Diabetes Mellitus Lecture Slides PDF

Module II: Endocrine Disorders Part 1 The Endocrine System  The nervous system and endocrine system are major controllers of homeostasis  The endocrine system consists of various glands that secrete hormones to maintain homeostasis  Hormone  A chemical messenger released in...

Module II: Endocrine Disorders Part 1 The Endocrine System  The nervous system and endocrine system are major controllers of homeostasis  The endocrine system consists of various glands that secrete hormones to maintain homeostasis  Hormone  A chemical messenger released in response to a change in the body’s internal environment  After secretion from endocrine glands, hormones enter the blood stream and are transported through out the body Endocrine Glands  Hypothalamus  Pituitary  Thyroid  Adrenal  Parathyroid  Pancreas  Ovary/Testes  Pineal  Thymus The Endocrine System  Hormonal balance is kept within a narrow range  Too much or too little results in profound physiologic changes  Processes regulated through negative feedback  Medications can be given that mimic hormones or block their effects if there is an underlying communication issue (disease state) Normal Regulation of Blood Glucose Regulation of Glucose  Glucose- “blood sugar”  Body’s primary energy source  Supplied to bloodstream through diet  Normal fasting levels (patients without DM) 70-110 mg/dL Pancreas  Hormones  Insulin released to decreased blood glucose levels  Glucagon released to increase blood glucose levels Regulation of Glucose - Hormones  Insulin  Hormone released from beta cells in pancreas to decrease glucose levels in blood  Needs to be present to allow glucose entry into cells  Insulin released is triggered by several factors  Glucose in blood  Incretins (GIP, GLP-1)  Glycogen- stored glucose in the liver Glucose  intestine  incretins released  pancreas releases insulin  glucose enters cells Regulation of Glucose cont.  Amylin  Co-secreted with insulin from the beta cells  Role in glycemic regulation:  Inhibits glucagon secretion  Slows gastric emptying  Promotes satiety which prevents post-prandial spikes in blood glucose  Eat food with carbohydrates Glucose enters blood stream and small intestine releases incretins Beta cells in Beta cells in pancreas release pancreas release insulin amylin Insulin presence Promotes satiety, slows allows glucose into gastric emptying, stops cells glucagon secretion Regulation of Glucose continued  Glucagon  Hormone released from alpha cells in pancreas to increase levels of glucose in blood  Glycogenolysis  In liver; stored glycogen is broken down and glucose is released into the bloodstream  Gluconeogenesis  In liver; turns fats/ proteins into endogenous glucose  Ketones: increase in free fatty acids in blood and ketones in the urine due to breakdown of lipids Diabetes Mellitus What is diabetes mellitus?  A disease in which the body’s ability to produce or respond to insulin is impaired resulting in elevated levels of glucose in the blood and urine  Can lead to serious acute and chronic complications Glucose Intolerance Disorders  Type 1 diabetes mellitus (T1DM)  Type 2 diabetes mellitus (T2DM)  Gestational diabetes Characteristics Type I Diabetes Type II Diabetes Etiology Autoimmune process Genetics, lifestyle Primary pathology Loss of pancreatic beta cells Insulin resistance, loss of incretin secretion of insulin effect, beta cell dysfunction Age of onset Usually childhood or adolescents Usually > 40 years Speed of onset Abrupt Gradual Prevalence 5-10% 90-95% Treatment Insulin replacement is Oral anti-diabetic, non-insulin mandatory with strict dietary injectable, or insulin in combination control with reduced calorie diet and exercise Blood glucose Levels fluctuate widely in More stable than Type I response to infection, exercise, and changes in insulin dose and caloric intake Body composition Usually thin and undernourished Frequently obese at diagnosis Ketosis Common, especially if insulin Uncommon dose is too low DM Manifestations  T1DM- more abrupt, may present in DKA  T2DM-Gradual onset  Hallmark symptoms: Polyuria, polydipsia, polyphagia  Fatigue  Vision changes, blurred vision  Non-healing sores  Frequent infections (genital, vaginal, skin and gums)  Numbness & tingling in legs and feet (peripheral neuropathy) Gestational Diabetes  Disorder of insulin resistance with onset during pregnancy (1-10% of pregnancies in the US)  Closely resembles T2DM  Most likely precipitated by placental hormones and weight gain during pregnancy  Risk factors  Obesity  Previous history of gestational diabetes  Previous offspring weighing more than 9 lb. at birth  Presence of glycosuria  Family history of T2DM Gestational Diabetes  Complications  Infant: