141

15: THE DIGESTION AND ABSORPTION OF FOOD

We are what we eat. This straightforward topic is interesting and relatively easy to teach.
This chapter goes into considerable mechanistic detail, which can be simplified if
warranted by time constraints.

Introduction
Teaching/Learning Objectives:
Students should be able to:
describe the composition of the gastrointestinal (GI) tract and the GI system.
list the four processes that accomplish the functions of the digestive system.

Overview: Functions of the Gastrointestinal Organs

Teaching/Learning Objectives:
Students should be able to:
describe the contributions of the mouth to the digestive process.
list the four functions of saliva.
recognize that the pharynx and esophagus conduct ingested material to the stomach.
describe the contributions of the stomach to the digestive process.
list the functions of the gastric secretions.
describe the contributions of the small intestines to the digestive process.
list the exocrine glands that empty into the small intestines, their respective
secretions, and their functions.
describe the contributions of the large intestines to the digestive process.
appreciate the volume of fluids secreted by these organs in the course of digesting
and absorbing food.

Structure of the Gastrointestinal Tract Wall

Teaching/Learning Objectives:
Students should be able to:
describe the structure of the GI tract wall from the mucosa, submucosa, muscularis
externa, and the serosa. Know what kinds of cells are found in these layers.
define villi, microvilli, brush border, and lacteal.
understand the importance of a large luminal surface area for intestinal function.
contrast how materials that enter lacteals and materials that enter the intestinal
capillaries reach the general circulation.
describe the role of Peyer's patches in the immune functions of the GI tract.

Digestion and Absorption

Teaching/Learning Objectives:
Students should be able to:
state the enzymes involved in carbohydrate digestion and where they are produced.
Describe the mechanism of carbohydrate absorption in the small intestine.
142 Instructor’s Manual for Vander’s Human Physiology, 10e

state the enzymes involved in protein digestion and where they are produced.
Describe the mechanisms in which proteins or their digestion products can be
absorbed from the small intestine.
describe the process of fat emulsification. State the sources of the emulsifiers.
Understand the importance of this process for efficient fat digestion.
discuss the properties of micelles and their role in fat absorption.
discuss the fate of the free fatty acids and monoglycerides that diffuse into intestinal
epithelial cells.
describe the properties of chylomicrons.
contrast the absorption of water-soluble and water-insoluble vitamins. Know the
function and understand the importance of intrinsic factor.
discuss how salts and water are absorbed in the small intestine.
discuss the role of ferritin in iron absorption.

Regulation of Gastrointestinal Processes

Teaching/Learning Objectives:
Students should be able to:
recognize that the control mechanisms of the gastrointestinal system regulate
conditions in the lumen of the tract, not in the internal environment. Understand
that, with few exceptions, gastrointestinal control mechanisms are governed not by
the nutritional state of the body, but rather by the volume and composition of the
luminal contents.
list the four stimuli that initiate gastrointestinal reflexes.
describe the role of the enteric nervous system in the gastrointestinal reflexes.
Recognize that the neural reflexes can be either short or long. Know that the central
nervous system can influence gastrointestinal processes by way of the autonomic
nervous system.
list the four major hormones that are known to control gastrointestinal functions.
State the location of the cells that secrete them, the stimuli for their secretion, and
their major functions.
recognize that the neural and hormonal control of gastrointestinal functions is
divisible into three phases—cephalic, gastric, and intestinal. Understand that these
phases are named for the site at which various stimuli initiate the reflex, and not for
the sites of effector activity.
describe the sequence of events that occurs during swallowing (deglutition).
describe the mechanism of gastric acid secretion by parietal cells. Discuss how this
secretion is controlled during the three phases of control. Discuss why increasing
the protein content of a meal increases the amount of acid secreted.
name the site of pepsinogen secretion. Know how the inactive precursor is converted
to active pepsin and the adaptive value of secretion of such an enzyme in inactive
form. Appreciate that most of the factors that stimulate or inhibit gastric acid
secretion have the same effect on pepsinogen secretion.
describe how gastric motility affects the digestion of food in the stomach.
Understand that the basic electrical rhythm of the stomach smooth muscle is set by
 Chapter 15 143

