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Nervous System > Dopamine Systems - 29 > Flashcards

Dopamine Systems - 29 Flashcards

1
Q

What is Dopamine?

A

A Monoamine neurotransmitter

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2
Q

What does dopamine do?

A

Translates thoughts into action : decision making, goal directed behavior, movement : affects mood

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3
Q

What are the pathways of the brand for Dopamine?

A

Mesocortial, Mesolithic, Nigrostriatal, Tuberoinfundibular, Chemoreceptors trigger zone

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4
Q

What is the Mesocortical pathway in control of?

A

Cognition

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5
Q

What is the Mesolithic pathway in control of?

A

Integration of emotional responses; “complex reward-oriented behavior”

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6
Q

What is the Nigrostriatal pathway in control of?

A

Motor; planning and execution; “automated behaviors”

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7
Q

What is the Tuberoinfundibular pathway in control of?

A

Inhibits prolactin release and regulates growth hormone release from the pituitary

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8
Q

What is the chemoreceptors trigger zone in control of?

A

Gag/vomit reflex - nausea

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9
Q

Where is dopamine synthesized?

A

In the pre-synaptic terminals

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10
Q

Where is dopamine stored?

A

In vesicles of the pre-synaptic terminals

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11
Q

What controls the release of dopamine?

A

Action potentials

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12
Q

What kind of receptors are dopamine receptors?

A

GPCRs

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13
Q

Are dopamine receptors excitatory or inhibitory?

A

They can be either

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14
Q

What does the dopamine transporter do?

A

Removes dopamine from the synapse for repackaging/use

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15
Q

What are the molecules of the dopamine pathway?

A

Tyrosine, L-DOPA, Dopamine, DOPAC, HVA

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16
Q

What are the enzymes of the Dopamine pathway?

A

Tyrosine hydroxylase, DOPA Decarboxylase, MAO, COMT

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17
Q

What are the steps of the Dopamine pathway?

A

Tyrosine (Tyrosine Hydroxylase) L-DOPA (DOPA Decarboxylase) Dopamine (MAO) DOPAC (COMT) HVA

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18
Q

What happens if you delete the Dopamine Transporter?

A

You’d have more dopamine in the clefts/increased motor activity

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19
Q

What is Parkinson’s Disease?

A

A neurodegenerative disease resulting from a loss of dopamine neurons

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20
Q

What would you notice in a brain with Parkinson’s?

A

Lack of pigmentation in the Substantia Nigra (no oxidation of dopamine)

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21
Q

What motor features do Parkinson’s Disease patients have?

A

“TRAP” : Tremor (when at rest) : Rigidity : A(Brady)kinesia (absense of movement) : Postural instability :::: Also, trouble swallowing, difficulty initiating walking, “masked” facial expressions

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22
Q

Does Parkinson’s Disease decrease life expectancy?

A

NO, but increased accidental death

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23
Q

What are some NON-motor symptoms of Parkinson’s?

A

Depression/anxiety, pain, speech/swallowing problems, sleep disturbances, autonomic symptoms

24
Q

What are examples of “autonomic symptoms” of Parkinson’s?

A

Constipation, orthostasis (lightheaded upon standing), sexual dysfunction, sweating abnormalities

25
Q

Who gets Parkinson’s?

A

1-2% over 65, 3-5% over 85; ~4% <50yrs

26
Q

Is there an increased risk of PD in relatives?

A

Slight increase in first-degree relatives

27
Q

T/F All cases of Parkinson’s Disease are related to an identified single gene

A

F - <10% of cases are related to an identified single gene

28
Q

What are environmental causes of Parkinson’s?

A

pesticides, head injury, infection, MPTP, Manganese (may be viral/bacterial!!!)

29
Q

What are some things that decrease the risk of Parkinson’s?

A

Smoking, and Caffeine

30
Q

What are the genetic causes of Parkinson’s Disease?

A

Increased risk in family members, multiple genetic risk factors

31
Q

How do we treat Parkinson’s?

