Stress Flashcards

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1
Q

def stressor

A

anything that knock’s you out of your homeostatic happy place *originates from a survival mechanism

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2
Q

When may your body need stress?

A
  • body needs it to stay alert
  • exercise
  • fever
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3
Q

What 2 hormones dominate the stress response?

A

adrenaline (norepinephrine) and cortisol

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4
Q

Who came up with the general adaptation syndrome and what does this mean?

A

-Selye
- “A common response to all stressors that help mobilize energy to help defeat the threat.”
- proposed stress to be a general response to any unpleasantries (through dropping mice and giving them stomach ulcers)

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5
Q

What physiological “fight/flight” responses do we see?

A
  • increased HR
  • increased BP
  • increased breathing rate
    *body mobilizes stored energy to convert into glucose and fuel muscles that need it
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6
Q

What turns on the “startle” stress response?

A
  • mediated by locus coeruleus
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7
Q

What turns on the “threat” stress response?

A
  • amygdala (responds to strong emotions like fear)
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8
Q

describe the pathway of stress activation

A
  • the amygdala or locus coeruleus independently or collectively activate the hypothalamus (this initiates 2 cascading stress axes that work simulatneously)
  • one fast (SAM axis) & 1 slow (HPA axis)
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9
Q

Provide the full name for the SAM axis and how it works:

A
  • sympathetic adreno-medullar axis
  • uses sympathetic nerves to activate the adrenal medulla
  • fast (bc using nerve responses), first-acting
  • activation of AM causes the rush of adrenaline/epinephrine into the blood stream
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10
Q

Why might slower/deep breathing help relax/turn off stress response?

A

reactivates parasympathetic system (rest + digest)

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11
Q

Provide the full name for the HPA axis and how it works:

A
  • hypothalmic pituitary adrenal axis
  • slower bc uses hormones
  • once hypothalamus gets activated, it releases CRH (corticotropin releasing hormone) which binds to receptors onthe pituitary gland that release ACTH (adrenocorticotropic hormone)
  • ACTH goes through blood to the adrenal cortex which gets activated and releases cortison
  • when cortisol rushed into the blood it helps release stored energy (most in liver and fat cells) for fight + flight
    *delayed response
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12
Q

Can the hypothalamus and stress responses be activated without the amygdala or locus coeruleus?

A

Yes! By any alterations in homeostasis

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13
Q

Exercise and psychological stress both activate the same processes… how do these differ in the way they activate it?

A

Exercise
- voluntary
- acute (mins to hours)
- minor strain
- easy to recover from

Psychological
- involuntary
- chronic - weeks, months, years (ex. money, relationship, work)
- major strain
- difficult to recover from (years with activated SAM and HPA is really straining to body, can cause brain damage)

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14
Q

def the cross-stressor hypothesis

A

voluntary exercise stress induces adaptations in the stress system that makes us more resilient to all stressors, even physiological ones

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15
Q

What did (Rimmele et al., 2007)’s study find in relation to cortisol, post-test anxiety and heart rate responses to psychosocial stress in trained and untrained men?

A

lower cortisol (HPA), lower anxiety and lower heart rate (SAM) in trained men
- exercise training = less reactive to stress

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16
Q

what does innocuous mean?

A

harmless

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17
Q

In a study on kinesophobia by (Pfingsten et al 2001), what was found as a result of telling participants certain exercises would be painful?

A
  • increase in fear rating
  • rating of pain increased by 20%
  • did not perform as many reps
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18
Q

def nocebo effect

A

negative effect produced by a sham treatment that cannot be attributed to the properties of the treatment itself and therefore, must be due to the patient’s belief in that treatment

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19
Q

Fear from innocuous cues can be conditioned through _

A

experience
(ex. Albert became afraid of anything white & fluffy after terrifying noise played with white mouse apprearance)

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20
Q

Equation for fear conditioning of a stress response:

A

CS (conditioned stimulus) +US (unconditioned stimulus) = CR (Conditioned Response)

CS = harmless stimulus (eventually evokes fear on it’s own)
US = thing that already has fear associated

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21
Q

def generalized anxiety disorder

A

excessive and exaggerated worry about everyday events for no apparent reason

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22
Q

def panic attacks

A

A sudden and intense fear that triggers a severe physical reaction when there is no real danger or threat

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23
Q

def phobia

A

An intense fear or aversion to a specific object or situation that may be harmless

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24
Q

def social anxiety

A

An intense fear of being negatively judged or scrutinized in a social setting even when it’s not true

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25
Q

How does the amygdala affect neurons?

