development of Gastro-intestinal system. pptx

Embryology

1. During the development of the primitive gut and its derivatives It is usually divided into four sections: The pharyngeal gut, or pharynx, extends from the buccopharyngeal membrane to the tracheobronchial diverticulum The foregut lies caudal to the pharyngeal tube and extends as far caudally as the liver outgrowth. The midgut begins caudal to the liver bud and extends to the junction of the right two-thirds and left third of the transverse colon in the adult . The hindgut extends from the left third of the transverse colon to the cloacal membrane

2. As a result of cephalo -caudal and lateral folding of the embryo, a portion of the endoderm-lined yolks ac cavity is incorporated into the embryo to form the primitive gut . In the cephalic and caudal parts of the embryo, the primitive gut forms a blind-ending tube, the foregut and hindgut , respectively. The middle part forms the midgut which remains temporally connected to the yolk sac by means of the vitelline duct, or yolk stalk

3. Endoderm forms the epithelial lining of the digestive tract and gives rise to the parenchyma of glands, such as the liver and pancreas. Muscle, connective tissue, and peritoneal components of the wall of the gut are derived from splanchnic mesoderm Portions of the gut tube and its derivatives are suspended from the dorsal and ventral body wall by mesenteries, (double layers of peritoneum) that enclose an organ and connect it to the body wall. Such organs are called intraperitoneal , whereas organs that lie against the posterior body wall and are covered by peritoneum on their anterior surface only (e.g., the kidneys) are considered retroperitoneal.

4. Peritoneal ligaments are double layers of peritoneum (mesenteries) that pass from one organ to another or from an organ to the body wall. Mesenteries and ligaments provide pathways for vessels, nerves, and lymphatics to and from abdominal viscera. Initially the foregut, midgut , and hindgut are in broad contact with the mesenchyme of the posterior abdominal wall.

5. By the fifth week however, the connecting tissue bridge has narrowed, and the caudal part of the foregut, the midgut , and a major part of the hindgut are suspended from the abdominal wall by the dorsal mesentery which extends from the lower end of the esophagus to the cloacal region of the hindgut. In the region of the stomach it forms the dorsal mesogastrium or greater omentum ; In the region of the duodenum it forms -the dorsal mesoduodenum ; and In the region of the colon it forms the dorsal mesocolon . Dorsal mesentery of the jejunal and ileal loops forms the mesentery proper.

6. Ventral mesentery, which exists only in the region of the terminal part of the esophagus, the stomach, and the upper part of the duodenum is derived from the septum transversum . Growth of the liver into the mesenchyme of the septum transversum divides the ventral mesentery into: ( a ) the lesser omentum , extending from the lower portion of the esophagus, the stomach, and the upper portion of the duodenum to the liver, ( b ) The f alciformligament , extending from the liver to the ventral bodywall .

7. At first the esophagus is short but with descent of the heart and lungs it lengthens rapidly The muscular coat, which is formed by surrounding splanchnic mesenchyme, is striated in its upper two-thirds and innervated by the vagus ; the muscle coat is smooth in the lower third and is innervated by the splanchnic plexus

8. Foregut DEVELOPMENT OF THE ESOPHAGUS When the embryo is approximately 4 weeks old, the respiratory diverticulum (lung bud) appears at the ventral wall of the foregut at the border with the pharyngeal gut. The tracheoesophageal septum gradually partitions this diverticulum from the dorsal part of the foregut. In this manner the foregut divides into a ventral portion, the respiratory primordium , and a dorsal portion, the esophagus

9. Esophageal Abnormalities Esophageal atresia and/or tracheoesophageal fistula results either from spontaneous posterior deviation of the tracheoesophageal septum or from some mechanical factor pushing the dorsal wall of the foregut anteriorly . In its most common form the proximal part of the esophagus ends as a blind sac,and the distal part is connected to the trachea by a narrow canal just above the bifurcation Other types of defects in this region occur much less frequently eg ,( atresias )obstruction of the passage the amniotic fluid into the intestinal tract of the fetus , resulting in accumulation of excess fluid in the amniotic sac ( polyhydramnios ). In addition to atresias , the lumen of the esophagus may narrow, producing esophageal stenosis, usually in the lower third.