metabolic abnormalities, stillbirth, macrosomia, and neonatal hypoglycemia  Mother: development of T2DM or insulin resistance later in life  Management through dietary counseling, exercise, and blood glucose/ketone monitoring; insulin may be needed  Evaluating Blood Glucose Levels Parameter Diagnostic Value Hemoglobin A1c > 6.5% ◦ Reflects blood glucose control over the lifespan of the RBC (90-120 days) ◦ Not affected by short-term variations in blood glucose Fasting plasma glucose (FPG) > 126 mg/dL [FPG= no caloric intake for > 8 hours] Two-hour plasma glucose during an oral > 200 mg/dL glucose tolerance test (OGTT) using 75g glucose in water Random plasma glucose, with classic > 200 mg/dL symptoms of hyperglycemia Correlation between estimated average blood glucose and HgbA1c http://www.diabetes.org/living-with-diabetes/treatment-and-care/blood-glucose-control/estimated-average- Recommendations for the Diabetic Patient  Glycemic Control  HgbA1c < 7%  Elderly or patients with a history of severe hypoglycemia may have a goal of < 8%  Fasting Plasma Glucose  Outpatient = 80-130mg/dL  Hospital = 140-180 mg/dL  Post-prandial (1-2 hours after a meal) < 180 mg/dL  Blood Pressure  < 130/80 mmHg or < 140/90 mmHg Recommendations for the Diabetic Patient  Lipids  Total Cholesterol < 200 mg/dL  LDL < 100 mg/dL  HDL > 60 mg/dL  Triglycerides < 150 mg/dL  Protein in urine  Kidney leaks small amounts of albumin into urine because of damage  Want albumin/creatinine ratio level to be 10% Severe renal or liver disease is present Painful neuropathy is present Undergoing surgery or diagnostic tests (NPO) Experiencing severe stress (infection or trauma) FYI- Some patients requiring acute treatment of hyperkalemia Mechanism of Promotes cellular uptake of glucose Action Converts glucose into glycogen Moves potassium into cells (with the glucose) Decreases HA1c more than any other medication Adverse Effects HYPOGLYCEMIA- monitor blood glucose with glucometer or continuous glucose monitoring (CGM) Hypokalemia, lipohypertrophy Times to know: onset of action (start of potential hypoglycemia) and peak concentration (worse signs of hypoglycemia)  Insulin Characteristics Category Drug Clarity Onset Injection Peak Duration Name Time Before Meal Bo Rapid-Acting Aspart Clear 5-20 15 1-3 hours 3-5 hours lu Lispro minutes minutes s Glulisine Short-Acting Regular Clear 30-60 30 2-4 hours 5-7 hours minutes minutes Ba Intermediate- NPH Cloudy 1-2 hours N/A 4-12 18-24 sa Acting hours hours l Long-Acting Glargine Clear 1-2 hours N/A Peakless 24 hours **Depending on what chart you look at, you may see slightly different times! Bolus- given before meals or as correction Basal- baseline control Time-effects of Exogenous Insulin Lehne, pg 666 Drug Class Insulin Route All types are given SQ Subcutaneous Regimens: Basal/Bolus Twice Daily Premixed Just basal insulin Insulin Pumps or patches Correctional Do not mix anything in the syringe with long-acting insulin glargine Only use insulin specific syringes that correspond with the insulin being administered and choose the correct needle for SQ Double-verify dose with another nurse prior to administration Gently rotate vial between palms to disperse the particles throughout the vial prior to withdrawing dose of insulin Rotate injections sites leaving 1 inch between administrations, use same general area for consistent absorption Regular insulin can be given IV push or IV infusion when needed (1 unit/ml in 0.9% NS) Insulin binds to IV tubing; 20-50 ml of insulin infusion should flow through the tubing and wasted  Sites of insulin administration: Instruct patients to systematically rotate injection sites and to allow 1 inch between sites to avoid lipohypertrophy http://media.pearsoncmg.com/ph/chet/chet_2015_nursing_mnls_and_rp/pharmacology/review/Mod_09/Lesson_02/LO3/LO3.html Lipohypertrophy Insulin Dosing Regimens  Basal/Bolus  Twice daily premixed  Just Basal  For T2DM in conjunction with oral medications for DM)  Continuous subcutaneous insulin infusion  Insulin pumps or pods  Less injections  Uses rapid acting insulin  Corrective  Corrects high blood glucose  Given in addition to usual dose  Used rapid or short acting insulin Basal/Bolus Insulin Regimen  Mimics the body’s normal response  Basal insulin (glargine or others) for 24-hour baseline coverage  Bolus insulin for meal coverage and as needed  Advantage: more flexible for patient mealtimes and mimics normal pancreas secretions  Disadvantage: multiple injections and cannot mix insulins Twice Daily Premix Regimen  Mixed Insulin (75/25, 70/30, etc.)  