Platelets (BMS 114) PDF

Platelets General Physiology Theoretical BMS 114  Platelets (Thrombocytes) Small, non-nucleated, granulated bodies. Formation: Bone marrow from megakaryocytes. Count: the normal platelet count is 300...

Platelets General Physiology Theoretical BMS 114  Platelets (Thrombocytes) Small, non-nucleated, granulated bodies. Formation: Bone marrow from megakaryocytes. Count: the normal platelet count is 300,000/mm3, thrombocytopenia platelet count less than 50000/mm3. Structure: A. Platelet Membrane: - It contains receptors for: collagen, Von Willebrand factor and fibrinogen. - It has a glycoprotein coat contains phospholipids, which form platelet factor 3 (PF3). B. Platelet Cytoplasm: 2 types of granules: ✓ dense granules: they contain non-protein substances, e.g. ADP ,serotonin, calcium. ✓ alpha granules: they contain proteins, e.g. platelet activation factor (PAF) and platelet derived growth factor (PDGF) (helps growth of endothelium i.e. wound healing). Platelet structure Alpha granules (non-protein): ADP, serotonin, calcium. Dense granules (protein): Platelet activation factor (PAF) & platelet derived growth factor (PDGF).  Hemostasis Definition: Stoppage of bleeding from injured blood vessel. Hemostasis steps: I. Vasoconstriction of injured blood vessel. II. Temporary platelet plug formation by platelet reactions. III. Blood clot formation to stabilize the temporary platelet plug. IV. Limitation reaction to dissolve clot after wound healing. I. Local Vasoconstriction Injury of a blood vessel is immediately followed by its constriction. This reduces the blood flow from the vessel. Vasoconstriction is due to: 1. Nervous reflexes: initiated by pain sensation from traumatized vessel 2. Local myogenic contraction: due to direct damage of the blood vessels 3. Chemical substances: serotonin and thromboxane A2 liberated from platelets cause vasoconstriction  II. Formation of Temporary Platelet Plug (Platelets reactions) 1. Platelet adhesion 2. Platelet activation 3. Release reaction 4. Platelet aggregation 5. Platelet fusion 6. Platelet procoagulant activity  II. Formation of Temporary Platelet Plug (Platelets reactions) 1. Platelet adhesion Normally platelets do not adhere to healthy blood vessels. However, when a blood vessel is cut, subendothelial collagen and von Willebrand factor are exposed, and platelets adhere to them by their membrane receptors. 2. Platelet activation Platelets swell, change their shape, put out pseudopodia, stick to other platelets and release of the platelet granules occurs. 3. Release reaction: when the contents of dense and alpha granules are released, they go into action: ADP: stimulates aggregation and activation of new platelets. Serotonin: stimulates vasoconstriction. PAF: stimulates aggregation and activation of new platelets. PDGF: stimulates the growth of the endothelial lining of blood vessels, helping their repair. Thromboxane A2: stimulates aggregation and activation of new platelets.  II. Formation of Temporary Platelet Plug (Platelets reactions) 4. Platelet aggregation: Released ADP and thromboxane A2 cause platelet aggregation at the site of injury. 5. Platelet procoagulant activity: Platelet release and aggregation results in exposure of PF3 on the platelet membrane. PF3 helps to start blood coagulation by activating some clotting factors. 6. Platelet fusion: Aggregated platelets undergo irreversible fusion.  Thromboxane A2 & prostacyclin formation PAF X Aspirin  Thromboxane A2 & prostacyclin formation Platelet activating factor (PAF) lead to the formation of arachidonic acid from membrane phospholipids, Arachidonic acid is then converted by cyclooxygenase to prostaglandin. In platelets, the enzyme thromboxane A2 synthase converts prostaglandin to thromboxane A2, which causes vasoconstriction, helps the release reaction and platelet aggregation. In endothelium the enzyme prostacyclin synthase converts prostaglandin to prostacyclin, which causes vasodilation, and decreases platelets release and aggregation and kept platelets plug localized. Aspirin inhibits cyclooxygenase. It therefore decreases the synthesis of both thromboxane A2 and prostacyclin. Therefore, the daily intake of small amounts of aspirin reduces clot formation and prevents myocardial infarctions.