10. Stenosis may be caused by incomplete recanalization, vascular abnorma lities , or accidents that compromise blood flow. Occasionally the esophagus fails to lengthen sufficiently and the stomach is pulled up into the esophageal hiatus through the diaphragm. The result is a congenital hiatal hernia.

11. DEVELOPMENT OF THE STOMACH -The stomach appears as a fusiform dilation of the foregut in the fourth week of development. -During the following weeks, its appearance and position change greatly as a result of the different rates of growth in various regions of its wall and the changes in position of surrounding organs. - Positional changes of the stomach are most easily explained by assuming that it rotates around a longitudinal and an antero posterior axis. -The stomach rotates 90◦ clockwise around its longitudinal axis, causing its left side to face anteriorly and its right side to face posteriorly. -Hence the left vagus nerve, initially innervating the left side of the stomach , now innervates the anterior wall; -Similarly the right vagus nerve innervates the posterior wall

12. - During this rotation the original posterior wall of the stomach grows faster than the anterior portion, forming the greater and lesser curvatures -The cephalic and caudal ends of the stomach originally lie in the midline , but during further growth the stomach rotates around an anteroposterior axis, -Such that the caudal or pyloric part moves to the right and upward and the cephalic or cardiac portion moves to the left and slightly downward. -The stomach thus assumes its final position, its axis running from above left to below right.

13. -Since the stomach is attached to the dorsal body wall by the dorsal mesogastrium and to the ventral body wall by the ventral mesogastrium , its rotation and disproportionate growth alter the position of these mesenteries . -Rotation about the longitudinal axis pulls the dorsal mesogastriumto the left, creating a space behind the stomach called the omental bursa (lesser peritoneal sac ). -This rotation also pulls the ventral mesogastrium to the right. As this process continues in the fifth week of development , the spleen primordium appears as a mesodermal proliferation between the two leaves of the dorsal mesogastrium .

14. -With continued rotation of the stomach, the dorsal mesogastrium lengthens,and the portion between the spleen and dorsal midline swings to the left and fuses with the peritoneum of the posterior abdominal wall. - The posterior leaf of the dorsal mesogastrium and the peritoneum along this line of fusion degenerate. -The spleen, which remains intraperitoneal , is then connected to the body wall in the region of the left kidney by the lienorenal ligament and to the stomach by the gastrolienal ligament

15. -Lengthening and fusion of the dorsal mesogastrium to the posterior body wall also determine the final position of the pancreas. - Initially the organ grows into the dorsal mesoduodenum , but eventually its tail extends into the dorsal mesogastrium . - Since this portion of the dorsal mesogastrium fuses with the dorsal body wall, the tail of the pancreas lies against this region. -Once the posterior leaf of the dorsal mesogastrium and the peritoneum of the posterior body wall degenerate along the line of fusion , the tail of the pancreas is covered by peritoneum on its anterior surface only and therefore lies in a retroperitoneal position. Organs , such as the pancreas, that are originally covered by peritoneum, but later fuse with the posterior body wall to become retroperitoneal, are said to be secondarily retroperitoneal .

