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The thin, single layer of cells than line a blood vessel is called the endothelium. (The walls of the smallest vessels, the capillaries, are comprised of the endothelium alone.) When the endothelium is intact and healthy, a clot, of course, should not form. A break in the endothelium allows platelets to contact collagen and the other factors that activate platelets. Coagulation reactions begin occurring more rapidly since tissue factor is exposed and the surface of activated platelets provides the environment for the activation of the cascade that ultimately converts prothrombin to thrombin. The developing clot consists of interlaced fibrin fibrils and activated platelets.

In addition to an actual break in the endothelium, various other situations can lead inappropriately to activated platelets. Injury to the endothelium, in general, tends to activate platelets. An important example here is a developing atherosclerotic plaque. Other examples include turbulent blood flow or damage to endothelium from an immunological cause.

Excessive activation of the blood coagulation reactions can results from stasis of blood flow in the veins of an immobilized or post-operative patient. The slow flow leads to the accumulation of activated clotting factors and tends to prevent their normal inactivation by the inhibitors described above. The handout discusses this further. The most dramatic example of hypercoagulability is disseminated intravascular coagulation, which can have many causes. As mentioned on a earlier page, certain serious, systemic inflections can trigger this state. It has the characteristics of a general, systemic inflammatory problem. Also, trauma, in general, potentially can lead to disseminated intravascular coagulation. Cancer can be another cause, probably through the entry of tissue factor into the blood. In all cases, many small clots form, blocking blood flow to widespread areas of the body. But since this is so widespread, it depletes platelets and clotting factors, leading to widespread hemorrhage. It is very easy for the sequence to fatal. Treatment involves reducing the tendency of the blood to clot with a drug such as heparin, while replacing the lost platelets and clotting factors. One cause of inadequate clotting is thrombocytopenia. Impaired clotting can be genetic due to lack of certain clotting factors (e.g. hemophilia) or lack of VWF. Or it can be due to impaired synthesis of clotting factors for other reasons. Vitamin K deficiency, which is required for the synthesis of several clotting factors, can be important here. Newborn infants, for example, may not have enough vitamin K.

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There are two major facets of the clotting mechanism - the platelets, and the thrombin system.

The platelets are tiny cellular elements, made in the bone marrow, that travel in the bloodstream waiting for a bleeding problem to develop. When bleeding occurs, chemical reactions change the surface of the platelet to make it "sticky." Sticky platelets are said to have become "activated." These activated platelets begin adhering to the wall of the blood vessel at the site of bleeding, and within a few minutes they form what is called a "white clot." (A clump of platelets appears white to the naked eye.)

The thrombin system consists of several blood proteins that, when bleeding occurs, become activated. The activated clotting proteins engage in a cascade of chemical reactions that finally produce a substance called fibrin. Fibrin can be thought of as a long, sticky string. Fibrin strands stick to the exposed vessel wall, clumping together and forming a web-like complex of strands. Red blood cells become caught up in the web, and a "red clot" forms.

A mature blood clot consists of both platelets and fibrin strands. The strands of fibrin bind the platelets together, and "tighten" the clot to make it stable.

In arteries, the primary clotting mechanism depends on platelets. In veins, the primary clotting mechanism depends on the thrombin system. But in reality, both platelets and thrombin are involved, to one degree or another, in all blood clotting.

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not B is a sorry way to answer a Plato question.

The answer is A :)

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plato is A :)

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Q: What is the sequance of events leading to the formation of a blood clot?
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