Acute pancreatitis results from premature activation of trypsinogen to trypsin within the pancreatic acinar cells, triggering autodigestion of the gland. Gallstones (40%) obstruct the ampulla of Vater causing bile reflux, while alcohol (40%) directly injures acinar cells and increases ductal permeability. Activated trypsin initiates a proteolytic cascade activating elastase (vessel wall destruction), phospholipase A2 (fat necrosis), and kallikrein (vasodilation, edema), leading to local inflammation, third-spacing, and potential systemic inflammatory response syndrome (SIRS). Chronic pancreatitis involves progressive fibrotic replacement of exocrine and endocrine tissue, resulting in malabsorption (steatorrhea) and eventual endocrine insufficiency (diabetes mellitus type 3c).