What are ulcers?

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Open sores; peptic ulcers develop on the mucous membranes that line the gastrointestinal tract and are caused by the excessive secretion of gastric juices, particularly from the pancreas into the intestine
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Causes and Symptoms

In the most general of terms, an ulcer is an open sore that does not respond readily to the normal processes of healing. It may occur on the skin itself or on internal mucous membranes. A corneal ulcer, for example, may occur as a result of infections stemming from local injuries of, or foreign objects lodged in, the eye. Circulatory disturbances associated with varicose veins or long periods in bed without sufficient body exercise can also cause skin ulcers. The latter form is sometimes referred to as bedsores.

The most commonly occurring ulcer, however, is the peptic ulcer, which occurs at various points in the gastrointestinal tract. Specifically, such ulcers affect the lower portion of the esophagus, the stomach (in which case the term “gastric” ulcer may be employed), and two locations in the small intestine: the duodenum and the jejunum. Approximately 10 percent of the general population in the United States and Western Europe is thought to suffer from peptic ulcers. A substantially higher percentage of the population may suffer from a condition that resembles ulcers in its symptomatic levels of discomfort and pain but that does not actually involve lesions. This condition is called nonulcerous dyspepsia.

When ulceration of the stomach or intestinal tissue advances past a certain stage, internal bleeding usually occurs. Reaction to this stage of deterioration may involve vomiting, in which case the granular bloody material that is expulsed resembles partially digested food and is brownish rather than red in color. This condition stems from the effect of acidic gastric juices on the blood that has been released. If bleeding from ulcers becomes evident through the presence of blood in the stools, the effect is different: the fecal material is black in color, a condition that was referred to in past generations as “tarry stool.”

Although modern medical science has identified the hydrochloric acid content of the gastric juice as the corrosive agent that causes ulcer sores in all these regions of the digestive system, the term “peptic ulcer” is still commonly used to refer to all ulcers. This label was first applied following the discovery, in 1836, of the enzyme pepsin, one of the first subcomponents of the gastric juice to be isolated in the laboratory.

In the twentieth century, the original contributions of physicians to the understanding of what ulcers are were combined with equally scientific observations of social and psychological factors that can bring about ulcers. Increasingly, many of these causes were associated with environmental and nervous emotional factors.

The likelihood of ulcers forming in the gastrointestinal tract is increased if an imbalance occurs in the normal functioning of a specific phase of the digestive process. That phase begins when, at the time that foods are taken into the mouth and swallowed, the body secretes gastric juice containing both acid and pepsin. The essential acid in gastric juice is hydrochloric acid, which is highly dangerous in its pure state and poisonous if swallowed directly. Pepsin is an enzyme produced in the lining of the stomach that has proteolytic, or protein-degrading, characteristics. Both these components in gastric juices are essential in the first stages of digestion to break down the foodstuffs in the stomach and to facilitate their passage into the small intestine, where other secretions from the liver and pancreas continue the process of digestion. In the case of the enzyme pepsin, it is secreted in an inactive chemical state; it therefore requires the presence of hydrochloric acid (also secreted in the stomach lining) to convert it chemically to an active state and an optimum degree of acidity (pH 1 to 3) for the digestive function it fulfills. If the chemical conversion of pepsin into an active digestive agent does not make use of all the hydrochloric acid that has been secreted, the excess acid is free to do damage to the sensitive tissue of the stomach or intestinal lining.

Ulcers can occur in any of several areas of the gastrointestinal tract when excessive amounts or imbalanced component proportions of gastric juice are secreted. In recent times, doctors established that a continuing state of nervousness or hostility can cause gastric juice to flow almost continuously. Such hypersecretion will damage the mucous membranes lining the digestive tract unless a more-or-less constant supply of food is taken in by the organism. Thus, the nervous eater who is constantly consuming foods may be unconsciously trying to control the potential development of ulcers in his or her gastrointestinal tract. The side effects on the body of constant nervous eating may be potentially as harmful as the localized effects associated with ulcers.

