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.
- T-Cell LymphomaThis is a sort of blood cancer in which there is a pathological increase in T-lymphocytes in the blood and lymph nodes and in other parts of the body, particularly the skin. Cf. Lymphoma.
- T-cellsalso T-lymphocytes
T-cells belong to the white blood cells. They are formed in bone marrow, lymph nodes, thymus and spleen and are responsible for cell-mediated immunity in the body. They possess receptors with the function of antibodies on their surface, which allow them to bind foreign substances directly, which they can then destroy.
- T-Helper CellsT-helper cells are specialised T-cells (T-lymphocytes) and are therefore white blood cells. T-helper cells support the B-cells in their function of producing antibodies and are also involved in the immune response themselves. During an HIV infection, the T-helper cells are themselves attacked by the virus, so that they are no longer capable of performing their function within the immune system. The course of the treatment of HIV is monitored by determining the number of T-helper cells. If the number drops below 250 per microlitre, the outlook is regarded as poor.
- T-Killer CellsAlso cytotoxic t-cells.
Special group of T-cells, which can directly destroy sick body cells. Their main function is to destroy infected cells or cells which have been malignantly transformed. They achieve this by recognising both the characteristics of body cells and of viruses or of malignant changes on the surface of the cells. They cannot only destroy sick cells, but also other cells of the immune system, which prevents an excessive immune response.
- T-LymphocytesCf. T-cells.
- T-Suppressor Cellsalso CD8+ Cells
Specialised T-cells which inhibit the activity of other cells of the immune system, particularly T-helper cells and B-cells. They serve to regulate the immune response and, for example, to stop an excessive immune response. In an HIV infection the T-suppressor cells first increase and then later decrease. There is a receptor on the surface of the T-suppressor cells which is known as the CD8 cell marker and which distinguishes them from T-helper cells, which bear the CD4 cell marker.
- tachycardiaa condition in which the resting heart rate exceeds 100 beats per minute (compared with the normal rate of 60 to 80 beats per minute ); tachycardia is a compensatory mechanism for hypoxia or inadequate tissue oxygenation
- TeleradiotherapyRadiation with a large distance between the radiation source and skin, e.g. in whole body radiotherapy. Cf. Radiotherapy.
- TestosteroneMost potent and most important male sex hormone (androgens). It is of decisive importance for the development of the male individual. Testosterone influences not only the development of the male sex organs, but also secondary male sexual characteristics, such as beard growth and muscular mass. It also steers sperm production. Testosterone is responsible for growth in length and the maturity of the skeleton. If the testosterone concentration in a man is too low, this is believed to favour osteoporosis. If the testosterone level in a woman is too high, this leads to symptoms of virilisation, such as increased hair growth in the male pattern, acne, a deeper voice and sometimes regression of the female sexual characteristics.
- thalassemiaThe term thalassemia denotes inherited disorders involving defective hematopoiesis. A gene defect results in the production of too little hemoglobin A, instead of which other globins are produced, which can accumulate in the body with toxic effect. In all forms of thalassemia the red blood cells have a shorter life span in the blood. The first clinical sign, usually noticed by the parents, is therefore pallor and anemia.
- Therapy Interruptionsee Interval Therapy.
- Therapy, AlternativeTherapy which does not use the methods of conventional medicine. Many alternative methods are scientifically controversial. The efficacy of some procedures (e.g. from traditional Chinese medicine) in some diseases has now been demonstrated or is now being examined (e.g. acupuncture)
- ThiazolidindionesThiazolidindiones are oral antidiabetic drugs which act as insulin sensitisers, which means that they improve the insulin-dependent cellular uptake of glucose. They stimulate certain glucose transporters and, for example, inhibit leptin, which is an insulin resistance factor. Use in type 2 diabetes.
- threoninean amino acid (C4H9NO3) that is found in various proteins; must be obtained from the diet
- thrombocytesblood platelets
- ThromboembolismThromboembolism is the acute occlusion of veins or arteries by a washed up thrombus. It is the most frequent form of embolism. Cf. thrombosis, lung embolism.
- ThrombolysisDissolution of a thrombus or embolism by the action of fibrinolytic drugs, which are drugs which dissolve thrombi. These either act in the whole body or are introduced directly into the site of occlusion with the vessel catheter , sometimes in combination with angioplasty (expansion of the occluded site with a balloon catheter). Thrombolysis is usually only short term and is followed by treatment with drugs to stop blood coagulation (anticoagulants).
