Development Of GIT PDF

Development of the Digestive System Primitive Gut – By the embryonic foldings with the incorporation of the yolk sac Development of Oral Cavity & Pharynx  Development of Oral Cavity Covered in the development of the face and baranchial apparatus With the...

Development of the Digestive System Primitive Gut – By the embryonic foldings with the incorporation of the yolk sac Development of Oral Cavity & Pharynx  Development of Oral Cavity Covered in the development of the face and baranchial apparatus With the rupture of bucopharyngeal membrane – Vestibule, including the gums develop from stomodium – Oral cavity proper develops from proximal part of primitive pharynx Boundary is just posterior to alveolar process  Developments of the salivary glands As invaginations of the oral epithelium into surrounding mesenchyme Parotid is ectodermal from stomodium Submandibular & sublingual glands are endodermal  Development of Esophagus Initially, at 4th wk is short Later elongates & reaches its final relative size by the 7th wk Epithelium proliferates & temporarily blocks the lumen, but reanalyzes by the end of embryonic period  Development of the Stomach At 4th week dilates and becomes fusiform Posterior border grows faster and becomes greater curvature Ventral border becomes lesser curvature Rotates 900 clockwise to the right around its longitudinal axis Also rotates around its anteroposterior axis  Development of the Duodenum Develops from caudal part of foregut & cranial part of midgut. Middle part grows rapidly to form a “C” shaped loop with a ventral convexity. Rotates 900 clockwise to the right, with the stomach Rests by its right side on posterior abdominal wall & becomes retroperitoneal.  Development of the Midgut Form a loop with a vntrantral convexity Apex is connected to the yolk sac by yolk sac stalk until 10th wk Cranial limb elongates much & coils Caudal limb elongates moderately & dilates Herniates during the 6th wk Rotates a total of 2700 counter clockwise, initially 900 during herniation and further twice 900 during return  Reduction of Midgut Herniation Cranial limb returns first passing posterior to the superior mesenteric artery to occupy left central position Caudal limb follows and lies superior, ventral & to the right of the cephalic limb derivatives. Cecum lags behind and temporarily occupies subhepatic region, but descends later forming hepatic flexure & ascending colon.  Development of the Appendix Develops as a narrow diverticulum from the distal end of cecal bud. As colon descends appendix frequently becomes retrocecal or retrocolic in position.  Development of the Hindgut Elongates & forms a loop with dorsal convexity Terminal part forms cloaca which is divided by urorectal septum into: – Urogenital sinus blocked by urogenital membrane ventrally – Anorectal canal blocked by anal membrane dorsally  Development of the Anal Canal Anal membrane ruptures & anorectal canal gives upper 2/3 - 1/2 of the anal canal up to the level of pectinate line. The lower 1/3 – 1/2 of the anal canal develops from the ectoderm lined proctoderm.  Development of the Liver As hepatic bud from apex of duodenal loop into septum transversum (ventral mesentery) Divides into: 1.Pars hepatica - larger & cranial - gives liver 2.Pars cystica - smaller & caudal - gives gallbladder Liver begins hematopoeitic function by 6th wk & bile production by 12th wk.  Development of the Pancreas 1. Dorsal pancreatic bud Appears 1st slightly cranial to hepatic bud Gives rise to upper part of head, neck, body & tail of pancreas 2. Ventral pancreatic bud From proximal region of hepatic bud Rotates along with duodenum to come & lie posterior to the dorsal pancreatic bud and fuse with it. Gives rise to uncinate process & lower part of head of pancreas  Pancreatic ducts 1. Main Pancreatic Duct (of Wirsung) – Formed by ducts of ventral pancreatic bud, distal part of dorsal pancreatic bud and their anastomsis – Form hepatopancreatic ampulla with the bile duct and opens into the major duodenal papilla 2. Accessory Pancreatic Duct (of Santorini) – By proximal part of duct of dorsal pancreatic bud – Opens into minor duodenal papilla, about 2 cm cranial to the major duodenal papilla  Development of the Mesenteries Ventral mesentery Develops from septum transversum Gives: 1. Lesser omentum between liver and stomach & duodenum as: Hepatogastric & hepatoduodenal ligaments 2. Falciform ligament between liver & ventral abdominal wall 3. Coronary & triangular ligaments between liver & diaphragm 4. Stroma and visceral peritoneum of liver Development of the Mesenteries Dorsal mesentery is divided into: 1. Dorsal mesentery of esophagus 2. Dorsal mesogastrium 3. Dorsal mesoduodenum 4. Mesentery proper 5. Dorsal mesocolon  Dorsal mesogastrium a) Gastrosplenic ligament b) Splenorenal ligament c) Omental bursa d) Greater omentum  Development of the omental bursa (lesser sac of peritoneum) By coalescence of small cavities in the dorsal mesogastrium and by the effect of rotation of the stomach Initially had a lower recess between the folds of the greater omentum  Development of the greater omentum Develops as double layered apron like fold of dorsal mesogastrium (totally has 4 layers) hanging down from the greater curvature of the stomach – Initially bound the lower recess of omental bursa – Later fuse and attach to the transverse colon Development of the dorsal mesoduodenum Largely disappears as duodenum becomes retroperitoneal  Development of the Mesentery proper Broad fan-shaped Run obliquely from left side of L2 vertebra to right iliosacral joint About 15cm long Development of the Dorsal mesocolon Develops into: Mesoappendix Transverse mesocolon Sigmoid mesocolon Ascending & descending colons becoming retroperitoneal  Molecular Regulation of Regional Specifications of the GIT Increasing gradients of retinoic acid (with least or no for pharynx cranially and highest for colon caudally) induce expression of the following transcription factors in the gut tube that initiate specifications: 1. CSOX2 for the esophagus and stomach 2. PDX1 for the duodenum 3. CDXC the small intestine 4. CDXA the large intestine and rectum  Molecular Regulation of Regional Specifications of the GIT Reciprocal epithelial–mesenchymal interaction stabilizes the initiated regional specifications of the GIT, where: – The GIT expresses SHH to stimulate the surrounding splanchnic mesoderm, which in turn expresses factors that determine the type of structure that specific region of the gut tube should develops to.  