pacemaker cells and that the force of contraction of the muscle is influenced by
hormones and neurotransmitters.
name the factors that stimulate and inhibit gastric emptying.
name the secretory products of the exocrine pancreas and the mechanisms
controlling their secretion. Describe how the inactive forms of the pancreatic
proteolytic enzymes are activated. Know the function of pancreatic bicarbonate in
the duodenum.
describe the major constituents of bile and their functions. Identify the constituents
that are destined to be excreted. Recognize the significance of the enterohepatic
circulation. Know how bile secretion is controlled. Know how bile flow into the
duodenum is controlled.
describe the different types of motility that occur in the small intestine, their
functions, and how they are controlled.
describe the functions of the large intestine and the bacteria inhabiting it. Discuss
the types of motility in the large intestine, and how they differ from those of the
small intestine. Understand the cause of flatus. Know the defecation reflex and how it
is consciously controlled.

Pathophysiology of the Gastrointestinal Tract

Teaching/Learning Objectives:
Students should be able to:
list the factors that normally prevent the stomach wall from being digested by acid
and proteolytic enzymes. Know the factors that may contribute to ulcer formation,
and the drugs used to treat ulcers.
describe the sequence of events that occurs during the vomiting reflex. Understand
the adaptive value of this reflex. Discuss the negative consequences of excessive
vomiting.
describe how gallstones are formed and the consequences of a gallstone blocking the
common bile duct.
know the cause and consequences of lactose intolerance.
differentiate between the causes of constipation and diarrhea. Understand the
consequences of severe diarrhea.

