anti-parkinson's

Question 1

what are we trying to tx in parkinson’s

Answer 1

to restore dopamie- dec sxs
dopamine defect seems to be the primary defect in the dz- but unclear what causes the neuron death
-often sxs don’t appear until 75% of dopamie is lost in the substantia nigra & corpus striata
-no cure for this dz, just relieve sxs

Question 2

levodopa

Answer 2

L-Dopa
a dopamine precursor converted to dopamine by dopa-decarboxylase
**unlike dopamine, L-Dopa can cross the BBB
**usu combined with a peripheral dopa-decarboxylase inhinitor(carbidopa, benserazide) to prevent premature conversion in adrenals or other tissues

Question 3

SE of levodopa

Answer 3

as with all dopaminergic drugs:

• N/V, anorexia- all induced by the stimulation of dopamine receptors in the GI & chemotrigger receptor zone(CTZ)
• hypotension, choreiform movements, insomnia, anxiety, visual hallucinations
• SE will usu develop over time and continued use of the drug- SE may be bad, but not as bad as the dz sxs
• effect works for about 5 yrs- effect will start shortening & become intermittent

Question 4

dopa-decarboxylase inhibitors

Answer 4

carbidopa or benserizide

prevent peripheral conversion of L-dopa to dopamine- allows for a lower initial dose & reduces peripheral SE

Question 5

common levodopa drugs with dopa-decarboxylase inhibitors

Answer 5

levodopa w/cabidopa/ sinemet
levodopa w/benserazide/ prolopa
levodopa w/both carbidopa & benserazide/ stalevo

Question 6

contraindications of levodopa

Answer 6

never use with MAOI’s- can lead to hypertensive crisis

• psychactric condtions like schizophrenia - may worsen psychotic sxs
• should not be given with a dopamine blocking psychotic

Question 7

L-dopa w/carbidopa/ sinemet

Answer 7

dopamine precursor with a peripheral dopamine decarboxylase inhibitor
for parkinson’s dz
MOA- L-dopa can cross the BBB- inc dopamine lvls in brain, esp substantia nigra
PO- TID, QID
SE- Nausea(less with carbidopa), hallucinations, nightmares, dyskinesias(uncontrolled movement), serpentine movements(chorea)

Question 8

dopamine agonists

Answer 8

used early in tx of parkinson’s- to delay initaiaion of L-dopa therapy- prolong tx time

• bind at: D1, D2, D3, D4 receptor sites
• bromocriptine/ parlodel
• carbergoline/ dostinex
• pergolide/ permax- no longer used in US(cardiac valve dysF)
• pramipexole/ mirapex- also used for restless leg
• ropinirole/ requip- also used for restless leg

Question 9

bromocriptine/ parlodel

Answer 9

dopamine agonist
for parkinson’s dz, prolactin secreting adenomas, acromegaly
MOA- non-dopamine agent that mimics dopamine, stimulates dopamine receptor sites
PO, crosses BBB
SE-nausea, hypertension or hypotension, confusion, hallucinations, HA, depression, dyskinesia, possible seizures. pulmonary fibrosis in extremely high doses

Question 10

benztropine/ cogentin

Answer 10

anticholinergic
for the cognitive sxs as well the tremor & drooling in early parkinson’s- DOES NOT TX MOVEMENT DO, used to diminish SE of antipsychotic drug
MOA- anticholinergic antagonist at muscarinic receptor sites
PO
SE- dry mouth, blurred vision, urinary retention, constipation, confusion, drowsiness, disorientation, memory impairment, visual hallucinaitons, exacerbation of pre-existing psychotic sxs

Question 11

amantadine/ symmetrel

Answer 11

anti-parkinson’s & anti-viral
tx’s early PD or late PD L-dopa related dyskinesias, anti influenza A
MOA- in PD related to antagonism of N-methyl-D-aspartate(NMDA) receptors- results in diminished dopamine reuptake
SE- light headedness, confusion, drowsiness, nightmares, dry mouth, constipation, urinary retention, N/V
-benefits are usu short lived- 6 months or less

Question 12

order of drug therapy for PD

Answer 12

4) L-dopa(sinemet)
3) bromocriptine
2) amandatine
1) anticholinergics

Question 13

surgical options

Answer 13

usu reserved for advanced dz

• neurostimulation
• pallidotomy
• thalamotomy
• fetal cell implantation