An assessment of the probable course and outcome of a disease.
Treatment is excision with a margin of normal tissue. The specimen must be examined histologically, and prognosis depends on the depth of invasion. Very super?cial melanomas carry an excellent outlook once removed, but deeper tumours may spread to regional lymph glands and beyond with fatal results. Public-awareness campaigns have led to the earlier presentation of melanomas in recent years, with corresponding bene?t. (See also SUNBURN.)... melanoma
Hodgkin’s disease The incidence is around four new cases per 100,000 population annually, with slightly more men than women contracting it. The ?rst incidence peak is in age group 20–35 and the second in age group 50–
70. The cause of Hodgkin’s is not known, although it is more common in patients from small families and well-educated backgrounds. The disease is three times more likely to occur in people who have had glandular fever (see MONONUCLEOSIS) but no link with the EPSTEIN BARR VIRUS has been established (see Burkitt’s lymphoma, below)
The disease is characterised histologically by the presence of large malignant lymphoid cells (Reed-Sternberg cells) in the lymph glands.
Clinically the lymph glands are enlarged, rubbery but painless; usually those in the neck or just above the CLAVICLE are affected. Spread is to adjacent lymph glands and in young people a mass of enlarged glands may develop in the MEDIASTINUM. The SPLEEN is affected in about one-third of patients with the disorder. Treatment is either with RADIOTHERAPY, CHEMOTHERAPY or both, depending on when the disease is diagnosed and the nature of the abnormal lymph cells. Cure rates are good, especially if the lymphoma is diagnosed early.
Non-Hodgkin’s lymphoma (NHL) This varies in its malignancy depending on the nature and activity of the abnormal lymph cells. The disease is hard to classify histologically, so various classi?cation systems have been evolved. High- and low-grade categories are recognised according to the rate of proliferation of abnormal lymph cells. No single causative factor has been identi?ed, although viral and bacterial infections have been linked to NHL, and genetic and immunological factors may be implicated. The incidence is higher than that of Hodgkin’s disease, at 12 new cases per 100,000 population a year, and the median age of diagnosis is 65–70 years. Suppression of the immune system that ocurs in people with HIV infection has been linked with a marked rise in the incidence of non-Hodgkin’s lymphoma and Hodgkin’s disease.
Most patients have painless swelling of one or more groups of lymph nodes in the neck or groin, and the liver and spleen may enlarge. As other organs can also be affected, patients may present with a wide range of symptoms, including fever, itching and weight loss. If NHL occurs in a single group of lymph nodes, radiotherapy is the treatment of choice; more extensive in?ltration of glands will require chemotherapy – and sometimes both types of treatment will be necessary. If these treatments fail, BONE MARROW TRANSPLANT may be carried out. Prognosis is good for low-grade NHL (75 per cent of patients survive ?ve years or more); in more severe types the survival rate is 40–50 per cent for two years.
Another variety of lymphoma is found in children in Africa, sometimes called after Burkitt, the Irish surgeon who ?rst identi?ed it. Burkitt’s lymphoma is a rapidly growing malignant tumour occurring in varying sites, and the Epstein Barr virus has a role in its origin and growth. A non-African variety of Burkitt’s lymphoma is now also recognised. CYTOTOXIC drug therapy is e?ective.... lymphoma
Bacterial meningitis is life-threatening: in the United Kingdom, 5–10 per cent of children who contract the disease may die. Most cases of acute bacterial meningitis in the UK are caused by two bacteria: Neisseria meningitidis (meningococcus), and Streptococcus pneumoniae (pneumococcus); other bacteria include Haemophilus in?uenzae (a common cause until virtually wiped out by immunisation), Escherichia coli, Mycobacterium tuberculosis (see TUBERCULOSIS), Treponema pallidum (see SYPHILIS) and Staphylococci spp. Of the bacterial infections, meningococcal group B is the type that causes a large number of cases in the UK, while group A is less common.
Bacterial meningitis may occur by spread from nearby infected foci such as the nasopharynx, middle ear, mastoid and sinuses (see EAR, DISEASES OF). Direct infection may be the result of penetrating injuries of the skull from accidents or gunshot wounds. Meningitis may also be a complication of neurosurgery despite careful aseptic precautions. Immuno-compromised patients – those with AIDS or on CYTOTOXIC drugs – are vulnerable to infections.
Spread to contacts may occur in schools and similar communities. Many people harbour the meningococcus without developing meningitis. In recent years small clusters of cases, mainly in schoolchildren and young people at college, have occurred in Britain.
Symptoms include malaise accompanied by fever, severe headache, PHOTOPHOBIA, vomiting, irritability, rigors, drowsiness and neurological disturbances. Neck sti?ness and a positive KERNIG’S SIGN appearing within a few hours of infection are key diagnostic signs. Meningococcal and pneumococcal meningitis may co-exist with SEPTICAEMIA, a much more serious condition in terms of death rate or organ damage and which constitutes a grave emergency demanding rapid treatment.
Diagnosis and treatment are urgent and, if bacterial meningitis is suspected, antibiotic treatment should be started even before laboratory con?rmation of the infection. Analysis of the CEREBROSPINAL FLUID (CSF) by means of a LUMBAR PUNCTURE is an essential step in diagnosis, except in patients for whom the test would be dangerous as they have signs of raised intracranial pressure. The CSF is clear or turbid in viral meningitis, turbid or viscous in tuberculous infection and turbulent or purulent when meningococci or staphylococci are the infective agents. Cell counts and biochemical make-up of the CSF are other diagnostic pointers. Serological tests are done to identify possible syphilitic infection, which is now rare in Britain.
Patients with suspected meningitis should be admitted to hospital quickly. General pracitioners are encouraged to give a dose of intramuscular penicillin before sending the child to hospital. Treatment in hospital is usually with a cephalosporin, such as ceftazidime or ceftriaxone. Once the sensitivity of the organism is known as a result of laboratory studies on CSF and blood, this may be changed to penicillin or, in the case of H. in?uenzae, to amoxicillin. Local infections such as SINUSITIS or middle-ear infection require treatment, and appropriate surgery for skull fractures or meningeal tears should be carried out as necessary. Tuberculous meningitis is treated for at least nine months with anti-tuberculous drugs (see TUBERCULOSIS). If bacterial meningitis causes CONVULSIONS, these can be controlled with diazepam (see TRANQUILLISERS; BENZODIAZEPINES) and ANALGESICS will be required for the severe headache.
Coexisting septicaemia may require full intensive care with close attention to intravenous ?uid and electrolyte balance, control of blood clotting and blood pressure.
Treatment of close contacts such as family, school friends, medical and nursing sta? is recommended if the patient has H. in?uenzae or N. meningitidis: RIFAMPICIN provides e?ective prophylaxis. Contacts of patients with pneumococcal infection do not need preventive treatment. Vaccines for meningococcal meningitis may be given to family members in small epidemics and to any contacts who are especially at risk such as infants, the elderly and immuno-compromised individuals.
The outlook for a patient with bacterial meningitis depends upon age – the young and old are vulnerable; speed of onset – sudden onset worsens the prognosis; and how quickly treatment is started – hence the urgency of diagnosis and admission to hospital. Recent research has shown that children who suffer meningitis in their ?rst year of life are ten times more likely to develop moderate or severe disability by the age of ?ve than contemporaries who have not been infected. (See British Medical Journal, 8 September 2001, page 523.)
Prevention One type of bacterial meningitis, that caused by Haemophilus, has been largely controlled by IMMUNISATION; meningococcal C vaccine has largely prevented this type of the disease in the UK. So far, no vaccine against group B has been developed, but research continues. Information on meningitis can be obtained from the Meningitis Trust and the Meningitis Research Foundation.... meningitis
Causes There is an inherited element: parents, children or siblings of schizophrenic sufferers have a one in ten chance of developing the disorder; a twin has a 50 per cent chance if the other twin has schizophrenia. Some BRAIN disorders such as temporal lobe EPILEPSY, tumours and ENCEPHALITIS seem to be linked with schizophrenia. Certain drugs – for example, AMPHETAMINES – can precipitate schizophrenia and DOPAMINE-blocking drugs often relieve schizophrenic symptoms. Stress may worsen schizophrenia and recreational drugs may trigger an attack.
Symptoms These usually develop gradually until the individual’s behaviour becomes so distrubing or debilitating that work, relationships and basic activities such as eating and sleeping are interrupted. The patient may have disturbed perception with auditory HALLUCINATIONS, illogical thought-processes and DELUSIONS; low-key emotions (‘?at affect’); a sense of being invaded or controlled by outside forces; a lack of INSIGHT and inability to acknowledge reality; lethargy and/or agitation; a disrespect for personal appearance and hygiene; and a tendency to act strangely. Violence is rare although some sufferers commit violent acts which they believe their ‘inner voices’ have commanded.
Relatives and friends may try to cope with the affected person at home, but as severe episodes may last several months and require regular administration of powerful drugs – patients are not always good at taking their medication
– hospital admission may be necessary.
Treatment So far there is no cure for schizophrenia. Since the 1950s, however, a group of drugs called antipsychotics – also described as NEUROLEPTICS or major tranquillisers – have relieved ?orid symptoms such as thought disorder, hallucinations and delusions as well as preventing relapses, thus allowing many people to leave psychiatric hospitals and live more independently outside. Only some of these drugs have a tranquillising e?ect, but their sedative properties can calm patients with an acute attack. CHLORPROMAZINE is one such drug and is commonly used when treatment starts or to deal with an emergency. Halperidol, tri?uoperazine and pimozide are other drugs in the group; these have less sedative effects so are useful in treating those whose prominent symptoms are apathy and lethargy.
The antipsychotics’ mode of action is by blocking the activity of DOPAMINE, the chemical messenger in the brain that is faulty in schizophrenia. The drugs quicken the onset and prolong the remission of the disorder, and it is very important that patients take them inde?nitely. This is easier to ensure when a patient is in hospital or in a stable domestic environment.
CLOZAPINE – a newer, atypical antipsychotic drug – is used for treating schizophrenic patients unresponsive to, or intolerant of, conventional antipsychotics. It may cause AGRANULOCYTOSIS and use is con?ned to patients registered with the Clorazil (the drug’s registered name) Patient Monitoring Service. Amisulpride, olanzapine, quetiapine, risperidone, sertindole and zotepine are other antipsychotic drugs described as ‘atypical’ by the British National Formulary; they may be better tolerated than other antipsychotics, and their varying properties mean that they can be targeted at patients with a particular grouping of symptoms. They should, however, be used with caution.
The welcome long-term shift of mentally ill patients from large hospitals to community care (often in small units) has, because of a lack of resources, led to some schizophrenic patients not being properly supervised with the result that they fail to take their medication regularly. This leads to a recurrence of symptoms and there have been occasional episodes of such patients in community care becoming a danger to themselves and to the public.
The antipsychotic drugs are powerful agents and have a range of potentially troubling side-effects. These include blurred vision, constipation, dizziness, dry mouth, limb restlessness, shaking, sti?ness, weight gain, and in the long term, TARDIVE DYSKINESIA (abnormal movements and walking) which affects about 20 per cent of those under treatment. Some drugs can be given by long-term depot injection: these include compounds of ?upenthixol, zuclopenthixol and haloperidol.
Prognosis About 25 per cent of sufferers recover fully from their ?rst attack. Another 25 per cent are disabled by chronic schizophrenia, never recover and are unable to live independently. The remainder are between these extremes. There is a high risk of suicide.... schizophrenia
Cancers are classi?ed according to the type of cell from which they are derived as well as the organ of origin. Hence cancers arising within the bronchi, often collectively referred to as ‘lung cancer’, include both adenocarcinomas, derived from epithelium (surface tissue), and carcinomas from glandular tissue. Sarcomas are cancers of connective tissue, including bone and cartilage. The behaviour of cancers and their response to therapy vary widely depending on this classi?cation as well as on numerous other factors such as how large the cancer is, how fast the cells grow and how well de?ned they are. It is entirely wrong to see cancer as a single disease entity with a universally poor prognosis. For example, fewer than one-half of women in whom breast cancer (see BREASTS, DISEASES OF) is discovered will die from the disease, and 75 per cent of children with lymphoblastic LEUKAEMIA can be cured.
