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21 Cards in this Set
- Front
- Back
Benztropine and Parkinson’s?
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MUSCARINIC CHOLINERGIC ANTAGONIST
Balances dopaminergic-cholinergic systems by reducing cholinergic dominance |
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Diphenhydramine and Parkinson’s?
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ANTIHISTAMINE
Central muscarinic blockade |
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Levodopa and Parkinson’s?
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Dopa precursor
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Levodopa + carbidopa and Parkinson’s?
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Levodopa – dopa precursor
Carbidopa – peripheral DOPA decarboxylase inhibitor |
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Bromocriptine, Pergolide, Pramiprexole and Parkinson’s?
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DOPA AGONISTS
Stimulates dopa receptors directly |
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Selegiline and Parkinson’s?
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MOA-B INHIBITOR
Elevates dopamine levels Also possible neuroprotective action |
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Entacapone and Parkinson’s?
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CATECHOL-O-METHYLTRANSFERASE INHIBITORS
Elevates Dopa levels Also possible neuroprotective action |
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Amantadine and Parkinson’s?
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ANTIVIRAL
May stimulate dopamine release |
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Drug treatment for Parkinson’s is ___________ not ____________.
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Symptomatic, NOT curative
Choice of treatment depends on many variables including symptom presentation, other concurrent health issues, and person’s age |
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Muscarinic cholinergic antagonists anti-Parkinsonian action?
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1. All have modest anti-parkinsonian action which is useful in the treatment of mild to moderate parkinsonism, or in combo w/ levodopa/carbidopa in pts w/ more severe parkinsonism
2. Also used in management in drug-induced parkinsonism in schizophrenic patients being treated w/ antipsychotic agents 3. Have modest beneficial effect on tremor and rigidity, little or no effect on bradykinesia BENZTROPINE |
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What are the side effects of anticholinergic agents?
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1. dry mouth
2. blurred vision 3. constipation and urinary retention 4. sedation and mental confusion |
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Anticholinergic agents are contra-indicated in pts with…?
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1. disturbances of bowel or bladder fxn
2. memory disorder 3. narrow angle glaucoma |
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Levodopa?
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Crosses the BBB
-- approx 95% of orally-admin levodopa is rapidly decarboxylated in the periphery to dopamine -- large doses are necessary to allow sufficient levodopa to cross BBB to elevate brain levels of Dopa |
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Levodopa S/Es?
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1. anorexia
2. nausea and vomiting 3. cardiac arrhythmias |
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Why do we use levodopa in combination with carbidopa?
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CARBIDOPA is a dopa decarboxylase inhibitor that does not cross the BBB, will block peripheral conversion of levodopa to dopamine
Results in a number of benefits 1. dose of levodopa can be decreased greatly 2. nausea and vomiting are largely eliminated 3. cardiac S/Es are diminished 4. effective doses of levodopa can be reached more quickly in the initial therapy 5. antagonism of therapeutic efficacy of levodopa by VitB6 is avoided. Pyridoxine enhances the effectiveness of decarboxylase No obvious pharm effects in pts w/ other neurological disorders or in normal individuals |
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Major side effect of levodopa?
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1. abnormal involuntary movements (dyskinesias) may develop w/ long-term therapy.
-- serious and dose-limiting side effect -- tolerance to dyskinesias does not develop 2. mild rxns occur early in therapy -- nervousness, insomnia -- anxiety, agitation and nightmares -- dose-limiting -- most common rxns are confusion and delirium -- severe depression w/ suicidal tendencies may occur -- other psychotic rxns include paranoid delusions and hallucinations MINOR (Keeton mentioned the two above; these are the others) cardiac arrhythmias and transient tachycardia due to action of dopamine on β-adrenergic receptors; occurs especially in patients w/ preexisting disturbances in cardiac fxn -- cardiac effects can be prevented by carbidopa or a β-adrenergic antagonist Orthostatic hypotension – occurs early in therapy and decrease in incidence w/ time Nausea and vomiting early in therapy and decrease in incidence w/ time. N/V result from an action of dopamine on the CTZ in the area postrema of the medulla, and are minimized by carbidopa |
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Bromocriptine?
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A dopamine receptor agonist w/ preference for the D2 subfamily of dopa receptors
Adjunctive therapy w/ levodopa/carbadopa in -- pts whose symptoms are not adequately controlled by levodopa/carbidopa -- pts experiencing “on-off phenomena” or “end of dose akinesia” b/c of its duration of action is longer than levodopa. |
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Other uses of bromocriptine?
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1. treatment of HYPERPROLACTINEMIA
-- increased serum levels of the hormone prolactin assoc w/ secreting tumors of the anterior pituitary -- with use of dopa antagonists, antipsychotic drugs in particular -- hyperprolactinemia assoc w/ amenorrhea and infertility in women, galactorrhea in both men and women 2. treatment of NEUROLEPTIC MALIGNANT SYNDROME -- NMS occurs in some pts being treated w antipsychotic drugs -- life-threatening and believed to result from extremely rapid blockade of postsynaptic dopamine receptors -- rapid decrease in dopaminergic activity can be reversed w/ dopa agonists such as bromocriptine -- give with dantrolene |
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MPTP-induced Parkinsonism?
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MPTP was produced initially as a byproduct of the synthesis of narcotic meperidine and was found to be the cause of parkinsonism in those who self-admin this illicit drug preparation
Converted by MAO-B to MPP+, which is extremely toxic to dopaminergic neurons, leading to their selective destruction in the substantia nigra Use of this drug in animals has provided a model for Parkinson’s disease |
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Etiology of Tourette’s syndrome?
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Characterized by multiple, complex involuntary mvmts including respiratory and vocal tics, such as grunting, barking, or compulsive utterances
Symptomatology of Tourette’s Syndrome is suggestive of dysfxn involving both basal ganglia and limbic structures |
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Treatment of Tourette’s syndrome?
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HALOPERIDOL
DOC in trtmt, but adverse effects of haloperidol, especially tardive dyskinesia, are a serious concern For ped populations, clonidine (alpha-adrenergic receptor antagonists) and risperidone (atypical antipsychotics) are effective and are preferred in order to avoid in children the development of tardive dyskinesia assoc w/ haloperidol |