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PMCOL 343 > parkinson > Flashcards

parkinson Flashcards

1
Q

what are 5 movement disorders

A 
tremor
chorea
athetosis
dystonia
tics
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2
Q

what is tremor

A

rhythmic oscillation around a joint

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3
Q

what is postural tremor

A

tremor while trying tp maintain posture

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4
Q

when is tremor associated with parkinsons (2 things)

A

rigidity and impairment of voluntery movement

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5
Q

what is intentional tremor

A

when you have a tremor when you want to move

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6
Q

which tremor is associated with essential (familial tremor)

A

postural tremor

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7
Q

what can intentional tremors be associated with (3 things)

A

lesions of brainstem (cerebellum), alcohol, drug toxicity

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8
Q

what does chorea mean (1 word)

A

dance

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9
Q

what types of movement characterize chorea

A

irregular, unpredictable movements

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10
Q

what does chorea do to voluntary activity

A

impair

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11
Q

which muscles are most affected by chorea

A

proximal muscles

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12
Q

what are some of the movements called in chorea and why

A

ballistic movements - more violent because they arise from proximal movements (like move whole arm instead of just hand)

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13
Q

is chorea hereditary

A

sometimes

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14
Q

what can cause chorea (3)

A

hereditary
general medical disorders
drug therapies

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15
Q

what is athetosis

A

slow writing movements (like twisting squirming controtions)

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16
Q

what is dystonia

A

sustained movement with abnormal posture

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17
Q

what causes athetosis (3)

A

perinatal (right before and after birth) damage, CNS lesions, drug treatments

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18
Q

what causes dystonia (3)

A

perinatal damage (right before and after birth), CNS lesions, drug treatments

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19
Q

what are Tics

A

sudden coordinated abnormal movements

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20
Q

what is tourettes syndrome

A

multiple chronic tics

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21
Q

what kind of drugs can induce parkinsons-like syndroms (2)

A

dopamine antagosnists or drugs that destroy DA releasing neurons

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22
Q

where do the Dopaminergic cells come from

A

substantia nigra compcta

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23
Q

where do the DA releasing cells project to (which neurons and where)

A

GABAergic cells in the striatum

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24
Q

what does DA do to GABAergic cells in striatum

A

inhibit

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25
Q

what does ACh do to GABAergic cells in striatum

A

excite

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26
Q

what causes parkinsons disease (which neurons are effected, what does this cause)

A

loss of DA releasing cells, less inhibition on GABA cells, so excess GABA release

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27
Q

what disease is characterized by a loss of nigral DA cells

A

parkinsons

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28
Q

what causes huntingtons disease (which neurons are effected, what does this cause)

A

Loss of cholinergic input, GABA cells die off, less GABA inhibition (so you get violent movements)

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29
Q

what disease is characterized by a loss of cholinergic input onto GABA cells in striatum

A

huntingtons

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30
Q

what disease is characterized by a loss GABA cells in striatum

A

huntingtons

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31
Q

what is another name for parkinsonism

A

paralysis agitans

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32
Q

what 4 things characterize parkinsons

A
  • rigidity
  • bradykinesia (slow movement)
  • tremor
  • postural instability
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33
Q

what usually causes parkinsons

A

unknown (idiopathic)

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34
Q

what may cause early onset parkinsons

A

genetics

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35
Q

is parkinsons progressive

A

yes

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36
Q

what is the frequency of the resting tremor

A

4-6Hz

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37
Q

what is the word for movements when the hands arent extended

A

“pill rolling”

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38
Q

what is the parkinsons gait +where flexion (3 places)

A

stooped posture, flexion at knees, hips and neck

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39
Q

what kind of steps do people with parkinsons take+ what is it like when they turn

A

small shuffling steps, emphasized when turning

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40
Q

is it difficult to initiate or change movements with parkinsons

A

yes

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41
Q

can you cure parkinsons

A

no

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42
Q

can you stop parkinsons progression

A

no

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43
Q

what % of neuron loss do you start getting parkinsons symptoms

A

80%

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44
Q

what is the primary therapy for Parkinson’s

A

enhance DA levels in striatum

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45
Q

what are 2 ways to enhance DA levels in the striatum (which drugs/ kind of drugs)

A

levodopa and dopamine agonists

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46
Q

what is secondary therapy for Parkinson’s

A

enhance DOPA entry into and persistance in brain

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47
Q

which drug helps enhance DOPA entry into brain + persistence in brain

A

carbidopa

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48
Q

what G protein for D1

A

Gs

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49
Q

what G protein for D2

A

Gi

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50
Q

what does D1 do to adenylyl cyclase

A

induce

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51
Q

where are D1 neurons located (2)

A
  • on DA neurons in nigra

- presynaptic terminals of cortical projections to striatum (glu receptive neurons)

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52
Q

what do D2 to adenylyl cyclaes activity

A

inhibit

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53
Q

where are D2 neurons located

A
  • postsynaptic on striatal GABA cells

- presynaptic on basal ganglia inputs to nigra

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54
Q

which effects of dopamine (agonism/anta) on which receptors can induce Parkinson’s symptoms (D1 D2)

