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At the site of vessel injury, platelets stick together and aggregate forming a plug, which is the beginning of forming a clot.
Describe the formation of a platelet plug
Platelets adhere to damaged endothelium to form platelet plug, temporarily sealing the break in the vessel wall.
Activated platelets release factors to stimulate further platelet activation, perpetuating plug formation in a positive feedback loop, and other factors that stimulate the coagulation cascade and maintain vasoconstriction.
Platelets adhere to the collagen fibers in the vessel wall due to the stimulus of von Willebrand factor, by becoming adhesive and filamentous.
During platelet aggregation, platelets bind to von Willebrand factor and fibrinogen to stick together and seal over the break in the endothelium.
The second critical step in hemostasis, which follows vasoconstriction, is platelet plug formation. COLLAGEN. There are three steps to platelet plug formation: platelet adherence, activation, and aggregation.
The first step of platelet plug formation is platelet adherence. Normally, the endothelial cells express molecules that inhibit platelet adherence and activation while platelets circulate through the blood vessels. These molecules include nitric oxide, prostacylcine (PGI2) and endothelial ADP-ase.
During an injury, sub-endothelial collagen from the extracellular matrix beneath the endothelial cells is exposed on the epithelium (as the normal epithelial cells are damaged and removed) which releases von Willebrand Factor (VWF). VWF causes the platelets to change form with adhesive filaments (extensions) which adhere to the sub-endothelial collagen on the endothelial wall.
After platelet adherence occurs, the sub-endothelial collagen binds to receptors on the platelet, which activates it. During platelet activation, the platelet releases a number of important cytokines and chemical mediators via degranulation. The released chemicals include ADP, VWF, thromboxane A2, platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), serotonin, and coagulation factors. The extra ADP and VWF is especially important because it causes other nearby platelets to ahere and activate as well, and release more ADP and VWF and the other chemicals of their own. For this reason, platelet plug formation is considered a positive feedback process because ADP and VWF levels are successively increased as more and more platelets activate to form the plug.
The other factors released during platelet activation perform other important functions. Thromboxane is an arachidonic acid derivative (similar to prostaglandins) that activates other platelets, maintains vasoconstriction. Serotonin is a short-lived inflammatory mediator with a vasoconstrictive effect that contributes to vascular changes associated with inflammation during an injury. PDGF and VEGF are involved in angiogenesis, the growth of new blood vessels and cell cycle proliferation (division) following injury. The coagulation factors include factor V and VIII, which are involved in the coagulation cascade that converts fibrinogen into fibrin mesh after platelet plug formation.
The final step of platelet plug formation is aggregation of the platelets into a barrier-like plug. Receptors on the platelet bind to VWF and fibrinogen molecules, which holds the platelets together. Platelets may also bind to subendothelial VWF to anchor them to the damaged endothelium. The completed plug will cover the damaged components of the endothelium and will stop blood from flowing out of it, but if the wound is large enough, blood will not coagulate until the fibrin mesh from the coagulation cascade is produced, which strengthens the platelet plug. If the wound is minor, the platelet plug may be enough to stop the bleeding without the coagulation cascade.