The process whereby blood clots.
The process by which blood changes from being liquid to being semi-solid and so stops flowing.
Blood clotting occurs in response to injury. The formation of the clot is a cascade of reactions involving both intrinsic and extrinsic factors. A deficiency of vitamin K prolongs the blood clotting time. Blood clots can also occur internally within the vascular system. The initiation signal for these clots is not completely known.
The process by which blood turns from a liquid into a semisolid mass to stop bleeding. It begins when an injury to a blood vessel exposes the blood to cells in the blood vessel’s lining. The blood cells known as platelets aggregate (adhere to one another) at the site of the injury. As the platelets aggregate, they trigger a cascade of reactions among various proteins known as coagulation factors, which results in the formation of a clot. The clot that seals the point of bleeding is made up of both the aggregated platelets and fibrin. When the wound heals, other proteins help dissolve the clot.
The mechanism of blood coagulation is crucial for controlling bleeding in cases of blood vessel injury. However, the occurrence of blood clots within significant blood vessels can result in a myocardial infarction (heart attack) or a stroke.
Upon the occurrence of blood vessel damage, an immediate constriction takes place to restrict blood flow to the affected region. This initiates a cascade of chemical reactions that culminate in the creation of a clot to seal the injury. Initially, platelets in the vicinity of the injury become activated, exhibiting adhesive properties as they adhere to the walls of the blood vessel. Subsequently, these activated platelets release chemical substances that activate coagulation factors. Collaborating with vitamin K, these factors act upon fibrinogen, a blood constituent, transforming it into fibrin. The fibrin strands intertwine, forming a mesh-like structure that ensnares red blood cells, ultimately leading to the formation of a clot.
There exist several mechanisms aimed at preventing the formation of undesired blood clots. These mechanisms encompass the action of prostacyclin, a type of prostaglandin that inhibits platelet aggregation, the initial step of blood clotting. Additionally, plasmin, a substance involved in fibrinolysis, works to break down fibrin. The continuous flow of blood aids in washing away active coagulation factors, while the liver serves to deactivate excessive coagulation factors, contributing to the prevention of clot formation.
Abnormalities in the process of blood clotting can lead to various bleeding disorders. Excessive clotting, known as thrombosis, can arise from inherited deficiencies or abnormalities in coagulation factors, the usage of oral contraceptives, reduced levels of coagulation-inhibiting enzymes, or sluggish blood flow in specific regions. The standard treatment for such conditions typically involves the administration of anticoagulant medications like heparin or warfarin.