Stress Flashcards

1
Q

stress

A

disturbance of homeostasis

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2
Q

systemic stressor

A

pose direct threat to survival

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3
Q

processive stressor

A

psychological, no direct threat
- asssociated w/ threats based on experience

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4
Q

__________ is the hub for two overlapping but distinct endocrine systems in stress response

A

adrenal gland

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5
Q

2 systems for stress response

A

HPA axis and adrenomedullary response

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6
Q

adrenomedullary response

A

immediate, non-specific
- fight or flight Cannon coined it
- catecholamines epinephrine and norepinephrine

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7
Q

HPA axis

A
  1. stressor causes CRH release from hypothalamus
  2. CRH travels to pituitary to release ACTH
  3. ACTH travels through bloodstream to adrenal cortex, targets zona fasciculata to stimulate release of GC’s like cortisol
  4. GC’s have many effects and targets
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8
Q

Selye’s main findings

A
  1. stress response is universal (same response regardless of type of stressor, and the same across species)
  2. chronic stress leads to illness
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9
Q

homeostatic concept cannot explain

A

anticipatory responses

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10
Q

allostasis

A

changing set point for homeostasis, allows us to function within changing conditions
- set points and responses to set points can change

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11
Q

example of acute vs chronic stress side effects that are related

A

acute: increased heart rate
chronic: hypertension

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12
Q

chronic stress on brain

A

affects hippocampus, amygdala, PFC, (etc)
- increase in neuroinflammation, decrease in neurogenesis

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13
Q

acute stress on brain

A

increase brain functioning, increase hippocampal neurogenesis (in rats), enhance memory 2 weeks after stress (integration of new hippocampal neurons into circuits)

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14
Q

does stress only affect hormones

A

no, also nervous and immune systems

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15
Q

basal GCs

A

steroid hormone released from adrenal cortex
- almost all vertebrate cells have receptors for them
- primary in humans is cortisol

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16
Q

cortisol

A

follows daily (diurnal) cycle
- highest right before wake, lowest during day (for us, opposite for mice bc they’re nocturnal)
- increases in response to stress and low blood glucose
- rhythm in adrenal gland is driven by ACTH release, which follows same rhythm

17
Q

Addison’s disease

A

decrease in cortisol and aldosterone
- damage/dysfunction of adrenal cortex
- weight loss, nausea, etc
- low levels of salt and glucose in blood
- treatment = cortisol agonist like prednisone, increase salt diet if aldosterone levels are low
- higher does in times of illness, injury, or stress

18
Q

Cushing’s disease

A

increased cortisol levels, increase in blood glucose levels
- weight gain, abdominal obesity, etc.
- treatment depends on cause, poss lower GC medication, surgery for tumours, etc

19
Q

dexamethasone is a cortisol

A

agonist

20
Q

GC in response to stress

A

takes longer to release, takes longer to affect targets
- early stress responses not bc of GC’s

21
Q

Munck’s hypothesis

A

cortisol at low doses (daily basal levels) is permissive, at high doses is suppressive
- same hormone can have different effects based on dose

22
Q

steps after a stressor

A
  • catecholamines - immediate increase in respiration and cardiovascular rates
  • immediate release of glucose and oxygen into blood
  • epinephrine - delivery of oxygen to tissues
  • glucocorticoids replenish energy reserves
  • endorphins stop pain responses
23
Q

Type 1

A

Mineralcorticoid receptors
- high affinity for cortisol
- basal, non-stress

24
Q

Type 2

A

Glucocorticoid receptors
- low affinity, active when cortisol levels are high, during stress

25
Q

permissive

A

basal levels of GCs enhance the actions of the first wave of stress-response hormones
- lack of GC’s sometime before stressor reduces a physiological resposne

26
Q

stimulatory

A

stress-induced GC levels enhance the actions of the first wave of stress-response hormones
- elimination of stress-induced GC levels decreases physiological response to stressor

27
Q

suppressive

A

stress-induced GC levels inhibit the actions of the first wave of stress-responseive hormones
- eliminations of stress-induced GC increases stress response

28
Q

mother rat stress and son testosterone peak

A

shifter (to earlier), lead to impaired secual behaviour

29
Q

increase LG =

A

increase in serotonin tone in hippocampus, increase in transcription factor NGFI-A

demethylation of GR exon 1, acetylation of histones around GR in hippocampus -> better gene expression, more GR in hippocampus, regulate stress response

30
Q

low LG =

A

methylation at exon 17 gene region of GR gene, NFGI-A couldn’t bind as well = lower GR in hippocampi, worse stress response regulation

31
Q

bullied twin =

A

increased DNA methylation at CpG8 on SERT = decreased cortisol response