412 Depression Flashcards

1
Q

core features of depression

A
  • dysphoria (prolonged sadness)
  • irritability (excessive sensitivity, hostility, moodiness)
  • anhedonia (loss of pleasure or interest in previously enjoyable activities)
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2
Q

symptom vs. syndrome vs. disorder

A
  • symptom: feeling of emotion or sadness (common)
  • syndrome: cluster of common symptoms (extreme on dimension of negative mood/affect)
  • disorder: syndrome that has been occurring for a certain amount of time and occurring with impairment in functioning
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3
Q

DMDD differential diagnosis

A
  • cannot be diagnosed concurrently with ODD or Bipolar
  • DMDD was created for kids who were being diagnosed with BP but only presenting with irritability
  • DMDD is more chronic irritability, while BP is more phasic
  • more intense irritability than you might see in MDD/PDD
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4
Q

evidence for DMDD

A
  • applying new criteria to existing data = hazy boundaries, not good at identifying those with the disorder
  • DMDD not well differentiated from CD or ODD
  • not much difference in symptom severity or functional impairment with or without the disorder
  • DMDD diagnosis showed poor stability
  • very high comorbidity (also meeting criteria for ODD, which can’t be diagnosed concurrently)
  • validity is questionable, high risk of over-diagnosis (irritability is very common in child development)
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5
Q

epidemiology of DMDD

A
  • limited studies before DSM-5 inclusion showed highest rates of symptoms in preschoolers
  • highest co-occurrence with depressive disorders and ODD (higher rates of social impairment, school suspension, service use, poverty)
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6
Q

categorical vs. dimensional depression

A
  • many kids and teens have subclinical depression
  • still show significant impairment
  • at greater risk for developing depression and other disorders/difficulties
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7
Q

epidemiology of MDD

A
  • 1% or preschool-age kids
  • 2% of elementary-school kids
  • 11% of adolescents
  • racial ethnic differences: Latinx youth and Black youth more likely to experience mood disorders, but white youth more likely to receive Tx (lower SES, discrimination)
  • lack of gender differences in childhood, and divergence increases after 15
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8
Q

possible explanations for the gender gap

A

(1) girls more likely to seek help (gender difference found in community samples, but there isn’t necessarily a difference)
(2) biological factors (onset of gender disaprity emerges during puberty, earlier puberty = depression but only in girls, puberty may sensitize girls to stress)
(3) puberty may create stress for girls (changes in physical appearance, sex-role identification), especially interpersonal stress (peer rejection, conflict, generating stress) because girls are invested in their relationships
(4) cognition: negative attributions (but this appears to be equal for boys and girls)
(5) coping: girls tend to ruminate or co-ruminate

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9
Q

preschool depression

A
  • earlier onset associated with more severe and chronic depression later (and higher rates of ADHD and anxiety at school age)
  • 2-week duration criteria not as relevant for preschoolers (even if not met, still associated with MDD 2 years later)
  • depressed 4-6 year-olds show altered brain activity (more amygdala activity when viewing emotional faces, like you see in adults) - dirupted amygdala functioning could be a biomarker or a consequence of depression throughout lifetime
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10
Q

biological factors

A
  • high (but lots of variability) heritability estimates (35-75%)
  • early exposure to stress can sensitize to later stress (stress reactivity)
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11
Q

stress reactivity

A
  • depression in moms associated with higher cortisol levels which can affect fetus
  • number of months a woman is depressed is associated with child’s elevated cortisol levels at 6-7 years
  • epigenetic transmission of biological processes
  • transmission of altered stress physiology postnatal through breastmilk
  • early experiences (sensitive period) with caregivers important for attachment (maternal depression may be associated with problematic parenting which alters child’s stress reactivity)
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12
Q

social-cognitive processing in depression

A
  • negative encoding biases (attentional, toward sadness/negative affect)
  • interpretation (negative attributional biases, unconscious pattern of response)
  • response search not as important, but still tend to identify fewer assertive responses
  • response decision: report themselves as less able to carry out assertive strategies (and as less effective) and think avoidant strategies are better
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13
Q

interpretation biases study

A
  • looking at high-risk population (cognition as a risk factor)
  • blending two words acoustically (neutral-negative, neutral-positive) to make the result a 50-50 chance of hearing either word
  • at-risk girls showed a preference for depression-related negative words (but not threat words), control group showed a preference for positive words
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14
Q

interpersonal theories of depression

A
  • less prosocial, less assertive, more avoidant and withdrawn, kids may be more hostile and aggressive
  • responding to interpersonal challenges in problematic ways
  • difficult to maintain healthy and close friendships with depression (less support, less social skill training)
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15
Q

stress exposure models of depression

A
  • depression caused by exposure to stress
  • peer rejection leads to depression
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16
Q

stress generation models of depression

A
  • higher depression leads to higher stress exposure
  • symptoms impact your interactions, and those difficulties cause interpersonal problems which exacerbate symptoms
  • depressed kids get rejected more
17
Q

evidence for stress generation models

A
  • clinical interview to place participants into 4 groups: depressed only, externalizing only, both, control
  • assessed life stress experiences and rated them in terms of severity, extent to which child contributed to the event (independent or dependent), interpersonal/non-interpersonal
  • depression associated with dependent and interpersonal stress
  • externalizing associated with dependent and non-interpersonal
  • neither was associated with independent
  • comorbid had highest levels of interpersonal and non-interpersonal
18
Q

co-rumination

A
  • dwelling on problems without solving them with a friend
  • associated with better friendships, but also with more negative mood
  • dwelling on negative affect with a friend = negative mood, but not friendship quality
  • rehashing the problem and speculating about what might happen = better friendship, but not negative mood
19
Q

reassurance seeking

A
  • initially, friends are happy to provide reassurance, but people keep seeking because they think they don’t mean it
  • over time, this becomes irritating and invalidating
  • which leads to friendship withdrawal and peer rejection
  • associated with unstable friendships
20
Q

contagion

A
  • your own depressive symptoms predict your friend’s depressive symptoms
  • co-rumination is the mediating mechanism
21
Q

