Physical and Behavioral Indicators of High Stress

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Physical and Behavioral Indicators of High Stress

Physical and Behavioral Indicators of High Stress
Physical and Behavioral Indicators of High Stress

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22 UNIT I Pathophysiologic Processes

transport into the cells (insulin resistance), the pathophysiologic basis for type 2 diabetes. Elevated cortisol levels also directly increase insulin resistance. Additionally, obesity is associated with the production of proinflammatory cytokines such as TNF-α, IL-1, and IL-6, which also have been connected to diabetes.

In acute stress, activation of the immune system allows for the coordinated defense of the body from damage. At first, leukocytosis and immune function, including phagocytosis and antibody production, may be enhanced to protect the body from foreign invaders (e.g., bacteria and viruses), but then is followed quickly by immunosuppression. Chronic activation of the stress mediators produces immunosuppression and increases the risk of infection and has been implicated in the development of autoimmune diseases and some cancers. Such overactiva- tion also prolongs existing infections and the development of secondary infections. Research supports the hypothesis that physical and emotional stress and dysfunctional coping mechanisms impair both antibody and T-cell–mediated responses to viruses and antiviral and antibacterial vaccines. Stressors of more than 1 month’s duration have been found to be the greatest predictors of the development of colds. Cumulated evidence, in both human and animal models, supports the premise that stress-induced dysregulation of the cellular and humoral arms of the immune system increases risk of infectious disease. Stress has been found by numerous studies to accelerate the progression of HIV infection.

Immune dysregulation can also include the excessive production of cytokines that promote the inflammatory response. Both physical and psychological stressors have been found to accomplish this, sensitizing the overall inflammatory response so that subsequent activations are markedly increased. Early life stress such as low SES and childhood

inflammation associated with stress, have been linked with memory loss, cognitive decline, and the development of Alzheimer disease. Emerging research indicates that males and females may show different patterns of brain structure remodeling in response to chronic stress. Estrogen may exert neuroprotective effects.

Stress hormones have been found to be elevated and dysregulated in major depressive illness. Increased cortisol secretion, decreased testosterone levels in men and women, and increased levels of growth hormone and proinflammatory cytokines have been documented in major depressive illness. Depression is common with chronic diseases such as fibromyalgia and multiple sclerosis, and the elevated cortisol levels associated with allostatic overload may be significant to the progression of some of the diseases. Another condition, PTSD, also appears to be associated with heightened sympathetic-adrenal-medullary responses as well as alterations in the HPA axis. Evidence suggests cortisol and norepinephrine help promote long-term memory consolidation and retention of traumatic and fearful events; however, administration of beta-blockers such as propranolol that interfere with the effects of norepinephrine has been shown to reduce the incidence of PTSD symptoms in many cases.

Allostatic mediators activate and maintain energy reserves, which are initially meant to be helpful in managing stressors. Nonetheless, obesity (especially abdominal obesity), diabetes, atherosclerosis, metabolic syndrome, osteoporosis and bone demineralization, and other diseases, as well as accelerated aging, are associated with their chronic activation. The food-seeking behavior initiated by cortisol is beneficial in the short term, but when cortisol levels are increased by chronic stress of either a physiologic or a psychological origin, this adaptation gone awry results in obesity. Obesity is a risk factor for decreased effectiveness of glucose

NERVOUS SYSTEM Neuropsychological manifestations