Week 10 Flashcards

1
Q

Stress

A

• Any stimulus that disrupts the body’s internal balance (i.e.,
physiological homeostasis)
• Any deviation from homeostasis
• The mental and physical state induced by a stressor
Stress – the state
Stressor – the thing that causes the state
Stress Response – the link between the stressor and stress

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2
Q

The Stress Response

A

• Fight or flight – survival mechanism – react quickly to life threatening
situation
• Rapid recognition of potentially harmful stimuli to mobilize the
defence responses
• An array of neural and endocrine systems that mobilise physiological
and psychological resources allowing response to the present
challenge to homeostasis and overall well being
• Complex but orchestrated and rapid
• The stress response is incredibly ancient evolutionarily
• All vertebrates respond to stressful situations by releasing hormones,
such as epinephrine and glucocorticoids
➢ Mobilize energy resources
➢ Increase blood pressure
➢ Turn off everything that’s not essential to surviving right now -
digestion, growth, reproduction
➢ Think more clearly
➢ Learning and memory are enhanced
➢ Sensory thresholds sharpened

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3
Q

Good Stress / Bad Stress

A

If stress is so good, then why the bad rap?
• All stressors – single stress response – Evolution is a tinkerer!!
• Many modern life stressors are not life threatening
• Many modern life stressors are social
• Many modern life stressors are psychological
• We neither fight nor flee
If stress is so good, then why the bad rap?
• Worries, social pressure, sitting in traffic
• All elicit the same stress response as
escaping a tiger – release of epinephrine
and cortisol
• Stress response evolved to get you out
of a bad situation
• Short term adaptive, long term harmful

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4
Q

Good Stress / Bad Stress- If stress is so good, then why the bad rap?

A
• Good stress – mild,
transient, not a complete
loss of control
• Bad stress – severe or
chronic and coupled with
lack of predictability or
perceived lack of control
• Chronic psychological
stress implicated in ill
health
Optimal good stress:
• Occurs in a safe environment
• Is transient and mild
• Involves a plausible but not
guaranteed reward
• You have control
• Results in arousal, alertness,
stimulation
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5
Q

Good Stress / Bad Stress- Bad stress – severe or chronic and coupled with lack of predictability or
perceived lack of control

A
• What if the stressor is
always there?
• What if you can’t get away?
• What if you believe that
nothing you do will change
things anyway?
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6
Q

Good Stress / Bad Stress- Long-term

A

The long-term activation of the stress-response system and the
overexposure to cortisol and other stress hormones that follows can
disrupt almost all your body’s processes
➢ Digestive problems
➢ Headaches
➢ Heart disease
➢ Sleep problems
➢ Weight gain
➢ Immune system impairment
➢ Accelerated chromosomal DNA aging (telomeres)
➢ Memory and concentration impairment
➢ Anxiety, depression, and other mental health issues

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7
Q

Stress- Introduction

A
Bad
-Visual System
Scotoma
Cataracts
Glaucoma
Retinal detachment
Cortical blindness
Colour blindness
Macular degeneration
Retinoblastoma
-Attention
Contralateral Neglect
-Auditory System
Sensorineural
deafness
-Pain
Congenital Insensitivity
to Pain
-Motor System
Motor Neuron Disease
Good
-Performance Enhancing
-Beneficial
-Rise to a challenge
-Protective
-Keeps you alive
-Adaptive
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8
Q

Bad Stress

A
-77% regularly experience
physical symptoms caused by
stress
-48% reported lying awake at
night due to stress
-One in seven
Australians will
experience depression
in their lifetime
-One in five Australians have
taken time off work in the
past 12 months because they
felt stressed, anxious,
depressed or mentally
unhealthy
-One quarter of
Australians will
experience an anxiety
condition in their
lifetime
-73% regularly experience
psychological symptoms caused
by stress
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9
Q

Gastric Ulcers

A

• Lesions of stomach lining leading to pain, bloating, nausea
• One of the first psychosomatic disorders - stress
• Warren and Marshall – H. Pylori
• Marshall ingested and developed
gastritis and ulcers
• H. Pylori – 90% of ulcers
• Nobel Prize in 2005
But most people have H. Pylori and only 10% get an ulcer
• Another factor increases susceptibility
of stomach wall to damage from H.
Pylori
• H. Pylori attacks the stomach wall, but
usually this is easily fixed
• Unless stomach (more generally
digestive) operations have been turned
right down to deal with a threat
• Stress

