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Session 4 Pharm- 3

Pharm -3- Parkinson Disease Drugs

T/F women suffer from Parkinson's disease more than men F
T/F most pts develop Parkinson's at age 40 F most develop after age 50
What is a resting tremor palsy like movement of hands and head that disappear with purposeful movement
What is bradykinesia associated with Parkinson's disease pt has difficulty initiating movement and controlling fine movements (cog wheeling, festinating, shuffling gait)
What are the symptoms of Parkinson's disease resting tremors, akinesia or rigidity, bradykinesia, postural instability
What is the pathophysiology of Parkinson's disease loss of dopaminergic substantia nigra neurons
T/F in Parkinson's disease you have an excess of Ach in the corpus striatum T dopamine is an inhibitory signal without you get excess Ach in the corpus striatum because the cells are not inhibited properly
What are the common health problems in Parkinson's patients anxiety, depression, sleep disturbances, dementia, autonomic dysfunction (urinary frequency/urgency, sexual dysfunction)
Is parkinsonism the same thing as Parkinson's disease No it is just symptoms like Parkinson's disease without actual loss of substantia nigra
What are some common causes of parkinsonism viral infections, head trauma, stroke, drugs that are dopamine antagonists
What are the 4 methods to try and restore function in Parkinson's disease 1. neurotransmitter replacement, 2 Dopamine receptor agonist, 3 Decrease dopamine metabolism (COMT and MAO), 4 Cholinergic muscarinic antagonists
What are the commonly used drugs to replace dopamine Levodopa (L-Dopa) and Carbidopa/Levodopa (Sinemet)
What place in Parkinson's therapy does bromocriptine play dopamine receptor agonist
Name the 4 dopamine receptor agonists bromocriptine, cabergoline, ropinirole, Pramipexole
What type of drug is tolcapone COMT inhibitor decreases dopamine metabolism
What type of drug is Entacapone COMT inhibitor decreases dopamine metabolism
What type of drug is Selegiline MAOB inhibitor
What type of drug is Rasagiline MAOB inhibitor
What type of drug is Trihexyphenydyl Cholinergic muscarinic Antagonist
What type of drug is benzatropine Cholinergic muscarinic Antagonist
What type of drug is Diphenhydramine Cholinergic muscarinic Antagonist
T/F exogenous dopamine can cross the BBB F that is why L-Dopa is administered which is a dopamine precursor
What is the most effective tx for motor symptoms of Parkinson's dis Levodopa
Why is Levodopa combined with carbidopa carbidopa inhibits peripheral amino acid decarboxylase making sure Levodopa doesn't get converted to dopamine before it crosses the BBB it also reduces the s/e of nausea and vomiting because it reduces dopamine in the serum
What adjunct can be given with levodopa to prevent the s/e of nausea and vomiting from too much dopamine in the serum Carbidopa
How long does the therapeutic benefits of L-DOPA typically last 2-5 years this is because initially the nigrostriatal neurons that remain can buffer the dopamine picking up the L-Dopa and storing and converting in with time the degeneration continues pt can't respond to L-dopa
What are the most common s/e of L-Dopa N/V, Hypotension from vasodilation, cardiac arrhythmias from increase in release of nor Epi and CNS effects of dyskinesia, day time sleepiness
There are some behavioral s/e of taking L-Dopa what are they hallucinations and confusion from excess dopamine in messolimbic pathway this is more common in elderly
What drugs can be given to address the s/e of hallucination and confusion that L-Dopa may cause Atypical Antipsychos like clozapine and quetiapine
What s/e can L-Dopa have on the eye Mydriasis and precipitatation of acute glaucoma (probably from increased nor Epi in sympathetic terminals
Why do you need to stop nonspecific MAOIs before giving L-Dopa combining L-Dopa with MAOIs like phenelzine and tranylcypromine can cause life threatening hypertensive crisis and hyperpyrexia
What advantage does Dopamine agonists have over Dopamine replacement does not depend on enzymatic conversion for activity (IE doesn't depend on nigrostriatal neurons to be functioning) Last longer than L-DOPA (8-12 hr half life)
What is the disadvantage with Dopamine Receptor agonists Increased rate of hallucinations and hypotension as compared to L-DOPA
What are the first generation dopamine receptor agonists Bromocriptine (Parlodel)
What is the 2nd gen dopamine receptor agonist Cabergoline (selective for D2 receptor)
What is the non ergot selective D2 receptor agonist meds Ropirinole(Requip), Pramipexole Mirapex), and Apomorphine
Why do you want to start bromocriptine at low doses to start tx can cause profound hypotension
What s/e does bromocriptine have Hypotension, Nausea and Fatigue (usually transient)
What advantage do the non ergot D2 receptor agonist have over ergot derived Initiate more quickly reach therapeutic doses in a week or less but cause hallucinations and somnolence
What do you need to be aware of when dosing Pramipexole in pts since it is excreted unchanged if they have kidney disease you need to adjust the dose
Why are the dopamine receptor agonist taking over as first line tx for Parkinson disease over L-DOPA they show less incidence of on/off effects and less degeneration of dopaminergic neurons
What is the MOA of COMT inhibitors block peripheral conversion of L-Dopa to methyl dopa increasing L-Dopa that reaches CNS,
Which of the COMTS Tolcapone (Tasmar) or Entacapone (COMTAN) also inhibits COMT in the CNS as well as periphery Tolcapone (Tasmar)
What are the s/e of Tolcapone (Tasmar) Nausea, Orthostatic hypotension, confusion and hallucinations. Hepatotoxicity in 2% of pts monitor this
Which drug Tolcapone (Tasmar) or Entacapone (Comtan) both COMT inhibitors has a longer duration of action Tolcapone the half-life of entacapone is only 2hrs
Does Entacapone (Comtan) require hepatic monitoring No it is not hepatotoxic like Tolcapone
Why would you give MAO-B inhibitor Selegiline (Eldepryl) over the non selective MAO inhibitors if they both fulfill the same role in inhibiting peripheral metabolism of Levodopa does not cause hypertensive crisis like the nonselective MAOIs
Your pt is no longer responding to Levodopa and is in advanced Parkinson disease would it be beneficial to add selegiline to their tx why or why not No- it increases the adverse motor and cognitive effects of L-DOPA therapy in later or advanced Parkinson disease. It should be used in early tx of disease where it is actually neuroprotective
Why would you use Muscarinic Antagonists in Parkinson Disease tx useful as an adjunct to treat parkinsonian activity
What are the s/e of using the Muscarinic Antagonists Sedation and Mental Confusion, Blurred vision (cycloplegia) use caution in pts with narrow angle glaucoma, Constipation and urinary retention
What was Amantadine (Symmetrel) originally made for prophylaxis and tx of influenza as an antiviral
What is the MOA of amantadine (Symmetrel) in Parkinson disease blocks NMDA glutamate receptors to block excitotoxicity (remember dopamine is typically and inhibitory signal this would mimic that) It also alters dopamine release in the striatum and has anticholinergic properties
T/F Amantadine is very effective in tx all stages of Parkinson disease F- effects are modest used as initial therapy for mild PD
What are the s/e of Amantadine Dizziness, Lethargy, Sleep Disturbances, Anticholinergic Effects, N/V (Mild and reversible)
Created by: smaxsmith