THROMBOSIS

Dr. Afsar Saeed Shaikh

M.B.B.S, M.Phil. Assistant Professor of Chemical PathologyPathology Department, KEMU, Lahore.

INTRODUCTION NORMAL HEMOSTASIS

1) Maintain blood in fluid form in normal blood vessels2) induce a rapid & localized hemostatic plug formation at the site of vascular injury

THROMBOSIS ‘Pathologic opposite to hemostasis’

INTRODUCTION DEFINATION:

‘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.’

INTRODUCTION ETIOLOGY:

Endothelial Injury Abnormal Blood Flow Hypercoagubality

Virchow Triad

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

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

1: Direct endothelial injury; physical loss of endothelium

2: Dysfunctional endothelium (Imbalance of anticoagulant and pro-coagulant properties of endothelium) Continued…….

Dysfunctional Endothelium

1. Stress of hypertension2. Bacterial endotoxins3. Turbulent flow over scarred

valves4. Hypercholesterolemia5. Products absorbed from

cigarette smoke 6. Irradiation.

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

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

Ulcerative atherosclerotic plaques

Aortic & arterial aneurysms MI Mitral valve stenosis Hyperviscosity syndrome Sickle cell anemia

3. Hypercoagubility Important but less frequent

contributor ‘Any alteration of the

coagulation pathways that predisposes to thrombosis’

Causes of Hypercoagubality

PRIMARY (Genetic) Common:

Mutation in factor V geneMutation in prothrombin gene

Rare:Antithrombin III deficiencyProtein C def.Protein S def.

Causes of Hypercoagubality

Secondary (Acquired) High Risk:

Prolonged bed restMI, Cancer, DICAtrial fibrillationTissue damageProsthetic cardiac valveAntiphospholipid antibody

syndrome

Causes of Hypercoagubality

Secondary (Acquired) Low Risk:

CardiomyopathyNephrotic syndromePregnancy, Oral

contraceptivesSickle cell anemiaSmoking

Types of Thrombi

Types: Arterial Thrombi Venous Thrombi Mural Thrombi Red Thrombi (Stasis thrombi) White Thrombi (Gray-white)

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 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

THANK YOU!

Fate of Thrombi

Propagation Embolization Dissolution Organization and recanalization