Stress Flashcards

1
Q

alarm reaction

A

initial response to stress
sympathetic NS
HPA axis

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2
Q

sympathetic NS

A

norepinephrine released from adrenal medulla
fast

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3
Q

HPA axis

A

cortisol released from adrenal cortex
slow

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4
Q

individual differences

A

early stressful experiences can allow for later resilience
more significant early life stress

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5
Q

stress immunization

A

due to comfort after the stress

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6
Q

significant early life stress

A

greater stress responses, learning deficits, long-lasting changes in brain- less adult neurogenesis, less adrenal steroid receptors

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7
Q

negative affective disorders

A

negative affect
genetic risk
chronic, lower grade stressors

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8
Q

negative affect

A

experiences world in negative terms
higher levels of distress, anxiety, dissatisfaction
low subjective sense of well being

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9
Q

genetic risk

A

many genes contribute to susceptibility

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10
Q

chronic, lower grade stressors

A

increase risk for anxiety disorders or depression

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11
Q

general adaptation to stress theory

A

alarm
resistance
exhaustion

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12
Q

alarm

A

body mobilizes to confront threat

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13
Q

resistance

A

body actively copes with threat

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14
Q

exhaustion

A

if threat continues the body’s resources become depleted

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15
Q

dysregulation can lead to negative affective disorders

A

chronic stress produces excess alarm and resistance
contribute to development of negative affective disorders

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16
Q

less adaptation to stress in negative affect

A

end of stressful event - HPA axis turns off negative feedback loop
neuropsychiatric issues- HPA axis has more difficulty turning off negative feedback loop

17
Q

PTSD patients size of hippocampi

A

PTSD patients have a smaller hippocampus than people without PTSD

18
Q

does stress shrink HPC to produce PTSD? or are smaller HPC a risk for developing PTSD?

A

twin study- both twins have smaller hippocampus- higher risk for developing PTSD

19
Q

PTSD involves a type of learned fear

A

if tone has a regular pattern, animal will habituate
chronic, unpredictable stressor (tone) will continue to elicit “freezing”

20
Q

model of PTSD

A

original trauma
subsequent stressors produced heightened alarm stress response
triggers traumatic memory (via amygdala)
over time, traumatic memory associations and physiological response are strengthened

21
Q

original trauma activates

A

locus coeruleus- norepinephrine
ventral tegmental area- dopamine
corticotropin-releasing hormone
low road/high road-> amygdala

22
Q

depression brain changes

A

greater brain activity in PFC and amygdala
persists after depression period over
electroconvulsive therapy/repetitive transcranial magnetic stimulation
smaller hippocampus

23
Q

depression neurotransmitter activity

A

reduced monoamine transmitter activity
serotonin, norepinephrine, dopamine
selective serotonin reuptake inhibitors (SSRIs)
serotonin-norepinephrine reuptake inhibitors (SNRIs)
ketamine, psilocybin?

24
Q

co-morbitity of anxiety and depression

A

have very similar symptoms and things that can make a person develop the disorder
may not be directly linked to each other but may have the same genetic causes and environmental causes

25
Q

co-morbitity

A

when two disease traits co-occur at a frequency that is higher than expected based upon the base rates of the two alone