The Nurse Practitioner's series on commonly billed diagnoses in primary care outpatient settings continues with type 2 diabetes mellitus (T2DM).1,2 This article will explore pathophysiology, clinical manifestations, diagnostic tests, and treatments based on the current best-available evidence.
Over 34 million people in the US are affected by diabetes.3,4 Approximately 26.9 million (10.5% of the US population) of those people have a diagnosis of diabetes, but another 7.3 million people remain undiagnosed.3 About 90% to 95% of those affected have T2DM.3 This number is expected to grow exponentially as US adults continue to live longer; the prevalence of diabetes increases with age.3,5 T2DM is associated with many preventable macrovascular and microvascular complications including myocardial infarction, cerebrovascular accident, end-stage renal disease, retinopathy, and foot ulcers. The CDC's 2017 Diabetes Report Card notes that diabetes is the seventh leading cause of death in the US.6 In 2017, the total cost of diabetes including medical costs and indirect costs such as lost work wages totaled approximately $327 billion.3,7
The pathogenesis of T2DM is multifactorial with several organs involved. Hyperglycemia, as a result of insulin resistance and impaired insulin secretion by the beta islet cells of the pancreas, is the predominant characteristic resulting from both genetic and environmental influences.8,9 Age, obesity, hypertension, physical inactivity, poor diet, and family history are the most prevalent risk factors in the development of T2DM.4,8
Insulin resistance is the substandard response of insulin-sensitive tissues, particularly the liver, muscle, and adipose tissue, to insulin.8 As insulin resistance increases, insulin levels rise, but the glucose level remains essentially normal, resulting in a state of hyperinsulinemia. Reduced beta cell mass and function develops and leads to a deficiency of insulin activity, eventually giving rise to prolonged hyperglycemia.8 Glucose inhibition by the pancreatic alpha cells is impeded, increasing secretion of glucagon and elevating glucagon concentrations in T2DM.8,9 Prolonged hyperglycemia promotes destruction of pancreatic beta cells, which results in fasting hyperglycemia as hepatic gluconeogenesis increases secondary to glucagon production.8,9 As hyperglycemia persists, further beta cell destruction is imminent.9
Insulin resistance is exacerbated by elevated levels of free fatty acids and proinflammatory cytokines associated with traits such as aging and obesity.9 Free fatty acids are produced in adipose tissue and interfere with intracellular insulin recognition, decrease tissue response to insulin, and cause beta cell death.8,9 Proinflammatory cytokines inherent with obesity have been linked to induction of insulin resistance and beta cell dysfunction along with comorbid conditions such as nonalcoholic fatty liver disease, atherosclerosis, and dyslipidemia.8,9
Gastrointestinal (GI) tissues are involved in the pathophysiology of T2DM via the actions of the incretins: glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide. These two hormones are released from the GI tract in response to food intake. Typically, incretin hormones will increase synthesis and secretion of insulin, aid in beta cell regeneration, and protect against beta cell damage.8 In T2DM, GLP-1 sensitivity is reduced, limiting the natural ability of GLP-1 to inhibit glucagon secretion and promote insulin secretion postprandially.8 Without appropriate gut hormone response, the satiating effects of insulin are unable to be produced, causing appetite dysregulation and weight gain, which can further exacerbate T2DM and its complications.8,9
The kidneys are designed to effectively filter and reabsorb glucose; most is reabsorbed by the sodium-glucose cotransporter 2 (SGLT2).9 A pathophysiologic action of the kidneys in the presence of hyperglycemia is to reabsorb more glucose.8 This leads to renal microvascular damage and significant renal complications.8,9
An important note regarding the sequence of the pathophysiologic mechanisms causing T2DM is that they tend to occur jointly rather than sequentially. Although insulin resistance is insufficient to independently cause T2DM, it is the strongest predictor of T2DM development and the primer for the cascade of negative health effects associated with this diagnosis.
History, physical exam, and diagnosis
A patient's health history is important to identify risk factors that are amenable to the development of T2DM. A thorough history should include the patient's family and social history, including family members diagnosed with any form of diabetes, and nutrition and physical activity habits. If evaluating a female patient, identifying a history of gestational diabetes mellitus during pregnancies is a risk factor for T2DM and should prompt screening at least every 3 years for life.4 If evaluating a patient with known T2DM, it is important to discuss their diabetes history and personal history of complications and/or comorbid conditions, obtain information about prescription and nonprescription medications, assess lifestyle and behavior patterns, and evaluate psychosocial conditions.4
Although patients may be asymptomatic, it is imperative to complete and document a review of systems specific for T2DM, inquiring about the presence of symptoms such as headache, fatigue, pruritus, numbness and tingling, and blurred vision.4,9 The classic symptoms of hyperglycemia including polyuria, polydipsia, and polyphagia may seem insignificant to patients with or without the diagnosis of T2DM and should be asked about at every visit. Frequent infections, slow wound healing, and/or vaginitis in women are common patient complaints that warrant investigation into diabetes as the potential underlying cause. Cardiovascular complaints such as chest pain may precipitate a diagnosis of T2DM or a related complication. NPs should ask questions specific to neurologic and renal symptoms to appropriately evaluate for common complications of diabetes.
