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
Nutritional Profile Energy value (calories per serving): Moderate Protein: High Fat: Low Saturated fat: Low Cholesterol: None Carbohydrates: High Fiber: Very high Sodium: Low Major vitamin contribution: Vitamin B6, folate Major mineral contribution: Iron, magnesium, zinc
About the Nutrients in This Food Beans are seeds, high in complex carbohydrates including starch and dietary fiber. They have indigestible sugars (stachyose and raffinose), plus insoluble cellulose and lignin in the seed covering and soluble gums and pectins in the bean. The proteins in beans are limited in the essential amino acids methionine and cystine.* All beans are a good source of the B vitamin folate, and iron. One-half cup canned kidney beans has 7.5 g dietary fiber, 65 mcg folate (15 percent of the R DA), and 1.6 mg iron (11 percent of the R DA for a woman, 20 percent of the R DA for a man). Raw beans contain antinutrient chemicals that inactivate enzymes required to digest proteins and carbohydrates. They also contain factors that inactivate vitamin A and also hemagglutinins, substances that make red blood cells clump together. Cooking beans disarms the enzyme inhibi- tors and the anti-vitamin A factors, but not the hemagglutinins. However, the amount of hemagglutinins in the beans is so small that it has no mea- surable effect in your body. * Soybeans are t he only beans t hat contain proteins considered “complete” because t hey contain sufficient amounts of all t he essent ial amino acids. The Folate Content of ½ Cup Cooked Dried Beans
Bean | Folate (mcg) |
Black beans | 129 |
Chickpeas | 191 |
Kidney beans canned | 65 |
Navy beans | 128 |
Pinto beans | 147 |
The Most Nutritious Way to Serve This Food Cooked, to destroy antinutrients. With grains. The proteins in grains are deficient in the essential amino acids lysine and isoleucine but contain sufficient tryptophan, methionine, and cystine; the proteins in beans are exactly the opposite. Together, these foods provide “complete” proteins. With an iron-rich food (meat) or with a vitamin C-rich food (tomatoes). Both enhance your body’s ability to use the iron in the beans. The meat makes your stomach more acid (acid favors iron absorption); the vitamin C may convert the ferric iron in beans into ferrous iron, which is more easily absorbed by the body.
Diets That May Restrict or Exclude This Food Low-calcium diet Low-fiber diet Low-purine (antigout) diet
Buying This Food Look for: Smooth-skinned, uniformly sized, evenly colored beans that are free of stones and debris. The good news about beans sold in plastic bags is that the transparent material gives you a chance to see the beans inside; the bad news is that pyridoxine and pyridoxal, the natural forms of vitamin B6, are very sensitive to light. Avoid: Beans sold in bulk. Some B vitamins, such as vitamin B6 (pyridoxine and pyridoxal), are very sensitive to light. In addition, open bins allow insects into the beans, indicated by tiny holes showing where the bug has burrowed into or through the bean. If you choose to buy in bulk, be sure to check for smooth skinned, uniformly sized, evenly colored beans free of holes, stones, and other debris.
Storing This Food Store beans in air- and moistureproof containers in a cool, dark cabinet where they are pro- tected from heat, light, and insects.
Preparing This Food Wash dried beans and pick them over carefully, discarding damaged or withered beans and any that float. (Only withered beans are light enough to float in water.) Cover the beans with water, bring them to a boil, and then set them aside to soak. When you are ready to use the beans, discard the water in which beans have been soaked. Some of the indigestible sugars in the beans that cause intestinal gas when you eat the beans will leach out into the water, making the beans less “gassy.”
What Happens When You Cook This Food When beans are cooked in liquid, their cells absorb water, swell, and eventually rupture, releasing the pectins and gums and nutrients inside. In addition, cooking destroys antinutri- ents in beans, making them more nutritious and safe to eat.
How Other Kinds of Processing Affect This Food Canning. The heat of canning destroys some of the B vitamins in the beans. Vitamin B is water-soluble. You can recover all the lost B vitamins simply by using the liquid in the can, but the liquid also contains the indigestible sugars that cause intestinal gas when you eat beans. Preprocessing. Preprocessed dried beans have already been soaked. They take less time to cook but are lower in B vitamins.
Medical Uses and/or Benefits Lower risk of some birth defects. As many as two of every 1,000 babies born in the United States each year may have cleft palate or a neural tube (spinal cord) defect due to their moth- ers’ not having gotten adequate amounts of folate during pregnancy. The current R DA for folate is 180 mcg for a woman and 200 mcg for a man, but the FDA now recommends 400 mcg for a woman who is or may become pregnant. Taking a folate supplement before becoming pregnant and continuing through the first two months of pregnancy reduces the risk of cleft palate; taking folate through the entire pregnancy reduces the risk of neural tube defects. Lower risk of heart attack. In the spring of 1998, an analysis of data from the records for more than 80,000 women enrolled in the long-run ning Nurses Health Study at Har vard School of Public Health/ Brigham and Woman’s Hospital in Boston demonstrated that a diet providing more than 400 mcg folate and 3 mg vitamin B6 a day from either food or supple- ments, more than t wice the current R DA for each, may reduce a woman’s risk of heart attack by almost 50 percent. A lthough men were not included in the analysis, the results are assumed to apply to them as well. NOT E : Beans are high in B6 as well as folate. Fruit, green leaf y vegetables, whole grains, meat, fish, poultr y, and shellfish are good sources of vitamin B6. To reduce the levels of serum cholesterol. The gums and pectins in dried beans and peas appear to lower blood levels of cholesterol. Currently there are two theories to explain how this may happen. The first theory is that the pectins in the beans form a gel in your stomach that sops up fats and keeps them from being absorbed by your body. The second is that bacteria in the gut feed on the bean fiber, producing short-chain fatty acids that inhibit the production of cholesterol in your liver. As a source of carbohydrates for people with diabetes. Beans are digested very slowly, produc- ing only a gradual rise in blood-sugar levels. As a result, the body needs less insulin to control blood sugar after eating beans than after eating some other high-carbohydrate foods (such as bread or potato). In studies at the University of Kentucky, a bean, whole-grain, vegetable, and fruit-rich diet developed at the University of Toronto enabled patients with type 1 dia- betes (who do not produce any insulin themselves) to cut their daily insulin intake by 38 percent. Patients with type 2 diabetes (who can produce some insulin) were able to reduce their insulin injections by 98 percent. This diet is in line with the nutritional guidelines of the American Diabetes Association, but people with diabetes should always consult with their doctors and/or dietitians before altering their diet. As a diet aid. Although beans are high in calories, they are also high in bulk (fiber); even a small serving can make you feel full. And, because they are insulin-sparing, they delay the rise in insulin levels that makes us feel hungry again soon after eating. Research at the University of Toronto suggests the insulin-sparing effect may last for several hours after you eat the beans, perhaps until after the next meal.
Adverse Effects Associated with This Food Intestinal gas. All legumes (beans and peas) contain raffinose and stachyose, complex sug- ars that human beings cannot digest. The sugars sit in the gut and are fermented by intestinal bacteria which then produce gas that distends the intestines and makes us uncomfortable. You can lessen this effect by covering the beans with water, bringing them to a boil for three to five minutes, and then setting them aside to soak for four to six hours so that the indigestible sugars leach out in the soaking water, which can be discarded. Alternatively, you may soak the beans for four hours in nine cups of water for every cup of beans, discard the soaking water, and add new water as your recipe directs. Then cook the beans; drain them before serving. Production of uric acid. Purines are the natural metabolic by-products of protein metabo- lism in the body. They eventually break down into uric acid, sharp cr ystals that may concentrate in joints, a condition known as gout. If uric acid cr ystals collect in the urine, the result may be kidney stones. Eating dried beans, which are rich in proteins, may raise the concentration of purines in your body. Although controlling the amount of purines in the diet does not significantly affect the course of gout (which is treated with allopurinol, a drug that prevents the formation of uric acid cr ystals), limiting these foods is still part of many gout regimens.
Food/Drug Interactions Monoamine oxidase (MAO) inhibitors. Monoamine oxidase inhibitors are drugs used to treat depression. They inactivate naturally occurring enzymes in your body that metabolize tyramine, a substance found in many fermented or aged foods. Tyramine constricts blood vessels and increases blood pressure. If you eat a food containing tyramine while you are taking an M AO inhibitor, you cannot effectively eliminate the tyramine from your body. The result may be a hypertensive crisis. Some nutrition guides list dried beans as a food to avoid while using M AO inhibitors.... beans
Nutritional Profile Energy value (calories per serving): Moderate to high Protein: Moderate to high Fat: Low to high Saturated fat: High Cholesterol: Low to high Carbohydrates: Low Fiber: None Sodium: High Major vitamin contribution: Vitamin A, vitamin D, B vitamins Major mineral contribution: Calcium
About the Nutrients in This Food Cheese making begins when Lactobacilli and/or Streptococci bacteria are added to milk. The bacteria digest lactose (milk sugar) and release lactic acid, which coagulates casein (milk protein) into curds. Rennet (gastric enzymes extracted from the stomach of calves) is added, and the mixture is put aside to set. The longer the curds are left to set, the firmer the cheese will be. When the curds are properly firm, they are pressed to squeeze out the whey (liquid) and cooked. Cooking evaporates even more liquid and makes the cheese even firmer.* At this point, the product is “fresh” or “green” cheese: cottage cheese, cream cheese, farmer cheese. Making “ripe” cheese requires the addition of salt to pull out more moisture and specific organisms, such as Penicil- lium roquefort for Roquefort cheese, blue cheese, and Stilton, or Penicillium cambembert for Camembert and Brie. The nutritional value of cheese is similar to the milk from which it is made. All cheese is a good source of high quality proteins with sufficient amounts of all the essential amino acids. Cheese is low to high in fat, mod- erate to high in cholesterol. * Natural cheese is cheese made direct ly from milk. Processed cheese is natural cheese melted and combined wit h emulsifiers. Pasteurized process cheese foods contain ingredients t hat allow t hem to spread smoot hly; t hey are lower in fat and higher in moisture t han processed cheese. Cholesterol and Saturated Fat Content of Selected Cheeses Mozzarella Source: USDA, Nutritive Value of Foods, Home and Garden Bullet in No. 72 (USDA, 1989). All cheeses, except cottage cheese, are good sources of vitamin A. Orange and yellow cheeses are colored with carotenoid pigments, including bixin (the carotenoid pigment in annatto) and synthetic beta-carotene. Hard cheeses are an excellent source of calcium; softer cheeses are a good source; cream cheese and cottage cheese are poor sources. The R DA for calcium is 1,000 mg for a woman, 1,200 mg for a man, and 1,500 mg for an older woman who is not on hormone- replacement therapy. All cheese, unless otherwise labeled, is high in sodium.
