Diabetes mellitus is a group of metabolic disorders that are characterized by chronically high blood sugar, resulting from defects of the secretion of insulin, insulin action, or both. There are two main types of diabetes. Type 1 diabetes is also called insulin dependent diabetes mellitus (IDDM) and is caused by a lack of insulin secretion by the beta cells of the pancreas. Types 2 diabetes, or non-insulin dependent diabetes mellitus (NIDDM), is caused by decreased sensitivity to insulin (Belonwu et al., 2013). “The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of different organs, especially the eyes, kidneys, nerves, heart, and blood vessels (American Diabetes Association, 2013).”
Prevalence of Diabetes Mellitus in U.S. and Risk Factors (Orlando)
The prevalence of both diagnosed and undiagnosed diabetes in the United States is remarkably high. An estimated 30.3 million people of all ages—or 9.4% of the U.S. population—had diabetes in 2015. This includes 30.2 million adults aged 18 years or older (12.2% of all U.S. adults), and 7.2 million (23.8%) of those adults were unaware of having diabetes (National Diabetes Statistics Report, 2017). The percentage of adults with diabetes increase with age; 25.2% of those were aged 65 years or older. Compared to non-Hispanic whites, the age-adjusted prevalence of diagnosed and undiagnosed diabetes was higher among Asians, non-Hispanic blacks, and Hispanics during 2011–2014 (National Diabetes Statistics Report, 2017). The World Health Organization predicted that the worldwide prevalence of diabetes will have almost doubled by the year 2030. That’s 177 million people in the year 2000 to 370 million (Belonwu et al., 2013)
It is estimated that 23.1 million people—or 7.2% of the U.S. population—have been diagnosed with diabetes. This includes 132,000 children and adolescents younger than 18 years of age (0.18% of the total U.S. population younger than age 18 years) and 193,000 children and adolescents younger than 20 years of age (0.24% of the total U.S. population younger than age 20 years). Type 2 diabetes is the predominant form of diabetes and accounts for at least 90% of all cases of diabetes mellitus (Belonwu, et al., 2013). About 5% of people with diabetes are estimated to have type 1 diabetes (National Diabetes Statistics Report, 2017).
The Centers for Disease Control and Prevention (CDC, 2017) state that a person is at risk for prediabetes if he/she is overweight, age 45 years or older, has a parent, brother, or sister with type 2 diabetes, is physically active less than 3 times a week, has ever had gestational diabetes, or gave birth to a baby who weighed more than 9 pounds. African Americans, Hispanic/Latino Americans, American Indians, Alaska Natives, some Pacific Islanders, and Asian Americans are also at higher risk. A person is at risk for developing type 2 diabetes if he/she has prediabetes and also all of the other aforementioned risk factors. The American Diabetes Association (2017) also say that smoking, high blood pressure, high cholesterol, and high blood glucose puts an adult at risk for diabetes type 2. Risk factors for type 1 diabetes are not as clear as they are for prediabetes and type 2 diabetes. Known risk factors for type 1 diabetes are family history, having a parent, brother, or sister with type 1 diabetes, and age. A person can get type 1 diabetes at any age, but it’s more likely to develop when you’re a child, teen, or young adult. In the United States, whites are more likely to develop type 1 diabetes than African Americans and Hispanic/Latino Americans. (National Diabetes Statistics Report, 2017).
Etiology and Pathophysiology of the Disease (Orlando)
IDDM is the result of an autoimmune response to the proteins of the islets cells of the pancreas (Belonwu et. al., 2013). The selective destruction of insulin producing pancreatic beta-cells leads to type 1 diabetes. Research shows that there is a robust connection between IDDM and other endocrine autoimmunity; and that there is an increased incidence of autoimmune diseases in family members of IDDM patients (Belonwu et al., 2013). The three types of autoantibodies that known to cause IDDM are islet cytoplasmic antibodies (ICCA), islet cell surface antibodies (ICSA), and specific antigenic targets of islet cells. The presence of antibodies to ICCA is a strong indicator of future development of IDDM. ICSA positive results are shown in 80% of type 1 diabetics while some type 2 diabetics have also been identified. The presence of antibodies to glutamic acid decarboxylase (GAD) is also a strong predictor of future development of IDDM in high risk populations. Anti-insulin antibodies (IAA) have also been identified in IDDM patients (Belonwu et al., 2013).