16. As a result of rotation of the stomach about its anteroposterior axis, the dorsal mesogastrium bulges down forms a double-layered sac extending over the transverse colon and small intestinal loops like an apron. This double-leafed apron is the greater omentum ; later its layers fuse to form a single sheet hanging from the greater curvature of the stomach. The posterior layer of the greater omentum also fuses with the mesentery of the transverse colon

17. The lesser omentum and falciform ligament form from the ventral mesogastrium , which itself is derived from mesoderm of the septum transversum . When liver cords grow into the septum, it thins to form the peritoneum of the liver, the falciform ligament, extending from the liver to the ventral body wall, and the lesser omentum , extending from the stomach and upper duodenum to the liver

18. -The free margin of the falciform ligament contains the umbilical vein which is obliterated after birth to form the round ligament of the liver ( ligamentum teres hepatis ). - The free margin of the lesser omentum connecting the duodenum and liver ( hepatoduodenal ligament) contains the bile duct, portal vein, and hepatic artery (portal triad). This free margin also forms the roof of the epiploic foramen of Winslow, which is the opening connecting the omental bursa (lesser sac) with the rest of the peritoneal cavity (greater sac)

19. Stomach Abnormalities -Pyloric stenosis occurs when the circular and, to a lesser degree, the longitudinal musculature of the stomach in the region of the pylorus hypertrophies. - One of the most common abnormalities of the stomach in infants, pyloric stenosis is believed to develop during fetal life. -There is an extreme narrowing of the pyloric lumen, and the passage of food is obstructed, resulting in severe vomiting. there are few cases the pylorus is atretic . Other malformations of the stomach, such as duplications and a prepyloric septum, are rare

20. DEVELOPMENT OF THE DUODENUM The terminal part of the foregut and the cephalic part of the midgut form the duodenum . The junction of the two parts is directly distal to the origin of the liver bud. As the stomach rotates, the duodenum takes on the form of a C-shaped loop and rotates to the right. This rotation, together with rapid growth of the head of the pancreas, swings the duodenum from its initialmidline position to the left side of the abdominal cavity

21. During the second month, the lumen of the duodenum is obliterated by proliferation of cells in its walls . However , the lumen is recanalized shortly thereafter. Since the foregut is supplied by the celiac artery and the midgut is supplied by the superior mesenteric artery, the duodenum is supplied by branches of both arteries

22. The duodenum and head of the pancreas press against the dorsal body wall , and the right surface of the dorsal mesoduodenum fuses with the adjacent peritoneum . Both layers subsequently disappear, and the duodenum and head of the pancreas become fixed in a retroperitoneal position. The entire pancreas thus obtains a retroperitoneal position. The dorsal mesoduodenum disappears entirely except in the region of the pylorus of the stomach, where a small portion of the duodenum (duodenal cap) retains its mesentery and remains intraperitoneal .

23. DEVELOPMENT OF LIVER AND GALLBLADDER The liver primordium appears in the middle of the third week as an outgrowth of the endodermal epithelium at the distal end of the foregut This outgrowth, the hepatic diverticulum, or liver bud, consists of rapidly proliferating cells that penetrate the septum transversum , that is, the mesodermal plate between the pericardial cavity and the stalk of the yolk sac. While hepatic cells continue to penetrate the septum, the connection between the hepatic diverticulum and the foregut (duodenum ) narrows , forming the bile duct.

24. A small ventral outgrowth is formed by the bile duct, and this outgrowth gives rise to the gallbladder and the cystic duct. During further development, epithelial liver cords intermingle with the vitelline and umbilical veins, which form hepatic sinusoids. Liver cords differentiate into the parenchyma (liver cells) and form the lining of the biliary ducts . Hematopoietic cells, Kupffer cells, and connective tissue cells are derived from mesoderm of the septum transversum

25. When liver cells have invaded the entire septum transversum , so that the organ bulges caudally into the abdominal cavity mesoderm of the septum transversum lying between the liver and the foregut and the liver and ventral abdominal wall becomes membranous, forming the lesser omentum and falciform ligament, respectively. Together , having formed the peritoneal connection between the foregut and the ventral abdominal wall, they are known as the ventral mesogastrium

26. Mesoderm on the surface of the liver differentiates into visceral peritoneum except on its cranial surface. In this region, the liver remains in contact with the rest of the original septum transversum . This portion of the septum , which consists of densely packed mesoderm, will form the central tendon of the diaphragm. The surface of the liver that is in contact with the future diaphragm is never covered by peritoneum; it is the bare area of the liver

27. In the 10th week of development the weight of the liver is approximately 10%of the total body weight. Although this may be attributed partly to the large numbers of sinusoids, another important factor is its hematopoietic function. Large nests of proliferating cells, which produce red and white blood cells, lie between hepatic cells and walls of the vessels. This activity gradually subsides during the last 2 months of intrauterine life, and only small hematopoietic islands remain at birth. The weight of the liver is then only 5%of the total body weight.

