Alzheimer's + Parkinson's Flashcards
re: our neurotransmitters, what is considered our “break pedal” / inhibitory NT? what is considered our “gas pedal”/ excitatory NT?
break pedal: dopamine
gas pedal: acetylcholine
what NT is decreased with parkinson’s disease?
dopamine
which is why we see tremors and issues with movement
the 2 major categories of drug therapy for PD are working on what?
manipulating either dopamine or acetylcholine
drug therapy for PD is based on what?
SYMPTOMS (b/c PD cannot be treated; we can only manage the symptoms)
what type of drug agents are used most commonly with PD?
dopaminergic agents (promote activation of dopamine receptors = get more dopamine to the brain)
dopaminergic agents help to improve what?
quality of life/functionality/mobility/ADLs
what are the 5 dopaminergic agents for PD therapy? (classes, not names)
- dopamine replacement
- dopamine agonists
- COMT inhibitors
- MAO-B inhibitors
- antiviral
what is the prototype for dopamine replacement drugs? + what is MOA?
levodopa / carbidopa
MOA: promote dopamine SYNTHESIS
what is prototype of dopamine agonists? + what is MOA?
pramipexole
MOA: DIRECT activation of dopamine receptors
what is prototype of COMT inhibitors? + what is MOA?
entaCAPONE
“CAPONE gets his meal COMPT”
MOA: blocks breakdown of levodopa = increased amt of levodopa that enters brain = enhanced effects of levodopa
what is prototype of MAO-B inhibitors? + what is MOA?
selegiline (“suh-leh-juh-leen”)
“My bAd, B - there’s no breakdown of dopaMINE with selegiLINE”
MOA: inhibits breakdown of DOPAMINE
what is prototype of antiviral for PD therapy? what is MOA?
amantadine
AntivirAl = AmAntAdine
MOA: promotes DOPAMINE RELEASE (from hypothalamus)
what is our most effective drug for PD? (reported that 75% of patients experience 50% reduction in symptoms)
levodopa/carbidopa
levodopa is usually given as combo with what? and why? (3 reasons)
levodopa + carbidopa
- decreases the breakdown of levodopa via DDC enzyme
- allows more to cross BBB*
- allows us to use lower doses of levodopa
when will we see effects of levodopa therapy? how long can they last?
can be months! + a 5 year MAX
delayed full effect + also doesn’t last
what is the MOA of levodopa?
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 ◡̈
what are the SE of levodopa/carbidopa? (6 - start with brain –> GU)
- CNS effects
- psychosis
- dyskinesia (head + neck most common)
- CV
- N/V
- dark sweat + urine
CPDCND
how can we mitigate the SE of N/V of levodopa/carbidopa? (2)
- give with food
2. avoid high protein meals (spread protein throughout the day)
what CV SE might we see with levodopa/carbidopa? (2)
- dysrhythmias
2. orthostatic hypotension
describe the “acute loss of effect” with levodopa/carbidopa therapy - (“wearing off” + “on-off effects) + how can we mitigate these effects?
“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!! ***
what is our 1st line therapy for mild to moderate symptoms of PD? (class + prototype)
dopamine agonists
pramipexole
why are dopamine agonists (pramipexole) used more commonly with younger population?
more serious side effects + these patients are “more likely to handle them better”
when using pramipexole as a monotherapy, what SE might you see? (7 - start with brain –> overall body)
- hallucinations **
- daytime somnolence (sleep attacks) **
- insomnia
- dizziness
- nausea
- constipation
- weakness
**most common
what medication might we pair with pramipexole? and what SE might we see with this combo? (3)
levodopa
- orthostatic hypotension
- dyskinesia
- increased hallucinations
(SE are from levodopa, i think, correct me if i’m wrong please!!)
what is the RARE instance that might occur with pramipexole therapy?
pathologic gambling + other compulsive behaviours
what is the MOA of COMT inhibitors?
increases amt of levodopa that enters brain (by preventing the breakdown of levodopa via COMT enzyme)
what drug class is known as the levodopa “boosters” and is commonly used with levodopa/carbadopa? what’s our prototype?
COMT inhibitors
entacapone
“capone gets a boost from all the cocaine”
what drug class increases the half life of levodopa?
COMT inhibitors
they prevent breakdown of levodopa - they’re also known as levodopa BOOSTERS
what are SE of entacapone? (7 - brain –> GU)
think increased levodopa
- hallucinations
- impulse control
- orthostatic hypotension
- dyskinesias
- sleep disturbances
- nausea
- urine color changes
“capone HIOD SNU to get rid of you”
what is considered our 2nd and 3rd line drugs for treatment of PD?
MAO-B inhibitors
what drug can we give with levodopa to reduce the “wearing-off” effect?
selegiline
MAO-B inhibitor
what drug suppresses the destruction of dopamine that’s derived from levodopa?
selegiline
MAO-B inhibitor
what are the SE of selegiline? (4)
overlap with other PD drugs
- insomnia (give in AM)
- orthostatic hypotension
- dizziness
- GI
what is our prototype for our antiviral drug for PD?
amantadine
how long will it take to see effects of amantadine + how long will they last?
effects within 2-3 days
ONLY last several months
what is the MOA of antivirals for PD therapy?
promote dopamine release
what drug may be used for dyskinesias caused by levodopa?
amantadine
antiviral
what are the SE of amantadine? (3)
- CNS
- anticholinergic (can’t pee, can’t see, can’t spit, can’t shit)
- livedo reticularis = mottling of skin
“crazy AMANTA with the crazy skin CAN’T do anything” / “antiviral = anticholinergic”
what education should we provide our patients about livedo reticularis r/t amantadine therapy?
it usually starts within a month of therapy, but is is benign!
what drug class is used to reduce tremors + rigidity?
think of your break and gas pedals r/t NTs
anticholinergics (2nd line therapy)
anticholinergics are blocking ACh, which is your gas pedal, so this will reduce tremors and rigidity
what is our prototype for anticholinergic drugs for PD therapy?
benztropine
“you can’t pee, [can’t see], can’t spit + can’t shit in a BENZ”
what are SE of benztropine?
(it’s an anticholinergic)
can’t pee, can’t see, can’t spit, can’t shit
what are the 2 drug classes used for alzheimer’s disease?
No Confusion =
- NMDA receptor antagonists
- cholinesterase inhibitors
what is the MOA of cholinesterase inhibitors?
inhibit cholinesterase from breaking down acetylcholine, making more ACh available
ACh important for memory
what are our 1st line drugs for Alzheimer’s Disease? + what is prototype?
cholinesterase inhibitors
donepezil
“DONE with alzheimers, give me a PEZ”
what are the SE of donepezil? (4)
(parasympathomimetics)
- N/V/D
- dizziness + HA
- bronchoconstriction
- bradycardia
fainting + fall risk
what drug-drug interactions exist with donepezil?
anticholinergic drugs
this opposes the parasymathomimetic effects of donepezil
how many days are needed to achieve steady state of donepezil?
15 days!! (70 hour half life!!)
how should donepezil be dosed + administered?
dose: start low + go slow
admin: late in day; can be with or without food
what is the MOA of NMDA receptor antagonists?
regulate calcium influx into neurons (in AD, too much calcium enters in)
what drug class is indicated for moderate to severe AD?
NMDA receptor antagonists
what is prototype for NMDA antagonists?
memantine (Namenda)
what are NMDA receptor antagonists usually given with?
cholinesterase inhibitor
what are the SE of memantine? (4)
Well tolerated or not?
very well tolerated
dizziness, HA, confusion, constipation
