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WINTER 2024 > 337 M1 > Flashcards

337 M1 Flashcards

1
Q

Wakefield’s Harmful Dysfunction

A
  • harmful: value based on social norms
  • dysfunction: failure of an organ system to perform according to its evolutionary design
  • the cause of symptoms must be mental to be a ‘mental disorder’
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2
Q

Skeptical view

A
  • Thomas Szasz
  • mental disorder is a label to justify medical intervention in a socially undesirable behaviour
  • labels result in stigma and social control
  • mental disorder should be an extension of physical and only be applicable to physical lesions
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3
Q

Pure Value Concept view

A
  • mental and physical disorders are judgments of desirability
  • disorder is a deviation from an ideal state
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4
Q

As Biological Disadvantage

A
  • purely biological
  • decreases survival and reproductive fitness
  • must also include statistical deviance view
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5
Q

Lillienfeld critique

A
  • questions what is natural function (the primary function of an organ system) and what is a by-product
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6
Q

Widiger proposal

A
  • disorders are constructs that must be measured indirectly
  • conceptualization will evolve as knowledge evolves
  • multimodal: latent constructs are multiply determined and multiply expressed (a single etiology would be ideal, but is unlikely)
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7
Q

five factors necessary for a valid classification system

A
  1. Clinical description: common clustered signs and symptoms
  2. Course: similar trajectory
  3. Treatment response
  4. Family history: should run in families
  5. Laboratory studies: biological and psychophysiological associations
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8
Q

challenges of a categorical system

A
  1. Heterogeneity: people in one group should look similar to each other and different from people in a separate group (this isn’t always the case)
  2. Comorbidity: 50% of people with one disorder meet criteria for another; how do you know which problem to treat first? Will affect Tx, severity, and prognosis
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9
Q

DSM-I and DSM-II

A
  • 1952 and 1968
  • few categories with no requirement for number of symptoms
  • based on psychoanalytic definitions
  • a first attempt to standardize
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10
Q

DSM-III and DSM-III-TR

A
  • 1980 and 1987
  • based on a medical model
  • empirical (not psychoanalytic, based on symptoms instead of etiology)
  • based on a consensus of professionals to define inclusion/exclusion criteria and duration
  • multi-axial classification
    I: Major Clinical Disorders (the problem to treat)
    II: Personality Disorders (not to treat, but could affect axis I)
    III: Medical Conditions
    IV: Psychosocial Stressors (context)
    V: Global Assessment of Functioning (somewhat arbitrary)
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11
Q

DSM-IV

A
  • 1994 and 2000
  • introduced distress and impairment as factors
  • gave a definition of mental illness
  • polythetic approach: certain signs and symptoms are neither necessary or sufficient
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12
Q

DSM-5

A
  • 2013
  • removes multi-axial system
  • some diagnoses get dimensional criteria
  • new categories (OCD, PTSD is moved to Trauma)
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13
Q

what could comorbidities be due to

A
  • chance (partly)
  • sampling bias (more severe clinical populations)
  • diagnostic criteria (overlap between diagnoses)
  • multiformity (comorbid disorders represent a third independent disorder)
  • causal (one disorder is a risk factor for another)
  • shared etiology causes multiple disorders
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14
Q

which disorders are where in HiTOP

A
  • SAD: internalizing - fear
  • Agoraphobia: internalizing - fear
  • Phobias: internalizing - fear
  • Panic: internalizing - fear
  • OCD: internalizing - fear
  • MDD: internalizing - distress
  • GAD: internalizing - distress
  • PTSD: internalizing - distress
  • Bipolar: internalizing - mania AND thought - mania (also closely related to psychosis)
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15
Q

