8) Stress Flashcards

1
Q

What is stress (chronic vs acute)?

A
  • is common, universal and frequent
  • difficult to define bc everyday stress and complaints differ from scientific definition
  • duality: may be relevant BUT can make us sick

Chronic stress = makes us sick, play a role in etiology of several diseases and disorders

Acute stress = can potentially be helpful, highly functional and evolutionary successful biological system

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2
Q

Different causes and consequences: Claude Bernard (1865)

A

homeostatis –> is an adaptive response to an external stimulus

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3
Q

Different causes and consequences: Walter Cannon (1925)

A

fight-or-flight response

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4
Q

Definition and Model: Hans Selye (1956): General adaptation syndrome

(Course of acute stress to chronic stress)

A

stressor = stress-eliciting stimulus

stress response = non-specific response fo the body to any demand, behavioural and physiological response
- response within object, inherent to its structure (derived from physics)
- everything that is challenging, elicits some response

stress = interaction between stressor and stress response

Short term stress leads to resistance BUT after long time to exhaustion
1) Alarm: acute physical adaptation response
- cortisol, adrenaline, noradrenaline
- shifts resoucres, fight or flight response
2) Resistance: reduce stress, solve situation and restore body to initial state
- cortisol
- after long time bio resources depleted
3) Exhaustion: when no return to normal functioning occurred, body resources depleted –> no restauration to initial state
- leads to disease and disorder

Model Restrictions:
- external stimulus fixed and invaried
- different levels of measurements that only correlate poorly
- very physiologically focused, left out psychological implications

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5
Q

Definition and Model: Lazarus (1980s): Transactional model of stress

A

stress = response to an ‘imbalance between demands and resources’
-> if pressure exceeds one’s ability to cope

Simple Model:
Stressor –> leads to appraisal –> leads to stress response

Tries to overcome prior model’s shortcomings
- complex interaction between demands and resouces –> if not able to cope, stress response
- higher subjective component –> people differ in interpretation

  1. Environment and stressors –> filtered and selected
  2. influences person individually
  3. Primary appraisal –> stimulus can be irrelevant, positive or dangerous
  4. Secondary appraisal –> only if deemed dangerous
    - analysis of available resources: if sufficient not stress, IF insufficient: STRESS
  5. Stress
  6. Coping –> overcoming stress
    - emotion or problem focused
  7. Reappraisal –> pacing and learning
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6
Q

What is stress (definition)?

A

= real or interpreted threat to the physiological and psychological integrity
- results in physiological and behavioural responses

= stress is a condition in which an individual is aroused by an aversive situation
- hostile employer, unpaid bills, predator or pawshock

  • magnitude of stress and its physiological consequences are greatly influenced –> by the individual’s perception of its ability to control the presence or intensity of the stimulation
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7
Q

Stress response: Brain and body

A

Image:
- increased blood flow to brain
- increased production of catecholamines (epinephrin/adrenaline, norepinephrine/noradrenaline, dopamine)
–> facilitates cognitive performance

  • pupils dilate/peripheral vision is reduced
  • heart rate increases
  • faster, deeper breathing
  • increased blood flow to large muscle groups
  • adrenal hormones (cortisol and DHEA) released, resulting in increased energy mobilisation
  • digestion slows dramatically
  • blood pressure increases

Other responses:
- increased perspiration to cool body
- increased muscle tension to prepare for fight or flight
- increased inflammation
- increased blood pressure
- decreased saliva production
- speed up of metabolism
- blood flow from skin surface is diverted to larger muscle groups and brain
- body extremities can change temperature

Reactions:
- increased alterness, short term strength, ability to handle stress
- heightened ability to focus
- increased oxygen to the brain
- faster, deeper breathing
- heightened sense of smell
–> body and mind are hyper-alert

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8
Q

Autonomic nervous system (ANS) and HPA system: ANS

A
  • two major systems for stress: ANS and HPA system

ANS
- short-term response, fight-or-flight
- sympathetic ANS (parasympathetic = rest and digest)

