A nurse is administering aspirin (ASA), a nonselective COX inhibitor, to a client who has rheumatoid arthritis. What are some of the specific indications of aspirin in this condition?

According to various sources, aspirin is a nonselective COX inhibitor that blocks the production of prostaglandins that are involved in inflammation, pain, fever, and platelet aggregation¹²³⁴. Aspirin is used to relieve the symptoms of rheumatoid arthritis (RA), such as joint swelling, stiffness, and pain¹²³⁴. Aspirin also has antiplatelet effects that can prevent cardiovascular events, such as myocardial infarction and stroke, in patients with RA who have an increased risk of atherosclerosis²³. However, aspirin does not modify the course or progression of RA, and it may cause gastrointestinal bleeding, ulceration, and perforation, as well as hypersensitivity reactions, renal impairment, and Reye's syndrome¹²³⁴. Therefore, aspirin should be used with caution and under medical supervision in patients with RA.

The other options are incorrect because:

B. It prevents cardiovascular events such as myocardial infarction and stroke by inhibiting platelet aggregation and thromboxane synthesis.

This option is wrong because it is not a specific indication of aspirin in rheumatoid arthritis, but a general indication of aspirin in patients with or at risk of cardiovascular disease . Aspirin can prevent cardiovascular events by inhibiting platelet aggregation and thromboxane synthesis, but this effect is not related to the treatment of rheumatoid arthritis symptoms, such as inflammation, pain, and fever . However, aspirin may have a secondary benefit of reducing the cardiovascular risk in patients with rheumatoid arthritis who have an increased risk of atherosclerosis .

C. It treats gouty arthritis by inhibiting the enzyme xanthine oxidase and reducing the production of uric acid.

This option is wrong because it describes the mechanism of action and indication of allopurinol, not aspirin . Allopurinol is a drug that treats gouty arthritis by inhibiting the enzyme xanthine oxidase and reducing the production of uric acid, which causes inflammation and pain in the joints . Aspirin does not inhibit xanthine oxidase or reduce uric acid levels, and it is not used to treat gouty arthritis . In fact, aspirin may worsen gouty arthritis by interfering with the renal excretion of uric acid and increasing its concentration in the blood .

D. It induces labor by stimulating uterine contractions and cervical ripening by blocking the production of prostaglandins.

This option is wrong because it describes the mechanism of action and indication of misoprostol, not aspirin . Misoprostol is a synthetic prostaglandin that induces labor by stimulating uterine contractions and cervical ripening . Aspirin does not induce labor, but rather blocks the production of prostaglandins that are involved in inflammation, pain, fever, and platelet aggregation

Celecoxib is a selective COX-2 inhibitor that blocks the production of prostaglandins that are involved in pain and inflammation, but spares the COX-1 enzyme that is responsible for protecting the stomach lining and platelet function¹²³⁴⁵. Therefore, celecoxib has less gastrointestinal toxicity than nonselective COX inhibitors, such as ibuprofen and naproxen, that inhibit both COX-1 and COX-2 enzymes¹²³⁴⁵. However, celecoxib still carries some risk of gastrointestinal bleeding and ulceration, especially in patients with a history of peptic ulcer disease, concomitant use of anticoagulants or corticosteroids, or high doses or long-term use of celecoxib¹²³⁴⁵. Therefore, the lowest effective dose and the shortest duration of treatment should be used, and patients should be monitored for signs and symptoms of gastrointestinal adverse events¹²³⁴⁵.

The other options are incorrect because:

B. The drug has more anti-inflammatory and analgesic effects than nonselective COX inhibitors because it blocks both COX-1 and COX-2 enzymes.

This option is wrong because celecoxib is a selective COX-2 inhibitor that does not block COX-1, which is involved in the production of prostaglandins that have anti-inflammatory and analgesic effects . Therefore, celecoxib has less anti-inflammatory and analgesic effects than nonselective COX inhibitors that block both COX-1 and COX-2 enzymes .

C. The drug has less cardiovascular risk than nonselective COX inhibitors because it inhibits vasodilatory and antiplatelet prostaglandins produced by COX-2 in the endothelium.

This option is wrong because celecoxib has more cardiovascular risk than nonselective COX inhibitors because it inhibits the production of prostacyclin, a prostaglandin that has vasodilatory and antiplatelet effects, while leaving the synthesis of thromboxane A2, a prostaglandin that promotes platelet aggregation, vasoconstriction, and smooth-muscle proliferation, unchanged or increased . This imbalance may favor thrombosis and vasoconstriction in the blood vessels and increase the risk of cardiovascular events, such as heart attacks and strokes . Therefore, celecoxib should be used with caution in patients with a history or risk factors for cardiovascular disease, and the lowest effective dose and the shortest duration of treatment should be used .

D. The drug has more antipyretic and antiplatelet effects than nonselective COX inhibitors because it blocks the production of prostaglandins involved in fever and platelet aggregation.

This option is wrong because celecoxib has less antipyretic and antiplatelet effects than nonselective COX inhibitors because it does not block the production of prostaglandins involved in fever and platelet aggregation . Celecoxib is a selective COX-2 inhibitor that spares the COX-1 enzyme that is responsible for protecting the stomach lining and platelet function