Summary

This document is an educational resource about Diabetes Mellitus, including glucose metabolism, the pancreas, insulin function, feedback mechanisms, and different types of diabetes.

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Chapter 20 Integrated Pathophysiologic Concepts: DIABETES MELLITIS Glucose Metabolism: A&P Review What do our cells use glucose (simple form of sugar) for? ________________________ Glucose is the preferred and primary source of _______ for all tissue cells. How does glucose get into the...

Chapter 20 Integrated Pathophysiologic Concepts: DIABETES MELLITIS Glucose Metabolism: A&P Review What do our cells use glucose (simple form of sugar) for? ________________________ Glucose is the preferred and primary source of _______ for all tissue cells. How does glucose get into the cells? ____________________________________ What is stored glucose called?_____________ Where is it stored? _________________ What are the hormones of glucose metabolism? ______________ and _________________. They are produced by the _________________. How does each function? A&P Review Pancreas Endocrine Function: secretes hormones – Insulin: Role in glucose metabolism? – Glucagon: Role in glucose metabolism? Exocrine Function – Digestive enzymes – Alkaline fluids Anatomy review: Islets of Langerhans – Alpha cells (produce glucagon) – Beta cells (produce insulin) – Delta cells (produce somatostatin—inhibitory hormone) Function of Insulin Anabolic (__________) building up hormone Binds to insulin receptor on cells and opens the glucose channels. Required for the uptake of glucose by cells such as liver, muscle, and adipose cells. cells can make ATP Promotes protein synthesis Promotes formation/storage of lipids (prevents breakdown of fats) triglycerride level high Facilitates transport of potassium, phosphate, and magnesium into the cells A&P review: Feedback Mechanisms— Glucose homeostasis Insulin increases when blood level of the following increase: – Blood glucose, amino acids, potassium, phosphate, magnesium, glucagon, and gastrin. Insulin binds to ________ receptor to open the ___________ glucose channels to let in these products in the blood Insulin decreases when there is – Low blood glucose, high insulin levels, and stimulation of alpha cells (why?) ________ glucogon production Glucagon – Released when glucose levels are low. Breaks down glycogen in liver—>so glucose blood levels will rise Diabetes Mellitus Definition: a disease in which the body’s ability to produce or respond to the hormone insulin is impaired, resulting in abnormal metabolism of carbohydrates and elevated levels of glucose in the blood and urine. Type 1 Type 2 Gestational Pathophysiology of Diabetes mellitus Remember insulin is required for glucose to move into cells – Normal – Type 1 beta cells destroyed -insulin production_____ destroyed so no insulin – Type II Insulin resistance à Elevated glucose and insulin levels àPancreas eventually wears out Diabetes mellitus Type II Diagnosis Fasting blood sugar >126 Random BS >200 normal fasting 80-100 **HgA1C is gold standard blood test for diagnosis and for monitoring control to known when to adjust medications. life span of RBC is 120 days: check every 3 months for A1C What is HgA1C? Glucose binds to hemoglobin. Gives us a 3 month average of blood glucose levels “photo album” A1C of 6.5 is diagnostic for diabetes. A1C of 5.7-6.4 is prediabetic stage Clinical manifestations of Diabetes Symptoms: (know definitions) Polydipsia excessive thirst urine output Polyuria trying to get rid of glucose hunger Polyphagia Glycosuria sugar in urine high urine output Unintentional weight loss Sign: hyperglycemia= elevated glucose Diabetes mellitus Type 1 beta Pathophysiology: Destruction of ______cells so production of _______ insulin is ________. low How does this affect glucose utilization by cells?