{"id":5097,"date":"2025-11-26T20:27:14","date_gmt":"2025-11-27T01:27:14","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=5097"},"modified":"2025-12-07T21:48:56","modified_gmt":"2025-12-08T02:48:56","slug":"endocrine-dysfunction","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/endocrine-dysfunction\/","title":{"raw":"9p5 Endocrine Homeostasis and Dysfunction","rendered":"9p5 Endocrine Homeostasis and Dysfunction"},"content":{"raw":"<strong>Main Functions of Key Hormones<\/strong>\r\n<ul>\r\n \t<li>Proper hormone levels are vital; underproduction or insensitivity results in dysfunction.<\/li>\r\n \t<li><strong>Excess production<\/strong> can cause tissue damage or abnormal growth.<\/li>\r\n<\/ul>\r\n<h1><strong>Common Endocrine Disorders Overview<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Growth hormone deficiency:<\/strong> Causes less growth in childhood.<\/li>\r\n \t<li><strong>Excess growth hormone:<\/strong> Causes excessive height or acromegaly.<\/li>\r\n \t<li><strong>ADH deficiency:<\/strong> Known as <strong>diabetes insipidus<\/strong>:\r\n<ul>\r\n \t<li>Causes\u00a0<strong>excess urination<\/strong>\u00a0(polyuria).<\/li>\r\n \t<li>Leads to\u00a0<strong>dehydration<\/strong>\u00a0and\u00a0<strong>thirst<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Excess ADH:<\/strong> Causes <strong>SIADH<\/strong>:\r\n<ul>\r\n \t<li>Leads to water retention, weight gain, and possible edema.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Thyroid hormone imbalance:<\/strong>\r\n<ul>\r\n \t<li><strong>Hypothyroidism:<\/strong>\u00a0Slows metabolic processes, causes cold intolerance, developmental delays.<\/li>\r\n \t<li><strong>Hyperthyroidism:<\/strong>\u00a0Speeds up metabolism, causes heat intolerance, weight loss, Graves' disease.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Parathyroid hormone imbalance:<\/strong>\r\n<ul>\r\n \t<li><strong>Hypoparathyroidism:<\/strong>\u00a0Bones become overly dense, neurological issues.<\/li>\r\n \t<li><strong>Hyperparathyroidism:<\/strong>\u00a0Bones weaken and become brittle, neurological issues.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h2><strong>Type I Diabetes Mellitus (Insulin Deficiency)<\/strong><\/h2>\r\n<ul>\r\n \t<li><strong>Type 1:<\/strong> Autoimmune destruction of pancreatic beta cells.\r\n<ul>\r\n \t<li>Results in\u00a0<strong>insufficient insulin production<\/strong>.<\/li>\r\n \t<li>Without insulin cells of the body are unable to\u00a0insert GLUT4 glucose transporters into their cell membranes to allow for glucose uptake by cells.\r\n<ul>\r\n \t<li>Causes high blood glucose levels<\/li>\r\n \t<li>Causes lipolysis which increases blood lipid levels<\/li>\r\n \t<li>Causes gluconeogenesis and glycogenolysis which increases blood glucose levels<\/li>\r\n \t<li>Causes glucosuria, polyuria, dehydration, polydipsia, and polyphagia<\/li>\r\n \t<li>Can cause ketoacidosis and electrolyte imbalances<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>Causes\u00a0<strong>high blood glucose<\/strong> levels, which are toxic to blood vessel walls.<\/li>\r\n \t<li>Affects all cells requiring glucose<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1>Type II Diabetes Mellitus (Insulin Insensitivity \/ Resistance)<\/h1>\r\n<ul>\r\n \t<li><strong>Type II:\u00a0<\/strong> Insulin insensitivity, leads to cells being less responsive to insulin and unable to insert GLUT4 glucose transporters into their cell membranes to allow for glucose uptake by cells.\r\n<ul>\r\n \t<li>Causes high blood glucose levels<\/li>\r\n \t<li>Causes lipolysis which increases blood lipid levels<\/li>\r\n \t<li>Causes gluconeogenesis and glycogenolysis which increases blood glucose levels<\/li>\r\n \t<li>Causes glucosuria, polyuria, dehydration, polydipsia, and polyphagia<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Excess Insulin Production<\/strong><\/h1>\r\nRare, but results in <strong>low blood glucose<\/strong> levels, risking <strong>hypoglycemia<\/strong> and <strong>brain dysfunction<\/strong>.