Download Development of Digestive System

Development of Digestive System
Origin (fig 3-5)

Due to longitudinal (cephalocaudal) & lateral folding of embryo, endoderm-linked yolk sac cavity is
incorporated into embryo to form primitive gut.
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Development of primitive gut can be discussed in 4 sections:
1.
Pharyngeal gut or pharynx
2.
Foregut (fm pharynx to liver outgrowth)
3.
Midgut (fm liver bud to junction % R 2/3 to L 1/3 transverse colon)
4.
Hindgut (fm 1/3 transverse colon to cloacal membrane)
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Endoderm forms epithelial lining and parenchyma of glands (liver & pancreas)
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Mesoderm forms muscular & peritoneal component of gut
Foregut
Esophagus (fig 7)
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At week 4, respiratory diverticulum (lung bud) appears at the ventral wall of foregut.
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It gradually separated from the dorsal part of the foregut by the esophagotracheal septum.
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So, the dorsal portion of foregut becomes the esophagus.
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Initially short, but due to descent of heart & lung, it lengthens rapidly.
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Upper 2/3 is striated muscle coated (innervated by vagus), lower 1/3 is by smooth muscle (innervated by
splanchnic px)
Esophageal Atresia (fig 8-10)
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Cause: -
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spontaneous deviation of esophagotracheal septum in post direction
mechanical factor pushing dorsal wall of foregut anteriorly
most common form: prox pt of eso end as blind sac, distal pt connect to trachea just above bifurcation (fig
10.1)
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atresia prevent passage of amniotic fluid into gut, cause accumulation of amniotic fluid (polyhydramnios)
Esophageal Stenosis (not required)
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occur in lower 1/3
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caused by incomplete re-canalization or vascular abnormality or accident that restrict blood flow
Congenital Hiatal Hernia (not required)
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eso fail to lengthen, so stomach pulled upward into esophageal hiatus through diaphragm
Stomach (fig 11-15)
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Due to different rates of growth in various regions of stomach wall and change in position of surrounding
organs, the appearance and position of stomach change greatly.
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The stomach is assumed to rotate around a longitudinal & an anteroposterior axis.
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Around the longi axis, stomach rotates 90º clockwise, causing the left side to face anteriorly (& R face post).
So the L vagus which innervate the L side of stomach initially, now innervate the ant wall.
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During the rotation, the original post wall of stomach grow faster than the ant portion, this result in formation of
greater and lesser curvatures. (fig 12)
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The cephalic & caudal ends of stomach originally located in the midline, but it rotates around the
anteroposterior axis (fig 13), so the pyloric pt moves to the right & upward and the cardiac portion moves to left
and slightly downward.
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Mesogastrium (fig 14-15)

The stomach is attached to the body wall by dorsal & ventral mesogastrium.

The rotation and disproportionate growth of stomach alter the position of these mesentries.

Rotation abt longi axis pull the dorsal meso to the left, creating the lesser sac (omental bursa) behind the
stomach. This rotation also pull the ventral meso to the right.

Due to the rotation abt anteroposterior axis, dorsal meso bulges in downward direction. It continues to
grow and form a double-layered sac (greater omentum) extending over the transverse colon & small
intestine. The sac finally fuse to form “single sheet” hanging from greater curvature. Post layer of greater
omentum also fuse with mesentery of T.colon.

