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Parkinsons Disease Flashcards

1
Q

What are 3 words to describe Parkinsons?

A

chronic
progressive
neurodegenerative

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2
Q

What is the most common movement disorder?

A

Parkinsons

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3
Q

Describe the pathophysiology of Parkinsons.

A

caused by progressive death of dopamine-producing neurons in the substantia nigra (part of the basal ganglia)
-death of DA neurons = messages telling the body how and when to move are delivered slowly or incompletely
-individual is unable to initiate and control movements in a normal way

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4
Q

What is the role of dopamine in movement?

A

important for smooth, coordinated, controlled movements

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5
Q

What is the etiology of Parkinsons?

A

unknown
some decline of dopaminergic neurons occurs with aging
-Parkinsons is an acceleration of that process

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5
Q

What are the two components of the substantia nigra?

A

pars compacta: DA producing
pars reticulata: GABA neurons

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6
Q

What are the risk factors for Parkinsons?

A

family history
pesticide exposure
repeated head injuries

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7
Q

What are the protective factors against Parkinsons?

A

smoking
high coffee consumption
intensive exercise

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8
Q

What are the hallmark movement symptoms of Parkinsons?

A

TRAP
-tremor
-rigidity
-akinesia/bradykinesia
-postural instability
3 S’s: slow, stiff, shaky

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9
Q

Describe the diagnosis of Parkinsons.

A

clinical diagnosis
Movement Disorder Society Clinical Diagnostic Criteria:
-must be present: bradykinesia
-at least 1 of: rest tremor or rigidity
-supportive: response to DA tx, levodopa-induced dyskinesias, olfactory loss

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10
Q

What is the takeaway regarding the presentation of Parkinsons?

A

a heterogenous disorder with substantial variations in clinical presentation

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11
Q

Describe the distinguishing features of Parkinsons.

A

tremor-predominant subtype:
-often younger patients
-typically have a slower, more benign course of progression
akinetic/rigid subtype:
-often have a more rapid rate of progression of motor sx
-particularly in older patients

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12
Q

What is the key feature of the other Parkinsonisms?

A

they do not respond to levodopa

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13
Q

What are some medications that can cause Parkinsonisms?

A

typical neuroleptics
atypical neuroleptics
-safer alts: clozapine, quetiapine
antinauseants/prokinetics
-safer alt: domperidone
miscellaneous: lithium, valproic acid

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14
Q

What are some “other” clinical features of Parkinsons?

A

often precede motor symptoms:
-hyposmia
-constipation
-depression
-fatigue
-REM Sleep Behavior Disorder
early in disease course:
-micrographia
-hypophonia
-dry eyes
-flat affect
later symptoms:
-sexual dysfunction
-sialorrhea
-autonomic dysfunction
-psychiatric disturbances (delusions/hallucinations)
-cognitive impairment and dementia

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15
Q

What are some principles of treatment for Parkinsons?

A

no PD treatment modifies disease progression
symptomatic treatment only
progressive - therefore ongoing medication changes and adjustments will be needed

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16
Q

What are the goals of therapy for Parkinsons?

A

reduce signs and symptoms of Parkinsons
minimize complications of drug therapy
maintain independence
improve/maintain QoL

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17
Q

What are the non-pharm treatments for Parkinsons?

A

physical therapy
occupational therapy
speech therapy
dental/vision/hearing care
psychological support
surgery

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18
Q

What are the classes of medications for Parkinsons?

A

levodopa
dopamine agonists
MAO-B inhibitors
amantadine
COMT inhibitors
anticholinergics

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19
Q

What does pharmacotherapy of Parkinsons focus on?

A

increasing dopamine levels (directly or indirectly)

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20
Q

What is the effective cornerstone of treatment for Parkinsons?

A

levodopa

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21
Q

What is levodopa always given with?

A

decarboxylase inhibitor
-carbidopa or benserazide

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22
Q

What is the role of carbidopa or benserazide when used with levodopa?

A

prevents conversion of levodopa to DA outside of the brain
-enhances efficacy
-reduces AE
neither carbidopa nor benserazide can cross the BBB

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23
Q

What is the MOA of levodopa?

