The medical term for vomiting blood.
Causes It is likely that there is some abrasion, or break, in the lining membrane (or mucosa) of the stomach and/or duodenum, and that it is gradually eroded and deepened by the acidic gastric juice. The bacterium helicobacter pylori is present in the antrum of the stomach of people with peptic ulcers; 15 per cent of people infected with the bacterium develop an ulcer, and the ulcers heal if H. pylori is eradicated. Thus, this organism has an important role in creating ulcers. Mental stress may possibly be a provocative factor. Smoking seems to accentuate, if not cause, duodenal ulcer, and the drinking of alcohol is probably harmful. The apparent association with a given blood group, and the fact that relatives of a patient with a peptic ulcer are unduly likely to develop such an ulcer, suggest that there is some constitutional factor.
Symptoms and signs Peptic ulcers may present in di?erent ways, but chronic, episodic pain lasting several months or years is most common. Occasionally, however, there may be an acute episode of bleeding or perforation, or obstruction of the gastric outlet, with little previous history. Most commonly there is pain of varying intensity in the middle or upper right part of the abdomen. It tends to occur 2–3 hours after a meal, most commonly at night, and is relieved by some food such as a glass of milk; untreated it may last up to an hour. Vomiting is unusual, but there is often tenderness and sti?ness (‘guarding’) of the abdominal muscles. Con?rmation of the diagnosis is made by radiological examination (‘barium meal’), the ulcer appearing as a niche on the ?lm, or by looking at the ulcer directly with an endoscope (see FIBREOPTIC ENDOSCOPY). Chief complications are perforation of the ulcer, leading to the vomiting of blood, or HAEMATEMESIS; or less severe bleeding from the ulcer, the blood passing down the gut, resulting in dark, tarry stools (see MELAENA).
Treatment of a perforation involves initial management of any complications, such as shock, haemorrhage, perforation, or gastric outlet obstruction, usually involving surgery and blood replacement. Medical treatment of a chronic ulcer should include regular meals, and the avoidance of fatty foods, strong tea or co?ee and alcohol. Patients should also stop smoking and try to reduce the stress in their lives. ANTACIDS may provide symptomatic relief. However, the mainstay of treatment involves four- to six-week courses with drugs such as CIMETIDINE and RANITIDINE. These are H2 RECEPTOR ANTAGONISTS which heal peptic ulcers by reducing gastric-acid output. Of those relapsing after stopping this treatment, 60–95 per cent have infection with H. pylori. A combination of BISMUTH chelate, amoxycillin (see PENICILLIN; ANTIBIOTICS) and METRONIDAZOLE – ‘triple regime’ – should eliminate the infection: most physicians advise the triple regime as ?rst-choice treatment because it is more likely to eradicate Helicobacter and this, in turn, enhances healing of the ulcer or prevents recurrence. Surgery may be necessary if medical measures fail, but its use is much rarer than before e?ective medical treatments were developed.... duodenal ulcer
Bleeding into or around the brain is a major concern following serious head injuries, or in newborn infants following a di?cult labour. Haemorrhage is classi?ed as arterial – the most serious type, in which the blood is bright red and appears in spurts (in severe cases the patient may bleed to death within a few minutes); venous – less serious (unless from torn varicose veins) and easily checked, in which the blood is dark and wells up gradually into the wound; and capillary, in which the blood slowly oozes out of the surface of the wound and soon stops spontaneously. Haemorrhage is also classi?ed as primary, reactionary, and secondary (see WOUNDS). Severe haemorrhage causes SHOCK and ANAEMIA, and blood TRANSFUSION is often required.
When a small artery is cut across, the bleeding stops in consequence of changes in the wall of the artery on the one hand, and in the constitution of the blood on the other. Every artery is surrounded by a ?brous sheath, and when cut, the vessel retracts some little distance within this sheath and a blood clot forms, blocking the open end (see COAGULATION). When a major blood vessel is torn, such spontaneous closure may be impossible and surgery is required to stop the bleeding.
