Sensory, Neuro, Nursing Practice Flashcards

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
i am the medical term of ringing of the ears
tinnitus
26
i am the medical term for the room is spinning
vertigo
27
i am a symptom that occurs when there is fluid in the ear compressing the 8th cranial nerve
vertigo
28
i am the reason the patient is a high fall risk
vertigo
29
i can cause a patient grief, depression and may also lead to suicidal ideation
tinnitus
30
i am ostosclerosis
conductive hearing loss
31
i am caused by otitis media with effusion
conductive hearing loss
32
i am caused by poor eustachian tube function
conductive hearing loss
33
i am caused by impacted cerumen
conductive hearing loss
34
i am caused by tumors in the ear
conductive hearing loss
35
i am caused by objects in the ear
conductive hearing loss
36
i hear better in noisy environment
conductive hearing loss (bone better than air)
37
my treatment plan is to either treat the cause or wear a hearing aide
conductive hearing loss
38
i am the most common type of permanent hearing loss
sensorineural hearing loss
39
i cannot be fixed by surgery or medicine
sensorinerual
40
i am caused by illness or genetics
snesoriunerual
41
i am caused by loud noises like concert, gun firing, construction, factory work, etc..
sensorineural
42
i am caused by ototoxicity
sensorineural i
43
i am vancomycin. i caused what kind of damage
sensorineural/toxicity
44
i am gentamycin i cause what kind of damage
sensorineural/toxicity
45
I am Aspirin I cause what kind of damage
sensorineural/toxicity
46
I am furosemide i can cause what kind damage?
sensorineural/toxicity
47
48. I am Quinine I cause what kind of damage
sensorineural/toxicity
48
49. I am caused by presbycusis (aging
sensorineural
49
51. My signs and symptoms include: Vertigo, Tinnitus, and Fluctuating hearing
meniere's syndrome
50
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.
meniere's syndrome
51
53. My surgical intervention includes a resection of the vestibular nerve or a total removal
(Meniere’s syndrome)
52
54. 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.
(Meniere’s syndrome)
53
55. For me you should assess for early detection to prevent permanent damage
nursing care/education
54
56. For me you should educate patients and have them teach back to ensure understanding
(Nursing care/ education)
55
57. I must be taught about adequate nutrition and hydration to ensure that I can maintain oil and sebaceous glands to maintain hearing.
nursing care/education
56
58. I must be taught about medication regimens
(nursing care/education)
57
59. I must be taught about surgery if necessary
(nursing care/ education)
58
60. You should never shout at me
hearing deficit
59
what you should do when a patient has a hearing deficit?
talk low and slow
60
1. The nurse is developing a teaching plan for a client with glaucoma. Which instruction should the nurse include in the plan of care?
1. Eye medication will need to be administered for life.
61
What is Cranial nerve #8 responsible for?
Auditory (vestibulocochlear) is responsible for balance and hearing.
62
What clinical manifestations are associated with hearing loss?
Ineffective communication, Decreased interaction, withdrawal, suspicion, loss of self-esteem and insecurity.
63
How do you check if a patient with hearing loss understood what you were communication to them?
Have the patient teach back. Also, have a family/friend at bedside to also get education.
64
What part of the ear is affected if the patient has conductive hearing loss?
Outer and middle ear
65
What part of the ear is affected if the patient has sensorineural hearing loss?
Inner ear damage (nerve pathways)
66
What are two of the priority symptoms that we are assessing for with hearing loss that is caused by compression of cranial nerve #8?
Tinnitus and vertigo
67
What is tinnitus and what is your priority assessment for the patient suffering with tinnitus?
Ringing of the ears can cause suicidal ideation.
68
What is Vertigo and what is your priority assessment for the patient suffering with vertigo?
Room is spinning while the patient is still. Patient is a high fall risk.
69
What are the some of the causes of Conductive hearing loss?
Otitis media with effusion, poor eustachian tube function, impacted cerumen, tumors, objects present, middle ear disease, otosclerosis
70
What are some of the causes of Sensorineural hearing loss?
Illness, genetics, loud noises, ototoxicity, and aging
71
What medications cause ototoxicity in sensorineural hearing loss?
