(obstetrician’s hand) the appearance of the hand in a carpopedal *spasm (see also tetany). The wrist is flexed, the fingers are tightly adducted, and the thumb is apposed across the palm.
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
Cause Asthma runs in families, so that parents with asthma have a strong risk of having children with asthma, or with other atopic (see ATOPY) illnesses such as HAY FEVER or eczema (see DERMATITIS). There is therefore a great deal of interest in the genetic basis of the condition. Several GENES seem to be associated with the condition of atopy, in which subjects have a predisposition to form ANTIBODIES of the IgE class against allergens (see ALLERGEN) they encounter – especially inhaled allergens.
The allergic response in the lining of the airway leads to an in?ammatory reaction. Many cells are involved in this in?ammatory process, including lymphocytes, eosinophils, neutrophils and mast cells. The cells are attracted and controlled by a complex system of in?ammatory mediators. The in?amed airway-wall produced in this process is then sensitive to further allergic stimuli or to non-speci?c challenges such as dust, smoke or drying from the increased respiration during exercise. Recognition of this in?ammation has concentrated attention on anti-in?ammatory aspects of treatment.
Continued in?ammation with poor control of asthma can result in permanent damage to the airway-wall such that reversibility is reduced and airway-narrowing becomes permanent. Appropriate anti-in?ammatory therapy may help to prevent this damage.
Many allergens can be important triggers of asthma. House-dust mite, grass pollen and animal dander are the commonest problems. Occupational factors such as grain dusts, hard-metals fumes and chemicals in the plastic and paint industry are important in some adults. Viral infections are another common trigger, especially in young children.
The prevalence of asthma appears to be on the increase in most countries. Several factors have been linked to this increase; most important may be the vulnerability of the immature immune system (see IMMUNITY) in infants. High exposure to allergens such as house-dust mite early in life may prime the immune system, while reduced exposure to common viral infections may delay the maturation of the immune system. In addition, maternal smoking in pregnancy and infancy increases the risk.
Clinical course The major symptoms of asthma are breathlessness and cough. Occasionally cough may be the only symptom, especially in children, where night-time cough may be mistaken for recurrent infection and treated inappropriately with antibiotics.
The onset of asthma is usually in childhood, but it may begin at any age. In childhood, boys are affected more often than girls but by adulthood the sex incidence is equal. Children who have mild asthma are more likely to grow out of the condition as they go through their teenaged years, although symptoms may recur later.
The degree of airway-narrowing, and its change with time and treatment, can be monitored by measuring the peak expiratory ?ow with a simple monitor at home – a peak-?ow meter. The typical pattern shows the peak ?ow to be lowest in the early morning and this ‘morning dipping’ is often associated with disturbance of sleep.
Acute exacerbations of asthma may be provoked by infections or allergic stimuli. If they do not respond quickly and fully to medication, expert help should be sought urgently since oxygen and higher doses of drugs will be necessary to control the attack. In a severe attack the breathing rate and the pulse rate rise and the chest sounds wheezy. The peak-?ow rate of air into the lungs falls. Patients may be unable to talk in full sentences without catching their breath, and the reduced oxygen in the blood in very severe attacks may produce the blue colour of CYANOSIS in the lips and tongue. Such acute attacks can be very frightening for the patient and family.
Some cases of chronic asthma are included in the internationally agreed description CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) – a chronic, slowly progressive disorder characterised by obstruction of the air?ow persisting over several months.
Treatment The ?rst important consideration in the treatment of asthma is avoidance of precipitating factors. When this is a speci?c animal or occupational exposure, this may be possible; it is however more di?cult for house-dust mite or pollens. Exercise-induced asthma should be treated adequately rather than avoiding exercise.
Desensitisation injections using small quantities of speci?c allergens are used widely in some countries, but rarely in the UK as they are considered to have limited value since most asthma is precipitated by many stimuli and controlled adequately with simple treatment.
There are two groups of main drugs for the treatment of asthma. The ?rst are the bronchodilators which relax the smooth muscle in the wall of the airways, increase their diameter and relieve breathlessness. The most useful agents are the beta adrenergic agonists (see ADRENERGIC RECEPTORS) such as salbutamol and terbutaline. They are best given by inhalation into the airways since this reduces the general side-effects from oral use. These drugs are usually given to reverse airway-narrowing or to prevent its onset on exercise. However, longer-acting inhaled beta agonists such as salmeterol and formoterol or the theophyllines given in tablet form can be used regularly as prevention. The beta agonists can cause TREMOR and PALPITATION in some patients.
The second group of drugs are the antiin?ammatory agents that act to reduce in?ammation of the airway. The main agents in this group are the CORTICOSTEROIDS. They must be taken regularly, even when symptoms are absent. Given by inhalation they have few side-effects. In acute attacks, short courses of oral steroids are used; in very severe disease regular oral steroids may be needed. Other drugs have a role in suppressing in?ammation: sodium cromoglycate has been available for some years and is generally less e?ective than inhaled steroids. Newer agents directed at speci?c steps in the in?ammatory pathway, such as leukotriene receptor-antagonists, are alternative agents.
Treatment guidelines have been produced by various national and international bodies, such as the British Thoracic Society. Most have set out treatment in steps according to severity, with objectives for asthma control based on symptoms and peak ?ow. Patients should have a management plan that sets out their regular treatment and their appropriate response to changes in their condition.
Advice and support for research into asthma is provided by the National Asthma Campaign.
See www.brit-thoracic.org.uk
Prognosis Asthma is diagnosed in 15–20 per cent of all pre-school children in the developed world. Yet by the age of 15 it is estimated that fewer than 5 per cent still have symptoms. A study in 2003 reported on a follow-up of persons born in 1972–3 who developed asthma and still had problems at the age of nine. By the time these persons were aged 26, 27 per cent were still having problems; around half of that number had never been free from the illness and the other half had apparently lost it for a few years but it had returned.... asthma
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
The outer coat consists of the sclera and the cornea; their junction is called the limbus. SCLERA This is white, opaque, and constitutes the posterior ?ve-sixths of the outer coat. It is made of dense ?brous tissue. The sclera is visible anteriorly, between the eyelids, as the ‘white of the eye’. Posteriorly and anteriorly it is covered by Tenons capsule, which in turn is covered by transparent conjunctiva. There is a hole in the sclera through which nerve ?bres from the retina leave the eye in the optic nerve. Other smaller nerve ?bres and blood vessels also pass through the sclera at di?erent points. CORNEA This constitutes the transparent, colourless anterior one-sixth of the eye. It is transparent in order to allow light into the eye and is more steeply curved than the sclera. Viewed from in front, the cornea is roughly circular. Most of the focusing power of the eye is provided by the cornea (the lens acts as the ‘?ne adjustment’). It has an outer epithelium, a central stroma and an inner endothelium. The cornea is supplied with very ?ne nerve ?bres which make it exquisitely sensitive to pain. The central cornea has no blood supply – it relies mainly on aqueous humour for nutrition. Blood vessels and large nerve ?bres in the cornea would prevent light from entering the eye. LIMBUS is the junction between cornea and sclera. It contains the trabecular meshwork, a sieve-like structure through which aqueous humour leaves the eye.
The middle coat (uveal tract) consists of the choroid, ciliary body and iris. CHOROID A highly vascular sheet of tissue lining the posterior two-thirds of the sclera. The network of vessels provides the blood supply for the outer half of the retina. The blood supply of the choroid is derived from numerous ciliary vessels which pierce the sclera in front and behind. CILIARY BODY A ring of tissue extending 6 mm back from the anterior limitation of the sclera. The various muscles of the ciliary body by their contractions and relaxations are responsible for changing the shape of the lens during ACCOMMODATION. The ciliary body is lined by cells that secrete aqueous humour. Posteriorly, the ciliary body is continuous with the choroid; anteriorly it is continuous with the iris. IRIS A ?attened muscular diaphragm that is attached at its periphery to the ciliary body, and has a round central opening – the pupil. By contraction and relaxation of the muscles of the iris, the pupil can be dilated or constricted (dilated in the dark or when aroused; constricted in bright light and for close work). The iris forms a partial division between the anterior chamber and the posterior chamber of the eye. It lies in front of the lens and forms the back wall of the anterior chamber. The iris is visible from in front, through the transparent cornea, as the ‘coloured part of the eye’. The amount and distribution of iris pigment determine the colour of the iris. The pupil is merely a hole in the centre of the iris and appears black.
The inner layer The retina is a multilayered tissue (ten layers in all) which extends from the edges of the optic nerve to line the inner surface of the choroid up to the junction of ciliary body and choroid. Here the true retina ends at the ora serrata. The retina contains light-sensitive cells of two types: (i) cones – cells that operate at high and medium levels of illumination; they subserve ?ne discrimination of vision and colour vision; (ii) rods – cells that function best at low light intensity and subserve black-and-white vision.
The retina contains about 6 million cones and about 100 million rods. Information from them is conveyed by the nerve ?bres which are in the inner part of the retina, and leave the eye in the optic nerve. There are no photoreceptors at the optic disc (the point where the optic nerve leaves the eye) and therefore there is no light perception from this small area. The optic disc thus produces a physiological blind spot in the visual ?eld.
The retina can be subdivided into several areas: PERIPHERAL RETINA contains mainly rods and a few scattered cones. Visual acuity from this area is fairly coarse. MACULA LUTEA So-called because histologically it looks like a yellow spot. It occupies an area 4·5 mm in diameter lateral to the optic disc. This area of specialised retina can produce a high level of visual acuity. Cones are abundant here but there are few rods. FOVEA CENTRALIS A small central depression at the centre of the macula. Here the cones are tightly packed; rods are absent. It is responsible for the highest levels of visual acuity.
The chambers of the eye There are three: the anterior and posterior chambers, and the vitreous cavity. ANTERIOR CHAMBER Limited in front by the inner surface of the cornea, behind by the iris and pupil. It contains a transparent clear watery ?uid, the aqueous humour. This is constantly being produced by cells of the ciliary body and constantly drained away through the trabecular meshwork. The trabecular meshwork lies in the angle between the iris and inner surface of the cornea. POSTERIOR CHAMBER A narrow space between the iris and pupil in front and the lens behind. It too contains aqueous humour in transit from the ciliary epithelium to the anterior chamber, via the pupil. VITREOUS CAVITY The largest cavity of the eye. In front it is bounded by the lens and behind by the retina. It contains vitreous humour.
Lens Transparent, elastic and biconvex in cross-section, it lies behind the iris and in front of the vitreous cavity. Viewed from the front it is roughly circular and about 10 mm in diameter. The diameter and thickness of the lens vary with its accommodative state. The lens consists of: CAPSULE A thin transparent membrane surrounding the cortex and nucleus. CORTEX This comprises newly made lens ?bres that are relatively soft. It separates the capsule on the outside from the nucleus at the centre of the lens. NUCLEUS The dense central area of old lens ?bres that have become compacted by new lens ?bres laid down over them. ZONULE Numerous radially arranged ?bres attached between the ciliary body and the lens around its circumference. Tension in these zonular ?bres can be adjusted by the muscles of the ciliary body, thus changing the shape of the lens and altering its power of accommodation. VITREOUS HUMOUR A transparent jelly-like structure made up of a network of collagen ?bres suspended in a viscid ?uid. Its shape conforms to that of the vitreous cavity within which it is contained: that is, it is spherical except for a shallow concave depression on its anterior surface. The lens lies in this depression.
Eyelids These are multilayered curtains of tissue whose functions include spreading of the tear ?lm over the front of the eye to prevent desiccation; protection from injury or external irritation; and to some extent the control of light entering the eye. Each eye has an upper and lower lid which form an elliptical opening (the palpebral ?ssure) when the eyes are open. The lids meet at the medial canthus and lateral canthus respectively. The inner medial canthus is ?xed; the lateral canthus more mobile. An epicanthus is a fold of skin which covers the medial canthus in oriental races.
Each lid consists of several layers. From front to back they are: very thin skin; a sheet of muscle (orbicularis oculi, whose ?bres are concentric around the palpebral ?ssure and which produce closure of the eyelids); the orbital septum (modi?ed near the lid margin to form the tarsal plates); and ?nally, lining the back surface of the lid, the conjunctiva (known here as tarsal conjunctiva). At the free margin of each lid are the eyelashes, the openings of tear glands which lie within the lid, and the lacrimal punctum. Toward the medial edge of each lid is an elevation known as the papilla: the lacrimal punctum opens into this papilla. The punctum forms the open end of the cannaliculus, part of the tear-drainage mechanism.
