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Atherosclerosis and Thrombus Formation
Thrombus Formation I -- Platelet Activation
 Rupture
of the atherosclerotic plaque exposes the subendothelial collagen
to the bloodstream [Kumar V, et al. Basic Pathology. 5th Edition.
Philadelphia, W.B. Saunders Co., 1992]. On contact with
collagen, platelets become activated, with platelet adhesion,
secretion of platelet contents, and platelet aggregation at
the site of injury. The activated platelet surface is
an essential catalytic surface for several coagulation reactions
that generate thrombin, a key factor in the coagulation sequence
[D'Souza D, et al. Lancet. 1994;344:991].
Platelets adhere to exposed subendothelium through
interaction with a variety of platelet surface receptors,
the most important of which is GP-Ib-IX [Hirsch J, et al.
In: Colman RW, et al (eds). Hemostasis and Thrombosis: Basic
Principles and Clinical Practice, Third Edition. Philadelphia,
J.B. Lipincott Company, 1994:1151]. This glycoprotein
is the main receptor for the subendothelial protein ligand
von Willebrand factor (vWF).
Platelet aggregation requires the platelet membrane
glycoprotein integrin receptor (GP IIb-IIIa), which -- at
least under low fluid shear stress conditions -- is involved
in calcium-dependent interplatelet bridging by bound fibrinogen.
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Stroke Education
