Diabetes Mellitus Persuasive
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Is a multisystem disease related to abnormal insulin production, impaired insulin utilization, or both. Diabetes Mellitus is a serious health problem throughout the world. It is the 5th leading cause of death in the U.S. It is the leading cause of heart disease, stroke, adult blindness, and nontraumatic lower limb amputations.
Etiology and Pathophysiology
Current theories link the cause of diabetes, singly or in combination, to genetic, autoimmune, viral, and environmental factors (obesity, stress). Regardless of its cause, diabetes is primarily a disorder of glucose metabolism related to absent or insufficient insulin supplies and/or poor utilization of the insulin that is available. The two most common types of diabetes are classified as type I or type II diabetes mellitus. Gestational diabetes and secondary diabetes are other classifications of diabetes commonly seen in clinical practice
Normal Insulin Metabolism
Insulin is a hormone produced by the B cells in the islets of Langerhans of the pancreas. Under normal conditions, insulin is continuously released into the bloodstream in small pulsatile increments (a basal rate), with increased release (bolus) when food is ingested. The activity of released insulin lowers blood glucose and facilitates a stable, normal glucose range of approximately 70 to 120 mg/dl. The average amount of insulin secreted daily by and adult is approx. 40 to 50 U, or 0.6 U/kg of body weight.
Other hormones (glucagons, epinephrine, growth hormone, and cortisol) work to oppose the effects of insulin and are often referred to as counterregulatory hormones. These hormones work to increase blood glucose levels by stimulating glucose production and output by the liver and by decreasing the movement of glucose into the cells. Insulin and the these counterregulatory hormones provide a sustained but regulated release of glucose for energy during food intake and periods of fasting and usually maintain blood glucose levels within the normal range. An abnormal production of any or all of these hormones may be present in diabetes.
Insulin is released from the pancreatic B cells as its precursor, proinsulin, and is then routed through the liver. Proinsulin is composed of two polypeptide chains, chain A and chain B, which are linked by the C-peptide chain. The presence of C peptide in serum and urine is a useful indicator of B cell function.
Insulin promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell. The rise in plasma insulin after a meal stimulates storage of glucose as glycogen in liver and muscle, inhibits gluconeogenesis, enhances fat deposition in adipose tissue, and increases protein synthesis. The fall in insulin level during normal overnight fasting facilitates the release of stored glucose from the liver, protein form muscle, and fat from adipose tissue. For this reason insulin is known as the anabolic or storage hormone.
Skeletal muscle and adipose tissue have specific receptors for insulin and are considered insulin-dependent tissues. Other tissues (brain, liver, blood cells) do not directly depend on insulin for glucose transport but require an adequate glucose supply for normal function. Although liver cells are not considered insulin-dependent tissue, insulin receptor sites on the liver facilitate the hepatic uptake of glucose and its conversion to glycogen.
Type I Diabetes Mellitus
Formally known as “juvenile onset” or “insulin dependent” diabetes, type I diabetes mellitus most often occur in people who are under 30 years of age, with a peak onset between ages 11 and 13. The rate of type I diabetes is 1.5 to 2 times higher in whites than nonwhites, with a similar incidence among males and females. Typically, it is seen in people with a lean body type, although it can occur in people who are overweight.
Etiology and Pathophysiology
Type I diabetes results from progressive destruction of pancreatic B cells due to an autoimmune process in susceptible individuals. Autoantibodies to the islet cells cause a reduction of 80% to 90% of normal B cell function before hyperglycemia and other manifestations occur. A genetic predisposition and exposure to a virus are factors that may contribute to the pathogenesis of type I diabetes.
Predisposition to type I diabetes is believed to be related to human leukocyte antigens (HLAs). When an individual with certain HLA types is exposed to viral infections, the B cells of the pancreas are destroyed, either directly or through an autoimmune process. The HLA types associated with an increased risk of type I diabetes include HLA-DR3 and HLA-DR4.
Onset of Disease
Type I diabetes is associated with a long preclinical period. The islet cell autoantibodies responsible for B cell destruction are present for months to years before the onset of symptoms. Manifestations of type I diabetes develop when the person’s pancreas can no longer produce insulin. Once this occurs, the onset of symptoms is usually rapid, and the patient comes to the emergency department with impending or actual ketoacidosis. The cpatient usually has a history of recent and sudden weight loss, as well as the classic symptoms of polydipsia (excessive thirst), polyuria (frequent urination), and polyphagia (excessive hunger).
