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PowerPoint® Lecture Slides
prepared by
Janice Meeking,
Mount Royal College
CHAPTER
23
The Digestive
System: Part B
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Pharynx
• Oropharynx and laryngopharynx
• Allow passage of food, fluids, and air
• Stratified squamous epithelium lining
• Skeletal muscle layers: inner longitudinal,
outer pharyngeal constrictors
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Esophagus
• Flat muscular tube from laryngopharynx to
stomach
• Pierces diaphragm at esophageal hiatus
• Joins stomach at the cardiac orifice
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Esophagus
• Esophageal mucosa contains stratified
squamous epithelium
• Changes to simple columnar at the stomach
• Esophageal glands in submucosa secrete
mucus to aid in bolus movement
• Muscularis: skeletal superiorly; smooth
inferiorly
• Adventitia instead of serosa
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(a)
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Mucosa
(contains a stratified
squamous epithelium)
Submucosa (areolar
connective tissue)
Lumen
Muscularis externa
• Longitudinal layer
• Circular layer
Adventitia (fibrous
connective tissue)
Figure 23.12a
Mucosa
(contains a stratified
squamous epithelium)
(b)
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Figure 23.12b
Go to GI Diseases (Esophagus)
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Digestive Processes: Mouth
• Ingestion
• Mechanical digestion
• Mastication is partly voluntary, partly reflexive
• Chemical digestion (salivary amylase and
lingual lipase)
• Propulsion
• Deglutition (swallowing)
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Deglutition
• Involves the tongue, soft palate, pharynx,
esophagus, and 22 muscle groups
• Buccal phase
• Voluntary contraction of the tongue
• Pharyngeal-esophageal phase
• Involuntary
• Control center in the medulla and lower pons
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Bolus of food
Tongue
Uvula
Pharynx
Bolus
Epiglottis
Epiglottis
Glottis
Trachea
Bolus
Esophagus
1 Upper esophageal sphincter is
contracted. During the buccal phase, the
tongue presses against the hard palate,
forcing the food bolus into the oropharynx
where the involuntary phase begins.
Relaxed muscles
2 The uvula and larynx rise to prevent food
from entering respiratory passageways. The
tongue blocks off the mouth. The upper
esophageal sphincter relaxes, allowing food
to enter the esophagus.
4 Food is moved
through the esophagus
to the stomach by
peristalsis.
Circular muscles
contract
Bolus of food
3 The constrictor muscles of the
pharynx contract, forcing food
into the esophagus inferiorly. The
upper esophageal sphincter
contracts (closes) after entry.
Relaxed
muscles
5 The gastroesophageal
sphincter opens, and food
enters the stomach.
Longitudinal muscles
contract
Gastroesophageal
sphincter closed
Gastroesophageal
sphincter opens
Stomach
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Figure 23.13
Bolus of food
Tongue
Pharynx
Epiglottis
Glottis
Trachea
1 Upper esophageal sphincter is contracted. During
the buccal phase, the tongue presses against the hard
palate, forcing the food bolus into the oropharynx
where the involuntary phase begins.
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Figure 23.13, step 1
Bolus
3 The constrictor muscles of the pharynx contract,
forcing food into the esophagus inferiorly. The upper
esophageal sphincter contracts (closes) after entry.
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Figure 23.13, step 3
Uvula
Bolus
Epiglottis
Esophagus
2 The uvula and larynx rise to prevent food from
entering respiratory passageways. The tongue blocks
off the mouth. The upper esophageal sphincter
relaxes, allowing food to enter the esophagus.
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Figure 23.13, step 2
Relaxed muscles
Circular muscles
contract
4 Food is moved through
the esophagus to the
stomach by peristalsis.
Bolus of food
Longitudinal muscles
contract
Gastroesophageal
sphincter closed
Stomach
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Figure 23.13, step 4
Relaxed
muscles
5 The gastroesophageal
sphincter opens, and food
enters the stomach.
Gastroesophageal
sphincter opens
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Figure 23.13, step 5
Bolus of food
Tongue
Uvula
Pharynx
Bolus
Epiglottis
Epiglottis
Glottis
Trachea
Bolus
Esophagus
1 Upper esophageal sphincter is
contracted. During the buccal phase, the
tongue presses against the hard palate,
forcing the food bolus into the oropharynx
where the involuntary phase begins.
