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THROMBOSIS

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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THROMBOSIS

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  1. THROMBOSIS Dr. Afsar Saeed Shaikh M.B.B.S, M.Phil. Assistant Professor of Chemical Pathology Pathology Department, KEMU, Lahore.

  2. INTRODUCTION • 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’

  3. 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.’

  4. INTRODUCTION • ETIOLOGY: • Endothelial Injury • Abnormal Blood Flow • Hypercoagubality

  5. Virchow Triad

  6. 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

  7. Endothelial Injury • Sites : • Within cardiac chamber (e.g. following M.I) • Over ulcerative atherosclerotic plaques • At the site of inflammatory or traumatic vascular injury

  8. 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…….

  9. Dysfunctional Endothelium • Stress of hypertension • Bacterial endotoxins • Turbulent flow over scarred valves • Hypercholesterolemia • Products absorbed from cigarette smoke • Irradiation.

  10. 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

  11. 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

  12. Clinical Settings of Abnormal Blood Flow • Ulcerative atherosclerotic plaques • Aortic & arterial aneurysms • MI • Mitral valve stenosis • Hyperviscosity syndrome • Sickle cell anemia

  13. 3. Hypercoagubility • Important but less frequent contributor • ‘Any alteration of the coagulation pathways that predisposes to thrombosis’

  14. 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.

  15. Causes of Hypercoagubality • Secondary (Acquired) • High Risk: Prolonged bed rest MI, Cancer, DIC Atrial fibrillation Tissue damage Prosthetic cardiac valve Antiphospholipid antibody syndrome

  16. Causes of Hypercoagubality • Secondary (Acquired) • Low Risk: Cardiomyopathy Nephrotic syndrome Pregnancy, Oral contraceptives Sickle cell anemia Smoking

  17. Types of Thrombi • Types: • Arterial Thrombi • Venous Thrombi • Mural Thrombi • Red Thrombi (Stasis thrombi) • White Thrombi (Gray-white)

  18. 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

  19. 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

  20. THANK YOU!

  21. Fate of Thrombi • Propagation • Embolization • Dissolution • Organization and recanalization

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