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Sensory, Neuro, Nursing Practice > Sensory, Neuro, Nursing Practice > Flashcards

Sensory, Neuro, Nursing Practice Flashcards

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1
Q

smell

A

I olfactory

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2
Q

visual acuity

A

II optic

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3
Q

opening of eyelids, eye movement upward/medial, upward/lateral, medial, downward/lateral

A

III oculomotor

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4
Q

eye movement (downward/medial)

A

IV trochlear

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5
Q

facial sensation, chewing movement

A

V Trigeminal

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6
Q

eye movement (lateral)

A

VI abducenes

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7
Q

facial muscle movement (except chewing muscle) and eyelid closing

A

VII facial

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8
Q

hearing and balance

A

VIII auditory (vestibulocochlear)

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9
Q

taste on the posterior third of the tongue

A

IX glossopharyngeal

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10
Q

uvula (palate muscle) swallowing)

A

X vagus

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11
Q

shoulder shrug

A

XI accessory

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12
Q

tongue movement

A

XII hypoglossal

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13
Q

i can lead to ineffective communication

A

hearing deficit

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14
Q

i can lead to decrease interaction, withdrawl, suspicion, loss of self-esteem and insecurity

A

hearing deficit

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15
Q

i affect the outer and middle ear

A

conductive

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16
Q

i affect the inner ear and affect nerve pathways

A

sensorineural

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17
Q

i affect the inner, middle, and outer ear

A

mixed

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18
Q

i am an assessment tool used to look at the ear

A

otoscope

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19
Q

i am an assessment test used that compares air conduction to bone conduction

A

rinne’s test

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20
Q

i am normal when air conduction is louder than bone conduction

A

rinne’s positive

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21
Q

i am abnormal when bone conduction is louder than air conduction

A

rinne’s negative

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22
Q

i am an assessment test when conducted i will strike 512htz tuning fork an place on my forhead

A

weber’s

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23
Q

i am abnormal when a tuning fork is on my forehead and the sound is different in my two ears

A

weber’s test

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24
Q

i am normal when tuning fork is on my forehead and can equally be heard in both ears

A

weber’s test

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25
Q

i am the medical term of ringing of the ears

A

tinnitus

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26
Q

i am the medical term for the room is spinning

A

vertigo

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27
Q

i am a symptom that occurs when there is fluid in the ear compressing the 8th cranial nerve

A

vertigo

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28
Q

i am the reason the patient is a high fall risk

A

vertigo

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29
Q

i can cause a patient grief, depression and may also lead to suicidal ideation

A

tinnitus

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30
Q

i am ostosclerosis

A

conductive hearing loss

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31
Q

i am caused by otitis media with effusion

A

conductive hearing loss

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32
Q

i am caused by poor eustachian tube function

A

conductive hearing loss

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33
Q

i am caused by impacted cerumen

A

conductive hearing loss

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34
Q

i am caused by tumors in the ear

A

conductive hearing loss

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35
Q

i am caused by objects in the ear

A

conductive hearing loss

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36
Q

i hear better in noisy environment

A

conductive hearing loss (bone better than air)

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37
Q

my treatment plan is to either treat the cause or wear a hearing aide

A

conductive hearing loss

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38
Q

i am the most common type of permanent hearing loss

A

sensorineural hearing loss

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39
Q

i cannot be fixed by surgery or medicine

A

sensorinerual

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40
Q

i am caused by illness or genetics

A

snesoriunerual

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41
Q

i am caused by loud noises like concert, gun firing, construction, factory work, etc..

A

sensorineural

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42
Q

i am caused by ototoxicity

A

sensorineural i

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43
Q

i am vancomycin. i caused what kind of damage

A

sensorineural/toxicity

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44
Q

i am gentamycin i cause what kind of damage

A

sensorineural/toxicity

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45
Q

I am Aspirin I cause what kind of damage

A

sensorineural/toxicity

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46
Q

I am furosemide i can cause what kind damage?

A

sensorineural/toxicity

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47
Q
  1. I am Quinine I cause what kind of damage
A

sensorineural/toxicity

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48
Q
  1. I am caused by presbycusis (aging
A

sensorineural

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49
Q
  1. My signs and symptoms include: Vertigo, Tinnitus, and Fluctuating hearing
A

meniere’s syndrome

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50
Q

interventions include: prevent injury during Vertigo attacks, provide bed rest in a quiet environment, provide assistance with walking, instruct the patient to move their head slowly to prevent worsening of the Vertigo, initiate sodium and fluid restrictions as prescribed, instruct the patient to stop smoking, instructed patient to avoid watching television because the flickering of lights may exacerbate symptoms, allow the patient to rest; And control Vertigo nausea in vomiting, mild diuretics may be prescribed to decrease endolymphatic volume, inform the patient about vestibular rehabilitation as prescribed.

A

meniere’s syndrome

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51
Q
  1. My surgical intervention includes a resection of the vestibular nerve or a total removal
A

(Meniere’s syndrome)

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52
Q
  1. My post-operative interventions- packing and dressings on the ear. Speak to the patient on the side of the unaffected ear. Perform neurological assessments. Maintain safety. Assess when ambulating. Encourage the patient to use a bedside commode rather than ambulating to the bathroom. Administer anti- vertigo and anti-emetic medications as prescribed.
A

(Meniere’s syndrome)

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53
Q
  1. For me you should assess for early detection to prevent permanent damage
A

nursing care/education

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54
Q
  1. For me you should educate patients and have them teach back to ensure understanding
A

(Nursing care/ education)

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55
Q
  1. I must be taught about adequate nutrition and hydration to ensure that I can maintain oil and sebaceous glands to maintain hearing.
A

nursing care/education

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56
Q
  1. I must be taught about medication regimens
A

(nursing care/education)

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57
Q
  1. I must be taught about surgery if necessary
A

(nursing care/ education)

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58
Q
  1. You should never shout at me
A

hearing deficit

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59
Q

what you should do when a patient has a hearing deficit?

A

talk low and slow

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60
Q
  1. The nurse is developing a teaching plan for a client with glaucoma. Which instruction should the nurse include in the plan of care?
A
  1. Eye medication will need to be administered for life.
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61
Q

What is Cranial nerve #8 responsible for?