Relaxed muscles
2 The uvula and larynx rise to prevent food
from entering respiratory passageways. The
tongue blocks off the mouth. The upper
esophageal sphincter relaxes, allowing food
to enter the esophagus.
4 Food is moved
through the esophagus
to the stomach by
peristalsis.
Circular muscles
contract
Bolus of food
3 The constrictor muscles of the
pharynx contract, forcing food
into the esophagus inferiorly. The
upper esophageal sphincter
contracts (closes) after entry.
Relaxed
muscles
5 The gastroesophageal
sphincter opens, and food
enters the stomach.
Longitudinal muscles
contract
Gastroesophageal
sphincter closed
Gastroesophageal
sphincter opens
Stomach
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Figure 23.13
Stomach: Gross Anatomy
• Cardiac region (cardia)
• Surrounds the cardiac orifice
• Fundus
• Dome-shaped region beneath the diaphragm
• Body
• Midportion
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Stomach: Gross Anatomy
• Cardiac region (cardia)
• Surrounds the cardiac orifice
• Fundus
• Dome-shaped region beneath the diaphragm
• Body
• Midportion
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Stomach: Gross Anatomy
• Pyloric region: antrum, pyloric canal, and pylorus
• Pylorus is continuous with the duodenum through the
pyloric valve (sphincter)
• Greater curvature
• Convex lateral surface
• Lesser curvature
• Concave medial surface
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Cardia
Esophagus
Muscularis
externa
• Longitudinal layer
• Circular layer
• Oblique layer
Lesser
curvature
Fundus
Serosa
Body
Lumen
Rugae of
mucosa
Greater
curvature
Duodenum
(a)
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Pyloric
Pyloric
canal
antrum
Pyloric sphincter
(valve) at pylorus
Figure 23.14a
Stomach: Gross Anatomy
• Lesser omentum
• From the liver to the lesser curvature
• Greater omentum
• Drapes from greater curvature
• Anterior to the small intestine
• The omenta have fat deposits and lots of
lymph nodes. The immune cells and
macrophages in the omenta police the
peritoneal cavity. The omenta can wall off
peritoneal infections.
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Greater and Lesser Omentums
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• ANS nerve supply to stomach
• Sympathetic via splanchnic nerves and celiac plexus
• Parasympathetic via vagus nerve
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• Blood supply to Stomach
• Celiac trunk – branches go to liver, stomach,
spleen, pancreas
• Veins of the hepatic portal system
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Inferior vena cava
(not part of hepatic
portal system)
Hepatic veins
Liver
Hepatic portal
vein
Small intestine
Gastric veins
Spleen
Inferior vena cava
Splenic vein
Right gastroepiploic
vein
Inferior
mesenteric vein
Superior
mesenteric vein
Large intestine
Rectum
(c) The hepatic portal circulation.
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Figure 19.29c
Diaphragm
Abdominal
aorta
Inferior
phrenic
arteries
Celiac Trunk
L. gastric artery
Common
hepatic
artery
Celiac
trunk
Splenic
artery
Middle
suprarenal
arteries
R. gastric
artery
Hepatic L
artery
proper
Gastroduodenal R
artery
R. gastroepiploic
artery
L. gastroepiploic artery
Middle Intestinal arteries
colic
artery
Superior
mesenteric
artery
R.
colic
artery
Renal
arteries
Gonadal
arteries
Ileocolic artery
Sigmoidal
arteries
Inferior
mesenteric
artery
L. colic
artery
Lumbar
arteries
(a) Schematic flowchart.
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Superior rectal
artery
Median sacral artery
Common iliac arteries
Figure 19.24a
Liver (cut)
Inferior vena cava
Diaphragm
Esophagus
Celiac trunk
Common hepatic
artery
Hepatic artery
proper
Gastroduodenal
artery
Right gastric artery
Gallbladder
Left gastric
artery
Stomach
Splenic artery
Pancreas
(major portion lies
posterior to stomach)
Right
gastroepiploic
artery
Superior
mesenteric
mesenteric
Duodenum
Abdominal aorta
Left
gastroepiploic
artery
Spleen
(b) The celiac trunk and its major branches. The left half of the liver has been removed.
