The pathophysiology of diabetes

The pathophysiology of diabetes

Introduction
Learning basic knowledge of the pathophysiology of diabetes depends on knowledge of glucose metabolism and insulin action. Food consumption, the breakdown of carbohydrates into glucose, glucose in the intestine. Glucose is absorbed in the blood glucose levels of elevated blood. This increased blood sugar, stimulating insulin secretion from pancreatic β-cells. Most cells require insulin, allowing glucose to enter. Insulin binding to specific cell receptors, promoting cell glucose, using glucose as energy. The increase in pancreatic insulin secretion at lower levels of blood glucose results in cellular glucose and subsequent use. Lowering of blood sugar, which results in secretion of insulin.

If the change of the production and secretion of insulin, disease, blood glucose kinetics will change. If the reduction of the production of insulin, glucose in the cells is suppressed, resulting in hyperglycemia. The target cells of insulin secretion from the pancreas, but not the correct, you will see the same effect. If the increased secretion of insulin, glucose levels in the blood can become too low (hypoglycaemia), large amounts of glucose into cells of tissues in the blood of small debris.

After the meal, the amount of glucose decomposition of carbohydrates often exceeds cellular glucose. Excess glucose stored as glycogen in the liver as a deposit and ready for future use. The energy required, storage of glycogen in the liver is converted to glucose by glycogenolysis, the elevated blood glucose level, and provides the energy source of the desired cell. The liver produces glucose from fat (fatty acid) and proteins (amino acids), via the process of gluconeogenesis. Glycogenolysis and gluconeogenesis, to improve the levels of blood sugar. Therefore, the blood glucose monitoring complex interactions between the gastrointestinal tract, pancreas, liver.

A variety of hormones can affect blood sugar. Insulin is the blood glucose level just lower of the hormone. Counter-regulatory hormones such as glucagon, catecholamines, growth hormone, thyroid hormone, glucocorticoids increase blood glucose levels, as well as all acts of the other effects.


Diabetes mellitus type 1

The basic pathophysiologic defects of type 1 diabetes is an autoimmune islet β-cell destruction. This destruction, the person has an absolute deficiency of insulin and insulin is not in production. Is considered to be triggered by environmental events, such as viral infections autoimmune destruction of pancreatic β cells. Genetically certain predisposing factors that increase risk, such as autoimmune phenomena.

The incidence of type 1 diabetes is usually sudden. It usually occurs before the age of 30, at any age, but may be diagnostic. Most patients with type 1 diabetes with normal weight or lean body. Because patients with type 1 diabetes, the insulin-producing pancreas no longer entirely dependent on exogenous insulin injections for survival. People with type 1 diabetes are highly susceptible to diabetic ketoacidosis. Because the pancreas does not produce insulin, glucose can not enter the cell and remains in the blood. In order to meet the energy needs of the cells, lipolysis lipolysis, free glycerol and free fatty acids. The conversion of glycerol to glucose for cellular use. Fatty acid concentration is converted into a ketone-ketone, bodily fluids and to reduce the hydrogen ion concentration (pH). The download ketonuria, and accompanied by lots of water. The ketones in the accumulation of body fluids, the lower the pH, electrolyte loss, dehydration, excessive urination, and give rise to changes in bicarbonate buffer system in diabetic ketoacidosis (DKA). Untreated DKA can lead to coma or death.

Many patients initially diagnosed with type 1 diabetes, diabetic ketoacidosis hospitalized. Diabetes or known pressure during infection can lead to CAD. However, more often, from blood glucose daily in poor control of the outcome of diabetic ketoacidosis. Several days or longer, due to the insufficient administration of insulin or an excess of glucose uptake remains severe hyperglycemia patients are prone to develop diabetic ketoacidosis.



