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444-Oncology and Neurology > Parkinson's disease > Flashcards

Parkinson's disease Flashcards

1
Q

describe PD

A

a chronic, progressive neuro disorder characterized by tremor, bradykinesia, rigidity, and postural instability

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2
Q

what are some genetic factors that could lead to PD

A

parkin gene
alpha synuclein

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3
Q

what are some toxin exposures that could lead to PD

A

exogenous: well waste, farming, heavy metals
endogenous: free radicals, infection, iron

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4
Q

what factors increase risk of PD

A

age
rural residence, farming, pesticides
frequent consumption of dairy

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5
Q

what are protective factors of PD

A

cigarette smoking
coffee, tea, caffeine
possibly: diet, hormones, vascular, meds

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6
Q

drugs that can cause secondary parkinsonism include

A

dopamine blockers: AP, metoclopramide
dopamine depletors: methyldopa, reserpine

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7
Q

medical causes of secondary parkinsonism

A

normal pressure hydrocephalus (NPH)
infarction
infection
trauma
any lesions/ neoplasms to substantia nigra

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8
Q

which of the following is false about parkinson’s
1. affects race equally if in same community
2. hallmark features include resting tremor, rigidity, bradycardia, postural instability
3. smoking decreases risk
4. frequent dairy consumption increases risk

A

2- bradykinesia

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9
Q

what are the hallmark features of parkinson’s

A

resting tremor
bradykinesia
rigidity
postural instability

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10
Q

should PK pts take vit e or CoQ10 for neuroprotection

A

no

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11
Q

T or F: dopaminergic tx are neuroprotective

A

F

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12
Q

what is often the first sign of PK dx

A

olfactoy changes- may lose some sense of smell

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13
Q

is the LD challenge recommended for PK screening

A

no because it can change movement in normal people

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14
Q

PK dx must have

A

bradykinesia + at least 1 of tremor or rigidity + 2 supportive criteria (olfactory loss, dramatic response to dopaminergic tx)

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15
Q

what is the exclusion criteria + red flags for PK dx (give 2 examples)

A

exclusion: restricted to lower limbs, tx with dopamine blocker at onset

red flags: rapid progression, absence of nonmotor features at 5yrs

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16
Q

most patients with PK will die from

A

infections + complications from immobility

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17
Q

the prognosis for PK pt dx at midlife is

A

15-20yrs

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18
Q

what is stage 1 of PK

A

unilateral involvement only

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19
Q

what is stage 5 of PK

A

wheelchir bound/ bedridden unless assisted

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20
Q

list 3 outcomes of importance in PK tx

A

imaging techniques
time to change in management (time to start LD, amount of increase/ decrease in (LD dose)
time to clinical event (first dopaminergic complications, time to motor fluctuations)
caregiver burden
changes in clinical scales
HRQL (PD specific instruments)
economics

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21
Q

what is the difference between ADL and IADL

A

ADL = basic functions you do every day like eating, dressing, washing
IADL = not daily, but still essential like banking, laundry, cleaning

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22
Q

what are some nonpharm PD tx

A

rehab (PT, OT, SLP)
tech (computer based, VR, AI)

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23
Q

3 guidelines for PD rehab

A

refer to dietician for advise
advise to take vit D supplement
advise not to take OTC dietary supplements without first consulting HCP

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24
Q

give the 3 guidelines for early pharm tx in PD

A

LD may be started at lowest dose possible for sx in early PD
DA may be titrated to effective dose in early PD
MAO-Bi may be used as sx tx for early PD

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25
Q

adjunct may be added to LD if pt develops _____ or _______ despite optimal LD tx

A

dyskinesias or motor fluctuations

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26
Q

what is the preferred initial PD tx

A

LD

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27
Q

DA may be used for early PD in

A

<60yrs + high risk of dyskinesias

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28
Q

when to avoid DA in PD

A

> 70yrs, Hx ICD, preexisting cog impairment, excessive daytime sleepiness, hallucinations

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29
Q

MO-B inhibitors may be prescribed as initial dopaminergic tx for ___________ in pts with early PD

A

mild motor sx

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30
Q

which has more motor benefits? LD or MOBi

A

LD

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31
Q

which 2 MAOi are irreversible

A

selegiline, rasagiline

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32
Q

selegiline and rasagiline may be used as

A

initial monotx or as an adjunct to LD

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33
Q

safinamide may be used as

A

adjunct to LD

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34
Q

which MAOi’s active metabolites are amphetamines

A

selegiline

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35
Q

which MAObi should be avoided in older adults

A

selegiline

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36
Q

DA indications

A

used in early disease to minimize use of LD
used in late disease as adjunct to LD

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37
Q

characteristics of older DA agents include (4)

A

less receptor sensitivity
low cost
high ADR
adjunct

38
Q

characteristics of newer DA agents include (4)

A

receptor specificity (D2-4)
high cose
lwoer ADR
adjunct or monotx

39
Q

how to titrate DA dose

A

titrate slowly q1-2wks to effective dose

40
Q

how should you decrease LD dose once a DA is added

A

decrease up to 25%

41
Q

list 3 DA SEs

A

N/V
orthostasis
psychiatric conditions (2x LD) + hallucintions
syncope, excessive daytime sleepiness, insomnia, dyskinesias, addiction disorders

42
Q

DA benefits are usually clinically significant for

A

1yr

43
Q

which is more expensive, DA or LD

A

DA

44
Q

which form of LD is used for PD

A

L form

45
Q

starting, max, and usual ceiling dose of LD

A

start = 100/25 TID
max = 1500mg LD/d
usual ceiling dose = 800mg LD/d

46
Q

what is the min dose of carbidopa to be used with LD? why is it added?