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Figure 19.24b
Falciform ligament
Liver
Gallbladder
Spleen
Stomach
Ligamentum teres
Greater omentum
Small intestine
Cecum
(a)
The Ligamentum Teres Hepatis is the remnant of the umbilical vein
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Figure 23.30a
Stomach: Microscopic Anatomy
• Four tunics
• Muscularis and mucosa are modified
• Muscularis externa
• Three layers of smooth muscle
• Inner oblique layer allows stomach to churn,
mix, move, and physically break down food
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Liver
Gallbladder
Lesser omentum
Stomach
Duodenum
Transverse colon
Small intestine
Cecum
Urinary bladder
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(b)
Figure 23.30b
Surface
epithelium
Mucosa
Lamina propria
Submucosa
(contains submucosal
plexus)
Muscularis externa
(contains myenteric
plexus)
Serosa
Muscularis
mucosae
Oblique layer
Circular layer
Longitudinal
layer
(a) Layers of the stomach wall (l.s.)
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Stomach wall
Figure 23.15a
Stomach: Microscopic Anatomy
• Mucosa
• Simple columnar epithelium composed of
mucous cells – they produce a cloudy two
layer coat of alkaline mucus which the surface
layer consists of a viscous-insoluble mucus
that traps bicarbonate-rich fluid beneath it
• The smooth lining is lined with dotted Gastric
pits that lead into gastric glands that produce
the various gastric juices
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• The cells forming the walls of the gastric pits
are primarily mucous cells – but the gastric
gland cells differ in the different regions of the
stomach.
• Cardia (entrance) and pylorus (exit) are
primarily mucus secreting cells
• Pyloric Antrum produce mucus and hormones
(enteroendocrine cells)
• Fundus and body – where most chemical
digestion occurs produce the majority of
stomach secretions
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Gastric pits
Surface epithelium
(mucous cells)
Gastric
pit
Mucous neck cells
Parietal cell
Chief cell
Gastric
gland
Enteroendocrine cell
(b) Enlarged view of gastric pits and gastric glands
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Figure 23.15b
Gastric Glands
• Cell types
• Mucous neck cells (secrete thin, acidic mucus)
• Parietal cells
• Chief cells
• Enteroendocrine cells
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Pepsinogen
HCl
Pepsin
Mitochondria
Parietal cell
Chief cell
Enteroendocrine
cell
(c) Location of the HCl-producing parietal cells and
pepsin-secreting chief cells in a gastric gland
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Figure 23.15c
Gastric Gland Secretions
• Glands in the fundus and body produce most of the
gastric juice
• Parietal cell secretions
• HCl
•  pH 1.5–3.5 denatures protein in food, activates
pepsin, and kills many bacteria
• Intrinsic factor
• Glycoprotein required for absorption of vitamin B12
in small intestine
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Gastric Gland Secretions
• Chief cell secretions
• Inactive enzyme pepsinogen
• Activated to pepsin by HCl and by pepsin itself
(a positive feedback mechanism)
• Chief cells also secrete insignificant amounts
of gastric lipase
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Gastric Gland Secretions
• Enteroendocrine cells
• Secrete chemical messengers into the lamina
propria
• Paracrines
• Serotonin and histamine
• Hormones
• Somatostatin and gastrin
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Mucosal Barrier
• Layer of bicarbonate-rich mucus
• Tight junctions between epithelial cells
• Damaged epithelial cells are quickly replaced
by division of stem cells – that reside where
the gastric pits join the gastric glands.
• The surface epithelia are replaced every three
to six days
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Homeostatic Imbalance
• Gastritis: inflammation caused by anything
that breaches the mucosal barrier
• Peptic or gastric ulcers: erosion of the
stomach wall
• Most are caused by Helicobacter pylori
bacteria
• Go to GI Diseases PowerPoint
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Bacteria
Mucosa
layer of
stomach
(a) A gastric ulcer lesion
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(b) H. pylori bacteria
Figure 23.16
Digestive Processes in the Stomach
• Physical digestion
• Denaturation of proteins
• Enzymatic digestion of proteins by pepsin
(and rennin in infants)
• Secretes intrinsic factor required for
absorption of vitamin B12
• Lack of intrinsic factor  pernicious anemia
• Delivers chyme to the small intestine
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Regulation of Gastric Secretion
•
Gastric Secretion has three phases – (1) Cephalic (2)
Gastric and (3) Intestinal.
