Cirrhosis represents the final common pathway of chronic liver injury, characterized by diffuse fibrosis, regenerative nodules, and distortion of hepatic vasculature. The hepatic stellate cell is the key mediator of fibrogenesis, transforming from a quiescent vitamin A-storing cell to an activated myofibroblast that produces excess collagen. Portal hypertension develops when the hepatic venous pressure gradient (HVPG) exceeds 5 mmHg; clinically significant portal hypertension occurs at ≥10 mmHg, and variceal hemorrhage risk increases at ≥12 mmHg. Decompensation is defined by the development of ascites, variceal hemorrhage, encephalopathy, or jaundice. The clinician must calculate MELD-Na scores for transplant prioritization, prescribe evidence-based pharmacotherapy for each complication, manage primary and secondary variceal prophylaxis, initiate SBP prophylaxis, and coordinate multidisciplinary hepatology care including transplant evaluation.