I. Structure and Innervation of the Gastrointestinal Tract
A. Structure of the gastrointestinal (GI) tract (Figure 6-1)
1* Epithelial cells
- are specialized in different
of the GI tract for secretion or ab-
2. Muscularis mucosa
-Contraction causes a change in the
surface area for secretion or ab-
3. Circular muscle
- Contraction causes a decrease
of the lumen of the GI
4. Longitudinal muscle
- Contraction causes shortening of a segment of the GI tract.
5. Submucosal plexus (Meissner's plexus) and myenteric plexus
- comprise the enteric nervous system of the GI tract.
Figure 6-1. Structure of the gastrointestinal (Gi) tract.
- integrate and coordinate the
motility, secretory, and endocrine functions
B. Innervation of the GI tract
- The autonomic nervous system (ANS)
the GI tract comprises both extrin-
1. Extrinsic innervation
(parasympathetic and sympathetic ner-
- Efferent fibers carry
information from the brain stem and spinal cord
-Afferent fibers carry
information from chemoreceptors and
a. Parasympathetic nervous system
- is usually excitatory on the functions of the GI tract.
- is carried via the vagus and pelvic nerves.
- Preganglionic parasympathetic
fibers synapse in the myenteric and
- Cell bodies in the ganglia of
plexuses then send information to
(1) The vagus
esophagus, stomach, pancreas,
- Reflexes in which both afferent
efferent pathways are con-
(2) The pelvic
innervates the lower large intestine, rectum,
b. Sympathetic nervous system
- is usually inhibitory on the functions of the GI tract.
- Fibers originate in the spinal cord between T-8 and L-2.
- Preganglionic sympathetic
cholinergic fibers synapse in the preverte-
- Postganglionic sympathetic
adrenergic fibers leave the prevertebral
- Cell bodies in the ganglia of
plexuses then send information to
2. Intrinsic innervation (enteric nervous system)
- coordinates and relays
from the parasympathetic and sympa-
- uses local reflexes to relay information within the GI tract.
- controls most functions of
tract, especially motility and secretion,
a. Myenteric plexus (Auerbach's plexus)
- primarily controls the motility of the GI smooth muscle.
b. Submucosal plexus (Meissner's plexus)
- primarily controls secretion and blood flow.
- receives sensory information
chemoreceptors and mechanorecep-
Regulatory Substances in the
Gastrointestinal Tract (Figure
A. GI hormones (Table 6-1)
- are released from endocrine
in the GI mucosa into the portal circulation,
- Four substances meet all of
requirements to be considered "official" GI
-contains 17 amino acids ("little gastrin")-
- Little gastrin is the form secreted in response to a meal.
- All of the biologic activity
gastrin resides in the four C-terminal
- "Big gastrin" contains
it is not a dimer of little
a. Actions of gastrin
(1) Increases H4 secretion by the gastric parietal cells- Gastrin is
far more potent than histamine in stimulating gastric H4 secretion.
(2) Stimulates growth
gastric mucosa and growth of mucosa
Figure 6-2. Gastrointestinal (GI) hormones, paracrines, and neurocrines.
Table 6-1. Summary of Gastrointestinal (GI) Hormones
CCK = cholecystokinin; GIP = gastric inhibitory peptide; GRP = gastrin-releasing peptide.
b. Stimuli for secretion of gastrin
- Gastrin is secreted from the G
of the gastric antrum in response
- Gastrin is secreted in response to the following:
(1) Small peptides and amino acids in the lumen of the stomach
- The most potent stimuli for
secretion are phenylalanine
(2) Distention of the stomach
(3) Vagal stimulation,
mediated by gastrin-releasing peptide
- Atropine does not block
mediated gastrin secretion be-
c. Inhibition of gastrin secretion
- H+ in the lumen
the stomach inhibits gastrin release. This
d. Zollinger-Ellison syndrome
- occurs when gastrin is secreted by non-p-cell tumors of the pancreas.
- contains 33 amino acids.
- is homologous to gastrin.
- The five C-terminal amino acids are the same in CCK and gastrin.
- The biologic activity of CCK resides in the C-terminal heptapeptide.
