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? (7 - start with brain –> GU)
- CNS effects
- psychosis
- dyskinesia (head + neck most common)
- CV
- N/V
- dark sweat + urine
- melanoma
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!!)
