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G.LUFUKUJA
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As a result of cephalocaudal and lateral folding of the
embryo, a portion of the endoderm-lined yolk sac cavity is
incorporated into the embryo to form the primitive gut.
Two other portions of the endoderm-lined cavity, the yolk
sac and the allantois, remain outside the embryo
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In the cephalic and caudal parts of the embryo, the primitive gut
forms a blind-ending tube, the foregut and hindgut, respectively.
The middle part, the midgut, remains temporally connected to
the yolk sac by means of the vitelline duct, or yolk stalk
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(Esophagus (distal end)
Respiratory tract (lower respiratory tract)
Stomach
Duodenum (proximal half)
Liver
Gallbladder
Pancreas
Spleen - The spleen arises from the mesodermal
dorsal mesentery but it is supplied by the
foregut (i.e. the celiac artery)
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Duodenum (distal half)
Jejunum
Ileum
Cecum
Appendix
Ascending colon
Hepatic flexure of colon
Transverse colon (proximal two-thirds)
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the distal third of the transverse colon
the splenic flexure,
the descending colon,
sigmoid colon,
Rectum and
the upper part of the anal canal
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Endoderm forms the epithelial lining of the digestive
tract and gives rise to the parenchyma of glands, such
as the liver and pancreas.
Muscle, connective tissue, and peritoneal components
of the wall of the gut are derived from splanchnic
mesoderm.
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When the embryo is approximately 4 weeks old, the
respiratory primordium (lung buds) begins to develop.
It begins as a laryngotracheal groove on the ventral
aspect of the primitive foregut (primordial pharynx).
The tracheoesophageal septum gradually partitions this
diverticulum from the dorsal part of the foregut. In this
manner the foregut divides into a ventral portion, the
respiratory primordium, and a dorsal portion, the
esophagus
LUFUKUJA GEORGE
Monday, May 22, 2017
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At first the esophagus is short, but with descent of the
heart and lungs it lengthens rapidly. The muscular coat,
which is formed by surrounding splanchnic mesenchyme,
is striated in its upper two-thirds and innervated by the
vagus; the muscle coat is smooth in the lower third and
is innervated by the splanchnic plexus
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Esophageal atresia and/or tracheoesophageal fistula results either
from spontaneous posterior deviation of the tracheoesophageal
septum or from some mechanical factor pushing the dorsal wall of the
foregut anteriorly. In its most common form the proximal part of the
esophagus ends as a blind sac, and the distal part is connected to the
trachea by a narrow canal just above the bifurcation
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Esophageal Stenosis
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Atresia of the esophagus prevents normal passage of amniotic
fluid into the intestinal tract, resulting in accumulation of excess
fluid in the amniotic sac (polyhydramnios). In addition to
atresias, the lumen of the esophagus may narrow, producing
esophageal stenosis, usually in the lower third. Stenosis may be
caused by incomplete recanalization
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Occasionally the esophagus fails to lengthen sufficiently and the
stomach is pulled up into the esophageal hiatus through the
diaphragm. The result is a congenital hiatal hernia.
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Portions of the gut tube and its derivatives are
suspended from the dorsal and ventral body wall by
mesenteries, double layers of peritoneum that
enclose an organ and connect it to the body wall.
Such organs are called intraperitoneal, whereas
organs that lie against the posterior body wall and
are covered by peritoneum on their anterior surface
only
(e.g.,
the
kidneys)
are
considered
retroperitoneal.
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Peritoneal ligaments are double layers of peritoneum
(mesenteries) that pass from one organ to another or from
an organ to the body wall.
Mesenteries and ligaments provide pathways for vessels,
nerves, and lymphatics to and from abdominal viscera
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The stomach appears as a fusiform dilation of the
foregut in the fourth week of development.
During the following weeks, its appearance and position
change greatly as a result of the different rates of growth
in various regions of its wall and the changes in position
of surrounding organs.
Positional changes of the stomach are most easily
explained by assuming that it rotates around a
longitudinal and an anteroposterior axis
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4th–8thweek the developing stomach grows in all directions to
become a sac-like structure
5thweek–the dorsal border grows faster than the ventral border
giving rise to the greater and lesser curvatures, respectively. 1st
Rotation– In the 5th week, the stomach rotates 90° clockwise
around its longitudinal axis so that the original dorsal side
becomes the left side, left becomes ventral, ventral – right and
right - dorsal.
(note: LT &RT VAGUS)
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The cephalic and caudal ends of the stomach originally lie
in the midline, but during further growth the stomach
rotates (2nd 90° Rotation : In the 7th week ) around
an anteroposterior axis, such rotation the caudal or pyloric
part moves to the right and upward and the cephalic or
cardiac portion moves to the left and slightly
downward. The stomach thus assumes its final position,
its axis running from above left to below right.
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Since the stomach is attached to the dorsal body wall
by the dorsal mesogastrium and to the ventral body
wall by the ventral mesogastrium, its rotation and
disproportionate growth alter the position of these
mesenteries.
