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THROMBOSIS. Dr. Afsar Saeed Shaikh M.B.B.S, M.Phil. Assistant Professor of Chemical Pathology Pathology Department, KEMU, Lahore. INTRODUCTION. NORMAL HEMOSTASIS 1) Maintain blood in fluid form in normal blood vessels

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Dr. Afsar Saeed Shaikh

M.B.B.S, M.Phil.

Assistant Professor of Chemical Pathology

Pathology Department, KEMU, Lahore.




    1) Maintain blood in fluid form in normal blood vessels

    2) induce a rapid & localized hemostatic plug formation at the site of vascular injury


    ‘Pathologic opposite to hemostasis’




    ‘An inappropriate activation of normal hemostatic processes, such as the formation of a blood clot in uninjured vasculature or thrombotic occlusion of a vessel after relatively minor injury.’




    • Endothelial Injury

    • Abnormal Blood Flow

    • Hypercoagubality

Virchow triad

Virchow Triad

1 endothelial injury

1. Endothelial Injury

  • General:

    • A dominant influence

    • Can act without combination with other factors

    • Important factor where normally high flow rates hampers thrombus formation e.g. arterial circulation & heart chambers

Endothelial injury

Endothelial Injury

  • Sites :

    • Within cardiac chamber (e.g. following M.I)

    • Over ulcerative atherosclerotic plaques

    • At the site of inflammatory or traumatic vascular injury

Mechanism of endothelial injury

Mechanism of Endothelial Injury

  • 1: Direct endothelial injury; physical loss of endothelium

  • 2: Dysfunctional endothelium (Imbalance of anticoagulant and pro-coagulant properties of endothelium)


Dysfunctional endothelium

Dysfunctional Endothelium

  • Stress of hypertension

  • Bacterial endotoxins

  • Turbulent flow over scarred valves

  • Hypercholesterolemia

  • Products absorbed from cigarette smoke

  • Irradiation.

1 abnormal blood flow

1. Abnormal Blood Flow

  • Turbulence:

    • Arterial & cardiac thrombosis

    • A cause of endothelial injury

    • Also causes countercurrents and local pockets of stasis

  • Stasis:

    • Venous thrombi

    • Acts by disturbing normal blood flow

Mechanism of abnormal blood flow

Mechanism of Abnormal Blood Flow

  • Normal blood flow; laminar

  • Turbulence & stasis disrupt normal laminar blood flow

  • Bring platelets in contact with endothelium

  • Prevent dilution of clotting factors

  • Retard the inflow of inhibitors

  • Promote endothelial cell activation

Clinical settings of abnormal blood flow

Clinical Settings of Abnormal Blood Flow

  • Ulcerative atherosclerotic plaques

  • Aortic & arterial aneurysms

  • MI

  • Mitral valve stenosis

  • Hyperviscosity syndrome

  • Sickle cell anemia

3 hypercoagubility

3. Hypercoagubility

  • Important but less frequent contributor

  • ‘Any alteration of the coagulation pathways that predisposes to thrombosis’

Causes of hypercoagubality

Causes of Hypercoagubality

  • PRIMARY (Genetic)

  • Common:

    Mutation in factor V gene

    Mutation in prothrombin gene

  • Rare:

    Antithrombin III deficiency

    Protein C def.

    Protein S def.

Causes of hypercoagubality1

Causes of Hypercoagubality

  • Secondary (Acquired)

  • High Risk:

    Prolonged bed rest

    MI, Cancer, DIC

    Atrial fibrillation

    Tissue damage

    Prosthetic cardiac valve

    Antiphospholipid antibody syndrome

Causes of hypercoagubality2

Causes of Hypercoagubality

  • Secondary (Acquired)

  • Low Risk:


    Nephrotic syndrome

    Pregnancy, Oral contraceptives

    Sickle cell anemia


Types of thrombi

Types of Thrombi

  • Types:

  • Arterial Thrombi

  • Venous Thrombi

  • Mural Thrombi

  • Red Thrombi (Stasis thrombi)

  • White Thrombi (Gray-white)

Morphology of thrombi

Morphology of Thrombi

  • Arterial:

  • Usually occlusive

  • Firmly attached to the injured artery wall

  • Gray-white and friable

  • Composed of a meshwork of platelets, fibrin, erythrocytes, and degenerating leukocytes

Morphology of thrombi1

Morphology of Thrombi

  • Venous:

  • Invariably occlusive

  • Not firmly attached to the artery wall

  • Red in color and not friable but wet like a in-vitro clot

  • Contain more erythrocytes as compare to arterial thrombi



Fate of thrombi

Fate of Thrombi

  • Propagation

  • Embolization

  • Dissolution

  • Organization and recanalization

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