Chapter 20 Diabetes PDF
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Saint Mary's College
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This document contains lecture notes covering integrated pathophysiologic concepts related to diabetes mellitus. It details glucose metabolism, the function of the pancreas and insulin, and feedback mechanisms related to glucose homeostasis.
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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 _______ ATP for all tissue cells. How does glucose get...
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 _______ ATP for all tissue cells. How does glucose get into the cells? ____________________________________ insulin is a hormone required for the uptake of glucose What is stored glucose called?_____________ glycogen Where is it stored? _________________ the Liver 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 (__________) up hormone building 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. so cells can makeATP Promotes protein synthesis Promotes formation/storage of lipids (prevents breakdown of fats) satrig high Facilitates transport of potassium, phosphate, and magnesium into the cells helps 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 ___________ to let in these products in glucose the blood shannels Insulin decreases when there is – Low blood glucose, high insulin levels, and stimulation of alpha cells (why?) glucagon ________ Glucagon produition – Released when glucose levels are low. Breaks down glycogen in liver—>so what is glucagons role glucose blood level 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 o Pathophysiology of Diabetes mellitus Remember insulin is required for glucose to move into cells – Normal destroyed – Type 1 Beta cells -insulin production_____ destroyed – Type II not well fit's but Insulin resistance à Elevated glucose and insulin levels àPancreas eventually wears out have enough in the bloodcells we don't glucose so produce more insulin Diabetes mellitus Type II Diagnosis Fasting blood sugar >126 Random BS >200 normal tasting 80 100 **HgA1C is gold standard blood test for diagnosis and for monitoring control to known when to adjust medications. tells us How much sugar has beenhanging in blood 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 know these Symptoms: (know definitions) Polydipsia excessive thirst Polyuria excessive urination p urine Polyphagia excessive Hunger p sugar in urine Glycosuria excess glucose in urine Unintentional weight loss dit highurine output elevated glucose Sign: hyperglycemia= significant elevation in blood glucoselevel F it is not normalto haveglucose in urine g Diabetes mellitus Type 1 Pathophysiology: Destruction of ______cells Beta so production of _______ insulin is ________. decrease impaired How does this affect glucose utilization by cells?________________ cellsareunabletouptakeglucose Increased alpha cell function leads to: g____________ lucagon 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_____ 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 product of fat breakdown by A can use as energywhen no or littleglucose -Ketones can accumulate from lipid breakdown…… Fats à Ketones being used as an energy source because absent in cells glucose______________ Ketones produced faster than they are used and excreted This leads to keto___________ acidosis = DKA______________ diabetic ketoacidosis Signs: Kussmaul respirations respiratory system tries to compensate __________ by _________________ exhaling more CO2 -“fruity breath” (ketones) Complications: Diabetic Ketoacidosis (DKA) Video on Bb Insufficient insulin ______à_____hyper glycemiaàacidosis Who gets it? ______________ A ketone Type Etiology and pathophysiology? Beta cell _________ destruction viral? Genetic? Autoimmune? Triggers: increased demand _____ for insulin as in stress, infection, excess food, inadequate insulin intake, pregnancy Rate of onset: _____________ fast Lipolysisàketones for energy sourceàcan’t excrete enoughàacidosis polyphagia Clinical Manifestation?the 3 polys: _______________, significant polyuria polydip elev. _______, glucose k________ etone formation Body’s response/ compensation: _________________________ respirator CO2 exhale Complications: decreased LOC, coma, death Treatment: correct acidosis, return glucose levels to normal, fluids, electrolytes, preserve perfusion K then electrolyte imbalances watch video 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. to know the ammount of Why?______________ insulive needed 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 pump that gives insuline 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 Gradual onset Now frequently seen in younger age groups diet is exercise Thought to be caused by resistance insulin _____________ 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 Etiology: deficiency of ______ insulin (but is still being produced) resistance insulin Symptoms: 3 polys, dehydration, wt loss, hyperglycemia, weakness, tremors, neuro changes, glucosuria Complications: dehydration, seizure, coma Treatment: careful fluid replacement, electrolyte replacement Emergency Situations Hyperglycemia Hypermolar in androgen production A insulin Diabetes Type II Treatment Approaches protein fat balance lower carbs Nutrition Exercise builds repairs insulin receptors 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 t.isim ablation know Metformin how it 8 3 y Type 2 Diabetes Mellitus Treatment (continued) If not controlled with oral medications and the non-insulin injectables Start Insulin Janovia trigger body own mechanisms insulin gigat – Fast acting to lower Blood sugar p – Short acting – Intermediate – Long acting Goal: maintain optimal blood glucose levels: HbA1