A

Auditory (vestibulocochlear) is responsible for balance and hearing.

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62
Q

What clinical manifestations are associated with hearing loss?

A

Ineffective communication, Decreased interaction, withdrawal, suspicion, loss of self-esteem and insecurity.

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63
Q

How do you check if a patient with hearing loss understood what you were communication to them?

A

Have the patient teach back. Also, have a family/friend at bedside to also get education.

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64
Q

What part of the ear is affected if the patient has conductive hearing loss?

A

Outer and middle ear

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65
Q

What part of the ear is affected if the patient has sensorineural hearing loss?

A

Inner ear damage (nerve pathways)

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66
Q

What are two of the priority symptoms that we are assessing for with hearing loss that is caused by compression of cranial nerve #8?

A

Tinnitus and vertigo

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67
Q

What is tinnitus and what is your priority assessment for the patient suffering with tinnitus?

A

Ringing of the ears can cause suicidal ideation.

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68
Q

What is Vertigo and what is your priority assessment for the patient suffering with vertigo?

A

Room is spinning while the patient is still. Patient is a high fall risk.

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69
Q

What are the some of the causes of Conductive hearing loss?

A

Otitis media with effusion, poor eustachian tube function, impacted cerumen, tumors, objects present, middle ear disease, otosclerosis

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70
Q

What are some of the causes of Sensorineural hearing loss?

A

Illness, genetics, loud noises, ototoxicity, and aging

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71
Q

What medications cause ototoxicity in sensorineural hearing loss?

A
  1. Vancomycin 2. Gentamycin 3. Cisplatin 4. Aspirin 5. Furosemide 6. Quinine
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72
Q

Sensorineural is permanent hearing loss that cannot be fixed by surgery or medicine?

A

True.

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73
Q

What is Meniere’s disease?

A

Refers to the dilation of the endolymphatic system by overproduction or decrease reabsorption of endolymphatic fluid. (Basically, too much fluid causing pressure on cranial nerve #8.

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74
Q

What treatments can be done for a patient with Meniere’s disease?

A

Mild diuretics, vestibular rehabilitation, surgery.

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75
Q

What communication technique is the most effective for a patient with hearing loss?

A

Talk Low and Slow. Can also use written instructions for patient.

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76
Q

What part of the eye do you administer eye drops?

A

Nasolacrimal duct/conjunctival sac.

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77
Q

How long do you hold pressure on the inner eye after administering eye drops?

A

At least 15 seconds.

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78
Q

Why do you want to apply pressure to the nasolacrimal duct/ conjunctiva after administering eye drops?

A

To prevent systemic absorption (Decrease of blood pressure and heart rate)

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79
Q

What are the four leading causes of blindness?

A

Age related macular degeneration, Cataract, Diabetic Retinopathy, Glaucoma.

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80
Q

What is Cranial nerve #2 responsible for?

A

Optic nerve is responsible for the visual acuity.

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81
Q

What is Cranial nerve # 3 responsible for?

A

Oculomotor is responsible for opening of eyelids, eye movement upward/medial, upward/lateral, medial, downward/lateral.

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82
Q

What is Cranial nerve #4 responsible for?

A

Trochlear nerve is responsible for eye movement downward/medial)

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83
Q

What is Cranial nerve #6 responsible for?

A

Abducens nerve is responsible for eye movement lateral

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84
Q

What is Cranial nerve #7 responsible for?

A

Facial nerve is responsible for facial muscle movement (except chewing), and eyelid closing.

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85
Q
  1. What is Cataract defined as?
A

Opacification of the lens.

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86
Q

What is the number one risk factor for cataracts?

A
  1. Age is the number one risk factor followed by diabetes mellitus, UV light, 2nd use of corticosteroids, and trauma.
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87
Q
  1. What safety education do you want to provide the patient diagnosed with cataracts?
A
  1. Do not drive at night because of low visibility from light not being able to go through. There will be a glare/Halo around light sources at nighttime.
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88
Q
  1. What is the treatment for cataracts?
A
  1. Surgery
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89
Q
  1. If the patient has any unexpected complications after cataract surgery, what should you do?
A
  1. Call the surgeon even if it is just pain!
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90
Q
  1. What part of the vision does glaucoma affect?
A
  1. Peripheral vision (Glaucoma, Peripheral) Gatorade and Powerade
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91
Q
  1. What is the difference between open and closed glaucoma?
A
  1. Open is gradual IOP build up. Closed is a rapid buildup 24-48 hour to fix before permanent damage.
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92
Q
  1. What part of the vision does macular degeneration affect?
A
  1. Central vision (Macular-McDonald’s, Central Chick fila)
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93
Q
  1. What is the difference between dry and wet macular degeneration?
A
  1. Dry is drusen buildup that is gradual. Wet is drusen with hemorrhage and neovascularization that is rapid.
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94
Q
  1. Is there a cure for macular degeneration?
A
  1. No cure just slowing of progression.
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95
Q
  1. For a type I diabetic when should they have an eye appointment?
A
  1. Within 5 years of diagnosis and then yearly.
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96
Q
  1. For a type 2 diabetic, when should they have an eye appointment?
A
  1. Upon diagnosis and then yearly.
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97
Q

what are some subjective data questions?

A

health info, birth history, TBI, stroke, degenerative disease, medications, surgery or other treatments, growth and developmental history, functional health patter, sleep rest pattern

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98
Q

what are some objective data?

A

physical examination
cranial nerve function
motor function
sensory function
reflexes

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99
Q

how do you do the assessment of the nervous system?

A

follow logical sequence
higher level of neurologic function to lower level
constant comparison of findings

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100
Q

what will patients present with if having altered mental and speech status?

A

confusion/memory
-loc
-appearance and behavior
-speech
-cognitive function
-constructional ability

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101
Q

what is the first indication that a patients neurologic function has declined?

A

a change in loc

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102
Q

what is alert?

A

awake and responsive, follows commands

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103
Q

what is lethargic?

