{"id":5117,"date":"2025-11-26T23:16:25","date_gmt":"2025-11-27T04:16:25","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=5117"},"modified":"2025-12-07T21:47:34","modified_gmt":"2025-12-08T02:47:34","slug":"type-i-diabetes-mellitus","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/type-i-diabetes-mellitus\/","title":{"raw":"9p9 Type I Diabetes Mellitus","rendered":"9p9 Type I Diabetes Mellitus"},"content":{"raw":"<h1><strong>Overview<\/strong><\/h1>\r\n<ul>\r\n \t<li>Also called\u00a0<strong>insulin-dependent diabetes mellitus<\/strong>\u00a0(IDDM).<\/li>\r\n \t<li>Formerly known as\u00a0<strong>juvenile diabetes<\/strong>\u00a0due to early onset, typically during childhood.<\/li>\r\n \t<li>Less common than Type II, accounting for about\u00a0<strong>10%<\/strong>\u00a0of diabetes cases.<\/li>\r\n \t<li>Usually <strong>more severe<\/strong> because of\u00a0<strong>acute complications<\/strong>\u00a0if blood glucose is not well-controlled.<\/li>\r\n \t<li><strong>Body weight:<\/strong>\u00a0Usually\u00a0<strong>thin<\/strong>\u00a0due to increased catabolism caused by lack of insulin.<\/li>\r\n<\/ul>\r\n<h1><strong>Causes<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Autoimmune destruction<\/strong> of pancreatic beta cells in the islets of Langerhans.<\/li>\r\n \t<li>Leads to\u00a0<strong>little or no insulin production<\/strong>.<\/li>\r\n \t<li>Thought to be triggered by several possible factors:\r\n<ul>\r\n \t<li><strong>Viral exposures:<\/strong>\u00a0Epstein-Barr virus, cytomegalovirus, mumps.<\/li>\r\n \t<li><strong>Genetics:<\/strong> Runs in families (family history)<\/li>\r\n \t<li><strong>Geographic factors:<\/strong>\u00a0Higher prevalence away from the equator, e.g., Finland.<\/li>\r\n \t<li>Not linked to\u00a0<strong>obesity<\/strong>\u00a0(unlike Type II).<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Typical Onset:<\/strong><\/h1>\r\n<ul>\r\n \t<li>Rapid development in children.<\/li>\r\n \t<li>Can occur in adults as a\u00a0<strong>latent autoimmune diabetes<\/strong>\u00a0variant.<\/li>\r\n<\/ul>\r\n<h1><strong>Pathophysiology:<\/strong><\/h1>\r\n<ul>\r\n \t<li>Lack of\u00a0<strong>insulin<\/strong> prevents <strong>glucose entry<\/strong> into cells,\r\n<ul>\r\n \t<li>as cell's require insulin to insert GLUT4 glucose transporters into their cell membranes.<\/li>\r\n \t<li>leading to <strong>high blood<\/strong> <strong>glucose levels<\/strong>\u00a0(<strong>hyperglycemia<\/strong>).<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Cells<\/strong>\u00a0become\u00a0<strong>starved for glucose<\/strong>, impairing ATP production.<\/li>\r\n \t<li>Excess glucose\u00a0<strong>diffuses into urine<\/strong>, drawing water and causing\u00a0<strong>polyuria<\/strong>,\u00a0causing<\/li>\r\n \t<li><strong>Dehydration<\/strong>\u00a0triggers\u00a0<strong>thirst<\/strong>\u00a0(polydipsia).<\/li>\r\n \t<li>The body responds by\u00a0<strong>breaking down proteins and fats<\/strong>\u00a0for energy:\r\n<ul>\r\n \t<li><strong>Gluconeogenesis<\/strong>: Produces glucose from proteins and fats.<\/li>\r\n \t<li><strong>Lipolysis<\/strong>: Leads to high\u00a0<strong>lipid levels<\/strong>\u00a0(<strong>lipidemia<\/strong>).<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<strong>Effects on the Body<\/strong>\r\n<ul>\r\n \t<li><strong>Muscle wasting<\/strong>\u00a0due to protein breakdown.<\/li>\r\n \t<li><strong>High blood lipids<\/strong>\u00a0increase risk of\u00a0<strong>atherosclerosis<\/strong>.<\/li>\r\n \t<li><strong>Ketone production<\/strong>\u00a0causes\u00a0<strong>ketosis<\/strong>\u00a0and potentially\u00a0<strong>ketoacidosis<\/strong>:\r\n<ul>\r\n \t<li>Blood becomes\u00a0<strong>acidic<\/strong>.<\/li>\r\n \t<li>Ketones and glucose are\u00a0<strong>excreted in urine<\/strong>\u00a0(ketonuria and glucosuria).