Ulcers are crater-like sores (generally 1/4 inch to 3/4 inch in diameter, but sometimes 1 to 2 inches in diameter) which form in the lining of the stomach (called gastric ulcers), just below the stomach at the beginning of the small intestine in the duodenum (called duodenal ulcers) or less commonly in the esophagus (called esophageal ulcers).
In general, ulcers in the stomach and duodenum are referred to as peptic ulcers.
The stomach is a bag of muscle that crushes and mixes food with the digestive "juices" - hydrochloric acid and pepsin. If the lining of the stomach (or duodenum) is damaged in one place or another, the acid and pepsin go to work on the lining as they would on food, breaking it down as though to digest it.
An ulcer is the result of an imbalance between aggressive and defensive factors. On one hand, too much acid and pepsin can damage the stomach lining and cause ulcers. On the other hand (and more commonly), the damage comes first from some other causes, making the stomach lining susceptible to even an ordinary level of gastric acid.
If a person does not receive treatment for ulcers, it could lead to a bleeding ulcer (the ulcer has eaten into blood vessels and the blood has seeped into the digestive tract), a perforated ulcer (the ulcer has eaten a hole in the wall of the stomach or duodenum and bacteria and partially digested food has spilled into the hole, causing inflammation) or a narrowing and obstruction of the intestinal opening preventing food from leaving the stomach and entering the small intestine.
The stomach defends itself from hydrochloric acid and pepsin by creating a mucus coating (that shields stomach tissue), by producing bicarbonate and by circulating blood to the stomach lining to aid in cell renewal and repair. If any of these functions are impaired it can lead to the formation of an ulcer.
The primary cause of ulcers is the bacterium called Helicobacter pylori (H. pylori). H. pylori is a spiral-shaped bacterium found in the stomach. Unlike other bacterium, H. pylori is able to twist through the layer of mucous that protects the stomach cavity and attach to cells on the surface of the stomach wall, where it produces urease, an enzyme that generates ammonia.
Urease generates substances that neutralize the stomach's acid and allows H. pylori to thrive. H. pylori weakens the stomach's defenses by thinning the mucous coating of the stomach, making it more susceptible to the damaging effects of acid and pepsin; inflaming the area; poisoning nearby cells and producing more stomach acid.
Although H. pylori is the primary cause of ulcers, there are other factors that play a role in ulcer development. These factors are the use of nonsteroidal anti-inflammatory drugs (NSAIDs), a person's lifestyle and the stomach's inability to defend itself against digestive fluids, hydrochloric acid and pepsin.
NSAIDs such as aspirin, ibuprofen (Motrin, Advil, Nuprin), naproxen (Naprosyn, Anaprox), or piroxicam (Feldene) interfere with the stomach's ability to produce mucus and bicarbonate (a chemical produced in the stomach that neutralizes and breaks down the hydrochloric acid and pepsin into substances less harmful).
NSAIDs also affect blood flow to the stomach, hinder cell repair and cause the stomach's defense mechanisms to fail.
Lifestyle factors such as smoking, drinking caffeine, consuming alcohol and stress are also associated with ulcers.
Smoking slows the healing of ulcers and makes them likely to recur.
Caffeine stimulates acid secretion in the stomach, thus aggravating the pain of an existing ulcer.
Studies on alcohol consumption and ulcers have been less conclusive, although alcoholic cirrhosis has been linked to an increased risk of ulcers, and heavy drinking has been shown to delay the healing of ulcers.
Although emotional stress is no longer thought to be a cause of ulcers, people with ulcers often report that emotional stress increases ulcer pain. However, physical stress increases the risk of developing gastric ulcers.
There may be no symptoms of ulcers or the individual may experience:
A gnawing or burning pain in the abdomen between the breastbone and the navel. The pain is usually worse a couple of hours after a meal or in the middle of the night when the stomach is empty.
Loss of appetite
Loss of weight
Tiredness (a symptom of a bleeding ulcer)
Weakness (a symptom of a bleeding ulcer)
Blood in vomit or stool. When blood is in the stool, it appears tarry or black (symptom of a bleeding ulcer).
