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Psych370 > 18.2 - Depressive disorders > Flashcards

18.2 - Depressive disorders Flashcards

1
Q

what is anhedonia

A

loss of cap to experience pleasure

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2
Q

How extreme can depression be

A

can become impossible to meet requirements

  1. keep a job
  2. maintain social contacts
  3. to eat
  4. maintain acceptable levels of personal hygiene
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3
Q

what are two common symptoms associated with depression

A

sleep disturbances

suicidal ideation

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4
Q

how long do depressive symptoms need to persist before one cab ne diagnosed with clinical or major depression

A

2 weeks

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5
Q

Explain the case of S.B

A
  • initially - excessive sleep, problems with focus, suicidal ideation, delusions - believed he was stupid and disliked, felt persecuted
  • became more severe: memory and attentional impairments affected ability to read/ delusional ideas and suicidal ideation constantly
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6
Q

what are the two general categories of depression

A
  1. reactive - triggered by a negative experience

2. endogenous - depression w no apparent cause

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7
Q

what is the LTP of depression

A

10%

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8
Q

gender differences in depression prev?

A

women 2x more likely to be diagnose

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9
Q

what is the current explanation fo why women have 2x higher prevalence of depression

A

unclear, but maybe gonadal-hormone related?

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10
Q

what is the lifetime risk of completed suicide in someone diagnosed with depression

A

4-15% depending on the study

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11
Q

at what age can you become depressed?

A

any, effects kids, adolescents and adults

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12
Q

does depression tend to present alone?

A

no, often comorbid with anxiety and heart disorders and diabetes

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13
Q

what are the two solid findings about genetic factors in depression

A
  1. twin studies - heritability estimate between 30 and 40%
  2. genome sequencing of those w recurrent major depressive disorder - identified 2 loci on chromosome 10 as contributors to the risk
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14
Q

where has most of the research on the causal role of experience in depression focussed?
- what is the believed mechanim of these?

A

role of stress and trauma - epigenetic mechanism are heavy mediators of depression onset in those susceptible

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15
Q

what are the two subtyp[es of MDD whose causes are more apparent?

A
  1. SAD - depression and lethargy recur during seasons - typically winter
  2. Peripartum depression - intense, sustained depression experience by some women during pregnancy or right after birth
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16
Q

what are the two lines of evidence that suggest SAD is caused by a reduction in sunlight

A
  1. incidence is higher in Alaska (9%) than Florida (1%) (winter days are shorter and less bright up north)
  2. light therapy is often effective in reducing symptoms
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17
Q

In what percentage of pregnancies do we see permpartum depression

A

~19%

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18
Q

what are the 5 major classes of drugs used to treat depressive disorders

A
  1. monoamine oxidase inhibitors (MAO inhibitors)
  2. tricyclic antidepressants
  3. selective monoamine reuptake inhibitors
  4. atypical antidepressants
  5. NMDA receptor antagonists
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19
Q

what was the first antidepressant, and what class was it

A

iproniazid (initially designed to treat suberculosis)

- monoamine agonist

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20
Q

explain the mechanism of action of Iproniazid

A

monoamine agonist by inhibiting the activity of monoamine oxidase (MAO)
- these enzymes break down monoamine neurotransmitters in the neuronal cytoplasm

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21
Q

what is the most dangerous side effect of MAO inhibits

A

the cheese effect - foods that contain the amine tyramine

  • tyramine elevates blood pressure
  • tyramine is typically metabolized rapidly in the liver by MAO
  • with MAO inhibited, they risk a massive spike in blood pressure
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22
Q

why are tricyclics named as they are

A
  1. antidepressant actin

2. chemical structures include three carbon rings

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23
Q

what was the first tricyclic antidepressant

A

imipramine, initially thought to be antipsychotic - not the case

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24
Q

what is the mechanism of tricyclics

A

block the reuptake of serotonin and norepinephrine

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25
Q

are tricyclics safer than MAO inhibitors?

