A term describing a part of the body nearer to a central point of reference, such as the trunk.
For example, the fingers are distal to the arm.
The opposite of distal is proximal.... distal
Bone fractures These occur when there is a break in the continuity of the bone. This happens either as a result of violence or because the bone is unhealthy and unable to withstand normal stresses.
SIMPLE FRACTURES Fractures where the skin remains intact or merely grazed. COMPOUND FRACTURES have at least one wound which is in communication with the fracture, meaning that bacteria can enter the fracture site and cause infection. A compound fracture is also more serious than a simple fracture because there is greater potential for blood loss. Compound fractures usually need hospital admission, antibiotics and careful reduction of the fracture. Debridement (cleaning and excising dead tissue) in a sterile theatre may also be necessary.
The type of fracture depends on the force which has caused it. Direct violence occurs when an object hits the bone, often causing a transverse break – which means the break runs horizontally across the bone. Indirect violence occurs when a twisting injury to the ankle, for example, breaks the calf-bone (the tibia) higher up. The break may be more oblique. A fall on the outstretched hand may cause a break at the wrist, in the humerus or at the collar-bone depending on the force of impact and age of the person. FATIGUE FRACTURES These occur after the bone has been under recurrent stress. A typical example is the march fracture of the second toe, from which army recruits suffer after long marches. PATHOLOGICAL FRACTURES These occur in bone which is already diseased – for example, by osteoporosis (see below) in post-menopausal women. Such fractures are typically crush fractures of the vertebrae, fractures of the neck of the femur, and COLLES’ FRACTURE (of the wrist). Pathological fractures also occur in bone which has secondary-tumour deposits. GREENSTICK FRACTURES These occur in young children whose bones are soft and bend, rather than break, in response to stress. The bone tends to buckle on the side opposite to the force. Greenstick fractures heal quickly but still need any deformity corrected and plaster of Paris to maintain the correction. COMPLICATED FRACTURES These involve damage to important soft tissue such as nerves, blood vessels or internal organs. In these cases the soft-tissue damage needs as much attention as the fracture site. COMMINUTED FRACTURES A fracture with more than two fragments. It usually means that the injury was more violent and that there is more risk of damage to vessels and nerves. These fractures are unstable and take longer to unite. Rehabilitation tends to be protracted. DEPRESSED FRACTURES Most commonly found in skull fractures. A fragment of bone is forced inwards so that it lies lower than the level of the bone surrounding it. It may damage the brain beneath it.
HAIR-LINE FRACTURES These occur when the bone is broken but the force has not been severe enough to cause visible displacement. These fractures may be easily missed. Symptoms and signs The fracture site is usually painful, swollen and deformed. There is asymmetry of contour between limbs. The limb is held uselessly. If the fracture is in the upper
limb, the arm is usually supported by the patient; if it is in the lower limb then the patient is not able to bear weight on it. The limb may appear short because of muscle spasm.
Examination may reveal crepitus – a bony grating – at the fracture site. The diagnosis is con?rmed by radiography.
Treatment Healing of fractures (union) begins with the bruise around the fracture being resorbed and new bone-producing cells and blood vessels migrating into the area. Within a couple of days they form a bridge of primitive bone across the fracture. This is called callus.
The callus is replaced by woven bone which gradually matures as the new bone remodels itself. Treatment of fractures is designed to ensure that this process occurs with minimal residual deformity to the bone involved.
Treatment is initially to relieve pain and may involve temporary splinting of the fracture site. Reducing the fracture means restoring the bones to their normal position; this is particularly important at the site of joints where any small displacement may limit movement considerably.
with plaster of Paris. If closed traction does not work, then open reduction of the fracture may
be needed. This may involve ?xing the fracture with internal-?xation methods, using metal plates, wires or screws to hold the fracture site in a rigid position with the two ends closely opposed. This allows early mobilisation after fractures and speeds return to normal use.
External ?xators are usually metal devices applied to the outside of the limb to support the fracture site. They are useful in compound fractures where internal ?xators are at risk of becoming infected.
Consolidation of a fracture means that repair is complete. The time taken for this depends on the age of the patient, the bone and the type of fracture. A wrist fracture may take six weeks, a femoral fracture three to six months in an adult.
