management:**\n\n- Patients should be managed in specialist services, with input from multiple specialities often required for different manifestations\n- Prompt management of ocular disease in particular is key to minimise the risk of sight loss\n- Physiotherapy, occupational therapy and/or podiatry input may be helpful for joint disease or functional impairment e.g. in neuro-Behcets\n- Patients should be educated on the disease and on self-management, for example for mouth ulcers:\n- Maintain good oral hygiene\n- Attend regular dental appointments\n- Use topic antiseptics e.g. chlorhexidine mouthwash\n- Avoid foods that cause irritation\n- Patients should be regularly assessed for both disease extent, overall disease activity and quality of life \n- Clinical psychology input is key for general emotional support and focused interventions to support self-management and address distress\n- Neuropsychology assessment should be carried out for all patients with neuro-Behcets\n\n**Medical management:**\n\n- Systemic steroids with a steroid-sparing agent (e.g. methotrexate or azathioprine) are first-line for ocular Behcets\n- Oral and genital ulcers may be treated with potent topical steroids (combined preparations with antibiotics and antifungals are also available)\n- Colchicine is a second-line option for mucocutaneous lesions, and the first-line treatment for arthritis and arthralgia\n- Second-line treatments for joint disease include intra-articular or oral steroids or NSAIDs\n- Gastrointestinal Behcets is managed with similar medications to inflammatory bowel disease, with 5-aminosalicylic acid, azathioprine and 6-mercaptopurine all first line options as well as steroids for flares\n- Neuro-Behcets should be treated with high-dose steroids +/- cyclophosphamide or anti-tumour necrosis factor (TNF) biologics\n- Patients with deep vein thrombosis should not be anticoagulated due to the risk of adverse effects - steroids and azathioprine or anti-TNF agents are first-line\n\n**Surgical and interventional management:**\n\n- Emergency surgery may be required for complications such as major GI bleeding or perforation\n- Stenting or surgery may be required for arterial involvement e.g. aneurysms\n\n# Complications\n\n- Visual loss\n- GI bleeding \n- GI perforation\n- Acute ischaemia of limbs or organs due to vasculitis or thrombosis\n- Acute coronary syndrome\n- Aneurysm rupture (e.g. in the lungs or the brain)\n- Seizures\n- Cognitive impairment is common especially in neuro-Behcets\n- Psychological distress including depression and anxiety\n\n# Prognosis\n\n- The typical disease course is with flares of disease with intervening periods of remission\n- The disease often becomes less active over time\n- Mortality is generally low but is higher in men and patients with an early age of onset\n- However death may occur due to neurological, GI or cardiovascular involvement\n- Immunosuppressive treatments are also associated with significant risks e.g. of infection \n\n# References\n\n[Behcets UK Factsheets](https://behcetsuk.org/behcets-medical-factsheets/)\n\n[British Association of Dermatologists and British Society for Rheumatology living guideline](https://academic.oup.com/rheumatology/advance-article/doi/10.1093/rheumatology/keae438/7753993)\n\n[The International Criteria for Behcets Disease](https://behcetsuk.org/wp-content/uploads/2018/06/ICBD-New-Criteria-2013.pdf)\n\n[Patient UK - Behcet's Disease](https://patient.info/doctor/behcets-disease-pro)\n\n[Radiopaedia - Behcet's Disease](https://radiopaedia.org/articles/behcet-disease-2?lang=gb)\n\n[DermNet NZ - Behcet's Disease](https://dermnetnz.org/topics/behcet-disease)",
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"question": "A 35-year-old Turkish man presents to accident and emergency with painful erythematous sclera and blurred vision of his right eye. He has had something similar in the past however it was not painful and resolved without treatment. \n\nHe also describes 3 episodes of self-terminating painful oral and genital ulcers in the past year and ongoing bilateral arthralgia in his proximal joints.\n\n\nObservations are normal. On examination, he has a globally erythematous right sclera. Vision is 6/12 in right, 6/6 in left (baseline 6/6 bilaterally). He has four well-circumscribed aphthous ulcers in his oral cavity and two further ulcers on the glans and shaft of his penis.\n\nWhat is the most likely diagnosis?",
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"explanation": "Given this patient's new neurology findings he should have urgent radiotherapy within 24hrs to prevent permanent neurological damage. While dexamethasone is a crucial part of management of MSCC and cauda equina syndrome, we should not wait for a trial of dexamethasone as there is a risk of permanent neurological damage if the cord is not decompressed",
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"explanation": "This will almost certainly be done while an inpatient to determine the progression of this patient's prostate cancer. However given this patient's new neurology findings, he requires urgent therapy to relieve his spinal cord compression to prevent permanent neurological damage",
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"explanation": "# Summary\n\nSpinal cord compression (SCC) is a medical emergency that can lead to permanent neurological disability. It causes symptoms of weakness and sensory disturbance below the level of the compression, back pain deep and bladder and bowel involvement (incontinence, constipation or retention). Upper motor neurone signs are seen. Causes include trauma, malignancy (especially metastatic spinal cord compression), disc prolapse or compression by an abscess or epidural haematoma. An MRI of the whole spine is the key investigation. Management depends on the underlying cause; high dose steroids and referral to neurosurgery for consideration of decompression are key. \n\n\n# Definition\n\nSpinal cord compression (SCC) is a form of myelopathy caused by pressure on the cord by a variety of causes. It causes an upper motor neurone lesion, unlike the lower motor neurone signs seen in cauda equina syndrome, where compression is below the level of L1. \n\n\n# Epidemiology\n\n- Spinal cord injury affects approximately 15.4 million people globally\n- Trauma causes the most cases worldwide, with falls, road traffic accidents and violence being the most common precipitants\n- In the UK, there are around 4400 new cases of spinal cord injury per year\n- Metastatic spinal cord compression (MSCC) is the leading cause in the UK \n- In around a quarter of patients, MSCC is their first presentation of malignancy \n\n\n# Aetiology\n\n- **Trauma** - typically due to vertebral fractures or dislocation of facet joints; the cord may be severed in significant trauma\n- **Malignancy i.e. MSCC** - either due to pathological collapse of vertebrae or compression by growing tumours\n- **Infection** including abscess formation and chronic infections such as tuberculosis \n- **Epidural haematoma** where blood accumulates in the epidural space, compressing the cord\n- **Intervertebral disc prolapse** although this is much more rare than lumbar disc prolapses causing cauda equina syndrome\n\n\n\n\n# Signs and Symptoms\n\n**Symptoms include:**\n\n\n- Back pain, which is typically:\n- Severe\n- Progressive\n- Aggravated by straining e.g. coughing\n- Difficulty walking\n- Weakness below the level compressed (typically bilateral and symmetrical)\n- Numbness below the level compressed\n- Urinary or faecal incontinence\n- Urinary retention\n- Constipation\n\n\n**Signs seen (below the level of the lesion):**\n\n\n- Hypertonia\n- Hyperreflexia (although reflexes may be absent at the level compressed)\n- Clonus\n- Upgoing plantars\n- Sensory loss (a \"sensory level\")\n\n\nSymptoms and signs of an underlying cause may also be present, e.g. weight loss and fatigue in a patient with MSCC, fevers in a patient with tuberculosis. \n\n\n# Differential Diagnosis\n\n- **Transverse Myelitis** causes inflammation of the cord that presents similarly to SCC; it may be seen in the context of chronic demyelinating diseases such as Multiple Sclerosis or Neuromyelitis Optica (where other manifestations e.g. optic neuritis may be present)\n- **Cauda Equina Syndrome** is usually caused by herniation of a lumbar disc compressing the cauda equina; bowel and bladder disturbances may be present but signs are lower motor neurone (e.g. flaccid rather than spastic paralysis)\n- **Peripheral Neuropathy** also causes symptoms of weakness and sensory loss, signs are lower motor neurone rather than upper and distribution differs depending on aetiology (e.g. symptoms often unilateral in compression neuropathies)\n- **Spinal metastases** and other causes of back pain (e.g. musculoskeletal), especially if the predominant symptom is pain with minimal neurological symptoms and signs\n- **Sciatica** refers to pain in the lower back, buttocks and posterior legs caused by nerve root compression usually secondary to disc herniation in the lumbar spine; weakness can also occur but MRI will differentiate this from SCC\n\n\n# Investigations\n\nAn **MRI whole spine** is the key investigation\n\n\n- The whole spine should be imaged as there may be compression at multiple levels\n- In cases of suspected MSCC, this should be done within 24 hours as per NICE guidelines\n- Patients with suspected spinal metastases (e.g. back pain) with no neurological signs or symptoms suggestive of MSCC should have their MRI within 1 week\n\n\nIn some cases other imaging modalities may be used, e.g. **whole-body CT** in the context of major trauma. CT may also be used in patients for whom MRI is contraindicated.\n\n\nOther investigations indicated depend on the presentation and suspected aetiology:\n\n\n- Do a **bladder scan** if suspected urinary retention \n- An **ECG** and **baseline blood tests** should be done in anticipation of possible emergency surgical decompression (including a **group and save** and **clotting**)\n- In cases where MSCC is the first presentation of malignancy, further investigations are required to determine where the primary cancer is (guided by history and examination)\n- This may include further imaging e.g. a CT of the chest, abdomen and pelvis\n- Bloods may be done for tumour markers e.g. PSA in men\n- Biopsy is usually required to confirm the diagnosis\n\n# Management\n\n- Management depends on the underlying cause as well as the patient's background \n- Patients with traumatic spinal cord injuries should be transferred to a major trauma centre\n- General principles include:\n- Immobilise the patient and nurse with spinal precautions (e.g. log-rolling)\n- Regular repositioning to prevent pressure ulceration in immobile patients\n- Analgesia for pain\n- VTE prophylaxis \n- Catheterise if in urinary retention\n- Counselling and rehabilitation is key, with multidisciplinary input (e.g. physiotherapy) \n\n**Using MSCC as an example:**\n\n- Start high-dose steroids (usually 16mg dexamethasone initially) in patients with suspected MSCC - this reduces oedema helping to relieve compression\n- A proton pump inhibitor (PPI) should also be given to prevent peptic ulceration caused by steroids\n- Blood glucose should be monitored for hyperglycaemia secondary to steroids\n- Refer to neurosurgery urgently for consideration of surgical decompression (other options include vertebroplasty or kyphoplasty)\n- Patients unsuitable for surgery may have radiotherapy for spinal metastases - this can also be used as an adjuvant after surgery\n- Spinal braces may be used in patients not suitable for surgery to help with pain management and spinal stability\n- Oncology input is key both for diagnosis in patients without a known malignancy and for ongoing management (e.g. chemotherapy)\n\n\n# NICE Guidelines\n\n\n[NICE - Spinal injury: assessment and initial management](https://www.nice.org.uk/guidance/ng41/)\n\n\n[NICE - Spinal metastases and metastatic spinal cord compression](https://www.nice.org.uk/guidance/ng234)\n\n\n# References\n\n[Patient UK - Spinal Cord Compression](https://patient.info/doctor/spinal-cord-compression)\n\n\n[World Health Organisation - Spinal Cord Injury](https://www.who.int/news-room/fact-sheets/detail/spinal-cord-injury)",
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"explanation": "Tumour lysis syndrome (TLS) is a potentially fatal complication from chemotherapy. It is more likely seen in cancers with high cell turnover rates, particularly haematological malignancies, e.g. lymphomas and leukaemias, but other solid tumours have also been associated with TLS. It is caused by tumour cells being lysed during treatment and releasing their contents into the blood, producing similar electrolyte abnormalities as rhabdomyolysis. It results in hyperkalaemia, hyperphosphataemia, hypocalcaemia, and hyperuricaemia (high blood uric acid). The patient has presented with symptoms that could be consistent with TLS, although it has been four weeks since his last cycle of chemotherapy and so this is very unlikely. His blood markers are also not consistent with TLS, and so this would be an unlikely cause for this patient's symptoms",
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"explanation": "In primary hypoparathyroidism, PTH is low, calcium is low, and phosphate is high. This is because of reduced osteoclastic activity in bone and so reduced serum calcium produced from bone reabsorption. Low PTH would also result in reduced reabsorption of calcium in the distal tubules and collecting ducts (reduces serum calcium), and reduced inhibition of reabsorption of phosphate from tubular fluid (increases serum phosphate)",
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"explanation": "The patient's symptoms are most likely caused by his hypercalcaemia. It rarely presents with _all_ of \"stones, moans, groans, and psychic overtones\" and often presents solely as lethargy or confusion. Non-small cell lung cancers often can cause hypercalcaemia due to tumour secretion of parathyroid-related protein (PTHrP). This acts in the same way as parathyroid hormone (PTH), activating parathyroid hormone receptors in tissue which results in increased osteoclastic bone resorption (with or without bone metastases), increased renal tubular absorption of calcium, and decreased reabsorption of phosphate in the kidney. The body's normal homeostatic mechanisms are still intact, and so secretion of PTH from the parathyroid gland is reduced to combat the patient's hypercalcaemia. Alkaline phosphatase is increased because of increased osteoclastic bone resorption. This patient's palpitations and new ECG findings can also be explained by hypercalcaemia. ECG findings found in hypercalcaemia are short QT interval, prolonged PR-interval (1st degree heart block), and Osborn waves.\n \n\n This patient has likely also developed an acute kidney injury (AKI) secondary to dehydration from hypercalcaemia - driven by forced diuresis and reduced oral intake from nausea/confusion. NB: The patient may not volunteer polyuria unless asked directly. While the patient does have raised urea, likely from pre-renal AKI, this would not usually elicit cognitive dysfunction at this concentration.\n \n\n This patient does have iron-deficiency anaemia, although this is very common in patients with cancer. There is no evidence of acute haemorrhage to cause this patient's confusion and a mildly increased urea gives further evidence against having had an upper gastrointestinal haemorrhage",
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"explanation": "In primary hypoparathyroidism, PTH is low, calcium is low, and phosphate is high. This is because of reduced osteoclastic activity in bone and so reduced serum calcium produced from bone reabsorption. Low PTH would also result in reduced reabsorption of calcium in the distal tubules and collecting ducts (reduces serum calcium), and reduced inhibition of reabsorption of phosphate from tubular fluid (increases serum phosphate)",
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"explanation": "This patient does have iron-deficiency anaemia, although this is very common in patients with cancer. There is no evidence of acute haemorrhage to cause this patient's confusion and a mildly increased urea gives further evidence against having had an upper gastrointestinal haemorrhage. Patients often compensate very well with chronic anaemia and may have few or no symptoms. They may complain of general lethargy and shortness of breath on exertion with haemoglobin (Hb) in the 80s, but without signs of acute haemorrhage, this is unlikely to cause confusion",
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"comment": "why is PTH low if PTH is being secreted causing high calcium?",
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"comment": "The tumour secretes parathyroid-related protein not PTH. This causes a rise in calcium similar to if there was a rise in PTH. This results in negative feedback on the parathyroid and the body is like, 'hey I don't need to increase calcium' so PTH levels from the parathyroid fall to very low levels.",
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"explanation": "# Summary\n\nConfusion is a common issue in oncology, with diverse causes including metabolic disturbances, infections, and metastatic spread to the brain. It is crucial to identify and treat underlying factors, as confusion can distress patients and families. Delirious patients face higher risks of falls and complications, requiring careful management strategies.\n\n\n# Differentials of confusion in oncology\n\nConfusion is a common presenting complaint within general medicine and oncology. Confusion seen in the context of a cancer patient alters the likelihood of certain causes of confusion.\n\nThere are a diverse range of causes for confusion in oncology patients:\n\n- **Metabolic disturbance** (hypoglycaemia, hypercalcaemia): this may present acutely or subacutely. Patients often have concurrent symptoms such as feeling hungry or shaky for hypoglycaemia and very thirsty or GI upset for hypercalcaemia.\n- **Neutropenic sepsis**: this is an oncological emergency and may be difficult to spot, as many usual signs of infection may be absent. In any patient with known or suspected neutropenia presenting with confusion, neutropenic sepsis should be top of the differential list.\n- **Infection** (pneumonia, UTI): patients may have localising symptoms of infection. For example, a cough or dysuria. However patients may present atypically so always consider whether sepsis could be causing the confusion, even in the absence of typical signs.\n- **Metastatic spread to the brain**: typically, this is subacute onset and associated with headache, visual disturbances and/or focal neurology. The most common cancers to spread to the brain are lung, breast, colorectal, melanoma and renal cell carcinoma. Therefore have a low threshold for suspecting metastases especially in these cancers.\n- **Anaemia**: this may be difficult to diagnose clinically, as cancer and its treatment causes fatigue for most patients. A full blood count is a useful investigation to rule out anaemia and neutropenia.\n- Other causes of delirium, including **pain, constipation and medications**. It is important to rule out these reversible causes of confusion. This can be elicited in the history and medication review, and treatment can make a significant difference to the patient's mental status and quality of life.\n\n# Management\n\nIt is important to recognise and treat the underlying cause of confusion. This can be distressing for the patient and relatives alike.\n\nPatients with delirium (acute confusional state) are at increased risk of falls, increased mortality and morbidity. Environmental modifications can help reduce confusion, as well as optimising reversible factors and falls risk reduction measures. Pharmacological management is reserved for when non-pharmacological measures do not work or when a patient is agitated towards the end of life.\n\n# NICE guidelines\n\n[NICE CKS: Delirium](https://cks.nice.org.uk/topics/delirium/)\n\n# References\n\n[Marie Curie: Delirium in palliative care](https://www.mariecurie.org.uk/professionals/palliative-care-knowledge-zone/symptom-control/delirium)",
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"question": "A 65-year-old man is brought to A&E with progressive confusion over the past week, lethargy and sleepiness. He is disoriented and reports occasional palpitations. He has a 60-pack-year smoking history and was diagnosed with non-small cell lung cancer nine months ago, and has completed multiple cycles of chemotherapy and radiotherapy, with the last cycle four weeks ago.\n\n\nHe is tachycardic, apyrexial, and has dry mucous membranes. His chest is clear, abdomen is soft and non-tender, with no focal neurology. \n\n\nECG shows new 1st degree heart block; urine dip is clear. Chest X-ray shows a known left hilar mass.\n\n\n\nBloods tests:\n\n\n|Serum|Result|Reference Range|\n|---------------------------|------|-----------------------------|\n|Haemoglobin|82|130 - 170 mg/dL|\n|White Cell Count|4.1|3.0 - 10.0 x 10⁹ /L|\n|Platelets|180|150 - 400 x 10⁹/L|\n|Mean Cell Volume|71|80 - 96 fL|\n|Urea|10.1|2.5 - 7.8 mmol/L|\n|Creatinine|170|60 - 120 µmol/L|\n|eGFR|37|≥ 60 mL/min/1.73m<sup>2</sup>|\n|Iron|5.6|14 - 31 μmol/L|\n|Total Iron Binding Capacity|35|54 - 75 μmol/L|\n|Corrected Calcium|3.6|2.2 - 2.6 mmol/L|\n|Magnesium|0.65|0.7 - 1.0 mmol/L|\n|Phosphate|0.4|0.8 - 1.5|\n|Parathyroid Hormone|0.1|1.6 - 8.5 pmol/L|\n\n\nWhat is the most likely cause of this patient's symptoms?",
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"explanation": "The main concern in patients on chemotherapy with pyrexia is neutropenic sepsis. This is defined as a temperature of greater than 38.0°C, OR any symptoms and/or signs of sepsis, in a person with absolute neutrophil count of 0.5 x 10⁹/L or lower.\n \n\n These patients are severely immunosuppressed and cannot mount the normal immune response to infection that others can. They can look and feel completely well for some time, with relatively normal observations, before rapidly becoming unwell and deteriorating. Low threshold are needed to treat aggressively early and take cultures from any possible source to help guide choice of step-down antibiotics",
