NSAIDs: aspirin-exacerbated respiratory disease: practice question

A Pharmacology 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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Pharmacology · NSAIDs: aspirin-exacerbated respiratory disease

Sample item

A 35-year-old asthmatic with nasal polyps develops severe wheezing within an hour of taking aspirin. What is the underlying mechanism?

AIgE-mediated mast cell degranulation to aspirin as an antigenBCOX inhibition shunts arachidonic acid to the lipoxygenase pathway, increasing cysteinyl leukotrienesCDirect muscarinic stimulation of bronchial smooth muscleDRelease of bradykinin through ACE inhibition

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

The answer and the reasoning

B. COX inhibition shunts arachidonic acid to the lipoxygenase pathway, increasing cysteinyl leukotrienes

In aspirin-exacerbated respiratory disease, blocking cyclooxygenase diverts arachidonate toward leukotriene synthesis, and the excess cysteinyl leukotrienes cause bronchoconstriction. It is a pharmacological, non-IgE reaction, and montelukast is helpful.

Option by option

A. IgE-mediated mast cell degranulation to aspirin as an antigen
The reaction is not IgE mediated, though it resembles allergy.
B. COX inhibition shunts arachidonic acid to the lipoxygenase pathway, increasing cysteinyl leukotrienes (correct)
Correct. Leukotriene shunting explains the reaction.
C. Direct muscarinic stimulation of bronchial smooth muscle
Aspirin has no muscarinic agonist action.
D. Release of bradykinin through ACE inhibition
Aspirin does not inhibit ACE or raise bradykinin.

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.

Questions about this Pharmacology question

What is the answer to this Pharmacology question?

The best answer is B, COX inhibition shunts arachidonic acid to the lipoxygenase pathway, increasing cysteinyl leukotrienes. In aspirin-exacerbated respiratory disease, blocking cyclooxygenase diverts arachidonate toward leukotriene synthesis, and the excess cysteinyl leukotrienes cause bronchoconstriction.

Why is "IgE-mediated mast cell degranulation to aspirin as an antigen" not the answer?

The reaction is not IgE mediated, though it resembles allergy.

Why is "Direct muscarinic stimulation of bronchial smooth muscle" not the answer?

Aspirin has no muscarinic agonist action.

Why is "Release of bradykinin through ACE inhibition" not the answer?

Aspirin does not inhibit ACE or raise bradykinin.

What concept does this question test?

It tests NSAIDs: aspirin-exacerbated respiratory disease in Pharmacology. It is a pharmacological, non-IgE reaction, and montelukast is helpful.

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 NSAIDs: aspirin-exacerbated respiratory disease?

Learn drugs as classes, then the exception in each class that an examiner would pick. Then use the flashcards and the other Pharmacology 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.