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Neuroscience > Depression > Flashcards

Depression Flashcards

1
Q

What is neurology?

A

→ Branch of medicine, diagnosis & treatment of nervous system disorders

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2
Q

What is psychiatry?

A

→ Branch of medicine, diagnosis & treatment of disorders that affect the mind and psyche

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3
Q

What is human behaviour a product of?

A

→ Product of brain activity

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4
Q

What is the brain a product of?

A

→ Genetics and environment

→ Experience

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5
Q

What is depressive disorder?

A

→ A low state marked by significant levels of sadness
→ lack of energy

→ low self worth
→ Guilt
→ related syndromes

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6
Q

What is a major depressive disorder?

A

→ A severe pattern of depression that is disabling and not caused by factors such as drugs or a medical condition

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7
Q

What are characteristics of affective disorders?

A

→ Disorders of mood rather than thought/cognition

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8
Q

What is unipolar depression?

A

→ mood swings in one direction

→ most common depressive illness

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9
Q

How many unipolar depression cases are caused by the environment?

A

→ 75%

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10
Q

How many cases of unipolar depression are caused by genetics?

A

→ 25%

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11
Q

What is bipolar depression?

A

→ Oscillation between depression and mania

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12
Q

What is mania?

A

→ Excessive exuberance
→ enthusiasm

→ self confidence
→impulsive actions
→ aggression
→ irritability
→ delusions of grandiose
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13
Q

What are the criteria used for depression diagnosis?

A

→ DSM-IV or ICD-10

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14
Q

What are the criteria for depression?

A

→ Five or more of the symptoms during the same 2 week period

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15
Q

What are the emotional symptoms of depression?

A

→ Apathy
→ pessimism

→ negativity
→ low self esteem
→ feeling guilty
→ loss of motivation
→ indecisiveness
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16
Q

What are the biological symptoms of depression?

A

→ Reduced activity
→ Loss of libido

→ Sleep disturbance
→ Loss of appetite

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17
Q

What are the animal models of depression?

A

→ Learned helplessness

→ mother infant separation is reversed by antidepressants

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18
Q

What is the gender bias in depression?

A

→ It affects twice as many females as males

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19
Q

What is the lifetime prevalence of depression in men and women?

A

→ 10-25% in women

→ 5-12% in men

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20
Q

When does the first depressive episode happen?

A

→ late adolescence

→ early adulthood

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21
Q

What is depression comorbid with?

A

→ terminal and chronic illness
→ thyroid dysfunction

→ neurological disease
→ stroke
→ drug abuse

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22
Q

How many depressed individuals will attempt suicide?

A

→ 20%

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23
Q

If one twin has depression what is the probability that the other will get it too?

A

→ 40-50%

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24
Q

What are environmental factors that may lead to depression?

A

→ loss
→ Environmental stressors

→ Social isolation

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25
Q

What is the monoamine theory for depression?

A

→ that there is a deficit of monoamines
→ 5-HT

→ dopamine
→ NA

26
Q

What is the evidence for the monoamine theory?

A

→ Overall reduced activity of dopaminergic and serotonergic systems
→ Reserpine depletes the brain of NA and 5-HT and induces depression

→ main antidepressant drugs increase amines in the brain

27
Q

What is the evidence against the monoamine theory?

A

→ It is difficult to show deficits in the brain of NA and 5-HT
→ most antidepressants take several weeks to work but increase in amines is acute

→ some antidepressants are weak and have no effect on amine uptake
→ cocaine blocks amine uptake but has no antidepressant effect
→ increase in 5-HT is linked to aggression and not depression

28
Q

What is the neuroendocrine theory?

A

→ there is hypersensitivity to the HPA axis

29
Q

What neurons input to the hypothalamus?

A

→ noradrenergic

→ 5-HT

30
Q

Describe how cortisol is produced?

A

→ Hypothalamus releases CRH (corticotropin releasing hormone)
→ CRH acts on the pituitary - release of adrenocorticotropic hormone (ACTH)

→ Cortisol release from the adrenal cortex in response to increased ACTH in the blood

31
Q

What does CRH do?

A

→ mimics depression like symptoms

32
Q

What is cortisol and CRH like in depressed patients?

A

→ Cortisol is higher

→ increased CRH in CSF

33
Q

What suppresses and increases the HPA axis?

A

→ hippocampus suppresses HPA

→ Amygdala increases HPA

34
Q

What are glucocorticoid receptor gene expression regulated by?

A

→ Early experience

35
Q

What causes glucocorticoid receptor expression in the brain?

A

→ tactile stimulation after birth activates 5-HT pathways to the hippocampus
→ it triggers a long lasting increase in the expression of glucocorticoid receptors in the hippocampus

36
Q

How do SSRIs affect glucocorticoid receptor expression i the hippocampus?

