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BLOOD CLOTTING
COAGULATION (BLOOD CLOTTING) 2 basic pathways: 1. Extrinsic pathway - initiated by substances released by damaged blood vessels or surrounding tissues outside the blood 2. Intrinsic pathway - begins in the blood – involved in clotting blood outside of body In the body both pathways are usually triggered by the same vessel-damaging events A pivotal molecule in both mechanisms is a phospholipid PF3 on the surfaces of aggregated platelets Each pathway requires Ca++ and steps which cascade toward factor X-from this point on they are the same In both pathways a series of plasma proteins, especially beta-globulins, play major roles Called blood clotting factors (most are inactive forms of proteolytic enzymes) Most are in plasma, a few are released by platelets and one is released by damaged tissue Most are designated by Roman numerals (I-XIII) – numbered according to the order of discovery An important difference between the pathways is their speed of action Extrinsic pathway is very quick-clotting can occur in as little as 15 seconds Intrinsic pathway - is more complex than extrinsic pathway Usually requires 2-6 minutes to cause clotting 3 basic stages in clotting: 1. Formation of prothrombin activator 2. Conversion of prothrombin into thrombin 3. Conversion of fibrinogen into fibrin Extrinsic clotting Named because formation of prothrombin activator is initiated by substances released by damaged blood vessels or tissues outside the blood The initiating substance is tissue thromboplastin or tissue factor (TF) Thromboplastin, factor VII and Ca++ activate factor X Factor X reacts with factor V and Ca++ to form prothrombin activator Prothrombin activator and Ca++ convert prothrombin (Factor II) into thrombin Prothrombin activator + Ca++ Prothrombin------------------------------------------------------------------thrombin (factor XIII)
Thrombin + Ca++ Fibrinogen (factor I)---------------------------------------------------------fibrin Fibrinogen - protein produced by liver - high molecular weight (largest plasma protein) Thrombin - enzyme that converts soluble fibrinogen to insoluble fibrin threads Threads of fibrin form a mesh that traps RBCs and plasma The clot then undergoes contraction and pulls edges of damaged vessel together Serum (defibrinated plasma) is squeezed out - most in 30-60 minutes Intrinsic clotting - blood clots when drawn from circulation and left to stand Can be triggered by contact with glass which activates clotting factor XII (Hageman or glass factor)-named after an engineer, Hageman, who had a deficiency of this factor and died of a pulmonary embolism Pathway named because formation of prothrombin activator is initiated by a substance within the blood (a tissue factor found on endothelial cells and monocytes) Intravascular clotting sometimes results from factors that activate the intrinsic pathway Ex. antigen - antibody reactions or septicemia due to bacterial toxins Deficiencies in the intrinsic pathway are associated with a number of hereditary bleeding diseases - especially Factor VIII in hemophilia A Intrinsic pathway is initiated when blood comes in contact with collagen in damaged blood vessels This causes activation of Factor XII (Hageman) and damage to platelets, resulting in release of phospholipids by platelets Factor XII activates Factor XI which activates Factor IX (Christmas factor) Factor IX acts together with factor VIII, Ca++ and platelet phospholipids to activate Factor X (Stuart) Factor X reacts with platelet phospholipids, factor V and Ca++ to form prothrombin activator Prothrombin activator converts prothrombin into thrombin Thrombin causes more platelets to adhere to each other, resulting in release of more platelet phospholipids (positive feedback cycle) Prothrombin is inactive precursor of thrombin Protein formed in the liver and is in the plasma in excess amounts Blood clots normally, even when the amount. of prothrombin is reduced by 50% or more Synthesis of prothrombin by the liver requires vitamin K Some foods (especially green leafy vegetables) contain vitamin K, but it is also synthesized in large intestine by certain bacteria Antibiotics which wipe out the intestinal flora may lead to vitamin K deficiency Vitamin K is required for synthesis of factors VII, IX, and X as well as prothrombin Newborn may have a deficiency and be prone to hemorrhage since vitamin K is not readily passed from mother to fetus Hence the need for giving it to the newborn and mothers before delivery Vitamin K is fat soluble - inadequate fat absorption due to lack of bile salts will limit it Ex. If bile ducts become obstructed, a vitamin K deficiency develops Blood with a deficiency of vitamin K shows lowered prothrombin and delayed clotting time Patients with obstructive jaundice are given vitamin K as a preoperative safeguard FACTORS THAT OPPOSE CLOTTING Endothelium lining blood vessels carries a negative charge that repels platelets and various clotting factors - prevents clotting Clotting occurs all the time throughout the body To prevent clotting, antithrombin (Factor III) (alpha globulin) is present in plasma and inactivates thrombin and factor X Other anticoagulants in blood: Alpha-2 –macroglobulin inactivates thrombin and plasmin Alpha-1- antitrypsin inhibits factor XI Protein C inactivates factors V and VIII and stimulates plasminogen activators |
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