1-year prevalences of disorders from most common to least

A
  • MDD
  • SAD (specific phobias may be 2nd most common)
  • PTSD
  • GAD
  • Panic
  • PDD
  • OCD
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16
Q

lifetime prevalences of disorder categories from most to least common

A
  • anxiety disorder
  • mood disorder
  • substance use disorders
  • prevalence for any disorder is 46%
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17
Q

vulnerability-stress correlations

A
  • demonstrate that diatheses and stress aren’t independent
  • stress generation: people who are more vulnerable may behave in ways that increase their stress
  • scars: having had one illness may change your view of the world which can exacerbate your stress
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18
Q

etiological heterogeneity

A
  • there are many pathways to disorder
  • captured by dimensional diathesis-stress models: low diathesis might still be capable of developing disorders at high enough levels of stress (not all-or-none like the original categorical diathesis-stress model)
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19
Q

differentiation between syndrome, disorder, disease

A
  • syndrome: cluster of signs and symptoms that tend to co-occur, but pathology and etiology aren’t well-understood
  • disorder: syndromes that cannot be explained by other conditions
  • disease: most understood - both pathology and etiology
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20
Q

endophenotype approach vs. exophenotype approach

A
  • endo: focus on identifying reliable biomarkers or lab indicators that are only present in the disordered population
  • exo: focus on traditional signs and symptoms (DSM’s approach)
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21
Q

follow-up design

A
  • start with people who are already ill and follow-up over time (prospective)
  • studying the natural course of a disorder
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22
Q

high-risk design

A
  • start with a sample likely to develop psychopathology and follow-up over time (prospective)
  • temporal ordering
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23
Q

vulnerability marker

A
  • should be present before, during, and after the illness
  • if only after, could be a scar
  • if it resolves with the illness, could be a subthreshold presentation
  • should be over-represented in high-risk populations
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24
Q

case control design

A

compare group with disorder to group without disorder (useful for rare disorders)

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25
Q

cohort design

A

single large sample, some of whom have the disorder (to compare to many control groups, useful when the disorder is common)

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26
Q

family studies

A
  • identify proband and assess their family members
  • rates of illness should be higher than in the general population
  • family tends to have subthreshold presentations (we inherit traits or predispositions, not disorders)
  • coaggregation: disorders run in families in a nonspecific way (depression and anxiety coaggregate in familires)
  • can suggest a genetic role but doesn’t prove it (move to adoption studies)
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27
Q

adoption studies

A
  • parent as proband: find the kids they gave up for adoption to see if they’re ill
  • adoptee as proband: compare their adopted/biological families to disentangle environment/genetic contributions
  • cross-fostering: kids of parents without a disorder raised in families of people with disorders compare to kids of parents with disorders raised in families of people without disorders
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28
Q

twin studies

A
  • gives an additive genetic component (A) that is roughly the difference between the Mz concordance and Dz concordance
  • common environment: shared environment
  • unique environment: nonshared environment
  • heritability estimate is sample-specific and varies according to environment - tends to increase with age and is higher when there’s less environmental variance
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29
Q

endophenotypes

A
  • intermediate between genotype and phenotype
  • must correlate with illness in the population
  • must not be state-dependent
  • must be heritable (more in Mz than Dz)
  • must see family similarities
  • must be more present in families than in the general population
  • must be specific to a particular illness (ideally)
  • able to be measured
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30
Q

fear

A

response to a real/perceived threat (prep for action) that is current, response is immediate and not mediated by conscious thought)

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31
Q

panic

A

physiologically similar to fear but evoked without an identifiable or current threat

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32
Q

anxiety

A

future-oriented (feeling threatened by potential occurrences that have not yet happened)

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33
Q

epidemiology of specific phobias

A
  • 2F:1M
  • tends to have childhood onsets, but kids usually outgrow them (except for agoraphobia which onsets in 30s)
  • high comorbidity with other anxiety disorders and depression
  • prevalence is 12.5% for specific and 1.5% for agoraphobia
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34
Q

etiological models of specific phobias

A
  • classical conditioning: averse learning experiences = acquired fears (doesn’t explain all cases)
  • fears maintained through operant conditioning (avoidance is negatively reinforced and fear cannot be disconfirmed - two-factor model)
  • evolutionary preparedness: evolved sensitivity to certain stimuli
  • immunizing effect of prior experience (kids have very little experience with anything)
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35
Q