Three main principles are applicable in the control of a severe external haemorrhage: (a) direct pressure on the bleeding point or points;
(b) elevation of the wounded part; (c) pressure on the main artery of supply to the part.
Control of internal haemorrhage is more dif?cult than that of external bleeding. First-aid measures should be taken while professional help is sought. The patient should be laid down with legs raised, and he or she should be reassured and kept warm. The mouth may be kept moist but no ?uids should be given. (See APPENDIX 1: BASIC FIRST AID.)... haemorrhage
Habitat: West Bengal, Madhya Pradesh, Maharashtra, Orissa, Andhra Pradesh, Western Ghats.
English: Utrasum Bead tree.Ayurvedic: Rudraaksha, Panch- mukhi.Siddha/Tamil: Rudraaksham.Action: Fruit—used for epileptic fits and headache. Powdered fruits (0.5 g) mixed with warm water are given two/three times daily in asthma. Stem bark— hypoglycaemic.
The Ayurvedic Pharmacopoeia of India indicated the use of the seed in hypertension, insomnia, psychoneurosis and mental diseases.The fruits contain palmitic, iso- palmitic, linoleic and myristic acids. Leaves gave alkaloids—rudrakine, (+)- elacocarpine and (+)-iso-elacocarpine; phenolics—quercetin, gallic acid and ellagic acid. EtOH (50%) extract of stem bark—hypoglycaemic. Aqueous extract of fruits—sedative, hy- potensive, spasmolytic, anticonvul- sant, choleretic, bronchodilatory and cardiostimulant.The fruit of E. oblongus Mast. non- Gaertn., synonym E. glandulosus Wall. ex Merrill (Western Ghats) is used in mental disorders and tetanus.Dosage: Seed—1-2 g. (API Vol. IV.)Siddha/Tamil: Ruthracham, Pagumbar.Folk: Rudirak, Bhutali.Action: Bark—stomachic, antibil- ious. Used in haematemesis. Nut— antiepileptic, antirheumatic.
The leaves gave quercetin, kaempfer- ol, gallic acid and ethylgallate.... elaeocarpus ganitrusAcute gastritis is an in?ammatory reaction of the gastric mucosa to various precipitating factors, ranging from physical and chemical injury to infections. Acute gastritis (especially of the antral mucosas) may well represent a reaction to infection by a bacterium called Helicobacter pylori. The in?ammatory changes usually go after appropriate antibiotic treatment for the H. pylori infection. Acute and chronic in?ammation occurs in response to chemical damage of the gastric mucosa. For example, REFLUX of duodenal contents may predispose to in?ammatory acute and chronic gastritis. Similarly, multiple small erosions or single or multiple ulcers have resulted from consumption of chemicals, especialy aspirin and antirheumatic NONSTEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS).
Acute gastritis may cause anorexia, nausea, upper abdominal pain and, if erosive, haemorrhage. Treatment involves removal of the o?ending cause.
Chronic gastritis Accumulation of cells called round cells in the gastric mucosal characterises chronic gastritis. Most patients with chronic gastritis have no symptoms, and treatment of H. pylori infection usually cures the condition.
Atrophic gastritis A few patients with chronic gastritis may develop atrophic gastritis. With or without in?ammatory change, this disorder is common in western countries. The incidence increases with age, and more than 50 per cent of people over 50 may have it. A more complete and uniform type of ATROPHY, called ‘gastric atrophy’, characterises a familial disease called PERNICIOUS ANAEMIA. The cause of the latter disease is not known but it may be an autoimmune disorder.
Since atrophy of the corpus mucosa results in loss of acid- and pepsin-secreting cells, gastric secretion is reduced or absent. Patients with pernicious anaemia or severe atrophic gastritis of the corpus mucosa may secrete too little intrinsic factor for absorption of vitamin B12 and so can develop severe neurological disease (subacute combined degeneration of the spinal cord).
