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depression Flashcards

1
Q

2 ways of treating depression?

A

CBT or pharmacotherapy

-side effects to drugs

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2
Q

what can cause depression?

A
  • premature death

- disability

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3
Q

2 types of depression?

A

unipolar or bipolar

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4
Q

explain unipolar depression

A

most common type, mood swings in 1 direction
75% of cases are reactive/environmental
25% of cases are genetic

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5
Q

explain bipolar depression

A

less common, oscillation between depression and mania, mood swings in 2 directions

  • mania is excessive exuberance, self confidence, aggression, irritability
  • more based on genetics
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6
Q

depressive disorder

A

low state, feelings of guilt, sadness, low self worth

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7
Q

major depressive disorder

A

severe pattern of depression that is disabling, not caused by factors like drugs/general medical condition

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8
Q

what is the name of major depressive disorder that is chronic?

A

dysthymic disorder

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9
Q

is diagnosing depression easy?

A

no

you can do a clinical interview and ask questions, and use the book

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10
Q

what is DSM IV?

A

what psychiatrists use to diagnose a person with any mental illness

  • need 5 or more of the symptoms present in the same 2 week period
    eg. significant weight loss, insomnia, feeling of low self worth, recurrent thoughts of death, low energy, not able to concentrate
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11
Q

how can the symptoms of depression be categorised?

A

emotional symptoms
-pessimism, loss of motivation, low self esteem, indecisiveness

biological symptoms
-decreased appetite, sleep disturbance, loss of libido

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12
Q

how does depression differ between males and females?

A

affects twice as many females

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13
Q

how does depression differ between age groups?

A

1st episode of depression usually late adolescence/early adulthood

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14
Q

suicide

A

20% of depressed patients attempt suicide

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15
Q

depression and comorbidity

A

depression is often comorbid with other psychiatric conditions
-eg. cancer, pain

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16
Q

name some medical conditions where you would find depression:

A
  • terminal illness
  • chronic illness
  • neurological disease
  • stroke
  • drug abuse
  • parkinsons disease
  • anxiety
17
Q

what are comorbid?

A

depression and anxiety

18
Q

is there a genetic predisposition to depression, and how do we know this?

A

yes there is, we know this because of twin studies

-the environment also plays a role

19
Q

explain the monoamine theory of depression

A

depression is caused by monoamine deficiencies

  • reduced activity of noradrenergic/serotonergic systems
  • antidepressant drugs increase amine concentration in the brain
20
Q

explain the neuroendocrine theory of depression

A

depression is caused by hypersensitivity of the HPA axis

  • stress activates the hypothalamus to release CRH, ant pit releases ACTH, adrenal cortex (zona fasiculata) releases cortisol
  • HPA activated in situations which normally wouldn’t even be considered stressful
  • results in increased basal cortisol levels
  • increased CRH levels have been found in cerebrospinal fluid, and increased plasma cortisol levels in depressed patients
  • decreased hippocampal glucocorticoid receptors
21
Q

what controls the HPA?

A

HPA releases cortisol, which acts positively on the hippocampus
-hippocampus inhibits the HPA
-amygdala stimulates the HP
so, hyperactive amygdala or hypoactive hippocampus can cause depression

22
Q

role of tactile stimulation?

A

tactile stimulation after birth activates 5-HT pathways to the hippocampus
-5-HT triggers long lasting increase in the expression of glucocorticoid receptor gene
-therefore, increase in glucocorticoid receptors in hippocampus
this is why abused/neglected babies can end up with mental illnesses

23
Q

how do SSRIs affect glucocorticoid receptors?

A

they increase glucocorticoid receptors in hippocampus

24
Q

hippocampus and pre frontal cortex

A

neuronal loss and decreased neuronal activity in depression

25
Q

what does 5-HT promote?

A

neurogenesis during development (BDNF)

BDNF promotes survival of cells in the brain

26
Q

how does exercise have an anti-depressant effect?

A

increased BDNF levels, therefore increased neurogenesis

27
Q

chronic stress consequences

A
  1. increased cortisol levels will stimulate the detrimental gene transcription response
  2. increase glutamate release, hyper activation of NMDA receptors, causing excitotoxicity neuronal death and depression
28
Q

what inhibits the detrimental gene transcription response?

A

activation of alpha 2 or 5HT-1A

-ie high levels of NA or serotonin

29
Q

treatments for affective disorders?

A
  • ECT

- Psychotherapy (CBT)

30
Q

ECT

A

electroconvulsive therapy,

  • localised electrical stimulation
  • evidence of neurogenesis but side effect of MEMORY LOSS
31
Q

psychotherapy

A

treats mild-moderate depression

  • overcome negative views
  • based on the idea that social interaction has a big anti-depressant effect
32
Q

all drugs that treat depression work by….

A

increasing NA or serotonin levels
-neurons get activated, NA released and binds to post-synaptic receptors, gets back inside the neurones via NA transporter

33
Q

drugs treatments

A 
Monoamine Oxidase Inhibitors (MAOIs)
Tricyclic Antidepressant Drugs (TCAs)
Selective Serotonin Re-uptake Inhibitors (SSRIs)
mixed 5HT/NA reuptake inhibitors (SNRIs)
NA reuptake inhibitors
34
Q

Tricyclic antidepressants (TCAs)

A
  • block reuptake of 5HT and NA, increase levels of these 2 in the synaptic cleft
  • down regulation of presynaptic receptors and therefore increase in transmitter release
  • long time to produce effects
  • good but not ideal
  • cardiovascular effects
  • also affects other receptors eg. muscarinic
35
Q

Monoamine Oxidase Inhibitors (MAOIs)

A
  • increased cytoplasm levels of 5HT/NA, increased leakage of these 2 monoamines
  • increased levels in the synaptic cleft
36
Q

Selective Serotonin Re-uptake Inhibitors (SSRIs)

A

5-HT reuptake inhibitor

  • Increase in 5HT in synaptic cleft
  • autoreceptors down regulated
37
Q

benefits and consequences of Selective Serotonin Re-uptake Inhibitors (SSRIs):

A

no cardiovascular problems because they don’t affect NA, but side effects include:

  • insomnia and sexual dysfunction due to activation of 5-HT2A receptor
  • nausea, diarrhoea and headache due to 5-HT3 receptor activation
38
Q

how long does the anti-depressant effect take?

A

antidepressant effect takes several weeks

39
Q

how do anti-depressants dampen down the HPA hyperactivity?

A

Increased hippocampal glucocorticoid receptor expression

Neuro (21 decks)

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