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adults > MS, MG, Guillain-Barre, cranial nerve and PNS disorders > Flashcards

MS, MG, Guillain-Barre, cranial nerve and PNS disorders Flashcards

1
Q

terminology

ataxia

A

impaired coordinationof movement during voluntary movement

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2
Q

terminology

diplopia

A

the awareness of two images of the same object occuring in one or both eyes

generally occurs with MG

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3
Q

terminology

dysphagia

A

difficulty swallowing

seen with parkinsons, MG, ALS, MS

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4
Q

terminology

dysphonia

A

voice impairment or altered voice production

nasallly tone

seen with MS and MG

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5
Q

terminology

neuropathy

A

general term indicating a disorder of the the nervous system

numbness, tingling, burning

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6
Q

terminology

ptosis

A

drooping of the eyelids

seen with MG

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7
Q

terminology

spasticity

A

muscular hypertonicity with increased resistance to stretch often associated with weakness, increased deep tendon reflexes, and diminished superficial reflexes

CNS related, jerky movements

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8
Q

name some infectious neurologic disorders

A
  • meningitis
  • brain abscesses
  • encephalitis
  • creutzfeldt-jakob disease

all of these lead to change in LOC
can use lumbar puncture, CT, MRI

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9
Q

describe meningitis

A
  • inflammation os meninges
  • originates through blood or invasive procedures
  • clinical manifestations include HA, neck rigidity, phtotophobia, and rash
  • diagnostic testing includes CT, lumbar puncture, C&S of CSF
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10
Q

describe brain absecesses

A
  • frequent in immunocompromised/bacteria can cause
  • clinical manifestations - HA (worse in AM), mental status changes
  • diagnostics: CT/MRI, drainage of abscess
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11
Q

describe encephalitis

A
  • inflammation of the brain tissue (increased ICP -> cushings triad)
  • causes: viruses, arthropod vectors
  • clinical manifestations: HA, fever, confusion, hallucinations, focal seizures
  • diagnostics: EEG, CT, MRI, lumbar puncture, PCR (polymerase chain reaction)
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12
Q

describe creutzfeldt-jakob disease

A
  • group of infectios disorders: mad cow disease (infected meat with prions, lie dormant)
  • originates through blood or invasive procedures
  • clinical manifestations: psychiatric symptoms, uncoordinated movements, memory loss
  • diagnostics: brain biopsy, EEG, MRI, lumbar puncture
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13
Q

what is multiple sclerosis

A
  • progressive demyelinating disease of the CNS
  • impaired nerve impulses in spine and brain

the demyelenation of axons can affect the eyes, muscles, grasp, digestion, urinary spasms, neurogenic bladder, and speech

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14
Q

who is at a higher risk of multiple sclerosis

A
  • peak age 25-35 years
  • women twice as likely as men
  • prevalent in colder climates
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15
Q

describe the cause of multiple sclerosis

A

exact cause is unknown but there are theories like:
- may be immunogenetic viral infection - epstein-barr virus
- HLA gene on chromosone 6

potential risk factors include:
- smoking
- lack of vitamin D
- epstein-barr virus

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16
Q

is multiple sclerosis predictable?

A

nope it is unpredictable in nature

  • variable pathophysiology
  • no two patients are alike in care needs
  • demyelination disrupts nerve impulses
  • plaques develop on demylinated axons
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17
Q

what are the four typical courses of multiple sclerosis

A
  • relapsing remitting: most common, manifestations remit with little or no progression
  • seondary progressive: gradual neurologic deterioration
  • primary progressive: gradual continuous deterioration
  • progressve relapsing: gradual deterioration with occasional superimposed relapses (never go back to baseline)
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18
Q

what are some clinical manifestations of multiple sclerosis

A

symptoms vary depending on location of the lesion

  • main symptoms: fatigue, depression, weakness, paresthesia, ataxia, loss of balance, spasticity, pain
  • visual disturbances: blurred vision, diplopia, loss of peripheral vision, scotoma (patchy blindness), total blindness
  • bladder/bowel dysfunction: hesitancy, frequency, urgency, retention, and constipation
  • sexual dysfunction
  • dysarthria
  • dysphagia
  • mood changes
  • cognitive impairment
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19
Q