Thus, the heptapeptide contains the
sequence that is homologous to gas-
a. Actions of CCK
(1) Stimulates contraction
(2) Stimulates pancreatic enzyme secretion.
secretin-induced stimulation of pancreatic HC03~ se-
(4) Stimulates growth of the exocrine pancreas.
(5) Inhibits gastric
emptying. Thus, meals containing fat stimulate
b. Stimuli for the release of CCK
- CCK is released from the I
of the duodenal and jejunal
(1) Small peptides and amino acids
(2) Fatty acids and monoglycerides
- Triglycerides do not stimulate the
release of CCK because they
- contains 27 amino acids.
- is homologous to
the twenty-seven amino acids
- All of the amino acids are required for biologic activity.
a. Actions of secretin
- are coordinated to reduce the
amount of H+ in the lumen of the small
HC03" secretion and increases
(2) Stimulates HCCV and H20
(3) Inhibits H+ secretion by gastric parietal cells.
b. Stimuli for the release of secretin
- Secretin is released by the S cells of the duodenum in response to:
(1) H+ in the lumen of the duodenum
(2) Fatty acids in the lumen of the duodenum
- contains 42 amino acids.
- is homologous to secretin and glucagon.
a. Actions of GIP
release. In the presence of an oral glucose
(2) Inhibits H+
secretion by gastric parietal cells (as is implied in
b. Stimuli for the release of GIP
- GIP is secreted by the duodenum and jejunum.
- GIP is the only GI hormone
released in response to fat, protein,
- are released from endocrine cells in the GI mucosa.
- diffuse over short distances to act on target cells located in the GI tract.
- The GI paracrines are somatostatin and histamine.
-is secreted by cells throughout the
tract in response to H+ in the
- inhibits the release of all GI hormones.
- inhibits gastric H+ secretion.
- is secreted by mast cells of the gastric mucosa.
- increases gastric H+
secretion directly and by potentiating the effects
- are synthesized in neurons of
GI tract, moved by axonal transport down
- Neurocrines then diffuse across the synaptic cleft to a target cell.
-The GI neurocrines are vasoactive
- contains 28 amino acids and is homologous to secretin.
- is released from neurons in
mucosa and smooth muscle of the GI
-produces relaxation of GI smooth muscle.
- stimulates pancreatic HCCV
secretion and inhibits gastric H+
- is secreted by pancreatic
cell tumors and is presumed to mediate
2. GRP (bombesin)
- is released from vagus nerves that innervate the G cells.
Figure 6-3. Gastrointestinal
slow waves superimposed by action potentials. Action potentials produce
- stimulates gastrin release from G cells.
3* Enkephalins (met-enkephalin and leu-enkephalin)
- are secreted from nerves in
mucosa and smooth muscle of the GI
- stimulate contraction of
smooth muscle, particularly the lower
- inhibit intestinal
and electrolytes. This action forms
III. Gastrointestinal Motility
- Contractile tissue of the GI
is almost exclusively unitary smooth muscle,
- Depolarization of circular
leads to contraction of a ring of smooth
- Depolarization of longitudinal
leads to contraction in the longitudinal
- Phasic contractions occur
antrum, and small intes-
- Tonic contractions occur
sphincter, orad stomach,
A. Slow waves (Figure 6-3)
- are oscillating
potentials inherent to the smooth muscle
- are not action
potentials, although they determine the pattern of
1. Mechanism of slow wave production
- is the cyclic activation and
deactivation of the cell membrane Na+-K+
- Depolarization during each
wave brings the membrane poten-
- Action potentials, produced
of the background of slow waves, then
2. Frequency of slow waves
- varies along the GI tract,
constant and characteristic for each part
- is not influenced by neural
hormonal input. In contrast, the frequency
- sets the maximum frequency
contractions for each part of the
- is lowest in the stomach (3
highest in the
B. Chewing, swallowing, and esophageal peristalsis
- lubricates food by mixing it with saliva.
- decreases the size of food
particles to facilitate swallowing and to begin
- The swallowing reflex is coordinated
Fibers in the
- The following sequence of events is involved in swallowing:
a. The nasopharynx closes and, at the same time, breathing is inhibited.
b. The laryngeal
contract to close the glottis and elevate the
с Peristalsis begins in the
the food bolus toward
relaxes to permit the food bolus to enter the esophagus.
