DEVELOPMENT OF THE GUT

Dr J.O. Ezugworie

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 GUT TUBE : INTRODUCTION.

• Formed by incorporation of endoderm lined yolk sac

into the embryo
• Cephalocaudal and lateral folding of the embryo is
the cause of incorp0rating the endoderm.
• The gut tube or primitive gut has 4 sections
- Pharyngeal gut or pharynx - from oropharyngeal
membrane to the respiratory diverticulum.
- Foregut –caudal to the pharynx, up to the liver
bud.
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 GUT TUBE : INTRODUCTION
- Mid-gut-caudal to the foregut ,up to the junction
of the proximal 2/3 and distal 1/3 third (left) of
the transverse colon.
- Hindgut- From the left third of the transverse
colon to the cloacal membrane.
Endoderm forms the epithelial lining of the digestive
tract .
The splanchnic or visceral mesoderm forms the
muscle ,connective tissue and peritoneal
components of the wall of the gut.
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 DEVELOPMENTOF THE FOREGUT
DEVELOPMENT OF THE OESOPHAGUS.
• 4th week event in the foregut.
• From the dorsal portion of the foregut at the border
with the pharyngeal gut.
• Tracheo-esophageal septum separates the dorsal
portion from the ventral portion which forms the
lung bud.
• The short oesophagus rapidly increases in length
with the descent of the heart and lungs.

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 DEVELOPMENTOF THE FOREGUT
• Visceral mesenchyme forms striated muscle in the
upper 2/3 of the oesophagus (nerve-vagus)
• And smooth muscle in the lower 1/3 (nerve,
splanchnic plexus).

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 STOMACH
• Fusiform dilation of the foregut in the midline
by 4th week of development close the
respiratory diverticulum in the thorax.
• The shape and position change overtime due
to:
 Various parts of the stomach wall growing at
different rates.
 Change in position of the surrounding organs.

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 STOMACH
 Positional changes (assumption) - rotation around a
longitudinal and an anterio-posterior axis.
• Rotation, 90 degrees clockwise ,longitudinal axis -
7th week
- Left side faces anteriorly ( Left vagus- anterior
stomach wall)
- Right side faces posteriorly (right vagus- post wall)
• Original posterior wall, faster growth—greater
curvature

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 STOMACH
• Original anterior wall, slow growth—lesser curvature
• During further growth
• Rotation, anterio-posterior axis -8th week,
• The caudal or pyloric end moves to the right and
upwards
• The cephalic or cardiac portion moves to the left and
slightly downward

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 STOMACH
• Stomach rotation and disproportionate
growth alter the position of these
mesenteries
Rotation, longitudinal axis
• Pulls the dorsal mesogastrium to the
left, and
• Creating the omental bursa (lesser
peritoneal sac) –a space behind the
stomach,
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 STOMACH

• Also the ventral mesogastrium is pulled to

the right
Rotation , anterior - posterior axis
• The dorsal mesogastrium bulges down
forming a double layered sac—the greater
omentum.
- The layers later fuse.

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 DEVELOPMENT OF THE DUODENUM
• Formed by the terminal part of the foregut and the
cephalic part of the mid-gut.
• The junction of the two parts, just distal to the
origin of liver bud
• The duodenum becomes C-shaped as a result of the
rotation of the stomach.
• The duodenum then rotates to the right.
• This rotation and rapid growth of the head of the
pancreas swing the duodenum from the midline to
the right.
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 DEVELOPMENT OF THE DUODENUM
• 2nd month of the development:
- The lumen of the duodenum is obliterated by
proliferation of epithelial cells .
- Recanalisation shortly afterwards.
- Dorsal meso-duodenum disappears except at
the duodenal cap
* Superior mesenteric artery supplies the
duodenum.
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 DEVELOPMENT OF THE MIDGUT
• In the 5th week of development:
A short mesentery suspends mid-gut from the
posterior abdominal wall.
The vitelline duct or yolk stalk joins the mid-
gut with the yolk sac
• Mid-gut development is characterized by
formation of the intestinal loop.

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 DEVELOPMENT OF THE MIDGUT
• Apex of the loop, where vitelline duct joins it
to yolk sac.
• The cephalic limb develops into the distal part
of duodenum , the jejunum and part of the
ileum.
• The caudal limb, into lower portion of the
ileum, the caceum, the appendix, the
ascending colon, and the proximal two-thirds
of the transverse colon.
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 PHYSIOLOGICAL UMBILICAL HERNIATION

• By 6th week,
• Due to rapid elongation of the intestinal loop,
and expansion of the liver:
• Abdominal cavity becomes too small
• Intestinal loops enter the extra-embryonic
cavity in the umbilical cord.