1. Vancomycin 2. Gentamycin 3. Cisplatin 4. Aspirin 5. Furosemide 6. Quinine
72
Sensorineural is permanent hearing loss that cannot be fixed by surgery or medicine?
True.
73
What is Meniere’s disease?
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.
74
What treatments can be done for a patient with Meniere’s disease?
Mild diuretics, vestibular rehabilitation, surgery.
75
What communication technique is the most effective for a patient with hearing loss?
Talk Low and Slow. Can also use written instructions for patient.
76
What part of the eye do you administer eye drops?
Nasolacrimal duct/conjunctival sac.
77
How long do you hold pressure on the inner eye after administering eye drops?
At least 15 seconds.
78
Why do you want to apply pressure to the nasolacrimal duct/ conjunctiva after administering eye drops?
To prevent systemic absorption (Decrease of blood pressure and heart rate)
79
What are the four leading causes of blindness?
Age related macular degeneration, Cataract, Diabetic Retinopathy, Glaucoma.
80
What is Cranial nerve #2 responsible for?
Optic nerve is responsible for the visual acuity.
81
What is Cranial nerve # 3 responsible for?
Oculomotor is responsible for opening of eyelids, eye movement upward/medial, upward/lateral, medial, downward/lateral.
82
What is Cranial nerve #4 responsible for?
Trochlear nerve is responsible for eye movement downward/medial)
83
What is Cranial nerve #6 responsible for?
Abducens nerve is responsible for eye movement lateral
84
What is Cranial nerve #7 responsible for?
Facial nerve is responsible for facial muscle movement (except chewing), and eyelid closing.
85
26. What is Cataract defined as?
Opacification of the lens.
86
What is the number one risk factor for cataracts?
27. Age is the number one risk factor followed by diabetes mellitus, UV light, 2nd use of corticosteroids, and trauma.
87
28. What safety education do you want to provide the patient diagnosed with cataracts?
28. 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.
88
29. What is the treatment for cataracts?
29. Surgery
89
30. If the patient has any unexpected complications after cataract surgery, what should you do?
30. Call the surgeon even if it is just pain!
90
31. What part of the vision does glaucoma affect?
31. Peripheral vision (Glaucoma, Peripheral) Gatorade and Powerade
91
32. What is the difference between open and closed glaucoma?
32. Open is gradual IOP build up. Closed is a rapid buildup 24-48 hour to fix before permanent damage.
92
33. What part of the vision does macular degeneration affect?
33. Central vision (Macular-McDonald’s, Central Chick fila)
93
34. What is the difference between dry and wet macular degeneration?
34. Dry is drusen buildup that is gradual. Wet is drusen with hemorrhage and neovascularization that is rapid.
94
35. Is there a cure for macular degeneration?
35. No cure just slowing of progression.
95
36. For a type I diabetic when should they have an eye appointment?
36. Within 5 years of diagnosis and then yearly.
96
37. For a type 2 diabetic, when should they have an eye appointment?
37. Upon diagnosis and then yearly.
97
what are some subjective data questions?
health info, birth history, TBI, stroke, degenerative disease, medications, surgery or other treatments, growth and developmental history, functional health patter, sleep rest pattern
98
what are some objective data?
physical examination cranial nerve function motor function sensory function reflexes
99
how do you do the assessment of the nervous system?
follow logical sequence higher level of neurologic function to lower level constant comparison of findings
100
what will patients present with if having altered mental and speech status?
confusion/memory -loc -appearance and behavior -speech -cognitive function -constructional ability
101
what is the first indication that a patients neurologic function has declined?
a change in loc
102
what is alert?
awake and responsive, follows commands
103
what is lethargic?
sleepy but arousable, drowsy, delayed responss, may drift to sleep
104
what is dysarthria?
difficulty articulating
105
what are the three areas of memory loss?
long term or remote memory recall or recurent memory immediate or new memory
106
what is the best score on the glasgow coma scale?
15
107
what is the worst score on the glasgow coma scale?
