NSAIDs relieve dysmenorrhea primarily by inhibiting which enzyme involved in prostaglandin synthesis?

• A. Inhibition of lipoxygenase.
• B. Inhibition of cyclooxygenase.
• C. Activation of prostacyclin synthase.
• D. Blockade of leukotriene receptors.

Answer: (B)

NSAIDs relieve dysmenorrhea by blocking cyclooxygenase, the enzyme that converts arachidonic acid into prostaglandins responsible for uterine contractions and pain. By inhibiting cyclooxygenase, prostaglandin production drops, leading to reduced uterine tone and cramping. The lipoxygenase pathway makes leukotrienes, which are not the primary drivers of menstrual cramps, so inhibiting it isn’t the main action of NSAIDs. Activating prostacyclin synthase would raise a different prostaglandin (PGI2) and isn’t how NSAIDs produce analgesia. Blocking leukotriene receptors targets leukotrienes rather than prostaglandins, so it doesn’t explain NSAID effects on dysmenorrhea.