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PD Flashcards

1
Q

What is the pathophysiology of parkinson’s?

A

Loss of SNc dopamine neurons
Increase of striatal cholinergic interneuron activity
Lewy bodies
Oxidative stress

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2
Q

What is the clinical presentation of PD?

A

Slow and progressive (sx onset is associated with degree of neuronal loss and spread of Lewy bodies through certain parts of the brain)

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3
Q

What are the cardinal features of PD?

A

Bradykinesia
Resting tremor (pill rolling/hands predominate)
Muscle rigidity
Gait dysfunction, postural instability - occurs later in disease

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4
Q

What are the motor sx of PD?

A 
Decreased dexterity 
Diminished arm swing when walking
Dysarthria
Dysphagia
Shuffling gait
Festinating gait
Flexed posture
"freezing" at initiation of movement
Hypomimia (reduced facial animation)
Hypophonia
Micrographia
Slow turning
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5
Q

What are the autonomic sx of PD?

A 
Bladder and sphincter disturbances
Consitpation
Diaphoresis
Orthostatic BP changes
Paroxysmal flushing
Sexual disturbances
Sialorrhea
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6
Q

What are the mental status changes in PD?

A 
Anxiety
Depression
Bradyphrenia (slow thought)
Confused state
Dementia
Hallucinations/psychosis
Sleep disturbance
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7
Q

What are other sx in PD?

A 
Fatigability
Oily skin
Pedal edema
Seborrhea
Weight loss
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8
Q

What are the goals for PD treatment?

A

Manage motor/non-motor sx so patients can maintain QOL.

Preserve ability to perform ADLs, improve mobility, minimize AEs or treatment complications.

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9
Q

When is treatment initiated in patients with PD?

A

When sx start to interfere with activities of daily living, employment, or WOL

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10
Q

What leads to cholinergic activity?

A

Decline in dopaminergic neurons/activity to increase in cholinergic activity

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11
Q

What is considered the most effective PD therapy?

A

Levodopa

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12
Q

What are limitations to levodopa?

A

Motor fluctuations
Dyskinesia
Neuropsychiatric complications
Often debilitating and difficult to manage

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13
Q

What may be initiate for mild-moderate PD?

A

Rasagiline or DAs (better SEs)

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14
Q

What is the drawback to starting MAOIs or DAs for mild-moderate PD?

A

Expensive

Less effective

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15
Q

What components of PD are not treated?

A

Freezing
Falling
Dementia

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16
Q

What therapy has been studied and shows benefit in PD?

A

Exercise

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17
Q

What are non-pharm interventions for PD?

A

Nutrition

Exercise

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18
Q

What are PD patients at an increased risk for when it comes to nutrition?

A

Poor nutrition
Weight loss
Loss of muscle mass

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19
Q

What are nutrition interventions for PD?

A

Encourage fluid and fiber intake to prevent/treat constipation
Adequate Ca intake for bone health
Take levodopa on empty stomach 1 hour before or after meals

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20
Q

What is L-dopa the precursor of?

A

Dopamine

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21
Q

Why do we give L-dopa and not dopamine for PD?

A

L-dopa crosses the BBB

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22
Q

Where is L-dopa converted?

A

Centrally - results in efficacy

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23
Q

What is the MOA of L-dopa?

A

Converted to dopamine by L-amino acid decarboxylase (L-AAD)

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24
Q

What are the most effective medications from least to most?

A

Anticholinergics/amantadine
COMTi/MAOIs
DA
Levodopa/carbidopa

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25
Q

What causes AE from levodopa?

A

Resulting from peripheral conversion of levodopa to dopamine by L-AAD

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26
Q

What are the AEs of levodopa alone?

A

N/V
Cardiac arrhythmias
Postural hypotension

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27
Q

What AE is associated with end-of-dose “wear off” of levodopa?

A

Motor complications

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28
Q

What class is carbidopa in?