In essence, what happens when an ulcer begins to form is that the acid and pepsin in the gastric juice begin to digest membrane tissue in the gastrointestinal tract itself. Normally, the stomach has a series of internal defenses to combat localized attacks by active gastric juice against its own sensitive membranes. In the first place, the mucous lining of the internal organs themselves forms a sort of barrier between membrane tissue and the combined food-gastric juice content of the functioning organ.

The cells of the stomach lining also secrete a natural antacid in the form of bicarbonate of soda. If the normal presence of these two protective agents is insufficient to prevent deterioration of the stomach or intestinal lining, a more active struggle ensues in the area where an ulcer has begun to develop. Surface cells begin to constrict to form a more resistant surface area around the nascent lesion. If the process does not proceed too rapidly, damaged cells may be replaced by healthy cells in the immediate area of the lesion.

Even more specialized reactions in the area of ulceration are associated with prostaglandins, which are chemical agents in the stomach lining that stimulate increased blood flow to nourish besieged cells. Prostaglandins can also bring about higher levels of antacid production and mucus accumulation where they are needed most.

With one notable and fairly rare exception, known as the Zollinger-Ellison syndrome (excessive production of acid), almost all cases of stomach ulcers (gastric ulcers) occur as a result of dysfunction in the defensive systems described above. As for duodenal (upper small intestine) ulcers, it appears that only about a third of all cases stem from higher-than-normal secretions of acid.

Doctors are not in full agreement regarding the way in which certain externally introduced substances may cause, or seriously contribute to, ulcers. Most have concluded, however, that a “big three” of clearly abusive substances—cigarettes, alcohol, and some over-the-counter drugs, especially aspirin—play a significant role. Cigarette smoking has been linked with the slowing down of essential body functions that either provide defenses against ulcers or contribute to their healing. One such function is the rate of blood flow itself, which is vital for the nourishment of cells that may be under attack by ulcers. Other side effects of smoking may include reduced production of prostaglandins, which make important contributions to the defensive reaction of the body against ulcerations.

As for the other potentially abusive agents, alcohol and certain over-the-counter or otherwise common drugs, it is the latter that are almost universally condemned for their negative effects on the proper functioning of the gastrointestinal system.

Alcohol, for its part, apparently does nothing to stimulate excessive acid production in the stomach. It does, however, interfere with the healing processes that are so vital in combating ulcers.

While caffeine is not usually considered to be an over-the-counter drug, it is known to be an important stimulator of acid secretions. Some doctors consider it to be second only to aspirin as a negative “foreign agent” affecting the sensitive mechanism of digestion in the stomach and small intestine.

Another common drug, aspirin, shares a dubious reputation in this respect with a number of other drugs classified as nonsteroidal anti-inflammatory drugs (NSAIDs) that are used to treat arthritis and other muscular or joint inflammations.

There is a widespread consensus that the occurrence of ulcers may be linked to external agents that are taken into the body. The simplest evidence of this hypothesis revolves around associations that have been established between the bacillus Helicobacter pylori and ulcerous conditions in the stomach and intestines.

Doctors had observed the presence of this bacillus (along with many others) in the human stomach for at least a century. Studies by the Australian researchers Bernard Marshall and J. R. Warner, however, noted that a very high percentage (nearly 100 percent) of patients diagnosed as having ulcers also had substantial traces of H. pylori.

Treatment and Therapy

As the debate over the role of H. pylori in causing ulcers took form in the early 1990s, those researchers who wanted to find proof that medicine was on the verge of a major breakthrough organized a full campaign to prescribe drugs that were known to kill the suspect bacillus.

It is now clear that H. pylori is a major contributing factor not only in ulcer development but also in the extremely high recurrence rate of relapse in healed patients. Because of the inflammation that the infecting organism causes in the stomach and duodenal linings, normal protective mechanisms break down. Once these barriers that protect the lining from damage by the acid and enzymes used in digesting food are gone, the process of ulceration begins. Even after the ulcer has healed, very high rates of recurrence are found unless the bacterial infection is eradicated.

