Type 2 diabetes epidemic increases use of oral anti-diabetic agents.
PATHOPHYSIOLOGY OF TYPE 2 DIABETES
Insulin resistance is the major pathophysiologic process that causes type 2 diabetes. As the disease progresses, pancreatic insulin deficiency plays an additional role in the pathogenesis of the condition. Cellular insensitivity to insulin puts strain on the pancreas to secrete increasing insulin amounts. Greater than normal amounts of insulin are required to achieve glycemic control. Eventually the pancreas becomes exhausted and cannot continue to secrete insulin in amounts commensurate with blood glucose levels. Blood glucose levels climb as the pancreas dysfunctions and ceils continually resist insulin.
Cellular insensitivity to insulin deters the entry of glucose into the cells, but the exact mechanism by which cells become insensitive to insulin is unknown. As the cells resist the effect of insulin, glucose accumulates in the bloodstream and hyperglycemia results. Eventually, because the cellular intake of glucose is deficient, the body perceives this as starvation. The liver then plays a key role as a compensatory organ. Hepatic glycogen stores break down through the process of glycogenolysis, which further raises blood glucose. After glycogen is depleted, the liver begins synthesizing glucose from amino acids and fats through the process of gluconeogenesis; this leads to further increases in blood glucose levels.
Breakdown of fat stores occurs to a minimal extent in type 2 diabetes due to the presence of some insulin. The presence of insulin inhibits lipolysis and consequent formation of fatty acids. Because fatty acids are normally the source of ketone formation, minimal formation of ketones occurs in type 2 diabetes (unlike type 1 diabetes) (Kumar, Abbas, & Fausto, 2005; McPhee, Lingappa, Ganong, & Lange, 2000) (see Figure 1).
[FIGURE 1 OMITTED]
Obesity is a major contributing factor to the development of type 2 diabetes. Fat ceils are particularly resistant to insulin action; the greater the adiposity of an individual, the greater the insulin resistance (Peters, 2000). For this reason, weight loss can improve glucose control dramatically in type 2 diabetes.
DIAGNOSIS AND TREATMENT OF TYPE 2 DIABETES
Type 2 diabetes usually develops gradually without overtly apparent symptoms. Most individuals experience years of high blood glucose levels prior to diagnosis of type 2 diabetes. In fact, upon diagnosis, 50% of individuals have already endured prolonged levels of elevated blood glucose which have caused microvascular and neurological damage (Shutta & Schwartz, 2001).
Type 2 diabetes is diagnosed mainly by a fasting blood glucose which exceeds 126 mg/dl on two separate primary care visits. Random blood glucose values greater than 200 mg/dl are also indicative of the disease. Glucose intolerance, a fasting blood glucose of greater than 110 mg/dl, is usually seen prior to the development of type 2 diabetes (American Diabetes Association [ADA], 2001).
Once the diagnosis is established, the patient must monitor his or her blood sugar vigilantly using a glucometer at least twice a day. These blood glucose levels are the determining factor for individualized patient treatment. The newest glucometers can store information so the clinician can review the patient's blood glucose levels retrospectively. Treatment also is based on evaluating the patient's level of glycemic control over the preceding 2 to 3 months via the hemoglobin A1c (HbA1c) laboratory test. HbA1c is a measure of the percentage of glycosylated hemoglobin in the bloodstream, which has developed due to hyperglycemic episodes. The ideal value of HbA1c is < 6.5% (ADA, 2001) (see Table 1).
BASIC TREATMENT OF TYPE 2 DIABETES
Treatment of type 2 diabetes traditionally has involved a stepwise approach which begins with lifestyle modification, mainly diet and exercise. Weight loss and increased activity are highly effective for blood glucose control. However, among many individuals, weight loss and increased activity levels are not sustainable.
Oral anti-diabetic agents are initiated when lifestyle modification proves insufficient. However, oral agents are most effective when individuals also maintain weight control and exercise. Oral agent combinations can be used if glycemic control is inadequate on monotherapy.
