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Thrombosis

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a haemodynamic disorder which has serious consequences. useful for pathology students and health-concerned people.

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Thrombosis

  1. 1. DEFINITION  THROMBOSIS is the formation of a clotted mass of blood within the cardiovascular system.  The clotted mass is called as THROMBUS. THROMBUS BLOOD CLOT 1- Involves wall of blood vessels, formed elements of blood & blood clotting system. 1- Involves only blood clotting system. 2- composed of platelets and fibrin. 2- composed of fibrin only. 3- may be life-threatening. 3- mostly life saving.
  2. 2. THROMBUS – GROSS PATHOLOGY
  3. 3. THROMBUS – MICROSCOPIC PATHOLOGY
  4. 4. Antithrombotic & prothrombotic property of endothelial cells
  5. 5. AETIOLOGY:-
  6. 6. 1- Endothelial injury :-  Trauma  Bacteria- Toxins by Erysipelothrix, Streptococcus, Staphylococcus, Coryanobacterium  Virus- Hog cholera virus thrombosis in spleen  Parasites- Strongylus vulgaris in anterior mesenteric artery of horse  Tumours invading endothelium Normal endothelium is thromboresistant, but when injured the highly thrombogenic subendothelium is exposed and promotes adhesion of fibrin and platelets.
  7. 7. 2- Abnormal bloodflow:-  RBC , WBC – Heavier axial stream Platelets – Lighter plasmatic / laminar stream  When blood flow slows down, platelets beingd the outermost in the blood stream, fall out to the periphery and stick to endothelium by virtue of their adhesive property.  Cause of slow bloodflow – Stasis and turbulence 1- chronic venous congestion 2- aged and debilitated animals 3- vericose vein- nasal submucosa in cattle, scrotal plexus of horse, large veins of broad ligament of bovine uterus 4- congestive heart failure
  8. 8. 3- Hypercoagulability :-  Increase in level of fibrinogen, prothrombin, factor VIIa, VIIIa, Xa  Increse in number of platelets  Decrease in levels of antithrombin III, protein C and fibrinolysin Hepatic disease - formation of prothrombin Bile deficiency in intestine - less absorption of Vit-K
  9. 9. Pathogenesis :-  Endothelial injury – platelets adhere to subendothelial collagen  Platelets secretes ADP and thromboxane A2  Plateles expose phospholipid complex – activates intrinsic coagulation pathway  Tissue factor from injured endothelium – activates extrinsic coagulation pathway  ADP – reversible primary hemostatic plug ADP, thrombin, TXA2 – irreversible secondary plug  Fibrin deposition around platelets
  10. 10. Classification :- (A) According to location-  1-Cardiac thrombus Valvular thrombus- in valves – Erysipelothrix infection in pig Mural thrombus – in wall of heart – Clostridium infection in cattle  2- Arterial thrombus - Strongylus vulgaris in anterior mesenteric artery of horse  3- Venous thrombus – more common in human  4- Capillary thrombus  5- Lymphatic thrombus
  11. 11. VALVULAR THROMBUS MURAL THROMBUS
  12. 12.  (B) According to location within the blood vessel :-  Lateral thrombus – one side of BV  Occluding thrombus – entire circumference of BV  Saddle thrombus – at bifurcation of BV  Canalised thrombus – new blood channels through the clot  (C) According to infective agent :-  Septic thrombus – contains bacteria  Parasitic thrombus – contains parasites  Aseptic thrombus – no bacteria or parasites  (D) According to colour :-  Pale or white thrombus – in rapid blood flow, only platelets  Red thrombus – in slow blood flow, fibrin attach to platelets  Mixed thrombus – most common  Laminated thrombus – alternate layers of white and red
  13. 13. WHITE AND RED THROMBI
  14. 14. Fate of thrombus :-  Propagation  Emboli formation – foreign body floating in the blood  Abcessation – when pyogenic bacteria present  Dissolution – by fibrinolytic activity  Organisation and recanalisation  Calcification
  15. 15. Effects:-  Negligible effect in vessels which are not required or where sufficient colateral circulation is present or in large vessels  Passive congestion and edema – as obstruction in venous return  Infarction – Thrombosis in end arteries lead to ischemic necrosis  Gangrene of limbs and intestine  Interference with cardiac function  Colic  Lameness  Septicemia or pyemia  Sudden death in coronary artery thrombosis
  16. 16. Rudolf Virchow

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