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Clin Med IV Exam II > Motor disorders/ Demyelinating diseases > Flashcards

Motor disorders/ Demyelinating diseases Flashcards

1
Q

Acute onset motor disorders can be what

A

vascular vs toxic/metabolic

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2
Q

Subactue onset motor disorders are what

A
  • neoplastic
  • infectious
  • inflammatory
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3
Q

Chronic onset motor disorders are what

A
  • neoplastic
  • hereditary
  • endocrine
  • degenerative
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4
Q

Disorders of what are not accompanied by altered sensation

A
  • anterior horn cells
  • neuromuscular junction
  • muscles
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5
Q

Myasthenia gravis

A

neuromuscular disorder characterized by weakness and fatigability of skeletal muscles

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6
Q

Defect in MG

A

decrease in the number of available AChRs at neuromuscular junctions d/t anti-body mediated autoimmune attack

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7
Q

Is ACh normally released in MG

A

YES but the decreased number of receptors causes failure to trigger muscle action potentials

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8
Q

What plays a role in the autoimmune response of MG

A

thymus

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9
Q

Peak incidence of MG

A

women in 20s and 30s

men in their 50s and 60s

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10
Q

Cardinal features of MG

A

weakness and fatigability of muscles

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11
Q

What can “unmask” MG

A
  • menses
  • pregnancy
  • antibiotics
  • CCB
  • phenytoin
  • lithium

exacerbates symptoms

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12
Q

What muscles are involved early in MG

A

cranial muscles, particularly lids and extraocular muscles

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13
Q

First presenting complaints on MG

A
  • diplopia

- ptosis

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14
Q

What is especially prominent in MuSK antibody- positive MG

A

bulbar weakness

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15
Q

If weakness remains restricted to the extraocular muscles for 3 years—>

A

it will most likely not progress to the limbs (ocular MG)

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16
Q

Are deep tendon reflexes presevered in MG

A

YES

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17
Q

Proximal or distal muscle weakness in MG?

A

mostly proximal

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18
Q

Sx’s of MG

A
  • diplopia
  • ptosis
  • dysarthria
  • lower extremity weakness
  • generalized weakness
  • dysphagia
  • upper extremity weakness
  • masticatory weakness
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19
Q

PE for MG

A
  • quantitative testing of muscle strength
  • forward arm abduction time
  • vital capacity (breathing)
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20
Q

Labs for MG

A
  • anti AChR radioimunoassay (neg doesnt not r/o MG)
  • repetitive nerve stimulation
  • single fiber electromyography
  • Edrophonium chloride
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21
Q

Mainstay of MG treatment

A

Pyridostigmine

30-120mg every 4 hrs

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22
Q

What can overmedication in MG cause

A

increase in weakness that will not be effected by edrophonium

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23
Q

When would you use a long acting anticholinesterase drug for MG?

A

used at bedtime for pts with persistent severe weakness upon awakening

*Mestinon

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24
Q

Cholinergic crisis

A
  • pallor
  • sweating
  • nausea
  • vomiting
  • salivation
  • colicky abd pain
  • miosis
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25
Q

Glycopyrrolate, propantheline, or hyscyamine are what? What do they cause?

A

anticholinergic drugs

decrease bowel motility and salivation

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26
Q

When should a thymectomy be used for treatment of MG

A

in all pts with thymoma

  • pts younger than 60
  • pts older than 60 with weakness not restricted to extraocular muscles
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27
Q

When is Azthioprine used

A

severe of progressive disease despite thymectomy and tx w/ AChIs and corticosteriods

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28
Q

How long does it make azithioprine to work

A

up to 1 year

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29
Q

When is plasmapheresis used for MG

A

in pts that are deteriorating rapidly or in crisis

special circumstances–> before surgery that will produce respiratory compromise

30
Q

Instead of plasmapheresis what could you use in a sick pt with MG

A

IV immunoglobulins

31
Q

Mycophenolate

A

inhibits proliferation of T and B cells in pts with MG which allows steroid dose to be lowered

32
Q

Cerebral palsy

A

chronic static impairment of muscle tone, strength, coordination, movements that happens around birth

33
Q

Signs and symptoms of CP

A
  • spasticity of the limbs
  • ataxia
  • dyskinetic movement disorder
  • persistent hypotonia without spacitiy
34
Q

What other neurological diseases are associated with CP

A
  • seizures
  • mild/severe retardation
  • varying degrees of language, vision and sensory disorders
35
Q

