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Pronunciations anticoagulants asparaginase embolism fibrin hematoma hemostasis pulmonary embolism purpura telangiectasia thrombin thrombocytopenia thrombolytic ticlopidine warfarin

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 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 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. 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.

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.

Blood Clots: Plugging the Breaks

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.

Drugs and Blood Clots: A Complicated Relationship The relationship between drugs and the body's ability to control bleeding (hemostasis) is complicated. The body's ability to form blood clots is vital to hemostasis, but too much clotting increases the risk of a heart attack, stroke, or pulmonary embolism. Many drugs, either intentionally or unintentionally, affect the body's ability to form blood clots. Some people are at high risk of forming blood clots and are intentionally given drugs to decrease the risk. Drugs may be given that reduce the stickiness of platelets, so that they will not clump together to block a blood vessel. Aspirin Some Trade Names ECOTRIN ASPERGUM , ticlopidine Some Trade Names TICLID , clopidogrel Some Trade Names PLAVIX , abciximab Some Trade Names REOPRO , and tirofiban Some Trade Names AGGRASTAT are examples of drugs that interfere with the activity of platelets. Other people at risk of forming blood clots may be given an anticoagulant, a drug that inhibits the action of blood proteins called clotting factors. Although often called "blood thinners," anticoagulants do not really thin the blood. Commonly used anticoagulants are warfarin Some Trade Names COUMADIN , given by mouth, and heparin, given by injection. People who take these drugs must be under close medical supervision. Doctors monitor the effects of these drugs with blood tests that measure the time it takes for a clot to form, and they adjust the dose on the basis of test results. Doses that are too low may not prevent clots, while doses that are too high may cause severe bleeding. Another type of anticoagulant, low-molecular-weight heparin, does not require as much supervision. Lepirudin Some Trade Names REFLUDAN , bivalirudin, and argatroban Some Trade Names ARGATROBAN are newer types of anticoagulants that directly act on thrombin, a protein that helps induce clotting. If a person already has a blood clot, a thrombolytic (fibrinolytic) drug can be given to help dissolve the clot. Thrombolytic drugs, which include streptokinase Some Trade Names STREPTASE and tissue plasminogen activator, are sometimes used to treat heart attacks and strokes caused by blood clots. These drugs may save lives, but they can also put the person at risk of severe bleeding. Surprisingly, heparin, a drug given to reduce the risk of clot formation, sometimes has an unintended activating effect on platelets that increases the risk of clotting (heparin-induced thrombocytopenia). Estrogen, alone or in oral contraceptives, can have the unintended effect of causing excessive clot formation. Certain drugs used to treat cancer (chemotherapy drugs), such as asparaginase Some Trade Names ELSPAR , can also increase the risk of clotting.

Last full review/revision May 2006 by Joel L. Moake, MD