Symptoms: skin hot, dry and flushed. High temperature and high humidity dispose. Sweating mechanism disorganised. Delirium, headache, shock, dizziness, possible coma, nausea, profuse sweating followed by absence of sweat causing skin to become hot and dry; rapid rise in body temperature, muscle twitching, tachycardia, dehydration.
Treatment. Hospital emergency. Reduce temperature by immersion of victim in bath of cold water. Wrap in a cold wet sheet. Lobelia, to equalise the circulation. Feverfew to regulate sweating mechanism. Yarrow to reduce temperature. Give singly or in combination as available.
Alternatives. Tea. Lobelia 1; Feverfew 2; Yarrow 2. Mix. 2 teaspoons to each cup boiling water; infuse 15 minutes. Half-1 cup freely. Vomiting to be regarded as favourable.
Tinctures. Combine: Lobelia 1; Pleurisy root 2; Valerian 1. Dose: 1-2 teaspoons in water every 2 hours. Decoction. Irish Moss; drink freely.
Practitioner. Tincture Gelsemium BPC (1973). Dose: 0.3ml (5 drops).
Alternate hot and cold compress to back of neck and forehead. Hot Chamomile footbath.
Diet. Irish Moss products. High salt. Abundant drinks of spring water.
Supplements. Kelp tablets, 2 thrice daily. Vitamin C (1g after meals thrice daily). Vitamin E (one 500iu capsule morning and evening).
Vitamin C for skin protection. Increasing Vitamin C after exposure to the sun should help protect against the sun’s ultra violet rays, as skin Vitamin C levels were shown to be severely depleted after exposure. (British Journal of Dermatology 127, 247-253) ... heatstroke
The start of ‘dehydration’ is signalled by a person becoming thirsty. In normal circumstances, the drinking of water will relieve thirst and serious dehydration does not develop. In a temperate climate an adult will lose 1.5 litres or more a day from sweating, urine excretion and loss of ?uid through the lungs. In a hot climate the loss is much higher – up to 10 litres if a person is doing hard physical work. Even in a temperate climate, severe dehydration will occur if a person does not drink for two or three days. Large losses of ?uid occur with certain illnesses – for example, profuse diarrhoea; POLYURIA in diabetes or kidney failure (see KIDNEYS, DISEASES OF); and serious blood loss from, say, injury or a badly bleeding ULCER in the gastrointestinal tract. Severe thirst, dry lips and tongue, TACHYCARDIA, fast breathing, lightheadedness and confusion are indicative of serious dehydration; the individual can lapse into COMA and eventually die if untreated. Dehydration also results in a reduction in output of urine, which becomes dark and concentrated.
Prevention is important, especially in hot climates, where it is essential to drink water even if one is not thirsty. Replacement of salts is also vital, and a diet containing half a teaspoon of table salt to every litre of water drunk is advisable. If someone, particularly a child, suffers from persistent vomiting and diarrhoea, rehydration therapy is required and a salt-andglucose rehydration mixture (obtainable from pharmacists) should be taken. For those with severe dehydration, oral ?uids will be insu?cient and the affected person needs intravenous ?uids and, sometimes, admission to hospital, where ?uid intake and output can be monitored and rehydration measures safely controlled.... dehydration
It usually arises in alcoholics after withdrawal or abstinence from alcohol.
Early symptoms include restlessness, agitation, trembling, and sleeplessness.
The person may develop a rapid heartbeat, fever, and dilation of the pupils.
Sweating, confusion, hallucinations, and convulsions may also occur.
Treatment consists of rest, rehydration, and sedation.
Vitamin injections, particularly of thiamine (see vitamin B complex), may be given.... delirium tremens
(See anxiety; anxiety disorders.)... generalized anxiety disorder
Excessive sweating may be caused by hot weather, exercise, or anxiety. In some cases it is due to an infection, thyrotoxicosis, hypoglycaemia, or a nervous system disorder. Usually, the disorder has no known cause, and begins at puberty, disappearing by the mid-20s or early 30s.
If hyperhidrosis is persistent and cannot be controlled by antiperspirants, surgery may be considered to destroy the nerve centres that control sweating.... hyperhidrosis
The condition may be caused by excessive sweating; in some cases, it is a sign of kidney failure.... oliguria
The chief object of perspiration is to maintain an even body temperature by regulating the heat lost from the body surface. Sweating is therefore increased by internally produced heat, such as muscular activity, or external heat. It is controlled by two types of nerves: vasomotor, which regulate the local blood ?ow, and secretory (part of the sympathetic nervous system) which directly in?uence secretion.
Eccrine sweat is a faintly acid, watery ?uid containing less than 2 per cent of solids. The eccrine sweat-glands in humans are situated in greatest numbers on the soles of the feet and palms of the hands, and with a magnifying glass their minute openings or pores can be seen in rows occupying the summit of each ridge in the skin. Perspiration is most abundant in these regions, although it also occurs all over the body.
Apocrine sweat-glands These start functioning at puberty and are found in the armpits, the eyelids, around the anus in association with the external genitalia, and in the areola and nipple of the breast. (The glands that produce wax in the ear are modi?ed apocrine glands.) The ?ow of apocrine sweat is evoked by emotional stimuli such as fear, anger, or sexual excitement.
Abnormalities of perspiration Decreased sweating may occur in the early stages of fever, in diabetes, and in some forms of glomerulonephritis (see KIDNEYS, DISEASES OF). Some people are unable to sweat copiously, and are prone to HEAT STROKE. EXCESSIVE SWEATING, OR HYPERIDROSIS, may be caused by fever, hyperthyroidism (see THYROID GLAND, DISEASES OF), obesity, diabetes mellitus, or an anxiety state. O?ensive perspiration, or bromidrosis, commonly occurs on the hands and feet or in the armpits, and is due to bacterial decomposition of skin secretions. A few people, however, sweat over their whole body surface. For most of those affected, it is the palmar and/or axillary hyperhidrosis that is the major problem.
Conventional treatment is with an ANTICHOLINERGIC drug. This blocks the action of ACETYLCHOLINE (a neurotransmitter secreted by nerve-cell endings) which relaxes some involuntary muscles and tightens others, controlling the action of sweat-glands. But patients often stop treatment because they get an uncomfortably dry mouth. Aluminium chloride hexahydrate is a topical treatment, but this can cause skin irritation and soreness. Such antiperspirants may help patients with moderate hyperhidrosis, but those severely affected may need either surgery or injections of BOTULINUM TOXIN to destroy the relevant sympathetic nerves to the zones of excessive sweating.... perspiration
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
Causes The disease is caused by the bacillus Clostridium tetani, found generally in earth and dust and especially in places where animal manure is collected. Infection usually follows a wound, especially a deeply punctured or gunshot wound, with the presence of some foreign body. It is a hazard in war and also among farmers, gardeners and those in the construction industry. The bacillus develops a toxin in the wound, which is absorbed through the motor nerves into the spinal cord where it renders the nerves excitable and acutely sensitive to mild stimuli.
Symptoms Most commonly appearing within four to ?ve days of the wound, the patient’s symptoms may be delayed for several weeks – by which time the wound may have healed. Initially there is muscle sti?ness around the wound followed by sti?ness around the jaw, leading to lockjaw, or trismus. This extends to the muscles of the neck, back, chest, abdomen, and limbs, leading to strange, often changing, contorted postures, accompanied by frequent seizures – often provoked by quite minor stimuli such as a sudden noise. The patient’s breathing may be seriously affected, in severe cases leading to ASPHYXIA; the temperature may rise sharply, often with sweating; and severe pain is common. Mental clarity is characteristic adding to the patient’s anxiety. In severe infections death may be from asphyxia, PNEUMONIA, or general exhaustion. More commonly, the disease takes a chronic course, leading to gradual recovery. Outcome depends on several factors, chie?y the patient’s immune status and age, and early administration of appropriate treatment.
Tetanus may occur in newborn babies, particularly when birth takes place in an unhygienic environment. It is particularly common in the tropics and developing countries, with a high mortality rate. Local tetanus is a rare manifestation, in which only muscles around the wound are affected, though sti?ness may last for several months. STRYCHNINE poisoning and RABIES, although similar in some respects to tetanus, may be easily distinguished by taking a good history.
Prevention and treatment The incidence of tetanus in the United Kingdom has been almost abolished by the introduction of tetanus vaccine (see IMMUNISATION). Children are routinely immunised at two, three and four months of age, and boosters are given later in life to at-risk workers, or those travelling to tropical parts.
Treatment should be started as soon as possible after sustaining a potentially dangerous wound. An intravenous injection of antitoxin should be given immediately, the wound thoroughly cleaned and PENICILLIN administered. Expert nursing is most important. Spasms may be minimised by reducing unexpected stimuli, and diazepam (see BENZODIAZEPINES; TRANQUILLISERS) is helpful. Intravenous feeding should be started immediately if the patient cannot swallow. Aspiration of bronchial secretions and antibiotic treatment of pneumonia may be necessary.... tetanus
Causes: oxygen starvation, lactic acid build-up. A common cause is depletion of salt from excessive sweating. Night cramps may be due to impaired blood supply or mineral deficiency: Calcium, Iron, Magnesium. Spasm takes many forms: writer’s, swimmer’s, pianist’s, harpist’s, trumpeter’s, hornplayer’s or emotional stress due to tightening of the facial muscles (German Chamomile). Athlete’s cramp from mechanical stress may be relieved by Cramp Bark as well as manipulation. Repetitive strain injury (RSI).
Cramp of the heart muscle is known as angina (Cramp Bark, Motherwort). Where due to spasm of blood vessels from atherosclerosis it may take the form of intermittent claudication (Prickly Ash bark, Cramp bark, Nettles, Vitamin E). For cramp in the back (Cramp bark, Ligvites); stomach (Fennel, Cardamoms, Turkey Rhubarb); womb (Squaw vine, Wild Yam, Cramp bark); kidney and bladder (Horsetail); muscles (Devil’s Claw).
Alternatives. Teas. Mild cases. Any one: German Chamomile, Lime flowers, Holy Thistle, Motherwort, Silverweed, Skullcap, St John’s Wort, Betony.
Combination: equal parts, Skullcap, German Chamomile, Motherwort. 1 heaped teaspoon to each cup boiling water; infuse 5-10 minutes. 1 cup thrice daily or as necessary.
Decoction. More severe cases. Any one: Cramp bark, Valerian, Peruvian bark, Wild Yam, Prickly Ash bark.