3
108
what are the subtle indications that deterioration is occuring in the neurologic status?
headache restlessness irrability being unusally quiet slurred speech change in orientation level
109
how to access light touch?
you can use a cotton ball and touch the patient
110
how to access for pain?
have a patient close their eyes and touvh areas of the body
111
how to access discrimination?
ask the patient to close their eyes and to identify what object you are using to touch the patient
112
how to access muscle tone?
finger to nose; hee; to shin pronate and supine both hands posture, gait risk for falling
113
what is a csf analysis?
provides information about a variety of cns diseases
114
how should CSF look like?
clear, colorless, odorless, and free of red blood cells, contain little protein
115
how can a patient be positioned for a CSF analysis?
lying side position or sitting position
116
what is the preop for a lumbar puncture?
-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
117
what is post of for a lumbar puncture?
-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)
118
what is a cerebral angiogram?
serial x-ray visualization of intracranial and extracranial blood vessels perfomed to detect vascular lesions (aneurysms, hematoma, AVM)
119
what nursing assessment do you do for a pt going for a cerebral angiogram?
withhold meal; need pt to stay very still
120
what do you monitor post op of cerebral angiogram?
monitor neurologic signs maintain bed rest for 6 hours monitor for bleeding report any neuro status change
121
what is a ct scan?
distinguishes bone, soft tissue. and fluids provide a rapid means of obtaining radiographic images of the brain
122
what is an mri used for?
to detect stokes, ms, tumors, trauma, hermiation, and seizures
123
what is a pet scan?
measures metabolic activity of brain to assess cell death or damage -for patients with stroke, AD, seizure disorders, PD, and tumors
124
what is a myelogram?
x-ray of spinal cord and vertebral column -injection of contrast into subarachnoid space, used to detect lesions -herniated or ruptured disc -spinal tumor
125
what is an electroencephalography?
EEG -electrical activity of brain recorded using scalp electrodes -evaluate seizure disorders, cerebral disease, bran injury, brain death
126
how to prepare for an EEG?
-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
127
what is an electromyography?
EMG -recording of electrical activity associated with innervation of skeletal muscle
128
what is a nerve conduction studies?
stimulating peripheral nerves at several points along its course and recording muscle action potential or sensory action potentiona
129
what is ischemia in brain?
inadequate blood flow to a part of the brain
130
what is hemorrhage in brain?
bleeding into the brain that results in death of brain cells
131
what causes a stroke?
disruption in the blood supply to part of the brain
132
what is FAST?
face drooping arm weakness speech difficulty time is critical
133
what is the patho of a stroke?
regardless of the cause, the underlying event is deprivation of oxygen and nutrients
134
what are non-modifiable stroke risk factors?
age gender: more common in men ethnicity: higher incidence in african americans hereditary: family history
135
what are modifiable stroke risk factors?
HTN** history of TIA cardiovascular disease diabetes smoking, alcohol, substance abuse birth control pills, hormone replacement obesity sleep apnea
136
what kind of strokes are there?
transient ischemic attack (TIA) ischemic (thrombotic, embolic) hemorrhagic (intracerebral, subarachnoid)
137
what is a TIA?
-transient episode of neurologic dysfunction -serve as a warning sign of further cerebrovascular disease -no way to predict outcome
138
what is a embolic stroke?
-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
139
are symptoms with an embolic stroke fast or slow?
slow and warning signs are less common, prognosis is related to amount of brain tissue deprived
140
what is a thrombotic stroke?
-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
what is a hemorrhagic stroke?
bleeding into brain tissue -intracerebral or intraparenchymal hemorrhage -subarachnoid space or ventricles subarachnoid or intraventricular hemorrhage
142
is prognosis good or poor with a hemorrhagic stroke?
poor
143
what is an intracerebral hemorrhage?
bleeding within the brain caused by rupture of a vessel -sudden onset of symotoms -progession over minutes to hours because of ongoing bleeding
144
what is the most common cause of intracerebral hemorrhage?
HTN
145
what are the clinical manifestations of an intracerebral hemorrhage?
neuro deficits headache n/v decrease loc hypertension
146
what is a subarachnoid hemorrhage?
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
what would you administer a calcium channel blocker for (nimodipine)
cerebral vasospasm
148
what is permissive hypertension?
keeping blood pressure increased so that blood flow can supply damaged parts of brain.