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"explanation": "# Summary\n\nNeutropenic sepsis is a serious infection that can occur in immunocompromised patients. According to NICE, in patients undergoing cancer treatment, it is identified by a temperature exceeding 38<sup>o</sup>C or any signs of infection, coupled with a neutrophil count below 0.5 x 10<sup>9</sup>/l. This condition is most prevalent among those receiving anticancer therapies and is considered an oncological emergency. Risk factors include severe or prolonged neutropenia, advanced malignancies, and certain medical comorbidities. Clinical presentation may be subtle, necessitating a high index of suspicion for any febrile immunocompromised patient. Prompt investigation and management, including the sepsis six protocol and early senior input, are crucial, as untreated neutropenic sepsis carries a significant risk of mortality and complications from treatment, such as multi-drug resistant infections.\n\n\n\n# Definition\n\nIn simple terms, neutropenic sepsis can be defined as the presence of both:\n\n- Neutropenia, a low number of neutrophils in the blood.\n- Sepsis, defined as a dysregulated response to infection causing life-threatening organ dysfunction.\n\nNICE define neutropenic sepsis in patients receiving anticancer treatment as a temperature **above 38<sup>o</sup>C or any other signs of infection and a neutrophil count of less than 0.5x10<sup>9</sup>/l**.\n\nIt most commonly occurs in people receiving anticancer therapy, and is an oncological emergency. It can also occur in immunocompromise due to other causes, for example immunosuppression, HIV infection or congenital immunodeficiency syndromes.\n\nNeutropenic fever is another commonly used term. It refers to a single temperature reading of above 38.3<sup>o</sup>C or two consecutive readings above above 38<sup>o</sup>C for two hours, along with a known or expected neutrophil count of less than 0.5x10<sup>9</sup>/l, and carries a greater risk of sepsis.\n\n***In practice, any fever in the context of known or suspected neutropenia is a medical emergency which can be life-threatening if not treated promptly.***\n\n# Aetiology\n\nRisk factors for neutropenic sepsis include:\n\n- Severe and/or prolonged neutropenia\n- Extremes of age\n- Previous febrile neutropenia\n- Haematological or advanced malignancy\n- Prolonged hospital admission or previous surgery\n- Medical comorbidities\n- Indwelling lines\n- Concurrent corticosteroids\n\nPathogens which can cause neutropenic sepsis include:\n\n- Gram-positive bacteria: Staphylococci sp. (including *S. aureus* & *S. epidermidis*), Enterococcus sp. and Streptococci sp.\n- Gram-negative bacteria: *Escherichia coli*, Klebsiella sp., Enterobacter sp. and *Pseudomonas aeruginosa*\n- Fungal infections with *Candida* or *Aspergillus* species\n- Viral infections\n\n# Signs and symptoms\n\nClinical features of neutropenic sepsis may be very difficult to distinguish, as neutropenic patients do not have a normal immune response. Therefore, you should have a low threshold for suspecting neutropenic sepsis in any immunocompromised person who becomes unwell. Clinical features may include:\n\n- Focal signs of infection, for example dysuria, productive cough, diarrhoea\n- Physiological derangement, including fever or hypothermia, elevated respiratory rate, tachycardia, hypotension, skin colour changes, altered mental state\n- Any concern from the patient or relative\n\n# Differential diagnosis\n\n- **Sepsis** causing neutropenia: the person will have presented with symptoms of sepsis first and had a normal or high white cell count, before subsequently developing a neutropenia due to the infection.\n- **Drug fever** can occur with many pharmacological agents. Patients may have associated eosinophilia, rash, hepatic or renal derangement. Tests for infection would be negative.\n- **Tumour fever**: this is a low-grade fever caused by progression of a malignancy causing inflammation. Tests for infection would be negative and tumour fevers do not respond to antibiotics.\n- **Venous thromboembolism**: patients would typically have concurrent symptoms of a deep vein thrombosis or pulmonary embolism (painful swollen leg, chest pain respectively). Definitive diagnosis would be via doppler ultrasound or the leg or CT angiogram of the chest.\n\n\n# Investigations\n\nIt is important to initiate investigations and management for neutropenic sepsis as soon as it is suspected. Initial investigations to request alongside an A-E assessment are:\n\n- Bedside: full set of observations, blood gas, glucose measurement, urine dip, ECG\n- Bloods: FBC, CRP, U&E's, LFT's, clotting, lactate\n- Cultures: blood cultures, urine, sputum, any indwelling lines or other potential sources of infection\n- Imaging: chest X-ray, and any further imaging related to the potential source of infection as appropriate\n\n# Management\n\n**For any patient with suspected neutropenic sepsis, adopt an A-E approach, initiate the sepsis six and seek early senior input.**\n\nThis will include:\n\n- Giving **oxygen** to maintain saturations above 94%\n- IV access to give **fluids** to maintain blood pressure, take bloods and give antibiotics\n- Giving IV broad-spectrum **antibiotics** according to local guidelines, to be given within an hour. Often, this is piperacillin/tazobactam.\n- Close **monitoring** of urine output, observations with a NEWS2 chart, and the patient's overall clinical condition.\n- **Senior** input may be the consultant on call for immediate management, but the relevant specialty, for example acute oncology, should also be contacted as soon as possible.\n\nNeutropenic patients can become very unwell very quickly. **Critical care** input may be required, and patients should be discussed with them early.\n\nFor further details of the sepsis six, please see the *Sepsis* page.\n\n# Complications\n\nUntreated, neutropenic sepsis has a high mortality rate.\n\nComplications of treatment with broad-spectrum antibiotics include:\n\n- Fungal infections, local and systemic\n- *C. difficile* infection\n- Multi-drug resistant infections, which are much more difficult to treat\n\n# NICE guidelines\n\n\n[NICE CKS: Neutropenic sepsis](https://cks.nice.org.uk/topics/neutropenic-sepsis/)\n\n# References\n\n[BMJ Best Practice: Febrile neutropenia](https://bestpractice.bmj.com/topics/en-gb/950)",
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"question": "A 44-year-old woman presents with a temperature of 38.1°C, 3 days after starting cycle 2 of chemotherapy for advanced colorectal cancer. She had T3a rectal cancer resected 8 weeks ago with an end colostomy.\n\nShe feels well, with normal observations. Examination shows moist, oral mucosa, a clear chest, a soft, non-tender abdomen, and a pink, warm colostomy producing type 5 stool. No focal neurological signs, meningism, rash, or cellulitis are present.\n\nInvestigations:\n\nUrine dip: Clear\nBeta-hCG: Negative\nChest X-ray: Unremarkable\n \n \n\n| Serum | Result | Reference Range |\n| ------------------------------------ | ------ | ------------------- |\n| Haemoglobin | 95 | 115-155 mg/dL |\n| White Cell Count | 2.1 | 3.0 - 10.0 x 10⁹ /L |\n| Platelets | 160 | 150 - 400 x 10⁹/L |\n| Neutrophils | 0.5 | 2.0 - 7.5 x 10⁹ /L |\n| Sodium | 135 | 135 - 146 mmol/L |\n| Potassium | 3.6 | 3.5 - 5.3 mmol/L |\n| Urea | 2.8 | 2.5 - 7.8 mmol/L |\n| Creatinine | 45 | 60 - 120 µmol/L |\n| eGFR | >90 | \\> 60 mL/min/1.73m2 |\n| C reactive protein | 25 | < 5 mg/L |\n| Lactate | 1.2 | 0.20-1.80 mmol/L |\n \n \n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "Always make sure in these questions, and in practice, to calculate the full 24 hour dose of oral morphine e.g. 2x90mg given the twice daily dosing",
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"name": "30-40mg oral morphine sulfate immediate release as required, 4-hourly",
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"explanation": "This would be an appropriate starting dose for a patient who is opioid-naïve, although this patient is already on high-strength long-acting morphine for her cancer pain and so breakthrough doses must be calculated appropriately",
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"explanation": "Breakthrough dose of morphine in adults with cancer is calculated by dividing the 24-hour dose of oral morphine by 6. Usually a range is required and so the range should be approximately 1/10th-1/6th of the 24-hour total morphine dose.\n \n\n The principal is the same for all opioids, although it is best practice to convert the full 24 hour dose of opioids to the corresponding _oral_ morphine dose, and then convert back to the desired drug and route. This is of use when the long-acting drug is different to the breakthrough drug e.g. oral oxycodone breakthrough with a buprenorphine patch.\n \n\n The total dose of oral morphine in this case is 180mg/24hrs. 1/6th of this is 30mg and 1/10th of this is 18mg. For practicality in administration, this has been rounded to 20-30mg",
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"comment": "i was always taught 1/6th of background makes up a breakthrough dose - so seeing 2 answers with 30 mg really isn't that helpful",
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"comment": "Max breakthrough dose is 1/6th of maintenance, so you really shouldn't be giving anything higher than 30mg",
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"comment": "1/6 - 1/10 is the range",
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"explanation": "# Summary\n\nMedications in end-of-life care focus on alleviating distressing symptoms in patients nearing death. A holistic approach is vital, considering physical, emotional, and social aspects of symptoms, often involving a multidisciplinary team. For pain management, the WHO pain ladder guides pharmacological strategies, with morphine as the primary strong opioid. Specific treatments for other symptoms depend on the underlying cause and it is important to consider reversible causes and non-pharmacological measures.\n\n\n\n# Definition\n\nMedications used in end of life care aim to relieve distressing symptoms which may appear in the last days, weeks, or months of life. They are commonly prescribed as 'anticipatory' or 'just in case' medications for a patient known to be nearing the end of life.\n\n\nThey can be administered:\n\n\n- Orally - if the patient is safely able to swallow\n- Subcutaneously - via single dose or continuous syringe pump\n- Transdermally - especially for stable symptoms and if available\n- Intramuscularly - less common\n- Intravenously - less common, but may be helpful if a patient already has access\n\n## A note on holistic care\n\nIn palliative care, and in medicine, it is important to consider all symptoms in context. There are many different aspects to symptoms. These include the physical cause, the patient's beliefs about their illness and symptoms, social contributors and impacts, their emotional and behavioural responses. Holistic assessment and management are crucial, which is why the multidisciplinary team is so important. \n\nFor example, a patient may have been prescribed very effective analgesia but is unable to administer medicines themselves. They may also have a very strong emotional response to pain or believe that they deserve their symptoms. They may benefit from a package of care or financial support for terminal illness which a social worker could help with, or an occupational therapist to help with activities of daily living. Counselling may give the patient a space to explore their feelings around their symptoms and their illness, while spiritual support could alleviate some existential distress. These additional interventions work alongside pharmacological therapy to optimise a person's quality of life through their illness.\n\nThis chapter focuses on medications for symptoms towards the end of life, but it is crucial to remember that each patient has a different combination of needs which requires an individual assessment and management plan, often with input from a range of health and social care professionals.\n\n# Pain\n\n\nInitial pharmacological management of pain should follow the WHO pain ladder. Once patients have reached the top of this ladder (requiring regular strong opioids), careful optimisation is necessary to ensure the right level of pain relief while minimising side effects.\n\n- Morphine is the first-line strong opioid analgesic. This can be given as a modified release or immediate release form. \n- Generally, patients would have a regular 'background' dose based on their 24-hour requirements, plus a PRN dose available for **breakthrough pain.** PRN doses are usually 1/6-1/10 of the 24 hour dose. Analgesia requirements should be reviewed regularly, for example every 24 hours.\n- Alternatives to morphine may be necessary for patients with poor renal function. These include oxycodone, alfentanyl or buprenorphine.\n- When prescribing opioid analgesia consider co-prescribing a regular laxative and an as-required anti-emetic. Monitor for signs of opioid toxicity (respiratory depression, sedation, myoclonus) and switch to alternatives or dose reduce as necessary.\n\nWhen switching analgesia, it is helpful to convert the dose first to oral morphine before converting to the desired medication. Please note that different routes also have different equivalent doses, so it is always safest to check guidelines.\n\n\nThe following table shows dose equivalents of 10mg oral morphine\n\n\n| Analgesic/Route | Dose | Conversion Factor |\n| ----------------------------- | ------- | ----------------- |\n| Codeine/tramadol/dihydrocodeine oral | 100mg | x10 |\n| Diamorphine IM/IV/Subcut | 3mg | x3.3 |\n| Morphine IM/IV/Subcut | 5mg | x2 |\n| Oxycodone oral\\* | 5mg\\* | x2\\* |\n| Oxycodone Subcut\\* | 2.5mg\\* | x4\\* |\n| Alfentanil Subcut | 0.3mg | x30 |\n\n\n*NB - oral oxycodone potency is between 1.3-2x that of oral morphine. Different trusts will adopt different guidance on which you should use. If in doubt, always opt for the lower dose and titrate up.\n\n\n# Breathlessness\n\nConsider non-pharmacological measures for breathlessness first. For example, sitting the patient up, opening a window or setting up a fan can all help.\n\nPharmacological management may involve low-dose opioids, benzodiazepines or therapeutic oxygen, and should be tailored to the patient.\n\n\n# Nausea and vomiting\n\nIt is important to consider the likely cause of nausea and vomiting, as medications target different parts of the vomiting pathway. Perform a full assessment to determine the likely cause of the nausea and vomiting. Consider parenteral routes of administration - patients may have severe gastrointestinal disturbance or at least may not be able to keep down oral antiemetics long enough to be effective.\n\nThe following table shows the primary site of activity and side effects of commonly used antiemetics:\n\n| Antiemetic | Receptor activity | Side effects & cautions | Useful for |\n|---|---|---|---|\n| Metoclopramide | Dopamine antagonist | Extrapyramidal symptoms, drowsiness, restlessness, diarrhoea. Do not give with antimuscarinics or in mechanical bowel obstruction | Gastric stasis, functional bowel obstruction |\n| Cyclizine | Histamine, acetylcholine antagonist | Drowsiness, antimuscarinic | Raised intracranial pressure, vestibular dysfunction |\n| Hyoscine | Acetylcholine antagonist | Antimuscarinic | Motion sickness |\n| Haloperidol | Dopamine antagonist | Less common in palliative care doses | Chemical |\n| Levomepromazine | Dopamine, histamine, acetylcholine, 5HT2 antagonist | Sedation, postural hypotension, antimuscarinic |Broad range |\n| Ondansetron | 5HT3 antagonist | Constipation, arrhythmias, movement disorder | Cytotoxic-related |\n\n- For chemically-mediated symptoms (for example medications, metabolic derangemenet), aim to treat the underlying cause. Antiemetics that may be helpful include haloperidol, metoclopramide or levomepromazine.\n- For nausea and vomiting due to raised intracranial pressure, cyclizine is usually used first-line. Dexamethasone or radiotherapy may be helpful to reduce the pressure-associated symptoms.\n- For patients with vestibular disturbance (for example symptoms associated with movement), cyclizine usually used first-line. Alternatives include hyoscine hydrobromide.\n- For patients with bowel obstruction, seek specialist advice. If due to peristaltic failure, review medications and consider starting metoclopramide (providing there is no colic). Likewise for gastric stasis, consider metoclopramide. For patients with mechanical obstruction and/or colic, do not give metoclopramide. Exclude constipation, give cyclizine for nausea and treat colic with hyoscine butylbromide.\n- If nausea and vomiting is due to compression from an abdominal or pelvic tumour, cyclizine should be used first-line.\n- For anxiety-related nausea and vomiting, begin with non-pharmacological measures for anxiety, such as CBT. A benzodiazepine or levomepromazine would be first-line pharmacological options.\n\n# Agitation\n\nAs with other symptoms, aim to manage reversible causes of agitation and possible delirium first. Consider non-pharmacological measures such as environmental modification. For patients in their last days of life, haloperidol or low-dose midazolam may be prescribed. Often, this is done as part of anticipatory prescribing.\n\n\n# Respiratory tract secretions\n\nRespiratory tract secretions often occur in the last days of life as a person becomes less able to clear their airways. They are rarely a cause of distress to the patient, but may be upsetting for family members or those close to the patient. An antimuscarinic such as hyoscine butylbromide or glycopyrronium bromide may be prescribed for noisy respiratory secretions.\n\n\n# NICE guidelines\n\n\n[NICE Guidance: Care of dying adults in the last days of life](https://www.nice.org.uk/guidance/ng31)\n\n[NICE CKS: Palliative care - general issues](https://cks.nice.org.uk/topics/palliative-care-general-issues/)\n\n[NICE CKS: Palliative care - dyspnoea](https://cks.nice.org.uk/topics/palliative-care-dyspnoea/)\n\n[NICE CKS: Palliative care - nausea and vomiting](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative care - secretions](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative cancer care - pain](https://cks.nice.org.uk/topics/)\n\n# References\n\n[Pallcare.info](https://www.pallcare.info/book.php)\n\n[BNF: Ondansetron](https://bnf.nice.org.uk/drugs/ondansetron/#drug-action)\n\n[BNF: Nausea and labyrinth disorders](https://bnf.nice.org.uk/treatment-summaries/nausea-and-labyrinth-disorders/)\n\n[BNF: Prescribing in palliative care](https://bnf.nice.org.uk/medicines-guidance/prescribing-in-palliative-care/)",
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"question": "A 75-year-old woman with metastatic mesothelioma presents with progressive shortness of breath and uncontrolled pleuritic chest pain. Her eGFR is 85mL/min/1.73m<sup>2</sup> and her liver function tests are all within normal range.\n\n\nShe currently takes 900mg gabapentin TDS, 1g paracetamol QDS, 80mg modified standard release morphine sulfate (long acting) BD, and 75mg amitriptyline ON. S She is currently using all her prescribed as-needed oral morphine doses and frequently requests her next dose due to ongoing pain.\n\n\nYou decide to increase her modified standard release morphine sulfate dose to 90mg twice daily. Calculate the most appropriate breakthrough oral morphine sulfate immediate release dose for this new regime.",
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"explanation": "This patient is on 90mg twice daily of morphine sulfate modified release and has used 4 doses of 30mg morphine immediate release, equating to a total of 300mg oral morphine sulfate in24hrs.\n \n\n Morphine sulfate accumulates in renal failure with eGFR <45mL/min/1.73m2 and so the choice of opioid should be changed to one with less renal excretion.\n \n\n In patient such as this one, with eGFR 10-30mL/min/1.73m2, the most common choice is oxycodone.\n \n\n To convert between opioids, always convert to the 24hr dose of oral morphine from the current opioid regime and then convert to the new drug of choice.\n \n\n If you are unsure, always look up conversions online or in your local trust guidance. The following table shows dose equivalents of 10mg oral morphine\n \n\n| Analgesic/Route | Dose | Conversion Factor |\n| -------------- | ------- | ----------------- |\n| Codeine/tramadol/dihydrocodeine oral | 100mg | x10 |\n| Diamorphine IM/IV/Subcut | 3mg | ÷3.3 |\n| Morphine IM/IV/Subcut | 5mg | ÷2 |\n| Oxycodone oral\\* | 6.6mg\\* | ÷1.5\\* |\n| Oxycodone Subcut\\* | 5mg\\* | ÷2\\* |\n| Alfentanil Subcut | 0.3mg | ÷30 |\n \n\n \\*NB - oral oxycodone potency is between 1.3-2x that of oral morphine. Different trusts will adopt different guidance on which you should use. If in doubt, always opt for the lower dose and titrate up.\n \n\n This patient is on 300mg/24hrs oral morphine equating to 150mg subcutaneous oxycodone/24hrs. Breakthrough analgesia dose is calculated 1/10th-1/6th the 24hr dose. This equates to 15mg-25mg subcutaneous oxycodone as required.\n \n\n Paracetamol is not available as a subcutaneous injection and so must be given orally or IV. Often when patients approach the end of their life intravenous medications are stopped or converted to other routes to avoid repetitive cannulations",
