A 55-year-old chronic alcoholic presents with sudden severe upper abdominal pain radiating to the back, vomiting, and elevated serum lipase (6x upper limit of normal). CT scan shows pancreatic necrosis involving 40% of the gland with peripancreatic fat stranding. The RANSON criteria score is 4. Which sequence of pathological events is MOST correct in severe acute pancreatitis?

• A Islet cell destruction → glucagon release → vasodilation → fat necrosis
• B Acinar cell injury → duct obstruction → activation of trypsinogen to trypsin within pancreas → autodigestion → sterile necrosis → systemic SIRS ✓
• C Pancreatic lipase release → saponification of peripancreatic fat → hypocalcemia → acinar cell death
• D Trypsin activation → duct rupture → ascites formation → protein-losing enteropathy

Explanation

The central event in acute pancreatitis is premature intrapancreatic activation of trypsinogen to trypsin (normally activated only in the duodenal lumen). Trypsin then activates other zymogens (elastase, phospholipase A2, lipase), causing autodigestion of the gland — characteristic fat necrosis (with chalky-white saponification due to calcium soap formation from lipase) and coagulative necrosis of parenchyma. Systemic activation of inflammatory mediators causes SIRS, ARDS, and multi-organ failure. Hypocalcemia occurs due to calcium chelation by free fatty acids (saponification), which is an important prognostic marker in Ranson criteria.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.