It is believed that its inhibition of COX-2 results in anti-inflammatory effects.
It is believed to have pain-killing effects due to its inhibition of both COX-1 and COX-2.
It is believed to reduce fever via blockage of Prostaglandin E2 (PGE2) via inhibition of COX.
Prostaglandin E1 (PGE1) is responsible for patency of the ductus arteriosus. The NSAID indomethacin is given to block PGE1 and close the PDA.
NSAIDS reversibly inhibit COX-1 and COX-2 and results in inhibition of production of prostaglandins (PG) and thromboxanes (TX). Each NSAID has small differences in COX-1 and COX-2 inhibition.
Through inhibition of COX, endoperoxides cannot turn into prostaglandins (PGs). This prevents PGs from performing their role in inflammatory responses, pain processing and fever production.
This drug reaction can result in acute or chronic interstitial nephritis characterized by fever, rash, hematuria and CVA tenderness.
Prostaglandins (PGs) produced by COX-1 help maintain the protective GI mucosal barrier in the stomach and intestines. Blockage of these PGs via COX-1 inhibition can result in gastric ulcers.
NSAIDS inhibit vasodilatory prostaglandins (PGs) which can result in decreased renal blood flow and renal damage.
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