adj. describing characteristics that are expressed differently in the two sexes but are controlled by genes not on the sex chromosomes, e.g. baldness in men.
Many people with epilepsy do not have any symptoms between seizures. Some people experience an aura shortly before. In some cases, a stimulus such as a flashing light triggers a seizure. Epileptic seizures may occur more frequently in times of illness or stress.
Epileptic seizures can be classified into two groups: generalized and partial. Generalized seizures cause loss of consciousness and may affect all areas of the brain. There are two types: grand mal and absence (petit mal) seizures. During a grand mal seizure, there may be an aura initially, then the bodybecomes stiff and consciousness is lost; breathing may be irregular or may stop briefly, then the body jerks uncontrollably. The person may be disorientated for hours afterwards and have no memory of the event. Prolonged grand mal seizures are potentially life-threatening. Absence seizures occur mainly in children. Periods of altered consciousness last for only a few seconds and there are no abnormal movements of the body. This type of seizure may occur hundreds of times daily.
Partial seizures are caused by abnormal electrical activity in a more limited area of the brain. They may be simple or complex. In simple partial seizures, consciousness is not lost and an abnormal twitching movement, tingling sensation, or hallucination of smell, vision, or taste occurs, lasting several minutes. In complex partial seizures, also known as temporal lobe epilepsy, conscious contact with the surroundings is lost. The sufferer becomes dazed and may behave oddly. Typically, the person remembers little, if any, of the event.
Diagnosis is made from examination of the nervous system and an EEG.
CT scanning or MRI of the brain and blood tests may also be carried out.
Anticonvulsant drugs usually stop or reduce the frequency of seizures.
Surgery may be considered if a single area of brain damage is causing the seizures.
Epilepsy that develops during childhood may disappear following adolescence.... epilepsy
A few patients with primary amenorrhoea have an abnormality of their CHROMOSOMES or malformation of the genital tract such as absecence of the UTERUS (see TURNER’S SYNDROME). A gynaecological examination will rarely disclose an IMPERFORATE HYMEN in a young girl who may also complain of regular cycles of pain like period pains.
There are many causes of secondary amenorrhoea and management requires dealing with the primary cause. The commonest cause is pregnancy. Disorders of the HYPOTHALAMUS and related psychological factors such as anorexia nervosa (see EATING DISORDERS) also cause amenorrhoea, as can poor nutrition and loss of weight by extreme dieting. It is common in ballet dancers and athletes who exercise a great deal, but can also be triggered by serious illnesses such as tuberculosis or malaria. Excess secretion of prolactin, either due to a micro-adenoma (see ADENOMA) of the PITUITARY GLAND or to various prescription drugs will produce amenorrhoea, and sometimes GALACTORRHOEA as well. Malfunction of other parts of the pituitary gland will cause failure to produce GONADOTROPHINS, thus causing ovarian failure with consequent amenorrhea. In CUSHING’S SYNDROME, amenorrhoea is caused by excessive production of cortisol. Similarly, androgen-production abnormalities are found in the common POLYCYSTIC OVARY SYNDROME. These conditions also have abnormalities of the insulin/glucose control mechanisms. Taking the contraceptive pill is not now considered to provoke secondary amenorrhoea but OBESITY and HYPOTHYROIDISM are potential causes.
When the cause is weight loss, restoring body weight may alone restore menstruation. Otherwise, measuring gonadotrophic hormone levels will help show whether amenorrhoea is due to primary ovarian failure or secondary to pituitary disease. Women with raised concentrations of serum gonadotrophic hormones have primary ovarian failure. When amenorrhoea is due to limited pituitary failure, treatment with CLOMIPHENE may solve the problem.... amenorrhoea
Because amphetamines inhibit appetite, they rapidly achieved a reputation for slimming purposes. However, they should not be used for this purpose; their dangers far outweigh their advantages.... amphetamines
Habitat: Throughout India, from Himachal Pradesh to Assam and Mizoram, and all over southern India.
English: Creat.Ayurvedic: Kaalmegha, Bhuunimba, Bhuuminimbaka, Vishwambharaa, Yavtikta, Kalpanaatha, Kiraata-tikta (var.).Unani: Kiryaat.Siddha/Tamil: Nilavembu.Action: Hepatoprotective, cholin- ergic, antispasmodic, stomachic, anthelmintic, alterative, blood purifier, febrifuge. It acts well on the liver, promoting secretion of bile. Used in jaundice and torpid liver, flatulence and diarrhoea of children, colic, strangulation of intestines and splenomegaly; also for cold and upper respiratory tract infections.
Key application: As bitter tonic, febrifuge and hepatoprotective. (Indian Herbal Pharmacopoeia.)Kaalmegha, officinal in IP, consists of dried leaves and tender shoots, which yield not less than 1% andro- grapholide on dry-weight basis.Several active constituents have been identified from the leaf and rhizome, including andrographolide, deoxyan- drographolide and other diterpenes.Andrographolide exhibited strong choleretic action when administered i.p. to rats. It induces increase in bile flow together with change in physical properties of bile secretion. It was found to be more potent than sily- marin.Andrographolide was found to be almost devoid of antihepatitis-B virus surface antigen-like activity (when compared with picroliv.)The leaf and stem extracts of Kaal- megha/andrographolide given s.c. or orally did not change blood sugar level of normal or diabetic rats.Alcoholic extract of the plant exhibited antidiarrhoeal activity against E. coli enterotoxins in animal models.Clinical evidence of effectiveness of andrographis in humans is limited to the common cold. Preliminary evidence suggests that it might increase antibody activity and phagocytosis by macrophages, and might have mast cell-stabilizing and antiallergy activity. (Natural Medicines Comprehensive Database, 2007.)The herb is contraindicated inbleed- ing disorders, hypotension, as well as male and female sterility (exhibited infertility in laboratory animals).Dosage: Whole plant—5-10 ml juice; 50-100 ml decotion; 1-3 g powder. (CCRAS.)... andrographis panicultataNutritional 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 Protein: Low (cocoa powder) High (chocolate) Fat: Moderate Saturated fat: High Cholesterol: None Carbohydrates: Low (chocolate) High (cocoa powder) Fiber: Moderate (chocolate) High (cocoa powder) Sodium: Moderate Major vitamin contribution: B vitamins Major mineral contribution: Calcium, iron, copper
About the Nutrients in This Food Cocoa beans are high-carbohydrate, high-protein food, with less dietary fiber and more fat than all other beans, excepting soy beans. The cocoa bean’s dietary fiber includes pectins and gums. Its proteins are limited in the essential amino acids lysine and isoleucine. Cocoa butter, the fat in cocoa beans, is the second most highly saturated vegetable fat (coconut oil is number one), but it has two redeeming nutritional qualities. First, it rarely turns rancid. Second, it melts at 95°F, the temperature of the human tongue. Cocoa butter has no cholesterol; neither does plain cocoa powder or plain dark chocolate. Cocoa beans have B vitamins (thiamine, riboflavin, niacin) plus min- erals (iron, magnesium, potassium, phosphorus, and copper). All chocolate candy is made from chocolate liquor, a thick paste pro- duce by roasting and grinding cocoa beans. Dark (sweet) chocolate is made of chocolate liquor, cocoa butter, and sugar. Milk chocolate is made of choc- olate liquor, cocoa butter, sugar, milk or milk powder, and vanilla. White * These values apply to plain cocoa powder and plain unsweetened chocolate. Add- ing other foods, such as milk or sugar, changes these values. For example, there is no cholesterol in plain bitter chocolate, but there is cholesterol in milk chocolate. chocolate is made of cocoa butter, sugar, and milk powder. Baking chocolate is unsweetened dark chocolate. The most prominent nutrient in chocolate is its fat. Fat Content in One Ounce of Chocolate
| Saturated fat (g) | Monounsaturated fat (g) | Polyunsaturated fat (g) | Cholesterol (mg) | |
| Dark (sweet) | ||||
| chocolate | 5.6 | 3.2 | 0.3 | 0 |
| Milk chocolate | 5.9 | 4.5 | 0.4 | 6.6 |
| Baking chocolate | 9 | 5.6 | 0.3 | 0 |
| White chocolate | 5.5 | 2.6 | 0.3 | 0 |
The Most Nutritious Way to Serve This Food With low-fat milk to complete the proteins without adding saturated fat and cholesterol. NOTE : Both cocoa and chocolate contain oxalic acid, which binds with calcium to form cal- cium oxalate, an insoluble compound, but milk has so much calcium that the small amount bound to cocoa and chocolate hardly matters. Chocolate skim milk is a source of calcium.
Diets That May Restrict or Exclude This Food Antiflatulence diet Low-calcium and low-oxalate diet (to prevent the formation of calcium oxalate kidney stones) Low-calorie diet Low-carbohydrate diet Low-fat diet Low-fat, controlled-cholesterol diet (milk chocolates) Low-fiber diet Potassium-regulated (low-potassium) diet
Buying This Food Look for: Tightly sealed boxes or bars. When you open a box of chocolates or unwrap a candy bar, the chocolate should be glossy and shiny. Chocolate that looks dull may be stale, or it may be inexpensively made candy without enough cocoa butter to make it gleam and give it the rich creamy mouthfeel we associate with the best chocolate. (Fine chocolate melts evenly on the tongue.) Chocolate should also smell fresh, not dry and powdery, and when you break a bar or piece of chocolate it should break cleanly, not crumble. One exception: If you have stored a bar of chocolate in the refrigerator, it may splinter if you break it without bringing it to room temperature first.
Storing This Food Store chocolate at a constant temperature, preferably below 78°F. At higher temperatures, the fat in the chocolate will rise to the surface and, when the chocolate is cooled, the fat will solidif y into a whitish powdery bloom. Bloom is unsightly but doesn’t change the chocolate’s taste or nutritional value. To get rid of bloom, melt the chocolate. The chocolate will turn dark, rich brown again when its fat recombines with the other ingredients. Chocolate with bloom makes a perfectly satisfactory chocolate sauce. Dark chocolate (bitter chocolate, semisweet chocolate) ages for at least six months after it is made, as its flavor becomes deeper and more intense. Wrapped tightly and stored in a cool, dry cabinet, it can stay fresh for a year or more. Milk chocolate ages only for about a month after it is made and holds its peak flavor for about three to six months, depending on how carefully it is stored. Plain cocoa, with no added milk powder or sugar, will stay fresh for up to a year if you keep it tightly sealed and cool.
What Happens When You Cook This Food Chocolate burns easily. To melt it without mishap, stir the chocolate in a bowl over a pot of hot water or in the top of a double boiler or put the chocolate in a covered dish and melt it in the microwave (which does not get as hot as a pot on the store). Simple chemistry dictates that chocolate cakes be leavened with baking soda rather than baking powder. Chocolate is so acidic that it will upset the delicate balance of acid (cream of tartar) and base (alkali = sodium bicarbonate = baking soda) in baking powder. But it is not acidic enough to balance plain sodium bicarbonate. That’s why we add an acidic sour-milk product such as buttermilk or sour cream or yogurt to a chocolate cake. Without the sour milk, the batter would be so basic that the chocolate would look red, not brown, and taste very bitter.
How Other Kinds of Processing Affect This Food Freezing. Chocolate freezes and thaws well. Pack it in a moistureproof container and defrost it in the same package to let it reabsorb moisture it gave off while frozen.
Medical Uses and/or Benefits Mood elevator. Chocolate’s reputation for making people feel good is based not only on its caffeine content—19 mg caffeine per ounce of dark (sweet) chocolate, which is one-third the amount of caffeine in a five-ounce cup of brewed coffee—but also on its naturally occurring mood altering chemicals phenylethylalanine and anandamide. Phenylethylalanine is found in the blood of people in love. Anandamide stimulates areas of your brain also affected by the active ingredients in marijuana. (NOTE : As noted by the researchers at the Neurosci- ences Institute in San Diego who identified anandamide in chocolate in 1996, to get even the faintest hint of marijuana-like effects from chocolate you would have to eat more than 25 pounds of the candy all at once.) Possible heart health benefits. Chocolate is rich in catechins, the antioxidant chemicals that give tea its reputation as a heart-protective anticancer beverage (see tea). In addition, a series of studies beginning with those at the USDA Agricultural Research Center in Peoria, Illinois, suggest that consuming foods rich in stearic acid like chocolate may reduce rather than raise the risk of a blood clot leading to a heart attack. Possible slowing of the aging process. Chocolate is a relatively good source of copper, a mineral that may play a role in slowing the aging process by decreasing the incidence of “protein glycation,” a reaction in which sugar molecules ( gly = sugar) hook up with protein molecules in the bloodstream, twisting the protein molecules out of shape and rendering them unusable. This can lead to bone loss, rising cholesterol, cardiac abnormalities, and a slew of other unpleasantries. In people with diabetes, excess protein glycation may be one factor involved in complications such as loss of vision. Ordinarily, increased protein glyca- tion is age-related. But at the USDA Grand Forks Human Nutrition Research Center in North Dakota, agricultural research scientist Jack T. Saari has found that rats on copper-deficient diets experience more protein glycation at any age than other rats. A recent USDA survey of American eating patterns says that most of us get about 1.2 mg copper a day, considerably less than the Estimated Safe and Adequate Daily Dietary Intake (ESADDI) or 1.5 mg to 3 mg a day. Vegetarians are less likely to be copper deficient because, as Saari notes, the foods highest in copper are whole grains, nuts, seeds, and beans, including the cocoa bean. One ounce of dark chocolate has .25 mg copper (8 –17 percent of the ESADDI).
Adverse Effects Associated with This Food Possible loss of bone density. In 2008, a team of Australian researchers at Royal Perth Hos- pital, and Sir Charles Gairdner Hospital published a report in the American Journal of Clinical Nutrition suggesting that women who consume chocolate daily had 3.1 percent lower bone density than women who consume chocolate no more than once a week. No explanation for the reaction was proposed; the finding remains to be confirmed. Possible increase in the risk of heart disease. Cocoa beans, cocoa powder, and plain dark chocolate are high in saturated fats. Milk chocolate is high in saturated fats and cholesterol. Eating foods high in saturated fats and cholesterol increases the amount of cholesterol in your blood and raises your risk of heart disease. NOTE : Plain cocoa powder and plain dark chocolate may be exceptions to this rule. In studies at the USDA Agricultural Research Center in Peoria, Illinois, volunteers who consumed foods high in stearic acid, the saturated fat in cocoa beans, cocoa powder, and chocolate, had a lower risk of blood clots. In addition, chocolate is high in flavonoids, the antioxidant chemicals that give red wine its heart-healthy reputation. Mild jitters. There is less caffeine in chocolate than in an equal size serving of coffee: A five- ounce cup of drip-brewed coffee has 110 to 150 mg caffeine; a five-ounce cup of cocoa made with a tablespoon of plain cocoa powder ( 1/3 oz.) has about 18 mg caffeine. Nonetheless, people who are very sensitive to caffeine may find even these small amounts problematic. Allergic reaction. According to the Merck Manual, chocolate is one of the 12 foods most likely to trigger the classic food allergy symptoms: hives, swelling of the lips and eyes, and upset stomach.* The others are berries (blackberries, blueberries, raspberries, strawberries), corn, eggs, fish, legumes (green peas, lima beans, peanuts, soybeans), milk, nuts, peaches, pork, shellfish, and wheat (see wheat cer ea ls).
