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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
Antiemetic of choice in PD
Domperidone
26
List the Dopamine agonists according to whether they are ergot derivatives or not
Ergot: Bromocriptine, Cabergoline, Pergolide (Go go Mo) Non-ergot derivatives: Ropinirole, Pramipexole, Rotigotine (TD), Apomorphine (SC) (PRRA)
27
Compare the F of DA agonists between ergot and non-ergot (EDA, nEDA). State a reason why is this observed
nEDA > EDA Due to EDA extensive first-pass metabolism
28
Which of the DA agonists require decreased dose in LIVER impairment? State whether is it an EDA or nEDA
Ropinirole (metabolism mainly in liver) nEDA
29
Which of the DA agonists require decreased dose in RENAL impairment? State whether is it an EDA or nEDA
Pramipexole (largely unchanged in urine) nEDA
30
PERIPHERAL DOPAMINERGIC AE of DA agonist | hint: similar to LevoD
1. NNV 2. Leg Edema 3. Orthostatic hypotension (less in Ropi) 4. EDA only: Fibrosis
31
CNS DOPAMINERGIC AE of DA agonist | hint: similar to LevoD
1. Hallucinations (visual > auditory) 2. Somnolence + day-time sleepiness (Ropi + Prami) 3. Compulsive behaviours (E.g. Gamble, shop, eat)
32
Compared to EDA, what advantage does nEDA has in terms of AE?
1. Less Fibrosis | 2. Less Valvular Heart Disease (caused by Pergolide)
33
TWO advantages of DA agonists over LevoD
1. Longer DoA = less frequent administration | 2. Less motor complications
34
One DISadvantage of DA agonist over LevoD
More AE (both peripheral and CNS dopaminergic AE)
35
What is the most common clinical use of DA agonist?
For younger patients, to delay levoD-induced motor complications
36
Dosage forms for Pramipexole and Ropinirole available in Singapore
IR and SR tabs
37
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?
# Choose Rasagiline. For Selegiline: - H metabolised to amphetamines - Stimulating, may cause insomnia before bed
38
Are MAO-BI effective as monotherapy?
Yes
39
Class of drug for Selegiline and Rasagiline
IRREVERSIBLE MAO-BI
40
Drug interactions with MAO-BI that washout periods are recommended?
SSRI, SNRI, TCA | basically serotoninergic agents and TCA
41
The most significant food interaction with MAO-BI
Tyramine
42
MAO-BI place in therapy for the management of PD?
1. Monotherapy | 2. More for young onset PD
43
Rank the efficacy of MAO-BI, DA agonists and LevoD
LevoD ≈ DA agonist > MAO-BI
44
Duration of action (short, med or long) of MAO-BI and the reason
Long duration | - Due to slow MAO regeneration
45
General properties of MAOBI compared to LevoD and DA agonists
Milder everything | i.e. less efficacy and improvement, but less motor complications and AE as well
46
Can COMT be used as monotherapy?
No, requires concurrent levodopa
47
Mechanism of COMT-I
- 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
One unique SE of entacapone which must counsel patient
Urine discolouration (orange)
49
List the drug interactions with COMT-I
1. Fe, Ca: avoid concurrent use 2. Warfarin: increased anticoagulant effect 3. Others: Catecholamine, nonselective MAOI
50
When COMT-I is given, why may a reduction in levoD dose be required
May cause spike in [LevoD] and may cause dyskinesia
51
Must LFTs be monitored with the use of entacapone?
No need, but just take note, use with caution in hepatic impairment
52
Unlike Entacapone, what are the properties of Tolcapone?
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
What does Stalevo contain?
Levo + Carbi + Entacapone
54
Purpose of anti-M in PD. List the two main anti-M used
Control tremor 1. Benztropine 2. Trihexyphenidyl
55
Anti-M that cannot be used to manage sx in PD, and why.
1. Ipratropium: Cannot Cross BBB 2. Hyoscine N-butylbromie (HNBB): Cannot Cross BBB 3. Tolterodine: Limited systemic absorption (accumulates at bladder)
56
Proposed mechanism of Amantadine. Hence, what is Amantadine classified as?
1. NMDA antagonist 2. Anti-M 3. Upreg D2R = increased sensitivity to D2 - Classified as: NMDA antagonists (NMDAA)
57
Drug class of Memantine. is it used in PD?
NMDAA. No
58
Dosing regimen of NMDAA (Amantadine) and reason for such regimen
2 doses, 2nd dose in afternoon due to stimulating effect (avoid insomnia at night) (similar to Selegiline, a MAOBI)
59
One significant SE of NMDAA
Livedo reticularis: Spiderweb pattern on arms and legs | - Refer to doctor if it occurs
60
Place of NMDAA in management of PD
1. Adjunct | 2. Manage LevoD-induced dyskinesias (NEW!!)
61
Distinguish between Parkinsonism and PD
Parkisonism: - Drug/toxin-induced - Also got vascular Parkinsonism
62
Distinguish between drug-induced Parkinsonism and PD in terms of sx
Parkinsonism: 1. Usually bilateral 2. Sx improve when drug withdrawn (unlike PD) 3. Tx by withdrawing offending drug (unlike PD)
63
LevoD is ineffective in Vascular parkinsonism. Why?
Caused by infarct/lesions, nothing relating to DA
64
Name some drugs/drug classes that can cause drug-induced parkinsonism
1. D2 antagonists: Antipsychotics 2. DA depleters and synthesis blockers 3. CCBs 4. Antidepressants
65
Best Tx for drug-induced parkinsonism
Prevention

Therapeutics IV (9 decks)

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