3* Esophageal motility
- The esophagus propels the swallowed food into the stomach.
- Sphincters at either end of
esophagus prevent air from entering the
- The upper one third of the esophagus is striated muscle.
- Because the esophagus is
the thorax, intraesophageal pressure
- The following sequence of
occurs as food moves into and down
a. As part of the swallowing reflex, the upper esophageal sphincter
relaxes to permit swallowed food to enter the esophagus.
b. The upper esophageal
then contracts so that food will not
с A primary peristaltic
contraction creates an area of high pressure
cL A secondary peristaltic
esophagus of any
e. As the food bolus
lower end of the esophagus, the lower
f. The orad region of the stomach relaxes ("receptive relaxation") to
allow the food bolus to enter the stomach.
4. Clinical correlations of esophageal motility
a. Gastric reflux
(heartburn) may occur if the tone of the lower esopha-
b. Achalasia may occur
the lower esophageal sphincter does not relax
С Gastric motility
- The stomach has three layers
smooth muscle—the usual longitudinal and
- The stomach has three anatomic divisions—the fundus, body, and antrum.
- The orad region of
fundus and the proximal body.
- The caudad region of
stomach includes the antrum and the distal body.
1. "Receptive relaxation"
- is a vagovagal
initiated by distention of the stomach and
- The orad region of the
relaxes to accommodate the in-
- CCK participates in
"receptive relaxation" by increasing the distensibil-
2. Mixing and digestion
- The caudad region of the
contracts to mix the food with gastric
a. Slow waves in
caudad stomach occur at a frequency of 3-5 waves/
b. If threshold is
during the slow waves, action potentials are
c. A wave of
contraction closes the distal antrum. Thus, as the caudad
are increased by vagal stimulation and de-
e. Even during fasting, contractions
3. Gastric emptying
- The caudad region of the
contracts to propel food into the duo-
a. The rate of gastric
is fastest if the stomach contents are
b. Fat inhibits gastric
gastric emptying time)
c. Н+ in the
inhibits gastric emptying via direct neural
D. Small intestinal motility
- The small intestine functions
the digestion and absorption of nutrients.
- As in the stomach, slow
basic electrical rhythm, which occurs
smooth muscle con-
1. Segmentation contractions
- mix the intestinal contents.
- A section of small intestine
contracts, sending the intestinal contents
- This back-and-forth
2. Peristaltic contractions
- are highly coordinated and propel
through the small intes-
- Contraction occurs behind
bolus and, simultaneously, relax-
- The peristaltic reflex is coordinated by the enteric nervous system.
3. Gastroileal reflex
- is mediated by the extrinsic ANS and possibly by gastrin.
- The presence of food in the
triggers increased peristalsis in the
Б. Large intestinal motility
- Fecal material moves from the
to the colon (i.e., through the ascending,
- Haustra, or sac-like
segments, appear after contractions of the large in-
1. Cecum and proximal colon
- When the proximal colon is
distended with fecal material, the ileocecal
proximal colon mix the contents
b. Mass movements occur
3 times/day and cause the colonic
2. Distal colon
- Because most colonic water
absorption occurs in the proximal colon, fecal
3. Rectum, anal canal, and defecation
- The sequence of events for defecation is as follows:
a. As the rectum fills with
material, it contracts and the internal anal
b. Once the
filled to about 25% of its capacity, there is an urge
с When it is convenient to
anal sphincter is
- Intra-abdominal pressure is
expiring against a closed
4. Gastrocolic reflex
- The presence of food in
stomach increases the motility of the colon
a. The gastrocolic
has a rapid parasympathetic component that
b. A slower, hormonal component is mediated by CCK and gastrin.
5. Disorders of large intestinal motility
a. Emotional factors
strongly influence large intestinal motility via the
disease), the absence of the co-
- A wave of reverse peristalsis
begins in the small intestine, moving the GI
-The gastric contents are eventually
pushed into the esophagus. If the upper
- The vomiting center in
medulla is stimulated by tickling the back
- The chemoreceptor trigger
in the fourth ventricle is activated
IV. Gastrointestinal Secretion (Table 6-2)
A. Salivary secretion
a. Initial starch
digestion by a-amylase (ptyalin) and initial triglyc-
b. Lubrication of ingested food by mucus
CCK = cholecystokinin; GIP = gastric inhibitory peptide.
