HSB Development of Digestive System PDF

MICROSCOPIC HSB LEARNING OBJECTIVES 1. Discuss development of the Digestive system 2. Enumerate derivatives of the primitive gut – foregut, midgut and hindgut 3. Discuss common congenital anomalies resulting from abnormal development of...

MICROSCOPIC HSB LEARNING OBJECTIVES 1. Discuss development of the Digestive system 2. Enumerate derivatives of the primitive gut – foregut, midgut and hindgut 3. Discuss common congenital anomalies resulting from abnormal development of the digestive system CASE 1: A 2 y/o boy is brought to the emergency room with fever, vomiting and abdominal pain. The mother told the attending physician that these symptoms began 12 hours ago and have progressively worsened. She also noticed that his stool and diaper were colored with bright red blood. Laboratory results showed that hematocrit and hemoglobin were on the low end of normal. Abdominal radiology showed a bowel obstruction that appears related to an abnormal intestinal outpocketing connected to the anterior abdominal wall. CASE 2: After his birth, a newborn was placed in the hospital’s nursery room. Within 24 hours, the newborn developed abdominal distention and his vomitus contained bile. It was also noted that he had failed to pass meconium during this time. Physical examination of the newborn at birth revealed normal findings. PRIMITIVE GUT PRIMITIVE GUT Formed from the incorporation of the dorsal part of the yolk sac into the embryo Craniocaudal and Lateral folding of the embryo 4th week Trans by: Alog, Benavidez, Costales, Dimasuhid, Flauta, Lasmarias, Masangkay | 1 Course | Date glands would come from the endoderm ESOPHAGUS The digestive tract is divided based on vascular supply into: ESOPHAGUS FOREGUT – Coeliac trunk a single tube, initially, that would be your tracheoesophageal MIDGUT – Superior Mesenteric artery region. Now that tube will be divided into 2 HINDGUT – Inferior Mesenteric artery parts by your tracheoesophageal septum, which will then be divided by 6th week. Once it divides in the 6th week, you will now FOREGUT DERIVATIVES have 2 separate tubes. Anteriorly that would be your Esophagus and Stomach laryngotracheal tube, posteriorly that would be the esophagus. Duodenum ( proximal to the opening of bile duct) Liver, Biliary apparatus ( hepatic ducts, Gallbladder and Bile ANOMALIES duct ) and Pancreas Supplied by Celiac artery ESOPHAGEAL ATRESIA MIDGUT DERIVATIVES If something would happen to the septum, it has not divided completely, you’re gonna have esophageal atresia Small intestine, including most of the duodenum There is failure of recanalization (8th week) likewise failure Cecum, Vermiform appendix, Ascending colon, and the of your tracheoesophageal septum to separate; associated right half to two thirds of the Transverse colon with TEF Supplied by Superior mesenteric artery All of the intestinal tubes, the majority of them, will become a solid structure initially. The digestive tract is a solid HINDGUT DERIVATIVES structure initially then it will recanalize afterwards. That solid Left one third to one half of the transverse colon structure is secondary to the proliferation of your epithelial Descending colon and Sigmoid colon lining, so it will recanalize to form a tubular structure Rectum and Superior part of the Anal canal afterwards so that food can pass through your intestinal Supplied by Inferior mesenteric artery tract Failure of recanalization that should be finished by 8th NOTES: week, you may have esophageal atresia and 85% of them The intestinal tract will be made up of 4 layers: Mucosa, also have TEF as a compensatory mechanism Submucosa, Musuclaris, and Adventitia Signs: The germ layer derivative of the epithelial lining and the ○ Polyhydramnios – accumulation of excessive amount of amniotic fluid Trans by: log, Benavidez, Costales, Dimasuhid, Flauta, Lasmarias, Masangkay | 2 Course | Date ○ Fetus unable to swallow amniotic fluid – cannot pass to the intestine for absorption and transfer through the placenta to the maternal blood for disposal Newborns with esophageal atresia usually appear healthy, and their first swallows are normal; but fluid returns through the nose and mouth and respiratory distress occurs ESOPHAGEAL ATRESIA ESOPHAGEAL STENOSIS lumen is narrowed (8th week); involves the midportion – maybe caused by hypertrophy of the submucosal/ muscularis externa or incomplete recanalization TRACHEOESOPHAGEAL FISTULA Abnormal communication between the trachea and esophagus Associated with Esophageal atresia Results from improper division of the foregut by the tracheoesophageal septum Clinical features of TEF: ○ Excessive accumulation of saliva or mucus in the nose and mouth ○ Episodes of gagging and cyanosis after swallowing milk Because the gastric contents now will go to the lungs ○ Abdominal distention after crying Gas from respiratory tract will accumulate in your intestinal tract ○ Reflux of gastric contents into the lungs, causing Pneumonitis TRACHEOESOPHAGEAL FISTULA A. Esophageal atresia with a TEF at distal end ( most common – 85 to 90 % of cases ) B. TEF only C. Esophageal atresia with a TEF at proximal end D. Esophageal atresia with a TEF at distal and proximal ends Trans by: log, Benavidez, Costales, Dimasuhid, Flauta, Lasmarias, Masangkay | 3 Course | Date STOMACH MESENTERY Week 4 – fusiform dilatation – primitive stomach Dorsal part grows faster than ventral part – resulting to greater and lesser curvatures Rotates 90 degrees clockwise HYPERTROPHIC PYLORIC STENOSIS muscularis externa in the pyloric region hypertrophies – narrow pyloric lumen that obstructs the passage of food Associated clinically with projectile vomiting after feeding and a small palpable mass at the right costal margin Trans by: log, Benavidez, Costales, Dimasuhid, Flauta, Lasmarias, Masangkay | 4 Course | Date Double bubble sign (White Arrow) – radiographic finding Hypertrophic Pyloric Stenosis found in Duodenal Atresia DUODENUM LIVER LIVER = part of the FOREGUT Hepatic Diverticulum Upper duodenum – caudal portion of the foregut ○ Endodermal lining of the Foregut forms an Lower duodenum – cranial most part of the midgut outgrowth ○ into the surrounding mesoderm of the Septum Transversum ⇒ appears in the middle 3rd week ○ Cranial part → Liver ○ Caudal part → Gall Bladder, Cystic duct ○ Can be seen on the Ventral Wall of the foregut. A. Duodenal stenosis – incomplete recanalization (5th– 6th weeks); involves 3rd and 4th portion B. Duodenal atresia – 2nd and 3rd portion; - “double bubble sign” 5th – 10th week = Rapidly growth Liver Stenosis = narrow lumen ○ Fetus accommodates/compensates with - For Atresia, no lumen. rapid growth of the liver. A case of abdominal obstruction in GIT = Request for 6th week = Occurs Physiologic Herniation abdominal x-ray. Herniation goes down to the Umbilical Cord (Yolk Sac) to intestinal tubes. as it goes down, it rotates to 90 degrees counterclockwise 11th Week = Return to Cavity, returns another 90 degree counterclockwise = Total 180 Degrees Trans by: log, Benavidez, Costales, Dimasuhid, Flauta, Lasmarias, Masangkay | 5 Course | Date Connection between the hepatic diverticulum and the 1:10,000 (85%) foregut narrows to form the Bile duct; an outgrowth of the failure of bile duct to canalize ( starts at 5th week ) bile duct gives rise to Gallbladder rudiment and Cystic results from liver infection during late fetal life duct jaundice occurs soon after birth Rx. by surgical correction PANCREAS Fig. 1: BILIARY SYSTEM = SYSTEM OF DUCTS 12th week = Formation of Bile Ducts Has Right and Left Hepatic Ducts = ○ Union of L&R ducts = Common Hepatic Duct From the Gallbladder, Cystic duct is branched to Common Hepatic Duct Cystic and Common hepatic ducts unite = ○ Forms the Common Bile Duct. PANCREAS Main Pancreatic Duct and Common Bile Duct unite = Develops from the dorsal and ventral pancreatic buds ○ Open to the 2nd part of duodenum. that originate from the endodermal lining of the foregut. Hematopoietic cells, Kupffer cells, and connective tissue you have 2 the ventral and dorsal pancreatic bud. cells - derived from mesoderm of the Septum Dorsal pancreatic bud appears first transversum. 