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Critical Care > Test 3 > Flashcards

Test 3 Flashcards

1
Q

If O2 goes down what do vessels do

A

Vasodilate

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2
Q

If O2 goes up what do vessels do

A

Constrict

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3
Q

Is a knife low or high velocity

A

Low

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4
Q

Most common skull fracture

A

Linear

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5
Q

What type of fracture looks like you cracked an egg

A

Comminuted

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6
Q

What is the halo effect

A

When blood encircled by a yellowish stain is seen in dressing or bed linen

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7
Q

What is battles sign

A

Bruising behind the ear

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8
Q

Clinical presentation of basilar fracture

A

Battle sign and raccoon eyes

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9
Q

Potential infectious complication of basilar fracture

A

Meningitis

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10
Q

Examples of focal primary brain injuries

A

Contusions, hematomas, penetrating injuries

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11
Q

Example of diffuse primary brain injury

A

Diffuse axonal injury

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12
Q

Recovery with diffuse axonal injury

A

No or minimal recovery

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13
Q

What type of bleed is epidural hematoma

A

Usually arterial, may or may not be able to stop

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14
Q

What type of bleed is subdural hematoma

A

Venous, slow bleed

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15
Q

Most common secondary brain injury

A

Cerebral ischemia

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16
Q

Outcome with secondary brain injury

A

When secondary injury takes hold it is hard to resolve

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17
Q

Components of cranial vault

A

Brian tissue, blood, CSF

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18
Q

Normal ICP

A

0-15 mmHg

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19
Q

Increased ICP?

A

20 mmHg of greater from more than 5 minutes

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20
Q

What is the Monroe Kellie Hypothesis

A

Increase in any component requires decrease in one or both of other components to maintain ICP

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21
Q

Neuro #1 priority

A

Oxygenated blood to brain cells

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22
Q

Is herniation a early or late sign

A

Late

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23
Q

Best tool for objective assessment of LOC

A

Glasgow coma scale

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24
Q

Components of Glasgow coma scale

A

Eye opening, verbal response, motor response

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25
Q

Early signs neurological change of increased ICP

A

LOC change, weakness

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26
Q

Late signs of neurological changes of increased ICP

A

Stupor, coma, pupil changes (non responsive), posturing

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27
Q

Early vital sign change of increased ICP

A

Hypertension

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28
Q

Late vital sign change of increased ICP

A

Cushings triad

  • systolic Hypertension with widening pulse pressure
  • bradycardia
  • irregular respirations
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29
Q

What is Cushings triad

A
  • systolic Hypertension with widening pulse pressure
  • bradycardia
  • irregular respirations (sign of irreversible damage)
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30
Q

With what Glasgow coma scale score do we indicate ICP monitoring

A

3-8

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31
Q

CPP=

A

CPP=MAP-ICP

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32
Q

Normal CPP

A

70-100 mmHg

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33
Q

Examples of osmotic diuretics

A

Mannitol and hypertonic saline 3%

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34
Q

Normal serum osmolality

A

275-295 mOsm/L

2x normal sodium

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35
Q

What is Nicardipine

A

Calcium channel blocker can be used to control hypertension without effecting cerebral vasculature

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36
Q

3 types of incomplete lesions

A

Anterior cord syndrome, central cord syndrome, and Brown-Sequard syndrome

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37
Q

C1 to C3 usually

A

Ventilator dependent

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38
Q

PCO2 is a potent ________

A

Vasodilator

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39
Q

Hallmark early sign of shock in pediatric patients

A

Tachycardia

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40
Q

Late sign of shock in pediatric patients

A

Hypotension

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41
Q

What is Kehrs sign

A

Left shoulder pain from diaphragm injury in spleen injury in children

42
Q

Trajectories of women in penetrating trauma? Men?

A

Women-downward

Men-upward force

43
Q

What lobe would memory and hearing loss relate to

A

Temporal

44
Q

What lobe has the primary functions of thinking, planning, judgment?

