PHAR 340 Lecture Notes - Lecture 28: Janus Kinase 3, Probenecid, Indometacin

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Autoimmune disease w limited joint function due to inflame synovial memb, destruction of bone, cartilage. Chemically heterogeneous, diverse mechanisms of action, some treat symptoms + some are dmards. Cox inhibitors that suppress symptoms (decr inflame, pain + fever-antipyretic) but dn stop disease progression. Cause decr in il-1, free radicals, interfere w ca-mediated intra signaling. Indomethacin: nsaid, efficacious, potent and standard for comparison, toxic in 35-50% of ppl causes headache. Naproxen t1/2 14 hrs so effects and toxicity last longer. Acetaminophen: not anti-inflam so not really a nsaid. Cox-2 inhibitor: just celecoxib now, less gi toxicity but cv toxicity. Low dose for fever+ pain, t1/2=3-5hrs (1st order) High dose for anti-inflam w apparent t1/2>12 hours (0 order) Gastric intolerance: mucosal irritation, inhibits protective effects of pg so get enteric coated asa problems. Airway constriction shifts aa from cox to lox pathway. Renal failure possible in patients w compromised renal function bc renal blood flow depends on pgs.

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