CNS pharmacology - Antidepressants

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  • Created by: Jess
  • Created on: 15-05-14 15:52
What are the physical signs of depression?
Pain, digestive/respiratory difficulties.
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What is the aetiology of depression?
A neurochemical imbalance caused by genetic and/or environmental factors.
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Outline the biological amine theory.
Depression is caused by the functional deficit of transmitters whilst mania is due to excess. Evidence for the following amines: 5-HT, NA and dopamine. Can be triggered by differrent events in different people.
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Where is drug treatment aimed at increased transmission targeted?
Inhibit reuptake, inhibit metabolism and enhance release.
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How can reuptake be inhibited in a NA neuron?
Inhibit the transporter at the presynaptic terminal clearing it from the synaptic cleft.
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How do tricyclic antidepressants work?
By inhibiting the NA reuptake transporter. Not specific - antagonist at several receptors giving different clinical effects.
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Name a tricyclic antidepressant.
Sedative - clomipramine, amitriptyline, dosulepin. Non-sedative - imipramine, lofepramine, nortriptyline.
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What are SSRIs?
Selective Serotonin Re-uptake Inhibitors.
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Give an example of an SSRI.
Citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline.
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How do monoamine oxidase inhibitors (MAOI) work?
Inhibit MAO that usually breaks down NA making more available for synaptic activity. Generally irreversible (only one reversible - moclobemide)
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Give an example of a MAOI.
Phenelzine, isocarboxazid, tranylcypromine.
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How can antidepressants enhance neurotransmitter release?
Alpha 2 adrenoceptor antagonists such as mirtazapine take away the negative feedback at the presynaptic terminal that would usually regulate (inhibit) release.
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What are the two mechanisms thought to underly the slow clinical efficacy of antidepressants?
Neuronal adaptation and neurogenesis.
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Outline the method of neuronal adaptation.
Cells have homeostatic mechanisms to turn down the excitation. Receptors can get turned off or endocytosed. Is a reduction in presynaptic autoreceptors or reuptake transporters required for clinical efficacy?
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Outline the method of neurogenesis.
Evidence that chronic AD treatment enhances serotonin activation that drives production of neurotrophins which produces new nerve cells in the hippocampus.
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What is the treatment for manic episodes/bipolar disorder?
Acute control: benzodiazepines, antipsychotics carbamzapine, valproic acid. Long term mood stabilisation - lithium carbonate, lithium citrate.
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How does lithium exert its action?
Inhibiting the enzyme inositol monophosphatase that is responsible for forming inositol to be reused following the G alpha q pathway.Uncompetitive inhibition - more active the pathway, greater the inhibition.
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What is amphetamine?
Indirectly acting sympathomimetic structurally related to noradrenaline.
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What is the mechanism of action of amphetamine?
Has weak action on postsynaptic adrenoceptors. Taken up by uptake 1 and displaces NA inside the vesicles, taken in by VMAT. NA builds up inside the cell until it leaks out. Mainly cytosolic NA not exocytosed. Stimulates the system.
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What are the clinical uses of amphetamine?
CNS stimulant in narcolepsy - prevent excessive daytime sleepiness. Used in ADHD - mechanism unclear (maybe dopaminergic pathways).
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Card 2

Front

What is the aetiology of depression?

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A neurochemical imbalance caused by genetic and/or environmental factors.

Card 3

Front

Outline the biological amine theory.

Back

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Card 4

Front

Where is drug treatment aimed at increased transmission targeted?

Back

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Card 5

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How can reuptake be inhibited in a NA neuron?

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