A 50-year-old chronic alcoholic presents with acute pancreatitis. The mechanism of pancreatic acinar cell injury in alcohol-induced acute pancreatitis primarily involves:
- A Direct toxic effect of ethanol metabolites causing premature intracellular activation of trypsinogen ✓
- B Gallstones obstructing the pancreatic duct and causing bile reflux
- C Parasympathetic hyperstimulation causing excessive zymogen secretion
- D Autoimmune attack by IgG4-positive plasma cells on pancreatic ductal epithelium
Correct answer: A. Direct toxic effect of ethanol metabolites causing premature intracellular activation of trypsinogen
Explanation
Alcohol and its metabolites (acetaldehyde, fatty acid ethyl esters) directly injure acinar cells by causing premature co-localization and fusion of zymogen granules with lysosomes (co-localization hypothesis), resulting in intracellular activation of trypsinogen to trypsin within the acinar cell itself — initiating the autodigestive cascade. Gallstone pancreatitis involves ductal obstruction and possibly bile reflux, but this is the mechanism for gallstone (not alcohol) pancreatitis. IgG4 plasma cells are the hallmark of autoimmune pancreatitis (Type 1).
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.