juvenil diabetes: 5 definition

Definition
Diabetes mellitus is juveniles the manifests diabetes mellitus before age 15 years; therefore have a more fun use the term juvenile ONSET Diabetes.
Diabetes mellitus type 1 is one of the types of chronic diseases in children is caused by a lack of insulin due to the amount of damage to the pancreas beta cells produce insulin.
Diabetes mellitus type I is one of the two main types of diabetes mellitus, marked with symptoms of sudden ONSET, insulinopenia, and dependence on insulin eksogen to extend life; ONSET peak age is 12 years old, although ONSET can at any age. This is due to lack of insulin production by beta pancreas, which can be derived from viral infection, autoimmune reaction, and may be genetic factors, islet cell antibody can usually be detected at diagnosis. When inadequate control, lack of insulin causes hiperglikemik, protein solutions, and the production of substances that cause keton increase fat metabolism, and hiperglikemia cause gkukosuria excess flow, diuresis osmotik, hiperosmolaritas, dehydration and ketoasidosis diabetik. This is accompanied by the angiopati on the blood vessel, especially a small (microangiopathy) that the retina, kidneys and membrane basemen arteriol to the entire body. Other symptoms include poliuria, polidipsia, polifagia, lose weight, parestesia, the view that vague, and iritabilitas; if not, continue to be ketoasidosis diabetik Nausea and vomiting, stupor, coma, and potentially fatal hiperosmolar. Is also called insulin-dependent d. mellitus, juvenile or juvenile-ONSET d. mellitus, type I and d. mellitus.

Diabetes mellitus type 1 - first called insulin-dependent diabetes (IDDM, insulin-dependent insulin "), or diabetic children, characterized by loss of beta cells produce insulin in the islands Langerhans pancreas so that the lack of insulin occurs in the body. This type of diabetes can be suffered by children and adults. (3)
Diabetes mellitus type I with marked insulinopenia and heavy dependence on eksogen insulin to prevent ketosis and to stay alive; therefore diabetes is also called diabetes mellitus insulin-dependent (diabetes mellitus insulin-dependent (IDDM)). Historical natural this disease indicates that there is no phase-insulin-dependent, praketotik, both before and after the initial diagnosis. While there, especially starting at the children, the disease can occur at any time in ages. Therefore, terms such as juvenile diabetes, diabetes tends to ketosis, and insulin must be replaced brittle diabetes type I or IDDM. Diabetes type I is clearly different because the relationship with histokompatibilitas antigen (HLA); the antibody against sitoplasma components and cell-surface component of the cell islands in the circulation; antibody against insulin in the absence of expose against eksogen previous insulin injection; antibody against dekarboksilase acid glutamate (glutamate acid decarboxylase (GAD)), the enzyme acid change glutamat clabber aminobutirat gamma (gamma aminobutyric acid (GABA)), found excessive inervasi on the island of pancreas; infiltration limfosit island early in the disease and other diseases autoimmune. With some exceptions, in the diabetic child is insulin-dependent and in category type I.

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juvenil diabetes: 4 insulin

Insulin
Insulin is a hormone that consists of a series of amino acid, is produced by beta cells pancreas gland. In normal circumstances, when there is excitement in the beta cells, insulin sintesis and then sekresi in blood according to the needs of the body for the regulation of blood glucose.
Insulin synthesis begins in the form of preproinsulin (insulin precursor hormone) on the reticulum endoplasmic beta cells. With the help of enzyme peptidase, preproinsulin to pro insulin solution so that the form, which is then gathered in the bubble-bubble (secretory vehicle) in these cells. Here, with the help of enzyme peptides, apart into pro insulin and insulin C-peptide (C-peptide) that they are ready to sekresi at the same time through the cell membrane.
Physiological mechanism of the above, is required for glucose metabolism during the process, in relation to the function of insulin in the process of glucose utilization in the body. Blood glucose level is increased, the main components that provide stimulus to the beta cells produce insulin, although some types of amino acids and drugs, can also have the same effect. Mechanism synthesis and insulin sekresi after the stimulus to the beta cell is quite complex, and can not fully be understood clearly.

