Nose and paranasal sinuses: aspirin-exacerbated respiratory disease mechanism: practice question

A ENT 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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ENT · Nose and paranasal sinuses: aspirin-exacerbated respiratory disease mechanism

Sample item

A 38-year-old with asthma and recurrent nasal polyps develops wheeze and profuse rhinorrhoea 40 minutes after taking ibuprofen. What is the underlying mechanism?

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

The answer and the reasoning

B. COX-1 inhibition diverting arachidonic acid to excess leukotriene synthesis

In aspirin-exacerbated respiratory disease, blocking cyclo-oxygenase-1 removes prostaglandin E2, which normally restrains inflammation, and shunts arachidonic acid down the 5-lipoxygenase pathway to cysteinyl leukotrienes. These cause bronchoconstriction and sinonasal swelling. It is not a true allergy, so skin tests are not useful.

Option by option

  • A. IgE-mediated mast cell degranulation to the drug

    This is an idiosyncratic pharmacological reaction, not IgE-mediated hypersensitivity.

  • B. COX-1 inhibition diverting arachidonic acid to excess leukotriene synthesis (correct)

    Correct. COX-1 inhibition raises leukotrienes and lowers protective prostaglandin E2.

  • C. Overproduction of prostaglandin E2

    Prostaglandin E2 is reduced, not raised, by these drugs.

  • D. Direct complement activation by the drug

    Complement activation is not the mechanism of this reaction.

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 ENT question

What is the answer to this ENT question?

The best answer is B, COX-1 inhibition diverting arachidonic acid to excess leukotriene synthesis. In aspirin-exacerbated respiratory disease, blocking cyclo-oxygenase-1 removes prostaglandin E2, which normally restrains inflammation, and shunts arachidonic acid down the 5-lipoxygenase pathway to cysteinyl leukotrienes.

Why is "IgE-mediated mast cell degranulation to the drug" not the answer?

This is an idiosyncratic pharmacological reaction, not IgE-mediated hypersensitivity.

Why is "Overproduction of prostaglandin E2" not the answer?

Prostaglandin E2 is reduced, not raised, by these drugs.

Why is "Direct complement activation by the drug" not the answer?

Complement activation is not the mechanism of this reaction.

What concept does this question test?

It tests Nose and paranasal sinuses: aspirin-exacerbated respiratory disease mechanism in ENT. These cause bronchoconstriction and sinonasal swelling. It is not a true allergy, so skin tests are not useful.

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 Nose and paranasal sinuses: aspirin-exacerbated respiratory disease mechanism?

Learn tuning fork results and audiogram patterns by sketching them. Then use the flashcards and the other ENT 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.