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 tyra- mine, a substance found in many fermented or aged foods. Tyramine constricts blood vessels and increases blood pressure. Caffeine is a substance similar to tyramine. If you consume excessive amounts of a caffeinated food, such as cocoa or chocolate, while you are taking an M AO inhibitor, the result may be a hypertensive crisis. False-positive test for pheochromocytoma. Pheochromocytoma, a tumor of the adrenal gland, secretes adrenalin, which the body converts to VM A (vanillylmandelic acid). VM A is excreted in urine, and, until recently, the test for this tumor measured the level of VM A in the urine. In the past, chocolate and cocoa, both of which contain VM A, were eliminated from the patient’s diet prior to the test lest they elevate the level of VM A in the urine and produce a false-positive result. Today, more finely drawn tests usually make this unnecessary. * The evidence link ing chocolate to allergic or migraine headaches is inconsistent. In some people, phenylet hylamine (PEA) seems to cause headaches similar to t hose induced by t yramine, anot her pressor amine. The PEA-induced headache is unusual in t hat it is a delayed react ion t hat usually occurs 12 or more hours after t he chocolate is eaten.... chocolate
This technique is used when normal methods of attempted CONCEPTION or ARTIFICIAL INSEMINATION with healthy SEMEN have failed. In the UK, assisted-conception procedures are governed by the Human Fertilisation & Embryology Act 1990, which set up the Human Fertilisation & Embryology Authority (HFEA).
Human Fertilisation & Embryology Act 1990 UK legislation was prompted by the report on in vitro fertilisation produced by a government-appointed committee chaired by Baroness Warnock. This followed the birth, in 1978, of the ?rst ‘test-tube’ baby.
This Act allows regulation monitoring of all treatment centres to ensure that they carry out treatment and research responsibly. It covers any fertilisation that uses donated eggs or sperm (called gametes) – for example, donor insemination or embryos (see EMBRYO) grown outside the human body (known as licensed treatment). The Act also covers research on human embryos with especial emphasis on foolproof labelling and immaculate data collection.
Human Fertilisation & EmbryologyAuthority (HFEA) Set up by the UK government following the Warnock report, the Authority’s 221 members inspect and license centres carrying out fertilisation treatments using donated eggs and sperm. It publishes a code of practice advising centres on how to conduct their activities and maintains a register of information on donors, patients and all treatments. It also reviews routinely progress and research in fertility treatment and the attempted development of human CLONING. Cloning to produce viable embryos (reproductive cloning) is forbidden, but limited licensing of the technique is allowed in specialist centres to enable them to produce cells for medical treatment (therapeutic cloning).
In vitro fertilisation (IVF) In this technique, the female partner receives drugs to enhance OVULATION. Just before the eggs are released from the ovary (see OVARIES), several ripe eggs are collected under ULTRASOUND guidance or through a LAPAROSCOPE. The eggs are incubated with the prepared sperm. About 40 hours later, once the eggs are fertilised, two eggs (three in special circumstances) are transferred into the mother’s UTERUS via the cervix (neck of the womb). Pregnancy should then proceed normally. About one in ?ve IVF pregnancies results in the birth of a child. The success rate is lower in women over 40.
Indications In women with severely damaged FALLOPIAN TUBES, IVF o?ers the only chance of pregnancy. The method is also used in couples with unexplained infertility or with male-factor infertility (where sperms are abnormal or their count low). Women who have had an early or surgically induced MENOPAUSE can become pregnant using donor eggs. A quarter of these pregnancies are multiple – that is, produce twins or more. Twins and triplets are more likely to be premature. The main danger of ovarian stimulation for IVF is hyperstimulation which can cause ovarian cysts. (See OVARIES, DISEASES OF.)... assisted conception
Nutritional Profile Energy value (calories per serving): Low Protein: Trace Fat: Trace Saturated fat: None Cholesterol: None Carbohydrates: Trace Fiber: Trace Sodium: Low Major vitamin contribution: None Major mineral contribution: None
About the Nutrients in This Food Coffee beans are roasted seeds from the fruit of the evergreen coffee tree. Like other nuts and seeds, they are high in proteins (11 percent), sucrose and other sugars (8 percent), oils (10 to 15 percent), assorted organic acids (6 percent), B vitamins, iron, and the central nervous system stimulant caffeine (1 to 2 percent). With the exceptions of caffeine, none of these nutrients is found in coffee. Like spinach, rhubarb, and tea, coffee contains oxalic acid (which binds calcium ions into insoluble compounds your body cannot absorb), but this is of no nutritional consequence as long as your diet contains adequate amounts of calcium-rich foods. Coffee’s best known constituent is the methylxanthine central ner- vous system stimulant caffeine. How much caffeine you get in a cup of coffee depends on how the coffee was processed and brewed. Caffeine is Caffeine Content/Coffee Servings Brewed coffee 60 mg/five-ounce cup Brewed/decaffeinated 5 mg/five-ounce cup Espresso 64 mg/one-ounce serving Instant 47 mg/rounded teaspoon
The Most Nutritious Way to Serve This Food In moderation, with high-calcium foods. Like spinach, rhubarb, and tea, coffee has oxalic acid, which binds calcium into insoluble compounds. This will have no important effect as long as you keep your consumption moderate (two to four cups of coffee a day) and your calcium consumption high.
Diets That May Restrict or Exclude This Food Bland diet Gout diet Diet for people with heart disease (regular coffee)
Buying This Food Look for: Ground coffee and coffee beans in tightly sealed, air- and moisture-proof containers. Avoid: Bulk coffees or coffee beans stored in open bins. When coffee is exposed to air, the volatile molecules that give it its distinctive flavor and richness escape, leaving the coffee flavorless and/or bitter.
Storing This Food Store unopened vacuum-packed cans of ground coffee or coffee beans in a cool, dark cabinet—where they will stay fresh for six months to a year. They will lose some flavor in storage, though, because it is impossible to can coffee without trapping some flavor- destroying air inside the can. Once the can or paper sack has been opened, the coffee or beans should be sealed as tight as possible and stored in the refrigerator. Tightly wrapped, refrigerated ground coffee will hold its freshness and flavor for about a week, whole beans for about three weeks. For longer storage, freeze the coffee or beans in an air- and moistureproof container. ( You can brew coffee directly from frozen ground coffee and you can grind frozen beans without thawing them.)
Preparing This Food If you make your coffee with tap water, let the water run for a while to add oxygen. Soft water makes “cleaner”-tasting coffee than mineral-rich hard water. Coffee made with chlorinated water will taste better if you refrigerate the water overnight in a glass (not plastic) bottle so that the chlorine evaporates. Never make coffee with hot tap water or water that has been boiled. Both lack oxygen, which means that your coffee will taste flat. Always brew coffee in a scrupulously clean pot. Each time you make coffee, oils are left on the inside of the pot. If you don’t scrub them off, they will turn rancid and the next pot of coffee you brew will taste bitter. To clean a coffee pot, wash it with detergent, rinse it with water in which you have dissolved a few teaspoons of baking soda, then rinse one more time with boiling water.
What Happens When You Cook This Food In making coffee, your aim is to extract flavorful solids (including coffee oils and sucrose and other sugars) from the ground beans without pulling bitter, astringent tannins along with them. How long you brew the coffee determines how much solid material you extract and how the coffee tastes. The longer the brewing time, the greater the amount of solids extracted. If you brew the coffee long enough to extract more than 30 percent of its solids, you will get bitter compounds along with the flavorful ones. (These will also develop by let- ting coffee sit for a long time after brewing it.) Ordinarily, drip coffee tastes less bitter than percolator coffee because the water in a drip coffeemaker goes through the coffee only once, while the water in the percolator pot is circulated through the coffee several times. To make strong but not bitter coffee, increase the amount of coffee—not the brewing time.
How Other Kinds of Processing Affect This Food Drying. Soluble coffees (freeze-dried, instant) are made by dehydrating concentrated brewed coffee. These coffees are often lower in caffeine than regular ground coffees because caffeine, which dissolves in water, is lost when the coffee is dehydrated. Decaffeinating. Decaffeinated coffee is made with beans from which the caffeine has been extracted, either with an organic solvent (methylene chloride) or with water. How the coffee is decaffeinated has no effect on its taste, but many people prefer water-processed decaf- feinated coffee because it is not a chemically treated food. (Methylene chloride is an animal carcinogen, but the amounts that remain in coffees decaffeinated with methylene chloride are so small that the FDA does not consider them hazardous. The carcinogenic organic sol- vent trichloroethylene [TCE], a chemical that causes liver cancer in laboratory animals, is no longer used to decaffeinate coffee.)
Medical Uses and/or Benefits As a stimulant and mood elevator. Caffeine is a stimulant. It increases alertness and concentra- tion, intensifies muscle responses, quickens heartbeat, and elevates mood. Its effects derive from the fact that its molecular structure is similar to that of adenosine, a natural chemical by-product of normal cell activity. Adenosine is a regular chemical that keeps nerve cell activ- ity within safe limits. When caffeine molecules hook up to sites in the brain when adenosine molecules normally dock, nerve cells continue to fire indiscriminately, producing the jangly feeling sometimes associated with drinking coffee, tea, and other caffeine products. As a rule, it takes five to six hours to metabolize and excrete caffeine from the body. During that time, its effects may vary widely from person to person. Some find its stimu- lation pleasant, even relaxing; others experience restlessness, nervousness, hyperactivity, insomnia, flushing, and upset stomach after as little as one cup a day. It is possible to develop a tolerance for caffeine, so people who drink coffee every day are likely to find it less imme- diately stimulating than those who drink it only once in a while. Changes in blood vessels. Caffeine’s effects on blood vessels depend on site: It dilates coronary and gastrointestinal vessels but constricts blood vessels in your head and may relieve headache, such as migraine, which symptoms include swollen cranial blood vessels. It may also increase pain-free exercise time in patients with angina. However, because it speeds up heartbeat, doc- tors often advise patients with heart disease to avoid caffeinated beverages entirely. As a diuretic. Caffeine is a mild diuretic sometimes included in over-the-counter remedies for premenstrual tension or menstrual discomfort.
Adverse Effects Associated with This Food Stimulation of acid secretion in the stomach. Both regular and decaffeinated coffees increase the secretion of stomach acid, which suggests that the culprit is the oil in coffee, not its caffeine. Elevated blood levels of cholesterol and homocysteine. In the mid-1990s, several studies in the Netherlands and Norway suggested that drinking even moderate amounts of coffee (five cups a day or less) might raise blood levels of cholesterol and homocysteine (by-product of protein metabolism considered an independent risk factor for heart disease), thus increas- ing the risk of cardiovascular disease. Follow-up studies, however, showed the risk limited to drinking unfiltered coffees such as coffee made in a coffee press, or boiled coffees such as Greek, Turkish, or espresso coffee. The unfiltered coffees contain problematic amounts of cafestol and kahweol, two members of a chemical family called diterpenes, which are believed to affect cholesterol and homocysteine levels. Diterpenes are removed by filtering coffee, as in a drip-brew pot. Possible increased risk of miscarriage. Two studies released in 2008 arrived at different conclusions regarding a link between coffee consumption and an increased risk of miscar- riage. The first, at Kaiser Permanente (California), found a higher risk of miscarriage among women consuming even two eight-ounce cups of coffee a day. The second, at Mt. Sinai School of Medicine (New York), found no such link. However, although the authors of the Kaiser Permanente study described it as a “prospective study” (a study in which the research- ers report results that occur after the study begins), in fact nearly two-thirds of the women who suffered a miscarriage miscarried before the study began, thus confusing the results. Increased risk of heartburn /acid reflux. The natural oils in both regular and decaffeinated coffees loosen the lower esophageal sphincter (LES), a muscular valve between the esopha- gus 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 esophagus. If the LES does not close efficiently, the stomach contents reflux and cause heartburn, a burning sensation. Repeated reflux is a risk factor for esophageal cancer. Masking of sleep disorders. Sleep deprivation is a serious problem associated not only with automobile accidents but also with health conditions such as depression and high blood pres- sure. People who rely on the caffeine in a morning cup of coffee to compensate for lack of sleep may put themselves at risk for these disorders. Withdrawal symptoms. Caffeine is a drug for which you develop a tolerance; the more often you use it, the more likely you are to require a larger dose to produce the same effects and the more likely you are to experience withdrawal symptoms (headache, irritation) if you stop using it. The symptoms of coffee-withdrawal can be relieved immediately by drinking a cup of coffee.
