Development of Foregut.dk

Development of Foregut
DR.DEEPAK N.KHEDEKAR
Assistant Professor.
DEPARTMENT OF ANATOMY.
LTMMC &GH MUMBAI

OBJECTIVES
• Derivatives
• Blood supply
• Embryological basis of various clinical
condition

DEVELOPMENT OF FOREGUT
Development of Esophagus
Development of Stomach & Omental Bursa
Development of Duodenum
Development of Liver and Biliary Apparatus
Development of Pancreas
Development of Spleen

DEVELOPMENT OF
GUT TUBE
 Alimentary system is
the digestive tract
from the mouth to
the anus with all its
associated glands and
organs.
 Primordia of
Alimentary system:
Develops from
Pharyngeal arches
Primitive gut

INTRODUCTION-PRIMORDIAL GUT
Time period : Forms during the 4th week
Events:
• Head, caudal eminence (tail), and lateral
folds incorporate the dorsal part of the
umbilical vesicle (yolk sac) into the
embryo .
• Initially closed at its cranial end by the
oropharyngeal m. , and at its caudal end
by the cloacal m.

HISTOGENESIS- PRIMORDIAL GUT
• Endoderm- Gives rise to most of the gut,
epithelium, and glands.
• Ectoderm of the stomodeum and anal pit-gives rise
to epithelium at the cranial and caudal ends of the
alimentary tract.

FOREGUT DERIVATIVES
Primordial pharynx and its derivatives:
Lower Respiratory system
Esophagus and stomach
Duodenum, prox .to the opening of the bile duct
Liver, biliary apparatus (hepatic ducts, gall bladder,
and bile duct), and pancreas
• Foregut derivatives (other than the pharynx, Lower
respiratory tract, and most of the esophagus) are
supplied by the Celiac trunk- the artery of the
foregut

1.DEVELOPMENT OF ESOPHAGUS
• Develops from the foregut
• Develops caudal to the pharyneal gut .
• Partitioning of the trachea from the esophagus
by the trache-oesophageal septum.
• Initially, it is short ,elongates rapidly, mainly
because of the growth and relocation of the
heart and lungs.

1.DEVELOPMENT OF ESOPHAGUS
Time period : Starts @4th wk, reaches final
length by the 7th wk.
• Epithelium and glands are derived from
endoderm.
Events:
1.Epithelium proliferates and obliterates the
lumen
2.Recanalization of the solid lumen normally
occurs by the end of the 8th week.

1.DEVELOPMENT OF ESOPHAGEAL MUSCLES
Development of Muscles:
Striated muscle (muscularis externa) of the
upper third is derived from mesenchyme in the
4th and 6th pharyngeal arches.
Smooth muscle- in the lower third, develops
from the surrounding splanchnic mesenchyme.
• Both types are innervated by vagus nerves ,
which supply the caudal pharyngeal arches .

TRANS-DIFFERENTIATION
• Myogenic regulatory factors trans-
differentiate of smooth muscle cells in the
superior part of the esophagus to striated
muscle, which is dependent on.

1.Developmental Anaomalies
of
Oespphagus

1.1 ESOPHAGEAL ATRESIA
Blockage (atresia) of the esophageal lumen :
• Incidence - 1 in 3000 to 4500 live births.
• Approx. 1/3 of affected are premature baby.
• 90% Association with tracheoesophageal fistula
Causes:
Deviation of the tracheoesophageal septum in a
posterior direction.
Incomplete separation of the oesophagus from
the laryngotracheal tube.
• Isolated esophageal atresia (5%–7% of cases)
results from failure of recanalization.

1.2.ESOPHAGEAL STENOSIS
• Narrowing of the lumen:
• Occur anywhere along the Oesophagus,
• Usually occurs in its distal third
• Either as a web or a long segment with a thread-
like lumen.
CAUSES:
• Incomplete recanalization of the oesophagus
• From a failure of esophageal blood vessels to
develop in the affected area.

