Q&A session - master this first Flashcards

To pass the exam

1
Q

Stress

What is Stress?

A

Stressor = stressful stimulus
Strain = body’s response to the stressor

Conditions of stress:
1. Physical => direct material or bodily challenges
2. Psychological => how one perceives circumstances in their lives

Examining stress:
- Can be a stimulu, the response to the stimulus and the transaction (the interaction between the stimulus and the response).

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2
Q

Stress

General adaptation syndrome

The 3 stages

A
  1. Alarm reaction: fight or flight response to an emergency
    - Mobilizes the body’s resources.
    - Fast acting arousal => Sympathetic NS activates adrenal glands that releases epinephrine and norepinephrine which activates the HPA axis and releases cortisol.
  2. Stage of resistance: HPA axiss predominates if the stressor continues.
    - Adaptation to the stressor
    - Physiological arousal is higher than normal and hormones are trying to be replenished.
    - Stage could make individuals vulnarable to health problems.
  3. Stage of exhaustion: prolonged arousal is costly
    - Immune system is weakened.
    - Body’s energy reserves are depleted.
    - Stress continues to damage the internal organs
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3
Q

Stress

Transaction model (Folkman)

Lecture

A

The interpretation of stressful events is more important than the events themselves

  1. Primary appraisal: how does this affect me? (irrelevant-relevant, good-bad)
  2. Secondary appraisal: what types of resources do I have in order to deal with it? Am i capable? (sufficient-insufficient)
  3. Stressful appraisal - factors. (Personal, situational,
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4
Q

Stress

HPA axis

A
  1. Stressor stimulates the release of Adrenocorticotropic hormone (ACTH) from the anterior pituitary gland.
  2. ACTH triggers the release of glucorticoids frm the adrenal cortex
  3. Glucorticoids (cortisol) produces the many compoennts of the stress response.

Pathway:
- Hypothalamus => CRH => Anterior pituitary => ACTH => Adrenal cortex => Cortisol

Long-term stress

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5
Q

Stress

The Sympathetic Adrenomedullary system (SAM)

A
  1. Stressor activates the sympathetic nervous system
  2. The system releases epinephrine and norepinephrine from the adrenal medulla - adrenaline.
  • Short term process => fight or flight stress
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6
Q

Stress

Inducing stress in the lab

TSST, MAST, SSSP

A
  1. The Trier Social Stress Test: fake induced speech with a math task in between - audience has a neutral-cold attitude and are interruptive with faults.
    - High stress before the speech.
  2. The masstricht Acute Stress Test: hand immersion task followed by math - no audience.
    - High stress during hand immersion
  3. Simple Singing Stress Procedure: video of singing and believed to be judged - no audience.
    - High stress before signing.
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7
Q

Stress

Stress Inoculation Training Treatment

The three phases

A
  1. Conceptualization phase: education of stress, threat appraisal, breakdown of big stressors.
  2. Skills acquisition phase: coping skills, cognitive and behavioural skills, individually tailored to the needs of patients.
  3. Application phase: using the skills, failure management, peer training, booster sessions.

Effects:
- Lower stress levels before performance compared to control groups.

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8
Q

Experimental approaches

LeDoux - the 2 roads of fear

Lecture

A
  1. High road: thalamus > visual cortex (site of awareness) > amygdala = slow, fine-grained, precise.
  2. Low road: thalamus > amygdala = fast, coarse, evolutionary advantage, irrational phobias.
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9
Q

Experimental approaches

Measuring attentional biases

Dot probe, emotional stroop,

A
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10
Q

Experimental approaches

The amygdala

A
  • The fear hub
  • It damaged - fear responses are inexistant.
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11
Q

Experimental approaches

Fear conditioning - Classical conditioning

Lecture

A

Fear learning
1. An unconditioned stimulus (stimulus, event) is associated with a unconditioned response (emotion and physiological response.
2. This is associated with a conditioned stimulus (previously neutral) to a conditioned response.

Terms:
- US = biologically aversive stimulus
- CS+ = stimulus that predicts the presence of a US.
- CS- = stimulus that predicts the absence of a US.
- CR = conditioend responses to the CS

Example: Alex was bitten by a dog, later showing intense reactions to dogs.
- CS = Dog (initially neutral)
- US = Dog bite (biologically aversive)
- CS-US pairing = Getting bitten by a dog
- CR = fear reaction in response to the CS (dog)

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12
Q

Experimental approaches

Criticism of Fear conditioning + how are they addressed?