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PHYSIOLOGICAL UMBILICAL HERNIATION

**Rotation of the midgut as it grows.

• Ileum, jejunum, form coiled loops.
• Superior mesenteric artery is the axis of
rotation.
• Rotation, counter clockwise, 270 degrees
when completed
• During herniation—about 90 degrees rotation

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 PHYSIOLOGICAL UMBILICAL HERNIATION

Retraction ---180 degrees rotation the large

intestine also lengthens, but no coiling
Retraction of the herniated loops
• By the 10th week
• Responsible factors, not precisely known.

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 PHYSIOLOGICAL UMBILICAL HERNIATION

• Regression of mesonephric kidney, decreased

growth of the liver and expansion of the
abdominal cavity – possible factors.
• First to re-enter - proximal portion of the
jejunum—lies on the left side.
Later returning loops - lie more and more to the
right.

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DEVELOPMENT OF CAECUM & APPENDIX

• Caecal bud—last to return –lies on the right

upper quadrant , below the liver (right lobe)
• The caecal bud, about the 6th week, appears as
a conical dilation of the caudal limb of the
primary intestinal loop,
• It descends into the right iliac fossa.

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DEVELOPMENT OF CAECUM & APPENDIX

• And places the ascending colon & hepatic flexure

on the right side of the abdominal cavity.
Appendix
- During the descent, the distal end of the caecal
bud forms narrow diverticulum - the appendix.
- The final position of the appendix is frequently
posterior to the caecum or the colon– retrocaecal
or retrocolic

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MESSENTERIES OF THE INTENSTINAL LOOPS
MESSENTERY PROPER
• Profound changes with rotation and coiling of the
loops
• The dorsal mesentery twists around the origin of the
superior mesenteric artery as the caudal limb moves
to the right.
• The mesenteries of the ascending and descending
colons press against the peritoneum of the
posterior abdominal wall.
• These peritoneal layers fuse to make the ascending
and descending colons retroperitoneal
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MESSENTERIES OF THE INTENSTINAL LOOPS
MESSENTERY PROPER
• The transverse mesocolon fuses with the
posterior wall of the greater omentum, still
mobile
• The mesentery of jejuno-ileal loop is
continous with that of ascending colon.
• This obtains a new line of attachment( from
the duodenal cap to the ileo-ceacal junction)
as the ascending colon become.
retroperitoneal.
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 DEVELOPMENT OF THE HINDGUT
The hindgut includes
• The distal third of the transverse colon
• The sigmoid colon
• The rectum ,and
• The upper part of the anal canal

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 DEVELOPMENT OF THE HINDGUT
1 The distal end of the hindgut enters into the
primitive anorectal canal (posterior region of
the cloaca).
2 The urorectal septum divides the cloaca into an
anterior portion and a posterior portion
• The allantois enters into the anterior portion
(the primitive urogenital sinus).
• The upper two thirds of the anal canal is
derived from the endoderm of the hindgut
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 DEVELOPMENT OF THE HINDGUT
• The lower one third is derived from ectoderm
in the region of the proctodeum
• The ectoderm on the surface of the cloaca
proliferates and invaginates to create the anal
pit
• At the end of 7th week, the cloaca membrane
(anal membrane)ruptures.
• This makes the upper and lower parts of the
anal canal continuous.
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 DEVELOPMENT OF THE HINDGUT
• Pectinate line is the junction between the
endodermal and ectodermal regions of the anal
canal
• At this point, the epithehum changes to squamous
• Above the line, the blood supply is from the
superior rectal artery –from inferior mesenteric
artery
• Below the line, inferior rectal arteries ,branches of
the internal pudendal arteries.

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 HINDGUT ABNORMALITIES
• Rectourethral fistula
• Rectovaginal fistula
• Caused by abnormal formation of the cloaca
and /or the urorectal septum
• The abnormality is such that the opening of
the hindgut shifts anteriorly, to open into the
urethra or vagina.

