MNT_1_Module_7._NT_in_MD_DM(2).pdf

Medical Nutrition Therapy 1 Module 7: Nutrition Therapy in Metabolic Disorders: Diabetes Mellitus Learning Outcomes: Upon completion of this module, you will be able to: Describe diabetes mellitus and identify the types...

Medical Nutrition Therapy 1 Module 7: Nutrition Therapy in Metabolic Disorders: Diabetes Mellitus Learning Outcomes: Upon completion of this module, you will be able to: Describe diabetes mellitus and identify the types Describe the symptoms of diabetes mellitus Explain the relationship of insulin to diabetes mellitus Discuss appropriate nutritional management of diabetes mellitus. Discuss the complications of diabetes mellitus and its dietary management Demonstrate ability to plan menus. Learning Guide Teaching Learning Activities (TLA) Resources 1. Read Module 7: Nutrition  Module 7: Nutrition Therapy in Therapy in Metabolic Disorder: Metabolic Disorder: Diabetes Diabetes Mellitus Mellitus  Self-Assessment Questions 2. Answer: Self-Assessment Questions  Self-Assessment Questions 3. Compare to SAQs answer key Answer Key 4. Answer Online Quiz  Quiz 5. Perform Task Activity 7-1: Case  Case Study: “Managing Type 2 Study “Managing Type 2 Diabetes” Diabetes”  Reference books  Computer or laptop, internet 1|Page Introduction Hundreds of years ago, a Greek physician named it diabetes, which means “to flow through,” because of the large amounts of urine generated by victims. Later, the Latin word mellitus, which means “honeyed,” was added because of the amount of glucose in the urine. Diabetes mellitus is a group of diseases characterized by high blood glucose concentrations resulting from defects in insulin secretion, insulin action, or both. Abnormalities in the metabolism of carbohydrate, protein, and fat are also present. Persons with diabetes have bodies that do not produce or respond to insulin, a hormone produced by the β-cells of the pancreas that is necessary for the use or storage of body fuels. Without effective insulin, hyperglycemia (elevated blood glucose) occurs, which can lead to serious complications and premature death; but, people with diabetes can take steps to control the disease and lower the risk of complications. Assigning a type of diabetes to an individual often depends on the circumstances present at the time of diagnosis, and many individuals do not easily fit into a single category. Thus it is less important to label the particular type of diabetes than it is to understand the pathogenesis of the hyperglycemia and to treat it effectively (ADA, 2006). What is clear, however, is the need to intervene early with lifestyle interventions, beginning with prediabetes and continuing through the disease process. In 1997 recommendations were made to eliminate the terms insulin-dependent diabetes mellitus (IDDM) and noninsulin dependent diabetes mellitus NIDDM) and to keep the terms type 1 and type 2 diabetes and to use Arabic rather than Roman numerals. Key Terms  Dawn phenomenon a natural increase in morning blood glucose levels and insulin requirements that occurs in people with and without diabetes but tends to be more marked in people with diabetes; possibly caused by a diurnal variation in growth hormone, cortisol, or catecholamines.  Diabetic ketoacidosis (DKA) severe, uncontrolled diabetes resulting from insufficient insulin, in which ketone bodies (acids) build up in the blood; if left untreated (with immediate administration of insulin and fluids), DKA can lead to coma and even death  Endogenous insulin an insulin produced within the body  Exogenous insulin an insulin produced outside the body  Gestational diabetes mellitus (GDM) glucose intolerance, the onset or first recognition of which occurs during pregnancy  Gluconeogenesis is the making of glucose from a noncarbohydrate source.  Glycemic index (GI) a measurement of the relative area under the postprandial glucose curve of 50 g of digestible carbohydrates compared with 50 g of a standard food, either glucose or white bread  Honeymoon phase the period after the initial diagnosis of type 1 diabetes when there may be some recovery of B-cell function and a temporary decrease in exogenous insulin requirement. 