Incidence In most western countries, cancer is the second most important cause of death after heart disease and accounts for 20–25 per cent of all deaths. In the United Kingdom in 2003, more than 154,000 people died of malignant disease. There is wide international variation in the most frequently encountered types of cancer, re?ecting the importance of environmental factors in the development of cancer. In the UK as well as the US, carcinoma of the BRONCHUS is the most common. Since it is usually inoperable at the time of diagnosis, it is even more strikingly the leading cause of cancer deaths. In women, breast cancer was for a long time the most common malignant disease, accounting for a quarter of all cancers, but ?gures for the late 1990s show that lung cancer now heads the incidence list – presumably the consequence of a rising incidence of smoking among young women. Other common sites are as follows: males – colon and rectum, prostate and bladder; females – colon and rectum, uterus, ovary and pancreas.
In 2003, of the more than 154,000 people in the UK who died of cancer, over 33,000 had the disease in their respiratory system, nearly 13,000 in the breast, over 5,800 in the stomach and more than 2,000 in the uterus or cervix, while over 4,000 people had leukaemia. The incidence of cancer varies with age; the older a person is, the more likely it is that he or she will develop the disease. The over-85s have an incidence about nine times greater than those in the 25–44 age group. There are also di?erences in incidence between sexes: for example, more men than women develop lung cancer, though the incidence in women is rising as the effects of smoking work through. The death rate from cancer is falling in people under 75 in the UK, a trend largely determined by the cancers which cause the most deaths: lung, breast, colorectal, stomach and prostate.
Causes In most cases the causes of cancer remain unknown, though a family history of cancer may be relevant. Rapid advances have, however, been made in the past two decades in understanding the di?erences between cancer cells and normal cells at the genetic level. It is now widely accepted that cancer results from acquired changes in the genetic make-up of a particular cell or group of cells which ultimately lead to a failure of the normal mechanisms regulating their growth. It appears that in most cases a cascade of changes is required for cells to behave in a truly malignant fashion; the critical changes affect speci?c key GENES, known as oncogenes, which are involved in growth regulation. (See APOPTOSIS.)
Since small genetic errors occur within cells at all times – most but not all of which are repaired – it follows that some cancers may develop as a result of an accumulation of random changes which cannot be attributed to environmental or other causes. The environmental factors known to cause cancer, such as radiation and chemicals (including tar from tobacco, asbestos, etc.), do so by increasing the overall rate of acquired genetic damage. Certain viral infections can induce speci?c cancers (e.g. HEPATITIS B VIRUS and HEPATOMA, EPSTEIN BARR VIRUS and LYMPHOMA) probably by inducing alterations in speci?c genes. HORMONES may also be a factor in the development of certain cancers such as those of the prostate and breast. Where there is a particular family tendency to certain types of cancer, it now appears that one or more of the critical genetic abnormalities required for development of that cancer may have been inherited. Where environmental factors such as tobacco smoking or asbestos are known to cause cancer, then health education and preventive measures can reduce the incidence of the relevant cancer. Cancer can also affect the white cells in the blood and is called LEUKAEMIA.
Treatment Many cancers can be cured by surgical removal if they are detected early, before there has been spread of signi?cant numbers of tumour cells to distant sites. Important within this group are breast, colon and skin cancer (melanoma). The probability of early detection of certain cancers can be increased by screening programmes in which (ideally) all people at particular risk of development of such cancers are examined at regular intervals. Routine screening for CERVICAL CANCER and breast cancer (see BREASTS, DISEASES OF) is currently practised in the UK. The e?ectiveness of screening people for cancer is, however, controversial. Apart from questions surrounding the reliability of screening tests, they undoubtedly create anxieties among the subjects being screened.
If complete surgical removal of the tumour is not possible because of its location or because spread from the primary site has occurred, an operation may nevertheless be helpful to relieve symptoms (e.g. pain) and to reduce the bulk of the tumour remaining to be dealt with by alternative means such as RADIOTHERAPY or CHEMOTHERAPY. In some cases radiotherapy is preferable to surgery and may be curative, for example, in the management of tumours of the larynx or of the uterine cervix. Certain tumours are highly sensitive to chemotherapy and may be cured by the use of chemotherapeutic drugs alone. These include testicular tumours, LEUKAEMIA, LYMPHOMA and a variety of tumours occurring in childhood. These tend to be rapidly growing tumours composed of primitive cells which are much more vulnerable to the toxic effects of the chemotherapeutic agents than the normal cells within the body.
Unfortunately neither radiotherapy nor currently available chemotherapy provides a curative option for the majority of common cancers if surgical excision is not feasible. New e?ective treatments in these conditions are urgently needed. Nevertheless the rapidly increasing knowledge of cancer biology will almost certainly lead to novel therapeutic approaches – including probably genetic techniques utilising the recent discoveries of oncogenes (genes that can cause cancer). Where cure is not possible, there often remains much that can be done for the cancer-sufferer in terms of control of unpleasant symptoms such as pain. Many of the most important recent advances in cancer care relate to such ‘palliative’ treatment, and include the establishment in the UK of palliative care hospices.
Families and patients can obtain valuable help and advice from Marie Curie Cancer Care, Cancer Relief Macmillan Fund, or the British Association of Cancer United Patients.
www.cancerbacup.org.uk
www.mariecurie.org.uk... cancer
Patients often have a poor sleep pattern, waking exhausted. Unexplained headache, urinary frequency and abdominal symptoms are common, but no cause has been found. Patients generally score highly on measures of anxiety and DEPRESSION. Fibromyalgia is not an ideal description; idiopathic di?use-pain syndrome and non-restorative sleep disorder are increasingly preferred terms.
Clinical ?ndings are generally unremarkable; most important is the presence of multiple hyperalgesic tender sites (e.g. low cervical spine, low lumbar spine, suboccipital muscle, mid upper trapezius, tennis-elbow sites, upper outer quadrants of buttocks, medial fat pad of knees). In ?bromyalgia, hyperalgesia (excessive discomfort) is widespread and symmetrical, but absent at sites normally non-tender. Claims by patients to be tender all over are more likely to be due to fabrication or psychiatric disturbance. OSTEOARTHRITIS and periarticular syndrome are much more common and should be excluded, together with other conditions, such as hypothyroidism (see THYROID GLAND, DISEASES OF), SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) and in?ammatory myopathy (see MUSCLES, DISORDERS OF), which may present with similar symptoms.
Cause There is no investigational evidence of in?ammatory, metabolic or structural abnormality, and the problem seems functional rather than pathological. SEROTONIN de?ciency has a signi?cant role in ?bromyalgia syndrome.
Management Controlled trials have con?rmed the usefulness of low-dose AMITRIPTYLINE or DOTHIEPIN together with a graded exercise programme to increase aerobic ?tness. How this works is still unclear; its e?cacy may be due to its normalising effects on the sleep centre or ‘pain gating’ (reduction of pain sensation) at the spinal-cord level. Prognosis is often poor. Nevertheless, suitable advice and training can help most patients to learn to cope better with their condition and avoid unnecessary investigations and drug treatments.... fibromyalgia syndrome
Structure Each tooth is composed of enamel, dentine, cement, pulp and periodontal membrane. ENAMEL is the almost translucent material which covers the crown of a tooth. It is the most highly calci?ed material in the body, 96–97 per cent being composed of calci?ed salts. It is arranged from millions of long, six-sided prisms set on end on the dentine (see below), and is thickest over the biting surface of the tooth. With increasing age or the ingestion of abrasive foods the teeth may be worn away on the surface, so that the dentine becomes visible. The outer sides of some teeth may be worn away by bad tooth-brushing technique. DENTINE is a dense yellowish-white material from which the bulk and the basic shape of a tooth are formed. It is like ivory and is harder than bone but softer than enamel. The crown of the tooth is covered by the hard protective enamel and the root is covered by a bone-like substance called cement. Decay can erode dentine faster than enamel (see TEETH, DISORDERS OF – Caries of the teeth). CEMENT or cementum is a thin bone-like material which covers the roots of teeth and helps hold them in the bone. Fibres of the periodontal membrane (see below) are embedded in the cement and the bone. When the gums recede, part of the cement may be exposed and the cells die. Once this has happened, the periodontal membrane can no longer be attached to the tooth and, if su?cient cement is destroyed, the tooth-support will be so weakened that the tooth will become loose. PULP This is the inner core of the tooth and is
composed of a highly vascular, delicate ?brous tissue with many ?ne nerve-?bres. The pulp is very sensitive to temperature variation and to touch. If the pulp becomes exposed it will become infected and usually cannot overcome this. Root-canal treatment or extraction of the tooth may be necessary. PERIODONTAL MEMBRANE This is a layer of ?brous tissue arranged in groups of ?bres which surround and support the root of a tooth in a bone socket. The ?bres are interspersed with blood vessels and nerves. Loss of the membrane leads to loss of the tooth. The membrane can release and re-attach the ?bres to allow the tooth to move when it erupts, or (to correct dental deformities) is being moved by orthodontic springs.
Arrangement and form Teeth are present in most mammals and nearly all have two sets: a temporary or milk set, followed by a permanent or adult set. In some animals, like the toothed whale, all the teeth are similar; but in humans there are four di?erent shapes: incisors, canines (eye-teeth), premolars (bicuspids), and molars. The incisors are chisel-shaped and the canine is pointed. Premolars have two cusps on the crown (one medial to the other) and molars have at least four cusps. They are arranged together in an arch in each jaw and the
cusps of opposing teeth interdigitate. Some herbivores have no upper anterior teeth but use a pad of gum instead. As each arch is symmetrical, the teeth in an upper and lower quadrant can be used to identify the animal. In humans, the quadrants are the same: in other words, in the child there are two incisors, one canine and two molars (total teeth 20); in the adult there are two incisors, one canine, two premolars and three molars (total 32). This mixture of tooth-form suggests that humans are omnivorous. Anatomically the crown of the tooth has mesial and distal surfaces which touch the tooth next to it. The mesial surface is the one nearer to the centre line and the distal is the further away. The biting surface is called the incisal edge for the anterior teeth and the occlusal surface for the posteriors.
Development The ?rst stage in the formation of the teeth is the appearance of a down-growth of EPITHELIUM into the underlying mesoderm. This is the dental lamina, and from it ten smaller swellings in each jaw appear. These become bell-shaped and enclose a part of the mesoderm, the cells of which become specialised and are called the dental papillae. The epithelial cells produce enamel and the dental papilla forms the dentine, cement and pulp. At a ?xed time the teeth start to erupt and a root is formed. Before the deciduous teeth erupt, the permanent teeth form, medial to them. In due course the deciduous roots resorb and the permanent teeth are then able to push the crowns out and erupt themselves. If this process is disturbed, the permanent teeth may be displaced and appear in an abnormal position or be impacted.
Eruption of teeth is in a de?nite order and at a ?xed time, although there may be a few months’ leeway in either direction which is of no signi?cance. Excessive delay is found in some congenital disorders such as CRETINISM. It may also be associated with local abnormalities of the jaws such as cysts, malformed teeth and supernumerary teeth.
The usual order of eruption of deciduous teeth is:
Middle incisors 6–8 months Lateral incisors 8–10 months First molars 12–16 months Canines (eye-teeth) 16–20 months Second molars 20–30 months
The usual order of eruption of permanent teeth is:
First molars 6–7 years Middle incisors 6–8 years Lateral incisors 7–9 years Canines 9–12 years First and second premolars 10–12 years Second molars 11–13 years Third molars (wisdom teeth) 17–21 years
The permanent teeth of the upper (top) and lower (bottom) jaws.
Teeth, Disorders of
Teething, or the process of eruption of the teeth in infants, may be accompanied by irritability, salivation and loss of sleep. The child will tend to rub or touch the painful area. Relief may be obtained in the child by allowing it to chew on a hard object such as a toy or rusk. Mild ANALGESICS may be given if the child is restless and wakens in the night. A serious pitfall is to assume that an infant’s symptoms of ill-health are due to teething, as the cause may be more serious. Fever and ?ts (see SEIZURE) are not due to teething.
Toothache is the pain felt when there is in?ammation of the pulp or periodontal membrane of a tooth (see TEETH – Structure). It can vary in intensity and may be recurring. The commonest cause is caries (see below) when the cavity is close to the pulp. Once the pulp has become infected, this is likely to spread from the apex of the tooth into the bone to form an abscess (gumboil – see below). A lesser but more long-lasting pain is felt when the dentine is unprotected. This can occur when the enamel is lost due to decay or trauma or because the gums have receded. This pain is often associated with temperature-change or sweet foods. Expert dental advice should be sought early, before the decay is extensive. If a large cavity is accessible, temporary relief may be obtained by inserting a small piece of cotton wool soaked, for example, in oil of cloves.
