Symptoms, Causes, Diabetes Mellitus Type 1, 2, 3, 4, Complications and TreatmentDiabetes mellitus is a metabolic disorder caused by many factors, with chronic hyperglycemia simtoma form and impaired metabolism of carbohydrates, fats and proteins, as a result of:
* Deficiency of insulin secretion, insulin activity, or both
* Glucose transporter deficiency.
* Or both.
Various diseases, syndromes and simtoma can be triggered by diabetes mellitus, such as: Alzheimer's disease, ataxia-telangiectasia, Down syndrome, Huntington's disease, mitochondrial disorders, miotonis dystrophy, Parkinson disease, Prader-Willi syndrome, Werner syndrome, Wolfram syndrome, leukoaraiosis, dementia, hypothyroidism, hyperthyroidism, hypogonadism, and others.
Common Symptoms
Simtoma further hyperglycemia induces other three classic symptoms:
* Polyuria - frequent urination
* Polydipsia - always feel thirsty
* Polyphagia - always hungry
* Weight loss, often only in diabetes mellitus type 1
and after long term without adequate care, can trigger a variety of chronic complications, such as:
* Disturbance in the eye with the potential result in blindness,
* Disorders of the kidneys to result in renal failure
* Cardiovascular disorders, accompanied by basement membrane lesions which can be determined by examination using electron microscopy,
* Interference with the nervous system to autonomic nerve dysfunction, foot ulcers, amputations, Charcot joint and sexual dysfunction,
and other symptoms such as dehydration, ketoacidosis, ketonuria and hyperosmolar non-ketotik which can result in stupor and coma.
* Susceptible to infection.
The word itself refers to diabetes mellitus in simtoma called glycosuria, or diabetes, which occurs if the patient does not immediately get treatment.
Classification
World Health Organization (WHO) classifies forms of diabetes mellitus based on the care and simtoma:
1. Type 1 diabetes, including ketoacidosis simtoma until the destruction of beta cells in the pancreas that caused or led to autoimmunity, and are idiopathic. Diabetes mellitus with unclear pathogenesis, such as cystic fibrosis or deficient mitochondria, are not included in this classification.
2. Type 2 diabetes, caused by a deficiency of insulin secretion, often accompanied by insulin resistance syndrome
3. Gestational diabetes, including gestational impaired glucose tolerance, GIGT and gestational diabetes mellitus, GDM.
and according to clinical stage without consideration of the pathogenesis, made into:
4. Diabetes requiring insulin for survival, as in the case of C-peptide deficiency.
5. Diabetes requiring insulin for control. At this stage, endogenous insulin secretion is not sufficient to achieve normoglicemia symptoms, if not accompanied by additional hormones from outside the body.
6. Not insulin requiring diabetes.
Fourth grade at the clinical stage classification similar to IDDM (English: insulin-dependent diabetes mellitus), were fifth and sixth stage is the classification of NIDDM (English: non-insulin-dependent diabetes mellitus). IDDM and NIDDM is a classification listed in the International Nomenclature of Diseases in 1991 and revisions to the 10th International Classification of Diseases in 1992.
Malnutrion-related classification of diabetes mellitus, MRDM, no longer used because, although malnutrition can affect the expression of several types of diabetes, up to now has not found evidence of malnutrition or protein deficiency can lead to diabetes. Subtype MRDM; Protein-deficient pancreatic diabetes mellitus, PDPDM, PDPD, PDDM, is still regarded as a form of malnutrition-induced diabetes mellitus and require further research. Whereas the other subtypes, Fibrocalculous pancreatic diabetes, FCPD, classified as exocrine pancreatic disease in fibrocalculous pancreatopathy trajectory that induces diabetes mellitus.
Classification of Impaired Glucose Tolerance, IGT, is now defined as the stage of the defective glucose regulation, as can be observed in all types of abnormalities hiperglisemis. But no longer considered diabetic.
Classification of Impaired Fasting glycaemia, IFG, introduced as the ratio simtoma fasting blood sugar is higher than the upper limit of normal range, but still below the ratio determined as the basis for the diagnosis of diabetes.
