In medical terms, a temporary loss or impairment of consciousness that occurs in some forms of epilepsy, typically generalized absence (petit mal) seizures in childhood.
A few patients with primary amenorrhoea have an abnormality of their CHROMOSOMES or malformation of the genital tract such as absecence of the UTERUS (see TURNER’S SYNDROME). A gynaecological examination will rarely disclose an IMPERFORATE HYMEN in a young girl who may also complain of regular cycles of pain like period pains.
There are many causes of secondary amenorrhoea and management requires dealing with the primary cause. The commonest cause is pregnancy. Disorders of the HYPOTHALAMUS and related psychological factors such as anorexia nervosa (see EATING DISORDERS) also cause amenorrhoea, as can poor nutrition and loss of weight by extreme dieting. It is common in ballet dancers and athletes who exercise a great deal, but can also be triggered by serious illnesses such as tuberculosis or malaria. Excess secretion of prolactin, either due to a micro-adenoma (see ADENOMA) of the PITUITARY GLAND or to various prescription drugs will produce amenorrhoea, and sometimes GALACTORRHOEA as well. Malfunction of other parts of the pituitary gland will cause failure to produce GONADOTROPHINS, thus causing ovarian failure with consequent amenorrhea. In CUSHING’S SYNDROME, amenorrhoea is caused by excessive production of cortisol. Similarly, androgen-production abnormalities are found in the common POLYCYSTIC OVARY SYNDROME. These conditions also have abnormalities of the insulin/glucose control mechanisms. Taking the contraceptive pill is not now considered to provoke secondary amenorrhoea but OBESITY and HYPOTHYROIDISM are potential causes.
When the cause is weight loss, restoring body weight may alone restore menstruation. Otherwise, measuring gonadotrophic hormone levels will help show whether amenorrhoea is due to primary ovarian failure or secondary to pituitary disease. Women with raised concentrations of serum gonadotrophic hormones have primary ovarian failure. When amenorrhoea is due to limited pituitary failure, treatment with CLOMIPHENE may solve the problem.... amenorrhoea
Three forms: major (grand mal); temporal lobe; and minor (petit mal). In petit mal the period of unconsciousness consists of brief absences lasting less than 15 seconds.
Treatment. Orthodox medical: Carbamazepine, phenytoin and many other drugs.
Alternatives. BHP (1983) recommends: Grand mal: Passion flower, Skullcap, Verbena. Petit mal: Hyssop. Standard central nervous system relaxants are Hops, Lobelia, Passion flower, Vervain, Valerian, Skullcap. Wm Boericke used Mugwort. Peony leaf tea had a long traditional use. In nearly all epileptics there is functional heart disturbance (Hawthorn, Lily of the Valley, Motherwort). Mistletoe can help in the struggle to control seizures and improve the quality of life.
Two important remedies are Skullcap and Passion flower. Both work quickly without risk of respiratory arrest. If dose by mouth is not possible insert gelatin capsules containing powders, per rectum, child or adult lying prone. This method is particularly suitable for feverish convulsions or Grand mal.
Repeat after 5 minutes if patient continues in convulsion. Where neither of these powders are available, Chamomile, Valerian or Mistletoe may be used.
“The remedy I have relied on most,” writes C.I. Reid, MD (Ellingwood’s Journal) “is Passion flower. Use this alone or in combination with Gelsemium – more often alone. I cannot say I obtain an absolutely curative effect, but the spasms disappear and do not return while the remedy is continued. It has none of the unpleasant effects of other medicines. I give the liquid extract in doses from 25-30 drops, 3-4 times daily, for continued use. It may be given more frequently for convulsions.”
Alfred Dawes, MNIMH. Green tincture of Mistletoe, 3-5 drops. Or, combine equal parts: Liquid Extract Skullcap, Valerian and Black Horehound.
Finlay Ellingwood MD combines White Bryony, Prickly Ash, Skullcap and St John’s Wort.
Samuel Thomson MD. Lobelia 2; Cayenne 1; (antispasmodic drops) given at the premonitary stage. 1-2 teaspoons.
Edgar Cayce. Passion flower tea. Hot Castor oil packs.
Excess acidity and intestinal toxaemia. There is considerable opinion that these trigger an attack. Combination: Liquid Extracts – Skullcap 15ml; Mistletoe 10ml; Meadowsweet 10ml; Elderflowers 10ml. Two 5ml teaspoons in water thrice daily.
West African Black Pepper. (Piper guineense) is used by traditional Nigerian healers to good effect. Associated with imperfect menstruation. Liquid Extracts, single or in combination: Black Cohosh, Life root, Lobelia. Dose: 5-15 drops thrice daily.
Associated with mental weakness. Liquid Extract Oats (avena sativa). 2-3 teaspoons in water thrice daily.
Aromatherapy. (Complex partial seizures) Massage with essential oils found to be beneficial. (The Lancet, 1990, 336 (8723) 1120)
Diet. Salt-free lacto-vegetarian. Oatmeal porridge. A cleansing 8-day grape juice fast has its advocates. Vitamin E. In 24 epileptic children refractory to anti-epileptic drugs (AEDs) with generalised tonic- clonic and other types of seizures, addition of Vitamin E 400iu daily to existing AEDs was accompanied by a significant reduction in 10 of 12 cases. (Epilepsy 1989; 30(1): 84-89)
Supportives: osteopathic or chiropractic adjustments.
Note: A number of Italian physicians linked a salt-rich diet with epileptic fits. Number and violence diminished when discontinued and did not recur for weeks. Dr W.P. Best found that, in children, circumcism made a valuable contribution.
Drug-dependency. Herbal medication may offer a supportive role to primary medical treatment. Under no circumstances should sufferers discontinue basic orthodox treatments except upon the advice of a physician.
Information. British Epilepsy Association, 40 Hanover Square, Leeds LS3 1BE, UK. Send SAE.
To be treated by or in liaison with a qualified medical practitioner. ... epilepsy
The speciality of anaesthesia broadly covers its provision for SURGERY, intensive therapy (intensive care), chronic pain management, acute pain management and obstetric analgesia. Anaesthetists in Britain are trained specialists with a medical degree, but in many countries some anaesthetists may be nurse practitioners working under the supervision of a medical anaesthetist.
The anaesthetist will assess the patient’s ?tness for anaesthesia, choose and perform the appropriate type of anaesthetic while monitoring and caring for the patient’s well-being, and, after the anaesthetic, supervise recovery and the provision of post-operative pain relief.
Anaesthesia may be broadly divided into general and local anaesthesia. Quite commonly the two are combined to allow continued relief of pain at the operation site after the patient awakens.
General anaesthesia is most often produced by using a combination of drugs to induce a state of reversible UNCONSCIOUSNESS. ‘Balanced’ anaesthesia uses a combination of drugs to provide unconsciousness, analgesia, and a greater or lesser degree of muscle relaxation.
A general anaesthetic comprises induction, maintenance and recovery. Historically, anaesthesia has been divided into four stages (see below), but these are only clearly seen during induction and maintenance of anaesthesia using inhalational agents alone.
(1) Onset of induction to unconsciousness
(2) Stage of excitement
(3) Surgical anaesthesia
(4) Overdosage
Induction involves the initial production of unconsciousness. Most often this is by INTRAVENOUS injection of a short-acting anaesthetic agent such as PROPOFOL, THIOPENTONE or ETOMIDATE, often accompanied by additional drugs such as ANALGESICS to smooth the process. Alternatively an inhalational technique may be used.
Maintenance of anaesthesia may be provided by continuous or intermittent use of intravenous drugs, but is commonly provided by administration of OXYGEN and NITROUS OXIDE or air containing a volatile anaesthetic agent. Anaesthetic machines are capable of providing a constant concentration of these, and have fail-safe mechanisms and monitors which guard against the patient’s receiving a gas mixture with inadequate oxygen (see HYPOXIC). The gases are adminstered to the patient via a breathing circuit either through a mask, a laryngeal mask or via ENDOTRACHEAL INTUBATION. In recent years, concerns about side-effects and pollution caused by volatile agents have led to increased popularity of total intravenous anaesthesia (TIVA).
For some types of surgery the patient is paralysed using muscle relaxants and then arti?cially ventilated by machine (see VENTILATOR). Patients are closely monitored during anaesthesia by the anaesthetist using a variety of devices. Minimal monitoring includes ELECTROCARDIOGRAM (ECG), blood pressure, PULSE OXIMETRY, inspired oxygen and end-tidal carbon-dioxide concentration – the amount of carbon dioxide breathed out when the lungs are at the ‘empty’ stage of the breathing cycle. Analgesic drugs (pain relievers) and local or regional anaesthetic blocks are often given to supplement general anaesthesia.
Volatile anaesthetics are either halogenated hydrocarbons (see HALOTHANE) or halogenated ethers (iso?urane, en?urane, des?urane and sevo?urane). The latter two are the most recently introduced agents, and produce the most rapid induction and recovery – though on a worldwide basis halothane, ether and chloroform are still widely used.
Despite several theories, the mode of action of these agents is not fully understood. Their e?cacy is related to how well they dissolve into the LIPID substances in nerve cells, and it is thought that they act at more than one site within brain cells – probably at the cell membrane. By whatever method, they reversibly depress the conduction of impulses within the CENTRAL NERVOUS SYSTEM and thereby produce unconsciousness.
At the end of surgery any muscle relaxant still in the patient’s body is reversed, the volatile agent is turned o? and the patient breathes oxygen or oxygen-enriched air. This is the reversal or recovery phase of anaesthesia. Once the anaesthetist is satis?ed with the degree of recovery, patients are transferred to a recovery area within the operating-theatre complex where they are cared for by specialist sta?, under the supervision of an anaesthetist, until they are ready to return to the ward. (See also ARTIFICIAL VENTILATION OF THE LUNGS.) Local anaesthetics are drugs which reversibly block the conduction of impulses in nerves. They therefore produce anaesthesia (and muscle relaxation) only in those areas of the body served by the nerve(s) affected by these drugs. Many drugs have some local anaesthetic action but the drugs used speci?cally for this purpose are all amide or ester derivatives of aromatic acids. Variations in the basic structure produce drugs with di?erent speeds of onset, duration of action and preferential SENSORY rather than MOTOR blockade (stopping the activity in the sensory or motor nerves respectively).
The use of local rather than general anaesthesia will depend on the type of surgery and in some cases the unsuitability of the patient for general anaesthesia. It is also used to supplement general anaesthesia, relieve pain in labour (see under PREGNANCY AND LABOUR) and in the treatment of pain in persons not undergoing surgery. Several commonly used techniques are listed below:
LOCAL INFILTRATION An area of anaesthetised skin or tissue is produced by injecting local anaesthetic around it. This technique is used for removing small super?cial lesions or anaesthetising surgical incisions.
NERVE BLOCKS Local anaesthetic is injected close to a nerve or nerve plexus, often using a peripheral nerve stimulator to identify the correct point. The anaesthetic di?uses into the nerve, blocking it and producing anaesthesia in the area supplied by it.
SPINAL ANAESTHESIA Small volumes of local anaesthetic are injected into the cerebrospinal ?uid through a small-bore needle which has been inserted through the tissues of the back and the dura mater (the outer membrane surrounding the spinal cord). A dense motor and sensory blockade is produced in the lower half of the body. How high up in the body it reaches is dependent on the volume and dose of anaesthetic, the patient’s position and individual variation. If the block is too high, then respiratory-muscle paralysis and therefore respiratory arrest may occur. HYPOTENSION (low blood pressure) may occur because of peripheral vasodilation caused by sympathetic-nerve blockade. Occasionally spinal anaesthesia is complicated by a headache, perhaps caused by continuing leakage of cerebrospinal ?uid from the dural puncture point.
EPIDURAL ANAESTHESIA Spinal nerves are blocked in the epidural space with local anaesthetic injected through a ?ne plastic tube (catheter) which is introduced into the space using a special needle (Tuohy needle). It can be used as a continuous technique either by intermittent injections, an infusion or by patient-controlled pump. This makes it ideal for surgery in the lower part of the body, the relief of pain in labour and for post-operative analgesia. Complications include hypotension, spinal headache (less than 1:100), poor e?cacy, nerve damage (1:12,000) and spinal-cord compression from CLOT or ABSCESS (extremely rare).... anaesthesia
Menstruation depends upon a functioning ovary (see OVARIES) and this upon a healthy PITUITARY GLAND. The regular rhythm may depend upon a centre in the HYPOTHALAMUS, which is in close connection with the pituitary. After menstruation, the denuded uterine ENDOMETRIUM is regenerated under the in?uence of the follicular hormone, oestradiol. The epithelium of the endometrium proliferates, and about a fortnight after the beginning of menstruation great development of the endometrial glands takes place under the in?uence of progesterone, the hormone secreted by the CORPUS LUTEUM. These changes are made for the reception of the fertilised OVUM. In the absence of fertilisation the uterine endometrium breaks down in the subsequent menstrual discharge.
Disorders of menstruation In most healthy women, menstruation proceeds regularly for 30 years or more, with the exceptions connected with childbirth. In many women, however, menstruation may be absent, excessive or painful. The term amenorrhoea is applied to the condition of absent menstruation; the terms menorrhagia and metrorrhagia describe excessive menstrual loss – the former if the excess occurs at the regular periods, and the latter if it is irregular. Dysmenorrhoea is the name given to painful menstruation. AMENORRHOEA If menstruation has never occurred, the amenorrhoea is termed primary; if it ceases after having once become established it is known as secondary amenorrhoea. The only value of these terms is that some patients with either chromosomal abnormalities (see CHROMOSOMES) or malformations of the genital tract fall into the primary category. Otherwise, the age of onset of symptoms is more important.
The causes of amenorrhoea are numerous and treatment requires dealing with the primary cause. The commonest cause is pregnancy; psychological stress or eating disorders can cause amenorrhoea, as can poor nutrition or loss of weight by dieting, and any serious underlying disease such as TUBERCULOSIS or MALARIA. The excess secretion of PROLACTIN, whether this is the result of a micro-adenoma of the pituitary gland or whether it is drug induced, will cause amenorrhoea and possibly GALACTORRHOEA as well. Malfunction of the pituitary gland will result in a failure to produce the gonadotrophic hormones (see GONADOTROPHINS) with consequent amenorrhoea. Excessive production of cortisol, as in CUSHING’S SYNDROME, or of androgens (see ANDROGEN) – as in the adreno-genital syndrome or the polycystic ovary syndrome – will result in amenorrhoea. Amenorrhoea occasionally follows use of the oral contraceptive pill and may be associated with both hypothyroidism (see under THYROID GLAND, DISEASES OF) and OBESITY.
Patients should be reassured that amenorrhoea can often be successfully treated and does not necessarily affect their ability to have normal sexual relations and to conceive. When weight loss is the cause of amenorrhoea, restoration of body weight alone can result in spontaneous menstruation (see also EATING DISORDERS – Anorexia nervosa). Patients with raised concentration of serum gonadotrophin hormones have primary ovarian failure, and this is not amenable to treatment. Cyclical oestrogen/progestogen therapy will usually establish withdrawal bleeding. If the amenorrhoea is due to mild pituitary failure, menstruation may return after treatment with clomiphene, a nonsteroidal agent which competes for oestrogen receptors in the hypothalamus. The patients who are most likely to respond to clomiphene are those who have some evidence of endogenous oestrogen and gonadotrophin production. IRREGULAR MENSTRUATION This is a change from the normal monthly cycle of menstruation, the duration of bleeding or the amount of blood lost (see menorrhagia, below). Such changes may be the result of an upset in the balance of oestrogen and progesterone hormones which between them control the cycle. Cycles may be irregular after the MENARCHE and before the menopause. Unsuspected pregnancy may manifest itself as an ‘irregularity’, as can an early miscarriage (see ABORTION). Disorders of the uterus, ovaries or organs in the pelvic cavity can also cause irregular menstruation. Women with the condition should seek medical advice. MENORRHAGIA Abnormal bleeding from the uterus during menstruation. A woman loses on average about 60 ml of blood during her period; in menorrhagia this can rise to 100 ml. Some women have this problem occasionally, some quite frequently and others never. One cause is an imbalance of progesterone and oestrogen hormones which between them control menstruation: the result is an abnormal increase in the lining (endometrium) of the uterus, which increases the amount of ‘bleeding’ tissue. Other causes include ?broids, polyps, pelvic infection or an intrauterine contraceptive device (IUD – see under CONTRACEPTION). Sometimes no physical reason for menorrhagia can be identi?ed.
Treatment of the disorder will depend on how severe the loss of blood is (some women will become anaemic – see ANAEMIA – and require iron-replacement therapy); the woman’s age; the cause of heavy bleeding; and whether or not she wants children. An increase in menstrual bleeding may occur in the months before the menopause, in which case time may produce a cure. Medical or surgical treatments are available. Non-steroidal anti-in?ammatory drugs may help, as may tranexamic acid, which prevents the breakdown of blood clots in the circulation (FIBRINOLYSIS): this drug can be helpful if an IUD is causing bleeding. Hormones such as dydrogesterone (by mouth) may cure the condition, as may an IUD that releases small quantities of a PROGESTOGEN into the lining of the womb.
Traditionally, surgical intervention was either dilatation and curettage of the womb lining (D & C) or removal of the whole uterus (HYSTERECTOMY). Most surgery is now done using minimally invasive techniques. These do not require the abdomen to be cut open, as an ENDOSCOPE is passed via the vagina into the uterus. Using DIATHERMY or a laser, the surgeon then removes the whole lining of the womb. DYSMENORRHOEA This varies from discomfort to serious pain, and sometimes includes vomiting and general malaise. Anaemia is sometimes a cause of painful menstruation as well as of stoppage of this function.
In?ammation of the uterus, ovaries or FALLOPIAN TUBES is a common cause of dysmenorrhoea which comes on for the ?rst time late in life, especially when the trouble follows the birth of a child. In this case the pain exists more or less at all times, but is aggravated at the periods. Treatment with analgesics and remedying the underlying cause is called for.
Many cases of dysmenorrhoea appear with the beginning of menstrual life, and accompany every period. It has been estimated that 5–10 per cent of girls in their late teens or early 20s are severely incapacitated by dysmenorrhoea for several hours each month. Various causes have been suggested for the pain, one being an excessive production of PROSTAGLANDINS. There may be a psychological factor in some sufferers and, whether this is the result of inadequate sex instruction, fear, family, school or work problems, it is important to o?er advice and support, which in itself may resolve the dysmenorrhoea. Symptomatic relief is of value.... menstruation
Male-pattern baldness, the most common form of alopecia, is hereditary and most often affects men. Normal hair is lost initially from the temples and crown and is replaced by fine, downy hair; the affected area gradually widens. Other hereditary forms are rare. They may be due to an absence of hair roots or abnormalities of the hair shaft.
In generalized alopecia, the hair falls out in large amounts. Causes include various forms of stress, such as surgery, prolonged illness, or childbirth. Many anticancer drugs cause temporary alopecia. The hair regrows when the underlying cause is corrected.
Localized alopecia may be due to permanent skin damage (for example, by burns or radiotherapy) or trauma to the hair roots by styling or, rarely, trichotillomania (a disorder in which sufferers pull out their hair). The most common type of localized hair loss is alopecia areata, which is an autoimmune disorder. There is no specific treatment, but the hair usually regrows within a few months. Alopecia universalis is a rare, permanent form of alopecia areata that causes loss of all the hair on the scalp and body, including the eyelashes and eyebrows. Skin diseases such as scalp ringworm (see tinea), lichen planus, lupus erythematosus, and skin tumours may also cause localized hair loss.
