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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 to maintain posture (eg. standing still), also exists as benign essential familial tremor

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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

what can intentional tremors be associated with (3 things)

A

lesions of brainstem (cerebellum), alcohol, drug toxicity

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7
Q

what does chorea mean (1 word)

A

dance

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8
Q

what types of movement characterize chorea

A

irregular, unpredictable movements

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9
Q

what does chorea do to voluntary activity

A

impair proximal muscle, resulting in violent movement

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10
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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11
Q

what can cause chorea (3)

A

hereditary
general medical disorders
drug therapies

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12
Q

what is athetosis

A

slow involuntary writhing movements (like twisting squirming controtions)

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13
Q

what is dystonia

A

sustained movement with abnormal posture

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14
Q

what causes dystonia and athetosis (3)

A

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

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15
Q

what are Tics

A

sudden coordinated abnormal movements

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16
Q

what is tourettes syndrome

A

multiple chronic tics

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17
Q

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

A

dopamine antagosnists or drugs that destroy DA releasing neurons (MPTP)

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18
Q

where do the Dopaminergic cells come from

A

substantia nigra compcta

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19
Q

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

A

GABAergic cells in the striatum

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20
Q

what does DA do to GABAergic cells in striatum

A

inhibit

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21
Q

what does ACh do to GABAergic cells in striatum

A

excite

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22
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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23
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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24
Q

what is another name for parkinsonism

A

paralysis agitans

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25
Q

what 4 things characterize parkinsons

A
  • rigidity
  • bradykinesia (slow movement)
  • tremor
  • postural instability
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26
Q

what usually causes parkinsons

A

unknown (idiopathic)

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27
Q

what may cause early onset parkinsons

A

genetics

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28
Q

is parkinsons progressive

A

yes

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29
Q

what is the frequency of the resting tremor

A

4-6Hz

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30
Q

what is the word for Parkinsonian movements when the hands arent extended

A

“pill rolling”

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31
Q

what is the parkinsons gait? describe 3 characteristics

A

stooped posture, flexion at knees, hips and neck, small shuffling steps, emphasized when turning, difficulty initiating movement

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32
Q

can you cure parkinsons

A

no

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33
Q

can you stop parkinsons progression

A

no

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34
Q

what is the primary therapy for Parkinson’s

A

enhance DA levels in striatum

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35
Q

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

A

levodopa and dopamine agonists

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36
Q

what is secondary therapy for Parkinson’s

A

enhance DOPA entry into and persistance in brain

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37
Q

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

A

carbidopa

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38
Q

what G protein for D1

A

Gs

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39
Q

what G protein for D2

A

Gi

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40
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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41
Q

where are D2 neurons located

A
  • postsynaptic on striatal GABA cells

- presynaptic on basal ganglia inputs to nigra

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42
Q

which DA receptor action of dopamine are antiparkinsonian

A

D2 agonists

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43
Q

do you need D1 or D2 action to do antiparkinsons therapy

A

mostly D2 but some D1 is needed

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44
Q

does dopamine pass the BBB

A

no

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45
Q

why does dopamine activation of D2 receptors have antiParkinson’s effects

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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46
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

47
Q

what is Levodopa’s relation to DA

A

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

48
Q

what step of DA synthesis does levodopa bypass

A

the rate-limiting step (tyrosine hydroxylase)

49
Q

does levodopa penetrate the BBB (how much)

A

yes at 1-10%

50
Q

where is levodopa transformed into DA

A

in the brain and periphery

51
Q

why is levodopa allowed to enter the brain

A

because it looks like an amino acid

52
Q

where is levodopa absorbed

A

in the small intestine

53
Q

why dont you want to take levodopa with food

A

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

54
Q

when do plasma concentrations of levodopa peak in the blood (how long, time)? what is the plasma 1/2 life of levodopa?

A

1-2 hours. half life: 1-3 hours with variability

55
Q

what are the metabolites of levodopa (2)

A
  • homovanillic acid HVA

- DOPAC (dihydroxyphenylacetic acid)

56
Q

what % of unmetabolized levodopa enters the brain

A

1-3%

57
Q

what kind of drug is coadministered with levodopa

A

periphreal DOPA decarboxylase inhibitor

58
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

59
Q

what is Carbidopa’s relation to the dopamine pathway

A

it is structurally similar to DOPA

60
Q

what is the mechanism of action of carbidopa

A

inhibits DOPA-decarboxylase, preventing breakdown of levadopa in the peripheries before it enters the brain

61
Q

what turns L-DOPA into dopamine

A

dopa decarboxylase

62
Q

how is carbidopa given in treatment

A

ratio of 1:10 or 1:4 with levodopa

63
Q

what does carbidopa permit with levodopa

A

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

64
Q

what is sinemet

A

carbidopa + levodopa

65
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

(since efficacy of levodopa decreases with treatment)

