Clotting begins when vascular endothelial cells are damaged. This damage can occur because of pre-existing health conditions, trauma, or randomly.
Platelets respond to endothelial cell damage by binding to the exposed collagen from the site of damage. This occurs through a cell adhesion ligand called von Willebrand factor.
Platelets recruit other platelets to aggregate at the site of damage through stimulation factors released during adhesion to the damaged endothelial cells.
More platelets are attracted to the site of damage, which allows the clot to form and grow in size. This prevents pathological loss of blood plasma through the damaged area.
Fibrinogen is a blood plasma protein that is activated by thrombin and turned into fibrin which is insoluble. Fibrin helps link platelets together.
Fibrin seals a clotted area by linking the platelets together. The appearance of fibrin is similar to a "mesh."
In order to prevent other pathological conditions, like infarction, the blood clot must dissolve once the endothelial cells have been repaired.
The liver produces many of the clotting factors that participate in the cascade resulting in fibrin activation and sealing of the blood clot.
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