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
What is the monoamine theory for depression?
→ that there is a deficit of monoamines → 5-HT → dopamine → NA
26
What is the evidence for the monoamine theory?
→ 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
What is the evidence against the monoamine theory?
→ 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
What is the neuroendocrine theory?
→ there is hypersensitivity to the HPA axis
29
What neurons input to the hypothalamus?
→ noradrenergic | → 5-HT
30
Describe how cortisol is produced?
→ 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
What does CRH do?
→ mimics depression like symptoms
32
What is cortisol and CRH like in depressed patients?
→ Cortisol is higher | → increased CRH in CSF
33
What suppresses and increases the HPA axis?
→ hippocampus suppresses HPA | → Amygdala increases HPA
34
What are glucocorticoid receptor gene expression regulated by?
→ Early experience
35
What causes glucocorticoid receptor expression in the brain?
→ 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
How do SSRIs affect glucocorticoid receptor expression i the hippocampus?
→ they increase it
37
Lack of what receptor is associated with depression and why ?
→ 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
What is the neurogenesis theory for depression?
→ Evidence of neuronal loss and decrease in neuronal activity in the hippocampus and prefrontal cortex
39
What promotes neurogenesis?
→ ECT | → antidepressants
40
What promotes neurogenesis during development?
5-HT via BDNF (brain derived neurotrophic factor)
41
What increases BDNF?
→ SSRIs
42
What increases in the cortex of depressed people?
→ glutamate
43
Why does glutamate cause depression?
→ excessive glutamate leads to neurotoxicity which leads to neuronal death
44
Describe how excitotoxicity occurs
→ Chronic stress causes a big release of glutamate → Hyperactivation of NMDA receptors → Excitotoxicity occurs leading to neuronal loss
45
Describe how neurogenesis occurs mediated by NA and 5HT
→ 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
What is an adverse effect of ECT?
→ Memory loss
47
What does psychotherapy help with?
→ overcoming negative views
48
What do tricyclic antidepressants do?
→ block reuptake of NA and 5-HT
49
What is an example of an SSRI?
→ Fluoxetine
50
What is an example of an NA selective reuptake inhibitor?
→ reboxetine
51
What do MAOI do?
``` → 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
What does lithium do?
→ Stabilises mood | →Li+ like Na+ gets into neurons but stays there=> depolarisation
53
What are psychological treatment?
→Cognitive behaviour therapy | →Interpersonal therapy.
54
Why are SSRI recommended first?
much safer and fewer side-effects
55
What are MAO-I associated with?
→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
What are reversible MAOIs?
→RIMA →Accumulation of NA displaces the RIMA allowing degradation of excess NA →RIMAs safer and selective RIMAs (e.g moclobemide) better tolerated
57
What does chronic treatment of TCAs cause?
→downregulation of (β1) & 5-HT2 ⍺2, 5-HT1A/1D (autoR) →Also affect mACh, HR, 5HTR
58
What does chronic action of SSRIs cause?
→ 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
Why are SSRIs safer and better tolerated?
Lack of anticholinergic effect and no cardiotoxicity – better compliance and recommended for long term use Broader therapeutic profile
60
What are side effects of SSRIs?
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
What are examples of future development of AD?
→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
What is lithium's mode of action?
→inhibits enzymes involved in signal transduction (IP3, phosphorylation, GSK3, hormone induced cAMP inhibition)