The individual with type I diabetes requires a supply of insulin from an outside source (exogenous insulin), such as an injection, in order to sustain life. Without insulin, the patient will develop diabetic ketoacidosis (DKA), a life-threatening condition resulting in metabolic acidosis. During this time, the patient requires very little injected insulin because B cell mass remains sufficient for glucose control as the
progressive destruction continues to occur. Eventually, as more B cells are destroyed, blood glucose levels increase, more insulin is needed, and the honeymoon period ends. This usually lasts 3 to 12 months, after which the person will require insulin on a permanent basis.
Type II Diabetes Mellitus
Type II diabetes mellitus is, by far, the most prevalent type of diabetes, accounting for over 90% of patients with diabetes. Type II usually occurs in people over 40 years of age, and 80% to 90% of patients are overweight at the time of diagnosis. It has a tendency to run in families and probably has a genetic basis. Prevalence of this type of diabetes is greater in some ethnic population. The highest rates occur among Native Americans, who are about three times as likely to have type 2 diabetes as non-Hispanic whites of similar age.
Prevalence of type 2 diabetes increase with age, with about half of the people diagnosed being older than 55. k
Etiology and Pathophysiology
In type II diabetes, the pancreas usually continues to produce some endogenous (self-made) insulin. However, the insulin that is produced is either insufficient for the needs of the body/or is poorly utilized by the tissues. In contrast, there is a virtual absence of endogenous insulin in type I diabetes. The presence of endogenous insulin is the major pathophysiologic distinction between type I and type II diabetes.
Genetic mutations that lead to insulin resistance and a higher risk for obesity have been found in many people with type 2 diabetes. It is likely that multiple genes are involved in this complex, multifactorial disorder.
Three major metabolic abnormalities have a role in the development of type 2 diabetes. The first factor is insulin resistance, which is a condition in which body tissues do not respond to the action of insulin. This is due to insulin receptors that are either unresponsive to the action of insulin and/or insufficient in number. Most insulin receptors are located on skeletal muscle, fat, and liver cells. When insulin is not properly used, the entry of glucose into the cell is impeded, resulting in hyperglycemia. In the early stages of insulin resistance, the pancreas responds to high blood glucose by producing greater amounts of insulin (if B cell function is normal). This creates a temporary state of hyper-insulinemia that coexists with the hyperglycemia.
A second factor in the development of type 2 diabetes is a marked decrease in the ability of the pancreas to produce insulin, as the B cells become fatigued from the compensatory overproduction of insulin. Impaired glucose tolerance (IGT), often called prediabetes, usually occurs when the alteration in B cell function is mild. IGT is a condition in which blood glucose levels are higher than normal but not high enough for a diagnosis of diabetes.
A third factor is inappropriate glucose production by the liver. Instead of properly regulating the release of glucose in response to blood levels, the liver does so in a haphazard way that does not correspond a primary factor in the development of type 2 diabetes.
Insulin Resistance Syndrome
A cluster of abnormalities that act synergistically to greatly increase the risk for cardiovascular disease. Insulin resistance syndrome is characterized by elevated insulin levels, high levels of triglycerides, decreased levels of high-density lipoproteins, increased levels of low-density lipoproteins, and hypertension. Risk factors for insulin resistance syndrome include central obesity, sedentary lifestyle, polycystic ovary syndrome, urbanization/Westernization, ethnicity, family history, gestational diabetes, and increased age. Overweight people with IGT can prevent or delay the onset of diabetes through a program of weight loss and regular physical activity.
Onset of Disease
Disease onset in type 2 diabetes is usually gradual. The person may go for many years with undetected hyperglycemia that might produce few, if any, symptoms. If the patient with type 2 diabetes has marked hyperglycemia (500 to 1000), a sufficient endogenous insulin supply may prevent DKA from occurring. However, osmotic fluid and electrolyte loss related to hyperglycemia may become severe and lead to hyperosmolar coma.
Gestational diabetes develops during pregnancy and occurs in about 4% of pregnancies in the U.S. It is detected at 24 to 28 weeks of gestation (6-7 months), usually following an oral glucose tolerance test (OGTT). Women with gestational diabetes have a higher risk for cesarean delivery, perinatal death, and neonatal complications. Although most women with gestational diabetes will have normal glucose levels within 6 weeks postpartum, their risk for developing type 2 diabetes in 5 to 10 years is increased. Nutritional therapy is considered to be the first-line therapy. If nutritional therapy alone does not achieve desirable fasting blood glucose levels, insulin therapy is usually indicated.