Complications of fractures are fairly common. In non-union, the fracture does not unite
– usually because there has been too much mobility around the fracture site. Treatment may involve internal ?xation (see above). Malunion means that the bone has healed with a persistent deformity and the adjacent joint may then develop early osteoarthritis.
Myositis ossi?cans may occur at the elbow after a fracture. A big mass of calci?ed material develops around the fracture site which restricts elbow movements. Late surgical removal (after 6–12 months) is recommended.
Fractured neck of FEMUR typically affects elderly women after a trivial injury. The bone is usually osteoporotic. The leg appears short and is rotated outwards. Usually the patient is unable to put any weight on the affected leg and is in extreme pain. The fractures are classi?ed according to where they occur:
subcapital where the neck joins the head of the femur.
intertrochanteric through the trochanter.
subtrochanteric transversely through the upper end of the femur (rare). Most of these fractures of the neck of femur
need ?xing by metal plates or hip replacements, as immobility in this age group has a mortality of nearly 100 per cent. Fractures of the femur shaft are usually the result of severe trauma such as a road accident. Treatment may be conservative or operative.
In fractures of the SPINAL COLUMN, mere damage to the bone – as in the case of the so-called compression fracture, in which there is no damage to the spinal cord – is not necessarily serious. If, however, the spinal cord is damaged, as in the so-called fracture dislocation, the accident may be a very serious one, the usual result being paralysis of the parts of the body below the level of the injury. Therefore the higher up the spine is fractured, the more serious the consequences. The injured person should not be moved until skilled assistance is at hand; or, if he or she must be removed, this should be done on a rigid shutter or door, not on a canvas stretcher or rug, and there should be no lifting which necessitates bending of the back. In such an injury an operation designed to remove a displaced piece of bone and free the spinal cord from pressure is often necessary and successful in relieving the paralysis. DISLOCATIONS or SUBLUXATION of the spine are not uncommon in certain sports, particularly rugby. Anyone who has had such an injury in the cervical spine (i.e. in the neck) should be strongly advised not to return to any form of body-contact or vehicular sport.
Simple ?ssured fractures and depressed fractures of the skull often follow blows or falls on the head, and may not be serious, though there is always a risk of damage which is potentially serious to the brain at the same time.
Compound fractures may result in infection within the skull, and if the skull is extensively broken and depressed, surgery is usually required to check any intercranial bleeding or to relieve pressure on the brain.
The lower jaw is often fractured by a blow on the face. There is generally bleeding from the mouth, the gum being torn. Also there are pain and grating sensations on chewing, and unevenness in the line of the teeth. The treatment is simple, the line of teeth in the upper jaw forming a splint against which the lower jaw is bound, with the mouth closed.
Congenital diseases These are rare but may produce certain types of dwar?sm or a susceptibility to fractures (osteogenesis imperfecta).
Infection of bone (osteomyelitis) may occur after an open fracture, or in newborn babies with SEPTICAEMIA. Once established it is very di?cult to eradicate. The bacteria appear capable of lying dormant in the bone and are not easily destroyed with antibiotics so that prolonged treatment is required, as might be surgical drainage, exploration or removal of dead bone. The infection may become chronic or recur.
Osteomalacia (rickets) is the loss of mineralisation of the bone rather than simple loss of bone mass. It is caused by vitamin D de?ciency and is probably the most important bone disease in the developing world. In sunlight the skin can synthesise vitamin D (see APPENDIX 5: VITAMINS), but normally rickets is caused by a poor diet, or by a failure to absorb food normally (malabsorbtion). In rare cases vitamin D cannot be converted to its active state due to the congenital lack of the speci?c enzymes and the rickets will fail to respond to treatment with vitamin D. Malfunction of the parathyroid gland or of the kidneys can disturb the dynamic equilibrium of calcium and phosphate in the body and severely deplete the bone of its stores of both calcium and phosphate.
Osteoporosis A metabolic bone disease resulting from low bone mass (osteopenia) due to excessive bone resorption. Su?erers are prone to bone fractures from relatively minor trauma. With bone densitometry it is now possible to determine individuals’ risk of osteoporosis and monitor their response to treatment.
By the age of 90 one in two women and one in six men are likely to sustain an osteoporosis-related fracture. The incidence of fractures is increasing more than would be expected from the ageing of the population, which may re?ect changing patterns of exercise or diet.
