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PR3153: Central Nervous System > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

What are the different types of PD

A
  • Idiopathic PD (most often)
  • Parkinson’s plus (less data on what agents work eg. levodopa):
    Multiple system atrophy (aka Shy-Drager syndrome)
    Progressive supranuclear palsy
    Corticobasal degeneration
    Lewy body disease
  • Parkinsonism (manifestation of the syndrome? Different MOA from idiopathic PD)
    Drug-induced, toxin-induced
    Vascular
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2
Q

What are the 4 characteristic features of PD

A

Tremor - resting tremor (not doing anything)
Rigidity - muscular rigidity (cogwheel hypertonic? Increase contraction)
Akinesia - slowness & poverty of movement
Postural instability (gait)

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3
Q

How to diagnose PD?

A
  • 2 of the 3 cardinal signs must be present
  • Tremor: resting tremor (disappears with movement), increases with stress
  • Rigidity: “ratchet”- like stiffness (cogwheel rigidity); also lead pipe rigidity
  • Akinesia/bradykinesia: subjective sense of weakness, loss of dexterity, difficulty using kitchen tools, loss of facial expression, reduced blinking, difficulty getting out of bed/chair, difficulty turning while walking.
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4
Q

What features appear at initial presentation of idiopathic PD

A
  • Asymmetric
  • Positive response to levodopa or apomorphine
  • Postural Instability (& falls)- not present at diagnosis
  • Less rapid progression (rapid= H&Y 3 in 3 years)
  • Autonomic dysfunction– not present
  • Neuroimaging- ??
  • Impaired olfaction (?)
  • Honeymoon period of 1st 3 yrs whr even w diagnosis, dont need/minimal pharmacological intervention, pt still can lead normal life.
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5
Q

What happens to pt as PD progresses

A
  • Unable to perform basic ADLs (or to perform them safely):
    Mobility (walking, using stairs) - increase falls
    Feeding self
    Grooming, personal hygiene
    Toileting
    Showering/bathing
    Continence (bowel and bladder)
  • Choking (swallowing problems)
  • Pneumonia
  • Falls
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6
Q

What is the greatest burden of PD

A

Costs

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7
Q

What are the features of early/young onset PD <40y/o

A
  • Slower disease progression
  • Features:
    < Cognitive decline
    Earlier motor complications
    Dystonia is common initial presentation vs falls & freezing in late-onset
  • Dopamine agonists used in preference to levodopa
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8
Q

What is goals of tx for PD

A

No cure
Manage symtpoms
Maintain function and autonomy
No treatment for PD has ever been shown to be “neuroprotective”

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9
Q

What are the classes of drugs for PD Tx

A

Increase central dopamine, dopaminergic transmission:
- Levodopa + DCI
- Dopamine agonists
- MAO B inhibitors
- COMT inhibitors

Correct imbalance in other pathways
- Anticholinergics
- NMDA antagonists

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10
Q

What is nonpharm tx for PD

A

PT (help them move):
- Stretching, transfers, posture
- Walking (draw a line or shine a light then they walk towards it to “unfreeze” them)

OT:
- Mobility aids, home &
- Workplace safety
- Speech & swallowing (how big can they swallow? Can crush?)
- Surgery

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11
Q

Which drug is most effective for treating PD smx

A

Levodopa

Esp bradykinesia & rigidity
Less effective for speech, postural reflex & gait disturbances

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12
Q

Can dopamine be used as a treatment? Why?

A

No, it does not cross the blood-brain- barrier

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13
Q

SE of levodopa

A

N/V (take with meals), orthostatic hypotn, drowsiness, sudden sleep onset, hallucinations, psychosis, dsykinesias

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14
Q

How does levodopa work?

A

Peripheral conversion of levodopa to dopamine: Is catalysed by DOPA decarboxylase, MAO, COMT

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15
Q

Why are DCI (benserazide, carbidopa) added to levodopa?

A

Increased bioavailability, prevents break down on levodopa outside of BBB

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16
Q

What type of meals affect absorption of levodopa

A

Absorption ↓ with high fat or high protein meals.

Counselling: space apart from heavy meal.

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17
Q

Does DCI cross BBB?

A

No

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18
Q

What is dose of levodopa

A

75-100mg daily

DCI : levodopa
either 1:4 or 1:10

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19
Q

What is the “On-off” phenomenon?

A
  • ON = response to levodopa (helps gain mobility -> so less adherence issues),
  • OFF = no response to levodopa
  • Unpredictable, not related to dose/dosing interval (cant tweak dosing regimen)
  • “throwing a light switch”
  • Mechanism unclear
  • Difficult to control with meds
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20
Q

What is the “wearing off” complication and how to manage it

A
  • Effect of levodopa wanes before the end of the dosing interval
  • Shortened “ON” time
  • Associated with disease progression
  • Management:
    Modify times of administration, and/or
    Replace with modified-release preparations at the appropriate time
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21
Q

What is dyskinesias motor complications and how to manage?

A
  • Can be unpredictable like “on-off” even if you flatten the peak dose so add amantadine
  • Involuntary, uncontrollable
  • Twitching, jerking
  • Peak dose dyskinesia
  • Dystonia
  • Management : add amantadine; replace specific doses with modified-release levodopa
22
Q

How to dose adjustment when switching btw immediate release and controlled release forms?

