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Krystan: Semester Two Nursing School > 2850 Pathophysiology Exam Four > Flashcards

2850 Pathophysiology Exam Four Flashcards

(106 cards)

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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
what can cause faulty valves in deep leg veins?
trauma central obesity pregnancy prolonged standing
26
what is the result of valve damage in leg veins?
impaired venous return and high venous pressure, which causes stasis and pooling of blood
27
how does venous congestion impact capillary filtration?
it inhibits movement of fluid and waste out of interstitial spaces
28
what are clinical presentations of venous insufficiency?
``` thin shiny skin dusky discoloration edema poor healing reduced or absent hair on legs ```
29
why is hair reduced or absent with venous insufficiency?
insufficient nutrient supply to that area
30
what is stasis dermatitis?
circumferential dusky discoloration around the legs
31
what causes stasis dermatitis?
buildup of hemosiderin in tissues
32
why does edema occur with venous insufficiency?
stasis increases the hydrostatic pressure, so fluid moves from the vascular space to the interstitial space
33
venous ulcers are caused by..
venous insufficiency
34
what pathophysiologic changes are found with venous stasis ulcers?
sluggish circulation poor tissue oxygenation deprivation of cellular nutrients impaired waste removal
35
what are clinical presentations of venous ulcers?
``` dark red coloration uneven margins very painful lots of edema and drainage possible necrosis ```
36
what is peripheral artery disease?
arteriosclerosis of peripheral arteries
37
what are risk factors for PAD?
``` age (over 45 for men, over 55 for women) hypertension high fat diet sedentary lifestyle obesity family history hyperlipidemia ```
38
what other conditions are associated with increased incidence of PAD?
``` diabetes smoking CKD cancer hypercoagulation disorders ```
39
what causes PAD?
reduced arterial bloodflow to periphery, causing tissue ischemia
40
what arteries are commonly affected in PAD?
carotid artery and femoral arteries
41
intermittent claudication
cramping leg pain associated with PAD
42
why does intermittent claudication occur?
reduced arterial blood flow
43
what happens when lack of circulation due to arterial obstruction occurs?
imbalance between tissue demand for oxygen and blood supply available
44
what can the patient do to decrease leg pain associated with intermittent claudication?
stop exercising
45
describe the reperfusion injury that occurs with peripheral arterial disease
free radicals are produced, causing oxidative stress, which causes further injury to the vascular bed and alterations in muscle metabolism
46
what conditions in a patient history are significant predisposing factors for PAD?
``` signs and symptoms of arteriosclerosis hypertension hyperlipidemia diabetes coronary artery disease MI ```
47
what are manifestations common to peripheral arterial disorders?
``` diminished or absent pulses palpable coolness paresthesias pallor pain in legs upon exertion ```
48
what are risk factors for pressure injuries?
``` poor nutrition impaired mobility diminished sensation impaired circulation moisture infection impaired cognition reduced oxygen in blood ```
49
how does pressure contribute to pressure injury?
it compresses small blood vessels, reducing blood flow to an area
50
how does shear contribute to pressure injury?
it deforms adipose tissue and muscle and reduces blood flow to an area, damaging the vascular bed
51
what is an example of shear?
a patient sliding down in bed (one layer of skin sliding against another)
52
how does friction contribute to pressure injury?
it damages the outer protective epidermal layer
53
what is an example of friction?
sliding a patient up in bed (skin dragging across a surface)
54
how does moisture contribute to pressure injury?
macerates the skin and decreases the pressure needed to produce an ulceration
55
what are skin findings when ischemia first occurs?
skin will be pale and cool, and vasodilation will occur when the pressure is relieved
56
what is reactive hyperemia?
relieving pressure on the ischemic area and the area vasodilating, causing it to flush bright red
57
with reactive hyperemia, redness for what length of time indicates tissue damage?
over 30 minutes
58
stage 1 pressure injury
intact skin, non-blanchable redness, discolored for over 30 minutes after pressure is relieved
59
stage 2 pressure injury
partial thickness loss of dermis, open and shallow with a pink wound bed, no slough
60
stage 3 pressure injury
deep crater with full thickness skin loss, damage and/or necrosis of subcutaneous tissue is present, possible undermining
61
stage 4 pressure injury
full thickness with extensive damage, bone/tendon/cartilage exposed or palpable, slough is present
62
deep tissue injury
skin is intact but discolored, area is very painful, damage amount under tissue is uncertain
63
what is an unstagable pressure injury?
full thickness skin loss but the base is obscured by slough or eschar