149
what can happen because of the hemorrhagic stroke?
neuro and systemic complications cerebral vasospasm hyponatremia myocardia ischemia and infarction, ARDS
150
clinical manifestation of a thrombotic stroke?
-typically no decreased LOC within the first 24 hours -symptoms get progressively worse as infarction and edema increase
151
what are clinical manifestation of an embolic stroke?
-sudden severe symptoms -warning signs are less common -patient remains conscious and may have a headache
152
what are the clinical manifestation of a hemorrhagic stroke?
-sudden onset of symptoms -symptoms progress over minutes to hours due to ongoing bleeding
153
what are the manifestations of right brain damage?
-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
what are the manifestations of left brain damage?
-paralyzed on right side: hemiplegia -impaired speech/language aphasias -slow performance, cautious -aware of deficits: depression, anxiety -impaired comprehension related to language, math
155
what are motor deficits from a stroke?
hemiplegia heiparesis ataxia
156
what are communication deficits from a stroke?
dysarthria dysphagia aphagia
157
what the cognitive impairment manifestations caused of a stroke
memory loss decrease attention span poor reasoning altered judgment
158
what are the psychological effects caused of stroke?
loss of self control depression emotional liability elimination problems
159
which sided stroke more likely to cause problems in spatial-percetual orientation?
stroke on right side
160
what is agnosia?
inability to recognize object by touch or hearing
161
what is apraxia?
inability to move a body part or not processing
162
what diagnostic confirms a stroke?
CT or MRI
163
What does a CT scan or MRI help when diagnosing a stroke?
-indicate size and location of lesion -differentiate between ischemic and hemorrhagic stroke
164
what are some preventive therapy for managing stroke?
healthy diet wt control regular exercise no smoking limited alcohol consumption bp managment routine health assessment
165
what medication is given for patient with TIA?
aspirin, 81mg/day oral anticoagulation for patients with A-fib warfarin statins, antihypertensives
166
what can TPA be administered?
within 3-4.5 hours of symptoms
167
what is the medical management of ischemic stroke?
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
who is not a candidate for TPA?
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
what does a patient need to have when administering TPA?
2 18g large bore IV folly fall precaution telesitter
170
what are the surgical treatment for ischemic stroke?
carotid endarterectomy carotid stenting
171
what are the surgical treatments for hemorrhagic stroke?
aneurysm clipping, coiling resection of arteriovenous malformation (AMV)
172
what is a carotid endarterectomy?
removing of plaque in the carotid artery to improve blood flow
173
what are the nursing interventions for stroke patients?
support resp system frequent neuro exam monitor cardiovascular system monitor musculoskeletal system monitor for skin breakdown monitor for constipation promote normal bladder function
174
how to achieve self care?
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
what is a seizure?
sudden abnormal, excessive electrical discharge of neurons in the brain -multiple neuros fire at a rate much faster than normal
176
what are metabolic disturbances associated with seizures?
acidosis electrolyte imbalance hypoglycemia hypoxia alcohol or barbiturate withdrawal dehydration or water intoxication
177
what are extracranial disorders associated with seizures?
hypertension heart, lung, liver, kidney disease systemic lupus erythematosus diabetic mellitus septicemia
178
what causes seizures?
idiopathic generalized epilepsy
179
what is epilepsy?
disease with continuing predisposition to seizures with consequences -neurobiologic -psychologic -social
180
how is epilepsy detected?
EEG
181
what is the patho of epilepsy?
group of abnormal neurons spontaneous firing where seizure originates pattern of spread/extent of involvment scar tissue
182
why is it important to locate seizure?
for successful surgical intervention
183
what is generalized seizure?
everywhere in the brain
184
what is focal seizure?
localized on particular side of the brain
185
what is a simple focal seizure?
pt is not going to lose LOC
186
what is complex focal seizure?
pt loses LOC
187
what are generalized seizure?
tonic-clonic absence myoclonic atonic tonic clonic
188
what are the phases of seizure?
prodromal phase aural phase ictal phase postictal phase
189
what is the prodromal phase?
sensation of behavior changes, they feel that its about to happen
190
what is the aural phase?
sensory warning
191
what is the ictal phase?
seizure phase, when it starts and ends
192
what is postictal phase?
recovery phase after the seizure
193
what are triggers of seizures?
lack of sleep, bright flashing, abrupt alcohol withdraw/intoxication, dehydration/water intoxication, electrolyte disbalances, stress, extreme physical activity
194
what is tonic clonic seizure?
