Diabetes Mellitus (Dm)

Diabetes mellitus (DM) is based on a malfunction in insulin secretion and / or on a peripheral insulin resistance varying degrees, leading to hyperglycemia. The early symptoms are due to the hyperglycemia and polyuria, polydipsia, and weakness. Phases of polyphagia, and blurred vision occur. Late complications include vascular disease, peripheral neuropathy, nephropathy, and predisposition to infection. The diagnosis is made by measuring the plasma glucose concentration. The therapy consists of a healthy diet, exercise and drugs that reduce glucose levels. These drugs include insulin and oral antihyperglycemic drugs. Complications can be delayed with adequate glycemic control or prevented; heart disease remains the leading cause of death in DM.

There are various forms of diabetes mellitus (DM) – type 1 and type 2, which can be distinguished from each other by a combination of certain characteristics (see Table: General characteristics of the diabetes type 1 and diabetes type 2). Terms that describe the age of onset (juvenile or adult) or type of treatment (insulin- or non-insulin dependent), should no longer be used because there is overlap, both in terms of age at onset of the disease and in terms of therapy.

Diabetes mellitus (DM) is based on a malfunction in insulin secretion and / or on a peripheral insulin resistance varying degrees, leading to hyperglycemia. The early symptoms are due to the hyperglycemia and polyuria, polydipsia, and weakness. Phases of polyphagia, and blurred vision occur. Late complications include vascular disease, peripheral neuropathy, nephropathy, and predisposition to infection. The diagnosis is made by measuring the plasma glucose concentration. The therapy consists of a healthy diet, exercise and drugs that reduce glucose levels. These drugs include insulin and oral antihyperglycemic drugs. Complications can be delayed with adequate glycemic control or prevented; heart disease remains the leading cause of death in the DM There are various forms of diabetes mellitus (DM) – type 1 and type 2, which can be distinguished by a combination of certain characteristics from each other (see table. General features of diabetes type 1 and diabetes type-2). Terms that describe the age of onset (juvenile or adult) or type of treatment (insulin- or non-insulin dependent), should no longer be used because there is overlap, both in terms of age at onset of the disease and in terms of therapy. The disorder of glucose metabolism (impaired glucose tolerance or impaired fast glucose see table: Diagnostic criteria for diabetes mellitus and abnormal glucose metabolism) is an intermediate or transitional form between normal glucose metabolism and DM, which is more common with advancing age. This disorder is already an important risk factor for DM. It can be made many years before the actual start of the DM. The reduced glucose tolerance is associated with an increased risk of cardiovascular disorders, diabetic microvascular complications but are not very frequent (microalbuminuria and / or retinopathy develop at 6 to 10%). is assessment of the blood glucose level based on conventional or SI units A1c hemoglobin etiology type 1 insulin production is missing due to autoimmune ? cell destruction of the pancreas in diabetes type 1 (formerly juvenile or insulin-dependent DM was called): Clinical calculator due to autoimmune destruction of the pancreatic ?-cells, insulin secretion severely limited. The destruction is probably triggered by environmental factors in genetically susceptible patients. The destruction of subclinical over months and years until the ?-cells are reduced to the extent that the secreted insulin levels are no longer sufficient to maintain plasma glucose levels under control. A normally Diabetes Type 1 develops in childhood or early adolescence and was until recently the most common before age 30 diagnosed form of DM Nevertheless, a DM can also develop in adulthood. Latent autoimmune diabetes in adults , LADA. This is initially often referred to as diabetes type 2. Some cases of diabetes type 1, especially among the dark-skinned population, do not appear innately as autoimmune, but are considered to be idiopathic. Diabetes Type 1 accounts for <10% of DM cases. The pathogenesis of the autoimmune ? cell destruction includes only been partially clarified interactions between predisposing genes, autoantigens and environmental factors. Predisposing genes can be found on the one hand the so-called major histocompatibility complex (major histocompatibility complex, MHC) -. Especially HLA-DR3, DQB1 * 0201 and HLA-DR4, DQB1 * 0302 in> 90% of patients with diabetes type -1 are available – and the other outside the MHC, where they regulate insulin production and processing, and determine the risk of DM in conjunction with the genes of the MHC. Predisposing genes are more common than others in some populations. Thus, the higher prevalence of diabetes type 1 in some ethnic groups (Scandinavian, Sardinian) is explained. Autoantigens are glutamic acid decarboxylase, insulin, insulinoma-associated protein, zinc transporter ZnT8 and other proteins of the ?-cells. It is believed that these proteins are exposed to or during the normal ?-cell turnover or ?