Diabetes Diabetes is a chronic (lifelong) disease marked by high levels of sugar in the blood.

Causes Insulin is a hormone produced by the pancreas to control blood sugar. Diabetes can be caused by too little insulin, resistance to insulin, or both. To understand diabetes, it is important to first understand the normal process by which food is broken down and used by the body for energy. Several things happen when food is digested: y y A sugar called glucose enters the bloodstream. Glucose is a source of fuel for the body. An organ called the pancreas makes insulin. The role of insulin is to move glucose from the bloodstream into muscle, fat, and liver cells, where it can be used as fuel.

People with diabetes have high blood sugar. This is because: y y y Their pancreas does not make enough insulin Their muscle, fat, and liver cells do not respond to insulin normally Both of the above

There are three major types of diabetes: y Type 1 diabetes is usually diagnosed in childhood. Many patients are diagnosed when they are older than age 20. In this disease, the body makes little or no insulin. Daily injections of insulin are needed. The exact cause is unknown. Genetics, viruses, and autoimmune problems may play a role. Type 2 diabetes is far more common than type 1. It makes up most of diabetes cases. It usually occurs in adulthood, but young people are increasingly being diagnosed with this disease. The pancreas does not make enough insulin to keep blood glucose levels normal, often because the body does not respond well to insulin. Many people with type 2 diabetes do not know they have it, although it is a serious condition. Type 2 diabetes is becoming more common due to increasing obesity and failure to exercise. Gestational diabetes is high blood glucose that develops at any time during pregnancy in a woman who does not have diabetes. Women who have gestational diabetes are at high risk of type 2 diabetes and cardiovascular disease later in life.

Diabetes affects more than 20 million Americans. Over 40 million Americans have pre-diabetes (early type 2 diabetes). There are many risk factors for type 2 diabetes, including: y y y y y y y y y y Age over 45 years A parent, brother, or sister with diabetes Gestational diabetes or delivering a baby weighing more than 9 pounds Heart disease High blood cholesterol level Obesity Not getting enough exercise Polycystic ovary disease (in women) Previous impaired glucose tolerance Some ethnic groups (particularly African Americans, Native Americans, Asians, Pacific Islanders, and Hispanic Americans)

Symptoms High blood levels of glucose can cause several problems, including: y y y y y y Blurry vision Excessive thirst Fatigue Frequent urination Hunger Weight loss

However, because type 2 diabetes develops slowly, some people with high blood sugar experience no symptoms at all. Symptoms of type 1 diabetes: y y y y y y Fatigue Increased thirst Increased urination Nausea Vomiting Weight loss in spite of increased appetite

Patients with type 1 diabetes usually develop symptoms over a short period of time. The condition is often diagnosed in an emergency setting. Symptoms of type 2 diabetes: y y y y y Blurred vision Fatigue Increased appetite Increased thirst Increased urination

Exams and Tests A urine analysis may be used to look for glucose and ketones from the breakdown of fat. However, a urine test alone does not diagnose diabetes. The following blood tests are used to diagnose diabetes: y Fasting blood glucose level -- diabetes is diagnosed if higher than 126 mg/dL on two occasions. Levels between 100 and 126 mg/dL are referred to as impaired fasting glucose or prediabetes. These levels are considered to be risk factors for type 2 diabetes and its complications. Hemoglobin A1c test -- this test has been used in the past to help patients monitor how well they are controlling their blood glucose levels. In 2010, the American Diabetes Association recommended that the test be used as another option for diagnosing diabetes and identifying pre-diabetes. Levels indicate: o Normal: Less than 5.7% o Pre-diabetes: Between 5.7% - 6.4% o Diabetes: 6.5% or higher Oral glucose tolerance test -- diabetes is diagnosed if glucose level is higher than 200 mg/dL after 2 hours. (This test is used more for type 2 diabetes.)

Random (non-fasting) blood glucose level -- diabetes is suspected if higher than 200 mg/dL and accompanied by the classic diabetes symptoms of increased thirst, urination, and fatigue. (This test must be confirmed with a fasting blood glucose test.)