Tablets/capsules. Black Cohosh, Cramp bark, Prickly Ash bark, Devil’s Claw, Wild Yam, Ligvites. Combination. Equal parts, Butterburr and Cramp bark. Dose: powders 500mg (two 00 capsules or one- third teaspoon thrice daily); Liquid extracts: one 5ml teaspoon. Tinctures: 1-2 teaspoons. Thrice daily or as necessary.
John William Fyfe MD. “After 20 years broken sleep from leg cramps a patient found relief with 15 drops Liquid Extract Black Haw, thrice daily for 3-4 days.” This was used successfully in his practice for over 30 years.
Aromatherapy. Massage oil. 3 drops Marjoram, 3 drops Basil, in 2 teaspoons Almond or other vegetable oil. Or: Cypress oil, Mustard bath for feet.
Diet. See food sources of Calcium, Iron and Magnesium.
Supplements. Daily. B-complex 100mg; B6 100mg; Dolomite tablets (1000mg); Vitamin E (400iu); Vitamin C (2g); Calcium ascorbate (800mg); Magnesium 300mg (450mg, pregnancy). Zinc (25mg).
For cramp of pregnancy – see PREGNANCY. ... cramp
“There is an increasing amount of evidence,” writes Dr D. Addy, Consulting Paediatrician, “that fevers may enhance the defence mechanism against infection. There is little evidence that fever itself is harmful except in 3 per cent of children who are prone to develop febrile convulsions.”
When a fever is identified (scarlet fever, measles, etc) specific treatment with agents of proven efficacy are required. See appropriate entries. For unidentified fever, before the doctor comes, diaphoretics (Yarrow, etc) may be given to induce sweating to relieve tension on lungs and other internal organs. Also, diuretics (Yarrow, etc) stimulate elimination of wastes through the kidneys. Two herbs, Elderflowers and Peppermint, given at the chill stage have probably saved lives of tens of thousands from fever. A timely laxative to clean out stomach and bowels may favourably reduce temperature.
Perseverance with strong Nettle tea may also assist the work of the awaited practitioner. Excellent for simple fevers is the formula: Liquid Extracts: Elderflowers 1oz; Peppermint quarter of an ounce; Cinnamon quarter of an ounce; Skullcap 1oz. One 5ml teaspoon in hot water every 2 hours until fever abates – patient in bed. Sponge down body with vinegar and water. Patient should not leave bed until temperature falls. Abundant Vitamin C drinks, fresh lemon, orange juice.
A fever may be accompanied by: flushed face, rapid breathing, headache, hot skin, shivering, thirst and sweating.
Discharges are often a necessary part of the cure. Once toxins are eliminated by skin, kidneys, bowel or by respiration, symptoms abate and a feeling of well-being appears. It is often a turning point towards recovery: the body is trying to throw off toxins and poisons. A fever is an effort of the system to fight back. ... fever
Alternatives. Agnus Castus, Ho-Shou-Wu, Black Cohosh, Damiana, Goldenseal, Lime flowers, Lobelia, Mistletoe, Rue, Sarsaparilla, Shepherd’s Purse, Wild Yam, Chamomile tea. Teas, tablets, liquid extracts, powders, tinctures.
Official treatment may include oestrogenic preparations (HRT) with risks of blood clotting and thrombosis.
Non-hormonal relief: combination.
Tea, equal parts, Lime flowers, Motherwort, Wild Carrot. 2 teaspoons to each cup boiling water; infuse 5-15 minutes. 1 cup freely.
Liquid extracts. Formula. Black Cohosh half; Mistletoe 1; Agnus Castus 1. Dosage: 1 teaspoon thrice daily in water.
Tinctures: same formula, double dose.
Evening Primrose (capsules).
Wessex traditional. Hawthorn flowers and leaves 4; Hops 1. 2 teaspoons to each cup boiling water; infuse 5-10 minutes; 1 cup freely.
Diet. Lacto-vegetarian.
Supplement. Vitamin E, 400iu morning and evening. ... hot flushes
The local effects of the tumour commonly cause headache and, less frequently, impairment of vision, particularly of the temporal ?eld of vision, as a result of pressure on the nerves to the eye. The tumour may damage the other pituitary cells giving rise to gonadal, thyroid or adrenocortical insu?ciency. The disease often becomes obvious in persons over about 45 years of age; they may also complain of excessive sweating, joint pains and lethargy. The diagnosis is con?rmed by measuring the level of growth hormone in the serum and by an X-ray of the skull which usually shows enlargement of the pituitary fossa.
Treatment The most e?ective treatment is surgically to remove the pituitary adenoma. This can usually be done through the nose and the sphenoid sinus, but large adenomas may need a full CRANIOTOMY. Surgery cures about 80 per cent of patients with a microadenoma and 40 per cent of those with a large lesion; the rate of recurrence is 5–10 per cent. For recurrences, or for patients un?t for surgery or who refuse it, a combination of irradiation and drugs may be helpful. Deep X-ray therapy to the pituitary fossa is less e?ective than surgery but may also be helpful, and recently more sophisticated X-ray techniques, such as gamma knife irradiation, have shown promise. Drugs – such as BROMOCRIPTINE, capergoline and quiangoline, which are dopamine agonists – lower growth-hormone levels in acromegaly and are particularly useful as an adjunct to radiotherapy. Drugs which inhibit growth-hormone release by competing for its receptors, octeotride and lanreotride, also have a place in treatment.
See www.niddk.nih.gov/health/endo/pubs/ acro/acro.htm
www.umm.edu/endocrin/acromegaly.htm... acromegaly
Insulin-dependent and non-insulindependent diabetes have a varied pathological pattern and are caused by the interaction of several genetic and environmental factors.
Insulin-dependent diabetes mellitus (IDDM) (juvenile-onset diabetes, type 1 diabetes) describes subjects with a severe de?ciency or absence of insulin production. Insulin therapy is essential to prevent KETOSIS – a disturbance of the body’s acid/base balance and an accumulation of ketones in the tissues. The onset is most commonly during childhood, but can occur at any age. Symptoms are acute and weight loss is common.
Non-insulin-dependent diabetes mellitus (NIDDM) (maturity-onset diabetes, type 2 diabetes) may be further sub-divided into obese and non-obese groups. This type usually occurs after the age of 40 years with an insidious onset. Subjects are often overweight and weight loss is uncommon. Ketosis rarely develops. Insulin production is reduced but not absent.
A new hormone has been identi?ed linking obesity to type 2 diabetes. Called resistin – because of its resistance to insulin – it was ?rst found in mice but has since been identi?ed in humans. Researchers in the United States believe that the hormone may, in part, explain how obesity predisposes people to diabetes. Their hypothesis is that a protein in the body’s fat cells triggers insulin resistance around the body. Other research suggests that type 2 diabetes may now be occurring in obese children; this could indicate that children should be eating a more-balanced diet and taking more exercise.
Diabetes associated with other conditions (a) Due to pancreatic disease – for example, chronic pancreatitis (see PANCREAS, DISORDERS OF); (b) secondary to drugs – for example, GLUCOCORTICOIDS (see PANCREAS, DISORDERS OF); (c) excess hormone production
– for example, growth hormone (ACROMEGALY); (d) insulin receptor abnormalities; (e) genetic syndromes (see GENETIC DISORDERS).
Gestational diabetes Diabetes occurring in pregnancy and resolving afterwards.
Aetiology Insulin-dependent diabetes occurs as a result of autoimmune destruction of beta cells within the PANCREAS. Genetic in?uences are important and individuals with certain HLA tissue types (HLA DR3 and HLA DR4) are more at risk; however, the risks associated with the HLA genes are small. If one parent has IDDM, the risk of a child developing IDDM by the age of 25 years is 1·5–2·5 per cent, and the risk of a sibling of an IDDM subject developing diabetes is about 3 per cent.
Non-insulin-dependent diabetes has no HLA association, but the genetic in?uences are much stronger. The risks of developing diabetes vary with di?erent races. Obesity, decreased exercise and ageing increase the risks of disease development. The risk of a sibling of a NIDDM subject developing NIDDM up to the age of 80 years is 30–40 per cent.
Diet Many NIDDM diabetics may be treated with diet alone. For those subjects who are overweight, weight loss is important, although often unsuccessful. A diet high in complex carbohydrate, high in ?bre, low in fat and aiming towards ideal body weight is prescribed. Subjects taking insulin need to eat at regular intervals in relation to their insulin regime and missing meals may result in hypoglycaemia, a lowering of the amount of glucose in the blood, which if untreated can be fatal (see below).
Oral hypoglycaemics are used in the treatment of non-insulin-dependent diabetes in addition to diet, when diet alone fails to control blood-sugar levels. (a) SULPHONYLUREAS act mainly by increasing the production of insulin;
(b) BIGUANIDES, of which only metformin is available, may be used alone or in addition to sulphonylureas. Metformin’s main actions are to lower the production of glucose by the liver and improve its uptake in the peripheral tissues.
Complications The risks of complications increase with duration of disease.
Diabetic hypoglycaemia occurs when amounts of glucose in the blood become low. This may occur in subjects taking sulphonylureas or insulin. Symptoms usually develop when the glucose concentration falls below 2·5 mmol/l. They may, however, occur at higher concentrations in subjects with persistent hyperglycaemia – an excess of glucose – and at lower levels in subjects with persistent hypo-glycaemia. Symptoms include confusion, hunger and sweating, with coma developing if blood-sugar concentrations remain low. Re?ned sugar followed by complex carbohydrate will return the glucose concentration to normal. If the subject is unable to swallow, glucagon may be given intramuscularly or glucose intravenously, followed by oral carbohydrate, once the subject is able to swallow.
Although it has been shown that careful control of the patient’s metabolism prevents late complications in the small blood vessels, the risk of hypoglycaemia is increased and patients need to be well motivated to keep to their dietary and treatment regime. This regime is also very expensive. All risk factors for the patient’s cardiovascular system – not simply controlling hyperglycaemia – may need to be reduced if late complications to the cardiovascular system are to be avoided.
Diabetes is one of the world’s most serious health problems. Recent projections suggest that the disorder will affect nearly 240 million individuals worldwide by 2010 – double its prevalence in 1994. The incidence of insulin-dependent diabetes is rising in young children; they will be liable to develop late complications.
Although there are complications associated with diabetes, many subjects live normal lives and survive to an old age. People with diabetes or their relatives can obtain advice from Diabetes UK (www.diabetes.org.uk).
