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