A

sleepy but arousable, drowsy, delayed responss, may drift to sleep

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104
Q

what is dysarthria?

A

difficulty articulating

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105
Q

what are the three areas of memory loss?

A

long term or remote memory
recall or recurent memory
immediate or new memory

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106
Q

what is the best score on the glasgow coma scale?

A

15

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107
Q

what is the worst score on the glasgow coma scale?

A

3

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108
Q

what are the subtle indications that deterioration is occuring in the neurologic status?

A

headache
restlessness
irrability
being unusally quiet
slurred speech
change in orientation level

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109
Q

how to access light touch?

A

you can use a cotton ball and touch the patient

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110
Q

how to access for pain?

A

have a patient close their eyes and touvh areas of the body

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111
Q

how to access discrimination?

A

ask the patient to close their eyes and to identify what object you are using to touch the patient

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112
Q

how to access muscle tone?

A

finger to nose; hee; to shin
pronate and supine both hands
posture, gait
risk for falling

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113
Q

what is a csf analysis?

A

provides information about a variety of cns diseases

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114
Q

how should CSF look like?

A

clear, colorless, odorless, and free of red blood cells, contain little protein

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115
Q

how can a patient be positioned for a CSF analysis?

A

lying side position or sitting position

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116
Q

what is the preop for a lumbar puncture?

A

-pt to be relaxed
-strict aseptic technique is mandatory by all personnel
-contraindicated in all clients with increased ICP
-contraindicated in clients with skin infection at or near puncture site

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117
Q

what is post of for a lumbar puncture?

A

-bed rest in flat position for 4-8 hours
-encourage fluids to facilitate CSF production
-administer analgesics as ordered if headache occurs
-monitor neurologic signs
-watch for signs of chemical or bacterial meningitis (fever, stiff neck, photophobia)

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118
Q

what is a cerebral angiogram?

A

serial x-ray visualization of intracranial and extracranial blood vessels perfomed to detect vascular lesions (aneurysms, hematoma, AVM)

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119
Q

what nursing assessment do you do for a pt going for a cerebral angiogram?

A

withhold meal; need pt to stay very still

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120
Q

what do you monitor post op of cerebral angiogram?

A

monitor neurologic signs
maintain bed rest for 6 hours
monitor for bleeding
report any neuro status change

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121
Q

what is a ct scan?

A

distinguishes bone, soft tissue. and fluids
provide a rapid means of obtaining radiographic images of the brain

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122
Q

what is an mri used for?

A

to detect stokes, ms, tumors, trauma, hermiation, and seizures

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123
Q

what is a pet scan?

A

measures metabolic activity of brain to assess cell death or damage
-for patients with stroke, AD, seizure disorders, PD, and tumors

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124
Q

what is a myelogram?

A

x-ray of spinal cord and vertebral column
-injection of contrast into subarachnoid space, used to detect lesions
-herniated or ruptured disc
-spinal tumor

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125
Q

what is an electroencephalography?

A

EEG
-electrical activity of brain recorded using scalp electrodes
-evaluate seizure disorders, cerebral disease, bran injury, brain death

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126
Q

how to prepare for an EEG?

A

-may be sleep deprived on night before to increase change of recording a seizure activity
-tranquilizers & stimulants should be withheld 24-48 hours before test
-coffee, tea, chocolate, and cola drinks omitted in meal before test
-meal is not omitted because altered blood glucose level can change brain wave pattern
-remove all metal
-procedure takes 45-60 min
-assure pt test does not cause electrical shock

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127
Q

what is an electromyography?

A

EMG
-recording of electrical activity associated with innervation of skeletal muscle

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128
Q

what is a nerve conduction studies?

A

stimulating peripheral nerves at several points along its course and recording muscle action potential or sensory action potentiona

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129
Q

what is ischemia in brain?

A

inadequate blood flow to a part of the brain

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130
Q

what is hemorrhage in brain?

A

bleeding into the brain that results in death of brain cells

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131
Q

what causes a stroke?

A

disruption in the blood supply to part of the brain

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132
Q

what is FAST?

A

face drooping
arm weakness
speech difficulty
time is critical

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133
Q

what is the patho of a stroke?

A

regardless of the cause, the underlying event is deprivation of oxygen and nutrients

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134
Q

what are non-modifiable stroke risk factors?

A

age
gender: more common in men
ethnicity: higher incidence in african americans
hereditary: family history

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135
Q

what are modifiable stroke risk factors?

A

HTN**
history of TIA
cardiovascular disease
diabetes
smoking, alcohol, substance abuse
birth control pills, hormone replacement
obesity
sleep apnea

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136
Q

what kind of strokes are there?

A

transient ischemic attack (TIA)
ischemic (thrombotic, embolic)
hemorrhagic (intracerebral, subarachnoid)

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137
Q

what is a TIA?

A

-transient episode of neurologic dysfunction
-serve as a warning sign of further cerebrovascular disease
-no way to predict outcome

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138
Q

what is a embolic stroke?

A

-embolus that lodges and occludes the cerebral artery it is either from infarction and edema
-most common from the heart, less common from long bone Fx
(endocardial layer of heart)
-remain conscious, complain of headache

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139
Q

are symptoms with an embolic stroke fast or slow?

A

slow and warning signs are less common, prognosis is related to amount of brain tissue deprived

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140
Q

what is a thrombotic stroke?

A

-occurs from injury to a blood vessel wall and formation of a blood clot
-results from thrombosis or narrowing of a blood vessel
-associated with DM & HTN
-can proceed a TIA

141
Q

what is a hemorrhagic stroke?

A

bleeding into brain tissue
-intracerebral or intraparenchymal hemorrhage
-subarachnoid space or ventricles
subarachnoid or intraventricular hemorrhage

142
Q

is prognosis good or poor with a hemorrhagic stroke?

A

poor

143
Q

what is an intracerebral hemorrhage?

A

bleeding within the brain caused by rupture of a vessel
-sudden onset of symotoms
-progession over minutes to hours because of ongoing bleeding

144
Q

what is the most common cause of intracerebral hemorrhage?

A

HTN

145
Q

what are the clinical manifestations of an intracerebral hemorrhage?

