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21 Cards in this Set

  • Front
  • Back
Benztropine and Parkinson’s?

Balances dopaminergic-cholinergic systems by reducing cholinergic dominance
Diphenhydramine and Parkinson’s?

Central muscarinic blockade
Levodopa and Parkinson’s?
Dopa precursor
Levodopa + carbidopa and Parkinson’s?
Levodopa – dopa precursor

Carbidopa – peripheral DOPA decarboxylase inhibitor
Bromocriptine, Pergolide, Pramiprexole and Parkinson’s?

Stimulates dopa receptors directly
Selegiline and Parkinson’s?

Elevates dopamine levels

Also possible neuroprotective action
Entacapone and Parkinson’s?

Elevates Dopa levels

Also possible neuroprotective action
Amantadine and Parkinson’s?

May stimulate dopamine release
Drug treatment for Parkinson’s is ___________ not ____________.
Symptomatic, NOT curative

Choice of treatment depends on many variables including symptom presentation, other concurrent health issues, and person’s age
Muscarinic cholinergic antagonists anti-Parkinsonian action?
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

What are the side effects of anticholinergic agents?
1. dry mouth
2. blurred vision
3. constipation and urinary retention
4. sedation and mental confusion
Anticholinergic agents are contra-indicated in pts with…?
1. disturbances of bowel or bladder fxn
2. memory disorder
3. narrow angle glaucoma
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
Levodopa S/Es?
1. anorexia

2. nausea and vomiting

3. cardiac arrhythmias
Why do we use levodopa in combination with carbidopa?
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
Major side effect of levodopa?
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
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.
Other uses of bromocriptine?
-- 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

-- 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
MPTP-induced Parkinsonism?
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
Etiology of Tourette’s syndrome?
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
Treatment of Tourette’s syndrome?

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