Increased risks are present of (a) heart disease, (b) peripheral vascular disease, and (c) cerebrovascular disease.
Diabetic eye disease (a) retinopathy, (b) cataract. Regular examination of the fundus enables any abnormalities developing to be detected and treatment given when appropriate to preserve eyesight.
Nephropathy Subjects with diabetes may develop kidney damage which can result in renal failure.
Neuropathy (a) Symmetrical sensory polyneuropathy; damage to the sensory nerves that commonly presents with tingling, numbness of pain in the feet or hands. (b) Asymmetrical motor diabetic neuropathy, presenting as progressive weakness and wasting of the proximal muscles of legs. (c) Mononeuropathy; individual motor or sensory nerves may be affected. (d) Autonomic neuropathy, which affects the autonomic nervous system, has many presentations including IMPOTENCE, diarrhoea or constipation and postural HYPOTENSION.
Skin lesions There are several skin disorders associated with diabetes, including: (a) necrobiosis lipoidica diabeticorum, characterised by one or more yellow atrophic lesions on the legs;
(b) ulcers, which most commonly occur on the feet due to peripheral vascular disease, neuropathy and infection. Foot care is very important.
Diabetic ketoacidosis occurs when there is insu?cient insulin present to prevent KETONE production. This may occur before the diagnosis of IDDM or when insu?cient insulin is being given. The presence of large amounts of ketones in the urine indicates excess ketone production and treatment should be sought immediately. Coma and death may result if the condition is left untreated.
Symptoms Thirst, POLYURIA, GLYCOSURIA, weight loss despite eating, and recurrent infections (e.g. BALANITIS and infections of the VULVA) are the main symptoms.
However, subjects with non-insulindependent diabetes may have the disease for several years without symptoms, and diagnosis is often made incidentally or when presenting with a complication of the disease.
Treatment of diabetes aims to prevent symptoms, restore carbohydrate metabolism to as near normal as possible, and to minimise complications. Concentration of glucose, fructosamine and glycated haemoglobin in the blood are used to give an indication of blood-glucose control.
Insulin-dependent diabetes requires insulin for treatment. Non-insulin-dependent diabetes may be treated with diet, oral HYPOGLYCAEMIC AGENTS or insulin.
Insulin All insulin is injected – mainly by syringe but sometimes by insulin pump – because it is inactivated by gastrointestinal enzymes. There are three main types of insulin preparation: (a) short action (approximately six hours), with rapid onset; (b) intermediate action (approximately 12 hours); (c) long action, with slow onset and lasting for up to 36 hours. Human, porcine and bovine preparations are available. Much of the insulin now used is prepared by genetic engineering techniques from micro-organisms. There are many regimens of insulin treatment involving di?erent combinations of insulin; regimens vary depending on the requirements of the patients, most of whom administer the insulin themselves. Carbohydrate intake, energy expenditure and the presence of infection are important determinants of insulin requirements on a day-to-day basis.
A new treatment for diabetes, pioneered in Canada and entering its preliminary clinical trials in the UK, is the transplantation of islet cells of Langerhans from a healthy person into a patient with the disorder. If the transplantation is successful, the transplanted cells start producing insulin, thus reducing or eliminating the requirement for regular insulin injections. If successful the trials would be a signi?cant advance in the treatment of diabetes.
Scientists in Israel have developed a drug, Dia Pep 277, which stops the body’s immune system from destroying pancratic ? cells as happens in insulin-dependent diabetes. The drug, given by injection, o?ers the possibility of preventing type 1 diabetes in healthy people at genetic risk of developing the disorder, and of checking its progression in affected individuals whose ? cells are already perishing. Trials of the drug are in progress.... diabetes mellitus
The most widely prescribed type of antidepressants are the tricyclics, so-called because their molecular structure includes three rings. The other commonly used types are named after the actions they have on chemicals in the brain: the SELECTIVE SEROTONIN-REUPTAKE INHIBITORS (SSRIS) and the MONOAMINE OXIDASE INHIBITORS (MAOIS) – see also below. All types of antidepressant work in similar ways. Tricyclic antidepressants have cured depression in millions of people, but they can cause unpleasant side-effects, particularly in the ?rst couple of weeks. These include SEDATION, dry mouth, excessive sweating, CONSTIPATION, urinary problems, and impotence (inability to get an erection). Up to half of all people prescribed tricyclic drugs cannot tolerate the side-effects and stop treatment before their depression is properly treated. More seriously, tricyclics can upset the rhythm of the heart in susceptible people and should never be given in the presence of heart disease.
The SSRIs are newer, coming into wide use in the late 1980s. They increase the levels in the brain of the chemical messenger SEROTONIN, which is thought to be depleted in depression. Indeed, the SSRIs are as e?ective as tricyclics and, although they can cause nausea and excessive sweating at ?rst, they generally have fewer side-effects. Their main disadvantage, however, is that they cost much more than the most commonly used tricyclic, amitriptyline. On the other hand, they are more acceptable to many patients and they cause fewer drop-outs from treatment – up to a quarter rather than a half. The money saved by completed, successful treatment may outweigh the prescribing costs. SSRIs have been reported as associated with an increased risk of suicide.
Another group of antidepressants, the MAOIs, have been in use since the late 1950s.
They are stimulants, rather than sedatives, and are particularly helpful for people who are physically and mentally slowed by depression. They work well but have one big disadvantage – a dangerous interaction with certain foods and other drugs, causing a sudden and very dangerous increase in blood pressure. People taking them must carry an information card explaining the risk and listing the things that they should avoid. Because of this risk, MAOIs are not used much now, except when other treatments have failed. A new MAOI, moclobemide, which is less likely to interact and so cause high blood pressure, is now available.
LITHIUM CARBONATE is a powerful antidepressant used for intractable depression. It should be used under specialist supervision as the gap between an e?ective dose and a toxic one is narrow.
St John’s Wort is a popular herbal remedy which may be e?ective, but which is handicapped by di?erences of strength between di?erent preparations or batches. It can interact with a number of conventional drugs and so needs to be used cautiously and with advice.
In general, antidepressants work by restoring the balance of chemicals in the brain. Improved sleep and reduced anxiety are usually the ?rst signs of improvement, particularly among people taking the more sedative tricyclic drugs. Improvement in other symptoms follow, with the mood starting to lift after about two weeks of treatment. Most people feel well by three months, although a few residual symptoms, such as slowness in the mornings, may take longer to clear up. People taking antidepressants usually want to stop them as soon as they feel better; however, the risk of relapse is high for up to a year and most doctors recommend continuing the drugs for around 4–6 months after recovery, with gradual reduction of the dose after that.
Withdrawal reactions may occur including nausea, vomiting, headache, giddiness, panic or anxiety and restlessness. The drugs should be withdrawn gradually over about a month or longer (up to six months in those who have been on maintenance treatment).
A wide range of antidepressant drugs is described in the British National Formulary. Examples include:
Tricyclics: amitryptyline, imipramine, doxepin.
MAOIs: phenelzine, isocarboxazid.
SSRIs: citalopram, ?uoxetine, paraxtene. (Antidepressant drugs not in these three
groups include ?upenthixol, mertazapine and venlafaxine.)... antidepressant drugs
Rarely, an enlarged gland may be the result of cancer in the thyroid.
Treatment A symptomless goitre may gradually disappear or be so small as not to merit treatment. If the goitre is large or is causing the patient di?culty in swallowing or breathing, it may need surgical removal by partial or total thyroidectomy. If the patient is de?cient in iodine, ?sh and iodised salt should be included in the diet.
Hyperthyroidism is a common disorder affecting 2–5 per cent of all females at some time in their lives. The most common cause – around 75 per cent of cases – is thyrotoxicosis (see below). An ADENOMA (or multiple adenomas) or nodules in the thyroid also cause hyperthyroidism. There are several other rare causes, including in?ammation caused by a virus, autoimune reactions and cancer. The symptoms of hyperthyroidism affect many of the body’s systems as a consequence of the much-increased metabolic rate.
Thyrotoxicosis is a syndrome consisting of di?use goitre (enlarged thyroid gland), over-activity of the gland and EXOPHTHALMOS (protruding eyes). Patients lose weight and develop an increased appetite, heat intolerance and sweating. They are anxious, irritable, hyperactive, suffer from TACHYCARDIA, breathlessness and muscle weakness and are sometimes depressed. The hyperthyroidism is due to the production of ANTIBODIES to the TSH receptor (see THYROTROPHIN-STIMULATING HORMONE (TSH)) which stimulate the receptor with resultant production of excess thyroid hormones. The goitre is due to antibodies that stimulate the growth of the thyroid gland. The exoph-
thalmos is due to another immunoglobulin called the ophthalmopathic immunoglobulin, which is an antibody to a retro-orbital antigen on the surface of the retro-orbital EYE muscles. This provokes in?ammation in the retro-orbital tissues which is associated with the accumulation of water and mucopolysaccharide which ?lls the orbit and causes the eye to protrude forwards.
Although thyrotoxicosis may affect any age-group, the peak incidence is in the third decade. Females are affected ten times as often as males; the prevalence in females is one in 500. As with many other autoimmune diseases, there is an increased prevalence of autoimmune thyroid disease in the relatives of patients with thyrotoxicosis. Some of these patients may have hypothyroidism (see below) and others, thyrotoxicosis. Patients with thyrotoxicosis may present with a goitre or with the eye signs or, most commonly, with the symptoms of excess thyroid hormone production. Thyroid hormone controls the metabolic rate of the body so that the symptoms of hyperthyroidism are those of excess metabolism.
The diagnosis of thyrotoxicosis is con?rmed by the measurement of the circulating levels of the two thyroid hormones, thyroxine and TRIIODOTHYRONINE.
