Diabetes mellitus (DM) is a group of metabolic diseases of the lipid, and protein metabolism vaglehidradniya that result from defects in insulin secretion, insulin action (sensitivity), or both.
Most diabetic patients fall into one of two broad categories: type 1 diabetes characterized by an absolute lack of insulin and Toe 2 DM defined by DigoPaul as the presence of insulin resistance compensated with inadequate increase in insulin secretion. Women who develop diabetes during pregnancy due to stress klafifitsirat as developed gestational diabetes. In summary, a small number of patients with DM (2-3%) diabetes is caused by infuktsii, drugs, endocrinopathies, pancreatic dysfunction and known genetic defects.
Etiologic classification of DM is presented below:
Type 1 diabetes: beta-cell destruction leading to absolute insulin deficiency
- Immune mediated
Type 2 ZD: can vary from predominantly insulin rezistentin type with relative insulin deficiency to predominantly insulin sekretoren defect with insulin RESISTANCE
Other specific types:
- Genetic defects in beta cell function
o Chromosomes 20q – MODY 1
about Chromosomes 7b – FASHION 2
o Chromosomes 12q – MODY 3
o Хромозома 13q–MODY 4
o Хромозома 17q–MODY 5
o Хромозома 2q–MODY 6
- Genetic defects in insulonovoto action
o Type 1 insulin resistance
o Lipotrofen diabetes
o Синдром на Rabson–Mendelhall
- Disease of the exocrine pancreas
o Injury / pankreatektomiya
o Cystic Fibrosis
o Fibrokalkulozna pancreatopathy
o Cushing’s Syndrome
- Drug induced
o Nicotinic acid
o Atypical antipsychotics
o Thyroid hormones
o Alpha interferon
o Congenital rubella
- Other syndromes genitichni
o Down Syndrome
o Syndrome Wolfram
o Syndrome Klaynfertel
Type 1 diabetes mellitus
This form of diabetes is a consequence of autoimmune distruktsiya of pancreatic beta cells. The markers of the autoimmune destruction are: (1) antibodies to ostovnite cells; (2) GAD antibodies, and (3) antibodies to insulin. These markers are present in 90% of patients. Young patsienti have fast beta-cell destruction and maniferstirat first pot usually with ketoacidosis, while adults relatively long time maintain sufficient insulin secretion to prevent ketoacidosis and in this case we are talking about later-onset autoimmune diabetes in adults ( LADA).
Type 2 diabetes mellitus
This form of diabetes is characterized by the presence of insulin resistance and rarely a start relative lack of insulin secretion.
Comparison between type 1 and type 2 DM is given in the table below
|Type 1 diabetes (insulin-dependent)||Type 2 DM insulin independent|
|epidemiology||Patients are usually under 30 years of age||Patients are usually over the age of 30 years|
|ancestral||HLA DR3 & DR4 in over 90% of cases||No HLA association
About 50% concordance in identical twins
|pathogenesis||Autoimmune desease||No inummi violations
|clinical features||insulin deficiency
Patients always nazhdayat of administration of insulin
|Partial insulin deficiency. May develop hyperosmolar state.|
|biochemistry||With the disappearance of the peptide||With persistent peptide|
Gestational Diabetes Mellitus
This type of diabetes is defined as glucose intolerance diagnosed for the first time during pregnancy.
Other specific types of diabetes
MODY diabetes is characterized by impaired insulin secretion in the absence of insulin resistance. Patients develop hyperglycemia at an early age. The disease is autosomal dominant as unasleduva
The incidence of type 2 DM is increasing and is on track to become a pandemic (about 8% of people over age 20 develop type 2 DM).
Type 1 diabetes accounts for 10% of all cases diagnosittsiran TA. It should be borne in mind that the evolution of the beta cell autoimmunity observed in about 10% of the population, but only 1% of these patients develop diabetes mellitus.
Markers of autoimmunity observed in 14-33% of patients with type 2 diabetes and the disease they are developing with rapid development of insulin dependence.
