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Thrombosis - Pathology by Dr.Pawan
The document discusses thrombosis, including the process of thrombus formation, types of blood clots, and associated pathophysiological mechanisms like Virchow's triad. It describes the roles of platelets and the coagulation system in hemostasis and thrombus formation, along with various predisposing and risk factors, such as endothelial injury and hypercoagulability. Additionally, it covers the morphology, effects, and potential fates of thrombi, along with the clinical implications of venous and arterial thrombi.
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Thrombosis - Pathology by Dr.Pawan
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- 3. Process of formationof solid mass in circulation from the constituents of flowing blood. The mass is called as THROMBUS.
- 4. Bloodclot • Mass of coagulated blood formedin vitro. • E.g. in a test tube. Hematoma • Extra vascular accumulation of blood clot. • E.g. into the tissues. Haemostaticplugs • blood clot formed in healthy individual at the site of bleeding. • E.g. in injury to blood vessel.
- 5. Ischemic injury Thromboembolism. Thrombi maybe life threatening by
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- 7. Virchows triad Endothelial injury Abnormalblood flow Hypercoagulability. OTHER PROCESSES Activation of platelets Activation of clotting system
- 8. 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.
- 9. Vascular Injury Major significancein formation of arterial, cardiac thrombi. Exposes sub endothelial connective tissue. Vasoconstriction of small blood vessels. Collagen, fibronectin, Elastin To reduce Blood Loss
- 10. Predisposing factors Endothelial injuryin MI , myocarditis , Cardiac Surgery. Ulcerated plaques in advanced atherosclerosis. Arterial diseases. D.M. Chemical agents Endogenous : Endotoxins , hypercholesterolemia Exogenous : Cigarette smoke
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- 13. Exposes the underlyingbasement membrane ECM Platelets adhere to the ECM via vWF through Gp1B receptors Platelets provide a phospholipids surface for coagulation Activation of platelet cause degranulation , secretes calcium that activates coagulation proteins ADP which mediates further platelet aggregation TXA2 which increases platelet activation and cause vasoconstriction.
- 14. Contd… ADP primary haemostatic plugby activating Gp IIb - IIIa receptors fibrinogen binding and cross linking. The formation of definitive secondary plug requires activation of thrombin to cleave fibrinogen and form polymerized fibrin via the coagulation cascade.
- 15. ROLE OF COAGULATION SYSTEM Conversionof plasma fibrinogen into solid mass of fibrin. Both haemostatic & thrombus formation. Cascade of 3 pathways.
- 17. Act onclotting factors to oppose formation of thrombin. e.g.antithrombin III, Protein C , C1 inactivator. Regulation of coagulation factor Protease inhibitors
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- 19. ALTERATIONS OF BLOODFLOW Central stream (leucocytes & red cells) platelets Peripheral stream (cell-free plasma zone) Normal axial flow Margination & Pavementing
- 20. Turbulence (unequal flow) Stasis(slowing)
- 21. HYPERCOAGUBILITY OF BLOOD primary(genetic) factors Common • Factor V mutation (factor V Leiden) • Prothrombin mutation • 5,10-Methylenetetrahydrofolate reductase • Increased levels of factors VIII, IX, XI, or fibrinogen Rare • Antithrombin III deficiency • Protein C & S deficiency.
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- 23. MI, CHF, Cardiomyopathy Atherosclerosis,Aneurysms. Nephrotic syndrome, Polycythaemia. Hyper estrogenic states (pregnancy and postpartum) Oral contraceptive use Tissue injury (surgery, fracture, burn) Sickle cell anemia shock secondary (acquired) factors Clinical conditions
- 24. Hypercoagubility may occurby coagulation factors e.g. fibrinogen, Prothrombin platelet count & adhesiveness. coagulation inhibitors e.g. Antithrombin III, fs products.
- 25. Morphology of athrombus GROSS
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- 27. ORIGIN OF THROMBI Commonin atrial appendages (right atrium, mitral, aortic valves) – Infective Endocarditis Mural & Non-Occlusive. Ball-valve thrombus : large round thrombus obstructing mitral valve Agonal thrombi – shortly before death – occur either or both ventricles. CARDIAC THROMBI
- 28. Feature Arterialthrombi Venousthrombi Bloodflow 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
- 29. Feature ArterialThrombi VenousThrombi Developmen t Usuallymural, 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 of 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
- 30. Occlusive thrombus Alternating layersof a) platelets and fibrin b) red blood cells ARTERIAL THROMBI
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- 32. CAPILLARY THROMBI Minute thrombicomposed mainly composed of packed red cells are formed in capillaries in acute inflammatory lesions, vasculitis, DIC.
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- 34. thrombus Fibrinolytic system Release of plasmin Dissolve & resolution. RESOLUTION Fibrinolyticactivity can be accentuated by administration of thrombolytic substances. (e.g. urokinase, streptokinase) .
- 35. ORGANISATION Phagocytic cells appear.Phagocytose fibrin & cell debris. Proteolytic enzymes liberated leukocytes and endothelial cells, digests coagulum. Capillaries grow into thrombus & fibroblasts invade thrombus. Fibro vascular granulation tissue formed , dense & less vascular covered over by endothelial cells. Recanalisation occurs.
- 38. Large cardiacthrombi : 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
- 39. Venous thrombi(Phlebothrombosis) Thromboembolism Oedema Poor wound healing Skin ulcer Painful thrombosed veins (Thrombophlebitis) Painful white leg (phlegma alba dolens)
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