It is believed to reduce fever via blockage of Prostaglandin E2 (PGE2).
It is believed to have pain-killing effects due to its inhibition of both COX-1 and COX-2.
Due to its antiplatelet effects, aspirin has been demonstrated to be effective for prevention of MI and ischemic stroke in those with existing cardiovascular disease (CVD) and those without CVD.
Aspirin irreversibly inhibit COX-1 and COX-2 and results in inhibition of production of prostaglandins (PG) and thromboxanes (TX).
This prevents PGs from performing their role in inflammatory responses, pain processing and fever production and TXs from causing platelet aggregation.
Aspirin is classified as an NSAID but it performs irreversible, not reversible inhibition of COX-1 and COX-2.
Administration of aspirin to children with viral infection is associated with microvesicular steatosis of hepatocytes, hepatoencephalopathy and potentially death. Causality has not yet been established.
Chronic aspirin toxicity can occur in individuals chronically taking 3g or more daily. This may result in ringing in the ears (tinnitus) possibly due to activation of cochlear NMDA receptors.
PG’s produced by COX-1 help maintain the protective GI mucosal barrier in the stomach and intestines. Blockage of these PG’s via COX-1 inhibition can result in gastric ulcers.
Aspirin toxicity can result in initial respiratory alkalosis due to hyperventilation and then metabolic acidosis. This presents as a mixed respiratory alkalosis and metabolic acidosis.
Aspirin can cause renal ischemia due to decreased renal blood flow, renal papillary necrosis or interstitial nephritis (acute or chronic).
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