Dec 31, 2015
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