IDDM is caused when circulating insulin is extremely low or absent, plasma glucagon is elevated, and the pancreatic beta cells fail to respond to all insulin-secretory stimuli. Insulin has effects on glucose metabolism, lipid metabolism, and protein metabolism. The destruction of the insulin-secreting cells of the islets of Langerhans causes insulin deficiency. Absolute insulin deficiency causes disruption of glucose uptake into muscle and adipose cells, and an absence of inhibition of hepatic glucose production, lipolysis, and increased catabolism of protein. These disruptions lead to hyperglycemia, hypertriglyceridemia, and an increased rate of protein degradation. Extreme insulin deficiency leads to osmotic diuresis and dehydration as well as elevated free fatty acid levels and diabetic ketoacidosis (DKA). Muscle wasting is observed in patients with uncontrolled IDDM and results from the inability to stimulate amino acid uptake and protein synthesis and inhibit protein degradation. (American Association of Clinical Endocrinologists: Diabetes Resource Center, 2017).
NIDDM is a disorder caused by a combination of genetic factors related to impaired insulin secretion, insulin resistance, and environmental factors such as obesity, lack of exercise, overeating, and stress (Belonwu et al., 2013). These factors induce insulin resistance, impair insulin secretion, and increases glucagon production. Plasma glucose is maintained within a narrow range by homeostatic interaction between tissue sensitivity to insulin and insulin secretion. The consequence of the breakdown of these mechanisms is type 2 diabetes. (Belonwu, et al., 2013) Since impaired insulin secretion and insulin resistance develops slowly, the disease progressively worsens over time due to chronic hyperglycemia. (AACE, 2017) “Insulin released in response to β-cell stimulation mediates uptake of glucose, amino acids, and fatty acids by insulin-sensitive tissues. In turn, these tissues feedback information to islet cells about their need for insulin. The mediator of this process has not been identified, but probably includes integration between the brain and humoral system. If insulin resistance is present, as often happens in people with obesity, β cells increase insulin output to maintain normal glucose tolerance. However, if β cells are incapable of this task, plasma concentrations of glucose increase (Cooper, et al., 2014).”
Signs and symptoms (Summer)
Clinical manifestations that present with diabetes mellitus type 1 and type 2, may differ from patient to patient depending on the onset of disease. The initial manifestation that may present is hyperglycemia. Patients suffering from hyperglycemia can experience multiple symptoms such as polyuria, polydipsia, unintentional weight loss, and/or ketonemia. Polyuria occurs when the serum glucose concentration rises above 180 mg/dL, exceeding the renal threshold for glucose, which leads to increased urinary glucose excretion. Glycosuria causes osmotic diuresis and hypovolemia (Levitsky, and Misra, 2017). Weight loss is a symptom experienced by half the patient population diagnosed with diabetes. This occurs as a result of hypovolemia and increased catabolism. Insulin deficiency in diabetics impairs glucose utilization in the skeletal muscle and increases fat and muscle breakdown. Initially, appetite is increased, but over time, diabetics are more thirsty than hungry, and ketosis leads to nausea and anorexia, contributing to weight loss (Levitsky, and Misra, 2017). Polydipsia occurs due to increased serum osmolality from hyperglycemia and hypovolemia. Despite the hypovolemia, patients may not have signs of dehydration (Levitsky, and Misra, 2017).
As blood sugars remain elevated, other symptoms of hyperglycemia can occur including candidiasis, visual disturbances cataracts, and perineal candidiasis. Perineal candidiasis is fairly common, especially among young children and girls. Visual disturbances are also common because of alterations in the osmotic milieu of the lens, and to a lesser extent the aqueous and vitreous humors leading to changes in refractive index. (Levitsky, and Misra, 2017).
