GOOD MORNING…

Development of digestive system.

DEVELOPMENT OF NOSE:
At the end of the fourth week, five
swellings (facial primordia) appear
around the primitive mouth (stomodeum)
The frontonasal process
The paired maxillary processes
 The paired mandibular processes.

On each side of the median plane in the ventrolateral part of frontonasal process,
surface ectoderm thickens to form an ectodermal elevation the olfactory placode.

The olfactory placodes invaginate into the underlying mesoderm to form olfactory
pits or nasal pits.

The mesenchyme around margins of nasal pits

proliferates to form horseshoe shaped elevations.

Medial half of horseshoe-shaped

elevation is called medial nasal process and
Lateral half is called lateral nasal process.
 Development of Palate

Embryologically the palate consists of two parts: primary palate and secondary
palate

The primary palate develops from the frontonasal process and secondary palate
develops from the maxillary processes.

Development of palate begins in the sixth week and completes by the end of the twelfth
week. The palate develops in two stages:
1. Development of primary palate
2. Development of secondary palate.
 Development of Primary Palate:

The primary palate is formed by fusion of two medial nasal processes of the frontonasal
process.
The fusion of these processes (at a deeper level) forms a wedge-shaped mass of
mesenchyme opposite upper jaw carrying four incisor teeth called primary palate. It
ossifies to form premaxilla.
 Development of Secondary Palate:

It is formed by fusion of two shelf-like outgrowths called palatine shelves from inner aspects
of the maxillary processes. The palatine shelves appear in the sixth week of development.

Initially they grow downward and medially on each side of and below the tongue.
Later, during the seventh and eighth week they assume horizontal position
above the tongue and fuse with each other to form the secondary palate.
The posterior parts of these processes that extend posteriorly beyond the nasal
septum fail to ossify and form the soft palate, including its soft conical projection—uvula.
 Development of palate

Palatine shelf – from maxillary prominence. Palate after the removal

Vertical in position, on either side of the of the lower jaw
tongue
Development of palate
 Development of palate

Tongue has moved downwards Palatine shelves horizontal,

and palatine shelves horizontal observe the nasal septum
Development of palate
Development of palate
Palate and its components
 Unilateral cleft lip, jaw
Unilateral cleft lip
Normal and extending to the
extending to nose
incisive foramen

Bilateral cleft involving Isolated cleft palate Cleft palate combined

lip and jaw with anterior cleft lip
 Development of Teeth:

The teeth develop in relation to alveolar process involving reciprocal induction

between neural crest mesenchyme and overlying ectodermal oral epithelium.
Stages of Development of Tooth The ectodermal epithelium overlying the
upper convex border of the alveolar process
becomes thickened and
projects into underlying mesoderm to form
the dental lamina.

The dental lamina now proliferates at ten

sites to produce local swellings called tooth
buds (enamel organs) that grow into the
underlying mesenchyme.

The mass of underlying neural crest

mesenchyme invaginates the tooth
bud/enamel organ. As a result, the enamel
organ becomes cap shaped. This mass of
mesenchyme that invaginates the tooth bud
is called dental papilla.

The enamel organs differentiate into three

layers:
1. Outer cell layer called outer enamel epithelium
2. Inner cell layer called inner enamel epithelium
3. Central core of loosely arranged cells called enamel
reticulum.
The cells of the enamel organ that line the dental papilla (cells of the inner layer enamel
epithelium) become columnar and are now called ameloblasts.

The mesodermal cells of dental papilla

adjacent to ameloblasts arrange themselves as
a continuous epithelial layer. The cells of this
layer are called odontoblasts.

The ameloblasts derived from inner enamel

epithelium of the enamel organ form the
enamel and
the odontoblasts derived from dental papilla
form the dentine and dental pulp.