•
Some are more stimulatory – Cephalic and Gastric and one
is more inhibitory – Intestinal Phase
•
Neural (vagus and enteric plexus) and hormonal
mechanisms control the secretions
1. Cephalic (reflex) phase: last just a few minutes prior to
food entry into the stomach. It occurs even if you don’t
actually get the food – if you desire the food and are not
depressed or have a lack of appetite
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Gastric Phase
• Lasts approximately 3–4 hours after food
enters the stomach
• Stimuli for this phase is gastric distention,
peptides, and low acidity
• Gastric Distention activates stretch receptors
and initiates both local (myenteric) reflexes
and vagovagal – both stimulate acetylcholine
release
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Gastrin (1)
• Gastrin is secreted by G-cells in the Pyloric
Antrum in accordance with chemical stimuli and
neural stimuli
• The chemical stimuli for Gastrin secretion are
partially digested proteins, caffeine, and rising
alkaline pH. High acidity less than a pH of 2
inhibits Gastrin secretion
• Gastric stimulates release of enzymes, also
Histamine from the enterochromaffin cells – but
its main targets are the Parietal cells in body of
the stomach that secrete HCl- prodding them to
secrete increased amounts of HCl
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Gastrin (2)
• When protein products enter the stomach, the
pH generally rises due to the proteins
buffering H+.
• The rising pH stimulates Gastrin which causes
HCl to spew out thus denaturing the proteins.
The more proteins the more Gastrin.
• As proteins are decomposed the acidity rises
and Gastrin is inhibited
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Gastrin (3)
• In addition to G-cells being stimulated
chemically – they are also stimulated neurally.
The parasympathetic turns on secretion via
acetylcholine from the Vagus and
Sympathetic turns it off
• The vagus was activated in the Cephalic
Phase and Gastric Phase due to stomach
distention
• Emotional upset, fear, anxiety, and anything
that triggers the fight and flight response turns
off Gastric secretion.
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Stimulatory events
Cephalic
phase
Gastric
phase
1 Sight and thought
of food
Cerebral cortex
Conditioned reflex
2 Stimulation of
taste and smell
receptors
Hypothalamus
and medulla
oblongata
1 Stomach
distension
activates
stretch
receptors
Vagovagal
reflexes
1 Presence of low
pH, partially digested
foods, fats, or
hypertonic solution
in duodenum when
stomach begins to
empty
Stimulate
Inhibit
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Medulla
Vagus
nerve
Vagus
nerve
Local
reflexes
2 Food chemicals
G cells
(especially peptides and
caffeine) and rising pH
activate chemoreceptors
Intestinal
phase
Inhibitory events
Gastrin
release
to blood
Intestinal
(enteric)
gastrin
release
to blood
Lack of
stimulatory
impulses to
parasympathetic
center
Cerebral
cortex
Gastrin
secretion
declines
G cells
Overrides
parasympathetic
controls
Sympathetic
nervous
system
activation
1 Excessive
acidity
(pH <2)
in stomach
2 Emotional
upset
Stomach
secretory
activity
Enterogastric
reflex
Brief
effect
1 Loss of
appetite,
depression
Local
reflexes
Vagal
nuclei
in medulla
Pyloric
sphincter
1 Distension
of duodenum;
presence of
fatty, acidic,
hypertonic
chyme, and/or
irritants in
the duodenum
2 Distension;
Release of intestinal
presence of
hormones (secretin,
cholecystokinin, vasoactive fatty, acidic,
partially
intestinal peptide)
digested food
in the
duodenum
Figure 23.17
Regulation and Mechanism of HCl Secretion
• Three chemicals (ACh, histamine, and
gastrin) stimulate parietal cells through
second-messenger systems
• All three are necessary for maximum HCl
secretion
• Antihistamines block H2 receptors and
decrease HCl release
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Secondary Messenger Systems for HCl
release
• Acetylcholine and Gastrin increase
intracellular Calcium levels.
• Histamine released by the enterochromaffinlike cells in response to Gastrin and to a
lesser extent by Ach acts through the cyclic
AMP system.
