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The normal range (99% of population analyzed) for platelets in healthy white people is 150,000 to 450,000 per cubic millimeter (a mm 3 equals a microliter). Platelet concentration is measured either manually using a hemocytometer, or by placing blood in an automated platelet analyzer using electrical impedance, such as a Coulter counter. 10.3 Drugs that stimulate platelet production.10.2 Drugs that suppress platelet function.9.2 Altered platelet function (thrombocytopathy).5.2.3.4 Platelet-coagulation factor interactions: coagulation facilitation.An arterial thrombus may partially obstruct blood flow, causing downstream ischemia, or may completely obstruct it, causing downstream tissue death.
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This type of thrombosis arises by mechanisms different from those of a normal clot: namely, extending the fibrin of venous thrombosis extending an unstable or ruptured arterial plaque, causing arterial thrombosis and microcirculatory thrombosis. Normal platelets can respond to an abnormality on the vessel wall rather than to hemorrhage, resulting in inappropriate platelet adhesion/activation and thrombosis: the formation of a clot within an intact vessel. A disorder of platelet function is called a thrombocytopathy or a platelet function disorder.
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Elevated platelet concentration is called thrombocytosis, and is either congenital, reactive (to cytokines), or due to unregulated production: one of the myeloproliferative neoplasms or certain other myeloid neoplasms. Low platelet concentration is called thrombocytopenia, and is due to either decreased production or increased destruction. Following the rupture of the blood vessel wall, the platelets are exposed and they adhere to the collagen in the surrounding connective tissue. The platelet cell membrane has receptors for collagen. Platelets also participate in both innate and adaptive intravascular immune responses. Some would add the subsequent retraction and platelet inhibition as fourth and fifth steps to the completion of the process and still others would add a sixth step, wound repair. These processes may overlap: the spectrum is from a predominantly platelet plug, or "white clot" to a predominantly fibrin, or "red clot" or the more typical mixture. Formation of this platelet plug (primary hemostasis) is associated with activation of the coagulation cascade, with resultant fibrin deposition and linking (secondary hemostasis). Third, they connect to each other through receptor bridges: aggregation.
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Second, they change shape, turn on receptors and secrete chemical messengers: activation. First, platelets attach to substances outside the interrupted endothelium: adhesion. They gather at the site and, unless the interruption is physically too large, they plug the hole. One major function of platelets is to contribute to hemostasis: the process of stopping bleeding at the site of interrupted endothelium. A healthy adult typically has 10 to 20 times more red blood cells than platelets. The smear is used to examine platelets for size, shape, qualitative number, and clumping. On a stained blood smear, platelets appear as dark purple spots, about 20% the diameter of red blood cells. The platelets congregate around the wound in order to create a cap to stop blood flow out of the tissue. As more platelets gather around the opening, they produce more ligands to amplify the response. The ligands, denoted by letter L, signal for platelets (P) to migrate towards the wound (Site A).