The ameloblasts (enamel frame) form enamel in the form of long prisms over the dentin. As
the amount of enamel increases, the ameloblasts move towards the outer enamel
epithelium. As a result, enamel reticulum and outer enamel epithelium disappear.
After the enamel is fully formed ameloblasts also
regress, leaving only a thin membrane—the
dental cuticle. After the eruption of tooth, this
membrane is gradually sloughed off.

The outer and inner enamel epithelia come

together at the neck of the tooth where they
form a fold—the Hertwig’s epithelial root
sheath. This sheath grows in the mesenchyme
and initiates the formation of the root.

As more and more dentine is produced, the pulp

cavity narrows and forms the pulp canal through
which nerve and vessels pass.

The inner cells of dental sac differentiate into

cementoblasts that produce the cementum (a
specialized bone).

The mesenchyme cells of the outside cement

layer give rise to the periodontal ligament
Early in the fourth week of intrauterine development, a series of surface elevations
appear in the lateral wall of primitive pharynx caudal to stomodeum. These
elevations are termed pharyngeal arches.

Initially the pharyngeal arches are confined in the lateral wall of the primitive pharynx.
But gradually they extend ventrally and fuse with their counterparts of the opposite
side in floor of the primitive pharynx to form horseshoe-shaped cylindrical bars.

Initially there are six arches. The fifth arch is small and rudimentary, and soon
disappears. Thus, only five pharyngeal arches remain.
The pouches between them on the inner aspect of the pharyngeal wall are termed
pharyngeal pouches and
grooves between them on the outer aspect of the pharyngeal wall are called
pharyngeal clefts.

1. Pharyngeal arches: Five in number and present in the lateral wall and floor of the
primitive pharynx. made up of mesoderm
2. Pharyngeal clefts (grooves): Four in number and present externally between the arches.
They are lined by ectoderm.
3. Pharyngeal pouches: Four in number and located internally between the two pharyngeal
arches. They are lined by endoderm.
4. Pharyngeal membranes: Four in number and located between the two adjacent arches
where pharyngeal cleft and pouches are opposed to each other.
 Components of a Pharyngeal Arch

● A core of mesoderm derived from paraxial mesoderm and neural crest cells. It is
covered externally by ectoderm and internally by endoderm.
● A cartilaginous bar/rod derived from neural crest mesenchyme.
● A pharyngeal arch artery that arises from corresponding horn of aortic sac (truncus
arteriosus) of primitive heart.
● A nerve derived from hind brain vesicle.
 The nerve of arch:
Morphologically each pharyngeal
arch is supplied by two nerves.
The nerve that runs along cranial
border of the arch is known as
post-trematic nerve and nerve
that runs along its caudal border
is called pretrematic nerve.
Muscles of the Pharyngeal Arches:
Cartilages of the Pharyngeal Arches:
Cartilages of the Pharyngeal Arches:
Cartilages of the Pharyngeal Arches:
Arteries of Pharyngeal Arches:
Pharyngeal Arch: summary
Pharyngeal Pouches:
Pharyngeal Pouches:
Pharyngeal Clefts (Grooves):
 Development of Tongue:
The tongue develops in the floor of developing mouth from first, second, third, and
fourth pharyngeal arches.

At the end of the fourth week of intrauterine life (IUL), a small median triangular
swelling called tuberculum impar develops in the floor of primitive pharynx, just
cranial to foramen cecum.*

Soon after the appearance of tuberculum

impar the two lateral oval swellings called
lingual swellings develop one on each
side of tuberculum impar

Caudal to tubercular impar a second large

median swelling called hypobranchial
eminence develops in the floor of primitive
pharynx in relation to second, third, and
fourth pharyngeal arches.
The hypobranchial eminence soon
subdivides into large cranial part and
small caudal part.
Development of Tongue:
 Development of Various Parts of Tongue:

The two lateral lingual swellings overgrow the

tuberculum impar and merge with each other to
form anterior two-third of the tongue.
The line of fusion of two lingual swellings in the
median plane forms median sulcus on the
dorsal surface of the tongue.

The tuberculum impar does not form any

recognizable part of the adult tongue.

