Development of GIT -II

By Dr. Aarushi Jain

MS ANATOMY
GMC KOTA
Development of Alimentary
System part 1(FOREGUT)
By Dr. Aarushi Jain
MS ANATOMY
GMC KOTA
 AN52.6 Describe the development and congenital
anomalies of: Foregut, Midgut & Hindgut

• SLO:
1. DESCRIBE THE DEVELOPMENT OF OESOPHAGUS
AND APPLIED ASPECT
2. EXPLAIN THE EMBRYOLOGICAL BASIS OF
HYPERTROPHIC PYLORIC STENOSIS
3. DERIVATIVES OF MESENTRIES AND LESSER
OMENTUM.
4. FORMATION OF LIVER AND SPLEEN
5. EMBRYOLOGICAL BASIS OF ANNULAR PANCREAS
 Introduction
Development of the gut tube proper involves
1. Continuous elongation,
2. Herniation past the body wall,
3. And rotation and folding for efficient packing
into the body cavity, and
4. Histogenesis and
5. Functional maturation
 Folding of embryo
• Longitudinal and
Transverse folding of
the embryo in the 3rd
and 4th weeks converts
the flat trilaminar
embryonic disc into a
trilaminar, elongated
cylinder
FORMATION OF PRIMITIVE GUT
 The alimentary tract
develops from the primitive
gut.
 On the formation of head
and tail folds, the part of
definitive yolk sac gets
trapped within the embryo.
 This trapped part forms the
primitive gut.
PARTS OF PRIMITIVE GUT
 Developing primitive gut
communicates with
1. Yolk sac through the
Anterior intestinal portal
vitellointestinal duct.
2. Allantoic diverticulum.
 The cranial part of the gut that
Posterior
intestinal
portal
lies in the head fold is foregut.
 The caudal part of gut that lies in
the tail fold is hindgut.
 The part of gut that
communicates with
vitellointestinal duct is midgut.
BLOOD SUPPLY VIA MESENTRIES
• The primitive gut is
supplied by coeliac
artery for the foregut,
• superior mesenteric
artery for the midgut
• and inferior mesenteric
artery for the hindgut
Histogenesis of the GIT
• Endoderm forms the epithelial
lining of the digestive tract and
gives rise to the specific cells (the
parenchyma) of glands, such as
hepatocytes and the exocrine and
endocrine cells of the pancreas.
• Stroma (connective tissue) for the
glands is derived from visceral
mesoderm.
• Muscle, connective tissue and
peritoneal components of the
wall of the gut also are derived
from visceral mesoderm
 Recanalisation
• Early in development,
the epithelial lining of
the gut tube proliferates
rapidly and obliterates
the lumen.
• Later, recanalization
occurs.
Intraperitoneal, retroperitoneal and
secondarily retroperitoneal organs
 MESENTRY
• Mesentery is a collection of
connective tissues that
maintains the gut tube and its
derivatives in their normal
anatomical positions.
• In the abdomen, dorsal
mesentery extends from the
lower portion of the esophagus
to the rectum as a continuous
sheet of tissue attached to the
posterior body wall and
providing a pathway for blood
vessels, lymphatics, and nerves
to the gut tube and its
derivatives.
PARTS OF MESENTRY
• the dorsal mesogastrium
• greater omentum,
• mesoduodenum,
• Mesentery proper to the
small intestine,
• mesocolon,
• mesoappendix,
• mesosigmoid,
• and mesorectum.
 Foregut
Tracheoesophageal groove

