Multiple Sclerosis Flashcards

1
Q

What happens to the brain with the natural course of MS?

A

brain atrophy

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2
Q

What is most likely responsible for disability in MS?

A

Axonal involvement

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3
Q

Diagnosis of MS depends on demonstrating what?

A

attacks of neurologic dysfunction disseminated in time and space

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4
Q

Most patients with MS begin as what type?

A

Relapsing- Remitting

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5
Q

Untreated pts w/ RRMS typically progress to what type of MS?

A

Progressive

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6
Q

Name four interferons used for MS treatment.

A

Avonex, Rebif, Betaseron, Extavia

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7
Q

Name three treatments for acute MS

A

Corticosteroids, plasmaphoresis, ACTH

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8
Q

What is the MOA of interferons in MS

A

inhibit T cell activation, shift from Th1 to Th2 (non-inflammatory), inhibit lymphocyte movement into CNS, apoptosis of T cells, IFN antagonism

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9
Q

What interferons are high dose, low dose?

A

Avonex - low dose

Rebif, Extavia, Betasteron- high dose

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10
Q

What are added benefits of Rebif over other interferons?

A

reduces disability

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11
Q

What two interferons work on IFN beta-1a?

A

Rebif, Avonex

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12
Q

What two interferons work on IFN beta-1b?

A

Extavia, Betasteron

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13
Q

Of the interferons what has the greatest likelihood of causing Neutralizing antibodies?

A

Betasteron

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14
Q

SE of avonex

A

lesser than other corticosteroids because lesser dose
mild anemia, elevated LFTs, hypothyroid
monitor LFTs every 6 months

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15
Q

SE of Rebif, Betasteron, Extavia

A

anemia, leukopenia, elevated LFTs, hypothyroid, menstrual irregularities, depression
monitor LFTs every 3 months

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16
Q

What are interferons used to treat?

A

RRMS

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17
Q

What is MOA of glatiramer acetate (Copaxone)?

A

causes T cell apoptosis, induces anti-inflammatory Th2 cells, induces regulatory T cells

18
Q

What problem occurs with NAB caused by use of an IFN?

A

All IFNs can no longer be used to treat because of cross reactivity

19
Q

When should you begin treating MS?

A

EARLY, before diagnosis with MS but high risk of developing MS by MRI criteria

20
Q

SE of glatiramer acetate (copaxone)?

A

mild injection site reaction

Anxiety-like reactions- chest tightness, SOB (Not related to heart problem)

21
Q

What isglatiramer acetate (copaxone) used to treat?

A

RRMS

22
Q

What is Natalizumab used to treat?

A

RRMS, considered 3rd line now with oral agents in use

23
Q

What are the SE of natalizumab?

A

PML (jc virus)
acute uticaria
systemic hypersensitivity reaction

headache, dizziness, fatigue, arthralgia, rigors

More common in pts with NAB

24
Q

When would you use ACTH?

A

treat acute MS attack in person with allergy to corticosteroids or poor IV access

25
Q

MOA of Natalizumab?

A

Binds VLA4 inhibiting leukocyte migration across BB barrier

26
Q

What is fingolimod used to treat?

A

RRMS

27
Q

Fingolimod MOA?

A

prodrug, sequesters circulating lymphocytes in secondary lymphoid organs via internalization of receptors on lymphocytes

28
Q

SE of Fingolimod?

A
Bradycardia and heart block (EKG for 6 hrs)
Macular edema (eye exam before treatment adn at 3 months)--> don't use in Diabetics 

Reduced FEV1, increased LFTs, lymphopenia, leukopenia, asthenia, back pain, blurred vision, headache dizziness, infections

29
Q

What must a patient be immune to before prescription of Fingolomid?

A

VZV

30
Q

What is teriflunomide (Aubagio) use to treat?

A

RRMS

31
Q

MOA of teriflunomide (Aubagio)?

A

Selective dihydro-orotate dehydrogenase inhibitor

blocks de-novo pyramidine synthesis, reducing T and B cell proliferation and function in response to autoantigens

32
Q

SE of teriflunomide (Aubagio)?

A

hepatotoxicity, teratogenicity, nausea, decreased hair density

33
Q

Dimethyl fumarate MOA?

A

activates Nrf2 pathway and induces antioxidant enzyme production (decreases oxidative stress)
Induces TH1–> Th2 shift

34
Q

SE of dimethyl fumarate?

A

N/V/D, stomach pain, flushing

35
Q

What are SE of corticosteroid use?

A

ST: insomnia, mood changes, fluid retention, epigastric pain, hypertension
LT: osteoporosis, cushingoid, secondary malignancies

36
Q

In regards to MS what does a Gd+ lesion and a T2 lesion represent?

A

Gd+ lesions are new lesions that convert to Th2 after 2 months

37
Q

Name four immunosuppressants used to treat SPMS?

A

Azathioprine, Methotrexate, Cyclophosphamide, Mycophenolate mofetil

38
Q

SE of immunosuppressants?

A

Systemic toxicity, monitor for blood changes

39
Q

What is Mitoxantrone used to treat?

A

SPMS and RRMS (2nd line)

40
Q

SE of Mitoxantrone?

A

Cardiac toxicity- decreased LVEF and irreversible CHF, risk increases w/ cumulative dosing

Acute leukemia

N/V, alopecia, increased infection risk, menstrual irregularities

41
Q

MOA of Mitoxantrone?

A

Broad immune suppression of macrophages, B & T cells. Reduces disease progression and disability.