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Diabetes Mellitus (DM) – Chapter 46
A group of diseases characterized by hyperglycemia caused by defects in insulin secretion, insulin action, or both. Affects nearly 34.1 million people in the United States; one third of the cases are undiagnosed. Prevalence is increasing. Ethnic and racial minority populations are disproportionately affected.
Classification of
Diabetes
Type 1 diabetes Type 2 diabetes Gestational diabetes Prediabetes Latent autoimmune diabetes of adults (LADA) Diabetes associated with other conditions or syndromes
Functions of Insulin
Transports and metabolizes glucose for energy. Stimulates storage of glucose in the liver and muscle as glycogen. Signals the liver to stop the release of glucose. Enhances storage of dietary fat in adipose tissue. Accelerates transport of amino acids into cells. Inhibits the breakdown of stored glucose, protein, & fat.
Type 1 Diabetes
Pathophysiology
Insulin-producing beta cells in the pancreas are destroyed by a combination of genetic, immunologic, and/or environmental factors. o In addition to genetic and immunologic components, environmental factors such as viruses or toxins that may initiate destruction of the beta cell continue to be investigated. Results in decreased insulin production, unchecked glucose production by the liver, and fasting hyperglycemia. Affects 5% to 10% of adults with diabetes.
When excess glucose is excreted in the urine, it is accompanied by excessive loss of fluids and electrolytes. o This is called osmotic diuresis. Fat breakdown occurs, resulting in an increased production of ketone bodies, a highly acidic substance formed when the liver breaks down free fatty acids in the absence of insulin. Diabetic ketoacidosis (DKA) is a metabolic derangement that occurs most commonly in persons with type 1 diabetes and results from a deficiency of insulin; highly acidic ketone bodies are formed, and metabolic acidosis occurs. o The three major metabolic derangements are hyperglycemia, ketosis, and metabolic acidosis. o DKA is commonly preceded by a day or more of polyuria, polydipsia, nausea, vomiting, and fatigue with eventual stupor and coma if not treated. o The breath has a characteristic fruity odor due to the presence of ketoacids.
Type 2 Diabetes
Pathophysiology
Insulin resistance and impaired insulin secretion. o Insulin resistance refers to a decreased tissue sensitivity to insulin. The exact mechanisms that lead to insulin resistance and impaired insulin secretion in type 2 diabetes are unknown, although genetic factors are thought to play a role. Affects 90% to 95% of adults with diabetes, onset at or over age 30 years, increasing in children r/t obesity. Slow, progressive glucose intolerance. Obesity usually presents at diagnosis. To overcome insulin resistance and to prevent the buildup of glucose in the blood, increased amounts of insulin must be secreted to maintain the glucose level at a normal or slightly elevated level. If the beta cells cannot keep up with the increased demand for insulin, the glucose level rises, and type 2 diabetes develops. Insulin resistance may also lead to metabolic syndrome, which is a constellation of symptoms, including hypertension, hypercholesterolemia, abdominal obesity, and other abnormities. Despite the impaired insulin secretion that is characteristic of type 2 diabetes, there is enough insulin present to prevent the breakdown of fat and the accompanying production of ketone bodies. o Therefore, DKA does not typically occur in type 2 diabetes. o Uncontrolled type 2 diabetes may lead to another acute problem – Hyperglycemic hyperosmolar syndrome (HHS) If the patient experiences symptoms, they are frequently mild and may include: o Fatigue o Irritability o Polyuria
Medical Management of Diabetes
Main goal is to normalize insulin activity & blood glucose levels to reduce the development of complications. The ADA now recommends HgbA1c less than 6.5%. Diabetes management has five components: o Nutritional therapy o Exercise o Monitoring o Pharmacologic therapy o Education The therapeutic goal for diabetes management is to achieve euglycemia (normal blood glucose levels) without hypoglycemia while maintaining a high quality of life.
