Care of Patients with Diabetes Mellitus

Chapter 67 Care of Patients with Diabetes Mellitus



Margaret Elaine McLeod



Learning Outcomes



Safe and Effective Care Environment



1. Assess the person who has diabetes for specific current and ongoing factors that pose threats to safety.


2. Administer insulin and other antidiabetic agents in a safe and accurate manner.


3. Apply the principles of infection control in the care of patients with diabetes.


4. Individualize patient teaching methods for diabetes management.


5. Teach patients and families the safe use of insulin injection equipment and glucose monitoring equipment.


6. Teach patients with peripheral neuropathy how to avoid injury.


Health Promotion and Maintenance



7. Encourage everyone to prevent type 2 diabetes by achieving and maintaining ideal weight and participating in regular exercise.


8. Teach all patients with diabetes how to self-manage their disease.


9. Teach the patient and family about the manifestations and emergency treatment of hypoglycemia and hyperglycemia.


Psychosocial Integrity



10. Allow the patient the opportunity to express concerns regarding the diagnosis of diabetes or the treatment regimen.


11. Explain all procedures, restrictions, drugs, and follow-up care to the patient and family.


12. Refer patients newly diagnosed with diabetes to local resources and support groups.


Physiological Integrity



13. Compare the risk factors, age of onset, manifestations, and pathologic mechanisms of type 1 and type 2 diabetes mellitus.


14. Explain the effects of insulin on carbohydrate, protein, and fat metabolism.


15. Explain how to mix different kinds of insulin together.


16. Evaluate laboratory data to determine effectiveness of the prescribed dietary, drug, and exercise therapies for diabetes.


17. Explain how to perform foot assessment and foot care for the patient with diabetes.


18. Collaborate with members of the health care team to provide care for patients with diabetic ketoacidosis (DKA) or hyperglycemic-hyperosmolar state (HHS).


image


http://evolve.elsevier.com/Iggy/


Animation: Insulin Function


Answer Keys for NCLEX Examination Challenges and Decision-Making Challenges


Audio Glossary


Audio Key Points


Concept Map Creator


Concept Map: Diabetes Mellitus—Type 2


Review Questions for the NCLEX® Examination


Diabetes mellitus (DM) is a chronic metabolic disease that requires lifelong behavioral and lifestyle changes. A collaborative approach helps the patient successfully manage the disease. As part of the team, you will plan, organize, and coordinate care with other health care team members to provide care and education and promote the patient’s health and well-being.


Diabetes is a major public health problem, and its complications, especially hypertension and hyperlipidemia (high blood lipid levels), cause many serious health problems. In the United States, diabetes mellitus (DM) is a leading cause of blindness, end-stage kidney disease, and foot or leg amputations. Many people have undiagnosed diabetes and, among those who are diagnosed, many have continuous high blood glucose levels. The complications of DM can be greatly reduced with glycemic (blood glucose) control along with management of hypertension and hyperlipidemia. Thus nursing priorities focus on helping the patient with diabetes achieve and maintain lifestyle changes that prevent long-term complications by keeping blood glucose levels and cholesterol levels as close to normal as possible (Young, 2011).



Pathophysiology



Classification of Diabetes


For all types of diabetes mellitus (DM), the main feature is chronic hyperglycemia (high blood glucose level) resulting from problems with insulin secretion, insulin action, or both. The disease is classified by the underlying problem causing a lack of insulin and the severity of the insulin deficiency. Table 67-1 outlines the types of DM.