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"explanation": "# Summary\n\nMedications in end-of-life care focus on alleviating distressing symptoms in patients nearing death. A holistic approach is vital, considering physical, emotional, and social aspects of symptoms, often involving a multidisciplinary team. For pain management, the WHO pain ladder guides pharmacological strategies, with morphine as the primary strong opioid. Specific treatments for other symptoms depend on the underlying cause and it is important to consider reversible causes and non-pharmacological measures.\n\n\n\n# Definition\n\nMedications used in end of life care aim to relieve distressing symptoms which may appear in the last days, weeks, or months of life. They are commonly prescribed as 'anticipatory' or 'just in case' medications for a patient known to be nearing the end of life.\n\n\nThey can be administered:\n\n\n- Orally - if the patient is safely able to swallow\n- Subcutaneously - via single dose or continuous syringe pump\n- Transdermally - especially for stable symptoms and if available\n- Intramuscularly - less common\n- Intravenously - less common, but may be helpful if a patient already has access\n\n## A note on holistic care\n\nIn palliative care, and in medicine, it is important to consider all symptoms in context. There are many different aspects to symptoms. These include the physical cause, the patient's beliefs about their illness and symptoms, social contributors and impacts, their emotional and behavioural responses. Holistic assessment and management are crucial, which is why the multidisciplinary team is so important. \n\nFor example, a patient may have been prescribed very effective analgesia but is unable to administer medicines themselves. They may also have a very strong emotional response to pain or believe that they deserve their symptoms. They may benefit from a package of care or financial support for terminal illness which a social worker could help with, or an occupational therapist to help with activities of daily living. Counselling may give the patient a space to explore their feelings around their symptoms and their illness, while spiritual support could alleviate some existential distress. These additional interventions work alongside pharmacological therapy to optimise a person's quality of life through their illness.\n\nThis chapter focuses on medications for symptoms towards the end of life, but it is crucial to remember that each patient has a different combination of needs which requires an individual assessment and management plan, often with input from a range of health and social care professionals.\n\n# Pain\n\n\nInitial pharmacological management of pain should follow the WHO pain ladder. Once patients have reached the top of this ladder (requiring regular strong opioids), careful optimisation is necessary to ensure the right level of pain relief while minimising side effects.\n\n- Morphine is the first-line strong opioid analgesic. This can be given as a modified release or immediate release form. \n- Generally, patients would have a regular 'background' dose based on their 24-hour requirements, plus a PRN dose available for **breakthrough pain.** PRN doses are usually 1/6-1/10 of the 24 hour dose. Analgesia requirements should be reviewed regularly, for example every 24 hours.\n- Alternatives to morphine may be necessary for patients with poor renal function. These include oxycodone, alfentanyl or buprenorphine.\n- When prescribing opioid analgesia consider co-prescribing a regular laxative and an as-required anti-emetic. Monitor for signs of opioid toxicity (respiratory depression, sedation, myoclonus) and switch to alternatives or dose reduce as necessary.\n\nWhen switching analgesia, it is helpful to convert the dose first to oral morphine before converting to the desired medication. Please note that different routes also have different equivalent doses, so it is always safest to check guidelines.\n\n\nThe following table shows dose equivalents of 10mg oral morphine\n\n\n| Analgesic/Route | Dose | Conversion Factor |\n| ----------------------------- | ------- | ----------------- |\n| Codeine/tramadol/dihydrocodeine oral | 100mg | x10 |\n| Diamorphine IM/IV/Subcut | 3mg | x3.3 |\n| Morphine IM/IV/Subcut | 5mg | x2 |\n| Oxycodone oral\\* | 5mg\\* | x2\\* |\n| Oxycodone Subcut\\* | 2.5mg\\* | x4\\* |\n| Alfentanil Subcut | 0.3mg | x30 |\n\n\n*NB - oral oxycodone potency is between 1.3-2x that of oral morphine. Different trusts will adopt different guidance on which you should use. If in doubt, always opt for the lower dose and titrate up.\n\n\n# Breathlessness\n\nConsider non-pharmacological measures for breathlessness first. For example, sitting the patient up, opening a window or setting up a fan can all help.\n\nPharmacological management may involve low-dose opioids, benzodiazepines or therapeutic oxygen, and should be tailored to the patient.\n\n\n# Nausea and vomiting\n\nIt is important to consider the likely cause of nausea and vomiting, as medications target different parts of the vomiting pathway. Perform a full assessment to determine the likely cause of the nausea and vomiting. Consider parenteral routes of administration - patients may have severe gastrointestinal disturbance or at least may not be able to keep down oral antiemetics long enough to be effective.\n\nThe following table shows the primary site of activity and side effects of commonly used antiemetics:\n\n| Antiemetic | Receptor activity | Side effects & cautions | Useful for |\n|---|---|---|---|\n| Metoclopramide | Dopamine antagonist | Extrapyramidal symptoms, drowsiness, restlessness, diarrhoea. Do not give with antimuscarinics or in mechanical bowel obstruction | Gastric stasis, functional bowel obstruction |\n| Cyclizine | Histamine, acetylcholine antagonist | Drowsiness, antimuscarinic | Raised intracranial pressure, vestibular dysfunction |\n| Hyoscine | Acetylcholine antagonist | Antimuscarinic | Motion sickness |\n| Haloperidol | Dopamine antagonist | Less common in palliative care doses | Chemical |\n| Levomepromazine | Dopamine, histamine, acetylcholine, 5HT2 antagonist | Sedation, postural hypotension, antimuscarinic |Broad range |\n| Ondansetron | 5HT3 antagonist | Constipation, arrhythmias, movement disorder | Cytotoxic-related |\n\n- For chemically-mediated symptoms (for example medications, metabolic derangemenet), aim to treat the underlying cause. Antiemetics that may be helpful include haloperidol, metoclopramide or levomepromazine.\n- For nausea and vomiting due to raised intracranial pressure, cyclizine is usually used first-line. Dexamethasone or radiotherapy may be helpful to reduce the pressure-associated symptoms.\n- For patients with vestibular disturbance (for example symptoms associated with movement), cyclizine usually used first-line. Alternatives include hyoscine hydrobromide.\n- For patients with bowel obstruction, seek specialist advice. If due to peristaltic failure, review medications and consider starting metoclopramide (providing there is no colic). Likewise for gastric stasis, consider metoclopramide. For patients with mechanical obstruction and/or colic, do not give metoclopramide. Exclude constipation, give cyclizine for nausea and treat colic with hyoscine butylbromide.\n- If nausea and vomiting is due to compression from an abdominal or pelvic tumour, cyclizine should be used first-line.\n- For anxiety-related nausea and vomiting, begin with non-pharmacological measures for anxiety, such as CBT. A benzodiazepine or levomepromazine would be first-line pharmacological options.\n\n# Agitation\n\nAs with other symptoms, aim to manage reversible causes of agitation and possible delirium first. Consider non-pharmacological measures such as environmental modification. For patients in their last days of life, haloperidol or low-dose midazolam may be prescribed. Often, this is done as part of anticipatory prescribing.\n\n\n# Respiratory tract secretions\n\nRespiratory tract secretions often occur in the last days of life as a person becomes less able to clear their airways. They are rarely a cause of distress to the patient, but may be upsetting for family members or those close to the patient. An antimuscarinic such as hyoscine butylbromide or glycopyrronium bromide may be prescribed for noisy respiratory secretions.\n\n\n# NICE guidelines\n\n\n[NICE Guidance: Care of dying adults in the last days of life](https://www.nice.org.uk/guidance/ng31)\n\n[NICE CKS: Palliative care - general issues](https://cks.nice.org.uk/topics/palliative-care-general-issues/)\n\n[NICE CKS: Palliative care - dyspnoea](https://cks.nice.org.uk/topics/palliative-care-dyspnoea/)\n\n[NICE CKS: Palliative care - nausea and vomiting](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative care - secretions](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative cancer care - pain](https://cks.nice.org.uk/topics/)\n\n# References\n\n[Pallcare.info](https://www.pallcare.info/book.php)\n\n[BNF: Ondansetron](https://bnf.nice.org.uk/drugs/ondansetron/#drug-action)\n\n[BNF: Nausea and labyrinth disorders](https://bnf.nice.org.uk/treatment-summaries/nausea-and-labyrinth-disorders/)\n\n[BNF: Prescribing in palliative care](https://bnf.nice.org.uk/medicines-guidance/prescribing-in-palliative-care/)",
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"question": "A 72-year-old man with metastatic colorectal cancer and chronic kidney disease is admitted with sepsis. After three days of treatment, he deteriorates. Following discussions, the decision is made to discontinue antibiotics and fluids, focusing on end-of-life care.\n\nHis current analgesia is paracetamol 1g QDS, morphine sulfate modified release (long-acting) 90mg BD, and morphine sulfate immediate release oral liquid (short acting) 30mg PRN, 4-hourly. He has used 4 doses of the PRN oral morphine in 24hrs.\n\n\nHis eGFR is 22 mL/min/1.73m². The patient asks if his oral medications can be reduced or converted to a syringe driver due to difficulty swallowing.\n\nWhich of the following prescriptions would be most suitable for this patient?",
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"explanation": "This patient most likely has chronic lymphocytic leukaemia. Immunophenotyping detects tumour markers in peripheral blood by labelling the white blood cells with antibodies directed against cell surface proteins. This allows for differentiation of leukaemic cells to show which specific type of leukaemia the patient has and so which treatment would be most appropriate",
"id": "33023",
"label": "a",
"name": "Immunophenotyping",
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"explanation": "Chronic lymphocytic leukaemia can be subcategorised using immunophenotyping and flow cytometry from peripheral blood. Therefore, evaluation of bone marrow biopsy is not usually necessary unless there is diagnostic doubt from the former tests",
"id": "33025",
"label": "c",
"name": "Bone marrow biopsy",
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"explanation": "Iron studies are commonly used to investigate the cause of anaemia and will likely be done in this patient as they are anaemic, but it is not the next best investigation for their leukaemia",
"id": "33027",
"label": "e",
"name": "Iron studies",
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"explanation": "Chronic lymphocytic leukaemia can be subcategorised using immunophenotyping and flow cytometry from peripheral blood. Evaluation of lymph node biopsy is not usually necessary unless there is diagnostic doubt from the former tests",
"id": "33024",
"label": "b",
"name": "Lymph node biopsy",
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"explanation": "Serum electrophoresis is commonly used to investigate multiple myeloma or monoclonal gammopathy of uncertain significance (MGUS). While chronic lymphocytic leukaemia may produce IgM paraproteinaemia, it is not routinely used in its diagnosis",
"id": "33026",
"label": "d",
"name": "Serum electrophoresis",
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"comment": "Quesbook notes mention bone marrow biopsy but not immunophenotyping ",
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"explanation": "# Summary\n\nChronic Lymphocytic Leukaemia (CLL) is a mature B-cell neoplasm characterized by the accumulation of monoclonal B lymphocytes in the blood, bone marrow, and lymphoid tissues. The CLL cells accumulate because they survive for a very long time, rather than because they divide at an accelerated rate. It is therefore an indolent disease of deregulated programmed cell death. It primarily affects older adults and often progresses slowly. CLL may be asymptomatic, but common symptoms include fatigue, lymphadenopathy, and hepatosplenomegaly. Diagnosis is confirmed through blood counts, flow cytometry, and genetic tests. Treatment is typically indicated for symptomatic or progressive disease and may involve chemotherapy, targeted therapy, and stem cell transplantation.\n\n# Definition\n\nChronic Lymphocytic Leukaemia (CLL) is a haematologic malignancy characterized by the accumulation of mature monoclonal B lymphocytes in the blood, bone marrow, and lymphoid tissues. These abnormal B cells are often slow-growing and crowd out healthy blood cells.\n\n\n# Epidemiology\n\nCLL is most common in men over the age of 60 years – incidence is 50 per 100,000 individuals after the age of 70 years and it is the most common leukaemia in Western countries\n\n# Aetiology\n\nThe precise cause of CLL is not well-defined, but genetic and environmental factors may contribute to its development. A family history of CLL or exposure to certain chemicals may be associated with an increased risk.\n\n\n# Signs and Symptoms \n\nCLL typically presents asymptomatically, but patients may present with:\n\n- Non-tender symmetrical lymphadenopathy\n- Hepatosplenomegaly\n- B symptoms – weight loss, night sweats and fever \n\nFeatures of marrow failure (infection, anaemia and bleeding) are less common than in acute leukaemias.\n\n# Differential Diagnosis\n\n- **Hairy Cell Leukaemia (HCL):** HCL is another mature B-cell leukaemia and may share some clinical features with CLL. However, the distinct hairy appearance of leukaemic cells in HCL helps differentiate the two.\n- **Small Lymphocytic Lymphoma (SLL):** SLL is closely related to CLL and is considered the tissue-based counterpart. Differentiating between CLL and SLL depends on whether the predominant site of involvement is in the blood or lymph nodes.\n- **Infections:** Some infectious diseases, such as infectious mononucleosis, can mimic lymphadenopathy and other symptoms of CLL.\n\n# Investigations \n\n- The most common initial blood result is an **incidental lymphocytosis** (80% of cases)\n- **Blood film** shows smudge cells – cells damaged as the film is made because they lack a cytoskeletal protein\n- **Immunophenotype** of the cells is CD5 and CD23 positive, FMC negative, CD22 and surface immunoglobulin weak\n- Chromosomal abnormalities are found in approximately 50% of patients \n- Direct antiglobulin test can be positive – AIHA can complicate CLL\n- Hypogammaglobulinaemia is common in advanced disease\n\n[lightgallery]\n\n- Other tests include bone marrow biopsy, which will show lymphocytic infiltration of mature lymphocytes, with some smear cells\n\nNICE advise considering an urgent FBC (within 48h) to assess for leukaemia in adults with any of the following:\n\n* Pallor\n* Persistent fatigue\n* Unexplained fever\n* Unexplained persistent or recurrent infection\n* Generalized lymphadenopathy\n* Unexplained bruising\n* Unexplained bleeding\n* Unexplained petechiae\n* Hepatosplenomegaly\n\n# Staging\n\nThe disease is often staged using Binet's system based on lymphoid tissue enlargement, haemoglobin and platelets.\n\n# Management \n\n- Treatment depends on the stage and activity of the disease i.e. rapidly progressive, bulky, with disabling systemic symptoms or there is associated cytopenias or shortened lymphocyte doubling time. \n- There is no evidence that intervening with treatment at an earlier, asymptomatic phase is beneficial. So often, watchful monitoring is often useful at this stage.\n- Traditionally, intensive chemotherapy including rituximab was first-line therapy. This has now changed in the world of targeted pathway inhibitors superseding chemotherapy. \n- In a patient with no co-morbidities and TP53 intact, +/- mutated IGHV mutated status, we can now start with Venetoclax (selective inhibitor of B-cell lymphoma-2, BCL-2)-Obinutuzumab (anti-CD20 monoclonal antibody) (Ven-O) upfront. \n- In fit patients with TP53 mutational disruption or any IGHV mutated status, first-line therapy is with Acalabrutinib (bruton tyrosine kinase inhibitor) +/- Obinutuzumab or upfront Ibrutinib (tyrosine kinase inhibitor, TKI) monotherapy. \n- Allogeneic stem cell transplant should be considered in those fit patients who have failed at least 2 of : chemoimmunotherapy, BTKi, BCL2i or have Richter’s transformation (sudden transformation into a significantly more aggressive form of large cell lymphoma). \n- If they are high-risk patients (TP53 disrupted), then an allogenic transplant can be considered after the failure of these therapies.\n- Steroids and monoclonal antibody treatments (eg. rituximab) may be useful in autoimmune haemolytic disease. \n- Prevention or treatment of infection with antibiotics or immunoglobulins is also part of the management. \n\n# Complications\n\n* **Infections:** Patients with CLL are at an increased risk of infections due to compromised immune function.\n* **Transformation to Diffuse Large B-Cell Lymphoma (Richter Transformation):** A small percentage of CLL patients may experience aggressive transformation to a high-grade lymphoma, which has a poor prognosis.\n* **Autoimmune Haemolytic Anaemia:** Some CLL patients may develop autoimmune complications, such as heamolytic anaemia or immune thrombocytopenia.\n\n# Prognosis \n\nCLL is a very variable disease: 1/3 of cases don't progress, 1/3 of cases progress slowly, and 1/3 of cases progress actively. \n\nFactors that affect prognosis are: \n\n- Disease stage \n- Atypical lymphocyte morphology\n- Lymphocyte doubling time <12 months\n- Bone marrow trephine showing diffuse involvement\n- Chromosomal/genetic abnormalities, in particular TP53\n- Unmutated immunoglobulin VH (IGVH) gene status\n- Male sex\n- High expression CD38\n\nGiven the improvement in the CLL therapeutic landscape, CLL prognosis now has a median 5-year survival at 87%.\n\nA small proportion of patients with CLL will progress to a more aggressive type with:\n\n- Refractoriness to treatment\n- Increase in systemic symptoms and disease bulk, plus a change in morphological features, specifically 'high-grade lymphomatous (Richter's) transformation'. \n\n\n\n# NICE Guidelines \n\n[NICE 2ww for Haematological Cancers](https://cks.nice.org.uk/topics/haematological-cancers-recognition-referral/management/referral-for-haematological-cancer/#refer-an-adult-for-suspected-leukaemia)",
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"learningPoint": "Immunophenotyping in chronic lymphocytic leukemia (CLL) is a diagnostic process that uses flow cytometry to identify specific cell surface markers, such as CD5, CD19, CD20, and CD23, to confirm the presence of clonal B-cell populations and distinguish CLL from other lymphoid disorders.",
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"question": "A 72-year-old man presents to the GP with 3 months of general fatigue, malaise, and night sweats.\n\n\nBloods reveal the following:\n\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|78 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|16.3x10<sup>9</sup>/L|3.0 - 10.0|\n|Neutrophils|3.1x10<sup>9</sup>/L|2.0 - 7.5|\n|Lymphocytes|8.2x10<sup>9</sup>/L|1.5 - 4.0|\n\n\nPeripheral blood film shows smudge cells and small mature lymphocytes with round nuclei and clumped chromatin.\n\n\nGiven the likely diagnosis, which of the following is the next best investigation?",
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"explanation": "Methylphenidate is not recommended in conduct disorder but is occasionally used in attention deficit hyperactive disorder (ADHD) to control challenging behaviour",
"id": "33140",
"label": "c",
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"explanation": "This would be appropriate if the child had a co-existing mental health problem, a neurodevelopmental condition, or learning disability, or if there was any indication of underlying mental health disorder",
"id": "33139",
"label": "b",
"name": "Refer to Child and Adolescent Mental Health Services (CAMHS)",
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"explanation": "This child is exhibiting behaviour typical of conduct disorder. Child-focused programmes are usually offered to children aged 9-14 with conduct disorder, involving group social and cognitive behavioural problem-solving exercises with rehearsal and feedback to improve behaviour",
"id": "33138",
"label": "a",
"name": "Refer to child-focused programmes",
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"__typename": "QuestionChoice",
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"explanation": "In parent training programmes, parenting skills are improved by using modelling, rehearsing, and feedback. Parent training is usually focused on children younger than 11 years old and so would unlikely be suggested in this scenario",
"id": "33142",
"label": "e",
"name": "Refer the father to parent training programmes",
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"explanation": "A health and social care assessment assesses what help and support can be provided at home, such as disability equipment and adaptations to the home, organising respite, and arrangements for parenting classes. In this case, there is no information suggesting they require functional adaptations to their home. Parent training is usually focused on children younger than 11 years old and so would unlikely be suggested in this scenario",
"id": "33141",
"label": "d",
"name": "Refer for a health and social care assessment by social services",
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"comment": "Patient.info \"Community-based help\nIf the behavioural problems are severe and persistent or a conduct disorder is suspected, ask your GP for advice.\n\nAntisocial behaviours are commonly seen in specialist services. If specialist help is needed, the GP will make a referral to your local child and adolescent mental health service (CAMHS). This specialist team will work together with you, the school and other community groups to support you and your child.\"",
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"comment": "I'm also sure that a lot of oppositional defiant disorders (<18y/o) are co-morbid with mood/mental health disorders ",
