Which components make up Virchow's Triad associated with deep vein thrombosis?

Which components make up Virchow's Triad associated with deep vein thrombosis?

• A. Arterial injury, endothelial dysfunction, dehydration
• B. Venous dilation, leukocytosis, hypercoagulability
• C. Venous stasis, endothelial injury, hypercoagulable state
• D. Platelet aggregation, vasoconstriction, leukopenia

Answer: (C)

Virchow's Triad describes three conditions that promote venous thrombosis: venous stasis, endothelial injury, and a hypercoagulable state. When blood flow in the veins slows (venous stasis), there’s more time for clotting factors to accumulate and interact with the endothelium, increasing clot formation. Endothelial injury exposes pro-thrombotic surfaces like collagen and tissue factor, triggering platelet adhesion and the coagulation cascade. A hypercoagulable state means the blood is inherently more prone to clot, due to inherited mutations or acquired conditions such as cancer, pregnancy, estrogen therapy, or inflammatory states. Together, these factors create a prothrombotic environment in the venous system, leading to deep vein thrombosis. Other options mix processes that aren’t central to this venous triad—arterial injury and dehydration relate more to arterial thrombosis or systemic effects, venous dilation alters flow but isn’t a component of the triad, and leukocytosis/leukopenia or vasoconstriction aren’t core elements of Virchow’s Triad.

Virchow's Triad describes three conditions that promote venous thrombosis: venous stasis, endothelial injury, and a hypercoagulable state. When blood flow in the veins slows (venous stasis), there’s more time for clotting factors to accumulate and interact with the endothelium, increasing clot formation. Endothelial injury exposes pro-thrombotic surfaces like collagen and tissue factor, triggering platelet adhesion and the coagulation cascade. A hypercoagulable state means the blood is inherently more prone to clot, due to inherited mutations or acquired conditions such as cancer, pregnancy, estrogen therapy, or inflammatory states. Together, these factors create a prothrombotic environment in the venous system, leading to deep vein thrombosis.

Other options mix processes that aren’t central to this venous triad—arterial injury and dehydration relate more to arterial thrombosis or systemic effects, venous dilation alters flow but isn’t a component of the triad, and leukocytosis/leukopenia or vasoconstriction aren’t core elements of Virchow’s Triad.