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444-Oncology and Neurology > MS > Flashcards

MS Flashcards

1
Q

there is an increase of MS prevalence
1. in males in the last decade
2. in northern communities
3. in children in alberta
4. in those >50yrs old in the last 10 years

A

2

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2
Q

what is the most common nontraumatic neurolgoical disability in people of working age

A

MS

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3
Q

which of the following is false about MS
1. most adults with dx say that sx started in childhood
2. it is the most common nontraumatic neurolgoical disability in people of retirement age
3. incidence is increasing in women (3;1), likely due to women entering workforce
4. the exact cause is unknown

A

2- of working age

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4
Q

3 possible mechanisms of MS

A

overactive immune disease resulting in
1. Breakdown of myelin and inadequate myelin repair
2. Degeneration / progression
3. B and T cell mediation

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5
Q

list 3 possible causes of MS

A

childhood obesity, less sun exposure, smoking, environment, genes, infections (EBV/ mono)

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6
Q

2 characteristics of MS

A

chronic inflammation in brain, spinal cord, optic nerves
slow degeneration, resulting in axonal loss

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7
Q

what is the emerging immunopath view of MS

A

T cells active, but B cells independent in also releasing cytokines

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8
Q

current immunomod tx for MS focuses on

A

preventing the demyelination

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9
Q

list 3 sx of MS

A

sensory, weakness, bladder and bowel, coordination, impaired vision, depression, cognition, fatigue, heat intolerance, balance/ gait, sexual dysfunction, pain, paroxysmal

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10
Q

what is considered a relapse of MS

A

=>24hrs of symptoms, a clinical event of MS inflammation

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11
Q

what are the 4 subtypes of MS

A

relapsing-remitting
2 progressive
1 progressive
progressive relapse

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12
Q

rank the MS subtypes from least to most common

A

progressive relapse
1 progressive
2 progerssive
relapsing remitting

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13
Q

______________disability doesn’t get worse between relapses but after each relapse it can end up worse than before

A

relapsing remitting

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14
Q

steady progression to worse disease state after relapse-remitting subtype

A

2 progressive

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15
Q

no relapses, just slow progression in MS is considered _________ subtype

A

1 progressive

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16
Q

Relapses occur, followed by full or partial recovery, but nerve damage continues and symptoms become increasingly disabling is _____________ subtype

A

progressive relapse

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17
Q

what is MS prodrome

A

various sx with ↑ physician encounters and rx drug use
Fatigue, pain, headache, low mood, anxiety, bladder issues, infections

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18
Q

what is considered radiologic isolated MS syndrome

A

no hx of MS sx but MRI looks like MS lesions

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19
Q

when radiologic isolated sx is noted, 50% of pts will have a clinical event of MS within ___yrs

A

50% in 10ysr

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20
Q

what is a clinically isolated sx of MS

A

1st spell of demyelintion

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21
Q

the natural hx of MS includes an increase in _________, __________, _________ and decreases in _______ and ______

A

increase in axonal damage, disability, progression
decrease in inflammation, # of relapses

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22
Q

the recent change to milder courses of MS is due to

A

Changes in diagnostic criteria, MS epidemiology, early + appropriate disease modifying therapies (DMT), improved general health in populations, tx of comorbidities (ex- HPTN, smoking, lipids, depression/anx)

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23
Q

later start of disease modifying therapies after MS onset, results in

A

increased LT disability

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24
Q

list 3 MS red flags

A

New neurologic sx (tingling, weakness, balance issues, dizziness, double vision, loss of vision)
Signs of infection
Intolerance to medication, medication SEs

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25
Q

how to quicken recovery from MS relapse

A

steroids IV/PO

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26
Q

what is classified as an MS relapse

A

> 24hrs of inflammation/ demyelination sx

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27
Q

4 steps in treating MS relapse

A
  1. screen for UTI and infections
  2. stop inflammation with rest, IV methylprednisolone or PO prednisone
  3. counsel on coping strategies
  4. sx management
  5. prevent more inflammation
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28
Q

what steroids are used for tx of MS relapse

A

IV methylprednisolone 1g daily F3-5d
PO prednisone 650mg BID F3d (give sleep aid)

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29
Q

is there a difference between PO and IV high dose steroids (prednisone) for MS?