A

→ they increase it

37
Q

Lack of what receptor is associated with depression and why ?

A

→ Decreased glucocorticoid receptors in the hippocampus (cortisol)
→ more cortisol is needed to bind and negatively feedback to the hippocampus

→ hippocampus downregulates the HPA axis

38
Q

What is the neurogenesis theory for depression?

A

→ Evidence of neuronal loss and decrease in neuronal activity in the hippocampus and prefrontal cortex

39
Q

What promotes neurogenesis?

A

→ ECT

→ antidepressants

40
Q

What promotes neurogenesis during development?

A

5-HT via BDNF (brain derived neurotrophic factor)

41
Q

What increases BDNF?

A

→ SSRIs

42
Q

What increases in the cortex of depressed people?

A

→ glutamate

43
Q

Why does glutamate cause depression?

A

→ excessive glutamate leads to neurotoxicity which leads to neuronal death

44
Q

Describe how excitotoxicity occurs

A

→ Chronic stress causes a big release of glutamate
→ Hyperactivation of NMDA receptors

→ Excitotoxicity occurs leading to neuronal loss

45
Q

Describe how neurogenesis occurs mediated by NA and 5HT

A

→ Noradrenaline acts on alpha 2 receptors
→ 5-HT acts on 5-HT1A receptors

→ these cause beneficial gene transcription
→ increased neurogenesis and inhibition of neural apoptosis

46
Q

What is an adverse effect of ECT?

A

→ Memory loss

47
Q

What does psychotherapy help with?

A

→ overcoming negative views

48
Q

What do tricyclic antidepressants do?

A

→ block reuptake of NA and 5-HT

49
Q

What is an example of an SSRI?

A

→ Fluoxetine

50
Q

What is an example of an NA selective reuptake inhibitor?

A

→ reboxetine

51
Q

What do MAOI do?

A 
→ block the degradation of 5-HT and NA
→increases [NA/5-HT]cytoplasm 
 and increases leakage of amine
→Increases [NA/5-HT] in synaptic cleft
→increases [5-HT] > [NA] > [DA]
52
Q

What does lithium do?

A

→ Stabilises mood

→Li+ like Na+ gets into neurons but stays there=> depolarisation

53
Q

What are psychological treatment?

A

→Cognitive behaviour therapy

→Interpersonal therapy.

54
Q

Why are SSRI recommended first?

A

much safer and fewer side-effects

55
Q

What are MAO-I associated with?

A

→food and drug interactions
→Tyramine (in cheese and wine) acts as indirect sympathomimetic and increases NA release
→Excess NA destroyed by MAO – if blocked NA will accumulate
→NA accumulation (Increases headache, intracranial haemorrhage => elevation in BP => severe hypertension)
→MAOIs not specific – reduce metabolism of opioid analgesics and alcohol

56
Q

What are reversible MAOIs?

A

→RIMA
→Accumulation of NA displaces the RIMA allowing degradation of excess NA

→RIMAs safer and selective RIMAs (e.g moclobemide) better tolerated

57
Q

What does chronic treatment of TCAs cause?

A

→downregulation of (β1) & 5-HT2
⍺2, 5-HT1A/1D (autoR)

→Also affect mACh, HR, 5HTR

58
Q

What does chronic action of SSRIs cause?

A

→ increases [5-HT] down regulation of 5-HT1A/1D
autoreceptors, disinhibition of 5-HT
neuron, inc. 5-HT release

→increased 5-HT release down regulates
post synaptic 5-HT receptors
‘normalising’

59
Q

Why are SSRIs safer and better tolerated?

A

Lack of anticholinergic effect and no cardiotoxicity – better compliance and recommended for long term use

Broader therapeutic profile

60
Q

What are side effects of SSRIs?

A

Insomnia & sexual dysfunction (5-HT2)

→Nausea; GI distress; headache (5-HT3)

→Increased risk of suicidal behaviour under 18

→Not used in combination with
TCA, MAO-I
(inhibits TCA metabolism)
(serotonin syndrome/tremor, seizures, hyperthermia, CV collapse)

61
Q

What are examples of future development of AD?

A

→Drugs affecting monoamine transmission

→Drugs affecting Ion channels

  • nACh agonist, antagonist, partial agonist
  • NMDA blockers (ketamine), could cause psychosis

→ Cortisol receptor antagonist, M1/M2 agonist, NK1/NK2 antagonists

62
Q

What is lithium’s mode of action?

A

→inhibits enzymes involved in signal transduction (IP3, phosphorylation, GSK3, hormone induced cAMP inhibition)

Neuroscience (21 decks)

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