Among other effects, aspirin inhibits thromboxane activity.How will this affect platelet plug formation?
Among other effects, aspirin inhibits thromboxane activity.
How will this affect platelet plug formation?
Aspirin is an antipyretic and anti-inflammatory agent. It prolongs the bleeding time and inhibits platelet aggregation. Aspirin reduces the risk of myocardial infarction, non-fatal stroke and vascular death. It inhibits platelet aggregation by inhibiting platelet thromboxane A2, reducing thrombus formation on the site of injury.
The platelet plug is formed by thrombin and fibrinogen. Aspirin acetylates cyclooxygenase-1 (COX-1) that inhibits thromboxane A2 synthesis. The COX 1 gene is a lipid platelet agonist that is decreased by aspirin that impairs platelets' aggregation. The thrombin formation is reduced, and clot permeability is increased, leading to the dissolution of the clot. The effect is impaired platelet function, decreased tissue factor (TF), acetylation of fibrinogen and fibrin clot lysis.
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