Disorders of the Stomach
Gastritis—Inflammation of the Gastric Mucosa. Mild to moderate chronic gastritis isexceedingly common in the population as a whole, especially in the middle to later years of adult life.
The inflammation of gastritis may be only superficial and therefore not very harmful, or it can penetrate deeply into the gastric mucosa, in many long-standing cases causing almost complete atrophy of the gastric mucosa. In a few cases, gastritis can be acute and severe, with ulcerative excoriation of the stomach mucosa by the stomach’s own peptic secretions.
Research suggests that much gastritis is caused by chronic bacterial infection of the gastric mucosa. This often can be treated successfully by an intensive regimen of antibacterial therapy.
In addition, certain ingested irritant substances can be especially damaging to the protective gastric mucosal barrier—that is, to the mucous glands and to the tight epithelial junctions between the gastric lining cells— often leading to severe acute or chronic gastritis. Two of the most common of these substances are excesses of alcohol or aspirin.
Gastric Barrier and Its Penetration in Gastritis. Absorp-tion of food from the stomach directly into the blood is normally slight. This low level of absorption is mainly caused by two specific features of the gastric mucosa: (1) it is lined with highly resistant mucous cells that secrete a viscid and adherent mucus and (2) it has tight junctions between the adjacent epithelial cells. These two together plus other impediments to gastric absorp-tion are called the “gastric barrier.”
The gastric barrier normally is resistant enough to dif-fusion so that even the highly concentrated hydrogen ions of the gastric juice, averaging about 100,000 times the concentration of hydrogen ions in plasma, seldom diffuse even to the slightest extent through the lining mucus as far as the epithelial membrane itself. In gas-tritis, the permeability of the barrier is greatly increased. The hydrogen ions do then diffuse into the stomach epithelium, creating additional havoc and leading to a vicious circle of progressive stomach mucosal damage and atrophy. It also makes the mucosa susceptible to digestion by the peptic digestive enzymes, thus fre-quently resulting in gastric ulcer.
Gastric Atrophy. In many people who have chronic gas-tritis, the mucosa gradually becomes more and more atrophic until little or no gastric gland digestive secre-tion remains. It is also believed that some people develop autoimmunity against the gastric mucosa, this also leading eventually to gastric atrophy. Loss of the stomach secretions in gastric atrophy leads to achlorhy-dria and, occasionally, to pernicious anemia.
Achlorhydria (and Hypochlorhydria). Achlorhydriameans simply that the stomach fails to secrete hydrochloric acid; it is diagnosed when the pH of the gastric secretions fails to decrease below 6.5 after maximal stimulation. Hypochlorhydria means dimin-ished acid secretion. When acid is not secreted, pepsin also usually is not secreted; even when it is, the lack of acid prevents it from functioning because pepsin requires an acid medium for activity.
Pernicious Anemia in Gastric Atrophy. Perniciousanemia is a common accompaniment of gastric atrophy and achlorhydria. Normal gastric secretions contain a glycoprotein called intrinsic factor, secreted by the same parietal cells that secrete hydrochloric acid. Intrinsic factor must be present for adequate absorption of vitamin B12 from the ileum. That is, intrinsic factor com- bines with vitamin B12 in the stomach and protects it from being digested and destroyed as it passes into the small intestine. Then, when the intrinsic factor–vitamin B12 complex reaches the terminal ileum, the intrinsic factor binds with receptors on the ileal epithelial surface. This in turn makes it possible for the vitamin B12 to be absorbed.
In the absence of intrinsic factor, only about 1/50 of the vitamin B12 is absorbed. And, without intrinsic factor, an adequate amount of vitamin B12 is not made available from the foods to cause young, newly forming red blood cells to mature in the bone marrow. The result is pernicious anemia.