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Dynamics II > Neurodegenerative Disorders > Flashcards

Neurodegenerative Disorders Flashcards

1
Q

What are neurodegenerative disorders characterized as?

A

the progression and the irreversible loss of neurons in specific regions

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2
Q

What is selective vulnerability?

A

the idea that there are specific neurons in the brain that cause specific neurodegenerative disorders

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3
Q

Where are the neurons that are affected in PD?

A

neurons in the substantia nigra

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4
Q

Where are the neurons that are affected in AD?

A

neurons in the hippocampus and the neocortex

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5
Q

Where are the neurons that are affected in HD?

A

neurons in the neostriatum

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6
Q

Where are the neurons that are affected in ALS?

A

spinal cord and cortical neurons

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7
Q

What are the two common cellular mechanisms in neurodegenerative disorders?

A
  1. misfolded proteins
  2. excitotoxicity
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8
Q

What is excitotoxicity?

A

excessive amount of glutamate that causes cell death

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9
Q

What is Parkinson’s Disease?

A

neurodegenerative disorder that has an increase in lew body structures (misfolded alpha-synuclein) in the substantia nigra that causes the loss of coordination and problems with movement

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10
Q

What are the symptoms of PD?

A

“TRAP” T-tremors, R-Rigidity, A-Akinesia, P-postural instability

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11
Q

What is the etiology of PD?

A

loss of dopamine, which leads to less inhibition of Ach , which causes abnormal signaling which causes an imbalance of impaired mobility

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12
Q

What is the goal of PD therapeutic strategy?

A

to increase the amount of dopamine and relief of symptoms, but it does not reverse PD

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13
Q

What are the classes of drugs to treat PD?

A
  1. Dopamine precursors
  2. Inhibitors of GI and peripheral L-dopa metabolism
  3. Dopamine receptor agonists
  4. NMDA-receptor antagonists
  5. Antimuscarinic agents
  6. Multimodal agents
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14
Q

How do dopamine precursors work?

A

give L-dopa to increase the amount of dopamine in the CNS because it can cross the blood brain barrier and metabolizes into dopamine

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15
Q

How do Levodopa metabolism inhibitors work?

A

the goal is to get dopamine out of the periphery which causes side effects and there are multiple ways to do this

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16
Q

How does carbidopa work?

A

DOPA decarboxylase inhibitor, stops L-dopa from being metabolized in the periphery; increases the concentration of L-dopa and a better chance to reach the CNS

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17
Q

How does Levodopa/Carvidopa work?

A

usually given in combination so L-dopa reaches the CNS and Carvidopa inhibits the enzyme that metabolizes L-dopa causing a dopamine concentration in the periphery

18
Q

What is unique about Pimavanserin (Nuplazid)?

A

helps with patients that have a combination of hallucinations and delusions associated with PD

19
Q

What is the MOA of Pimavanserin?

A

inverse agonist and antagonist for seritonin receptors which is good because it does not affect Dopamine concentration

20
Q

What is the purpose of COMT Inhibitors?

A

inhibits the metabolism of L-Dopa by COMT to 3-O methyl dopa

21
Q

What is the goal of COMT inhibitors?

A

increases L-dopa chances of reaching the CNS to then get metabolized to dopamine lowering the amount of side effects; decreasing the “wearing-off” symptoms

22
Q

What is unique about Entacapone?

A
  • short duration of action out of the COMT inhibitors
  • periphery effects only (does not cross the BBB)
23
Q

What is unique about Tolcapone?

A
  • long duration of action out of the COMT inhibitors
  • periphery effects and CNS effects (can cross the BBB)
  • has a harsh adverse effects of fulminating hepatic necrosis
24
Q

What is the goal of selective MAO Type B Inhibitors?

A
  • decrease the metabolism of dopamine leading to the longevity of dopamine in the CNS
25
Q

Where are MAO Type B enzymes located?

A

in the brain (CNS); specifically in the straitum

26
Q

What is unique about Selegiline?

A
  • irreversible MAO Type B Inhibitor
  • metabolized by methamphetamine and amphetamine
27
Q

What is unique about Rasagiline (Azilect)?

A
  • irreversible MAO Type B Inhibitor
  • 5 times the potency of Selegiline
  • not metabolized by amphetamine-type metabolites
28
Q

What are the advantages of Dopamine-Receptor Agonists?

A
  • one a day dosing
  • improves adherence
29
Q

What is the goal of Dopamine-Receptor Agonists?

A
  • alleviate motor deficits
  • for early diseases (mainly)
  • drugs that act like dopamine
30
Q

What are two examples of Dopamine-Receptor Agonists?

A
  • Ropinirole (Requip)
  • Pramipexole (Mirapex)
31
Q

What is the goal of NMDA-Receptor Antagonists?

A

increases the amount of dopamine in the synaptic cleft because of the inhibition of reuptake or inhibition of glutamate receptors lowering excitation

32
Q

When are NMDA-Receptor Antagonists used?

A

in early stages

33
Q

What are the advantages of NMDA-Receptor Antagonists?

A
  • fewer side effects
  • useful for dyskinesia and tremors
  • more effective than anticholinergics
34
Q

What is a disadvantage of NMDA-Receptor Antagonists?

A
  • tolerance is developed quickly
35
Q

What is the goal of Muscarinic Receptor Antagonists?

A

restoring the balance of striatal dopamine and acetylcholine

36
Q

When are Muscarinic Receptor Antagonists used?

A

early disease or adjunct therapy

37
Q

What are the side effects of Muscarinic Receptor Antagonists?

A

SLUDGEM

38
Q

What is the goal of Benztropine (Cogentin)?

A

restoring balance by increasing the amount of dopamine by inhibiting the receptor that produces Ach

39
Q

What is the goal of Multimodal MAO?

A

trying to manage the motor symptoms and motor fluctuation

40
Q

What is the purpose of Dopaminergic Multimodal MOA?

A

-selective and reversible MAO-B
- dopamine reuptake inhibition

41
Q

What is the purpose of Non-Dopaminergic Multimodal MOA?

A

reduces the excessive release of glutamate

Dynamics II (6 decks)

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