Orbit The bony cavity within which the eye is held. The orbits lie one on either side of the nose, on the front of the skull. They a?ord considerable protection for the eye. Each is roughly pyramidal in shape, with the apex pointing backwards and the base forming the open anterior part of the orbit. The bone of the anterior orbital margin is thickened to protect the eye from injury. There are various openings into the posterior part of the orbit – namely the optic canal, which allows the optic nerve to leave the orbit en route for the brain, and the superior orbital and inferior orbital ?ssures, which allow passage of nerves and blood vessels to and from the orbit. The most important structures holding the eye within the orbit are the extra-ocular muscles, a suspensory ligament of connective tissue that forms a hammock on which the eye rests and which is slung between the medial and lateral walls of the orbit. Finally, the orbital septum, a sheet of connective tissue extending from the anterior margin of the orbit into the lids, helps keep the eye in place. A pad of fat ?lls in the orbit behind the eye and acts as a cushion for the eye.
Conjunctiva A transparent mucous membrane that extends from the limbus over the anterior sclera or ‘white of the eye’. This is the bulbar conjunctiva. The conjunctiva does not cover the cornea. Conjunctiva passes from the eye on to the inner surface of the eyelid at the fornices and is continuous with the tarsal conjunctiva. The semilunar fold is the vertical crescent of conjunctiva at the medial aspect of the palpebral ?ssure. The caruncle is a piece of modi?ed skin just within the inner canthus.
Eye muscles The extra-ocular muscles. There are six in all, the four rectus muscles (superior, inferior, medial and lateral rectus muscles) and two oblique muscles (superior and inferior oblique muscles). The muscles are attached at various points between the bony orbit and the eyeball. By their combined action they move the eye in horizontal and vertical gaze. They also produce torsional movement of the eye (i.e. clockwise or anticlockwise movements when viewed from the front).
Lacrimal apparatus There are two components: a tear-production system, namely the lacrimal gland and accessory lacrimal glands; and a drainage system.
Tears keep the front of the eye moist; they also contain nutrients and various components to protect the eye from infection. Crying results from excess tear production. The drainage system cannot cope with the excess and therefore tears over?ow on to the face. Newborn babies do not produce tears for the ?rst three months of life. LACRIMAL GLAND Located below a small depression in the bony roof of the orbit. Numerous tear ducts open from it into predominantly the upper lid. Accessory lacrimal glands are found in the conjunctiva and within the eyelids: the former open directly on to the surface of the conjunctiva; the latter on to the eyelid margin. LACRIMAL DRAINAGE SYSTEM This consists of: PUNCTUM An elevated opening toward the medial aspect of each lid. Each punctum opens into a canaliculus. CANALICULUS A ?ne tube-like structure run-ning within the lid, parallel to the lid margin. The canaliculi from upper and lower lid join to form a common canaliculus which opens into the lacrimal sac. LACRIMAL SAC A small sac on the side of the nose which opens into the nasolacrimal duct. During blinking, the sac sucks tears into itself from the canaliculus. Tears then drain by gravity down the nasolacrimal duct. NASOLACRIMAL DUCT A tubular structure which runs down through the wall of the nose and opens into the nasal cavity.
Visual pathway Light stimulates the rods and cones of the retina. Electrochemical messages are then passed to nerve ?bres in the retina and then via the optic nerve to the optic chiasm. Here information from the temporal (outer) half of each retina continues to the same side of the brain. Information from the nasal (inner) half of each retina crosses to the other side within the optic chiasm. The rearranged nerve ?bres then pass through the optic tract to the lateral geniculate body, then the optic radiation to reach the visual cortex in the occipital lobe of the brain.... eye
Hin: Gular, Umar
Ben: Jagya dumurMal, Tam,Kan: AthiTel: Udambaramu, PaidiGular fig, Cluster fig or Country fig, which is considered sacred, has golden coloured exudate and black bark. It is distributed all over India. Its roots are useful in treating dysentery. The bark is useful as a wash for wounds, highly efficacious in threatened abortions and recommended in uropathy. Powdered leaves mixed with honey are given in vitiated condition of pitta. A decoction of the leaves is a good wash for wounds and ulcers. Tender fruits (figs) are used in vitiated conditions of pitta, diarrhoea, dyspepsia and haemorrhages. The latex is administered in haemorrhoids and diarrhoea (Warrier et al, 1995). The ripe fruits are sweet, cooling and are used in haemoptysis, thirst and vomiting (Nadkarni, 1954; Aiyer et al, 1957; Moos, 1976). Nalpamaradi coconut oil, Candanasava, Valiya Arimedastaila, Dinesavalyadi Kuzhambu, Abhrabhasma, Valiya candanaditaila, etc. are some important preparations using the drug (Sivarajan et al, 1994).It is a moderate to large-sized spreading laticiferous, deciduous tree without many prominent aerial roots. Leaves are dark green and ovate or elliptic. Fruit receptacles are 2-5cm in diameter, sub- globose or pyriform arranged in large clusters on short leafless branches arising from main trunk or large branches. Figs are smooth or rarely covered with minute soft hairs. When ripe, they are orange, dull reddish or dark crimson. They have a pleasant smell resembling that of cedar apples. The bark is rusty brown with a fairly smooth and soft surface, the thickness varying from 0.5-2cm according to the age of the trunk or bark. Surface is with minute separating flakes of white tissue. Texture is homogeneously leathery (Warrier et al, 1995).Stem-bark gives gluanol acetate, -sitosterol, leucocyanidin-3-O- -D-glucopyrancoside, leucopelargonidin-3-O- -D-glucopyranoside, leucopelargonidin -3-O- -L-rhamnopyranoside, lupeol, ceryl behenate, lupeol acetate and -amyrin acetate. Stem- bark is hypoglycaemic and anti-protozoal. Gall is CVS active. Bark is tonic and used in rinder pest diseases of cattle. Root is antidysenteric and antidiabetic. Leaf is antibilious. Latex is antidiarrhoeal and used in piles. Bark and syconium is astringent and used in menorrhagia (Husain et al, 1992).2. Ficus microcarpa Linn. f. syn. F. retusa auct. Non. Linn.San: Plaksah; Hin,Ben: Kamarup;Mal: Ithi, Ithiyal;Tam: Kallicci, Icci;
Kan: Itti;
Tel: PlaksaPlaksah is the Ficus species with few branches and many adventitious roots growing downward. It is widely distributed throughout India and in Sri Lanka, S. China, Ryuku Isles and Britain. Plakasah is one of the five ingredients of the group panchvalkala i.e, five barks, the decoction of which is extensively used to clear ulcers and a douche in leucorrhoea in children. This decoction is administered externally and internally with satisfactory results. Plaksah is acclaimed as cooling, astringent, and curative of raktapitta doshas, ulcers, skin diseases, burning sensation, inflammation and oedema. It is found to have good healing property and is used in preparation of oils and ointments for external application in the treatment of ulcers (Aiyer and Kolammal, 1957). The stem-bark is used to prepare Usirasava, Gandhataila, Nalpamaradi taila, Valiya marmagulika, etc. (Sivarajan et al, 1994). The bark and leaves are used in wounds, ulcers, bruises, flatulent colic, hepatopathy, diarrhoea, dysentery, diabetes, hyperdipsia, burning sensation, haemaorrhages, erysipelas, dropsy, ulcerative stomatitis, haemoptysis, psychopathy, leucorrhoea and coporrhagia (Warrier et al,1995) F. microcarpa is a large glabrous evergreen tree with few aerial roots. Leaves are short- petioled, 5-10cm long, 2-6cm wide and apex shortly and bluntly apiculate or slightly emarginate. Main lateral nerves are not very prominent and stipules are lanceolate. Fruit receptacles are sessile and globose occurring in axillary pairs. It is yellowish when ripe without any characteristic smell. Bark is dark grey or brown with a smooth surface except for the lenticels. Outer bark is corky and crustaceous thin and firmly adherent to inner tissue. Inner bark is light and flesh coloured with firbrous texture (Warrier et al, 1995). It is also equated with many other species of the genus. viz. F. Singh and Chunekar, 1972; Kapoor and Mitra, 1979; Sharma, 1983).The bark contains tannin, wax and saponin. Bark is antibilious. Powdered leaves and bark is found very good in rheumatic headache. The bark and leaves are astringent, refrigerant, acrid and stomachic.3. Ficus benghalensis Linn.Eng: Banyan tree; San: Nyagrodhah, Vatah;Hin: Bat, Bargad;Ben: Bar, Bot; Mar: Vada; Mal: Peral, Vatavriksham;Tam: Alamaram, Peral;Kan: Ala;Tel: Peddamarri;Guj: VadBanyan tree is a laticiferous tree with reddish fruits, which is wound round by aerial adventitious roots that look like many legs. It is found in the Sub-Himalayan tract and Peninsular India. It is also grawn throughout India. It is widely used in treatment of skin diseases with pitta and rakta predominance. Stem-bark, root -bark, aerial roots, leaves, vegetative buds and milky exudate are used in medicine. It improves complexion, cures erysepelas, burning sensation and vaginal disorders, while an infusion of the bark cures dysentery, diarrhoea, leucorrhoea, menorrhagia, nervous disorders and reduces blood sugar in diabetes. A decoction of the vegetative buds in milk is beneficial in haemorrhages. A paste of the leaves is applied externally to abcesses and wounds to promote suppuration, while that of young aerial roots cure pimples. Young twigs when used as a tooth brush strengthen gum and teeth (Nadkarni, 1954; Aiyer and Kolammal, 1957; Mooss,1976). The drug forms an important constituent of formulations like Nalpamaradi Coconut oil, Saribadyasava, Kumkumadi taila, Khadi ra gulika, Valiyacandanadi taila, Candanasava, etc. (Sivarajan et al, 1994). The aerial roots are useful in obstinate vomiting and leucorrhoea and are used in osteomalacia of the limbs. The buds are useful in diarrhoea and dysentery. The latex is useful in neuralgia, rheumatism, lumbago, bruises, nasitis, ulorrhagia, ulitis, odontopathy, haemorrhoids, gonorrhoea, inflammations, cracks of the sole and skin diseases (Warrier et al, 1995).It is a very large tree up to 30m in height with widely spreading branches bearing many aerial roots functioning as prop roots. Bark is greenish white. Leaves are simple, alternate, arranged often in clusters at the ends of branches. They are stipulate, 10-20cm long and 5-12.5cm broad, broadly elliptic to ovate, entire, coriaceous, strongly 3-7 ribbed from the base. The fruit receptacles are axillary, sessile, seen in pairs globose, brick red when ripe and enclosing male, female and gall flowers. Fruits are small, crustaceous, achenes, enclosed in the common fleshy receptacles. The young bark is somewhat smooth with longitudinal and transverse row of lenticels. In older bark, the lenticels are numerous and closely spaced; outer bark easily flakes off. The fresh cut surface is pink or flesh coloured and exudes plenty of latex. The inner most part of the bark adjoining the wood is nearly white and fibrous (Warrier et al, 1995).The bark yields flavanoid compounds A, B and C; A and C are identified as different forms of a leucoanthocyanidin and compound B a leucoanthocyanin. All the 3 were effective as hypoglycaemic agents. Leaves give friedelin, -sitosterol, flavonoids- quercetin-3-galactoside and rutin. Heart wood give tiglic acid ester of taraxasterol. Bark is hypoglycemic, tonic, astringent, antidiarrhoeal and antidiabetic. Latex is antirheumatic. Seed is tonic. Leaf is diaphoretic. Root fibre is antigonorrhoeic. Aerial root is used in debility and anaemic dysentery (Husain et al, 1992)..4. Ficus religiosa Linn.Eng:Peepal tree, Sacred fig; San:Pippalah, Asvatthah; Hin:Pippal, Pipli, Pipar; Mal:ArayalBen: Asvatha;Tam: Arasu, Asvattam;Kan: Aswatha;Tel: Ravi; Mar: Ashvata, PimpalaPeepal tree or Sacred fig is a large deciduous tree with few or no aerial roots. It is common throughout India, often planted in the vicinity of the temples. An aqueous extract of the bark has an antibacterial activity against Staphylococcus aureus and Escherichia coli. It is used in the treatment of gonorrhoea, diarrhoea, dysentery, haemorrhoids and gastrohelcosis. A paste of the powdered bark is a good absorbent for inflammatory swellings. It is also good for burns. Leaves and tender shoots have purgative properties and are also recommended for wounds and skin diseases. Fruits are laxative and digestive. The dried fruit pulverized and taken in water cures asthma. Seeds are refrigerant and laxative. The latex is good for neuralgia, inflammations and haemorrhages (Warrier et al, 1995). Decoction of the bark if taken in honey subdues vatarakta (Nadkarni, 1954; Aiyer and Kolammal, 1957; Mooss, 1976; Kurup et al, 1979). The important preparations using the drug are Nalpamaradi taila, Saribadyasava, Candanasava, Karnasulantaka, Valiyamarma gulika etc (Sivarajan et al, 1994). branches bearing long petioled, ovate, cordate shiny leaves. Leaves are bright green, the apex produced into a linear-lanceolate tail about half as long as the main portion of the blade. The receptacles occurring in pairs and are axillary, depressed globose, smooth and purplish when ripe. The bark is grey or ash coloured with thin or membranous flakes and is often covered with crustose lichen patches. The outer bark is not of uniform thickness, the middle bark in sections appear as brownish or light reddish brown. The inner part consists of layers of light yellowish or orange brown granular tissue (Warrier et al, 1995).Bark gives -sitosterol and its glucoside. Bark is hypoglycaemic. Stem bark is antiprotozoal, anthelmintic and antiviral. Bark is astringent, antigonorrheic, febrifuge, aphrodisiac and antidysenteric. Syconium, leaf and young shoot is purgative (Husain et al, 1992).Agrotechnology: Ficus species can be cultivated in rocky areas, unused lands, or other wastelands of the farmyard. The plant is vegetatively propagated by stem cuttings. A few species are also seed propagated. Stem cuttings of pencil thickness taken from the branches are to be kept for rooting. Rooted cuttings are to be transplanted to prepared pits. No regular manuring is required. Irrigation is not a must as a plant is hardy. The plant is not attacked by any serious pests or diseases. Bark can be collected after 15 years. Ficus species generally has an economic life span of more than hundred years. Hence bark can be regularly collected from the tree. Root, bark, leaves, fruits and latex form the economic parts (Prasad et al,1995).... ficusIn blood transfusion, the person giving and the person receiving the blood must belong to the same blood group, or a dangerous reaction will take place from the agglutination that occurs when blood of a di?erent group is present. One exception is that group O Rhesus-negative blood can be used in an emergency for anybody.