2|Page   Hyperglycemia excessive glucose in the blood (generally 180 mg/dl or above) caused by too little insulin, insulin resistance, or increased food intake; symptoms include frequent urination, increased thirst, weight loss, and often tiredness or fatigue  Hypoglycemia (or insulin reaction) low blood glucose level (70 mg/dl or less) caused by the administration of excessive insulin or insulin secretagogues too little food, delayed or missed meals or snacks, increased exercise or other physical activity, or alcohol intake without food.  Insulin a hormone released from the β-cells of the pancreas that enables cells to metabolize and stores glucose and other fuels.  Polydipsia excessive thirst  Polyuria excessive urination  Pre-diabetes (impaired glucose homeostasis) blood glucose concentrations that are higher than normal but not yet high enough to be diagnosed as diabetes, sometimes referred to as impaired glucose tolerance (IGT) or impaired fasting glucose (IFG); risk factor for future diabetes and cardiovascular disease.  Type I diabetes a type of diabetes that usually occurs in persons younger than 30 years of age but can occur at any age; previously known as insulin-dependent diabetes mellitus (IDDM) or juvenile-onset diabetes.  Type 2 diabetes a type of diabetes usually occurring in persons older than 30 years of age, previously known as noninsulin-dependent diabetes mellitus (NIDDM) or maturity onset diabetes; now also frequently diagnosed in youth and Young adults. Endocrine System The endocrine system is the collection of glands that produce hormones that regulate metabolism, growth and development, tissue function, sexual function, reproduction, sleep, and mood, among other things. The endocrine system is made up of the pituitary gland, thyroid gland, parathyroid glands, adrenal glands, pancreas, ovaries (in females) and testicles (in males). The word endocrine derives from the Greek words "endo," meaning within, and "crinis," meaning to secrete. The endocrine system affects almost every organ and cell in the body. Hormone levels that are too high or too low indicate a problem with the endocrine system. Hormone diseases also occur if your body does not respond to hormones in the appropriate ways. Stress, infection and changes in the blood's fluid and electrolyte balance can also influence hormone levels. The most common endocrine diseases are: Diabetes and Hypothyroidism. 3|Page  Figure 7-1 Endocrine System Diabetes Mellitus Diabetes Mellitus is the name for a group of serious and chronic disorders affecting the metabolism of carbohydrates. Characterized by elevated blood glucose concentrations and disordered insulin metabolism Etiology: The etiology (cause) of diabetes is not confirmed. Although it appears that diabetes may be genetic, environmental factors also may contribute to its occurrence. For example, viruses or obesity may precipitate the disease in people who have a genetic predisposition. The World Health Organization indicates that the prevalence of the disease is increasing worldwide, especially in areas showing improvement in living standards. 4|Page Classification and pathophysiology Pre-diabetes. Fasting or glucose tolerance test results above normal, but not diagnostic of diabetes. These persons should be monitored closely because they have an increased risk of developing diabetes. The amount of glucose in the blood normally rises after a meal. The pancreas reacts by providing insulin. As the insulin circulates in the blood, it binds to special insulin receptors on cell surfaces. This binding causes the cells to accept the glucose. The resulting reduced amount of glucose in the blood in turn signals the pancreas to stop sending insulin. Pre-diabetes is a stage of impaired glucose homeostasis that includes IFG and GT is called pre-diabetes. People with pre-diabetes have impaired fasting glucose (IFG), impaired glucose tolerance (IGT), or both. Individuals with pre-diabetes are at high risk for future diabetes and CVD. Type 1 Diabetes Mellitus (Insulin Dependent Diabetes Mellitus IDDM) – β-cell destruction, a disorder in which the body cannot produce enough insulin, typically appears at a young age. Insulin injection is required. – Usually develop during childhood or adolescence, and symptoms may appear abruptly in previously healthy children. – Classic symptoms are polyuria, polydipsia, weight loss, and weakness or fatigue. – Ketoacidosis – acidosis due to excessive