Alcohol, fatty & autoimmune liver disease flashcards
19 high-yield MRCP Part 1 cards from the Intellect Medicos Gastroenterology & Hepatology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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Which transaminase pattern is typical of alcoholic liver disease?
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AST higher than ALT, classically in a ratio of more than 2:1 (with raised GGT and MCV).
Why? Alcohol damages mitochondria (rich in AST) and causes pyridoxine deficiency, which lowers ALT more. In viral hepatitis and MASLD, ALT is usually higher than AST.
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In severe alcoholic hepatitis (Maddrey discriminant function 32 or more), what drug treatment is considered?
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Oral prednisolone 40 mg daily for 28 days, if there is no active infection or GI bleeding.
Why? Steroids can improve short-term survival in severe disease. Response is checked with the Lille score at day 7: if 0.45 or more, stop prednisolone.
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Alcoholic hepatitis histology shows ballooned hepatocytes, neutrophil infiltrate and ______, with pericellular 'chicken-wire' fibrosis.
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Mallory–Denk bodies
Why? Mallory–Denk bodies are clumps of damaged cytokeratin filaments inside injured hepatocytes.
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What defines MASLD (formerly NAFLD)?
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Hepatic steatosis plus at least one cardiometabolic risk factor, with no other cause of liver disease and alcohol below harmful levels.
Why? Risk factors: overweight/obesity, type 2 diabetes, dyslipidaemia, hypertension. Insulin resistance is central.
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In NAFLD/MASLD, NICE uses the ______ blood test: a score of 10.51 or above indicates advanced fibrosis.
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enhanced liver fibrosis (ELF)
Why? ELF measures hyaluronic acid, procollagen III peptide and TIMP-1. Below 10.51, retest every 3 years in adults.
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In NAFLD/MASLD, NICE uses the enhanced liver fibrosis (ELF) blood test: a score of ______ indicates advanced fibrosis.
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10.51 or above
Why? ELF measures hyaluronic acid, procollagen III peptide and TIMP-1. Below 10.51, retest every 3 years in adults.
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What is the most important treatment for MASLD?
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Weight loss – aim for 7–10% of body weight – through diet and exercise.
Why? Weight loss reduces steatosis, inflammation and even fibrosis. Pioglitazone (especially in diabetes) or vitamin E can be considered in secondary care for advanced fibrosis.
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Autoimmune hepatitis type 1 (adults) is linked to ______ antibodies; type 2 (children, more aggressive) to anti-LKM1 antibodies.
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ANA and anti-smooth muscle
Why? AIH also shows a raised IgG and interface hepatitis with plasma cells on biopsy, typically in young women with other autoimmune disease.
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Autoimmune hepatitis type 1 (adults) is linked to ANA and anti-smooth muscle antibodies; type 2 (children, more aggressive) to ______ antibodies.
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anti-LKM1
Why? AIH also shows a raised IgG and interface hepatitis with plasma cells on biopsy, typically in young women with other autoimmune disease.
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What is the first-line treatment of autoimmune hepatitis?
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A corticosteroid (prednisolone) plus azathioprine.
Why? Immunosuppression controls the T-cell attack on hepatocytes; azathioprine is steroid-sparing and continues as maintenance. Liver transplant is for liver failure.
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Drug-induced liver injury is hepatocellular if ALT is at least ______ × ULN and cholestatic if ALP is at least 2 × ULN.
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5
Why? The pattern helps identify the likely culprit drug.
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Drug-induced liver injury is hepatocellular if ALT is at least 5 × ULN and cholestatic if ALP is at least ______ × ULN.
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2
Why? The pattern helps identify the likely culprit drug.
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Which commonly used antibiotic is a classic cause of cholestatic jaundice that may appear weeks after the course ends?
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Co-amoxiclav (the clavulanic acid component).
Why? The reaction can be delayed up to about 6 weeks. Flucloxacillin causes a similar delayed cholestatic hepatitis.
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Which antibody is positive in about 95% of patients with primary biliary cholangitis?
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Anti-mitochondrial antibody (AMA, M2 subtype).
Why? PBC is autoimmune destruction of small intrahepatic bile ducts, mostly in middle-aged women. IgM is raised and ALP/GGT are high.
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What is the first-line drug treatment for primary biliary cholangitis?
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Ursodeoxycholic acid (UDCA).
Why? UDCA is a hydrophilic bile acid that improves bile flow and slows progression.
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What is the first-line diagnostic test for primary sclerosing cholangitis, and the classic finding?
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MRCP – multifocal strictures and dilatations of the bile ducts ('beading').
Why? PSC is a large-duct disease, so it is seen on cholangiography; AMA is negative, p-ANCA is often positive.
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Which malignancy is most strongly associated with primary sclerosing cholangitis?
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Cholangiocarcinoma.
Why? Chronic biliary inflammation drives malignant change. PSC also raises the risk of gallbladder and colorectal cancer.
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What is the treatment of an amoebic liver abscess?
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Metronidazole (or tinidazole), followed by a luminal agent such as paromomycin or diloxanide furoate.
Why? Metronidazole kills invasive trophozoites; the luminal agent clears cysts from the gut to prevent relapse. Surgery is rarely needed.
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Why is diagnostic needle aspiration of a suspected hydatid liver cyst avoided?
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Spillage of cyst contents can cause anaphylaxis (and seed new cysts).
Why? Echinococcus cysts (from dogs/sheep) show eggshell calcification and daughter cysts. Treatment is albendazole with surgery, or a planned percutaneous drainage technique (PAIR) under albendazole cover in selected cysts.