Myocardial infarction, pulmonary embolism, occlusive arterial disease.
Tendency to bleed, pregnancy (up to week 18), high blood pressure (hypertension), stroke, danger of bleeding from large ulcers, large wounds, previous operations and injections into a muscle.
- ThrombosisComplete or partial occlusion of arteries or veins or cavities of the heart by blood coagulation, followed by the formation of clots, which are aggregates of thrombocytes (blood platelets) and fibrin. This is a large water-insoluble protein which has many crosslinks and which is the final product of blood coagulation.
Mode of origin
Three essential factors support the formation of a thrombus or blood clot: 1. Damage to the vessel walls, e.g. from inflammation, arteriosclerosis or injury from external force; 2. decreased blood velocity, e.g. in varicose veins, operation, inadequate pumping by the heart; 3. Changes in blood composition, e.g. increased tendency to clot, increased tendency of the thromboyctes to aggregate.
- thromboticrelating to thrombosis
- ThrombusBlood clot arising from blood coagulation in the vessels or on the wall of the heart, e.g. in the atrium. Cf. embolism, thrombosis, thrombolysis
1. A stratified or white thrombus arises from deposition of blood platelets (thrombocytes) on a defect in the vessel wall. It consist of a framework of piles of thrombocytes which are surrounded by fibrin. This is a large water-insoluble protein which has many crosslinks and which is the final product of blood coagulation. The thrombus remains fixed to the vessel wall and rarely occurs in isolation. 2. An agglutinative or red thrombus arises as a result of blood coagulation when the blood flows too slowly or not at all. Sheets of fibrin form parallel to the vessel and between these are red and white blood cells (erythrocytes and leucocytes) in the same distribution as in blood. The agglutinative thrombus totally fills the vessel, with occlusion or obliteration, but does not stick to the vessel wall. Bits of it can therefore easily be released and there is danger of embolism. 3. Mixed thrombus. Consist of a head area (stratified thrombus) and a tail area (agglutinative thrombus)
- Throttled kidneyName for kidney with abnormal perfusion, leading to high blood pressure (see renal hypertension). The low perfusion can lead to atrophied kidneys.
- Thrush OesophagitisThrush oesophagitis is an infection of the oesophagus with the fungus Candida albicans. The disease mostly occurs in patients with a weakened immune system, particularly HIV patients. It tends to occur repeatedly. It is treated with antibiotics.
- ThymusGland which lies behind the sternum and which is part of the immune system. The thymus is mostly active in childhood and decreases in size after puberty. The T-cells which are used for cell-mediated immunity are given their specific stamp in the thymus.
- Thyreocalcitoninsee calcitonin
- ThyroidGlandula thyroidea
This is a gland which forms hormones and which lies under the larynx. It covers the front half of the circumference of the windpipe and is butterfly-shaped. The weight in adults is 20-60 g. The thyroid uses iodide from the blood to form the hormones triiodothyronine (T3) and thyroxine (T4) in a series of steps. These are released into the blood as required. The thyroid also forms the hormone calcitonin.
The hormones T3 and T4 increase oxygen consumption in the tissues and thus basic metabolism and heat production. They affect carbohydrate, protein and fat metabolism. The consequences of this include effects on growth and development. Calcitonin is important in calcium metabolism. It inhibits calcium release from bones and reduces calcium blood concentration in this way.
The release of the hormones T3 and T4 is regulated by the hormones of the hypothalamus (TRH) and the pituitary (TSH). The concentrations of T3 and T4 in blood have feedback effects on the hypothalamus and pituitary, which then react by releasing more or less TRH or TSH.
- Thyroid CarcinomaMost frequent form of the malignant thyroid tumour, about 1% of all tumours in the thyroid.
Symptoms: In 95% of cases the thyroid carcinoma is first noticed as a nodular enlargement of the thyroid (malignant goitre). Signs of the disease include rapid occurrence and growth of a nodule in the thyroid, hoarseness, breathing problems and difficulties in swallowing, particularly in patients who are under 60. The thyroid nodules are often firm to the touch, painless and have adhered to the skin above them. Whistling sounds when breathing can develop (if the tumour presses on the windpipe). Sometimes the so-called Horner syndrome develops. This means that in one eye the pupil is reduced in size, the lid sags and the eye ball is depressed.
