Bleeding diatheses may be caused by congenital or acquired defects in the vasculature, platelets, or the coagulation proteins. Congenital or acquired defects or deficiencies of platelets usually manifest as superficial petechial and ecchymotic hemorrhages (especially of mucous membranes), epistaxis, melena, or prolonged bleeding at injection and incision sites, whereas congenital or acquired deficiencies in coagulation proteins usually manifest clinically as delayed deep tissue hemorrhage, hematoma formation, and bleeding into joints and body cavities.
Pathologic thrombosis may occur because of primary or inherited disorders of anticoagulant protein factors or because of secondary or acquired disorders. Collectively, these conditions are called hypercoagulable states. Systemic syndromes, such as disseminated intravascular coagulation, that enhance platelet responsiveness to agonists and alter the balance between anticoagulant and procoagulant protein factors or that increase the reactivity of endothelium are more common in animals than inherited disorders.