Alveolar abscess, dental abscess or gumboil This is an ABSCESS caused by an infected tooth. It may be present as a large swelling or cause trismus (inability to open the mouth). Treatment is drainage of the PUS, extraction of the tooth and/or ANTIBIOTICS.
Caries of the teeth or dental decay is very common in the more a?uent countries and is most common in children and young adults. Increasing awareness of the causes has resulted in a considerable improvement in dental health, particularly in recent years; this has coincided with a rise in general health. Now more than half of ?ve-year-old children are caries-free and of the others, 10 per cent have half of the remaining carious cavities. Since the start of the National Health Service, the emphasis has been on preventive dentistry, and now edentulous patients are mainly found among the elderly who had their teeth removed before 1948.
The cause of caries is probably acid produced by oral bacteria from dietary carbohydrates, particularly re?ned sugar, and this dissolves part of the enamel; the dentine is eroded more quickly as it is softer (see TEETH – Structure). The exposed smooth surfaces are usually protected as they are easily cleaned during normal eating and by brushing. Irregular and overcrowded teeth are more at risk from decay as they are di?cult to clean. Primitive people who chew coarse foods rarely get caries. Fluoride in the drinking water at about one part per million is associated with a reduction in the caries rate.
Prolonged severe disease in infancy is associated with poor calci?cation of the teeth, making them more vulnerable to decay. As the teeth are formed and partly calci?ed by the time of birth, the diet and health of the mother are also important to the teeth of the child. Pregnant mothers and children should have a good balanced diet with su?cient calcium and vitamin
D. A ?brous diet will also aid cleansing of the teeth and stimulate the circulation in the teeth and jaws. The caries rate can be reduced by regular brushing with a ?uoride toothpaste two or three times per day and certainly before going to sleep. The provision of sweet or sugary juices in an infant’s bottle should be avoided.
Irregularity of the permanent teeth may be due to an abnormality in the growth of the jaws or to the early or late loss of the deciduous set (see TEETH – Development). Most frequently it is due to an imbalance in the size of the teeth and the length of the jaws. Some improvement may take place with age, but many will require the help of an orthodontist (specialist dentist) who can correct many malocclusions by removing a few teeth to allow the others to be moved into a good position by means of springs and elastics on various appliances which are worn in the mouth.
Loosening of the teeth may be due to an accident or in?ammation of the GUM. Teeth loosened by trauma may be replaced and splinted in the socket, even if knocked right out. If the loosening is due to periodontal disease, the prognosis is less favourable.
Discoloration of the teeth may be intrinsic or extrinsic: in other words, the stain may be in the calci?ed structure or stuck on to it. Intrinsic staining may be due to JAUNDICE or the antibiotic tetracycline. Extrinsic stain may be due to tea, co?ee, tobacco, pan (a mixture of chuna and betel nuts wrapped in a leaf), iron-containing medicines or excess ?uoride.
Gingivitis or in?ammation of the gum may occur as an acute or chronic condition. In the acute form it is often part of a general infection of the mouth, and principally occurs in children or young adults – resolving after 10–14 days. The chronic form occurs later in life and tends to be progressive. Various microorganisms may be found on the lesions, including anaerobes. Antiseptic mouthwashes may help, and once the painful stage is past, the gums should be thoroughly cleaned and any calculus removed. In severe conditions an antibiotic may be required.
Periodontal disease is the spread of gingivitis (see above) to involve the periodontal membrane of the tooth; in its ?orid form it used to be called pyorrhoea. In this, the membrane becomes damaged by the in?ammatory process and a space or pocket is formed into which a probe can be easily passed. As the pocket becomes more extensive, the tooth loosens. The loss of the periodontal membrane also leads to the loss of supporting bone. Chronic in?ammation soon occurs and is di?cult to eradicate. Pain is not a feature of the disease but there is often an unpleasant odour (halitosis). The gums bleed easily and there may be DYSPEPSIA. Treatment is largely aimed at stabilising the condition rather than curing it.
Dental abscess is an infection that arises in or around a tooth and spreads to involve the bone. It may occur many years after a blow has killed the pulp of the tooth, or more quickly after caries has reached the pulp. At ?rst the pain may be mild and intermittent but eventually it will become severe and a swelling will develop in the gum over the apex of the tooth. A radiograph of the tooth will show a round clear area at the apex of the tooth. Treatment may be by painting the gum with a mild counter-irritant such as a tincture of aconite and iodine in the early stages, but later root-canal therapy or apicectomy may be required. If a swelling is present, it may need to be drained or the o?ending teeth extracted and antibiotics given.
Injuries to teeth are common. The more minor injuries include crazing and the loss of small chips of enamel, and the major ones include a broken root and avulsion of the entire tooth. A specialist dental opinion should be sought as soon as possible. A tooth that has been knocked out can be re-implanted if it is clean and replaced within a few hours. It will then require splinting in place for 4–6 weeks.
Prevention of dental disease As with other disorders, prevention is better than cure. Children should be taught at an early age to keep their teeth and gums clean and to avoid re?ned sugars between meals. It is better to ?nish a meal with a drink of water rather than a sweetened drink. Fluoride in some of its forms is useful in the reduction of dental caries; in some parts of the UK natural water contains ?uoride, and in some areas where ?uoride content is low, arti?cial ?uoridation of the water supply is carried out. Overcrowding of the teeth, obvious maldevelopment of the jaw and persistent thumbsucking into the teens are all indications for seeking the advice of an orthodontist. Generally, adults have less trouble with decay but more with periodontal disease and, as its onset is insidious, regular dental inspections are desirable.... teeth
Cause Asthma runs in families, so that parents with asthma have a strong risk of having children with asthma, or with other atopic (see ATOPY) illnesses such as HAY FEVER or eczema (see DERMATITIS). There is therefore a great deal of interest in the genetic basis of the condition. Several GENES seem to be associated with the condition of atopy, in which subjects have a predisposition to form ANTIBODIES of the IgE class against allergens (see ALLERGEN) they encounter – especially inhaled allergens.
The allergic response in the lining of the airway leads to an in?ammatory reaction. Many cells are involved in this in?ammatory process, including lymphocytes, eosinophils, neutrophils and mast cells. The cells are attracted and controlled by a complex system of in?ammatory mediators. The in?amed airway-wall produced in this process is then sensitive to further allergic stimuli or to non-speci?c challenges such as dust, smoke or drying from the increased respiration during exercise. Recognition of this in?ammation has concentrated attention on anti-in?ammatory aspects of treatment.
Continued in?ammation with poor control of asthma can result in permanent damage to the airway-wall such that reversibility is reduced and airway-narrowing becomes permanent. Appropriate anti-in?ammatory therapy may help to prevent this damage.
Many allergens can be important triggers of asthma. House-dust mite, grass pollen and animal dander are the commonest problems. Occupational factors such as grain dusts, hard-metals fumes and chemicals in the plastic and paint industry are important in some adults. Viral infections are another common trigger, especially in young children.
The prevalence of asthma appears to be on the increase in most countries. Several factors have been linked to this increase; most important may be the vulnerability of the immature immune system (see IMMUNITY) in infants. High exposure to allergens such as house-dust mite early in life may prime the immune system, while reduced exposure to common viral infections may delay the maturation of the immune system. In addition, maternal smoking in pregnancy and infancy increases the risk.
Clinical course The major symptoms of asthma are breathlessness and cough. Occasionally cough may be the only symptom, especially in children, where night-time cough may be mistaken for recurrent infection and treated inappropriately with antibiotics.
The onset of asthma is usually in childhood, but it may begin at any age. In childhood, boys are affected more often than girls but by adulthood the sex incidence is equal. Children who have mild asthma are more likely to grow out of the condition as they go through their teenaged years, although symptoms may recur later.
The degree of airway-narrowing, and its change with time and treatment, can be monitored by measuring the peak expiratory ?ow with a simple monitor at home – a peak-?ow meter. The typical pattern shows the peak ?ow to be lowest in the early morning and this ‘morning dipping’ is often associated with disturbance of sleep.
Acute exacerbations of asthma may be provoked by infections or allergic stimuli. If they do not respond quickly and fully to medication, expert help should be sought urgently since oxygen and higher doses of drugs will be necessary to control the attack. In a severe attack the breathing rate and the pulse rate rise and the chest sounds wheezy. The peak-?ow rate of air into the lungs falls. Patients may be unable to talk in full sentences without catching their breath, and the reduced oxygen in the blood in very severe attacks may produce the blue colour of CYANOSIS in the lips and tongue. Such acute attacks can be very frightening for the patient and family.
Some cases of chronic asthma are included in the internationally agreed description CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) – a chronic, slowly progressive disorder characterised by obstruction of the air?ow persisting over several months.
Treatment The ?rst important consideration in the treatment of asthma is avoidance of precipitating factors. When this is a speci?c animal or occupational exposure, this may be possible; it is however more di?cult for house-dust mite or pollens. Exercise-induced asthma should be treated adequately rather than avoiding exercise.
Desensitisation injections using small quantities of speci?c allergens are used widely in some countries, but rarely in the UK as they are considered to have limited value since most asthma is precipitated by many stimuli and controlled adequately with simple treatment.
There are two groups of main drugs for the treatment of asthma. The ?rst are the bronchodilators which relax the smooth muscle in the wall of the airways, increase their diameter and relieve breathlessness. The most useful agents are the beta adrenergic agonists (see ADRENERGIC RECEPTORS) such as salbutamol and terbutaline. They are best given by inhalation into the airways since this reduces the general side-effects from oral use. These drugs are usually given to reverse airway-narrowing or to prevent its onset on exercise. However, longer-acting inhaled beta agonists such as salmeterol and formoterol or the theophyllines given in tablet form can be used regularly as prevention. The beta agonists can cause TREMOR and PALPITATION in some patients.
The second group of drugs are the antiin?ammatory agents that act to reduce in?ammation of the airway. The main agents in this group are the CORTICOSTEROIDS. They must be taken regularly, even when symptoms are absent. Given by inhalation they have few side-effects. In acute attacks, short courses of oral steroids are used; in very severe disease regular oral steroids may be needed. Other drugs have a role in suppressing in?ammation: sodium cromoglycate has been available for some years and is generally less e?ective than inhaled steroids. Newer agents directed at speci?c steps in the in?ammatory pathway, such as leukotriene receptor-antagonists, are alternative agents.
Treatment guidelines have been produced by various national and international bodies, such as the British Thoracic Society. Most have set out treatment in steps according to severity, with objectives for asthma control based on symptoms and peak ?ow. Patients should have a management plan that sets out their regular treatment and their appropriate response to changes in their condition.
Advice and support for research into asthma is provided by the National Asthma Campaign.
See www.brit-thoracic.org.uk
Prognosis Asthma is diagnosed in 15–20 per cent of all pre-school children in the developed world. Yet by the age of 15 it is estimated that fewer than 5 per cent still have symptoms. A study in 2003 reported on a follow-up of persons born in 1972–3 who developed asthma and still had problems at the age of nine. By the time these persons were aged 26, 27 per cent were still having problems; around half of that number had never been free from the illness and the other half had apparently lost it for a few years but it had returned.... asthma
Tumours All masses cause varying combinations of headache and vomiting – symptoms of raised pressure within the inexpansible bony box formed by the skull; general or localised epileptic ?ts; weakness of limbs or disordered speech; and varied mental changes. Tumours may be primary, arising in the brain, or secondary deposits from tumours arising in the lung, breast or other organs. Some brain tumours are benign and curable by surgery: examples include meningiomas and pituitary tumours. The symptoms depend on the size and situation of the mass. Abscesses or blood clots (see HAEMATOMA) on the surface or within the brain may resemble tumours; some are removable. Gliomas ( see GLIOMA) are primary malignant tumours arising in the glial tissue (see GLIA) which despite surgery, chemotherapy and radiotherapy usually have a bad prognosis, though some astrocytomas and oligodendronogliomas are of low-grade malignancy. A promising line of research in the US (in the animal-testing stage in 2000) suggests that the ability of stem cells from normal brain tissue to ‘home in’ on gliomal cells can be turned to advantage. The stem cells were chemically manipulated to carry a poisonous compound (5-?uorouracil) to the gliomal cells and kill them, without damaging normal cells. Around 80 per cent of the cancerous cells in the experiments were destroyed in this way.
