TAILIEUCHUNG - Chapter 109. Disorders of Platelets and Vessel Wall

Hemostasis is a dynamic process in which the platelet and the blood vessel wall play key roles. Platelets become activated upon adhesion to von Willebrand factor (vWF) and collagen in the exposed subendothelium after injury. Platelet activation is also mediated through shear forces imposed by blood flow itself, particularly in areas where the vessel wall is diseased, and is also affected by the inflammatory state of the endothelium. The activated platelet surface provides the major physiologic site for coagulation factor activation, which results in further platelet activation and fibrin formation. . | Chapter 109. Disorders of Platelets and Vessel Wall Hemostasis is a dynamic process in which the platelet and the blood vessel wall play key roles. Platelets become activated upon adhesion to von Willebrand factor vWF and collagen in the exposed subendothelium after injury. Platelet activation is also mediated through shear forces imposed by blood flow itself particularly in areas where the vessel wall is diseased and is also affected by the inflammatory state of the endothelium. The activated platelet surface provides the major physiologic site for coagulation factor activation which results in further platelet activation and fibrin formation. Genetic and acquired influences on the platelet and vessel wall as well as on the coagulation and fibrinolytic systems determine whether normal hemostasis or bleeding or clotting symptoms will result. The Platelet Platelets are released from the megakaryocyte likely under the influence of flow in the capillary sinuses. The normal blood platelet count is 150 000-450 000 pL. The major regulator of platelet production is the hormone thrombopoietin TPO which is synthesized in the liver. Synthesis is increased with inflammation and specifically by interleukin 6. TPO binds to its receptor on platelets and megakaryocytes by which it is removed from the circulation. Thus a reduction in platelet and megakaryocyte mass increases the level of TPO which then stimulates platelet production. Platelets circulate with an average life span of 7-10 one-third of the platelets reside in the spleen and this number increases in proportion to splenic size although the platelet count rarely decreases to 40 000 pL as the spleen enlarges. Platelets are physiologically very active but are anucleate and thus they have limited capacity to synthesize new proteins. Normal vascular endothelium contributes to preventing thrombosis by inhibiting platelet function Chap. 59 . When vascular endothelium is injured these inhibitory effects are

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