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DPT 620: Neuro > The Evaluation of Persons with Brain Injury > Flashcards

The Evaluation of Persons with Brain Injury Flashcards

1
Q

the pt presentation with CVA can vary based on what factors?

A

cause of stroke

area of infarct

setting

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2
Q

what are the 2 types of stroke?

A

ischemic and hemorrhagic

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3
Q

which stroke is more common?

A

ischemic stroke

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4
Q

what is the most common area of infarct?

A

MCA (middle cerebral artery)

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5
Q

a stroke of the cerebellum will result in what deficits?

A

coordination deficits

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6
Q

what is the focus of acute/subacute CVA care?

A

medical stability (hemodynamics, respiratory fxn)

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7
Q

in acute/subacute stroke rehab, which is more common, flaccid or spastic hemiplegia?

A

flaccid hemiplegia

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8
Q

what are the characteristics of chronic CVA care?

A

stable but CV impaired

spastic hemiplegia

loss of fractionated movement

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9
Q

what is normal CBF?

A

60

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10
Q

what is the threshold for synaptic transmission for CBF?

A

20

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11
Q

what is the CBF levels indicative of irreversible damage?

A

12

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12
Q

what is the CBF range for reversible damage/suboptimal fxn?

A

12-20

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13
Q

what is the CBF range for adequate function?

A

20-60

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14
Q

why will a pt’s BP be kept high post CVA?

A

to increase perfusion

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15
Q

what is the penumbra?

A

the area of vulnerability around the dead tissue post CVA that is silent, not dead from a lack of blood flow

with adequate restoration of perfusion, it can be reversed

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16
Q

what are the characteristics of a left hemisphere lesion?

A

difficulty communicating

difficulty processing info in a sequential, linear manner

cautious, anxious, and disorganized when trying new tasks

realistic in appraisal of problems

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17
Q

what are the characteristics of a right hemisphere lesion?

A

difficulty in spatial-perceptual tasks

overestimation of their abilities (decreased awareness of limitations)

may have L neglect and even pusher

geographically challenged

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18
Q

what are common s/s following a stroke?

A

impaired motor control (flaccidity vs spasticity, decreased activation on the involved side, decreased contralateral strength)

impaired sensation and proprioception

limited ability to ambulate

limited postural stability

limited fxnal mobility

limited ability to perform self-care and ADLs

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19
Q

what are some less common, lesion-specific s/s following a stroke?

A

impaired language and communication

dysphagia (deep and posterior, more severe)

impaired cognition/memory

impaired behavioral control and judgement

visual/perceptual deficits ; unilateral neglect

apraxia (sequencing issue)-premotor injury

limbic: fear, emotional lability, depression

impaired B/B control

pain (MSK, neuro)

sleep disturbances

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20
Q

is the issue post CVA more so strength or activation of muscles?

A

activation of muscles

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21
Q

what is the first step in treatment post CVA?

A

postural alignment!!!

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22
Q

what are the primary impairments in CVA?

A

changes in muscle tone, muscle activation, muscle strength, and sensation

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23
Q

what are the muscle tones that can result from CVA?

A

flaccidity, hypotonicity, and spasticity

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24
Q

what are the deficits in muscle activation that can result from CVA?

A

poor initiation, muscle sequencing, timing, or firing

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25
Q

what are the deficits in muscle strength that can result from CVA?

A

flaccid paralysis or weakness, contralateral weakness

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26
Q

what are the deficits in sensation that can result from CVA?

A

varying degrees of light touch, nociception, static, and dynamic position sense

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27
Q

what secondary impairments can result from CVA?

A

changes in postural alignment, stability, and/or mobility

atypical movement synergies

clinical hypertonicity

changes in muscle and soft tissue length

pain, edema, skin integrity, vascular integrity (DVT)

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28
Q

what is clinical hypertonicity?

A

not spasticity, but movement related phenomenon where more movement and effort leads to increased tone

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29
Q

what are composite impairments that can result from CVA?

A

functional movement deficits

undesirable functional compensations and learned non-use

pain

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30
Q

in the hours to days following CVA, what happens?

A

flaccid hemiplegia

electrical silence

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31
Q

when does the most significant recovery occur post CVA?

A

the 1st 6 months

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32
Q

what are the key components of interventions post-CVA?

A

make the interventions skilled, task-specific, goal directed

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33
Q

how long post CVA can pts generally make improvements?