64
slough
tan, black, or brown leathery necrotic tissue
65
eschar
tan, yellow, or green necrotic tissue
66
primary intention healing
simple, rapid healing of a wound with clearly lacerated and defined edges. no gap in tissue present
67
example of primary intention wound
surgical incision
68
secondary intention healing
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
what pathophysiologic process differentiates primary intention healing from secondary?
contraction phase caused by myofibroblasts pulling the wound together
70
what types of wound heal by tertiary intention?
pressure ulcers, burns, or wounds with contamination or a lot of missing deep tissue
71
what are some common requirements for tertiary intention wounds?
skin grafts and sterile packing (wound may be left open for several days and then allowed to close)
72
why is protein necessary for wound healing?
its necessary for cellular regeneration and connective tissue synthesis
73
why are carbohydrates necessary for wound healing?
it can be a good energy source to spare protein for the healing process
74
why are fats necessary for wound healing?
they are an essential component of cell membranes that are being synthesized
75
why are adequate arterial and venous circulation necessary for wound healing?
to bring a rich supply of nutrients and oxygen to the wound and adequately remove waste from the wound by venous return
76
how does oxygen facilitate wound healing?
oxygen facilitates collagen synthesis and WBC function
77
why do elderly patients heal less efficiently?
they are naturally more immunosuppressed and prone to infection aging skin reduced collagen synthesis more secondary conditions that reduce blood flow
78
why do diabetic patients often have delayed wound healing?
lack of sensation and circulation in extremities | diabetes reduces abilities of neutrophils and macrophages, hindering inflammation process
79
why do corticosteroids inhibit wound healing?
they suppress inflammation process and inhibit collagen synthesis
80
what is the single most important cause of delayed wound healing?
infection (causes perpetual inflammation)
81
what procedures are necessary to facilitate optimal healing of an infected wound?
vigorous irrigation, cleansing, and removal of necrotic tissue and foreign matter
82
what is the prevalence of major depressive disorder?
17%
83
depression: pathophysiology
mutation in the serotonin transporter gene, causing serotonin deficiency
84
what other neurotransmitters can be out of balance in depression?
dopamine and norepinephrine
85
what areas of the brain are affected in depression and how are they affected?
increased activity in the neocortex and decreased activity in the limbic system
86
what is required for diagnosis of a major depressive episode?
symptoms lasting two weeks or longer and interfering with daily functional activities
87
what are risk factors for depression?
``` 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
what kinds of psychiatric disorders often accompany depression?
substance use disorders eating disorders anxiety disorders
89
what are common clinical manifestations of depression?
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
what is the prevalence of ADHD?
diagnosed in about 5% of kids, with 50-70% experiencing symptoms into adulthood
91
pathophysiology of ADHD
genetics, environmental, and neurological factors interfering with neurotransmitter encoding and transmission
92
risk factors for ADHD
``` 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
clinical manifestations of ADHD
``` 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
what is substance abuse disorder?
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
abruptly stopping using a substance in substance abuse can lead to...
withdrawal
96
what is the most dangerous substance to withdraw from and why?
alcohol, because it can cause heart attacks (especially in older adults)
97
pathophysiology of substance abuse
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
what are risk factors for substance abuse disorder?
age (adolescence) | family history
99
what are general clinical manifestations of substance use disorder?
euphoria and sedation (depending on which substance is being used)
100
what is bipolar disorder?
a cyclic disorder characterized by alternating periods of depression and mania
101
what are pathophysiologic brain changes seen with bipolar disorder?
increased response in amygdala to emotional cues and changes in temporal lobe activity
102
what are risk factors for bipolar?
genetics
103
manifestations of type 1 bipolar?
``` mania lasting one week or more psychotic features poses potential harm to self or others hyperactive and hyperverbal doesn't sleep impulsivity flamboyance ```
104
what is the main problem/characteristic of type 1 bipolar?
mania
105
manifestations of type 2 bipolar?
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
what is the main problem/characteristic of type 2 bipolar?
depression

Krystan: Semester Two Nursing School (13 decks)

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