Klein’s theory of panic

A
  • physiological sensations becomes the CS that was paired with a full-blown panic attack (the CR)
  • leads to reinforcement through avoidance
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36
Q

epidemiology of panic disorder

A
  • 2F:1M
  • 4-5% lifetime prevalence
  • onset is about 24 years and very abrupt (rare before adolescence and after middle age)
  • heritability estimate about 30-40%
  • very comorbid with other Axis I disorders (and personality disorders common too)
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37
Q

Clark’s theory of panic

A
  • catastrophic misinterpretation of bodily sensations = more arousal = vicious cycle (initial symptoms are usually internally-generated, but could be due to caffeine, cocaine, etc.)
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38
Q

anxiety sensitivity

A
  • trait-like fear about sensations related to anxiety
  • belief that if you keep having the panic symptoms, your health will eventually decline
  • more likely to panic when you experience anxiety
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39
Q

behavioural signs of PD

A
  • safety behaviours: maladaptive coping contributes to maintenance of PDP
  • interoceptive avoidance: avoidance of internal symptoms that reproduce high arousal (caffeine, having sex, saunas)
  • experiential avoidance: distraction from anxiety sx, thought suppression
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40
Q

temperament relation to panic

A
  • neuroticism, negative affectivity
  • fear of fear could lead to behaviours that exacerbate stress
  • related to anxiety sensitivity
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41
Q

etiology ideas from reading about panic

A
  • anxious attachment (unpredictable/unresponsive caregiver) = anxiety disorders
  • respiratory disease is common (could be a diathesis)
  • reduced amygdala volume
  • increased HPA reactivity to environmental cues (difficulty differentiating between threat and safety cues)
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42
Q

treatment for PD

A
  • CBT: panic control treatment uses cognitive aspects, conditioning, behavioural exposure (Clark’s model is more focused on cognitions)
  • ACT useful if you use behavioural exposure
  • exposure + relaxation + breathing training
  • SSRIs most useful, benzos also effective (both have withdrawal effects that could prompt relapse)
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43
Q

epidemiology of GAD

A
  • 2F:1M
  • 5-6% (lifetime) or 3.1% (6-month)
  • onset is around 30 years, but highly variable
  • gradual onset
  • very chronic (similar to personality disorders)
  • high comorbidities (controversial diagnosis because of this - could just be conceptualized as negative affectivity that predisposes generally to psychopathology)
  • trait anxiety runs in families, so does GAD
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44
Q

differentiation of GAD from MDD

A
  • GAD: attentional biases toward threat
  • MDD: more likely to have memory biases
  • MDD: low positive affect (people with GAD can experience joy, but both have tendencies toward high negative affect)
  • MDD: precipitating event is humiliation vs. GAD: precipitating event is danger events
  • MDD: emotion context insensitivity (ECI), disengagement from the environment
  • GAD: hyperresponsivity to threat and normal responses to positive stimuli
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45
Q

temporal course MDD and GAD

A
  • extreme goal-focus in GAD = burnout = motivational disengagement in MDD
  • uncertainty about future in GAD = certainty about negative future in MDD
  • beliefs of helplessness in GAD = hopelessness in MDD
  • Or MDD could be a stressor, so after recovery people worry to prevent another episode
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46
Q

cognitive avoidance

A
  • rather than feel fear, worry about what to do about fear
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47
Q