<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Signs and Symptoms:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Polydipsia:<\/strong>\u00a0 Increased <strong>thirst<\/strong> (due to dehydration)<\/li>\r\n \t<li><strong>Polyphagia:<\/strong>\u00a0 Increased <strong>hunger<\/strong><\/li>\r\n \t<li><strong>Polyuria:<\/strong>\u00a0 Increased <strong>urine volume<\/strong> (due to <strong>glucosuria<\/strong> and osmotic diuresis)<\/li>\r\n \t<li>Fatigue (due to cell's reduced ability to uptake glucose)<\/li>\r\n \t<li>Blurred vision (due to retinopathies and diabetic cataracts)<\/li>\r\n \t<li>Slowed healing of wounds (due to cell's reduced ability to uptake glucose)<\/li>\r\n<\/ul>\r\n<h2><strong>Diagnostic Blood Tests:<\/strong><\/h2>\r\n<ol>\r\n \t<li><strong>Glycated hemoglobin (A1c) test<\/strong>\r\n<ul>\r\n \t<li>Measures the percentage of hemoglobin with blood sugar attached.<\/li>\r\n \t<li>Reflects\u00a0<strong>blood glucose control over 2-3 months<\/strong>.<\/li>\r\n \t<li>Levels\u00a0<strong>above 6.5%<\/strong>\u00a0suggest diabetes.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Random blood sugar test<\/strong>\r\n<ul>\r\n \t<li>Blood sample taken randomly, regardless of fasting.<\/li>\r\n \t<li>Blood glucose\u00a0<strong>above 110 mg\/dL<\/strong>\u00a0indicates abnormality.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Fasting blood sugar test<\/strong>\r\n<ul>\r\n \t<li>Fasting for 12 hours before testing.<\/li>\r\n \t<li>Normal:\u00a0<strong>&lt;100 mg\/dL<\/strong>.<\/li>\r\n \t<li>Diabetic:\u00a0<strong>&gt;125 mg\/dL<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ol>\r\n<h1><strong>Treatments:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Insulin injections<\/strong>\u00a0are essential.<\/li>\r\n \t<li>No known\u00a0<strong>preventive\u00a0cause\u00a0or cure<\/strong>; management focuses on blood sugar control.\r\n<ul>\r\n \t<li><strong>Note:<\/strong>\u00a0 Pancreatic transplants are challenging, and are not curative as the underlying cause of autoimmune destruction of the pancreatic beta cells by auto-antibodies and WBCs still exists.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Complications of Uncontrolled Diabetes and Risk of Long-Term Damage:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Blood vessel damage<\/strong>\u00a0leads to:\r\n<ul>\r\n \t<li><strong>Atheromas<\/strong>\u00a0formation.<\/li>\r\n \t<li><strong>Vascular damage<\/strong> affecting organs. and putting person at risk for:\r\n<ul>\r\n \t<li><strong>Cardiovascular disease:<\/strong>\u00a0Stroke, heart attack, peripheral vascular disease.<\/li>\r\n \t<li><strong>Kidney failure<\/strong>\u00a0(due to nephropathy).<\/li>\r\n \t<li><strong>Nerve damage:<\/strong> Neuropathy<\/li>\r\n \t<li><strong>Pregnancy complications:<\/strong>\u00a0Stillbirths and miscarriages.<\/li>\r\n \t<li><strong>Increased risk of amputations<\/strong>\u00a0due to ischemia and gangrene.<\/li>\r\n \t<li><strong>Eye damage:<\/strong> Leading to blindness (diabetic retinopathy).<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n&nbsp;\r\n<ul>\r\n \t<li><strong>Blurred Vision or Vision Loss:\u00a0<\/strong>\r\n<ul>\r\n \t<li>also due to development of diabetic (sugar) cataracts<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Summary<\/strong><\/h1>\r\n<ul>\r\n \t<li>In\u00a0<strong>Type I<\/strong>,\u00a0<strong>autoimmune destruction<\/strong>\u00a0results in\u00a0<strong>insulin deficiency<\/strong>.<\/li>\r\n \t<li><strong>Autoimmune origin<\/strong> causes destruction of beta cells in pancreatic islets of Langerhans.<\/li>\r\n \t<li><strong>Blood glucose regulation<\/strong>\u00a0is severely impaired.<\/li>\r\n \t<li><strong>Rapid onset in children<\/strong>, generally non-obese.<\/li>\r\n \t<li>Requires\u00a0<strong>lifelong insulin therapy<\/strong>.<\/li>\r\n \t<li>Precursors and triggers are still under study.<\/li>\r\n \t<li>The condition leads to\u00a0<strong>vascular damage<\/strong>\u00a0affecting multiple organs and systems, emphasizing the importance of tight blood glucose control.