Parkinson's disease Flashcards by Linda Chen

describe PD

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

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what are some genetic factors that could lead to PD

parkin gene
alpha synuclein

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what are some toxin exposures that could lead to PD

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

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what factors increase risk of PD

age
rural residence, farming, pesticides
frequent consumption of dairy

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what are protective factors of PD

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

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drugs that can cause secondary parkinsonism include

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

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medical causes of secondary parkinsonism

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

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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

2- bradykinesia

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what are the hallmark features of parkinson’s

resting tremor
bradykinesia
rigidity
postural instability

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should PK pts take vit e or CoQ10 for neuroprotection

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T or F: dopaminergic tx are neuroprotective

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what is often the first sign of PK dx

olfactoy changes- may lose some sense of smell

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is the LD challenge recommended for PK screening

no because it can change movement in normal people

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PK dx must have

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

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

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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most patients with PK will die from

infections + complications from immobility

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the prognosis for PK pt dx at midlife is

15-20yrs

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what is stage 1 of PK

unilateral involvement only

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what is stage 5 of PK

wheelchir bound/ bedridden unless assisted

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list 3 outcomes of importance in PK tx

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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what is the difference between ADL and IADL

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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what are some nonpharm PD tx

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

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3 guidelines for PD rehab

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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give the 3 guidelines for early pharm tx in PD

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

dyskinesias or motor fluctuations

what is the preferred initial PD tx

DA may be used for early PD in

<60yrs + high risk of dyskinesias

when to avoid DA in PD

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

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

mild motor sx

which has more motor benefits? LD or MOBi

which 2 MAOi are irreversible

selegiline, rasagiline

selegiline and rasagiline may be used as

initial monotx or as an adjunct to LD

safinamide may be used as

adjunct to LD

which MAOi's active metabolites are amphetamines

selegiline

which MAObi should be avoided in older adults

selegiline

DA indications

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

characteristics of older DA agents include (4)

less receptor sensitivity low cost high ADR adjunct

characteristics of newer DA agents include (4)

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

how to titrate DA dose

titrate slowly q1-2wks to effective dose

how should you decrease LD dose once a DA is added

decrease up to 25%

list 3 DA SEs

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

DA benefits are usually clinically significant for

1yr

which is more expensive, DA or LD

which form of LD is used for PD

L form

starting, max, and usual ceiling dose of LD

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

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

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

list the 4 LD products

sinemet prolopa stalevo duodopa

sinemet IR and CR onset

IR = 30min CR = 2h

pros of IR sinemet

rapid, immediate effect ca nbe crushed, chewed lower cost

CR sinemet pros

controls late stage complications lower peaks can be split

cons of IR sinemet

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

cons of CR sinemet

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

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

IR rather than CR

dopamine metabolism produces

free radicles

characteristics of LD tx in early PD

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

characteristics of LD in late PD

short duration of target clinical response on time associated with dyskinesias

which COMTi is emergency release

tolcapone

what is entacapone

peripheral enzyme inhibitor (COMTi) dosed with each LD dose

COMTi can reduce LD by ____ on average

25%

COMTi suggested early use wit hLD to ___________

decrease oxidative stress by lowering LD dose

SE of COMTi

excessive LD

COMTi intx

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

T or F; LD has disease modifying effects

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

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

LD < DA

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

LD, DA, DA, LD, DA

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

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

dopaminergic EDS counselling

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

waht is the EDS

epworth sleep scale

impulse control disorders in PD are due to

dopamine increases from meds in the striatum

6 RF for ICD

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

how to manage ICD

less aggressive DA use, slower titration DBS may be considered

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

anticholinergics in PD is useful in

tremor or dystonia in younger pts

amantadine was traditionally used in

influenza

amantadine use in

young pts, early tx

amantadine itnx

additive eff with anticholinergics

which NHPs contain Ldopa

ashwaganda

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

2- can still try but ask first

what is wearing off phenomenon

LD effect not lasting

what is on off phenomenon

changes in absorption, intx

dyskinesias on PD tx is due to

sensitization of receptors

dystonias in PD tx is due to

acute lack of dopamine

wearing off phenomenon onset

delayed (years)

on off phenomenon onset

delayed

dyskinesias onset from PD tx

early or delayed

dystonias onset from PD tx

early or delayed

what is a surgical intervention to PD

deep brain stimulation thalamotomy medial pallidotomy fecal transplantation

challenges to DBS

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