A

Decarboxylase inhibitor

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29
Q

What is the starting L-dopa dose for relief of disability?

A

200-300 mg/d

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30
Q

What is the upper range of L-dopa doses for severe parkinsonism?

A

800-1000mg/d

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31
Q

Is there a hard max dose of L-dopa?

A

No

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32
Q

What dose of carbidopa is needed to prevent peripheral AEs of L-dopa?

A

75mg/d

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33
Q

What is the max dose of carbidopa?

A

200mg/d

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34
Q

What is peak plasma concentration for L-dopa variability usually attributed to?

A

Erratic gastric emptying

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35
Q

What can affect gastric emptying?

A

Meals delay

Antacids promote

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36
Q

Where is L-dopa primarily absorbed?

A

Duodenum

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37
Q

Is L-dopa protein bound?

A

No

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38
Q

What is the elimination 1/2 life for L-dopa alone?

A

1 hour

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39
Q

What is the elimination 1/2 life of L-dopa/carbidopa?

A

1.5 hours

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40
Q

What is the elimination 1/2 life of L-dopa/carbidopa + COMTi?

A

2-2.5 hours

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41
Q

Why do we increase the dose of controlled and extended release sinemet?

A

Not absorbed well?

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42
Q

Do we start with controlled or immediate release sinemet?

A

Immediate

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43
Q

Why would we switch to controlled release sinemet?

A

Motor sx

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44
Q

Will all patients eventually receive sinemet?

A

Yes

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45
Q

What formulations does L-dopa/carbidopa come as for use in feeding tubes?

A

Gel (Duopa)

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46
Q

What are the non-ergot derivative DAs?

A

Pramipexole
Ropinirole
Rotigotine (transdermal patch)

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47
Q

What are the AEs of DAs?

A 
N/V
Sedation
Imuple control disorders (gambling, pathologic shopping etc)
Daytime sedation including:
Sleep attacks
Lightheadedness & postural hypotension
Hallucinations
Vivid dreams
Confusion
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48
Q

What is the ergot derivative DA?

A

Bromocriptine

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49
Q

Which DA requires renal dose adjustment?

A

Pramipexole

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50
Q

Why is bromocriptine no longer used?

A

Increased risk of pulmonary fibrosis

Lower efficacy compared to other DAs

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51
Q

How long do most patients use DA monotherapy?

A

A few years before requiring L-dopa

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52
Q

When are DAs used as L-dopa adjunct therapy?

A

With a deteriorating response to L-dopa
Experiencing fluctuations in L-dopa response
Experiencing motor fluctuations

53
Q

What do DAs reduce the frequency of?

A

“off” epsiodes

54
Q

What drug class produces a levodopa sparing affect?

A

DA

55
Q

What is apomorphine?

A

Short acting injectable used for acute, intermittent treatment of “off” episodes of PD in patients already receiving levodopa therapy

56
Q

Where is apomorphine given?

A

Setting where BP can be monitored continuously

57
Q

What apoprophine dose do we give first?

A

a 0.2mL (2mg) test dose

58
Q

How often do we monitor the apomorphine test dose?

A

Monitor supine and standing BP predose, 20, 40, 60 minutes postdose

59
Q

If apomorphine is tolerated, how do we titrate?

A

Begin with 0.2mL as needed, and increase by 0.1mL if necessary

60
Q

What do we do if the first apomorphine dose is ineffective?

A

Do not redose

61
Q

What are AEs of apomorphine?

A 
N/V --> severe
Hypotension
Injection site reactions
Dyskinesia
Hallucinations
62
Q

How do we prophylax for apomorphine n/v?

A

Trimethobenzamide (antiemetic) should be initiated 3 days before test dose and continue for at least 2 months

63
Q

What is the MOA of MAOIs?

A

Irreversible selective MAOI that block dopamine breakdown and can modestly extend the duration of action of levodopa

64
Q

How long can MAOIs extend levodopa duration of action?