Diabetes occurs in some people because of another medical condition or due to the treatment of a medical condition that causes abnormal blood glucose levels. Conditions that may cause secondary diabetes include Cushing syndrome, hyperthyroidism, and the use of parenteral nutrition. Commonly used medications that can induce diabetes in some people include corticosteroids (prednisone), phenytoin (Dilantin), and atypical antipsychotics (clozapine). Secondary diabetes usually resolves when the underlying condition is treated.
Type I Diabetes Mellitus
Because the onset of type I is rapid, the initial manifestations are usually acute. The classic symptoms are polyuria (frequent urination), polydipsia (excessive thirst), and polyphagia (excessive hunger). The osmotic effect of glucose produces the manifestations of polydipsia and polyuria . Polyphagia is a consequence of cellular malnourishment when insulin deficiency prevents utilization of glucose for energy. Weight loss may occur as the body cannot get glucose and turns to other energy sources, such as fat and protein. Weakness and fatigue may also be experienced, as body cells lack needed energy from glucose. Ketoacidosis, a complication associated with untreated type I, is associated with additional clinical manifestation.
Type II Diabetes Mellitus
The clinical manifestations of type 2 are often nonspecific, although it is possible that an individual with type 2 diabetes will experience some of the classic symptoms associated with type I. Some of the more common manifestations associated with type 2 diabetes include fatigue, recurrent infections, prolonged wound healing, and visual changes.
Regardless of the type, the diagnosis of diabetes mellitus can be made through one of three methods. Diagnosis must be confirmed on a subsequent day by any of the three methods.
Fasting plasma glucose level exceeding 126 mg/dl (7.0 mmol/L).
Random, or casual, plasma glucose measurement exceeding 200 mg/dl (11.1 mmol/L), plus manifestations of diabetes, such as polyuria, polydipsia, and unexplained weight loss. Casual is defined as any time of day without regard to the time of the last meal.
Two-hour OGTT level exceeding 2oo mg/dl (11.1 mmol/L), using a glucose load of 75 g.
The fasting plasma glucose test, confirmed by repeat testing on another day, is the preferred method of diagnosis. When overy symptoms of hyperglycemia (polyuria, polydipsia, and polyphagia) coexist with fasting plasma glucose levels of 126 mg/dl (7.0 mmmol/L) or greater, further testing using the oral glucose tolerance test may not be necessary to make a diagnosis.
Measurement of glycosylated hemoglobin, also known as the hemoglobin A1c (A1C) test, is useful in determining glycemic levels over time. The test works by showing the amount of glucose that has been attached to hemoglobin molecule increases and remains attached to the red blood cell (RBC) for the life of the cell (approx. 120 days). Therefore a glycosylated hemoglobin test indicates the overall glucose control for the previous 90 to 120 days. All patients with diabetes should have regular assessments of A1C done. People with diabetes who can maintain near-normal A1C levels over time have a greatly reduced risk for the development of retinopathy, nephropathy, and neuropathy. The ideal goal is 7.0% or less.
The goals of diabetes management are to reduce symptoms, promote well-being, prevent acute complications of hyperglycemia, and delay the onset and progression of long-term complications, These goals are likely to be met when the patient is able to maintain blood glucose levels as near to normal as possible. Patient teaching, which enables the patient to become the most active participant in his or her own care, is essential for a successful treatment plan. Nutritional therapy, drug therapy, exercise, and self-monitoring of blood glucose are the tools used in the management of diabetes. The two types of glucose-lowering agents used in the treatment of diabetes are insulin and oral agents. All individuals with type 1 diabetes require insulin. For some people with type 2 diabetes, a regimen of proper nutrition, regular physical activity, and maintenance of desirable body weight will be sufficient to attain an optimal level of blood glucose control. For the majority, however, drug therapy will be necessary.
Drug Therapy: Insulin
Exogenous (injected) insulin is needed when a patient has inadequate insulin to meet specific metabolic needs and the combination of nutritional therapy, exercise, and OAs cannot maintain a satisfactory blood glucose level. Exogenous insulin is required for the management of type I diabetes. Exogenous insulin is required for the management of type I diabetes. Exogenous insulin may be prescribed for the patient with type 2 who cannot control blood glucose by other means, especially during periods of severe stress, such as illness or surgery.