Treatments for male-pattern baldness include hair transplants or drug treatments with minoxidil or finasteride.... alopecia
Congenital azoospermia may be due to a chromosomal abnormality such as Klinefelter’s syndrome; failure of the testes to descend into the scrotum; absence of the vasa deferentia (ducts that carry sperm from the testes to the seminal vesicles); or cystic fibrosis.
In some males, azoospermia may be the result of hormonal disorders affecting the onset of puberty. Another cause is blockage of the vasa deferentia, which may follow a sexually transmitted infection, tuberculosis, or surgery on the groin. Azoospermia can also be the result of damage to the testes. This can follow radiotherapy, treatment with certain drugs, and prolonged exposure to heat, or the effects of occupational exposure to toxic chemicals.
If the cause is treatable, sperm production may restart. However, in some cases, the testes will have been permanently damaged.... azoospermia
Ethosuximide may cause nausea and vomiting and, in rare cases, affects production of blood cells in bone marrow (see anaemia, aplastic).... ethosuximide
It may be due to absence of tooth buds at birth or the result of damage to developing tooth buds by infection or other widespread disease.
If only a few teeth are missing, a bridge can fill the gap; if all the teeth are missing, a denture is needed.... anodontia
Symptoms: skin hot, dry and flushed. High temperature and high humidity dispose. Sweating mechanism disorganised. Delirium, headache, shock, dizziness, possible coma, nausea, profuse sweating followed by absence of sweat causing skin to become hot and dry; rapid rise in body temperature, muscle twitching, tachycardia, dehydration.
Treatment. Hospital emergency. Reduce temperature by immersion of victim in bath of cold water. Wrap in a cold wet sheet. Lobelia, to equalise the circulation. Feverfew to regulate sweating mechanism. Yarrow to reduce temperature. Give singly or in combination as available.
Alternatives. Tea. Lobelia 1; Feverfew 2; Yarrow 2. Mix. 2 teaspoons to each cup boiling water; infuse 15 minutes. Half-1 cup freely. Vomiting to be regarded as favourable.
Tinctures. Combine: Lobelia 1; Pleurisy root 2; Valerian 1. Dose: 1-2 teaspoons in water every 2 hours. Decoction. Irish Moss; drink freely.
Practitioner. Tincture Gelsemium BPC (1973). Dose: 0.3ml (5 drops).
Alternate hot and cold compress to back of neck and forehead. Hot Chamomile footbath.
Diet. Irish Moss products. High salt. Abundant drinks of spring water.
Supplements. Kelp tablets, 2 thrice daily. Vitamin C (1g after meals thrice daily). Vitamin E (one 500iu capsule morning and evening).
Vitamin C for skin protection. Increasing Vitamin C after exposure to the sun should help protect against the sun’s ultra violet rays, as skin Vitamin C levels were shown to be severely depleted after exposure. (British Journal of Dermatology 127, 247-253) ... heatstroke
Causes (female). Absence of menses, dry vaginal entrance, tension, stress, tiredness, deformed or retroverted womb, cervical polyps, inflammation of the cervix or ovaries, fibroids, cystic ovaries, diabetes, drugs, steroids, psychogenic factors. Women who use intra-uterine devices may become infertile from tubal infection. The Pill affects fertility. Vitamin E deficiency. Professor Richard Morisset (World Health Organisation) asserts STD’s account for more than 50 per cent infertility in women. Alcohol is a factor.
Causes (male). Inadequate seman, testicular or prostate infection, orchitis (from past mumps), kidney failure, chronic lung disease from smoking, thyroid deficiency, liver and other infections, calcium or Vitamin E deficiency. Low sperm count is found in regular drinkers of alcohol. 30 per cent cases of infertility are found to be due to the male.
“Women who drink more than one cup of coffee a day may find it harder to become pregnant.” (American study reported in The Guardian, 28.12.88)
“Vegetarian women have lower levels of oestrogen. The amount of fibre women eat is believed to affect oestrogen levels in their blood.” (Dr Elwyn Hughes, University of Wales Institute of Science and Technology)
“Drinking more than four cups of coffee a day and smoking more than 20 cigarettes could be a dangerous combination for male fertility.” (Research study, North Carolina, USA)
Women whose mothers smoked when they were pregnant are only 50 per cent as fertile as women who were not exposed (when in the uterus) to a mother’s tobacco smoke. (C. Weinberg, “Reduced Fecundity in Women with Prenatal exposure to cigarette smoking.” American Journal of Epidemiology 1989; 129 p1072)
Margarine has been implicated in low sperm counts.
Alternatives. Endocrine balancers.
Female. Tea. Equal parts: herbs – Motherwort, Agnus Castus and Oats. Mix. 2 teaspoons to each cup boiling water; infuse 15 minutes. Dose, 1 cup 2-3 times daily.
Tablets: Agnus Castus, dosage as on bottle.
Liquid Extracts: equal parts Agnus Castus and Helonias: 1 teaspoon in water 2-3 times daily.
Maria Treben: 25 drops fresh Mistletoe juice in water, on empty stomach, night and morning.
External: Castor oil abdominal packs twice weekly.
Male. Ginseng, Gotu Kola, or the traditional combination of Damiana, Saw Palmetto and Kola. Tablets, liquid extracts, powders or tinctures. Tinctures (practitioner): Capsicum Fort BPC 5ml; Saw Palmetto (1:5) 10ml; Damiana (1:5) 50ml; Prickly Ash (1:5) 10ml. Aqua to 100ml. 1 teaspoon in water, thrice daily. (Arthur Hyde FNIMH)
An orange a day helps keep sperm OK. (Important role of Vitamin C – New Scientist 1992 NO.1812 p20)
Fasting. Mrs A. Rylin, Sweden, had been trying to conceive for 2 years. Conventional medicine proved ineffective until both she and her husband decided to fast for ten days. Within a month she conceived. Other successes reported.
Diet. (For both partners) Vitamin A foods. Wholefoods, oatmeal products (breakfast oats, etc). Regular raw food days. No alcohol. The key mineral for infertility is zinc, a deficiency of which may be made up with bran which is not only high in zinc but in soluble fibre. Not to eat any green peas, which are mildly contraceptive.
Supplements. Daily. Vitamin C (1 gram). Vitamin E (500iu). One B-complex tablet, including B6. The calcium ion is the key regulator of human sperm function – Calcium Lactate 300mg (2 tablets thrice daily at meals). Zinc – 2 tablets or capsules at night. Folic acid, 400mcg. Dolomite. Iron.
Notes. Consider Vitamin B12 and Iron deficiency when evaluating anaemia in infertile couples.
20 percent of men suffer infertility and produce high levels of superoxide radicals in their semen. Vitamin E, an antioxidant, is believed to mop up their superoxide radicals.
Observe sign of zinc deficiency: white flecks on nails. ... infertility
When an individual is on a ventilator, the criteria for diagnosing brain death are based on clear evidence of irreversible damage to the brain; persistent deep coma; no attempts at breathing when the patient is taken off the ventilator; and lack of brainstem function.
(See also death, sudden; mortality.)... death
Many sufferers make use of a radio, television, cassette player, or headphones to block out the noise in their ears.
A tinnitus masker, a hearingaid type device that plays white noise (a random mixture of sounds at a wide range of frequencies), may be effective.... tinnitus
Treatment with growth hormone from infancy helps girls with Turner’s syndrome to achieve near normal height. Coarctation of the aorta is treated surgically. Treatment with oestrogen drugs induces menstruation, but it does not make affected girls fertile.... turner’s syndrome
the cervix; the upper part opens into the fallopian tubes. The inside is lined with endometrium. The uterus expands in size during pregnancy to accommodate the growing baby. At full-term, the powerful uterine muscles expel the baby via the birth canal (see childbirth). After the menopause, the endometrium atrophies (becomes thinner) and the uterine muscle and connective tissue are reduced.
Conditions that affect the uterus include congenital disorders, such as malformation or absence of the uterus; tumours, including polyps, fibroids, and cancer of the endometrium (see uterus, cancer of); infections, causing endometritis; and hormonal disorders. (See also uterus, prolapse of; uterus, retroverted.)... uterus
Both HIV-1 and HIV-2 are predominantly sexually transmitted and both are associated with secondary opportunistic infections. However, HIV-2 seems to result in slower damage to the immune system. HIV-1 is known to mutate rapidly and has given rise to other subtypes.
HIV is thought to have occurred in humans in the 1950s, but whether or not it infected humans from another primate species is uncertain. It became widespread in the 1970s but its latency in causing symptoms meant that the epidemic was not noticed until the following decade. Although it is a sexually transmitted disease, it can also be transmitted by intravenous drug use (through sharing an infected needle), blood transfusions with infected blood (hence the importance of e?ective national blood-screening programmes), organ donation, and occupationally (see health-care workers, below). Babies born of HIV-positive mothers can be infected before or during birth, or through breast feeding.
Although HIV is most likely to occur in blood, semen or vaginal ?uid, it has been found in saliva and tears (but not sweat); however, there is no evidence that the virus can be transmitted from these two body ?uids. There is also no evidence that HIV can be transmitted by biting insects (such as mosquitoes). HIV does not survive well in the environment and is rapidly destroyed through drying.
Prevalence At the end of 2003 an estimated 42 million people globally were infected with HIV – up from 40 million two years earlier. About one-third of those with HIV/AIDS are aged 15–24 and most are unaware that they are carrying the virus. During 2003 it is estimated that 5 million adults and children worldwide were newly infected with HIV, and that 3 million adults and children died. In Africa in 2003,
3.4 million people were newly infected and 2.3 million died, with more than 28 million carrying the virus. HIV/AIDS was the leading cause of death in sub-Saharan Africa where over half of the infections were in women and 90 per cent of cases resulted from heterosexual sex. In some southern African countries, one in three pregnant women had HIV.
In Asia and the Paci?c there were 1.2 million new infections and 435,000 deaths. The area with the fastest-growing epidemic is Eastern Europe, especially the Russian Federation where in 2002 around a million people had HIV and there were an estimated 250,000 new infections, with intravenous drug use a key contributor to this ?gure. Seventy-?ve per cent of cases occurred in men, with male-to-male sexual transmission an important cause of infection, though heterosexual activity is a rising cause of infection.
At the end of 2002 the UK had an estimated 55,900 HIV-infected adults aged between 15 and 59. More than 3,600 individuals were newly diagnosed with the infection in 2000, the highest annual ?gure since the epidemic started
– in 1998 the ?gure was 2,817 and in 1999 just over 3,000 (Department of Health and Communicable Disease Surveillance Centre). The incidence of AIDS in the UK has declined sharply since the introduction of highly active antiretroviral therapy (HAART) and HIV-related deaths have also fallen: in 2002 there were 777 reported new AIDS cases and 395 deaths, compared with 1,769 and 1,719 respectively in 1995. (Sources: UNAIDS and WHO, AIDS Epidemic Update, December 2001; Public Health Laboratory Services AIDS and STD Centre Communicable Disease Surveillance and Scottish Centre for Infection and Environmental Health, Quarterly Surveillance Tables.)
Poverty is strongly linked to the spread of AIDS, for various reasons including lack of health education; lack of e?ective public-health awareness; women having little control over sexual behaviour and contraception; and, by comparison with the developed world, little or no access to antiretroviral drugs.
Pathogenesis The cellular target of HIV infection is a subset of white blood cells called T-lymphocytes (see LYMPHOCYTE) which carry the CD4 surface receptor. These so-called ‘helper T-cells’ are vital to the function of cell-mediated immunity. Infection of these cells leads to their destruction (HIV replicates at an enormous rate – 109) and over the course of several years the body is unable to generate suf?cient new cells to keep pace. This leads to progressive destruction of the body’s immune capabilities, evidenced clinically by the development of opportunistic infection and unusual tumours.
Monitoring of clinical progression It is possible to measure the number of viral particles present in the plasma. This gives an accurate guide to the likely progression rate, which will be slow in those individuals with fewer than 10,000 particles per ml of plasma but progressively more rapid above this ?gure. The main clinical monitoring of the immune system is through the numbers of CD4 lymphocytes in the blood. The normal count is around 850 cells per ml and, without treatment, eventual progression to AIDS is likely in those individuals whose CD4 count falls below 500 per ml. Opportunistic infections occur most frequently when the count falls below 200 per ml: most such infections are treatable, and death is only likely when the CD4 count falls below 50 cells per ml when infection is developed with organisms that are di?cult to treat because of their low intrinsic virulence.
Simple, cheap and highly accurate tests are available to detect HIV antibodies in the serum. These normally occur within three months of infection and remain the cornerstone of the diagnosis.
Clinical features Most infected individuals have a viral illness some three weeks after contact with HIV. The clinical features are often non-speci?c and remain undiagnosed but include a ?ne red rash, large lymph nodes, an in?uenza-like illness, cerebral involvement and sometimes the development of opportunistic infections. The antibody test may be negative at this stage but there are usually high levels of virus particles in the blood. The antibody test is virtually always positive within three months of infection. HIV infection is often subsequently asymptomatic for a period of ten years or more, although in most patients progressive immune destruction is occurring during this time and a variety of minor opportunistic infections such as HERPES ZOSTER or oral thrush (see CANDIDA) do occur. In addition, generalised LYMPHADENOPATHY is present in a third of patients and some suffer from severe malaise, weight loss, night sweats, mild fever, ANAEMIA or easy bruising due to THROMBOCYTOPENIA.
The presentation of opportunistic infection is highly variable but usually involves either the CENTRAL NERVOUS SYSTEM, the gastrointestinal tract or the LUNGS. Patients may present with a sudden onset of a neurological de?cit or EPILEPSY due to a sudden onset of a STROKE-like syndrome, or epilepsy due to a space-occupying lesion in the brain – most commonly TOXOPLASMOSIS. In late disease, HIV infection of the central nervous system itself may produce progressive memory loss, impaired concentration and mental slowness called AIDS DEMENTIA. A wide variety of opportunistic PROTOZOA or viruses produces DYSPHAGIA, DIARRHOEA and wasting. In the respiratory system the commonest opportunistic infection associated with AIDS, pneumonia, produces severe shortness of breath and sometimes CYANOSIS, usually with a striking lack of clinical signs in the chest.
In very late HIV infection, when the CD4 count has fallen below 50 cells per ml, infection with CYTOMEGALOVIRUS may produce progressive retinal necrosis (see EYE, DISORDERS OF) which will lead to blindness if untreated, as well as a variety of gastrointestinal symptoms. At this stage, infection with atypical mycobacteria is also common, producing severe anaemia, wasting and fevers. The commonest tumour associated with HIV is Kaposi’s sarcoma which produces purplish skin lesions. This and nonHodgkin’s lymphoma (see LYMPHOMA), which is a hundred times more frequent among HIV-positive individuals than in the general population, are likely to be associated with or caused by opportunistic viral infections.
Prevention There is, as yet, no vaccine to prevent HIV infection. Vaccine development has been hampered
by the large number of new HIV strains generated through frequent mutation and recombination.
because HIV can be transmitted as free virus and in infected cells.
because HIV infects helper T-cells – the very cells involved in the immune response. There are, however, numerous research pro
grammes underway to develop vaccines that are either prophylactic or therapeutic. Vaccine-development strategies have included: recombinant-vector vaccines, in which a live bacterium or virus is genetically modi?ed to carry one or more of the HIV genes; subunit vaccines, consisting of small regions of the HIV genome designed to induce an immune response without infection; modi?ed live HIV, which has had its disease-promoting genes removed; and DNA vaccines – small loops of DNA (plasmids) containing viral genes – that make the host cells produce non-infectious viral proteins which, in turn, trigger an immune response and prime the immune system against future infection with real virus.
In the absence of an e?ective vaccine, preventing exposure remains the chief strategy in reducing the spread of HIV. Used properly, condoms are an extremely e?ective method of preventing exposure to HIV during sexual intercourse and remain the most important public-health approach to countering the further acceleration of the AIDS epidemic. The spermicide nonoxynol-9, which is often included with condoms, is known to kill HIV in vitro; however, its e?ectiveness in preventing HIV infection during intercourse is not known.
Public-health strategies must be focused on avoiding high-risk behaviour and, particularly in developing countries, empowering women to have more control over their lives, both economically and socially. In many of the poorer regions of the world, women are economically dependent on men and refusing sex, or insisting on condom use, even when they know their partners are HIV positive, is not a straightforward option. Poverty also forces many women into the sex industry where they are at greater risk of infection.
Cultural problems in gaining acceptance for universal condom-use by men in some developing countries suggests that other preventive strategies should also be considered. Microbicides used as vaginal sprays or ‘chemical condoms’ have the potential to give women more direct control over their exposure risk, and research is underway to develop suitable products.
Epidemiological studies suggest that male circumcision may o?er some protection against HIV infection, although more research is needed before this can be an established public-health strategy. Globally, about 70 per cent of infected men have acquired the virus through unprotected vaginal sex; in these men, infection is likely to have occurred through the penis with the mucosal epithelia of the inner surface of the foreskin and the frenulum considered the most likely sites for infection. It is suggested that in circumcised men, the glans may become keratinised and thus less likely to facilitate infection. Circumcision may also reduce the risk of lesions caused by other sexually transmitted disease.
Treatment AIDS/HIV treatment can be categorised as speci?c therapies for the individual opportunistic infections – which ultimately cause death – and highly active antiretroviral therapy (HAART) designed to reduce viral load and replication. HAART is also the most e?ective way of preventing opportunistic infections, and has had a signi?cant impact in delaying the onset of AIDS in HIV-positive individuals in developed countries.
Four classes of drugs are currently in use. Nucleoside analogues, including ZIDOVUDINE and DIDANOSINE, interfere with the activity of the unique enzyme of the retrovirus reverse transcriptase which is essential for replication. Nucleotide analogues, such as tenofovir, act in the same way but require no intracellular activation. Non-nucleoside reverse transcriptase inhibitors, such as nevirapine and EFAVIRENZ, act by a di?erent mechanism on the same enzyme. The most potent single agents against HIV are the protease inhibitors, such as lopinavir, which render a unique viral enzyme ineffective. These drugs are used in a variety of combinations in an attempt to reduce the plasma HIV viral load to below detectable limits, which is achieved in approximately 90 per cent of patients who have not previously received therapy. This usually also produces a profound rise in CD4 count. It is likely, however, that such treatments need to be lifelong – and since they are associated with toxicities, long-term adherence is di?cult. Thus the optimum time for treatment intervention remains controversial, with some clinicians believing that this should be governed by the viral load rising above 10,000 copies, and others that it should primarily be designed to prevent the development of opportunistic infections – thus, that initiation of therapy should be guided more by the CD4 count.
It should be noted that the drug regimens have been devised for infection with HIV-1; it is not known how e?ective they are at treating infection with HIV-2.
HIV and pregnancy An HIV-positive woman can transmit the virus to her fetus, with the risk of infection being particularly high during parturition; however, the risk of perinatal HIV transmission can be reduced by antiviral drug therapy. In the UK, HIV testing is available to all women as part of antenatal care. The bene?ts of antenatal HIV testing in countries where antiviral drugs are not available are questionable. An HIV-positive woman might be advised not to breast feed because of the risks of transmitting HIV via breastmilk, but there may be a greater risk associated with not breast feeding at all. Babies in many poor communities are thought to be at high risk of infectious diseases and malnutrition if they are not breast fed and may thus be at greater overall risk of death during infancy.
Counselling Con?dential counselling is an essential part of AIDS management, both in terms of supporting the psychological wellbeing of the individual and in dealing with issues such as family relations, sexual partners and implications for employment (e.g. for health-care workers). Counsellors must be particularly sensitive to culture and lifestyle issues. Counselling is essential both before an HIV test is taken and when the results are revealed.