Osteoporosis may be classi?ed as primary or secondary. Primary consists of type 1 osteoporosis, due to accelerated trabecular bone loss, probably as a result of OESTROGENS de?ciency. This typically leads to crush fractures of vertebral bodies and fractures of the distal forearm in women in their 60s and 70s. Type 2 osteoporosis, by contrast, results from the slower age-related cortical and travecular bone loss that occurs in both sexes. It typically leads to fractures of the proximal femur in elderly people.
Secondary osteoporosis accounts for about 20 per cent of cases in women and 40 per cent of cases in men. Subgroups include endocrine (thyrotoxicosis – see under THYROID GLAND, DISEASES OF, primary HYPERPARATHYROIDISM, CUSHING’S SYNDROME and HYPOGONADISM); gastrointestinal (malabsorption syndrome, e.g. COELIAC DISEASE, or liver disease, e.g. primary biliary CIRRHOSIS); rheumatological (RHEUMATOID ARTHRITIS or ANKYLOSING SPONDYLITIS); malignancy (multiple MYELOMA or metastatic CARCINOMA); and drugs (CORTICOSTEROIDS, HEPARIN). Additional risk factors for osteoporosis include smoking, high alcohol intake, physical inactivity, thin body-type and heredity.
Individuals at risk of osteopenia, or with an osteoporosis-related fracture, need investigation with spinal radiography and bone densitometry. A small fall in bone density results in a large increase in the risk of fracture, which has important implications for preventing and treating osteoporosis.
Treatment Antiresorptive drugs: hormone replacement therapy – also valuable in treating menopausal symptoms; treatment for at least ?ve years is necessary, and prolonged use may increase risk of breast cancer. Cyclical oral administration of disodium etidronate – one of the bisphosphonate group of drugs – with calcium carbonate is also used (poor absorption means the etidronate must be taken on an empty stomach). Calcitonin – currently available as a subcutaneous injection; a nasal preparation with better tolerance is being developed. Calcium (1,000 mg daily) seems useful in older patients, although probably ine?ective in perimenopausal women, and it is a safe preparation. Vitamin D and calcium – recent evidence suggests value for elderly patients. Anabolic steroids, though androgenic side-effects (masculinisation) make these unacceptable for most women.
With established osteoporosis, the aim of treatment is to relieve pain (with analgesics and physical measures, e.g. lumbar support) and reduce the risk of further fractures: improvement of bone mass, the prevention of falls, and general physiotherapy, encouraging a healthier lifestyle with more daily exercise.
Further information is available from the National Osteoporosis Society.
Paget’s disease (see also separate entry) is a common disease of bone in the elderly, caused by overactivity of the osteoclasts (cells concerned with removal of old bone, before new bone is laid down by osteoblasts). The bone affected thickens and bows and may become painful. Treatment with calcitonin and bisphosphonates may slow down the osteoclasts, and so hinder the course of the disease, but there is no cure.
If bone loses its blood supply (avascular necrosis) it eventually fractures or collapses. If the blood supply does not return, bone’s normal capacity for healing is severely impaired.
For the following diseases see separate articles: RICKETS; ACROMEGALY; OSTEOMALACIA; OSTEOGENESIS IMPERFECTA.
Tumours of bone These can be benign (non-cancerous) or malignant (cancerous). Primary bone tumours are rare, but secondaries from carcinoma of the breast, prostate and kidneys are relatively common. They may form cavities in a bone, weakening it until it breaks under normal load (a pathological fracture). The bone eroded away by the tumour may also cause problems by causing high levels of calcium in the plasma.
EWING’S TUMOUR is a malignant growth affecting long bones, particularly the tibia (calfbone). The presenting symptoms are a throbbing pain in the limb and a high temperature. Treatment is combined surgery, radiotherapy and chemotherapy.
MYELOMA is a generalised malignant disease of blood cells which produces tumours in bones which have red bone marrow, such as the skull and trunk bones. These tumours can cause pathological fractures.
OSTEOID OSTEOMA is a harmless small growth which can occur in any bone. Its pain is typically removed by aspirin.
OSTEOSARCOMA is a malignant tumour of bone with a peak incidence between the ages of ten and 20. It typically involves the knees, causing a warm tender swelling. Removal of the growth with bone conservation techniques can often replace amputation as the de?nitive treatment. Chemotherapy can improve long-term survival.... bone, disorders of
Insulin-dependent and non-insulindependent diabetes have a varied pathological pattern and are caused by the interaction of several genetic and environmental factors.
