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3153 Psychiatry > IC17 Parkinson's Disease > Flashcards

IC17 Parkinson's Disease Flashcards

1
Q

What are the 3 types of parkinson’s disease?

A
  1. Idiopathic PD (most common)
  2. Drug induced Parkinsonism
  3. Early/young onset PD
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2
Q

What is idiopathic PD? What are the risk and protective factors of IPD?

A
  1. Idiopathic PD (most common)
    o neurodegenerative disease
    o slightly more common in men
    o age ↑
    o Smoking & caffeine ↓
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3
Q

How does young onset PD differ from normal PD?
Which medication is usually given to them?

A
  1. Early/young onset PD
    a. Slower disease progression
    b. Less cognitive decline
    c. More motor complications
    d. Dystonia
    e. Dopamine agonist preferred
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4
Q

What are the cardinal symptoms of PD?
What are the criteria for diagnosing PD?

A

For diagnosis – based on clinical signs, physical examination, history
2 of the 3 cardinal symptoms must be present:

  1. Tremors at rest
  2. Rigidity
    a. Cogwheel rigidity
    b. Lead pipe rigidity
  3. Akinesia / Bradykinesia
    a. Slowness and poverty of movement
    b. Loss of dexterity
    c. Loss of facial expression
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5
Q

What are the 4 characteristic features of PD?

A

Cardinal Motor Symptoms of PD
4 characteristic features: (TRAP)

  1. Tremors at rest
  2. Rigidity
    a. Cogwheel rigidity
    b. Lead pipe rigidity
  3. Akinesia / Bradykinesia
    a. Slowness and poverty of movement
    b. Loss of dexterity
    c. Loss of facial expression
  4. Postural instability
    a. Gait, postural issues
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6
Q

What are the features of initial presentation of PD?

A

At initial presentation, features of idiopathic PD:

  1. Asymmetric
  2. Positive response to levodopa/apomorphine
  3. Less rapid progression in 1st 3 years
  4. NO postural instability/falls
  5. NO autonomic dysfunction
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7
Q

What are the features of idiopathic PD as disease progresses?

A

As disease progress, features of idiopathic PD:

  1. Inability to perform basic ADL
    a. Mobility, feeding self, grooming, personal hygiene, toileting, showering, continence
  2. Choking (inability to swallow)
  3. Pneumonia (aspiration pneumonia)
  4. Falls
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8
Q

What are the tools/assessment used to measure disease progression?
What are the stages of PD? (both qns are optional)

A

Measuring disease progression:

  1. Hoehn and Yahr Staging
  2. MDS-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS)
    I: unilateral TRA
    II: bilateral
    III: Postural instability
    IV: Severe disability, falls, dependency, cognitive decline, but can still walk and stand
    V: Wheelchair / bed bound
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9
Q

*Name the non-motor symptoms of idiopathic PD. (9)

A

5 non-motor symptoms of PD (more distressing)
need to name some of the non-motor symptoms of idiopathic PD

  1. Dementia
  2. Depression
  3. Psychosis
  4. REM sleep behaviour disorder
  5. Constipation
  6. GI motility
  7. Orthostatic hypotension (midodrine can help)
  8. Sialorrhea
  9. Fatigue
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10
Q

What is the patho of PD?

A

Pathophysiology of PD

  • Neuroinflammation
  • Loss of dopaminergic neurons in substantia nigra (Neurodegeneration)
  • Misfolded alpha-syno-nuclei proteins –> lewy bodies
  • Glutamate causes neurotoxicity
    o Glutamate –> binds to NMDA receptors –> encourage cell death
    o Causes and maintains levodopa-induced dyskinesia
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11
Q

How does drug-induced PD differ from IPD?
How to manage PD after drug-induced PD is managed?

A
  • Sx tends to be bilateral
  • Response to levodopa is poor
  • Withdrawal of drug leads to improvement of sx in 8 weeks
  • Management: withdrawal of offending drug
  • May unmask underlying PD –> use anticholinergic / amantadine to address this
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12
Q

*What are the high and intermediate potential drugs causing DIP?

A
  • Need to know high and intermediate potential drugs causing DIP:

o high potential

  1. Dopamine antagonist e.g. FGA, SGA (at higher doses), tetrabenazine
  2. Alpha-methyldopa
  3. Cinnarizine

o Intermediate potential

  1. Antiseizures e.g. valproate, phenytoin, levetiracetam
  2. Antiemetic e.g. metoclopramide, prochlorperazine
  3. Lithium
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13
Q

What are the goals of PD?

A

Goal of treatment:

  1. Manage symptoms
  2. Maintain function and autonomy
  3. NO treatment is neuroprotective
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14
Q

What are the possible med options for PD?