CBT model of depression

A
  • based on diathesis-stress model
  • depression maintained through negative cognitive and behavioural processes
  • target depressogenic thinking, low reinforcement and negative life events, skill deficits
  • automatic thoughts and behavioural inhibition
22
Q

emotional spirals in depression (CBT)

A
  • negative events breed negative moods = negative behaviours = negative thoughts and low expectations for the future
  • spirals can also be positive, so you have to disrupt the negative downward spiral and facilitate positive triggers
23
Q

cognitive techniques in CBT

A
  • identify automatic thoughts and challenge them
  • bring thoughts in line with the event instead of solely negative or reframing them positively
  • observe thoughts, feelings & behaviour, consider alternative explanations, solve problems rationally
  • orientation toward therapy as an experiment (try something to see if it works)
  • match developmental level (insight and abstract thinking)
24
Q

behavioural techniques in CBT

A
  • keep track of mood and activity, develop a list of rewarding activities (that produce pride and pleasure)
  • change habits (addressing environmental obstacles and skill deficits)
  • monitor how mood is being affected by these changes
25
Q

predictors of positive outcomes for CBT

A
  • combined behavioural activation and thought challenging
  • involving parents in the intervention
  • efficacy goes down as severity increases
26
Q

cultural CBT study

A
  • comparing interventions for depression in non-WEIRD samples
  • CBT, economic, integrated all led to reduced symptoms in low/middle income countries
  • interpersonal trending toward effectiveness, but not reliable yet
27
Q

antidepressant medications

A
  • much more widely documented in adults, some don’t work at all/less in children (brain development/metabolism differences)
28
Q

tricyclics

A
  • prevent reuptake of serotonin and NE or increasing responsiveness of receptors
  • not effective in youth
29
Q

monamine oxidase inhibitors

A
  • MAO (enzyme) should break down neurotransmitters, so blocking them will increase their levels in the synapse
  • some mixed evidence of efficacy
  • potentially fatal side effects (tyramine)
30
Q

selective serotonin reuptake inhibitors

A
  • specifically focused on serotonin
  • evidence for fluoxetine efficacy in teens
  • not fatal in overdose
  • some negative side effects
  • takes weeks to work
31
Q

serotonin and norepinephrine reuptake inhibitors

A
  • also block NE
  • still takes weeks to work
32
Q

black-box warning for SSRIs

A
  • suggestion of increased risk of suicide
  • warns of dangerous side effects
  • data from all RCTs using antidepressants showed higher levels of suicidality compared to placebo (no deaths from suicide)
  • other studies show decreased rates of suicidality
  • more recent studies found no association between use of Prozac and higher suicidal ideation in teens
33
Q

media coverage study of suicide and SSRIs

A
  • investigating whether media coverage and warning labels lead to lower use of SSRIs and increased suicide risk
  • looking specifically at psychotropic poisoning (underestimate of SAs)
  • found decreases in prescriptions after the FDA warning
  • found an increase in psychotropic poisonings after the warning
  • no change in completed suicide before and after
34
Q

course of action for using SSRIs for youth

A
  • discuss risk and benefit: could increase risk of suicidal ideation (could increase your energy which makes you more likely to proceed with an attempt)
  • leaving depression untreated can also increase risk of suicide
  • SSRIs are efficacious all around the world for treating depression
35
Q

treating depression in preschoolers

A
  • diagnosis in preschool is still new, so not much data
  • limited data on psychiatric drugs
  • version of parent-management training focusing on helping parents manage their children’s moods
  • helping kids increase positive mood (so there is less room for negative)
  • therapy is first-line, but if it persists, fluoxetine has the best risk-benefit profile (and continuously monitor)
36
Q

Treatment for Adolescents with Depression (TADS)

A
  • at the time of the study, CBT had some evidence but lots of room to improve the treatment, meds were being increasingly used, combined was being used but no idea if this was actually helpful
  • sample was 439 youths with moderate-severe MDD
  • SSRI and combined group did better post-treatment than placebo or CBT alone
  • CBT was most helpful for suicidality (combined and CBT alone groups vs. SSRIs and placebo)
37
Q

explanations for results in TADS

A
  • CBT didn’t outperform a pill placebo
  • CBT might not work in a more severe sample (it worked better in sub-clinical presentations)
  • treatment manual was very flexible (clinicians using different CBT methods, so some participants could have received more helpful skills)
38
Q

TADS follow-up

A
  • after 12 weeks, unblinded placebo and SSRI groups (people who were still depressed in the placebo group received treatment)
  • after 36 weeks from the start (no more control group), all groups were equal
  • could just be time (MDD episodes are cyclical and we don’t have a control group)
  • could be that CBT takes longer to show positive effects
  • 1-year post-treatment (returned to treatment as usual), participants were maintaining gains on depression and suicidality