MSK/Derm drugs Flashcards
aspirin moa
irreversibly inhibits COX-1 and COX-2 by covalent acetylation, which decreases synthesis of both TXA2 and PGs; increases bleeding time until new platelets are produced; no effect on PT, PTT;
aspirin toxicity
gastric ulceration, tinnitus
chronic use - acute renal failure, interstitial nephritis, and upper GI bleeding; risk of Reye syndrome in children treatment with aspirin for viral infection;
stimulates respiratory centers causing hyperventilation and respiratory alkalosis
NSAIDs
ibuprofen, naproxen, indomethacin, ketorolac, diclofenac
NSAID moa
reversible inhibit COX-1 and COX-2; block PG synthesis
NSAID toxicity
interstitial nephritis, gastric ulcer, renal ischemia (PGs dilate afferent arteriole)
celecoxib moa
reversibly inhibits COX-2; found in inflammatory cells and vascular endothelium and mediates inflammation and pain; spares COX-1, which helps maintain the gastric muscosa; spares platelet function
celecoxib toxicity
high risk of thrombosis; allergy
acetaminophen moa
reversible inhibits COX in the CNS; inactivated peripherally
acetaminophen toxicity
overdose produces hepatic necrosis - NAPQI depletes GSH and forms toxic tissue adducts in the liver
acetaminophen OD antidote
n-acetylcysteine
bisphosphonates moa
pyrophosphate analogs, bind hydroxyapatitie in bone, inhibiting osteoclast activity
bisphosphonate toxicity
corrosive esophagitis, osteonecrosis of the jaw
allopurinol moa
inhibits xanthine oxidase, decreasing the conversion of xanthine to uric acid;
allopurinol use
chronic gout prevention; used in lymphoma and leukemia to prevent tumor lysis; increases concentrations of 6-MP and azothioprine (normally metab by xanthine oxidase)
febuxostat moa
inhibits xanthine oxidase
