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Neuro - Week 4 > Multiple Sclerosis Therapeutics > Flashcards

Multiple Sclerosis Therapeutics Flashcards

1
Q

Immune response to this virus may produce anti-MOG (myelin oligodendrocyte glycoprotein)

A

EBV

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2
Q

This drug is the treatment for acute attack of MS

A

IV methylprednisolone (high dose)

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3
Q

IV methylprednisolone is used in the treatment for this course of MS

A

Acute attack

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4
Q

The MOA of this drug used for MS acute attacks may be decreased edema in the area of demyelination

A

IV methylprednisolone

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5
Q

Adverse effects of this MS drug for acute attacks are numerous and includes sleep disturbances, metallic taste, GI upset, and hyperglycemia

A

IV methylprednisolone

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6
Q

Immunomodulation may be key function of this MS drug through binding to type 1 interferon receptors and activating tyrosine kinase pathways

A

Interferon beta

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7
Q

Immunomodulation may be key function of Interferon for MS through binding to type 1 interferon receptors and activating these pathways

A

Tyrosine kinase

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8
Q

This MS drug intensifies depression, contraindicated in patients with untreated depression

A

Interferon beta

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9
Q

About half of patients taking this MS drug develop neutralizing antibodies, making the product less effective

A

Interferon beta (lower incidence with 1a)

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10
Q

Does interferon beta 1a or 1b have a lower incidence of developing neutralizing antibodies?

A

1a

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11
Q

This MS drug is a random peptide of L-alanine, L-glutamic acid, L-lysine and L-tyrosine

A

Glatiramer

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12
Q

This MS drug may mimic antigenic properties of myelin basic protein

A

Glatiramer

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13
Q

This MS drug may serve as a decoy to locally-generated autoantibodies

A

Glatiramer

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14
Q

What is the MOA of Glatiramer in MS?

A

May serve as a decoy (mimics myelin basic protein)

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15
Q

This MS drug has a relatively mild adverse effects profile, but injection site reactions are common
(One time reaction of chest tightening, flushing, and dyspnea)

A

Glatiramer

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16
Q

Glatiramer is a random peptide of L-alanine, L-glutamic acid, L-lysine and L-tyrosine, and may mimic the antigenic properties of this protein

A

Myelin basic protein
(serving as a decoy)

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17
Q

This MS drug binds VLA-4 and blocks its interaction with CNS endothelium vascular cell adhesion molecules thus denying lymphocytes access to the CNS

A

Natalizumab

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18
Q

Natalizumab binds this and blocks its interaction, denying lymphocytes access to the CNS

A

VLA-4

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19
Q

Natalizumab binds VLA-4, blocking the entry of these into the CNS

A

Lymphocytes

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20
Q

Natalizumab binds VLA-4 and blocks its interaction with this

A

CNS endothelium vascular cell adhesion molecules

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21
Q

This MS drug is prescribed and administered via the TOUCH program

A

Natalizumab

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22
Q

Natalizumab is prescribed and administered via this program

A

TOUCH

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23
Q

This MS drug may cause Progressive Multifocal Leukoencephalopathy

A

Natalizumab

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24
Q

Natalizumab adverse effects include causing this condition, which arises from a viral infection characterized by inflammation of white matter

A

Progressive multifocal leukoencephalopathy (PML)

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25
Q

What are the Big 4 adverse effects of monoclonal antibodies?

A

Increased risk of infection, cancer, heart failure, and hypersensitivity

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26
Q

What MS drug’s MOA results in lymphocytes being unable to access the CNS?

A

Natalizumab

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27
Q

Appropriate use, autoimmunity, infusion reactions, malignancies are black box for this MS drug

A

Alemtuzumab

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28
Q

This is the only FDA-approved drug for Primary-progressive MS

A

Ocrelizumab

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29
Q

Ocrelizumab is the only FDA-approved drug for this MS course

A

Primary-progressive MS

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30
Q

This MS drug is a monoclonal antibody that targets B cells (anti-CD20)

A

Ocrelizumab

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31
Q

What is the MOA of Ocrelizumab?

A

Anti-CD20 (targets B cells)

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32
Q

Upon phosphorylation by sphingosine kinase 2, this MS drug acts as a potent agonist of sphingosine 1-phosphate receptors (S1PR)

A

Fingolimod

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33
Q

Upon phosphorylation by this, fingolimod acts as a potent agonist of sphingosine 1-phosphate receptors (S1PR)

A

Sphingosine kinase 2

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34
Q

Upon phosphorylation by sphingosine kinase 2, fingolimod acts as a potent agonist of these receptors

A

Sphingosine 1-phosphate receptors (S1PR)

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35
Q

Activation of this receptor by Fingolimod sequesters circulating lymphocytes in lymph nodes and reduces infiltration of T cells and macrophages into CNS

A

Sphingosine 1-phosphate receptors (S1PR)

36
Q

S1PR activation by Fingolimod has this effect

A

Sequesters circulating lymphocytes
Reduces infiltration of T cells and macrophages into CNS

37
Q

The action of this MS drug results in the sequestering of circulating lymphocytes and reduced infiltration of T cells and macrophages into CNS

A

Fingolimod

38
Q

Fatal varicella-zoster infections can occur with this MS drug

A

Fingolimod

39
Q

Bradycardia and altered cardiac conduction slowing are adverse effects of this MS drug

A

Fingolimod

40
Q

Macular edema is an adverse effect of this MS drug

A

Fingolimod

41
Q

This adverse effect of Fingolimod should be monitored closely for 6 hours after first dose