Health-care workers Health-care workers may be at risk of occupational exposure to HIV, either through undertaking invasive procedures or through accidental exposure to infected blood from a contaminated needle (needlestick injury). Needlestick injuries are frequent in health care – as many as 600,000 to 800,000 are thought to occur annually in the United States. Transmission is much more likely where the worker has been exposed to HIV through a needlestick injury or deep cut with a contaminated instrument than through exposure of mucous membranes to contaminated blood or body ?uids. However, even where exposure occurs through a needlestick injury, the risk of seroconversion is much lower than with a similar exposure to hepatitis C or hepatitis B. A percutaneous exposure to HIV-infected blood in a health-care setting is thought to carry a risk of about one infection per 300 injuries (one in 1,000 for mucous-membrane exposure), compared with one in 30 for hepatitis C, and one in three for hepatitis B (when the source patient is e-antigen positive).
In the event of an injury, health-care workers are advised to report the incident immediately where, depending on a risk assessment, they may be o?ered post-exposure prophylaxis (PEP). They should also wash the contaminated area with soap and water (but without scrubbing) and, if appropriate, encourage bleeding at the site of injury. PEP, using a combination of antiretroviral drugs (in a similar regimen to HAART – see above), is thought to greatly reduce the chances of seroconversion; it should be commenced as soon as possible, preferably within one or two hours of the injury. Although PEP is available, safe systems of work are considered to o?er the greatest protection. Double-gloving (latex gloves remove much of the blood from the surface of the needle during a needlestick), correct use of sharps containers (for used needles and instruments), avoiding the resheathing of used needles, reduction in the number of blood samples taken from a patient, safer-needle devices (such as needles that self-blunt after use) and needleless drug administration are all thought to reduce the risk of exposure to HIV and other blood-borne viruses. Although there have been numerous cases of health-care workers developing HIV through occupational exposure, there is little evidence of health-care workers passing HIV to their patients through normal medical procedures.... aids/hiv
Atherosclerosis is due to the deposition of CHOLESTEROL into the walls of arteries. The process starts in childhood with the development of fatty streaks lining the arteries. In adulthood these progress, scarring and calcifying to form irregular narrowings within the arteries and eventually leading to blockage of the vessel. The consequence of the narrowing or blockage depends on which vessels are involved
– diseased cerebral vessels cause strokes; coronary vessels cause angina and heart attacks; renal vessels cause renal failure; and peripheral arteries cause limb ischaemia (localised bloodlessness).
Risk factors predisposing individuals to atherosclerosis include age, male gender, raised plasma cholesterol concentration, high blood pressure, smoking, a family history of atherosclerosis, diabetes and obesity.
Arteritis occurs in a variety of conditions that produce in?ammation in the arteries. Examples include syphilis – now rare in Britain
– which produces in?ammation of the aorta with subsequent dilatation (aneurysm formation) and risk of rupture; giant cell arteritis (temporal arteritis), a condition usually affecting the elderly, which involves the cranial arteries and leads to headache, tenderness over the temporal arteries and the risk of sudden blindness; Takayasu’s syndrome, predominantly affecting young females, which involves the aortic arch and its major branches, leading to the absence of pulse in affected vessels; and polyarteritis nodosa, a condition causing multiple small nodules to form on the smaller arteries. General symptoms such as fever, malaise, weakness, anorexia and weight loss are accompanied by local manifestations of ischaemia (bloodlessness) in di?erent parts of the body.... arteries, diseases of
Symptoms In most cases, death from asphyxia is due to insu?ciency of oxygen supplied to the blood. The ?rst signs are rapid pulse and gasping for breath. Next comes a rise in the blood pressure, causing throbbing in the head, with lividity or blueness of the skin, due to failure of aeration of the blood, followed by still greater struggles for breath and by general CONVULSIONS. The heart becomes overdistended and gradually weaker, a paralytic stage sets in, and all struggling and breathing slowly cease. When asphyxia is due to charcoal fumes, coal-gas, and other narcotic in?uences, there is no convulsive stage, and death ensues gently and may occur in the course of sleep.
Treatment So long as the heart continues to beat, recovery may be looked for with prompt treatment. The one essential of treatment is to get the impure blood aerated by arti?cial respiration. Besides this, the feeble circulation can be helped by various methods. (See APPENDIX 1: BASIC FIRST AID – Choking; Cardiac/respiratory arrest.)... asphyxia
Insulin-dependent and non-insulindependent diabetes have a varied pathological pattern and are caused by the interaction of several genetic and environmental factors.
Insulin-dependent diabetes mellitus (IDDM) (juvenile-onset diabetes, type 1 diabetes) describes subjects with a severe de?ciency or absence of insulin production. Insulin therapy is essential to prevent KETOSIS – a disturbance of the body’s acid/base balance and an accumulation of ketones in the tissues. The onset is most commonly during childhood, but can occur at any age. Symptoms are acute and weight loss is common.
Non-insulin-dependent diabetes mellitus (NIDDM) (maturity-onset diabetes, type 2 diabetes) may be further sub-divided into obese and non-obese groups. This type usually occurs after the age of 40 years with an insidious onset. Subjects are often overweight and weight loss is uncommon. Ketosis rarely develops. Insulin production is reduced but not absent.
A new hormone has been identi?ed linking obesity to type 2 diabetes. Called resistin – because of its resistance to insulin – it was ?rst found in mice but has since been identi?ed in humans. Researchers in the United States believe that the hormone may, in part, explain how obesity predisposes people to diabetes. Their hypothesis is that a protein in the body’s fat cells triggers insulin resistance around the body. Other research suggests that type 2 diabetes may now be occurring in obese children; this could indicate that children should be eating a more-balanced diet and taking more exercise.
Diabetes associated with other conditions (a) Due to pancreatic disease – for example, chronic pancreatitis (see PANCREAS, DISORDERS OF); (b) secondary to drugs – for example, GLUCOCORTICOIDS (see PANCREAS, DISORDERS OF); (c) excess hormone production
– for example, growth hormone (ACROMEGALY); (d) insulin receptor abnormalities; (e) genetic syndromes (see GENETIC DISORDERS).
Gestational diabetes Diabetes occurring in pregnancy and resolving afterwards.
Aetiology Insulin-dependent diabetes occurs as a result of autoimmune destruction of beta cells within the PANCREAS. Genetic in?uences are important and individuals with certain HLA tissue types (HLA DR3 and HLA DR4) are more at risk; however, the risks associated with the HLA genes are small. If one parent has IDDM, the risk of a child developing IDDM by the age of 25 years is 1·5–2·5 per cent, and the risk of a sibling of an IDDM subject developing diabetes is about 3 per cent.
Non-insulin-dependent diabetes has no HLA association, but the genetic in?uences are much stronger. The risks of developing diabetes vary with di?erent races. Obesity, decreased exercise and ageing increase the risks of disease development. The risk of a sibling of a NIDDM subject developing NIDDM up to the age of 80 years is 30–40 per cent.
Diet Many NIDDM diabetics may be treated with diet alone. For those subjects who are overweight, weight loss is important, although often unsuccessful. A diet high in complex carbohydrate, high in ?bre, low in fat and aiming towards ideal body weight is prescribed. Subjects taking insulin need to eat at regular intervals in relation to their insulin regime and missing meals may result in hypoglycaemia, a lowering of the amount of glucose in the blood, which if untreated can be fatal (see below).
Oral hypoglycaemics are used in the treatment of non-insulin-dependent diabetes in addition to diet, when diet alone fails to control blood-sugar levels. (a) SULPHONYLUREAS act mainly by increasing the production of insulin;
(b) BIGUANIDES, of which only metformin is available, may be used alone or in addition to sulphonylureas. Metformin’s main actions are to lower the production of glucose by the liver and improve its uptake in the peripheral tissues.
Complications The risks of complications increase with duration of disease.
Diabetic hypoglycaemia occurs when amounts of glucose in the blood become low. This may occur in subjects taking sulphonylureas or insulin. Symptoms usually develop when the glucose concentration falls below 2·5 mmol/l. They may, however, occur at higher concentrations in subjects with persistent hyperglycaemia – an excess of glucose – and at lower levels in subjects with persistent hypo-glycaemia. Symptoms include confusion, hunger and sweating, with coma developing if blood-sugar concentrations remain low. Re?ned sugar followed by complex carbohydrate will return the glucose concentration to normal. If the subject is unable to swallow, glucagon may be given intramuscularly or glucose intravenously, followed by oral carbohydrate, once the subject is able to swallow.
Although it has been shown that careful control of the patient’s metabolism prevents late complications in the small blood vessels, the risk of hypoglycaemia is increased and patients need to be well motivated to keep to their dietary and treatment regime. This regime is also very expensive. All risk factors for the patient’s cardiovascular system – not simply controlling hyperglycaemia – may need to be reduced if late complications to the cardiovascular system are to be avoided.
Diabetes is one of the world’s most serious health problems. Recent projections suggest that the disorder will affect nearly 240 million individuals worldwide by 2010 – double its prevalence in 1994. The incidence of insulin-dependent diabetes is rising in young children; they will be liable to develop late complications.
Although there are complications associated with diabetes, many subjects live normal lives and survive to an old age. People with diabetes or their relatives can obtain advice from Diabetes UK (www.diabetes.org.uk).
Increased risks are present of (a) heart disease, (b) peripheral vascular disease, and (c) cerebrovascular disease.
Diabetic eye disease (a) retinopathy, (b) cataract. Regular examination of the fundus enables any abnormalities developing to be detected and treatment given when appropriate to preserve eyesight.
Nephropathy Subjects with diabetes may develop kidney damage which can result in renal failure.
Neuropathy (a) Symmetrical sensory polyneuropathy; damage to the sensory nerves that commonly presents with tingling, numbness of pain in the feet or hands. (b) Asymmetrical motor diabetic neuropathy, presenting as progressive weakness and wasting of the proximal muscles of legs. (c) Mononeuropathy; individual motor or sensory nerves may be affected. (d) Autonomic neuropathy, which affects the autonomic nervous system, has many presentations including IMPOTENCE, diarrhoea or constipation and postural HYPOTENSION.
Skin lesions There are several skin disorders associated with diabetes, including: (a) necrobiosis lipoidica diabeticorum, characterised by one or more yellow atrophic lesions on the legs;
(b) ulcers, which most commonly occur on the feet due to peripheral vascular disease, neuropathy and infection. Foot care is very important.
Diabetic ketoacidosis occurs when there is insu?cient insulin present to prevent KETONE production. This may occur before the diagnosis of IDDM or when insu?cient insulin is being given. The presence of large amounts of ketones in the urine indicates excess ketone production and treatment should be sought immediately. Coma and death may result if the condition is left untreated.
Symptoms Thirst, POLYURIA, GLYCOSURIA, weight loss despite eating, and recurrent infections (e.g. BALANITIS and infections of the VULVA) are the main symptoms.
However, subjects with non-insulindependent diabetes may have the disease for several years without symptoms, and diagnosis is often made incidentally or when presenting with a complication of the disease.
Treatment of diabetes aims to prevent symptoms, restore carbohydrate metabolism to as near normal as possible, and to minimise complications. Concentration of glucose, fructosamine and glycated haemoglobin in the blood are used to give an indication of blood-glucose control.
Insulin-dependent diabetes requires insulin for treatment. Non-insulin-dependent diabetes may be treated with diet, oral HYPOGLYCAEMIC AGENTS or insulin.
Insulin All insulin is injected – mainly by syringe but sometimes by insulin pump – because it is inactivated by gastrointestinal enzymes. There are three main types of insulin preparation: (a) short action (approximately six hours), with rapid onset; (b) intermediate action (approximately 12 hours); (c) long action, with slow onset and lasting for up to 36 hours. Human, porcine and bovine preparations are available. Much of the insulin now used is prepared by genetic engineering techniques from micro-organisms. There are many regimens of insulin treatment involving di?erent combinations of insulin; regimens vary depending on the requirements of the patients, most of whom administer the insulin themselves. Carbohydrate intake, energy expenditure and the presence of infection are important determinants of insulin requirements on a day-to-day basis.
A new treatment for diabetes, pioneered in Canada and entering its preliminary clinical trials in the UK, is the transplantation of islet cells of Langerhans from a healthy person into a patient with the disorder. If the transplantation is successful, the transplanted cells start producing insulin, thus reducing or eliminating the requirement for regular insulin injections. If successful the trials would be a signi?cant advance in the treatment of diabetes.
Scientists in Israel have developed a drug, Dia Pep 277, which stops the body’s immune system from destroying pancratic ? cells as happens in insulin-dependent diabetes. The drug, given by injection, o?ers the possibility of preventing type 1 diabetes in healthy people at genetic risk of developing the disorder, and of checking its progression in affected individuals whose ? cells are already perishing. Trials of the drug are in progress.... diabetes mellitus
Adrenal glands These two glands, also known as suprarenal glands, lie immediately above the kidneys. The central or medullary portion of the glands forms the secretions known as ADRENALINE (or epinephrine) and NORADRENALINE. Adrenaline acts upon structures innervated by sympathetic nerves. Brie?y, the blood vessels of the skin and of the abdominal viscera (except the intestines) are constricted, and at the same time the arteries of the muscles and the coronary arteries are dilated; systolic blood pressure rises; blood sugar increases; the metabolic rate rises; muscle fatigue is diminished. The super?cial or cortical part of the glands produces steroid-based substances such as aldosterone, cortisone, hydrocortisone, and deoxycortone acetate, for the maintenance of life. It is the absence of these substances, due to atrophy or destruction of the suprarenal cortex, that is responsible for the condition known as ADDISON’S DISEASE. (See CORTICOSTEROIDS.)
Ovaries and testicles The ovary (see OVARIES) secretes at least two hormones – known, respectively, as oestradiol (follicular hormone) and progesterone (corpus luteum hormone). Oestradiol develops (under the stimulus of the anterior pituitary lobe – see PITUITARY GLAND below, and under separate entry) each time an ovum in the ovary becomes mature, and causes extensive proliferation of the ENDOMETRIUM lining the UTERUS, a stage ending with shedding of the ovum about 14 days before the onset of MENSTRUATION. The corpus luteum, which then forms, secretes both progesterone and oestradiol. Progesterone brings about great activity of the glands in the endometrium. The uterus is now ready to receive the ovum if it is fertilised. If fertilisation does not occur, the corpus luteum degenerates, the hormones cease acting, and menstruation takes place.
The hormone secreted by the testicles (see TESTICLE) is known as TESTOSTERONE. It is responsible for the growth of the male secondary sex characteristics.
Pancreas This gland is situated in the upper part of the abdomen and, in addition to the digestive enzymes, it produces INSULIN within specialised cells (islets of Langerhans). This controls carbohydrate metabolism; faulty or absent insulin production causes DIABETES MELLITUS.
Parathyroid glands These are four minute glands lying at the side of, or behind, the thyroid (see below). They have a certain e?ect in controlling the absorption of calcium salts by the bones and other tissues. When their secretion is defective, TETANY occurs.
Pituitary gland This gland is attached to the base of the brain and rests in a hollow on the base of the skull. It is the most important of all endocrine glands and consists of two embryologically and functionally distinct lobes.
The function of the anterior lobe depends on the secretion by the HYPOTHALAMUS of certain ‘neuro-hormones’ which control the secretion of the pituitary trophic hormones. The hypothalamic centres involved in the control of speci?c pituitary hormones appear to be anatomically separate. Through the pituitary trophic hormones the activity of the thyroid, adrenal cortex and the sex glands is controlled. The anterior pituitary and the target glands are linked through a feedback control cycle. The liberation of trophic hormones is inhibited by a rising concentration of the circulating hormone of the target gland, and stimulated by a fall in its concentration. Six trophic (polypeptide) hormones are formed by the anterior pituitary. Growth hormone (GH) and prolactin are simple proteins formed in the acidophil cells. Follicle-stimulating hormone (FSH), luteinising hormone (LH) and thyroid-stimulating hormone (TSH) are glycoproteins formed in the basophil cells. Adrenocorticotrophic hormone (ACTH), although a polypeptide, is derived from basophil cells.
The posterior pituitary lobe, or neurohypophysis, is closely connected with the hypothalamus by the hypothalamic-hypophyseal tracts. It is concerned with the production or storage of OXYTOCIN and vasopressin (the antidiuretic hormone).
PITUITARY HORMONES Growth hormone, gonadotrophic hormone, adrenocorticotrophic hormone and thyrotrophic hormones can be assayed in blood or urine by radio-immunoassay techniques. Growth hormone extracted from human pituitary glands obtained at autopsy was available for clinical use until 1985, when it was withdrawn as it is believed to carry the virus responsible for CREUTZFELDT-JAKOB DISEASE (COD). However, growth hormone produced by DNA recombinant techniques is now available as somatropin. Synthetic growth hormone is used to treat de?ciency of the natural hormone in children and adults, TURNER’S SYNDROME and chronic renal insu?ciency in children.
Human pituitary gonadotrophins are readily obtained from post-menopausal urine. Commercial extracts from this source are available and are e?ective for treatment of infertility due to gonadotrophin insu?ciency.
The adrenocorticotrophic hormone is extracted from animal pituitary glands and has been available therapeutically for many years. It is used as a test of adrenal function, and, under certain circumstances, in conditions for which corticosteroid therapy is indicated (see CORTICOSTEROIDS). The pharmacologically active polypeptide of ACTH has been synthesised and is called tetracosactrin. Thyrotrophic hormone is also available but it has no therapeutic application.
HYPOTHALAMIC RELEASING HORMONES which affect the release of each of the six anterior pituitary hormones have been identi?ed. Their blood levels are only one-thousandth of those of the pituitary trophic hormones. The release of thyrotrophin, adrenocorticotrophin, growth hormone, follicle-stimulating hormone and luteinising hormone is stimulated, while release of prolactin is inhibited. The structure of the releasing hormones for TSH, FSH-LH, GH and, most recently, ACTH is known and they have all been synthesised. Thyrotrophin-releasing hormone (TRH) is used as a diagnostic test of thyroid function but it has no therapeutic application. FSH-LH-releasing hormone provides a useful diagnostic test of gonadotrophin reserve in patients with pituitary disease, and is now used in the treatment of infertility and AMENORRHOEA in patients with functional hypothalamic disturbance. As this is the most common variety of secondary amenorrhoea, the potential use is great. Most cases of congenital de?ciency of GH, FSH, LH and ACTH are due to defects in the hypothalamic production of releasing hormone and are not a primary pituitary defect, so that the therapeutic implication of this synthesised group of releasing hormones is considerable.
GALACTORRHOEA is frequently due to a microadenoma (see ADENOMA) of the pituitary. DOPAMINE is the prolactin-release inhibiting hormone. Its duration of action is short so its therapeutic value is limited. However, BROMOCRIPTINE is a dopamine agonist with a more prolonged action and is e?ective treatment for galactorrhoea.