A

Up to 1 hour of “on” time during the day

65
Q

What do MAOIs decrease the formation of?

A

Free radicals (possible neuroprotective effect)

66
Q

Which MAOI is approved for initial monotherapy or adjunct to levodopa for PD treatment?

A

Rasagiline

67
Q

Which MAOI can be used as adjunctive treatment to levodopa for PD?

A

Selegiline

68
Q

What are AEs of MAOIs?

A 
Dyskinesia
Hallucinations
Delusions
Nausea
Orthostatic hypotension
69
Q

What are DDIs for MAOIs?

A

MAO-B receptors have less than MAO-A receptors

70
Q

How is rasagiline administered?

A

Once daily

71
Q

How is rasagiline metabolized?

A

To relatively inactive metabolite and is devoid of amphetamine like side effects

72
Q

How is selegiline metabolized?

A

Metabolites are amphetamine type and can cause insomnia and jitteriness (negates theorized neuroprotective effect)

73
Q

What is the brand of levodopa/carbidopa/entacapone?

A

Stalevo

74
Q

What is Entacapone dosing?

A

200mg with each levodopa/carbidopa dose

75
Q

What is the max number of entacapone doses per day?

A

8

76
Q

What is the class for entacapone?

A

COMT-inhibitors (catechol-O-methyl transferase inhibitors)

77
Q

What is the MOA of COMT-i?

A

Prevent conversion of levodopa to its metabolite 3-O-methyldopa (3OMD), thuse extending the effects of each levodopa dose

78
Q

Can entacapone be used alone?

A

No, only effect when used with levodopa

79
Q

What is entacapone used for?

A

Managing motor fluctuations

80
Q

Where does entacapone work?

A

Inhibits COMT in periphery only

81
Q

What are the AEs of entacapone?

A 
Dyskinesia
Hallucinations
Confusion
Nausea
Orthostatic hypotension
Brownish-orange urine discoloration
82
Q

What are the SE of tolcapone?

A

Severe and fatal hepatotoxicity
Strict liver monitoring required
Must sign a consent form

83
Q

When would patients take tolcapone?

A

Not responding to entacapone

84
Q

What drugs are anticholinergic?

A

Benztropine

Trihexyphenidyl

85
Q

Where do the anticholinergics work?

A

Centrally

86
Q

What are anticholinergic MOA?

A

Blocks excessive cholinergic activity involved in PD pathology in the CNS at muscarinic sites

87
Q

What PD features do anticholinergics not treat?

A

Bradykinesia

Gait disturbances

88
Q

What PD feature might anticholinergics help with?

A

Dystonia

89
Q

What is the efficacy of anticholinergics in PD?

A

Tremor is similar to DA

90
Q

What are the AEs of anticholinergics?

A 
Blurred vision
Confusion
Constipation
Dry mouth
Memory difficulty
Sedation
Urinary retention
91
Q

What is the limiting factor for anticholinergics?

A

Can try to reduce dose but may need to continue

92
Q

What is the ideal patient for anticholinergic therapy?

A

Younger and cognitively intact

Can be used with other therapies for PD

93
Q

What is an NMDA receptor antagonist?

A

Amantadine

94
Q

What is NMDA mainly used for/?

A

tremor

95
Q

What is NMDA somewhat effective for?

A

Rigidity and bradykinesia

96
Q

What is amantadine effective in suppressing?

A

Levodopa induced dyskinesia

97
Q

What are the AEs for amantadine

A

Confusion in elderly at HD
Sedation and vivid dreams
Dry mouth
Livedo reticularis (diffuse mottling of the skin)
Hallucinations
Rare SE include depression, anxiety, dizziness, psychosis, and confusion

98
Q

How is amantadine adjusted?

A

Renally

99
Q

Which PD drug is best used for short term monotherapy?

A

Amantadine d/t tansient modest efficacy

100
Q

What is the brand and dose of benztropine?