с. Protection of the mouth
esophagus by dilution and buffering of
2. Composition of saliva
a. Saliva is characterized by:
(1) High volume (relative to the small size of the salivary glands)
(2) High K+ and HC03- concentrations
(3) Low Na+ and CI- concentrations
(5) Presence of a-amylase, lingual lipase, and kallikrein
b. The composition of saliva varies with the salivary flow rate (Figure 6-4).
(1) At the lowest flow
the lowest osmolarity and
(2) At the highest flow
4 ml/min), the composition of
3. Formation of saliva (Figure 6-5)
- Saliva is formed by three major
glands—the parotid, submaxillary,
Figure 6-4. Composition of saliva as a function of salivary flow rate.
Figure 6-5. Modification of saliva by ductal cells.
- The structure of
to a bunch of grapes. The acinus
- When saliva production is
stimulated, myoepithelial cells that line the
a. The acinus
- produces an initial saliva with a composition similar to plasma.
- This initial saliva is isotonic
and has the same Na+, K+, CI-, and HC03-
b. The ducts
- modify the initial saliva by the following processes:
(1) The ducts reabsorb Na+
and CI-; therefore, the concentrations
(2) The ducts secrete
and HC03-; therefore, the concentrations
(3) Aldosterone acts
ductal cells to increase the reabsorption
(4) Saliva becomes
hypotonic in the ducts because the ducts are
(5) The effect
on saliva composition is explained by
- Thus, at high flow rates,
most like the initial secretion
- At low flow rates, saliva
initial secretion from
-The only ion that does not "fit"
4. Regulation of saliva production (Figure 6-6)
- Saliva production is
the parasympathetic and sympathetic
- Saliva production is unique
it is increased by both parasympa-
a. Parasympathetic stimulation (cranial nerves VII and IX)
- increases saliva
transport processes in
- Cholinergic receptors on acinar and ductal cells are muscarinic.
Figure 6-6. Regulation of
secretion. ACh = acetylcholine; cAMP = cyclic adenosine monophosphate;
-The second messenger is inositol
- Anticholinergic drugs (e.g., atropine)
inhibit the production of saliva
b. Sympathetic stimulation
- increases the production
saliva and the growth of salivary
- Receptors on acinar and ductal cells are p-adrenergic.
-The second messenger is cyclic
с Saliva production
- is increased (via
activation of the parasympathetic nervous system)
- is decreased (via
inhibition of the parasympathetic nervous system)
B. Gastric secretion
1. Gastric cell types and their secretions (Table 6-3 and Figure 6-7)
Table 6-3. Gastric Cell Types and Their Secretions
Part of Stomach
Stimulus for Secretion
Vagal stimulation (ACh)
Vagal stimulation (ACh)
Vagal stimulation (via
Inhibited by somatostatin
Inhibited by H+ in
Vagal stimulation (ACh)
ACh = acetylcholine; GRP = gastrin-releasing peptide.
Gastrin - -
Figure 6-7. Gastric cell types and their functions.
- Parietal cells, located in the body, secrete HC1 and intrinsic factor,
- Chief cells, located in the body, secrete pepsinogen.
- G cells, located in the antrum, secrete gastrin.
2. Mechanism of gastric H+ secretion (Figure 6-8)
- Parietal cells secrete
the lumen of the stomach and, con-
a. In the parietal cells, C02
and H20 are converted to H+ and HC03~,
b. H+ is
the lumen of the stomach by the H+-K+ pump
- The drug omeprazole inhibits
H+,K+-ATPase and blocks H+ se-
с The HCO3" produced
absorbed into the bloodstream in
- If vomiting occurs,
gastric H+ never arrives in the small intestine,
3. Stimulation of gastric H+ secretion (Figure 6-9)
a. Vagal stimulation
- increases H+ secretion by a direct pathway and an indirect pathway.
- In the direct path, the vagus
- In the indirect path, the vagus
Figure 6-8. Simplified mechanism of H+ secretion by gastric parietal cells.