\r\n<h1><strong>Summary<\/strong><\/h1>\r\n<ul>\r\n \t<li>Endocrine disorders often result from hormone underproduction or target tissue insensitivity.<\/li>\r\n \t<li>Recognizing symptoms helps in diagnosing and treating these issues through hormone supplements or blockers.<\/li>\r\n \t<li>Maintaining hormone balance is crucial for health and proper physiological functioning.<\/li>\r\n<\/ul>\r\n&nbsp;\r\n\r\n&nbsp;\r\n\r\nThis table illustrates the clinical implications of endocrine dysfunction.\r\n<table class=\"grid\" style=\"border-collapse: collapse;width: 100%\" border=\"0\">\r\n<tbody>\r\n<tr>\r\n<td style=\"width: 19.6787%\"><strong>Hormone<\/strong><\/td>\r\n<td style=\"width: 20.3481%\"><strong>Underproduction of Hormone or Tissue Insensitivity to Hormone<\/strong><\/td>\r\n<td style=\"width: 19.411%\"><strong>Signs and Symptoms<\/strong><\/td>\r\n<td style=\"width: 21.0174%\"><strong>Overproduction of Hormone or Hypersensitivity to Hormone<\/strong><\/td>\r\n<td style=\"width: 19.411%\"><strong>Signs and Symptoms<\/strong><\/td>\r\n<\/tr>\r\n<tr>\r\n<td style=\"width: 19.6787%\"><strong>Growth Hormone (GH)<\/strong><\/td>\r\n<td style=\"width: 20.3481%\">Pituitary gland growth failure<\/td>\r\n<td style=\"width: 19.411%\">Delayed growth; Abnormal fat distribution; Low blood glucose hours after a meal<\/td>\r\n<td style=\"width: 21.0174%\">Gigantism (if GH overproduction occurs during childhood);\r\n\r\nAcromegaly (if GH overproduction occurs during adulthood)<\/td>\r\n<td style=\"width: 19.411%\">Excessive growth in height during childhood;\r\n\r\nExcessive thickness of bone during adulthood<\/td>\r\n<\/tr>\r\n<tr>\r\n<td style=\"width: 19.6787%\"><strong>Antidiuretic (ADH) <\/strong><\/td>\r\n<td style=\"width: 20.3481%\">Diabetes insipidus<\/td>\r\n<td style=\"width: 19.411%\">Polyuria, dehydration, thirst<\/td>\r\n<td style=\"width: 21.0174%\">SIADH (Syndrome of Inappropriate ADH secretion)<\/td>\r\n<td style=\"width: 19.411%\">Increased body weight and water content<\/td>\r\n<\/tr>\r\n<tr>\r\n<td style=\"width: 19.6787%\"><strong>Thyroxine (T4) Triiodothyronine (T3)<\/strong><\/td>\r\n<td style=\"width: 20.3481%\">Hypothyroidism;\r\n\r\nInfantile hypothyroidism;\r\n\r\nMyxedema<\/td>\r\n<td style=\"width: 19.411%\">Low metabolic rate; Low body temperature; Impaired physical &amp; mental development<\/td>\r\n<td style=\"width: 21.0174%\">Hyperthyroidism;\r\n\r\nGraves Disease<\/td>\r\n<td style=\"width: 19.411%\">High metabolic Rate; High body temperature<\/td>\r\n<\/tr>\r\n<tr>\r\n<td style=\"width: 19.6787%\"><strong>Parathyroid Hormone<\/strong><\/td>\r\n<td style=\"width: 20.3481%\">Hypoparathyroidism<\/td>\r\n<td style=\"width: 19.411%\">Muscular weakness;\r\n\r\nNeurological problems;\r\n\r\nFormation of dense bones and tetany due to low blood Ca2+ levels (because osteoclast activity it too low!)<\/td>\r\n<td style=\"width: 21.0174%\">Hyperparathyroidism<\/td>\r\n<td style=\"width: 19.411%\">Neurologic, mental, muscular problems due to high blood Ca2+ levels and weak and brittle bones (because osteoclast activity it too high!)<\/td>\r\n<\/tr>\r\n<tr>\r\n<td style=\"width: 19.6787%\"><strong>Insulin<\/strong><\/td>\r\n<td style=\"width: 20.3481%\">Type 1 Diabetes Mellitus (autoimmune disease)<\/td>\r\n<td style=\"width: 19.411%\">High blood glucose, high blood lipid levels, increased lipolysis in adipose cells, increased glycogenolysis, increased gluconeogenesis, glycosuria, ketonemia, polyuria, polyphagia, polydipsia<\/td>\r\n<td style=\"width: 21.0174%\">Excess insulin production or administration<\/td>\r\n<td style=\"width: 19.411%\">Low blood glucose levels, possibly causing coma<\/td>\r\n<\/tr>\r\n<tr>\r\n<td style=\"width: 19.6787%\"><\/td>\r\n<td style=\"width: 20.3481%\"><\/td>\r\n<td style=\"width: 19.411%\"><\/td>\r\n<td style=\"width: 21.0174%\"><\/td>\r\n<td style=\"width: 19.411%\"><\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>","rendered":"<p><strong>Main Functions of Key Hormones<\/strong><\/p>\n<ul>\n<li>Proper hormone levels are vital; underproduction or insensitivity results in dysfunction.