Cause
Possible induction of type 2 diabetes from a variety of hormonal abnormalities, such as hormone secretion of the adrenal glands, pituitary and thyroid are observational studies that are worthy of leaves at this time. For example, the onset of IGT and diabetes mellitus often referred to by the related hiperkortisolisme or acromegaly and Cushing's syndrome.
Hormone hypersecretion of GH in acromegaly and Cushing's syndrome often results in insulin resistance, both in the liver and other organs, with hyperinsulinemia and hyperglycemia simtoma, which have an impact on cardiovascular disease and result in death.
GH does have an important role in glucose metabolism by stimulating glukogenesis and lipolysis, and increased levels of blood glucose and fatty acids. In contrast, insulin-like growth factor 1 (IGF-I) increases sensitivity to insulin, especially in striated muscle. However, in acromegaly, an increase in the ratio of IGF-I can not reduce insulin resistance, due to excess GH.
Therapy with somatostatin could reduce excess GH in some people, but because it also inhibits the secretion of insulin from the pancreas, this therapy will lead to complications in glucose tolerance.
While the hormone cortisol hypersecretion in hiperkortisolisme that causes visceral obesity, insulin resistance, and dyslipidemia, leading to hyperglycemia and decrease glucose tolerance, the occurrence of insulin resistance, stimulation of gluconeogenesis and glycogenolysis. When bersinergis with cofactors hypertension, hypercoagulable, may increase cardiovascular risk.
Hormone hypersecretion also occur in the thyroid gland in the form of tri-iodotironina with hyperthyroidism which causes abnormal glucose tolerance.
In patients with neuroendocrine tumors, changes in glucose tolerance caused by insulin hiposekresi, as occurs in patients with pancreatic surgery, phaeochromocytoma, glukagonoma and somatostatinoma.
Hormone hypersecretion is suspected also induces another type of diabetes, namely type 1. Synergy sitokina shaped hormone, interferon-gamma and TNF-α, found to carry signals for beta cell apoptosis, both in vitro and in vivo. Apoptosis of beta cells also occur due to the mechanism of Fas-FasL, and / or hypersecretion of cytotoxic molecules, such as granzyme and perforin; in addition to hyperactivity of T cells and CD4-CD8-.
Diabetes Mellitus Type 1
Diabetes mellitus type 1, juvenile diabetes (in English: childhood-onset diabetes, juvenile diabetes, insulin-dependent diabetes mellitus, IDDM) is diabetes that occurs due to the reduced ratio of insulin in the blood circulation due to the loss of insulin-producing beta cells in the islands Langerhans of the pancreas. IDDM can be suffered by children and adults.
Until now IDDM can not be prevented and can not be cured, even with diet and exercise. Most people with type 1 diabetes have health and good weight when the disease began suffered. In addition, the sensitivity and response to insulin is generally normal in this type of diabetes, especially in the early stages.
The most common cause of loss of beta cells in type 1 diabetes is the autoimmune reaction that destroys error pancreatic beta cells. Autoimmune reactions can be triggered by an infection in the body.
Currently, type 1 diabetes can only be treated by using insulin, with careful monitoring of blood glucose levels through blood testing monitors. Basic treatment of type 1 diabetes, even for the earliest stages, is replacement of insulin. Without insulin, ketosis and diabetic ketoacidosis can lead to coma and even death can result. Emphasis is also given on lifestyle adjustments (diet and exercise). Apart from giving injections in general, it also allows administration of insulin through a pump, which allows for feedback of insulin 24 hours a day at dose levels that have been determined, it is also possible dose (a bolus) of insulin is needed at meal times. And it is also possible for the administration of insulin input through "an inhaled powder."
Treatment of type 1 diabetes must continue. Treatment will not affect normal activities, if sufficient awareness, appropriate care, and discipline in the examination and treatment started. Average glucose levels for patients with type 1 diabetes should be as close as possible to the normal rate (80-120 mg / dl, 4-6 mmol / l). Some physicians suggest up to 140-150 mg / dl (7 - 7.5 mmol / l) for those with problems with a lower number, such as "frequent hypoglycemic events." [citation needed] A reading above 200 mg / dl (10 mmol / l) are often accompanied by discomfort and urination too often leading to dehydration. [citation needed] A reading above 300 mg / dl (15 mmol / l) usually require immediate treatment and can lead to ketoacidosis. that low levels of blood glucose, called hypoglycemia, can cause loss consciousness.