Treatment There are several e?ective treatments for thyrotoxicosis. ANTITHYROID DRUGS These drugs inhibit the iodination of tyrosine and hence the formation of the thyroid hormones. The most commonly used drugs are carbimazole and propylthiouricil: these will control the excess production of thyroid hormones in virtually all cases. Once the patient’s thyroid is functioning normally, the dose can be reduced to a maintenance level and is usually continued for two years. The disadvantage of antithyroid drugs is that after two years’ treatment nearly half the patients will relapse and will then require more de?nitive therapy. PARTIAL THYROIDECTOMY Removal of three-quarters of the thyroid gland is e?ective treatment of thyrotoxicosis. It is the treatment of choice in those patients with large goitres. The patient must however be treated with medication so that they are euthyroid (have a normally functioning thyroid) before surgery is undertaken, or thyroid crisis and cardiac arrhythmias may complicate the operation. RADIOACTIVE IODINE THERAPY This has been in use for many years, and is an e?ective means of controlling hyperthyroidism. One of the disadvantages of radioactive iodine is that the incidence of hypothyroidism is much greater than with other forms of treatment. However, the management of hypothyroidism is simple and requires thyroxine tablets and regular monitoring for hypothyroidism. There is no evidence of any increased incidence of cancer of the thyroid or LEUKAEMIA following radio-iodine therapy. It has been the pattern in Britain to reserve radio-iodine treatment to those over the age of 35, or those whose prognosis is unlikely to be more than 30 years as a result of cardiac or respiratory disease. Radioactive iodine treatment should not be given to a seriously thyrotoxic patient. BETA-ADRENOCEPTOR-BLOCKING DRUGS Usually PROPRANOLOL HYDROCHLORIDE: useful for symptomatic treatment during the ?rst 4–8 weeks until the longer-term drugs have reduced thyroid activity.
Hypothyroidism A condition resulting from underactivity of the thyroid gland. One form, in which the skin and subcutaneous tissues thicken and result in a coarse appearance, is called myxoedema. The thyroid gland secretes two hormones – thyroxine and triiodothyronine – and these hormones are responsible for the metabolic activity of the body. Hypothyroidism may result from developmental abnormalities of the gland, or from a de?ciency of the enzymes necessary for the synthesis of the hormones. It may be a feature of endemic goitre and retarded development, but the most common cause of hypothyroidism is the autoimmune destruction of the thyroid known as chronic thyroiditis. It may also occur as a result of radio-iodine treatment of thyroid overactivity (see above) and is occasionally secondary to pituitary disease in which inadequate TSH production occurs. It is a common disorder, occurring in 14 per 1,000 females and one per 1,000 males. Most patients present between the age of 30 and 60 years.
Symptoms As thyroid hormones are responsible for the metabolic rate of the body, hypothyroidism usually presents with a general sluggishness: this affects both physical and mental activities. The intellectual functions become slow, the speech deliberate and the formation of ideas and the answers to questions take longer than in healthy people. Physical energy is reduced and patients frequently complain of lethargy and generalised muscle aches and pains. Patients become intolerant of the cold and the skin becomes dry and swollen. The LARYNX also becomes swollen and gives rise to a hoarseness of the voice. Most patients gain weight and develop constipation. The skin becomes dry and yellow due to the presence of increased carotene. Hair becomes thinned and brittle and even baldness may develop. Swelling of the soft tissues may give rise to a CARPAL TUNNEL SYNDROME and middle-ear deafness. The diagnosis is con?rmed by measuring the levels of thyroid hormones in the blood, which are low, and of the pituitary TSH which is raised in primary hypothyroidism.
Treatment consists of the administration of thyroxine. Although tri-iodothyronine is the metabolically active hormone, thyroxine is converted to tri-iodothyronine by the tissues of the body. Treatment should be started cautiously and slowly increased to 0·2 mg daily – the equivalent of the maximum output of the thyroid gland. If too large a dose is given initially, palpitations and tachycardia are likely to result; in the elderly, heart failure may be precipitated.
Congenital hypothyroidism Babies may be born hypothyroid as a result of having little or no functioning thyroid-gland tissue. In the developed world the condition is diagnosed by screening, all newborn babies having a blood test to analyse TSH levels. Those found positive have a repeat test and, if the diagnosis is con?rmed, start on thyroid replacement therapy within a few weeks of birth. As a result most of the ill-effects of cretinism can be avoided and the children lead normal lives.
Thyroiditis In?ammation of the thyroid gland. The acute form is usually caused by a bacterial infection elsewhere in the body: treatment with antibiotics is needed. Occasionally a virus may be the infectious agent. Hashimoto’s thyroiditis is an autoimmune disorder causing hypothyroidism (reduced activity of the gland). Subacute thyroiditis is in?ammation of unknown cause in which the gland becomes painful and the patient suffers fever, weight loss and malaise. It sometimes lasts for several months but is usually self-limiting.
Thyrotoxic adenoma A variety of thyrotoxicosis (see hyperthyroidism above) in which one of the nodules of a multinodular goitre becomes autonomous and secretes excess thyroid hormone. The symptoms that result are similar to those of thyrotoxicosis, but there are minor di?erences.
Treatment The ?rst line of treatment is to render the patient euthyroid by treatment with antithyroid drugs. Then the nodule should be removed surgically or destroyed using radioactive iodine.
Thyrotoxicosis A disorder of the thyroid gland in which excessive amounts of thyroid hormones are secreted into the bloodstream. Resultant symptoms are tachycardia, tremor, anxiety, sweating, increased appetite, weight loss and dislike of heat. (See hyperthyroidism above.)... goitre
Arrhythmias An abnormal rate or rhythm of the heartbeat. The reason is a disturbance in the electrical impulses within the heart. Sometimes a person may have an occasional irregular heartbeat: this is called an ECTOPIC beat (or an extrasystole) and does not necessarily mean that an abnormality exists. There are two main types of arrhythmia: bradycardias, where the rate is slow – fewer than 60 beats a minute and sometimes so slow and unpredictable (heartblock) as to cause blackouts or heart failure; and tachycardia, where the rate is fast – more than 100 beats a minute. A common cause of arrhythmia is coronary artery disease, when vessels carrying blood to the heart are narrowed by fatty deposits (ATHEROMA), thus reducing the blood supply and damaging the heart tissue. This condition often causes myocardial infarction after which arrhythmias are quite common and may need correcting by DEFIBRILLATION (application of a short electric shock to the heart). Some tachycardias result from a defect in the electrical conduction system of the heart that is commonly congenital. Various drugs can be used to treat arrhythmias (see ANTIARRHYTHMIC DRUGS). If attacks constantly recur, the arrhythmia may be corrected by electrical removal of dead or diseased tissue that is the cause of the disorder. Heartblock is most e?ectively treated with an arti?cial CARDIAC PACEMAKER, a battery-activated control unit implanted in the chest.
Cardiomyopathy Any disease of the heart muscle that results in weakening of its contractions. The consequence is a fall in the e?ciency of the circulation of blood through the lungs and remainder of the body structures. The myopathy may be due to infection, disordered metabolism, nutritional excess or de?ciency, toxic agents, autoimmune processes, degeneration, or inheritance. Often, however, the cause is not identi?ed. Cardiomyopathies are less common than other types of heart diseases, and the incidence of di?erent types of myopathy (see below) is not known because patients or doctors are sometimes unaware of the presence of the condition.
The three recognised groups of cardiomyopathies are hypertrophic, dilated and restrictive.
•Hypertrophic myopathy, a familial condition, is characterised by great enlargement of the muscle of the heart ventricles. This reduces the muscle’s e?ciency, the ventricles fail to relax properly and do not ?ll suf?ciently during DIASTOLE.
In the dilated type of cardiomyopathy, both ventricles overdilate, impairing the e?ciency of contraction and causing congestion of the lungs.
In the restrictive variety, proper ?lling of the ventricles does not occur because the muscle walls are less elastic than normal. The result is raised pressure in the two atria (upper cavities) of the heart: these dilate and develop FIBRILLATION. Diagnosis can be di?cult and treatment is symptomatic, with a poor prognosis. In suitable patients, heart TRANSPLANTATION may be considered. Disorders of the heart muscle may also be
caused by poisoning – for example, heavy consumption of alcohol. Symptoms include tiredness, palpitations (quicker and sometimes irregular heartbeat), chest pain, di?culty in breathing, and swelling of the legs and hands due to accumulation of ?uid (OEDEMA). The heart is enlarged (as shown on chest X-ray) and ECHOCARDIOGRAPHY shows thickening of the heart muscle. A BIOPSY of heart muscle will show abnormalities in the cells of the heart muscle.
Where the cause of cardiomyopathy is unknown, as is the case with most patients, treatment is symptomatic using DIURETICS to control heart failure and drugs such as DIGOXIN to return the heart rhythm to normal. Patients should stop drinking alcohol. If, as often happens, the patient’s condition slowly deteriorates, heart transplantation should be considered.
Congenital heart disease accounts for 1–2 per cent of all cases of organic heart disease. It may be genetically determined and so inherited; present at birth for no obvious reason; or, in rare cases, related to RUBELLA in the mother. The most common forms are holes in the heart (atrial septal defect, ventricular septal defect – see SEPTAL DEFECT), a patent DUCTUS ARTERIOSUS, and COARCTATION OF THE AORTA. Many complex forms also exist and can be diagnosed in the womb by fetal echocardiography which can lead to elective termination of pregnancy. Surgery to correct many of these abnormalities is feasible, even for the most severe abnormalities, but may only be palliative giving rise to major diffculties of management as the children become older. Heart transplantation is now increasingly employed for the uncorrectable lesions.
Coronary artery disease Also known as ischaemic heart disease, this is a common cause of symptoms and death in the adult population. It may present for the ?rst time as sudden death, but more usually causes ANGINA PECTORIS, myocardial infarction (heart attack) or heart failure. It can also lead to a disturbance of heart rhythm. Factors associated with an increased risk of developing coronary artery disease include diabetes, cigarette smoking, high blood pressure, obesity, and a raised concentration of cholesterol in the blood. Older males are most affected.
Coronary thrombosis or acute myocardial infarction is the acute, dramatic manifestation of coronary-artery ischaemic heart disease – one of the major killing diseases of western civilisation. In 1999, ischaemic heart disease was responsible for about 115,000 deaths in England and Wales, compared with 153,000 deaths in 1988. In 1999 more than 55,600 people died of coronary thrombosis. The underlying cause is disease of the coronary arteries which carry the blood supply to the heart muscle (or myocardium). This results in narrowing of the arteries until ?nally they are unable to transport su?cient blood for the myocardium to function e?ciently. One of three things may happen. If the narrowing of the coronary arteries occurs gradually, then the individual concerned will develop either angina pectoris or signs of a failing heart: irregular rhythm, breathlessness, CYANOSIS and oedema.
If the narrowing occurs suddenly or leads to complete blockage (occlusion) of a major branch of one of the coronary arteries, then the victim collapses with acute pain and distress. This is the condition commonly referred to as a coronary thrombosis because it is usually due to the affected artery suddenly becoming completely blocked by THROMBOSIS. More correctly, it should be described as coronary occlusion, because the ?nal occluding factor need not necessarily be thrombosis.
