Eicosanoids: aspirin-exacerbated asthma: practice question

A Biochemistry 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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Biochemistry · Eicosanoids: aspirin-exacerbated asthma

Sample item

A 35-year-old woman with asthma and nasal polyps develops severe wheezing 30 minutes after taking aspirin. Which mechanism best explains this?

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

The answer and the reasoning

B. COX inhibition diverts arachidonic acid to the 5-lipoxygenase pathway, raising cysteinyl leukotrienes

Aspirin and other NSAIDs irreversibly or reversibly inhibit cyclooxygenase, reducing prostaglandins such as bronchoprotective PGE2. Arachidonic acid is shunted to 5-lipoxygenase, increasing LTC4, LTD4 and LTE4, which are potent bronchoconstrictors. The reaction is pharmacological and not IgE-mediated, and leukotriene receptor antagonists such as montelukast help.

Option by option

  • A. Aspirin inhibits 5-lipoxygenase and so removes leukotrienes

    Aspirin does not inhibit lipoxygenase; if it did, wheezing would not worsen.

  • B. COX inhibition diverts arachidonic acid to the 5-lipoxygenase pathway, raising cysteinyl leukotrienes (correct)

    Correct. Shunting to leukotriene synthesis explains the bronchospasm.

  • C. Aspirin increases synthesis of bronchoprotective PGE2

    Aspirin lowers PGE2, and loss of its bronchoprotective effect contributes to the reaction.

  • D. Aspirin directly triggers IgE-mediated degranulation of mast cells

    The reaction is not IgE mediated, since there is no prior sensitisation to aspirin as an allergen.

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 Biochemistry question

What is the answer to this Biochemistry question?

The best answer is B, COX inhibition diverts arachidonic acid to the 5-lipoxygenase pathway, raising cysteinyl leukotrienes. Aspirin and other NSAIDs irreversibly or reversibly inhibit cyclooxygenase, reducing prostaglandins such as bronchoprotective PGE2.

Why is "Aspirin inhibits 5-lipoxygenase and so removes leukotrienes" not the answer?

Aspirin does not inhibit lipoxygenase; if it did, wheezing would not worsen.

Why is "Aspirin increases synthesis of bronchoprotective PGE2" not the answer?

Aspirin lowers PGE2, and loss of its bronchoprotective effect contributes to the reaction.

Why is "Aspirin directly triggers IgE-mediated degranulation of mast cells" not the answer?

The reaction is not IgE mediated, since there is no prior sensitisation to aspirin as an allergen.

What concept does this question test?

It tests Eicosanoids: aspirin-exacerbated asthma in Biochemistry. Arachidonic acid is shunted to 5-lipoxygenase, increasing LTC4, LTD4 and LTE4, which are potent bronchoconstrictors. The reaction is pharmacological and not IgE-mediated, and leukotriene receptor antagonists such as montelukast help.

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 Eicosanoids: aspirin-exacerbated asthma?

Build one table of enzyme deficiency, disease, inheritance and key finding, then revise it by spaced recall. Then use the flashcards and the other Biochemistry 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.