Causes: The causes are unknown. The risk of thyroid carcinoma may be increased by irradiation (for example during radiotherapy), particularly in childhood.
Diagnosis: Palpation, ultrasound, X-ray investigation of the thyroid with the help of radioactive substances which concentrate in tumours (thyroid scintigraphy), removal of cells from the suspicious region through the skin with a fine needle (fine needle biopsy). Possibly X-ray of the ribcage, computer tomography, nuclear spin resonance, laboratory tests of changes in thyroid hormones.
Therapy: All, or almost all, the thyroid is removed by operation, depending on the size and position of the tumour. Lymph nodes and neighbouring tissue are also removed. Radiotherapy may be performed after the operation. After the thyroid has been removed, the thyroid hormones are administered as tablets. The operation may damage a glottal nerve, which leads to hoarseness, or the parathyroid glands, which can disturb the calcium and phosphate balance.
Prognosis: The 5-year survival with good therapy is 10-90% of patients, depending on the malignancy of the tumour.
- Thyroid TumoursBenign and malignant tumours of the thyroid.
The following forms are distinguished:
Benign thyroid tumours: Tumours which originate from gland tissue, which can produce thyroid hormones. Benign tumours only rarely become malignant, but are often difficult to distinguish from malignant tumours.
Malignant thyroid tumours: these occur about twice as often in women as in men and are mostly thyroid carcinoma.
- ThyroiditisThyroiditis is inflammation of the thyroid. Acute inflammation of the thyroid can for example be caused by infection with HIV.
- titrateto gradually increase or decrease the dose of a drug until the target dose or the desired effect is achieved
- TNM ClassificationClassification of the stages of malignant tumours, as suggested by the Union internationale contre le cancer (Abb. UICC). T (tumour) stands for the size of the primary tumour, N (nodule) for the lack or presence of neighbouring lymph node metastases and M (metastases) that of distant metastases (see metastases). The addition of number denotes the size of the malignancy within the body (e.g. T1, T2 , N0, N1 , M0, M1).
A TNM classification can be made on the basis of the results of physical investigations, X-ray and endoscopy results and other relevant investigations. An additional category, C (for certainty), indicates the reliability of the findings. A second type of TNM classification is made after the operation and the examination of the tissue taken. This may change or complement the initial TNM classification, for example, with the category P (determination of the stage in tissue from the operation) or category G (degree of malignancy determined in the tissue). As an example, the TNM classification of a 2-5 cm large mammary carcinoma adhering lightly to the skin or chest muscle, with extensive and adherent lymph node metastases and with distant metastases: T2 N3 M1. The TNM categories used for gynaecological tumours have been defined so that they agree with the stages recognised by the FIGO (abb. Fédération Internationale de Gynécologie et d´Obstétrique). Cf. Tumour Classification.
- TonsilsThe tonsils are part of the lymphatic tissue. They lie in the pharynx and thus at the gate of entry of many foreign substances. They form a ring shaped defence, the lymphatic tonsillar ring. A distinction is made between 1. Palatine tonsils, 2. Pharyngeal tonsil, 3. Tubal tonsils and 4. Tongue (lingual) tonsils.
- TranscriptaseAn enzyme which is capable of transmitting into ribonucleic acid. the genetic information which is coded in the structures of desoxyribonucleic acid (DNA) This step is necessary to translate the genetic information from DNA into proteins. Cf. Transcriptase, reverse.
- Transcriptase, ReverseAn enzyme which occurs in retroviruses (see Retroviridae), which can transcribe into DNA the genetic information which is encoded in the structures of ribonucleic acid (RNA). This enzyme makes it possible for viruses to multiply.
- TranscriptionTransfer of the genetic information stored in DNA to RNA, which is supported by certain enzymes (RNA-polymerases). In higher cells (eukaryotes), transcription occurs in the cell nucleus. The resulting so-called primary transcript is complementary to the DNA matrix at a molecular level.
- transferrina protein in blood plasma capable of combining with ferric ions and transporting iron in the body
- transferrin saturationa measure of the degree to which iron atoms are bound to transferrin
- Transfusion HepatitisTransfusion hepatitis is acute inflammation of the liver caused by transmission of hepatitis C viruses in infected blood (Hepatitis, acute). It often takes a chronic course.
