Term
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Definition
| NSAID (sort of). Rapidly absorbed from stomach and small intestine. t1/2 = 15 mins. Irreversibly binds to COX-1. Analgesic effects due to COX3 in brain. Also, anti-pyretic and anti-inflam. TOX: GI, platlet inhibition, hypersensitivity, Reyes Syndrome, Can treat pain, but mostly used to decrese risk of CVD. Platlet aggreation decreased bc COX-1 normally stimulates thromboxane which increases aggretation. |
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Term
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Definition
| NSAID (sort of). Asprin metabolite. T1/2 = 3+ hrs. Binds COX1+2, but reversibly. Metabolized in liver. Highly bound to albumin. |
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Term
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Definition
| NSAID. Well absorbed in GI tract. T1/2 is short = 2 hrs, quickly cleared. Well tolerated. Tox: GI, renal, hepatic, rash. |
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Term
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Definition
| NSAID. Long duration, t1/2 = 12-17hrs. 7 hrs analgesic, 12 hrs inflam. Renal elimination. Use: gout, migrane, osteoarthritis, pain, tendonitis, bursitis, rheumatoid disorders. (inflam conditions). Tox: GI, renal, hepatic, rash. |
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Term
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Definition
| NSAID. analgesic, antipyritic, antiinflam. VV strong drug, with lots of toxicities. Tox: GI, CNS (headache, vertigo, somulance), GI, renal, hepatic, rash. Use: Not used for pain anymore, used to close a patent ductus arteriosus. |
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Term
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Definition
| NSAID. Rapidly absorbed Gi tract. t1/2 = 3-4 hrs. Weak COX1 and 2 inhibitor, mostly COX3 inhibitor in brain!. Analgesic, anti-pyretic, little anti-inflam. 5 percent metabolized by P450s and glutathione. if this pathway is overloaded, can lead to buildup of toxic intermediate and hepatic failute. CAREFUL with alcohol, uses up glutathione. 90 percent sulfated and gluconorided, no toxicity. |
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Term
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Definition
| Use in treatment of acetominophen toxicity. Increases glutathione stores, combines directly with NAPGI as a glutathione substitute and releases nontoxic NAPQI. Enchances nontoxic sulfate conjugation. |
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Term
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Definition
| NSAID. COX-2 selective inhibitor. All others pulled be FDA bc increased risk of MI and stroke. COX 2 normally stimulates prostacyclin I2, which is a thromboxane antagonist, decreasing clotting. COX2 inhibitors INCREASE clotting. |
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