A

Bradycardia and altered cardiac conduction slowing

42
Q

Fingolimod can cause fatal infections from this virus

A

Varicella-zoster

43
Q

Fatal varicella-zoster infections, Bradycardia and altered cardiac conduction slowing, Macular edema, and Reduction in pulmonary function are adverse effects of this MS drug

A

Fingolimod

44
Q

This MS drug requires first dose monitoring for bradycardia

A

Fingolimod

45
Q

Fingolimod requires first dose monitoring for this adverse effect

A

Bradycardia

46
Q

Both siponimod and ozanimod have better adverse effect profiles so far, than this MS drug

A

Fingolimod

47
Q

Is Fingolimod an agonist or antagonist of sphingosine 1-P receptors?

A

Potent agonist

48
Q

This test is required before starting Findolimod therapy

A

Electrocardiogram

49
Q

Electrocardiagram is required before therapy with this MS drug

A

Fingolimod

50
Q

This MS drug should be avoided in patients with arrhythmias or antiarrhythmic drug therapy

A

Fingolimod

51
Q

Before starting this MS drug, chickenpox history or vaccination should be confirmed

A

Fingolimod

52
Q

Presumed MOA of this MS drug is pyrimidine synthesis inhibition to reduce T and B cell activation, proliferation and function

A

Teriflunomide

53
Q

What is the MOA of Teriflunomide?

A

Inhibits pyrimidine synthesis
(reducing T and B cell activation, proliferation and function)

54
Q

Teriflunomide inhibits synthesis of this

A

Pyrimidines

55
Q

Teriflunomide inhibits pyrimidine synthesis to reduce activation, proliferation and function of these 2 cell types

A

T and B cells

56
Q

Liver enzyme changes and hepatotoxicity are black box warnings of this MS drug

A

Teriflunomide

57
Q

Fingolimod reduces the infiltration of these two types of cells into the CNS

A

T cells and macrophages

58
Q

This MS drug is contraindicated in pregnancy

A

Teriflunomide

59
Q

Liver enzyme changes and hepatotoxicity, Bone marrow suppression, Neuropathy and renal toxicity are adverse effects of this MS drug

A

Teriflunomide

60
Q

Teriflunomide is contraindicated in this

61
Q

This is the primary metabolite of Dimethyl fumarate

A

Monomethyl fumarate

62
Q

Is the primary metabolite of Dimethyl fumarate (monomethyl fumara) an active agent?

A

Yes - both are

63
Q

Flushing is an adverse effect of this MS drug

A

Dimethyl fumarate

64
Q

What is the main adverse effect of Dimethyl fumarate, which is reduced when taken with food?

65
Q

Is flushing reduced or increased when Dimethyl fumarate is taken with food?

66
Q

How can you reduce the adverse effect of flushing with use of Dimethyl fumarate?

A

Take with food

67
Q

This drug is primarily used as antineoplastic agent, but also slows the worsening of neurologic disability in MS

A

Mitoxantrone

68
Q

What is the MOA of Mitoxantrone in MS?

A

General suppression of T cells, B cells, and macrophages that attack myelin

69
Q

What is the MOA of Mitoxantrone in immunosuppression?

A

Inhibition of DNA and RNA synthesis through intercalation of G-C base pairs

70
Q

This drug that can be used to treat MS has immunosuppression action, which ultimately breaks the DNA chain, interferes with RNA function, and interferes with topoisomerase II function

A

Mitoxantrone

71
Q

MOA of Mitoxantrone in MS is related to the general suppression of these 3 types of cells

A

T cells, B cells and macrophages

72
Q

MOA of Mitoxantrone in immunosuppression is inhibition of DNA and RNA synthesis, through this

A

Intercalation of G-C base pairs

73
Q

This drug that can be used for MS, intercalates G-C base pairs to inhibit DNA and RNA synthesis

A

Mitoxantrone

74
Q

Mitoxantrone immunosuppression breaks the DNA chain, interferes with RNA function, and also interferes with the function of this enzyme

A

Topoisomerase II

75
Q

This MS drug has cardiac toxicity, with a lifetime cumulative dose of 140 mg/m^2 (about 12 doses)

A

Mitoxantrone

76
Q

Why does Mitoxantrone have a lifetime cumulative dose?

A

Due to its cardiac toxicity

77
Q

This MS drug has risk of leukemia

A

Mitoxantrone

78
Q

Mitoxantrone has risk of developing this cancer
(about 1 in 145 patients)

79
Q

Are disease modifying therapies for MS approved for pregnancy or breastfeeding?

A

No - none of them are

80
Q

This MS drug has powerful steroidal anti-inflammatory action

A

Methylprednisolone

81
Q

This MS drug is a sphingosine 1-P receptor modulator that sequesters lymphocytes in lymph nodes

A

Fingolimod

82
Q

This MS drug is toxic to bone marrow, liver, kidney, and is very teratogenic

A

Teriflunomide

83
Q

Flushing, bone marrow depression, and liver toxicity are adverse effects of this MS drug

A

Dimethyl fumarate

84
Q

This MS drug activates antioxidant pathway

A

Dimethyl fumarate

85
Q

A patient in renal failure should not receive this MS drug

A

Teriflunomide
(due to renal toxicity adverse effect)

86
Q

Flu-like symptoms are common with this MS drug

A

Interferon B

Neuro - Week 4 (9 decks)

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