Insulin is generally the last step in the therapeutic approach to control type 2 diabetes. After diet, exercise, and oral anti-diabetic agents fail to control the individual's blood glucose, insulin is added to the regimen. Treatment is modified to achieve a Hgb A1C value less than or equal to 6.5% (Reasoner, 2002).
GLYCEMIC CONTROL BY ORAL ANTI-DIABETIC AGENTS
Different categories of oral anti-diabetic agents have various mechanisms of action, pharmacokinetics, and possible side effects. Although monotherapy with an oral anti-diabetic agent and lifestyle modification are effective in controlling blood glucose in some individuals, combination therapy is indicated more often. A combination of an oral anti-diabetic agent and insulin is used commonly to obtain the best glycemic control. According to data from the landmark United Kingdom Prospective Diabetes Study (UKPDS), a high number of individuals on single-drug therapy demonstrate ineffective glycemic control over time (UKPDS Group, 1998).
Oral anti-diabetic agents aim to control the three glycemic indices of diabetes:
* glycosylated hemoglobin
* fasting blood glucose
* postprandial glucose
However, the agents differ in their effects on the indices. Good control of the key glycemic indices greatly diminishes the risk of adverse events in patients with type 2 diabetes, as demonstrated in the UKPDS.
Because hyperglycemia is the major source of acute and long-term complications in type 2 diabetes, strict glycemic control is essential. Values for preprandial (fasting), postprandial (after meals), and bedtime blood glucose have been delineated by the ADA (2001) (see Table 2). The individual with type 2 diabetes should understand the use of a glucometer and attempt to maintain blood glucose levels in the range recommended by the ADA.
CATEGORIES OF ORAL ANTI-DIABETIC AGENTS
Available oral agents include insulinotropic agents (sulfonylureas and meglitinides), biguanides, alpha-glucosidase inhibitors, and thiazolidinediones (glitazones). Within the literature, terms vary for these drug categories; meglitinides are often referred to as glitinides and thiazolinediones are sometimes referred to as glitazones (see Table 3).
Insulinotropic agents stimulate pancreatic insulin secretion. Biguanides and thiazolidinediones are insulin sensitizers, making body tissues less resistant to insulin. Alpha-glucosidase inhibitors block intestinal absorption of carbohydrates. Each category of oral agent has different sites of action, pharmacokinetics, and possible side effects (see Table 3).
The bignanide metformin (Glucophage[R], Fortamet[R]) is first line therapy for patients with type 2 diabetes. Metformin inhibits hepatic glucose production, thereby antagonizing fasting hyperglycemia. It also enhances muscle cell insulin sensitivity. There is no direct effect on the pancreas; to obtain an effect, the patient needs some ability to secrete endogenous insulin. Metformin also lowers cholesterol and triglycerides by reducing the hepatic synthesis of very low density lipoprotein cholesterol (VLDL-C). Metformin is most effective when used in combination with sulfonylureas, thiazolinediones, or insulin, and has replaced the sulfonlyureas as first-line therapy (Schutta & Schwartz, 2001).
Lactic acidosis, a rare serious metabolic imbalance, can result from accumulation of metformin, and can occur whenever there is significant tissue hypoperfusion and hypoxemia. The majority of cases of lactic acidosis have occurred in patients with diabetes and hepatic disease, renal insufficiency, heart failure, dehydration, or sepsis. Patients should be cautioned about excessive alcohol intake because alcohol potentiates the effect of metformin on lactate metabolism. Lactic acidosis is a medical emergency which requires immediate discontinuation of the drug. Treatment of lactic acidosis requires intensive medical management and may involve hemodialysis. Metformin should he discontinued temporarily in patients who require vascular radiocontrast studies or surgery.
