Neuro: Pharm - Parkinson Dz Flashcards
Pathology in Parkinsons:
loss of dopaminergic neurons and excess cholinergic activity
Bromocriptine: MOA
DA agonist (ergot)
Pramipexole: MOA
DA agonist (non-ergot) non-ergots are preferred
Ropinrole: MOA
DA agonist (non-ergot) non-ergots are preferred
Amantadine: MOA, others uses, toxicity
increase DA release
also used as antiviral against influenza A and rubella
toxicity = ataxia
L-dopa/carbidopa: MOA
converted to DA in CNS
Selegeline: MOA
selective MAO type B inhibitor, prevents breakdown of DA
Entacapone: MOA
COMT inhibitor - prevents L-dopa degradation -> increases DA availability
Tolcapone: MOA
COMT inhibitor - prevent L-dopa degradation -> increases DA availability
Benztropine: MOA, uses
Antimuscarinic
improves tremor and rigidity but has little effect on bradykinesia
Levodopa: MOA
increases level of DA in brain
Unlike DA, levodopa can cross BBB and is converted by Dopa decarboxylase in the CNS to DA.
Carbidopa: MOA
Peripheral decarboxylase inhibitor, is given with L-dopa to increase the bioavailability of L-dopa in the brain and to limit peripheral side effects.
Levodopa: uses
Parkinson disease
Levodopa toxicity
Arrhythmias from increased peripheral formation of catecholamines. Long-term use can lead to dyskinesia following administration (“on-off” phenomenon), akinesia between doses.
Selegiline: MOA
Selectively inhibits MAO-B, which preferentially metabolizes DA over NE and 5-HT, thereby increasing availability of DA.
Also has antioxidant properties
