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5. thrombosis and embolism Slide 1 5. thrombosis and embolism Slide 2 5. thrombosis and embolism Slide 3 5. thrombosis and embolism Slide 4 5. thrombosis and embolism Slide 5 5. thrombosis and embolism Slide 6 5. thrombosis and embolism Slide 7 5. thrombosis and embolism Slide 8 5. thrombosis and embolism Slide 9 5. thrombosis and embolism Slide 10 5. thrombosis and embolism Slide 11 5. thrombosis and embolism Slide 12 5. thrombosis and embolism Slide 13 5. thrombosis and embolism Slide 14 5. thrombosis and embolism Slide 15 5. thrombosis and embolism Slide 16 5. thrombosis and embolism Slide 17 5. thrombosis and embolism Slide 18 5. thrombosis and embolism Slide 19 5. thrombosis and embolism Slide 20 5. thrombosis and embolism Slide 21 5. thrombosis and embolism Slide 22 5. thrombosis and embolism Slide 23 5. thrombosis and embolism Slide 24 5. thrombosis and embolism Slide 25 5. thrombosis and embolism Slide 26 5. thrombosis and embolism Slide 27 5. thrombosis and embolism Slide 28 5. thrombosis and embolism Slide 29 5. thrombosis and embolism Slide 30
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superficial introduction to the topic for bachelor level

