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NSAIDs lecture

NSAIDs lecture notes

What is the mechanism of action of Aspirin? It irreversity inhibits COX1 and COX2, thereby inhibiting PGI2(prostacyclin), PGE2(prostaglandins) and TXA2(THromboxane)
What is the clinical use of aspirin in low doses? <300mg/day: dereases platelet aggregation
What is the clinical use of aspirin in intermediate doses? 300-2400mg/day:antipyretic and analgesic
What is the clincial use of aspirin in high dosage? anti-inflammatory
What are some of the side effects of aspirin? Gastric upset, chronic use can lead to renal failure, interstitial nephritis and upper GI bleeding, Reyes syndrome.
What does PGI2(prostacyclin) do? decreases platelet aggregation, vasodilation, decreases uterine tone
What does PGE2(prostaglandins) do? decreases vascular tone, increases pain, uterine tone, and temperature
What does TXA2(Thromboxane) do? Increases platelet aggregation and causes vasoconstriction
Name some of the traditional NSAIDs? Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac
What are the clinical uses of NSAIDs? Antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a PDA.
What are the side effects of NSAIDs? AntRenal damage, GI distress, ulcers, aplastic anemia
What is the name of the COX-2 inhibitor? celecoxib
Is celecoxib better than aspirin in it's antiplatelet effect? No
What is the MOA of celecoxib? Inhibits COX-2 which is found on in inflammatory cells/vascular endothelium. Spares COX-1 which maintains the gastric mucosa - thus doesn't have the corrosive effects of other NSAIDS on the GI.
What is the usage of celecoxib? RA and OA
What are the side effects of celecoxib? increases risk of thrombosis, sulfa allergy, less toxicity to GI muosa
Created by: villagejoker