Summary

This document provides information about diabetes mellitus, including its types (type 1 and 2), risk factors, etiology, pathophysiology, and treatment. It also describes insulin's role in the body and its relation to blood glucose.

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Diabetes Mellitus What is Diabetes Mellitus? Chronic multisystem disease characterized by hyperglycemia from abnormal insulin production, impaired insulin use, or both. Diabetes is the leading cause of End stage renal disease, adult blindne...

Diabetes Mellitus What is Diabetes Mellitus? Chronic multisystem disease characterized by hyperglycemia from abnormal insulin production, impaired insulin use, or both. Diabetes is the leading cause of End stage renal disease, adult blindness, and nontraumatic lower limb amputations. Risk Factors Family History Previously identified as glucose intolerant(gestational diabetes, prediabetic) Hispanic Age >45 Obesity Given birth to an infant >9 pounds Etiology and Pathophysiology Type 1 or type 2 Can be caused by a multitude of factors the most popular being genetic, environmental, or autoimmune(type 1) Insulin is a hormone made by the β cells in the islets of Langerhans of the pancreas. Under normal conditions, insulin is continuously released into the bloodstream in small amounts, with increased release when food is ingested. Insulin lowers blood glucose and facilitates a stable, normal glucose range of about 70 to 120 mg/dL. Insulin promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell. ******GLUCOSE SHOULD BE IN THE CELL NOT IN THE BLOOD. INSULIN IS THE KEY TO ALLOW GLUCOSE INTO THE CELL AND OUT OF THE BLOODSTREAM!!!!***** Other hormones (glucagon, epinephrine, growth hormone [GH], cortisol) work against the effects of insulin. They are counterregulatory hormones.The counterregulatory hormones and insulin work together to maintain blood glucose levels within the normal range by regulating the release of glucose for energy during food intake and periods of fasting. Different roles that insulin play in the body: ○ Promotes glucose transport in skeletal muscles and adipose tissue(used for energy) ○ Inhibits gluconeogenesis(making of glucose) ○ Increases protein synthesis Type 1 Diabetes: Insulin Dependent Diabetes Mellitus Autoimmune disorder which the body develops antibodies against insulin and/or the pancreatic cells do not make insulin The result of the destruction of the beta cells in the pancreas, the only cells in the body that make insulin. Because Langerhan cells are destroyed, insulin can no longer be made Diabetes that is present usually within the first few years of life or diagnosed during school age. Signs and Symptoms: ○ Most common signs/symptoms are POLYDIPSIA (excessive thirst), POLYURIA(excessive urine), POLYPHAGIA (excessive hunger) - HYPERGLYCEMIA ○ fatigue/weakness due to the body’s inability to get energy from glucose ○ GI symptoms: N/V - body’s attempt to get rid of excess glucose ○ Weight-loss Treatment: ○ Exogenous insulin required (insulin from outside source to maintain life) ○ Type 2 Diabetes: Non-Insulin Dependent Diabetes Mellitus Combination of inadequate insulin production to control blood glucose and cellular resistance to insulin Gradual onset of disease Diagnosed on routine lab testing w/ elevated glucose or A1C levels ○ A1C of 6.5% or higher- measures the amount glycosylated hemoglobin as a percentage of total hemoglobin( For example, 6.5% means 6.5% of the total hemoglobin has glucose attached to it) When blood glucose levels are elevated over time, the amount of glucose attached to Hgb increases. Therefore, A1C provides a measurement of blood glucose levels over the previous 2 to 3 months, with increases in the Hb A1C reflecting elevated blood glucose levels. ○ Fasting plasma glucose (FPG) level of 126 mg/dL (7.0 mmol/L) or greater. Fasting is defined as no caloric intake for at least 8 hours ○ A 2-hour plasma glucose level of 200 mg/dL (11.1 mmol/L) or greater during an OGTT, using a glucose load of 75 g ○ In a patient with classic symptoms of hyperglycemia (polyuria, polydipsia, unexplained weight loss) or hyperglycemic crisis, a random plasma glucose level of 200 mg/dL (11.1 mmol/L) or greater Prediabetes Person diagnosed with prediabetes is at risk of developing type 2 diabetes Impaired glucose tolerance (IGT), impaired fasting glucose (IFG) or both Glucose levels are elevated but not high enough to meet the diagnosis for diabetes IGT-2 hour oral glucose tolerance test (OGTT) values are 140 to 199 Usually no symptoms Patient Teaching ○ Have glucose and A1C checked regularly. The ADA identifies an A1C goal for patients with diabetes of less than 7.0%. The American College of Endocrinology recommends an A1C of less than 6.5%. ○ Monitor for symptoms of diabetes such as fatigue, frequent infections, or slow-healing wounds ○ Maintain a healthy weight, exercise regularly and make healthy food choices Gestational Diabetes Develops during pregnancy Higher risk for Cesarean delivery High risk include women who are obese, are of advanced maternal age, or have a family history of diabetes. Women with an average risk for gestational diabetes are screened using an OGTT at 24 to 28 weeks of gestation. Most women with gestational diabetes have normal glucose levels within 6 weeks postpartum Diagnostics:(Can be used for all Types but mostly secondary onset**) ○ Fasting plasma glucose If fasting glucose is over 126, then DM is present ○ Hemoglobin A1C: Gives average of glucose levels for the past three months Glucose sticks to RBCs A1c measures the sugar that sticks throughout the RBC lifespan(120 days) ○ Estimated Average Glucose(eAG): A calculated conversion of HbA1c Its reported in mg/dL, the same units as blood glucose Puts the A1c in terms they can understand to emphasize teaching point of lowering sugar ○ Urine glucose, ketones, and protein levels: The presence of