Calcium Content of Cheese | ||
Cheese | Serving | Calcium (mg) |
Blue | oz. | 150 |
Camembert | wedge | 147 |
Cheddar | oz. | 204 |
Cottage cheese | ||
creamed | cup | 135 |
uncreamed | cup | 46 |
Muenster | oz. | 203 |
Pasteurized processed American | oz. | 174 |
Parmesan grated | tbsp. | 69 |
Provolone | oz. | 214 |
Swiss | oz. | 272 |
The Most Nutritious Way to Serve This Food With grains, bread, noodles, beans, nuts, or vegetables to add the essential amino acids miss- ing from these foods, “complete” their proteins, and make them more nutritionally valuable.
Diets That May Restrict or Exclude This Food Antiflatulence diet Controlled-fat, low-cholesterol diet Lactose- and galactose-free diet (lactose, a disaccharide [double sugar] is composed of one unit of galactose and one unit of glucose) Low-calcium diet (for patients with kidney disease) Sucrose-free diet (processed cheese)
Buying This Food Look for: Cheese stored in a refrigerated case. Check the date on the package. Avoid: Any cheese with mold that is not an integral part of the food.
Storing This Food Refrigerate all cheese except unopened canned cheeses (such as Camembert in tins) or grated cheeses treated with preservatives and labeled to show that they can be kept outside the refrigerator. Some sealed packages of processed cheeses can be stored at room temperature but must be refrigerated once the package is opened. Wrap cheeses tightly to protect them from contamination by other microorganisms in the air and to keep them from drying out. Well-wrapped, refrigerated hard cheeses that have not been cut or sliced will keep for up to six months; sliced hard cheeses will keep for about two weeks. Soft cheeses (cottage cheese, ricotta, cream cheese, and Neufchatel) should be used within five to seven days. Use all packaged or processed cheeses by the date stamped on the package. Throw out moldy cheese (unless the mold is an integral part of the cheese, as with blue cheese or Stilton).
Preparing This Food To grate cheese, chill the cheese so it won’t stick to the grater. The molecules that give cheese its taste and aroma are largely immobilized when the cheese is cold. When serving cheese with fruit or crackers, bring it to room temperature to activate these molecules.
What Happens When You Cook This Food Heat changes the structure of proteins. The molecules are denatured, which means that they may be broken into smaller fragments or change shape or clump together. All of these changes may force moisture out of the protein tissue, which is why overcooked cheese is often stringy. Whey proteins, which do not clump or string at low temperatures, contain the sulfur atoms that give hot or burned cheese an unpleasant “cooked” odor. To avoid both strings and an unpleasant odor, add cheese to sauces at the last minute and cook just long enough to melt the cheese.
How Other Kinds of Processing Affect This Food Freezing. All cheese loses moisture when frozen, so semisoft cheeses will freeze and thaw better than hard cheeses, which may be crumbly when defrosted. Drying. The less moisture cheese contains, the less able it is to support the growth of organ- isms like mold. Dried cheeses keep significantly longer than ordinary cheeses.
Medical Uses and/or Benefits To strengthen bones and reduce age-related loss of bone density. High-calcium foods protect bone density. The current recommended dietary allowance (R DA) for calcium is still 800 mg for adults 25 and older, but a 1984 National Institutes of Health (NIH) Conference advisory stated that lifelong protection for bones requires an R DA of 1,000 mg for healthy men and women age 25 to 50 ; 1,000 mg for older women using hormone replacement therapy; and 1,500 mg for older women who are not using hormones, and these recommendations have been confirmed in a 1994 NIH Consensus Statement on optimal calcium intake. A diet with adequate amounts of calcium-rich foods helps protect bone density. Low-fat and no-fat cheeses provide calcium without excess fat and cholesterol. Protection against tooth decay. Studies at the University of Iowa (Iowa City) Dental School confirm that a wide variety of cheeses, including aged cheddar, Edam, Gouda, Monterey Jack, Muenster, mozzarella, Port Salut, Roquefort, Romano, Stilton, Swiss, and Tilsit—limit the tooth decay ordinarily expected when sugar becomes trapped in plaque, the sticky film on tooth surfaces where cavity-causing bacteria flourish. In a related experiment using only cheddar cheese, people who ate cheddar four times a day over a two-week period showed a 20 percent buildup of strengthening minerals on the surface of synthetic toothlike material attached to the root surfaces of natural teeth. Protection against periodontal disease. A report in the January 2008 issue of the Journal of Periodontology suggests that consuming adequate amounts of dairy products may reduce the risk of developing periodontal disease. Examining the dental health of 942 subjects ages 40 to 79, researchers at Kyushu University, in Japan, discovered that those whose diets regularly included two ounces (55 g) of foods containing lactic acid (milk, cheese, and yogurt) were significantly less likely to have deep “pockets” (loss of attachment of tooth to gum) than those who consumed fewer dairy products.
Adverse Effects Associated with This Food Increased risk of heart disease. Like other foods from animals, cheese is a source of choles- terol and saturated fats, which increase the amount of cholesterol circulating in your blood and raise your risk of heart disease. To reduce the risk of heart disease, the USDA /Health and Human Services Dietary Guidelines for Americans recommends limiting the amount of cholesterol in your diet to no more than 300 mg a day. The guidelines also recommend limit- ing the amount of fat you consume to no more than 30 percent of your total calories, while holding your consumption of saturated fats to more than 10 percent of your total calories (the calories from saturated fats are counted as part of the total calories from fat). Food poisoning. Cheese made from raw (unpasteurized) milk may contain hazardous microorganisms, including Salmonella and Listeria. Salmonella causes serious gastric upset; Lis- teria, a flulike infection, encephalitis, or blood infection. Both may be life-threatening to the very young, the very old, pregnant women, and those whose immune systems are weakened either by illness (such as AIDS) or drugs (such as cancer chemotherapy). In 1998, the Federal Centers for Disease Control (CDC) released data identif ying Listeria as the cause of nearly half the reported deaths from food poisoning. Allergy to milk proteins. Milk is one of the foods most frequently implicated as a cause of allergic reactions, particularly upset stomach. However, in many cases the reaction is not a true allergy but the result of lactose intolerance (see below). Lactose intolerance. Lactose intolerance—the inability to digest the sugar in milk—is an inherited metabolic deficiency that affects two thirds of all adults, including 90 to 95 percent of all Orientals, 70 to 75 percent of all blacks, and 6 to 8 percent of Caucasians. These people do not have sufficient amounts of lactase, the enzyme that breaks the disaccharide lactose into its easily digested components, galactose and glucose. When they drink milk, the undi- gested sugar is fermented by bacteria in the gut, causing bloating, diarrhea, flatulence, and intestinal discomfort. Some milk is now sold with added lactase to digest the lactose and make the milk usable for lactase-deficient people. In making cheese, most of the lactose in milk is broken down into glucose and galactose. There is very little lactose in cheeses other than the fresh ones—cottage cheese, cream cheese, and farmer cheese. Galactosemia. Galactosemia is an inherited metabolic disorder in which the body lacks the enzymes needed to metabolize galactose, a component of lactose. Galactosemia is a reces- sive trait; you must receive the gene from both parents to develop the condition. Babies born with galactosemia will fail to thrive and may develop brain damage or cataracts if they are given milk. To prevent this, children with galactosemia are usually kept on a protective milk- free diet for several years, until their bodies have developed alternative pathways by which to metabolize galactose. Pregnant women who are known carriers of galactosemia may be advised to give up milk and milk products while pregnant lest the unmetabolized galactose in their bodies cause brain damage to the fetus (damage not detectable by amniocentesis). Genetic counseling is available to identif y galactosemia carriers and assess their chances of producing a baby with the disorder. Penicillin sensitivity. People who experience a sensitivity reaction the first time they take penicillin may have been sensitized by exposure to the Penicillium molds in the environment, including the Penicillium molds used to make brie, blue, camembert, roquefort, Stilton, and other “blue” cheeses.
Food/Drug Interactions Tetracycline. The calcium ions in milk products, including cheese, bind tetracyclines into insoluble compounds. If you take tetracyclines with cheese, your body may not be able to absorb and use the drug efficiently. Monoamine oxidase (MAO) inhibitors. Monoamine oxidase inhibitors are drugs used to treat depression. They inactivate naturally occurring enzymes in your body that metabolize tyra- mine, a substance found in many fermented or aged foods. Tyramine constricts blood ves- sels and increases blood pressure. If you eat a food such as aged or fermented cheese which is high in tyramine while you are taking an M AO inhibitor, your body may not be able to eliminate the tyramine. The result may be a hypertensive crisis.
