MS Flashcards

0
Q

what do the IFNbeta’s do? (7 fncs)

A
  1. inhibit Tcell activation, promotes its apoptosis
  2. th1–> th2 via cytokines production switch
  3. inhibits lymphocyte movmt into CNS
  4. antiproliferative effect
  5. anti-viral
  6. IFN-g antagonism
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1
Q

the 4 interferon betas (IFN-b) used to tx RRMS (relapsing remitting MS). indicate if they are 1a or 1b

A

IFN1a: avonex and rebif
IFN1b: betaseron and extavia

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2
Q

what are considered high dose IFNb’s? (3)

A

rebif, betaseron, extavia

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3
Q

1st line tx for RRMS

A

rebif

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4
Q

IFNb that forms least Nab

A

avonex

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5
Q

IFNb that forms most Nab

A

betaseron

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6
Q

all ____ produce these SEs: flue like, minor irritation at injection site, anemia. which one produces TCP?

A

IFNb’s. rebif also has TCP

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7
Q

anemia
inc LFT
hypothyroidism

A

all IFNb’s: avonex, rebif, betaseron, extavia

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8
Q
  1. which 2 IFNb’s decrease progression and disability?

2. which 2 IFNbs have no effect on disease progression?

A
  1. avonex and rebif

2. betaseron and extavia

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9
Q

myelin basic protein analog

A

glatiramer acetate

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10
Q

used to also tx____; this is a mix of 4 myelin basic proteins (MBPs) that causes:

  1. T cell apoptosis (looks like MBP)
  2. induces Th2 from Th1 switch
  3. induces Treg with induction of anergy
  4. neuroprotection
A

glatiramer acetate

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11
Q

only active in CNS; reduces relapse by 1/3 of used early, modest reduction in MRI lesion and reduce atrophy; no effect on dz progression

A

glatiramer acetate

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12
Q

mild SE: injection site rx, anxiety attack like rx, chest tightness, SOB

A

glatiramer acetate

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13
Q

monoclonal ab that binds VLA4 (integrin subunit) and inhibits leukocyte migration to BBB

A

natalizumab

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14
Q

second line for RRMS

A

natalizumab

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15
Q

natalizumab puts pt at risk for ____ infection, resulting in ____. also acute urticaria, HSR (infusion rxn)

A

JC virus; PML

16
Q

can induce ab’s to this drug, causing it to not work for RRMS

A

natalizumab

17
Q

prodrug that helps sequester circulation lymphocytes in secondary lymphoid organs via internalization of SIP receptors in lymphocytes (but have no effect on lymphocyte induction, prolif, memory fnc);;;;used for tx ___

A

fingolimod (sphingosine-1-P analog)

-RRMS

18
Q

major SE of fingolimod?

A
  • brady, heartblock (EKG monitor first 6hrs)
  • macular edema

also: reduced FEV1, inc LFTs, lymphopenia, leukpenia, asthenia, back pain, blurred vision/HA/dizz, infections

19
Q

to admin fingolimod, need to make sure pt is what?

A

VZV immune

20
Q
  1. Immunomodulators (5)

2. immunosuppressants (5)

A
  1. the IFNb’s, glatiramer acetate, natalizumab, fingolimod, dimethyl fumarate
  2. teriflunomide, mitoxantrone, azathioprine, methotrexate, cyclophosphamide, mycophenolate mofetil
21
Q

immunomodulator that enhances the nrf2 pathway (which inc antiox enzymes to dec ox stress), and Th1–>Th2 shift

A

dimethylfumarate

22
Q

tx psorasis and dec progression of MS; SE: rash/flushing, n/v/d/pain

A

dimethyl fumarate

23
Q

IS that selective dihydro-orotate dehydrogenase inhibitor (blocks denovo pyramidine synthesis, reduces B+T prolif);

  • func against autoag’s
  • preserves replication and fnc of cells living on salvage pathway (hematopoietic cells, memory cells)
A

teriflunomide

24
Q

hepatotoxicity, teratogenicity in animals

A

teriflunomide

25
Q

first line injectables for RRMS

A

teriflunomide

26
Q

broad immune suppression of b,t,macrophages,
dec relapses
reduces progression and disability
-SPMS (secondary progressive MS), RRMS (2nd line)

A

mitoxantrone

27
Q

dose-dependent cardiac toxicity (dec LVEF, irrev CHF), acute leukemia;
-thus, have a life time limit (depends of LVEF)

A

mitoxantrone

28
Q

4 IS that tx SPMS (resistant, or as comb with other therapies)

A
  1. azathioprine
  2. methotrexante
  3. cyclophosphamide
  4. mycophenolate mofetil
    (AMcycMyc)
29
Q

all IS have systemic tox:

  1. methotrexate
  2. cyclophosphamide
  3. mycophenolate mofetil
  4. terflunomide
A
  1. liver and pul fibrosis
  2. hemorrhagic cystitis
  3. PML, lymphomas, skin malign, RBC aplasia
  4. hepatotox, teratogenicity
30
Q

corticosteroid for IS

A

methylprednisone

31
Q

unclear mech but may involve suppression of both B and T cells, may reduce cytokine release

A

methylprednisone

32
Q

used for acute MS attack, SPMS

shortens acute attack duration, speeds recovery

A

methylprednisone

33
Q

short term: insomnia, mood changes, fluid retention, epigastric pain, HTN
long term: osteoporosis, cushingoid, secondary malign

A

methylprednisone

34
Q

give during acute MS attack if the pt is allergic to corticosteroids or have poor IV access; or if MTP doesnt work

A

ACTH

35
Q

use this during acute MS that’s not responsive to MTP

A

plasmapharesis