Patients with atrophic gastritis often have bacterial colonisation of the upper alimentary tract, with increased concentration of nitrite and carcinogenic N-nitroso compounds. These, coupled with excess growth of mucosal cells, may be linked to cancer. In chronic corpus gastritis, the risk of gastric cancer is about 3–4 times that of the general population.
Postgastrectomy mucosa The mucosa of the gastric remnant after surgical removal of the distal part of the stomach is usually in?amed and atrophic, and is also premalignant, with the risk of gastric cancer being very much greater than for patients with duodenal ulcer who have not had surgery.
Stress gastritis Acute stress gastritis develops, sometimes within hours, in individuals who have undergone severe physical trauma, BURNS (Curling ulcers), severe SEPSIS or major diseases such as heart attacks, strokes, intracranial trauma or operations (Cushing’s ulcers). The disorder presents with multiple super?cial erosions or ulcers of the gastric mucosa, with HAEMATEMESIS and MELAENA and sometimes with perforation when the acute ulcers erode through the stomach wall. Treatment involves inhibition of gastric secretion with intravenous infusion of an H2-receptorantagonist drug such as RANITIDINE or FAMOTIDINE, so that the gastric contents remain at a near neutral pH. Despite treatment, a few patients continue to bleed and may then require radical gastric surgery.
Gastric ulcer Gastric ulcers were common in young women during the 19th century, markedly fell in frequency in many western countries during the ?rst half of the 20th century, but remained common in coastal northern Norway, Japan, in young Australian women, and in some Andean populations. During the latter half of this century, gastric ulcers have again become more frequent in the West, with a peak incidence between 55 and 65 years.
The cause is not known. The two factors most strongly associated with the development of duodenal ulcers – gastric-acid production and gastric infection with H. pylori bacteria – are not nearly as strongly associated with gastric ulcers. The latter occur with increased frequency in individuals who take aspirin or NSAIDs. In healthy individuals who take NSAIDs, as many as 6 per cent develop a gastric ulcer during the ?rst week of treatment, while in patients with rheumatoid arthritis who are being treated long term with drugs, gastric ulcers occur in 20–40 per cent. The cause is inhibition of the enzyme cyclo-oxygenase, which in turn inhibits the production of repair-promoting PROSTAGLANDINS.
Gastric ulcers occur especially on the lesser curve of the stomach. The ulcers may erode through the whole thickness of the gastric wall, perforating into the peritoneal cavity or penetrating into liver, pancreas or colon.
Gastric ulcers usually present with a history of epigastric pain of less than one year. The pain tends to be associated with anorexia and may be aggravated by food, although patients with ‘prepyloric’ ulcers may obtain relief from eating or taking antacid preparations. Patients with gastric ulcers also complain of nausea and vomiting, and lose weight.
The principal complications of gastric ulcer are haemorrhage from arterial erosion, or perforation into the peritoneal cavity resulting in PERITONITIS, abscess or ?stula.
Aproximately one in two gastric ulcers heal ‘spontaneously’ in 2–3 months; however, up to 80 per cent of the patients relapse within 12 months. Repeated recurrence and rehealing results in scar tissue around the ulcer; this may cause a circumferential narrowing – a condition called ‘hour-glass stomach’.
The diagnosis of gastric ulcer is con?rmed by ENDOSCOPY. All patients with gastric ulcers should have multiple biopsies (see BIOPSY) to exclude the presence of malignant cells. Even after healing, gastric ulcers should be endoscopically monitored for a year.
Treatment of gastric ulcers is relatively simple: a course of one of the H2 RECEPTOR ANTAGONISTS heals gastric ulcers in 3 months. In patients who relapse, long-term inde?nite treatment with an H2 receptor antagonist such as ranitidine may be necessary since the ulcers tend to recur. Recently it has been claimed that gastric ulcers can be healed with a combination of a bismuth salt or a gastric secretory inhibitor
for example, one of the PROTON PUMP INHIBITORS such as omeprazole or lansoprazole
together with two antibiotics such as AMOXYCILLIN and METRONIDAZOLE. The long-term outcome of such treatment is not known. Partial gastrectomy, which used to be a regular treatment for gastric ulcers, is now much more rarely done unless the ulcer(s) contain precancerous cells.
