Thrombosis - Pathology by Dr.Pawan

A Presentation on Thrombosis - Pathology point of view
Based on Harshmohan and Robbins - Textbook of Pathology

1. GOOD AFTERNOON

2. THROMBOSIS By , Pawan Kumar B

3. Thrombi may be life threatening by

4. PATHOPHYSIOLOGY

5. Virchows triad OTHER PROCESSES

6. Endothelium Antithrombotic factors Antiplatelet Adenosine diphosphatase (  ADP) Prostacyclin and nitric oxide (also vasodilatation) Anticoagulant Heparin-like molecules (activate antithrombin III) Thrombomodulin (activates protein C) Protein S synthesis Fibrinolytic t-PA Procoagulant factors Production of vWF Production of tissue factor Binding of factors IXa & Xa .

7. Vascular Injury Collagen, fibronectin, Elastin To reduce Blood Loss

8. Predisposing factors

9. Role of platelets

10. Contd…

11. Contd… The formation of definitive secondary plug requires activation of thrombin to cleave fibrinogen and form polymerized fibrin via the coagulation cascade .

12. ROLE OF COAGULATION SYSTEM

13. Act on clotting factors to oppose formation of thrombin. e.g.antithrombin III, Protein C , C1 inactivator. Regulation of coagulation factor Protease inhibitors

14. Fibrinolytic System

15. ALTERATIONS OF BLOOD FLOW Central stream (leucocytes & red cells) platelets Peripheral stream ( cell-free plasma zone ) Normal axial flow Margination & Pavementing

16. Turbulence (unequal flow ) Stasis (slowing)

17. HYPERCOAGUBILITY OF BLOOD

18. Hypercoagulable states secondary (acquired) factors RISK FACTORS

19. secondary (acquired) factors Clinical conditions

20. Hypercoagubility may occur by

21. Morphology of a thrombus GROSS

22. MICROSCOPY

23. ORIGIN OF THROMBI CARDIAC THROMBI

24. Feature Arterial thrombi Venous thrombi Blood flow Formed in rapidly flowing blood of arteries & heart Slow moving blood in veins Sites Common in aorta ,coronary, cerebral, iliac, femoral, renal & mesenteric arteries. Common in superficial varicose veins, deep leg veins, popliteal, femoral & iliac veins Thrombogenesis Formed following endothelial cell injury . e.g. in atherosclerosis Formed following venous stasis e.g. in abdominal operations, child-birth VASCULAR THROMBI

25. Feature Arterial Thrombi Venous Thrombi Development Usually mural, not occluding the lumen completely, may propagate Usually occlusive, take the cast of vessel in which formed, may propagate in both directions Macroscopy Grey-white, friable with lines of Zahn on surface. Red-blue with fibrin strands & lines of Zahn . Microscopy Distinct lines o f Zahn composed of platelets, with entangled red and white blood cells Lines of Zahn with more abundant red cells. Effects Ischemia leading to infarcts . e.g. in heart brain etc Thromboemboilsm, oedema, skin ulcers, poor wound hearing

26. Occlusive thrombus Alternating layers of platelets and fibrin red blood cells ARTERIAL THROMBI

27. VENOUS THROMBI

28. CAPILLARY THROMBI Minute thrombi composed mainly composed of packed red cells are formed in capillaries in acute inflammatory lesions, vasculitis, DIC.

29. Thrombosis

30. RESOLUTION Fibrinolytic activity can be accentuated by administration of thrombolytic substances. (e.g. urokinase, streptokinase) .

31. ORGANISATION

32. Large cardiac thrombi : Sudden death by mechanical obstruction of blood flow or Thromboembolism. Arterial thrombi : Ischemic necrosis may lead to gangrene. Coronary artery thrombosis may lead to sudden death. Capillary thrombi : DIC. Clinical effects

33. Venous thrombi (Phlebothrombosis)

34. THANK YOU… 