<P> 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 coagulation, blood changing from a liquid to a gel . Intact blood vessels are central to moderating blood's tendency to form clots . The endothelial cells of intact vessels prevent blood clotting with a heparin - like molecule and thrombomodulin 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 . </P> <P> The word hemostasis (/ ˌhiːmoʊˈsteɪsɪs /, sometimes / ˌhiːˈmɒstəsɪs /) uses the combining forms hemo - and - stasis, New Latin from Ancient Greek αἱμο - haimo - (akin to αἷμα haîma), "blood", and στάσις stásis, "stasis", yielding "motionlessness or stopping of blood". </P> <P> 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-endothelium surface . 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: </P> <Ol> <Li> Vascular spasm (Vasoconstriction) - Vasoconstriction is produced by vascular smooth muscle cells, and is the blood vessel's first response to injury . The smooth muscle cells are controlled by vascular endothelium, which releases intravascular signals to control the contracting properties . When a blood vessel is damaged, there is an immediate reflex, initiated by local sympathetic pain receptors, which helps promote vasoconstriction . The damaged vessels will constrict (vasoconstrict) which reduces the amount of blood flow through the area and limits the amount of blood loss . Collagen is exposed at the site of injury, the collagen promotes platelets to adhere to the injury site . Platelets release cytoplasmic granules which contain serotonin, ADP and thromboxane A2, all of which increase the effect of vasoconstriction . The spasm response becomes more effective as the amount of damage is increased . Vascular spasm is much more effective in smaller blood vessels . </Li> <Li> Platelet plug formation - Platelets adhere to damaged endothelium to form a platelet plug (primary hemostasis) and then degranulate . This process is regulated through thromboregulation . Plug formation is activated by a glycoprotein called Von Willebrand factor (vWF), which is found in plasma . Platelets play one of major roles in the hemostatic process . When platelets come across the injured endothelium cells, they change shape, release granules and ultimately become' sticky' . Platelets express certain receptors, some of which are used for the adhesion of platelets to collagen . When platelets are activated, they express glycoprotein receptors that interact with other platelets, producing aggregation and adhesion . Platelets release cytoplasmic granules such as adenosine diphosphate (ADP), serotonin and thromboxane A2 . Adenosine diphosphate (ADP) attracts more platelets to the affected area, serotonin is a vasoconstrictor and thromboxane A2 assists in platelet aggregation, vasoconstriction and degranulation . 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 . This is referred to as primary hemostasis . </Li> <Li> Clot formation - Once the platelet plug has been formed by the platelets, the clotting factors (a dozen proteins that travel along the blood plasma in an inactive state) are activated in a sequence of events known as' coagulation cascade' which leads to the formation of Fibrin from inactive fibrinogen plasma protein . Thus, a Fibrin mesh is produced all around the platelet plug to hold it in place; this step is called "Secondary Hemostasis". During this process some red and white blood cells are trapped in the mesh which causes the primary hemostasis plug to become harder: the resultant plug is called as' thrombus' or' Clot' . Therefore' blood clot' contains secondary hemostasis plug with blood cells trapped in it . 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 . </Li> </Ol>

Steps for stopping a break in the vascular system