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Gastrointestinal Anatomy and

Physiology
Rowena A. Abante MD
Jan. 27, 2009
 The
gastrointestinal
system consists of
the
gastrointestinal
tract and
associated
glandular organs
that produce
secretions
Physiologic
Functions
Topic outline
I. Structure and innervation of the GIT
II. Regulatory substances in the GIT
III. Gastrointestinal motility
IV. Gastrointestinal secretion
V. Digestion and absorption
VI.
Topic outline
I. Structure and innervation of the GIT
II. Regulatory substances in the GIT
III. Gastrointestinal motility
IV. Gastrointestinal secretion
V. Digestion and absorption
VI.
The structure of the GIT varies greatly from region

to region, but common features exists in the


overall organization of the tissues

Structure of the GIT

• Mucosa
 Consists of an epithelium, the lamina propia, and
muscularis mucosae
Epithelial cells are specialized for secretion or absorption
Contraction of the muscularis mucosae causes a change in
surface area for secretion or absorption

Structure of the GIT

• Submucosa
Consists largely of loose connective tissue with collagen
and elastin fibers
Glands may be present in some regions


Structure of the GIT

• Muscularis externa
Inner circular , outer longitudinal
Contraction of the circular muscle causes a decrease in
diameter of the lumen of the GIT
Contraction of the longitudinal muscle causes shortening
of a segment of the GIT

Structure of the GIT

• Serosa
Consists mainly of connective tissue covered with a layer
of squamous mesothelial cells


Innervation of the GIT
The autonomic nervous system of the GI tract

comprises both extrinsic and intrinsic nervous


system

1.Extrinsic innervation
 Parasympathetic and sympathetic NS
2.Intrinsic innervation
Enteric NS
Innervation of the GIT: Extrinsic
• Afferent fibers carry sensory information from
chemoreceptors and mechanoreceptors in the
GI tract to the brain stem and spinal cord

• Efferent fibers carry information from the
brainstem and spinal cord to the GI tract
Innervation of the GIT: Extrinsic
1.Parasympathetic NS

▫ Usually excitatory on the functions of the GIT



▫ Innervation of the GIT down to the level of the
transverse colon is provided by the vagus
nerve

▫ The remainder of the colon, the rectum, and the
anus receive from fibers of the pelvic nerves

Innervation of the GIT: Extrinsic
1.Sympathetic NS
2.
▫ Usually inhibitory on the functions of the GIT

▫ Fibers originate in the spinal cord between T8 and
L2

▫ Preganglionic sympathetic cholinergic fibers synapse
in the prevertebral ganglia

▫ Postganglionic sympathetic adrenergic fibers leave
the prevertebral ganglia and synapse in the
myenteric and submucosal plexuses
Innervation of the GIT: Intrinsic
• Coordinates and relays information from the
PNS and SNS to the GI tract

• Uses local reflexes to relay information within
the GI tract

• Controls most functions of the GIT, especially
motility and secretion, even in the absence of
the extrinsic innervation
Innervation of the GIT: Intrinsic
1.Myenteric plexus
▫ Auerbach’s plexus
▫ Primarily controls the motility of the GI smooth
muscle

2.Submucosal plexus
▫ Meissner’s plexus
▫ Primarily controls the secretion and blood flow
▫ Receives sensory information from chemoreceptors
and mechanoreceptors in the GI tract
3.
Topic outline
I. Structure and innervation of the GIT
II. Regulatory substances in the GIT
III. Gastrointestinal motility
IV. Gastrointestinal secretion
V. Digestion and absorption
VI.
The functions of the GIT are regulated and
coordinated by hormones, paracrine agonists and
neurons.

