Therapeutics - Parkinsons Flashcards by amanda kastel

define parkinsons and name some symptoms

progressive neurologic disorder

tremors, rigidity, postural instability, bradykinesia (slow movement)

How well did you know this?

Not at all

Perfectly

what are dopamine levels like in parkinsons patients

where? what about acetylcholine levels?

low

in substantia nigra

high acetylcholine (so excess cholinergic activity)

How well did you know this?

Not at all

Perfectly

true or false

most parkinsons is idiopathic

true - no known cause

How well did you know this?

Not at all

Perfectly

some things that can induce parkinsons

heavy metals
pesticides
MPTP
CO
drugs (1st gen antipsychotics, metoclopramide, phenothiazides)

How well did you know this?

Not at all

Perfectly

true or false

parkinsons can occur after encephalitis

true

How well did you know this?

Not at all

Perfectly

early and late MOTOR parkinsons symptoms

early - cogwheel rigidity, soft voice, shuffling gair, bradykinesia, pill-rolling tremors

late - freezing, postural imbalance, hard to swallow and talk - get some cognitive deficits

How well did you know this?

Not at all

Perfectly

name some autonomic symptoms of parkinsons

orthostatic hypotension
constipation
hard to pee
extreme sweating
seborrhea

How well did you know this?

Not at all

Perfectly

effect of parkinsons on blood pressure

can cause orthostatic hypotension - even when just sitting down

How well did you know this?

Not at all

Perfectly

hyposmia

nonmotor parkinsons symptom - loss of smell

How well did you know this?

Not at all

Perfectly

2 symptoms of parkinsons that may actually occur before the patient is even diagnosed

hyposmia (hard to smell)
REM sleep disorder

How well did you know this?

Not at all

Perfectly

when a patient is “on” in parkinsons, is the medication working or not working

working - symptoms are controlled

How well did you know this?

Not at all

Perfectly

short term and long term goals for parkinsons treatment

short term - control symptoms, increase functionality

long term - limit complications, maintain effective treatment

How well did you know this?

Not at all

Perfectly

trueor false

there are several disease-modifying treatments for parkinsons

FALSE- none

only symptomatic relief

How well did you know this?

Not at all

Perfectly

a patient has some parkinsons symptoms with early PD (less than 5 years)… but not causing disability

what is the approach??

ie - a tremor in nondominant hand

wait and see approach – hold off for now

bc once we start levodopa, limited amount of time that the patient will respond

but if pt has significant issues — start LEVODOPA

How well did you know this?

Not at all

Perfectly

in general, initial treatment with ____ provides more benefit to dopamine agonists

levodopa

How well did you know this?

Not at all

Perfectly

what is considered “early” parkinsons

less than 5 years

How well did you know this?

Not at all

Perfectly

a patient is initially started on a MAO-B inhibitor for parkinsons

what will they need in the future

will need additional treatment within 2-3 years — diff from patients who are started on levodopa or dopamine agonist

How well did you know this?

Not at all

Perfectly

3 potential initial options for early PD

levodopa
dopamine agonist
MAO B inhibitor

How well did you know this?

Not at all

Perfectly

true or false

dopamine agonists are more likely to cause dyskinesias than levodopa

FALSE - levodopa is more likely to cause dyskinesia

How well did you know this?

Not at all

Perfectly

for early PD:

levodopa vs levodopa + entacapone vs IR levodopa

which is most effective

all equally effective

How well did you know this?

Not at all

Perfectly

which has a higher risk of impulse control disorders — dopamine agonists or levodopa?

dopamine agonists have higher risk

How well did you know this?

Not at all

Perfectly

if a patient is less than 60 years old with PD, explain the thought process behind what treatment to start

may start with a dopamine agonist over levodopa

younger people can tolerate the CNS SE of dopamine agonists more….. and also the patient is gonna be living with PD for a long time - want to try to wait to use levodopa

How well did you know this?

Not at all

Perfectly

patient has a history of cognitive impairment and PD

what should we start with

start with levodopa

How well did you know this?

Not at all

Perfectly

patient has a history of MOOD DISORDERS and PD

what should we start with

levodopa

How well did you know this?

