Term
|
Definition
MOA: 95% broken down in periphery, therefore admin with carbidopa.
Use: Parkinsons, no longterm use
Tox: N, CV(incr bp), hallucinations, dyskinesias |
|
|
Term
|
Definition
MOA: peripheral dopa decarboxylase Inhib, inhibs AAAD from breaking down L-dopa to dopa in blood
Use: parkinsons
TOX: doesn't cross BBB (actually good) |
|
|
Term
|
Definition
MOA: COMT Inhib. (COMT breaks down L-dopa in peripheral blood)
USE: Parkinsons, increase L-dopa that enters BBB |
|
|
Term
| Sinemet (L-dopa+ Carbidopa) |
|
Definition
| MOA: L-dopa gets in thru LNAAT(BBB), carbidopa blocks AAAD in periphery-->get more L-dopa as opposed to giving Tyr. We don't do this bc TH is rls in Dopa biosyn |
|
|
Term
|
Definition
MOA: D3>D2 Dopa R agonist(non ergot)
Use: monotx or w/ Ldopa. Don't depend on NS Dopa neuron fx bc bid to Dopa R,
Tox: N, orthostatic, hypotension, hallucinations, not as effective as L dopa for PD sx
PHARM: oral abs, renal clearance unchang |
|
|
Term
|
Definition
MOA: D3>D2 Dopa R Agonist
Use don't depend on NS Dop neuron Fx bc directly bind dopa R, use early on
Tox: N, hypotension, hallucinations, not as effective as Ldopa for PD Sx |
|
|
Term
|
Definition
MOA: anticholinergic, dopa releasing agent, NMDA antagonist
Use: modest Anti-PD action
Tox: dizziness, lethargy, sleep prob |
|
|
Term
|
Definition
MOA: Monoamine Oxidase B Inhib, inhib dopa breakdown w/in n. terminal, so more can be packaged and released.
Use: early PD prior to L dopa or adjunct
TOX: selective for MAOB at low dose, inhib MAOA & B at high dose. L-dopa+nonsel MAOI=stop NT breakdown, hypertension |
|
|
Term
|
Definition
MOA: Muscarinic R Antagonist
Use: modest anti PD |
|
|