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"explanation": "# Summary\n \nConduct disorder is a diagnosis characterised by persistent behaviour in patients under 18 that repeatedly violates the rights of others and demonstrates a disregard for societal norms. Key signs include demonstration of physical aggression, destructive behaviour, and stealing. Primary investigations into conduct disorder often involve psycho-social assessments and physical examinations to rule out potential differential diagnoses such as Oppositional Defiant Disorder (ODD) or Attention-Deficit/Hyperactivity Disorder (ADHD). Management strategies typically involve a combination of psychotherapy, family therapy, and in some cases, pharmacological treatments.\n \n\n# Definition\n \nConduct disorder is a psychological diagnosis given to patients under the age of 18 years old who consistently exhibit behaviours and attitudes that disrespect and violate the rights of others, often breaching societal norms and rules, and interfering with the patient's ability to live a normal life. \n \n\n# Epidemiology\n \nWhile the prevalence rates can vary, conduct disorder is found in 4.6% of 5-19-year-olds in England according to an NHS survey in 2017. Higher rates were observed in boys (5.8%) compared to girls (3.4%). It is most common in those ages 11-16 and is less common to onset after age 16. It is also more common amongst white British compared to Black/Black British or Asian/Asian British populations. \n\nThe disorder is more common in urban areas and among families with lower socioeconomic status. Looked after children in foster care or children's homes show higher rates of conduct disorder. \n\n\n# Aetiology\n \nThe aetiology of conduct disorder is multifactorial, involving a complex interplay of genetic, environmental, and psychological factors. These can include a family history of mental health disorders, childhood maltreatment or neglect, peer influence, and underlying neurological abnormalities. \n \n\n# Signs and Symptoms\n \n\nThe key clinical manifestations of conduct disorder are:\n \n\n - Persistent and serious violation of rules, societal norms, and the rights of others\n - Physical aggression directed towards people and animals\n - Destructive behaviour, such as arson or vandalism\n - Deceitfulness or theft\n - Serious violation of rules, such as truancy or running away from home\n \n\n# Differential Diagnosis\n \n\nIn evaluating conduct disorder, several other disorders should be considered, including:\n \n\n - **Oppositional Defiant Disorder (ODD)**: Presents with angry and irritable mood, argumentative and defiant behaviour, but usually lacks the severe aggression, violation of societal norms, and respect for the rights of others seen in conduct disorder.\n - **Attention-Deficit/Hyperactivity Disorder (ADHD)**: Characterised by a persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development. This can be distinguished from conduct disorder by the absence of consistent antisocial behaviours.\n - **Mood Disorders**: Depressive and bipolar disorders can sometimes be associated with disruptive behaviours. However, in these conditions, mood symptoms predominate and there is usually no persistent pattern of violation of the rights of others.\n \n\n# Investigations\n \n\nInvestigations for conduct disorder primarily involve psycho-social assessments by CAMHS, which include:\n \n\n - Interviews with the child and parents to gather a comprehensive developmental, familial, and social history\n - Observations of the child’s behaviour in various settings\n - Use of standardised assessment tools and questionnaires (Strengths and Difficulties Questionnaire) \n - Physical examination and other tests to rule out medical conditions that could contribute to the behaviour\n \n\n# Management\n \n\nManagement strategies for conduct disorder may include:\n \n\n - **Psychotherapy**: Cognitive-behavioral therapy (CBT) can be effective in helping the child to control their anger and improve their problem-solving skills.\n - **Family therapy**: This can help improve family interactions and communication, which in turn can reduce symptoms of conduct disorder. \n - **Parent training programmes**: Use modelling, rehearsal and feedback to improve parenting skills. \n - **Pharmacological treatments**: Not used first line, but in some cases medications may be used to manage comorbid conditions or specific problematic behaviours, such as impulsivity, aggression, or mood symptoms.\n - **School-based interventions**: These may also be beneficial in promoting positive behaviours and reducing disruptive behaviours.\n \n\n# Prognosis\n \n\nThe prognosis of conduct disorder is generally poor:\n \n\n - Around 50% of children with conduct disorder develop antisocial personality disorder\n - Around 50% develop substance misuse issues\n - Around 40% become recurring young offenders\n\nYounger age of behavioural problems increases the risk of the patient becoming involved with crime. \n \n \n# NICE Guidelines\n \n [NICE Guideline on Antisocial behaviour and Conduct Disorders in children and Young People: recognition and Management](https://www.nice.org.uk/guidance/cg158) \n \n\n# References\n \n[Royal College of Psychiatrists \" Behavioural problems and conduct disorder\"](https://www.rcpsych.ac.uk/mental-health/parents-and-young-people/information-for-parents-and-carers/behavioural-problems-and-conduct-disorder-for-parents)\n\n [Information on Conduct Disorder](https://patient.info/childrens-health/behavioural-problems-and-conduct-disorder)\n \n [WHO Conduct Disorder](https://applications.emro.who.int/docs/EMRPUB_leaflet_2019_mnh_217_en.pdf)",
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"question": "A 12-year-old boy is brought to the GP by his father for 12 months of recurrent vandalism, frequent theft of other children's property, repeated episodes of lying to his teachers, and has started smoking. His son does not feel his behaviour is problematic. He often becomes \"uncontrollable\" at home breaking dishes and furniture with no guilt or remorse in harming others.\n\nHe has no history of mental health problems and there is no indication of an underlying mental health disorder. He does not have any developmental disorders or learning disabilities.\n\nWhich of the following is the most appropriate next management step?",
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"explanation": "This patient has multiple risk factors for MI, including diabetes, hypertension and obesity. Diaphoresis (sweating) and nausea are both important symptoms to recognise as potential indicators of cardiac pathology. They can also present with shortness of breath as the primary symptom. In addition, older male patients are the most likely demographic to experience MI without chest pain",
"id": "33253",
"label": "a",
"name": "Myocardial infarction (MI)",
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"__typename": "QuestionChoice",
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"explanation": "DKA occurs more often in type 1 diabetes compared with type 2, however, some patients with type 2 diabetes are ketone producing. It would be unlikely for ketoacidosis to cause collapse without first experiencing notable vomiting, confusion or drowsiness, none of which are mentioned in the stem",
"id": "33257",
"label": "e",
"name": "Diabetic ketoacidosis (DKA)",
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"explanation": "A TIA is characterised by sudden onset neurological deficit that usually lasts for minutes to hours, but resolves within 24 hours. A TIA could be an explanation for a patient presenting following a collapse. However, it is not classically preceded by an extended period of symptoms from other systems, such as nausea and sweating",
"id": "33255",
"label": "c",
"name": "Transient ischaemic attack (TIA)",
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"explanation": "This patient does have a risk factor for pulmonary embolism in his obesity, but his risk profile for a MI is greater. In addition, there are no other identifiable triggers for pulmonary embolism in the history, such as recent long distance travel or immobility",
"id": "33254",
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"explanation": "It is always important to consider arrhythmia as a potential cause of collapse. However, there is no mention of preceding palpitations, shortness of breath or pre-syncopal episodes. Given the diaphoresis, nausea and risk factors for MI, this would be a more likely explanation",
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"explanation": "# Summary\r\n\r\nAcute coronary syndrome (ACS) refers to a set of symptoms and signs that occur due to reduced blood flow to the heart at rest. It encompasses 3 distinct diagnoses: unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). In the case of infarction, this is a medical emergency requiring urgent treatment. ACS is most commonly caused by the rupture of atherosclerotic plaques in coronary arteries leading to further narrowing, and potentially complete occlusion, of these critical blood vessels. Diagnosis involves clinical evaluation, ECGs, and troponin levels. Treatment strategies differ for STEMI and NSTEMI/unstable angina but include oxygen therapy if hypoxic, antiplatelet medication, glyceryl trinitrates, morphine, and percutaneous coronary intervention (PCI). Post-MI management includes aspirin, dual antiplatelet therapy, beta-blockers, ACE inhibitors, high-dose statins, and cardiac rehabilitation. There are many complications to be aware of post-ACS and these include arrhythmias, heart failure, and cardiac tamponade, and others.\r\n\r\n# Definition \r\n\r\nAcute coronary syndrome is a set of symptoms and signs that occur due to decreased blood flow to the heart at rest. It broadly refers to three distinct diagnoses: unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI). \r\n\r\n# Epidemiology \r\n\r\nIn the UK, there are over 80,000 hospital admissions due to ACS every year. Coronary artery disease remains the largest cause of death in the UK. \r\n\r\n# Pathophysiology\r\n\r\nCoronary artery disease refers to the narrowing of coronary arteries by atherosclerosis and plaque formation. In stable angina, when the demand for myocardial oxygen increases with exertion, narrowed coronary arteries cannot meet this increased demand leading to myocardial ischaemia and pain. Conversely, in ACS, the symptoms occur at rest. This is because there is sudden plaque rupture and clot formation in the narrowed coronary arteries. If there is partial occlusion of the coronary artery this leads to ischaemia and chest pain at rest (unstable angina). If the coronary artery becomes more occluded or fully occluded this leads to significant hypoperfusion of the myocardium and ultimately leads to infarction (death) of the myocardial tissue (NSTEMI or STEMI). \r\n\r\n# Risk Factors\r\n\r\nCoronary artery disease and the development of plaques can be attributed to non-modifiable and modifiable risk factors. Modifiable risk factors must be addressed in the management of IHD. \r\n\r\n* Non-modifiable:\r\n * Age\r\n * Male sex\r\n * Family history\r\n * Ethnicity (particularly South Asians)\r\n* Modifiable:\r\n * Smoking\r\n * Hypertension\r\n * Hyperlipidaemia\r\n * Hypercholesterolaemia\r\n * Obesity\r\n * Diabetes\r\n * Stress\r\n * High fat diets\r\n * Physical inactivity\r\n\r\n# Classification \r\n\r\nAcute coronary syndrome can be split up into three distinct diagnoses: \r\n\r\n1. **Unstable angina**: caused by partial occlusion of a coronary artery. Troponin negative chest pain with normal/abnormal ECG signs. \r\n2. **Non-ST Elevation Myocardial Infarction**: caused by severe but incomplete occlusion of a coronary artery. Troponin positive chest pain without ST elevation. \r\n3. **ST-Elevation Myocardial Infarction**: caused by complete occlusion of a coronary artery. Troponin positive chest pain with ST elevation on ECG. \r\n\r\n*Myocardial Ischaemia vs. Myocardial Infarction and the Release of Troponin*\r\n\r\nIt is important at this stage to distinguish between angina (stable angina is on exertion and unstable angina is at rest) and myocardial infarction. Angina refers to myocardial ischaemia that causes chest pain but does not lead to the death of myocardial tissue and does not lead to a troponin rise. In myocardial infarction, the hypoperfusion of the myocardium is so profound that it leads to the death of myocardial tissue. It is when there is myocardial tissue death that troponin is released into the bloodstream and a troponin rise is found on blood tests.\r\n\r\n*Type 2 Myocardial Infarction* \r\n\r\nIt is also important to mention that some patient may have myocardial infarctions due to cardiac hypoperfusion for other reasons (e.g. severe sepsis, hypotension, hypovolaemia or coronary artery spasm). These are usually termed type 2 myocardial infarctions and may not require the conventional treatment outlined below. \r\n\r\n# Symptoms and Signs\r\n\r\n* Chest pain - the classical presentation can be considered in terms of the SOCRATES mnemonic:\r\n * Site - Central/left sided\r\n * Onset - Sudden\r\n * Character - Crushing ('like someone is sitting on your chest')\r\n * Radiation - Left arm, neck and jaw\r\n * Associated symptoms - Nausea, sweating, clamminess, shortness of breath, sometimes vomiting or syncope\r\n * Timing - Constant\r\n * Exacerbating/relieving factors - Worsened by exercise/exertion and may be improved by GTN\r\n * Severity - Often extremely severe\r\n* Atypical presentations may include:\r\n * Epigastric pain\r\n * No pain (more common in elderly and **patients with diabetes**):\r\n * Acute breathlessness\r\n * Palpitations\r\n * Acute confusion\r\n * Diabetic hyperglycaemic crises\r\n * Syncope\r\n\r\n# Differential Diagnoses\r\n\r\nIt is important to remember that there are non-MI causes of chest pain and these should be considered when making a diagnosis:\r\n\r\n* Cardiac\r\n * Myocarditis\r\n * Pericarditis\r\n * Cardiomyopathy\r\n * Valvular disease\r\n * Cardiac trauma\r\n* Pulmonary\r\n * PE\r\n * Pneumonia\r\n * Pneumothorax\r\n* Vascular\r\n * Aortic dissection\r\n* GI\r\n * Oesophageal spasm\r\n * Oesophagitis\r\n * Peptic ulcer\r\n * Pancreatitis\r\n * Cholecystitis\r\n* MSK\r\n * Rib fracture\r\n * Costochondritis\r\n * Muscle injury\r\n * Herpes zoster\r\n\r\n# Diagnosis of ACS \r\n\r\nDiagnosis depends on a combination of clinical, ECG and biochemical findings which helps distinguish between the various types of ACS.\r\n\r\n* Unstable angina - cardiac chest pain at rest + abnormal/normal ECG + **normal troponin**.\r\n* NSTEMI - cardiac chest pain at rest + abnormal/normal ECG (but not ST-elevation) + **raised troponin**\r\n* STEMI - cardiac chest pain at rest + **persistent ST-elevation/new LBBB** (note that there is no need for a troponin in this case).\r\n\r\n## Diagnosis of STEMI\r\n\r\n* ST segment elevation **>2mm** in adjacent chest leads\r\n* ST segment elevation **>1mm** in adjacent limb leads\r\n* New left bundle branch block (LBBB) with chest pain or suspicion of MI\r\n\r\n## Diagnosis of NSTEMI\r\n\r\nDiagnosis of NSTEMI requires two of the following:\r\n\r\n* Cardiac chest pain\r\n* Newly abnormal ECG which does not demonstrate ST-elevation e.g. ST depression, T wave inversion or non-specific changes. \r\n* Raised troponin (with no other reasonable explanation)\r\n\r\n# Investigations\r\n\r\n## Bedside \r\n\r\n* ECG \r\n\t* Looking for ST-elevation, LBBB or other ST abnormalities\r\n\t* This is the most important investigation and should not be delayed for other investigations (e.g. bloods) because this will define immediate management.\r\n\t* If an ECG shows STEMI then troponin is essentially irrelevant and the patient requires immediate treatment.\r\n\r\n## Bloods \r\n\r\n* Troponin: performed **at least 3 hours** after pain starts. It will also need to be repeated (usually 6 hours after the first level) in order to demonstrate a dynamic troponin rise. \r\n* Renal function: good renal function is required for coronary angiogram +/- PCI due to the use of contrast. \r\n* HbA1c and lipid profile: looking for modifiable risk factors for coronary artery disease. \r\n* FBC and CRP - rule out infectious causes of chest pain\r\n* D-dimer - may be used in _appropriate_ patients to rule out PE. *Be very careful about who you do a D-dimer on!*\r\n\r\n## Imaging \r\n\r\n* CXR: should be completed in all those presenting with a chest symptoms. It will help to rule out other causes of chest pain (e.g. pneumothorax) and look for complications of a large MI (e.g. pulmonary oedema in acute heart failure). \r\n\r\n# ECG Interpretation - Cardiac Territories and Affected Vessels\r\n\r\nThe importance of a 12-lead ECG is that it allows one to view electrical activity of the heart from different \"views\". In MI (particularly STEMI) this allows you to understand which territory (and therefore which vessel) is being affected.\r\n\r\n| Location of ST elevation | Area of myocardium | Coronary artery |\r\n| -------------------------- | ------------------ | -------------------- |\r\n| II, III, aVF | Inferior | RCA |\r\n| V1-2 | Septal | Proximal LAD |\r\n| V3-4 | Anterior | LAD |\r\n| V5-6 | Apex | Distal LAD/ LCx/ RCA |\r\n| I, aVL | Lateral | Lcx |\r\n| V7-V9 (ST depression V1-3) | Posterolateral | RCA/ LCx |\r\n\r\n\r\nRCA: right coronary artery, LAD: left anterior descending, LCx: Left circumflex\r\n\r\n[lightgallery]\r\n\r\n[lightgallery2]\r\n\r\n[lightgallery3]\r\n\r\n[lightgallery4]\r\n\r\n\r\nNSTEMIs may also show T wave abnormalities (such as ST depression and T wave inversions) in vascular territories as above. However, changes can also often not include all the specific leads of that territory in an NSTEMI.\r\n\r\n# Troponin Interpretation\r\n\r\nTroponin is a myocardial protein that is released into the bloodstream when cardiac myocytes are damaged. Serum levels typically rise **3 hours** after myocardial infarction begins.\r\n\r\nDifferent hospitals have differing guidelines (and assays) for interpretations of results. In general there are three groups of troponin levels:\r\n\r\n* Low - definitely no myocardial cell death. The patient is not having an MI although they may be experiencing unstable angina.\r\n* Mildly raised - This is an equivocal result and may be due to other non-MI related factors (see below). These patients usually need a <u>6-12 hour repeat test</u>.\r\n * If repeat troponin is raised on the repeat they are having an MI.\r\n * If repeat troponin is stable or falling then they are unlikely to be having an MI.\r\n* Definitely raised with sequential dynamic troponin rises - MI confirmed (be aware of the possibility of a Type 2 MI)\r\n\r\n## Non-ACS causes of a raised troponin\r\n\r\nAlthough troponin is often used diagnose myocardial infarction, there are in fact many causes of a raised troponin:\r\n\r\n* Myocardial infarction\r\n* Pericarditis\r\n* Myocarditis\r\n* Arrythmias\r\n* Defibrillation\r\n* Acute heart failure\r\n* Pulmonary embolus\r\n* Type A aortic dissection\r\n* Chronic kidney disease\r\n* Prolonged strenuous exercise\r\n* Sepsis\r\n\r\nIt is therefore critical to have good clinical grounds to test a troponin in order to avoid unnecessary treatments and investigations.\r\n\r\n# Management\r\n\r\nAcute management depends on the type of acute coronary syndrome. It is broadly split into the management of STEMI and the management of NSTEMI/unstable angina. \r\n\r\n# Management of STEMI\r\n\r\n[lightgallery5]\r\n\r\nFor emergencies, always follow A-E structure. \r\n\r\n1. Targeted oxygen therapy (aiming for sats >90%)\r\n2. Loading dose of **PO aspirin 300mg**\r\n - Note that some hospital protocols will also call for a loading dose of a second anti-platelet agent such as clopidogrel (300mg) or ticagrelor (180mg)\r\n - For those going on to have PCI, NICE guidance suggests adding prasugrel (if not on anti-coagulation) or clopidogrel (if on anti-coagulation)\r\n3. **Sublingual GTN spray** - for symptom relief\r\n4. **IV morphine/diamorphine** - in addition this causes vasodilation reducing preload on the heart\r\n5. Primary percutaneous coronary intervention (PPCI) for those who:\r\n - Present **within 12 hours of onset of pain** AND\r\n - Are **<2 hours** since <u>first medical contact</u>\r\n\r\nRemember that (particularly in STEMI) _time is heart_ therefore urgent treatment, escalation, and delivery of PPCI is critical to good outcomes.\r\n\r\n# Management of NSTEMI/Unstable Angina\r\n\r\n[lightgallery6]\r\n\r\nFor emergencies, always follow A-E structure. \r\n\r\n1. Targeted oxygen therapy (aiming for sats >90%)\r\n2. Loading dose of **PO aspirin 300mg** and fondaparinux\r\n * Patients should have their 6 month mortality score (often the GRACE score) calculated as early as possible - all those who are anything other than lowest risk should also be given **prasugrel or ticagrelor** unless they have a high risk of bleeding where **PO clopidogrel 300mg** is more appropriate.\r\n3. **Sublingual GTN spray** - for symptom relief\r\n4. **IV morphine/diamorphine** - in addition this causes vasodilation reducing preload on the heart\r\n5. Start antithrombin therapy such as **treatment dose low molecular weight heparin** or **fondaparinux** if they are for an immediate angiogram\r\n6. Patients with <u>high 6 month risk of mortality</u> should be offered an angiogram within 96 hours of symptom onset.\r\n\r\nNote that management of unstable angina is similar to that of NSTEMI with aspirin for all patients and fondaparinux and early angiography for those at high risk.\r\n\r\n# Post-MI management\r\n\r\n[lightgallery7]\r\n\r\n* ALL patients post-MI patients should be started on the following 5 drugs:\r\n 1. **Aspirin 75mg OM** + second anti-platelet (**clopidogrel 75mg OD** or **ticagrelor 90mg OD**)\r\n 2. **Beta blocker (normally bisoprolol)**\r\n 3. **ACE-inhibitor (normally ramipril)**\r\n 4. **High dose statin (e.g. Atorvastatin 80mg ON)**\r\n* All patients should have an **ECHO** performed to assess systolic function and any evidence of heart failure should be treated.\r\n* All patients should be referred to **cardiac rehabilitation**.\r\n* Patients who have been treated without angiography should be considered for ischaemia testing to assess for inducible ischaemia. \r\n\r\n# Complications\r\n\r\n* Ventricular arrhythmia\r\n* Recurrent ischaemia/infarction/angina\r\n* Acute mitral regurgitation\r\n* Congestive heart failure\r\n* 2nd, 3rd degree heart block\r\n* Cardiogenic shock\r\n* Cardiac tamponade\r\n* Ventricular septal defects\r\n* Left ventricular thrombus/aneurysm\r\n* Left/right ventricular free wall rupture\r\n* Dressler's Syndrome\r\n* Acute pericarditis\r\n\r\n## Ventricular Arrhythmias\r\n\r\n* Ventricular arrhythmias can occur as a consequence of MI, during cardiac catheterisation, or after reperfusion.\r\n* Most post-MI ventricular arrhythmias are short lived and self-resolve.\r\n* However if sustained VT or VF occurs they should be treated as per the Advanced Life Support protocols.\r\n\r\n## Recurrent Ischaemia/Infarction/Angina\r\n\r\n* Occasionally inserted stents can thrombose requiring reintervention.\r\n* New infarcts can occur in different vascular territories - this is less likely in the age of PCI where all territory are imaged during the procedure.\r\n* Angina and chest pain can continue for some time after an MI and is more common in NSTEMI patients.\r\n\r\n## Congestive Heart Failure\r\n\r\n* Heart failure can occur as a consequence of impairment heart muscle function secondary to ischaemia.\r\n* It should be treated as any other acute heart failure.\r\n* Ventricular function may improve over months as the heart muscle recovers.\r\n\r\n## Heart Block\r\n\r\n* Various levels of heart block are common - particularly following **inferior** infarcts (because the right coronary artery supplies the SAN).\r\n* These may be treated with:\r\n * Simple observation (as many will revert back to sinus rhythm)\r\n * Transcutaneous/venous pacing (if symptomatic)\r\n * Permanent pacing (if failing to resolve)\r\n\r\n## Left Ventricular Thrombus/Aneurysm\r\n\r\n* Aneurysm can occur following an anterior MI where the myocardium can be susceptible to wall stress leading to an aneurysm.\r\n* It may be silent, cause arrhythmias or embolic events.\r\n* It is definitely diagnosed on ECHO but ECG may show persisting ST elevation.\r\n* Thrombus can form either within an above described aneurysm or around hypokinetic regions of the myocardium.\r\n* Thrombi can embolise causing complications such as stroke, acute limb ischaemia and mesenteric ischaemia.\r\n\r\n## Left/Right Ventricular Free Wall Rupture\r\n\r\n* Necrosis of the free walls of either ventricle can lead to rupture allowing blood into the pericardial space.\r\n* This leads to a rapid tamponade and normally leads to cardiac arrest/death within seconds.\r\n* Treatment includes pericardiocentesis and surgery but prognosis is extremely poor.\r\n\r\n## Acute Mitral Regurgitation\r\n\r\n* This can occur because of papillary muscle rupture and carries a poor prognosis. Occurs commonly due to infero-osterior MI. \r\n* This presents with:\r\n * Pansystolic murmur heard best at the apex\r\n * Severe and sudden heart failure\r\n* It is diagnosed on echocardiogram and may require surgical correction.\r\n\r\n## Ventricular Septal Defect\r\n\r\n* Interventricular septal rupture is a short-term complications of myocardial infarction.\r\n* Rupture caused by an anterior infarct is generally apical and simple.\r\n* Rupture caused by an inferior infarct is generally basal and more complex.\r\n* Without reperfusion, septal rupture typically occurs within the first week after the infarction.\r\n* Features of septal rupture include:\r\n * Shortness of breath\r\n * Chest pain\r\n * Heart failure\r\n * Hypotension\r\n * Harsh, loud pan-systolic murmur along the left sternal border.\r\n * Palpable parasternal thrill.\r\n* Diagnosis is with echocardiogram.\r\n* Patients are managed with emergency cardiac surgery.\r\n\r\n## Dressler's syndrome\r\n\r\n* Dressler's syndrome or post-infarction pericarditis typically presents with persistent fever and pleuritic chest pain **2-3 weeks** or up to a few months after an MI.\r\n* Note that patients can get pericarditis immediately following MI which is NOT considered Dressler's syndrome.\r\n* Symptoms usually resolve after several days.\r\n* Occasionally it can also present with features of pericardial effusion and has become relatively uncommon since the introduction of PCI.\r\n* Management: **high dose aspirin**\r\n\r\n# Prognosis \r\n\r\nDue to the development of PPCI and post-MI care (cardiac rehabilitation) the mortality rates following myocardial infarction continue to decline. Those patients who go on to develop heart failure after myocardial infarction have a significantly worse prognosis than those who do not. \r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines for Unstable Angina and NSTEMI](https://www.nice.org.uk/guidance/cg94)\r\n\n[NICE Guidelines for STEMI](https://www.nice.org.uk/guidance/cg167)\r\n\r\n# References\r\n\r\n[Patient UK Information on Acute Coronary Syndrome](<https://patient.info/doctor/acute-coronary-syndrome-pro>)",