A

IR to CR : generally ↑ dose needed (~25%,-50%)
CR to IR : generally ↓ dose needed

23
Q

Sustained released forms are useful for __

A

↓ stiffness upon waking

24
Q

Examples of sustained released forms

A

Sinemet SR
Madopar HBS

25
Q

What DDI with levodopa?

A

Pyridoxine:
- Cofactor for dopa decarboxylase
- Generally not a problem if levodopa is administered with a DCI but do be aware of the possibility of interactions with High dose B6 for haematological problems or in high potency vit B complex tabs

Iron: Affects absorption of levodopa -> space out administration

Protein: Affects absorption of levodopa -> space out administration

Dopamine antagonists:
- Metoclopramide, prochlorperazine (N&V)
- Antiemetic of choice in PD = domperidone (for GI motility)
- 1st gen antipsychotics - if possible, avoid unless thr is indication then R vs B, which is more pressing issue to tackle
- Risperidone

26
Q

Examples of dopamine agonists

A

Cabergoline
Ropinirole
Pramipexole

27
Q

Peripheral SE of dopamine agonists

A

N&V
Orthostatic hypotension
Leg edema

28
Q

Central SE of dopamine agonists

A
  • Hallucinations (usually visual > auditory)
  • Somnolence, day-time sleepiness (similar to levo due to similar MOA)
  • Compulsive behaviours:
    Gambling, shopping, eating, hypersexuality
    Act on reward system
    Caregivers need to watch out! Then stop drug
29
Q

CV SE of dopamine agonists

A

Fibrosis:
- Pulmonary, pericardiac, retro-peritoneal
- May be partially reversible upon withdrawal
- Lower risk with non-ergot agents

Valvular heart disease:
Incidence appears to be greater with ergot-derived agents (∴not used often now)

30
Q

Dopamine agonists vs levodopa place in therapy?

A
  • < motor complications than levodopa but…
  • > hallucinations, sleep disturbances, leg oedema, orthostatic hypotension
  • No clinically significant differences in efficacy between agents
  • Frequently preferred over levodopa in younger patients: to maximise treatment options and delay the onset of levodopa- induced motor complications (unless rly bothered by tx)
31
Q

Dopamine agonists place in therapy?

A
  • Monotherapy In Young-onset PD
  • Adjunct to levodopa in moderate/severePD
  • Management Of Motor Complications Caused By Levodopa -> can give lower dose
  • Neuroprotection, disease modification??
32
Q

Which PD drug is available as transdermal patch?

A

Rotigotine

33
Q

Examples of MAO-B inhibitors for PD

A

Selegiline, rasagiline

34
Q

What is MAO-Bi place in therapy?

A

Effective as monotherapy in early stages

35
Q

Dose of selegiline

A

5mg OM to BD (second dose in afternoon)

36
Q

Dose of rasagiline

A

0.5 to 2mg once daily

37
Q

DDI with MAOBi

A
  • SSRIs, SNRIs, TCAs: Wash out periods recommended
  • Pethidine, tramadol,
  • Linezolid
  • Dextromethorphan
  • Dopamine
  • Sympathomimetics : nasal decongest eg. pseudoephedrine, phenylephrine
  • Another MAOi
38
Q

Food interactions with MAOBi

A

tyramine, cheeses, meat, soy sauce

39
Q

Among levodopa, dopamine agonists and MAOBi, which has more improvements in motor smx and more motor complications?

A

Levodopa

40
Q

Example of Catechol-O-Methyl Transferase Inhibitors (COMT-i)

A

Entacapone

41
Q

DDI with entacapone

A
  • Iron, calcium,
  • Avoid concurrent nonselective MAOi (but safe with MAO- Bi, caution with selective MAO-Ai)
  • any catecholamine drug
  • Enhance anticoagulant effect of warfarin
42
Q

SE of entacapone

A

Diarrhoea, urine discolouration (orange),
dyskinesia upon initiation, orthostatic hypotn, N/V

43
Q

Which drug must Entacapone be taken with

A

Levodopa

44
Q

Anticholinergics place in therapy

A

Limited use, primarily used to control temors

45
Q

Example of anticholinergic used in PD

A

Benzhexol

46
Q

NMDA antagonists place in therapy

A

Adjunctive, manage levodopa-induced dyskinesia

47
Q

SE of NMDA antagonist

A

Nausea, light headedness, insomnia, confusion, hallucinations, livedo reticularis

48
Q

What complementary medicines have shown some effect for PD

A

Co-enzyme Q10
Creatine
Vit E
Gluthathione
Riboflavin
Lipoic acid
Acetyl carnitine
Curcumin

49
Q

How to differentiate drug induced parkinsonism vs PD

A

Smx tend to occur bilaterally in DIP
Withdrawal of the drug usually leads to improvement in 80% of smx in 8wks

50
Q

Examples of drugs that can induce parkinsonism

A

High risk:
Typical antipsychotics
Atypical antipsychotics
a-methyldopa
Cinnarizine

Intermediate risk:
Valproate, phenytoin, levetiracetam
Prochlorperazine, metoclopramide
Diltiazem, verapamil
Lithium

PR3153: Central Nervous System (9 decks)

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