Chapter 46

1. Chapter 46 Diabetes Mellitus and Hypoglycemia

2. Learning Objectives • Describe the role of insulin in the body. • Explain the pathophysiology of diabetes mellitus and hypoglycemia. • Describe the signs and symptoms of diabetes mellitus and hypoglycemia. • Explain tests and procedures used to diagnose diabetes mellitus and hypoglycemia. • Discuss treatment of diabetes mellitus and hypoglycemia. • Explain the difference between type 1 and type 2 diabetes mellitus.

3. Learning Objectives • Differentiate between acute hypoglycemia and diabetic ketoacidosis. • Describe the treatment of a patient experiencing acute hypoglycemia or diabetic ketoacidosis. • Describe the complications of diabetes mellitus. • Identify nursing interventions for a patient diagnosed with diabetes mellitus or hypoglycemia. • Identify nursing interventions for a patient diagnosed with ketoacidosis.

4. Diabetes Mellitus

5. Pathophysiology Chronic disorder of impaired metabolism with vascular and neurologic complications Key feature is elevated blood glucose, called hyperglycemia Blood glucose level normally regulated by insulin, a hormone produced by beta cells in the islets of Langerhans located in the pancreas

6. Type 1 Absence of endogenous insulin Formerly called juvenile-onset diabetes because it most commonly occurs in juveniles and young adults An autoimmune process, possibly triggered by a viral infection, destroys beta cells, the development of insulin antibodies, and the production of islet cell antibodies (ICAs) Affected people require exogenous insulin for the rest of their lives

7. Type 2 Inadequate endogenous insulin and body’s inability to properly use insulin Beta cells respond inadequately to hyperglycemia; results in chronically elevated blood glucose Continuous high glucose level in the blood desensitizes the beta cells; they become less responsive to the elevated glucose More common in adults; increasing in children Controlled by diet and exercise; may require oral hypoglycemic agents or exogenous insulin

8. Role of Insulin Glucose Insulin stimulates active transport of glucose into cells If insulin absent, glucose remains in the bloodstream Blood becomes thick, which increases its osmolality Increased osmolality stimulates the thirst center Increased fluid does not pass into body tissues; high serum osmolality retains fluid in the bloodstream As blood passes through the kidneys, some glucose eliminated Osmotic force created by glucose draws extra fluid and electrolytes with it, causing abnormally increased urine volume

9. Role of Insulin Fatty acids Promotes fatty acid synthesis and conversion of fatty acids into fat, which is stored as adipose tissue Also spares fat by inhibiting breakdown of adipose tissue and mobilization of fat and by inhibiting the conversion of fats to glucose Without adequate insulin, fat stores break down and increased triglycerides are stored in the liver Increased fatty acids in the liver can triple the production of lipoproteins; promotes atherosclerosis

10. Role of Insulin Protein Enhances protein synthesis in tissues and inhibits the conversion of protein into glucose Amino acids are admitted into cells; enhances rate of protein formation while preventing protein degradation Without adequate insulin, protein storage halts; large amounts of amino acids dumped into the bloodstream High levels of plasma amino acids place people with diabetes at risk for development of gout Changes in protein metabolism lead to extreme weakness and poor organ functioning

11. Etiology An autoimmune malfunction may cause complete destruction of the islets of Langerhans in the pancreas, creating type 1 diabetes Islet cell antibodies are identified in more than 80% of all people with type 1 diabetes at the time of diagnosis

12. Figure 46-1

13. Risk Factors Obesity Sedentary lifestyle Family history of diabetes Age 40 years and older History of gestational DM History of delivering infant weighing more than 10 lb African American (33% higher risk for type 2 DM) Latin American/Hispanic (>300% higher risk for type 2 DM) American Indians (33%-50% higher risk for type 2 DM)

14. Risk Factors Metabolic syndrome Thought to be a precursor to diabetes Impaired glucose tolerance, high serum insulin, hypertension, elevated triglycerides, low HDL cholesterol, altered size and density of LDL cholesterol Believed that metabolic syndrome is a chronic low-grade inflammatory process affecting endothelial tissue Long-term effects: atherosclerosis, ischemic heart disease, left ventricular hypertrophy, type 2 DM Research directed at learning how to detect this syndrome early and what interventions might slow or arrest the progress

15. Long-Term Complications

16. Microvascular Complications Retinopathy Pathological changes in the retina that are associated with DM Nephropathy Kidney damage

