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Wien Aufnahmeprüfung M.Sc. Psychologie 2020 > Stress and Health > Flashcards

Flashcards in Stress and Health Deck (21)
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What are some important stress related terms/concepts?

  • stressor: the perceived threat to an organism
  • stress response: the response to that stressor
  • situational stereotypy: the degree to which a situation evokes different patterns of biologic responses
    • e.g.  vigilance response; involving sympethatic nervous system (SNS) and activive inhibition, or fight or flight response with increased autonomic and hormonal activities
  • response stereotypy: individual difference in stress response to same situation (pattern)


Why may adverse effects of chronic stress be particularly common in humans?

  • possibly, via high capacity for symbolic thinking which may elicit persistent stress response


What are some psychologically relevant stressors with adverse effects in childhood. What are its effects?

  • maltreatment/abuse: leads to dysregulation of affect, provocative behaviours, avoidance of intimacy, disturbances in attachment
  • childhood sexual abuse survivors: increased general stress, personality disorders more prevalent, associated with negative views toward learning
  • children of divorced parents: increased antisocial behaviour, anxiety, depression.
  • exposure to non-responsive environments: leading to learned helplessness
  • exposure to war/terrorism: PTSD, depression. (70% of childreen in Kuwait reported ptsd-symptoms after Gulf War. In lebanon 40% of children had PTSD like symptoms symptoms 10 years after the war


What role do neo-natal experiences play in the development of response stereotypy?

neonatal experiences in rats were shown to have long-term effects in cognitive-emotional responses:

  • rats with nurturing mothers have increased levels of serotonine activity compared with rats raised by less nurturing mothers
    • increased serotonine activity lead to increased expression of glucocorticoid receptor gene (e.g. receptor for cortisol)
    • this lead to improved glucocorticoid feedback into the SNS. These rats (if female) became themselves highly nurturing mothers and low-anxiety adults
  • those rats that were seperated from their moms a few hour a day had highly active HPA-axes and elevated SNS arousal


Please explain the variability of stress responses

  • Due to differences in situations (situational stereotypy):
    • intensity or severity of stressor
    • controllability
    • features that influence appraisals and cognitive responses
    • usually, multiple stressors have more sever health consequences (e.g. work stress in combination with threat or high demand with low control)
  • due to personal differences
    • rsik factors:
      • having prior psychiatric history
      • neuroticism
      • being female etc.
      • levels of neuroticism and reactivity correlates with event proneness
    • protective factors:
      • coping resources
        • social support (fare better after natural disaster, infarcts)
        • self-esteem, (lower cortisol responses to acute stressors)
        • optimism
      • finding meaning (e.g. political activists were better able to handle torture in Turkey than those that were noot)


What are particularly harmful stressors for major depression and generlaised and anxiety?

And for PTSD?

  • depression and GAD:
    • dimensions of loss
    • humiliation
    • and danger
  • for PTSD:
    • injury
    • damage to property
    • loss of resources
    • bereavement
    • perceived life threat


What makes a stress response adaptive?

If its short term (selye, 1956)

  1. stress hormones make energy stores available for immediate use
  2. new pattern of energy distribution emerges
    • energy is diverted to tissues i.p skeletaal muscles and brain
    • immune cells are activate; sent to battle stations
    • less important activities are suspended (e.g. digestion and production of growth and gonadal hormones
      • eating growth and sexual activity may be destructive in life or death situations


How does the stress response work hormonally?

  1. Stress hormones are produced by the SNS
    • (SNS stimulates adrenal medulla to produce catecholamines (epineprine).
  2. and (simultaneously) by the hypothalamic-pituitary adreno-cortical axis (HPA-Axis) -
    • paraventricular nucleus of hypothalamus produces corticotrophin releasing factor
    • which stimulates the pituitary to produce adrenocorticotropin
    • which stimulates adrenal cortex to secrete cortisol
  3. catecholamines and cortisol increase available sources of energy by promoting lipolysis and conversion of glycogen into glucose (i.e. blood sugar)
    • Lipolysis is the process of breaking down fats into usable sources of energy (e.g. fatty acids, glycerol)


How does the cardiovascular and immunal stress response look like?

