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Pharm III - Exam 2 > Parkinson's > Flashcards

Parkinson's Flashcards

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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
Use of Rasagiline in PD
- Monotherapy in early PD | - Or in combo w/LD in advanced disease
26
What is preferred in PD - Selegiline or Rasagiline?
Rasagiline
27
What is preferred in PD - Selegiline or Rasagiline?
Rasagiline
28
When Rasagiline is added to LD in advanced PD, what is the effect?
- Improves motor fluctuations | - Reduces "off time"
29
Which MAO-B inhibitor does NOT have tyramine interactions?
Rasagiline
30
Which MAO-B inhibitor does NOT have tyramine interactions?
Rasagiline
31
Drug interactions with Rasagiline
- Serotonin syndrome | - Does NOT have tyramine interactions like Selegiline
32
How is amantadine used in PD?
- Antiviral agent w/mild therapeutic effect in PD - Improves bradykinesia, rigidity, tremor - MOA unclear
33
When is amantadine used in PD?
Early stages when mild symptoms occur
34
When is amantadine used in PD?
Early stages when mild symptoms occur
35
Disadvantage of Amantadine
Tachyphylaxis develops within 4-8 weeks
36
How should Amantadine be discontinued?
Do NOT d/c abruptly - taper gradually to avoid Parkinsonism
37
How should Amantadine be discontinued?
Do NOT d/c abruptly - taper gradually to avoid Parkinsonism
38
How are anticholinergics used in PD?
- 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
Which agents are used in PD specifically for their anticholinergic effects?
Benztropine mesylate | Trihexyphenidyl
40
How should anticholinergics be d/c?
NOT abruptly due to potential withdrawal reactions
41
How should anticholinergics be d/c?
NOT abruptly due to potential withdrawal reactions
42
How are PD patients affected by combo therapy of DA and LD?
Less likely to develop dyskinesias and motor fluctuations
43
How are patients affected by combo therapy of DA and LD?
Less likely to develop dyskinesias and motor fluctuations
44
Dosing of dopamine agonists
- Best determined by slow titration - May take 4-8 weeks to see beneficial effects - Remains effective throughout advanced stages
45
What are Ergot derivatives?
- Dopamine agonists - Rarely used in PD - Agents are bromocriptine, pergolide (removed from market d/t cardiac valve fibrosis)
46
What are Ergot derivatives?
- Dopamine agonists - Rarely used in PD - Agents are bromocriptine, pergolide (removed from market d/t cardiac valve fibrosis)
47
What are non-Ergot derivatives?
- Dopamine agonists used in PD treatment | - Pramipexole, Ropinirole, Rotigotine, Apomorphine
48
Rare ADRs of non-ergot derivatives
- Risk for daytime somnolence and sleep attacks - Hypersexuality - Pathological behaviors
49
Rare ADRs of non-ergot derivatives
- Risk for daytime somnolence and sleep attacks - Hypersexuality - Pathological behaviors
50
Dosing and administration of Ropinirole
- IR, ER formulations | - Titrate cautiously in hepatic impairment
51
Dosing and administration of Ropinirole
- IR, ER formulations | - Titrate cautiously in hepatic impairment
52
What is Rotigotine indicated for?
Early stage idiopathic PD and advanced stages
53
ADRs of Rotigotine
- Application site reactions - NV - Somnolence - Dizzy - Hallucinations, abnormal dreaming
54
ADRs of Rotigotine
- Application site reactions - NV - Somnolence - Dizzy - Hallucinations, abnormal dreaming
55
Dosing and administration of Apomorphine
- Must use antiemetic as prophylaxis due to significant NV - Must start with test dose and is given 3-5 times/day - SQ injection
56
Which PD agent requires using an antiemetic beforehand?
Apomorphine (dopamine agonist)
57
Which PD agent requires using an antiemetic beforehand?
Apomorphine (dopamine agonist)
58
Which drugs should NOT be used with Apomorphine and why?
- Serotonin blockers (e.g. ondansetron) | - Combo can result in severe hypotension
59
PK of Apomorphine
- 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
PK of Apomorphine
- 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
What is the cornerstone of PD treatment?
Levodopa (LD) - nearly all patients will require supplementation with LD
62
How is LD metabolized?
- 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
Why is carbidopa/levodopa effective in PD?
- 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
What is carbidopa?
- 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
What is carbidopa?
- 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
ADRs of carbidopa/levodopa
- NV - Orthostasis - Confusion - Postural hypotension - Vivid dreams - Wearing off fluctuations - Dyskinesias

Pharm III - Exam 2 (3 decks)

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