A

Frontal

45
Q

What lobe has the primary function of sensory function

A

Parietal

46
Q

What type of posturing when a patient has rigid extension and pronation of arms and legs

A

Decebrate

47
Q

Normal GFR

A

80-125 ml/min

48
Q

What is the GFR

A

How fast are the kidneys able to filter our blood

49
Q

Normal phosphorus

A

2.4-4.1

50
Q

Normal magnesium

A

1.5-2.5

51
Q

How much of the cardiac output goes to the kidneys

A

20-25%

52
Q

Afferent vs. efferent

A

Afferent- in toward a system

Efferent- out away from a system

53
Q

ADH and aldosterone deal with what

A

Water reabsorption

54
Q

What happens if patient is acidotic

A

Kidneys form ammonia and excrete extra hydrogen ions

55
Q

What happens if a patient is alkalotic

A

Increased bicarb excretion

56
Q

What is enuresis

A

Kid pees the bed at night

57
Q

Hallmark signs of AKI

A

Azotemia and oliguria

58
Q

A sudden decline in function resulting in disturbances of fluid, electrolyte, and acid-base balance

A

Acute Kidney Injury

59
Q

What is azotemia

A

Increased BUN and creatinine

60
Q

What is oliguria

A

Urine output of less than 0.5 ml/kg/hr

61
Q

When a child is less than 2 can they not be potty trained

A

Not neurologically developed enough to control bladder

62
Q

What is the most common cause of AKI in critical care patient

A

Sepsis

63
Q

Causes of AKI

A

Prerenal, intrarenal, postrenal

64
Q

Prerenal cause AKI

A

Before the kidney and it is a perfusion issue

65
Q

Intrarenal causes of AKI

A

In the kidney, act on kidney tissue, acute tubular necrosis most common, contrast induced nephropathy is another cause

66
Q

Most common cause of intrarenal AKI

A

Acute tubular necrosis

67
Q

What kind of cause is contrast induced nephropathy

A

Intrarenal cause

68
Q

Drug to protect kidneys from dye

A

Mucomyst

69
Q

Postrenal causes of AKI

A

Obstruction of some sort, urine is sitting in kidney so increased intratubular pressure=decreased GFR, hydronephrosis

70
Q

What are the three phases of AKI

A

Imitation, maintenance, recovery

71
Q

In what stage is intrinsic renal damage established

A

Maintenance phase

72
Q

How long may recovery phase take in AKI

A

4-6 months

73
Q

Normal BUN/creatinine ratio

A

10:1-20:1

74
Q

Normal creatinine clearance

A

84-134 ml/min

75
Q

Normal GFR

A

80-125 ml/min

76
Q

What is the GFR

A

How fast are the kidneys able to filter our blood

77
Q

Normal phosphorus

A

2.4-4.1

78
Q

Normal magnesium

A

1.5-2.5

79
Q

How much of the cardiac output goes to the kidneys

A

20-25%

80
Q

Afferent vs. efferent

A

Afferent- in toward a system

Efferent- out away from a system

81
Q

ADH and aldosterone deal with what

A

Water reabsorption

82
Q

What happens if patient is acidotic

A

Kidneys form ammonia and excrete extra hydrogen ions

83
Q

What happens if a patient is alkalotic

A

Increased bicarb excretion

84
Q

What is enuresis

A

Kid pees the bed at night

85
Q

Hallmark signs of AKI

A

Azotemia and oliguria

86
Q

A sudden decline in function resulting in disturbances of fluid, electrolyte, and acid-base balance

A

Acute Kidney Injury

87
Q

What is azotemia

A

Increased BUN and creatinine

88
Q

What is oliguria

A

Urine output of less than 0.5 ml/kg/hr

89
Q

When a child is less than 2 can they not be potty trained

A

Not neurologically developed enough to control bladder

90
Q

What is the most common cause of AKI in critical care patient

A

Sepsis

91
Q

Causes of AKI

A

Prerenal, intrarenal, postrenal

92
Q

Prerenal cause AKI

A

Before the kidney and it is a perfusion issue

93
Q

Intrarenal causes of AKI

A

In the kidney, act on kidney tissue, acute tubular necrosis most common, contrast induced nephropathy is another cause

94
Q

Most common cause of intrarenal AKI

A

Acute tubular necrosis

95
Q

What kind of cause is contrast induced nephropathy

A

Intrarenal cause

96
Q

Drug to protect kidneys from dye

A

Mucomyst

97
Q

Postrenal causes of AKI

A

Obstruction of some sort, urine is sitting in kidney so increased intratubular pressure=decreased GFR, hydronephrosis

98
Q

What are the three phases of AKI

A

Imitation, maintenance, recovery

99
Q

In what stage is intrinsic renal damage established

A

Maintenance phase

100
Q

How long may recovery phase take in AKI

A

4-6 months

101
Q

Normal BUN/creatinine ratio

A

10:1-20:1

102
Q

Normal creatinine clearance

A

84-134 ml/min

Critical Care (4 decks)

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