Stress Flashcards
Define a stressor
Anything that disrupts physiological balance
Define the stress response
Biological response triggered by the body to re-establish the balance (following an actual or perceived threat)
Define distress
A biological state where the stress response has a deleterious effect upon the individuals welfare
What are the 4 main categories of stressor?
- Enviromental - temperature extremes, noise/vibration, famine/drought, smell
- Physiological - wounds, disease/infection, injury(castration/dehorning/tail docking)
- Social - dominancy disputes (fighting/subordination), solitary confinement
- Pyschological - restraint, lack of control, anxiety/fear
What did Walter Cannon study in 1900s? Who else investigated stress physiology after him?
Homeostasis
Role of adrenaline in stress physiology
Fight or flight response
Hans Selye 1950s - role of GCs in stress physiology, general adaptation syndrome
What was discovered about the stress response?
It is NON-SPECIFIC
- Selye discovered that application of a wide variety of stressors -> peptic ulcers, ^adrenal glands, v immune system
Other than negative stimuli, what may cause a stress response?
Positive experiences like playing, mating
Give Chrousos (1998) definition of the homeostatic concept of stress
“Stress is the recognition by the body of a stressor and threatened state of homeostasis, adaptive responses are the body’s attempt to counteract the stressor and re-establish homeostasis”
What are the problems associated with homeostatic concept of stress?
- individual differences in stressor perception
- pyschological stressors (eg. public speaking/claustrophobia)
- ^GC/SNS triggered by pleasure too
- Optimum homeostatic parameters shift (eg. running v sleep)
Give an alternative definition of stress to Chrousos (1998) definition
Kim and DIamond 2002 - “A condition in which individuals are aroused by aversive stimuli - the extent of the stress is determined by the individuals perception of control over the aversive stimuli
What are the 3 stages of the adaptive stress response?
- Recognition - appriasal and interpretation based on previous experience
- Biological response - defence eg. behavioural change
- Return of biological function to baseline
What may modify the adaptive stress response?
Modifiers
- experience
- genetics
- social relationships
- age
- health
- control
What are the two main components of the biological response?
- SAM axis
- Catecholamines (mainly NA) from SNS
- Catecholamines (mainly A) from adrenal medulla
> Latency: Seconds - HPA axis
- GCs from adrenal cortex
> Latency: Minutes
What are the 2 types of corticosterone receptor?
Type 1 - MR - high affinity - activated by low GC - Homeostasis Type 2 - GR - low affinity - only activated by high GC - Stress, abnormal behaviour
What is the evolutionary advantage to the stress response?
When activated in response to a real threat, rediverts resources from non-essential energy expensive processes to those that promote immediate survival (eg. muscles/brain) - HIGJLY ADAPTIVE
- system deactivates once crisis is averted
Give 6 physiological actions of the stress response
- ^energy availability and blood glucose
- v insulin secretion -> ^ glucagon production
- ^ gluconeogensis (GC/A/NA,) ^ lipolysis (GC) - mobilisation from existing stores - ^O2 availability
- ^resp rate (A/NA) - ^blood flow to muscles
- ^HR (A/NA)
- ^BP (A/NA)
- ^Blood Volume (ADH) - v Pain perception (“SIA”)
- endorphins - Inhibition of non-survival systems
- v Digestion (A/NA)
- v growth (GC)
- v immune function (GC) - v inflam and Ab production but migration of some immune cells to the skin surface
- v reproduction (PRL) - Enhanced alertness/sensory function/memory
- (A/NA/ADH)
Why does sustained stress cause pathological states?
Sustianed stress due to frequent activation/un-terminated stress responses/activatino due to psychological/social stress -> habituation of stressor, adaptation to deal with stressor -> exhaustion and ^ likelihood of disease.
Novel stressor will still initiate a normal stress response.
Who discovered the “general adaption syndrome”? Outline the 3 stages.
Selye 1936 - Rats housed at low temperatures
- [2 days] Alarm reaction - ^adrenal cortex, veasinophil, altrphy of thymus/spleen/lymph
- [2 weeks] Resistance - no symptoms, cold adapted
- [2 months] - Exhausiton - died due to 2ry infection
Who proposed the model of animal stress with 3 layers
- recognition of a threat to homeostasis
- stress response
- consequences of stress (“distress/pathological state”)
Moberg 2000
What are the consequences of chronic stress? What is the main cause of these?