Metformin is available commonly as 500 mg tablets and should be taken with meals once or twice daily as directed (Medical Economics, 2005). It is not recommended for children, or pregnant or nursing women. Renal function should be monitored and metformin should be discontinued in renal insufficiency. Blood levels of metformin increase with concomitant use of drugs which are secreted by renal tubules. Metformin's interactions with other drugs may predispose to hyperglycemia. The clinician should consult the Physician's Desk Reference[R] (PDR) for the long list of medications which interact with metformin prior to prescribing the drug. Metformin is used in combination formulations with other classes of oral ant-diabetic agents. Avandamet[R] (thiazolinedione and metformin) and Glucovance[R] (glyburide and metformin) are examples of these drug combinations.
Thiazolinediones (TZDs) induce changes in genetic transcription processes within muscle cell nuclei which, in turn, make cells more sensitive to insulin. TZDs also inhibit hepatic glucose production. The two drugs currently available are pioglitazone (Actos[R]) and rosiglitazone (Avandia[R]). TZDs can be used as monotherapy or in combination with other oral anti-diabetic drugs. A combination formulation is Avandamet[R] (TZD and metformin).
Generally the TZDs inhibit platelet aggregation and lower blood pressure which are beneficial cardiovascular effects. However, TZDs often increase total cholesterol and raise LDL cholesterol levels. For this reason, TZDs may not be suitable for individuals with diabetes who also have dyslipidemia (Granberry & Fonseca, 2005). As an exception, Chipkin (2005) showed that pioglitazone lowers total cholesterol and triglycerides, and raises HDL cholesterol.
TZDs should not be used in persons with liver impairment, and liver enzymes should be monitored closely while taking this drug. Because drug levels can increase in heart failure, these medications should not be used in severe heart failure. TZDs may antagonize effectiveness of oral contraceptives, and resumption of ovulation can occur in premenopausal women. These drugs should not be used in pregnancy or children. Glycemic control can be disrupted with concomitant administration of ketoconazole. Once-daily dosage of 15 mg to 45 mg is the usual regimen (Medical Economics, 2005).
Insulinotropic Agents: Sulfonylureas and Meglitinides (Glitinides)
Sulfonylureas. Sulfonylureas are known as insulinotropic agents, insulin releaser agents, or secretogogues because they stimulate the pancreas to secrete insulin. To obtain maximum benefit, the patient needs to have functional pancreatic beta cells which secrete endogenous insulin. As pancreatic function wanes with progression of time in type 2 diabetes, sulfonylureas become less effective.
Sulfonylureas have fallen out of favor as first-line therapeutic agents with the advent of biguanides. Many practitioners refrain from using sulfonylureas because they raise blood insulin levels; high insulin levels are associated with weight gain and vascular injury. In the 1960s and 1970s, the University Group Diabetes Program (UGDP) study proposed that tolbutamide, an older sulfonylurea, increased cardiovascular risk. The UGDP study, a long-term clinical trial, found tolbutamide-treated patients had a rate of cardiovascular mortality 2.5 times that of patients treated with diet alone (Bradley, Dolger, Forsham, & Seltzer, 1975; Medical Economics, 2005). However, these results have been disputed by many experts (Meier, Gallwitz, Schmidt, Mugge, & Nauck, 2004; Schwartz & Meinert, 2004). The 1998 landmark United Kingdom Prospective Diabetes Study found no increase in coronary artery disease in patients treated with sulfonylureas compared to diet (UKPDS Group, 1998). The findings of the UKPDS seem to have settled this controversy.
The side effect of weight gain with sulfonylurea use is problematic because insulin resistance increases with adiposity. Weight gain is a major cause of drug failure and withdrawal from therapy. Sulfonylureas have little or no beneficial effect on lipids (Chipkin, 2005).
Hypoglycemia is a common side effect of sulfonylureas, particularly in patients who skip meals. Exercise, alcohol ingestion, or combination therapy increases risk of hypoglycemia. Hypoglycemia may be difficult to identify in older adults, especially those on beta adrenergic blockers (Medical Economics, 2005). Beta adrenergic blockers diminish hypoglycemic symptoms. For the patient taking a sulfonylurea, vigilant blood glucose monitoring is essential.