Food/Drug Interactions Drugs that make it harder to metabolize caffeine. Some medical drugs slow the body’s metabolism of caffeine, thus increasing its stimulating effect. The list of such drugs includes cimetidine (Tagamet), disulfiram (Antabuse), estrogens, fluoroquinolone antibiotics (e.g., ciprofloxacin, enoxacin, norfloxacin), fluconazole (Diflucan), fluvoxamine (Luvox), mexi- letine (Mexitil), riluzole (R ilutek), terbinafine (Lamisil), and verapamil (Calan). If you are taking one of these medicines, check with your doctor regarding your consumption of caf- feinated beverages. Drugs whose adverse effects increase due to consumption of large amounts of caffeine. This list includes such drugs as metaproterenol (Alupent), clozapine (Clozaril), ephedrine, epinephrine, monoamine oxidase inhibitors, phenylpropanolamine, and theophylline. In addition, suddenly decreasing your caffeine intake may increase blood levels of lithium, a drug used to control mood swings. If you are taking one of these medicines, check with your doctor regarding your consumption of caffeinated beverages. Allopurinol. Coffee and other beverages containing methylxanthine stimulants (caffeine, theophylline, and theobromine) reduce the effectiveness of the antigout drug allopurinol, which is designed to inhibit xanthines. Analgesics. Caffeine strengthens over-the-counter painkillers (acetaminophen, aspirin, and other nonsteroidal anti-inflammatories [NSAIDS] such as ibuprofen and naproxen). But it also makes it more likely that NSAIDS will irritate your stomach lining. Antibiotics. Coffee increases stomach acidity, which reduces the rate at which ampicillin, erythromycin, griseofulvin, penicillin, and tetracyclines are absorbed when they are taken by mouth. (There is no effect when the drugs are administered by injection.) Antiulcer medication. Coffee increases stomach acidity and reduces the effectiveness of nor- mal doses of cimetidine and other antiulcer medication. False-positive test for pheochromocytoma. Pheochromocytoma, a tumor of the adrenal glands, secretes adrenalin, which is converted to VM A (vanillylmandelic acid) by the body and excreted in the urine. Until recently, the test for this tumor measured the levels of VM A in the patient’s urine and coffee, which contains VM A, was eliminated from patients’ diets lest it elevate the level of VM A in the urine, producing a false-positive test result. Today, more finely drawn tests make this unnecessary. Iron supplements. Caffeine binds with iron to form insoluble compounds your body cannot absorb. Ideally, iron supplements and coffee should be taken at least two hours apart. Birth control pills. Using oral contraceptives appears to double the time it takes to eliminate caffeine from the body. Instead of five to six hours, the stimulation of one cup of coffee may last as long as 12 hours. 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 vessels and increases blood pressure. Caffeine is a substance similar to tyramine. If you consume excessive amounts of a caffeinated beverage such as coffee while you are taking an M AO inhibitor, the result may be a hypertensive crisis. Nonprescription drugs containing caffeine. The caffeine in coffee may add to the stimulant effects of the caffeine in over-the-counter cold remedies, diuretics, pain relievers, stimulants, and weight-control products containing caffeine. Some cold pills contain 30 mg caffeine, some pain relievers 130 mg, and some weight-control products as much as 280 mg caffeine. There are 110 –150 mg caffeine in a five-ounce cup of drip-brewed coffee. Sedatives. The caffeine in coffee may counteract the drowsiness caused by sedative drugs; this may be a boon to people who get sleepy when they take antihistamines. Coffee will not, however, “sober up” people who are experiencing the inebriating effects of alcoholic beverages. Theophylline. Caffeine relaxes the smooth muscle of the bronchi and may intensif y the effects (and/or increase the risk of side effects) of this antiasthmatic drug.... coffee
Adrenal glands These two glands, also known as suprarenal glands, lie immediately above the kidneys. The central or medullary portion of the glands forms the secretions known as ADRENALINE (or epinephrine) and NORADRENALINE. Adrenaline acts upon structures innervated by sympathetic nerves. Brie?y, the blood vessels of the skin and of the abdominal viscera (except the intestines) are constricted, and at the same time the arteries of the muscles and the coronary arteries are dilated; systolic blood pressure rises; blood sugar increases; the metabolic rate rises; muscle fatigue is diminished. The super?cial or cortical part of the glands produces steroid-based substances such as aldosterone, cortisone, hydrocortisone, and deoxycortone acetate, for the maintenance of life. It is the absence of these substances, due to atrophy or destruction of the suprarenal cortex, that is responsible for the condition known as ADDISON’S DISEASE. (See CORTICOSTEROIDS.)
Ovaries and testicles The ovary (see OVARIES) secretes at least two hormones – known, respectively, as oestradiol (follicular hormone) and progesterone (corpus luteum hormone). Oestradiol develops (under the stimulus of the anterior pituitary lobe – see PITUITARY GLAND below, and under separate entry) each time an ovum in the ovary becomes mature, and causes extensive proliferation of the ENDOMETRIUM lining the UTERUS, a stage ending with shedding of the ovum about 14 days before the onset of MENSTRUATION. The corpus luteum, which then forms, secretes both progesterone and oestradiol. Progesterone brings about great activity of the glands in the endometrium. The uterus is now ready to receive the ovum if it is fertilised. If fertilisation does not occur, the corpus luteum degenerates, the hormones cease acting, and menstruation takes place.
The hormone secreted by the testicles (see TESTICLE) is known as TESTOSTERONE. It is responsible for the growth of the male secondary sex characteristics.
Pancreas This gland is situated in the upper part of the abdomen and, in addition to the digestive enzymes, it produces INSULIN within specialised cells (islets of Langerhans). This controls carbohydrate metabolism; faulty or absent insulin production causes DIABETES MELLITUS.
Parathyroid glands These are four minute glands lying at the side of, or behind, the thyroid (see below). They have a certain e?ect in controlling the absorption of calcium salts by the bones and other tissues. When their secretion is defective, TETANY occurs.
Pituitary gland This gland is attached to the base of the brain and rests in a hollow on the base of the skull. It is the most important of all endocrine glands and consists of two embryologically and functionally distinct lobes.
The function of the anterior lobe depends on the secretion by the HYPOTHALAMUS of certain ‘neuro-hormones’ which control the secretion of the pituitary trophic hormones. The hypothalamic centres involved in the control of speci?c pituitary hormones appear to be anatomically separate. Through the pituitary trophic hormones the activity of the thyroid, adrenal cortex and the sex glands is controlled. The anterior pituitary and the target glands are linked through a feedback control cycle. The liberation of trophic hormones is inhibited by a rising concentration of the circulating hormone of the target gland, and stimulated by a fall in its concentration. Six trophic (polypeptide) hormones are formed by the anterior pituitary. Growth hormone (GH) and prolactin are simple proteins formed in the acidophil cells. Follicle-stimulating hormone (FSH), luteinising hormone (LH) and thyroid-stimulating hormone (TSH) are glycoproteins formed in the basophil cells. Adrenocorticotrophic hormone (ACTH), although a polypeptide, is derived from basophil cells.
The posterior pituitary lobe, or neurohypophysis, is closely connected with the hypothalamus by the hypothalamic-hypophyseal tracts. It is concerned with the production or storage of OXYTOCIN and vasopressin (the antidiuretic hormone).
PITUITARY HORMONES Growth hormone, gonadotrophic hormone, adrenocorticotrophic hormone and thyrotrophic hormones can be assayed in blood or urine by radio-immunoassay techniques. Growth hormone extracted from human pituitary glands obtained at autopsy was available for clinical use until 1985, when it was withdrawn as it is believed to carry the virus responsible for CREUTZFELDT-JAKOB DISEASE (COD). However, growth hormone produced by DNA recombinant techniques is now available as somatropin. Synthetic growth hormone is used to treat de?ciency of the natural hormone in children and adults, TURNER’S SYNDROME and chronic renal insu?ciency in children.
Human pituitary gonadotrophins are readily obtained from post-menopausal urine. Commercial extracts from this source are available and are e?ective for treatment of infertility due to gonadotrophin insu?ciency.
The adrenocorticotrophic hormone is extracted from animal pituitary glands and has been available therapeutically for many years. It is used as a test of adrenal function, and, under certain circumstances, in conditions for which corticosteroid therapy is indicated (see CORTICOSTEROIDS). The pharmacologically active polypeptide of ACTH has been synthesised and is called tetracosactrin. Thyrotrophic hormone is also available but it has no therapeutic application.
HYPOTHALAMIC RELEASING HORMONES which affect the release of each of the six anterior pituitary hormones have been identi?ed. Their blood levels are only one-thousandth of those of the pituitary trophic hormones. The release of thyrotrophin, adrenocorticotrophin, growth hormone, follicle-stimulating hormone and luteinising hormone is stimulated, while release of prolactin is inhibited. The structure of the releasing hormones for TSH, FSH-LH, GH and, most recently, ACTH is known and they have all been synthesised. Thyrotrophin-releasing hormone (TRH) is used as a diagnostic test of thyroid function but it has no therapeutic application. FSH-LH-releasing hormone provides a useful diagnostic test of gonadotrophin reserve in patients with pituitary disease, and is now used in the treatment of infertility and AMENORRHOEA in patients with functional hypothalamic disturbance. As this is the most common variety of secondary amenorrhoea, the potential use is great. Most cases of congenital de?ciency of GH, FSH, LH and ACTH are due to defects in the hypothalamic production of releasing hormone and are not a primary pituitary defect, so that the therapeutic implication of this synthesised group of releasing hormones is considerable.
GALACTORRHOEA is frequently due to a microadenoma (see ADENOMA) of the pituitary. DOPAMINE is the prolactin-release inhibiting hormone. Its duration of action is short so its therapeutic value is limited. However, BROMOCRIPTINE is a dopamine agonist with a more prolonged action and is e?ective treatment for galactorrhoea.
Thyroid gland The functions of the thyroid gland are controlled by the pituitary gland (see above) and the hypothalamus, situated in the brain. The thyroid, situated in the front of the neck below the LARYNX, helps to regulate the body’s METABOLISM. It comprises two lobes each side of the TRACHEA joined by an isthmus. Two types of secretory cells in the gland – follicular cells (the majority) and parafollicular cells – secrete, respectively, the iodine-containing hormones THYROXINE (T4) and TRI-IODOTHYRONINE (T3), and the hormone CALCITONIN. T3 and T4 help control metabolism and calcitonin, in conjunction with parathyroid hormone (see above), regulates the body’s calcium balance. De?ciencies in thyroid function produce HYPOTHYROIDISM and, in children, retarded development. Excess thyroid activity causes thyrotoxicosis. (See THYROID GLAND, DISEASES OF.)... endocrine glands
The outer coat consists of the sclera and the cornea; their junction is called the limbus. SCLERA This is white, opaque, and constitutes the posterior ?ve-sixths of the outer coat. It is made of dense ?brous tissue. The sclera is visible anteriorly, between the eyelids, as the ‘white of the eye’. Posteriorly and anteriorly it is covered by Tenons capsule, which in turn is covered by transparent conjunctiva. There is a hole in the sclera through which nerve ?bres from the retina leave the eye in the optic nerve. Other smaller nerve ?bres and blood vessels also pass through the sclera at di?erent points. CORNEA This constitutes the transparent, colourless anterior one-sixth of the eye. It is transparent in order to allow light into the eye and is more steeply curved than the sclera. Viewed from in front, the cornea is roughly circular. Most of the focusing power of the eye is provided by the cornea (the lens acts as the ‘?ne adjustment’). It has an outer epithelium, a central stroma and an inner endothelium. The cornea is supplied with very ?ne nerve ?bres which make it exquisitely sensitive to pain. The central cornea has no blood supply – it relies mainly on aqueous humour for nutrition. Blood vessels and large nerve ?bres in the cornea would prevent light from entering the eye. LIMBUS is the junction between cornea and sclera. It contains the trabecular meshwork, a sieve-like structure through which aqueous humour leaves the eye.
The middle coat (uveal tract) consists of the choroid, ciliary body and iris. CHOROID A highly vascular sheet of tissue lining the posterior two-thirds of the sclera. The network of vessels provides the blood supply for the outer half of the retina. The blood supply of the choroid is derived from numerous ciliary vessels which pierce the sclera in front and behind. CILIARY BODY A ring of tissue extending 6 mm back from the anterior limitation of the sclera. The various muscles of the ciliary body by their contractions and relaxations are responsible for changing the shape of the lens during ACCOMMODATION. The ciliary body is lined by cells that secrete aqueous humour. Posteriorly, the ciliary body is continuous with the choroid; anteriorly it is continuous with the iris. IRIS A ?attened muscular diaphragm that is attached at its periphery to the ciliary body, and has a round central opening – the pupil. By contraction and relaxation of the muscles of the iris, the pupil can be dilated or constricted (dilated in the dark or when aroused; constricted in bright light and for close work). The iris forms a partial division between the anterior chamber and the posterior chamber of the eye. It lies in front of the lens and forms the back wall of the anterior chamber. The iris is visible from in front, through the transparent cornea, as the ‘coloured part of the eye’. The amount and distribution of iris pigment determine the colour of the iris. The pupil is merely a hole in the centre of the iris and appears black.
The inner layer The retina is a multilayered tissue (ten layers in all) which extends from the edges of the optic nerve to line the inner surface of the choroid up to the junction of ciliary body and choroid. Here the true retina ends at the ora serrata. The retina contains light-sensitive cells of two types: (i) cones – cells that operate at high and medium levels of illumination; they subserve ?ne discrimination of vision and colour vision; (ii) rods – cells that function best at low light intensity and subserve black-and-white vision.
The retina contains about 6 million cones and about 100 million rods. Information from them is conveyed by the nerve ?bres which are in the inner part of the retina, and leave the eye in the optic nerve. There are no photoreceptors at the optic disc (the point where the optic nerve leaves the eye) and therefore there is no light perception from this small area. The optic disc thus produces a physiological blind spot in the visual ?eld.
The retina can be subdivided into several areas: PERIPHERAL RETINA contains mainly rods and a few scattered cones. Visual acuity from this area is fairly coarse. MACULA LUTEA So-called because histologically it looks like a yellow spot. It occupies an area 4·5 mm in diameter lateral to the optic disc. This area of specialised retina can produce a high level of visual acuity. Cones are abundant here but there are few rods. FOVEA CENTRALIS A small central depression at the centre of the macula. Here the cones are tightly packed; rods are absent. It is responsible for the highest levels of visual acuity.
The chambers of the eye There are three: the anterior and posterior chambers, and the vitreous cavity. ANTERIOR CHAMBER Limited in front by the inner surface of the cornea, behind by the iris and pupil. It contains a transparent clear watery ?uid, the aqueous humour. This is constantly being produced by cells of the ciliary body and constantly drained away through the trabecular meshwork. The trabecular meshwork lies in the angle between the iris and inner surface of the cornea. POSTERIOR CHAMBER A narrow space between the iris and pupil in front and the lens behind. It too contains aqueous humour in transit from the ciliary epithelium to the anterior chamber, via the pupil. VITREOUS CAVITY The largest cavity of the eye. In front it is bounded by the lens and behind by the retina. It contains vitreous humour.
Lens Transparent, elastic and biconvex in cross-section, it lies behind the iris and in front of the vitreous cavity. Viewed from the front it is roughly circular and about 10 mm in diameter. The diameter and thickness of the lens vary with its accommodative state. The lens consists of: CAPSULE A thin transparent membrane surrounding the cortex and nucleus. CORTEX This comprises newly made lens ?bres that are relatively soft. It separates the capsule on the outside from the nucleus at the centre of the lens. NUCLEUS The dense central area of old lens ?bres that have become compacted by new lens ?bres laid down over them. ZONULE Numerous radially arranged ?bres attached between the ciliary body and the lens around its circumference. Tension in these zonular ?bres can be adjusted by the muscles of the ciliary body, thus changing the shape of the lens and altering its power of accommodation. VITREOUS HUMOUR A transparent jelly-like structure made up of a network of collagen ?bres suspended in a viscid ?uid. Its shape conforms to that of the vitreous cavity within which it is contained: that is, it is spherical except for a shallow concave depression on its anterior surface. The lens lies in this depression.
Eyelids These are multilayered curtains of tissue whose functions include spreading of the tear ?lm over the front of the eye to prevent desiccation; protection from injury or external irritation; and to some extent the control of light entering the eye. Each eye has an upper and lower lid which form an elliptical opening (the palpebral ?ssure) when the eyes are open. The lids meet at the medial canthus and lateral canthus respectively. The inner medial canthus is ?xed; the lateral canthus more mobile. An epicanthus is a fold of skin which covers the medial canthus in oriental races.
