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Health Psych - Kin 2G03 > Stress > Flashcards

Stress Flashcards

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1
Q

what is an acute stressor? give 3 examples of physical and psychological stressors

A

something that disrupts homeostatic balance (hormones involved are adrenaline and cortisol)
ex:
- getting chased by bear
- writing an assignment that’s due tomorrow that you haven’t started yet

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2
Q

what did the Selye experiment demonstrate for the experimental and control rats? conclusions?

A

Selye handled rats poorly and they all dev’t stomach ulcers (experimental and control)
- he concluded that they were all experiencing a stress response since unpleasant situations seemed to make them sick

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3
Q

what is general adaptation syndrome? why did psychologists not like this theory?

A

our body produces the same physiological response to any stressor that knocks us out of homeostatic balance

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4
Q

parasympathetic nervous system vs. sympathetic nervous system

A

parasympathetic NS: innervates all systems of the body, rest and digest functions, main NT is ACh released from the brain to the periphery of the body

sympathetic NS: responsible for fight or flight response, increase in HR, BP, etc.
- main NT is ACh from spine to intermediate ganglion and then adrenaline/epinephrine and norepinephrine from intermediate ganglion to target cells

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5
Q

what role does the locus coeruleus play in the stress response?
what NT does it release?

A

releases norepinephrine in response to stress

  • LC receives input from env’t, sends signals to thalamus which activates it even more and interacts with the hippocampus (memory) & amygdala (fear processing)
  • LC regulates homeostasis and allostasis of stress response
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6
Q

describe the SAM axis and how it contributes to the stress response

A
  • a rapid stress response that triggers fight or flight
  • hypothalamus activates sympathetic NS which activates adrenal medulla to release epinephrine into the blood where it reaches target cells, all unnecessary functions are shut down
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7
Q

describe the HPA axis and how it contributes to the stress response

A

elicits a slower, more sustained response through hormone release
- hypothalamus is activated, releases corticotropin releasing hormone (CRH), targets pituitary gland to release adrenocorticotropic hormone (ACTH) that targets the adrenal cortex to release cortisol into the blood which increases blood glucose to provide energy for fight or flight

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8
Q

how are the SAM and HPA axes different?

A
  • SAM is fast but short response bc uses nerve conduction

- HPA is slower but longer lasting response to stress since is uses hormones

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9
Q

what impact does epinephrine have on the body?

A
  • shuts down all unnecessary functions so that energy can be used for quick reaction to threats (increase HR, BP, breathing rate)
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10
Q

what impact does cortisol have on the body?

A
  • increases blood glucose by mobilizing stored energy from the liver and adipose to provide energy for flight or flight response
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11
Q

describe the Trier Social Stress Test (TSST)

A

an experiment designed to test how well people cope under pressure
- normal cortisol levels were measured before and the stress response was activated

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12
Q

how does the Trier Social Stress Test (TSST) impact the stress system? does the stress response depend for elite sportsmen, amateur sportsmen or untrained men? is the response to cortisol a function of mineralocorticoid receptors or glucocorticoid receptors?

A

stress system was activated

  • if someone is an elite athlete, they have less cortisol (stress) response to the psychological stressor and also return to normal faster
  • GR involved in response to cortisol
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13
Q

immediate stressor

how does this have an impact on the stress response

A

stressors that happen which you are not prepared for

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14
Q

anticipated stressor

how does this have an impact on the stress response

A

stressors that you’ve conditioned yourself to be stressed about so you fear them
- ie could come from having a bad experience with something

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15
Q

how do you acquire fear to an innocuous stimulus?

A

through presentation of the CS with the US, the subject will eventually elicit the CR with only the presentation of the CS

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16
Q

how do the hippocampus and amygdala contribute to fear conditioning? how do they interface w the stress system? how are they different?

A
  • the amygdala and hippocampus are related to the stress response
  • amygdala responsible for fear response which activates HPA axis (stress response)
  • hippocampus involved in memory and learning of the associated fear/stress response - requires fear response from amygdala first since it activates the amygdala which activates the HPA
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17
Q

what type of fear conditioning would be influenced if you lesion the amygdala?

