Stress Flashcards

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1
Q

STRESS

A
  • stressor = threatening/demanding event/situation (ie. predator presence/social competition/extreme weather)
  • stress response = stressors triggering coordinated physiological/psychological/beh changes
  • vertebrates stress = activation of 2 neuroendocrine protection systems:
    1. SAS (sympatho-adrenergic system) = rapid/short-term/catecholamine (adrenaline/noradrenaline) mediated
    2. HPA (hypothalamic-pituitary-adrenal axis) = long-term/glucocorticoid (cortisol) mediated
  • together orchestrate response to potentially harmful/life-threatening situations
  • involve bi-directional body communication
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2
Q

SAS (SYMPATHO-ADRENERGIC SYSTEM)

A

hypothalamus -> nerve impulses -> spinal cord -> adrenal medulla -> catecholamine release (epinephrine/norepinephrine)

  • increased HR/BP/metabolism
  • liver converts glycogen to glucose; glucose release
  • bronchiole dilation
  • blood flow pattern changes -> ^alertness/decreased digestive activity/decreased urine output
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3
Q

HPA (HYPOTHALAMIC-PITUITARY-ADRENAL AXIS)

A

CRH (corticotropin-releasing hormone) -> anterior pituitary corticotrope cells release ACTH -> blood target -> adrenal cortex -> mineralocorticoid/glucocorticoid release

  • sodium/water retention in kidneys
  • ^ blood volume/BP/gluconeogensis
  • decreased insulin sensitivity/GH/T3/immune response/fat & protein mobilisation
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4
Q

STRESS RESPONSE STAGES

A

SELYE (1932)

  1. ALARM REACTION
    - pituitary-adrenal system perceives stressor
    - SAS prepares body for action/FVF
    - HPA releases energy stores
  2. RESISTANCE STAGE
    - body attempts physiological balance re-establishment
    - if stressor persists, stress hormones/arousal remain ^
  3. EXHAUSTION STAGE
    - prolonged stress eventually depletes resources/exhausts body’s defences
    - stress-related illnesses develop
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5
Q

ALARM REACTION

A
  • prompted by sudden/unexpected stressor appearances
  • startle = non-specific immediate beh response
  • followed by FVF = specific beh responses
  • physiological changes accompany (ie. ^BP/tachycardia (rapid HR)/tachypnoea (rapid breathing))
  • above = active coping mechanisms for threat control
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6
Q

AR: SAS

A
  • alarm reaction primarily linked to SAS (sympatho-adrenergic system)
  • activates brainstem nuclei/vagal nerve/adrenal medulla
  • adrenal medulla releases adrenaline (wide effect range)/noradrenaline (stimulates muscle alpha receptors; contraction redirects blood to essential organs/^BP)
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7
Q

ADRENALINE

A
  • raises HR/muscle blood flow
  • reduces blood flow to skin/intestines
  • stimulates glycogenolysis via liver (glycogen broken to glucose = ^ blood sugar)
  • causes adipose tissue to release fat into blood
  • widens bronchioles (lung air passageways)
  • dilates pupils
  • assists body to escape from/deal w/stress
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8
Q

AR: HPA

A
  • ACTH stimulates adrenal cortex to release cortisol/other steroids
  • engages slower-acting passive coping mechanisms (useful w/FVF = ineffective)
  • adaptively redirects energy:
  • direct oxygen/nutrients to brain
  • stimulates lipolysis (fat breakdown)/gluconeogenesis (glucose production)
  • inhibits growth/reproduction
  • suppresses immune system
  • contains inflammatory responses
  • enhances arousal/vigilance/cog
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9
Q

RESISTANCE STAGE

A

DEIZNER et al (1997)

  • if stressor successfully handled, body restores homeostasis; feedback loops return stress hormones to baseline levels/recovery
  • may see reduced impact of stressor w/repeated exposures BUT severe/uncontrollable/long-lasting aversive events may lead to sustained HPA activation = chronic stress response
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10
Q

EXHAUSTION STAGE

A
  • stress-related illness process includes:
    1. sugars mobilised; energy never stored (muscle wasting; fatigue; increased diabetes risk)
    2. hypertension (^BP) maintained (blood vessel damage)
    3. digestion suppressed (peptic ulcers; irritable bowel syndrome)
    4. suppressed growth (psychogenic dwarfism; bone decalcification)
    5. suppressed reproduction (disrupted ovulation; impotence; libido loss)
    6. suppressed immunity/inflammation (long-term immunosuppression; increased disease susceptibility)
    7. altered cog/sensory threshold (neural degeneration in hippocampus/pre-frontal cortex; impaired learning/memory retrieval)
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11
Q

