Parkinsons Flashcards

1
Q

common age and gender in parkinsons

A

male

diagnosed age 66 usually

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2
Q

the four motor features

A
bradykinesia 
tremor at rest
rigidity 
postural instability 
*must have bradykinesia
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3
Q

describe the tremor at rest

A

rhythmic
asymmetric - doesnt affect both sides equally
pill rolling
feet, lip, jaw
may disappear with voluntary movement and sleep
worsens with mental stress

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4
Q

describe the rigidity

A

lead pipe, cogwheel
neck, trunk, limbs
resistance to passive movement of the limbs

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5
Q

describe bradykinesia

A

slowness of all movements

difficulty initiating movement

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6
Q

describe postural instability

A

later presentation
shuffling gait
narrow base
freezing and falls

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7
Q

main difference in symptoms between motor cortex disorders

A

no muscle weakness

just a communication issue

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8
Q

other clinical features

A
depression
dementia
sleep disturbance
difficultly smelling
micrographia 
dysphagia
lack of expression -hypomimia
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9
Q

what happens in the substantia nigra

A

low dopamine causes parkinsons
high dopamine causes dyskinesia
cells start to die in parkinsons

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10
Q

what is the substantion nigra responsible for

A

controls movements and connects to the motor cortex

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11
Q

how does the nigrostriatal pathway achieve smooth muscle movement

A

ach (inhibitory) and dopamine(excitatory) are in balance

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12
Q

what happens when there is much more ach than dopamine

A

movement becomes jerky and stiff

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13
Q

drugs that can cause parkinson like motor symptoms

A

typical antipsychotics - block all 4 pathways
atypical antipsycotics - selectively block dopamine in mesolimbic pathway
Gi agents - metoclopramide
SSRI
valproic acid
old antihypertensives

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14
Q

4 types of extrapyramidal symptoms

A

dystonia
akathisia
pseudoparkinsonism
tardive dyskinesia

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15
Q

risk factors for drug induced parkinsonism

A

old
femal
high dose of offending drug
history of movement disorder

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16
Q

signs its drug induce parkinsonism

A

symmetric presentation***
onset within a few weeks of starting drug
may take 2-6months to resolve after

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17
Q

what is drug induced neuroleptic malignant syndrome

A

life threatening
due to sudden decrease in dopaminergic transmission
dopamine blocker&raquo_space;»decrease in dopamine transmission or sudden withdrawal from dopamine enhancer

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18
Q

FARM symptoms of neuroleptic malignant syndrome

A

fever
autonomic instability - sweat, HR, BP
rigidity
mental status changes

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19
Q

when do symptoms appear in parkinsons

A

once there is loss of 60-80% of pigmented neurons in the substantia nigra

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20
Q

5 ways to treat parkinsons

A
dopamine precursor
dopamine agonist
NMDA receptor antagonist
COMT or MOAB inhibitor 
block acetylcholine
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21
Q

goals of therapy

A

preserve ability to perform activities of daily living
min AE and treatment complications
improve non motor features

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22
Q

what warrants therapu

A

when diability interferes with social emotional or work life

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23
Q

why dont we treat early mild symptoms

A

ldopa is the best drug but loses effect over time so want to save it

24
Q

anticholinergic MOA

A

block acetylcholine, relative increase in dopamine

25
amantadine MOA
NMDA antagonist | increases dopamine release
26
MAO-B inhibtor MOA
reduce dopamine breakdown in the cns
27
COMT inhibitor MOA
reduce levodopa breakdown in GI | prolongs half life and increase bioavailability
28
dopamine agonist MOA
directly stimulates dopamine receptors
29
levodopa MOA
converted to dopamine by dopa decarboxylase
30
why cant dopamine just be directly gicen
cant cross the BBB
31
when to use anticholinergics (benztropine)
generally people <60 due to the AE and modest efficacy
32
anticholinergic AE
``` constipation dry mouth eye infections urinary retention blurred vision cognitive impairment headache increased HR overheating ```
33
do you have to taper benztropine
yes over 1 week
34
indication for amantadine
modest effect used early for tremor used alter to reduce ldopa dyskinesia better tolerated in yount patients due to stimulatory effects (normally used for MS fatigue)
35
AE of amantadine
``` confusion, insomnia, nervous anticholinergic GI hypotension livedo reticularis *take in AM ```
36
what is livedo reticularis
reversible diffuse purple red skin in the extremeties not an issue just cosmetic
37
role of MAOBi
early for monotherapy | add on to levodopa to extend on time
38
is tyramine intake a concern wtih selegiline and rasagiline
no
39
AE of selegiline
``` insomnia hallucination confusion orthostatic hypotension take in AM *bc converted to methamphetamine ```
40
AE of rasagiline
GI - take with food
41
which drugs prevent dopamine degradation in the peripheray
comt inhibitors | DDC inhibitors
42
why do comt inhibitors have no effect wihtout levodopa
only role is to prevent dopamine from being broken dow
43
comt inhibitor role
mild improvement prevode 1-2 hr on time longer for levodopa later used as an add on
44
entacapone is a
COMT inhibitor | not covered *
45
AE of COMT inhibitors
``` NV brown orange urine/sweat sweating diarrhea dyskinesia hypotension ```
46
ergot derived dopamine agonist and why its not used
bromocriptine | cardiac valve disease
47
examples of non ergot agonists
pramipexole ropinirole rotigotine
48
rold of dopamine agonists
alone in mild | adjunct to levodopa in patients with motor fluctuations
49
adv and dis of dopamine agonist
less motor complications than levodopa but more AE
50
rotigotine form
patch | not covered*
51
dopamine agonist AE
``` nausea cognitive impairment lower extremity edema impulsivity sleep attacks - caution driving increase levodopa induced dyskinesias ```
52
dose initiation and taper with dopamine agonist
initiate low dose and increase over 4-6 weeks to prevent AE | abrupt withdrawal causes NMS
53
benefits of levodopa
improves disability prolongs ability to work reduced mortality rate
54
primary concern with dopamine
dyskinesias
55
dopamine decarboixylase inhibitors MOA
allows ldopa to cross BBB prevents conversion in periphery also minimizes peripheral AE
56
examples of dopamine decarboxylase inhibitors
carbidopa | benserazide