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juvenil diabetes: 3 blood glucose

Diabetes mellitus is a deficiency causes hormone insulin, which functions utilize glucose as a source of energy and fat sintesa. The result is the cumulative glucose in the blood (hiperglikemia) and finally through the urine without ekskresi used (glycosuria). Therefore, urine production is increased and the patient must urinate often, feeling very thirsty, decreased body weight and feel tired.

Blood glucose
Glukoneogenesis body will meet the interests of glucose at the time of carbohydrate is not available in sufficient amount of glucose in food. Supply continuously required as a source of energy, particularly for the nervous system and eritrosit. Failure on the glukoneogenesis usually fatal result. Blood glucose level below the critical value will cause disfungsi brain that can lead to coma and death. Glucose also needed in the network as adipose source gliseda- glyseril, and may have a role in maintaining the level of compound in the citric acid cycle in the body in many networks. Even in circumstances in which supply most of the fat calorie needs for the organism, the particular needs of basaltic will glucose there. Glucose is one - one of the baker's energy supply for the muscles in order anaerobe. This element is a precursor of milk sugar (lactose) in the breast gland and is actively taken by the fetus. In addition, the mechanism glukoneogenesis in use to clean the various products of metabolism other network in the blood, such as lactate produced by muscle and eritrosit, and glycerol that it continuously produced by the network adiposa. Propionat, namely acid fat glukogenik in the main produce in the process of carbohydrate digest by ruminant animals, is important for substrate glukoneogenesis body in this animal species.
Most of the carbohydrate in food that is most of the glucose will be formed. Carbohydrate foods are digested in the active residues containing glucose, and galaktosa will fruktosa in the offshore in intestinum. Elements in this nutrient transport into the vena porta hepar through hepar. Galaktosa and fruktosa immediately in a change in glucose hepar.

Glucose in the form of various compound glukogenik the glukoneogenesis. This compound can be in the grade in 2 categories:
(1) compound that includes the conversion into glucose net directly without re-cycle, which means, as some amino acids and propionate, and
(2) compound which is a partial result of glucose metabolism in certain network and the in transport in the kidney and hepar for synthesis back into glucose. Thus, the compound that laktat through glucose oxidation in muscle and order by eritrosit, will be taken in hepar and kidney for glucose re-made so that the element is available for circulation through oxidation in the network. This process is known as Cori cycle or cycles lactate acid. Glycerol 3-phosphate for synthesis triasilgriserol network adipose derived from blood glucose. Asilgliserol compound on the network adiposa continue to experience in the hydrolysis to form free gliserol that can not be in use by the network and thus adipose will be diffuse out and into the blood. This free Gliserol will converted into glucose through a mechanism glukoneogenesis in hepar and kidney.
Between acid-amino acid is transported from muscle to hepar in during the famine was the most dominant alanine. This then produces postulate cycle alanine the glucose-glucose recycling result of hepar to muscle with the piruvat, which was followed by transmitting a alanine, and transportation alanine to hepar, and then followed by glukoneogenesis back into glucose. Net transfer of amino nitrogen from muscle to hepar and free energy from the muscles to hepar thus can be done. Energy needed for glucose synthesis in the hepar of piruvat derived from acid-oxidation fatty acid. Also be formed from glucose glycogen hearts through glikogenolisis.

On deficiency insulin there is a heavy acceleration lipolisis. This resulted in the increase rate triasil-gliserol plasma (hiperlipidemia). Few asetil-KoA can metabolise through the citric acid cycle, so the rest must be converted into acid-keto acid (ketonemia) and some excrested(ketonuria). Because glikolisis blocked, enzyme glucose 6-phosphate that the acceleration of glikogenolisis will changed into glucose. This together with the acceleration glukoneogenesis result hiperglikemia (due to increased amino acid and which have increased the amount of enzyme PEPCK). Insulin is basically the reverse of all this. (Murray, 1999)

