(Transcribed from Dr. Martin’s lecture,16 Mar 2000 by Brian Buschman)
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The process of GI development is set in motion in the fourth week by the embryonic folding. Just about every step in this process begins in the fourth week. The folding will enclose part of the yolk sac but for now it remains outside of the embryo. The folding also creates three layers of the gut:
1) An inner endodermal lining.
2) The middle layer is made of splanchnic mesoderm.
3) The outer layer (serosa or adventitia) forms from ectoderm.
The gut develops in three parts the first being the foregut. It forms the GI tract from the mouth to just after the major duodenal papillae as well as the respiratory tract. The abdominal foregut is supplied by the celiac trunk. It receives it’s parasympathetic innervation from the vagus nerve and sympathetic from the greater splanchnic nerve (T5-9). It gives rise to:
1) The parts of the mouth that are not of neural crest origin.
2) The lower respiratory system.
3) The esophagus, stomach and the first part of the duodenum.
4) The pancreas, liver, gallbladder and the associated duct system.
The trachea and the esophagus begin as a single tube and are separated by the development of the tracheoesophageal septum. The esophageal part rapidly elongates and it’s epithelium proliferates and obliterates the lumen. Under normal conditions the lumen recanalizes around the 8th week.
The epithelia and associated glands are formed from endoderm.
It’s muscularis externa is striated in the upper third and innervated by SVE (bronchiomotor, voluntary) fibers of the vagus nerve. The lower third is smooth muscle innervated by GVE (parasympathetic) fibers of the vagus nerve. The middle third is a gradual transition from one to the other.
In about one of 4500 births there is atresia of the esophagus. Most of the cases involve a blind ended proximal segment and a fistula connecting the distal segment to the trachea. It will usually go undetected during development because there is still a path for amniotic fluid to make it to the gut for absorption but respirator distress is encountered with the first drinks of milk as it goes down the trachea. If there is esophageal atresia without the fistula then polyhydraminous will result since there will be no path for absorption of amniotic fluid.
Again, in the fourth week, a dilation in the foregut occurs which will develop into the stomach. The dorsal boarder glows faster then the ventral boarder resulting in the lesser and greater curvatures of the stomach.
The stomach develops in the midline and then rotates 90o clockwise to assume it’s current position. The right and left vagus will now innervate the posterior and anterior walls respectively. This also pulls the mesogastrium to the left to create the ornamental cavity.
The most common foregut anomaly is pyloric stenosis which results from hypertrophy of the muscles of (usually of the circular layer) of the pyloris. The clinical sign is projectile vomiting in the infant and it is five times more common in males then females.
In the fourth week the distal part of the foregut and proximal part of the midgut join just distal to the major duodenal papilla and form a C-shaped tube. The lumen becomes smaller but will later return to a normal diameter.
Stenosis is the partial occlusion of the lumen due to incomplete recanalization of the duodenum. It results in forceful vomiting like in pyloric stenosis.
Duodenal atresia is the complete closure of the lumen and will result in polyhydraminous. It can be either before or after the entrance of the common bile duct. If it is in the foregut (before the duct) then there will be no signs of bile in the amniotic fluid when polyhydraminous is detected. If it’s a post-ductal atresia there will be bile present in the amniotic fluid after the 12th week.
The liver develops from a swelling of the caudal foregut on the ventral side known as the liver bud or hepatic diverticulum. It penetrates the septum transversum which will form part of the diaphragm ad well as the hemopoetic cells, Kuffer cells and connective tissue of the liver. Initially the lobes are the same size but during development the right becomes much larger.
During the 6th week of development the liver takes over the job of hemopoesis from the allantois and will eventually pass it on to the spleen. It begins to produce bile about the 12th week.
The caudal part of the hepatic diverticulum develops into the gallbladder and cystic duct. Initially the common bile duct attached ventrally to the duodenum but as the duodenum rotates it is taken dorsally. This is why the common bile duct passes posterior to the duodenum.
As the liver bulges into it’s position it acquires the umbilical vein which will become the falciform ligament in the adult. It also develops intraperitoneally and grows to the posterior abdominal wall where it’s peritoneum collects into the coronary ligament (or triangular ligaments) and forms the bare area between itself and the posterior abdominal wall.
Biliary atresia is the most common form of liver anomaly. It’s is noticed by jaundice and must either be surgically corrected or requires liver transplant.
The pancreas develops from two buds. The larger dorsal bud and the smaller ventral bud. The ventral bud is somewhat attached to the hepatic diverticulum. As the duodenum rotates the ventral bud is carried back to and merges with the dorsal bud. The major pancreatic duct comes from the ventral bud and connects to the common bile duct because the common site of origin. The duct of the dorsal bud may become the accessory pancreatic duct and give the minor duodenal papillae inferior to the major pancreatic papillae.
