Chapter 52 Diabetes mellitus: complications
For ease of discussion, complications are divided into three groups: acute, chronic and infectious.
Acute complications
Diabetic ketoacidosis. Lipolysis is a characteristic of insulin lack (Ch. 51). Released free fatty acids are converted in the liver to ketone bodies (e.g. acetoacetate, acetone and 3-hydroxybutyrate). These substances are acidic and release hydrogen ions, causing metabolic acidosis. The combination of excess ketone bodies (ketosis) and acidosis is called ketoacidosis, and is usually seen in type 1 diabetes.
Hyperosmolar non-ketotic syndrome. This condition typically occurs in older patients with type 2 diabetes. It is characterized by hyperglycaemia and dehydration. A typical scenario is a patient who does not drink enough water to compensate for the urinary losses through osmotic diuresis; the consequence is a rise in serum osmolality. Ketoacidosis is minimal or absent.
Hypoglycaemia. This is a complication seen in treated diabetics who take insulin (or occasionally other hypoglycaemic agents) in excess of requirements. The resultant fall in blood glucose can cause mental symptoms, hunger, palpitations, sweating, abnormalities of behaviour and convulsions. In severe hypoglycaemia, patients may present with coma, but this must not be confused with the coma caused by ketoacidosis in untreated diabetes.
Chronic complications
Glycosylation of proteins. Glucose can bind to proteins by chemical reactions that do not depend on enzymes (non-enzymatic glycosylation), and this process may be important in the pathogenesis of diabetic complications (Fig. 3.52.1). The amount of non-enzymatically glycosylated protein in the body is directly proportional to the level of blood glucose. This phenomenon is exploited in the glycosylated haemoglobin (HbA1c) test, in which the level of circulating HbA1c is used as a measure of the average blood glucose over the previous few weeks, and thus as an indication of the control of blood glucose achieved by a diabetic patient.
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