Note: the space behind the stomach called the omental
bursa (lesser peritoneal sac)
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Formation of omental bursa…
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GREATER OMENTUM
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Pyloric stenosis occurs when the circular and, to a lesser degree, the
longitudinal musculature of the stomach in the region of the pylorus
hypertrophies. One of the most common abnormalities of the stomach in
infants, pyloric stenosis is believed to develop during fetal life. There is an
extreme narrowing of the pyloric lumen, and the passage of food is obstructed,
resulting in severe vomiting. In a few cases the pylorus is atretic.
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The terminal part of the foregut and the cephalic part of the
midgut form the duodenum, thus receives a dual blood supply from
foregut and midgut arteries (celiac and superior mesenteric)
As the stomach rotates, the duodenum takes on the form of a Cshaped loop and rotates to the right.
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During the second month, the lumen of the duodenum is
obliterated by proliferation of cells in its walls.
However, the lumen is recanalized shortly thereafter
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Is the partial occlusion of the duodenal lumen. Usually
results from incomplete recanalization of the duodenum
resulting from defective vacuolization.
Because of the stenosis, the stomach’s contents (usually
containing bile) are often vomited.
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Duodenal Atresia
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During early duodenal development, the lumen fails to
occur and a short distance of the duodenum become
occluded.
In infants with duodenal atresia, vomiting begins a few
hours after birth.
The vomitus almost contains bile.
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The liver primodium appears in the middle of the third week as an
outgrowth of the endodermal epithelium at the distal end of the
foregut.
The hepatic diverticulum, or liver bud, consists of rapidly
proliferating cells that penetrate the septum transversum, that is,
the mesodermal plate between the pericardial cavity and the stalk of
the yolk sac.
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While hepatic cells continue to penetrate the septum, the
connection between the hepatic diverticulum and the foregut
(duodenum) narrows, forming the bile duct.
A small ventral outgrowth is formed by the bile duct, and this
outgrowth gives rise to the gallbladder and the cystic duct.
Hematopoietic cells, Kupffer cells, and connective tissue cells
are derived from mesoderm of the septum transverse mesoderm.
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In the 10th week of development the weight of the liver is
approximately 10%of the total body weight.
hematopoietic function.
Large nests of proliferating cells, which produce red and white
blood cells, lie between hepatic cells and walls of the vessels. This
activity gradually subsides
during the last 2 months of intrauterine life, and only small
hematopoietic islands remain at birth. The weight of the liver is
then only 5%of the total body weight
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Molecular Regulation of Liver Induction
Fibroblast growth factors (FGFs) secreted by cardiac
mesoderm. Thus, the cardiac mesoderm “instructs” gut endoderm
to express liver specific genes by inhibiting an inhibitory factor of
these same genes.
Liver and Gallbladder Abnormalities Variations in liver
lobulation are common but not clinically significant,
Accessory hepatic ducts and duplication of the
gallbladder are also common and usually asymptomatic
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The pancreas is formed by two buds originating from the
endodermal lining of the duodenum
Whereas the dorsal pancreatic bud is in the dorsal mesentery, the
ventral pancreatic bud is close to the bile duct When the
duodenum rotates to the right and becomes C-shaped, the ventral
pancreatic bud moves dorsally in a manner similar to the shifting of
the entrance of the bile duct
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The ventral bud forms the uncinate process and inferior part of
the head of the pancreas
The remaining part of the gland is derived from the dorsal bud.
The main pancreatic duct (of Wirsung) is formed by the distal
part of the dorsal pancreatic duct and the entire ventral pancreatic
duct
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In the third month of fetal life, pancreatic islets (of Langerhans)
develop from the parenchymatous pancreatic tissue and scatter
throughout the pancreas.
Insulin secretion begins at approximately the fifth month.
Glucagon- and somatostatin-secreting cells also develop from
parenchymal cells.
Splanchnic mesoderm surrounding the pancreatic buds forms the
pancreatic connective tissue
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Annular pancreas
 The ventral pancreatic bud
consists of two components
that normally fuse and rotate
around the duodenum.
 Occasionally,
however, the
right portion of the ventral
bud migrates along its
normal route, but the left
migrates in the opposite
direction.
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this
manner,
the
duodenum is surrounded by
pancreatic tissue which may
produce
duodenal
obstruction.
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Spleen is derived from the dorsal mesogastrium, not
from the gut tube endoderm.
Late 4th week, a mesenchymal condensation develops
in the dorsal mesogastrium of the lesser sac.
5th week, the condensation differentiates into the
spleen.
Accessory spleens may also develop near the primary
spleen.
