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Pharmacotherapy III > MS - Pharmacology Rochet > Flashcards

MS - Pharmacology Rochet Flashcards

1
Q

What drugs are used for acute attacks of MS?

A

Methylprednisolone
Prednisone
ACTH

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2
Q

What are corticosteroids MOA?

A

Upregulating anti-inflammatory genes
Down-regulating inflammatory genes
Alleviating edema

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3
Q

What are the interferons MOA?

A

Inhibit autoreactive lymphocytes

Inhibit BBB penetration via MMP

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4
Q

What are ADEs of interferons?

A

Well-tolerated

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5
Q

Interferons delay what?

A

Conversion of CIS to clinical MS

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6
Q

T/F: Interferons have a risk for neutralizing antibodies

A

True

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7
Q

What is the MOA of glatiramer acetate?

A

Inhibits autoreactive lymphocytes

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8
Q

What are autoreactive lymphocytes?

A

DCs and T cells

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9
Q

Glatiramer acetate delays what?

A

Conversion of CIS to MS

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10
Q

T/F: Glatiramer acetate has a risk for neutralizing antibodies

A

False

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11
Q

What type of structure is glatiramer acetate?

A

polypeptide

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12
Q

Glatiramer acetate mimics antigenic properties of _________

A

myelin basic protein

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13
Q

What is unique about fingolimod’s structure?

A

Lipid tail

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14
Q

Fingolimod is a ______ receptor agonist

A

Sphingosine 1-phosphate

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15
Q

What is fingolimod’s MOA?

A

Stimulate oligodendrocyte survival & remyelination

Interfere w/lymphocytes moving out of lymphoids

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16
Q

T/F: Fingolimods are superior to IFN-Beta

A

True

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17
Q

What are fingolimods side effects?

A

Cardiotoxicity
Fatal viral encephalitis
PML

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18
Q

What is natalizumab’s MOA?

A

antibody against a4 integrin

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19
Q

What does a4 integrin normally do? (MOA?)

A

Pair with B1 integrin to make VLA-4, which binds to VCAM-1 to get B and T cells into periphery

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20
Q

T/F: Natalizumab has superior effects compared to first-line DMDs

A

True

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21
Q

Side effects of natalizumab?

A 
Allergic reactions (from neutralizing antibodies)
PML!!!!
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22
Q

Mitoxantrone has what MOA?

A

Cytotoxic - causes DNA strand breaks and delays DNA repair

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23
Q

How doe mitoxantrone delay DNA repair?

A

Inhibition of topoisomerase II

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24
Q

T/F: Mitoxantrone is used to treat SPMS

A

True

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25
Q

What are mitoxantrone’s side effects?

A

Cardiotoxicity

Malignancy

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26
Q

Which drug can be used as induction therapy initially?

A

Mitoxantrone

27
Q

Teriflunomide has what MOA?

A

Cytotoxic - inhibits pyrimidine biosynthesis

28
Q

What enzyme does teriflunomide inhibit?

A

Dihydroorotate dehydrogenase

29
Q

Teriflunomide’s ADEs?

A

Hepatotoxicity

Teratogenicity

30
Q

How does teriflunomide affect MS?

A

Reduces relapse rates

MRI endpoints

31
Q

Demithyl fumurate structure?

A

two esters attached by double bound (esterified carboxylic acid)

32
Q

Dimethyl fumarate MOA?

A

Metabolized by esterases to active Nrf2 antioxidant responses
Promotes remyelination
Suppresses activated T cells and DCs

33
Q

Side effects of dimethyl fumarate?

A
  • PML

- Lymphocytopenia

34
Q

What is the Nrf2 antioxidant response pathway?

A

Nrf2 normally degraded by Keap1 (ubiquitylation)
Keap1 modified during oxidative stress - inhibited
Nrf2 accumulates, enters nucleus, activates transcription of antioxidant response element (ARE) genes
Genes under ARE make glutathione and detoxify

35
Q

Nrf2 activates genes regulated by what element ?

A

ARE - antioxidant response element

36
Q

Keap1 is covalently modified on what residues by oxidative stress?

A

Cysteine residues

37
Q

How is Nrf2 normally inactivated?

A

ubiquitylation by Keap1

38
Q

Genes under control of ARE are part of what response?

A

Phase II

39
Q

What is neutrophin?

A

Antioxidant released by glial cells (astrocytes)

40
Q

Nrf2 pathway increases ____ in astrocytes which travels to _____ and interacts with _____

A

Increases GSH; travels to neurons; interacts with ROS and RNS

41
Q

Alemtuzumab targets ____

A

CD52

42
Q

Alemtuzumab is effective in early phase or degenerative phase of MS?

A

early phase

43
Q

Rituximab targets ___ on ___

A

CD20 on B cells

44
Q

Rituximab stops ___MS and may be effective for ___ MS

A

RRMS may be PPMS

45
Q

Daclizumab targets ____

A

CD25

46
Q

Firategrast MOA?

A

a4 integrin - B and T cells can’t get into CNS

47
Q

T/F: Firategrast reduces MRI Gd lesions

A

True

48
Q

T/F: Firategrast reduces relapse rates

A

False - little effect on relapse rates

49
Q

Amiloride MOA

A

Antagonizes ASIC-1 channel – calcium channel

50
Q

Amiloride is used in patients with ___MS

A

PPMS

51
Q

Laquinimod MOA

A

Up-regulates BNDF –> neuroprotection

Immunomodulatory effects

52
Q

LINGO-1 Antagonist MOA

A

Interfers with LINGO-1, negative regulator of OPC differentiation

53
Q

Cladribine structure

A

Like DNA

54
Q

Cladribine MOA

A

Phosphorylated to 2-chloro-dATP, which damages DNA and interfers with DNA metabolism–> lymphocyte depletion

55
Q

What cells is cladribine converted to 2-chloro-dATP in?

A

Lymphocytes, monocytes

56
Q

What ROA does cladribine have?

A

Oral

57
Q

What cells does daclizumab binding affect?

A

T cells (via CD25 on IL-2 receptor)

58
Q

How does daclizumab affect MS?

A

Decrease in relapse and new lesions

59
Q

Daclizumab ROA?

A

SC q month

60
Q

Contraindication to daclizumab?

A

Hepatotoxicity

Infections, skin rash

61
Q

Ocrelizumab MOA

A

Targets CD20 - on mature B cells only

62
Q

T/F: Ocrelizumab does not affect disease progessio in PPMS

A

FALSE - decrease progression of PPMS!

63
Q

T/F: Ocrelizumab increases relapse rate in RRMS

A

False - Decrease relapse rate!

64
Q

Ocrelizumab MOA?

A

Infusion

Pharmacotherapy III (12 decks)

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