A

neuro deficits
headache
n/v
decrease loc
hypertension

146
Q

what is a subarachnoid hemorrhage?

A

intracranial bleeding int cerebrospinal fluid-filled space between arachnoid an pia mater
-often caused by rupture of cerebral aneurysm, trauma, or illicit drug use
-Circle of Willis
-incidence increase with age; higher in women
-silent killer

147
Q

what would you administer a calcium channel blocker for (nimodipine)

A

cerebral vasospasm

148
Q

what is permissive hypertension?

A

keeping blood pressure increased so that blood flow can supply damaged parts of brain.

149
Q

what can happen because of the hemorrhagic stroke?

A

neuro and systemic complications
cerebral vasospasm
hyponatremia
myocardia ischemia and infarction, ARDS

150
Q

clinical manifestation of a thrombotic stroke?

A

-typically no decreased LOC within the first 24 hours
-symptoms get progressively worse as infarction and edema increase

151
Q

what are clinical manifestation of an embolic stroke?

A

-sudden severe symptoms
-warning signs are less common
-patient remains conscious and may have a headache

152
Q

what are the clinical manifestation of a hemorrhagic stroke?

A

-sudden onset of symptoms
-symptoms progress over minutes to hours due to ongoing bleeding

153
Q

what are the manifestations of right brain damage?

A

-paralyzed left side: hemiplegia
-left sided neglect
-spatial-perceptual deficits
-tends to deny or minimize problem
-rapid performance, short attention span
-impulsive, safety problems
-impaired judgment
-impaired time concept

154
Q

what are the manifestations of left brain damage?

A

-paralyzed on right side: hemiplegia
-impaired speech/language aphasias
-slow performance, cautious
-aware of deficits: depression, anxiety
-impaired comprehension related to language, math

155
Q

what are motor deficits from a stroke?

A

hemiplegia
heiparesis
ataxia

156
Q

what are communication deficits from a stroke?

A

dysarthria
dysphagia
aphagia

157
Q

what the cognitive impairment manifestations caused of a stroke

A

memory loss
decrease attention span
poor reasoning
altered judgment

158
Q

what are the psychological effects caused of stroke?

A

loss of self control
depression
emotional liability
elimination problems

159
Q

which sided stroke more likely to cause problems in spatial-percetual orientation?

A

stroke on right side

160
Q

what is agnosia?

A

inability to recognize object by touch or hearing

161
Q

what is apraxia?

A

inability to move a body part or not processing

162
Q

what diagnostic confirms a stroke?

A

CT or MRI

163
Q

What does a CT scan or MRI help when diagnosing a stroke?

A

-indicate size and location of lesion
-differentiate between ischemic and hemorrhagic stroke

164
Q

what are some preventive therapy for managing stroke?

A

healthy diet
wt control
regular exercise
no smoking
limited alcohol consumption
bp managment
routine health assessment

165
Q

what medication is given for patient with TIA?

A

aspirin, 81mg/day
oral anticoagulation for patients with A-fib
warfarin
statins, antihypertensives

166
Q

what can TPA be administered?

A

within 3-4.5 hours of symptoms

167
Q

what is the medical management of ischemic stroke?

A

thrombolytic therapy within 3 hours of s/s of ischemic stroke
-noncontrast CT of head
-blood test for coagulation studies
-screening for history for GI bleeding, stroke, or head trauma

168
Q

who is not a candidate for TPA?

A

a pt with head trauma in the past 3 months
-major surgery in the last 14 days
-active bleeding within 22 days
or if 3-4.5 hours have passed within the time frame

169
Q

what does a patient need to have when administering TPA?

A

2 18g large bore IV
folly
fall precaution
telesitter

170
Q

what are the surgical treatment for ischemic stroke?

A

carotid endarterectomy
carotid stenting

171
Q

what are the surgical treatments for hemorrhagic stroke?

A

aneurysm clipping, coiling
resection of arteriovenous malformation (AMV)

172
Q

what is a carotid endarterectomy?

A

removing of plaque in the carotid artery to improve blood flow

173
Q

what are the nursing interventions for stroke patients?

A

support resp system
frequent neuro exam
monitor cardiovascular system
monitor musculoskeletal system
monitor for skin breakdown
monitor for constipation
promote normal bladder function

174
Q

how to achieve self care?

A

encourage to assist in personal hygiene as soon as able to sit up
-dress with affected side
-dressing-better balance sitting up
-improve morale if fully dressed
-using clothing size larger than normal
-place on affected side-dress first

175
Q

what is a seizure?

A

sudden abnormal, excessive electrical discharge of neurons in the brain
-multiple neuros fire at a rate much faster than normal

176
Q

what are metabolic disturbances associated with seizures?

A

acidosis
electrolyte imbalance
hypoglycemia
hypoxia
alcohol or barbiturate withdrawal
dehydration or water intoxication

177
Q

what are extracranial disorders associated with seizures?

A

hypertension
heart, lung, liver, kidney disease
systemic lupus erythematosus
diabetic mellitus
septicemia

178
Q

what causes seizures?

A

idiopathic generalized epilepsy

179
Q

what is epilepsy?

A

disease with continuing predisposition to seizures with consequences
-neurobiologic
-psychologic
-social

180
Q

how is epilepsy detected?

A

EEG

181
Q

what is the patho of epilepsy?

A

group of abnormal neurons
spontaneous firing
where seizure originates
pattern of spread/extent of involvment
scar tissue

182
Q

why is it important to locate seizure?

A

for successful surgical intervention

183
Q

what is generalized seizure?

A

everywhere in the brain

184
Q

what is focal seizure?

A

localized on particular side of the brain

185
Q

what is a simple focal seizure?

A

pt is not going to lose LOC

186
Q

what is complex focal seizure?

A

pt loses LOC

187
Q

what are generalized seizure?

A

tonic-clonic
absence
myoclonic
atonic
tonic
clonic

188
Q

what are the phases of seizure?

A

prodromal phase
aural phase
ictal phase
postictal phase

189
Q

what is the prodromal phase?

A

sensation of behavior changes, they feel that its about to happen

190
Q

what is the aural phase?