The process of maintaining a stable glucose level in the blood is one of the homeostasis mechanisms that set the fine and also the one where hepar, network ekstrahepatik and took some hormone. Cell heart cells appear to be passed with a glucose-free (through the GLUT transporter 2), while cells outside the network ekstrahepatik (outside the island of Langerhans pancreas) is relatively not permeable. As a result, crossing through the membrane into the cell phase-speed barrier in the process of glucose in the network ekstrahepatik, glucose and the process fosforilasi quickly by heksokinase at the time of entry in cells. Conversely, enzyme activity and concentration of some compound that may be important to provide a far more direct or to the expenditure of glucose in hepar. However, the concentration of glucose in the blood are important factors that control the speed of glucose in the hepar and ekstrahepatik network. Role of various glikosa the transporter protein found in the cell membrane and each have 12 pieces of transmembran.

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juvenil diabetes: 2 etiology

Epidemiology
DM is a disease with great consequences to health and social. Not only because of the high prevalence of complications, but because cronic and a high death rate.
Prevalence of DM in the world continues to increase. In 1995, prevalence 4.0%. In the year 2025 is estimated to be 5.4%. In developing countries increased prevalence is more light. In 1995 it was found 84 million cases of DM and in the year 2025 this figure will increase to 228 million.
The occurrence of diabetes was 7 years before diagnosis, so morbidity and early mortality occurred in cases that are not detected.

Etiology and Pathogenesis
Developments in understanding the etiology and pathogenesis DM revitedthe previous classification. Although all types of DM by the hyperglycemia, but pathogenesis occurrence hyperglycemia very different. 2005 American Diabetes Association (ADA) to make the classification, the diabetes is type 4, among others, type 1 DM, type 2 DM, type DM, and DM in pregnancy. Diagnostic criteria of DM, according to the ADA in 2005 is:
1. When blood sugar 200 mg / dl if the typical complaints,
2. Fasting blood sugar 126 mg / dl.
3. Plasma glucose level 200 mg / dl at 2 hours after glucose load at 75 grams TTGO.
Diabetes mellitus is not a single form, but presumably is a heterogeneous group of aberration is the difference between the pattern and the genetic mechanism and etiology patofisiologi other disturbances that cause glucose tolerance. National Diabetes Data Group has put the classification category and diabetes glucose intolerance based on the knowledge of the present. This classification has been accepted and supported by various diabetes associations around the world by researchers and Pediatrics. Three main forms of diabetes and some forms of carbohydrate intolerance were identified: Type I Diabetes (Diabetes mellitus Juvenil), type II diabetes, and secondary diabetes.

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juvenil diabetes: 1 definition

Diabetes Melitus(DM) according to the American Diabetes Association (ADA) in 2005, is a group of diseases characterized metabolic with hyperglycemia happens because sekresi aberration insulin, insulin work or both.
Hyperglycemia chronicles on diabetes-related long-term damage, disfungsi, and failure of various organs, especially eyes, kidneys, nerves, heart and blood vessel.
According to the WHO in 1980, DM is a set of muscle problems and the chemical, which is a result of a number of factors which gained deficiency relative or absolute insulin and insulin function disturbances, in particular family, related to the aterosklerosis quickened, and is predisposisi for the occurrence of aberration, such as specific mikrovaskuler retinopati, nefropati.
Diabetes is a syndrome melitus energy homeostasis disruption caused by insulin or deficiency by deficiency work and lead to carbohydrate metabolism, protein and fat is not normal. This is an aberration metabolic-interference endocrine the children and teenagers the most prevalent with important consequences on the physical and emotional development.
metabolism, protein and fat due to lack sekresi insulin or insulin resistance in the network. This occurs in the form of a main type 1 d. mellitus and type 2 d. mellitus, different things in the cause, pathology, genetic, age ONSET, and handling.

Diabetes mellitus is a disease that causes interference metabolic carbohydrate metabolism, fat, protein and as a result of the lack of effective insulin.
Diabetes mellitus, diabetes or diabetes is a chronic disturbance of metabolism, especially concerning glucose in the body. However, the metabolism of fat and protein is also subject to (Lat. = continuance diabetes, mellitus = honey sweet).

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