Diabetes Mellitus Type 2
Diabetes mellitus type 2 (English: adult-onset diabetes, obesity-related diabetes, non-insulin-dependent diabetes mellitus, NIDDM) is a type of diabetes mellitus that occurs is not caused by the ratio of insulin in the blood circulation, but is a metabolic disorder caused by mutations in many genes, including those expressing β cell dysfunction, impaired insulin secretion, the cell resistance to insulin caused by the dysfunction of GLUT10 with hormone resistin cofactors that cause tissue cells, mainly in the liver becomes less sensitive to insulin as well as RBP4 that suppress absorption of glucose by striated muscle, but increases the secretion of blood sugar by the liver. Mutation of these genes often occurs on chromosome 19 which is the densest of chromosomes found in humans.
In NIDDM found that high expression of SGLT1, the ratio of RBP4 and resistin hormone high, [an increase in metabolic rate glycogenolysis and gluconeogenesis in the liver, decreased the rate of increase in the rate of oxidation and esterification reactions in the liver.
NIDDM can also be caused by dyslipidemia , lipodystrophy, and insulin resistance syndrome.
In the early stages of disorder that arises is the reduced sensitivity to insulin, which is marked by rising levels of insulin in the blood. Hyperglycemia can be treated with anti-diabetic drugs that improve insulin sensitivity or reduce glucose production from the liver, but the more severe the disease , insulin secretion was diminished, and occasionally required insulin therapy. There are several theories that say the exact cause and mechanism of this resistance, but central obesity is known to predispose to insulin resistance, in connection with the expenditure of adipokines ( its a group of hormones) that damage the glucose tolerance. Obesity is found in approximately 90% of patients developed the world's diagnosis with type 2 diabetes. Other factors include incubate and family history, although in the last decade has steadily increased starting to affect teenagers and children.
Type 2 diabetes can occur without any symptoms prior to diagnosis. Type 2 diabetes usually, initially, treated by changing physical activity (exercise), diet (generally a reduction of carbohydrate intake), and through weight reduction. These can restore insulin sensitivity, even when weight loss / weight is modest, for example, around 5 kg (10 to 15 lb), most especially when it is in abdominal fat deposits. The next step, if necessary, treatment with oral [[antidiabetic drugs. [As / When / Because] insulin production is initially unimpaired treatment, oral (often used in combination) can still be used to improve insulin production (eg, sulfonylureas) and regulate the release / release that do not fit on glucose by the liver (and attenuate insulin retaliation to some degree (eg, metformin), and substantially attenuate insulin retaliation (eg, thiazolidinediones). If this fails, insulin therapy will be required to maintain normal or near normal glucose levels. A an orderly way of life of blood glucose checks is recommended in many cases, most particularly and most necessary when taking medication.
A dipeptidyl peptidase 4 inhibitor sitagliptin called, was recently allowed to be used as a treatment for type 2 diabetes mellitus. Such dipeptidyl peptidase 4 inhibitor to another, sitagliptin will open up opportunities for the development of tumors or cancer cells.
A typical phenotype is shown by NIDDM in humans is a deficiency in mitochondrial oxidative metabolism in striated muscle. In contrast, tri-iodotironina hormone induces biogenesis in mitochondria and promotes the synthesis of ATP synthase in complex V, increase activity of cytochrome c oxidase in complex IV, lower reactive oxygen species, reduce oxidative stress, is the hormone melatonin increases the production of ATP in the mitochondria and increases the activity of respiratory chain, especially in complex I, III and IV. Together with the insulin, the three form a cycle of this hormone that regulates mitochondrial oxidative phosphorylation in striated muscle. On the other hand, metalotionein which inhibits the activity of GSK-3beta reduces the risk of cardiac muscle deficiency in diabetics.
Simtoma that occurs in NIDDM could be reduced dramatically, followed by a reduction in body weight after intestinal bypass surgery. It is known as a result of increased secretion of hormones inkretin, but experts have not been able to determine whether this method can provide healing for NIDDM with changes in glucose homeostasis.
