- Aspirin is the prototype NSAID and functions by irreversibly inhibiting cyclooxygenases (COXs) the enzymes that convert Arachidonic Acid to a variety of prostoglandins and thromboxanes. Aspirin is one of the most commonly used drugs, displaying antipyretic, anti-inflammatory, analgesic, and platelet inhibiting effects. However, the drug can display a number of important adverse GI, respiratory, and renal effects. Toxic doses can lead to ototoxicity and potentially fatal metabolic acidosis
- The platelet inhibitory properties of aspirin result from its irreversible inhibition of COX-1 the enzyme responsible for generating Thromboxane A2 during during platelet activation. As described in Platelet Plugging, release of Thromboxane A2 from an activated platelet promotes the activation of nearby platelets thus facilitating platelet aggregation. Because aspirin is an irreversible inhibitor of COX-1, platelets are affected for their lifetime while in the circulation and thus the platelet inhibitory effects of the drug diminish only with the synthesis of new platelets, taking roughly 7-10 days. Coagulation is not affected; consequently, while bleeding time is increased due to reduced platelet function, the coagulation parameters of PT/PTT remain unchanged.