Drugs For Parkinsons Disease (24) Flashcards

1
Q

Parkinsons disease affects

A

Dopamine producing neurons in the brain

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2
Q

Symptoms of Parkinson’s are caused by

A

An imbalance of dopamine and acetylcholine

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3
Q

Dopamine vs ACh in Parkinson’s

A

Dopamine: inhibitory

ACh: excitatory

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4
Q

Direct vs indirect drugs affecting the dopamine system

A

Direct: dopamine receptor agonists

Indirect: levodopa-carbidopa selegiline amantidine

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5
Q

Precursor to dopamine

A

Levodopa

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6
Q

MAOI prevents

A

DA metabolism

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7
Q

Anticholingeric agents example

A

Benztropine

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8
Q

BBB does not allow

A

Exoganeously supplied dopamine to enter, but it does allow levodopa

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9
Q

Levodopa is taken up by

A

Dopaminergic terminal and converted into dopamine and then released

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10
Q

Levodopa therapy is aimed at

A

Increasing dopamine release form surviving DA neurones

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11
Q

Levodopa therapy maintains function mobility for

A

Years
-prolongs quality of life and expectancy

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12
Q

How long does it take for full therapeutic response

A

Several months

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13
Q

Therapy for Parkinson’s does not

A

Cure or stop progression of disease

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14
Q

As PD progresses

A

It becomes more and more difficult to control symptoms with levodopa

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15
Q

Where is levodopa metabolized outside of CNS

A

GI and liver

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16
Q

Combination therapy with levodopa therapy

A

Carbidopa

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17
Q

Why is carbidopa given if it Cant cross the BBB?

A

Prevents levodopa breakdown in the periphery

18
Q

Levodopa can also be metabolized by COMT, how does one stop this

A

Use COMT inhibitors

19
Q

Example of COMT inhibitors

A

Entacapone

20
Q

Entacapone

A

Inhibits COMT
-more levodopa available to enter brain
-used to reduce on-off phenomenon

21
Q

Wearing off effect of levodopa therapy

A

Gradual loss
-subtherapeutic levels near end of dosing interval

22
Q

On off phenomenon

A

Abrupt loss of drug effect even at high drug levels
-lasts from minutes to hours
-unknown reason

23
Q

AE of levodopa

A

-nausea and vomiting
-dyskinesia
-CV
-psychosis

24
Q

Dyskinesia as AE of levodopa

A

Involuntary muscle movements
-oral, facial muscle, writhering and flinging movement of arms and legs

25
Dopaminergic therapy
Prevents DA metabolism -MAO B inhibitor -inhibiting DA breakdown in neurones
26
MAO-B inhibitor
Selegiline
27
Amantadine
Promotes DA release from nerve endings
28
selegiline
Irreversible MAOI that selectively inhibits MAO-B
29
Selegiline is a
MAO-B inhibitor
30
Selegiline causes an increase
In the levels of dopaminergic stimulation in the CNS
31
Selegiline indications
Milder symptoms or earlier
32
Selegiline has a ___ agent and it is helpful
Adjunctive agent, helping response to levodopa flucting on-off
33
AE of Selegiline
Mild: nausea, abdominal pain, dry mouth, lightheaded mess, dizziness, insomnia,
34
Indirect dopaminergic therapy: amantadine
Release of dopamine from the storage sites at the end of nerve cells that are still intact
35
Indirect dopaminergic therapy: amantadine also blocks
The reputable of dopamine into the nerve endings
36
Indirect dopaminergic therapy: amantadine does not
Stimulate dopamine receptors directly
37
Indirect dopaminergic therapy: amantadine may help with
Levodopa induced dyskinesias
38
Direct acting dopaminergic therapy
DA receptor agonists -directly stimulate dopamine receptors
39
What is the first line treatment for PD in younger patients, mild/moderate symptoms, reduce wearing off effect, less effective than levodopa
Dopaminergic therapy
40
Anticholingeric drugs do not relieve
Bradykinesia