(Latin) A fortunate woman; in mythology, the goddess of fortune and chance
Fortunah, Fortuin, Fortuyn, Fortunata, Fortunatus
Fortunah, Fortuin, Fortuyn, Fortunata, Fortunatus
DDT has thus had a wide use in medicine, public health, veterinary medicine, horticulture, and agriculture. Unfortunately, the indiscriminate use of DDT is potentially hazardous, and its use is now restricted or banned in several countries, including the United Kingdom.
The danger of DDT is that it enters the biological food chain with the result that animals at the end of the food chain such as birds or predators may build up lethal concentrations of the substance in their tissues.
In any case, an increasing number of species of insects were becoming resistant to DDT. Fortunately, newer insecticides have been introduced which are toxic to DDT-resistant insects, but there are doubts whether this supply of new insecticides can be maintained as insects develop resistance to them.... dichlorodiphenyl trichloroethane
– there may be epidemics spread by the bite of mosquitoes or ticks.
The clinical features begin with in?uenza-like symptoms – aches, temperature and wretchedness; then the patient develops a headache with drowsiness, confusion and neck sti?ness. Severely ill patients develop changes in behaviour, abnormalities of speech, and deterioration, sometimes with epileptic seizures. Some develop paralysis and memory loss. CT (see COMPUTED TOMOGRAPHY) and MRI brain scans show brain swelling, and damage to the temporal lobes if the herpes virus is involved. ELECTROENCEPHALOGRAPHY (EEG), which records the brainwaves, is abnormal. Diagnosis is possible by an examination of the blood or other body ?uids for antibody reaction to the virus, and modern laboratory techniques are very speci?c.
In general, drugs are not e?ective against viruses – antibiotics are of no use. Herpes encephalitis does respond to treatment with the antiviral agent, aciclovir. Treatment is supportive: patients should be given painkillers, and ?uid replacement drugs to reduce brain swelling and counter epilepsy if it occurs. Fortunately, most sufferers from encephalitis make a complete recovery, but some are left severely disabled with physical defects, personality and memory disturbance, and epileptic ?ts. Rabies is always fatal and the changes found in patients with AIDS are almost always progressive. Except in very speci?c circumstances, it is not possible to be immunised against encephalitis.
Encephalitis lethargica is one, now rare, variety that reached epidemic levels after World War I. It was characterised by drowsiness and headache leading on to COMA. The disease occasionally occurs as a complication after mumps and sometimes affected individuals subsequently develop postencephalitic PARKINSONISM.... encephalitis
Fawsta, Faustina, Faustine, Faustyna, Faustyne, Fausteena, Fausteene, Fawstina, Fawstine, Fawstyna, Fawstyne, Fawsteena, Fawsteene... fausta
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
Breast feeding Unless there is a genuine contraindication, every baby should be breast fed. The nutritional components of human milk are in the ideal proportions to promote the healthy growth of the human newborn. The mother’s milk, especially colostrum (the ?uid secreted before full lactation is established) contains immune cells and antibodies that increase the baby’s resistance to infection. From the mother’s point of view, breast feeding helps the womb to return to its normal size and helps her to lose excess body fat gained during pregnancy. Most importantly, breast feeding promotes intimate contact between mother and baby. A ?nal point to be borne in mind, however, is that drugs taken by a mother can be excreted in her milk. These include antibiotics, sedatives, tranquillisers, alcohol, nicotine and high-dose steroids or vitamins. Fortunately this is rarely a cause of trouble. (See also main entry on BREAST FEEDING.)
Arti?cial feeding Unmodi?ed cows’ milk is not a satisfactory food for the human newborn and may cause dangerous metabolic imbalance. If breast feeding is not feasible, one of the many commerciallly available formula milks should be used. Most of these are made from cows’ milk which has been modi?ed to re?ect the composition of human milk as closely as possible. For the rare infant who develops cows’-milk-protein intolerance, a milk based on soya-bean protein is indicated.
Feeding and weight gain The main guide as to whether an infant is being adequately fed is the weight. During the ?rst days of life a healthy infant loses weight, but should by the end of the second week return to birth weight. From then on, weight gain should be approximately 6oz. (170g) each week.
The timing of feeds reffects social convention rather than natural feeding patterns. Among the most primitive hunter-gatherer tribes of South America, babies are carried next to the breast and allowed to suckle at will. Fortunately for developed society, however, babies can be conditioned to intermittent feedings.
As the timing of breast feeding is ?exible – little or no preparation time being required – mothers can choose to feed their babies on demand. Far from spoiling the baby, demand feeding is likely to lead to a contented infant, the only necessary caution being that a crying baby is not always a hungry baby.
