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