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Fap 331 stress
Fap 331 stress
Fap 331 stress
Fap 331 stress
Fap 331 stress
Fap 331 stress
Fap 331 stress
Fap 331 stress
Fap 331 stress
Fap 331 stress
Fap 331 stress
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Fap 331 stress

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  • 1. Stress1) Define stress making sure to include both physiologic and psychologic factors that can play a role (T762, M312) a) According to Hans Selye: a state or condition of the body produced by “diverse nocuous agents” and manifested by a syndrome of changes – general adaptation syndrome (GAS) which produces the stress triad: i) Enlarged adrenal cortex ii) Atrophy of thymus gland and other lymphatic organs iii) Bleeding ulcers in stomach and duodenal lining b) A person experiences stress, physical or psychological, when a demand exceeds a person’s coping abilities. c) Stressors: any agent or stimulus that produces stress i) Response depends on perception – varies among individuals ii) Any extreme stimuli: too much or too little of anything (1) Physical: i.e. extreme temperature – hot or cold (2) Psychological: i.e. extreme lack of social contact stimuli iii) Often injurious, unpleasant or painful but not always (1) Seyle’s quote: a painful blow and a passionate kiss can be equally stressful iv) Anything a person perceives as a threat – real or imagined (1) Arouses fear or anxiety (2) Includes emotion of grief v) Reactions and stress response varies between individuals and in one individual at different times vi) Prenatal stress (1) Occurs in developing fetus (2) i.e. fetal alcohol syndrome2) Describe the structure and function of the autonomic nervous system (M432-441, T475-485) a) Structure i) Considered part of efferent division of the Peripheral Nervous System (PNS) ii) Carries efferent signals to the autonomic or visceral effectors: cardiac muscle, smooth muscle, glandular epithelia and adipose and other tissues iii) Consists of 2 efferent divisions (1) Sympathetic Nervous System (a) Preganglionic neurons start in thoracic and lumbar segments of spinal cord- (b) Sometimes referred to as thoracolumbar division (c)
  • 2. (2) Parasympathetic Nervous System (a) Preganglionic neurons are in the brainstem or sacral cord (b) Referred to as craniosacral division b) Function i) Major functions include: heartbeat regulation, smooth muscle contraction, glandular secretion, metabolism control to maintain homeostasis. (1) Sympathetic nervous system functions: (a) Mobilize energy stores in times of need – fight-or-flight (b) Increased heart and respiratory rate and strength of cardiac muscle contraction (c) Vasodilation of vessels to the heart , skeletal muscles, respiratory airways (d) Vasoconstriction of vessels to digestive and other organs, and of spleen and other blood reservoirs (e) Increased conversion of glycogen to glucose and breakdown of stored fats (f) Increased sweating (2) Parasympathetic Nervous System functions (a) Slow heart and respiratory rate (b) Promote digestion and elimination (c) Considered the system for “rest and repair.”3) Describe the three stages of the general adaptation syndrome (GAS) response and relate to the timing of the development of disease. (M312, T763-764) a) Alarm stage: i) Increased activity of sympathetic nervous system ii) Increased secretion of cortisol by adrenal cortex, and of norepinephrine by adrenal medulla iii) Marked reduction of lymphocytes and eosinophils = decreased immune response and allergic response iv) Increased mobilization of fats and tissue proteins = hyperglycemia b) Resistance or adaptation stage i) Adrenal cortex and medulla return to normal rates of hormone secretion ii) Sympathetic activity returns to normal iii) Successful adaptation to stressor c) Exhaustion stage i) Occurs when stress is extremely severe or occurs over a long time ii) First increased cortisol secretion then markedly decreased iii) Onset stress triad – hypertrophied adrenal cortex, atrophied lymphatic organs, bleeding ulcers
  • 3. iv) Body can no longer cope with stressor – may lead to death d) Relationship to development of disease i) Seyle believed the Stage of Exhaustion marked the onset of disease ii) He referred to these as “diseases of adaptation”4) Describe the current contribution of research to our understanding of Seyle’s GAS response (T766, figure 22-6) (M314, 315, figure 10-2 ) a) Stress is being defined more specifically as any stimulus that directly or indirectly stimulates neurons of the hypothalamus to release corticotropin-releasing hormone (CRH) and to send stimulating impulses to sympathetic centers and posterior pituitary. This activity triggers many responses that together are referred to as “stress syndrome” or “stress response.” b) Some effects are immediate(sympathetic activity – fight or flight) and some are longer term (hormonal effects.) c) See figure 22-6 on page T767 and compare to figure 22-5 on page T766.5) Define homeostasis (T19) a) The relative constancy of the normal body’s internal (fluid) environment i) Homeo = same or equal ii) Stasis = standing still b) The maintenance of relatively constant internal conditions despite changes in either the internal or the external environment