what are some gerontologic considerations for multiple sclerosis

A
  • high risk of med interactions
  • monitor closely for toxicities d/t altered pharmacokinetics
  • lots of meds are hard on the liver
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20
Q

describe the diagnosis of multiple sclerosis

A
  • patient history: clinical presentation (partial diagnosis)
  • imaging: presence of plaques on MRI
  • lab findings: lumbar puncture to check CSF for presence of oligoclonal banding
  • urodynamic studies: underling bladder dysfunction
  • evoked potentials of optic pathways and auditory system: slowed never conduction
  • neuropsychological testing: detects cognitive impairments
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21
Q

what is the goal of treatment for multiple sclerosis

A

slow progression of the disease, manage symptoms, and treat acute exacerbations

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22
Q

describe pharmacologic disease modifying therapies for relapsing-remitting MS

A

interferon Beta: suppress immune system
glatiramer: used speicifically for relapsing-remitting MS, works by stopping the body from damaging its own nerve cells
methylprednisolone: for exacerbations, watch glucose Q6, suppresses immune system

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23
Q

MS drugs

whats used for spasticity

A
  • baclofen
  • tizanidine
  • dantrolene
  • benzos
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24
Q

MS drugs

whats used for anxiety

A

benzodiazepines - diazepam
also used for spasticity

25
Q

MS drugs

whats used for fatigue

A

amantadine

26
Q

MS drugs

whats used for bladder issues

A

anticholinergics

tell em to piss and shit before giving this

27
Q

what are some nonpharmacological treatments for MS

A

individualized care plan
- physical, functional, and emotional/social needs
- safety (increased risk for falls)
- mobility (ROM)
- bowel and bladder control

28
Q

describe myasthenia gravis

A

Autoimmune disease affecting the myoneural junction characterized by varying degrees of weakness of voluntary muscles
- Antibodies directed at acetylcholine receptor sites impair transmission of impulses across the myoneural junction (80%)
- Resulting in less stimulation → Voluntary muscle weakness
- May have thymic hyperplasia or thymic tumor

29
Q

when are the two peaks of onset for myasthenia gravis

A
  • 20-30yrs for women
  • after 50 for men
30
Q

whats the hallmark symptom of myasthenia gravis

A

increased weakness with sustained muscle contraction that improves after periods of rest

31
Q

what are the clinical manifestations of myasthenia gravis

A
  • ocular manifestations are most common (80%): ptosis and diplopia
  • weakness of muscles of face and throat: expressionless face, difficulty swallowing, difficulty chewing
  • dysphonia: nasally voice
  • may also affect extremities, trunk, neck, and breathing
  • degree of weakness varies from local to generalized
  • symptoms vary in type and degree
32
Q

describe the diagnosis of myasthenia gravis

A
  • history
  • clinical presentation
  • physical exam (cant maintain contraction)
  • neurological exam
  • diagnostic tests
33
Q

what diagnostic tests are used in the diagnosis of myasthenia gravis

A
  • anticholinesterase inhibitor test
  • ice test (used for patienrs with asthma or cardiac conditions)
  • blood tests (positive for acetylcholine receptor antibodies)
  • nerve conduction tests
  • EMG
  • MRI to assess for enlarged thymus gland
34
Q

describe anticholinesterase inhibitor test

A
  • edrophonium (tensilon test) IV: improve 30 seconds after injection lasting 5 mins
  • neostigmine for diagnostic purposes

atropine is antidote for both drugs

35
Q

describe the treatment of myasthenia gravis

A
  • pharmacological
  • surgical
  • others given with exacerbations: intravenous immune globulin, therapeutic plasma exchange
36
Q

what pharmacological therapy is used for myasthenia gravis

A
  • anticholinesterase agent: pyridostigmine (generally given 4x/day to help control weakness)
  • immunosuppressive drugs: corticosteroids (reduce levels of serum Ach receptor antibodies, sx get worse b4 getting better)
  • cytotoxic drugs: azathioprine (reduces receptor antibody levels; adverse effects are leukopenia and liver toxicity)
37
Q

what surgical therapies may be used for myasthenia gravis

A

thymectomy

38
Q

describe therapautic plasma exchange (aka plasmapheresis) for myasthenia gravis exacerbations