LECTURE OUTLINE
I. Overview of the gastrointestinal (GI) system
A. Structures (GI tract plus glandular organs) (Figs. 15-1, 15-3)
B. Functions of the system: motility, secretion, digestion, and absorption (Figs. 15-2, 15-3)
II. GI tract wall
A. Functions of GI epithelial cells: endocrine and exocrine secretion (Fig. 15-6)
B. Mucosa of small intestine—specialized for absorption
III. Digestion and absorption of food
A. Carbohydrates
B. Proteins
C. Fats
1. Emulsification by bile salts (Fig. 15-9, 15-10)
144 Instructor’s Manual for Vander’s Human Physiology, 10e
2. Digestion by lipase and formation of micelles (Fig. 15-11)
3. Formation of chylomicrons and absorption into lacteals (Fig. 15-12)
IV. Regulation of GI processes
A. Neural regulation
B. Hormonal regulation
C. Phases of GI control (Figs. 15-20, 15-24)
D. Regulated processes: Functions of the
1. Mouth, pharynx, and esophagus (Figs. 15-14, 15-15)
2. Stomach (Fig. 15-16)
3. Small intestine
4. Pancreas
5. Liver
6. Large intestine
V. Pathophysiologies of the GI tract
CHAPTER 15 REVIEW QUESTIONS
1. List the four processes that accomplish the
functions of the gastrointestinal system.
Digestion, secretion, absorption, and motility.
2. List the primary functions performed by each of
the organs in the gastrointestinal system.
The mouth and pharynx: Chewing and the
initiation of the swallowing reflex.
Salivary glands: Secrete saliva, which moistens and
lubricates food and begins the digestion of
carbohydrates.
Esophagus: Moves food to the stomach by peristaltic
waves; secretes mucus for lubrication of food bolus.
Stomach: Stores, mixes, dissolves, and continues the
digestion of food; regulates the emptying of food into
the small intestine. Secretes HCl, which solubilizes
food particles and kills microbes; pepsin, a protein-
digesting enzyme; and mucus, which lubricates and
protects the epithelial surface.
Pancreas (exocrine portion): Secretes enzymes that
digest carbohydrates, fats, proteins, and nucleic
acids; and bicarbonate, which neutralizes the HCl
entering the small intestine from the stomach.
Liver: Secretes bile, which contains: bile salts, which
solubilize (emulsify) water-insoluble fats;
bicarbonate, which neutralizes HCl entering the
small intestine from the stomach; bilirubin and other
bile pigments that are waste products for excretion
in the feces; and many endogenous and foreign
organic molecules as well as trace metals for
excretion in the feces. Has many nondigestive
functions as well.
Gallbladder: Stores and concentrates bile between
meals.
Small intestine: Major site of digestion and
absorption of most substances; mixes and propels
contents. Produces digestive enzymes; secretes salt
and water to maintain fluidity of intestinal contents,
and mucus to provide lubrication.
Large intestine: Stores and concentrates undigested
matter; absorbs salt and water; mixes and propels
contents; performs defecation; secretes mucus for
lubrication.
3. Approximately how much fluid is secreted into
the gastrointestinal tract each day compared
with the amount of food and drink ingested?
How much of this appears in the feces?
Approximately 1500 ml of saliva, 2000 ml of gastric
secretions, 500 ml of bile, and 1500 ml of intestinal
secretions for a total of 7000 ml are secreted into the
GI tract each day, compared with the ingestion of
1200 ml of water and 800 g of food. All but 100 ml
of water and 50 g of solids is normally absorbed into
the blood; the remainder appears in the feces.
4. What structures are responsible for the large
surface area of the small intestine?
The intestinal mucosa is folded and has finger-like
projections called villi that extend from the luminal
surface. The surface of each villus is covered with a
layer of epithelial cells whose surface membranes
form small projections called microvilli. The
combination of folded mucosa, villi, and microvilli
increases the surface area of the small intestine
about 600-fold over that of a flat-surfaced tube
having the same length and diameter.
Chapter 15
5. Where does the venous blood go after leaving
the small intestine?
The venous drainage from the small intestine goes to
the liver via the hepatic portal vein. There it flows
through a second capillary network before leaving
the liver to return to the heart.
6. Identify the enzymes involved in carbohydrate
digestion and the mechanism of carbohydrate
absorption in the small intestine.
Digestible polysaccharides (starch and glycogen) are
broken down to maltose (glucose-glucose
disaccharides) by amylase, which is secreted by the
salivary glands and the pancreas. Maltose, along
with ingested sucrose (glucose-fructose) and
lactose (glucose-galactose), must be broken down to
monosaccharides by enzymes located on the luminal
membranes of the small-intestine epithelial cells.
The monosaccharides are then transported across the
intestinal epithelium into the blood. Fructose enters
the epithelial cells by facilitated diffusion, while
glucose and galactose undergo secondary active
transport coupled to sodium. These
monosaccharides all then leave the epithelial cells
and enter the blood by way of facilitated diffusion
transporters in the basolateral membranes of the