TABLE 67-1 CLASSIFICATION OF DIABETES MELLITUS



















Type 1 Diabetes


• Beta-cell destruction leading to absolute insulin deficiency


• Autoimmune


• Idiopathic

Type 2 Diabetes


• Ranges from insulin resistance with relative insulin deficiency to secretory deficit with insulin resistance

Other Specific Conditions Resulting in Hyperglycemia


• Genetic defects of beta-cell function


• Genetic defects in insulin action


• Diseases of the exocrine pancreas: pancreatitis, trauma, neoplasia, cystic fibrosis, hemochromatosis


• Endocrinopathies: acromegaly, Cushing’s disease, glucagonoma, pheochromocytoma, hyperthyroidism, aldosteronism


• Drug or chemical-induced conditions (from use of pentamidine, nicotinic acid, glucocorticoids, thyroid hormone, diazoxide, beta-adrenergic agents, thiazides, phenytoin, interferon-alpha, other drugs)


• Infections: congenital rubella, cytomegalovirus, human immune deficiency virus


• Uncommon forms of immune-related diabetes


• Other genetic syndromes associated with diabetes: Down syndrome, Klinefelter syndrome, Turner’s syndrome, Huntington disease, and others

Gestational Diabetes Mellitus (GDM)


• Glucose intolerance with onset or first recognition during pregnancy


Data from American Diabetes Association (ADA). (2010a). Position statement: Diagnosis and classification of diabetes mellitus, Diabetes Care, 33(Suppl. 1), 62-69.



The Endocrine Pancreas


The pancreas has mostly exocrine functions that are related to digestion and endocrine functions that are related to blood glucose control. The endocrine portion of the pancreas has about 1 million small glands, the islets of Langerhans, scattered through the organ. The two types of islet cells important to glucose control are the alpha cells, which secrete glucagon, and the beta cells, which produce insulin and amylin. Glucagon is a “counterregulatory” hormone that has actions opposite those of insulin. It prevents hypoglycemia (low blood glucose levels) by triggering the release of glucose from cell storage sites. Insulin prevents hyperglycemia by allowing body cells to take up, use, and store carbohydrate, fat, and protein.


Active insulin is a protein made up of 51 amino acids. It is initially produced as inactive proinsulin, a prohormone that contains an additional amino acid chain (the C-peptide chain). Proinsulin is converted into active insulin by removal of the C-peptide (Fig. 67-1).


image

FIG. 67-1 Proinsulin, secreted by and stored in the beta cells of the islets of Langerhans in the pancreas, is transformed by the liver into active insulin. Insulin attaches to receptors on target cells, where it promotes glucose transport into the cells through the cell membranes.


About 40 to 50 units of insulin is secreted daily directly into liver circulation in a two-step manner. It is secreted at low levels during fasting (basal insulin secretion) and at increased levels after eating (prandial). An early burst of insulin secretion occurs within 10 minutes of eating. This is followed by an increasing release that lasts until the blood glucose level is normal.



Glucose Homeostasis


Glucose is the main fuel for central nervous system (CNS) cells. Because the brain cannot produce or store much glucose, it needs a continuous supply from circulation to prevent neuronal dysfunction and cell death. Other organs can use both glucose and fatty acids to generate energy. Glucose is stored inside cells as glycogen in the liver and muscles, and free fatty acids are stored as triglyceride in fat cells. Fat is the most efficient means of storing energy. Fat has 9 calories of stored energy per gram. Protein and carbohydrate have only 4 calories per gram. During a prolonged fast or after illness or injury, proteins are broken down and some of the amino acids are converted into glucose.


Several organs and hormones play a role in maintaining glucose homeostasis. During the fasting state, when the stomach is empty, blood glucose is maintained between 60 and 150 mg/dL (3.3 and 8.3 mmol/L) by a balance between glucose uptake by cells and glucose production by the liver. Insulin plays a pivotal role in this process.


Movement of glucose into some cells requires the presence of specific carrier proteins, glucose transport (GLUT) proteins and insulin. Insulin is like a “key” that opens “locked” membranes to glucose, allowing glucose in the blood to move into cells to generate energy. Insulin starts this action by binding to insulin receptors on the cell membranes, which changes membrane permeability to glucose.