Each lid consists of several layers. From front to back they are: very thin skin; a sheet of muscle (orbicularis oculi, whose ?bres are concentric around the palpebral ?ssure and which produce closure of the eyelids); the orbital septum (modi?ed near the lid margin to form the tarsal plates); and ?nally, lining the back surface of the lid, the conjunctiva (known here as tarsal conjunctiva). At the free margin of each lid are the eyelashes, the openings of tear glands which lie within the lid, and the lacrimal punctum. Toward the medial edge of each lid is an elevation known as the papilla: the lacrimal punctum opens into this papilla. The punctum forms the open end of the cannaliculus, part of the tear-drainage mechanism.
Orbit The bony cavity within which the eye is held. The orbits lie one on either side of the nose, on the front of the skull. They a?ord considerable protection for the eye. Each is roughly pyramidal in shape, with the apex pointing backwards and the base forming the open anterior part of the orbit. The bone of the anterior orbital margin is thickened to protect the eye from injury. There are various openings into the posterior part of the orbit – namely the optic canal, which allows the optic nerve to leave the orbit en route for the brain, and the superior orbital and inferior orbital ?ssures, which allow passage of nerves and blood vessels to and from the orbit. The most important structures holding the eye within the orbit are the extra-ocular muscles, a suspensory ligament of connective tissue that forms a hammock on which the eye rests and which is slung between the medial and lateral walls of the orbit. Finally, the orbital septum, a sheet of connective tissue extending from the anterior margin of the orbit into the lids, helps keep the eye in place. A pad of fat ?lls in the orbit behind the eye and acts as a cushion for the eye.
Conjunctiva A transparent mucous membrane that extends from the limbus over the anterior sclera or ‘white of the eye’. This is the bulbar conjunctiva. The conjunctiva does not cover the cornea. Conjunctiva passes from the eye on to the inner surface of the eyelid at the fornices and is continuous with the tarsal conjunctiva. The semilunar fold is the vertical crescent of conjunctiva at the medial aspect of the palpebral ?ssure. The caruncle is a piece of modi?ed skin just within the inner canthus.
Eye muscles The extra-ocular muscles. There are six in all, the four rectus muscles (superior, inferior, medial and lateral rectus muscles) and two oblique muscles (superior and inferior oblique muscles). The muscles are attached at various points between the bony orbit and the eyeball. By their combined action they move the eye in horizontal and vertical gaze. They also produce torsional movement of the eye (i.e. clockwise or anticlockwise movements when viewed from the front).
Lacrimal apparatus There are two components: a tear-production system, namely the lacrimal gland and accessory lacrimal glands; and a drainage system.
Tears keep the front of the eye moist; they also contain nutrients and various components to protect the eye from infection. Crying results from excess tear production. The drainage system cannot cope with the excess and therefore tears over?ow on to the face. Newborn babies do not produce tears for the ?rst three months of life. LACRIMAL GLAND Located below a small depression in the bony roof of the orbit. Numerous tear ducts open from it into predominantly the upper lid. Accessory lacrimal glands are found in the conjunctiva and within the eyelids: the former open directly on to the surface of the conjunctiva; the latter on to the eyelid margin. LACRIMAL DRAINAGE SYSTEM This consists of: PUNCTUM An elevated opening toward the medial aspect of each lid. Each punctum opens into a canaliculus. CANALICULUS A ?ne tube-like structure run-ning within the lid, parallel to the lid margin. The canaliculi from upper and lower lid join to form a common canaliculus which opens into the lacrimal sac. LACRIMAL SAC A small sac on the side of the nose which opens into the nasolacrimal duct. During blinking, the sac sucks tears into itself from the canaliculus. Tears then drain by gravity down the nasolacrimal duct. NASOLACRIMAL DUCT A tubular structure which runs down through the wall of the nose and opens into the nasal cavity.
Visual pathway Light stimulates the rods and cones of the retina. Electrochemical messages are then passed to nerve ?bres in the retina and then via the optic nerve to the optic chiasm. Here information from the temporal (outer) half of each retina continues to the same side of the brain. Information from the nasal (inner) half of each retina crosses to the other side within the optic chiasm. The rearranged nerve ?bres then pass through the optic tract to the lateral geniculate body, then the optic radiation to reach the visual cortex in the occipital lobe of the brain.... eye
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
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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
Cause Asthma runs in families, so that parents with asthma have a strong risk of having children with asthma, or with other atopic (see ATOPY) illnesses such as HAY FEVER or eczema (see DERMATITIS). There is therefore a great deal of interest in the genetic basis of the condition. Several GENES seem to be associated with the condition of atopy, in which subjects have a predisposition to form ANTIBODIES of the IgE class against allergens (see ALLERGEN) they encounter – especially inhaled allergens.
The allergic response in the lining of the airway leads to an in?ammatory reaction. Many cells are involved in this in?ammatory process, including lymphocytes, eosinophils, neutrophils and mast cells. The cells are attracted and controlled by a complex system of in?ammatory mediators. The in?amed airway-wall produced in this process is then sensitive to further allergic stimuli or to non-speci?c challenges such as dust, smoke or drying from the increased respiration during exercise. Recognition of this in?ammation has concentrated attention on anti-in?ammatory aspects of treatment.
Continued in?ammation with poor control of asthma can result in permanent damage to the airway-wall such that reversibility is reduced and airway-narrowing becomes permanent. Appropriate anti-in?ammatory therapy may help to prevent this damage.
Many allergens can be important triggers of asthma. House-dust mite, grass pollen and animal dander are the commonest problems. Occupational factors such as grain dusts, hard-metals fumes and chemicals in the plastic and paint industry are important in some adults. Viral infections are another common trigger, especially in young children.
The prevalence of asthma appears to be on the increase in most countries. Several factors have been linked to this increase; most important may be the vulnerability of the immature immune system (see IMMUNITY) in infants. High exposure to allergens such as house-dust mite early in life may prime the immune system, while reduced exposure to common viral infections may delay the maturation of the immune system. In addition, maternal smoking in pregnancy and infancy increases the risk.
Clinical course The major symptoms of asthma are breathlessness and cough. Occasionally cough may be the only symptom, especially in children, where night-time cough may be mistaken for recurrent infection and treated inappropriately with antibiotics.
The onset of asthma is usually in childhood, but it may begin at any age. In childhood, boys are affected more often than girls but by adulthood the sex incidence is equal. Children who have mild asthma are more likely to grow out of the condition as they go through their teenaged years, although symptoms may recur later.
The degree of airway-narrowing, and its change with time and treatment, can be monitored by measuring the peak expiratory ?ow with a simple monitor at home – a peak-?ow meter. The typical pattern shows the peak ?ow to be lowest in the early morning and this ‘morning dipping’ is often associated with disturbance of sleep.
Acute exacerbations of asthma may be provoked by infections or allergic stimuli. If they do not respond quickly and fully to medication, expert help should be sought urgently since oxygen and higher doses of drugs will be necessary to control the attack. In a severe attack the breathing rate and the pulse rate rise and the chest sounds wheezy. The peak-?ow rate of air into the lungs falls. Patients may be unable to talk in full sentences without catching their breath, and the reduced oxygen in the blood in very severe attacks may produce the blue colour of CYANOSIS in the lips and tongue. Such acute attacks can be very frightening for the patient and family.
Some cases of chronic asthma are included in the internationally agreed description CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) – a chronic, slowly progressive disorder characterised by obstruction of the air?ow persisting over several months.
Treatment The ?rst important consideration in the treatment of asthma is avoidance of precipitating factors. When this is a speci?c animal or occupational exposure, this may be possible; it is however more di?cult for house-dust mite or pollens. Exercise-induced asthma should be treated adequately rather than avoiding exercise.
Desensitisation injections using small quantities of speci?c allergens are used widely in some countries, but rarely in the UK as they are considered to have limited value since most asthma is precipitated by many stimuli and controlled adequately with simple treatment.
There are two groups of main drugs for the treatment of asthma. The ?rst are the bronchodilators which relax the smooth muscle in the wall of the airways, increase their diameter and relieve breathlessness. The most useful agents are the beta adrenergic agonists (see ADRENERGIC RECEPTORS) such as salbutamol and terbutaline. They are best given by inhalation into the airways since this reduces the general side-effects from oral use. These drugs are usually given to reverse airway-narrowing or to prevent its onset on exercise. However, longer-acting inhaled beta agonists such as salmeterol and formoterol or the theophyllines given in tablet form can be used regularly as prevention. The beta agonists can cause TREMOR and PALPITATION in some patients.
The second group of drugs are the antiin?ammatory agents that act to reduce in?ammation of the airway. The main agents in this group are the CORTICOSTEROIDS. They must be taken regularly, even when symptoms are absent. Given by inhalation they have few side-effects. In acute attacks, short courses of oral steroids are used; in very severe disease regular oral steroids may be needed. Other drugs have a role in suppressing in?ammation: sodium cromoglycate has been available for some years and is generally less e?ective than inhaled steroids. Newer agents directed at speci?c steps in the in?ammatory pathway, such as leukotriene receptor-antagonists, are alternative agents.
Treatment guidelines have been produced by various national and international bodies, such as the British Thoracic Society. Most have set out treatment in steps according to severity, with objectives for asthma control based on symptoms and peak ?ow. Patients should have a management plan that sets out their regular treatment and their appropriate response to changes in their condition.
Advice and support for research into asthma is provided by the National Asthma Campaign.
See www.brit-thoracic.org.uk
Prognosis Asthma is diagnosed in 15–20 per cent of all pre-school children in the developed world. Yet by the age of 15 it is estimated that fewer than 5 per cent still have symptoms. A study in 2003 reported on a follow-up of persons born in 1972–3 who developed asthma and still had problems at the age of nine. By the time these persons were aged 26, 27 per cent were still having problems; around half of that number had never been free from the illness and the other half had apparently lost it for a few years but it had returned.... asthma
Nutritional Profile Energy value (calories per serving): Moderate Protein: Moderate Fat: Low Saturated fat: Low Cholesterol: None Carbohydrates: High Fiber: High Sodium: Low Major vitamin contribution: B vitamins, folate Major mineral contribution: Iron, potassium
About the Nutrients in This Food Barley is a high-carbohydrate food, rich in starch and dietary fiber, particu- larly pectins and soluble gums, including beta-glucans, the fiber that makes cooked oatmeal sticky. The proteins in barley are incomplete, limited in the essential amino acid lysine. Barley is a good source of the B vitamin folate. One-half cup cooked barley has 4.5 grams dietary fiber and 12.5 mg folate (3 percent of the R DA for healthy adults).
The Most Nutritious Way to Serve This Food With a calcium-rich food and with a food such as legumes or meat, milk, or eggs that supplies the lysine barley is missing.
Diets That May Restrict or Exclude This Food Gluten-free diet
Buying This Food Look for: Clean, tightly sealed boxes or plastic bags. Stains indicate that something has spilled on the box and may have seeped through to con- taminate the grain inside. * Values are for pearled barley.
Storing This Food Store barley in air- and moisture-proof containers in a cool, dark, dry cabinet. Well protected, it will keep for several months with no loss of nutrients.
Preparing This Food Pick over the barley and discard any damaged or darkened grains.
What Happens When You Cook This Food Starch consists of molecules of the complex carbohydrates amylose and amylopectin packed into a starch granule. When you cook barley in water, its starch granules absorb water mol- ecules, swell, and soften. When the temperature of the liquid reaches approximately 140°F, the amylose and amylopectin molecules inside the granules relax and unfold, breaking some of their internal bonds (bonds between atoms on the same molecule) and forming new bonds between atoms on different molecules. The result is a network that traps and holds water molecules. The starch granules swell and the barley becomes soft and bulky. If you continue to cook the barley, the starch granules will rupture, releasing some of the amylose and amylopectin molecules inside. These molecules will attract and immobilize some of the water molecules in the liquid, which is why a little barley added to a soup or stew will make the soup or stew thicker. The B vitamins in barley are water-soluble. You can save them by serving the barley with the liquid in which it was cooked.
How Other Kinds of Processing Affect This Food Pearling. Pearled barley is barley from which the outer layer has been removed. Milling, the process by which barley is turned into flour, also removes the outer coating (bran) of the grain. Since most of the B vitamins and fiber are concentrated in the bran, both pearled and milled barley are lower in nutrients and fiber than whole barley. Malting. After barley is harvested, the grain may be left to germinate, a natural chemical process during which complex carbohydrates in the grain (starches and beta-glucans) change into sugar. The grain, now called malted barley, is used as the base for several fermented and distilled alcohol beverages, including beer and whiskey.
Medical Uses and/or Benefits To reduce cholesterol levels. The soluble gums and pectins in barley appear to lower the amount of cholesterol circulating in your blood. There are currently two theories to explain how this might work. The first theory is that the pectins form a gel in your stomach that sops up fats and keeps them from being absorbed by your body. The second is that bacteria living in your gut may feed on the beta-glucans in the barley to produce short-chain fatty acids that slow the natural production of cholesterol in your liver. Barley is very rich in beta-glucans; some strains have three times as much as oats. It also has tocotrienol, another chemical that mops up cholesterol.... barley
13.
The ?rst type of damage occurs as an acute episode in which one or more severe blows leads to loss of consciousness and occasionally to death. Death in the acute phase is usually due to intracranial haemorrhage and this carries a mortality of 45 per cent even with the sophisticated surgical techniques currently available. The second type of damage develops over a much longer period and is cumulative, leading to the atrophy of the cerebral cortex and brain stem. The repair processes of the brain are very limited and even after mild concussion it may suffer a small amount of permanent structural damage. Brain-scanning techniques now enable brain damage to be detected during life, and brain damage of the type previously associated with the punch-drunk syndrome is now being detected before obvious clinical signs have developed. Evidence of cerebral atrophy has been found in relatively young boxers including amateurs and those whose careers have been considered successful. The tragedy is that brain damage can only be detected after it has occurred. Many doctors are opposed to boxing, even with the present, more stringent medical precautions taken by those responsible for running the sport. Since the Royal College’s survey in 1969, the British Medical Association and other UK medical organisations have declared their opposition to boxing on medical grounds, as have medical organisations in several other countries.
In 1998, the Dutch Health Council recommended that professional boxing should be banned unless the rules are tightened. It claimed that chronic brain damage is seen in 40–80 per cent of boxers and that one in eight amateur bouts end with a concussed participant.
There is currently no legal basis on which to ban boxing in the UK, although it has been suggested that an injured boxer might one day sue a promoter. One correspondent to the British Medical Journal in 1998 suggested that since medical cover is a legal requirement at boxing promotions, the profession should consider if its members should withdraw participation.... boxing injuries
Lactic acid (CH3.CHOH.COOH) is produced in the body during muscular activity, the lactic acid being derived from the breakdown of GLYCOGEN. Muscle fatigue is associated with an accumulation of lactic acid in the muscle. Recovery follows when enough oxygen gets to the muscle, part of the lactic acid being oxidised and most of it then being built up once more into glycogen.... lactic acid
Cytotoxic drugs are used either singly or in combination, when an enhanced response is the aim. Chemotherapy of cancer is a complex process and should be supervised by an oncologist in co-operation with physicians, surgeons, radiotherapists and radiologists as appropriate.
