GI physiology: mucosal defence: 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: mucosal defence

Sample item

A 58-year-old man taking diclofenac for arthritis presents with epigastric pain and an antral ulcer. Which mechanism of mucosal damage is most directly responsible?

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

The answer and the reasoning

C. Inhibition of COX-1, with reduced prostaglandin-mediated mucus, bicarbonate and mucosal blood flow

Prostaglandins E2 and I2 produced by COX-1 stimulate mucus and bicarbonate secretion, maintain mucosal blood flow and inhibit acid secretion. NSAIDs inhibit COX-1 and remove these defences, so acid and pepsin injure the mucosa. Misoprostol, a prostaglandin E1 analogue, or proton pump inhibitors can be used for gastroprotection.

Option by option

  • A. Direct stimulation of gastrin release from antral G cells

    NSAIDs do not directly stimulate gastrin release.

  • B. Inhibition of the H-K ATPase of parietal cells

    H-K ATPase inhibition reduces acid and is the action of proton pump inhibitors, which would heal ulcers.

  • C. Inhibition of COX-1, with reduced prostaglandin-mediated mucus, bicarbonate and mucosal blood flow (correct)

    Loss of prostaglandin-mediated protection is the main NSAID mechanism.

  • D. Increased secretion of intrinsic factor

    Intrinsic factor secretion is unrelated to NSAID ulceration.

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 C, Inhibition of COX-1, with reduced prostaglandin-mediated mucus, bicarbonate and mucosal blood flow. Prostaglandins E2 and I2 produced by COX-1 stimulate mucus and bicarbonate secretion, maintain mucosal blood flow and inhibit acid secretion.

Why is "Direct stimulation of gastrin release from antral G cells" not the answer?

NSAIDs do not directly stimulate gastrin release.

Why is "Inhibition of the H-K ATPase of parietal cells" not the answer?

H-K ATPase inhibition reduces acid and is the action of proton pump inhibitors, which would heal ulcers.

Why is "Increased secretion of intrinsic factor" not the answer?

Intrinsic factor secretion is unrelated to NSAID ulceration.

What concept does this question test?

It tests GI physiology: mucosal defence in Physiology. NSAIDs inhibit COX-1 and remove these defences, so acid and pepsin injure the mucosa. Misoprostol, a prostaglandin E1 analogue, or proton pump inhibitors can be used for gastroprotection.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. 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: mucosal defence?

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.