<\/li>\n<li><strong>Excess production<\/strong> can cause tissue damage or abnormal growth.<\/li>\n<\/ul>\n<h1><strong>Common Endocrine Disorders Overview<\/strong><\/h1>\n<ul>\n<li><strong>Growth hormone deficiency:<\/strong> Causes less growth in childhood.<\/li>\n<li><strong>Excess growth hormone:<\/strong> Causes excessive height or acromegaly.<\/li>\n<li><strong>ADH deficiency:<\/strong> Known as <strong>diabetes insipidus<\/strong>:\n<ul>\n<li>Causes\u00a0<strong>excess urination<\/strong>\u00a0(polyuria).<\/li>\n<li>Leads to\u00a0<strong>dehydration<\/strong>\u00a0and\u00a0<strong>thirst<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Excess ADH:<\/strong> Causes <strong>SIADH<\/strong>:\n<ul>\n<li>Leads to water retention, weight gain, and possible edema.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Thyroid hormone imbalance:<\/strong>\n<ul>\n<li><strong>Hypothyroidism:<\/strong>\u00a0Slows metabolic processes, causes cold intolerance, developmental delays.<\/li>\n<li><strong>Hyperthyroidism:<\/strong>\u00a0Speeds up metabolism, causes heat intolerance, weight loss, Graves&#8217; disease.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Parathyroid hormone imbalance:<\/strong>\n<ul>\n<li><strong>Hypoparathyroidism:<\/strong>\u00a0Bones become overly dense, neurological issues.<\/li>\n<li><strong>Hyperparathyroidism:<\/strong>\u00a0Bones weaken and become brittle, neurological issues.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h2><strong>Type I Diabetes Mellitus (Insulin Deficiency)<\/strong><\/h2>\n<ul>\n<li><strong>Type 1:<\/strong> Autoimmune destruction of pancreatic beta cells.\n<ul>\n<li>Results in\u00a0<strong>insufficient insulin production<\/strong>.<\/li>\n<li>Without insulin cells of the body are unable to\u00a0insert GLUT4 glucose transporters into their cell membranes to allow for glucose uptake by cells.\n<ul>\n<li>Causes high blood glucose levels<\/li>\n<li>Causes lipolysis which increases blood lipid levels<\/li>\n<li>Causes gluconeogenesis and glycogenolysis which increases blood glucose levels<\/li>\n<li>Causes glucosuria, polyuria, dehydration, polydipsia, and polyphagia<\/li>\n<li>Can cause ketoacidosis and electrolyte imbalances<\/li>\n<\/ul>\n<\/li>\n<li>Causes\u00a0<strong>high blood glucose<\/strong> levels, which are toxic to blood vessel walls.<\/li>\n<li>Affects all cells requiring glucose<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1>Type II Diabetes Mellitus (Insulin Insensitivity \/ Resistance)<\/h1>\n<ul>\n<li><strong>Type II:\u00a0<\/strong> Insulin insensitivity, leads to cells being less responsive to insulin and unable to insert GLUT4 glucose transporters into their cell membranes to allow for glucose uptake by cells.\n<ul>\n<li>Causes high blood glucose levels<\/li>\n<li>Causes lipolysis which increases blood lipid levels<\/li>\n<li>Causes gluconeogenesis and glycogenolysis which increases blood glucose levels<\/li>\n<li>Causes glucosuria, polyuria, dehydration, polydipsia, and polyphagia<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Excess Insulin Production<\/strong><\/h1>\n<p>Rare, but results in <strong>low blood glucose<\/strong> levels, risking <strong>hypoglycemia<\/strong> and <strong>brain dysfunction<\/strong>.<\/p>\n<h1><strong>Summary<\/strong><\/h1>\n<ul>\n<li>Endocrine disorders often result from hormone underproduction or target tissue insensitivity.<\/li>\n<li>Recognizing symptoms helps in diagnosing and treating these issues through hormone supplements or blockers.<\/li>\n<li>Maintaining hormone balance is crucial for health and proper physiological functioning.<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>This table illustrates the clinical implications of endocrine dysfunction.