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
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2
Q

drug most likely to cause GI ADE

A

non-selective NSAIDs

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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
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4
Q

drug most likely to cause renal ADE

A
  • Indomethacin most likely

- Sulindac (and possibly salsalate) least likely

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5
Q

Hematologic

A
  • Decreased platelet aggregation: Cyclooxygenase inhibition results in decreased synthesis of thromboxane A2
  • Aplastic anemia, agranulocytosis, and thrombocytopenia rarely reported
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6
Q

drug most likely to cause hematologic ADE

A
  • Indomethacin most likely

- Cox2 inhibitors – does not do this

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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
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8
Q

drug most likely to cause cardiovascular ADE

A

Cox2 inhibitors most likely (but PRECISION trial debunked this)

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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
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10
Q

What are the risk factors for NSAID nephrotoxicity?

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