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Pharm 323 Spring 22 > Alzheimer's + Parkinson's > Flashcards

Alzheimer's + Parkinson's Flashcards

1
Q

re: our neurotransmitters, what is considered our “break pedal” / inhibitory NT? what is considered our “gas pedal”/ excitatory NT?

A

break pedal: dopamine

gas pedal: acetylcholine

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2
Q

what NT is decreased with parkinson’s disease?

A

dopamine

which is why we see tremors and issues with movement

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3
Q

the 2 major categories of drug therapy for PD are working on what?

A

manipulating either dopamine or acetylcholine

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4
Q

drug therapy for PD is based on what?

A

SYMPTOMS (b/c PD cannot be treated; we can only manage the symptoms)

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5
Q

what type of drug agents are used most commonly with PD?

A

dopaminergic agents (promote activation of dopamine receptors = get more dopamine to the brain)

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6
Q

dopaminergic agents help to improve what?

A

quality of life/functionality/mobility/ADLs

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7
Q

what are the 5 dopaminergic agents for PD therapy? (classes, not names)

A
  1. dopamine replacement
  2. dopamine agonists
  3. COMT inhibitors
  4. MAO-B inhibitors
  5. antiviral
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8
Q

what is the prototype for dopamine replacement drugs? + what is MOA?

A

levodopa / carbidopa

MOA: promote dopamine SYNTHESIS

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9
Q

what is prototype of dopamine agonists? + what is MOA?

A

pramipexole

MOA: DIRECT activation of dopamine receptors

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10
Q

what is prototype of COMT inhibitors? + what is MOA?

A

entaCAPONE

“CAPONE gets his meal COMPT”

MOA: blocks breakdown of levodopa = increased amt of levodopa that enters brain = enhanced effects of levodopa

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11
Q

what is prototype of MAO-B inhibitors? + what is MOA?

A

selegiline (“suh-leh-juh-leen”)

“My bAd, B - there’s no breakdown of dopaMINE with selegiLINE”

MOA: inhibits breakdown of DOPAMINE

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12
Q

what is prototype of antiviral for PD therapy? what is MOA?

A

amantadine

AntivirAl = AmAntAdine

MOA: promotes DOPAMINE RELEASE (from hypothalamus)

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13
Q

what is our most effective drug for PD? (reported that 75% of patients experience 50% reduction in symptoms)

A

levodopa/carbidopa

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14
Q

levodopa is usually given as combo with what? and why? (3 reasons)

A

levodopa + carbidopa

  1. decreases the breakdown of levodopa via DDC enzyme
  2. allows more to cross BBB*
  3. allows us to use lower doses of levodopa
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15
Q

when will we see effects of levodopa therapy? how long can they last?

A

can be months! + a 5 year MAX

delayed full effect + also doesn’t last

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16
Q

what is the MOA of levodopa?

A

converts to dopamine in the brain

side note: combining it with carbidopa prevents this conversion happening in the bloodstream, so more dopamine can reach brain ◡̈

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17
Q

what are the SE of levodopa/carbidopa? (6 - start with brain –> GU)

A
  1. CNS effects
  2. psychosis
  3. dyskinesia (head + neck most common)
  4. CV
  5. N/V
  6. dark sweat + urine

CPDCND

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18
Q

how can we mitigate the SE of N/V of levodopa/carbidopa? (2)

A
  1. give with food

2. avoid high protein meals (spread protein throughout the day)

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19
Q

what CV SE might we see with levodopa/carbidopa? (2)

A
  1. dysrhythmias

2. orthostatic hypotension

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20
Q

describe the “acute loss of effect” with levodopa/carbidopa therapy - (“wearing off” + “on-off effects) + how can we mitigate these effects?

A

“wearing off” : happens at the end of the dosing interval = give dose ON TIME; can also administer selegiline**

“on-off” : abrupt loss of effect; can happen @ any time; starts working again randomly = avoid high protein meals!! ***

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21
Q

what is our 1st line therapy for mild to moderate symptoms of PD? (class + prototype)

A

dopamine agonists

pramipexole

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22
Q

why are dopamine agonists (pramipexole) used more commonly with younger population?

A

more serious side effects + these patients are “more likely to handle them better”

23
Q

when using pramipexole as a monotherapy, what SE might you see? (7 - start with brain –> overall body)

A
  1. hallucinations **
  2. daytime somnolence (sleep attacks) **
  3. insomnia
  4. dizziness
  5. nausea
  6. constipation
  7. weakness

**most common

24
Q

what medication might we pair with pramipexole? and what SE might we see with this combo? (3)

A

levodopa

  1. orthostatic hypotension
  2. dyskinesia
  3. increased hallucinations

(SE are from levodopa, i think, correct me if i’m wrong please!!)

