Duke PA Parkinson's Pharmacology
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| non-pharmocologic therapies for Parkinson's disease | exercise, mental therapy
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| surgical treatment for parkinson's disease | thalamotomy, pallidotomy, deep brain stimulation
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| pharmocologic therapies for parkinson's disease | increase endogenous dopamine, dopamine agonists, anticholinergics, NMDA antagonists
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| therapies to increase endogenous dopamine | levodopa, peripheral decarboxylase inhibitors (PDI), catechol-O-methyl-transferase (COMT) inhibitors, monoamine oxidase B (MAO-B) inhibitors
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| dopamine agonists classes | nonergot, ergot
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| precursor of dopamine | levodopa
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| most effective drug for Parkinson's | levodopa
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| levodopa is converted to dopamin by | dopa decarboxylase enzyme
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| why not just give dopamine | peripheral dopamine results in adverse effects, and it will not cross the blood brain barrier
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| peripheral decarboxylase inhibitor | carbidopa
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| carbidopa is given with levodopa to __ | block peripheral conversion of levodopa to dopamine
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| contraindication for levodopa+carbidopa (sinemet) | narrow angle glaucoma
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| overdose of levodopa+carbidopa (sinemet) can lead to | palpitations, arrhythmias, spasms, hypo/hypertension
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| when a patient is on levodopa+carbidopa (sinemet) monitor | blood pressure, symptoms, dyskinesias, mental status
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| levodopa+carbidopa (sinemet) is best absorbed | on an empty stomach
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| COMT Inhibitors | tolcapone (Tasmar), entacapone (Comtan)
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| COMT inhibitors must be given with __ to have an effect | levodopa+carbidopa (Sinemet
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| what is COMT | enzyme that metabolizes catecholamines and levodopa
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| what do COMT inhibitors do | prevent peripheral conversion of levodopa, increase levodopa half life, and increase levodopa bioavalability
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| there have been reporst of __ with Tolcapone | fatal liver injury
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| d/c tolcapone if there is | elevation in LFT's or signs and symptoms of hepatic failure
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| strict __ monitoring with tolcapone | LFT
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| MAO-B inhibitors | selegiline (Eldepryl), Rasagiline (Azilect)
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| MAO breaks down | dopamine, norepinephrine, epinephrine, serotonin, tyramines
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| MAO-B inhibitor contraindications | meperidine, opioids, other MAO inhibitors
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| when giving MOA-B inhibitors monitor | blood pressure, and parkinson's symptoms
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| Nonergot dopamine agonists | pramipexole (Mirapex), ropinirole (ReQuip), rotigotine (Neupro), apomorphin (Apokyn)
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| Ergot dopamine agonists | pergolide (Permax), Bromocriptine (Parlodel)
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| dopamine agonist MOA | stimulate postsynaptic dopamine receptors within the corpus striatum
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| when patients are on dopamine agonists monitor for | signs and symptoms of orthostatic hypotension
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| anticholinergics | trihecyphenidyl (Artane), benztropine (cogentin), diphenhydramine (Benadryl)
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| diphenhydramine (Benadryl) is effective against tremor but not __ | bradykinesia or other IPD symptoms
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| MOA of anticholinergics | blocks the excitatory neurotransmitter acetylcholine
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| anticholinergic contraindications | narrow-able glaucoma, pyloric or duodenal obstruction, stenosing peptic ulcers, bladder neck obstructions, achalasia, myasthenia gravis
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| anticholinergics are poor agents for patients with | cognitive dysfunction
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| NMDA antagonists | amantadine (symmetrel)
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| NMDA antagonists MOA | exact mechanism unkown, inhibits dopamine reuptake
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| NMDA antagonists may decrease | mental altertness
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| NMDA antagonists precautions | liver disease, eczematoid dermatitis, psychosis, h/o seizures, renal dysfunction, edema/CHF patients, avoid with angle closure glaucoma
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| the TRAP symptoms are | Tremor, Rigidity, Akinesia/bradykinesia, postural disturbacnes
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| absence of movement | akinesia
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| drugs induced parkinsonism can be caused by __ | dopamine receptor blockers (antipsychotics), antiemetics (metoclopramide, prochlorperazine), dopamine storage depletors (reserpine)
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| secondary causes of parkinsonism | drug induced, toxins, strokes, traumatic lesions, normal pressure hydrocephalus
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| parkinson's disease is a disorder of the __ system | extrapyramidal
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| in parkinson's disease dopamine is outweighed by __ | acetylcholine
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| dopamine inhibits release of __ | acetylcholine
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| when there is less dopamine there is a relative increase in __ | acetylcholine
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| __ has multiple drug interactions | levodopa + Carbidopa
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| too much dopamine stimulation can cause | dyskinesias
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| advise patients on Levodopa+Carbidopa to __ | rise carefully from lying/sitting position
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| when converting IR to SR levodopa-carbidopa increase total daily dose by __% | 30
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| COMT inhibitor that works both peripherally and centrally | Tolcapone (Tasmar)
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| COMT inhibitor that works only peripherally | Entacapone (Comtan)
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| enzyme that metabolizes catecholamines and levodopa | COMT
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| Drug that prevents peripheral conversion of levodopa to 3-OMD | COMT inhibitors (entacapone, tolcapone)
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| MAO-B inhibitors adverse drug effects | insomnia (selegiline only), dizziness, n/v, xerostomia, dyskinesias, mood changes, headache, hypotension
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| Insomnia is an AE of which MAO-B inhibitor only | selegiline (Eldepryl)
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| MAO-B inhibitor that does not cause insomnia | rasagiline (Azilect)
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| avoid administering __ late in the day | selegiline (Eldypryl)
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| Dopamine agonist common AE's | nausea, sedation, light headedness, dizziness, vivid dreams, postural hypotension, dyskinesia
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| dose limiting AE's of dopamine agonists | confusion, hallucinations, daytime sedation
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| peripheral AE's for anticholinergics | blurred vision, urinary retention, xerostomia, constipation
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| central AE's for anticholinergics | confusion, impairment of memory, hallucinations, delusions
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| Anticholinergics are not recommended for the __ | elderly
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| NMDA AE's | Sedation, vivid dreams, xerostomia, livedo reticularis, edema, depression, hallucinations, anxiety, dizziness, confusion
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| NMDA's that will go away with time | sedation, vivid dreams
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| rose colored lacelike discoloration of lower extremities seen with amantadine therapy. this is not a harmful AE. | livedo reticularis
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