thrombosis dr. afsar saeed shaikh m.b.b.s, m.phil. assistant professor of chemical pathology...
TRANSCRIPT
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THROMBOSIS
Dr. Afsar Saeed Shaikh
M.B.B.S, M.Phil. Assistant Professor of Chemical PathologyPathology Department, KEMU, Lahore.
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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’
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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.’
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INTRODUCTION ETIOLOGY:
Endothelial Injury Abnormal Blood Flow Hypercoagubality
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Virchow Triad
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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
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Endothelial Injury
Sites : Within cardiac chamber (e.g.
following M.I) Over ulcerative atherosclerotic
plaques At the site of inflammatory or
traumatic vascular injury
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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…….
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Dysfunctional Endothelium
1. Stress of hypertension2. Bacterial endotoxins3. Turbulent flow over scarred
valves4. Hypercholesterolemia5. Products absorbed from
cigarette smoke 6. Irradiation.
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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
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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
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Clinical Settings of Abnormal Blood Flow
Ulcerative atherosclerotic plaques
Aortic & arterial aneurysms MI Mitral valve stenosis Hyperviscosity syndrome Sickle cell anemia
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3. Hypercoagubility Important but less frequent
contributor ‘Any alteration of the
coagulation pathways that predisposes to thrombosis’
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Causes of Hypercoagubality
PRIMARY (Genetic) Common:
Mutation in factor V geneMutation in prothrombin gene
Rare:Antithrombin III deficiencyProtein C def.Protein S def.
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Causes of Hypercoagubality
Secondary (Acquired) High Risk:
Prolonged bed restMI, Cancer, DICAtrial fibrillationTissue damageProsthetic cardiac valveAntiphospholipid antibody
syndrome
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Causes of Hypercoagubality
Secondary (Acquired) Low Risk:
CardiomyopathyNephrotic syndromePregnancy, Oral
contraceptivesSickle cell anemiaSmoking
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Types of Thrombi
Types: Arterial Thrombi Venous Thrombi Mural Thrombi Red Thrombi (Stasis thrombi) White Thrombi (Gray-white)
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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
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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
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THANK YOU!
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Fate of Thrombi
Propagation Embolization Dissolution Organization and recanalization