Blood clots form when the blood changes from a liquid to a gel-like or semi-solid state. This process is called coagulation or clotting. There are a few key steps that lead to clot formation:
Injury to Blood Vessels
Often, the first step is some sort of injury to a blood vessel. This can be a cut or tear in the vessel wall that exposes the blood to surfaces that trigger clotting. It could also be damage to the inside of the blood vessel, which roughens the surface and makes clotting more likely. Certain medical conditions like atherosclerosis can damage blood vessels and predispose a person to clot formation.
When a blood vessel is injured, platelets in the blood get activated. Platelets are disk-shaped cell fragments that circulate in the blood and are essential for normal clotting. When activated, they change shape, becoming spiky and sticky. They also release chemical messengers into the blood that recruit more platelets and promote clotting.
Platelet Adhesion and Aggregation
Activated platelets begin to stick to the site of injury, as well as to each other. This process is enhanced by von Willebrand factor (vWF), a protein that helps platelets adhere to surfaces. As more and more platelets aggregate, they form a platelet plug that provides the initial stability to the clot.
The coagulation cascade is a series of chemical reactions involving blood proteins called clotting factors. This cascade is initiated by the exposure of blood to injured tissue and platelet factors. It results in the production of thrombin, an enzyme that converts fibrinogen in the blood into long strands of fibrin that stabilize the clot.
Fibrin Mesh Formation
Thrombin cleaves fibrinogen into fibrin molecules. These fibrin molecules polymerize to form long fibrous strands that create a mesh-like structure. This fibrin mesh traps platelets, blood cells and plasma to create a stabilized clot.
Clot Stabilization and Maturation
As the clot develops, thrombin also activates Factor XIII, which creates bonds between fibrin strands to further stabilize the clot. Over hours to days, the clot gradually shrinks as fibroblasts replace the fibrin mesh with collagen, fully maturing the clot.
Once a clot is no longer needed, the body has a mechanism to break it down called fibrinolysis. Plasmin, an enzyme, degrades the fibrin mesh. Various regulators keep this process in check so clots don’t break down too quickly before wound healing is complete.
Key Factors That Initiate Clotting
There are several key factors that can initiate the clotting process:
- Endothelial injury – Damage to the lining of blood vessels exposes the blood to collagen and other surfaces that trigger platelets to activate.
- Turbulent blood flow – Areas where blood flow is irregular can cause platelet activation. This is why blood clots often form in the heart atrial fibrillation.
- Contact with foreign materials – Contact between blood and artificial surfaces like plastics and metals can activate clotting.
- Tissue factor – This protein is released when tissues are damaged and activates the coagulation cascade.
- Cancer – Tumor cells can release substances into the blood and make it more prone to clotting.
- Infection and inflammation – The immune system’s inflammatory response on an injury or infection can shift the hemostatic balance towards clot formation.
- Pregnancy – Increased estrogen and other changes during pregnancy increase clotting factors and the risk of clotting.
- Genetic factors – Mutations in genes that regulate clotting can cause the blood to clot too easily.
- Medications – Certain prescription drugs like oral contraceptives can increase clotting factors.
- Sitting for long periods
In summary, the first step to clot formation is usually some event that causes injury and activates platelets. Platelet activation then initiates a cascade of events including platelet aggregation, coagulation factor activation, fibrin formation, and clot maturation and stabilization. Regulating this process properly is essential to prevent excessive clotting on one hand while maintaining normal hemostasis on the other.