  1. Stress signal in hypothalamus sends nerve impulse to spinal cord (sympathetic system)
  2. signal is sent further via preganglionic sympathetic fibers to Adrenal Medulla
  3. Adrenal medualla secretes aminoacid-based hormones –> release of catecholamines: adrenaline/epinephrine or noradrenaline/norepinephrine
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9
Q

Autonomic nervous system (ANS) and HPA system: HPA systems

A
  • two major systems for stress: ANS and HPA

Hypothalamic-Piturary-Adrenal (HPA) system
1. stress signal to hypothalamus (hypothalamic paraventricular nuclei (PVN)) –> release of Corticotrophin Releasing Hormone (CHR) to hypophyseal portal system
2. Corticotroph cells of anterior pituary release AdrenoCorticoTrophic Hormone (ACTH) into blood stram
3. ACTH is transported to adreneal gland (adrenal cortex) via systemic circulation (kidneys) –> release of sterioid hormones (Cortisol: Mineralocorticoids and Glucocorticoids)
4. Cortisols cross brain-blood-barrier, closed feedback loop (signal at hypothalamus)

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10
Q

What is the function of the HPA

A
  • delay of +30min to hours after stress stimuli

Permissive, suppressive, stimulatory and preparative actions?
1) the physiological function of increased glucocorticoid levels
- NOT to protect agansit the source of stress itself
- BUT against the normal defense reactions that are activated by stress

2) glucocorticoids accomplish this function by turning off those defense reactions
–> preventing them from overshooting and themselves threatening homeostasis

3) glucocorticoids are required to limit the water damage caused by the fire brigade

–> downregulation to avoid too much damage

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11
Q

Involvement of GR and MR

A
  • MR-genomic does not really play a role in stress
  • MR-nongenomic and GR-genomic play a role
  • HPA is divided into MR and GR

MR:
- activation, appraisal and decision making
–> appraisal of the situation and/or for response selection
–> encoding and memory of the situation for future use
–> predictability, apparaisal and risk assessment, reactivity and flexibility, onset stress reaction
=> part of initial stress response

GR:
- recovery, adaptation and homeostasis
–> redistribution of resources towards cortical network
–> consolidation of memory and behavioural adaptation
–> prevents the initial reaction from overshooting
–> controllability, memory storage, adaptation, turn-off stress reaction

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12
Q

Psychological effects of stress

A

Learning and memory
- 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 behaviour and ingroup bias –> especially in women
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13
Q

What type of measure can be taken to induce stress in the lab?

A

physiological
psychosocial
drug maipulation

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14
Q

Laboratory stress induction: Physiological

A

For example:
- hand in cold water for 3min
- ANS response, less effect on HPA
- immediate and short term effect
- usually induced directly before testing task

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15
Q

Laboratory stress induction: Psychosocial

A

For example:
- fake interview with ‘trained observers’ who evaluate the participant
- participant gets 5min to prepare, 15min in total
- gold-standard elicits HPA response, takes longer to develop –> peak in cortisol

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16
Q

Laboratory stress induction: Drug manipulation

A
  • no direct stress but drugs elicit ANS response (adrenaline or noradrenaline) or HPA response (cortisol)
17
Q

How to measure stress?

A
  • standardised questionnaires
  • measurements:
    > blood pressure
    > heart rate
    > electrodermal activity
    > stress hormones in hair (chronic stress leads to metabolites in hair), blood, saliva
18
Q

Chronic stress and effects of glucocorticoids

A
  • more exhaustion phases
  • longer activations and lack of adaptation

anti-inflammatory
- too much glucocorticoids
> increased infections
> increased cancer progression
> increased ageing
> decreased efficacy of vaccination
> decreased wound healing

pro-inflammatory
- too little glucocorticoids
> increased autoimmune diseases
> increased inflammation
> increased pain

19
Q

Major depressive disorder and stress

A
  • MDD is one of the most prevalent mental disorders
  • main symptoms are depressed mood and/or loss of interest and pleasure
    –> cognitive problems including memory disturbances are also frequent
  • biological, psychological and soical factors play a role in the development of MDD
    –> suggesting that depression results when a preexisting vulnerability is activated by stressful life events

HPA axis
- 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