Dietary Management
Nutrition, meal planning, weight control, and increased activity are the foundation of diabetes management. Management goals: o Control of total caloric intake to attain or maintain a reasonable body weight o Control of blood glucose levels o Normalization of lipids and blood pressure to prevent heart disease o To prevent, or at least slow, the rate of development of the chronic complications of diabetes by modifying nutrient intake and lifestyle. o To address individual nutrition needs, taking into account personal and cultural preferences and willingness to change. o To maintain the pleasure of eating by only limiting food choices when indicated by scientific evidence. Nurse's role: o Be knowledgeable about dietary management o Communicate with dietician or other management specialists o Reinforce patient understanding o Support dietary and lifestyle changes
Meal Planning
Consider food preferences, lifestyle, usual eating times, and cultural and ethnic background. Review diet history and need for weight loss, gain, or maintenance.
Caloric requirements and calorie distribution throughout the day; exchange lists o Carbohydrates: 50% to 60% carbohydrates; emphasize whole grains In general, carbohydrate foods have the greatest effect on blood glucose levels because they are more quickly digested than other foods and are converted into glucose rapidly. o Fat: 20% to 30% This approach may help reduce risk factors such as increased serum cholesterol levels, which are associated with the development of coronary artery disease—the leading cause of death and disability among people with diabetes. o Nonanimal sources of protein (e.g., legumes, whole grains) and increase fiber Refer to Table 46-2 for exchange list.
Glycemic Index
Combining starchy foods with protein and fat slows absorption and glycemic response. Raw or whole foods tend to have lower responses than cooked, chopped, or pureed foods. Eat whole fruits rather than juices; this decreases glycemic response because of fiber (slowing absorption). Adding food with sugars may produce lower response if eaten with foods that are more slowly absorbed.
Other Dietary Concerns
Alcohol o Large amounts can be converted to fats, increasing the risk for DKA. o Alcohol consumption may lead to excessive weight gain (from the high caloric content of alcohol), hyperlipidemia, and elevated glucose levels (especially with mixed drinks and liqueurs). o Patient education regarding alcohol intake must emphasize moderation in the amount of alcohol consumed. o Moderate intake is considered to be one alcoholic beverage per day for women and two per day for men. o Lower-calorie or less-sweet drinks (e.g., light beer, wine) and food intake along with alcohol consumption are advised. Nutritive & nonnutritive sweeteners o The nutritive sweeteners contain calories, and the nonnutritive sweeteners have few or no calories in the amounts normally used. o Nutritive sweeteners include: Fructose (fruit sugar), sorbitol, and xylitol, all of which provide calories in amounts similar to those in sucrose (table sugar). They cause less elevation in blood sugar levels than sucrose does and are often used in sugar-free foods. Sweeteners containing sorbitol may have a laxative effect. o Nonnutritive sweeteners have minimal or no calories. They are used in food products and are also available for table use. They produce minimal or no elevation in blood glucose levels, and the U.S. Food and Drug Administration (FDA) lists them as safe for people with diabetes. Misleading food labels o Foods labeled “sugarless” or “sugar-free” may still provide calories equal to those of the equivalent sugar-containing products if they are made with nutritive sweeteners. o Therefore, these foods should not be considered “free” foods to be eaten in unlimited quantity, because they can elevate blood glucose levels.
