EMBRYO-LC11-Embryonic Development of Gastrointestinal System.docx.pdf

OUTLINE I. DIVISIONS OF GUT TUBE II. MOLECULAR REGULATION OF GUT TUBE DEVELOPMENT III. MESENTERIES IV. FOREGUT V. MOLECULAR REGULATION OF LIVER INDUCTION VI. PANCREAS VII. MIDGUT...

OUTLINE I. DIVISIONS OF GUT TUBE II. MOLECULAR REGULATION OF GUT TUBE DEVELOPMENT III. MESENTERIES IV. FOREGUT V. MOLECULAR REGULATION OF LIVER INDUCTION VI. PANCREAS VII. MIDGUT VIII. HINDGUT IX. CLINICAL CORRELATIONS I. DIVISIONS OF GUT TUBE Cephalocaudal and Lateral folding: Endoderm Incorporation = primitive gut ○ foregut ○ midgut ○ hindgut the GI tract is derived from the endoderm, in particular; they came Figure 2. Sagittal section of the embryo at various stages of development from the primitive gut demonstrating the effect of cephalocaudal and lateral folding on the position of Midgut remains temporally connected to yolk sac by vitelline duct the endoderm-lined cavity. Note the formation of the foregut, midgut, and as the consequence of the cephalocaudal and lateral body folding, hindgut. (A) Presomite embryo. (B) Embryo with seven somites. (C) Embryo with the endoderm is incorporated into the embryo, resulting to the 14 somites. (D) At the end of the first month. formation of the primitive gut, leaving the embryo with a gut suspended by a dorsal mesentery PRIMITIVE GUT: FROM DORSAL PART OF THE YOLK SAC dorsal mesentery = yolk sac + allantois that remains outside Pharyngeal gut/pharynx: from oropharyngeal membrane to respiratory diverticulum (head and neck) foregut: extends up to the liver midgut: after liver but up to junction of left 3rd of transverse colon hindgut: from left 3rd of transverse colon to cloacal membrane GENERALITIES the epithelium of and the parenchyma of glands associated with the digestive tract (e.g., liver and pancreas) are derived from endoderm gland stroma: from visceral/splanchnic mesoderm the muscular walls of the digestive tract (lamina propria, muscularis mucosae, submucosa, muscularis externa, adventitia and/or serosa) 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 however, a process of recanalization restores the lumen II. MOLECULAR REGULATION OF GUT TUBE DEVELOPMENT RETINOIC ACID CONCENTRATION GRADIENT pharynx vs colon RA comes from the pharynx, that is exposed to little to no RA; the colon sees the highest concentration of RA causes TF (transcription factors) expression in the gut ○ SOX2: esophagus and stomach ○ PDX1: duodenum ○ CDXC: small intestine ○ CDXA: large intestine and rectum endodermal cells secretes sonic hedgehog (SHH) Figure 1. Visual representation of the divisions of the Gut Tube mesoderm then expresses HOX genes This initial patterning is stabilized by reciprocal interactions between the endoderm and visceral mesoderm adjacent to the gut tube. As seen in Figure 2B, the pericardial cavity is enlarging, and is moving medially until such time that it forms an evagination (see Figure 2C and 2D), eventually TRANSCRIPTION FACTORS forming the yolk sac. SHH secreted from the endoderm for epithelial-mesenchymal interaction ○ Determines the specific gut structure Page 1 of 9 [EMBRYOLOGY] 1.11 Embryonic Development of Gastrointestinal System – Dr. Gail Domecq T. Tanawit ○ SHH expression upregulates factors in the mesoderm that DORSAL MESENTERY then determine the type of structure that forms from the dorsal mesogastrium gut tube greater omentum ○ in the caudal limit of the midgut, SHH expression mesoduodenum establishes a nested expression of HOX genes in the mesentery mesoderm mesocolon HOX genes influence cephalic-caudal regions of the gut tube mesoappendix ○ formation of component of mid and hind gut mesosigmoid ○ HOX 9-10: small intestine mesorectum ○ HOX 9-11: cecum ○ HOX 9-12: large intestine ○ HOX 9-13: cloaca Figure 5. Primitive dorsal and ventral mesenteries. The liver is connected to the ventral abdominal wall and to the stomach by the falciform ligament and lesser Figure 3. Molecular regulation of gut development: Color-coded diagram that omentum, respectively. The superior mesenteric artery runs through the indicates genes responsible for initiating regional specification of the gut into mesentery proper and continues toward the yolk sac as the vitelline