-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
how long does the tonic phase last
10-20 seconds
196
how long does the clonic phase last
30-40 seconds
197
what is the postictal phase of a tonic clonic seizure
-muscle soreness, fatigue -patient may sleep for hours -may not feel normal for hours to days **No memory of seizure
198
what is typical absence seizure?
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
what is atypical absence seizure?
-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
what is a atonic seizure?
-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
what is tonic seizure?
-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
what is clonic seizure?
-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
what is focal seizure?
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
what is simple focal seizure?
-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
what is complex focal seizure?
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
what is psychogenic nonepileptic seizure
-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
what is status epilepticus
-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
what are the complications of status epilepticus?
-medical emergency -most frequent in infants and elderly -may result in permanent brain damage or death
209
what are the complications of seizures on lifestyle?
-depression -social stigma still exists -discrimination in employment and educational opportunities -driving sanctions (3monthts)
210
what diagnositc assessment can be done for seizure?
history and physical seizure history
211
is their a cure for seizures?
no, goal of therapy is to prevent seizures with minimal drug side effects
212
what are the primary drugs of treatment of tonic-clonic and focal onset seizure?
-phenytoin (dilantin) -carbamazepine (tegretol) -valporic acid (depakote)
213
how do AED work?
suppress discharge of neurons within a seizure focus -suppress propagation of seizure activity from the focus to the other areas of the brain
214
what is the MOA of AED?
-suppression of sodium influx -suppression of calcium influx -promotion of potassium efflux -blockade of receptors for glutamate -potentiation of GABA
215
what should you monitor when administering AED medication?
plasma drug level
216
what medication is most widely used for AED and 1st drug to suppress seizure w/o depressing the entire CNS?
phenytoin (dilantin)
217
what does phenytoin (dilantin) help?
active against partial and generalized tonic-clonic seizures serves as prototype for the traditional AED
218
what is the MOA of phenytoin (dilantin)
causes selective inhibition of sodium channels
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what are the effects on the CNS from phenytoin (dilantin)
-nystagmus, sedation, ataxia, diplopia, cognitive impairment **gingival hyperplasia
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what are drug interactions with phenytoin (dilantin)
-decrease effects on oral contraceptive, warfarin, glucocorticoids -increase dilantin leavels: diazepam, isoniazid, cimetidine, alcohol, valporic acid decrease dilantin levels: carbamazepine, phenobarbital, alcohol
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should you administer phenytoin with or without food
with food
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what is the MOA in carbamazepine (tegretol)
same as phenytoin but minimal effects on cognitive function -used for bipolar disorder and trigeminal neuralgia
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what are the side effects of carbamazepine (tegretol)
bone marrow suppression
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what is valporic acid (depakene, depakote)
1st line drug for all partial and generalized seizures -used for bipolar disorder and migraine prevention
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what are the adverse effects of valporic acid (depakene,depakote)
hepatoxicity, pancreatitis
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what is phenobarbital?
one of the oldest AED, effective and inexpensive -belongs to the barbiturate family -can cause physical dependence -decrease effect of warfarin and birth control
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what are the side effects of phenobarbital?
