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Aspirin inhibits the COX enzyme. It results in less TXA2 and PGI2 being produced. TXA2 is prothrombotic whereas PGI2 is antithrombotic. The TXA2 pathway is more susceptible to aspirin as the drug has a greater affinity for COX-1 enzymes which are more predominant in platelets. Platelets are also unable to generate new COX enzymes due to having no nucleus while endothelial cells can generate new COX 1 and 2 enzymes. In addition, the platelets in the liver get exposed to the greatest concentrations of aspirin as opposed to endothelial cells in other parts of the body.

Aspirin is used to reduce the risk of myocardial infarction in patients with unstable angina and to reduce the risk of stroke in patients with transient ischaemic attacks. It can also increase the survival rate of those who had an acute myocardial infarction. The drug may cause damage to the stomach.

Warfarin is a vitamin K eposide reductase inhibitor. By inhibiting vitamin K eposide reductase, vitamin K cannot be reduced. This reduced vitamin K is an essential cofactor for gamma-carboxylase to turn the Glu of factor X into Gla. Without Clu, calcium ions cannot bind to it to cause factor X to undergo conformation change to interact with the tissue factor and VIIa cofactor.

Warfarin is used to prevent venous thrombosis and pulmonary embolism. It can be used after myocardial infractions for these purposes. Side effects of warfarin include increased bleeding risks.

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Q: What are the differences between the mechanisms of action therapeutic uses and adverse reactions of aspirin and warfarin in the treatment of thrombotic disorders?
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