Cirrhosis represents irreversible hepatic fibrosis where regenerative nodules replace normal lobular architecture. Portal hypertension develops when fibrotic tissue increases intrahepatic vascular resistance (sinusoidal pressure >5 mmHg gradient). This drives formation of portosystemic collaterals, most dangerously esophageal varices. Decreased hepatocyte mass reduces albumin synthesis (oncotic pressure falls, causing ascites and edema), clotting factor production (coagulopathy), bile conjugation (jaundice), and ammonia metabolism to urea (hepatic encephalopathy). Hepatorenal syndrome occurs when severe portal hypertension causes splanchnic vasodilation, reducing effective circulating volume and triggering renal vasoconstriction. The nurse must manage fluid overload with diuretics, titrate lactulose for encephalopathy, monitor for variceal hemorrhage, coordinate paracentesis, and implement bleeding precautions.