| Agglutinogens | Agglutinins | Frequency | |
| in the | in the | in Great | |
| Group | erythrocytes | plasma | Britain |
| AB | A and B | None | 2 per cent |
| A | A | Anti-B | 46 per cent |
| B | B | Anti-A | 8 per cent |
| O | Neither | Anti-A and | 44 per cent |
| A nor B | Anti-B | ||
Rhesus factor In addition to the A and B agglutinogens (or antigens), there is another one known as the Rhesus (or Rh) factor – so named because there is a similar antigen in the red blood corpuscles of the Rhesus monkey. About 84 per cent of the population have this Rh factor in their blood and are therefore known as ‘Rh-positive’. The remaining 16 per cent who do not possess the factor are known as ‘Rh-negative’.
The practical importance of the Rh factor is that, unlike the A and B agglutinogens, there are no naturally occurring Rh antibodies. However, such antibodies may develop in a Rh-negative person if the Rh antigen is introduced into his or her circulation. This can occur (a) if a Rh-negative person is given a transfusion of Rh-positive blood, and (b) if a Rh-negative mother married to a Rh-positive husband becomes pregnant and the fetus is Rh-positive. If the latter happens, the mother develops Rh antibodies which can pass into the fetal circulation, where they react with the baby’s Rh antigen and cause HAEMOLYTIC DISEASE of the fetus and newborn. This means that, untreated, the child may be stillborn or become jaundiced shortly after birth.
As about one in six expectant mothers is Rh-negative, a blood-group examination is now considered an essential part of the antenatal examination of a pregnant woman. All such Rh-negative expectant mothers are now given a ‘Rhesus card’ showing that they belong to the rhesus-negative blood group. This card should always be carried with them. Rh-positive blood should never be transfused to a Rh-negative girl or woman.... blood groups
before descending, behind it, through the chest cavity. It terminates in the abdomen by dividing into the 2 common iliac arteries of the legs.
The aorta is thick-walled and has a large diameter in order to cope with the high pressure and large volume of blood passing through it. (See also arteries, disorders of; circulatory system.)... aorta
Ben: Kalmegh
Mal: Nilaveppu, Kiriyattu Tam: Nilavempu Kan: KreataImportance: Kalmegh, the Great or Green Chiretta is a branched annual herb. It is useful in hyperdipsia, burning sensation, wounds, ulcers, chronic fever, malarial and intermittent fevers, inflammations, cough, bronchitis, skin diseases, leprosy, pruritis, intestinal worms, dyspepsia, flatulence, colic, diarrhoea, dysentery, haemorrhoids and vitiated conditions of pitta (Warrier et al, 1993). It is used to overcome sannipata type of fever, difficulty in breathing, hemopathy due to the morbidity of kapha and pitta, burning sensation, cough, oedema, thirst, skin diseases, fever, ulcer and worms. It is also useful in acidity and liver complaints (Aiyer and Kolammal, 1962). The important preparations using the drug are Tiktakagheta, Gorocandi gulika, Candanasava, Panchatiktam kasaya, etc. (Sivarajan et al, 1994). A preparation called “Alui” is prepared by mixing powdered cumin (Cuminium cyminum) and large cardamom (Amomum subulatum) in the juice of this plant and administered for the treatment of malaria (Thakur et al, 1989). It is also a rich source of minerals.Distribution: The plant is distributed throughout the tropics. It is found in the plains of India from U.P to Assam, M.P., A.P, Tamil Nadu and Kerala, also cultivated in gardens.Botany: Andrographis paniculata (Burm.f.) Wall ex.Nees belongs to the family Acanthaceae. It is an erect branched annual herb, 0.3-0.9m in height with quadrangular branches. Leaves are simple, lanceolate, acute at both ends, glabrous, with 4-6 pairs of main nerves. Flowers are small, pale but blotched and spotted with brown and purple distant in lax spreading axillary and terminal racemes or panicles. Calyx-lobes are glandular pubescent with anthers bearded at the base. Fruits are linear capsules and acute at both ends. Seeds are numerous, yellowish brown and sub-quadrate (Warrier et al,1993).Another species of Andrographis is A. echioides (Linn.) Nees. It is found in the warmer parts of India. The plant is a febrifuge and diuretic. It contains flavone-echiodinin and its glucoside-echioidin (Husain et al, 1992).Agrotechnology: The best season of planting Andrographis is May-June. The field is to be ploughed well, mixed with compost or dried cowdung and seedbeds of length 3m, breadth 1/2m and 15cm height are to be taken at a distance of 3m. The plant is seed propagated. Seeds are to be soaked in water for 6 hours before sowing. Sowing is to be done at a spacing of 20cm. Seeds may germinate within 15-20 days. Two weedings, first at one month after planting and the second at 2 month after planting are to be carried out. Irrigation during summer months is beneficial. The plant is not attacked by any serious pests or diseases. Flowering commences from third month onwards. At this stage, plant are to be collected, tied into small bundles and sun-dried for 4-5 days. Whole plant is the economic part and the yield is about 1.25t dried plants/ha (Prasad et al, 1997).Properties and activity: Leaves contain two bitter substances lactone “andrographolid” and “kalmeghin”. The ash contains sodium chloride and potassium salts. Plant is very rich in chlorophyte. Kalmeghin is the active principle that contains 0.6% alkaloid of the crude plant. The plant contains diterpenoids, andrographolide, 14-deoxy-11-oxo-andrographolide, 14-deoxy-11,12-dihydroandrographolide, 14-deoxy andrographolide and neoandrographolide (Allison et al, 1968). The roots give flavones-apigenin-7,4-dio-O-methyl ether, 5-hydroxy-7,8,2’,3’- tetramethoxyflavone, andrographin and panicolin and -sitosterol (Ali et al, 1972; Govindachari et al, 1969). Leaves contain homoandrographolide, andrographosterol and andrographone.The plant is vulnerary, antipyretic, antiperiodic, anti-inflammatory, expectorant, depurative, sudorific, anthelmintic, digestive, stomachic, tonic, febrifuge and cholagogue. The plant is antifungal, antityphoid, hepatoprotective, antidiabetic and cholinergic. Shoot is antibacterial and leaf is hypotensive(Garcia et al, 1980). This is used for the inflammation of the respiratory tract. In China, researchers have isolated the andrographolide from which soluble derivative such as 14-deoxy-11, 12-dehydro-andrographolide which forms the subject of current pharmacological and clinical studies. Apigenin 7,4’-O-dimethyl ether isolated from A. paniculata exhibits dose dependent, antiulcer activity in shay rat, histamine induced ulcer in guinea pigs and aspirin induced ulcers in rats. A crude substance isolated from methanolic extract of leaves has shown hypotensive activity. Pre-treatment of rats with leaf (500mg/kg) or andrographolide (5mg/kg) orally prevented the carbon tetrachloride induced increase of blood serum levels of glutamate-oxaloacetate transaminase in liver and prevented hepatocellular membrane.... green chiretta(iii) blockage of the circulation of CSF. Such disturbances in the circulation of the ?uid may be due to congenital reasons (most commonly associated with SPINA BIFIDA), to MENINGITIS, or to a tumour.
Symptoms In children, the chief symptoms observed are the gradual increase in size of the upper part of the head, out of all proportion to the face or the rest of the body. The head is globular, with a wide anterior FONTANELLE and separation of the bones at the sutures. The veins in the scalp are prominent, and there is a ‘crackpot’ note on percussion. The normal infant’s head should not grow more than 2·5 cm (1 inch) in each of the ?rst two months of life, and much more slowly subsequently; growth beyond this rate should arouse suspicions of hydrocephalus, so medical professionals caring for infants use centile charts for this purpose.
The cerebral ventricles are widely distended, and the convolutions of the brain ?attened, while occasionally the ?uid escapes into the cavity of the cranium, which it ?lls, pressing down the brain to the base of the skull. As a consequence of such changes, the functions of the brain are interfered with, and in general the mental condition of the patient is impaired. Untreated, the child is dull and listless, irritable and sometimes suffers from severe mental subnormality. The special senses become affected as the disease advances, especially vision, and sight is often lost, as is also hearing. Towards the end, paralysis is apt to occur.
Treatment Numerous ingenious operations have been devised for the treatment of hydrocephalus. The most satisfactory of these utilise unidirectional valves and shunts (tubes), whereby the cerebrospinal ?uid is bypassed from the brain into the right atrium of the heart or the peritoneal cavity. The shunt may have to be left in position inde?nitely.... hydrocephalus
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
Rheumatic fever is now extremely uncommon in developed countries, but remains common in developing areas. Diagnosis is based on the presence of two or more major manifestations – endocarditis (see under HEART, DISEASES OF), POLYARTHRITIS, chorea, ERYTHEMA marginatum, subcutaneous nodules – or one major and two or more minor ones – fever, arthralgia, previous attacks, raised ESR, raised white blood cell count, and ELECTROCARDIOGRAM (ECG) changes. Evidence of previous infection with streptococcus is also a criterion.
Clinical features Fever is high, with attacks of shivering or rigor. Joint pain and swelling (arthralgia) may affect the knee, ankle, wrist or shoulder and may migrate from one joint to another. TACHYCARDIA may indicate cardiac involvement. Subcutaneous nodules may occur, particularly over the back of the wrist or over the elbow or knee. Erythema marginatum is a red rash, looking like the outline of a map, characteristic of the condition.
Cardiac involvement includes PERICARDITIS, ENDOCARDITIS, and MYOCARDITIS. The main long-term complication is damage to the mitral and aortic valves (see HEART).
The chief neurological problem is chorea (St Vitus’s dance) which may develop after the acute symptoms have subsided.