Post laryngeal part

Pre laryngeal part

Pharynx and floor of mouth Esophagus, stomach, liver, gallbladder,

pancreas, upper Duodenum till
hepatopancreatic duct
 Midgut

Precaecal part Post caecal part

Cecum,
Lower Duodenum,
Appendix, Ascending
Jejunum, Ileum
Colon, Proximal 2/3
Of The Transverse Colon
 HINDGUT
Allantoenteric diverticulum
Pre allantoic Post
allantoic
part
Distal one-third of the
transverse colon, Rectum,
descending colon, And upper anal
sigmoid colon, canal
Foregut
Oesophagus
 In the lower part of the pharynx, a
laryngotracheal groove appears
that later form tracheobronchial
(respiratory) diverticulum.
 Tracheoesophageal septum
divides the part of foregut caudal
to tracheobronchial diverticulum in
ventral trachea and dorsal
oesophagus.
 Small oesophagus elongates due to
the formation of neck and descent
of the diaphragm, lungs and heart.
Oesophagus
 • Occurs when the
Esophageal atresia tracheoesophageal septum
deviates too far dorsally, causing
the esophagus to end as a closed
tube.
• About 33% of patients with
esophageal atresia also have other
congenital defects associated with
the vater (vertebral defects, anal
atresia, tracheoesophageal fistula,
and renal defects) or vacterl
(similar to vater but also
cardiovascular defects and upper
limb defects) syndrome.
• It is associated clinically with
polyhydramnios (fetus is unable to
swallow amniotic fluid) and
 Highlight of Ten’s
• There are ten alphabets in the word oesophagus.
• The length of the oesophagus is ten inches
• It pierces the diaphragm at the level of 10th
thoracic vertebra.
• If number ten catheter is passed in a newborn
and in case, it gets obstructed at mark ten at the
level at the lips, diagnosis of the
tracheoesophageal fistula is confirmed.
 Esophageal stenosis
• When the lumen of the esophagus is narrowed
• Usually involves the midesophagus.
Caused by
1. Submucosal/muscularis externa hypertrophy,
2. Remnants of the tracheal cartilaginous ring within
the wall of the esophagus,
3. Or a membranous diaphragm obstructing the
lumen probably due to incomplete recanalization.
Achalasia
• Occurs due to the loss of
ganglion cells in the
myenteric (auerbach) plexus
• Characterized by the failure
to relax the lower
esophageal sphincter, which
will cause progressive
dysphagia and difficulty in
swallowing
• Bird-beak deformity seen in
barium swallow.
Esophageal duplication
• Occurs most commonly due
to a congenital esophageal
cyst, which is usually found
(60% of the cases) in the
lower esophagus.
• Duplication cysts may lie on
the posterior aspect of the
esophagus, where they
protrude into the posterior
mediastinum or within the
wall of the esophagus (i.E.,
Intramural).
STOMACH
 present
below
STOMACH (4TH WEEK) septum
tranversum

Thoracic foregut elongate at 26th day

Fusiform dilation

Dorsolateral wall grows>ventral

Superior
Future greater curvature expansion to Future lesser curvature
form cardiac
and fundus
end Moves to right and
90degree rotation around vertical axis right vagus becomes
dorsal
Moves to left and
the left vagus
becomes ventral 90 degree rotation around Cardiac end moves left
anteroposterior axis downwards

pyloric end moves right upwards

 Factors for rotation of stomach
1. Rapid enlargement of right lobe of liver so
spleen also moves towards left
2. Active growth process so to shift dorsal
mesogastrium to shift to left
What is the result
• Bend the presumptive duodenum
into a C shape
• Displace it to the right until it lies
against the dorsal body wall
becoming secondarily
retroperitoneal
• Recess dorsal to the stomach called
the lesser sac of the peritoneal
cavity.
• Rest of the peritoneal cavity is now
called the greater sac
• Reduces the communication
between the greater and lesser sacs
of the peritoneal cavity to a narrow
canal lying just posterior to the
lesser omentum. This canal is called
the epiploic foramen of Winslow.
 Formation of Greater Omentum
• Lesser sac enlarges due to
progressive expansion of the
dorsal mesogastrium.
• Large, suspended fold of
mesogastrium, called the
greater omentum, hangs from
the dorsal body wall and the
greater curvature of the
stomach and drapes over more
inferior organs of the
abdominal cavity .
• The posterior layer of the
greater omentum also fuses
with mesentery of the
transverse colon
 RECESSES OF LESSER SAC
• Portion of the lesser sac
directly dorsal to the stomach
is now called the upper
recess of the lesser sac,
• Cavity within the greater
omentum is called the lower
recess of the lesser sac.
• The lower recess is
obliterated during fetal life as
the anterior and posterior
folds of the greater omentum
fuse together.
 Mesentries of stomach
Dorsal mesogastrium
Ventral mesogastrium derived
from septum transversum Developing spleen in its fold

Growth of liver in Gastrosplenic

septum transversum ligament leinorenal

Falciform ligament Lesser omentum

 Congenital Hypertrophic Pyloric Stenosis

 Congenital defect due to the hypertrophy of circular muscle

layer at the pylorus.
 Pyloric stenosis is one of the most common abnormalities
of the stomach in infants.
 Incidence: 1 in every 150 male infants and 1 in every 750
female infants.
 Presentation: Newborn is normal until first feed.
 Newborn present projectile forceful vomiting after 2–3 hours
of first feed. Vomitus does not contain bile.
 Treatment: Surgical correction.

