HB - Stress and Coping Flashcards
1
Q
PHYSIOLOGICAL/AUTONOMIC IMPACT OF STRESS
A
- Physiological/Autonomic
- Muscle tension
- Hypervigilance (irritability, anxiety)
- Digestive upset (stomach churning)
- Difficulty sleeping
-
Adrenaline
- Fight or Flight response
- GI slows/stops
- Sweat glands activated
- Muscle tension
- Pulse and BP increases
- Pupils dilate
-
Cortisol
- Increased appetite
- Increase blood sugar from
- Protein/Fat catabolism
- Decrease peripheral glucose utilization
- Depressed immune system
2
Q
EPIGENTIC IMPACT OF STRESS
A
-
Epigenetic
- Genomic expression of cortisol receptors in the hippocampus modified by early life trauma
- Decreased expression –> increased stress response
- Genomic expression of cortisol receptors in the hippocampus modified by early life trauma
3
Q
HOLMES-RAHE INDEX
A
- Social readjustment scale that lists and ranks major stressors that are weighted by “life change units”
- Qualifies the relative importance of life changes in terms of distress or “morbidity load” on an individual<!--StartFragment-->
- Studied the relationship between stress and illness
- Life-stress scale of 43 ranked events
- Increased life units of stress = increased likelihood of illness’
- H&R score correlates with illness
- Low (<100) = 30-35% likelihood of illness
- High (201 - 300) = 80%
- Moderate (101 - 200) = 50%
4
Q
STRESS
A
- Acute stress - immediate ANS response to protect and heal body
- Chronic stress - adaptive mechanisms overwhelmed –> disease and dysfunction
- Stress activates endocrine system –> cortisol production<!-- -->Inflammation<!-- -->Cycle: cytokine production –> further cortisol production<!-- -->Medical illness<!-- -->Immune response<!-- -->Cycle: cytokine production
5
Q
EFFECTS OF CHRONIC STRESS
A
-
Metabolic
- Excess glucocorticoids
- Decreased sensitivity to insulin
- Increase in blood sugar
- Increase in blood fat
- Increased risk for metabolic syndromes
-
Inflammatory/Immune
- Acute stress –> activation of immune response
- Chronic stress
- Impaired production & activity of B and T cells
- Shrinkage of thymus
- Decreased immune response (viral infection, cancer)
- Contribute to increased risk of AI disease (MS, RA, Thyroiditis)
- Psychoneuroimmunology
- Immune suppression or activation can be classically conditioned
-
Cardiovascular
- Chronically elevated adrenaline and cortisol
- Chronic high BP and HR
- Decreased compliance/distensibility of BVs
- Increased clotting
- Spastic BVs –> angina
- Increase blood fat levels
- Inflammation
-
Cancer
- No clear evidence of cancer-stress link in humans
-
Reproductive
- Glucocorticoids inhibit (via - feedback cycle) LH and FSH
- Inhibition of testosterone/estrogen release
- Decreased fertility/sexual functioning
6
Q
STRESS AND TELOMERES
A
- Higher stress = shorter telomeres –> manifestations of age-related diseases:
- Macular degeneration (vision loss)
- Atherosclerosis
- Impaired wound healing
- Heart disease
- Grey hair
- Wrinkles
7
Q
STRESS VS EXERCISE
A
- Moderate exercise = increased telomere length
- Intense exercise = inversely related with telomere length
- Temporary increase endorphins, dopamine, and serotonin during exercise –> calm and focus
- Stimulation of Brain Derived Neurotrophic Factor which basically =’s an SSRI
8
Q
STAGES OF STRESS RESPONSE
A
- Alarm Stage: adaptive defenses mobilized
- Resistance Stage: attempt to cope/adapt
- Exhaustion Stage: demand exceeds available resources; defensive efforts fail
9
Q
ACUTE VS CHRONIC STRESS
A
-
Acute: protects and heals the body
- Immediate sympathetic nervous system activation –> fight or flight response
- Energy mobilization (storage is halted)
- Increased HR, BP, and respiration
- Immune system activation
- Non-critical functions stopped to make all resources available to cope with stress
-
Chronic: body’s adaptive mechanism can be overwhelmed
- Results in disease and dysfunction
10
Q
YERKES-DODSON LAW
A
