Neurodegenerative Flashcards

1
Q

Parkinson’s Disease is a neurodegenerative disorder of the extrapyramidal system associated with neurotransmission of the balance of ____ and ____ in the striatum

A

dopamine and acetylcholine (ACh)

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2
Q

Pramipexole (Mirapex)

Mechanism of action

A

Dopamine agonist

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3
Q

Levodopa/carbidopa (Dopar) (Sinemet)

Mechanism of action

A

Dopamine precursor

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4
Q

Entacapone (Comtan)

Mechanism of action

A

Blocks COMT (enzyme that breaks down L-Dopa)

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5
Q

What is the most effective drug for Parkinson’s and what is the biggest downside of it?

A

Levodopa is most effective, but long-term use carries a higher risk for disabling dyskinesias

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6
Q

What is levodopa given in combination with?

A

Carbidopa

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7
Q

What is an important food-drug interaction for Levodopa?

A

Neutral amino acids compete with levodopa for intestinal absorption and for transport across the blood-brain barrier. High protein foods will reduce therapeutic effects

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8
Q

What does carbidopa reduce the incidence of?

A

-Adverse cardiac effects
-Nausea/vomiting

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9
Q

Levodopa

Adverse effects

A

-Orthostatic hypotension
-Dyskinesias
-Psychosis
-Nausea/vomiting
-Sudden “off phenomenon”

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10
Q

What helps with the “off phenomenon” in with Levodopa?

A

Can be reduced with dopamine agonists, COMT inhibitors

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11
Q

Levodopa/carbidopa drug interactions

A

First generation antipsychotics

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12
Q

What does carbidopa do?

A

Increases available levodopa in the CNS and allows for 75% decrease in levodopa dosage, therefore it reduces cardiovascular and GI adverse effects

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13
Q

How long does it take for Parkinson’s drugs to take effect?

A

Up to a month

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14
Q

Pramipexole (Mirapex)

Adverse effects

A

-Nausea
-Dizziness
-Daytime somnolence
-Rare instances of “sleep attacks”

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15
Q

What is the pathophysiology of Alzheimer’s?

A

Degeneration of neurons
-Early in the hippocampus
-Later in the cerebral cortex

Reduced cholinergic transmission
-Levels of ACh 90% below normal

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16
Q

What are risk factors for AD?

A

-Age
-Family history
-Female
-Head injury
-Low educational level
-Production of apoE4
-Estrogen/progestin therapy
-Tobacco use
-Sedentary lifestyle

17
Q

How is AD diagnosed?

A

-One episodic memory impairment
-One AD biomarker (MRI, PET scan)

18
Q

What is the goal of drug therapy in AD?

A

Drugs make the neurons that are still functional work a little better for a period of time

19
Q

How well do AD drugs work?

A

Drugs yield improvement that is statistically significant but clinically marginal

20
Q

______ inhibitors may delay or slow progression of the AD but will not stop it

A

Cholinesterase

21
Q

Cholinesterase inhibitors

Drug interactions

A

Drugs that block cholinergic receptors reduce the response to cholinesterase inhibitors - antihistamines, TCAs, conventional antipsychotics

22
Q

Cholinesterase inhibitors

A

Donepezil (Aricept) and Rivastigmine (Exelon)

23
Q

Patch prescribed for AD

A

Rivastigmine

24
Q

AD drugs - Cholinesterase inhibitors - Donepezil and Rivastigmine

Adverse effects

A

Bradycardia (uncommon)
Orthostatic hypotension (uncommon)
GI
Dizziness
Headaches

25
Q

Memantine (Namenda)

Mechanism of action

A

NMDA receptor antagonist

26
Q

Memantine (Namenda)

Indication

A

Moderate to severe AD

27
Q

Drugs for neuropsychiatric symptoms in AD

A

atypical antipsychotics - Risperidone (Risperdal) and olanzapine (Zyprexa)