Tyramine Content of Cheeses High Boursault, Camembert, Cheddar, Emmenthaler, Stilton Medium to high Blue, brick, Brie, Gruyère, mozzarella, Parmesan, Romano, Roquefort Low Processed American cheese Very little or none Cottage and cream cheese Sources: The Medical Letter Handbook of Adverse Drug Interactions (1985); Handbook of Clinical Dietetics ( The A merican Dietet ic Associat ion, 1981). False-positive test for pheochromocytoma. Pheochromocytomas (tumors of the adrenal glands) secrete adrenalin that is converted by the body to vanillyl-mandelic acid ( VM A) and excreted in the urine. Tests for this tumor measure the level of VM A in the urine. Since cheese contains VM A, taking the test after eating cheese may result in a false-positive result. Ordinarily, cheese is prohibited for at least 72 hours before this diagnostic test.... cheese
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
Rarely, an enlarged gland may be the result of cancer in the thyroid.
Treatment A symptomless goitre may gradually disappear or be so small as not to merit treatment. If the goitre is large or is causing the patient di?culty in swallowing or breathing, it may need surgical removal by partial or total thyroidectomy. If the patient is de?cient in iodine, ?sh and iodised salt should be included in the diet.
Hyperthyroidism is a common disorder affecting 2–5 per cent of all females at some time in their lives. The most common cause – around 75 per cent of cases – is thyrotoxicosis (see below). An ADENOMA (or multiple adenomas) or nodules in the thyroid also cause hyperthyroidism. There are several other rare causes, including in?ammation caused by a virus, autoimune reactions and cancer. The symptoms of hyperthyroidism affect many of the body’s systems as a consequence of the much-increased metabolic rate.
Thyrotoxicosis is a syndrome consisting of di?use goitre (enlarged thyroid gland), over-activity of the gland and EXOPHTHALMOS (protruding eyes). Patients lose weight and develop an increased appetite, heat intolerance and sweating. They are anxious, irritable, hyperactive, suffer from TACHYCARDIA, breathlessness and muscle weakness and are sometimes depressed. The hyperthyroidism is due to the production of ANTIBODIES to the TSH receptor (see THYROTROPHIN-STIMULATING HORMONE (TSH)) which stimulate the receptor with resultant production of excess thyroid hormones. The goitre is due to antibodies that stimulate the growth of the thyroid gland. The exoph-
thalmos is due to another immunoglobulin called the ophthalmopathic immunoglobulin, which is an antibody to a retro-orbital antigen on the surface of the retro-orbital EYE muscles. This provokes in?ammation in the retro-orbital tissues which is associated with the accumulation of water and mucopolysaccharide which ?lls the orbit and causes the eye to protrude forwards.
Although thyrotoxicosis may affect any age-group, the peak incidence is in the third decade. Females are affected ten times as often as males; the prevalence in females is one in 500. As with many other autoimmune diseases, there is an increased prevalence of autoimmune thyroid disease in the relatives of patients with thyrotoxicosis. Some of these patients may have hypothyroidism (see below) and others, thyrotoxicosis. Patients with thyrotoxicosis may present with a goitre or with the eye signs or, most commonly, with the symptoms of excess thyroid hormone production. Thyroid hormone controls the metabolic rate of the body so that the symptoms of hyperthyroidism are those of excess metabolism.
The diagnosis of thyrotoxicosis is con?rmed by the measurement of the circulating levels of the two thyroid hormones, thyroxine and TRIIODOTHYRONINE.
Treatment There are several e?ective treatments for thyrotoxicosis. ANTITHYROID DRUGS These drugs inhibit the iodination of tyrosine and hence the formation of the thyroid hormones. The most commonly used drugs are carbimazole and propylthiouricil: these will control the excess production of thyroid hormones in virtually all cases. Once the patient’s thyroid is functioning normally, the dose can be reduced to a maintenance level and is usually continued for two years. The disadvantage of antithyroid drugs is that after two years’ treatment nearly half the patients will relapse and will then require more de?nitive therapy. PARTIAL THYROIDECTOMY Removal of three-quarters of the thyroid gland is e?ective treatment of thyrotoxicosis. It is the treatment of choice in those patients with large goitres. The patient must however be treated with medication so that they are euthyroid (have a normally functioning thyroid) before surgery is undertaken, or thyroid crisis and cardiac arrhythmias may complicate the operation. RADIOACTIVE IODINE THERAPY This has been in use for many years, and is an e?ective means of controlling hyperthyroidism. One of the disadvantages of radioactive iodine is that the incidence of hypothyroidism is much greater than with other forms of treatment. However, the management of hypothyroidism is simple and requires thyroxine tablets and regular monitoring for hypothyroidism. There is no evidence of any increased incidence of cancer of the thyroid or LEUKAEMIA following radio-iodine therapy. It has been the pattern in Britain to reserve radio-iodine treatment to those over the age of 35, or those whose prognosis is unlikely to be more than 30 years as a result of cardiac or respiratory disease. Radioactive iodine treatment should not be given to a seriously thyrotoxic patient. BETA-ADRENOCEPTOR-BLOCKING DRUGS Usually PROPRANOLOL HYDROCHLORIDE: useful for symptomatic treatment during the ?rst 4–8 weeks until the longer-term drugs have reduced thyroid activity.
Hypothyroidism A condition resulting from underactivity of the thyroid gland. One form, in which the skin and subcutaneous tissues thicken and result in a coarse appearance, is called myxoedema. The thyroid gland secretes two hormones – thyroxine and triiodothyronine – and these hormones are responsible for the metabolic activity of the body. Hypothyroidism may result from developmental abnormalities of the gland, or from a de?ciency of the enzymes necessary for the synthesis of the hormones. It may be a feature of endemic goitre and retarded development, but the most common cause of hypothyroidism is the autoimmune destruction of the thyroid known as chronic thyroiditis. It may also occur as a result of radio-iodine treatment of thyroid overactivity (see above) and is occasionally secondary to pituitary disease in which inadequate TSH production occurs. It is a common disorder, occurring in 14 per 1,000 females and one per 1,000 males. Most patients present between the age of 30 and 60 years.
Symptoms As thyroid hormones are responsible for the metabolic rate of the body, hypothyroidism usually presents with a general sluggishness: this affects both physical and mental activities. The intellectual functions become slow, the speech deliberate and the formation of ideas and the answers to questions take longer than in healthy people. Physical energy is reduced and patients frequently complain of lethargy and generalised muscle aches and pains. Patients become intolerant of the cold and the skin becomes dry and swollen. The LARYNX also becomes swollen and gives rise to a hoarseness of the voice. Most patients gain weight and develop constipation. The skin becomes dry and yellow due to the presence of increased carotene. Hair becomes thinned and brittle and even baldness may develop. Swelling of the soft tissues may give rise to a CARPAL TUNNEL SYNDROME and middle-ear deafness. The diagnosis is con?rmed by measuring the levels of thyroid hormones in the blood, which are low, and of the pituitary TSH which is raised in primary hypothyroidism.
Treatment consists of the administration of thyroxine. Although tri-iodothyronine is the metabolically active hormone, thyroxine is converted to tri-iodothyronine by the tissues of the body. Treatment should be started cautiously and slowly increased to 0·2 mg daily – the equivalent of the maximum output of the thyroid gland. If too large a dose is given initially, palpitations and tachycardia are likely to result; in the elderly, heart failure may be precipitated.
Congenital hypothyroidism Babies may be born hypothyroid as a result of having little or no functioning thyroid-gland tissue. In the developed world the condition is diagnosed by screening, all newborn babies having a blood test to analyse TSH levels. Those found positive have a repeat test and, if the diagnosis is con?rmed, start on thyroid replacement therapy within a few weeks of birth. As a result most of the ill-effects of cretinism can be avoided and the children lead normal lives.
Thyroiditis In?ammation of the thyroid gland. The acute form is usually caused by a bacterial infection elsewhere in the body: treatment with antibiotics is needed. Occasionally a virus may be the infectious agent. Hashimoto’s thyroiditis is an autoimmune disorder causing hypothyroidism (reduced activity of the gland). Subacute thyroiditis is in?ammation of unknown cause in which the gland becomes painful and the patient suffers fever, weight loss and malaise. It sometimes lasts for several months but is usually self-limiting.
Thyrotoxic adenoma A variety of thyrotoxicosis (see hyperthyroidism above) in which one of the nodules of a multinodular goitre becomes autonomous and secretes excess thyroid hormone. The symptoms that result are similar to those of thyrotoxicosis, but there are minor di?erences.
Treatment The ?rst line of treatment is to render the patient euthyroid by treatment with antithyroid drugs. Then the nodule should be removed surgically or destroyed using radioactive iodine.
Thyrotoxicosis A disorder of the thyroid gland in which excessive amounts of thyroid hormones are secreted into the bloodstream. Resultant symptoms are tachycardia, tremor, anxiety, sweating, increased appetite, weight loss and dislike of heat. (See hyperthyroidism above.)... goitre
K
Diagram of glomerulus (Malpighian corpuscle).
Fortunately the body has two kidneys and, as most people can survive on one, there is a good ‘functional reserve’ of kidney tissue.
Symptoms Many patients with kidney disorders do not have any symptoms, even when the condition is quite advanced. However,
others experience loin pain associated with obstruction (renal colic) or due to infection; fevers; swelling (oedema), usually of the legs but occasionally including the face and arms; blood in the urine (haematuria); and excess quantities of urine (polyuria), including at night (nocturia), due to failure of normal mechanisms in the kidney for concentrating urine. Patients with chronic renal failure often have very di?use symptoms including nausea and vomiting, tiredness due to ANAEMIA, shortness of breath, skin irritation, pins and needles (paraesthesia) due to damage of the peripheral nerves (peripheral neuropathy), and eventually (rarely seen nowadays) clouding of consciousness and death.
