Bleeding Tendency

In any bleeding episodes, there will be a breach in the continuity of the blood vessel walls involved. Therefore, in the physiologic or normal situations, the damaged segment of the vessel wall will initiate the repair by enlisting the help of both the platelets and the clotting proteins. Platelets are small blood cells that can be activated and aggregated to form a platelet plug to seal the vessel wall breach. The platelet plug will also provide a conducive surface upon which the clotting proteins can react. The clotting proteins, once activated, will ultimately culminate in the laying down of a fiber network over the initial platelet plug. This fiber network serves to strengthen the platelet plug in sealing the vessel breach. However, once the inciting agents have been eliminated and the underlying vessel damages repaired, the fiber network and platelet plug will be removed. Therefore in anyone who has an abnormal or pathological bleeding tendency, it may result from abnormalities in the a) vessel walls, b) platelets, and/or c) clotting proteins.

Causes of bleeding tendency

There are many causes to vessel defects eg. hereditary (ie Ehlers Danlos syndrome), nutrient deficiency (i.e. Vitamin C deficiency), drug induced (ie steroid induced), aging (senile purpura), certain infections (ie streptococcal, meningococcal infections), malignancies (i.e. lymphoma, leukemia), etc.

The platelet disorders are often subdivided into either quantitative (ie thrombocytopenia) or qualitative problems ( i.e. platelet dysfunction). The former can be a result of decreased platelet production in the bone marrow or an increased destruction/loss of platelets in the peripheral blood stream. The causes can likewise be a primary platelet disorder (e.g. hereditary, nutrient deficiency, infections, drug induced, etc.) or secondary to other disease states affecting the marrow or peripheral blood (e.g. other malignancies, autoimmune disorder, etc).

Clotting defects can either be due to an abnormal production or an accelerated removal of the fiber clots. The common cause of defective production is the hereditary deficiency of clotting factors (e.g. hemophilia, von Willebrand disease, etc). The problem with an accelerated removal of fiber clots is by far very rare, but nevertheless, could still result from a deficiency of the regulatory proteins in clot removal (e.g. plasminogen activator inhibitor deficiency).