production of ketone bodies – is sometimes the first sign of disease. Type 1 diabetes, formerly known as insulin-dependent diabetes mellitus or juvenile diabetes, is characterized by the absence of insulin. It occurs from an autoimmune response that damages or destroys pancreatic beta cells, leaving them unable to produce insulin. Interaction between genetic susceptibility and environmental factors, such as viral infection, is thought to be responsible for type 1 diabetes (Fowler, 2010). The genetic predisposition to type 1 diabetes is the result of the combination of HLA-DQ coded genes for disease susceptibility offset by genes that are related to disease resistance (ADA, 2006). However, the genetic factors that confer susceptibility or protection remain unclear. Type 1 diabetes has two forms: immune-mediated diabetes mellitus and idiopathic diabetes mellitus. Immunemediated diabetes mellitus results from an autoimmune destruction of the β-cells of the pancreas, the only cells in the body that make the hormone insulin that regulates blood glucose. Idiopathic type I diabetes mellitus refers to forms of the disease that have no known etiology. Although only a minority of persons with type I diabetes fall into this category of those who do, most are of African or Asian origin (ADA, 2006). There is no known way to prevent type 1 diabetes. All people with type 1 diabetes require exogenous insulin for survival. Although type 1 diabetes can occur at any age, it is most often detected in children and adolescents. The classic symptoms of polyuria, polydipsia, and polyphagia appear abruptly. Sometimes, the first sign of the disease is ketoacidosis. Type 1 diabetes accounts for 5% to 10% of all diagnosed diabetes cases. 5|Page Type II Diabetes Mellitus (Non-Insulin Dependent Diabetes Mellitus NIDDM). A progressive disorder in which body cells become less responsive to insulin, not enough insulin is produced. – This condition tends to occur as a consequence of obesity to respond to insulin. – Genetics – Poor eating habits, sedentary lifestyles, increased obesity, aging population. – 45-years of age develop Type 2 diabetes, previously referred to as non–insulin-dependent diabetes or adult-onset diabetes, can occur at any age and accounts for 90% to 95% of diagnosed cases of diabetes. Unlike type 1 diabetes, in which there is a relatively abrupt and absolute end to insulin production, type 2 diabetes is a slowly progressive disease characterized by a combination of insulin resistance and relative insulin deficiency (Fowler, 2010). When cells do not respond to insulin as they should, the pancreas compensates by secreting higher than normal levels of insulin. This period of impaired glucose tolerance/impaired fasting glucose is known as prediabetes: glucose levels are normal or slightly elevated to levels below the criteria for diabetes and insulin levels are increased. Over time, chronic hyperinsulinemia leads to a decrease in the number of insulin receptors on the cells and a further reduction in tissue sensitivity to insulin. Insulin production progressively falls to a deficient level, and frank type 2 diabetes develops. Because hyperglycemia develops gradually in type 2 diabetes and is often not severe enough for patients to recognize any of the classic diabetes symptoms, type 2 diabetes may go undiagnosed for years. Many patients will have already developed complications by the time of diagnosis (Ahmad and Crandall, 2010). Risk factors for type 2 diabetes appear is Figure 7-2. Overweight and obesity are strongly correlated with the development of type 2 diabetes and may be responsible for the growing epidemic (Fowler, 2010). Other risks are increasing age, lack of physical activity, and race/ ethnicity. Abdominal obesity, abnormal serum lipid levels (low high- density lipoprotein cholesterol and/or high triglycerides), and hypertension are additional risks that are shared with the risk of cardiovascular disease. Figure 7-2 Risk Factors for Type 2 Diabetes 6|Page Gestational Diabetes Mellitus (GDM) Gestational diabetes mellitus (GDM) is hyperglycemia that develops during pregnancy, usually around the 24th week of gestation. Women who meet the standard criteria for diabetes at their first prenatal visit are diagnosed with overt diabetes, not GDM. Diabetes increases risks in