Hemostasis or haemostasis is a process which causes bleeding to stop, meaning to keep blood within a damaged blood vessel (the opposite of hemostasis is hemorrhage). It is the first stage of wound healing. This involves blood changing from a liquid to a gel. Intact blood vessels are central to moderating blood’s tendency to clot. The endothelial cells of intact vessels prevent blood clotting with a heparin-like molecule andthrombomodulin and prevent platelet aggregation with nitric oxide and prostacyclin. When endothelial injury occurs, the endothelial cells stop secretion of coagulation and aggregation inhibitors and instead secrete von Willebrand factor which initiate the maintenance of hemostasis after injury. Hemostasis has three major steps: 1) vasoconstriction, 2) temporary blockage of a break by a platelet plug, and 3) blood coagulation, or formation of a fibrin clot. These processes seal the hole until tissues are repaired.
PROCESS
Hemostasis occurs when blood is present outside of the body or blood vessels. It is the instinctive response for the body to stop bleeding and loss of blood. During hemostasis three steps occur in a rapid sequence. Vascular spasm is the first response as the blood vessels constrict to allow less blood to be lost. In the second step, platelet plug formation, platelets stick together to form a temporary seal to cover the break in the vessel wall. The third and last step is called coagulation or blood clotting. Coagulation reinforces the platelet plug with fibrin threads that act as a “molecular glue”. Platelets are a large factor in the hemostatic process. They allow for the creation of the “platelet plug” that forms almost directly after a blood vessel has been ruptured. Within seconds of a blood vessel’s epithelial wall being disrupted platelets begin to adhere to the sub-endotheliumsurface. It takes approximately sixty seconds until the first fibrin strands begin to intersperse among the wound. After several minutes the platelet plug is completely formed by fibrin. Hemostasis is maintained in the body via three mechanisms:
1. Vascular spasm – Damaged blood vessels constrict. Vascular spasm is the blood vessels’ first response to injury. The damaged vessels will constrict (vasoconstrict) which reduces the amount of blood flow through the area and limits the amount of blood loss. This response is triggered by factors such as a direct injury to vascular smooth muscle, chemicals released by endothelial cells and platelets, and reflexes initiated by local pain receptors. The spasm response becomes more effective as the amount of damage is increased. Vascular spasm is much more effective in smaller blood vessels.
2. Platelet plug formation – Platelets adhere to damaged endothelium to form platelet plug (primary hemostasis) and then degranulate. This process is regulated through thromboregulation. Platelets play one of the biggest factors in the hemostatic process. Being the second step in the sequence they stick together (aggregation) to form a plug that temporarily seals the break in the vessel wall. As platelets adhere to the collagen fibers of a wound they become spiked and much stickier. They then release chemical messengers such as adenosine diphosphate (ADP), serotonin and thromboxane A2. These chemicals are released to cause more platelets to stick to the area and release their contents and enhance vascular spasms. As more chemicals are released more platelets stick and release their chemicals; creating a platelet plug and continuing the process in a positive feedback loop. Platelets alone are responsible for stopping the bleeding of unnoticed wear and tear of our skin on a daily basis.
The second stage of hemostasis involves platelets that move throughout the blood. When the platelets find an exposed area or an injury, they begin to form what is called a platelet plug. The platelet plug formation is activated by a glycoprotein called the Von Willebrand factor (vWF), which are found in the body’s blood plasma. When the platelets in the blood are activated, they then become very sticky so allowing them to stick to other platelets and adhere to the injured area.
There are a dozen proteins that travel along the blood plasma in an inactive state and are known as clotting factors. Once the platelet plug has been formed by the platelets, the clotting factors begin creating the Blood Clot. When this occurs the clotting factors begin to form a collagen fiber called fibrin. Fibrin mesh is then produced all around the platelet plug, which helps hold the fibrin in place. Once this begins, red and white blood cells become caught up in the fibrin mesh which causes the clot to become even stronger.
3. Blood coagulation – Clots form upon the conversion of fibrinogen to fibrin, and its addition to the platelet plug (secondary hemostasis). Coagulation: The third and final step in this rapid response reinforces the platelet plug. Coagulation or blood clotting uses fibrin threads that act as a glue for the sticky platelets. As the fibrin mesh begins to form the blood is also transformed from a liquid to a gel like substance through involvement of clotting factors and pro-coagulants. The coagulation process is useful in closing up and maintaining the platelet plug on larger wounds. The release of Prothrombin also plays an essential part in the coagulation process because it allows for the formation of a thrombus, or clot, to form. This final step forces blood cells and platelets to stay trapped in the wounded area. Though this is often a good step for wound healing, it has the ability to cause severe health problems if the thrombus becomes detached from the vessel wall and travels through the circulatory system; If it reaches the brain, heart or lungs it could lead to stroke, heart attack, or pulmonary embolism respectively. However, without this process the healing of a wound would not be possible.
DISORDERS
The body’s hemostasis system requires careful regulation in order to work properly. If the blood does not clot sufficiently, it may be due to bleeding disorders such ashemophilia; this requires careful investigation. Over-active clotting can also cause problems; thrombosis, where blood clots form abnormally, can potentially causeembolisms, where blood clots break off and subsequently become lodged in a vein or artery.
Hemostasis disorders can develop for many different reasons. They may be congenital, due to a deficiency or defect in an individual’s platelets or clotting factors. A number of disorders can be acquired as well.