Chronic rheumatic heart disease occurs subsequently in at least half of those who have had rheumatic fever with carditis. The heart valve usually involved is the mitral; less commonly the aortic, tricuspid and pulmonary. The lesions may take 10–20 years to develop in developed countries but sooner elsewhere. The heart valves progressively ?brose and ?brosis may also develop in the myocardium and pericardium. The outcome is either mitral stenosis or mitral regurgitation and the subsequent malfunction of this or other heart valves affected is chronic failure in the functioning of the heart. (see HEART, DISEASES OF).
Treatment Eradication of streptococcal infection is essential. Other features are treated symptomatically. PARACETAMOL may be preferred to ASPIRIN as an antipyretic in young children. One of the NON-STEROIDAL ANTIINFLAMMATORY DRUGS (NSAIDS) may bene?t the joint symptoms. CORTICOSTEROIDS may be indicated for more serious complications.
Patients who have developed cardiac-valve abnormalities require antibiotic prophylaxis during dental treatment and other procedures where bacteria may enter the bloodstream. Secondary cardiac problems may occur several decades later and require replacement of affected heart valves.... rheumatic fever
Blood pressure is measured using a sphygmomanometer and is expressed as millimetres of mercury (mmHg).
Blood pressure varies with age, between individuals, and at different times in the same individual but a healthy young adult usually has a blood pressure reading, at rest, of about 120/80 (that is 120 mmHg systolic and 80 mmHg diastolic).
Abnormally high blood pressure is called hypertension; abnormally low pressure is termed hypotension.... blood pressure
The left carotid arises from the aorta and runs up the neck on the left side of the trachea (windpipe). The right carotid arises from the subclavian artery (which branches off the aorta) and follows a similar route on the right side of the
neck. Just above the level of the larynx (voice-box), each carotid artery divides to form an external carotid artery and an internal carotid artery. The external arteries have multiple branches that supply most tissues in the face, scalp, mouth, and jaws; the internal arteries enter the skull to supply the brain and eyes. At the base of the brain, branches of the 2 internal carotids and the basilar artery join to form a ring of vessels called the circle of Willis. Narrowing of these vessels may be associated with transient ischaemic attack (TIA); obstruction of them causes a stroke. carpal tunnel syndrome Numbness, tingling, and pain in the thumb, index finger, and middle fingers caused by compression of the median nerve at the wrist. Symptoms may be worse at night. The condition results from pressure on the nerve where it passes into the hand via a gap (the “carpal tunnel’’) under a ligament at the front of the wrist. It is common among keyboard users. It also occurs without obvious cause in middleaged women, and is associated with pregnancy, initial use of oral contraceptives, premenstrual syndrome, rheumatoid arthritis, myxoedema, and acromegaly.
The condition often disappears without treatment.
Persistent symptoms may be treated with a corticosteroid drug injected under the ligament, or the ligament may be cut to relieve pressure on the nerve.... carotid artery
does not develop in all people infected with. The interval between infection and the development of is highly variable. Without treatment, around half of those people infected will develop within 8–9 years.
is transmitted in body fluids, including semen, blood, vaginal secretions, and breast milk. The major methods of transmission are sexual contact (vaginal, anal, or oral), blood to blood (via transfusions or needle-sharing in drug users), and mother to fetus. has also been transmitted through blood products given to treat haemophilia, artificial insemination by donated semen, and kidney transplants; but improved screening has greatly reduced these risks. is not spread by everyday contact, such as hugging or sharing crockery. The virus enters the bloodstream and infects cells that have a particular receptor, known as the CD4 receptor, on their surface. These cells include a type of white blood cell (a CD4 lymphocyte) responsible for fighting infection and cells in other tissues such as the brain. The virus reproduces within the infected cells, which then die, releasing more virus particles into the blood. If the infection is left untreated, the number of CD4 lymphocytes falls, resulting in greater susceptibility to certain infections and some types of cancer.
Some people experience a short-lived illness similar to infectious mononucleosis when they are first infected with. Many individuals have no obvious symptoms; some have only vague complaints, such as weight loss, fevers, sweats, or unexplained diarrhoea, described as -related complex.
Minor features of infection include skin disorders such as seborrhoeic dermatitis. More severe features include persistent herpes simplex infections, oral candidiasis (thrush), shingles, tuberculosis, and shigellosis. may also affect the brain, causing a variety of neurological disorders, including dementia.
Certain conditions, known as AIDSdefining illnesses, are characteristic of full-blown. These include cancers (Kaposi’s sarcoma and lymphoma of the brain), and various infections (pneumocystis pneumonia, cytomegalovirus infection, toxoplasmosis, diarrhoea due to CRYPTOSPORIDIUM or ISOSPORA, candidiasis, disseminated strongyloidiasis, and cryptococcosis), many of which are described as opportunistic infections.
Confirmation of infection involves testing a blood sample for the presence of antibodies to. Diagnosis of fullblown is based on a positive test along with the presence of an AIDSdefining illness.
The risk of infection with can be reduced by practising safer sex. Intravenous drug users should not share needles. There is a small risk to health workers handling infected blood products or needles, but this risk can be minimized by safe practices.
Treatment of infection with a combination of antiviral drugs can slow the disease’s progress, and may prevent the development of full-blown. The 2 main types of antiviral drug used are protease inhibitors, such as indinavir, and reverse transcriptase inhibitors such as zidovudine. Treatment is also available for -defining illnesses.... aids
Rectal bleeding and discomfort on defaecation are the most common features. Prolapsing haemorrhoids often produce a mucous discharge and itching around the anus. A complication of prolapse is thrombosis and strangulation; this can cause extreme pain.
Diagnosis is usually by proctoscopy. Mild cases are controlled by drinking plenty of fluids, eating a high-fibre diet, and establishing regular toilet habits. Rectal suppositories and creams containing corticosteroid drugs and local anaesthetics reduce pain and swelling. More troublesome haemorrhoids may be treated by sclerotherapy, cryosurgery, or by banding, in which a band is tied around the haemorrhoid, causing it to wither and drop off. A haemorrhoidectomy is generally required for prolapsing haemorrhoids.... haemorrhoids
strains: type A has been the cause of pandemics in the last century.
Types A and B produce classic flu symptoms; type C causes a mild illness that is indistinguishable from a common cold. The illness usually clears up completely within 7–10 days. Rarely, flu takes a severe form, causing acute pneumonia that may be fatal within a day or 2 even in healthy young adults. Type B infections in children sometimes mimic appendicitis, and they have been implicated in Reye’s syndrome. In the elderly and those with lung or heart disease, influenza may be followed by a bacterial infection such as bronchitis or pneumonia. Analgesic drugs (painkillers) help to relieve aches and pains and reduce fever. The antiviral drug amantadine may be given if the person is elderly or has another lung condition. Antibiotic drugs may be used to combat secondary bacterial infection.
Flu vaccines, containing killed strains of the types A and B virus currently in circulation, are available, but have only a 60–70 per cent success rate.
Immunity is short-lived, and vaccination (recommended for older people and anyone suffering from respiratory or circulatory disease) must be repeated annually.... influenza
The small intestine is about 6.5 m in length and has 3 sections: the duodenum, the jejunum and the ileum. Partially digested food from the stomach is forced along the intestine by peristalsis.
The small intestine is concerned with the digestion and absorption of food. Digestive enzymes and bile are added to the partly digested food in the duodenum via the bile and pancreatic ducts (see biliary system). Glands within the walls of each section of the small intestine produce mucus and other enzymes, which help to break down the food. Blood vessels in the intestinal walls absorb nutrients and carry them to the liver for distribution to the rest of the body.
The large intestine is about 1.5 m long. The main section, the colon, is divided into an ascending, a transverse, a descending, and a pelvic portion (the sigmoid colon). The appendix hangs from a pouch (the caecum) between the small intestine and the colon. The final section before the anus is the rectum.Unabsorbed material leaves the small intestine as liquid and fibre.
As this material passes through the large intestine, water, vitamins, and mineral salts are absorbed into the bloodstream, leaving faeces made up of undigested food residue, fat, various secretions, and bacteria.
The faeces are compressed and pass into the rectum for evacuation.... intestine
The main symptom is swelling of the legs and face due to oedema. Also, fluid may collect in the chest cavity, resulting in pleural effusion, or in the abdomen, causing ascites. Diarrhoea, lethargy, and anorexia may occur.
Treatment is of the underlying condition.
A low-sodium diet may be recommended, and diuretic drugs may be given to reduce oedema.
If the concentration of protein in the blood is very low, protein may need to be given intravenously.... nephrotic syndrome
of reducing pain and providing nursing care until the oesophagus heals.
Reflux oesophagitis is due to poor function of the muscles in the lower oesophagus, which permits the stomach’s acidic contents to rise back into the oesophagus (see acid reflux). The main symptom, heartburn, may be worsened by alcohol, smoking, and obesity. Poor function of the lower oesophagus may be linked with a hiatus hernia. Treatment focuses on diet and lifestyle changes. Antacid drugs help to reduce acidity. Surgical treatment may be necessary for a hiatus hernia.
Barrett’s oesophagus, a complication of reflux oesophagitis, may lead to cancer. Severe, chronic oesophagitis can cause an oesophageal stricture.... oesophagitis
Severe acute pancreatitis may lead to hypotension, heart failure, kidney failure, respiratory failure, cysts, and ascites. Chronic pancreatitis may also lead to the development of ascites and cysts, as well as bile duct obstruction and diabetes mellitus.
A diagnosis may be made by blood tests, abdominal X-rays, ultrasound scanning, CT scanning, MRI, or ERCP. Acute pancreatitis is treated with intravenous infusion of fluids and salts and opioid analgesic drugs. In some cases, the gut may be washed out with sterile fluid, or a pancreatectomy may be performed and any gallstones that are present removed. Treatment for the chronic form is with painkillers, insulin, pancreatin, and, in some cases, pancreatectomy.... pancreatitis
The main dietary sources are fruits and vegetables. Considerable amounts of vitamin C are lost when foods are processed, cooked, or kept warm.
Mild deficiency of vitamin C may result from a serious injury or burn, major surgery, the use of oral contraceptives, fever, or continual inhalation of carbon monoxide (from traffic fumes or tobacco smoke). It may cause weakness, general aches, swollen gums, and nosebleeds. More serious deficiency is usually caused by a very restricted diet. Severe deficiency leads to scurvy and anaemia.
If the daily dose of vitamin C exceeds about 1g, it may cause nausea, stomach cramps, diarrhoea, or kidney stones
(see calculi, urinary tract).... vitamin c
Various processes that can occur include in?ammation, ulceration, infection or tumour. Abdominal disease may be of rapid onset, described as acute, or more long-term when it is termed chronic.
An ‘acute abdomen’ is most commonly caused by peritonitis – in?ammation of the membrane that lines the abdomen. If any structure in the abdomen gets in?amed, peritonitis may result. Causes include injury, in?ammation of the Fallopian tubes (SALPINGITIS), and intestinal disorders such as APPENDICITIS, CROHN’S DISEASE, DIVERTICULITIS or a perforated PEPTIC ULCER. Disorders of the GALLBLADDER or URINARY TRACT may also result in acute abdominal pain.
General symptoms of abdominal disease include:
Pain This is usually ill-de?ned but can be very unpleasant, and is termed visceral pain. Pain is initially felt near the mid line of the abdomen. Generally, abdominal pain felt high up in the mid line originates from the stomach and duodenum. Pain that is felt around the umbilicus arises from the small intestine, appendix and ?rst part of the large bowel, and low mid-line pain comes from the rest of the large bowel. If the diseased organ secondarily in?ames or infects the lining of the abdominal wall – the PERITONEUM – peritonitis occurs and the pain becomes more de?ned and quite severe, with local tenderness over the site of the diseased organ itself. Hence the pain of appendicitis begins as a vague mid-line pain, and only later moves over to the right iliac fossa, when the in?amed appendix has caused localised peritonitis. PERFORATION of one of the hollow organs in the abdomen – for example, a ruptured appendix or a gastric or duodenal ulcer (see STOMACH, DISEASES OF) eroding the wall of the gut – usually causes peritonitis with resulting severe pain.
The character of the pain is also important. It may be constant, as occurs in in?ammatory diseases and infections, or colicky (intermittent) as in intestinal obstruction.