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10
Q

Main Characters

A

Hypothalamus
Pituitary
Amygdala
Adrenal Cortex- Releases cortisol - the major
glucocorticoid in humans
Adrenal Medulla- Releases epinephrine (also
known as adrenaline

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11
Q

The Stress Response

A

• The stress response is incredibly ancient evolutionarily
• All vertebrates – fish, birds, reptiles, mammals
• Encounter a stressor – any perceived threat - a tiger, a mean boss, a
worrying thought
• Sensory information to the amygdala – interprets – if perceive a
threat then signal hypothalamus
• Secrete hormones (epinephrine and glucocorticoids) to respond

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12
Q

Two pathways

A
Sympathetic-adrenal-medullary
(SAM) system
Fast response
Short acting
Epinephrine
Jump start
Hypothalamus-pituitary-adrenal
(HPA) axis
Slow response
Lasting
Cortisol
Keep things going
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13
Q

The Stress Response

A

SAM

HPA

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14
Q

SAM System

A

Efferent Nerves

  • Parasympathetic Nervous system
  • Sympathetic Nervous System
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15
Q

ANS Efferents

A
Change the body’s internal state
Sympathetic
• Fight or flight
• Stimulate organs and
release hormones to
wind things up
• Mobilise energy sources
• Increase blood flow and
respiration
• Suppress non-essentials
From chest, mid-lower back
Parasympathetic
• Rest and digest
• Counteract sympathetic
to wind things down
• Stimulate digestion and
restorative functions
• Conserve energy
From brain, lower back
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16
Q

SAM System

A

• Direct adrenergic innervation of organs (epinephrine and norepinephrine)
• Stimulate the adrenal medulla to release epinephrine into bloodstream –
efficient to replace neural activity for sustained response
• Very fast response – before conscious awareness
• Wind things up and supress non-essentials but also senses sharpen, improve
mood, encourage creative thinking, problems feel more like challenges
• SNS slow to shut down – need to actively counteract - PSNS
• No ill effects from the short-term response (although persistent epinephrine
surges can damage blood vessels)

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17
Q

HPA Axis

A

• As initial surge of epinephrine subsides, the hypothalamus activates
the second component of the stress response system
• Release of cortisol by adrenal cortex
• Measure of circulating cortisol most common physiological measure
of stress
• Primary function – increase blood glucose
• Support an extended fight or flight response

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18
Q

HPA Axis - Cortisol

A

• Important steroid hormone – almost all cells in the body have cortisol
receptors
• Sleep/wake cycle
• Low blood sugar
• Stress
• Metabolic effects
• Release glucose stores in muscle and liver
• Modifies fat and protein metabolism – fatty acid mobilisation and
gluconeogenesis (create more glucose)
• Alters immune system responses
• Reduce inflammation
• Hyperactivity results in immune suppression
• Suppresses the digestive system, the reproductive system and growth
processes
• Negative feedback control – cortisol acts on both the hypothalamus and the
pituitary to turn the HPA axis DOWN

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19
Q

Three Determinants of HPA Activity

A

Three main determinants of HPA axis activity control the amount of
cortisol a person is exposed to during adulthood
• Genetic factors
• Early-life environment
• Current life stress
Also, sex and age differences in stress response

20
Q

Three Determinants of HPA Activity

Genetic factors

A

• DNA variations in genes encoding neurotransmitters involved in HPA
axis regulation.
• Heritable influences account for 62% of the variance in basal
glucocorticoid levels

21
Q

Three Determinants of HPA Activity

Early-life environment

A

• Pre and post-natal influences
• Maternal stress modifies HPA axis responsivity of infant and adult offspring
• Childhood trauma associated with alterations in HPA axis function
• Animal models show neonatal stress results in a epigenetic modification of a
receptor gene with long-lasting effects on cortisol responsivity - rats that
received poor maternal care showed deficits in receptors in the
hippocampus and impaired shut off of the HPA stress response
• Mild to moderate early life stressors enhance HPA regulation and promotes
life long resilience to stress

