<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>
<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>
which is the correct sequence of events when skin is cut and bleeding occurs
which is the correct sequence of events when skin is cut and bleeding occurs
Vascular spasm ( Vasoconstriction ) Platelet plug formation Clot formation
Vascular spasm ( Vasoconstriction ) Platelet plug formation Clot formation