ype 2 diabetes mellitus consists of an

ype 2 diabetes mellitus consists of an array of dysfunctions characterized by hyperglycemia and resulting from the combination of resistance to insulin action, inadequate insulin secretion, and excessive or inappropriate glucagon secretion. Poorly controlled type 2 diabetes is associated with an array of microvascular, macrovascular, and neuropathic complications. Microvascular complications of diabetes include retinal, renal, and possibly neuropathic disease. Macrovascular complications include coronary artery and peripheral vascular disease. Diabetic neuropathy affects autonomic and peripheral nerves. Unlike patients with type 1 diabetes mellitus, patients with type 2 are not dependent on insulin for life. This distinction was the basis for the older terms for types 1 and 2, insulin dependent and non-insulin dependent diabetes. However, many patients with type 2 diabetes are ultimately treated with insulin. Because they retain the ability to secrete some endogenous insulin, they are considered to require insulin but not to depend on insulin. Nevertheless, given the potential for confusion due to classification based on treatment rather than etiology, the older terms have been abandoned. Another older term for type 2 diabetes mellitus was adult-onset diabetes. Currently, because of the epidemic of obesity and inactivity in children, type 2 diabetes mellitus is occurring at younger and younger ages. Although type 2 diabetes mellitus typically affects individuals older than 40 years, it has been diagnosed in children as young as 2 years of age who have a family history of diabetes. In many communities, type 2 diabetes now outnumbers type 1 among children with newly diagnosed diabetes. Diabetes mellitus is a chronic disease that requires long-term medical attention to limit the development of its devastating complications and to manage them when they do occur. It is a disproportionately expensive disease; in the United States in 2012, the direct and indirect costs of diagnosed diabetes were estimated to be $245 billion; people with diagnosed diabetes had average medical expenditures 2.3 times those of people without diabetes. This article focuses on the diagnosis and treatment of type 2 diabetes and its acute and chronic complications, other than those directly associated with hypoglycemia and severe metabolic disturbances, such as hyperosmolar hyperglycemic state (HHS) and diabetic ketoacidosis (DKA). For more information on those topics, research on your own Hyperosmolar Hyperglycemic State and Diabetic Ketoacidosis. Medication Summary Pharmacologic therapy of type 2 diabetes has changed dramatically in the last 10 years, with new drugs and drug classes becoming available. These drugs allow for the use of combination oral therapy, often with improvement in glycemic control that was previously beyond the reach of medical therapy. Agents used in diabetic therapy include the following: Biguanides Sulfonylureas Insulins Amylinomimetics Bile acid sequestrants Dopamine agonists Traditionally, diet modification has been the cornerstone of diabetes management. Weight loss is more likely to control glycemia in patients with recent onset of the disease than in patients who are significantly insulinogenic. Medications that induce weight loss, such as orlistat, may be effective in highly selected patients but are not generally indicated in the treatment of the average patient with type 2 diabetes mellitus. Patients who are symptomatic at initial presentation with diabetes may require transient treatment with insulin to reduce glucose toxicity (which may reduce beta-cell insulin secretion and worsen insulin resistance) or an insulin secretagogue to rapidly relieve symptoms such as polyuria and polydipsia. Type 2 diabetes mellitus consists of an array of dysfunctions characterized by hyperglycemia and resulting from the combination of resistance to insulin action, inadequate insulin secretion, and excessive or inappropriate glucagon secretion. Research other resources, to help identify various cutaneous, ophthalmologic, vascular, and neurologic manifestations of DM. Signs and symptoms of DM Many patients with type 2 diabetes are asymptomatic. Clinical manifestations include the following: Classic symptoms: Polyuria, polydipsia, polyphagia, and weight loss Blurred vision Lower extremity paresthesia Yeast infections (e.g., balanitis in men) Diagnosis Diagnostic criteria by the American Diabetes Association (ADA) include the following: [1] A fasting plasma glucose (FPG) level of 126 mg/dL (7.0 mmol/L) or higher, or A 2-hour plasma glucose level of 200 mg/dL (11.1 mmol/L) or higher during a 75-g oral glucose tolerance test (OGTT), or A random plasma glucose of 200 mg/dL (11.1 mmol/L) or higher in a patient with classic symptoms of hyperglycemia or hyperglycemic crisis. Whether a hemoglobin A1c (HbA1c) level of 6.5% or higher should be a primary diagnostic criterion or an optional criterion remains a point of controversy. Indications for