22
Q

Three Determinants of HPA Activity

Current Life Stress

A

• Severe, chronic stress in adulthood alter HPA axis dynamics and
increase the cortisol burden
• Chronic stress triggers a shift in the normal circadian rhythm of
cortisol release – increased baseline
• Makes the HPA axis more sensitive, resulting in higher cortisol
exposure or greater cortisol burden following each stressful episode

23
Q

• Severe, chronic stress in adulthood alter HPA axis dynamics and
increase the cortisol burden
• Chronic stress triggers a shift in the normal circadian rhythm of
cortisol release – increased baseline
• Makes the HPA axis more sensitive, resulting in higher cortisol
exposure or greater cortisol burden following each stressful episode

A

• Romania under Ceausescu (1960’s to 1989) – contraception and
abortion forbidden; childless couples taxed – high birth rate
• Huge number of children to orphanages – horrific conditions –
isolation, neglect, maltreatment
• Failed to meet even the most basic needs of the children
• Intense and pervasive stress during development
• McLaughlin et al. (2015) – 138 children – 3 groups – orphanage;
orphanage but removed to high quality foster care; local controls
• Electrocardiogram, impedance cardiograph, and neuroendocrine data
collected during laboratory based challenge tasks
• Main finding – blunted SAM and HPA responses to lab stressors –
both social and non-social
• Normal response if removed into foster care before 24 months –
critical period

24
Q

Chronic Stress

A

Adaptive
• Mobilise energy stores
• Increase blood supply
• Enhanced cognition
• Enhanced immunity, reduced
inflammation
• Suppression of growth
• Suppression of digestion
• Suppression of reproduction
Disorder
• Metabolic dysfunction, inefficient energy use, muscle wasting, type 2 diabetes
• Stress hypertension, atherosclerosis,
heart disease
• Memory loss, disconnection of neural networks, reduced neurogenesis, selective neurodegeneration
• Amygdala expansion → increased anxiety
• Depletion of dopamine → anhedonia → depression
• Increased risk of some infectious diseases (probably no increase in cancer risk)
• Osteoporosis, osteoarthritis,
psychogenic dwarfism
• Increased risk of ulcers, increased fat deposition
• Females – irregular cycles, loss of cycles, failure of implantation; males – decreased testosterone, erectile dysfunction; everyone – loss of libido

25
Q

Psychosocial Short Stature

A

• Extreme stress and emotional deprivation endured during childhood
• Symptoms appear after age two and continue into the early teenage years
• Failure to thrive despite adequate nutrition - short stature, immature
skeletal age, and improper body weight for height
• Low growth hormone but resistant to treatment with GH
• When a child leaves an abusive home environment, growth hormone
insufficiency can be reversed.
• Undergo rapid “catch-up growth” to what is likely their genetically
predetermined height.

26
Q

Brain - Cortisol Damage

A

Chronic stress negatively impacts the brain in many ways
• Mediated by cortisol
• Acts directly on receptors and indirectly via excitatory
neurotransmitters, BDNF, other intra- and extracellular mediators
• Structural remodelling (plasticity) of
• Hippocampus
• Amygdala
• Prefrontal Cortex
• Remodelling is reversible, but more difficult with age

27
Q

Brain - Cortisol Damage

Hippocampus

A

• Contextual information about the circumstances under which stress response has
been activated in the past - contributes to threat appraisal by the amygdala;
important in learning and memory, and in regulation of mood
• HC particularly susceptible to stress – high density of glucocorticoid receptors
• Reduce dendritic branching; reduce adult neurogenesis; modify synapse
structure; loss of grey matter
• May be a protective function against permanent damage
• Disrupt performance of HC dependent tasks
• HC part of system that tells HT to turn off cortisol – loss of regulation

28
Q

Brain - Cortisol Damage

Amygdala

A

• Amygdala based fear circuitry mediates defensive behaviours and
physiological responses to danger
• Emotional significance of sensory signals learned and maintained
• Opposite effect than on HC - increase plasticity and expansion of
dendritic processes
• Bad since increases fear acquisition and decrease extinction – learn
more readily to be afraid and less readily detect safety – anxiety
disorder

29
Q

Brain - Cortisol Damage

Prefrontal Cortex

A

• Provides top-down control of emotional responses and amygdala
restraint
• Dendritic shrinkage in mPFC - impaired cognitive flexibility
• Dendritic expansion in OFC - salience of reward or punishment so
possibly increased vigilance to possible new stressors
• Impaired amygdala restraint during stress