A

Limitations:
- Ethical considerations
- No direct experience of CS-US pairing = not all patients have a history of fear conditioning, ex: not all dog phobic have gotten attacked by a dog => fear learning via instructions or observational learning or revaluating the US.
- Not everyone develops a phobia/PTSD after CS-US pairing => prior experience (latent inhibition), individual differences.

Advantages:
- Controlled for various confounding variables.
- Controlled environments
- Intensity of threat (US) can be manipulated

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13
Q

Experimental approaches

Fear vs Anxiety

A

Anxiety:
- anticipation of potential threat.
- Unknown source of threat.
- General feeling of apprehension about possible danger.
- Future oriented
- Hypervigilance
- Long-term

Fear:
- Response to a specific, known, stimulus.
- Imminent threat.
- Selective attention to threat.
- Mobilization (HR accelaration, elevated blood pressure)
- Fight or flight response.

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14
Q

Experimental approaches

Extinction learning

A

To repeatedly present the CS+ alone

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15
Q

Experimental approaches

Return of fear

Lecture

A
  1. Contextual renewal:
  • Acquisition > extinction > renewal test
  1. Spontaneous recovery
  2. Reinstatement
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16
Q

PTSD

Elher’s and Clarks cognitive model

A
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17
Q

PTSD

Emotional processing theory (FOA)

Lecture

A
18
Q

PTSD

Brain changes

Lecture

A
19
Q

PTSD

EMDR

A
20
Q

Panic Disorder

Clark’s cognitive model

A
21
Q

Panic Disorder

Gorman’s biological model

A
22
Q

Panic Disorder

Threat-Imminence model

A
23
Q

Panic Disorder

Revised causal model of PD

A
24
Q

Panic Disorder

Interoceptve exposure

A
25
Q

Panic Disorder

In-vivo treatment

A
26
Q

Generalised anxiety disorder

Intolerance of uncertainty model

A
27
Q

Generalised anxiety disorder

Metacognitive model

A
28
Q

Generalised anxiety disorder

Intolerance of uncertainty therapy

A
29
Q

Generalised anxiety disorder

Metacognitive Therapy

A
30
Q

Generalised anxiety disorder

Behavioural differences between healthy and GAD

A
31
Q

Social anxiety disorder

DSM-5 criteria

Lecture

A
  1. Fear about one or more social situations.
  2. The fear will act/show anxiety symptoms that will be negatively evaluated by others.
  3. The situation almost provokes the fear.
  4. The situations are avoided.
  5. The fear is out of proportion.
  6. The fear is persistent (6 months or more).
  7. Causes distress and impairment in more than one context.
  8. It not attributable to physiological effects of a substance.
32
Q

Social anxiety disorder

Processing social evaluative situations model

6 steps

Lecture

A
  1. Social situation activates an assumption. Ex: people will make fun of me for giving this speech.
  2. This activates the perception of social danger. Ex: People will laugh at me.
  3. This activates as sense of Self as a social object/the center of attention. Ex: i can feel my face getting red and hands being sweaty.
  4. Symptoms start to show. Ex: I actually start sweating and being visibly red.
  5. Safety behaviours are activated. Ex: squeezing my hands so nobody can see they are shaking.
  6. The anxiety is maintained and the cycle repeats itself.
33
Q

Social anxiety disorder

Integrated etiological and maintenance model

5 components

Lecture

A
  1. The extent to which social evaluative stimuli are threatening to someone > continuous scale.
  2. Factors that influence the SET model: inherited tendencies (temperaments), parent behaviours (learning), peer experiences (negative evaluation), life events, culture.
  3. Cognitive processes: self-focus, anticipation and attention towards threat.
  4. Behavioural processes: avoidance (to eliminate the threat but always comes back in the future), safety behaviours (reinforce fear), cognitive avoidance (worsen symptoms).
  5. All the components together lead to interference in life and social anxiety disorder.
34
Q

Social anxiety disorder

SAD developping during Adolescence

Lecture

A
  1. Begins with seperation anxiety in 5 years old and develops fully at 13 years old on average.
  2. Adolescents are focused on peers.
  3. The gap between the amygdala development (early) and prefrontal regions (later) is the reason for SAD in adolescents => they can respond intensely to emotions but cannot control them yet.
  4. The social brain => automatic and instinctive social responses to understand and read people’s behaviours
35
Q

Social anxiety disorder

Adapting SAD models for adolescents.