epithelial cells.
7. List three ways in which proteins or their
digestion products can be absorbed from the
small intestine.
1) The amino acids produced by the complete
digestion of protein in the small intestine enter the
epithelial cells by secondary active transport coupled
to sodium. There are multiple transporters with
different specificities for the 20 types of amino acids.
2) Short chains of two or three amino acids are also
absorbed by a secondary active-transporter that is
coupled to the hydrogen-ion gradient. Within the
epithelial cell, these di- and tripeptides are
hydrolyzed to amino acids, which then leave the cell
and enter the blood through a facilitated diffusion
carrier in the basolateral membranes.
3) Very small amounts of intact proteins are able to
cross the intestinal epithelium and gain access to the
interstitial fluid. They do so by a combination of
endocytosis and exocytosis. The absorptive capacity
for intact proteins is much greater in infants than in
adults.
8. Describe the process of fat emulsification.
The fats in ingested foods are insoluble in water and
aggregate into large lipid droplets in the upper
portion of the stomach. Since pancreatic lipase is a
water-soluble enzyme, its digestive action in the
small intestine can take place only at the surface of a
145
lipid droplet. If most of the ingested fat remained in
large lipid droplets, the rate of lipid digestion would
be very slow. The rate of digestion is substantially
increased by the process of emulsification, which is
the division of the large lipid droplets into much
smaller droplets, thereby increasing their surface
area and accessibility to lipase action.
The emulsification of fat requires (1) the
mechanical disruption of the large fat droplets into
smaller droplets and (2) an emulsifying agent, which
acts to prevent the smaller droplets from
reaggregating back into large droplets. The
mechanical disruption is provided by contractile
activity, occurring in the lower portion of the
stomach and in the small intestine. Phospholipids
in foods and phospholipids and bile salts secreted
in the bile provide the emulsifying agents.
Phospholipids and bile salts (which are formed
from cholesterol in the liver) are amphipathic
molecules. The nonpolar portions of these molecules
associate with the nonpolar interior of the lipid
droplets, leaving the polar portions of the
amphipathic molecules exposed at the water surface.
There they repel other lipid droplets that are
similarly coated with these emulsifying agents,
thereby preventing their reaggregation into larger
fat droplets.
The coating of the lipid droplets with these
emulsifying agents, however, impairs the
accessibility of the water-soluble lipase to its lipid
substrate. To overcome this problem, the pancreas
secretes a protein called colipase, which is
amphipathic and lodges on the lipid droplet surface.
Colipase binds the lipase enzyme, holding it on the
surface of the lipid droplet.
9. What is the role of micelles in fat absorption?
Micelles are similar in structure to emulsion
droplets but are much smaller. Micelles consist of
bile salts, fatty acids, monoglycerides, and
phospholipids all clustered together with the polar
ends of each molecule oriented toward the micelle’s
surface and the nonpolar portions forming the
micelle’s core.
Although fatty acids and monoglycerides have
an extremely low solubility in water, a few molecules
do exist in solution and are free to diffuse across the
lipid portion of the luminal plasma membranes of the
epithelial cells lining the small intestine. Micelles,
containing the products of fat digestion, are in
equilibrium with the small concentration of fat
digestion products that are free in solution. Thus,
micelles are continuously breaking down and
reforming. When a micelle breaks down, its contents
are released into the solution and become available to
diffuse across the intestinal lining. As the
146 Instructor’s Manual for Vander’s Human Physiology, 10e
concentrations of free lipids fall, because of their
diffusion into epithelial cells, more lipids are released
into the free phase as micelles break down. Thus, the
micelles provide a means of keeping most of the
insoluble fat-digestion products in small soluble
aggregates, while at the same time replenishing the
small amount of products that are free in solution
and able to diffuse into the intestinal epithelium.
10. Describe the movement of fat digestion
products from the intestinal lumen to a lacteal.
As described above, fatty acids and monoglycerides
leave the intestinal lumen and enter the intestinal
epithelial cells by diffusing through the lipid portion
of the cells’ luminal plasma membranes. Once inside
the cells, these fat digestion products are
resynthesized into triacylglycerols in the agranular
endoplasmic reticulum. This process lowers the
concentration of cytosolic free fatty acids and
monoglycerides and thus maintains a diffusion
gradient for these molecules into the cell. Within
this organelle, the resynthesized fat aggregates into
small droplets coated with amphipathic proteins that
perform an emulsifying function similar to that of
