Medical Management - Parkinson's Flashcards

1
Q

medical management

A

primary importance in PD

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2
Q

PD is

A

dynamic dz

not a static presentation

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3
Q

what must we do w/ medical management

A

must constantly re-evaluate and change dosing and timing of meds

as the sxs change and the dx progresses

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4
Q

what does the pt experience w/ meds

A

changing response to meds and dz’s progression

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5
Q

medical management strategies

A

block acetylcholine

replace dopamine

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6
Q

block acetylcholine

A

anticholinergics

effective for tremor only

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7
Q

block acetylcholine –> S/E

A

confusion

decrease memory

hallucinations

dry mouth

constipation

urinary retention

orthostasis

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8
Q

replace dopamine

A

sinemet

amantadine

dopamine agonists

enzyme inhibitors

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9
Q

sinemet –> replace dopamine

A

L-dopa carbidopa

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10
Q

what are some sxs caused by

A

decreased dopamine

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11
Q

dopamine replacement therapy aimed at

A

replacing the deficient NT

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12
Q

does dopamine cross the BBB

A

no

but L-Dopa (its precursor) does

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13
Q

what is L-dopa delivered w/

A

carbidopa = sinemet

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14
Q

what does sinemet inhibit

A

the release of L-dopa in the peripheral tissue

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15
Q

what does sinemet do

A

increases its release into the brain

decreases the amount of L-dopa needed (cutting down the side effects)

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16
Q

sinemet (levadopa/carbidopa)limits

A

limits bradykinesia, rigidity and tremor

17
Q

what doesnt levadopa/carbidopa treat

A

motor planning deficits

postural instability

non-motor sxs

18
Q

what happens overtime –> levadopa/carbidopa

A

therapeutic windown gets smaller and toxic window gets bigger

19
Q

S/E levadopa/carbidopa

A

dyskinesia

dystonia

on/off motor fluctuations

20
Q

50-60% of pts on L-dopa

A

will have motor complications w/in 5 yrs

21
Q

dopamine agonists

A

bromocriptine (parlodel)

pergolide (permax)

22
Q

what happens when dopamine agonists and added to sinemet

A

decrease clinical fluctuations

23
Q

what do dopamine agonists do

A

boosts output of remaining substantia nigra cells

24
Q

neuroprotective drugs

A

MAOs

25
Q

MAOs

A

monoamine oxidase inhibitors (MAOs)

26
Q

what do MAOs control

A

neuronal degradation can be controlled w/ anti-oxidase

which controls the synthesis and elimination of free radicals

27
Q

hypothesis –> MAOs

A

in PD –> there is increased production or decrease defense against free radicals in the SN

accelerating cell death

28
Q

type of MAO

A

selegiline

29
Q

selegiline

A

inhibits the enzyme that breaks down dopamine

30
Q

what does selegiline limit

A

free radical production during dopamine metabolism

31
Q

what must selegiline rescue

A

damaged but viable dopaminergic neurons

32
Q

what may early use of selegiline do

A

decrease the need for sinemet

early in the course of the dz

33
Q

what do anticholinergic drugs do

A

restore the balance of acetylcholine and dopamine

34
Q

anticholinergic drugs

A

parsidol

cogentin

akinetin

artane

35
Q

when are anticholinergic drugs used

A

less frequently than others

36
Q

when is the use of anticholinergic drugs more useful

A

early in the dz

when tremor is the most prominent problem

37
Q

amantadine has

A

dopaminergic and anticholinergic properties

38
Q

what dos amantadine do

A

stimulates the release of dopamine

from surviving presynaptic terminals in the striatum

39
Q

what does amantine affect

A

rigidity and bradykinesia

but not tremor