A patient with bronchial asthma develops worsening bronchoconstriction after being given aspirin. The underlying mechanism is:

• A Aspirin stimulates H1 receptors on bronchial smooth muscle, causing bronchoconstriction
• B Aspirin inhibits phosphodiesterase, reducing cAMP and causing bronchoconstriction
• C Aspirin directly activates mast cell TLR-2 receptors, triggering bronchoconstriction
• D COX inhibition by aspirin diverts arachidonic acid to the 5-lipoxygenase pathway, increasing cysteinyl leukotriene synthesis ✓

Explanation

Aspirin-exacerbated respiratory disease (Samter's syndrome) results from COX-1 inhibition redirecting arachidonic acid away from prostaglandin synthesis toward the 5-lipoxygenase pathway. This generates excess cysteinyl leukotrienes (LTC4, LTD4, LTE4), which are potent bronchoconstrictors and promote mucus secretion. Patients with this condition often also have nasal polyps and chronic rhinosinusitis. The leukotriene pathway is the mechanism, not direct receptor activation.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.