Tom Borkovec

A
  • worry = cognitive avoidance about low-probability events
  • when those events don’t occur, they believe their worry was effective, so they keep worrying to keep preventing the bad outcomes
  • worry is a verbal/cognitive process that buffers form emotional arousal (no vivid imagery = cannot change fear structure)
  • thought suppression = more intrusive worry = increases sense of lack of control = more worry
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48
Q

intolerance of uncertainty in GAD

A
  • core feature of GAD
  • tendency to react negatively to ambiguous situations (preferring a negative outcome to an uncertain one)
  • causal role in exacerbation of worry
  • information-processing bias (more recall of ambiguous situations and more likely to interpret them negatively)
49
Q

metacognition view of GAD

A
  • Type I worry: about daily events
  • Type II worry: worry about worry
  • belief that worry is a positive coping strategy, so they use it, but when they feel they can’t cope with a stressor = Type II worry = belief that worry is uncontrollable
50
Q

mood-as-input view of GAD

A
  • implementing an ‘as many as you can’ strategy to response generation + negative mood = more perseveration (so the cycle continues)
51
Q

treatments for GAD

A
  • CBT (most effective)
  • relaxation training, psychoeducation, identifying triggers of worry, imaginal/in vivo exposure
  • cognitive restructuring: targeting beliefs about worry, intolerance of uncertainty, negative problem-solving orientation, cognitive avoidance
  • client preference for meds or behavioural Tx (CBT is better for long-term outcomes, but otherwise they’re similar)
  • SSRIs, benzos, SNRIs, psychotropics to boost GABA, second-generation antipsychotics
52
Q

epidemiology of SAD

A
  • 2F:1M (gender differences emerge in adolescence)
  • 12% prevalence (2nd most common anxiety disorder, 3rd most common overall)
  • high comorbidity with anxiety and depression (high self-criticism) - SAD may act as a risk factor
  • lower prevalence in East Asian countries and among Hispanic and non-white populations (could be due to measurement problems)
  • onset age around 16 (social re-orientation and importance of peer judgment in adolescence)
  • moderately heritable
53
Q

Clark and Wells cognitive theory of SAD

A
  • social situations activate negative beliefs about their social competency
  • negative schemas interfere with their interpretation of the situation = see more danger and threat = more anxious = rejection is viewed as even more likely = more anxious
  • internal self-focus during social interactions so they can’t focus on others’ judgments (which acts a safety/avoidance behaviour) and makes them less socially competent
  • biased memory toward negative experiences which reinforces a negative self-schema
54
Q

post-event processing in SAD

A

biased rumination that confirms negative beliefs

55
Q

research paradigms SAD

A
  • Stroop task: cannot disengage attention from social threat words
  • dot-probe paradigm: attending preferentially to threat stimulus
  • attentional biases could also be shifting away from threat (which can lead to missing positive cues from others)
56
Q

biases in SAD

A
  • judgment: self-critical, overestimate the likelihood of negative outcomes
  • memory: especially when info is personally relevant, negative intrusive memories of social situations
  • imagery: in third person = negative view of the self = more anxiety (contributes to maintenance)
57
Q

risk factors in childhood for SAD

A
  • parental anxiety
  • insecure attachment = negative peer relations, interpersonal difficulties
  • childhood maltreatment = negative, global, stable inferential style
  • controlling/critical parenting
  • accommodating parenting = behavioural inhibition is reinforced
58
Q

CBT for SAD

A
  • cognitive restructuring
  • in vivo exposure
  • Clark and Wells cognitive therapy: shifting attention externally, decreasing safety and avoidance behaviours
59
Q

biological interventions for SAD

A
  • SSRIs and SNRIs
  • benzos (as-needed adjunct)
  • MAOIs (last resort)
  • atypical antipsychotics, anticonvulsants
60
Q

obsessions

A
  • intrusive and inappropriate (ego-dystonic)
  • recognized to be your own thoughts (not thought-insertion)
  • contamination, uncertainty, aggressive, symmetry/exactness, sexual (less common in kids), somatic
  • never act on obsessions, but still cause distress
61
Q

compulsions

A
  • attempts to neutralize or suppress obsessions (to decrease anxiety)
  • washing/cleaning, checking, repeating, mental (prayers, voluntary thoughts)
62
Q

