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Pharmacotherapeutics IV CA2 > Parkinsons > Flashcards

Parkinsons Flashcards

1
Q

What are the 3 cardinal symptoms of PD?

A

Tremor (resting tremor), rigidity and akinesia/bradykinesia.

Diagnosis is where 2 of the 3 cardinal signs must be present.

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2
Q

How does PD affect basic ADL?

A
  • mobility issues (walking, using the stairs)
  • feeding oneself
  • grooming, personal hygiene
  • toileting
  • showering
  • continence (bowel and bladder)
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3
Q

What is the goal of managing PD?

A
  • manage symptoms
  • maintain function and autonomy
    (no treatment for PD is neuroprotective)
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4
Q

What are the 4 classes of medications used to treat PD motor symptoms?

A
  • levodopa + DCI
  • dopamine agonists
  • MAOB-inhibitors
  • COMT inhibitors
  • anticholinergics
  • NMDA antagonists
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5
Q

What are some non motor symptoms of PD?

A
  • dementia
  • depression/psychosis
  • sleep disorders
  • sialorrhoea (salivation)
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6
Q

What agent is preferred in early/young onset PD?

A

Dopamine agonists in preference to levodopa

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7
Q

What are the non-pharmacological treatments used in PD?

A
  • physiotherapy
  • occupational therapy
  • speech therapy and swallowing
  • surgery
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8
Q

What is the most effective drug for treatment of PD symptoms?

A

Levodopa

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9
Q

Why can’t dopamine be used as a treatment?

A

Does not cross the BBB

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10
Q

How is levodopa converted to dopamine?

A

You want it to occur in the brain.

However, peripheral conversion of levodopa to dopamine can occur, catalyzed by DOPA decarboxylase, MAO and COMT -> causes nausea/vomiting and hypotension.

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11
Q

What is the absorption of levodopa affected by?

A

Absorption decreases with high fat or high protein meals. Separate administration by 2 hours.

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12
Q

What are DOPA decarboxylase inhibitors?

A

Benserazide and carbidopa

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13
Q

What are the adverse effects of levodopa?

A
  • nausea/vomiting (from peripheral conversion)
  • orthostatic hypotension
  • drowsiness, sudden sleep onset
  • hallucinations, psychosis
  • dyskinesia (within 3-5 years of initiating levodopa)
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14
Q

What is the on-off phenomenon for levodopa?

A

On - response to levodopa
Off - no response to levodopa
(unpredictable)

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15
Q

What is the wearing off phenomenon for levodopa?

A

effect of levodopa wanes before the end of the dosing interval -> modify time of administration or replace with modified release preparations

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16
Q

How do we manage dyskinesia from levodopa?

A

add amantadine; replace specific doses with modified release levodopa

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17
Q

How is the bioavailabilty like for sustained release levodopa?

A

Lower bioavailability than immediate release -> need to adjust doses when converting vice versa.

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18
Q

What are the 4 drug interactions for levodopa?

A
  • Pyridoxine: cofactor for dopa decarboxylase. take note if high dose B6 for haematological problems or in high potency vit B complex tabs
  • Iron: affects absorption of levodopa -> space out
  • Protein (food and protein powder) -> affect absorption, space out
  • Anti-dopaminergic drugs: metoclopramide, prochlorperazine (antiemetic of choice in PD is domperidone); FGA and risperidone
19
Q

What are examples of dopamine agonists?

A

Ergot derivatives:

  • bromocriptine
  • cabergoline
  • pergolide

Non-ergot derivatives:

  • ropinirole
  • pramipexole
  • rotigotine (transdermal) -> used in dysphagia in PD patients
  • apomorphine (SC)
20
Q

What special elimination parameters do we need to take note for ropinirole and pramipexole?

A

Ropinirole: mainly metabolized by the liver to inactive metabolites -> adjust in hepatic impairment
Pramipexole: excreted largely unchanged in the urine -> dose adjust acc to renal function

21
Q

What are the adverse effects of dopamine agonists?

A 
Dopaminergic: 
nausea, vomiting 
orthostatic hypotension 
leg edema 
hallucinations
somnolence
day time sleepiness
compulsive behaviours

Non-dopaminergic:
fibrosis (lower risk with non ergot agents)
valvular heart disease (lower risk for non ergot agents)

22
Q

What is the place in therapy for dopamine agonists?

A

Preferred over levodopa in younger patients to maximize treatment options and delay the onset of levodopa-induced motor complications. (used as monotherapy in young onset PD)

adjunct to levodopa in moderate/severe PD

23
Q

What are examples of MAOB-inhibitors?

A

Selegiline and rasagiline -> both irreversible enzyme inhibitors -> short half life but long duration of action

24
Q

Place in therapy for MAOB-i?

A

effective as monotherapy in early stages;

adjunct in later stages

25
Q

What is selegiline metabolized to?

A

To amphetamines which are stimulating and have no effect on MAOB.

26
Q

Is rasagiline metabolized to amphetamines?

A

NO

27
Q

What are the drug interactions for MAOBi?

A

SSRI, SNRI and TCAs -> washout period is recommended

28
Q

What is a counselling point for MAOB-i?

A

Avoid tyramine rich foods

29
Q

What are examples of COMTi?

A

Entacapone and tolcapone

30
Q

What is the place in therapy for COMTi?

A
  • Not effective without concurrent levodopa treatment.

- decreases “off” time

31
Q

What are some drug interactions of entacapone?

A
  • iron, calcium
  • avoid concurrent MAOi
  • catecholamine drug
  • enhance anticoagulant effect of warfarin
32
Q

What are the adverse effects of entacapone?

A
  • diarrhoea
  • urine discolouration (orange)
  • use with caution in hepatic impairment, but monitoring of LFTs generally not required
  • may cause dyskinesia upon initiation -> may require a lowering of levodopa dose
  • may potentiate orthostatic hypotension and nausea/vomiting
33
Q

What is the difference between tolcapone and entacapone?

A
  • more potent and longer duration of effect than entacapone

- however, causes liver issues -> need to monitor LFTs

34
Q

What is the place in therapy for anticholinergics in PD?

A
  • primarily used to control tremors
35
Q

What are examples of NMDA antagonists in PD?

A
  • amantadine

- memantine

36
Q

What are the adverse effects of NMDA antagonists?

A
  • nausea
  • light-headedness
  • insomnia
  • confusion
  • hallucinations
  • livedo reticularis
37
Q

What is the place in therapy for NMDA antagonists?

A
  • used as an adjunct to levodopa to manage levodopa-induced dyskinesias
38
Q

What are the two types of parkinsonism?

A
  • vascular parkinsonism

- drug-induced parkinsonism

39
Q

What drugs can cause drug-induced parkinsonism?

A
  • dopamine receptor blockers (FGA antipsychotics eg haloperidol and prochlorperazine, amisulpride & SGA at higher doses eg risperidone, olanzapine and aripiprazole)
  • cinnarizine
  • valproate
40
Q

How to treat drug induced parkinsonism?

A

Remove offending drug

41
Q

What is Parkinson Hyperpyrexia Syndrome (PHS)?

A
  • caused by changes in dopaminergic treatment
42
Q

How to manage PHS?

A
  • If cause is reduced dopaminergic medications, reinstate previous treatment and increase dose of levodopa gradually.
  • Dantrolene and bromocriptine
43
Q

What are some complications of PD?

A
  • aspiration pneumonia (impaired swallowing)
  • dopamine agonist withdrawal
  • psychosis
  • dyskinesia

Pharmacotherapeutics IV CA2 (5 decks)

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