DEVELOPMENT OF STOMACH
Time Period: During the 4th week,
Events:
• Slight dilation (fusiform enlargement) in caudal
(distal part) of the foregut indicates the site of the
primordium of the stomach.
• Dilation is oriented in the median plane .
• Primordial stomach enlarges and broadens ventro-
dorsally.
• During the next 2 weeks, the dorsal border of the
stomach grows faster than its ventral border;
• Dorsal border - greater curvature of the stomach

2.DEVELOPMENT OF STOMACH
• Initially the distal part of the foregut is a tubular
structure
Time period: 4th wk, a slight dilation indicates the site of
the primordium of the stomach.
• Dilation first appears as a fusiform enlargement of the
caudal (distal part) of the foregut and is initially oriented
in the median plane.
Primordial stomach -enlarges and broadens ventro-
dorsally.
• Next 2 weeks - Dorsal border of the stomach grows
faster than its ventral border.
• Dorsal border developing greater curvature of the
stomach .

2.ROTATION OF STOMACH
• Occurs due to enlargement of the mesentery and
adjacent organs, growth of the stomach walls.
• Stomach enlarges and acquires its final shape
• Slowly rotates 90 degrees in a clockwise direction
(viewed from the cranial end) around its longitudinal axis.

2.EFFECTS OF ROTATION ON THE STOMACH
• Ventral border -(lesser curvature) moves to right.
• Dorsal border -(greater curvature) moves to left.
• Left side - Ventral surface.
• Right side - Dorsal surface.
• After rotation, stomach assumes its final position
• Long axis -Transverse to the long axis of the body .
Rotation and growth of the stomach explain why the
left vagus nerve supplies the anterior wall of the
adult stomach and the right vagus nerve
innervates its posterior wall.

2.ROTATION OF STOMACH
 Before rotation-
• Cranial and caudal ends of the stomach are in the
median plane
 During rotation-
• Cranial region -moves to left & slightly inferiorly,
• Caudal region moves to the right & superiorly

2.MESENTERIES OF
STOMACH
MESOGASTRIUM
Dorsal mesentery-
• Suspend Stomach from
the dorsal wall of the
abdominal cavity
• Lies originally in the
median plane
• Carried to the left
during rotation of the
stomach and
formation of the
omental bursa or
lesser sac of
peritoneum
• Contains the spleen
and celiac artery.

2.MESENTERIES OF STOMACH
• Primordial ventral mesogastrium attaches to
the stomach, duodenum to the liver and
ventral abdominal wall

OMENTAL BURSA
• Pouch-like bursa facilitates movements of the
stomach.
• Large recess of the peritoneal cavity.
• Lies between stomach and posterior abdominal wall.
FORMATION:
• Isolated clefts develop in the mesenchyme forming
the thick dorsal mesogastrium.
• Clefts soon coalesce to form a single cavity, the
omental bursa or lesser peritoneal sac .
• Rotation of the stomach pulls the dorsal
mesogastrium to the left, thereby enlarging the
bursa, Expands transversely and cranially

OMENTAL BURSA
• Superior part is cut off as the diaphragm
develops, forming a closed space—infracardiac
bursa.
• If it persists, it lies medial to base of right lung.
• Inferior region of the superior part of the
omental bursa persists as the superior recess of
the omental bursa

OMENTAL BURSA
• As the stomach enlarges, the omental bursa
expands and acquires an inferior recess of the
omental bursa between the layers of the
elongated dorsal mesogastrium—the greater
omentum.
• Inferior recess disappears as the layers of the
greater omentum fuse .
• Omental bursa communicates with the
peritoneal cavity through an opening—the
Omental foramen or Epiploic foaramen

