The Digestion and Absorption of Food
ulcers, the ulcers tend to recur if the
Helicobacter pylori
ria are not removed.
Despite popular notions, the role of stress in produc-
ing ulcers remains unclear. Once the ulcer has been formed,
however, emotional stress can aggravate it by increasing acid
Vomiting is the forceful expulsion of the contents of the stom-
ach and upper intestinal tract through the mouth. Like swal-
lowing, vomiting is a complex refl ex coordinated by a region
in the brainstem medulla oblongata, in this case known as the
vomiting center.
Neural input to this center from receptors
in many different regions of the body can initiate the vomit-
ing refl ex. For example, excessive distension of the stomach or
small intestine, various substances acting upon chemorecep-
tors in the intestinal wall or in the brain, increased pressure
within the skull, rotating movements of the head (motion sick-
ness), intense pain, and tactile stimuli applied to the back of
the throat can all initiate vomiting. The
area postrema
in the
brain, which is outside the blood-brain barrier, is sensitive to
toxins in the blood and can initiate vomiting. There are many
chemicals (
) that can stimulate vomiting via receptors
in the stomach, duodenum, or brain. A powerful household
emetic is
syrup of ipecac,
which stimulates vomiting by a dual
action on the enteric mucosa and the brain.
What is the adaptive value of this refl ex? Obviously,
the removal of ingested toxic substances before they can be
absorbed is benefi cial. Moreover, the nausea that usually accom-
panies vomiting may have the adaptive value of conditioning
the individual to avoid the future ingestion of foods contain-
ing such toxic substances. Why other types of stimuli, such as
those producing motion sickness, have become linked to the
vomiting center is not clear.
Vomiting is usually preceded by increased salivation,
sweating, increased heart rate, pallor, and nausea. The events
leading to vomiting begin with a deep breath, closure of the
glottis, and elevation of the soft palate. The abdominal mus-
cles then contract, raising the abdominal pressure, which is
transmitted to the stomach’s contents. The lower esophageal
sphincter relaxes, and the high abdominal pressure forces
the contents of the stomach into the esophagus. This initial
sequence of events, which can occur repeatedly without expul-
sion via the mouth, is known as
Vomiting occurs
when the abdominal contractions become so strong that the
increased intrathoracic pressure forces the contents of the
esophagus through the upper esophageal sphincter.
Vomiting is also accompanied by strong contractions in
the upper portion of the small intestine—contractions that tend
to force some of the intestinal contents back into the stomach
for expulsion. Thus, some bile may be present in the vomitus.
Excessive vomiting can lead to large losses of the water
and salts that normally would be absorbed in the small intes-
tine. This can result in severe dehydration, upset the body’s salt
balance, and produce circulatory problems due to a decrease
in plasma volume. The loss of acid from vomiting results in a
metabolic alkalosis (Chapter 14). A variety of antiemetic drugs
can suppress vomiting.
As described earlier, bile contains not only bile salts but also
cholesterol and phospholipids, which are water-insoluble and
are maintained in soluble form in the bile as micelles. When
the concentration of cholesterol in the bile becomes high in
relation to the concentrations of phospholipid and bile salts,
cholesterol crystallizes out of solution, forming
This can occur if the liver secretes excessive amounts of choles-
terol or if the cholesterol becomes overly concentrated in the
gallbladder as a result of salt and water absorption. Although
cholesterol gallstones are the most frequently encountered gall-
stones in the Western world, the precipitation of bile pigments
can also occasionally be responsible for gallstone formation.
Why some individuals develop gallstones and others do
not is still unclear. Women, for example, have about twice the
incidence of gallstone formation as men, and Native Americans
have a very high incidence compared with other ethnic groups
in the United States.
If a gallstone is small, it may pass through the common
bile duct into the intestine with no complications. A larger
stone may become lodged in the opening of the gallbladder,
causing painful contractile spasms of the smooth muscle. A
more serious complication arises when a gallstone lodges in
the common bile duct, thereby preventing bile from entering
the intestine. A large decrease in bile can decrease fat diges-
tion and absorption. Furthermore, impaired absorption of the
fat-soluble vitamins A, D, K, and E can occur, leading to, for
example, clotting problems (vitamin K defi ciency) and calcium
malabsorption (due to vitamin D defi ciency). The fat that is
not absorbed enters the large intestine and eventually appears
in the feces (a condition known as
). Furthermore,
bacteria in the large intestine convert some of this fat into
fatty acid derivatives that alter salt and water movements, lead-
ing to a net fl ow of fl uid into the large intestine. The result is
diarrhea and fl uid loss.
Because the duct from the pancreas joins the common
bile duct just before it enters the duodenum, a gallstone that
becomes lodged at this point prevents both bile and pancre-
atic secretions from entering the intestine. This results in
failure both to neutralize acid and to adequately digest most
organic nutrients, not just fat. The end result is severe nutri-
tional defi ciencies.
The buildup of very high pressure in a blocked common
bile duct is transmitted back to the liver and interferes with
the further secretion of bile. As a result, bilirubin, which is
normally secreted into the bile by uptake from the blood in
the liver, accumulates in the blood and diffuses into tissues,
producing a yellowish coloration of the skin and eyes known
It should be emphasized, however, that bile duct obstruc-
tion is not the only cause of jaundice. Bilirubin accumulation in
the blood can occur if hepatocytes are damaged by liver disease
and therefore fail to secrete bilirubin into the bile. It can also
occur if the level of bilirubin in the blood exceeds the capacity
of the normal liver to secrete it, as in diseases that result in an
increased breakdown of red blood cells—
hemolytic jaundice
At birth, the liver’s capacity to secrete bilirubin is not fully
developed. During the fi rst few days of life this may result
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