Mechanism of antiplatelet drugs | Hematology | Blood Physiology | Pharmacology

Physiology lecture explains primary hemostasis i.e platelet plug formation with the steps involved in platelet plug formation, i.e platelet adhesion, platelet activation, and platelet aggregation.

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It also explains its pathology and the pharmacology of antiplatelet drugs.
What are the antiplatelet drugs? What is the physiological basis of the actions of antiplatelet drugs? In what situations are antiplatelet drugs used and why?

The process of hemostasis consists of three steps: vasospasm, platelet plug formation and clot formation.

Platelet plug formation:
Platelet adhesion: At site of vessel injury the endothelial cells are injured and there is exposure of sub endothelial collagen. At the site, von Willebrand factor (vWF) binds to the sub endothelial collagen. On the surface of the platelets there is a protein known as GP 1B which has affinity for the vWF. Now this process of binding of GP 1b platelet receptor with von willebrand factor is known as platelet adhesion.

Platelet activation: Because of the binding of GP 1b platelet receptor with von willebrand factor, there is change in shape of the platelets and they release the contents of the alpha and dense granules into the blood that is ADP, thromboxane A2. This is known as platelet activation.

Platelet aggregation: ADP and TXA2 act on the platelets themselves. Because of this there is change in affinity of another protein present on the surface of platelet that is GP 2b3a. Once that affinity increases, platelets binds to fibrinogen and there is cross linking between the platelets. So this process of platelets binding with other platelets is known as platelet aggregation.

Diseases:
Qualitative platelet disorders: Number of platelets is normal but there is a decrease in platelet function
1. Decrease in von Willebrand factor occurs in inherited disease which is autosomal dominant. It will affect platelet adhesion
2. Abnormal gp1B receptor (Bernard Soulier Syndrome): Platelet adhesion cannot occur.
3.Abnormal GP 2b 3a (Glanzman's thrombasthenia): Platelet aggregation is defective

Quantitative disorders:
Decrease in number of platelets like in infections e.g. dengue, idiopathic thrombocytopenic purpura.

Use of antiplatelets: Wen there is excessive platelet plug formation
1. ADP receptor antagonists: Clopidogrel.
2. Formation of thromboxane A2 is blocked by aspirin.
3. GpIIbIIIa receptors antagonist : Abciximab so it interferes with platelet aggregation


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