Portal hypertension in cirrhosis results from increased intrahepatic resistance (structural: fibrosis, nodular distortion; dynamic: stellate cell contraction from decreased nitric oxide and increased endothelin-1) and increased portal blood flow (splanchnic vasodilation from excessive nitric oxide production in the mesenteric circulation). When the hepatic venous pressure gradient (HVPG) exceeds 10 mmHg, portosystemic collaterals develop at sites of portal-systemic anastomosis: esophageal varices (left gastric vein → esophageal veins), caput medusae (paraumbilical veins), hemorrhoids (superior → inferior rectal veins), and retroperitoneal shunts. Splanchnic vasodilation reduces effective arterial blood volume, triggering RAAS activation, sympathetic nervous system stimulation, and ADH release, causing renal sodium and water retention (ascites) and ultimately hepatorenal syndrome.