Stress Flashcards
alarm reaction
initial response to stress
sympathetic NS
HPA axis
sympathetic NS
norepinephrine released from adrenal medulla
fast
HPA axis
cortisol released from adrenal cortex
slow
individual differences
early stressful experiences can allow for later resilience
more significant early life stress
stress immunization
due to comfort after the stress
significant early life stress
greater stress responses, learning deficits, long-lasting changes in brain- less adult neurogenesis, less adrenal steroid receptors
negative affective disorders
negative affect
genetic risk
chronic, lower grade stressors
negative affect
experiences world in negative terms
higher levels of distress, anxiety, dissatisfaction
low subjective sense of well being
genetic risk
many genes contribute to susceptibility
chronic, lower grade stressors
increase risk for anxiety disorders or depression
general adaptation to stress theory
alarm
resistance
exhaustion
alarm
body mobilizes to confront threat
resistance
body actively copes with threat
exhaustion
if threat continues the body’s resources become depleted
dysregulation can lead to negative affective disorders
chronic stress produces excess alarm and resistance
contribute to development of negative affective disorders
less adaptation to stress in negative affect
end of stressful event - HPA axis turns off negative feedback loop
neuropsychiatric issues- HPA axis has more difficulty turning off negative feedback loop
PTSD patients size of hippocampi
PTSD patients have a smaller hippocampus than people without PTSD
does stress shrink HPC to produce PTSD? or are smaller HPC a risk for developing PTSD?
twin study- both twins have smaller hippocampus- higher risk for developing PTSD
PTSD involves a type of learned fear
if tone has a regular pattern, animal will habituate
chronic, unpredictable stressor (tone) will continue to elicit “freezing”
model of PTSD
original trauma
subsequent stressors produced heightened alarm stress response
triggers traumatic memory (via amygdala)
over time, traumatic memory associations and physiological response are strengthened
original trauma activates
locus coeruleus- norepinephrine
ventral tegmental area- dopamine
corticotropin-releasing hormone
low road/high road-> amygdala
depression brain changes
greater brain activity in PFC and amygdala
persists after depression period over
electroconvulsive therapy/repetitive transcranial magnetic stimulation
smaller hippocampus
depression neurotransmitter activity
reduced monoamine transmitter activity
serotonin, norepinephrine, dopamine
selective serotonin reuptake inhibitors (SSRIs)
serotonin-norepinephrine reuptake inhibitors (SNRIs)
ketamine, psilocybin?
co-morbitity of anxiety and depression
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
co-morbitity
when two disease traits co-occur at a frequency that is higher than expected based upon the base rates of the two alone