Thyroid gland The functions of the thyroid gland are controlled by the pituitary gland (see above) and the hypothalamus, situated in the brain. The thyroid, situated in the front of the neck below the LARYNX, helps to regulate the body’s METABOLISM. It comprises two lobes each side of the TRACHEA joined by an isthmus. Two types of secretory cells in the gland – follicular cells (the majority) and parafollicular cells – secrete, respectively, the iodine-containing hormones THYROXINE (T4) and TRI-IODOTHYRONINE (T3), and the hormone CALCITONIN. T3 and T4 help control metabolism and calcitonin, in conjunction with parathyroid hormone (see above), regulates the body’s calcium balance. De?ciencies in thyroid function produce HYPOTHYROIDISM and, in children, retarded development. Excess thyroid activity causes thyrotoxicosis. (See THYROID GLAND, DISEASES OF.)... endocrine glands
Non-speci?c back pain is probably the result of mechanical disorders in the muscles, ligaments and joints of the back: torn muscles, sprained LIGAMENTS, and FIBROSITIS. These disorders are not always easy to diagnose, but mild muscular and ligamentous injuries are usually relieved with symptomatic treatment – warmth, gentle massage, analgesics, etc. Sometimes back pain is caused or worsened by muscle spasms, which may call for the use of antispasmodic drugs. STRESS and DEPRESSION (see MENTAL ILLNESS) can sometimes result in chronic backache and should be considered if no clear physical diagnosis can be made.
If back pain is severe and/or recurrent, possibly radiating around to the abdomen or down the back of a leg (sciatica – see below), or is accompanied by weakness or loss of feeling in the leg(s), it may be caused by a prolapsed intervertebral disc (slipped disc) pressing on a nerve. The patient needs prompt investigation, including MRI. Resting on a ?rm bed or board can relieve the symptoms, but the patient may need a surgical operation to remove the disc and relieve pressure on the affected nerve.
The nucleus pulposus – the soft centre of the intervertebral disc – is at risk of prolapse under the age of 40 through an acquired defect in the ?brous cartilage ring surrounding it. Over 40 this nucleus is ?rmer and ‘slipped disc’ is less likely to occur. Once prolapse has taken place, however, that segment of the back is never quite the same again, as OSTEOARTHRITIS develops in the adjacent facet joints. Sti?ness and pain may develop, sometimes many years later. There may be accompanying pain in the legs: SCIATICA is pain in the line of the sciatic nerve, while its rarer analogue at the front of the leg is cruralgia, following the femoral nerve. Leg pain of this sort may not be true nerve pain but referred from arthritis in the spinal facet joints. Only about 5 per cent of patients with back pain have true sciatica, and spinal surgery is most successful (about 85 per cent) in this group.
When the complaint is of pain alone, surgery is much less successful. Manipulation by physiotherapists, doctors, osteopaths or chiropractors can relieve symptoms; it is important ?rst to make sure that there is not a serious disorder such as a fracture or cancer.
Other local causes of back pain are osteoarthritis of the vertebral joints, ankylosing spondylitis (an in?ammatory condition which can severely deform the spine), cancer (usually secondary cancer deposits spreading from a primary tumour elsewhere), osteomyelitis, osteoporosis, and PAGET’S DISEASE OF BONE. Fractures of the spine – compressed fracture of a vertebra or a break in one of its spinous processes – are painful and potentially dangerous. (See BONE, DISORDERS OF.)
Backache can also be caused by disease elsewhere, such as infection of the kidney or gall-bladder (see LIVER), in?ammation of the PANCREAS, disorders in the UTERUS and PELVIS or osteoarthritis of the HIP. Treatment is e?ected by tackling the underlying cause. Among the many known causes of back pain are:
Mechanical and traumatic causes
Congenital anomalies. Fractures of the spine. Muscular tenderness and ligament strain. Osteoarthritis. Prolapsed intervertebral disc. Spondylosis.
In?ammatory causes
Ankylosing spondylitis. Brucellosis. Osteomyelitis. Paravertebral abscess. Psoriatic arthropathy. Reiter’s syndrome. Spondyloarthropathy. Tuberculosis.
Neoplastic causes
Metastatic disease. Primary benign tumours. Primary malignant tumours.
Metabolic bone disease
Osteomalacia. Osteoporosis. Paget’s disease.
Referred pain
Carcinoma of the pancreas. Ovarian in?ammation and tumours. Pelvic disease. Posterior duodenal ulcer. Prolapse of the womb.
Psychogenic causes
Anxiety. Depression.
People with backache can obtain advice from www.backcare.org.uk... backache
Habitat: Throughout India in tropical areas; also cultivated in hedges.
English: Butterfly Pea, Winged- leaved Clitoria, Mezereon.Ayurvedic: Girikarnikaa, Aparaa- jitaa, Aasphota, Girimallikaa, Girikanyaa, Kokilaa,Yonipushpaa, Vishnukraantaa. (Evolvulus alsi- noides Linn. is also known as Vishnukraantaa, Vishnukranti). Used as Shankhapushpi in the South.Unani: Mezereon Hindi.Siddha/Tamil: Kakkanam.Folk: Koyal (Punjab).Action: Root—cathartic like jalap. Roots cause gripe and tenesmus, hence not recommended as purgative. Used in ascites. Root bark—diuretic (infusion used in irritation of bladder and urethra). Root juice—given in cold milk to liquefy phlegm in chronic bronchitis. The root, bark, seeds and leaves—used for gastric acidity. The root is administered with honey as a general tonic to children for improving mental faculty.
The Ayurvedic Pharmacopoeia of India recommends the dried leaf in migraine, psychoneurosis and mania.An alcoholic extract of the plant showed sedative and hypothermic effect in rodents.Rats, fed with ethanol extract of flowers, showed a significantly lowered serum sugar level in experimentally induced diabetes.The seeds contain a nucleoprotein with its amino acid sequence similar to insulin, but for the absence of his- tidine, threonine, proline and crystine.Seeds gave cinnamic acid, flavonol gly- coside. Leaves contain glycosides of kaempferol.In South India, the seeds and roots constitute the drug Shankhapushpi, used as a nervine tonic. In other regions, Canscora decussata, Convolvulus pluricaulis, Evolvulus alsinoides and Lavendula bipinnata are used as Shan- khapushpi.Dosage: Root—1-3 g powder (API Vol. II); dried leaf—2-5 g; seed—1- 3 g. (API Vol. IV.)... clitoria ternateaArrhythmias 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
Many modi?cations have been devised of the basic steroid molecule in an attempt to keep useful therapeutic effects and minimise unwanted side-effects. The main corticosteroid hormones currently available are CORTISONE, HYDROCORTISONE, PREDNISONE, PREDNISOLONE, methyl prednisolone, triamcinolone, dexamethasone, betamethasone, paramethasone and de?azacort.
They are used clinically in three quite distinct circumstances. First they constitute replacement therapy where a patient is unable to produce their own steroids – for example, in adrenocortical insu?ciency or hypopituitarism. In this situation the dose is physiological – namely, the equivalent of the normal adrenal output under similar circumstances – and is not associated with any side-effects. Secondly, steroids are used to depress activity of the adrenal cortex in conditions where this is abnormally high or where the adrenal cortex is producing abnormal hormones, as occurs in some hirsute women.
The third application for corticosteroids is in suppressing the manifestations of disease in a wide variety of in?ammatory and allergic conditions, and in reducing antibody production in a number of AUTOIMMUNE DISORDERS. The in?ammatory reaction is normally part of the body’s defence mechanism and is to be encouraged rather than inhibited. However, in the case of those diseases in which the body’s reaction is disproportionate to the o?ending agent, such that it causes unpleasant symptoms or frank illness, the steroid hormones can inhibit this undesirable response. Although the underlying condition is not cured as a result, it may resolve spontaneously. When corticosteroids are used for their anti-in?ammatory properties, the dose is pharmacological; that is, higher – often much higher – than the normal physiological requirement. Indeed, the necessary dose may exceed the normal maximum output of the healthy adrenal gland, which is about 250–300 mg cortisol per day. When doses of this order are used there are inevitable risks and side-effects: a drug-induced CUSHING’S SYNDROME will result.
Corticosteroid treatment of short duration, as in angioneurotic OEDEMA of the larynx or other allergic crises, may at the same time be life-saving and without signi?cant risk (see URTICARIA). Prolonged therapy of such connective-tissue disorders, such as POLYARTERITIS NODOSA with its attendant hazards, is generally accepted because there are no other agents of therapeutic value. Similarly the absence of alternative medical treatment for such conditions as autoimmune haemolytic ANAEMIA establishes steroid therapy as the treatment of choice which few would dispute. The use of steroids in such chronic conditions as RHEUMATOID ARTHRITIS, ASTHMA and DERMATITIS needs careful assessment and monitoring.
Although there is a risk of ill-effects, these should be set against the misery and danger of unrelieved chronic asthma or the incapacity, frustration and psychological trauma of rheumatoid arthritis. Patients should carry cards giving details of their dosage and possible complications.
The incidence and severity of side-effects are related to the dose and duration of treatment. Prolonged daily treatment with 15 mg of prednisolone, or more, will cause hypercortisonism; less than 10 mg prednisolone a day may be tolerated by most patients inde?nitely. Inhaled steroids rarely produce any ill-e?ect apart from a propensity to oral thrush (CANDIDA infection) unless given in excessive doses.
General side-effects may include weight gain, fat distribution of the cushingoid type, ACNE and HIRSUTISM, AMENORRHOEA, striae and increased bruising tendency. The more serious complications which can occur during long-term treatment include HYPERTENSION, oedema, DIABETES MELLITUS, psychosis, infection, DYSPEPSIA and peptic ulceration, gastrointestinal haemorrhage, adrenal suppression, osteoporosis (see BONE, DISORDERS OF), myopathy (see MUSCLES, DISORDERS OF), sodium retention and potassium depletion.... corticosteroids
Blunt injuries These may cause haemorrhage inside the eye, cataract, retinal detachment or even rupture of the eye (see also EYE, DISORDERS OF). Injuries from large blunt objects – for example, a squash ball – may also cause a ‘blow-out fracture’ of the orbital ?oor resulting in double vision. Surgical treatment may be required depending on the patient’s speci?c problems.
Chemical burns Most chemical splashes cause conjunctivitis and super?cial keratitis in the victim (see EYE, DISORDERS OF); both conditions are self-limiting. Alkalis are, however, more likely to penetrate deeper into the eye and cause permanent damage, particularly to the cornea. Prompt irrigation is important. Further treatment may involve testing the pH of the tears, topical antibiotics and CORTICOSTEROIDS, and vitamin C (drops or tablets – see APPENDIX 5: VITAMINS), depending on the nature of the injury.
Corneal abrasion Loss of corneal epithelium (outermost layer). Almost any sort of injury to the eye may cause this. The affected eye is usually very painful. In the absence of other problems, the epithelium heals rapidly: small defects may close within 24 hours. Treatment conventionally consists of antibiotic ointment and sometimes a pad over the injured eye.
Foreign bodies Most foreign bodies which hit the eye are small and are found in the conjunctival sac or on the cornea; most are super?cial and can be easily removed. A few foreign bodies penetrate deeper and may cause infection, cataract, retinal detachment or haemorrhage within the eye. The foreign body is usually removed and the damage repaired; nevertheless the victim’s sight may have been permanently damaged. Particularly dangerous activities include hammering or chiselling on metal or stone; people carrying out these activities (and others, such as hedge-cutting and grass-strimming) should wear protective goggles.... eye injuries
K
Diagram of glomerulus (Malpighian corpuscle).
Fortunately the body has two kidneys and, as most people can survive on one, there is a good ‘functional reserve’ of kidney tissue.
Symptoms Many patients with kidney disorders do not have any symptoms, even when the condition is quite advanced. However,
others experience loin pain associated with obstruction (renal colic) or due to infection; fevers; swelling (oedema), usually of the legs but occasionally including the face and arms; blood in the urine (haematuria); and excess quantities of urine (polyuria), including at night (nocturia), due to failure of normal mechanisms in the kidney for concentrating urine. Patients with chronic renal failure often have very di?use symptoms including nausea and vomiting, tiredness due to ANAEMIA, shortness of breath, skin irritation, pins and needles (paraesthesia) due to damage of the peripheral nerves (peripheral neuropathy), and eventually (rarely seen nowadays) clouding of consciousness and death.
Signs of kidney disease include loin tenderness, enlarged kidneys, signs of ?uid retention, high blood pressure and, in patients with end-stage renal failure, pallor, pigmentation and a variety of neurological signs including absent re?exes, reduced sensation, and a coarse ?apping tremor (asterixis) due to severe disturbance of the body’s normal metabolism.
Renal failure Serious kidney disease may lead to impairment or failure of the kidney’s ability to ?lter waste products from the blood and excrete them in the urine – a process that controls the body’s water and salt balance and helps to maintain a stable blood pressure. Failure of this process causes URAEMIA – an increase in urea and other metabolic waste products – as well as other metabolic upsets in the blood and tissues, all of which produce varying symptoms. Failure can be sudden or develop more slowly (chronic). In the former, function usually returns to normal once the underlying cause has been treated. Chronic failure, however, usually irreparably reduces or stops normal function.
Acute failure commonly results from physiological shock following a bad injury or major illness. Serious bleeding or burns can reduce blood volume and pressure to the point where blood-supply to the kidney is greatly reduced. Acute myocardial infarction (see HEART, DISEASES OF) or pancreatitis (see PANCREAS, DISORDERS OF) may produce a similar result. A mismatched blood transfusion can produce acute failure. Obstruction to the urine-?ow by a stone (calculus) in the urinary tract, a bladder tumour or an enlarged prostate can also cause acute renal failure, as can glomerulonephritis (see below) and the haemolytic-uraemia syndrome.
HYPERTENSION, DIABETES MELLITUS, polycystic kidney disease (see below) or AMYLOIDOSIS are among conditions that cause chronic renal failure. Others include stone, tumour, prostatic enlargement and overuse of analgesic drugs. Chronic failure may eventually lead to end-stage renal failure, a life-threatening situation that will need DIALYSIS or a renal transplant (see TRANSPLANTATION).
Familial renal disorders include autosomal dominant inherited polycystic kidney disease and sex-linked familial nephropathy. Polycystic kidney disease is an important cause of renal failure in the UK. Patients, usually aged 30–50, present with HAEMATURIA, loin or abdominal discomfort or, rarely, urinary-tract infection, hypertension and enlarged kidneys. Diagnosis is based on ultrasound examination of the abdomen. Complications include renal failure, hepatic cysts and, rarely, SUBARACHNOID HAEMORRHAGE. No speci?c treatment is available. Familial nephropathy occurs more often in boys than in girls and commonly presents as Alport’s syndrome (familial nephritis with nerve DEAFNESS) with PROTEINURIA, haematuria, progressing to renal failure and deafness. The cause of the disease lies in an absence of a speci?c ANTIGEN in a part of the glomerulus. The treatment is conservative, with most patients eventually requiring dialysis or transplantation.
Acute glomerulonephritis is an immune-complex disorder due to entrapment within glomerular capillaries of ANTIGEN (usually derived from B haemolytic streptococci – see STREPTOCOCCUS) antibody complexes initiating an acute in?ammatory response (see IMMUNITY). The disease affects children and young adults, and classically presents with a sore throat followed two weeks later by a fall in urine output (oliguria), haematuria, hypertension and mildly abnormal renal function. The disease is self-limiting with 90 per cent of patients spontaneously recovering. Treatment consists of control of blood pressure, reduced ?uid and salt intake, and occasional DIURETICS and ANTIBIOTICS.
Chronic glomerulonephritis is also due to immunological renal problems and is also classi?ed by taking a renal biopsy. It may be subdivided into various histological varieties as determined by renal biospy. Proteinuria of various degrees is present in all these conditions but the clinical presentations vary, as do their treatments. Some resolve spontaneously; others are treated with steroids or even the cytotoxic drug CYCLOPHOSPHAMIDE or the immunosuppressant cyclosporin. Prognoses are generally satisfactory but some patients may require renal dialysis or kidney transplantation – an operation with a good success rate.
Hydronephrosis A chronic disease in which the kidney becomes greatly distended with ?uid. It is caused by obstruction to the ?ow of urine at the pelvi-ureteric junction (see KIDNEYS – Structure). If the ureter is obstructed, the ureter proximal to the obstruction will dilate and pressure will be transmitted back to the kidney to cause hydronephrosis. Obstruction may occur at the bladder neck or in the urethra itself. Enlargement of the prostate is a common cause of bladder-neck obstruction; this would give rise to hypertrophy of the bladder muscle and both dilatation of the ureter and hydronephrosis. If the obstruction is not relieved, progressive destruction of renal tissue will occur. As a result of the stagnation of the urine, infection is probable and CYSTITIS and PYELONEPHRITIS may occur.
Impaired blood supply may be the outcome of diabetes mellitus and physiological shock, which lowers the blood pressure, also affecting the blood supply. The result can be acute tubular necrosis. POLYARTERITIS NODOSA and SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) may damage the large blood vessels in the kidney. Treatment is of the underlying condition.
Infection of the kidney is called pyelonephritis, a key predisposing factor being obstruction of urine ?ow through the urinary tract. This causes stagnation and provides a fertile ground for bacterial growth. Acute pyelonephritis is more common in women, especially during pregnancy when bladder infection (CYSTITIS) spreads up the ureters to the kidney. Symptoms are fever, malaise and backache. Antibiotics and high ?uid intake are the most e?ective treatment. Chronic pyelonephritis may start in childhood as a result of congenital deformities that permit urine to ?ow up from the bladder to the kidney (re?ux). Persistent re?ux leads to recurrent infections causing permanent damage to the kidney. Specialist investigations are usually required as possible complications include hypertension and kidney failure.
Tumours of the kidney are fortunately rare. Non-malignant ones commonly do not cause symptoms, and even malignant tumours (renal cell carcinoma) may be asymptomatic for many years. As soon as symptoms appear – haematuria, back pain, nausea, malaise, sometimes secondary growths in the lungs, bones or liver, and weight loss – urgent treatment including surgery, radiotherapy and chemotherapy is necessary. This cancer occurs mostly in adults over 40 and has a hereditary element. The prognosis is not good unless diagnosed early. In young children a rare cancer called nephroblastoma (Wilm’s tumour) can occur; treatment is with surgery, radiotherapy and chemotherapy. It may grow to a substantial size before being diagnosed.
Cystinuria is an inherited metabolic defect in the renal tubular reabsorption of cystine, ornithine, lysine and arginine. Cystine precipitates in an alkaline urine to form cystine stones. Triple phosphate stones are associated with infection and may develop into a very large branching calculi (staghorn calculi). Stones present as renal or ureteric pain, or as an infection. Treatment has undergone considerable change with the introduction of MINIMALLY INVASIVE SURGERY (MIS) and the destruction of stone by sound waves (LITHOTRIPSY).... kidneys, diseases of
The only certain sign of death, however, is that the heart has stopped beating. To ensure that this is permanent, it is necessary to listen over the heart with a stethoscope, or directly with the ear, for at least ?ve minutes. Permanent stoppage of breathing should also be con?rmed by observing that a mirror held before the mouth shows no haze, or that a feather placed on the upper lip does not ?utter.
In the vast majority of cases there is no dif?culty in ensuring that death has occurred. The introduction of organ transplantation, however, and of more e?ective mechanical means of resuscitation, such as ventilators, whereby an individual’s heart can be kept beating almost inde?nitely, has raised diffculties in a minority of cases. To solve the problem in these cases the concept of ‘brain death’ has been introduced. In this context it has to be borne in mind that there is no legal de?nition of death. Death has traditionally been diagnosed by the irreversible cessation of respiration and heartbeat. In the Code of Practice drawn up in 1983 by a Working Party of the Health Departments of Great Britain and Northern Ireland, however, it is stated that ‘death can also be diagnosed by the irreversible cessation of brain-stem function’. This is described as ‘brain death’. The brain stem consists of the mid-brain, pons and medulla oblongata which contain the centres controlling the vital processes of the body such as consciousness, breathing and the beating of the heart (see BRAIN). This new concept of death, which has been widely accepted in medical and legal circles throughout the world, means that it is now legitimate to equate brain death with death; that the essential component of brain death is death of the brain stem; and that a dead brain stem can be reliably diagnosed at the bedside. (See GLASGOW COMA SCALE.)
