2. Development of G.I.T
Overview – 1a
• Primitive gut, (derived from
endodermal yolk sac); Wk4
• Premitive gut extends from
bucco-pharyngeal
membrane to cloacal
membrane*
• Communicates with
remaining y/sac via vitello-
intestinal duct
• Foregut; Mid-gut; Hindgut*
Assignment 7.1
1. Summarize the G.I.T
development:(when,
what, where, how,
why, which)?*
2. What are the
components of the
foregut, mid-gut and
hindgut?
3. Development of G.I.T
Overview – 1b
• G.I.T develops from primitive
gut that is derived from the
dorsal part of endodermal
yolk sac.
• Tubular primitive gut:
extends in the median plane
from buccopharyngeal
membrane at its cranial end to
cloacal membrane at its caudal
end.
freely communicates with the
remaining yolk sac by the
vitello-intestinal duct.
• The upper one-third
part of the esophagus
has striated
musculature,
• Middle one-third has
mixed (striated and
smooth) musculature,
and
• Lower one-third has
smooth musculature as
in the rest of the gut.
4. Development of G.I.T
Overview – 1c
Foregut:
• Comprises cranial and
caudal portions
• Cranial portion gives rise
to the pharynx
• Caudal portion becomes
lower oesophagus,
stomach and cranial half of
duodenum
Foregut components:
(Summary)
• Pharynx,
• Trachea
• Lower oesophagus,
• Stomach,
• Duodenum (cranial
half)
5. Development of G.I.T
Overview – 1d
Midgut Components:
• Midgut endoderm gives
rise to mucosae of:
Duodenum (2nd half)
Jejunum,
Ileum,
Ascending colon and
Transverse Colon (two
thirds of)
• Midgut endoderm forms
elongating loop resulting in
physiological umbilical
hernia
• Midgut loop rotates
anticlockwise; first
rotation is 90° as loop
enters umbilical cord;
further 180° as it returns
to abdominal cavity
• Occurs 6-10 wks of
development
6. Development of G.I.T
Overview – 1e
• Hindgut endorm:
Gives rise to mucosae
of lower third of
transverse colon,
descending and sigmoid
colon, rectum and
upper half of anal canal
Also gives rise to part of
the lining of urinary
tract
• HIndgut Components:
Transverse colon (lower
third)
Descending colon
Sigmoid colon
Rectum
Anal Canal (Upper half)
7. Development of G.I.T
Overview – 1f
Development of foregut:
• Trachea; Esophagus development*:
Histological composition of adult
human G.I.T*
Embryological derivatives of G.I.T
epithelia glands and viscera*
Recanalization*
• Stomach development*
• Liver development*
• Gall bladder & Extra-hepatic bile
ducts development*
• Upper Duodenum development*
Assignment 7.2
1. From histology viewpoint, what are
the components of adult human
G.I.T?
2. Where are the foregut G.I.T
components derived from?*
3. When and how does recanalization
occur?
4. Account for the development of the
entire foregut.
8. Development of G.I.T
Overview – 1g
Clinical Relevance:
• Malformations of:
Trachea*
Oesophagus, Pylorus*
Stomach *
Gall bladder and Extra-
hepatic ducts *
Liver *
Pancreas *
Assignment 7.3
1. Enumerate the clinical
abnormalities of the
foregut .*
2. Describe their clinical
presentations of the
foregut malformations*
3. How are the foregut
malformations
managed?
12. Development of G.I.T
Clinical : Foregut Anomalies - 1
• a. Esophageal atresia (Picture opposite;
posterior view, which shows that the
esophagus terminates blindly in a blunted
esophageal pouch (arrow) :
Occurs when the tracheoesophageal
septum deviates too far dorsally, causing
the esophagus to end as a closed tube.
About 33% of patients with esophageal
atresia also have other congenital defects
associated with the VATER (vertebral
defects, anal atresia, tracheoesophageal
fistula, and renal defects) or VACTERL
(similar to VATER plus cardiovascular defects
and upper limb defects) syndromes.
EA is associated clinically with
polyhydramnios (the fetus is unable to
swallow amniotic fluid) and a
tracheoesophageal fistula.
