Medical Concepts

  NON PHARMACOLOGICAL THERAPY  MNT Glycemic Index Dietary supplements Weight measurements Physical Activity Psychological assessment Immunizations 2.GLYCEMIC INDEX " The Glycemic index of a carbohydrate containing food is determined by comparing the glucose excursions after consuming 30g of test food with glucose excursions after consuming 50g of reference food (white bread) " Glycemic Index= Blood glucose area under the curve (3hr) for test food / Blood glucose area under the curve (3hr) for reference food Low glycemic index foods have value of 53 or less and include many fruits, vegetables, grainy breads, legumes, etc. High glycemic index foods have value of 70 or greater and include baked potatoes, white bread, etc. 3.DIETARY SUPPLEMENTS Patients may seek and use dietary supplements in the treatment of diabetes.  Remember, despite the popular notion, there is no "diabetes specific diet". Data from randomized controlled trials seem to support the efficacy of Coc

 NON PHARMACOLOGICAL THERAPY  MNT Glycemic Index Dietary supplements Weight measurements Physical Activity Psychological assessment Immunizations 1. MEDICAL NUTRITION THERAPY (MNT)  " Medical Nutrition Therapy (MNT) is a term used by the ADA to describe the optimal condition of caloric intake with other aspects of diabetes therapy (Insulin, Exercise, Weight loss)". The ADA has issued recommendations for three types of MNT: Primary prevention measures of MNT are directed at preventing or delaying the onset of type 2 Diabetes in high-risk individuals (obese or with pre-diabetes) by promoting weight reduction. Secondary prevention measures of MNT are directed at preventing or delaying-related complications in diabetic individuals by improving glycemic control. Tertiary prevention measures of MNT are directed at managing diabetes-related complications (cardiovascular disease, neuropathy) in diabetic individuals. Despite the popular notion, there is not any " Diabetic diet

  GOAL OF THERPY The goals of treatment of DM includes; Reducing, controlling and managing long-term microvascular, macrovascular and neuropaathic complications. Preserving beta cell function. Preventing acute complications from increased Blood glucosel level. Minimizing hypoglycemic episodes. Maintaining patient quality of life. --Two landmark trials, THE DIABETES CONTROL AND COMPLICATION TRIAL (DCCT) and THE UNITED KINGDOM PROSPECTIVE DIABETES STUDY(UKPDS), showed that lowering blood glucose levels decreased the risk of developing chronic complications. --A near normal blood glucose level can be achieved with appropriate patient education , lifestyle modification and medications . --Proper care of DM requires goal setting and assessment for glycemic control , self-monitoring of blood glucose (SMBG) monitoring of blood glucose pressure , and lipid levels , regular monitoring for the development of complications , dietary and exercise lifestyle modifications and proper medication us

 CLINICAL PRESENTATION AND DIAGNOSIS OF DM 2. SCREENING American Diabetes Association (ADA) recommends routine screening for T2 DM every 3 years in all adults starting at 45 years of age. Testing of T2 DM should be considered in any adult, regardless of their age, who have a BMI greater than or equal to 25kg/m2. The ADA does not currently recommend widespread screening for T1 DM because of the relatively low incidence in the general population, although measurement of Islet antibodies may be appropriate for high-risk individuals. 3.GESTATIONAL DIABETES: "Gestational diabetes is the glucose intolerance in women during pregnancy". All pregnant women who have risk factors for T2 DM should be screened for undiagnosed T2 DM at their first prenatal visit using standard diagnostic criteria.  Any women found to have diabetes in the early point at pregnancy is considered to have T2 DM or GDM. All other pregnant women, not currently known to have DM should be screened for GDM with a 75

  METABOLIC SYNDROME AND INCRETIN EFFECT METABOLIC SYNDROME: "Insulin resistance has been associated with a number of other cardiovascular risks , including Abdominal obesity , Hypertension , Dyslipidemia , Hypercoagulation , and Hyperinsulinemia . The clustering of these risk factors has been termed as Metabolic syndrome." The most widely used criteria to define metabolic syndrome were established by the National Cholesterol Education Program Adult Treatment Panel III Guidelines . INCRETIN EFFECT Incretins: are a group pf metabolic hormone that stimulate a decrease in blood Glucose levels. Incretin hormones are: GLP-1, GIP. Incretins are gut hormones that are secreted from entero-endocrine cells into blood within minutes after eating (present in GIT, Stomach, and Pancreas). A great deal of research is occurring today to develop compounds that enhance the incretin effect, either by mimicking its action or y enabling incretin hormones, to remain physiologically active for lon

