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Nursing 102 > Nervous system Exam #2 > Flashcards

Nervous system Exam #2 Flashcards

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1
Q

What is biofeedback?

A

conservative form of Tx for ppl who suffer from chronic HA. Learn to control body functions that are usually involuntary (ie HR, BP, body temp)

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2
Q

How do nerve blocks work?

A

local anesthetic is injected to inhibit neural pathways

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3
Q

What is neuroablation?

A

permanent nerve destruction to stop nerve impulse transmission permanently

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4
Q

What is chemical ablation?

A

destruction of nerves after admin of chemical agent

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5
Q

What is thermal ablation?

A

use of extreme temps to ablate nerves, cryoablation (cold) or radiofrequency (hot)

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6
Q

What is a cordotomy?

A

sever the spinothalmic tract

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7
Q

What is a tractectomy?

A

sever the spinal tract at the level of the brain stem, dorsal route (sensory) affected only, not ventral (motor)

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8
Q

What is deep brain stimulation?

A

electrodes in brain are connected to implant in chest wall sends impulses to target location to block nerve impulses

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9
Q

What kind of neuroaugmentation is used to Tx seizure disorders?

A

vagal nerve stimulation

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10
Q

Where do inflammatory brain conditions most often originate from?

A

the bloodstream

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11
Q

What is meningitis?

A

inflammation of the meninges

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12
Q

Pathophysiology of meningitis?

A

organism travels to CNS via blood, damages BBB, infects CSF which leads to an increased production of CSF (IICP), protein spills in, less glucose enters

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13
Q

How is bacterial meningitis spread?

A

URI

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14
Q

What is the primary difference between viral & bacterial meningitis?

A

viral is self-limiting, bacterial = medical emergency

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15
Q

What are S/Sx of bacterial meningitis?

A

HEADACHE (earliest sign)

fever, N/V, stiff neck, photophobia

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16
Q

What are 3 classic signs of bacterial meningitis?

A
  1. nuchal rigidity
  2. Positive brudzinski’s sign
  3. Positive Kernig
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17
Q

What is nuchal rigidity?

A

stiff & painful neck, forced flexion = pain & muscle spasms

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18
Q

What is a + Brudzinski’s sign?

A

when examiner flexes pts neck, involuntary knee & hip flexion

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19
Q

What is a + Kernig sign?

A

when pt laying supine with hip flexed, examiner cannot straighten knee

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20
Q

What are S/Sx of IICP?

A

altered mental state

seizures, BP RR HR changes, coma, death

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21
Q

How do you Dx bacterial meningitis?

A

most significant Dx = LP for CSF analysis: cloudy, purulent, increased protein & WBC’s, low glucose

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22
Q

How do you Tx bacterial meningitis?

A

large doses of IV ABX STAT (after cultures drawn), isolation & symptomatic Tx

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23
Q

What is waterhourse-friderichsen syndrome?

A

severe vascular dysfunction

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24
Q

What is the rationale for using decadron for meningitis?

A

decrease cerebral edema = reduces mortality & hearing loss

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25
Q

What is encephalitis?

A

acute inflammation of brain tissue caused by a virus, can be transmitted from mosquitos & ticks

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26
Q

Pathophysiology of encephalitis?

A

virus enters host and accesses CNS, via circulation, where it causes diffuse cortex inflammation

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27
Q

S/Sx of encephalitis?

A

mild to severe, flu-like Sx + IICP Sx (mental changes from minimal to coma, seizures, memory less, motor disturbances)

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28
Q

Which virus should you suspect for adults over 50 with encephalitis or meningitis in summer or early fall?

A

west nile virus

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29
Q

How do you Dx encephalitis?

A

Hx of recent travel or viruses, MRI, CT, PET looking for inflamed tissue, PCR test & Ig M

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30
Q

Tx for encephalitis?

A

antivirals & dexamethasone (decadron) to reduce inflammation

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31
Q

What is a brain abscess?

A

localized collections of pus within brain tissue

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32
Q

Pathophysiology of brain abscess?

A

localized infection causes tissue necrosis & pus formation causes liquidification, becomes encapsulated in a thick fibrous wall

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33
Q

How do brain abscesses reach the brain?