When a person’s blood sugar becomes significantly high, two complications can occur. These complications are called diabetic ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS). DKA is more common in type 1 diabetes, but can occur in Type 2 diabetes as well. The symptoms of DKA include polyuria, polydipsia, and weight loss. Patients with ketoacidosis may also present with a fruity-smelling breath, kussmaul respirations, drowsiness, lethargy and altered mental status. HHS is seen more in patients with T2DM, but can occur in type I diabetics. HHS is caused by hyperglycemia (plasma glucose above 600 mg/dL), hyperosmolality and severe dehydration. This condition usually presents with little or no ketonuria. Although, HHS is less commonly seen than DKA it has a high morbidity and mortality if not adequately treated (Laffel and Svoren, 2017).
Diagnostic Tests & Procedures (Summer)
To confirm a diagnosis of DM, lab tests can be performed. The screenings tests for diabetes include hemoglobin A1C (A1C), fasting plasma glucose (FPG), and an oral glucose tolerance test (OGTT). The hemoglobin A1C is a screening test for that measures the amount of blood glucose levels over a 3-month span. An A1C level above 6.5 percent, is confirmative to a diagnosis of diabetes. An A1C level between 5.7 and 6.4 percent indicates prediabetes. A diagnosis of prediabetes put the patient at a greater risk for developing diabetes. FPG is a blood draw performed after a person has fasted for over 8 hours. A FPG reading that is higher than126 mg is indicative of diabetes. A person is diagnosed with prediabetes if their FPG is over 100 mg/dl. An oral glucose tolerance test (OGTT) can be used as part of the diagnostic process. This test can detect the development of DM eve when FPG is not elevated. The patient is asked to ingest a drink high in sugar. The patient will wait for two hours and then a blood draw is performed to measure the plasma glucose. A Plasma glucose above 200 mg/dL is reveals diabetes. Plasma glucose above 140 mg/dL to 199 mg/dL indicates prediabetes (Levitsky and Misra, 2017).
In order to plan care for a patient with diabetes, it is crucial to differentiate between T1DM and T2DM. Currently, there is not a set criteria or diagnostic test that can distinguish between T1DM and T2DM. Therefore, clinicians rely on a combination of patient history, symptoms, and diagnostic testing. The patient history collected includes: weight, age, genetics, and family history. Weight is an important data collection because patients with T2DM are usually obese, with a body mass index above the 95th percentile. Patients with T1DM usually experience weight loss and are not obese. Patient’s age is considered a distinguishing marker due to the fact that Patients with T2DM generally experience symptoms after puberty and patients with T1DM often have symptoms earlier. About 45 percent of children with T1DM present before 10 years of age and children with T2DM present after the age of 10. Assessing genetics is important due to the fact that patients with T2DM frequently have acanthosis nigricans, hypertension, dyslipidemia, and polycystic ovary syndrome (in girls); these symptoms are rare in T1DM. Family history data is also collected. Studies show in patients diagnosed with T2DM, 75 to 90 percent have a close relative diagnosed as well. In contrast, only 10 percent of patients with T1DM have a close family member diagnosed with T1DM. Laboratory tests are another helpful way to distinguish between T1DM and T2DM. Lab tests for antibodies are drawn from patients with diabetes. Although, testing for antibodies does not directly distinguish between the two types of diabetes it does help with data collection. Patients with T1DM have shown the presence of circulating, islet-specific, pancreatic autoantibodies against glutamic acid decarboxylase (GAD65), the 40K fragment of tyrosine phosphatase (IA2), insulin, and/or zinc transporter 8 (ZnT8). A patient without the presence of pancreatic enzymes can still be diagnosed with T1D. Another lab test performed are Insulin and C-peptide levels. Diabetics with high fasting insulin and C-peptide levels suggest T2DM. In T1dm plasma glucose levels are low or in the normal range (Levitsky and Misra, 2017).