<\/p>\n<table class=\"grid\" style=\"border-collapse: collapse;width: 100%\">\n<tbody>\n<tr>\n<td style=\"width: 19.6787%\"><strong>Hormone<\/strong><\/td>\n<td style=\"width: 20.3481%\"><strong>Underproduction of Hormone or Tissue Insensitivity to Hormone<\/strong><\/td>\n<td style=\"width: 19.411%\"><strong>Signs and Symptoms<\/strong><\/td>\n<td style=\"width: 21.0174%\"><strong>Overproduction of Hormone or Hypersensitivity to Hormone<\/strong><\/td>\n<td style=\"width: 19.411%\"><strong>Signs and Symptoms<\/strong><\/td>\n<\/tr>\n<tr>\n<td style=\"width: 19.6787%\"><strong>Growth Hormone (GH)<\/strong><\/td>\n<td style=\"width: 20.3481%\">Pituitary gland growth failure<\/td>\n<td style=\"width: 19.411%\">Delayed growth; Abnormal fat distribution; Low blood glucose hours after a meal<\/td>\n<td style=\"width: 21.0174%\">Gigantism (if GH overproduction occurs during childhood);<\/p>\n<p>Acromegaly (if GH overproduction occurs during adulthood)<\/td>\n<td style=\"width: 19.411%\">Excessive growth in height during childhood;<\/p>\n<p>Excessive thickness of bone during adulthood<\/td>\n<\/tr>\n<tr>\n<td style=\"width: 19.6787%\"><strong>Antidiuretic (ADH) <\/strong><\/td>\n<td style=\"width: 20.3481%\">Diabetes insipidus<\/td>\n<td style=\"width: 19.411%\">Polyuria, dehydration, thirst<\/td>\n<td style=\"width: 21.0174%\">SIADH (Syndrome of Inappropriate ADH secretion)<\/td>\n<td style=\"width: 19.411%\">Increased body weight and water content<\/td>\n<\/tr>\n<tr>\n<td style=\"width: 19.6787%\"><strong>Thyroxine (T4) Triiodothyronine (T3)<\/strong><\/td>\n<td style=\"width: 20.3481%\">Hypothyroidism;<\/p>\n<p>Infantile hypothyroidism;<\/p>\n<p>Myxedema<\/td>\n<td style=\"width: 19.411%\">Low metabolic rate; Low body temperature; Impaired physical &amp; mental development<\/td>\n<td style=\"width: 21.0174%\">Hyperthyroidism;<\/p>\n<p>Graves Disease<\/td>\n<td style=\"width: 19.411%\">High metabolic Rate; High body temperature<\/td>\n<\/tr>\n<tr>\n<td style=\"width: 19.6787%\"><strong>Parathyroid Hormone<\/strong><\/td>\n<td style=\"width: 20.3481%\">Hypoparathyroidism<\/td>\n<td style=\"width: 19.411%\">Muscular weakness;<\/p>\n<p>Neurological problems;<\/p>\n<p>Formation of dense bones and tetany due to low blood Ca2+ levels (because osteoclast activity it too low!)<\/td>\n<td style=\"width: 21.0174%\">Hyperparathyroidism<\/td>\n<td style=\"width: 19.411%\">Neurologic, mental, muscular problems due to high blood Ca2+ levels and weak and brittle bones (because osteoclast activity it too high!)<\/td>\n<\/tr>\n<tr>\n<td style=\"width: 19.6787%\"><strong>Insulin<\/strong><\/td>\n<td style=\"width: 20.3481%\">Type 1 Diabetes Mellitus (autoimmune disease)<\/td>\n<td style=\"width: 19.411%\">High blood glucose, high blood lipid levels, increased lipolysis in adipose cells, increased glycogenolysis, increased gluconeogenesis, glycosuria, ketonemia, polyuria, polyphagia, polydipsia<\/td>\n<td style=\"width: 21.0174%\">Excess insulin production or administration<\/td>\n<td style=\"width: 19.411%\">Low blood glucose levels, possibly causing coma<\/td>\n<\/tr>\n<tr>\n<td style=\"width: 19.6787%\"><\/td>\n<td style=\"width: 20.3481%\"><\/td>\n<td style=\"width: 19.411%\"><\/td>\n<td style=\"width: 21.0174%\"><\/td>\n<td style=\"width: 19.411%\"><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n","protected":false},"author":1370,"menu_order":11,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[],"contributor":[60],"license":[57],"class_list":["post-5097","chapter","type-chapter","status-web-only","hentry","contributor-zoe-soon","license-cc-by-nc-sa"],"part":63,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5097","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":4,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5097\/revisions"}],"predecessor-version":[{"id":5251,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5097\/revisions\/5251"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/63"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5097\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=5097"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=5097"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=5097"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=5097"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}