Gastrointestinal physiology: Helicobacter pylori and gastrin: 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 · Gastrointestinal physiology: Helicobacter pylori and gastrin

Sample item

A 40-year-old man with duodenal ulcer has antral-predominant Helicobacter pylori infection, a raised fasting gastrin and high acid output. A secretin stimulation test does not raise gastrin. What is the mechanism of the hypergastrinaemia?

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

The answer and the reasoning

A. Antral inflammation reduces somatostatin from D cells, removing inhibition of gastrin release

Antral infection lowers D-cell somatostatin and raises antral pH through ammonia production, both of which release G cells from inhibition. Gastrin and acid output rise, favouring duodenal ulcer. In a gastrinoma secretin paradoxically raises gastrin; here it does not.

Option by option

  • A. Antral inflammation reduces somatostatin from D cells, removing inhibition of gastrin release (correct)

    Correct. Reduced somatostatin disinhibits gastrin release.

  • B. Increased secretin release from duodenal S cells

    Secretin inhibits gastrin release in normal subjects.

  • C. Destruction of parietal cells causing achlorhydria

    Achlorhydria raises gastrin but would lower acid output, which is not seen here.

  • D. Autonomous gastrin secretion by a pancreatic tumour

    A gastrinoma would show a gastrin rise after secretin.

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, Antral inflammation reduces somatostatin from D cells, removing inhibition of gastrin release. Antral infection lowers D-cell somatostatin and raises antral pH through ammonia production, both of which release G cells from inhibition.

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

Secretin inhibits gastrin release in normal subjects.

Why is "Destruction of parietal cells causing achlorhydria" not the answer?

Achlorhydria raises gastrin but would lower acid output, which is not seen here.

Why is "Autonomous gastrin secretion by a pancreatic tumour" not the answer?

A gastrinoma would show a gastrin rise after secretin.

What concept does this question test?

It tests Gastrointestinal physiology: Helicobacter pylori and gastrin in Physiology. Gastrin and acid output rise, favouring duodenal ulcer. In a gastrinoma secretin paradoxically raises gastrin; here it does not.

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 Gastrointestinal physiology: Helicobacter pylori and gastrin?

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.