characterize homeostasis c) The ability of the body to maintain homeostasis serves as a basis for understanding mechanisms of disease. d) See figure 1-12 that depicts the the body’s internal environment and systems involved in maintenance of homeostasis.6) Describe the role of catecholamines in the neuroendocrine response to stress. (M314 -316) a) The catecholamines involved are epinephrine and norepinephrine. i) Epinephrine is released from the adrenal medulla after stimulation by the sympathetic nervous system. (80%) ii) Norepinephrine is released from the locus ceruleus in the brainstem as well as the adrenal medulla (20%) b) Catecholamines mimic direct sympathetic stimulation i) Norepinephrine during stress: (1) Increases blood pressure via vasoconstrition (2) Dilates the pupils (3) Causes pilerection (4) Increases sweat gland action in armpits and palms
  • 4. ii) Epinephrine during stress: (1) Greater influence on cardiac action and metabolic regulation (2) Enhances myocardial contractility,increases heart rate, and increases venous return to the heart = increases cardiac output and blood pressure. (3) Dilates skeletal muscle blood vessels = increases oxygenation (4) Metabolically: causes transient hyperglycemia by: (a) Promoting gluconeogenesis and glycogenolysis in the liver (b) Inhibiting glycogen breakdown (c) Decreasing glucose uptake in the muscles and organs (d) Decreasing insulin release from pancreas (5) Mobilizes free fatty acids and cholesterol by: (a) Stimulating lipolysis and freeing triglycerides and fatty acids from fat stores (b) Inhibiting the degradation of circulation cholesterol to bile acids iii) Catecholamines are immunosuppressive (1) Increase numbers of NK cells but decreased responsiveness of T and B lymphocytes (2) Effect lasts only 2 hours after injection of epinephrine so to be immunosuppressive levels must be chronically elevated.7) Describe the role of cortisol in the neuroendocrine response to stress. (M316-317) a) Stress stimulates hypothalamus  releases CRH  anterior pituitary releases ACTH ACTH stimulates adrenal cortex to release cortisol. b) Cortisol effects are widespread and permissive with catecholamines resulting in: i) Increased blood glucose ii) Increased blood pressure and cardiac output iii) Increased blood levels of amino acids via protein catabolism in muscle iv) Decreased circulating lymphocytes, eosinophils, moncytes/macrophages  decreased immune and allergic responses v) Decreased protein synthesis  atrophy of lymphoid tissue and immunosuppression c) See table 10-4 page 317 for more detailed outline. 8. Describe the role of endorphins, growth hormone, prolactin, and testosterone in the stress response. a. Endorphins are proteins found in the brain that have pain-relieving capabilities like opiates and they are released into blood as part of the response to stressful stimuli such as traumatic injury and acute, intense
  • 5. stress situation (i.e. parachute jumping). In inflamed tissue, endorphin receptors on peripheral sensory nerves get activated to relive pain and in hemorrhage, b (beta) endorphin levels from the pituitary gland increase to inhibit blood pressure increase. (325 McCance)b. Growth hormone (Somatotropin) is synthesized from anterior pituitary gland and from lymphocytes and mononuclear phagocytic cells. GH affects protein, lipid, and carbohydrate metabolism and counters effects of insulin. It is involved in tissue repair and may participate in the growth and function of the immune system. GH levels increase in the blood in response to stressful physical and psychological stimuli (i.e. cardiac catherization, electroshock therapy, gastroscopy, surgery, fever, physical exercise, taking exam, viewing violent or sexually arousing films, etc). Prolonged activation of stress response (chronic stress) leads to suppression of GH. (325 McCance)c. Prolactin is released from anterior pituitary gland and other extrapituitary tissue sites including lymphoid cells. Prolactin is necessary for lactation and breast development and its receptors are present in liver, kidney, intestine, and adrenals. Prolactin levels in plasma increases as a result of stressful stimuli (i.e. surgery, pelvic exam, motion sickness, after taking exam, and after receiving sexual stimulation). Unlike GH, prolactin shows little change after exercise but similar to GH, prolactin increases with intense stimuli. Prolactin acts as a second messenger for interleukin-2 (IL-2) and have a positive influence on B cell activation and differentiation for immune function. (325 McCance)d. Testosterone is secreted by Leydig cells and it regulates male secondary sex characteristics and libido. Its level decreases after physiological and psychological stressful stimuli (i.e. ether/anestheria, surgery, marathon running, mountain climbing, respiratory failure, burn, CHF, rigorous combat training, etc) by cortisol and b (beta) endorphin. Individuals with acute illnesses, such as respiratory failure, burns, and CHF, show a marked reduction in testosterone. Estrogen depresses T cell-depended immune function and enhances B cell function but androgen suppresses both T and B cells responses leading to greater susceptibility to sepsis and mortality in males than in females.