A

no- PO is less expensive and more convenient

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30
Q

what are disease modifying therapies

A

LT tx to modify disease course, delay accumulation of disability- no direct impact on sx

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31
Q

Early intensive therapy sees a reduced 5yr rate of disability compared to___________

A

escalation therapy

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32
Q

list the conventional escalation treatment ladder

A

watchful waiting
immunomodulators
IRT
higher efficacy tx

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33
Q

list the early top down tx series

A

higher efficacy
IRT
watchful waiting
retreat and/ or immunomodulators

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34
Q

patients with milder MS, lower risk of progression should use the ________ strategy, starting with the following tx first

A

escalation
immunomodulators, teriflunomide

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35
Q

in pts with some RF or poor responders to immunomodulaors (high risk of progression), the ________ should be used, starting with the following meds

A

escalataion
Natalixumab
fingolimod/ sphingosine 1 phosphate inhibitors
Alemtuzumab, ocrelizumab
Cladribine
Ofatumumab

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36
Q

in pts with aggressive disease, _________ strategy should be used with the following meds used first

A

De-escalation strategy

Alemtuzumab
Ocrelizumab
Cladribine
Ofatumumab

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37
Q

what are the 3 immunomodulator maintenance therapies for MS

A

BIFN, GA, DMF

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38
Q

BIFN MOA

A

↓peripheral activation of T cells, stops lymphocytes from crossing BBB

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39
Q

GA MOA

A

↓peripheral activation of T cells, modulates immune system to T2 state, ↓ central inflammatory cascade in brain

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40
Q

BIFN and GA efficacy

A

~33% relapse reduction

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41
Q

BIFN SEs

A

flu like sx, liver effects, leukopenia

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42
Q

GA SEs

A

rash, panic reaction

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43
Q

DMF metabolic byproduct + the SE associated with the byproduct

A

nicotinic acid- facial flushing

44
Q

how to treat facial flushing from DMF

A

ASA pre treatment

45
Q

DMF efficaacy

A

50% relapse reduction

46
Q

teriflunomide MOA

A

Antimetabolite- interferes with de novo synthesis of pyrimidines, blocks cell replication in rapidly dividing cells, inhibits proliferation of activated T and B cells in periphery

47
Q

name the 4 immunosuppressive/ maintenance tx for MS

A

teriflunomide
natalizumab
sphingosine-I-phosphate inhibitors
B cell depleters

48
Q

teriflunomide is generally used for ____________

A

those that are milder with MS or older pts

49
Q

teriflunomide itnx

A

CYP2C8i, amiodarone, live vaccines, immunosuppressants

50
Q

in women on teriflunomide, if they want to get pregnant, what must be done?

A

stop teri
washout with colestyramine or activated charcol

51
Q

natalizumb MOA

A

Anti Trafficking agent: stops lymphocytes from crossing BBB and attacking the myelin
blocks a4 integrin subunit with VCAM-1 at BBB (can’t adhere and roll through blood vessel walls)

52
Q

natalizumab intx

A

ßIFN, immunosuppressives

53
Q

which drug requires stratification for JC virus
1. teriflunomide
2. natalizumab
3. ocrelizumab
4. alemtuzumab

54
Q

which MS meds can be used in pregnancy?

A

BIFN, GA
natalizumab

55
Q

natalizumab AEs include

A

infusion reactions
rebound effect if stopped suddenly
increase in liver enzymes
rare severe brain infections from JC virus reactivation

56
Q

-imod class

A

Sphingosine-I-phosphate inhibitors

57
Q

Sphingosine-I-phosphate inhibitors MOA

A

inhibits migration of T cells from lymphoid tissues and target organs including CNS
antitrafficking, maintenance

58
Q

sphingosine -I-phosphate inhibitors interact with

A

antiarrhythmics, immunosuppressants, BB, drugs that ↑ QT interval (ex- antidepressants), avoid live vaccines

59
Q

which med decreases HR with first dose
1. siponimod
2. natalizumab
3. ofatumumab
4. BIFN

A

10- sphingosine -i-phosphate inhibitors

60
Q

what is the only tx approved for secondary progressive MS

61
Q

Sphingosine-I-phosphate inhibitor SEs

A

Rebound effect
Avoid in pregnancy and BF (teratogenic)
Liver eff, low WBCs, infections (shingles- vaccinate prior to initiation)
Eye- macular edema

62
Q

SEs specific to fingolimod

A

basal cell carcinoma
bradycardia
HPTN

63
Q

B cell depletors for MS include

A

ocrelizumab, ofatumumab

64
Q

B cell depleters MOA

A

bind to CD20 on surface of B cells = lysis

65
Q

B cell depleters intx

A

immunosuppressants, live vaccines

66
Q

what is the 1st tx for active primary progressive MS

A

ocrelizumab

67
Q

B cell depleter efficacy

A

Prevent 60% relapses + most new MRI lesions

68
Q

B cell depleter SEs

A

Infusion rxn (ocrelizumb)
Infections (zoster)
Cardiac events
Cancers (breast)
Can’t use in pregnancy