A

sensory warning

191
Q

what is the ictal phase?

A

seizure phase, when it starts and ends

192
Q

what is postictal phase?

A

recovery phase after the seizure

193
Q

what are triggers of seizures?

A

lack of sleep, bright flashing, abrupt alcohol withdraw/intoxication, dehydration/water intoxication, electrolyte disbalances, stress, extreme physical activity

194
Q

what is tonic clonic seizure?

A

-characterized by loss of consciousness and falling
-body stiffens (tonic) with subsequent jerking of extremities (clonic)
-cyanosis, excessive salivation, tongue or cheek biting, and incontinence may occur

195
Q

how long does the tonic phase last

A

10-20 seconds

196
Q

how long does the clonic phase last

A

30-40 seconds

197
Q

what is the postictal phase of a tonic clonic seizure

A

-muscle soreness, fatigue
-patient may sleep for hours
-may not feel normal for hours to days
**No memory of seizure

198
Q

what is typical absence seizure?

A

usually occurs only in children and rarely beyond adolescence
-can be precipitated by flashing lights and hyperventilation
-“daydreaming”
-patient unresponsive when spoken to during seizure
-few seconds

199
Q

what is atypical absence seizure?

A

-characterized by staring spell with other manifestation
-eyeblinking, jerking movement of the lips, repetitive finger movement
-last as much as 30 seconds
-usually continue into adulthood

200
Q

what is a atonic seizure?

A

-involve tonic episode or paroxysmal loss of muscle tone
-begins suddenly and person falls
-last less than 15 seconds
-person usually remains conscious
-can resume normal activity immediatly
-great risk for head injury
-drop attack

201
Q

what is tonic seizure?

A

-involve sudden onset of maintained increased tone in the extensor muscle
-often occurs in sleep
-affect both sides of body
-usually last less than 20 seconds
-consciousness is usually preserved

202
Q

what is clonic seizure?

A

-begin with loss of consciousness and sudden loss of muscle tone
-followed by rhythmic limb jerking that may or may not be symmetric
-relatively rare

203
Q

what is focal seizure?

A

also called partial or partial focal
-begin specific region of cortex in one hemisphere of brain
-produce manifestations based on function of area of the brain
-divided according to clinical expression

204
Q

what is simple focal seizure?

A

-person remains conscious and alert
-experiences unusual feelings or sensations that can take many forms
-sudden and unexplainable feelings of joy, anger, sadness, or nausea
-may hear, smell, taste, see or feel things that are not real

205
Q

what is complex focal seizure?

A

patients have loss of consciousness or alteration in awareness
-eyes remain open but cannot interact
-may displace strange behavior
-automatisms-repetitive, purposeless action
-do not remember an activity started before or coninued during seizure
-30seconds-2 minutes (long time)

206
Q

what is psychogenic nonepileptic seizure

A

-imitate seizures but are triggered by emotional events
-proper diagnosis usually requires used of video EEG-monitoring
-Hx of emotional or physical abuse or traumatic events often emerges

207
Q

what is status epilepticus

A

-state of continuous seizure activity or condition when seizures recur in rapid succession without return to consciousness between seizure
-any seizure lasting longer than 5 minutes
-neurologic emergency
-can occur with any type of seizure

208
Q

what are the complications of status epilepticus?

A

-medical emergency
-most frequent in infants and elderly
-may result in permanent brain damage or death

209
Q

what are the complications of seizures on lifestyle?

A

-depression
-social stigma still exists
-discrimination in employment and educational opportunities
-driving sanctions (3monthts)

210
Q

what diagnositc assessment can be done for seizure?

A

history and physical
seizure history

211
Q

is their a cure for seizures?

A

no, goal of therapy is to prevent seizures with minimal drug side effects

212
Q

what are the primary drugs of treatment of tonic-clonic and focal onset seizure?

A

-phenytoin (dilantin)
-carbamazepine (tegretol)
-valporic acid (depakote)

213
Q

how do AED work?

A

suppress discharge of neurons within a seizure focus
-suppress propagation of seizure activity from the focus to the other areas of the brain

214
Q

what is the MOA of AED?

A

-suppression of sodium influx
-suppression of calcium influx
-promotion of potassium efflux
-blockade of receptors for glutamate
-potentiation of GABA

215
Q

what should you monitor when administering AED medication?

A

plasma drug level

216
Q

what medication is most widely used for AED and 1st drug to suppress seizure w/o depressing the entire CNS?

A

phenytoin (dilantin)

217
Q

what does phenytoin (dilantin) help?

A

active against partial and generalized tonic-clonic seizures
serves as prototype for the traditional AED

218
Q

what is the MOA of phenytoin (dilantin)

A

causes selective inhibition of sodium channels

219
Q

what are the effects on the CNS from phenytoin (dilantin)

A

-nystagmus, sedation, ataxia, diplopia, cognitive impairment
**gingival hyperplasia

220
Q

what are drug interactions with phenytoin (dilantin)

A

-decrease effects on oral contraceptive, warfarin, glucocorticoids
-increase dilantin leavels: diazepam, isoniazid, cimetidine, alcohol, valporic acid
decrease dilantin levels: carbamazepine, phenobarbital, alcohol

221
Q

should you administer phenytoin with or without food

A

with food

222
Q

what is the MOA in carbamazepine (tegretol)

A

same as phenytoin but minimal effects on cognitive function
-used for bipolar disorder and trigeminal neuralgia

223
Q

what are the side effects of carbamazepine (tegretol)

A

bone marrow suppression

224
Q

what is valporic acid (depakene, depakote)

A

1st line drug for all partial and generalized seizures
-used for bipolar disorder and migraine prevention

225
Q

what are the adverse effects of valporic acid (depakene,depakote)

A

hepatoxicity, pancreatitis

226
Q

what is phenobarbital?

A

one of the oldest AED, effective and inexpensive
-belongs to the barbiturate family
-can cause physical dependence
-decrease effect of warfarin and birth control

227
Q

what are the side effects of phenobarbital?