  • 6. 9. Diagram the major interactions of the nervous, endocrine, and immune system in the stress response including all of the major chemical mediators. See pages 314-315 McCance Stressor-> limbic system -> SNS (brainstem (locus ceruleus)) -> Adrenal medulla -> norepienphrine (w/albumin) norepinephrine: increase sweat gland action, goosebumps, immune effect (increased blood pressure), increased contraction of arteriole smooth muscle, pupil dilation Stressor-> limbic system -> SNS (PVN -> LC) -> norepienphrine epinephrine: bronchodilation, increase force and rate of cardiac contraction (increase CO), increase lipolysis (increase circulating free fatty acids) -> increase circulating free fatty acids, pancreas decrease insulin-> decreased glucose uptake, increased glycagon-> increased glucogenesis, liver decreases glycogen synthesis, and increase glycogenolysis Stressor -> Hypothalamus-> Anterior Pituitary -> b-endorphins, ACTH,Prolactin, GH b (beta) endorphins: decreased pain sensation prolactin: lactation and breast development GH: increased protein synthesis, lypolysis, increased gluconeogenesis, decreased glucose uptake in muscle and adipose, decreased insulin sensitivity, increased IGH-1 ACTH-> adrenal cortex-> Cortisol-> increase blood glucose (liver), increase BP and CO, increase catabolism in muscle-> increased amino acids, increased circulating PMNs, antiimflammatory effects, promotes lypolysis in extremities, decreased lutenizing hormone (estradiol, testosterone), promotes lipogenesis in face and trunk, decreased protein synthesis-> atrophy of lymphoid tissue (immunosuppression, decreased eosinophils, lymphocytes, and macrophages) Stressor -> Hypothalamus-> Posterior Pituitary -> Vasopressin, ADH, oxytocin Vasopressin/ADH: increases water absorption in the kidney Oxytocin: increase milk let-down and uterine contraction
  • 7. 10. Discuss 3 specific links between the immune system and the neuroendocrine response to stress. 1) direct effect of CNS neuropeptides on immune cells: Neuropeptides and neuroendocrine hormones may directly control biochemical events affecting cell proliferation, differentiation, and fx or may indirectly control immune cell behavior by affecting the production of cytokines. (323) 2) stress-induced endocrine products influence immune cell and neurologic cell fx: Hypothalamic-pituitary-adrenal (HPA) axis may produce indirect effect on the CNS that modulate immune response. Increased level of circulating glucocorticoids (GCSs) may be an important mechanism in stress-related immune structure alterations and in suppression of immune system. The GCS level increases are attributable to pituitary ACTH production- a result of increased hypothalamic CRH then it increases the cortisol secretion. Cortisol fees bac to inhibit further cytokine release by macrophages and monocytes. (322) 3) immune cell products (cytokines) affect nervous and endocrine cells fx through direct and indirect pathways: Lymphocytes also are known to produce ACTH and endorphins in small amounts, which probably influence immune response in an autocrine or paracrine manner in the microenvironment of an ongoing immune response. The T cell growth factor (IL-2) can up-regulate pituitary ACTH. Immune- derived cytokines have significan influence on neuroendocrine fx, with evidence for direct and indirect cytokine effects on nervous and adrenal cell fxs. (323)Pathophysiology
  • 8. 1. Identify the physiologic rationale for the following clinical manifestation of stress: tachycardia, elevated blood pressure, dilated pupils, elevated blood sugar, pallor. (314-316 McCance) a. Tachycardia: stressor activates limbic system, which stimulates SNS to releases norepinephrine to increase contraction of arteriole smooth muscle and epinephrine increases force and rate of cardiac contraction. b. Elevated BP: stressor activates limbic system, SNS stimulated to release norepinephrine that increases BP by constricting smooth muscle in all blood vessels. Cortisol stimulates rennin release from kidneys. Increased renin increases BP by increasing extracellular volume (increase in blood plasma, lymph, interstitial fluid). Posterior pituitary releases ADH and adrenal cortex releases aldosterone that increase water retention that can also contribute to increased BP. c. Dilated pupils: eye dilation is controlled by parasympatheric and sympathetic nerve system. Like the mechanism of tachycardia, norepinephrine from stimulated SNS dilates pupils. d. Elevated blood sugar: both epinephrine and cortisol can elevate blood sugar. Epinephrine decreases glycogen sythesis, increase gluconeogenesis, and increases