Gen Path L9, 10, & 13

  1. shock is characterized by ________; it can be caused by ________ or by __________. The consequences are _________ and _________.
    • systemic hypoperfusion of tissues
    • diminished cardiac output
    • reduced effective circulating blood volume
    • impaired tissue perfusion
    • cellular hypoxia
  2. Types of Shock
    • Cardiogenic shock results from low cardiac output due to myocardial pump failure, caused by eg. myocardial damage (infarction), ventricular arrhythmias, extrinsic compression (cardiac tamponade), or outflow obstruction (e.g., pulmonary embolism)
    • Hypovolemic shock results from low cardiac output due to loss of blood or plasma volume (e.g., due to hemorrhage or fluid loss from severe burns)
    • Septic shock results from arterial vasodilation and venous blood pooling that stems from the systemic immune response to microbial infection.
    • Neurogenic shock results from loss of vascular
    • tone associated with anesthesia or secondary to a spinal cord injury.
    • Anaphylactic shock results from systemic vasodilation and increased vascular permeability that is triggered by an immunoglobulin E–mediated hypersensitivity reaction
  3. Stages of shock
    • initial nonprogressive stage - reflex compensatory mechanisms activated, vital organ perfusion maintained. neurohumoral mechanisms -> tachycardia, peripheral vasoconstriction (septic
    • shock initially causes cutaneous vasodilation), renal fluid conservation
    • progressive stage - tissue hypoperfusion, onset of worsening circulatory and metabolic derangement, including acidosis. widespread tissue hypoxia -> lactic acidosis -> blunts vasomotor response -> arterioles dilate -> Peripheral pooling
    • irreversible stage - severe cellular and tissue injury, survival impossible
  4. Shock of any form can lead to hypoxic tissue injury if not corrected.
  5. Septic shock is caused by the host response to bacterial or fungal infections; it is characterized by endothelial cell activation, vasodilation, edema, disseminated intravascular coagulation, and metabolic derangements.
  6. causes of edema
    • Increased Hydrostatic Pressure
    • Reduced Plasma Osmotic Pressure - albumin lost (nephrotic syndrome) or synthesized in inadequate (severe liver disease, protein malnutrition)
    • Lymphatic Obstruction - result of inflammatory or neoplastic condition
    • Sodium and Water Retention
  7. Edema is the result of the movement of fluid from the vasculature into the interstitial spaces; the fluid may be protein-poor (______) or protein-rich (_______).
    • transudate
    • exudate
  8. Petechiae
    hemorrhage 1 to 2 mm in diameter
  9. Purpura
    3 to 5 mm hemorrhages
  10. Ecchymoses
    1 to 2 cm subcutaneous hematomas (colloquially called bruises)
  11. Thrombus development usually is related to one or more components of Virchow’s triad:
    • endothelial injury - e.g., by toxins, hypertension, inflammation, or metabolic products
    • abnormal blood flow, stasis or turbulence - e.g., aneurysms, atherosclerotic plaque
    • hypercoagulability: either primary (e.g., factor V Leiden, increased prothrombin synthesis, antithrombin III defciency) or secondary (e.g., bed rest, tissue damage, malignancy)
  12. Thrombi may propagate, resolve, become organized, or embolize; Thrombosis causes tissue injury by local vascular occlusion or by distal embolization
  13. Fat Embolism
    • Soft tissue crush injury or rupture of marrow vascular sinusoids (long bone fracture) releases microscopic fat globules into the circulation and cause embolism. a small portion of which is fatal.
    • Fat microemboli occlude pulmonary and cerebral microvasculature, both directly and by triggering platelet aggregation. exacerbated by fatty acid release from lipid globules -> local toxic endothelial injury. Platelet activation and granulocyte recruitment (with free radical, protease, and eicosanoid release) complete the vascular assault.
  14. Air Embolism
    • Serious if trapped in coronary artery or cerebral arterial circulation
    • Small venous gas emboli generally fine
    • decompression sickness - also causes Grecian bend (muscle) and choke (respiratory), caisson disease (bone)
  15. Pulmonary emboli derive primarily from lower-extremity deep vein thrombi; their effects depend mainly on the size of the embolus and the location in which it lodges.
  16. Systemic emboli derive primarily from cardiac mural or valvular thrombi, aortic aneurysms, or atherosclerotic plaques.
  17. Pulmonary infarction is a common clinical complication, bowel infarction often is fatal, and ischemic necrosis of distal extremities (gangrene) causes substantial morbidity in the diabetic population.
  18. Arterial thrombosis or embolism underlies the vast majority of infarctions.
Card Set
Gen Path L9, 10, & 13
Gen Path L9, 10, & 13 Hemodynamic Disturbances