In many cases, insulin injections are given two or more times daily to control the blood glucose level. Blood glucose monitoring: o Individualize treatment regimen to obtain optimal blood glucose control o Self-monitoring of blood glucose (SMBG) levels has dramatically altered diabetes care Categories of insulin: o Rapid acting o Short acting: regular insulin o Intermediate acting: NPH insulin o Long acting: No peak o Rapid-acting inhalation powder: Afrezza
Insulin Regimen
Insulin preparations vary according to time course of action, source, and manufacturer. Table 46-4 describes several insulin regimens and the advantages and disadvantages of each. Two general approaches to insulin therapy: o Conventional o Intensive
Complication of Insulin Therapy
Local allergic reactions o A local allergic reaction (redness, swelling, tenderness, and induration or a 2- to 4-cm wheal) may appear at the injection site 1 to 2 hours after the administration of insulin. Reactions usually resolve in a few hours or days. If they do not resolve, another type of insulin can be prescribed. Systemic allergic reactions o Systemic allergic reactions to insulin are rare. When they do occur, there is an immediate local skin reaction that gradually spreads into generalized urticaria (hives). These rare reactions are occasionally associated with generalized edema or anaphylaxis. The treatment is desensitization, with small doses of insulin given in gradually increasing amounts using a desensitization kit. Insulin lipodystrophy o Lipodystrophy refers to a localized reaction, in the form of either lipoatrophy or lipohypertrophy, occurring at the site of insulin injections. Lipoatrophy is the loss of subcutaneous fat; it appears as slight dimpling or more serious pitting of subcutaneous fat. The use of human insulin has almost eliminated this disfiguring complication. o Lipohypertrophy, the development of fibrofatty masses at the injection site, is caused by the repeated use of an injection site. If insulin is injected into scarred areas, absorption may be delayed. This is one reason that rotation of injection sites is so important. Patients should avoid injecting insulin into these areas until the hypertrophy disappears. Resistance to injected insulin. o Patients may develop insulin resistance and require large insulin doses to control symptoms of diabetes. In most patients with diabetes who take insulin, immune antibodies develop and bind the insulin, thereby decreasing the insulin available for use. All insulins cause some antibody production in humans. Morning hyperglycemia (Chart 46-5)
Methods of Insulin Delivery
Traditional subcutaneous injections Insulin pens
Jet injectors Insulin pumps Future: Implantable insulin pumps
Educating Patients in Insulin Self-Management
For patients with newly diagnosed type 2 diabetes, emphasis is initially placed on meal planning, exercise, and weight loss if applicable. Those who are starting to take oral antidiabetic agents need to know about detecting, preventing, and treating hypoglycemia. If diabetes has gone undetected for many years, the patient may already be experiencing some chronic complications from diabetes. o Therefore, for some patients with newly diagnosed type 2 diabetes, basic diabetes education must include information on preventive skills, such as foot care & eye care. Use and action of insulin Symptoms of hypoglycemia and hyperglycemia o Required actions Blood glucose monitoring Self-injection of insulin Insulin pump use Which insulin agent is rapid acting? a. Regular b. Glargine detemir c. Aspart d. NPH Rationale: Aspart is a rapid-acting insulin, as are lispro and glulisine. Rapid-acting insulins are used for rapid reduction of glucose level, to treat postprandial hyperglycemia, and/or to prevent nocturnal hypoglycemia.
Oral Antidiabetic Agents
Used for patients with type 2 diabetes who require more than diet and exercise alone. Combinations of oral drugs may be used. Major side effect: hypoglycemia. Nursing interventions: o Monitor blood glucose for hypoglycemia and other potential side effects. Patient education Table 46-
Acute Complications of
Diabetes
o Subcutaneous or intramuscular glucagon (1 mg) o 25 to 50 mL of 50% dextrose solution IV Mild Hypoglycemia (Tremors, Shakiness, Diaphoresis, Excessive hunger, Pallor, Tachycardia, Paresthesia) o 10 to 15 grams of Carbohydrate Moderate Hypoglycemia (H/A, Mood swings, Drowsiness, Slurred speech, Double vision, impair judgment, irritability) o 20 to 30 grams carbohydrates, Glucagon,1 mg, SC or IM Severe Hypoglycemia (Disorientation, Sz. Unconsciousness) o 10 to 25grams of Glucose (as 50% or 25% of IV dextrose) o Glucagon, 1 mg IM or IV Cold & clammy, I need some candy; hot & dry, my sugar is high.