Signs of kidney disease include loin tenderness, enlarged kidneys, signs of ?uid retention, high blood pressure and, in patients with end-stage renal failure, pallor, pigmentation and a variety of neurological signs including absent re?exes, reduced sensation, and a coarse ?apping tremor (asterixis) due to severe disturbance of the body’s normal metabolism.
Renal failure Serious kidney disease may lead to impairment or failure of the kidney’s ability to ?lter waste products from the blood and excrete them in the urine – a process that controls the body’s water and salt balance and helps to maintain a stable blood pressure. Failure of this process causes URAEMIA – an increase in urea and other metabolic waste products – as well as other metabolic upsets in the blood and tissues, all of which produce varying symptoms. Failure can be sudden or develop more slowly (chronic). In the former, function usually returns to normal once the underlying cause has been treated. Chronic failure, however, usually irreparably reduces or stops normal function.
Acute failure commonly results from physiological shock following a bad injury or major illness. Serious bleeding or burns can reduce blood volume and pressure to the point where blood-supply to the kidney is greatly reduced. Acute myocardial infarction (see HEART, DISEASES OF) or pancreatitis (see PANCREAS, DISORDERS OF) may produce a similar result. A mismatched blood transfusion can produce acute failure. Obstruction to the urine-?ow by a stone (calculus) in the urinary tract, a bladder tumour or an enlarged prostate can also cause acute renal failure, as can glomerulonephritis (see below) and the haemolytic-uraemia syndrome.
HYPERTENSION, DIABETES MELLITUS, polycystic kidney disease (see below) or AMYLOIDOSIS are among conditions that cause chronic renal failure. Others include stone, tumour, prostatic enlargement and overuse of analgesic drugs. Chronic failure may eventually lead to end-stage renal failure, a life-threatening situation that will need DIALYSIS or a renal transplant (see TRANSPLANTATION).
Familial renal disorders include autosomal dominant inherited polycystic kidney disease and sex-linked familial nephropathy. Polycystic kidney disease is an important cause of renal failure in the UK. Patients, usually aged 30–50, present with HAEMATURIA, loin or abdominal discomfort or, rarely, urinary-tract infection, hypertension and enlarged kidneys. Diagnosis is based on ultrasound examination of the abdomen. Complications include renal failure, hepatic cysts and, rarely, SUBARACHNOID HAEMORRHAGE. No speci?c treatment is available. Familial nephropathy occurs more often in boys than in girls and commonly presents as Alport’s syndrome (familial nephritis with nerve DEAFNESS) with PROTEINURIA, haematuria, progressing to renal failure and deafness. The cause of the disease lies in an absence of a speci?c ANTIGEN in a part of the glomerulus. The treatment is conservative, with most patients eventually requiring dialysis or transplantation.
Acute glomerulonephritis is an immune-complex disorder due to entrapment within glomerular capillaries of ANTIGEN (usually derived from B haemolytic streptococci – see STREPTOCOCCUS) antibody complexes initiating an acute in?ammatory response (see IMMUNITY). The disease affects children and young adults, and classically presents with a sore throat followed two weeks later by a fall in urine output (oliguria), haematuria, hypertension and mildly abnormal renal function. The disease is self-limiting with 90 per cent of patients spontaneously recovering. Treatment consists of control of blood pressure, reduced ?uid and salt intake, and occasional DIURETICS and ANTIBIOTICS.
Chronic glomerulonephritis is also due to immunological renal problems and is also classi?ed by taking a renal biopsy. It may be subdivided into various histological varieties as determined by renal biospy. Proteinuria of various degrees is present in all these conditions but the clinical presentations vary, as do their treatments. Some resolve spontaneously; others are treated with steroids or even the cytotoxic drug CYCLOPHOSPHAMIDE or the immunosuppressant cyclosporin. Prognoses are generally satisfactory but some patients may require renal dialysis or kidney transplantation – an operation with a good success rate.
Hydronephrosis A chronic disease in which the kidney becomes greatly distended with ?uid. It is caused by obstruction to the ?ow of urine at the pelvi-ureteric junction (see KIDNEYS – Structure). If the ureter is obstructed, the ureter proximal to the obstruction will dilate and pressure will be transmitted back to the kidney to cause hydronephrosis. Obstruction may occur at the bladder neck or in the urethra itself. Enlargement of the prostate is a common cause of bladder-neck obstruction; this would give rise to hypertrophy of the bladder muscle and both dilatation of the ureter and hydronephrosis. If the obstruction is not relieved, progressive destruction of renal tissue will occur. As a result of the stagnation of the urine, infection is probable and CYSTITIS and PYELONEPHRITIS may occur.
Impaired blood supply may be the outcome of diabetes mellitus and physiological shock, which lowers the blood pressure, also affecting the blood supply. The result can be acute tubular necrosis. POLYARTERITIS NODOSA and SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) may damage the large blood vessels in the kidney. Treatment is of the underlying condition.
Infection of the kidney is called pyelonephritis, a key predisposing factor being obstruction of urine ?ow through the urinary tract. This causes stagnation and provides a fertile ground for bacterial growth. Acute pyelonephritis is more common in women, especially during pregnancy when bladder infection (CYSTITIS) spreads up the ureters to the kidney. Symptoms are fever, malaise and backache. Antibiotics and high ?uid intake are the most e?ective treatment. Chronic pyelonephritis may start in childhood as a result of congenital deformities that permit urine to ?ow up from the bladder to the kidney (re?ux). Persistent re?ux leads to recurrent infections causing permanent damage to the kidney. Specialist investigations are usually required as possible complications include hypertension and kidney failure.
Tumours of the kidney are fortunately rare. Non-malignant ones commonly do not cause symptoms, and even malignant tumours (renal cell carcinoma) may be asymptomatic for many years. As soon as symptoms appear – haematuria, back pain, nausea, malaise, sometimes secondary growths in the lungs, bones or liver, and weight loss – urgent treatment including surgery, radiotherapy and chemotherapy is necessary. This cancer occurs mostly in adults over 40 and has a hereditary element. The prognosis is not good unless diagnosed early. In young children a rare cancer called nephroblastoma (Wilm’s tumour) can occur; treatment is with surgery, radiotherapy and chemotherapy. It may grow to a substantial size before being diagnosed.
Cystinuria is an inherited metabolic defect in the renal tubular reabsorption of cystine, ornithine, lysine and arginine. Cystine precipitates in an alkaline urine to form cystine stones. Triple phosphate stones are associated with infection and may develop into a very large branching calculi (staghorn calculi). Stones present as renal or ureteric pain, or as an infection. Treatment has undergone considerable change with the introduction of MINIMALLY INVASIVE SURGERY (MIS) and the destruction of stone by sound waves (LITHOTRIPSY).... kidneys, diseases of
Treatment The best treatment is prompt surgical removal of the diseased appendix, usually with antibiotic cover. If performed early, before rupture occurs, APPENDICECTOMY is normally straightforward and recovery swift. If the appendix has already ruptured and there is abscess formation or free intra-abdominal pus, surgery is still the best treatment but postoperative complications are more likely, and full recovery may be slower.... appendicitis
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: Cultivated in most parts of India.
English: Bengal Gram, Chick pea.Ayurvedic: Chanaka, Chanakaa, Harimantha, Vajimantha, Jivan, Sakal-priya.Unani: Nakhud.Siddha/Tamil: Kadalai, Mookkuk- kadalai.Action: Antibilious, hypoc- holesteremic, antihyperlipidemic, antistress. Acid exudate from the plant—used in indigestion, diarrhoea, dysentery. Seed coat extract—diuretic, antifungal (externally). Dry leaf—refrigerant.
Supplementation of gram in wheat based diet helps in lysine absorption which is otherwise a limiting amino acid in cereal based diets. Germination improves mineral bioavailability. In germinated gram flour, there is significant increase in nutritional quality of protein and very significant increase in ascorbic acid.The seeds contain pangamic acid, the stemina building, antistress and antihyperlipidemic principle of gram. Gram is given as preventive diet to atherosclerosis patients because of its rich phosphorus content.Isoflavones, biochanin A and for- monetin exhibited hypolipidermic activity in rats. Total flavonoids reduced serum and liver cholesterol in rats.Seeds reduced postprandial plasma glucose in human.... cicer arietinumTumours 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
Nutritional Profile Energy value (calories per serving): High Protein: Low Fat: High Saturated fat: High Cholesterol: High Carbohydrates: Low Fiber: None Sodium: Low (unsalted butter) High (salted butter) Major vitamin contribution: Vitamin A, vitamin D Major mineral contribution: None
About the Nutrients in This Food Butterfat is 62 percent saturated fatty acids, 35 percent monounsaturated fatty acids, and 4 percent polyunsaturated fatty acids. One tablespoon of butter has 11 g of fat, 7.1 g of saturated fat, and 31 mg cholesterol, and 1,070 IU vitamin A (46 percent of the R DA for a woman, 36 percent of the R DA for a man). The vitamin A is derived from carotenoids in plants eaten by the milk-cow.
Diets That May Restrict or Exclude This Food Low-cholesterol, controlled-fat diet Sodium-restricted diet (salted butter)
Buying This Food Look for: Fresh butter. Check the date on the package.