Clinical examination and brain scanning (CT, or COMPUTED TOMOGRAPHY; magnetic resonance imaging (MRI) and functional MRI) are safe, accurate methods of demonstrating the tumour, its size, position and treatability.
Strokes When a blood vessel, usually an artery, is blocked by a clot, thrombus or embolism, the local area of the brain fed by that artery is damaged (see STROKE). The resulting infarct (softening) causes a stroke. The cells die and a patch of brain tissue shrinks. The obstruction in the blood vessel may be in a small artery in the brain, or in a larger artery in the neck. Aspirin and other anti-clotting drugs reduce recurrent attacks, and a small number of people bene?t if a narrowed neck artery is cleaned out by an operation – endarterectomy. Similar symptoms develop abruptly if a blood vessel bursts, causing a cerebral haemorrhage. The symptoms of a stroke are sudden weakness or paralysis of the arm and leg of the opposite side to the damaged area of brain (HEMIPARESIS), and sometimes loss of half of the ?eld of vision to one side (HEMIANOPIA). The speech area is in the left side of the brain controlling language in right-handed people. In 60 per cent of lefthanders the speech area is on the left side, and in 40 per cent on the right side. If the speech area is damaged, diffculties both in understanding words, and in saying them, develops (see DYSPHASIA).
Degenerations (atrophy) For reasons often unknown, various groups of nerve cells degenerate prematurely. The illness resulting is determined by which groups of nerve cells are affected. If those in the deep basal ganglia are affected, a movement disorder occurs, such as Parkinson’s disease, hereditary Huntington’s chorea, or, in children with birth defects of the brain, athetosis and dystonias. Modern drugs, such as DOPAMINE drugs in PARKINSONISM, and other treatments can improve the symptoms and reduce the disabilities of some of these diseases.
Drugs and injury Alcohol in excess, the abuse of many sedative drugs and arti?cial brain stimulants – such as cocaine, LSD and heroin (see DEPENDENCE) – can damage the brain; the effects can be reversible in early cases. Severe head injury can cause localised or di?use brain damage (see HEAD INJURY).
Cerebral palsy Damage to the brain in children can occur in the uterus during pregnancy, or can result from rare hereditary and genetic diseases, or can occur during labour and delivery. Severe neurological illness in the early months of life can also cause this condition in which sti? spastic limbs, movement disorders and speech defects are common. Some of these children are learning-disabled.
Dementias In older people a di?use loss of cells, mainly at the front of the brain, causes ALZHEIMER’S DISEASE – the main feature being loss of memory, attention and reasoned judgement (dementia). This affects about 5 per cent of the over-80s, but is not simply due to ageing processes. Most patients require routine tests and brain scanning to indicate other, treatable causes of dementia.
Response to current treatments is poor, but promising lines of treatment are under development. Like Parkinsonism, Alzheimer’s disease progresses slowly over many years. It is uncommon for these diseases to run in families. Multiple strokes can cause dementia, as can some organic disorders such as cirrhosis of the liver.
Infections in the brain are uncommon. Viruses such as measles, mumps, herpes, human immunode?ciency virus and enteroviruses may cause ENCEPHALITIS – a di?use in?ammation (see also AIDS/HIV).
Bacteria or viruses may infect the membrane covering the brain, causing MENINGITIS. Viral meningitis is normally a mild, self-limiting infection lasting only a few days; however, bacterial meningitis – caused by meningococcal groups B and C, pneumococcus, and (now rarely) haemophilus – is a life-threatening condition. Antibiotics have allowed a cure or good control of symptoms in most cases of meningitis, but early diagnosis is essential. Severe headaches, fever, vomiting and increasing sleepiness are the principal symptoms which demand urgent advice from the doctor, and usually admission to hospital. Group B meningococcus is the commonest of the bacterial infections, but Group C causes more deaths. A vaccine against the latter has been developed and has reduced the incidence of cases by 75 per cent.
If infection spreads from an unusually serious sinusitis or from a chronically infected middle ear, or from a penetrating injury of the skull, an abscess may slowly develop. Brain abscesses cause insidious drowsiness, headaches, and at a late stage, weakness of the limbs or loss of speech; a high temperature is seldom present. Early diagnosis, con?rmed by brain scanning, is followed by antibiotics and surgery in hospital, but the outcome is good in only half of affected patients.
Cerebral oedema Swelling of the brain can occur after injury, due to engorgement of blood vessels or an increase in the volume of the extravascular brain tissue due to abnormal uptake of water by the damaged grey (neurons) matter and white (nerve ?bres) matter. This latter phenomenon is called cerebral oedema and can seriously affect the functioning of the brain. It is a particularly dangerous complication following injury because sometimes an unconscious person whose brain is damaged may seem to be recovering after a few hours, only to have a major relapse. This may be the result of a slow haemorrhage from damaged blood vessels raising intracranial pressure, or because of oedema of the brain tissue in the area surrounding the injury. Such a development is potentially lethal and requires urgent specialist treatment to alleviate the rising intracranial pressure: osmotic agents (see OSMOSIS) such as mannitol or frusemide are given intravenously to remove the excess water from the brain and to lower intracranial pressure, buying time for de?nitive investigation of the cranial damage.... brain, diseases of
Chronic bronchitis is typi?ed by chronic productive cough for at least three months in two successive years (provided other causes such as TUBERCULOSIS, lung cancer and chronic heart failure have been excluded). The characteristics of emphysema are abnormal and permanent enlargement of the airspaces (alveoli) at the furthermost parts of the lung tissue. Rupture of alveoli occurs, resulting in the creation of air spaces with a gradual breakdown in the lung’s ability to oxygenate the blood and remove carbon dioxide from it (see LUNGS). Asthma results in in?ammation of the airways with the lining of the BRONCHIOLES becoming hypersensitive, causing them to constrict. The obstruction may spontaneously improve or do so in response to bronchodilator drugs. If an asthmatic patient’s airway-obstruction is characterised by incomplete reversibility, he or she is deemed to have a form of COPD called asthmatic bronchitis; sufferers from this disorder cannot always be readily distinguished from those people who have chronic bronchitis and/ or emphysema. Symptoms and signs of emphysema, chronic bronchitis and asthmatic bronchitis overlap, making it di?cult sometimes to make a precise diagnosis. Patients with completely reversible air?ow obstruction without the features of chronic bronchitis or emphysema, however, are considered to be suffering from asthma but not from COPD.
The incidence of COPD has been increasing, as has the death rate. In the UK around 30,000 people with COPD die annually and the disorder makes up 10 per cent of all admissions to hospital medical wards, making it a serious cause of illness and disability. The prevalence, incidence and mortality rates increase with age, and more men than women have the disorder, which is also more common in those who are socially disadvantaged.
Causes The most important cause of COPD is cigarette smoking, though only 15 per cent of smokers are likely to develop clinically signi?cant symptoms of the disorder. Smoking is believed to cause persistent airway in?ammation and upset the normal metabolic activity in the lung. Exposure to chemical impurities and dust in the atmosphere may also cause COPD.
Signs and symptoms Most patients develop in?ammation of the airways, excessive growth of mucus-secreting glands in the airways, and changes to other cells in the airways. The result is that mucus is transported less e?ectively along the airways to eventual evacuation as sputum. Small airways become obstructed and the alveoli lose their elasticity. COPD usually starts with repeated attacks of productive cough, commonly following winter colds; these attacks progressively worsen and eventually the patient develops a permanent cough. Recurrent respiratory infections, breathlessness on exertion, wheezing and tightness of the chest follow. Bloodstained and/or infected sputum are also indicative of established disease. Among the symptoms and signs of patients with advanced obstruction of air?ow in the lungs are:
RHONCHI (abnormal musical sounds heard through a STETHOSCOPE when the patient breathes out).
marked indrawing of the muscles between the ribs and development of a barrel-shaped chest.
loss of weight.
CYANOSIS in which the skin develops a blue tinge because of reduced oxygenation of blood in the blood vessels in the skin.
bounding pulse with changes in heart rhythm.
OEDEMA of the legs and arms.
decreasing mobility.
Some patients with COPD have increased ventilation of the alveoli in their lungs, but the levels of oxygen and carbon dioxide are normal so their skin colour is normal. They are, however, breathless so are dubbed ‘pink pu?ers’. Other patients have reduced alveolar ventilation which lowers their oxygen levels causing cyanosis; they also develop COR PULMONALE, a form of heart failure, and become oedematous, so are called ‘blue bloaters’.
Investigations include various tests of lung function, including the patient’s response to bronchodilator drugs. Exercise tests may help, but radiological assessment is not usually of great diagnostic value in the early stages of the disorder.
Treatment depends on how far COPD has progressed. Smoking must be stopped – also an essential preventive step in healthy individuals. Early stages are treated with bronchodilator drugs to relieve breathing symptoms. The next stage is to introduce steroids (given by inhalation). If symptoms worsen, physiotherapy – breathing exercises and postural drainage – is valuable and annual vaccination against INFLUENZA is strongly advised. If the patient develops breathlessness on mild exertion, has cyanosis, wheezing and permanent cough and tends to HYPERVENTILATION, then oxygen therapy should be considered. Antibiotic treatment is necessary if overt infection of the lungs develops.
Complications Sometimes rupture of the pulmonary bullae (thin-walled airspaces produced by the breakdown of the walls of the alveoli) may cause PNEUMOTHORAX and also exert pressure on functioning lung tissue. Respiratory failure and failure of the right side of the heart (which controls blood supply to the lungs), known as cor pulmonale, are late complications in patients whose primary problem is emphysema.
Prognosis This is related to age and to the extent of the patient’s response to bronchodilator drugs. Patients with COPD who develop raised pressure in the heart/lung circulation and subsequent heart failure (cor pulmonale) have a bad prognosis.... chronic obstructive pulmonary disease (copd)
Rarely, an enlarged gland may be the result of cancer in the thyroid.
Treatment A symptomless goitre may gradually disappear or be so small as not to merit treatment. If the goitre is large or is causing the patient di?culty in swallowing or breathing, it may need surgical removal by partial or total thyroidectomy. If the patient is de?cient in iodine, ?sh and iodised salt should be included in the diet.
Hyperthyroidism is a common disorder affecting 2–5 per cent of all females at some time in their lives. The most common cause – around 75 per cent of cases – is thyrotoxicosis (see below). An ADENOMA (or multiple adenomas) or nodules in the thyroid also cause hyperthyroidism. There are several other rare causes, including in?ammation caused by a virus, autoimune reactions and cancer. The symptoms of hyperthyroidism affect many of the body’s systems as a consequence of the much-increased metabolic rate.
Thyrotoxicosis is a syndrome consisting of di?use goitre (enlarged thyroid gland), over-activity of the gland and EXOPHTHALMOS (protruding eyes). Patients lose weight and develop an increased appetite, heat intolerance and sweating. They are anxious, irritable, hyperactive, suffer from TACHYCARDIA, breathlessness and muscle weakness and are sometimes depressed. The hyperthyroidism is due to the production of ANTIBODIES to the TSH receptor (see THYROTROPHIN-STIMULATING HORMONE (TSH)) which stimulate the receptor with resultant production of excess thyroid hormones. The goitre is due to antibodies that stimulate the growth of the thyroid gland. The exoph-
thalmos is due to another immunoglobulin called the ophthalmopathic immunoglobulin, which is an antibody to a retro-orbital antigen on the surface of the retro-orbital EYE muscles. This provokes in?ammation in the retro-orbital tissues which is associated with the accumulation of water and mucopolysaccharide which ?lls the orbit and causes the eye to protrude forwards.
Although thyrotoxicosis may affect any age-group, the peak incidence is in the third decade. Females are affected ten times as often as males; the prevalence in females is one in 500. As with many other autoimmune diseases, there is an increased prevalence of autoimmune thyroid disease in the relatives of patients with thyrotoxicosis. Some of these patients may have hypothyroidism (see below) and others, thyrotoxicosis. Patients with thyrotoxicosis may present with a goitre or with the eye signs or, most commonly, with the symptoms of excess thyroid hormone production. Thyroid hormone controls the metabolic rate of the body so that the symptoms of hyperthyroidism are those of excess metabolism.
The diagnosis of thyrotoxicosis is con?rmed by the measurement of the circulating levels of the two thyroid hormones, thyroxine and TRIIODOTHYRONINE.
