2850 Pathophysiology Exam Four Flashcards

1
Q

what is the gold standard for a brain death determination?

A

neurological exam

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2
Q

what conditions must be ruled out before determining brain death?

A
severe electrolyte imbalance
severe acid base issue
endocrine abnormalities 
core temperature below 89.6 degrees
hypotension
drug intoxication
poisoning
neuromuscular blockade
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3
Q

what is “locked in syndrome”?

A

a rare neurological disorder where all voluntary muscles are paralyzed except muscles controlling eye movement. This must be ruled out before declaring brain death

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4
Q

what does a clinical neurological exam assess a patient for when trying to determine brain death?

A

coma
apnea
absence of brainstem reflexes

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5
Q

how will absence of brainstem reflexes be manifest in the pupils?

A

pupils round or oval and dilated 4-6 mm with no response to bright light

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6
Q

how will an absence of brain stem reflexes be manifest in corneal reflex?

A

there will be no blinking when the corneal edge is touched with a cotton ball

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7
Q

what is cold caloric stimulation? How does it play into determining brainstem reflexes?

A

irrigating the ear canal with ice water after tilting the head 30 degrees. No neck or eye deviation towards the cold stimulus indicates brain death/lack of brain stem reflexes

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8
Q

how is bronchial suctioning used to determine brain death?

A

patient is suctioned, and if no coughing occurs as a response, it indicates brain death

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9
Q

explain apneic diffusion oxygenation

A

This is done to determine brain death in ventilated patients. The vent is turned off, patients are preoxygenated to eliminate respiratory nitrogen, and the climbing PaCO2 is used to attempt to get spontaneous respirations

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10
Q

how is depth of coma assessed?

A

presence or absence of motor response to painful stimulus

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11
Q

how is patient’s reaction to pain determined when assessing coma depth?

A

pressing on the supraorbital nerve, pinching the sternum, or pressing on the nailbed

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12
Q

what is meant by end of life?

A

final phase of a patient’s illness where death is imminent and no further life-saving measures are to be taken

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13
Q

death rattle

A

noisy, wet sounding respirations caused by mouth breathing and accumulation of mucus in the airway

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14
Q

when does the death rattle occur?

A

very near the end of life, usually only the last few hours

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15
Q

why does the death rattle occur?

A

the patient has increasing difficulty swallowing or coughing up secretions

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16
Q

cheyne-stokes respirations

A

alternating periods of apnea and deep, rapid breathing

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17
Q

what are changes in the cardiovascular system as death approaches?

A

increased heart rate, then weaker and slower pulse as the patient approaches death
irregular heart rhythm
decreased BP
slower medication absorption (may need increased dose)

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18
Q

what are musculoskeletal changes as death approaches?

A
loss of ability to move/extreme weakness
loss of gag reflex
difficulty swallowing
jaw sagging 
speech difficulty 
posture and alignment difficulty
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19
Q

what are integumentary changes as death approaches?

A

mottling of skin
cold and clammy skin
cyanosis (especially nose, nail beds, and knees)
waxlike skin very close to death

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20
Q

putrefaction

A

action of bacteria on tissues of dead body, leading to discoloration, gas production, and a foul odor

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21
Q

autolysis

A

breakdown of body cells due to lysozymes beginning to digest dead tissues

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22
Q

rigor mortis

A

post-mortem muscle stiffening (begins 1-2 hours after death and usually passes by about 24 hours after death)

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23
Q

livor mortis

A

purple-red discoloration in dependent parts of the body due to gravitational blood pooling after the heart stops

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24
Q

what does chronic venous insufficiency occur from?

A

damage to valves in the deep veins of the legs

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25
Q

what can cause faulty valves in deep leg veins?

A

trauma
central obesity
pregnancy
prolonged standing

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26
Q

what is the result of valve damage in leg veins?

A

impaired venous return and high venous pressure, which causes stasis and pooling of blood

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27
Q

how does venous congestion impact capillary filtration?

A

it inhibits movement of fluid and waste out of interstitial spaces

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28
Q

what are clinical presentations of venous insufficiency?

A
thin shiny skin
dusky discoloration
edema
poor healing
reduced or absent hair on legs
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29
Q

why is hair reduced or absent with venous insufficiency?

A

insufficient nutrient supply to that area

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30
Q

what is stasis dermatitis?

A

circumferential dusky discoloration around the legs

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31
Q

what causes stasis dermatitis?

A

buildup of hemosiderin in tissues

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32
Q

why does edema occur with venous insufficiency?

A

stasis increases the hydrostatic pressure, so fluid moves from the vascular space to the interstitial space

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33
Q

venous ulcers are caused by..

A

venous insufficiency

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34
Q

what pathophysiologic changes are found with venous stasis ulcers?