Persons with diabetes need to have their hemoglobin A1c (HbA1c) level checked every 3 - 6 months. The HbA1c is a measure of average blood glucose during the previous 2 - 3 months. It is a very helpful way to determine how well treatment is working. Have your cholesterol and triglyceride levels checked each year (aim for LDL levels below 100 mg/dL). Treatment The immediate goals are to treat diabetic ketoacidosis and high blood glucose levels. Because type 1 diabetes can start suddenly and have severe symptoms, people who are newly diagnosed may need to go to the hospital. The long-term goals of treatment are to: y y y Prolong life Reduce symptoms Prevent diabetes-related complications such as blindness, heart disease, kidney failure, and amputation of limbs

These goals are accomplished through: y y y y y y y Blood pressure and cholesterol control Careful self testing of blood glucose levels Education Exercise Foot care Meal planning and weight control Medication or insulin use

There is no cure for diabetes. Treatment involves medicines, diet, and exercise to control blood sugar and prevent symptoms. LEARN THESE SKILLS Basic diabetes management skills will help prevent the need for emergency care. These skills include: y y y y y y y y How to recognize and treat low blood sugar (hypoglycemia) and high blood sugar (hyperglycemia) What to eat and when How to take insulin or oral medication How to test and record blood glucose How to test urine for ketones (type 1 diabetes only) How to adjust insulin or food intake when changing exercise and eating habits How to handle sick days Where to buy diabetes supplies and how to store them

After you learn the basics of diabetes care, learn how the disease can cause long-term health problems and the best ways to prevent these problems. Review and update your knowledge, because new research and improved ways to treat diabetes are constantly being developed.

SELF-TESTING If you have diabetes, your doctor may tell you to regularly check your blood sugar levels at home. There are a number of devices available, and they use only a drop of blood. Self-monitoring tells you how well diet, medication, and exercise are working together to control your diabetes. It can help your doctor prevent complications. The American Diabetes Association recommends keeping blood sugar levels in a range based on your age. Discuss these goals with your doctor and diabetes educator. Before meals: y y y y 70 - 130 mg/dL for adults 100 - 180 mg/dL for children under age 6 90 - 180 mg/dL for children 6 - 12 years old 90 - 130 mg/dL for children 13 - 19 years old

At bedtime: y y y y Less than 180 mg/dL for adults 110 - 200 mg/dL for children under age 6 100 - 180 mg/dL for children 6 - 12 years old 90 - 150 mg/dL for children 13 - 19 years old

WHAT TO EAT You should work closely with your health care provider to learn how much fat, protein, and carbohydrates you need in your diet. A registered dietician can help you plan your dietary needs. People with type 1 diabetes should eat at about the same times each day and try to be consistent with the types of food they choose. This helps to prevent blood sugar from becoming extremely high or low. People with type 2 diabetes should follow a well-balanced and low-fat diet. See: Diabetes diet HOW TO TAKE MEDICATION Medications to treat diabetes include insulin and glucose-lowering pills called oral hypoglycemic drugs. People with type 1 diabetes cannot make their own insulin. They need daily insulin injections. Insulin does not come in pill form. Injections are generally needed one to four times per day. Some people use an insulin pump. It is worn at all times and delivers a steady flow of insulin throughout the day. Other people may use inhaled insulin. See also: Type 1 diabetes Unlike type 1 diabetes, type 2 diabetes may respond to treatment with exercise, diet, and medicines taken by mouth. There are several types of medicines used to lower blood glucose in type 2 diabetes. See also: Type 2 diabetes Medications may be switched to insulin during pregnancy and while breastfeeding. Gestational diabetes may be treated with exercise and changes in diet.

