is both a qualitative and quantitative abnormality

inhibits thrombin and factors IX, X, XI, XII, plasmin, protein C

autosomal dominant; manifests before the age of 35

manifestation: lower extremity thrombophlebitis and pulmonary embolism

laboratory feature:

Type I: deficient antigen and functional activity Type II: deficient in functional activity only

autosomal dominant; manifests before the age of 30

manifestation: recurrent superficial deep vein thrombophlebitis and frequent pulmonary emboli

laboratory feature:

manifestations: recurrent venous thrombosis together with immunologic protein S level of 30-60%

laboratory feature:

impairment of fibrinolytic system → buildup of fibrin → thrombus

principle: defective release of TPA, deficiency XII, circulating inhibitors plasminogen activators

quantitative and functional abnormalities of plasminogen

manifestations: recurrent thrombosis

rigid fibrin resistant to the fibrinolytic enzyme system

autosomal recessive; early in life

manifestation: arterial and venous thrombosis

acquired immunoglobulin directed against phospholipids secondary to prostacyclin inhibition

SLE and other autoimmune disorders, neoplasms, drug therapy

laboratory feature:

increased in factors:

decreased in:

post-operative state:

malignancy

pregnancy

Oral contraceptive use or Estrogen

increased number

increased aggregation response to ADP, collagen and epinephrine

increased level of beta-thromboglobulin and PF4

DM, hyperlipidemia, myeloproliferative disorders, heparin induced platelet agglutination

artificial/foreign surfaces → increased adhesion & aggregation of platelets → activation of coagulation system

abnormal vascular surfaces → disrupts normal antithrombotic function of EC

abnormal blood flow → causes vascular EC damage through local hypoxia & slow removal of activated clotting factors from site of vascular injury

Antitrombin III (AT III)

Protein C

Plasmin