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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.
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.
Injury causes damaged tissue cells to produce prothrombin activator. This, along with a clotting factor produced by the sticky platelets (cell fragments) at the damaged site, cause prothrombin + calcium to make thrombin (blood protein). All the while fibrinogen is stimulated to make fibrin (blood protein). 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.
Coagulation of the blood begins with the activation of platelets - protoplasmic bodies that aid in the clotting of blood. These particles are part of blood composition at all times, but only coagulate when a blood vessel is injured. The injury triggers chemical signals which in turn draw collagen and platelets to the site of the wound and eventually build a structure to prevent blood loss.
Step 1: Conversion of the soluble plasma protein fibrinogen.Step 2: Fibrin threads stick to exposed surfaces of damaged blood vessels.Step 3: Serum, a plasma minus the clotting factors is present.Step 4: Once formed, more clotting is supported.
The protein fibrin is found in the blood and it has a necessary role in blood clotting.Thrombin, another protein, is found in blood. It is an enzyme that speeds up the rate of blood clotting. Thrombin and fibrin work hand in hand during the process of blood clotting.
Damaged tissue has a vvery low resolution. Proceed with caution.
it can damaged our tissue
damaged tissue can be reqaired by the .
If this clotting occurs in the larger arteries, it results in major tissue damage.
Anthrax attacks the cells that create the connective tissue in our blood cells. This means that there is no clotting of the blood.