artery. esophagus, stomach, duodenum, etc. Figure 6. Transverse sections through embryos at various stages of development. (A) The intraembryonic cavity, bordered by visceral and somatic layers of lateral Figure 4. Molecular regulation of gut development: Drawings showing an plate mesoderm, is in open communication with the extraembryonic cavity. (B) example from the midgut and hindgut regions indicating how early gut The intraembryonic cavity is losing its wide connection with the extraembryonic specification is stabilized. cavity. (C) At the end of the fourth week, visceral mesoderm layers are fused in the midline and form a double-layered membrane (dorsal mesentery) between -Stabilization is effected by epithelia-mesenchymal interactions between gut right and left halves of the body cavity. Ventral mesentery exists only in the endoderm and surrounding visceral (splanchnic) mesoderm. Endoderm cells region of the septum transversum (not shown) initiate the stabilization process by secreting SHH, which establishes a nested expression of HOX genes in the mesoderm. This interaction results in a genetic VENTRAL MESENTERY cascade that regulates specification of each gut region as is shown for small and from septum transversum large intestine regions in these diagrams (See Figure 4). with liver growth to septum ○ ventral mesogastrium (lesser omentum) ○ falciform ligament III. MESENTERIES continuous with dorsal mesentery primitive gut is connected to posterior abdominal wall mesenchyme visceral vs. parietal peritoneum and narrows by 5th week peritoneal reflection: junction between organ and inner posterior dorsal mesentery (from fusion of mesodermal layers) takes over abdominal wall ○ from esophagus to rectum ○ double layer membrane One consequence of the tail folding is the incorporation of the allantois ○ nerve, blood vessels, and lymphatic pathway allantois forms the cloaca primitive dorsal and ventral mesenteries distal allantois remain in connecting stalk by day 35 the connecting stalk and the yolk sac talk fuse to form the - intraperitoneal organs: organs that are enclosed by double layers of umbilical cord peritoneum, are connected to the body wall - retroperitoneal organs: organs that lie against the posterior body PRIMITIVE GUT wall and are covered by peritoneum on their anterior surface only stomodeum: ectoderm at cranial end of gut (e.g., kidneys) foregut: endoderm and splanchnic mesoderm midgut: endoderm and splanchnic mesoderm hindgut: endoderm and splanchnic mesoderm Page 2 of 9 [EMBRYOLOGY] 1.11 Embryonic Development of Gastrointestinal System – Dr. Gail Domecq T. Tanawit proctodeum: anal pit- ectoderm at caudal end of GI tract. the cephalic and caudal ends are derived from the ectoderm Foregut, midgut and hindgut are derived from the splanchnic mesoderm ○ splanchnic mesoderm derivatives: inner circular and outer duodenum muscle layers IV. FOREGUT Derivatives: Pharynx (with derivatives tonsils, tongue, salivary glands, etc.) Lower respiratory system Esophagus Stomach Duodenum (proximal to distal bile duct) Figure 8. Successive stages in development of the respiratory diverticulum and Liver, Biliary system and pancreas esophagus through partitioning of the foregut. A. At the end of the third week [lateral view]. B,C. During the fourth week [ventral view]. DEVELOPMENT OF THE ESOPHAGUS The cephalic foregut is partitioned by the tracheoesophageal septum Clinical correlation/s: [4th weeks onward] (refer to figure 8). ○ Esophageal atresia and/or tracheoesophageal fistula Tracheoesophageal septum gradually partitions this diverticulum results either from spontaneous posterior deviation of the from the dorsal part of the foregut (refer to figure 9). tracheoesophageal septum or from some mechanical Formation of esophagus (refer to figure 8 and 9): factor pushing the dorsal wall of the foregut anteriorly. a. The respiratory diverticulum (lung bud) appears at the ○ Atresia - prevents normal passage of amniotic fluid into ventral wall of the foregut at the border with the the intestinal tract, resulting in accumulation of excess pharyngeal gut at 4 weeks old. fluid in amniotic sac [polyhydramnios]. b. Tracheoesophageal septum gradually partitions this ○ Esophageal stenosis - narrowing of the lumen of the