32
 Clinical scenario
A mother brings her 1-month-old son into the clinic,
complaining of her son “vomiting all over the place
when he tries to eat something.” She said her son’s
vomiting looks like it was “shot out of a cannon.”
Relevant physical findings include a small, nontender,
palpable mass on the right costal margin.
Relevant laboratory findings include barium swallow
radiograph showing a narrow pyloric channel and
abdominal ultrasound showing a hypertrophic pylorus.
Which of the following is the most likely diagnosis
 Duodenum
• The terminal part of the foregut and the cephalic part of the midgut form the
duodenum
• Junction of the two parts is directly distal to the origin of the liver bud
• Stomach rotation and rapid growth of the head of the pancreas, swings the
duodenum from its initial midline position to the right side of the abdominal
cavity.
• Most of the duodenum become attached to the posterior body wall.
• A small portion of the distal region of the duodenum (duodenal cap) retains an
extension of mesentery and remains unattached to the posterior body wall.
 Blood supply
- Proximal part (derived from foregut) – is supplied
by branches of coeliac trunk.
- Distal part (derived from midgut) – is supplied by
branches of superior mesenteric artery.
 Anomalies of Duodenum
1.Duodenal stenosis: Incomplete recanalisation → Partial
occlusion of lumen → produces duodenal stenosis. Newborn
baby with duodenal stenosis vomits feed that contains bile. MCQ
2.Duodenal atresia: Complete occlusion of lumen. Duodenal
atresia is the most common intestinal atresia. Duodenal atresia
produces polyhydramnios. On ultrasonography, the distended
gas-filled stomach and duodenum produces double-bubble
sign. MCQ
3.Duodenal diverticula: usually arises from the second part of
the duodenum.
LIVER, GALL BLADDER, PANCREAS AND
SPLEEN
 Development of Liver and Gallbladder
1. The endodermal lining of the foregut
forms an outgrowth called the hepatic
diverticulum into the surrounding
mesoderm of the septum transversum.
2. Cords of hepatoblasts (called hepatic
cords) from the hepatic diverticulum
grow into the mesoderm of the septum
transversum.
3. The hepatic cords arrange themselves
around the vitelline veins and
umbilical veins, which course through
the septum transversum and form the
hepatic sinusoids.
4. The liver bulges into the abdominal
cavity, thereby stretching the septum
transversum to form the ventral
mesentery, consisting of the falciform
ligament and the lesser omentum.
 LIGAMENTS
5. The falciform ligament
contains the left umbilical
vein, which regresses after
birth to form the ligamentum
teres.
6. The lesser omentum can be
divided into the hepatogastric
ligament and hepatoduodenal
ligament.
7. The hepatoduodenal ligament
contains the bile duct, portal
vein, and hepatic artery (i.e.,
portal triad).
 Gall bladder and bile duct
1. The connection
between the hepatic
diverticulum and the
foregut narrows to
form the bile duct.
2. An outgrowth from the
bile duct gives rise to
the gallbladder
rudiment and cystic
duct
 Derivatives of Ventral Mesentery
Liver contacts with septum transversum

Peritoneal reflection Cranial part of Caudal part of

on inferior surface of mesentry is absent ventral mesentry
diaphragm encircles as liver is direct
contact with central
bare area like crown Visceral peritoneum
tendon
1
Bare area of liver
2
Coronary ligament
Anastomoses between hepatic
3 portal vessels and the systemic
Falciform ligament veins of the diaphragm