- Transfusion LawLaw which regulates the transmission of blood or blood components from one human to another. One aim of this is to stop diseases from being transmitted.
- transient ischemic attacka temporary reduction in the blood supply to an area of the brain , usually associated with partial blockage of an artery; neurological symptoms vary with the site and extent of the blockage
- transitional cell carcinomaa malignant tumour of the kidney that begins in the renal pelvis (the junction of ureter and kidney) and accounts for 5% to 10% of kidney tumours; also called urothelial carcinoma
- translationsynthesis of a protein sequence based on an mRNA sequence
- Treatment, PalliativePalliative treatment in contrast to cure, e.g. in the treatment of tumours which can no longer be removed by operation, or which have formed metastases, so that cure is not possible.
- Triacylglycerolssee triglycerides
- Triglyceridesalso known as triacylglcerols or neutral fats. Dietetic name: fats.
Triglycerides consist of three fatty acids, which are esterified with glycerol. They are taken up with food and split in the intestine into glycerol and free fatty acids. They are reassembled to triglycerides in the intestinal mucous membrane and transported through the lymph vessels as chylomicrons (small lipoprotein particles). They are bound in the blood to lipoproteins. Triglycerides can also be formed directly in the body, particularly in the liver, kidneys and heart muscle. These triglycerides are transported in blood as VLDL (Very Low Density Lipoproteins). Triglycerides are especially important for the body as sources of energy. They are stored as depot fat. For pathological increases in triglycerides see hypertriglyceridaemia, hyperlipoproteinaemia. Cf. lipolysis, digestion of neutral fats.
- TumourA locally restricted increase in tissue volume (growth, blastoma, neoplasia) which comes from excessive growth of endogenous tissue. The excessive growth occurs spontaneously, is uninhibited to differing degrees, is free from regulation from other parts of the body and is irreversible. This growth is generally connected to the loss of certain cell and tissue functions and is only partially or not at all under the physiological control of the organism.
Classification: 1. according to the origin of the tissue, 2. according to the biological behaviour: a) Benign tumours: these grow slowly, possess clear borders, are sometimes encapsulated in connective tissue and usually remain at their site of origin. b) Malignant tumours: These grow rapidly, do not have clear borders, and when they grow they penetrate into and destroy neighbouring tissue. They frequently form metastases. C) Semimalignant tumours. These penetrate and destroy when they grow, but do not form metastases. Benign tumours can become malignant, which means that they may be a sort of transition stage in the malignant transformation of normal cells.
In the extended sense, a tumour is any localised swelling from the accumulation of aqueous fluid in tissue (oedema), acute and chronic inflammation, restricted dilatation of an artery (aneurysm) or swelling of an organ as a result of inflammation (e.g. the so-called spleen tumour).
- Tumour AntigensAlso tumour-associated or tumour-specific antigens.
Antigens which appear in certain cell structures (cell nucleus, cytoplasm) or on the surface of tumour cells and which are also often detectable in the serum of tumour patients.
The formation of tumour antigens may be triggered by the genes of tumour viruses (e.g. Epstein Barr virus in Burkitts lymphoma and nasopharyngeal carcinoma, cf. viruses, oncogenic) or by genes of the affected cell.
Tumour antigens can be detected by specific tests, which are mostly based on antigen-antibody reactions. The occurrence of tumour antigens on the surface of tumour cells can trigger a reaction from the immune system. The control and amplification of this is the aim of the immune therapy of tumours. Antibodies and immunocompetent cells can only react with tumour antigens which are situated on the cell membrane. Tumour antigens which occur in blood serum can be exploited for diagnostic purposes as tumour markers.
- Tumour CellsCells of malignant tumours which arise from malignant changes in normal body cells. Various typical characteristic are striking in the diagnosis of cells of this sort, e.g. unusual size and/or shape of the cell nucleus, a change in the number of chromosomes and extreme variations in cell size and shape.
- Tumour ClassificationI. According to biological behaviour: 1. Benign tumours: Growths with normally developed cells and slow growth which displaces other tissues; 2. Malignant tumours with pathologically altered cells. These mostly grow rapidly into the surroundings, infiltrate and destroy neighbouring tissue and form metastases; 3. Semimalignant tumours with the tissue characteristics of malignant tumours and locally infiltrating growth, however mostly without metastases.