Types of Insulin
In the past, purified preparations of insulin made from beef and pork pancreas were used. However, human insulin is now the most widely used type of insulin. Human insulin is not directly harvested from human organs, but is derived from common bacteria (Escherichia coli) or yeast cells using recombinant DNA technology. The major advantage of human insulin is cost-effectiveness and decreased likelihood of causing an allergic reaction to animal insulin or additives to regular insulin.
Insulin differs in regard to onset, peak of action, and duration. The specific properties of each type of insulin are matched with the patient’s diet and activity. All insulin preparations start with regular insulin as a base. By adding zinc, acetate buffers, and protamine to insulin in various ways, the onset of activity, peak, and duration times can be manipulated. Zinc is added to make lente insulin, and zinc and protamine are added to make NPH. These additives can cause an allergic reaction at the injection site.
The timing of insulin administration in relation to meals is important. Regular insulin should be taken 30 to 45 minutes before meals to ensure the onset of action in conjunction with meal absorption. (table 47-4)
Types of Insulin
Rapid-acting insulin lispro (Humalog)
Short-acting insulin regular (Humulin R, Novolin R,
Intermediate-acting NPH (Humulin N, Novolin N)
Lente (Humulin L, Novolin L)
Long-acting ultralente (Humalin U)
Combination therapy NPH/regular 70/30 (Humalin
70/30, Novolin 70/30)
NPH/regular 50/50 (Humulin
50/50) NPH/lispro 75/25
(Humalog Mix 75/25)
The criteria for selection are based on the type of diabetes and the required, desired, and feasible levels of glycemic control.
Synthetic rapid-acting insulin’s include lispro (Humalog) and aspart insulin (Novolog). They have an onset of action of approx. 5 to 15 min. (as compared with 30 to 60 min for regular insuslin). Rapid-acting insulin is considered to be the type that best mimics natural insulin secretion in response to a meal. It is injected at the time of the meal to within 15 min of the meal. Another longer-acting insulin must also be used as basal background insulin, because the duration of rapid-acting insulin is so short.
Insulin glargine (Lantus) is a long-acting insulin that is released steadily and continuously and does not have a peak of action. It is used for once-daily sub Q administration at bedtime in patients with type I and type 2 diabetes who require basal (long acting) insulin for the control of hyperglycemia. Glargine must not be diluted or mixed with any other insulin or solution.
Short- or rapid-acting insulin is often mixed with a longer-acting insulin to provided both mealtime and basal coverage without having to administer two separate injections. Patients may mix themselves or may use a commercially premixed formula.
As a protein, insulin requires special storage considerations. Heat and freezing alter the insulin molecule. Insulin vials that the patient is currently using may be left at room temperature for up to 4 weeks unless the room temp is higher than 86 degrees or below freezing. Insulin can be stored in the refrigerator.
Prefilled syringes are stable for up to 30 days when stored in the refrigerator. Syringes prefilled with a cloudy solution should be stored in a vertical position with the needle pointed up to avoid clumping of suspended insulin binders in the needle.
Administration of Insulin
Because insulin is inactivated by gastric juices, it cannot be taken orally. Injection is the only route of administration currently approved for self-administration. Routine administration of insulin is most commonly done by means of SQ injection, although IV administration of regular insulin can be done when immediate onset of action is desired.
The speed with which peak serum concentrations are reached varies with the anatomic site for injection. The fastest absorption is from the abdomen, followed by the arm, thigh, and buttock. The patient should be cautioned about injecting into a site that is to be exercised. Exercise of the area containing the injection site together with the increased body heat generated by the exercise may increase the rate of absorption and speed the onset of insulin action. Lipodystrophy=a condition that produces lumps and dents in the skin from repeated injection in the same spot, the use of human insulin reduces this risk. Patients are advised to rotate the injection within one particular site, such as the abdomen. Most commercial insulin is available as U100, indicating that 1ml contains 100 U of insulin. U100 insulin must be used with a U100-marked syringe. Disposable plastic insulin syringes are available in a variety of sizes. Patients should be cautioned to check dosage lines carefully when changing syringe types because some use a scale of 1 U increments and others use a 2 U increment.
An insulin pen is a compact portable device that serves the same function as a needle and syringe but is handier to use. It usually comes preloaded with insulin. The advantage is that they are less “medical” looking. A new type of pen is the InDuo, which combines an insulin pen and a blood glucose monitor.
