1. NBME REVIEW topic: g.i embryology.
By: Dr Abiodun Mark Akanmode.

2. Introduction i
The digestive tract starts developing from the primitive gut.
The primitive gut tube is divided into 3 main sections: -Foregut(pharynx - duodenum) -Midgut(duodenum - proximal 2/3rd of the T.colon) -Hindgut(distal 1/3rd of the T.colon - anal canal above the pectinate line)

3. Introduction ii
The epithelium and the parenchyma of glands associated with the digestive tract (e.g., liver and pancreas) are derived from endoderm.
The muscular walls of the digestive tract are derived from splanchnic mesoderm.
During the solid stage of development the endoderm of the gut tube proliferates until the gut is a solid tube.
A process of recanalization restores the lumen

5. Foregut: esophagus
At 4 wks the respiratory diverticulum(lung bud) arises from the ventral wall of the foregut.
The tracheoesophageal septum seperates the ventral lung bud from the dorsal esophagus.
The upper 2/3rd is innervated by the vagus nerve.
The lower 1/3rd is innervated by the splanchnic plexus.

6. stomach.
This arises as a fusiform dilation of the foregut also around the 4th week.
It is initially oriented in the median plane and suspended from the dorsal wall of the abdominal cavity by the dorsal mesentery.
During development the stomach rotates 90˚ thus around its longitudinal plane thus causing the left side to face anteriorly and the right side posteriorly.
Rotation of the stomach creates the omental bursa or lesser peritoneal sac.
Thus the left vagus innervates the anterior part and the right vagus innervates the posterior part.

7. Stomach development & rotation.

8. Foregut: duodenum.
The terminal part of the foregut and the cephalic part of the midgut forms the duodenum.
The duodenum acquires its C-shaped loop as the stomach rotates.
Because of its location at the junction of the foregut and the midgut, branches of both the celiac trunk and the superior mesenteric artery supply the duodenum

9. Foregut: liver & gallbladder.
The liver develops from endodermal cells that form the hepatic diverticulum.
The hepatic diverticulum divides into a cranial part, which forms the parenchyma of the liver, and the caudal part, which gives rise to the gallbladder and cystic duct. 
The hemopoietic cells, Kupffer cells, and connective tissue of the liver are derived from mesenchyme in the septum transversum.
By the 10th wk of development, the liver weight approximately 10% of total body weight.
Blood formation (hemopoiesis) begins in the liver during the sixth week of development, and bile formation begins in the twelfth week.

10. FOREGUT: PANCREAS.
The pancreas develops from two outgrowths of the endodermal epithelium, the dorsal pancreatic bud and the ventral pancreatic bud.
During rotation of the gut these primordial come together to form a single pancreas.
The ventral pancreatic bud forms the uncinate process and part of the head, while the dorsal pancreatic bud forms the remainder of the head, body, and tail of the pancreas.
Insulin secretion begins at approx 5th month.

11. Pancreatic development & rotation.

12. Midgut: The midgut communicates with the yolk sac via the yolk stalk.
 As the midgut forms, it elongates into a U-shaped loop (midgut loop) that temporarily projects into the umbilical cord (physiological umbilical herniation)
 The cranial limb of the midgut elongates rapidly during development and forms the jejunum and cranial portion of the ileum.
The caudal limb forms the cecum, appendix, caudal portion of the ileum, ascending colon, and proximal two-thirds of the transverse colon.
The midgut loop rotates 270° counterclockwise around the superior mesenteric artery as it retracts into the abdominal cavity during the tenth week of development.

13. Midgut: physiologic umbilical herniation.

14. Hindgut:
The hindgut is defined to begin where the blood supply changes from the superior mesenteric artery to the inferior mesenteric artery, i.e. at the distal third of the transverse colon.

15. Clinical correlates: esophageal atresia.

17. Clinical correlates: pyloric stenosis.
Overgrowth of the longitudinal muscle fibers of the pylorus creates a marked thickening of the pyloric region of the stomach. 
This condition affects approximately 1/150 male infants.
The resulting stenosis of the pyloric canal obstructs passage of food into the duodenum, and as a result after feeding the infant expels the contents of the stomach with considerable force (projectile vomiting).

19. Clinical correlates: Meckel’s Diverticulum
A remnant of the proximal part of the yolk stalk that fails to degenerate during the early fetal period results in a finger- like blind pouch that projects from the ileum.
While this condition occurs in about 1/50 people, it is usually asymptomatic and only occasionally leads to abdominal pain and/or rectal bleeding.

20. Clinical correlates: omphalocele.
This involves the herniation of the abdominal visceral through an enlarges umbilical ring.
The etiology of the defect is a failure of the bowel to return from physiologic herniation during the 6th-10th weeks.
Omphalocele occurs in 2.5/10,000 births and its associated with a high rate of mortality and severe malformation of the heart and neural tube.
Approx half of all children born with omphalocele have chromosomal abnomalities.

22. Clinical correlates: gastroschisis.
This is the herniation of the abdominal content through the body wall directly into the amniotic cavity.
It usually occurs lateral to the umbilicus on the right.
Unlike omphalocele, gastroschisis is not covered by peritoneum or amnion.
Gastroschisis occurs in 1/10000 births and its increasing in frequency especially among young women who abuse cocaine.

24. Clinical correlates: MALROTATION OF THE MIDGUT.
 Malrotation also predisposes the infant to a volvulus of the midgut, wherein the intestines bind and twist around a short mesentery.  
Volvulus usually interferes with the blood supply to a section of the intestines, and can lead to necrosis and gangrene.

25. Clinical correlates: congenital megacolon.
This results from the failure of neural crest cells to migrate and form the myenteric plexus in the sigmoid colon and rectum.
The resulting lack of innervation results in loss of peristalsis, fecal retention, and abdominal distention.
Mutation of the RET gene a tyrosine kinase receptor involved in neural crest migration can result in congenital megacolon.
In 80% of cases the rectum is mostly involved.

27. Other hindgut abnomalities.
Anorectal Agenesis: Abnormal formation of the urorectal septum causes the rectum to end as a blind sac above the puborectalis muscle.
Anal Agenesis: Abnormal formation of the urorectal septum causes the rectum to end as a blind sac below the puborectalis muscle.
Imperforate Anus:The anal membrane fails to break down before birth.
The anus must be reconstructed surgically, with severity depending on the thickness of the intervening tissue.

28. Problems to solve.
1. 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? 2. 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? 3. At birth a baby girl has meconium in her vagina and no anal opening. What type of birth defect does she have?

30. References: Lange medical embryology.
Kaplan anatomy lecture series 2013 edition.
First aid step 1: 2011,2013,2015 editions.
Images: Google images.