A

infection by direct extension: most common (from ear, tooth, mastoid or sinus infections)
trauma or neurosurgery
bloodstream

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34
Q

Which organisms are usually responsible for brain abscesses?

A

staph & strep

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35
Q

S/Sx of brain abscess:

A

HA, fever, chills, LOC changes + Focal S/Sx depending on location of abscess

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36
Q

How do you Dx & Tx brain abscess?

A

WBC & ESR, cultures, CT/MRI

large doses ABX, craniotomy if ABX not effective

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37
Q

What is prognosis for unTx’ed brain abscess?

A

100% mortality

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38
Q

What is neurosyphilis?

A

inadequately Tx’ed syphillis, not contagious!

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39
Q

Dx for neurosyphilis?

A

RPR (rapid plasma regain) often tested when anyone presents with neuro S/Sx

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40
Q

S/Sx of neurosyphilis?

A

progressive ataxia, lightening pain, slapping gait, Charcot’s joints, loss of DTR

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41
Q

What is Tx for neurosyphilis?

A

Penicillin (neurodeficits will remain!)

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42
Q

What is diff between primary (functional) & secondary (organic) HA?

A 
Primary = HA is primary problem (migraine, cluster or tension HA)
Secondary = results from a medical condition (Sx of another problem)
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43
Q

What causes tension HA?

A

stress/tension

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44
Q

Which is the most common type of HA?

A

tension

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45
Q

What are S/Sx of tension HA?

A

bilateral pain, c/o pressure/tightness, photo/phonosensitivty

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46
Q

How do you Tx tension HA?

A 
Abortive = OTC NSAIDS, muscle relaxers, sedatives, tranquilizers or narcotics (severe)
preventative = antidepressants, Beta-blockers, selective serotonin uptake inhibitors
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47
Q

What is pathophysiology of migraine?

A

neurovascular events cause vessel dilation, constriction & spasm. hyperexcitable neurons in cerebral cortex (particularly occipital lobe)

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48
Q

S/Sx of migraine:

A

unilateral mod-severe pain, usually over 1 eye or ear, throbbing synchronized to pulse accompanied by photo/phonosensitivity & N/V

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49
Q

What triggers migraines?

A

foods containing tyramine, some medications (nitro & estrogen) & bright lights, smells or menses

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50
Q

What is an aura?

A

a sensation that precedes HA & signals onset (often visual)

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51
Q

What are phases of migraines?

A

Prodromal = experiences consistent Sx that often precede HA (food cravings, mood swings) Diff from aura
Second Phase = time pt experiences HA
Third phase = HA termination phase, pain subsiding

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52
Q

What are Tx for migraines?

A

OTC NSAIDS for mild

for severe = triptans

53
Q

How do triptans work? & what are S/Es?

A

affects serotonin receptors to inhibit neurogenic inflammation & cause cranial vasoconstriction
S/E = flushing, tingling or hot sensation

54
Q

What are cluster HA?

A

severe HA caused by hypothalmic dysfunction

55
Q

What are S/Sx of cluster HA?

A

unilateral pain focused around 1 eye, burning sharp severe stabbing pain, occur in rhythmic pattern (same time, same season for wks-months)

56
Q

What is an abortive Tx for cluster HA

A

100% O2 by face mask

57
Q

What is a seizure?

A

paroxysmal, uncontrolled electrical d/c of neurons that interrupts normal function and causes abnormal motor, sensory and autonomic activity

58
Q

How are seizures Dx?

A

Hx of head trauma, illness, birth injury etc
EEG (not definitive)
CT, MRI, cerebral angiogroaphy, MRA

59
Q

What are 2 major classes of seizures?

A

partial & generalized

60
Q

What is the most common type of seizure?

A

generalized tonic-clonic seizure

61
Q

What does tonic mean? clonic?

A 
tonic = muscle stiffness
clonic = abrupt jerky movements & loss of muscle tone
62
Q

Where do generalized seizures occur?

partial?

A 
generalized = always involve abnormal firing on both sides of brain
partial = unliateral manifestations due to localized focal abnormality (can spread into generalized seizure)
63
Q

What is the ictal phase?