28. Another important function of the liver begins at approximately the 12 th week , when bile is formed by hepatic cells . Meanwhile , since the gallbladder and cystic duct have developed and the cystic duct has joined the hepatic duct to form the bile duct, bile can enter the gastrointestinal tract. As a result, its contents take on a dark green color. Because of positional changes of the duodenum, the entrance of the bile duct gradually shifts from its initial anterior position to a posterior one, and consequently, the bile duct passes behind the duodenum

29. Liver and Gallbladder Abnormalities Variations in liver lobulation are common but not clinically significant, Accessory hepatic ducts and duplication of the gallbladder are also common and usually asymptomatic. However , they become clinically important under pathological conditions. In some cases the ducts, which pass through a solid phase in their development, fail to recanalize . This defect , extrahepatic biliary atresia, occurs in 1/15,000 live births.

30. Among patients with extrahepatic biliary atresia, 15 to 20% have patent proximal ducts and a correctable defect, but the remainder usually die unless they receive a liver transplant. Another problem with duct formation lies within the liver itself; it is intrahepatic biliary duct atresia and hypoplasia. This rare abnormality (1/100,000 live births) may be caused by fetal infections. It may be lethal but usually runs an extended benign course.

31. Development of the PANCREAS The pancreas is formed by two buds originating from the endodermal lining of the duodenum. Whereas the dorsal pancreatic bud is in the dorsal mesentery the ventral pancreatic bud is close to the bile duct. When the duodenum rotates to the right and becomes C-shaped, the ventral pancreatic bud moves dorsally in a manner similar to the shifting of the entrance of the bile duct Finally the ventral bud comes to lie immediately below and behind the dorsal bud.

32. Later the parenchyma and the duct systems of the dorsal and ventral pancreatic buds fuse. The ventral bud forms the uncinate process and inferior part of the head of the pancreas. The remaining part of the gland is derived from the dorsal bud. The main pancreatic duct (of Wirsung ) is formed by the distal part of the dorsal pancreatic duct and the entire ventral pancreatic duct.

33. The proximal part of the dorsal pancreatic duct either is obliterated or persists as a small channel, the accessory pancreatic duct (of Santorini ).. The main pancreatic duct, together with the bile duct, enters the duodenum at the site of the major papilla; the entrance of acessory duct (when present) is at the site of the minor papilla. In about 10% of cases the duct system fails to fuse,and the original double system persists

34. In the third month of fetal life, pancreatic islets (of Langerhans) develop from the parenchymatous pancreatic tissue and scatter throughout the pancreas. Insulin secretion begins at approximately the fifth month. Glucagon- and somatostatin -secreting cells also develop from parenchymal cells. Splanchnicmesoderm surrounding the pancreatic buds forms the pancreatic connective tissue.

35. The ventral pancreatic bud consists of two components that normally fuse and rotate around the duodenum so that they come to lie below the dorsal pancreatic bud. -Occasionally , however, the right portion of the ventral bud migrates along its normal route, but the left migrates in the opposite direction. -In this manner, the duodenum is surrounded by pancreatic tissue, and an annular pancreas is formed. -The malformation sometimes constricts the duodenum and causes complete obstruction. -

36. Accessory pancreatic tissue may be anywhere from the distal end of the esophagus to the tip of the primary intestinal loop. Most frequently it lies in the mucosa of the stomach and in Meckel’s diverticulum, where it may show all of the histological characteristics of the pancreas itself.

