1. List 3 examples of the pathogenesis of thrombosis
    • 1. endothelial injury
    • 2. alteration in blood flow
    • 3. hypercoagulability
  2. explain endothelial cell injury in terms of thrombosis
    loss of barrier between blood and extracellular matrix, increased prothrombic activity caused by hemodynamic stress
  3. Explain the alteration in blood flow in terms of thrombosis
    • 1. turbulence induces endothelial dysfunction and activation
    • 2. stasis causes platelets move to periphery of vessel lumen. This allows for concentration of clotting factors important in the formation of venous thrombi
  4. explain inherited and aquired reasons for hypercoagulability in terms of thrombosis
    • Inherited: Factor V Leiden mutation, prothrombin mutation, deficiencies of anticoagulant protein (antithrombin III)
    • Aquired: prolonged bed rest, extensive tissue damage, cancer, pregnancy
  5. explain Factor V Leiden mutation
    produces a factor v that cannot be degraded by protein c
  6. describe morphology of arterial thrombi
    occur at sites of turbulence or endothelial cell injury. they have white appearance with distinct lines of Zahn and may be occlusive or mural. lodge in smaller arteries causing infarction.
  7. what is an NBTE?
    non-bacterial thrombotic endocarditis: sterile thrombi on heart valve
  8. describe morphology of venous thrombi
    dark red color with no clear lines of zahn. form in deep veins of the legs.
  9. what are the 4 fates of thrombi?
    • 1. propagation (enlargement by fibrin/platelet deposition)
    • 2. embolization (entire thrombus dislodges or piece breaks loose)
    • 3. dissolution (lysis by fibrinolytic activity)
    • 4. organization (deposition of collagen to replace fibrin and recanalization to reestablish flow)
  10. Describe DIC (disseminated intravascular coagulation) and possible causes
    depletion of coagulation factors and platelets via widespread activation of coagulation cascades. associated with widespread formation of microthrombi and risk of hemorrhage. conditions causing DIC include gram negative infection, obstetric complications, neoplasm, shock and massive injury.
  11. Describe Embolism
    solid, liquid, or gas carried from one point to another point in the vascular system
  12. thombi from deep veins in the legs usually lodge where?
    pulmonary arteries
  13. what are 5 consequences of pulmonary thromboemboli?
    • 1. no clinical manifestation (no ischemia due to double blood supply)
    • 2. pulmonary hemorrhage and hematemesis due to ischemic injury without infarction
    • 3. pulmonary infarction
    • 4. sudden death due to large emboli obstructing a large pulmonary artery or straddling the bifurcation of the pulmonary arterial trunk (saddle embolus)
    • 5. gradual obstruction that leads to pulmonary hypertension
  14. describe paradoxical embolus
    embolus that arises in a systemic vein and crosses a communication from the venous side to the arterial side of circulation, usually through a patent foramen ovale or atrial septal defect.
  15. describe systemic embolization
    origin is usually left atrium, left ventricle or ulcerated atherosclerotic plaque. can travel to any systemic artery.
  16. describe 4 "other" types of emboli
    • fat: fracture of large long bone or soft tissue injury
    • air: decompression sickness
    • amniotic fluid
    • atherosclerotic
  17. define infarction
    ischemic necrosis in an organ due to arterial obstruction
  18. describe a Red (hemorrhagic) infarct
    can be caused by venous occlusion, loose tissue, infarction followed by reflow of blood into the area
  19. describe a white infarct
    occurs with arterial occlusions in solid organs
  20. list 3 morphologic characteristics of infarcts
    • 1. wedge-shaped with point of wedge at site of arterial obstruction
    • 2. infarcts usually followed by acute inflammation
    • 3. infarcts in the brain result in liquefactive necrosis
  21. define shock
    systemic hypoperfusion of tissues
  22. list/define 5 types of shock
    • 1. cardiogenic: loss of pumping capacity of the heart
    • 2. hypovolemic: blood loss
    • 3. septic: bacterial infection
    • 4. anaphaylactic: IgE hypersensitivity
    • 5. neurogenic: loss of vascular tone
  23. what are the clinical manifestions of septic shock?
    • 1. vasodilation
    • 2. hypotension
    • 3. reduced myocardial contractility
  24. describe the pathogenesis of septic shock
    LPS of Gm- binds to receptor on monocytes causing release of IL-1 and TNF, as well as secondary cytokines.
  25. list 3 stages of shock
    • 1. nonprogressive
    • 2. progressive
    • 3. irreversible
  26. define non-progressive shock
    maintenance of tissue perfusion by tachycardia, renal conservation of water, redistrobution of blood to vital organs via peripheral vasoconstriction
  27. define progressive shock
    inadequate perfusion with metabolic imbalances such as acidosis and increased lactic acid. acidosis reduces vasomotor response to sympathetic stimulation leading to pooling of blood and reduced perfusion. hypoxic injury to endothelium results in DIC.
  28. define irreversible shock
    tissue injury that cannot be reversed by reperfusion
  29. list 7 pathologic changes in shock for brain, heart, kidney, lungs, adrenals, GI, and liver
    • 1. Brain: ischemic necrosis of neurons in the brain
    • 2. Heart: necrosis in the heart
    • 3. Kidney: necrosis of tubular epithelial cells in the kidney (acute tubular necrosis)
    • 4. Lungs: diffuse alveolar damage in the lungs due to endothelial injury (ARDS)
    • 5. Adrenals: depletion of lipids in adrenal cortex
    • 6. GI: mucosal hemorrhage and necrosis in the intestines
    • 7. Liver: necrosis of the liver
  30. 7 clinical manifestations of shock
    • 1. tachycardia
    • 2. tachypnea
    • 3. hypotension
    • 4. clammy skin
    • 5. decreased urinary output
    • 6. confusion
    • 7. low blood pH (acidosis) and elevated lactic acid
Card Set
Overview of Thrombosis, Embolism, Infarction, Shock