Alternate delivery methods
Continuous subcutaneous insulin infusion can be administered using an insulin pump, a small battery-operated device that resembles a standard paging device in size and appearance. Usually worn on the belt, the pump is connected via a small plastic tube to a catheter inserted into the sub Q tissue in the abdominal wall. Every 2 to 3 days the insertion site is changed and the pump is refilled with insulin and reprogrammed. It is programmed to deliver a continuous infusion of short-acting insulin 24 hours a day, known as the “basal rate”. At mealtime, the user programs the pump to deliver a bolus infusion of insulin appropriate to the amount of carbohydrate ingested and to bring down high premeal blood glucose, if necessary. Its major advantage is the potential for tight glucose control. It also offers the benefit of a more normal lifestyle, allowing users more flexibility with meal and activity patterns. The insertion site should be checked daily for redness and swelling.
An alternative to the insulin pump is intensive insulin therapy, which consists of multiple daily insulin (MDI) injections together with frequent self-monitoring of blood glucose. The goal is to achieve a near-normal glucose level of 80 to 120 mg/dl before meals.
Problems with Insulin Therapy
Hypoglycemia, allergic reactions, lipodystrophy, and Somogyi effect are the problems associated with insulin therapy.
Local inflammatory reactions to insulin may occur, such as itching, erythema, and burning around the infection site. Local reactions may be self-limiting within 1 to 3 months or may improve with a low dose of antihistamine. A true insulin allergy is a systemic response with urticaria and possibly anaphylactic shock generally resulting from the use of animal insulins. Usually rare, particularly since human insulin has become available.
Lipodystrophy (hypertrophy or atrophy of SQ tissue) may occur if the same injection sites are used frequently. Hypertrophy, a thickening of the SQ tissue, eventually regresses if the patient does not use the site for at least 6 months. The use of hypertrophied sites may result in erratic insulin absorption. Most common associated with beef or beef and pork insulin and rarely with human insulin. Site rotation on a daily or weekly basis is not
necessary with human insulin.
Somogyi effect-Wide differences in early morning (low) and fasting (high) glucose levels. Usually accruing in the hours of sleep, It produces a decline in blood glucose level in response to too much insulin. Counterregulatory hormones are released, stimulating lipolysis, gluconeogenesis, and glycogenolysis, which in turn produce rebound hyperglycemia and ketosis. The danger of his effect is that when blood glucose levels are measured in the morning, hyperglycemia is apparent and the patient may increase the insulin dose. It is associated with the occurrence of undetected hypoglycemia during sleep, although it can happen at any time.
The patient may report headaches on awakening and may recall night sweats or nightmares. If suspected pt. may be advised to check glucose levels between 2 to 4am to determine if hypoglycemia is present at that time. If it is, the insulin dosage affecting the early morning blood glucose is reduced.
The Dawn phenomenon is characterized by hyperglycemia that is present on awakening in the morning due to the release of counterregulatory hormones in the predawn hours. It has been suggested that growth hormone and/or cortisol are possible factors in the occurrence. This affects the majority of people with diabetes and tends to be most severe when growth hormone is at its peak in adolescence and young adulthood.
Careful assessment is required to document each phenomenon because the treatment for each differs. The tx. For Somogyi effect is less insulin. The tx. For dawn phenomenon is an adjustment in the timing of insulin admin. or an increase in insulin.
Drug Therapy: Oral Agents
Oral agents (OAs) are not insulin, but they work to improve the mechanisms by which insulin and glucose are produced and used by the body. For any of the OAs to be effective, the patient must have some circulating endogenous insulin. There are currently no OAs for the tx of type 1 diabetes. OAs may be used in combination with agents from other classes or with insulin to achieve blood glucose targets.
Five classes of oral medications are available to improve diabetes control for patients with type 2 diabetes.
Sulfonylureas-have been widely used to treat type 2 diabetes since the 1950s. They are called first generation or second generation depending on when they were introduced into clinical use in the US. The first generation of these drugs used in the tx. of diabetes mellitus includes tolbutamide (Orinase), acetohexamide (Dymelor), tolazamide (Tolinase), and chlorpropamide (Diabinese). The second generation of sulfonylureas includes glipizide (Glucotrol, Glucotrol XL), glyburide (Micronase, DiaBeta, Glynase), and glimepiride (Amaryl). Second-generation drugs have fewer adverse effects and are more potent by weight, but they are more expensive.
