USMLE-Rx Step 1 Qmax Challenge #1594

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USMLE-Rx Step 1 Qmax Challenge #1594A 57-year-old man has arthritis, which is treated with a cycloocygenase (COX)-2 inhibitor. He presents to the emergency department with sudden-onset shortness of breath and chest pain which radiates to his jaw and left arm.

Which of the following best explains why the patient may have been better off using aspirin for his arthritis instead of selective COX-2 inhibitors?

KEY: (+ denotes an in increase in concentration and – denotes a decrease in concentration, PGI2 = prostaglandin I2, TxA2 = thromboxane A2)

A. A
B. B
C. C
D. D
E. E


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4 thoughts on “USMLE-Rx Step 1 Qmax Challenge #1594”

  1. A thromboxane A2 (TXA2) and prostacyclin (PGI2) . These hormones are labile metabolites of arachidonic acid. TXA2 is generated by blood platelets, while PGI2 is produced by vascular endothelium. TXA2 is a potent vasoconstrictor. It also initiates the release reaction, followed by platelet aggregation. PGI2 is a vasodilator, especially potent in coronary circulation. It also inhibits platelet aggregation by virtue of stimulation of platelet adenyl cyclase. A balance between formation and release of PGI2, TXA2 and/or cyclic endoperoxides in circulation is of utmost importance for the control of intra-arterial thrombi formation and possibly plays a role in the pathogenesis of atherosclerosis.

  2. E)
    The probable diagnosis is drug-induced mi

    Arachidonic Acid ——-COX-1—-> TXA2
    Arachidonic Acid ——-COX-2—-> PGI2

    Selective COX-2 inhibitors would decrease PGI2 and thus increase risk for vasoconstriction and platelet aggregation without affecting levels of TXA2.

    Nonselective COX inhibitor (ASPIRIN) inhibits production of both TXA2 & PGI2 in earlier stage.

  3. B, ASA inhibits both COX, so we can rule out D. selective COX2 inhibitor increases risk of MI. How? In the arachidonic acid pathway they inhibit the production of PGE-2 that causes fever and pain. Substrate accumulates, all that substrates goes to he other side of the pathway stimulating the production of tromboxane A2 that is platelet agregating substance.

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