Four points are important in determining the time that has elapsed since death. HYPOSTASIS, or congestion, begins to appear as livid spots on the back, often mistaken for bruises, three hours or more after death. This is due to the blood running into the vessels in the lowest parts. Loss of heat begins at once after death, and the body has become as cold as the surrounding air after 12 hours – although this is delayed by hot weather, death from ASPHYXIA, and some other causes. Rigidity, or rigor mortis, begins in six hours, takes another six to become fully established, remains for 12 hours and passes o? during the succeeding 12 hours. It comes on quickly when extreme exertion has been indulged in immediately before death; conversely it is slow in onset and slight in death from wasting diseases, and slight or absent in children. It begins in the small muscles of the eyelid and jaw and then spreads over the body. PUTREFACTION is variable in time of onset, but usually begins in 2–3 days, as a greenish tint over the abdomen.... death, signs of
Varieties Haemorrhoids are classi?ed into ?rst-, second- and third-degree, depending on how far they prolapse through the anal canal. First-degree ones do not protrude; second-degree piles protrude during defaecation; third-degree ones are trapped outside the anal margin, although they can be pushed back. Most haemorrhoids can be described as internal, since they are covered with glandular mucosa, but some large, long-term ones develop a covering of skin. Piles are usually found at the three, seven and eleven o’clock sites when viewed with the patient on his or her back.
Causes The veins in the anus tend to become distended because they have no valves; because they form the lowest part of the PORTAL SYSTEM and are apt to become over?lled when there is the least interference with the circulation through the portal vein; and partly because the muscular arrangements for keeping the rectum closed interfere with the circulation through the haemorrhoidal veins. An absence of ?bre from western diets is probably the most important cause. The result is that people often strain to defaecate hard stools, thus raising intra-abdominal pressure which slows the rate of venous return and engorges the network of veins in the anal mucosa. Pregnancy is an important contributory factor in women developing haemorrhoids. In some people, haemorrhoids are a symptom of disease higher up in the portal system, causing interference with the circulation. They are common in heart disease, liver complaints such as cirrhosis or congestion, and any disease affecting the bowels.
Symptoms Piles cause itching, pain and often bleeding, which may occur whenever the patient defaecates or only sometimes. The piles may prolapse permanently or intermittently. The patient may complain of aching discomfort which, with the pain, may be worsened.
Treatment Prevention is important; a high-?bre diet will help in this, and is also necessary after piles have developed. Patients should not spend a long time straining on the lavatory. Itching can be lessened if the PERINEUM is properly washed, dried and powdered. Prolapsed piles can be replaced with the ?nger. Local anaesthetic and steroid ointments can help to relieve symptoms when they are relatively mild, but do not remedy the underlying disorder. If conservative measures fail, then surgery may be required. Piles may be injected, stretched or excised according to the patient’s particular circumstances.
Where haemorrhoids are secondary to another disorder, such as cancer of the rectum or colon, the underlying condition must be treated – hence the importance of medical advice if piles persist.... haemorrhoids
Types In adults, three types of jaundice occur. They are all the result of disturbance in the mechanism by which HAEMOGLOBIN from the breakdown of ageing red blood cells (erythrocytes) is not properly processed in the liver. Normally the breakdown product of this haemoglobin – bilirubin – is made water-soluble in the liver and excreted via the bile ducts into the small intestine, where it colours the stools dark brown. HAEMOLYTIC JAUNDICE In this type, the amount of bilirubin produced is too much for the liver to deal with, the excess usually being the result of an abnormal level of haemoglobin from the breakdown of blood cells. This haemolytic anaemia, as it is known, has several causes (see ANAEMIA). HEPATOCELLULAR JAUNDICE In this disorder, bilirubin builds up in the blood because liver cells have been damaged or have died – usually as a result of a viral infection (there are four types) causing HEPATITIS, or of liver failure. OBSTRUCTIVE JAUNDICE Also called cholestatic jaundice, this type is characterised by the inability of bile to be discharged from the liver because the bile ducts are blocked as a result of gall-stones (see under GALL-BLADDER, DISEASES OF) or a growth. Sometimes the ducts are absent (atresia) or have been destroyed in the liver as a result of CIRRHOSIS.
Symptoms Yellowness, appearing ?rst in the whites of the eyes and later over the whole skin, is the symptom that attracts notice. Indigestion, nausea, poor appetite and general malaise are other symptoms. The skin may itch, and the faeces are pale because of the absence of bile.
Treatment The essential step is to treat the underlying cause if possible: for instance, gallstones, if these be the cause of the jaundice. Comprehensive laboratory investigations are usually required, and supportive measures are needed. (See also LIVER, DISEASES OF.).... jaundice
Occupational health includes both mental and physical health. It is about compliance with health-and-safety-at-work legislation (and common law duties) and about best practice in providing work environments that reduce risks to health and safety to lowest practicable levels. It includes workers’ ?tness to work, as well as the management of the work environment to accommodate people with disabilities, and procedures to facilitate the return to work of those absent with long-term illness. Occupational health incorporates several professional groups, including occupational physicians, occupational health nurses, occupational hygienists, ergonomists, disability managers, workplace counsellors, health-and-safety practitioners, and workplace physiotherapists.
In the UK, two key statutes provide a framework for occupational health: the Health and Safety at Work, etc. Act 1974 (HSW Act); and the Disability Discrimination Act 1995 (DDA). The HSW Act states that employers have a duty to protect the health, safety and welfare of their employees and to conduct their business in a way that does not expose others to risks to their health and safety. Employees and self-employed people also have duties under the Act. Modern health-and-safety legislation focuses on assessing and controlling risk rather than prescribing speci?c actions in di?erent industrial settings. Various regulations made under the HSW Act, such as the Control of Substances Hazardous to Health Regulations, the Manual Handling Operations Regulations and the Noise at Work Regulations, set out duties with regard to di?erent risks, but apply to all employers and follow the general principles of risk assessment and control. Risks should be controlled principally by removing or reducing the hazard at source (for example, by substituting chemicals with safer alternatives, replacing noisy machinery, or automating tasks to avoid heavy lifting). Personal protective equipment, such as gloves and ear defenders, should be seen as a last line of defence after other control measures have been put in place.
The employment provisions of the DDA require employers to avoid discriminatory practice towards disabled people and to make reasonable adjustments to working arrangements where a disabled person is placed at a substantial disadvantage to a non-disabled person. Although the DDA does not require employers to provide access to rehabilitation services – even for those injured or made ill at work – occupational-health practitioners may become involved in programmes to help people get back to work after injury or long-term illness, and many businesses see the retention of valuable sta? as an attractive alternative to medical retirement or dismissal on health grounds.
Although a major part of occupational-health practice is concerned with statutory compliance, the workplace is also an important venue for health promotion. Many working people rarely see their general practitioner and, even when they do, there is little time to discuss wider health issues. Occupational-health advisers can ?ll in this gap by providing, for example, workplace initiatives on stopping smoking, cardiovascular health, diet and self-examination for breast and testicular cancers. Such initiatives are encouraged because of the perceived bene?ts to sta?, to the employing organisation and to the wider public-health agenda. Occupational psychologists recognise the need for the working population to achieve a ‘work-life balance’ and the promotion of this is an increasing part of occupational health strategies.
The law requires employers to consult with their sta? on health-and-safety matters. However, there is also a growing understanding that successful occupational-health management involves workers directly in the identi?cation of risks and in developing solutions in the workplace. Trade unions play an active role in promoting occupational health through local and national campaigns and by training and advising elected workplace safety representatives.
Occupational medicine The branch of medicine that deals with the control, prevention, diagnosis, treatment and management of ill-health and injuries caused or made worse by work, and with ensuring that workers are ?t for the work they do.
Occupational medicine includes: statutory surveillance of workers’ exposure to hazardous agents; advice to employers and employees on eliminating or reducing risks to health and safety at work; diagnosis and treatment/management of occupational illness; advice on adapting the working environment to suit the worker, particularly those with disabilities or long-term health problems; and advice on the return to work and, if necessary, rehabilitation of workers absent through illness. Occupational physicians may play a wider role in monitoring the health of workplace populations and in advising employers on controlling health hazards where ill-health trends are observed. They may also conduct epidemiological research (see EPIDEMIOLOGY) on workplace diseases.
Because of the occupational physician’s dual role as adviser to both employer and employee, he or she is required to be particularly diligent with regards to the individual worker’s medical CONFIDENTIALITY. Occupational physicians need to recognise in any given situation the context they are working in, and to make sure that all parties are aware of this.
Occupational medicine is a medical discipline and thus is only part of the broader ?eld of occupational health. Although there are some speci?c clinical duties associated with occupational medicine, such as diagnosis of occupational disease and medical screening, occupational physicians are frequently part of a multidisciplinary team that might include, for example, occupational-health nurses, healthand-safety advisers, ergonomists, counsellors and hygienists. Occupational physicians are medical practitioners with a post-registration quali?cation in occupational medicine. They will have completed a period of supervised in-post training. In the UK, the Faculty of Occupational Medicine of the Royal College of Physicians has three categories of membership, depending on quali?cations and experience: associateship (AFOM); membership (MFOM); and fellowship (FFOM).
Occupational diseases Occupational diseases are illnesses that are caused or made worse by work. In their widest sense, they include physical and mental ill-health conditions.
In diagnosing an occupational disease, the clinician will need to examine not just the signs and symptoms of ill-health, but also the occupational history of the patient. This is important not only in discovering the cause, or causes, of the disease (work may be one of a number of factors), but also in making recommendations on how the work should be modi?ed to prevent a recurrence – or, if necessary, in deciding whether or not the worker is able to return to that type of work. The occupational history will help in deciding whether or not other workers are also at risk of developing the condition. It will include information on:
the nature of the work.
how the tasks are performed in practice.
the likelihood of exposure to hazardous agents (physical, chemical, biological and psychosocial).
what control measures are in place and the extent to which these are adhered to.
previous occupational and non-occupational exposures.
whether or not others have reported similar symptoms in relation to the work. Some conditions – certain skin conditions,
for example – may show a close relationship to work, with symptoms appearing directly only after exposure to particular agents or possibly disappearing at weekends or with time away from work. Others, however, may be chronic and can have serious long-term implications for a person’s future health and employment.
Statistical information on the prevalence of occupational disease in the UK comes from a variety of sources, including o?cial ?gures from the Industrial Injuries Scheme (see below) and statutory reporting of occupational disease (also below). Neither of these o?cial schemes provides a representative picture, because the former is restricted to certain prescribed conditions and occupations, and the latter suffers from gross under-reporting. More useful are data from the various schemes that make up the Occupational Diseases Intelligence Network (ODIN) and from the Labour Force Survey (LFS). ODIN data is generated by the systematic reporting of work-related conditions by clinicians and includes several schemes. Under one scheme, more than 80 per cent of all reported diseases by occupational-health physicians fall into just six of the 42 clinical disease categories: upper-limb disorders; anxiety, depression and stress disorders; contact DERMATITIS; lower-back problems; hearing loss (see DEAFNESS); and ASTHMA. Information from the LFS yields a similar pattern in terms of disease frequency. Its most recent survey found that over 2 million people believed that, in the previous 12 months, they had suffered from an illness caused or made worse by work and that
19.5 million working days were lost as a result. The ten most frequently reported disease categories were:
stress and mental ill-health (see MENTAL ILLNESS): 515,000 cases.
back injuries: 508,000.
upper-limb and neck disorders: 375,000.
lower respiratory disease: 202,000.
deafness, TINNITUS or other ear conditions: 170,000.
lower-limb musculoskeletal conditions: 100,000.
skin disease: 66,000.
headache or ‘eyestrain’: 50,000.
traumatic injury (includes wounds and fractures from violent attacks at work): 34,000.
vibration white ?nger (hand-arm vibration syndrome): 36,000. A person who develops a chronic occu
pational disease may be able to sue his or her employer for damages if it can be shown that the employer was negligent in failing to take reasonable care of its employees, or had failed to provide a system of work that would have prevented harmful exposure to a known health hazard. There have been numerous successful claims (either awarded in court, or settled out of court) for damages for back and other musculoskeletal injuries, hand-arm vibration syndrome, noise-induced deafness, asthma, dermatitis, MESOTHELIOMA and ASBESTOSIS. Employers’ liability (workers’ compensation) insurers are predicting that the biggest future rise in damages claims will be for stress-related illness. In a recent study, funded by the Health and Safety Executive, about 20 per cent of all workers – more than 5 million people in the UK – claimed to be ‘very’ or ‘extremely’ stressed at work – a statistic that is likely to have a major impact on the long-term health of the working population.
While victims of occupational disease have the right to sue their employers for damages, many countries also operate a system of no-fault compensation for the victims of prescribed occupational diseases. In the UK, more than 60 diseases are prescribed under the Industrial Injuries Scheme and a person will automatically be entitled to state compensation for disability connected to one of these conditions, provided that he or she works in one of the occupations for which they are prescribed. The following short list gives an indication of the types of diseases and occupations prescribed under the scheme:
CARPAL TUNNEL SYNDROME connected to the use of hand-held vibrating tools.
hearing loss from (amongst others) use of pneumatic percussive tools and chainsaws, working in the vicinity of textile manufacturing or woodworking machines, and work in ships’ engine rooms.
LEPTOSPIROSIS – infection with Leptospira (various listed occupations).
viral HEPATITIS from contact with human blood, blood products or other sources of viral hepatitis.
LEAD POISONING, from any occupation causing exposure to fumes, dust and vapour from lead or lead products.
asthma caused by exposure to, among other listed substances, isocyanates, curing agents, solder ?ux fumes and insects reared for research.
mesothelioma from exposure to asbestos.
In the UK, employers and the self-employed have a duty to report all occupational injuries (if the employee is o? work for three days or more as a result), diseases or dangerous incidents to the relevant enforcing authority (the Health and Safety Executive or local-authority environmental-health department) under the Reporting of Injuries, Diseases and Dangerous Occurrences Regulations 1995 (RIDDOR). Despite this statutory duty, comparatively few diseases are reported so that ?gures generated from RIDDOR reports do not give a useful indication of the scale of occupational diseases in the UK. The statutory reporting of injuries is much better, presumably because of the clear and acute relationship between a workplace accident and the resultant injury. More than 160,000 injuries are reported under RIDDOR every year compared with just 2,500 or so occupational diseases, a gross underestimate of the true ?gure.
There are no precise ?gures for the number of people who die prematurely because of work-related ill-health, and it would be impossible to gauge the exact contribution that work has on, for example, cardiovascular disease and cancers where the causes are multifactorial. The toll would, however, dwarf the number of deaths caused by accidents at work. Around 250 people are killed by accidents at work in the UK each year – mesothelioma, from exposure to asbestos at work, alone kills more than 1,300 people annually.
The following is a sample list of occupational diseases, with brief descriptions of their aetiologies.
Inhaled materials
PNEUMOCONIOSIS covers a group of diseases which cause ?brotic lung disease following the inhalation of dust. Around 250–300 new cases receive bene?t each year – mostly due to coal dust with or without silica contamination. SILICOSIS is the more severe disease. The contraction in the size of the coal-mining industry as well as improved dust suppression in the mines have diminished the importance of this disease, whereas asbestos-related diseases now exceed 1,000 per year. Asbestos ?bres cause a restrictive lung disease but also are responsible for certain malignant conditions such as pleural and peritoneal mesothelioma and lung cancer. The lung-cancer risk is exacerbated by cigarette-smoking.
Even though the use of asbestos is virtually banned in the UK, many workers remain at risk of exposure because of the vast quantities present in buildings (much of which is not listed in building plans). Carpenters, electricians, plumbers, builders and demolition workers are all liable to exposure from work that disturbs existing asbestos. OCCUPATIONAL ASTHMA is of increasing importance – not only because of the recognition of new allergic agents (see ALLERGY), but also in the number of reported cases. The following eight substances are most frequently linked to occupational asthma (key occupations in brackets): isocyanates (spray painters, electrical processors); ?our and grain (bakers and farmers); wood dust (wood workers); glutaraldehyde (nurses, darkroom technicians); solder/colophony (welders, electronic assembly workers); laboratory animals (technicians, scientists); resins and glues (metal and electrical workers, construction, chemical processors); and latex (nurses, auxiliaries, laboratory technicians).
The disease develops after a short, symptomless period of exposure; symptoms are temporally related to work exposures and relieved by absences from work. Removal of the worker from exposure does not necessarily lead to complete cessation of symptoms. For many agents, there is no relationship with a previous history of ATOPY. Occupational asthma accounts for about 10 per cent of all asthma cases. DERMATITIS The risk of dermatitis caused by an allergic or irritant reaction to substances used or handled at work is present in a wide variety of jobs. About three-quarters of cases are irritant contact dermatitis due to such agents as acids, alkalis and solvents. Allergic contact dermatitis is a more speci?c response by susceptible individuals to a range of allergens (see ALLERGEN). The main occupational contact allergens include chromates, nickel, epoxy resins, rubber additives, germicidal agents, dyes, topical anaesthetics and antibiotics as well as certain plants and woods. Latex gloves are a particular cause of occupational dermatitis among health-care and laboratory sta? and have resulted in many workers being forced to leave their profession through ill-health. (See also SKIN, DISEASES OF.)
Musculoskeletal disorders Musculoskeletal injuries are by far the most common conditions related to work (see LFS ?gures, above) and the biggest cause of disability. Although not all work-related, musculoskeletal disorders account for 36.5 per cent of all disabilities among working-age people (compared with less than 4 per cent for sight and hearing impairment). Back pain (all causes – see BACKACHE) has been estimated to cause more than 50 million days lost every year in sickness absence and costs the UK economy up to £5 billion annually as a result of incapacity or disability. Back pain is a particular problem in the health-care sector because of the risk of injury from lifting and moving patients. While the emphasis should be on preventing injuries from occurring, it is now well established that the best way to manage most lower-back injuries is to encourage the patient to continue as normally as possible and to remain at work, or to return as soon as possible even if the patient has some residual back pain. Those who remain o? work on long-term sick leave are far less likely ever to return to work.
Aside from back injuries, there are a whole range of conditions affecting the upper limbs, neck and lower limbs. Some have clear aetiologies and clinical signs, while others are less well de?ned and have multiple causation. Some conditions, such as carpal tunnel syndrome, are prescribed diseases in certain occupations; however, they are not always caused by work (pregnant and older women are more likely to report carpal tunnel syndrome irrespective of work) and clinicians need to be careful when assigning work as the cause without ?rst considering the evidence. Other conditions may be revealed or made worse by work – such as OSTEOARTHRITIS in the hand. Much attention has focused on injuries caused by repeated movement, excessive force, and awkward postures and these include tenosynovitis (in?ammation of a tendon) and epicondylitis. The greatest controversy surrounds upper-limb disorders that do not present obvious tissue or nerve damage but nevertheless give signi?cant pain and discomfort to the individual. These are sometimes referred to as ‘repetitive strain injury’ or ‘di?use RSI’. The diagnosis of such conditions is controversial, making it di?cult for sufferers to pursue claims for compensation through the courts. Psychosocial factors, such as high demands of the job, lack of control and poor social support at work, have been implicated in the development of many upper-limb disorders, and in prevention and management it is important to deal with the psychological as well as the physical risk factors. Occupations known to be at particular risk of work-related upper-limb disorders include poultry processors, packers, electronic assembly workers, data processors, supermarket check-out operators and telephonists. These jobs often contain a number of the relevant exposures of dynamic load, static load, a full or excessive range of movements and awkward postures. (See UPPER LIMB DISORDERS.)
