Chapter 9 Stress and Disease

Allostasis

-"Stability through change" -brain continuously monitors for future events and anticipates what is required from neuroendocrine and autonomic system

Hypothalamic-Pituitary-Adrenal (HPA) Axis

-Nervous system: Hypothalamus secretes corticotropin-releasing hormone (CRH), Pituitary releases adrenocorticotropin hormone (ACTH) -Endocrine System: adrenals secrete cortisol and catecholamines -Immune system: multiple alterations secondary to cortisol and catecholamines

Cortisol Effects

-Used therapeutically as powerful anti-inflammatory/ immunosuppressive agents -influence virtually all immune cells -elevated levels my decrease innate immunity and increase autoimmune response

Cortisol

-abnormal elevations linked to obesity, sleep deprivation, lipid abnormalities, hypertension, diabetes, atherosclerosis, and loss of bone density -secretion during stress inhibits initial inflammatory effects -promotes resolution and repair -shown to induce T-cell apoptosis

More Neuroendocrine Regulation

-cortisol and catecholamines: decrease cellular immunity while increasing humoral immunity and increase acute inflammation -CRH-relased peripherally proinflammatory: vasodilation and increased vascular permeability thyroid hormone decrease: suppression of growth and reproduction= conserve energy -Neuropeptide Y (NPY): sympathatic neruotransmitter causing tissue remodeling (atherosclerosis)

Dr. Hans Selye

-descover a new sex hormone -injected ovarian extracts into rats -the changes were: 1-enlargement of the adrenal gland 2-decreased lymphocytes (damage to lymph structures) 3-development of bleeding ulcers in stomach and duodenal lining -he called these changes stressors

Stress-age syndrome

-excitability changes in the limbic system and hypothalamus -increased catecholamines, ADH, ACTH and cotisol -decreased testosterone, thyroxiine, and other hormones -alterations of opioid peptides -immunodepression -pattern of chronic inflammation -alterations in lipoproteins -hypercoagulation of the blood -free radical damage of cells

Stress-induced Hormone alterations: estrogen

-exerts a calming effect during stressful stiumations

Stress-induced Hormone alterations: Melatonin

-increased during stress response

psychosocial distress

-manifests as physiologic, emotional, cognitive and behavior changes - at risk for immunologic deficits -aggression associated with changes in T and B cell numbers

Coping

-may be adaptive or maladaptive -strategies beneficial when problem focused and when social support is sought -maladaptive coping may contribute to adverse health effects

stress and interventions

-meditation -mindfulness -imagery -massage -biofeedback -support groups -stress management techniques

Stress

-perceived or anticipated threat that disrupts a person's well-being or homeostasis -may be from psychologic/emotional/physical/physiologic stimuli that trigger stress response -everyone experiences stress when a demand exceeds a person's coping abilities -starts with a stimulus that the brain perceives as stressful and in turn promotes adaptational and survival-related physiologic responses

Stress-induced Hormone alterations: Oxytocin

-produced by the hypothalamus during labor and lactation -promotes bonding and social attachment -produced during orgasm -reduced anxiety (stressed women cannot labor or bond)

Stress-induced Hormone alterations: B-endorpines

-proteins found in the brain that have pain-relieving capabilities -released in response to stressor -hemorrhage increases levels to inhibit BP increases or delays compensatory changes -Growth hormone (somatotropin) chronic stress decreases growth hormone

Psychoneuroimmunology (PNI)

-psycho: consciousness -Neuro: CNS -immune: immune modulation by psychosocial stressors leads directly to health outcomes

Pyschologic Mediators

-reactive response -anticipatory response -conditional response

Stress-induced Hormone alterations: Testosterone

-regulates male secondary sex characteristics and libido -testosterone levels decrease after stressful stimuli

Neuroendocrine Regulation: Catecholamines

-released from adrenal medulla: Epi released which binds with both a and b receptors -a-adrenergic receptors -B-adrenergic receptors -mimic direct sympathetic stimulation

Neuroendocrine Regulation: Cortisol (hydrocortisone)

-secreted during stress -reaches all tissues -activated by adrenocorticotropic hormone (ACTH) -stimulates gluconeogenesis -elevates blood glucose levels -affects protein metabolism -powerful anti-inflammatory and immunosuppressive agent

Role of immune system

-stress directly related to proinflammatory cytokines -linked between stress, immune function and disease/cancer -immune system affected by neuroendocrine factors -stress response decreases T cell cytotoxicity and B cell function

Stress, Personality, Coping and Illness

-stress is not an independent entity but a system of interdependent processes -individualized response -personality characteristics also are associated with individual differences in appraisal and response to stressors -adverse consequences of stress may be minimized by coping -psychologic distress predictive of psychologic, social, and physical health outcomes: PTSD

General Adaptation Syndrome (GAS)

1-Alarm stage: stressor triggers the hypothalamic-pituitary-adrenal (HPA) axis which activates the sympathetic nervous system and arousal of body defenses 2-resistance/adaptation stage: begins with the actions of adrenal hormones and mobilization contributes to fight or flight 3-Exhaustion state: (allostatic overload) occurs only if stress continues and adaptation is not successful this leads to stress-related disorders

Allostatic Overload

Overactivation of adaptive system highly individualized