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Pharmacology II Quiz 6 > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

0
Q

Classic primary symptoms of PD

A

Tremor
Rigidity
Bradykinesias

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1
Q

Cause of Parkinson’s Disease (PD)

A

Changes in the substantia nigra and striatum occur and decreased levels dopamine are a result.

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2
Q

MOA PD

A

Dopamine disappears in presynaptic terminal and post synaptic cleft.

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3
Q

PD Drug therapy aims to

A

Increase amount of dopamine in the CNS

Decrease acetylcholine levels or block acetylcholine

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4
Q

When dopamine decreases acetylcholine…

A

… increases

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5
Q

How do you decide pharmacological therapy for PD?

A

Note nothing provides neuroprotection.

Choose either Levodopa or dopamine agonist.

Levodopa predominates in the market and is the “old” one in the crowd.

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6
Q

Levodopa is never prescribed…

A

… by itself.

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7
Q

What are the keys to managing PD therapy

A

Individualized - Provider’s judgement.

No therapy is disease-modifying. It will continue to progress as it is a progressive disease.

When to initiate:

- A diagnosis or symptom manifestation? - When you have a definitive diagnosis.
- Levodopa- start early or delay? -
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8
Q

Why wouldn’t you start Levodopa too early?

A

Levodopa must turn into Dopamine (A to B) and throws off extra electrons causing damage to surrounding tissues. If you start therapy early and buy the theory of free radical formation it could quite possible make PD worse.

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9
Q

Dopamine Precurser Class Drug

A

L-Dopa

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10
Q

MOA of Levodopa

A

Levodopa passes the blood brain barrier (Dopamine cannot!) into the CNS and brain where it needs to work.

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11
Q

What percentage of Levodopa ends up in the brain?

A

1-3%

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12
Q

Where does metabolism of levodopa occur?

A

Outside CNS

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13
Q

How can you improve Levodopa penetration into the brain?

A

Make the dose smaller - 10% can enter the brain and less metabolism occurs in the GI tract or peripheral tissues (toxicity).

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14
Q

How is the extended release tablet of Levodopa absorbed?

A

Extended release is less completely absorbed.

Start with immediate release then review options for combined therapy.

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15
Q

What is notable about discontinue Levodopa (dopamine precurser)?

A

Abrupt withdrawal may result in neuroleptic malignant syndrome.

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16
Q

Immediate release Levodopa may cause…

A

… waxing and waning.

Motor fluctuations, dyskinesias, abnormal cramps/postures (dystonia)

Good days vs bad days which is due to progressive degeneration of dopamine terminals.

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17
Q

To decrease waxing and waning…

A

… you can add immediate release Levodopa to the extended release Levodopa.

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18
Q

Adverse Drug Reactions of Levodopa

A

Nausea

Somnolence, dizziness, headache.

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19
Q

Older patients on levodopa may experience…

A

… confusion, hallucinations, delusions, agitation, psychosis.

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20
Q

Does Levodopa cause neurotoxicity?

A

Possibly

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21
Q

Dopamine Precursor class drug

A

Levodopa/carbidopa

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22
Q

Levodopa/carbidopa

A

Levodopa/carbidopa
X/X dose (variable)
every 8 hours

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23
Q

Dopamine Agonists

A

Pramipexole (Mirapex)
Ropinirole (Requip)
Rotigotine (Neupro)

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24
Q

On the prescription for levodopa/carbedopa the smaller number is for …

A

carbedopa

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25
Q

Which dopamine agonists comes as a patch?

A

Rotigotine (Neupro)

26
Q

MOA of dopamine agonists

A

Exploit structure activity relationship.

Molecules look like dopamine and pass through the blood brain barrier.

NOT DONE - COMPLETE

27
Q

Choice agent of dopamine agonists

A

Dopamine agonist patients more likely to develop side effects when compared to levodopa use - Pt more likely to discontinue therapy.

28
Q

Do dopamine agonists have withdrawal syndrome?

A

Yes - same as dopamine precurser.

29
Q

ADRs of Dopamine Agonists

A 
Postural hypotension
Hallucinations
Nausea
Somnolence
Worsen dyskinesias

Unique side effect: Induces compulsive behavior.

