NSAIDs and Acetaminophen Flashcards
MOA of NSAIDs?
ameliorate pain and inflammation through reversible (Except aspirin) inhibition of cyclooxygenase enzyme (COX)
How are most NSAIDs metabolized?
hepatically with the exception of ketorolac, which is 58% unchanged in urine
Which leads to platelet inhibition: Inhibition of COX1 or COX2?
COX1 inhibition causes platelet inhibition and increaesd bleeding time. GI toxicity as well.
Which NSAID has shortest half-life?
diclofenac (tiny dick)
Which NSAID has longest half-life?
piroxicam (peer off into the distance)
Which NSAID has lowest risk of GI toxicity?
ibuprofen
Which NSAID has highest risk of GI toxicity?
ketorolac
What factors contribute to an NSAIDs GI toxicity?
half-life and COX selectivity (more COX1 inhibition=more GI toxicity)
What can be given with NSAIDs to reduce GI toxicity?
H2 receptor antagonists, misoprostol, or proton pump inhibitors (PPIs). PPIs are most effective because they better suppress acid.
How do NSAIDs cause cardiovascular events?
NSAIDs inhibit platelets but only for a short duration, whereas aspirin inhibits permanently (7-10 days). NSAIDs will compete with aspirin and result in decreased protection, thus more thrombotic events and CV damage in patients who need the inhibition
Which NSAID is seemingly cardioprotective and has no interaction with aspirin?
na interactions so naproxen protects
What can a combo of aspirin and ibuprofen cause?
increased CV risk
What effects do NSAIDs have on BP?
they increase BP
Which BP drugs can have adverse effects with NSAIDS?
ACEI’s and ARB’s
How do NSAIDs cause acute renal toxicity?
they inhibit PGI2 and E2, which help maintain renal bloodflow and GFR