Storing This Food Store butter in the refrigerator, tightly wrapped to protect it from air and prevent it from picking up the odors of other food. Even refrigerated butter will eventually turn rancid as its fat molecules combine with oxygen to produce hydroperoxides that, in turn, break down into chemicals with an unpleasant flavor and aroma. This reaction is slowed (but not stopped) by cold. Because salt retards the combination of fats with oxygen, salted butter stays fresh longer than plain butter. (Lard, which is pork fat, must also be refrigerated. Lard has a higher proportion of unsaturated fats than the butter. Since unsaturated fats combine with oxygen more easily than saturated fats, lard becomes rancid more quickly than butter.)
Preparing This Food To measure a half-cup of butter. Pour four ounces of water into an eight-ounce measuring cup, then add butter until the water rises to the eight-ounce mark. Scoop out the butter, use as directed in recipe.
What Happens When You Cook This Food Fats are very useful in cooking. They keep foods from sticking to the pot or pan; add fla- vor; and, as they warm, transfer heat from the pan to the food. In doughs and batters, fats separate the flour’s starch granules from each other. The more closely the fat mixes with the starch, the smoother the bread or cake will be. Heat speeds the oxidation and decomposition of fats. When fats are heated, they can catch fire spontaneously without boiling first at what is called the smoke point. Butter will burn at 250°F.
How Other Kinds of Processing Affect This Food Freezing. Freezing slows the oxidation of fats more effectively than plain refrigeration; frozen butter keeps for up to nine months. Whipping. When butter is whipped, air is forced in among the fat molecules to produce a foam. As a result, the whipped butter has fewer calories per serving, though not per ounce.
Adverse Effects Associated with This Food Increased risk of heart disease. Like other foods from animals, butter contains cholesterol and saturated fats. Eating butter increases the amount of cholesterol circulating in your blood and raise your risk of heart disease. To reduce the risk of heart disease, USDA /Health and Human Services Dietary Guidelines for Americans recommends limiting the amount of cholesterol in your diet to no more than 300 mg a day. The guidelines also recommend limit- ing the amount of fat you consume to no more than 30 percent of your total calories, while holding your consumption of saturated fats to no more than 10 percent of your total calories (the calories from saturated fats are counted as part of the total calories from fat). Increased risk of acid reflux. Consuming excessive amounts of fats and fatty foods loosens the lower esophageal sphincter (LES), a muscular valve between the esophagus and the stomach. When food is swallowed, the valve opens to let food into the stomach, then closes tightly to keep acidic stomach contents from refluxing (flowing backwards) into the esopha- gus. If the LES does not close efficiently, the stomach contents reflux to cause heartburn, a burning sensation. Repeated reflux is a risk factor for esophageal cancer.... butter
Also called acute coryza or upper respiratory infection, the common cold is characterised by in?ammation of any or all of the airways – NOSE, sinuses (see SINUS), THROAT, LARYNX, TRACHEA and bronchi (see BRONCHUS). Most common, however, is the ‘head cold’, which is con?ned to the nose and throat, with initial symptoms presenting as a sore throat, runny nose and sneezing. The nasal discharge may become thick and yellow – a sign of secondary bacterial infection – while the patient often develops watery eyes, aching muscles, a cough, headache, listlessness and the shivers. PYREXIA (raised temperature) is usual. Colds can also result in a ?are-up of pre-existing conditions, such as asthma, bronchitis or ear infections. Most colds are self-limiting, resolving in a week or ten days, but some patients develop secondary bacterial infections of the sinuses, middle ear (see EAR), trachea, or LUNGS.
Treatment Symptomatic treatment with ANTIPYRETICS and ANALGESICS is usually su?cient; ANTIBIOTICS should not be taken unless there is de?nite secondary infection or unless the patient has an existing chest condition which could be worsened by a cold. Cold victims should consult a doctor only if symptoms persist or if they have a pre-existing condition, such as asthma which could be exacerbated by a cold.
Most colds result from breathing-in virus-containing droplets that have been coughed or sneezed into the atmosphere, though the virus can also be picked up from hand-to-hand contact or from articles such as hand towels. Prevention is, therefore, di?cult, given the high infectivity of the viruses. No scienti?cally proven, generally applicable preventive measures have yet been devised, but the incidence of the infection falls from about seven to eight years – schoolchildren may catch as many as eight colds annually – to old age, the elderly having few colds. So far, despite much research, no e?ective vaccines have been produced.... cold, common
Blunt injuries These may cause haemorrhage inside the eye, cataract, retinal detachment or even rupture of the eye (see also EYE, DISORDERS OF). Injuries from large blunt objects – for example, a squash ball – may also cause a ‘blow-out fracture’ of the orbital ?oor resulting in double vision. Surgical treatment may be required depending on the patient’s speci?c problems.
Chemical burns Most chemical splashes cause conjunctivitis and super?cial keratitis in the victim (see EYE, DISORDERS OF); both conditions are self-limiting. Alkalis are, however, more likely to penetrate deeper into the eye and cause permanent damage, particularly to the cornea. Prompt irrigation is important. Further treatment may involve testing the pH of the tears, topical antibiotics and CORTICOSTEROIDS, and vitamin C (drops or tablets – see APPENDIX 5: VITAMINS), depending on the nature of the injury.
Corneal abrasion Loss of corneal epithelium (outermost layer). Almost any sort of injury to the eye may cause this. The affected eye is usually very painful. In the absence of other problems, the epithelium heals rapidly: small defects may close within 24 hours. Treatment conventionally consists of antibiotic ointment and sometimes a pad over the injured eye.
Foreign bodies Most foreign bodies which hit the eye are small and are found in the conjunctival sac or on the cornea; most are super?cial and can be easily removed. A few foreign bodies penetrate deeper and may cause infection, cataract, retinal detachment or haemorrhage within the eye. The foreign body is usually removed and the damage repaired; nevertheless the victim’s sight may have been permanently damaged. Particularly dangerous activities include hammering or chiselling on metal or stone; people carrying out these activities (and others, such as hedge-cutting and grass-strimming) should wear protective goggles.... eye injuries
Staphylococcal food poisoning occurs after food such as meat products, cold meats, milk, custard and egg products becomes contaminated before or after cooking, usually through incorrect handling by humans who carry S. aureus. The bacteria produce an ENTEROTOXIN which causes the symptoms of food poisoning 1–8 hours after ingestion. The toxin can withstand heat; thus, subsequent cooking of contaminated food will not prevent illness.
Heat-resistant strains of Cl. perfringens cause food poisoning associated with meat dishes, soups or gravy when dishes cooked in bulk are left unrefrigerated for long periods before consumption. The bacteria are anaerobes (see ANAEROBE) and form spores; the anaerobic conditions in these cooked foods allow the germinated spores to multiply rapidly during cooling, resulting in heavy contamination. Once ingested the bacteria produce enterotoxin in the intestine, causing symptoms within 8–24 hours.
Many di?erent types of Salmonella (about 2,000) cause food poisoning or ENTERITIS, from eight hours to three days after ingestion of food in which they have multiplied. S. brendeny, S. enteritidis, S. heidelberg, S. newport and S. thompson are among those commonly causing enteritis. Salmonella infections are common in domesticated animals such as cows, pigs and poultry whose meat and milk may be infected, although the animals may show no symptoms. Duck eggs may harbour Salmonella (usually S. typhimurium), arising from surface contamination with the bird’s faeces, and foods containing uncooked or lightly cooked hen’s eggs, such as mayonnaise, have been associated with enteritis. The incidence of human S. enteritidis infection has been increasing, by more than 15-fold in England and Wales annually, from around 1,100 a year in the early 1980s to more than 32,000 at the end of the 1990s, but has since fallen to about 10,000. A serious source of infection seems to be poultry meat and hen’s eggs.
Although Salmonella are mostly killed by heating at 60 °C for 15 minutes, contaminated food requires considerably longer cooking and, if frozen, must be completely thawed beforehand, to allow even cooking at a su?cient temperature.
Enteritis caused by Campylobacter jejuni is usually self-limiting, lasting 1–3 days. Since reporting of the disease began in 1977, in England and Wales its incidence has increased from around 1,400 cases initially to nearly 13,000 in 1982 and to over 42,000 in 2004. Outbreaks have been associated with unpasteurised milk: the main source seems to be infected poultry.
ESCHERICHIA COLI O157 was ?rst identi?ed as a cause of food poisoning in the early 1980s, but its incidence has increased sharply since, with more than 1,000 cases annually in the United Kingdom in the late 1990s. The illness can be severe, with bloody diarrhoea and life-threatening renal complications. The reservoir for this pathogen is thought to be cattle, and transmission results from consumption of raw or undercooked meat products and raw dairy products. Cross-infection of cooked meat by raw meat is a common cause of outbreaks of Escherichia coli O157 food poisoning. Water and other foods can be contaminated by manure from cattle, and person-to-person spread can occur, especially in children.
Food poisoning associated with fried or boiled rice is caused by Bacillus cereus, whose heat-resistant spores survive cooking. An enterotoxin is responsible for the symptoms, which occur 2–8 hours after ingestion and resolve after 8–24 hours.
Viruses are emerging as an increasing cause of some outbreaks of food poisoning from shell?sh (cockles, mussels and oysters).
The incidence of food poisoning in the UK rose from under 60,000 cases in 1991 to nearly 79,000 in 2004. Public health measures to control this rise include agricultural aspects of food production, implementing standards of hygiene in abattoirs, and regulating the environment and process of industrial food production, handling, transportation and storage.... food poisoning
Bacterial meningitis is life-threatening: in the United Kingdom, 5–10 per cent of children who contract the disease may die. Most cases of acute bacterial meningitis in the UK are caused by two bacteria: Neisseria meningitidis (meningococcus), and Streptococcus pneumoniae (pneumococcus); other bacteria include Haemophilus in?uenzae (a common cause until virtually wiped out by immunisation), Escherichia coli, Mycobacterium tuberculosis (see TUBERCULOSIS), Treponema pallidum (see SYPHILIS) and Staphylococci spp. Of the bacterial infections, meningococcal group B is the type that causes a large number of cases in the UK, while group A is less common.