A

no conditioning would occur if the amygdala was damaged since we can’t have the fear response without it

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18
Q

what type of fear conditioning would be influenced if you lesion the hippocampus?

A

we could learn to fear a response but would not be able to make a more complex association (contextual cueing requires hippocampus)

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19
Q

learned helplessness

A

a freeze response that is developed when individuals under a lot of stress learn there is nothing they can do about their situation

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20
Q

describe the learned helplessness paradigm. what are the 2 conditions? what happens in phase 1 and phase 2? how is learned helplessness measured?

A

2 dogs - one shocked with control and one shocked without control

  • dogs who were shocked with control were more likely to try and escape and got our faster in a box where the floor shocked them
  • dogs shocked without control will remain in shocking part of the box bc they learned that they have no control over their stressful situation
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21
Q

is the stress response on or off when experiencing learned helplessness? is the behavioural response typical or atypical and why?

A

stress response is on and can remain on when experiencing learned helplessness, cortisol levels remain high
- the behavioural response is typical of that exhibited with their stress but they learn to stop exhibiting their typical behaviour but still experience the stress - causes allostatic loac

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22
Q

give 3 examples of things that could cause learned helplessness in humans

A
  • repeatedly studying hard for a test and failing it
  • someone who feels antisocial feels that there is nothing she can do about it so it makes them even more antisocial
  • someone experiencing feelings of anxiety or depression may feel as though they can’t do anything about them and so they don’t try and do anything to fix the situation
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23
Q

epigenetics

A

external modifications to DNA that turn genes on or off

  • these modifications don’t change the genes themselves, they just affect how the DNA is read and therefore the proteins that are produced
  • relevant bc our genetics can determine how we respond to stressors
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24
Q

what are HLG and LLG mothers? what was the best evidence for an impact of the environment on stress response?

A

HGL = high locking and grooming mothers
- rats that create a low stress response in their pups by grooming their pups

LGL = low licking and grooming mothers are unattentive and neglect their pups and produce pups that are more stressed as adults

  • cross fostering rat pups from one mother to another showed that regardless of who their biological mother is, the strong influence of the rats’ mother (env’t) played the largest role on whether the rats were stressed adults or not
25
Q

how does allostatic response differ from a homeostatic response?

A

allostatic response puts body dramatically out of normal range to meet the demands of the env’t
- cortisol maintains allostasis

homeostatic response keeps things in the body regulated to maintain a constant state

26
Q

allostatic load
what is it?
what causes it?
what are the consequences?

A

when the allostatic response is overstimulated, the body’s stress response doesn’t come back down to normal
- this requires a lot more energy than just maintaining homeostasis and can damage the body if this occurs for long periods of time without time for recovery

27
Q

how does the stress response shut off?

A

by negative feedback loop:

  • the HPA axis starts from the hypothalamus which releases CRH that acts on pituitary to release ACTH that acts on the adrenal cortex to release cortisol
  • this cortisol then inhibits the release of ACTH from the pituitary and CRH from the hypothalamus which works to bring cortisol levels back to normal
28
Q

glucocorticoid receptors (GRs)

A

set recovery rate

  • not occupied at rest
  • have low affinity for cortisol
  • only occupied when cortisol levels are high
  • more GR = faster recovery (really only occupied when stress levels are high)
29
Q

mineralocorticoid receptors (MRs)

A

set baseline levels for cortisol

  • have a high affinity for cortisol (binds it even at lower levels)
  • always occupied
  • more MR = lower baseline cortisol levels
30
Q

MRs and GRs main location

A

both founds densely packed in hippocampus at baseline and in response to a stressor
- therefore, the hippocampus regulates both baseline and recovery cortisol levels

31
Q

glucocorticoid receptors (GRs) FUNCTION

A
  • receptors that bind cortisol out of the blood into cells that compress it
  • found on the pituitary and hypothalamus that cortisol bind to and shuts down the production of the hormones that each of the structures produce therefore the production of cortisol decreases and cortisol uptake increases
  • also found in hippocampus so cortisol binds to the GRs there and the hippocampus inhibits the hypothalamus also (shut off HPA)
32
Q

how do early life stressors influence the genetic expression of MRs and GRs? is this caused by genetics or epigenetics?

