NSAIDS, Acetaminophen Flashcards
mechanism: acetylation of COX-1 AND COX-2, decreased prostaglandin synthesis
clinical application: analgesia, antypyretic, anti-inflammatory and antithrombotic in low dose
P: longer than pharmakokinetic half-life of drug due to irreversible COX inhibition
Toxicities: GI, Nephro, increased bleeding time, bronchoconstriction, tinnitus, hyperventilation, metabolic acidosis, hyperthermia, coma
Aspirin(salicylate)
mechanism: REVERSIBLE inhibition of COX-1 and COX-2 results in decreased prostaglandin synthesis
clinical application: analgesia, antipyretic, and anti-inflammatory, closure of PDA
P: rapid metabolism and renal elimination
Toxicities: GI, Nephro, reaction due to increased leukotrienes, interference with ASPIRIN’S antithrombotic action
Ibuprofen(non selective NSAID)
mechanism: SELECTIVE, REVERSIBLE inhibition of COX-2 results in decreased prostaglandin synthesis
clinical application: analgesia, antipyretic
P:hepatic conjugation
Toxicity: Nephro, reaction due to increased leukotrienes, LESS risk of GI toxicity, GREATER risk of thrombosis
Celecoxib(COX-2 inhibitor)
mechanism: unknown, WEAK COX inhibitor
clinical application: analgesia, antipyretic
P: hepatic conjugation
Toxicities: Hepatotoxicity in overdose (antidote is ACETYLCYSTEINE), hepatotoxicity more likely with chronic ALCOHOL consumption, which induces P45O enzymes
Acetaminophen
mechanism: conventional synthetic CYTOTOXIC to rapidly dividing immune cells due to inhibition of DIHYDROFOLATE REDUCTASE
clinical application: anticancer, rheumatic disorders
P: Renal elimination
Toxicities: nausea, mucosal ulcers, hema, hepa, teratogenicity
Methotrexate(DMARDs)
mechanism: Inhibition of MICROTUBULE assembly decreases MACROPHAGE migration and phagocytosis
clinical application: Chronic and acute gout, familial MEDITERRANEAN fever
P:Oral drug
Toxicities:Diarrhea, severe liver and kidney damage in overdose
Colchicine(Microtubule assembly inhibitor)
mechanism: Inhibition of renal reuptake of uric acid
clinical application: Chronic gout, prolongation of
antimicrobial drug action
P: Oral drug
Toxicities: exacerbation of ACUTE GOUT,
hypersensitivity reactions, inhibits renal tubular secretion of weak acids such as methotrexate
Probenecid(Uricosurics)
similar to probenecid
Sulfinpyrazone
mechanism: Active metabolite irreversibly inhibits
xanthine oxidase and lowers production of uric acid
clinical application: Chronic gout, adjunct to cancer chemotherapy
P: Activated by XANTHINE OXIDASE • oral drug
Toxicities: GI upset, hypersensitivity reactions, BONE MARROW suppression
Allopurinol (Xanthine oxidase inhibitors)
reversible inhibitor of xanthine oxidase
Febuxostat
mechanism: recombinant mammalian uricase coverts uric acid to the soluble allantoin
clinical application: chronic REFRACTORY gout
P: IV
Toxicities: rapid change in uric acid levels can precipitate gout flare, prophylaxis with NSAIDS or colchicine
Pegloticase(Uricase)
