Transcript Document

THROMBOSIS
Dr. Afsar Saeed Shaikh
M.B.B.S, M.Phil.
Assistant Professor of Chemical Pathology
Pathology Department, KEMU, Lahore.
INTRODUCTION
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NORMAL HEMOSTASIS
1) Maintain blood in fluid form
in normal blood vessels
2) induce a rapid & localized
hemostatic plug formation at the
site of vascular injury
THROMBOSIS
‘Pathologic opposite to
hemostasis’
INTRODUCTION
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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
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ETIOLOGY:
Endothelial Injury
 Abnormal Blood Flow
 Hypercoagubality

Virchow Triad
1. Endothelial Injury
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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
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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
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1: Direct endothelial injury;
physical loss of endothelium
2: Dysfunctional endothelium
(Imbalance of anticoagulant and
pro-coagulant properties of
endothelium)
Continued…….
Dysfunctional Endothelium
1.
2.
3.
4.
5.
6.
Stress of hypertension
Bacterial endotoxins
Turbulent flow over scarred valves
Hypercholesterolemia
Products absorbed from cigarette
smoke
Irradiation.
1. Abnormal Blood Flow
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Turbulence:
Arterial & cardiac thrombosis
 A cause of endothelial injury
 Also causes countercurrents and
local pockets of stasis
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Stasis:
Venous thrombi
 Acts by disturbing normal blood
flow
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Mechanism of Abnormal Blood
Flow
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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
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Ulcerative atherosclerotic plaques
Aortic & arterial aneurysms
MI
Mitral valve stenosis
Hyperviscosity syndrome
Sickle cell anemia
3. Hypercoagubility
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Important but less frequent
contributor
‘Any alteration of the coagulation
pathways that predisposes to
thrombosis’
Causes of Hypercoagubality
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PRIMARY (Genetic)
Common:
Mutation in factor V gene
Mutation in prothrombin gene
Rare:
Antithrombin III deficiency
Protein C def.
Protein S def.
Causes of Hypercoagubality
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Secondary (Acquired)
High Risk:
Prolonged bed rest
MI, Cancer, DIC
Atrial fibrillation
Tissue damage
Prosthetic cardiac valve
Antiphospholipid antibody syndrome
Causes of Hypercoagubality
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Secondary (Acquired)
Low Risk:
Cardiomyopathy
Nephrotic syndrome
Pregnancy, Oral contraceptives
Sickle cell anemia
Smoking
Types of Thrombi
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Types:
Arterial Thrombi
Venous Thrombi
Mural Thrombi
Red Thrombi (Stasis thrombi)
White Thrombi (Gray-white)
Morphology of Thrombi
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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
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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
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Propagation
Embolization
Dissolution
Organization and recanalization