The development of cells in a part to which they have been carried by metastasis. Can also be used to describe bacteria establishing and multiplying on a particular part of the body.
Among the smallest and simplest microorganisms are the viruses. First described as ?lterable agents, and ranging in size from 20–30 nm to 300 nm, they may be directly visualised only by electron microscopy. They consist of a core of deoxyribonucleic or ribonucleic acid (DNA or RNA) within a protective protein coat, or capsid, whose subunits confer a geometric symmetry. Thus viruses are usually cubical (icosahedral) or helical; the larger viruses (pox-, herpes-, myxo-viruses) may also have an outer envelope. Their minimal structure dictates that viruses are all obligate parasites, relying on living cells to provide essential components for their replication. Apart from animal and plant cells, viruses may infect and replicate in bacteria (bacteriophages) or fungi (mycophages), which are damaged in the process.
Bacteria are larger (0·01–5,000 µm) and more complex. They have a subcellular organisation which generally includes DNA and RNA, a cell membrane, organelles such as ribosomes, and a complex and chemically variable cell envelope – but, unlike EUKARYOTES, no nucleus. Rickettsiae, chlamydia, and mycoplasmas, once thought of as viruses because of their small size and absence of a cell wall (mycoplasma) or major wall component (chlamydia), are now acknowledged as bacteria; rickettsiae and chlamydia are intracellular parasites of medical importance. Bacteria may also possess additional surface structures, such as capsules and organs of locomotion (?agella) and attachment (?mbriae and stalks). Individual bacterial cells may be spheres (cocci); straight (bacilli), curved (vibrio), or ?exuous (spirilla) rods; or oval cells (coccobacilli). On examination by light microscopy, bacteria may be visible in characteristic con?gurations (as pairs of cocci [diplococci], or chains [streptococci], or clusters); actinomycete bacteria grow as ?laments with externally produced spores. Bacteria grow essentially by increasing in cell size and dividing by ?ssion, a process which in ideal laboratory conditions some bacteria may achieve about once every 20 minutes. Under natural conditions, growth is usually much slower.
Eukaryotic micro-organisms comprise fungi, algae, and protozoa. These organisms are larger, and they have in common a well-developed internal compartmentation into subcellular organelles; they also have a nucleus. Algae additionally have chloroplasts, which contain photosynthetic pigments; fungi lack chloroplasts; and protozoa lack both a cell wall and chloroplasts but may have a contractile vacuole to regulate water uptake and, in some, structures for capturing and ingesting food. Fungi grow either as discrete cells (yeasts), multiplying by budding, ?ssion, or conjugation, or as thin ?laments (hyphae) which bear spores, although some may show both morphological forms during their life-cycle. Algae and protozoa generally grow as individual cells or colonies of individuals and multiply by ?ssion.
Micro-organisms of medical importance include representatives of the ?ve major microbial groups that obtain their essential nutrients at the expense of their hosts. Many bacteria and most fungi, however, are saprophytes (see SAPROPHYTE), being major contributors to the natural cycling of carbon in the environment and to biodeterioration; others are of ecological and economic importance because of the diseases they cause in agricultural or horticultural crops or because of their bene?cial relationships with higher organisms. Additionally, they may be of industrial or biotechnological importance. Fungal diseases of humans tend to be most important in tropical environments and in immuno-compromised subjects.
Pathogenic (that is, disease-causing) microorganisms have special characteristics, or virulence factors, that enable them to colonise their hosts and overcome or evade physical, biochemical, and immunological host defences. For example, the presence of capsules, as in the bacteria that cause anthrax (Bacillus anthracis), one form of pneumonia (Streptococcus pneumoniae), scarlet fever (S. pyogenes), bacterial meningitis (Neisseria meningitidis, Haemophilus in?uenzae) is directly related to the ability to cause disease because of their antiphagocytic properties. Fimbriae are related to virulence, enabling tissue attachment – for example, in gonorrhoea (N. gonorrhoeae) and cholera (Vibrio cholerae). Many bacteria excrete extracellular virulence factors; these include enzymes and other agents that impair the host’s physiological and immunological functions. Some bacteria produce powerful toxins (excreted exotoxins or endogenous endotoxins), which may cause local tissue destruction and allow colonisation by the pathogen or whose speci?c action may explain the disease mechanism. In Staphylococcus aureus, exfoliative toxin produces the staphylococcal scalded-skin syndrome, TSS toxin-1 toxic-shock syndrome, and enterotoxin food poisoning. The pertussis exotoxin of Bordetella pertussis, the cause of whooping cough, blocks immunological defences and mediates attachment to tracheal cells, and the exotoxin produced by Corynebacterium diphtheriae causes local damage resulting in a pronounced exudate in the trachea.
Viruses cause disease by cellular destruction arising from their intracellular parasitic existence. Attachment to particular cells is often mediated by speci?c viral surface proteins; mechanisms for evading immunological defences include latency, change in viral antigenic structure, or incapacitation of the immune system – for example, destruction of CD 4 lymphocytes by the human immunode?ciency virus.... microbiology
Acute 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
However, calling a condition psychosomatic implies something more – the primacy of the psyche over the soma. Going back to the in?uential theories and practice of PSYCHOANALYSIS as expounded from the 1930s, many diseases have been proposed as the result of psychological factors.These have included PEPTIC ULCER, ULCERATIVE COLITIS, ASTHMA, PSORIASIS and others. In this view, much physical disorder is due to repressed or excessive emotions. Likewise it is also argued that whereas some people express psychological distress via psychological symptoms (such as anxiety, depression and so on), others develop physical symptoms instead – and that they are also at greater risk of physical disease.
The trouble with this view is that medical advances repeatedly show that it goes too far. Stress certainly causes physical symptoms – for example, DYSPEPSIA – but the belief that it caused peptic ulcers vanished with the discovery of the true cause: colonisation of the stomach by the bacterium, Helicobacter pylori. Of course, stress and social adversity affect the risk of many diseases. For example, the incidence of heart disease among UK government employees (civil servants) has been shown to be in?uenced by their social class and their degree of job satisfaction. But we do not know how this works. Some argue that social adversity and stress in?uence how the heart functions (‘He died of a broken heart’). Stress can also affect IMMUNITY but it cannot cause AIDS/HIV and we do not know if there is a link running from stress to abnormal immune function to actual illness.
We can say that psychological factors provoke physical symptoms, and often even explain how this can happen. For example, when you are anxious you produce more epinephrine (adrenaline), which gives rise to chest pain, ‘butter?ies in the stomach’ and PALPITATION. These symptoms are not ‘all in the mind’, even if the trigger is a psychological one. People who are depressed are more likely to experience nearly every physical symptom there is, but especially pain and fatigue. Taken as a whole, psychologically induced symptoms are an enormous burden on the NHS and probably responsible for more doctor visits and sickness absence than any other single cause. Also we can be con?dent that social adversity and stress powerfully in?uence the outcome of many illnesses; likewise, a vast range of unhealthy activities and behaviours such as smoking, excessive alcohol intake, excessive eating, and so on. But we must be careful not to assume that our emotions directly cause our illnesses.... psychosomatic diseases
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