The Digestion and Absorption of Food
557
antibiotics that inhibit other species of bacteria as well as the
disease-causing bacteria.
Other bacterial products include gas (
atus
), which is a
mixture of nitrogen and carbon dioxide, with small amounts of
the gases hydrogen, methane, and hydrogen sulfi de. Bacterial
fermentation of undigested polysaccharides produces these
gases in the colon (except for nitrogen, which is derived from
swallowed air), at the rate of about 400 to 700 ml/day.
Certain foods (beans, for example) contain large amounts of
carbohydrates that cannot be digested by intestinal enzymes
but are readily metabolized by bacteria in the large intestine,
producing large amounts of gas.
Motility and Defecation
Contractions of the circular smooth muscle in the large intes-
tine produce a segmentation motion with a rhythm consider-
ably slower (one every 30 min) than that in the small intestine.
Because of the slow propulsion of the large intestine contents,
material entering the large intestine from the small intestine
remains for about 18 to 24 h. This provides time for bacteria
to grow and multiply. Three to four times a day, generally fol-
lowing a meal, a wave of intense contraction known as a
mass
movement
spreads rapidly over the transverse segment of the
large intestine toward the rectum. This usually coincides with
the gastroileal refl ex. Unlike a peristaltic wave, in which the
smooth muscle at each point relaxes after the wave of con-
traction has passed, the smooth muscle of the large intestine
remains contracted for some time after a mass movement. The
large intestine is innervated by parasympathetic and sympathetic
nerves. Parasympathetic input increases segmental contractions,
whereas sympathetic input decreases colonic contractions.
The
anus,
the exit from the rectum, is normally closed
by the
internal anal sphincter,
composed of smooth muscle,
and the
external anal sphincter,
composed of skeletal muscle
under voluntary control. The sudden distension of the walls of
the rectum produced by the mass movement of fecal material
into it initiates the neurally mediated
defecation refl
ex.
The conscious urge to defecate, mediated by mechano-
receptors, accompanies distension of the rectum. The refl ex
response consists of a contraction of the rectum, relaxation of
the internal anal sphincter, but
contraction
of the external anal
sphincter (initially), and increased peristaltic activity in the
sigmoid colon. Eventually, a pressure is reached in the rectum
that triggers refl ex
relaxation
of the external anal sphincter,
allowing the feces to be expelled.
Brain centers can, however, via descending pathways to
somatic nerves to the external anal sphincter, override the refl ex
signals that eventually would relax the sphincter, thereby keep-
ing the external sphincter closed and allowing a person to delay
defecation. In this case, the prolonged distension of the rec-
tum initiates a reverse peristalsis, driving the rectal contents
back into the sigmoid colon. The urge to defecate then sub-
sides until the next mass movement again propels more feces
into the rectum, increasing its volume and again initiating
the defecation refl ex. Voluntary control of the external anal
sphincter is learned during childhood. Spinal cord damage
can lead to a loss of voluntary control over defecation.
Defecation is normally assisted by a deep breath, fol-
lowed by closure of the glottis and contraction of the abdomi-
nal and thoracic muscles, producing an increase in abdominal
pressure that is transmitted to the contents of the large intes-
tine and rectum. This maneuver (termed the Valsalva maneu-
ver) also causes a rise in intrathoracic pressure, which leads to
a transient rise in blood pressure followed by a fall in pressure
as the venous return to the heart is decreased. The cardiovas-
cular changes resulting from excessive strain during defecation
may precipitate a stroke or heart attack, especially in consti-
pated elderly people with cardiovascular disease.
Pathophysiology of the
Gastrointestinal Tract
Because the end result of gastrointestinal function is the absorp-
tion of nutrients, salts, and water, most malfunctions of this
organ system affect either the nutritional state of the body or
its salt and water content. The following are a few examples of
disordered gastrointestinal function.
Ulcers
Considering the high concentration of acid and pepsin secreted
by the stomach, it is natural to wonder why the stomach does
not digest itself. Several of the factors that protect the walls of
the stomach from being digested include: (1) The surface of the
mucosa is lined with cells that secrete a slightly alkaline mucus
that forms a thin layer over the luminal surface. Both the pro-
tein content of mucus and its alkalinity neutralize hydrogen
ions in the immediate area of the epithelium. Thus, mucus
forms a chemical barrier between the highly acidic contents of
the lumen and the cell surface. (2) The tight junctions between
the epithelial cells lining the stomach restrict the diffusion of
hydrogen ions into the underlying tissues. (3) Damaged epi-
thelial cells are replaced every few days by new cells arising by
the division of cells within the gastric pits.
At times, these protective mechanisms can prove inade-
quate, and erosion (
ulcers
) of the gastric surface can develop.
Ulcers can occur not only in the stomach but also in the lower
part of the esophagus and in the duodenum. Indeed, duode-
nal ulcers are about 10 times more frequent than gastric ulcers,
affecting about 10 percent of the U.S. population. Damage to
blood vessels in the tissues underlying the ulcer may cause bleed-
ing into the gastrointestinal lumen (
Figure 15–34
). On occa-
sion, the ulcer may penetrate the entire wall, resulting in leakage
of the luminal contents into the abdominal cavity. A device
used to diagnose gastric and duodenal ulcers is the
endoscope
(see Figure 15–34). This uses either fi beroptic or video tech-
nology to directly visualize the gastric and duodenal mucosa.
Furthermore, the endoscopist can apply local treatments and
take samples of tissue (
biopsy
) during upper endoscopy. Similar
devices can be used to visualize the colon (fl exible
sigmoidos-
copy
or
colonoscopy
) and the bronchi (
bronchoscopy
).
Ulcer formation involves breaking the mucosal barrier
and exposing the underlying tissue to the corrosive action of
acid and pepsin, but it is not always clear what produces the
initial damage to the barrier. Although acid is essential for
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