Glimepiride (Amary[R]), glyburide (Diabeta[R], Micronase[R]), chlorpropamide (Diabenese[R]), and glipizide (Glucotrol[R], Glynase[R]) are commonly prescribed sulfonylureas. These drugs should be taken with breakfast or the first main meal of the day. Clinicians will titrate the dosage of medication according to blood glucose results. When these drugs are initiated, frequent blood glucose monitoring is necessary to adjust the dosage.
Because sulfonylureas are composed of sulfa compounds, they are contraindicated in persons allergic to sulfa. These drugs should not be taken in ketoacido sis, renal or liver impairment, or pituitary or adrenal insufficiency. The long list of drug interactions with sulfonylureas requires clinicians to consult the PDR before prescribing these drugs for individuals who take other medications.
Meglitinides (glitinides). Meglitinides (glitinides) stimulate the pancreas to secrete insulin. The action of meglitinides, as with sulfonylureas, is dependent on functional beta ceils of the pancreas. Meglitinides differ from sulfonylureas in that they offer more flexibility in glucose control for the patient. These agents are shortacting, rapidly excreted, and taken with meals. They are absorbed rapidly from the G1 tract and excreted primarily by the kidney. Meglitinides should be taken with meals or up to 30 minutes before meals, making a common drug regimen 3 times a day. Repaglinide (Prandin[R]) and nateglinide (Starlix[R]) are meglitinides which can be used as monotherapy or in combination with another class of oral anti-diabetic agent (Medical Economics, 2005).
These drugs effectively control postprandial hyperglycemia. Recent investigations suggest that postprandial elevations in blood glucose contribute most to rises in HbA1c and cardiovascular disease (Diabetes Epidemiology: Collaborative Analysis of Diagnostic Criteria in Europe [DECODE], 1999). As the role of postprandial hyperglycemia has assumed heightened importance in diabetes management, these drugs have taken on new significance (Avignon & Monnier, 2000).
To prevent hypoglycemia, patients should be cautioned to skip doses of meglitinides when not eating meals. Because of their rapid onset and shorter duration of action, they cause less incidences of postprandial hypoglycemia than sulfonylureas. They do not cause the weight gain associated with sulfonylureas.
The alpha-glucosidase inhibitors acarbose (Precose[R]) and miglitol (Glyset[R]) delay absorption of carbohydrates by reversibly blocking the enzyme alpha-glucoside hydrolase at the intestinal border. This drug acts locally in the GI tract and is not absorbed systemically in significant amounts. Acarbose prevents a large rise in postprandial glucose, a fact that has become more significant in light of research linking postprandial hyperglycemia to risk of cardiovascular mortality (DECODE, 1999). Hyperglycemia after meals is more deleterious to the arterial endothelium than high fasting blood glucose levels. Clinical trials have shown that therapies that reduce postprandial blood glucose reduce cardiovascular risk (Karasik, 2005). The correlation between vascular injury and postprandial hyperglycemia has refocused treatment priorities.
The individual should be advised to take acarbose at the beginning of each meal, three times a day (Medical Economics, 2005). Dietary instructions, exercise recommendations, and regular testing of blood glucose are essential during treatment with acarbose. Intestinal adsorbents and digestive enzyme preparations can reduce the effect of acarbose. Digoxin levels also may be altered by co-administration of acarbose.
Acarbose does not cause hypoglycemia by itself, but it can lead to this complication in combination formulations. Interactions with diuretics, corticosteroids, oral contraceptives, thyroid medications, sympathomimetic agents, and calcium channel blockers can cause hyperglycemia. GI symptoms are the most common side effects of acarbose due to undigested carbohydrates in the lower intestine. Liver and renal impairment can occur with high doses of acarbose.