The ventral meso form the falciform ligament and the lesser omentum.
Duodenum
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Form by terminal part of foregut & cephalic part of midgut.
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As the stomach rotate, duodenum take on the form of a C-shaped loop and rotate to the right.
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The rotation, with rapid growth of head of pancreas, cause duodenum swing against the dorsal body wall, and
the right surface of dorsal meso fuse with the peritoneum. Both layer disappear & duodenum & head of
pancreas becomes retroperitoneal. Small portion of duodenum remains intraperitoneal. (book 14.16)
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During the 2nd month, the lumen is obliterated by proliferation of cells in walls. The lumen is recanlized (fig 19)
shortly.
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Duodenum is supplied by branches of celiac art & SMA.
Liver (fig 20-21)
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The liver bud (hepatic diverticulum) appear in the mid week 3 as outgrowth of endodermal epithelium of distal
end of foregut.
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It consists of rapidly proliferating cells that penetrate the septum transversum (the mesodermal plate between
pericardial cavity & the stalk of yolk sac)
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As hepatic cells penetrate the septum, connection % liver bud & foregut (duodenum) narrows, forming bile
duct.
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Bile duct gives rise to a ventral outgrowth which is the cystic duct & gallbladder.
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Initially, the entrance of bile duct is in anterior position, with position change of duodenum, it will gradually shift
to posterior position, and the bile duct pass behind the duodenum.
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For further development, epithelial liver cords mix with vitelline & umbilical vein, forming hepatic sinusoid.
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Liver cords differentiate into parenchyma & form the lining of biliary ducts.
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Hematopoietic cells, Kupffer cells & c.t. are from mesoderm of septum transversum
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When liver cells invade the whole septum, mesoderm of septum becomes membranous, forming lesser
omentum & falciform lig.
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Mesoderm on liver surface  visceral peritoneum
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The cranial surface is not cover by peritoneum, instead it contact with the septum transversum. The septum
consist of mesoderm and form tendinous diaphragm. The space of liver in contact with diaphragm becomes
the bare area of liver.
Pancreas (fig 22-23)
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Form by 2 buds: dorsal pancreatic bud in dorsal mesentery & ventral bud close to bile duct
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When duodenum rotate to right and becomes C-shape, the ventral bud migrate dorsally similar to shifting of
entrance of bile duct. Finally ventral bud lie below the dorsal bud.
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Later, parenchyma and duct system of dorsal & ventral buds fuse
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Ventral bud  uncinate process & inf pt of head
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Dorsal bud  remaining part of pancreas
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Main pancreatic duct formed by distal pt of dorsal pancreatic duct & entire ventral duct
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Prox pt of dorsal duct will be obliterated or persist as accessory pancreatic duct
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Main pancreatic duct + bile duct enter duodenum at major papilla, accessory duct enter at minor papilla
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(X) Islets of Langerhans develop from parenchymatous pancreatic tissue in mth 3, insulin secretion start at
mth 5
Midgut
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Week 5, midgut is suspend from the dorsal abd wall by mesentery and communicate with the yolk sac by yolk
stalk / vitelline duct
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The midgut begin just distal to entrance of bile duct into duodenum & terminate at the junction of 2/3
transverse colon, whole midgut supplied by SMA
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Development of midgut is shown by rapid elongation of gut (particularly the cephalic limb) & mesentery,
resulting the 1º intestinal loop. The apex remains open with the yolk sac by yolk stalk.
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Cephalic limb  distal pt of duodenum, jejunum & pt of ileum.
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Caudal limb  lower pt of ileum, cecum, appendix, ascending colon & 2/3 transverse colon
1. Physiological Herniation (fig 3-6)
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At week 6, due to rapid growth & expansion of liver, the abdominal cavity becomes too small to hold the
intestinal loop, so it enter the extraembryonic coelom in the umbilical cord.
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The gut returns to abd cavity at week 12
2. Rotation of Midgut (fig 11-13)
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As the gut lengthen, the 1º intestinal loop rotate around the axis formed by SMA anti-clockwise about 270º
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During rotation, elongation of gut continue, and jejunum & ileum form a number of coiled loops. Though the
large intestine grow in length, it cannot form a coiling pattern.
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Rotation occurs during herniation (90º, fig 13.1) and during return of intestinal loops into abd cavity (180º, fig
13.2)
3. Return of Herniated loops
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Week 10, herniated loop begin to return that MAY due to regression of mesonephric kidney, reduced liver
growth & actual expansion of abd cavity
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Prox portion of jejunum is the 1st part to enter the abd cavity & lie on the left side, the later returning loop
gradually settle more to right, cecal bud (appear at week 6) is last pt to enter
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At first, cecal bud is located in the right upper quadrant just below the right liver lobe.
