Diseases of the endocrine portion of the pancreas

Diabetes mellitus and tumors from the endocrine cells of the islets of Langerhans (insulinoma, gastrinoma) are referred to diseases of ECPR.
Diabetes mellitus is a chronic disease caused by absolute or relative insulin deficiency, leading to disruption of all types of metabolism, primarily carbohydrate. Diabetes mellitus is the most common endocrine disease that, according to WHO, affects more than 100 million people worldwide. It should be noted that the incidence of diabetes mellitus (DM) in economically developed countries is increasing annually by 6-10%. In this regard, diabetes, along with cardiovascular diseases and cancer diseases, was included in the group of diseases that are the most frequent causes of death and disability of patients.
Diabetes is a Greek word used to refer to diseases involving the formation of a large amount of urine, polyuria. Diabetes in Greek is a siphon or the process of fluid flow through. In the XVIII century, it was found that in most cases of diabetes, urine contains sugar, and this type of diabetes was called diabetes mellitus – diabetes melitus from Latin mellitus (sweetened with honey) as opposed to diabetes insipidus – diabetes insipidus, in which polyuria is not combined with glucosuria.
SD classification. In accordance with the WHO classification (1999), type I diabetes is identified, which is manifested by destruction of the & # 946; cells of pancreatic islets with absolute insulin deficiency (autoimmune and idiopathic);Type II diabetes, which is based on changes in & # 946; cells, leading to insufficiency and insulin resistance; other specific types of diabetes – genetic defects in the action of insulin, unusual forms of immune mediated diabetes;gestational diabetes (pregnant diabetes).
In diabetes type I, there are two types: immune and non-immune. The basis of immune diabetes is destruction of & # 946; -cells by cells of the immune system. In most cases, antibodies to glutamate decarboxylase (marker & # 946; cells of islets of Langerhans), GAD65, islet cells or insulin are detected. The disease is strictly associated with tissue antigens HLA2RH, HLADR3 and other autoimmune diseases, such as Graves’ disease, Hashimoto, Addison. Non-immune type I diabetes is secondary and complicates, for example, pancreatitis.

Type II diabetes mellitus (insulin-independent diabetes) is a group of heterogeneous disorders of carbohydrate metabolism and this explains the lack of a unified generally accepted theory of the pathogenesis of this disease. Genetic aspects of NIDDM in the development of the disease are confirmed by the following facts: in identical twins, NIDDM almost always develops (95-100%), but the genetic defect that determines the development of NIDDM is not yet fully decoded. However, there are facts showing that two independent genes are involved in the pathogenesis of NIDDM: one is responsible for the violation of insulin secretion, and the second is responsible for the development of insulin resistance. The option of having a common defect in the glucose recognition system of &-cells or peripheral tissues is also considered, as a result of which there is either a decrease in glucose transport or a decrease in the glucose-stimulated response of-cells. The risk of developing type II diabetes increases from 2 to 6 times in the presence of diabetes in parents or next of kin. The risk of developing NIDDM is doubled in obesity I grade, 5 times in moderate obesity, in cases of grade III obesity, the risk increases 10 times! Of particular importance for the development of NIDDM is obesity with the deposition of fat in the abdominal area – abdominal fat distribution. It should be noted that this fat distribution is more closely related to the development of metabolic disorders, including hyperinsulinemia, hypertension, hypertriglyceridemia, insulin resistance and type II diabetes, than the peripheral fat distribution or its distribution in typical parts of the body.

In recent years, the hypothesis of a “deficient” phenotype has attracted considerable interest: malnutrition during the prenatal period or early postnatal period is one of the main reasons for the slow development of the endocrine function of the pancreas and susceptibility to NIDDM.
Metabolic disorders in diabetes type I are diverse: insulin deficiency leads to hyperglycemia, glycosuria, polyuria, a decrease in circulating blood volume, the development of diabetic coma. Insulin deficiency leads to increased lipolysis, increased fatty acid levels, and ketoacidosis.
The classic symptoms of type I diabetes are polyuria, polydipsia, polyphagia with paradoxical weight loss. The main visceral manifestations of diabetes are peripheral and autonomic neuropathy, as well as vascular changes.