A

sluggish circulation
poor tissue oxygenation
deprivation of cellular nutrients
impaired waste removal

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35
Q

what are clinical presentations of venous ulcers?

A
dark red coloration
uneven margins
very painful
lots of edema and drainage 
possible necrosis
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36
Q

what is peripheral artery disease?

A

arteriosclerosis of peripheral arteries

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37
Q

what are risk factors for PAD?

A
age (over 45 for men, over 55 for women)
hypertension
high fat diet
sedentary lifestyle 
obesity
family history 
hyperlipidemia
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38
Q

what other conditions are associated with increased incidence of PAD?

A
diabetes
smoking
CKD
cancer
hypercoagulation disorders
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39
Q

what causes PAD?

A

reduced arterial bloodflow to periphery, causing tissue ischemia

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40
Q

what arteries are commonly affected in PAD?

A

carotid artery and femoral arteries

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41
Q

intermittent claudication

A

cramping leg pain associated with PAD

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42
Q

why does intermittent claudication occur?

A

reduced arterial blood flow

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43
Q

what happens when lack of circulation due to arterial obstruction occurs?

A

imbalance between tissue demand for oxygen and blood supply available

44
Q

what can the patient do to decrease leg pain associated with intermittent claudication?

A

stop exercising

45
Q

describe the reperfusion injury that occurs with peripheral arterial disease

A

free radicals are produced, causing oxidative stress, which causes further injury to the vascular bed and alterations in muscle metabolism

46
Q

what conditions in a patient history are significant predisposing factors for PAD?

A
signs and symptoms of arteriosclerosis
hypertension
hyperlipidemia
diabetes
coronary artery disease 
MI
47
Q

what are manifestations common to peripheral arterial disorders?

A
diminished or absent pulses
palpable coolness
paresthesias
pallor
pain in legs upon exertion
48
Q

what are risk factors for pressure injuries?

A
poor nutrition
impaired mobility 
diminished sensation 
impaired circulation 
moisture 
infection
impaired cognition
reduced oxygen in blood
49
Q

how does pressure contribute to pressure injury?

A

it compresses small blood vessels, reducing blood flow to an area

50
Q

how does shear contribute to pressure injury?

A

it deforms adipose tissue and muscle and reduces blood flow to an area, damaging the vascular bed

51
Q

what is an example of shear?

A

a patient sliding down in bed (one layer of skin sliding against another)

52
Q

how does friction contribute to pressure injury?

A

it damages the outer protective epidermal layer

53
Q

what is an example of friction?

A

sliding a patient up in bed (skin dragging across a surface)

54
Q

how does moisture contribute to pressure injury?

A

macerates the skin and decreases the pressure needed to produce an ulceration

55
Q

what are skin findings when ischemia first occurs?

A

skin will be pale and cool, and vasodilation will occur when the pressure is relieved

56
Q

what is reactive hyperemia?

A

relieving pressure on the ischemic area and the area vasodilating, causing it to flush bright red

57
Q

with reactive hyperemia, redness for what length of time indicates tissue damage?

A

over 30 minutes

58
Q

stage 1 pressure injury

A

intact skin, non-blanchable redness, discolored for over 30 minutes after pressure is relieved

59
Q

stage 2 pressure injury

A

partial thickness loss of dermis, open and shallow with a pink wound bed, no slough

60
Q

stage 3 pressure injury

A

deep crater with full thickness skin loss, damage and/or necrosis of subcutaneous tissue is present, possible undermining

61
Q

stage 4 pressure injury

A

full thickness with extensive damage, bone/tendon/cartilage exposed or palpable, slough is present

62
Q

deep tissue injury

A

skin is intact but discolored, area is very painful, damage amount under tissue is uncertain

63
Q

what is an unstagable pressure injury?

A

full thickness skin loss but the base is obscured by slough or eschar

64
Q

slough

A

tan, black, or brown leathery necrotic tissue

65
Q

eschar

A

tan, yellow, or green necrotic tissue

66
Q

primary intention healing

A

simple, rapid healing of a wound with clearly lacerated and defined edges. no gap in tissue present

67
Q

example of primary intention wound

A

surgical incision

68
Q

secondary intention healing

A

healing of a wound with extensive loss of tissue where regeneration of that same tissue cannot occur. scar tissue formation and epidermal thinning are present

69
Q

what pathophysiologic process differentiates primary intention healing from secondary?

A

contraction phase caused by myofibroblasts pulling the wound together

70
Q

what types of wound heal by tertiary intention?

A

pressure ulcers, burns, or wounds with contamination or a lot of missing deep tissue

71
Q

what are some common requirements for tertiary intention wounds?

A

skin grafts and sterile packing (wound may be left open for several days and then allowed to close)

72
Q

why is protein necessary for wound healing?

