Chapter 23
The Digestive System
869
23
danger posed by ulcers is perforation of the stomach wall, lead-
ing to peritonitis and, perhaps, massive hemorrhage.
For years, ulcers were blamed on factors that increased
HCl production or reduced mucus secretion, including aspi-
rin and nonsteroidal anti-inflammatory drugs (NSAIDs such
as ibuprofen), smoking, spicy food, alcohol, coffee, and stress.
Although acid conditions
are
necessary for ulcers to form, acid-
ity in itself is not sufficient to cause them. Ninety percent of
recurrent ulcers are the work of a certain strain of acid-resistant,
corkscrew-shaped
Helicobacter pylori
bacteria (Figure 23.16b),
which burrow like a drill bit through the mucus and destroy
the protective mucosal layer, leaving denuded areas. Even more
troubling are studies that link this bacterium to some stomach
cancers.
More than half of the population harbors
H. pylori
, but these
pathological effects occur in only 10–20% of infected individu-
als. Te antimicrobial activity of gastric mucin appears to pro-
tect most of us from
H. pylori
’s invasive attacks.
A breath test can easily detect the presence of
H. pylori
. A
simple two-week-long course of antibiotics kills the embedded
bacteria, promotes healing of the ulcers, and prevents recur-
rence. For active ulcers, a blocker for H
2
(histamine) receptors
may also help because it inhibits HCl secretion by blocking his-
tamine’s effects.
Te relatively few peptic ulcers not caused by
H. pylori
gener-
ally result from long-term use of NSAIDs. In such noninfectious
cases, H
2
-receptor blocker drugs such as cimetidine (±agamet)
and ranitidine (Zantac) are the therapy of choice.
Check Your Understanding
24.
What structural modification of the stomach wall underlies
the stomach’s ability to mechanically break down food?
25.
Two substances secreted by cells of the gastric glands are
needed to produce the active protein-digesting enzyme
pepsin. What are these substances and which cells secrete
them?
26.
Which protective substances or activities make up the so-
called mucosal barrier?
For answers, see Appendix H.
Digestive Processes in the Stomach
Explain how gastric secretion and stomach motility are
regulated.
Define and account for the alkaline tide.
Except for ingestion and defecation, the stomach is involved
in the whole “menu” of digestive activities. Besides serving as
a holding area for ingested food, the stomach continues the
demolition job begun in the oral cavity by further degrading
food both physically and chemically. It then delivers chyme, the
product of its activity, into the small intestine.
Protein digestion begins in the stomach and is the main type
of enzymatic breakdown that occurs there. HCl produced by
stomach glands denatures dietary proteins in preparation for
gastric pits join the gastric glands. Te stomach surface epi-
thelium of mucous cells is completely renewed every three to
six days, but the more sheltered glandular cells deep within
the gastric glands have a much longer life span.
Homeostatic Imbalance
23.8
Anything that breaches the gel-like mucosal barrier causes in-
flammation of the stomach wall, a condition called
gastritis
.
Persistent damage to the underlying tissues can promote
peptic
ulcers
, specifically called
gastric ulcers
when they are erosions
of the stomach wall
(Figure 23.16a)
. Te most distressing
symptom of gastric ulcers is gnawing epigastric pain that seems
to bore through to your back. Te pain typically occurs 1–3
hours a²er eating and is o²en relieved by eating again. Te
Bacteria
Mucosa
layer of
stomach
(a) A gastric ulcer lesion
(b)
H. pylori
bacteria
Figure 23.16
Photographs of a gastric ulcer and the
H. pylori
bacteria that most commonly cause it.
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