In general, a newborn will require feeding every two to four hours and, if well, is unlikely to sleep for more than six hours. After the ?rst months, a few lucky parents will ?nd their infant sleeping through the night.
Weaning Weaning on to solid foods is again a matter of individuality. Most babies will become dissatis?ed with a milk-only diet at around six months and develop enthusiasm for cereal-based weaning foods. Also at about this time they enjoy holding objects and transferring them to their mouths – the mouth being an important sense organ in infants. It is logical to include food items that they can hold, as this clearly brings the baby pleasure at this time. Introduction of solids before the age of four months is unusual and best avoided. The usual reason given for early weaning is that the baby appears hungry, but this is unlikely to be the case; crying due to COLIC, for example, is more probable. Some mothers take the baby’s desire to suck – say, on their ?nger – as a sign of hunger when this is, in fact, re?ex activity.
Delaying the start of weaning beyond nine months is nutritionally undesirable. As weaning progresses, the infant’s diet requires less milk. Once established on a varied solid diet, breast and formula milks can be safely replaced with cows’ milk. There is, however, no nutritional contraindication to continued breast feeding until the mother wishes to stop.
It is during weaning that infants realise they can arouse extreme maternal anxiety by refusing to eat. This can lead to force-feeding and battles of will which may culminate in a breakdown of the mother-child relationship. To avoid this, parents must resist the temptation to coax the child to eat. If the child refuses solid food, the meal should be taken away with a minimum of fuss. Children’s appetites re?ect their individual genetic structure and a well child will eat enough to grow and maintain satisfactory weight gain. If a child is not eating properly, weight gain will be inadequate over a prolonged period and an underlying illness is the most likely cause. Indeed, failure to thrive is the paediatrician’s best clue to chronic illness.
Advice on feeding Many sources of con?icting advice are available to new parents. It is impossible to satisfy everyone, and ultimately it is the well-being of the mother and infant and the closeness of their relationship that matter. In general, mothers should be wary of rigid advice. An experienced midwife, health visitor or well-baby-clinic nursing sister are among the most reliable sources of information.
Protein Fat per Sugar Calories per cent cent per cent per cent
Human milk 1·1 4·2 7·0 70 Cows’ milk 3·5 3·9 4·6 66
Composition of human and cows’ milk... infant feeding
Odile, Odilia, Odolia, Odilea, Odola, Odalis, Odalys... odila
Viral infections by any of hepatitis A, B, C, D, or E viruses and also CYTOMEGALOVIRUS (CMV), EPSTEIN BARR VIRUS, and HERPES SIMPLEX.
Autoimmune disorders such as autoimmune chronic hepatitis, toxins, alcohol and certain drugs – ISONIAZID, RIFAMPICIN, HALOTHANE and CHLORPROMAZINE.
WILSON’S DISEASE.
Acute viral hepatitis causes damage throughout the liver and in severe infections may destroy whole lobules (see below).
Chronic hepatitis is typi?ed by an invasion of the portal tract by white blood cells (mild hepatitis). If these mononuclear in?ammatory cells invade the body (parenchyma) of the liver tissue, ?brosis and then chronic disease or cirrhosis can develop. Cirrhosis may develop at any age and commonly results in prolonged ill health. It is an important cause of premature death, with excessive alcohol consumption commonly the triggering factor. Sometimes, cirrhosis may be asymptomatic, but common symptoms are weakness, tiredness, poor appetite, weight loss, nausea, vomiting, abdominal discomfort and production of abnormal amounts of wind. Initially, the liver may enlarge, but later it becomes hard and shrunken, though rarely causing pain. Skin pigmentation may occur along with jaundice, the result of failure to excrete the liver product BILIRUBIN. Routine liver-function tests on blood are used to help diagnose the disease and to monitor its progress. Spider telangiectasia (caused by damage to blood vessels – see TELANGIECTASIS) usually develop, and these are a signi?cant pointer to liver disease. ENDOCRINE changes occur, especially in men, who lose their typical hair distribution and suffer from atrophy of their testicles. Bruising and nosebleeds occur increasingly as the cirrhosis worsens, and portal hypertension (high pressure of venous blood circulation through the liver) develops due to abnormal vascular resistance. ASCITES and HEPATIC ENCEPHALOPATHY are indications of advanced cirrhosis.
Treatment of cirrhosis is to tackle the underlying cause, to maintain the patient’s nutrition (advising him or her to avoid alcohol), and to treat any complications. The disorder can also be treated by liver transplantation; indeed, 75 per cent of liver transplants are done for cirrhosis. The overall prognosis of cirrhosis, however, is not good, especially as many patients attend for medical care late in the course of the disease. Overall, only 25 per cent of patients live for ?ve years after diagnosis, though patients who have a liver transplant and survive for a year (80 per cent do) have a good prognosis.