17. Macrovascular Complications Accelerated atherosclerotic changes in the person with diabetes Associated with coronary artery disease (CAD), cerebral vascular accidents (CVA or stroke), and peripheral vascular disease (PVD)

18. Long-Term Complications

19. Neuropathic Complications Neuropathy: pathologic changes in nerve tissue Mononeuropathy affects a single nerve or group of nerves Polyneuropathy involves both sensory and autonomic nerves Autonomic neuropathy affects the sympathetic and parasympathetic nervous systems

20. Hypoglycemic Unawareness The usual symptoms of tachycardia, palpitations, tremor, sweating, and nervousness may be absent Patient may suddenly have changes in mental status as the first sign of hypoglycemia

21. Long-Term Complications Foot complications of diabetes May have foot problems associated with neuropathy, inadequate blood supply, or a combination Mechanical irritation Thermal injury Chemical irritation

22. Long-Term Complications: Prevention Diabetes Control and Complications Trial (DCCT): intensive treatment of type 1 DM delayed the onset or slowed the progress of diabetic retinopathy, nephropathy, and neuropathy Outcome of United Kingdom Prospective Diabetes Study (UKPDS): similar benefits of tight control with type 2 DM

23. Long-Term Complications: Prevention ADA recommends Blood pressure: <130 systolic, <80 diastolic Total cholesterol: <200 mg/dL LDL: <100 mg/dL HDL: >45 mg/dL for men (>55 mg/dL for women) Triglyceride: <150 mg/dL

24. Acute Emergency Complications

25. Acute Hypoglycemia Dangerous drop in blood glucose Causes Taking too much insulin, not eating enough food or not eating at the right time, an inconsistent pattern of exercise Gastroparesis, renal insufficiency, and certain drugs including aspirin and beta-adrenergic blockers

26. Acute Hypoglycemia Signs and symptoms Adrenergic: shakiness, nervousness, irritability, tachycardia, anxiety, lightheadedness, hunger, tingling or numbness of the lips or tongue, and diaphoresis Neuroglucopenia: drowsiness, irritability, impaired judgment, blurred vision, slurred speech, headaches, and mood swings progressing to disorientation, seizures, and unconsciousness

27. Acute Hypoglycemia Treatment Give patient 10 to 15 g of quick-acting carbohydrates Repeat every 15-30 minutes until blood glucose is >70 mg/dL for adults, 80 to 100 mg/dL for older adults and children If patient is unable to swallow, an IM or subcutaneous injection of 1 mg of glucagon or an IV dose of 50 mL of 50% dextrose should be given as ordered or per protocol

28. Diabetic Ketoacidosis (DKA) Life-threatening emergency caused by a relative or absolute deficiency of insulin Early signs and symptoms Anorexia, headache, and fatigue As condition progresses, classic symptoms of polydipsia, polyuria, and polyphagia develop If untreated, patient becomes dehydrated, weak, and lethargic with abdominal pain, nausea, vomiting, fruity breath, increased respiratory rate, tachycardia, blurred vision, and hypothermia

29. Diabetic Ketoacidosis (DKA) Late signs Air hunger (Kussmaul’s respirations), coma, and shock Death can result without prompt medical care

30. Diabetic Ketoacidosis (DKA) Treatment aimed at correction of three main problems Dehydration Electrolyte imbalance Acidosis

31. Hyperglycemic Hyperosmolar Nonketotic Syndrome Patient goes into a coma from extremely high glucose levels (>600 mg/dL) There is no evidence of elevated ketones Pancreas produces enough insulin to prevent breakdown of fatty acids and formation of ketones, but not enough to prevent hyperglycemia Persistent hyperglycemia causes osmotic diuresis, resulting in loss of fluid and electrolytes Dehydration and hypernatremia develop May be caused by the same factors that trigger ketoacidosis

32. Medical Diagnosis One or more of the following criteria on two separate occasions is considered DM Polyuria, polydipsia, polyphagia, unexplained weight loss plus random glucose level >200 mg/dL Fasting serum glucose level >126 mg/dL (after at least an 8-hour fast) Two-hour postprandial glucose level >200 mg/dL during oral glucose tolerance test (OGTT) under specific guidelines. Test must use a glucose load of 75 g of anhydrous glucose dissolved in water