epidemiology of OCD

A
  • 1.5% lifetime prevalence
  • slightly more common in males in childhood, but slightly more common in females in adulthood
  • age of onset is about 19 years
  • usually with gradual onset (often childhood onset)
  • very chronic (full remission is rare)
63
Q

cognitive models of OCD

A
  • while intrusive thoughts are very common, people with OCD consider them to be very upsetting + feel responsible and self-blame for any possible negative outcomes (which makes the thought more upsetting until they must perform the ritual to decrease anxiety)
  • negative affectivity increases rates of intrusive thoughts
  • deficits in STM: constantly re-checking because they can’t remember if they’ve already checked
  • poor reality testing: difficulty distinguishing between real and imagined events (convinced that thoughts are true)
64
Q

intolerance of uncertainty in OCD

A
  • believe they lack sufficient coping mechanisms or problem-solving skills to deal with threats
  • compulsions are an attempt to increase certainty about outcomes
65
Q

moral TAF

A

belief that unwanted disturbing thoughts are just as bad as the actions themselves

66
Q

likelihood TAF

A

belief that having a thought will increase the chance that the outcome will occur (which makes disturbing thoughts even more upsetting)

67
Q

neutralizing obsessional thoughts study

A
  • attempts to undo or prevent thoughts (checking, crossing out, lighting on fire)
  • neutralizing immediately = decrease in anxiety and decrease in desire to neutralizing
  • delayed neutralizing = desire to neutralize remains, but anxiety decreases naturally
  • neutralizing isn’t just driven by anxiety, but by a sense of responsibility
68
Q

disgust proneness

A
  • especially associated with contamination subtype, but also hoarding, ordering, other specific phobias
  • runs in families, also has a learning component (vicarious)
  • OCD more likely to believe there’s a danger of contamination (false alarm)
  • difficult to extinguish the aversive conditioning, so can be difficult to treat
69
Q

cognitive-behavioural models of OCD

A
  • maladaptive beliefs (inflated responsibility, need to control thoughts, intolerance of uncertainty)
  • intrusive thoughts appraised as significant
  • operant conditioning helps maintain the disorder
70
Q

treatment for OCD

A
  • exposure and response prevention shows 50-70% improvement
  • in vivo/imaginal exposure to provoke anxiety, but let anxiety subside naturally and don’t engage in rituals (helps to facilitate extinction)
  • within-session habituation (anxiety decreases within one session) and between-session habituation (anxiety is initially lower with every session)
  • inhibitory learning: new safety associations are being created
  • SSRIs, tricyclics show 20-40% reductions (convenient but modest)
71
Q

epidemiology of PTSD

A
  • 2F:1M (but rates of trauma are equivalent across genders)
  • 7-8% prevalence (but rates of trauma are 50-60%)
  • highest risk of PTSD is associated with assault and violence (but still PTSD only develops in 50% of people)
  • rates vary culturally (may be due to time of measurement effects), predominant/distressing symptoms vary culturally
72
Q

predictors of PTSD

A
  • gender
  • familial psychopathology
  • history of psychopathology
  • internalizing sx in childhood (negative affectivity)
  • childhood or previous traumas
  • lower IQ
  • nature of trauma (proximity, duration, risk to life, intention, psychological factors during the experience, *dissociation most important)
  • level of social support following trauma (but PTSD tends to erode social networks)
73
Q

results of the co-twin PTSD study

A
  • similar abnormalities in ExP+ and UxP+ that aren’t present in the other pair of twins which suggests the vulnerability factor hypothesis
  • slight differences between ExP+ and UxP+ suggest the worsening course hypothesis
  • symptom severity was correlated with hippocampal volume in the same person and in their co-twin
74
Q

hypotheses about hippocampal volumes in PTSD

A

(1) scar hypothesis: caused by trauma
(2) risk factor for trauma exposure (selecting dangerous environments)
(3) vulnerability factor for developing PTSD following a trauma (SUPPORTED)
(4) consequence of exposure to trauma (NOT SUPPORTED)
(5) manifestation/sign of PTSD
(6) product of a sequel or complication of PTSD (worsening course - SUPPORTED)