25
Q

what is the RARE instance that might occur with pramipexole therapy?

A

pathologic gambling + other compulsive behaviours

26
Q

what is the MOA of COMT inhibitors?

A

increases amt of levodopa that enters brain (by preventing the breakdown of levodopa via COMT enzyme)

27
Q

what drug class is known as the levodopa “boosters” and is commonly used with levodopa/carbadopa? what’s our prototype?

A

COMT inhibitors

entacapone

“capone gets a boost from all the cocaine”

28
Q

what drug class increases the half life of levodopa?

A

COMT inhibitors

they prevent breakdown of levodopa - they’re also known as levodopa BOOSTERS

29
Q

what are SE of entacapone? (7 - brain –> GU)

think increased levodopa

A
  1. hallucinations
  2. impulse control
  3. orthostatic hypotension
  4. dyskinesias
  5. sleep disturbances
  6. nausea
  7. urine color changes

“capone HIOD SNU to get rid of you”

30
Q

what is considered our 2nd and 3rd line drugs for treatment of PD?

A

MAO-B inhibitors

31
Q

what drug can we give with levodopa to reduce the “wearing-off” effect?

A

selegiline

MAO-B inhibitor

32
Q

what drug suppresses the destruction of dopamine that’s derived from levodopa?

A

selegiline

MAO-B inhibitor

33
Q

what are the SE of selegiline? (4)

overlap with other PD drugs

A
  1. insomnia (give in AM)
  2. orthostatic hypotension
  3. dizziness
  4. GI
34
Q

what is our prototype for our antiviral drug for PD?

A

amantadine

35
Q

how long will it take to see effects of amantadine + how long will they last?

A

effects within 2-3 days

ONLY last several months

36
Q

what is the MOA of antivirals for PD therapy?

A

promote dopamine release

37
Q

what drug may be used for dyskinesias caused by levodopa?

A

amantadine

antiviral

38
Q

what are the SE of amantadine? (3)

A
  1. CNS
  2. anticholinergic (can’t pee, can’t see, can’t spit, can’t shit)
  3. livedo reticularis = mottling of skin

“crazy AMANTA with the crazy skin CAN’T do anything” / “antiviral = anticholinergic”

39
Q

what education should we provide our patients about livedo reticularis r/t amantadine therapy?

A

it usually starts within a month of therapy, but is is benign!

40
Q

what drug class is used to reduce tremors + rigidity?

think of your break and gas pedals r/t NTs

A

anticholinergics (2nd line therapy)

anticholinergics are blocking ACh, which is your gas pedal, so this will reduce tremors and rigidity

41
Q

what is our prototype for anticholinergic drugs for PD therapy?

A

benztropine

“you can’t pee, [can’t see], can’t spit + can’t shit in a BENZ”

42
Q

what are SE of benztropine?

A

(it’s an anticholinergic)

can’t pee, can’t see, can’t spit, can’t shit

43
Q

what are the 2 drug classes used for alzheimer’s disease?

A

No Confusion =

  1. NMDA receptor antagonists
  2. cholinesterase inhibitors
44
Q

what is the MOA of cholinesterase inhibitors?

A

inhibit cholinesterase from breaking down acetylcholine, making more ACh available

ACh important for memory

45
Q

what are our 1st line drugs for Alzheimer’s Disease? + what is prototype?

A

cholinesterase inhibitors

donepezil

“DONE with alzheimers, give me a PEZ”

46
Q

what are the SE of donepezil? (4)

A

(parasympathomimetics)

  1. N/V/D
  2. dizziness + HA
  3. bronchoconstriction
  4. bradycardia

fainting + fall risk

47
Q

what drug-drug interactions exist with donepezil?

A

anticholinergic drugs

this opposes the parasymathomimetic effects of donepezil

48
Q

how many days are needed to achieve steady state of donepezil?

A

15 days!! (70 hour half life!!)

49
Q

how should donepezil be dosed + administered?

A

dose: start low + go slow
admin: late in day; can be with or without food

50
Q

what is the MOA of NMDA receptor antagonists?

A

regulate calcium influx into neurons (in AD, too much calcium enters in)

51
Q

what drug class is indicated for moderate to severe AD?

A

NMDA receptor antagonists

52
Q

what is prototype for NMDA antagonists?

A

memantine (Namenda)

53
Q

what are NMDA receptor antagonists usually given with?

A

cholinesterase inhibitor

54
Q

what are the SE of memantine? (4)

Well tolerated or not?

A

very well tolerated

dizziness, HA, confusion, constipation

Pharm 323 Spring 22 (18 decks)

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