A

Links them together strongly, makes it very hard to forget things associated with strong emotions

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26
Q

How does the amygdala function in anxiety and why might this be problematic?

A
  • once any “threat” is detected, the stress response is activated to warn all the body tissues without delay
  • the amygdala stays on until the threat is gone (but worries can sometimes never fully go away)
  • amygdala also has no way of telling the body what the nature of the threat is, so there may be a heightened response to something that is not truly dangerous.
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27
Q

Are the amygdala and hippocampus necessary for fear conditioning? (Bechara et al 1995)

A
  • Hippocampus not necessary, see similar patterns of fear responses (unless context-related fear)
  • Amygdala very critical for fear conditioning
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28
Q

What are the 3 steps for basic fear conditioning?

A

habituation (CS), acquisition (CS + US = CS), extinction (CS)

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29
Q

What are the 5 steps for context-related fear conditioning?

A

habituation, acquisition, extinction (change rooms), reinstate, (change rooms), recovery

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30
Q

Linking of fear to context is largely due to _ (brain area)

A

hippocampus

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31
Q

describe the brain regions involved in fear conditioning

A
  • hippocampus (context-specific threat) activates amygdala to initiate fear, which integrates info and interface with hypothalamus which starts the 2-axis stress response
  • the PFC is able to control the more primitive parts of the brain (3 mentioned above) * why mindfulness can help stress, inhibits the amygdala
    *in an anxiety disorder, PFC can’t communicate with amygdala anymore
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32
Q

When does learned helplessness happen?

A

when a person is conditioned to believe that a bad situation is unchangeable or inescapable
*often occurs due to repeated stress, we get freeze instead of fight/flight

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33
Q

describe the shutter box experiment

A
  • 1 side wired with electricity, other side is not
  • dog doesn’t even try to cross small barrier because of the uncontrollable stressor
    *only dogs shocked without control learn helplessness
  • dogs shocked with control of a red button to stop shocks escapes
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34
Q

What is the effect of exercise on learned helplessness?

A

exercising decreases “freeze” responses, take less time to leave (escape latency)
- mice shutter box experiment

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35
Q

More “freeze” responses are associated with _

A

learned helplessness

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36
Q

How does exercise affect the SAM axis?

A
  • exercise turns the SAM axis “on” and “off”
  • intensity of exercise dictates how stress-provoking it is (moderate increases adrenaline a little, high a lot)
  • adrenaline drops very quickly during recovery
  • cortisol takes longer to peak & drop in recovery period, stays elevated (can help turn off the sam axis & hpa to refill glycogen stores)
37
Q

def allostasis

A

-stability through change
- rapid but gradual internal changes to meet demands of changing external environment
- the body is not fixed to certain homeostasis, homeostatic set point changes

38
Q

def allostatic load

A

stress overload, body grows weaker rather than stronger
- more likely to occur with chronic psychological stress or combined stressors because it is involuntary and uncontrollable

39
Q

How is cortisol production shut off? What is this calles?

A

-as cortisol rises, it binds to it’s receptors located on the pituitary gland and hypothalamus
- when cortisol binds, it stops the next step in the cascade of cortisol production
- this is called negative feedback loop

40
Q

Which 2 receptors can cortisol bind to?

A

Mineralocorticoid Receptors (MRs)
- high affinity for cortisol, occupied all the time
- sets baseline levels
- more MRs = lower baseline

Glucocorticoid Receptors (GRs)
- low affinity for cortisol (only bind when cortisol is high)
- occupied when CORT is high
- sets recovery rate
- more GR = faster recovery

41
Q

What brain area contains the most glucocorticoid receptors?

A

hippocampus

42
Q

How do GRs inhibit the 2 axes? Aka “master off-switch”

A

When GRs bind to the hippocampus, it inhibits the hypothalamus directly which stops the 2 stress response axes

43
Q

Why do individuals react differently to stressors?

A

-some have more GRs, recover faster from stressful events and less likely to suffer from allostatic load
- earlylife stressful environment (high and low licking and grooming mouse mom crossfostering study)
*partly built into biology!

44
Q

What effect does chronic life stress have on GR number in the brain?

A

reduces GRs
- GRs saturated all the time and stress “off-switch” not working, become corticoresistant and cortisol remains in the blood
*exercise can protect brain against chronic early life stress

45
Q

What role does BDNF play in stress?