Causes The precise cause is not known, but a wide range of factors play a part in inducing coronary artery disease. Heredity is an important factor. The condition is more common in men than in women; it is also more common in those in sedentary occupations than in those who lead a more physically active life, and more likely to occur in those with high blood pressure than in those with normal blood pressure (see HYPERTENSION). Obesity is a contributory factor. The disease is more common among smokers than non-smokers; it is also often associated with a high level of CHOLESTEROL in the blood, which in turn has been linked with an excessive consumption of animal, as opposed to vegetable, fats. In this connection the important factors seem to be the saturated fatty acids (low-density and very low-density lipoproteins [LDLs and VLDLs] – see CHOLESTEROL) of animal fats which would appear to be more likely to lead to a high level of cholesterol in the blood than the unsaturated fatty acids of vegetable fats. As more research on the subject is carried out, the arguments continue about the relative in?uence of the di?erent factors. (For advice on prevention of the disease, see APPENDIX 2: ADDRESSES: SOURCES OF INFORMATION, ADVICE, SUPPORT AND SELFHELP.)
Symptoms The presenting symptom is the sudden onset, often at rest, of acute, agonising pain in the front of the chest. This rapidly radiates all over the front of the chest and often down over the abdomen. The pain is frequently accompanied by nausea and vomiting, so that suspicion may be aroused of some acute abdominal condition such as biliary colic (see GALLBLADDER, DISEASES OF) or a perforated PEPTIC ULCER. The victim soon goes into SHOCK, with a pale, cold, sweating skin, rapid pulse and dif?culty in breathing. There is usually some rise in temperature.
Treatment is immediate relief of the pain by injections of diamorphine. Thrombolytic drugs should be given as soon as possible (‘rapid door to needle time’) and ARRHYTHMIA corrected. OXYGEN is essential and oral ASPIRIN is valuable. Treatment within the ?rst hour makes a great di?erence to recovery. Subsequent treatment includes the continued administration of drugs to relieve the pain; the administration of ANTIARRHYTHMIC DRUGS that may be necessary to deal with the heart failure that commonly develops, and the irregular action of the heart that quite often develops; and the continued administration of oxygen. Patients are usually admitted to coronary care units, where they receive constant supervision. Such units maintain an emergency, skilled, round-the-clock sta? of doctors and nurses, as well as all the necessary resuscitation facilities that may be required.
The outcome varies considerably. The ?rst (golden) hour is when the patient is at greatest risk of death: if he or she is treated, then there is a 50 per cent reduction in mortality compared with waiting until hospital admission. As each day passes the prognosis improves with a ?rst coronary thrombosis, provided that the patient does not have a high blood pressure and is not overweight. Following recovery, there should be a gradual return to work, care being taken to avoid any increase in weight, unnecessary stress and strain, and to observe moderation in all things. Smoking must stop. In uncomplicated cases patients get up and about as soon as possible, most being in hospital for a week to ten days and back at work in three months or sooner.
Valvular heart disease primarily affects the mitral and aortic valves which can become narrowed (stenosis) or leaking (incompetence). Pulmonary valve problems are usually congenital (stenosis) and the tricuspid valve is sometimes involved when rheumatic heart disease primarily affects the mitral or aortic valves. RHEUMATIC FEVER, usually in childhood, remains a common cause of chronic valvular heart disease causing stenosis, incompetence or both of the aortic and mitral valves, but each valve has other separate causes for malfunction.
Aortic valve disease is more common with increasing age. When the valve is narrowed, the heart hypertrophies and may later fail. Symptoms of angina or breathlessness are common and dizziness or blackouts (syncope) also occur. Replacing the valve is a very e?ective treatment, even with advancing age. Aortic stenosis may be caused by degeneration (senile calci?c), by the inheritance of two valvular leaflets instead of the usual three (bicuspid valve), or by rheumatic fever. Aortic incompetence again leads to hypertrophy, but dilatation is more common as blood leaks back into the ventricle. Breathlessness is the more common complaint. The causes are the same as stenosis but also include in?ammatory conditions such as SYPHILIS or ANKYLOSING SPONDYLITIS and other disorders of connective tissue. The valve may also leak if the aorta dilates, stretching the valve ring as with HYPERTENSION, aortic ANEURYSM and MARFAN’S SYNDROME – an inherited disorder of connective tissue that causes heart defects. Infection (endocarditis) can worsen acutely or chronically destroy the valve and sometimes lead to abnormal outgrowths on the valve (vegetations) which may break free and cause devastating damage such as a stroke or blocked circulation to the bowel or leg.
Mitral valve disease leading to stenosis is rheumatic in origin. Mitral incompetence may be rheumatic but in the absence of stenosis can be due to ISCHAEMIA, INFARCTION, in?ammation, infection and a congenital weakness (prolapse). The valve may also leak if stretched by a dilating ventricle (functional incompetence). Infection (endocarditis) may affect the valve in a similar way to aortic disease. Mitral symptoms are predominantly breathlessness which may lead to wheezing or waking at night breathless and needing to sit up or stand for relief. They are made worse when the heart rhythm changes (atrial ?brillation) which is frequent as the disease becomes more severe. This leads to a loss of e?ciency of up to 25 per cent and a predisposition to clot formation as blood stagnates rather than leaves the heart e?ciently. Mitral incompetence may remain mild and be of no trouble for many years, but infection must be guarded against (endocarditis prophylaxis).
Endocarditis is an infection of the heart which may acutely destroy a valve or may lead to chronic destruction. Bacteria settle usually on a mild lesion. Antibiotics taken at vulnerable times can prevent this (antibiotic prophylaxis) – for example, before tooth extraction. If established, lengthy intravenous antibiotic therapy is needed and surgery is often necessary. The mortality is 30 per cent but may be higher if the infection settles on a replaced valve (prosthetic endocarditis). Complications include heart failure, shock, embolisation (generation of small clots in the blood), and cerebral (mental) confusion.
PERICARDITIS is an in?ammation of the sac covering the outside of the heart. The sac becomes roughened and pain occurs as the heart and sac rub together. This is heard by stethoscope as a scratching noise (pericardial rub). Fever is often present and a virus the main cause. It may also occur with rheumatic fever, kidney failure, TUBERCULOSIS or from an adjacent lung problem such as PNEUMONIA or cancer. The in?ammation may cause ?uid to accumulate between the sac and the heart (e?usion) which may compress the heart causing a fall in blood pressure, a weak pulse and circulatory failure (tamponade). This can be relieved by aspirating the ?uid. The treatment is then directed at the underlying cause.... heart, diseases of
Cramp Painful spasm of a muscle usually caused by excessive and prolonged contraction of the muscle ?bres. Cramps are common, especially among sportsmen and women, normally lasting a short time. The condition usually occurs during or immediately following exercise as a result of a build-up of LACTIC ACID and other chemical by-products in the muscles
– caused by the muscular e?orts. Cramps may occur more frequently, especially at night, in people with poor circulation, when the blood is unable to remove the lactic acid from the muscles quickly enough.
Repetitive movements such as writing (writer’s cramp) or operating a keyboard can cause cramp. Resting muscles may suffer cramp if a person sits or lies in an awkward position which limits local blood supply to them. Profuse sweating as a result of fever or hot weather can also cause cramp in resting muscle, because the victim has lost sodium salts in the sweat; this disturbs the biochemical balance in muscle tissue.
Treatment is to massage and stretch the affected muscle – for example, cramp in the calf muscle may be relieved by pulling the toes on the affected leg towards the knee. Persistent night cramps sometimes respond to treatment with a drug containing CALCIUM or QUININE. If cramp persists for an hour or more, the person should seek medical advice, as there may be a serious cause such as a blood clot impeding the blood supply to the area affected.
Dystrophy See myopathy below.
In?ammation (myositis) of various types may occur. As the result of injury, an ABSCESS may develop, although wounds affecting muscle generally heal well. A growth due to SYPHILIS, known as a gumma, sometimes forms a hard, almost painless swelling in a muscle. Rheumatism is a vague term traditionally used to de?ne intermittent and often migratory discomfort, sti?ness or pain in muscles and joints with no obvious cause. The most common form of myositis is the result of immunological damage as a result of autoimmune disease. Because it affects many muscles it is called POLYMYOSITIS.
Myasthenia (see MYASTHENIA GRAVIS) is muscle weakness due to a defect of neuromuscular conduction.
Myopathy is a term applied to an acquired or developmental defect in certain muscles. It is not a neurological disease, and should be distinguished from neuropathic conditions (see NEUROPATHY) such as MOTOR NEURONE DISEASE (MND), which tend to affect the distal limb muscles. The main subdivisions are genetically determined, congenital, metabolic, drug-induced, and myopathy (often in?ammatory) secondary to a distant carcinoma. Progressive muscular dystrophy is characterised by symmetrical wasting and weakness, the muscle ?bres being largely replaced by fatty and ?brous tissue, with no sensory loss. Inheritance may take several forms, thus affecting the sex and age of victims.
The commonest type is DUCHENNE MUSCULAR DYSTROPHY, which is inherited as a sex-linked disorder. It nearly always occurs in boys.
Symptoms There are three chief types of myopathy. The commonest, known as pseudohypertrophic muscular dystrophy, affects particularly the upper part of the lower limbs of children. The muscles of the buttocks, thighs and calves seem excessively well developed, but nevertheless the child is clumsy, weak on his legs, and has di?culty in picking himself up when he falls. In another form of the disease, which begins a little later, as a rule at about the age of 14, the muscles of the upper arm are ?rst affected, and those of the spine and lower limbs become weak later on. In a third type, which begins at about this age, the muscles of the face, along with certain of the shoulder and upper arm muscles, show the ?rst signs of wasting. All the forms have this in common: that the affected muscles grow weaker until their power to contract is quite lost. In the ?rst form, the patients seldom reach the age of 20, falling victims to some disease which, to ordinary people, would not be serious. In the other forms the wasting, after progressing to a certain extent, often remains stationary for the rest of life. Myopathy may also be acquired when it is the result of disease such as thyrotoxicosis (see under THYROID GLAND, DISEASES OF), osteomalacia (see under BONE, DISORDERS OF) and CUSHING’S DISEASE, and the myopathy resolves when the primary disease is treated.
Treatment Some myopathies may be the result of in?ammation or arise from an endocrine or metabolic abnormality. Treatment of these is the treatment of the cause, with supportive physiotherapy and any necessary physical aids while the patient is recovering. Treatment for the hereditary myopathies is supportive since, at present, there is no cure – although developments in gene research raise the possibility of future treatment. Physiotherapy, physical aids, counselling and support groups may all be helpful in caring for these patients.
