Pancreatitis

Acute pancreatitis involves premature intracellular activation of trypsinogen to trypsin, initiating a proteolytic cascade that autodigests pancreatic parenchyma. The two predominant etiologies are biliary (gallstone impaction at the ampulla of Vater, 40%) and alcoholic (direct acinar cell toxicity, 30%). Trypsin activation triggers complement and kinin cascades, releasing proinflammatory cytokines (TNF-α, IL-1β, IL-6) that produce a systemic inflammatory response. Third-space fluid losses can exceed 6-8 liters in severe cases. The revised Atlanta classification distinguishes mild (no organ failure), moderately severe (transient organ failure <48 hours), and severe (persistent organ failure >48 hours) pancreatitis. Chronic pancreatitis results in progressive fibrosis with loss of exocrine function (steatorrhea, malabsorption) and endocrine function (pancreatogenic diabetes, type 3c). The clinician must classify severity using validated scoring systems, prescribe goal-directed fluid therapy, manage complications including infected necrosis, and coordinate long-term enzyme replacement and lifestyle modification.