<\/li>\r\n<\/ul>","rendered":"<h1><strong>Overview<\/strong><\/h1>\n<ul>\n<li>Also called\u00a0<strong>insulin-dependent diabetes mellitus<\/strong>\u00a0(IDDM).<\/li>\n<li>Formerly known as\u00a0<strong>juvenile diabetes<\/strong>\u00a0due to early onset, typically during childhood.<\/li>\n<li>Less common than Type II, accounting for about\u00a0<strong>10%<\/strong>\u00a0of diabetes cases.<\/li>\n<li>Usually <strong>more severe<\/strong> because of\u00a0<strong>acute complications<\/strong>\u00a0if blood glucose is not well-controlled.<\/li>\n<li><strong>Body weight:<\/strong>\u00a0Usually\u00a0<strong>thin<\/strong>\u00a0due to increased catabolism caused by lack of insulin.<\/li>\n<\/ul>\n<h1><strong>Causes<\/strong><\/h1>\n<ul>\n<li><strong>Autoimmune destruction<\/strong> of pancreatic beta cells in the islets of Langerhans.<\/li>\n<li>Leads to\u00a0<strong>little or no insulin production<\/strong>.<\/li>\n<li>Thought to be triggered by several possible factors:\n<ul>\n<li><strong>Viral exposures:<\/strong>\u00a0Epstein-Barr virus, cytomegalovirus, mumps.<\/li>\n<li><strong>Genetics:<\/strong> Runs in families (family history)<\/li>\n<li><strong>Geographic factors:<\/strong>\u00a0Higher prevalence away from the equator, e.g., Finland.<\/li>\n<li>Not linked to\u00a0<strong>obesity<\/strong>\u00a0(unlike Type II).<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Typical Onset:<\/strong><\/h1>\n<ul>\n<li>Rapid development in children.<\/li>\n<li>Can occur in adults as a\u00a0<strong>latent autoimmune diabetes<\/strong>\u00a0variant.<\/li>\n<\/ul>\n<h1><strong>Pathophysiology:<\/strong><\/h1>\n<ul>\n<li>Lack of\u00a0<strong>insulin<\/strong> prevents <strong>glucose entry<\/strong> into cells,\n<ul>\n<li>as cell&#8217;s require insulin to insert GLUT4 glucose transporters into their cell membranes.<\/li>\n<li>leading to <strong>high blood<\/strong> <strong>glucose levels<\/strong>\u00a0(<strong>hyperglycemia<\/strong>).<\/li>\n<\/ul>\n<\/li>\n<li><strong>Cells<\/strong>\u00a0become\u00a0<strong>starved for glucose<\/strong>, impairing ATP production.<\/li>\n<li>Excess glucose\u00a0<strong>diffuses into urine<\/strong>, drawing water and causing\u00a0<strong>polyuria<\/strong>,\u00a0causing<\/li>\n<li><strong>Dehydration<\/strong>\u00a0triggers\u00a0<strong>thirst<\/strong>\u00a0(polydipsia).<\/li>\n<li>The body responds by\u00a0<strong>breaking down proteins and fats<\/strong>\u00a0for energy:\n<ul>\n<li><strong>Gluconeogenesis<\/strong>: Produces glucose from proteins and fats.<\/li>\n<li><strong>Lipolysis<\/strong>: Leads to high\u00a0<strong>lipid levels<\/strong>\u00a0(<strong>lipidemia<\/strong>).<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p><strong>Effects on the Body<\/strong><\/p>\n<ul>\n<li><strong>Muscle wasting<\/strong>\u00a0due to protein breakdown.<\/li>\n<li><strong>High blood lipids<\/strong>\u00a0increase risk of\u00a0<strong>atherosclerosis<\/strong>.<\/li>\n<li><strong>Ketone production<\/strong>\u00a0causes\u00a0<strong>ketosis<\/strong>\u00a0and potentially\u00a0<strong>ketoacidosis<\/strong>:\n<ul>\n<li>Blood becomes\u00a0<strong>acidic<\/strong>.<\/li>\n<li>Ketones and glucose are\u00a0<strong>excreted in urine<\/strong>\u00a0(ketonuria and glucosuria).<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Signs and Symptoms:<\/strong><\/h1>\n<ul>\n<li><strong>Polydipsia:<\/strong>\u00a0 Increased <strong>thirst<\/strong> (due to dehydration)<\/li>\n<li><strong>Polyphagia:<\/strong>\u00a0 Increased <strong>hunger<\/strong><\/li>\n<li><strong>Polyuria:<\/strong>\u00a0 Increased <strong>urine volume<\/strong> (due to <strong>glucosuria<\/strong> and osmotic diuresis)<\/li>\n<li>Fatigue (due to cell&#8217;s reduced ability to uptake glucose)<\/li>\n<li>Blurred vision (due to retinopathies and diabetic cataracts)<\/li>\n<li>Slowed healing of wounds (due to cell&#8217;s reduced ability to uptake glucose)<\/li>\n<\/ul>\n<h2><strong>Diagnostic Blood Tests:<\/strong><\/h2>\n<ol>\n<li><strong>Glycated hemoglobin (A1c) test<\/strong>\n<ul>\n<li>Measures the percentage of hemoglobin with blood sugar attached.