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BCN Exam 3 > Anti-Parkinson's Drugs > Flashcards

Anti-Parkinson's Drugs Flashcards

1
Q

What percent of dopamine neurons have been lost before the symptoms of Parkinsons (PD) appear?

A

70-80%

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2
Q

What are the symptoms of Parkinsons Disease (PD)?

A

Tremor at rest

Bradykinesia (slow movements), difficulty starting movements, rigidity, short fast steps, small handwriting, blank face

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3
Q

The subtantia nigra supplies what structures with dopamine?

A

Straitum (Caudate and putamen)

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4
Q

Why is L-Dopa preferred over pure dopamine to give to a pt ?

A

L-Dopa crosses the BBB much more easily than dopamine

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5
Q

What occurs when D1 receptors are activated?

A

Inc cAMP and stimulates the direct pathway (putaminal/GABA/substance P/dynorphin) that project to medial globus pallidus

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6
Q

What occurs when D2 receptors are activated?

A

Dec cAMP, inhibits the indirect pathway (putaminal GABA/enkephalin) thta projects to lateral globus pallidus

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7
Q

Which dopamine neuron plays the major role in PD therapy?

A

D2

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8
Q

What are the characteristics of Levodopa?

A

Rapid symptomatic benefits, well tolerated, continues to work throughout the disease course, usually combined with carbidopa

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9
Q

Why is carbidopa used in conjunction with levodopa?

A

Allows the largest amount of levodopa to become dopa as possible (keeps the levodopa from entering and be digested by the GI system)

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10
Q

What are the side effects of Levodopa?

A

Not effective for gait imbalance, freezing, or postural instability, N&V, hallucination, illusions, somnolence, edema, compulsions

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11
Q

What is the levodopa sparing strategy used in early PD?

A

The younger the pt, avoid using levodopa so they do not develop complications sooner
Start with a dopamine agonist, amantadine, or anti-cholinergic

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12
Q

At what age can you start a person with PD on levodopa?

A

65 or older

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13
Q

What are the positive effects of dopamine agonists?

A

Effective for tremor, rigidity, and bradykinesia
Action largely via activation of striatal DR receptors
More protective against motor flux and dyskinesias

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14
Q

Which treatment has the shortest half life?

A

L-dopa

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15
Q

What are the characteristics of pramipexole?

A

8-12 hr half life, renal clearance, 1.5-4.5 mg/day

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16
Q

What are the characteristics of ropinirole?

A

4-6 hr half life, hepatic clearance, 3-24 mg/day

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17
Q

What are the dopamine agonists?

A

Bromocriptine (1980), pramipexole, and ropinirole (1997, non-ergots)

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18
Q

Where are the dopamine agnoists for bromocroptine?

A

D2 and partial D1

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19
Q

Where are the dopamine agnoists for pramipexole?

A

Non-ergoline at D3 > D2

20
Q

Where are the dopamine agnoists for ropinirole?

A

Non-ergoline at D2 > D3

21
Q

Where are the dopamine agnoists for rotigotine?

A

Mostly D2 (but also 3,4, and 5)

22
Q

What are the benefits to dopamine agonists?

A

Stimulates dopamine receptors directly, independent of dopamine terminal function, reduces risk for dyskinesia, no effected by diet protein, delays motor complications

23
Q

What are the characteristics of Levodopa?

A

Rapid symptomatic benefits, well tolerated, continues to work throughout the disease course, usually combined with carbidopa, crosses BBB

24
Q

What are the positive effects of dopamine agonists?

A

Effective for tremor, rigidity, and bradykinesia, long half life
Action largely via activation of striatal D2 receptors
More protective against motor flux and dyskinesias

25
Q

What are the limitations of dopamine agonists?

A

Careful titration of doses, N&V, hallucinations, illusions, somnolence, edema, compulsions

26
Q

What is the downside to dopamine agonists?

A

Less effective than levodopa, ineffective for gait imbalances, freezing, and postural instability
More sedating and neurophyschotic

27
Q

What are the side effects of L-dopa?

A

Development of motor complications within 5 years of disease

Dyskinsia and Dystonia, motor fluctuations

28
Q

How can you extend the benefit of levodopa?

A

Inc dose per admin

Add dopamine agnoist, monoamine oxidase B inhibitor, catechol-O-methyl transfer inhibitor

29
Q

What are the levodopa and DA metabolism inhibitors for PD treatment?

A

Levodopa, carbidopa, tolcapone, selegiline

30
Q

Describe parcopa.

A

Carbidopa/levodopa combo

Dissolves orally w/o water, tastes minty, can be taken as a booster, and should be taken upon waking up

31
Q

What is the monoamineoxidase-B (MAO-B) inhibitor?

A

Selegiline

32
Q

what is the function of a MAO-B inhibitor?

A

Inhibits dopamine metabolism, enhances L-dopa transport, produce a small benefits alone, metabolized to amphetamine and methamphetamine, possible neuoprotection

33
Q

What is a side effect of selegiline?

A

Motor complications

34
Q

What is rasagiline?

A

An irreversible inhibitor of MAO-B, selectively inhibits enzyme that metabolizes dopamine
Enhances L-dopa, possible neuroprotection

35
Q

What does the inhibiton of COMT do in PD?

A

(Entacapone)

Extends duration of L-dopa (doesn’t raise levels), dopaminergic diarrhea, urine discoloration, not so hepatotoxic

36
Q

What is the role of COMT in the body?

A

Converts L-dopa and dopamine to 3-OMD

37
Q

Describe amantadine.

A

Enhances synthesis, release or reuptake of dopamine from surviving neurons
Reduces dyskinesia

38
Q

What are the three antimuscarinic agents?

A

Benztropine, trihexyphenidyl, biperiden

39
Q

What are the adverse effects of antimuscarinic agents?

A

Dry mouth, intraocular pressure, interference with GI peristalsis

40
Q

What was amantadine originally made for?

A

As an antiviral to protect for influenza type A

41
Q

What are some side effects of amantadine?

A

Ankle edema, livedo reticularis, and confusion/hallucinations

42
Q

Describe apomorphine.

A

High affinity for D4 (also 2,3,5 at receptors), very potent, short acting (60 min), needs to be injected

43
Q

What are the side effects to the apomorphine injection?

A

Dyskinesia, nausea, skin irritation, low blood pressure

44
Q

What is deep brain stimulation?

A

Surgical treatment for PD, creates a mini lesion using electrical stimuation

45
Q

What are the targets for deep brain stimulation?

A

Lateral globus pallidus and subthalamic nucleus

BCN Exam 3 (8 decks)

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