NSAID adverse effects

Question 1

GI

Answer 1

• Caused by direct acid damage and prostaglandin inhibition
• To prevent esophageal injury, take NSAID upright with sufficient liquid (≥ 120 mL) & not immediately before bedtime

Question 2

drug most likely to cause GI ADE

Answer 2

non-selective NSAIDs

Question 3

Renal

Answer 3

• NSAIDs block production of PG which decreases the body’s compensatory mechanism to keep the body euvolemic
• Prolonged renal ischemia may lead to chronic renal insufficiency or papillary necrosis
• Can also impair diuretic effect and blood pressure control

Question 4

drug most likely to cause renal ADE

Answer 4

• Indomethacin most likely

- Sulindac (and possibly salsalate) least likely

Question 5

Hematologic

Answer 5

• Decreased platelet aggregation: Cyclooxygenase inhibition results in decreased synthesis of thromboxane A2
• Aplastic anemia, agranulocytosis, and thrombocytopenia rarely reported

Question 6

drug most likely to cause hematologic ADE

Answer 6

• Indomethacin most likely

- Cox2 inhibitors – does not do this

Question 7

Cardiovascular

Answer 7

• COX-1 regulates thromboxane, COX-2 regulates prostacyclin; theoretically, blocking COX-2 and not COX1 could increase platelet aggregation
• All NSAIDs have potential for increasing risk for cardiovascular events and gastrointestinal bleeding

Question 8

drug most likely to cause cardiovascular ADE

Answer 8

Cox2 inhibitors most likely (but PRECISION trial debunked this)

Question 9

What are risk factors for hepatic ADE’s with NSAIDs?

Answer 9

• advanced age
• decreased renal function
• multiple drug use
• higher drug doses
• increased duration of therapy
• juvenile arthritis
• systemic lupus erythematosus (SLE)
• RA

Question 10

What are the risk factors for NSAID nephrotoxicity?

Answer 10

• intrinsic renal disease (Cr >=2)
• > = 65, HTN
• CHF
• diuretics
• ACEi