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PHRM 845 > (3.4) Pharmacotherapy of MS > Flashcards

(3.4) Pharmacotherapy of MS Flashcards

1
Q

What is dissemination in time (DIT)?

A
  • Time between evidence of new lesions in subsequent MRIs (30 days)
  • Damage that has happened more than once
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2
Q

What is dissemination in space (DIS)?

A
  • Need for >1 T2 lesions appearing in at least 2 of 4 MS typical CNS regions (cortical, periventricular, infratentorial, spinal cord)
  • Damage that is in more than once place
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3
Q

What is clinically isolated syndrome (CIS)?

A
  • Descriptor of a first demyelinating event involving the optic nerve, cerebrum, cerebellum, brainstem, or spinal cord
  • Most will develop MS within 20 years
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4
Q

What is relapsing remitting MS (RRMS)?

A

Consists of relapses w partial or complete remission between relapses
- Most will become progressive type over time

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5
Q

What % of diagnoses is RRMS?

A

80-90%

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6
Q

What is secondary progressive MS (SPMS)?

A

About 80% of RRMS pts will progress to SPMS, consisting of fewer relapses w continuing disability

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7
Q

What is primary progressive MS (PPMS)?

A

Progressive form from onset w minor improvements or periods of stability

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8
Q

What % of pts have PPMS?

A

10-15%

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9
Q

How common is PPMS?

A

More common in pts diagnosed in later years (>50 years of age)

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10
Q

What is progressive relapsing MS (PRMS)?

A

Steadily worsening disease from onset w later, clear, acute relapses

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11
Q

Is there recovery and remission from PRMS?

A

May be some recovery from acute attacks, but no remission between relapses

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12
Q

How common is PRMS?

A

PRMS is the least common form (about 5% of diagnoses)

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13
Q

What is the first line tx of acute attacks?

A

High dose corticosteroid tx; oral or IV based on inpt or outpt setting

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14
Q

What is the inpatient setting corticosteroid given for tx of acute attacks?

A

Methylprednisolone 500-1000mg IV daily for 3-7 days, w or without an oral taper over 1-3 weeks

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15
Q

What is the outpatient setting corticosteroid given for tx of acute attacks?

A

Oral prednisone 1250mg every other day x5 doses w/o need for taper

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16
Q

What is another option for tx of acute attacks?

A

Adrenocorticotropic hormone (H.P. Achtar) or plasma exchange

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17
Q

Patients w optic neuritis should receive what acute attacks tx?

A

IV methylprednisolone

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18
Q

What causes progressive multifocal leukoencephalopathy (PML)?

A

Reactivation of dormant John Cunningham Virus (JCV)

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19
Q

MS patients must be tested for what and why?

A

Patients must be tested for JCV antibodies to check for PML

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20
Q

What type of vaccines are preferred for pts w MS?

A

Inactivated vaccines

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21
Q

Which type of vaccines are not recommended in MS pts and why?

A

Live, attenuated vaccines are not recommended bc the ability to cause the disease is weakened, but not eliminated

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22
Q

What MS medication do you NEVER use together w live virus vaccines?

A

Alemtuzumab

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23
Q

Which vaccine should be considered by MS pts who have never had chicken pox?

A

Varicella vaccines, especially if they may start a MS medication that suppresses cell-mediated immunity (like fingolimod, alemtuzumab)

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24
Q

What are important counseling tips of dimethyl fumarate, diroximel fumarate, and monomethyl fumarate’s dosage form?

A
  • The capsule SHOULD NOT be opened and sprinkled on food
  • Do not chew or crush
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25
Q

What should be monitored when using dimethyl fumarate, diroximel fumarate, and monomethyl fumarate?

A
  • Monitor LFTs (Hepatotoxicity)
  • Monitor CBC w differential (neutropenia)
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26
Q

What is associated with dimethyl fumarate, diroximel fumarate, and monomethyl fumarate?

A

Associated w PML

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27
Q

What is a common SE of dimethyl fumarate, diroximel fumarate, and monomethyl fumarate and how can it be relieved?

A
  • Can cause flushing
  • May take aspirin 30 minutes prior to dose to reduce risk of it happening
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28
Q

What medications are in the sphingosine-1-phosphate receptor modulators?

A

Fingolimod, ozanimod, ponesimod, siponimod

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29
Q

A pt has failed to tolerate a S1P receptor modulator. Can they take a different one?

A

No, DO NOT switch between S1P receptor modulators

30
Q

What are CIs w S1P receptor modulators?

A
  • Past arrhythmia diagnosis
  • Any of the following CV diagnoses in the past 6 months: MI, unstable angina, stroke/TIA, class 3/4 HF
31
Q

What are the monitoring parameters of S1P receptor modulators?

A
  • Monitor CBC bc of increased risk of infection
  • Pts should have routine eye exams bc of macular edema
32
Q

What happens when a S1P receptor modulator is discontinued?

A

D/c can result in significant worsening of MS sxs

33
Q

Why must pts who’ve taken their 1st dose of S1P receptor modulators be monitored for 6 hours?