A

epigenetics

  • acetylation
  • methylation
  • attentive mothering causes epigenetic changes that cause methyl groups to be added and more GRs are produced
  • inattentive mothering causes additions of methyl groups cases methyl groups to be added and less GRs are produced
  • this happens in the hippocampus
33
Q

acetylation

A

adding acetyl groups to histones loosens that chromosome from histone allowing it to be more easily read and transcribed

34
Q

methylation

A

adding a methyl group to the nucleotide cytosine inhibits gene expression (stops transcription)

35
Q

what is tuberculosis (TB)?

A

an infectious disease transmitted by airborne pathogens

  • people with TB during epidemic in the 1900s were sent to sanitoriums where 50% of them died
  • not everyone exposed to TB bacteria, got the TB disease
36
Q

how did Holmes at al test the link b/w psychological stress and susceptibility to TB? describe the details of the study

A
  • looked at employees of TB sanitorium, comparing 20 who got TB and 20 who did not (all were exposed to it)
  • those with greater psychological stresses were more susceptible to getting TB
  • limitations: extraneous factors, correlation ≠ causation
37
Q

how does psychological stress turn on the stress response?

A

psychological stress activates peripheral stress response (HPA and SAM axis) via the amygdala and hippocampus

38
Q

when is psychological stress good and when is it bad?

A
  • good in acute instances where it can help us get a task done
  • bad when psychological stress is chronic since it causes allostatic load
39
Q

how does the activation of the amygdala change in response to chronic stress? anxiety? what impact does this have on the stress system?

A
  • amygdala activity is higher in response to chronic stress, so there is constant activation of the stress response through fear (seen in individuals with social phobias)
  • leads to allostatic load which can lead to breakdown of mental and physical systems
40
Q

what are cytokines?

A

cells that belong to the T-cell grouping of WBC

  • categorized as Th1 or Th2
  • balance changes in response to stress
41
Q

what are Th1 and Th2 cells?

A

cytokines, important to the immune response

- balance of these is affected by stress

42
Q

how does a chronic psychological stressor influence the immune system? does this influence total WBC count? why or why not?

A

epinephrine and cortisol can alter Th1 and Th2 (cytokines) balance when the NT act on lymph nodes

43
Q

how did Cohen et al test the link b/w psychological stress and susceptibility of viral infection? describe the details of the study

A
  • people asked to rate their psychological stress level and then exposed to cold virus
  • of the individuals who reported less stress, v. few of them developed the cold
  • 50% of the individuals who reported high levels of stress developed the cold
  • limitation: measured total WBC count when cytokine (Th1 and Th2) balance was changing, which would not be observed when measuring total WBC therefore the results could not be explained
44
Q

how did Kang and Fox test the link b/w psychological stress and susceptibility to viral infection? describe the details of the study

A
  • testing students stress levels before exams and during exams using a questionnaire
  • observed diff cytokine levels
  • when stressed (exams) Th1 counts were much lower as a result of stress, causing us to be more susceptible to infection
  • when stressed Th2 levels were much higher
  • determined that the balance b/w cytokine types is important for our health
45
Q

contrast Th1 and Th2 cytokines.

A

Th1 types: IL-2, IFN-y
T helper 1

Th2 types: IL-6, IL-4
T helper 2

46
Q

what roles do Th1 and Th2 cytokines play in immune function?

A

Th1: cell-mediated immunity (lysosomes) provide immune protection against bacteria, viruses, cancer

Th2: humoral (extracellular) immunity (antigens)
provide immune protection against parasites such as malaria

47
Q

what happens to the immune response when there is too much or too little of either Th1 or Th2 cytokine?

