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Unit 3: Pharm - Liza > Multiple Sclerosis > Flashcards

Multiple Sclerosis Flashcards

1
Q

What are the goals of current therapies for MS?

A

shorten relapses, reduce severity of relapse, reduce accumulation of disability, prevent disease, reverse disability (promote remyelination), alleviate symptoms

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2
Q

What is the most successful type of current MS therapy?

A

Immunomodulators

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3
Q

What are the three agents used to tx acute MS?

A

Methylprednisone (Corticosteroids), ACTH, Plasmapharesis

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4
Q

How does Methylpredinisone act and what other drug is given with it?

A

Unclear MOA (suppresses both T and B cells and may reduce cytokine release) and it shortens acute attack to hasten recovery. It is given IV with oral prednisone taper

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5
Q

What are the short and long term side effects of taking methylprednisone

A

short term: insomnia, mood changes, fluid retention, epigastric pain, HTN

long term: osteroporosis, cushingoid, secondary malignancies

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6
Q

Why would you administer Plasmapharesis?

A

helps w/acute MS attacks nonresponsive to methylprednisone

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7
Q

Why would you give ACTH? What is it’s drawback?

A

For acute MS attacks if patient allergic to corticosteroids or with poor IV access (can be injected SC or IM). Drawback = expensive!

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8
Q

Name the 4 beta interferons used to treat relapse remitting MS (RRMS)

A

Avonex, Rebif, Betaseron, Extavia

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9
Q

What are the proposed MOA’s for all of the beta interferons?

A

inhibit T-cell activation, shift from Th1 to Th2, inhibit lymphocyte migration into CNS, anti-proliferative effect, apoptosis of autoreactive T cells, anti-viral, IFN-gamma antagonism, don’t cross BBB

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10
Q

Which of the IFN-betas is considered low dose? What are it’s effects?

A

Avonex; shown to decerase relapse rate by 1/3 and reduce MRI lesions and decrease disability/brain atrophy

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11
Q

Which of the IFN-betas are considered high dose and of these, which are considered more efficacious than low dose Avonex?

A

Rebif (more efficacious), Betaseron (more efficacious), Extavia

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12
Q

Which two IFN betas don’t have effect on disease progression despite decreasing relapse rate and enhancing lesions on MRI?

A

Betaseron and Extavia

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13
Q

What are the side effects of the IFN-beta-1a Rebif and the IFN-beta-1b Betaseron and Extavia

A

flu-like symptoms, injection site reactions, anemia, menstrual irregularities, depression, increased LFTs and hypothyroidism (monitor every 3 months)

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14
Q

Which of the IFN-B have the least neutralizing antibodies that form and which have the most?

A

Least: Avonex

Most: Betaseron

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15
Q

What are the side effects of Avonex?

A

mild anemia, increased LFT (monitor every 6 months), hypothyroid, flu-like symptoms and minor irritation at injection site <>

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16
Q

What type of drug is Glatiramer acetate and what are its possible mechanisms of action?

A

it’s a Myelin basic protein analog (mixture of 4 AA’s); it causes T-cell apoptosis since it looks like MBP, induces anti-inflammatory shift from Th1 to Th2, induces Treg with induction of anergy, and possible neuroprotction

17
Q

What are the effects of Glatiramer acetate on RRMS?

A

acts in CNS (not peripherally); decreases relapse rate by 1/3 and has modest effect on MRI activity but NO effect on disease progression; decreases brain atrophy

18
Q

Are the side effects of Glatiramer acetate mild or severe?

A

MIld: injection site reactions, anxiety like reactions (chest tightness, SOB)

19
Q

What do the studies say for 1st line treatments in terms of when to tx MS patients and what type of dosage to use?

A

Treat EARLY! High dose interferons are superior! More frequent dosing!

20
Q

What would the professor recommend as an overall good 1st line therapy?

A

Rebif over Avonex (more efficacious), Rebif over Betaseron (less neutralizing antibodies), Rebif over Copaxone (Glatiramer acetate) re: MRI effects. Ultimately depends on patient tolerance of side effects and # of injections

21
Q

What type of drug is Natalizumab and what’s it’s MOA?

