To treat or prevent abnormal blood clotting, doctors must understand the multifaceted aspects of the clotting mechanism. The following explanation is greatly simplified, but is designed to provide a basic understanding of how the many drugs used to treat clotting problems work, and some basis for assessing the treatments your doctor may prescribe for you.
How does the blood clot?
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.
How the Blood Clots - using a coronary artery as an example.
Figure 1. A coronary artery is shown that has an atherosclerotic plaque ("AP") partially occluding the lumen (opening) of the artery. Platelets within the blood are shown ("P"). The flow of blood through the artery is indicated by the long arrow. The patient with this artery likely has stable angina.Figure 2. The atherosclerotic plaque has developed an ulcer ("U").
Figure 3. The platelets have been activated (i.e., made "sticky") by their exposure to the ulcerated plaque. They begin to aggregate (to stick) to the surface of the ulcer.