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Blood
capillary
Chief cell
CO2
CO2 + H2O
Carbonic
H2CO3 anhydrase
H+
K+
Stomach lumen
H+-K+
ATPase
H+
K+
HCO3–
Alkaline
tide
HCI
Parietal cell
HCO3–
Cl–
Cl–
HCO3–- Cl–
antiporter
Cll–
Interstitial
fluid
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Figure 23.18
Regulation of Gastric Secretion
3. Intestinal phase: brief stimulatory effect as
partially digested food enters the duodenum,
followed by inhibitory effects (enterogastric
reflex and enterogastrones)
Some actions are excitatory and some are
inhibitory
As partially digested foods fill the initial part of the
small intestine (duodenum). This action
stimulates the release of intestinal Gastrin.
This stimulates the stomach to continue its
secretory activity. However, this action is
brief.
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• The action is brief due to the fact that as the intestines fill with
chyme containing large amounts of H+, fats, partially digested
proteins and various irritating substances, the inhibitory
component is triggered in the form of the enterogastric reflex
• The enterogastric reflex is a trio of reflexes that (1) inhibit the
vagal nuclei in the medulla (2) inhibit local reflexes and (3)
activate sympathetic fibers that cause the pyloric sphincter to
tighten and prevent further food entry.
• The purpose of this inhibitory action is to not fill the
duodenum with excess acidity and match the small intestines
processing time.
• Additionally there is a release of several intestinal hormones
– termed enterogastrones (Secretin, Cholecystokinin, and
Vasoactive Intestinal Peptide). All are inhibitory on the
stomach.
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Response of the Stomach to Filling
• Stretches to accommodate incoming food
• Reflex-mediated receptive relaxation
• Coordinated by the swallowing center of the
brain stem and mediated by the vagus
nerves acting on Serotonin and Nitric Oxide
releasing enteric neurons
• Gastric accommodation
• Plasticity (stress-relaxation response) of
smooth muscle
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• Small rippling waves in the body and fundus of
stomach where good (food storage) chemical digestion
occur
• Waves get stronger in pyloric antrum. The pyloric
region which holds about 30 cc of chyme acts as a
dynamic filter that allows only liquids and small
particles to pass through the barely open pyloric valve
during the digestive process.
• Normally each peristaltic wave reaching the pyloric
muscle squirts only 3 cc or less of chyme into the small
intestines. Because the contraction also closes the
pyloric valve, which is normally partially relaxed, the
rest (27 cc) goes back into the stomach to be better
mixed.
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Gastric Contractile Activity
• The intensity of peristaltic waves can be
changed but the rate is constant – about 3
waves per minute.
• Pacemaker cells (cells of Cajal) located in the
longitudinal muscle layer – automatically
depolarize and repolarize setting the cyclic
slow waves – also known as the Basic
electrical rhythm (BER)
• The smooth muscle cells are connected by
gap junctions to the rest of muscularis – the
waves are efficiently transmitted.
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• The pacemakers set the maximum rate of
contraction, but they do not initiate the
contractions or regulate the force.
• They generate subthreshold depolarization
waves, which are then ignited (enhanced by
further depolarization and brought to
threshold) by neural and hormonal factors.
• Factors that increase the strength of
contractions are the same factors that
enhance stomach secretions.
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Gastric Contractile Activity
• Most vigorous near the pylorus
• Chyme is either
• Delivered in ~ 3 ml spurts to the duodenum, or
• Forced backward into the stomach
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Pyloric
valve
closed
1 Propulsion: Peristaltic
waves move from the
fundus toward the
pylorus.
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Pyloric
valve
closed
2 Grinding: The most
vigorous peristalsis and
mixing action occur
close to the pylorus.
Pyloric
valve
slightly
opened
3 Retropulsion: The pyloric
end of the stomach acts as a
pump that delivers small
amounts of chyme into the
duodenum, simultaneously
forcing most of its contained
material backward into the
stomach.
Figure 23.19
Regulation of Gastric Emptying
• The stomach usually empties completely within 4
hours after a meal.
• The larger the meal (more stomach distention) and
the more liquid the meal is – the faster it empties.
• Fluids pass quickly through the stomach.