diverticulum from the dorsal part of the foregut esophagus usually in the lower third. Stenosis may be c. Foregut divides into a ventral portion, the respiratory caused by incomplete recanalization, vascular primordium, and a dorsal portion, the esophagus. abnormalities, or accidents that compromise blood flow. Initially short (figure 8: A) but lengthens as the heart and lungs ○ Congenital hiatal hernia - failure of the esophagus to descend (figure 8: B). lengthen sufficiently, pulling up the stomach into the Muscular coat by surrounding mesenchyme is: esophageal hiatus through the diaphragm ⅓ striated : vagus (upper two-thirds) ⅔ smooth: splanchnic plexus (lower third) The upper part of your esophagus is voluntary therefore ⅓ part is vagus, proceeding down it would be splanchnic in nature Figure 7. Embryos during the fourth [A] and fifth [B] weeks of development showing formation of the gastrointestinal tract and the various derivatives Figure 9. Variations of esophageal atresia and/or tracheoesophageal fistula in originating from the endodermal germ layer. order of their frequency of appearance: [A] 90%, [B] 4%, [C] 4%, [D] 1%, and [E] 1%. DEVELOPMENT OF THE STOMACH During the 4th week caudal foregut begins to dilate (fusiform dilation in close approximation to the respiratory diverticulum in the primitive thoracic region) Diaphragmatic hernia - failure in lengthening of the esophageal region in the abdominal cavity below the diaphragm causing the stomach to remain in the thoracic cavity compressing the lungs. Initiate oriented in the median plate Rotation of the stomach ○ as the stomach grows; the ventral surface rotates to the right Page 3 of 9 [EMBRYOLOGY] 1.11 Embryonic Development of Gastrointestinal System – Dr. Gail Domecq T. Tanawit the dorsal border moves to the left Omental bursa/lesser peritoneal sac - space behind the Growth of the stomach stomach due to the rotation. ○ During the next two weeks Spleen from mesoderm proliferation in dorsal mesoderm dorsal wall of stomach grows faster than the Lienorenal reflection - peritoneum that connects spleen ventral wall giving rise to greater and lesser to the posterior body wall in the region of the left kidney curvature Gastrolienal reflection - connects spleen to the posterior body wall in the region of the stomach Figure 11. A. The positions of the spleen, stomach, and pancreas at the end of the fifth week. Note the position of the spleen and pancreas in the dorsal mesogastrium. B. Position of spleen and stomach at 11th week. Note formation of the omental bursa [lesser peritoneal sac]. Figure 10. A, B, and C. Rotation of the stomach along its longitudinal axis as seen anteriorly. D and E. Rotation of the stomach around the anteroposterior Greater omentum axis. Note the change in position of the pylorus and cardia. ○ from downward growth of dorsal mesogastrium. ○ initially as two layers and fuse forming a single sheet As the stomach grows: hanging from the greater curvature of the stomach ○ the left side becomes the ventral surface ○ Posterior layer fuses with mesentery of the transverse ○ the right side becomes the dorsal surface colon Cranial region moves inferiorly and to the left Clinical correlation/s: Caudal region moves superiorly and to the right ○ Pyloric stenosis Long axis of stomach becomes nearly transverse hypertrophy of circular and or longitudinal Innervation of the gastrointestinal tract muscle in pylorus Vagus 3- 5 after birth the rotation of the stomach leaves the Erythromycin left vagus nerve on the ventral surface of the stomach Projectile narrowing (anterior vagal trunk) right vagus nerve in the dorsal surface of the DEVELOPMENT OF THE DUODENUM stomach (posterior vagal trunk) derived from terminal foregut up to the bile duct (first and second Arteries parts) since the foregut distal to the esophagus is cephalic midgut from bile duct to jejunum supplied by the celiac artery, branches of this growth of the duodenum artery supply the stomach ○ grows as a C-shaped loop that projects ventrally. Attachment rotation of the duodenum ○ Dorsal mesogastrium - attachment to the dorsal body wall ○ as the stomach rotates so does the duodenum ○ Ventral mesogastrium - attachment to the ventral body ○ as the duodenal loop