Ailments and Situations - Ulcer - Causes - Peptic Ulcer

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Ailments and Situations - Ulcer
- Bedsore
- Canker
- Leg Ulcer
- Peptic Ulcer
- Symptoms and Signs - Bedsore
- Symptoms and Signs - Canker
- Symptoms and Signs - Leg Ulcer
- Symptoms and Signs - Peptic Ulcer
- Causes - Bedsore
- Causes - Canker
- Causes - Leg Ulcer
- Causes - Peptic Ulcer
- What to Expect - Bedsore
- What to Expect - Canker
- What to Expect - Leg Ulcer
- What to Expect - Peptic Ulcer
- Remedies - Bedsore
- Remedies - Canker Sore
- Remedies - Leg Ulcer
- Remedies - Peptic Ulcer
- Actions and Remedy Listings - Bedsore
- Actions and Remedy Listings - Canker
- Actions and Remedy Listings - Leg Ulcer
- Actions and Remedy Listings - Peptic Ulcer
- See also
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Peptic Ulcer

Over-secretion of gastric acid is generally not the cause of peptic ulcer formation. Although the gastric acid required to digest food is very corrosive, with a pH of 1 to 3, the stomach has a number of protective factors in place to prevent ulcer formation, even with acid over-secretion. The lining of the stomach and duodenum is covered by a layer of mucous called mucin. Other protective factors include the constant renewal of intestinal cells and the secretion of factors that neutralize acid when it contacts the stomach or intestinal lining.

Peptic ulcers occur when the protective factors that line the stomach or duodenum are damaged. Historically it was thought that over-secretion of stomach acid was the culprit. Current theories, however, focus on Helicobacter pylori infection and non-steroidal anti-inflammatory drug (NSAID) use, such as acetylsalicylic acid, et cetera. Smoking, alcohol consumption, nutrient deficiencies, stress, food allergies, and steroid use can also compromise the protective factors.

H. pylori infects 50% of the population over the age of fifty. This bacterium is found in 91% to 100% of people with duodenal ulcers and 70% of people with gastric ulcers. Factors that contribute to H. pylori infection include decreased gastric acid secretion and low antioxidant content of the gastrointestinal (GI) lining.

NSAID use is associated with an increased risk of developing a peptic ulcer. Daily use of aspirin and other NSAIDs is often prescribed for the prevention of heart attack and stroke. This can also increase the risk of GI bleeding from a peptic ulcer.

Smoking plays a significant role in the occurrence and severity of peptic ulcers. Smoking increases peptic ulcer frequency, decreases response to therapy, and increases the chance of dying due to complications of peptic ulcers. Smoking increases the back-flow of bile into the stomach, which irritates the lining of both the stomach and duodenum. Bicarbonate secretion by the pancreas (to neutralize gastric acid) also decreases, while the passage of food from the stomach to duodenum increases. In addition, the chronic anxiety and psychological stress associated with smoking often increase the severity of ulcers.

NSAID use combined with smoking further complicates matters. The NSAID causes the ulcer, while smoking stimulates gastric output to worsen symptoms and severity.

Stress seems to play a role in the development of peptic ulcers. The amount of stress a person is under is not as important as how they deal with the stress. It is often found that people who repress their emotions may have an increase in incidence of peptic ulcers.

Food allergies can also cause peptic ulcers and milk consumption tends to lead to a number of problems. Pasteurized milk increases stomach acid secretion and higher milk consumption has been associated with a higher incidence of peptic ulcer formation. This is rather paradoxical, considering many people find symptomatic relief of peptic ulcers after drinking a glass of milk.