Stress and the Body Flashcards
1
Q
stress
1. stressor
2. general adaptation syndrome
3. purpose of stress
A
- stressor any stimulus that disrupts homeostasis; release of adrenaline and cortisol to stim body to respond to stressor
- rats exposed to diff stressors dev ulcers; body reacts in same way to all stressors; general response is to liberate glucose into bloodstream, increase HR, BP, and breathing rate to increase fuel metabolism to supply body with E to respond to stress
- acutely is helpful to respond and adapt but if chronic then dmg health
2
Q
stress response
A
- startle due to stressor activates locus coreuleus, if threat is detected then LC activates amygdala; amygdala activate hypothalamus
- fast response hypothalamus sends signals via sympathetic nerves to adrenal medulla to release Epi/adrenaline to induce sympathetic response to flight or fight
- slow response, hypothalamus releases CCRH to pituitary gland to release ACTH adrenal cortex, release cortisol into blood, signal release of glucose and lipids from liver and adipose tissue to supply E
3
Q
exercise and psychological stress
1. comp
2. cross-stressor hypothesis
3. trained v. untrained men during stress response
A
- exercise is voluntary, acute stressor with minor strain, easy to recover from and with sufficient rest, adaptation occur; psychological stress is involuntary, chronic, major strain that is difficult to recover from
- voluntary exercise stress induces positive adaptations to stress sys, for higher resilience to all stressors
- cortisol (HPA), HR (SAM,), state anxiety all lower in trained men than untrained men during trier social stress test showing more resilience to stress on all aspects of stress response
4
Q
fear conditioning
1. pain and exercise
2. nocebo effect and health
3. classical conditioning
A
- when told that exercise will cause a bit of pain, feel increased fear and pain perception and; control group (not told exercise will cause pain) pain and fear decrease slightly
- negative effect produced by sham treatment due to patient’s belief; ethical concerns that disclosing negative side effects to patients will cause them to feel the side affects and increase anxiety
- learn to fear innocuous things by conditioning people to associate an conditioned stimulus with an unconditioned (natural physiological response) to produce a conditioned response (fear) to the CS\
5
Q
anxiety and conditioning
1. GAD
2. panic attacks
3. phobia
4. social anxiety
A
- anxiety disorders can originate from conditioned fear and be triggered for no real reason
- GAD excessive worry about everyday events for no reason
- panic attack is sudden irrational intense fear that triggers severe physical reaction
- phobia is intense fear/aversion to something with no apparent threat
- intense fear of being judged/scrutinized in social setting even when not true
6
Q
brain and fear conditioning
1. how phobias are formed
2. amygdala, fear, and anxiety
3. role of the hippocampus in fear conditioning
4. prefrontal cortex in fear response
A
- neurons that fire together form synapses, fear forms powerful synapses
- amygdala detects threat, fear conditioning, activating stress response until threat is gone; in people with anxiety, amygdala v. reactive to anything, stress response always active
- hippocampus plays role in memory and context; associates context with fear, activates amygdala
- responsible for threat expression, inhibiting and cognitive regulation of threat inhibition; can inhibit amygdala to decrease stress response; in anxiety, can’t provide rational response to fear, weak PFC inhibition, fear unregulated in amygdala, produce large stress response
7
Q
learned helplessness
1. overview
2. preventing learned helplessness
A
- conditioned to believe that bad situation is unchangeable or inescapable as response to chronic stress thus stay in situation (freeze); even intermittent relieve of stressor increases chance of attempting to change or escape
- gaining control over situation and getting regular exercise
8
Q
allostasis
1. exercise on SAM comp HPA
2. allostasis and exercise
3. allostatic load
A
- SAM increase Epi greatly with high intensity and decrease quickly as soon as recovery begins; HPA slower to increase cortisol and slower to decrease
- ability to adapt changing environment; with repeated exposure to exercise, push homeostatic set point to withstand more stress; exercise is controllable measure to push allostasis
