Hemostamia is a series of processes that take place inside the blood vessels to retain blood fluid without clots or bleeding.
Educationally, hemostasis takes place in three stages that develop quickly and in a coordinated manner and mainly affect the platelets and proteins responsible for coagulation and fibrillation.
Hemostase occurs in a didactic way in three dependent and simultaneous stages.
Hemostamia begins as soon as the blood vessel is damaged. In response to the injury, a vasoconstriction of the injured vessel occurs to decrease local blood flow and thus prevent bleeding or thrombosis.
At the same time, the platelets are activated and attached to the ship’s endothelium using the von Willebrand factor. The platelets then change shape to release their contents to the plasma, which has the function of recruiting more platelets to the site of the lesion, and begin to adhere to each other, forming the primary platelet cap, which has a temporary effect. .
Learn more about platelets and their functions
At the same time as primary hemostatics occurs, the coagulation cascade is activated, causing the activation of the proteins responsible for coagulation. As a result of the coagulation cascade, fibrin forms, which strengthens the primary platelet layer, making it more stable.
Coagulation factors are proteins that circulate in the blood in its inactive form, but that are activated according to the needs of the body and have the ultimate goal of transforming fibrinogen into fibrin, fundamental to the process of blood stagnation.
Fibrillalysis is the third stage of hemostasis and consists of a process of gradual destruction of the hemostatic plug to restore normal blood circulation. This process is mediated by plasmin, which is a protein derived from plasminogen and whose function is to degrade fibrin.
Changes in hemostasis can be detected by specific blood tests, such as:
In addition to these tests, your doctor may recommend others, such as measuring clotting factors, for example, to make it possible to know if there is a deficiency of a clotting factor that may interfere with the hemostatic process.