EXERCISE Regular exercise is especially important for people with diabetes. It helps with blood sugar control, weight loss, and high blood pressure. People with diabetes who exercise are less likely to experience a heart attack or stroke than those who do not exercise regularly. Here are some exercise considerations: y y y y y y y y Always check with your doctor before starting a new exercise program. Ask your doctor or nurse if you have the right footwear. Choose an enjoyable physical activity that is appropriate for your current fitness level. Exercise every day, and at the same time of day, if possible. Monitor blood glucose levels before and after exercise. Carry food that contains a fast-acting carbohydrate in case you become hypoglycemic during or after exercise. Carry a diabetes identification card and a cell phone in case of emergency. Drink extra fluids that do not contain sugar before, during, and after exercise.

You may need to change your diet or medication dose if you change your exercise intensity or duration to keep blood sugar levels from going too high or low. FOOT CARE People with diabetes are more likely to have foot problems. Diabetes can damage blood vessels and nerves and decrease the body's ability to fight infection. You may not notice a foot injury until an infection develops. Death of skin and other tissue can occur. If left untreated, the affected foot may need to be amputated. Diabetes is the most common condition leading to amputations. To prevent injury to the feet, check and care for your feet every day.

Type 2 Diabetes Mellitus: Update on Diagnosis, Pathophysiology, and Treatment Richard J. Mahler and Michael L. Adler SIXTEEN million individuals in the United States with type 2 diabetes mellitus and an additional 3040 million with impaired glucose tolerance result in health care costs exceeding 100 billion dollars annually . Treatment is predominantly directed at microvascular and macrovascular complications . In type 1 diabetes mellitus the relationship between glycemic control and microvascular complications has been well established . The relationship between tight glycemic control and microvascular disease in type 2 diabetes mellitus appears to be established in the recently completed United Kingdom prospective diabetes study . Despite the morbidity and mortality associated with retinopathy, nephropathy, and neuropathy, cardiovascular disease remains the leading cause of death in type 2 diabetes mellitus . Consequently, the treatment of confounding risk factors of obesity, hypertension, and hyperlipidemia assumes major importance and must be coordinated with good glycemic control for reduction in total mortality in type 2 diabetes mellitus . Based on the emerging relationship between the degree of glycemic control and microvascular complications as well as the contribution of hyperglycemia in the development of macrovascular disease, it is the purpose of this review to summarize the current state of knowledge to provide a rational basis for the treatment of type 2 diabetes mellitus. Classification of type 2 Diabetis Mellitus

The definition of type 2 diabetes mellitus, previously termed noninsulin-dependent diabetes mellitus, was recently modified by the American Diabetes Association. Several criteria may be used independently to establish the diagnosis: 1) a 75-g oral glucose tolerance test with a 2-h value of 200 mg/dL or more, 2) a random plasma glucose of 200 mg/dL or more with typical symptoms of diabetes, or 3) a fasting plasma glucose of 126 mg/dL or more on more than one occasion. Fasting glucose values are preferred for their convenience, reproducibility, and correlation with increased risk of microvascular complications. The term impaired fasting glucose has been defined as fasting plasma glucose of 110 or more and 125 mg/dL or less. Impaired glucose tolerance (IGT) is defined as a 2-h plasma glucose value of 140 or more and of less than 200 mg/dL during an oral glucose tolerance . Individuals with impaired fasting glucose and IGT are considered to be at high risk for the development of diabetes and macrovascular disease . Although one third of these patients will eventually develop diabetes, dietary modification and exercise can lower the risk of progression from impaired glucose tolerance to type 2 diabetes; and may also prevent the development of IGT in nondiabetic individuals at high risk . Pharmacological agents may also be of benefit in limiting the progression from IGT to diabetes . Pathophysiology

Type 2 diabetes mellitus is a heterogeneous disorder with varying prevalence among different ethnic groups. In the United States the populations most affected are native Americans, particularly in the desert Southwest, HispanicAmericans, and Asian-Americans . The pathophysiology of type 2 diabetes mellitus is characterized by peripheral insulin resistance, impaired regulation of hepatic glucose production, and declining -cell function, eventually leading to -cell failure. The primary events are believed to be an initial deficit in insulin secretion and, in many patients, relative insulin deficiency in association with peripheral insulin resistance .

