HEMOSTASIS AND ITS STEPS

HEMOSTASIS AND ITS STEPS

1. HEMOSTASIS SHARFUNNISA.S.H. I M.SC. HN & AZMATHULLAH I M.Sc.MGMD

2. INTRODUCTION Hemostasis combines the terms “ hemo ” (meaning “blood”) and “stasis” (meaning “standing still”). Haemostasis refers to the spontaneous arrest or prevention of bleeding from the injured/damaged vessels by the physiological process

3. STEPS Hemostasis involves three main steps Vasoconstriction, Formation of temporary haemostatic plug and Formation of the definitive haemostatic clot.

4. 1. VASOCONSTRICTION Immediately after injury, the blood vessel constrict and decreases the loss of blood from the damaged portion When the blood vessel is cut ,the endothelial is damaged and the collagen is exposed. Platelets adhere to this collagen and get activated and produces vasoconstrictor Initial vasoconstriction is caused by direct effect of injury on the vascular smooth muscles. The initial vasoconstriction is transient but is maintained for several minutes or even hours by humoral facilitation due to release 5HT (5- hydroxytryptamine ) (serotonin) and other vasoconstrictors.

5. 2. PLATELET PLUG FORMATION Formation of a temporary haemostatic plug by the platelets at the site of injury involves following steps: Platelet adhesions Platelet activation Platelet aggregation

6. PLATELET ADHESION Following injury, platelets come in contact with the damaged collagen fibres and endothelial cells of the vessel wall and change their characteristics. That is, they begin to swell and assume irregular forms with large number of pseudopodia protruding from the surface. The contractile proteins of the platelets contract forcibly and cause release of granules that contain multiple factors. They become sticky and therefore adhere to the collagen of damaged cell wall and to the damaged endothelium. Aspirin prevents platelet aggregation by inhibiting formation of thromboxane A2. Therefore, aspirin in low doses is of value in preventing myocardial infarction.

7. PLATELET ACTIVATION The platelets secrete large quantities of ADP and thromboxane A2, which act on the nearby platelets and cause their activation. Stickiness of these additional platelets causes them to adhere to originally activated platelets. In this way, a vicious cycle is initiated which leads to activation and adherence of large number of platelets.

8. PLATELET AGGREGATION The large numbers of activated sticky platelets stick to each other forming platelets aggregation. Platelets aggregation is also increased by platelet activatingfactor , a cytokine secreted by neutrophils, monocytes and platelet cell membrane lipids. Platelet aggregation initiates a series of reactions which result in formation of thromboxane A2 and prostacyclin from the platelet membrane phospholipids.

9. FORMATION OF TEMPORARY HEMOSTATIC PLUG The platelets adherence and aggregation ultimately lead to the formation of platelet plug. At first, it is a fairly loose plug but is successful in blocking the blood loss if the vascular opening is small. Inhibition of further plug formation: Prostacyclin formed from the membrane phospholipids inhibits thromboxane formation and thus curtail the process of further plug formation. This reaction keeps the platelets plug localized, i.e. prevents intravascular spread of plug.

10. FORMATION OF DEFINITIVE HAEMOSTATIC PLUG The temporary platelet plug is converted into the definitive haemostatic plug by the process of clot formation (blood coagulation) which involves a complex series of events. Platelets play an important role in the formation of the intrinsic prothrombin activator which is responsible for initiating the process of clot formation. Note. The blood clot formed at the site of injury results in a tight unyielding seal or the so-called definitive haemostatic plug.

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