rotates it to the right wall; part of septum transversum; mesoderm becomes ○ eventually comes to lie in a retroperitoneal position. thinner as liver grows in the region forming two parts of Duodenal cap - small portion of the distal region of the duodenum ventral mesentery: retaining an extension of mesentery that remains unattached to the Lesser omentum posterior body wall. liver attachment of stomach during the 5th and 6th weeks Portal pedicle - connection to the duodenum; ○ the duodenal lumen becomes lugged by epithelial cells thickening on the free margin connecting the ○ later recanalized duodenum and liver Blood supply: Portal pedicle contains: ○ Foregut - celiac artery ○ Portal triad - bile duct, portal vein, hepatic ○ Midgut - superior mesenteric artery artery ○ Duodenum - celiac artery and superior mesenteric artery ○ Roof of the epiploic foramen (of Winslow) - opening connecting the omental bursa (lesser sac) with the rest of the peritoneal cavity (greater sac). Falciform ligament liver connection of ventral body wall contains umbilical vein on the free margin ligamentum teres hepatis - round ligament of liver obliterated after birth Page 4 of 9 [EMBRYOLOGY] 1.11 Embryonic Development of Gastrointestinal System – Dr. Gail Domecq T. Tanawit Accessory hepatic ducts and duplication of the gallbladder ○ common and usually asymptomatic ○ clinically important under pathological conditions Extrahepatic biliary atresia ○ occurs in 1/15,000 live births ○ 15% to 20% have patent proximal ducts and a correctable defect, but the remainder usually die unless they receive a liver transplant Intrahepatic biliary duct atresia and hypoplasia ○ problem with duct formation within the liver itself ○ rare abnormality [1/100,000 live births] ○ may be caused by fetal infections ○ may be lethal but usually runs an extended benign course Figure 12. Upper portion of the duodenum showing the solid stage [A] and cavity formation [B] produced by recanalization. DEVELOPMENT OF THE LIVER During the 3rd week the liver buds develops ○ Liver bud also known as hepatic diverticulum - consists of rapidly proliferating cells that penetrate the septum transversum Endodermal cells grow toward septum transversum (the mesodermal plate between the pericardial cavity and the stalk of the yolk sac) Endodermal cords (epithelial liver cords) mix with cells of vitelline Figure 14. A. Obliteration of the bile duct resulting in distention of the and umbilical veins (hepatic sinusoids) to form liver parenchyma - gallbladder and the hepatic ducts distal to the obliteration. B. Duplication of the forms the lining of the biliary duct gallbladder. Hematopoietic cells, Kupffer cells and connective tissue cells are derived from mesoderm of septum transversum V. MOLECULAR REGULATION OF LIVER INDUCTION Liver function ○ early function is hematopoiesis ○ activity diminishes during the last 2 months of gestation All of the foregut endoderm has the potential to express liver-specific genes and to differentiate into liver tissue. DEVELOPMENT OF THE BILE DUCT ○ this expression however is blocked by factors produced by As the liver develops, the epithelium between the liver and the surrounding tissues (ectoderm, noncardiac mesoderm, foregut narrows and forms the bile duct. and particularly notochord) Narrow connection between the hepatic diverticulum and the foregut (duodenum) as a result of the penetration of hepatic cells to septum. DEVELOPMENT OF THE GALLBLADDER a diverticulum develops from the bile duct (small ventral outgrowth) giving rise to the gallbladder and the cystic duct bile duct biomes solid, then the lumen opens again Figure 15. Diagram of the cardiac and hepatic-forming regions illustrating induction of liver development The action of these inhibitors is blocked in the prospective hepatic region by: ○ Fibroblast Growth Factors (FGF2) from cardiac mesoderm and blood vessel-forming endothelial cells Figure 13. Transverse sections through the region of the duodenum at various adjacent to the gut tube at the site of liver bud outgrowth stages of development. At first, the duodenum and head of the pancreas are cardiac mesoderm together with neighboring located in the median plane [A], but later, they swing to the right and become