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Pharm III - Exam 2 > Parkinson's > Flashcards

Parkinson's Flashcards

1
Q

Epidemiology of Parkinson’s

A
  • 2:1 males

- 50-80 yo

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2
Q

Etiology of Parkinson’s

A
  • Exact cause unknown (idiopathic MC)
  • No clear triggers identified
  • 10-15% have 1st or 2nd degree relative
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3
Q

Pathophys of Parkinson’s

A
  • Progressive depletion of dopaminergic neurions in substantia nigra of basal ganglia
  • 70 to 80% of dopamine lost by the time a patient presents w/symptoms
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4
Q

How much dopamine has been lost by the time a patient shows symptoms of Parkinson’s?

A

70-80%

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5
Q

Relation of ACh and Parkinson’s

A

Functional increase in ACh occurs which causes characteristic tremor

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6
Q

What is found postmortem in Parkinson’s?

A

Lewy bodies (spherical, abnormal aggregates of protein) are found in remaining dopamine cells in substantia nigra

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7
Q

Core clinical characteristics of PD

A
  • Bradykinesia and akinesia
  • Tremor (unilateral, at rest)
  • Rigidity
  • Postural instability
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8
Q

How is PD diagnosed?

A

Bradykinesia and at least 1 of:

  • Limb muscle rigidity
  • Resting tremor
  • Postural instability
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9
Q

What is the definitive diagnosis of PD?

A

At least 2 characteristics present AND positive response to anti-Parkinson’s pharmacotherapy

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10
Q

Predictors of PD progression

A
  • Older age at onset
  • Rigidity or hypokinesia as presenting symptom
  • Male
  • Presence of comorbidities (stroke, auditory defects, visual impairments)
  • Decreased response to dopamine
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11
Q

Pharmacotherapy options for PD

A
  • MAO-B inhibitors
  • Amantadine
  • Anticholinergic (symptom relief)
  • Dopamine agonists
  • Carbidopa/levodopa
  • COMT inhibitors
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12
Q

Pharmacotherapy options for PD

A
  • MAO-B inhibitors
  • Amantadine
  • Anticholinergic (symptom relief)
  • Dopamine agonists
  • Carbidopa/levodopa
  • COMT inhibitors
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13
Q

Levodopa as 1st line treatment of PD?

A
  • Controversial
  • Provides significant improvement in motor function BUT long term is eventually a/w gradual loss of efficacy, dyskinesias, motor fluctuations
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14
Q

What is 1st line tx of PD if patient is older, has cognitive impairment, or has mod-severe functional impairment?

A

Levodopa

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15
Q

What is 1st line tx of PD?

A
  • Depends on patient age and function
  • Younger pt: MAO-B inhibitor OR dopamine
  • Older pt: Levodopa
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16
Q

MOA of Selegiline

A
  • Irreversible MAO-B inhibitor

- Provides mild relief of symptoms

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17
Q

MOA of Selegiline

A
  • Irreversible MAO-B inhibitor

- Provides mild relief of symptoms

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18
Q

How does Selegiline use relate to LD use?

A
  • Using Selegiline can delay the need to start LD by 9 months
  • Allows for lower doses of LD (by as much as 1/2) when used in combo
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19
Q

What is Selegiline’s use in PD treatment?

A

Use it early on - beneficial effects do not last long term

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20
Q

What is Selegiline’s use in PD treatment?

A

Use it early on - beneficial effects do not last long term

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21
Q

Selegiline and neuroprotection

A
  • Does NOT seem to provide neuroprotection
  • Metabolized into a neurotoxic amphetamine derivative
  • Can cause insomnia and jitteriness
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22
Q

ADRs of Selegiline

A
  • Dyskinesias
  • Orthostasis
  • Serotonin syndrome w/other sympathomimetics or serotonergic agents
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23
Q

ADRs of Selegiline

A
  • Dyskinesias
  • Orthostasis
  • Serotonin syndrome w/other sympathomimetics or serotonergic agents
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24
Q

Rasagiline MOA

A

2nd generation irreversible selective inhibitor of MAO-B

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25
Q

Use of Rasagiline in PD

A
  • Monotherapy in early PD

- Or in combo w/LD in advanced disease

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26
Q

What is preferred in PD - Selegiline or Rasagiline?

A

Rasagiline

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27
Q

What is preferred in PD - Selegiline or Rasagiline?

A

Rasagiline

28
Q

When Rasagiline is added to LD in advanced PD, what is the effect?

A
  • Improves motor fluctuations

- Reduces “off time”

29
Q

Which MAO-B inhibitor does NOT have tyramine interactions?

A

Rasagiline

30
Q

Which MAO-B inhibitor does NOT have tyramine interactions?

A

Rasagiline

31
Q

Drug interactions with Rasagiline

A
  • Serotonin syndrome

- Does NOT have tyramine interactions like Selegiline

32
Q

How is amantadine used in PD?

A
  • Antiviral agent w/mild therapeutic effect in PD
  • Improves bradykinesia, rigidity, tremor
  • MOA unclear
33
Q

When is amantadine used in PD?

A

Early stages when mild symptoms occur

34
Q

When is amantadine used in PD?