A

crosses BBB –> converted to DA via decarboxylase

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24
Describe the effectiveness of levodopa.
initially, universally effective for: -bradykinesia -rigidity -respond in days, max 2 weeks variable effect: tremor less likely to help with: -poor balance -non motor sx
25
What can decrease the bioavailability of levocarb?
protein iron antacids
26
How should levocarb be initiated?
titrate slowly to prevent nausea/dizziness
27
How should levocarb be discontinued?
need to taper off slowly due to risk of NMS
28
Why is controlled release levocarb rarely used?
delayed and unpredictable onset -rarely used apart from overnight
29
What are the adverse effects of levocarb?
nausea, stomach upset dizziness/orthostasis fatigue vivid dreams confusion/hallucinations (later stages)
30
What can occur with levodopa therapy after ~5 years of treatment?
wearing off (med not lasting as long as it used to) on-off phenomena (fine one min, not fine the next min) freezing dyskinesias (abnormal, involuntary movements) -due to increases sens of brain to levodopa as PD progresses -commonly limbs and trunk -common shortly after a dose
31
What are some of the new formulations of levodopa?
Duodopa (intestinal gel) Vyalev (SQ infusion) inhaled capsules *designed to address limitations of oral admin*
32
How is Duodopa delivered?
enteral (PEG-J tube) -delivers constant low doses
33
What is the benefit of Duodopa?
reduces off time by 2h/day without increasing dyskinesias
34
How is Vyalev delivered?
continuous subcut infusion -delivers low and constant doses
35
What are the adverse effects of Vyalev?
injection site rxns dyskinesias psychosis
36
What is the use of the inhaled levodopa capsules?
prn for unexpected off-periods or delayed onset -onset: 10 minutes -duration: 1 hour
37
What are examples of dopamine agonists?
ergot derivatives: bromocriptine, cabergoline -basically never used due to CV + pulmonary toxicity non-ergot derivates: pramipexole, ropinirole, rotigotine
38
What is the MOA of dopamine agonists?
mimic the effects of DA by binding to post-synaptic DA receptors
39
What is the place in therapy for dopamine agonists?
may be used as initial therapy in young pts (<60) -"save" levodopa for later not preferred in older adults due to poor tolerability -may be used as add on once motor complications develop if refractory/intolerant to other options used for restless legs syndrome (hs)
40
How do dopamine agonists compare to levodopa in terms of efficacy and tolerability?
less effective for motor symptoms than levodopa more side effects less risk of motor complications seen with levodopa
41
What are the adverse effects of dopamine agonists?
more common with levodopa: -nausea/GI upset -orthostatic hypotension -confusion -fatigue -hallucinations drowsiness, sudden sleep attacks leg swelling impulse control disorder - up to 15% of pts -pathological gambling -hypersexual behavior -compulsive shopping -DA dysregulation syndrome
42
How should dopamine agonists be discontinued?
taper slowly --> NMS risk
43
What is apomorphine?
very potent DA agonist used for rescue therapy (freezing) -comes as injectable or SL
44
What is the role of MAO?
enzyme that breaks down DA, other NTs, and amines -MAO A: breaks down NE and 5HT preferentially -MAO B: breaks down DA and other amines preferentially
45
What are examples of MAO-B inhibitors?
rasagiline selegiline
46
When do MAO-B inhibitors lose their selectivity?
at 2-5x the recommended therapeutic dose -no need to restrict dietary tyramine at doses used for PD
47
What is the place in therapy for MAO-B inhibitors?
can be used as monotherapy if symptoms are mild can be used later in disease course for motor complications with levodopa therapy (rasagiline) -wearing off, freezing
48
How do MAO-B inhibitors compare to levodopa in terms of efficacy and safety?
less effective than levodopa fewer adverse effects and less frequent dosing
49
What are the side effects of MAO-B inhibitors?
generally well tolerated -nausea, headache, insomnia
50
What is the risk of combining an MAO-B inhibitor with an SSRI/SNRI?
unlikely to cause serotonin syndrome at recommended doses -lowest effective dose should be used *avoid DM in patients taking MAO-B inhibitors*
51
What is an example of a COMT inhibitor?
entacapone
52
What is the MOA of entacapone?
blocks COMT in periphery = more levodopa gets to brain
53
How should entacapone be given?
MUST be given with levodopa -has no effect on its own -used for prolonging the action of levodopa once motor complications develop (wearing off, freezing)
54
What should be done to the dose of levodopa when entacapone is started?
decrease levodopa dose by 30% -to minimize dyskinesia
55
What are the adverse effects of entacapone?
nausea, diarrhea may turn urine and sweat an orangey-brown colour
