Lecture 1: Introduction Flashcards

1
Q

How can stress be defined?

A

Means a variety of things like a negative situation, feeling of pressure, tension or negative emotion. Psychological definition: stress can occur when demands are appraised as exceeding a person’s resources to cope

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2
Q

What are stressors?

A

External or internal events that may trigger stress responses. These can be acute stressors, chronic stressors, daily hassles, traumatic stressors and role strain

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3
Q

What are the different types of stress responses?

A

This is how we respond to a stressor, which can be cognitive, affective, behavioural and physiological responses. There is not always a strong association between these. In a repressive coping style will show no emotional distress but show physiological responses

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4
Q

What are the two waves when responding to stress?

A

Involves a quick first wave which is the fight or flight response involving the sympathetic branch of the autonomic nervous system. The second wave is slower and involves the endocrine pathways of the hypothalamic-pituitary adrenal axis.

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5
Q

How exactly does the sympathetic nervous system work?

A

It prepares the body to prepare for immediate action. The adrenal medulla is stimulated to produce stress hormones like adrenaline and noradrenaline which stimulates the heart and lungs away from unnecessary functions

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6
Q

How does the HPA axis work?

A

The hypothalamus releases corticotropin releasing factor which leads to a release of cortisol and other hormones from the adrenal cortex.

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7
Q

What is the role of cortisol?

A

A steroid and critical stress hormone which results in an increase in blood sugar levels and metabolic rate which influences regulation of blood pressure, immune system and inflammatory response. Cortisol can return to normal levels after a stressful period but prolonged periods can lead to dysregulation and chronically elevated levels of cortisol. Can result in Cushing’s syndrome

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8
Q

What has research found about stronger stress responses?

A

Usually occurs in more novel, unpredictable or uncontrollable situations. Chronic stress on physical frailty was fully mediated by perceived control, but trying to gain control over a situation that is uncontrollable can lead to more stress

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9
Q

Stress responsivity

A

How people respond physiologically to stress which is genetically determined but early environment is important for shaping responses to stressors -> fetal programming. Nature and nurture shown through dandelion and orchid children study. Dandelion- those highly responsive and in high adversity had more illness than those highly responsive in low adversity. Orchid- less responsive had a similar risk of illness not dependent on the environment.

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10
Q

Tend and befriend response

A

Animals and humans tending to offspring and seeking out others for safety and comfort-> women more likely to use. Oxytocin and endogenous opioids have been found to play a role in affiliative behaviours and attachment to others. Opioid system involved in reducing physical pain and reducing separation distress while oxytocin linked to reduced physiological stress responses and psychological distress. Fight-flight responses good for threatening events but tend-befriend to buffer long-term negative impact of stressors

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11
Q

How do the SNS and HPA axis affect the immune system?

A

SNS- increases immune system activity like natural killer cells
HPA axis- suppresses immune activity through production of cortisol which has an anti-inflammatory effect, reducing white blood cells and cytokine release

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12
Q

How do different types of stress influence immune responses?

A
  • short stressors lead to an acute increases immune response and redistribution of cells for immediate defence
  • brief stressors for several days can influence the function of the immune system from cellular immunity to humoral immunity to protect against infection
  • chronic stressors results in poorer immune function in general
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13
Q

What are the 3 processes of appraisal?

A
  • primary appraisal is the demands of the situation being evaluated as benign or stressful
  • secondary appraisal is a person evaluating their resources and capacity to cope
  • reappraisal is that after a coping strategy a person reconsiders the situation
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14
Q

What has research found about the appraisal approach?

A

Appraisal of pain as threatening was linked with more impairment and psychological distress. While appraisals of pain as challenging linked to more pain tolerance and active coping.

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15
Q

Interactional model

A

Interaction between person, environment, appraisal, coping and other psychosocial factors. Seen as a dynamic process

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16
Q

Why is it difficult to establish pathways between stress and health?

A
  • huge variation in how people respond to stressors which can be influenced by resilience, coping, social support, allostatic load
  • unclear whether the cause of an illness is due to stress or other factors
  • the effect of stress on health can be due to behavioural, emotional or physical responses to stressors which can then cause disease
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17
Q

Allostasis

A

Process of regulating our physiological state to achieve stability or homeostasis. Frequent activation or chronic activation can result in a high allostatic load. A prolonged response is when they are in a continually high state-> long-term strain. Or when an allostatic system does not respond so other systems to overcompensate. If acute stressors are repeated with lack of adaptation, can lead to stress responses

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18
Q

What is resilience and what has research found about it?