Table 1 shows the main differential diagnostic characters of diabetes type I and II.
Pathomorphology of diabetes. Regardless of the form of diabetes in most patients with diabetes for decades, morphological changes in the vessels of the microvasculature (increased permeability of the basement membranes, plasmogram, hyalinosis of small arteries and capillaries of the muscles, skin, retina, nerve trunks) are detected. Such changes in the vessels of the microvasculature are included in the concept of diabetic microangiopathy. The main cause of microangiopathy is hyperglycemia. The morphological manifestations of diabetic microangiopathy in the kidneys are most pronounced and have specific characteristics. They are represented by diabetic glomerulonephritis and glomerulosclerosis, which are based on the proliferation of mesangial cells in response to the clogging of mesangium by metabolic products and immune complexes. In the final, the hyalinosis of mesangia and the death of glomeruli (Kimelstil-Willesen syndrome) develop.

Macroangiopathy is manifested by atherosclerosis of muscular and muscular-elastic arteries.
Changes in the pancreas in diabetes affect the pancreatic islets (they decrease in size, the number of islets decreases); the pancreas itself is reduced in size, there is its lipomatosis and sclerosis.
Typically, a change in the liver in diabetes in the form of its increase, liver cell obesity (fatty degeneration of hepatocytes), glycogen in the liver cells is not detected.
In the pancreatic islets, leukocyte infiltration is detected, most often in the form of lymphoid infiltration, which is localized both inside the islets (insulitis) and around them. Insulitis is more commonly detected in young patients with a short history of the disease. Another option, eosinophilic insulitis, is typical of newborns with diabetes who die immediately or shortly after birth (NIDDM).
In patients with NIDDM, amyloidosis can be detected in the islets of the pancreas, then sclerosis and fibrosis of the islets naturally develops. Patients with a long-existing diabetes develop peripheral neuropathy, affecting the motor and sensory nerves of the lower extremities. Morphologically, neuropathy is characterized by damage to Schwann’s nerve shells, destruction of myelin and damage to axons. In some cases, peripheral neuropathy is accompanied by a violation of the innervation of the pelvic organs (autonomic neuropathy); clinically in patients with dysfunction of the intestine, bladder, impotence.
Tumors from the endocrine cells of the islets of Langerhans. Pancreatic islets (islets of Langerhans) are scattered throughout the pancreas, but most of them are in the distal part (tail). Tumors from the cells of the islets of Langerhans are relatively rare and may be benign and malignant, functioning and nonfunctioning. Insulin-producing, gastrin-producing tumors, type and glucagon, are distinguished from functioning adenomas.

The insulin-producing tumor (insulinoma) is derived from & # 946; cells of the islets of Langerhans and is usually located in the distal 2/3 of the pancreas, less often can be localized in the head of the gland. In cases of ectopia of the pancreatic islets in the wall of the duodenum 12, the tumor is localized in the wall of the intestine. Insulinoma produces a large amount of insulin, with the result that the patient develops hypoglycemia, which is accompanied by dizziness, weakness, eccentric behavior, and in severe cases, coma. 50% insulin is benign. Most of them are solitary tumors, however, in 5% of cases, patients suffer from meningitis syndrome. Microscopically insulinoma has a solid structure, consists of cells similar to the cells of the islets of Langerhans. Sometimes dystrophic changes, hemorrhages and necrosis are observed in the tumor, which are located in the center of the tumor growth. Insulinoma can be malignant, which is manifested by signs of germination of the capsule and vessel walls, the appearance of mitoses and metastases in the regional lymph nodes and the liver.

Gastrinoma (gastrin-producing tumor) is localized both in the pancreas and in the wall of the duodenum. With it, patients develop Zollinger-Ellison syndrome. Gastrin, produced by tumor cells, causes hyperplasia of the parietal cells of the stomach, resulting in the formation of hydrochloric acid increases by 20 times, which leads to the development of multiple peptic ulcers of the stomach. 60-70% of gastrin are malignant tumors, in 5-10% of patients, meningitis syndrome is detected.
VIPoma (vipoma) – a tumor growing from cells that produce vasoactive intestinal polypeptide (VIP). When hyperproduction of this polypeptide by tumor cells develops water diarrhea syndrome. In patients with this disease, hypokalemia and achlorhydria are noted, these electrolyte disorders can lead the patient to death. Vipoma most often (80%) are malignant tumors.

Glucagonoma is a tumor from; cells of the islets of Langerhans. Clinically causes the development of the syndrome, including diabetes mellitus, skin necrosis, stomatitis and anemia. Most of the glucagon are malignant tumors.

local_offerevent_note January 17, 2020

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