A

YES

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26
Q

what is the mechanism of SSRIs

A

serotonin agonists - block the reuptake of serotonin from synapses

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27
Q

what was the first SSRI to be developed (both names)

A

fluoxetine (Prozac)

28
Q

what drug is fluoxetine molecularly similar to

A

imipramine - fluoxetine is no more effective than tricyclics

29
Q

why is fluoxetine and SSRIs so popular (2)

A
  1. fewer side effects than tricyclics and MEO inhibitors

2. act against a wider range of psychological disorders (not just depression)

30
Q

what did the success of SSRIs cause

A

the introduction of the selective norepinephrine reuptake inhibitors (SNRIS)

31
Q

what is an example of an SNRI

A

reboxetine

32
Q

how effective are SNRIs

A

as effect as SSRIs

33
Q

are there any other forms of selective (x) uptake inhibitors that are effective?
- give an example

A

yes, those that block the uptake of more than one monoamine neurotransmitter
- venlafaxine

34
Q

are atypical antidepressants all similar in some way?

A

no, catch all class for those that are not SSRIs, Mao inhibs or tricyclics

35
Q

what are the two examples of atypical antidepressants

A
  1. bupropion - various effects on NTs

2. agomelatine - melatonin receptor antagonist

36
Q

explain the mechanisms of action of bupropion

A
  1. dopamine reuptake inhibitor
  2. Norepinephrine reuptake inhibitor
  3. nicotinic-acytlcholine receptor blocker
37
Q

what is the mechanim of NMDA receptor antagonists

A

block the glutamate NMDA receptor

38
Q

what is an example of an NMDA receptor antagonist that has been shown to be very effective

A

Ketamine, dissociative hallucinogen

- single, low doses of ketamine reduce depression very fast, even in those who’ve been experiencing it for over 1 week

39
Q

what has the fact that ketamine has so many piss poor side effects caused

A

the search for more selective NMDA receptor antagonists that have fewer side effects

40
Q

is there any large difference between the effectiveness of the different classes?

A

Not so much, MAO, tricyclics, SMRIs are all about even at 50% improvement rate

41
Q

what fact reduces the positivity of antidepressant drug effects

A

25% of the 50% of participants who improve on the drugs can be attributed to placebo

42
Q

what types of depression are antidepressants most effective in

A

severe depression - those who are mildly effected tend not to improve more than placebo, but they do in fact work in severe cases

43
Q

what are the consistent findings from structural MRI studies of the brains of patients with depression (general finding plus 4 specific regions )

A

reductions in graymatter volumes in…

  1. PFC
  2. hippocampus
  3. amygdala
  4. cingulate cortex
44
Q

do only people who have depression experience the gray matter loss associated with the disorder

A

No, even those who are just genetically predisposed to it

45
Q

are gray matter reductions in the only negative outcomes of depression on brain
- in what brain area are these findings most consistent

A

No, also white matter reductions in several brain areas

- PFC baby

46
Q

where have fMRI studies found atypical activity in the brain? (6)
- are these just local, or are there other types of activity differences?

A
  1. frontal cortex
  2. cingulate cortex
  3. insular cortex
  4. amygdala
    5 thalamus
    6 striatum
  5. relation among the activity of these structures is atypical during a variety of cognitive states
47
Q

describe the monoamine theory of depression

A

depression is associated with the underacitvity at serotonergic and noradrenergic synapses

48
Q

what is the monoamine theory of depression nalrgely based on

A

the fact that MAO inhibs, tricyclic, and SRIS, SNRIs are all agonists of serotonin, norepinephrine, or both

49
Q

where do we get the other piece of support for the monoamine theory of depression?
what do the findings imply

A
  1. autopsy studies - norepinephrine and serotonin receptors are found more numerous in those who had clinical depression and had not received. treatment
  2. implicates a deficit in monoamine release bc when insufficient amount of a neurotransmitter is released at a synapse, there is usually a compensatory increase in the number of receptors for that NT
50
Q

what is up-regulation

A

the compensatory increase in the number of receptors for a NT that has been released in insufficient quantities

