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
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 ...
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