Autoimmune hepatitis is a type that most commonly occurs in women between 20 and 40 years of age. The cause is unknown and it has been suggested that the disease has several immunological subtypes. Symptoms are similar to other viral hepatitis infections, with painful joints and AMENORRHOEA as additional symptoms. Jaundice and signs of chronic liver disease usually occur. Treatment with CORTICOSTEROIDS is life-saving in autoimmune hepatitis, and maintenance treatment may be needed for two years or more. Remissions and exacerbations are typical, and most patients eventually develop cirrhosis, with 50 per cent of victims dying of liver failure if not treated. This ?gure falls to 10 per cent in treated patients.
Viral hepatitis The ?ve hepatic viruses (A to E) all cause acute primary liver disease, though each belongs to a separate group of viruses.
•Hepatitis A virus (HAV) is an ENTEROVIRUS
which is very infectious, spreading by faecal contamination from patients suffering from (or incubating) the infection; victims excrete viruses into the faeces for around ?ve weeks during incubation and development of the disease. Overcrowding and poor sanitation help to spread hepatitis A, which fortunately usually causes only mild disease.
Hepatitis B (HBV) is caused by a hepadna virus, and humans are the only reservoir of infection, with blood the main agent for transferring it. Transfusions of infected blood or blood products, and injections using contaminated needles (common among habitual drug abusers), are common modes of transfer. Tattooing and ACUPUNCTURE may spread hepatitis B unless high standards of sterilisation are maintained. Sexual intercourse, particularly between male homosexuals, is a signi?cant infection route.
Hepatitis C (HCV) is a ?avivirus whose source of infection is usually via blood contacts. E?ective screening of blood donors and heat treatment of blood factors should prevent the spread of this infection, which becomes chronic in about 75 per cent of those infected, lasting for life. Although most carriers do not suffer an acute illness, they must practise life-long preventive measures.
Hepatitis D (HDV) cannot survive independently, needing HBV to replicate, so its sources and methods of spread are similar to the B virus. HDV can infect people at the same time as HBV, but it is capable of superinfecting those who are already chronic carriers of the B virus. Acute and chronic infection of HDV can occur, depending on individual circumstances, and parenteral drug abuse spreads the infection. The disease occurs worldwide, being endemic in Africa, South America and the Mediterranean littoral.
Hepatitis E virus (HEV) is excreted in the stools, spreading via the faeco-oral route. It causes large epidemics of water-borne hepatitis and ?ourishes wherever there is poor sanitation. It resembles acute HAV infection and the patient usually recovers. HEV does not cause chronic infection. The clinical characteristics of the ?ve hepatic
viruses are broadly similar. The initial symptoms last for up to two weeks (comprising temperature, headache and malaise), and JAUNDICE then develops, with anorexia, nausea, vomiting and diarrhoea common manifestations. Upper abdominal pain and a tender enlarged liver margin, accompanied by enlarged cervical lymph glands, are usual.
As well as blood tests to assess liver function, there are speci?c virological tests to identify the ?ve infective agents, and these are important contributions to diagnosis. However, there is no speci?c treatment of any of these infections. The more seriously ill patients may require hospital care, mainly to enable doctors to spot at an early stage those developing acute liver failure. If vomiting is a problem, intravenous ?uid and glucose can be given. Therapeutic drugs – especially sedatives and hypnotics – should be avoided, and alcohol must not be taken during the acute phase. Interferon is the only licensed drug for the treatment of chronic hepatitis B, but this is used with care.
Otherwise-?t patients under 40 with acute viral hepatitis have a mortality rate of around
0.5 per cent; for those over 60, this ?gure is around 3 per cent. Up to 95 per cent of adults with acute HBV infection recover fully but the rest may develop life-long chronic hepatitis, particularly those who are immunode?cient (see IMMUNODEFICIENCY).
Infection is best prevented by good living conditions. HVA and HVB can be prevented by active immunisation with vaccines. There is no vaccine available for viruses C, D and E, although HDV is e?ectively prevented by immunisation against HBV. At-risk groups who should be vaccinated against HBV include:
Parenteral drug abusers.
Close contacts of infected individuals such as regular sexual partners and infants of infected mothers.
Men who have sex with men.
Patients undergoing regular haemodialysis.