Cancer of the stomach Cancer of the stomach is common and dangerous and, worldwide, accounts for approximately one in six of all deaths from cancer. There are marked geographical di?erences in frequency, with a very high incidence in Japan and low incidence in the USA. In the United Kingdom around 33 cases per 100,000 population are diagnosed annually. Studies have shown that environmental factors, rather than hereditary ones, are mainly responsible for the development of gastric cancer. Diet, including highly salted, pickled and smoked foods, and high concentrations of nitrate in food and drinking water, may well be responsible for the environmental effects.
Most gastric ulcers arise in abnormal gastric mucosa. The three mucosal disorders which especially predispose to gastric cancer include pernicious anaemia, postgastrectomy mucosa, and atrophic gastritis (see above). Around 90 per cent of gastric cancers have the microscopic appearance of abnormal mucosal cells (and are called ‘adenocarcinomas’). Most of the remainder look like endocrine cells of lymphoid tissue, although tumours with mixed microscopic appearance are common.
Early gastric cancer may be symptomless and, in countries like Japan with a high frequency of the disease, is often diagnosed during routine screening of the population. In more advanced cancers, upper abdominal pain, loss of appetite and loss of weight occur. Many present with obstructive symptoms, such as vomiting (when the pylorus is obstructed) or di?culty with swallowing. METASTASIS is obvious in up to two-thirds of patients and its presence contraindicates surgical cure. The diagnosis is made by endoscopic examination of the stomach and biopsy of abnormal-looking areas of mucosa. Treatment is surgical, often with additional chemotherapy and radiotherapy.... stomach, diseases of
In?ammation of the liver, or HEPATITIS, may occur as part of a generalised infection or may be a localised condition. Infectious hepatitis, which is the result of infection with a virus, is one of the most common forms. Many di?erent viruses can cause hepatitis, including that responsible for glandular fever (see MONONUCLEOSIS). Certain spirochaetes may also be the cause, particularly that responsible for LEPTOSPIROSIS, as can many drugs. Hepatitis may also occur if there is obstruction of the BILE DUCT, as by a gall-stone.
Cirrhosis of the liver A disorder caused by chronic damage to liver cells. The liver develops areas of ?brosis or scarring; in response, the remaining normal liver cells increase and form regeneration nodules. Those islands of normality, however, suffer from inadequate blood supply, thus adversely affecting liver function. Alcohol is the most common cause of cirrhosis in the United Kingdom and the USA, and the incidence of the disorder among women in the UK has recently risen sharply as a consequence of greater consumption of alcohol by young women in the latter decades of the 20th century. In Africa and many parts of Asia, infection with hepatitis B virus is a common cause. Certain drugs – for example, PARACETAMOL – may damage the liver if taken in excess. Unusual causes of cirrhosis include defects of the bile ducts, HAEMOCHROMATOSIS (raised iron absorption from the gut), CYSTIC FIBROSIS, cardiac cirrhosis (the result of heart failure causing circulatory congestion in the liver), and WILSON’S DISEASE (raised copper absorption).
Symptoms Some people with cirrhosis have no signs or symptoms and the disease may be diagnosed at a routine medical examination. Others may develop jaundice, OEDEMA (including ascites – ?uid in the abdomen), fever, confusion, HAEMATEMESIS (vomiting blood), loss of appetite and lethargy. On examination, cirrhotic patients often have an enlarged liver and/ or SPLEEN, and HYPERTENSION. Liver function tests, cholangiography (X-ray examination of the bile ducts) and biopsy of liver tissue will help to reach a diagnosis.
Treatment Nothing can be done to repair a cirrhosed organ, but the cause, if known, must be removed and further advance of the process thus prevented. In the case of the liver, a high-protein, high-carbohydrate, low-fat diet is given, supplemented by liver extract and vitamins B and K. The consumption of alcohol should be banned. In patients with liver failure and a poor prognosis, liver TRANSPLANTATION is worthwhile but only after careful consideration.