Lecture

A
  • Activating assumptions => mental imagery
  • Processing self as a social object => very common, associated with higher self-consciousness.
  • Safety behaviours => requires parents to step in.
  • Factors => parenting factors, friendships/peer victimisation, social media.
36
Q

Social anxiety disorder

Attentional bias modification treatment

Lecture

A

Modification of the dot probe task => gamified.
Results: all kids show less anxiety but more prominent in the active condition.

37
Q

Social anxiety disorder

Clark and wells’ cognitive model

4 dysfunctional patterns

A

The interaction between innate behavioural predispositions and life experiences => perceiving the world as dangerous.

Dyfunctional patterns:
1. Attention inward bias: attention to inner thoughts/feelings - subjective and confirms their experience = enhances anxiety.
2. Safety behaviours: behaviours to avoid negative evaluation from others - often increases anxiety.
3. Cognitive distortions: overestimating negative judgement from others - constant monitoring of behaviours = hyper-vigilance and impaired social performance.
4. Attentional bias: anticipatory anxiety before and negative reflection after.

38
Q

Social anxiety disorder

Rapee’s cognitive behavioural model

3, factors, 5 dysfunctional processes

A

SAD exists on a continuum.
Factors that influence the dysfunctional processes:
1. Genetic factors
2. Negative evaluation bias
3. Acceptance in society

Dysfunctional patterns:
1. Social situations
2. Avoidant behaviours:
3. Negative self-image:
4. Negative evaluation:
5. Post-event processing:

39
Q

Social anxiety disorder

Similarities and differences between Clark and Rapee’s models

A

Similarities:
1. Importance of avoidance behaviours.
2. Attentional resources to the threatening assessment of others.
3. Cognitions: distorted representation of the self, unrealistically high standards for own performance and consequences.

Differences:
1. Attentional focus: internal (clark) and external (rapee)
2. Safety behaviours: core problem (clark), avoidance is more problematic (rapee).
3. Treatment: tackle safety behaviours + shift focus outward (clark), tackle the avoidance and direct attention to mental representations + indicators.

40
Q

Social anxiety disorder

Cognitive biases in SAD

4 biases

A
  1. interpretation & judgment biases: interpreting ambiguous social cues as negative/threatening.
  • Cognitive bias modification => repeatedly exposing individual to ambiguous information to encourage positive interpretations.
  1. Selective attention bias: focus on negative information while ignoring positive/neutral ones.
  • Unconscious: adaptive to detecting threats for survival => stroop task and dot probe = faster response to threatening stimuli.
  • Conscious: focus on negative aspects of themselves related to social performance => stroop task/dot probe/face-in-the-crowd = faster response to threatening stimuli / CBM paradigm: train attention away from threatening stimuli.
  1. Post-event processing: ruminating on negative aspects of performance after the interaction => reinforces negative beliefs.
  • CBT to change biases.
  1. Implicit associations bias: associating social cues with negative outcomes => low self-esteem.
  • CBM to lower implicit rejection associations.

CBT + CBM can change bias and lead to reovery.

41
Q

Social anxiety disorder

Maladaptive behaviours in SAD

4 behaviours

A
  1. Avoidance: avoidance of social cues
  • Approach-avoidance task/crowd stimuli study/gaze direction manipulation study = supported slower appraoch to threatening stimuli
  1. Interpersonal distance: maintaining more interpersonal space than needed.
  • Virtual reality study = supported slower appraoch to threatening stimuli
  1. Behavioural and facial mimicry: less facial mimicry => cannot understand others’ affective states.
  • EMG study = supported diminished appraoch to threatening stimuli
  1. Social skills: deficits in acquiring social skill, social performance, fluency and anxious behaviour.
    * Measure social behaviour and facial blood flow.