A

drowsiness, interfers with metabolism of vitamin d & k
toxicity: nystagmus and ataxia

228
Q

what is oxcarbazepine (trileptal)

A

-derivative of carbamazepine
-for management of partial seizures

229
Q

what is the MOA of oxcarbazepine (trileptal)

A

blockade of voltafe-sensitive sodium channels

230
Q

what are the side effects of oxcarbazepine (trileptal)

A

dizziness, drowsiness, avoid driving & other hazardous activities

231
Q

what is lamotrigine (lamitical)

A

-broad spectrum of antiseizure activity
-bipolar disorder
-life threatening rash
-risk for suicide

232
Q

what is the MOA of lamotrigine (lamictal)

A

blocks sodium and calcium channels

233
Q

what is gabapentin (neurontin)

A

-adjunct therapy for partial seizures
-off label use: neuropathic pain, prophylaxis of migraine, fibromyalgia, and post meopausal hot flashes
-very well tolerated

234
Q

what are the side effects of gabapentin (neurontin)

A

somnolence, dizziness, ataxia, fatigue, nystagmus, and peripheral edema

235
Q

what is pregablin (lyrica)

A

useful for neuropathic pain, posttherpetic neuralgia
-is regulated under the controlled substance act
-adjunct therapy for partial seizure
-can cause angioedema

236
Q

what is levetiracetam (keppra)

A

does not interact with other AED
-MOA: unkown
-good at controlling seizures

237
Q

what is topiramate (topamax)

A

broad spectrum antiseizure agent

238
Q

what is lorazepam (ativan)

A

-1st line management
-effect last up to 72 hours
-usual dose 4mg IV @ rate of 2mg/min

239
Q

what is diazepam (valium)

A

-short duration, must be administered repeatedly, 5-10 mg IV every 5 to 10 mins @5mg/min (not exceed 30 mg)

240
Q

which medications are management of acute seizures and status epilepticus

A

-lorazepam (ativan) 1st line management
-diazepam (valium)
-phenytoin (dilantin)
-fosphenytoin (cerebyx)

241
Q

what are the interprofessional care for AED?

A

-many of the antiseizure drugs have a long half-life
-can be given 1-2 times per day
-antiseizure drugs should not be discontinued abruptly as this many cause seizre

242
Q

what is the surgical consideration for focal seizure?

A

neurosurgery

243
Q

what is the surgical consideration for gneralized seizures?

A

vagal nerve stimulation

244
Q

what are the diagnosis of eplipesy?

A

seizure diary
eeg

245
Q

how can a patient be a candidate for surgery with seizures?

A

patient has to have defined site of seizure orgin
-laser ablation
-radiosurgery
-hemispherectomy

246
Q

what does SEIZURE stand for?

A

S-turn pt to the side
E-ensure safetly (rails/pads)
I-initiate oxygen therapy
Z- zero restraints
U-undo tight clothing
R-record the seizure
E-evaluate post seizure

247
Q

what is multiple scleroisis?

A

a chronic, unpredictable, progressive, degenerative disorder of the CNS
***characterized by segmental demyelination of nerve fibers of brain and spinal cord

248
Q

what are the causes of multiple sclerosis?

A

unkown

249
Q

what is multiple sclerosis characterized by?

A

characterized by periods of remission and exacerbation
-affects mostly women between 20-50 -more progressive when diagnosed at age >50

250
Q

what is the primary problem with multiple scleroisis?

A

autoimmune response

251
Q

what are the possible factors of multiple scleroisis?

A

infection, smoking, physical injury, emotional stress, excessive fatigue, postpartum, poor state health

252
Q

what is the etiology and patho of multiple scleroisis?

A

-chronic inflammation
-demyelination
-gliolis (scarring in the cns
-immune system attacks the myelin sheath

253
Q

what kind of tremors are in multiple scleroisis?

A

intention tremors

254
Q

what are the clinical manifestation of MS?

A

-mental status decreases, decrease concentration, attention deficit, memory loss
-depression and unstable mood
-limb weakness, loss of coordination and balance
-visual disturbances, blurred vision, color distortions, vision loss, eye pain
-loss of sensation, speech impediment, tremors or dizziness
-muscle spasms, fatigue, numbness, tinglining and prickling pain
-bladder and bowel dysfunction

255
Q

what are motor manifestations of MS?

A

-weakness or paralysis of limbs and trunk
-spasticity of muscles
-scanning of speech

256
Q

what is the impaired bowel and bladder and function manifestations?

A

-constipation
-variable urinary problems
-spastic bladder
-flaccid bladder

257
Q

what are the clinical manifestations of MS in sexual dysfunction?

A

-erectile dysfunction
-decreased libido
-painful intercourse

258
Q

what are clinical manifestations of cognitive manifestations?

A

-short-term memory attention
-information, processing
-attention, planning
-visual perception
-word finding

259
Q

what are the definitve test for MS?

A

no test
but MRI to check for plaque
CSF analysis
evoked potential studies
neuropsychological testing
sexual history

260
Q

what do they use to diagnose MS?

A

-evidence of at least 2 inflammatory demyelinating lesions in at least 2 different locations within the CNS
-damage or attack occurring at different times (usually >1month apart)
-all other possible diagnosis must have been ruled out

261
Q

what are the goal treatments for MS?

A

delay progression of disease, manage chronic symptoms, and treat acute exacerbations

262
Q

what is the drug therapy used for in MS?

A

-decrease the frequency and severity of relapses
-reduce the development of brain lesions
-decrease future disability

263
Q

what is the disease modifying drug I in MS?

A

-drugs that suppress the immune system to modify disease progression,. prevent relapse

264
Q

what are immunomodulators in MS?

A

-treatment should begin as soon as diagnosed
-modify the disease progression and prevent relapses

265
Q

what is the interferon beta used for in patients with MS?

A

-reduces the frequency and severity of attacks
-reduces the number and size of lesions detectable with MRI
-delays progression of disability

266
Q

what are the adverse effects of interferon beta?

A

-flu like reactions
-hepatotoxicity
-myelosuppression
-injection site reactions
-depression
-suicidal thoughts
-drug interactions

267
Q

how are the interferon beta medication for MS prepared?

A

-dispensed as single use syringes and vials

268
Q

what are the two immunosuppressants for MS?