The education and management of these children raise many diffculties. Much help in dealing with these problems can be obtained from Muscular Dystrophy Campaign.
Myositis ossi?cans, or deposition of bone in muscles, may be congenital or acquired. The congenital form, which is rare, ?rst manifests itself as painful swellings in the muscles. These gradually harden and extend until the child is encased in a rigid sheet. There is no e?ective treatment and the outcome is fatal.
The acquired form is a result of a direct blow on muscle, most commonly on the front of the thigh. The condition should be suspected whenever there is severe pain and swelling following a direct blow over muscle. The diagnosis is con?rmed by hardening of the swelling. Treatment consists of short-wave DIATHERMY with gentle active movements. Recovery is usually complete.
Pain, quite apart from any in?ammation or injury, may be experienced on exertion. This type of pain, known as MYALGIA, tends to occur in un?t individuals and is relieved by rest and physiotherapy.
Parasites sometimes lodge in the muscles, the most common being Trichinella spiralis, producing the disease known as TRICHINOSIS (trichiniasis).
Rupture of a muscle may occur, without any external wound, as the result of a spasmodic e?ort. It may tear the muscle right across – as sometimes happens to the feeble plantaris muscle in running and leaping – or part of the muscle may be driven through its ?brous envelope, forming a HERNIA of the muscle. The severe pain experienced in many cases of LUMBAGO is due to tearing of one of the muscles in the back. These conditions are usually relieved by rest and massage. Partial muscle tears, such as occur in sport, require more energetic treatment: in the early stages this consists of the application of an ice or cold-water pack, ?rm compression, elevation of the affected limb, rest for a day or so and then gradual mobilisation (see SPORTS MEDICINE).
Tumours occur occasionally, the most common being ?broid, fatty, and sarcomatous growths.
Wasting of muscles sometimes occurs as a symptom of disease in other organs: for example, damage to the nervous system, as in poliomyelitis or in the disease known as progressive muscular atrophy. (See PARALYSIS.)... muscles, disorders of
The so-called ultra-short-wave diathermy (or short-wave diathermy, as it is usually referred to) has replaced the original long-wave diathermy, as it is produced consistently at a stable wave-length (11 metres) and is easier to apply. In recent years microwave diathermy has been developed, which has a still higher oscillating current (25,000 million cycles per second, compared with 500 million for short-wave diathermy).
When the current passes, a distinct sensation of increasing warmth is experienced and the temperature of the body gradually rises; the heart’s action becomes quicker; there is sweating with increased excretion of waste products. The general blood pressure is also distinctly lowered. The method is used in painful rheumatic conditions, both of muscles and joints.
By concentrating the current in a small electrode, the heating effects immediately below this are very much increased. The diathermy knife utilises this technique to coagulate bleeding vessels and cauterise abnormal tissue during surgery.... diathermy
Internal: White Willow bark, Red Sage.
External: Essential oils of Sage, Pine, Rosemary, Lavender. Blended with fresh lemon juice are marketed as a gentle spray without aerosol (Weleda). Zinc and Castor oil cream or ointment.
Bath preparations made from these oils; herbal soaps, massage oils. ... anti-perspirants
HYPERGLYCAEMIA. See: DIABETES. To reduce sugar in blood – Guar gum. HYPERHIDROSIS. Excessive sweating. See: PERSPIRATION. ... hypergalactia
Pseudoacanthosis nigricans is a much more common condition, usually seen in dark-complexioned people who are overweight. In this form, the skin in fold areas is both thicker and darker than the surrounding skin, and there is usually excessive sweating in affected areas. The condition may improve with weight loss.... acanthosis nigricans
In high doses, amfetamines can cause tremor, sweating, anxiety, and sleeping problems. Delusions, hallucinations, high blood pressure, and seizures may also occur. Prolonged use may produce tolerance and drug dependence.
Amfetamines are often abused for their stimulant effect.... amfetamine drugs
Without food and drink the body rapidly becomes thinner and lighter as it draws upon its stored energy reserves, initially mainly fat. Body temperature gradually falls, and muscle is progressively broken down as the body struggles to maintain its vital functions. Dehydration, leading to cardiovascular collapse, inevitably follows unless a basic amount of water is taken – particularly if the body’s ?uid output is high, such as may occur with excessive sweating.
After prolonged fasting the return to food should be gradual, with careful monitoring of blood-pressure levels and concentrations of serum ELECTROLYTES. Feeding should consist mainly of liquids and light foods at ?rst, with no heavy meals being taken for several days.... fasting
Severe poisoning from ingestion of fungi is very rare, since relatively few species are highly toxic and most species do not contain toxic compounds. The most toxic species are those containing amatoxins such as death cap (Amanita phalloides); this species alone is responsible for about 90 per cent of all mushroom-related deaths. There is a latent period of six hours or more between ingestion and the onset of clinical effects with these more toxic species. The small intestine, LIVER and KIDNEYS may be damaged – therefore, any patient with gastrointestinal effects thought to be due to ingestion of a mushroom should be referred immediately to hospital where GASTRIC LAVAGE and treatment with activated charcoal can be carried out, along with parenteral ?uids and haemodialysis if the victim is severely ill. In most cases where effects occur, these are early-onset gastrointestinal effects due to ingestion of mushrooms containing gastrointestinal irritants.
Muscarine is the poisonous constituent of some species. Within two hours of ingestion, the victim starts salivating and sweating, has visual disturbances, vomiting, stomach cramps, diarrhoea, vertigo, confusion, hallucinations and coma, the severity of symptoms depending on the amount eaten and type of mushroom. Most people recover in 24 hours, with treatment.
‘Magic’ mushrooms are a variety that contains psilocybin, a hallucinogenic substance. Children who take such mushrooms may develop a high fever and need medical care. In adults the symptoms usually disappear within six hours.
Treatment If possible, early gastric lavage should be carried out in all cases of suspected poisoning. Identi?cation of the mushroom species is a valuable guide to treatment. For muscarine poisoning, ATROPINE is a speci?c antidote. As stated above, hospital referral is advisable for people who have ingested poisonous fungi.... fungus poisoning
The operation is sometimes still done if the patient has failed to respond to dietary treatment and treatment with H2-blocking drugs (see CIMETIDINE; RANITIDINE) along with antibiotics to combat Helicobacter pylori, an important contributary factor to ulcer development. Partial gastrectomy is usually accompanied by VAGOTOMY, which involves cutting the VAGUS nerve controlling acid secretion in the stomach. Among the side-effects of gastrectomy are fullness and discomfort after meals; formation of ulcers at the new junction between the stomach and duodenum which may lead to GASTRITIS and oesophagitis (see OESOPHAGUS, DISEASES OF); dumping syndrome (nausea, sweating and dizziness because the food leaves the stomach too quickly after eating); vomiting and diarrhoea. The side-effects usually subside but may need dietary and drug treatment.... gastrectomy
Homeostasis regulates conditions such as temperature and acidity by negative feedback.
For example, when the body overheats, sweating is stimulated until the temperature returns to normal.
Homeostasis also involves the regulation of blood pressure and blood glucose levels.... homeostasis
Heat collapse is characterised by fatigue, giddiness, and temporary loss of consciousness. It is accompanied by HYPOTENSION and BRADYCARDIA; there may also be vomiting and muscular cramps. Urinary volume is diminished. Recovery is usual.
Heat exhaustion is characterised by increasing weakness, dizziness and insomnia. In the majority of sufferers, sweating is defective; there are few, if any, signs of dehydration. Pulse rate is normal, and urinary output good. Body temperature is usually 37·8–38·3 °C.
Heat cramps (usually in the legs, arms or back, and occasionally involving the abdominal muscles) are associated with hard physical work at a high temperature. Sweating, pallor, headache, giddiness and intense anxiety are present. Body temperature is only mildly raised.
Heat hyperpyrexia is heralded by energy loss and irritability; this is followed by mental confusion and diminution of sweating. The individual rapidly becomes restless, then comatose; body temperature rises to 41–42 °C or even higher. The condition is fatal unless expertly treated as a matter of urgency.
Treatment With the ?rst two syndromes, the affected individual must be removed immediately to a cool place, and isotonic saline administered – intravenously in a severe case. The fourth syndrome is a medical emergency. The patient should be placed in the shade, stripped, and drenched with water; fanning should be instigated. He or she should be wrapped in a sheet soaked in cool water and fanning continued. When rectal temperature has fallen to 39 °C, the patient is wrapped in a dry blanket. Immediately after consciousness returns, normal saline should be given orally; this usually provokes sweating. The risk of circulatory collapse exists. Convalescence may be protracted and the patient should be repatriated to a cool climate. Prophylactically, personnel intended for work in a tropical climate must be very carefully selected. Adequate acclimatisation is also essential; severe physical exertion must be avoided for several weeks, and light clothes should be worn. The diet should be light but nourishing, and ?uid intake adequate. Those performing hard physical work at a very high ambient temperature should receive sodium chloride supplements. Attention to ventilation and air-conditioning is essential; fans are also of value.... heat stroke
If you’re looking for a special herbal tea, you can try pipsissewa tea. It has a pleasant taste, slightly bitter, like most herbal teas, but also a bit sweet. Also, it comes with many health benefits. Read to find out more!
About Pipsissewa Tea
Pipsissewa tea is made from the pipsissewa plant, also known as Umbellate Wintergreen or Prince’s pine. It is a small, evergreen perennial plant, usually found in the dry woodlands or sandy soils of Southern Canada and northern United States.
The plant can grow up to 30cm tall. It usually has 4 evergreen, shiny leaves with a toothed margin; they’re arranged one opposite the other on the stem. It has 4-8 flowers, either pink or white, which bloom during summer.
The pipsissewa plant is used to make root beer. It can also be used to flavor candies and soft drinks.
How to prepare Pipsissewa Tea
You only need a few minutes to prepare a cup of pipsissewa tea. Put a tablespoon of herbs in the cup, then pour freshly boiled water over it. Let it steep for 2-4 minutes; then, strain the drink. Sweeten it with milk or honey, if you wish.
Pipsissewa Tea Benefits
Pipsisewa, as a plant, contains many important constituents which are also transferred to the pipsissewa tea. Some of them are hydroquinones (for example, arbutin), flavonoids, triterpenes, methyl salicylate, phenols, essential oils, and tannins. They have many health benefits.