= GCs usual cause
> Metabolic system
- energy mobilised constantly
- inefficient lypolsis and gluconeogenesis
- hyperglyceamia -> diabetes
- weakness/fatigue
- myopathy
> CV system
- ^ CV tone
- myocardial damage
- hypertension
- atheroscelrosis -> stroke/heart disease
> GIT
- inhibited -> loss of appetite, weight loss
- gastric ulcers
> Wound healing and immune system inhibited
- ^risk of infection/parasitism/AI disease
> Repro system inhibited
- Anovulation/lack of behavioural oestrus
- v Testosterone/impotency
- Loss of libido
> Growth inhibited
- weight loss/stunted growth
- ^ risk of fractures and osteoporosis
> Brain
- altered cognition and sensory thresholds
- hippocampal damage and cognitive impairment
When may some of the usual signs of chronic stress not be seen?
Highly prolific bred farm animals may not show reproduction related problems
How may subclinical stress cause problems?
Multiple sub-clinical stressors “combine” and cause pathological stress
- Animals kept in captivity and wild animals in degraded habitats particularly vulnerable to subclinical stress
Give 2 examples of sub clinical stress causing problems.
- Wild freshwater fish populations
- low oxygen levels -> no obvious clinical signs
- low level toxin -> no obvious clinical signs
> if exposed to both concurrently -> “unexplained” mortality - pigs sensitive to sequential aversive stimuli
- aggressive challenges by pen mates, tail bitten, transferred to sick pen roughly, loaded onto truck fro transport -> stress levels elevate each time until unacceptable -> collapse and death
What do Broom and Johnson (1993) argue?
“Stress overtaxes control systems to the point where fitness is reduced”
- BUT this exemts many stimuli generally considered stressful
> stress implies poor welfare but poor welfare can exist without stress
Who developed the idea of an allostatic load?
McEwan and Wingfield 2003
Define allostasis
Achieving stability through physiological or behavioural change eg. alteration in baseline reap rate/HR/metabolism
- sleeping/walking
- neonate/adult
- pregnant/non-pregnant
- summer/winter
Define an allostatic state
Entered when regulatory system operates at an altered level in response to environmental challenge or change
Define allostatic load
Cumulative costs incurred by the body during allostasis
Define allostatic overload
Demand exceeds capacity to cope (-ve energy balance)
- > emergency life history stage
eg. birds laying eggs - would normally find more food and deal with allostatic load, but if food is scarce -> overload
What are the 2 ways of measuring stress?
Behaviour
Physiological measures
What behavioural measures can be used to identify stress?
- Change in behaviour
- Detrimental behaviour eg. feather plucking/self harm
- Stereotypies
- Indicators of pain
What physiological measures can be taken to identify stress?
> HR
- ^ emotional response (SNS)
- v freeze response (PNS)
- Arryhthmias
- Changes in HR during stressor exposure
BP ^ with chronic stress
Resp rate ^ with chronic stress
Body temp ^ core, v peripheral (SNS and adrenal cortex activity)
Immune system function
- WBCs eg. H:L ratio
- Ab production following Ag challenge v with stress
Adrenal hormones (acute stress)
- SAM (catecholamines released v quickly and metabolised v quickly)
- HPA (collect blood <5mins or urine/saliva GC later)
How may the HPA axis be investigated to look at chronic stress?
Sensitisation and desensitisation - chronic stress -> > ^GC (normal stress response) > ^^^GC (sensitisation) > baseline GC (habituation) > baseline, but novel stressor -> ^^^GC (sensitisation)
Give examples where ^ plasma GC have been found
- pigs in high stocking densities
- calves in crates
- dairy cattle subjected to social mixing/overcrowding
- sows that lost aggressive encounters
What are the problems associated with measuring stress?
- no single measure will apply to all stressors
- SAM/HPA can be activated by non-stressors
- sample methodology can confound results by being stressful
- Diurnal cycle of GC secretion
- Interbreed differences in GC response eg. chickens may be flighty or calm but HR^ same
- Inter-individual response influenced by modifiers (eg. coping system when confronted may differ between dogs, still equally stressed)
Give 3 examples of the effects of prenatal stress
Lay 1997 - cattle transport stress -> ^GC and ^HR at 150d restraint test
Clarke 1994 - rhesus monkeys stress -> v birth weight, developmental delay, attentional deficit, v social behaviour, v cognition, ^ stress responsiveness
Levine 1967 - rats stress -> v emotional response to novelty and v HPA response to stress
What did Liu 1997 investigate?
Epigenetics of rat rearing - if raised by calm, nurturing mother -> calm, nurturing adult
If raised by anxious, non-nurtering mother -> anxious, non nurturing adult
> ^Type 2 corticosterone receptors due to ^ licking
How does predictability affect stress responsiveness? Outline a study.
If stimuli are predictable and of constant intensity -> Habituation
If stimuli are unpredictable or of varying intensity -> Anxiety as animal cannot prepare or predict the next stimulus
eg. Weiss 1972 - rats given random or predictable (light cue) shocks
> random group - ^GC, stomach ulcers, disrupted immune system due to ^ anxiety
> control group knew they were safe when light wasn’t on