Doctors have a number of options available for diagnosing ulcers, such as performing endoscopic and x-ray examinations, as well as testing for H. pylori. Endoscopy is a diagnostic procedure that gives the doctor a direct view of the upper digestive tract from within the body itself. By means of an instrument called a fiber-optic endoscope, the doctor is able to illuminate and follow the same path that food takes, examining the esophagus, stomach and duodenum from within. Along the way, the doctor will look closely at inflamed, ulcerated or infected areas, as well as growths and malformations.
If the doctor suspects ulcers, an upper GI (gastrointestinal) series (x-rays) of the esophagus, stomach and duodenum will usually be performed. The patient will swallow a chalky liquid that contains barium, which makes the ulcer visible on the x-ray.
The doctor may also order a gastroscopy, in which a flexible tube-shaped device with a special light-conducting properties will be put down the throat to enable the doctor to see the ulcer and obtain tissue samples for microscopic examination to determine if the ulcer is cancerous.
Confirming the presence of H. pylori is important in diagnosing an ulcer because elimination of H. pylori is likely to cure the ulcer. H. pylori can be detected using a blood, breath or tissue test. The blood test uses a blood sample to identify and measure H. pylori antibodies. Approved in 1996, the Meretek UBT Breath Test requires that a person first drink a liquid or swallow a capsule containing a small amount of a protein. The person is then asked to blow through a straw into a balloon. A lab technician checks the exhaled air for evidence of the H. pylori bacteria. If the doctor previously performed an endoscopy, the tissue obtained through that procedure is cultured and watched for growth of H. pylori organisms.
Along with reducing stress and modifying lifestyle, doctors treat gastric and duodenal ulcers with several types of medicines, including H2-blockers, proton-pump inhibitors and mucosal protective agents. When treating H. pylori, these medications are used in combination with antibiotics. If medication is ineffective or complications arise, surgery may be required.
H2-blockers reduce the amount of acid that the stomach makes. These medicines include cimetidine (Tagamet), ranitidine (Zantac), famotidine (Pepcid) and nizatidine (Axid). A single bedtime dose starts healing a duodenal ulcer in four weeks and a gastric ulcer in six to eight weeks.
Proton-pump inhibitors modify the stomach's production of acid by stopping the stomach's acid pump - the final step of acid secretion. The recently approved and now available drug, omeprazole (Prilosec), is 10 times more powerful in suppressing stomach acid production than the H2-blockers, able to promote duodenal ulcer healing in two to four weeks. This potent acid-inhibitor can suppress about 95 percent of stomach acid production. It is especially useful for treating people whose ulcers fail to respond to H2-receptor blockers or other medications and those with Zollinger-Ellison syndrome.
Mucosal protective agents protect the stomach's mucous lining from acid. The prescription medications are sucralfate (Sulcrate or Carafate) and misoprostol (Cytotec). The non-prescription medications are antacids (such as Tums and Rolaids) and bismuth subsalicylate (Pepto-Bismol).
Antibiotics. With the discovery of the link between ulcers and H. pylori peptic ulcers can be treated by a short course of combined high dose antibiotic therapy rather than acid-suppression alone. Without antibacterial therapy, there is a 75 percent chance of the ulcer reccurring. With antibacterial therapy, there is a 1 percent chance of the ulcer reccurring. There are two types of combination therapies currenly being used: triple therapy and dual therapy.
Triple therapy involves:
Metronidazole (Flagyl)*, an antibiotic taken four times a day
Tetracycline (Achromycin or Sumycin)**, an antibiotic taken four times a day
Pepto-Bismol taken four times a day
This regimen lasts two weeks. This treatment is 90 percent effective in destroying the H. pylori bacteria and in reducing the risk of recurrence. (*doctor may substitute amoxicillin (Amoxil or Trimox); **doctor may substitute clarithromycin (Biaxin))
Dual therapy involves:
Amoxicillin two to four times a day or Biaxin three times a day
Prilosec two times a day
This regimen lasts two weeks. This treatment is 80 percent effective in destroying the H. pylori bacteria and in reducing the risk of recurrence.
The most common types of surgery for ulcers are vagotomy, antrectomy and pyloroplasty.
Vagotomy involves cutting the vagus nerve that transmits messages from the brain to the stomach. This interruption reduces acid secretion.
Antrectomy removes the lower part of the stomach (antrum) which produces a hormone that stimulates the stomach to secrete digestive juices. This enlarges the opening into the duodenum and small intestine (pyloris), enabling contents to pass more freely from the stomach.
Pyloroplasty may be performed with a vagotomy.