Clinical meaning
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).
Diagnosis & workup
Diagnostics & workup: - Serum lipase (preferred) >3x upper limit of normal is diagnostic - Serum amylase (less specific, also elevated in parotitis, bowel obstruction) - CT abdomen with IV contrast (Balthazar scoring for severity at 72 hrs) - MRCP for suspected biliary etiology or recurrent pancreatitis - Right upper quadrant ultrasound to evaluate for gallstones - Triglyceride level to rule out hypertriglyceridemia-induced pancreatitis - CRP at 48 hours (>150 mg/L predicts severe disease) - BUN, hematocrit trending for hemoconcentration (severity marker) - BISAP or Ranson criteria for prognostication