Haemostasis is the ability to stop the flow of blood in an event of external injury or a breach in a reasonably sized vessel within minutes without affecting the rest of blood flow in the body. The haemostasis consists of four main processes vascular response, platelet response, Coagulation and Fibrinolysis. But when haemostasis is not stopped and goes overactive or get activated inappropriately activated can cause thrombosis and few other complications. The first three step in haemostasis is rapid the first step is vascular spasm or vasoconstriction in which the blood vessels constrict to allow less blood to flow and be lost. In the second step, the platelet sticks together to form a platelet plug to cover the break in the vessel. …show more content…
Fibrin is not present in our blood but it floats around with a protein attached to it which is basically fibrinogen, so it is converted to fibrin by Coagulation cascade. There are many proteins in our blood known as the coagulation factors or serine protease that circulate as inactive zymogens, upon the activation of this zymogens it initiates a coagulation cascade. There are two coagulation pathways involved in the secondary haemostasis called the extrinsic and intrinsic coagulation pathways both of which lead to a common pathway the activation of factor X, thrombin and the final product fibrin. The intrinsic pathway or contact activation pathway starts when factor XII also known as Hageman factor is activated. In intrinsic pathway, once in contact with the activated platelets, the platlets promote the activation of FXll to form FXlla which activates FXl to FXla which activates FlX to FlXa which has a co-factor FVlla and together activates FX to FXa which then with its cofactor FVa make thrombin which then helps to make …show more content…
The FVlla than activates FX to form FXa, which combines with its cofactor FVa and helps convert prothrombin to thrombin. Thrombin then activates other components of the coagulation cascade like FVll, FV, FXl and FVlll and converts fibrinogen to fibrin. because of the continued activations of FVlll and FXl by thrombin in both the pathways the coagulation cascade is maintained until it is down-regulated by the anticoagulation pathway. Thrombin also activates Factor Xlll which help fibrin to form covalent bonds that create a linkage between the fibrin polymers to form an insoluble fibrin network or mesh. The thrombin also produces antithrombin and plasmin which work as the negative feedback in this process and stops the clot going out of