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"explanation": "# Summary\r\n\r\nHeart failure (HF) is a clinical syndrome characterised by the heart's inability to pump enough blood to meet the body's needs. It is a common condition primarily affecting the elderly population. HF can be classified based on various factors, such as the type of dysfunction (systolic or diastolic), the onset (acute or chronic), and the severity of symptoms (NYHA classification). The clinical features of HF differ depending on whether it primarily affects the left or right ventricle, but broadly include fatigue, shortness of breath, and peripheral oedema. Diagnosis involves evaluating symptoms, NT-pro-BNP levels, and echocardiography. Management includes lifestyle modifications, medical therapy, and, in some severe cases, cardiac resynchronisation therapy. The prognosis for HF varies, but approximately 50% of those diagnosed are alive at 5 years.\r\n\r\n# Definition \r\n\r\nHeart failure (HF), also known as congestive heart failure (CHF) and congestive cardiac failure (CCF), is defined as the failure of the heart to generate sufficient cardiac output to meet the metabolic demands of the body.\r\n\r\n# Epidemiology \r\n\r\n* HF is common: the prevalence in the UK is estimated at 1-2%.\r\n\r\n* HF primarily affects the elderly population: the average age of diagnosis is 75 years old. The incidence of HF has been increasing with the ageing population.\r\n\r\n* In Europe and North America the most common causes are coronary artery disease, hypertension, and valvular disease.\r\n\r\n* Although Chagas disease is a rare cause in Europe and North America, it is a significant cause of heart failure in Central/South America.\r\n\r\n# Pathophysiology\r\n\r\nThe pathophysiology for HF is diverse and depends on the aetiology of the HF. \r\n\r\n# Classification \r\n\r\nHF can be classified in different ways. It can be classified as being low output vs. high output HF, predominantly systolic or diastolic dysfunction, whether the process has been acute or chronic, or by the severity of symptoms (and consideration for predominantly left or right ventricle features). \r\n\r\n## Low-output HF vs. High-output HF \r\n\r\nLow-output HF is much more common than high-output HF. Low-output HF occurs when cardiac output is reduced due to a primary problem with the heart and the heart is unable to meet the body's needs. Conversely, high-output HF refers to a heart that has a normal cardiac output, but there is an increase in peripheral metabolic demands that the heart is unable to meet. \r\n\r\nThe common causes of low-output HF will be further discussed below. Common causes of high-output HF include: \r\n\r\n* Anaemia\r\n* Arteriovenous malformation\r\n* Paget's disease\r\n* Pregnancy\r\n* Thyrotoxicosis\r\n* Thiamine deficiency (wet Beri-Beri)\r\n\r\nThese can be remembered with the AAPPTT mnemonic. \r\n\r\n## Systolic vs. Diastolic HF\r\n\r\nSystolic dysfunction refers to an impairment of ventricular contraction. The ventricles are able to fill well, but the heart is unable to pump the blood sufficiently out of the ventricle due to impaired myocardial contraction during systole (reduced ejection fraction). Common causes include: ischaemic heart disease, dilated cardiomyopathy, myocarditis or infiltration (haemochromatosis or sarcoidosis). \r\n\r\nIn comparison, diastolic dysfunction refers to the inability of the ventricles to relax and fill normally, hence the heart is still able to pump well but pumps out less blood per contraction due to reduced diastolic filling (preserved ejection fraction). Common causes include: uncontrolled chronic hypertension (significant left ventricular hypertrophy reduces filling of the left ventricle), hypertrophic cardiomyopathy, cardiac tamponade, and constrictive pericarditis. \r\n\r\n## Acute vs. Chronic HF \r\n\r\nHF can also be classified according to the time of onset. Acute HF occurs with new-onset HF symptoms (acute mitral regurgitation following an MI) or an acute deterioration in a patient with known, chronic HF. In comparison, chronic HF progresses more slowly and may take many years to develop. \r\n\r\n## Severity of Symptoms\r\n\r\n**New York Heart Association (NYHA) Classification of HF**\r\n\r\nThe NYHA Classification system is used to classify HF through the severity of symptoms. It runs from Class I (no limitation) to Class IV (discomfort at rest). \r\n\r\n* Class I - no limitation in physical activity, and activity does not cause undue fatigue, palpitations or dyspnoea.\r\n* Class II - slight limitation of physical activity, and comfort at rest. Ordinary physical activity causes fatigue, palpitations and/or dyspnoea.\r\n* Class III - marked limitation in physical activity, but comfort at rest. Minimal physical activity causes fatigue (less than ordinary).\r\n* Class IV - inability to carry on any physical activity without discomfort, with symptoms occurring at rest. If any activity takes place, discomfort increases.\r\n\r\n# Symptoms and Signs\r\n\r\nThe clinical features of HF can be considered according to the ventricle most impacted. However, a common presenting complaint for all types of heart failure is **fatigue**. \r\n\r\n\r\n## Clinical features of left heart failure (LHF)\r\n\r\nLHF, or left ventricular failure (LVF), causes pulmonary congestion (pressure builds up in the LHS of the heart and there is backpressure to the lungs) and systemic hypoperfusion.\r\n\r\n### Symptoms \r\n\r\n* Shortness of breath on exertion\r\n* Orthopnoea\r\n* Paroxysmal nocturnal dyspnoea\r\n* Nocturnal cough (± pink frothy sputum)\r\n* **Fatigue**\r\n\r\n### Signs \r\n\r\n* Tachypnoea\r\n* Bibasal fine crackles on auscultation of the lungs\r\n* Cyanosis\r\n* Prolonged capillary refill time \r\n* Hypotension\r\n* Less common signs: pulsus alternans (alternating strong and weak pulse), S3 gallop rhythm (produced by large amounts of blood striking compliant left ventricle), features of functional mitral regurgitation. \r\n\r\n## Clinical features of right heart failure \r\n\r\nRight heart failure causes venous congestion (pressure builds up behind the right heart) and pulmonary hypoperfusion (reduced right heart output).\r\n\r\n### Symptoms \r\n\r\n* Ankle swelling \r\n* Weight gain \r\n* Abdominal swelling and discomfort \r\n* Anorexia and nausea \r\n\r\n### Signs\r\n\r\n* Raised JVP\r\n* Pitting peripheral oedema (ankle to thighs to sacrum)\r\n* Tender smooth hepatomegaly\r\n* Ascites\r\n* Transudative pleural effusions (typically bilaterally)\r\n\r\n*NB. Sometimes left-sided heart failure can lead to pulmonary congestion which in turn also pushes the right ventricle into failure. In these cases, signs and symptoms of both left and right-sided heart failure may be present. This is congestive cardiac failure.* \r\n\r\n# Differential Diagnoses\r\n\r\n* **Chronic Obstructive Pulmonary Disease (COPD)** \r\n\t* **Similarities**: both may present with dyspnoea (and significant respiratory distress) and fatigue. \r\n\t* **Differences**: in heart failure, the shortness of breath is typically worse on lying flat (orthopnoea) and may be accompanied by paroxysmal nocturnal dyspnoea and peripheral oedema. Shortness of breath in COPD tends to be worse with exertion and is likely accompanied by other symptoms including chronic productive cough, wheeze and a significant smoking history. \r\n\r\n* **Acute Respiratory Distress Syndrome** \r\n\t* **Similarities**: both may present with shortness of breath, tachypnoea and respiratory distress. Both lead to the accumulation of fluid in the lungs and impaired gaseous exchange leading to hypoxaemia. \r\n\t* **Differences**: the underlying pathology between the two is different. Heart failure is a result of raised pressures in pulmonary capillaries, whereas ARDS is usually due to increased pressures in pulmonary capillaries secondary to a large insult (e.g. pneumonia, aspiration, or trauma). They can be distinguished by taking pulmonary capillary wedge pressures. \r\n\r\n* **Renal Failure** \r\n\t* **Similarities**: fluid retention and peripheral overload. \r\n\t* **Differences**: other signs and symptoms will allow distinction between HF and renal failure. In the latter, you may find uraemic symptoms(nausea, anorexia, uraemic flap) and potentially signs of renal replacement therapy. \r\n\r\n* **Liver Failure** \r\n\t* **Similarities**: fluid retention and peripheral overload especially ascites. \r\n\t* **Differences**: liver failure patients will present with other signs and symptoms including jaundice, hepatic encephalopathy and chronic liver disease signs (gynaecomastia, spider naevi, and excoriations). \r\n\r\n\r\n# Investigations\r\n\r\nIf a stable patient is presenting to the GP with suspected chronic heart failure, investigations should be carried out as per NICE guidelines. \r\n\r\n**1st line = NT-pro-BNP level**\r\n\r\nNT-pro-BNP is released by the ventricles in response to myocardial stretch. It has a high negative predictive value.\r\n\r\nInterpret NT-pro-BNP results as follows: \r\n\r\n* >2000ng/L (236pmol/L): refer urgently for specialist assessment and TTE <2 weeks. \r\n* 400-2000ng/L (47-236pmol/L): refer for specialist assessment and TTE <6 weeks. \r\n* If <400ng/L: diagnosis of heart failure is less likely. \r\n\r\n**Arrange a 12-lead ECG in all patients** \r\n\r\nECG may be normal or hint at underlying aetiology (ischaemic changes or arrhythmias). \r\n\r\n**Transthoracic echocardiogram (TTE)**\r\n\r\nAn echocardiogram will confirm the presence and degree of ventricular dysfunction.\r\n\r\n* Ventricular dysfunction is normally measured by the ejection fraction (EF). \r\n * EF <40% = HF with reduced ejection fraction (HFrEF, systolic dysfunction). \r\n * EF >40% but with raised BNP = HF with preserved ejection fraction (HFpEF, diastolic dysfunction).\r\n * EF 50-70% with normal BNP = normal. \r\n\r\n**Other Investigations:** \r\n\r\n* **Bloods**: U&E (renal function for medication and hyponatraemia), LFTS (deranged LFTs suggest hepatic congestion), TFTs (hyperthyroidism and high-output HF), glucose and lipid profile (modifiable CV risk factors)\r\n\r\n* **CXR**: CXR findings in heart HF can be remembered by the ABCDEF mnemonic:\r\n * A: **Alveolar** oedema (with 'batwing' perihilar shadowing)\r\n * B: **Kerley B** lines (caused by interstitial oedema)\r\n * C: **Cardiomegaly** (cardiothoracic ratio >0.5)\r\n * D: upper lobe blood **diversion**\r\n * E: **Pleural effusions** (typically bilateral transudates)\r\n * F: **Fluid in the horizontal fissure**\r\n\r\n[lightgallery]\r\n\r\n[lightgallery1] \r\n\r\n# Management\r\n\r\n## Conservative management\r\n\r\n* Weight loss if BMI >30. \r\n* Smoking cessation \r\n* Salt and fluid restriction - improves mortality\r\n* Supervised exercise-based group rehabilitation programme for people with heart failure. \r\n\r\nOffer annual influenza and one-off pneumococcal vaccinations for patients diagnosed with heart failure. \r\n\r\n## Medical management\r\n\r\n**Symptom management**: \r\n\r\n* For fluid overload, prescribe loop diuretics (e.g. furosemide or bumetanide). These do not affect overall mortality from heart failure. \r\n\r\n\r\n**Management which improves mortality**:\r\n \r\n1st line = ACE-I and beta-blocker \r\n\r\n* Consider ARB if intolerant to ACE-I. \r\n* Consider hydralazine if intolerant to ACE-I/ARB. \r\n\r\nIf symptoms persist and NYHA Class 3 or 4 consider adding:\r\n\r\n* Aldosterone antagonists = spironolactone or eplerenone. \r\n* Hydralazine and a nitrate for Afro-Caribbean patients. \r\n* Ivabradine if in sinus rhythm and impaired EF. \r\n* Digoxin = useful in those with AF. This <u>worsens</u> mortality but improves morbidity.\r\n\r\nNICE also advices seeking specialist guidance for prescribing **SGLT2 inhibitors** (dapagliflozin or empagliflozin). These should be given in symptomatic chronic heart failure with preserved or reduced ejection fraction, or as an add-on for patients already optimised with ACE-i/ARB/sacubitril-valsartan (i.e. combination), beta-blockers and aldosterone antagonists.\r\n\r\n**BASH Mnemonic**\r\n\r\n* BASH medications demonstrate a mortality benefit in patients with HFrEF = Beta-blockers, ACE-inhibitors/ARB, Spironolactone and Hydralazine. \r\n* There are no medications that improve mortality in diastolic heart failure. \r\n\r\n[lightgallery2]\r\n\r\n# Surgical/Interventional management \r\n\r\n* Cardiac resynchronisation therapy\r\n* Implantable cardiac defibrillators (ICDs) are indicated if the following criteria are fulfilled: \r\n * QRS interval <120ms, high risk sudden cardiac death, NYHA class I-III\r\n * QRS interval 120-149ms without LBBB, NYHA class I-III\r\n * QRS interval 120-149ms with LBBB, NYHA class I\r\n\r\n## Adverse effects of heart failure medications\r\n\r\nThe common side-effects for different heart failure medications are listed below\r\n\r\n* **Beta blockers**: Bradycardia, hypotension, fatigue, dizziness\r\n* **ACE inhibitors**: Hyperkalaemia, renal impairment, dry cough, lightheadedness, fatigue, GI disturbances, angioedema\r\n* **Spironolactone**: Hyperkalaemia, renal impairment, gynaecomastia, breast tenderness/hair growth in women, changes in libido\r\n* **Furosemide**: Hypotension, hyponatraemia/kalaemia,\r\n* **Hydralazine/nitrates**: Headache, palpitations, flushing\r\n* **Digoxin**: Dizziness, blurred vision, GI disturbances\n* **SGLT-2 inhibitors:** Thrush, UTIs, DKA in patients with pre-existing diabetes\r\n\r\n# Prognosis \r\n\r\nIt is estimated that >50% of people diagnosed with HF will survive after 5 years. Approximately 35% will be alive in 10 years. \r\n\r\n# NICE Guidelines\r\n\r\n[NICE Guidelines on Acute Heart Failure](https://www.nice.org.uk/guidance/cg187/chapter/1-Recommendations)\n\n[NICE Guidelines on Chronic Heart Failure](https://cks.nice.org.uk/topics/heart-failure-chronic)\r\n\r\n# References \r\n\r\n[2022 Stat Pearls Summary of Congestive Heart Failure](https://www.ncbi.nlm.nih.gov/books/NBK430873)",
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"question": "A 91 year old woman presents to the general practice (GP) with shortness of breath and peripheral oedema to the mid-thighs which has been worsening for the past month. The shortness of breath is worse on exertion and when lying flat - as a result she reports often waking up very breathless in the night and having to sleep propped up on 4 pillows, where previously she only used 2. She is a heavy smoker with a 70 pack year history and has a past medical history of myocardial infarction 10 years previously.\n\nWhat is the most likely cause of this acute breathlessness?",
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"explanation": "# Summary \r\n\r\nBroad complex tachycardia refers to dysrhythmias with a heart rate greater than 100 beats per minute and a QRS complex broader than 120 milliseconds. This term encompasses life-threatening rhythms such as ventricular tachycardia (VT) and ventricular fibrillation (VF). VT is a regular, broad complex tachycardia and may be with or without a pulse. In contrast, VF is irregular and is always pulseless. Pulseless VT and VF must be managed according to the ALS algorithm and require immediate defibrillation and administration of medications like adrenaline and amiodarone, whilst managing pulsed VT involves synchronised shocks and amiodarone. SVT with aberrancy, a condition where supraventricular tachycardia occurs in the presence of bundle-branch block, can mimic VT and should be treated cautiously.\r\n\r\n# Definition \r\n\r\nBroad complex tachycardias are dysrhythmias that have a heart rate greater than 100bpm and a QRS complex that is greater than 120ms. The most common broad complex tachycardias are ventricular tachycardia or ventricular fibrillation. \r\n\r\n# Ventricular Tachycardia (VT)\r\n\r\nA regular broad complex tachycardia. It can occur with a pulse or it may be pulseless. \r\n\r\nECG features include: \r\n\r\n* Tachycardia (>100 beats per minute)\r\n* Absent p waves\r\n* Monomorphic regular broad QRS complexes (>120ms)\r\n\r\n[lightgallery]\r\n\r\n# Management of VT \r\n\r\n## Pulseless VT \r\n\r\nIf there is no pulse the patient should be managed according to the Advanced Life Support algorithm. \r\n\r\n* Pulseless VT is a shockable rhythm so a 200J bi-phasic **unsynchronised** shock should be administered. \r\n* IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock.\r\n* Adrenaline should be administered every 3-5 minutes thereafter. \r\n\r\n## Pulsed VT with Adverse Features\r\n\r\nIf the patient has a pulse but is demonstrating adverse features (shock, syncope, myocardial ischaemia, or heart failure) the patient should be managed according to Resuscitation Council Tachyarrhythmia algorithm. \r\n\r\n* Administer synchronised DC shocks (up to 3 attempts). If the patient is conscious this will require sedation or anaesthesia. \r\n* Expert help should guide amiodarone administration (300mg IV over 10-20 minutes followed by 900mg infusion over 24 hours). \r\n\r\n## Pulsed VT with No Adverse Features \r\n\r\nIf the patient has a pulse and is not demonstrating adverse features then the Resuscitation Council Tachyarrhythmia algorithm should be followed. \r\n\r\n* Amiodarone 300mg IV over 10-60 minutes. \r\n* If this is ineffective then administer synchronised DC shocks (up to 3 attempts). If the patient is conscious this will require sedation or anaesthesia. \r\n* *N.B. if there has been a previous certain diagnosis of SVT with aberrancy treat as for regular narrow complex tachycardias*\r\n\r\n# Ventricular fibrillation (VF) \r\n\r\nAn irregular broad complex tachycardia. This is always a pulseless rhythm.\r\n\r\nECG features include: \r\n\r\n* Tachycardia >100bpm \r\n* QRS complexes are polymorphic and irregular (>120ms)\r\n\r\n[lightgallery1]\r\n\r\n# Management of VF\r\n\r\nThe patient should be managed according to the Advanced Life Support algorithm. \r\n\r\n* VF is a shockable rhythm so a 200J bi-phasice **unsynchronised** shock should be administered. \r\n* IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock.\r\n* Adrenaline should be administered every 3-5 minutes thereafter.\r\n\r\n# Other Broad Complex Tachycardias \r\n\r\nInclude: \r\n\r\n* Torsades des pointes: see section. \r\n* SVT with aberrancy: occurs when a patient with a bundle-branch block goes into SVT. It can be difficult to distinguish between VT and an SVT with aberrancy. The safest approach is to treat as VT. \r\n\r\n[lightgallery2]\r\n\r\n# NICE Guidelines\r\n\n[NICE CKS Guidelines for Cardiac Arrest and ALS](<https://cks.nice.org.uk/topics/cardiac-arrest-out-of-hospital-care/management/advanced-life-support-adult/>)\r\n\r\n# References\r\n[Resuscitation Council UK Adult Tachycardia Algorithm](<https://www.resus.org.uk/sites/default/files/2021-04/Tachycardia%20Algorithm%202021.pdf>)\r\n\r\n[Resuscitation Council UK Adult ALS Algorithm](<https://www.resus.org.uk/sites/default/files/2021-04/Adult%20Advanced%20Life%20Support%20Algorithm%202021.pdf>)",
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"question": "A 30 year old man has a cardiac arrest whilst playing rugby and is brought into the emergency department (ED) by ambulance. Cardiopulmonary resuscitation (CPR) is ongoing and it is time for a rhythm check.\n\nWhich rhythm can be identified on this ECG trace?\n\n[lightgallery]",
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"explanation": "This ECG is describing complete or third degree heart block which can cause severe and symptomatic bradycardia. In patients with heart block that are severely symptomatic, or with the more dangerous forms of heart block that threaten to progress to ventricular standstill (second degree type 2 and complete/third degree) treatment with a PPM is needed. This device provides the \"pace\" for the ventricles, which the atria are not providing",
