Coagula§£o Intravascular Disseminada

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  • Coagulao Intravascular Disseminada

    Verso Original:Keith Lewis, MDVerso Portuguesa:Alzira Sarmento, MDPaula Rocha, MDUCINP do Hospital Maria Pia,Porto - Portugal

    1uci@hmariapia.min-saude.pt

  • CIDSndrome adquirido caracterizado por coagulao intravascular generalizada.A coagulao sempre o evento inicial.A morbilidade e mortalidade relacionam-se com a extenso da trombose intravascular.Causas mltiplas

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    Trombose

    Fibrina

    Glbulos rubros

    Plaquetas

    Thrombi can occlude blood vessels and interfere with normal blood supply to various parts of the body. Consequences of thrombosis and embolization include:

    Myocardial infarction Stroke

    Deep vein thrombosis Pulmonary embolus

    In this scanning electron photomicrograph, the fibrin "mesh" of cross-linked fibrin monomers can be seen as a white stringlike substance trapping red blood cells in a fresh clot.The red cells are not sticking together; they are being held together by fibrin. Much the same process occurs early in clot development, when platelet aggregates are held together by fibrinogen, which stabilizes the first hemostatic plug.

    Up to this point in the program, the discussion has been about the hemostatic mechanism. Merely looking at the blood clot in this photograph, it isn't possible to tell if it's a hemostatic "plug" or a thrombus.

    Normally, coagulation occurs in response to injury and serves a protective purpose. However, when the thrombogenic factors predominate, intravascular thrombosis may occur. Thrombi may form in any part of the vascular system, including veins, arteries, the heart, and the microcirculation. The complications of thrombosis are caused either by the effects of local obstruction or distant obstruction from the embolization of thrombotic material.

    A clot, or fragment of a clot, which becomes dislodged from its site of origin is known as an embolus. Emboli generally do not stop flowing until they come to a narrow point in the circulatory system. Thus emboli originating in large arteries or in the left side of the heart eventually plug smaller arteries or arterioles while emboli originating in the venous system or in the right side of the heart flow into the vessels of the lung.

    Colman RW, Hirsh J, Marder VJ, Salzman EW. Overview of hemostasis. In: Colman RW, Hirsh J, Marder VJ, Salzman EW, eds. Hemostasis and thrombosis, 3rd ed. Philadelphia: J.B. Lippincott, 1994 pp 6,13,14.

    Thrombi can occlude blood vessels and interfere with normal blood supply to various parts of the body. Consequences of thrombosis and embolization include:

    Myocardial infarction Stroke

    Deep vein thrombosis Pulmonary embolus

    In this scanning electron photomicrograph, the fibrin "mesh" of cross-linked fibrin monomers can be seen as a white stringlike substance trapping red blood cells in a fresh clot.The red cells are not sticking together; they are being held together by fibrin. Much the same process occurs early in clot development, when platelet aggregates are held together by fibrinogen, which stabilizes the first hemostatic plug.

    Up to this point in the program, the discussion has been about the hemostatic mechanism. Merely looking at the blood clot in this photograph, it isn't possible to tell if it's a hemostatic "plug" or a thrombus.

    Normally, coagulation occurs in response to injury and serves a protective purpose. However, when the thrombogenic factors predominate, intravascular thrombosis may occur. Thrombi may form in any part of the vascular system, including veins, arteries, the heart, and the microcirculation. The complications of thrombosis are caused either by the effects of local obstruction or distant obstruction from the embolization of thrombotic material.

    A clot, or fragment of a clot, which becomes dislodged from its site of origin is known as an embolus. Emboli generally do not stop flowing until they come to a narrow point in the circulatory system. Thus emboli originating in large arteries or in the left side of the heart eventually plug smaller arteries or arterioles while emboli originating in the venous system or in the right side of the heart flow into the vessels of the lung.

    Colman RW, Hirsh J, Marder VJ, Salzman EW. Overview of hemostasis. In: Colman RW, Hirsh J, Marder VJ, Salzman EW, eds. Hemostasis and thrombosis, 3rd ed. Philadelphia: J.B. Lippincott, 1994 pp 6,13,14.

  • Reviso da HemostaseCascata da coagulaoEndotlio vascularMecanismos anticoagulantesSistema fibrinolticoPlaquetasDinmica de fluxo

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    Hemostase

    Subendothelial matrix

    Platelets

    Hemostatic plug

    Fibrin

    Endothelial cell

    RBC

    WBC

    WBC

    Hemostasis refers to the prevention of blood loss. In the body, this is accomplished by vasoconstriction and coagulation. Undue bleeding is controlled and the fluidity of the blood is maintained by counterbalances within the coagulation and fibrinolytic systems. Blood vessel injury or disruption, platelet defects, abnormalities of the normally circulating anticoagulants and fibrinolytic mechanisms may upset the balance between fibrinolysis and coagulation.

