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Pathology · Inflammation: arachidonic acid metabolites
Sample itemA 35-year-old man with chronic rhinosinusitis, nasal polyps and asthma develops severe bronchospasm after taking aspirin. Which mediators are overproduced because of the pharmacological block of arachidonic acid metabolism?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. Cysteinyl leukotrienes LTC4, LTD4 and LTE4
Aspirin irreversibly inhibits cyclooxygenase, so arachidonic acid is diverted to the 5-lipoxygenase pathway. The excess cysteinyl leukotrienes cause bronchoconstriction, mucus secretion and increased vascular permeability. Loss of the protective bronchodilator prostaglandin E2 contributes, and leukotriene receptor antagonists such as montelukast are useful.
Option by option
A. Cysteinyl leukotrienes LTC4, LTD4 and LTE4 (correct)
Correct. Shunting down the lipoxygenase pathway raises cysteinyl leukotrienes, which are potent bronchoconstrictors.
B. Thromboxane A2
Thromboxane A2 is also a cyclooxygenase product, and aspirin reduces its platelet synthesis.
C. Prostacyclin PGI2
Prostacyclin is a cyclooxygenase product, so aspirin decreases it.
D. Prostaglandin E2
Prostaglandin E2 is reduced by cyclooxygenase inhibition, and its loss removes a bronchodilating effect.
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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