drowsiness, interfers with metabolism of vitamin d & k toxicity: nystagmus and ataxia
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what is oxcarbazepine (trileptal)
-derivative of carbamazepine -for management of partial seizures
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what is the MOA of oxcarbazepine (trileptal)
blockade of voltafe-sensitive sodium channels
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what are the side effects of oxcarbazepine (trileptal)
dizziness, drowsiness, avoid driving & other hazardous activities
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what is lamotrigine (lamitical)
-broad spectrum of antiseizure activity -bipolar disorder -life threatening rash -risk for suicide
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what is the MOA of lamotrigine (lamictal)
blocks sodium and calcium channels
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what is gabapentin (neurontin)
-adjunct therapy for partial seizures -off label use: neuropathic pain, prophylaxis of migraine, fibromyalgia, and post meopausal hot flashes -very well tolerated
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what are the side effects of gabapentin (neurontin)
somnolence, dizziness, ataxia, fatigue, nystagmus, and peripheral edema
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what is pregablin (lyrica)
useful for neuropathic pain, posttherpetic neuralgia -is regulated under the controlled substance act -adjunct therapy for partial seizure -can cause angioedema
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what is levetiracetam (keppra)
does not interact with other AED -MOA: unkown -good at controlling seizures
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what is topiramate (topamax)
broad spectrum antiseizure agent
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what is lorazepam (ativan)
-1st line management -effect last up to 72 hours -usual dose 4mg IV @ rate of 2mg/min
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what is diazepam (valium)
-short duration, must be administered repeatedly, 5-10 mg IV every 5 to 10 mins @5mg/min (not exceed 30 mg)
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which medications are management of acute seizures and status epilepticus
-lorazepam (ativan) 1st line management -diazepam (valium) -phenytoin (dilantin) -fosphenytoin (cerebyx)
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what are the interprofessional care for AED?
-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
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what is the surgical consideration for focal seizure?
neurosurgery
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what is the surgical consideration for gneralized seizures?
vagal nerve stimulation
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what are the diagnosis of eplipesy?
seizure diary eeg
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how can a patient be a candidate for surgery with seizures?
patient has to have defined site of seizure orgin -laser ablation -radiosurgery -hemispherectomy
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what does SEIZURE stand for?
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
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what is multiple scleroisis?
a chronic, unpredictable, progressive, degenerative disorder of the CNS ***characterized by segmental demyelination of nerve fibers of brain and spinal cord
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what are the causes of multiple sclerosis?
unkown
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what is multiple sclerosis characterized by?
characterized by periods of remission and exacerbation -affects mostly women between 20-50 -more progressive when diagnosed at age >50
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what is the primary problem with multiple scleroisis?
autoimmune response
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what are the possible factors of multiple scleroisis?
infection, smoking, physical injury, emotional stress, excessive fatigue, postpartum, poor state health
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what is the etiology and patho of multiple scleroisis?
-chronic inflammation -demyelination -gliolis (scarring in the cns -immune system attacks the myelin sheath
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what kind of tremors are in multiple scleroisis?
intention tremors
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what are the clinical manifestation of MS?
-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
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what are motor manifestations of MS?
-weakness or paralysis of limbs and trunk -spasticity of muscles -scanning of speech
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what is the impaired bowel and bladder and function manifestations?
-constipation -variable urinary problems -spastic bladder -flaccid bladder
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what are the clinical manifestations of MS in sexual dysfunction?
-erectile dysfunction -decreased libido -painful intercourse
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what are clinical manifestations of cognitive manifestations?
-short-term memory attention -information, processing -attention, planning -visual perception -word finding
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what are the definitve test for MS?
no test but MRI to check for plaque CSF analysis evoked potential studies neuropsychological testing sexual history
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what do they use to diagnose MS?
-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
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what are the goal treatments for MS?
delay progression of disease, manage chronic symptoms, and treat acute exacerbations
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what is the drug therapy used for in MS?
-decrease the frequency and severity of relapses -reduce the development of brain lesions -decrease future disability
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what is the disease modifying drug I in MS?
-drugs that suppress the immune system to modify disease progression,. prevent relapse
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what are immunomodulators in MS?
-treatment should begin as soon as diagnosed -modify the disease progression and prevent relapses
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what is the interferon beta used for in patients with MS?
-reduces the frequency and severity of attacks -reduces the number and size of lesions detectable with MRI -delays progression of disability
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what are the adverse effects of interferon beta?
-flu like reactions -hepatotoxicity -myelosuppression -injection site reactions -depression -suicidal thoughts -drug interactions
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how are the interferon beta medication for MS prepared?
-dispensed as single use syringes and vials
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what are the two immunosuppressants for MS?
-mitoxantrone -cladribine
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what are mitoxantrone and cladribine used for with a pt with MS?
more toxic than immunomodulators produces greater suppression of immune function -helps with relapse
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what does mitoxantrone help with in pts with MS?
