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THROMBOSIS

THROMBOSIS. DEFINITION - PROCESS OF FORMATION OF SOLID MASS IN CIRCULATION FROM THE CONSTITUENTS OF FLOWING BLOOD THE MASS IS THROMBUS THE DANGER BEING- ISCHEMIC INJURY THROMBOEMBOLISM. VENOUS THROMBUS. DEEP VEIN THROMBUS. RUPTURED ATHEROSCLEROTIC PLAQUE WITH THROMBUS.

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THROMBOSIS

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  1. THROMBOSIS DEFINITION- PROCESS OF FORMATION OF SOLID MASS IN CIRCULATION FROM THE CONSTITUENTS OF FLOWING BLOOD • THE MASS IS THROMBUS • THE DANGER BEING- ISCHEMIC INJURY THROMBOEMBOLISM.

  2. VENOUS THROMBUS

  3. DEEP VEIN THROMBUS

  4. RUPTURED ATHEROSCLEROTIC PLAQUE WITH THROMBUS

  5. FRESH THROMBUS

  6. SADDLE THROMBUS

  7. ENDOTHELIAL DAMAGE

  8. THROMBUS IN A VESSEL

  9. PATHOPHYSIOLOGY OF THROMBUS VIRCHOW’S TRIAD- 1. ENDOTHELIAL INJURY 2. ALTERATION IN BLOOD FLOW 3. HYPERCOAGULABILITY OF THE BLOOD

  10. 1.ENDOTHELIUM • INTACT ENDOTHELIUM HAS FOLLOWING FUNCTIONS - 1.PROTECTS FLOWING BLOOD FROM THROMBOGENIC EFFECTS OF SUBENDOTHELIUM 2.ELABORATION OF ANTITHROMBOTIC FACTORS- A.HEPARIN LIKE SUBSTANCE WHICH ACCELERATES THE FUNCTION OF ANTITHROMBIN III & INACTIVATES SOME COAGULATION FACTORS.

  11. ENDOTHELIUM • B. THROMBOMODULIN –CONVERTS THROMBIN TO ACTIVATOR OF PROTEIN C,AN ANTICOAGULANT. • C. INHIBITORS OF PLATELET AGGREGATION SUCH AS ADPase,PGI 2 OR PROSTACYCLIN • D. PLASMINOGEN ACTIVATOR- FIBRINOLYTIC ACTIVITY

  12. ENDOTHELIUM 3. RELEASE PROTHROMBOTIC FACTORS LIKE A. THROMBOPLASTIN OR TISSUE FACTOR

  13. ENDOTHELIUM • B. von WILLEBRAND FACTOR-CAUSE ADHERENCE OF PLATELETS TO SUBENDOTHELIUM • C.PLATELET ACTIVATING FACTOR-ACTIVATOR & AGGREGATOR OF PLATELETS • D.INHIBITOR OF PLASMINOGEN ACTIVATOR THAT SUPPRESSES FIBRINOLYSIS

  14. ENDOTHELIAL INJURY • MAJOR CAUSE OF THROMBI OF HEART & ARTERIES IS ENDOTHELIAL INJURY • CLINICAL CONDITIONS WHERE ENDOTHELIAL INJURY IS SEEN A. MYOCARDIAL INFARCTION, B. MYOCARDITIS, C. CARDIAC SURGERY, D. PROSTHETIC VALVES

  15. CAUSES OF ENDOTHELIAL INJURY E. ULCERATED PLAQUES, F. HAEMODYNAMIC STRESS IN HYPERTENSION, G. ARTERIAL DISEASES, H. DIABETES MELLITUS,

  16. CAUSES OF ENDOTHELIAL INJURY I. ENDOGENOUS CHEMICAL AGENTS- HYPERCHOLESTEROLAEMIA, ENDOTOIXINS, J. EXOGENOUS CHEMICAL AGENTS-CIGARETTE SMOKE

  17. 2.PLATELETS PLAY A CENTRAL ROLE IN NORMAL HAEMOSTASIS ADHESION TO SUBENDOTHELIAL COLLAGEN Von WILLEBRANDS FACTOR IS REQUIRED FOR PLATELET ADHESION - PLATELET ACTIVATION- PLATELET RELEASE REACTION- GRANULES ARE RELEASED

  18. ROLE OF PLATELETS PLATELET AGGREGATION BY ADP FROM DENCE BODIES (PLATELET GRANULES) – TEMPORARY HAEMOSTATIC PLUG

  19. 3.COAGULATION SYSTEM 1. INTRINSIC PATHWAY- CONTACT WITH ABNORMAL SURFACE - ACTIVATION OF F-12 & SEQUENTIAL INTERACTIONS OF FACTORS XI, IX, VIII & FINALLY F- X

  20. 3.COAGULATION SYSTEM 2. IN THE EXTRINSIC PATHWAY - TISSUE DAMAGE-RELEASE OF TISSUE FACTOR OR THROMBOPLASTIN WHICH INTERACT WITH F – VII AND CALCIUM IONS – ACTIVATES FACTOR X

  21. COAGULATION SYSTEM 3. COMMON PATHWAY-BEGINS WHERE BOTH INTRINSIC & EXTRINSIC PATHWAYS CONVERGE TO ACTIVATE FACTOR X WHICH FORMS COMPLEX WITH F - Va & PLATELET FACTOR 3 IN THE PRESENCE OF CALCIUM IONS.