Regulatory substances: GI hormones
• Released from endocrine cells in the GI mucosa
into the portal circulation, enter the general
circulation, and have physiologic functions on
target cells

• GI hormones
1.Gastrin
2.Cholecystokinin (CCK)
3.Secretin
4.Gastric Inhibitory Peptide (GIP)
Regulatory substances: GI hormones
Summary of GI hormones
Hormones Site of Stimulus for secretion Actions
secretion
Gastrin G cells of Small peptides and amino acids inc gastric H+ secretion
stomach Distention of stomach Stimulates growth of gastric mucosa

Vagus

Inhibited by H+ in stomach

CCK I cells of Small peptides and amino acids Stimulates contraction of gallbladder and relaxation of
duodenum and Fatty acids the sphincter of Oddi
jejunum Inc pancreatic enzyme and HCO3- secretion

Inc growth of exocrine pancreas/gallbladder

Inhibits gastric emptying

Secretin S cells of H+ in the duodenum Inc pancreatic HCO3 secretion


duodenum Fatty acids in duodenum Inc biliary HCO3 secretion
Dec gastric H+ secretion

GIP Duodenum and Fatty acids, amino acids, and oral Inc insulin secretion
jejunum glucose Dec gastric H+ secretion
Regulatory substances: Paracrines
• Released from endocrine cells in the GI mucosa

• Diffuse over short distances to act on target cells


located in the GI tract

1. somatostatin

2. histamine


Regulatory substances: Paracrines
1.Somatostatin
▫ Secreted by cells throughout the GI tract in response
to H+ in the lumen
▫ Secretion is inhibited by vagal stimulation
▫ Inhibits the release of ALL GI hormones
▫ Inhibits H+ secretion

2.Histamine
▫ Secreted by mast cells of the gastric mucosa
▫ Inc gastric H+ secretion directly and by potentiating
the effects of gastrin and H+ secretion
Regulatory substances: Neurocrines
• Synthesized in neurons of the GIT, moved by
axonal transport down the axon, and released
by action potentials in the nerves
• Then diffuse across the synaptic cleft to a target
cell

1.Vasoactive intestinal polypeptide (VIP)
2.Gastrin-releasing peptide (GRP)
3.Enkephalins
Regulatory substances: Neurocrines
1. VIP
▫ Homologous to secretin
▫ Released from neurons in the mucosa and smooth muscle of the GIT
▫ Produces relaxation of GI muscle , including the LES

2. GRP
▫ Released from vagus nerves that innervate the G cells
▫ Stimulates gastrin release from G cells

3. Enkephalins
▫ Secreted from nerves in the mucosa and smooth muscle of the GIT
▫ Stimulate contraction of GI smooth muscle (LES, pyloric, ileocecal
sphincters)
▫ Inhibits intestinal secretion of fluid and electrolytes
Topic outline
I. Structure and innervation of the GIT
II. Regulatory substances in the GIT
III.Gastrointestinal motility
IV. Gastrointestinal secretion
V. Digestion and absorption
VI.
Gastrointestinal motility
• Contractile tissue of the GIT is almost exclusvely
unitary smooth muscle, with the exception of
the pharynx, upper 1/3 of the esophagus, and
external anal sphincter, all of which are striated
muscles



Gastrointestinal motility
• Depolarization of circular muscle leads to
contraction of a ring of smooth muscle and a
decrease in the diameter of that segment of the
GIT

• Depolarization of longitudinal muscle leads to
contraction in the longitudinal direction and a
decrease in length of that segment of the GIT

Gastrointestinal motility
• Phasic contractions occur in the esophagus, gastric
antrum, and small intestine

• Tonic contraction occur in the LES, orad stomach,


and ileocecal and internal anal sphincters
GI motility: slow waves
• Are oscillating membrane
potentials inherent to the
smooth muscle cells of
some parts of the GIT

• Occur spontaneously

• Originate in the interstitial
cells of Cajal, which
serves as the pacemaker
of GI smooth muscle

GI motility: slow waves
1. Mechanism of slow wave production

▫ Is the cyclic activation and deactivation of the cell membrane Na+-K+


pump

▫ Depolarization during each slow waves brings the membrane potential
of smooth muscle cells closer to threshold and, therefore,
increases the probability that action potentials will occur.