A

Treat the symptoms. Improve function/QoF. Replace brain dopamine (give L-Dopa)

32
Q

What can you do to slow/reverse the effects of Parkinson’s?

A

There is no known treatment to slow or reverse the progression of Parkinson’s

33
Q

What things can PD treatment help with?

A

Treat bradykinesia/rigidity, tremor, sometimes postural/gait treated

34
Q

What drug is given to replace Dopamine?

A

L-DOPA (Levodopa)

35
Q

Why cant we just give Dopamine instead of the precursor?

A

Dopamine will be broken down in the periphery before getting into the brain.

36
Q

What treatments are there that are aimed at the dopamine system?

A

Replace Dopamine : Enhance Dopamine : Dopamine receptor agonists

37
Q

How do you enhance Dopamine?

A

Prevent the conversion of L-DOPA to Dopamine in the periphery (Dopamine cant pass BBB)

38
Q

What drugs “enhance dopamine”?

A

Carbidopa, Entacapone, Rasagiline, Selegiline, and Low dose cocaine

39
Q

What is the name for the drug that combines Carbidopa and Levodopa? Why would you do this?

A

Sinemet; Carbidopa stops the breakdown of L-DOPA in the periphery, and Levodopa IS L-DOPA

40
Q

What is an example of a dopamine receptor agonist?

A

Pramipexole

41
Q

What effects does Levodopa have?

A

CNS effects: Reduced bradykinesia/rigidity, antidepressant ::: Endocrine effects: decreased prolactin release ::: GI: Nausea/vomiting (take w/ food) ::: CARDIOVASCULAR SYSTEM: Orthostatic hypotension, cardiac stimulation

42
Q

How do the motor complication of Parkinson’s progress from early to advanced?

A

Early: Long-duration of L-DOPA effect with little dyskinesias ::: Moderate: Short-duration of effect with some dyskinesias ::: Advanced: Short-duration with consistent dyskinesias

43
Q

What are some of the Pros and Cons to using a Dopamine Receptor Agonist?

A

Lasts longer than Levodopa (smooths wearing off feeling when used together); More side effects

44
Q

What are some side effects of Dopamine Receptor Agonists?

A

Sleep attacks, Impulse Control Disorders (compulsive gambling…)

45
Q

What are som “other Pharmacological approaches” to PD?

A

Benztropine (Cogentin) and Amantadine (Symmetrel)

46
Q

What is Benztropine?

A

Cogentin; Muscarinic antagonist : cognitive side effects/fatigue

47
Q

What is Amantadine?

A

Symmetrel; antiviral; increases dopamine release/reduces reuptake

48
Q

What is the most modern treatment for Parkinson’s? When is it used?

A

Deep Brain Stimulation : when pharmacological therapies fail

49
Q

Contraindications for Deep Brain Stimulation:

A

Cognitive impairment; postural instability; uncontrolled depression

50
Q

What is Huntington’s Disease?

A

Neurodegenerative disorder: Genetic disease

51
Q

What inheritance is there for Huntington’s?

A

Autosomal dominant: Trinucleotide repeat on Chromosome 4

52
Q

When does Huntington’s onset?

A

Between 20-40

53
Q

What are some characteristics of Huntington’s?

A

Demonstrates anticipation; Psychiatric disturbances (1st); Chorea; dystonia; dementia/DEATH

54
Q

What is Chorea?

A

Jerky/involuntary movements of the shoulder/hips/face

55
Q

What are some psychiatric symptoms of Huntington’s?

A

Depression, psychosis, bipolar

56
Q

How do we treat Huntington’s?

A

Treat Chorea with Dopamine ANTAGONISTS ::: Treat bradykinesia/rigidity with Dopamine AGONISTS

57
Q

What are the main dental implication of Huntington’s and Parkinson’s?

A

Exam difficulty, hygiene, and drug interactions

Nervous System (10 decks)

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