A nurse is evaluating a client who has fever and is receiving acetaminophen (Tylenol), a nonsalicylate NSAID. What are some of the outcomes that indicate the effectiveness of the therapy?

This is because ketorolac can cause gastrointestinal, renal, and cardiovascular effects as a result of its nonselective inhibition of cyclooxygenase (COX) enzymes². COX enzymes are responsible for producing prostaglandins that have different functions in different tissues. By blocking both COX-1 and COX-2 enzymes, ketorolac can interfere with the protective, regulatory, and homeostatic roles of prostaglandins in various organs². Therefore, the nurse should consider the following points when administering this drug:

A. ssas

It should be given orally with food or milk to minimize gastrointestinal irritation: This is because ketorolac can cause gastrointestinal effects such as nausea, vomiting, ulceration, bleeding, and perforation by blocking the production of prostaglandins that protect the gastric mucosa from acid and pepsin²³. The nurse should advise the client to take ketorolac with food or milk, avoid alcohol and tobacco, report any signs of gastrointestinal bleeding (such as black or tarry stools, abdominal pain, vomiting blood), and use the lowest effective dose for the shortest duration possible²³.

B. asdasd

It should be given intravenously slowly over 15 to 30 minutes to prevent hypotension or thrombophlebitis: This is because ketorolac can cause hypotension by blocking the production of prostaglandins that regulate blood pressure and vascular tone² . It can also cause thrombophlebitis by irritating the vein wall and causing inflammation and clot formation² . The nurse should monitor the client's blood pressure and infusion site during and after the administration of ketorolac and report any signs of hypotension (such as dizziness, fainting, blurred vision) or thrombophlebitis (such as redness, swelling, pain, warmth) to the doctor² .

C. asfdeaf

It should be given for short-term use only (up to 5 days) to avoid renal impairment or gastrointestinal bleeding: This is because ketorolac can cause renal impairment by blocking the production of prostaglandins that maintain renal blood flow, glomerular filtration rate, sodium excretion, and water balance² . It can also cause gastrointestinal bleeding by blocking the production of prostaglandins that inhibit platelet aggregation and promote hemostasis²³. The risk of these effects is higher in those with preexisting renal impairment, heart failure, liver cirrhosis, dehydration, or hypovolemia, and those who use diuretics or anticoagulants²³ . The nurse should monitor the client's fluid intake and output, body weight, electrolytes, and renal function tests, and report any signs of renal dysfunction (such as oliguria, anuria, edema) or gastrointestinal bleeding (such as black or tarry stools, abdominal pain, vomiting blood) to the doctor²³ .

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