Physiology · GIT Physiology (Secretions, Hormones, Motility, Absorption)

A 48-year-old man with recurrent jejunal ulceration has fasting serum gastrin of 1200 pg/mL. He has steatorrhoea, yet faecal fat studies show his pancreatic lipase output after secretin stimulation is normal. The most likely explanation for his steatorrhoea is:

  • A Autoimmune destruction of I cells reducing CCK release
  • B Competitive inhibition of micelle formation by excess gastrin itself
  • C Acid inactivation of pancreatic lipase and precipitation of bile salts in the duodenum due to pH below 4
  • D Secondary lymphangiectasia obstructing lacteal drainage of chylomicrons
Correct answer: C. Acid inactivation of pancreatic lipase and precipitation of bile salts in the duodenum due to pH below 4

Explanation

In Zollinger-Ellison syndrome the massive acid load lowers duodenal pH below the optimum for lipase and precipitates glycine-conjugated bile salts, destroying mixed micelles even though enzyme secretion is normal. The pancreas works fine; the environment inactivates its products. This is why high-dose PPI therapy corrects the steatorrhoea.

Reference: Ganong's Review of Medical Physiology, 26th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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