Selected health professionals, including laboratory sta? dealing with blood samples and products.... hepatitis
Cause The disease is caused by a VIRUS of the in?uenza group. There are at least three types of in?uenza virus, known respectively as A, B and
C. One of their most characteristic features is that infection with one type provides no protection against another. Equally important is the ease with which the in?uenza virus can change its character. It is these two characteristics which explain why one attack of in?uenza provides little, if any, protection against a subsequent attack, and why it is so di?cult to prepare an e?ective vaccine against the disease.
Epidemics of in?uenza due to virus A occur in Britain at two- to four-year intervals, and outbreaks of virus B in?uenza in less frequent cycles. Virus A in?uenza, for instance, was the prevalent infection in 1949, 1951, 1955 and 1956, whilst virus B in?uenza was epidemic in 1946, 1950, 1954 and, along with virus A, in 1958–59. The pandemic of 1957, which swept most of the world, although fortunately not in a severe form, was due to a new variant of virus A
– the so-called Asian virus – and it has been suggested that it was this variant that was responsible for the pandemics of 1889 and 1918. Since 1957, variants of virus A have been the predominating causes of in?uenza, accompanied on occasions by virus B.
In 1997 and 2004, outbreaks of Chinese avian in?uenza caused alarm. The in?uenza virus had apparently jumped species from birds
– probably chickens – to infect some people. Because no vaccine is available, there was a risk that this might start an epidemic.
Symptoms The incubation period of in?uenza A and B is 2–3 three days, and the disease is characterised by a sudden onset. In most cases this is followed by a short, sharp febrile illness of 2–4 days’ duration, associated with headache, prostration, generalised aching, and respiratory symptoms. In many cases the respiratory symptoms are restricted to the upper respiratory tract, and consist of signs of irritation of the nose, pharynx and larynx. There may be nosebleeds, and a dry, hacking cough is often a prominent and troublesome symptom. The fever is usually remittent and the temperature seldom exceeds 39·4 °C (103 °F), tending to ?uctuate between 38·3 and 39·4 °C (101 and 103 °F).
The most serious complication is infection of the lungs. This infection is usually due to organisms other than the in?uenza virus, and is a complication which can have serious results in elderly people.
The very severe form of ’?u which tends to occur during pandemics – and which was so common during the 1918–19 pandemic – is characterised by the rapid onset of bronchopneumonia and severe prostration. Because of the toxic e?ect on the heart, there is a particularly marked form of CYANOSIS, known as heliotrope cyanosis.
Convalescence following in?uenza tends to be prolonged. Even after an attack of average severity there tends to be a period of weakness and depression.
Treatment Expert opinion is still divided as to the real value of in?uenza vaccine in preventing the disease. Part of the trouble is that there is little value in giving any vaccine until it is known which particular virus is causing the infection. As this varies from winter to winter, and as the protection given by vaccine does not exceed one year, it is obviously not worthwhile attempting to vaccinate the whole community. The general rule therefore is that, unless there is any evidence that a particularly virulent type of virus is responsible, only the most vulnerable should be immunised – such as children in boarding schools, elderly people, and people who suffer from chronic bronchitis or asthma, chronic heart disease, renal failure, diabetes mellitus or immunosuppression (see under separate entries). In the face of an epidemic, people in key positions, such as doctors, nurses and those concerned with public safety, transport and other public utilities, should be vaccinated.
For an uncomplicated attack of in?uenza, treatment is symptomatic: that is, rest in bed, ANALGESICS to relieve the pain, sedatives, and a light diet. A linctus is useful to sooth a troublesome cough. The best analgesics are ASPIRIN or PARACETAMOL. None of the sulphonamides or the known antibiotics has any e?ect on the in?uenza virus; on the other hand, should the lungs become infected, antibiotics should be given immediately, because such an infection is usually due to other organisms. If possible, a sample of sputum should be examined to determine which organisms are responsible for the lung infection. The choice of antibiotic then depends upon which antibiotic the organism is most sensitive to.... influenza
Saidah, Sa’ida, Sayida, Saeida, Saedah, Said, Sayide, Sayidea, Sayda, Saydah, Saeda... saida
There are also more than 200 identi?ed disorders described as inborn errors of metabolism. Some cause few problems; others are serious threats to an individual’s life. Individual disorders are, fortunately, rare – probably one child in 10,000 or 100,000; overall these inborn errors affect around one child in 1,000. Examples include GALACTOSAEMIA, PHENYLKETONURIA, porphyrias, TAY SACHS DISEASE and varieties of mucopolysaccharidosis, HOMOCYSTINURIA and hereditary fructose (a type of sugar) intolerance.... metabolic disorders
Anxiety neurosis, or anxiety state, constitutes the most common form of neurosis; fortunately it is also among the most responsive to treatment. Once the neurosis develops, sufferers are in a state of persistent anxiety and worry, ‘tensed up’, always fatigued and unable to sleep at night. In addition, there are often physical complaints – for example, palpitations, sweating, apparent discomfort on swallowing (‘globus’), and headache.