A

2-3 years

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34
Q

t/f: interventions have to be salient to the pt

A

true

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35
Q

what % recover to near complete fxning?

A

10%

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36
Q

what % recover fxnally with mild impairment?

A

25%

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37
Q

what % experience moderate to severe impairments?

A

40%

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38
Q

what % require placement and 24 hrs care?

A

10%

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39
Q

what % die as a result of CVA?

A

15%

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40
Q

t/f: early intervention yields more potent results

A

true

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41
Q

what is one of the main determinants of synaptogenesis?

A

training, specifically experience-induced or fxn-induced cortical reorganization

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42
Q

t/f: the cortex has the capacity to change structure and fxn during training and enriched environments

A

true

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43
Q

t/f: the anatomy of the damage, time since damage, age of pt, and amount of therapy received influences changes that can be made

A

true

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44
Q

t/f: the secondary motor areas become more fxnally relevant w/damage to the primary motor cortex, but can’t fully compensate

A

true

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45
Q

what is involved in acute care d/c planning?

A

chart review, labs/imaging/meds/social hx, MD orders, nursing report, AIDET, systems review, and fxnal assessment

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46
Q

what is involved in d/c planning for chronic CVA?

A

observation, AIDET, interviewing, HPI/imaging, meds, social/PLOF, ROS, systems review, examination

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47
Q

what do we want to know in acute CVA care?

A

date, type, location

current med stability, parameters

initial presenting symptoms and severity

timing of medical intervention

hx of management to date

trajectory of recovery

presence of complications

current vs previous status, prognosis

optimal d/c setting given status and supports

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48
Q

what do we want to know in chronic CVA care?

A

date, type, and location

current presenting symptoms and severity; summary of progression

medical interventions, w/complications

what type of Rx (medical, PT, OT, SLP) has pt received

desired goals

limiting factors

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49
Q

what social info is critical to obtain or ask for?

A

social hx and level of function

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50
Q

what are the screenings in acute CVA care?

A

medical stability

alertness

cognition and ability to follow commands

communication

perception

sensory and motor fxn

postural control and functional status

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51
Q

if a pt has HTN (>165/95mmHg) what is their risk for stroke?

A

6x increased risk

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52
Q

if a pt has heart disease, what is their risk for stroke?

A

2-6x increased risk

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53
Q

if a pt has A-fib, what is their risk for stroke?

A

increased risk of ischemic stroke, DVT, edema

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54
Q

what is the risk for a pt that has HF w/ or w/o reduced ejection fraction (EF)?

A

reduced exercise tolerance

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55
Q

if a pt has DM, what is their risk for stroke?

A

3-6x increased risk

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56
Q

what are the 5 components of metabolic syndrome?

A

increased waist circumference, increased BP, decreased HDL, increased triglycerides, increased fasting glucose

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57
Q

if a pt with metabolic syndrome has all 5 components present, what is their stroke risk?

A

5 fold stroke risk

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58
Q

what CV conditions increase risk for stroke?

A

HTN, heart disease, A-fib, HF

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59
Q

what endocrine disorders increase stroke risk?

A

DM, metabolic syndrome, obesity, and hypothyroidism

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60
Q

what neurologic conditions increase stroke risk?

A

hx of stroke, TIA, tumor, or brain injury

sleep fxns

cognitive decline (is dementia)

behavioral/psychological changes

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61
Q

what pulmonary conditions increase stroke risk?

A

smoking

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62
Q

what are precautions for CVA in acute care?

A

b4 seeing the pts, obtain and follow the physician’s orders regarding bed rest, activity, and vital signs parameters

pre-plan your sequence and equipment, assistance needs, and safety plan

monitor vital signs for all individuals

implement fall precautions

monitor pt’s pain and fatigue

plan ahead in regards to neglect and impulsivity

monitor for PT vulnerability (potential abuse)

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63
Q

pts with flaccid hemiplegia may be at risk for what?

A

shoulder pain and dysfunction

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64
Q

what critical evaluation limitations can greatly impact your eval?

A

beginning postural alignment

alertness, cognition, communication

behavior, attention, judgement, motivation

perception, neglect

motor sequencing and planning issues (apraxia)

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65
Q

what should be done at the start of a CVA intervention?

A

postural adjustments (esp the pelvis)

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66
Q

what is included in the neuro section of the systems review?