5th – 8th weeks BILIARY ATRESIA As the duodenum rotates to the right and becomes C-shaped, the ventral pancreatic bud is carried dorsally with the bile duct – soon lies posterior to the dorsal pancreatic bud and later fuses with it Main pancreatic duct is formed by the union of the distal part of the dorsal pancreatic duct and the entire ventral pancreatic duct Proximal part of the dorsal pancreatic duct usually obliterates, but it may persist as an accessory pancreatic Fig. 1: Biliary Atresia of 4 types duct Type I: atresia of the common bile duct Type IIa: common hepatic duct Type IIb: common bile, common hepatic, and cystic duct Type III: common bile, cystic, and hepatic ducts up to the porta hepatis. (Majority of Cases) ○ A subtype present in over 90% of patients with biliary atresia ○ Causes Jaundice in babies Extrahepatic biliary atresia obstruction of the ducts at or superior to the porta hepatis Trans by: log, Benavidez, Costales, Dimasuhid, Flauta, Lasmarias, Masangkay | 6 Course | Date INTESTINAL LOOP Main duct of Wirsung – ventral and dorsal bud Accessory duct (Santorini) – dorsal bud Ventral pancreatic bud forms most of the head of the pancreas, including the uncinate process Dorsal pancreatic bud forms the remainder of the pancreas - head, body and tail. If I ask you, anlage of the body and tail of the pancreas? Dorsal Pancreatic Bud. supplied by what artery? Celiac Artery ANNULAR PANCREAS Probably results from the growth of a bifid ventral pancreatic bud around the duodenum, parts then fuse with the dorsal bud forming a pancreatic ring Anomaly produces complete obstruction / atresia or partial obstruction / stenosis of the duodenum MIDGUT Superior mesenteric artery Primary intestinal cranial distal duodenum loops jejunum upper ileum caudal lower ileum cecum, appendix asc. colon, 2/3 transverse 6th week – physiologic herniation (secondary to your Liver) 90o counterclockwise rotation 10th – 12th week re-enters abdomen 180o rotation during reduction So it will rotate, once it rotate fully, the appendix is gonna be on the right. Trans by: log, Benavidez, Costales, Dimasuhid, Flauta, Lasmarias, Masangkay | 7 Course | Date JEJUNUM & ILEUM UMBILICAL HERNIA So it should enter the abdomen fully. The umbilical area will close at 26th week and after birth 5-15 weeks after the umbilical cord has been cut. But if there are intestinal contents you may have persistence Umbilical Hernia. JEJUNUM & ILEUM Jejunum (proximal 2/5 ), begins at the duodenojejunal flexure and the ileum (distal 3/5) ,ends at the ileocecal junction 6 to 7 meters long Jejunum lies in the LUQ; ileum lies in the RLQ OMPHALOCELE Intestinal loop outside the body covered WITH protective sac. GASTROSCHISIS occurs when there is a defect in the ventral abdominal wall – there is massive evisceration of the intestines; incomplete closure of the lateral folds; NO protective sac; common in males DIVISIONS The worst will be called Gastroschisis, Intestinal loop Cecum outside, and DO NOT HAVE a protective sac. This is an Appendix emergent condition. Colon ○ ascending ○ transverse ○ descending ○ sigmoid Rectum Anal canal Trans by: log, Benavidez, Costales, Dimasuhid, Flauta, Lasmarias, Masangkay | 8 Course | Date True diverticulum that is located approximately 2 ft from the ileocecal junction, occurs in about 2% of the population, about 2 inches long and may contain ectopic gastric or pancreatic cells Bleeding associated with ulceration of the ectopic cells, obstruction and pain that is referred over the area of umbilicus or may mimic