Figure 6-9. Agents and second
messengers that stimulate H+ secretion in gastric parietal
cells. ACh = acetylcho-
- Atropine, a
muscarinic antagonist, inhibits H+ secretion
- Vagotomy eliminates both pathways.
- is released from mast cells
gastric mucosa and diffuses to the
- stimulates H+
by activating H2 receptors on the parietal
- The second messenger for histamine is cAMP.
drugs, such as cimetidine, inhibit H+ secretion
- is released in response to
meal (small peptides, distention of
- stimulates H+
by interacting with an unidentified receptor
- The second messenger for
the parietal cell has not been
d. Potentiating effects of ACh,
histamine, and gastrin on H+ se-
- Potentiation occurs
the response to simultaneous administra-
- Potentiation of gastric H+
secretion can be explained, in part, because
(1) Histamine potentiates the actions of ACh and gastrin in
stimulating H+ secretion.
- Thus, H2 receptor
blockers (e.g., cimetidine) are particularly
(2) ACh potentiates the
of histamine and gastrin in
- Thus, muscarinic receptor
such as atropine, block both
4. Inhibition of gastric H+ secretion
- Negative feedback mechanisms
H+ by the pari-
a. Low pH (< 3.0) in the stomach
- inhibits gastrin secretion and thereby inhibits H+ secretion.
- After a meal is ingested, H+
secretion is stimulated by the mechanisms
b. Chyme in the duodenum
- inhibits H+ secretion both directly and via hormonal mediators.
- The hormonal mediators are GIP
fatty acids in the duode-
5. Pathophysiology of gastric H+ secretion
a* Gastric ulcers
- If the normal protective
the stomach is damaged, the pres-
- H+ secretion is decreased, not increased (as might be assumed).
- Gastrin levels are
feedback) in patients
b. Duodenal ulcers
- are more common than gastric ulcers.
- H+ secretion is
higher than normal and is responsible, along with
- Gastrin levels in response to a meal are higher than normal*
- Parietal cell mass is
the trophic effect of
c. Zollinger-Ellison syndrome
- occurs when a gastrin-secreting
- Н+ secretion
unabated because the gastrin secreted by pan-
6. Drugs that block H+ secretion are used in the treatment of ulcers
(see Figure 6-9).
- blocks H+
inhibiting cholinergic muscarinic receptors on
- blocks H2
thereby inhibits histamine stimulation of H+
- is particularly effective in
reducing H+ secretion because it not only
- directly inhibits H+,K+-ATPase and H+ secretion.
- contains a high concentration of HC03 , whose purpose is to neutralize the
acidic chyme that reaches the
1. Composition of pancreatic secretion
a. Pancreatic juice is characterized by:
(1) High volume
(2) Virtually the same Na+ and K+ concentrations as plasma
(3) Much higher HC03~ concentration than plasma
(4) Much lower CI" concentration than plasma
(6) Pancreatic lipase, amylase, and proteases
b. The composition of the
component of pancreatic secretion varies
Figure 6-10. Composition of pancreatic secretion as a function of pancreatic flow rate.
-At low flow rates, the
secretes an isotonic fluid that is
- At high flow rates, the
fluid that is
- Regardless of the flow rate, pancreatic secretions are isotonic.
2, Formation of pancreatic secretion (Figure 6-11)
- Like the salivary glands, the
exocrine pancreas resembles a bunch of
- The acinar cells of the exocrine pancreas make up most of its weight.
a. Acinar cells
- produce a small volume of
pancreatic secretion, which is mainly
b. Ductal cells
- modify the initial pancreatic
secretion by secreting HC03" and ab-
- Because the pancreatic ducts
water, H20 moves
3. Regulation of pancreatic secretion
- is secreted by the S cells of
duodenum in response to H+ in the
- acts on the pancreatic ductal cells to increase HC03~ secretion.
- Thus, when H+ is
delivered from the stomach to the duodenum, secretin
- The second messenger for secretin is cAMP.
- is secreted by the I cells of
duodenum in response to small peptides,
- acts on the pancreatic
cells to increase enzyme secre-
Figure 6-11. Modification of pancreatic secretion by ductal cells.