Insulin exerts many effects on metabolism and cellular processes in different body tissues and organs. The main metabolic effects of insulin are to stimulate glucose uptake in skeletal muscle and heart muscle and to suppress liver production of glucose and very-low-density lipoprotein (VLDL). In the liver, insulin promotes the production and storage of glycogen (glycogenesis) at the same time that it inhibits glycogen breakdown into glucose (glycogenolysis). It increases protein and lipid (fat) synthesis and inhibits ketogenesis (conversion of fats to acids) and gluconeogenesis (conversion of proteins to glucose). In muscle, insulin promotes protein and glycogen synthesis. In fat cells, it promotes triglyceride storage. Overall, insulin keeps blood glucose levels from becoming too high and helps keep blood lipid levels in the normal range.


In the fasting state (not eating for 8 hours), insulin secretion is suppressed, which leads to increased gluconeogenesis in the liver and kidneys, along with increased glucose generation by the breakdown of liver glycogen. In the fed state, insulin released from pancreatic beta cells reverses this process. Instead, glycogen breakdown and gluconeogenesis are inhibited. At the same time, insulin also enhances glucose uptake and use by cells and reduces both fat breakdown (lipolysis) and protein breakdown (proteolysis). When more glucose is present in liver cells than can be metabolized for energy or stored as glycogen, insulin causes the excess glucose to be converted to free fatty acids (FFAs). These extra FFAs are deposited as fat in fat cells.


Glucose in the blood after a meal is controlled by the emptying rate of the stomach and delivery of nutrients to the small intestine where they are absorbed into circulation. Incretin hormones (e.g., GLP-1), secreted in response to the presence of food in the stomach, have several actions. They increase insulin secretion, inhibit glucagon secretion, and slow the rate of gastric emptying, thereby preventing hyperglycemia after meals.


Counterregulatory hormones increase blood glucose by actions opposite those of insulin when more energy is needed. Glucagon is the main counterregulatory hormone. Other hormones that increase blood glucose levels are epinephrine, norepinephrine, growth hormone, and cortisol. The combined actions of insulin and counterregulatory hormones (discussed in the next section) keep blood glucose levels in the range of 60 to 100 mg/dL (3.3 to 5.6 mmol/L) to support brain functions. When glucose levels fall, insulin secretion stops and glucagon is released. Glucagon causes the release of glucose from the liver. Liver glucose is made through breakdown of glycogen to glucose (glycogenolysis) and conversion of amino acids into glucose (gluconeogenesis). When liver glucose is unavailable, the breakdown of fat (lipolysis) and the breakdown of proteins (proteolysis) provide fuel for energy.



Absence of Insulin


Insulin is needed to move glucose into most body tissues. The lack of insulin in diabetes, from either a lack of production or a problem with insulin use at its cell receptor, prevents some cells from using glucose for energy. The body then breaks down fat and protein in an attempt to provide energy and also increases the levels of counterregulatory hormones in an attempt to make glucose from other sources. Table 67-2 outlines the body’s response to insufficient insulin.


TABLE 67-2 PHYSIOLOGIC RESPONSE TO INSUFFICIENT INSULIN







• Decreased glycogenesis (conversion of glucose to glycogen)


• Increased glycogenolysis (conversion of glycogen to glucose)


• Increased gluconeogenesis (formation of glucose from non-carbohydrate sources, such as amino acids and lactate)


• Increased lipolysis (breakdown of triglycerides to glycerol and free fatty acids)


• Increased ketogenesis (formation of ketones from free fatty acids)


• Proteolysis (breakdown of protein with amino acid release in muscles)


Without insulin, glucose builds up in the blood, causing hyperglycemia, which is high blood glucose levels. Hyperglycemia causes fluid and electrolyte imbalances, leading to the classic symptoms of diabetes: polyuria, polydipsia, and polyphagia.