37. development of the Midgut In the 5-week-old embryo, the midgut is suspended from the dorsal abdominal wall by a short mesentery and communicates with the yolk sac by way of the vitelline duct or yolk stalk. In the adult the midgut begins immediately distal to the entrance of the bile duct into the duodenum and terminates at the junction of the proximal two-thirds of the transverse colon with the distal third. Over its entire length the midgut is supplied by the superior mesenteric artery

38. Development of the midgut is characterized by rapid elongation of the gut and its mesentery, resulting in formation of the primary intestinal loop. At its apex, the loop remains in open connection with the yolk sac by way of the narrow vitelline duct. The cephalic limb of the loop develops into the distal part of the duodenum, the jejunum, and part of the ileum. The caudal limb becomes the lower portion of the ileum, the cecum, the appendix, the ascending colon, and the proximal two-thirds of the transverse colon

39. PHYSIOLOGICAL HERNIATION Development of the primary intestinal loop is characterized by rapid elongation, particularly of the cephalic limb. As a result of the rapid growth and expansion of the liver, the abdominal cavity temporarily becomes too small to contain all the intestinal loops So they enter the extra embryonic cavity in the umbilical cord during the sixth week of development (physiological umbilical herniation)

40. ROTATION OF THE MIDGUT Coincident with growth in length, the primary intestinal loop rotates around an axis formed by the superior mesenteric artery. When viewed from the front, this rotation is counterclockwise, and it amounts to approximately 270◦ when it is complete. Even during rotation, elongation of the small intestinal loop continues, and the jejunum and ileum form a number of coiled loops. The large intestine likewise lengthen considerably but does not participate in the coiling phenomenon. Rotation occurs during herniation (about 90◦) as well as during return of the intestinal loops into the abdominal cavity

41. RETRACTION OF HERNIATED LOOPS During the 10th week, herniated intestinal loops begin to return to the abdominal cavity . Although the factors responsible for this return are not precisely known , it is thought that regression of the mesonephric kidney, reduced growthof the liver, and expansion of the abdominal cavity play important roles. The proximal portion of the jejunum, the first part to reenter the abdominal cavity , comes to lie on the left side. The later returning loops gradually settle more and more to the right.

42. The cecal bud, which appears at about the sixth week as a small conical dilation of the caudal limb of the primary intestinal loop, is the last part of the gut to reenter the abdominal cavity. Temporarily it lies in the right upper quadrant directly below the right lobe of the liver. From here it descends into the right iliac fossa, placing the ascending colon and hepatic flexure on the right side of the abdominal cavity. During this process the distal end of the cecal bud forms a narrow diverticulum, the appendix. Since the appendix develops during descent of the colon, its final position frequently is posterior to the cecum or colon. These positions of the appendix are called retrocecal or retrocolic , respectively

43. MESENTERIES OF THE INTESTINAL LOOPS The mesentery of the primary intestinal loop, the mesentery proper, undergoes profound changes with rotation and coiling of the bowel. When the caudal limb of the loop moves to the right side of the abdominal cavity, the dorsal mesentery twists around the origin of the superior mesenteric artery. Later , when the ascending and descending portions of the colon obtain their definitive positions, their mesenteries press against the peritoneum of the posterior abdominal wall

44. After fusion of these layers, the ascending and descending colons are permanently anchored in a retroperitoneal position . The appendix, lower end of the cecum, and sigmoid colon, however , retain their free mesenteries. The fate of the transverse mesocolon is different. It fuses with the posterior wall of the greater omentum but maintains its mobility. Its line of attachment finally extends from the hepatic flexure of the ascending colon to the splenic flexure of the descending colon

45. The mesentery of the jejunoileal loops is at first continuous with that of the ascending colon. When the mesentery of the ascending mesocolon fuses with the posterior abdominal wall, the mesentery of the jejunoileal loops obtains a new line of attachment that extends from the area where the duodenum becomes intraperitoneal to the ileocecal junction