• Solids take longer in that they need to be processed
more
• The rate of gastric emptying depends not only on the
stomach but just as much on the small intestines
processing time. Too much release into the small
intestine (too much stretch) initiates the enterogastric
reflex.
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Gastric Emptying
• Carbohydrate-rich chyme moves quickly
through the duodenum
• Fatty chyme remains in the duodenum
6 hours or more
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Presence of fatty, hypertonic,
acidic chyme in duodenum
Duodenal enteroendocrine cells
Chemoreceptors and
stretch receptors
Secrete
Enterogastrones
(secretin,
cholecystokinin,
vasoactive intestinal
peptide)
Duodenal
stimuli
decline
Initial stimulus
Physiological response
Result
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Target
Via short
reflexes
Enteric
neurons
Contractile force and
rate of stomach
emptying decline
Via long
reflexes
CNS centers
sympathetic
activity;
parasympathetic
activity
Stimulate
Inhibit
Figure 23.20
Vomiting and Gastroparesis
• Vomiting is caused by many factors – with the
most common being extreme stretching of the
stomach and/or intestines. Other factors are
bacterial toxins, excessive alcohol, spicy
foods, and certain drugs.
• Both bloodborne molecules and sensory
impulses going to the emetic center in the
medulla initiate the events for vomiting.
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Gastroparesis
• Gastroparesis, also called delayed gastric
emptying, is a medical condition consisting of a
paresis (partial paralysis) of the stomach,
resulting in food remaining in the stomach for a
longer period of time than normal. Normally, the
stomach contracts to move food down into the
small intestine for digestion. The vagus nerve
controls these contractions. Gastroparesis may
occur when the vagus nerve is damaged and the
muscles of the stomach and intestines do not
work normally. Food then moves slowly or stops
moving through the digestive tract.
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Causes
• Gastroparesis may be chronic or transient; transient
gastroparesis may arise in acute illness of any kind, with the
use of certain cancer treatments or other drugs which affect
digestive action, or due to anorexia nervosa, bulimia and
other abnormal eating patterns.
• Chronic gastroparesis is frequently due to autonomic
neuropathy. This may occur in people with type 1 diabetes or
type 2 diabetes. The vagus nerve becomes damaged by
years of high blood glucose, resulting in gastroparesis.
Gastroparesis has also been associated with various
autoimmune diseases and syndromes, such as fibromyalgia
and Parkinson's disease, and may occur as part of a
mitochondrial disorder.
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Small Intestine: Gross Anatomy
• Major organ of digestion and absorption
•
2–4 m (20 feet long in cadaver but 7 -13 feet
long in living person); extends from pyloric
sphincter to ileocecal valve – approximately 200
square meters of surface area (doubles tennis
court)
•
Subdivisions
1. Duodenum (retroperitoneal) 10 inches
2. Jejunum (attached posteriorly by mesentery) 8
feet
3. Ileum (attached posteriorly by mesentery) 12 feet
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• The Ligament of Treitz (named after Václav
Treitz) connects the duodenum of the small
intestines to the diaphragm. It contains a
slender band of skeletal muscle from the
diaphragm and a fibromuscular band of
smooth muscle from the horizontal and
ascending parts of the duodenum. When it
contracts, the suspensory muscle of the
duodenum widens the angle of the
duodenojejunal flexure, allowing movement of
the intestinal contents
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Mouth (oral cavity)
Tongue
Esophagus
Liver
Gallbladder
Duodenum
Jejunum
Small
intestine Ileum
Anus
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Parotid gland
Sublingual gland Salivary
Submandibular
glands
gland
Pharynx
Stomach
Pancreas
(Spleen)
Transverse colon
Descending colon
Ascending colon
Large
Cecum
intestine
Sigmoid colon
Rectum
Vermiform appendix
Anal canal
Figure 23.1
Duodenum
• The bile duct and main pancreatic duct
• Join at the hepatopancreatic ampulla
• Enter the duodenum at the major duodenal
papilla
• Are controlled by the hepatopancreatic
sphincter
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Right and left
hepatic ducts
of liver
Cystic duct
Common hepatic duct
Bile duct and sphincter
Accessory pancreatic duct
Mucosa
with folds
Gallbladder
Major duodenal
papilla
Hepatopancreatic
ampulla and sphincter
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Tail of pancreas
Pancreas
Jejunum
Duodenum
Main pancreatic duct
and sphincter
Head of pancreas
Figure 23.21
Structural Modifications
• Increase surface area of proximal part for
nutrient absorption
• Circular folds (plicae circulares) 1 cm tall –
permanent folds of mucosae and submucosa
• Villi – 1 mm high
• Microvilli
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Structural Modifications
• Circular folds
• Permanent (~1 cm deep)
• Force chyme to slowly spiral through lumen
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Vein carrying blood to
hepatic portal vessel
Muscle
layers
Circular
folds
Villi
Lumen
(a)
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Figure 23.22a
Structural Modifications
• Villi (gives a velvety look)
• Motile fingerlike extensions (~1 mm high) of
the mucosa
• Villus epithelium
• Simple columnar absorptive cells
(enterocytes)
• Goblet cells
• In the core of each villus is a dense capillary
bed and a wide lymph capillary called a
lacteal.