-cell injury (eg., By infection) released, which is primarily a cell-mediated immune response (with the destruction of ?-cells insulitis ) ends triggers. Glucagon secreting ?-cells remain unaffected. Antibodies against autoantigens, which can be found in the serum, the answer to the ?-cell destruction appear to be and not its cause. Various types of virus (including coxsackie, rubella, cytomegalovirus, Epstein-Barr viruses and retroviruses) have a been implicated in diabetes type 1 with the occurrence. Viruses can directly infect and destroy ? cells, or they cause the ?-cell destruction indirectly by exposing autoantigens activate autoreactive lymphocytes or molecular sequences of autoantigens, which stimulate an immune response mimic (molecular mimicry). Other mechanisms are possible. The diet may play a role. The early infants with dairy products (especially cow’s milk and the milk protein ?-casein), high nitrate levels in drinking water and a low vitamin D intake have been associated with an increased risk for type 1 DM. Early (<4 months) or late (> 7 months) supply of gluten or grain increases the risk of an islet cell autoantibody production. (Was formerly diabetes adult or non-insulin dependent DM) identifies the mechanisms of these associations are unklar.Typ 2 Insulin Resistance In diabetes type 2, insulin secretion is inadequate because patients have developed a resistance to insulin. The hepatic resistance to insulin leads to the inability to suppress hepatic glucose production and peripheral insulin resistance affects the peripheral glucose uptake. These mechanisms result in fasting and postprandial hyperglycemia. Frequently, the insulin levels are very high, especially in the early stages of the disease. Later in the disease, insulin production may decrease, leading to a further worsening hyperglycemia. The disease usually develops in adults and is more common in advancing age. Up to one in three adults has> 65 years impaired glucose tolerance. In older adults, the plasma glucose levels reach higher values ??than in younger adults, especially after meals high in carbohydrate content of the meal. The glucose levels also need more time until they are back to normal, in part because of increased accumulation of visceral and abdominal fat and decreased muscle mass. has become epidemic since obesity in childhood diabetes Type 2 is increasingly in children: 40-50% of new-onset DM cases in children are attributable to the type of the second About 90% of all adults with DM have a diabetes type-2. There is clear evidence of genetic determinants, to which the high prevalence of the disease within certain ethnic groups indicates (especially with the Indians, Latin Americans and Asians) and with relatives of existing sufferers. Although several genetic polymorphisms have been identified in recent years, there is no single gene could be identified as responsible for the most common forms of diabetes type-2. The pathogenesis is complex and not fully understood. Hyperglycemia then develops when insulin resistance can not be compensated by increased insulin secretion. Although insulin resistance is characteristic for patients who are at risk for, or a manifestation of diabetes type 2, it is also in diabetes type 2 evidence of ?-cell dysfunction and decreased insulin secretion, including reduced insulin secretion first response to iv Infusion of glucose, loss of the normal pulsatile insulin secretion, an increase in the Proinsulinsekretion as an indication of an impaired insulin production and accumulation of Inselzellamyloidpolypeptid, a protein which is normally secreted along with insulin. Hyperglycemia itself can affect insulin secretion, since high glucose levels desensitize ?-cells and / or a ?-cell dysfunction (glucose toxicity) cause, or both. Normally, it takes years to adapt these changes in insulin resistance. Obesity and weight gain are important determinants of insulin resistance in diabetes type-2. There are genetic influences, but in the manifestation Also the diet, the amount of physical activity and lifestyle reflect. The failure to suppress lipolysis in adipose tissue, increases plasma levels of free fatty acids, which in turn affect the insulin-dependent glucose transport and glycogen synthase in muscles. Adipose tissue as an endocrine organ sets various mediators (adipocytokines) free, the preferred (adiponectin) or as a side effect (tumor necrosis factor ?, IL-6, leptin, resistin) influence the glucose metabolism. Intrauterine growth retardation and low birth weight were also associated with insulin resistance in later life and show that adverse prenatal environmental influences glucose metabolism beeinflussen.Verschiedene other DM types are various other causes that are responsible for a small percentage of DM cases, genetic defects of ? cell function, insulin action and the mitochondrial DNA (eg MODY = maturity onset diabetes of youth.); Diseases of the pancreas (e.g., cystic fibrosis, pancreatitis, hemochromatosis.); Endocrinopathies (. For example, Cushing syndrome, acromegaly); Toxins (. Vacor for example, a means for controlling rats); and drug-induced diabetes mellitus, in particular by glucocorticoids, ?