The cytotoxic drugs include:
(1) The alkylating agents which act by damaging DNA, thus interfering with cell reproduction. Cyclophosphamide, ifosfamide, chlorambucil, kelphalan, busulphan, thiotepa and mustine are examples of alkylating agents.
(2) There are a number of cytotoxic antibiotics used in the treatment of cancer – doxorubicin, bleomycin, dactinomycin, mithramycin and amsacrine are examples. They are used primarily in the treatment of acute leukaemia and lymphomas.
(3) Antimetabolites – these drugs combine irreversibly with vital enzyme systems of the cell and hence prevent normal cell division. Methotrexate, cytarabine, ?uorouracil, mercaptopurine and azathioprine are examples.
(4) Another group of cytotoxic drugs are the vinca alkaloids such as vincristine, vinblastine and vindesima.
(5) Platinum compounds such as carboplatin, cisplatin and oxaliplatin are e?ective. All of them are given intravenously, but the latter two tend to have more unpleasant side-effects. Carboplatin and cisplatin are useful in the treatment of solid tumours. Carboplatin, a derivative of cisplatin, is given intravenously in ovarian cancer and in small-cell lung cancer. Better tolerated than cisplatin, the drug causes less nausea and vomiting, nephrotoxicity, neurotoxicity and ototoxicity. Where platinum-containing therapy has failed, intravenous treatment with paclitaxel may be tried. With only a limited success rate, it is relatively toxic and should be carefully supervised; responses, however, are sometimes prolonged.
Also of increasing importance in treating cancer are interferons. These are naturally occurring proteins with complex effects on immunity and cell function. Although toxic, with numerous adverse effects, they have shown some anti-tumour e?ect against certain lymphomas and solid tumours.... cytotoxic
Habitat: Throughout India, particularly in waste place.
English: Thornapple, Downy Datura.Ayurvedic: Dhattuura, Dhuurta, Dhastura, Unmatta, Shivapriya, Harapriya, Hema, Haatta, Dhustuu- ra, Dhustuuraka, Kanaka, Maatula. Also equated with Raaj-dhatuura. (white var.)Unani: Dhaturaa.Siddha/Tamil: Oomatthai, Karu- voomatthai.Action: Various plant parts are used in headache, hemiplegia, epilepsy, delirium, convulsions, cramps, rigid thigh muscles, rheumatism. Leaf— antitumour, antirheumatic. Leaf and corolla—anti-inflammatory. Flower—antiasthmatic. Seed, leaf and root—anticatarrhal, febrifuge, antidiarrhoeal, antidermatosis; also used in cerebral complications. Seeds—used in asthma. Limited use in kinetosis (excessive salivation, nausea and vomiting).
Along with other therapeutic applications, The Ayurvedic Pharmacopoeia ofIndia indicated the use of the whole plant in dysuria and alopecia.The plant accumulates more hyos- cine than hyoscyamine. Hyoscine content of dried leaves and flowering tops—between 0.02-0.55%. Alkaloid content of leaves—0.55%; stem—0.4%; seeds—0.19%; pericarps—0.8%; root at flowering of the plant—0.77%.Hyoscine in large doses causes delirium and coma.Dosage: Seed—30-60 mg. (API Vol. III.)... datura metelDoctors make the diagnosis of depression when they believe a patient to be ill with the latter condition, which may affect physical health and in some instances be life-threatening. This form of depression is common, with up to 15 per cent of the population suffering from it at any one time, while about 20 per cent of adults have ‘medical’ depression at some time during their lives – such that it is one of the most commonly presenting disorders in general practice. Women seem more liable to develop depression than men, with one in six of the former and one in nine of the latter seeking medical help.
Manic depression is a serious form of the disorder that recurs throughout life and is manifested by bouts of abnormal elation – the manic stage. Both the manic and depressive phases are commonly accompanied by psychotic symptoms such as delusions, hallucinations and a loss of sense of reality. This combination is sometimes termed a manic-depressive psychosis or bipolar affective disorder because of the illness’s division into two parts. Another psychiatric description is the catch-all term ‘affective disorder’.
Symptoms These vary with the illness’s severity. Anxiety and variable moods are the main symptoms in mild depression. The sufferer may cry without any reason or be unresponsive to relatives and friends. In its more severe form, depression presents with a loss of appetite, sleeping problems, lack of interest in and enjoyment of social activities, tiredness for no obvious reason, an indi?erence to sexual activity and a lack of concentration. The individual’s physical and mental activities slow down and he or she may contemplate suicide. Symptoms may vary during the 24 hours, being less troublesome during the latter part of the day and worse at night. Some people get depressed during the winter months, probably a consequence of the long hours of darkness: this disorder – SEASONAL AFFECTIVE DISORDER SYNDROME, or SADS – is thought to be more common in populations living in areas with long winters and limited daylight. Untreated, a person with depressive symptoms may steadily worsen, even withdrawing to bed for much of the time, and allowing his or her personal appearance, hygiene and environment to deteriorate. Children and adolescents may also suffer from depression and the disorder is not always recognised.
Causes A real depressive illness rarely has a single obvious cause, although sometimes the death of a close relative, loss of employment or a broken personal relationship may trigger a bout. Depression probably has a genetic background; for instance, manic depression seems to run in some families. Viral infections sometimes cause depression, and hormonal disorders – for example, HYPOTHYROIDISM or postnatal hormonal disturbances (postnatal depression) – will cause it. Di?cult family or social relations can contribute to the development of the disorder. Depression is believed to occur because of chemical changes in the transmission of signals in the nervous system, with a reduction in the neurochemicals that facilitate the passage of messages throughout the system.
Treatment This depends on the type and severity of the depression. These are three main forms. PSYCHOTHERAPY either on a one-to-one basis or as part of a group: this is valuable for those whose depression is the result of lifestyle or personality problems. Various types of psychotherapy are available. DRUG TREATMENT is the most common method and is particularly helpful for those with physical symptoms. ANTIDEPRESSANT DRUGS are divided into three main groups: TRICYCLIC ANTIDEPRESSANT DRUGS (amitriptyline, imipramine and dothiepin are examples); MONOAMINE OXIDASE INHIBITORS (MAOIS) (phenelzine, isocarboxazid and tranylcypromine are examples); and SELECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRIS) (?uoxetine – well known as Prozac®, ?uvoxamine and paroxetine are examples). For manic depression, lithium carbonate is the main preventive drug and it is also used for persistent depression that fails to respond to other treatments. Long-term lithium treatment reduces the likelihood of relapse in about 80 per cent of manic depressives, but the margin between control and toxic side-effects is narrow, so the drug must be carefully supervised. Indeed, all drug treatment for depression needs regular monitoring as the substances have powerful chemical properties with consequential side-effects in some people. Furthermore, the nature of the illness means that some sufferers forget or do not want to take the medication. ELECTROCONVULSIVE THERAPY (ECT) If drug treatments fail, severely depressed patients may be considered for ECT. This treatment has been used for many years but is now only rarely recommended. Given under general anaesthetic, in appropriate circumstances, ECT is safe and e?ective and may even be life-saving, though temporary impairment of memory may occur. Because the treatment was often misused in the past, it still carries a reputation that worries patients and relatives; hence careful assessment and counselling are essential before use is recommended.
Some patients with depression – particularly those with manic depression or who are a danger to themselves or to the public, or who are suicidal – may need admission to hospital, or in severe cases to a secure unit, in order to initiate treatment. But as far as possible patients are treated in the community (see MENTAL ILLNESS).... depression
Psychiatrists like to categorise mental illnesses because mental signs and symptoms do occur together in clusters or syndromes, each tending to respond to certain treatments. The idea that illnesses can be diagnosed simply by recognising their symptom patterns may not seem very scienti?c in these days of high technology. For most common mental illnesses, however, this is the only method of diagnosis; whatever is going wrong in the brain is usually too poorly understood and too subtle to show up in laboratory tests or computed tomography scans of the brain. And symptom-based definitions of mental illnesses are, generally, a lot more meaningful than the vague lay term ‘nervous breakdown’, which is used to cover an attack of anything from AGORAPHOBIA to total inability to function.
There is still a lot to learn about the workings of the brain, but psychiatry has developed plenty of practical knowledge about the probable causes of mental illness, ways of relieving symptoms, and ways of aiding recovery. Most experts now believe that mental illnesses generally arise from di?erent combinations of inherited risk and psychological STRESS, sometimes with additional environmental exposure – for example, viruses, drugs or ALCOHOL.
The range of common mental illnesses includes anxiety states, PHOBIA, DEPRESSION, alcohol and drug problems, the EATING DISORDERS anorexia and bulimia nervosa, MANIC DEPRESSION, SCHIZOPHRENIA, DEMENTIA, and a group of problems related to coping with life that psychiatrists call personality disorders.
Of these mental illnesses, dementia is the best understood. It is an irreversible and fatal form of mental deterioration (starting with forgetfulness and eventually leading to severe failure of all the brain’s functions), caused by rapid death of brain cells and consequent brain shrinkage. Schizophrenia is another serious mental illness which disrupts thought-processes, speech, emotions and perception (how the brain handles signals from the ?ve senses). Manic depression, in which prolonged ‘highs’ of extremely elevated mood and overexcitement alternate with abject misery, has similar effects on the mental processes. In both schizophrenia and manic depression the sufferer loses touch with reality, develops unshakeable but completely unrealistic ideas (delusions), and hallucinates (vividly experiences sensations that are not real, e.g. hears voices when there is nobody there). This triad of symptoms is called psychosis and it is what lay people, through fear and lack of understanding, sometimes call lunacy, madness or insanity.
The other mental illnesses mentioned above are sometimes called neuroses. But the term has become derogatory in ordinary lay language; indeed, many people assume that neuroses are mild disorders that only affect weak people who cannot ‘pull themselves together’, while psychoses are always severe. In reality, psychoses can be brief and reversible and neuroses can cause lifelong disability.
However de?ned and categorised, mental illness is a big public-health problem. In the UK, up to one in ?ve women and around one in seven men have had mental illness. About half a million people in Britain suffer from schizophrenia: it is three times commoner than cancer. And at any one time, up to a tenth of the adult population is ill with depression.
Treatment settings Most people with mental-health problems get the help they need from their own family doctor(s), without ever seeing a psychiatrist. General practictitioners in Britain treat nine out of ten recognised mental-health problems and see around 12 million adults with mental illness each year. Even for the one in ten of these patients referred to psychiatrists, general practitioners usually handle those problems that continue or recur.
Psychiatrists, psychiatric nurses, social workers, psychologists, counsellors and therapists often see patients at local doctors’ surgeries and will do home visits if necessary. Community mental-health centres – like general-practice health centres but catering solely for mental-health problems – o?er another short-cut to psychiatric help. The more traditional, and still more common, route to a psychiatrist for many people, however, is from the general practititioner to a hospital outpatient department.
Specialist psychiatric help In many ways, a visit to a psychiatrist is much like any trip to a hospital doctor – and, indeed, psychiatric clinics are often based in the outpatient departments of general hospitals. First appointments with psychiatrists can last an hour or more because the psychiatrist – and sometimes other members of the team such as nurses, doctors in training, and social workers – need to ask lots of questions and record the whole consultation in a set of con?dential case notes.
Psychiatric assessment usually includes an interview and an examination, and is sometimes backed up by a range of tests. The interview begins with the patient’s history – the personal story that explains how and, to some extent, why help is needed now. Mental-health problems almost invariably develop from a mixture of causes – emotional, social, physical and familial – and it helps psychiatrists to know what the people they see are normally like and what kind of lives they have led. These questions may seem unnecessarily intrusive, but they allow psychiatrists to understand patients’ problems and decide on the best way to help them.
The next stage in assessment is the mental-state examination. This is how psychiatrists examine minds, or at least their current state. Mental-state examination entails asking more questions and using careful observation to assess feelings, thoughts and mental symptoms, as well as the way the mind is working (for example, in terms of memory and concentration). During ?rst consultations psychiatrists usually make diagnoses and explain them. The boundary between a life problem that will clear up spontaneously and a mental illness that needs treatment is sometimes quite blurred; one consultation may be enough to put the problem in perspective and help to solve it.
Further assessment in the clinic may be needed, or some additional tests. Simple blood tests can be done in outpatient clinics but other investigations will mean referral to another department, usually on another day.
Further assessment and tests
PSYCHOLOGICAL TESTS Psychologists work in or alongside the psychiatric team, helping in both assessment and treatment. The range of psychological tests studies memory, intelligence, personality, perception and capability for abstract thinking. PHYSICAL TESTS Blood tests and brain scans may be useful to rule out a physical illness causing psychological symptoms. SOCIAL ASSESSMENT Many patients have social diffculties that can be teased out and helped by a psychiatric social worker. ‘Approved social workers’ have special training in the use of the Mental Health Act, the law that authorises compulsory admissions to psychiatric hospitals and compulsory psychiatric treatments. These social workers also know about all the mental-health services o?ered by local councils and voluntary organisations, and can refer clients to them. The role of some social workers has been widened greatly in recent years by the expansion of community care. OCCUPATIONAL THERAPY ASSESSMENT Mental-health problems causing practical disabilities – for instance, inability to work, cook or look after oneself – can be assessed and helped by occupational therapists.
Treatment The aims of psychiatric treatment are to help sufferers shake o?, or at least cope with, symptoms and to gain or regain an acceptable quality of life. A range of psychological and physical treatments is available.
COUNSELLING This is a widely used ‘talking cure’, particularly in general practice. Counsellors listen to their clients, help them to explore feelings, and help them to ?nd personal and practical solutions to their problems. Counsellors do not probe into clients’ pasts or analyse them. PSYCHOTHERAPY This is the best known ‘talking cure’. The term psychotherapy is a generalisation covering many di?erent concepts. They all started, however, with Sigmund Freud (see FREUDIAN THEORY), the father of modern psychotherapy. Freud was a doctor who discovered that, as well as the conscious thoughts that guide our feelings and actions, there are powerful psychological forces of which we are not usually aware. Applying his theories to his patients’ freely expressed thoughts, Freud was able to cure many illnesses, some of which had been presumed completely physical. This was the beginning of individual analytical psychotherapy, or PSYCHOANALYSIS. Although Freud’s principles underpin all subsequent theories about the psyche, many di?erent schools of thought have emerged and in?uenced psychotherapists (see ADLER; JUNGIAN ANALYSIS; PSYCHOTHERAPY). BEHAVIOUR THERAPY This springs from theories of human behaviour, many of which are based on studies of animals. The therapists, mostly psychologists, help people to look at problematic patterns of behaviour and thought, and to change them. Cognitive therapy is very e?ective, particularly in depression and eating disorders. PHYSICAL TREATMENTS The most widely used physical treatments in psychiatry are drugs. Tranquillising and anxiety-reducing BENZODIAZEPINES like diazepam, well known by its trade name of Valium, were prescribed widely in the 1960s and 70s because they seemed an e?ective and safe substitute for barbiturates. Benzodiazepines are, however, addictive and are now recommended only for short-term relief of anxiety that is severe, disabling, or unacceptably distressing. They are also used for short-term treatment of patients drying out from alcohol.