A

-mitoxantrone
-cladribine

269
Q

what are mitoxantrone and cladribine used for with a pt with MS?

A

more toxic than immunomodulators
produces greater suppression of immune function
-helps with relapse

270
Q

what does mitoxantrone help with in pts with MS?

A

-decreases the neurologic disability and clinical replases
-binds with DNA and inhibits topoisomerase

271
Q

what are the adverse effects of mitoxantrone?

A

-myelosuppression
cardiotoxicity
fetal harm
-reversible hair loss, injury to mucosa, n/v, amenorrhea, allergy , green urine tine and sclera

272
Q

what are the drugs that help manage exacerbation with pt with MS?

A

-corticosteroids (methylprednosolone, prednisone
-helps treate acture exacerbation
-reduce edema and acute inflammation at the site of demyelination

273
Q

what is PD?

A

-chronic, progressive neurodegenerative disease of the CNS
-manifesting primarily in motor dysfunction
-primary idiopathic origin

274
Q

what is the etiology and patho of PD?

A

-exact cause is unknown
-possibly a result between environmental factors and persons genetic makeup

275
Q

what are the secondary/atypical parkinsons?

A

-exposure to chemicals and metals
-drug-induced (prescribed, illicit)

276
Q

what does PD lack in the brain?

A

-lack of dopamine
-degeneration of dopamine producing neurons in substantia nigra of midbrain
-disrupts dopamine-acetycholine balance in basal ganglia
-essential for normal functioning of extrapyramidal motor system

277
Q

what is TRAP?

A

Tremor
Rigidity
Akinesia/Bradykensia
Postural instability

278
Q

is head bopping a part of PD?

A

NO

279
Q

what are the beginning stages of PD?

A

mild tremor, slight limp, decrease arm sling

280
Q

what are later stages of PD?

A

shuffling, propulsive gait with arms flexed, loss of postural reflexed

281
Q

what are the clinical manifestions of PD in tremor?

A

-often first sign
-pill rolling hand tremor
-diaphragm, tongue, lips, jaw may be involved
-initially minimal
-more prominent at rest
-aggravated by emotional stress, increase concentration

282
Q

what are the clinical manifestations of rigidity in PD?

A

-increase resistance to passive ROM when limbs are moved through their ROM
-cogwheel rigidity
jerky quality
like intermittent catches in passive movement of a joint
-sustained muscle contraction
complaints of soreness
feeling tired and achy
pain in the head, upper body, spine, and legs
-slowness of movement

283
Q

what is akinesia?

A

absence of loss of control of voluntary muscle movements

284
Q

what is bradykinesia?

A

slowness of movement
particularly evident in the loss of automatic movements

285
Q

what is the postural instability in propulsion and retropulsion?

A

-unable to stop self from going forward
-unable to stop self from going backwards
increased fall risk

286
Q

what are other clinical manifestations of PD with the loss of automatic movements?

A

-stooped posture
-masked face
-drooling
-festination (shuffling gate)
HIGH RISK FOR ASPIRATION

287
Q

what is the appearance of a patient with PD?

A

-blank facial expression
-forward tilt to posture
-slow, montonous, slurred speech
-tremor
-short, shuffling gate

288
Q

what are the nonmotor symptoms of PD?

A

-depression, anxiety, apathy
-fatigue
-inability to plan/poor attention
-pain
-urinar incontinence and constipation
-erectile dysfunction
-memory changes

289
Q

what are the sleep problems in a patient with PD?

A

-difficulty staying asleep
-restless sleep
-nightmares
-drowsiness during the day
-REM sleep behavior disorder
-violent dreams, potentially dangerous motor activity during REM sleep

290
Q

what are the complications of PD?

A

-motor symptoms
-weakness
-neurologic process
-neurosychiatric problems
-dementia often results

291
Q

what can dysphagia cause in a person with PD?

A

malnutrition and aspiration

292
Q

how are patients diagnosed with PD?

A

-presence of 2 or more cardinal manifestations of TRAP
-positive response to the antiparkinsonian drug
-medical Hx, presenting symptoms, neuro exam

293
Q

what are the drug therapy for PD helping with?

A

-aimed with correcting imbalance of neurotransmitter within the CNS
-enhance or release supply of DA
-block the effects of overactive cholingeric neuros in the striatum (anticholinergics)

294
Q

what are the therapeutic goals in drug therapy for PD?

A

-ideal treatment that reverses neuronal degeneration or prevent further degeneration does not exist

295
Q

what are the two major drugs for PD?

A

Dopaminergic agents and anticholinergic agents

296
Q

what are the dopaminergic agents used for in PD?

A

-most commonly used
-promote activation of dopamine receptprs
-levadopa

297
Q

what are the anticholinergic agents used for in PD?

A

-prevent activation of cholinergic receptors
-benztropine (cogentin)

298
Q

what is the dopamine replacement medication?

A

levadopa

299
Q

what does levadopa help with?

A

highly effective, but benefits diminished overtime
-orally administed; rapidly absorbed from the small intestine
-food delays absorption (amino acids)
-high protein food reduce therapeutic effects

300
Q

what should not be taken with levadopa?

A

high protein foods

301
Q

what is the MOA of levadopa/carbidopa (sinemet)

A

levadopa is converted to dopamine in the CNS. Carbidopa prevents peripheral destruction of levodopa. converted to dopamine in basal ganglia

302
Q

what are the adverse effects of levadopa/carbidopa (sinemet)

A

n/v
dyskinesias
postural hypotension
dysruthmias
psychosis
impulse control
darkened sweat and urine
loss of effect

303
Q

what is pramipexole used for?

A

-1st line drug or supplement to levadopa
used alone in early PD and with levadopa in advance pd

304
Q

what are the adverse effects of pramipexole

A

sleep attacks
nausea
dizziness
daytime somnolence
insomina
constopation
weakness and hallucinations

305
Q

what are the anticholinergic (trihexiphenidyl and benztropine

A

-blocks muscarinc receptors in the striatium
decrease activity of ach

306
Q

what should selegiline be given with

A

with lunch or breakfast

307
Q

what is deep brain stimulation

A

most common surgical treatment
reversibel and programmable
decrease increase neuronal activity produced by DA

308
Q

what is ablation surgery

A

located target destroy area of the brain affected by PD

309
Q

what is ALS?

