Parkinson's Disease Pharmacology (HOYT)
Frontal cortex
Basal ganglia
Nucleus accumbens
Substantia nigra
Striatum
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Tyrosine; striatum
Tyrosine; substantia nigra
Tyrosine; basal ganglia
Tryptophan; striatum
Tryptophan; substantia nigra
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Almost complete loss of dopamine neurons from substantia nigra and the striatum
Neuronal degeneration and depigmentation
Appearance of intracellular inclusions called Lewy bodies in dopamine neurons
Two of the above
All of the above
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Primary Parkinson's disease
Secondary Parkinson's disease
Both forms have similar prevalence
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Drug side effects (e.g. antipsychotics and reserpine)
Viral infections (encephalitis lethargica)
Myocardial infarction
Stroke
Repetitive head trauma
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Hyperactivity of the remaining dopaminergic neurons
Increased rate of transmitter turnover
Increase in the number of dopamine receptors - "Denervation hypersensitivity"
Two of the above
None of the above, these are all compensatory mechanisms
D1
D2
D3
D4
D5
Inhibitory; increase
Inhibitory; decrease
Excitatory; increase
Excitatory; decrease
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Inhibition of potassium channels
Activation of potassium channels
Inhibition of voltage-sensitive calcium channels
Activation of voltage-sensitive calcium channels
Activation of sodium channels
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Dopamine-beta hydroxylase
DOPA decarboxylase
Aromatic amino acid decarboxylase
Tyrosine hydroxylase
None of the above
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True
False
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D1
D2
D3
D4
D5
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Remove GABA
Replace dopamine
Mimic action of dopamine
Increase release of dopamine/inhibit NMDA receptor
Antagonize acetylcholine
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