Swelling The commonest cause of abdominal swelling in women is pregnancy. In disease, swelling may be due to the accumulation of trapped intestinal contents within the bowel, the presence of free ?uid (ascites) within the abdomen, or enlargement of one or more of the abdominal organs due to benign causes or tumour.
Constipation is the infrequent or incomplete passage of FAECES; sometimes only ?atus can be passed and, rarely, no bowel movements occur (see main entry for CONSTIPATION). It is often associated with abdominal swelling. In intestinal obstruction, the onset of symptoms is usually rapid with complete constipation and severe, colicky pain. In chronic constipation, the symptoms occur more gradually.
Nausea and vomiting may be due to irritation of the stomach, or to intestinal obstruction when it may be particularly foul and persistent. There are also important non-abdominal causes, such as in response to severe pain or motion sickness.
Diarrhoea is most commonly due to simple and self-limiting infection, such as food poisoning, but may also indicate serious disease, especially if it is persistent or contains blood (see main entry for DIARRHOEA).
Jaundice is a yellow discoloration of the skin and eyes, and may be due to disease in the liver or bile ducts (see main entry for JAUNDICE).
Diagnosis and treatment Abdominal diseases are often di?cult to diagnose because of the multiplicity of the organs contained within the abdomen, their inconstant position and the vagueness of some of the symptoms. Correct diagnosis usually requires experience, often supplemented by specialised investigations such as ULTRASOUND. For this reason sufferers should obtain medical advice at an early stage, particularly if the symptoms are severe, persistent, recurrent, or resistant to simple remedies.... abdomen, diseases of
Habitat: Tropical jungles throughout India, especially in the Deccan.
Ayurvedic: Saptalaa, Shitalaa, Saatalaa, Shrivalli, Kantvalli.Unani: Shikaakaai, Kharunb Nabti.Siddha/Tamil: Seekai, Sigakai.Folk: Ban-Reethaa.Action: Febrifuge, expectorant, emetic, spasmolytic, diuretic, antidiarrhoeal. Leaves—an infusion is given in malarial fever. Pods and seeds—decoction is used to remove dandruff (known as Shikaakaai), extensively used as a detergent. An ointment is used for skin diseases. Bark—extract is used in leprosy.
The bark yields a saponin which, on hydrolysis, yields lupeol, alpha- spinasterol and acacic acid lactone. Pods also yield saponins (20.8%). Sugars identified are glucose, arabinose and rhamnose.The leaves contain alkaloids, nicotine and colycotomine, a triterpenoid saponin and oxalic, tartaric, citric, suc- cinic and ascorbic acids.The bark saponins are spermicidal, also haemolytic and spasmolytic. A decoction of pods relieves biliousness and acts as a purgative.The ethanolic extract of unripe pods yields a glycosidal fraction (0.28%) which exhibits anti-inflammatory activity. It also shows significant antibacterial activity.The plant acts as an antiseptic agent for curing sores, gums and loose teeth.The flowers are the source of Cassie perfume.The main constituents of the flowers are benzyl, anisic, decylic and cuminic aldehydes, as well as traces of geraniol, farnesol and linalool.... acacia concinnaBoth 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
See www.rospa.com... accidental death
Habitat: Assam, Bengal, southwards to Andhra Pradesh and western Ghats.
English: Kadam.Ayurvedic: Kadamba, Priyaka, Vrtta-pushpa, Nipa, Halipriya. Kadambaka is equated with Adina cordifolia.Siddha/Tamil: Venkadambu, Vellai Kadambam.Action: Stembark—febrifugal, antidiuretic, anthelmintic, hypo- glycaemic. Fruit—cooling; anti- catarrhal, blood purifier, analgesic.
Family: Moraceae.Habitat: Western Ghats from Konkan southwards to Trivandrum, up to 600 m.
English: Sacking tree, Upas tree.Ayurvedic: Valkala vrksha.Siddha/Tamil: Aranthelli, Mara-uri, Nettavil.Folk: Jangali Lakuch, Jasund, Chaandakudaa.Action: Seed—febrifuge, antidysen- teric (in minute doses). Latex— circulatory stimulant (in minute doses.)
The latex contains a series of poisonous cardenolides, of which alpha- and/or beta-antiarin are the main components. The total amount of crystalline cardiac glycosides in the latex ranges from 0.1 to 2.5%; alpha-antiarin from 0.0 to 1.38% and beta-antiarin from 0.075 to 1.44%. Antiarins are said to act on the heart more powerfully than digitalin. Beta-antiarin is more potent than alpha-antiarin.Latex, in small quantities, is a mild cardiac and circulatory stimulant, whereas in large quantities it acts as a myocardial poison. It stimulates intestinal and uterine contractions.As many as 34 Kedde-positive substances were reported in the seed sample from Indonesia. The latex sample showed the presence of 29 Kedde- positive substances.... antiaris toxicariaThe drugs are much more e?ective in the treatment and prevention of venous clotting – for example, deep vein thrombosis (DVT), see under VEINS, DISEASES OF – than in preventing thrombosis formation in arteries with their fast-?owing blood in which thrombi contain little ?brin (against which the anticoagulants work) and many PLATELETS.
The main anticoagulants now in use are the natural agent HEPARIN (a quick-acting variety and a low-molecular-weight long-acting type); synthetic oral anticoagulants such as WARFARIN and the less-often-used acenocoumarol and PHENINDIONE; and antiplatelet compounds such as ASPIRIN, clopidogrel dipyridamole and ticlopidines. Fondaparinux is an extract of heparin which can be given once daily by injection; ximelagatran, an inhibitor of thrombin, is being trialled as the ?rst new oral anticoagulant since heparin.
Patients taking anticoagulants need careful medical monitoring and they should carry an Anticoagulant Card with instructions about the use of whatever drug they may be receiving – essential information should the individual require treatment for other medical conditions as well as for thrombosis.... anticoagulants
Habitat: Found all over India, ascending to 300 m.
English: Elephant Creeper.Ayurvedic: Vriddhadaaruka, Vriddhadaaru, Vriddhadaaraka, Bastaantri, Sthavira, Sthaviradaaru, Atarunadaaru, Samudrashosha. (Seeds of Salvia plebeia R. Br. are also known as Samudrashosha.)Unani: Samunder sokh.Siddha/Tamil: Ambgar, Samuddira- pacchaiFolk: Bidhaaraa.Action: Root—aphrodisiac (considered as a rejuvenator), nervine (used in diseases of nervous system, sexual disorders), diuretic (used in strangury), antirheumatic. Seeds—hypotensive, spasmolytic. Leaves—used externally in skin diseases (ringworm, eczema, boils, swellings); rubefacient, topically stimulant.
The seeds contain hallucinogenic ergoline alkaloids, the main ones being ergine and isoergine. EtOH (50%) extract of seeds exhibits hypotensive activity. (Seeds of all species of Argyreia contain ergoline alkaloids and are hypotensive.) Leaves of Argyreia sp. contain sitosterol and are antiphlogistic.In Indian medicine, A. speciosa is not used as a single drug for sexual disorders in men, but as a supporting drug for exerting its antiphlogistic, spasmolytic and hypotensive actions on the central nervous system. The drug, in itself, did not show anabolic- cum-androgen-like or spermogenetic activity experimentally.Ipomoea petaloidea Chois and Ipo- moea biloba Forskofthe Convolvulacae family are also used as Vriddhadaaru.In Western herbal medicine, Hawaiian Baby Woodrose is equated with Argyreia nervosa (synonym Argyreia speciosa; grows in Florida, California and Hawaii). The seed is used for pain relief and as a hallucinogen.The seeds contain hallucinogens including ergonovine, isoergine (isoly- sergic acid amide) and ergine (lysergic acid amide). Four to eight seeds are equivalent to 10-100 mcg of LSD, a potent serotonin-1A (5-HT1A) agonist. The effects last 6-8 h. (Natural Medicines Comprehensive Database, 2007.)Dosage: Root—3-5 g powder.(CCRAS.)... argyreia speciosaThe most widely prescribed type of antidepressants are the tricyclics, so-called because their molecular structure includes three rings. The other commonly used types are named after the actions they have on chemicals in the brain: the SELECTIVE SEROTONIN-REUPTAKE INHIBITORS (SSRIS) and the MONOAMINE OXIDASE INHIBITORS (MAOIS) – see also below. All types of antidepressant work in similar ways. Tricyclic antidepressants have cured depression in millions of people, but they can cause unpleasant side-effects, particularly in the ?rst couple of weeks. These include SEDATION, dry mouth, excessive sweating, CONSTIPATION, urinary problems, and impotence (inability to get an erection). Up to half of all people prescribed tricyclic drugs cannot tolerate the side-effects and stop treatment before their depression is properly treated. More seriously, tricyclics can upset the rhythm of the heart in susceptible people and should never be given in the presence of heart disease.
The SSRIs are newer, coming into wide use in the late 1980s. They increase the levels in the brain of the chemical messenger SEROTONIN, which is thought to be depleted in depression. Indeed, the SSRIs are as e?ective as tricyclics and, although they can cause nausea and excessive sweating at ?rst, they generally have fewer side-effects. Their main disadvantage, however, is that they cost much more than the most commonly used tricyclic, amitriptyline. On the other hand, they are more acceptable to many patients and they cause fewer drop-outs from treatment – up to a quarter rather than a half. The money saved by completed, successful treatment may outweigh the prescribing costs. SSRIs have been reported as associated with an increased risk of suicide.
Another group of antidepressants, the MAOIs, have been in use since the late 1950s.
They are stimulants, rather than sedatives, and are particularly helpful for people who are physically and mentally slowed by depression. They work well but have one big disadvantage – a dangerous interaction with certain foods and other drugs, causing a sudden and very dangerous increase in blood pressure. People taking them must carry an information card explaining the risk and listing the things that they should avoid. Because of this risk, MAOIs are not used much now, except when other treatments have failed. A new MAOI, moclobemide, which is less likely to interact and so cause high blood pressure, is now available.
LITHIUM CARBONATE is a powerful antidepressant used for intractable depression. It should be used under specialist supervision as the gap between an e?ective dose and a toxic one is narrow.
St John’s Wort is a popular herbal remedy which may be e?ective, but which is handicapped by di?erences of strength between di?erent preparations or batches. It can interact with a number of conventional drugs and so needs to be used cautiously and with advice.
In general, antidepressants work by restoring the balance of chemicals in the brain. Improved sleep and reduced anxiety are usually the ?rst signs of improvement, particularly among people taking the more sedative tricyclic drugs. Improvement in other symptoms follow, with the mood starting to lift after about two weeks of treatment. Most people feel well by three months, although a few residual symptoms, such as slowness in the mornings, may take longer to clear up. People taking antidepressants usually want to stop them as soon as they feel better; however, the risk of relapse is high for up to a year and most doctors recommend continuing the drugs for around 4–6 months after recovery, with gradual reduction of the dose after that.
Withdrawal reactions may occur including nausea, vomiting, headache, giddiness, panic or anxiety and restlessness. The drugs should be withdrawn gradually over about a month or longer (up to six months in those who have been on maintenance treatment).
A wide range of antidepressant drugs is described in the British National Formulary. Examples include:
Tricyclics: amitryptyline, imipramine, doxepin.
MAOIs: phenelzine, isocarboxazid.
SSRIs: citalopram, ?uoxetine, paraxtene. (Antidepressant drugs not in these three
groups include ?upenthixol, mertazapine and venlafaxine.)... antidepressant drugs
This technique is used when normal methods of attempted CONCEPTION or ARTIFICIAL INSEMINATION with healthy SEMEN have failed. In the UK, assisted-conception procedures are governed by the Human Fertilisation & Embryology Act 1990, which set up the Human Fertilisation & Embryology Authority (HFEA).
Human Fertilisation & Embryology Act 1990 UK legislation was prompted by the report on in vitro fertilisation produced by a government-appointed committee chaired by Baroness Warnock. This followed the birth, in 1978, of the ?rst ‘test-tube’ baby.
This Act allows regulation monitoring of all treatment centres to ensure that they carry out treatment and research responsibly. It covers any fertilisation that uses donated eggs or sperm (called gametes) – for example, donor insemination or embryos (see EMBRYO) grown outside the human body (known as licensed treatment). The Act also covers research on human embryos with especial emphasis on foolproof labelling and immaculate data collection.
