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Pharm > Parkinson's > Flashcards

Parkinson's Flashcards

1
Q

usual time of diagnosis of parkinson’s

A

55-65

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2
Q

when patients are symptomatic, they’ve already lost how many dopamine neurons in the brain?

A

70-80%

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3
Q

dopamine
What is it
Where is it

A

an inhibitory NT in the extra pyramidal system

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4
Q

what is the excitatory NT in the EPS?

A

acetylcholine

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5
Q

when dopaminergic activity decreases,

A

cholinergic activity dominates - resulting in motor disturbances

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6
Q

which area in the EPS is most affected by Parkinson’s?

A

the dopamine neurons in the substantial nigra (the lewy bodies)

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7
Q

extrapyramidal system responsible for (3)

A

movement,
dampens erratic motions,
maintains muscle tone and posture.

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8
Q

the dopamine cell bodies are located in ______ and project to _________

A

the midbrain in the substantial nigra. they project to the dorsal striatum.

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9
Q

dopamine pathways in the brain (3)

A

nigrostriatal
mesolimbic and mesocortical
tuberoinfundibular

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10
Q

dopamine signaling and cholinergic signaling in a normal brain

A

there is a balance between them which results in controlled movement

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11
Q

in the Parkinson’s brain

A

the neurons that supply dopamine to the striatum degenerate leading to unopposed cholinergic signaling. results in disturbed movement.

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12
Q

direct and indirect pathway originate from

A

distinct populations of gaba neurons in the striatum

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13
Q

direct pathway activation does what?

A

promotes movement

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14
Q

indirect pathway activation

A

inhibits movement

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15
Q

dopamine receptor subtypes

A

d1 and d2

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16
Q

d1 receptors are expressed on

A

on gaba neurons in the striatum that form the DIRECT pathway

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17
Q

d2 receptors are expressed

A

expressed exclusively on gaba neurons in the striatum that form the INDIRECT pathway

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18
Q

dopamine receptor agonists used to treat Parkinson’s disease are all

A

selective D2 receptor agonists

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19
Q

why are dopamine receptor agonists used?

A

analogous to replacing dopamine on direct pathway, dampening indirect pathway activity.

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20
Q

drug related Parkinsonism may be seen with

A

antipsychotics
anti emetics
metoclopramide

(all dopamine receptor antagonists)

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21
Q

MPTP

A

neurotoxin which destroys dopamine nerve terminals

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22
Q

rotenone and paraquat

A

pesticides which resemble MPTP. used to be commonly used in agriculture and farming.

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23
Q

TRAP signs and symptoms of Parkinson’s disease

motor

A

T - tremor (“pill rolling”)
R - rigidity
A - akinesia or bradykinesia
P - postural instability and abnormal gait

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24
Q

SOAP signs and symptoms of parkinson’s

non motor

A

S - sleep disturbance
O - other/misc
A - autonomic (urinary, sweating)
P - psychologic

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25
Q

new parkinson’s drug for parkinson’s psychosis. controversial because it hasn’t been properly vetted and patients have noted worsening symptoms.

A

Pimavanzserin

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26
Q

therapeutic goals of pharmacotherapy for parkinson’s

A

improve ability to carry out ADLs and to improve the non motor symptoms associated with the disease

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27
Q

classes of Parkinson’s disease treatments (5)

A 
inhibitors of MAO B
dopamine receptor agonists
amantadine
anticholinergics
dopamine augmentation/precursor (levidopa)
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28
Q

drugs that are used to enhance levidopa (2)

A

inhibitor of dopa decarboxylase (carbidopa)

inhibitor of COMT (metabolizes levodopa)

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29
Q

major goal of therapy

A

increase dopamine activity in the brain

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30
Q

gold standard for parkinson’s

A

levodopa/carbodopa

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31
Q

levopdopa is

A

the precursor to dopamine in the brain

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32
Q

MAO B inhibitors do what

A

stop dopamine breakdown

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33
Q

specific symptoms of parkinson’s can mainly be treated with

A

anti cholinergics

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34
Q

mild symptoms of Parkinson’s can be treated with what drug class?