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Cecum descend into the right iliac fossa, placing the ascending colon & hepatic flexure on the right. During
descending, primitive appendix form at the distal end of cecal bud. As appendix form during descending, finally
the appendix is located post to cecum or colon.
4. Fixation of gut
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The mesentery of primary intestinal loop (mesentery proper) undergoes changes with rotation & coiling of the
loops.
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When the caudal limb moves to the right side of abd, the dorsal mesentery twists around the origin of SMA.
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When ascending & descending colon obtain the final position, their mesentery press against the peritoneum of
the post abd wall.
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Fusion of these layers occurs and asc & des colon permanently anchored in a retroperitoneal position.
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Appendix, lower end of cecum, sigmoid colon retain in free mesentery.
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For transverse colon, it fuse with the post wall of greater omentum BUT remains its mobility. The line of
attachment extend from the hepatic to splenic flexure.
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For the jujunoileal loops, it is at first continuos with asc colon. When the asc mesocolon fuse with the post abd
wall, the meso of jujunoileal loops obtains a new line of attachment that extend from the area where
duodenum becomes intraperitoneal to the ileocecal junction
Omphalocele (fig 8-10)
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Involves herniation of abd viscera (include liver, S & L intestine, stomach, spleen or gallbladder) through an
enlarged umbilical ring and are covered by amnion.
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The origin of this defect is a failure of bowel to return to the body cavity from physiological herniation during
week 6-10
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High rate of mortality occur
Abnormality abt Vitelline duct (fig 16-18)
a. Meckel's diverticulum
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A few ppl has a small portion of vitelline duct persist, forming an outpocket of ileum, which known as Meckel's
diverticulum.
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It's located 40-60cm from the ileocecal valve on the antimensenteric border of ileum.
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Usually it does not cause any symptom, except when it contains pancreatic tissue or gastric mucosa, that will
cause ulceration & bleeding.
b. Vitelline fistula (fig 17.4)
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The vitelline duct remains patent over the entire length, forming a direct communication between the umbilicus
and the intestinal tract
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Fecal discharge may found at the umbilicus
c. Vitelline Cyst (fig 17.2)
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both ends of vitelline duct are transformed into fibrous cord, while the middle portion forms a large cyst
Nonrotation (fig 19)
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Due to rotation
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When this occurs, colon & cecum are the first portion of gut to return from umbilical cord, so they settle on the
amounts to 90º anti-clockwise
L side of the abd cavity, resulting in left-side colon
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It may resulting twisting of intestine (volvulus, fig 21) and limited blood flow.
Reverse rotation
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occur when primary loop rotate 90º in clockwise direction
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in such condition, tran. colon pass behind the duodenum and lie behind the SMA
Duplication of intestinal loops
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occur anywhere along the length of the gut, most located in region of ileum
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vary from long segment to small diverticulum
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origin unknown, may result from abnormal proliferation of gut parenchyma
Hindgut
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gives rise to the distal 1/3 of trans. colon, desc colon, sigmoid colon, rectum & the upper pt of anal canal.
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Endoderm of hindgut also form the internal lining of bladder and urethra.
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During further development, a transverse ridge, the urorectal septum arise in the angle between the allantois
and the hindgut.
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The septum grow caudally, dividing the cloaca into anterior portion (primitive urogenital sinus) & posterior pt
(anorectal canal) (fig 2.1)
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At week 7, urorectal septum reaches the cloacal membrane, perineal body is formed. (fig 2.3) The cloacal
membrane is then divided into anal membrane & urogenital membrane.
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The anal membrane is surrounded by mesenchymal swelling located at the bottom of an ectodermal
depression known as anal pit. (fig 3.1)
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In week 9, the anal membrane ruptures, an open pathway is formed between the rectum and the outside. (fig
3.2)
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So, upper part of anal canal is endodermal origin and supply by IMA, lower third of anal canal is ectodermal
origin and supply by (middle) rectal arteries fm internal pudendal artery.
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Pectinate line is form at the junction, the epithelium change from columnar to squamous.
Retoanal Atresia (fig 4-11)
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When there's incomplete formation of hindgut, imperforate anus with or without fistula connecting urogenital
system occurs.
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Classified as high (usually with fistula) and low (no fistula) deformities
Aganglionic megacolon (Hirschspung's disease, fig 12-17)
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Due to absence of parasympathetic ganglia in the bowel wall which derived from neural crest cells that migrate
from the neural fold to the bowel wall.
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In most case, rectum is involved, and most extend to sigmoid
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Only 3% involve the entire colon.