Polyuria is frequent and excessive urination and results from an osmotic diuresis caused by excess glucose in the urine. As a result of diuresis, sodium, chloride, and potassium are excreted in the urine and water loss is severe. Dehydration results, and polydipsia (excessive thirst) occurs. Because the cells receive no glucose, cell starvation triggers polyphagia (excessive eating). Despite eating vast amounts of food, the person remains in starvation until insulin is available to move glucose into the cells.


With insulin deficiency, fats break down, releasing free fatty acids. Conversion of fatty acids to ketone bodies (small acids) provides a backup energy source. Because ketone bodies, or “ketones,” are abnormal breakdown products of fatty acids, they collect in the blood when insulin is not available, leading to metabolic acidosis.


The dehydration that occurs with diabetes leads to hemoconcentration (an increased blood concentration), hypovolemia (a decreased blood volume), hyperviscosity (thick, concentrated blood), poor tissue perfusion, and hypoxia (poor tissue oxygenation), especially to the brain. Hypoxic cells do not metabolize glucose efficiently, the Krebs’ cycle is blocked, and lactic acid increases, causing more acidosis.


The excess acids caused by absence of insulin increase hydrogen ion (H+) and carbon dioxide (CO2) levels in the blood, causing metabolic acidosis. These products trigger the respiratory centers of the brain to increase the rate and depth of respiration in an attempt to excrete more carbon dioxide and acid. This type of breathing is known as Kussmaul respiration. Acetone is exhaled, giving the breath a “fruity” odor. When the lungs can no longer offset acidosis, the blood pH drops. Arterial blood gas studies show a metabolic acidosis (decreased pH with decreased arterial bicarbonate [image] levels) and compensatory respiratory alkalosis (decreased partial pressure of arterial carbon dioxide [PaCO2]).


Insulin lack initially causes potassium depletion. With the increased fluid loss from hyperglycemia, excessive potassium is excreted in the urine, leading to low serum potassium levels. High serum potassium levels may occur in acidosis because of the shift of potassium from inside the cells to the blood. Serum potassium levels in DM, then, may be low (hypokalemia), high (hyperkalemia), or normal, depending on hydration, the severity of acidosis, and the patient’s response to treatment. Chapter 14 discusses acid-base balance and acidosis in more detail.



image Nclex Examination Challenge


Health Promotion and Maintenance


The client newly diagnosed with diabetes asks why he is always so thirsty. What is the nurse’s best response?



A. “The extra glucose in the blood increases the blood sodium level, which increases your sense of thirst.”


B. “Without insulin, glucose is excreted rather than used in the cells. The loss of glucose directly triggers thirst, especially for sugared drinks.”


C. “The extra glucose in the blood makes the blood thicker, which then triggers thirst so that the water you drink will dilute the blood glucose level.”


D. “Without insulin, glucose combines with blood cholesterol, which damages the kidneys, making you feel thirsty even when no water has been lost.”



Acute Complications of Diabetes


Three glucose-related emergencies can occur in patients with diabetes:



• Diabetic ketoacidosis (DKA) caused by lack of insulin and ketosis


• Hyperglycemic-hyperosmolar state (HHS) caused by insulin deficiency and profound dehydration


• Hypoglycemia from too much insulin or too little glucose


All three problems require emergency treatment and can be fatal if treatment is delayed or incorrect. These problems and their interventions are described later.



Chronic Complications of Diabetes


Diabetes mellitus (DM) can lead to health problems and early death because of changes in large blood vessels (macrovascular) and small blood vessels (microvascular) in tissues and organs. Complications result from poor tissue circulation and cell death. Macrovascular complications, including coronary heart disease, cerebrovascular disease, and peripheral vascular disease, lead to increased early death. Microvascular complications of blood vessel structure and function lead to nephropathy (kidney dysfunction), neuropathy (nerve dysfunction), and retinopathy (vision problems). Explanations for these diabetic vascular complications include:



• Chronic hyperglycemia thickens basement membranes, which causes organ damage.


• Glucose toxicity directly or indirectly affects functional cell integrity.


