Q1. A serum-ascites albumin gradient (SAAG) of 15 g/L indicates: A. Portal hypertension B. Peritoneal malignancy C. Tuberculous peritonitis D. Nephrotic syndrome ANSWER: A — portal hypertension. Why: a SAAG of 11 g/L or more indicates portal hypertension, most often from cirrhosis. A low gradient points to malignancy, TB, pancreatitis or nephrotic syndrome. LEARNING POINT: the gradient, not the ascitic protein, is the discriminating measurement.

Q2. Which finding in cirrhosis reflects PORTAL HYPERTENSION rather than synthetic failure? A. Prolonged prothrombin time B. Low serum albumin C. Splenomegaly with thrombocytopenia D. Jaundice ANSWER: C — splenomegaly with thrombocytopenia. Why: portal congestion enlarges the spleen, which then sequesters platelets (hypersplenism). A, B, D: all reflect lost synthetic or metabolic function. LEARNING POINT: sort every complication into "not working" or "blood not flowing through".

Q3. A cirrhotic patient with ascites is admitted confused. No fever, soft abdomen, creatinine risen from 80 to 150. The most important immediate investigation is: A. Serum ammonia B. Diagnostic ascitic tap C. CT head D. Repeat LFTs ANSWER: B — diagnostic ascitic tap. Why: SBP in cirrhosis is frequently painless and afebrile, presenting only as encephalopathy or renal impairment. Ascitic neutrophils ≥ 250/mm³ make the diagnosis. A: ammonia correlates poorly and does not change management. LEARNING POINT: decompensation is precipitated — find the trigger rather than treating the symptom alone.

Q4. A cirrhotic with an INR of 2.0 is NOT bleeding and requires a paracentesis. Regarding fresh frozen plasma: A. Give it routinely to correct the INR first B. It is not routinely required — haemostasis is rebalanced and the INR overstates bleeding risk C. Give it only if platelets are also low D. Give twice the usual dose ANSWER: B. Why: cirrhosis reduces both procoagulant and anticoagulant factors. The INR measures only one side, so it does not predict bleeding as it does in other patients, and these patients also thrombose. LEARNING POINT: do not transfuse to correct a number that is not measuring what you think it measures.

Q5. A cirrhotic patient presents with haematemesis. In addition to resuscitation, terlipressin and endoscopy, which is ESSENTIAL? A. Prophylactic antibiotics B. High-volume transfusion to Hb 12 g/dL C. Intravenous vitamin K alone D. Immediate TIPS in all cases ANSWER: A — prophylactic antibiotics. Why: every cirrhotic with a GI bleed should receive antibiotics, which reduce infection, rebleeding and mortality. B: over-transfusion raises portal pressure and can worsen bleeding; a restrictive strategy is preferred. LEARNING POINT: the most commonly omitted correct answer in this scenario.

Q6. A cirrhotic with ascites takes ibuprofen for a week. Creatinine rises from 90 to 250 with a bland urinalysis. The mechanism is: A. Direct tubular toxicity from ibuprofen B. Loss of prostaglandin-mediated renal vasodilation in a circulation dependent on it C. Obstructive uropathy D. Glomerulonephritis ANSWER: B. Why: in advanced cirrhosis, splanchnic vasodilation reduces effective circulating volume, and renal perfusion becomes dependent on prostaglandin-mediated vasodilation. NSAIDs block prostaglandin synthesis and precipitate renal failure. D: would give an active sediment, not a bland one. LEARNING POINT: NSAIDs should be avoided in cirrhosis. This is also a classic route into hepatorenal syndrome.

Q7. For secondary prevention after a variceal bleed, which beta-blocker is appropriate? A. Bisoprolol B. Atenolol C. Propranolol D. Metoprolol ANSWER: C — Propranolol (non-selective). Why: reducing portal pressure requires beta-2 blockade — unopposed alpha-mediated splanchnic vasoconstriction reduces portal inflow. Cardioselective agents block only beta-1 and do not achieve this. A, B, D: all cardioselective. LEARNING POINT: the same selectivity logic as the beta-blockers chapter, applied to a different organ.