Tri 7 Endocrinology #7725 Test 5 Summer 2000 Dr. Sanders 1 DIABETES (American diabetes association clinical practice recommendations 1998). This is relatively prominent. There is plenty of fund raising to “cure” the disease. 30-40% of people have DM and don’t know it. Our textbook is relatively current, but some tests are obsolete. Over the years there were a number of diagnostic schemes to detect DM. You either have it or you don’t. DM is common that chiropractors see – they will either have it or they will develop it. Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Note, hyperglycemia is not DM. Hyperglycemia: 1) there is a defect in insulin production 2) there is a problem in insulin action 3) both. CLASSIFICATION OF DIABETES MELLITUS AND OTHER CATEGORIES OF GLUCOSE REGULATION – the expert committee on the diagnosis and classification of diabetes mellitus. CLASSIFICATION OF DM: Type 1 – idiopathic. Type 2 – idiopathic. Other specific types (caused by an identifiable process). Gestational DM – idiopathic. The terms insulin-dependent DM and non-insulin-dependent DM and their acronyms, IDDM AND NIDDM, are eliminated. The terms type 1 and type 2 are retained, with Arabic numerals being used rather than roman numerals. TYPE 1: encompasses the vast majority of cases that are primarily due to pancreatic islet -cell destruction and that are prone to ketoacidosis. While most type 1 diabetes is characterized, in the majority of cases, by the presence of islet cell, GAD, IA-2, IA-3, (insulin autoantibodies) that identify the autoimmune process that leads to -cell destruction. In some subjects, no evidence of autoimmunity is present. These cases are classified as type 1 idiopathic, though we know the mechanisms, the cause is unknown. Had the label of insulin dependent, juvenile onset, and others. TYPE 2: includes the most prevalent (85-90%) form of diabetes, which results from insulin resistance with or without an insulin secretory defect. OTHER – these cause secondary forms of DM: Genetic defects of -cell function Diseases of the pancreas Drug/chemical induced Uncommon immune forms Genetic defects in insulin activity Endocrinopathies Infections Other genetic syndromes Tri 7 Endocrinology #7725 Test 5 Summer 2000 Dr. Sanders 2 GESTATIONAL DM – defined as any degree of glucose intolerance with onset or first recognition during pregnancy. This is not a case of a diabetic that becomes pregnant, it is a person that becomes pregnant and develops DM that may or may not resolve. GDM complicates ~4% of all pregnancies in the U.S., resulting in ~135,000 cases annually. The prevalence may range from 1-14% of pregnancies, depending on the population studied. Maternal complications related to GDM also include an increased rate of cesarean delivery and chronic hypertension. Although many patients diagnosed with GDM sill not develop diabetes later in life, others will be diagnosed many years postpartum as having type 1 diabetes, type 2 diabetes, IFG (intolerance of fasting glucose), or IGT (impaired glucose tolerance). IMPAIRED GLUCOSE TOLERANCE – the stage termed impaired glucose tolerance (IGT) has been retained. MALNUTRITION-RELATED DM – this class of DM is eliminated. While it appears that malnutrition may influence the expression of other types of diabetes, the evidence that diabetes can be directly caused by protein deficiency is not convincing. It is more likely a result of genetics that expressed itself through frank starvation. DIAGNOSTIC CRITERIA FOR DM (National Diabetes Data group 3/98). Three ways to diagnose diabetes are possible: 1. Symptoms (polyuria, polydipsia, polyphagia, etc) with casual plasma glucose >200. Casual is defined as any time of day without regard to time since last meal. 2. FBG >126 mg/dL; fasting is defined as no caloric intake for at least 8 hours. There are challenges to this diagnostic criteria. Though our text says 140, in the past six months it changed to 126. There are three types of glucose: normal (was 80-120), diagnostic (140), and the “in-betweeners”… what was discovered, was that people in the 126 to 139 range tended to develop complications. 3. An OGTT (oral glucose tolerance test) with the 2 hour post-load value >200mg/dL. This is a rare test anymore and you can not perform it on an ill patient. This is not reproducible, if over age 65 it doesn’t work. Symptoms and casual glucose >200mg/dL or FBG>126mg/dL or 2hr (OGTT)>200mg/dL. Each must be confirmed by repeat testing. FBG<110mg/dL = normal fasting glucose. FBG>110 and <126mg/dL = IFG FBG>126mg/dL = provisional diagnosis of diabetes. 