Human Fertilisation & EmbryologyAuthority (HFEA) Set up by the UK government following the Warnock report, the Authority’s 221 members inspect and license centres carrying out fertilisation treatments using donated eggs and sperm. It publishes a code of practice advising centres on how to conduct their activities and maintains a register of information on donors, patients and all treatments. It also reviews routinely progress and research in fertility treatment and the attempted development of human CLONING. Cloning to produce viable embryos (reproductive cloning) is forbidden, but limited licensing of the technique is allowed in specialist centres to enable them to produce cells for medical treatment (therapeutic cloning).
In vitro fertilisation (IVF) In this technique, the female partner receives drugs to enhance OVULATION. Just before the eggs are released from the ovary (see OVARIES), several ripe eggs are collected under ULTRASOUND guidance or through a LAPAROSCOPE. The eggs are incubated with the prepared sperm. About 40 hours later, once the eggs are fertilised, two eggs (three in special circumstances) are transferred into the mother’s UTERUS via the cervix (neck of the womb). Pregnancy should then proceed normally. About one in ?ve IVF pregnancies results in the birth of a child. The success rate is lower in women over 40.
Indications In women with severely damaged FALLOPIAN TUBES, IVF o?ers the only chance of pregnancy. The method is also used in couples with unexplained infertility or with male-factor infertility (where sperms are abnormal or their count low). Women who have had an early or surgically induced MENOPAUSE can become pregnant using donor eggs. A quarter of these pregnancies are multiple – that is, produce twins or more. Twins and triplets are more likely to be premature. The main danger of ovarian stimulation for IVF is hyperstimulation which can cause ovarian cysts. (See OVARIES, DISEASES OF.)... assisted conception
Uses Its main use is in gout, for which colchicine, the active principle of colchicum, in doses of 0·5 mg every one or two hours until the pain is relieved, followed by 0·5 mg thrice daily for about a week, is the form generally employed.... colchicum
Toxins. In conditions such as chronic glomerulonephritis (see KIDNEYS, DISEASES OF) and URAEMIA there is a severe anaemia due to the e?ect of the disease upon blood formation.
Drugs. Certain drugs, such as aspirin and the non-steroidal anti-in?ammatory drugs, may cause occult gastrointestinal bleeding.... defective blood formation
The dependence that most concerns modern society is one in which individuals become dependent on or addicted to certain substances such as alcohol, drugs, tobacco (nicotine), caffeine and solvents. This is often called substance abuse. Some people become addicted to certain foods or activities: examples of the latter include gambling, computer games and use of the Internet.
The 28th report of the World Health Organisation Expert Committee on Drug Dependence in 1993 de?ned drug dependence as: ‘A cluster of physiological, behavioural and cognitive phenomena of variable intensity, in which the use of a psychoactive drug (or drugs) takes on a high priority. The necessary descriptive characteristics are preoccupation with a desire to obtain and take the drug and persistent drug-seeking behaviour. Psychological dependence occurs when the substance abuser craves the drug’s desirable effects. Physical dependence occurs when the user has to continue taking the drug to avoid distressing withdrawal or abstinence symptoms. Thus, determinants and the problematic consequences of drug dependence may be biological, psychological or social and usually interact.’
Di?erent drugs cause di?erent rates of dependence: TOBACCO is the most common substance of addiction; HEROIN and COCAINE cause high rates of addiction; whereas ALCOHOL is much lower, and CANNABIS lower again. Smoking in the western world reached a peak after World War II with almost 80 per cent of the male population smoking. The reports on the link between smoking and cancer in the early 1960s resulted in a decline that has continued so that only around a quarter of the adult populations of the UK and USA smokes. Globally, tobacco consumption continues to grow, particularly in the developing world with multinational tobacco companies marketing their products aggressively.
Accurate ?gures for illegal drug-taking are hard to obtain, but probably approximately 4 per cent of the population is dependent on alcohol and 2 per cent on other drugs, both legal and illegal, at any one time in western countries.
How does dependence occur? More than 40 distinct theories or models of drug misuse have been put forward. One is that the individual consumes drugs to cope with personal problems or diffculties in relations with others. The other main model emphasises environmental in?uences such as drug availability, environmental pressures to consume drugs, and sociocultural in?uences such as peer pressure.
By contrast to these models of why people misuse drugs, models of compulsive drug use – where individuals have a compulsive addiction
– have been amenable to testing in the laboratory. Studies at cellular and nerve-receptor levels are attempting to identify mechanisms of tolerance and dependence for several substances. Classical behaviour theory is a key model for understanding drug dependence. This and current laboratory studies are being used to explain the reinforcing nature of dependent substances and are helping to provide an explanatory framework for dependence. Drug consumption is a learned form of behaviour. Numerous investigators have used conditioning theories to study why people misuse drugs. Laboratory studies are now locating the ‘reward pathways’ in the brain for opiates and stimulants where positive reinforcing mechanisms involve particular sectors of the brain. There is a consensus among experts in addiction that addictive behaviour is amenable to e?ective treatment, and that the extent to which an addict complies with treatment makes it possible to predict a positive outcome. But there is a long way to go before the mechanisms of drug addiction are properly understood or ways of treating it generally agreed.
Effects of drugs Cannabis, derived from the plant Cannabis sativa, is a widely used recreational drug. Its two main forms are marijuana, which comes from the dried leaves, and hashish which comes from the resin. Cannabis may be used in food and drink but is usually smoked in cigarettes to induce relaxation and a feeling of well-being. Heavy use can cause apathy and vagueness and may even cause psychosis. Whether or not cannabis leads people to using harder drugs is arguable, and a national debate is underway on whether its use should be legalised for medicinal use. Cannabis may alleviate the symptoms of some disorders – for example, MULTIPLE SCLEROSIS (MS) – and there are calls to allow the substance to be classi?ed as a prescribable drug.
About one in ten of Britain’s teenagers misuses volatile substances such as toluene at some time, but only about one in 40 does so regularly. These substances are given o? by certain glues, solvents, varnishes, and liquid fuels, all of which can be bought cheaply in shops, although their sale to children under 16 is illegal. They are often inhaled from plastic bags held over the nose and mouth. Central-nervous-system excitation, with euphoria and disinhibition, is followed by depression and lethargy. Unpleasant effects include facial rash, nausea and vomiting, tremor, dizziness, and clumsiness. Death from COMA and acute cardiac toxicity is a serious risk. Chronic heavy use can cause peripheral neuropathy and irreversible cerebellar damage. (See SOLVENT ABUSE (MISUSE).)
The hallucinogenic or psychedelic drugs include LYSERGIC ACID DIETHYLAMIDE (LSD) or acid, magic mushrooms, ecstasy (MDMA), and phencyclidine (PCP or ‘angel’ dust, mainly used in the USA). These drugs have no medicinal uses. Taken by mouth, they produce vivid ‘trips’, with heightened emotions and perceptions and sometimes with hallucinations. They are not physically addictive but can cause nightmarish bad trips during use and ?ashbacks (vivid reruns of trips) after use, and can probably trigger psychosis and even death, especially if drugs are mixed or taken with alcohol.
Stimulant drugs such as amphetamine and cocaine act like adrenaline and speed up the central nervous system, making the user feel con?dent, energetic, and powerful for several hours. They can also cause severe insomnia, anxiety, paranoia, psychosis, and even sudden death due to convulsions or tachycardia. Depression may occur on withdrawal of these drugs, and in some users this is su?ciently deterrent to cause psychological dependence. Amphetamine (‘speed’) is mainly synthesised illegally and may be eaten, sni?ed, or injected. Related drugs, such as dexamphetamine sulphate (Dexedrine), are prescribed pills that enter the black market. ECSTASY is another amphetamine derivative that has become a popular recreational drug; it may have fatal allergic effects. Cocaine and related drugs are used in medicine as local anaesthetics. Illegal supplies of cocaine (‘snow’ or ‘ice’) and its derivative, ‘crack’, come mainly from South America, where they are made from the plant Erythroxylon coca. Cocaine is usually sni?ed (‘snorted’) or rubbed into the gums; crack is burnt and inhaled.
Opiate drugs are derived from the opium poppy, Papaver somniferum. They are described as narcotic because they induce sleep. Their main medical use is as potent oral or injectable analgesics such as MORPHINE, DIAMORPHINE, PETHIDINE HYDROCHLORIDE, and CODEINE. The commonest illegal opiate is heroin, a powdered form of diamorphine that may be smoked, sni?ed, or injected to induce euphoria and drowsiness. Regular opiate misuse leads to tolerance (the need to take ever larger doses to achieve the same e?ect) and marked dependence. A less addictive oral opiate, METHADONE HYDROCHLORIDE, can be prescribed as a substitute that is easier to withdraw.
Some 75,000–150,000 Britons now misuse opiates and other drugs intravenously, and pose a huge public-health problem because injections with shared dirty needles can carry the blood-borne viruses that cause AIDS/HIV and HEPATITIS B. Many clinics now operate schemes to exchange old needles for clean ones, free of charge. Many addicts are often socially disruptive.
For help and advice see APPENDIX 2: ADDRESSES: SOURCES OF INFORMATION, ADVICE, SUPPORT AND SELF-HELP – National Dugs Helpline.
(See ALCOHOL and TOBACCO for detailed entries on those subjects.)... dependence
Astigmatism (See ASTIGMATISM.)
Blepharitis A chronic in?ammation of the lid margins. SEBORRHOEA and staphylococcal infection are likely contributors. The eyes are typically intermittently red, sore and gritty over months or years. Treatment is di?cult and may fail. Measures to reduce debris on the lid margins, intermittent courses of topical antibiotics, steroids or systemic antibiotics may help the sufferer.
Blepharospasm Involuntary closure of the eye. This may accompany irritation but may also occur without an apparent cause. It may be severe enough to interfere with vision. Treatment involves removing the source of irritation, if present. Severe and persistent cases may respond to injection of Botulinum toxin into the orbicularis muscle.
Cataract A term used to describe any opacity in the lens of the eye, from the smallest spot to total opaqueness. The prevalence of cataracts is age-related: 65 per cent of individuals in their sixth decade have some degree of lens opacity, while all those over 80 are affected. Cataracts are the most important cause of blindness worldwide. Symptoms will depend on whether one or both eyes are affected, as well as the position and density of the cataract(s). If only one eye is developing a cataract, it may be some time before the person notices it, though reading may be affected. Some people with cataracts become shortsighted, which in older people may paradoxically ‘improve’ their ability to read. Bright light may worsen vision in those with cataracts.
The extent of visual impairment depends on the nature of the cataracts, and the ?rst symptoms noticed by patients include di?culty in recognising faces and in reading, while problems watching television or driving, especially at night, are pointers to the condition. Cataracts are common but are not the only cause of deteriorating vision. Patients with cataracts should be able to point to the position of a light and their pupillary reactions should be normal. If a bright light is shone on the eye, the lens may appear brown or, in advanced cataracts, white (see diagram).
While increasing age is the commonest cause of cataract in the UK, patients with DIABETES MELLITUS, UVEITIS and a history of injury to the eye can also develop the disorder. Prolonged STEROID treatment can result in cataracts. Children may develop cataracts, and in them the condition is much more serious as vision may be irreversibly impaired because development of the brain’s ability to interpret visual signals is hindered. This may happen even if the cataracts are removed, so early referral for treatment is essential. One of the physical signs which doctors look for when they suspect cataract in adults as well as in children is the ‘red re?ex’. This is observable when an ophthalmoscopic examination of the eye is made (see OPHTHALMOSCOPE). Identi?cation of this red re?ex (a re?ection of light from the red surface of the retina –see EYE) is a key diagnostic sign in children, especially young ones.
There is no e?ective medical treatment for established cataracts. Surgery is necessary and the decision when to operate depends mainly on how the cataract(s) affect(s) the patient’s vision. Nowadays, surgery can be done at any time with limited risk. Most patients with a vision of 6/18 – 6/10 is the minimum standard for driving – or worse in both eyes should
E
bene?t from surgery, though elderly people may tolerate visual acuity of 6/18 or worse, so surgery must be tailored to the individual’s needs. Younger people with a cataract will have more demanding visual requirements and so may opt for an ‘earlier’ operation. Most cataract surgery in Britain is now done under local anaesthetic and uses the ‘phaco-emulsi?cation’ method. A small hole is made in the anterior capsule of the lens after which the hard lens nucleus is liqui?ed ultrasonically. A replacement lens is inserted into the empty lens bag (see diagram). Patients usually return to their normal activities within a few days of the operation. A recent development under test in the USA for children requiring cataract operations is an intra-ocular ?exible implant whose magnifying power can be altered as a child develops, thus precluding the need for a series of corrective operations as happens now.