A

MAO-B inhibitors

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35
Q

2 examples of MAO-B inhibitors

A

selegiline

rasagiline

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36
Q

for more severe Parkinson’s symptoms, what medication combos may be used? (2)

A

levodopa and carbidopa

levodopa and dopamine receptor agonist

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37
Q

which is a stronger drug, levodopa or carbidopa?

A

levodopa

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38
Q

levodopa compared to dopamine recept agonists

A

levodopa is more effective but long term use carries a higher risk for dyskinesias

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39
Q

what medication should be tried first in mod-severe parkinson’s

A

dopamine receptor agonists for as long as possible before changing to levodopa

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40
Q

why is it recommended to wait as long as possible before starting levodopa?

A

long term use carries higher risk for dyskinesias

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41
Q

once the dopamine receptor agonists are no longer effective for symptom management, what med should be introduced?

A

levodopa.

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42
Q

“off” time defined

A

periods of the day when levodopa is not working well, causing a worsening of symptoms/bradykinesia/akinesia

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43
Q

“off” time

explained

A

unexplainable. it is not related to falling concentrations of the drug. it is a phenomenon where for certain parts of the day, the drug is not effective.

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44
Q

“on” times

A

periods off sufficient control of symptoms with levodopa

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45
Q

as Parkinson’s disease progresses, what happens with “off” times

A

they become longer and longer

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46
Q

MAO-B inhibitor stands for

A

monoamine oxidase B inhibitor

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47
Q

COMT inhibitor stands for

A

catechol-O-methyltransferase inhibitors

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48
Q

if symptoms are severe and unrelieved with medications, what may need to be considered

A

surgery like DBS

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49
Q

what is MAO-B’s role in the brain?

A

metabolism/inactivation of dopamine

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50
Q

what is the MoA of MAO-B inhibitors?

A

inhibit MAO-B, thus increasing dopamine levels in the striatum.

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51
Q

How are MAO-Bs like rasagiline or seligiline used? (2)

A

alone for milder Parkinson’s
or
in combo with levodopa to reduce off times

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52
Q

downside of MAO-B inhibitors

A

efficacy declines within 12-24 months

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53
Q

side effect unique to selegiline

A

insomnia due to its metabolites

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54
Q

active metabolites of selegiline which cause insomnia in patients

A

amphetamine

d-amphetamine

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55
Q

patient education for selegiline

A

take med before noon bc of insomnia risk

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56
Q

anti muscarinic/anti cholinergic drugs for parkinson’s

A

for mild symptoms in younger patients

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57
Q

indications for anticholinergics in parkinson’s

A

mild disease
younger patients (<60)
decrease tremor

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58
Q

which anticholinergics may you see in parkinson’s? (2)

A

benztropine

trihexyphenidyl

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59
Q

anticholinergics vs dopamine agonists

A

less effective but better tolerated in younger patients

60
Q

use of amantadine as mono therapy in parkinson’s

A

tremor if mild

61
Q

amantadine can also be used in combo with

A

levodopa/carbidopa

62
Q

amantadine may be used as an alternative to

A

anticholinergics in older patients with mild symptoms

63
Q

dosing of amantadine

A

dose adjust for renal sufficiency

64
Q

efficacy of amantadine

A

diminished after a few months, requiring drug holiday

65
Q

drug holiday for amantadine

A

efficacy can be restored after 1-2 week drug holiday and reintroduction.

66
Q

first line drugs for parkinson’s

A

dopamine agonists

67
Q

dopamine agonist MoA

A

directly activate D2 receptors in the brain

68
Q

which is more efficacious, D2 agonist or levodopa?

A

levodopa

69
Q

levodopa is the precursor to

A

dopamine

70
Q

levodopa to dopamine

A

levodopa is converted to dopamine in the dopamine terminals via enzymatic conversion

71
Q

in order for levodopa to work, you need to have

A

dopamine terminals in the striatum

72
Q

loss of dopamine terminals in parkinson’s means what for levodopa?