Insulin-dependent diabetes mellitus (IDDM) (juvenile-onset diabetes, type 1 diabetes) describes subjects with a severe de?ciency or absence of insulin production. Insulin therapy is essential to prevent KETOSIS – a disturbance of the body’s acid/base balance and an accumulation of ketones in the tissues. The onset is most commonly during childhood, but can occur at any age. Symptoms are acute and weight loss is common.
Non-insulin-dependent diabetes mellitus (NIDDM) (maturity-onset diabetes, type 2 diabetes) may be further sub-divided into obese and non-obese groups. This type usually occurs after the age of 40 years with an insidious onset. Subjects are often overweight and weight loss is uncommon. Ketosis rarely develops. Insulin production is reduced but not absent.
A new hormone has been identi?ed linking obesity to type 2 diabetes. Called resistin – because of its resistance to insulin – it was ?rst found in mice but has since been identi?ed in humans. Researchers in the United States believe that the hormone may, in part, explain how obesity predisposes people to diabetes. Their hypothesis is that a protein in the body’s fat cells triggers insulin resistance around the body. Other research suggests that type 2 diabetes may now be occurring in obese children; this could indicate that children should be eating a more-balanced diet and taking more exercise.
Diabetes associated with other conditions (a) Due to pancreatic disease – for example, chronic pancreatitis (see PANCREAS, DISORDERS OF); (b) secondary to drugs – for example, GLUCOCORTICOIDS (see PANCREAS, DISORDERS OF); (c) excess hormone production
– for example, growth hormone (ACROMEGALY); (d) insulin receptor abnormalities; (e) genetic syndromes (see GENETIC DISORDERS).
Gestational diabetes Diabetes occurring in pregnancy and resolving afterwards.
Aetiology Insulin-dependent diabetes occurs as a result of autoimmune destruction of beta cells within the PANCREAS. Genetic in?uences are important and individuals with certain HLA tissue types (HLA DR3 and HLA DR4) are more at risk; however, the risks associated with the HLA genes are small. If one parent has IDDM, the risk of a child developing IDDM by the age of 25 years is 1·5–2·5 per cent, and the risk of a sibling of an IDDM subject developing diabetes is about 3 per cent.
Non-insulin-dependent diabetes has no HLA association, but the genetic in?uences are much stronger. The risks of developing diabetes vary with di?erent races. Obesity, decreased exercise and ageing increase the risks of disease development. The risk of a sibling of a NIDDM subject developing NIDDM up to the age of 80 years is 30–40 per cent.
Diet Many NIDDM diabetics may be treated with diet alone. For those subjects who are overweight, weight loss is important, although often unsuccessful. A diet high in complex carbohydrate, high in ?bre, low in fat and aiming towards ideal body weight is prescribed. Subjects taking insulin need to eat at regular intervals in relation to their insulin regime and missing meals may result in hypoglycaemia, a lowering of the amount of glucose in the blood, which if untreated can be fatal (see below).
Oral hypoglycaemics are used in the treatment of non-insulin-dependent diabetes in addition to diet, when diet alone fails to control blood-sugar levels. (a) SULPHONYLUREAS act mainly by increasing the production of insulin;
(b) BIGUANIDES, of which only metformin is available, may be used alone or in addition to sulphonylureas. Metformin’s main actions are to lower the production of glucose by the liver and improve its uptake in the peripheral tissues.
Complications The risks of complications increase with duration of disease.
Diabetic hypoglycaemia occurs when amounts of glucose in the blood become low. This may occur in subjects taking sulphonylureas or insulin. Symptoms usually develop when the glucose concentration falls below 2·5 mmol/l. They may, however, occur at higher concentrations in subjects with persistent hyperglycaemia – an excess of glucose – and at lower levels in subjects with persistent hypo-glycaemia. Symptoms include confusion, hunger and sweating, with coma developing if blood-sugar concentrations remain low. Re?ned sugar followed by complex carbohydrate will return the glucose concentration to normal. If the subject is unable to swallow, glucagon may be given intramuscularly or glucose intravenously, followed by oral carbohydrate, once the subject is able to swallow.
