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Neuro Med > Exam 6: Basal Ganglia Pharmacology > Flashcards

Exam 6: Basal Ganglia Pharmacology Flashcards

1
Q

What is an example of a hypokinetic disorder

A

Parkinson disease

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2
Q

What is an example of hyperkinetic disorder

A

Huntington’s disease

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3
Q

What is progressively lost in parkinson disease

A

Progressive loss of dopaminergic neurons in substantia nigra pars compacta

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4
Q

What does less dopamine in the striatum result in?

A

Decreased direct pathway activity, increased indirect pathway activity, lose coordinated direct/indirect activity. Marked increase in inhibition of thalamus, reduced excitation of motor cortex

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5
Q

What are the genetic components of Parkinson disease?

A

alpha-synuclein (SNCA), LRRK2, parkin, others

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6
Q

What are symptoms of parkinson disease?

A

Bradykinesia, muscle rigidity, resting tremor, impair postural balance

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7
Q

What is the current therapeutic strategy for parkinson’s disease?

A

treat symptoms only, restoring dopaminergic activity

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8
Q

Why can’t you treat PD patients with dopamine?

A

It does not cross the BBB

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9
Q

T/F: Levodopa is a prodrug

A

True

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10
Q

What converts levodopa to dopamine?

A

L-aromatic amino acid decarboxylase (AAAD)

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11
Q

Why does only 5% of levodopa enter the CNS?

A

Significant AAAD activity in GI tract

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12
Q

What can high levels of peripheral dopamine cause?

A

nausea, orthostatic hypertension

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13
Q

What is the action of carbidopa?

A

inhibits AAAD in the periphery, reducing levodopa dose by nearly 75%

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14
Q

What is Levodopa and Carbidopa called in compound?

A

Sinemet

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15
Q

What is the mechanism of levodopa

A

Activates D1 receptors (activates direct pathway), Acivates D2 receptors (inhibits indirect pathway)

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16
Q

When is levodopa most effective in the progression of PD?

A

early in therapy

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17
Q

What is the overall effect of levodopa on a PD patients disease?

A

decreased akinesia, rigidity, and tremor

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18
Q

Why is levodopa less effective over time?

A

progressive loss of dopaminergic neurons

19
Q

Describe the interaction of L-DOPA and presynaptic neurons

A

store in presynaptic dopaminergic terminals of striatum and released gradually

20
Q

What can occur with treatment of L-DOPA as dopaminergic neurons are lost?

A

dyskinesia

21
Q

What are dyskinesias?

A

abnormal involuntary movements

22
Q

When do “on period dyskinesia” occur?

A

During times of peak dose (high plasma levels of levodopa) with maximal antiparkinsonian relief

23
Q

When does diphasic dyskinesia occur while dosing levodopa?

A

onset and offset of the levodopa effect coinciding rising and falling plasma levodopa levels

24
Q

What occurs in diphasic dyskinesia?

A

repetitive, slow movements of the lower limbs often coinciding with tremor in the upper limbs

25
Q

What occurs during “off” period dystonia?

A

fixed and painful postures more frequently affecting the feet

26
Q

What occurs during “on” period dyskinesia

A

brief, abrupt, irregular, unpredictable movements (chorea) predominantly involving the neck, trunk and upper limbs

27
Q

What can be done to decrease the “wearing off phenomenon”

A

increase dose, decrease dosing interval, add COMT inhibitor

28
Q

What are adverse effects of levodopa

A

confusion, anxiety, agitation, insomnia, nightmares, depression, psychotic reactions, orthostatic hypotension, nausea, vomiting, anorexia

29
Q

What drug decreases peripheral metabolism of levodopa by COMT?

A

COMT inhibitor: entacapone

30
Q

What does entacapone do in terms of levodopa effects?

A

smoother response, more prolonged “on” time

31
Q

What are adverse effects related to with entacapone treatment?

A

adverse effects are related to increased plasma L-DOPA

32
Q

What class of monoamine oxidase enzymes do we target with MAOIs. What does it do? What is an example?

A

MAO-B, which primarily metabolized dopamine. Selegiline

33
Q

When is treatment with MAOIs useful?

A

effective early in PD as monotherapy or combined with L-DOPA

34
Q

what is the benefit of using a dopamine receptor agonist?

A

bypasses the conversion of L-DOPA to dopamine

35
Q

What are the adverse effects of dopamine receptor agonists? What helps to lower these effects?

A

response fluctuations, dyskinesia, lower with L-DOPA therapy

36
Q

What are examples of dopamine receptor agonists?

A

Pramipexole, ropinirole

37
Q

T/F: muscarinic antagonists be used to treat PD? Example?

A

True; atropine

38
Q

What is the known mechanism of amantadine (symmetrel)

A

antiviral; NMDA receptor antagonist, decrease release/reuptake of dopamine, antimuscarinic

39
Q

What are adverse effects of amantadine (symmetrel)?

A

agitation, confusion, excitement, restlessness, insomnia, halucinations

40
Q

What are surgical interventions of PD?

A

pallidotomy- alleviates akinesia, rigidity, and drug-induced dyskinesia; thalamotomy- ameliorates tremor

41
Q

What are symptoms of Huntington’s disease?

A

Hyperkinetic disorder; uncontrolled rapid, jerky movements

42
Q

What is the etiologic mechanism of Huntington’s disease?

A

degeneration of striatal neurons projecting to GPe; leads to: increased GPe activity (GABA), decreased STN nucleus activity (glutamate), decreased GPi activity (GABA), loss of thalamic inhibition, increased thalamic excitatory drive

43
Q

What are the genetic problems of Huntington’s?

A

expanded CAG (polyglutamine) repeats in huntington gene, autosomal dominant neuronal degeneration resulting in death in 10-20 years

Neuro Med (39 decks)

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