Bacterial meningitis may occur by spread from nearby infected foci such as the nasopharynx, middle ear, mastoid and sinuses (see EAR, DISEASES OF). Direct infection may be the result of penetrating injuries of the skull from accidents or gunshot wounds. Meningitis may also be a complication of neurosurgery despite careful aseptic precautions. Immuno-compromised patients – those with AIDS or on CYTOTOXIC drugs – are vulnerable to infections.
Spread to contacts may occur in schools and similar communities. Many people harbour the meningococcus without developing meningitis. In recent years small clusters of cases, mainly in schoolchildren and young people at college, have occurred in Britain.
Symptoms include malaise accompanied by fever, severe headache, PHOTOPHOBIA, vomiting, irritability, rigors, drowsiness and neurological disturbances. Neck sti?ness and a positive KERNIG’S SIGN appearing within a few hours of infection are key diagnostic signs. Meningococcal and pneumococcal meningitis may co-exist with SEPTICAEMIA, a much more serious condition in terms of death rate or organ damage and which constitutes a grave emergency demanding rapid treatment.
Diagnosis and treatment are urgent and, if bacterial meningitis is suspected, antibiotic treatment should be started even before laboratory con?rmation of the infection. Analysis of the CEREBROSPINAL FLUID (CSF) by means of a LUMBAR PUNCTURE is an essential step in diagnosis, except in patients for whom the test would be dangerous as they have signs of raised intracranial pressure. The CSF is clear or turbid in viral meningitis, turbid or viscous in tuberculous infection and turbulent or purulent when meningococci or staphylococci are the infective agents. Cell counts and biochemical make-up of the CSF are other diagnostic pointers. Serological tests are done to identify possible syphilitic infection, which is now rare in Britain.
Patients with suspected meningitis should be admitted to hospital quickly. General pracitioners are encouraged to give a dose of intramuscular penicillin before sending the child to hospital. Treatment in hospital is usually with a cephalosporin, such as ceftazidime or ceftriaxone. Once the sensitivity of the organism is known as a result of laboratory studies on CSF and blood, this may be changed to penicillin or, in the case of H. in?uenzae, to amoxicillin. Local infections such as SINUSITIS or middle-ear infection require treatment, and appropriate surgery for skull fractures or meningeal tears should be carried out as necessary. Tuberculous meningitis is treated for at least nine months with anti-tuberculous drugs (see TUBERCULOSIS). If bacterial meningitis causes CONVULSIONS, these can be controlled with diazepam (see TRANQUILLISERS; BENZODIAZEPINES) and ANALGESICS will be required for the severe headache.
Coexisting septicaemia may require full intensive care with close attention to intravenous ?uid and electrolyte balance, control of blood clotting and blood pressure.
Treatment of close contacts such as family, school friends, medical and nursing sta? is recommended if the patient has H. in?uenzae or N. meningitidis: RIFAMPICIN provides e?ective prophylaxis. Contacts of patients with pneumococcal infection do not need preventive treatment. Vaccines for meningococcal meningitis may be given to family members in small epidemics and to any contacts who are especially at risk such as infants, the elderly and immuno-compromised individuals.
The outlook for a patient with bacterial meningitis depends upon age – the young and old are vulnerable; speed of onset – sudden onset worsens the prognosis; and how quickly treatment is started – hence the urgency of diagnosis and admission to hospital. Recent research has shown that children who suffer meningitis in their ?rst year of life are ten times more likely to develop moderate or severe disability by the age of ?ve than contemporaries who have not been infected. (See British Medical Journal, 8 September 2001, page 523.)
Prevention One type of bacterial meningitis, that caused by Haemophilus, has been largely controlled by IMMUNISATION; meningococcal C vaccine has largely prevented this type of the disease in the UK. So far, no vaccine against group B has been developed, but research continues. Information on meningitis can be obtained from the Meningitis Trust and the Meningitis Research Foundation.... meningitis
Grade of obesity
BMI (W/H2) III >40 II 30–40 I 25–29·9 not obese <25
Causes Whatever the causes of obesity, the fact remains that energy intake (in the form of food and drink) must exceed energy output (in the form of activity and exercise) over a suf?ciently long period of time.
Obesity tends to aggregate in families. This has led to the suggestion that some people inherit a ‘thrifty’ gene which predisposes them to obesity in later life by lowering their energy output. Indeed, patients often attribute their obesity to such a metabolic defect. Total energy output is made up of the resting metabolic rate (RMR), which represents about 70 per cent of the total; the energy cost of physical activity; and thermogenesis, i.e. the increase in energy output in response to food intake, cold exposure, some drugs and psychological in?uences. In general, obese people are consistently found to have a higher RMR and total energy output, per person – and also when expressed against fat-free mass – than do their lean counterparts. Most obese people do not appear to have a reduced capacity for thermogenesis. Although a genetic component to obesity remains a possibility, it is unlikely to be great or to prevent weight loss from being possible in most patients by reducing energy intake. Environmental in?uences are believed to be more important in explaining the familial association in obesity.
An inactive lifestyle plays a minor role in the development of obesity, but it is unclear whether people are obese because they are inactive or are inactive because they are obese. For the majority of obese people, the explanation must lie in an excessive energy intake. Unfortunately, it is di?cult to demonstrate this directly since the methods used to assess how much people eat are unreliable. For most obese people it seems likely that the defect lies in their failure to regulate energy intake in response to a variety of cognitive factors (e.g. ease of ?tting of clothes) in the long term.
Unfortunately, it can be possible to identify by the time of their ?rst birthday, many of the children destined to be obese.
Rarely, obesity has an endocrine basis and is caused by hypothyroidism (see under THYROID GLAND, DISEASES OF), HYPOPITUITARISM, HYPOGONADISM or CUSHING’S SYNDROME.
Symptoms Obesity has adverse effects on MORBIDITY and mortality (see DEATH RATE) which are greatest in young adults and increase with the severity of obesity. It is associated with an increased mortality and/or morbidity from cardiovascular disease, non-insulin-dependent diabetes mellitus, diseases of the gall-bladder, osteoarthritis, hernia, gout and possibly certain cancers (i.e. colon, rectum and prostate in men, and breast, ovary, endometrium and cervix in women). Menstrual irregularities and ovulatory failure are often experienced by obese women. Obese people are also at greater risk when they undergo surgery. With the exception of gallstone formation, weight loss will reduce these health risks.
Treatment Creation of an energy de?cit is essential for weight loss to occur, so the initial line of treatment is a slimming diet. An average de?cit of 1,000 kcal/day (see CALORIE) will produce a loss of 1 kg of fat/week and should be aimed for. Theoretically, this can be achieved by increasing energy expenditure or reducing energy intake. In practice, a low-energy diet is the usual form of treatment since attempts to increase energy expenditure, either by physical exercise or a thermogenic drug, are relatively ine?ective.
Anorectic drugs, gastric stapling and jaw-wiring are sometimes used to treat severe obesity. They are said to aid compliance with a low-energy diet by either reducing hunger (anorectic drugs) or limiting the amount of food the patient can eat. Unfortunately, the long-term e?ectiveness of gastric stapling is not known, and it is debatable whether the modest reduction in weight achieved by use of anorectic drugs is worthwhile – although a new drug, ORLISTAT, is becoming available that reduces the amount of fat absorbed from food in the gastrointestinal tract. For some grossly obese patients, jaw-wiring can be helpful, but a regain of weight once the wires are removed must be prevented. These procedures carry a risk, so should be done only if an individual’s health is in danger.... obesity
The condition is more common in women, because it is usually associated with wearing narrow, pointed, high-heeled shoes, but it may be caused by an inherited weakness in the joint.
A hallux valgus often leads to formation of a bunion or to osteoarthritis in the joint, causing pain and limiting foot movement.
Severe deformity may be corrected by osteotomy or arthrodesis.... hallux valgus
Pityriasis alba is a mild form of chronic eczema (see DERMATITIS) occurring mainly in children on the face and in young adults on the upper arms. It is characterised by round or oval ?aky patches which are paler than the surrounding skin due to partial loss of MELANIN pigment. The appearance is more dramatic in dark-skinned or suntanned subjects. Moisturising cream often su?ces, but 1 per cent HYDROCORTISONE cream is more e?ective.
Pityriasis rosea is a common self-limiting eruption seen mainly in young adults. It usually begins as a solitary red ?aky patch (often misdiagnosed as ringworm). Within a week this ‘herald patch’ is followed by a profuse symmetrical eruption of smaller rose-pink, ?aky, oval lesions on the trunk and neck but largely sparing the limbs and face. Itching is variable. The eruption usually peaks within 3 weeks and fades away leaving collarettes of scale, disappearing within 6–7 weeks. It rarely recurs and a viral cause is suspected but not proved. It is not contagious and there is no speci?c treatment, but crotamiton cream (Eurax) may relieve discomfort.... pityriasis
Prescriptions. While specimen combinations appear for each specific disease in this book, medicines from the dispensary may be varied many times during the course of treatment. The practitioner will adapt a prescription to a patient’s individual clinical picture by adding and subtracting agents according to the changing basic needs of the case. For instance, a first bottle of medicine or blend of powders may include a diuretic to clear the kidneys in preparation for the elimination of wastes and toxins unleashed by active ingredients.
The reader should never underestimate the capacity of herbal medicine to regenerate the human body, even from the brink of disaster.