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In the 5-week-old embryo, the midgut is suspended
from the dorsal abdominal wall by a short
mesentery and communicates with the yolk sac by
way of the vitelline duct or yolk stalk
By the fifth week of embryological life,
the ileum begins to grow longer at a very fast rate,
forming a U-shaped fold called the primary
intestinal loop. The loop grows so fast in length
that it outgrows the abdomen and protrudes
through the umbilicus. At its apex, the loop
remains in open connection with the yolk sac by
way of the narrow vitelline duct
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PHYSIOLOGICAL HERNIATION
Development of the primary intestinal loop is
characterized by rapid elongation, particularly of the
cephalic limb. As a result of the rapid growth and
expansion of the liver, the abdominal cavity temporarily
becomes too small to contain all the intestinal loops, and
they enter the extraembryonic cavity in the umbilical
cord during the sixth week of development
(physiological umbilical herniation)
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The cephalic limb of the loop develops into the distal part of the
duodenum, the jejunum, and part of the ileum. The caudal limb
becomes the lower portion of the ileum, the cecum, the appendix, the
ascending colon, and the proximal two-thirds of the transverse colon
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During the herniation process the primary intestinal loop rotates. When
viewed from the front, this rotation is counterclockwise, around the axis
of the superior mesenteric artery (dorsoventral axis) and it amounts to
approximately 270◦ when it is complete
At 8th week, the first rotation is complete. At the same time the
lengthening jejunum and ileum (midgut) develop into a series of folds
called the jejunal-ileal loops.
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By week 10, the loop retracts back into the abdomen. As the
intestinal loop re-enters the abdomen it rotates an additional 180°
counterclockwise. By 11th week, rotation and retraction are
complete.
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During the 10th week, herniated intestinal loops begin to
return to the abdominal cavity.
Although the factors responsible for this return are not
precisely
known,itisthoughtthatregressionofthemesonephrickidney,redu
cedgrowth of the liver, and expansion of the abdominal cavity
play important roles.
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Ileal Diverticulum
An ileal diverticulum (of Meckel) is a remnant of the proximal part
of the embryonic yolk stalk, the diverticulum usually appears as a
finger-like pouch. It may be free (74%) or attached to the
umbilicus (26%). Although its mucosa is mostly ileal in type, it
may also include areas of acid-producing gastric tissue,
pancreatic tissue, or jejunal or colonic mucosa.
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Reversed Rotation.
In very unusual cases, the mid gut loop rotates in a clockwise
rather than a counterclockwise direction.
As a result, the duodenum lies anterior to the superior
mesenteric artery rather than posterior to it, and the transverse
colon lies posterior instead of anterior to it.
In this infant the transverse colon may be obstructed by pressure
from the superior mesenteric artery.
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Embryological Errors
Abnormal rotation of the intestinal loop may result in twisting of
the intestine (volvulus) and a compromise of the blood supply.
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Subhepatic Cecum and Appendix.
If the cecum adheres to the inferior surface of the
liver when it returns to the abdomen, it will be drawn
superiorly as the liver diminishes in size, as a result
the cecum remains in its fetal position.
The subhepatic cecum and appendix may
be seen in adults and create a problem in
the diagnosis of appendicitis and during
the surgical removal of the appendix
(Appendectomy).
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Omphalocele
 Failure of midgut return.
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Involves herniation of abdominal viscera through an
enlarged umbilical ring.
The viscera, which may include liver, small and large
intestines, stomach, spleen, or gallbladder, are
covered by amnion.
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Gastroschisis
Represents a congenital defect characterized by
a defect in the anterior abdominal wall through
which the abdominal contents freely protrude
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The hindgut gives rise to the distal third of the
transverse colon, the descending colon, the sigmoid,
the rectum, and the upper part of the anal canal.
The endoderm of the hindgut also forms the internal
lining of the bladder and urethra.
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The terminal portion of the hindgut enters into the
posterior region of the cloaca or the primitive anorectal
canal.
The allantois enters into the anterior portion or the
primitive urogenital sinus. A layer of mesoderm, the
urorectal septum, separates the region between the
allantois and hindgut.
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The urorectal septum septum is derived from
the merging of mesoderm covering the yolk
sac and surrounding the allantois.
As the embryo grows and caudal folding
continues, the tip of the urorectal septum
comes to lie close to the cloacal membrane.
The transverse line of fusion between the
septum and cloacal membrane forms the
perineal body.
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The ectodermal cloaca behind the perineal
body presents a surface depression, the
proctodeum or the anal pit.
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At the end of the seventh week, the cloacal membrane
ruptures, creating the anal opening for the hindgut
and a ventral opening for the urogenital sinus.
At this time, proliferation of ectoderm closes the
caudalmost region of the anal canal.
During the ninth week, this region recanalizes.
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The anal canal is developed from two sources; Upper
part from the endodermal cloaca & Lower par from the
ectodermal proctodeum.
At this line, the epithelium changes from columnar in
upper anal canal to stratified squamous epithelium in
lower anal canal.
Thus, the upper part of the anal canal is supplied by
the the superior rectal artery a continuation of the
inferior mesenteric artery
The lower part of the anal canal is supplied by inferior
rectal arteries, branches of the internal pudendal
arteries..
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Imperforate anus
Rectoanalatresias,and fistulas
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1.
2.
3.
Prenatal ultrasound showed polyhydramnios at 36
weeks, and at birth the infant had excessive fluids
in its mouth and difficulty breathing. What birth
defect might cause these conditions?
Prenatal ultrasound at 20 weeks revealed a
midline mass that appeared to contain intestines
and was membrane bound. What diagnosis would
you make, and what would be the prognosis for
this infant?
At birth a baby girl has meconium in her vagina
and no anal opening. What type of birth defect
does she have, and what was its embryological
origin?
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