- potentiates the effect of
on ductal cells to stimulate HC03~
- The second messenger for CCK
is IP3 and increased intracellular
c. ACh (via vagovagal reflexes)
- is released in response to H+,
- stimulates enzyme
acinar cells and, like CCK,
4. Cystic fibrosis
- is a disorder of pancreatic secretion.
- results from a defect in CI"
channels that is caused by a mutation in the
- is associated with a deficiency
D. Bile secretion and gallbladder function (Figure 6-12)
1. Composition and function of bile
- Bile contains bile salts,
and bile pigments
a* Bile salts
- are amphipathic molecules
Figure 6-12. Recirculation of bile acids from the ileum to the liver. CCK = cholecystokinin.
- aid in the intestinal
absorption of lipids by emulsifying
- Above a critical micellar concentration, bile salts form micelles.
- Bile salts are positioned on
outside of the micelle, with their
- Free fatty acids and
are present in the inside of the
2. Formation of bile
- Bile is produced continuously by hepatocytes.
- Bile drains into the hepatic
and is stored in the gallbladder for
- Choleretic agents increase the formation of bile.
- Bile is formed by the following process:
a. Primary bile acids (cholic acid and chenodeoxycholic acid) are
synthesized from cholesterol by hepatocytes.
- In the intestine, bacteria
a portion of each of the primary bile
- Synthesis of new bile acids
as needed, to replace bile acids
b. The bile acids are
with glycine or taurine to form their
с Electrolytes and H20 are added to the bile.
d. During the interdigestive
the gallbladder is relaxed, the sphinc-
e. Bile is concentrated in
result of isosmotic reab-
3. Contraction of the gallbladder
- is released in response to small
and fatty acids in the
- tells the gallbladder that
needed to emulsify and absorb lipids
- causes contraction of the
gallbladder and relaxation of the
- causes contraction of the gallbladder.
4. Recirculation of bile acids to the liver
- The terminal ileum
Na+-bile acid cotransporter, which is a
- Because bile acids are not
recirculated to the liver until they reach the
- After ileal resection, bile
the liver, but
V. Digestion and Absorption (Table 6-4)
- Carbohydrates, protein, and
are digested and absorbed in the small in-
- The surface area for
the small intestine is greatly increased by
1. Digestion of carbohydrates
- Only monosaccharides are
absorbed. Carbohydrates must be di-
Table 6-4. Summary of Digestion and Absorption
a. a-Amylases (salivary
b. Maltase, a-dextrinase,
sucrase in the intestinal brush border
c. Lactase, trehalase,
sucrase degrade their respective disaccharides
- Lactase degrades lactose to glucose and galactose.
- Trehalase degrades trehalose to glucose.
- Sucrase degrades sucrose to glucose and fructose.
2. Absorption of carbohydrates (Figure 6-13)
a. Glucose and galactose
- are transported from the
lumen into the cells by Na+-depen-
- are then transported from cell to blood by facilitated diffusion.
- The Na+-K+
pump in the basolateral membrane keeps the intracellular
- Poisoning the Na+-K+
pump inhibits glucose and galactose absorption
- is transported exclusively by
facilitated diffusion; therefore, it cannot
3. Clinical disorders of carbohydrate absorption
- Lactose intolerance results
brush border lactase
1. Digestion of proteins
Figure 6-13. Mechanism of
absorption of monosaccharides by intestinal epithelial cells. Glucose
- degrade proteins by hydrolyzing interior peptide bonds.
- hydrolyze one amino acid at a
from the С terminus of proteins
- is not essential for protein digestion.
- is secreted as pepsinogen by the chief cells of the stomach.
- Pepsinogen is activated to pepsin by gastric H+.
- The optimum pH for pepsin is between 1 and 3.