▫ Action potentials, produced on the background of slow waves, then
initiate contraction of smoth muscle cells
GI motility: slow waves
2. Frequency of slow waves

▫ Varies along the GIT, but is constant and characteristic for each
part of the GIT

▫ Not influenced by hormonal nor neural input, in contrast, the
frequency of the action potentials that occur on top of the
slow waves is modified by neural and hormonal influences

▫ Sets the maximum frequency of contractions for each part of
the GIT

▫ Is lowest in the stomach (3sw/min), and highest in the
duodenum (12sw/min)
GI motility: Chewing
• Lubricates food by mixing it with saliva

• Decreases the size of food particles to facilitate
swallowing and to begin the digestive process
GI motility: Swallowing
• The swallowing reflex is coordinated in the
medulla.

• Fibers in the vagus and glossopharyngeal nerves
carry information between the GIT and the
medulla

GI motility: Swallowing
• Swallowing can be initiated
voluntary, but thereafter
it is almost entirely under
reflex control.

• The swallowing reflex is a
rigidly ordered sequence
of events that propels
food from the mouth to
the stomach.

• This reflex also inhibits
respiration and prevents
entry of food into the
trachea during
swallowing

GI motility: esophageal motility
• The esophagus contains a
gradient of muscle, from all
skeletal at the top to all
smooth at the bottom.

• Innervation: vagus

• After the food is swallowed, the
esophagus functions as a
conduit to move the food
from the pharynx to the
stomach.

•Sphincters at either end of the esophagus prevent air from entering the upper
• esophagus and gastric acid from entering the lower esophagus.
GI motility: esophageal motility
GI motility: esophageal motility
• The following sequence of events occurs as food moves into and down the
esophagus:

1. UES relaxation to permit swallowed food to enter the esophagus
2.
3. UES contraction to prevent reflux of food into the pharynx
4.
5. A primary peristaltic contraction moves down the esophagus and propels the
food bolus along
6.
7. A second peristaltic contraction clears the esophagus from any remain food
8.
9. LES relaxation, vagally mediated via VIP
10.
GI motility: esophageal motility
GI motility: gastric motility

• The stomach has 3 layers of
smooth muscle- the usual
longitudinal and circular
and a third oblique layer



• The stomach has 3
anatomical divisions-
fundus, body, antrum

GI motility: gastric motility
• The orad region includes
the fundus and the
proximal body.
▫ This region contains the
oxyntic glands and is
responsible for receiving
the ingested meal.

• The caudad region icludes


the antrum and the distal
body.
▫ This region is responsible
for contractions that mix
food and propel it into
the duodenum.
GI motility: gastric motility
1. Receptive relaxation
▫ A vagovagal reflex that is initiated by distention of the
stomach and is abolished by vagotomy
▫ Orad region relaxes to accomodate the ingested meal
▫ CCK participates by increasing distensibility of the
stomach

2.Mixing and digestion
▫ Caudad region contracts to mix the food with gastric
secretion and begins the process of digestion
▫ The size of food particles are reduced

GI motility: gastric motility
 3. Gastric emptying

▫ Caudad region contracts to propel food


into the duodenum

▫ The rate of gastric emptying is fastest
when the stomach contents are
isotonic. If the stomach contents
are hypotonic or hypertonic,
gastric emptying is slowed.

▫ Fats inhibits gastric emptying by
stimulating release of CCK

▫ H+ in the duodenum inhibits gastric
emptying via direct neural reflexes
GI motility: gastric motility
• Regulation of gastric emptying

▫ Chyme entering the duodenum activates intestinal receptors.

▫ This leads to increased contraction of the duodenum and decreased
contraction of the stomach (Delayed Gastric Emptying)

▫ Secretin, CCK, and GIP (enterogastrone) are released by the
duodenum and feed back on the stomach to slow down.
GI motility: small intestinal motility
GI motility: small intestinal motility
GI motility: small intestinal motility
• The SI functions in the digestion and absorption of nutrients.

• Slow waves set the basic electrical rhythm which occurs at a
frequency of 12sw/min.

