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5. thrombosis; hemodynamic disorders

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5. thrombosis; hemodynamic disorders

  1. 1. Hemodynamic Disorders Hemodynamic Disorders  Edema  Edema  Hyperemia and Congestion  Hyperemia and Congestion  Hemorrhage  Hemorrhage  Hemostasis and Thrombosis  Hemostasis and Thrombosis  Embolism  Embolism  Infarction  Infarction  Shock  Shock 1 Dr. Krishna Tadepalli, MD, www.mletips.com
  2. 2. THROMBOSIS -Virchow triad 2 Dr. Krishna Tadepalli, MD, www.mletips.com
  3. 3. Thrombosis Thrombosis  Clot in an inappropriate site ––uninjured blood vessel  Clot in an inappropriate site uninjured blood vessel  DIC (Disseminated Intravascular coagulation)- multiple fibrin  DIC (Disseminated Intravascular coagulation)- multiple fibrin thrombi thrombi  Pathogenesis = Virchow’s triad  Pathogenesis = Virchow’s triad  1. Endothelial injury  loss of balance between Pro & Anti  1. Endothelial injury  loss of balance between Pro & Anti thrombotic effects of EC towards Pro; ↑Hemodynamic stresses ((HTN, thrombotic effects of EC towards Pro; ↑Hemodynamic stresses HTN, Turbulent blood flow); other damaging factors (Homocystinuria, Turbulent blood flow); other damaging factors (Homocystinuria, ↑Cholesterol, smoking) ↑Cholesterol, smoking)  2. Blood flow alterations  Turbulence (leads to EC injury, Stasis;  2. Blood flow alterations  Turbulence (leads to EC injury, Stasis; Turbulence & Stasis lead to  Platelet activation, Clotting factor Turbulence & Stasis lead to  Platelet activation, Clotting factor activation and accumulation, ↓inflow of clotting factor inhibitors, pts. activation and accumulation, ↓inflow of clotting factor inhibitors, pts. with AS, Aneurysms, Sickle cell, Hyper viscosity syndromes with AS, Aneurysms, Sickle cell, Hyper viscosity syndromes  3. Hypercoagulabulity  can be primary (genetic) or secondary  3. Hypercoagulabulity  can be primary (genetic) or secondary (acquired) (acquired) 3 Dr. Krishna Tadepalli, MD, www.mletips.com
  4. 4.  Hypercoagulabulity  Hypercoagulabulity  1. Primary  suspect in aapatient <50 yr old with  1. Primary  suspect in patient <50 yr old with recurrent thrombi in the absence of acquired risk factors recurrent thrombi in the absence of acquired risk factors  A). Most common ones  Mutations (point) in  A). Most common ones  Mutations (point) in Factor V & Factor II ((Prothrombin) Genes; lead to Factor V & Factor II Prothrombin) Genes; lead to venous thrombi (DVT), venous thrombi (DVT),  B). Rare ones Homocystinuria ((cause ↓Anti B). Rare ones Homocystinuria cause ↓Anti- thrombin III & Endothelial Thombomodulin  lead to thrombin III & Endothelial Thombomodulin  lead to Arterial & Venous thrombi, Atherosclerosis) Arterial & Venous thrombi, Atherosclerosis) 4 Dr. Krishna Tadepalli, MD, www.mletips.com
  5. 5.  Hypercoagulabulity  Hypercoagulabulity  22.Secondary  Drugs, Autoimmune diseases  . Secondary  Drugs, Autoimmune diseases  A). Heparin induced Thrombocytopenia  in 5% of users of un A). Heparin induced Thrombocytopenia  in 5% of users of un- fractionated (High Molecular weight) heparin, produce anti –platelet factor fractionated (High Molecular weight) heparin, produce anti –platelet factor 44antibodies, also cause platelet dysfunction (bleeding), replaced by low antibodies, also cause platelet dysfunction (bleeding), replaced by low molecular weight heparin molecular weight heparin  B). Anti-Phospholipid Antibody syndrome  can be Primary  B). Anti-Phospholipid Antibody syndrome  can be Primary (without underlying cause) or Secondary ((SLE, Drugs, infections) (without underlying cause) or Secondary SLE, Drugs, infections)  Cause  Anti body against Phospholipid (cardiolipin) or epitopes of  Cause  Anti body against Phospholipid (cardiolipin) or epitopes of Prothrombin Prothrombin  In vitro ––Ab inhibits clot formation but in Vivo, promotes clotting.  In vitro Ab inhibits clot formation but in Vivo, promotes clotting.  