Chalazion A ?rm lump in the eyelid relating to a blocked meibomian gland, felt deep within the lid. Treatment is not always necessary; a proportion spontaneously resolve. There can be associated infection when the lid becomes red and painful requiring antibiotic treatment. If troublesome, the chalazion can be incised under local anaesthetic.
Conjunctivitis In?ammation of the conjunctiva (see EYE) which may affect one or both eyes. Typically the eye is red, itchy, sticky and gritty but is not usually painful. Redness is not always present. Conjunctivitis can occasionally be painful, particularly if there is an associated keratitis (see below) – for example, adenovirus infection, herpetic infection.
The cause can be infective (bacteria, viruses or CHLAMYDIA), chemical (e.g. acids, alkalis) or allergic (e.g. in hay fever). Conjunctivitis may also be caused by contact lenses, and preservatives or even the drugs in eye drops may cause conjunctival in?ammation. Conjunctivitis may addtionally occur in association with other illnesses – for example, upper-respiratory-tract infection, Stevens-Johnson syndrome (see ERYTHEMA – erythema multiforme) or REITER’S SYNDROME. The treatment depends on the cause. In many patients acute conjunctivitis is self-limiting.
Dacryocystitis In?ammation of the lacrimal sac. This may present acutely as a red, painful swelling between the nose and the lower lid. An abscess may form which points through the skin and which may need to be drained by incision. Systemic antibiotics may be necessary. Chronic dacryocystitis may occur with recurrent discharge from the openings of the tear ducts and recurrent swelling of the lacrimal sac. Obstruction of the tear duct is accompanied by watering of the eye. If the symptoms are troublesome, the patient’s tear passageways need to be surgically reconstructed.
Ectropion The lid margin is everted – usually the lower lid. Ectropion is most commonly associated with ageing, when the tissues of the lid become lax. It can also be caused by shortening of the skin of the lids such as happens with scarring or mechanical factors – for example, a tumour pulling the skin of the lower lid downwards. Ectropion tends to cause watering and an unsightly appearance. The treatment is surgical.
Entropion The lid margin is inverted – usually the lower lid. Entropion is most commonly associated with ageing, when the tissues of the lid become lax. It can also be caused by shortening of the inner surfaces of the lids due to scarring – for example, TRACHOMA or chemical burns. The inwardly directed lashes cause irritation and can abrade the cornea. The treatment is surgical.
Episcleritis In?ammation of the EPISCLERA. There is usually no apparent cause. The in?ammation may be di?use or localised and may affect one or both eyes. It sometimes recurs. The affected area is usually red and moderately painful. Episcleritis is generally not thought to be as painful as scleritis and does not lead to the same complications. Treatment is generally directed at improving the patient’s symptoms. The in?ammation may respond to NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS) or topical CORTICOSTEROIDS.
Errors of refraction (Ametropia.) These will occur when the focusing power of the lens and cornea does not match the length of the eye, so that rays of light parallel to the visual axis are not focused at the fovea centralis (see EYE). There are three types of refractive error: HYPERMETROPIA or long-sightedness. The refractive power of the eye is too weak, or the eye is too short so that rays of light are brought to a focus at a point behind the retina. Longsighted people can see well in the distance but generally require glasses with convex lenses for reading. Uncorrected long sight can lead to headaches and intermittent blurring of vision following prolonged close work (i.e. eye strain). As a result of ageing, the eye becomes gradually long-sighted, resulting in many people needing reading glasses in later life: this normal process is known as presbyopia. A particular form of long-sightedness occurs after cataract extraction (see above). MYOPIA(Short sight or near sight.) Rays of light are brought to a focus in front of the retina because the refractive power of the eye is too great or the eye is too short. Short-sighted people can see close to but need spectacles with concave lenses in order to see in the distance. ASTIGMATISMThe refractive power of the eye is not the same in each meridian. Some rays of light may be focused in front of the retina while others are focused on or behind the retina. Astigmatism can accompany hypermetropia or myopia. It may be corrected by cylindrical lenses: these consist of a slice from the side of a cylinder (i.e. curved in one meridian and ?at in the meridian at right-angles to it).
Keratitis In?ammation of the cornea in response to a variety of insults – viral, bacterial, chemical, radiation, or mechanical trauma. Keratitis may be super?cial or involve the deeper layers, the latter being generally more serious. The eye is usually red, painful and photophobic. Treatment is directed at the cause.
Nystagmus Involuntary rhythmic oscillation of one or both eyes. There are several causes including nervous disorders, vestibular disorders, eye disorders and certain drugs including alcohol.
Ophthalmia In?ammation of the eye, especially the conjunctiva (see conjunctivitis, above). Ophthalmia neonatorum is a type of conjunctivitis that occurs in newborn babies. They catch the disease when passing through an infected birth canal during their mother’s labour (see PREGNANCY AND LABOUR). CHLAMYDIA and GONORRHOEA are the two most common infections. Treatment is e?ective with antibiotics: untreated, the infection may cause permanent eye damage.
Pinguecula A benign degenerative change in the connective tissue at the nasal or temporal limbus (see EYE). This is visible as a small, ?attened, yellow-white lump adjacent to the cornea.
Pterygium Overgrowth of the conjunctival tissues at the limbus on to the cornea (see EYE). This usually occurs on the nasal side and is associated with exposure to sunlight. The pterygium is surgically removed for cosmetic reasons or if it is thought to be advancing towards the visual axis.
Ptosis Drooping of the upper lid. May occur because of a defect in the muscles which raise the lid (levator complex), sometimes the result of ageing or trauma. Other causes include HORNER’S SYNDROME, third cranial nerve PALSY, MYASTHENIA GRAVIS, and DYSTROPHIA MYOTONICA. The cause needs to be determined and treated if possible. The treatment for a severely drooping lid is surgical, but other measures can be used to prop up the lid with varying success.
Retina, disorders of The retina can be damaged by disease that affects the retina alone, or by diseases affecting the whole body.
Retinopathy is a term used to denote an abnormality of the retina without specifying a cause. Some retinal disorders are discussed below. DIABETIC RETINOPATHY Retinal disease occurring in patients with DIABETES MELLITUS. It is the commonest cause of blind registration in Great Britain of people between the ages of 20 and 65. Diabetic retinopathy can be divided into several types. The two main causes of blindness are those that follow: ?rst, development of new blood vessels from the retina, with resultant complications and, second, those following ‘water logging’ (oedema) of the macula. Treatment is by maintaining rigid control of blood-sugar levels combined with laser treatment for certain forms of the disease – in particular to get rid of new blood vessels. HYPERTENSIVE RETINOPATHY Retinal disease secondary to the development of high blood pressure. Treatment involves control of the blood pressure (see HYPERTENSION). SICKLE CELL RETINOPATHY People with sickle cell disease (see under ANAEYIA) can develop a number of retinal problems including new blood vessels from the retina. RETINOPATHY OF PREMATURITY (ROP) Previously called retrolental ?broplasia (RLF), this is a disorder affecting low-birth-weight premature babies exposed to oxygen. Essentially, new blood vessels develop which cause extensive traction on the retina with resultant retinal detachment and poor vision. RETINAL ARTERY OCCLUSION; RETINAL VEIN OCCLUSION These result in damage to those areas of retina supplied by the affected blood vessel: the blood vessels become blocked. If the peripheral retina is damaged the patient may be completely symptom-free, although areas of blindness may be detected on examination of ?eld of vision. If the macula is involved, visual loss may be sudden, profound and permanent. There is no e?ective treatment once visual loss has occurred. SENILE MACULAR DEGENERATION (‘Senile’ indicates age of onset and has no bearing on mental state.) This is the leading cause of blindness in the elderly in the western world. The average age of onset is 65 years. Patients initially notice a disturbance of their vision which gradually progresses over months or years. They lose the ability to recognise ?ne detail; for example, they cannot read ?ne print, sew, or recognise people’s faces. They always retain the ability to recognise large objects such as doors and chairs, and are therefore able to get around and about reasonably well. There is no e?ective treatment in the majority of cases. RETINITIS PIGMENTOSAA group of rare, inherited diseases characterised by the development of night blindness and tunnel vision. Symptoms start in childhood and are progressive. Many patients retain good visual acuity, although their peripheral vision is limited. One of the characteristic ?ndings on examination is collections of pigment in the retina which have a characteristic shape and are therefore known as ‘bone spicules’. There is no e?ective treatment. RETINAL DETACHMENTusually occurs due to the development of a hole in the retina. Holes can occur as a result of degeneration of the retina, traction on the retina by the vitreous, or injury. Fluid from the vitreous passes through the hole causing a split within the retina; the inner part of the retina becomes detached from the outer part, the latter remaining in contact with the choroid. Detached retina loses its ability to detect light, with consequent impairment of vision. Retinal detachments are more common in the short-sighted, in the elderly or following cataract extraction. Symptoms include spots before the eyes (?oaters), ?ashing lights and a shadow over the eye with progressive loss of vision. Treatment by laser is very e?ective if caught early, at the stage when a hole has developed in the retina but before the retina has become detached. The edges of the hole can be ‘spot welded’ to the underlying choroid. Once a detachment has occurred, laser therapy cannot be used; the retina has to be repositioned. This is usually done by indenting the wall of the eye from the outside to meet the retina, then making the retina stick to the wall of the eye by inducing in?ammation in the wall (by freezing it). The outcome of surgery depends largely on the extent of the detachment and its duration. Complicated forms of detachment can occur due to diabetic eye disease, injury or tumour. Each requires a specialised form of treatment.
Scleritis In?ammation of the sclera (see EYE). This can be localised or di?use, can affect the anterior or the posterior sclera, and can affect one or both eyes. The affected eye is usually red and painful. Scleritis can lead to thinning and even perforation of the sclera, sometimes with little sign of in?ammation. Posterior scleritis in particular may cause impaired vision and require emergency treatment. There is often no apparent cause, but there are some associated conditions – for example, RHEUMATOID ARTHRITIS, GOUT, and an autoimmune disease affecting the nasal passages and lungs called Wegener’s granulomatosis. Treatment depends on severity but may involve NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS), topical CORTICOSTEROIDS or systemic immunosuppressive drugs.
Stye Infection of a lash follicle. This presents as a painful small red lump at the lid margin. It often resolves spontaneously but may require antibiotic treatment if it persists or recurs.
Sub-conjunctival haemorrhage Haemorrhage between the conjunctiva and the underlying episclera. It is painless. There is usually no apparent cause and it resolves spontaneously.
Trichiasis Inward misdirection of the lashes. Trichiasis occurs due to in?ammation of or trauma to the lid margin. Treatment involves removal of the patient’s lashes. Regrowth may be prevented by electrolysis, by CRYOTHERAPY to the lid margin, or by surgery.
For the subject of arti?cial eyes, see under PROSTHESIS; also GLAUCOMA, SQUINT and UVEITIS.... eye, disorders of
Habitat: Distributed in Northwestern Himalayas.
English: Common Barberry, True Barberry.Ayurvedic: Daruharidraa (var.).Folk: Chatrod, Kashmal.Action: Root and bark—used for ailments of gastrointestinal tract, liver, gallbladder, kidney and urinary tract, respiratory tract, also as a febrifuge and blood purifier.