Although it has been shown that careful control of the patient’s metabolism prevents late complications in the small blood vessels, the risk of hypoglycaemia is increased and patients need to be well motivated to keep to their dietary and treatment regime. This regime is also very expensive. All risk factors for the patient’s cardiovascular system – not simply controlling hyperglycaemia – may need to be reduced if late complications to the cardiovascular system are to be avoided.
Diabetes is one of the world’s most serious health problems. Recent projections suggest that the disorder will affect nearly 240 million individuals worldwide by 2010 – double its prevalence in 1994. The incidence of insulin-dependent diabetes is rising in young children; they will be liable to develop late complications.
Although there are complications associated with diabetes, many subjects live normal lives and survive to an old age. People with diabetes or their relatives can obtain advice from Diabetes UK (www.diabetes.org.uk).
Increased risks are present of (a) heart disease, (b) peripheral vascular disease, and (c) cerebrovascular disease.
Diabetic eye disease (a) retinopathy, (b) cataract. Regular examination of the fundus enables any abnormalities developing to be detected and treatment given when appropriate to preserve eyesight.
Nephropathy Subjects with diabetes may develop kidney damage which can result in renal failure.
Neuropathy (a) Symmetrical sensory polyneuropathy; damage to the sensory nerves that commonly presents with tingling, numbness of pain in the feet or hands. (b) Asymmetrical motor diabetic neuropathy, presenting as progressive weakness and wasting of the proximal muscles of legs. (c) Mononeuropathy; individual motor or sensory nerves may be affected. (d) Autonomic neuropathy, which affects the autonomic nervous system, has many presentations including IMPOTENCE, diarrhoea or constipation and postural HYPOTENSION.
Skin lesions There are several skin disorders associated with diabetes, including: (a) necrobiosis lipoidica diabeticorum, characterised by one or more yellow atrophic lesions on the legs;
(b) ulcers, which most commonly occur on the feet due to peripheral vascular disease, neuropathy and infection. Foot care is very important.
Diabetic ketoacidosis occurs when there is insu?cient insulin present to prevent KETONE production. This may occur before the diagnosis of IDDM or when insu?cient insulin is being given. The presence of large amounts of ketones in the urine indicates excess ketone production and treatment should be sought immediately. Coma and death may result if the condition is left untreated.
Symptoms Thirst, POLYURIA, GLYCOSURIA, weight loss despite eating, and recurrent infections (e.g. BALANITIS and infections of the VULVA) are the main symptoms.
However, subjects with non-insulindependent diabetes may have the disease for several years without symptoms, and diagnosis is often made incidentally or when presenting with a complication of the disease.
Treatment of diabetes aims to prevent symptoms, restore carbohydrate metabolism to as near normal as possible, and to minimise complications. Concentration of glucose, fructosamine and glycated haemoglobin in the blood are used to give an indication of blood-glucose control.
Insulin-dependent diabetes requires insulin for treatment. Non-insulin-dependent diabetes may be treated with diet, oral HYPOGLYCAEMIC AGENTS or insulin.
Insulin All insulin is injected – mainly by syringe but sometimes by insulin pump – because it is inactivated by gastrointestinal enzymes. There are three main types of insulin preparation: (a) short action (approximately six hours), with rapid onset; (b) intermediate action (approximately 12 hours); (c) long action, with slow onset and lasting for up to 36 hours. Human, porcine and bovine preparations are available. Much of the insulin now used is prepared by genetic engineering techniques from micro-organisms. There are many regimens of insulin treatment involving di?erent combinations of insulin; regimens vary depending on the requirements of the patients, most of whom administer the insulin themselves. Carbohydrate intake, energy expenditure and the presence of infection are important determinants of insulin requirements on a day-to-day basis.
A new treatment for diabetes, pioneered in Canada and entering its preliminary clinical trials in the UK, is the transplantation of islet cells of Langerhans from a healthy person into a patient with the disorder. If the transplantation is successful, the transplanted cells start producing insulin, thus reducing or eliminating the requirement for regular insulin injections. If successful the trials would be a signi?cant advance in the treatment of diabetes.
Scientists in Israel have developed a drug, Dia Pep 277, which stops the body’s immune system from destroying pancratic ? cells as happens in insulin-dependent diabetes. The drug, given by injection, o?ers the possibility of preventing type 1 diabetes in healthy people at genetic risk of developing the disorder, and of checking its progression in affected individuals whose ? cells are already perishing. Trials of the drug are in progress.... diabetes mellitus
K
Diagram of glomerulus (Malpighian corpuscle).