2 hour post-load of glucose (2h PG)<140 = normal glucose tolerance 2 hour PG >140 AND <200 mg/Dl = IGT 2 hour PG>200 mg/dL = provisional diagnosis of diabetes (the diagnosis must be confirmed). HbAlc measurement is not currently recommended for diagnosis of diabetes. Tri 7 Endocrinology #7725 Test 5 Summer 2000 Dr. Sanders 3 THE DISEASE Several pathogenic processes are involved in the development of diabetes. DM is a multisystemic disease primarily affecting the nervous and vascular systems. This is where chiropractic comes in to help. These range from autoimmune destruction of the -cells of the pancreas with consequent insulin deficiency to abnormalities that result in resistance to insulin action. The basis of the abnormalities in carbohydrate, fat, and protein metabolism in diabetes is deficient action of insulin on target tissues. Deficient insulin action results from inadequate insulin secretion and/or diminished tissue responses to insulin at one or more points in the complex pathways of hormone action. Impairment of insulin secretion and defects in insulin action frequently coexist in the same patient, and it is often unclear which abnormality, if either alone, is the primary cause of the hyperglycemia. Symptoms of marked hyperglycemia include: polyuria, polydipsia, weight loss, polyphagia, blurred vision. As physicians, our responsibility is to find, recognize, and diagnose the process. COMPLICATIONS Acute metabolic – the patient will die without treatment. This is what the diabetic works to prevent on a daily basis. Hypoglycemia – the most frequent; 10-25% of patients, more common in type 1. Ketoacidosis – most often in recognized diabetics; hyperglycemia, acidosis, osmotic diuresis, abdominal pain, anorexia, nausea. This is a killer. Nonketotic hyperosmolar syndrome - >320mOsm/L, >600mg/dL, dehydration; caused by lack of fluid intake. This is also a killer. Chronic - common denominator is nerves and vessels. Retinopathy – diabetes is the leading cause of blindness in persons aged 3 years. Blindness occurs 20 times more frequently in diabetic patients than in others. Is most often seen after the disease has been manifest for at least 15 years. Approximately 10-15% of type 1 diabetic patients become legally blind whereas in type 2 diabetic patients the risk is approximately half that value. The primary cause of visual loss is retinopathy. Regardless of the type of diabetes, the severity of retinopathy increases with increasing duration of the disease. The earliest retinopathic changes are classified as nonproliferative retinopathy. These lesions generally do not affect visual acuity. Proliferative retinopathy is characterized by the growth of fine … new blood vessels and fibrous tissue from the inner retinal surface … optic nerve head. Prevalence rates of both non-proliferative and proliferative retinopathy are higher in type 1 than in type 2 diabetes. Nephropathy – end stage renal disease (ESRD) from diabetic nephropathy is a major cause of death, particularly in type 1 diabetes, in which it affects 30-35% of patients. Diabetes is the leading cause and accounts for one third of the ESRD cases in the united states. In patients destined to develop ESRD, gross proteinuria (greater than 0.3 gram of albumin per day) begins approximately 15 years after the diagnosis of diabetes. Neuropathy – symptomatic, potentially disabling neuropathy affects nearly 50% of diabetic patients. It may be symmetrical or focal and often involves the autonomic nervous system as well. The prevalence of symmetrical neuropathy is similar in type 1 and 2 diabetes, whereas focal neuropathy is most common in older type 2 diabetes. Tri 7 Endocrinology #7725 Test 5 Summer 2000 Dr. Sanders 4 Distal sensorimotor neuropathy – this syndrome, characterized by axonal loss, is the most common presentation of diabetic neuropathy. The process involves all somatic nerves but has a distinct … predilection for distal sites, i.e. the distal sensorimotor nerves of the feet and hands. Patients complain of numbness and tingling in the extremities, especially the feet. Diabetic foot – the syndrome is characterized by plantar ulcers that heal slowly and follow apparently insignificant trauma. In severe cases, gangrene may be a complication and amputation the outcome. Diabetes accounts for about one half of non-traumatic limb amputations. Atherocsclerosis – involving the arteries of the heart, lower extremities, and brain is the major cause of death from diabetes. The atherosclerotic process is indistinguishable from that affecting the non-diabetic population but begins earlier and is more severe. The predilection of atherosclerosis is uniformly observed over the entire spectrum of diabetes – from difficult-to-control insulin dependent patients to patients with mild hyperglycemia requiring insulin. The risk of MI is 2 to 3 fold greater in diabetes. Hypertension. TREATMENT GOALS Short term A. Restore metabolic control to as close to normal as possible. B. Improve sense of well-being. Long term - Minimize risk of diabetic complications: accelerated atherosclerosis, microangiopathy (retinopathy, nephropathy), neuropathy. LIFESTYLE MODIFICATIONS FOR THE PATIENT WITH DIABETES Diet 1. Weight reduction (when appropriate). This increases the receptor density as the cell size reduces. 2. Carbohydrates: 45-60% (depending on severity of diabetes and triglyceride). 3. Restriction of saturated fat (to < 10% of calories). 4. Increased monounsaturated fat (depending on the need to limit carbohydrate. 5. Decreased cholesterol intake to <300 mg per day. 6. Sodium restriction in patients prone to HTN. Exercise 1. Type: aerobic strongly preferred. Avoid heavy lifting, straining, and Valsalva maneuvers that raise BP. 2. Intensity: increase pulse rate to at least 120-140, depending on the age and cardiovascular state of the patient. 3. Frequency: 3-4 days per week. 4. Duration: 20-30 minutes preceded and followed by stretching and flexibility exercises for 5-10 minutes.