33. Medical Diagnosis Prediabetes Individuals with impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) Individuals should receive education on weight reduction and increasing physical activity

34. Medical Diagnosis Oral glucose tolerance test Diet of 150 to 300 g carbohydrate for 3 days before test Night before test, patient fasts after midnight Morning of test, blood drawn for fasting serum glucose Patient then given a drink (Glucola) containing 75 g of carbohydrates and instructed to remain quiet Blood drawn at 30 minutes and 1 hour after the ingestion of glucose. After these two samples, blood is drawn at hourly intervals until the test is completed

35. Medical Treatment Nutritional management Medical nutrition therapy (MNT) is an important part of diabetes management; should be included in diabetes self-management education Because of complexity of nutritional management, a registered dietitian should be part of the diabetes management team, and the individual with diabetes should be included in decision making

36. Medical Treatment Exercise Effective adjunct for people with diabetes Aids in weight loss, improves cardiovascular conditioning, improves insulin sensitivity, and promotes a sense of well-being Exercising muscle uses glucose at 20 times the rate of a muscle at rest and does not require insulin

37. Insulin Therapy All patients with type 1 disease need insulin injections; some patients with type 2 disease may eventually need insulin Insulins classified by source and course of action Source: human, pork, or beef (beef is being phased out) Course of action: rapid acting, short acting, intermediate acting, and long acting All rapid-acting and short-acting insulins are clear The other insulins are cloudy

38. Figure 46-2

39. Insulin Therapy Route Oral: insulin cannot be given orally because it is rendered useless in the gastrointestinal tract Subcutaneously: all insulins can be given subcutaneously Intravenously: ONLY regular insulin can be given intravenously Inhalation: a form of insulin that can be taken by inhalation has recently been approved, but it is not yet widely used

40. Insulin Therapy Concentrations U-100 insulin has 100 units/mL Most commonly used U-500 insulin has 500 units/mL Used only in emergencies and for patients who are extremely insulin resistant U-40 insulin has 40 units/mL Not available in the United States

41. Insulin Therapy Premixed insulin products Contain both Regular and NPH insulin 70% NPH and 30% Regular insulin 50% NPH and 50% Regular insulin 75% NPH and 25% Lispro

42. Insulin Therapy Dosing schedules Conventional therapy Typically uses a combination of a short-acting and an intermediate- or long-acting insulin Intensive therapy To achieve tight control; may require 3 or 4 injections daily Continuous subcutaneous insulin infusion Patient has indwelling subcutaneous catheter connected to an external portable infusion pump; pump delivers Regular insulin continuously

43. Insulin Therapy Insulin mixing Two types can be mixed in one syringe to avoid two injections Insulin injection Site rotation helps prevent lipohypertrophy or lipoatrophy Absorption rate varies with different body sites American Diabetes Association recommends rotating sites within one anatomic area rather than moving among all areas See Figure 46-3

44. Figure 46-3

45. Insulin Therapy Insulin pump Needle is inserted subcutaneously in an appropriate part of the anatomy Pump is programmed to deliver a steady trickle of insulin throughout the day and can provide a bolus of insulin at mealtimes

46. Figure 46-4

47. Insulin Therapy Intranasal route Only 10% of the drug is absorbed through the nasal mucosa, making it relatively expensive to use Nasal irritation is a frequent side effect Only Regular insulin is given intranasally Insulin catheter Indwelling subcutaneous catheters may be placed in the abdomen to permit repeated insulin injections without repeated needlesticks

48. Oral Hypoglycemic Agents If patients with type 2 DM unable to control blood glucose with nutrition and exercise, physician may prescribe oral hypoglycemics Sulfonylureas (three generations), alpha-glucosidase inhibitors, biguanides, thiazolidinediones, D-phenylalanines, meglitinides Combination oral medications ACTOplus met (pioglitazone and metformin), Avandamet (rosiglitazone and metformin), Avandaryl (rosiglitazone and glimepiride), Glucovance (glyburide and metformin), Metaglip (glipizide and metformin)

49. Self-Monitoring of Blood Glucose Allows patients to monitor blood glucose levels to regulate their diet, exercise, and medication regimens to remain euglycemic Portable electronic glucose meters have largely replaced other methods of self-monitoring

50. Glycosylated Glucose Levels Glycosylated hemoglobin (HbA1c) reflects glucose levels over the past few months Fructosamine levels reflect those over several weeks