DEPRESSION Flashcards

1
Q

list some things depression is characterized by

A
unhappy mood 
guilt 
worthlessness 
loss of interest, motivation, appetite, pleasure 
concentration difficulty
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2
Q

depression is pathological when

A

symptoms are disproportionate or prolonged

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3
Q

costs of depression to society and individual

A

increased suicide risk
impacts family
lost productivity costs

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4
Q

prevalence

A

15-20%

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5
Q

why are women more likely to get diagnosed with depression

A

post partum
menopause
more likely to seek treatment

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6
Q

what precedes depression

A

increased stress and anxiety

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7
Q

individuals with depression tend to have

A

increased cort and crf levels

crf promotes cortisol release

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8
Q

Cushing syndrome

A

high levels of gluccorticoids and makes individuals more prone to depression

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9
Q

describe the dexamethasone suppression test

A

dexamethasone stimulates cort receptors in the same way cort does, telling the body that there is lots of cort production and so it leads to the HPA axis to stop producing it.

in depressed patients, production levels do not drop, negative feedback fails

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10
Q

neural abnormalities in depression

A
  1. increased amygdala and PFC activity could be due to disrupted regulation of amygdala by PFC
  2. reduced hippocampal levels which is a brake on the HPA axis
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11
Q

Glucocorticoid hypothesis

A

early life stress increases CRF expression in hypothalamus, which increases amygdala sensitivity to stress and decreases glucocorticoid receptors in hippocampus

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12
Q

three animal depression models

A
  1. chronic mild stress - rodents exposed to multiple different stressors (cold temp, wet be doing, restraint, sudden sound noise) for 1-3 weeks)
  2. Chronic social defeat - intruder that is dominant
  3. early maternal separation - separate young form mothers for brief periods daly during first few weeks of life
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13
Q

3 behavioural tests for depression animals

A
  1. forced swim/tail suspension
  2. social avoidance
  3. sucrose preference
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14
Q

The monoamine hypothesis of depression

A

depression is the result of abnormal reductions in brain monoamine (mostly 5ht and NE) levels
supporting evidence
1. came to this conclusion because reserpine which reduces monaomien levels induces depression and
2. monoamine oxidase inhibitors which block metabolism of monoamines and increase brain levels alleviate depression.
3. SSRI prozac found to be effective at treating depression
4. Tricyclic antidepressant imipramine (blocks monoamine reupatke) alleviates depression

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15
Q

problems with monoamine hypothesis

A
  1. antidepressants increase monoamine levels quickly yet takes a while to see reduction in symptoms
  2. not all depressed patients respond to increased monoamine levels large placebo effect
  3. depletion of 5ht or NE does not cause depressive phenotype in animal models
  4. tryptophan depletion induces symptoms in unmedicated patients but NOT healthy subjects without family history of depression (so just low serotonin levels do not cause depression )
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16
Q

5HT and depression

A
  1. sert polymorphisms linked to some forms of depression. higher 5HT causes reduced firing of 5ht via auto receptor mediated inhibition
  2. suicide victims and depressed patients show lower 5ht metabolite/precursor levels
  3. depressed individuals have higher levels of postsynaptic 5ht2 (compensatory)
  4. depressed individuals have reduced sensitivity to 5ht agonists.
17
Q

acute vs long term SSRI affects

A

acute: reduces 5ht release
long term: increases 5ht release by downregulating autoreceptors so these can increase synaptic 5ht release. repeated treatment also increases sensitivty of post 5ht receptors in pfc and hippocampus

18
Q

consistent findings of NE

A

untreated depressed patients show increase in a2 receptors which may attenuate NE release

19
Q

chronic antidepressant treatment does what

A

down regulated B-receptors for NE which parallels onset of therapeutic response so its important.

20
Q

monoamine oxidase inhibitors

A

blocks MAO which breaks down monoamines
unpleasant side effects: BP changes, sleep disturbances, overeating/weight gain
more dangerous: drugs that enhance NE function have more intense effect like cold meds.
Elevated tyramine causes more NE and so not allowed to eat cheese with it
MAO inhibit other liver enzymes which degrade drugs like alcohol for example p450

21
Q

TCA

A

block reuptake transporters. neurons must be firing for this
side effets - block histamine which is usually involved in arousal so causes sedation and fatigue.
dry mouth, constipation, urine retention
block a1 receptors, when combined with NE reuptake blocking can have dangerous side effects
low TI

22
Q

SSRIs

A

most commonly used less side effects
increases activation of 5ht receptors
side effects: anxiety, movement disorders, nausea, headache, insomnia, sexual dysfunction

23
Q

serotonin syndrome

A

dangerous effects when SSRIS combined with other 5ht agonist or drugs that interfere with SSRI metabolism
agitation, disorientation, ataxia, spasms, fever, shivering, diarrhea, increased BP/heart rate

24
Q

SSRI withdrawal

A

fatigue, insomnia, vivid dreams, increased anxiety, irritability

25
Q

treatments for treatment resistant depression

A

ketamine - non competitive NMDA antagonist. reduces symptoms by 70% after psychosis dissipates.

26
Q

treatments for bipolar disorder

A

lithium carbonate
elevates brain tryptophan and 5ht levels. reduces DA and NE activity by enhancing reupatek and reudcing release
side effects: increased thirst, urination, concentration and memory impairments, fate, tremor, weight gain
low TI

27
Q

cyclothymia

A

milder form of BPD patients cycle between dysthymia (mild depression) and hypomania (increased energy)