Starting with A for "ACE inhibitor" and continuing through to Y for "Yolk Sac Tumour", we give you succinct explanations for scientific and medical terms in clear and simple words.
- Type 2 diabetesDefinition
also known as diabetes mellitus type 2
Type 2 diabetes is a chronic progressive disease of the islet cells in the pancreas which produce insulin, leading to a permanent increase in concentrations of blood sugar (hyperglycaemia). The disease mostly develops in older people and is therefore known as adult-onset diabetes. Forms: Type 2a without and type 2b with overweight. A large proportion of type 2 diabetics are overweight.
The syndrome is not uniform. The lack of sensitivity to insulin can be inherited or acquired. The essential factor in the development of the disease is often pathological overweight and the connected way of life, particularly when the overweight is coupled to protracted high blood sugar and fat concentrations and high blood pressure (cf. metabolic syndrome).
Course of the disease
The first symptom is the reduced sensitivity of the target tissue (such as the muscles) to insulin, the hormone which reduces blood sugar (insulin resistance). This is coupled to relative or absolute insulin deficiency, often together with protracted and excessive nutritional intake of glucose. The effects of low levels of insulin include reduction in cellular glucose uptake, reduction in glucose oxidation to produce energy, inhibition of the formation of glycogen and increase in the production of cholesterol. Insulin deficiency blocks cellular absorption of glucose and causes a general decrease in sugar oxidation (so-called low utilisation). At the same time, glucose formation (glucogenesis) is increased. The coupling of these two processes leads to the symptoms of type 2 diabetes. There are interconnected complex disturbances in carbohydrate, fat and protein metabolism and electrolyte, water and acid-base balance. The reduced efficacy of insulin together with the raised blood sugar lead to excessive insulin production. With time, raised insulin concentrations coupled to insulin resistance exhaust the ability of the islets of Langerhans to produce insulin, so that finally less insulin is produced. In this way type 2 diabetes can become insulin-dependent, in other words treatment with insulin required.
The symptoms depend on the extent and duration of the insulin deficiency. The condition often develops slowly and may not be noticed. Once the blood glucose concentrations are too high for reabsorption, glucose is excreted in the urine (glucosuria); dehydration and abnormal thirst develop. The dehydration and the resulting rise in blood salt concentrations can lead to temporary visual problems. Further symptoms include weakness in mild cases, but may extend to hyperosmolar coma (cf. diabetic coma).
In the long term, the condition causes abnormalities in the perfusion of small arterial blood vessels. This then can lead to damage to the eyes and visual impairment (diabetic retinopathy), to impairment in renal function (diabetic glomerulosclerosis), to neurological disease and, for example, to diabetic foot. Disease of the intermediate and larger arteries is mostly seen as arteriosclerosis, with increased risks of stroke and occlusive arterial disease, coronary heart disease and myocardial infarct. Cf. diabetic angiopathies.
In healthy individuals blood sugar concentrations are about 110 mg/dl, rising to 140 mg/dl after food. Blood or possibly urine samples may be used to detect increases in blood sugar. Blood glucose concentrations measured at least 8 hours after the last food (fasting blood sugar) may normally not lie above 126 mg/dl. Otherwise diabetic metabolism can be assumed. Glucose is excreted in the urine (glucosuria) at blood sugar concentrations from about 180 mg/dl. Detection with a test strip is possible. Further diagnostic measures include the glucose tolerance test, in which blood sugar concentrations are measured with blood or urine samples under standard conditions.
The aim of the therapy is the optimal metabolic control. If possible, blood sugar should be under 140 mg/dl, both fasting and after food. Alternatively glycohaemoglobins (HbA1c) can be reduced to less than 7.0 to 7.5%. Initially it is attempted to reach these goals with basic treatment - weight loss when there is overweight, diet and physical activity. Drug treatment should only be started two to four months after these measures have been exhausted. The exception here is the patient with acute complications or severely abnormal metabolism with ketoacidosis and dehydration.
2. Sulphonylureas increase the release of body insulin and are the first-line drugs for patients with type 2a diabetes, i.e. no overweight but absolute insulin deficiency. The first-line drugs for patients with type 2b diabetes (overweight patients) are drugs to reduce blood sugar.
3. Overweight patients with raised blood insulin from increased insulin production (hyperinsulinism) can be successfully treated with combinations of different drugs to reduce blood sugar. These can complement each other and overcome insulin resistance.
4. Treatment with insulin should not be too late. A single injection with insulin in the morning or evening, in addition to previous treatment, may be adequate for a long time. This combination may fail to produce adequate control of blood sugar, particularly if there are late complications. If this is the case, conventional or intense conventional insulin therapy must be attempted. Additional treatment with oral antidiabetic drugs is then usually no longer necessary.
5. New Developments: 1. Like sulphonylureas, aminoacid analogues cause rapid and intense release of insulin. Their duration of action may be shorter, which could lead to less protracted increases in insulin levels after meals. 2. Insulin sensitisers increase muscular insulin sensitivity, hepatic gluconeogenesis and blood fat values, reducing the risk of arteriosclerosis. They also tend to lower blood pressure. They can quite generally prevent the development of the metabolic syndrome in type 2 diabetes.
Structural training programs based on behavioural therapeutic concepts have been developed to overcome the severe psychic stress caused by the disease. These include basic knowledge of the disease and instruction on hygiene, foot care, nutrition and drug treatment (particularly insulin). Loss of potency and libido impair the quality of life and self-confidence and require special attention.
1. Independent control of metabolism, including urinary glucose concentrations in simple cases and blood sugar during insulin treatment. 2. Insulin-dependent patients can adjust the dose of insulin themselves with the help of measurements of blood sugar. 3. Expert foot care and continual control of the feet for calluses, sites of pressure and wounds may prevent the development of the diabetic foot. Regular control of the back of the eye can lead to the recognition of early changes which can develop to diabetic retinopathy and sight loss.
Measures for prevention (or improvement): 1. Weight loss from a marked reduction in calorie intake often leads to a dramatic improvement in overall metabolism. 2. Important components of treatment and prevention include carbohydrate-rich food (ca. 50% of total energy), a high proportion of fats with unsaturated fatty acids (olive or rape oil), strict restriction to the intake of saturated fatty acids (milk or slaughter fat) and high levels of roughage. 3. Oats-fruit days or rice-fruit days are very effective in the treatment of newly diagnosed and relatively mild cases. 4. 20-30 Minutes endurance training each day (jogging, walking, swimming or cycling) can bring great improvements in both the general condition and in the insulin sensitivity of the musculature. 5. Regular control of the blood sugar concentration.
Glossary entries: Roche and Walter de Gruyter, Berlin