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5. thrombosis and embolism

  1. 1. Thrombosis And Embolism Dr. Saugat Chapagain
  2. 2. Thrombosis
  3. 3.  Thrombus a solid mass consisting of blood constituents within the blood vessel; attached to the point of origin.  Thrombosis  the process of…  Clot  mass of coagulated blood  Haematoma  extravascular accumulation of blood clot  Haemostatic plugs  normal clots to control bleeding Thrombus and Thrombosis
  4. 4.  Virchow’s Triad  Endothelial injury  Altered blood flow (stasis/ turbulence)  Hypercoagulability of blood Pathophysiology
  5. 5. Coagulation cascade
  6. 6.  Vascular injury exposes subendothelial thrombogenic connective tissues (collagen, elastin, fibronectin, laminin and glycosaminoglycans)  Initial vasoconstriction to reduce blood loss.  Tissue factors initiate extrinsic pathway  Collagen initiate intrinsic pathway. Endothelial injury
  7. 7.  Ulcerated plaque in advanced atherosclerosis.  Haemodynamic stress in HTN  Arterial diseases  Diabetes mellitus  Endogenous chemical agents (hypercholesterolemia)  Exogenous chemical agents (smoking)  TAO  Bacterial toxins  Trauma  IV cannulation  Radiation injury  Turbulent flow of blood in aneurysm  Mural thrombus following cardiac abnormality Causes of endothelial injury
  8. 8.  Turbulence: unequal flow (arterial); may aggravate vascular injury as well.  Stasis: slowing (venous)  Blood cells and platelets migrate to periphery and pavement the endothelium  Normal flow has:  Central fast moving red and white blood cells.  Slow moving laminar stream of platelets.  Peripheral slowest moving cell-free plasma. Alteration of blood flow
  9. 9. Effects:  Prevent dilution by fresh flowing blood of activated clotting factors.  Disrupt laminar blood flow and bring platelets in contact of endothelium  Retard the inflow of clotting factor inhibitors and permit thrombosis  Promote endothelial cell activation Examples:  DVT of lower limbs  Mural thrombus  Thrombosis in aneurism
  10. 10. Favoured by:  Smoking  Ageing  Use of OCPs  Obesity Causes:  Increased coagulation factors  Increased platelet count and adhesiveness  Decreased levels of coagulation inhibitors Hypercoagulability
  11. 11. Primary (genetic)  Deficiency of anti thrombin  Deficiency of protein C or S  Defects in fibrinolysis  Mutation of factor V Secondary (acquired)  Risk factors:  Advanced age  Sedentary life style  Immobilization  Smoking  Clinical conditions leading to thrombosis:  Heart diseases (MI, CHF, RHD)  Vascular diseases (atherosclerosis, aneurysms, varicosities)  Hypercoagulibility (polycythemia, dehydration, nephrotic syndrome)  Shock  Late pregnancy and puerperium  drugs Factors favoring thrombosis
  12. 12.  Gross:  Shape and size depends on origin  Arterial  white and mural (firm and pale)  Venous  red and occlusive(soft, red and gelatinous)  Mixed/ laminated – alt white and red layers separated by line of ZAHN.  Microscopic:  Lines of Zahn seen where visible  Collection of cells and fibrin Morphology
  13. 13. Based on colour and components:  Pale – primarily platelets  Red – primarily RBCs  Mixed – visible lines of zahn Based on site and mode of formation:  Occlusive  Mural – occurs in heart chambers/ aorta/ major arteries Based on infection:  Bland – non infected  Septic – infected. Types
  14. 14.  Resolution – plasmin may dissolve the thrombus completely  Organization – eventually covered by endothelial cells after granulation tissue formation (or calcification/ ossification)  Propagation – enlargement of size may block important vessels.  Thromboembolism – detachment and released into blood stream Fate of thrombus
  15. 15. Embolism
  16. 16.  The process of partial or complete obstruction of some part of the CVS by any mass carried in the circulation.  Commonly thromboembolism (90%) What is it?
  17. 17.  Depending on matter of embolus  Solid- thrombus, atheroma, malignant cell, parasites, foreign bodies.  Liquid- fat globules, amniotic fluid, bone marrow  Gasseous- air, other gasses  Depending on infection:  Bland  Septic  Depending on source of emboli:  Cardiac emboli from left side of the heart – vegetations of endocarditis, atrial appendages  Arterial – in systemic arteries of brain, spleen, kidney and intestine.  Venous – in pulmonary arteries  Lymphatic emboli TYPE
  18. 18.  A detached thrombus or a part of thrombus.  Site of lodgement:  Arterial (systemic)  Venous  Pulmonary THROMBOEMBOLISM
  19. 19.  Most common and fatal form.  Occlusion of the pulmonary arterial tree.  Pulmonary thrombosis (rare) ETIOLOGY  More common in bed ridden patients. Causes:  Thrombi originating from large veins of lower legs (popliteal, femoral and iliac)  Less common sources ( varicosities of superficial veins, pelvic veins) PULMONARY THROMBOEMBOLISM
  20. 20. Detachment of thrombus  thromboembolism  drains into right atrium.  Large thrombus is impacted at the bifurcation of main pulmonary artery (saddle embolus) or on RV or its outflow tract.  If large embolus fragments  small embolus impacts in a number of vessels (esp. on lower lobes of lungs)  Paradoxical embolism – passage of embolus from rt. heart to lt. heart via ASD or VSD. Pathogenesis
  21. 21.  Sudden death – d/t massive pulm. Embolism.  Acute cor pulmonale – RHF d/t pulmonary HTN  Pulm. Infarction – obstruction of small pulm. arteries.  Pulm. Haemorrhage – central pulm. Haemorrhage d/t obstruction of flow in endarteries.  Resolution – 60-80 % by fibrinolysis.  Pulm. HTN, chronic cor-pulmonale and pulm. Atreriosclerosis. Consequences
  22. 22.  Arterial embolism  Esp. originating in LV (MI, cardiomyopathy, RHD, congenital heart disease, IE, prosthetic valves) Site of origin:  Heart (80%)  Aorta – thrombi over ulcerated atheroma in aortic aneurysm  Paradoxical – rt.  lt. in ASD or VSD  Idiopathic – 10-15% Systemic thromboembolism
  23. 23.  Infarction – kidney, spleen, mesentery  Stroke – brain (10%)  Upper and lower extremeties- peripheral vascular diseases, gangrene, etc. Effects
  24. 24.  Embolism of fat globules.  Obstruction by fragments of adipose tissue  fat tissue embolism. Etiology  Traumatic –  Trauma to bones, trauma to soft tissue  Non traumatic –  Burns, DM, fatty liver, pancreatitis, decompression sickness. Fat embolism
  25. 25.  Mechanical obstruction – micro aggregates of fat causes obstruction of vessels.  Chemmical injury – FFA causes toxic injury.  Thrombocytopenia – d/t coating of fat globules with platelets. Consequences  Pulmonary fat embolism  Systemic fat embolism (in case of ASD/ VSD) Pathogenesis
  26. 26.  Air, nitrogen and other gases,  Air embolism – entry of air due to trauma, injury or surgery.  Decompression sickness/ caisson’s disease, diver’s palsy or aeroembolism seen in deep sea divers. Causes:  During delivery or abortion  Acquired/ accidental pneumothorax  Haemodialysis  Accidental opening of large veins  Angiography  Cardiothoracic surgery / trauma Gas Embolism
  27. 27.  Most serious, unpredictable and unpreventable cause of maternal mortality.  Amniotic fluid may contain – epithelial squames, vernix caseosa, lanugo hair, bile from meconium and mucus s/s  Sudden respiratory distress and dyspnoea  Deep cyanosis  CV shock  Convulsions  Coma  Unexpected death Amniotic fluid embolism
  28. 28.  Mechanical blockage of pulmonary circulation in extensive embolism  Anaphylactic reaction to components  DIC d/t liberation of thromboplastin  Haemorrhagic manifestations d/t thrombocytopenia and afibrinogenaemia. Cause of death
  29. 29. Thank you
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superficial introduction to the topic for bachelor level

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