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11 Cards in this Set
- Front
- Back
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Agonize dopamine (D2) receptors
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Ergots - Bromocriptine
Non-Ergots (preferred) - Pramipexole, ropinirole |
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Increase dopamine
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Amantadine - antiviral that increases dopamine release
L-dopa - bradykinesia and rigidity are reversed quickly, but doesn't do much for tremor With carbidopa - inhibits conversion of L-dopa to dopa in the peripheral tissues |
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Prevent dopamine breakdown
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Selegiline - selective MAO type B inhibitor - delays clinical progression of PD
Used with COMT inhibitors: Entacapone and tolcapone - prevent L-Dopa degradation |
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Curb excess cholinergic activity
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Benztropine - improves tremor and rigidity, but has little effect on bradykinesia
Trihexyphenidyl - inhibits central muscarinic receptors |
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What converts L-dopa to dopamine?
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dopa decarboxylase
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How does carbidopa work?
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It inhibits the peripheral dopa decarboxylases, so less L-dopa is converted to dopamine in the periphery, allowing more L-dopa to make it into the CNS
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Long term use of L-dopa causes what?
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Dyskinesia following administration and akinesia between doses.
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Why is selegiline's specific inhibition of MAO type B important?
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MAO type B preferentially degrades dopamine over NE or 5-HT
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What is the plan with approaching PD?
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Try combinations of:
Selegiline Anticholinergics Amantadine until they no longer control symptoms, then introduce Levodopa and carbidopa |
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Desctibe the "on-off"phenomena
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An unpredictable and dose-independent characteristic of advanced parkinsons... no clear etiology... minimized with constant dosings
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Describe the "wearing-off" phenomena
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D/t progressive destruction of the striatonigral dopaminergic neurons over time. This response is dose-dependent and predictable.
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