Platelets and minimises blood loss until platelets

Platelets are not complete cells but are fragments of cells from larger cells known as megakaryocytes, a platelet is 2 to 4µm in diameter, approximately 1000 platelets are produced from a single megakaryocyte (Lauralee Sherwood, 2016). Platelets are functional for an average of ten days, once the ten day expire they are removed from circulation by tissue microphages and are replaced by new platelets from the bone marrow (Lauralee Sherwood, 2016).Platelets are essential for haemostasis, which is the process of stopping bleeding from a ruptured vessel. For bleeding to commence from a vessel, a rupture in the vessel wall must be present and the pressure gradient must be greater in the vessel to force the blood out. When a cut or vessel is ruptured the vessel immediately constricts. The constriction of the blood vessel or vascular spasm slows the flow of blood through the defected vessel and minimises blood loss until platelets can arrive to the damaged site (Lauralee Sherwood, 2016). Platelets do not normally adhere to the smooth endothelial lining of blood vessels, but they can adhere to damaged vessel walls. Once the endothelial lining is disrupted due to vessel injury, the platelets which are always present in the plasma adhere to the exposed collagen, collagen is a fibrous protein in the connective tissue which underlays the endothelial lining (Lauralee Sherwood, 2016). Von Willebrand Factor (vWF) has binding sites to which the moving platelets attach by means of receptors on the cells surface. VWF also serves as a bridge between the injured vessel wall and the platelets. The adherence prevents the platelets from being swept away in the circulation. The layer of platelets adhered with one another, this the foundation of a haemostatic platelet plug at the defected site (Lauralee Sherwood, 2016). Collagen activates the bound platelets, normally platelets have a smooth surface and are of disc shaped but once activated platelets are activated they quickly reorganise their actin cytoskeletal to develop spikey processes which aid in the adherence process as seen in Figure 2 3. Activated platelets also release chemicals from their storage granules, one of these chemicals is adenosine diphosphate (ADP), this ADP causes the surface of nearby platelets to become sticky aiding in the platelet aggregation and reinforces the injured vessel wall (Lauralee Sherwood, 2016). This platelet plug is limited only to the defected zone and does not spread to the nearby undamaged vascular tissue due to the inability to adhere to the smooth endothelial wall.


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