the bile salts.
The exit of these fat droplets from the cell follows
the same pathway as a secreted protein. Vesicles
containing the droplet pinch off the endoplasmic
reticulum, are processed through the Golgi
apparatus, and eventually fuse with the plasma
membrane, releasing the fat droplet into the
interstitial fluid. These extracellular fat droplets,
called chylomicrons, then pass into the
lacteals—the lymphatic capillaries in the intestinal
villi. Lacteals have large slit pores between their
endothelial cells through which the chylomicrons can
pass into the lymph.
11. How does the absorption of fat-soluble vitamins
differ from that of water-soluble vitamins?
The fat-soluble vitamins follow the same pathway for
absorption as do the products of fat digestion. They
are solubilized in micelles and are packaged with
triacylglycerols in the lipid droplets that become
chylomicrons.
Most water-soluble vitamins are absorbed by
diffusion or by mediated transport and pass through
the basolateral membrane of intestinal cells into the
capillaries. Vitamin B12 is different in that it is a
very large, charged molecule and, in order to be
absorbed, must first bind to a protein called intrinsic
factor that is secreted by the acid-secreting cells in
the stomach. Intrinsic factor with bound vitamin
B12 then binds to specific sites on the epithelial cells
in the lower portion of the ileum, where vitamin B12
is absorbed by endocytosis.
12. Specify two conditions that may lead to failure
to absorb vitamin B12.
Failure to absorb vitamin B12 would result from a
failure of the stomach cells to secrete intrinsic factor,
or from the surgical removal of the stomach or the
lower part of the ileum.
13. How are salts and water absorbed in the small
intestine?
Sodium ions, which are the most abundant solute in
chyme, are absorbed from the small (and large)
intestine by a primary active process. Following the
“downhill” entry of sodium from the lumen into the
epithelial cell via cotransport with other transported
solutes, Na, K-ATPase pumps located in the
basolateral membrane actively transport sodium out
of the cell. Chloride and bicarbonate ions are
absorbed with the sodium ions. Other minerals
present in smaller concentrations, such as
potassium, magnesium, and calcium, are also
absorbed by active transport.
Intestinal epithelial cells are very permeable to
water. Water follows the absorption of the salts
along the osmotic gradient that is set up by active
salt absorption.
14. Describe the role of ferritin in the absorption of
iron.
The iron ions that are actively transported into
intestinal epithelial cells are mostly incorporated into
ferritin, a protein-iron complex that functions as an
intracellular iron store. The absorbed iron that is
not bound to ferritin is released on the blood side
where it circulates throughout the body bound to the
plasma protein transferrin. Most of the iron bound
to ferritin in the epithelial cells is released back into
the intestinal lumen when the cells at the tips of the
villi disintegrate, and it is excreted in the feces.
Iron absorption depends on the body’s iron
content. When body stores are ample, the increased
concentration of free iron in the plasma and
intestinal epithelial cells leads to an increased
transcription of the gene coding for the ferritin
protein and thus an increased synthesis of ferritin.
This results in the increased binding of iron in the
intestinal epithelial cells and a reduction in the
amount of iron released into the blood. When the
body stores drop, the production and hence the
concentration of intestinal ferritin decreases, thereby
increasing the amount of unbound iron released into
the blood.
15. List the four types of stimuli that initiate most
gastrointestinal reflexes.
Chapter 15
1) Distention of the gastrointestinal tract wall by
the volume of the luminal contents.
2) Chyme osmolarity.
3) Chyme acidity.
4) Chyme concentration of specific digestion
products.
16. Describe the location of the enteric nervous
system and its role in both short and long
reflexes.
The enteric nervous system is composed of two nerve
networks, the myenteric plexus in the muscularis
externa, and the submucous plexus in the
submucosa of the gastrointestinal tract wall. These
neurons either synapse with other neurons in the
plexuses or end near smooth muscles, glands, and
epithelial cells—i.e., effector cells. This innervation
permits neural reflexes that are completely within
the tract. In addition, nerve fibers from both the
sympathetic and parasympathetic branches of the
autonomic nervous system enter the intestinal tract
and synapse with neurons in both plexuses. Via
these pathways, the CNS can influence the motility
and secretory activity of the gastrointestinal tract.
Thus, two types of neural reflex arcs exist: (1) short
reflexes from receptors through the nerve plexuses
to effector cells; and (2) long reflexes from receptors
in the tract to the CNS by way of afferent nerves and
back to the nerve plexuses and effector cells by way
of autonomic nerve fibers.
17. Name the four established gastrointestinal
hormones and state their major functions.
