Chronic Liver Disease Complications Flashcards
7 cards from real Internal Medicine Exam practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.
Read the first 7 Chronic Liver Disease Complications flashcards as text
A cirrhotic patient develops sudden onset of right-sided pleural effusion. Thoracentesis reveals transudative fluid with SAAG >1.1. No pulmonary pathology is identified. What is the diagnosis?
Answer: Hepatic hydrothorax
Hepatic hydrothorax is a transudative pleural effusion (usually right-sided) caused by passage of ascitic fluid through diaphragmatic defects in cirrhotic patients.
Which of the following best explains thrombocytopenia in patients with cirrhosis and portal hypertension?
Answer: Splenic sequestration due to splenomegaly
Splenomegaly from portal hypertension causes splenic sequestration of platelets, and reduced thrombopoietin synthesis by the liver also contributes.
A patient with cirrhosis develops rapidly progressive renal failure. Terlipressin plus albumin is started. What is the proposed mechanism of terlipressin in hepatorenal syndrome?
Answer: Causes splanchnic vasoconstriction, reducing portal pressure and improving renal perfusion
Terlipressin is a vasopressin analogue that constricts splanchnic vasculature, reduces portal hypertension-driven vasodilation, and improves systemic and renal perfusion.
Which screening test is recommended every 6 months for hepatocellular carcinoma surveillance in patients with cirrhosis?
Answer: Liver ultrasound with or without AFP
AASLD guidelines recommend abdominal ultrasound every 6 months, with optional AFP, for HCC surveillance in cirrhotic patients.
A cirrhotic patient develops bilateral lower extremity edema and tense ascites. Serum albumin is 1.9 g/dL. Which mechanism primarily drives ascite formation in this scenario?
Answer: Sinusoidal hypertension and splanchnic vasodilation with sodium and water retention
The "peripheral vasodilation hypothesis" holds that portal hypertension-driven splanchnic vasodilation leads to RAAS and SNS activation, causing renal sodium and water retention and ascites formation.
A 58-year-old with hepatitis C cirrhosis is prescribed rifaximin for secondary prophylaxis of hepatic encephalopathy. What is rifaximin's primary mechanism of action?
Answer: Non-absorbable antibiotic that reduces ammonia-producing gut bacteria
Rifaximin is a non-absorbable antibiotic that reduces the ammonia-producing gut bacteria, lowering portal ammonia load and decreasing recurrent encephalopathy episodes.
Which of the following best describes the 'washout' appearance of hepatocellular carcinoma on contrast-enhanced MRI?
Answer: Arterial phase hyperenhancement followed by portal/delayed phase hypoenhancement
The LI-RADS criteria define HCC's hallmark as arterial hyperenhancement (APHE) followed by washout (hypoenhancement) in portal venous or delayed phases.