The posterior one-third of the

tongue including circumvallate
papillae develops from cranial part of
hypobranchial eminence

The posterior most part of the

tongue and epiglottis develop from
the caudal part of the hypobranchial
eminence.
Development of Various Parts of Tongue:
 The muscles of tongue:
The muscles of tongue develop from myoblasts that migrate into developing
tongue from the occipital myotomes.

The hypoglossal nerve —the nerve of occipital myotomes—accompanies the

myoblasts during their migration to the pharyngeal arches and innervates the
muscles of tongue as they develop.
The digestive tract (gastrointestinal tract) develops from primitive gut that is derived
from the dorsal part of endodermal yolk sac.

The primitive gut forms during the fourth week of intrauterine life by the incorporation
of a larger portion of the yolk sac (umbilical vesicle) into the embryonic disc during
craniocaudal and lateral folding of embryo.
The tubular primitive gut extends in the median plane from buccopharyngeal
membrane at its cranial end to cloacal membrane at its caudal end.
It freely communicates with the remaining yolk sac by the vitellointestinal duct.

The part of gut cranial to this communication is called foregut, part caudal to this
communication is called hindgut, and part intervening between foregut and hindgut
is called midgut.
The cranial end of foregut is
separated from the stomodeum
by buccopharyngeal membrane
while caudal end of hindgut is
separated from the proctodeum by
cloacal membrane.

At later stage of development buccopharyngeal and cloacal membranes rupture, and

gut communicates to exterior at its both ends.

The mucosa is derived from endoderm.

The muscular, connective tissues, and

other layers of wall of the digestive tract
are derived from splanchnopleuric
mesoderm surrounding the primitive gut.
While the primitive gut is being formed the
midline artery, dorsal aorta, gives off a
series of ventral branches to the gut.

Those in the region of midgut run right up

to the yolk sac and are, therefore, termed
vitelline arteries. Later most of these
ventral branches of dorsal aorta disappear
and only three of them remain:

one of foregut (the celiac artery),

one of midgut (the superior mesenteric
artery), and
one of hindgut (the inferiormesenteric
artery)
Esophagus:
The esophagus develops from the part of foregut
between the pharynx and the stomach.

Ventrally at the pharyngoesophageal junction, the

foregut presents a median laryngotracheal groove.

The groove bulges forward and caudally to form

tracheobronchial (respiratory) diverticulum.

The tracheoesophageal septum

divides the foregut caudal to the pharynx into the
esophagus and trachea
1. Esophageal atresia: It occurs due to failure
of recanalization of the developing esophagus.

The esophageal atresia is often associated with

tracheoesophageal fistula.
It is produced by extreme posterior deviation of
tracheoesophageal septum.

In esophageal atresia, the fetus is unable to

swallow amniotic fluid; hence there is an abnormal
increase in the amount of amniotic fluid producing
a clinical condition called polyhydramnios.

The newborn with esophageal atresia accepts the

first feed (viz., milk or fluid diet) normally, but
when givens ubsequent feed, it regurgitates
through the mouth and nose; and may cause
respiratory distress and cyanosis.

The surgical correction (treatment) gives 85%

survival rate.
2. Esophageal stenosis:
In this anomaly, the lumen of the esophagus is narrow usually in lower third part. It
is caused by incomplete esophageal recanalization and vascular abnormalities.

3. Tracheoesophageal fistula:
It occurs due to failure of separation of tracheobronchial diverticulum from
esophagus due to nonformation of tracheoesophageal septum .
In most of the cases (85%) the lower segment of esophagus communicates with the
trachea.

4. Achalasia cardia:
It occurs due to failure of relaxation of the musculature in the lower part of the
esophagus following loss of ganglionic cells in Aurbach’s plexus. Clinically patient
complains of difficulty in swallowing. On barium swallow, the lower part of esophagus
presents pencil-shaped narrowing (bird beak deformity).

