Platelet aggregation

Platelet aggregation is a crucial process in the formation of a blood clot. It involves the clumping together of platelets in the blood under certain physiological or pathological conditions. This process is an essential part of hemostasis, the cessation of blood loss from a damaged vessel, and is also involved in the development of thrombosis.

Mechanism of Platelet Aggregation

Platelet aggregation is initiated by the activation of platelets. This can occur due to a variety of stimuli, including exposure to subendothelial collagen, thrombin, adenosine diphosphate (ADP), and thromboxane A2. Upon activation, platelets change shape from spherical to spiky, and the glycoprotein receptors on their surface undergo changes that allow them to bind to fibrinogen, a protein that bridges adjacent platelets, leading to aggregation.

Role in Hemostasis

In hemostasis, platelet aggregation plays a key role in the formation of the primary hemostatic plug. This is a temporary blockage of a break in the blood vessel wall, formed by aggregated platelets. The primary plug is then stabilized by the formation of a fibrin mesh, which is the result of the coagulation cascade.

Role in Thrombosis

While platelet aggregation is essential for hemostasis, excessive or inappropriate aggregation can lead to thrombosis, the formation of a blood clot within a blood vessel. This can result in serious conditions such as stroke, myocardial infarction, and pulmonary embolism.

Antiplatelet Drugs

Antiplatelet drugs are used to inhibit platelet aggregation and prevent thrombosis. These include aspirin, which inhibits the production of thromboxane A2, and clopidogrel, which blocks ADP receptors on the platelet surface.

See Also

• Coagulation
• Hemostasis
• Thrombosis
• Antiplatelet drug