WEIGHT LOSS AGENTS AND TYPE 2 DIABETES
The weight-loss drug sibutramine (Meridia[R]) has shown effectiveness in type 2 diabetes. Sibutramine acts on the central nervous system to induce satiety through inhibition of serotonin and norepinephrine uptake. It also inhibits norepinephrine reuptake, which increases sympathetic discharge, heart rate, and BP. Sibutramine significantly decreases fasting blood glucose, HbA1c levels, and plasma triglycerides, and raises HDL cholesterol levels in obese individuals with type 2 diabetes (Heath, Chong, Weinstein, & Seaton, 1999). Due to the sympathetic side effects, this drug should not be prescribed for some individuals, such as those with hypertension or cardiovascular disease.
Orlistat (Xenical[R]), another weight loss medication, has shown similar improvements in glucose control after weight loss. However, orlistat acts by inhibiting fat absorption and thus has many GI side effects (Hollander, Lucas, Hauptman, Boldrin, & Segal, 1999). In general, the effectiveness of weight loss medications confirms the contribution of obesity to the pathogenesis of type 2 diabetes and the importance of weight loss for improved glycemic control.
NURSING IMPLICATIONS OF ORAL ANTI-DIABETIC AGENTS
Patient Education: Key Task Of the Nurse
Because nurses in all clinical settings will care for patients with diabetes, they require "state of the art" knowledge of treatment. Prevention of hyperglycemia is the most significant aim of treatment in diabetes, in part because postprandial hyperglycemia is most influential in forming long-term complications (Rossetti, 1995). The more thorough the patient education, the better chance the patient has for attaining glycemic control.
The ADA (2001) recommends that patients with diabetes receive medical care from an integrated team of health care professionals, including physicians, nurses, nurse practitioners, nutritionists, pharmacists, and mental health professionals. Nurses who are prepared as certified diabetes educators are often central to the care of patients. Nurses in general are key clinicians involved in educating the patient about self-monitoring of blood glucose, medication administration, and the signs and detrimental effects of poor glycemic control. Patients need to understand how the health of their heart, kidneys, eyes, and lower extremities can be affected negatively by hyperglycemia. They also need to understand their susceptibility to infections and poor wound healing. Yearly influenza vaccine and periodic pneumococcal vaccine are recommended (ADA, 2004). Nurses also can reinforce the lifestyle modifications of diet, weight control, and daily exercise. Numerous patient education materials are available from the American Diabetes Association (www.diabetes.org).
Patients must have a demonstration of glucometer use and understand the meanings of blood glucose values. They should be given simple written materials and have the opportunity to demonstrate use of the glucometer for the nurse. Patients should feel comfortable with the operation of a glucometer because use of this device will be a daily necessity. Most patients will learn use of the lancet, glucose strips, and glucometer by repeated practice with nurse support.
Patients should receive instruction about symptoms related to hyperglycemia and hypoglycemia. Extreme stress, acute illnesses, fever, infections, or surgery can cause dramatic alterations in blood glucose levels. Polyuria (excess urination) and polydipsia (excess thirst) are the key symptoms of hyperglycemia in type 2 diabetes. With vigilant blood glucose monitoring, hyperglycemia can be avoided. If blood glucose reaches high levels, patients should contact their physicians as soon as possible for instructions.
Patients need to be aware that tachycardia (palpitations), diaphoresis (excessive perspiration), tremulousness, headache, difficulty concentrating, and anxiety can be symptoms of hypoglycemia. The patient should carry sources of glucose for hypoglycemic episodes. Ingesting candy, crackers, or orange juice may be somewhat effective to reverse hypoglycemia, but these sources take a prolonged time to be absorbed into the bloodstream. Quickly absorbable forms of glucose specifically are available as over-the-counter preparations for diabetes.
With any anti-diabetic agent, concomitant use of beta-adrenergic blockers may increase risk of hypoglycemia and mask symptoms of hypoglycemia (Medical Economics, 2005). Beta-blockers antagonize hepatic glycogenolysis and blunt the sympathetic nervous system responses of associated with hypoglycemia.