Gastrin: Stimulates acid secretion and motility of
the stomach (major functions) as well as its growth.
Also stimulates growth of the exocrine pancreas and
the small intestine, motility of the intestinal ileum,
and mass movement in the large intestine.
Cholecystokinin (CCK): Stimulates pancreatic
enzyme secretion, contraction of the gall bladder,
and the relaxation of the sphincter of Oddi. Inhibits
stomach acid secretion and motility (major
functions). Also potentiates the stimulation by
secretin of pancreatic and liver bicarbonate secretion,
and stimulates growth of the exocrine pancreas.
Secretin: Stimulates secretion of bicarbonate by the
pancreas and liver. Inhibits stomach acid secretion
and motility (major functions). Also potentiates
CCK’s stimulation of pancreatic enzyme secretion
and stimulates growth of the exocrine pancreas.
Glucose-dependent insulinotropic peptide (GIP):
Stimulates insulin secretion.
(A fifth hormone, somatostatin, inhibits the secretion
of gastric acid, histamine, and gastrin in the stomach
and the secretion of insulin and glucagon by the
endocrine pancreas.)
147
18. Describe the neural reflexes leading to
increased salivary secretion.
The secretion of saliva is controlled by both
sympathetic and parasympathetic neurons. Both
systems stimulate salivary secretion, with the
parasympathetics producing the greater response. In
the absence of food, a low rate of salivary secretion
keeps the mouth moist. In the presence of food,
salivary secretion increases markedly. This reflex
response is initiated by chemoreceptors and pressure
receptors in the walls of the mouth and on the
tongue. Stimulation of these receptors reflexly
activates, by way of afferent neurons, autonomic
neuronal input to the salivary glands, stimulating
increased salivary-gland blood flow and secretion of
saliva.
19. Describe the sequence of events that occur
during swallowing.
Swallowing (deglutition) is a complex reflex
initiated when pressure receptors in the walls of the
pharynx are stimulated by food or drink forced into
the rear of the mouth by the tongue. These receptors
send afferent impulses to the swallowing center in
the medulla oblongata. This center then elicits
swallowing via efferent fibers to the muscles in the
pharynx and esophagus as well as to the respiratory
muscles.
As the ingested material moves into the
pharynx, the soft palate is elevated and lodges
against the back wall of the pharynx, preventing food
from entering the nasal cavity. Impulses from the
swallowing center inhibit respiration, raise the
larynx, and close the glottis, keeping food from
moving into the trachea. As the tongue forces the
food farther back into the pharynx, the food tilts a
flap of tissue , the epiglottis, backward to cover the
closed glottis.
The esophageal phase of swallowing begins with
relaxation of the upper esophageal sphincter.
Immediately after the food has passed, the sphincter
closes, the glottis opens, and breathing resumes.
Once in the esophagus, the food is moved toward the
stomach by a progressive wave of muscle
contractions that proceeds along the esophagus,
compressing the lumen and forcing the food ahead of
it. These waves of contraction are called peristaltic
waves. The lower esophageal sphincter opens
and remains relaxed throughout the period of
swallowing, allowing the arriving food to enter the
stomach. After the food has passed, the sphincter
closes, resealing the junction between the esophagus
and the stomach.
148 Instructor’s Manual for Vander’s Human Physiology, 10e
20. List the cephalic, gastric, and intestinal phase
stimuli that stimulate or inhibit acid secretion
by the stomach.
Cephalic phase: The sight, smell, taste, and chewing
of food cause increased secretion of HCl by stomach
parietal cells.
Gastric phase: The distention of the stomach by the
volume of ingested material and the presence of
peptides and amino acids further stimulate gastric
acid secretion. Increased acid concentration inhibits
acid secretion in a negative-feedback manner.
Intestinal phase: Increased acid concentration,
osmolarity, and fatty acid and amino acid
concentrations in the duodenum and the distention
of it, all reflexly inhibit gastric acid secretion.
21. Describe the function of gastrin and the factors
controlling its secretion.
Gastrin stimulates the secretion of HCl by the
parietal cells of the stomach, and it also stimulates
the secretion of histamine. (Other functions of
gastrin are given in the answer to Question 7.) Its
secretion is stimulated by enteric neuron activity
responding to increased parasympathetic activity
and to gastric phase stimuli—i.e., increased luminal
distention and the presence of amino acids and
peptides in the stomach lumen. Gastrin secretion is
also stimulated directly by amino acids and peptides,
and is inhibited by HCl by way of somatostatin.
22. By what mechanism is pepsinogen converted to
pepsin in the stomach?
The acidity in the stomach’s lumen alters the shape
of the inactive precursor pepsinogen, exposing its
active site so that this site can act on other
pepsinogen molecules to break off a small chain of
amino acids from their ends. This cleavage converts
