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Neuro Rehab 2 > Myasthenia Gravis > Flashcards

Myasthenia Gravis Flashcards

1
Q

what is myasthenia gravis

A

LMN myopathic disorder w NM junction pathophysiology

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2
Q

what is the pathophysiology of MG

A

autoimmune dz

antibodies produced against ACh receptors of postsynaptic membrane at the NMJ

bind to ACh receptors and causes destruction

ACh unable to bind to post-synaptic membrane

dec amp in end-plate potentials

dec action potentials and weak ms contraction

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3
Q

is MG hereditary

A

not a genetic health condition

however, inc risk of MG if there is an autoimmune d/o (thyroid dz, RA, lupus) in the family

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4
Q

what are 3 possible etiologies of MG

A

inc risk if autoimmune in fam
viral/bacterial trigger
thymus gland link

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5
Q

how has MG been possibly linked to thymus gland as an etiology

A

thymus gland involved w immune cell production
- programs T cells to recognize self vs non-self

tumor of thymus gland or thymic hyperplasia seen in people w MG
- possible that T cell malfunction results in autoimmune attack

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6
Q

what is the general pattern seen in the demographics of prevalence of MG

A

more common in <50yo F
more common in >50yo M

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7
Q

why can it be difficult to initially dx MG

A

fluctuation in sx
- sx may also be mild at first

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8
Q

how is MG dx

A

presence of Ab in antibody testing + clinical presentation* confirms dx

*clinical s/sx
differentials r/o
- psych d/o
- stroke/TIA
- MS
- ALS
- other NM d/o

(don’t need antibody testing to be dx w MG - can be dx based of clinical sx w differentials r/o)

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9
Q

what is antibody testing for MG

A

antibodies (Ab) against ACh receptors present in 90% of pts w MG (seropositive)

seronegative doesn’t fully r/o MG

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10
Q

what are all the dx tests for MG

A

antibody testing
blood serum testing
EMG studies
Tensilon test
MRI/CT of thymus

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11
Q

what would EMG studies show in MG

A

rapidly declining action potential in ms upon repeated nerve stim

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12
Q

what does tensilon (edrophonium) test for in MG

A

rapid acting cholinesterase inhibitor admin via IV
- produces temp inc in strength of contraction

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13
Q

how are clinical subgroups of MG organized

A

age of onset
- neonate, juvenile, early, late
seroneg MG (no Ab)
location of weakness
- thymus tumor, eye, generalized

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14
Q

what are clinical features of MG

A

facial, eye neck weakness
- asymmetrical, fluctuating
ptosis
weakness of oropharyn ms
- dysphag, dysart, nas speech
impacts respiratory ms
fatigue/weakness w activity

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15
Q

what is the most common motor sx

A

ptosis

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16
Q

how does fatigue and weakness often present in MG and how is this an education point for us

A

worse w activity
relieved by rest

provide ed on pacing
more strenuous activities early in day, allow rest breaks

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17
Q

what is a key feature of how sx present in MG

A

sx (esp ptosis) becomes more pronounced w fatigue as they get tired throughout the day

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18
Q

what are aggravating factors for MG

A

emotional stress
systemic illness
thyroid d/o
pregnancy
menstrual cycle
inc body temp
meds

19
Q

what meds can be aggravating factors in MG and why

A

ms relaxants
- dec strength of contractions, exacerbates

milk of magnesia
- related to substances in ms contraction (mg)

local anesthetics
some antibiotics

20
Q

what is the most common and primary sx in MG at time of dx

A

ocular sx

21
Q

what is the course of MG

A

fluctuating, overall progressive
- periods of active and inactive states

progression from ocular to generalized sx w/i 2yr period

diurnal changes - sx worse at night

nadir w/i 1-3yrs of onset

22
Q

what is the average length of remission if pt w MG were to go into remission

A

5yr

23
Q

what is the prognosis for someone w MG

A

good
- not rapidly progressive or fatal in most people
- better outcomes if dx early and treated early

24
Q

how is MG severity related to antibody testing

A

inc severity in seropositive MG

  • but better px w early thymectomy (thymus tumors or hyperplasia often removed)
  • thymectomy benefit may dec w age of onset
25
Q

how does px vary between thymoma and non-thymoma MG

A

similar severity and outcomes

sorry trick question mamas

26
Q

what is the main source of mortality in MG

A

myasthenic crisis
- acute, severe flare
- more common in women
- cause respiratory failure
- rare

27
Q

what are medical management options for MG

A

cholinesterase inhibitors
thymectomy
corticosteroids
immunosuppressants
plasma exchange and IVIg

28
Q

how does cholinesterase inhibitors work to manage MG

A

prevent degradation of ACh
- can’t help w binding site so inc level of ACh in NMJ so that more ACh is available and circulating

29
Q

typical outcomes for ocular MG

A

low disability rate
respond well to drug therapy
high rate of spontaneous remission

30
Q

what are side effects of cholinesterase inhibitors

A

abdominal cramps
diarrhea
excessive saliva production

usually not severe or troublesome enough for people to go off meds

31
Q

who is a thymectomy contraindicated in for MG

A

children

32
Q

who is a thymectomy controversial in for MG

A

ocular MG
- if ocular only sx, rare to prescribe this surgery

33
Q

when will you see the best outcomes from a thymectomy in MG

A

people <60yo
early in dz process

34
Q

what are typical outcomes for a thymectomy in MG

A

70-80% have inc strength or dec need for meds
- remission rate of 33-38% but not immediate

35
Q

why are corticosteroids used in medical management of MG

A

dec autoantibody synthesis
anti-inflammatory effects

36
Q

what types of medical management strategies are more short term / for an acute crisis in MG

A

corticosteroids
immunosuppressants
plasma exchange and IVIg

would want to switch to other meds after (cholinesterase inhibitors)

37
Q

what are SE of corticosteroids in MG

A

OP
wt gain
high BP
GI disturbances

want to avoid taking these long term

38
Q

why are immunosuppressants used in management of MG

A

lessen autoimmune attack

39
Q

what is a risk w the use of immunosuppressants in managing MG

A

inc risk of infection

40
Q

what is the efficacy of plasma exchange and IVIg in managing MG

A

fast acting and effective
- but temp effects

more effective if combined w drug therapy

41
Q

what PT intervention is indicated to prevent/dec severity of a myasthenia crisis

A

inspiratory ms training

42
Q

what does evidence say ab PT and MG

A

lack of evidence to support specific interventions

43
Q

what are PT strategies for MG

A

breathing exercises
submax resistive therex w low reps
aerobic exercise

44
Q

what are the goals/purposes of PT in MG

A

PT = minimize effects
prevent disuse atrophy
focus on function/participate

goal is to educate people on need for frequent rest periods and pacing as sx worsen w repetitive use and w day

Neuro Rehab 2 (48 decks)

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