Acknowledgements. I am indebted to my distinguished mentor, Edgar Gerald Jones, Mansfield, Nottinghamshire, England, to whom I owe more than I could ever repay. I am indebted also to the National Institute of Medical Herbalists, and to the British Herbal Medicine Association, both of which bodies have advanced the cause of herbal medicine. I have drawn heavily upon the British Herbal Pharmacopoeias 1983 and 1990, authentic publications of the BHMA, and have researched major works of ancient and modern herbalism including those pioneers of American Eclectic Medicine: Dr Samuel Thomson, Dr Wooster Beach, Dr Finlay Ellingwood and their British contemporaries. All made a vital contribution in their day and generation. I have endeavoured to keep abreast of the times, incorporating the latest scientific information at the time of going to press. For the purposes of this book I am especially indebted to my friend Dr John Cosh for checking accuracy of the medical material and for his many helpful suggestions.
A wealth of useful plants awaits further investigation. Arnica, Belladonna and Gelsemium are highly regarded by European physicians. It is believed that these plants, at present out of favour, still have an important role in medicine of the future. The wise and experienced clinician will wish to know how to harness their power to meet the challenge of tomorrow’s world.
Perhaps the real value of well-known alternative remedies lies in their comparative safety. Though largely unproven by elaborate clinical trials, the majority carry little risk or harm. Some have a great potential for good. The therapy is compatible with other forms of treatment.
The revival of herbal medicine is no passing cult due to sentimentality or superstition. It indicates, rather, a return to that deep devotion to nature that most of us have always possessed, and which seems in danger of being lost in the maze of modern pharmacy. It is an expression of loyalty to all that is best from
the past as we move forward into the 21st century with a better understanding of disease and its treatment. I believe the herbal profession has a distinguished and indispensible contribution to make towards the conquest of disease among peoples of the world, and that it should enjoy a place beside orthodox medicine.
Who are we to say that today’s antibiotics and high-tech medicine will always be available? In a world of increasing violence, war and disaster, a breakdown in the nation’s health service might happen at any time, thus curtailing production of insulin for the diabetic, steroids for the hormone-deficient, and anti-coagulants for the thrombotic. High-technology can do little without its specialised equipment. There may come a time when we shall have to reply on our own natural resources. It would be then that a knowledge of alternatives could be vital to survival. ... self medication
Condition also caused by a spasm in the coronary circulation. ‘Strangling pain in the chest’, lasting 2 to 10 minutes. Aggravated by diabetes, anaemia, goitre, high blood pressure and stress.
Is it angina? Important evidence is the association of the pain with exercise and its relief by rest. Pain is similar to intermittent claudication (pain in the calf muscle). Sense of constriction in front of chest: may radiate to the jaw or left arm.
Atherosclerosis (hardening of the arteries) is caused by cholesterol deposits hindering blood flow. It is the work of the practitioner to unclog blocked arteries where possible.
Phytotherapy may increase exercise capacity, reduce the number of angina attacks, and is known to enjoy a low incidence of unwanted side-effects.
Alternatives. Teas. Chamomile, Hawthorn, Motherwort, Lime Flowers, Hops, Oats (avena), Orange Tree leaves.
Tablets/capsules. Cayenne, Hawthorn, Lobelia, Prickly Ash.
Powders. Formula. Equal parts: Hawthorn berries, Opuntia (Cactus flowers), Mistletoe, Motherwort. Dose: 750mg (three 00 capsules or half a teaspoon) thrice daily.
Liquid extracts: Formula: Equal parts: Cactus, Hawthorn, Prickly Ash. Dose: 1-2 teaspoons. Thrice daily.
Tinctures: Formula. Hawthorn BHP (1983) 30ml; Motherwort BHP (1983) 30ml; Prickly Ash bark BHP (1983) 20ml; Tincture Capsicum Fort BPC 1934: 0.25ml. Dose: 5ml in water thrice daily.
Practitioner. Alternatives:–
1. Tincture Aconite, BPC 1949 : 2-5 drops (0.12 to 0.3ml) when necessary.
2. Liquid extract: Lobelia BHP (1983): 10-30 drops every 20 minutes when necessary.
3. Formula. Tincture Selenicereus grand (preferably fresh plant) 1oz; Tincture Ginger quarter of an ounce. Dose: 15-30 drops every 15 minutes.
4. Formula. Liquid extract: Prickly Ash bark 20ml; Liquid extract: Cactus 20ml. Mix. Dose: 5-20 drops when necessary. (A. Barker, FNIMH)
5. Emergency. Tincture Gelsemium BPC 1973. Dose: 5 drops (0.3ml).
Diet: See: DIET – HEART AND CIRCULATION. Vitamin E reduces the risk of angina. ... angina
Kittens proved the greatest hazard, particularly those with fleas. Local inflammation with glandular swelling and fever. Organism: usually Pasteurella multocida. Often with great weakness. One of the commonest causes of swollen glands in the USA.
Treatment. Poke root to combat infection of the glandular system. Echinacea to increase powers of resistance.
Alternatives. Tablets/capsules. Poke root. Echinacea. Wild Yam.
Powders. Formula: Echinacea 2; Gum Myrrh half; Goldenseal half. Dose: 500mg (two 00 capsules or one-third teaspoon) every 3 hours.
Tinctures. Formula. Echinacea 2; Poke root 1; Goldenseal half. Mix. One teaspoon in water every 3 hours.
Dosage for children: see – DOSAGE.
Topical. Apply Tea Tree oil diluted. May be diluted many times. Vitamin C. 1g morning and evening.
Calcium ascorbate powder. 1g morning and evening. ... cat scratch fever
Misleading claims and the use of such words as “organic”, “wholesome”, “natural” or “biological” cannot be accepted on product labels. The Licensing Authority treats herbal manufacturers no differently than manufacturers of allopathic products for serious conditions.
The Advertising Standards Authority does not allow quotation of any medicinal claims, except where a Product Licence (PL) has been authorised by the Licensing Authority.
All labels must include: Name of product (as on Product Licence), description of pharmaceutical form (tablet, mixture etc), Product Licence No., Batch No., quantity of each active ingredient in each unit dose in metric terms; dose and directions for use; quantity in container (in metric terms); “Keep out of reach of children” or similar warning; Name and address of Product Licence Holder; expiry date (if applicable); and any other special warnings. Also to appear: excipients, method/route of administration, special storage instructions, and precautions for disposal, if any.
Where licences are granted, the following words should appear on the label of a product: “A herbal product traditionally used for the symptomatic relief of . . .”. “If symptoms persist see your doctor.” “Not to be used in pregnancy” (where applicable). “If you think you have . . . consult a registered medical practitioner before taking this product.” “If you are already receiving medical treatment, tell your doctor that you are taking this product.” These warnings are especially necessary should symptoms persist and be the start of something more serious than a self-limiting condition.
Herbal preparations should be labelled with the additives and colourings they contain, if any. This helps practitioners avoid prescribing medicines containing them to certain patients on whom they may have an adverse reaction.
Labels of medicinal products shall comply with the Medicines (Labelling) Regulations 1976 (SI 1976 No. 1726) as amended by the Medicines (Labelling) Amendment Regulations 1977 (SI 1977 No. 996), the Medicines (Labelling) Amendment Regulations 1981 (SI 1981 No. 1791) and the Medicines (Labelling) Amendment Regulations 1985 (SI 1985 No. 1558).
Leaflets issued with proprietory medicinal products shall comply with the requirements of the Medicines (Leaflets) Regulations 1977 (SI 1977 No. 1055).
See also: ADVERTISING: CODE OF PRACTICE. BRITISH HERBAL MEDICINE ASSOCIATION. ... labelling of herbal products
Causes: faulty absorption of fats, bacterial or viral infection, nervous bowel, anxiety or psychosomatic disturbance, malfunction of the thyroid gland, etc.
Looseness of the bowels may sometimes occur as an acute cleansing eliminative effort by Nature to expel wastes and impurities. Dehydration can be serious in children. For presence of mucous or blood in the stool refer to DIFFERENTIAL DIAGNOSIS.
Differential diagnosis. Crohn’s disease, Gastroenteritis, Diverticulosis, Ulcerative colitis, Dysentery, Salmonella.
Travel diarrhoea: ‘blight of holiday and business trips abroad’ due to E. Coli. Acute, usually non- persistent self-limiting condition. Ginger, crystallised or powder in capsules or tablets is known to reduce the incidence in high risk areas.
Imported bloody diarrhoeas – salmonella, shigella or amoebic infections should receive special investigation by a competent authority, a consultant in infectious diseases. First-aid until the practitioner comes: 2-5 drops oil of Peppermint in water.
Children’s diarrhoea. Re-hydration after severe loss of fluids – glass of water containing 1 teaspoon salt and 2 teaspoons sugar.
Over 13,000 children die from this preventable disease every day, many in the developing countries. This simple combination of sugar and salt prevents dehydration, the most common cause of death from acute diarrhoea, and has helped save tens of thousands of lives.
Alternatives. Rest. Avoid caffeine and alcohol drinks. Plenty of astringent herb teas to reduce the associated hyperperistalsis. Children – half-dose.
Teas. Any one of the following: Agrimony, Avens, Burmarigold, Black Walnut leaves, Burnet (greater or garden), Ground Ivy, Ladysmantle, Hops (nervous bowel), Plantain, Peppermint, Periwinkle (vinca major), Meadowsweet, Silverweed, Shepherd’s Purse, Tormentil. Sage. Formulae: (1) equal parts; Raspberry leaves, Agrimony, Avens. Or (2) equal parts; Raspberry leaves, Plantain, Silverweed. 2 teaspoons to each cup boiling water; infuse 5-15 minutes. Half-1 cup freely. For nerve exhaustion: add a sprinkle of Valerian.
