Depression and antidepressants

three types of affective dissorder
Unipolar depression, bipolar, Seasonal affective disorder
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Features of unipolar depression
1.4% incidence, females > men, 75% reactive.
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How is unipolar depression diagnosed
Five or more symptoms present during the same 2 week period representing a change from previous funcitoning
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10 areas of symptoms
1. mood. 2. Pleasure. 3. weight. 4. Sleep. 5. psychomotor, 6. energy levels. 7. self worth, 8. concentration, 9. suicide
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The neurotransmitters involved in depression
noradrenaline and serotonin
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More about noradrenaline and depression
It's involved in drive and motivation, and there is post-mortem evidence for depression.
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Where is serotonin found and what is it involved in?
Dorsal and ventral raphe - control of mood, anxiety, sleep, libido, food intake, pain perception (inc.)
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Three options for treatment of depression
Psychology therapies, antidepressant drugs, electroconvulsive therapy
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Describe the monoamine hypothesis
depression is caused by functional deficits of monoamine transmitters in certain areas of the brain (mania = functional excess).
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Support for the monoamine hypothesis - things that INCREASE mood
Tricyclic antidepressants - block uptake of NA and 5HT. Moaoi's - block metabolism of NA/5HT
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Support for the monoamine hypothesis - things that decrease mood.
a-methyl tyrosine inhibits NA synthesis. Methyldopa inhibits NA synthesis
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Drugs that DONT support the monoamine hypothesis
amphetamine which releases NA and blocks uptake, has no effect on depression. Cocaine also inhibits NA reuptake and has no effect.
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Drugs that increase monoamine synthesis and don't have an effect on depression
tryptophan 5HT synthesis, and has only been shown to increase mood sometimes. L-DOPA has no effect.
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5HT ant/agonists and the monoamine hypothesis
methysergide is a 5ht antagonist that has no effect. iprinidole is a 5ht antagonist that increases mood
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Describe the HPA axis
hypothalamic nuclei recieve NA and 5HT inputs, which causes it to release CRH onto the anterior pituitary, which releases ACTH which stimulates cortisol release from the adrenal cortex
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What is different in the HPA axis in depressed patients
High cortisol levels (increased CRH), reduced growth hormone, increase prolactin.
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What test can be given for depression
dexamthasone suppression test, depressed patients fail to respond
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BDNF and depression
In depressed people there is reduced BDNF or malfunction of TrkB - some antidepressants increase BDNF
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What is seen in the cortex of depressed patients
elevated cortical GLU levels - some antidepressants reduce glutamate levels or depress NMDA receptor function
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LTP and depression
antidepressants both depress and facilitate LTP
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Areas where neurons are lost in depression
hippcampus and prefrontal cortex. this is an effect mimicked by chronic stress or an increase in glucocorticoids
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One way to promote neurogenesis
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The 5 classes of antidepressant. See if you can draw the table
MOAO-I, tricyclic antidepressants, SSRIs, noradrenalineSRI's, serotonin and noradrenaline reuptake inhibitors, Noradrengergic and specific serotonergic antidepressants
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Card 2


Features of unipolar depression


1.4% incidence, females > men, 75% reactive.

Card 3


How is unipolar depression diagnosed


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Card 4


10 areas of symptoms


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Card 5


The neurotransmitters involved in depression


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