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Antiplatelet therapy with one or more of these drugs decreases the ability of blood clots to form by interfering with the platelet activation process in primary hemostasis. Antiplatelet drugs can reversibly or irreversibly inhibit the process involved in platelet activation resulting in decreased tendency of platelets to adhere to one another ...
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.
Platelet storage pool deficiency is a family of clotting disorders characterized by deficient granules in platelets. Individuals with these disorders have too few or abnormally functioning alpha granules , delta granules , or both alpha and delta granules and are therefore unable to form effective clots, which leads to prolonged bleeding.
Other causes of reactive thrombocythemia include: post surgery, iron deficiency, drugs, and rebound effect after bone marrow suppression. [8] Research suggests that thrombocytosis can also occur after physical exercise, and is triggered by hemoconcentration and the release of platelets from the liver, lungs and spleen. [3] [9]
Platelet donation therapy is frequently needed by cancer patients, because chemotherapy for such patients can render them unable to generate platelets of their own. The basic principles of automatic platelet apheresis are the same as in the manual procedure, but the whole procedure is performed by a computer-controlled machine.
Platelet plug formation: Platelets adhere to damaged endothelium to form a platelet plug (primary hemostasis) and then degranulate. This process is regulated through thromboregulation. Plug formation is activated by a glycoprotein called von Willebrand factor (vWF), which is found in plasma. Platelets play one of major roles in the hemostatic ...
The incidence of bone marrow failure is triphasic: one peak at two to five years during childhood (due to inherited causes), and two peaks in adulthood, between 20 and 25 years old and after 60 years old (from acquired causes). [14] One in ten individuals with bone marrow failure have unsuspected Fanconi anemia (FA). [14]
The underlying mechanism for the deleterious effect proposes that endothelial cells lining the microvasculature in the body express COX-2, whose selective inhibition results in levels of prostaglandin I2 (PGI2, prostacyclin) down-regulated relative to thromboxane (since COX-1 in platelets is unaffected).