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Parkinson's disease

Antiparkinson drugs

QuestionAnswer
signs and symptoms of PD are due to the progressive degeneration of the inhibitory dopaminergic pathway projecting from? substantia nigra to the caudate nucleus
a tremor often present in Parkinson's Disease at rest but disappears during purposeful movement? "pill rolling" tremor
what is Bradykinesia in PD? decreased spontaneous movement, loss of normal associated movement,slow initiation of movement
Why do PD patients have rigidity? due to increased muscle tone
What type of posture and gait do PD patients have? progressive stooped position with a shuffling gait
What types of psychological changes are seen in PD patients? depression and dementia
Why do some PD patient seem to have excessive oral secretions? there is a deficiency of dopamine, allowing cholinergic dominance
immediate precursor of dopamine which will cross the blood brain barrier? levodopa
levodopa MOA? Levodopa augments the supply of dopamine in surviving presynaptic terminals
selegiline MOA? inhibits the inactivation of dopamine by the B subtype of monoamine oxidase (MAO-B) thereby decreasing catabolism of dopamine. (Must keep doses below 10mg/day for it will inhibit MOA-A which can cause problems with tyramine ingestion)
amantadine MOA? promotes the presynaptic release of dopamine from intact neurons and blocks NMDA (N-methyl-D-aspartic acid) receptors
What else is amantadine used for? an antiviral treatment for Influenza A
Why not use dopamine for the treatment of PD instead of L-dopa? dopamine cannot cross the BBB but L-dopa can. L-dopa or levadopa is the metabolic precursor (prodrug) to dopamine.
What are the side effects of l-dopa? nausea, vomiting, postural hypotension, arrhythmias, tachycardia
What is administered concurrently with l-dopa to minimize side effects? carbidopa; allows treatment with lower dose of L-dopa which thus decrease side effects
carbidopa MOA? inhibits DOPA decarboxylase in the periphery therby increasing the proportion of L-dopa entering the brain
levodopa-carbidopa Sinemet
Ergot-derived dopamine agonists? bromocriptine(Parlodel) & pergolide(Permax)& pramipexole(Mirapex)
What is the MOA of anticholinergic drugs on PD? blocks the unopposed action of cholinergic effects on striatal cholinergic interneurons which are disinhibited in the absence of dopaminergic stimulation
Anticholinergics used in PD? benztropine (Cogentin), trihexyphenydyl(Artane) & procyclidine (Kemadrin)
PD is associated with degeneration of which neuronal pathway? the nigrostriatal dopamine pathway
The primary goal in the treatment of PD is the stimulation of dopamine receptors in what brain region? neostriatum; the terminal field of the nigrostriatal pathway
Therapeutic effects of l-dopa? decreased tremor; decreased rigidity; improved mental function & sense of well-being
Problems with long term treatment with l-dopa include? hypersexuality; hallucinations; fluctuations in efficacy & dystonias and dyskinesias
What dietary recommendations would you make to your PD patient taking Sinemet? to take their daily protein in one meal separate from the l-dopa medications because L-dopa is an amino acid, the protein in their food will compete with the uptake of L-dopa and it will be poorly absorbed.
"on -off" syndrome is? oscillations in performance of the medication involving rapid changes from from akinesia to dyskinesia
How does "end-of-dose" syndrome differ from "on-off" syndrome? in "end-of-dose" the medication is wearing off and it responds to taking more drug whereas "on-off" syndrome does not respond to additional medication
In starting benztropine on your patient who is taking sinemet, what would you include in your education? the dose of anticholinergic (benztropine) should be separated from the dose of sinemet (L-dopa/carbidopa) because benztropine will slow gastric emptying and causing further degradation of the L-dopa making less of it available for absorption
Name 2 COMT inhibitors? tolcapone (Tasmar) & entacapone (Comtan)
COMTs MOA? inhibits the enzyme COMT (catechol-O-methyltransferase) which inactivates l-dopa and dopamine thereby increasing the duration of action of l-dopa and dopamine
Whats the difference between tolcapone and entacapone? tolcapone is highly lipid soluble and crosses the BBB, entacapone does not. Also there are problems with hepatotoxity with tolcapone, not entacapone.
What are the ADRs of the COMTs? diarrhea, bright yellow discoloration of urine, increased l-dopa side effects
Your PD patient on Sinemet is having "end-of-dose" syndrome, what could you add? COMTs medication; increases the duration of action of L-dopa and dopamine
l-dopa / carbidopa / entacapone Stalevo
Non-ergot dopamine agonist MOA? direct stimulation of the dopamine receptor AND they slow cellular metabolism which slows progression of the disease by 30%
Name 2 non-ergot dopamine agonists? Ropinirole (Requip) and pramipexole (Mirapex)
In addition to PD, what else is ropinirole (Requip) used for? restless leg syndrome
What is the difference between the ergot-derived and the non-ergot dopamine agonists? the ergot-derived hit more of the different dopamine receptors and can cause hallucinations (LSD is an ergot) whereas the non-ergot hit D3>D2 and have less SEs.
Your patient is late in the progression of PD, what drug might you add to control dyskinesias that are occurring with the l-dopa therapy? amantadine (Symmetrel)
What are the side effects of amantadine? Hallucinations, confusion, and nightmares, Insomnia, dizziness, lethargy, slurred speech
What is livido reticularis? seen in long term use of amantadine it is the "net-like" mottling on the skin caused by localized vasoconstriction
What is selegiline metabolically converted to? amphetamine, should not be given late in day - may cause insomnia
What drug algorithm would you follow for a newly diagnosed PD patient? L-dopa/carbidopa &/or dopamine agonist > COMT inhibitor > anticholinergics
Created by: psfisher50 on 2006-08-07



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