Type 2 diabetes mellitus

Diabetics approximately 90% of Americans suffer from type 2 diabetes. The incidence of type 2 diabetes is higher in African Americans, Native Americans, Hispanic Americans, Pacific Islanders than in Caucasians. Most type 2 diabetes are overweight, most of them were diagnosed in adults. Type 2 diabetes is a series of genetic factors than type 1 saw. Although the concordance rate between monozygotic twins with type 1 diabetes is approximately 30-50%, and the tax rate is approximately 90% of patients with type 2 diabetes. Although type 2 diabetes has a strong genetic predisposition, not a single genetic defect has been found. Besides the impact of genetic risk factors and acquired for type 2 diabetes, obesity, age and inactive lifestyle.

Type 2 diabetes does not mean basic defect pathophysiological autoimmune destruction of pancreatic β cells. In contrast, type 2 diabetes characterized in that the three obstacles by the following: (1) the outer peripheral resistance to insulin, especially in muscle cells, (2) to increase the production of glucose by the liver ( 3) changing the secretion of pancreatic insulin. Increased insulin resistance tissue usually occurs first, and optionally followed by impaired insulin secretion. Pancreas to produce insulin, but the insulin resistance to prevent inappropriate use at the cellular level. Glucose can not enter target cells, and accumulate in the blood, resulting in hyperglycemia. High blood sugar often stimulate the development and increase the production of insulin secretion by the pancreas, diabetes type 2 patients tend to have an excessive production of insulin (hyperinsulinemia). Through the years, the insulin-producing pancreas typically reduced below normal levels. Besides blood sugar in type 2 diabetes patients tend to have a group of diseases known as the syndrome of insulin resistance or syndrome X

Obesity contributes significantly to insulin resistance, even in the absence of diabetes. In fact, weight loss is the cornerstone of the treatment of obese patients with type 2 diabetes. Weight loss typically reduce insulin resistance. Obesity can also be seen in young individuals of type 2 diabetes in the last 10-20 years, the incidence has increased dramatically in the United States. Once thought to be a disease of adults, type 2 diabetes is directly related to the increase in the average weight of children and young adults, young America during this time.

Usually a slow onset of type 2 diabetes may remain undiagnosed for years. About half of people with type 2 diabetes who do not know their own disease. Unfortunately, the nature of the disease insidious to allow negative impact applied early prolonged hyperglycemia major organ systems. Many patients with type 2 diabetes is diagnosed, the complications of diabetes. Survival does not require exogenous insulin in patients with type 2 diabetes, because insulin is still produced. However, insulin injections are usually an integral part of the medical treatment of type 2 diabetes. Unlike type 1 diabetes, type 2 diabetes, individuals are generally resistant, the CAD, the insulin your pancreas is usually sufficient to prevent the development and production of ketone bodies generated. Physiological stress can cause severe diabetic ketoacidosis in patients with type 2 diabetes. In the long term can result in severe acidosis nonketotic hyperosmolar hyperglycemia. Hyperglycemia resulting from the excretion of large amounts of glucose, accompanied by the loss of water. If fluid is not replaced, can lead to dehydration, acidosis and electrolyte imbalance.



Gestational diabetes

Gestational diabetes occurred 4% of pregnancies in the United States. It usually occurs in the third trimester of pregnancy, and a significant increase in perinatal morbidity and mortality.11 correct diagnosis and treatment of gestational diabetes improve pregnancy outcomes. , Pathophysiology of gestational diabetes and insulin resistance and type 2 diabetes. Most patients with gestational diabetes return to normal glucose tolerance after delivery, but women with a history of gestational diabetes, 30-50% in 10 years, the development of type 2 diabetes.

Impaired glucose tolerance and fasting glucose
The condition known as impaired glucose tolerance (IGT) and impaired fasting glucose (IFG), which represents between diabetes and metabolic status normal blood sugar. IFG increased fasting glucose levels, food intake, usually have a normal level. IGT with normal glucose tolerance, most of the time, but hyperglycemia can become large glucose load. IGT and IFG not considered clinical entity, in contrast, is a risk factor for diabetes in the future. IFG and IGT pathophysiological mainly involves endogenous insulin secretion and insulin resistance, and in most patients is normal. Approximately 30% and 40% IGT and IFG and personal development within 10 years after the onset of type 2 diabetes.