Congenital vascular abnormalities (vessel wall structure defects). Defects of the actual blood vessel are poorly defined and difficult to test. Hereditary telangiectasia is the most commonly recognized vascular abnormality. Laboratory studies are normal, so the diagnosis must be made from clinical signs and symptoms. Patients frequently report epistaxis and symptoms of anemia. Another abnormality is congenital hemangiomas (Kasabach–Merritt syndrome).

Acquired abnormalities of the vessel wall structure. Causes include Henoch–Schönlein purpura as an allergic response to infection or drugs, diabetes, rickettsial diseases, septicemia, and amyloidosis present with some degree of vascular abnormalities. Purpura can also be associated with steroid therapy and easy bruising in females (infectious purpura), or it can be a result of drug use.

Hereditary connective tissue disorders. These include Ehlers–Danlos syndrome (hyperplastic skin and hyperflexible joints) and pseudoxanthoma elasticum (rare connective tissue disorder).

Acquired connective tissue defects. These can be caused by scurvy (vitamin C deficiency) or senile purpura.

Qualitative platelet abnormalities. These disorders can be divided into subclasses:

1. Thrombocytopenia (platelet count less than 150 × 10³/mm³) is caused by decreased production of platelets, increased use or destruction of platelets, or hypersplenism. Contributing factors include bone marrow disease, autoimmune diseases, DIC, bacterial or viral infection, chemotherapy, radiation therapy, multiple transfusions, and certain drugs (e.g., NSAIDs, thiazides, estrogens).

2. Thrombocytosis (elevated platelet count) is caused by hemorrhage, iron-deficiency anemia, inflammation, or splenectomy.

3. Thrombocythemia (platelet count more than 1000 × 10³/mm³ or more than 1000 × 10⁹/L) is caused by granulocytic leukemia, polycythemia vera, or myeloid metaplasia.

Quantitative platelet abnormalities. These are associated with Glanzmann thrombasthenia, a hereditary autosomal recessive disorder that can produce severe bleeding, especially with trauma and surgical procedures. Platelet factor 3 differences associated with aggregation, adhesion, or release defects may be manifested in storage pool disease, May–Hegglin anomaly, Bernard–Soulier syndrome (autosomal recessive coagulopathy), and Wiskott–Aldrich syndrome. Dialysis and use of drugs such as aspirin, other antiinflammatory agents, dipyridamole, and prostaglandin E also can be tied to platelet abnormalities.

Congenital coagulation abnormalities. These include hemophilia A and B (deficiencies of factors VIII and IX, respectively), rare autosomal recessive traits (hemophilia C), and autosomal dominant traits (e.g., von Willebrand disease).

Acquired coagulation abnormalities. These are associated with several disease states and are much more common than inherited deficiencies.

1. Circulatory anticoagulant activity may be evident in the presence of antifactor VIII, RA, immediate postpartum period, SLE, or multiple myeloma.

2. Vitamin D deficiency may be caused by oral anticoagulants, biliary obstruction and malabsorption syndrome, or intestinal sterilization by antibiotic therapy. Newborns are prone to vitamin D deficiency.

3. DIC causes continuous production of thrombin, which, in turn, consumes the other clotting factors and results in uncontrolled bleeding.

4. Primary fibrinolysis is the situation whereby isolated activation of the fibrinolytic mechanism occurs without prior coagulation activity, as in streptokinase therapy, severe liver disease, prostate cancer, or, more rarely, electroshock.

5. Most coagulation factors are manufactured in the liver. Consequently, in liver disease, the extent of coagulation abnormalities is directly proportional to the severity of the liver disease.