الفهرس 
THROMBOPOIESISOnly 14 pages are availabe for public view
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Abstract
latelets are small anucleate disc shaped particles shed from the cytoplasm of megakaryocytes, which is the only polyploidy haematopoietic cell.
Once the platelets have been filled with its organelles and granule content they will be released via the megakaryocytic cytoplasmic extensions called the proplatelet tips
Platelets contain four distinguishable storage granule types, the α granule, the dense granule, the lysosomes & the microperoxisomes. These granules are filled with biologically active proteins that greatly contribute to platelet functions.
On platelet activation by an agonist such as collagen or thrombin the granules migrate to cell surface & release their granule content in varying quantities depending on the strength of the agonist.
Platelet surface membrane glycoproteins which belong to several receptor families including: integrins, leucine-rich GPs, immunoglobulin cell adhesion molecules, and selectin, together with the secretory granules enables the platelets to perform their boivital role in hemostasis, they arrest bleeding from damaged blood vessels by plugging the defect and formation of primary hemostatic plug. Platelets perform this task via platelet adhesion to the wounded area, platelet activation, platelet secretion of their secretory granule content and platelet aggregation.
Platelets have also been found to play a role in systemic diseases, Although platelet aggregation is crucial to stop bleeding from an injured vessel, platelets also form aggregates on ruptured atherosclerotic plaques, consequently triggering thrombus formation that can completely block blood flow, causing myocardial infarction, stroke, and other thrombotic disorders.
Antiplatelet agents that inhibit platelet activation adhesion or aggregation e.g aspirin, clopidogrel are used as prophylactic and therapeutic treatment for these systemic diseases.
Abnormalities in platelet granule content (e.g.Gray platelet syndrome) or in surface membrane glycoprotein receptors (e.g.Glanzmann thrombasthenia) result in a variety of congenital disorders manifested by bleeding diathesis of variable degrees.
Platelet functions can also be affected by systemic diseases (e.g. uremia), hematological disorders (e.g.chronic myeloproliferative disorders) and drugs (e.g.NSAIDs).
Treatment of platelet disorders is mainly by platelet transfusion if there is severe bleeding, while mild cases can be treated by desmopressin or recombinant factor VIIa.
Recently the potential for gene therapy by altering megakaryocytes gives hope for treating platelet disorders.