69
Q

4 phases of immune reconstitution tx for MS

A
  1. abnormal immune system at baseline
  2. reduction phase after giving agent
  3. repopulation phase
  4. reconstitution phase
70
Q

what is a major pro of immune reconstitution tx

A

can hit hard in the beginning then let the immune system grow back = not immunocomp in LT

71
Q

what are 2 immune reconstitution meds

A

alemtuzumab
cladribine

72
Q

alemtuzumab MOA

A

Humanized monoclonal Ab, targets CD52 (lymphocytes and monocytes) = T cell physis by antibody mediated cytotoxicity and complement cell lysis

73
Q

alemtuzumab works in the
1. CNS
2. periphery
3. BBB

74
Q

alemtuzumab is used mainly
1. for those with aggressive MS
2. as a gentler agent for older pts
3. for pts with milder course of MS
4. 2+3

75
Q

how many infusions of alemtuzumab is usually used

A

2, some require a 3rd or 4th

76
Q

alemtuzumab infusion schedule

A

Consecutive infusion for 5 days 1st yr, then 3 days 2nd yr

77
Q

alemtuzumab AEs

A

Infusion reaction, rash, HA
Rare carotid dissection/ stroke
Infections (zoster)
Delayed autoimmune disorder
Thyroid papillary ca

78
Q

which therapy can not be used in BF
1. BIFN
2. GA
3. Natalizumab
4. alemtuzumab

79
Q

pts on alemtuzumab may get pregnant ____ after infusion

80
Q

cladribine MOA

A

immune cell depleting agent (sustained reduction of T and B lymphocytes), immune reconstitution tx, works in periphery

81
Q

a senior pt has a mod course of MS and has failed immunomodulators. they refuse injections and would like a tx that is PO. what is the best option
1. alemtuzumab
2. cladribine
3. teriflunomide
4. fingolimod

82
Q

cladribine SEs

A

opportunistic infections until immune system grows back
nausea, HA, cold sores ,rash, fever, hair thinning, abd pain, flu and flu like sx

83
Q

pts may get pregnant _____ after cladribine

84
Q

sx of MS are
1. highly variable
2. usually MS specific
3. affect M>F
4. come and go with all subtypes

85
Q

how to treat fatigue in MS

A

Amantadine
Non Sedating antidepressants (citalopram, wellbutrin)
4-aminopyridine (Fampridine = fampyra)
Dextroamphetamine (adderall XR)

86
Q

how to treat gait changes in MS

A

Multidisciplinary, exercise
Fampridine (sustained form of 4-amino-pyridine)

87
Q

fampridine is a

A

potassium channel blocker that strengthens signal down the nerve + improves walking speed

88
Q

how to treat spasticity in MS (nonpharm)

A

stretching
splinting
exercise/ yoga

89
Q

pharm tx for spasticity in MS

A

baclofen, tizanidine, BZDs, gabapentin, dantrolene, botox injections, cannabinoids, phenol injections (most have withdrawal/ tolerance)
Baclofen pump

90
Q

what should be monitored in treating spasticity in MS with meds like baclofen, BZDs, phenol injections, botox, etc

A

sedation, weakness, cognitive slowing, can worsen gait/ transfers

91
Q

a spastic bladder is

A

small and tight

92
Q

flaccid bladder is

A

large, difficult to empty

93
Q

medications for bladder dysfunction in MS include

A

solifenacin/ darifenacin
mirabegron
oxybutynin agents
amitriptyline
DDAVP nasal spray
tolterodine
botox injections

94
Q

what may be used to treat large and flaccid bladder (nonpharm)

A

catherizataion

95
Q

what is dyssynergia

A

bladder and sphincter contraction

96
Q

which drug has hx with psoriatic arthritis

97
Q

which drug causes facial flushing

98
Q

which MS agent is an antimetabolite that interferes with pyrimidine synthesis + T and B cells in periphery

A

teriflunomide

99
Q

which of the following inhibits T and B cells in the periphery
1. BIFN
2. GA
3. teriflonomide
4. all of the above

A

3 only
1 + 2 are T cell inhibitors only

100
Q

DMF formulation

101
Q

teriflunomide formulation

102
Q

which MS drug is blocks a4 integrin subunit with VCAM-1 at the BBB

A

natalizumab

103
Q

which MS drug can reactivate JC virus

A

natalizumab

104
Q

-mods are

A

sphingosine-i-phosphate inhibitors

105
Q

which class of MS drugs decreases HR with first doses

A

sphingosine-i-phosphate inhibitors

106
Q

what ist he 1st tx for active primary progressive MS

A

ocrelizumab

107
Q

can you use alemtuzumab while breastfeeding

444-Oncology and Neurology (22 decks)

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