A

signs of seizures or hydrocephalus

screen of CNs

swallowing fxns

mentation

communication

behavior

motor fxns

executive fxns

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67
Q

what are the 5 breathing patterns to be aware of?

A

eupnea

bradypnea

biot’s respirations

cheyne-strokes respirations

apnea

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68
Q

what is eupnea?

A

normal respiration w/ equal rate and depth

12-20 breaths/min

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69
Q

what is bradypnea?

A

slow respirations

<10 breaths/min

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70
Q

what are Biot’s respirations?

A

irregular respiration of variable depth (usually shallow), alternating w/periods of apnea

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71
Q

what are Cheyne-Strokes respirations?

A

gradual increase in depth of respiration followed by gradual decrease and then a periods of apnea

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72
Q

what is apnea?

A

absence of breathing

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73
Q

why does hemorrhagic CVA pose concern for respiration?

A

the bleed can expand and shift structures and put pressure on the BS (respiratory and vital fxns)

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74
Q

why would acute CVA BP be higher?

A

doctors often set it higher to increase perfusion

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75
Q

anyone with dysphagia should have what vital sign monitored?

A

temperature

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76
Q

what are s/s to watch for aspiration and swallowing dysfunction?

A

excessive drooling, wet/gurgly voice, frequent coughing/choking

poor oral food management, pocketing of food

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77
Q

what are the interventions for aspiration/swallowing dysfunctions?

A

referral to SLP

positioning for meals

precautions pertaining to oral intake should be implemented where indicated

monitor and inform

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78
Q

what is the primary auditory cortex responsible for?

A

auditory discrimination

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79
Q

what is the secondary auditory cortex responsible for?

A

classification of sounds (language vs other sounds)

80
Q

what is wernicke’s area responsible for?

A

auditory comprehension, vocabulary

81
Q

what is the role of the subcortical connections?

A

to connect broca’s and wernicke’s area

82
Q

what is broca’s area responsible for?

A

instructions for language output

83
Q

what is the oral and throat region of the sensorimotor cortex responsible for?

A

cortical output to speech muscles

84
Q

what are strategies for Broca’s aphasia?

A

allow for supplemental time

if you know what they’re talking about, provide the 1st letter of the word or a sentence completion cue

ask the pt to DESCRIBE the object they’re unable to think of (look, fxn, location)

ask pt to gesture the sue of the object

reading aloud may be fluent

songs and automatic language

85
Q

what aphasia can understand but can’t communicate?

A

Broca’s

86
Q

t/f: pts with broca’s aphasia tend to get frustrated

A

true

87
Q

what are strategies for wernicke’s aphasia?

A

limit verbal commands

avoid open ended ?s

ask the pt to GESTURE the use of the object

reading/writing are not going to be effective

88
Q

which aphasia will the pt not understand what you’re saying, speak in gibberish, and pretent that they understand you?

A

Wernicke’s aphasia

89
Q

what are strategies for dysarthria?

A

proximal stability for controlled mobility

proper breathing support

increased volume of speech

decreased rate of speech

hard articulatory contacts

increased oral cavity opening

short phrasing

allow supplemental time

90
Q

what are strategies for verbal apraxia?

A

focus on improved motor production

repeating sounds and practicing the correct mouth movements

encourage the pt to speak slowly ‘‘silent rehearsal

rest breaks

visual model

allow supplemental time

more severe=AAC

encourage use of hand gestures, writing, pointing to letters/pictures, and a computer

91
Q

what are commonalities in aphasia strategies?

A

short phrases

speak slowly

avoid complex commands and questions

repeat as needed

modeling

visual cues

decreased external stimuli

allow supplemental time

difficulty understanding what they’ve read

92
Q

what is included in a functional assessment?

A

changing and maintaining body position (transfers, bed mobility, bending, squatting, sitting, standing)

walking and moving (short, long, terrain change, stairs, obstacles, etc)

93
Q

what should be considered in assessing levels of assistance?

A

how much of the tasks can the pt complete themselves

what makes the pt successful (time, facilitation, cues, sequencing, assitance)

ind, sup v, CG, min A, mod A, Max A, dep

% performed

94
Q

what predicts d/c during acute hospitalization?

A

AM-PAC “6 click”

95
Q

t/f: the AM-PAC “6 click” is done like the Berg Balance, asking the patient to perform each task

A

false, it is done based on observations during the visit

96
Q

what does the AM-PAC “6 click” evaluate?