________________ cells cant get glucose in cell Increased alpha cell function leads to: g____________ lucogon leads to ____________ glucose in blood Etiology: g______ enetic Environmental triggers: _________-à viral a_________ utoimmune Most serious type; usually occurs in childhood or young adulthood Clinical Manifestations: hyperglycemia, polydipsia, polyphagia, polyuria, unintentional weight loss. Ketone level_____high Why? (next slide) Diagnostic criteria H&P, clinical manifestations, elevated blood glucose (fasting and otherwise), elev. A1C lab, ketones in urine, autoantibiodies to islet cells and GAD enzyme (in B cells) Diabetes mellitus Type 1 Complications -Ketones can accumulate from lipid breakdown…… Fats à Ketones being used as an energy source because glucose______________ absent in cells Ketones produced faster than they are used and excreted This leads to keto___________ acidosis metabolic = DKA______________ diabeteic keto acidosis Signs: Kussmaul respirations respiratory system tries to __________ compensate by _________________ exhaling more -“fruity breath” (ketones) Complications: Diabetic Ketoacidosis (DKA) Video on Bb Insufficient ______à_____ insulin hyper glycemiaàacidosis Who gets it? ______________ type Etiology and pathophysiology? Beta cell _________ destruction viral? Genetic? Autoimmune? Triggers: increased _____ demandfor insulin as in stress, infection, excess food, inadequate insulin intake, pregnancy Rate of onset: _____________ fast Lipolysisàketones for energy sourceàcan’t excrete enoughàacidosis Clinical Manifestation?the 3 polys: polyuria, _______________, polydipsia, significant elev. _______, glucose k________ etones formationpolyphaisa Body’s response/ compensation: _________________________ respirator - Complications: decreased LOC, coma, death Treatment: correct acidosis, return glucose levels to normal, fluids, electrolytes, preserve perfusion electrolytes imbalances K+ pee out Complication of Insulin Deficiency in Type 1 Diabetes Diabetic ketoacidosis Diabetes mellitus Type 1 Treatment Treatment of Type I: 1. Requires daily injections of insulin. Why? Types of insulin: 2. And carbohydrate counting. Why?______________ to know how much insulin to give 3. exercise also critical part of treatment! Insulin pumps and continuous glucose monitoring (CGMs) systems have transformed diabetes care and management!! A continuous glucose monitor (CGM) tracks blood glucose levels using a sensor under the skin. Wirelessly sends the information to a smartphone or on an insulin infusion pump. calculates how much insulin is needed and signals the insulin infusion pump Types of insulin pumps. when insulin needs to be 1. worn outside the body. Insulin delivered. goes through a catheter (has a The insulin infusion needle that is inserted under the pump will deliver small skin and stays several days. doses of insulin throughout the day when blood glucose 2. attaches directly to the skin levels are not in target range. and gives insulin. Replaced every few days. https://www.niddk.nih.gov/health- information/diabetes/overview/managing- diabetes/artificial-pancreas Diabetes mellitus Type 2 Most common form of diabetes Gradual onset Now frequently seen in younger age groups Thought to be caused by insulin _____________ resistance and wearing out of the beta cells of the Islets of Langerhans in the pancreas Type 2 Diabetes Concept Map Clinical Manifestations May have: Polyuria Polydipsia Polyphagia Glucosuria Weight loss (in severe) COMPLICATIONS of Diabetes TYPE II video on Bb Hyperosmolar Hyperglycemia Non Ketototic Syndrome (HHNK) (includes diabetic coma): extreme hyperglycemia (600mg/dl +!) most commonly with Type II DM stress response, increased carbs, insulin resistance, infection or with certain medications Hyperosmolarity d/t excess glucose; low fluid So H20 moves from __________ intracellular to _________ extracellular Osmotic diuresis dehydrated cells Etiology: deficiency of ______ insulin (but is still being produced) increase insulin reistance Symptoms: 3 polys, dehydration, wt loss, hyperglycemia, weakness, tremors, neuro changes, glucosuria Complications: dehydration, seizure, coma Treatment: careful fluid replacement, electrolyte replacement Diabetes Type II Treatment Approaches Nutrition protein, fat balance Exercise increases insulin sensitivity Medication combinations (oral and non-insulin injectables and insulins) that improve insulin sensitivity, insulin secretion, decrease hepatic glucose output, slow digestion, increase excretion of glucose, etc. etc. Medications interfere with pathways that lead to hyperglycemia Type 2 Diabetes Mellitus Treatment (continued) If not controlled with oral medications and the non-insulin injectables Start Insulin like ozempic januvia – Fast acting – Short acting – Intermediate – Long acting Goal: maintain optimal blood glucose levels: HbA1

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