2.DEVELOPMENTAL
ANAOMALIES
OF
STOMACH

2.1.HYPERTROPHIC PYLORIC STENOSIS
• Affects one in 150 males and one in 750 females.
• Marked muscular thickening of the pylorus, Distal
sphincteric region of the stomach
• Circular and the longitudinal muscles in the
pyloric region are hypertrophied.
• Results in severe stenosis of the pyloric canal and
obstruction of the passage of food, the stomach
becomes markedly distended.
• Surgical relief of the pyloric obstruction
(pyloromyotomy) is the usual treatment

2.2.HYPERTROPHIC PYLORIC STENOSIS

3.DEVELOPMENT OF DUODENUM
Time period: Begins to in the 4th wk
Develops from:
From Caudal part of the foregut*
Cranial part of the midgut**, and
Splanchnic mesenchyme associated with these
parts of the primordial gut
• Junction of the two parts*,** of the duodenum is
just distal to the origin of the bile duct .
• Developing duodenum grows rapidly, forming a
C-shaped loop that projects ventrally .

Rotation-
• Rotation of duodenal loop to the right due to
stomach rotation.
• Becomes retroperitoneal as pressed against
the posterior wall of the abdominal cavity
• Supplied by branches of the celiac (foregut )
and superior mesenteric arteries (midgut)
that supply these parts of the primordial gut.

• Period: 5th and 6th weeks
Events :
Proliferation of epithelial cells
Lumen becomes progressively smaller and is
temporarily obliterated.
Vacuolation occurs as the epithelial cells
degenerate;
Duodenum becomes recanalized by the end of
the embryonic period .
Ventral mesentery disappeared.

3.DEVELPOPMENT OF DUODENUM
4th week 5th week

3.1.DUODENAL ATRESIA
• Rare disease, consist of complete occlusion of
the duodenal lumen
• If complete recanalization of the lumen fails to
occur, a short segment of the duo-denum is
occluded .
• Blockage occurs at the junction of the bile and
pancreatic ducts ( hepato-pancreatic ampulla )
• Occasionally the blockage involves the
horizontal (third) part of the duodenum.
• Investigation suggests an autosomal recessive
inheritance.

3.2.DUODENAL STENOSIS
• Partial occlusion of the lumen
• Results from incomplete recanalization
• Most stenoses involve the horizontal (third) and/or
ascending (fourth) parts of the duodenum.

4.DEVELOMENT
OF
LIVER
AND
BILLIARY TREE

4.DEVELOPMENT OF HEPATOBILIARY APPARATUS
Time period: 4th wk.
 Molecular Event: Wnt/β-catenin signaling
pathway plays a key role in this process.
Events:
• Arise as a ventral outgrowth from the distal
foregut.
• Hepatic diverticulum and ventral bud of the
pancreas develop from embryonic endoderm
• FGFs (fibroblast growth factors) secreted by the
developing heart, interact with the bipotential cells
and induce formation of the hepatic diverticulum.

4.DEVELOPMENT OF LIVER
 Events:
 Diverticulum extends into the septum
transversum, a mass of splanchnic mesoderm
between the developing heart and midgut.
Septum transv. forms ventral mesogastrium
Hepatic diverticulum enlarges, divides into 2
parts as it grows between the layers of the
ventral mesogastrium
Larger cranial part - Primordium of the liver
Smaller caudal part - Gallbladder

HEPATIC DIVERTICULUM
Proliferating Endodermal cells forms :
Interlacing cords of hepatocytes
Lining of the intrahepatic part of the biliary A.
Hepatic cords anastomose around endothelium-lined
spaces, the primordia of the hepatic sinusoids.
• Vascular endothelial growth factor Flk-1 (VEGF-Flk-1)
signals for the early morphogenesis of the hepatic
sinusoids (primitive vascular system).
• Fibrous and hematopoietic tissue and Kupffer cells of
the liver are derived from mesenchyme in the septum
transversum.

DEVELOPMENT OF LIVER,5TH WEEK
• Quantity of oxygenated blood flowing through umbilical
v. into the liver determines the development and
functional segmentation of the liver.