Nurses need to take an accurate history of all the medications of the patient. There are many possible drug-drug interactions between oral anti-diabetic agents and other categories of drugs. The possible side effect of lactic acidosis associated with metformin is of particular importance. Anytime a patient requires intravenous radio-opaque dye, metformin should be discontinued in the days preceding the procedure. Lactic acidosis is a medical emergency which can occur in dehydration, sepsis, heart failure, renal impairment, and other conditions. With any oral anti-diabetic agent, thorough patient education regarding specific dosing schedules and potential side effects are a necessary nursing intervention.
Nurses across all health settings will encounter patients with diabetes, and they should have a holistic understanding of the pathogenesis, complications, and pharmacotherapy of this disease. A wide number of oral anti-diabetic agents are used for treating type 2 diabetes. Each class of drug has a distinctive mode of action and possible side effects. Certain oral antidiabetic agents demonstrate cardioprotective effects on lipids and blood pressure. Oral agents often are used in combination because different agents can offer synergistic means of glycemic control. Patient education, a key nursing intervention, promotes independent health maintenance and prevention of complications among individuals with type 2 diabetes.
American Diabetes Association (ADA). (2001). Clinical practice recommendations. Diabetes Care, 24(Suppl. 1), $34.
American Diabetes Association (ADA). (2004). Standards of medical care in diabetes. Diabetes Care, 27(Suppl. 1), S15-S35.
Avignon, A., & Monnier, L. (2000). Specific effect of postprandial glycemic peaks on HbA1c and angiopathy. Diabetes & Metabolism, 26(Suppl. 2), 12-15.
Bradley, R.E, Dolger, H, Forsham, P.H., & Seltzer, H. (1975). Settling the UGDP controversy. Journal of the American Medical Association, 232(8), 813-817.
Chipkin, S.R. (2005). How to select and combine oral agents for patients with type 2 diabetes mellitus. American Journal of Medicine, 118(5A), 4S-13S.
Diabetes Epidemiology: Collaborative Analysis of Diagnostic Criteria in Europe (DECODE). (1999). Lancet, 354, 617-621.
Granberry, M.C., & Fonseca, V.A. (2005). Cardiovascular risk factors associated with insulin resistance: Effects of oral antidiabetic agents. American Journal of Cardiovascular Drugs, 5(3), 201-209.
Heath, M.J., Chong, E., Weinstein, S.P., & Seaton, T.B. (1999). Sibutramine enhances weight loss and improves glycemic control and plasma lipid profile in obese patients with type 2 diabetes mellitus. Diabetes, 48(Suppl. 1), 1-A550.
Hollander, R, Lucas, C., Hauptman, J., Boldrin, M.N., & Segal, K.R. (1999). Orlistat reduces body weight and cardiovascular disease risk factors in obese men and women with type 2 diabetes. Diabetes, 48(Suppl. 1), 1-A550.
Karasik, A. (2005). Glycaemic control is effective for cardiovascular risk reduction across the type 2 diabetes continuum. Annals of Medicine, 37(4), 250-258.
Kumar, V., Abbas, A.K., & Fausto, N. (2005). Robbins & Cotran Pathologic Basis of Disease (7th ed.). Philadelphia: Elsevier Saunders.
McPhee, S.J., Lingappa, V.R., Ganong, W.F., & Lange, J.D. (2000). Pathophysiology of disease: An introduction to clinical medicine (3rd ed.). New York: Lange Medical/McGraw Hill.
Medical Economics. (2005). Physician's desk reference. Montvale, N J: Author.
Meier, J.J., Gallwitz, B., Schmidt, W.E., Mugge, A., & Nauck, M.A. (2004). Is impairment of ischaemic preconditioning by sulfonylurea drugs clinically important? Heart, 90(1), 9-12.
Mokdad, A.H., Ford, E.S., Bowman, B.A., Nelson, D.E., Engelgau, M.M., Vinicor, F., et al. (2000). Diabetes trends in the U.S: 1990-1998. Diabetes Care, 23, 1278-1283.