Diabetic Ketoacidosis (DKA)
Absence or inadequate amount of insulin resulting in abnormal metabolism of carbohydrate, protein, and fat. Clinical features Hyperglycemia Dehydration Acidosis Physiology/Pathophysiology: Refer to Figure 46- o Diabetic ketoacidosis (DKA) is a metabolic derangement that occurs most commonly in persons with type 1 diabetes and results from a deficiency of insulin; highly acidic ketone bodies are formed, and metabolic acidosis occurs. The three major metabolic derangements are hyperglycemia, ketosis, and metabolic acidosis. DKA is commonly preceded by a day or more of polyuria, polydipsia, nausea, vomiting, and fatigue with eventual stupor and coma if not treated. The breath has a characteristic fruity odor due to the presence of ketoacids.
Clinical Manifestations
Onset: slow (4-10 hours) around 12 pm to 5pm Insulin Durations History: Too little or lack of insulin, GI upset, febrile illness, skipping doses of insulin, infection, surgery, stress, puberty, pregnancy and inability to respond to an increased need. Signs and symptoms: o Breath smells sweet like juicy fruit gum o Tachycardia o Hypotension o Acidosis o High Blood Sugar o Hyperkalemia Needs: Hydration, Insulin and Replacement Tx.
Assessment of DKA
Blood glucose levels between 250 and 800 mg/dL. Severity of DKA not only due to blood glucose level. Ketoacidosis is reflected in low serum bicarbonate, low pH; low PCO2 reflects respiratory compensation (Kussmaul respirations).
Ketone bodies in blood and urine. Electrolytes vary according to degree of dehydration; increase in creatinine, Hct, BUN.
Management of DKA
Rehydration with IV fluid. IV continuous infusion of regular insulin. Reverse acidosis and restore electrolyte balance. Note: rehydration leads to increased plasma volume and decreased K; insulin enhances the movement of K+ from extracellular fluid into the cells. Monitor blood glucose, renal function and urinary output, ECG, electrolyte levels, VS, lung assessments for signs of fluid overload.
Hyperglycemic Hyperosmolar Syndrome (HHS)
Hyperosmolar hyperglycemia is caused by a lack of sufficient insulin; ketosis is minimal or absent. Hyperglycemia causes osmotic diuresis, loss of water and electrolytes, hypernatremia, and increased osmolality. Manifestations include hypotension, profound dehydration, tachycardia, and variable neurologic signs caused by cerebral dehydration. High mortality rate.
Management of HHS
Rehydration Insulin administration Monitor fluid volume and electrolyte status Prevention Diagnosis and management of diabetes Assess and promote self-care management skills
Long-term Complications of Diabetes
Macrovascular: accelerated atherosclerotic changes; coronary artery disease, cerebrovascular disease, peripheral vascular disease. Microvascular: microangiopathy; diabetic retinopathy (refer to Table 46-7), nephropathy. Neuropathic: peripheral neuropathy, autonomic neuropathies, hypoglycemic unawareness, neuropathy, sexual dysfunction. True or False: Diabetes leads to only microvascular complications. Rationale: Long-term complications of diabetes can affect almost every organ system of the body and are a major cause of disability. The general categories of long-term diabetic complications are macrovascular disease, microvascular disease, and neuropathy.
Macrovascular Complications
Coronary artery disease o Death is 2 to 4 X’s ↑ o Women 3-4 x’s > risk factor (esp. in their 50’s & 60y/o)
Replace carbohydrates with liquid ones if the client is unable to eat. Call MD if client has vomiting over 4 hours. Travel Keep snack for emergencies (raisins, nuts, crackers, hard candy). Letter giving medical background. In case of illness (notify family physician, family/next of kin). Always wear medical ID tag. Carry two packages of glucagon. Have spare prescriptions for medication. Main Considerations o Changes in activity level Changes in daily schedule I.E., timing of meals, changes in time zone. Patient should inform airline if special meal is needed. Keep medications and diabetic supplies with you in a carry-on luggage. Always have your doctor’s number, insurance card and emergency number. Storage & Safety Tips Keep used bottle of insulin at room temperature. Store extra bottles in the refrigerator. Gently roll the bottle between your hands before filling the syringe. Do not use past the expiration date. Rotate sites. Draw regular insulin first when mixing (Note: clear to cloudy).
