Coagulation

Coagulation is a synonymous term for Coagulation. This can mean the coagulation of blood, lymph or proteins. There is also the electrocoagulation procedure in high-frequency surgery.

What is the coagulation?

Blood coagulation on the one hand and the coagulation of proteins on the other hand are medically relevant. The clotting of blood or lymph is also called Hemostasis designated. Hemostasis is responsible for stopping bleeding. Hemostasis can be divided into two sub-processes. The primary hemostasis is called hemostasis, the secondary hemostasis is called blood clotting.

Protein coagulation plays a role in the development of coagulation necrosis. Such necroses are found, for example, when exposed to heat or acids.

Function & task

The coagulation of blood is a vital function of the body. Only thanks to coagulation can excessive blood escape from the vessels in the event of injuries. In addition, the coagulation creates the prerequisite for wound healing.

Hemostasis begins immediately after the injury. When a blood vessel is injured, blood leaks out and comes into contact with the surrounding connective tissue. The blood platelets (thrombocytes) adhere to the collagen fibers of the connective tissue. This process is known as platelet adhesion.

The von Willebrand factor creates a connection between the individual blood platelets so that the wound is covered with a thin layer. The process of adhesion activates the platelets. They release various substances which, among other things, induce coagulation. In addition, the platelets aggregate and form a plug that temporarily closes the wound. However, this white thrombus is not particularly stable. Plasma hemostasis with blood coagulation is required for a tighter seal.

The plasmatic hemostasis or secondary hemostasis is the phase of blood clotting. This can be divided into different phases. In the activation phase, the platelets are activated. This happens through contact with the connective tissue. The contact converts the coagulation factor VII into its active form and some thrombin is formed.

When sufficient thrombin has been formed, a complex of factors IV and VIII is activated. This activator complex in turn activates the important factor X. The activation phase ends with the formation of active thrombin.

The coagulation phase follows. The enzymatic active thrombin cleaves various chemical units from fibrinogen in the coagulation phase. This creates fibrin. The fibrin is deposited between the platelets so that stable bonds are formed. This stabilizes the entire thrombus. Red blood cells (erythrocytes) are also deposited in the fibrin-platelet network. The white thrombus becomes a red thrombus.

The platelets contract, pulling the fibrin network. As a result, the wound edges contract and the wound is closed. Connective tissue cells can, however, still penetrate the wound. They are responsible for wound healing.

Illnesses & ailments

The coagulation of the blood can be disturbed in any phase of the coagulation. Each of these various disorders ultimately leads to an increased tendency to bleed. Primary haemostasis can be impaired if there is a severe platelet deficiency. One speaks here of thrombocytopenia. This can be the result of leukemia or an infectious disease, for example.

The most common congenital disorder of primary hemostasis is Willebrand-Juergens syndrome. In most cases, however, the blood clotting is only slightly impaired, so that many people affected are not aware of their disease.

Furthermore, coagulation disorders can occur if there are no coagulation factors. The best-known example of diseases of this type is hemophilia.It is also known as hemophilia. The most common forms of hemophilia are hemophilia A and hemophilia B. In hemophilia A, coagulation factor VIII is absent, in hemophilia B, coagulation factor XI is absent. These disorders are innate.

However, coagulation can also be impaired by a lack of vitamin K. If there is a vitamin K deficiency, the coagulation factors II, VII, IX and X can no longer be produced in sufficient quantities by the liver. Since most of the coagulation factors are produced in the liver, problems with coagulation and thus increased bleeding can also occur in liver diseases.

Life-threatening, however, are not only coagulation disorders that lead to an increased tendency to bleed, but also disorders in which blood clotting occurs abnormally. An example of such a disorder is disseminated intravascular coagulopathy (DIC). This consumption coagulopathy usually occurs as a complication of various clinical pictures. Consumption coagulopathy can occur in the context of shock, severe blood poisoning, extensive burns or birth complications. DIC is initiated by pathologically increased levels of histamine, serotonin, adrenaline, by the destruction of blood platelets or by bacterial toxins.

Coagulation factors are increasingly consumed and the formation of tiny blood clots (microthrombi) occurs. These clog the vessels. The lungs, kidneys and heart are particularly affected. In the second stage of the disease, there is a decrease in blood platelets and clotting factors. Fibrinolysis follows. Due to the lack of platelets and clotting factors, the body can no longer close damaged blood vessels. The result is uncontrolled bleeding (hemorrhagic diathesis). While thrombi have formed in some places due to the increased coagulation, bleeding occurs in other places. In the final stage of DIC, the full image of a shock emerges.