- When the pH is > 5, pepsin
denatured. Thus, in the intestine, as
d. Pancreatic proteases
- include trypsin,
elastase, carboxypeptidase A, and car-
- are secreted in inactive
are activated in the small intestine
(1) Trypsinogen is activated
to trypsin by a brush border enzyme,
(2) Trypsin then converts
chymotrypsinogen, proelastase, and procar-
(3) After their digestive work
complete, the pancreatic proteases
2. Absorption of proteins (Figure 6-14)
- Digestive products of protein can
amino acids, dipep-
a. Absorption of free amino acids
cotransport occurs in the luminal mem-
Figure 6-14. Mechanism of
absorption of amino acids, dipeptides, and tripeptides by intestinal
- The amino acids are then
transported from cell to blood by facilitated
-There are four separate
acidic, basic, and
b. Absorption of dipeptides and tripeptides
- is faster than absorption of free amino acids.
cotransport of dipeptides and tripeptides also
- After the dipeptides and
tripeptides are transported into the intestinal
- The amino acids are then
transported from cell to blood by facilitated
1. Digestion of lipids
(1) In the
stomach, mixing breaks lipids into droplets to increase the
(2) Lingual lipases digest
triglycerides to mono-
(3) CCK slows gastric
emptying. Thus, delivery of lipids from the
b. Small intestine
(1) Bile acids emulsify
intestine, increasing the
(2) Pancreatic lipases hydrolyze
(3) The hydrophobic products
lipid digestion are solubilized in mi-
2. Absorption of lipids
a. Micelles bring the
products of lipid digestion into contact with the
b. In the intestinal
the products of lipid digestion are reesterified to
- Lack of apoprotein В results
inability to transport chylomicrons
c. Chylomicrons are
transported out of the intestinal cells by exocytosis.
3, Malabsorption of lipids—steatorrhea
- can be caused by any of the following:
a. Pancreatic disease (e.g.,
b. Hypersecretion of
gastric H+ secretion is increased
с Ileal resection, which
a depletion of the bile acid pool because
d. Bacterial overgrowth, which
e. Decreased number of
cells for lipid absorption (tropical
f. Failure to synthesize
apoprotein B, which leads to the inability to
D. Absorption and secretion of electrolytes and H20
- Electrolytes and H20
cells by either cellular
- Tight junctions attach
one another at the luminal
- The permeability of the tight
junctions varies with the type of epithelium.
1. Absorption of NaCl
a. Na+ moves into
intestinal cells, across the luminal membrane, and
(1) Passive diffusion (through Na+ channels)
(2) Na+-glucose or Na+-amino acid cotransport
(3) Na+-Cl" cotransport
(4) Na+-H+ exchange
-in the small intestine, Na+-glucose
- In the colon, passive
Na+ channels is most important.
b. Na+ is
out of the cell against its electrochemical gradient by
c. CI absorption
absorption throughout the GI tract by
(1) Passive diffusion by a paracellular route
(2) Na+-Cl" cotransport
2. Absorption and secretion of K+
a. Dietary K+
is absorbed in the small intestine by passive diffusion
b. K+ is actively secreted
by a mechanism similar to that
-As in the distal tubule, K+
secretion in the colon is stimulated by
- In diarrhea, K+
secretion by the colon is increased because of a flow
3. Absorption of H20
- is secondary to solute absorption.
- is isosmotic in the small
intestine and gallbladder. The mechanism
- In the colon, H20
in the small intestine,
4. Secretion of electrolytes and H20 by the intestine
- The GI tract also secretes electrolytes from blood to lumen.
-The secretory mechanisms are
the crypts. The absorptive
a. CI" is the primary ion
secreted into the intestinal lumen. It is
secreted into the lumen by passively following CI". H20
с Vibrio cholerae (cholera
causes diarrhea by stimulating CI"
- Cholera toxin binds to
the luminal membrane of crypt
- Intracellular cAMP increases;
result, CI" channels in the luminal
- Na+ and H20
lumen and lead to secretory di-
- Some strains of Escherichia
cause diarrhea by a similar mech-
E. Absorption of other substances
a. Fat-soluble vitamins (A,
are incorporated into micelles
b. Most water-soluble
by Na+-dependent co-
c. Vitamin B12
absorbed in the ileum and requires intrinsic
- The vitamin B12-intrinsic
receptor on the
- Gastrectomy results
loss of gastric parietal cells as the source
- absorption in the small
depends on the presence of adequate
- Vitamin D deficiency or
renal failure results in inadequate intesti-
- is absorbed as heme iron (iron
- Free Fe2+
the blood bound to transferrin, which trans-
- Iron deficiency is the most
cause of anemia.