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Clotting Mechanism and what helps to absorb clots pg 908-909 in text book Important proteins in the alpha and

beta fractions are the clotting factors which are made in the liver. Clotting factors including fibrinogen remain in an inactive form in the blood plasma until activated by the clotting cascade. Clotting Cascade: -First the tissue is injured resulting in: The extrinsic pathway is activated by the release of thromboplastin from the injured tissue. As a result prothrombin is converted to thrombin, which in turn catalyzes (modify/ increase) the conversion of fibrinogen to fibrin. The intrinsic pathway is activated sequentially until fibrin is ultimately formed. This is a slower process, but is most often responsible for clotting in vivo. As the injured cell is repaired and again covered with endothelial cell (inner layer of blood vessel), the fibrin clot is no longer needed. Fibrin is digested in via two systems: plasma fibrinolytic system and the cellular fibrinolytic system. Plasminogen is required to lyse (break down) the fibrin.

When the clot is no longer needed, after blood vessel is healed, the Plasminogen is activated to form plasmin. Plasmin then digests the fibrinogen and fibrin. The breakdown products are referred to as fibrin degradation products, are released into circulation. With this system clots are dissolved as tissue is repaired, and the vascular system returns to its normal state. Following damage to a blood vessel, vascular spasm occurs to reduce blood loss while other mechanisms also take effect: Blood platelets congregate at the site of damage and amass to form a platelet plug. This is the beginning of the process of the blood "breaking down" from is usual liquid form in such a way that its constituents play their own parts in processes to minimize blood loss

Thrombolytic medications are approved for the immediate treatment of stroke and heart attack. The most commonly used drug for thrombolytic therapy is tissue plasminogen activator (tPA) According to the American Heart Association, you have a better chance of surviving and recovering from a heart attack if you receive a thrombolytic drug within 12 hours after the heart attack starts. Ideally, you should receive thrombolytic medications within the first 90 minutes after arriving at the hospital for treatment. Thrombolytics work by dissolving a major clot quickly. This helps restart blood flow to the heart and helps prevent damage to the heart muscle. Thrombolytics can stop a heart attack that would otherwise be deadly. The drug restores some blood flow to the heart in most patients. However, the blood flow may not be completely normal and there may still be a small amount of muscle damaged. Additional therapy, such as cardiac catheterization or angioplasty, may be needed. Thrombolytics are not given to someone who is having a hemorrhagic stroke. They could worsen the stroke by causing increased bleeding. __________________________________________________________________________________________________ Blood Clotting is one of three mechanisms that reduce the loss of blood from broken blood vessels. 3 mechanisms are: Vascular Spasm - The smooth muscle in blood vessel walls contracts immediately the blood vessel is broken. This response reduces blood loss for some time, while the other hemostatic mechanisms become active. Platelet Plug Formation - When blood platelets encounter a damaged blood vessel they form a "platelet plug" to help to close the gap in the broken blood vessel. The key stages of this process are: platelet adhesion, platelet release reaction, and platelet aggregation

Blood Clotting (Coagulation) - As described below:

Following damage to a blood vessel, vascular spasm occurs to reduce blood loss while other mechanisms also take effect: Blood platelets congregate at the site of damage and amass to form a platelet plug. This is the beginning of the process of the blood "breaking down" from is usual liquid form in such a way that its constituents play their own parts in processes to minimise blood loss. Blood normally remains in its liquid state while it is within the blood vessels but when it leaves them the blood may thicken and form a gel (coagulation).

Blood clotting (technically "blood coagulation") is the process by which (liquid) blood is transformed into a solid state. This blood clotting is a complex process involving many clotting factors (incl. calcium ions, enzymes, platelets, damaged tissues) activating each other. The three stages of this process are: 1. Formation of Prothrombinase 2. Prothrombinase can be formed in two ways, depending of which of two "systems" or "pathways" apply. Intrinsic System o This is initiated by liquid blood making contact with a foreign surface, i.e. something that is not part of the body; or Extrinsic System o This is initiated by liquid blood making contact with damaged tissue. Both the intrinsic and the extrinsic systems involve interactions between coagulation factors. These coagulation factors have individual names but are often referred to by a standardised set of Roman Numerals, e.g. Factor VIII (antihaemophilic factor), Factor IX (Christmas factor). 3. Prothrombin converted into the enzyme Thrombin Prothrombinase (formed in stage 1.) converts prothrombin, which is a plasma protein that is formed in the liver, into the enzyme thrombin. Fibrinogen (soluble) converted to Fibrin (insoluble) In turn, thrombin converts fibrinogen (which is also a plasma protein synthesized in the liver) into fibrin. Fibrin is insoluble and forms the threads that bind the clot. Consequences of Blood Clotting Problems: If blood clots too quickly/easily then thrombosis may occur. This is blood clotting in an unbroken blood vessel, which is dangerous and can lead to strokes or heart-attacks. Conversely, if blood takes too long to clot hemorrhage may occur. In this case much blood may be lost from the blood vessels, which is also dangerous. The hereditary disorder haemophilia is a condition in which certain coagulation factors are missing from the blood, as a result of which the blood cannot form clots (without medical intervention).

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