APC (with<unk>  S as a cofactor) degrades Factor Va and Factor VIIIa.<unk><unk>  is the inability of<unk>  C to cleave Factor Va and/or Factor VIIIa, which allows for longer duration of thrombin generation and may lead to a hypercoagulable state. This may be hereditary or acquired. The best known and most common hereditary form is Factor V Leiden, which is responsible for more than 95% of cases. Other genetic causes include Factor V Cambridge (VThr306) and the factor V HR2 haplotype (A4070G mutation). Acquired forms of<unk><unk>  occur in the presence of elevated Factor VIII concentrations. Antiphospholipid antibodies, pregnancy, and certain forms of estrogen therapy, such as ethinylestradiol-containing birth control pills, have been found to produce acquired<unk><unk> .
Activated protein C resistance
Protein C deficiency
Factor VII deficiency
COAT platelet defect
Primary fibrinogenolysis
Factor XII deficiency
Factor XIII deficiency
Antithrombin III deficiency