Key application: Listed by German Commission E among unapproved herbs.An extract with 80% berberine and additional alkaloids stimulated the bile secretion of rats by 72%. (PDR.) As cholagogue. (The British Herbal Pharmacopoeia.)The main alkaloid is berberine (well tolerated up to 0.5 g). Berries are safe.Bererine in small doses stimulates the respiratory system; poisonings have been observed from overdoses. Poisonings from the total herb have not been reported. (German Commission E.)Berberine is bactericidal, amoebici- dal and trypanocidal. Berberine is an- tidiarrhoeal, asitentersinto the cytosol or binds to the cell membrane and inhibits the catalytic unit of andenylate cyclase. It is active in vitro and in animals against cholera.Berberine stimulates bile secretion and shows sedative, hypotensive, anti- convulsant and uterine stimulant activity in animals. Alkaloid bermarine is also strongly antibacterial. It has been shown to increase white blood cell and platelet counts in animals with iatro- genic leukocytopaenia.Berberine, berbamine and jatror- rhizine are hypotensive and sedative.Many of the alkaloids are antineo- plastic.The alkaloid berbamine (50 mg three times daily for 1-4 weeks) helped reverse leukopaenia induced by benzene, cancer chemotherapy or radiotherapy in a clinical study. (Francis Brinker.)Berberine, when combined with pyrimethamine, was more effective than combinations with other antibiotics in treating chloroquine-resistant malaria. (Sharon M. Herr.)... berberis vulgarisThe cells produce the main constituents of MUCUS.... goblet cell
Habitat: Native to Central America, often cultivated in Madhya Pradesh and South India.
English: Annatto.Ayurvedic: Sinduri, Sinduriyaa.Siddha/Tamil: Jabara, Manjitti.Action: Plant—astringent, antibil- ious, antiemetic, blood purifier. Leaves—infusion is given in jaundice, also in dysentery. Externally, scar-preventive. Root bark— febrifuge, antiperiodic. Seed pulp— haemostatic, antidysenteric, diuretic, laxative. Fruit—antidysenteric.
An antimicrobial constituent, mas- linic acid, alongwith gallic acid and pyrogallol, has been isolated from the leaves. Alcoholic extract of the leaves completely inhibited Micrococcus pyo- genes, but was inactive against E. coli. The aqueous extract, however, showed partial inhibition against E. coli. The aqueous extract also showed potent inhibitory activity towards lens aldose re- ductase, which plays an important role in the management of diabetic complications. The activity is attributed to a flavonoid, isoscutelarein.Bixin, the main constituent of seed coat, shows cytostatic effect on the growth of human lymphoma cells. Bixin also has a hyperglycaemic effect and may disturb blood glucose control.... bixa orellanaArrhythmias 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
Tumours All masses cause varying combinations of headache and vomiting – symptoms of raised pressure within the inexpansible bony box formed by the skull; general or localised epileptic ?ts; weakness of limbs or disordered speech; and varied mental changes. Tumours may be primary, arising in the brain, or secondary deposits from tumours arising in the lung, breast or other organs. Some brain tumours are benign and curable by surgery: examples include meningiomas and pituitary tumours. The symptoms depend on the size and situation of the mass. Abscesses or blood clots (see HAEMATOMA) on the surface or within the brain may resemble tumours; some are removable. Gliomas ( see GLIOMA) are primary malignant tumours arising in the glial tissue (see GLIA) which despite surgery, chemotherapy and radiotherapy usually have a bad prognosis, though some astrocytomas and oligodendronogliomas are of low-grade malignancy. A promising line of research in the US (in the animal-testing stage in 2000) suggests that the ability of stem cells from normal brain tissue to ‘home in’ on gliomal cells can be turned to advantage. The stem cells were chemically manipulated to carry a poisonous compound (5-?uorouracil) to the gliomal cells and kill them, without damaging normal cells. Around 80 per cent of the cancerous cells in the experiments were destroyed in this way.
Clinical examination and brain scanning (CT, or COMPUTED TOMOGRAPHY; magnetic resonance imaging (MRI) and functional MRI) are safe, accurate methods of demonstrating the tumour, its size, position and treatability.
Strokes When a blood vessel, usually an artery, is blocked by a clot, thrombus or embolism, the local area of the brain fed by that artery is damaged (see STROKE). The resulting infarct (softening) causes a stroke. The cells die and a patch of brain tissue shrinks. The obstruction in the blood vessel may be in a small artery in the brain, or in a larger artery in the neck. Aspirin and other anti-clotting drugs reduce recurrent attacks, and a small number of people bene?t if a narrowed neck artery is cleaned out by an operation – endarterectomy. Similar symptoms develop abruptly if a blood vessel bursts, causing a cerebral haemorrhage. The symptoms of a stroke are sudden weakness or paralysis of the arm and leg of the opposite side to the damaged area of brain (HEMIPARESIS), and sometimes loss of half of the ?eld of vision to one side (HEMIANOPIA). The speech area is in the left side of the brain controlling language in right-handed people. In 60 per cent of lefthanders the speech area is on the left side, and in 40 per cent on the right side. If the speech area is damaged, diffculties both in understanding words, and in saying them, develops (see DYSPHASIA).
Degenerations (atrophy) For reasons often unknown, various groups of nerve cells degenerate prematurely. The illness resulting is determined by which groups of nerve cells are affected. If those in the deep basal ganglia are affected, a movement disorder occurs, such as Parkinson’s disease, hereditary Huntington’s chorea, or, in children with birth defects of the brain, athetosis and dystonias. Modern drugs, such as DOPAMINE drugs in PARKINSONISM, and other treatments can improve the symptoms and reduce the disabilities of some of these diseases.
Drugs and injury Alcohol in excess, the abuse of many sedative drugs and arti?cial brain stimulants – such as cocaine, LSD and heroin (see DEPENDENCE) – can damage the brain; the effects can be reversible in early cases. Severe head injury can cause localised or di?use brain damage (see HEAD INJURY).
Cerebral palsy Damage to the brain in children can occur in the uterus during pregnancy, or can result from rare hereditary and genetic diseases, or can occur during labour and delivery. Severe neurological illness in the early months of life can also cause this condition in which sti? spastic limbs, movement disorders and speech defects are common. Some of these children are learning-disabled.
Dementias In older people a di?use loss of cells, mainly at the front of the brain, causes ALZHEIMER’S DISEASE – the main feature being loss of memory, attention and reasoned judgement (dementia). This affects about 5 per cent of the over-80s, but is not simply due to ageing processes. Most patients require routine tests and brain scanning to indicate other, treatable causes of dementia.
Response to current treatments is poor, but promising lines of treatment are under development. Like Parkinsonism, Alzheimer’s disease progresses slowly over many years. It is uncommon for these diseases to run in families. Multiple strokes can cause dementia, as can some organic disorders such as cirrhosis of the liver.
Infections in the brain are uncommon. Viruses such as measles, mumps, herpes, human immunode?ciency virus and enteroviruses may cause ENCEPHALITIS – a di?use in?ammation (see also AIDS/HIV).
Bacteria or viruses may infect the membrane covering the brain, causing MENINGITIS. Viral meningitis is normally a mild, self-limiting infection lasting only a few days; however, bacterial meningitis – caused by meningococcal groups B and C, pneumococcus, and (now rarely) haemophilus – is a life-threatening condition. Antibiotics have allowed a cure or good control of symptoms in most cases of meningitis, but early diagnosis is essential. Severe headaches, fever, vomiting and increasing sleepiness are the principal symptoms which demand urgent advice from the doctor, and usually admission to hospital. Group B meningococcus is the commonest of the bacterial infections, but Group C causes more deaths. A vaccine against the latter has been developed and has reduced the incidence of cases by 75 per cent.
If infection spreads from an unusually serious sinusitis or from a chronically infected middle ear, or from a penetrating injury of the skull, an abscess may slowly develop. Brain abscesses cause insidious drowsiness, headaches, and at a late stage, weakness of the limbs or loss of speech; a high temperature is seldom present. Early diagnosis, con?rmed by brain scanning, is followed by antibiotics and surgery in hospital, but the outcome is good in only half of affected patients.
Cerebral oedema Swelling of the brain can occur after injury, due to engorgement of blood vessels or an increase in the volume of the extravascular brain tissue due to abnormal uptake of water by the damaged grey (neurons) matter and white (nerve ?bres) matter. This latter phenomenon is called cerebral oedema and can seriously affect the functioning of the brain. It is a particularly dangerous complication following injury because sometimes an unconscious person whose brain is damaged may seem to be recovering after a few hours, only to have a major relapse. This may be the result of a slow haemorrhage from damaged blood vessels raising intracranial pressure, or because of oedema of the brain tissue in the area surrounding the injury. Such a development is potentially lethal and requires urgent specialist treatment to alleviate the rising intracranial pressure: osmotic agents (see OSMOSIS) such as mannitol or frusemide are given intravenously to remove the excess water from the brain and to lower intracranial pressure, buying time for de?nitive investigation of the cranial damage.... brain, diseases of
Acute bronchitis is due to an acute infection – viral or bacterial – of the bronchi. This is distinguished from PNEUMONIA by the anatomical site involved: bronchitis affects the bronchi whilst pneumonia affects the lung tissue. The infection causes a productive cough, and fever. Secretions within airways sometimes lead to wheezing. Sometimes the speci?c causative organism may be identi?ed from the sputum. The illness is normally self-limiting but, if treatments are required, bacterial infections respond to a course of antibiotics.
Chronic bronchitis is a clinical diagnosis applied to patients with chronic cough and sputum production. For epidemiological studies it is de?ned as ‘cough productive of sputum on most days during at least three consecutive months for not less than two consecutive years’. Chronic bronchitis is classi?ed as a CHRONIC PULMONARY OBSTRUCTIVE DISEASE (COPD); chronic ASTHMA and EMPHYSEMA are the others.
In the past, industrial workers regularly exposed to heavily polluted air commonly developed bronchitis. The main aetiological factor is smoking; this leads to an increase in size and number of bronchial mucous glands. These are responsible for the excessive mucus production within the bronchial tree, causing a persistent productive cough. The increased number of mucous glands along with the in?ux of in?ammatory cells may lead to airway-narrowing: when airway-narrowing occurs, it slows the passage of air, producing breathlessness. Other less important causative factors include exposure to pollutants and dusts. Infections do not cause the disease but frequently produce exacerbations with worsening of symptoms.
Treatments involve the use of antibiotics to treat the infections that produce exacerbations of symptoms. Bronchodilators (drugs that open up the airways) help to reverse the airway-narrowing that causes the breathlessness. PHYSIOTHERAPY is of value in keeping the airways clear of MUCUS. Cessation of smoking reduces the speed of progression.... bronchitis
Habitat: Western temperate Himalayas from 2,500 to 4,000 m.
English: American cowslip, Marsh Marigold, Water Buttercup.Folk: Mamiri (Punjab).Family: Theaceae.Habitat: Cultivated in Assam, Darjeeling, Travancore, the Nilgiris, Malabar, Bengal, Dehra Dun and Kumaon.
English: Tea.Unani: Chaai, Shaahi, Shaayi.Siddha/Tamil: Thaeyilai.Action: Stimulant, diuretic, astringent. In China, used for diarrhoea and dysentery (causes gastrointestinal upsets and nervous irritability when consumed in excess). Green tea: anticancer effects have been observed in Chinese green tea, Camellia thea, extract; the extract of Japanese green tea showed antihepatotoxic effects.
Important constituents of leaf buds and very young leaves are: caffeine, with a much smaller amount of other xanthines (theophylline and theo- bromine); tannins (the main tannin in green tea is (-)-epigallocatechin); flavonoids, quercetin, kaempferol. The stimulant and diuretic are due to caffeine content, the astringency due to the tannins.Drinking tea lowers thiamine and thiamine diphosphate losses in urine and blood serum respectively but increases niacin losses. Hot water extract of black tea facilitates Ca absorption in the body experimentally. Tea may decrease zinc bioavailability.The tea, if added to the meal, significantly lower the availability of iron. Milk is as effective as ascorbic acid in countering the depressing effect of tea on iron availability (in vitro).The green tea catechin inhibited car- cinogenesis in small intestines when given during or after carcinogen treatment to experimental rats. (-)-epi- gallocatechin gallate and theaflavin di- gallate from green tea inhibited the in- fectivity of both influenza A and B virus (in vitro).Green tea, when added to a lard- cholesterol diet, decreased the cholesterol and triglyceride levels in fowls. Tea polyphenols exhibit hypocholes- terolaemic activity.Tea polyphenols—(-)-epicatechin gallate, (-)-epigallocatechine galate, theaflavin monogallate A or B, and or theaflavin digallate—are used for treating hyperglycaemia.Saponins from tea are used as an- tiulcer agents.Concurrent use of tea and beta- adrenergic agonists may increase the risk of cardiac arrhythmias. Caffeine, a component of tea, may increase insulin resistance. (Sharon M. Herr.)... camellia sinensis
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