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Platelets arise from megakaryocytic precursors in the bone marrow. Maturation and production is regulated by several general cytokines and the more specific platelet growth factor, thrombopoietin. Platelet production occurs through the specialized process of endomitosis, by which DNA replicates without cell division, resulting in the polyploid nuclei characteristic of megakaryocytes.1 Proplatelet extensions form from megakaryocytic cytoplasm; once granule and cytoplasmic organization is complete, platelets are released from the ends of the proplatelet structures. After leaving the marrow, approximately one third of the platelet mass is sequestered in the spleen, while the other two thirds circulate with a life span of 7 to 10 days. Thrombopoiesis is balanced by platelet senescence and consumption to maintain a normal blood platelet count (150,000–400,000/mm3) via the plasma thrombopoietin level. Platelets have an average diameter of 2.0 to 5.0 mm and typical mean platelet volumes of 6 to 10 femtoliters.1 Their external surface consists of a lipid bilayer containing a variety of structural glycoproteins. The anuclear cytoplasm contains dense granules, which store calcium, serotonin, adenosine diphosphate (ADP), and adenosine triphosphate (ATP), and the more numerous alpha granules, which contain other biologically active proteins including fibrinogen, von Willebrand factor, factor V, and other adhesive molecules.

Circulating platelets fulfill many critical hemostatic functions, including adhesion to sites of vascular injury, amplification of the platelet response, secretion of mediators of hemostasis, and aggregation via fibrinogen binding. After vascular injury, these processes lead to formation of a platelet plug, which constitutes primary hemostasis. Platelets also play a central role in activation of the coagulation cascade, or secondary hemostasis (eFig. 439.1). Platelets potentiate secondary hemostasis by providing a phospholipid (cofactor) surface on which several key coagulation reactions can take place. For example, the activated platelet surface accelerates the conversion of prothrombin to thrombin by several hundred-thousandfold.2

eFigure 439.1.

The role of platelets in hemostasis. A: With vessel injury, circulating unactivated platelets tether to exposed subendothelial matrix via specific platelet receptors (circles and rods). B: With progressive adhesion, platelets undergo activation, shape change, and exposure of other activated receptors (crosses), culminating in formation of the platelet plug. C: At the activated platelet surface (crescentic forms), phosphatidylserine (a coagulation cofactor) is preferentially exposed at the outer membrane leaflet, thereby potentiating the activation of factor X to factor Xa and factor II (prothrombin) to factor IIa (thrombin). Thrombin is the critical enzyme that allows formation of the fibrin clot. Factors VIII and IX, the proteins that are deficient in hemophilia A and hemophilia B, respectively, are cofactor (in its activated form, factor VIIIa) and zymogen (factor IXa is the active enzyme) for the initial reaction depicted in C. Factor VIII normally circulates in the plasma bound to von Willebrand factor. Roman numerals signify coagulation proteins, functioning as either zymogens (circles), enzymes (excised circles), or cofactors (ovals).

(From Yee DL. Platelets as modifiers of clinical phenotype in hemophilia. ...

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