CNS Meds: Parkinson's Disease Flashcards

1
Q

Describe how Parkinson’s disease (PD) affects the body

A
  • PD progressively affects a person’s ability to control movement
  • PD also negatively impacts how a person feels, thinks, sleeps, and talks.
  • Common symptoms

tremors, bradykinesia (slow movement), stiff muscles, stooped posture, etc.

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2
Q

Recall the effects of dopamine in the brain

A
  • reward
  • pleasure, euphoria
  • motor function **
  • compulsion
  • perservation
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3
Q

Explain the role of the striatum in the brain

A

Corpus striatum is a part of the basal ganglia of the brain and coordinates movement of the body

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4
Q

Recite 2 parts of the brain that send information to the striatum

A

Striatum receives information from 2 sources:

neocortex & substantia nigra

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5
Q

Identify the part of the brain that delivers dopamine to the striatum

A

Substantia nigra

Substantia nigra neurons are an important source of dopamine for striatum

In PD, the neurons connecting the substantia nigra die – cutting off dopamine supply!

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6
Q

Describe the non-motor symptoms that a dopamine deficit causes

A

autonomic disturbances (quite a lot!)
depression
psychosis and dementia
flat affect

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7
Q

Discuss the neurotransmitter imbalance that leads to the symptoms of Parkinson’s disease

A

Parkinson’s is essentially imbalance!

Imbalance between dopamine (DOPA) and acetylcholine (Ach) in the brain –> not enough dopamine

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8
Q

Why dopamine is not directly given to Parkinson’s patients

A

Dopamine cannot cross the blood brain barrier

We can only give drugs that help increase dopamine levels in the brain or act like dopamine in the brain –> there are 6 types of Parkinson’s Drugs!!!

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9
Q

Explain how monoamine oxidase type B (MAO-B) inhibitors help restore dopamine levels

A

There will be less MAO-B
–> we can conserve dopamine in the brain

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10
Q

Explain how N-methyl-D-aspartate (NDMA) glutamate inhibitors help restore dopamine levels

A

NMDA-type glutamate blocker will block the action of glutamate to increase dopamine release

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11
Q

Explain how dopamine agonist inhibitors help restore dopamine levels

A

mimic dopamine and binds to dopamine receptors of neurons

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12
Q

Explain how dopamine prodrugs help restore dopamine levels

A

Levodopa (prodrug) can cross BBB and replaces missing dopamine in the brain

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13
Q

Explain how carbidopa decarboxylase inhibitors help restore dopamine levels

A

Carbidopa works by preventing levodopa from being broken down before it reaches the brain

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14
Q

Explain how catechol-O-methyltransferase (COMT) inhibitors help restore dopamine levels

A

COMT inhibitors act by blocking the action of enzymes that break down levodopa and extending the duration of its action in the brain

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15
Q

Explain how anticholinergics help restore dopamine levels

A

Anticholinergics block the activity of Ach

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16
Q

Select the best drug class for treating mild PD symptoms

A

MAO-B inhibitor

***conserve what you already have!

17
Q

Select the drug class that is most effective for more severe PD symptoms

A

L-DOPA (combined with carbidopa)

Dopamine agonist

***when the symptoms get severe, we want to make more dopamine available!

18
Q

How to manage times when medications “wear off” in Parkinson’s disease

A

“Off times” can be reduced with:

  • dopamine agonists
  • COMT inhibitors
  • MAO-B inhibitors
19
Q

Explain how levodopa increases dopamine levels in the brain of patients with Parkinson’s disease (PD)

A

Levodopa can cross BBB by active transport system in the brain
–> neurons in the striatum will uptake the levodopa
–> levodopa converted to dopamine in the striatum

20
Q

Describe how carbidopa can maximize the effect of levodopa

A

Levodopa and carbidopa are like French fries & ketchup–they are better together!!

Although carbidopa cannot cross BBB, it can slow down the breakdown (decarboxylation) of levodopa in intestines
–> more L-DOPA can cross BBB, carbidopa reduces dosage of L-DOPA by 75%

21
Q

Tell how the effects of levodopa and carbidopa change over time

A

Sadly, they are effective for the first 2 years, then decline after 3-5 years

22
Q

Recall a common side effect of levodopa and carbidopa use

A

Patients can develop dyskinesia…

23
Q

What do you need to teach patient and family when taking levodopa and carbidopa

A

Not to eat high protein meals with the medication

***dietary protein compete for protein transport across BBB

24
Q

List CNS side effects of PD meds

A
  • anxiety, agitation
  • difficulty with memory or higher level thinking
  • difficulty sleeping
  • psychosis, hallucination
25
Q

List behavioral side effects of PD meds

A
  • impulsiveness
  • loss of moral compass
  • gambling, over-eating, alcohol abuse, etc.
26
Q

List cardiovascular side effects of PD meds

A

risk of orthostatic hypotension (take adequate fluid and salt!)

irregular heartbeat or “fluttering (palpitation)”

27
Q

Tell how levodopa affects the gastrointestinal (GI) tract

A

nausea and vomiting

**dopamine receptors on medulla get activated

28
Q

Recall how levodopa and carbidopa affect the genitourinary (GU) system and skin

A

It can darken saliva, sweat, or urine

Also, it can active malignant melanoma –> patients should be screened for skin cancer regularly

29
Q

List ways in which PD medication side effects can be reduced

A
  • working with healthcare provider to adjust dosage
  • take amantadine
  • deep brain stimulation
30
Q

List two dangerous drug interactions of levodopa, as well as its beneficial drug interaction

A

Dangerous: first generation antipsychotics, MAO inhibitors

Beneficial: anticholinergic medication

31
Q

Describe the reasons it can be dangerous to administer 1st-generation antipsychotics with levodopa

A

FGA will block dopamine receptors in the striatum –> decrease therapeutic effects of L-DOPA.

32
Q

Identify the potential risk of combining levodopa with monoamine oxidase inhibitors (MAOIs)

A

risk of developing hypertensive crisis