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Therapeutics IV > Mngt PD - Concepts > Flashcards

Mngt PD - Concepts Flashcards

1
Q

Describe the three cardinal sx of PD. How many of them must be present before dx of PD can be established?

A
  1. Tremor (resting)
    - Resting tremors, disappears with movement
    - Increases with stress
  2. Rigidity:
    - Cogwheel rigidity
    - Leadpipe rigidity
  3. Akinesia/Bradykinesia
    - Sense of weakness
    - Loss dexterity
    - Loss facial expression
    etc.

Dx Criteria: 2 of 3 MUST be present

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2
Q

List the ADLs (Activities of daily living) that PD can affect

A
  1. Mobility
  2. Feeding self
  3. Grooming
  4. Toileting
  5. Showering/bathing
  6. Continence
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3
Q

Describe how PD leads to increased risk of morbidity, if left uncontrolled and untreated

A
  1. Choking, may lead to pneumonia
    - Impaired swallowing
  2. Falls, due to weakness
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4
Q

What are the goals of managing PD

A
  1. Manage sx

2. Maintain function and autonomy

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5
Q

Can PD be cured or prevented? Explain your answer

A
  • No: DA cannot be replaced, and hence cannot be cured

- No prevention, as no tx has shown to be neuroprotective

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6
Q

In the treatment of PD, is pharmacologic or non-pharmacologic tx more important?

A

Both are equally important

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7
Q

List the Non-Pharmacological management of PD

A
  1. Physiotherapy (e.g. stretch, posture, walk)
  2. Occupational therapy (E.g. mobility aids, home and workplace safety)
  3. Speech and swallowing
  4. Surgery (e.g. Deep Brain stimulation for severe cases)
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8
Q

List drug classes, and at least one example from each, that are used in the management of PD

A
  1. Levodopa + DCI
  2. Dopamine agonists: Pramipexole
  3. MAO-BI: Rasagiline
  4. COMT-I: Entacapone (-capone)
  5. Anticholinergics (Trihexylphenidyl)
  6. NMDA antagonists (Amantadine)

(1-4: Increase DA, 5-6 correct imbalance other ways)

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9
Q

Which classes of drugs used in PD are NOT the best at relieving sx?

A
  1. Anticholinergics

2. NMDA antagonist

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10
Q

Gold standard drug for PD. Explain your answer

A

Levodopa: Most effective for sx relief, especially Bradykinesia and Rigidity

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11
Q

Why is levodopa, instead of DA itself, used to treat PD

A

DA cannot cross BBB

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12
Q

Purpose of adding a decarboxylase inhibitor (DCI) with levodopa

A

Minimise conversion of levodopa to DA in the PERIPHERY, hence avoiding:

  • NNV
  • HyPOtension
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13
Q

Levodopa has decreased absorption with high fat or high protein meals. What is the clinical implication of this?

A

Take 2-4h apart from food, and plan meals and drug consumption properly if NGT

(coz patient requires high protein diet in PD)

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14
Q

Dosage ratio of levodopa:DCI for different preparation

A

Levodopa:DCI

  • 4:1 (Sinemet, Madopar)
  • 10:1 (Sinemet)

(e.g. Sinemet 25mg carbidopa + 250mg levo)

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15
Q

The three AE of Levodopa, in terms of decreasing severity

A
  1. Dyskinesias: onset 3-5y after initiation
  2. Psychosis, Hallucinations
  3. Drowsiness, sudden sleep onset

(Psychosis: due to excess D. Recall that psychosis is caused by excess NT. Since Levodopa adds DA to brain, may be in excess hence cause psychosis)

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16
Q

Describe the “on-off” phenomenon in levodopa tx. What are its problems and mechanisms?

A
  • ON = response to levoD = relieved sx
  • OFF = no response

Problem: Difficult to control with meds

  • Unpredictable,
  • No dose relation
  • Unclear mechanism
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17
Q

Describe the “wearing off” effect

A

Big idea: Shortened “ON” time

  • Associated with disease progression
  • “Wearing off” = Effect of LevoD wanes bef end of dosing interval
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18
Q

What are the ways to manage “wearing off” effect in LevoD tx?