Pipsissewa teais often recommended in the treatment for infections of the urinary tract, such as cystitis, painful urination, bladder and kidney stones, kidney inflammation, prostatitis, gonorrhea, and urethritis. It can also be used to treat arthritis, gout and rheumatism.
Drinking pipsissewa tea will help your body expel various infectious microorganisms. It can increase sweating in order to treat fever diseases. It is also often included in the treatment for ailments of the respiratory tract, such as colds, whooping cough, and bronchitis.
Pipsissewa tea can be used topically, as well. It can be used with blisters, tumors, and swellings. Also, you can use it as an eye wash if you’ve got sore eyes.
Pipsissewa Tea Side Effects
It is not well-known if pipsissewa tea can affect women during pregnancy or breast feeding. However, it’s considered safe not to drink it, just in case it might affect the baby.
It is best not to drink pipsissewa tea if you’re taking medication for the intestine, or if you’ve got iron deficiency.
Drinking a large amount of pipsissewa tea can also lead to a few side effects. The symptoms you might get are: diarrhea, nausea, vomiting, headaches, and loss of appetite.
You’ll definitely enjoy drinking pipsissewa tea, both for its pleasant taste and because of the health benefits it has.
... have a cup of pipsissewa teaTreatment of acute hypoglycaemia depends upon the severity of the condition. Oral carbohydrate, such as a sugary drink or chocolate, may be e?ective if the patient is conscious enough to swallow; if not, glucose or GLUCAGON by injection will be required. Comatose patients who recover after an injection should then be given oral carbohydrates. An occasional but dangerous complication of coma is cerebral oedema (see BRAIN, DISEASES OF – Cerebral oedema), and this should be considered if coma persists. Emergency treatment in hospital is then needed. When the patient has recovered, management of his or her diabetes should be assessed in order to prevent further hypoglycaemic attacks.... hypoglycaemic coma
Hypohidrosis is a feature of hypohidrotic ectodermal dysplasia, a rare, inherited, incurable condition that is characterized by reduced sweating and is accompanied by dry, wrinkled skin, sparse hair, small, brittle nails, and conical teeth.
Other causes of hypohidrosis include exfoliative dermatitis and some anticholinergic drugs.... hypohidrosis
Habitat: Native to Europe and temperate Asia. Occurs in West Himalyas from Kashmir to Kumaon.
English: Hyssop.Ayurvedic: Dayaa-kunji. (Nepeta longibractea is also equated with Zuufaa, Dayaa-kunji.)Unani: Zuufaa, Zuufaa Yaabis.Folk: Diyaanku (Laddakh).Action: Stimulant, carminative, sedative, antispasmodic, diuretic, pectoral. Used for bronchitis, coughs and colds. Induces heavy sweating in fevers, increases blood pressure. Emmenagogue. Used externally for bruises, discoloured contusions and cuts.
Key application: As expectorant. (The British Herbal Pharmacopoeia.)Hyssop contains terpenoids, including marrubiin; a volatile oil consisting mainly of camphor, pinocamphone and beta-pinene; flavonoids, gluco- sides, tannins and resin. Marrubiin is a strong expectorant. The plant also contains ursolic acid, an anti- inflammatory principle. The alcoholic extract of the aerial parts at flowering yields an active antioxidant compound, rosmanol-9-ethyl ether. Its activity is much greater than butylat- ed hydroxytoluene. The extract of the plant showed weak hepatoprotective activity against CCl4-induced toxicity in albino mice.Pinocamphone and isopinocam- phone are toxic constituents of the essential oil. Wild plants from Ku- maon (Uttaranchal) shows presence of very small amounts of pinocam- phone (0.61%) in essential oil, as compared to Himalayan hyssop (38.44%) and cultivated North American hyssop (42.66%). The essential oil can induce epileptic seizures.... hyssopus officinalisAn excessive accumulation of monoamines can induce a dangerous reaction characterised by high blood pressure, palpitations, sweating and a feeling of su?ocation. Hence the care with which MAOI drugs are administered. What is equally important, however, is that in no circumstances should a patient receiving any MAOI drug eat cheese, yeast preparations such as Marmite, tinned ?sh, or high game. The reason for this ban is that all these foodstu?s contain large amounts of tyramine which increases the amount of certain monoamines such as noradrenaline in the body. (See MENTAL ILLNESS.)
There are also certain drugs, such as AMPHETAMINES and PETHIDINE HYDROCHLORIDE, which must not be taken by a patient who is receiving an MAOI drug. The MAOIs of choice are phenelzine or isocarboxazid because their stimulant effects are less than those of other MAOIs, making them safer.... monoamine oxidase inhibitors (maois)
Anxiety neurosis, or anxiety state, constitutes the most common form of neurosis; fortunately it is also among the most responsive to treatment. Once the neurosis develops, sufferers are in a state of persistent anxiety and worry, ‘tensed up’, always fatigued and unable to sleep at night. In addition, there are often physical complaints – for example, palpitations, sweating, apparent discomfort on swallowing (‘globus’), and headache.
Obsessional neuroses are much less common and constitute only about 5 per cent of all neuroses. Like other neuroses, they usually develop in early adult life. (See MENTAL ILLNESS.)... neurosis
Stinging capsules discharge when jellyfish tentacles are touched.
Usually, the sting causes only a mildly painful or itchy rash, but some jellyfish and Portuguese men-of-war (other members of the same group) can cause a severe sting.
Rarely, venom may cause vomiting, sweating, breathing difficulties, and collapse.
Dangerous species live mainly in tropical waters.
Antivenoms may be available.... jellyfish stings
Motion sickness is caused by the effect of repetitive movement on the organ of balance in the inner ear. Factors such as anxiety, a fume-laden atmosphere, or the sight of food may make the condition worse. So, too, can focusing on nearby objects; sufferers should look at a point on the horizon.
Motion sickness may be prevented or controlled by antiemetic drugs or by acupressure bands worn on the wrist.... motion sickness
Possible adverse effects of neostigmine include nausea and vomiting, increased salivation, abdominal cramps, diarrhoea, blurred vision, muscle cramps, sweating, and twitching.... neostigmine
The nervous system can be likened to a computer. The central processing unit – which receives, processes and stores information and initiates instructions for bodily activities – is called the central nervous system: this is made up of the brain and SPINAL CORD. The peripheral nervous system – synonymous with the cables that transmit information to and from a computer’s processing unit – has two parts: sensory and motor. The former collects information from the body’s many sense organs. These respond to touch, temperature, pain, position, smells, sounds and visual images and the information is signalled to the brain via the sensory nerves. When information has been processed centrally, the brain and spinal cord send instructions for action via motor nerves to the ‘voluntary’ muscles controlling movements and speech, to the ‘involuntary’ muscles that operate the internal organs such as the heart and intestines, and to the various glands, including the sweat glands in the skin. (Details of the 12 pairs of cranial nerves and the 31 pairs of nerves emanating from the spinal cord are given in respective texts on brain and spinal cord.)
Functional divisions of nervous system As well as the nervous system’s anatomical divisions, the system is divided functionally, into autonomic and somatic parts. The autonomic nervous system, which is split into sympathetic and parasympathetic divisions, deals with the automatic or unconscious control of internal bodily activities such as heartbeat, muscular status of blood vessels, digestion and glandular functions. The somatic system is responsible for the skeletal (voluntary) muscles (see MUSCLE) which carry out intended movements initiated by the brain – for example, the activation of limbs, tongue, vocal cords (speech), anal muscles (defaecation), urethral sphincters (urination) or vaginal muscles (childbirth). In addition, many survival responses – the most powerfully instinctive animal drives, which range from avoiding danger and pain to shivering when cold or sweating when hot – are initiated unconsciously and automatically by the nervous system using the appropriate neural pathways to achieve the particular survival reaction required.
The complex functions of the nervous system include the ability to experience emotions, such as excitement and pleasure, anxiety and frustration, and to undertake intellectual activities. For these experiences an individual can utilise many built-in neurological programmes and he or she can enhance performance through learning – a vital human function that depends on MEMORY, a three stage-process in the brain of registration, storage and recall. The various anatomical and functional divisions of the nervous system that have been unravelled as science has strived to explain how it works may seem confusing. In practical terms, the nervous system works mainly by using automatic or relex reactions (see REFLEX ACTION) to various stimuli (described above), supplemented by voluntary actions triggered by the activity of the conscious (higher) areas of the brain. Some higher functions crucial to human activity – for example, visual perception, thought, memory and speech – are complex and subtle, and the mechanisms are not yet fully understood. But all these complex activities rest on the foundation of relatively simple electrochemical transmissions of impulses through the massive network of billions of specialised cells, the neurones.... nervous system
Side effects include insomnia, sweating, and dizziness on standing.... reboxetine
There may also be nausea, vomiting, sweating, and blood in the urine.
Treatment is usually with bed rest, plenty of fluids, and injections of an analgesic drug, such as pethidine.... renal colic
Overdose causes hyperventilation, tinnitus, sweating, abnormal bleeding, biochemical disturbances, and, in severe cases, convulsions and coma.... salicylate drugs
Many species are not dangerous, but some in North Africa, southern , South America, the Caribbean, and India are highly venomous.
Some stings may cause only mild pain and tingling; but in more venomous species severe pain, restlessness, sweating, diarrhoea, and vomiting can occur.
Stings are rarely fatal in adults but require prompt attention.
If pain is the only symptom, analgesics and a cold compress may be enough.
In severe cases, antivenom may be needed.... scorpion stings
Thirst is stimulated by an increased concentration of salt, sugar, or certain other substances in the blood. As the blood passes through the hypothalamus in the brain, special nerve receptors are stimulated, inducing the sensation of thirst. Thirst is also stimulated if blood volume decreases as a result of sweating, vomiting, diarrhoea, severe bleeding, or extensive burns. Thirst may also be caused by a dry mouth.... thirst
Shock may result from loss of blood or plasma volume. This may occur as a result of haemorrhage or severe diarrhoea and vomiting. It may also result from peripheral pooling of blood due to such causes as TOXAEMIA or ANAPHYLAXIS. The toxaemia is commonly the result of a SEPTICAEMIA in which leakage through capillaries reduces circulating blood volume. Another form is called cardogenic shock, and is due to failure of the heart as a pump. It is most commonly seen as a result of myocardial infarction (see under HEART, DISEASES OF).