A

we need a balance to remain healthy

  • too much Th1 results in autoimmune diseases (ex. MS, cancer)
  • Th1 decreases when stressed
  • too much Th2 results in allergies
  • Th2 increases with stress
48
Q

how does chronic stress impact Th1/Th2 cytokines and your susceptibility to various diseases?

A

chronic stress increases Th2 and decreases Th1 so our immunity against viruses, bacteria, cancer will decrease and we may develop allergy flare-up

49
Q

describe Descartes mind-body dualism and explain how it influenced mental health treatment

A
  • the idea that the mind is a separate entity from the body

- this changed medicine from being mystic to the biomedical model that we know today

50
Q

what is psychoneuroimmunology?

A

the effect of the mind on health and resistance to disease

- also how our physical illnesses can have an impact on our psychological mood

51
Q

what is sickness behaviour?

A
  • when you’re sick, you don’t feel like doing anything, have low energy, and would rather be socially isolated
  • looks like depressive symptoms
52
Q

what causes sickness behaviour? why might it be adaptive?

A
  • caused by a heightened where cytokines recruit other immune cells to the site of infection which creates inflammation there (when this happens in the brain, the response is amplified and this is where sickness behaviour comes from)
  • may be adaptive because it limits the chances of us going out and infecting others with our illnesses
53
Q

how does heightened amygdala activity influence your behaviour?
name a mental health illness with heightened amygdala activity

A

since the amygdala is involved in emotional regulation, and cytokines can influence it, a heightened immune response can alter our emotional behaviour by acting on the amygdala
- ex. individuals w social phobias have heightened amygdala response, leading them to social withdrawl

54
Q

what is the classical biomedical view re: the root cause of depression?
what is the evidence that suggests this may not be the cause of depression in all cases?

A
  • lack of serotonin in the forebrain
  • there may be inflammatory pathways that could be driving depressive symptoms for people that have nothing to do with serotonin availability; evidence is that the drugs that target serotonin don’t help everyone with their depressive symptoms
55
Q

describe the 3 studies discussed in class linking depression and
inflammation. what are the key limitations of those studies? which study
provides the strongest evidence for a causal link between inflammation and
depression and why?

A

Evan et al study: people w chronic inflammatory diseases showed greater depressive symptoms than the general population

Musselman et al study showed that long term cytokine therapy (as treatment for cancer pts) correlated with increase in depression rate over time

  • both of these studies involved subjects who were already sick (confounding variable)

best evidence: Miller at al study shows that inflammation (IL-6) is greater in (healthy) individuals who showed depressive symptoms than the control group

56
Q

what is SSRI?

A

selective serotonin reuptake inhibitors
- classic treatment for depression meant to block transporters that recycle serotonin so that serotonin stays in the synapse longer and hopefully creates positive mood

57
Q

what is the difference b/w an SSRI responder and SSRI non-responder? how do their levels of cytokines differ at baseline and could this be useful as a screening tool for responder type?

A
  • SSRI responders: SSRIs relieve their depressive symptoms
  • SSRI non-responders do not experience relief from their depressive symptoms when they take SSRIs (30%)
  • study suggests that the SSRI non responders could be the individuals with high inflammation that causes their depressive symptoms (drugs for arthritis reduce inflammation and also relieve depressive symptoms)
58
Q

describe the details of the study by Rethorst et al

A
  • TNF-alpha (a cytokine) causes depression-like effects on the body
  • this cytokine is elevated in individuals with known inflammatory diseases
  • study shows that exercise seems to lower TNF-a/depressive symptoms over time (12 weeks)
  • those who started with high levels of inflammation seemed to benefit the most from from exercise
59
Q

does exercise improve mood by reducing inflammation? (“Emily’s thesis”)

A

studied uni students for a full academic term until exams

  • over a 6 week period, students who didn’t exercise became significantly more depressed before exams which was protected from by both moderate intensity and HIIT exercise
  • stress, depression and anxiety were all reduced by moderate intensity exercise and HIIT but moderate was best

Health Psych - Kin 2G03 (3 decks)

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