People diagnosed with hyperglycemia can have differential diagnoses. Before diagnosing a person with diabetes, it is important to rule out other causative actors. Some other disorders that can cause hyperglycemia include septic shock or other critical illnesses, certain medications, pancreatic disorders, and endocrine disorders.
Medical and Nursing Management (Raheel)
Diabetes fundamentally increases the risk of developing various cardiovascular problems, including coronary artery disease, heart attack, stroke, narrowing of the arteries and high blood pressure (Abdullah et al., 2010). Furthermore, excess sugar can also potentially injure the walls of smaller blood vessels that sustain nerves, especially in the legs leading to peripheral neuropathy (Abdullah et al., 2010). Eventually, prevailing levels of insulin in type 2 diabetic patients are not enough to contest with increased levels of blood glucose (hyperglycemia) due to insulin receptor insensitivity thereby, requiring greater amounts of insulin for uptake of glucose into the cells. Normalized glucose levels decrease the overall risk of developing many of the complications associated with diabetes and remain a priority for any individual suffering from diabetes (Abdullah et al., 2010).
The primary treatment for type 1 diabetic remains centered around insulin therapy due to the destruction of pancreatic beta cells and requires a combination of at least two or more types of insulin with varying dose requirements based on the personal caloric and metabolic needs (Narayan, 2006). In addition to insulin therapy, type 1 diabetics require referral to a dietician for nutritional education and are encouraged to maintain a healthy body weight (Narayan, 2006). Lastly, self-monitoring of blood glucose remains an essential part of diabetes management in type 1 diabetes. It is recommended that testing of blood glucose levels be done four to seven times a day, usually before breakfast, afternoon, before lunch, evening meal and before bedtime as well as before and after intense physical activity (Narayan, 2006). Analysis of the different types of insulin will be discussed in greater details in the later section of this paper.
Currently, an assortment of approaches can be implemented for stabilizing and maintaining normal blood glucose levels. The common trait shared among both medical and nursing management disease involves preliminary diagnosis and aggressive supervision of the disease in the earliest stages (Malin et al., 2012). The first-line of treatment recommended for newly diagnosed type 2 diabetic patients are exercise, weight loss and oral anti-hyperglycemic medications. Overall, the three interventions all focus on improving glycemic control (Schinner, 2009). In regards to drug interventions, most recent research findings indicate that diet and exercise along with administration of metformin continue to be the first line of treatment after new diagnosis of both pre-diabetes and diabetes in patients with type 2 diabetes. The primary and added benefit of metformin includes weight loss, improvement in insulin receptor sensitivity and inhibition of advancement of pre-diabetes into type 2 diabetes (Malik et al., 2010). The mechanism by which metformin increases insulin sensitivity is directly rooted in the ability of this drug to galvanize skeletal AMP-activated protein kinase (AMPK) (Malin et al., 2012).
Current state of research also indicates the use and benefits of metformin in decreasing the development of cancer. A metal-analysis research by Thakkar et al. (2013) analyzed primary data from various research studies and concluded that “metformin use decreases while sulfonylurea (a different anti-diabetic medication) use is associated with an increased cancer risk with type 2 diabetic mellitus patients.” However, the authors indicated a need for large-scale randomized control trials before implementation into the medical practice (Thakkar et al., 2013).
Oral Anti-Hyperglycemic Medications (Raheel)
Diet, exercise and weight loss are always encouraged as initial line of treatment in newly diagnosed diabetic patients. However, in patients whose A1C levels are greater than 7.5-8% initiation of oral diabetes medications is recommended. Metformin as discussed earlier remains the first line of treatment (Pleuvry, 2008). Patients in whom metformin is contraindicated (impaired renal function, current hepatic impairment, alcohol abuse) can be started on sulfonylurea such as Glipizide. Sulfonylurea work by causing the pancreases to release more insulin by inhibiting potassium channels that are sensitive to ATP (Pleuvry, 2008).