glucose in the urine indicates ketosis of fat cells due to increased sugar in the blood but no sugar IN the cells Protein castings in the urine can indicate damage to kidneys due to increased breakdown of sugar over a chronic amount of time ○ Serum Cholesterol Testing for other risk factors like Atherosclerosis Types of Insulin Storage of Insulin As a protein, insulin has special storage considerations. Extreme temperatures alter the insulin molecule and can make it less effective. Insulin vials and pens in use may be left at room temperature for up to 4 weeks Teach patients to avoid prolonged exposure to direct sunlight or extreme hot/cold weather Store prefilled insulin syringes with 2 types; 30 days for 1 Store unopened insulin vials and pens in the refrigerator. Administration of Insulin Routine doses of insulin are given by subcutaneous injection. Regular insulin can be given IV when immediate onset of action is desired. Insulin is not taken orally because it is inactivated by gastric fluids. The fastest subcutaneous absorption is from the abdomen, followed by the arm, thigh, and buttock. Teach patients to rotate the injection within and between sites to prevent excess bruising Most commercial insulin is available as U100. This means that 1 mL contains 100 U of insulin. U100 insulin must be used with a U100-marked syringe. Insulin injections are typically given at a 45-90-degree angle. Insulin Pump: An insulin pump delivers a continuous subcutaneous short-acting insulin infusion through a small device worn on the belt, in a pocket, or under clothing. All insulin pumps are programmed to deliver a continuous infusion of rapid-acting insulin, known as the basal rate. Basal insulin can be temporarily increased or decreased based on carbohydrate intake, activity changes, or illness. People who have insulin pumps: ○ A person who failed to control diabetes on other regimens ○ Pregnant ○ Quality of life Risk of infection at site if not rotated every 24-48 hours Problems with Insulin Therapy Hypoglycemia: ○ Treatment includes administering glucagon 0.5-2mg (IM). After 20 minutes with no progression, administer again ○ When aroused, give 45 mg of carbs to replace glycogen stores Allergic Reactions: ○ Local inflammatory reactions to insulin may occur, such as itching, erythema, and burning around the injection site. ○ Local reactions may be self-limiting within 1 to 3 months or may improve with a low dose of antihistamine. Lipodystrophy ○ Lipodystrophy (loss of subcutaneous fatty tissue) may occur if the same injection sites are used frequently. Somogyi Effect ○ Hyperglycemia in the morning may be due to the Somogyi effect. ○ A high dose of insulin causes a decline in blood glucose levels during the night. As a result, counterregulatory hormones (e.g., glucagon, epinephrine, GH, cortisol) are released. The danger of this effect is that when blood glucose levels are measured in the morning, hyperglycemia is apparent and the patient (or the HCP) may increase the insulin dose. ○ If a patient has morning hyperglycemia, checking blood glucose levels between 2:00 and 4:00 AM for hypoglycemia Treatment- The treatment for Somogyi effect is a bedtime snack, reducing the dose of insulin, or both. Dawn Phenomenon ○ The dawn phenomenon is also characterized by hyperglycemia that is present on awakening. ○ The treatment for the dawn phenomenon is an increase in insulin or an adjustment in administration time. Drugs Therapy Drug: MOA: Nursing Considerations: Biguanides: Metformin The primary action of metformin is causes moderate weight loss; can to reduce glucose production by be used for people with type 2 the liver. diabetes and prediabetes who are overweight or obese. a-Glucosidase Inhibitors: Glyset, Works in the small intestine to slow Taken with the first bite of each Precose carb metabolism and delays main meal, they are most effective glucose absorption in lowering postprandial blood glucose. Their effectiveness is measured by checking 2-hour postprandial glucose levels. Sulfonylureas: Glucotrol, Glynase Stimulates the pancreatic cells to Most common side effect is secrete more insulin and hypoglycemia peripheral cells’ sensitivity to insulin Meglitinides: Prandin Stimulates the of insulin from the Hypoglycemia is a common side pancreatic islet cells; rapid acting effect Interprofessional Care: Patient and caregiver teaching and follow-up programs Nutrition therapy: ○ MyPlate was developed by the U.S. Department of Agriculture (USDA) to represent national nutrition guidelines for people with or without diabetes. ○ Starch, bread, fruit, milk and food groups raise blood sugar ○ Low carbs, lean meats, and vegetables are good sources to maintain a healthy diet and maintain a safe sugar range Nursing Care: ○ Patient education!!! Medication compliance, medication admin instruction, foot care, diet Acute Complications of Diabetes Diabetic Ketoacidosis (DKA) DKA is a serious condition that proceeds rapidly and must be treated promptly that is caused by a profound deficiency of insulin. It is characterized by hyperglycemia, ketosis, acidosis, and dehydration. WHY?? ○ Hyperglycemia: cells don’t have insulin to allow glucose in. This forces the body to use fat cells to break down glucose for energy ○ Ketoacidosis: the after-effect of fat cells being broken down for glucose stores ○ Dehydration: cells are hungry! They have no food so the body goes into severe dehydration. This is also caused by the hyperosmolarity in the extracellular fluid and NOT in the cells. The overload of sugar in ECF leads to vomiting in an attempt to excrete excess sugar. DKA Clinical Manifestations Dehydration Lethargy SWEET FRUITY BREATH (HALLMARK!!!!) KUSSMAUL RESPIRATIONS (RAPID, DEEP BREATHING W/ DYSPNEA)- body’s attempt to reverse metabolic acidosis by exhaling CO2 (respiratory compensation) Labs- Blood Glucose >250, pH

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