vascular endothelial cells “instructs” gut attached to the posterior abdominal wall [B]. endoderm to express liver-specific genes by inhibiting an inhibitory factor of these same CLINICAL CORRELATION/S: genes Variations in liver lobulation ○ common but not clinically significant Page 5 of 9 [EMBRYOLOGY] 1.11 Embryonic Development of Gastrointestinal System – Dr. Gail Domecq T. Tanawit ○ Bone Morphogenetic Proteins (BMPs), secreted by the Expression of the paired homeobox genes PAX4 and PAX6 specifies septum transversum, which enhances the competence of the endocrine cell lineage, such that cells expressing both genes prospective liver endoderm to respond to FGF2 become insulin, somatostatin, and pancreatic polypeptide cells; ○ Both aids in liver (hepatocytes) and biliary cell lineage whereas those expressing only PAX6 become a (glucagon) cells. differentiation ○ Regulated by hepatocyte nuclear transcription factor (HNF MOLECULAR REGULATION OF PANCREAS DEVELOPMENT 3 and 4) Islet of Langerhans develop from parenchymatous tissue during the Once the “instruction” is received, cells in the 3rd month of gestation. liver field differentiate into both hepatocytes ○ They scatter throughout the pancreas and biliary cell lineages, a process that is at least partially regulated by hepatocyte nuclear Transcription factors involved in the formation of pancreas: transcription factors (HNF3 and 4). PAX 4 and PAX 6 specify cells to become: ○ β (insulin) cells ○ δ (somatostatin) cells ○ 𝛾 (pancreatic polypeptide) cells VI. PANCREAS PAX 6 only: ○ 𝛼 (glucagon) cells Originates from two pancreatic buds: Insulin secretion begins at 5 months of gestation. Dorsal pancreatic bud in dorsal mesentery Glucagon and somatostatin-secreting cells also develop from Ventral pancreatic bud is near the bile duct. parenchymal cells. Visceral mesoderm surrounding the pancreatic buds forms the pancreatic connective tissue. VII. MIDGUT In the 5-week 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. Supplied by the superior mesenteric artery. During early development there is a rapid growth of both midguts and its mesentery. Cephalic and Caudal limbs of the midgut Figure 16. Dorsal and ventral pancreatic bud development During rotation of the duodenum the ventral bud moves dorsally. Ventral bud will lie caudal and posterior to the dorsal bud. Ventral bud forms uncinate process and inferior pancreatic head. Dorsal bud makes up rest of gland Main pancreatic duct is formed from dorsal and ventral pancreatic duct. 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 the accessory duct (when present) is at the site of the minor papilla. Figure 18. Development of Midgut. Midgut forms a primary intestinal loop. Loop remains in connection with the yolk sac. Connection is called the vitelline duct. If vitelline duct persists, it is called a Meckel’s diverticulum. 1) PHYSIOLOGICAL UMBILICAL HERNIATION a) 6th week abdominal cavity cannot contain the gut. Figure 17. Stages in development of pancreas (A) 30 days - approx. 5mm (B) 35 b) Midgut migrates into the umbilical cord days - approx. 7mm. 2) RETURN TO THE MIDGUT FGF2 and ACTIVIN (a TGF-B family member) a) Midgut returns at 10-12 weeks ○ Secreted by the notochord Reasons: ○ Repress SHH in endoderm to become pancreas - Regression of mesonephric kidney As a result, Pancreatic and Duodenal hemeobox 1 (PDX) gene - Reduced liver growth upregulated. Page 6 of 9 [EMBRYOLOGY] 1.11 Embryonic Development of Gastrointestinal System – Dr. Gail Domecq T. Tanawit - Increased size of the abdominal cavity b) First to return: Jejunum (on the left side), while the other VIII. HINDGUT parts return, they are placed on the right side. c) Last to return: Cecum (on the right side, under the liver). DEVELOPMENT OF THE HINDGUT Then, it descends and forms the ascending colon and Terminal portion is in contact with the ectoderm via cloacal plate or hepatic flexure. cloacal membrane. d) Distal end of the cecal bud forms the appendix. Membrane is endoderm of hindgut and ectoderm via anal pit. Cloaca is an expanded portion of the hindgut. 