Coping and Stress (5 questions) Flashcards
Good stress
circuit activation –> return to normal at end of stress
Mild stress: what happen?
- desensitize circuits –> experience based resilience;
- 5HT ↑’s availability of BDNF, preventing or reversing neuron loss
- hippocampus vulnerable to these losses
Chronic stress: what happens?
- turns off BDNF genes –> ↓creation/maintenance of neurons & connections –> synapse loss or apoptosis (loss of the whole neuron)
- Stress and cortisol exposure decrease BDNF expression and can cause hippocampal atrophy, similar to atrophy that occurs in depression
What is BDNF?
- Brain Derived Neurotrophic Factor
- A protein; member of neurotrophins – r/t NGF or nerve growth factor
- Found in brain & periphery
- Supports neuron survival, encourages growth/differentiation of new neurons and synapses.
- Active in hippocampus, cortex, basal forebrain – r/t learning, memory, higher thinking
- Neurotrophins help to stimulate and control neurogenesis and BDNF is very active
- In animal models, exercise increases BDNF secretion in hippocampus
Cortisol vs corticosterone
Cortisol is the predominant glucocorticoid in humans (and is produced in the adrenal zona fasciculata), whereas corticosterone is less abundant in humans, but is the dominant glucocorticoid in rodents (in humans it is produced in the zonae fasciculata AND glomerulusa).
Defining stress
- Stress – response to pressures of daily life or threats to well being; adrenaline response (fight or flight)
- Motivates; increase productivity
- Minor interference with life
- Coping strategies used to resolve; able to problem solve
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Defining fear
- Fear: response to a known threat –prepares us
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Defining anxiety
- Anxiety: unknown, vague response; may be expressed physically; a negative outcome of stress
- Fear & Anxiety are part of the same circuit
Stress vs anxiety
- Reaction is greater than typical response
- Requires help to relieve
- Usual coping ineffective
- Unable to problem solve
- Anxiety can be: mild, moderate, severe or panic level
- Selye: General Adaptation Syndrome (GAS)
Levels of anxiety
Acute anxiety (severe), Panic, Chronic anxiety (moderate)
Physiological symptoms of acute anxiety (severe)
Tachycardia, palpitations, hyperventilation, fainting, dizzy, blurred vision, trembling, diarrhea, headaches, insomnia, nausea, freq urination
Emotional symptoms of acute anxiety
Irritability, anger, crying, withdrawal, clinging, critical of self/others, inadequacy, Insecurity, powerlessness,
Cognitive symptoms of acute anxiety (severe)
- Preoccupied
- Distracted
- Inattentive
- Attends only to a specific detail
Physiological symptoms of panic
All the symptoms of severe acute anxiety PLUS
- Aimless/random behavior (run, shout)
- Immobility
- Unable to speak
Emotional symptoms of panic
- Feelings of dread
- Like dying
- Terror
- Eeriness
- Feel unreal
Cognitive symptoms of Panic
- Delusions
- Hallucinations
- Poor reality testing
Physiological symptoms of chronic anxiety (moderate)
- Jumpy
- Daytime fatigue
- Sleep disturbance
- Heartburn, belching
- Muscle tension
- Sweaty palms
- Flushed, dry mouth
- Frequent sighing
Emotional symptoms of chronic anxiety (moderate)
- Nervousness
- Irritability
- Loneliness
Cognitive symptoms of chronic anxiety (moderate)
- Ruminating
- Worrying
- Attend only to details, immediate task
Fight or flight response
- Epinephrine & NE secretion from adrenal medulla and sympathetic nervous system enables mobilization
- Sympathetic nervous system triggered and within seconds effects: heart rate, bp, metabolism, respiration, decreased digestion enable successful mobilization to survive threats
Selye’s GAS
General Adaptation Syndrome (GAS)
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Alarm: SAM & HPA activation:
- Mobilization!
- Resistance: Attempt to adapt to threat:Less than optimal function. If we cannot adapt…
- Exhaustion: Unable to adapt or function; Illness or death if threat not resolved
SAM: sympathetic adrenal medullary response
What is allostasis?
process of achieving stability (homeostasis) through adaptive physiologic or behavior change. Good in short term. Possibly damaging if not “shut off”
- e.g., adrenalin, glucocorticoids, cytokines act on organs/tissue
What is allostatic load?
cost of wear and tear from repeated activation of stress responses. Leads to physical and emotional disease (atrophy of neurons compromising hippocampus function)
3 types of allostatic load
- Frequent stressors (frequency of events determine amt of load)
- Failure to turn off physiologic responses (autonomic, neuroendocrine)
- Failure to respond adequately to a challenge (ex: increased inflammatory cytokine activity b/c HPA activity does not contain)
Axes involved in fight or flight
- Sympathetic-adrenal-medullary (SAM) axis activation
- Hypothalamic-pituitary-adrenal (HPA) axis activation
increase of sympathetic activity, cortisol, and proinflammatory cytokines
decline in parasympathetic activity
Stress response: what happens when we perceive a threat?
Thalamus → Amygdala. Lateral amygdala receives sensory input (ex: fear) → to central nucleus of amygdala → output activates HPA axis & sympathetic ns
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Hypothalamus secretes:
- CRH → triggers ACTH release from anterior pituitary → triggers stress hormone release (glucocoritcoids, i.e. cortisol) from adrenal cortex
- β-endorphin (mitigates pain reduction) → stimulates epinephrine release from adrenal medulla;
- AVP also released from hypothalamus
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Hippocampus has adrenal steroid receptors:
- Type I: mineralocorticoid; Type II: glucocorticoid
- Produces excitation, if prolonged can lead to excitotoxicity/damage
Which produces a faster reaction, HPA or SAM?
SAM
Describe the hormonal cascade involved in HPA activation
- Corticotrophin releasing hormone (CRH) secreted in hypothalamus →
- AP, which releases ACTH →
- Through bloodstream to adrenal cortex, which releases glucocorticoids (cortisol) →
- Cortisol feeds back, slowing release of ACTH & CRH
HPA: effect of cortisol
- mobilizes energy
- Increases CV tone
- Suppresses anabolic activity (reproduction, digestion, growth, immunity)
- Increased release in early AM hrs → prepare for day
- Acute/Chronic Stress
Role of hippocampus in HPA axis
inhibitory (turns HPA down)
HPA: feedback mechanisms image
SAM axis activation
- RAPID response to stress → prepares body to react
- Catecholamines (Epi, NE) released by adrenal medulla →
- ↑ heart rate, ↑ respiration, ↑ blood flow, ↑ BP, ↑ glucose
- ↓ digestive activity
- Counterbalanced with Parasympathetic activity
PNS: role
freeze/hide behaviors; direct innervation of organs – promote vegetative function and decreased physiologic arousal
PNS vs SNS
counteract one another - in most people - only small % have both high or both low
SNS: what are the two paths of the F or F response coordinated by the Locus Coeruleus?
- Fast: direct noradrenergic innervation of visceral organs
- Slow: hormonal path from adrenal medulla → epi & NE and Increased: heart rate, respiration, glucose, blood flow to muscle