A

seizure phase

64
Q

what is the aural phase?

A

sensory warning

65
Q

What is an absence seizure?

A

childhood seizure - brief staring spell lasting just a few seconds. Can be precipitated by blinking/flashing lights (video games!!)

66
Q

What is an atonic seizure?

A

sudden loss of muscle tone, person drops to the floor unconscious, but will usually regain consciousness before they hit the ground

67
Q

What is an atypical absence seizure?

A

staring spell with peculiar behavior and post-seizure confusion

68
Q

What are 2 subdivisions of partial seizures?

A

simple partial seizures (alert) & complex partial seizures (altered LOC)

69
Q

Describe simple partial seizure

A

no loss of consciousness
last < 1 min
Sx are uniliateral: may be sensory (olfactory hallucinations), motor (involuntary movements) or autonomic (increased HR or flushing)

70
Q

Describe complex partial seizure

A

last longer than 1 min, changes in LOC, occur in temporal lobe, may have automatisms (repetitive movements)

71
Q

Describe generalized tonic-clonic seizures

A

Loss OC, tonic, clonic, last 2-5 min, may experience cyanosis, excess salivation, tongue/cheek biting, incontinence

72
Q

What is TODS?

A

transient period of paralysis after a seizure

73
Q

What are 3 criteria for surgery to Tx seizure? and what do they do remove during surgery?

A

3 criteria = confirm Dx, Failed drug trial, identify type of seizure
Surgery = remove epileptic focus to prevent spread

74
Q

What is status epilepticus?

A

continuous seizure w o return to consciousness between. medical emergency b/c neurons become exhausted, leads to permanent brain damage

75
Q

What are 2 primary interventions during status epilepticus?

A

maintain airway & gain IV access

76
Q

Tx for status epilepticus?

A

IV antiepileptics

77
Q

What is Parkinson’s?

A

slowly progressive neurologic movement disorder

78
Q

Patho of parkinson’s:

A

decreased dopamine levels due to destruction of dopamine producing cells, leads to imbalance between dopamine & Ach

79
Q

What are 3 cardinal signs of Parkinson’s?

A

Tremors, rigidity, bradykinesia

80
Q

Dx Parkinson’s:

A

2 out of 3 cardinal signs & trial with anti-parkinson’s meds to look for improvements

81
Q

What is Tx medication for Parkinson’s?

A

Levodopa, dopamine agonists, anticholinergics

82
Q

How does deep brain stimulation help with Parkinson’s?

A

delivers electrical stimulation to inhibit neuronal activity.

83
Q

What is Huntington’s disease?

A

Disease of nervous system that results in involuntary choreiform movements and mental status changes

84
Q

Which gender does Huntington’s affect more?

A

Men & women equally

85
Q

Which gene is responsible for Huntington’s disease?

A

HD gene: IT 15

86
Q

What is patho of Huntington’s?

A

HD gene causes a deficiency in GABA and Ach which = excess dopamine.

87
Q

What are clinical manifestations of Huntington’s disease?

A

chorea & intellectual decline

88
Q

How is Huntington’s Dx?

A

presentation of characteristics, family Hx & genetic testing

89
Q

How do you Tx Huntington’s?

A

No cure or Tx to halt or reverse disease, only symptomatic Tx
Xenazine decreases dopamine availability
Neuroepieptics = calming effect

90
Q

What is MS?

A

chronic, degenerative autoimmune disorder that affects the myelin sheath & conduction pathways of CNS

91
Q

Patho of MS:

A

chronic inflammation leads to myelin sheath damage & gliosis which inhibits impulses in CNS. 1st T cells activated, disrupt BBB barrier, later inflammation within CNS causes demylenation, scarring & axon damage

92
Q

What is the most common & severe Sx of MS?

A

fatigue.

93
Q

What are other Sx of MS:

A

impaired movement, stiffness, gait problems, tremors w activity, hyperactive DTR, poor balance, visual disturbances, parasthesias, vertigo, tinnitus, Pain, ST memory loss

94
Q

What are classifications of MS?

A

relapsing remitting, Secondary progressive, primary progressive, progressive relapsing

95
Q

what happens to people w MS during pregnancy?