There is a distal esophageal connection with
the trachea at the carina (arrowhead).
13. Development of G.I.T
Clinical : Foregut Anomalies - 2
• b. Esophageal stenosis
(Figure opposite; shows the stratified
squamous epithelial lining of the esophagus
and submucosal glands)* Note that a
portion of the muscular wall contains
remnants of cartilage (arrow), which
contributes to a stenosis.)
• Esophageal stenosis:
Occurs when the lumen of the
esophagus is narrowed and usually
involves the midesophagus.
The stenosis may be caused by
submucosal/muscularis externa
hypertrophy, remnants of the
tracheal cartilaginous ring within
the wall of the esophagus, a
membranous diaphragm
obstructing the lumen probably
due to incomplete recanalization.
14. Development of G.I.T
Clinical : Foregut Anomalies - 3
• c. Esophageal duplication:
(Figure opposite; yhe barium esophagram
demonstrates a large intramural duplication cyst
in the proximal esophagus (dashed lines). The
cyst shows acute angles with the esophageal
lumen, indicating its intramural location)
Esophageal duplication: occurs
most commonly due to a
congenital esophageal cyst, which
is usually found (60% of the cases)
in the lower esophagus.
Duplication cysts may lie on the
posterior aspect of the esophagus,
where they protrude into the
posterior mediastinum or within
the wall of the esophagus (i.e.,
intramural).
15. Development of G.I.T
Clinical : Foregut Anomalies - 4
• d. Vascular compression of the
esophagus
(Figure opposite; the barium
esophagram in the same patient reveals
an oblique compression of the
esophagus (arrow) due to the
anomalous right subclavian artery)
The compression occurs due the
abnormal origin of the right
subclavian artery due to
developmental anomalies of the
aortic arches
The anomalous right subclavian
artery passes from the aortic
arch behind the esophagus and
may cause dysphagia
(“dysphagia lusoria”).
16. Development of G.I.T
Clinical : Foregut Anomalies - 5
• e. Achalasia Cardia:
Achalasia occurs due to the
loss of ganglion cells in the
myenteric plexus (Auerbach)
and is characterized by the
failure to relax the lower
esophageal sphincter, which
causes progressive dysphagia
and difficulty in swallowing
(Figure opposite; the barium esophagram of
the distal esophagus in the figure shows a
long, narrowed segment (“bird beak”) of the
esophagus secondary to muscular hypertrophy
in long-standing achalasia
17. Development of G.I.T
Clinical : Foregut Anomalies - 6a
Esophageal (hiatal) Hernia:
• Esophageal (hiatal) hernia,
is thought to be due to
congenital shortness of the
esophagus. Upper portions
of the stomach are
retained in the thorax, and
the stomach Is constricted
at the level of the
diaphragm.
18. Development of G.I.T
Clinical : Foregut Anomalies - 6b
Esophageal Hiatal hernia.
• Extreme left figure:
Shows the normal relationship of the
gastroesophageal (GE) junction,
stomach, esophagus, and diaphragm.
• Middle figure:
Shows a sliding hiatal hernia, in
which the stomach immediately
below the GE junction is seen to
prolapse through the diaphragmatic
hiatus into the chest.
• Extreme right figure:
Shows a paraesophageal hernia in
which the cardia or fundus of the
stomach prolapses through the
diaphragmatic hiatus, leaving the GE
junction within the esophageal cavity.
19. Development of G.I.T
Clinical: Foregut Anomalies - 6c
Para-Esophageal (Hiatal
)hernia
A paraesophageal hernia is
seen on an upper
gastrointestinal radiograph
series.
Note that the
gastroesophageal (GE)
junction remains below the
diaphragm.
(Picture Courtesy of David Y Graham,
MD. )
20. Development of G.I.T
Clinical : Foregut Anomalies - 6d
Hiatal hernia. This image is a barium
radiograph view of a large para-
esophageal hernia. GE = gastro-
esophageal. (Courtesy of David Y Graham,
MD.)
Hiatal hernia. This barium radiograph shows
a large paraesophageal hernia in which the
entire stomach is seen in the chest cavity.
(Courtesy of David Y Graham, MD. )