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"explanation": "# Summary\r\n\r\nHeart block refers to an obstruction in the electrical conduction system of the heart. This obstruction can occur at various points in the conduction system, including the sinoatrial node, atrioventricular node, Bundle of His, or bundle branches. Atrioventricular heart block specifically affects the conduction between the atria and ventricles. The severity of heart block can range from first degree, which is generally benign, to second degree (Mobitz Type I and II), to complete (third degree) heart block, which requires immediate management with a permanent pacemaker due to the risk of asystole. The underlying causes and management strategies differ for each type of heart block.\r\n\r\n# Definition \r\n\r\nHeart block occurs due to an obstruction in the electrical conduction system of the heart. It can occur anywhere along the conduction system of the heart from the sinoatrial node to the atrioventricular node to the Bundle of His or within the bundle branches themselves. \r\n\r\nSinoatrial node block rarely leads to symptoms as the atrioventricular node acts as a secondary pacemaker. Bundle branch blocks are a form of heart block but they are discussed in a separate section. The rest of this section will discuss atrioventricular block in more detail. \r\n\r\nPatients with atrioventricular heart block may be asymptomatic or may present with fatigue, lightheadeness, syncope, shortness of breath and most seriously in cardiac arrest or with sudden death. \r\n\r\n# First Degree Heart Block\r\n\r\n## Definition\r\n\r\nThis is caused by prolonged conduction of electrical activity through the AV node. It can be identified on ECG by finding a PR interval >200ms.\r\n\r\n[lightgallery]\r\n\r\n## Causes\r\n\r\n* High vagal tone: e.g. athletes\r\n* Acute inferior MI\r\n* Electrolyte abnormalities: e.g. hyperkalaemia\r\n* Drugs: e.g. NHP-CCBs, beta-blockers, digoxin, cholinesterase inhibitors\r\n\r\n## Management\r\n\r\nFirst degree heart block itself is benign and does not need treating. However, any pathological underlying cause should be reversed.\r\n\r\n# Second Degree Heart Block \r\n\r\nSecond degree heart block is split into Mobitz Type I and Mobitz Type II heart block. \r\n\r\n# Mobitz Type I\r\n\r\n## Definition\r\n\r\nWenckebach phenomenon or Mobitz type I is a type of second degree heart block that is usually due to reversible conduction block at the AV node. It is characterised by progressive lengthening of the PR interval which results in a P wave that fails to conduct a QRS.\r\n\r\n[lightgallery1]\r\n\r\n## Causes\r\n\r\n* MI (mainly inferior)\r\n* Drugs such as beta/calcium channel blockers, digoxin\r\n* Professional athletes due to high vagal tone\r\n* Myocarditis\r\n* Cardiac surgery\r\n\r\n## Management\r\n\r\nIt is generally asymptomatic and does not require any specific management as the risk of high AV block/complete heart block is low. If symptoms do arise, ECG monitoring may be required, precipitating drugs must be stopped and if they are bradycardic with adverse features they should be treated with atropine.\r\n\r\n# Mobitz Type II\r\n\r\n## Definition\r\n\r\nMobitz type II block is a type of second degree AV block where there are intermittent non-conducted P waves. The _PR interval is constant_ (may be normal or prolonged) and there may no pattern or fixed ratios such as 2:1 or 3:1 block. It is usually caused by conduction system failure, especially at the His-Purkinje system.\r\n\r\nIn most cases there is a broad QRS indicating a distal block in the His-Purkinje system and many patients have pre-existing left bundle branch block/bifascicular block.\r\n\r\n[lightgallery2]\r\n\r\n## Causes\r\n\r\n* Infarction: particularly anterior MI which damages the bundle branches\r\n* Surgery: mitral valve repair or septal ablation\r\n* Inflammatory/autoimmune: rheumatic heart disease, SLE, systemic sclerosis, myocarditis\r\n* Fibrosis: Lenegre's disease\r\n* Infiltration: sarcoidosis, haemochromatosis, amyloidosis\r\n* Medication: beta-blockers, calcium channel blockers, Digoxin, amiodarone\r\n\r\n## Management\r\n\r\nDefinitive management is with a permanent pacemaker as these <u>_patients are at risk of complete heart block_</u> and at risk of becoming haemodynamically unstable.\r\n\r\n# Complete (Third degree) Heart Block\r\n\r\n## Definition\r\n\r\nComplete heart block occurs when atrial impulses fail to be conducted to the ventricles. Sufficient cardiac output may be secondary to a ventricular or junctional escape rhythm.\r\n\r\nECG shows severe bradycardia and complete dissociation between the P waves and the QRS complexes. These patients are at high risk of asystole, ventricular tachycardia and cardiac arrest. \r\n\r\n[lightgallery3]\r\n\r\n## Causes\r\n\r\n* Myocardial infarction: especially inferior\r\n* Drugs acting at the AVN: beta blockers, dihydropyridine calcium channel blockers, or adenosine\r\n* Idiopathic fibrosis\r\n\r\n## Management\r\n\r\nManagement of complete (third degree) heart block is via the acute bradycardia guideline (see below). Permanent pacemaker insertion is eventually required due to the risk of sudden death.\n\nAcute management:\n\nFor emergencies, always follow an A-E structure. Identify reversible causes (dyselectrolytaemias, drugs, cardiac causes etc.) \r\n\r\n*If there are adverse signs (e.g. shock, syncope, heart failure, myocardial ischaemia):* \r\n\r\n* **1st line** = **500 micrograms atropine IV**\r\n * Atropine blocks the vagal nerve which increases firing rate of the SAN. \r\n* **2nd line** = if the first dose of atropine is not working can consider giving additional doses of atropine 500mcg up to 3mg until response. Alternatively, **transcutaenous pacing** or **isoprenaline** or **adrenaline** or **alternative drugs** including aminophylline, adrenaline, glucagon (in beta-blocker or calcium channel blocker overdose). \r\n\r\n*If there are no adverse signs but a risk of asystole, or a satisfactory response to 500mcg atropine:*\r\n\r\n* Risk of asystole: recent asystole, mobitz type II block, complete heart block + broad QRS, ventricular pauses >3s. \r\n* **1st line** = administer **500 micrograms atropine IV**. Alternatively, **transcutaenous pacing** or **isoprenaline** or **adrenaline** or **alternative drugs** including aminophylline, adrenaline, glucagon (in beta-blocker or calcium channel blocker overdose). \r\n\r\n*If there are no adverse signs and there is no risk of asystole*\r\n\r\n* Observe\r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines on Pacing](<https://www.nice.org.uk/guidance/ta88/chapter/2-clinical-need-and-practice>) \r\n\r\n# References\r\n\r\n[Life in the Fast Lane Heart Block ECG Summary](https://litfl.com/heart-block-and-conduction-abnormalities/)\r\n\r\n[Resuscitation Council Adult Bradycardia Algorithm](<https://www.resus.org.uk/sites/default/files/2020-05/G2015_Adult_bradycardia.pdf>)",
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"explanation": "# Summary\r\n\r\nStable angina, characterised by chest pain triggered by myocardial ischemia, is most commonly caused by coronary artery disease. Typical anginal chest pain is described as an exertional chest discomfort that may radiate to the jaw/neck/arm and that is alleviated by rest (<5 minutes) or with GTN spray. Diagnosis involves investigations such as ECG, blood tests, and CT coronary angiogram. Management includes conservative measures to optimise cardiovascular risk factors, medical treatment with anti-anginal medications, and revascularisation options like coronary artery bypass graft or percutaneous coronary intervention in cases not controlled by medical therapy.\r\n\r\n# Definition \r\n\r\nTypical anginal chest pain is defined by the following 3 features:\r\n\r\n1. Constriction/heavy discomfort to chest that may radiate to the jaw/neck/arm.\r\n2. Brought on by exertion.\r\n3. Alleviated by rest (<5 minutes) or GTN spray. \r\n\r\n3/3 features = typical angina pain \r\n\r\n2/3 features = atypical angina pain\r\n\r\n0-1/3 features = non-anginal pain \r\n\r\n# Epidemiology \r\n\r\nA 2020 Health Survey for England estimated prevalence in all UK adults as 3%, increasing to a prevalence of 10–12% in women aged 65–84 years and 12–14% in similarly aged men. \r\n\r\n# Pathophysiology\r\n\r\nStable angina occurs as a result of a mismatch of myocardial oxygen supply and demand. Most commonly, stable angina is due to coronary artery disease. Coronary artery disease refers to the narrowing of coronary arteries by atherosclerosis and plaque formation. When demand for myocardial oxygen increases with exertion, narrowed coronary arteries cannot meet this increased demand leading to myocardial ischaemia and pain. \r\n\r\nOther rarer causes of stable angina include anaemia, aortic stenosis, or hypertrophic cardiomyopathy.\r\n \r\n# Classification \r\n \r\nStable angina pain can be considered by its limitations on day-to-day activity:\r\n\r\n* Class I: no angina with normal physical activity. Strenuous activity may cause symptoms. \r\n* Class II: angina pain causes slight limitation on normal physical activity. \r\n* Class III: angina causes marked limitation on normal physical activity. \r\n* Class IV: angina occurs with any physical activity and may occur at rest (see unstable angina). \r\n\r\n# Symptoms and Signs\r\n\r\n* Central, constricting chest pain that radiates to neck/jaw/arm. \r\n* Exertional chest pain that is relieved on rest/GTN. \r\n* Associated symptoms: nausea, vomiting, clamminess or sweating. \r\n\r\nStable angina may have no clinical signs on examination at rest.\r\n\r\n# Differential Diagnoses \r\n\r\n* **Acute Coronary Syndrome (ACS)** \r\n\t* **Similarities**: cardiac-sounding chest pain as a presenting complaint for both. Similar patient profile with significant risk factors for coronary artery disease. \r\n\t* **Differences**: stable angina only occurs on exertion and is alleviated by rest. ACS chest pain occurs at rest. \r\n\r\n* **Gastro-oesophageal reflux disease (GORD)** \r\n\t* **Similarities**: both may present with central chest discomfort/pain. \r\n\t* **Differences**: discomfort in stable angina commonly described as a squeezing or pressure-like pain brought on by exertion. GORD-related chest discomfort often described as a burning sensation that is triggered by certain foods, alcohol, or lying down. \r\n\r\n* **Costochondritis** \r\n\t* **Similarities**: both present with chest pain. \r\n\t* **Differences**: costochondritis refers to inflammation of the cartilage connecting ribs to the sternum. The pain is described as sharp and can be reproduced by pressing on the chest wall. \r\n\r\n* **Pleuritic Chest Pain e.g. Pulmonary Embolism, Pneumonia** \r\n\t* **Similarities**: both present with chest pain or discomfort. \r\n\t* **Differences**: pleuritic chest pain is often described as sharp and worse on inspiration. Pleuritic chest pain will also be accompanied by clinical features relating to the underlying cause e.g. productive cough, fevers, risk factors for VTE, or a hot swollen calf. \r\n\r\nOther differential diagnoses include anxiety, aortic dissection (radiates to the back), and other causes of musculoskeletal chest pain. \r\n\r\n# Investigations\r\n\r\nOnce atypical/typical anginal pain is suspected: \r\n\r\n**Routine investigations in primary care**: \r\n\r\n* ECG - to assess for ischaemic changes or previous MI. \r\n* Bloods - FBC and TFTs (to exclude anaemia and hyperthyroidism respectively which can exacerbate angina symptoms).\r\n* Consider cardivascular risk factors: hypertension, hypercholesterolaemia, diabetes mellitus, smoking. \r\n\r\n**1st line investigations**\r\n\r\n* CT coronary angiogram (CT CA)- indicated if typical/atypical angina pain or if ECG shows ischaemic changes in chest pain with <2 angina features.\r\n\r\n**2nd line investigations** \r\n\r\nIf CTCA is inconclusive the patient may undergo functional imaging: \r\n\r\n* Stress echocardiogram \r\n* Myocardial perfusion SPECT \r\n* Cardiac MRI\r\n\r\n**3rd line investigations**\r\n\r\nInvasive coronary angiography can be performed if there are inconclusive results from non-invasive testing.\r\n\r\n# Management\r\n\r\n## Conservative management\r\n\r\nConservative management involves the optimisation of cardiovascular risk factors to reduce the atherosclerotic process. \r\n\r\n* Smoking cessation\r\n* Glycaemic control\r\n* Hypertension\r\n* Hyperlipidaemia\r\n* Weight loss\r\n* Alcohol intake \r\n\r\n## Medical management \r\n\r\n* Secondary prevention: aspirin 75mg OD and statin 80mg ON. \r\n* GTN spray for symptom relief: inform patient of side-effects (headache, flushing, dizziness) and to repeat dose if pain not stopped after 5 minutes. \r\n\r\n*Emergency help should be sought if pain not subsided after 2 doses of GTN as this may indicate acute coronary syndrome.* \r\n\r\n**Anti-anginal medications**\r\n\r\n**1st line** = beta-blocker (bisoprolol) OR calcium channel blocker (verapamil or diltiazem). *Do not combine due to risk of heart block*. \n\nIf taking a beta-blocker and symptoms are uncontrolled, switch to, or add, a long-acting dihydropyridine calcium-channel blocker (CCB), such as amlodipine, modified-release nifedipine. If taking a non-dyhydropyridine calcium channel blocker already, switch to a beta blocker.\r\n\r\nIf neither can be tolerated, consider a long-acting nitrate (ISMN), ivabradine, nicorandil or ranolazine. \r\n\r\n**2nd line** = beta-blocker (bisoprolol) AND long-acting dihydropyridine calcium channel blocker (amlodipine or nifedipine)\r\n\r\n**3rd line** = beta-blocker (bisoprolol) AND long-acting dihydropyridine calcium channel blocker AND long-acting nitrate.\r\n\r\nA 3rd medication should only be added if the patient is symptomatic despite 2 anti-anginal drugs. At this stage, revascularisation with PCI or CABG must be considered. \r\n\r\n## Revascularisation\r\n\r\nRevascularisation with coronary artery bypass graft (CABG) or percutaneous coronary intervention (PCI) must be considered in patients with: \r\n\r\n* Symptoms which are not controlled by optimal medical management.\r\n* Complex 3 vessel disease and/or significant left main stem on CTCA. \r\n\r\n# NICE Guidelines\n\r\n[NICE Guidance on Cardiac-Sounding Chest Pain](<https://www.nice.org.uk/guidance/cg95/chapter/Recommendations>) \r\n\n[NICE Guidance on Stable Angina](<https://www.nice.org.uk/guidance/cg126/chapter/Guidance>) \r\n\r\n# References\r\n\r\n[Patient UK Information on Stable Angina](<https://patient.info/doctor/stable-angina-2>) ",
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"explanation": "# Summary\r\n\r\nAortic stenosis (AS) is characterised by the narrowing of the aortic valve, which restricts blood flow from the left ventricle to the aorta and the rest of the body. It is a common valvular pathology, with severe aortic stenosis having an estimated prevalence of 3% in those over 75 years old. The condition can be caused by senile calcification, congenital bicuspid valve, rheumatic heart disease, or supravalvular stenosis. Mild-to-moderate aortic stenosis may be asymptomatic, but severe cases present with symptoms such as syncope, angina, and dyspnoea. Diagnosis is confirmed through echocardiography. Management of asymptomatic AS is usually conservative and patients require regular echocardiograms. Symptomatic AS requires medical treatment to optimise symptoms and consideration for surgical or interventional interventions. Severe, symptomatic aortic stenosis carries a high risk of mortality without intervention, and prompt treatment is crucial. \r\n\r\n# Definition \r\n\r\nAortic stenosis (AS) refers to the narrowing and tightening of the aortic valve leading to reduced blood flow from the left ventricle into the aorta and ultimately to the rest of the body. \r\n\r\n# Epidemiology \r\n\r\nFor individuals over 75 years old, the prevalence of severe aortic stenosis is estimated at 3%. It is a common valvular pathology. \r\n\r\n# Pathophysiology\r\n\r\nNormally, the aortic valve opens to allow blood to be pumped from the left ventricle into the aorta and to the rest of the body during systole. In aortic stenosis, there is a narrowing of the aortic valve which means that the left ventricle has to generate more pressure to enable sufficient blood to cross the aortic valve and pass into the aorta. Initially, this leads to left ventricular hypertrophy as the left side of the heart compensates for the narrowing. Over time, the left ventricle can no longer compensate and the left ventricle will start to enlarge, the ejection fraction will reduce, and this will ultimately leads to reduced cardiac output.\r\n\r\n# Cause \r\n\r\nCauses of AS include: \r\n\r\n* Senile calcification: most common cause in those >65y/o. \r\n* Congenital bicuspid valve: most common cause in those <65y/o.\r\n* Rheumatic heart disease \r\n* William's syndrome: supravalvular stenosis \r\n\r\n# Symptoms\r\n\r\nLike with all valvular pathologies, mild-to-moderate aortic stenosis may be asymptomatic and may be picked up incidentally on cardiac auscultation or on echocardiogram. \r\n\r\nThe symptoms of severe AS can be remembered by the mnemonic 'SAD'. \r\n\r\n* **S**yncope \r\n* **A**ngina \r\n* **D**yspnoea \r\n\r\nOther symptoms include: pre-syncope, palpitations, left ventricular heart failure symptoms (exertional dyspnoea, orthopnoea, PND) or can present in cardiac arrest/sudden cardiac death. \r\n\r\n# Signs\r\n\r\n* Slow-rising carotid pulse\r\n* Narrow pulse pressure\r\n* Heaving, non-displaced apex beat (can be displaced if there is left ventricular hypertrophy)\r\n* Ejection systolic murmur\r\n * Heard best at the second intercostal space on the right\r\n * Can be described as \"harsh\"\r\n * Radiates to the carotids\r\n* Soft S2 heart sound: absent S2 corresponds with severity\r\n* Ejection click may be heard in some cases (early systolic)\r\n\r\n# Investigations\r\n\r\n## Bedside\r\n\r\n* **ECG:** LVH, left axis deviation, and poor R wave progreesion. \r\n\r\n## Imaging\r\n\r\n* **CXR:** cardiomegaly and evidence of pulmonary oedema. Occasionally, a calcified aortic valve is visible. \r\n* **Echocardiogram: definitive diagnosis**. \r\n\t* Definitive diagnosis of aortic stenosis. \r\n\t* Severity of AS can be quantified with doppler echocardiography. AS is classified as severe if it meets the following parameters: \r\n\t\t* Peak gradient > 40 mmHg (note, in severe left ventricular dysfunction, a low peak gradient can be falsely reassuring)\r\n\t\t* Valve area < 1.0cm x<sup>2</sup>\r\n\t\t* Aortic jet velocity >4 m/s\r\n* **Exercise testing:** may be used in physically active patients to assess the true severity of asymptomatic patients with echocardiography confirmed AS. \r\n* **Cardiac MRI:** can be used to provide additional, more details information regarding valve morphology, dimensions of the aortic root and the extent of valve calcification. \r\n\r\n# Management\r\n\r\n## Conservative \r\n\r\nTiming of intervention is crucial as many cases remain asymptomatic and stable and may not require treatment at all. \r\n\r\nPatients who do not meet the criteria for intervention should have regular echocardiography follow-up, with severe AS being monitored every 6 months, mild-to-moderate AS monitored yearly, and younger patients can be monitored every two to three years.\r\n\r\n## Medical \r\n\r\nMedical management of AS involves symptom management of left ventricular failure with diuretics and optimising heart failure medications with beta-blockers and ACE-I etc. Isolated medical therapy should only be used in those who are not suitable for intervention. \r\n\r\n## Surgical and Interventional \r\n\r\nIntervention in AS is indicated in the following patients:\r\n\r\n* All patients with symptomatic aortic stenosis \r\n* Asymptomatic patients with a left ventricular ejection fraction (LVEF) < 55%\r\n* Asymptomatic patients with an LVEF > 50% who are physically active, and who have symptoms or a fall in blood pressure during exercise testing\r\n* Asymptomatic patients with an LVEF > 50% who have the following risk factors\r\n * Aortic valve peak velocity > 5m/s x<sup>2</sup>\r\n * Severe calcification and peak velocity progression >= 0.3m/s x<sup>2</sup>\r\n * Markedly elevated BNP levels (more than twice upper limit) without other explanation\r\n * Severe pulmonary hypertension (pulmonary artery systolic pressure > 60mmHg)\n * Aortic valve area less than 0.6 cm<sup>2 \n\r\n\r\nChoices of intervention are **transcatheter aortic valve implantation (TAVI)** or **surgical aortic valve replacement (SAVR)**.\r\n\r\n* TAVI is favoured with patients with severe comorbidities, previous heart surgery, frailty, restricted mobility, and those older than 80 years of age.\r\n* SAVR is favoured for patients who are low risk and younger.\r\n\r\n# Complications\r\n\r\nAortic stenosis if left untreated can lead to LV failure. It is also implicated in sudden cardiac death. \r\n\r\n# Prognosis \r\n\r\nSevere, symptomatic AS patients are at a very high risk of sudden-death. It is estimated that these patients have a mortality rate of 50% at 1 year. It is essential that these patients are identified and treated swiftly. \r\n\r\n# Aortic sclerosis\r\n\r\nAortic sclerosis is an asymptomatic condition that can be incidentally revealed through physical examination or via echocardiogram. It is caused by age-related senile degeneration of the valve.\r\n\r\n## Clinical findings\r\n\r\nClassic findings are an ejection systolic murmur that _does not radiate to the carotids_, there is normal S2, pulse character and volume.\r\n\r\nIt can be defined as an irregular aortic leaflet thickening and focal increased echogenicity, but is distinguished from aortic stenosis because there is no impairment of valve leaflet excursion, and peak doppler velocities are normal or only minimally elevated (markedly elevated in stenosis)\r\n\r\n# NICE Guidelines\n\r\n[NICE Guidelines for Valvular Heart Disease](https://www.nice.org.uk/guidance/ng208/chapter/recommendations##References:)\r\n\r\n# References \r\n\r\n[BMJ Aortic Stenosis Summary](<https://www.bmj.com/content/380/bmj-2022-070511>)",
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"explanation": "Flecainide is classically used to cardiovert patients who have acutely gone into atrial fibrillation. It has an emerging role in the management of SVT; however would still not be used before attempting vagal manoeuvres. It is contraindicated if there is known structural heart disease",
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"explanation": "The first line treatment that should be attempted in patients with SVT to cardiovert back to sinus rhythm is vagal manoeuvres. These include the Valsalva manoeuvre (in practice, this is often getting the patient to blow into a closed syringe) or carotid massage",
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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 29 year old man presents to the emergency department (ED) with palpitations and vomiting. His ECG shows supraventricular tachycardia (SVT) at a rate of 170 beats per minute. The patient is stable with no adverse features.\n\nWhat is the first line treatment for this patient?",
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"explanation": "Once establishing if the patient is conscious/rousable, an assessment of airway would be the next priority",