[Link] esophagus:
It occurs when esophagus fails to elongate during development. When the
esophagus fails to elongate, the stomach is pulled up into the esophageal hiatus of
diaphragm causing congenital hiatal hernia.
Stomach:
The stomach appears as a fusiform dilatation of foregut distal to the esophagus in the
fourth week of intrauterine life (IUL).

This dilatation presents a ventral border and dorsal border, a left surface and
right surface, and an upper end and a lower end.
Change in Shape and Position of Stomach :
The change in shape of stomach occurs due to differential growth in its different
regions.

Dorsal border grows much more than ventral border and forms greater curvature of
the stomach, while the ventral border forms lesser curvature of the stomach.

The changes in position of the stomach can be easily explained by assuming that it
rotates twice:
(a)around a longitudinal axis and (b) around an anteroposterior axis.
 Rotation of
stomach:

● First the stomach rotates 90° clockwise around its longitudinal axis.
As a result, its left surface now faces anteriorly and forms anterior surface.
Similarly, its right surface faces posteriorly to form posterior surface.

For this reason left vagus nerve initially supplying the left surface of stomach now
supplies its anterior surface and right vagus nerve initially supplying the right surface
now supplies its posterior surface.

● The cephalic and caudal ends of stomach originally lie in the midline
Now the stomach rotates around its anteroposterior axis.

As a result, the cardiac end of stomach originally lying in the midline moves to
the left and slightly downward, and

The pyloric end originally lying in the midline moves to the right and slightly
upward.
 Change in the Mesenteries of the Stomach Due to its Rotation

The dorsal border provides attachment to dorsal mesentery (dorsal mesogastrium)

that extends from the stomach to posterior abdominal wall.

The ventral border provides attachment to ventral mesentery (ventral mesogastrium)

that extends from the stomach to septum transversum and anterior abdominal wall.
 Change in the Mesenteries of the Stomach Due to its Rotation

When liver develops in the septum transversum, the ventral mesogastrium is

divided in two parts.
The part extending from the stomach to the liver is called lesser omentum, and the
part extending between the liver and anterior abdominal wall is called falciform
ligament of the liver.
 Change in the Mesenteries of the Stomach Due to its Rotation

When the spleen develops from mesoderm lying between the two layers of dorsal
mesogastrium.

The dorsal mesogastrium is divided in two parts.

The part extending from greater curvature (fundus) of the stomach to spleen forms
the gastrosplenic ligament,
While the part extending from spleen to posterior abdominal wall forms the
lienorenal ligament.
The dorsal mesogastrium attached to rest of greater curvature elongates
and forms a large apron-like fold of peritoneum called greater omentum.
 Change in the Mesenteries of the Stomach Due to its Rotation

The rotation of stomach along its longitudinal axis pulls the dorsal mesogastrium to
the left, creating a space behind the stomach called lesser sac of peritoneum
(omental bursa)
Duodenum:
The duodenum develops from two sources (dual origin):
(a) proximal half is derived from foregut and (b) distal half is derived from midgut.

(a) The first and second part of duodenum up

to the opening of common bile duct develop
from foregut,

(b) the second part of the duodenum below the

opening of common bile duct along with third
and fourth part develop from midgut.

The developing duodenum forms a loop

that is attached to posterior abdominal wall
by a mesentery called mesoduodenum

Initially development of the lumen of the

duodenum is obliterated by the proliferation of
endodermal cells.
Later on cells in the lumen disintegrate and the
duodenum gets recanalized.
Development of Midgut Derivatives:
The superior mesenteric artery, the
artery of midgut, runs posteroanteriorly
through the middle of the mesentery of
the midgut loop.