A

mobility and independence w/mobility

97
Q

are unilateral or BL ADs better post-stroke?

A

BL

98
Q

what is wrong with using a hemiwalker post stroke?

A

it tends to promote asymmetry and non use of the involved side

99
Q

t/f: a walker is often used post-stroke and can have a platform to position the hand in a way that doesn’t promote increased tone

A

true

100
Q

what is taken into account for prescription of assistive technology?

A

motor fxn, prognosis, and ambulatory status

101
Q

when a pt is d/c home, home health, or outpatient, do we prescribe ADs?

A

yes

102
Q

when a pt is d/c to IFR to home or subacute to home, do we prescribe ADs?

A

sometimes

103
Q

when a pt is d/c to ECF and/or are non-ambulatory, do we prescribe ADs?

A

nope!

104
Q

how do we leave pts when we finish the bedside eval?

A

symmetrical (if possible upright) and with the call bell in reach

communicate how you leave the pt

105
Q

in acute care, what is the exam/screening of mental functions consisting of?

A

A and O x4, commands, observation for other signs of impaired mental fxns [Mini cog]

106
Q

in chronic care, what is the exam/screening of mental functions consisting of?

A

systems review (A and O x4, commands), MoCA

107
Q

what are some orientation deficit strategies?

A

introduce and explain why you are there (point to your name badge)

ask about the circumstances of their injury and fill in as needed (once they can tell you about their stroke, you don’t have to focus on cognition anymore bc you have it)

make eye contact to ensure you have their attention

108
Q

what are some executive function deficit strategies?

A

may need to help them “get started” or to keep them going

may need to re-direct if impulsive or perseverative (repetative words, actions, etc)

break things down to assist them w/sequencing or organizing their thoughts and actions

may be unaware of their errors/safety issues, so provide concrete feedback

109
Q

what are some attention deficits strategies?

A

decrease extraneous noise/stimuli as much as possible

say pt’s name prior to providing verbal info

make and ensure eye contact when speaking

keep questions and instructions simple

change activity as appropriate

one activity/step at a time

forced choices

rest breaks

incorporate problem solving

pt/caregiver education for carryover

110
Q

when using attention deficit strategies, what do you document?

A

document the time the pt can attend to the type of task

if cues are provided, count the # of cues/time

111
Q

what are some memory deficit strategies?

A

realize they may not be able to recall case hx info or even personal info (check to rule out confabulation)

face to face communication

use less words (declarative) and more procedural

repetition

rehearsal

write important info down

set timers/alarms

set schedule

pt/caregiver education for carryover

break things down into smaller units and repeat, repeat, repeat

112
Q

what is confabulation?

A

when a pt fills in the void when they can’t remember a story

113
Q

what should be documented with memory deficit strategies?

A

of cues, % content remembered

114
Q

what is hemi-spatial neglect?

A

pt can’t tell where their body is in space

115
Q

what CVA would cause hemi-spatial neglect?

A

R parietal lobe lesion

116
Q

what is hemi-body neglect?

A

pt can’t feel one side of their body

117
Q

what spatial relations may be present post-stroke?

A

difficulty in perceiving the relationship bw self and objects in the environment

118
Q

what are agnosias?

A

inability to recognize incoming info despite in tact sensory capacities

119
Q

what is anosognisia?

A

pt is unaware of their illness

120
Q

what is somatognosia?

A

pt is unaware of one’s own body

121
Q

if you move towards a pt’s neglectful side and they track you, is it mild or severe?

A

more likely mild

122
Q

if you move towards a pt’s neglectful side and they can’t track you, is it mild or severe?

A

more likely severe

123
Q

what should be documented with neglect?

A

what resting neglect is

what it takes to improve it and much it improves

how long attention is maintained

124
Q

t/f: for a pt with neglect, position yourself in the L visual field if possible, or position where the pt can remain engaged visually

A

true

125
Q

what are some problem-solving strategies?

A

have the pt verbalize possible solutions to a given activity

have the pt verbalize appropriate solutions to a given activity

immediately bring unsafe/inappropriate actions to the pts attention

ask the pt what the safest and most effective solution

pt/caregiver education for carryover

126
Q

what should be documented for problem-solving strategies?

A

the # of cues or % of the task the pt can complete w/ or w/o cues

127
Q

what are strategies for poor safety awareness. impulsivity, anosognosia, and somatognosia?

