The clot plot: Stop the bleeding

The human body relies on a constant flow of blood carrying oxygen and other vital nutrients through the blood vessels to the cells.  Blood must be kept liquid so that it can easily travel through the arteries, veins and capillaries.  But, it must also be able to form a clot to prevent blood loss if a vessel is damaged.  

The process that leads to blood clotting (coagulation) is very complex.  It starts when the cells that line a blood vessel are damaged.  In a healthy blood vessel, these cells help to keep the blood vessel open and prevent the blood from spontaneously clotting; in other words, a healthy lining is anticoagulant or anti-clotting.  Damage to a vessel causes the release of chemicals that set into motion a chain reaction of specific proteins designed to promote clotting.  

Most of these clotting factors (numbered I through XIII) are made in the liver.  They are always floating around in the blood stream; however, they are generally in an inactive state.  This means they cannot cause the blood to clot unless they are activated by another factor.  This way, they are not causing widespread and perpetual clotting of the blood in our bloodstream.
The initial player in blood clotting is the platelet.  The damaged vessel lining cells produce a factor called von Willebrand factor to attract platelets to adhere to the damaged area.  Attached platelets in turn release chemicals to attract many more platelets to the site.  This clump of platelets forms a temporary plug to stop bleeding.  Next, a soluble substance called fibrinogen attaches to this platelet plug.    

While the plug is being formed, clotting factors are being activated by one another on the surface of the adhered platelets.  The sole purpose of the clotting factor cascade is to change the soluble fibrinogen into insoluble fibrin.  Fibrin strands link together within the plug to produce a more stable clot.  

If any step in the clotting process is interrupted, bleeding cannot be properly stopped.  This is what happens in hereditary diseases such as hemophilia.  Individuals with Hemophilia A lack the ability to produce proper amounts of clotting factor VIII.  This leads to a gap in the clotting chain reaction and, therefore, prolonged bleeding if the individual gets injured.  Medical treatment involves giving these individuals intravenous clotting factor.  

Medications are used to prevent blood clotting as well.  Heart attacks and strokes can be caused by blockage of blood flow to the heart muscle or to the brain by clot formation within the arteries.  Aspirin and clopidogrel (Plavix) are given as “blood thinners” to at-risk individuals because they interfere with the platelet’s ability to stick to the vessel wall and to stick to other platelets.  

Warfarin (Coumadin) is also commonly used as a blood thinner, especially in patients who have atrial fibrillation, have an artificial heart valve, or in those who have developed a blood clot in the leg.  It works by inactivating the enzyme that converts vitamin K to its active state.  Activated vitamin K is responsible for modifying several of the clotting factors so that they can properly interact in the clotting cascade.  In the presence of warfarin or without vitamin K, the blood cannot clot properly.  

The content in this column is for informational purposes only.  Consult your physician for appropriate individual treatment.  Dr. Reynolds practices Family Medicine in Chesterfield.


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