Abscess of the liver When an ABSCESS develops in the liver, it is usually a result of amoebic DYSENTERY, appearing sometimes late in the disease – even after the diarrhoea is cured (see below). It may also follow upon in?ammation of the liver due to other causes. In the case of an amoebic abscess, treatment consists of oral metronidazole.
Acute hepatic necrosis is a destructive and often fatal disease of the liver which is very rare. It may be due to chemical poisons, such as carbontetrachloride, chloroform, phosphorus and industrial solvents derived from benzene. It may also be the cause of death in cases of poisoning with fungi. Very occasionally, it may be a complication of acute infectious hepatitis.
Cancer of the liver is not uncommon, although it is rare for the disease to begin in the liver – the involvement of this organ being usually secondary to disease situated somewhere in the stomach or bowels. Cancer originating in the liver is more common in Asia and Africa. It usually arises in a ?brotic (or cirrhotic) liver and in carriers of the hepatitis B virus. There is great emaciation, which increases as the disease progresses. The liver is much enlarged, and its margin and surface are rough, being studded with hard cancer masses of varying size, which can often be felt through the abdominal wall. Pain may be present. Jaundice and oedema often appear.... liver, diseases of
Menstruation. The regular monthly loss of blood which women sustain as a result of menstruation always puts a strain on the blood-forming organs. If this loss is excessive, then over a period of time it may lead to quite severe anaemia.
Childbirth. A considerable amount of blood is always lost at childbirth; if this is severe, or if the woman was anaemic during pregnancy, a severe degree of anaemia may develop.
Bleeding from the gastrointestinal tract. The best example here is anaemia due to ‘bleeding piles’ (see HAEMORRHOIDS). Such bleeding, even though slight, is a common cause of anaemia in both men and women if maintained over a long period of time. The haemorrhage may be more acute and occur from a DUODENAL ULCER or gastric ulcer (see STOMACH, DISEASES OF), when it is known as haematemesis.
Certain blood diseases, such as PURPURA and HAEMOPHILIA, which are characterised by bleeding.... loss of blood
Habitat: Cultivated all over India as a food crop.
English: Rice.Ayurvedic: Shaali, Vrihidhaanya, Tandula, Nivara.Unani: Biranj Saathi.Action: Rice-water (a water decoction of rice)—demulcent and refrigerant in febrile and inflammatory diseases and in dysuria. Also used as a vehicle for compound preparations used for gynaecological disorders. It is regarded as cooling in haematemesis and epistaxis, and as diuretic.
The green clum or stalks—recommended in biliousness. Ash of the straw—used in the treatment of wounds and discharges. Lixiviated ash of straw is used as anthelmintic and in nausea.The Ayurvedic Pharmacopoeia ofIn- dia recommends the dried root in dy- suria and lactic disorders.The pigments occurring in coloured types of rice are a mixture of monogly- cosides of cyanidin and delphinidin. The dark Puttu Rice of India contains a diglycosidic anthocyanin.Dosage: Root—50 g for decoction. (API, Vol. II.)... oryza sativaTo strengthen veins – Gentian. To enhance resistance – Echinacea. To counter failing strength – Ginseng. To promote granulation – Comfrey. To restore lacerated nerves – St John’s Wort. Nettles are a well-known traditional anti-haemorrhagic.
If bleeding is serious, control with firm finger pressure. Any one of the following may be used in the form of teas, tinctures, powders, etc.
Bowels. Ladies Mantle, Avens, Horsetail, Shepherd’s Purse, Tormentil, Raspberry leaves, Yarrow, Cranesbill, Bilberry.
Gums. Tea. Equal parts: Horsetail, St John’s Wort. (Maria Treben) Or:– Paint gums with Tincture Myrrh, Blood root, Goldenseal or Marigold.
Post-partum. (After child-birth) Goldenseal BHP (1983); Lady’s Mantle BHP (1983).