DEVELOPMENT OF LIVER
Events;
• 5th to 10th wks-Rapid growth of liver , fills a
large part of the upper abdominal cavity
• 6th week- Hematopoiesis begins, giving the
liver a bright reddish appearance
• 9th wk- liver -approx 10% of the total wt of fetus
• 12th wk -Bile formation by hepatic cells begins .
• Initially, the right and left lobes are approx.
same size, but the right lobe becomes larger .

CAUDAL PART OF THE HEPATIC DIVERTICULUM
• Forms gallbladder, and the stalk of the diverticulum
forms the cystic duct .
• Initially, Extrahepatic biliary apparatus is occluded with
epithelial cells, but it is later canalized because of
vacuolation resulting from degeneration of these cells.
• Stalk connecting the hepatic and cystic ducts to the
duodenum becomes the bile duct.
• Initially, this duct attaches to the ventral aspect of the
duodenal loop; however, as the duodenum grows and
rotates, the entrance of the bile duct is carried to the
dorsal aspect of the duodenum .
• Bile entering the duodenum through the bile duct after
the 13th week gives the meconium (intestinal contents)
a dark green color.

VENTRAL MESENTERY
• Thin, double-layered membrane gives rise to:
• 1.Lesser omentum - passing from the liver to the
lesser curvature of the stomach (hepatogastric
ligament) and from the liver to the duodenum
(hepatoduodenal ligament)
• 2.Falciform ligament, extending from the liver to
the ventral abdominal wall
• Umbilical vein - passes in the free border of the
falciform ligament
• Liver is covered by peritoneum except for the
bare area that is in direct contact with the
diaphragm

• Minor variations are common, but congenital
anomalies of the liver are rare.
• Variations of the hepatic ducts, bile duct, and
cystic duct are common and clinically significant.

4.ANOMALIES OF
HEPATOBILLARY
APPARATUS
• Accessory hepatic ducts-
5% of the population.
• Accessory ducts are narrow
channels running from the
right lobe of the liver into
the anterior surface of the
body of the gallbladder.
• In some cases, the cystic
duct opens into an
accessory hepatic duct
rather than into the
common hepatic duct.

4.EXTRAHEPATIC BILIARY ATRESIA
• Most serious anomaly (one in 5000 -20,000 live births)
• Most common form-(85% of cases) is obliteration of the bile
ducts at or superior to the porta hepatis
• S/S: Jaundice , acholic (clay colored ) stools , dark colored urine
appears,70% of those treated, the disease continues to
progress.

DEVELOPMENT OF PANCREAS
• Develops from
dorsal and ventral
pancreatic buds
of endodermal
cells,
• Develops between
the layers of the
mesentery which
arise from the
caudal of the
foregut .
Most of the pancreas is derived from
the larger dorsal pancreatic bud,
which appears first and develops a
slight distance cranial to the ventral
bud.

VENTRAL PANCREATIC BUD
• Develops near the entry of the bile duct into the
duodenum, between the layers of the ventral mesentery.
• Carried dorsally with the bile duct as the duodenum
rotates to the right and becomes C shaped.
• Lies posterior to the dorsal pancreatic bud and later
fuses with it.

PANCREATIC DUCT SYSYEM
Ventral pancreatic bud- forms the
Uncinate process
Part of the head of the pancreas.
• As the foregut rotate, the pancreas comes to lie
along the dorsal abdominal wall.
• fusion of pancreatic buds causes their ducts
anastomose.
Pancreatic duct is formed from -
Duct of the ventral bud and the
Distal part of the duct of the dorsal bud .

PANCREATIC DUCT SYSYEM
• Proximal part of the duct of the dorsal bud
persists as an accessory pancreatic duct that
opens into the minor duodenal papilla,
• Minor duodenal papilla located
approximately 2 cm cranial to the main duct.
• Two ducts often communicate with each
other.
• In approximately 9% of people, the pancreatic
ducts fail to fuse, resulting in two ducts.