A
  • done in specialty area
  • central line used, pull blood out and take out plasma then give antibodies
  • used daily for a couple weeks
39
Q

what are some possible triggers of a myasthenia crisis

A
  • resp infection
  • med changes/sudden withdrawal of meds
  • surgery
  • pregnancy
  • stress on the body
  • spontaneously
40
Q

what are some symptoms of myasthenia crisis

A
  • severe generalized muscle weakness
  • severe resp/cyanosis
  • sudden rise in BP secondary to hypoxia
  • increased HR
  • absent cough and swallow reflexes
  • increased secretions (salivation, diaphoresis, tearing)
  • restlessness, dysarthria
  • bowel/bladder incontinence
41
Q

whats the treatment for myasthenia crisis

A
  • increase meds
  • may need mechanical vent
42
Q

what is a cholinergic crisis

A

excess of acetylcholine (over medication)

43
Q

what are some symptomgs of cholinergic crisis

A
  • severe abd cramps
  • bronchospasms
  • N/V
  • increased secretions
  • increased weakness
  • blurred vision
44
Q

whats the treatment of cholinergic crisis

A
  • discontinue all cholinergic meds until symptoms subside
  • provide ventilation support
  • atropine 1mg to reverse side effects of meds
45
Q

will the majority of patients with myasthenia gravis live normal life expectancy?

A

yep

46
Q

what is guillain-barre

A

acute inflammatory demyeleinating polyneuropathy affecting the peripheral nervous system

47
Q

what are some causes of guillain-barre

A
  • autoimmune response a viral infection
  • often preceded by URI or GI infection (1-4wks)
  • various potential viruses like campylobacter jejuni, cytomegalovirus, epstein barr, and others
48
Q

what are some types of guillain-barre

A
  • ascending (most common): starts at feet and works its way up
  • purely motor
  • descending
  • miller fisher syndrome (rare)
  • acute pan-automatic neuropathy
49
Q

what are the characteristics of ascending weakness guillain-barre

A
  • starts in lower extremities
  • paresthesia - hands and feet
  • pain
  • hyporeflexia
  • can involve paralysis up to and including resp system
50
Q

what are the three phases of guillain-barre

A
  • initial acute: 1-3wks after viral infection (be very aware)
  • plateau: 2-4wks, stops progressing
  • recovery occurs in a descending pattern (usually maximal recovery within 6mo (up to 2 yrs)

excellant prognosis, 70% make full recovery

51
Q

whats included in the diagnosis of guillain-barre

A
  • history: type of infection, resp status, recent weakness
  • clinical presentation
  • CSF examination (lumbar puncture)
  • EMG (assess muscle response)
52
Q

whats included in the medical treatment of guillain-barre

A
  • considered a medical emergency
  • focus of therapy is resp and supportive care
  • therapeutic plasma exchange
53
Q

whats included in nursing management of guillain-barre

A
  • vitals
  • resp assessments
  • assess and manage swallowing
  • intake and output (SIADH - retaining fluids)
  • mobility (prevent contractures)
  • pain (meds)
  • preventing complications (monitor skin, VTE risk, EKG, pneumonia, and aspiration risk)
54
Q

what cranial nerve does trigeminal neuralgia affect

A

V

55
Q

describe trigeminal neuralgia

A
  • affects cranial nerve V
  • causes sudden pain in face and facial contraction
  • use anticonvulsants to relieve pain -> calms nerves down
56
Q

what cranial nerve does bells palsy affect

A

VII

57
Q

describe bells palsy

A
  • affects cranial nerve VII
  • inflammation of the nerve and paralysis of facial muscle
  • drooping face
  • treat with steroids and check sugar
58
Q

describe peripheral neuropathies

A
  • numbness, tingling, burning in hands and feet
  • both motor and sensory
  • most common cause is diabetes
  • untreated: atrophy, weakness, and decreased reflexes
59
Q

describe mononeuropathy

A
  • one nerve
  • like carpal tunnel

adults (51 decks)

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