Lungs. Haemoptysis. Blood spitting. Blood root, Beth root, Lungwort, Mullein, Horsetail, St John’s Wort, Cranesbill. Bur-Marigold. Sage. Mouse Ear, Bugleweed. Nettle tea is a good stand-by.
Post-menopausal bleeding: Internal: Raspberry leaves, Ladies Mantle, Shepherd’s Purse. Plantain tea as an injection. Plugs of cotton wool saturated with Witch Hazel. To be investigated by a competent authority.
Mucous surfaces: tongue, mouth, throat, gullet. Marigold, Yarrow, Rue, Clematis erecta, Life root.
Blood root (tincture: 10-15 drops in water). Ice to suck.
Nose. Witch Hazel. Nettles. Vinegar water: to snuff into nostrils. Apply sponge soaked in cold water to back of the neck. Or: plug nose with Witch Hazel saturated cotton wool.
Hymen. See entry.
Skin. Superficial. Buckwheat, Marigold, Daisy, Tormentil, Witch Hazel, Blood root (tincture),.
Stomach. Haematemesis. The vomit of blood has the appearance of coffee grounds and is a symptom of gastric ulcer. Teas: Avens, Meadowsweet, Yarrow, Bur-Marigold, Cranesbill, Mullein.
Decoctions: Cranesbill root, Beth root, Oak bark.
After Surgery. After tissue excisions, blood clotting or wound-healing disorders for safe haemostasis: Beth root, Cranesbill root, Lady’s Mantle, St John’s Wort.
Blood in the urine. See: HAEMATURIA.
Bleeding of menses: See: MENSTRUATION.
IUD bleeding. Bleeding from intra-uterine devices: Injection: teas – Lady’s Mantle, Cranesbill, Tormentil, Marigold.
Vitamin E supplementation (International Journal of Fertility, Vol 28. 1983) Suggested dose: One 500iu capsule morning and evening.
Retinal haemorrhage. Buckwheat tea. Vitamin C: 1-3g daily. Evening Primrose oil.
Red cell stimulators: Yellow Dock root, Red Clover, Gentian.
White cell stimulators: Liquorice, Ginseng (Siberian) and Korean, Goldenseal, Echinacea.
Vitamins. C. D. K. P.
Minerals. Calcium, Iron, Selenium, Zinc.
Note: Any new episode of bleeding (rectal, gastric, etc) in those 45 and over should be investigated in hospital. Alteration of bowel habit, with bleeding, in young people should lead to referral to a doctor. ... bleeding
The major cause of peptic ulcers is
HELICOBACTER PYLORI bacterial infection, which can damage the lining of the stomach and duodenum, allowing the acid stomach contents to attack it. Analgesic drugs, alcohol, excess acid production, and smoking can also damage the stomach lining. Ulcers can also form in the oesophagus, when acidic juice from the stomach enters it (see acid reflux), and in the duodenum.
There may be no symptoms, or there may be burning or gnawing pain in the upper abdomen. Other possible symptoms include loss of appetite, nausea, and vomiting. The ulcer may also bleed. If severe, it may result in haematemesis
(vomiting of blood) and melaena, and is a medical emergency. Chronic bleeding may cause iron-deficiency anaemia. Rarely, an ulcer may perforate the wall of the digestive tract and lead to peritonitis.
An ulcer is usually diagnosed by an endoscopy of the stomach and duodenum; less commonly, a barium meal (see barium X-ray examination) is performed. Tests will be carried out to see whether the individual is infected with the HELICOBACTER bacterium. If this is the case, a combination of antibiotics and an ulcerhealing drug will be given. A further test may be done to check that treatment has been successful. If HELICOBACTER is not detected – for example, in ulcers caused by nonsteroidal anti-inflammatory drugs (NSAIDs) – treatment is with proton pump inhibitors or H-blockers, and the NSAIDs will be stopped. Surgery is now rarely needed for peptic ulcers, except to treat complications such as bleeding or perforation.... peptic ulcer
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