<\/li>\n<li>Reflects\u00a0<strong>blood glucose control over 2-3 months<\/strong>.<\/li>\n<li>Levels\u00a0<strong>above 6.5%<\/strong>\u00a0suggest diabetes.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Random blood sugar test<\/strong>\n<ul>\n<li>Blood sample taken randomly, regardless of fasting.<\/li>\n<li>Blood glucose\u00a0<strong>above 110 mg\/dL<\/strong>\u00a0indicates abnormality.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Fasting blood sugar test<\/strong>\n<ul>\n<li>Fasting for 12 hours before testing.<\/li>\n<li>Normal:\u00a0<strong>&lt;100 mg\/dL<\/strong>.<\/li>\n<li>Diabetic:\u00a0<strong>&gt;125 mg\/dL<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n<h1><strong>Treatments:<\/strong><\/h1>\n<ul>\n<li><strong>Insulin injections<\/strong>\u00a0are essential.<\/li>\n<li>No known\u00a0<strong>preventive\u00a0cause\u00a0or cure<\/strong>; management focuses on blood sugar control.\n<ul>\n<li><strong>Note:<\/strong>\u00a0 Pancreatic transplants are challenging, and are not curative as the underlying cause of autoimmune destruction of the pancreatic beta cells by auto-antibodies and WBCs still exists.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Complications of Uncontrolled Diabetes and Risk of Long-Term Damage:<\/strong><\/h1>\n<ul>\n<li><strong>Blood vessel damage<\/strong>\u00a0leads to:\n<ul>\n<li><strong>Atheromas<\/strong>\u00a0formation.<\/li>\n<li><strong>Vascular damage<\/strong> affecting organs. and putting person at risk for:\n<ul>\n<li><strong>Cardiovascular disease:<\/strong>\u00a0Stroke, heart attack, peripheral vascular disease.<\/li>\n<li><strong>Kidney failure<\/strong>\u00a0(due to nephropathy).<\/li>\n<li><strong>Nerve damage:<\/strong> Neuropathy<\/li>\n<li><strong>Pregnancy complications:<\/strong>\u00a0Stillbirths and miscarriages.<\/li>\n<li><strong>Increased risk of amputations<\/strong>\u00a0due to ischemia and gangrene.<\/li>\n<li><strong>Eye damage:<\/strong> Leading to blindness (diabetic retinopathy).<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n<ul>\n<li><strong>Blurred Vision or Vision Loss:\u00a0<\/strong>\n<ul>\n<li>also due to development of diabetic (sugar) cataracts<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Summary<\/strong><\/h1>\n<ul>\n<li>In\u00a0<strong>Type I<\/strong>,\u00a0<strong>autoimmune destruction<\/strong>\u00a0results in\u00a0<strong>insulin deficiency<\/strong>.<\/li>\n<li><strong>Autoimmune origin<\/strong> causes destruction of beta cells in pancreatic islets of Langerhans.<\/li>\n<li><strong>Blood glucose regulation<\/strong>\u00a0is severely impaired.<\/li>\n<li><strong>Rapid onset in children<\/strong>, generally non-obese.<\/li>\n<li>Requires\u00a0<strong>lifelong insulin therapy<\/strong>.<\/li>\n<li>Precursors and triggers are still under study.<\/li>\n<li>The condition leads to\u00a0<strong>vascular damage<\/strong>\u00a0affecting multiple organs and systems, emphasizing the importance of tight blood glucose control.<\/li>\n<\/ul>\n","protected":false},"author":1370,"menu_order":15,"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-5117","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\/5117","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":13,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5117\/revisions"}],"predecessor-version":[{"id":5247,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5117\/revisions\/5247"}],"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\/5117\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=5117"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=5117"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=5117"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=5117"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}