PHYS - NEURO > 18. DEPRESSION > Flashcards

18. DEPRESSION Flashcards

(18 cards)

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1
Q

What are affective disorders & give examples?

A
  • Affective disorders are disorders of mood rather than thought or cognition
  • They are the main cause of premature death or disability
  • Depression is the most common affective disorder
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2
Q

What are the two types of depression?

A
  1. UNIPOLAR DEPRESSION

2. BIPOLAR DEPRESSION

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3
Q

What is unipolar depression?

A
  • Mood swings occur in one direction
  • Most common type of depression
  • Mainly due to environment
  • 25% of cases due to genetics
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4
Q

What is bipolar depression?

A
  • Bipolar depression is characterised by oscillations between mania & depression
  • Mania can be impulsive actions, aggression, irritability, excessive exuberance
  • Tends to run in families, mainly due to genetics
  • Onset is in early adulthood
  • Two types of bipolar depression
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5
Q

What are the two types of bipolar depression?

A
  • TYPE 1 = More mania episodes with or without depression

- TYPE 2 = Depression with hypomania

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6
Q

What criteria is used to diagnose depression?

A
  • DCM 5 for diagnosis where 5 out of 8 symptoms must be present including depressed mood & loss of interest
  • ICD 10 is the criteria for the symptoms
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7
Q

What are the emotional symptoms of depression according to ICD-10?

A
  • Apathy, pessimism, negativity
  • Loss of motivation, feeling guilty
  • Low self esteem
  • Indecisiveness
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8
Q

What are the biological symptoms of depression according to ICD-10?

A
  • Reduced activity
  • Loss of appetite
  • Loss of libido
  • Sleep disturbance
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9
Q

What are the three theories of depression?

A
  1. MONOAMINE THEORY
  2. NEUROENDOCRINE THEORY
  3. NEUROPLASTICITY THEORY
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10
Q

What does the monoamine theory of depression suggest?

A
  • The Monoamine theory of depression suggests that depression is due to a deficiency in monoamines such as NA, DA & 5HT
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11
Q

What is the supporting evidence for the monoamine theory?

A
  • Reserpine depletes NA & 5HT which induces depression

- Antidepressants increase the levels of monoamines in the brain

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12
Q

What is the evidence against the monoamine theory?

A
  • Antidepressants take several weeks to work but the increase in monoamines is acute
  • Cocaine inhibits the uptake of monoamine but it doesn’t have an antidepressant effect
  • Low levels of serotonin are associated with aggression rather than depression
  • Antidepressants have a weak uptake on monoamine uptake
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13
Q

What does the neuroendocrine theory suggest?

A
  • The neuroendocrine theory suggests that hypersensitivity of the HPA axis leads to excessive cortisol which is responsible for depression, without a stimuli
  • Excessive cortisol can cause detrimental gene expression resulting in apoptosis of neurons -> depression
  • Noradrenergic & serotonergic neurones project into the hypothalamus
  • Hypothalamus produces CRH, Pituitary produces ACTH, Adrenal gland produces cortisol
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14
Q

What two brain structures project into the hypothalamus?

A
  • Amygdala
  • Hippocampus
  • The amygdala stimulates the HPA axis to produce cortisol
  • But the hippocampus stimulates the HPA axis to inhibit cortisol release
  • High levels of cortisol feedback to the hippocampus which causes a inhibitory output on the hypothalamus
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15
Q

What happens to hippocampal feedback to the hypothalamus in depression?

A
  • There’s an increase in cortisol in the plasma & CRH in the CSF of depressed patients
  • Decreased hippocampal feedback to the hypothalamus, it’s impaired meaning cortisol levels aren’t reduced
  • There’s down regulation of glucocorticoid receptors in the hypothalamus, meaning less cortisol activates the hippocampus so the inhibitory output is reduced
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16
Q

What happens to the HPA axis due to maternal deprivation?

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A
  • Maternal deprivation = downregulation of glucocorticoid receptors in hippocampus
  • Cortisol binds to these receptors, but it’s not enough to activate hippocampus
  • Results in a reduced inhibitory output of the hippocampus to the HPA
  • HPA isn’t inhibited, so cortisol levels continue to rise
17
Q

How can maternal deprivation predispose individuals to depression?

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A
  • Downregulation of glucocorticoid receptors on hippocampus results in reduced negative feedback to the HPA
  • This means that the HPA is less sensitive to high cortisol levels so continues to produce cortisol
  • Overactivation of HPA axis predisposes individuals to depression
18
Q

What is the effect of nurturing on the HPA axis?

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A
  • Nurturing or tactile stimulation activates serotonergic pathways projecting into the hippocampus
  • Serotonin causes a long-lasting increase in gene expression for the glucocorticoid receptors
  • Upregulation of the glucocorticoid receptors in the hippocampus mean that it can respond to cortisol levels and feedback to the HPA accordingly
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