A

Bradycardia may occur - do an ECG at baseline and end of observation period

34
Q

Which S1P receptor modulator should not be used w an MAOi?

A

Ozanimod

35
Q

What is required for siponimod before prescribing?

A

CYP2C9 genotype testing required before prescribing

36
Q

What are SEs of glatiramer acetate?

A
  • Injection SEs immediately post injection
  • Flushing, sweating, dyspnea, chest pain, anxiety, itching
37
Q

What is a counseling tip that must be done w glatiramer acetate and why?

A

Pts MUST rotate injection sites bc likely permanent lipoatrophy may occur

38
Q

Pt reports chest pain after using glatiramer acetate. Is this clinically significant?

A

Not usually clinically significant, unless pt has PMH of CV risk

39
Q

Can glatiramer acetate be used during pregnancy?

A
  • May be preferred if tx is necessary in pregnancy
  • Teratogenic effects are unknown
40
Q

What is a common SE of interferons and how can this risk be reduced?

A
  • Flu-like sxs can occur after injection
  • Decrease risk by pre-treating w acetaminophen or NSAID, dosing in evening/at bedtime and gradual dose titration
41
Q

What are psychiatric SEs of interferons?

A

Depression, suicidal thinking

42
Q

What are monitoring parameters w interferons?

A

Monitor LFTs and TSH - elevated liver function tests and thyroid dysfunction

43
Q

What drugs are in the monoclonal antibodies class for tx of MS?

A

Alemtuzumab, Natalizumab, Ocrelizumab

44
Q

What are possible severe AEs of alemtuzumab?

A

Possible fatal infusion rxns and autoimmune conditions

45
Q

What is alemtuzumab associated w?

A

Associated w increased risk of malignancies

46
Q

What is CI in alemtuzumab?

A

CI in pts w HIV infection bc of prolonged decreased CD4 count

47
Q

What is Natalizumab associated w?

A

Significant association w PML

48
Q

What differentiates ocrelizumab from the other monoclonal antibodies?

A

Ocrelizumab is the only drug FDA-approved for PPMS

49
Q

What is CI w ocrelizumab?

A

CI in active hepatitis B

50
Q

What is ocrelizumab associated w?

A

Associated w increased risk of malignancies

51
Q

What should be completed before starting monoclonal antibody tx?

A

Complete vaccinations at least 6 weeks before

52
Q

What can be used to premedicate before starting monoclonal antibody dose?

A

Steroid, antihistamine, acetaminophen

53
Q

Use of teriflunomide in pregnancy.

A

CONTRAINDICATED
- For accelerated elimination, cholestyramine or activated charcoal for 11 days

54
Q

Use of mitoxantrone in pregnancy.

A

Contraceptive required for tx, pregnancy test before each infusion

55
Q

Use of fingolimod in pregnancy.

A

Contraception during tx and for at least 2 months after d/c

56
Q

Use of ozanimod in pregnancy.

A

Contraception during tx and for at least 3 months after d/c

57
Q

Use of ponesimod in pregnancy.

A

Contraception during tx and for at least 7 days after d/c

58
Q

Use of siponimod in pregnancy.

A

Contraceptive during tx and for least 10 days after d/c

59
Q

Use of ocrelizumab in pregnancy.

A

Contraceptive during tx and for at least 6 months after d/c

60
Q

Use of caldribine in pregnancy.

A
  • Contraceptive required + barrier method for at least 6 months after d/c
  • CI in breastfeeding
61
Q

What happens to the relapses of MS during pregnancy and after pregnancy?

A

Rates of relapses of MS decreases during pregnancy, increases for first 3 months post-partum, then returns to pre-pregnancy rate

62
Q

What is the pseudobulbar affect?

A

Frequent and inappropriate episodes of crying, laughing, or both, unrelated to actual mood

63
Q

What is the cause of pseudobulbar affect?

A
  • Cause unknown
  • May be related to disruption of neural pathways from brainstem to cerebellum
64
Q

What is used to tx pseudobulbar affect?

A

Neudexta (dextromethorphan/quinidine)

65
Q

What is the MOA of dextromethorphan in Neudexta?

A

Agonist at sigma-1 receptors

66
Q

What is the MOA of quinidine in Neudexta?

A

A P450 2D6 inhibitor that blocks the conversion of dextromethorphan to dextrorphan, allowing dextromethorphan to reach CNS

67
Q

What lifestyle modifications help w gait abnormalities/walking speed?

A

Physical training, gait training, exercise

68
Q

What drug therapy treats gait abnormalities/walking speed?

A

Dalfampridine (Ampyra)

69
Q

What is the MOA of dalfampridine?

A

Blocks K channels and prevents repolarization of cell, which prolongs action potentials and nerve impulse transmission in demyelinated area, which may improve walking speed

70
Q

Which formulation of dalfampridine is preferred?

A

ER

71
Q

What are possible SEs of dalfampridine ER?

A

UTIs, insomnia, dizziness, headache, nausea

72
Q

Why is the dalfampridine ER formulation preferred over the IR?

A

IR dosage form and dose escalation is associated w seizures; IR dosage form CI in pts w hx of seizures

PHRM 845 (48 decks)

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