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Clinical 2.0 winter > Parkinsons > Flashcards

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
Q

amantadine MOA

A

NMDA antagonist

increases dopamine release

26
Q

MAO-B inhibtor MOA

A

reduce dopamine breakdown in the cns

27
Q

COMT inhibitor MOA

A

reduce levodopa breakdown in GI

prolongs half life and increase bioavailability

28
Q

dopamine agonist MOA

A

directly stimulates dopamine receptors

29
Q

levodopa MOA

A

converted to dopamine by dopa decarboxylase

30
Q

why cant dopamine just be directly gicen

A

cant cross the BBB

31
Q

when to use anticholinergics (benztropine)

A

generally people <60 due to the AE and modest efficacy

32
Q

anticholinergic AE

A 
constipation 
dry mouth 
eye infections
urinary retention
blurred vision 
cognitive impairment
headache 
increased HR 
overheating
33
Q

do you have to taper benztropine

A

yes over 1 week

34
Q

indication for amantadine

A

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
Q

AE of amantadine

A 
confusion, insomnia, nervous
anticholinergic
GI 
hypotension 
livedo reticularis 
*take in AM
36
Q

what is livedo reticularis

A

reversible diffuse purple red skin
in the extremeties
not an issue just cosmetic

37
Q

role of MAOBi

A

early for monotherapy

add on to levodopa to extend on time

38
Q

is tyramine intake a concern wtih selegiline and rasagiline

A

no

39
Q

AE of selegiline

A 
insomnia
hallucination 
confusion
orthostatic hypotension 
take in AM 
*bc converted to methamphetamine
40
Q

AE of rasagiline

A

GI - take with food

41
Q

which drugs prevent dopamine degradation in the peripheray

A

comt inhibitors

DDC inhibitors

42
Q

why do comt inhibitors have no effect wihtout levodopa

A

only role is to prevent dopamine from being broken dow

43
Q

comt inhibitor role

A

mild improvement
prevode 1-2 hr on time longer for levodopa
later used as an add on

44
Q

entacapone is a

A

COMT inhibitor

not covered *

45
Q

AE of COMT inhibitors

A 
NV 
brown orange urine/sweat 
sweating
diarrhea
dyskinesia 
hypotension
46
Q

ergot derived dopamine agonist and why its not used

A

bromocriptine

cardiac valve disease

47
Q

examples of non ergot agonists

A

pramipexole
ropinirole
rotigotine

48
Q

rold of dopamine agonists

A

alone in mild

adjunct to levodopa in patients with motor fluctuations

49
Q

adv and dis of dopamine agonist

A

less motor complications than levodopa but more AE

50
Q

rotigotine form

A

patch

not covered*

51
Q

dopamine agonist AE

A 
nausea
cognitive impairment
lower extremity edema 
impulsivity 
sleep attacks - caution driving 
increase levodopa induced dyskinesias
52
Q

dose initiation and taper with dopamine agonist

A

initiate low dose and increase over 4-6 weeks to prevent AE

abrupt withdrawal causes NMS

53
Q

benefits of levodopa

A

improves disability
prolongs ability to work
reduced mortality rate

54
Q

primary concern with dopamine

A

dyskinesias

55
Q

dopamine decarboixylase inhibitors MOA

A

allows ldopa to cross BBB
prevents conversion in periphery
also minimizes peripheral AE

56
Q

examples of dopamine decarboxylase inhibitors

A

carbidopa

benserazide

Clinical 2.0 winter (28 decks)

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