3) ROTATION OF THE MIDGUT Cloaca receives the allantois (sac filled fluid with embryonic and a) The Midgut rotates around the superior mesenteric extra embryonic tissues which play a role for gas exchange and artery. waste). b) This rotation is counterclockwise. c) Even during rotation, elongation of the small intestinal HINDGUT loop continues, and the jejunum and ileum form a Distal 3rd of TC, DC, samoyed, rectum and upper anal canal. number of coiled loops. Endoderm of the hindgut also forms the internal lining of the bladder d) THe large intestine likewise lengthens considerably but and urethra. does not participate in the coiling phenomenon. Terminal hindgut enters urogenital sinus. e) Rotation occurs during herniation. Allantois also enter urogenital sinus. f) 90 degrees during herniation Urorectal septum (mesoderm separating allantois and hindgut) g) 180 degrees during the return comes in contact with the cloacal membrane. Return of the intestinal loops into the Cloacal membrane is the boundary between ectoderm and abdominal cavity endoderm. h) A total of 270 degrees Cloacal membrane ruptures at 7th week = anal opening and rest degenerate for continuity of canal. Lower third is ectoderm derived (protodeum), proliferate and invaginate = anal pit. Junction between ectoderm and endoderm = pectinate line, epithelium changes. (From columnar to stratified squamous epithelium) IX. CLINICAL CORRELATIONS 1) MESENTERY DEFECTS a) Volvulus of the Cecum and Colon ascending portion of the colon fails to attach to the posterior abdominal wall, a mobile colon results which may allow it to twist upon. b) Retrocolic Hernia formed when entrapment of portions of the small intestine posterior to the ascending portion of the colon occurs. 2) BODY WALL DEFECTS Figure 19. Rotation of midgut in weeks 6, 8, 9, 11, and up to fetal period. a) Omphalocele involves herniation of abdominal viscera through an enlarged umbilical ring. may include liver, small and large intestines, stomach, spleen, or gallbladder which are covered by amnion. origin of defect is from the failure of the bowel to return to the body cavity from its physiological herniation during 6th to 10th weeks. Approximately 15% of live infants have chromosomal abnormalities. an abdominal wall defect at the base of the umbilical cord (umbilicus); the infant is born with sac protruding through the defect which contains small intestine, liver, and large intestine. Failure of the intestine to return after a physiologic herniation. The herniated loop is covered by an amnion. The return of physiologic herniation happens on the 6th to 10th weeks of gestation Incidence rate: 2.5/10,000 births. Mortality: 25%. Omphalocele is associated with other anomalies: (1) Cardiac anomalies: 50%. Most common Figure 20. Rotation of midgut in relation with its other parts. (2) Neural Tube defects: 40% Factors increasing the risk of omphalocele: INNERVATION OF THE GUT TUBE (1) Alcohol Vagal neural crest cells innervate the gut tube. (2) Tobacco Additional lumbosacral neural crest cells innervate the hindgut. (3) Selective serotonin reuptake inhibitors (SSRIs) (4) Obesity Page 7 of 9 [EMBRYOLOGY] 1.11 Embryonic Development of Gastrointestinal System – Dr. Gail Domecq T. Tanawit 4) GUT ROTATION DEFECTS Malrotation of the intestinal loop may result in twisting of the intestine [volvulus] and a compromise of the blood supply. Normal: the primary intestinal loop rotates 270° counterclockwise. Rotation amounts to 90° only in 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 Figure 21. Newborns with omphalocele more and more to the right, resulting in a left-sided colon. b) Gastroschisis ○ Reversed rotation of the intestinal loop refers to a protrusion of abdominal contents through the body occurs when the primary loop wall directly into the amniotic cavity. rotates 90° clockwise. It occurs lateral to the umbilicus usually on the right, and the the transverse colon passes behind defect is most likely due to abnormal closure of the body wall the duodenum and lies behind the around the connecting stalk. superior mesenteric artery. Volvulus [rotation of the bowel] resulting in a compromised ○ Duplications of intestinal loops and cysts blood supply may, however, kill large regions of the intestine and occur anywhere along the length lead to fetal death. of the gut tube. found in the region ○ no amnion covering the intestines of the ileum. ○ Incidence rate: 1/10,000 5) GUT ATRESIA AND STENOSIS occur anywhere along the intestine. Most occur in the duodenum, fewest occur in the colon, and equal numbers occur in the jejunum and ileum [1/1,500 births]. Atresia in the upper duodenum is probably due to a lack of recanalization distal portion. Duodenum caudally stenosis and Atresia caused by vascular “accidents” that resulted in compromised blood flow and tissue necrosis in a section of the gut resulting in the defects. Accidents caused by malrotation, volvulus, gastroschisis, omphalocele, and other factors, Figure 22. A newborn with gastroschisis. Misexpression of some HOX genes and of genes and receptors in the FGF family result in gut Atresia. 3) VITELLINE DUCTS ○ Apple peel atresia a) Meckel diverticulum or ileal diverticulum accounts for 10% of Atresias. 2% to 4% of people, a small portion of the vitelline duct persists, atresia is in the proximal jejunum, forming an outpocketing of the ileum adult approximately 40 to and the intestine is short, with the 60 cm from the ileocecal valve on the antimesenteric border of portion distal to the lesion coiled the ileum, does not usually cause any symptoms. around a mesenteric remnant. b) Enterocystoma, Or A Vitelline Cyst Triangulation Or Volvulus Heterotopic pancreatic tissue or gastric mucosa, cause ulceration, bleeding, or even perforation. Both ends of the vitelline duct transform into fibrous cords, and the middle portion forms a large cyst. c) Umbilical Fistula Intestinal loops may twist around the fibrous strands and become obstructed fecal discharge may then be found at the umbilicus Meconium: first fecal discharge of the baby Figure 24. Apple peel atresia, which occurs in the jejunum and accounts for 10% of bowel atresias. The affected portion of the bowel is coiled around a remnant of mesentery. 6) HINDGUT ABNORMALITIES a) Rectourethral and rectovaginal fistulas occur in l/5,000 live births caused by abnormalities in formation of the cloaca and/or the urorectal septum. Figure 23. A newborn with umbilical fistula Page 8 of 9 [EMBRYOLOGY] 1.11 Embryonic Development of Gastrointestinal System – Dr. Gail Domecq T. Tanawit For example, if the cloaca is too small or if the Answer Key urorectal septum does not extend far enough 1. A caudally, then opening of the hindgut shifts 2. B anteriorly leading to an opening of the hindgut 3. Foregut, Midgut, and Hindgut into the urethra or vagina. 4. Splanchnopleuric mesoderm 5. B b) Rectoanal fistulas and atresias 6. Gut Atresia leave a narrow tube or fibrous remnant 7. D connected to the perineal surface. 8. D due to misexpression of genes during 9. B epithelial—mesenchymal signaling. 10. C c) Imperforate anus the anal membrane fails to breakdown. REFERENCES 1. Reference: Langman, J., & Sadler, T. W. (2012). Langman's medical embryology. 12 ed. Philadelphia: Wolters Kluwer Health. Pp. 23-24 2. Moore, K. L., N., P. T. V., & Torchia, M. G. (2020). The developing human: Clinically oriented embryology. Elsevier. 3. PPT - Doc Gail Tanawit TEST YOURSELF 1. What is the gene responsible for the development of the small intestine? a. 9-10 HOX gene and CDXC b. SHH and HOX gene c. 9-13 HOX gene PDX1 d. 9-11 HOX gene CDx1 2. Period in which the umbilical cord was formed? a. day 45 b. day 35 c. day 43 d. day 50 3. What are the regions of the primitive gut tube? 4. What is mesentery derived from? 5. What do mesenteries and ligaments provide paths for? a. Muscular tissues b. Vessels, nerves and lymphatics c. Oesophagus and Cloacal region d. Skeletal tissues 6. Caused by the misexpression of some HOX genes and of genes and receptors in the FGF? 7. Cells that form the enteric nervous system? a. ectodermal cells b. mesodermal cells c. endodermal cells d. Neural crest cells 8. This are the causes of fetal duodenal obstructions except a. Duodenal atresia b. Duodenal web c. AOTA d. NOTA 9. These cells are regarded as the pacemakers of the gastrointestinal tract. a. SA cells b. Interstitial cells of Cajal c. Neural crest cells d. Pluripotent stem cells 10. How does midgut rotate as it retracts into the abdomen a. Rotate 90 degrees counterclockwise b. Rotate 90 degrees clockwise c. Rotate 180 degrees counterclockwise d. Rotate 180 degrees clockwise Page 9 of 9