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Pathopharm Final > 10: Adult Burns & Shock (Part 1) > Flashcards

10: Adult Burns & Shock (Part 1) Flashcards

1
Q

MODS is initiated and perpetuated by

A

uncontrolled systemic inflammatory and stress responses.

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2
Q

burns are a form of trauma with

A

wide-reaching effects on all organ systems.

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3
Q

the physiologic response of burns is dependent on

A

the extent of burn surface involvement and the depth of tissue destruction.

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4
Q

shock is a condition during which

A

the cardiovascular system fails to perfuse the tissues adequately; causes general and widespread impairment of cellular metabolism.

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5
Q

common pathways in all types of shock (3)

A
  • Impaired cellular metabolism (d/t decreased O2 & nutrient delivery)
  • Usually w/ increased O2/nutrient demand & consumption
  • Decreased removal of cellular waste products
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6
Q

cause of cardiogenic shock

A

heart failure

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7
Q

neurogenic/vasogenic shock cause

A

Alterations in smooth muscle tone

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8
Q

Anaphylactic shock is caused by

A

hypersensitivity

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9
Q

septic shock is caused by

A

infection

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10
Q

hypovolemic shock is caused by

A

insufficient intravascular fluid

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11
Q

clinical manifestations of shock

A

Weak, cold, hot, nauseated, dizzy, confused, afraid, thirsty, short of breath, and generally “feeling sick”

Decreased blood pressure, cardiac output, and urinary output

Increased respiratory rate

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12
Q

treatment of shock

A

Oxygenation: Absolute necessity in all shock states
Correct or remove underlying cause
Provide supportive therapy

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13
Q

in shock, metabolism shifts from ____________ to ____________

A

shift from aerobic to anaerobic

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14
Q

how does shock impair cellular metabolism?

A

impaired O2 use, regardless of cause

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15
Q

shock causes accumulation of ____________ in the cell (2)

A

sodium and chloride

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16
Q

what exits the cell in shock

A

potassium

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17
Q

shock activates what pathway

A

coagulation

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18
Q

shock causes the release of ____________ enzyme

A

lysosomal

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19
Q

how is glucose use changed during shock

A

impaired glucose use, cells shifting to glycogenolysis, gluconeogenesis, lipolysis

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20
Q

gluconeogenesis causes…

A

proteins to be used for fuel, thus no longer available for maintaining cellular structure, function, repair, and replication

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21
Q

shock causes toxic ____________ and ____________ production

A

ammonia and urea

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22
Q

metabolic acidosis features what kind of mechanism

A

compensatory

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23
Q

what does the compensatory mechanism of metabolic acidosis do

A

Enables cardiac and skeletal muscles to use lactic acid as a fuel source but only for a limited time

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24
Q

what happens to the heart in cardiogenic shock

A

Inability of the heart to pump adequate blood to tissues and end organs from any cause

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25
Q

what causes cardiogenic shock

A

myocardial ischemia, myocardial infarction

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26
Q

Cardiogenic shock causes persistent hypotension and tissue hypoperfusion caused by

A

cardiac dysfunction in the presence of adequate intravascular volume and left ventricular filling pressure

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27
Q

cardiogenic shock is a (↑/ ↓) in cardiac output

A

decrease

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28
Q

As cardiac output decreases, what compensatory adaptive responses are activated? (3)

A

Renin-angiotensin, neurohormonal, and sympathetic nervous system

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29
Q

what do the compensatory responses of cardiogenic shock cause (3)

A

Fluid retention, systemic vasoconstriction, and tachycardia.

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30
Q

catecholamines increase (2)

A

contractility and heart rate

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31
Q

cardiogenic shock activates the ____________ response

A

inflammatory

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32
Q

cardiogenic shock diagram

A
33
Q

what happens to the heart in cardiogenic shock

A

Increased myocardial requirements burden the already failing heart.

The heart can no longer pump an adequate volume of blood with sufficient force to perfuse the tissues.

34
Q

clinical manifestation of cardiogenic shock

A

Chest pain, dyspnea, and faintness, along with feelings of impending doom

35
Q

classic hallmarks of cardiogenic shock

A

Tachycardia, tachypnea, hypotension, jugular venous distention, dysrhythmia, and low measured cardiac output

36
Q

tx of cardiogenic shock

A

Intraaortic balloon counterpulsation (IABP) or percutaneous or ventricular assist devices (VADS)

Implantable VADS, pacemakers, or internal defibrillator devices

37
Q

fibrinolytic therapies

for cardiogenic shock

A

disintegrate coronary thrombus

38
Q

examples of percutaneous interventions

for cardiogenic shock

A

Balloon angioplasty, stent placement, and thrombectomies

39
Q

surgeries for cardiogenic shock

A

Coronary artery bypass, ventriculoplasty, or heart transplantation

40
Q

hypovolemic shock patho

A

Insufficient intravascular fluid volume
Loss of whole blood, blood plasma, or interstitial fluid; or fluid sequestration

