Diabetic Ketoacidosis (DKA) PDF - Western Sydney University

Endocrine Disorders- Diabetic Ketoacidosis  Important Copyright Notice for Western Sydney University Students The material in this presentation has been made available to you by and on behalf of Western Sydney University for your personal use and study only. The material contained in this...

Endocrine Disorders- Diabetic Ketoacidosis  Important Copyright Notice for Western Sydney University Students The material in this presentation has been made available to you by and on behalf of Western Sydney University for your personal use and study only. The material contained in this recorded lecture is subject to copyright protection. You may not make any further copies and share the recorded lectures in whole or in part by any hardcopy, digital and or online technologies.  Alterations of Pancreatic function Patton, K., Thibodeau, G., Anatomy and Physiology, 2016  Insulin glycolysis Glucose Adenosine Tri Phosphate (ATP) irreversible glycogenesis Glucose Glycogen (stored in liver and muscle) reversible lipogenesis Glucose lipids (stored in adipose – long-term) irreversible Functions of Insulin List, Sarah, Understanding Pathophysiology, 2019.  Glucagon glycogenolysis Glycogen Glucose reversible gluconeogenesis Amino Acids Glucose reversible ketogenesis Fatty acids/lipids ketone bodies ( to be used only by brain and heart) irreversible Marieb, E. N., & Hoehn, K. (2016).  Diabetes “Diabetes is a group of metabolic disease characterized by increased glucose levels in the blood resulting from defects in insulin secretion, insulin action or both” (Farrell & Dempsey, 2016 pg. 1110) Common types Type 1 DM Type 2 DM Gestational diabetes latent autoimmune diabetes in adults (LADA) maturity onset diabetes of the young  Risk factors & Etiology Type I DM (absolute insulin deficiency) o Environmental and genetic factors o Viruses like coxasie virus o Autoimmune response Type II DM (insulin resistance with an insulin secretory deficit) Obesity Sedentary lifestyle Family history of diabetes Age 45 years and older History of GDM History of delivering infant weighing more than 9 lb Ethnicity derived from Alaskan Native, American Indian, Asian American, Hispanic/Latino, African descent, Native Hawaiian or Pacific Islander Polycystic ovary syndrome Cardiovascular disease and hypertension Presence of acanthosis nigricans or other conditions associated with insulin resistance  Lack of sufficient production of insulin  Inability of receptors to take up insulin  Production of “useless” improper insulin (defective)  Consumption of excess CHO and refined sugars Metabolic Effects  Decreased utilization of glucose Excess glucose remains in blood liver unable to store, kidneys excrete glucose glucose is osmodiuretic meaning draws water along with it  Increased fat metabolism  Increased protein metabolism Key clinical features in Diabetes Mellitus Farrell & Dempsey, 2016  Major Chronic complications of diabetes Molecular explorations through biology and medicine  Acute Emergency Complications of Diabetes 1) Acute Hypoglycemia Dangerous drop in blood glucose Response of the nervous system to inadequate glucose for cell function shakiness, nervousness, irritability, tachycardia, anxiety, lightheadedness, hunger, tingling or numbness of the lips or tongue, and diaphoresis If treatment is delayed Neuroglycopenia (caused by a shortage of glucose to the brain) Drowsiness, irritability, impaired judgment, blurred vision, slurred speech, headaches, and mood swings progressing to disorientation, seizures, and unconsciousness Progresses to convulsions, coma, and death 2) Diabetic Ketoacidosis Diabetic Ketoacidosis (DKA) is a life-threatening emergency caused by a relative deficiency (ineffective amount of insulin) or absolute deficiency (lack of insulin) in addition to elevated counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone ) Most likely to occur when diabetes is undiagnosed; when the patient does not take enough insulin; when the patient with uncontrolled type1 DM exercises too vigorously; or when the patient experiences stress linked to illness, infection, surgery, or emotions  Ketoacidosis is a problem primarily with type 1 DM. It occurs when ketone bodies accumulate as the result of the breakdown of fats for energy associated with inadequate insulin.  Ketoacidosis can occur in individuals with type 2 DM when severe hyperglycaemia is associated with another acute condition, such as sepsis or a myocardial infarction.  