Parkinson's Flashcards
What causes Parkinson’s?
loss of nigrostriatal dopamine neurons
What is key in providing clinical improvement?
activation of D2 dopamine receptor
How is PD diagnosed?
bradykinesia plus 2 or more of following:
- limb muscle rigidity
- resting tremor
- posutral instability
- micrographia
also responsiveness to L-dopa
Modified Hoehn and Yahr Staging
- staging from 0 to 5 where 0 is no sign of dz and 5 is w/c bound and bedridden
- PD is progressive and sxs worsen over time
Tx Goals
- maintain independence, ADLs, QOL
- alleviate sxs
- minimize development of response fluctuations
- limit medication-related adverse effects
Possible Tx Approaches
- lifestyle changes, nutrition, exercise
- pharmacologic intervention
- surgical treatment
What is the most effective tx for PD?
levodopa/carbidopa
Levodopa/Carbidopa MOA
increases DA in CNS
Why is levodopa used instead of straight dopamine?
-levodopa crosses BBB but DA does not
Amantadine
-antiviral w/ mild therapeutic effects in PD
Amantadine MOA
- NMDA receptor antagonist
- blocks glutamate (excitatory NT) transmission
- promotes DA release
What can happen if amantadine is abruptly discontinued?
rebound PD
Name 2 MAO-B inhibitors.
selegiline and rasagiline
MAO-B Inhibitor MOA
- prevent breakdown of DA
- rasagiline may be neuroprotective and neurorestorative
Drug Interactions of MAO-B Inhibitors
- TCA, SSRI, SNRI, meperidine: CNS toxicity, HTN, increased temp, death
- MAOI: HTN crisis
- tyramine containing foods: risk of HTN crisis
Name 2 catechol-o-methyltransferase (COMT) inhibitors.
entacapone and tolcapone