Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PSYC 342 > Lecture 11 Stress Basics > Flashcards

Lecture 11 Stress Basics Flashcards

1
Q

Three physiological stress systems

A
  • Parasympathetic Nervous system
  • Sympathetic Nervous system
  • Hypothalamus-Pituitary Adrenal Axis (HPA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Nor =

A

in the CNS (for the purposes of this course)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

CNS vs HPA

A

CNS is much faster

HPA lasts longer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

SNS

A

Spine > Medulla > Adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

The Hypothalamus Pituitary Adrenal Axis: Major stress axis of the organism

A

HPA axis is relevant to stress

CNS > Hypothalamus > CRH > Anterior pituitary > ACTH > Adrenal Cortex > Free cortisol

Has a third order feedback loop that limits it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Free vs. Bound Cortisol

A
  • CBG is a binding globulin
  • Binds steroid hormones
  • Regulates the amount that can bind to receptors

Hence we are mostly interested in FREE CORTISOL levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Characteristics of the HPA

A

There is a baseline level of HPA activity
-Every 60-90 mins there is a pulse timed via negative feedback

Ultradian rhythm =more than once per day

When there is psychological stress = additional secretory burst

Circadian rhythm
daily pattern, nadir around midnight
peak in the morning to help us get up

Third Order feedback loop
like the HPG axis we know and love

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Functional Tests of The HPA Axis

5 tests

A

(1) CRH
(2) ACTH
Both stimulate the system to increase cortisol
-Cannot cross the BBB but can cause Cortisol release via the adrenal cortex
-This can cross the BBB and exert negative feedback
-If these are administered constantly, they will overwhelm negative feedback

(3) Dexamethasone
Metabolite of cortisol
Decreases pituitary activity

(4)Combined DEX / CRH
Stimulates ACTH and inhibits - this tells you about pituitary function
-baseline (circadian rhythm) testing
-Do in AM at wake before stressors exert an influence

(5) Stress test
Lab controlled, standard stressor
-Watch the HPA axis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Glucocorticoid receptors (GCs) : DISTRIBUTION

A

Both types:

  • Present in hippocampus
  • Present in amygdala
  • Present in hypothalamus
  • Present in pituitary

Type 1
-Provides positive feedback
Not present elsewhere in the cortex

Type 2
-Provides negative feedback
Present in high concentrations in cortex, especially the frontal lobes

The balance of these receptors determines the effect inn the 4 common regions. Outside this, always has inhibitory effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Processive vs systematic

A

Neurons in hippocampus, amygdala, frontal cortex, hypothalamus, brainstem
-projections to hypothalamus to regulate HPA

Differentiate processive vs systematic stressors: how fast is response needed?

  • Ether hypoxia immediate (systemic)
  • Midterm not death inducing (processive)

Systematic direct activation
Processive indirect effects
through GABA modulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Systematic direct activation

A

Brainstem

Something life threatening e.g. hypoxia
Does not need appraising
Pain/hot/cold/hypoxia
PVN > Increased HPA activity
Direct excitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Processive indirect effects

through GABA modulation

A

GABA neurons in the Preoptic area and the Hypothalamus have inhibit the PVN

These neurons:

(1) Receives excitatory input from the Ventral Hippocampus and PFC
- Increases the activity of GABA neurons
- Therefore indirectly excites the HPA axis
- More stress = more inhibition of the cortex and so less excitation of the GABA neurons
- More stress at the PVN

(2) Receives Inhibitory input from the amygdala
- When this activity is high, less GABA activity and therefore less inhibition of the PVN
- More stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Type 2 GC receptors

A
  • Are in the cortex
  • More circulating cortisol leads to more inhibition of the cortex’s excitatory effect on the POA of the hypothalamus.
  • This area has GABA projections to the PVN
  • This lack of cortical situation drops the activity of the GABA neurons
  • Hence activity at the PVN increases

So there is more stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Lazarus: Primary / secondary appraisal

A

Stress can be good or bad

Demand > Resources: stress (distress)
-This type of stress is bad

Resources > Demand: challenge (eustress)
-This type is good (i.e. prep for midterm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

The stress appraisal theory

A

Environmental event is appraised

Primary - based on past XP and beliefs > threat or challenge or Benign

If benign, ignore

If threat go to secondary appraisal

Secondary appraisal
-What resources, options and effectiveness do I have
-Do I have enough
Perception matters here

Decide how to act (or not!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Biopsychosocial model of stress

A

Extended Lazarus work
2 stress responses and interaction with perception
Events perceived as challenge or threat?

