PSYC 336 Exam Flashcards

1
Q

global burden of depression

A

“common cold” of mental disorders

so common

more costly than some medical disorders

276 mill people- crossculturally; twice as many women

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2
Q

epidemiology of depression

A

lifetime prevalence 17%
accounts for 70% of suicides
increases suicide rate 4 fold

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3
Q

major depressive disorder criteria

A

5+ symptoms present for at least 2 weeks
1 has to be either depressed mood or loss of interest
- depressed mood

  • loss of interest/pleasure (anhedonia)
  • change in appetite and/or weight
  • insomnia or hypersomnia
  • psychomotor agitation or retardation
  • fatigue or loss of energy
  • concentration problems and/or indecisiveness
  • worthlessness or guilt
  • suicidal ideation, intent, or action

huge heterogeneity of symptoms, presents challenge for developing etiology model and treatment models

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4
Q

“depression” in the global south

A

DSM criteria based on the manifestation of depression in area of the world where only 10% of world’s population lives

manifests differently in other cultures

Kufungisisa in Zimbawe - “thinking too much”

‘tension’ in India- somatic symptoms (ex. headaches)

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5
Q

Depression course (and draw them)

A

episodic (70-80%)
- 50% one (swoop)
- 50% multiple episodes

persistent (20-30%)
- persistent MDD (persistent at least to years)
- “double depression” (always feeling some depression), currently in episode
- “dysthymia” (chronic minor depression)
- “double depression” not currently in episode

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6
Q

single lifetime episode depression (SLEDs)

A

the lifetime course of 50% of those with episodic depression

should it be treated differently? maybe not; shouldn’t give $ treatments unnecessarily, better treatment if identified

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7
Q

depression is a multietiological disorder

A

SLEDS
- life circumstances

PERSISTENT
- underlying vulnerability

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8
Q

ACES

A

questionnaire; higher score associated with worse outcomes

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9
Q

building a depression model (draw and explain)

A

look at ipad

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10
Q

relation of early life stress to the onset of depression and anxiety disorders

A

review on slides ** make sure correct in notes **

takeaway: emotional abuse looks differently when it’s moms vs dads and who the kid is

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11
Q

relation of child maltreatment to severity of depression

A

those with a child maltreatment history and major depression have:

  • younger age at onset
  • poorer premorbid functioning
  • greater severity of symptoms
  • more persistent or recurrent coure
  • more treatment resistance
  • higher comorbidities
    ** emotional and sexual abuse are strongest predictors
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12
Q

resilience to early life stress

A

4 year longitudinal study of high schoolers at risk for dropout
- violence exposure and family conflict were strong risk factors for increasing depression over time
- support from mother significantly buffered these effects and was associated with lowering of depression of time

eisman 2015

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13
Q

Dr Cleopatra Caldwell

A

not everyone who experiences early life stress develops depression

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14
Q

the cognitive model of depression

A

the manner in which an event or stimulus is appraised or evaluated determines the type, intensity, and persistence of the experienced emotion

it’s not the stimulus itself that causes the response; it’s the manner it’s appraised/thoughts about it that causes the response

S > R

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15
Q

Dr Aaron T Beck (beck)

A

famous, revolutionized field of psych
was a freudian psychologist where there was a focus of S>R behaviour

but Beck was looking at what happened between S >R in the mind

***Beck says that cognitions determine the type, intensity etc of our emotions

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16
Q

levels of depressotypic cognition

A

AUTOMATIC THOUGHTS
(“she doesn’t like me”)
- highest level of cognition
- conscious
- running commentary in mind
- not necessarily negative
- cog theory- get ppl to be aware and evaluate accuracy of thoughts

INTERMEDIARY BELIEFS / ASSUMPTIONS
(“if someone gets close to me, they’ll reject me”)

CORE BELIEFS / SCHEMA
(“i’m unloveable”)

17
Q

cognitive schemas

A

hypothetical structures containing the stored representation of beliefs that are abstracted from sensory experiences
- guide the selection, encoding, organization, storage and retrieval of information
- we have schemas of things we’ve experienced in life which guide how we approach new situations

depressotypic schemas

18
Q

depressotypic schemas

A

enduring, rigid, and complex negative beliefs about the self, personal world and future that are resistant to change despite the presentation of disconfirming information

enduring- persists despite other experiences
rigid- hard to argue against
complex- everything wrapped up into complex bundle
resistant to change

19
Q

does negative cognition cause depression (study, explain findings and how they did it)

A

temple-wisconsin project (Alloy 2006)

1st year students given measures of negative cognitive schema content and negative cognitive style - rumination

students with no history of depression were divided into groups and followed for 4 years
- high cog risk
- low cog risk

high risk more likely to develop major depression as well as experiencing subthreshold symptoms

high risk also predicted recurrence

findings specific to depression, not anxiety disorder

20
Q

vulnerability model: early life stress affects the development of the HPA axis

A

purpose of the HPA axis is to release cortisol and other neurochemicals to enable fight or flight during acute life threatening events

goal is to release cortisol but then shut off when the threat is gone

it’s not developed to deal with chronic “human made” stressors

early life stressors can tune the HPA axis to become more sensitive; affects development of the HPA axis

21
Q

cortisol kills brain cells: glucocorticoid toxicity model

A

hypocampus: hold short term memories and transfer them to long term; emotional processes, including anxiety and avoidance behaviours

amygdala: links emotions to many other brain abilities, especially memories, learning and sensations

22
Q

Dr McEwen

A

the cortisol that’s released kills brain cells particularly in the hippocampus and amygdala

23
Q

consequences of cortisol toxicity

A

smaller amygdala and hippocampal volume

disrupted connectivity between amygdala and hippocampus and the cortex

  • rumination: when there’s not as much connectivity there’s repetitive rumination bc frontal cortex isn’t dampening it
  • impaired extinction of painful memories: painful memories consisting, harder to integrate
  • emotional dysregulation: problems with control