MOLECULAR STUDIES
Ventral pancreas develops from a
Bipotential cell population in the ventral
region of the duodenum where the
transcription factor PDX1 is expressed.
FGF-2, which is secreted by the developing
heart
Dorsal pancreatic bud develops from
Notochord secreting activin
FGF-2,

HISTOGENESIS OF PANCREAS
• Parenchyma -derived from the endoderm of the
pancreatic buds, which forms a network of tubules.
• Pancreatic acini - begin to develop from cell clusters
around the ends of these tubules (primordial
pancreatic ducts).
• Pancreatic islets -develop from groups of cells that
separate from the tubules and lie between the acini.
• chemokine SDF-1, controls formation and branching
of the tubules.
• Expression of Ngn-3 (neurogenin-3) is required for
differentiation of pancreatic islet endocrine cells.

HISTOGENESIS OF PANCREAS
• Insulin secretion begins during 10 wks.
• Glucagon- and somatostatin-containing cells develop
before differentiation of beta-cells.
• Glucagon- detected in fetal plasma at 15 weeks.
• CT sheath and interlobular septa develop from the
surrounding splanchnic mesenchyme.
• In maternal DM, the insulin-secreting beta cells in
the fetal pancreas are chronically exposed to high
levels of glucose. As a result, these cells undergo
hypertrophy to increase the rate of insulin secretion.

ANOMALIES OF PANCREAS
• Ectopic pancreas –
• often located in the wall of the stomach,
duodenum, or jejunum.
• Can present with obstruction, bleeding, or
even as cancer.

ANNULAR PANCREAS
• Is rare anomaly
• Ring-like or annular part of the pancreas
consists of a thin, flat band of pancreatic
tissue
• Surrounds the descending or second part of
the duodenum.
• Cause obstruction of the duodenum.
• Infants present with symptoms of complete or
partial bowel obstruction.

ANNULAR PANCREAS
• Blockage of the duodenum develops if
pancreatitis develops in the annular pancreas.
• Associated with Down syndrome, intestinal
malrotation , and cardiac defects.
• Females are affected more frequently than
males.
• Probably results from the growth of a bifid
ventral pancreatic bud around the duodenum.

ANNULAR PANCREAS
• Parts of the bifid ventral bud then fuse with
the dorsal bud, forming a pancreatic ring.
• Surgical intervention may be required for
management of this condition.

SPLENIC PRIMORDIUM
• Derived from a mass of mesenchymal cells
located between the layers of the dorsal
mesogastrium.
• Begins to develop during the 5th wk,
• Capsulin, a basic transcription factor, and
homeobox genes regulate the development

SPLENIC PRIMORDIUM
• Lobulated in the fetus, lobules normally
disappear before birth.
• Notches in the superior border of the adult
spleen are remnants of the grooves of lobules.
• Stomach rotation causes the left surface of the
mesogastrium fuses with the peritoneum over the
left kidney.
• Dorsal attachment of the Lienorenal ligament .
• Splenic artery follows a tortuous course posterior
to the omental bursa

SPLENIC PRIMORDIUM
 Mesenchymal cells in the differentiate to form
Capsule,
Connective tissue framework, and
Parenchyma of the spleen.
• Spleen functions as a hematopoietic center until
late fetal life;
• However,it retains its potential for blood cell
formation even in adult life.

ANOMALIES-ACCESSORY SPLEENS
(POLYSPLENIA)
• Small splenic masses (1cm in diam.) of splenic
tissue may exist in one of the peritoneal folds,
Hilum of the spleen,
Tail of the pancreas, or
Gastrosplenic ligament.
• Accessory spleens (polysplenia) are usually
isolated but may be attached to the spleen by
thin bands.
• Occurs in approximately 10% of people.

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