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Diabetes is a chronic, progressive disease associated with significant morbidity and mortality. Fortunately, several long-term, prospective studies have demonstrated how proper medical management can significantly reduce the risks associated with diabetes. Based on these studies, the American Diabetes Association and American Association of Clinical Endocrinologists set forth standards and guidelines for the medical management of diabetes. The recommendations clearly outline a multifactorial plan for managing diabetes, but they do not provide specific recommendations for selection and titration of pharmacological treatment. Published reports suggest that specialists are adept at using complex drug regimens to reach the goals set forth in the guidelines, but primary care practitioners could benefit from treatment algorithms that guide the management of drug regimens for diabetes. This article briefly reviews the pharmacological management of type 2 diabetes and describes our experience developing a treatment algorithm for use within a managed care plan.
Diabetes is a chronic, progressive disease associated with significant morbidity and mortality. Patients with uncontrolled type 2 diabetes experience significant microvascular and macrovascular complications, which occur even in relatively asymptomatic individuals. With respect to microvascular complications, ∼16–21% of patients with diabetes experience retinopathy, 12–23% nephropathy, and 20–40% neuropathy.1 The risk of macrovascular complications, such as cardiovascular disease (CVD), cerebrovascular disease, and peripheral vascular disease, is several times higher in patients with type 2 diabetes than in nondiabetic patients.
Several landmark studies clearly document that patients who aggressively control their blood glucose levels are less likely to develop complications associated with diabetes.2,3 Based on these studies, the American Diabetes Association (ADA)4 and American Association of Clinical Endocrinologists (AACE)5 set goals for the outcome of medical intervention as a hemoglobin A1c (A1C) value of < 7 and 6.5%, respectively; preprandial plasma glucose levels of 90–130 mg/dl; and peak postprandial plasma glucose levels of < 180 mg/dl.3 One of the landmark studies, the U.K. Prospective Diabetes Study,2 conclusively demonstrated that for every percentage point decrease in A1C (e.g., from 8 to 7%), there was a 35% reduction in the risk of microvascular complications. In addition, research shows that reducing risk factors for CVD, such as diabetes, effectively prevents or slows CVD. With respect to reaching these goals, the guidelines emphasize lifestyle modifications (e.g., diet and exercise), patient education, and regular follow-up to prevent or delay complications.
diabetes and high blood pressure diet causes (☑ josh axe) | diabetes and high blood pressure diet how do you get ithow to diabetes and high blood pressure diet for Excellus BlueCross BlueShield is a nonprofit independent licensee of the BlueCross BlueShield Association and is New York''s standards allow any agent to be used for first-line treatment and do not address appropriate adjustments for patients outside their glycemic goals. Reports in the literature suggest that well-defined protocols for the use of oral agents in the management of diabetes would produce better results,1,6–10 and the experience of our DMP concurs with these reports.
In nondiabetic patients, glucose homeostasis is mediated by the stimulation of insulin secretion from the β-cells in the pancreas, which acts to suppress the endogenous hepatic production of glucose and stimulate glucose uptake in the peripheral tissues (e.g., muscle and fat). In patients with type 2 diabetes, which accounts for ∼90–95% of the diagnosed cases of diabetes, there is some the 1 last update 06 Aug 2020 degree of resistance to insulin in the hepatic and peripheral tissues, and the β-cells have a diminished ability to secrete insulin. It is unclear which mechanism plays the dominant role in the pathology of type 2 diabetes and the associated complications.11In nondiabetic patients, glucose homeostasis is mediated by the stimulation of insulin secretion from the β-cells in the pancreas, which acts to suppress the endogenous hepatic production of glucose and stimulate glucose uptake in the peripheral tissues (e.g., muscle and fat). In patients with type 2 diabetes, which accounts for ∼90–95% of the diagnosed cases of diabetes, there is some degree of resistance to insulin in the hepatic and peripheral tissues, and the β-cells have a diminished ability to secrete insulin. It is unclear which mechanism plays the dominant role in the pathology of type 2 diabetes and the associated complications.11
In the United States, there the 1 last update 06 Aug 2020 are five main classes of oral medications approved for the treatment of type 2 diabetes (Table 1) as monotherapy or combination therapy for patients who are not able to control their diabetes with diet and exercise alone.In the United States, there are five main classes of oral medications approved for the treatment of type 2 diabetes (Table 1) as monotherapy or combination therapy for patients who are not able to control their diabetes with diet and exercise alone.
Oral Agents Approved for Treatment of Type 2 Diabetes in the United States
Secretagogues act by increasing the secretion of insulin from the β-cells in the pancreas. The effect of higher plasma insulin concentrations suppresses hepatic glucose production and facilitates glucose uptake by the muscles.12,13 Most patients receiving monotherapy with secretagogues will eventually require a second agent from another class because the production of insulin by β-cells eventually declines, and stimulating the β-cells no longer improves insulin secretion.
diabetes and high blood pressure diet natural treatment cure (🔴 youngest age in pediatrics) | diabetes and high blood pressure diet go awayhow to diabetes and high blood pressure diet for Secretagogues have a neutral or slightly beneficial effect on plasma lipid levels. The major concern is the potential for hypoglycemia and weight gain, although the nonsulfonylurea agent repaglinide is thought to have a lower incidence of hypoglycemia than the sulfonylureas.14 Some evidence suggests that the actual incidence of hypoglycemia resulting from treatment with any agent is of minor significance in comparison with the incidence of hypoglycemia associated with lifestyle changes.1,14 Regardless, some patients will be at higher risk than others, and the relative risk should be considered.
