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How Blood Clots

by Joel L. Moake, MD

Hemostasis is the body's way of stopping injured blood vessels from bleeding. Hemostasis includes clotting of the blood. Too much clotting can block blood vessels that are not bleeding. Consequently, the body has control mechanisms to limit clotting and dissolve clots that are no longer needed. An abnormality in any part of this system that controls bleeding 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 severe blood loss. When clotting is excessive, small blood vessels in critical places can become clogged with clots. Clogged vessels in the brain can cause strokes, and clogged vessels leading to the heart can cause heart attacks. 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 involves three major processes:

  • Narrowing (constriction) of blood vessels

  • Activity of cell-like blood particles that help in blood clotting (platelets)

  • Activity of proteins found in blood that work with platelets to help the blood clot (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. 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's 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.

Blood Clots: Plugging the Breaks

When an injury causes a blood vessel wall to break, platelets are activated. They change shape from round to spiny, stick to the broken vessel wall and each other, and begin to plug the break. They also interact with other blood proteins to form fibrin. Fibrin strands form a net that entraps more platelets and blood cells, producing a clot that plugs the break.

Formation of a clot also involves activation of a sequence of blood clotting factors that generate thrombin. 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.

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.

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