Assignments: NRS-430V, NRS-429VN, NRS-434VN and NRS-428VN

May 12, 2022
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Assignments NRS-430V, NRS-429VN, NRS-434VN and NRS-428VN

Assignments: NRS-430V, NRS-429VN, NRS-434VN and NRS-428VN

This is a writing-intensive course. The professional capstone practicum project offers students the opportunity to propose a resolution to an issue or problem significant to nursing practice within a clinical environment. Students identify, design, and propose an evidence-based solution within a health care organization with guidance from faculty and a preceptor in the field. The proposal must reflect synthesis and integration of course content and professional practice. Development of the capstone project is guided by the baccalaureate program student learning outcomes. Clinical hours: 100. Prerequisites: NRS-430V, NRS-429VN, NRS-434VN, NRS-428VN, HLT-362V, NRS-433V, PHI-413V, NRS-451VN, NRS-410V, and NRS-440VN.

NRS-430V, NRS-429VN, NRS-434VN and NRS-428VN


Diabetes can be classified into the following general categories:

  1. Type 1 diabetes (due to autoimmune β-cell destruction, usually leading to absolute insulin deficiency)

  2. Type 2 diabetes (due to a progressive loss of β-cell insulin secretion frequently on the background of insulin resistance)

  3. Gestational diabetes mellitus (GDM) (diabetes diagnosed in the second or third trimester of pregnancy that was not clearly overt diabetes prior to gestation)

  4. Specific types of diabetes due to other causes, e.g., monogenic diabetes syndromes (such as neonatal diabetes and maturity-onset diabetes of the young [MODY]), diseases of the exocrine pancreas (such as cystic fibrosis), and drug- or chemical-induced diabetes (such as with glucocorticoid use, in the treatment of HIV/AIDS, or after organ transplantation)

This section reviews most common forms of diabetes but is not comprehensive. For additional information, see the American Diabetes Association (ADA) position statement “Diagnosis and Classification of Diabetes Mellitus” (1).

Type 1 diabetes and type 2 diabetes are heterogeneous diseases in which clinical presentation and disease progression may vary considerably. Classification is important for determining therapy, but some individuals cannot be clearly classified as having type 1 or type 2 diabetes at the time of diagnosis. The traditional paradigms of type 2 diabetes occurring only in adults and type 1 diabetes only in children are no longer accurate, as both diseases occur in both cohorts. Occasionally, patients with type 2 diabetes may present with diabetic ketoacidosis (DKA), particularly ethnic minorities (2). Children with type 1 diabetes typically present with the hallmark symptoms of polyuria/polydipsia, and approximately one-third present with DKA (3). The onset of type 1 diabetes may be more variable in adults, and they may not present with the classic symptoms seen in children. Although difficulties in distinguishing diabetes type may occur in all age-groups at onset, the true diagnosis becomes more obvious over time.

In October 2015, the ADA, JDRF, the European Association for the Study of Diabetes, and the American Association of Clinical Endocrinologists convened the Differentiation of Diabetes by Pathophysiology, Natural History, and Prognosis Research Symposium (4). The goals of the symposium were to discuss the genetic and environmental determinants of type 1 and type 2 diabetes risk and progression, to determine appropriate therapeutic approaches based on disease pathophysiology and stage, and to define research gaps hindering a personalized approach to treatment. The experts agreed that in both type 1 and type 2 diabetes, various genetic and environmental factors can result in the progressive loss of β-cell mass and/or function that manifests clinically as hyperglycemia. Once hyperglycemia occurs, patients with all forms of diabetes are at risk for developing the same complications, although rates of progression may differ. They concluded that the identification of individualized therapies for diabetes in the future will require better characterization of the many paths to β-cell demise or dysfunction.

Characterization of the underlying pathophysiology is much more developed in type 1 diabetes than in type 2 diabetes. It is now clear from studies of first-degree relatives of patients with type 1 diabetes that the persistent presence of two or more autoantibodies is an almost certain predictor of clinical hyperglycemia and diabetes. The rate of progression is dependent on the age at first detection of antibody, number of antibodies, antibody specificity, and antibody titer. Glucose and A1C levels rise well before the clinical onset of diabetes, making diagnosis feasible well before the onset of DKA. Three distinct stages of type 1 diabetes can be identified (Table 2.1) and serve as a framework for future research and regulatory decision making (4,5).