Physical agents A number of physical agents cause occupational ill-health of which the most important is occupational deafness. Workplace noise exposures in excess of 85 decibels for a working day are likely to cause damage to hearing which is initially restricted to the vital frequencies associated with speech – around 3–4 kHz. Protection from such noise is imperative as hearing aids do nothing to ameliorate the neural damage once it has occurred.
Hand-arm vibration syndrome is a disorder of the vascular and/or neural endings in the hands leading to episodic blanching (‘white ?nger’) and numbness which is exacerbated by low temperature. The condition, which is caused by vibrating tools such as chain saws and pneumatic hammers, is akin to RAYNAUD’S DISEASE and can be disabling.
Decompression sickness is caused by a rapid change in ambient pressure and is a disease associated with deep-sea divers, tunnel workers and high-?ying aviators. Apart from the direct effects of pressure change such as ruptured tympanic membrane or sinus pain, the more serious damage is indirectly due to nitrogen bubbles appearing in the blood and blocking small vessels. Central and peripheral nervous-system damage and bone necrosis are the most dangerous sequelae.
Radiation Non-ionising radiation from lasers or microwaves can cause severe localised heating leading to tissue damage of which cataracts (see under EYE, DISORDERS OF) are a particular variety. Ionising radiation from radioactive sources can cause similar acute tissue damage to the eyes as well as cell damage to rapidly dividing cells in the gut and bone marrow. Longer-term effects include genetic damage and various malignant disorders of which LEUKAEMIA and aplastic ANAEMIA are notable. Particular radioactive isotopes may destroy or induce malignant change in target organs, for example, 131I (thyroid), 90Sr (bone). Outdoor workers may also be at risk of sunburn and skin cancers. OTHER OCCUPATIONAL CANCERS Occupation is directly responsible for about 5 per cent of all cancers and contributes to a further 5 per cent. Apart from the cancers caused by asbestos and ionising radiation, a number of other occupational exposures can cause human cancer. The International Agency for Research on Cancer regularly reviews the evidence for carcinogenicity of compounds and industrial processes, and its published list of carcinogens is widely accepted as the current state of knowledge. More than 50 agents and processes are listed as class 1 carcinogens. Important occupational carcinogens include asbestos (mesothelioma, lung cancer); polynuclear aromatic hydrocarbons such as mineral oils, soots, tars (skin and lung cancer); the aromatic amines in dyestu?s (bladder cancer); certain hexavalent chromates, arsenic and nickel re?ning (lung cancer); wood and leather dust (nasal sinus cancer); benzene (leukaemia); and vinyl chloride monomer (angiosarcoma of the liver). It has been estimated that elimination of all known occupational carcinogens, if possible, would lead to an annual saving of 5,000 premature deaths in Britain.
Infections Two broad categories of job carry an occupational risk. These are workers in contact with animals (farmers, veterinary surgeons and slaughtermen) and those in contact with human sources of infection (health-care sta? and sewage workers).
Occupational infections include various zoonoses (pathogens transmissible from animals to humans), such as ANTHRAX, Borrelia burgdorferi (LYME DISEASE), bovine TUBERCULOSIS, BRUCELLOSIS, Chlamydia psittaci, leptospirosis, ORF virus, Q fever, RINGWORM and Streptococcus suis. Human pathogens that may be transmissible at work include tuberculosis, and blood-borne pathogens such as viral hepatitis (B and C) and HIV (see AIDS/HIV). Health-care workers at risk of exposure to infected blood and body ?uids should be immunised against hapatitis B.
Poisoning The incidence of occupational poisonings has diminished with the substitution of noxious chemicals with safer alternatives, and with the advent of improved containment. However, poisonings owing to accidents at work are still reported, sometimes with fatal consequences. Workers involved in the application of pesticides are particularly at risk if safe procedures are not followed or if equipment is faulty. Exposure to organophosphate pesticides, for example, can lead to breathing diffculties, vomiting, diarrhoea and abdominal cramps, and to other neurological effects including confusion and dizziness. Severe poisonings can lead to death. Exposure can be through ingestion, inhalation and dermal (skin) contact.
Stress and mental health Stress is an adverse reaction to excessive pressures or demands and, in occupational-health terms, is di?erent from the motivational impact often associated with challenging work (some refer to this as ‘positive stress’). Stress at work is often linked to increasing demands on workers, although coping can often prevent the development of stress. The causes of occupational stress are multivariate and encompass job characteristics (e.g. long or unsocial working hours, high work demands, imbalance between e?ort and reward, poorly managed organisational change, lack of control over work, poor social support at work, fear of redundancy and bullying), as well as individual factors (such as personality type, personal circumstances, coping strategies, and availability of psychosocial support outside work). Stress may in?uence behaviours such as smoking, alcohol consumption, sleep and diet, which may in turn affect people’s health. Stress may also have direct effects on the immune system (see IMMUNITY) and lead to a decline in health. Stress may also alter the course and response to treatment of conditions such as cardiovascular disease. As well as these general effects of stress, speci?c types of disorder may be observed.
Exposure to extremely traumatic incidents at work – such as dealing with a major accident involving multiple loss of life and serious injury
(e.g. paramedics at the scene of an explosion or rail crash) – may result in a chronic condition known as post-traumatic stress disorder (PTSD). PTSD is an abnormal psychological reaction to a traumatic event and is characterised by extreme psychological discomfort, such as anxiety or panic when reminded of the causative event; sufferers may be plagued with uncontrollable memories and can feel as if they are going through the trauma again. PTSD is a clinically de?ned condition in terms of its symptoms and causes and should not be used to include normal short-term reactions to trauma.... occupational health, medicine and diseases
Pregnancy lasts about 280 days and is calculated from the ?rst day of the last menstrual period – see MENSTRUATION. Pregnancy-testing kits rely on the presence of the hormone beta HUMAN CHORIONIC GONADOTROPHIN (b HCG) which is excreted in the woman’s urine as early as 30 days from the last menstrual period. The estimated date of delivery can be accurately estimated from the size of the developing fetus measured by ULTRASOUND (see also below) between seven and 24 weeks. ‘Term’ refers to the time that the baby is due; this can range from 38 weeks to 41 completed weeks.
Physical changes occur in early pregnancy – periods stop and the abdomen enlarges. The breasts swell, with the veins becoming prominent and the nipples darkening. About two in three women will have nausea with a few experiencing such severe vomiting as to require hospital admission for rehydration.
Antenatal care The aim of antenatal care is to ensure a safe outcome for both mother and child; it is provided by midwives (see MIDWIFE) and doctors. Formal antenatal care began in Edinburgh in the 1930s with the recognition that all aspects of pregnancy – normal and abnormal – warranted surveillance. Cooperation between general practitioners, midwives and obstetricians is now established, with pregnancies that are likely to progress normally being cared for in the community and only those needing special intervention being cared for in a hospital setting.
The initial visit (or booking) in the ?rst half of pregnancy will record the history of past events and the results of tests, with the aim of categorising the patients into normal or not. Screening tests including blood checks and ultrasound scans are a routine part of antenatal care. The ?rst ultrasound scan is done at about 11 weeks to date the pregnancy, with a further one done at 20 weeks – the anomaly scan – to assess the baby’s structure. Some obstetric units will check the growth of the baby with one further scan later in the pregnancy or, in the case of twin pregnancies (see below), many scans throughout. The routine blood tests include checks for ANAEMIA, DIABETES MELLITUS, sickle-cell disease and THALASSAEMIA, as well as for the blood group. Evidence of past infections is also looked for; tests for RUBELLA (German measles) and SYPHILIS are routine, whereas tests for human immunode?ciency virus (see AIDS/ HIV below) and HEPATITIS are being o?ered as optional, although there is compelling evidence that knowledge of the mother’s infection status is bene?cial to the baby.
Traditional antenatal care consists of regular appointments, initially every four weeks until 34 weeks, then fortnightly or weekly. At each visit the mother’s weight, urine and blood pressure are checked, and assessment of fetal growth and position is done by palpating the uterus. Around two-thirds of pregnancies and labours are normal: in the remainder, doctors and midwives need to increase the frequency of surveillance so as to prevent or deal with maternal and fetal problems.
Common complications of pregnancy
Some of the more common complications of pregnancy are listed below.
As well as early detection of medical complications, antenatal visits aim to be supportive and include emotional and educational care. Women with uncomplicated pregnancies are increasingly being managed by midwives and general practitioners in the community and only coming to the hospital doctors should they develop a problem. A small number will opt for a home delivery, but facilities for providing such a service are not always available in the UK.
Women requiring more intensive surveillance have their management targeted to the speci?c problems encountered. Cardiologists will see mothers-to-be with heart conditions, and those at risk of diabetes are cared for in designated clinics with specialist sta?. Those women needing more frequent surveillance than standard antenatal care can be looked after in maternity day centres. These typically include women with mildly raised blood pressure or those with small babies. Fetal medicine units have specialists who are highly skilled in ultrasound scanning and specialise in the diagnosis and management of abnormal babies still in the uterus. ECTOPIC PREGNANCY Chronic abdominal discomfort early in pregnancy may be caused by unruptured ectopic pregnancy, when, rarely, the fertilised OVUM starts developing in the Fallopian tube (see FALLOPIAN TUBES) instead of the uterus. The patient needs hospital treatment and LAPAROSCOPY. A ruptured ectopic pregnancy causes acute abdominal symptoms and collapse, and the woman will require urgent abdominal surgery. URINARY TRACT INFECTIONS These affect around 2 per cent of pregnant women and are detected by a laboratory test of a mid-stream specimen of urine. In pregnancy, symptoms of these infections do not necessarily resemble those experienced by non-pregnant women. As they can cause uterine irritability and possible premature labour (see below), it is important to ?nd and treat them appropriately. ANAEMIA is more prevalent in patients who are vegetarian or on a poor diet. Iron supplements are usually given to women who have low concentrations of HAEMOGLOBIN in their blood (less than 10.5 g/dl) or who are at risk of becoming low in iron, from bleeding, twin pregnancies and those with placenta previa (see below). ANTEPARTUM HAEMORRHAGE Early in pregnancy, vaginal bleedings may be due to a spontaneous or an incomplete therapeutic ABORTION. Bleeding from the genital tract between 24 completed weeks of pregnancy and the start of labour is called antepartum haemorrhage. The most common site is where the PLACENTA is attached to the wall of the uterus. If the placenta separates before delivery, bleeding occurs in the exposed ‘bed’. When the placenta is positioned in the upper part of the uterus it is called an abruption. PLACENTA PRAEVIA is sited in the lower part and blocks or partly blocks the cervix (neck of the womb); it can be identi?ed at about the 34th week. Ten per cent of episodes of antepartum bleeding are caused by placenta previa, and it may be associated with bleeding at delivery. This potentially serious complication is diagnosed by ultrasound scanning and may require a caesarean section (see below) at delivery. INCREASED BLOOD PRESSURE, associated with protein in the urine and swelling of the limbs, is part of a condition known as PRE-ECLAMPSIA. This occurs in the second half of pregnancy in about 1 in 10 women expecting their ?rst baby, and is mostly very mild and of no consequence to the pregnancy. However, some women can develop extremely high blood pressures which can adversely affect the fetus and cause epileptic-type seizures and bleeding disorders in the mother. This serious condition is called ECLAMPSIA. For this reason a pregnant woman with raised blood pressure or PROTEIN in her urine is carefully evaluated with blood tests, often in the maternity day assessment unit. The condition can be stopped by delivery of the baby, and this will be done if the mother’s or the fetus’s life is in danger. If the condition is milder, and the baby not mature enough for a safe delivery, then drugs can be used to control the blood pressure. MISCARRIAGE Also called spontaneous abortion, miscarriage is the loss of the fetus. There are several types:
threatened miscarriage is one in which some vaginal bleeding occurs, the uterus is enlarged, but the cervix remains closed and pregnancy usually proceeds.
inevitable miscarriage usually occurs before the 16th week and is typi?ed by extensive blood loss through an opened cervix and cramp-like abdominal pain; some products of conception are lost but the developing placental area (decidua) is retained and an operation may be necessary to clear the womb.
missed miscarriages, in which the embryo dies and is absorbed, but the decidua (placental area of uterine wall) remains and may cause abdominal discomfort and discharge of old blood.
THERAPEUTIC ABORTION is performed on more than 170,000 women annually in England and Wales. Sometimes the woman may not have arranged the procedure through the usual health-care channels, so that a doctor may see a patient with vaginal bleeding, abdominal discomfort or pain, and open cervix – symptoms which suggest that the decidua and a blood clot have been retained; these retained products will need to be removed by curettage.
Septic abortions are now much less common in Britain than before the Abortion Act (1967) permitted abortion in speci?ed circumstances. The cause is the passage of infective organisms from the vagina into the uterus, with Escherichia coli and Streptococcus faecalis the most common pathogenic agents. The woman has abdominal pain, heavy bleeding, usually fever and sometimes she is in shock. The cause is usually an incomplete abortion or one induced in unsterile circumstances. Antibiotics and curettage are the treatment. INTRAUTERINE GROWTH RETARDATION describes a slowing of the baby’s growth. This can be diagnosed by ultrasound scanning, although there is a considerable margin of error in estimates of fetal weight. Trends in growth are favoured over one-o? scan results alone. GESTATIONAL DIABETES is a condition that is more common in women who are overweight or have a family member with diabetes. If high concentrations of blood sugar are found, e?orts are made to correct it as the babies can become very fat (macrosomia), making delivery more di?cult. A low-sugar diet is usually enough to control the blood concentration of sugars; however some women need small doses of INSULIN to achieve control. FETAL ABNORMALITIES can be detected before birth using ultrasound. Some of these defects are obvious, such as the absence of kidneys, a condition incompatible with life outside the womb. These women can be o?ered a termination of their pregnancy. However, more commonly, the pattern of problems can only hint at an abnormality and closer examination is needed, particularly in the diagnosis of chromosomal deformities such as DOWN’S (DOWN) SYNDROME (trisomy 21 or presence of three 21 chromosomes instead of two).
Chromosomal abnormalities can be de?nitively diagnosed only by cell sampling such as amniocentesis (obtaining amniotic ?uid – see AMNION – from around the baby) done at 15 weeks onwards, and chorionic villus sampling (sampling a small part of the placenta) – another technique which can be done from 12 weeks onwards. Both have a small risk of miscarriage associated with them; consequently, they are con?ned to women at higher risk of having an abnormal fetus.
Biochemical markers present in the pregnant woman’s blood at di?erent stages of pregnancy may have undergone changes in those carrying an abnormal fetus. The ?rst such marker to be routinely used was a high concentration of alpha-fetol protein in babies with SPINA BIFIDA (defects in the covering of the spinal cord). Fuller research has identi?ed a range of diagnostic markers which are useful, and, in conjunction with other factors such as age, ethnic group and ultrasound ?ndings, can provide a predictive guide to the obstetrician – in consultation with the woman – as to whether or not to proceed to an invasive test. These tests include pregnancy-associated plasma protein assessed from a blood sample taken at 12 weeks and four blood tests at 15–22 weeks – alphafetol protein, beta human chorionic gonadotrophin, unconjugated oestriol and inhibin A. Ultrasound itself can reveal physical ?ndings in the fetus, which can be more common in certain abnormalities. Swelling in the neck region of an embryo in early pregnancy (increased nuchal thickness) has good predictive value on its own, although its accuracy is improved in combination with the biochemical markers. The e?ectiveness of prenatal diagnosis is rapidly evolving, the aim being to make the diagnosis as early in the pregnancy as possible to help the parents make more informed choices. MULTIPLE PREGNANCIES In the UK, one in 95 deliveries is of twins, while the prevalence of triplets is one in 10,000 and quadruplets around one in 500,000. Racial variations occur, with African women having a prevalence rate of one in 30 deliveries for twins and Japanese women a much lower rate than the UK ?gure. Multiple pregnancies occur more often in older women, and in the UK the prevalence of fertility treatments, many of these being given to older women, has raised the incidence. There is now an o?cial limit of three eggs being transferred to a woman undergoing ASSISTED CONCEPTION (gamete intrafallopian transfer, or GIFT).
Multiple pregnancies are now usually diagnosed as a result of routine ultrasound scans between 16 and 20 weeks of pregnancy. The increased size of the uterus results in the mother having more or worse pregnancy-related conditions such as nausea, abdominal discomfort, backache and varicose veins. Some congenital abnormalities in the fetus occur more frequently in twins: NEURAL TUBE defects, abnormalities of the heart and the incidence of TURNER’S SYNDROME and KLINEFELTER’S SYNDROME are examples. Such abnormalities may be detected by ultrasound scans or amniocentesis. High maternal blood pressure and anaemia are commoner in women with multiple pregnancies (see above).
The growth rates of multiple fetuses vary, but the di?erence between them and single fetuses are not that great until the later stages of pregnancy. Preterm labour is commoner in multiple pregnancies: the median length of pregnancy is 40 weeks for singletons, 37 for twins and 33 for triplets. Low birth-weights are usually the result of early delivery rather than abnormalities in growth rates. Women with multiple pregnancies require more frequent and vigilant antenatal assessments, with their carers being alert to the signs of preterm labour occurring. CEPHALOPELVIC DISPROPORTION Disparity between the size of the fetus and the mother’s pelvis is not common in the UK but is a signi?cant problem in the developing world. Disparity is classi?ed as absolute, when there is no possibility of delivery, and relative, when the baby is large but delivery (usually after a dif?cult labour) is possible. Causes of absolute disparity include: a large baby – heavier than 5 kg at birth; fetal HYDROCEPHALUS; and an abnormal maternal pelvis. The latter may be congenital, the result of trauma or a contraction in pelvic size because of OSTEOMALACIA early in life. Disproportion should be suspected if in late pregnancy the fetal head has not ‘engaged’ in the pelvis. Sometimes a closely supervised ‘trial of labour’ may result in a successful, if prolonged, delivery. Otherwise a caesarean section (see below) is necessary. UNUSUAL POSITIONS AND PRESENTATIONS OF THE BABY In most pregnant women the baby ?ts into the maternal pelvis head-?rst in what is called the occipito-anterior position, with the baby’s face pointing towards the back of the pelvis. Sometimes, however, the head may face the other way, or enter the pelvis transversely – or, rarely, the baby’s neck is ?exed backwards with the brow or face presenting to the neck of the womb. Some malpositions will correct naturally; others can be manipulated abdominally during pregnancy to a better position. If, however, the mother starts labour with the baby’s head badly positioned or with the buttocks instead of the head presenting (breech position), the labour will usually be longer and more di?cult and may require intervention using special obstetric forceps to assist in extracting the baby. If progress is poor and the fetus distressed, caesarean section may be necessary. HIV INFECTION Pregnant women who are HIV positive (see HIV; AIDS/HIV) should be taking antiviral drugs in the ?nal four to ?ve months of pregnancy, so as to reduce the risk of infecting the baby in utero and during birth by around 50 per cent. Additional antiviral treatment is given before delivery; the infection risk to the baby can be further reduced – by about 40 per cent – if delivery is by caesarean section. The mother may prefer to have the baby normally, in which case great care should be taken not to damage the baby’s skin during delivery. The infection risk to the baby is even further reduced if it is not breast fed. If all preventive precautions are taken, the overall risk of the infant becoming infected is cut to under 5 per cent.