PE findings with CP

A
  • spasticity
  • hyperreflexia
  • ataxia
  • involuntary movements
  • microcephaly
  • hemiplegia–>affected limb smaller
  • cataracts, retinopathy
36
Q

Treatment of CP

A
  • PT, OT, ST
  • botulism/meds –> spasticity of medication
  • tx of seizures

can improve with age if mild

37
Q

Mean age of onset of Tourettes

A

5 years old, males more than females

38
Q

What is a Tic

A

sudden, brief, uncontrollable repetitive, non rhythmic, stereotyped, purposeless movements or vocalizations

39
Q

What can precede tics

A

premonitory sensations or unpleasant somatosensory sx

40
Q

What can trigger tourettes or make it worse

A
  • worsened by anxiety or excitement

- can be triggered by physical experiences

41
Q

Do tics go away while sleeping

A

no

42
Q

Diagnosing tourettes

A

vocal and motor tics for 1 year

MRI or EEG to r/o other conditions

43
Q

Tx of tourettes

A

no real treatment

  • can use neuroleptics to suppress tics
  • alpha adrenergic agonists
  • ADHD Rx
  • behavioral treatments
44
Q

Multiple sclerosis

A

autoimmune disorder in which the body attacks and destroys the fatty tissues that insulate nerves/axon

45
Q

What part of the NS does MS affects

A

central NS and causes inflammation of white matter in the brain that forms plaques

46
Q

MS is a ___ disease

A

demyelinating

47
Q

Myelin is rich in what

A

lipid and proteins

48
Q

Symptoms of MS

A
  • fatigue
  • depression
  • memory changes
  • pain, spascitiy
  • vertigo, dizziness
  • tremor
  • double vision/vision loss
  • weakness
  • numbness/tingling, ataxia
49
Q

What causes remission of MS

A

remodeling of the demyelinated axonal plasma membrane allowing for more sodium channels to permit conduction despite myelin loss

50
Q

Diagnosis of MS

A
  • need to have 2 episodes of symptoms that occur in different points in time
  • absence of other treatable causes for the sx’s
  • LP, MRI
  • blood tests
  • evoked potentials
51
Q

What do evoked potentials detect

A

slow or abnormal conduction in response to visual or auditory stimuli

52
Q

LP in MS

A

mild pleocytosis and mild elevated total protein

53
Q

What lab finding can be found in patients with MS

A

IgG

54
Q

Primary diagnostic tool for MS

A

MRI (look for plaques)

55
Q

Disease modifying rx for MS

A
  • interferon beta 1a
  • interferon beta 1b
  • glatiramer acetate

*used for relapsed remitting MS

56
Q

Side effects of interferon

A

flu like symptoms, skin irritation

57
Q

Side effects of glatiramer acetate

A

skin erythema, rash, dyspnea, transient chest pain

58
Q

Tx for secondary progressive MS

A

INF-B1b and mitoxantrone

59
Q

When is mitoxantrone bad

A

if a patient has a low EF, Cardiotoxic!

60
Q

What is given for an MG flare

A
  • plasma exhange

- steriods

61
Q

Tx for systemic spasticity in MS

A
  • baclofen

- cyclobenzaprine

62
Q

Tx for optic neuritis in Ms

A
  • methylprednisolone

- oral corticosteriods

63
Q

Tx for tremor in MS

A
  • propranolol

- primidone

64
Q

Guillain-Barre syndrome is

A

an acute inflammatory demyelinating polyneuopathy

65
Q

Precipitating factors for Guillain-Barre

A
  • bacteria
  • CMV
  • HIB
  • EBV
  • surgery
  • trauma
  • malignancy
66
Q

Most common infection causing Guillain-Barre in the US

A

campylobacter jejuni

67
Q

Two subtypes of GBS

A
  • antibody injury to myelin sheath

- antibody injures axonal membrane

68
Q

Sx of GBS due to Zika

A
  • symmetric muscle weakness in lower limbs
  • incapacity to walk
  • areflexia
  • facial palsy
  • trouble swallowing
  • paresthesia
69
Q

What features need to be present for diagnosis of GBS

A
  • progressive weakness in legs and arms

- areflexia in weak limbs

70
Q

Diagnostics for GBS

A
  • LP

- nerve conduction studies

71
Q

Tx for GBS

A
  • IV IG

- plasmapheresis

Clin Med IV Exam II (8 decks)

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