HemoDynamics

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Author:
julieaburch
ID:
47344
Filename:
HemoDynamics
Updated:
2010-11-04 23:03:34
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Pathology
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Description:
Hemodynamics
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  1. Active bleeding into extravascular tissues or spaces resulting from disruption of the integrity of vascular walls
    Hemorrhage
  2. Hemorrhage into skin
    petechiae (pinpoint)
  3. Hemorrhage into mucous membranes
    Purpura
  4. Hemorrhage into serosal surfaces
    Ecchymoses
  5. Coughing of blood from lungs
    Hemoptysis
  6. Vomiting of blood
    Hematemesis
  7. Dark "tarry" blood in the stool
    Melena
  8. Bright red blood in the stool
    Hematochezia
  9. The body's intrinsic ability to slow down or stop hemorrhage
    Hemostasis
  10. An intravascular blood coagulum formed as a method to achieve hemostasis.
    Thrombus
  11. The formation of an extravascular coagulum or a postmortem intravascular coagulum formed only from the plasma coagulation factors
    Blood Clot
  12. Measures the time it takes blood to clot by the intrinsic pathway
    Partial Thromboplastin Time (PTT)
  13. Measures the time it takes for blood to clot by the extrinsic pathway
    Prothrombin Time (PT)
  14. Test that identifies the degradation product of cross-linked fibrin and is used as an indicator of active fibrinolyses
    D-Dimer Test
  15. Virchow's Triad (predisposing factors to a life-threatening thrombus)
    • 1. Alteration of Vascular Endothelim
    • 2. Alteration of Blood Flow
    • 3. Alterations of Blood Components
  16. Type of thrombi that form most frequently in areas of artherosclerotic damage to the vessel wall or, in the heart, over areas of previous myocardial infarction. Tend to develop alternating layers (lines of Zahn) of fibrin adn aggregated platelets, which gives these thrombi a grey, laminated appearance (white thrombus)
    Arterial Thrombi
  17. Cardiac and aortic thrombi firmly attached to underlying vessel wall. Generally non-occlusive.
    Mural Thrombi
  18. Type of thrombi that usually form in areas of blood stasis. Most clinically significant of these form in deep leg veins. Most are the result of sluggish blood flow, so tend to be occlusive and do not develop lines of Zahn. RBCs remain trapped within the developing thrombus and this produces a dark red-blue appearance (red thrombus)
    Venous Thrombi
  19. This type of thrombi is usually due to local endothelial damage. Generally consist of platelets and fibrin and are not grossly visible
    Capillary Thrombi
  20. Reestablished vascular flow through an occlusive thrombus
    Recanalization
  21. A thrombus that has fragmented and detached completely from its place of origin to tumble through the circulation
    Thromboembolus
  22. These form a perfect cast of the vessel in which they form, do not contain lines of Zahn, are not firmly attached to the vessel wall, have a "currant-jelly" and/or "chicken fat" appearance, adn do not break apart easily
    Post-mortem Blood Clots
  23. The process of tissue necrosis secondary to an abrupt reduction in tissue oxygenation. Usually the result of a sudden interference with the arterial blood supply to a tissue, but may be due to obstruction of venous drainage or to conditions that decrease the oxygen carrying capacity of blood.
    Infarction/Infarcts
  24. In tissues with a single blood supply without significant anastomoses (kidneys, spleen, heart, etc.), occlusion of an artery results in coagulation necrosis of the tissues supplied by that artery. Blood perfusion of the tissue is interrupted. What color of infarct results?
    Pale Infarct
  25. Tissues that have a single blood supply with rich anastomoses (small bowel) or that have a dual blood supply (lung, liver) are somewhat protected against abrupt hypoxia due to the alternate blood source. If necrosis does occur, however, that alternate blood source may lead into the necrotic tissue, resulting in what color of infarct?
    Red (hemorrhagic) Infarct
  26. True or False:
    Infarcts due to arterial occlusion tend to be wedge-shaped with the apex located close to the point of obstruction
    True
  27. An acquired disorder involving a coagulation abnormality. Numerous fibrin thrombi are formed consuming platelets, fibrinogen, and coagulation factors and secondarily activating the fibrinolytic system. The microthrombi may lead to microinfarcts of the affected tissue, acute tubular necrosis of the kidneys, and hemolytic anemia. Shock is a frequent complication
    Disseminated Intravascular Coagulation (DIC)
  28. The process in which a free-floating mass is carried through the vascular system to a point distant to its site of origin or entry. The vast majority are fragments of preexisting thrombi. Infarction of tissue distal to the point of impact may occur
    Embolization
  29. 80-85% of this type of emboli arise from mural thrombi in the left ventricle or left atrial appendage of the heart. May or may not cause infarction. Major sites of impaction include lower extremities, brain, kidney, and spleen.
    Systemic (Arterial) Emboli
  30. Although rare, if a right-to-left shunt is present in the heart (patent foramen ovale, atrial or ventricular septal defect), a venous embolus can gain access into the systemic circulation. This is called?
    Paradoxical Embolus
  31. The third most common cause of sudden death.
    Pulmonary (venous) Thrombi
  32. These type of emboli most frequently occur after long-bone trauma when marrow fat is exposed to the venous circulation.
    Fat Emboli
  33. This type of emboli may result from abortion procedures, traumatic pneumothorax, Caisson's disease, etc. May cause "air lock" in the right heart
    Air Emboli
  34. The inadequate perfusion and resultant hypoxia of body tissues
    Shock
  35. Type of shock resulting from acute loss of blood or fluid from the circulation. May be due to hemorrhage, burns, vomiting, diarrhea, etc.
    Hypovolemic Shock
  36. Type of shock resulting from the inability of the heart to maintain adequate output. May be due to myocardial infarcts, cardiac tamponade, pulmonary emboli, etc.
    Cardiogenic Shock
  37. Type of shock that involves the pooling of blood in peripheral vasculature leading to a central "hypovolemia" adn hypoperfusion of vital organs
    Vascular Shock
  38. Type of vascular shock involving the inability to maintain peripheral vascular muscle tone with subsequent peripheral pooling of blood. May be due to CNS injury, drugs, etc.
    Neurogenic Vascular Shock
  39. Type of vascular shock that involves severe gram-negative bacterial infections that produce endotoxins that cause peripheral vascular pooling. Resulting shock may also be complicated by direct toxic damage to the vessels and by DIC
    Septic (Endotoxic) Shock
  40. Type of vascular shock that involves hypersensitivity reactions which lead to widespread vasodilation (causing peripheral vascular pooling) and increased capillary permeability with fluid loss from the vasculature. Can lead to hypovolemia and hypoperfusion of vital organs
    Anaphylactic Vascular Shock

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