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 HINDGUT ABNORMALITIES
Examples—
the cloaca being too small
 urorectal septum ,not extending enough
caudally
• Rectoanal fistula
• Rectoanal atresias
• The opening or fibrous remnant connected to
the perineal surface
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 HINDGUT ABNORMALITIES
• Cause probably---mis-expression of genes
during epithelial- mesenchymal signalling
• Imperforate anus- occurs when anal membrane
fails to rupture
• Congenital megacolon: Due to an absence of
parasympathetic ganglia in the bowel wall
(Aganglionic megacolon or Hirschprung
diseases.)
• Rectum is involved in most cases
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 HINDGUT ABNORMALITIES
• In 80% ,the effect extends to the midpoint of
the sigmoid
• In 10 to 20%—the transverse colon and right
side colonic segments
• In 3%---the entire colon ,involved,
• Cause : Mutatims in RET gene, a tyrosine
kinase receptor in neural crest cells ,then
migration to the wall of the bowels

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 EOSOPHAGEAL ABNORMOLITIES

• Eosophageal atresia
• Tracheo-eosophageal fistula: causes:-
 Spontaneous tracheoeosophageal septum
posterior deviation
 Machanical pushing of the dorsal wall of the
forgut anteriorly
1. E.g proximal part ,ends as a blind sac and distal
part ,connected to the trachea---(the most
common form,)
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 EOSOPHAGEAL ABNORMOLITIES
• Oesophageal atresia----polyhydramnis
• Oesophageal stenosis—usually in the lower
third
I. incomplete recanalisation
II. Vascular abnormalities
III. Accident limiting blood flow
• Short oesophagus :failure to lengthen leads
to –congenital hiatal hernia.
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 STOMACH ABNORMALITIES
• Pyloric steno
• Hypertrophy of the muscles of the region of
the pylorus (circular –longitudinal)
• One of the most common seen in infant .
• Projectile vomiting 3 to 5days after birth.
Develop during fetal life and after .
• Erythromycin—a risk factor in the newborn.
• Duplication of stomach
• Prepyloric septum
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 GUT ROTATION DEFECTS
 Left sided colon
• Only 90 degrees rotation
• Colon or caecum return first ,settle on the left
 Reversed rotation of the intestinal loop
• 90 degrees clockwise rotation
• Transverse colon ,behind the duodenum and superior
mesenteric artery.
 Duplications of the intestinal loops and cysts
• Ileum—most frequent site.
• 33% associated with other defects e.g intestinal atresias,
imperforate anus gastroschisis,and omphalocele Causes
Abnormal proliferations of gut parenchyme.
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 ABNOMALITIES OF THE MESENTERIES
• Mobile checum
Persistence of a portion of the mesocolon
• Volvulus
Mesentery of the ascending colon fails to fuse with the
perifoneum of the posterior abdominal wall.
Rerocolic pocket
Incomplete fusion of the mesentery
• Retrocolic hernia
Portions of the small intestine entraped behind the
mesocolon.
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 ABNOMALITIES OF THE MESENTERIES
BODY WALL DEFFECT
• Omphalocele :in 25:10,000 births
• Amnion covers the herniated viscera :liver.
• Small and large intestines, stomach, spleen,
gallbladder.
• High rate of mortality 25%
• Severe malformations: cardiac abnormalities in
50%—NTDS (40),chromosomal abnormalities
15%of cases
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 ABNOMALITIES OF THE MESENTERIES
Gastroschisis; /; 1:10,000 births;9 frequency
• Abdominal viscera—into amniotic cavity
• Lateral to umbilicus, usually to the right? Due to
abnormal closure of the body wall around the
connecting stalk.
• Viscera not covered by peritoneum or amnion
• Not associated with chromosomal abnormalities or
other severe defects
• Survival rate—excellent
• Associated with volvulus.
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 VITELLINE DUCT ABNORMALITIES
• Meckel’s diverticulum (ileal diverticulum)
Persistence of a small portion of the vitelline
duct
In 2 to 4% of people
 40 to 60cm from the ileocaecal valve
Antimesenteric. border of the ileum
Usually ,no symptoms.
• May contain:
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 VITELLINE DUCT ABNORMALITIES
 Heterotopic pancreatic tissue
 Gastric mucosa(ulceration bleeding or perforation)
• Enterocytoma or vitelline cyst
 Large cyst in the middle of fibrous cord of the duct.
• Strangulation or volvulus around the fibrous cord
of the duct
• Umbilical fistula or vitelline fistula
 Patent vitelline duct over the entire length.

