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There are certain glycoproteins present on the platelet surface that takes part in platelet adhesion and aggregation. Also the collagen receptors present on the platelet can directly bind to subendothelial collagen further anchoring the adhesion. After initial adhesion, platelets are activated releasing factors that promote platelet aggregation. This aggregation occurs mostly by inter platelet interaction of Gp IIb/IIIa receptors present on the surface membrane. All these events lead to platelet plug formation. (Harrison 2005, p337) To stabilize the initial platelet plug, fibrin meshwork is required which only becomes available after series of activation of various clotting factors. The activation of these clotting factors is like a cascade reaction in which one activates the other until a loop is formed. There are two distinct pathways; extrinsic and intrinsic pathways. Tissue factor (TF) initiates coagulation by activating classic extrinsic pathway, whereas, intrinsic pathway play a role in propagation of the cascade. All this activation takes place mostly at the phospholipid membranes of the platelets. Tissue factor responsible for initiation is expressed by damaged and exposed components of the vessel wall as well as released by platelets and monocytes. Coagulation process ultimately activates thrombin from its inactive state which in turn converts fibrinogen into fibrin. These fibrins then arrange in an orderly manner, providing a mesh work that anchor the platelets and form a fibrin clot at the site of injury. (Harrison 2005, pp.337-339) 2. Three major components of Virchow’s triad include stasis, hypercoagulability and endothelial injury. This triad basically explains the haemostatic mechanisms that promote thrombus formation. Stasis is the interruption to the normal blood flow or obstruction in the circulatory system. Immobility, venous insufficiency and mitral stenosis are few causes which promote stasis of blood. Heart arrhythmias can also lead to turbulence of blood, interrupting the normal flow. Stasis allows the settlement of clotting factors and platelets, thereby, promoting thrombosis. Muscle contraction is a major force that moves the venous blood towards heart against gravity. Therefore, immobility results in pooling and stasis of blood in the lower extremity and is an important cause of deep venous thrombosis. (Torshin 2007, p55) Damage to vascular endothelium is a very strong promoter of thrombus formation. Thrombus formation at the site of vascular injury is a normal physiological mechanism that aims to prevent any blood loss. Endothelial injury results in platelet adhesion and aggregation with the release of tissue factor that activates the coagulation cascade ultimately forming the fibrin meshwork that anchors the platelets and form a thrombus. Common causes of vascular endothelial injury include long standing hypertension, inflammation and trauma. (Torshin 2007, p55) There are many factors that can predispose to hypercoagulability state such as pregnancy, use of oral contraceptive pills, sepsis, trauma etc. Most importantly any pathology that increase blood viscosity or increase cellular components of plasma can lead to hypercoagulable state. Polycythemia and myeloproliferative disorders are few examples. Similarly factors deficiency of factors that inhibit coagulation can promote thrombus formation. (Torshin 2007, pp.55-56) 3: Three major compo ...Show more
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Summary

Haematology Instructor University Haemostasis 1: Vascular injury initiates various multistep processes to ensure that a clot is formed at the site of injury to prevent any loss of blood. Two important steps involved in the prevention of blood loss and repair include platelet plug and fibrin clot formation…
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