Preparatory Mindset

The liver has remarkable regenerative capacity — that's why patients often present LATE when damage is extensive. Think in terms of: hepatitis (inflammation → viral, alcoholic, drug-induced), cirrhosis (fibrosis → end-stage), and liver failure (loss of synthetic AND metabolic function). Key labs: ALT/AST (hepatocellular damage), ALP/GGT (cholestasis), bilirubin (excretion), PT/INR (synthetic function).

Core Concepts

• Liver has synthetic (albumin, clotting factors), metabolic (bilirubin, ammonia, drug metabolism), and excretory (bile) functions.


• Hepatitis: inflammation from viruses (HAV, HBV, HCV), alcohol, drugs.


• Cirrhosis: irreversible fibrosis → nodular regeneration → portal hypertension.


• Portal hypertension → varices (bleeding), ascites (fluid), splenomegaly, portosystemic shunts (encephalopathy).


• Jaundice: pre-hepatic (unconjugated bilirubin, hemolysis), hepatic (mixed), post-hepatic (conjugated, obstruction).


• Liver enzymes: ALT/AST (hepatocellular), ALP/GGT (cholestasis)..

High-Yield Points

• ALT/AST: hepatocellular damage (AST:ALT >2 in alcoholic hepatitis)


• ALP/GGT: cholestasis (obstruction)


• Bilirubin: unconjugated (hemolysis, Gilbert) vs conjugated (obstruction, hepatocellular)


• PT/INR: measures synthetic function — prolonged in liver failure


• Cirrhosis → portal hypertension → varices, ascites, splenomegaly


• Hepatic encephalopathy: ammonia hypothesis — treated with lactulose

Topic Summary

Liver pathology ranges from acute hepatitis (reversible) to cirrhosis (irreversible fibrosis) to liver failure (loss of function). Jaundice, ascites, coagulopathy, and encephalopathy are key clinical features.