ANTIDEPRESSANT DRUGS like amitriptyline and ?uoxetine are given to lift depressed mood and to relieve the physical symptoms that sometimes occur in depression, such as insomnia and poor appetite. The side-effects of antidepressants are mostly relatively mild, when recommended doses are not exceeded – although one group, the monoamine oxidase inhibitors, can lead to sudden and dangerous high blood pressure if taken with certain foods.
Manic depression virtually always has to be treated with mood-stabilising drugs. Lithium carbonate is used in acute mania to lower mood and stop psychotic symptoms; it can also be used in severe depression. However lithium’s main use is to prevent relapse in manic depression. Long-term unwanted effects may include kidney and thyroid problems, and short-term problems in the nervous system and kidney may occur if the blood concentration of lithium is too high – therefore it must be monitored by regular blood tests. Carbamazepine, a treatment for EPILEPSY, has also been found to stabilise mood, and also necessitates blood tests.
Antipsychotic drugs, also called neuroleptics, and major tranquillisers are the only e?ective treatments for relieving serious mental illnesses with hallucinations and delusions. They are used mainly in schizophrenia and include the short-acting drugs chlorpromazine and clozapine as well as the long-lasting injections given once every few weeks like ?uphenazine decanoate. In the long term, however, some of the older antipsychotic drugs can cause a brain problem called TARDIVE DYSKINESIA that affects control of movement and is not always reversible. And the antipsychotic drugs’ short-term side-effects such as shaking and sti?ness sometimes have to be counteracted by other drugs called anticholinergic drugs such as procyclidine and benzhexol. Newer antipsychotic drugs such as clozapine do not cause tardive dyskinesia, but clozapine cannot be given as a long-lasting injection and its concentration in the body has to be monitored by regular blood tests to avoid toxicity. OTHER PHYSICAL TREATMENTS The other two physical treatments used in psychiatry are particularly controversial: electroconvulsive therapy (ECT) and psychosurgery. In ECT, which can be life-saving for patients who have severe life-threatening depression, a small electric current is passed through the brain to induce a ?t or seizure. Before the treatment the patient is anaesthetised and given a muscle-relaxing injection that reduces the magnitude of the ?t to a slight twitching or shaking. Scientists do not really understand how ECT works, but it does, for carefully selected patients. Psychosurgery – operating on the brain to alleviate psychiatric illness or di?cult personality traits – is extremely uncommon these days. Stereo-tactic surgery, in which small cuts are made in speci?c brain ?bres under X-ray guidance, has super-seded the more generalised lobotomies of old. The Mental Health Act 1983 ensures that psychosurgery is performed only when the patient has given fully informed consent and a second medical opinion has agreed that it is necessary. For all other psychiatric treatments (except another rare treatment, hormone implantation for reducing the sex drive of sex o?enders), either consent or a second opinion is needed – not both. TREATMENT IN HOSPITAL Psychiatric wards do not look like medical or surgical wards and sta? may not wear uniforms. Patients do not need to be in their beds during the day, so the beds are in separate dormitories. The main part of most wards is a living space with a day room, an activity and television room, quiet rooms, a dining room, and a kitchen. Ward life usually has a certain routine. The day often starts with a community meeting at which patients and nurses discuss issues that affect the whole ward. Patients may go to the occupational therapy department during the day, but there may also be some therapy groups on the ward, such as relaxation training. Patients’ symptoms and problems are assessed continuously during a stay in hospital. When patients seem well enough they are allowed home for trial periods; then discharge can be arranged. Patients are usually followed up in the outpatient clinic at least once.
TREATING PATIENTS WITH ACUTE PSYCHIATRIC ILLNESS Psychiatric emergencies – patients with acute psychiatric illness – may develop from psychological, physical, or practical crises. Any of these crises may need quick professional intervention. Relatives and friends often have to get this urgent help because the sufferer is not ?t enough to do it or, if psychotic, does not recognise the need. First, they should ring the person’s general practitioner. If the general practitioner is not available and help is needed very urgently, relatives or friends should phone the local social-services department and ask for the duty social worker (on 24-hour call). In a dire emergency, the police will know what to do.
Any disturbed adult who threatens his or her own or others’ health and safety and refuses psychiatric help may be moved and detained by law. The Mental Health Act of 1983 authorises emergency assessment and treatment of any person with apparent psychiatric problems that ful?l these criteria.
Although admission to hospital may be the best solution, there are other ways that psychiatric services can respond to emergencies. In some districts there are ‘crisis intervention’ teams of psychiatrists, nurses, and social workers who can visit patients urgently at home (at a GP’s request) and, sometimes, avert unnecessary admission. And research has shown that home treatment for a range of acute psychiatric problems can be e?ective.
LONG-TERM TREATMENT AND COMMUNITY CARE Long-term treatment is often provided by GPs with support and guidance from psychiatric teams. That is ?ne for people whose problems allow them to look after themselves, and for those with plenty of support from family and friends. But some people need much more intensive long-term treatment and many need help with running their daily lives.
Since the 1950s, successive governments have closed the old psychiatric hospitals and have tried to provide as much care as possible outside hospital – in ‘the community’. Community care is e?ective as long as everyone who needs inpatient care, or residential care, can have it. But demand exceeds supply. Research has shown that some homeless people have long-term mental illnesses and have somehow lost touch with psychiatric services. Many more have developed more general long-term health problems, particularly related to alcohol, without ever getting help.
The NHS and Community Care Act 1990, in force since 1993, established a new breed of professionals called care managers to assess people whose long-term illnesses and disabilities make them unable to cope completely independently with life. Care managers are given budgets by local councils to assess people’s needs and to arrange for them tailor-made packages of care, including services like home helps and day centres. But co-ordination between health and social services has sometimes failed – and resources are limited – and the government decided in 1997 to tighten up arrangements and pool community-care budgets.
Since 1992 psychiatrists have had to ensure that people with severe mental illnesses have full programmes of care set up before discharge from hospital, to be overseen by named key workers. And since 1996 psychiatrists have used a new power called Supervised Discharge to ensure that the most vulnerable patients cannot lose touch with mental-health services. There is not, however, any law that allows compulsory treatment in the community.
There is ample evidence that community care can work and that it need not cost more than hospital care. Critics argue, however, that even one tragedy resulting from inadequate care, perhaps a suicide or even a homicide, should reverse the march to community care. And, according to the National Schizophrenia Fellowship, many of the 10–15 homicides a year carried out by people with severe mental illnesses result from inadequate community care.
Further information can be obtained from the Mental Health Act Commission, and from MIND, the National Association for Mental Health. MIND also acts as a campaigning and advice organisation on all aspects of mental health.... mental illness
Clinically, the lymphatic ?lariases characteristically cause ELEPHANTIASIS (lymphoedema); onchocerciasis gives rise to ophthalmic complications (river-blindness), rashes and subcutaneous nodules; loaiasis causes subcutaneous ‘Calabar swellings’ and subconjunctival involvement; and dracontiasis predisposes to secondary bacterial infections (usually involving the lower limbs). Diagnosis is by ?nding the relevant ?larial nematode, either in blood (day and night ?lms should be examined), or in one or other of the body ?uids. An EOSINOPHILIA is often present in peripheral blood. Serological diagnosis is also of value. In onchocerciasis, skin-snips and the Mazotti reaction are valuable adjuncts to diagnosis.
The mainstay of chemotherapy consists of diethylcarbamazine (aimed predominantly at the larval stage of the parasite). However, ivermectin (not available in the UK) is e?ective in onchocerciasis, and metronidazole or one of the benzimidazole compounds have limited value in dracontiasis. Suramin has been used to kill adult ?larial worms. Prevention consists of eradication of the relevant insect vector.... filariasis
Nutritional Profile Energy value (calories per serving): Low Protein: Low Fat: Low Saturated fat: Low Cholesterol: Low Carbohydrates: None Fiber: None Sodium: Low Major vitamin contribution: None Major mineral contribution: None
About the Nutrients in This Food Although gelatin is made from the collagen (connective tissue) of cattle hides and bones or pig skin, its proteins are limited in the essential acid tryptophan, which is destroyed when the bones and skin are treated with acid, and is deficient in several others, including lysine. In fact, gelatin’s proteins are of such poor quality that, unlike other foods of animal origin (meat, milk), gelatin cannot sustain life. Laboratory rats fed a diet in which gelatin was the primary protein did not grow as they should; half died within 48 days, even though the gelatin was supplemented with some of the essential amino acids. Plain gelatin has no carbohydrates and fiber. It is low in fat. Flavored gel- atin desserts, however, are high in carbohydrates because of the added sugar.
The Most Nutritious Way to Serve This Food With a protein food rich in complete proteins. Gelatin desserts whipped with milk fit the bill.
Diets That May Restrict or Exclude This Food Low-carbohydrate diet (gelatin desserts prepared with sugar) Low-sodium diet (commercial gelatin powders) Sucrose-free diet (gelatin desserts prepared with sugar) * Values are for prepared unsweetened gelat in.
Buying This Food Look for: Tightly sealed, clean boxes.
Storing This Food Store gelatin boxes in a cool, dry cabinet.
Preparing This Food Commercial unflavored gelatin comes in premeasured 1-tablespoon packets. One tablespoon of gelatin will thicken about two cups of water. To combine the gelatin and water, first heat ¾ cup water to boiling. While it is heating, add the gelatin to ¼ cup cold liquid and let it absorb moisture until it is translucent. Then add the boiling water. (Flavored fruit gelatins can be dissolved directly in hot water.)
What Happens When You Cook This Food When you mix gelatin with hot water, its protein molecules create a network that stiffens into a stable, solid gel as it squeezes out moisture. The longer the gel sits, the more intermo- lecular bonds it forms, the more moisture it loses and the firmer it becomes. A day-old gel is much firmer than one you’ve just made. Gelatin is used as a thickener in prepared foods and can be used at home to thicken sauces. Flavored gelatin dessert powders have less stiffening power than plain gelatin because some of their protein has been replaced by sugar. To build a layered gelatin mold, let each layer harden before you add the next.... gelatin
Action: Astringent, expectorant, diuretic (mild), antispasmodic, stimulant. Of limited use because of pyrrolizidine alkaloids.
Uses: Inflammation of urinary tract, gravel, skin disorders. Gall bladder disorders, bronchitis, asthma, whooping cough. Migraine of liver origin.
Preparations: 1 teaspoon crushed root steeped in each cup cold water overnight. Next day warm, not boil, and strain. Half cup thrice daily.
Petaforce. (Vogel & Webb) capsules, 25mg Butterburr extract.
Neurochol (Brenner). Combines Butterburr and Wormwood. ... butterbur
Alternatives of limited efficacy: see entry – CORTICOSTEROIDS. These are known to produce increased output of adrenal hormones by their cortisone-like effect. ... cortisone
Gene therapy is currently used to treat disorders caused by a fault in a single recessive gene, when the defect can remedied by introducing a normal ALLELE. Treating disorders caused by dominant genes is more complicated. CYSTIC FIBROSIS is an example of a disease caused by a recessive gene, and clinical trials are taking place on the e?ectiveness of using LIPOSOMES to introduce the normal gene into the lungs of someone with the disorder. Trials are also underway to test the e?ectiveness of introducing tumour-suppressing genes into cancer cells to check their spread.
Gene therapy was ?rst used in 1990 to treat an American patient. Eleven European medical research councils (including the UK’s) recommended in 1988 that gene therapy should be restricted to correcting disease or defects, and that it should be limited to somatic cells. Interventions in germ-line cells (the sperm and egg) to e?ect changes that would be inherited, though technically feasible, is not allowed (see CLONING; HUMAN GENOME).... gene therapy
The Council is funded by doctors’ annual fees and is responsible to the Privy Council. Substantial reforms of the GMC’s structure and functions have been and are still being undertaken to ensure that it operates e?ectively in today’s rapidly evolving medical and social environment. In particular, the Council has strengthened its supervisory and disciplinary functions, and among many changes has proposed the regular revalidation of doctors’ professional abilities on a periodic basis. The Medical Register, maintained by the GMC, is intended to enable the public to identify whom it is safe to approach to obtain medical services. Entry on the Register shows that the doctor holds a recognised primary medical quali?cation and is committed to upholding the profession’s values. Under revalidation requirements being ?nalised, in addition to holding an initial quali?cation, doctors wishing to stay on the Register will have to show their continuing ?tness to practise according to the professional attributes laid down by the GMC.
Once revalidation is fully established, there will be four categories of doctor:
Those on the Register who successfully show their ?tness to practise on a regular basis.
Those whose registration is limited, suspended or removed as a result of the Council’s disciplinary procedures.
Those who do not wish to stay on the Register or retain any links with the GMC.
Those, placed on a supplementary list, who do not wish to stay on the main Register but who want to retain a formal link with the medical profession through the Council. Such doctors will not be able to practise or prescribe.... general medical council (gmc)
Stress and anxiety are probably the most common causes of headache and, where possible, the reasons – overwork, family problems, unemployment, ?nancial diffculties, etc. – should be tackled. An unpleasant environment such as tra?c pollution or badly ventilated or overcrowded working conditions may provoke headaches in some people, as may excessive smoking or ca?eine intake. MIGRAINE is a characteristic and often disabling type of headache; high blood pressure may cause the condition (see HYPERTENSION); and, occasionally, refractive errors of the eyes (see EYE, DISORDERS OF) are associated with headaches. SINUS infections are often characterised by frontal headaches. Rheumatism in the muscles of the neck and scalp produce headaches; fever is commonly accompanied by a headache; and sunstroke and HEAT STROKE customarily result in headaches. Finally, diseases in the brain such as meningitis, tumours and HAEMORRHAGE may ?rst manifest themselves as persistent or recurrent headaches.
Treatment Obtaining a reliable diagnosis – with the help of further investigations, including CT (see COMPUTED TOMOGRAPHY) or MRI scanning when indicated – should always be the initial aim; treatment in most cases should then be aimed at the underlying condition. Particular concerns include headache that worsens at night or in the early morning; ever-increasing headaches; those associated with abnormal neurological signs on examination; or those associated with ?ts (see FIT).
