Hemostatic disorders are classified into the following clinical syndromes: thrombotic, hemorrhagic and thrombo-hemorrhagic syndromes.
THROMBOTIC SYNDROME
Immobilization after surgery, chronic congestive heart failure, atherosclerotic vascular disease, a malignancy and pregnancy predispose to thrombosis. Endothelial injury is a trigger of thrombosis. Other factors such as abnormal blood flow, increased platelet number, hypercoagulability, dysfibrinogenemias and fibrinolytic defect play a certain role in thrombosis. Slowing of blood flow, especially in veins, or thrombocytosis are considered as important factors of thrombosis. Mechanisms of thrombosis are described in fig. 22.
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Fig. 22. Mechanisms of thrombosis
Atherosclerotic lesion, hemodynamic stress associated with hypertension, bacterial endotoxins, virus and immune complexes are the most common causes of endothelial injury. Some drugs may damage blood vessels by causing allergic reactions.
Turbulence
Turbulence contributes to arterial and cardiac thrombosis by reducing the local release of prostacyclin (prostaglandin 12). In venous vessels, stasis or slowdown of blood stream prevent the dilution of the activated coagulation factors by fresh blood.
Hypercoagulability
Hypercoagulability is a risk factor that predisposes to thrombosis. A point mutation in the plasma clotting factor V makes the molecule of factor V resistant to degradation by activated protein C. This mutation may account for 25% of inherited prethrombotic states, and approximately 3% of the population worldwide is heterozygous for this mutation. In heterozygous state patients with protein C and protein S defects show disease if they have less than 50% of normal molecules. In contrast, slight reduction of plasma antithrombin III content increases the risk of thrombosis.