Fortunately the body has two kidneys and, as most people can survive on one, there is a good ‘functional reserve’ of kidney tissue.
Symptoms Many patients with kidney disorders do not have any symptoms, even when the condition is quite advanced. However,
others experience loin pain associated with obstruction (renal colic) or due to infection; fevers; swelling (oedema), usually of the legs but occasionally including the face and arms; blood in the urine (haematuria); and excess quantities of urine (polyuria), including at night (nocturia), due to failure of normal mechanisms in the kidney for concentrating urine. Patients with chronic renal failure often have very di?use symptoms including nausea and vomiting, tiredness due to ANAEMIA, shortness of breath, skin irritation, pins and needles (paraesthesia) due to damage of the peripheral nerves (peripheral neuropathy), and eventually (rarely seen nowadays) clouding of consciousness and death.
Signs of kidney disease include loin tenderness, enlarged kidneys, signs of ?uid retention, high blood pressure and, in patients with end-stage renal failure, pallor, pigmentation and a variety of neurological signs including absent re?exes, reduced sensation, and a coarse ?apping tremor (asterixis) due to severe disturbance of the body’s normal metabolism.
Renal failure Serious kidney disease may lead to impairment or failure of the kidney’s ability to ?lter waste products from the blood and excrete them in the urine – a process that controls the body’s water and salt balance and helps to maintain a stable blood pressure. Failure of this process causes URAEMIA – an increase in urea and other metabolic waste products – as well as other metabolic upsets in the blood and tissues, all of which produce varying symptoms. Failure can be sudden or develop more slowly (chronic). In the former, function usually returns to normal once the underlying cause has been treated. Chronic failure, however, usually irreparably reduces or stops normal function.
Acute failure commonly results from physiological shock following a bad injury or major illness. Serious bleeding or burns can reduce blood volume and pressure to the point where blood-supply to the kidney is greatly reduced. Acute myocardial infarction (see HEART, DISEASES OF) or pancreatitis (see PANCREAS, DISORDERS OF) may produce a similar result. A mismatched blood transfusion can produce acute failure. Obstruction to the urine-?ow by a stone (calculus) in the urinary tract, a bladder tumour or an enlarged prostate can also cause acute renal failure, as can glomerulonephritis (see below) and the haemolytic-uraemia syndrome.
HYPERTENSION, DIABETES MELLITUS, polycystic kidney disease (see below) or AMYLOIDOSIS are among conditions that cause chronic renal failure. Others include stone, tumour, prostatic enlargement and overuse of analgesic drugs. Chronic failure may eventually lead to end-stage renal failure, a life-threatening situation that will need DIALYSIS or a renal transplant (see TRANSPLANTATION).
Familial renal disorders include autosomal dominant inherited polycystic kidney disease and sex-linked familial nephropathy. Polycystic kidney disease is an important cause of renal failure in the UK. Patients, usually aged 30–50, present with HAEMATURIA, loin or abdominal discomfort or, rarely, urinary-tract infection, hypertension and enlarged kidneys. Diagnosis is based on ultrasound examination of the abdomen. Complications include renal failure, hepatic cysts and, rarely, SUBARACHNOID HAEMORRHAGE. No speci?c treatment is available. Familial nephropathy occurs more often in boys than in girls and commonly presents as Alport’s syndrome (familial nephritis with nerve DEAFNESS) with PROTEINURIA, haematuria, progressing to renal failure and deafness. The cause of the disease lies in an absence of a speci?c ANTIGEN in a part of the glomerulus. The treatment is conservative, with most patients eventually requiring dialysis or transplantation.
Acute glomerulonephritis is an immune-complex disorder due to entrapment within glomerular capillaries of ANTIGEN (usually derived from B haemolytic streptococci – see STREPTOCOCCUS) antibody complexes initiating an acute in?ammatory response (see IMMUNITY). The disease affects children and young adults, and classically presents with a sore throat followed two weeks later by a fall in urine output (oliguria), haematuria, hypertension and mildly abnormal renal function. The disease is self-limiting with 90 per cent of patients spontaneously recovering. Treatment consists of control of blood pressure, reduced ?uid and salt intake, and occasional DIURETICS and ANTIBIOTICS.
