Virchows Triad

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Hemostasis A) Primary Hemostasis = weak platelet plug 1. Vascular Damage 2. Transient vasoconstriction of damaged vessels (mediated by re exive neuronal stimulation + endothelin release Endothelins: *21-amino acid vasoconstricting peptides produced primarily in the endothelium *have a key role in vascular homeostasis. *are among the strongest vasoconstrictors known *endothelins are implicated in vascular diseases ex: heart, general circulation and brain 3. Platelet Adhesion: a. vWF binds exposed subendothelial collagen -vWF @ Weibel-Palade Bodies @ Endothelial Cells -vWF @ a-Granules of platelets b. Platelets bind vWF using GPIb Receptor 4. Platelet degranulation: adhesion induces shape change in platelets and degranulation of platelet mediators a. ADP is released from dense platelet granules: promotes exp[osure of GP2b/3a receptors on platelets b. TXA2 is synthesized by platelet COX1 (TXA2 promotes PLATELET AGGREGATION) 5. Platelet Aggregation a. Platelets cross link using GP2b/3a receptors and Fibrinogen from the plasma 6. This platelet plug is weak, the coagulaiton cascade stabilizes it B) Secondary Hemostasis =stabilized platelet plug, mediated by the Coagulation Cascade 1. Coagulation cascade generates Thrombin 2. Thrombin converts brinogen to brin, stabilizing the platelet plug #platelet- brin thrombus 3. Coagulation Cascade Activators Coagulation Cascade requires 1. Exposure to activating substances a. Extrinsic Pathway: exposure to Tissue Thromboplastin activates factor 7a b. Intrinsic Pathway: subendothelial collagen activates factor 12a 2. Phospholipids @ platelet surface 3. Calcium derived from platelet dense granules 1) Circulatory Stasis Varicose Veins Venous obstruction (Tumor, Pregnancy-fetus--X IVC) A-Fib: clots around valve LV-dysfunction 3) Hypercoagulative state Cancer Pregnancy: hormones (estrogen) Estrogen therapy: postmenopausal Estrogen therapy: The PILL --> clotting Trauma or Surgery of lower extremity Inamitory bowel disease Nephrotic syndrome: urinating antithrombin 3 Sepsis Inhereted THROMBOPHILLIA VIRCHOWS Triad (more than one is what causes problems) 2) Vascular wall injury Trauma or surgery Venepuncture Chemical irritation Heart valve replacment Athlersclerosis Indwelling catheters Hemodynamic Derangements DD wk2 Hemodynamic Derangements Introduction To Atherosclerosis Thrombosis And Embolization FLOW GRADIENT VASOCONSTRICTION BY VSM -SLOW BLOOD FLOW -SLOWS BLOOD LOSS -MOVES PLATELETS CLOSER TO ENDOTHELIAL SURFACE 1) Reexive vasoconstriction: sympathetic 2) platelet mediated vasconstriction Vasoactive substances dense granules NPE, 5HT ...

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Transcript of Virchows Triad

  • Hemostasis

    A) Primary Hemostasis = weak platelet plug1. Vascular Damage

    2. Transient vasoconstriction of damaged vessels(mediated by re exive neuronal stimulation + endothelin releaseEndothelins:

    *21-amino acid vasoconstricting peptides produced primarily in the endothelium *have a key role in vascular homeostasis. *are among the strongest vasoconstrictors known*endothelins are implicated in vascular diseases ex: heart, general circulation and brain

    3. Platelet Adhesion:a. vWF binds exposed subendothelial collagen

    -vWF @ Weibel-Palade Bodies @ Endothelial Cells-vWF @ a-Granules of platelets

    b. Platelets bind vWF using GPIb Receptor

    4. Platelet degranulation: adhesion induces shape change in platelets and degranulation of platelet mediatorsa. ADP is released from dense platelet granules: promotes exp[osure of GP2b/3a receptors on plateletsb. TXA2 is synthesized by platelet COX1

    (TXA2 promotes PLATELET AGGREGATION)

    5. Platelet Aggregationa. Platelets cross link using GP2b/3a receptors and Fibrinogen from the plasma

    6. This platelet plug is weak, the coagulaiton cascade stabilizes it

    B) Secondary Hemostasis =stabilized platelet plug, mediated by the Coagulation Cascade1. Coagulation cascade generates Thrombin

    2. Thrombin converts brinogen to brin, stabilizing the platelet plug#platelet- brin thrombus

    3. Coagulation Cascade ActivatorsCoagulation Cascade requires

    1. Exposure to activating substancesa. Extrinsic Pathway: exposure to Tissue Thromboplastin activates factor 7ab. Intrinsic Pathway: subendothelial collagen activates factor 12a

    2. Phospholipids @ platelet surface3. Calcium derived from platelet dense granules

    1) Circulatory Stasis Varicose Veins Venous obstruction (Tumor, Pregnancy-fetus--X IVC) A-Fib: clots around valve LV-dysfunction

    3) Hypercoagulative state Cancer Pregnancy: hormones (estrogen) Estrogen therapy: postmenopausal Estrogen therapy: The PILL --> clotting Trauma or Surgery of lower extremity In!amitory bowel disease Nephrotic syndrome: urinating antithrombin 3 Sepsis Inhereted THROMBOPHILLIA

    VIRCHOWS Triad(more than one is what causes problems)

    2) Vascular wall injury Trauma or surgery Venepuncture Chemical irritation Heart valve replacment Athlersclerosis Indwelling catheters

    Hemodynamic Derangements

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    DD wk2Hemodynamic DerangementsIntroduction To AtherosclerosisThrombosis And Embolization

    FLOW GRADIENT

    VASOCONSTRICTION BY VSM -SLOW BLOOD FLOW-SLOWS BLOOD LOSS-MOVES PLATELETS CLOSER TO ENDOTHELIAL SURFACE

    1) Re!exive vasoconstriction: sympathetic2) platelet mediated vasconstriction

    Vasoactive substances dense granulesNPE, 5HT ...