A

Resilience is having a swift recovery from stressful events, sustainability of purpose in adversity and growth or new learning from adversity. At least 50% of people have experienced some kind of trauma but only 10% suffer from PTSD

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19
Q

How can emotions and emotional disposition influence resilience?

A

Positive emotional states and positive dispositions are linked with reduced mortality. Depression, anger and hostility are linked with CVD and mortality. Those with more neuroticism report more pain and somatic symptoms with no consistent link with heart disease, cancer or mortality

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20
Q

How can coping influence resilience?

A

Coping strategies that enable a person to feel more in control can increase positive emotions and decrease negative emotions which is linked to resilience. No style is better than another, it depends on the situation

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21
Q

How can social relationships and social support influence resilience?

A

Negative relationships like those involving abuse or conflict are some of the most potent stressors. Parents and children found to have similar responses to stress also through attachment, if abandoned then can lead to insecure and chaotic responses to stressors. Linked to improved health outcomes and 50% increase in survival rates, having stronger outcomes than other risk factors. Presence of others during stressful tasks can reduce SNS and HPA axis responses but depends on other factors as well. Presence of others more important than actual support received.

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22
Q

What are the types of coping?

A

Emotion-focused strategides concentrates on reducing distress while problem-focused strategies is on dealing with the problem. Approach coping strategies deal with the situation proactively so is more active. While avoidant coping strategies avoid the problem so more emotion-focussed.

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23
Q

What are the main symptoms of burnout?

A
  • emotional exhaustion (depletion, worn out, physical exhaustion)
  • depersonalization (unfeeling and impersonal, lack of engagement with others)
  • reduced personal accomplishment (poor sense of effectiveness, involvement, commitment and poor belief in ability to change environment)
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24
Q

What is engagement?

A

Involves high levels of vigour, dedication and absorption and linked to good performance

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25
Q

What is burn out linked to?

A

Poor performance, high job dissatisfaction, abseentism and staff turnover. Linked to younger age, alcohol, tobacco use, medication. In Europe more to do with negative attitudes to work while in USA burnout linked to work-life conflict and poor coping strategies.

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26
Q

How does burnout risk work?

A

It operates at 3 levels: individual level (healthy lifestyle/behaviours, good coping), individual and environment (social support structures, person-organisation fit) and organizational level (working conditions, organisation of work, design). To prevent this, positive organisational culture and staff engagement can be improved

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27
Q

Which students are most likely to develop burnout later in life?

A

Those who are disorganised, poor time management, feel overwhelmed, unsure of demands of different tasks, self-critical, neurotic, perfectionists, imposter, and female more likely to have stress and burnout

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28
Q

What are the different ways of managing stress?

A

Strategies aim to reduce arousal and build coping skills. 2 approaches: focussing on physical and mental relaxation such as yoga, mindfulness or those that focus on cognition and behaviour like psychoeducation, cognitive restructuring, stress inoculation.

29
Q

What is stress inoculation?

A

Exposes people to potential stressors and training them so that they have some protection in the future and work effectively in those conditions

30
Q

What are the main aspects of resilience found?

A
  • attitudes and perspectives like remaining interested, developing self-awareness and personal limitations
  • balance and prioritisation like setting limits and honouring the self
  • practice management style so good business management and staff
  • supportive relations like personal relationships and good communication
31
Q

What is the major stressful life event checklist?

A

These scales assess the number of major events that a person reports in a year usually with each event adding to the total stress burden. The Life Events and Difficulties schedule is an example. The threat of an event is assessed and compared to ratings of similar events which could lead to a risk for a certain disease

32
Q

What are the 4 theoretical perspectives for a stressful event?

A
  • adaptation which suggests that each additional event adds to the overall burden of change and positive events can also lead to change
  • for there to be stress there needs to be harm or threat (imminence of harm, intensity, duration, uncontrollability found to be important) but maximum risk can be enough and not cumulative
  • when a situation is demanding, resulting in psychological distress but decision latitude and control is insufficient
  • interruption of goals like maintaining physical integrity and psychological wellbeing
33
Q

Which approach is the most accepted?