Chronic glomerulonephritis is also due to immunological renal problems and is also classi?ed by taking a renal biopsy. It may be subdivided into various histological varieties as determined by renal biospy. Proteinuria of various degrees is present in all these conditions but the clinical presentations vary, as do their treatments. Some resolve spontaneously; others are treated with steroids or even the cytotoxic drug CYCLOPHOSPHAMIDE or the immunosuppressant cyclosporin. Prognoses are generally satisfactory but some patients may require renal dialysis or kidney transplantation – an operation with a good success rate.
Hydronephrosis A chronic disease in which the kidney becomes greatly distended with ?uid. It is caused by obstruction to the ?ow of urine at the pelvi-ureteric junction (see KIDNEYS – Structure). If the ureter is obstructed, the ureter proximal to the obstruction will dilate and pressure will be transmitted back to the kidney to cause hydronephrosis. Obstruction may occur at the bladder neck or in the urethra itself. Enlargement of the prostate is a common cause of bladder-neck obstruction; this would give rise to hypertrophy of the bladder muscle and both dilatation of the ureter and hydronephrosis. If the obstruction is not relieved, progressive destruction of renal tissue will occur. As a result of the stagnation of the urine, infection is probable and CYSTITIS and PYELONEPHRITIS may occur.
Impaired blood supply may be the outcome of diabetes mellitus and physiological shock, which lowers the blood pressure, also affecting the blood supply. The result can be acute tubular necrosis. POLYARTERITIS NODOSA and SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) may damage the large blood vessels in the kidney. Treatment is of the underlying condition.
Infection of the kidney is called pyelonephritis, a key predisposing factor being obstruction of urine ?ow through the urinary tract. This causes stagnation and provides a fertile ground for bacterial growth. Acute pyelonephritis is more common in women, especially during pregnancy when bladder infection (CYSTITIS) spreads up the ureters to the kidney. Symptoms are fever, malaise and backache. Antibiotics and high ?uid intake are the most e?ective treatment. Chronic pyelonephritis may start in childhood as a result of congenital deformities that permit urine to ?ow up from the bladder to the kidney (re?ux). Persistent re?ux leads to recurrent infections causing permanent damage to the kidney. Specialist investigations are usually required as possible complications include hypertension and kidney failure.
Tumours of the kidney are fortunately rare. Non-malignant ones commonly do not cause symptoms, and even malignant tumours (renal cell carcinoma) may be asymptomatic for many years. As soon as symptoms appear – haematuria, back pain, nausea, malaise, sometimes secondary growths in the lungs, bones or liver, and weight loss – urgent treatment including surgery, radiotherapy and chemotherapy is necessary. This cancer occurs mostly in adults over 40 and has a hereditary element. The prognosis is not good unless diagnosed early. In young children a rare cancer called nephroblastoma (Wilm’s tumour) can occur; treatment is with surgery, radiotherapy and chemotherapy. It may grow to a substantial size before being diagnosed.
Cystinuria is an inherited metabolic defect in the renal tubular reabsorption of cystine, ornithine, lysine and arginine. Cystine precipitates in an alkaline urine to form cystine stones. Triple phosphate stones are associated with infection and may develop into a very large branching calculi (staghorn calculi). Stones present as renal or ureteric pain, or as an infection. Treatment has undergone considerable change with the introduction of MINIMALLY INVASIVE SURGERY (MIS) and the destruction of stone by sound waves (LITHOTRIPSY).... kidneys, diseases of
The contents of the pelvis are the urinary bladder and rectum in both sexes; in addition the male has the seminal vesicles and the prostate gland surrounding the neck of the bladder, whilst the female has the womb, ovaries, and their appendages.
A second meaning is as in renal pelvis – that part of the collecting system proximal to the URETER which collects urine from the renal pyramids (see KIDNEYS).... pelvis
DNA (deoxyribonucleic acid) the genetic material of nearly all living organisms, which controls heredity and is located in the cell nucleus (see chromosome; gene). DNA is a *nucleic acid composed of two strands made up of units called *nucleotides (see illustration). The two strands are wound around each other into a double helix and linked together by hydrogen bonds between the bases of the nucleotides (see base pairing). The genetic information of the DNA is contained in the sequence of bases along the molecule (see genetic code); changes in the DNA cause *mutations. The DNA molecule can make exact copies of itself by the process of *replication, thereby passing on the genetic information to the daughter cells when the cell divides.... dmsa
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