Shock, Mods, and Burns

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Author:
servinggod247
ID:
290324
Filename:
Shock, Mods, and Burns
Updated:
2014-11-30 23:46:07
Tags:
pathophysiology
Folders:
pathophysiology
Description:
pathophysiology
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  1. definition of shock
    cells not recieving adequate o2 or unable to use o2
  2. what happens when body doesnt have glucose
    • uses glycogenolysis 
    • gluconeogenesis 
    • lypolysis as alternatives for fuel generation
  3. glycogenolysis
    breakdown of glycogen to glucose
  4. gluconeogenesis
    glycogen formation from fatty acids and proteins rather than from glucose
  5. lypolysis
    fat breakdown
  6. Cardiogenic shock
    heart failure

    • R/T:
    • Myocardial ischemia
    • MI
    • CHF
    • Myocardial or pericardial infections
  7. hypovolemic shock
    insufficient intravascular fluid volume

    • R/T: Loss of whole blood plasma or interstitial fluid
    • Third spacing
  8. Anaphylactic shock
    immunologic alterations 

    • R/T:
    • hypersensitivity leading to vasodilation and peripheral pooling
  9. Neurogenic shock
    Neural alterations of vascular tone

    • R/T:
    • Imbalance of sympathetic or parasympathetic stimulation of vascular smooth muscle causing vasodilation
    • Decreased systemic vascular resistance of smooth muscle

    Nitric oxide synthesis and metabolic acidosis activate k+ channels of plasma membrane of vascular smooth muscle

    Prevents CA+ which mediates norepinephrine and agniotensin II induced vasoconstrictors from entering cell
  10. Multiple organ dysfunction syndrome
    progressive failure of 2 or more organ systems r/t a systemic inflammatory response after a severe illness or injury
  11. primary MODS
    immediate local or mid systemic response
  12. secondary MODS
    uncontrollable, excessive systemic inflammatory response syndrome (SRIS) that develops after a latent period and results in organ dysfunction
  13. First degree burn
    • epidermis only 
    • skin function intact
    • tactile and pain sensors
    • blisters may be present after 24 hours
  14. Second degree burn SUPERFICIAL PARTIAL THICKNESS
    • destruction of epidermis and dermis
    • no skin dysfunction 
    • tactile and pain sensors intact
    • blisters present within minutes
  15. Second degree Deep partial thickness
    • destruction of epidermis and dermis
    • skin function lost
    • tactile and pain sensors diminished
    • blisters may or may not appear, a flat dehydrated layer that lifts off in sheets
  16. third degree full thickness
    • destruction of epidermis, dermis and SQ tissue
    • no skin function
    • no tactile or pain sensors
    • blisters are rare: a flat dehydrated layer that lifts off easily
  17. IN BURNS: capillary bed opens in burn area and
    entire capillary system
  18. IN BURNS: increased capillary permeability leads to
    hypovolemic shock and massive edema
  19. IN BURNS: survival depends on
    impact on cellular level's metablic and immunologic responses
  20. IN BURNS: almost immediate hypermetabolic state induced that persists until
    wound closure...persistent elevation of core body temperature
  21. IN BURNS: evaporative water loss _____ times normal during early phase of injury
    20
  22. IN BURNS: hypercoagulable state develops; elevated plasma fibrinogen concentration in presence of
    shortened prothrombin time and activated partial thromboplastin time
  23. IN BURNS: Immunosupression and increased susceptiblity to
    potetnially fatal systemic burn wound sepsis
  24. IN BURNS: natural resistance to infection in burn wounds depends on
    nonspecific immune system and relies on phagocytes to leave bloodstream and migrate to site of infection
  25. burned pt's serum contains inhibitor of complement conversion that leads to
    decreased opsonization of bacteria and less polymorphonuclear neutrophil chemotaxis

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