STRESS TRIGGERS

A
  • any stimulus can be stressor if perceived to threaten homeostasis & activates HPA axis
  • most naturally occurring stressors involve factor combo
    SYSTEMIC (“ACTUAL”) STRESSORS
  • visceral nociceptors
  • somatic nociceptors
  • inflammatory signals
  • baroreceptor/osmoreceptor stimulation
    NEUROGENIC (“ANTICIPATED”) STRESSORS
  • HPA activation in physiological challenge absence
  • predator anticipation/recognition
  • dangers associated w/novel environment
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12
Q

ST: COSPECIFICS

A

SAPOLSKY (2005)
- dominance interactions in baboons
- dominant male’s testosterone recovers more rapidly after stressful event
- subordinate males display ^ circulating cortisol levels
- dominance beh often subtle (threats > direct aggression)
CARLSON et al (2006)
- meerkat pup begging
- adults long-term contributions to pup feeding = + correlated w/cortisol plasma levels
- pup begging both ^ plasma cortisol levels/pup feeding via male helpers

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13
Q

MODERN STRESS TRIGGERS

A
  • modern environment stressors = difficult to avoid -> high chronic stress rates:
    1. job related (high pressure/long hours/inconvenient shifts)
    2. financial worries
    3. transport (traffic jams/dangerous driving/public transport)
    4. global pandemic/environmental destruction/racial inequality
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14
Q

EUSTRESS VS DISTRESS

A

EUSTRESS
- perturbation can be dealt w/effectively
- beneficial stress response quickly terminated once homeostasis restores
DISTRESS
- chronic hypo/hyperactivation of HPA axis
- may be harmful/lead to abnormal beh

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15
Q

EUSTRESS/DISTRESS BALANCE

A
  • quality/intensity tips balance
  • individual characteristics challenged by stressor:
    1. genetic predisposition
    2. past history/experience
    3. development age/stage
  • stimuli interpretation varies between/within individuals; may be associated w/emotional state (ie. anxiety/arousal)
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16
Q

YERKES-DODSON LAW

A
  • feeling a little stressed can be good
  • arousal improves performance up to optimal point
  • past this point, performance begins decrease
  • task-dependent precise pattern
17
Q

COGNITIVE & COPING APPRAISAL

A

LAZARUS’S TRANSACTIONAL THEORY (1966)

  • dynamic relationship between environmental demands (stressors)/individual’s psychological resources for dealing w/them (coping ability)
  • distress (negative stress) = from perceived imbalance between demands/resources
18
Q

COGNITIVE APPRAISAL

A
  • personal factors = goals/personal resources/beliefs
  • situational factors = demands/constraints/opportunities
    PRIMARY APPRAISAL
  • significance in personal goals/values/self-belief terms
  • aka. “is the situation irrelevant/beneficial/threatening/challenging to me?”
    SECONDARY APPRAISAL
  • ability to control situation/wellbeing importance
  • aka. “what can/should I do about it?”
19
Q

COGNITIVE APPRAISAL PROCESS

A

LAZARUS & FOLKMAN (1984)
situation/event -> primary appraisal -> perceived threat -> secondary appraisal -> perception of coping ability w/threat/inability to cope -> positive stress/distress

20
Q

STRESS IMMUNISATION

A

LEVINE et al (1967)

  • exposure to stressors in early life -> greater resilience
  • rat pup handling
  • human handling = mildly stressful event
  • early life handling = lower cortisol secretion in response to stressful events
  • maternal licking ^ post handling
  • offspring of mother exhibiting higher grooming/licking rates = ^ stressor resilient
  • long-term maternally deprived pups = ^ stress response associated w/adrenal steroid receptor changes
21
Q

SUMMARY

A
  • stress response orchestrated by 2 neuroendocrine protection systems:
    1. SAS (sympatho-adrenergic system) activates FVF via adrenaline/noradrenaline (rapid)
    2. HPA (hypothalamic-pituitary-adrenal axis) redirects energy via cortisol (slower)
  • Selye’s general adaptation syndrome identified 3 key stages of stress response: alarm/resistance/recovery/exhaustion
  • chronic stress response w/sustained HPA activation can cause stress-related illness
  • eustress = successful execution/termination of stress response; distress = environmental stressors exceed psychological coping resources
  • stress immunisation = exposure to mild stressors early in life builds greater stressor resilience later