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FOUNDATION OVERVIEW

Diabetes mellitus (DM) is a group of metabolic disorders characterized by high blood glucose as well as altered fat and protein metabolism that results from defects in insulin secretion, insulin action (sensitivity), or both. Type 1 diabetes mellitus (T1DM) characterized by insulin deficient and type 2 diabetes mellitus (T2DM) characterized by insulin resistance combined with beta cell dysfunction. Additional subclasses include gestational diabetes mellitus (GDM) and secondary diabetes associated with hormonal syndromes, medications, and diseases of the pancreas. The key differences between T1DM and T2DM are the pathophysiology, etiology of hyperglycemia, and clinical presentation; however, both are associated with microvascular and macrovascular complications.

T1DM is a cellular-mediated autoimmune process that destroys pancreatic β-cells resulting in insulin deficiency. Due to the lack of insulin, glucose is not able to be used as energy. The onset of symptoms leading to the diagnosis of T1DM is abrupt and includes polydipsia, polyuria, polyphagia, weight loss, or ketoacidosis. T2DM is impaired insulin secretion and insulin resistance at sites such as the liver, muscles, and adipocytes. Patients with T2DM can produce insulin, but the amount may not be sufficient to keep up with the body’s glucose metabolism, or the insulin that is produced may not work appropriately at its receptor sites. There are multiple risk factors for the development of T2DM, including family history; obesity (ie, ≥20% over ideal body weight, or body mass index [BMI] ≥25 kg/m2); chronic physical inactivity; history of impaired glucose tolerance (IGT), impaired fasting glucose (IFG), or hemoglobin A1c (HbA1c) 5.7% to 6.4%; hypertension (≥140/90 mm Hg in adults); high-density lipoprotein (HDL) cholesterol less than or equal to 35 mg/dL (≤0.91 mmol/L) and/or a triglyceride level more than or equal to 250 mg/dL (≥2.83 mmol/L); history of vascular disease; presence of acanthosis nigricans; and polycystic ovary disease. Additionally, the prevalence of T2DM increases with age and varies widely among racial and ethnic populations. The prevalence of T2DM is especially high in Native Americans, Hispanic Americans, African Americans, Asian Americans, and Pacific Islanders. While the prevalence of T2DM increases with age, the disorder is increasingly being diagnosed in adolescence. The increased incidence of T2DM in adolescence and young adults has been attributed to an increase in overweight/obesity and sedentary lifestyle, in addition to genetic predisposition.

The clinical presentations of T1DM and T2DM are different. Most patients (75%) develop T1DM before age 20 years, but it can develop at any age. Individuals with T1DM are often thin and are prone to ketoacidosis if insulin is withheld or under conditions of severe physiological stress. Symptoms, such as polyuria, polydipsia, polyphagia, weight loss, and lethargy, are common at the time of initial presentation. In the outpatient setting, some patients present with vague complaints of weight loss and fatigue but other symptoms may not be apparent unless a comprehensive history is taken. Twenty percent to forty percent of patients with T1DM present with diabetic ketoacidosis (DKA) after several days ...

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