Acute pancreatitis results from premature activation of pancreatic enzymes (particularly trypsinogen to trypsin) within the pancreatic parenchyma, leading to autodigestion. The two most common etiologies are gallstones (40%) impacting the ampulla of Vater and causing bile reflux into the pancreatic duct, and alcohol (40%) causing direct toxic injury to acinar cells and increased zymogens. Premature trypsin activation triggers a cascade: trypsin activates other zymogens (elastase, phospholipase, lipase), elastase digests blood vessel walls causing hemorrhage, lipase digests peripancreatic fat causing fat necrosis and saponification (calcium binding to fatty acids, causing hypocalcemia), and phospholipase damages cell membranes. The massive inflammatory response releases cytokines (TNF-alpha, IL-1, IL-6) into systemic circulation, potentially causing SIRS, multiorgan failure, and ARDS. Cullen sign (periumbilical ecchymosis) and Grey Turner sign (flank ecchymosis) indicate retroperitoneal hemorrhage from severe necrotizing pancreatitis. Ranson criteria at admission and at 48 hours predict severity and mortality.