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bmb test 1 > B7-092 Multiple Sclerosis > Flashcards

B7-092 Multiple Sclerosis Flashcards

1
Q

most common demyelinating disease affecting the central nervous system

A

multiple sclerosis

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2
Q

CNS myelin comes from

A

oligodentrites

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3
Q

PNS myelin comes from

A

Schwann cells

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4
Q

what kind of deficit pattern does MS cause?

A

multifocal

discrete areas of transient inflammatory deyelination

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5
Q

MS is thought to result from […] response to antigens in myelin

A

autoimmune

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6
Q

damaged myelin disrupts […]

A

saltatory conduction

(slows/stops propagation at nodes of Ranier)

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7
Q

people living in what areas of the world have the highest risk of getting MS?

A

temperate zones (northern US, Europe, Canada)

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8
Q

when migrating from a high-risk to low-risk area, chances of getting MS decrease if migration occurred before what age?

A

20

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9
Q

late infection with […] provides a 3-fold increased risk of developing MS

A

EBV

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10
Q

shares epitopes with myelin basic protein

A

EBV

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11
Q

theories of geographical distribution of MS [3]

A

hygiene hypothesis
molecular mimicry (EBV)
low levels of vitamin D

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12
Q

signs and symptoms of MS are dependent on

A

location of lesion

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13
Q

common symptomatic locations of MS plaques [3]

A

optic nerve
brain stem/cerebellum
spinal cord

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14
Q

asymptomatic lesions commonly occur where?

A

cerebral hemispheres

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15
Q

diagnostic criteria for MS

A

two or more lesion of the CNS separated in space and time without other explanation

(can use MacDonald criteria to account for radiologic findings)

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16
Q

supportive findings of MS [3]

A

multifocal white matter lesions on MRI
CSF oligoclonal bands
CSF pleocytosis <50 cells

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17
Q

inflammation around penetrating venules that run perpendicular to the ventricles

A

dawson fingers

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18
Q

many people have T2 hyperintensities on MRI but without [….], they should not be diagnosed with MS

A

clinical abnormalities

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19
Q

what would you expect to seen on CSF analysis in an MS patient

A

oligoclonal bands
elevated IgG
elevated IgG index
maybe elevated protein
maybe elevated WBC

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20
Q

85% of MS patients have what type?

A

relapsing-remitting MS

(50% of these patients develop secondary progressive MS)

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21
Q

15% of MS patients have what type?

A

primary progressive MS

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22
Q

symptoms develop over hours or days
can worsen for several weeks
slowly subside over several weeks or months

A

relapsing remitting MS

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23
Q

recurrence of previously experienced symptoms not related to current inflammation
often seen in the setting of systemic infection (UTI, pneumonia)

A

psedoexacerbation

no steroids

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24
Q

gradual progression
spinal myelopathy is common

A

progressive MS

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25
Q

progressive course following a relapsing remitting course

A

secondary progressive MS

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26
Q

first presentation of neurological symptoms from inflammatory demyelination

A

clinically isolated syndrome

(often a retrospective diagnosis, can be monofocal or multifocal)

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27
Q

used to guide prognosis of MS

A

expanded disability status scale (EDSS)

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28
Q

poor prognostic factors for MS [7]

A

male
older age
multifocal
onset with motor, cerebellar, bladder/bowel symptoms
high frequency of relapses
severe relapses
high lesion load on MRI

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29
Q

used to shorten the duration of relapse

A

high dose steroids

(not used in pseudo exacerbation)

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30
Q

treatment for MS related fatigue

A

methylphenidate

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31
Q

treatment for MS spasticity

A

baclofen (oral or pump)

32
Q

MOA: suppression of gamma interferon

A

beta interferon

33
Q

MOA: competes with MBP for antigen presentation

A

glatiramer acetate

34
Q

MOA: inhibits pyrimidine synthesis inhibiting clonal expansion lymphocytes

A

teriflunomide

35
Q

MOA: decreases lymphocyte proliferation through Nrf2 pathway

A

dimethyl fumurate

36
Q

MOA: sphingosine-1-phosphate receptor modulator trapping lymphocytes in lymph nodes