A

D2 antagonists of dopamine

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55
Q

which DA receptor action of dopamine are antiparkinsonian

A

D2

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56
Q

do you need D1 or D2 action to do antiparkinsons therapy

A

mostly D2 but some D1 is needed

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57
Q

does dopamine pass the BBB

A

no

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58
Q

why are D2 actions of dopamine antiParkinson’s

A

because D2 activation on striatal GABA cells inhibits extra GABA release (less GABA release so less of the Parkinson’s stiffness)

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59
Q

why does D2 antagonism induce Parkinson’s like symptoms

A

because D2 agonism helps reduce GABA release. D2 antagonism is similar to the death fo DA releasing neurons

60
Q

what is Levodopa’s relation to DA

A

it is a metabolic precursor to DA synthesis (AMD bypasses the rate-limiting synthesis step)

61
Q

what step of DA synthesis does levodopa bypass

A

the rate-limiting step

62
Q

does levodopa penetrate the BBB (how much)

A

yes at 1-10%

63
Q

where is levodopa transformed into DA

A

in the brain and periphery

64
Q

why is levodopa allowed to enter the brain

A

because it looks like an amino acid

65
Q

where is levodopa absorbed

A

in the small intestine

66
Q

how easily is levadopa absorbed

A

fast and easy

67
Q

why dont you want to take levodopa with food

A

because the amino acids from food with compete with levodopa with transporter

68
Q

how does levodopa get absorbed into the blood

A

absorbed in the small intestine via amino acid transporters

69
Q

when do plasma concentrations of levodopa peak in the blood (how long, time)

A

1-2 hours

70
Q

what is the plasma 1/2 life of levodopa

A

1-3 hours (considerable variability)

71
Q

what are the metabolites of levodopa (2)

A
  • homovanillic acid HVA

- DOPAC (dihydroxyphenylacetic acid)

72
Q

what % of unmetabolized levodopa enters the brain

A

1-3%

73
Q

what is the therapeutic goal of levodopa use

A

increase levodopa into the CNS

74
Q

what kind of drug is coadministered with levodopa

A

periphreal DOPA decarboxylase inhibitor

75
Q

why would you want to administer a periphreal DOPA decarboxylase inhibitor with levodopa

A

to help prevent its breakdown outside the brain so more can come in

76
Q

what is Carbidopa’s relation to the dopamine pathway

A

it is structurally similar to DOPA

77
Q

what is the mechanism of action of carbidopa

A

inhibits DOPA-decarboxylase

78
Q

what are the intermediates between tyrosine and dopamine

A

just DOPA (L-DOPA)

79
Q

what turns L-DOPA into dopamine

A

dopa decarboxylase

80
Q

how is carbidopa given in treatment

A

ratio of 1:10 or 1:4 with levodopa

81
Q

what does carbidopa permit with levodopa

A

up to 10% of levodopa to enter the brain (increases levodopa entering into brain)

82
Q

what is sinemet

A

carbidopa + levodopa

83
Q

what is the ratio of carbidopa and levodopa in sinemet

initial treatment and final

A

25 carbidopa:100 levodopa

increases to

25 carbidopa:250 levodopa

(efficacity of levodopa decreases with treatment)

84
Q

how does the effect of levodopa change with treatment

A

it decreases inefficacy

85
Q

what drugs do you often add to sinemet in advanced stages

A

add dopaminergics

86
Q

what are some gastrointestinal effects of levodopa (3)

A

nausea vomit weight loss

87
Q

what causes vomiting with levodopa

A

DA action at the vomiting center

88
Q

where is the vomiting centre

A

in CNS but outside BBB

89
Q

why is there more vomiting centre activation with levodopa

A

because levodopa increases DA which activates the vomiting center

90
Q

what are 3 ways to help prevent the GI issues of levodopa

A
  • smaller more frequent doses
  • using carbidopa too
  • antacids
91
Q

do antiemetic phenothiazines help with GI issues with levodopa

A

no

92
Q

what are cardiovascular effects of levodopa

A

tachycardia, arrhythmia, postural hypotension

93
Q

what causes the adverse cardio effects of levodopa

A

increase catecholamine formation in periphery

94
Q

what can help counteract the cardio effects of levodopa and how

A

carbidopa because it reduces the circulating dopamine

95
Q

what % of people get dyskinesias with levodopa

A

80%

96
Q

why does dyskinesia vary with levodopa use

A

because its dose-related with individual responses

97
Q

what can help the dyskinesias with levodopa

A
  • improvement with levodopa alone
  • drug holidays
  • surgery (reduce doses of levodopa needed)
98
Q

what are the adverse behavioural effects of levodopa (6)

A

depression, anxiety, agitation, confusion, delusions, mood changes

99
Q

are there more of lessBEHAVIOURAL effects with just levodopa or levodopa and a DDC inhibitor (carbidopa)