- Pathologic gambling.
- Compulsive shopping.
- Compulsive sexual behavior.
30
Q

Requip XL

A

Requip XL
12 mg
two tablets once a day

31
Q

Dopamine Agonist class drug

A

Requip XL

32
Q

MAO-B inhibitors

A

Rasagiline (Azilect)

Selegeline (Eldepryl)

33
Q

MOA of MAO-B inhibitors

A

MAO-B can break down dopamine products. If you inhibit MAO-B free-floating dopamine is less likely to be broken down.

Inhibition of enzyme MAO-B.
More dopamine available to support nerve transmission.

34
Q

Does MAO-B monotherapy reduce disease progression?

A

By themselves they do not have the same effect as other products (dopamine precursors, dopamine agonists).

Is this a neuroprotective agent? Maybe? No one can prove it occurs but some clinicians try to add it on early as it is a complimentary agent.

35
Q

Do MAO-B inhibitors increase cancer risk?

A

Increased cancer risk accompanies Parkinson’s - probably not the drug.

36
Q

Drug interactions for MAO-B inhibitors

A

Tramadol
Methadone
Cyclobenzaprine
St.John’s Wart

MAO-B increases drug effect of these drugs as they are not metabolized and can cause toxicity.

37
Q

ADRs of MAO-B inhibitors

A

Insomnia, nervousness confusion
Nausea
Orthostatic hypotension

38
Q

When should you take your MAO-B? Soledjeline

A

Morning and Lunchtime

39
Q

MAO-B inhibitor class drug

A

Azilect

40
Q

Azilect

A

Azilect
1 mg
once daily

41
Q

What does Amantadine do?

A 
Old drug - no one really does research on it and it may...
increase dopamine release
inhibit dopamine reuptake
stimulate dopamine receptors
etc...
42
Q

Kinetics of Amentidine

A

Renal dose adjustment with lowest level dosing at 200 mg every 7 days

43
Q

Benefits of Amantidine

A

Transient
Short-term treatment in mild disease
Temporary “add-on” in advance Parkinsons

Not used in frontline therapy.

44
Q

If the PD patient’s primary complaint is rigidity prescribe…

A

Amentidine

45
Q

ADRs of Amentidine

A

Pretty well toelrated with low sie effect profile:
-CNS: Confusion, hallucinations, nightmares. Caution with patients with pre-existing psychiatric diagnoses.
Anke edema
Livedo
NOT DONE

46
Q

Amantadine

A

Amantadine
100 mg
Twice a day

47
Q

Anticholinergics

A

Benztropine (Cogentin)

Trihexyphenidyl (Artane)

48
Q

MOA of anticholinergics

A

Blocks acetylcholine receptor.

49
Q

What must you dopamine and acetylcholine levels?

A

Level them out. As dopamine decreases you must decrease acetylcholine.

50
Q

Anticholinergics work well when trying to…

A

… control tremor.

51
Q

Be careful using anticholinergics when…

A

… the pt has a CV condition.

52
Q

Anticholinergics are good for…

A

Slow resting tremor.

Monotherapy in patients less than 70 yo with no significant akinesia or gait disturbance.

53
Q

ADRs of anticholinergics

A

Tachycardia
Constipation, urinary retention
Hypotension
CNS effects such as disorientation, hallucinations, toxic psychosis

54
Q

Anticholinergic class drug

A

Trihexyphenidyl

55
Q

Trihexyphenidyl

A

Trihexyphenidyl
2 mg
XXXXX

56
Q

COMT inhibitors MOA

A

Stop COMT from breaking down dopamine

57
Q

COMT Inhibitors

A

Tolcapone (Tasmar)

Entacapone (Comtan)

58
Q

COMTs are always combined with…

A

.. Levodopa.

59
Q

When do you use a COMT inhibitor?

A

Always an addition to levodopa/carbidopa.

Assist when motor fluctuations; “off” periods

60
Q

ADRs of COMT inhibitors

A

Heightened reactions from levodopa/carbidopa

Historic issue with hepatotoxicity

61
Q

Practice parameters for Parkinson’s Disease from American Academy of Neurology

A

Reduction of “off” time: use rasagiline, entacapone, pramipexole, Ropinirole.

No one agent is better than the others.

Dyskinesias? Consider amantadine.

Levodopa does not appear to accelerate disease progression.

No treatments are neuroprotective.

No evidence that vitamins can improve motor function.

Exercise may help improve motor function, speech therapy may improve speech volume.

62
Q

Treatment of depression, psychosis, and dementia in Parkinson disease:

A

Screening tools should be used for detection of depression.

Screening tools should be used for detection of dementia.

Pharmacology II Quiz 6 (5 decks)

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