The biguanides act by suppressing basal hepatic glucose production and enhancing insulin uptake by the muscle. The fasting blood glucose level will begin to decrease within 3–5 days after initiating therapy, but the full effect takes 1–2 weeks. Biguanides reduce plasma triglycerides and LDL cholesterol levels. Metformin is the only agent in any of the oral antidiabetic drug classes that can reduce both microvascular and macrovascular complications when used as monotherapy for the treatment of type 2 diabetes.2,3 Most patients treated with metformin maintain a consistent weight or lose weight. The incidence of hypoglycemia associated with metformin is rare because metformin does not increase insulin secretion. Biguanides are contraindicated in patients with renal disease or dysfunction, congestive heart failure that requires pharmacological treatment, and acute or chronic metabolic acidosis.15
Thiazolidinediones (TZDs) rejuvenate β-cell activity and act to improve sensitivity to insulin.15–17 The fasting blood glucose levels begin to decrease within 5–7 days, but the maximum potential of a given dose is not reached for 3–4 weeks. TZDs when used alone or in combination with other medications for diabetes can cause fluid retention and exacerbate or lead to congestive heart failure. Liver toxicity occurs in some patients, so liver function must be monitored monthly.
α-Glucosidase inhibitors decrease postprandial glucose levels by delaying the digestion of carbohydrates and absorption of glucose. Although it does not reverse any pathophysiological defects, slowing the rate of absorption of glucose is thought to give the β-cells more time to secrete the necessary insulin. α-Glucosidase inhibitors must be taken with the first bite of food. The effect of this class of drugs on lipid profiles and body weight is neutral. The major side effects are gastrointestinal in nature.
There are a few new classes of drugs, such as synthetic amylin hormone (pramlintide) and incretin mimetics (exenatide). There are also some combination products new to the market. Because they are relatively new, they are not included in any of the algorithms published in the literature. But based on preliminary data, these injectable agents (e.g., exenatide and pramlintide) will likely be secondline therapy.18 It is assumed that combination products are used when appropriate per an algorithm because the pharmacology suggests that combinations should be used when a patient has been stabilized on both medications individually.
When developing a pharmacological treatment strategy for patients with type 2 diabetes, it is important to remember that glucose disposition is part of a complex metabolic and cardiovascular system that includes dys-lipidemia, hypertension, obesity, and coagulability, among others morbidities.19 The goals for A1C are general, and it is expected that goals for each patient be customized based on a complete assessment of the patient. Aggressive glycemic control is appropriate in some patients, whereas the risk of hypoglycemia, weight gain, or other complications necessitates less aggressive goals in other patients, such as those with limited life expectancy, those who are very young or old, and those with select comorbidities. In addition, the presence and severity of comorbidities vary among patients and over time within a single patient. Thus, regular reassessment is required.
Once treatment goals have been individualized, several patient-specific factors should also be considered when selecting a drug regimen. Such factors include differences in how the medications work, the potential for hypoglycemia, time to onset of action, estimated time spent outside of goals, potential compliance with the regimen, and the patient''s physician to consider insulin therapy because of her A1C > 10%. M.S. was not assessed for insulin resistance or metabolic syndrome at her physician''s case shows how the algorithm could be used for newly diagnosed patients, but some patients enter the algorithm after first-line assessment, as described below.
M.J. is a 53-year-old man who has been living with type 2 diabetes for 10 years. He is currently on a regimen consisting of a biguanide and a TZD. Initially, he had good blood glucose control, with fasting plasma glucose levels between 90 and 120 mg/dl. His A1C has ranged from 6.2 to 7.0%. At M.J.''s physician requested a nutritional consultation; ran standard laboratory tests, including a lipid panel, liver function tests, and A1C; and asked M.J. to continue to monitor his blood glucose at home. At the followup visit, M.J.''s primary care practitioner took an aggressive but appropriate approach to gain control of M.J.''minipanel-dialog-wrapper''minipanel-dialog-link-link''minipanel-dialog-link-mini''display:none''minipanel-dialog-wrapper''minipanel-dialog-link-link''minipanel-dialog-link-mini''display:none''minipanel-dialog-wrapper''minipanel-dialog-link-link''minipanel-dialog-link-mini''display:none''panels-ajax-pane-title''new-40''panels-ajax-pane panels-ajax-pane-new-40''new-40''panels-ajax-pane panels-ajax-pane-new-4''new-4''panels-ajax-pane panels-ajax-pane-new-5''new-5''highwire-cite highwire-citation-jcore-title-only''highwire-cite-title''highwire-cite highwire-citation-jcore-title-only''highwire-cite-title''highwire-cite highwire-citation-jcore-title-only''highwire-cite-title''highwire-list-footer'>Show more Feature Articles