75
Q

dual-representation theory of PTSD

A
  • autobiographical memories (verbally-accessible VAM): info consciously attended-to before, during, after trauma
  • situationally-accessible memories (SAM): unconsious information not easily accessed
76
Q

social-cognitive theory of PTSD

A
  • trauma can modify important beliefs about personal invulnerability, the world as a meaningful and predictable place, and the self as positive/worthy
  • can affect agency, safety, trust, power/control, esteem, intimacy
  • individuals will engage in (1) assimilation, alter interpretation of event, (2) accommodation, alter original belief slightly, or (3) overaccommodation, alter belief drastically
77
Q

conservation of resources theory

A
  • traumatic stress occurs when most important resources are threatened (well-being, sense of trust)
78
Q

treatment of PTSD

A
  • CBT is best, includes prolonged exposure (PE) to habituate to anxety and block negative reinforcement from avoidance
  • cognitive processing therapy (CPT) targets unhelpful thoughts without a behavioural component
  • stress-inoculation therapy (SIT) and present-centered therapy (PCT) focus on non-trauma
  • biological: SSRI, SNRI, antiadrenergics, mood stabilizers, anticonvulsants (benzos aren’t effective)
  • 40-80% remission with large drop out rates (avoidance)
79
Q

epidemiology of MDD vs. bipolar

A
  • MDD: 2F: 1M
  • bipolar: F=M
  • MDD 10-20x more common than bipolar
  • bipolar has earlier onset, more episodes, poorer outcomes
80
Q

Watson & Clark tripartite model

A
  • to explain overlap between MDD and anxiety disorders
  • depression-specific: anhedonia (few people with anxiety show this sx)
  • anxiety-specific: physiological hyperarousal (may be better applied to panic/phobias)
  • overlap: general distress/negative affectivity
  • cannot explain all cases (SAD)
81
Q

epidemiology of depression

A
  • 2F:1M
  • MDD lifetime prevalence is 16-17%
  • PDD lifetime prevalence is 3-6%
  • rates tend to be lower in East Asian countries
  • PDD rates are higher in industrialized countries
  • presentation varies culturally: somatic complaints in Asian, Latin American, North African countries
82
Q

MDD course

A
  • onset teens/mid-20s (can be preceded by low grade chronic depression)
  • episodes last 5-6 months on average
  • 20% of episodes are longer than 2 years
  • 50% of people who have one episode will have at least another
  • most people relapse (average of 5-6 episodes over lifetime)
83
Q

PDD course

A
  • very chronic
  • high likelihood of remission with relapse
  • common to have PDD with intermittent episodes of MDD
84
Q

family studies of MDD and bipolar

A
  • proband with MDD = family more likely to have MDD, not bipolar
  • proband with bipolar = family more likely to have bipolar and MDD
  • some disorders run more cleanly in families, there is some overlap
85
Q

McGuffin twin study design and conclusions

A
  • Mz and Dz index twins with bipolar or MDD, then find their co-twins to see if they have mood disorders, MDD, or bipolar
  • Bipolar appears more heritable (suggests 70% heritability)
  • suggests 96% heritability of mood disorders in general (mood disorders have a genetic component)
  • suggests 52% heritability of MDD
86
Q

Kendler twin study

A
  • higher heritability estimates in female twins which suggests more genetic factors in girls
87
Q

Parker’s parental bonding instrument

A
  • Dimension 1: care, nurturance
  • dimension 2: overprotection, control
  • low care frequently reported, overprotection less so
  • interaction between low care and high overprotection is especially important
88
Q

behavioural models of depression

A
  • behavioural inhibition (cause) = receive less positive reinforcement from the environment = even less likely to engage in those behaviours (avoidance - negative reinforcement)
  • interpersonal deficits can also decrease the amount of positive reifnrocement
  • anhedonia = amotivation = avoidance because lack of energy and activities aren’t rewarding anyway
  • cognitive factors: low self-esteem = high negative affect = high self-criticism = bad social performance (which confirms belief of low self-esteem)
89
Q