Table 2.1

Staging of type 1 diabetes (4,5)

The paths to β-cell demise and dysfunction are less well defined in type 2 diabetes, but deficient β-cell insulin secretion frequently in the setting of insulin resistance appears to be the common denominator. Characterization of subtypes of this heterogeneous disorder have been developed and validated in Scandinavian and Northern European populations, but have not been confirmed in other ethnic and racial groups. Type 2 diabetes is primarily associated with insulin secretory defects related to inflammation and metabolic stress among other contributors including genetic factors. Future classification schemes for diabetes will likely focus on the pathophysiology of the underlying β-cell dysfunction and the stage of disease as indicated by glucose status (normal, impaired, or diabetes) (4).


Diabetes may be diagnosed based on plasma glucose criteria, either the fasting plasma glucose (FPG) or the 2-h plasma glucose (2-h PG) value after a 75-g oral glucose tolerance test (OGTT) or A1C criteria (1,6) (Table 2.2).

Table 2.2

Criteria for the diagnosis of diabetes

FPG, 2-h PG after 75-g OGTT, and A1C are equally appropriate for diagnostic testing. It should be noted that the tests do not necessarily detect diabetes in the same individuals. The efficacy of interventions for primary prevention of type 2 diabetes (7,8) has primarily been demonstrated among individuals with impaired glucose tolerance (IGT), not for individuals with isolated impaired fasting glucose (IFG) or for those with prediabetes defined by A1C criteria.

The same tests may be used to screen for and diagnose diabetes and to detect individuals with prediabetes. Diabetes may be identified anywhere along the spectrum of clinical scenarios: in seemingly low-risk individuals who happen to have glucose testing, in individuals tested based on diabetes risk assessment, and in symptomatic patients.

Fasting and 2-Hour Plasma Glucose

The FPG and 2-h PG may be used to diagnose diabetes (Table 2.2). The concordance between the FPG and 2-h PG tests is imperfect, as is the concordance between A1C and either glucose-based test. Numerous studies have confirmed that, compared with FPG and A1C cut points, the 2-h PG value diagnoses more people with diabetes.


The A1C test should be performed using a method that is certified by the NGSP ( and standardized or traceable to the Diabetes Control and Complications Trial (DCCT) reference assay. Although point-of-care A1C assays may be NGSP certified, proficiency testing is not mandated for performing the test, so use of point-of-care assays for diagnostic purposes is not recommended but may be considered in the future if proficiency testing is performed and documented.

The A1C has several advantages compared with the FPG and OGTT, including greater convenience (fasting not required), greater preanalytical stability, and less day-to-day perturbations during stress and illness. However, these advantages may be offset by the lower sensitivity of A1C at the designated cut point, greater cost, limited availability of A1C testing in certain regions of the developing world, and the imperfect correlation between A1C and average glucose in certain individuals. National Health and Nutrition Examination Survey (NHANES) data indicate that an A1C cut point of ≥6.5% (48 mmol/mol) identifies one-third fewer cases of undiagnosed diabetes than a fasting glucose cut point of ≥126 mg/dL (7.0 mmol/L) (9).

When using A1C to diagnose diabetes, it is important to recognize that A1C is an indirect measure of average blood glucose levels and to take other factors into consideration that may impact hemoglobin glycation independently of glycemia including age, race/ethnicity, and anemia/hemoglobinopathies.


The epidemiological studies that formed the basis for recommending A1C to diagnose diabetes included only adult populations. Therefore, it remains unclear if A1C and the same A1C cut point should be used to diagnose diabetes in children and adolescents (9,10).


A1C levels may vary with race/ethnicity independently of glycemia (11,12). For example, African Americans may have higher A1C levels than non-Hispanic whites despite similar fasting and postglucose load glucose levels (13). Though there is some conflicting data, African Americans may also have higher levels of fructosamine and glycated albumin and lower levels of 1,5-anhydroglucitol, suggesting that their glycemic burden (particularly postprandially) may be higher (14,15). The association of A1C with risk for complications appears to be similar in African Americans and non-Hispanic whites (16).

Hemoglobinopathies/Red Blood Cell Turnover

Interpreting A1C levels in the presence of certain hemoglobinopathies may be problematic. For patients with an abnormal hemoglobin but normal red blood cell turnover, such as those with the sickle cell trait, an A1C assay without interference from abnormal hemoglobins should be used. An updated list of interferences is available at

In conditions associated with increased red blood cell turnover, such as pregnancy (second and third trimesters), hemodialysis, recent blood loss or transfusion, or erythropoietin therapy, only blood glucose criteria should be used to diagnose diabetes.

