Professional Documents
Culture Documents
nal System
Development
Matt Velkey
matt.velkey@duke
.edu
454A Davison
Gastrulation:
Epiblast cells
migrate through the
primitive streak.
Definitive (embryonic)
endoderm cells
displace
the hypoblast.
Mesoderm spreads
between endoderm
and ectoderm.
Endoderm
cloacal membrane
folding,
mesoderm is
recruited to gut
wall
Derivatives of gu
Foregut:
pharynx
esophagus
stomach
proximal duodenum
thyroid
parathyroid glands
tympanic cavity
trachea, bronch
liver, gallbladder
pancreas
Midgut:
proximal duodenum to
right half of
transverse
colon
Hindgut:
left half of
transverse
colon to anus
urinary bladder
4th week
5th week
note
Esophagus
Stomach
Stomach Duod.
Carlson fig 15
Fetus
Wheaters fig 1
Regional Organogenesis:
Esophagus
Region of foregut just caudal
to lung bud develops into
esophagus errors in forming
the esophagotracheal septa
and/or re-canalization lead to
tracheoesophageal fistulas
and/or esophageal atresia,
respectively.
Endodermal lining is stratified
columnar and proliferates such
that the lumen is obliterated;
patency of the lumen
established by re-canalization
errors in this process lead to
esophageal stenosis
Larsens fig
5th week
14-22
7th week
9th week
4th week
Regional Organogenesis:
Stomach
5th week
6th week
Greater omentum
rd
month
3rd month
3rd month
Stomach appears first as a fusiform dilation of the foregut endoderm which undergoes a 90 rotation
such that the left side moves ventrally and the right side moves dorsally (the vagus nerves follow this
rotation which is how the left vagus becomes anterior and the right vagus becomes posterior).
Differential growth establishes the greater and lesser curvatures; cranio-caudal rotation tips the
pylorus superiorly
Dorsal AND ventral mesenteries of the stomach are retained to become the greater and lesser omenta,
respectively
Caudal end of the stomach separated from the duodenum by formation of the pyloric sphincter (dependent
on factors such as SOX-9, NKX-2.5, and BMP-4 signaling) errors in this process lead to pyloric
stenosis.
Pyloric
Stenosis
Rather common malformation:
present in 0.5% - 0.1% of
infants
Characterized by very forceful
(aka projectile), non-bilious
vomiting ~1hr. after feeding
(when pyloric emptying would
occur).
NOTE: the presence of bile would
indicate POST-duodenal blockage of
some sort.
Langmans fig 14
Regional Organogenesis:
Liver & Pancreas
ventral
pancreas
Langmans fig 14-22
ALL foregut endoderm has the potential to develop into either liver or pancreas but local
signals repress these fates (mesodermal Wnts Liver; mesodermal Wnts + endodermal Shh
Pancreas)
FGFs and BMPs from cardiac mesoderm and septum transversum inhibit Wnt signaling, but the
endoderm still expresses Shh and thus develops into liver.
Meanwhile, endoderm just caudal to liver bud is out of reach from the FGFs and BMPs but
still sees Wnts, so the tissue does NOT become liver.
Unlike the rest of the endoderm,
it does NOT express Shh and so develops into pancreas.
Rotation of
the duodenum
brings the
ventral and
dorsal
pancreas
together
Larsens fig 14-09
3rd month
retroperitoneal vs.
secondarily
retroperitoneal
Absent or incomplete
secondary rotation
Development of the
hindgut
imperforate anus
anal atresia
rectourethral fistula
rectovesical fistula
Carlson fig 15
some
Hirschprung
Disease
(congenital
Occurs in ~1:5000
Caused
by failure
megacolon)
births
of
vagal neural crest cells
to migrate into a portion
of the colon
Denervated region
tonically constricted
(role of myenteric plexus
is largely INHIBITORY)
Upstream regions become
distended (hence
megacolon)
Surgically repaired by
removing affected region