30
Q

Turning the Stress Response OFF

A

• Basic mechanism – Parasympathetic Nervous System
• Post threat, PSNS rapidly dampens stress response and cortisol levels
fall
• Direct innervation of organs (acetylcholine) and hormones to the
adrenal cortices to supress cortisol
• BUT … hierarchical dominance of SNS over PSNS – often requires
conscious effort to initiate relaxation response
• Relaxation response can be triggered – deep abdominal breathing,
focus on word, visualisation, yoga, etc
Conscious control of the stress response – prefrontal cortex
• Amygdala response not very nuanced – all or none qualities of defensive
reactions
• Amygdala threat appraisal is negatively biased – missing a real threat is worse
than misinterpreting something non-threatening
• Moderate stress levels - PFC activates inhibitory amygdala neurons
• Cognitive reinterpretation of stimuli possible
• Threatening or exciting
• Overwhelming or challenging
• BUT … intense stress - excessive NE output suppresses PFC restraint on the
amygdala- amygdala storm

31
Q

Stress and Social Bonds

A

• Compared to most animals, humans not that great at fighting or fleeing - no sharp teeth, claws or thick hide, pretty slow
• Fight and flight both potentially leave young at risk – human young particularly vulnerable - stress response must protect offspring in times of danger and not just the individual
• Under conditions of threat, people come together to protect one another - impulse to affiliate part of the human stress response
• Humans evolved to use social relationships as a primary resource to
deal with stressful times – tend and befriend
• Social affiliation – release of oxytocin
• Oxytocin reduces cortisol response to stress and supresses HPA axis
• Oxytocin reduces threat induced amygdala activation and fear conditioning
• To exhibit a social response to stress, arousal must be controlled to avoid
aggression or flight
• Supportive contacts reduce stress response but hostile or unsupportive
increase it
• Affiliation is vital so expect systems to maintain it – sensitive to social threats
and loss of social contact

32
Q

Social Isolation

A

• More than one in six people report feeling lonely in any given year and 1.5
million people have been lonely for a decade or more (Household, Income
and Labour Dynamics in Australia (HILDA))
• Social isolation is stressful – we are built to be social
• Being lonely is stressful
• Without social support stress is less manageable
• Unmanaged stress becomes chronic
• Chronic stress impairs systems that deal with stress
• Higher levels of loneliness are associated with higher levels of social
interaction anxiety, less social interaction, poorer psychological wellbeing
and poorer quality of life
• Increased risk of mortality - 26%
• Physical symptoms - lack of energy, sleep problems, diet problems,
headaches, illness, aches and pains and worsening of medical conditions
• Poor mental health including depression, lower levels of self-worth, life
satisfaction and subjective wellbeing
• Substance abuse

33
Q

Amygdala

A
Amygdala based fear circuitry mediates defensive behaviours and
physiological responses to danger
• All sensory input – indirect
and direct
• Emotional significance of
sensory signals learned and
maintained
• PFC inputs – suppress fear
• HC inputs – mediate
learning about context of
fear related events (esp.
location)
Amygdala based fear circuitry mediates defensive behaviours and
physiological responses to danger
• Brain stem outputs control
emotional responses
(behavioural and
physiological) – HT for
SAM/HPA responses; PAG
for defensive responses
• Cortical outputs influence
cognitive function –
attention, perception,
memory, decision making
34
Q

Anxiety

A

• Fear– adaptive response to threat and usually transient
• Anxiety– longer lasting response to signals or vague indications –
adaptive arousal, vigilance, preparedness increases good for
surviving danger
• Hyperarousal (exaggerated startle response); heightened SNS arousal
and motor tension
• Adaptive since motivates effective coping behaviours
• Fear is good and anxiety is good

35
Q

Anxiety Disorders

A

• BUT … if it persists or occurs out of proportion to possible threat –
disorder
• Chronic fear in the absence of direct threat – common psychological
correlate of stress
• Maladaptive since disrupts normal functioning
• 5 classes of anxiety disorder – generalized, phobic, panic, OCDs, PTSD
• Generalized, phobic, panic, and OCDs run in families – twin studies
suggest substantial genetic component