A

lou gehrig disease
it is progressive, rare, incurable degenerative disease involving the motor system
affects more men that women
median age of onset 55

310
Q

what is the patho of ALS

A

-rapidly progessing, fatal CNS disease affects voluntary muscle control
-does not impair sense or ability to think
-affects diaphragm and chest wall

311
Q

what is the etiology of ALS

A

about 10% of ALS is genetics
smoking
athleticism
metals
solvents
radiation
electromagnetic fields
pesticides
viruses

312
Q

what are the clinical manifestations of ALS

A

-muscle cramps or stiffness
muscle weakness
slurred speech
difficulty swallowing
-loss of muscle tone

313
Q

upper motor neuron damage in ALS

A

associated with spasticity

314
Q

lower motor neuron damage in ALS

A

associated with flaccidity

315
Q

what are early symptoms of ALS

A

tongue atrophy
dysphagia
dysarthria

316
Q

what are the late symptoms of ALS

A

nasal quality of speech
fasciculation of the face
spasticity
weakness of the hands and arms
muscle atrophy
eventual respiratory muscle involvement

317
Q

what are the diagnositcs for ALS

A

no single test can be used to diagnose
-based on s&S
-emg and nerve conduction studies
-ct scan and/mri of neck and head
-lumbar puncture
-genetic testing
swallow studies

318
Q

what is Riluzole (rilutek) for ALS?

A

delayed need for tracheostomy by 3-6 months
well tolerated

319
Q

what is the MOA of riluzole (rilutek)

A

reduce damage to motor neurons by decreasing the release of glutamate

320
Q

what is the adverse effects of riluzole

A

asthenia, GI reactions, dizziness, vertigo, somnolence, decreased lung function, neutropenia, and liver injury
Taken PO, BID

321
Q

what is edaravone (radivaca) for ALS

A

shown to slow the loss of physical function in early stages of ALS

322
Q

what is the MOA edaravone (radivaca)

A

unknown in the treatment of ALS, but believed to relieve the effects of oxidative stress, a likely factor in progression of ALS

323
Q

what is the adverse effect of edaravone (radivaca)

A

hives; swelling of lips, tongue, or face; fainting; breathing problems; wheezing; trouble swallowing; dizziness; itching; asthma attack
Given IV in 14-day cycles

324
Q

what are the complications of ALS?

A

Aspiration
Respiratory failure
Pneumonia
Pressure ulcers
Deep Vein Thrombosis (DVT)
Pulmonary embolism (PE)
Constipation, contractures
Depression
Weigh loss
Loss of ability for self care

325
Q

what do speech pathologist do?

A

swallow assessment and treatment
speech and language
cognitive assessment and treatment

326
Q

what are the phases of swallowing?

A

oral
pharyngeal
esophageal

327
Q

difficulty swallowing

A

dysphagia

328
Q

what are the cognitive dysphagia

A

dementia
head injury
lethargic or obtunded patients

329
Q

what are the nurses role in dysphagia management?

A

Good history (RN assessment forms)
Good oral mechanism exam
Swallow screen (3oz water observation)
Observation with meals and medications
Assistance with oral care **
Assistance with feeding **
Hasten referrals to other professionals

330
Q

what are the signs and symptoms for dysphagia?

A

Cannot manage oral secretions (drooling, gurgly)
Difficulty chewing, prolonged chewing
Pocketing of food in buccal cavities
Holding food in mouth for long periods
Excessive drooling during meals
Absent swallow (know how to palpate)
Coughing/choking or throat clearing after swallows
Wet, gurgly voice after swallows
Pain with swallowing
Swallowing many times for small bolus

331
Q

what are the top three risk factors for aspiration pneumonia?

A

dependence on others for feeding
dependence on other for oral care
missing or decaying teeth

332
Q

what are other indicators for dysphagia

A

tube feeding
multiple medical diagnosis
chronic reflux

333
Q

what is intact with ALS?

A

Cognitive function is intact while body is giving away

334
Q

what is silent aspiration?

A

Aspirated material is undetected by a desensitized trachea
Consequently, no reflexive cough is triggered to protect the airway
Results in false negative Bedside swallow evaluation
If suspected, an MBS/VFSS or FEES study would be better able to identify the aspiration

335
Q

what are feeding/swallowing precautions?

A

Chin-tuck
Thickened liquids
Follow-up swallows
Straws v. No straws
Throat clearing
“General Precautions”

336
Q

what are the special diets?

A

Clear liquid
Full liquid
International Dysphagia Diets
Regular
Restrictions as prescribed by RD or MD!

337
Q

what are the frazier water protocol?

A

It is tool that allows and encourages patients at high risk of aspiration to have ice and water throughout the day.

338
Q

what are the communication disorders?

A

motor speech disorders
language disorders
cognitive-communicative disorders

339
Q

what is an expressive aphagia?

A

brain doesn’t process what you’re saying

340
Q

what is SBAR?

A

situation
background
assessment
recommendation

341
Q

what is pdsa

A

plan -idea for action
do -make the change
study -test it and collect data
act- adjust actions

342
Q

what is core team?

A

nursing

343
Q

what is contigency teams?

A

code blue, physician, respiratory, pharmacy, rapid response

344
Q

what is magnet culture?

A

visionary nursing leadership
-having someone is backing them up
strong nursing representation at the top levels of managment
building an environment that encourages participatation
enpowering nurses in patient care
showing superior patient outcomes

345
Q

how does healthcare information technology help?

A

direct access, decrease in medical errors, decrease in duplicate orders, reduce mistakes in reading hand written

346
Q

what does professional nursing look like to you?

A

caring for patient in a dignified way

347
Q

what is step?

A

status of patient
team members
enviroment
progress towards goal

348
Q

what is picot

A

population/patient/problem
intervention
comparision/contorl
outcome
time

349
Q
A

Sensory, Neuro, Nursing Practice (1 decks)

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