  • energy is distributed to the organs that need it by increasing blood pressre and conrtacting certain blood vessels while dilating others
  • There are two hemodynamic mechanism to increase blood pressure:
    1. myocardial mechanism: increase blood pressure through enhanced cardiac output (increase in HR and stroke volume output)
    2. vascular mechanism: constrict vasculature, hence increasing blood pressure
  • specific stressors tend to elicit one of the two mechanisms:
    • stressors that require active coping (e.g. giviing a speech) elicit myocardial response
    • stressors that require vigilant coping mechanism (keeping food in bucket of ice water) tend to elicit vascular response
  • these mechanisms seems to be evolutionarily adaptive:
    • cardiac response facilitates active coping by shunting blood to skeletal muscles - fight-flight response
    • situations that do not require decisive action but instead need skeletal muscle inhibition and vigilance (freeze-response) vascular mechanism is adaptive
      • shunts away blood from periphery to internal orans in case one ecxperiences a wound
  • also immune system is responing by macrophages and natural killer cells depart from lymphatic tissue and spleen to bloodstream (temorarily raising number of immune cells in blood; leukocytosis)
    • then wander to battle stations e.g. skin where wounds are likely


What are the cardial consequences of Chronic Stress?

  • acture stress response becomes maladaptive if it is continuously activated (Selye 1956)
  • chronic SNS activation leads to:
    • sustained blood pressure elevation
      • forces heart to work harder causing hypertrophy of left ventricle, over time elevated BP, damaged arteries, plaque
    • vascular hypertrophy; i.e. muscles that constrict the vasculature thicken leading to
      • elevated RBP and
      • response stereotypy
      • or a tendency to respond to all stressors with a vascular response


What are hormonal consequences of a Chronic Stress Response?

  • immunity is suppressed through elevated basal levels of stress hormones directly affecting ccytokine profiles
    • cytokines are communicatory molecules produced by immune cells.
    • there are three types of cytokines:
      1. Proinflammatory cytokines that mediate acute inflammatory reactions
      2. Th 1 cytokines mediate cellular immunity by stimulating jatural killer cells and cytotoxic T cells
      3. Th 2 cytokines mediate humoral immunity by stimulating B cells to produce antibodies (they "tag" extracellular cells, e.g. bacteria)
    • stressors such as examination can lead to a Th2 shift (increase in Th2 cells relative to Th1 cells) which suppresses cellular immunity in favor of humoral immunity.
    • more chronic stressors can lead to suppression of humora (Th2) and cellular (Th1) immunity
  • intermediate and chronic stressors are realted to slower wound healing, recovery from surgery, antibody responsesantiviral deficits
  • particularly problematic for the elderly who may have immunoscenescence (gradual loss of immune function due to age)


Stress and Cardiovascular disease.

  • Occupational gradient in Coronary Heart Disease (CHD): men with lowest socioeconomic status have poorest health outcomes
    • variance can be accounted for with lack of perceived job control, also smoking, alcohol use and sedentary lifestyle, behaviours that may be facilitated via stress
    • for men: work stress seems to predict CHD and hypertension
    • among women with existing CHD marital stress seems to be predicting poor prognosis
  • atherosclerotic CHD (Kaplan et al., 1982): studied male cynomolgus monkeys:
    • stressor: reorganising group every three months so they have new companions and moderate atherogenic diet for all monkeys
    • were assessed for their relative dominance
    1. socially dominant monkey iin unstable groups had more atherosclerosis than socially less dominant monkeys
    2. socially dominant males in unstable groups had more atherosclerosis than their counterparts in stable, unchanging groups
    3. heart-rate reactivity to threat of capture predicted atherosclerosis
    4. SNS blocking agent decreased progression of atherosclerosis
  • findings that affiliative social behaviour decreased progresseion of atheroclerosis even if the rabits had a genetic predisposition and stable groups exhibited koore such behaviour compared to changing groups


Stress and Upper Respiratory Disease (Cold).

  • stress predicts scusceptibility to common cold
    • maybe they just spend more time outside?
  • people that were quarantined and exposed to Rhinovirus and had been exposed to life-stress were more likely to catch a cold (events lasting longer than a month), those that had shorter stress did not catch it more often


Human Immunodeficiency Virus and Stress

  • faster HIV progression to AIDS associated with cumulative stressors, use of denial as coping, lower satisfaction with social support and elevated cortisol levels.


Stress and Inflammation, The Immune System and Physiscal Health.

  • despite its immunosuppressive effects, stress is also associated with exacerbatioons of autoimmune disease and CHD
    • acute stress response includes activation of cells to innate immune system (effect mediated by pro-inflammatory cytokines)
    • in chronic stress cortisol eventually suppresses proinflammatory cytokine production, in people with autoimmune disease or CHD stress lead to a chronic activation of the proinflammatory cytokine production
  • Miller et al. (2002) glucocorticoid-resistance model argues thatimmune-cells become resistent to effects of cortisol through reduction of cortisol receptors.
    • so cortisol cannot suppress inflammation, stress will promote proinflammatory cytokine production indefinetly
  • implications for rheumatoid arthritis were excessive inflammation leads to joint damage, swellimg pain and reduced morbidity
  • in multiple sclerosis (MS) overactive immune system targets myeline surround nerves eventually leading to blindness and paralysis
  • in CHD. immune system responds to vascular injury just like any other wound: immune cells infiltrate artery wall which can eventually lead to thrombosis (i.e. clot)
  • elevated inflammatory markers as C-reactivity protein (CRP) predicts heart attack
  • CRP has been associated with major depressive episodes in men


In what way is sickness behaviour adaptive and when is it not?

