Hemostasis is a term used to describe hemostasis. After a vessel is injured, various physiological processes occur to stop the bleeding.
What is hemostasis?
In hemostasis, the body stops bleeding that results from injuries to blood vessels. This prevents large amounts of blood from escaping. As part of hemostasis, the body brings bleeding caused by injuries to blood vessels to a halt. This prevents the escape of large amounts of blood. Hemostasis can be divided into two processes. However, both are closely related and interact with each other. Primary hemostasis is responsible for stopping bleeding after about one to three minutes. It is in turn divided into the three steps of vasoconstriction, platelet adhesion and platelet aggregation. Primary hemostasis is followed by secondary hemostasis, which takes about six to ten minutes. Here, too, three different phases (activation phase, coagulation phase and retraction phase) are distinguished. Disturbances in hemostasis can manifest as a tendency to bleed or as inadequate hemostasis.
Function and role
Primary hemostasis is the phase of hemostasis. Immediately after injury, the injured vessels contract. This process is called vasoconstriction. Vasoconstriction results in a narrowed vessel lumen in front of the injury. This slows blood flow in the injured area. Platelets attach to certain components of the injured vessel walls. Glycoprotein receptor Ib and / or glycoprotein receptor Ic/IIA are required for this adhesion reaction. The adhesion of platelets leads for an initial provisional covering of the wound. By these mechanisms, the bleeding is stopped after one to three minutes. Secondary hemostasis is the phase of actual blood clotting. In three steps, the provisional closure is replaced by a more stable fibrin net. Platelet contact with external factors activates various clotting factors. Negatively charged surfaces are found, for example, in glass or stainless steel. The activated clotting factors initiate a clotting cascade. If the coagulation cascade is set in motion in this way, there is an underlying activation of the intrinsic system. The extrinsic coagulation system is activated by the contact of blood with injured tissue. Here, too, a coagulation cascade follows. At the end of the coagulation cascade, enzymatically active thrombin is present in both the intrinsic and extrinsic systems. This causes polymerization of the fibrin. Fibrin is formed from the inactive fibrinogen. The so-called factor XIII ensures that the individual fibrin threads bind together. In this way, the platelet plug formed in the primary phase is stabilized and the wound closure is solidified. The resulting plug is called a red thrombus. The thrombin also causes the actin-myosin skeleton of the platelets to contract. The platelets contract, pulling the edges of the wound together. This causes the wound to close. The contraction of the wound and platelet-derived growth factor (PDGF) promote the immigration of connective tissue cells. From this point on, wound healing begins. So, in summary, hemostasis is a vital process that provides hemostasis in injuries. This prevents the excessive loss of blood. At the same time, the conditions for rapid healing of the wound are created.
Diseases and ailments
Disorders of hemostasis can lead to inadequate hemostasis and excessive hemostasis and coagulation, respectively. The causes of these defects are at the level of fibrinolysis, platelets, or coagulation itself. Diseases associated with an increased tendency to bleed fall under the term “hemorrhagic diathesis.” Hemorrhagic diatheses can be divided into four groups according to their pathomechanisms: Thrombocytopathies, Thrombocytopenias, Coagulopathies and Vascular Hemorrhagic Diatheses. Hemorrhagic diatheses include conditions such as hemophilia A, hemophilia B, Osler disease, Schönlein-Henoch purpura, hypersplenism, consumptive coagulopathy, and Willebrand-Jürgens syndrome. Characteristic for all these diseases is an increased bleeding tendency.In this case, the bleeding is either too long, too severe or caused by even the smallest injuries. In the hemophilic hemorrhage type, the hemorrhages are very extensive and relatively sharply limited. Bleeding into joints or muscles is typical here. Large-area bruising occurs after trivial injuries. These hemorrhages occur in diseases such as hemophilia A or hemophilia B. In thrombocytopenias or vascular diatheses, the bleeding occurs in the form of petechiae or purpura. Petechiae are small pinpoint hemorrhages of the skin or mucous membranes. In purpura, there are multiple small-spot skin hemorrhages. Diseases associated with excessive hemostasis are called thrombophilias. Here, there is an increased tendency to thrombosis. Hypercoagulability can be detected by laboratory diagnosis. Thrombophilias can be congenital or acquired. Acquired risk factors for the development of thrombophilia include obesity, smoking, pregnancy, estrogen-containing contraceptives, heart failure, and immobility after surgery or prolonged illness. Genetic risk factors include antithrombin deficiency, protein C deficiency, or protein S deficiency. In hemophilia, blood clots can form in all vessels of the body. However, the preferred locations are the deep veins of the legs. Thromboses often go unnoticed. Even severe thromboses that later lead to pulmonary embolism are often asymptomatic. With pronounced venous thrombosis, the ankles, lower leg or the entire leg swells. The affected extremity is also warm. The skin is taut. The feeling of tightness and pain may also occur throughout the leg. The most dangerous complication of thrombosis is pulmonary embolism. Here, the thrombus travels from the leg into the arteries of the lung, causing a life-threatening vascular occlusion.