The use of thiazolidinedione (TZD) is recommend for patients that have contraindications to both metformin and sulfonylurea. TZDs (Pioglitazone) work to increase insulin sensitivity consequently, increasing glucose uptake among body cells (Pleuvry, 2008). Nevertheless, caution must be taken due to the increase risk of heart failure, fractures and increase in bladder cancer with this medication. Other injectable and oral diabetic medication such as sodium-glucose co-transporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) agonists, alpha-glucosidaseand inhibitors dipeptidyl peptidase-4 (DPP-4) inhibitors are recommended as adjuvant therapy in combination with other diabetic medication and insulin therapy (Tucker, 2009).
Insulin Therapy (Raheel)
Insulin is a hormone that is secreted by the pancreases after food consumption in small bursts. Individuals with diabetes have defective insulin receptor sensitivity and require greater levels of insulin in order to decrease blood glucose levels. Individuals whose blood sugar can no longer be controlled through diet, exercise, and oral anti-hyperglycemic medication, exogenous insulin is often the only remaining medication of choice (Tucker, 2009). The main side-effect of insulin administration is hypoglycemia. The signs and symptoms associated with hypoglycemia are irritability, hunger, confusion, lethargy, impaired vision, sweating and death when blood glucose levels drop below 50mg/dL (Tucker, 2009).
Insulin administration is dependent on the weight, metabolic and caloric needs of the individual. Rapid acting insulin (Humalog, Novalog) have an onset of 10 to 30-minutes with a peak of 30 minutes to 3-hours. Shorting acting insulin (Regular) are taken about 30- minutes before meal and work over 2-hours. Intermediated acting insulin (NPH), take approximately 3 hours to work but have 24 hours of efficacy and are usually combined with short and long acting medications. Lastly, long acting insulin (Lantus) starts working in 1-hour and can be efficacious over a 24-hour period. It is usually combined with rapid and short acting insulin and is taken once or twice a day (Tucker, 2009).
Nursing Interventions and Management (Raheel)
Nurses and nurse practitioners are often the first healthcare providers to engage and educate diabetic patients regarding self-management, regulation and stabilization of blood glucose levels. Moreover, diabetes management also requires extensive and continuous self-care activity on the part of the patient. Therefore, it is vital that nurses and nurse practitioners maintain the appropriate skill set in evaluating applicable nursing interventions particularly concerning newly diagnosed diabetic patients (Saudek et al., 2009). The role of physical activity as a suitable nursing intervention can additionally be incorporated into patient education and teaching protocols. This intervention is cost effective, therapeutic and significant in controlling blood glucose levels and the consequence of proper and timely nursing interventions, have wide implications on the patient’s physical, mental and economic outlook (Levich, 2011).
In the clinical setting, ambulation and range-of-motion exercises are important in preventing pressure ulcers, bed sores and deep vein thrombosis. Likewise, ambulation and aerobic exercise are just as important in the health of a diabetic patient outside of the acute care setting (Weinberger et al., 1995). Moreover, research also indicates, the benefit of exercise in improving glucose control in diabetic patients is highest when used in the earliest phase of the disease process (Malin, 2012). It is therefore vital, that the appropriate nursing process from assessment, evaluation and intervention occur at the earliest phase of the disease for healthier patient outcome (Weinberger et al., 1995).
Conclusion (Raheel)
The American Diabetes Association (2013) estimates that the cost of health care for diabetic patients is $245 billion dollars a year and around 43% of this cost can be credited to hospital inpatient treatments due to both primary and secondary complications of diabetes (ADA, 2013). Additional costs of treatment related to diabetes complications outside the clinical setting are estimated to be 18% of total health prescription expenditure. The above stated cost analysis for providing care to a diabetic patient is significant (ADA, 2013). The implications are evident since the expected number of newly diagnosed type 2 diabetes is predicted to increase. Exercise, in any form, especially in recently diagnosed type 2 diabetic patient can serves as a primary and cost-effective measure and act as a beneficial first nursing intervention likely to improve patient outcome in the clinical setting and beyond. (American Diabetes Association, 2013).