If failure of adequate blood ?ow to vital organs is prolonged, the effects can be disastrous. The ischaemic intestine permits the transfer of toxic bacterial products and proteins across its wall into the blood; renal ISCHAEMIA prevents the maintenance of a normal electrolyte and acid-base balance.
Treatment If the shock is a result of haemorrhage or diarrhoea or vomiting, replacement of blood, lost ?uid and electrolytes is of prime importance. If it is due to septicaemia, treatment of the infection is of paramount importance, and in addition, intravenous ?uids and vasopressor drugs will be required. Cardiogenic shock is treated by attention to the underlying cause. Full intensive care is likely to be required, and arti?cial ventilation and DIALYSIS may both be needed.... shock
Habitat: Kashmir, Himachal Pradesh and Garhwal at 25003,000 m; cultivated in Kashmir and neighbouring regions.
English: Kuth, Costus.Ayurvedic: Kushtha, Kusht, Vaapya, Kaashmira, Gada, Rug, Ruk, Aamaya, Paalaka. (Substitute: Pushkara Muula, Inula racemosa.)Unani: Qust.Siddha/Tamil: Kostum, Kottam.Folk: Sugandha-Kuutth.Action: Root—antispasmodic, expectorant, carminative, astringent, antiseptic. An ingredient of prescriptions for dyspepsia, asthma, cough, chronic rheumatism, skin diseases. Applied locally to wounds and ulcerations. Powdered root, mixed with mustard oil, is applied to scalp in prurigo.
The Ayurvedic Pharmacopoeia of India recommends the root in cough, bronchitis, dyspnoea; erysipelas and gout.The root (containing both the essential oil and alkaloid, saussurine) is used for asthma, particularly of vagotonic type. It produces a definite relaxtion of the bronchioles. The relief obtained is comparable to that of conventional bronchodilators without side effects, like a rise in blood pressure, sweating or headache even on repeated administration.Saussurine depresses parasympa- thetic nervous system. The aminoacid- sesquiterpene adducts, saussureami- nes A, B and C show antiulcer effect. The aqueous extract of the root exhibits antianginal activity.Essential oil inhibits peristalic movement of the gut. It is absorbed from the gastro-intestinal tract and partly excreted by lungs producing an expectorant action and partly by the kidneys producing diuretic effect. (In Western herbal, Kuth essential oil is not prescribed internally.)Kuth roots contain resinoids (6%), and essential oil (1.5%), alkaloid (0.05%) inulin (18%), saussurea lactone (20-25%), a fixed oil and minor constituents like tannin and sugars. Roots obtained from Kashmir are, in general, richer in essential oil content than roots obtained from Garhwal and Nepal. The roots of Punjab variety gave cos- tunolide, dehydrocostuslactone, costic acid, palmitic and linoleic acids, beta- sitosterol and alpha-cyclocostunolide. The Kashmir variety, in addition, gave alantolactone, beta-cyclocostunolide and iso-alantolactone.The essential oil of the roots exhibit strong antiseptic and disinfectant activity against Streptococcus and Staphy- lococcus.Costus speciosus Sm. synonym Banksea speciosa, also known as Kush- tha, is a different herb of Zingiberaceae family. Rhizomes and stems yield dios- genin.Dosage: Root—0.2-1.0 g powder. (API, Vol. I.)... saussurea lappaSyncope can also result when the venous return to the heart is impaired as a result of a rise in intrathoracic pressure. This may happen after prolonged vigorous coughing – the so-called COUGH SYNCOPE – or when elderly men with prostatic hypertrophy strain to empty their bladder. This is known as micturition syncope. Syncope is particularly likely to occur when the arterial blood pressure is unusually low. This may result from overtreatment of HYPERTENSION with drugs or it may be the result of diseases, such as ADDISON’S DISEASE, which are associated with low blood pressures. It is important that syncope be distinguished from EPILEPSY.... syncope
Habitat: Waste places and on roadsides, particularly near buildings.
Features ? The tough, wiry, quadrangular, many-branched stem averages eighteeninches high. Roughish, pinnately-lobed, serrate leaves grow distantly and opposite in pairs ; the upper ones clasp the stem. while the lower ones are stalked. Small, light lilac-coloured flowers bloom in May, along thin, wiry spikes. Very bitter in taste, a slightly aromatic odour is given off when rubbed.Action: Nervine, tonic, emetic and sudorific.
The herb was held in high repute by those who brought the Thomsonian system to this country. Coffin, writing ninety years ago, says ? "As an emetic it ranks next to lobelia ; it is also one of the strongest sweating medicines in nature. It is good for colds, coughs and pain in the head, and some years ago was highly esteemed as a remedy for consumption. As an emetic it supersedes the use of antimony and ipecacuanha, to both of which it is superior, since it not only produces all the good effects ascribed to the others, but it operates without any of the dangerous consequences that ever attend the use of antimonial preparations, and cramps, and even death have been known to follow their use. . . . Vervain will relieve and cure those complaints in children which generally accompany teething; it likewise destroys worms. Administered as a tea, it powerfully assists the pains of labour ; as a diuretic it increases the urinary discharge."The ounce to pint infusion is now used, and taken in wineglass doses. As a nervine, Scullcap and Valerian are usually added.... vervainIn its course from the base of the skull to the lumbar region, the cord gives o? 31 nerves on each side, each of which arises by an anterior and a posterior root that join before the nerve emerges from the spinal canal. The openings for the nerves formed by notches on the ring of each vertebra have been mentioned under the entry for spinal column. To reach these openings, the upper nerves pass almost directly outwards, whilst lower down their obliquity increases, until below the point where the cord ends there is a sheaf of nerves, known as the cauda equina, running downwards to leave the spinal canal at their appropriate openings.
The cord is a cylinder, about the thickness of the little ?nger. It has two slightly enlarged portions, one in the lower part of the neck, the other at the last dorsal vertebra; and from these thickenings arise the nerves that pass to the upper and lower limbs. The upper four cervical nerves unite to produce the cervical plexus. From this the muscles and skin of the neck are mainly supplied, and the phrenic nerve, which runs down through the lower part of the neck and the chest to innervate the diaphragm, is given o?. The brachial plexus is formed by the union of the lower four cervical and ?rst dorsal nerves. In addition to nerves to some of the muscles in the shoulder region, and others to the skin about the shoulder and inner side of the arm, the plexus gives o? large nerves that proceed down the arm.
The thoracic or dorsal nerves, with the exception of the ?rst, do not form a plexus, but each runs around the chest along the lower margin of the rib to which it corresponds, whilst the lower six extend on to the abdomen.
The lumbar plexus is formed by the upper four lumbar nerves, and its branches are distributed to the lower part of the abdomen, and front and inner side of the thigh.
The sacral plexus is formed by parts of the fourth and ?fth lumbar nerves, and the upper three and part of the fourth sacral nerves. Much of the plexus is collected into the sciatic nerves, the largest in the body, which go to the legs.
The sympathetic system is joined by a pair of small branches given o? from each spinal nerve, close to the spine. This system consists of two parts, ?rst, a pair of cords running down on the side and front of the spine, and containing on each side three ganglia in the neck, and beneath this a ganglion opposite each vertebra. From these two ganglionated cords numerous branches are given o?, and these unite to form the second part – namely, plexuses connected with various internal organs, and provided with numerous large and irregularly placed ganglia. The chief of these plexuses are the cardiac plexus, the solar or epigastric plexus, the diaphragmatic, suprarenal, renal, spermatic, or ovarian, aortic, hypogastric and pelvic plexuses.
The spinal cord, like the brain, is surrounded by three membranes: the dura mater, arachnoid mater, and pia mater, from without inwards. The arrangement of the dura and arachnoid is much looser in the case of the cord than their application to the brain. The dura especially forms a wide tube which is separated from the cord by ?uid and from the vertebral canal by blood vessels and fat, this arrangement protecting the cord from pressure in any ordinary movements of the spine.
In section the spinal cord consists partly of grey, but mainly of white, matter. It di?ers from the upper parts of the brain in that the white matter (largely) in the cord is arranged on the surface, surrounding a mass of grey matter (largely neurons – see NEURON(E)), while in the brain the grey matter is super?cial. The arrangement of grey matter, as seen in a section across the cord, resembles the letter H. Each half of the cord possesses an anterior and a posterior horn, the masses of the two sides being joined by a wide posterior grey commissure. In the middle of this commissure lies the central canal of the cord, a small tube which is the continuation of the ventricles in the brain. The horns of grey matter reach almost to the surface of the cord, and from their ends arise the roots of the nerves that leave the cord. The white matter is divided almost completely into two halves by a posterior septum and anterior ?ssure and is further split into anterior, lateral and posterior columns.
Functions The cord is, in part, a receiver and originator of nerve impulses, and in part a conductor of such impulses along ?bres which pass through it to and from the brain. The cord contains centres able to receive sensory impressions and initiate motor instructions. These control blood-vessel diameters, eye-pupil size, sweating and breathing. The brain exerts an overall controlling in?uence and, before any incoming sensation can affect consciousness, it is usually ‘?ltered’ through the brain.
Many of these centres act autonomously. Other cells of the cord are capable of originating movements in response to impulses brought direct to them through sensory nerves, such activity being known as REFLEX ACTION. (For a fuller description of the activities of the spinal cord, see NEURON(E) – Re?ex action.)
The posterior column of the cord consists of the fasciculus gracilis and the fasciculus cuneatus, both conveying sensory impressions upwards. The lateral column contains the ventral and the dorsal spino-cerebellar tracts passing to the cerebellum, the crossed pyramidal tract of motor ?bres carrying outgoing impulses downwards together with the rubro-spinal, the spino-thalamic, the spino-tectal, and the postero-lateral tracts. And, ?nally, the anterior column contains the direct pyramidal tract of motor ?bres and an anterior mixed zone. The pyramidal tracts have the best-known course. Starting from cells near the central sulcus on the brain, the motor nerve-?bres run down through the internal capsule, pons, and medulla, in the lower part of which many of those coming from the right side of the brain cross to the left side of the spinal cord, and vice versa. Thence the ?bres run down in the crossed pyramidal tract to end beside nerve-cells in the anterior horn of the cord. From these nerve-cells other ?bres pass outwards to form the nerves that go direct to the muscles. Thus the motor nerve path from brain to muscle is divided into two sections of neurons, of which the upper exerts a controlling in?uence upon the lower, while the lower is concerned in maintaining the muscle in a state of health and good nutrition, and in directly calling it into action. (See also NERVE; NERVOUS SYSTEM.)... spinal cord