Chemistry Reference
In-Depth Information
Figure 2.1
Mechanism of thrombosis. The platelet activation mechanisms and acti-
vation of the coagulation system synergize in thrombus formation. Platelets
have different cell-surface receptors that are activated by specific agonists.
Upon activation, these receptors trigger intracellular signal transduction
mechanisms, resulting in the activation of integrin receptors GP IIb/IIIa.
Activated GP IIb/IIIa receptors bind to the RGD motif of fibrinogen,
thereby cross-linking activated platelets which leads to platelet aggregation.
Among the various platelet surface receptors, PAR-1 (thrombin receptor)
is by far the most potent inducer of platelet activation. Concurrent with
platelet activation, the coagulation process is also triggered by the exposure
of tissue factor to blood, resulting in the production of thrombin. In its
procoagulant role, thrombin cleaves soluble fibrinogen to fibrin which
cross-links to form an insoluble fibrin meshwork that traps aggregated
platelets and other plasma particles, leading to a growing thrombus.
chain of events leads to the aggregation of platelets. Depending on the nature of
the vascular injury, this may develop into either a normal hemostasis or a
pathologic condition (the latter resulting in vascular thrombosis, ischemic
stroke, etc.). The underlying platelet events constitute a complex series of
biochemical and cellular processes that can be classified as adhesion of platelets
to damaged vessel wall, activation of platelets, secretion of granular contents
from activated platelets, and aggregation of platelets.
23,24
The adhesion of platelets to denuded endothelium represents the primary
hemostatic response to vessel wall injury.
25
When endothelial layer disruption
occurs as a result of a vascular trauma, platelets adhere to the exposed endo-
thelium to form a discontinuous platelet monolayer. The adhered platelets
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