A

The threat or harm approach, the goal interruption and decision latitude have less evidence but can be seen as a subset. Adaptation approach has not held up in research

34
Q

What are the pathways that can link stressful event exposure to disease?

A

Affective regulation (more fear, anxiety, depression), health behaviours (poor nuitrition, no exercise, alcohol) and neurohormonal systems and direct innervation of tissues by autonomic nervous system.

35
Q

Stress and common illnesses

A
  • those with depression were more likely to have experienced a stressful life event
  • increased risk of CVD with more stress (more fat, dysregulated lipid and glucose, inflammation, higher resting blood pressure). Acute stressors can trigger cardiac events
  • chronic enduring events can increase risk of developing illness to infection, like being exposed to a virus and those who had more stressful life events were more likely to have an infection. Same with HIV/AIDS
  • inconsistent findings with cancer, one study found that more stressful life events led to poorer survival and higher mortality rates
36
Q

What is critical incident debriefing?

A

The client would talk about their thoughts and feelings and symptoms which the therapist would try to normalize. But has found to have little effect on PTSD and depression or that it can make it worse.

37
Q

What is puzzling about people being exposed to stressful events?

A

Many people that have been through a stressful event did not develop a cold, did not experience depression. The percentage of these can change depending on the stressor exposure and psychopathology outcome but most do not suffer from mental health problems

38
Q

Why are some people more resilient to stressful events?

A

Some have more perceived control, greater self-efficacy, and less negative affectivity and rumination, access to social resources can all promote resilience

39
Q

In what way are stressful events not random?

A

Influenced by individual differences in environment and psychological characteristics. Such as in low SES environments there can be more frequent and severe stressor exposure. Greater neuroticism and a negative attributional style can lead to more interpersonal conflicts and experiencing more stressful life events. Individual stressful events can trigger sequences of other events and can even be passed on across generations

40
Q

Why is stressful event exposure not the proximate cause of disease?

A

In healthy people, stressful events may not trigger pathogenesis, events could influence the ability to fight pathogens or exacerbate premorbid processes. Baseline does not fully rule out all other unidentified signs of illness. What could be stressor triggered could actually be stressor triggered progression of a previously unidentified disease. Stressful events can tip the balance of a vulnerable system

41
Q

Which types of stressful events are particularly potent?

A

Interpersonal problems like conflict with a spouse, death of a loved one etc. Interpersonal issues which threaten an individual’s social status has been linked to adverse health outcomes. Those experiencing social rejection showed a decrease in anti-inflammatory gene signalling. Employment difficulties also has implications for role identity and social status which was linked to negative health outcomes-> strongest predictor of developing illness

42
Q

What are chronic events?

A
  • with exposure there are more chances of the stressor being at points of vulnerability which increases wear and tear
  • includes persistent chronic stressors like job stress, parental conflict and chronic intermittent stressors like sexual difficulties
  • there can be chronic exposure sequences which are events that occur over an extended period of time due to an initiating event like divorce, job loss
43
Q

What are the aspects of chronic events that result in increased risk over time instead of adaptation?

A
  • continued effects of exposure more likely to occur when events are severely threatening
  • random intermittent events can inhibit habituation
  • underlying biological process which leads to stressor-elicited changes
44
Q

Why are acute events still important?

A

These can still exacerbate pre-existing disease, and traumatic events like rape are acute but the duration of the appraisal, the affective response and physical effects should all be considered

45
Q

What has been found about cumulative risk?

A

That the more events occur, the greater the risk but no direct evidence whether due to amount of change or threat. Others argue that a moderate/severe threat is enough to put people at risk and other events do not increase the risk. This could be due to issues with defining the content of events

46
Q

How have these issues with categorization been overcome?

A

By trying to sort the events into domains and counting the number of domains in which there are issues. But it is unclear whether an event needs to meet a threshold or be clustered together

47
Q

What is the role of chronic background stressors?

A

Mixed results about greater sensitization due to chronic background stress and so more responsive to other acute events.

48
Q

How can time impact the negative impacts of stress?

