Cirrhosis

Cirrhosis is the final common pathway of chronic liver injury: ongoing inflammation and hepatocyte death trigger fibrosis, and the liver's architecture is progressively replaced by bands of scar tissue surrounding regenerative nodules. The result is a shrunken, firm, nodular liver that can neither perform its metabolic functions nor allow blood to flow through it normally.

The leading causes are chronic alcohol use, chronic viral hepatitis (hepatitis B and C), and metabolic dysfunction-associated steatotic liver disease (fatty liver disease); less common causes include autoimmune hepatitis, hemochromatosis, Wilson disease, and biliary diseases. Whatever the insult, the fibrotic remodeling is largely irreversible once established.

Cirrhosis produces two overlapping problem sets. Loss of hepatocyte function causes decreased albumin (edema), impaired clotting factor synthesis (bleeding), jaundice, and failure to detoxify ammonia (hepatic encephalopathy). Scarring also raises resistance to portal blood flow, producing portal hypertension — the source of esophageal varices, ascites, splenomegaly, and caput medusae. Compensated cirrhosis may be silent for years; decompensation is marked by variceal bleeding, ascites, or encephalopathy, and cirrhosis also predisposes to hepatocellular carcinoma.

The USMLE Step 1 tests cirrhosis extensively — its causes, the pathophysiology of portal hypertension, and the mechanism behind each complication. The CCMA exam covers cirrhosis among the accessory organ diseases a medical assistant should recognize, including its association with alcohol use and hepatitis.