Treatment of Parkinsons Flashcards
Levodopa (L-dopa)
- Inactive precursor of Dopamine
- Easily crosses the BBB & can be synthesized into Dopamine in the BBB where it’s taken up by surviving dopamine neurons
- It’s metabolism increases levels of NE, Epi & DA (can lead to central/ peripheral effects
Central Effects: Impact on the mesa-limbic system
-Too high levels of DA= psychosis, anxiety, insomnia
Peripheral Effects: Hypertension; Tachycardia
-Can stimulate the chemorecetive zone (emesis)
- DA inhibits the release of PRL (can cause hyperprolactemia- not usually a problem in the elderly)
- Hyperstimulation of DA-R’s–> Dyskinesia
Cardidopa/ Benserazide:
- Decarboxylase Inhibitors
- ->To be administered with L-dopa to inhibit aromatic amino acid decarboxylase
- Overcomes peripheral adverse effects of L-dopa
Entracapone (Comptan):
- Inhibits peripheral COMT (COMT breaks down DA)
- Administered with L-Dopa + Caridopa or Benserazide to prevent DA metabolism by COMT
Selegiline:
-Monoamine Oxidase Inhibitor
(Inhibits the breakdown of DA)
-Delays disease progression from 10-12 months up to 18 months.
-Administered with L-dopa to reduce the amount of L-dopa needed (eventually, L-dopa stops working)
Bromocriptine:
Dopamine receptor antagonist
-Shown to improve parkinson symptoms when administered to L-dopa + carbidopa or benserazide
T1/2= 5 hours
Pramipexole, Ropinrol and Rotigotine
Newer DA Antagonists
-Fewer adverse effects than Bromocriptine
Benzotropine/ Trihexyphenidyl:
Muscarinic ACh antagonist
Rasagiline:
Newer MAO- Inhibitor
- Increases free radical scavengers & inhibits apoptosis
- Less AE’s than Selegiline
M30:
- ->Activated iron chelator/ MAO- inhibitor
- Neuroprotective/ anti- apoptotic properties
- Multifunctional, non- toxic Fe chelator
- Selective irreversible inhibitor of both MAO-A/B
- ->Improves oxidative damage!