Hemorrhage or burns or emesis or diuresis

41
Q

compensatory mechanisms for hypovolemic shock

A

Compensatory vasoconstriction, increased systemic vascular resistance (SVR), and afterload

to improve blood pressure and perfusion to core organs

42
Q

hypovolemic shock chart

A
43
Q

hypovolemic shock clinical manifestations (3)

A
  • Poor skin turgor, thirst, oliguria
  • Low systemic and pulmonary preloads
  • Rapid heart rates
44
Q

tx of hypovolemic shock (2)

A

Prompt control of hemorrhage
Fluid replacement

45
Q

neurogenic shock patho

A

Widespread vasodilation occurs from an imbalance between parasympathetic and sympathetic simulation.

46
Q

neurogenic shock causes persistent vasodilation and creates relative….

A

hypovolemia

47
Q

in neurogenic shock ________ is unchanged but the amount of space containing the blood has increased

A

blood volume

48
Q

in neurogenic shock pressure in the vessels is inadequate to drive nutrients across capillary membranes, therefore…

A

nutrient delivery to cells is impared

49
Q

neurogenic shock can be caused by (3)

A

severe pain and stress, anesthesia, and depressant drugs.

50
Q

neurogenic shock flow chart

A
51
Q

neurogenic shock clinical manifestations (2)

A

Very low SVR, bradycardia

52
Q

tx of neurogenic shock

A

decrease pain level

53
Q

anaphylactic shock is the outcome of…

A

widespread hypersensitivity to an allergen that triggers a reaction known as anaphylaxis.

54
Q

in anaphylactic shock ,an allergen causes

A

an extensive immune and inflammatory response.

Massive vasodilation follows with a fluid shift into the interstitium.

55
Q

anaphylactic shock is a widespread hypersensitivity reaction that leads to…(3)

A

vaso-dilation, peripheral pooling, and relative hypovolemia

56
Q

anaphylactic shock chart

A
57
Q

anaphylactic shock clinical manifestations

A

Anxiety, difficulty breathing, gastrointestinal (GI) cramps, edema, hives (urticaria), sensations of burning or itching of the skin, fever, and hemolysis.

58
Q

treatment of anaphylactic shock begins with

A

removal of the antigen if possible

59
Q

epinephrine for anaphylactic shock

A

Decreases mast cell and basophil degranulation, causing vasoconstriction; reverses airway constriction.

60
Q

use of IV volume expanders (LRs) in anaphylactic shock

A

Reverses relative hypovolemia

61
Q

use of antihistamines and steroids in anaphylactic shock

A

stops inflammatory reaction

62
Q

____________ initiate septic shock

A

infectious processed

63
Q

6 most common septic shock infection sites

A

the lungs, bloodstream, intravascular catheter, intra-abdominal, urinary tract, and a surgical wound.

64
Q

cause the host to initiate the inflammatory process

A

Bacteremia, endotoxins, and exotoxins

65
Q

inflammatory process activates ….(4)

A

Activates the complement, coagulation, and kinin systems and cellular immunity.

66
Q

the inflammatory process initiates and promotes widespread…

A

vasodilation

67
Q

this looks important!

A
68
Q

septic shock progression

A
69
Q

septic shock clinical manifestations

A

Persistent low arterial pressure, low SVR from vasodilation, and an alteration in oxygen extraction by all cells.

70
Q

treatment of septic shock

A

Check lactate level; obtain blood cultures; start antibiotic and antifungal medications; implement fluid challenge; and achieve goals for blood pressure, central venous pressure, and central venous oxygen saturation.

71
Q

initial vasopressor of choice in septic shock

A

norepinephrine

72
Q

MODS is a progressive dysfunction of

A

two or more organ systems from an uncontrolled inflammatory response to a severe illness or injury.

73
Q

MODS can cause (2)

A

organ failure and death

74
Q

2 most common causes of MODS

A

shock and sepsis

75
Q

other causes of MODS

A

Trauma, burns, acute respiratory disorder (ARDS), major surgery, circulatory shock, necrotic tissue, disseminated intravascular coagulation (DIC), acute renal failure, acute pancreatitis

76
Q

those at greatest risk for MODS (3)

A

Older adults

Those with significant tissue injury or preexisting disease

Those in whom resuscitation from the initiating illness or injury has been delayed or is inadequate

77
Q

MODS mortality rate

A

Is 54% when two organ systems are affected.

Mortality rate increases to 100% with the failure of five systems.

78
Q

primary MODS

A

Injury is directly associated with a specific insult: Hypoperfusion.

79
Q
A

Pathopharm Final (8 decks)

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