Beck’s cognitive triad

A
  • negative views about self = negative views about the world = negative views about the future (these schemas act as a diathesis, filter information)
  • schemas contribute to negative automatic thoughts containing cognitive distortions
90
Q

cognitive distortions

A
  • all-or-nothing
  • arbitrary inference (drawing negative conclusions without evidence)
  • overgeneralization
  • selective abstraction (not seeing the whole picture)
  • magnification/minimization
  • personalization (bad things happen because of you)
  • emotional reasoning (something is true because of the strength of the emotion)
91
Q

Seligman’s learned helplessness

A
  • learn early on that our behaviour is useless to change a situation, so we should stop expending effort to try (doesn’t explain why depressed people feel guilty for bad things happening)
  • revision: we make internal, global, stable attributions when we feel like we lack control over a situation
92
Q

self-referent encoding task (SRET)

A
  • lab study for memory biases seen in depression (preferential recall for negative words that they endorsed as describing them)
  • we don’t see these memory biases in people with anxiety
  • sometimes also seen in at-risk populations
93
Q

attentional biases in depression

A
  • faster at finding threat in a safe environment and slower at finding safety cues in a threatening environment
  • stroop task: difficulty disengaging from threatening or sad words
  • dot-probe task
  • dischotic listening: difficulty inhibiting distractor information when it’s related to loss, sadness, threat
  • less evidence for attentional than more memory biases
94
Q

integrated view of depression

A
  • diathesis can be biological (genetic, neurochemical (monoamines), endocrine (stress response), immunology (inflammation response), neural connectivity)
  • can be behavioural (avoidance)
  • can be cognitive (distortions, schemas)
  • can be emotional (reactivity, regulation)
95
Q

treatment of depression

A
  • behavioural: decreasing unpleasant and increasing pleasant events (behavioural activation)
  • CBT: identify and challenge automatic thoughts, cognitive errors, negative core beliefs
  • interpersonal therapy: identifying and correcting lapses in interpersonal functioning
  • somatic: ECT, transcranial stimulation, deep brain stimulation, MAOIs, TCAs, SSRIs, SNRIs
  • PDD especially can benefit from continued pharmacotherapy and psychotherapy
96
Q

psychotic symptoms in bipolar

A
  • mood congruent (delusions of grandeur for mania, guilt and sin for depression)
  • mood incongruent (thought insertion/mind control for mania, anything happy for depression)
  • psychotics sx should only occur during the episode to still be considered bipolar, otherwise it’s schizoaffective
97
Q

epidemiology of bipolar

A
  • lifetime prevalence is 2-4%, stable worldwide
  • cyclothymia prevalence is 4-5%
  • 5-10% with depression will convert to bipolar
  • episodes last about 2 months (but duration can decrease with tx)
  • poor prognosis if mixed states or rapid cycling
  • relapse rate: 7-9 times over lifetime
98
Q

treatment for bipolar and MDD

A
  • bipolar: lithium as mood stabilizer with anticonvulsants (has a lot of noncompliance)
  • MDD: antidepressants (which can trigger mania in bipolar)
99
Q

goal-attainment etiological model

A
  • stress in prior 6 months predictive of onset and relapse
  • goal-attainment events can also trigger mania: get really happy = get dysregulated = no productive bx = downward spiral
  • elevated reward sensitivity (NAcc activation, more reactive to successes - predictor of severe course)
100
Q

kindling etiological model

A
  • need a high-level stressor to provoke the first episode = brain changes to be more vulnerable = need less stress for the next episode until no stress is required to provoke mania
101
Q