A

worse with both drugs than just levodopa

100
Q

what are some drugs that can help with the behavioural effects of levodopa

A

some antipsychotics

101
Q

what 2 things cause/effect the fluctuation of response of levodopa

A
  • increasing frequency with treatment

- some related to timing of doses (wearing-off, end-of dose akinesa)

102
Q

what is the on-off phenomenon

A

periods of akinesia alternate with mobility and dyskenesia (sudden, sometimes unpredictable changes in a PD patient’s symptoms, varying between mobility (usually with dyskinesia) and immobility)

103
Q

what is the mechanism of the on-off phenomenon

A

its unknown

104
Q

what are 2 ways to help reduce on-off phenomenon

A

reduce protein intake (DA is a tyrosine derivative)

controlled release sinemet or COMT inhibitors

105
Q

is on-off phenomenon related to dose timing

A

no

106
Q

what are drug holidays and the point of them

A

taking breaks to help reduce adverse effects

107
Q

are drug holidays good for on-off phenomenon

A

it can help for some people

108
Q

what happens with abrupt cessation of levodopa

A

severe akinesia

109
Q

what happens if you do drug holiday then start again with a low dose

A

there will be fewer averse effects than before

110
Q

how long do the benefits of drug holidays last

A

not long

111
Q

what 3 benefits of using DA agonists

A
  • they dont have potentially toxic metabolites
  • they do not compete with other substances for transporters
  • they are receptor selective
112
Q

how do you use dopamine agonists in treatment

A

with adjuct to levodopa/carbidopa, or to gradually replace to levodopa

113
Q

what are 2 examples of dopamine agonists

A

bromocriptine and pergolide

114
Q

which receptor does bromocriptine bind

A

agonist at D2

115
Q

which receptor does pergolide bind

A

mixed D1 and D2 agonist

116
Q

is pergolide or bromocriptine better

A

pergolide

117
Q

what do bromocriptine and pergolide do to the required dose of levodopa

A

lower

118
Q

what are the adverse effects of bromocriptine and pergolide

A

similar to levodopa but less sever (but mental symptoms are worse)

119
Q

which dopamine agonists are the ergot derivatives

A

bromocriptine and pergolide (older ones)

120
Q

which dopamine agonists are the older drugs

A

bromocriptine and pergolide

121
Q

which dopamine agonists are the newer drugs

A

pramipexole and ropinirole

122
Q

why are bromocriptine and pergolide able to stick around longer

A

because they are not shaped like a.a. unlike levodopa

123
Q

how are pramipexole and ropinirole used in parkinsons therapy

A

they can be prescribed alone

124
Q

how are bromocriptine and pergolide used in therapy

A

often given with levodopa

125
Q

which DA receptors does pramipexole bind

A

D3 (D2 class) agonist

126
Q

which DA receptors does ropinirole bind

A

pure D2 agonist

127
Q

what are the adverse effects like for pramipexole and ropinirole

A

similar to levodopa

128
Q

what are 2 benefits of using pramipexole

A

effective in advances parkinsons

possible neuroprotective effect

129
Q

what does MAO B metabolize

A

dopamine

130
Q

what is selegiline do

A

blocks MAO B

131
Q

when is selegiline used in treatment and how

A

with levodopa when its effects start declining

132
Q

what are some contraindications for selegiline

A

patients that use TCAs or SSRIs

133
Q

what does COMT do

A

metabolizes levodopa

134
Q

what happens to COMT levels with more DDC inhibition

A

increase levels

135
Q

which drug may also have antioxidant antiapoptotic effects in animals

A

selegiline (dont worry if dont know)

136
Q

what are 2 examples of COMT inhibitors

A

tolcapone and entacapone

137
Q

where does tolcapone act

A

centrally and peripheral (hepatotoxic)

138
Q

where does entacapone act

A

only peripherally

139
Q

what are some side effects of tolcapone and entacapone +1 really bad one

A

similar to levodopa, diarrhea, orange urine, orthostatic hypotension

tolcapone is hepatotoxic

140
Q

which of tolcapone and entacapone is hepatotoxic

A

tolcapone

141
Q

how does tolcapone and entacapone reduce the amount of levodopa needed

A

(COMT inhibitors)
increases its half life
increases levels of 3OMD which competes for transporters taking levodopa into blood (?idk)

142
Q

what is amantadine

A

antiviral

143
Q

how does amantadine work

A

blocks NMDA receptor on cholinergic neurons, may increase release brain dopamine

144
Q

what are some bad things about using amantadine in parkinsons

A

it has lots of adverse effects

145
Q

when are using anticholinergics the best for parkinsons

A

when the tremor is the main symptoms

146
Q

when are using anticholinergics not great for parkinsons

A

if its rigidity or bradykineasia

147
Q

why can anticholinergics be good for parkinsons

A

because a lack of DA release means overbalance of cholinergic excitation in the basal ganglia

PMCOL 343 (31 decks)

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