glycogenolysis in the liver to increase blood glucose in the system. CRH from hypothalamus stimulates anterior pituitary to make ACTH, then it stimulates adrenal cortex to increase the prduction of cortisol. Like epinephrine, cortisol stimulates liver to increase gluconeogenesis to increase blood glucose in the blood. e. Pallor: paleness in skin or mucous membrane is presented by sympathetic activity. It goes hand-in-hand with clammy and moist skin and it is affected by the vasoconstricting effect of norepinephrine. Vasocontriction decreases amount of erythrocytes in the cutanous system. (http://www.wrongdiagnosis.com/symptom/pallor.htm)2. Distinguish between effective and ineffective coping for stress
  • 9. a. Effective coping: adaptive coping strategies, especially those that are problem-focused and those that encourage seeking social support, are beneficial during stressful experiences. b. Ineffective coping: cannot manage stress demand and can lead to change in behavior resulting in potentially adverse health effects (i.e. increased smoking, change in eating habits), disturbance in sleep-wake cycle (sleep deprivation and circadian disruption affect respiratory and immune system function). It may exacerbate the effects of distress on health, thus augmenting potential for illness.3. Describe the relationship between stress and disease by analyzing the impact of stress on the following diseases: a. Coronary Artery Disease: Stress increases SNS activity, which releases epinephrine to mobilize free fatty acids and cholesterol by stimulating lipolysis, freeing triglycerides and fatty acids from fat stores, and inhibiting the degradation of circulating cholesterol to bile acids. This causes the increase in circulating free fatty acids, trigylcerides, and cholesterol and they attach on the walls of coronary arteries then the plaque accumulates over time. b. HTN: Stress increases sympathetic activity, which increases norepinephrine to constrict the vessels in blood reservoirs and dilate vessels in skeletal muscle, it increase rate and stroke volume of heart contraction for increased cardiac output, then increases systolic BP. (see Elevated BP for additional info) The chronic stress can cause cardiovascular disease, mainly arthrosclerosis due to plaque formation in the arterial blood vessels (see CAD above for mechanism) c. Peptic ulcer disease: Stress increases sympathetic activity that decreases secretion by digestive glands, decreases peristalsis, and decreased mucosal blood flow. Addionally, cortisol contributes in gastric ulceration. Stress affects hypothalamus and the anterior pituitary produces ACTH and it activates the adrenal cortex to secrete cortisol into the plasma. Among many functions of costisol, it
  • 10. promotes enough gastric secretion to cause unlceration of the gastric mucous.4. If given a case study be prepared to identify the clinical manifestation of stress, discuss the scientific rationale for these findings, and identify abnormal labs that may be stress related. Hx: • Heart palpitation/tachycardia- due to norepinephrine increasing contraction of arteriole smooth muscle and epinephrine increasing force and rate of cardiac contraction. • Dyspnea- epinephrine induces brochodilation • Indigestion (GERD)- too much gastric secretion • Constipation- decreases peristalsis by SNS • Insomnia- pineal gland blocks the production of melatonin • Diaphoresis- norepinephrine increases sweat gland action • Alertness- increased glucose arouses CNS • Unhealing wound/sores and infections - cortisol’s action on immunosuppresion • Dark yellow urine- Vasopressin/ADH/aldosterone prevents fluid loss • Decrease in libido- cortisol and b-endorphins decrease testosterone • Fatigue- patient reached stage of exhaustion by breaking down the compensatory mechanisms and homeostasis Examination: • Dilated pupil- the SNS produces norepinephrine to dilate pupils • Elevated blood pressure- see 1b • Elevated glucose- see 1d • Elevated GH- by stimulation of anterior pituitary
  • 11. • Elevated CRH- by stimulation of hypothalamus• Elevated ACTH- by stimulation of anterior pituitary• Elevated albumin- catacholamines circulate bound to albumin• Elevated free fatty acids- epinephrine increases lypolysis to circulate free fatty acids• Elevated blood level of amino acids (total serum protein (?))- cortisol increases protein catabolism for amino acid accessibility• Increased parasites in stool sample- cortisol’s effect on immunosuppression increases parasite growth in stool• Decreased WBC (decreased lymphocytes, monocytes, eosinophils)

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