-Cell dysfunction is initially characterized by an impairment in the first phase of insulin secretion during glucose stimulation and may antedate the onset of glucose intolerance in type 2 diabetes . Initiation of the insulin response depends upon the transmembranous transport of glucose and coupling of glucose to the glucose sensor. The glucose/glucose sensor complex then induces an increase in glucokinase by stabilizing the protein and impairing its degradation. The induction of glucokinase serves as the first step in linking intermediary metabolism with the insulin secretory apparatus. Glucose transport in -cells of type 2 diabetes patients appears to be greatly reduced, thus shifting the control point for insulin secretion from glucokinase to the glucose transport system . This defect is improved by the sulfonylureas . Later in the course of the disease, the second phase release of newly synthesized insulin is impaired, an effect that can be reversed, in part at least in some patients, by restoring strict control of glycemia. This secondary phenomenon, termed desensitization or -cell glucotoxicity, is the result of a paradoxical inhibitory effect of glucose upon insulin release and may be attributable to the accumulation of glycogen within the -cell as a result of sustained hyperglycemia . Other candidates that have been proposed are sorbital accumulation in the -cell or the nonenzymatic glycation of -cell proteins. Other defects in -cell function in type 2 diabetes mellitus include defective glucose potentiation in response to nonglucose insulin secretagogues, asynchronous insulin release, and a decreased conversion of proinsulin to insulin. An impairment in first phase insulin secretion may serve as a marker of risk for type 2 diabetes mellitus in family members of individuals with type 2 diabetes mellitus and may be seen in patients with prior gestational diabetes . However, impaired first phase insulin secretion alone will not cause impaired glucose tolerance. Autoimmune destruction of pancreatic -cells may be a factor in a small subset of type 2 diabetic patients and has been termed the syndrome of latent autoimmune diabetes in adults. This group may represent as many as 10% of Scandinavian patients with type 2 diabetes and has been identified in the recent United Kingdom study, but has not been well characterized in other populations . Glucokinase is absent within the -cell in some families with maturity-onset diabetes of young . However, deficiencies of glucokinase have not been found in other forms of type 2 diabetes .
B-cell

In summary, the delay in the first phase of insulin secretion, although of some diagnostic import, does not appear to act independently in the pathogenesis of type 2 diabetes. In some early-onset patients with type 2 diabetes (perhaps as many as 20%) there may be a deficiency in insulin secretion that may or may not be due to autoimmune destruction of the -cell and is not due to a deficiency in the glucokinase gene. In the great majority of patients with type 2 diabetes ( 80%), the delay in immediate insulin response is accompanied by a secondary hypersecretory phase of insulin release as a result of either an inherited or acquired defect within the -cell or a compensatory response to peripheral insulin resistance. Over a prolonged period of time, perhaps years, insulin secretion gradually declines, possibly as a result of intraislet accumulation of glucose intermediary metabolites . In view of the decline in -cell mass, sulfonylureas appear to serve a diminishing role in the long term management of type 2 diabetes . Unanswered is whether amelioration of insulin resistance with earlier detection or newer insulin-sensitizing drugs will retard the progression of -cell failure, obviating or delaying the need for insulin therapy.
Insulin Resistance

Emanating from the prismatic demonstration by Yalow and Berson of the presence of hyperinsulinism in type 2 diabetes, insulin resistance has been considered to play an integral role in the pathogenesis of the disease . Recent critical reviews, however, have questioned the primacy, specificity, and contribution of insulin resistance to the disease state . As chronic hyperinsulinemia inhibits both insulin secretion and action , and hyperglycemia can impair both the insulin secretory response to glucose as well as cellular insulin sensitivity , the precise relation between