Challenge (DemandsResources): SNS adrenalin, HPA cortisol

Avoidance (Demands>Resources so ignore): SNS not activated, HPA extended activation

17
Q

Threat/Challenge/Chronic threat system responses

A

Threat
(Demands exceed resources)
HPA + SNS activation

Challenge
(Demands do not exceed resources)
HPA not activated
SNS activated

Chronic Threat
(Demands chronically exceed resources)
HPA super activated
SNS not

(Might avoid a problem in this case)

18
Q

Chronic stress

A

If chronic, HPA becomes hyperactivated while SNS no longer active
-Blood pressure remains elevated
Blood glucose elevated

-Believed to cause tissue and organ damage
Associated with Psychopathology (e.g., Depression)

  • Future theories added individual differences
  • Adaptive callibration model in reading
19
Q

Scientific evidence for the models

A

Challenging to collect data

  • Stress and resources are subjective
  • A “standard” stressor can be interpreted in many ways
  • Linking early life stress (organization) to current response (activation)

Problems:
Laboratory vs. real-life stressors
Stress markers
Coherence of stress responses among systems and with experience of stress
(do physiological measures map onto subjective ones?)

WHAT DO YOU MEASURE!

20
Q

Laboratory versus real-life stressors: the Trier Social Stress Test

A

(1) Public speaking
(2) Doing math out loud with people watching and judging

HPA axis response - fast ACTH increase, slower cortisol increase

21
Q

Necessary measures include…

3 types of thing

A

(1) Measures of HPA activity:
CRH, ACTH, Cortisol (Corticosterone)

(2) Measures of SNS activity:
Adrenaline, Noradrenaline, Alpha-amylase (metabolite of adrenaline), Heart rate variability

(3) Measure of subjective stress
Survey/questionnaires

22
Q

Coherence among stress systems

A

At a stressor, there is an immediate spike in SNS activity

  • This drops off over 10 mins
  • Cortisone is slower to increase
  • Peaks at 22 mins
  • The SNS measures are dropping when COrtisol is peaking
23
Q

Do the two systems add or are the compensatory for one another (Study 1 - dexa)

A

(Study 1)

  • Dexamethasone suppresses HPA
  • G1 Dexa G2 Control
  • Do TSST

SNS (HR)
In control = activates
In G1 MASSIVE activation

HPA (Cortisol)
In control = activates
In G1 = no activation

Subjective Stress
In control = rise
In G1 = Very big rise

Conclusion
When HPA inhibited, SNS compensates and this is what drives subjective stress

24
Q

Do the two systems add or are the compensatory for one another (Study 2 - propanolol)

A 
G1 Propranolol (drops SNS)
Control - nothing

SNS
G1 - no activation
Control - normal

HPA
G1 Large increase
Control - normal

Subjective stress
G1 - lower subjective stress
Control - normal

Conclusion

When SNS is dropped, HPA compensates by cos SNS is what drives subjective stress this is lower when SNS s inhibited

25
Q

Coherence among stress systems: individual differences

A

Examine cortisol amylase and early life exposure to stressors
-Parental Bonding Inventory and Childhood Trauma Questionnaire Trier Inventory of Chronic Stress

Took only participants scoring higher than specific cut-off

Relationship between ELA and the response of stress system

Administered the Trier Social Stress Test

RESULTS

There was higher A Amlysae (SNS) in high Early Life Event groups

In Low ELA = normal

The ratio Amylase-Over-Cortisol shows this most accurately

Low cortisol activation in high ELA groups

26
Q

Blunted Cortisol Response

A

In response to ELA the bodies stress system is organized differently and you see a lower Cortisol response to stress lifelong

We do not know in what direction (does this cause high SNS and so low HPA or the other way around)

27
Q

AOC

A

AOC correlates with many aspects of chronic stress

Better than sAA Cort, or COA

28
Q

Coherence among stress systems: individual differences

A

Supports complimentary stress theories

There is still evidence for additive ones too

AOC correlates with many aspects of chronic stress
Better than sAA Cort, or COA

New measure of bio stress that correlates with psyc stress so use this

ELA leads to blunted HPA because of high SNS activation or other way around

29
Q

Glucocorticoid cascade hypothesis

A

Allostasis is the maintenance of homeostasis via change
-It has a price

Allostatic load (glucocorticoid cascade)

  • The physiological cost of increasing and decreasing stress all the time
  • Influenced by many things (such as genes/individual differences)
  • Looked at stress and ageing
  • Chronic stress leads to overactivation of receptors
  • Get downregulated
  • Negative feedback has less receptors to act on
  • So cortisol levels increase

What follows? Immunosuppression, muscle atrophy, osteoporosis, hyperglycemia, atherosclerosis, diabetes

The insensitivity causes a viscous circle

Supposed to be mediated via HPA axis activity
neurotoxic effects of glucocorticoids in the brain

30
Q

The glucocorticoid cascade hypothesis:

Cell damage in the CNS?

A

Glucocorticoids cross cell membranes and change protein production

Some repress growth factors
Some increase apoptotic factors

These combined lead to increased apoptosis

Proposed mechanisms of damage:
modulation of mRNA
inhibition of glucose transport
potentiation of excitatory amino acids

However, hippocampal ‘loss’ even in Cushing’s is reversible

no higher AD incidence after hypercortisolemia

So you can recover

PSYC 342 (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions