Cirrhosis & its complications flashcards
17 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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Name the five components of the Child–Pugh score.
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Bilirubin, albumin, prothrombin time (INR), ascites and encephalopathy.
Why? Each scores 1–3; total grades cirrhosis as Child's A (5–6), B (7–9) or C (10+), which predicts survival.
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A serum–ascites albumin gradient (SAAG) of 11 g/L or more indicates what?
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Portal hypertension (e.g. cirrhosis, cardiac ascites, Budd–Chiari).
Why? High hydrostatic pressure pushes out fluid with little protein, so the serum–ascites albumin difference is large. A low SAAG suggests peritoneal disease (malignancy, TB), pancreatitis or nephrotic syndrome.
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What is the first-line diuretic for ascites due to cirrhosis?
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Spironolactone (an aldosterone antagonist), with furosemide added if needed.
Why? Cirrhotic ascites is driven by secondary hyperaldosteronism and sodium retention. Also restrict dietary sodium (about 2 g/day).
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After large-volume paracentesis of more than 5 litres, what is given and at what dose?
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Human albumin solution (20%), 8 g per litre of ascites removed.
Why? Albumin prevents post-paracentesis circulatory dysfunction and renal failure.
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Which ascitic fluid result diagnoses spontaneous bacterial peritonitis?
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Ascitic neutrophil count of 250 cells/mm³ or more.
Why? Start treatment immediately – do not wait for culture. The most common organism is E. coli.
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What is the first-line treatment of spontaneous bacterial peritonitis?
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IV third-generation cephalosporin (cefotaxime or ceftriaxone) plus IV albumin.
Why? Albumin reduces the risk of hepatorenal syndrome and death. Ciprofloxacin is the alternative in penicillin allergy (avoid a quinolone if the patient was already on quinolone prophylaxis).
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Under NICE NG50 (2023), when should antibiotics be considered to PREVENT a first episode of SBP in cirrhosis with ascites?
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Not routinely. Consider them only if the person is at high risk (e.g. ascitic protein 15 g/L or less, Child–Pugh score above 9 or MELD above 16), or if an infection would seriously affect their care (e.g. awaiting transplant or TIPSS).
Why? NICE found no overall benefit from routine prophylaxis and worries about resistance and fluoroquinolone harms. If given, follow local microbiology advice and continue until the ascites resolves.
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What is the first-line drug for hepatic encephalopathy, and how does it work?
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Lactulose – it acidifies the colon, converting ammonia (NH₃) to non-absorbable ammonium (NH₄⁺), and speeds transit.
Why? Less ammonia reaches the brain. Always look for and treat the precipitant (infection, GI bleed, constipation, electrolytes, sedatives).
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Which antibiotic is added to lactulose to prevent recurrent hepatic encephalopathy?
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Rifaximin.
Why? It is a poorly absorbed antibiotic that reduces ammonia-producing gut bacteria.
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What is the first-line drug treatment of hepatorenal syndrome (HRS-AKI)?
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Terlipressin plus IV albumin (after stopping diuretics and treating precipitants such as SBP).
Why? Terlipressin reverses splanchnic vasodilatation and albumin expands volume, improving renal perfusion. Liver transplant is the only cure.
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What is the most common complication after a TIPSS procedure?
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Hepatic encephalopathy.
Why? The shunt lets ammonia-rich portal blood bypass the liver. Severe encephalopathy is therefore a contraindication, along with severe heart failure and sepsis.
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A 32-year-old woman with polycythaemia vera develops sudden RUQ pain, tender hepatomegaly and ascites. What is the first-line investigation?
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Doppler ultrasound of the hepatic veins.
Why? This is Budd–Chiari syndrome (hepatic venous outflow obstruction). Doppler shows absent or reduced hepatic vein flow, thrombus and collaterals.
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How are people with cirrhosis screened for hepatocellular carcinoma?
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Liver ultrasound every 6 months, with or without serum AFP.
Why? Small tumours found early can be resected, ablated or transplanted. A lesion of 1 cm or more, or rising AFP, needs multiphase CT or MRI.
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In the BCLC staging of HCC, very early/early disease is treated with resection, ablation or transplant; intermediate (BCLC B) with ______; advanced (BCLC C) with systemic therapy.
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transarterial chemoembolisation (TACE)
Why? BCLC combines tumour burden, liver function and performance status. In the UK, first-line systemic options include atezolizumab plus bevacizumab (Child–Pugh A, ECOG 0–1) or durvalumab plus tremelimumab; lenvatinib is another option.
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In the BCLC staging of HCC, very early/early disease is treated with resection, ablation or transplant; intermediate (BCLC B) with transarterial chemoembolisation (TACE); advanced (BCLC C) with ______.
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systemic therapy
Why? BCLC combines tumour burden, liver function and performance status. In the UK, first-line systemic options include atezolizumab plus bevacizumab (Child–Pugh A, ECOG 0–1) or durvalumab plus tremelimumab; lenvatinib is another option.
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King's College criteria for transplant in paracetamol-induced liver failure: arterial pH below ______ after resuscitation, OR all of INR above 6.5, creatinine above 300 µmol/L and grade 3–4 encephalopathy.
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7.3
Why? These identify patients unlikely to survive without urgent transplant.
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King's College criteria for transplant in paracetamol-induced liver failure: arterial pH below 7.3 after resuscitation, OR all of INR above ______, creatinine above 300 µmol/L and grade 3–4 encephalopathy.
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6.5
Why? These identify patients unlikely to survive without urgent transplant.