NSAIDS Flashcards
NSAIDS
aspirin (acetylsalicyclic acid, sodium salicylate, mesalamine), piroxicam, Ibuprofen/naproxen, indomethacin, diclofenac/ketorolac, celecoxib, and actaminophen
Thromboxane A3
critical to platelet aggregation formation of clots
PGI2
inhibits gastric secretion, vasodilator, venodilar,inhibitor of platelet aggregation
PGE2 and PGF2alpha
promote secretion of protective mucus as stomach lining, vasodilation in kidney
Aspirin
irreversibly acetylates and inactives cyclooxygenase (COX-1)
COX-1 and 2
produces prostanoids such as TXA which induces platelet aggregation
Celecoxib
Selective COX-2 inhibitor, reversible, anti-inflammatory/antipyretic/analgesic, do not share antiplatelet actions of COX-1 inhibitors
All other NSAIDS but Aspirin and Celecoxib
piroxicam, Ibuprofen/naproxen, indomethacin, diclofenac/ketorolac. All are COX inhibitors, non selective, reversible
NSAIDS renal effects
block prostaglandins on afferent arteriole and reduce GFR
Acetaminophen
NOT AN NSAID but relieves paina nd fever. analgesic and antipyretic choice for children. weak COX1/2 inhibitor and inhibits prostaglandin synthesis in CNS
Piroxicam
NSAID, cox inhibitor, long half life (50 hours)
Ibuprofen
NSAID, cox inhibitor, effective in closing patent ductus arteriosus in preterm infants, less GI toxicity than other nsaids
Naproxen
NSAID, cox inhibitor, topical prep and ophthalmic solution available, more GI tox than ibuprofen but less than aspirin, 14 hour half life
Indomethacin
NSAID, cox inhibitor, inhibits Phospholipase A2 as well, very potent and considered when one of less toxic agent are ineffective, used to accellerate closure of patent arteriosus
Diclofenac
NSAID, cox inhibitor, ophthalmic and topical delivery