51
Q

what two lines of evidence have challenged the monoamine theory of depression

A
  1. disc that monoamine agonists are not very effective for most depressed patients, and even when they are, they’re only a little better than placebo
  2. discovery that other NTs like GABA, glutamate and acetylcholine play a role in the development of depression
52
Q

explain the theoretical justficiaiton for the neuroplasticity theory of depression

A

developed from the fact that monoamine agonists tend to only become effective after a few weeks after medication onset
- agonist effects at monoaminergic synapses is not the critical therapeutic mechanism - downstream increase? in neuroplasticitiy is the real mechanism

53
Q

how does the neuroplasticity theory of depression explain its ethology

A
  • depression results from a decrease of neuroplastic processes in brain structures that leads to neuron loss and other neural pathology
54
Q

what two kinds oil research have provided general support for the neuroplasticity theory of depression

A
  1. studies showing that stress and depression are assoc with the disruption of neuroplastic processes
  2. studies showing antidepressants are associated with an enhancement of neuroplastic processes
55
Q

what are the two examples of disrupted Neuroplastic processes in stress and depression

A
  1. reduction in the synthesis of neurotrophins

2. decrease in adult hippocampal neurogenesis

56
Q

what are the three examples of the increased neuroplastic processes after antidepressant treatments

A
  1. increase in neurotrophic synth
  2. increase in synaptogeneis
  3. increase in adult hippocampal neurogenesis
57
Q

which neurotrophic factor has been of particular interest to researchers, and why?

A

Brain derived neurotropic factor (BDNF)

- treatments that improve depression (pharm and nonpharm) increase BDNF levels in patients who show improvements

58
Q

what has the discovery that treatments that improve depression (pharm and nonpharm) increase BDNF levels in patients who show improvements led to (3)

A
  1. the proposal that decreased blood levels of BDNF is a biomarker for depression
  2. increased blood levels of BDNF as a biomarker for successful completion
  3. antidepressants increase blood levels of BDNF which increases neuroplastic processes that lead to the alleviation of depression
59
Q

what are the two treatments involving brain stimulation in depression

A
  1. repetetive transcranial magnetic stimulation

2. deep brain stimulation

60
Q

describe repetetive transcranial magnetic stimulation (rTMS)

A

form of transcranial mag stim that involves the noninvasive delivery of receptive magnetic pulses
- either high frequency, ie 5 per second (high frequency TMS) or low frequency (1/second) (low frequency)
delivered to specific cortical areas (typically PFC)

61
Q

what do we think high frequency TMS does

A

stimulates activity within the brain region to which it is appleid

62
Q

what do we think low frequency TMS does

A

inhibits activity within the brain regions to which it is applied

63
Q

what have metaanaluysis about rTMS shown

A

reliable improvement of depressive symptoms after either high or low frequency rTMS when compared with sham rTMS

64
Q

describe deep brain stimulation

A

chronic brain stimulation through an implanted electrode

- shown to be effective on patients whose depression did not respond to other treatments

65
Q

explain Loranzo and colleagues study of DBS

A

implanted the tip of a stimulation electrode into an area of white matter of the anterior cingulate gyrus in the medial PFC

  • delivered continual pulses of electrical stimulation that couldn’t be detected by patients
  • all 20 patients selected bc they had repeatedly failed to respond to conventional treatment
  • 60% SHOWEDE SUBSTANTIAL IMPROVEMENT
  • 35% WERE LARGELY SYMPTOM FREE
  • IMPROVEMETNS LASTER FOR AT LEAST A YEAR
  • replicated in other centres
66
Q

what do most researchers contend is the cause of our problems with treating depression

A

the diagnostic tools were using generate a large heterogeneous group of patients - misguiding research
- need more precise diagnostic tools

Psych370 (37 decks)

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