inhibiting the formation of prothrombin activator and the action of thrombin on fibrinogen
formation of prothrombin activator
formation of prothrombin activator
inhibiting the formation of prothrombin activator and the action of thrombin on fibrinogen
These are the three phases:Phase 1: Formation of prothrombin activatorThe prothrombin activator is formed through intrinsic and/or extrinsic pathway. Usually it is formed by both. Its formation is triggered by tissue-damaging events and it involves a series of procoagulants. Each pathway cascades towards Factor X (i.e. the Stuart Factor) that complexes with Ca2+, platelet factor 3 (PF3), and Factor V to form the prothrombin activator.The intrinsic pathway is triggered by negatively charged surfaces of activated platelets, collagen, and glass and it uses factors present within the blood. As for the extrinsic pathway, it is triggered by exposure to tissue factor (Factor III). The extrinsic pathway bypasses several steps of the intrinsic pathway so it is faster. Once the prothrombin activator is formed, the clot forms in 10-15 seconds.Phase 2: Prothrombin's conversion to thrombinThe prothrombin activator catalyses the transformation of prothrombin to thrombin.Phase 3: Fibrinogen conversion to fibrinThrombin (Factor II) converts soluble fibrinogen to the solid fibrin. The fibrin formed will cause the plasma to become a gel-like trap for formed elements, forming the structural basis of the clot. The thrombin along with Ca2+ activates Factor XIII to cross-link fibrin. This will strengthen and stabilise the clot.
Thrombin
it is the activator device
prothrombin time, hematocrit
Injury causes damaged tissue cells to produce prothrombin activator. This, along with clotting factor produced by the sticky platelets at the damaged site, cause prothrombin + calcium to make thrombin. All the while fibrinogen is stimulated to make fibrin. The fibrin ensnares RBCs to form the clot with the platelets. All factors have to be there for the clotting to occur. Lack of any of them causes bleeding disorders.
Injury cause damaged tissue cells to produce prothrombin activator. This, along with clotting factor produced by the sticky platelets at the damaged site, cause prothrombin + calcium to make thrombin. All the while, fibrinogen is stimulated to make fibrin. The fibrin ensnares RBCs to form the clot with the platelets.All factors have to be there for the clotting to occur. Lack of any of them causes bleeding disorders.
difference between activator and inhibitor
The INR has basically replaced the prothrombin time, or PT.