A

flingolimod/siponimod

37
Q

MOA: anti-alpha 4 integrin antibody preventing lymphocytes from crossing BBB

A

natalizumab

38
Q

MOA: purine nucleoside analog cytotoxic to lymphocytes

A

cladribine

39
Q

MOA: anti CD52 antibody causing prolonged lymphocyte depletion

A

alemtuzumab

40
Q

MOA: anti CD20 antibody depleting B cells

A

rituximab/ocrelizumab

41
Q

side effects: beta interferon

A

flu like symptoms

42
Q

side effects: glatiramer acetate

A

injection site reaction

43
Q

side effects: teriflunomide

A

liver dysfunction, hair loss

44
Q

side effects: dimethyl fumurate

A

lymphopenia, liver dysfunction

45
Q

side effects: fingolimod/siponimod

A

first dose bradycardia
herpes virus infections
rare PML

46
Q

side effects natalizumab

A

higher risk of PML
rebound

47
Q

side effects: cladribine

A

liver toxicity
risk of infection
rare PML

48
Q

side effects: alemtuzumab

A

risk of autoimmunity
infections

49
Q

side effects: rituximab

A

infections
malignancy
rare PML

50
Q

interferes with antigen presentation

A

glatiramer acetate

51
Q

prevent clonal expansion [2]

A

teriflunomide
dimethyl fumurate

52
Q

prevent the movement of lymphocytes from the lymph node into circulation

A

fingolimod
siponimod

53
Q

prevent the movement of lymphocytes from the circulation to brain

A

natalizumab

(rebound phenomenon if suddenly stopped since all the lymphocytes can suddenly move in)

54
Q

kill lymphocytes [3]

A

cladribine
alemtuzumab
rituximab

55
Q

main function of myelin

A

enable saltatory conduction

56
Q

[…] loss is a pathological feature of MS

A

axon

57
Q

are DMARDs helpful for secondary progressive MS?

A

no

58
Q

what happens to the action potentials where the disease has caused demyelination?

A

the action potential conduction is slower and can even be blocked when the signal are moving faster (increased temperature)

59
Q

pathology of what parts of the nervous system can result from MS? [4]

A

axonal transection
brain atrophy
demyelination
neuronal degeneration

60
Q

radiographic hallmark of acute MS lesion

A

gadolinium T1 enhancing lesion due to breakdown of the BBB

61
Q

immunotherapy is effective for what type of MS?

A

relapsing-remitting

62
Q

what MRI finding are you less likely to see in progressive forms of MS?

A

gadolinium T1 enhancement (hallmark of acute lesions)

63
Q

treatment for secondary progressive MS?

A

supportive -can use steroids to shorten duration and provide symptom management

DMARDs are not effective

64
Q

red flags for psuedo exacerbation [2]

A

recent infection
symptoms they’ve had before

65
Q

90% of MS patients will have […] in the CSF

A

oligoclonal bands

66
Q

what feature of MS accounts for reduced processing speeds

A

demyelination

67
Q

main pathological feature that leads to demyelination

A

perivenular inflammation

68
Q

T2 hyperintensities in the corpus callosum emanting from the ventricles

A

Dawson’s fingers

69
Q

a few scattered white matter lesions are normal in people over what age?

A

50

does not confer risk of MS

70
Q

symptoms continuously worsen from onset of disease
no history of clear cut attacks

A

primary progressive MS

71
Q

A progression of RR-MS characterized by continuous worsening of neurological function that occurs independently of exacerbation events

A

secondary progressive MS

72
Q

Exacerbations occur.
Symptoms remit almost completely between exacerbations.

A

relapsing-remitting MS

73
Q

how long can an MS relapse last?

A

average 6-8 weeks

Note: this is from Dr. Google, I just wanted an idea of when to consider progression, please don’t stake your test score on it haha

74
Q

concordance rate of MS in monozygous twins

A

30%

75
Q

represent antibodies generated within the CNS

A

oligoclonal bands

76
Q

concordance rate of MS in dizygotic twins

A

7%

77
Q

concordance rate of MS in siblings

A

about 3%

bmb test 1 (17 decks)

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