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BSC2086_ Chapter 17

Two systems—the nervous and endocrine communicate with neurotransmitters and hormones - Regulate homeostasis
Endocrine system glands, tissues, and cells that secrete hormones
Hormones chemical messengers that are transported by the bloodstream
Exocrine glands Have ducts Extracellular effects
Endocrine glands No ducts Intracellular effects
Major Organs of the Endocrine System Pineal gland Pituitary gland Hypothalamus Thyroid gland Thymus Adrenal gland Pancreas Gonads: Ovary (female) Testis (male) Parathyroid glands
Comparison of Nervous and Endocrine Systems Both serve for internal communication - Nervous: both electrical and chemical - Endocrine: only chemical Speed and persistence of response - Nervous: fast - Endocrine: slow
Comparison of Nervous and Endocrine Systems Adaptation to long-term stimuli - Nervous: quickly - Endocrine: slowly Area of effect - Nervous: targeted and specific (one organ) - Endocrine: general, widespread effects (many organs)
Major Chemical Classes of Hormones Steroid hormones Monoamines Peptide hormones
Monoamines Thyroxine Epinephrine
Steroid hormones Testosterone Estradiol
Peptide hormones Angiotensin II Oxytocin Antidiuretic hormone
Hormones stimulate only those cells that have receptors for them
Receptors On plasma membrane, in the cytoplasm, or in the nucleus
Receptors act like switches turning on metabolic pathways when hormone binds to them
Hydrophilic hormones - Cannot penetrate into target cell - Must stimulate physiology indirectly - Most monoamines and peptides
Hydrophobic hormones - Penetrate plasma membrane and enter nucleus - Act on the genes changing target cell physiology - Estrogen, progesterone, thyroid hormone
Synergistic effects Synergism between FSH and testosterone on sperm production
Permissive effects Estrogen prepares uterus for action of progesterone
Antagonistic effects Insulin lowers blood glucose and glucagon raises it
Hypothalamic hormones - Gonadotropin-releasing hormone - Thyrotropin-releasing hormone - Corticotropin-releasing hormone - Prolactin-inhibiting hormone - Growth hormone-releasing hormone - Somatostatin
Anterior lobe hormones - Follicle-stimulating hormone - Luteinizing hormone - Thyroid-stimulating hormone (thyrotropin) - Adrenocorticotropic hormone - Prolactin - Growth hormone
Neurohypophysis ( Posterior Pituitary) hormones Produced in hypothalamus (released by PP) - Oxytocin - Antidiuretic hormone (ADH, vasopressin)
Positive Feedback TRH->TSH->TH->Target organ
GH - induces the liver and other tissue to produce growth stimulants called insulin-like growth factors (IGF-I AND IGF-II) or somatomedins
Somatomedins stimulate target cells in diverse tissue - Mostly IGF-I - IGF-II important in fetal growth
Mechanisms of GH-IGF - Protein synthesis - Lipid metabolism (protein sparring effect) - Carbohydrate metabolism ( glucose sparring effect) - Electrolyte Balance
Stress caused by any situation that upsets homeostasis and threatens one's physical or emotional well-being - Injury, surgery, infection, intense exercise, pain, grief, depression, anger, etc.
General adaptation syndrome (GAS) Three stages: - Alarm reaction (epinephrine and norepinephrine) - Stage of resistance (cortisol) - Stage of exhaustion (can lead to death)
Pituitary Disorders Head trauma affects pituitary gland's ability to secrete ADH - Diabetes insipidus
GH Disorders - Hypersecretion when young: gigantism - Hyposecretion when young: pituitary dwarfism - Hypersecretion as adult: acromegaly
Thyroid Disorders Goiter Myxedema Graves disease
Goiter any pathological enlargement of the thyroid gland
Myxedema Hypothyroidism
Graves disease Hyperthyroidism - may have bulging eyes later
Adrenal Disorders Cushing syndrome Addison's Disease
Cushing syndrome excess cortisol secretion - Hyperglycemia, hypertension, weakness, edema
Addison's Disease insufficient gluco- and mineralocorticoids
Diabetes Mellitus - Disruption of fuel metabolism due to hyposecretion or inaction of insulin - Elevated blood glucose, glucose and ketones in urine
Polyuria increased urine
Polydipsia thirst
Polyphagia hunger
Type 1 (IDDM)—5-10% Treated with insulin
Type 2 (NIDDM)—90-95% - Problem is insulin resistance (target cells do not respond) - Treated with weight-loss program and exercise
Pathogenesis — cells cannot absorb glucose, rely on fat and proteins for energy - Fat catabolism increases free fatty acids and ketones in blood - Ketoacidosis (ketones decr pH)
Created by: 624817371005582
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