A

it becomes less effective

73
Q

unlike levodopa, dopamine agonists

A

do not rely on enzymatic conversion to be active

74
Q

levodopa and dietary proteins

A

dietary proteins compete with levodopa for active transporters to cross the BBB

75
Q

if you eat a protein rich meal and take levodopa at the same time,

A

reduced of absorption of levodopa through GI lumen and decreased availability of transporter to pump levodopa to brain.

76
Q

dopamine agonists have a ____ incidence of response failure as compared to levodopa

A

lower

77
Q

which drug is less likely to cause dyskinesias, dopamine agonist or levodopa?

A

dopamine agonist

78
Q

two types of dopamine receptor agonists

A

derivatives of ergot

non-ergot derivatives

79
Q

adverse effect unique to pramipexole and not other D2 agonists

A

sleep attacks

80
Q

why do d2 agonists cause impulse control disorders?

A

because dopamine signaling is increased in the frontal cortex. you lose inhibitory control over impulsive behaviors.

81
Q

d2 agonists and MAO b inhibitors may be

A

neuro protective when started early

82
Q

Ropinirole mono therapy

A

for mild symptoms

83
Q

ropinirole for more advanced symptomatology will be

A

given with levodopa/carbidopa

84
Q

for a more active patient who may still be working, which med would be better between pramipexole and ropinirole?

A

ropinirole because there is less risk for sleep effects

85
Q

pramipexole elimination

A

entirely by kidneys

86
Q

ropinirole elimination

A

hepatic metabolism

87
Q

what may be a determining factor between pramipexole and ropinirol?

A

renal and liver function

88
Q

when is rotigotine appropriate?

A

in early stage disease

89
Q

rotigotine route and rationale

A

transdermal patch

PO goes through significant first pass effect

90
Q

how often is rotigotine patch changed

A

q24 hours

91
Q

how often can rotigotine be titrated?

A

weekly

92
Q

adverse effects of rotigotine?

and which is more prominent of rotigotine among the d2 agonists?

A 
sleep disorders
dizziness
headache
hallucinations
dyskinesia
nausea/vomiting*
93
Q

route of apomorphine

A

SC injection

94
Q

drug interactions of apomorphine: ondansetron

A

severe hypotension

95
Q

drug interactions of apomorphine: anti htn

A

cancels the anti htn effect

96
Q

ekg abnormalities with apomorphine

A

causes tachycardia and cardiac dysrhythmias. be careful when given with drugs which prolong QTC

97
Q

severe adverse effect of apomorphine and intervention

A

severe nausea.

start anti emetic 3 days prior, but not a 5HT3 antagonist like ondansetron

98
Q

apomorphine sexual side effects

A

enhanced erections and arousal/promiscuity

99
Q

cornerstone of PD treatment since the 1960s

A

levodopa

100
Q

if a patient with parkinson’s is given levodopa and does not respond

A

they do not have Parkinson’s disease

101
Q

pt education for levodopa regarding clinical effect

A
  • full therapeutic response will not be seen for several months
  • beneficial effects will diminish over time
102
Q

levodopa therapeutic window

A

narrows over time as disease progresses

103
Q

how long is levodopa typically beneficial for? and then what?

A

2-5 years

pre treatment state may return in 5-8 years from initiation of treatment

104
Q

most troubling adverse effect of levodopa

A

drug induced dyskinesias

105
Q

all patients with PD, at some point, will require

A

levodopa

106
Q

levodopa is always combined with

A

carbidopa

107
Q

acute loss of effect of levodopa

A

drug wears off near the end of the dosing interval, indicating the drug level has declined to subtherapeutic level

108
Q

how to minimize wearing off of levodopa

A
  • shorten the dose interval
  • give a drug that prolongs levodopa’s half life
  • give direct acting dopamine agonist
109
Q

drug used for prolonging levodopa’s half life

A

entacapone

110
Q

wearing off vs off time

A

wearing off occurs when levodopa’s therapeutic levels have fallen to subtherapeutic, for instance at the end of the dosing interval.

off times are an unexplainable phenomenon where levodopa stops working for a few minutes to up to 2 hours. this is not related to plasma levels.