False positive test with syphilis antigens ((cardiolipin)  False positive test with syphilis antigens cardiolipin)  Mechanism  inhibit PGI2, Platelet activation, interfere with Protein  Mechanism  inhibit PGI2, Platelet activation, interfere with Protein C activity C activity  Clinical  in aaclassic case, female with recurrent miscarriages,  Clinical  in classic case, female with recurrent miscarriages, recurrent arterial & venous thrombi, cardiac vegetations (Libman -recurrent arterial & venous thrombi, cardiac vegetations (Libman Sack’s), Thrombocytopenia Sack’s), Thrombocytopenia  Rx  Anticoagulants in early stages, Immunosuppressant in advanced  Rx  Anticoagulants in early stages, Immunosuppressant in advanced 5 Dr. Krishna Tadepalli, MD, www.mletips.com
  6. 6. Thrombus - Morphology Arterial Arterial  Almost always arise from  Almost always arise from heart heart  Grow in retrograde  Grow in retrograde fashion (direction of fashion (direction of flow) flow)  Forms at site of  Forms at site of Endothelial injury (AS), Endothelial injury (AS), turbulence (aneurysms) turbulence (aneurysms)  Pale/ white  Pale/ white  Lines of Zahn  Lines of Zahn  Firmly adherent to vessel  Firmly adherent to vessel wall wall  From emboli  Cause  From emboli  Cause infarctions (lower infarctions (lower extremities ––75%, Brain, extremities 75%, Brain, Kidney, spleen) Kidney, spleen) Venous Venous • Deep veins (popleteal  • Deep veins (popleteal  Femoral Iliac), Femoral Iliac), • Antigrade (towards heart• Antigrade (towards heartdirection of flow) direction of flow) • At site of stasis (lower • At site of stasis (lower extremities) extremities) • • • • • • Red //dark Red dark No lines of Zahn No lines of Zahn Loosely attached (easily Loosely attached (easily embolize) embolize) • Emboli cause Pulmonary • Emboli cause Pulmonary embolism ((silent in 50% embolism silent in 50% of pts.) of pts.) 6 Dr. Krishna Tadepalli, MD, www.mletips.com
  7. 7.  ? Arterial or venous thrombus  ? Arterial or venous thrombus 7 Dr. Krishna Tadepalli, MD, www.mletips.com
  8. 8. Thrombus - Morphology • Venous • Venous • Loosely attached • Loosely attached (easily embolize) (easily embolize) • Red/ dark • Red/ dark • Post mortem clot • Post mortem clot • Not attached • Not attached • Chicken fat • Chicken fat supernatant supernatant 8 Dr. Krishna Tadepalli, MD, www.mletips.com
  9. 9.  Thrombi on heart valves --Vegetations  Thrombi on heart valves Vegetations  1. Infective acute ((staph. aureus), sub acute ((strep.  1. Infective acute staph. aureus), sub acute strep. viridians), cause infective Endocarditis (IE) viridians), cause infective Endocarditis (IE)  2. Sterile   2. Sterile   A). Autoimmune ––pts. With SLE ––Libman sack’s  A). Autoimmune pts. With SLE Libman sack’s ((unique with vegetations on both Atrial & Ventricular unique with vegetations on both Atrial & Ventricular surfaces of valve) surfaces of valve)  B). Others  cancers, hypercoagulable states etc.,  B). Others  cancers, hypercoagulable states etc.,  Thrombi – Clinical features (by occlusion or  Thrombi – Clinical features (by occlusion or embolization) embolization)  Arterial – infarctions ((also called gangrene in lower limbs),  Arterial – infarctions also called gangrene in lower limbs),  Venous- DVT  PE  Venous- DVT  PE  Thrombi – Clinical course  Thrombi – Clinical course  Fresh or recent propagation, embolization, resolution  Fresh or recent propagation, embolization, resolution  Old  organization (inflammation, Fibrosis), Re  Old  organization (inflammation, Fibrosis), Re -canalization -canalization 9 Dr. Krishna Tadepalli, MD, www.mletips.com
  10. 10. Thrombi – Clinical course 10 Dr. Krishna Tadepalli, MD, www.mletips.com
  11. 11. Thrombus Arterial Venous 11 Dr. Krishna Tadepalli, MD, www.mletips.com
  12. 12. Organization & Recanalization H&E-stained section Stain for elastic tissue 12 Dr. Krishna Tadepalli, MD, www.mletips.com

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