• Chronic ischemia in small blood vessels causes connective tissue hypoxia and microischemia.


Chronic high blood glucose levels are the main cause of microvascular complications and allow premature development of macrovascular complications. Additional risk factors that contribute to poor health outcomes for people with DM include smoking, physical inactivity, increased body weight, hypertension, and excessive blood levels of cholesterol and other fats. Many of these factors can be modified to reduced complications related to DM.


The Diabetes Control and Complications Trial (DCCT) showed that hyperglycemia is a critical factor for long-term complications in patients with type 1 DM. Intensive therapy aiming for blood glucose levels as close to normal as possible delays the onset and progression of retinopathy, nephropathy, neuropathy, and macrovascular disease. Additional studies show that intensive therapy with lowered blood glucose levels delays the onset of retinopathy, nephropathy, and neuropathy in patients with type 2 DM. A strong relationship exists between microvascular complications and blood glucose levels. For every percentage point decrease in HbA1c (hemoglobin A1c), a 35% reduction in the risk for kidney and eye complications has been shown.



Macrovascular Complications



Cardiovascular Disease


Diabetes mellitus (DM) is associated with a reduced life span, largely as a result of cardiovascular disease (CVD). Most patients with DM die as a result of a thrombotic event, usually myocardial infarction (MI). DM also affects the heart muscle, causing both systolic and diastolic heart failure. Left ventricular dysfunction with heart failure and fatal cardiac dysrhythmias are more common after MI in patients with DM.


Patients with diabetes, those with prediabetes, and those with metabolic syndrome are at increased risk for CVD. This excess risk affects women to a greater degree than men and is influenced by the patient’s ethnic group. The Adult Treatment Panel III of the National Cholesterol Education Program recommends that diabetes be considered a “coronary heart disease risk equivalent” and a target for aggressive reduction of risk factors.


Patients with DM often also have the traditional cardiovascular risk factors of obesity, hypertension, dyslipidemia, and sedentary lifestyle. Cigarette smoking and a positive family history greatly increase risk for CVD. Kidney disease, indicated by albuminuria (presence of albumin in the urine), increases the risk for coronary heart disease and mortality from MI. Patients with DM often have higher levels of C-reactive protein (CRP), an acute-phase inflammatory marker associated with increased risk for cardiovascular problems and death.


Cardiovascular complication rates can be reduced through aggressive management of hyperglycemia, hypertension, and hyperlipidemia. The American Diabetes Association (ADA) recommends that blood pressure be maintained below 130/80 mm Hg and that low-density lipoprotein (LDL) cholesterol remain below 100 mg/dL (2.60 mmol/L) for patients without manifestations of CVD and to less than 70 mg/dL (1.8 mmol/L) for patients with manifestations of CVD (ADA, 2010b). Diets high in saturated fat raise total cholesterol and LDL cholesterol levels, which increase the risk for coronary artery disease. Lifestyle modifications that focus on reducing saturated fat, trans fat, and cholesterol intake; increasing intake of omega-3 fatty acids, fiber, and plant sterols; weight loss (if indicated); and increasing physical activity are recommended to improve the lipid profile for patients with DM (ADA, 2010b).


Priority nursing actions focus on interventions to reduce modifiable risk factors associated with CVD, such as smoking cessation, diet, exercise, blood pressure control, maintenance of prescribed aspirin use, and maintenance of prescribed lipid-lowering drug therapy.

< div class='tao-gold-member'>

Related posts:

  1. End-of-Life Care
  2. Assessment of the Hematologic System
  3. Assessment of the Cardiovascular System
  4. Care of Patients with Noninfectious Lower Respiratory Problems

Stay updated, free articles. Join our Telegram channel
Tags:
Jul 18, 2016 | Posted by in NURSING | Comments Off on Care of Patients with Diabetes Mellitus

Full access? Get Clinical Tree
Get Clinical Tree app for offline access