Pharm -3- Parkinson Disease Drugs
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| T/F women suffer from Parkinson's disease more than men | F
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| T/F most pts develop Parkinson's at age 40 | F most develop after age 50
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| What is a resting tremor | palsy like movement of hands and head that disappear with purposeful movement
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| What is bradykinesia associated with Parkinson's disease | pt has difficulty initiating movement and controlling fine movements (cog wheeling, festinating, shuffling gait)
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| What are the symptoms of Parkinson's disease | resting tremors, akinesia or rigidity, bradykinesia, postural instability
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| What is the pathophysiology of Parkinson's disease | loss of dopaminergic substantia nigra neurons
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| 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
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| What are the common health problems in Parkinson's patients | anxiety, depression, sleep disturbances, dementia, autonomic dysfunction (urinary frequency/urgency, sexual dysfunction)
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| Is parkinsonism the same thing as Parkinson's disease | No it is just symptoms like Parkinson's disease without actual loss of substantia nigra
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| What are some common causes of parkinsonism | viral infections, head trauma, stroke, drugs that are dopamine antagonists
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| 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
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| What are the commonly used drugs to replace dopamine | Levodopa (L-Dopa) and Carbidopa/Levodopa (Sinemet)
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| What place in Parkinson's therapy does bromocriptine play | dopamine receptor agonist
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| Name the 4 dopamine receptor agonists | bromocriptine, cabergoline, ropinirole, Pramipexole
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| What type of drug is tolcapone | COMT inhibitor decreases dopamine metabolism
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| What type of drug is Entacapone | COMT inhibitor decreases dopamine metabolism
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| What type of drug is Selegiline | MAOB inhibitor
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| What type of drug is Rasagiline | MAOB inhibitor
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| What type of drug is Trihexyphenydyl | Cholinergic muscarinic Antagonist
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| What type of drug is benzatropine | Cholinergic muscarinic Antagonist
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| What type of drug is Diphenhydramine | Cholinergic muscarinic Antagonist
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| T/F exogenous dopamine can cross the BBB | F that is why L-Dopa is administered which is a dopamine precursor
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| What is the most effective tx for motor symptoms of Parkinson's dis | Levodopa
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| 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
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| What adjunct can be given with levodopa to prevent the s/e of nausea and vomiting from too much dopamine in the serum | Carbidopa
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| 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
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| 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
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| 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
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| 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
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| What s/e can L-Dopa have on the eye | Mydriasis and precipitatation of acute glaucoma (probably from increased nor Epi in sympathetic terminals
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| 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
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| 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)
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| What is the disadvantage with Dopamine Receptor agonists | Increased rate of hallucinations and hypotension as compared to L-DOPA
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| What are the first generation dopamine receptor agonists | Bromocriptine (Parlodel)
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| What is the 2nd gen dopamine receptor agonist | Cabergoline (selective for D2 receptor)
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| What is the non ergot selective D2 receptor agonist meds | Ropirinole(Requip), Pramipexole Mirapex), and Apomorphine
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| Why do you want to start bromocriptine at low doses to start tx | can cause profound hypotension
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| What s/e does bromocriptine have | Hypotension, Nausea and Fatigue (usually transient)
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| 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
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| 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
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| 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
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| What is the MOA of COMT inhibitors | block peripheral conversion of L-Dopa to methyl dopa increasing L-Dopa that reaches CNS,
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| Which of the COMTS Tolcapone (Tasmar) or Entacapone (COMTAN) also inhibits COMT in the CNS as well as periphery | Tolcapone (Tasmar)
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| What are the s/e of Tolcapone (Tasmar) | Nausea, Orthostatic hypotension, confusion and hallucinations. Hepatotoxicity in 2% of pts monitor this
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| 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
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| Does Entacapone (Comtan) require hepatic monitoring | No it is not hepatotoxic like Tolcapone
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| 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
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| 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
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| Why would you use Muscarinic Antagonists in Parkinson Disease tx | useful as an adjunct to treat parkinsonian activity
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| 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
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| What was Amantadine (Symmetrel) originally made for | prophylaxis and tx of influenza as an antiviral
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| 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
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| T/F Amantadine is very effective in tx all stages of Parkinson disease | F- effects are modest used as initial therapy for mild PD
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| What are the s/e of Amantadine | Dizziness, Lethargy, Sleep Disturbances, Anticholinergic Effects, N/V (Mild and reversible)
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