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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": "Corticosteroid inhalers are \"**preventer**\" inhalers; they take some time to have an effect. They act by reducing inflammation in the airways, which worsens airway obstruction",
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"explanation": "Short acting muscarinic antagonists play a more significant role in the management of chronic obstructive pulmonary disease (COPD), rather than asthma",
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"explanation": "Long-acting beta<sub>2</sub> agonists are typically used more for the prevention of asthma symptoms and are sometimes used in combination devices alongside inhaled corticosteroids",
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"name": "Long-acting beta<sub>2</sub> agonist",
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"explanation": "Inhaled short acting beta<sub>2</sub> agonists are \"**relievers**\" – these agents work quickly to relax smooth muscle in the airways and produce a bronchodilator effect, resulting in rapid relief of symptoms",
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"explanation": "# Summary\n\nAsthma is a common disease of the airways, involving reversible bronchoconstriction, hyperreactivity and chronic inflammation. When bronchoconstriction is triggered (an “asthma attack”), patients experience episodes of wheeze, dyspnoea, cough and chest tightness. Initial investigations for all adults with suspected asthma are fractional exhaled nitric oxide (FeNO) or a full blood count looking for eosinophilia. If neither of these are confirmatory, patients should be assessed with spirometry including bronchodilator reversibility. Management involves a stepwise approach to medications, starting with “reliever therapy” (usually short-acting beta-2 agonists such as salbutamol inhalers) in combination with “preventer therapy” medications including inhaled corticosteroids, leukotriene receptor antagonists and long-acting beta-2 agonist inhalers. Allergen avoidance, smoking cessation, regular peak flow monitoring and inhaler technique are all key to good asthma control.\n\n# Definition\n\nAsthma is a common disease in both adults and children, characterised by intermittent \"asthma attacks\" with wheeze, cough, shortness of breath and chest tightness. There are several underlying mechanisms that centre around reversible bronchoconstriction, hyperreactivity and chronic inflammation.\n\n# Epidemiology\n\nIn the UK, approximately 8 million people have been diagnosed with asthma, of which 5.4 million are on treatment. Onset is usually in childhood and some find symptoms remit with age, although relapse is possible after long periods of being well.\n\nOn average, three people die from an asthma attack each day in the UK. The majority of these deaths are preventable, with an estimated 7/10 people with asthma not receiving basic preventative care such as inhaler technique checks and a personalised asthma plan.\n\nPeople experiencing socioeconomic deprivation are more likely to have asthma and to have worse outcomes (e.g. higher rates of hospitalisation). This is multifactorial, with these groups more likely to be exposed to triggers such as smoking and air pollution, and to have lower health literacy and access to healthcare.\n\n# Pathophysiology\n\nAsthma is often associated with a personal and/or family history of atopy, including the atopic triad of asthma, allergic rhinitis, and eczema. In asthma, there is an exaggerated response to a wide range of triggers. These include:\n\n- Cold air and exercise\n- Pollution and cigarette smoke\n- Allergens such as animal dander, dust mites and pollen\n- Irritants such as perfumes, paints or air fresheners\n- Medications such as NSAIDs or beta-blockers\n\nThese trigger a type 1 hypersensitivity reaction which is mediated by IgE. T Helper 2 cells produce IL4, IL5 and IL13 cytokines which activate the humoral immune system, leading to the proliferation of eosinophils, mast cells and dendritic cells. These cells then produce more inflammatory mediators such as leukotrienes and histamine.\n\nThis inflammation contributes to airway hyperresponsiveness leading to bronchospasm, as well as mucus hypersecretion that also obstructs airways. Over time in severe asthma, airway remodelling mediated by fibroblasts causes chronic obstruction and thickening of smooth muscle.\n\n# Risk factors\n\n- Family history of asthma or atopy\n- Personal history of atopy (eczema, allergic rhinitis, allergic conjunctivitis)\n- Exposure to smoke, including maternal smoking in pregnancy\n- Respiratory infections in infancy\n- Prematurity and low birth weight\n- Obesity\n- Social deprivation\n- Occupational exposures (e.g. flour dust, isocyanates from paint)\n\n# Symptoms\n\n- Wheeze\n- Dyspnoea\n- Cough\n- Chest tightness\n\nThe above symptoms should be episodic and usually show **diurnal variation** (worse at night or in the early morning). The patient may be able to identify specific triggers as listed above.\n\n# Signs\n\nIn between asthma exacerbations, clinical examination may be normal. If asthma is poorly controlled or during an exacerbation, signs include:\n\n- Tachypnoea\n- Increased work of breathing\n- Hyperinflated chest\n- Expiratory polyphonic wheeze throughout the lung fields\n- Decreased air entry (if severe)\n\n\n# Differential diagnosis\n\n- **Bronchiectasis** - usually associated with a productive cough, patients get frequent chest infections and coarse crackles rather than wheeze predominate on examination.\n- **Vocal cord dysfunction** - shares many triggers with asthma, inspiration more difficult than expiration, may have stridor.\n- **Chronic obstructive pulmonary disease** - patients usually >35 years old with a significant smoking history, may overlap with asthma in some.\n- **Gastro-oesophageal reflux disease** - microaspiration of stomach acid due to reflux can cause episodes of cough and wheeze which mimic asthma (although these may coexist and reflux can trigger asthma exacerbations). Symptoms are often postural and related to eating.\n- **Eosinophilic Granulomatosis with Polyangiitis** (Churg-Strauss syndrome) - small vessel vasculitis associated with pANCA, aside from asthma symptoms include nasal polyps, sinusitis, purpuric rashes and peripheral neuropathy.\n\n# Investigations \n\n- **FeNO (fractional exhaled nitric oxide) testing:** offer this **or** blood eosinophil count to all adults to confirm eosinophilic airway inflammation, asthma can be diagnosed if this is >50 parts per billion.\n- **Full blood count** to check **eosinophil count:** offer this **or** FeNO first-line to all adults - asthma can be diagnosed if this is above the normal reference range.\n- If neither of these confirm asthma, **spirometry** with **bronchodilator reversibility** should be offered to confirm airway obstruction (i.e. FEV1/FVC<70%). A bronchodilator (e.g. salbutamol inhaler) is given and spirometry repeated to assess response to treatment. An improvement in FEV1 of 12% or more or 200ml is diagnostic of asthma.\n- If spirometry is delayed or not available, patients may be asked to monitor their peak flow twice a day for 2 weeks and keep a diary of the readings. This is then used to assess **peak flow variability** (the difference between the highest and lowest readings as a percentage of the average PEF). Variability >20% is a positive result.\n- If none of the above are confirmatory, patients may be referred to specialist services for a **direct bronchial challenge test**, where histamine or metacholine is inhaled to trigger bronchoconstriction. Airway hyperresponsiveness is assessed by looking at the concentration of the triggering medication required to cause a 20% decrease in FEV1 - 8mg/ml or less is a positive result.\n\nNote: All of the above tests may be falsely negative in patients treated with inhaled corticosteroids.\n\n# Management of Chronic asthma\n\nThe aim of chronic asthma management is to achieve complete control over symptoms, with no need for rescue medications and no restrictions on physical activity. All patients should have a personalised asthma action plan which should be reviewed at least annually. Components of management include:\n\n## Non-pharmacological\n\n- Teach good inhaler technique and review this regularly\n- Spacer devices can be used to optimise medication delivery\n- Regular peak flow monitoring\n- Smoking cessation\n- Advice on avoiding triggers where possible (e.g. allergens, certain medications)\n- Ensure vaccinations are up to date, including annual influenza vaccination\n- Assess for occupational asthma by asking if symptoms are better when the patient is away from work and arrange specialist referral if this is suspected\n\n## Pharmacological\n\n- Prescribe all patients a combination inhaler with a **long-acting beta-2 agonist** (LABA) i.e. formoterol and a low-dose **inhaled corticosteroid** (ICS) i.e. budesonide to use as a reliever inhaler (i.e. PRN) - this is referred to as anti-inflammatory reliever (AIR) therapy.\n- Patients who do not respond adequately to AIR therapy, who are highly symptomatic at presentation or who present with a severe asthma exacerbation should be started on a low-dose **maintenance and reliever therapy inhaler** (MART). MART is a combination inhaler with ICS and a fast-acting LABA (e.g. beclomethasone + formoterol which is also known as Fostair), which is used as both a reliever inhaler (PRN) and as maintenance treatment (usually twice daily).\n- The next step would be increasing the ICS dose from low to **moderate** in the MART inhaler.\n- At this stage if asthma is not controlled, check FeNO and blood eosinophil count and refer to specialist asthma services if either are raised.\n- If neither are raised, consider adding either a **leukotriene receptor antagonist** (LTRA) such as montelukast (this is a tablet taken every night) or a **long-acting muscarinic agonist** (LAMA) such as tiotropium.\n- One of these should be trialled for 8-12 weeks alongside the moderate-dose MART - if asthma is well-controlled it can be continued.\n- If there is some improvement in control but this is still inadequate, the other medication can be trialled in addition (i.e. moderate dose MART + LTRA + LAMA).\n- If control has not improved, stop the medication and try the other one - if this is not successful refer to specialist services.\n- Options in specialist clinics include therapies such as **biologics** (e.g. omalizumab, which targets IgE).\n\nOther than patients who are not responding to treatment, the following situations shold also prompt a secondary care referral:\n\n- Uncertainty regarding diagnosis\n- Suspected occupational asthma\n- Severe or life-threatening asthma requiring admission to hospital\n- Multiple exacerbations requiring oral steroid treatment per year\n\n# Acute asthma\n\nAcute asthma exacerbations are graded in severity as below:\n\n\n| Severity | Clinical Features |\n|-----------------------|-----------------------------------------------|\n| Moderate | PEFR > 50% of predicted or best |\n| | No features of severe/life-threatening asthma |\n| Severe | PEFR 33-50% of predicted or best |\n| | Heart rate > 110 |\n| | Respiratory rate > 25 |\n| | Unable to complete sentences in one breath. |\n| | Accessory muscle use |\n| Life-threatening | PEFR < 33% of predicted or best |\n| | Oxygen saturation < 92% or cyanosis |\n| | Altered conciousness/confusion |\n| | Exhaustion/poor respiratory effort |\n| | Cardiac arrhythmia |\n| | Hypotension |\n| | Silent chest |\n\n\n## Investigations \n\n- **Peak expiratory flow rate (PEFR)** to help assess severity as per the classification above and monitor response to treatment.\n- **Arterial blood gas** if the patient is hypoxic to assess oxygenation and ventilation in patients - CO2 is expected to be low due to hyperventilation and if this is raised this indicates the asthma attack is near fatal.\n- **Portable chest X-ray** if a trigger such as pneumonia or a complication such as pneumothorax is suspected clinically.\n\n## Management \n\n- Recognise that this may be a medical emergency, assess using an ABCDE approach and escalate early to senior colleagues/critical care if not responding to treatment\n- Titrate oxygen to maintain saturations of 94-98%\n- Nebulised salbutamol driven by oxygen (if out of hospital, give up to 10 puffs of inhaled salbutamol and call an ambulance if not responding)\n- If the attack is severe or life-threatening or if response to salbutamol has been poor, add nebulised ipratropium bromide\n- Give prednisolone 40-50mg orally, or IV hydrocortisone if the patient is unable to swallow\n- Can consider IV magnesium sulphate and/or aminophylline if the patient is not responding to nebulisers\n- If the patient continues to deteriorate despite maximal therapy, they may require intubation and ventilation in an intensive care setting (for example in cases of severe hypoxia or exhaustion)\n\nFollow up after an acute asthma attack is crucial, with NICE guidelines stating that patients should be reviewed within 2 days of discharge from hospital to assess their symptoms, inhaler technique and current management.\n\n# NICE Guidelines\n\n[NICE - Asthma: diagnosis, monitoring and chronic asthma management](https://www.nice.org.uk/guidance/ng245)\n\n# References\n\n[NICE CKS](https://cks.nice.org.uk/topics/asthma/)\n\n[Report on health inequalities and asthma](https://www.asthmaandlung.org.uk/sites/default/files/2023-03/auk-health-inequalities-final.pdf)\n\n[Guideline on severe asthma in primary care](https://www.pcrs-uk.org/sites/default/files/pcru/articles/2019-Autumn-Issue-18-SevereAsthmaReferral.pdf)\n\n\n\n",
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"question": "A 33 year old man presents to the GP complaining of chest tightness and a nocturnal cough. He is diagnosed with asthma.\n\nWhat is the first line inhaled agent used for relief of symptoms in asthma?",
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"__typename": "QuestionChoice",
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"explanation": "Examination findings in patients with lung cancer may include clubbing and a monophonic or harsh sounding wheeze. COPD is significantly more common than lung cancer",
"id": "33306",
"label": "d",
"name": "Lung cancer",
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"explanation": "Asthma is not as classically a disease of smokers compared with COPD. In addition, although asthma does cause wheeze (which tends to be polyphonic or \"musical\"), it does not cause hyper-expansion of the lungs",
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"name": "Asthma",
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"explanation": "Typical examination findings in ILD include fine end-expiratory crackles in the affected area (bases or apices depending on the cause of the fibrosis). You may also find clubbing and reduced chest expansion. This is a restrictive lung condition and as such, does not cause hyper-expansion of the lungs",
"id": "33304",
"label": "b",
"name": "Interstitial lung disease (ILD)",
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "COPD is directly linked to exposure to tobacco smoke or other pollutants (including direct and passive smoke inhalation). It is an obstructive condition which causes air trapping, leading to hyper-expanded lungs. This manifests in reduced expansion and hyper-resonance to percussion. COPD also commonly causes wheeze, particularly in times of acute exacerbation when there may be additional mucus clogging the already obstructed airways",
"id": "33303",
"label": "a",
"name": "Chronic obstructive pulmonary disease (COPD)",
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"__typename": "QuestionChoice",
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"explanation": "Most patients with bronchiectasis will have crackles on examination due to the presence of excess mucus in the airways. COPD is significantly more common than bronchiectasis",
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"label": "e",
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"explanation": "# Summary\n\nChronic obstructive pulmonary disease (COPD) is a chronic obstructive disease of the airways with the two main components being chronic bronchitis and emphysema. It usually develops due to smoking, with other risk factors including occupation exposures and air pollution. Patients present with breathlessness, a chronic productive cough and wheeze. Key investigations are spirometry (to confirm obstruction), full blood count (to identify anaemia or polycythaemia) and a chest X-ray to exclude lung cancer or other causes of symptoms. Management includes smoking cessation, pulmonary rehabilitation, consideration of long term oxygen therapy, inhaled or nebulised medical treatment and consideration of other medications e.g. mucolytics. Acute exacerbations of COPD may be infective or non-infective, and can be treated by increasing bronchodilator therapy, oral prednisolone and antibiotics (if an infective cause is suspected).\n\n# Definition\n\nChronic obstructive pulmonary disease (COPD) involves airway obstruction that is usually progressive. It encompasses both emphysema (where alveolar wall destruction leads to enlargement of the distal airspaces) and chronic bronchitis (persistent or recurrent productive cough usually due to mucus hypersecretion). \n\n# Epidemiology\n\nIn the UK 1.2 million people have a diagnosis of COPD, with an estimated 2 million people living with it undiagnosed. It is the 5th commonest cause of death in the UK, causing almost 30,000 deaths per year. \n\nAround 90% of COPD cases in the UK are caused by smoking, with household pollution being a bigger contributing factor in low and middle income countries.\n\n# Risk Factors\n\n- Tobacco smoking and passive smoke exposure\n- Marijuana smoking \n- Occupational exposure to dusts and fumes\n- Household air pollution from wood or coal burning\n- Alpha-1 antitrypsin deficiency\n\nPrognosis is variable, with the following factors associated with higher morbidity and mortality:\n\n- Poor exercise tolerance\n- Smoking\n- Low body mass index\n- Multi-morbidity and frailty\n- Exacerbations requiring admission to hospital or frequent exacerbations\n- Severe obstruction on spirometry (as measured by a lower FEV1)\n- Chronic hypoxia\n- Cor pulmonale\n\n# Pathophysiology\n\nChronic Bronchitis:\n\n- As a protective reaction to smoke or other pollutants, goblet cells hypersecrete mucus in the bronchi and bronchioles of the lungs.\nCilia are not able to remove the excess mucus and so it obstructs the small airways.\nOngoing inflammation causes remodelling and thickening of the airway walls that also contributes to obstruction.\n\nEmphysema:\n\n- Inflammation in the lungs is usually countered by antiproteases such as alpha-1 antitrypsin, however the activity of these is reduced by smoke and other pollutants. \n- Without sufficient antiprotease activity, proteolytic enzymes produced by inflammatory cells break down the walls of the alveoli.\n- This causes enlargement of the terminal airspaces and reduces the surface area available for gas exchange.\n\n# Classification\n\nThe Global Initiative for Chronic Obstructive Lung Disease (GOLD) classifies COPD severity using airflow limitation (as measured by FEV1), severity of symptoms and frequency of exacerbations. \n\n| GOLD Grade | Severity | Post-Bronchodilator FEV₁ (% Predicted) |\n|------------|--------------------------|----------------------------------------|\n| 1 | Mild | ≥ 80% |\n| 2 | Moderate | 50-79% |\n| 3 | Severe | 30-49% |\n| 4 | Very Severe | < 30% |\n\n\nThe two measures used to quantify symptom severity are the CAT (COPD Assessment Test) and the mMRC (modified Medical Research Council) dyspnoea scale which is given below:\n\n| Grade | Description |\n|-------|----------------------------------------------------------------------------------------------------|\n| 0 | I only get breathless with strenuous exercise. |\n| 1 | I get short of breath when hurrying on level ground or walking up a slight hill. |\n| 2 | On level ground, I walk slower than people of the same age because of breathlessness, or I have to stop for breath when walking at my own pace. |\n| 3 | I stop for breath after walking about 100 yards or after a few minutes on level ground. |\n| 4 | I am too breathless to leave the house, or I am breathless when dressing or undressing. |\n\n# Signs and symptoms\n\n- Shortness of breath that worsens with exertion\n- Reduced exercise tolerance\n- Chronic productive cough\n- Recurrent lower respiratory tract infections\n- Wheeze\n- In more advanced cases, systemic symptoms such as weight loss and fatigue may be present\n\nExamination may be normal, though signs may include:\n\n- Wheeze or crackles on auscultation\n- Accessory muscle usage\n- Pursed lip breathing (this creates a small amount of positive end expiratory pressure to prevent the alveoli from collapsing)\n- Cyanosis \n- Hyperinflation of the chest\n- Cachexia\n- Raised JVP and peripheral oedema (indicating cor pulmonale has developed)\n\n# Investigations\n\n- **Spirometry** - the diagnostic investigation for COPD and key to classification of severity, may be used to monitor progression of the disease. A FEV1/FVC ratio <0.7 confirms obstruction.\n\n- **Bloods** - Full blood count looking for polycythaemia (resulting from chronic hypoxaemia) or anaemia (usually anaemia of chronic disease), consider BNP to assess for heart failure (with an **echocardiogram** if suspected, alpha-1 antitrypsin in young patients/minimal smoking history/strong family history\n- **ECG** - the following ECG changes are often seen in advanced COPD with features of e.g. cor pulmonale, and include:\n\t- Right axis deviation\n\t- Prominent P waves in inferior leads\n\t- Inverted P waves in high lateral leads (I, aVL)\n\t- Low voltage QRS\n\t- Delayed R/S transition in leads V1-V6\n\t- P pulmonale\n\t- Right ventricular strain pattern\n\t- RBBB\n\t- Multifocal atrial tachycardia\n\n- **Chest X-ray** - used to rule out other causes of symptoms (e.g. lung cancer, bronchiectasis), may show features of COPD including hyperinflation of the chest with flattening of the hemidiaphragms and bullae.\n\n[lightgallery1]\n\n- **Sputum culture** - during exacerbations to target antibiotic therapy\n\n# Differential diagnosis\n\n- **Asthma:** may coexist with COPD, suspect if onset of symptoms <35, history of atopy, non-smoker, variable or nocturnal symptoms.\n- **Bronchiectasis:** copious secretions and coarse crepitations on examination, triggering factors include severe childhood respiratory tract infections.\n- **Heart Failure:** suspect in patients with ischaemic heart disease, may have orthopnoea and paroxysmal nocturnal dyspnoea.\n- **Interstitial Lung Disease:** dry rather than a productive cough, fine crackles on examination.