  22. COAGULATION SYSTEM • THIS COMPLEX ACTIVATES PROTHROMBIN (F-II) TO THROMBIN(F-IIa)

  23. REGULATORS OF COAGULATION SYSTEM • 1. PROTEASE INHIBITORS-ACT ON COAGULATION FACTORS & OPPOSE THE FORMATION OF THROMBIN - PROTEASE INHIBITORS ARE - ANTITHROMBIN III, PROTEIN C, C1 INACTIVATOR, α1-ANTITRYPSIN, α 2-MACROGLOBULIN

  24. REGULATORS OF COAGULATION SYSTEM 2. FIBRINOLYTIC SYSTEM- PLASMINOGENACTIVATOR CONVERTS PLASMINOGEN TO PLASMIN A FIBRINOLYTIC ENZYME RELEASING FIBRIN SPLIT PRODUCTS.

  25. 2.HYPERCOAGULABILITY OF THE BLOOD 1. NEPHROTIC SYNDROME 2. ADVANCED CANCER 3. EXTENSIVE TRAUMA,BURNS,PUERPERIUM.

  26. HYPERCOAGULABILITY OF THE BLOOD COAGULATION IS FAVOURED BY ADVANCED AGE,SMOKING,USE OF ORAL CONTRACEPTIVES & OBESITY.

  27. HYPERCOAGULABILITY OF THE BLOOD HYPERCOAGULABILITY MAY BE a . DUE TO INCREASE COAGULATION FACTORS, b. INCREASE IN PLATELET COUNT

  28. HYPERCOAGULABILITY OF THE BLOOD WITHINCREASE IN THEIR ADHESSIVENESS C. DECREASED LEVELS OF COAGULATION INHIBITORS SUCH AS ANTI -THROMBIN III,FIBRIN SPLIT PRODUCTS

  29. 3.ALTERATION OF BLOOD FLOW FORMATION OF ARTERIAL & CARDIAC THROMBI IS FACILITATED BY TURBULENCE IN BLOOD FLOW(NORMAL AXIAL FLOW IS DISTURBED) STASIS INITIATES THE VENOUS THROMBI EVEN WITHOUT ENDOTHELIAL INJURY.

  30. TYPES OF THROMBI AND THEIR MORPHOLOGY • THROMBI OCCUR IN HEART,ARTERIES,VEINS & CAPILLARIES • ARTERIAL THROMBI PRODUCE ISCHEMIA & INFARCTION • CARDIAC & VENOUS THROMBI CAUSE EMBOLISM.

  31. MORPHOLOGY OF THROMBI GROSS- VARIES IN SIZE,,SHAPE,COMPOSITION DEPENDING ON THE SITE OF ORIGIN

  32. MORPHOLOGY OF THROMBI ARTERIAL THROMBI ARE WHITE & MURAL, ARE FIRM & PALE • VENOUS THROMBI - RED & OCCLUSIVE, SOFT & GELATINOUS

  33. MORPHOLOGY OF THROMBI DEPENDS ON RATE OF FLOW OF BLOOD RAPID ARTERIAL & CARDIAC CIRCULATION- LINES OF ZAHN- ALTERNATE LAYERS OF LIGHT STAINING PLATELET AGGREGATES WITH FIBRIN & DARK STAINING LAYERS OF RED CELLS

  34. LINES OF ZAHN-

  35. LINES OF ZAHN-

  36. MORPHOLOGY OF THROMBI • SLOW MOVING FLOW IN VEINS- RED THROMBI- ABUNDANT RED CELLS, LEUCOCYTES & PLATELETS TRAPPED IN FIBRIN MESHWORK.

  37. VENOUS THROMBI

  38. RED THROBUS IN INFERIOR VENA CAVA

  39. THROMBUS IN A VESSEL

  40. RUPTURED ATHEROSCLEROTIC PLAQUE WITH THROMBUS

  41. ANTIMORTEM THROMBI & POSTMORTEM CLOTS • ANTIMORTEM THROMBI-GROSS- DRY,GRANULAR,FIRM,FRIABLE, ADHERENT TO VESSEL WALL,MAY OR MAY NOT FIT THEIR VASCULAR CONTOURS, LINES OF ZAHNS PRESENT

  42. ANTIMORTEM THROMBI & POSTMORTEM CLOTS • POSTMORTEM CLOT-GROSSLY GELATINOUS,SOFT, RUBBERY,NOT ATTACHED TO THE VESSEL WALL,TAKES THE SHAPE OF THE VESSEL WALL OR IT’S BIFURCATION, • THE SURFACE IS CHICKEN FAT YELLOW COVERING THE UNDERLYING RED CURRENT JELLY

  43. POSTMORTEM CLOT WITH CHICKEN FAT AND CURRENT JELLY APPEARANCE

  44. POSTMORTEM CLOT WITH CURRENT JELLY APPEARANCE

  45. FATE OF THROMBI 1.RESOLUTION- ACTIVATION OF FIBRINOLYTIC SYSTEM-RELEASE OF PLASMIN-DISSOLVE THE THROMBUS, PHAGOCYTES PHAGOCYTOSE THE THROMBUS , PROTEOLYTIC ENZYMES FROM LEUCOCYTES & ENDOTHELIUM DIGEST THE COAGULUM

  46. FATE OF THROMBI • 2.ORGANISATION - CAPILLARIES GROW, FIBROBLASTS GROW TO PRODUCE GRANULATION TISSUE- COLLAGENOUS TISSUE COVERED BY ENDOTHNELIUM- RECANALISATION HYALINISATION ,CALCIFICATION TO FORM PHLEBOLITHS.

  47. A THROMBOSIS OF A CORONARY ARTERY IS SHOWN HERE IN CROSS SECTION.

  48. RECANALISATION OF CORONARY ARTERY THROMBOSIS

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