A
  1. Modify times of administration

2. Replaced with modified-release preps at appropriate times

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19
Q

Explain the underlying mechanism that explains the changes in levodpa response that is associated with progression of PD, and its relation to the “wearing-off” effect

A

Three things to take note: Threshold, Response Threshold and Dyskinesia (MTC, MIC, DysK, toxic effect of MTC is dysK)

As PD progresses from early to advanced PD:

  • TI narrows, hence MTC decreased, MIC increased
  • [LevoD] required to reach MIC increases, but yet with that increase, may hit MTC and hence cause dysK
  • Since TI narrows, the time which [LevoD] is within TI decreases also, hence “wearing-off” faster as PD progresses
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20
Q

Describe the motor complications that is associated with the use of Levodopa.

A

Dyskinesia (dysK):

  • Involuntary twitching and jerking
  • Usually occur at peak-doses of LevoD (peak dose dysK)
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21
Q

Describe the management to levoD motor complications

A
  1. Add amantadine

2. Replace specific doses with modified-release levoD

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22
Q

Describe the dose adjustments between IR and CR of LevoD/DCI. Explain why is it adjusted in that specific way

A
  1. IR to CR: Increase dose (25-50%)
  2. CR to IR: decrease dose

Reason: CR lower bioavailability

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23
Q

What is one benefit of Levodopa in SR form?

A

Decrease stiffness on walking

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24
Q

Describe the drug interactions of LevoD, and how to manage it

A
  1. Fe , Protein (food, protein powder)
    - Affects absorption of levoD
    - Space out administration
  2. Anti-DA (e.g. Metoclopramide, prochlorperazine)
    - Use non Anti-DA antiemetic: Domperidone
  3. Pyridoxine: cofactor for dopa DCI
    - Not a problem
    - (high B6/ high potency vitB may cause Haematological problems)
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25
Q

Antiemetic of choice in PD

A

Domperidone

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26
Q

List the Dopamine agonists according to whether they are ergot derivatives or not

A

Ergot: Bromocriptine, Cabergoline, Pergolide
(Go go Mo)

Non-ergot derivatives: Ropinirole, Pramipexole, Rotigotine (TD), Apomorphine (SC)
(PRRA)

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27
Q

Compare the F of DA agonists between ergot and non-ergot (EDA, nEDA). State a reason why is this observed

A

nEDA > EDA

Due to EDA extensive first-pass metabolism

28
Q

Which of the DA agonists require decreased dose in LIVER impairment? State whether is it an EDA or nEDA

A

Ropinirole (metabolism mainly in liver)

nEDA

29
Q

Which of the DA agonists require decreased dose in RENAL impairment? State whether is it an EDA or nEDA

A

Pramipexole (largely unchanged in urine)

nEDA

30
Q

PERIPHERAL DOPAMINERGIC AE of DA agonist

hint: similar to LevoD

A
  1. NNV
  2. Leg Edema
  3. Orthostatic hypotension (less in Ropi)
  4. EDA only: Fibrosis
31
Q

CNS DOPAMINERGIC AE of DA agonist

hint: similar to LevoD

A
  1. Hallucinations (visual > auditory)
  2. Somnolence + day-time sleepiness (Ropi + Prami)
  3. Compulsive behaviours (E.g. Gamble, shop, eat)
32
Q

Compared to EDA, what advantage does nEDA has in terms of AE?

A
  1. Less Fibrosis

2. Less Valvular Heart Disease (caused by Pergolide)

33
Q

TWO advantages of DA agonists over LevoD

A
  1. Longer DoA = less frequent administration

2. Less motor complications

34
Q

One DISadvantage of DA agonist over LevoD

A

More AE (both peripheral and CNS dopaminergic AE)

35
Q

What is the most common clinical use of DA agonist?

A

For younger patients, to delay levoD-induced motor complications

36
Q

Dosage forms for Pramipexole and Ropinirole available in Singapore

A

IR and SR tabs

37
Q

A doctor asks you to advise him on whether selegiline or rasagiline should be given at bedtime for a patient. Which will you choose and why?

A

Choose Rasagiline.

For Selegiline:

  • H metabolised to amphetamines
  • Stimulating, may cause insomnia before bed
38
Q

Are MAO-BI effective as monotherapy?