Treatment There are several e?ective treatments for thyrotoxicosis. ANTITHYROID DRUGS These drugs inhibit the iodination of tyrosine and hence the formation of the thyroid hormones. The most commonly used drugs are carbimazole and propylthiouricil: these will control the excess production of thyroid hormones in virtually all cases. Once the patient’s thyroid is functioning normally, the dose can be reduced to a maintenance level and is usually continued for two years. The disadvantage of antithyroid drugs is that after two years’ treatment nearly half the patients will relapse and will then require more de?nitive therapy. PARTIAL THYROIDECTOMY Removal of three-quarters of the thyroid gland is e?ective treatment of thyrotoxicosis. It is the treatment of choice in those patients with large goitres. The patient must however be treated with medication so that they are euthyroid (have a normally functioning thyroid) before surgery is undertaken, or thyroid crisis and cardiac arrhythmias may complicate the operation. RADIOACTIVE IODINE THERAPY This has been in use for many years, and is an e?ective means of controlling hyperthyroidism. One of the disadvantages of radioactive iodine is that the incidence of hypothyroidism is much greater than with other forms of treatment. However, the management of hypothyroidism is simple and requires thyroxine tablets and regular monitoring for hypothyroidism. There is no evidence of any increased incidence of cancer of the thyroid or LEUKAEMIA following radio-iodine therapy. It has been the pattern in Britain to reserve radio-iodine treatment to those over the age of 35, or those whose prognosis is unlikely to be more than 30 years as a result of cardiac or respiratory disease. Radioactive iodine treatment should not be given to a seriously thyrotoxic patient. BETA-ADRENOCEPTOR-BLOCKING DRUGS Usually PROPRANOLOL HYDROCHLORIDE: useful for symptomatic treatment during the ?rst 4–8 weeks until the longer-term drugs have reduced thyroid activity.
Hypothyroidism A condition resulting from underactivity of the thyroid gland. One form, in which the skin and subcutaneous tissues thicken and result in a coarse appearance, is called myxoedema. The thyroid gland secretes two hormones – thyroxine and triiodothyronine – and these hormones are responsible for the metabolic activity of the body. Hypothyroidism may result from developmental abnormalities of the gland, or from a de?ciency of the enzymes necessary for the synthesis of the hormones. It may be a feature of endemic goitre and retarded development, but the most common cause of hypothyroidism is the autoimmune destruction of the thyroid known as chronic thyroiditis. It may also occur as a result of radio-iodine treatment of thyroid overactivity (see above) and is occasionally secondary to pituitary disease in which inadequate TSH production occurs. It is a common disorder, occurring in 14 per 1,000 females and one per 1,000 males. Most patients present between the age of 30 and 60 years.
Symptoms As thyroid hormones are responsible for the metabolic rate of the body, hypothyroidism usually presents with a general sluggishness: this affects both physical and mental activities. The intellectual functions become slow, the speech deliberate and the formation of ideas and the answers to questions take longer than in healthy people. Physical energy is reduced and patients frequently complain of lethargy and generalised muscle aches and pains. Patients become intolerant of the cold and the skin becomes dry and swollen. The LARYNX also becomes swollen and gives rise to a hoarseness of the voice. Most patients gain weight and develop constipation. The skin becomes dry and yellow due to the presence of increased carotene. Hair becomes thinned and brittle and even baldness may develop. Swelling of the soft tissues may give rise to a CARPAL TUNNEL SYNDROME and middle-ear deafness. The diagnosis is con?rmed by measuring the levels of thyroid hormones in the blood, which are low, and of the pituitary TSH which is raised in primary hypothyroidism.
Treatment consists of the administration of thyroxine. Although tri-iodothyronine is the metabolically active hormone, thyroxine is converted to tri-iodothyronine by the tissues of the body. Treatment should be started cautiously and slowly increased to 0·2 mg daily – the equivalent of the maximum output of the thyroid gland. If too large a dose is given initially, palpitations and tachycardia are likely to result; in the elderly, heart failure may be precipitated.
Congenital hypothyroidism Babies may be born hypothyroid as a result of having little or no functioning thyroid-gland tissue. In the developed world the condition is diagnosed by screening, all newborn babies having a blood test to analyse TSH levels. Those found positive have a repeat test and, if the diagnosis is con?rmed, start on thyroid replacement therapy within a few weeks of birth. As a result most of the ill-effects of cretinism can be avoided and the children lead normal lives.
Thyroiditis In?ammation of the thyroid gland. The acute form is usually caused by a bacterial infection elsewhere in the body: treatment with antibiotics is needed. Occasionally a virus may be the infectious agent. Hashimoto’s thyroiditis is an autoimmune disorder causing hypothyroidism (reduced activity of the gland). Subacute thyroiditis is in?ammation of unknown cause in which the gland becomes painful and the patient suffers fever, weight loss and malaise. It sometimes lasts for several months but is usually self-limiting.
Thyrotoxic adenoma A variety of thyrotoxicosis (see hyperthyroidism above) in which one of the nodules of a multinodular goitre becomes autonomous and secretes excess thyroid hormone. The symptoms that result are similar to those of thyrotoxicosis, but there are minor di?erences.
Treatment The ?rst line of treatment is to render the patient euthyroid by treatment with antithyroid drugs. Then the nodule should be removed surgically or destroyed using radioactive iodine.
Thyrotoxicosis A disorder of the thyroid gland in which excessive amounts of thyroid hormones are secreted into the bloodstream. Resultant symptoms are tachycardia, tremor, anxiety, sweating, increased appetite, weight loss and dislike of heat. (See hyperthyroidism above.)... goitre
Arrhythmias An abnormal rate or rhythm of the heartbeat. The reason is a disturbance in the electrical impulses within the heart. Sometimes a person may have an occasional irregular heartbeat: this is called an ECTOPIC beat (or an extrasystole) and does not necessarily mean that an abnormality exists. There are two main types of arrhythmia: bradycardias, where the rate is slow – fewer than 60 beats a minute and sometimes so slow and unpredictable (heartblock) as to cause blackouts or heart failure; and tachycardia, where the rate is fast – more than 100 beats a minute. A common cause of arrhythmia is coronary artery disease, when vessels carrying blood to the heart are narrowed by fatty deposits (ATHEROMA), thus reducing the blood supply and damaging the heart tissue. This condition often causes myocardial infarction after which arrhythmias are quite common and may need correcting by DEFIBRILLATION (application of a short electric shock to the heart). Some tachycardias result from a defect in the electrical conduction system of the heart that is commonly congenital. Various drugs can be used to treat arrhythmias (see ANTIARRHYTHMIC DRUGS). If attacks constantly recur, the arrhythmia may be corrected by electrical removal of dead or diseased tissue that is the cause of the disorder. Heartblock is most e?ectively treated with an arti?cial CARDIAC PACEMAKER, a battery-activated control unit implanted in the chest.
Cardiomyopathy Any disease of the heart muscle that results in weakening of its contractions. The consequence is a fall in the e?ciency of the circulation of blood through the lungs and remainder of the body structures. The myopathy may be due to infection, disordered metabolism, nutritional excess or de?ciency, toxic agents, autoimmune processes, degeneration, or inheritance. Often, however, the cause is not identi?ed. Cardiomyopathies are less common than other types of heart diseases, and the incidence of di?erent types of myopathy (see below) is not known because patients or doctors are sometimes unaware of the presence of the condition.
The three recognised groups of cardiomyopathies are hypertrophic, dilated and restrictive.
•Hypertrophic myopathy, a familial condition, is characterised by great enlargement of the muscle of the heart ventricles. This reduces the muscle’s e?ciency, the ventricles fail to relax properly and do not ?ll suf?ciently during DIASTOLE.
In the dilated type of cardiomyopathy, both ventricles overdilate, impairing the e?ciency of contraction and causing congestion of the lungs.
In the restrictive variety, proper ?lling of the ventricles does not occur because the muscle walls are less elastic than normal. The result is raised pressure in the two atria (upper cavities) of the heart: these dilate and develop FIBRILLATION. Diagnosis can be di?cult and treatment is symptomatic, with a poor prognosis. In suitable patients, heart TRANSPLANTATION may be considered. Disorders of the heart muscle may also be
caused by poisoning – for example, heavy consumption of alcohol. Symptoms include tiredness, palpitations (quicker and sometimes irregular heartbeat), chest pain, di?culty in breathing, and swelling of the legs and hands due to accumulation of ?uid (OEDEMA). The heart is enlarged (as shown on chest X-ray) and ECHOCARDIOGRAPHY shows thickening of the heart muscle. A BIOPSY of heart muscle will show abnormalities in the cells of the heart muscle.
Where the cause of cardiomyopathy is unknown, as is the case with most patients, treatment is symptomatic using DIURETICS to control heart failure and drugs such as DIGOXIN to return the heart rhythm to normal. Patients should stop drinking alcohol. If, as often happens, the patient’s condition slowly deteriorates, heart transplantation should be considered.
Congenital heart disease accounts for 1–2 per cent of all cases of organic heart disease. It may be genetically determined and so inherited; present at birth for no obvious reason; or, in rare cases, related to RUBELLA in the mother. The most common forms are holes in the heart (atrial septal defect, ventricular septal defect – see SEPTAL DEFECT), a patent DUCTUS ARTERIOSUS, and COARCTATION OF THE AORTA. Many complex forms also exist and can be diagnosed in the womb by fetal echocardiography which can lead to elective termination of pregnancy. Surgery to correct many of these abnormalities is feasible, even for the most severe abnormalities, but may only be palliative giving rise to major diffculties of management as the children become older. Heart transplantation is now increasingly employed for the uncorrectable lesions.
Coronary artery disease Also known as ischaemic heart disease, this is a common cause of symptoms and death in the adult population. It may present for the ?rst time as sudden death, but more usually causes ANGINA PECTORIS, myocardial infarction (heart attack) or heart failure. It can also lead to a disturbance of heart rhythm. Factors associated with an increased risk of developing coronary artery disease include diabetes, cigarette smoking, high blood pressure, obesity, and a raised concentration of cholesterol in the blood. Older males are most affected.
Coronary thrombosis or acute myocardial infarction is the acute, dramatic manifestation of coronary-artery ischaemic heart disease – one of the major killing diseases of western civilisation. In 1999, ischaemic heart disease was responsible for about 115,000 deaths in England and Wales, compared with 153,000 deaths in 1988. In 1999 more than 55,600 people died of coronary thrombosis. The underlying cause is disease of the coronary arteries which carry the blood supply to the heart muscle (or myocardium). This results in narrowing of the arteries until ?nally they are unable to transport su?cient blood for the myocardium to function e?ciently. One of three things may happen. If the narrowing of the coronary arteries occurs gradually, then the individual concerned will develop either angina pectoris or signs of a failing heart: irregular rhythm, breathlessness, CYANOSIS and oedema.
If the narrowing occurs suddenly or leads to complete blockage (occlusion) of a major branch of one of the coronary arteries, then the victim collapses with acute pain and distress. This is the condition commonly referred to as a coronary thrombosis because it is usually due to the affected artery suddenly becoming completely blocked by THROMBOSIS. More correctly, it should be described as coronary occlusion, because the ?nal occluding factor need not necessarily be thrombosis.
Causes The precise cause is not known, but a wide range of factors play a part in inducing coronary artery disease. Heredity is an important factor. The condition is more common in men than in women; it is also more common in those in sedentary occupations than in those who lead a more physically active life, and more likely to occur in those with high blood pressure than in those with normal blood pressure (see HYPERTENSION). Obesity is a contributory factor. The disease is more common among smokers than non-smokers; it is also often associated with a high level of CHOLESTEROL in the blood, which in turn has been linked with an excessive consumption of animal, as opposed to vegetable, fats. In this connection the important factors seem to be the saturated fatty acids (low-density and very low-density lipoproteins [LDLs and VLDLs] – see CHOLESTEROL) of animal fats which would appear to be more likely to lead to a high level of cholesterol in the blood than the unsaturated fatty acids of vegetable fats. As more research on the subject is carried out, the arguments continue about the relative in?uence of the di?erent factors. (For advice on prevention of the disease, see APPENDIX 2: ADDRESSES: SOURCES OF INFORMATION, ADVICE, SUPPORT AND SELFHELP.)
Symptoms The presenting symptom is the sudden onset, often at rest, of acute, agonising pain in the front of the chest. This rapidly radiates all over the front of the chest and often down over the abdomen. The pain is frequently accompanied by nausea and vomiting, so that suspicion may be aroused of some acute abdominal condition such as biliary colic (see GALLBLADDER, DISEASES OF) or a perforated PEPTIC ULCER. The victim soon goes into SHOCK, with a pale, cold, sweating skin, rapid pulse and dif?culty in breathing. There is usually some rise in temperature.
