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The PFA-100 (Platelet Function Assay — 100) is a system for analysing platelet function in which citrated whole blood is aspirated through a disposable cartridge containing an aperture within a membrane coated with either collagen and epinephrine or collagen and ADP. These agonists induce platelet adhesion, activation and aggregation, leading ...
They circulate in the blood of mammals and are involved in hemostasis, leading to the formation of blood clots. Platelets release thread-like fibers to form these clots. The normal range (99% of population analyzed) for platelets is 150,000 to 450,000 per cubic millimeter. [6] If the number of platelets is too low, excessive bleeding can occur.
Platelets are regulators of hemostasis and thrombosis. Platelets become active in the blood following vascular injury. Vascular injury causes platelets to stick to the cellular matrix that is exposed under the endothelium, form a platelet plug, and then form a thrombus. Platelets are essential in the formation of an occlusive thrombus and are ...
Platelet count increase as well as platelet survival after transfusion is related to the dose of platelets infused and to the patient's body surface area (BSA). Usually these values are less than what would be expected. Corrected platelet count increment (CCI) = platelet increment at one hr x BSA (m 2) / # platelets infused x 10 11
Hypercoagulable state (thrombophilia) results from defects in regulation of platelet or clotting factor function, and can cause thrombosis. Infectious disorders of blood Blood is an important vector of infection. HIV, the virus that causes AIDS, is transmitted through contact with blood, semen or other body secretions of an infected person.
Thrombopoietin is a glycoprotein hormone produced by the liver and kidney which regulates the production of platelets. It stimulates the production and differentiation of megakaryocytes, the bone marrow cells that bud off large numbers of platelets. [5] Megakaryocytopoiesis is the cellular development process that leads to platelet production.
Thrombocytopenia in hospitalized alcoholics may be caused by spleen enlargement, folate deficiency, and most frequently, the direct toxic effect of alcohol on production, survival time, and function of platelets. [23] Platelet count begins to rise after 2 to 5 days' abstinence from alcohol.
Exposure of blood to the subendothelial space initiates two processes: changes in platelets, and the exposure of subendothelial platelet tissue factor to coagulation factor VII, which ultimately leads to cross-linked fibrin formation. Platelets immediately form a plug at the site of injury; this is called primary hemostasis.