46. Abnormalities of the Mesenteries Normally the ascending colon, except for its most caudal part ( approximately 1 inch), fuses to the posterior abdominal wall and is covered by peritoneum on its anterior surface and sides. Persistence of a portion of the mesocolon gives +rise to a mobile cecum. In the most extreme form, the mesentery of the ascending colon fails to fuse with the posterior body wall. Such a long mesentery allows abnormal movements of the gut or even volvulus of the cecum and colon . Similarly , incomplete fusion of the mesentery with the posterior body wall may give rise to retrocolic pockets behind the ascending mesocolon . A retrocolic hernia is entrapment of portions of the small intestine behind the mesocolon .

47. Body Wall Defects Omphalocele involves herniation of abdominal viscera through an enlarged umbilical ring. The viscera, which may include liver, small and large intestines , stomach, spleen, or gallbladder, are covered by amnion . The origin of this defect is a failure of the bowel to return to the body cavity from its physiological herniation during the 6th to 10th weeks. Omphalocele occurs in 2.5/10,000 births and is associated with a high rate of mortality (25%) and severe malformations, such as cardiac anomalies (50 %) and neural tube defects (40%). Approximately half of live-born infants with omphalocele have chromosomal abnormalities

48. Gastroschisis is a herniation of abdominal contents through the body wall directly into the amniotic cavity. It occurs lateral to the umbilicusmusually on the right, through a region weakened by regression of the right umbilical vein, which normally disappears. Viscera are not covered by peritoneum or amnion, and the bowel may be damaged by exposure to amniotic fluid . Gastroschisis occurs in 1/10,000 births but is increasing in frequency,especially among young women; this increase may be related to cocaine use.

49. Unlike omphalocele , gastroschisis is not associated with chromosome abnormalities or other severe defects, so the survival rate is excellent. Volvulus ( rotation of the bowel) resulting in a compromised blood supply may, however , kill large regions of the intestine and lead to fetal death

50. Vitelline Duct Abnormalities In 2 to 4% of people, a small portion of the vitelline duct persists, forming an out pocketing of the ileum, Meckel’s diverticulum or ileal diverticulum. In the adult, this diverticulum, approximately 40 to 60 cm from the ileocecal valve on the antimesenteric border of the ileum, does not usually cause any symptoms. However , when it contains heterotopic pancreatic tissue or gastric mucosa, it may cause ulceration, bleeding, or even perforation

51. - Sometimes both ends of the vitelline duct transform into fibrous cords, and the middle portion forms a large cyst, an enterocystoma , or vitelline cyst. Since the fibrous cords traverse the peritoneal cavity, intestinal loops may twist around the fibrous strands and become obstructed, causing strangulation or volvulus. In another variation the vitelline duct remains patent over its entire length, forming a direct communication between the umbilicus and the intestinal tract. This abnormality is known as an umbilical fistula, or vitelline fistula. A fecal discharge may then be found at the umbilicus .

52. Gut Rotation Defects Abnormal rotation of the intestinal loop may result in twisting of the intestine (volvulus ) and a compromise of the blood supply. Normally the primary intestinal loop rotates 270 ◦ counter clockwise . Occasionally, however, rotation amounts to 90◦ only. When this occurs, the colon and cecum are the first portions of the gut to return from the umbilical cord, and they settle on the left side of the abdominal cavity. The later returning loops then move more and more to the right, resulting in left-sided colon.

53. Reversed rotation of the intestinal loop occurs when the primary loop rotates 90◦ clockwise. In this abnormality the transverse colon passes behind the duodenum and lies behind the superior mesenteric artery. Duplications of intestinal loops and cysts may occur anywhere along the length of the gut tube. They are most frequently found in the region of the ileum, where they may vary from a long segment to a small diverticulum. Symptoms usually occur early in life, and 33% are associated with other defects, such as intestinal atresias , imperforate anus, gastroschisis , and omphalocele . Their origin is unknown, although they may result from abnormal proliferations of gut parenchyma.

