Flashcards in Movement Disorders Meds Deck (13):
-SE of prolonged use?
Name:Levodopa/carbidopa (Sinememt) "GOLD STANDARD"
Effectiveness decreases after 3 years of tx and may return to pretreatment levels in 6-7yrs; relieves akinesia, rigidity, and tremor
SE: prolonged use may directly hasten the degeneration of dopamine neurons in the substantia nigra
MOA: levadopa is an immediate metabolic precursor to dopamine, penetrates the brain where its converted to dopamine. Carbidopa is given in conjunction to inhibit the conversion to dopamine before it reaches the BBB
--low BP, arrhythmia, GI effects, hair loss, dyskinesias**
--confusion, anxiety, vivid dreams, hallucinations
CI: concurrent use with MAOI's, psychotic pts, angle-closure glaucoma, hx of melanoma (melanoma is dopamine driven)
Class; MOA-B inhibitors
-Slegiline *may have neuroprotective properties*
MOA: stops the breakdown of dopamine
Adverse Effects: Insomnia(take in AM), jitteriness, dyskinesias, orthostatic hypotension
-TCAs, SSRIs, Demerol
Class: Dopamine Agonists
-bromocriptine(dont use much d/t fungus attacking heart valves)
MOA: wakes up receptor sites to increase dopamine utilization
*only use when sinemet effectiveness is declining as add on therapy, when we add this on we decrease sinemet.
-Nausea and constipation
-nightmares, hallucinations, psychosis
-pts with psychotic illness
Class: COMT inhibitors
Entacapone (Comtan), Tolcapone (Tasmar)
MOA: inhibits dopamine breakdown by selectively inhibiting COMT.
-involuntary muscle movements
-mental confusion/hallucination s
-cramps, Nausea, diarrhea
*try this for 2-3 weeks and if its not working then stop it and you dont do it again*
-when is this useful?
MOA: potentiates the dopaminergic function by influenciig the synthesis, release, or reuptake of dopamine.
-useful for early mild sx
-sedation, vivid dreams, dry mouth, depression, hallucinations
-Class: Ach Blocking
- Adverse effects
Trihexyphenidyl (Artane), Benztropine (Cogentin)
MOA: blocks Ach thereby blocking inhibition, so Ach not as effective in blocking dopamine.
-CNS: drowsiness, mental slowness, restlessness, confusion, hallucination
-SYstemic: dry mouth, blurred vision, consitpation, urinary retention
-BPH, obstructive GI dz, angle closure glaucoma
-Class: NMDA receptor inihibtors
Apomorphine (Apokyn) ??
Patient with mild parkinsons, what medication is used first line?
selegiline, this is the only medication that may provide benefit with slowing some progression of the dz
If experienceing the "wearing off effect" while taking sinemet what is the next best step?
how can you prevent this "wearing off effect"?
bridge therapy; add on COMT inhibitor*, MAOBs, dopamine agonists
-multiple small doses on empty stomach to maintain a constant level
-controlled release formulation
What are some causes of the wearing off effect?
-dz progresses beyond the ability of levodopa to control it
-become tolerant to prolonged exposure to dopamine
-dopamine neurons become incapable of storing dopamine and when the levodopa wears off there is no dopamine remaining.
-L-dopa itself accelerates the dz by producing oxygen free radicals, this increases injuries to the brain and dopamine degredation
Use: treat acute episodes of "hypermobility or freezing" give subQ
SE: profound nausea, must be given with antiemetic (NOT zofran, kytril b/c they block dopamine)
Symptomatic treatment of mild parkinsons is probably best avoided until there is some degree or disability or sx begin to have a significant impact on ADLs, T/F?