A

Monoclonal antibody; MOA: binds to VLA4 expressed on surface of all leukocytes to inhibit leukocyte migration across BBB

22
Q

What are some of the therapeutics and drawbacks of Natalizumab?

A

Therapeutics: decrease relapse rate by 2/3 and greatly reduces MRI lesions; only have to take 1/month

Drawbacks: drug doesn’t work if patients develop positive antibodies to Natalizumab; these pts also more commonly have side effects

23
Q

What are the side effects of Natalizumab?

A

PML (progressive multifocal leukencephalopathy) (JC virus)–>esp if immunosuppressed and + for anti-JC virus antibodies; systemic hypersensitivity reactions, urticaria, headaches, dizziness, fatigue, arthralgia, rigors

THUS this drug is considered 2nd, maybe even 3rd line for use

24
Q

What type of drug is Fingolimod and what is its MOA?

A

Sphingosine-1-phosphate analog (1st oral drug approved for MS); MOA: prodrug that sequesters circulating lymphocytes in secondary lymphoid organs via induction of intracellular internalization of receptors on lymphocytes (no effect on lymphocyte induction, proliferation or memory function)

25
Q

What are some of the important side effects of Fingolimod?

A

bradycardia and heart block (must do 6hr monitoring for 1st dose); macular edema (must do ophtho exam before and after 3 months); minor: reduced FEV1, inc LFTs, lymphopenia leukopenia, back pain, blurred vision, headache, dizzy, infections

26
Q

What must patients taking Fingolimod have antibodies to prior to taking the medication?

A

VZV

27
Q

What is the MOA for the immunosuppressant Teriflunomide?

A

selective dihydro-orotate dehydrogenase inhibitor that blocks de novo pyramidine synthesis, reducing T and B cell proliferation and function against auto antigens; preserves replication and function of cells living on salvage pathway (hematopoietic cells, memory cells)

28
Q

What are the pros and cons to taking Teriflunomide?

A

Pros: oral admin just as efficacious as 1st line injectables, overall relatively safe

Cons: hepatotoxicity and teratogenicity based on animal data

29
Q

What is the MOA of Dimethyl Fumarate?

A

Antiinflammatory effects: inhibits expression of adhesion molecules; induces Th1–>Th2 shift

Neuroprotective effects: activates Nrf2 pathway to induce antioxidant enzyme production and clear free radicals and protect against oxidative stress

30
Q

What are the side effects of Dimethyl Fumarate?

A

N/V, diarrhea, stomach pain, flushing, itching, redness

31
Q

What is observed in secondary progressive MS (SPMS) as compared to RRMS?

A

greater lesion burden, increased axonal loss w/comparable lesion burden, impaired recovery mechanisms, increased spinal cord/brain atrophy, disability progresses despite decline in MRI activity, new inflammatory activity–>disability progression

32
Q

What are the potential therapies for SPMS?

A

Mitoxantrone (only FDA approved therapy), Azathioprine, Methotrexate, Cyclophosphamide (all immunosuppressants)

33
Q

What class of drug is Mitoxantrone and what is it’s MOA?

A

Class: Anthracenedione; MOA: broad immunosuppression/modulation of B cells, T cells, and macrophages; decreases frequency of clinical relapse, reduces disease progression and reduces disability

34
Q

What are some side effects of Mitoxantrone?

A

cardiac toxicity (decrease in LVEF and irreversible CHF), can induce acute leukemia, N/V, alopecia, menstrual problems, increased susceptibility to infection

35
Q

How are the immunosuppressants Azathioprine, Methotrexate, and Cyclophosphamide used to treat MS and what are their side effects?

A

Used in SPMS where other drugs have been ineffective or as combination with other therapies; Side effects include systemic toxicity (requires blood monitoring)

36
Q

What are the therapies for primary progressive MS?

A

no FDA approved drugs yet; no trials w/immunosuppressants, pulse steroids perhaps, or IVIg

Unit 3: Pharm - Liza (14 decks)

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