56
What is the MOA of amantadine?
unclear in PD
57
What is the role of amantadine?
limited to treating bothersome dyskinesia later in disease course
58
What are the adverse effects of amantadine?
nausea, confusion, hallucinations, peripheral edema livedo reticularis *not as well tolerated in older adults due to cognitive effects*
59
What are examples of anticholinergics?
trihexyphenidyl benztropine procyclidine
60
What is the MOA of anticholinergics in Parkinsons?
decrease the amount of ACh in the brain to restore the DA/ACh balance in the striatum
61
What is the role of anticholinergics in Parkinsons?
effective mainly for tremor -not effective for other motor symptoms *not used often; poorly tolerated in older adults*
62
Do we always have to start pharmacotherapy at the initial diagnosis of Parkinsons?
no need to start if there is no functional impairment
63
What are some steps we can take with levodopa itself when levodopa is failing?
take on an empty stomach as consistently as possible add levocarb CR @ hs wearing off: increase dosing frequency dyskinesias: smaller, more frequent doses
64
What are some agents we can add on when levodopa is failing?
dyskinesias: -amantadine wearing-off: -COMT inhibitor, MAO-B inhibitor = decrease off-time by 1-1.5h/day -dopamine agonist = decrease off-time by 2h/day
65
What is the surgical treatment for Parkinsons?
deep brain stimulation
66
What is an under treated aspect of Parkinsons?
non-motor symptoms -can have a substantial impact on QoL
67
What are examples of non-motor symptoms in Parkinsons?
constipation depression autonomic dysfunction (ED, orthostasis, incontinence) hallucinations and delusions drooling sleep disorders
68
Describe constipation management in Parkinsons.
usual lifestyle: increase fiber, fluid, and exercise avoid constipating meds/OTCs domperidone can be considered to increase GI motility PEG considered 1st line for preventing and managing -may need to add stimulant on top if insufficient
69
Describe depression management in Parkinsons.
little evidence to guide depression management in PD generally managed similarly to patients without PD -bupropion not DOC due to additive dopaminergic effect -sertraline/citalopram/venlafaxine/duloxetine safe + effective re-evaluate need, deprescribe if possible -increased fall and orthostasis risk
70
What causes autonomic dysfunction in PD?
PD and PD drugs
71
What should be some of the first steps in evaluating orthostatic hypotension in Parkinsons?
review antihypertensives ensure adequate hydration review other meds stand slowly compression stockings increase salt intake
72
When do we consider drugs for orthostatic hypotension in Parkinsons? What are the options?
severe and refractory domperidone: -least evidence of efficacy but no supine HTN midodrine: -alpha 1 agonist -limited by supine HTN (take last dose >4h before bed) fludricortisone: -mineralocorticoid -limited by supine HTN
73
Describe urinary incontinence management in Parkinsons.
non-pharm preferred -regular toileting -assistive devices -decrease caffeine intake -decrease fluid intake in evening pharmacotherapy if refractory
74
Describe erectile dysfunction management in Parkinsons.
PDE5-inhibitors used 1st line apomorphine injections may be helpful
75
Describe sialorrhea management in Parkinsons.
chewing gum or soft candy can help trigger swallowing reflex ipratropium spray to mouth atropine eye drops given SL (usually tried first) refractory or atropine AEs --> Botox
76
Describe insomnia management in Parkinsons.
usual sleep hygiene measures adequate control of PD motor symptoms at night melatonin has some evidence of benefit doxepin or trazodone if refractory
77
What is REM Sleep Behavior Disorder?
loss of muscle atony during REM sleep individuals act out dreams - violent and can cause injury often predates diagnosis of PD
78
Describe management of REM Sleep Disorder.
avoid hs dosing of ADs (may worsen sx) if tx necessary: -melatonin (limited evidence) -clonazepam (best evidence)
79
Describe management of restless legs syndrome in Parkinsons.
screen for iron deficiency optimize dopaminergic therapy - consider hs DA agonist 2nd line: gabapentin, pregabalin
80
Do all hallucinations require treatment in Parkinsons patients?
not all do -if insight is preserved, infrequent, and not bothersome = pharmacotherapy not required
81
Describe management of hallucinations in Parkinsons.
slowly discontinue medications that may be contributing -amantadine, DA agonists, anticholinergics, sedatives avoid 1st gen APs, olanzapine, risperidone, aripiprazole clozapine: efficacy but not used due to agranulocytosis quetiapine: less evidence but does not worsen PD sx -start low and go slow

PHAR358 (20 decks)

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