Platelet plug
Platelet Plug
A Platelet plug or Platelet thrombus is a gathering of platelets in the blood. It forms at the site of a damaged blood vessel to prevent bleeding. It is the first step in the process of hemostasis, which is the cessation of blood loss from a damaged vessel.
Formation[edit | edit source]
The formation of a platelet plug, also known as primary hemostasis, begins when platelets adhere to the subendothelial collagen at the site of an injury. This adhesion is mediated by a glycoprotein in the platelet membrane, Glycoprotein Ib, which binds to von Willebrand factor (vWF) that has been bound to the exposed collagen.
Once adhered, the platelets change shape from spherical to stellate, and release the contents of their granules. This process is known as platelet activation. The granules contain substances such as ADP, thromboxane A2, and serotonin, which promote further platelet activation and recruitment.
The recruited platelets then aggregate, forming a platelet plug. This aggregation is mediated by fibrinogen and the platelet membrane glycoprotein Glycoprotein IIb/IIIa. The fibrinogen forms bridges between the glycoprotein IIb/IIIa receptors of different platelets, effectively sticking them together.
Role in Hemostasis[edit | edit source]
The platelet plug serves to temporarily block the site of injury and prevent further blood loss. However, it is not stable and can easily be dislodged. To stabilize the plug, the process of coagulation or secondary hemostasis takes place. This involves a cascade of enzymatic reactions that result in the formation of fibrin strands, which cross-link and form a stable clot over the platelet plug.
Clinical Significance[edit | edit source]
Abnormalities in platelet plug formation can lead to bleeding disorders such as von Willebrand disease and Bernard-Soulier syndrome. On the other hand, excessive platelet plug formation can result in thrombotic disorders such as deep vein thrombosis and myocardial infarction.
See Also[edit | edit source]
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