Over the years we have had many cancer patients come to our clinic, New Hope Unlimited, who have been diagnosed with blood clots after receiving chemotherapy. Most of the patients have no idea about blood clots or how they are formed. All they were told is that “this can be bad.”
The body’s way of stopping injured blood vessels from bleeding is called hemostasis. This includes clotting of the blood, but too much clotting can block blood vessels that are not bleeding. The body has control mechanisms that will limit clotting and dissolve clots that are no longer needed. If there is an abnormality in any part of this system that controls bleeding it can lead to excessive bleeding or clotting, which can be dangerous. Severe blood loss may be caused when clotting is poor and there is even a slight injury to a blood vessel. Small blood vessels in critical places can become clogged with clots when clotting is excessive. If these clogged vessels are in the brain it can cause strokes and those leading to the heart can cause heart attacks. Even pieces of clots from veins in the legs, pelvis or abdomen can travel through the bloodstream to the lungs and might block major arteries called pulmonary embolisms.
Three Major Hemostasis processes
These are the three major processes that hemostasis involves:
- Constriction (narrowing) of blood vessels
- Activity of cell-like blood particles that help in blood clotting called platelets
- Activity of proteins found in blood that work with platelets to help the blood clot
If there is an injured blood vessel it constricts and blood flows more slowly, hence clotting can start. Then at the same time the accumulating pool of blood outside the blood vessel presses against the vessel, helping to prevent further bleeding. When a blood vessel wall is damaged, a series of reactions activate the platelets so they stick to the injured area. The glue that holds platelets to the vessel wall is von Willebrand’s factor, a protein produced by the cells of the vessel wall. Collagen and thrombin, both proteins, act at the site of the injury to induce platelets to stick together. As they accumulate at the site, a mesh that plugs the injury is formed. Platelets change their shape from round to spiny and release proteins and other substances that entrap more platelets and clotting proteins in the enlarging plug that then becomes a blood clot.
This formation also involves activation of a sequence of blood clotting factors that generate thrombin that 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 strands add bulk to the developing clot and hold it in place to keep the vessel wall plugged.
The Role Of Anticoagulants
Some people are at high risk of forming these blood clots and are given drugs to decrease the risk, so they will not clump together to block a blood vessel. Some drugs that interfere with the activity of platelets are aspirin, ticlopidine, clopidogrel, abeiximab and tirofiban. An anticoagulant, a drug that inhibits the action of blood proteins called clotting factors or “blood thinners” (warfarin and heparin) may be given to those at risk of forming clots. These patients must be closely monitored when on these drugs and their dose closely watched. Surprisingly, estrogen can have the unintended effect of causing excessive clot formation and certain drugs to treat cancer as asparaginase can also increase the risk of clotting.
– Dr Fredda Branyon