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8 Cards in this Set
- Front
- Back
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Parkinson's Overview
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Disease of the basal ganglia.
Poverty of movement, rigidity and tremor. decreased levels of dopamine (caudate nucleus, putamen and globus pallidus.) Degeneration of the nigrostriatal tract. |
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The blood brain barrier
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Cannot replace dopamine directly as it does not cross the BBB.
Must use precursor (L-dopa). However L-dopa is peripherally metabolised, reducing effective dose. Given with peripheral decarboxylase inhibitor. |
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Aetiology of Parkinson's
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Cause of Parkinson's Disease is unknown.
Antipyschotic drugs block dopamine receptors and often produce a Parkinson's like syndrome. |
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Dopaminergic Drugs
MOA, Adverse Effects, Problems with long term treatment |
Levodopa with selective extracerebral decarboxylase inhibitor.
-MOA: L-dopa immediate precursor to dopamine. -Adverse Effects: Nausea and Vomiting. Psychiatric side effects: vivid dreams, hallucinations, psychotic states and confusion. Over stimulation of the mesolimbic or mesocortical dopamine receptors. -Problems with long-term treatment: Gradual recurrence of parkinsonian akinesia. Various dyskinesias may occur. 'on-off' cycling. |
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Dopamine Agonists
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Bromocriptine/Ropinirole
-Used in an effort to prevent 'on-off' cycling early in Parkinson's. -Used when l-dopa patients start exhibiting 'on-off' cycling. |
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Drugs causing dopamine release
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Amantadine has muscarinic blokcing actions and probably increases dopamine release. It has modest antiparkinsonian effects in a few patients, but tolerance soon occurs.
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MAOb and COMT inhibitors
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Selegiline selectively inhibits MAOb. Reduces metabolism of dopamine in the brain. Used in late disease as an adjunct. May increase mortalitiy.
Entacapone inhibits catechol-O-methyltransferase COMT. slows elimination of L-dopa. Used in late disease. |
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Anticholinergics
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Muscarinic antagonists - most improvement in early parkinson's.
Though have many neurological and physiological side effects. |