During the physical exam, it is important to note that abnormal findings may be absent in patients with newly diagnosed T2DM. Subtle signs of slow-healing wounds and recurring infections, especially yeast infections, may be present and should prompt lab evaluation. Acanthosis nigricans is a common incidental finding on exam that should also increase suspicion for T2DM. Consistent and accurate measurement of BP is imperative to identify high BP that can exacerbate cardiovascular risk associated with T2DM.4,9 Refer to the June issue of The Nurse Practitioner for an earlier article in this series focused on hypertension. It is essential to measure the atherosclerotic cardiovascular disease (ASCVD) risk in all patients with T2DM.10 Refer to the July issue of The Nurse Practitioner for an earlier article in this series focused on ASCVD. Due to the morbidity from T2DM related to macrovascular and microvascular complications and the frequency of delayed diagnosis, target organ damage is often present at the time of diagnosis.4,9
Examining a patient with known T2DM should include measurement of BP and body mass index (BMI) along with comprehensive fundoscopic, cardiovascular, integumentary, neurologic, and foot exams.4 At every outpatient visit, evaluate for signs of target organ damage, and consistent measurement of ASCVD risk.10
The onset of T2DM is insidious, and the majority of patients are asymptomatic at the time of their outpatient visit, with hyperglycemia noted on routine lab testing, prompting further evaluation.4 Screening is based on a variety of factors as outlined in the next section.
Early detection and prompt treatment may reduce T2DM complications, so routine screening is appropriate.4,9 Screening for prediabetes and diabetes should be considered for all individuals who have overweight or obesity and at least one other diabetes risk factor.4 (See Screening recommendations for prediabetes and diabetes.) In addition, all adults age 45 and older should be screened. Any one of the following screening tests is appropriate: glycosylated hemoglobin test (A1C), fasting plasma glucose, or an oral glucose tolerance test.4,6 If results are normal, testing may be repeated every 3 years.
A diagnosis of T2DM is based on a fasting blood glucose of ≥126 mg/dL, a 2-hour plasma glucose during a 75-g oral glucose tolerance test of ≥200 mg/dL, or an A1C of ≥6.5% or more.4
The following tests should be performed in all patients with newly diagnosed T2DM: A1C if the results are not available within the past 3 months, lipid profile, liver function tests, spot urinary albumin-to-creatinine ratio, serum creatinine and estimated glomerular filtration rate, and serum potassium levels in patients on an angiotensin-converting enzyme inhibitor, angiotensin II receptor blocker, or diuretic.9 Optional testing can include C-peptide if the diagnosis between type 1 diabetes mellitus and T2DM is unclear.9 The C-peptide level is normal or elevated in T2DM, while it is decreased in type 1.9
For patients with T2DM, A1C should be performed biannually or quarterly based on glycemic control, and lipid profile, liver function tests, spot urinary albumin-to-creatinine ratio, serum creatinine and estimated GFR, and vitamin B12 (if taking metformin) should be performed annually.4,9
T2DM treatment is complex, requiring ongoing office visits, education, and the use of chronic medications to prevent acute and chronic complications.4,9 Both nonpharmacologic and pharmacologic treatments may be necessary.
The glycemic recommendation from the American Diabetes Association (ADA) for nonpregnant adults with diabetes is an A1C of <7%.4 (See Recommended glycemic targets for nonpregnant adults.)