Treatment is immediate relief of the pain by injections of diamorphine. Thrombolytic drugs should be given as soon as possible (‘rapid door to needle time’) and ARRHYTHMIA corrected. OXYGEN is essential and oral ASPIRIN is valuable. Treatment within the ?rst hour makes a great di?erence to recovery. Subsequent treatment includes the continued administration of drugs to relieve the pain; the administration of ANTIARRHYTHMIC DRUGS that may be necessary to deal with the heart failure that commonly develops, and the irregular action of the heart that quite often develops; and the continued administration of oxygen. Patients are usually admitted to coronary care units, where they receive constant supervision. Such units maintain an emergency, skilled, round-the-clock sta? of doctors and nurses, as well as all the necessary resuscitation facilities that may be required.
The outcome varies considerably. The ?rst (golden) hour is when the patient is at greatest risk of death: if he or she is treated, then there is a 50 per cent reduction in mortality compared with waiting until hospital admission. As each day passes the prognosis improves with a ?rst coronary thrombosis, provided that the patient does not have a high blood pressure and is not overweight. Following recovery, there should be a gradual return to work, care being taken to avoid any increase in weight, unnecessary stress and strain, and to observe moderation in all things. Smoking must stop. In uncomplicated cases patients get up and about as soon as possible, most being in hospital for a week to ten days and back at work in three months or sooner.
Valvular heart disease primarily affects the mitral and aortic valves which can become narrowed (stenosis) or leaking (incompetence). Pulmonary valve problems are usually congenital (stenosis) and the tricuspid valve is sometimes involved when rheumatic heart disease primarily affects the mitral or aortic valves. RHEUMATIC FEVER, usually in childhood, remains a common cause of chronic valvular heart disease causing stenosis, incompetence or both of the aortic and mitral valves, but each valve has other separate causes for malfunction.
Aortic valve disease is more common with increasing age. When the valve is narrowed, the heart hypertrophies and may later fail. Symptoms of angina or breathlessness are common and dizziness or blackouts (syncope) also occur. Replacing the valve is a very e?ective treatment, even with advancing age. Aortic stenosis may be caused by degeneration (senile calci?c), by the inheritance of two valvular leaflets instead of the usual three (bicuspid valve), or by rheumatic fever. Aortic incompetence again leads to hypertrophy, but dilatation is more common as blood leaks back into the ventricle. Breathlessness is the more common complaint. The causes are the same as stenosis but also include in?ammatory conditions such as SYPHILIS or ANKYLOSING SPONDYLITIS and other disorders of connective tissue. The valve may also leak if the aorta dilates, stretching the valve ring as with HYPERTENSION, aortic ANEURYSM and MARFAN’S SYNDROME – an inherited disorder of connective tissue that causes heart defects. Infection (endocarditis) can worsen acutely or chronically destroy the valve and sometimes lead to abnormal outgrowths on the valve (vegetations) which may break free and cause devastating damage such as a stroke or blocked circulation to the bowel or leg.
Mitral valve disease leading to stenosis is rheumatic in origin. Mitral incompetence may be rheumatic but in the absence of stenosis can be due to ISCHAEMIA, INFARCTION, in?ammation, infection and a congenital weakness (prolapse). The valve may also leak if stretched by a dilating ventricle (functional incompetence). Infection (endocarditis) may affect the valve in a similar way to aortic disease. Mitral symptoms are predominantly breathlessness which may lead to wheezing or waking at night breathless and needing to sit up or stand for relief. They are made worse when the heart rhythm changes (atrial ?brillation) which is frequent as the disease becomes more severe. This leads to a loss of e?ciency of up to 25 per cent and a predisposition to clot formation as blood stagnates rather than leaves the heart e?ciently. Mitral incompetence may remain mild and be of no trouble for many years, but infection must be guarded against (endocarditis prophylaxis).
Endocarditis is an infection of the heart which may acutely destroy a valve or may lead to chronic destruction. Bacteria settle usually on a mild lesion. Antibiotics taken at vulnerable times can prevent this (antibiotic prophylaxis) – for example, before tooth extraction. If established, lengthy intravenous antibiotic therapy is needed and surgery is often necessary. The mortality is 30 per cent but may be higher if the infection settles on a replaced valve (prosthetic endocarditis). Complications include heart failure, shock, embolisation (generation of small clots in the blood), and cerebral (mental) confusion.
PERICARDITIS is an in?ammation of the sac covering the outside of the heart. The sac becomes roughened and pain occurs as the heart and sac rub together. This is heard by stethoscope as a scratching noise (pericardial rub). Fever is often present and a virus the main cause. It may also occur with rheumatic fever, kidney failure, TUBERCULOSIS or from an adjacent lung problem such as PNEUMONIA or cancer. The in?ammation may cause ?uid to accumulate between the sac and the heart (e?usion) which may compress the heart causing a fall in blood pressure, a weak pulse and circulatory failure (tamponade). This can be relieved by aspirating the ?uid. The treatment is then directed at the underlying cause.... heart, diseases of
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
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
According to the type of cells that predominate, leukaemia may be classi?ed as acute or chronic lymphoblastic leukaemia or myeloid leukaemia. Acute lymphoblastic leukaemia (ALL) is mostly a disease of childhood and is rare after the age of 25. Acute myeloid leukaemia is most common in children and young adults, but may occur at any age. Chronic lymphatic leukaemia occurs at any age between 35 and 80, most commonly in the 60s, and is twice as common in men as in women. Chronic myeloid leukaemia is rare before the age of 25, and most common between the ages of 30 and 65; men and women are equally affected. Around 2,500 patients with acute leukaemia are diagnosed in the United Kingdom, with a similar number annually diagnosed with chronic leukaemia.
Cause Both types of acute leukaemia seem to arise from a MUTATION in a single white cell. The genetically changed cell then goes through an uncontrolled succession of divisions resulting in many millions of abnormal white cells in the blood, bone marrow and other tissues. Possible causes are virus infection, chemical exposure, radiation and genetic background. The cause of chronic lymphocytic leukaemia is not known; the chronic myeloid version may have a genetic background.
Symptoms In acute cases the patient is pale due to anaemia, may have a purpuric rash due to lack of platelets, and may have enlarged lymphatic glands and spleen. The temperature is raised, and the condition may be mistaken for an acute infection (or may ?rst become apparent because the patient develops a severe infection due to a lack of normal white blood cells).
In the chronic type of the disease the onset is gradual, and the ?rst symptoms which occasion discomfort are either swelling of the abdomen and shortness of breath, due to painless enlargement of the spleen; or the enlargement of glands in the neck, armpits and elsewhere; or the pallor, palpitation, and other symptoms of anaemia which often accompany leukaemia. Occasional bleeding from the nose, stomach, gums or bowels may occur, and may be severe. Generally, there is a slight fever.
When the blood is examined microscopically, not only is there an enormous increase in the number of white cells, which may be multiplied 30- or 60-fold, but various immature forms are also found. In the lymphatic form of the disease, most white cells resemble lymphocytes, which, in healthy blood, are present only in small numbers. In the myeloid form, myelocytes, or large immature cells from the bone marrow, which are never present in healthy blood, appear in large numbers, and there may also be large numbers of immature, nucleated erythrocytes.
Treatment This varies according to the type of leukaemia and to the particular condition of the patient. Excellent results are being obtained in the control of ALL using blood transfusions, CHEMOTHERAPY, RADIOTHERAPY and bone-marrow TRANSPLANTATION. In the case of acute leukaemia, the drugs now being used include MERCAPTOPURINE, METHOTREXATE and CYCLOPHOSPHAMIDE. Blood transfusion and CORTICOSTEROIDS play an important part in controlling the condition during the period before a response to chemotherapy can be expected. Chemotherapy has almost completely replaced radiotherapy in the treatment of chronic leukaemia. For the myeloid form, BUSULFAN is the most widely used drug, replaced by hydroxyurea, mercaptopurine, or one of the nitrogen mustard (see NITROGEN MUSTARDS) derivatives in the later stages of the disease. For the lymphatic form, the drugs used are CHLORAMBUCIL, CYCLOPHOSPHAMIDE, and the nitrogen mustard derivatives.
Prognosis Although there is still no guaranteed cure, the outlook in both acute and chronic leukaemia has greatly improved – particularly for the acute form of the disease. Between 70 and 80 per cent of children with acute lymphoblastic leukaemia may be cured; between 20 and 50 per cent of those with acute myeloid leukaemia now have much-improved survival rates. Prognosis of patients with chronic lymphocytic leukaemia is often good, depending on early diagnosis.... leukaemia
In?ammation of the liver, or HEPATITIS, may occur as part of a generalised infection or may be a localised condition. Infectious hepatitis, which is the result of infection with a virus, is one of the most common forms. Many di?erent viruses can cause hepatitis, including that responsible for glandular fever (see MONONUCLEOSIS). Certain spirochaetes may also be the cause, particularly that responsible for LEPTOSPIROSIS, as can many drugs. Hepatitis may also occur if there is obstruction of the BILE DUCT, as by a gall-stone.
Cirrhosis of the liver A disorder caused by chronic damage to liver cells. The liver develops areas of ?brosis or scarring; in response, the remaining normal liver cells increase and form regeneration nodules. Those islands of normality, however, suffer from inadequate blood supply, thus adversely affecting liver function. Alcohol is the most common cause of cirrhosis in the United Kingdom and the USA, and the incidence of the disorder among women in the UK has recently risen sharply as a consequence of greater consumption of alcohol by young women in the latter decades of the 20th century. In Africa and many parts of Asia, infection with hepatitis B virus is a common cause. Certain drugs – for example, PARACETAMOL – may damage the liver if taken in excess. Unusual causes of cirrhosis include defects of the bile ducts, HAEMOCHROMATOSIS (raised iron absorption from the gut), CYSTIC FIBROSIS, cardiac cirrhosis (the result of heart failure causing circulatory congestion in the liver), and WILSON’S DISEASE (raised copper absorption).
Symptoms Some people with cirrhosis have no signs or symptoms and the disease may be diagnosed at a routine medical examination. Others may develop jaundice, OEDEMA (including ascites – ?uid in the abdomen), fever, confusion, HAEMATEMESIS (vomiting blood), loss of appetite and lethargy. On examination, cirrhotic patients often have an enlarged liver and/ or SPLEEN, and HYPERTENSION. Liver function tests, cholangiography (X-ray examination of the bile ducts) and biopsy of liver tissue will help to reach a diagnosis.
Treatment Nothing can be done to repair a cirrhosed organ, but the cause, if known, must be removed and further advance of the process thus prevented. In the case of the liver, a high-protein, high-carbohydrate, low-fat diet is given, supplemented by liver extract and vitamins B and K. The consumption of alcohol should be banned. In patients with liver failure and a poor prognosis, liver TRANSPLANTATION is worthwhile but only after careful consideration.
Abscess of the liver When an ABSCESS develops in the liver, it is usually a result of amoebic DYSENTERY, appearing sometimes late in the disease – even after the diarrhoea is cured (see below). It may also follow upon in?ammation of the liver due to other causes. In the case of an amoebic abscess, treatment consists of oral metronidazole.
Acute hepatic necrosis is a destructive and often fatal disease of the liver which is very rare. It may be due to chemical poisons, such as carbontetrachloride, chloroform, phosphorus and industrial solvents derived from benzene. It may also be the cause of death in cases of poisoning with fungi. Very occasionally, it may be a complication of acute infectious hepatitis.
Cancer of the liver is not uncommon, although it is rare for the disease to begin in the liver – the involvement of this organ being usually secondary to disease situated somewhere in the stomach or bowels. Cancer originating in the liver is more common in Asia and Africa. It usually arises in a ?brotic (or cirrhotic) liver and in carriers of the hepatitis B virus. There is great emaciation, which increases as the disease progresses. The liver is much enlarged, and its margin and surface are rough, being studded with hard cancer masses of varying size, which can often be felt through the abdominal wall. Pain may be present. Jaundice and oedema often appear.... liver, diseases of
Much more serious is spina bi?da cystica, in which the spinal-wall defect is accompanied by a protrusion of the spinal cord. This may take two forms: a meningocele, in which the MENINGES, containing CEREBROSPINAL FLUID, protrude through the defect; and a meningomyelocele, in which the protrusion contains spinal cord and nerves.