A

75mg/d
to prevent LD breakdown in periphery = allows same effect at lower doses = less vomiting potential

47
Q

list the 4 LD products

A

sinemet
prolopa
stalevo
duodopa

48
Q

sinemet IR and CR onset

A

IR = 30min
CR = 2h

49
Q

pros of IR sinemet

A

rapid, immediate effect
ca nbe crushed, chewed
lower cost

50
Q

CR sinemet pros

A

controls late stage complications
lower peaks
can be split

51
Q

cons of IR sinemet

A

multiple doses/ day
dependence on burst
peak related dyskinesias
more fluctuations in sx

52
Q

cons of CR sinemet

A

expensive
higher dose required
not chewed/ crushed
does not provide burst

53
Q

clinicians should initially prescribe ____ levodopa rather than ___ levodopa or levodopa/ carbidopa/ entacapone in pts with early PD

A

IR rather than CR

54
Q

dopamine metabolism produces

A

free radicles

55
Q

characteristics of LD tx in early PD

A

smooth, extended duration of target clinical response
low incidence of dyskinesias

56
Q

characteristics of LD in late PD

A

short duration of target clinical response
on time associated with dyskinesias

57
Q

which COMTi is emergency release

A

tolcapone

58
Q

what is entacapone

A

peripheral enzyme inhibitor (COMTi)
dosed with each LD dose

59
Q

COMTi can reduce LD by ____ on average

A

25%

60
Q

COMTi suggested early use wit hLD to ___________

A

decrease oxidative stress by lowering LD dose

61
Q

SE of COMTi

A

excessive LD

62
Q

COMTi intx

A

AD
drugs metabolized by COMT- dobutamine, epinephrine, methyldopa, isoproterenol

63
Q

T or F; LD has disease modifying effects

A

F

64
Q

T or F: there is no reason to delay LD tx

A

T

65
Q

rank the following based on how often they are stopped (lowest to highest): LD, MAOi, DA

A

LD < DA <MAOi

66
Q

LD vs DA
___ is better tolerated
____ has higher rates of SEs
_____ more likely to be stopped
____ has better sx control
____ have fewer motor complications

A

LD, DA, DA, LD, DA

67
Q

which has fewer LT complications, but is less efficacious
1. LD
2. DA

A

2

68
Q

which is better tolerated, better efficacy, but has higher motor complications
1. LD
2. DA

A

1

69
Q

dopaminergic EDS counselling

A

is present in 50% of drivers = warm pts, may have to stop driving for at least 1mth

70
Q

waht is the EDS

A

epworth sleep scale

71
Q

impulse control disorders in PD are due to

A

dopamine increases from meds in the striatum

72
Q

6 RF for ICD

A

young onset of PD, male, personality, unmarried Hx (fam, SU, psych), use of a DA

73
Q

how to manage ICD

A

less aggressive DA use, slower titration
DBS may be considered

74
Q

anti- ACh in PD
1. is a first line tx
2. is now rarely used
3. is useful in tremor or dystonia in older pts
4. may be used early in disease as adjuncts

A

2

75
Q

anticholinergics in PD is useful in

A

tremor or dystonia in younger pts

76
Q

amantadine was traditionally used in

A

influenza

77
Q

amantadine use in

A

young pts, early tx

78
Q

amantadine itnx

A

additive eff with anticholinergics

79
Q

which NHPs contain Ldopa

A

ashwaganda

80
Q

NHPs in PD
1. avoid all NHPs
2. overall weak evidence
3. must add on dietary restrictions
4. may use in place of DA tx

A

2- can still try but ask first

81
Q

what is wearing off phenomenon

A

LD effect not lasting

82
Q

what is on off phenomenon

A

changes in absorption, intx

83
Q

dyskinesias on PD tx is due to

A

sensitization of receptors

84
Q

dystonias in PD tx is due to

A

acute lack of dopamine

85
Q

wearing off phenomenon onset

A

delayed (years)

86
Q

on off phenomenon onset

A

delayed

87
Q

dyskinesias onset from PD tx

A

early or delayed

88
Q

dystonias onset from PD tx

A

early or delayed

89
Q

what is a surgical intervention to PD

A

deep brain stimulation
thalamotomy
medial pallidotomy
fecal transplantation

90
Q

challenges to DBS

A

not complete resolution of PD sx
complications like depression, behaviours, cog impirmenet

444-Oncology and Neurology (22 decks)

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