Physiology · Blood, hemostasis and basic immunity

Thrombosis and bleeding: Virchow's triad and hemostatic defects !

Mechanism
Exam priority: medium

Clots form where blood is slow, the vessel wall is damaged or the blood clots too easily. Bleeding happens when platelets or clotting factors fail.

Updated 2026-11-01

Also called: Virchow's triad, Bleeding disorders, Thrombophilia

See it in 3D: Great saphenous vein · Popliteal vein · Femoral artery · Liver

Key points

Virchow's triad: stasis (immobility, long travel, heart failure), endothelial injury (surgery, trauma, catheters), hypercoagulability (cancer, pregnancy, estrogen, inherited thrombophilia).
Venous thrombi are red (fibrin and red cells, low flow) → prevented with anticoagulants; arterial thrombi are white (platelet-rich, high shear on a ruptured plaque) → antiplatelet drugs.
A deep vein thrombus of the leg can embolize to the lungs: pulmonary embolism.
Platelet-type bleeding: skin and mucosa, petechiae, immediate. Factor-type bleeding: joints and muscles, large hematomas, delayed rebleeding.
DIC: widespread activation consumes platelets and factors → simultaneous microthrombi and bleeding.
Cirrhosis is 'rebalanced': low procoagulant factors and platelets, but also low proteins C and S and high factor VIII and vWF, so patients can bleed and clot.

What it is

Hemostasis is a balance between clotting and its brakes. Thrombosis appears when that balance tips inside an intact vessel, and Virchow's triad names the three ways it tips: stasis, endothelial injury and hypercoagulability. Bleeding disorders tip it the other way, and the pattern of bleeding tells whether platelets or clotting factors are at fault.

How it works, step by step

Stasis lets activated factors accumulate and keeps them from being diluted or cleared by the liver.
Low flow also lowers O₂ and shear at valve pockets of leg veins → endothelium becomes procoagulant.
Endothelial injury exposes tissue factor and collagen and removes thrombomodulin and prostacyclin.
Hypercoagulability adds more factors or fewer brakes (factor V Leiden, antithrombin or protein C/S deficiency, antiphospholipid antibodies, estrogen).
In veins, a fibrin-rich thrombus grows along the flow and can break off → embolus to the pulmonary arteries.
In arteries, plaque rupture exposes thrombogenic material under high shear → platelet-rich thrombus → infarction.
In bleeding disorders, a missing platelet function stops the first seal; a missing factor leaves a seal without fibrin that fails later.

Two ways to bleed

Feature	Platelet or vWF defect	Clotting factor defect
Typical sites	Skin, gums, nose, menses, gut	Joints, muscles, deep tissues
Skin lesions	Petechiae, small bruises	Large hematomas
Timing after a cut	Immediate	Delayed, recurs after hours
Examples	Thrombocytopenia, von Willebrand disease, aspirin	Hemophilia A and B, vitamin K deficiency, liver failure

Clinical notes

Long immobility (surgery, long bus or plane journeys, bed rest) and pregnancy are common risk settings for leg vein thrombosis.
Sepsis is a frequent trigger of DIC: cytokines induce tissue factor on monocytes and endothelium.
Newborns lack vitamin K; vitamin K prophylaxis at birth prevents factor-type bleeding in the first weeks.

Test yourself

Think of the answer, then tap the question to see it.

Why are anticoagulants preferred for venous thrombosis and antiplatelet drugs for arterial thrombosis?

Venous clots form at low flow and are mostly fibrin and red cells, driven by the coagulation cascade. Arterial clots form at high shear on plaques and are platelet-rich, driven by platelet activation.

Why does DIC cause both thrombosis and bleeding?

Systemic tissue factor activity forms microthrombi everywhere, consuming platelets, fibrinogen and factors; once these are used up and fibrinolysis is active, bleeding follows.

A patient bleeds into the knee joint hours after a minor injury. Which kind of defect is most likely?

A clotting factor defect such as hemophilia: the platelet plug forms, but without enough thrombin and fibrin it is not stabilized and bleeding restarts into deep tissues.

Why can a patient with cirrhosis and a high INR still develop portal vein thrombosis?

The liver also makes less protein C, protein S and antithrombin, factor VIII and vWF rise, and portal flow is slow, so hemostasis is rebalanced and can tip toward clotting.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

In Biochemistry

Vitamin K (phylloquinone)

In Pharmacology

← All of physiology

Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: Deep Venous Thrombosis (StatPearls (NCBI Bookshelf), 2024); Acute Pulmonary Embolism (StatPearls (NCBI Bookshelf), 2024); Hepatic Cirrhosis (StatPearls (NCBI Bookshelf), 2024); 18.5 Hemostasis (OpenStax (Rice University), 2022); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 37). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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