Conditions that lead to stasis, vascular injury, and hypercoagulability (Virchow’s triad) act as risk factors for DVT.
Acquired risk factors include older age, cancer, surgery, trauma, immobilization, hormone replacement therapy, oral contraceptive use, pregnancy, neurologic disease, cardiac disease, and antiphospholipid antibodies.
Hematologic disorders associated with DVT include disseminated intravascular coagulation, heparin-induced thrombocytopenia, antiphospholipid antibody syndrome, TTP, HUS, polycythemia vera, PNH, and essential thrombocythemia. Inflammatory bowel disease, systemic lupus erythematosus, and obesity are additionally associated with DVT.

Affecting procoagulant or fibrinolytic pathways:
The most common inherited risk factors for venous thrombosis are the factor V Leiden mutation and prothrombin 20210 mutations.
Other mutations predisposing an individual to venous thrombosis include inherited deficiency of protein C or S and mutations of fibrinogen, tissue plasminogen activator, thrombomodulin, or plasminogen activator inhibitor.
In contrast, arterial thrombosis occurs in the setting of platelet activation, and the genetic predisposition for arterial thrombosis includes mutations that affect platelet receptors or redox enzymes.

Ans. is ‘b’ i.e., Intravenous heparin therapy 
• Any venous thrombosis involving the femoropopliteal system is treated with full anticoagulation.
• Traditionally, the treatment of DVT centers around heparin treatment to maintain the PTT at 60 to 80 seconds, followed by warfarin therapy to obtain an INR of 2.5 to 3.0.
• This initial therapy usually is continued for at least 5 days, while oral vitamin K antagonists are being simultaneously administered.
Unfractionated Heparin
• UFH therapy is most commonly administered with an initial IV bolus of 80 units/kg or 5000 units.
• Initial bolus is followed by a continuous IV drip, initially at 18 units/kg per hour or 1300 units per hour.
• The half-life of IV UFH ranges from 45-90 minutes and is dose-dependent.
• Level of antithrombotic therapy should be monitored every 6 hours using aPTT, with the goal range of 1.5 to 2.5 times control values

The answer is C (Antibodies to factor VIII)

Antibodies to factor VIII should be suspected in a disorder presenting with ‘bleeding’ and not in presenting with recurrent thrombosis.

• ‘Antibodies against factor VIII should be suspected in any acquired severe bleeding disorder associated with a prolonged PTT’ — CMDT
• Factor VIII antibodies are distinguished from lupus anticoagulants by the presence of clinical bleeding.’

Major coagulation defects associated with venous thrombosis

Factor V Leiden (commonest association with DVT)

Antithrombin III deficiency Protein C deficiency

Protein S deficiency

Prothrombin gene mutation Homocyteinemia

Antiphospholipid antibody

Homocyteinemia and Antiphospholipid antibodies are also associated with arterial thrombi (others being associated with venous thrombosis only).

Ans. C i.e. Subungual hematoma

Deep venous thrombosis

Clinical presentation:

– Unilateral leg swelling,

– Local warmth,

– Erythema & Pain

• Non-invasive test to diagnose DVT: Duplex venous USG
• A drug used for DVT prophylaxis: Heparin

Treatment:

– Thrombolytic therapy,

– Bandaging etc. Homans sign in DVT: Forced dorsiflexion of the foot causes calf pain