Confirming the Diagnosis

Unless there is a clear clinical diagnosis (e.g., patient in a hyperglycemic crisis or with classic symptoms of hyperglycemia and a random plasma glucose ≥200 mg/dL [11.1 mmol/L]), a second test is required for confirmation. It is recommended that the same test be repeated without delay using a new blood sample for confirmation because there will be a greater likelihood of concurrence. For example, if the A1C is 7.0% (53 mmol/mol) and a repeat result is 6.8% (51 mmol/mol), the diagnosis of diabetes is confirmed. If two different tests (such as A1C and FPG) are both above the diagnostic threshold, this also confirms the diagnosis. On the other hand, if a patient has discordant results from two different tests, then the test result that is above the diagnostic cut point should be repeated. The diagnosis is made on the basis of the confirmed test. For example, if a patient meets the diabetes criterion of the A1C (two results ≥6.5% [48 mmol/mol]) but not FPG (<126 mg/dL [7.0 mmol/L]), that person should nevertheless be considered to have diabetes.

Since all the tests have preanalytic and analytic variability, it is possible that an abnormal result (i.e., above the diagnostic threshold), when repeated, will produce a value below the diagnostic cut point. This scenario is likely for FPG and 2-h PG if the glucose samples remain at room temperature and are not centrifuged promptly. Because of the potential for preanalytic variability, it is critical that samples for plasma glucose be spun and separated immediately after they are drawn. If patients have test results near the margins of the diagnostic threshold, the health care professional should follow the patient closely and repeat the test in 3–6 months.




  • Screening for prediabetes and risk for future diabetes with an informal assessment of risk factors or validated tools should be considered in asymptomatic adults. B

  • Testing for prediabetes and risk for future diabetes in asymptomatic people should be considered in adults of any age who are overweight or obese (BMI ≥25 kg/m2 or ≥23 kg/m2 in Asian Americans) and who have one or more additional risk factors for diabetes. B

  • For all people, testing should begin at age 45 years. B

  • If tests are normal, repeat testing carried out at a minimum of 3-year intervals is reasonable. C

  • To test for prediabetes, fasting plasma glucose, 2-h plasma glucose after 75-g oral glucose tolerance test, and A1C are equally appropriate. B

  • In patients with prediabetes, identify and, if appropriate, treat other cardiovascular disease risk factors. B

  • Testing for prediabetes should be considered in children and adolescents who are overweight or obese and who have two or more additional risk factors for diabetes. E


In 1997 and 2003, the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus (17,18) recognized a group of individuals whose glucose levels did not meet the criteria for diabetes but were too high to be considered normal. “Prediabetes” is the term used for individuals with IFG and/or IGT and/or A1C 5.7–6.4% (39–47 mmol/mol). Prediabetes should not be viewed as a clinical entity in its own right but rather as an increased risk for diabetes (Table 2.3) and cardiovascular disease (CVD). Prediabetes is associated with obesity (especially abdominal or visceral obesity), dyslipidemia with high triglycerides and/or low HDL cholesterol, and hypertension.

Table 2.3

Assignments NRS-430V, NRS-429VN, NRS-434VN and NRS-428VN

Assignments NRS-430V, NRS-429VN, NRS-434VN and NRS-428VN

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Criteria for testing for diabetes or prediabetes in asymptomatic adults


The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus (17,18) defined IFG as FPG levels between 100 and 125 mg/dL (between 5.6 and 6.9 mmol/L) and IGT as 2-h PG after 75-g OGTT levels between 140 and 199 mg/dL (between 7.8 and 11.0 mmol/L). It should be noted that the World Health Organization (WHO) and numerous other diabetes organizations define the IFG cutoff at 110 mg/dL (6.1 mmol/L).

As with the glucose measures, several prospective studies that used A1C to predict the progression to diabetes as defined by A1C criteria demonstrated a strong, continuous association between A1C and subsequent diabetes. In a systematic review of 44,203 individuals from 16 cohort studies with a follow-up interval averaging 5.6 years (range 2.8–12 years), those with A1C between 5.5 and 6.0% (between 37 and 42 mmol/mol) had a substantially increased risk of diabetes (5-year incidence from 9 to 25%). An A1C range of 6.0–6.5% (42–48 mmol/mol) had a 5-year risk of developing diabetes between 25 and 50% and a relative risk 20 times higher compared with A1C of 5.0% (31 mmol/mol) (19). In a community-based study of African American and non-Hispanic white adults without diabetes, baseline A1C was a stronger predictor of subsequent diabetes and cardiovascular events than fasting glucose (20). Other analyses suggest that A1C of 5.7% (39 mmol/mol) or higher is associated with a diabetes risk similar to that of the high-risk participants in the Diabetes Prevention Program (DPP) (21), and A1C at baseline was a strong predictor of the development of glucose-defined diabetes during the DPP and its follow-up (22).