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 GUT ATRESIAS AND STENOSES
• Anywhere along the intestine
• Most ,in the duodenum,
• Fewest, in the colon
• Equal numbers, in jejunum/ileum
• 1:1500 births
CAUSES.
• Lack of recanalization— upper duodenum
• Vascular accidents—distal portion of duodenum,

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 GUT ATRESIAS AND STENOSES
• malrotation, volvulus, gastroschisis,
omphalocele and others
• Gut differentiation problems
• 50% of cases—a region of the bowel is lost
• 20%—a fibrous cord remains
• 20%—narrowing,with thin diaphragm
segmenting the

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 GUT ATRESIAS AND STENOSES
• larger and smaller pieces of bowel
• 10%—stenoses and multiple atresia
• Apple peel atresia
• 10% of atresias
--- at proximal jejunum
---short intestine
---Intestine distal to the lesion coil around a mesenteric
remnant
---low birth weight in cases of extensive gut involvement

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 DEVELOPMENT OF THE LIVER
• 3rd week, hepatic bud (hepatic diverticulum) an out
growth of the endodermal epithelum or distal end of
the forgut (duodenum)
• Septum transversum, penetrated by the proliferating
cells of the liver bud, as the epithelial liver cord.
• With further development, the epithelial liver cord
intermingle with the vitelline and umbilical veins,
forming the hepatic sinusoids.
• The liver cords: paraenchyma of the liver (liver
cells),lining the biliary ducts
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 DEVELOPMENT OF THE LIVER
• Mesoderm of the septum transversum form the.
Haemopoietic cells; kupper cells; connective tissue
cells and the peritoneum covering the liver.
• By the 10th week of development:
• Liver weight –10% of the total body weight. Sinusoids
in large numbers
Haematopoietic function.
• By the 12th week:
 Hepatic cells—bile secretion
 Bile enter the GIT, contents dark green colour.
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 BILE DUCT ,GALL BLADDER AND CYSTIC
DUCT DEVELOPMENT
• Bile duct-Narrowed connection between the
liver bud and the forgut.
Position of the duct- first anterior and finally,
posterior to the duodenum.
• Gall bladder– A small ventral out growth from
the bile duct forms the gall bladder and cystic
duct.

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LIVER AND GALL BLADDER ABNORMALITIES

• Variations in liver lobulation—common

• Accessory hepatic ducts-common , usually
asymptomatic
• Duplication of the gall bladder- common,
usually asymptomatic
• Extrahepatic billary atresia---1:15,000births
15 to 20% patent proximal ducts, correctable
defect .
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LIVER AND GALL BLADDER ABNORMALITIES

• The remainder –usually fatal unless with liver

transplant.
• Intrahepatic billary duct atresia/hypoplasia-
rare(1: 100000 live births)
CAUSES
• Fetal infections
• Usually runs an extended benign course

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DEVELOPMENT OF THE PANCREAS
• Two buds, endodermal lining of the duodenum
• Dorsal pancreatic bud, into the dorsal mesentery
• Ventral pancreatic bud, close to the bile duct (two
components),with rotation of the duodenum
rotating to the right, and the becoming C-shaped.
• The ventral pancreatic bud moves dorsally to lie
just below and behind the dorsal bud.

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DEVELOPMENT OF THE PANCREAS
• The parenchyma and duct systems of the two
buds later fuse.
• The ventral bud—the uncenate process and
the inferior part of the head of the pancreas.
• The dorsal bud—the remaining part of the
gland.

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DEVELOPMENT OF THE PANCREAS
• The main pancreatic duct of the Wirsung:
dorsal part of the dorsal pancreatic duct and
the entire ventral pancreatic duct
• The accessory pancreatic duct(of Santorin: the
proximal part of the dorsal pancreatic duct
(where it fails to obliterate).
• The main pancreatic duct, with the bile duct,
enters the duodenum at the site of the major
papilla.
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DEVELOPMENT OF THE PANCREAS
• The accessory duct, when present, enters at
the site of the minor papilla,
• In 10% of the cases, the original double duct
system persists.
• By 3rd month of development, the parenchyma
of the pancreas forms the pancreatic islet (of
Langerhans).

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 DEVELOPMENT OF THE PANCREAS
• By the 5th month, insulin secretion begins.
• Glucogen –and somatostatin—secreting cells
• Formed by the parenchymal cells.
• The pancreatic connective tissue, by the
visceral mesoderm around the pancreatic
buds.

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 PANCREATIC ABNORMALITIES
• Annular pancreas—by the right and left
portions of the ventral pancreatic bud
migrating in opposite direction
• Accessory pancreatic tissue—anywhere
between the end of oesophagus to the top of
the intestinal loop: most frequent sites are:
• Mucosa of the stomach and Merkel’s
diverticulum.

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