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.
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