A
  1. Levodopa
  2. adjunct: carbidopa, benserazide, entacapone
  3. Dopamine agonist e.g. pramipexole, rotigotine, ropinirole
  4. MAO-Bi e.g. selegiline, rasagiline
  5. Anticholinergics e.g. trihexyphenidyl, benztropine
  6. NMDA receptor antagonist e.g. amantadine
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15
Q

What is the MOA and place in therapy of Levodopa?

A

MOA:

  • crosses BBB
  • converted to dopamine
  • Most effective in ↓bradykinesia & rigidity

Place in therapy:

  • monotherapy
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16
Q

What is the PK of levodopa? (optional?)

A

PK:

  • absorbed in proximal part of SI
  • ↓F (alone)
  • ↑F (w DCI)
  • absorbed by active saturable carrier system for large neutral a.a through BBB
  • ↓absorption by high fat / high protein meals (space apart from heavy meals)
  • short t1/2
17
Q

What is the DDI of levodopa?

A

DDI:
1) vit B6 (pyridoxine)
- cofactor of Decarboxylase
- generally not a problem if given w DCI
2) Iron
- affects absorption of levodopa → space out administration
3) Protein
- affects absorption of levodopa → space out administration
4) Dopamine antagonist
e.g. metoclopramide, prochlorperazine → use domperidone for antiemetic
e.g. FGA → avoid if possible
e.g. risperidone

18
Q

What are the ADRs of Levodopa?

A

Peripheral

1) N&V
2) Orthostatic Hypotension

Central
3) Drowsiness, sudden sleep onset
4) Hallucination, psychosis

5) Dyskinesia (onset within 3-5yrs)

19
Q

What is the MOA and place in therapy of DCI?

A

Decarboxylase Inhibitors
e.g. carbidopa, benserazide 75-100mg OD

Place in therapy:

  • Adjunct w levodopa
  • do NOT cross BBB
  • Levodopa:DCI
    1:4 (Sinemet, madopar)
    1:10 (Sinemet)
20
Q

What is the MOA and place in therapy of COMTi?
What is an impt counselling point of COMTi?

A

COMT inhibitors
e.g. entacapone

Stavelo (combi): L-dopa, carbidopa, entacapone

MOA:

  • reversible, selective COMT inhibitor
  • ↓ “off” time

Place in therapy:

  • Adjunct w levodopa +/-DCI (must take at the same time)
21
Q

What is the DDI of COMTi? (optional)

A

DDI (optional to know?):
1) Iron, calcium
2) Avoid non-selective MAOi (but safe w MAO-Bi, caution with selective MAO-Ai)
3) Catecholamine drugs
4) Warfarin

**Use with caution in hepatic impairment

22
Q

What are the ADRs of COMTi?

A

Entacapone

1) Diarrhea
2) Urine discoloration (orange)
3) May ↑levodopa’s ADR since less levodopa are metabolised e.g. N&V, dyskinesia, hypotension, hallucinations, daytime sleepiness → ↓levodopa dose

23
Q

What is the MOA and place in therapy of MAO-Bi?

A

MAO-B inhibitors e.g. selegiline, rasagiline

MOA:

  • irreversible MAO-B inhibitors
  • non-selective to MAO-B
  • NO neuroprotection

Place in therapy:

  • Monotherapy (early stages/ young onset PD)
  • not as great as levodopa & dopamine agonist
  • adjunct (later stages)
24
Q

What is the PK of MAO-Bi?
Thus, what needs to be counselled?
What is the dose of both MAO-Bi?

A

PK:

  • short t1/2 but long duration of action
  • Selegiline is hepatically metabolized to amphetamines → stimulating
    → Selegiline 5mg OM to BD (2nd dose in afternoon to avoid affecting sleep)
  • Rasagiline NOT metabolized to amphetamines → Rasagiline 0.5-2mg OD
25
Q

What is the DDI of MAO-Bi? (8)

A

DDI:

1) SSRI, SNRI, TCAs (need washout)
2) Pethidine, tramadol
3) linezolid
4) Dextromethorphan
5) Dopamine
6) Sympathomimetics e.g. pseudoephedrine, phenylephrine
7) Other MAOIs
8) Tyramine (cheese, soy sauce)

26
Q

What is the MOA and place in therapy of Dopamine agonist?

A

Dopamine agonist
e.g. pramipexole IR/SR, ropinirole IR/SR, rotigotine patch (exemption drug), apomorphine (rescue therapy for freezing episodes), ergot derivatives like pergolide (rarely used)

MOA:

  • bind to D2 receptors in basal ganglia
  • Pros: ↓motor complications, helps manage motor complications by ↓levodopa dose
  • Cons: ↑hallucinations, sleep disturbances, leg edema, orthostatic hypotension

Place in therapy:

  • monotherapy (esp in younger pts)
  • adjunct w levodopa (mod-sev PD)
27
Q

What is the PK of dopamine agonist (both ergot & non-ergot)?

