Renal and acid–base: NSAID plus ACE inhibitor in volume depletion: 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 · Renal and acid–base: NSAID plus ACE inhibitor in volume depletion

Sample item

A 70-year-old man with diarrhoea who takes an ACE inhibitor and ibuprofen develops acute kidney injury. Which combination of effects on glomerular arterioles explains the fall in GFR?

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

The answer and the reasoning

B. Loss of prostaglandin-mediated afferent dilatation and of angiotensin II efferent constriction

In volume depletion, GFR is held up by prostaglandin-mediated afferent dilatation and angiotensin II-mediated efferent constriction. An NSAID removes the first and an ACE inhibitor removes the second, so glomerular pressure collapses. The injury is haemodynamic and usually reverses when the drugs are stopped.

Option by option

  • A. Direct toxicity to the glomerular basement membrane

    This is haemodynamic and not a structural basement membrane injury.

  • B. Loss of prostaglandin-mediated afferent dilatation and of angiotensin II efferent constriction (correct)

    Correct. Both compensatory arteriolar responses are blocked, so filtration pressure falls.

  • C. Loss of angiotensin II afferent constriction and prostaglandin efferent dilatation

    Angiotensin II constricts the efferent arteriole predominantly; this pairing has the roles reversed.

  • D. Excess afferent dilatation with efferent dilatation

    Dilating both arterioles would not cause such a fall in GFR when volume is low.

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 B, Loss of prostaglandin-mediated afferent dilatation and of angiotensin II efferent constriction. In volume depletion, GFR is held up by prostaglandin-mediated afferent dilatation and angiotensin II-mediated efferent constriction.

Why is "Direct toxicity to the glomerular basement membrane" not the answer?

This is haemodynamic and not a structural basement membrane injury.

Why is "Loss of angiotensin II afferent constriction and prostaglandin effere…" not the answer?

Angiotensin II constricts the efferent arteriole predominantly; this pairing has the roles reversed.

Why is "Excess afferent dilatation with efferent dilatation" not the answer?

Dilating both arterioles would not cause such a fall in GFR when volume is low.

What concept does this question test?

It tests Renal and acid–base: NSAID plus ACE inhibitor in volume depletion in Physiology. An NSAID removes the first and an ACE inhibitor removes the second, so glomerular pressure collapses. The injury is haemodynamic and usually reverses when the drugs are stopped.

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 Renal and acid–base: NSAID plus ACE inhibitor in volume depletion?

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.