II. According to histology and genetics. This means that the tissues are named according to the tissue from which they originated: 1. Tumours from the epithelium, which arises from the external and internal blastodermic layer of the embryonic phase; a) benign tumours: e.g. adenomas, papillomas, polyps; b) malignant tumours: carcinomas; 2. Tumours from embryonic connective tissue (mesenchyme) a) benign tumours: e.g. lipomas, fibromas, osteomas, myomas, leiomyomas, rhabdomyomas, chondromas; b) malignant tumours: sarcomas; 3. Embryonal tumours from undifferentiated tissue: e.g. nephroblastomas, neuroblastomas, medulloblastomas, retinoblastomas, embryonal rhabdomyosarcomas, teratomas;
III. According to appearance, physiological changes and clinical course of the disease: There are various classifications for this, such as the TNM classification and grading.
- Tumour Destruction SyndromeMetabolic change after chemotherapy from the destruction of tumours of large mass or cell number. This syndrome mostly occurs in patients with cancers of the blood or of the system which forms the blood (hematopoietic system).
Symptoms: Include muscle cramp, irregular heart beat, abnormal renal function, which is caused by increased concentrations of uric acid, potassium and phosphate and a drop in serum calcium concentration.
Therapy: Administration of water and the drugs allopurinol and sodium bicarbonate.
- Tumour Irradiation, PreoperativeSupportive radiotherapy before a planned operation for malignant tumours.
Preoperative tumour irradiation should either decrease the size of the tumour, which may make a successful operation possible. Another possible aim is to devitalise or kill the tumour cells so that the risk of transferring the cells during the operation is reduced.
- Tumour Volume Doubling TimeTime in which the volume of the tumour doubles. A tumour which is clinically detectable has normally reached two thirds of its total growth time. For example the mammary carcinoma, the average tumour volume doubling time is believed to be 200 days, so that a palpable nodule (so-called early diagnosis) needs more than 15 years for its development. This is the reason that metastases are already detectable in about 20% of these cases.
- Tumour, bladderBladder tumours mostly originate from the cells which coat the bladder. They often lie at the base of the bladder, which is directed towards the perineum, but may also occur at the same time in different locations. They occur particularly frequently in older individuals. The most frequent forms are bladder papilloma and bladder carcinoma. Rarer forms are fibroma, myoma and neurofibroma. Typical signs of disease are blood in the urine (haematuria), infections of the urinary tract, frequent urinary urgency and possibly pain or feeling of pressure.
Diagnosis: The diagnosis is made on the basis of examining the cells in the urine, ultrasound, palpation, cystoscopy (mirror examination of the bladder), tissue sampling through the urethra and computer tomography.
It is necessary to distinguish this condition from carcinoma of the prostate, benign prostatic enlargement, stones in the bladder, rectal carcinoma which is growing into the bladder and gynaecological tumours.
- Tumour, Colonicsee Carcinoma, Colorectal.
- Tumour, IntestinalBenign and malignant tumours of the intestine (duodenum, small intestine, large intestine). cf. Carcinoma of the Colon, Colorectal Carcinoma.
- Tumour, Small IntestinalTumour in the small intestine.
Frequency: In all 5% of the tumours of the intestinal tract. Malignant tumours of the small intestine are about 1-3% of the malignant tumours of the digestive tract.
1. Benign tumours of the small intestine: tumours of the glands (adenomas), fat cells (lipomas), blood vessels (haemangiomas) or intestinal muscles (leiomyomas).
2. Malignant tumours of the small intestine: tumours of the glands (adenosarcomas), lymph nodes (malignant lymphoma), intestinal muscles (leiomyosarcoma) or certain cells which produce hormones (carcinoids).
Symptoms: Accumulation of air in the intestine or abdominal cavity (meteorism), seizures of pain, vomiting, palpable increase in size in the abdominal cavity. Constipation from constriction of the intestine, anaemia.
Diagnosis: X-ray investigation after enema with contrast medium, to improve the visibility of the structures in the intestine, X-ray imaging of the blood vessels (angiography), possibly operation to find the tumour.
Therapy: Operative removal of the affected section of the intestine, with malignant tumours this includes the neighbouring lymph nodes and connection of the two ends of the intestine which result.