Whether the cause is physical or stress-induced, used sensibly and for a limited period a low dose of aspirin or paracetamol may be helpful. In many cases of stress-induced headache, however, the most e?ective treatment is relaxation. There are many speci?c treatments for migraine and hypertension. Sinusitis is treated with antibiotics and sometimes by surgery.... headache
Most GPs work in groups of self-employed individuals, who contract their services to the local Primary Care Trust (PCT) – see below. Those in full partnership are called principals, but an increasing number now work as non-principals – that is, they are employees rather than partners in a practice. Alternatively, they might be salaried employees of a PCT. The average number of patients looked after by a full-time GP is 1,800 and the average duration of consultation about 10 minutes. GPs need to be able to deal with all common medical conditions and be able to recognise conditions that require specialist help, especially those requiring urgent action.
Until the new General Medical Services Contract was introduced in 2004, GPs had to take individual responsibility for providing ‘all necessary medical services’ at all times to their patient list. Now, practices rather than individuals share this responsibility. Moreover, the contract now applies only to the hours between
8.00 a.m. and 6.30 p.m., Mondays to Fridays; out-of-hours primary care has become the responsibility of PCTs. GPs still have an obligation to visit patients at home on weekdays in case of medical need, but home-visiting as a proportion of GP work has declined steadily since the NHS began. By contrast, the amount of time spent attending to preventive care and organisational issues has steadily increased. The 2004 contract for the ?rst time introduced payment for speci?c indicators of good clinical care in a limited range of conditions.
A telephone advice service, NHS Direct, was launched in 2000 to give an opportunity for patients to ‘consult’ a trained nurse who guides the caller on whether the symptoms indicate that self-care, a visit to a GP or a hospital Accident & Emergency department, or an ambulance callout is required. The aim of this service is to give the patient prompt advice and to reduce misuse of the skills of GPs, ambulance sta? and hospital facilities.
Training of GPs Training for NHS general practice after quali?cation and registration as a doctor requires a minimum of two years’ post-registration work in hospital jobs covering a variety of areas, including PAEDIATRICS, OBSTETRICS, care of the elderly and PSYCHIATRY. This is followed by a year or more working as a ‘registrar’ in general practice. This ?nal year exposes registrars to life as a GP, where they start to look after their own patients, while still closely supervised by a GP who has him- or herself been trained in educational techniques. Successful completion of ‘summative assessment’ – regular assessments during training – quali?es registrars to become GPs in their own right, and many newly quali?ed GPs also sit the membership exam set by the Royal College of General Practitioners (see APPENDIX 8: PROFESSIONAL ORGANISATIONS).
A growing number of GP practices o?er educational attachments to medical students. These attachments provide experience of the range of medical and social problems commonly found in the community, while also o?ering them allocated time to learn clinical skills away from the more specialist environment of the hospital.
In addition to teaching commitments, many GPs are also choosing to spend one or two sessions away from their practices each week, doing other kinds of work. Most will work in, for example, at least one of the following: a hospital specialist clinic; a hospice; occupational medicine (see under OCCUPATIONAL HEALTH, MEDICINE AND DISEASES); family-planning clinics; the police or prison services. Some also become involved in medical administration, representative medicopolitics or journalism. To help them keep up to date with advances and changes in medicine, GPs are required to produce personal-development plans that outline any educational activities they have completed or intend to pursue during the forthcoming year.
NHS GPs are allowed to see private patients, though this activity is not widespread (see PRIVATE HEALTH CARE).
Primary Care Trusts (PCTs) Groups of GPs (whether working alone, or in partnership with others) are now obliged by the NHS to link communally with a number of other GPs in the locality, to form Primary Care Trusts (PCTs). Most have a membership of about 30 GPs, working within a de?ned geographical area, in addition to the community nurses and practice counsellors working in the same area; links are also made to local council social services so that health and social needs are addressed together. Some PCTs also run ambulance services.
One of the roles of PCTs is to develop primary-care services that are appropriate to the needs of the local population, while also occupying a powerful position to in?uence the scope and quality of secondary-care services. They are also designed to ensure equity of resources between di?erent GP surgeries, so that all patients living in the locality have access to a high quality and uniform standard of service.
One way in which this is beginning to happen is through the introduction of more overt CLINICAL GOVERNANCE. PCTs devise and help their member practices to conduct CLINICAL AUDIT programmes and also encourage them to participate in prescribing incentive schemes. In return, practices receive payment for this work, and the funds are used to improve the services they o?er their patients.... general practitioner (gp)
waste (instead of the carbon dioxide from aerobic activity), sometimes causing muscle fatigue and pain.... anaerobic
Habitat: North-western Himalayas. Cultivated on limited scale in North Indian plains.
English: Egyptian Henbane.Ayurvedic: Paarsika-yavaani (related species), Turushkaa.Unani: Ajwaayin Khuraasaani, Shuukraan, Tukhm-bang.Folk: Vajra-bhang.Action: Sedative.
The leaves and flowering tops contain higher concentration of tropane alkaloids than other species of Hyoscy- amus, used as a source of hyoscine.... hyoscyamus muticusBlood accumulates in the liver, which swells.
Liver failure and portal hypertension result.
Treatment is aimed at removing the cause of the obstruction: this may be a blood clot, pressure on the veins from a liver tumour, or a congenital abnormality of the veins.
In most cases, treatment has only a limited effect and, unless a liver transplant can be done, the disease is fatal within 2 years.... budd–chiari syndrome
All movable joints involve four structures: the bones whose junction forms the joint; a layer of cartilage covering the ends of these, making them smooth; a ?brous sheath, the capsule, thickened at various points into bands or ligaments, which hold the bones together; and, ?nally, the synovial membrane, which lines the capsule and produces a synovial ?uid, lubricating the movements of the joint. In addition, the bones are kept in position at the joints by the various muscles passing over them and by atmospheric pressure. Where the ends of the bones do not quite correspond, a subsidiary disc of ?bro-cartilage may help to adapt the ends of the bones more perfectly to each other. Larger cavities may be ?lled by movable pads of fat under the synovial membrane, giving additional protection to the joint.
Varieties After this main division of joints into those which are ?xed and those movable, the movable joints may be further subdivided. In gliding joints, such as the wrist and ankle, the bones have ?at surfaces capable of only a limited amount of movement. In hinge joints, such as the elbow and knee, movement takes place around one axis. Ball-and-socket joints, exempli?ed by the shoulder and hip, allow free movement in any direction. Subsidiary varieties are named according to the shape of the bones which enter the joint.... joints
Habitat: Cultivated mainly in Madhya Pradesh, Uttar Pradesh, Maharashtra, Bihar and Rajasthan.
English: Linseed, Flax.Ayurvedic: Atasi, Umaa, Masrnaa, Nilapushpi, Kshumaa.Unani: Kattan.Siddha/Tamil: (Seed).Action: Seed—demulcent, emollient, laxative, antilipidemic, antitussive, pectoral (used in bronchitis and cough). Flowers—used as nervine and cardiac tonic. Oil— used in burns, skin injuries and sores.
Key application: Internally, for chronic constipation, for colons damaged by abuse of laxatives, irritable bowel syndrome, diverticular disease, symptomatic short-term treatment of gastritis and enteritis. Externally, for painful skin inflammations. (German Commission E, ESCOP, The British Herbal Pharmacopoeia.)The plant contains chlorogenic acid and its isomer. Also present are palmitic, stearic, oleic, linoleic acids, along with amino acids, and sugars. Linseed also contains mucilage (3-10%) in epidermis; fatty oil (30-40%); cyanogenic glycosides (0.05-00.1%) mainly linus- tatin, neolinustatin and linamarin; lig- nans; phenylpropane derivatives including linusitamarin. (Cyanogenic glycosides are not found toxic in therapeutic doses as these are broken down only to a limited extent in the body.)The seeds are an excellent source of dietary alpha-linolenic acid for modifying plasma and tissue lipids. Flaxseed preparations reduced atherogenic risk in hyperlipemic patients. (Cited in Expanded Commission E Monographs.)Human studies have indicated Flax- seed's use in atherosclerosis, hyperc- holesterolemia, lupus nephritis, chronic renal diseases and in cancer prevention (active principle: lignan precursor secoisolariciresinol diglycoside). (Sharon M. Herr. Also Am J Clin Nutr, 1999, 69, 395-402.)The PP glucose response to a 50 g carbohydrate load given as Flaxseed bread was found to be 27% lower when compared with regular white bread.Taking Flaxseed oil daily for 3 months did not improve symptoms of pain and stiffness in rheumatoid arthritis and no effect was observed on RA, such as C-reactive protein and ESR. (Natural Medicines Comprehensive Database, 2007.)The water-binding capacity and rhe- ological properties of linseed mucilage resembled those of guar gum.Dosage: Ripe seed—3-6 g powder. (API, Vol. I.) Flower-bud—3-6 g; oil—5-10 ml. (CCRAS.)... linum usitatissimumAffected children may appear normal at birth but, at 6–12 months of age, they develop cardiac abnormalities, umbilical hernia, skeletal deformities, and enlargement of the tongue, liver, and spleen.
Growth is limited and mental development slows.
If the condition is diagnosed in early infancy, a bone marrow transplant may be curative.... hurler’s syndrome
and lower teeth together. The wires are removed after about 6 weeks.... jaw, fractured
Breast reconstructive surgery (MAMMOPLASTY) may be done at the same time as the mastectomy – the preferred option – or, if that is not feasible, at a later date. Where the whole breast has been excised, some form of arti?cial breast (prosthesis) will be provided. This may be an external prosthesis ?tted into a specially made brassiere, or an internal implant – perhaps a silicone bag, though there has been controversy over the safety of this device. Reconstructive techniques involving the transfer of skin and muscle from nearby areas are also being developed. Post-operatively, patients can obtain advice from Breast Cancer Care.... mastectomy
Side-effects of paclitaxel include hypersensitivity, MYELOSUPPRESSION, cardiac ARRHYTHMIA and peripheral NEUROPATHY. Only a minority of patients respond to the drug, but when it works the results are often long-lasting.... paclitaxel
Many cases of pleurisy are associated with only a little e?usion, the in?ammation consisting chie?y in exudation of FIBRIN: to this form the term ‘dry pleurisy’ is applied. Further, pleurisy may be limited to a very small area – or, on the contrary, may affect, throughout a greater or less extent, the pleural surfaces of both lungs.
Causes Pleurisy is often associated with other forms of in?ammatory disease within the chest, more particularly PNEUMONIA, BRONCHIECTASIS, and tuberculosis; it occasionally accompanies PERICARDITIS. It may also be due to carcinoma of the lung, or be secondary to abdominal infections such as subphrenic abscess. Further, wounds or injuries of the thoracic walls are apt to set up pleurisy.
Symptoms The symptoms of pleurisy vary, being generally well marked, but sometimes obscure. DRY PLEURISY In the case of dry pleurisy, which is, on the whole, the milder form, the chief symptom is a sharp pain in the side, felt especially on breathing. Fever may or may not be present. There is a slight, dry cough, and breathing is quicker than normal and shallow. PLEURISY WITH EFFUSION is usually more severe than dry pleurisy, and, although it may in some cases develop insidiously, it is in general ushered in sharply by shivering and fever, like other acute in?ammatory diseases. Pain is felt in the side or breast, of a severe cutting or stabbing character. A dry cough usually occurs and breathing is painful and di?cult.
Treatment The treatment varies greatly with the form and severity of the attack. Bed rest, antibiotics, analgesics and antipyretics are advisable. A large pleural e?usion may need to be drained via an aspiration needle.... pleurisy
The concept of the dose-response is important for understanding the risk of exposure to a particular substance. This is embodied in a statement by Paracelsus (c.1493–1541): ‘All substances are poisons; there is none which is not a poison. The right dose di?erentiates a poison and a remedy.’
Poisoning may occur in a variety of ways: deliberate – SUICIDE, substance abuse or murder; accidental – including accidental overdose of medicines; occupational; and environmental
– including exposure during ?re.
Ingestion is the most common route of exposure, but poisoning may also occur through inhalation, absorption through the skin, by injection and through bites and stings of venomous animals. Poisoning may be described as acute, where a single exposure produces clinical effects with a relatively rapid onset; or chronic, where prolonged or repeated exposures may produce clinical effects which may be insidious in onset, cumulative and in some cases permanent.
Diagnosis of poisoning is usually by circumstantial evidence or elimination of other causes of the clinical condition of the patient. Some substances (e.g. opioids) produce a characteristic clinical picture in overdose that can help with diagnosis. In some patients laboratory analysis of body ?uids or the substance taken may be useful to determine or con?rm the o?ending agent. Routine assays are not necessary. For a very small number of poisons, such as paracetamol, aspirin, iron and lead, the management of the patient may depend on measuring the amount of poison in the bloodstream.
Accurate statistics on the incidence of poisoning in the UK are lacking. Mortality ?gures are more reliable than morbidity statistics; annually, well over 100,000 cases of poisoning are admitted to hospital. The annual number of deaths from poisoning is relatively small – about 300 – and in most cases patients die before reaching hospital. Currently, CARBON MONOXIDE (CO) is by far the most common cause of death due to poisoning. The most common agents involved in intentional or accidental poisoning are drugs, particularly ANALGESICS, ANTIDEPRESSANT DRUGS and SEDATIVES. Alcohol is also commonly taken by adults, usually in combination with drugs. Children frequently swallow household cleaners, white spirit, plant material – such as belladonna (deadly nightshade) and certain mushrooms; for example, death cap and ?y agaric – aftershave and perfume as well as drugs. If possible, the suspect container, drug or plant should be taken with the victim to the hospital or doctor. The use of child-resistant containers has reduced the number of admissions of children to hospital for treatment. Bixtrex® is an intensely bitter-tasting agent which is often added to products to discourage ingestion; however, not everybody is able to taste it, nor has any bene?cial e?ect been proven.
Treatment of poisoning usually begins with decontamination procedures. For ingested substances this may involve making the patient sick or washing the stomach out (GASTRIC LAVAGE): this is usually only worthwhile if performed soon after ingestion. It should be emphasised that salt (sodium chloride) water must never be given to induce vomiting, since this procedure is dangerous and has caused death. For substances spilt on the skin, the affected area should immediately be thoroughly washed and all contaminated clothing removed. Following eye exposure, the affected eye/s should be thoroughly irrigated with saline or water.
Treatment thereafter is generally symptomatic and supportive, with maintenance of the victim’s respiratory, neurological and cardiovascular systems and, where appropriate, monitoring of their ?uid and electrolyte balance and hepatic and renal function. There are speci?c antidotes for a few substances: the most important of these are PARACETAMOL, iron, cyanide (see CYANIDE POISONING), opioids (see OPIOID), DIGOXIN, insecticides and some heavy metals. Heavy-metal poisoning is treated with CHELATING AGENTS – chemical compounds that form complexes by binding metal ions: desferrioxamine and pencillinamine are two such agents. The number of people presenting with paracetamol overdose – a common drug used for attempted suicide – has fallen sharply since restrictions were placed on its over-thecounter sales.
