## Virchow's Triad and Thrombosis **Key Point:** Virchow's triad comprises three major factors that predispose to thrombosis: (1) endothelial injury, (2) abnormality of blood flow (stasis or turbulence), and (3) alterations in blood composition (hypercoagulability). ### The Three Components | Component | Examples | Mechanism | |-----------|----------|----------| | Endothelial injury | Atherosclerosis, trauma, surgery, indwelling catheters | Exposes tissue factor and von Willebrand factor; activates extrinsic pathway | | Abnormality of blood flow | Stasis (atrial fibrillation, venous obstruction), turbulence (atherosclerotic plaques) | Promotes platelet aggregation and fibrin deposition; reduces dilution of procoagulants | | Alterations in blood composition | Hypercoagulability (cancer, pregnancy, OCP use, thrombophilias) | Increased procoagulant factors or decreased anticoagulant factors | ### Why "Increased Platelet Adhesiveness" is NOT Part of Virchow's Triad **High-Yield:** Increased platelet adhesiveness is a *consequence* of endothelial injury and abnormal blood flow, not a primary component of Virchow's triad. The triad focuses on three *independent* predisposing factors, not the cellular responses that follow. **Clinical Pearl:** While platelet dysfunction or increased platelet reactivity can contribute to thrombosis, Virchow's triad specifically refers to the three macroscopic/systemic conditions that create a prothrombotic environment. Platelet adhesiveness changes occur *after* endothelial damage is already present. **Warning:** Students often confuse the consequences of Virchow's triad (platelet aggregation, fibrin deposition) with the triad itself. The triad is about the *conditions* that favor thrombosis, not the *mechanisms* of clot formation. [cite:Robbins 10e Ch 4]
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