Because so many people are infected with these common bacteria but not everyone develops ulcers, other contributing factors are clearly present. In the vulnerable patient, a combination of the well-known risk factors along with infection work together to bring about ulcers. It is now a routine treatment to administer antibiotics and stomach acid inhibitors simultaneously. Cure rate times and relapse rates have improved significantly.

Whatever the ultimate explanation concerning the causes of this surprisingly common ailment may be, the medical world remained, in the late twentieth century, devoted to the necessary use of a number of drugs to control the effects of gastric and peptic ulcers by fighting the flow of gastric juices that do the physical damage of ulceration. On the whole, these drugs, which are called histamine II blockers, aim at one objective: to block the formation of stomach acid. A similar effect is produced by several widely used (and markedly expensive) medicines that are prepared under commercial labels: Tagamet, Zantac, Pepcid, and Axid. Drugs in the class called acid pump inhibitors, such as Prilosec, also block stomach acid, but by a different and nearly complete method: they prevent the stomach cells from actually making the acid, in the final step before it is secreted into the stomach. These drugs are effective even in the most difficult cases of ulceration.

Much more complicated than the problem of treating normal cases of ulcers is the technical question of how to guard against the further deterioration of ulcers into different forms of gastrointestinal cancer. New forms of technology were being tested in the late twentieth century that allowed physicians to examine the inner mucous membranes of the intestines directly. One such device, called the fiber-optic endoscope, consists of a long tube that is passed through the esophagus and stomach to penetrate the upper portions of the small intestine. The fiber-optic endoscope not only views and photographs the surface areas affected by ulcers but also allows the physician to biopsy the tissue at the same time. This and other methods of diagnosis, although not available to all hospitals and clinics, and not mastered by all physicians who were trained in the pre-fiber-optic generation, represent enormous potential advances over the rather basic therapies developed during the previous century.

Perspective and Prospects

Long before modern scientific research techniques provided the medical world with a relatively precise idea of what causes ulcers and how to treat them, an entire literature on the disease had accumulated. It was apparently Hippocrates himself, in the fifth century BCE, who first studied the gastric hemorrhaging that can result from a peptic ulcer. Others, including the first century CE Roman Celsus, noted the favorable effect of prescribing a nonacid diet to patients suffering from ulcers. It was not until the eighteenth and nineteenth centuries, however, that doctors prepared the first clinical accounts of the effects of ulcers based on pathological studies.

Not much had changed by the early twentieth century regarding the attitude of physicians toward the role of acids in the stage-by-stage degenerative process of ulceration. The American doctor Bertram W. Sippy was often quoted after his famous 1912 statement to medical students that “where there is no acid, there is no ulcer.” The question of what caused the presence of excess acid in the intestines aside, medical science would try to come closer to being able to detect the actions of the “culprit at work.” To the general public, the advanced process of fiber-optic endoscopy gives the appearance of having been developed overnight in the last decades of the twentieth century. In fact, a number of necessary prestages had been pioneered all over the globe for more than a century.

As early as 1868, nearly thirty years before X-rays were discovered, German physician Adolf Kussmaul performed experiments that involved inserting a hollow lighted tube into patients’ stomachs. He was actually able to see the interior surface of the stomach with the naked eye. Later, also in Germany, in 1908, a doctor named Hammeter was able to display a gastric ulcer by using barium meal X-ray technology. At a certain point, still well before the advent of fiber-optic endoscopy, a technique called arteriography was employed to explore the extent of ulcer damage when hemorrhaging occurred. This method, which still complemented fiber-optic endoscopy into the 1990s, involves the injection, through a fine tube passing through key arteries, of a dye whose movement in the intestinal tissue is then traced by means of a rapid series of X-ray images.

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