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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
# MS drugs whats used for fatigue
amantadine
26
# MS drugs whats used for bladder issues
anticholinergics tell em to piss and shit before giving this
27
what are some nonpharmacological treatments for MS
individualized care plan - physical, functional, and emotional/social needs - safety (increased risk for falls) - mobility (ROM) - bowel and bladder control
28
describe myasthenia gravis
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
when are the two peaks of onset for myasthenia gravis
- 20-30yrs for women - after 50 for men
30
whats the hallmark symptom of myasthenia gravis
increased weakness with sustained muscle contraction that **improves after periods of rest**
31
what are the clinical manifestations of myasthenia gravis
- 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
describe the diagnosis of myasthenia gravis
- history - clinical presentation - physical exam (cant maintain contraction) - neurological exam - diagnostic tests
33
what diagnostic tests are used in the diagnosis of myasthenia gravis
- 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
describe anticholinesterase inhibitor test
- edrophonium (tensilon test) IV: improve 30 seconds after injection lasting 5 mins - neostigmine for diagnostic purposes atropine is antidote for both drugs
35
describe the treatment of myasthenia gravis
- pharmacological - surgical - others given with exacerbations: intravenous immune globulin, therapeutic plasma exchange
36
what pharmacological therapy is used for myasthenia gravis
- **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
what surgical therapies may be used for myasthenia gravis
thymectomy
38
describe therapautic plasma exchange (aka plasmapheresis) for myasthenia gravis exacerbations
- done in specialty area - central line used, pull blood out and take out plasma then give antibodies - used daily for a couple weeks
39
what are some possible triggers of a myasthenia crisis
- resp infection - med changes/sudden withdrawal of meds - surgery - pregnancy - stress on the body - spontaneously
40
what are some symptoms of myasthenia crisis
- 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
whats the treatment for myasthenia crisis
- increase meds - may need mechanical vent
42
what is a cholinergic crisis
excess of acetylcholine (over medication)
43
what are some symptomgs of cholinergic crisis
- severe abd cramps - bronchospasms - N/V - increased secretions - increased weakness - blurred vision
44
whats the treatment of cholinergic crisis
- discontinue all cholinergic meds until symptoms subside - provide ventilation support - atropine 1mg to reverse side effects of meds
45
will the majority of patients with myasthenia gravis live normal life expectancy?
yep
46
what is guillain-barre
acute inflammatory demyeleinating polyneuropathy affecting the **peripheral nervous system**
47
what are some causes of guillain-barre
- 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
what are some types of guillain-barre
- **ascending** (most common): starts at feet and works its way up - purely motor - descending - miller fisher syndrome (rare) - acute pan-automatic neuropathy
49
what are the characteristics of ascending weakness guillain-barre
- starts in lower extremities - paresthesia - hands and feet - pain - hyporeflexia - can involve paralysis up to and including resp system
50
what are the three phases of guillain-barre
- 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
whats included in the diagnosis of guillain-barre
- history: type of infection, resp status, recent weakness - clinical presentation - CSF examination (lumbar puncture) - EMG (assess muscle response)
52
whats included in the medical treatment of guillain-barre
- considered a medical emergency - focus of therapy is resp and supportive care - therapeutic plasma exchange
53
whats included in nursing management of guillain-barre
- 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
what cranial nerve does trigeminal neuralgia affect
V
55
describe trigeminal neuralgia
- affects cranial nerve V - causes sudden pain in face and facial contraction - use anticonvulsants to relieve pain -> calms nerves down
56
what cranial nerve does bells palsy affect
VII
57
describe bells palsy
- affects cranial nerve VII - inflammation of the nerve and paralysis of facial muscle - drooping face - treat with steroids and check sugar
58
describe peripheral neuropathies
- numbness, tingling, burning in hands and feet - both motor and sensory - most common cause is diabetes - untreated: atrophy, weakness, and decreased reflexes
59
describe mononeuropathy
- one nerve - like carpal tunnel

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