This section is from the book "Diet In Dyspepsia And Other Diseases Of The Stomach And Bowels", by William Tibbles. See also: 4 Weeks to Healthy Digestion.
Why does not the stomach digest itself? This question has been asked for centuries, many theories have been propounded to explain it, and still the puzzle remains. If an artificial gastric juice be prepared we know that it will digest meat, fish, and eggs or similar substances; these, however, are dead materials. If a living animal or a limb of such an animal be kept in an artificial gastric juice it will not be digested, except so far as the dead cuticle is concerned. But if the tissues of such an animal's limb be injured, there is no guarantee that they will not be digested; if the injury is sufficient to interfere with the nutrition of the skin and muscles they will certainly be digested. Living animals have been known to exist in the human stomach; thus the ordinary round worm, frogs, toads, and newts in their fully-developed condition, have been ejected by vomiting. Therefore it appears that the healthy living tissues contain some protective material which the injured tissues do not contain. It is argued that the living stomach also contains some protective material which, under ordinary circumstances, prevents the gastric juice from digesting it. It has been suggested that this protection is due to an antiferment secreted by the cells of the stomach; it has also been held that a free secretion of mucus forms a protecting varnish to the mucous membrane; and that the blood flowing constantly through its vessels is alkaline, while the gastric juice is acid, and one counteracts the other. Some of these theories are valueless. It is probably a sufficient protection that the tissues are living, like those of animals occasionally incarcerated within the stomach. If the nutrition of the cells of the stomach is low, or their vitality reduced by a deficient nerve supply or deficient circulation, neither the coating of mucus nor the alkalinity of the blood will protect the stomach entirely. A reduction of vitality in the cells of a small area may occur from many causes, and if they have not sufficient power to resist the poisonous effect of the small amount of hydrochloric acid, the cells would then be destroyed and digested by the gastric juice. Thus a sore place or ulcer is formed. Once started, such an ulcer, perhaps originally very minute, spreads by a continuance of the same circumstances. The reduction of vitality may be due to a deficiency of some normal ferment in the cells of that small area or to the formation of a particular toxin in them. Observations have shown that an ulcer can easily be produced by using a particular serum, which reduces the vitality of the cells - when the gastric juice contains a normal or supernormal amount of hydrochloric acid; if the proportion of acid is greater than usual the ulcer will be more extensive than when the gastric juice contains only the normal quantity of acid. In most cases of ulcer of the stomach the gastric juice is very acid (hyperchlorhydria); and whenever the vitality of the mucous membrane is reduced by a toxic substance the cells are liable to be attacked and digested by the gastric juice. That is the theory recently promulgated. But there are other feasible explanations. If a tiny focus of inflammation occurs in an enfeebled spot, as the result of septic infection or mechanical injury, an embolism may occur in a small bloodvessel and cause a tiny patch of necrosis. It is well known that acute gastric ulcers commonly occur in the course of ulcerative endocarditis and other infectious diseases where small emboli form in the gastric arteries. There may be no evidence of a severe septic disease. preceding an ordinary gastric ulcer; but there is abundant evidence of septic matter from the teeth and gums and of bacteria from the food finding their way into the stomach. There is also plenty of evidence that the food may contain hard particles of substances which by their mechanical action may cause local inflammation and predispose the tissues to embolism. It matters not, however, whether the death of the small piece of mucous membrane is due to septic embolism, mechanical irritation, or the absence of some normal antibody, there is the fact that a small piece of dead or diseased mucous membrane forms a slough and falls out or is digested, and an ulcer is left. An acute ulcer has a clean and punched-out appearance. There may be one or several, but it is strange that in men the primary ulcer is in the duodenum, and in women it is in the stomach. We are quite ignorant of the cause of this peculiarity or why one person should be subject to an ulcer and not another. Gastric is far more common than duodenal ulcer, for out of 1300 cases 90 per cent affected the stomach, and only 10 per cent the duodenum. The ulcers are curable by rest and careful feeding, but relapses are common. They may also be cured by surgical means; but it would be an error to suppose such means are a prevention against other ulcers, for it has been shown that relapses occur in 10 per cent of the cases operated on. When a first attack of ulcer occurs medical treatment should always be resorted to. Indeed, I should strongly recommend medical treatment to be tried first in every case. But when the disease is very chronic, haemorrhage occurring frequently, and no cure resulting from medicine and food, recourse must be had to surgery, and we should be thankful that such means exist for the removal of the ulcer. The persons most likely to be affected by gastric ulcer are young women. They are usually anaemic as the result of conditions which predispose to the ulcer. What those conditions are have not been finally settled. Sir Andrew Clark considered one of the chief elements was constipation; but many more girls suffer from constipation than from ulcer, and no clear connexion can be traced between them. Similar remarks apply to tight lacing, to which ulcers are sometimes attributed; but few men wear stays, and the occurrence of an ulcer in them is probably a coincidence. A sluggish circulation has been blamed for their occurrence, but we see perforating ulcers of the feet in people with a good circulation. It is probable that there is a special diathesis or constitutional state which predisposes to the formation of ulcers.
The chief symptoms of a chronic gastric ulcer are pain, vomiting after food, and haemorrhage. The pain begins soon after eating and lasts as long as there is food in the stomach. The painful area may be a spot small enough to be covered by a sixpence, or it may beimore diffused and radiate to the shoulder-blades. Vomiting relieves the pain, and is seldom absent in a well-marked case; it is exhausting by itself, and causes loss of strength and emaciation by removing much-needed food from the body. The vomited materials are more or less changed according to the length of time they have been in the stomach. They are often mixed with mucus, and contain an excess of hydrochloric acid; but in bad cases there is a persistent catarrh of the stomach, profuse secretion of mucus, a deficiency of hydrochloric acid, and an excess of organic acids. But pain and vomiting may be absent. In such cases the ulcer is only diagnosed when it penetrates a blood-vessel and causes haemorrhage; the bleeding may then be profuse and alarming. In cases where vomiting is constant there may be a slight oozing of blood from the granulated surface of the ulcer; but this may be sufficient to make the diagnosis of ulcer more accurate than when there is only pain and vomiting. A duodenal ulcer causes discomfort after food and the peculiar "hunger pain" which is characteristic of the disease; there may or may not be vomiting of food and blood, but more often there are mere traces of blood in the motions.
Although pain, vomiting, and bleeding from the stomach are the recognized indications of an ulcer, it cannot be denied that these symptoms may occur without an ulcer. Many patients have been operated on after profuse haemorrhage, and no ulcer could be found; other persons have died after profuse gastric haemorrhage, and no ulcer could be found at the post-mortem examination, nor any evidence that an ulcer had ever existed. Some of these people may have had the characteristic pain, vomiting, and bleeding for years, and the most that could be found was a patch of congested mucous membrane. The condition is called Gastrostaxis or Gastrorhexis.
 
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