54. Gut Atresias and Stenoses Atresias and stenoses may occur anywhere along the intestine.Most occurm in the duodenum, fewest occur in the colon, and equal numbers occur in the jejunum and ileum (1/1500 births). Atresias in the upper duodenum are probably due to a lack of recanalization. From the distal portion of the duodenum caudally, however, stenoses and atresias are most likely caused by vascular “accidents.” These accidents may be caused by malrotation,volvulus , gastroschisis , omphalocele , and other factors. As a result, blood supply to a region of the bowel is compromised and a segment dies, resulting in narrowing or complete loss of that region.

55. In 50% of cases a region of the bowel is lost, and in 20% a fibrous cord remains. In another 20% there is narrowing, with a thin diaphragm separating the larger and smaller pieces of bowel. Stenoses and multiple atresias account for the remaining 10% of these defects, with a frequency of 5% each. Apple peel atresia accounts for 10% of atresias . The atresia is in the proximal jejunum, and the intestine is short, with the portion distal to the lesion coiled around a mesenteric remnan . Babies with this defect have low birth weight and other abnormalities.

56. Hindgut The hindgut gives rise to the distal third of the transverse colon, the descending colon , the sigmoid, the rectum, and the upper part of the anal canal. The endoderm of the hindgut also forms the internal lining of the bladder and urethra The terminal portion of the hindgut enters into the posterior region of the cloaca , the primitive anorectal canal; the allantois enters into the,anterior portion , the primitive urogenital sinus The cloaca itself is an endoderm-lined cavity covered at its ventral boundary by surface ectoderm .

57. This boundary between the endoderm and the ectoderm forms the cloacal membrane . the region between the allantois and hindgutform the urogenital septum . This septum is derived from the merging of mesoderm covering the yolk sac and surrounding the allantois. As the embryo grows and caudal folding continues, the tip of the urorectal septum comes to lie close to the cloacal membrane, although the two structures never make contact.

58. At the end of the seventh week, the cloacal membrane ruptures, creating the anal opening for the hindgut and a ventral opening for the urogenital sinus. Between the two, the tip of the urorectal septum forms the perineal body. At this time , proliferation of ectoderm closes the caudalmost region of the anal canal. During the ninth week, this region recanalizes . Thus, the caudal part of the anal canal originates in the ectoderm, and it is supplied by the inferior rectal arteries, branches of the internal pudendal arteries. The cranial part of the anal canal originates in the endoderm and is supplied by the superior rectal artery, a continuation of the inferior mesenteric artery, the artery of the hindgut

59. Hindgut Abnormalities Rectoanal atresias , and fistulas, which occur in 1/5000 live births, are caused by abnormalities in formation of the cloaca. Thus , if the posterior portion of the cloaca is too small and consequently the posterior cloacal membrane is short , the opening of the hindgut shifts anteriorly. If the defect in the cloaca is small , the shift is small, causing a low opening of the hindgut into the vagina or urethra. If the posterior region of the cloaca is very small , the location of the hindgut opening shifts more anteriorly to a higher location.

60. Thus, rectoanal atresias and fistulas are due to ectopic positioning of the anal opening and not to defects in the urorectal septum. Low lesions are twice as common as high ones, with the intermediate variety being the least common. Approximately 50% of children with rectoanal atresias have other birth defects . With imperforate anus, there is no anal opening. This defect occurs because of a lack of recanalization of the lower portion of the anal canal.

61. Congenital megacolon is due to an absence of parasympathetic ganglia in the bowel wall ( aganglionic megacolon or Hirschsprung disease). These ganglia are derived from neural crest cells that migrate from the neural folds to the wall of the bowel. Mutations in the RET gene, a tyrosine kinase receptor involved in crest cell migration, can result in congenital megacolon . In most cases the rectum is involved, and in 80% the defect extends to the midpoint of the sigmoid. In only 10 to 20% are the transverse and right-side colonic segments involved, and in 3% the entire colon is affected.