Coagulation is a synonymous term for clotting. It may refer to the coagulation of blood, lymph, or proteins. In addition, there is the procedure of electrocoagulation in high-frequency surgery.
What is coagulation?
Coagulation is a synonymous term for clotting. It can refer to the coagulation of blood, lymph, or proteins. Medically relevant is on the one hand the coagulation of blood and on the other hand the coagulation of proteins. The coagulation of blood or lymph is also referred to as hemostasis. Hemostasis is responsible for stopping bleeding. Hemostasis can be divided into two sub-processes. Primary hemostasis is called hemostasis, and secondary hemostasis is called blood coagulation. Protein coagulation plays a role mainly in the development of coagulation necroses. Such necroses are found, for example, when exposed to heat or acid.
Function and role
Coagulation of blood is a vital function of the body. It is only thanks to coagulation that excessive leakage of blood from the vessels can be prevented in the event of injury. In addition, coagulation creates the prerequisite for wound healing. Immediately after the injury, hemostasis already begins. When a blood vessel is injured, blood escapes and comes into contact with the surrounding connective tissue. The blood platelets (thrombocytes) attach themselves to the collagen fibers of the connective tissue. This process is called platelet adhesion. The von Willebrand factor creates a connection between the individual platelets so that the wound is covered by a thin layer. The platelets are activated by the adhesion process. They release various substances that, among other things, induce coagulation. In addition, the platelets aggregate, forming a plug that temporarily closes the wound. However, this white thrombus is not particularly stable. For a firmer closure, plasmatic hemostasis with blood coagulation is needed. Plasmatic hemostasis or secondary hemostasis is the phase of blood coagulation. This can be divided into different phases. In the activation phase, platelets are activated. This occurs through contact with connective tissue. The contact converts clotting factor VII into its active form and some thrombin is formed. When sufficient thrombin has been produced, 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. This is followed by the coagulation phase. In the coagulation phase, the enzymatically active thrombin cleaves various chemical units from fibrinogen. This results in the formation of fibrin. The fibrin is deposited between the platelets, forming stable bonds. 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 and thus pull on the network of fibrin. As a result, the wound edges also contract and the wound is closed. Connective tissue cells, however, can still penetrate the wound. They are responsible for wound healing.
Diseases and complaints
Blood coagulation can be disrupted at any stage of clotting. The end result of each of these different disturbances is an increased tendency to bleed. Primary hemostasis may be impaired in the presence of severe platelet deficiency. This is referred to as thrombocytopenia. This can be the result of leukemia or an infectious disease, for example. The most common congenital disorder of primary hemostasis is Willebrand-Jürgens syndrome. In most cases, however, blood coagulation is only slightly impaired, so that many affected individuals are unaware of their condition. Furthermore, coagulation disorders can occur if coagulation factors are missing. The best-known example of this type of disease is hemophilia. It is also known as hemophilia. The most common forms of hemophilia are hemophilia A and hemophilia B. Hemophilia A lacks coagulation factor VIII, while hemophilia B lacks coagulation factor XI. These disorders are congenital. However, clotting can also be affected by a deficiency of vitamin K.In the case of vitamin K deficiency, coagulation factors II, VII, IX and X can no longer be produced by the liver in sufficient quantities. Since most clotting factors are produced in the liver, liver diseases can also lead to disorders of coagulation and thus to increased bleeding. However, not only coagulation disorders that lead to an increased tendency to bleed are life-threatening, but also disorders in which blood coagulation occurs abnormally. An example of such a disorder is disseminated intravascular coagulopathy (DIC). This consumptive coagulopathy usually occurs as a complication of various medical conditions. For example, consumption coagulopathy may occur in the setting of shock, severe sepsis, extensive burns, or birth complications. DIC is initiated by pathologically elevated levels of histamine, serotonin, epinephrine, by destruction of platelets or by bacterial toxins. Increased clotting factors are consumed and tiny blood clots (microthrombi) are formed. These clog the vessels. The lungs, kidneys and heart are particularly affected. In the second stage of the disease, there is a decrease in platelets and clotting factors. This is followed by fibrinolysis. 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). Thus, while thrombi have formed at some sites due to increased coagulation, bleeding occurs at other sites because of this. In the final stage of DIC, full-blown shock develops.