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• The villi are large and leaflike in the
duodenum and gradually narrow and shorten
along the length of the small intestine.
• A slip of smooth muscle in the villus core
allows it to alternatively shorten and lengthen.
• The pulsations (1) increase the contact
between the villus and contents of the
intestinal lumen making better absorption and
(2) milk lymph along the lacteals.
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Structural Modifications
• Microvilli
• Projections (brush border) of absorptive
cells
• Bear brush border enzymes – these
enzymes complete the digestive process
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Histology of Intestinal Wall
• Epithelium of the villus is largely simple
columnar absorptive cells bound by tight
junctions and richly endowed with microvilli.
• Goblet cells
• Between the villi are intestinal pits that lead
into tubular glands called intestinal crypts –
also known as the crypts of Lieberkühn.
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Intestinal Crypts
• Intestinal crypt epithelium
• Primarily composed of secretory cells that produce
intestinal juice – a watery mixture containing mucus that
serves as a carrier fluid for absorbing nutrients from chyme
• Enteroendocrine cells – source of the enterogastrones
(Secretin and CCK)
• Intraepithelial lymphocytes (IELs) – these are T-cells that
do not need priming – upon encountering antiges they
immediately release killing cytokines
• Release cytokines that kill infected cells
• Paneth cells – release defensins and lysozyme
• Stem cells – can differentiate – become specialized
absorptive cells, goblet cells, and enteroendocrine cells.
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• The stem cells migrate up to become the
epithelial cells – the existent epithelial cells
undergo apoptosis and are shed from the
villus tips, renewing the villus epithelium every
two days.
• but when the stem cells differentiate into
Paneth cells – they stay at the base
• The crypts decrease in number along the
length of the small intestine, but the goblet
cells become more abundant.
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Microvilli
(brush border)
Absorptive cells
Lacteal
Goblet cell
Blood
capillaries
Mucosa
associated
lymphoid tissue
Intestinal crypt
Muscularis
mucosae
Duodenal gland
(b)
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Vilus
Enteroendocrine
cells
Venule
Lymphatic vessel
Submucosa
Figure 23.22b
Submucosa
• Typical areolar connective tissue
• Contains individual and aggregated lymphoid
follicles
• Peyer’s patches (aggregated lymphoid follicles)
– increase in number as go towards end of
small intestine. They protect distal part against
bacteria since normal flora increases there.
• Also contains proliferating lymphocytes that
leave the intestine enter blood stream and then
return to home in the submucosa to produce
IgA
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Submucosal Duodenal Glands
• Duodenal (Brunner’s) glands of the duodenum
secrete alkaline mucus
• The glands help neutralize acidic chyme
moving in from the stomach
• When this protection is absent or insufficient –
duodenal ulcers can occur
• The muscularis of the small intestine is
bilayered and except for the duodenum which
is retroperitoneal and has an adventitia, the
external intestinal surface is covered by a
visceral peritoneum
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Intestinal Juice
• Normally secrete 1 to 2 ml of intestinal juice daily –
that facilitates transport and absorption of nutrients
• Secreted in response to distension or irritation of the
mucosa by hypertonic or acidic chyme.