A
  • (ergot derivatives) ↓F than other dopamine agonist due to 1st pass effects
  • ↑t1/2 & duration than levodopa
  • (ropinirole) ↑t1/2, metabolised in liver to inactive metabolites
  • (Pramipexole) ↑t1/2, excreted unchanged in kidney
28
Q

What are the ADRs of dopamine agonist?

A

Peripheral (similar to levodopa):

1) N&V
2) Orthostatic hypotension
3) Leg edema

Central:

1) Hallucinations (visual)
2) somnolence, daytime sleepiness
3) Compulsive behaviour e.g. gambling, shopping, eating → stop med

Ergot ADRs:

1) fibrosis → stop meds
2) valvular heart disease

29
Q

What is the place in therapy for anticholinergics?

A

Anticholinergics e.g. trihexyphenidyl, benztropine

Place in therapy:

  • Limited use
  • used to control tremor dominant symptoms
  • treat sialorrhea
30
Q

What is the PK of trihexyphenidyl?

A

↑F, ↑t1/2

31
Q

What are the ADRs of anticholinergics?

A

anticholinergic ADRs:)

32
Q

What is the MOA and place in therapy of NMDA receptor antagonist?

A

NMDA receptor antagonist
e.g. amantadine

MOA:

  • NMDA antagonist
  • anticholinergic
  • upregulates D2 receptors

Place in therapy:

  • Adjunct w levodopa
  • manage levodopa-induced dyskinesia
  • monotherapy
33
Q

What is the PK of NMDA receptor antagonist?
What is the DDI?
What is the counselling point when taking amantadine?

A

PK:

  • Renally excreted
  • can be stimulating (similar to selegiline) → 2nd dose in the afternoon

DDI:

1) Memantine

34
Q

What are the ADRs of amantadine?

A

1) Nausea
2) Light-headedness
3) Insomnia (stimulating)
4) Confusion
5) Hallucinations
6) Livedo reticularis (thrombosis)

35
Q

What are the motor complications of PD?
*What are the strategies to manage them?

A

Strategies to manage motor complications of PD
Motor complications of using Levodopa for PD:

  1. On-off response
    a. Unpredictable
    b. Management: hard to control w meds, can’t tweak regimen, Levodopa+carbidopa/benserazide, pramipexole, ropinirole, rotigotine, rasagiline, entacapone
  2. Wearing off response
    a. effects wanes off before the next dose
    b. shorter “on” time
    c. as disease progresses
    d. Management:
    i. Modify times of administration
    ii. Replace with modified release preparations at the appropriate time
    iii. Add COMTI e.g. entacapone can ↓ “off” time
  3. Dyskinesia
    a. Involuntary, uncontrollable, tweaking, jerking, dystonia
    b. Peak dose dyskinesia
    c. Management:
    i. Change to smaller doses but give at higher frequency (flatten dose)
    When already flatten peak, but PD progresses and dyskinesia becomes unpredictable and irreversible, then
    ii. Add amantadine (can ↓dyskinesia since anti-glutamate)
    iii. Replace specific doses with modified release levodopa (long duration, but low peak which is good)
36
Q

What are the benefits of using sustained release levodopa?
How to dose adjust when switching between IR to CR and vice versa?
What are the counselling points when giving sustained release levodopa?

A

Sustained release form of Levodopa:

  • Could be added on for the last dose of the day → Good for ↓stiffness on waking
  • Release levodopa over 4-6hrs
  • *↓F in sustained release form:
    o Dose adjustments needed when switching between immediate release and controlled release forms
    o IR to CR: gradually ↑dose (~25-50%)
    o CR to IR: gradually ↓dose
  • Sinemet SR: do NOT crush
  • Madopar HBS: do NOT open capsule
37
Q

What are the differences amongst levodopa, dopamine agonist, MAO-BI?

A

Efficacy Levodopa (1) Dopamine Agonist (2) MAO-BI (3)
Improvement in motor symptoms More Less Less
Improvement in ADL More Less Less
Motor complications More Less Less
ADRs^ Less More Less

^e.g. hallucinations, sleepiness, impulse control disorder

see page 49 of notes

38
Q

What are the non-pharm for PD?

A

Non-pharmacological PD:

  1. PT – stretching, transfer, posture, walking
  2. OT – mobility aids, home, workplace sfety
  3. ST – speech and swallowing
  4. Surgery

3153 Psychiatry (10 decks)

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