Not at all

Perfectly

if patient's PD disease is SEVERE, what should we start with

levodopa

initial therapy if the patient has TREMOR ONLY (no bradykinesia)

anticholinergics -- but only if the patient is younger!!!! dont like the anticholinergic side effects in older people

when may MAO-B inhibitors be used as initial therapy

really only for milder cases

which med is PRIMARILY for dyskinesia as an add on therapy

amantadine

true or false for PD, nonpharm treatment is just as important as pharmacologic

true exercise, PT, OT, speech therapy

3 potential add on therapies for PD

istradefylline amantadine (dyskinesia) COMT inhibitors

advanced therapy PD

surgical

2 MAO-B inhibitors that may be considered at diagnosis of PD if it is mild

rasagiline selegiline

true or false a dopamine agonist should only be started if the patient is under 60 what if over 60?

true if over 60 - start carbidopa/levodopa

after initial PD therapy, doses should be adjusted as needed and tolerated as the patient's symptoms get worse, what should be done

add another agent, then add COMT inhibitor

2 general concerns of PD/PD drugs

melanoma - should be checked by derm impulse control disorders (anthing that increases dopamine in the brain - includes BOTH dopamine agonists and levodopa) - urges to gamble, sexual urges, etc

MOA of MAO-B inhibitors

binds MAO-B enzyme - the enzyme that metabolizes (oxidizes) dopamine blocks breakdown of dopamine in the brain

name 3 MAO-B inhibitors

selegiline rasagiliine safinamide

4 drugs that should be used with caution with MAO-B inhibitors

tramadol meperidine DM SSRIS

which MAO-B inhibitor was originally thought to be neuroprotective but it was debunked

selegiline it was just symptomatic relief

only indication for ODT selegiline

in combo with levodopa later in the disease

important note when dosing all the MAO-B inhibitors

-DO NOT GO ABOVE THE MAX DOSE. will not be selective for B anymore. can go into hypertensive crisis

selegiline ADRs

hallucinations, confusion nausea INSOMNIA!!!!! - from the amphetamine-like metabolite

how can insomnia from selegiline be avoided

if PO version - dont give the 2nd dose after 2pm ODT formulation has less CNS stimulation

true or false transdermal selegiline can be used for parkinsons

FALSE - the transdermal form is only for depression

PO max dose selegiline ODT max dose selegiline why is it important not to go above these?

PO - 10mg ODT - 2.5mg loses specificity for MAO-B inhibition - can go into hypertensive crisis

use for rasagiline

monotherapy in early PD carbidopa/levodopa adjunct in moderate-advanced PD

max doses of rasagiline: -monotherapy -adjunct to levodopa

monotherapy - 1mg QD adjunt - 0.5mg but may increase to 1mg

advantages of rasagiline over selegiline

no amphetamine-like side effects (no insomnia) tyramine reaction unlikely (less CV side effects) overall - less CV and less CNS side effects

use of safinamide

as an adjunct to carbidopa-levidopa in patients with "off" episodes NOT USED AS MONOTHERAPY

true or false safinamide can be effective as monotherapy for PD

FALSE - not effective as monotherapy. only as adjunct to carb/lev in patients experiencing off episodes

what foods should be avoided with safinamide

very high tyramine concentration

dose of safinamide

50mg QD for 2 weeks increase to 100mg daily after that (100mg is MAX)

in what patients must safinamide be avoided

patients with severe hepatic impairment

safinamide ADRs

CNS depression dyskinesia impulse control disorder serotonin syndrome HTN

3 anticholinergics that may potentially be used for PD tremors in YOUNGER PATIENTS

diphenhydramine benztropine trihexyphenidyl

effect of anticholinergics on the heart

tachycardia

effect of anticholinergics on the eyes

dry eyes

any dose adjustments for amantadine?

in renal impairment (CrCl less than 60mL/min)

place in PD therapy for amantadine

in early disease or late, in combo with other agents monotherapy effect is short lived -- only 6 months

ADRs amantadine

CNS changes and similar anticholinergic effects levido reticularis (skin condition)

amantadine administration considerations

dont give after 2pm to avoid insomnia!!! also, older patients may not tolerate CNS side effects - not preferred

2 names of amantadine ER state what they're approved for

gocovri (capsule) - for dyskinesias and off episodes osmolex ER (tablet) - for PD and drug-induced EPS

differentiate between the dosing time of Gocovri vs Osmolex

QHS - gocovri qam - osmolex

dose adjustments for gocovri and osmolex

both - dose adjustment in CrCl less than 60, DO NOT USE in CrCl less than 15

true or false gocovri and osmolex are NOT interchangeable

true

____ is considered the mainstay of therapy for PD

levodopa

why is carbidopa given with levodopa

if we just give levodopa, it will get converted to dopamine in the periphery which we DONT WANT carbidopa prevents the peripheral conversion (breakdown) of levodopa into dopamine

___mg of carbidopa/day is needed to block the peripheral conversion of levodopa into dopamine

50-100mg

true or false carbidopa does not cross the BBB

true - this is good lveodopa does tho - which is good

2 formulations of carbidopa/levodopa for late stage PD to treat the motor fluctuations

enteral suspension for jejunal infusion SQ continuous infusion

Therapeutics - Parkinsons Flashcards

(71 cards)