A

most will see remission, or at least improvement, of Sx during pregnancy, but high risk for exacerbation postpartum

96
Q

What is the primary tool for Dxing MS?

A

MRI to visualize plaques and scarring

97
Q

What do MS meds do?

A

reduce plaques (# & size) & reduce frequency & duration of relapses

98
Q

What is primary MS med?

A

interferon injections

99
Q

What is Tx for acute exacerbation of MS?

A

ACTH (adrenocorticotropic hormone) IV

solu-medrol IV for 1-2 weeks

100
Q

What is ALS?

A

Amyotrophic Lateral Sclerosis is a rapidly progressive neurologic disorder that causes degeneration of UMN & LMN. leads to progressive debilitating muscle weakness

101
Q

ALS does not affect:

A

Senses, function, or intellect

102
Q

What is the most widely accepted theory behind ALS?

A

Protein mishandling. mishandled proteins build up & caused nerve cell damage

103
Q

Clinical manifestations of ALS:

A

initially muscle weakness & fatigue
then muscle twitching, spasticity & hyperreflexia
dysarthria, dysphagia, pain & resp difficulties

104
Q

What is the cause of death with ALS most often?

A

Respiratory failure

105
Q

What is the only med approved to Tx ALS?

A

glutamate antagonists (rilutek or riluzole)

106
Q

What is myasthenia gravis?

A

autoimmune, muscle fatigue & weakness caused by inadequate Ach receptor site stimulation due to Ach receptor antibodies

107
Q

Patho of MG:

A

Antibodies are produced that block Ach receptor sites, decreased available sites = not enough Ach stimulation to cause muscle contraction

108
Q

What is definitive Dx for MG?

A

tensilon test: assess muscle stength, IV admin of tensilon, reassess muscle strength. improved muscle strength = +MG

109
Q

Primary manifestation of MG?

A

muscle fatigue, worse at the end of the day

110
Q

which muscles are most affected w MG?

A

eyes, eyelids, & facial muscles

111
Q

What is a Simpson eye test?

A

when pt looks up for a few min eyelid will begin to droop bc of muscle fatigue

112
Q

What is 1st line of therapy for MG? 2nd line?

A

anticholinesterase drugs: Mestinon = most successful.

2nd = immunoglobulin G

113
Q

What are 2 complications of MG?

A

myasthenic crisis & cholinergic crisis

114
Q

What is Myasthenic crisis?

A

insufficient medication- under stimulation of Ach receptor sites by Ach

115
Q

What is cholinergic crisis?

A

excessive medication- excess stimulation of Ach receptor sites by Ach

116
Q

What are S/Sx of myasthenic & cholinergic crisis? What are primary concerns

A

ptosis, dyspnea, dysarthria & dysphagia. primary concerns = aspiration & resp insufficiency

117
Q

How do you Tx myasthenia crisis?

A

IV tensilon

118
Q

How do you Tx cholinergic crisis?

A

Atropine

119
Q

What is trigeminal neuralgia?

A

disease affecting the 5th cranial nerve (trigeminal)

120
Q

What are the 3 branches of the trigemnial nerve?

A

ophthalmic, maxillary & mandibular

121
Q

What are clinical manifestations of trigeminal neuralgia?

A

sudden, unilateral excruciating pain of the face

122
Q

What are trigger zones?

A

zones that will initiate pain with benign event

can be a draft, brushing teeth, touching face etc

123
Q

What is Dx for trigeminal neuralgia?

A

imaging to r/o other causes of pain

124
Q

What is Tx for trigeminal neuralgia?

A

anti-epileptics

125
Q

What is guillain barre syndrome?

A

acute autoimmune attack on myelin sheath of peripheral nerves, characterized by symmetrical ascending muscle weakness

126
Q

patho of guillain barre:

A

edema, inflammation & demyelination of nerves by antibodies

127
Q

in which direction does remyelination occur?

A

proximal to distal

128
Q

what is #1 complication of guillain barre?

A

respiratory failure

129
Q

what is therapy of choice for guillain barre?

A

IV immunoglobulin

Nursing 102 (9 decks)

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