Explain the major clinical consequences of portal hypertension in cirrhosis.

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Portal hypertension in cirrhosis stems from increased resistance to portal blood flow within the diseased liver, which raises portal venous pressure. That heightened pressure drives the main clinical problems: formation of portosystemic collaterals leading to varices, especially in the esophagus and stomach, which are prone to life‑threatening bleeding; accumulation of fluid in the abdomen (ascites) from increased hydrostatic pressure and neurohumoral sodium retention, along with reduced oncotic support from low albumin; and congestion of the spleen (splenomegaly) with hypersplenism, causing sequestration of blood cells and associated cytopenias. These interconnected changes explain why increased intrahepatic resistance translating into higher portal pressure results in variceal bleeding, ascites, and splenomegaly with hypersplenism—the major clinical consequences of portal hypertension in cirrhosis.