4 Hepatogatric ligament
Lesser omentum

Hepatoduodenal liagament
 ANOMALIES OF GALL BLADDER
1. Intrahepatic gall bladder occurs when the
gallbladder rudiment advances beyond the
hepatic diverticulum and becomes buried
within the substance of the liver.
2. Floating gall bladder occurs when the
gallbladder rudiment lags behind the hepatic
diverticulum and thereby becomes suspended
from the liver by a mesentery.
A floating gall bladder is at risk for torsion.
Developmental anomalies of the gall bladder
• which two( duplicated) ,
bilobed, diverticula, and
septated gall bladders
are found.
Developmental anomalies of the cystic duct
Biliary atresia
Defined as the obliteration of
extrahepatic and/or intrahepatic
ducts.
The ducts are replaced by fibrotic
tissue due to acute and chronic
inflammation.
Clinical findings include: progressive
neonatal jaundice with onset soon
after birth, white, clay-colored
stool, and dark-colored urine;
average survival time is 12–19
months with a 100% mortality
rate; can be treated by liver
transplantation.
 Development of Pancreas
1. The ventral pancreatic bud and dorsal
pancreatic bud are direct outgrowths
of foregut endoderm.
2. Within both pancreatic buds,
endodermal tubules surrounded by
mesoderm branch repeatedly to form
acinar cells and ducts (i.e., exocrine
pancreas).
3. Isolated clumps of endodermal cells
bud from the tubules and accumulate
within the mesoderm to form islet
cells (i.e., endocrine pancreas).
4. Because of the 90° clockwise rotation
of the duodenum, the ventral bud
rotates dorsally and fuses with the
dorsal bud to form the definitive adult
pancreas.
 DERIVATIVES OF BUDS
5. The ventral bud forms the
uncinate process and a portion
of the head of the pancreas.
6. The dorsal bud forms the
remaining portion of the head,
body, and tail of the pancreas.
7. The main pancreatic duct is
formed by the anastomosis of
the distal two-thirds of the
dorsal pancreatic duct (the
proximal one-third regresses)
and the entire ventral
pancreatic duct (48% incidence).
 Accessory pancreatic duct
• Develops when the
proximal one third of
the dorsal pancreatic
duct persists and opens
into the duodenum
through a minor
papillae at a site
proximal to the ampulla
of Vater (33%
incidence).
 Pancreas divisum
occurs when the distal
two-thirds of the dorsal
pancreatic duct and the
entire ventral pancreatic
duct fail to anastomose
and the proximal one-
third of the dorsal
pancreatic duct persists,
thereby forming two
separate duct systems.
Annular Pancreas
• Arises when the two lobes of a bilobed
ventral pancreatic bud (a normal
variation) migrate in opposite directions
around the duodenum to fuse with the
dorsal pancreatic bud, thereby forming a
ring of pancreatic tissue around the
duodenum and causing severe
duodenal obstruction.
• Newborns and infants are intolerant of
oral feeding and often have bilious
vomiting.
• Radiographic evidence of an annular
pancreas is indicated by a duodenal
obstruction, where a “double bubble”
sign is often seen due to dilation of the
stomach and distal duodenum
 Development of Spleen
• A mesenchymal condensation
develops in dorsal mesogastrium
of the lesser sac.
• The rotation of the stomach and
growth of the dorsal
mesogastrium translocates the
spleen to the left side of the
abdominal cavity.
• The rotation of the dorsal
mesogastrium also establishes a
mesenteric connection called the
renal-splenic ligament between
the spleen and the left kidney.
• The portion of the dorsal
mesentery between the spleen
and the stomach is called the
gastrosplenic ligament
 Anomalies of the Spleen
• Accessory splenic tissue is found around the
spleen, in the gastrosplenic ligament, greater
omentum and the left spermatic cord.
• After removal of the spleen the accessory
splenic tissues enlarge and take over the
function of the lost spleen.
• HAMARTOMAS
• CYSTS- TRUE OR FALSE
MIDGUT
 DERIVATIVES
• Supplied by the superior mesenteric artery
(SMA) and
• Include the lower duodenum, jejunum, ileum,
caecum, appendix, ascending colon, and
proximal two-third of the transverse colon.
Mixed rotation of gut
Recanalisation
Volvulus
Cytodifferentiation of gut epithelium
Hindgut- divisions of cloaca
Fate of allantois and urogenital sinus
Lower third of anorectal canal
Allantois
Hirchprungs disease