66
Q

how does the effect of levodopa change with treatment

A

it decreases inefficacy

67
Q

what drugs do you often add to sinemet in advanced stages

A

add dopaminergics

68
Q

what are some gastrointestinal effects of levodopa (3)

A

nausea vomit weight loss

69
Q

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

A
  • smaller more frequent doses
  • using carbidopa/perhipheral DDC inhibitors to decrease the amont of free DA in the periphery
  • antacids
70
Q

do antiemetic phenothiazines help with GI issues with levodopa

A

no

71
Q

what are cardiovascular effects of levodopa

A

tachycardia, arrhythmia, postural hypotension

72
Q

what causes the adverse cardio effects of levodopa

A

increase catecholamine formation in periphery (due to DA -> NA -> A)

73
Q

what can help counteract the cardio effects of levodopa and how

A

carbidopa/peripheral DDC inhibitors because it reduces the circulating dopamine

74
Q

why does dyskinesia vary with levodopa use

A

because its dose-related with individual responses

75
Q

what can help the dyskinesias with levodopa

A
  • improvement as patient gets used to levodopa treatment
  • drug holidays
  • surgery (reduce doses of levodopa needed)
76
Q

what are the adverse behavioural effects of levodopa (6)

A

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

77
Q

list 5 negative side effects of levadopa

A

GI related (nausea and vomiting)
CV (tachycardia)
Dyskinesias
Behavioral effects (depression, anxiety, delusion)
Fluctuations in response
On and Off phenomena

78
Q

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

A

some antipsychotics

79
Q

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

A
  • increasing frequency with treatment (levodopa become more ineffective)

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

80
Q

what is the on-off phenomenon

A

periods of akinesia alternate with mobility and dyskenesia (no movement and too much movement)

81
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

82
Q

what are drug holidays? why are they controversial

A

taking breaks to help reduce adverse effects
needs very careful supervision since stopping levodopa abruptly can lead to akinesia
benefits are short lived

83
Q

what 4 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
  • can be used in combination therapy with levodopa/carbidopa
84
Q

how do you use dopamine agonists in treatment

A

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

85
Q

what are 2 examples of dopamine agonists

A

bromocriptine and pergolide

86
Q

which receptor does bromocriptine bind

A

agonist at D2

87
Q

which receptor does pergolide bind

A

mixed D1 and D2 agonist

88
Q

is pergolide or bromocriptine better

A

pergolide

89
Q

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

A

lower

90
Q

what are the adverse effects of bromocriptine and pergolide

A

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

91
Q

name two ergot derivative dopamine agonists

A

bromocriptine and pergolide (older ones)

92
Q

which dopamine agonists are the older drugs

A

bromocriptine and pergolide

93
Q

name two non-ergot related dopamine agonists

A

pramipexole and ropinirole

94
Q

how are bromocriptine and pergolide used in therapy compared to pramipexole and ropinole

A

bromochiptine and pergolide are often given with levodopa
pramipexole and ropinole are given alone

95
Q

which DA receptors does pramipexole bind

A

D3 (D2 class) agonist

96
Q

which DA receptors does ropinirole bind

A

pure D2 agonist

97
Q

what are the adverse effects like for pramipexole and ropinirole

A

similar to levodopa

98
Q

what are 2 benefits of using pramipexole

A

effective in advanced parkinsons and firstline therapy for younger patients to protect remaining neurons

possible neuroprotective effect

99
Q

what does MAO B metabolize

A

dopamine

100
Q

what are selegiline/rasagiline

A

MAO B blocker

101
Q

name a MAO B inhibitors used in Parkinson’s treatment

A

Selegine

102
Q

when is selegiline used in treatment and how

A

with levodopa when its effects start declining

103
Q

what are some contraindications for selegiline

A

patients that use TCAs or SSRIs

104
Q

what does COMT do

A

metabolizes levodopa

105
Q

what happens to COMT levels with more DDC inhibition

A

increase levels (since there is excess L-DOPA lying around)

106
Q

what are 2 examples of COMT inhibitors

A

tolcapone and entacapone

107
Q

where does tolcapone act

A

centrally and peripheral (hepatotoxic)

108
Q

where does entacapone act

A

only peripherally

109
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

110
Q

how does tolcapone and entacapone reduce the amount of levodopa needed

A

(COMT inhibitors)
increases its half life by inhibiting L-DOPA breakdown

111
Q

what is amantadine

A

antiviral that blocks NMDA receptors on cholinergic neurons, may increase brain dopamine

112
Q

when are using anticholinergics the best for parkinsons

A

when the tremor is the main symptoms (NOT rigidity, brakykinesia)

113
Q

why can anticholinergics be good for parkinsons

A

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

PMCOL 343 (31 decks)

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