A

Congentin 0.5-0.4 1-2x/d

101
Q

What are the brands and doses of carbidopa/levodopa?

A

Sinemet 2-6x/d 300-1000
Sinemet CR 3-6x/d 400-1000
Rytary (ER) 3-5x/d 435-1170

102
Q

What are the brands and doses of DAs?

A

Pramipexole (Mirapex ER) 1.5-4.5 TID
Ropinorole (Requip) 8-24 TID
Rotigotine (Neuro patch) 2-8 Daily

103
Q

What is the brand and dose of entacapone?

A

Comtan 200-1600 w/levodopa

104
Q

What are the brands and doses of MAO-B inhibitors

A

Rasagiline (Azilect) 0.5-1 daily

Selegiline (Eldepryl) 5-10 BID

105
Q

What is the brand and dose for amantadine?

A

Symmetrel 200-300 BID

106
Q

What is the dose for stalevo?

A

600-1600 6-8 times daily

107
Q

What is the brand and dose of pimavanserin?

A

Nuplazid 34 daily

108
Q

If a patient has mild motor sx (any age) what is potential therapy options?

A

Consider rasagiline
Can add:
Amantadine
Anticholinergics (for tremor in younger, cognitively intact pts)

109
Q

If a patient has mild/mod motor sx and is < 60yo w/no cognitive impairment, what are potential therapy options?

A

DA (initial therapy or addition to establish regimen)

110
Q

If a patient has severe motor sx or is > 60yo or has cognitive impairment, what are potential therapy options?

A

Levodopa (inital therap or addition to established regimen)

111
Q

How do we adjust levodopa therapy with motor fluctuations?

A

Increase dosing frequency
Add MAO-B or COMTi
Add DA

112
Q

How do we adjust levodopa therapy if there is peak dose dyskinesia?

A

Reduce dopaminergic dose

Add amantadine

113
Q

What is the wearing off period of levodopa?

A

End of dose deterioration

114
Q

What are the possible treatments for wearing off?

A

Increase frequency of doses
Change to CR/ER formulation
Add DA, MAOI, COMTi, amantadine
SQ apomorphine

115
Q

What can cause drug-resistant off periods?

A

Delayed gastric emptying or absorption

116
Q

What are possible treatments of drug-resistant off periods?

A 
Give on empty stomach
Crush/chew and take on full glass of water
Avoid CD form; ER may be ok 
Switch to ODT formula
Increase dose and/or frequency
117
Q

What is the treatment of rapid fluctuations?

A

Add DA, MAOI, COMTi that decrease clearance of levodopa

Drug free period/drug holiday

118
Q

What are treatments of nocturnal off states and dystonia?

A

Bedtime dose of DA

ER form of levodopa or DA

119
Q

What is treatment of dystonia?

A

Baclofen/botox

120
Q

What are possible treatments for dykinesia?

A

Smaller, more frequent doses of levodopa
Use of sustained release product
Amantadine 200-400mg/d

121
Q

What drugs may worsen dyskinesia?

A

DA, COMTi, MAOI

122
Q

What is used to treat depression in PD?

A

Pramipexole
Consider MAOI as they are derived from antidepressants
TCA may be more effective than paroxetine/placebo

123
Q

How do we treat dementia in PD?

A

Cholinesterase inhibitors

124
Q

What are the preferred APXs for disruptive psychotic sx?

A

Pimavanserin
Quetiapine
Clozapine

125
Q

What is pimavanserin?

A

SGA indicated for PD suffering with hallucinations and delusions

126
Q

What is the MOA of pimavanserin?

A

Combined inverse agonist/antagonist at serotonin receptors; does not have affinity for dopamine receptors

127
Q

How is quetiapine used in PD hallucinations?

A

Bedtime dose at first, low dose, gradually increase weekly if needed

128
Q

What does clozapine work on in PD?

A

Motor sx and hallucinations

Neuro (13 decks)

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