-decreases the neurologic disability and clinical replases -binds with DNA and inhibits topoisomerase
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what are the adverse effects of mitoxantrone?
-myelosuppression cardiotoxicity fetal harm -reversible hair loss, injury to mucosa, n/v, amenorrhea, allergy , green urine tine and sclera
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what are the drugs that help manage exacerbation with pt with MS?
-corticosteroids (methylprednosolone, prednisone -helps treate acture exacerbation -reduce edema and acute inflammation at the site of demyelination
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what is PD?
-chronic, progressive neurodegenerative disease of the CNS -manifesting primarily in motor dysfunction -primary idiopathic origin
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what is the etiology and patho of PD?
-exact cause is unknown -possibly a result between environmental factors and persons genetic makeup
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what are the secondary/atypical parkinsons?
-exposure to chemicals and metals -drug-induced (prescribed, illicit)
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what does PD lack in the brain?
-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
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what is TRAP?
Tremor Rigidity Akinesia/Bradykensia Postural instability
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is head bopping a part of PD?
NO
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what are the beginning stages of PD?
mild tremor, slight limp, decrease arm sling
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what are later stages of PD?
shuffling, propulsive gait with arms flexed, loss of postural reflexed
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what are the clinical manifestions of PD in tremor?
-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
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what are the clinical manifestations of rigidity in PD?
-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
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what is akinesia?
absence of loss of control of voluntary muscle movements
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what is bradykinesia?
slowness of movement particularly evident in the loss of automatic movements
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what is the postural instability in propulsion and retropulsion?
-unable to stop self from going forward -unable to stop self from going backwards increased fall risk
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what are other clinical manifestations of PD with the loss of automatic movements?
-stooped posture -masked face -drooling -festination (shuffling gate) HIGH RISK FOR ASPIRATION
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what is the appearance of a patient with PD?
-blank facial expression -forward tilt to posture -slow, montonous, slurred speech -tremor -short, shuffling gate
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what are the nonmotor symptoms of PD?
-depression, anxiety, apathy -fatigue -inability to plan/poor attention -pain -urinar incontinence and constipation -erectile dysfunction -memory changes
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what are the sleep problems in a patient with PD?
-difficulty staying asleep -restless sleep -nightmares -drowsiness during the day -REM sleep behavior disorder -violent dreams, potentially dangerous motor activity during REM sleep
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what are the complications of PD?
-motor symptoms -weakness -neurologic process -neurosychiatric problems -dementia often results
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what can dysphagia cause in a person with PD?
malnutrition and aspiration
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how are patients diagnosed with PD?
-presence of 2 or more cardinal manifestations of TRAP -positive response to the antiparkinsonian drug -medical Hx, presenting symptoms, neuro exam
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what are the drug therapy for PD helping with?
-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)
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what are the therapeutic goals in drug therapy for PD?
-ideal treatment that reverses neuronal degeneration or prevent further degeneration does not exist
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what are the two major drugs for PD?
Dopaminergic agents and anticholinergic agents
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what are the dopaminergic agents used for in PD?
-most commonly used -promote activation of dopamine receptprs -levadopa
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what are the anticholinergic agents used for in PD?
-prevent activation of cholinergic receptors -benztropine (cogentin)
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what is the dopamine replacement medication?
levadopa
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what does levadopa help with?
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
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what should not be taken with levadopa?
high protein foods
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what is the MOA of levadopa/carbidopa (sinemet)
levadopa is converted to dopamine in the CNS. Carbidopa prevents peripheral destruction of levodopa. converted to dopamine in basal ganglia
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what are the adverse effects of levadopa/carbidopa (sinemet)
n/v dyskinesias postural hypotension dysruthmias psychosis impulse control darkened sweat and urine loss of effect
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what is pramipexole used for?
