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The extrinsic pathway is faster than the intrinsic pathway
True
Blood coagulation can occur either through an intrinsic or extrinsic pathway. The first step in either pathway begins with the production of Factor X,which marks the common pathway of coagulation.
This involves the clotting mechanism. There are two pathways the intrinsic pathway and the extrinsic pathway. The intrinsic pathway is caused by a damaged surface. The extrinsic pathway is caused by trauma. It has a number of steps. Each step involves an enzyme or factor. Prothrombin changes to thrombin. Fibrinogen changes to fibrin. That produces a cross-linked fibrin clot. This blocks further bleeding.
The Tannic acid helps to form a blood clot by contracting blood vessels. Amr ^_^Actually, blood clotting is the result of a "cascade" effect of different factors in the blood. Once activated they "domino" -- one activates the next in the chain -- until the blood clots. There are two pathways to blood clotting (coagulation) -- an intrinsic pathway and an extrinsic (external) pathway. Tannic acid acts to activate the extrinsic pathway and set the factor "cascade" in motion to clot the blood.
Blood clotting is also known as coagulation. On average, it occurs within 3 to 6 minutes of a blood vessel being damaged. There are two main ways for blood clotting to occur: the intrinsic pathway, and the rapid extrinsic pathway. Whichever pathway occurs the final result is always that blood plasma turns into a gel as a result of being combined with fibrin, and this forms a blood clot.
One is faster than the other.
Intrinsic pathway of coagulation (measured as PTT in laboratories).
Thrombin
yes.
There are the intrinsic and extrinsic pathways in clotting. The intrinsic pathway is initiated when blood comes in contact with damaged endothelium or collagen, and involves clotting factors XII, XI, IX, and VIII. The extrinsic pathway is activated when being exposed to tissue factor from tissue injury or the addition of thromboplastin to blood, and involves clotting factor VII. The two pathways meet at the point of clotting factor X activation to lead the final common pathway. From here, factor X is converted to prothrombin, prothrombin to thrombin, thrombin to fibrinogen, fibrinogen to fibrin, and finally fibrin to fibrin clot. Platelets, activated by thrombin, adhere to the damaged endothelium wall or collagen to form a plug. At the same time, they activate clotting factors VII and X. More platelets are stimulated by fibrin clots, resulting in reinforcing the formed clots.
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.