 PATHOPHYSIOLOGY OF DM IMPAIRED INSULIN SECRETION A pancreas with normal Beta cell function is able to adjust insulin production to maintain normal blood glucose levels. Hyperinsulinemia or high blood levels of insulin is an early finding of T2 DM. More insulin is secreted to maintain normal blood glucose levels until eventually the pancreas can no longer produce sufficient insulin. Impaired Beta cell function results in reduced ability to produce a first-phase insulin response sufficient to signal the liver to stop producing glucose after a meal. As DM progresses, large numbers of patients with T2DM eventually loses all beta cell function and require exogenous insulin to maintain the blood glucose levels.  INSULIN RESISTANCE Insulin resistance is the primary factor that differentiates T2DM from other forms of diabetes. Insulin resistance maybe present for several years prior to the diagnosis of DM. Insulin resistance occurs more significantly in skeletal muscles and liver. Insulin res

GENERAL MECHANISM OF ACTION OF INSULIN AND RELATE HORMONES The body's main fuel is Glucose. Glucose is stored in the liver and muscles as Glycogen.  Excess glucose is stored in the adipose tissues which yield fatty acids via lipolysis. In the fasting state, free fatty acids supply much of the energy needs of the body except for the CNS which requires Glucose to function normally. Proteins can also be converted to glucose via gluconeogenesis. RELEASE OF INSULIN AND GLUCAGON Insulin and Glucagon are produced in the pancreas by the Islets of Langerhans . Beta cells   make up 70%-90% of the Islets and produce Insulin and Amylin while the a-cells   produce glucagon. The main function of insulin is to decrease blood glucose levels. Glucagon, along with other counter-regulatory hormones such as growth factor, cortisol, and Epinephrine, increases Blood glucose levels.  The opposing actions of Glucagon and Insulin along with other counter-regulatory hormones maintain a normal fasting value

TYPES OF DIABETES MELLITUS 1. TYPE1 DM Type 1 DM is usually diagnosed before age 30 years, but it can develop at any age. T1DM is an autoimmune disease in which insulin producing B-cells are destroyed. The presence of Human Leucocyte Antigens (HLAs ) is associated with the development of T1DM. In addition, these individuals often develop Islet cell antibodies , Insulin Autoantibodies or Glutamic Acid decarboxylase autoantibodies . At the time of development of diagnosis of T1DM, it is usually believed that most of the patients have 80-90%loss of beta cells. The remaining beta cells function at the diagnosis creates a " HONEYMOON PERIOD" during which the blood glucose levels are easier to control, and smaller amounts of insulin are required. after this, the remaining beta cells function is completely lost, and the patients become completely deficient of insulin and hence require exogenous insulin.  2. TYPE1.5 DM:  Also referred as Latent autoimmune diabetes in Adults (LAD)

 DIABETES MELLITIS Definition: Diabetes Mellitus (DM) describes a group pf chronic metabolic  disorders characterized by hyperglycemia that may result in long-term microvascular, macrovascular and neuropathic complications. these complications contribute to diabetes being the leading cause of: a) new cases of blindness among adults b) end stage renal diseases c)non-traumatic lower limb amputations Etiology: The increasing prevalence is caused by three influences: 1. ethnicity        2. Lifestyle       3. Age Types: a) Type 1 DM b) Type 2 DM c) Type 1.5DM d) Gestational Diabetes Mellitus (GDM) ** In type 1 DM; the body fails to make insulin. In type 2 DM; body either develops resistance to insulin or not enough insulin is produced to lower the Blood glucose levels** Epidemiology The worldwide prevalence of DM has risen over past two decades with an estimation of 30 million cases in 1985 to 177 million cases in 2000. Based on current trends, >30million individuals will have diabetes b