A
  • Brain-Derived Neurotropic Factor
  • works like a protective coating from stress
  • surrounds the hippocampus, protecting GRs from stressor
  • moderate exercise increases this a little, high intensity increases a lot BUT supressed in chronic stress
46
Q

def epigenetics

A
  • external modifications to DNA that turn gener “on and off”
  • These modifications do not change the DNA sequence, but instead, they affect how the gene is “read”
    *can be altered by phychological stress and exercise
47
Q

Gene expression is determined by _

A

the packaging of DNA
- DNA tightly wound around histones, helps dna fit and express genes through allowing it to be read by transcription factors
- dna>rna>proteins>things like bdnf

48
Q

Do epigenetic changes affect the genetic code?

A

No, just alter gene expression

49
Q

What are some examples of epigenetic changes?

A
  • adding an acetyl group, loosens chromosome structure and makes it easier to read the underlying gene
  • methyl group physically inhibits gene expression by attaching to the nucleotide cytosine, gene can’t be read and protein can’t be made
50
Q

What is added to the GR gene during chronic stress and what can reverse this change?

A

chronic stress adds CH3 to the GR gene, but exercise removes them

51
Q

def tuberculosis

A
  • a respiratory condition but bacteria based
  • can be exposed but not get symptoms
52
Q

Holmes et al tested if stress can impact the ability to get infected with tuberculosis, what did they find?

A
  • studied employees of sanitoriums (20 each that did or did not get TB)
  • sorted by age, sex, race
  • people with stress before hand were more likely to develop TB
53
Q

Why do stressed-out cells trick the immune system?

A

Body cells “know the handshake”
- Foreign cells don’t, have pathogen associated molecular patterns (PAMPS)
- Stressed out cells have damage associated molecular patterns (DAMPS) that induce a sterile immune response, “too tense to perform handshake”

54
Q

def sterile immune response

A

no virus, cell damage evokes immune response

55
Q

A double-breach in immunity activates _ that _

A

inflammasomes
- increase inflammation a lot
- ex. stress only ok, infection only increases inflammatory cytokines, stress and infection increases cytokines by much more

56
Q

def inflammasomes

A

specialized immune cells triggered by 2x immunity breach

57
Q

Too much inflammation causes _

A

allostatic load
- stressed-out system more sensitive to allergens and viruses

58
Q

What is an elevated WBC count indicative of?

A

an infection being fought by the body

59
Q

Cohen et al investigated the impact of psychological rate of infection, describe some elements of the study and what they found

A

-420 healthy adults given nasal drops with respiratory virus
- the ppl with psych stress tended to get a cold
*WBC count didn’t change tho!

60
Q

Which cells are impacted by stress?

A

Th1 and Th2

61
Q

Describe Th1/Type 1 cells:

A
  • provide cellular immunity, can even kill cancerous cells
62
Q

Describe Th2/Type 2 cells”

A
  • provide humoral immunity, things that are circulating in the blood (ex. parasites, malaria)
63
Q

What can happen if TH1 and TH2 are not in balance?

A

too much Th1: cellular attack mode and autoimmune responses
too much Th2: can make you more sensitive to allergies

64
Q

Stress decreases the production of which type of cell?

A

Th1, decreases protection from viruses, bacteria
- can make Th2 cells more abundant, may be more succeptible to allergies

65
Q

In the study mentioned in class by Fox and Kang, what was observed with increasing levels of stress in students during exams as compared to midterms?

A
  • Th1 decreased (more succeptible to get sick, greater risk for infections)
  • Th2 increased (greater allergy risk)
66
Q

What influenced the western medicine and biomedical model of health for over 300 years?

A

Descartes mind-body dualism (treating the mind and body as seperate things)

67
Q

How does mind-body communication work?

A

Mind: consciousness, perception, thinking, and memory interact with the nervous system
- the nervous system then interacts with the immune system and endocrine system

68
Q

How can physical illness impact your physiological mood?

A

cause negative mood states by increasing inflammatory cytokines which interact with the amygdala to increase social withdrawal
- viruses, toxins and bacteria are sensed by TLR (toll-like receptors) and activate immune cells to produce cytokines
- the cytokines then cause inflammation (increased blood and immune cells) at the site of injury and interact with microglia in the brain, activating them to make cytokines
- brain becomes inflamed and interacts with amygdala which produces symptoms (fatigue, withdrawal, anorexia, fever)

69
Q

How can temporary sadness and social withdrawal be adaptive?