A

think it through b4 you act (you and the pt)

ask the pt what their deficits are

ask pt what has happened to them; point out deficits as needed

ask pt why they need to use an AD

incorporate problem solving

ask pt to verbalize the steps they intend to do b4 doing them

ask pt to perform each step slowly; even consider counting or verbalizing through the activity

engage pt in an activity (to a certain extent) if they’re insistent, they can perform despite deficits so that they may see they’re unable

pt/caregiver education for carryover

128
Q

what is the role of the BG in movement?

A

makes the efferent copy of the movement

129
Q

what is the role of the cerebellum in movement?

A

revision of movement

130
Q

which stroke subgroup experiences impulsivity and difficulty with problem solving?

A

R MCA or BS

131
Q

what population would benefit from sequencing strategies?

A

pts with impulsivity

132
Q

what are some sequencing strategies?

A

break down the whole task into parts

have PT verbalize steps to an activity prior to performing it

generate written steps

immediately point out incorrect steps

incorporate problem solving

pt/caregiver education for carryover

133
Q

what should be documented with sequencing strategies?

A

of cues in a given activity prep, initiation, or execution

134
Q

what are some motor planning and motor sequencing strategies for the pre-motor cortex?

A

breakdown whole tasks into parts

provide proximal stability for distal mobility

include stability as part of the movement sequence

135
Q

what are some motor planning and motor sequencing strategies for the SMA?

A

break down whole tasks into parts

use bi-manual activities

use demonstration, hand-over-hand, repetition

have pt ID movement sequence errors

incorporate problem solving

136
Q

what is the Yerkes-Dodson inverted-U principle?

A

bell curve that shows appropriate levels of arousal allowing for optimal motor performance

high/low arousal or limbic levels can deteriorate motor performance and limit ability to motor learn

137
Q

how can you examine for levels of arousal/limbic levels?

A

ANS responses of homeostatic state including HR, BP, RR, pupil dilation, and sweating

determination of pt reactivity, including degree and rate of response to stimulation (touch, sound, light, smell)

138
Q

what are some emotional-limbic effects of stroke?

A

apathy

euphoria

increased irritability/frustration

depression

social inappropriateness

pseudo-bulbar affect

139
Q

what is apathy?

A

shallow affect and blunted emotional responses

140
Q

what CVA would cause apathy?

A

L or frontal lobe injury

141
Q

t/f: euphoria is a common effect of stroke

A

false

142
Q

what CVA would result in increased irritability/frustration?

A

L CVA (R hemiplegia)

143
Q

t/f: depression is an extremely common effect of stroke

A

true

144
Q

what kind of depression is caused by stroke?

A

neurogenic depression

145
Q

t/f: there is a greater fxnal impairment at both admission and d/c with depression post-stroke

A

true

146
Q

t/f: pts with stroke and depression have a lower level of participation in the rehab process

A

true

147
Q

t/f: pts with stroke and depression experience similar gains over a the course of rehab

A

true

148
Q

t/f: pts with stroke and depression experience spontaneous resolution w/in several months of onset

A

true

149
Q

what is pseudobulbar affect?

A

emotional lability, emotional dysregulation, uncontrolled emotional outbursts that are random and obstructive

150
Q

can PBA be medically managed?

A

yes

151
Q

who can help with emotional-limbic effects of stroke?

A

neuropsychologist

152
Q

in the outpatient setting, what makes up the eval?

A

observation, AIDET, interview (HPI/imaging), meds, social/PLOF, ROS, systems review, exam

153
Q

does inpatient or outpatient use more evaluative functions?

A

outpatient

154
Q

what is evaluated in outpatient?

A

motor fxn, praxis (sequencing), strength, postural control and fxnal status, outcomes measures

155
Q

is inpatient or outpatient more focused on fxnal improvement?

A

outpatient

156
Q

what does the standard fxnal examination include?

A

movt assessment

levels of assistance

documentation

157
Q

what should be documented in the standard fxnal assessment

A

time, facilitation, cues, sequencing, assistance

158
Q

what levels of assistance may be documented?

A

indep, sup v, CG, min A, mod A, max A, dep

159
Q

what is the FIM?

A

fxnal independence measure

160
Q

t/f: the FIM takes into account the assisstance and time

A

true

161
Q

what measure is great for non-ambulatory patient?

