GI physiology: Zollinger-Ellison syndrome: practice question

A Physiology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Physiology · GI physiology: Zollinger-Ellison syndrome

Sample item

A 42-year-old man has recurrent duodenal and jejunal ulcers, and fatty, loose stools. Fasting gastrin is markedly raised and gastric pH is 1.5. Which mechanism best explains his steatorrhoea?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

A. Acid load lowers duodenal pH, which inactivates pancreatic lipase and precipitates bile salts

A gastrinoma secretes gastrin autonomously and drives massive acid output that overwhelms pancreatic bicarbonate neutralisation. The low intraluminal pH inactivates pancreatic lipase and precipitates bile acids, so micelle formation and fat digestion fail. Mucosal injury adds to the malabsorption, and proton pump inhibitors correct the diarrhoea.

Option by option

  • A. Acid load lowers duodenal pH, which inactivates pancreatic lipase and precipitates bile salts (correct)

    Excess acid inactivates lipase and bile salts in the small bowel lumen.

  • B. Loss of ileal bile salt absorption

    Ileal disease is not part of the syndrome; bile salt loss is not the cause.

  • C. Absence of secretin release from duodenal S cells

    Secretin release is stimulated by the acid, not absent.

  • D. Failure of pancreatic lipase secretion from acinar destruction

    The pancreas is structurally normal in this condition, and enzyme secretion is intact.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is A, Acid load lowers duodenal pH, which inactivates pancreatic lipase and precipitates bile salts. A gastrinoma secretes gastrin autonomously and drives massive acid output that overwhelms pancreatic bicarbonate neutralisation.

Why is "Loss of ileal bile salt absorption" not the answer?

Ileal disease is not part of the syndrome; bile salt loss is not the cause.

Why is "Absence of secretin release from duodenal S cells" not the answer?

Secretin release is stimulated by the acid, not absent.

Why is "Failure of pancreatic lipase secretion from acinar destruction" not the answer?

The pancreas is structurally normal in this condition, and enzyme secretion is intact.

What concept does this question test?

It tests GI physiology: Zollinger-Ellison syndrome in Physiology. The low intraluminal pH inactivates pancreatic lipase and precipitates bile acids, so micelle formation and fat digestion fail. Mucosal injury adds to the malabsorption, and proton pump inhibitors correct the diarrhoea.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study GI physiology: Zollinger-Ellison syndrome?

For each system, sketch the key graph (pressure–volume loop, oxygen dissociation curve, nephron handling) and explain it aloud. Then use the flashcards and the other Physiology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.