Coagulation System
The arrest of bleeding, also called blood clotting or hemostasis, is the ability of blood to provide closure to a wound.
The blood taken from the blood vessels "coagulates" spontaneously in the test tube within a few minutes. The blood changes from a liquid state to a gelatinous state with the participation of formed elements. The property of blood to coagulate outside the vascular system is an extremely vital process whose importance lies in protecting the body from loss of its blood fluid.
The wound plug, initially composed solely of thrombocytes, is not capable of permanently closing the injured vascular site. This is also a good thing, because otherwise such grafts could sometimes be formed too quickly. The complex coagulation system ensures that coagulation only takes place when it is really needed.
It is activated at the site of the injury at the same time as the complex platelet processes take place. Its clearly slower process ends in the formation of fibrin threads, which spin through the wound graft in a net-like manner and usually also deposit in the immediate vicinity of the graft, whereby abundant erythrocytes are included.
The final strength of the closure plug is achieved by the contraction of the platelets, which are "felted" with their pseudopodia and fibrin threads.
This process, which normally takes 5 - 7 minutes (coagulation time), involves platelets as well as a large number of plasmatic factors.
The actual coagulation process - like primary haemostasis - is triggered by the vessel and tissue injury and activated in two different ways:
- exogenous or extravascular way (Extrinsic System)
- endogenous or intravascular way (Intrinsic System)
On the exogenous path, activation takes place very quickly (within seconds), while on the endogenous path, activation takes place over a larger number of intermediate stages and takes longer (minutes). As a rule, both systems are involved in the normal coagulation process. The common final stage of the two activating systems finally makes prothrombin (factor II) and vitamin K formed in the liver is converted into thrombin. The thrombin thus formed is an enzyme, which also synthesizes the fibrinogen (factor I) and thus initiates the formation of fibrin.