When the damage to small blood vessels is observed there are two main steps which should be taken one is the hemostasis and another is the stoppage of bleeding. Hemostasis has two phases: primary hemostasis and secondary hemostasis.

The primary hemostasis is categorized by platelet adhesion, vascular contraction and the formation of a softaggregate plug. When an injury is occurred and it causes local contraction of vascular smooth muscle for temporary time period,

 

 

the vasoconstriction slows down the flow of blood and activating the platelet adhesion. The adhesion begins when subendothelium attaches to the von Willebrand factor. Platelets starts collecting at the injured surface and then the platelets are activated to contact with collagen. The collagen activated platelets then stretch out to cover the injured surface. The fibrinogen has many platelet binding sites. The fibrinogen and platelets aggregation build up to make a soft plug. This aggregation occurs after 20 seconds of injury. The primary hemostasis is of short period.

 

 

The secondary hemostasis is accountable for stabilization of soft clot and for the maintenance of vasoconstriction. The vasoconstriction is maintained by thromboxane, serotonin and prostaglandin. After this the soft plug is then solidified because of a complex interaction between enzymes, membrane and coagulation factors. The coagulation factors circulate in the body in an inactive form until the coagulation cascade in initiated. The coagulation factors are produced by the liver. This is a chain reaction and on completion of each and every step, another coagulation factor is activated which leads to the conversion of fibrinogen to fibrin.