    Blood normally circulates through endothelium-lined vessels without coagulation or platelet activation occurring and without appreciable hemorrhage. Injury to the endothelial cells triggers the hemostatic process, which typically begins with the attachment of platelets (Adhesion) to the damaged endothelium or exposed subendothelial proteins such as collagen and von Willebrand factor (vWf).

    The platelets then change form (Activate) and release factors that stimulate the clotting process. They also bind together (Aggregate). At the same time, plasma proteins may react with elements in the subendothelium, activating the contact phase of coagulation. Exposed fibroblasts and macrophages present tissue factor, a membrane protein, to the blood at the injured site, thereby triggering the Extrinsic phase of blood coagulation.

    Under normal conditions, hemostasis protects the individual from massive bleeding secondary to trauma. In abnormal states, life-threatening bleeding can occur or thrombosis can occlude the vascular tree. Hemostasis is influenced by a number of different factors including: (a) vascular extracellular matrix and alterations in endothelial reactivity, (b) platelets, (c) coagulation proteins, (d) inhibitors of coagulation, and (e) fibrinolysis.

    Cotran RS, Kumar V, Robbins SL, eds. Robbins pathologic basis of disease, 5th ed. Philadelphia: W.B. Saunders, 1994 pp 99-106.

    Goodnight S. Physiology of coagulation and the role of vitamin K. In: Ansell JE, Oertel LB, Wittkowsky AK, eds. Managing oral anticoagulation therapy, Gaithersburg: Aspen Publishers, 1997 pp 1B-1:1-5.

    Hemostasis refers to the prevention of blood loss. In the body, this is accomplished by vasoconstriction and coagulation. Undue bleeding is controlled and the fluidity of the blood is maintained by counterbalances within the coagulation and fibrinolytic systems. Blood vessel injury or disruption, platelet defects, abnormalities of the normally circulating anticoagulants and fibrinolytic mechanisms may upset the balance between fibrinolysis and coagulation.

    Blood normally circulates through endothelium-lined vessels without coagulation or platelet activation occurring and without appreciable hemorrhage. Injury to the endothelial cells triggers the hemostatic process, which typically begins with the attachment of platelets (Adhesion) to the damaged endothelium or exposed subendothelial proteins such as collagen and von Willebrand factor (vWf).

    The platelets then change form (Activate) and release factors that stimulate the clotting process. They also bind together (Aggregate). At the same time, plasma proteins may react with elements in the subendothelium, activating the contact phase of coagulation. Exposed fibroblasts and macrophages present tissue factor, a membrane protein, to the blood at the injured site, thereby triggering the Extrinsic phase of blood coagulation.

    Under normal conditions, hemostasis protects the individual from massive bleeding secondary to trauma. In abnormal states, life-threatening bleeding can occur or thrombosis can occlude the vascular tree. Hemostasis is influenced by a number of different factors including: (a) vascular extracellular matrix and alterations in endothelial reactivity, (b) platelets, (c) coagulation proteins, (d) inhibitors of coagulation, and (e) fibrinolysis.

    Cotran RS, Kumar V, Robbins SL, eds. Robbins pathologic basis of disease, 5th ed. Philadelphia: W.B. Saunders, 1994 pp 99-106.

    Goodnight S. Physiology of coagulation and the role of vitamin K. In: Ansell JE, Oertel LB, Wittkowsky AK, eds. Managing oral anticoagulation therapy, Gaithersburg: Aspen Publishers, 1997 pp 1B-1:1-5.

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  • Endotlio VascularEndotlio Vascular expressa: TrombomodulinaActivator do Plasminognio TecidularTromboplastina Tecidular/Factor Tecidular

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    *

    Hemostase

    Subendothelial matrix

    Platelets

    Hemostatic plug

    Fibrin

    Endothelial cell

    RBC

    WBC

    WBC

    Hemostasis refers to the prevention of blood loss. In the body, this is accomplished by vasoconstriction and coagulation. Undue bleeding is controlled and the fluidity of the blood is maintained by counterbalances within the coagulation and fibrinolytic systems. Blood vessel injury or disruption, platelet defects, abnormalities of the normally circulating anticoagulants and fibrinolytic mechanisms may upset the balance between fibrinolysis and coagulation.

    Blood normally circulates through endothelium-lined vessels without coagulation or platelet activation occurring and without appreciable hemorrhage.