A

its necessary for cellular regeneration and connective tissue synthesis

73
Q

why are carbohydrates necessary for wound healing?

A

it can be a good energy source to spare protein for the healing process

74
Q

why are fats necessary for wound healing?

A

they are an essential component of cell membranes that are being synthesized

75
Q

why are adequate arterial and venous circulation necessary for wound healing?

A

to bring a rich supply of nutrients and oxygen to the wound and adequately remove waste from the wound by venous return

76
Q

how does oxygen facilitate wound healing?

A

oxygen facilitates collagen synthesis and WBC function

77
Q

why do elderly patients heal less efficiently?

A

they are naturally more immunosuppressed and prone to infection
aging skin
reduced collagen synthesis
more secondary conditions that reduce blood flow

78
Q

why do diabetic patients often have delayed wound healing?

A

lack of sensation and circulation in extremities

diabetes reduces abilities of neutrophils and macrophages, hindering inflammation process

79
Q

why do corticosteroids inhibit wound healing?

A

they suppress inflammation process and inhibit collagen synthesis

80
Q

what is the single most important cause of delayed wound healing?

A

infection (causes perpetual inflammation)

81
Q

what procedures are necessary to facilitate optimal healing of an infected wound?

A

vigorous irrigation, cleansing, and removal of necrotic tissue and foreign matter

82
Q

what is the prevalence of major depressive disorder?

A

17%

83
Q

depression: pathophysiology

A

mutation in the serotonin transporter gene, causing serotonin deficiency

84
Q

what other neurotransmitters can be out of balance in depression?

A

dopamine and norepinephrine

85
Q

what areas of the brain are affected in depression and how are they affected?

A

increased activity in the neocortex and decreased activity in the limbic system

86
Q

what is required for diagnosis of a major depressive episode?

A

symptoms lasting two weeks or longer and interfering with daily functional activities

87
Q

what are risk factors for depression?

A
being female
age between 17 and 40
living in a rural area
accompanying psychiatric disorders 
hypothyroidism
genetics/family history
previous personal history of depression
88
Q

what kinds of psychiatric disorders often accompany depression?

A

substance use disorders
eating disorders
anxiety disorders

89
Q

what are common clinical manifestations of depression?

A

being sad for most of the day on most days
anhedonia
weight loss or gain
sleep disturbances (increase or decrease)
agitation
fatigue
anergia
feelings of guilt and worthlessness
diminished concentration and decisiveness
suicidal ideation
sluggish responses

90
Q

what is the prevalence of ADHD?

A

diagnosed in about 5% of kids, with 50-70% experiencing symptoms into adulthood

91
Q

pathophysiology of ADHD

A

genetics, environmental, and neurological factors interfering with neurotransmitter encoding and transmission

92
Q

risk factors for ADHD

A
school aged child
boys (4 times more likely than girls)
genetics
lead poisoning
maternal substance use during pregnancy 
low birth weight 
serious head injury
93
Q

clinical manifestations of ADHD

A
high energy levels
problems resisting temptation
disruptive behavior/interrupting
problems completing tasks
squirming
making lots of noise
trouble listening and following directions 
impulsivity 
problems reading social cues and situations
94
Q

what is substance abuse disorder?

A

repeated use of a certain substance leading to clinically significant impairment over a 12 month period and the person needing continued use of that substance to be able to function

95
Q

abruptly stopping using a substance in substance abuse can lead to…

A

withdrawal

96
Q

what is the most dangerous substance to withdraw from and why?

A

alcohol, because it can cause heart attacks (especially in older adults)

97
Q

pathophysiology of substance abuse

A

it is theorized that a gene variation in a dopamine receptor gene leads to a diminished number of dopamine receptors, predisposing someone addiction a way to compensate for dopamine insufficiency

98
Q

what are risk factors for substance abuse disorder?

A

age (adolescence)

family history

99
Q

what are general clinical manifestations of substance use disorder?

A

euphoria and sedation (depending on which substance is being used)

100
Q

what is bipolar disorder?

A

a cyclic disorder characterized by alternating periods of depression and mania

101
Q

what are pathophysiologic brain changes seen with bipolar disorder?

A

increased response in amygdala to emotional cues and changes in temporal lobe activity

102
Q

what are risk factors for bipolar?

A

genetics

103
Q

manifestations of type 1 bipolar?

A
mania lasting one week or more
psychotic features
poses potential harm to self or others
hyperactive and hyperverbal
doesn't sleep
impulsivity 
flamboyance
104
Q

what is the main problem/characteristic of type 1 bipolar?

A

mania

105
Q

manifestations of type 2 bipolar?

A

mania lasts for 4 days or less and is not as severe (hypomania)
no psychotic features
hypomania is noticeable but does not hinder social or occupational functioning

106
Q

what is the main problem/characteristic of type 2 bipolar?

A

depression