The primary action of the sulfonylureas is to increase insulin production from the pancreas. Therapy is generally more effective early in the course of type 2 diabetes. Prolonged use can cause decreased effectiveness.
Meglitinides-increase insulin production from the pancreas. But because they are more rapidly absorbed and eliminated, they offer a reduced potential for hypoglycemia. When taken just before meals, pancreatic insulin production increases during and after the meal, mimicking the normal blood glucose response to eating. Pt. should be instructed to take meglitinides anytime from 30 min before each meal right up to the time of the meal.
Biguanides- Metformin (Glucophage) is a biguanide glucoselowering agent. It can be used alone or with sulfonylureas, other OAs or insulin to treat type 2 diabetes. The primary action of metformin is to reduce glucose production by the liver. It also enhances insulin sensitivity at the tissue level and improves glucose transport into the cells. Besides being an effective blood glucose lowering agent, metformin has other advantages. Metformin is also used to treat prediabetes, especially in individuals who are obese and have
a Glucosidase inhibitors- Also known as “starch blockers”, these drugs work by slowing down the absorption of carbohydrate in the small intestine. Acarbose (Precose) and miglitol (Glyset) are the available drugs in this class. Taken with the first bite of each main meal, they are most effective in lowering post-prandial blood glucose. Effectiveness of these medications is measured by checking 2-hour postprandial glucose levels. Medications from this class are not effective against fasting hyperglycemia.
Thiazolidinediones- Sometimes referred to as “insulin sensitizers,” these agents include pioglitazone (Actos) and rosiglitazone (Avandia). They are most effective for people who have insulin resistance. They improve insulin sensitivity, transport, and utilization at target tissues. Because they do not increase insulin production, thiazolidinediones will not cause hypoglycemia when used alone, but the risk is still present when a thiazolidinedione is used in combination with a sulfonylurea or insulin. Patient taking these medications may experience a secondary benefit of improved lipid profiles and BP levels.
Other Drugs Affecting Blood Glucose Levels
Both the patient and the health care provider must be aware of drug interactions that can potentiate hypoglycemic and hyperglycemic effects. For example, B-adrenergic blockers can mask symptoms of hypoglycemia and prolong the hypoglycemic effects of insulin. Thiazide and loop diuretics can porentiate hyperclycemia by inducing potassium loss, although low-dose therapy with a thiazide is usually considered safe.
Is the cornerstone of care for the person with diabetes, it is alos the most challenging for many people. Achieving nutritional goals requires a coordinated team effort that takes into account the behavioral, cognitive, socioeconomic, cultural, and religious aspects of the person. A diabetes nurse educator and a registered dietitian, with expertise in diabetes management are recommended.
Recently issued guidelines from the ADA indicate that within the context of an overall healthy eating plan, a person with diabetes can eat the same foods as a person who does not have diabetes.
Type I Diabetes Mellitus
Meal planning should be based on the individual’s usual food intake and balanced with insulin and exercise patterns. The insulin regimen should be developed with the patients eating habits and activity pattern in mind. Pts. Using rapid-acting insulin can make adjustments in dosage before the meal based on the current of the meal. Intensified insulin therapy, such as multiple daily injections or the use of an insulin pump, allows considerable flexibility in food selection and can be adjusted for deviations from usual eating and exercise habits.
Type 2 Diabetes Mellitus
The emphasis for nutritional therapy in type 2 diabetes should be placed on achieving glucose, lipid, and blood pressure goals. Because 80-90% of people with type 2 diabetes are over weight, calorie reduction is a goal. A weight loss of 5% to 7% of body weight often improves glycemic control, even if desirable body weight is not achieved. Weight loss is best attempted by a moderate decrease in calories and an increase in caloric expenditure. Regular exercise and learning new behaviors and attitudes can help facilitate long-term lifestyle changes. Monitoring of blood glucose levels, A1C, lipids, and blood pressure provide feedback on how well the goals of nutritional therapy are being met.
The meal plan with diabetes does not prohibit the consumption of any one type of food. All food groups should be represented in a daily meal plan that is nutritionally balanced.
Protein- 15% to 20% of total daily calories.
Fat-less than 10% of daily calories from saturated fat. Cholesterol intake should be less than 300 mg/day.
