Hypertensive disorders: mechanism of aspirin prophylaxis: practice question

A OBG 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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OBG · Hypertensive disorders: mechanism of aspirin prophylaxis

Sample item

Low-dose aspirin reduces the risk of pre-eclampsia in high-risk women. Which mechanism explains this?

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

The answer and the reasoning

C. Selective inhibition of platelet thromboxane A2 synthesis, restoring the thromboxane-prostacyclin balance

In pre-eclampsia thromboxane A2, a vasoconstrictor and platelet aggregator, dominates over prostacyclin. Low-dose aspirin irreversibly inhibits platelet cyclo-oxygenase and spares endothelial prostacyclin, so the balance shifts towards vasodilatation. It is started early in the second trimester or before, in high-risk women.

Option by option

  • A. Inhibition of endothelial prostacyclin synthesis

    Aspirin does not inhibit endothelial prostacyclin at low dose; blocking it would worsen the imbalance.

  • B. Direct reduction of circulating sFlt-1

    Aspirin has no direct action on circulating sFlt-1.

  • C. Selective inhibition of platelet thromboxane A2 synthesis, restoring the thromboxane-prostacyclin balance (correct)

    Correct. Low doses inhibit platelet thromboxane while sparing prostacyclin.

  • D. Blockade of angiotensin II receptors in the uterine vessels

    Angiotensin receptor blockers act on the renin-angiotensin system and are contraindicated in pregnancy.

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 OBG question

What is the answer to this OBG question?

The best answer is C, Selective inhibition of platelet thromboxane A2 synthesis, restoring the thromboxane-prostacyclin balance. In pre-eclampsia thromboxane A2, a vasoconstrictor and platelet aggregator, dominates over prostacyclin.

Why is "Inhibition of endothelial prostacyclin synthesis" not the answer?

Aspirin does not inhibit endothelial prostacyclin at low dose; blocking it would worsen the imbalance.

Why is "Direct reduction of circulating sFlt-1" not the answer?

Aspirin has no direct action on circulating sFlt-1.

Why is "Blockade of angiotensin II receptors in the uterine vessels" not the answer?

Angiotensin receptor blockers act on the renin-angiotensin system and are contraindicated in pregnancy.

What concept does this question test?

It tests Hypertensive disorders: mechanism of aspirin prophylaxis in OBG. Low-dose aspirin irreversibly inhibits platelet cyclo-oxygenase and spares endothelial prostacyclin, so the balance shifts towards vasodilatation. It is started early in the second trimester or before, in high-risk women.

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 Hypertensive disorders: mechanism of aspirin prophylaxis?

Learn management algorithms as steps: PPH, eclampsia, ectopic pregnancy. Then use the flashcards and the other OBG 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.