DIABETES MELLITUS Diabetes is a systemic disease characterized by hyperglycemia, hyperlipidemia, and hyperaminoacidemia. Diabetes alters the metabolism of all the energy nutrients (carbohydrates, fats and proteins) and affects most organ systems, often leading to specific problems with microcirculation, neuropathic disorders, and an increased predisposition to atherosclerosis. In that, Diabetes can contribute to or cause the development of blindness, kidney disease, heart disease, leg pains and ulcers (often requiring amputation), complications of pregnancy etc. The two major forms of diabetes are Type I (insulin dependent or juvenile onset) and Type II (non-insulin dependent or maturity onset). They share a central feature: elevated blood sugar levels due to absolute or relative insufficiencies of insulin and/or cellular resistance to the actions of insulin. Insulin is a key regulator of blood glucose levels. After a meal, food is digested in the stomach and intestines; carbohydrates are broken down in to glucose (and other sugars), and proteins are broken down into amino acids. Glucose and amino acids are absorbed directly into the bloodstream, and their blood concentration levels rise. Normally, this triggers release of insulin from the beta cells of the pancreas. Insulin, in turn, increases the permeability of cells (especially muscle cells) to glucose and amino acids, where there are burned for energy, converted into proteins, or stored for later use. Insulin also facilitates storage of excess glucose as glycogen in the liver and muscle for later use when food nutrients are not available. As blood glucose levels fall to pre-meal levels, the pancreas reduces its production of insulin and the body uses its stored energy until the next meal provides additional nutrition. Type I: Insulin Dependent Diabetes Mellitus (IDDM) In Type I diabetes, the beta cells are gradually destroyed; eventually insulin deficiency is absolute. Without insulin, blood glucose levels rise excessively and hyperglycemia ensues. Glucose levels eventually rise above the “threshold” levels of absorption capability by the kidneys and glucose is lost in the urine. Water moves with glucose, which leads to polyuria. Type I diabetes is associated with an abrupt onset of symptoms such as weakness, weight loss, excessive hunger and thirst as well as physiologic signs of low to absent levels of insulin in the blood, proneness to ketosis, and (injected) insulin dependence. Type I diabetes is believed to be a progressive autoimmune disease which leads to destruction of the insulin secreting beta cells of the pancreas. It is suggested that genetic predisposition coupled with environmental factors trigger the autoimmune reaction. In most cases, it is felt that by the time symptoms are evident enough to seek medical attention, 80-90% of the beta cells have been destroyed. Type I Diabetes involves about 10% of the diabetic population. Up to 80,000 people in the U.S. are estimated to have type I diabetes with about 30,000 new cases being diagnosed each year. It primarily affects younger (under 40, typically in childhood) and thinner patients, but may be seen at any age. Type II: Non-Insulin Dependent Diabetes Mellitus (NIDDM) Type II disease usually has a more gradual onset and is associated with inadequate production of insulin and/or a reduced sensitivity or responsiveness of cells to the presence of insulin. Most type II diabetics produce variable, even normal amounts of insulin, but they have abnormalities in liver and muscle cells that resist its actions. Insulin attaches to receptor sites, but glucose does not get in. Many type II diabetics can control their disease with diet modifications, or with medications that stimulate insulin secretion from the pancreas. The condition often worsens, however, and (injected) insulin support becomes necessary. Type II Diabetes is caused by a complex interplay of genes, environment, insulin abnormalities (reduced secretion and resistance of cells), increased glucose production in the liver, and increased fat breakdown. Type II Diabetes tends to be more prevalent in persons who are overweight, and incidence increases with age. Early symptoms may be present or diagnosis may occur with routine screening. Symptoms include excessive thirst, increased urination, fatigue, and blurred vision and weight loss. Because diagnosis may be delayed, complications from the disease may already be present (retinopathy, foot ulcers, renal disease etc). Inheritance plays a much stronger role in Type II Diabetes. Autoimmunity is not a factor. Environmental factors, particularly obesity and a high carbohydrate diet will precipitate the disease in those who are already predisposed. Type II diabetes involves about 90% of the diabetic population; mainly in adulthood (over 40) and in the obese, but may be seen in young patients. About 16 million Americans have Type II diabetes and about half are unaware they have it. Diagnosis / Testing for Diabetes: Current medical guidelines recommend that everyone over 45 be tested regularly for Diabetes and that younger adults be tested when risk factors are present such as: 20% overweight, hypertension, low HDL levels, high triglyceride levels, family history etc. Current methods of testing for Diabetes include: Fasting Plasma Glucose: A simple blood test taken after 8 hours of fasting. Normally, the upper limit of glucose concentrations in the blood when fasting is 115 mg/dl. Diabetes is diagnosed when fasting glucose levels are above 126 mg/dl. Oral Glucose Tolerance Test: This is the most sensitive test for Diabetes. The test begins with a Fasting Plasma Glucose test. A second blood test is then performed two hours after the client drinks a special glucose rich solution. Normally, blood glucose levels will rise after drinking the solution, but will decrease after two hours (after the body would normally “burn” or store the excess glucose). In the Diabetic, the initial increase is excessive and remains high, generally above 200 mg/dl. Emergency Conditions Associated with Diabetes: Hypoglycemia [Also known as Insulin shock]: Hypoglycemia can be caused by administration of too much insulin, not enough food intake, excessive exercise or alcohol consumption (alcohol affects the liver’s ability to release stored glycogen). Usually, the condition is manageable but occasionally becomes quite severe or even life threatening, especially if the symptoms are not recognized by the patient. Mild symptoms include sweating, trembling, hunger, and rapid heartbeat. Severely low blood sugar levels can lead to neurologic symptoms: confusion, weakness, disorientation, combativeness, and in rare and worst-case scenarios, coma, seizure and death. Patients that are prone to hypoglycemic events are encouraged to carry hard candy, juice or sugar packets with them. In case of a hypoglycemic event, 3-5 pieces of candy, 2-3 sugar packets, or ½ cup of fruit juice should be given. If there is inadequate response within 15 minutes, additional oral sugar should be given or immediate medical attention should be sought. Ketoacidosis: Diabetic ketoacidosis is a life-threatening complication caused by insulin depletion that results in excessive blood glucose concentration levels. With extreme hyperglycemia, fat breakdown accelerates and increases the production of fatty acids. Fatty acids are converted into ketones which are toxic at high levels. Ketoacidosis is almost always associated with Type I Diabetes and is generally thought to be rare in Type II where some insulin is still present, although it is not impossible for a Type II diabetic to develop ketoacidosis. In Type I patients, ketoacidosis is almost always caused by noncompliance with treatment and is usually preceded by stressful events, especially illness. It is not clear what causes total insulin depletion or triggers ketoacidosis in Type II diabetics. Risk of ketoacidosis is much higher in adolescents because they are less likely to be fully compliant with treatment parameters. Symptoms of ketoacidosis include nausea and vomiting. Breathing may be abnormally deep and rapid with frequent sighing, and heart rate may be rapid. If the condition persists, coma, and eventual death may occur. Clinical Considerations: It is very difficult (clinically, without lab tests) to differentiate between these two conditions (presenting symptoms are similar). As a general rule, if your client destabilizes, ALWAYS GIVE SUGAR in an attempt to reverse the situation. Why?? The client is more likely to be hypoglycemic than hyperglycemic, in which case, giving them sugar will help raise their blood glucose levels and reverse their symptoms. If their symptoms do not reverse or improve, then assume hyperglycemia/ketoacidosis and call 911.