- States that performance and adaptive learning are optimal under moderate (rather than high or low) stress (arousal) conditions
- High stress interferes with performance
- Low stress leads to low motivation and lackluster performance
- Applied to specific learning situations
- Learning new or difficult tasks is optimal under low/moderate stress conditions
- Performance of well-learned tasks is optimal under high stress conditions
11
Q
ROLE OF AMYGDALA AND HIPPOCAMPUS
A
-
Amygdala = emergency response
- Arouses and motivates organism via sympatho-adrenomedullary (SAM) axis
- Activates the hypothalamus-pituitary-adrenal axis (HPA)
- Triggers catecholamine release and glucocorticoids
- Activates the hypothalamus-pituitary-adrenal axis (HPA)
- Arouses and motivates organism via sympatho-adrenomedullary (SAM) axis
-
Hippocampus/Prefrontal Cortex (PFC) = intelligence agency
- Modulates the amygdala by assessing relevant memories to determine an appropriate stress response –> fine tunes the acute stress response
12
Q
ROLE OF GLUCOCORTICOIDS
A
- Stress causes hypothalamus to secrete corticotropin-releasing hormone
- Transported to pituitary to stimulate secretion of adrenocorticotropic hormone (ACTH), beta endorphin (BE), and other hormones
- ACTH stimulates the adrenal cortex to release glucocorticoids which binds to glucocorticoid receptors in the brain to stimulates shutting down the stress response
- In chronic stress, GR function can become impaired –> no cease of stress response
13
Q
EVOLUTIONARY OBJECTIVE –> ILLNESS
A
- Common disease are the byproduct of the body adapting to challenges to maintain homeostasis
14
Q
EFFECTS OF CHRONIC STRESS OF METBOLIC, GROWTH, AND REPRODUCTIVE PROCESSES
A
-
Metabolic
- In chronic stress the acute stress response is constantly being turned on and off
- Nutrient stores are depleted faster than they are replaced
- Excess glucocorticoids can impair body’s ability to respond to insulin
- Increased blood glucose and fat levels
- Impedes oxygen flow and organ efficiency
- Can ultimately lead to Type II Diabetes and CAD
-
Metabolic syndrome
- Central obesity
- Insulin resistance
-
Growth
- Moderate stress –> facilitative effect on growth, optimizing:
- Pituitary secretion of GH
- Bone growth
- Cell division
- Nutrient distribution
- Chronic stress –> impaired growth and development
- Sympathetic nervous system activation, disrupts growth processes, digestion and metabolism)
- Inhibition of GH release because of
- Excess glucocorticoid levels reducing target cell sensitivity
- Impaired synthesis of new proteins and DNA in cell division
- Telomere shortening
- Moderate stress –> facilitative effect on growth, optimizing:
-
Reproductive
- High stress = high glucocorticoid levels = inhibition of LH and FSH
- Males: leads to inhibition of testosterone release and sperm production
- Can impede parasympathetic activation of penile erection
- Impotence/premature ejaculation
- Can impede parasympathetic activation of penile erection
- Females: inhibition of estrogen release and egg production
- Increased fat cell consumption –> impedes estrogen production
- Buildup of androgens –> amenorrhea
- Decreased progesterone + glucocorticoids block bone re-calcification –> osteoporosis
- Atherosclerosis –> impaired uterine wall nutrition
- Males: leads to inhibition of testosterone release and sperm production
- High stress = high glucocorticoid levels = inhibition of LH and FSH
15
Q
STRESS VS IMMUNE SYSTEM DISORDERS
A
- Acute stress activates the immune system
- Chronic stress –> depressed immune system
- Caused by excess glucocorticoid levels
- Impaired B and T cell production –> decreased thymus size
- Impaired natural killer cell activity
- Or chronic stress –> heightened immune system –> AI disorders
- Multiple sclerosis
- Pernicious anemia
- Rheumatoid arthritis (bacterial infection onset)
- Juvenile diabetes
- Allergies
- Thyroiditis (Hashimoto’s)
- Lupus erythematosus (viral infection onset)
