Stress Response and Coping

reactive response

response to a stressor that is currently happening and is triggered by perception of an immediate threat or challenge (like anxiety while taking an exam)

anticipatory response

stress response occurs before expected stressor as body prepares for a potential disruption in homeostasis (like stress the day before an exam)

conditioned response

a previously neutral stimulus becomes associated with a past stressful/threatening experience resulting in future exposure triggering a stress response (like phobias and PTSD)

psychological distress

unpleasant emotional response when demands are perceived as threatening or overwhelming

can stress contribute to the development or worsening of disease?

yes

allostasis

the body’s process of adapting to stress to maintain stability

allostatic load

the cumulative “wear and tear”on the body from repeated chronic stress

allostatic overload

occurs when body’s ability to adapt to ongoing stress is exceeded and may contribute to disease development or worsening of an existing disease

psychoneuroimmunologic (PNI) mediators

examines the interaction between psychological, nervous, endocrine, and immune systems and how stress influences immune response

can short-term stress temporarily enhance some immune responses?

yes

stress response

initiated when the brain perceives a real/perceived stressor and causes the CNS and endocrine systems to coordinate physiologic responses; activates the SNS and HPA Axis

sympathetic nervous system (SNS)

releases NE from sympathetic nerve endings and adrenal medulla releases Epi, producing a rapid fight-or-flight response that increases arousal, vigilance, HR, BP, and energy availability

HPA Axis

hypothalamus releases CRH (corticotropin releasing hormone) which stimulates release of ACTH (adrenocorticotropic hormone) from the anterior pituitary that stimulates the adrenal cortex to release cortisol

catecholamines

hormones produced by adrenal glands (primary ones are NE and Epi) and they are involved in the stress response, released in response to SNS activation and produce the fight-or-flight response

Norepinephrine (NE)

primarily released from sympathetic nerve endings; increases BP by constricting peripheral vessels, dilates pupils, causes piloerection, increases sweat gland action

Epinephrine (Epi)

primarily released from adrenal cortex; greater influence on cardiac action compared to NE, vasodilation, metabolic regulation that increases glucose levels

cortisol

glucocorticoid hormone released by the adrenal cortex and is stimulated by ACTH during HPA Axis activation, helps body adapt to prolonged/ongoing stress; gluconeogenesis, inc. protein breakdown, maintain BP and cardio. fxn, suppress infl./immune response

immune/inflammatory effects of chronic cortisol elevation

suppresses immune/inflammatory responses which increases susceptibility to infection and delays wound healing

metabolic effects of chronic cortisol elevation

persistent hyperglycemia, greater insulin resistance (so increased risk of diabetes), inc. central fat accumulation, metabolic syndrome/obesity, inc. protein breakdown contributes to myo wasting/weakness

cardiovascular effects of chronic cortisol elevation

can contribute to hypertension and may increase cardiovascular risk

cortisol immune system effects

helps regulate immune and inflammatory response in stress, suppresses production of proinflammatory cytokines, dec. activity of immune cells, but chronic elevation can suppress normal immune defenses

endorphins/enkephalins

naturally occurring opioid peptides produced by the body that decrease pain perception and make you feel happy/euphoric