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NEURO CLERKSHIP > MS, neuromuscular junction > Flashcards

MS, neuromuscular junction Flashcards

1
Q

is RRMS or PPMS more common in women than men

A

RRMS is- the progressive primary is about the same

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2
Q

what does the absolute diagnostic criteria for demonstration of dissemination of disease related events requires?

A

seperation of both time and place

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3
Q

clinically isolated demyelinating syndromes —what predicts whether it will become MS?

A

MRI- less risk if MRI is normal at start of CIDS

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4
Q

T-F–MS is almost always a LMN syndrome?

A

false, UMN

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5
Q

what has greater than sensitivity than MRI for MS?

A

CSF analysis

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6
Q

what is the CSF findings in MS?

A

elevated IgG index, IgG synthetic rate, oligoclonal bands (not found in blood)

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7
Q

what tech can help show lesiion demonstrated in space?

A

unilateral conduction delay of the P100 evoked potential

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8
Q

what standard screening tests should be conducted in someone with MS?

A

CBC, CMP, ESR, ANA, B12, infection or hypercoaguability measures
(ALL SHOULD BE NEGATIE IN STRAIGHT FORWARD MS)

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9
Q

separate MS attacks must have how long between them?

A

30day

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10
Q

What might cause a pseudo MS attack or worsening of symptoms?

A

high fever, vigorous exercise, hot water baths or showers or environmental heat

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11
Q

what major categories of illness make up the core differntials for MS?

A 
Inflammatory disease
infectious diseas
disease of myelin
vascular disease
misc.(spinocerebellar, arnold-chiari, B12, hashimoto, Leber's-mitoch)
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12
Q

T-F all MS gets worse over time?

A

trure

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13
Q

T-F men with later onset usually do worse than women in MS ?

A

true with more evident myelopathic symtpoms

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14
Q

T-F- MS cerebellar symptoms tend to do worse over time?

A

true

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15
Q

T-F—younger onset means worse long term with MS?

A

false

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16
Q

T-F- optic neuritis at onset for MS tends to have worse long term?

A

False

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17
Q

t-F intervals of MS attacks >1year fear well

A

True

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18
Q

do persistent ambulation difficulties arise sooner in progressive-from-onset or relapsing from onset?

A

progressive from onset

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19
Q

preg and breastfeeding makes MS worse?

A

false- usually a relative protected time. without breast feeding might be worse

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20
Q

how many patients with RRMS become SPMS after 10 years?

A

50%

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21
Q

How many RRMS patients wil need a walking aide 15-23 years later?

A

50%

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22
Q

review the list of disease modifying MS drugs

A

interferon beta, glatiramer acetate, mitoxantrone, natalizumab, fingolimod, teriflunomide, dimethyl fumarate

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23
Q

T-F–MS has a correlation between EBNA-1 IgG and gadolinium enhancing MRI lesions?

A

true

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24
Q

MS patients need what tests for diagnosis?

A

MRI and CSF for oligoclonal bands and IgG inde

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25
Q

review a list of common MS symptoms

A

neurogenic bladder, fatigue, spasticity, sexual dysfunction, depression

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26
Q

does ALS start limb or face symptoms first?

A

limb onset usually

27
Q

what are common ALS management things?

A

biPAP, feeding tube, communication devices, medications for drooling, ALS clinic rehab, clinical trials

28
Q

what is the mean time of after diabetes onset to development of neuropathy?

A

8 years
Type 1 longer
Type 2 may actually be before

29
Q

is burning pain or proprioception large myelinated fibers?

A

proprioception- pain is small unmyelinated

30
Q

does regulated blood glucose reverse polyneuropathy?

A

no but may lessen pain

31
Q

what medications do we use to treat neuropathy pain?

A

gabapentin, amitriptyline and pregabalin

32
Q

what are the common infections of guillane barre?

A

CMV, EBV, campy, Hib

33
Q

what are the antibodies against?

A

schwan cells/myelin

on peripheral nerves

34
Q

does guillane barre effect sensation or motor?

A

both and then may effect breathing, heart rate, urinary retention, ileus

35
Q

what does nerve conduction studies show for guillane barre?

A

demyelinating pattern

36
Q

what does CSF show in guillane barre?

A

elevated total protein and no or few WBCs

37
Q

what is Rx for guillane barre?

A

admit- monitor respiratory- may need IVIG or plasmapheresis

38
Q

although many improve with guillane barre with time, what may persist in 50%-

A

neuropathic signs- paresthesias and numbness

39
Q

what are antibodies of mysenthia gravis agains?

A

AcH receptors > reduction in action potentials of the muscle membrane and therefore muscle weakness

40
Q

what is the most common presenting symptom of myesthenia gravis?

A

ptosis and diplopia

41
Q

how do we diagnose myasthenia gravis?

A

blood test acetylcholine receptor antibodies

cholinesterase inhibitors like tensilon or prostigmine and weakness should improve

slow rate repetitive nerve stimulation > decrement

42
Q

what is symptomatic medication for myasthenia gravis?

A

pyridostigmine

43
Q

what is immunosuppresive treatment for myasthenia gravis?

A

prednisone, azathiprine, mycophenolate mofetil

44
Q

what is used to treat myasthenia in acute severe crisis?

A

IVIG plasmapharesis

45
Q

what organ may be removed to treat myasthenia gravis?

A

thmymectomy

46
Q

is lambert eaton presynaptic or post synaptic?

A

pre

47
Q

what are clinical features of lambert eaton?

A

fatiguing weakness, dry mouth, ED

48
Q

what is lambert eaton often associated with?

A

malignancy- small cell lung carcinoma

49
Q

how do we diagnose lambert eaton?

A

blood test P/Q ca channel antibodies, high rate repetitive nerve stimulation increment

50
Q

is botulism a pre or post synaptic disorder?

A

pre synaptic

51
Q

where do botulism symptoms start and then where do they fo?

A

bulbar then limbs and then respiratory

52
Q

what is management of botulism?

A

supportive- ICU vent feeding. antitoxin

53
Q

how do we diagnose polymyositis?

A

Creatine Kinase level elevation 50x

-muscle biopsy invasion of fibers by Tcells

54
Q

How do we treat molymyositis?

A

prednisone

55
Q

what is unique about dermatomyositis?

A

rashes- heliotrope rash-

56
Q

what is the difference in diagnostic biposy of dermatomyositis?

A

perivascular inflammatory infiltrates, perifascicular atrophy is pathognomonic

57
Q

what is the clinical hallmark of inclusion body myositis?

A

early weakness and atrophy of quads and forearms (wrist and finger flexors) and foot drop

58
Q

what does muscle biopsy of inclusion body myositis show?

A

endomysial inflammation with basophilic granular indclusions around the edges of vacuoles

59
Q

does inclusion body myositis respond to immunosupressors?

A

no

60
Q

what is the most common inherited neuromuscular disease in adults?

A

myotonic dystrophty- CTG

61
Q

why does myotonia occur in MD?

A

chloride channel abnormality

62
Q

where do we see muscle wasting in myotonic dystrophy?

A

temporal wasting

63
Q

what clinical features not related to muscle are often found with myotonic dystrphy,

A

cataracts, arrhythmias, hypogonadism, hypersomnia, frontal balding, retardation apathy

NEURO CLERKSHIP (7 decks)

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