A 50-year-old alcoholic man develops acute pancreatitis. The proposed mechanism linking alcohol to acinar cell injury involves:
- A Direct viral cytopathic effect on acinar cells
- B Premature activation of trypsinogen to trypsin within acinar cells by cathepsin B released from co-localised lysosomes ✓
- C Autoimmune IgG4 antibody-mediated destruction of acinar cells
- D Parasympathetic overstimulation causing excessive zymogen secretion
Correct answer: B. Premature activation of trypsinogen to trypsin within acinar cells by cathepsin B released from co-localised lysosomes
Explanation
In alcohol-induced acute pancreatitis, ethanol and its metabolites cause abnormal co-localisation of zymogen granules with lysosomes within acinar cells. Cathepsin B, a lysosomal cysteine protease, prematurely activates trypsinogen to trypsin inside the acinar cell, initiating a cascade of autodigestion by activating other zymogens (chymotrypsin, elastase, phospholipase). This 'intracellular activation' hypothesis is the dominant pathophysiological mechanism. Autoimmune mechanisms cause IgG4-related pancreatitis (type 1 autoimmune pancreatitis).
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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