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The Merck Manual--Second Home Edition logo
 
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Chapter 173. Bleeding and Clotting Disorders
Topics: Introduction | Hereditary Hemorrhagic Telangiectasia | Allergic Purpura | Thrombocytopenia | Von Willebrand's Disease | Hemophilia | Thrombophilia | Disseminated Intravascular Coagulation
 
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Introduction

An abnormality in any part of the system that controls bleeding (hemostasis) can lead to excessive bleeding or excessive clotting, both of which can be dangerous. When clotting is poor, even a slight injury to a blood vessel may lead to major blood loss. When clotting is uncontrolled, small blood vessels in critical places can become clogged with clots. Clogged vessels in the brain can cause strokes; clogged vessels leading to the heart can cause heart attacks; and pieces of clots from veins in the legs, pelvis, or abdomen can travel through the bloodstream to the lungs and block major arteries there (pulmonary embolism).

Hemostasis is the body's way of stopping injured blood vessels from bleeding. It involves three major processes: narrowing (constriction) of blood vessels, activity of platelets, and activity of blood clotting factors.

An injured blood vessel constricts so that blood flows out more slowly and clotting can start. At the same time, the accumulating pool of blood outside the blood vessel (a hematoma) presses against the vessel, helping prevent further bleeding.

click here to view the figure See the figure Blood Clots: Plugging the Breaks.

As soon as a blood vessel wall is damaged, a series of reactions activates platelets so that they stick to the injured area. The "glue" that holds platelets to the blood vessel wall is von Willebrand factor, a protein produced by the cells of the vessel wall. The proteins collagen and thrombin act at the site of the injury to induce platelets to stick together. As platelets accumulate at the site, they form a mesh that plugs the injury. The platelets change shape from round to spiny, and they release proteins and other substances that entrap more platelets and clotting proteins in the enlarging plug that becomes a blood clot.

Thrombin converts fibrinogen, a blood clotting factor that is normally dissolved in blood, into long strands of fibrin that radiate from the clumped platelets and form a net that entraps more platelets and blood cells. The fibrin strands add bulk to the developing clot and help hold it in place to keep the vessel wall plugged. Formation of a clot also involves activation of a sequence of blood clotting factors that generate thrombin.

The reactions that result in the formation of a blood clot are balanced by other reactions that stop the clotting process and dissolve clots after the blood vessel has healed. Without this control system, minor blood vessel injuries could trigger widespread clotting throughout the body--which actually happens in some diseases.

click here to view the sidebar See the sidebar Drugs and Blood Clots: A Complicated Relationship.

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