In traditional therapy, a flavonoid hesperidin and naringin-containing compounds, known to cause:
* An increase in glucokinase mRNA,
* An increase in GLUT4 expression in the liver and tissues
* An increase in peroxisomes proliferator gamma perceiving
* Increasing the ratio of plasma insulin, and leptin protein C
* Decrease in GLUT2 expression in liver
* Decrease in the ratio of plasma fatty acids and triglycerides in the liver
* Decrease in the ratio in plasma and liver cholesterol levels, among others, by pressing the 3-hydroxy-3-methylglutaryl-coenzyme reductase, acyl-CoA, cholesterol asiltransferase
* Decrease in fatty acid oxidation in the liver and palmitoyl karnitina activity, such as by reducing the synthesis of glucose-6 phosphatase dehydrogenase and fosfatidat fosfohidrolase
* Increase the rate of glycolysis path and / or decrease the rate of gluconeogenesis trajectory
're naringin alone, lower mRNA transcription karboksikinase phosphoenolpyruvate and glucose-6 phosphatase in the liver.
Hesperidin is an organic compound found in many types of citrus fruit, is naringin, found in many types of fruit wines.
Gestational diabetes mellitus (English: gestational diabetes, insulin-resistant type 1 diabetes, double diabetes, type 2 diabetes the which has progressed to require injected insulin, latent autoimmune diabetes of adults, type 1.5 "diabetes, type 3 diabetes, LADA) or diabetes mellitus that occurs only during pregnancy and recovery after childbirth, with the involvement of interleukin-6 and C reactive protein in the pathogenesis trajectory. [34] GDM may be harmful to the fetus or the mother's health, and about 20-50% of women with GDM survive.
Diabetes mellitus in pregnancy occurred in approximately 2-5% of all pregnancies. GDM is temporary in nature and can increase or disappear after delivery. GDM is curable, but requires careful medical supervision during pregnancy.
Although GDM is temporary, if not handled properly can harm the fetus or the mother's health. Risks that can be experienced by the baby include macrosomia (high infant weight / above normal), congenital heart disease and central nervous system abnormalities, and skeletal muscle defects. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. Hyperbilirubinemia may result from damage to red blood cells. In severe cases, death may occur before birth, most commonly occurs as a result of poor placental perfusion due to vascular damage. Induction of pregnancy may be indicated with decreased placental function. Cesarean surgery can be done if there are signs that the fetus is in danger or increased risk of injury associated with macrosomia, such as shoulder dystocia.
Complication
Long-term complications include cardiovascular disease (multiple risk), chronic renal failure (major cause of dialysis), retinal damage which can lead to blindness, and nerve damage that can cause impotence and gangrene with risk of amputation. More serious complications are more common when poor control of blood sugar levels.
Diabetic ketoacidosis
In patients with type I diabetes, symptoms develop suddenly and can develop rapidly into a condition called diabetic ketoacidosis. Sugar levels in the blood is high but because most of the cells can not use glucose without insulin, so these cells take energy from other sources. Fat cells are broken down and produces ketones, which are toxic chemical compounds that can cause the blood to become acidic (ketoacidosis). The early symptoms of diabetic ketoacidosis is thirst and frequent urination, nausea, vomiting, fatigue and abdominal pain (especially in children). Breathing becomes deep and rapid as the body attempts to repair the blood acidity. Patient breath smells like the smell of acetone. Without treatment, diabetic ketoacidosis could develop into a coma, sometimes within just a few hours. Even after starting insulin therapy, patients with type I diabetes may develop ketoacidosis if they miss a single injection of insulin, or experiencing stress due to infection, a serious accident or illness. Type II diabetics may not show symptoms for several years. If the more severe insulin deficiency, hence the symptoms of frequent urination and thirst. Ketoacidosis is rare. If the blood sugar levels are very high (up to more than 1,000 mg / dL, usually caused by stress, such as infections or drugs), then the patient will experience severe dehydration, which can cause mental confusion, dizziness , seizures and coma in a condition called hyperosmolar hyperglycemic, non-ketotik.
Hypoglycemia
Handling
Patients who are sufficiently controlled by the setting just is not having trouble eating when fasting. Patients who are sufficiently controlled with a single dose of the drug is also not difficult to fast. Drugs given during fasting. For controlled with oral hypoglycemic drugs (Oho) high doses, the drug is administered at a dose before Iftar meal is greater than the dose. For the use of insulin, insulin use medium term given when breaking it.
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