Peters, A. (2000). The clinical implications of insulin resistance. The American Journal of Managed Care, 6(13 Suppl.), S668-S674.
Reasoner, C.A. (2002). Aggressive control of type 2 diabetes using oral agents. Therapeutic spotlight. Supplement to Clinician Reviews. International Center for Postgraduate Education. New York: Jobson Publishing, LLC.
Rossetti, L. (1995). Glucose toxicity: The implications of hyperglycemia in the pathophysiology of diabetes mellitus. Clinical Investigations in Medicine, 18, 255-260.
Schutta, M.H., & Schwartz, S.S. (2001). Preventing diabetic complications by decreasing insulin resistance. Preventive Medicine in Managed Care, 2(1 Suppl.), S3-S16.
Schwartz, T.B., & Meinert, C.L. (2004). The UGDP controversy: Thirty-four years of contentious ambiguity laid to rest. Perspectives in Biologic Medicine, 47(4), 564-574.
United Kingdom Prospective Diabetes Study Group (UKPDS). (1998). Intensive blood glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet, 352, 837-853.
Teri Capriotti, DO, MSN, CRNP, is a Clinical Associate Professor, Villanova University, Villanova, PA.
Table 1. Diagnostic Criteria for Type 1 and Type 2 Diabetes Mellitus Fasting Blood Glucose Ideal < 100 mg/dl Impaired fasting glucose 110-125 mg/dl (pre-diabetes) Diagnose diabetes [greater than or equal to] 126 mg/dl Random Glucose or 2-Hour Postprandial Glucose Ideal < 140 mg/dl Impaired glucose tolerance 140 -199 mg/dl (pre-diabetes) Diagnose diabetes [greater than or equal to] 200 mg/dl Test for Blood Glucose Control over Last 3 Months Glycosylated hemoglobin (Hgb A1C) [less than or equal to] 6.5 % ideal Source: American Diabetes Association, 2004 Table 2. ADA Treatment Goals for Glycemic Control in Type 2 Diabetes * Preprandial blood glucose 80-120 mg/dl * Postprandial blood glucose < 180 mg/dl * Bedtime blood glucose 100-140 mg/dl * HbA1c [less than or equal to] 6.5% Source: American Diabetes Association, 2004 Table 3. Category, Name, and Action of Oral Anti-Diabetic Agents Brand Drug Category Generic Name Name Biguanide metformin Glucophage[R] Fortamete Insulinotropic glimepiride Amaryl[R] (sulfonylureas) glipizide Glucotrol[R] glyburide DiaBeta[R] chlorpropamide Diabenese[R] glibenclamide gliclazide Insulinotropic repaglinide Prandin[R] (meglitinides) Starlix[R] (also called nateglinide glitinides) Thiazolinedione pioglitazone Actos[R] (also called rosiglitazone Avandia[R] glitazones) Alpha-glucosidase acarbose Precose[R] inhibitors Miglitol[R] Most Common Possible Drug Category Main Action of Drug Side Effects Biguanide Inhibits hepatic glucose Hypoglycemia production Lactic acidosis Sensitizes body tissues Drug-drug interactions to insulin Decreases hepatic synthesis of cholesterol Insulinotropic Stimulates pancreas to Hypoglycemia (sulfonylureas) secrete insulin Sulfa allergy Weight gain Drug-drug interactions Insulinotropic Stimulates pancreas to Hypoglycemia/weight gain (meglitinides) secrete insulin less likely than (also called sulfonylureas glitinides) Drug-drug interactions Thiazolinedione Sensitizes body tissues Hypoglycemia (also called to insulin Deactivation of oral glitazones) contraceptives Drug-drug interactions Possible liver dysfunction May cause hyperlipidemia Inhibits platelet aggregation Alpha-glucosidase Delays absorption of Hypoglycemia inhibitors carbohydrates in the Gastrointestinal side intestine effects Drug-drug interactions
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|Title Annotation:||Nursing Pharmacology|
|Date:||Oct 1, 2005|
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