The superior mesenteric artery divides

the midgut loop into two segments:
1. Prearterial (proximal) segment
2. Postarterial (distal) segment

The prearterial segment is cranial

The midgut elongates to form a U-shaped and the postarterial segment is
primary intestinal loop. caudal.
This U-shaped loop is suspended from The postarterial segment near
posterior abdominal wall by a short the apex of midgut loop develops a
mesentery and at its apex, small conical diverticulum—the cecal
bud at its antimesenteric border.
it communicates with the yolk sac through
narrow vitellineduct / vitellointestinal
duct/yolk stalk.
Development of
Midgut Derivatives:
Rotation of Midgut Loop:

● Before rotation, the prearterial segment of

midgut loop,superior mesenteric artery, and
postarterial segmentof midgut loop, from above
to downward, lie in thevertical (sagittal) plane.

1. Before return into the abdominal cavity, the

prearterial segment of midgut loop undergoes
90° anticlockwise rotation.
As a result (as seen from the front), the
prearterial segment comes to the right and the
postarterial segment goes to the left.

The prearterial segment of midgut loop elongates

extensively and forms coils of jejunum and ileum,
which lie on the right side of superior mesenteric
artery, outside the abdominal cavity.
2. As these coils of jejunum and ileum return to the
abdominal cavity, the midgut loop undergoes
second 90° anticlockwise rotation

so that coils of jejunum and ileum (derived from

prearterial segment) pass behind the superior
mesenteric artery.

As a result, the duodenum goes behind the superior

mesenteric artery.

3. Lastly when the postarterial segment returns to

the abdominal cavity it undergoes third 90°
anticlockwise rotation.

As a result, cecum and an appendix that develop

from cecal bud now come to lie on the right side just
below the liver.
Final positions of intestinal loops:
The orientation of pre- and postarterial segments of midgut loop at different phases of
rotation (three 90° anticlockwise rotations)

● In order to return in the abdominal cavity, the midgut loop undergoes rotation of 90°
in anticlockwise direction thrice.

Thus, there is a total rotation of 270° out of which

first 90° rotation occurs within umbilicus (i.e., outside the abdominal cavity) and
remaining 180° rotation occurs within the abdominal cavity.
Development of Cecum and Appendix:

The cecum and appendix develop from cecal

bud—a conical dilatation that appears in the
postarterial segment of the midgut loop near its
apex (i.e., site of attachment of vitelline duct).

The proximal part of the bud grows rapidly

and forms cecum,

while its distal part remains narrow to form the

appendix.
 Change in Shape of Cecum and Appendix:

The growth of the

cecum after birth
leads to a change
in its shape and
change in position of
attachment of the
appendix.

At birth, the cecum is conical in shape and vermiform appendix is attached at its apex. Later
cecal growth results in formation of two saccules—one on either side.
The right saccule grows faster than the left. As a result, the apex of the cecum and the base of
the appendix is pushed towards left, nearer to ileocecal junction.
For this reason in adults, the base of the appendix is attached to posteromedial wall of the
cecum, near the ileocecal junction.

1. Conical (fetal) type (2%)

2. Infantile (quadrate) type (3%)
3. Normal type (80–90%)
4. Exaggerated type (4–5%).
Exomphalos or omphalocele:

This anomaly results from failure of coils of the small intestine to return into
abdominal cavity from their physiological herniation into extraembryonic celom
during sixth to tenth week of IUL.

Itoccurs in 2.5/10,000 births and could be associated with cardiac and neural tube
defects.
Clinically, it presents as a rounded mass protruding from the umbilicus. This mass
contains coils of the small intestine and is covered by a transparent amniotic
membrane.
Anomalies of vitellointestinal duct:
Vitellointestinal duct connects the apex of midgut loop to yolk sac.
Normally it disappears completely.
The failure to disappear completely or in part will produce following anomalies of
vitellointestinal duct.

(a) Meckel’s diverticulum:

A small part of vitellointestinal duct close to midgut (ileum) persists and forms the
Meckel’s diverticulum. It may be connected to the umbilicus
by a fibrous cord (the obliterated remaining part of vitellointestinal duct).
(b) Umbilical sinus :
It occurs when part of vitellointestinal
duct close to umbilicus persists, i.e., fails to
[Link] sinus communicates with the
umbilicus.

