Coagulation vs Clotting
Coagulation and clotting are the same phenomenon. Medical term is coagulation while the lay term is clotting. Clotting is an easy term and doctors also are not above using it.
Clot formation is one of the most important protective mechanisms in the body. It prevents exsanguinating bleeding and infection, and it is a critical step in wound healing. It provides the framework for the eventual migration of actively dividing epithelial cells and fibroblasts which precede wound healing.
When there is damage to a blood vessel, it exposes the highly reactive extracellular matrix material to the blood cells. There are many binding sites for blood cells in the extracellular material. Trauma damages the blood cells too. These events trigger platelet activation and aggregation. Damaged platelets and endothelial cells secrete inflammatory mediators which in turn activate blood cells to produce various potent chemicals. These chemicals, in turn, activate more platelets and lead to the formation of a platelet plug. This part of clotting is totally dependent on the number and function of the platelets. Therefore, low platelet amount (thrombocytopenia) or poor platelet function (thrombasthenia) causes delayed formation of the platelet plug. This can be detected by prolonged bleeding time test. A small prick is made on the earlobe, and the time it takes for the bleeding to stop first is taken as the bleeding time.
Next step of clotting is the proper coagulation cascade. Coagulation can occur along two major pathways. They are the intrinsic and the extrinsic pathway. There are various clotting factors produced by the liver and those are vital to the clotting process. Absence of these clotting factors interferes with clotting. Absence of factor VIII causes hemophilia A. Absence of factor IX causes hemophilia B (Christmas disease). (Read the Difference Between Hemophilia A and B). These disorders prolong prothrombin time test, which is the standard test done commonly to assess coagulation disorders.
The extrinsic pathway is also known as the tissue factor pathway. In trauma, when the tissues get damaged, a highly reactive tissue factor gets exposed. This activates factor X in the presence of factor VII and calcium ions. The intrinsic pathway involves a lot of clotting factors than the extrinsic pathway. It starts with factor XII getting activated after contact with damaged vascular endothelium. XIIa activates factor XI which in turn activates factor IX in the presence of factor VIII, calcium ions and phospholipids. Activated factor IXa activates factor X. Factor X activation marks the entry into the final step of the coagulation cascade, which is the common pathway.
Activated factor Xa converts prothrombin into thrombin in the presence of factor V, calcium ions and phospholipids. Thrombin converts fibrinogen into fibrin. Thrombin also activates factor XIII and helps with crosslinking fibrin. The result is a complex fibrin meshwork. Blood cells get attached to the meshwork and a definitive clot forms.