Respiratory organs, digestive system for diabetes. Diabetes mellitus with hemochromatosis

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Respiratory organs, digestive system for diabetes. Diabetes mellitus with hemochromatosis

Respiratory organs in diabetes mellitus change due to the dryness of the mucous membrane of the larynx, trachea, and bronchi. Alveoli of the lungs can undergo hyalinosis. A tendency to bronchitis, pneumonia, lung abscesses is detected. At a young age in diabetes mellitus, when the body’s resistance is reduced, often pulmonary tuberculosis develops as a concomitant disease. Diabetes mellitus with pulmonary tuberculosis is worse, the course of pulmonary tuberculosis is severe. Infiltrative forms, caverns, pneumonia are observed; pleurisy. Massive specific anti-tuberculosis therapy in combination with insulin therapy stops the tuberculosis process. 

Dry lips and mucous membranes of the oral cavity , cracks in the corners of the mouth, dry, coated raspberry-colored tongue can be seen in patients with severe diabetes mellitus. Patients at a young age have carious teeth that are easily destroyed and fall out. Gums are loosening (gingivitis, pyorrhea). The motor function of the stomach is disturbed. The mucous membrane of the stomach is hyperplastic. In violation of vascular permeability, bleeding is possible. In diabetes mellitus, cases of peptic ulcer are described. Patients complain of pain in the epigastric region. 

Nausea , vomiting are noted with ketoacidosis. The acidity of the gastric juice increases, the enzyme metabolism is disrupted. The external secretory function of the pancreas is reduced. Lipocaic substance is not produced sufficiently.

In some cases , achilles and hypacid gastritis can be noted in patients. Impaired enzyme metabolism promotes the development of enterocolitis. Fermentation and absorption of food in the intestine are disrupted, flatulence occurs.  

The liver is especially affected by diabetes . Pathological changes in all types of metabolism entail a violation of the liver. Insulin deficiency leads to a decrease in glycogen formation, an intensive release of glucose into the blood stream from the liver, and subsequent fatty infiltration. Insufficiency of lipocaic substance exacerbates the pathological state of fat metabolism in the liver and promotes ketosis. The pigment-forming function of the liver and the barrier are impaired. 

Degenerative changes occur in the liver cells and biliary dyskinesia is observed. Diabetic hepatitis is complicated by cholecystitis and reactive pancreatitis. Cirrhosis in patients with diabetes is relatively rare. 

Children with diabetes have Moriak syndrome, which is characterized by hepatomegaly, stunted growth and sexual development. Weight loss is not observed, more often subcutaneous layer is well defined. The course of diabetes is severe. Often there is high hyperglycemia, glucosuria and ketoacidosis. 

Heavy flows diabetes hemochromatosis – bronze diabetes, which is characterized by the triad. With bronze diabetes mellitus against the background of primary liver cirrhosis, hemochromatosis occurs with skin pigmentation. Excess iron in the blood leads to impregnation of parenchymal organs. Iron in the form of crystals is deposited in the islets of Langerhans, adrenal cortex, sex glands. Severe diabetes is exacerbated by increasing liver failure. Patients die in cases of diabetic and hepatic coma. In infectious hepatitis (Botkin’s disease), severe diabetes mellitus is often detected with a tendency to ketoacidosis.  

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