36
Q

Anxiety Disorders - Examples

A
  • Generalised Anxiety Disorder
  • Phobic
  • Panic
  • Obsessive Compulsive Disorders
  • Post Traumatic Stress Disorder
37
Q

• Generalised Anxiety Disorder

A
  • stress response and extreme feelings of anxiety in absence of obvious cause
  • chronic worry and vigilance not warranted by situation
  • heightened SNS arousal and motor tension
38
Q

• Phobic

A
  • intense excessive fear of specific stimuli

* similar to GAD but triggered by specific object or situation

39
Q

• Panic

A

• rapid onset extreme fear and severe stress symptoms
• panic attack – intense fear plus somatic symptoms – palpitations, shortness
of breath, sweating, dizzy

40
Q

• Obsessive Compulsive Disorders

A

• recurrent and uncontrollable anxiety producing thoughts (obsessions) and
impulses (compulsions)
• responding (eg washing hands) dissipates the anxiety
• behaviours intended to neutralize negative thoughts and emotions from
obsessions – resisting compulsions leads to high anxiety

41
Q

• Post Traumatic Stress Disorder

A

• recurrent and uncontrollable anxiety producing thoughts (obsessions) and
impulses (compulsions)
• responding (eg washing hands) dissipates the anxiety
• behaviours intended to neutralize negative thoughts and emotions from
obsessions – resisting compulsions leads to high anxiety

42
Q

Anxiety and Stress

A

• Anxiety disorders often triggered by stressful event
• Genetic – heritability 30-40% but timing and focus reflect particular
experience
• Stress and anxiety high comorbidity – both thought to involve
heightened emotional response to stress
• Stress disorder impacts the amygdala, HC and PFC - response to
incoming sensory information
• Amygdala and ACC implicated in anxiety from functional imaging
studies

43
Q

Depression

A

• Depression – affective disorder – disturbance of mood or emotion
• Prolonged feelings of sadness, emptiness, or hopelessness, loss of interest in
activities that were once enjoyed
• Changes in appetite (leading to overeating or not eating enough), changes in
sleeping patterns (sleeping too much or not being able to sleep), loss of energy,
and difficulty concentrating.
• Distinguish from normal sadness by severity, pervasiveness, duration, associated
symptoms
• Must have signs and symptoms nearly every day for at least 2 weeks
• Features vary widely – possibly multiple disorders with similar signs and
symptoms
• Monoamine theory – underactivity at serotonergic and noradrenergic
synapses
• MAO inhibitors, tricyclics, SSRIs and norepinephrine reuptake
inhibitors are all agonists of serotonin, norepinephrine or both
• But – inhibitory actions fast but weeks before effect on depressions -
rather than an absolute deficit, low 5-HT neurotransmission may
represent a risk factor for MDD
• Genetic - concordance 60% MZ twins, 15% DZ but no particular gene
linked variations in many genes, each with a small effect, combine to
increase the risk of developing depression.

44
Q

Depression and Stress

A

• Depression and stress interrelated – stress can precede depression and
depression is stressful
• Depression and chronic stress share symptomatic features and
biochemical changes
• Depressed release more stress hormones – increased HPA activation
and impaired HPA suppression (cortisol feedback system)
• Alterations in HPA axis functioning in recovered depressed patients and
at-risk individuals
• Enlargement of amygdala and increased activity
• Association between brain-derived neurotrophic factor (BDNF) levels
and depression (animal models of depression and depressed patients)
• Altered immune function in depression (suppression)
• Antidepressants increase neurogenesis

45
Q

Depression and Stress

Genetic-stress model

A

• Genetic susceptibility plus early stress sensitises system so over react
to mild stressors
• Environmental stressors reprogram biological systems through
epigenetic processes, such as DNA methylation, by altering the
expression of genes
• Stress shown to trigger attacks in sufferers rather than increasing
susceptibility in healthy – but, significant stressors appear to be more
frequently involved with initial episodes

46
Q

Stress Management

A

• Stress is good (until its bad)
• PSNS – should dampen the SNS, but can be activated – calm down, breathe,
teach the PSNS
• PFC – conscious amygdala control – is it really stressful? Is it really dangerous?
• (Perceived) control of the situation
• Fight or flight – use the stress response – exercise
• Escape the stressor
• Be with your people (and make sure you have people)