Meningocele is less common and has a good prognosis. HYDROCEPHALUS and neurological problems affecting the legs are rare, although the bladder may be affected. Treatment consists of surgery which may be in the ?rst few days of life or much later depending upon the precise situation; long-term follow-up is necessary to pick up any neurological problems that may develop during subsequent growth of the spine.
Meningomyelocele is much more serious and more common, accounting for 90 per cent of all cases. Usually affecting the lumbo-sacral region, the range of severity may vary considerably and, while early surgery with careful attention in a minor case may achieve good mobility, normal bladder function and intellect, a more extensive protrusion may cause complete ANAESTHESIA of the skin, with increased risk of trauma; extensive paralysis of the trunk and limbs, with severe deformities; and paralysis and insensitivity of the bladder and bowel. Involuntary movements may be present, and hydrocephalus occurs in 80 per cent of cases. The decision to operate can only be made after a full examination of the infant to determine the extent of the defect and any co-existent congenital abnormalities. The child’s potential can then be estimated, and appropriate treatment discussed with the parents. Carefully selected patients should receive long-term treatment in a special centre, where full attention can be paid to all their various problems.
There is growing evidence of the value of vitamin supplements before and during pregnancy in reducing the incidence of spina bi?da. Parents of affected infants may obtain help, advice, and encouragement from the Association for Spina Bi?da and Hydrocephalus which has branches throughout the country, or the Scottish Spina Bi?da Association.... spina bifida
Varieties Some are of an infective nature, as already stated; some arise as the result of injury, and several contributing factors are mentioned under the heading of CANCER.
Traditionally tumours have been divided into benign (simple) and malignant. Even benign tumours can be harmful, because their size or position may distort or damage nerves, blood vessels or organs. Usually, however, they are easily removed by surgery. Malignant tumours or cancers are harmful and potentially lethal, not just because they erode tissues locally but because many of them spread, either by direct growth or by ‘seeding’ to other parts – ‘metastasising’. Malignant tumours arise because of an uncontrolled growth of previously normal cells. Heredity, environmental factors and lifestyle all play a part in malignancy (see also ONCOGENES). Symptoms are caused by local spread and as a result of metastases. These cause serious local damage, for example, in the brain or lungs, as well as disturbing the body’s metabolism. Unless treated with CHEMOTHERAPY, RADIOTHERAPY or surgery or a combination of these, malignant tumours are ultimately fatal. Many, however, can now be cured. The original site and type of a malignant tumour usually determine the rate and extent of spread.
The type of cell and organ site determine the characteristics of a malignant tumour. The prognosis (outlook) for a patient with a malignant tumour depends largely upon how soon it is diagnosed. Staging criteria have been developed to assess the local and metastatic spread of a tumour, its size and also likely sensitivity to the types of available treatment. The ability to locate a tumour and its metastases accurately has vastly improved with the introduction of radionuclide and ULTRASOUND scanning, CT scanning and magnetic resonance imaging (MRI). Screening for cancers such as those in the breast, cervix, colorectal region and prostate help early diagnosis and usually improve treatment outcomes.
Tumours are now classed according to the tissues of which they are built, somewhat as follows:
simple tumours of normal tissue. hollow tumours or cysts, generally of simple nature.
malignant tumours: (a) of cellular structure, resembling the cells of skin, mucous membrane, or secreting glands; (b) of connective tissue.... tumour
Thrush is characterised by the presence of white patches on the mucous membrane which bleeds if the patch is gently removed. It is caused by the growth of a parasitic mould known as Candida albicans. Antifungal agents usually suppress the growth of candida. Candidal in?ltration of the mucosa is often found in cancerous lesions.
Leukoplakia literally means a white patch. In the mouth it is often due to an area of thickened cells from the horny layer of the epithelium. It appears as a white patch of varying density and is often grooved by dense ?ssures. There are many causes, most of them of minor importance. It may be associated with smoking, SYPHILIS, chronic SEPSIS or trauma from a sharp tooth. Cancer must be excluded.
Stomatitis (in?ammation of the mouth) arises from the same causes as in?ammation elsewhere, but among the main causes are the cutting of teeth in children, sharp or broken teeth, excess alcohol, tobacco smoking and general ill-health. The mucous membrane becomes red, swollen and tender and ulcers may appear. Treatment consists mainly of preventing secondary infection supervening before the stomatitis has resolved. Antiseptic mouthwashes are usually su?cient.
Gingivitis (see TEETH, DISEASES OF) is in?ammation of the gum where it touches the tooth. It is caused by poor oral hygiene and is often associated with the production of calculus or tartar on the teeth. If it is neglected it will proceed to periodontal disease.
Ulcers of the mouth These are usually small and arise from a variety of causes. Aphthous ulcers are the most common; they last about ten days and usually heal without scarring. They may be associated with STRESS or DYSPEPSIA. There is no ideal treatment.
Herpetic ulcers (see HERPES SIMPLEX) are similar but usually there are many ulcers and the patient appears feverish and unwell. This condition is more common in children.
Calculus (a) Salivary: a calculus (stone) may develop in one of the major salivary-gland ducts. This may result in a blockage which will cause the gland to swell and be painful. It usually swells before a meal and then slowly subsides. The stone may be passed but often has to be removed in a minor operation. If the gland behind the calculus becomes infected, then an ABSCESS forms and, if this persists, the removal of the gland may be indicated. (b) Dental, also called TARTAR: this is a calci?ed material which adheres to the teeth; it often starts as the soft debris found on teeth which have not been well cleaned and is called plaque. If not removed, it will gradually destroy the periodontal membrane and result in the loss of the tooth. (See TEETH, DISORDERS OF.)
Ranula This is a cyst-like swelling found in the ?oor of the mouth. It is often caused by mild trauma to the salivary glands with the result that saliva collects in the cyst instead of discharging into the mouth. Surgery may be required.
Mumps is an acute infective disorder of the major salivary glands. It causes painful enlargement of the glands which lasts for about two weeks. (See also main entry for MUMPS.)
Tumours may occur in all parts of the mouth, and may be BENIGN or MALIGNANT. Benign tumours are common and may follow mild trauma or be an exaggerated response to irritation. Polyps are found in the cheeks and on the tongue and become a nuisance as they may be bitten frequently. They are easily excised.
A MUCOCOELE is found mainly in the lower lip.
An exostosis or bone outgrowth is often found in the mid line of the palate and on the inside of the mandible (bone of the lower jaw). This only requires removal if it becomes unduly large or pointed and easily ulcerated.
Malignant tumours within the mouth are often large before they are noticed, whereas those on the lips are usually seen early and are more easily treated. The cancer may arise from any of the tissues found in the mouth including epithelium, bone, salivary tissue and tooth-forming tissue remnants. Oral cancers represent about 5 per cent of all reported malignancies, and in England and Wales around 3,300 people are diagnosed annually as having cancer of the mouth and PHARYNX.
Cancer of the mouth is less common below the age of 40 years and is more common in men. It is often associated with chronic irritation from a broken tooth or ill-?tting denture. It is also more common in those who smoke and those who chew betel leaves. Leukoplakia (see above) may be a precursor of cancer. Spread of the cancer is by way of the lymph nodes in the neck. Early treatment by surgery, radiotherapy or chemotherapy will often be e?ective, except for the posterior of the tongue where the prognosis is very poor. Although surgery may be extensive and potentially mutilating, recent advances in repairing defects and grafting tissues from elsewhere have made treatment more acceptable to the patient.... mouth, diseases of
However, calling a condition psychosomatic implies something more – the primacy of the psyche over the soma. Going back to the in?uential theories and practice of PSYCHOANALYSIS as expounded from the 1930s, many diseases have been proposed as the result of psychological factors.These have included PEPTIC ULCER, ULCERATIVE COLITIS, ASTHMA, PSORIASIS and others. In this view, much physical disorder is due to repressed or excessive emotions. Likewise it is also argued that whereas some people express psychological distress via psychological symptoms (such as anxiety, depression and so on), others develop physical symptoms instead – and that they are also at greater risk of physical disease.
The trouble with this view is that medical advances repeatedly show that it goes too far. Stress certainly causes physical symptoms – for example, DYSPEPSIA – but the belief that it caused peptic ulcers vanished with the discovery of the true cause: colonisation of the stomach by the bacterium, Helicobacter pylori. Of course, stress and social adversity affect the risk of many diseases. For example, the incidence of heart disease among UK government employees (civil servants) has been shown to be in?uenced by their social class and their degree of job satisfaction. But we do not know how this works. Some argue that social adversity and stress in?uence how the heart functions (‘He died of a broken heart’). Stress can also affect IMMUNITY but it cannot cause AIDS/HIV and we do not know if there is a link running from stress to abnormal immune function to actual illness.
We can say that psychological factors provoke physical symptoms, and often even explain how this can happen. For example, when you are anxious you produce more epinephrine (adrenaline), which gives rise to chest pain, ‘butter?ies in the stomach’ and PALPITATION. These symptoms are not ‘all in the mind’, even if the trigger is a psychological one. People who are depressed are more likely to experience nearly every physical symptom there is, but especially pain and fatigue. Taken as a whole, psychologically induced symptoms are an enormous burden on the NHS and probably responsible for more doctor visits and sickness absence than any other single cause. Also we can be con?dent that social adversity and stress powerfully in?uence the outcome of many illnesses; likewise, a vast range of unhealthy activities and behaviours such as smoking, excessive alcohol intake, excessive eating, and so on. But we must be careful not to assume that our emotions directly cause our illnesses.... psychosomatic diseases
Causes: hereditary background with deficiency of cell enzymes or cell membrane weakness; wrongly matched blood transfusion, environmental chemicals, food additives, colourings, drugs, infections. Symptoms. Pale face, sore tongue, headache, dizziness, palpitations, breathlessness, angina, weakness, loss of weight and appetite, jaundice (yellow skin), feverishness, vague aches and pains, enlarged spleen and pain under left ribs.
Treatment. Under hospital supervision.
Echinacea has a long reputation for regeneration of red blood cells: experience shows it beneficial for this type of anaemia. To assist control of symptoms: Gentian, Motherwort, Mugwort, Barberry, Hops, Saw Palmetto.
Bitter herbs stimulate the stomach, liver and pancreas. By increasing the appetite they benefit digestion and are given half an hour before meals by tea or decoction: Hops, Quassia chips, Angostura, Feverfew, Bogbean.
Formula. Tea. Milk Thistle 2; Betony 1; Hops 1. Mix. 1-2 teaspoon to each cup boiling water. Infuse 5-15 minutes. 1 cup, thrice daily.
Decoction. Echinacea 1; Sarsaparilla 1; Peruvian bark half; Saw Palmetto half. Mix. 2 teaspoons to 2 cups water, simmer gently 20 minutes. Half a cup, cold, thrice daily before meals.
For weak heart add one part Hawthorn; neurasthenia (Ginkgo); swelling of ankles (Lily of the Valley); loss of hormonal balance (Ginseng).
Prognosis. Surgical removal of spleen may be necessary.
Diet. Dandelion coffee, molasses, desiccated or fresh calves’ liver. Green leafy vegetables, dried beans, apricots. Shellfish, milk, eggs, Soya, meats. Supplements. Daily. Vitamin B12 1mg; Vitamin C, 1g; Folic acid 400mcg; Floradix. ... anaemia: haemolytic
Causes There is a major immunogenetic predisposition to rheumatoid arthritis in people carrying the HLA-DR4 antigen (see HLA SYSTEM). Other minor immunogenetic factors have also been implicated. In addition, there is a degree of familial clustering which suggests other unidenti?ed genetic factors. Genetic factors cannot alone explain aetiology, and environmental and chance factors must be important, but these have yet to be identi?ed.
Epidemiology Rheumatoid arthritis more commonly occurs in women from the age of 30 onwards, the sex ratio being approximately 4:1. Typical rheumatoid arthritis may occur in adolescence, but in childhood chronic SYNOVITIS usually takes one of a number of di?erent patterns, classi?ed under juvenile chronic arthritis.
Pathology The primary lesion is an in?ammation of the synovial membrane of joints. The synovial ?uid becomes diluted with in?ammatory exudate: if this persists for months it leads to progressive destruction of articular CARTILAGE and BONE. Cartilage is replaced by in?ammatory tissue known as pannus; a similar tissue invades bone to form erosions. Synovitis also affects tendon sheaths, and may lead to adhesion ?brosis or attrition and rupture of tendons. Subcutaneous and other bursae may be involved. Necrobiotic nodules also occur at sites outside synovium, including the subcutaneous tissues, the lungs, the pericardium and the pleura.