Classification Of Glucose Status
Levels of fasting glucose
o < 5.6 mmol\L
- Impaired glucose tolerance
or 5.6 – 6.9 mmol \ L
or > 7 mmol \ L
Glucose levels 2 hours after a glucose challenge
o < 7.8 mmol\L
- Impaired glucose tolerance
or 7.8-11.1 mmol \ L
or > 11.1 mmol \ L
Type 1 diabetes mellitus
Type 1 diabetes is characterized by an absolute lack of insulin. Most often this is due to immune-mediated destruction of pancreatic beta cells, but rarely unknown idiopathic process can also contribute to this. The pathogenesis of type 1 diabetes passes through the 4 steps: (1) long predkilnichen period covering 9 to 13 years during which they are available immune markers for autoimmune beta cell destruction; (2) hyperglycemia when 80-90% of the beta cells are destroyed; (3) The transient remission continued until 12-24 months; (4) clinically detectable disease which is associated with the risk of complications and death.
Autoimmune process is mediated by macrophages and T lymphocytes, which is accompanied by the presence of circulating antibodies to different beta cell antigens. The most frequently observed antibodies to these cells Langerhanovite Islands. Other antibodies to insulin, to glutamic acid decarboxylase to the island tyrosine phosphatase and others.
Therefore, there is no 100% concordance in twins factors Aquila medium such as infections, chemical agents dietarni agents and contribute to the expression of the disease.
Type 2 diabetes mellitus
Fasting 75% of the glucose content in noninsulin-dependent tissues such as brain and splanchnic tissues (liver and gastrointestinal organs). The remaining 25% of glucose metabolism takes place in the muscles and is insulin dependent. Fasting 85% of the production of glucose made by the liver, and the remaining 15% of kidneys. Postprandial glucose exogenous stimulate insulin secretion by pancreatic beta cells, subsequent hyperinsulinemia: (1) inhibits endogenous glucose production in the liver and (2) stimurila obartnoto uptake of glucose by peripheral tissues.
Dysfunction in insulin secretion: in type 2 DM beta cells are unable to maintain high levels of insulin ssekretsiya. This inzufitsientsiya that occurs after eating leads to increased glucose production by the liver at night and vosiki levels of fasting glucose morning.
Insulin resistance: its main site of expression is muscle tissue. Under normal conditions, the increase in plasma glucose levels of endogenous insulin resp.nivata muscles borne in themselves glucose at a rate of 10 mg / kg / minute. In patsienitte with type 2 insulin action on muscle tissue is zavabeno about 40 minutes on one side and the other side is reduced very capacity of muscles to absorb glucose about 50%.
Role of adipose tissue: the term “visceral fat” is described adipose tissue in the abdominal cavity (omentum, mesenteric, perinefralna and retroperitoneal adipose tissue). This visceral fat is endocrinologic much more active than subcutaneous and released as free fatty acids , and cytokines that fall into the portal circulation and cause liver stimurilane production of VLDL and reduce insulin sensitivity in peripheral tissues. This fat however proizvizhda and a hormone called “adiponectin” which decreased hepatic production and increases peripheral glukoza its utilization. In patients complete the production of this hormone by the visceral fat is suppressed.
CLINICAL PRESENTATION diabetes
Clinical presentations of type 1 and type 2 DM are very different.
Autoimmune type 1 diabetes can occur at any age. About 75% of patients develop it up to the age of 20, and the remaining 25% develop the disease as adults.
Symptoms of hyperglycemia include polyuria, polydipsia, increased appetite, frequent night urination and weight loss.
About 20-40% of patients with type 1 diabetes manifested first with diabetic tsetoatsidoza occurring a few days after onset of the above symptoms.
The clinical manifestation in patients with type 2 DM is gradual.
The clinical features of diabetes are sumarizirani in the table below:
|Type 1 diabetes mellitus||Type 2 diabetes mellitus|
|age||Mostly in ’30||Mostly over ’30|
|body habitus||weak patients||full patients|
|insulin resistance||missing||often available|
|autoantibodies||often available||rarely available|
|Symptoms of the disease||Available at diagnosis||often asymptomatic|
|Ketones in the diagnosis||available||missing|
|Need insulin therapy||immediate||Possible years after diagnosis|
|acute complications||diabetic ketoacidosis||Hiperosmoralna coma|
|Microvascular complications at the time of diagnosis||Not||often|
|Macrovascular complications at the time of diagnosis||rarely||often|