A

Yes

39
Q

Class of drug for Selegiline and Rasagiline

A

IRREVERSIBLE MAO-BI

40
Q

Drug interactions with MAO-BI that washout periods are recommended?

A

SSRI, SNRI, TCA

basically serotoninergic agents and TCA

41
Q

The most significant food interaction with MAO-BI

A

Tyramine

42
Q

MAO-BI place in therapy for the management of PD?

A
  1. Monotherapy

2. More for young onset PD

43
Q

Rank the efficacy of MAO-BI, DA agonists and LevoD

A

LevoD ≈ DA agonist > MAO-BI

44
Q

Duration of action (short, med or long) of MAO-BI and the reason

A

Long duration

- Due to slow MAO regeneration

45
Q

General properties of MAOBI compared to LevoD and DA agonists

A

Milder everything

i.e. less efficacy and improvement, but less motor complications and AE as well

46
Q

Can COMT be used as monotherapy?

A

No, requires concurrent levodopa

47
Q

Mechanism of COMT-I

A
  • In presence of DCI, COMT becomes major metaboliser of LevoD
  • COMT-I can inhibit that and increase efficacy and DoA of LevoD, by decreasing “OFF” time
48
Q

One unique SE of entacapone which must counsel patient

A

Urine discolouration (orange)

49
Q

List the drug interactions with COMT-I

A
  1. Fe, Ca: avoid concurrent use
  2. Warfarin: increased anticoagulant effect
  3. Others: Catecholamine, nonselective MAOI
50
Q

When COMT-I is given, why may a reduction in levoD dose be required

A

May cause spike in [LevoD] and may cause dyskinesia

51
Q

Must LFTs be monitored with the use of entacapone?

A

No need, but just take note, use with caution in hepatic impairment

52
Q

Unlike Entacapone, what are the properties of Tolcapone?

A
  1. More potent and longer DOA:
    - May require greater dose reduction in levoD
  2. Require LFTs monitoring: Every 2-4 weeks for SIX months)
    - i.e. initiation and after every dose increment
  3. Not available in Singapore
53
Q

What does Stalevo contain?

A

Levo + Carbi + Entacapone

54
Q

Purpose of anti-M in PD. List the two main anti-M used

A

Control tremor

  1. Benztropine
  2. Trihexyphenidyl
55
Q

Anti-M that cannot be used to manage sx in PD, and why.

A
  1. Ipratropium: Cannot Cross BBB
  2. Hyoscine N-butylbromie (HNBB): Cannot Cross BBB
  3. Tolterodine: Limited systemic absorption (accumulates at bladder)
56
Q

Proposed mechanism of Amantadine. Hence, what is Amantadine classified as?

A
  1. NMDA antagonist
  2. Anti-M
  3. Upreg D2R = increased sensitivity to D2
  • Classified as: NMDA antagonists (NMDAA)
57
Q

Drug class of Memantine. is it used in PD?

A

NMDAA. No

58
Q

Dosing regimen of NMDAA (Amantadine) and reason for such regimen

A

2 doses, 2nd dose in afternoon due to stimulating effect (avoid insomnia at night)

(similar to Selegiline, a MAOBI)

59
Q

One significant SE of NMDAA

A

Livedo reticularis: Spiderweb pattern on arms and legs

- Refer to doctor if it occurs

60
Q

Place of NMDAA in management of PD

A
  1. Adjunct

2. Manage LevoD-induced dyskinesias (NEW!!)

61
Q

Distinguish between Parkinsonism and PD

A

Parkisonism:

  • Drug/toxin-induced
  • Also got vascular Parkinsonism
62
Q

Distinguish between drug-induced Parkinsonism and PD in terms of sx

A

Parkinsonism:

  1. Usually bilateral
  2. Sx improve when drug withdrawn (unlike PD)
  3. Tx by withdrawing offending drug (unlike PD)
63
Q

LevoD is ineffective in Vascular parkinsonism. Why?

A

Caused by infarct/lesions, nothing relating to DA

64
Q

Name some drugs/drug classes that can cause drug-induced parkinsonism

A
  1. D2 antagonists: Antipsychotics
  2. DA depleters and synthesis blockers
  3. CCBs
  4. Antidepressants
65
Q

Best Tx for drug-induced parkinsonism

A

Prevention

Therapeutics IV (9 decks)

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