A
  • not gonna spread disease to other people if sickness is acute
70
Q

What’s the core neural component of pathoge-induced social withdrawal?

A

heightened amygdala activation

71
Q

def depression and give an assumed biological cause

A

an affected state of negative mood and low arousal lasting at least 2 weeks, lack of serotonin in the forebrain

72
Q

What are 3 factors that may lead someone to believe that physical illness causes depression?

A
  • chronic inflammatory diseases are associated with depressive symptoms (Evan et al., 2005)
    -12 weeks of cytokine therapy for cancer increased rates of mahor depression (Musselman et al., 2001)
  • Depressed individuals who are otherwise healthy have higher levels of pro-inflammatory cytokines (best evidence) (Miller et al., 2002)
73
Q

What is the mainstream treatment for depression? How does this work?

A

SSRIs (selective serotonin reuptake inhibitors)
- block the reabsorption of serotonin

74
Q

Why might SSRIs not work for someone with drug-resistant depression?

A
  • some people have persistently high levels of inflammation (higher baseline pro-inflammatory cytokine levels)
  • some forms of depression may be more associated with inflammation than lack of serotonin (treating inflammation may help reduce symptoms)
75
Q

What specific cytokine may be linked to depressive symptoms?

A

TNFalpha
- induces depression-like changes in brain function and behaviour

76
Q

How does exercise affect inflammation?

A
  • exercise is temporarily pro-inflammatory, this goes away because muscles release myokines which are anti-inflammatory
  • exercise tones stress responses so that you are less reactive to stressors
77
Q

What did the study by Rethorst et al, 2013 find in relation to exercise and clinically depressed individuals?

A

Clinically depressed people with high TNFalpha benefit most from exercise as compared with those with a lower TNF alpha at baseline, still saw a decrease in depressive symptoms though

78
Q

Does the dosage of exercise affect depression and inflammation? (Emily’s thesis study)

A
  • looked at 55 uni students
  • moderate intensity reduced depression, anxiety, and stress, while the control group reported increases in depression and anxiety
  • HIIT increased anx and stress, but reduced depressive symptoms
  • moderate intensity exercise can reduce TNF alpha to improve mood, while HIT did not.
    *dose matters!
79
Q

How can acute stress change the morphology of neurons in the brain?

A
  • with more exposure to stress, spinal density of neurons in the amygdala increases which makes it hypersensitive to stress
  • spinal density in the hippocampus and PFC, however, is reduced with chronic stress due to the chronically high levels of cortisol that change the neuroenvironment, toxic to neurons
  • neurons shrink in length and branch points and neurogenesis is prevented = hippocampus not functioning properly and takes a longer time to turn off stress response
80
Q

How is the pre-frontal cortex affected by stress?

A
  • in a similar way to hippocampus, spinal density decreases = worse at cognitive tasks and regulating emotions (PFC usually inhibits amygdala)
  • as a result, amygdala is able to launch larger and more frequent stress responses
81
Q

Who is Chris Waddell? What happened to him and how does his story relate to resiliency?

A
  • promising ski racer
  • sustained a spinal cord injury
  • became most decorated paralympic skier
  • became first paraplegic to summit Mt. Kilimanjaro
  • Waddell’s exercise training likely buffered the effects of his trauma (exercise increases BDNF to protect brain, also helps counteract decreasing neurogenesis)
82
Q

def resiliency

A

the capacity to withstand or to recover quickly from difficulties

83
Q

Perception of Health Matters! In Keller et al.’s study, what was found in relation to percieved affects of stress on people’s health vs risk of death

A
  • those who experienced a lot of stress but believed that it had a small effect on their health has a ~20% reduced risk of death
  • those who believed their stress had a large effect had a 43% increased risk of death
84
Q

Viewing stress as positive can improve_

A

cognitive functioning

85
Q

def trait mindfulness

A

one’s ability to purposely pay attention in the present moment, non-judgementally

86
Q

How does mindfulness meditation reduce psychological distress?

A

increasing PFC activity and inhibiting amygdala activity

87
Q

Are positive affirmation helpful?

A

Yes, but not to everyone

88
Q

How can CBT (cognitive behavioural therapy) help with psychological stress?

A

helps rewire the brain to help you rewrite the narrative about fear