Peptic ulcers are open sores that develop in the inside lining of the esophagus, stomach and upper portion of small intestine (duodenum) as a result of erosion from stomach acids. A peptic ulcer of the stomach is called a gastric ulcer of the duodenum, a duodenal ulcer; and of the esophagus, an esophageal ulcer. Peptic ulcers occur when the lining of these organs is corroded by the acidic digestive (peptic) juices which are secreted by the cells of the stomach. A peptic ulcer differs from erosion because it extends deeper into the lining of the esophagus, stomach, or duodenum and excites more of an inflammatory reaction from the tissues that are eroded. It is an ulcer of gastrointestinal tract at an area exposed to the acid pepsin mixture (APM). The mucosa of gastrointestinal tract (GIT) in this area is digested by pepsin (peptic digestion). It is most often caused by Helicobacter pylori infection. Vast majority of peptic ulcer occurs in
1. Stomach (Gastric ulcer).
2. First part of duodenum (Duodenal
3. Lower end of esophagus (as a result
of reflux from the stomach into the
: Peptic ulcer development
Components of Gastric Defense
A. Gastric mucus and bicarbonate
secretion by gastric mucosal cells: Gastric mucus forms a layer over the epithelium of mucosa. Mucosal cells of pyloric region secrete bicarbonate ions which remain in between the epithelial cells and the mucus and pH at this region is 6 or 7. In the luminalsurface of the mucus, the pH is low i.e. 2-3,
therefore the peptic activity is high,
digestion is possible. Near the epithelium, deep to the mucus layer, the pH is high therefore pepsin loses its activity.
Mechanical barrier offered by mucus
present over the surface of gastric
epithelium is an important component of defense. The mucus is thick and sticky, APM fails to penetrate it and no digestion of epithelial cells. Pepsin is big molecule and it requires good deal of space through which it transverse. Aspirin and non-steroidal anti- inflammatory agent can depolymerizes and causes loss of their stickiness and increases permeability to pepsin.
B. Presence of tight junction between epithelial cells of stomach and
duodenum: Presence of tight junction
between epithelial cells of stomach and
duodenum restrict the entry of material but high acidity of aspirin is better absorbed in stomach and damage the tight junction leads to peptic ulceration.
Components of Aggressive Mechanism:
1. Helicobacter pylori (H. Pylori): It is
gram –ve bacteria found in gastric and
duodenal mucosa of most person, particularly elderly. They, while in the
mucosa, split urea into ammonia and thus elevate the local pH and damage the local region of the mucosa by high alkalinity. In this way, they strongly help the peptic ulcer development (PUD).
2. Acid: Hydrochloric acid (HCl) is
secreted by the parietal cells of the gastric glands. Excess acid production from gastrinomas (it is a tumor in the pancreas or duodenum that secretes excess of gastrin leading to ulceration), tumors of parietal cells of stomach increases acid output.
3. Non-steroidal anti-inflammatory
drugs (NSAID): Non-steroidal anti- inflammatory drugs, such as aspirin, naproxen, ibuprofen, and many pain medications can irritate or inflame the lining of stomach and small intestine. Even safety coated aspirin and aspirin in powered form can frequently cause ulcers.
4. Stress: Emotional stress is no longer thought to be a cause of ulcers, however, people with ulcers often report that emotional stress increases ulcer pain. Physical stress may increase the risk of developing ulcers, particularly in the stomach. For example, people with injuries, such as severe burns, and people undergoing major surgery often require