-blockers, protease inhibitors and therapeutic doses of niacin. Pregnancy causes all women insulin resistance varying degrees, but few develop gestational diabetes (diabetes mellitus in pregnancy (gestational diabetes)). General features of diabetes type 1 and diabetes type 2 feature Type 1 Type 2 age of onset most frequently <30 years Most frequently> 30 years Associated obesity Unusual Very common tendency to ketoacidosis, which requires insulin treatment Yes No Plasma levels of endogenous insulin extreme low to undetectable Variable: low, normal or increased depending on the degree of insulin resistance and the defect in the insulin secretion occurring in both twins ? 50%> 90% associated with certain HLA-D antigens Yes no autoantibodies in the pancreas in diagnosis Yes, but not always present no Islet cell pathology insulitis, selective loss of most of ?-cells smaller, normal-appearing Islands; Amyloid (amylin) sequestration often susceptible to the development of diabetic complications (retinopathy, nephropathy, neuropathy, atherosclerotic cardiovascular disease) Yes hyperglycemia responds to oral antihyperglycemic drugs No Yes, initially in many patients Diagnostic criteria for diabetes mellitus and abnormal glucose metabolism test NormalImpaired glucose metabolism diabetes FPG (mg / dL [mmol / l]) <100 (<5.6) 100-125 (5.6 to 6.9) ?126 (? 7.0) OGTT (mg / dl [mmol / l]) <140 (<7.7) 140-199 (7.7 to 11.0) ? 200 (? 11.1) HbA1c (%) <5.7 5.7 to 6.4 ? 6.5PFG = Sober plasma glucose value; HbA1c = glycosylated hemoglobin; OGTT = oral glucose tolerance test, 2-h glucose levels. Symptoms and signs The most common symptoms of diabetes mellitus are those of hyperglycemia. The slight hyperglycemia early diabetes is often asymptomatic; Therefore, the diagnosis may be delayed for many years. A more severe hyperglycemia causes glycosuria and thus osmotic diuresis, which can lead to frequent urination, polyuria and polydipsia, which in turn can result in dehydration and orthostatic hypotension. Severe dehydration leads to weakness, fatigue and changes in the state of consciousness. Depending on the plasma glucose level and go the symptoms. A polyphagia may occur concomitantly to the symptoms of hyperglycemia, however, is not a typical symptom on the patient to complain. Hyperglycemia can also cause weight loss, nausea and vomiting, a limitation of vision and increased susceptibility to infection by bacteria and fungi. Patients with diabetes type-1 typically fall by symptomatic hyperglycemia and / or by a diabetic ketoacidosis (DKA, diabetic ketoacidosis (DKA)) on. Since insulin secretion can temporarily recover partially, many patients after the acute onset of the disease, a transient phase near-normal glucose levels. Patients with diabetes type 2 can be noticed by hyperglycemia, but are often asymptomatic, and their disease is only detected during routine testing. Your condition falls only after a routine check on or through the symptoms of late complications of diabetes, suggesting that the disease was undetected for a while. In some patients initially a hyperosmotic coma occurs, especially during periods of stress or if the glucose metabolism by drugs such. B. glucocorticoids is further restricted. Complications When blood sugar levels are poorly controlled for years, resulting in a variety of vascular primary symptoms that can affect both small and large vessels (micro- and macrovascular complications), or both. The mechanisms that lead to the development of vascular disease are varied such. B. glycosylation of serum and tissue proteins with the formation of so-called. "Advanced glycation end products" (AGE), Superoxidentstehung, activation of protein kinase C, an enzyme of the signaling cascade that increases the vascular permeability and disturbance of endothelial cause, accelerate the Hexosaminbiosynthese and Polyolkreislaufs, leading to accumulation of sorbitol in the tissues. Hypertension and dyslipidemia occur as part of a DM frequently. Arterial thrombosis micro, proinflammatory and prothrombotic effects of hyperglycemia and hyperinsulinemia affect the vascular autoregulation. An immune system disorder is another serious complication and occurs due to direct effects of hyperglycemia on cellular immunity. The three most common and most serious manifestations of DM caused by microvascular disorders: retinopathy nephropathy neuropathy Microvascular disorder impaired wound healing difficult, so can develop minor injuries to deep ulcerations with an increased risk of infection already, particularly in the lower extremities. A very good blood glucose control can prevent such complications. Once existing complications may be irreversible. Cellulitis (foot ulcer) © Springer Science + Business Media var model = {thumbnailUrl: '/-/media/manual/professional/images/496-cellulitis-with-foot-ulcer-slide-98a-springer-high_de.jpg?la= de & thn = 0 & mw = 350 ', imageUrl:' /-/media/manual/professional/images/496-cellulitis-with-foot-ulcer-slide-98a-springer-high_de.jpg?la=de&thn=0 ', title: 'cellulitis (foot ulcer) ", description:' u003Ca id = " v38396099 ""class = "" anchor "" u003e u003c / a u003e u003cdiv class = "" para "" u003e u003cp u003eEin patient with diabetes often develops a microvascular disorder that can severely impair wound healing

Health Life Media Team

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