Lifestyle modifications are the principal treatment modalities, both at diagnosis and throughout the disease process.12 Maintaining optimal weight by following a low-carbohydrate, high-fiber diet that is low in saturated fats and avoids trans fatty acids is imperative to lessen the burden of and potential for obesity that can further negatively affect patients with T2DM.9,12 The US Department of Health and Human Services recommends at least 150 minutes of moderate-intensity or 75 minutes of vigorous-intensity physical activity weekly to ensure positive clinical outcomes.12,13 Adequate sleep, behavioral support, and smoking cessation are also of great importance for treatment success.9,12 Documentation of patient-centered goal setting and adherence with lifestyle modifications are imperative for comprehensive T2DM care.4
Pharmacologic therapy for T2DM is required when lifestyle modifications do not result in adequate blood glucose control. Selecting a medication for glycemic control requires appropriate analysis of the risks and benefits of the agent according to patient age, comorbidities, and hypoglycemia risk.4,9,12 Individualized goals in conjunction with A1C levels aid in determining the need for monotherapy, dual therapy, or triple therapy.4,9,12
Due to the variety of pathophysiologic mechanisms involved in the disease, there is a plethora of pharmacologic therapies. Current therapy is based on a step approach centered around the patient's A1C levels. Therapy includes drugs that alter insulin action, stimulate insulin secretion, affect the absorption of glucose, mimic the effects of incretin, act as an insulin secretagogue, or suppress postprandial glucagon release.4,9,12 Insulin itself is a therapy for T2DM. Metformin is a biguanide that is effective in decreasing hepatic glucose production and intestinal absorption of glucose while increasing insulin sensitivity in peripheral tissues.14 It is recommended as first-line pharmacologic therapy for T2DM by both the American Association of Clinical Endocrinologists (AACE) and the ADA, but is not without contraindications and risks that require careful analysis.4,12 The AACE and ADA guidelines include GLP-1 receptor agonists, SGLT2 inhibitors, dipeptidyl peptidase 4 (DPP-4) inhibitors, thiazolidinediones, alpha glucosidase inhibitors, sulfonylureas, and insulin as potential options for monotherapy (if indicated), dual therapy, or triple therapy.4,12 AACE and ADA guidelines recommend starting with metformin as monotherapy, unless contraindicated, when the entry A1C level is <7.5%.4,12 An entry A1C of ≥7.5% (per AACE) or that is 1.5% to 2.0% above goal (per ADA) requires combination therapy with metformin, unless contraindicated, and another agent as mentioned above, such as a GLP-1 receptor agonist and/or an SGLT2 inhibitor.4,12 According to the AACE guideline, an entry A1C of >9.0%, especially if a patient is symptomatic, requires insulin, often basal, in addition to other agents as mentioned above.4,12 Being cognizant of the risks, benefits, and contraindications of each type of pharmacologic intervention is key in developing a patient-centered treatment plan that will promote adherence.
A referral to a certified diabetes care and education specialist to educate patients on the appropriate way to measure blood glucose outside of the office along with development of an individualized plan for lifestyle modifications is paramount. Patients should be instructed to perform home glucose monitoring and document their results. The log of home glucose values should be reviewed at every office appointment. This should be done in conjunction with telehealth counseling or clinical interventions.4 Initiating collaboration with specialty physicians, dietitians, exercise specialists, pharmacists, dentists, podiatrists, and mental health professionals allows for prevention and appropriate monitoring of T2DM complications.4,9
The International Classification of Diseases, 10th Revision, Clinical Modification (ICD-10-CM) is a morbidity classification published by a joint effort between the Centers for Medicare and Medicaid Services and the National Center for Health Statistics.15 The ICD-10-CM is the standard billing code system used to submit diagnosis codes for insurance reimbursement.
ICD-10-CM codes for diabetes mellitus are composite codes that express the type of diabetes, the body system affected, and the complications affecting that body system.15,16 The current coding expectations are to use as many codes as necessary to identify all the associated conditions and adequately describe all complications of the disease.15,16 The previous ICD-9-CM allowed for more “unspecified” codes related to diabetes mellitus, leading to a less scientific capture of the disease.16 The ICD-10-CM code E11.9, for T2DM, is submitted for patients who present without any known disease-related complications.15,16 To represent the highest level of specificity in coding, subcategories of T2DM are explored and assigned.15,16 For example, if a patient has T2DM with diabetic chronic kidney disease, then submit code E11.22.16 If a patient has T2DM with a foot ulcer, then submit code E11.621.16 Supportive information within the chart will provide justification for highly specified and correct coding. (See ICD codes.) The code with the highest specificity will increase reimbursement.
Implications for practice
The role of NPs in managing T2DM includes:19
- initial and ongoing assessment
- ordering labs and diagnostic testing
- pharmacologic and nonpharmacologic management per treatment guidelines
- patient education
- coordination of care–including referrals
- billing services for reimbursement of care and performance measurement.
NPs excel in aligning T2DM management with the Chronic Care Model, an effective model known for reducing the cumulative incidence of diabetes-related complications and all-cause mortality.19 This model emphasizes a person-centered, integrated long-term treatment approach with ongoing collaborative communication and goal setting with all team members.19 NPs are effective leaders of a multidisciplinary team approach to T2DM care with proven quality patient outcomes.20 NPs should be proficient in maintaining cost-effectiveness and appropriately using support from lay health coaches, navigators, and/or community health workers to truly tailor the care approach for individuals. NPs should employ active listening to elicit patient preferences and beliefs and guide patients in overcoming barriers to optimize their health outcomes and improve their health-related quality of life. NPs should consider the social, cultural, economic, and behavioral elements impacting a patient with T2DM, which allows for patient-specific treatment in an evidence-based, culturally sensitive way.19 Patients who actively play a role in the management of their T2DM have greater satisfaction with their care, which is linked to medication adherence and compliance with lifestyle modifications.19 These are some of the many ways in which NPs can lead the charge to promote positive change within their communities and among their patients with T2DM.