Seeds. Coriander, Caraway or Fenugreek. Half a teaspoon to each cup water, brought to boil; vessel removed as soon as boiling point is reached. Half-1 cup freely.
Decoctions. Any one of the following: Bayberry, Cranesbill (American), Rhatany root, Sweet Chestnut leaves, Oak bark, Wild Yam, Iceland Moss.
Powders. Any one: Calamus, Bayberry, Oak bark, Cinnamon, Black Catechu, Wild Yam. Add pinch of Ginger.
Tinctures. (1) Combine Bayberry 2; Ginger 1. Or (2) Combine Bayberry 1; Raspberry leaves 2. One to two 5ml teaspoons thrice daily after meals.
Tincture, or spirits of Camphor: 5-10 drops in water every 3-4 hours for severe depletion of body fluids. Adults only.
Aloe Vera. Scientific papers confirm efficacy.
Dr Finlay Ellingwood. Castor oil: 5 drops every 2 hours.
Bilberry juice. Half-1 cup freely.
Goldenseal. Antibacterial. 5-10 drops, tincture, 3-4 times daily. Adults only.
Diet. Avoid cow’s milk. 3-day fast on fruit juices and herb teas alone, followed by gruel made from Slippery Elm, Oatmeal or Arrowroot. Yoghurt. Bilberry fruit. Carob bean products: chocolate or other preparations. Ensure adequate fluid intake.
Supplementation. Vitamins A, B12, C, D. Minerals: Calcium, Iron, Magnesium, Potassium, Zinc. Preventative. 2 drops oil of Peppermint morning and evening. ... diarrhoea
Causes: smoking, mis-use of the voice in talking or singing (Ginseng).
Symptoms: voice husky or absent (aphonia). Talking causes pain. Self-limiting.
Treatment. Stop talking for 2 days. Care is necessary: neglect or ineffective treatment may rouse infection and invade the windpipe and bronchi resulting in croup.
Differential: croup is alerted by high fever and characteristic cough, requiring hospital treatment. Alternatives. Teas: Red Sage. Garden Sage. Thyme, wild or garden.
Effective combination: equal parts, Sage and Raspberry leaves. Used also as a gargle.
Tablets/capsules. Poke root. Lobelia. Iceland Moss.
Cinnamon. Tincture, essence or oil of: 3-5 drops in teaspoon honey.
Horseradish. 1oz freshly scraped root to steep in cold water for two hours. Add 2 teaspoons runny honey. Dose: 2-3 teaspoons every two hours.
Topical. Equal parts water/cider vinegar cold pack round throat. Renew when dry.
Traditional: “Rub soles of the feet with Garlic and lard well-beaten together, overnight. Hoarseness gone in the morning.” (John Wesley) Friar’s balsam.
Aromatherapy. Steam inhalations. Oils: Bergamot, Eucalyptus, Niaouli, Geranium, Lavender, Sandalwood.
Diet. Three-day fruit fast.
Supplements. Daily. Vitamin A (7500iu). Vitamin C (1 gram thrice daily). Beta carotene 200,000iu. Zinc 25mg. ... laryngitis, acute
To establish efficacy of treatment for a named specific disease by herbs, the DHSS requires scientific data presented to the Regulatory authorities for consideration and approval.
A product is not considered a herbal remedy if its active principle(s) have been isolated and concentrated, as in the case of digitalis from the Foxglove. (MAL 2. Guidance notes)
A herbal product is one in which all active ingredients are of herbal origin. Products that contain both herbal and non-vegetable substances are not considered herbal remedies: i.e. Yellow Dock combined with Potassium Iodide.
The British Government supports freedom of the individual to make an informed choice of the type of therapy he or she wishes to use and has affirmed its policy not to restrict the general availability of herbal remedies. Provided products are safe and are not promoted by exaggerated claims, the future of herbal products is not at risk. A doctor with knowledge and experience of herbal medicine may prescribe them if he considers that they are a necessary part of treatment for his patient.
Herbalism is aimed at gently activating the body’s defence mechanisms so as to enable it to heal itself. There is a strong emphasis on preventative treatment. In the main, herbal remedies are used to relieve symptoms of self-limiting conditions. They are usually regarded as safe, effective, well-tolerated and with no toxicity from normal use. Some herbal medicines are not advised for children under 12 years except as advised by a manufacturer on a label or under the supervision of a qualified practitioner.
World Health Organisation Guidelines
The assessment of Herbal Medicines are regarded as:–
Finished, labelled medicinal products that contain as active ingredients aerial or underground parts of plants, or other plant material, or combinations thereof, whether in the crude state or as plant preparations. Plant material includes juices, gums, fatty oils, essential oils, and any other substances of this nature. Herbal medicines may contain excipients in addition to the active ingredients. Medicines containing plant material combined with chemically defined active substances, including chemically defined, isolated constituents of plants, are not considered to be herbal medicines.
Exceptionally, in some countries herbal medicines may also contain, by tradition, natural organic or inorganic active ingredients which are not of plant origin.
The past decade has seen a significant increase in the use of herbal medicines. As a result of WHO’s promotion of traditional medicine, countries have been seeking the assistance of WHO in identifying safe and effective herbal medicines for use in national health care systems. In 1989, one of the many resolutions adopted by the World Health Assembly in support of national traditional medicine programmes drew attention to herbal medicines as being of great importance to the health of individuals and communities (WHA 42.43). There was also an earlier resolution (WHA 22.54) on pharmaceutical production in developing countries; this called on the Director-General to provide assistance to the health authorities of Member States to ensure that the drugs used are those most appropriate to local circumstances, that they are rationally used, and that the requirements for their use are assessed as accurately as possible. Moreover, the Declaration of Alma-Ata in 1978 provided for inter alia, the accommodation of proven traditional remedies in national drug policies and regulatory measures. In developed countries, the resurgence of interest in herbal medicines has been due to the preference of many consumers for products of natural origin. In addition, manufactured herbal medicines from their countries of origin often follow in the wake of migrants from countries where traditional medicines play an important role.
In both developed and developing countries, consumers and health care providers need to be supplied with up-to-date and authoritative information on the beneficial properties, and possible harmful effects, of all herbal medicines.
The Fourth International Conference of Drug Regulatory Authorities, held in Tokyo in 1986, organised a workshop on the regulation of herbal medicines moving in international commerce. Another workshop on the same subject was held as part of the Fifth International Conference of Drug Regulatory Authorities, held in Paris in 1989. Both workshops confined their considerations to the commercial exploitation of traditional medicines through over-the-counter labelled products. The Paris meeting concluded that the World Health Organisation should consider preparing model guidelines containing basic elements of legislation designed to assist those countries who might wish to develop appropriate legislation and registration.
The objective of these guidelines, therefore, is to define basic criteria for the evaluation of quality, safety, and efficacy of herbal medicines and thereby to assist national regulatory authorities, scientific organisations, and manufacturers to undertake an assessment of the documentation/submission/dossiers in respect of such products. As a general rule in this assessment, traditional experience means that long-term use as well as the medical, historical and ethnological background of those products shall be taken into account. Depending on the history of the country the definition of long-term use may vary but would be at least several decades. Therefore the assessment shall take into account a description in the medical/pharmaceutical literature or similar sources, or a documentation of knowledge on the application of a herbal medicine without a clearly defined time limitation. Marketing authorisations for similar products should be taken into account. (Report of Consultation; draft Guidelines for the Assessment of Herbal Medicines. World Health Organisation (WHO) Munich, Germany, June 1991) ... herbal medicine
With some forms of radiation, damage occurs when the radiation dose exceeds a certain limit, usually 1 sievert (Sv) (see radiation unit). This damage may include radiation dermatitis, cataracts, organ failure (which may occur many years later), or radiation sickness.
For other types of radiation damage, the risk that damage will occur increases with increasing doses of radiation. Cancer caused by radiation-induced mutation is the major example of this type of damage. Radioactive leaks from nuclear reactors can cause a rise in mutation rates, which may lead to an increase in cancers, such as leukaemias; to birth defects; and to hereditary diseases. Cancer usually develops years after exposure. Radiation damage can be controlled by limiting exposure. People exposed to radiation at work have their exposure closely monitored to ensure that it does not exceed safe limits. People of reproductive age or younger should have their reproductive organs shielded when having X-rays or radiotherapy.There is no evidence of radiation hazards with visual display units (VDUs).... radiation hazards
The wrist contains 8 bones (known collectively as the carpus) arranged in 2 rows, one articulating with the bones of the forearm, and the other connecting to the bones of the palm. Tendons connect the forearm muscles to the fingers and thumb, and arteries and nerves supply the muscles, bones, and skin of the hand and fingers.
Wrist injuries may lead to serious disability by limiting hand movement. A common injury in adults is Colles’ fracture, in which the lower end of the radius is fractured and the wrist and hand aredisplaced backwards. In young children, similar displacement results from a fracture through the epiphysis (growing end) of the radius. A sprain can affect ligaments at the wrist joint, but most wrist sprains are not severe. (See also carpal tunnel syndrome; wrist-drop; tenosynovitis; and osteoarthritis.)... wrist
Like tuberculosis, leprosy should be treated with a combination of antibacterial drugs, to overcome the problem of resistance developing to a single drug; the WHO advocates a combination of rifampicin and dapsone for six months to treat paucibacillary leprosy and these drugs with the addition of clofazimine for multibacillary leprosy, this multidrug therapy (MDT) to be continued for two years. Reconstructive surgery can repair some of the damage caused by the disease. A vaccine is being developed and tested.... leprosy