08 Stress Flashcards

1
Q

general adaptation syndrom (Seyle)

A
  • stress is the nonspecific response of the body to any demand
    3-stage model
  • alarm: fight-flight response, immediately after stressor appearance, immediate physiological response
  • resistance: keeping initial response under control
  • exhaustion: either exhaustion or recovery, if it can deal with it
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2
Q

What is a stressor, a stress response and stress

A
  • stressor: stress-eliciting stimulus
  • stress response: behavioral and physiological response
  • stress: interaction between both
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3
Q

Lazarus’ transactional model of stress

A
  • primary appraisal: interpretation of stimulus as positive, dangerous or irrelevant
  • if dangerous, secondary appraisal: analysis of available resources, sufficient or insufficient
  • if insufficient, stress elicited
  • coping: overcoming of the stress, problem-focused (change situation) or emotion-focused (change the relation)
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4
Q

short-term stress response of ANS

A
  • hypothalamus sends nerve impulses down the spinal cord via preganglionic sympathetic fibers to adrenal medulla which secretes adrenalin and noradrenalin
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5
Q

sympathetic vs. parasympathetic ANS

A
  • sympathetic: fight-or-flight response
  • parasympathetic: rest-and-digest
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6
Q

long-term stress response

A

hypothalamic-pituitary-adrenal (HPA) axis
- hypothalamus sends CRH (corticotropin-releasing hormones) to corticotropic cells in pituitary which release ACTH (adrenocorticotropic hormones) into blood stream
- transported to adrenal cortex which secretes steroid hormones and cortisol (mineralocorticoids and glucocorticoids)
- cortisol crosses BBB and closes feedback loop

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7
Q

function of HPA axis

A
  • delay of +30min to hours after stress
  • permissive, suppressive, stimulatory and preparative actions
  • regulatory system: controls normal defense reaction
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8
Q

mineralocorticoid receptors

A
  • mechanism: rapid nongenomic increase in glutamate release probability
  • timeframe/delay: minutes
  • hormonal dependence: shortly after stress, as long as corticosterone is high
  • functional relevance: enhanced brain activity in specific limbic areas, acquisition strategy, activation, appraisal of the situation and/or for response selection, encoding and memory of the situation for future use
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9
Q

glucocorticoid receptors

A
  • mechanism: slow transcriptional regulation of multiple genes
  • timeframe/delay: hours
  • hormonal dependence: some hours after stress, when corticosterone is low again
  • functional relevance: normalization of brain activity, preservation of encoded information, storage for future use, recovery, redistribution of resources towards cortical networks, consolidation of memory and behavioral adaptation, prevents initial reaction from overshooting
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10
Q

psychological effects of stress

A
  • enhanced consolidation of memory processing
  • impaired retrieval of memory
  • especially for emotionally arousing information
  • executive functions: impaired working memory and cognitive flexibility
  • shift from goal-directed to habitual control of action
  • riskier decision making with focus on immediate rewards
  • increased prosocial behavior and in-group bias, especially in women
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11
Q

stress measurements

A
  • physiological: blood pressure, heart rate, electrodermal activity
  • measurements of stress hormone concentrations (blood, saliva, hair)
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12
Q

chronic stress - effects of unbalanced glucocorticoids

A

too much glucocorticoids (anti-inflammatory):
- more infections
- lower efficacy of vaccination
- slower wound healing
- faster cancer progression
- faster aging
too little glucocorticoids (inflammatory):
- more autoimmune disease
- more inflammation
- more pain

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13
Q

chronic stress: neuroscientific findings

A

amygdala
- persistent dendritic growth and spine formation leading to hyper-responsiveness and symptom severity
hippocampus
- reversible dendritic atrophy and reduced neurogenesis leading to reduced volume and inverted correlation with symptom severity
medial PFC
- reversible dendritic atrophy and spine loss leading to hypo-responsiveness and inverted correlation with symptom severity

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14
Q

HPA axis in MDD

A
  • enhanced basal and stimulated cortisol release, high CRF in CSF, exaggerated ACTH response to CRF, impaired negative feedback of HPA axis
  • interpreted as reflecting an exaggerated CRF drive and/or as a reduction of functioning of GRs
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