- Tumours, BrainTumours within the skull. A distinction is made between primary brain tumours, which originate in the individual types of tissue in the brain (e.g. cerebral membranes, pituitary, nerve cells) and secondary tumours. These are either metastases* from other tumours or originate in the bone which surrounds the brain. There are four grades, depending on the malignant or benign character of the tumour.
Grade I: benign
Grade II: largely benign, survival time of 3-5 years after operation
Grade III: largely malignant, survival time of 2-3 years after operation
Grade IV: malignant, survival time of 6-15 months after operation
Frequency: Brain tumours make up 7-9% of all tumour diseases. Men are more often affected than women.
Symptoms: The symptoms depend on the site of the tumour and its rate of growth. Initially frequent symptoms are headaches, epileptic attacks, personality changes, loss of individual brain functions, such as abnormal speech and movement, and forgetfulness. Hydrocephalus (water in the brain) may develop later, because of difficulties in draining water from the brain. Other later symptoms include stroke, due to pressure on blood vessels and on the whole brain, as a result of pinching in the transition to the spinal chord. The diagnosis must distinguish this condition from inflammation, abnormal perfusion of the brain, atrophy of the brain, bleeding and parasitic diseases.
Diagnosis: Computer tomography or nuclear spin tomography of the skull (with or without contrast medium), imaging of the blood vessels (angiography) to diagnose the position and often also the type of tumour, extraction and microscopic examination of brain tissue and brain water and examination for so-called tumour markers (substances which can give indications about the presence, clinical course and prognosis of tumour diseases).
Therapy: Brain tumours are treated by operation or by radiotherapy and/or chemotherapy. If required, treatment may be started to lower the raised pressure in the brain or to treat epilepsy.
Prognosis: The chances of a cure depend on the type of tumour, how it grows and where it is situated.
- Tumours, SkinGeneral name for benign and malignant tumours which originate in all structures in the skin and in accessory tissues. Cf. Skin Cancer, Melanoma, malignant.
- Twin studyA twin study is a study which works with the so-called twins method.
- Twins methodMethod of clarifying whether and to what extent a characteristic is determined by hereditary or by environmental factors. This method is based on a comparison between the similarity or identity of a characteristic in (genetically identical) monozygotic ("identical") twins, in comparison with (partially genetically different) dizygotic ("non-identical") twins. If there is greater agreement or similarity in a characteristic with monozygotic twins and greater variability in dizygotic twins or in the general population, this speaks for the hereditary character of this characteristic.
- Type 1 diabetesalso known as diabetes mellitus type 1.
Sugar disease which results from the destruction of the beta- (or B-) cells of the pancreas. This disease mostly starts in children or young people and therefore used to be known as infantile or juvenile diabetes mellitus.
Diseases of the immune system, mostly caused by immune reactions against the body itself (autoimmune reactions). In this way antibodies are formed which destroy pancreatic tissue. The result is chronic absolute insulin deficiency. Type 1 diabetes is insulin-dependent from the start, which means that insulin must be administered. There is a hereditary tendency for type 1 diabetes to develop, so that an individual with diabetic parents has a higher risk of developing diabetes than an individual with healthy parents.
As a result of the lack of insulin, an acute and life-threatening condition often develops, with raised blood sugar concentrations (hyperglcyaemia). This can lead to glucose excretion in the urine (glucosuria) when the rate of renal resorption of glucose in the kidneys has been exceeded. Further symptoms are thirst, increased urination and increase in weight. The loss of water and the resulting increase in blood concentrations of salt can cause temporary visual disturbances. Further symptoms range from general weakness when the condition is mild to ketoacidotic coma (see 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.
Increased blood sugar concentrations, absolute insulin deficiency with insulin dependence, i.e. the body requires insulin. Type 1 and type 2 diabetes are mainly distinguished by detecting the autoantibodies in type 1. These destroy pancreatic tissue. Further diagnosis can for example be based on the glucose tolerance test, in which blood and urine concentrations are measured under standard conditions.
Insulin treatment: Blood sugar is measured before each insulin injection. The dose of insulin is then fixed on the basis of the blood sugar concentration and the size of the planned meal. The aim is the optimal control of blood sugar concentrations.
Complications: Danger of low blood sugar concentrations (hypoglycaemia). These can cause loss of consciousness and be life threatening.
- 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