• Parasympathetic stimulation increases intestinal smooth
muscle contraction; sympathetic stimulation decreases it.
GI motility: small intestinal motility
1.Segmental contractions
2.
▫ Mix the intestinal contents
▫ a section of the intestine contracts sending the chyme in both
orad and caudad directions
▫ This back-and-forward movement produced by segmentation
contraction causes mixing without net forward movement
of the chyme

GI motility: small intestinal motility
2. Peristaltic contractions

▫ Highly coordinated, and propel the chyme through the SI


toward the LI
▫ Contraction behind the bolus, and simultaneous relaxation in
front of the bolus cause the chyme to be propelled caudally.
GI motility: small intestinal motility
3. Gastroileal reflex

▫ mediated by the extrinsic NS and possibly by gastrin


▫ The presence of food in the stomach triggers peristalsis in the
ileum and relaxation of the ileocecal sphincter.
GI motility: large intestinal motility
GI motility: large intestinal motility
• Fecal material moves from the cecum to the
colon, to the rectum, and then to the anal canal

• Haustra, or sac-like segments, appear after
contractions of the large intestines


GI motility: large intestinal motility
1. Cecum and proximal colon
2.
▫ When the proximal colon is distended with fecal material,
ileocecal sphincter contracts to prevent reflux into the
ileum.
▫ Segmentation contractions in the proximal colon mix the
contents
▫ Mass movements occur 1-3x/day and cause the colonic content
to move distally for long distances (e.g. From the
transverse colon sigmoid colon

 Di
 stal colon
 
▫ ecause most colonic water
absorption occurs in the
proximal colon fecal
GI motility: large intestinal motility
 3. Rectum, anal canal, and defecation

▫ Sequence of events:
1.Rectum fills with fecalmaterial, contracts, and then
internal anal sphincter relaxes. (rectosphincteric
reflex)
2.
3.Once rectum is filled with 25% of its capacity
there is an urge to
defecate however
defecation is prevented
because the external anal
sphincter is tonicall
contracted
 
 hen it is convenient to
GI motility: large intestinal motility
4. Gastrocolic reflex

▫ The presence of food in the stomach increases


the motility of the colon and increases the
frequency of mass movements

▫ It has a rapid parasympathetic component taht
is initiated when the stomach is stretched by
food.

Topic outline
I. Structure and innervation of the GIT
II. Regulatory substances in the GIT
III. Gastrointestinal motility
IV.Gastrointestinal secretion
V. Digestion and absorption
VI.
GI secretion:
Summary of GI secretions
GI secretion Major characteristics Stimulated by Inhibited by
Saliva High HCO3 PNS Sleep
High K SNS Dehydration
Hypotonic Atropine

α αµ ψλ ασε
Λ ι ν γ υ αλ λ ι π ασε

Gastric secretion  HCl Gastrin Dec stomach pH


PNS Chyme in duodenum
Histamine Atropine

Cimetidine
 Pepsinogen  PNS Omeprazole
 Intrinsic factor 

Pancreatic secretion  High HCO3 Secretin


 Isotonic CCK
PNS

Pancreatic lipase,
  CCK
amylase,proteases  PNS
 

Bile Bile salts  CCK  Ileal resection


Bilirubin  PNS
Phospolipids

cholesterol
GI secretion: salivary secretion
• Functions of saliva
▫ Initial starch digestion by α α µ ψ λ α σ ε
(π τ ψ α λ ι ν ) α ν δ ι ν ι τ ι α λ
τ ρ ι γ λ ψχ ε ρ ι δ ε
δ ι γ ε στ ι ο ν β ψ λ ι ν γ υ αλ
λ ι π ασε
▫ Lubrication of ingested food by mucus
▫ protection of the mouth and esophagus by
dilution and buffering of ingested foods
GI secretion: salivary secretion
• Composition
▫ Characterized by:
 High volume
High K+ and HCO3 conc
Low Na and Cl conc
Hypotonicity
Presence of amylase, lingual lipase, and kallikrein
▫ At lowest flow rates, saliva has the lowest osmolarity
and lowest Na, Cl, and HCO3 conc, but has the
highest K conc.
▫ At the highest flow rates (up to 4ml/min), the
composition is closest to that of plasma