\n- **Lung cancer:** patients with COPD are usually at higher risk due to smoking history, need to investigate for malignancy in cases with a persistent cough/haemoptysis/weight loss.\n- **Tuberculosis:** similar symptoms, systemic manifestations include fevers and weight loss, consider in at-risk groups.\n\n# Management of Chronic COPD\n\n**Conservative:**\n\n- Patient education, ensure all patients have a personalised self-management plan\n- Smoking cessation support\n- Nutritional support and dietician referral if malnourished\n- Annual influenza and one-off pneumococcal vaccination\n- Pulmonary rehabilitation (refer if grade 3 and above on mMRC dyspnoea scale or a recent admission for an acute exacerbation)\n- Consider referral for respiratory physiotherapy to help with sputum clearance and breathing techniques\n\n**Medical:**\n\n\n- For patients whose activities are limited by breathlessness, start a short-acting beta-2 agonist (SABA, e.g. salbutamol) or short-acting muscarinic antagonist (SAMA, e.g. ipratropium) inhaler\n- The next step depends on if they have features of asthma or steroid responsiveness: if these are present then add a long-acting beta-2 agonist (LABA, e.g. formoterol) and an inhaled corticosteroid (ICS, e.g. beclomethasone). If these are not present then add a LABA and a long-acting muscarinic antagonist (LAMA, e.g. tiotropium). \n- If patients do not respond adequately to this, the third inhaler can then be trialled (i.e. all patients would be on a SABA/SAMA + LABA + LAMA + ICS).\n\nPatients who require further therapy should be referred to a specialist for ongoing management which may include oral steroids, oral theophylline or oral phosphodiesterase-4 inhibitors (e.g. roflumilast).\n\nManagement of stable COPD is can be tailored according to the patient’s clinical phenotype. The following groups are defined according to 2024 NICE guidance:\n\n**Group A**\n \n- **Definition**: Patients with minimal symptoms (mMRC grade 0–1 or CAT score <10) and no history of exacerbations requiring hospitalisation or oral corticosteroids in the last year. \n- **Management**:\n - Start with a **short-acting bronchodilator (SABA or SAMA)** as needed for symptom relief.\n - If symptoms are not controlled, consider switching to a long-acting bronchodilator: \n - **LAMA** or **LABA**, depending on individual tolerance and symptom profile. \n\n**Group B**\n \n- **Definition**: Patients with significant symptoms (mMRC grade ≥2 or CAT score ≥10) but no exacerbations requiring hospitalisation or oral corticosteroids in the last year. \n- **Management**: \n - Initiate treatment with a **LAMA** or **LABA** as maintenance therapy. \n - If symptoms persist despite monotherapy, escalate to **dual therapy (LABA + LAMA)**. \n\n**Group E**\n \n- **Definition**: Patients with frequent exacerbations (≥2 per year or ≥1 requiring hospitalisation) regardless of symptom burden. \n- **Management**: \n - First-line therapy is **LAMA** for exacerbation prevention. \n - If exacerbations persist, escalate to: \n\t - **Dual therapy (LABA + LAMA)**. \n\t - If asthmatic features or steroid responsiveness are present (e.g., eosinophilia or a history of asthma), consider **LABA + ICS**. \n - For patients who continue to experience exacerbations despite dual therapy, switch to **triple therapy (LABA + LAMA + ICS)**. \n\n\n\n| **Group** | **Phenotype** | **Initial Therapy** | **Escalation Therapy** | \n|-------------|--------------------------------|------------------------------|------------------------------------| \n| **Group A** | 0 or 1 moderate exacerbation not leading to hospitalisation | SABA or SAMA as needed | LAMA or LABA | \n| **Group B** | 0 or 1 moderate exacerbation not leading to hospitalisation| LAMA or LABA | LABA + LAMA | \n| **Group E** | 2 or more moderate exacerbations or 1 or more exacerbations leading to hospitalisation\t | LAMA | LABA + LAMA or LABA + LAMA + ICS | \n\n\nOther medical treatments that may be considered include:\n\n- Oral mucolytic therapy - for patients with a chronic cough productive of sputum.\n- Prophylactic antibiotics - in cases of frequent infective exacerbations, should be discussed with a specialist, a common choice would be azithromycin 3x per week.\n- Nebuliser therapy - for patients with disabling breathlessness despite optimised use of inhalers.\n- Long-term oxygen therapy (LTOT) - see below for more details\n\n\n**Surgical:**\n\n- In certain cases of severe COPD when patients have not responded to maximal medical therapies, surgical intervention may be considered. \n- Both the NICE recommended options involve lung volume reduction (which involves removing emphysematous areas of the lung so that the healthy lung can expand) - this can be done either by surgical resection or using bronchoscopy to site a one-way valve in one of the larger airways to collapse the diseased lung. \n\n### Long term oxygen therapy (LTOT)\n\n**The following patients should be referred for assessment for LTOT:**\n\n- Oxygen saturations <92% in air or cyanosis\n- FEV1 <30% predicted (consider referring if <49%)\n- Polycythaemia\n- Peripheral oedema or raised jugular venous pressure (suggesting cor pulmonale)\n\nThis assessment involves ensuring that patients are medically optimised and their COPD is stable (i.e. they’re not recovering from a recent exacerbation). Patients who are current smokers cannot be offered LTOT because of the risk of burns and fires. \n\nPatients then have two ABGs in air at least 3 weeks apart and the following patients should be offered LTOT (with the advice to use the oxygen for at least 15 hours per day):\n\n- PaO2 below 7.3kPa\n- PaO2 7.3-8kPa with any of secondary polycythaemia, peripheral oedema or pulmonary hypertension\n\n# Complications\n\n## Acute exacerbations\n\n- These present with worsening breathlessness, productive cough and wheeze, and patients may be febrile, tachycardic and tachypnoeic. \n- Patients who are clinically well may be treated at home with an increase in their usual inhalers, a short course of oral steroids (usually 30mg prednisolone for 5 days) and oral antibiotics if bacterial infection is suspected. \n- Those who have frequent exacerbations may be given a “rescue pack” of steroids and antibiotics to keep at home and start using in case of an exacerbation (alongside seeking medical help).\n\n- Patients requiring hospital admission should also receive steroids and antibiotics if indicated. \n- They may require nebulised bronchodilators, supplementary oxygen and in case of deterioration respiratory support with non-invasive ventilation may be required. \n- Advanced care planning and ensuring that escalation status is discussed with patients is therefore key, so that if they deteriorate to the point of needing intensive care support it is established whether or not this is appropriate and in line with their wishes.\n\n## Polycythaemia\n\n- Chronic tissue hypoxia as seen in COPD leads to a compensatory overproduction of erythropoietin, which leads to increased red blood cell production (i.e. secondary polycythaemia). \n- This causes an increase in blood viscosity that in turns increases risk of both arterial and venous thrombosis. \n\n\n## Cor Pulmonale\n\nCor pulmonale refers to right ventricular dilation or hypertrophy in response to pulmonary hypertension caused by chronic lung disease - COPD is not the only cause of this but it is the most common.\n\nThe pathophysiology is as follows:\n\n- Changes in the lungs and chronic hypoxaemia cause the walls of the pulmonary arteries to thicken.\n- This increases vascular resistance in the lungs.\n- The right ventricle then has to pump against greater resistance, which causes it to either dilate or hypertrophy.\n- Ultimately this leads to right heart failure, with resulting peripheral oedema, hepatomegaly and elevated jugular venous pressure (JVP).\n\nPeripheral oedema may be treated symptomatically with diuretics and long-term oxygen therapy has been shown to reduce morbidity and mortality. All patients with suspected cor pulmonale should be referred to secondary care.\n\n## Pneumothorax\n\n- COPD is a common cause of secondary pneumothoraces (i.e. a pneumothorax secondary to underlying lung disease). These occur when a bulla ruptures, releasing air into the pleural cavity. \n- Investigations and treatment are as per the BTS guidelines (see Pneumothorax chapter for more details).\n\n## Depression and anxiety\n- Over 1 in 3 people with COPD report symptoms of depression and anxiety so screening for this is important during patient reviews. \n- The COPD Assessment Test (CAT) can be used to assess the impact of COPD on everyday life. \n- Referral to psychological services for support may be appropriate, as well as holistic assessment and management.\n\n# NICE Guidelines\n\n[Click here for the NICE Guidelines](https://www.nice.org.uk/guidance/ng115)\n\n[NICE CKS - COPD](https://cks.nice.org.uk/topics/chronic-obstructive-pulmonary-disease/)\n\n# References\n\n[Patient UK - COPD](https://patient.info/doctor/chronic-obstructive-pulmonary-disease-pro)\n\n[GOLD report 2023](https://goldcopd.org/2023-gold-report-2/)\n\n[Radiopaedia - COPD](https://radiopaedia.org/articles/chronic-obstructive-pulmonary-disease-1?lang=gb)\n\n[Patient UK - Cor Pulmonale](https://patient.info/doctor/cor-pulmonale)",
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"question": "A 61 year old woman presents to the GP with shortness of breath which is limiting her ability to care for herself independently. She is no longer able to wash or dress herself without significant breathlessness.\n\nOn examination, the GP identifies:\n\nTar staining on the right hand, cachexia, increased work of breathing at rest, reduced chest expansion bilaterally, hyper-resonance to percussion bilaterally and bilateral expiratory wheeze.\n\nWhich clinical diagnosis is most likely, given the examination findings?",
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"explanation": "A CXR is not a diagnostic test for a pulmonary embolism, and in fact, is usually normal in these patients. When signs are present on the CXR (such as wedge shaped consolidation representing pulmonary infarction), it can be difficult to directly determine the cause (pneumonia could also explain this change)",
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"label": "b",
"name": "Chest X-ray (CXR)",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Spirometry does not have a role in the diagnosis of pulmonary embolism",
"id": "33312",
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"explanation": "This is the main alternative diagnostic imaging for patients with a contraindication to CTPA, such as severe renal impairment or contrast allergy. It is also used in pregnancy due to the lower radiation dose",
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"explanation": "This patient has a Wells score of 7: Heart rate of >100 (1.5), haemoptysis (1), recent immobilisation of at least 3 days in the last 4 weeks (1.5), PE is number one diagnosis, or equally likely (3). Haemodynamically stable patients with a high clinical probability of PE (more than 4 points) should be investigated with a CTPA unless contraindicated",
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"explanation": "A D-dimer would the first line test in patients with a Wells score of less than or equal to 4 (low probability of PE) and who are haemodynamically stable",
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"explanation": "# Definition\n\nA pulmonary embolism (PE) is when a blood clot in the pulmonary arterial vasculature develops, usually from an underlying deep vein thrombosis (DVT) of the lower limbs.\n\n# Epidemiology of pulmonary embolism (PE)\n\n2300 people died as a result of a pulmonary embolism in the UK in 2012, representing 2% of all deaths from lung diseases.\n\n# Presentation of a PE\n\n**Symptoms**\n\n- Sudden-onset shortness of breath, pleuritic chest pain, and haemoptysis (this is the 'typical' triad, although note that all three features are rarely present).\n\n- A massive pulmonary embolism may present with the above and syncope/shock.\n\n- A small pulmonary embolism may be asymptomatic.\n\n**Signs**\n\n- Classically tachypnoea, tachycardia and hypoxia is present. There may be low-grade pyrexia. Tachycardia may be the only presenting sign.\n\n- Note that a small pulmonary embolism may result in a normal examination.\n\n- A massive pulmonary embolism may present with hypotension, cyanosis, and signs of right heart strain (such as a raised JVP, parasternal heave, and loud P2).\n\nIt is important to look for signs of a concomitant deep vein thrombosis (a unilaterally swollen, tender calf).\n\n# ECG findings\n\nECG: Normal or sinus tachycardia. In a massive PE there may be evidence of right-heart strain (with P pulmonale, right axis deviation, right bundle branch block, and non-specific ST/T wave changes). The classic S1Q3T3 (deep S waves in lead I, pathological Q waves in lead III, and inverted T waves in lead III) is relatively uncommon (<20% of patients).\n\n# Blood tests in PE\n\nABG: This may be normal or show a type 1 respiratory failure (hypoxia without hypercapnia) and/or a respiratory alkalosis (due to hyperventilation secondary to hypoxia).\n\nRemember the baseline tests such as FBC (the patient may be anaemic if the PE has caused haemoptysis), CRP may be raised, U&E (to assess renal function before CTPA), clotting function (important if the patient is to be started on LMWH/Warfarin).\n\nSpecial tests include D-dimer (this is highly non-specific but has a 95% negative predictive value i.e. it is useful in ruling out a PE if negative).\n\n# Imaging Investigations in PE\n\nChest x-ray: this is typically normal in PE but possible findings include _Fleischner sign_ (an enlarged pulmonary artery), _Hampton's hump_ (a peripheral wedge shaped opacity), and _Westermark's sign_ (regional oligaemia). The chest x-ray is helpful in ruling out differentials (e.g. pneumonia, pneumothorax).\n\nCT pulmonary angiogram (CTPA): this is the diagnostic test of choice for a PE and will show a filling defect in the pulmonary vasculature. Note that a V/Q scan is preferred if the patient has renal impairment, contrast allergy or is pregnant.\n\nLower limb Duplex: helpful if a DVT is thought to be the cause of the PE (note this investigation is first-line - before a CTPA - in pregnancy).\n\nBedside echocardiogram: this is used if the patient is thought to have a massive PE (signs of right heart strain/hypotension), in order to assess suitability for thrombolysis.\n\n# Well's scoring system\n\nThe Well's score is a useful tool for risk stratifying patients with a suspected PE.\n\nPoints are allocated as follows:\n\n- 3 points:\n - Clinical signs and symptoms of a deep vein thrombosis (DVT)\n - If no alternative diagnosis is more likely than a PE\n- 1.5 points:\n - Tachycardia (heart rate >100 beats/minute)\n - If the patient has been immobile for more than 3 days or has had major surgery within the last month\n - If the patient has had a previous PE or DVT\n- 1 point:\n - If the patient presents with haemoptysis\n - If there is an active malignancy\n\nIf the Well's score is 4 or less the D-dimer should be measured. The D-dimer has a high negative predictive value but a low specificity so is only useful if the clinical suspicion of a PE is low.\n\nA low D-dimer excludes a PE. A raised D-dimer is an indication for diagnostic imaging (by CTPA or V/Q scan).\n\nIf the Well's score is more than 4 further diagnostic imaging is required. Low-molecular weight heparin is typically administered in the interim if the clinical suspicion of a PE is high (and should certainly be administered if there is delay in performing the CTPA).\n\n# Acute management of a PE\n\nIn the emergency department the patient should be assessed using the DR ABCDE approach:\n\n- Airway: likely to be patent.\n- Breathing: the patient may be tachypnoeic and hypoxic. Oxygen should be administered.\n- Circulation: the patient may be tachycardic. Signs of right heart strain are suggestive of a sub-massive PE. Hypotension is suggestive of a massive PE. Consider intravenous fluids if the systolic blood pressure is <90 mmHg.\n- Disability: likely to be unremarkable.\n- Exposure: the patient may have a low grade pyrexia. It is important to check for signs of a deep vein thrombosis (DVT). Consider analgesia at this stage if required.\n\nThrombolysis (an intravenous bolus of Alteplase) is indicated in a massive PE (features of haemodynamic instability). There is debate over whether it should be administered in a sub-massive PE.\n\n# Medical management of a PE\n\nAnticoagulation should be administered.\n\nIn the outpatient setting, direct oral anticoagulants such as apixaban or rivaroxaban should be started.\n\nIf neither of the above are suitable, dabigatran, edoxaban or warfarin can be considered. Low molecular weight heparin should be continued for at least 5 days and until 48 hours of therapeutic INR (>2) has been achieved if using warfarin. If using dabigatran or edoxaban then LMWH should be used for 5 day prior.\n\nThe duration of anticoagulation treatment depends on the aetiology of the PE. A provoked PE (identifiable risk factors e.g. surgery, peri-partum) should be treated for 3 months. An unprovoked PE should be treated for 6 months. If there is an ongoing cause (e.g. a thrombophilia) the patient should be treated for life.\n\nRecurrence of a VTE in a patient already on warfarin requires an increase in the target INR (to 3-4).\n\nIn the inpatient/emergency setting, low molecular weight heparin is usually started instead as it is shorter acting.\n\n# Interventional management of a PE\n\nEmbolectomy may be considered in patients with a massive PE when thrombolysis is contraindicated.\n\nAn inferior vena cava filter may be considered in patients with recurrent DVTs on Warfarin or patients in which anticoagulation is contraindicated.\n\n# References\n\n[Click for the NICE Guidelines](https://www.nice.org.uk/guidance/ng158)",
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"question": "A 31 year old woman presents to the emergency department (ED) with sudden onset breathlessness and one episode of haemoptysis. Last week she had a car accident, and she has spent the last 5 days resting in bed due to whiplash. She has no other past medical history. Her only regular medication is the combined oral contraceptive pill. Her observations are as follows:\n\nRespiratory rate 22, oxygen saturations 96% on room air, pulse 110, blood pressure 110/73, temperature 36.5\n\nThe ED doctor suspects pulmonary embolism (PE). What is the definitive diagnostic investigation for PE in this patient?",
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"explanation": "This pneumothorax has occurred in a patient with no prior lung disease and without a trigger. Additionally, this patient has many risk factors for pneumothorax, including smoking, his height and his age/gender combination",
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"name": "Primary spontaneous pneumothorax",
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"explanation": "A secondary spontaneous pneumothorax happens without a trigger in a patient with known underlying lung disease",
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"explanation": "In this patient's demographic, in the absence of any risk factors for thrombus formation, a pneumothorax would be a more likely cause for sudden onset pleuritic chest pain",
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"label": "e",
"name": "Pulmonary embolism",
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"explanation": "A patient with a tension pneumothorax would be clinically more unwell than this patient, whose observations are not significantly deranged. The lack of tracheal deviation makes this unlikely",
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"comment": "would this not be secondary as likely caused by marfans or associated CT disorder as he's \"noted to be very tall\" or does the condition have to be diagnosed before?",
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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 22 year old male presents to the emergency department (ED) with right sided pleuritic chest pain. This came on suddenly with no identifiable trigger. He is a smoker with a 10 pack year history and is noted to be very tall. He has no past medical history. His observations follow:\n\nRespiratory rate 22, oxygen saturations 97%, pulse rate 90, blood pressure, 114/70, temperature 36.8\n\nA chest x-ray visualises the right lung margin 2 centimetres from the chest wall, with absence of lung markings within this space. There is no evidence of tracheal deviation.\n\nWhat is the most likely diagnosis?",
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"explanation": "An AMTS forms part of CRB-65 assessment which is part of the recommended pathway for assessing severity of CAP in the GP context (recommended by both British Thoracic Society and National Institute for Health and Care Excellence (NICE)).\n\nCRB-65 is calculated as follows, scoring one point for each of the following:\n\n- C = confusion (defined as a AMTS score of ≤ 8, or new disorientation in person, place or time)\n- R = respiratory rate ≥ 30\n- B = systolic blood pressure <90 mmHg or diastolic blood pressure ≤60 mmHg\n- 65 = age ≥ 65 years\n\nA score of:\n\n- 0 = likely suitable for outpatient management\n- 1-2 = consider hospital referral\n- 3 or 4 = urgent hospital admission\n\nTherefore, the score helps to inform whether a patient should be referred to hospital or if management in the community is appropriate. Other patient factors should also be considered alongside the score, including the patient's age, previous and concurrent health conditions and oxygen saturations",
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"explanation": "A CXR would demonstrate the proportion of lung impacted by the infection, an important indicator of pneumonia severity. However, in the context of GP assessment this test is not routinely available, nor does it form part of the evidence-based scoring system for pneumonia severity assessment",
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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 59-year-old woman presents to the GP with a 3-day history of worsening cough, productive of green sputum, and notable fatigue. She diagnosed with a community acquired pneumonia (CAP).\n\nHer observations are as follows:\n\n- Respiratory rate 22\n- Oxygen saturations 97% on room air\n- Pulse 109\n- Blood pressure 109/67\n- Temperature 37.9°C\n\nWhat other factor needs to be considered to allow for evidenced-based severity grading of the pneumonia in this context?",
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