A

Early stages when mild symptoms occur

35
Q

Disadvantage of Amantadine

A

Tachyphylaxis develops within 4-8 weeks

36
Q

How should Amantadine be discontinued?

A

Do NOT d/c abruptly - taper gradually to avoid Parkinsonism

37
Q

How should Amantadine be discontinued?

A

Do NOT d/c abruptly - taper gradually to avoid Parkinsonism

38
Q

How are anticholinergics used in PD?

A
  • No longer mainstay tx
  • Reserved for use in early stages with resting tremor as initial presenting symptom w/minimal bradykinesia or rigidity
  • May be used monotherapy or in combo
39
Q

Which agents are used in PD specifically for their anticholinergic effects?

A

Benztropine mesylate

Trihexyphenidyl

40
Q

How should anticholinergics be d/c?

A

NOT abruptly due to potential withdrawal reactions

41
Q

How should anticholinergics be d/c?

A

NOT abruptly due to potential withdrawal reactions

42
Q

How are PD patients affected by combo therapy of DA and LD?

A

Less likely to develop dyskinesias and motor fluctuations

43
Q

How are patients affected by combo therapy of DA and LD?

A

Less likely to develop dyskinesias and motor fluctuations

44
Q

Dosing of dopamine agonists

A
  • Best determined by slow titration
  • May take 4-8 weeks to see beneficial effects
  • Remains effective throughout advanced stages
45
Q

What are Ergot derivatives?

A
  • Dopamine agonists
  • Rarely used in PD
  • Agents are bromocriptine, pergolide (removed from market d/t cardiac valve fibrosis)
46
Q

What are Ergot derivatives?

A
  • Dopamine agonists
  • Rarely used in PD
  • Agents are bromocriptine, pergolide (removed from market d/t cardiac valve fibrosis)
47
Q

What are non-Ergot derivatives?

A
  • Dopamine agonists used in PD treatment

- Pramipexole, Ropinirole, Rotigotine, Apomorphine

48
Q

Rare ADRs of non-ergot derivatives

A
  • Risk for daytime somnolence and sleep attacks
  • Hypersexuality
  • Pathological behaviors
49
Q

Rare ADRs of non-ergot derivatives

A
  • Risk for daytime somnolence and sleep attacks
  • Hypersexuality
  • Pathological behaviors
50
Q

Dosing and administration of Ropinirole

A
  • IR, ER formulations

- Titrate cautiously in hepatic impairment

51
Q

Dosing and administration of Ropinirole

A
  • IR, ER formulations

- Titrate cautiously in hepatic impairment

52
Q

What is Rotigotine indicated for?

A

Early stage idiopathic PD and advanced stages

53
Q

ADRs of Rotigotine

A
  • Application site reactions
  • NV
  • Somnolence
  • Dizzy
  • Hallucinations, abnormal dreaming
54
Q

ADRs of Rotigotine

A
  • Application site reactions
  • NV
  • Somnolence
  • Dizzy
  • Hallucinations, abnormal dreaming
55
Q

Dosing and administration of Apomorphine

A
  • Must use antiemetic as prophylaxis due to significant NV
  • Must start with test dose and is given 3-5 times/day
  • SQ injection
56
Q

Which PD agent requires using an antiemetic beforehand?

A

Apomorphine (dopamine agonist)

57
Q

Which PD agent requires using an antiemetic beforehand?

A

Apomorphine (dopamine agonist)

58
Q

Which drugs should NOT be used with Apomorphine and why?

A
  • Serotonin blockers (e.g. ondansetron)

- Combo can result in severe hypotension

59
Q

PK of Apomorphine

A
  • Onset is rapid (peaks within 60 mins)
  • Start with test dose and is given 3-5 times/day
  • NO oral dosing available, only SQ injection
60
Q

PK of Apomorphine

A
  • Onset is rapid (peaks within 60 mins)
  • Start with test dose and is given 3-5 times/day
  • NO oral dosing available, only SQ injection
61
Q

What is the cornerstone of PD treatment?

A

Levodopa (LD) - nearly all patients will require supplementation with LD

62
Q

How is LD metabolized?

A
  • In periphery, metabolized rapidly to dopamine
  • Dopamine does not cross BBB
  • LD alone is not effective because it requires high doses to get to brain and would cause significant NV
63
Q

Why is carbidopa/levodopa effective in PD?

A
  • Carbidopa is a peripheral decarboxylase inhibitor (decreases conversion of LD to dopamine in periphery)
  • Allows for LD to make it to the brain before becoming dopamine
  • Avoids significant NV
64
Q

What is carbidopa?

A
  • Peripheral decarboxylase inhibitor
  • Decreases conversion of LD to dopamine in the periphery
  • This allows for LD to get to brain before being converted to dopamine
  • 80% less LD dose required to achieve same effect
65
Q

What is carbidopa?

A
  • Peripheral decarboxylase inhibitor
  • Decreases conversion of LD to dopamine in the periphery
  • This allows for LD to get to brain before being converted to dopamine
  • 80% less LD dose required to achieve same effect
66
Q

ADRs of carbidopa/levodopa

A
  • NV
  • Orthostasis
  • Confusion
  • Postural hypotension
  • Vivid dreams
  • Wearing off fluctuations
  • Dyskinesias

Pharm III - Exam 2 (3 decks)

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