  • proinflammatory cytokines are sufficient to produce sickness symptoms
    • it is seen as a highly organised strategy to combat infection; they promote resistance and facilitate recovery
      • fatigue, decrease in activity to preserve energy and redirect toward enhancing immunity
      • also: malaise, diminished appetite and listlessness
      • limiting exploration, mating and foraging preserves energy and make risky encounters less likely
      • decreasing food-intake decreases iron-levels which bacteria use to replicate
  • sickness behaviour can become maladaptive when repeatedly or continuously activated
    • features can overlap with depression
    • patients with inflammatory diseases report higher levels of depression (MS, CHD) compared to those with non-inflammatory diseasses. proinflamatory diseases may mediate depression with proinflamatory cytokines


Allostasis and Allostatic Load

  • allostasis are changes in biological set-point that occur in life due to chronic stressors
  • costs of these is adjustment are referred to allostatic load
    • cumulative allostatic load may lead to chronic disease; but could also be caused by comorbidities (immunoscenscence, genetic predisposition, pathogen exposure etc.)
    • changes in set points: British soldiers in WWII had chronic elevation of bloos pressure (allostasis) but theey returned to normal after the war
    • individuals with e.g. chronic fatigue syndrome are much more affected by allostatic load (e.g. hurrican)


Behavioural Interventions in Chronic Disease

  • patients with chronic, life-threatening diseases confront daily stressors that undermine the most resilient coping strategies or overwhelm resources
  • Psycho-social internventions (e.g. cognitive-behavioural stress management - CBSM) improve quality of life, decrease stress and improve mood, improved perceived social support, facilitate problem-focused coping and change cognitive appraisals, decrease SNS arousal, decrease overuse of medication, may also improve disease progression


cStress and Morbidity, Mortality and Disease Progression

  • Psychosocial interventions decreased mortality and mobidity between 20 and 40%
  • Recurrent Coronary Prevention Project (RCPP) with group-based CBT decreased hostility annd depressed affectas well as composite medical end point of cardiac death + nonfatal MI
  • ENRICHDD clinical trial found decrease in depression and increase in perceived social support but no effct on medical end point death
    • secondary analysis found that cardiac arrest decreased around 40% for white men but null effect for minority women
    • RCPP trial consisted mostly of whit males
  • four factors were found to distinguish psychosocial interventions that were succesfull in improving survival:
    1. patients with same type and severity in each group
    2. creation of supportive environment
    3. educational component
    4. stress management and coping skills training
  • e.g. 6 weeks CBSM intervention increased survival + reduced stress, enhanced active coping and more NK cells cytotoxicity
  • psychosocial interventions could not decrease disease progression in AIDS but factors that are associated with disease progression:
    1. distress
    2. depressed affect
    3. denial coping
    4. low perceived social support
    5. elevated cortisol
  • group-based CBSM (CBT + relaxation)
     decreased stress related symptoms in HIV patients:
    • lower distress, anxiety and depressed mood
    • also lower anti-body titers of herpesviruses + higher levels of T-helper cells, NK cells and lymphocyte proliferation
    • cortisol
    • and epinephrine
    • improved percceived social support and coping skill  mediated the relationship



  • popular definition of stressful situations (Lazarus): a situation of which the demands exceed the resources of the individual
  • creatures face threat to homoeostasis which must be met with adaptive responses
    • societal level: Lackk of resources (inadequate insureance), pestilence, war, terrosrism etc.
    • individual levels: job stress, marital stress, unsafe school and neighbourhoos etc.
  • acute stress responses may be adaptive, especiall in young, healthy and optimistic individuals
    • if stressor is too strong and/or persistent and the individual is vulnerable (age, genes, constitutional factors etc.), poor coping skills or resources, than stress may lead to disease
    • relationship between stress and and disease may be mediated by endocrine-immune mechanisms


What were some early views on stress or its theoretical background?

  • Claude Bernard (1865) says that for survival it was critical to keep our "internal millieu" constant in the face of changing environments.
    • Canon (1929) called this "homeostasis"
    • Selye (1956) used the word "stress" to anything that threatens homeostasis