biological factors in bipolar

A
  • high norepinephrine in mania, low in depressive
  • decreased sensitivity of serotonin system = increase variability in dopamine system
  • high glutamate levels in PFC
102
Q

neural circuits in bipolar

A
  • hyperactive amygdala in mania
  • decreased connectivity between amygdala and PFC
  • lower PFC activation (inability to inhibit emotions, abnormal control of limbic structures)
  • impairments in emotional control circuits
  • hyperactive BG and striatal activation
103
Q

social rhythm stability hypothesis

A
  • inability to maintain daily rhythms, increased variability in circadian rhythms
  • fluctuations in sleep quality can trigger negative moods
  • bright light can trigger mania (disrupting circadian rhythms)
104
Q

stressor

A
  • external demand that presents a challenge to homeostasis/ability to maintain equilibrium
  • can be negative or positive, real or perceived
105
Q

stress

A
  • how the organism reacts physiologically/psychologically to the stressor
  • necessarily and sufficiently an interaction between the organism and its environment
106
Q

SAM system

A
  • sympathetic adrenomedullary system
  • hypothalamus signals = medulla secretes adrenaline and noradrenaline = fight-or-flight = peripheral excitation
  • immediate response
107
Q

HPA axis

A
  • hypothalamus-pituitary-adrenal axis
  • hypothalamus release corticotropin releasing hormone/factor = pituitary gland releases adrenocorticotropic hormone = adrenal cortex releases glucocorticoids = fight-or-flight (inhibit immune system)
108
Q

allostatic load

A

the amount of strain the stress system is under

109
Q

hippocampus

A
  • memory, stress regulation
  • strong reciprocal connections with the hippocampus and many cortisol receptors
  • acute stress decreases hippocampal activation
  • chronic stress decreases hippocampal volumes (cell death, fewer connections)
  • altered function of the hippocampus = cortisol hypersecretion (cannot dampen the cortisol response like it should)
110
Q

PFC

A
  • slow to develop, so it’s easier to inflict damage on it (vulnerable to effects of stress)
  • repeated stress = dendritic shortening
  • severe child abuse = decreased PFC volume (cell death, reduced connections)
111
Q

5 patterns associated with ELS

A
  1. common
  2. increases risk of lifetime mental disorder
  3. nonspecific risk factor
  4. increases risk of psychopathology throughout life
  5. explains 30% of disorder onsets
    - can disrupt brain development (maternal cortisol)
    - can lead to persistent dysregulation of stress response systems
112
Q

fetal programming

A
  • maternal stress passed to fetus via glucocorticoids (placenta), so infants develop hypersensitive stress response systems (increased baseline and reactive cortisol)
113
Q

factors that can buffer against stress

A
  • men doing the TSST with their female partner (doesn’t work for women unless the male partner is making physical contact)
  • pet ownership, doing the TSST with a dog
  • physical exercise can protect against hippocampal degeneration, can improve mood immediately
  • present-focused breath
114
Q

sleep deprivation effects on stress systems

A
  • increases allostatic load (increases blood pressure, and night cortisol)
  • can affect hippocampal volumes, alter mood and cognitive control
  • bad sleep hygiene can decrease sleep quality and duration
115
Q

reactivity hypothesis

A
  • larger heart rate responses and greater cortisol reactivity = future adverse health risks
  • also hyporesponsiveness of cortisol associated with adverse outcomes
  • stress-related circadian dysregulation (flatter diurnal cortisol slope)
116
Q

specificity models of ELS

A
  • effects of ELS differ depending on type of stress
  • doesn’t account for co-occurring ELS
117
Q

cumulative-risk models of ELS

A
  • doesn’t account for type, severity, chronicity
118
Q

dimensional models

A
  • experience-driven plasticity has specific influences on learning and neurodevelopment through synaptic pruning and myelination
  • threat/harshness, deprivation, unpredictability
  • measuring degrees of experiences in early life and making predictions about affective, cognitive, neural development that are similarly/differentially affected by these experiences

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