(c) Vitelline (umbilical) fistula :

It occurs when vitellointestinal duct fails to
obliterate along its entire extent.

This fistula communicates with ileum at one

end and opens to exterior at the umbilicus at
the other end.
Clinically, the ileal contents may be discharged
through the umbilicus.

(d) Vitelline cyst :

When small middle part of vitellointestinal
duct persists (i.e., fails to obliterate), it forms
cyst.
Anomalies due to errors of rotation of midgut loop

(a) Nonrotation: In this anomaly, the midgut

loop fails to rotate.
The caudal or postarterial segment returns first
in the abdominal cavity.
Hence, large intestine occupies the left side of
the abdominal cavity while the small intestine
derived from prearterial segment returns later
and occupies the right side of the abdominal
cavity.

(b) Partial rotation: In this anomaly, first 180° of rotation takes place normally
but last 90° of rotation does not take place. As a result, cecum and appendix,
instead of being on the right side of the abdominal cavity, are located just below
pylorus of stomach.

(c) Reversed rotation: In this anomaly, the midgut loop rotates clockwise instead
of anticlockwise. In this condition, transverse colon passes behind duodenum and
lies behind the superior mesenteric artery .
if ascending colon does not form or remains too short, the cecum does not descend
and remains permanently below the liver leading to congenital anomaly called
subhepatic cecum and appendix.

In cases of subhepatic cecum and appendix, the inflammation of appendix

(appendicitis) would cause tenderness in right hypochondrium that may lead to
mistaken diagnosis of cholecystitis (inflammation of gall bladder).
Development of Hindgut Derivatives:
1. Left one-third of transverse colon
2. Descending colon
3. Sigmoid colon
4. Rectum
5. Upper part of the anal canal.
 Development of Rectum;

The terminal dilated part of the hindgut distal to allantois is called cloaca.

It is divided into two parts by urorectal septum:

(a) a broad ventral part called primitive urogenital sinus and
(b) a narrow dorsal part is called primitive rectum.

The urogenital sinus gives rise to the urinary bladder and urethra, while the
primitive rectum gives rise to the rectum and upper part of the anal canal.
 Development of Anal Canal:
The anal canal develops from two sources: (a) hindgut and (b) proctodeum.

The upper half of the anal canal is endodermal in origin and develops from primitive
rectum.

Ecto
The lower half of the anal canal is endodermal in origin and develops from anal pit
called proctodeum.

Initially, the two parts are separated from each other by anal membrane. Later when
this membrane ruptures the two parts communicate with each other. The
site of anal membrane is represented by pectinate line in adults
Congenital megacolon (Hirschsprung’s disease)
In this anomaly, a segment of the colon is dilated.
However, it is the segment distal to dilatation that is abnormal.

In this abnormal segment, autonomic parasympathetic ganglia are absent in the

myenteric plexus.
As a result there is no peristalsis in this segment. Since contents of colon cannot
pass through this segment, the segment proximal to it grossly dilates.
Imperforate anus:
It is a clinical condition in which the lower part of gut (GIT) fails to communicate with
exterior.

a) The rectum and anal canal develop

normally but anal membrane fails to breakdown.
The anal membrane bulges out with accumulated
contents proximal to it. This is a minor form of
imperforated anus and can be corrected by
excision of the anal membrane.

( (b) The proctodeum remains a solid mass of

ectodermal cells, and there is a big gap between
it and upper part of the anal canal.

(c) The upper and lower parts of the anal canal remain separated by a gap.

(d) The anal canal is stenosed. In this condition, anal canal and anal orifice are
extremely narrow. It occurs when urorectal septum deviates dorsally as it reaches
cloacal membrane.
Rectal fistulae :
The rectal fistulae are frequently seen in association with the imperforated anus.

The common types of rectal fistulae are

(a) rectovaginal fistula,
(b) Rectovesical fistula,
(c) rectourethral fistula.

The rectal fistulae are usually associated with rectal atresia.

