NSAID adverse effects Flashcards
1
Q
GI
A
- Caused by direct acid damage and prostaglandin inhibition
- To prevent esophageal injury, take NSAID upright with sufficient liquid (≥ 120 mL) & not immediately before bedtime
2
Q
drug most likely to cause GI ADE
A
non-selective NSAIDs
3
Q
Renal
A
- 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
4
Q
drug most likely to cause renal ADE
A
- Indomethacin most likely
- Sulindac (and possibly salsalate) least likely
5
Q
Hematologic
A
- Decreased platelet aggregation: Cyclooxygenase inhibition results in decreased synthesis of thromboxane A2
- Aplastic anemia, agranulocytosis, and thrombocytopenia rarely reported
6
Q
drug most likely to cause hematologic ADE
A
- Indomethacin most likely
- Cox2 inhibitors – does not do this
7
Q
Cardiovascular
A
- 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
8
Q
drug most likely to cause cardiovascular ADE
A
Cox2 inhibitors most likely (but PRECISION trial debunked this)
9
Q
What are risk factors for hepatic ADE’s with NSAIDs?
A
- advanced age
- decreased renal function
- multiple drug use
- higher drug doses
- increased duration of therapy
- juvenile arthritis
- systemic lupus erythematosus (SLE)
- RA
10
Q
What are the risk factors for NSAID nephrotoxicity?
A
- intrinsic renal disease (Cr >=2)
- > = 65, HTN
- CHF
- diuretics
- ACEi