Low doses of aspirin prolong bleeding time by selec tively inhibiting synthesis of the following mediator in the platelets
Antiplatelet aggregation:- Mech of action:- Aspirin inhibits COX irreversibly and thus inhibits synthesis of PGs. NSAIDs inhibit synthesis of both proaggregatory (TXA2- synthesized in platelets) and anti- aggregatory (PGI2- synthesized by endothelium) prostanoids, but effect on platelet TXA2 predominates . At therapeutic doses most NSAIDs inhibit platelet aggregation, bleeding time is prolonged. Therefore aspirin exes anti- thrombotic effect for several days. Risk of surgical and anticoagulant associated bleeding is enhanced. These drugs should be stopped a week before any elective major surgeries to reduce the risk of bleeding. Ref:- kd tripathi; pg num:-194
Thromboxane A2
5-Hydroxytryptamine
Platelet activating factor
Prostacyclin
Autacoids