Summary Points

• Hypercoagulability refers to conditions that predispose an individual to thrombosis.

• Risk factors associated with hypercoagulability can be divided into those that are environmental, acquired, or inherited.

• Thrombosis is the formation of blood clots in the vasculature. Thrombosis can be arterial or venous.

• Arterial thrombosis is mainly composed of platelets with small amount of red cells and white cells, whereas venous thrombosis is composed of fibrin clot and red cells

• Thrombosis may result from vascular injury, platelet activation, coagulation activation, defect in fibrinolytic system, and defect in physiological inhibitors.

• Physiological thrombosis results from the body's natural response to vascular injury. It is localized and is formed to prevent excess blood loss.

• Pathological thrombosis includes deep venous thrombosis, arterial thrombosis, and pulmonary embolism. Pathological thrombosis may be caused by acquired or inherited conditions.

nase is not fibrin specific, and because it is antigenic, it may cause allergic reactions.

Bleeding is the most common complication associated with thrombolytic drugs. Thrombolytic therapy does not require monitoring, however, prior screening tests such as PT, aPTT, TT, fibrinogen, and platelet count may be helpful to predict patients who are at high risk of bleeding.3

• Thromboembolism is formed when clot is dislodged from the origination site and filtered out in the pulmonary circulation.

• Physiological anticoagulant is plasma protein and includes antithrombin, heparin cofactor II, protein C, and protein S.

• Antithrombin is made in the liver. It inhibits factors IIa, IXa, Xa, XIa, and XlIa. Heparin increases the inhibitory action of antithrombin.

• Protein C is a vitamin K-dependent protein made in the liver. Protein C is activated by thrombin-throm-bomodulin complex. Protein S is a cofactor for activation of protein C. Activated protein C deactivates factors Va and VIIIa.

• Inherited risk factors are associated with genetic mutations that result in deficiency of naturally occurring inhibitors such as protein C, protein S, or antithrombin; accumulation of procoagulant factors as in prothrombin G20210A; or clotting factor resistance to anticoagulant activities of physiological inhibitors as in activated protein C resistance.

• The majority (92%) of activated protein C resistance cases are inherited and are caused by mutation of factor V Arg506Gln, referred to as factor V Leiden.

A technical representative for a reference laboratory experienced severe pain behind his left knee 1 day after a visit to one of his laboratory accounts. He tried to pass it off as muscle pain because of a recent basketball game, but walking became difficult for him. Over the next 24 hours, he noticed that the area of pain became swollen, red, and even more sensitive. What is your clinical impression?


This patient may be experiencing deep vein thrombosis. Upon further questioning, it was discovered that the patient had done significant highway driving during the week; most of the time keeping his left knee in a bent position. He eventually went to the emergency department, where the thrombosis was diagnosed. His PT and aPTT results were normal, but his D-dimer results were higher than the normal range. A venogram demonstrated a clot behind the left knee. The patient was treated appropriately and started on a regimen of Coumadin with careful outpatient monitoring

Acquired thrombotic disorders are associated with underlying diseases or drugs.

Antiphospholipid syndrome is caused by antibodies against phospholipid-dependent coagulation assays such as aPTT, which was not corrected with 1:1 mix with normal plasma. The most common form of aPL antibodies are lupus anticoagulant (LA) and anticar-diolipin (ACA).

Laboratory tests for LA include aPTT or dRRVT; mixing studies, and confirmatory studies. Anticardiolipin antibodies are tested by ELISA.

Heparin-induced thrombocytopenia (HIT) is an immune-mediated thrombotic complication associated with heparin therapy. The antibody is produced against heparin-platelet factor 4 complexes.

Diagnostic tests for HIT include heparin-dependent platelet activation assays and detection of the antibody by ELISA.

Antithrombotic drugs include antiplatelet drugs, anticoagulant drugs, and thrombolytic drugs.

Aspirin is an antiplatelet drug that inhibits the cyclooxygenase (COX) enzyme and therefore prevents formation of thromboxane A2 (TXA2). TXA2 is a potent platelet-activating substance released from the activated platelets.

Heparin is a short-term anticoagulant drug. It is administered intravenously or intramuscularly. Heparin dosage is monitored by aPTT value to range from 1.5 to 2.5 times the mean of the laboratory control.

Coumadin is a vitamin K antagonist drug that inhibits the vitamin K-dependent coagulation factors (II, VII, IX, and X).

Coumadin is an oral anticoagulant that is administered as a long-term anticoagulant. It is monitored by PT/INR.

Thrombolytic drugs include tPA, urokinase, and streptokinase.

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