referred pain of inflamed appendix HINDGUT Inferior mesenteric artery ⅓ transverse colon, desc. colon, sigmoid colon, rectum, and superior part of anal canal Epithelium of urinary bladder and most of urethra Cloaca VOLVULUS Volvulus is the twisting of the intestine. This may cause obstruction CASE 1 A 2 y/o boy is brought to the emergency room with fever, vomiting and abdominal pain. The mother told the attending physician that At the terminal end of the hindgut is the blind pouch called these symptoms began 12 hours ago and have progressively Cloaca. worsened. She also noticed that his stool and diaper were colored The Cloaca will divide into 2 (by the urorectal septum). with bright red blood. Laboratory results showed that hematocrit ○ The ventral part of the cloaca will become the and hemoglobin were on the low end of normal. Abdominal urogenital sinus. radiology showed a bowel obstruction that appears related to an ○ The dorsal part will become the anorectal canal. abnormal intestinal outpocketing connected to the anterior The lower canal comes from another source which is the abdominal wall. proctodeum. a case of meckel’s diverticulum ○ Vascular supply: inferior rectal artery from internal pudendal artery Cloacal Sphincter MECKEL’S DIVERTICULUM ○ Anterior part (sup. transverse perineal it is also located in the right lower quadrant (RLQ) bulbospongiosus, ischiocavernous) it may mimic appendicitis ○ Posterior part (ext. anal sphincter) In cases of newborn (or even adult), if they have RLQ pain, you have to think first of the appendix. Next, rule out meckel’s diverticulum. Next, rule out urinary tract infection. ANAL CANAL Next, if it’s a female, rule out any ovarian conditions Upper – from Hindgut; endoderm ○ simple columnar epithelium Lower – from Proctodeum; ectoderm ○ stratified squamous nonkeratinized epithelium Junction – Pectinate line ○ divide the anal canal into superior (hindgut derivative) Trans by: log, Benavidez, Costales, Dimasuhid, Flauta, Lasmarias, Masangkay | 9 Course | Date Cloaca – terminal end of the hindgut which is partitioned by the urorectal septum into rectum and upper anal canal ○ urorectal septum separate cloaca into urogenital sinus and upper anal membrane Cloacal membrane is partitioned by the urorectal septum into the anal membrane and urogenital membrane IMPERFORATE ANUS 8th week – anal membrane ruptures ○ No anal opening 1/5000 more common in males secondary to abnormal development of the urorectal septum ○ The anorectal canal forms normally, but the anal membrane separating the ectodermal and endodermal portions of the anus is abnormally thick. This thickened anal membrane may fail to rupture or may rupture incompletely, resulting in imperforate anus or anal stenosis. HIRSCHSPRUNG’S DISEASE CASE 2: After his birth, a newborn was placed in the hospital’s nursery room. Within 24 hours, the newborn developed abdominal distention and his vomitus contained bile. It was also noted that he had failed to pass meconium during this time. Physical examination of the newborn at birth revealed normal findings RECTAL FISTULA Failure of migration of neural crest cells (Myenteric / Improper development of urorectal septum auerbach’s and Meissner’s plexus) leading to abnormal ○ Usually there is also no anal opening innervations of the bowel ○ There is a meconium passage. (Vagina in female, Most common cause of lower intestinal obstruction in Urethra in male) neonates Congenital Megacolon ○ absence of autonomic ganglion cells in Myenteric and Meissner’s plexus ○ 5th – 7th week Trans by: log, Benavidez, Costales, Dimasuhid, Flauta, Lasmarias, Masangkay | 10 Course | Date ○ Rectum and sigmoid colon ○ 33% of neonatal obstructions ○ 4 males:1 female ANAL OPENING MECONIUM PASSAGE IMPERFORATE None None ANUS RECTAL FISTULA None Yes CONGENITAL Yes None MEGACOLON Trans by: log, Benavidez, Costales, Dimasuhid, Flauta, Lasmarias, Masangkay | 11