Clinical features Rheumatoid arthritis varies from the very mild to the severely disabling. Many mild cases probably go undiagnosed. At least 50 per cent of patients continue to lead a reasonably normal life; around 25 per cent are signi?cantly disabled in terms of work and leisure activities; and a minority become markedly disabled and are limited in their independence. There is often an early acute phase, followed by substantial remission, but in other patients gradual step-wise deterioration may occur, with progressive involvement of an increasing number of joints.
The diagnosis of rheumatoid arthritis is largely based on clinical symptoms and signs. Approximately 70 per cent of patients have rheumatoid factor ANTIBODIES in the SERUM but, because of the large number of false positives and false negatives, this test has very little value in clinical practice. It may be a useful pointer to a worse prognosis in early cases if the level is high. X-RAYS may help in diagnosing early cases and are particularly helpful when considering surgery or possible complications such as pathological fracture. Patients commonly develop ANAEMIA, which may be partly due to gastrointestinal blood loss from antiin?ammatory drug treatment (see below).
Treatment involves physical, pharmacological, and surgical measures, together with psychological and social support tailored to the individual patient’s needs. Regular activity should be maintained. Resting of certain joints such as the wrist with splints may be helpful at night or to assist prolonged manual activities. Sound footwear is important. Early use of antirheumatic drugs reduces long-term disability. Drug treatment includes simple ANALGESICS, NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS), and slow-acting drugs including GOLD SALTS (in the form of SODIUM AUROTHIOMALATE), PENICILLAMINE, SULFASALAZINE, METHOTREXATE and AZATHIOPRINE.
The non-steroidal agents are largely e?ective in reducing pain and early-morning sti?ness, and have no e?ect on the chronic in?ammatory process. It is important, especially in the elderly, to explain to patients the adverse effects of NSAIDs, the dosage of which can be cut by prescribing paracetamol at the same time. Combinations of anti-rheumatic drugs seem better than single agents. The slow-acting drugs take approximately three months to act but have a more global e?ect on chronic in?ammation, with a greater reduction in swelling and an associated fall in erythrocyte sedimentation rate (ESR) and rise in the level of HAEMOGLOBIN. Local CORTICOSTEROIDS are useful, given into individual joints. Systemic corticosteroids carry serious problems if continued long term, but may be useful under special circumstances. Much research is currently going on into the use of tumour necrosis factor antagonists such as INFLIXIMAB and etanercept, but their precise role remains uncertain.... rheumatoid arthritis
Louse typhus, in which the infecting rickettsia is transmitted by the louse, is of worldwide distribution. More human deaths have been attributed to the louse via typhus, louse-borne RELAPSING FEVER and trench fever, than to any other insect with the exception of the MALARIA mosquito. Louse typhus includes epidemic typhus, Brill’s disease – which is a recrudescent form of epidemic typhus – and TRENCH FEVER.
Epidemic typhus fever, also known as exanthematic typhus, classical typhus, and louse-borne typhus, is an acute infection of abrupt onset which, in the absence of treatment, persists for 14 days. It is of worldwide distribution, but is largely con?ned today to parts of Africa. The causative organism is the Rickettsia prowazeki, so-called after Ricketts and Prowazek, two brilliant investigators of typhus, both of whom died of the disease. It is transmitted by the human louse, Pediculus humanus. The rickettsiae can survive in the dried faeces of lice for 60 days, and these infected faeces are probably the main source of human infection.
Symptoms The incubation period is usually 10–14 days. The onset is preceded by headache, pain in the back and limbs and rigors. On the third day the temperature rises, the headache worsens, and the patient is drowsy or delirious. Subsequently a characteristic rash appears on the abdomen and inner aspect of the arms, to spread over the chest, back and trunk. Death may occur from SEPTICAEMIA, heart or kidney failure, or PNEUMONIA about the 14th day. In those who recover, the temperature falls by CRISIS at about this time. The death rate is variable, ranging from nearly 100 per cent in epidemics among debilitated refugees to about 10 per cent.
Murine typhus fever, also known as ?ea typhus, is worldwide in its distribution and is found wherever individuals are crowded together in insanitary, rat-infested areas (hence the old names of jail-fever and ship typhus). The causative organism, Rickettsia mooseri, which is closely related to R. prowazeki, is transmitted to humans by the rat-?ea, Xenopsyalla cheopis. The rat is the main reservoir of infection; once humans are infected, the human louse may act as a transmitter of the rickettsia from person to person. This explains how the disease may become epidemic under insanitary, crowded conditions. As a rule, however, the disease is only acquired when humans come into close contact with infected rats.
Symptoms These are similar to those of louse-borne typhus, but the disease is usually milder, and the mortality rate is very low (about 1·5 per cent).
Tick typhus, in which the infecting rickettsia is transmitted by ticks, occurs in various parts of the world. The three best-known conditions in this group are ROCKY MOUNTAIN SPOTTED FEVER, ?èvre boutonneuse and tick-bite fever.
Mite typhus, in which the infecting rickettsia is transmitted by mites, includes scrub typhus, or tsutsugamushi disease, and rickettsialpox.
Rickettsialpox is a mild disease caused by Rickettsia akari, which is transmitted to humans from infected mice by the common mouse mite, Allodermanyssus sanguineus. It occurs in the United States, West and South Africa and the former Soviet Union.
Treatment The general principles of treatment are the same in all forms of typhus. PROPHYLAXIS consists of either avoidance or destruction of the vector. In the case of louse typhus and ?ea typhus, the outlook has been revolutionised by the introduction of e?cient insecticides such as DICHLORODIPHENYL TRICHLOROETHANE (DDT) and GAMMEXANE.
The value of the former was well shown by its use after World War II: this resulted in almost complete freedom from the epidemics of typhus which ravaged Eastern Europe after World War I, being responsible for 30 million cases with a mortality of 10 per cent. Now only 10,000–20,000 cases occur a year, with around a few hundred deaths. E?cient rat control is another measure which reduces the risk of typhus very considerably. In areas such as Malaysia, where the mites are infected from a wide variety of rodents scattered over large areas, the wearing of protective clothing is the most practical method of prophylaxis. CURATIVE TREATMENT was revolutionised by the introduction of CHLORAMPHENICOL and the TETRACYCLINES. These antibiotics altered the prognosis in typhus fever very considerably.... typhus fever
Prevention is best. Wipe over possible areas with whisky or Vodka following with Oil of St John’s Wort. Bed patients are encouraged to spend at least 2 or 3 hours out of bed daily. Many kinds of bed-care aids exist: inflatable rings, water beds and padded protection. Vitamin C deficiency exists in most cases. Treatment. Herbal antibiotics: Wild Indigo, Myrrh, Milk Thistle, Goldenseal, Echinacea, Marigold. Supportives: Comfrey, Sarsaparilla, Vitamin E.
Tablets/capsules. Goldenseal, Echinacea, Sarsaparilla.
Powders. Parts: Echinacea 2; Goldenseal 1; Liquorice 1. Dose: 750mg (three 00 capsules or half a teaspoon) thrice daily.
Tinctures. Wild Indigo 1; Echinacea 2; Goldenseal quarter. 1-2 teaspoons in water 3 times daily. Practitioner. Tincture Echinacea BHP (1983) 20ml; Tincture Goldenseal BPC (1949) 5ml; Tincture Marigold BPC (1934) 10ml. Low alcohol vodka to 100ml. Sig: 5ml (3i) tds aq. cal. AC. (Anonymous) Topical. Early stages: Comfrey poultice or ointment. Marshmallow and Slippery Elm ointment; Oil St John’s Wort, Rue tea. Fresh pulp of Aloe Vera. Later stages: Sunlight soap plaster. Official medicine at the turn of the century used Lassar’s paste or zinc and castor oil ointment which are still effective. Distilled extract of Witch Hazel. For threatened gangrene, skin breakdown with formation of slough: (1) Zinc and Castor oil ointment (or cream) plus a little powdered Myrrh. (2) Cold poultice of Comfrey powder. ... bedsores
Symptoms. Failing appetite, weight loss, flatulence, bowel symptoms, bladder disturbance, abdominal pain, clothes tight around the abdomen. The disease usually presents after the age of 45, users of contraceptives having a lower risk of development.
Risk of ovarian cancer has been related to women who consume too much animal fat and too little vegetable fat (JAM Nov. 1984). A similar risk is recorded in a report from Milan providing strong evidence of its relation to excessive coffee consumption.
Researchers at John Hopkin’s University, Baltimore, USA, report success with Taxol, extracted from the bark of the Pacific Yew Tree, given intravenously to 40 women with ovarian cancer resistant to other therapies, caused a 50 per cent decrease in size of the tumours. (New Scientist 1989, 1687, p37) Treatment. Should it be necessary to defer surgery or cytotoxic chemotherapy, any of the following alternatives may be taken with profit, or prescribed as secondary to primary treatment.
Tea. Equal parts: Agnus Castus, Gotu Kola, Red Clover. 1 heaped teaspoon to each cup boiling water; infuse 5-15 minutes. Drink freely.
Formula. Cramp bark 3; Liquorice 1; Thuja 1; Poke root half. Mix. Dose: Powders: 750mg (three 00 capsules or half a teaspoon). Liquid extracts: 1 teaspoon. Tinctures: 2 teaspoons. Thrice daily.
Vaginal pack. 8 parts Slippery Elm powder mixed with 1 part Thuja powder in a little water to form a paste; saturate tampon and insert.
Dr J. Christopher. For pre- and post-operative pain: Black Willow.
British Herbal Pharmacopoeia. Cramp bark for pain.
Diet. See: DIET – CANCER. Drinks of Violet leaf tea freely.
Supplements. Post-operative treatment should include Comfrey and Calcium to counter the loss of calcium on surgical removal, with possible brittle and broken bones in ageing women.
Note: When a potential lesion is found, a pelvic ultrasound scan may confirm.
Treatment by gynaecologist or oncologist. ... cancer – ovaries
Cause: Septicaemia or infected embolism conveyed from elsewhere – veins of the face, sinuses, head. May be a complication of meningitis.
Symptoms: headache, nausea, swelling of eyelids and forehead, pupils distended, veins of temples prominent, fever with severe constitutional disturbance.
Prognosis: usually fatal in the absence of orthodox antibiotics, but anti-staphylococcal herbs are helpful. Tinctures. Formula. Echinacea 3; Goldenseal 2; Myrrh (Tincture) 1. 1 teaspoon in water every 2 hours (acute). Thrice daily (chronic).
Treatment by or in liaison with general medical practitioner. ... cavernous sinus thrombosis
Symptoms: Influenza-like fever, breathlessness, cough.
Prognosis: Chronic lung damage and progressive disability.
Indicated: antifungals, antibiotics.
Alternatives. Teas. Marigold, Ground Ivy, Scarlet Pimpernel, Yarrow. 1 heaped teaspoon to each cup boiling water; infuse 5-15 minutes; 1 cup freely.
Tablets/capsules. Garlic, Echinacea, Goldenseal, Thuja.
Powders. Combine, parts, Echinacea 3; Goldenseal 1; Thuja 1. Dose: 500mg, (two 00 capsules or one- third teaspoon) thrice daily.
Decoction. Irish Moss, to promote expectoration and eliminate debris.
Tinctures. Alternatives. (1) Echinacea 2; Lobelia 1; Liquorice 1. (2) Equal parts: Wild Indigo, Thuja and Pleurisy root. (3) Echinacea 2; Marigold 1; Thuja half; Liquorice half. Dosage: two 5ml teaspoons in water thrice daily. Acute cases: every 2 hours.
Topical. Inhalation of Eucalyptus or Tea Tree oils.
Diet. See: DIET – GENERAL. Yoghurt in place of milk.
Note: Bronchodilators of little value. Those at risk should have an X-ray at regular intervals. ... farmer’s lung
The course and severity of the disease vary. Typically, a child passes unformed, pale, oily, foul-smelling faeces and may fail to thrive. Often, growth is stunted and the child has recurrent respiratory infections. Without prompt treatment, pneumonia, bronchitis, and bronchiectasis may develop, causing lung damage. Most male sufferers and some females are infertile. CF causes excessive loss of salt in sweat, and heatstroke and collapse may occur in hot weather.
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