Molecular Regulation of Liver Induction Expression of genes that could initiate development of liver in all regions of the foregut endoderm are normally remained inhibited by factors produced mainly by the notochord, but also ectoderm and noncardiac mesoderm.  Molecular Regulation of Liver Induction This is however, lifted only in the region of developing liver (hepatic field) by FGF2 secreted from cardiac mesoderm and vascular endothelial cells adjacent to the gut tube under the influence of BMPs from the septum transversum  Molecular Regulation of Pancreas Development The dorsal pancreatic bud is initiated by local repression of SHH in gut endoderm by FGF2 and activin produced from the notochord and endothelium of the dorsal aorta The ventral bud is induced by splanchnic mesoderm Congenital Anomalies of the Digestive System Congenital Anomalies of the Esophagus Short esophagus  by arrested descent associated with thoracic stomach. Congenital Anomalies of the Esophagus Esophageal stenosis  by incomplete recanalization Esophageal atresia  by failure of recanalization Congenital Anomalies of the Esophagus Various tracheoesophageal fistulae  by incomplete separation of trachea from esophagus. Congenital Anomalies of the Stomach Thoracic stomach Transposition of stomach to the right  by reversed rotation Pyloric stsenosis  by hypertrophy of mainly circular muscle layer of muscularis externa.  Congenital Anomalies of the Duodenum Duodenal stenosis By incomplete recanalization or pressure from annular pancreas Congenital Anomalies of the Duodenum Duodenal atresia By failure of recanalization Congenital Anomalies of the Midgut Congenital omphalocele  Because of failure of complete return of physiological umbilical herniation. Umbilical hernia  Herniation of abdominal content through imperfectly closed umbilicus. Gastroschisis  By incomplete closure of the lateral folds, causing herniation of the abdominal content. Congenital Anomalies of the Midgut Ileal (Meckel’s) diverticulum (omphalomenteric duct) – Remnant of proximal part of yolk stalk. – 40-50 cm proximal to ileocecal junction. Congenital Anomalies of the Midgut Nonrotation of midgut – Caudal limb of the midgut loop returns first after herniation. – Large intestine on left side & small intestine on right side.  Volvulus (twisting of the intestine) may occur. Congenital Anomalies of the Midgut Mixed rotation – Failure of completion of final 900 rotation. – Cecum is with mesentery & found over duodenum inferior to pylorus. – Volvulus may occurs. Congenital Anomalies of the Midgut Reversed rotation – Clockwise rotation of midgut & failure of fixation of the intestine. – Superior mesenteric artery compresses transverse colon. Congenital Anomalies of the Midgut Subhepatic cecum & appendix  Failure of cecum to descend into iliac fossa Congenital Anomalies of the Midgut Internal hernia  Herniation of small intestine into abnormal mesenteric sac during return from physiological herniation  Congenital Anomalies of the Midgut Midgut volvulus  Small intestine hangs by a narrow stalk causing midgut volvulus. Congenital Anomalies of the Midgut Duplication of the intestine – By defective recanalization – As cystic or tubular duplication Congenital Anomalies of the Midgut Mobile cecum – By incomplete fixation of ascending colon. – Volvulus of cecum may occur. Atresia & stenosis – By incomplete recanalization or defective blood supply.  Congenital Anomalies of the Hindgut Congenital Megacolon (Hirschsprung disease) – Dilatation of the colon just proximal to a region with no enteric ganglia. – Mostly in rectum & sigmoid colon.  Congenital Anomalies of the Hindgut Various types of: Anorectal agenesis & atresia – Because of incomplete split, incomplete recanalization or defective blood supply. – May be with fistula. Anal stenosis – Imperforate anus by failure of anal membrane to perforate Congenital Anomalies of the Hindgut Congenital Anomalies of the Hindgut  Congenital Anomalies of the Liver Extrahepatic bilary atresia – By failure of recanalization or infection. Double gallbladder – Pars cystica divides.  Congenital Anomalies of the Liver Absence of gallbladder – Failure of pars cystica to develop. Absence of cystic duct – Entire pars cystica develop into gallbladder. Abnormally long cystic duct – Cystic duct may open into bile duct near entrance into the duodenum. Accessory bile duct – A small bile duct may open directly from liver into gallbladder. Congenital Anomalies of the Pancreas Annular pancreas Because of bifid ventral pancreatic bud or fixation of ventral pancreatic bud. Congenital Anomalies of the Pancreas Separate ventral & dorsal pancreatic masses with separate ducts - By failure of anastomosis of ducts of the two pancreatic buds Ectopic pancreas - In the submucosa of stomach, duodenum, small intestine or Meckel’s diverticulum. Absence of ventral or dorsal pancreatic bud.