Antiparkinson drugs
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| 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 |
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Created by:
psfisher50
on 2006-08-07