glucose and insulin level as a surrogate measure of insulin resistance has been questioned. Lean type 2 diabetic patients over 65 yr of age have been found to be as insulin sensitive as their age-matched nondiabetic controls . Moreover, in the majority of type 2 diabetic patients who are insulin resistant, obesity is almost invariably present . As obesity or an increase in intraabdominal adipose tissue is associated with insulin resistance in the absence of diabetes, it is believed by some that insulin resistance in type 2 diabetes is entirely due to the coexistence of increased adiposity . Additionally, insulin resistance is found in hypertension, hyperlipidemia, and ischemic heart disease, entities commonly found in association with diabetes again raising the question as to whether insulin resistance results from different pathogenetic disease processes or is unique to the presence of type 2 diabetes . Prospective studies have demonstrated the presence of either insulin deficiency or insulin resistance before the onset of type 2 diabetes. Two studies have reported the presence of insulin resistance in nondiabetic relatives of diabetic patients at a time when their glucose tolerance was still normal . In addition, first degree relatives of patients with type 2 diabetes have been found to have impaired insulin action upon skeletal muscle glycogen synthesis due to both decreased stimulation of tyrosine kinase activity of the insulin receptor and reduced glycogen synthase activity . Other studies in this high risk group have failed to demonstrate insulin resistance, and in the same group, impaired early phase insulin release and loss of normal oscillatory pattern of insulin release have been described . Based upon these divergent studies, it is still impossible to dissociate insulin resistance from insulin deficiency in the pathogenesis of type 2 diabetes. However, both entities unequivocally contribute to the fully established disease. Liver The ability of insulin to suppress hepatic glucose production both in the fasting state and postprandially is normal in first degree relatives of type 2 diabetic patients. It is the increase in the rate of postprandial glucose production that heralds the evolution of IGT . Eventually, both fasting and postprandial glucose production increase as type 2 diabetes progresses. Hepatic insulin resistance is characterized by a marked decrease in glucokinase activity and a catalytic increased conversion of substrates to glucose despite the presence of insulin . Thus, the liver in type 2 diabetes is programmed to both overproduce and underuse glucose. The elevated free fatty acid levels found in type 2 diabetes may also play a role in increased hepatic glucose production . In addition, recent evidence suggests an important role for the kidney in glucose production via gluconeogenesis, which is unrestrained in the presence of type 2 diabetes . Therapy Diet. Diet therapy, although important for the prevention as well as the treatment of all stages of type 2 diabetes, continues to remain poorly understood and high controversial . When obesity coexists with hyperglycemia, as seen in the majority of individuals with type 2 diabetes, weight reduction is the major goal of dietary therapy . Traditional recommendations emphasize reduction of both the total and saturated fat content and replacement with complex carbohydrates to 5055% of the dietary calories. In type 2 diabetic patients, such diets may cause marked postprandial hyperglycemia. As there is considerable patient variability in the rate of glucose absorption, arduous attention to postprandial glucose monitoring and the addition of high fiber contents to the diet become critically important. Moreover, as the glycemic response of the diet is also dependent upon the texture and content of other food stuffs in the diet as well as the rate of intestinal motility, the diet as well as the stage and duration of type 2 diabetes have to be considered on an individual basis . Exercise. Exercise has been shown to be beneficial in the prevention of the onset of type 2 diabetes mellitus as well as in the improvement of glucose control as a result of enhanced insulin sensitivity . Decreased intraabdominal fat, an increase in insulin-sensitive glucose transporters (GLUT-4) in muscle, enhanced blood flow to insulin-sensitive tissues, and reduced free fatty acid levels appear to be the mechanisms by which exercise restores insulin sensitivity. In addition, exercise provides the added benefits of lowering blood pressure, improving myocardial performance, and lowering serum triglycerides while raising high density lipoprotein cholesterol levels.

Reaction

After reading the update on diabetes mellitus I was surprised that in america 16 million people are being diagnosed of type 2 diabetes mellitus and an additional 3040 million with impaired glucose tolerance result. Nowadays people need to modify their lifestyle for this is one of the risk factors in having diabetes, especially the diet. In America they have high rates of diabetes because the people their likes to eat fast food and sweets and most people are lazy to exercise which could help lower cholesterol and blood sugar. I always believe in the saying prevention is better than cure so to maintain and prevent such condition one must change their lifestyle, throw away all the bad habits that could harm the body, have adequate nutrition and a good exercise routine.

Update on Diabetes mellitus

Submitted By: Kyzyl Valencia BSN 3- B