mother and infant. It increases the risk of preeclampsia, caesarean delivery, and fetal macrosomia and also the risk of hypertension and diabetes after pregnancy (Catalano, Huston, Amini, and Kalhan, 1999). Some studies show that as many as 70% of women who develop GDM will develop type 2 diabetes within 10 years after delivery (Fowler, 2010). GDM increases the risk of newborn death, stillbirth, and infant hypoglycemia in the days after delivery. Occurs among pregnant with multiple pregnancies; – gave birth to > 8 –lbs. baby – increased BMI prior to pregnancy Table 7-1. Effect of Insulin Insufficiency on Nutrient Insulin normally promotes nutrient uptake after meals, as well as the synthesis of glycogen, triglycerides, and protein in liver, adipose, and muscle tissue. A defect in insulin metabolism inhibits these processes, leading to the effects shown in this table. Nutrient Effects of Insulin Insufficiency Carbohydrate  Decrease glucose uptake by muscle and adipose cells.  Decrease glycogen synthesis in the liver and muscle  Increased glycogen breakdown in the liver and muscle  Increased gluconeogenesis in the liver  Hyperglycemia Fat  Decreased triglyceride synthesis in adipose tissue.  Increased triglyceride breakdown in adipose tissue.  Increased fatty acid and triglyceride levels in the blood.  Increased production of ketone bodies in the liver. Protein  Decreased amino acid uptake by muscle cells.  Decreased synthesis of tissue protein.  Increased breakdown of tissue protein.  Muscle wasting and growth retardation Symptoms: Biochemical  Glycosuria. Presence of sugar in the urine; occurs when renal threshold for sugar is reached  Hyperglycemia. Elevated blood glucose level due to absolute or relative lack of insulin.  Ketosis or Acidosis. Accumulation of ketone bodies (intermediate products of fatty acid oxidation) due to rapid oxidation of fatty acids when the cells cannot utilize glucose effectively as a source of energy.  Ketonuria. Presence of ketone bodies in urine. 7|Page Clinical  Polyuria excessive urination, abnormally large volume of urine when the kidneys have to draw off liquid from the blood passing through it to dissolve the excess glucose that has to be excreted.  Polydipsia increased thirst, a response to the excessive loss of water through the urine.  Polyphagia increased appetite, resulting from the failure of the cells to utilize nutrients properly.  Dehydration. due to excessive urinary output which us not balanced by water intake.  Weight loss. Despite eating more than usual to relieve hunger, glucose does not enter the cell due to insulin resistance. The body uses alternative fuels stored in muscle and fat.  Blurred vision. if your blood sugar is too high, fluid may be pulled from the lenses of your eyes. This may affect the ability to focus.  Slow-healing sores or frequent infections. Due to decrease protein utilization.  Areas of darkened skin. Some people with type 2 diabetes have patches of dark velvety skin in the folds and creases of their bodies – usually in the armpits and neck. This condition, called acanthosisnigricans, may be a sign of insulin resistance.  Susceptibility to infections. Immune system is affected. Diagnosis of Diabetes 1. Random Blood glucose sample (one taken without regard to food intake) that exceeds 200 mg per 100 ml in a person with symptoms of diabetes. 2. Fasting Blood Sugar Test (FBS) (defined as no caloric intake for at least 8 hrs.) A blood glucose of 126 mg/100ml or greater. 3. Glucose tolerance test- is a measure of the ability of the patient to utilize a specific amount of glucose. It is used to establish a diagnosis of diabetes or impaired glucose tolerance in asymptomatic individuals whose FBS is between 100 and 125 ng/dL of plasma. 4. Glycosylated hemoglobin (HbA1C) – test provides a good index for monitoring overall diabetes control and therapeutic decisions can be based on this value. 5. Self-Monitoring Blood Glucose (SMBG)- allows persons who have diabetes to measure their blood glucose levels at home. 6. Urine Examination – is useful in testing the total volume, specific gravity, glucose and fatty acids. 8|Page  Table 7-2 Diagnostic Criteria for DM TEST DIAGNOSTIC HEALTHY GLYCEMIC TARGET CRITERIA TARGET (Recommended goal to reduce risk of long-term complications) ADA1 AACE2 IDF3 Hba1c (%) >6.5%