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| Acute Pancreatitis |
| Etiology • May be due to infection, ischemia, drug toxicity • Associated with alcohol and gallstones |
| Pathogenesis • Acinar cells release enzymes resulting in proteolysis, lipolysis and hemorrhage • Proposed mechanisms include duct obstruction leading to secondary acinar cell injury, direct acinar cell toxicity, or aberrant intracellular transport, |
| Epidemiology • Adults • 80% associated with alcohol or cholelithiasis |
| General Gross Description • Firm, edematous organ with foci of hemorrhage and yellow white fat necrosis • If completely necrotic will be soft, flabby and hemorrhagic |
| General Microscopic Description • Necrosis including fat with ghost-like cell outlines • Dense neutrophilic infiltrate • Hemorrhage |
| Clinical Correlation • Epigastric pain radiating to the back relieved by sitting up • Elevated pancreatic enzymes in serum • May be catastrophic with adult respiratory distress syndrome, DIC and shock |
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 899-902. |
| Acute Pancreatitis |
| Synopsis by: Melinda Sanders M.D. (T59000M41600)[52] |
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