The pancreatic tubule system is of endodermal origin. The acini develop at the end of the tubules. The islets of Langerhan develop away from the tubules. Being endocrine they have no need to be near the duct system
Anular pancreas is when the ventral pancreatic bud grows around the duodenum causing constriction. Patients with this condition have a higher rate of pancreatic and peptic ulcers.
The spleen does not develop from the foregut but do to it’s position in the dorsal mesogastrium is discussed here. It develops from mesenchyme cells. As the stomach rotates it pulls the dorsal mesogastrium to the left therefore moving the spleen from being dorsal to the stomach to being to it’s left. This is also why the spleen is considered to be secondarily retroperitoneal. This rotation forms the lienorenal ligament from the mesogastrium.
In late fetal life the spleen acquires hemopoesis function from the liver which it hands off to bone marrow around the time of birth. Even in adult life the spleen retains it’s hemopoetic ability incase needed.
The midgut forms the tube from just after the major duodenal papillae to the proximal 2/3 of the transverse colon. It is supplied by the inferior mesenteric vessels. It’s sympathetic nerve supply is still by the vagus but it’s parasympathetic supply is via the middle splanchnic nerve (T10-11).
It forms by a strange series of folds. It is suspended from the abdominal wall by the mesentery proper and from a U-shaped loop projecting out of the umbilicus and connection to the yolk sac by the yolk stalk. This is called physiological herniation. The loop is centered around the superior mesenteric artery. The look will undergo 90o of rotation counter clockwise around the artery. As the abdomen expands and more room is available it will return to the abdomen and in the process undergo another 180o rotation so the colon falls into the proper place.
The appendix usually lies either behind the colon (retrocolic) or behind the secum (retrosecal). About 2/3 of people have a retrosecal appendix.
Congenital omphalocele is when the midgut loops fail to return to the abdomen.
Meckel’s diverticulum is when a part of the yolk stalk persists as a connection to the ileum about 40-50 cm from the ilealsecal junction. It exists in about 3% of the population and is able to become inflamed like the appendix. In some cases it can also have a fistula to the umbilicus where fecal material will pass through the umbilicus.
Gastrochisis is a defect of the medial plane of the abdomen that allows abdominal viscera to hang out.
Left sided colon results from failure of the midgut to undergo the additional 180o rotation as it returns to the abdomen. It can be a problem if the abnormal position causes pinching against one of the arteries.
Reversed rotation, when the original 90o rotation happened in the clockwise position, will cause the transverse colon to pass posterior to the duodenum. It’s danger is possible occlusion or kinking of the arteries.
Atresia or stenosis of the gut would cause a considerable backup in the gut leading to excessive gastrointestinal distension and excessive vomiting in newborns.
The hindgut gives the distal 1/3 of the transverse colon and all tubes down to the anal canal and the endoderm of the bladder and most of the urethra. It gets it’s blood supply from the inferior mesenteric artery. It’s sympathetic supply is from S2-4 and it’s parasympathetic is by the lesser splanchnic (T12) and by lumber splanchnic nerves.
The terminal part of the hindgut enters what is called the cloaca which will separate into the urinary tract and the anal canal. It is closed from the outside by the cloacal membrane. The anal pit, of ectodermal origin, is outside the membrane and the hindgut inside. The urorectal septum divides the cloaca into the section for the bladder/urethra and the rectum.
The cloacal membrane will regress providing the anal canal. In the anal canal ridges will arise in the hindgut part called the anal columns of Morgagni. The pectinate line is the line at the bottom of the columns demarking the endoderm from the ectoderm. The endodermal part is supplies by superior mesenteric vessels and it’s nervous supply is only sensitive to stretch. It’s lymphatics drain into the inferior mesenteric nodes. The ectodermal part is supplied by the middle and inferior rectal vessels and it is sensitive to pain. It’s lymphatics drain into inferior mesenteric nodes. Therefore hemorrhoids in the ectodermal part will hurt like crazy but hemorrhoids in the endodermal part will not.
Imperforate anus is when the cloacal membranes fails to regress and forms a blockage of the anal canal.
Rectal atresia is the abnormal recanalization of the anal canal leading to a point where the canal is replaces by fibrous cord for a stretch.
Anorectal agenesis is where the rectum ends blindly. It often has a fistula to the bladder or urethra in males or vagina in females.
Congenital megacolon is the failure of the parasympathetic ganglia to develop due to some neonatal obstruction. This leads to lack of peristalsis and backing up of fecal matter causing distension of the colon.
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