A

the FIM

162
Q

on the FIM what scores show the largest gains in function?

A

admission FIM >37-72/126

163
Q

t/f: D/C deposition and FIM score on admission are significantly correlated

A

true

164
Q

a FIM score of <40/126 is likely to d/c where?

A

to LTC facility

165
Q

a FIM score of >80/126 is likely to d/c where?

A

home

166
Q

movement system dx is the impaired movement or motor control related to…

A

movement pattern coordination deficits

force production deficit

fractionated movement deficit

postural vertical deficit

sensory selection and weighting deficit

sensory detection deficit

hypokinesia

dysmetria

cognitive deficits

167
Q

______ performance discriminates the effects of stroke and is related to the potential for recovery

A

gait velocity

168
Q

t/f: when 10m gait velocity measured are stratefied into clinically meaningful fxnal ambulation classes, changes in velocity are clinically meaningful

A

true

169
Q

what is household ambulation gait velocity?

A

<0.4m/s

170
Q

what is limited community ambulation gait velocity?

A

0.4-0.8 m/s

171
Q

what is full community ambulation gait velocity?

A

> or =0.8 m/s

172
Q

t/f: transitioning to a higher class of ambulation is associated with substantially better fxn, QOL, mobility, and community participation

A

true

173
Q

why should we make gait training a priority?

A

bc very early mobilization after stroke fast tracks return to walking

174
Q

what is the ICF domain of the OPS?

A

body fxn

175
Q

what is the Orpington Prognostic Indicator (OPS)?

A

an assessment of stroke severity based on motor performance, proprioception, balance, and cognition

176
Q

OPS scores range from ___ to ____

A

1.6-6.8

177
Q

do higher OPS scores indicate greater or lesser deficit?

A

greater deficit

178
Q

each section of the OPS is graded from ____ to ____

A

0-1.2

179
Q

what is a 0 on the OPS?

A

normal performance

180
Q

the motor performance of the OPS is based upon what?

A

the Medical Research Council Grading for Power

181
Q

the cognitive component of the OPS is based on what?

A

the Hodkin’s Mental test

182
Q

what is mild to moderate OPS score?

A

<3.2

183
Q

what is moderate to moderately severe OPS score?

A

3.2-5.2

184
Q

what is severe to major OPS score?

A

> 5.2

185
Q

for OPS scores <3.2, what does it indicate?

A

high likelihood of returning home

186
Q

for OPS scores that fall bw 3.2-5.2, they generally respond better to what?

A

rehab

187
Q

for OPS scores >5.2, pts are typically dependent or independent?

A

dependent

188
Q

t/f: there is no MDC, MCID, or SEM established for the OPS

A

true

189
Q

what are the postural deviations of the pelvis

A

asymmetrical weight bearing with majority of the weight on the stronger side

in sitting, posterior pelvic tilt

in standing, unilateral retraction and elevation on the more affected side

190
Q

what are the postural deviations of the trunk?

A

with sacral sitting (post pelvic tilt) a flattened lumbar curve with exaggerated thoracic curve and forward head

lateral flexion with trunk shortening on the more affected side

191
Q

what are the postural deviations of the shoulders?

A

unequal height with more effected shoulder depressed

humeral subluxation with scapular downward rotation and lateral flexion of the trunk

scapular instability (winging) may be present

192
Q

what are the postural deviations of the head/neck?

A

protraction with lateral trunk flexion

lateral flexion of the head with rotation away from the more affected side

193
Q

what are the postural deviations of the UEs?

A

more affected UE typically held in a flexed adduction position, with IR and elbow flexion, forearm pronation, wrist and fingers flexion, and limb is NWB

stronger UE used for postural support

194
Q

what are the postural deviations of the LEs?

A

in sitting: more affected LE typically held in hip abduction and ER with hip and knee flexion (flexion synergy pattern)

in standing: more affected LE typically held in hip and knee extension with adduction and IR (scissoring pattern); ankle PF

unequal WB on feet, similar to pelvis in sitting

195
Q

when a pt is on what medication, will it change the BP parameters allowed by the physician within acute care?

A

thrombolytics like rt-PA

196
Q

what medication can mask a pt’s HR during exercise?

A

anti-hypertensives like ace-inhibitors, ɑ-blockers, ß-
blockers, CA++ channel blockers,
vasodilators, and diuretics

DPT 620: Neuro (13 decks)

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