Premature birth This is a birth that takes place before the end of the normal period of gestation, usually before 37 weeks. In practice, however, it is de?ned as a birth that takes place when the baby weighs less than 2·5 kilograms (5••• pounds). Between 5 and 10 per cent of babies are born prematurely, and in around 40 per cent of premature births the cause is unknown. Pre-eclampsia is the most common known cause; others include hypertension, chronic kidney disease, heart disease and diabetes mellitus. Multiple pregnancy is another cause. In the vast majority of cases the aim of management is to prolong the pregnancy and so improve the outlook for the unborn child. This consists essentially of rest in bed and sedation, but there are now several drugs, such as RITODRINE, that may be used to suppress the activity of the uterus and so help to delay premature labour. Prematurity was once a prime cause of infant mortality but modern medical care has greatly improved survival rates in developing countries.
Labour Also known by the traditional terms parturition, childbirth or delivery, this is the process by which the baby and subsequently the placenta are expelled from the mother’s body. The onset of labour is often preceded by a ‘show’ – the loss of the mucus and blood plug from the cervix, or neck of the womb; this passes down the vagina to the exterior. The time before the beginning of labour is called the ‘latent phase’ and characteristically lasts 24 hours or more in a ?rst pregnancy. Labour itself is de?ned by regular, painful contractions which cause dilation of the neck of the womb and descent of the fetal head. ‘Breaking of the waters’ is the loss of amniotic ?uid vaginally and can occur any time in the delivery process.
Labour itself is divided into three stages: the ?rst is from the onset of labour to full (10 cm) dilation of the neck of the womb. This stage varies in length, ideally taking no more than one hour per centimetre of dilation. Progress is monitored by regular vaginal examinations, usually every four hours. Fetal well-being is observed by intermittent or continuous monitoring of the fetal heart rate in relation to the timing and frequency of the contractions. The print-out is called a cardiotocograph. Abnormalities of the fetal heart rate may suggest fetal distress and may warrant intervention. In women having their ?rst baby (primigravidae), the common cause of a slow labour is uncoordinated contractions which can be overcome by giving either of the drugs PROSTAGLANDIN or OXYTOCIN, which provoke contractions of the uterine muscle, by an intravenous drip. Labours which progress slowly or not at all may be due to abnormal positioning of the fetus or too large a fetus, when prostaglandin or oxytocin is used much more cautiously.
The second stage of labour is from full cervical dilation to the delivery of the baby. At this stage the mother often experiences an irresistible urge to push the baby out, and a combination of strong coordinated uterine contractions and maternal e?ort gradually moves the baby down the birth canal. This stage usually lasts under an hour but can take longer. Delay, exhaustion of the mother or distress of the fetus may necessitate intervention by the midwife or doctor. This may mean enlarging the vaginal opening with an EPISIOTOMY (cutting of the perineal outlet – see below) or assisting the delivery with specially designed obstetric forceps or a vacuum extractor (ventouse). If the cervix is not completely dilated or open and the head not descended, then an emergency caesarean section may need to be done to deliver the baby. This procedure involves delivering the baby and placenta through an incision in the mother’s abdomen. It is sometimes necessary to deliver by planned or elective caesarean section: for example, if the placenta is low in the uterus – called placenta praevia – making a vaginal delivery dangerous.
The third stage occurs when the placenta (or afterbirth) is delivered, which is usually about 10–20 minutes after the baby. An injection of ergometrine and oxytocin is often given to women to prevent bleeding.
Pain relief in labour varies according to the mother’s needs. For uncomplicated labours, massage, reassurance by a birth attendant, and a warm bath and mobilisation may be enough for some women. However, some labours are painful, particularly if the woman is tired or anxious or is having her ?rst baby. In these cases other forms of analgesia are available, ranging from inhalation of NITROUS OXIDE GAS, injection of PETHIDINE HYDROCHLORIDE or similar narcotic, and regional local anaesthetic (see ANAESTHESIA).
Once a woman has delivered, care continues to ensure her and the baby’s safety. The midwives are involved in checking that the uterus returns to its normal size and that there is no infection or heavy bleeding, as well as caring for stitches if needed. The normal blood loss after birth is called lochia and generally is light, lasting up to six weeks. Midwives o?er support with breast feeding and care of the infant and will visit the parents at home routinely for up to two weeks.
Some complications of labour All operative deliveries in the UK are now done in hospitals, and are performed if a spontaneous birth is expected to pose a bigger risk to the mother or her child than a specialist-assisted one. Operative deliveries include caesarean section, forceps-assisted deliveries and those in which vacuum extraction (ventouse) is used. CAESAREAN SECTION Absolute indications for this procedure, which is used to deliver over 15 per cent of babies in Britain, are cephalopelvic disproportion and extensive placenta praevia, both discussed above. Otherwise the decision to undertake caesarean section depends on the clinical judgement of the specialist and the views of the mother. The rise in the proportion of this type of intervention (from 5 per cent in the 1930s to its present level of over 23 per cent
P
of the 600,000 or so annual deliveries in England) has been put down to defensive medicine
– namely, the doctor’s fear of litigation (initiated often because the parents believe that the baby’s health has suffered because the mother had an avoidably di?cult ‘natural’ labour). In Britain, over 60 per cent of women who have had a caesarean section try a vaginal delivery in a succeeding pregnancy, with about two-thirds of these being successful. Indications for the operation include:
absolute and relative cephalopelvic disproportion.
placenta previa.
fetal distress.
prolapsed umbilical cord – this endangers the viability of the fetus because the vital supply of oxygen and nutrients is interrupted.
malpresentation of the fetus such as breech or transverse lie in the womb.
unsatisfactory previous pregnancies or deliveries.
a request from the mother.
Caesarean sections are usually performed using regional block anaesthesia induced by a spinal or epidural injection. This results in loss of feeling in the lower part of the body; the mother is conscious and the baby not exposed to potential risks from volatile anaesthetic gases inhaled by the mother during general anaesthesia. Post-operative complications are higher with general anaesthesia, but maternal anxiety and the likelihood that the operation might be complicated and di?cult are indications for using it. A general anaesthetic may also be required for an acute obstetric emergency. At operation the mother’s lower abdomen is opened and then her uterus opened slowly with a transverse incision and the baby carefully extracted. A transverse incision is used in preference to the traditional vertical one as it enables the woman to have a vaginal delivery in any future pregnancy with a much smaller risk of uterine rupture. Women are usually allowed to get up within 24 hours and are discharged after four or ?ve days. FORCEPS AND VENTOUSE DELIVERIES Obstetric forceps are made in several forms, but all are basically a pair of curved blades shaped so that they can obtain a purchase on the baby’s head, thus enabling the operator to apply traction and (usually) speed up delivery. (Sometimes they are used to slow down progress of the head.) A ventouse or vacuum extractor comprises an egg-cup-shaped metal or plastic head, ranging from 40 to 60 mm in diameter with a hollow tube attached through which air is extracted by a foot-operated vacuum pump. The instrument is placed on the descending head, creating a negative pressure on the skin of the scalp and enabling the operator to pull the head down. In mainland Europe, vacuum extraction is generally preferred to forceps for assisting natural deliveries, being used in around 5 per cent of all deliveries. Forceps have a greater risk of causing damage to the baby’s scalp and brain than vacuum extraction, although properly used, both types should not cause any serious damage to the baby.
Episiotomy Normal and assisted deliveries put the tissues of the genital tract under strain. The PERINEUM is less elastic than the vagina and, if it seems to be splitting as the baby’s head
moves down the birth canal, it may be necessary to cut the perineal tissue – a procedure called an episiotomy – to limit damage. This is a simple operation done under local anaesthetic. It should be done only if there is a speci?c indication; these include:
to hasten the second stage of labour if the fetus is distressed.
to facilitate the use of forceps or vacuum extractor.
to enlarge a perineum that is restricted because of unyielding tissue, perhaps because of a scar from a previous labour. Midwives as well as obstetricians are trained
to undertake and repair (with sutures) episiotomies.
(For organisations which o?er advice and information on various aspects of childbirth, including eclampsia, breast feeding and multiple births, see APPENDIX 2: ADDRESSES: SOURCES OF INFORMATION, ADVICE, SUPPORT AND SELF-HELP.)... pregnancy and labour
Only a small minority of those exposed to M. leprae develop the disease. The incubation period is 3–5 years or longer. The major clinical manifestations involve skin and nerves: the former range from depigmented, often anaesthetic areas, to massive nodules; nerve involvement ranges from localised nerve swelling(s) to extensive areas of anaesthesia. Advanced nerve destruction gives rise to severe deformities: foot-drop, wrist-drop, claw-foot, extensive ulceration of the extremities with loss of ?ngers and toes, and bone changes. Eye involvement can produce blindness. Laryngeal lesions produce hoarseness and more serious sequelae. The diagnosis is essentially a clinical one; however, skin-smears, histological features and the lepromin skin-test help to con?rm the diagnosis and enable the form of disease to be graded.
Although the World Health Organisation had originally hoped to eliminate leprosy worldwide by 2000, that has proved an unrealistic target. The reason is an absence of basic information. Doctors are unable to diagnose the disorder before a patient starts to show symptoms; meanwhile he or she may have already passed on the infection. Doctors do not know exactly how transmission occurs or how it infects humans – nor do they know at what point a carrier of the bacterium may infect others. The incidence of new infections is still more than 650,000 cases a year or about 4.5 cases per 10,000 people in those countries worst affected by the disease.
Treatment Introduction of the sulphone compound, dapsone, revolutionised management of the disease. More recently, rifampicin and clofazimine have been added as ?rst-line drugs for treatment. Second-line drugs include minocycline, o?oxacin and clarithromycin; a number of regimens incorporating several of these compounds (multi-drug regimens – introduced in 1982) are now widely used. A three-drug regime is recommended for multi-bacillary leprosy and a two-drug one for parcibacillary leprosy. Dapsone resistance is a major problem worldwide, but occurs less commonly when multi-drug regimens are used. Older compounds – ethionamide and prothionamide
– are no longer used because they are severely toxic to the liver. Corticosteroids are sometimes required in patients with ‘reversal reaction’. Supportive therapy includes physiotherapy; both plastic and orthopaedic surgery may be necessary in advanced stages of the disease. Improvement in socio-economic conditions, and widespread use of BCG vaccination are of value as preventive strategies. Early diagnosis and prompt institution of chemotherapy should prevent long-term complications.... leprosy
The primary problem is seen as a change in structure of cartilage and BONE, rather than an in?ammatory SYNOVITIS. Osteoarthritis usually implies a loss of the central load-bearing area of articular hyaline cartilage, with outgrowth of cartilage at the articular margin and subsequent ossi?cation to form bony outgrowths known as OSTEOPHYTES. Osteophytes form with increasing age, whether or not there is signi?cant cartilage loss, and in the elderly may lead to local frictional symptoms, and in the spine, to nerve compression.
The condition has a wide range of causes, of which some, like dysplasia and trauma, are known and others have yet to be identi?ed. The main clinical problems occur in the hip and knee. The cartilage loss in the hip usually occurs in the sixth or seventh decade. It may affect both hips in fairly rapid succession, or only one hip; such patients often have no problems in other joints. Cartilage loss in the knee occurs from the ?fth decade onwards and is often associated with cartilage loss in small joints in the hand and elsewhere. Cartilage loss in the distal interphalangeal joints of the hand is associated with the formation of bony swellings known as Heberden’s nodes.
Treatment Management is largely directed at maintaining activity, with physical and social support as necessary. ANALGESICS may be of some value, particularly in the management of night pain. NON-STEROIDAL ANTIINFLAMMATORY DRUGS (NSAIDS) may help patients with early-morning sti?ness and may also reduce pain on movement and night pain. Their bene?t, however, tends to be less marked than in RHEUMATOID ARTHRITIS and their long-term usage has considerable toxicity problems. Advanced cartilage loss is best treated by joint replacement. Hip- and knee-joint replacements – with a wide variety of arti?cial joints – are now common surgical procedures which greatly improve the mobility of affected individuals. (See ARTHROPLASTY.)
People with arthritis and their relatives can obtain help and advice from Arthritis Care.... osteoarthritis
Rarely, the UTERUS may be completely absent as a result of abnormal development. In such patients secondary sexual development is normal but MENSTRUATION is absent (primary amennorhoea). The chromosomal make-up of the patient must be checked (see CHROMOSOMES; GENES): in a few cases the genotype is male (testicular feminisation syndrome). No treatment is available, although the woman should be counselled.
The uterus develops as two halves which fuse together. If the fusion is incomplete, a uterine SEPTUM results. Such patients with a double uterus (uterus didelphys) may have fertility problems which can be corrected by surgical removal of the uterine septum. Very rarely there may be two uteri with a double vagina.
The uterus of most women points forwards (anteversion) and bends forwards (ante?exion). However, about 25 per cent of women have a uterus which is pointed backwards (retroversion) and bent backwards (retro?exion). This is a normal variant and very rarely gives rise to any problems. If it does, the attitude of the uterus can be corrected by an operation called a ventrosuspension.
Endometritis The lining of the uterine cavity is called the ENDOMETRIUM. It is this layer that is partially shed cyclically in women of reproductive age giving rise to menstruation. Infection of the endometrium is called endometritis and usually occurs after a pregnancy or in association with the use of an intrauterine contraceptive device (IUCD – see CONTRACEPTION). The symptoms are usually of pain, bleeding and a fever. Treatment is with antibiotics. Unless the FALLOPIAN TUBES are involved and damaged, subsequent fertility is unaffected. Very rarely, the infection is caused by TUBERCULOSIS. Tuberculous endometritis may destroy the endometrium causing permanent amenorrhoea and sterility.
Menstrual disorders are common. Heavy periods (menorrhagia) are often caused by ?broids (see below) or adenomyosis (see below) or by anovulatory cycles. Anovulatory cycles result in the endometrium being subjected to unopposed oestrogen stimulation and occasionally undergoing hyperplasia. Treatment is with cyclical progestogens (see PROGESTOGEN) initially. If this form of treatment fails, endoscopic surgery to remove the endometrium may be successful. The endometrium may be removed using LASER (endometrial laser ablation) or electrocautery (transcervical resection of endometrium). Hysterectomy (see below) will cure the problem if endoscopic surgery fails. Adenomyosis is a condition in which endometrial tissue is found in the muscle layer (myometrium) of the uterus. It usually presents as heavy and painful periods, and occasionally pain during intercourse. Hysterectomy is usually required.
Oligomenorhoea (scanty or infrequent periods) may be caused by a variety of conditions including thyroid disease (see THYROID GLAND, DISEASES OF). It is most commonly associated with usage of the combined oral contraceptive pill. Once serious causes have been eliminated, the patient should be reassured. No treatment is necessary unless conception is desired, in which case the patient may require induction of ovulation.
Primary amenorrhoea means that the patient has never had a period. She should be investigated, although usually it is only due to an inexplicable delay in the onset of periods (delayed menarche) and not to any serious condition. Secondary amenorrhoea is the cessation of periods after menstruation has started. The most common cause is pregnancy. It may be also caused by endocrinological or hormonal problems, tuberculous endometritis, emotional problems and severe weight loss. The treatment of amenorrhoea depends on the cause.
Dysmenorrhoea, or painful periods, is the most common disorder; in most cases the cause is unknown, although the disorder may be due to excessive production of PROSTAGLANDINS.
Irregular menstruation (variations from the woman’s normal menstrual pattern or changes in the duration of bleeding or the amount) can be the result of a disturbance in the balance of OESTROGENS and PROGESTERONE hormone which between them regulate the cycle. For some time after the MENARCHE or before the MENOPAUSE, menstruation may be irregular. If irregularity occurs in a woman whose periods are normally regular, it may be due to unsuspected pregnancy, early miscarriage or to disorders in the uterus, OVARIES or pelvic cavity. The woman should seek medical advice.
Fibroids (leiomyomata) are benign tumours arising from the smooth muscle layer (myometrium) of the uterus. They are found in 80 per cent of women but only a small percentage give rise to any problems and may then require treatment. They may cause heavy periods and occasionally pain. Sometimes they present as a mass arising from the pelvis with pressure symptoms from the bladder or rectum. Although they can be shrunk medically using gonadorelin analogues, which raise the plasma concentrations of LUTEINISING HORMONE and FOLLICLE-STIMULATING HORMONE, this is not a long-term solution. In any case, ?broids only require treatment if they are large or enlarging, or if they cause symptoms. Treatment is either myomectomy (surgical removal) if fertility is to be retained, or a hysterectomy.
Uterine cancers tend to present after the age of 40 with abnormal bleeding (intermenstrual or postmenopausal bleeding). They are usually endometrial carcinomas. Eighty per cent present with early (Stage I) disease. Patients with operable cancers should be treated with total abdominal hysterectomy and bilateral excision of the ovaries and Fallopian tubes. Post-operative RADIOTHERAPY is usually given to those patients with adverse prognostic factors. Pre-operative radiotherapy is still given by some centres, although this practice is now regarded as outdated. PROGESTOGEN treatment may be extremely e?ective in cases of recurrence, but its value remains unproven when used as adjuvant treatment. In 2003 in England and Wales, more than 2,353 women died of uterine cancer.
Disorders of the cervix The cervix (neck of the womb) may produce an excessive discharge due to the presence of a cervical ectopy or ectropion. In both instances columnar epithelium – the layer of secreting cells – which usually lines the cervical canal is exposed on its surface. Asymptomatic patients do not require treatment. If treatment is required, cryocautery – local freezing of tissue – is usually e?ective.
Cervical smears are taken and examined in the laboratory to detect abnormal cells shed from the cervix. Its main purpose is to detect cervical intraepithelial neoplasia (CIN) – the presence of malignant cells in the surface tissue lining the cervix – since up to 40 per cent of women with this condition will develop cervical cancer if the CIN is left untreated. Women with abnormal smears should undergo colposcopy, a painless investigation using a low-powered microscope to inspect the cervix. If CIN is found, treatment consists of simply removing the area of abnormal skin, either using a diathermy loop or laser instrument.
Unfortunately, cervical cancer remains the most common of gynaecological cancers. The most common type is squamous cell carcinoma and around 4,000 new cases (all types) are diagnosed in England and Wales every year. As many as 50 per cent of the women affected may die from the disease within ?ve years. Cervical cancer is staged clinically in four bands according to how far it has extended, and treatment is determined by this staging. Stage I involves only the mucosal lining of the cervix and cone BIOPSY may be the best treatment in young women wanting children. In Stage IV the disease has spread beyond the cervix, uterus and pelvis to the URINARY BLADDER or RECTUM. For most women, radiotherapy or radical Wertheim’s hysterectomy – the latter being preferable for younger women – is the treatment of choice if the cancer is diagnosed early, both resulting in survival rates of ?ve years in 80 per cent of patients. Wertheim’s hysterectomy is a major operation in which the uterus, cervix, upper third of vagina and the tissue surrounding the cervix are removed together with the LYMPH NODES draining the area. The ovaries may be retained if desired. Patients with cervical cancer are treated by radiotherapy, either because they present too late for surgery or because the surgical skill to perform a radical hysterectomy is not available. These operations are best performed by gynaecological oncologists who are gynaecological surgeons specialising in the treatment of gynaecological tumours. The role of CHEMOTHERAPY in cervical and uterine cancer is still being evaluated.
Prolapse of the uterus is a disorder in which the organ drops from its normal situation down into the vagina. First-degree prolapse is a slight displacement of the uterus, second-degree a partial displacement and third-degree when the uterus can be seen outside the VULVA. It may be accompanied by a CYSTOCOELE (the bladder bulges into the front wall of the vagina), urethrocoele (the urethra bulges into the vagina) and rectocoele (the rectal wall bulges into the rear wall of the vagina). Prolapse most commonly occurs in middle-aged women who have had children, but the condition is much less common now than in the past when prenatal and obstetric care was poor, women had more pregnancies and their general health was poor. Treatment is with pelvic exercises, surgical repair of the vagina or hysterectomy. If the woman does not want or is not ?t for surgery, an internal support called a pessary can be ?tted – and changed periodically.