When a patient presents with an illness thought to be caused by exposure to substances at work, further exposure should be limited or prevented and investigations undertaken to determine the source and extent of the problem. Acutely poisoned workers will usually go to hospital, but those suffering from chronic exposure may attend their GP with non-speci?c symptoms (see OCCUPATIONAL HEALTH, MEDICINE AND DISEASES).
In recent years, legislation has been enacted in the UK to improve safety in the workplace and to ensure that data on the hazardous constituents and effects of chemicals are more readily available. These o?cial controls include the Control of Substances Hazardous to Health (COSHH) and the Chemicals (Hazard Information and Packaging) Regulations (CHIP) and are UK legislation in response to European Union directives.
The National Poisons Information Service is a 24-hour emergency telephone service available to the medical profession and provides information on the likely effects of numerous agents and advice on the management of the poisoned patient. The telephone numbers are available in the medical literature. In the UK this is not a public-access service. People who believe they, or their relatives, have been poisoned should seek medical advice from their GPs or attend their local hospital.
Toxbase The National Poisons Information Service provides a primary clinical toxicology database on the Internet: www.spib.axl.co.uk. This website provides information about routine diagnosis, treatment and management of people exposed to drugs, household products and industrial and agricultural products.
(See also APPENDIX 1: BASIC FIRST AID.)... poisons
Prostaglandins play an important part in the production of PAIN, and it is now known that ASPIRIN relieves pain by virtue of the fact that it prevents, or antagonises, the formation of certain prostaglandins. In addition, they play some, although as yet incompletely de?ned, part in producing in?ammatory changes. (See INFLAMMATION; NON-STEROIDAL ANTIINFLAMMATORY DRUGS (NSAIDS).)
Thus prostaglandins have potent biological effects, but their instability and rapid metabolism make them short-acting. They are produced but not stored by most living cells and act locally. The two most important prostaglandins are prostacycline and thromboxane: prostacycline is a vasodilator and an inhibitor of platelet aggregation; thromboxanes have the opposite effects and cause vasoconstriction and platelet aggregation. The NSAIDs act by blocking an ENZYME called cyclo-oxygenase which converts arachidonic acid to the precursors of the various prostaglandins. Despite their potent pharmacological properties, the role of prostaglandins in current therapeutics is limited and controversial. They have been used most successfully as an inhibitor of platelet aggregation in extra-corporeal haemoperfusion systems. The problems with the prostacyclines is that they have to be given intravenously as they are inactive by mouth, and continuous infusion is required because the drug is rapidly eliminated with a half-life of minutes. Side-effects tend to be severe because the drug is usually given at the highest dose the patient can tolerate. The hope for the future lies in the exploitation of the compound to generate, synthetically, stable orally active prostacycline analogues which will inhibit platelet aggregation and hence thrombotic events, and yet have minimal effects on the heart and blood vessels.... prostaglandins
Habitat: Cultivated in Kashmir at elevation of 760-2,400 m, also in Himachal Pradesh and Uttar Pradesh.
English: Almond.Ayurvedic: Vaataama, Vaataada.Unani: Baadaam Shireen, Loz.Siddha/Tamil: Vaadumai.Action: Kernels—nutritious, demulcent and stimulant nervine tonic; valuable in diets for peptic ulcer. Unripe fruits— astringent, applied to gums. Oil—nutritive, demulcent, slightly laxative.
Almond flour made from the residue left after expressing almond oil, and almond butter, is used for the preparation of starch-free diabetic food.The chief protein of almond is a globulin, amandin, an albumin is also reported. Amandin has a high arginine content (11.9%). The primary chemical difference between the sweet and bitter kernel lies in the high content (2.5-3.5%) of amygdalin in bitter kernel; the ripe sweet almond being free of this cyanogenetic glucoside. Owing to the presence of amygdalin, which on enzymatic hydrolysis yields hydrocyanic acid, the bitter almond is not fit for human consumption.The oil yield from bitter kernels is usually 38 to 45% and from sweet almond 44 to 55%. The bitter almond oil containing hydrocyanic acid finds limited use in medicine as an antispas- modic and sedative. Dissolved in 50 times water, it is applied externally in prurigo senilis. Hydrocyanic acid-free oil is used for flavouring purposes.Partial replacement of saturated fatty acids with almonds lowers total plasma cholesterol and low-density lipoprotein cholesterol.... prunus amygdalusS. haematobium causes CYSTITIS and haematuria – passage of blood in the urine; bladder cancer and ureteric obstruction, giving rise to hydronephrosis and kidney failure, are long-term sequelae in a severe case. S. mansoni can cause colonic symptoms and in a severe case, POLYPOSIS of the COLON; diarrhoea, which may be bloody, can be a presenting feature. In a heavy infection, eggs surrounded by granulomas are deposited in the liver, giving rise to extensive damage (pipe-stem ?brosis) associated with PORTAL HYPERTENSION, oesophageal varices, etc. However, unlike in CIRRHOSIS, hepatocellular function is preserved until late in the disease. S. japonicum (which is con?ned to the Far East, especially Indonesia) behaves similarly to S. mansoni infection; liver involvement is often more severe.
Diagnosis can be made by microscopic examination of URINE or FAECES. The characteristic eggs are usually detectable. Alternatively, rectal or liver BIOPSY are of value. Serological tests, including an ELISA (see ENZYME-LINKED IMMUNOSORBENT ASSAY (ELISA)), have now largely replaced invasive procedures used in making a parasitological diagnosis.
Treatment CHEMOTHERAPY has been revolutionised by the introduction of praziquantel (administered orally); this compound has no serious side-effects, although its cost may limit its use in developing countries. Oxamniquine is cheaper and e?ective in S. mansoni infection, although evidence of resistance has been recorded in several countries. Metriphonate is also relatively cheap and is of value in S. haematobium infection. Prevention is by complete avoidance of exposure to contaminated water; all travellers to infected areas should know about this disease. It is increasing in frequency as new expanses of fresh water appear as a result of irrigation schemes and dam projects. Molluscicides can be employed for snail-control.... schistosomiasis
Causes There is a major immunogenetic predisposition to rheumatoid arthritis in people carrying the HLA-DR4 antigen (see HLA SYSTEM). Other minor immunogenetic factors have also been implicated. In addition, there is a degree of familial clustering which suggests other unidenti?ed genetic factors. Genetic factors cannot alone explain aetiology, and environmental and chance factors must be important, but these have yet to be identi?ed.
Epidemiology Rheumatoid arthritis more commonly occurs in women from the age of 30 onwards, the sex ratio being approximately 4:1. Typical rheumatoid arthritis may occur in adolescence, but in childhood chronic SYNOVITIS usually takes one of a number of di?erent patterns, classi?ed under juvenile chronic arthritis.
Pathology The primary lesion is an in?ammation of the synovial membrane of joints. The synovial ?uid becomes diluted with in?ammatory exudate: if this persists for months it leads to progressive destruction of articular CARTILAGE and BONE. Cartilage is replaced by in?ammatory tissue known as pannus; a similar tissue invades bone to form erosions. Synovitis also affects tendon sheaths, and may lead to adhesion ?brosis or attrition and rupture of tendons. Subcutaneous and other bursae may be involved. Necrobiotic nodules also occur at sites outside synovium, including the subcutaneous tissues, the lungs, the pericardium and the pleura.
Clinical features Rheumatoid arthritis varies from the very mild to the severely disabling. Many mild cases probably go undiagnosed. At least 50 per cent of patients continue to lead a reasonably normal life; around 25 per cent are signi?cantly disabled in terms of work and leisure activities; and a minority become markedly disabled and are limited in their independence. There is often an early acute phase, followed by substantial remission, but in other patients gradual step-wise deterioration may occur, with progressive involvement of an increasing number of joints.
The diagnosis of rheumatoid arthritis is largely based on clinical symptoms and signs. Approximately 70 per cent of patients have rheumatoid factor ANTIBODIES in the SERUM but, because of the large number of false positives and false negatives, this test has very little value in clinical practice. It may be a useful pointer to a worse prognosis in early cases if the level is high. X-RAYS may help in diagnosing early cases and are particularly helpful when considering surgery or possible complications such as pathological fracture. Patients commonly develop ANAEMIA, which may be partly due to gastrointestinal blood loss from antiin?ammatory drug treatment (see below).
Treatment involves physical, pharmacological, and surgical measures, together with psychological and social support tailored to the individual patient’s needs. Regular activity should be maintained. Resting of certain joints such as the wrist with splints may be helpful at night or to assist prolonged manual activities. Sound footwear is important. Early use of antirheumatic drugs reduces long-term disability. Drug treatment includes simple ANALGESICS, NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS), and slow-acting drugs including GOLD SALTS (in the form of SODIUM AUROTHIOMALATE), PENICILLAMINE, SULFASALAZINE, METHOTREXATE and AZATHIOPRINE.
The non-steroidal agents are largely e?ective in reducing pain and early-morning sti?ness, and have no e?ect on the chronic in?ammatory process. It is important, especially in the elderly, to explain to patients the adverse effects of NSAIDs, the dosage of which can be cut by prescribing paracetamol at the same time. Combinations of anti-rheumatic drugs seem better than single agents. The slow-acting drugs take approximately three months to act but have a more global e?ect on chronic in?ammation, with a greater reduction in swelling and an associated fall in erythrocyte sedimentation rate (ESR) and rise in the level of HAEMOGLOBIN. Local CORTICOSTEROIDS are useful, given into individual joints. Systemic corticosteroids carry serious problems if continued long term, but may be useful under special circumstances. Much research is currently going on into the use of tumour necrosis factor antagonists such as INFLIXIMAB and etanercept, but their precise role remains uncertain.... rheumatoid arthritis
Sex education in schools is regarded as an e?ective way of reducing teenaged pregnancy, especially when linked with contraceptive services. Several studies have shown that it does not cause an increase in sexual activity and may even delay the onset of sexual relationships and lessen the number of partners. Programmes taught by youth agencies may be even more e?ective than those taught in the classroom – possibly because teaching takes place in small groups of volunteer participants, and the programmes are tailored to their target populations. Despite improvements in sex education, the United Kingdom has the highest incidence of teenaged pregnancies in the European Community.
Sex education, including information about AIDS/HIV and other sexually transmitted infections (STIs), is compulsory in all state-maintained secondary schools in England and Wales. The National Curriculum includes only biological aspects of AIDS/HIV, STIs and human sexual behaviour.
All maintained schools must have a written statement of their policy, which is available to parents. The local education authority, governing body and headteacher should ensure that sex education encourages pupils to have due regard to moral considerations and the value of family life. Sex-education policies and practices are monitored by the O?ce for Standards in Education (OFSTED) and the O?ce of HM Chief Inspector of Schools (OHMCI) as part of school inspections.... sex education
Dumbness is the inability to pronounce the sounds that make up words. DEAFNESS is the most important cause, being due to a congenital brain defect, or acquired brain disease, such as tertiary SYPHILIS. When hearing is normal or only mildly impaired, dumbness may be due to a structural defect such as tongue-tie or enlarged tonsils and adenoids, or to ine?cient voice control, resulting in lisping or lalling. Increased tension is a common cause of STAMMERING; speech disorders may occasionally be of psychological origin.
Normal speech may be lost in adulthood as a result of a STROKE or head injury. Excessive use of the voice may be an occupational hazard; and throat cancer may require a LARYNGECTOMY, with subsequent help in communication. Severe psychiatric disturbance may be accompanied by impaired social and communication skills. (See also VOICE AND SPEECH.)
Treatment The underlying cause of the problem should be diagnosed as early as possible; psychological and other specialist investigations should be carried out as required, and any physical defect should be repaired. People who are deaf and unable to speak should start training in lip-reading as soon as possible, and special educational methods aimed at acquiring a modulated voice should similarly be started in early childhood – provided by the local authority, and continued as required. Various types of speech therapy or PSYCHOTHERAPY may be appropriate, alone or in conjunction with other treatments, and often the ?nal result may be highly satisfying, with a good command of language and speech being obtained.
Help and advice may be obtained from AFASIC (Unlocking Speech and Language).... speech disorders
Structure
CORIUM The foundation layer. It overlies the subcutaneous fat and varies in thickness from 0·5–3.0 mm. Many nerves run through the corium: these have key roles in the sensations of touch, pain and temperature (see NEURON(E)). Blood vessels nourish the skin and are primarily responsible for regulating the body temperature. Hairs are bedded in the corium, piercing the epidermis (see below) to cover the skin in varying amounts in di?erent parts of the body. The sweat glands are also in the corium and their ducts lead to the surface. The ?brous tissue of the corium comprises interlocking white ?brous elastic bundles. The corium contains many folds, especially over joints and on the palms of hands and soles of feet with the epidermis following the contours. These are permanent throughout life and provide unique ?ngerprinting identi?cation. HAIR Each one has a root and shaft, and its varying tone originates from pigment scattered throughout it. Bundles of smooth muscle (arrectores pilorum) are attached to the root and on contraction cause the hair to stand vertical. GLANDS These occur in great numbers in the skin. SEBACEOUS GLANDS secrete a fatty substance and sweat glands a clear watery ?uid (see PERSPIRATION). The former are made up of a bunch of small sacs producing fatty material that reaches the surface via the hair follicle. Around three million sweat or sudoriparous glands occur all over the body surface; sited below the sebaceous glands they are unconnected to the hairs. EPIDERMIS This forms the outer layer of skin and is the cellular layer covering the body surface: it has no blood vessels and its thickness varies from 1 mm on the palms and soles to 0·1 mm on the face. Its outer, impervious, horny layer comprises several thicknesses of ?at cells (pierced only by hairs and sweat-gland openings) that are constantly rubbed o? as small white scales; they are replaced by growing cells from below. The next, clear layer forms a type of membrane below which the granular stratum cells are changing from their origins as keratinocytes in the germinative zone, where ?ne sensory nerves also terminate. The basal layer of the germinative zone contains melanocytes which produce the pigment MELANIN, the cause of skin tanning.
Nail A modi?cation of skin, being analagous to the horny layer, but its cells are harder and more adherent. Under the horny nail is the nail bed, comprising the well-vascularised corium (see above) and the germinative zone. Growth occurs at the nail root at a rate of around 0·5 mm a week – a rate that increases in later years of life.
Skin functions By its ability to control sweating and open or close dermal blood vessels, the skin plays a crucial role in maintaining a constant body temperature. Its toughness protects the body from mechanical injury. The epidermis is a two-way barrier: it prevents the entry of noxious chemicals and microbes, and prevents the loss of body contents, especially water, electrolytes and proteins. It restricts electrical conductivity and to a limited extent protects against ultraviolet radiation.
The Langerhans’ cells in the epidermis are the outposts of the immune system (see IMMUNITY), just as the sensory nerves in the skin are the outposts of the nervous system. Skin has a social function in its ability to signal emotions such as fear or anger. Lastly it has a role in the synthesis of vitamin D.... skin
Health Encyclopedia