Hence, it is reasonable to consider an A1C range of 5.7–6.4% (39–47 mmol/mol) as identifying individuals with prediabetes. Similar to those with IFG and/or IGT, individuals with A1C of 5.7–6.4% (39–47 mmol/mol) should be informed of their increased risk for diabetes and CVD and counseled about effective strategies to lower their risks (see Section 5 “Prevention or Delay of Type 2 Diabetes”). Similar to glucose measurements, the continuum of risk is curvilinear, so as A1C rises, the diabetes risk rises disproportionately (19). Aggressive interventions and vigilant follow-up should be pursued for those considered at very high risk (e.g., those with A1C >6.0% [42 mmol/mol]).

Table 2.4 summarizes the categories of prediabetes and Table 2.3 the criteria for prediabetes testing. The ADA diabetes risk test is an additional option for screening (Fig. 2.1). For recommendations regarding risk factors and screening for prediabetes, see pp. S17–S18 (“Screening and Testing for Type 2 Diabetes and Prediabetes in Asymptomatic Adults” and “Screening and Testing for Type 2 Diabetes and Prediabetes in Children and Adolescents”).

Table 2.4

Categories of increased risk for diabetes (prediabetes)*



  • Blood glucose rather than A1C should be used to diagnose the acute onset of type 1 diabetes in individuals with symptoms of hyperglycemia. E

  • Screening for type 1 diabetes with a panel of autoantibodies is currently recommended only in the setting of a research trial or in first-degree family members of a proband with type 1 diabetes. B

  • Persistence of two or more autoantibodies predicts clinical diabetes and may serve as an indication for intervention in the setting of a clinical trial. Outcomes may include reversion of autoantibody status, prevention of glycemic progression within the normal or prediabetes range, prevention of clinical diabetes, or preservation of residual C-peptide secretion. A


In a patient with classic symptoms, measurement of blood glucose is sufficient to diagnose diabetes (symptoms of hyperglycemia or hyperglycemic crisis plus a random plasma glucose ≥200 mg/dL [11.1 mmol/L]). In these cases, knowing the blood glucose level is critical because, in addition to confirming that symptoms are due to diabetes, it will inform management decisions. Some providers may also want to know the A1C to determine how long a patient has had hyperglycemia.

Immune-Mediated Diabetes

This form, previously called “insulin-dependent diabetes” or “juvenile-onset diabetes,” accounts for 5–10% of diabetes and is due to cellular-mediated autoimmune destruction of the pancreatic β-cells. Autoimmune markers include islet cell autoantibodies and autoantibodies to GAD (GAD65), insulin, the tyrosine phosphatases IA-2 and IA-2β, and ZnT8. Type 1 diabetes is defined by the presence of one or more of these autoimmune markers. The disease has strong HLA associations, with linkage to the DQA and DQB genes. These HLA-DR/DQ alleles can be either predisposing or protective.

The rate of β-cell destruction is quite variable, being rapid in some individuals (mainly infants and children) and slow in others (mainly adults). Children and adolescents may present with ketoacidosis as the first manifestation of the disease. Others have modest fasting hyperglycemia that can rapidly change to severe hyperglycemia and/or ketoacidosis with infection or other stress. Adults may retain sufficient β-cell function to prevent ketoacidosis for many years; such individuals eventually become dependent on insulin for survival and are at risk for ketoacidosis. At this latter stage of the disease, there is little or no insulin secretion, as manifested by low or undetectable levels of plasma C-peptide. Immune-mediated diabetes commonly occurs in childhood and adolescence, but it can occur at any age, even in the 8th and 9th decades of life.

Autoimmune destruction of β-cells has multiple genetic predispositions and is also related to environmental factors that are still poorly defined. Although patients are not typically obese when they present with type 1 diabetes, obesity should not preclude the diagnosis. Patients with type 1 diabetes are also prone to other autoimmune disorders such as Hashimoto thyroiditis, Graves disease, Addison disease, celiac disease, vitiligo, autoimmune hepatitis, myasthenia gravis, and pernicious anemia (see Section 3 “Comprehensive Medical Evaluation and Assessment of Comorbidities”).

Idiopathic Type 1 Diabetes

Some forms of type 1 diabetes have no known etiologies. These patients have permanent insulinopenia and are prone to ketoacidosis, but have no evidence of β-cell autoimmunity. Although only a minority of patients with type 1 diabetes fall into this category, of those who do, most are of African or Asian ancestry. Individuals with this form of diabetes suffer from episodic ketoacidosis and exhibit varying degrees of insulin deficiency between episodes. This form of diabetes is strongly inherited and is not HLA associated.

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