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Homeostasis and The Stress Response. Homeostasis. Homeostasis.
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Homeostasis • Definition: The tendency of an organism or a cell to regulate its internalconditions, usually by a system of feedbackcontrols, so as to stabilize health and functioning, regardless of the outside changing conditions. http://www.biology-online.org/dictionary/Homeostasis • Influences that tend to deregulate internal conditions are termed “stressors” • This is a different definition than we are used to hearing • Stressors can be physical, emotional, environmental, etc. • Compensatory mechanisms to counteract the effect(s) of stressors involve • Autonomic nervous system • Adrenal cortex • Renin-angiotensin-aldosterone system (RAAS) • Many others.
Stressors Anxiety Procedures Disease Old age Obesity Malnutrition Pain Fear Trauma Prolonged Exertion Heat Anger Low 02 supply Cold Noise Treatments Lack of sleep Surgery Drugs Radiation Infection
Neuroendocrine Pathways and Physiologic Responses to StressDescription
Neuroendrocrine Pathways and Physiologic Responses to StressDescription • Shows the different responses to stressors • May perceive stressor in the cerebral cortex or the stressor may be unconscious • Activating the RAS (the part of the brain that keeps up awake) – leads to increased muscle tension and alertness • Limbic system produces the emotional response • The locus ceruleus activates the ANS (sympathetic nervous system), which activates the adrenal medulla and the activation of the RAAS
Neuroendrocrine Pathways and Physiologic Responses to StressDiagram
Neuroendrocrine Pathways and Physiologic Responses to Stress (Corticotropin Releasing Factor) (Adrenocorticotropic Hormone) Activation of the RAAS Adapted from Porth, 2011, Essentials of Pathophysiology,3rd ed., Lippincott, p. 213
Activation of the Sympathetic Nervous System (SNS) • Heart rate • Blood pressure • Cool skin • All of the blood is being shunted away form the skin to the skeletal muscle • Diaphoresis to keep body cool • Pupil dilation • Blood glucose to have fuel for muscle • Peristalsis • Urine output • Do not want to devote metabolic energy to urine formation
Release of Norepinephrine Norepinephrine 1 1 2 1 Pupil Dilation Vasoconstriction of arteries and veins (↑Venous return to the heart/CO and ↑Blood Pressure) • Heart rate • Contractility • Release of renin • All of these increase blood • pressure
Epinephrine Released by • Adrenal Medulla • Activates alpha 1 and • alpha 2 as well as beta • 2 receptors Epinephrine 1 2 1 1 • Vasoconstriction • Blood pressure • Venous return/CO Pupil dilation 2 Dilation of skeletal muscle vascular beds and bronchi Heart rate Contractility Release of renin
Epinephrine 2 2 Lipolysis of triglycerides Degradation of cholesterol to bile Salts • Free fatty acids that can • be used for ATP synthesis • - maximizes energy • production Cholesterol to be available for the repair of cell membranes
Epinephrine 2 Skeletal Muscle 2 Protein breakdown/amino acid release Liver Gluconeogenesis Glycogen Breakdown Blood Glucose
Norepinephrine stimulates beta-1 receptors to cause: • Lipolysis of triglyerides – beta 2 • Vasoconstriction of blood vessels - alpha • Decreased heart rate – muscarinic receptors • Renin release
Release of Renin and ADH (Antidiuretic Hormone) • Renin is released in response to SNS stimulation of beta-1 receptors in the kidney • Release of renin initiates renin-angiotensin-aldosterone system (RAAS) • Angiotensin II causes vasoconstriction leading to Blood pressure • Aldosterone causes increased reabsorption of water in the kidneys causing venous return → cardiac output • Aldosterone has a steroid structure, like cortisol, and is referred to as a mineralocorticoid. ----------------------------------------------------------------------- • ADH (antidiuretic hormone) is released from the posterior pituitary in response to SNS stimulation • ADH causes increased reabsorption of water in the kidneys causing venous return → cardiac output
ReninAngiotensinAldosterone System (RAAS)Diagram Must know this!!! Porth, 2011, Essentials of Pathophysiology, 3rd ed., Lippincott, p. 420.
Hypothalamus-Anterior Pituitary Function Porth, 2007, Essential of Pathophysiology, 2nd ed., Lippincott, p. 666
Hypothalamus-Anterior Pituitary FunctionDescription • The hypothalamus and the anterior pituitary are important in the stress response • Cells release releasing factors that travel through the vessels and cause cells in the anterior pituitary to release tropic hormones • Go to target glands to release peripheral hormones • The hormone has a negative feedback on the anterior pituitary and the hypothalamus to decrease the hormone
Feedback Inhibition Diagram Porth, Essentials of Pathophysiology, 3rd ed., 2011, Lippincott, p.770.
Peripheral Glands Controlled by the Pituitary Porth, 2011, Essential of Pathophysiology, 3rded., Lippincott, p. 770
Regulation of Cortisol Synthesis and SecretionDescription • Adrenals do not store glucocorticoids • Amount released = amount made • Regulated by negative feedback loop • Circadian rhythm • bedtime, sleep, peak on awakening, during day • Stress increases CRH synthesis and release. • Some of the inputs into the hypothalamus include stress and circadian rhythms • Also regulated by negative feedback from cortisol in the periphery • Also acts on cells in the anterior pituitary • ACTH circulates all over the body, such as the adrenal cortex • Biological effects of cortisol are on nearly every body cell • Cortisol secretion is low at night, at its highest in the morning
Regulation of Cortisol Synthesis and Secretion Lehne, 2009, Pharmacology for Nursing Care, 7th ed., Elsevier, p. 711
Diurnal Secretion of Cortisol Stewart, Paul, 2003, The adrenal cortex in Larson, et al, eds., Williams’ Textbook of Endocrinology, Saunders. When we administer corticosteroids pharmacologically, we try to mimic this diurnal rhythm.
CortisolPhysiologic Effects • Carbohydrate metabolism • Fat metabolism • Protein metabolism • Cardiovascular • Central nervous system • Stress
CortisolCarbohydrate Metabolism • Carbohydrate Metabolism • Gluconeogenesis – the synthesis of new glucose molecules in the liver • Peripheral glucose utilization in the periphery • Increased gluconeogenesis and decreased peripheral glucose utilization will increase glucose levels in the body • glucose uptake muscle/adipose tissue • Promote glucose storage (glycogen) All these make glucose more available to the brain!
Glucocorts • Supplying the brain with glucose is essential for survival. • Glucocorts help meet this need with CHO metabolism thru the following 4 ways. • All 4 actions increase glucose availablility during fasting and thereby ensure the brain will not be deprived of its primary source of energy. • When present in chronically high levels for a prolonged period of time, glucocorts produce symptoms much like those of diabetics. • Pro metab: promote pro breakdown. • If present at high levels for prolonged pd of time, glucorts will cause a thinning of skin, muscle wasting, and negative nitrogen balance • Fat metab: glucocorts promote lipolysis (fat breakdown). • When present at high levels for an extended time, glucocorts cause fat redistribution, given the pt a potbelly, moon face, and buffalo hump on the back.
CortisolProtein Metabolism • Promote catabolism • Amino acids provide substrate for hepatic gluconeogenesis
CortisolFat Metabolism • Promote lipolysis • Increases the amount of energy that is available to the cells • Free fatty acids provide substrate for the Krebs cycle.