- increase allostatic load without sufficient rest/recovery, weakens body and no adaptation occurs; stressors all combine to increase allostatic load; when stressed can’t exercise as intensely, take longer to recover, and less fitness gans
9
Q
stress dynamics: recovering from HPA response
1. negative feedback
2. receptors
A
- cortisol binds to receptors in the hypothalamus and the pituitary gland provide negative feedback to inhibit cortisol release
- mineralocorticoid receptors have high affinity for cortisol, set baseline cortisol lvl; glucocorticoid receptors have low affinity for cortisol, only bind when cortisol lvls are high to remove cortisol from blood for recovery; hippocampus high in GR, can signal hypothalamus to inhibit cortisol release
10
Q
biological basis of stress sensitivity
1. overview
2. BDNF
3. epigenetics
A
- chronic early life stress reduces GR in the brain but can preserve GR using exercise to protect against stress
- exercise increase BDNF which supports GR, chronic stress decreases BDNF
- gene expression determined by the packaging of DNA, if exposed can be transcripted, if hidden not; acetylation loosens DNA, stim gene expression; methylation inhibit gene expression when methyl group attaches to cytosine to block transcription; chronic stress adds CH3 to GR gene, exercise removes them
11
Q
psychological stress and immunity
1. immune system and stressed cells
2. stress and infection
A
- body cells have normal molecular PRO patterns on their surface recognized by immune cells, foreign cells have pathogen associated molecular patterns (PAMP), stressed cells have damageAMP that induce sterile immune response to remove damaged cells
- stress combined with infection greatly increases inflammasomes, creating high inflammation and thus greater allostatic load, making a stressed-out immune sys more sensitive to allergens and errors in detecting viruses or bacteria
12
Q
stress and adaptive immune response
A
- T helper cell 1 and 2 important in adaptive immune response
- Th1 has cytokines IL1 and IFN gamma, use cell-mediated immunity vis DAMP/PAMP to protect against viruses, bacteria, and cancer, when too many autoimmunity
- Th2 has cytokines IL6, IL4, use extracellular immunity to protect against parasites, when too many allergies
- stressed immune system decrease T1 and increase T2 leading to increased risk of infection and greater risk of allergies
13
Q
- Decartes’ mind-body dualism
- Mind-body connection
- sickness behaviour
A
- idea that diseases of body and mind are separate and should be treated separately has great influence on western medicine and biomedical model; psychological influences on health are largely ignored
- mind and body communicate via NS, endocrine sys, and immune sys
- after infection heightened immune response, inflammasomes release cytokines to body to alert it of infection, cytokines in the brain activates the amydala causes sickness behaviour, where individual withdraws socially; can be adaptive in short term since less likely to spread illness and get more rest but prolonged negative mood state can lead to anxiety and depression
14
Q
rethinking depression
1. def and biomedical model
2. depression and chronic physical illness and
3. response to SSRI
4. exercise and depression
A
- depression is affected state of negative mood and low arousal for at least 2 weeks, assumed to be due to lack of serotonin in forebrain
- chronic inflammatory disease assoc with depressive symptoms, long term pro-inflammatory cytokine therapy increased rates of major depression
- classic treatment is SSRI to prevent reabsorption of serotonin to relieve depressive symptoms; 30% people are non-responders found to have high cytokine levels compared to responders and control (depression not due to low SER); treating with anti-inflammatories may reduce depressive symptoms
- MICT reduced TNF alpha (cytokine) to reduce depession, anxiety and stress to improve mood while control increased negative mood; HIIT increased anxiety and stress but decreased depression due to higher allostatic load; exercise is important in improving mood but amount matters
15
Q
acute stress and the brain
1. amygdala
2. hippocampus and PFC
A
- increase number of dendrites able to receive more signals, hyperactivity increasing anxiety even after 1 day exposure to acute stress
- decrease in BDNF decreases dendrites and branch points can’t send as many signal to inhibit amygdala, stress increases; reversible; loss of dendrites decreases memory formation and increases reactivity to stress in hippocampus and increases impulsion and negative emotions in PFC, potentially causing mental illness