 Liver:

The liver, the largest gland in the body, develops from following three sources:

1. Parenchyma of the liver is derived from endodermal hepatic bud of foregut.

2. Fibrous stroma of the liver is derived from mesenchyme of septum
transversum, a plate of intraembryonic mesoderm at the cranial edge of embryonic
disc.
3. Sinusoids of liver develop from absorbed and broken vitelline and umbilical veins
within the septum transversum.
Liver: The hepatic bud grows into the
ventral mesogastrium and through it
into the septum transversum

The bud soon divides into two parts: a

large cranial part called pars
hepatica and a small caudal part
called pars cystica.
The pars hepatica forms the liver,
while pars cystica forms the
gallbladder and cystic duct. The
part of bud proximal to pars cystica
forms common bile duct (CBD).

The pars hepatica further divides into

right and left portions that form right
and left lobes of the liver
respectively. Initially both lobes of the
liver are of equal size.
Liver:
 Congenital anomalies of the liver:

Riedel’s lobe:
It is a tongue-like extension from the right lobe of
the liver It develops as an extension of normal
hepatic tissue from the inferior margin of the right
lobe of the liver.

Polycystic disease of the liver:

The biliary tree within the liver (i.e., bile canaliculi and bile ductules) normally
connects them with the extrahepatic bile ducts. Failure of union of some of these
ducts may cause the formation of cysts within the liver.

Intrahepatic biliary atresia:

It is a very serious anomaly. The intrahepatic biliary atresia cannot be subjected
to surgical correction.
As a result, there are only two options for parents:
(a) to go for liver transplant of the child or (b) to let the child die.
Anomalies of gallbladder:
Anomalies of extrahepatic biliary ducts:
 Development of Pancreas:
The dorsal pancreatic bud arises from dorsal wall of foregut and grows between
two layers of the dorsal mesentery of duodenum

the ventral pancreatic bud arises from ventral wall of foregut in common with/or
close to the hepatic bud and grows between the two layers of ventral mesentery.

When the duodenum rotates to right and becomes C shaped, the ventral pancreatic
bud is on the right and the dorsal pancreatic bud is on the left of the duodenum

With rapid growth of right duodenal wall, the ventral pancreatic bud shifts from right to
left and lies just below the dorsal pancreatic bud.
 Development of Pancreas:

The dorsal and ventral pancreatic buds grow in size and fuse with each other to form
the pancreas.

The dorsal pancreatic bud forms the upper part of head, neck,body, and tail of
the pancreas
while ventral pancreatic bud forms the lower part of the head and uncinate
process of pancreas..
Development of Pancreas:
 Development of Ducts of the Pancreas:

Initially two parts of the pancreas derived

from two pancreatic buds have separate
ducts called dorsal and ventral
pancreatic ducts that open separately into
the duodenum.

Opening of dorsal pancreatic duct is about

2 cm proximal to opening of the ventral
pancreatic duct. The ventral pancreatic
duct opens in common with the bile duct
derived from the hepatic bud.
Now communication (anastomosis)
develops between the dorsal and ventral
pancreatic ducts.

The main pancreatic duct (duct of Wirsung) develops from:

(a) dorsal pancreatic duct distal to anastomosis between the two ducts,
(b) anastomosis (communication) between the two ducts, and
(c) Ventral pancreatic duct proximal to the anastomosis.
The proximal part of the dorsal pancreatic duct may persist as accessory
pancreatic duct (duct of Santorini).
Anomalies of pancreas:

1. Annular pancreas In this condition, the

pancreatic tissue completely surrounds second
part of the duodenum causing its obstruction.

The bifid ventral pancreatic bud fails to fuse to

form a single mass.

The two lobes (right and left) of the ventral

pancreatic bud grow and migrate in opposite
directions around the second part of the
duodenum and form a collar of pancreatic tissue.
2. Divided pancreas:

It occurs when the dorsal and ventral pancreatic buds fail to fuse with each other.
As a result, the two parts of pancreas derived from two buds remain separate
from each other.
Thank you…