Larger number is intermediate acting insulin; smaller number is rapid or regular insulin– must give right before meals twice daily  Advantages: less overall amount of injections  Disadvantages: potentially less control with dose changes  You can also manually draw up both singular insulins into one syringes (clear to cloudy)  When mixing rapid or regular insulin with NPH  Draw up shorter acting or regular first, then NPH  Prevents the possibility of accidentally injecting some of the longer acting insulin into the shorter acting vial  Clear (short)  Cloudy (intermediate) Drug Class Insulin Drug Sulfonylureas, pramlintide and alcohol have additive hypoglycemic Interactions effects with concurrent use Monitor serum glucose levels and adjust insulin or oral hypoglycemic medication doses accordingly Thiazide diuretics and glucocorticoids can raise blood glucose levels and counteract the effects of insulin Higher insulin doses may be needed Beta blockers can mask sympathetic response to hypoglycemia making it difficult to recognize Advise patients of the importance of self monitoring blood glucose Instruct patients to maintain regular eating schedule to ensure adequate glucose during time of hypoglycemic action Applies to oral medications that can cause hypoglycemia as well! Insulin Storage Unopened vials Store in refrigerator until expiration date Do not freeze Insulins premixed in Store 1-2 weeks in refrigerator; vertical with needles syringes pointing up Insulin vials being used Store at room temperature (59-86 ºF) avoiding sunlight and intense heat Insulin that is cold can make the injection more painful Discard after 30 days Sick Day Dosing  Insulin- never stop taking- use sick day dosing  Check blood glucose and ketones levels every 2 hours  Drink extra fluids to maintain hydration and flush ketones  Drink sugar or carbs depending on levels Drug Class Insulin Clinical Education Considerations Proper diet and exercise Adjusting insulin for diet changes and drug interactions Appearance and mixing of insulin Adjusting insulin for sick day dosing Ensure adequate glucose is available at time of onset of insulin and during peaks Appropriate insulin storage Monitoring blood glucose Monitoring ketones Appropriate management of hypoglycemia Wear a medical alert bracelet When to seek medical advice Blood glucose > 250 mg/dL for 2 checks Vomiting or diarrhea more than 6 hours High fever more than 24 hours Moderate-high ketones are present for more than 6 hours Ketones present over 12 hours Signs or symptoms of severe dehydration Abdominal or chest pain Acute Diabetes Mellitus Complications Hypoglycemia Diabetic ketoacidosis (DKA) Hyperglycemic hyperosmolar non-ketotic syndrome (HHS) Hypoglycemia  Low blood glucose < 70 mg/dL Treatment of Hypoglycemia  Conscious patients- give oral glucose  15/15 rule  Give 15-20 grams oral glucose  4 ounces (1/2 cup) juice  4 ounces (1/2 cup) non-diet soda  8 ounces of ski milk  3-4 glucose tabs; 1 glucose gel  2 packets of smarties  5-6 life savers  Recheck after 15 minutes and treat again if still hypoglycemic  Eat something to prevent further hypoglycemia Treatment of Hypoglycemia Continued  Unconscious or extremely low blood glucose- give parenteral route  Glucagon – intramuscular, subcutaneous (can also give intranasal)  Dextrose 50% intravenous Diabetic Ketoacidosis (DKA)  More common in T1DM but can occur in T2DM  Severe manifestation of insulin deficiency  Evolves quickly in T1DM, particularly children  Results in significant  Hyperglycemia, dehydration, ketoacidosis  Manifestations:  Polyuria Abdominal pain  Polydipsia Kaussmal respirations  Nausea, Vomiting Tachycardia  Dehydration Hyponatremia  Altered mental status Hyperkalemia  Coma Fruity (acetone) breath Management of DKA 1. Fluid & Electrolyte Replacement 2. IV Regular Insulin Therapy  Slowly stabilize blood glucose  Always must check potassium levels and supplement before insulin (if K+ is less than 3.3)  Once DKA resolved can be converted to SQ insulin once BG is < 200 mg/dL and signs of acidosis are gone 3. Correct severe acidosis  Diabetic Ketoacidosis (DKA) Hyperosmolar Hyperglycemic Nonketotic State (HHS) Association T1DM T2DM Mortality Rate Relatively lower Relatively higher Presentation Abdominal pain, polyuria, Fatigue, altered level of polydipsia, dehydration, consciousness, hyperviscosity Kussmaul breathing, acetone (increased risk of MI and (sweet) breath stroke), hypovolemia pH < 7.35, ketones present no ketones, normal pH, marked hyperglycemia Onset Hours Days Management Fluid replacement, IV regular Controlled rehydration, monitor insulin, potassium serum osmolality replacement  Increased hepatic Increased glucose production carbohydrate and loss of incretin intake / lack of exercise effect Increased blood Decreased Genetic peripheral Decreased glucose factors insulin secretion from T2DM glucose uptake (insulin resistance) pancreas