pepsinogen to pepsin, the fully active form.
23. Describe the factors that control gastric
emptying.
The factors that regulate acid secretion can also alter
gastric motility, and in the same direction. Thus,
gastrin in high concentration increases the force of
antral smooth-muscle contractions. Distension of
the stomach also increases the force of these
contractions through long and short reflexes
triggered by mechanoreceptors in the stomach wall.
In contrast, distension of the duodenum or the
presence of fat, high acidity, or hypertonic solutions
in its lumen all inhibit gastric emptying.
24. Describe the mechanisms controlling pancreatic
secretion of bicarbonate and enzymes.
The hormone secretin is the primary stimulant for
pancreatic bicarbonate secretion, and CCK is the
primary stimulant for the secretion of pancreatic
enzymes. These two hormones potentiate each
other’s actions. The major stimulus for secretin
release is increased acidity in the duodenum. The
major stimuli for CCK secretion are the presence of
fatty acids and amino acids in the duodenum.
25. How are pancreatic proteolytic enzymes
activated in the small intestine?
The inactive zymogens are activated by the
proteolytic enzyme trypsin, which is the active form
of the secreted trypsinogen. Tripsinogen is
activated to trypsin by the proteolytic enzyme
enterokinase, which is embedded in the luminal
plasma membranes of the intestinal epithelial cells.
26. List the major constituents of bile.
Bile contains: 1) bile salts; 2) lecithin, a
phospholipid; 3) bicarbonate ions and other salts;
4) cholesterol; 5) bile pigments and small amounts
of other metabolic end products; and 6) trace metals.
27. Describe the recycling of bile salts by the
enterohepatic circulation.
During the digestion of a fatty meal, most of the bile
salts entering the intestinal tract via the bile are
absorbed by specific sodium-coupled transporters in
the ileum. The absorbed bile salts are returned via
the hepatic portal vein to the liver, where they are
once again secreted into the bile. This recycling
pathway from the intestine to the liver and back to
the intestine is known as the enterohepatic
circulation.
28. What determines the rate of bile secretion by
the liver?
Bile-salt secretion is controlled by the concentration
of bile salts in the blood—the greater the plasma
concentration of bile salts, the greater their secretion
by the liver. Absorption of bile salts from the
intestine during the digestion of a meal leads to their
increased plasma concentration and thus to an
increased rate of bile salt secretion by the liver.
Some bile is always being secreted by the liver,
however.
29. Describe the effects of secretin and CCK on the
bile ducts and gall bladder.
CCK and, to a lesser extent, secretin stimulate the
gall bladder to contract, increasing bile flow into the
common bile duct, and the sphincter of Oddi
(hepatopancreatic duct sphincter) to relax,
allowing bile to flow from the common bile duct into
the duodenum.
Chapter 15
30. What causes water to move from the blood to
the lumen of the duodenum following gastric
emptying?
When the chyme entering the duodenum following
gastric emptying is hypertonic because of a high
concentration of solutes in the meal and because the
process of digestion breaks down large molecules into
many more smaller molecules, water will move the
lumen by osmosis from the isotonic plasma.
31. Describe the type of intestinal motility found
during and shortly after a meal and the type
found several hours after a meal.
The most common motion in the small intestine
during and shortly after a meal is a stationary
contraction and relaxation of intestinal segments,
with little apparent net movement toward the large
intestine. This rhythmical contraction and
relaxation of intestinal smooth muscle is called
segmentation, and allows for thorough mixing of
the chyme in the lumen and bringing it into contact
with the intestinal wall.
After most of a meal has been absorbed, the
segmenting contractions cease and are replaced by a
pattern of peristaltic activity called the migrating
motility complex. Beginning in the lower portion
of the stomach, repeated waves of peristaltic activity
travel about 2 ft along the small intestine and then
die out. This short segment of peristaltic activity
slowly migrates down the small intestine, taking
about 2 h to reach the large intestine. By the time
the migrating motility complex reaches the ilium,
new waves are beginning in the stomach, and the
process is repeated. Upon the arrival of a meal in the
stomach, the migrating motility complex rapidly
ceases in the intestine and is replaced by
segmentation.
32. Describe the production of flatus by the large
intestine.
Bacterial fermentation of undigested polysaccharides
in the colon produces flatus (gas), which is a mixture
of carbon dioxide, hydrogen, methane, and hydrogen
sulfide, and nitrogen from swallowed air.
33. Describe the factors that initiate and control
defecation.
The anus, the exit from the rectum, is normally
closed by the internal anal sphincter, which is
composed of smooth muscle, and the external anal
sphincter, which is composed of skeletal muscle