• Slightly alkaline (7.4 – 7.8) and isotonic with blood
plasma
• Largely water, enzyme-poor, due to the fact that
enzymes are limited to the intestinal enzymes
bound to brush border. It does contain contains
mucus – secreted by goblet cells and duodenal
glands
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Liver
• Largest gland in the body
• Four lobes—right, left, caudate, and quadrate
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Liver
• Falciform ligament
• Separates the (larger) right and (smaller) left
lobes
• Suspends liver from the diaphragm and
anterior abdominal wall
• Round ligament (ligamentum teres)
• Remnant of fetal umbilical vein along free
edge of falciform ligament
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Sternum
Nipple
Liver
Bare area
Falciform
ligament
Left lobe of liver
Right lobe
of liver
Gallbladder
(a)
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Round ligament
(ligamentum
teres)
Figure 23.24a
Sternum
Nipple
Liver
Lesser omentum
(in fissure)
Left lobe of liver
Porta hepatis
containing hepatic
artery (left) and
hepatic portal vein
(right)
Quadrate lobe
of liver
Ligamentum teres
Bare area
Caudate lobe
of liver
Sulcus for
inferior
vena cava
Hepatic vein
(cut)
Bile duct (cut)
Right lobe of
liver
Gallbladder
(b)
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Figure 23.24b
Liver: Associated Structures
• Lesser omentum anchors liver to stomach
• Hepatic artery and vein at the porta hepatis
• Bile ducts
• Common hepatic duct leaves the liver
• Cystic duct connects to gallbladder
• Bile duct formed by the union of the above two
ducts
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Right and left
hepatic ducts
of liver
Cystic duct
Common hepatic duct
Bile duct and sphincter
Accessory pancreatic duct
Mucosa
with folds
Gallbladder
Major duodenal
papilla
Hepatopancreatic
ampulla and sphincter
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Tail of pancreas
Pancreas
Jejunum
Duodenum
Main pancreatic duct
and sphincter
Head of pancreas
Figure 23.21
Liver: Microscopic Anatomy
• Liver lobules
• Hexagonal structural and functional units
• Filter and process nutrient-rich blood
• Composed of plates of hepatocytes (liver
cells)
• Longitudinal central vein
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(a)
Lobule
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(b)
Central vein
Connective
tissue septum
Figure 23.25a, b
Liver: Microscopic Anatomy
• Portal triad at each corner of lobule
• Bile duct receives bile from bile canaliculi
• Portal arteriole is a branch of the hepatic artery
• Hepatic venule is a branch of the hepatic portal
vein
• Liver sinusoids are leaky capillaries between
hepatic plates
• Kupffer cells (hepatic macrophages) in liver
sinusoids
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Interlobular veins
(to hepatic vein)
Central vein
Sinusoids
Bile canaliculi
Plates of
hepatocytes
Bile duct (receives
bile from bile
canaliculi)
Fenestrated
lining (endothelial
cells) of sinusoids
Portal vein
Hepatic
macrophages
in sinusoid walls
Bile duct
Portal venule
Portal arteriole
Portal triad
(c)
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Figure 23.25c
Liver: Microscopic Anatomy
• Hepatocyte functions (see MS Word Liver
Functions for complete list)
• Process bloodborne nutrients
• Store fat-soluble vitamins
• Perform detoxification
• Produce ~900 ml bile per day
• Stores glycogen
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Liver Regeneration
• The regenerative ability of the liver is
exceptional. It can regenerate to its former
size even if 70% is removed.
• Liver cells secrete VEGF (Vascular
Endothelial Growth Factor) which binds to
specific receptors on endothelial cells lining
the sinusoids.
• The endothelial cells proliferate and release
other growth factors, such as hepatocyte
growth factor (HGF) and interleukin 6.
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Bile
• Yellow-green, alkaline solution containing
• Bile salts: cholesterol derivatives that function
in fat emulsification and absorption
• Bilirubin: pigment formed from heme
• Cholesterol, neutral fats, phospholipids, and
electrolytes
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Bile
• Enterohepatic circulation
• Recycles bile salts
• Bile salts  duodenum  reabsorbed from
ileum  hepatic portal blood  liver 
secreted into bile
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The Gallbladder
• Thin-walled muscular sac on the ventral
surface of the liver
• Stores and concentrates bile by absorbing its
water and ions
• Releases bile via the cystic duct, which flows
into the bile duct
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