A
  • violations of the expected time course of certain events can have negative impacts
  • such as losing a spouse has even more negative outcomes earlier in life
  • adverse childhood experiences lead to an increased risk of developing illness later and also being exposed to more stressors over the life course
  • also works through generating long-term changes in biological process and behaviour
49
Q

How can gender roles influence the stressful events that women and men face?

A
  • men are encouraged to develop agentic goals from a young age while women are more likely to have communal goals
  • so the theory is that men face more achievement-related stressful experiences while women have more interpersonal stressful experiences (and experience stress more indirectly)
  • but there are mixed findings, partially due to closing the gap in work-related stressor exposure
50
Q

Differential risk for depression between men and women

A

Equal risk in childhood but female risk increases perhaps due to more sensitivity in social networks and stressful interpersonal life events which is linked to depression onset.

51
Q

What is the higher mortality risk linked with stress?

A

48% higher mortality risk and significant after controlling for other life style and risk factors

52
Q

What are the 3 approaches to understanding stress?

A

Stress as a stimulus (stressor assessed through questionnaire based assessments and exposure paradigms). stress as an evaluative process (stress perception) and stress as a response (stress response)

53
Q

What was found to be significant for the type of stressor?

A
  • total number of negative life events
  • total number of daily hassles
54
Q

How was acute stress measured?

A

With a complex task like mental arithmetic and amplifying components like time pressure, social evaluation and to avoid punishment/obtain rewards. Anxiety, heart rate and epinephrine found to go up

55
Q

Reactivity hypothesis

A

Exaggerated cardiovascular responses to acute stress is a risk factor for development of CVD disease. It is stable and can lead to long-term implications

56
Q

How is stress an evaluation process?

A

Primary appraisal - is situation harmful, threatening, challenging
Secondary appraisal, assess resources to choose a coping method
Emotion-focussed/problem-focussed coping

57
Q

Primacy of affect

A

Stress perceptions without conscious evaluation

58
Q

What did Brady’s experiment find?

A

That lack of control is a key determinant of stress

59
Q

Social- self preservation theory

A

Threats to self lead to a specific set of psychological and physiological reactions like feelings of low social worth and increases in cortisol
-> cortisol increased more when doing tasks with a greater audience

60
Q

How can stress be measured as a response?

A
  • self report through anxiety, anger, shame, depressed mood
  • physiology like immunity, endocrine, metabolic, cardiovascular
  • behaviour like restless, lethargy, under/over responsiveness
61
Q

2 wave defense response

A

Parasympathetic nervous system releases acetylcholine within seconds, SAM release adrenaline and noradrenaline
HPA axis releases ACTH
The neurotransmitters active receptors on adjacent cells, while hormones active receptors on distant cells

62
Q

Differences in how neurotransmitters and hormones work

A

Hormones work at a greater distance, slower/sustained temporal effects, systematic changes as they have integrative functions. Slow effects through gene transcription which leads to glucose production and memory consolidation.
Neurotransmitters have fast effects through receptor activation which can lead to muscle contraction, arousal vigilance

63
Q

How does the HPA axis work?

A

Hypothalamus release CRF
Anterior pituitary gland releases ACTH. The adrenal cortex releases cortisol which target cells receive and leads to a biological response

64
Q

Role of these systems

A

Immune system → immune suppression
Liver → gluconeogenesis
Adipose cells → fat metabolism
Adrenal medulla → adrenalin production
Hippocampus → declarative memory
Amygdala → fear memory

65
Q

How is the brain and stress hormones a reciprocal relationship?

A

The brain regulates release of stress hormones, and
stress hormones regulate the brain

66
Q

How do glucocorticoids enhance extinction-based therapy?

A

Less fear is reported after VR exposure therapy and reduced physiological responding after VR therapy

67
Q

Signs of parasympathetic withdrawal

A
  • dry mouth
  • trachicardia
  • slowed GI peristaltic
  • measured by heart rate variability
  • has activation with some stimuli like disgust, phobia, blood and fainting
68
Q

Signs of sympathetic activation

A

Increase in blood pressure, increase in heart rate, blood redistribution, increase in metabolism, increase in lipids and glucose levels. Outcome measures: norepinephrine in blood, salivary protein, skin conductance, pupil dilation and blood pressure/heart rate