under voluntary control. The sudden distension of
the walls of the rectum produced by the mass
movement of fecal matter into it initiates the
neurally mediated defecation reflex.
149
The conscious urge to defecate, mediated by
mechanoreceptors, accompanies distension of the
rectum. The reflex 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 reflex
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 reflex signals
that eventually would relax the sphincter, thereby
keeping it closed and allowing a person to delay
defecation. In this case, the prolonged distension of
the rectum initiates a reverse peristalsis, driving the
rectal contents back into the sigmoid colon. The
urge to defecate then subsides until the next mass
movement again propels more feces into the rectum,
increasing its volume and again initiating the
defecation reflex.
34. Why is the stomach’s wall normally not
digested by the acids and digestive enzymes in
the lumen?
Several factors protect the walls of the stomach from
being digested, including:
1) The surface of the mucosa is lined with cells that
secrete highly alkaline mucus, which forms a thin
layer over the luminal surface. Both the protein
content of the mucus and its alkalinity neutralize
hydrogen ions in the immediate area of the
epithelium. Thus, the mucus forms a chemical
barrier between the highly acid 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 epithelial cells are replaced every few
days by new cells arising by the division of cells
within the gastric pits.
35. Describe the process of vomiting.
Vomiting is the forceful expulsion of the contents of
the stomach and upper intestinal tract through the
mouth. Vomiting is a complex reflex coordinated by
a region of the medulla oblongata called the vomiting
center. Neural input to this center from receptors in
many different regions of the body can initiate the
vomiting reflex. Vomiting is usually preceded by
increased salivation, sweating, increased heart rate,
pallor, and feelings of nausea. The events leading to
vomiting begin with a deep inspiration, closure of
the glottis, and elevation of the soft palate. The
abdominal muscles then contract, raising the
abdominal pressure, which is transmitted to the
150 Instructor’s Manual for Vander’s Human Physiology, 10e
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 can occur repeatedly
without expulsion via the mouth and is known as
retching. 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 from which
they can be expelled.
36. What are the consequences of blocking the
common bile duct with a gallstone?
When a gallstone blocks the common bile duct, bile is
prevented from entering the small intestine. The
absence of bile in the intestine decreases the rate of
fat digestion and absorption, so that about half of the
ingested fat is not digested and passes on to the large
intestine and eventually appears in the feces.
Furthermore, bacteria in the large intestine convert
some of this fat into fatty acid derivatives that alter
salt and water movements, leading to a net flow of
fluid into the large intestine. The result is diarrhea
and fluid loss.
Since 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 pancreatic secretions from
entering the intestine. This results in failure both to
neutralize acid and to digest adequately most
organic nutrients, not just fat. The end result is
severe nutritional deficiencies.
The build up of pressure in a blocked common
bile duct inhibits further secretion of bile. As a
result, bilirubin, which is normally secreted into the
bile from the blood, accumulates in the blood and
diffuses into tissues, where it produces the yellowish
coloration of the skin and eyes known as jaundice.
37. What are the consequences of the failure to
digest lactose in the small intestine?
Lactose is the major carbohydrate in milk. Lack of
lactase in the small intestine inhibits the digestion
of lactose to glucose and galactose, and thus lactose
cannot be absorbed. Since the absorption of water
requires prior absorption of solute to provide an
osmotic gradient, the unabsorbed lactose prevents
some of the water from being absorbed. This lactose-
containing fluid is passed on to the large intestine,
where bacteria digest the lactose. They then
metabolize the released monosaccharides, producing
large quantities of flatus (which distends the colon,
producing pain) and short-chain fatty acids, which
cause fluid movement into the large intestine,
producing diarrhea.
38. Contrast the factors that cause constipation with
those that produce diarrhea.
Decreased motility of the large intestine is the
primary factor causing constipation. The longer the
fecal material remains in the large intestine, the
more water is absorbed from it and the harder and
drier the feces become, making defecation more
difficult. Thus, constipation tends to promote
constipation.
Diarrhea can result from decreased fluid
absorption, increased fluid secretion, or both. The
response to lactose in a lactose-intolerant person is
one example of diarrhea caused by decreased fluid
absorption. A number of bacterial, protozoan, and
viral diseases of the intestinal tract cause secretory
diarrhea.