DKA Onset Insulin or Insulin Demand Type I DM Infections Inflammation Intoxication Iatrogenic  Diabetic Ketoacidosis Pathophysiology Insulin Insulin Demand Glucose cannot enter the cells Stimulates Sympathetic Nervous System Lipolysis Releases adrenaline/noradrenaline Free fatty Acids Gluconeogenesis, glycogenolysis, lipolysis Ketone bodies e.g., acetoacetate glucose Releases H+ protons Osmotic diuresis Enters blood stream- Acidosis Dehydration  Diabetic Ketoacidosis Pathophysiology (Summary) Tissues cannot use glucose without insulin, resulting in an increase in serum glucose levels Excess glucose entering the renal tubules increases osmotic pressure Reabsorption of water, increasing urine output (i.e., osmotic diuresis) The patient voids large amounts of dilute urine (i.e., polyuria) The sympathetic nervous system responds to the cellular need for fuel by converting glycogen to glucose and manufacturing additional glucose (makes things worser) As glycogen stores are depleted, the body begins to burn fat and protein for energy. The breakdown of fat and protein for energy produces acidic substances called ketone bodies. As the ketones accumulate, the pH of the blood decreases and results in severe acidosis, which can be fatal.  DKA Clinical features and Pathophysiology link KETONE BODIES Dehydration Releases H+ protons Acidic environment Act on emetic center in medulla oblongata Acidic state Peripheral chemoreceptors Blood volume stimulated (BP) Nausea and vomiting Protons move from Extracellular space to intracellular Baroreceptors space Stimulates vagus nerve Stimulated In response, cells push K+ ions out for each H+ that enters Stimulates respiratory center SNS stimulated Hyperkalemia Respiratory Rate Vasoconstriction RAAS Cardiac Contractility Arrythmias Fruity breath Kussmaul’s respiration (acetone)  Clinical features of diabetic ketoacidosis Early signs and symptoms of DKA are anorexia, headache, and fatigue Progresses to polydipsia, polyuria, and polyphagia If untreated Patient becomes dehydrated, weak, and lethargic with abdominal pain, nausea, vomiting, fruity breath (because of ketone production), increased respiratory rate, tachycardia, blurred vision, and hypothermia Late signs are air hunger (seen as Kussmaul respirations: rapid and deep), coma, and shock If untreated Death  Management of Diabetic Ketoacidosis Main Goals: Correction of (1) dehydration, (2) electrolyte imbalance, and (3) acidosis Dehydration: Replace the fluid, which will aid the kidneys in eliminating excess glucose. Usually administer 1000 mL of normal saline to run over the first hour, followed by an additional 2000 to 8000 mL of intravenous fluids for the next 24 hours. Electrolyte Imbalance: Potassium shifts out of the cells, causing transient (temporary) hyperkalemia. The hyperkalemia associated with hyperglycemia should be treated with fluid replacement and insulin administration. Sodium deficiency is generally corrected by infusion of normal saline. Phosphate, magnesium, and calcium levels should also be monitored. Acidosis: Ketoacidosis is treated with the slow intravenous infusion of insulin. When the serum glucose level reaches 25 to 30 mmoL/L, dextrose solution is added. The intravenous insulin is given continuously or as a bolus until subcutaneous insulin can be given or else the patient may become ketoacidotic again. References Dunning, T., & Sinclair, A. J. (2020). Care of people with diabetes : A manual for healthcare practice. 5 th ed. John Wiley & Sons Ltd. Hooter, L. (2020). Diabetes and Hypoglycemia. In A. D. B. S. N. M. N. P. R. N. F. Linton & M. A. P. R. N. F. Matteson (Eds.), Medical-Surgical Nursing (pp. 967-995). https://doi.org/http://dx.doi.org/10.1016/B978-0-323-55459-6.00050-5 Kumar, A., (2020). Diabetes : Epidemiology, pathophysiology and clinical management (1st ed.). Taylor & Francis Ltd. Linton, F.& Matteson, F. (Eds.), Medical-Surgical Nursing (pp. 911-928). https://doi.org/http://dx.doi.org/10.1016/B978-0-323-55459-6.00047-5 List, S. (2019). Alterations of endocrine function across the life span. In J. A. Craft, C. J. Gordon, S. E. Huether, K. L. McCance, V. L. Brashers, & N. S. Rote (Eds.), Understanding Pathophysiology, ANZ Edition (pp. 255-278). https://doi.org/http://dx.doi.org/10.1016/B978-0-7295-4264-7.00011-X Patton, K. T. P., & Thibodeau, G. A. P. (2016). Endocrine glands. In K. T. P. Patton & G. A. P. Thibodeau (Eds.), Anatomy & Physiology (pp. 579-608). https://doi.org/http://dx.doi.org/10.1016/B978-0-323-29883-4.00038-X Western Sydney Local Health District. (2019). Department of Endocrinology. Inpatient Management of Diabetic Ketoacidosis. www.wslhd.health.nsw.gov.au>ArticleDocuments