Virchow’s triad

virchow’s triad


Virchow’s Triad refers to the three primary factors that contribute to the development of venous thrombosis (blood clot formation). It was proposed by Rudolf Virchow in the 19th century.


⚖️ Components of Virchow’s Triad

  1. Endothelial Injury
    • Damage to the vascular endothelium exposes subendothelial collagen and tissue factor, promoting clotting.
    • Causes: trauma, surgery, inflammation, hypertension, atherosclerosis, indwelling catheters.
  2. Stasis of Blood Flow
    • Sluggish or stagnant blood increases the risk of clot formation.
    • Causes: prolonged immobility (bed rest, long flights), heart failure, varicose veins, atrial fibrillation.
  3. Hypercoagulability
    • Abnormal tendency of blood to clot.
    • Causes: inherited thrombophilias (Factor V Leiden, Protein C/S deficiency), pregnancy, malignancy, oral contraceptives, dehydration, sepsis.

📊 Summary Table

Virchow’s TriadKey Examples
Endothelial InjuryTrauma, surgery, hypertension, atherosclerosis
Stasis of Blood FlowProlonged immobility, varicose veins, CHF, AF
HypercoagulabilityFactor V Leiden, pregnancy, malignancy, OCPs

🧠 Clinical Relevance

  • Explains the pathogenesis of Deep Vein Thrombosis (DVT), Pulmonary Embolism (PE), and other thromboembolic diseases.
  • Guides risk assessment and preventive strategies (anticoagulants, compression stockings, early mobilization).

1. Virchow’s Triad explains the pathogenesis of which condition?
Venous thrombosis
Arterial dissection
Aortic aneurysm
Pericardial effusion
Virchow’s triad describes the major risk factors for venous thromboembolism.
2. Which of the following is NOT part of Virchow’s Triad?
Endothelial injury
Stasis of blood flow
Vasospasm
Hypercoagulability
Vasospasm is not part of Virchow’s triad.
3. Endothelial injury contributes to thrombosis by:
Releasing nitric oxide
Exposing tissue factor and collagen
Increasing fibrinolysis
Reducing platelet adhesion
Endothelial damage exposes subendothelial collagen and tissue factor, promoting clotting.
4. Prolonged bed rest mainly predisposes to thrombosis due to:
Hypercoagulability
Endothelial injury
Stasis of blood flow
Arterial turbulence
Immobility leads to sluggish venous return, i.e. stasis.
5. Which of the following is an example of hypercoagulability?
Factor V Leiden mutation
Bed rest
Vascular trauma
Varicose veins
Inherited thrombophilia such as Factor V Leiden increases coagulability.
6. Pregnancy increases the risk of thrombosis mainly due to:
Hypercoagulability
Stasis only
Endothelial rupture
Hypocoagulability
Pregnancy is a hypercoagulable state.
7. Atrial fibrillation predisposes to thrombosis because of:
Endothelial injury
Hypercoagulability
Stasis of blood in atria
Vasospasm
AF causes blood stasis in atria, leading to clot formation.
8. Malignancy is associated with thrombosis due to:
Endothelial trauma
Hypercoagulability
Blood stasis
Fibrinolysis
Cancers release procoagulants, increasing risk of thrombosis.
9. Which of the following conditions is an example of endothelial injury?
Atherosclerosis
Pregnancy
Varicose veins
Dehydration
Atherosclerosis damages the endothelium, exposing subendothelial tissue.
10. Which of the following causes venous stasis?
Polycythemia
Endothelial trauma
Oral contraceptive use
Prolonged immobility
Immobility causes venous stasis by reducing calf muscle pump activity.
11. The triad was proposed by which scientist?
Rudolf Virchow
William Osler
Thomas Hodgkin
Robert Koch
Rudolf Virchow described this triad in the 19th century.
12. Which factor is shared between venous and arterial thrombosis?
Endothelial injury
Stasis
Hyperviscosity
Hypocoagulability
Endothelial injury promotes both arterial and venous thrombosis.
13. Which type of embolism is most directly linked to Virchow’s Triad?
Fat embolism
Air embolism
Pulmonary embolism
Amniotic embolism
Deep vein thrombosis caused by Virchow’s triad can embolize to lungs → PE.
14. Which inherited condition increases hypercoagulability?
Protein C deficiency
Iron deficiency
Vitamin D deficiency
Pernicious anemia
Protein C deficiency reduces anticoagulant activity, increasing clot risk.
15. Varicose veins predispose to thrombosis due to:
Stasis of blood
Hypercoagulability
Endothelial trauma
Low platelets
Varicosities slow venous return → stasis.
16. Oral contraceptive pills increase clot risk via:
Endothelial injury
Stasis
Hypercoagulability
Arterial turbulence
OCPs increase clotting factors and decrease anticoagulants → hypercoagulability.
17. Which of the following is the LEAST associated with Virchow’s Triad?
Immobilization
Cancer
Asthma
Pregnancy
Asthma is not a direct factor in Virchow’s triad.
18. Which factor contributes most in trauma patients?
Endothelial injury
Stasis
Hypercoagulability
Hypocoagulability
Trauma causes direct vascular injury leading to clot formation.
19. Nephrotic syndrome predisposes to thrombosis by:
Hypercoagulability due to loss of anticoagulant proteins
Endothelial rupture
Stasis alone
Fibrinolysis activation
Loss of antithrombin III and protein S in urine increases clotting tendency.
20. Preventive strategies against Virchow’s Triad include:
Compression stockings
Early mobilization
Anticoagulants
All of the above
All these strategies target different components of the triad to reduce clot risk.
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