Vertical section of female reproductive tract (viewed from front) showing sites of common gynaecological disorders.
Hysterectomy Many serious conditions of the uterus have traditionally been treated by hysterectomy, or removal of the uterus. It remains a common surgical operation in the UK, but is being superseded in the treatment of some conditions, such as persistent MENORRHAGIA, with endometrial ablation – removal of the lining of the uterus using minimally invasive techniques, usually using an ENDOSCOPE and laser. Hysterectomy is done to treat ?broids, cancer of the uterus and cervix, menorrhagia, ENDOMETRIOSIS and sometimes for severely prolapsed uterus. Total hysterectomy is the usual type of operation: it involves the removal of the uterus and cervix and sometimes the ovaries. After hysterectomy a woman no longer menstruates and cannot become pregnant. If the ovaries have been removed as well and the woman had not reached the menopause, hormone replacement therapy (HRT – see MENOPAUSE) should be considered. Counselling helps the woman to recover from the operation which can be an emotionally challenging event for many.... uterus, diseases of
Action: taenicide, astringent, stimulant. In absence of other remedies may be used for tape-worm. Use confined to veterinary medicine. Hardens soft gums. Treatment: for helminthiasis in dogs. To expel tape worms.
Preparations: Areca powder: dose, 1-4g. Liquid Extract; dose, 1-4ml. Thrice daily. ... areca nut
Tinctures. Formula. Echinacea 3; Goldenseal 1; Myrrh quarter. One teaspoon in water every 2 hours (acute) thrice daily (chronic). ... coxsackie infection
Infection is usually blood-born from dental abscess, tonsils, boil, or old wounds. Prompt modern hospital treatment is necessary to avoid thrombosis or necrosis of bone. Herbal medication can play a substantial supportive role. Differential diagnosis should exclude Infective Arthritis, Cellulitis, Rheumatic Fever, Leukaemia.
Symptoms. Affected bone painful and hot. Throbbing. Fever. Dehydration. Raised E.S.R. Severe general illness.
Treatment. Should enhance resistance as well as combat infection. Comfrey and Echinacea are principle remedies. Infected bone areas are not well supplied with blood, so oral antibiotics may not reach them; this is where topical herbal treatments can assist. Anti-bacterial drinks are available in the absence of conventional antibiotics.
To promote cell proliferation and callous formation: Comfrey root, Marigold, St John’s Wort, Arnica. (Madaus)
To stimulate connective tissue: Thuja.
Comfrey root. Potential benefit outweighs possible risk.
Teas. Nettles. Plantain. Silverweed, Yarrow. Boneset. Marigold petals. St John’s Wort. Comfrey leaves. Singly or in combination. Abundant drinks during the day.
Formula. Echinacea 2; Comfrey 1; Myrrh half; Thuja quarter. Dose – Liquid extracts: 2 teaspoons. Tinctures: 2-3 teaspoons. Powders: 750mg (three 00 capsules or half a teaspoon). Three or more times daily in water or honey.
Madaus: Tardolyt. Birthwort: a sodium salt of aristolochic acid.
Maria Treben: Yarrow and Fenugreek tea. Half cup Yarrow tea 4 times daily. To two of such cups, add half a teaspoon ground Fenugreek seeds.
Dr Finlay Ellingwood: Liquid Extract Echinacea 20-30 drops in water four times daily. And: Liquid Extract Lobelia 20-30 drops in water twice daily. Calcium Lactate tablets.
Topical. Comfrey root poultices to facilitate removal of pus, and to heal.
Diet. No solids. Fruit and milk diet for 5 days, followed by lacto-vegetarian diet. Herb teas as above. Plenty of water to combat dehydration.
Supplements. Daily. Vitamin B12 (50mcg), C (3g), D (500iu), E (1000iu). Calcium (1000-1500mg) taken as calcium lactate, Zinc.
General. Regulate bowels. Surgical treatment in a modern hospital necessary for removal of dead bone (sequestrum) and for adequate nursing facilities.
Treatment by a general medical practitioner or hospital specialist. ... osteomyelitis
It may be needed if the woman’s breasts are overfull (see engorgement).
A woman may want to express milk so that it can be given to the baby in her absence, or so that an infant unable to feed at the breast, due to prematurity, for example, can benefit from breast milk.
Milk can be expressed by hand or with a breast pump.... expressing milk
Among the smallest and simplest microorganisms are the viruses. First described as ?lterable agents, and ranging in size from 20–30 nm to 300 nm, they may be directly visualised only by electron microscopy. They consist of a core of deoxyribonucleic or ribonucleic acid (DNA or RNA) within a protective protein coat, or capsid, whose subunits confer a geometric symmetry. Thus viruses are usually cubical (icosahedral) or helical; the larger viruses (pox-, herpes-, myxo-viruses) may also have an outer envelope. Their minimal structure dictates that viruses are all obligate parasites, relying on living cells to provide essential components for their replication. Apart from animal and plant cells, viruses may infect and replicate in bacteria (bacteriophages) or fungi (mycophages), which are damaged in the process.
Bacteria are larger (0·01–5,000 µm) and more complex. They have a subcellular organisation which generally includes DNA and RNA, a cell membrane, organelles such as ribosomes, and a complex and chemically variable cell envelope – but, unlike EUKARYOTES, no nucleus. Rickettsiae, chlamydia, and mycoplasmas, once thought of as viruses because of their small size and absence of a cell wall (mycoplasma) or major wall component (chlamydia), are now acknowledged as bacteria; rickettsiae and chlamydia are intracellular parasites of medical importance. Bacteria may also possess additional surface structures, such as capsules and organs of locomotion (?agella) and attachment (?mbriae and stalks). Individual bacterial cells may be spheres (cocci); straight (bacilli), curved (vibrio), or ?exuous (spirilla) rods; or oval cells (coccobacilli). On examination by light microscopy, bacteria may be visible in characteristic con?gurations (as pairs of cocci [diplococci], or chains [streptococci], or clusters); actinomycete bacteria grow as ?laments with externally produced spores. Bacteria grow essentially by increasing in cell size and dividing by ?ssion, a process which in ideal laboratory conditions some bacteria may achieve about once every 20 minutes. Under natural conditions, growth is usually much slower.
Eukaryotic micro-organisms comprise fungi, algae, and protozoa. These organisms are larger, and they have in common a well-developed internal compartmentation into subcellular organelles; they also have a nucleus. Algae additionally have chloroplasts, which contain photosynthetic pigments; fungi lack chloroplasts; and protozoa lack both a cell wall and chloroplasts but may have a contractile vacuole to regulate water uptake and, in some, structures for capturing and ingesting food. Fungi grow either as discrete cells (yeasts), multiplying by budding, ?ssion, or conjugation, or as thin ?laments (hyphae) which bear spores, although some may show both morphological forms during their life-cycle. Algae and protozoa generally grow as individual cells or colonies of individuals and multiply by ?ssion.
Micro-organisms of medical importance include representatives of the ?ve major microbial groups that obtain their essential nutrients at the expense of their hosts. Many bacteria and most fungi, however, are saprophytes (see SAPROPHYTE), being major contributors to the natural cycling of carbon in the environment and to biodeterioration; others are of ecological and economic importance because of the diseases they cause in agricultural or horticultural crops or because of their bene?cial relationships with higher organisms. Additionally, they may be of industrial or biotechnological importance. Fungal diseases of humans tend to be most important in tropical environments and in immuno-compromised subjects.
Pathogenic (that is, disease-causing) microorganisms have special characteristics, or virulence factors, that enable them to colonise their hosts and overcome or evade physical, biochemical, and immunological host defences. For example, the presence of capsules, as in the bacteria that cause anthrax (Bacillus anthracis), one form of pneumonia (Streptococcus pneumoniae), scarlet fever (S. pyogenes), bacterial meningitis (Neisseria meningitidis, Haemophilus in?uenzae) is directly related to the ability to cause disease because of their antiphagocytic properties. Fimbriae are related to virulence, enabling tissue attachment – for example, in gonorrhoea (N. gonorrhoeae) and cholera (Vibrio cholerae). Many bacteria excrete extracellular virulence factors; these include enzymes and other agents that impair the host’s physiological and immunological functions. Some bacteria produce powerful toxins (excreted exotoxins or endogenous endotoxins), which may cause local tissue destruction and allow colonisation by the pathogen or whose speci?c action may explain the disease mechanism. In Staphylococcus aureus, exfoliative toxin produces the staphylococcal scalded-skin syndrome, TSS toxin-1 toxic-shock syndrome, and enterotoxin food poisoning. The pertussis exotoxin of Bordetella pertussis, the cause of whooping cough, blocks immunological defences and mediates attachment to tracheal cells, and the exotoxin produced by Corynebacterium diphtheriae causes local damage resulting in a pronounced exudate in the trachea.
Viruses cause disease by cellular destruction arising from their intracellular parasitic existence. Attachment to particular cells is often mediated by speci?c viral surface proteins; mechanisms for evading immunological defences include latency, change in viral antigenic structure, or incapacitation of the immune system – for example, destruction of CD 4 lymphocytes by the human immunode?ciency virus.... microbiology
German Chamomile tea. ... nervous stomach
Drugs given orally or topically may induce phototoxic reactions of various types. Thus, TETRACYCLINES exaggerate sunburn reactions. and the diuretic FRUSEMIDE may cause blistering reactions. Psoralens induce erythema and pigmentation. AMIODARONE also induces pigmentation. (See also PHOTOCHEMOTHERAPY.)
Phytophotodermatitis is a streaky, blistering photodermatosis typically seen on the limbs of children playing in grassy meadows in summer. The phototoxic reaction is caused by psoralens in weeds.
Berlocque dermatitis is a pattern of streaky pigmentation usually seen on women’s necks, caused by a reaction to psoralens in perfumes.
Certain rare metabolic diseases may lead to photosensitisation. They include the PORPHYRIAS and PELLAGRA. Other skin diseases such as lupus erythematosus (see under LUPUS) and ROSACEA may be aggravated by light exposure. Sometimes, in the absence of any of these factors, some people spontaneously develop a sensitivity to light causing various patterns of DERMATITIS or URTICARIA. The most common pattern is ‘polymorphic light eruption’ which typically appears within a day or two of arrival at a sunny holiday destination and persists until departure. Continuously exposed areas, such as the hands and face, may be ‘hardened’ and unaffected.
Treatment Appropriate clothing and headgear, sunscreen creams and lotions are the main preventative measures.... photodermatoses
(4) Absence of any other form of mental disorder that would explain the unusual behaviour. The corresponding American terminology is ‘antisocial personality disorder’. (See MENTAL ILLNESS.)... psychopathic
Super?cial re?exes comprise the sudden movements which result when the skin is brushed or pricked, such as the movement of the toes that results from stroking the sole of the foot.
Deep re?exes depend upon the state of mild contraction in which muscles are constantly maintained when at rest, and are obtained, as in the case of the knee-jerk (see below), by sharply tapping the tendon of the muscle in question.
Visceral re?exes are those connected with various organs, such as the narrowing of the pupil when a bright light is directed upon the EYE, and the contraction of the URINARY BLADDER when distended by urine.
Faults in these re?exes give valuable evidence as to the presence and site of neurological disorders. Thus, absence of the knee-jerk, when the patellar tendon is tapped, means some interference with the sensory nerve, nerve-cells, or motor nerve upon which the act depends – as, for example, in POLIOMYELITIS, or peripheral NEURITIS; whilst an exaggerated jerk implies that the controlling in?uence exerted by the BRAIN upon this re?ex mechanism has been cut o? – as, for example, by a tumour high up in the SPINAL CORD, or in the disease known as MULTIPLE SCLEROSIS (MS).... reflex action
Causes This disease is the result of de?ciency of vitamin D in the diet. Healthy bones cannot be built up without calcium (or lime) salts, and the body cannot use these salts in the absence of vitamin D. Want of sunlight and fresh air in the dwellings where children are reared is also of importance. Once a common condition in industrial areas, it had almost disappeared in Great Britain but has recurred in recent years, largely amongst children of Asian and African origin.
The periosteum – the membrane enveloping the bones – becomes in?amed, and the bone formed beneath it is defective in lime salts and very soft. Changes also occur at the growing part of the bone, the epiphyseal plate.
Symptoms The symptoms of rickets most usually appear towards the end of the ?rst year, and rarely after the age of ?ve. The children are often ‘snu?y’ and miserable.
Gradually, changes in the shape of the bones becomes visible, ?rst chie?y noticed at the ends of the long bones. The softened bones also tend to become distorted, the legs bending outwards and forwards so the child becomes bow-legged or knock-kneed. Changes occur in the ribs (‘rickets rosary’) and cranial bones, while teeth appear late and decay or fall out.
The disease usually ends in recovery with more or less of deformity and dwar?ng – the bones, although altered in shape, becoming ultimately ossi?ed.
Treatment The speci?c remedy is vitamin D in the form of calciferol (vitamin D2). A full diet is of course essential, with emphasis upon a su?cient supply of milk. Rickets is very rare in breast-fed children but it is a wise precaution to give breast-fed babies supplementary vitamin
D. After the child is weaned, the provision of suitable food is vital, supplemented with some source of vitamin D. Regular exposure to sunlight is desirable. Controversy exists as to whether vitamin D should be added in the manufacture of ?our, particularly of types used by the Asian community.
De?ciency of vitamin D in adults results in osteomalacia (see under BONE, DISORDERS OF). (See also APPENDIX 5: VITAMINS.)... rickets
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
Typically the patient complains of widespread severe itching, worse when the body is warm after a bath or in bed. Burrows are visible as wavy black lines 3–5 mm long in the skin of the hands, wrists or sides of the feet. The intensity of the rash depends on the immune response. Papules, pustules, crusts and excoriations are seen on the hands and there may be a widespread eczematous (see DERMATITIS) or urticarial (see URTICARIA) rash elsewhere. Papules or even nodules on the PENIS and SCROTUM are characteristic. In infants, burrows occur on the palms and soles. Diminished immune response in old age, DOWN’S (DOWN) SYNDROME, etc. lead to a type of scabies which is less itching and more scaly. Rarely, absence of immune response causes a mite-saturated, generalised scaly dermatitis (Norwegian scabies). Admission of such a patient to hospital may result in an outbreak of scabies in other patients, sta? and visitors caused by mite-infested airborne scale.
Treatment MALATHION 0·5 per cent aqueous lotion, or PERMETHRIN 5 per cent cream, applied to the whole body, except the head, for 24 hours and then washed o? cures the infection. In infants the head and neck should be included. The secondary eruption may take 2– 3 weeks to settle completely and 10 per cent crotamiton cream is used during this period. It is essential that all intimate contacts be treated simultaneously. FOMITES need not be treated.... scabies
Treatment involves surgery.
A colostomy may be needed initially before definitive surgery to construct an anus.... anus, imperforate
Lactase deficiency results in a reduced ability to digest lactose, also known as lactose intolerance.
The condition may be permanent, or may occur temporarily after gastroenteritis, particularly in young children.
Symptoms include abdominal cramps, bloating, flatulence, and diarrhoea, all of which are caused by the laxative effect of the undigested sugar in the intestines.
Treatment is with a lactose-free diet.... lactase deficiency
Imperforate anus, or absence of the anus, may occur in newly born children, and the condition is relieved by operation.
Itching at the anal opening is common and can be troublesome. It may be due to slight abrasions, to piles, to the presence of threadworms (see ENTEROBIASIS), and/or to anal sex. The anal area should be bathed once or twice a day; clothing should be loose and smooth. Local application of soothing preparations containing mild astringents (bismuth subgallate, zinc oxide and hamamelis) and CORTICOSTEROIDS may provide symptomatic relief. Proprietary preparations contain lubricants, VASOCONSTRICTORS and mild ANTISEPTICS.
Pain on defaecation is commonly caused by a small ulcer or ?ssure, or by an engorged haemorrhoid (pile). Haemorrhoids may also cause an aching pain in the rectum. (See also PROCTALGIA.)
Abscess in the cellular tissue at the side of the rectum – known from its position as an ischio-rectal abscess – is fairly common and may produce a ?stula. Treatment is by ANTIBIOTICS and, if necessary, surgery to drain the abscess.
Prolapse or protrusion of the rectum is sometimes found in children, usually between the ages of six months and two years. This is generally a temporary disorder. Straining at defaecation by adults can cause the lining of the rectum to protrude outside the anus, resulting in discomfort, discharge and bleeding. Treatment of the underlying constipation is essential as well as local symptomatic measures (see above). Haemorrhoids sometimes prolapse. If a return to normal bowel habits with the production of soft faeces fails to restore the rectum to normal, surgery to remove the haemorrhoids may be necessary. If prolapse of the rectum recurs, despite a return to normal bowel habits, surgery may be required to rectify it.
Tumours of small size situated on the skin near the opening of the bowel, and consisting of nodules, tags of skin, or cauli?ower-like excrescences, are common, and may give rise to pain, itching and watery discharges. These are easily removed if necessary. Polypi (see POLYPUS) occasionally develop within the rectum, and may give rise to no pain, although they may cause frequent discharges of blood. Like polypi elsewhere, they may often be removed by a minor operation. (See also POLYPOSIS.)
Cancer of the rectum and colon is the commonest malignancy in the gastrointestinal tract: around 17,000 people a year die from these conditions in the United Kingdom. Rectal cancer is more common in men than in women; colonic cancer is more common in women. Rectal cancer is a disease of later life, seldom affecting young people, and its appearance is generally insidious. The tumour begins commonly in the mucous membrane, its structure resembling that of the glands with which the membrane is furnished, and it quickly in?ltrates the other coats of the intestine and then invades neighbouring organs. Secondary growths in most cases occur soon in the lymphatic glands within the abdomen and in the liver. The symptoms appear gradually and consist of diarrhoea, alternating with attacks of constipation, and, later on, discharges of blood or blood-stained ?uid from the bowels, together with weight loss and weakness. A growth can be well advanced before it causes much disturbance. Treatment is surgical and usually this consists of removal of the whole of the rectum and the distal two-thirds of the sigmoid colon, and the establishment of a COLOSTOMY. Depending upon the extent of the tumour, approximately 50 per cent of the patients who have this operation are alive and well after ?ve years. In some cases in which the growth occurs in the upper part of the rectum, it is now possible to remove the growth and preserve the anus so that the patient is saved the discomfort of having a colostomy. RADIOTHERAPY and CHEMOTHERAPY may also be necessary.... rectum, diseases of
Sexual dysfunction may be due to physical or psychiatric disease, or it may be the result of the administration of drugs. The main group of drugs likely to cause sexual problems are the ANTICONVULSANTS, the ANTIHYPERTENSIVE DRUGS, and drugs such as metoclopramide that induce HYPERPROLACTINAEMIA. The benzodiazepine TRANQUILLISERS can reduce libido and cause failure of erection. Tricyclic ANTIDEPRESSANT DRUGS may cause failure of erection and clomipramine may delay or abolish ejaculation by blockade of alpha-adrenergic receptors. The MONOAMINE OXIDASE INHIBITORS (MAOIS) often inhibit ejaculation. The PHENOTHIAZINES reduce sexual desire and arousal and may cause di?culty in maintaining an erection. The antihypertensive drug, methyldopa, causes impotence in over 20 per cent of patients on large doses. The beta-adrenoceptorblockers and the DIURETICS can also cause impotence. The main psychiatric causes of sexual dysfunction include stress, depression and guilt.... sexual dysfunction
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