Carbohydrate-should constitute the remaining percentage of calories after determining protein and fat needs. Carbohydrates should include whole grains, fresh veg. and fresh fruits. Overall intake of simple sugar should be limited as much as possible, it consumption is acceptable in moderate amounts when counted as part of total carbohydrate intake.
Sodium- intake should be less than 2400mg/day.
Fiber-approx. 25 to 30g/day from a variety of food sources.
Alcohol is high in calories, has no nutritive value, and promotes hypertriglyceridemia. In addition, it has detrimental effects on the liver. The inhibitor effect of alcohol on glucose production by the liver can cause severe hypoglycemia in patients on insulin or oral hypoglycemic medications that increase insulin secretion. It can have adverse effects when used in conjuction with certain meds. Moderate alcohol consumption can sometimes be safely incorporated into the meal plan if blood glucose levels are well controlled and if the patient is not on medications that will cause adverse side effects. A pt. can reduce the risk for alcohol-induced hypoglycemia by eating carbohydrates when drinking alcohol. One drink is approx. 135 cal. Should drink alcohol with food, use sugar-free mixes, and drink dry, light wines.
The dietician initially teaches the principles of the nutrition therapy prescription. Nurses should be prepared to work with dietitians as part of interdisciplinary diabetes care team. The food guide pyramid is an appropriate teaching tool for people with diabetes. It helps the patient to visualize the recommended amounts of foods that should be eaten from each group of a daily basis. Another method of meal planning is to use the plate method. This helps the patient visualize the amount of veg., starch, and meat that should fill a 9 inch plate. Diet teaching should include the patient’s family and significant others if poss. More effective directing teaching efforts to the person who will be cooking.
Regular, consistent exercise is considered an essential part of diabetes management. Exercise increases insulin sensitivity and can have a direct effect on lowering the blood glucose levels. It also contributes to weight loss, which also decreases insulin resistance. The therapeutic benefits of regular physical activity may result in a decreased need for diabetes medicines in order to reach target blood glucose goals. Regular exercise may also help reduce triglyceride and LDL cholesterol levels, reduce blood pressure, and improve circulation.
Pts who use insulin, sulfonylueas, or meglitinides are at increased risk for hypoglycemia when there is an increase in physical activity. The glucose-lowering effects of exercise can last up to 48 hours after the activity, so it is possible for hypoglycemia to occur for that long after the activity. It is recommended that patients who use medications that can cause hypoglycemia schedule exercise about 1 hour after a meal, or that they have a 10 to 15 g carbohydrate snack before exercising. Several small carb snack can be taken every 30 min during exercise to prevent hypoglycemia. Pts at risk should always carry a fast-acting source of carbs such as glucose tablets or hard candies, when exercising. Exercise is best done after meals, when the blood glucose level is rising, self monitor before, during and after to determine effect of exercise.
Monitoring Blood Glucose
Self-monitoring of blood glucose
SMBG is a cornerstone of diabetes management. It enables the pt to make self-management decisions regarding diet, exercise, and medications. It is also important for detecting episodic hyperglycemia and hypoglycemia. Disposable lancets are usually used to obtain a small drop of capillary blood that is placed onto a reagent strip. Newer systems allow the user to collect blood from alternative sites such as the forearm. Plasma or venous samples are 10to12% higher than whole blood (finger stick). The chief advantage of SMBG is that it supplies immediate information about blood glucose levels that can be used to make adjustments in food intake, activity patterns, and medication dosages. Pts with type I typically test 4 times per day (before meals and at bedtime).
Is used as a tx option for patients with type I diabetes mellitus who have end-stage renal disease and who have had or plan to have a kidney transplant. Kidney and pancreas transplants are often done together. If renal failure is not present, the ADA recommends that pancreas transplantation should only be considered for patients who exhibit the following three criteria:
A history of frequent, acute, and severe metabolic complications (hypoglycemia, hyperglycemia, ketoacidosis) requiring medical attention
Clinical and emotional problems with exogenous insulin therapy that are so severe as to be incapacitating
Consistent failure of insulin-based management to prevent acute complications
Successful pancreas transplantation can improve the quality of life of people with diabetes, primarily by eliminating the need for exogenous insulin, frequent daily blood glucose measurements and many of the dietary restrictions imposed by the disorder. Pts who undergo pancreas transplantation require immunosuppression to prevent rejection of the graft and potential recurrence of the autoimmune process that might again destroy pancreatic islet cells.