BIOL 2420 Lecture Notes - Lecture 8: Peptic Ulcer, Gastric Mucosa, Proton-Pump Inhibitor
26 Apr 2018
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Unit 9 – Lecture 8
The Stomach Balances Digestion and Defense
- Under normal conditions
o Gastric mucosa protects itself from autodigestion by acid and enzymes with a mucus-
bicarbonate barrier
- Mucous cells – on the luminal surface and in the neck of gastric glands secrete both substances
o Mucus forms a physical barrier
o Bicarbonate creates a chemical buffer barrier underlying the mucus
- Research shows that
o Bicarbonate layer just above the cell surface in the stomach has a pH that is close to 7
▪ Despite the pH in the lumen being highly acidic at pH 2
o Mucus secretion is increased when the stomach is irritated
▪ Like by the ingestion of aspirin or alcohol
- Failure of the mucus-bicarbonate barrier
o Zollinger-Ellison syndrome
▪ Patients secrete excessive levels of gastrin
• Usually caused by gastrin-secreting tumors in the pancreas
▪ Hyperacidity in the stomach overwhelms the normal protective mechanisms and
cause a peptic ulcer
• In peptic ulcers, acid and pepsin destroy the mucosa, creating holes that
extend into the submucosa and muscularis of the stomach and duodenum
o Acid reflux into the esophagus can erode the mucosal layer here
- Excess acid secretion (dyspepsia) is an uncommon cause of peptic ulcers
o The most common causes are nonsteroidal anti-inflammatory drugs (NSAIDs)
▪ Like aspirin
o Helicobacter pylori
▪ Bacterium that creates inflammation of the gastric mucosa
- Primary therapy for excess acid secretion (dyspepsia) was ingestion of antacids (agents
neutralizing acid in the gastric lumen)
o Molecular biologists discovered the mechanism for acid secretion by parietal cells
▪ The potential for new therapies become obvious
- Today there are 2 classes of drugs used for therapy of dyspepsia
o H2 receptor antagonists
o Proton pump inhibitors that block the H+-K+-ATPase
Integrated Function: The Intestinal Phase
- Once chyme passes into the small intestine the intestinal phase of digestion begins
- Chyme entering the small intestine has undergone relatively little chemical digestion
o Entry must be controlled to avoid overwhelming the small intestine
o Motility in the small intestine is also controlled
- Intestinal contents are slowly propelled forward by a combination of segmental and peristaltic
contractions
o Mixes chyme with enzymes and expose digested nutrients to the mucosal epithelium for
absorption
- Forward movement of chyme through the intestine must be slow enough to allow digestion and
absorption to go to completion
o Parasympathetic innervation and the GI hormones gastrin and CCK promote intestinal
motility
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Document Summary
Under normal conditions: gastric mucosa protects itself from autodigestion by acid and enzymes with a mucus- bicarbonate barrier. Mucous cells on the luminal surface and in the neck of gastric glands secrete both substances: mucus forms a physical barrier, bicarbonate creates a chemical buffer barrier underlying the mucus. Failure of the mucus-bicarbonate barrier: zollinger-ellison syndrome, patients secrete excessive levels of gastrin, usually caused by gastrin-secreting tumors in the pancreas, hyperacidity in the stomach overwhelms the normal protective mechanisms and cause a peptic ulcer. In peptic ulcers, acid and pepsin destroy the mucosa, creating holes that extend into the submucosa and muscularis of the stomach and duodenum: acid reflux into the esophagus can erode the mucosal layer here. Excess acid secretion (dyspepsia) is an uncommon cause of peptic ulcers: the most common causes are nonsteroidal anti-inflammatory drugs (nsaids, like aspirin, helicobacter pylori, bacterium that creates inflammation of the gastric mucosa.