111
Q

entacapone is

A

a COMT inhibitor

112
Q

MoA levodopa

A

reduces symptoms by increasing dopamine synthesis in the striatum

113
Q

how does levodopa enter the brain

A

via an active transport system across the BBB

114
Q

once levodopa is in the brain

A

it enters dopamine nerve terminals in the striatum, where it will be synthesized into dopamine

115
Q

levodopa has no direct effects on its own, instead

A

it is converted to dopamine, its active form.

116
Q

levodopa helps to restore a proper balance between

A

dopamine and acetylcholine.

117
Q

active transporter for levodopa

A

L-amino acid transporter

118
Q

L-amino acid performs active transport for levodopa across the ____ and ____

A

GI mucosa

BBB

119
Q

what competes with levodopa for the L-amino acid transporter?

A

dietary protein

120
Q

when to take levodopa

A

1-2 hours before a meal

121
Q

why can’t we just give patients dopamine?

A
  • half life is too short

- can cause cardiac dysrhythmias

122
Q

why are levodopa and carbidopa always given together

A

carbidopa enhances the half life and bioavailability of levidopa by binding to and inhibiting dopa-d-carboxylase in the peripheral tissues, the enzyme that metabolizes levidopa

123
Q

carbidopa on its own

A

has no therapeutic effect

124
Q

does carbidopa cross the BBB?

A

No.

125
Q

carbidopa allows you to give ____ the dose of levodopa if it were given alone

A

1/5th

126
Q

why is carbidopa so important?

A

it allows you to use the lowest dose possible for as long as possible, delaying the development of dyskinesias.

127
Q

adverse effects of levodopa/carbidopa

A 
N/V
dyskinesias
dystonia
postural hypotension
psychosis
hallucination
vivid dreams
insomnia
somnolence
128
Q

trade off with levodopa/carbidopa

A

tremor may actually worsen but bradykinesia and rigidity will respond.

129
Q

effectiveness of levodopa/carbidopa over time

A

will decrease. dose will need to be increased.

130
Q

levodopa/carbidopa is contraindicated with what condition

A

narrow angle glaucoma

131
Q

what drugs do levodopa/carbidopa interact with?

A

anticholinergics

MAO-A inhibitors

132
Q

levodopa/carbidopa interact with anticholinergics because

A

anticholinergics delay gastric emptying, decreasing the absorption of levodopa/carbidopa

133
Q

levodopa/carbidopa and MAO-A inhibitors

A

HTN crisis

134
Q

inhaled levodopa

A

rescue med during off episodes

new development

135
Q

onset of action of inhaled levodopa

A

~10 min

136
Q

adverse effects of inhaled levodopa

A

cough
URI
nausea
discolored saliva

137
Q

MAOIs and inhaled levodopa

A

MAOIs need to be stopped ~2 weeks prior

138
Q

COMT inhibitors MoA

A

selective and reversible inhibitors of catechol-O-methyl transferase

139
Q

catechol I methyl transferase is an

A

enzyme capable of metabolizing peripheral levodopa

140
Q

COMT inhibitors and levodopa

A

prolong half life and duration of action of levodopa by decreasing peripheral levodopa metabolism.

141
Q

when catechol-O-methyl transferase (COMT) metabolizes levodopa, its metabolite can

A

compete with levodopa for the active transporter

142
Q

inhibiting COMT not only prolongs half life and duration of action of levodopa, but it also

A

reduces competition for the active transporter, getting levodopa into the brain faster

143
Q

COMT inhibitors, like entacapone, combined with levodopa

A

increases the duration of the on phase as well as reduces the wearing off phenomenon.

144
Q

example of COMT inhibitor

A

entacapone

145
Q

entacapone is used

A

to reduce the wearing off phenomenon of levodopa

146
Q

adverse effects of entacapone

A 
dyskinesias 
nausea
diarrhea
hallucination
orthostatic hypotension
urine discoloration

Pharm (31 decks)

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