Quiz 4 Flashcards

1
Q

What is the autoimmune theory?

A

Attach on the CNS leading to a disruption of the BBB
Migration of T lymphocytes into the CNS
T-lymphocytes attack myelin
Results in demyelination

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2
Q

What is RRMS?

A

Relapsing-Remitting MS

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3
Q

What is the most common form of MS at diagnosis?

A

RRMS

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4
Q

What are RRMS exacerbations?

A

Clearly defined

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5
Q

What happens to neurologic function in RRMS?

A

Acute worsening

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6
Q

Is there remission from RRMS?

A

Periods of partial/complete

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7
Q

If a patient has RRMS, what other form may it develop into w.in 10 years?

A

SPMS

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8
Q

What is SPMS?

A

Secondary progressive MS

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9
Q

What happens to SPMS QOL during progression?

A

Steadily worsening +/- flare ups

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10
Q

Does SPMS have remission?

A

Minor recoveries

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11
Q

What is PPMS?

A

Primary progressive MS

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12
Q

How does disease progress in PPMS?

A

Slow but continuous worsening of their disease from the onset

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13
Q

Are there any relapses in PPMS?

A

No

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14
Q

What is the rate of progression in PPMS?

A

Varies over time

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15
Q

What is the least common MS?

A

PRMS

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16
Q

What is PRMS?

A

Progressive relapsing MS

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17
Q

How does PRMS progress?

A

Steadily worsening disease from the onset

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18
Q

Are there any relapses in PRMS?

A

Clear acute relapses +/- recovery

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19
Q

How does PRMS contrast to RRMS?

A

Periods between relapses are characterized by continuing disease progression

20
Q

How do we treat acute exacerbations of MS?

A

HD methylprednisolone (500-1000mg/d) x 3-10 days

21
Q

What are the 1a treatments for MS?

A

Interferon beta
Glatiramer
Dimethyl fumarate

22
Q

What are the 1b treatments for MS?

A

Fingolimod

Teriflunomide

23
Q

What are the 1c treatments for MS?

A

Natalizumab

Ocrelizumab

24
Q

What are the 2nd line treatments for MS?

A

Mitoxantrone
Alemtuzumab
Daclizumab

25
Q

What are the treatments of MS spasticity?

A

Baclofen
Tizanidine
Dalfampridine

26
Q

What are the treatments of MS bladder sx?

A

Oxybutynin
Tolterodine
Dicyclomine

27
Q

What are the treatments of MS sensory sx?

A

CBZ
Gaba
VPA
TCAs

28
Q

What are the treatments of MS fatigue?

A

Amantadine
Modafinil
Methylphenidate

29
Q

What is the pathophysiology of PD?

A

Loss/degeneration of dopamine neurons -> relative increase of cholinergic interneuron activity (tremors)
Development of Lewy Bodies

30
Q

What are the cardinal features of PD?

A

Bradykinesia
Resting tremor
Muscle rigidity
Gait dysfunction, postural instability

31
Q

What are SEs of levodopa therapy?

A

Abnormal involuntary movements (motor complications)

  • Dyskinesia treatment
  • Peak too high, must dose adjust
32
Q

How do we treat dyskinesia d/t levodopa?

A

Smaller, more frequent doses of levodopa
Use sustained-release products
Amantadine 200-400mg QD

33
Q

What is the “off” effect d/t in levodopa therapy?

A

End of dose deterioration
Motor sx of PD breakthrough
Trough

34
Q

What is the management of the “off” effect?

A

Increase frequency of doses

Change to CR/ER formulation

35
Q

When is CR/ER levodopa formula more effective?

A

For HS dose

36
Q

What agents can be added to levodopa to get more steady dopamine effects?

A

DA, MAOI, COMT-i, or amantadine

37
Q

If a PD patient is having a severe “off” effect, what can be given?

A

SQ apomorphine

38
Q

What may cause drug resistant off periods

A

May be a result of delayed gastric emptying or absorption

39
Q

What are ways we can manage drug resistant off periods?

A
Give on an empty stomach
Crush/chew and take with a full glass of water
Avoid CR formulation
Switch to ODT
Increase dose and/or frequency
40
Q

How do we treat rapid on-off fluctuations?

A

Addition of DA, MAOI, COMT-i

Drug free period or drug holiday (rare)

41
Q

How do we have nocturnal off state?

A

HS dose of DA

ER formulation of levodopa/dopamine agonist

42
Q

What is the MOA of dimethyl fumarate?

A

Unknown
Thought to prevent damage of the brain and spinal cord through its antioxidant properties brought about by activation of the nuclear factor-like 2 pathway

43
Q

What is the dose of dimethyl fumarate?

A

120mg twice daily for 7 days then increase to MD of 240mg twice daily

44
Q

What is the BBW for dimethyl fumarate?

A

Increase risk of Progressive Multifocal Leukoencephalopathy (PML)

45
Q

What are common AEs of dimethyl fumarate?

A
Flushing
GI upset (ab pain, nausea, diarrhea), pruritus, rash, leukopenia
46
Q

What do we monitor in dimethyl fumarate?

A

CBC at baseline then every 6-12 months