GI secretion: salivary secretion
• Formation
▫ Formed by 3 major glands:
 Parotid
Submaxillary
Sublingual

▫ The acinus produces the
initial saliva with a
composition similar to
that of plasma (isotonic)

▫ The ducts modify the
initial isotonic saliva
making it hypotonic

GI secretion: salivary secretion
• Regulation of salivary production

▫ Salivary formation is unique in that it is increased by both


parasympathetic and sympathetic activity. Parasympathetic activity,
however is more important
▫ PNS- CN VII and IX
 By increasing the transport process in the acinar and ductal cells and
by causing vasodilatation
Anticholinergics inhibit production dr mouth
▫ N
  increasing production and growth
of salivar glands although
effects arer smaller than  N
stimulation
▫ thers
ncreased (via N b food in the
mouth smells conditioned
reflexes and nausea
Decreased (via inhibitio of N b
sleep dehdration fear
anticholinergics
GI secretion: Gastric secretion
Gastric mucosa

▫ Cardiac glandular
region
 Mucus secreting


▫ Oxyntic glandular
region
Acid secreting


▫ Pyloric glandular region
Gastrin and mucus
secreting
GI secretion: Gastric secretion
Gastric cell types and their

secretion

• Parietal cells
▫ Located in the body
▫ HCl, IF
▫ Stimuli: gastrin, vagal
(ACh), histamine

• Chief cells
▫ Located in the body
▫ Pepsinogen
▫ Stimulus: vagal (ACh)

GI secretion: Gastric secretion
Gastric cell types and their

secretion

• G cells
▫ Located in the antrum
▫ Gastrin
▫ Stimuli: vagal (ACh)
▫ Inhibited by:
somatostatin, H+

• Mucus cells
▫ Located in the antrum
▫ Mucus, pepsinogen
▫ Stimulus: vagal (ACh)
GI secretion: Gastric secretion
 Physiology

• Cholinergic input via the vagus nerve and
histaminergic input from local gastric sources are
the principal contributors to basal acid secretion.

• Stimulated gastric acid secretion occurs primarily in
three phases based on the site where the signal
originates (cephalic, gastric, and intestinal).
GI secretion: Gastric secretion
GI secretion: Gastric secretion
 Stimulation of gastric acid secretion

• Vagal
▫ Increases H+ secretion by direct and indirect pathway
▫ Direct: Vagus ch parietal cells
▫ Indirect: Vagus G cells gastrin parietal
cells
▫ nhibited b tropine via muscarinic
receptor

• Histamine
▫ Released from mast cells in the gastric mucosa
▫ Stimulates H+ secretion by activating H2 receptors on the parietal cell
membrane
▫ Inhibited by: H2 blockers ( Cimetidine)

• Gastrin
▫ Released in response to eating a meal
GI secretion: Gastric secretion
Inhibition of gastric acid secretion

• Negative feedback inhibits the secretion of H+by


parietal cells

• Low pH in the stomach


▫ Inhibits gastrin secretion
inhibiting G+ secretion

• Chyme in the duodenum



GI secretion: Pancreatic secretion
GI secretion: Pancreatic secretion
• Contains high conc of HCO3 the purpose is to
neutralize the acidic chyme that reaches the
duodenum

• Contains enzymes essential for the digestion of protein,


carbohydrate, and fat

• Regulates whole body metabolism via


▫ Insulin
▫ Glucagon
▫ Somatostatin


GI secretion: Pancreatic secretion
GI secretion: Pancreatic secretion
• Composition of pancreatic secretion
▫ High volume
▫ Virtually the same conc of Na and K as plasma
▫ Much higher HCO3 conc than plasma
▫ Isotonic
▫ Pancreatic lipase, amylase, and proteases

