Flashcards in Anti-Parkinson Deck (34):
concept: Why does increasing DOPA make sense
@ normal physiological context DOPA levels are negligilbe. since rate limiting step is tyrosine OHase above DOPA production, if you load up on substrate you can increased DA = good to go for parkinson hurrah.
Goal of therapy for Parkinson
want to decrease GABA -- normally DA stimulates GABA neurons and Ach decreased GABA -- so goal is to get more DA and less Ach so that GABA activity is increased
What happens when levidopa is decarboxylated in the periphery ie symptoms
Why does food slow the appearance of levidopa in the plasma?
amino acids compete with absorption from gut and transport from blood to brain
Wearing Off Phenomenon VRS On-Off Phenomenon
wearing off - fluctuations due to timing of levodopa administration
On-off phenomenon - fluctautions not due to timing of levodopa administration
How to treat the Offs of the ON Off phenomenon
What vitamin is contraindicated with levodopa and why
vitamin B6 because is a cofactor for DOPA decarboxylase and increases peripheral metabolism of levodopa
Why cant you use levodopa with a nonspecific MAO inhibitor
What type of meds and patients shouldnt be given levodopa
healthy people and ppl on antipsychotics or with mental disturbances
What eye probelms contraindicated levodopa
angle closure glaucoma
What heart problems are significinat?
can cause arrhtymias in cardiac patients
Name the ergot D2 agonist
Name the nonergot D2 agonists
Ropinirole (pin role = parkinson side effect ;))
Which nonergo D2 agonist is available only transdermal
Ergot side effects please :) only the bolded ones
Bromocriptine: pulmonary infiltrates
plueral and retroperitoneal fibrosis
erythromelalgia (bouts of pain cuased by temperature, turns red, usually hands and feet)
Nonergot side effects bolded please
Ropinirole (Ro-pin roll)
~*~Contraindications and be careful pateints for DA agonists
recent mi (causes arrhythmias)
periperal vascular disease (erytrmelalgia and vasospasm @ periphery)
puptic ulceration (makes em bleed)
Who cares about Apomorphine and why
rescue for OFF episodes of akinesia
emetogenic so give an antiemtic first
other effects i dont have time for- not bolded
Which MAO i are used as adjuncts for levodopa treatment?
selegiline - deprenyl
(new one, not listed in antidepressant lec) =
What is a concern about the metabolism of selegilin
metabolized to metamphetamine and amphetamine so can cause insomnia if take late in the day
Justify the use of Tolcapone (gangster) and Entacapone
Tolcapone and Entacapone inhibit COMT --> thus levodopa is not metabolized to 3-o-methyl dopa so there is no compeition for uptake of levodopa to the BBB or the intestine; when you use carbidopa it causes increase shunting of levodopa to its metabolite
Describe site of action of tolcapone and entacapone
tolcapone - in bbb and intestine
entacapone - periphery (enterocytes ie enta @ gut)
~*~A/se of tolcapone
fulminating hepatic necrosis; entacapone doesnt cause this so preferred.
~*~Antiviral with antiparkinsonism effects?
a) increases synthesis, release or reuptake of DA from **surviving neurons
Bolded side effect of Amantadine
Levido reticularis - clears spontaneously after 1 month of cessationg of tx
What good are antimuscarinics for Parkinson?
improve tremor and rigidity but not relaly bradykinesia (more central and due to DA... maybe)
When should you not use antimuscarins
Describe the first line regimen for Parkinson.
levodopa + carbidopa
Decribe what you'd give for second line treatment of Parkinson
ergot - bromocriptine
nonergot - pramipexole, ropinirole, rotigotine
Why would you add a COMT inhibitor or an MAOB inhibitor to levodopa?
to reduced motor fluctations for peopel with advanced disease
COMT inhibitors are teh CAPTONES
MAo-b are the GILINES
Why would you add an antimuscarinic to the treatment regimen @ parkinson?
control of tremor and drooling.
If I say CAPTONE you say?
control of adcanced disease
fulminating hepatic necrosis