-1st line drug or supplement to levadopa used alone in early PD and with levadopa in advance pd
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what are the adverse effects of pramipexole
sleep attacks nausea dizziness daytime somnolence insomina constopation weakness and hallucinations
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what are the anticholinergic (trihexiphenidyl and benztropine
-blocks muscarinc receptors in the striatium decrease activity of ach
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what should selegiline be given with
with lunch or breakfast
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what is deep brain stimulation
most common surgical treatment reversibel and programmable decrease increase neuronal activity produced by DA
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what is ablation surgery
located target destroy area of the brain affected by PD
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what is ALS?
lou gehrig disease it is progressive, rare, incurable degenerative disease involving the motor system affects more men that women median age of onset 55
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what is the patho of ALS
-rapidly progessing, fatal CNS disease affects voluntary muscle control -does not impair sense or ability to think -affects diaphragm and chest wall
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what is the etiology of ALS
about 10% of ALS is genetics smoking athleticism metals solvents radiation electromagnetic fields pesticides viruses
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what are the clinical manifestations of ALS
-muscle cramps or stiffness muscle weakness slurred speech difficulty swallowing -loss of muscle tone
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upper motor neuron damage in ALS
associated with spasticity
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lower motor neuron damage in ALS
associated with flaccidity
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what are early symptoms of ALS
tongue atrophy dysphagia dysarthria
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what are the late symptoms of ALS
nasal quality of speech fasciculation of the face spasticity weakness of the hands and arms muscle atrophy eventual respiratory muscle involvement
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what are the diagnositcs for ALS
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
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what is Riluzole (rilutek) for ALS?
delayed need for tracheostomy by 3-6 months well tolerated
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what is the MOA of riluzole (rilutek)
reduce damage to motor neurons by decreasing the release of glutamate
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what is the adverse effects of riluzole
asthenia, GI reactions, dizziness, vertigo, somnolence, decreased lung function, neutropenia, and liver injury Taken PO, BID
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what is edaravone (radivaca) for ALS
shown to slow the loss of physical function in early stages of ALS
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what is the MOA edaravone (radivaca)
unknown in the treatment of ALS, but believed to relieve the effects of oxidative stress, a likely factor in progression of ALS
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what is the adverse effect of edaravone (radivaca)
hives; swelling of lips, tongue, or face; fainting; breathing problems; wheezing; trouble swallowing; dizziness; itching; asthma attack Given IV in 14-day cycles
324
what are the complications of ALS?
Aspiration Respiratory failure Pneumonia Pressure ulcers Deep Vein Thrombosis (DVT) Pulmonary embolism (PE) Constipation, contractures Depression Weigh loss Loss of ability for self care
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what do speech pathologist do?
swallow assessment and treatment speech and language cognitive assessment and treatment
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what are the phases of swallowing?
oral pharyngeal esophageal
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difficulty swallowing
dysphagia
328
what are the cognitive dysphagia
dementia head injury lethargic or obtunded patients
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what are the nurses role in dysphagia management?
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
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what are the signs and symptoms for dysphagia?
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
what are the top three risk factors for aspiration pneumonia?
dependence on others for feeding dependence on other for oral care missing or decaying teeth
332
what are other indicators for dysphagia
tube feeding multiple medical diagnosis chronic reflux
333
what is intact with ALS?
Cognitive function is intact while body is giving away
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what is silent aspiration?
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
what are feeding/swallowing precautions?
Chin-tuck Thickened liquids Follow-up swallows Straws v. No straws Throat clearing “General Precautions”
336
what are the special diets?
Clear liquid Full liquid International Dysphagia Diets Regular Restrictions as prescribed by RD or MD!
337
what are the frazier water protocol?
It is tool that allows and encourages patients at high risk of aspiration to have ice and water throughout the day.
338
what are the communication disorders?
motor speech disorders language disorders cognitive-communicative disorders
339
what is an expressive aphagia?
brain doesn't process what you're saying
340
what is SBAR?
situation background assessment recommendation
341
what is pdsa
plan -idea for action do -make the change study -test it and collect data act- adjust actions
342
what is core team?
nursing
343
what is contigency teams?
code blue, physician, respiratory, pharmacy, rapid response
344
what is magnet culture?
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
how does healthcare information technology help?
direct access, decrease in medical errors, decrease in duplicate orders, reduce mistakes in reading hand written
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what does professional nursing look like to you?
caring for patient in a dignified way
347
what is step?
status of patient team members enviroment progress towards goal
348
what is picot
population/patient/problem intervention comparision/contorl outcome time
349