Obsessional neuroses are much less common and constitute only about 5 per cent of all neuroses. Like other neuroses, they usually develop in early adult life. (See MENTAL ILLNESS.)... neurosis
DIABETES INSIPIDUS, a condition characterised by the passing of a large volume of URINE every day, is due to lack of the antidiuretic hormone (see VASOPRESSIN). Enhanced production of the ADRENOCORTICOTROPHIC HORMONE (ACTH) leads to CUSHING’S SYNDROME. Excessive production of PROLACTIN by micro or macro adenomas (benign tumours) leads to hyperprolactinaemia and consequent AMENORRHOEA and GALACTORRHOEA. Some adenomas do not produce any hormone but cause effects by damaging the pituitary cells and inhibiting their hormone production.
The most sensitive cells to extrinsic pressure are the gonadotrophin-producing cells and the growth-hormone producing cells, so that if the tumour occurs in childhood, growth hormone will be suppressed and growth will slow. Gonadotrophin hormone suppression will prevent the development of puberty and, if the tumour occurs after puberty, will result in amenorrhoea in the female and lack of LIBIDO in both sexes. The thyroid-stimulating hormone cells are the next to suffer and the pressure effects on these cells will result in hypothyroidism (see under THYROID GLAND, DISEASES OF).
Fortunately the ACTH-producing cells are the most resistant to extrinsic pressure and this is teleologically sound as ACTH is the one pituitary hormone that is essential to life. However, these cells can suffer damage from intracellular tumours, and adrenocortical insu?ciency is not uncommon.
Information about these disorders may be obtained from the Pituitary Foundation.... pituitary-linked disorders
Treatment The patient should be kept quiet. Arti?cial respiration may be necessary and intravenous BENZODIAZEPINES to prevent convulsions may also be needed. (See POISONS; also APPENDIX 2: ADDRESSES: SOURCES OF INFORMATION, ADVICE, SUPPORT AND SELFHELP.)... strychnine
Mercury has an affinity for the central nervous system. Soon it concentrates in the kidney causing tubular damage. A common cause is the mercurial content (50 per cent) in the amalgam fillings in teeth which, under certain conditions, release a vapour. Fortunately, its use in dentistry is being superceded by an alternative composite filling.
A common cause of poisoning was demonstrated in 1972 when 6,000 people became seriously ill (600 died) from eating bread made from grain treated with a fungicide containing methylmercury. For every fungus in grain there is a mercuric compound to destroy it. The seed of all cereal grain is thus treated to protect its power of germination.
Those who are hypersensitive to the metal should as far as possible avoid button cells used in tape recorders, cassette players, watch and camera mechanisms. As the mercury cells corrode, the metal enters the environment and an unknown fraction is converted by micro organisms to alkylmercury compounds which seep into ground waters and eventually are borne to the sea. When cells are incinerated, the mercury volatilises and enters the atmosphere. (Pharmaceutical Journal, July 28/1984)
Mercury poisoning from inhalation of mercury fumes goes directly to the brain and pituitary gland. Autopsies carried out on dentists reveal high concentrations of mercury in the pituitary gland. (The Lancet, 5-27-89,1207 (letter))
Treatment. For years the common antidote was sulphur, and maybe not without reason. When brought into contact sulphur and mercury form an insoluble compound enabling the mercury to be more easily eliminated from the body. Sulphur can be provided by eggs or Garlic.
Old-time backwoods physicians of the North American Medical School used Asafoetida, Guaiacum and Echinacea. German pharmacists once used Bugleweed and Yellow Dock. Dr J. Clarke, USA physician recommends Sarsaparilla to facilitate breakdown and expulsion from the body.
Reconstructed formula. Echinacea 2; Sarsaparilla 1; Guaiacum quarter; Asafoetida quarter; Liquorice quarter. Dose: Liquid Extracts: 1 teaspoon. Tinctures: 2 teaspoons. Powders: 500mg (two 00 capsules or one-third teaspoon). Thrice daily.
Chelation therapy.
Formula. Tinctures. Skullcap 2-15 drops; Pleurisy root 20-45 drops; Horehound 5-40 drops. Mercurial salivation. Thrice daily. (Indian Herbology of North America, by Alma Hutchens) Dental fillings: replace amalgam with safe alternative – ceramic, etc. Evidence of a link between tooth fillings containing mercury and ME has caused the use of dental amalgam to be banned in Sweden. ... mercury poisoning
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