A deficiency in one or more coagulation factors will also cause abnormalities in hemostasis. The image to the right depicts the coagulation cascade. Notice how one factor eventually acts upon another to form a stabilized fibrin clot, the cascade's end product. Having an abnormally low level or a complete lack of a coagulation factor can cause the extrinsic, intrinsic, or common pathways to malfunction, resulting in dangerous hemorrhagic issues, including spontaneous bleeding.
Two of the most common factor deficiencies are factor VIII (hemophilia A) and factor IX (hemophilia B). Hemophilia A is present in two forms—congenital (inherited) and acquired. Congenital hemophilia A occurs when an individual is born with a factor VIII deficiency. Acquired hemophilia A occurs when an individual spontaneously produces an autoantibody to factor VIII, leaving the body unable to use the factor VIII that may be present. Hemophilia B is an inherited condition where the individual has a mutation of the factor IX gene and cannot produce adequate levels of this coagulation factor.
Patients sometimes have multiple factor deficiencies secondary to a primary condition, such as vitamin K deficiency, disseminated intravascular coagulation (DIC), and liver disease. Due to vitamin K deficiency, the liver cannot produce vitamin K-dependent coagulation factors. During liver disease, the liver may be unable to produce coagulation factors effectively. In DIC, the clotting processes are in overdrive and will consume the coagulation factors produced, leading to low levels of circulating coagulation factors.
