Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum from simple hepatic steatosis (fat accumulation in more than 5% of hepatocytes without significant inflammation) to non-alcoholic steatohepatitis (NASH, steatosis with lobular inflammation, hepatocyte ballooning, and progressive fibrosis) to cirrhosis and hepatocellular carcinoma. The pathogenesis is explained by the multiple-hit hypothesis: the first hit involves hepatic triglyceride accumulation driven by insulin resistance — hyperinsulinemia increases hepatic de novo lipogenesis via SREBP-1c activation while impairing fatty acid beta-oxidation and VLDL export. Subsequent hits include lipotoxicity from free fatty acids and their metabolites (diacylglycerols, ceramides, lysophosphatidylcholine) that activate hepatocyte endoplasmic reticulum stress, mitochondrial dysfunction, and oxidative stress through reactive oxygen species (ROS) generation. These processes trigger hepatocyte apoptosis and necroptosis, which activate Kupffer cells (resident hepatic macrophages) and hepatic stellate cells. Activated stellate cells transform into myofibroblasts and deposit extracellular matrix (collagen I and III), producing progressive fibrosis that is staged histologically from F0 (no fibrosis) through F4 (cirrhosis). Fibrosis stage is the strongest predictor of liver-related morbidity and mortality, making accurate staging essential. Non-invasive fibrosis assessment uses composite scoring systems (FIB-4 index combining...