• At low flow rates, it secretes an isotonic fluid that is composed
mainly of Na and Cl

• At high flow rates, it secretes an isotonic fluid that is composed


mainly of Na and HCO3

• Regardless of the flow rates, it secretes isotonic fluid


GI secretion: Pancreatic secretion
• Formation of pancreatic secretion
▫ Acinar cells
 Produce a small volume of initial pancreatic secretion, which
is mainly Na and Cl
▫ Ductal cells
Modify the initial pancreatic secretion by secreting HCO3 and
absorbing Cl via Cl-HCO3 excahnge mechanism in the
luminal membrane
Because the pancreatic ducts are permeable to water, H2O
moves into the lumen to make the pancreatic secretion
isotonic

• Stimulation of pancreatic secretion
▫ Secretin
▫ CCK
▫ AcH

GI secretion: Bile secretion and
Gallbladder function

• Composition and function of bile


▫ Bile contains bile salts, phospholipids, cholesterol, and bile pigments


• Formation of bile
▫ Bile is produced continuously by hepatocytes
▫ Bile drains into the hepatic ducts and is stored in the gallbladder for subsequent release.

GI secretion: Bile secretion and
Gallbladder function
• Primary bile acids
▫ cholic and chenodeoxycholic acids
▫ Synthesized from cholesterol by hepatocytes

• In the intestines, bacteria convert a portion of each of the primary
bile acids to secondary bile acids ( deoxycholic acid and
lithocholic acid

GI secretion: Bile secretion and
Gallbladder function
GI secretion: Bile secretion and
Gallbladder function
•Most bile acids are taken
up by distal ileum
epithelial cells by
2oactive transport
when they are no
longer needed for
digestion.

•They travel to the liver
via the portal vein and
are taken up by
hepatocytes through
the for recycling.

•They re-enter the bile
canaliculus through
the BSEP (bile salt
exchange pump)

Topic outline
I. Structure and innervation of the GIT
II. Regulatory substances in the GIT
III. Gastrointestinal motility
IV. Gastrointestinal secretion
V. Digestion and absorption
VI.
GI Digestion and Absorption
• Carbohydrates, proteins, and lipids are digested
and absorbed in the small intestines

• The surface area for absorption in the SI is
greatly increased by the presence of
brushborders
Summary of digestion and absorption
Nutrient Digestion Site of Mechanism of absorption
absorption

Carbohydrates To monosaccahrides SI  Na-dependent co-transport (glucose, galactose)


(glucose, galactose,  Facilitated Diffusion (fructose)
fructose)

Proteins To amino acids, SI  Na-dependent co-transport (amino acids)


dipeptides, tripeptides  H+ dependent co-transport (di- and tripeptides)

Lipids To fatty acids, SI Micelles form with bile salts in intestinal lumen
monoglycerides, Diffusion of fatty acids, mono glycerides, and cholesterol into cell

cholesterol Reesterification in cell to TG and phospholipids

Chylomicrons form in cell (requires apoprotein) and are transferred

to lymph

Fat-soluble SI  Micelles with bile salts


vitamins 

Water-soluble Ileum of SI  Na-dependent co-transport


vitamins
Vit B12 IF-Vit B12 complex

Bile acids Ileum of SI Na-dependent co-transport ; recirculated to liver


Ca+ SI  Vit D-dependent Ca binding protein
Fe+ Fe3+ is reduced to Fe 2+ SI Binds to apoferritin in cell
Circulates in blood bound to transferrin
GI Digestion and Absorption
• Absorption and secretion of water and
electrolytes
• Electrolytes and water may cross intestinal
epithelial cells by either cellular or paracellular

Thank you!
senesc
ent
RBC
Bilirubin Metabolism
s ma Bilirubin-
Macrophages Pla
heme Albumin
(spleen) Adduct
Bilirubin (indirect)

Urine Systemic Circulation

Feces (urobilin)
(stercobilin) Bilirubin Glucuronide

Portal Circ.

Urobilin
ogen Bile Duct
Intestinal Flora Hepatocyte

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