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How Blood Clots
Even a simple cut on your finger necessitates a long, complex chain of reactions to stop the flow of blood through blood clotting. If one of these sequential events fails, you’re on the way to the emergency room. And if the blood colt winds up in the wrong spot, you could be toast (stroke, thrombosis or heart attack).
Now we’re not going to cover all of the 80-plus reactions that occur in blood clotting, but we’re going to give you some idea how miraculous the process is. Here are the highlights:
Coagulators
Platelets
Platelets that flow in our bloodstream are the first and most crucial components of this process. These little cellular wonders are manufactured in the center of our bones (the bone marrow). When platelets come upon a leaking vein, they are programmed to become “sticky” and clump together (if you’re artery is cut, blood gushes out with such force that you’ll need a tourniquet or an ambulance), This platelet action is called primary hemostasis (cessation of blood loss from a damaged vessel).
Calcium
Calcium and phospholipid (a platelet membrane constituent) are required for the tenase and prothrombinase complexes to function.
Vitamin K
Vitamin K denotes a group of lipophilic, and hydrophobic, vitamins that are needed for the posttranslational modification of certain proteins, mostly required for blood coagulation.
Clotting Factors
Clotting factors (there are 30 of them), are proteins which immediately work to assist the coagulation function in a process called secondary hemostasis. Proteins in the blood plasma, called coagulation factors, respond in a complex cascade to form fibrin strands that strengthen the platelet plug by maintaining oncotic pressure. The most prominent is thrombin, a coagulation protein that converts soluble fibrinogen into insoluble strands of fibrin, as well as catalyzing many other coagulation-related reactions. Fibrous proteins are considered the most flexible fibers in nature, stretching to three times their length. These wonderful fibers form the scab over the cut.
If you lack any of these clotting factors, you are classified as having a blood coagulation disorder (such as Bernard-Soulier syndrome - when platelets lack a substance that sticks to the walls of blood vessels; Glanzmann's thrombasthenia - a condition caused by lack of a protein required for platelets to clump together; Factor II deficiency; Factor V deficiency, etc.)
Polyphosphate
Polyphosphate is a potent hemostatic regulator, accelerating blood clotting by activating the contact pathway and promoting the activation of factor V.
Inhibitors
Three mechanisms keep the coagulation cascade in check. Abnormalities can lead to an increased tendency toward thrombosis:
Protein C
Protein C is an important co-factor inhibitor, which degrades the co-factors FVa and FVIIIa. It is activated by thrombin with thrombomodulin and requires its co-enzyme Protein S to function. Quantitative or qualitative deficiency of either may lead to thrombophilia (a tendency to develop thrombosis). Impaired action of Protein C (activated Protein C resistance), for example by having the " Leiden" variant of Factor V or high levels of FVIII also may lead to a thrombotic tendency.
Antithrombin
Antithrombin is a serine protease inhibitor (serpin) that degrades the serine proteases; thrombin and FXa, as well as FXIIa, and FIXa. It is constantly active, but its adhesion to these factors is increased by the presence of heparan sulfate (a glycosaminoglycan) or the administration of heparins (different heparinoids increase affinity to F Xa, thrombin, or both).
Tissue Factor Pathway Inhibitor
Tissue factor pathway inhibitor (TFPI) inhibits F VIIa-related activation of F IX and F X after its original initiation.
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Sources: Health Information - National Institutes of Health (http://health.nih.gov)Wikipedia (http://en.wikipedia.org) Medline Dictionary (http://www.nlm.nih.gov/medlineplus) Healthfinder Library (http://healthfinder.gov/library)
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