Demyelination, Cohen Flashcards

1
Q

presenting Sx of MS

A

visual loss, diplopia, dysarthria, ataxia, paralysis, sensory loss, bladder and sexual dysfunction
loss of cognitive abilities

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2
Q

type of destruction in MS

A

myelin destruction in oligodendrocytes

axons destroyed

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3
Q

age onset MS

A

late 20s

female >M

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4
Q

gender prognosis MS

A

male worse prognosis

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5
Q

geography Ms

A

north equator more common

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6
Q

twin studies MS

A

more common in monozygotic than dizygotic

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7
Q

HLA MS

A

DR15

D3 D4

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8
Q

pathology MS

A
T cell mediated against CNS myelin
inflammation
some B cells
macrophages!
cytokines and chemokines
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9
Q

what cytokines and chemokines are released in MS

A

INF beta and gamma

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10
Q

tyeps of courses of MS

A

benign MS
relapsing remitting
secondary chroni
primary progressive

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11
Q

majority MS is what pattern

A

relapsing remitting

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12
Q

course of benign MS

A

small number of mild attacks and regain full function eventually

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13
Q

why are legs affected more in MS than arms

A

more myelin

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14
Q

what amount of attacks in first few years of MS suggests poor prognosis

A

> 1 attack/year

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15
Q

life expenctancy shortage in MS patients

A

5-10 years

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16
Q

Kurtzkes rule

A

90% disability in MS occurs within 10 years initial dx

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17
Q

Common Sx in first attack of MS

A

visual loss or double vision
weakness
paresthesia

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18
Q

Dx of MS

A

easier when patients have 2+ attacks of CNS dysfunction
MRI! old and new lesions
LP!!! most specific b/c oligoclonal bands

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19
Q

What shows recent area demyelination in CNS

A

MRI with gadolinium enhancement

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20
Q

Optic neuritis

A

sudden loss vision in one or both eyes
painful
lose pupillary reaction

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21
Q

what causes optic neuritis

A

swelling of nerve

very painful

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22
Q

Marcus Gunn reaction or Pupillary afferent defect

A

when flashlight quickly moved form normal eye to affected eye and seems to dilate

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23
Q

disc in optic neuritis

A

pallor

yellow coloring

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24
Q

what to give to patient with optic neuritis

A

IV corticosteroids

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25
Q

patients with optic neuritis tend to develop

A

MS

26
Q

Signs of internuclear ophthalmoplegia

A

adduction cannot reach medial edge
abductin goes part way with nystagmus
b/l

27
Q

location lesion of internuclear ophthalmoplegia

A

damage to medial longitudinal fasciculus in brain stem linking CN VI with contra CNIII

28
Q

causes of internuclear opthalmoplegia

A

MS

or brainstem stroke

29
Q

Diagnostic criteria MS

A

2+ attacks in brain or spinal cord at 2+ times

30
Q

MRI findings in MS

A

9+ hyperintense T2 lesions with 1+ gadolinium enhancing lesion
1+ lesion of cerebellum or brain stem
3+ periventricular lesions

31
Q

if almsot meet MRI findings MS in brain do what

A

MRI of cervical or thoracic to see discrete cord lesions

32
Q

lesions in brain are usually in what location compared to lateral ventricles in MS

A

right angles

33
Q

MS thoracic spine

A

<3 consecutive segment lesions

34
Q

LP os MS patient

A

oligoclonal bands IgG
increased levels myelin basic protein
increased wBC (not super high)

35
Q

Goal Tx MS

A

limit attacks and disability

36
Q

beta interferons used in MS

A

avenox
betaseron
rebif

37
Q

glatiramer actate is indicated for what form MS

A

relapsing remitting

acts as decoy for immune system

38
Q

use of Natalizumab

A

PML except have to stop if think have JC virus

39
Q

Fingolimod

A

once day capsule
limit circulation lymphocytes (keep inside lymph nodes)
muss less likely to cross BBB

40
Q

side effects fingolomid

A

cardiac: brady and CAD

41
Q

Tx for MS symptoms

A

antispasmodics
antidepressants
corticosteroids

42
Q

Neuromyelitis optica “Devic”

A

optic neuritis and spinal cord demyelination

not brain demyelination!!!!!

43
Q

MRI devics or NMO

A

> 3 vertebral segments show demyelination

44
Q

devics reaches C3 C4

A

respiratory crisis

45
Q

CSF in devic disease

A

seldom oligoclonal bands

>50 WBC

46
Q

Tx devic disease

A

corticosteroids!!
chronic with azathioprine!!
not INF

47
Q

Ab in devic disease

A

against aquaporin 4 channels which more common in optic nn and spinal cord

48
Q

age affected by NMO

A

young- very elderly

49
Q

bilateral optic neuritis more likley to be

A

NMO

50
Q

time frame NMO

A

shortly after infection

monophasic illness

51
Q

Acute inflammatory demyelinating Polyneuropathy

A

Guillain Barre
after infection (upper respiratory or GI)
rapidly progressive paralysis
ascending

52
Q

where is immune attack in guillain barre

A

roots of peripheral and sometimes CN
usually just motor not sensory
DTR completely lost

53
Q

death in guillain barre

A

respiratory arrest

54
Q

Nerve conduction in guillain barre

A

dec velocity and delayred F waves

55
Q

LP in guillain barre

A

high high CSF protein
slight elevation WBC
cellular chemical dissociation

56
Q

meningitis encephalitis LP

A

both WBC and protein increased!

57
Q

outcome guillian barre

A

full recovery in weeks to mo

soemtimes permanent weakness or pain

58
Q

Chronic Inflammtory Demyleinating Polyneuropathy

A
slower
3-6 mo
mild weakness
dec reflexes
increased CSF protein
59
Q

Tx Chronic Inflammatory Demyelinating Polyneuropathy

A

oral corticosteroids
plasma exchange
IVIgG

60
Q

does guillain barre respond to corticosteroids

A

no

61
Q

Tx Guillain barre

A

plasma exchange
IV IgG
most effective if begun within first 3 weeks!!!!!!