diabetes screening in asymptomatic adults includes the following: [2] Sustained blood pressure >135/80 mm Hg [3] Overweight and 1 or more other risk factors for diabetes (e.g. first-degree relative with diabetes BP >140/90 mm Hg, and HDL < 35 mg/dL and/or triglyceride level >250 mg/dL) [4] ADA recommends screening at age 45 years in the absence of the above criteria Management Goals of treatment are as follows: Microvascular (i.e., eye and kidney disease) risk reduction through control of glycemia and blood pressure. Macrovascular (i.e., coronary, cerebrovascular, peripheral vascular) risk reduction through control of lipids and hypertension, and smoking cessation Metabolic and neurologic risk reduction through control of glycemia Recommendations for the treatment of type 2 diabetes mellitus from the European Association for the Study of Diabetes (EASD) and the American Diabetes Association (ADA) place the patient’s condition, desires, abilities, and tolerances at the center of the decision-making process. The EASD/ADA position statement contains 7 key points: 1. Individualized glycemic targets and glucose-lowering therapies 2. Diet, exercise, and education as the foundation of the treatment program 3. Use of metformin as the optimal first-line drug unless contraindicated 4. After metformin, the use of 1 or 2 additional oral or injectable agents, with a goal of minimizing adverse effects if possible 5. Ultimately, insulin therapy alone or with other agents if needed to maintain blood glucose control 6. Where possible, all treatment decisions should involve the patient, with a focus on patient preferences, needs, and values 7. A major focus on comprehensive cardiovascular risk reduction The 2013 ADA guidelines for SMBG frequency focus on an individual’s specific situation rather than quantifying the number of tests that should be done. The recommendations include the following: 1. Patients on intensive insulin regimens 2. Perform SMBG at least before meals and snacks, as well as occasionally after meals; at bedtime; before exercise and before critical tasks (e.g., driving); when hypoglycemia is suspected 3. after treating hypoglycemia until normoglycemia is achieved. Patients using less frequent insulin injections or noninsulin therapies – Use SMBG results to adjust to food intake, activity, or medications to reach specific treatment goals; clinicians must not only educate these individuals on how to interpret their SMBG data, but they should also reevaluate the ongoing need for and frequency of SMBG at each routine visit. Approaches to prevention of diabetic complications include the following: 1. HbA1c every 3-6 months 2. Yearly dilated eye examinations 3. Annual microalbumin checks 4. Foot examinations at each visit 5. Blood pressure < 130/80 mm Hg, lower in diabetic nephropathy 6. Statin therapy to reduce low-density lipoprotein cholesterol Questions 1. What is the pathophysiology of type 2 diabetes mellitus (DM)? 2. What are the signs and symptoms of type 2 diabetes mellitus (DM)? 3. What are the ADA diagnostic criteria for type 2 diabetes mellitus (DM)? 4. When should asymptomatic adults be screened for type 2 diabetes mellitus (DM)? 5. What are the main goals of treatment for type 2 diabetes mellitus (DM)? 6. What are the EASD-ADA treatment guidelines for type 2 diabetes mellitus (DM)? 7. What are the ADA guidelines for self-monitoring of blood glucose (SMBG) frequency? 8. Which interventions may help prevent or limit the complications of diabetes mellitus (DM)? 9. What are the characteristics of type 2 diabetes mellitus (DM)? 10. What are the common vascular and neuropathic complications of type 2 diabetes mellitus (DM)? 11. How are type 1 and type 2 diabetes mellitus (DM) differentiated? 12. What is the total annual cost in the U.S. for management of diabetes mellitus (DM)? 13. How does type 2 diabetes mellitus (DM) develop? 14. What two factors must be present for type 2 diabetes mellitus (DM) to occur? 15. How does prolonged type 2 diabetes mellitus (DM) affect the pancreas? 16. What is the role of beta-cell dysfunction in the pathophysiology of type 2 diabetes mellitus (DM)? 17. How does insulin resistance affect glucose tolerance in type 2 diabetes mellitus (DM)? 18. Which genes increase the risk for developing type 2 diabetes mellitus (DM)? 19. What is the role of amino acid metabolism in the pathology of type 2 diabetes mellitus (DM)? 20. How do the complications of diabetes mellitus (DM) differ by type? 21. Which lipid abnormalities contribute to cardiovascular risk in type 2 diabetes mellitus (DM)? 22. How does insulin resistance affect lipid accumulation and how is it managed? 23. When does cardiovascular risk increase in the pathology of type 2 diabetes mellitus (DM)? 24. How does type 2 diabetes mellitus (DM) accelerate cognitive decline, and what is the relationship of coronavirus disease 2019 (COVID-19) to diabetes? 25. At what BMI does the risk for type 2 diabetes mellitus (DM) increase?

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