Development of the GI Tract Flashcards
Yolk Sac Endoderm
Gives rise to gut epithelium and glands
Stomodeum and Proctodeum
Primitive mouth and anal pit. The ectoderm of these develops into the epithelium at the cranial and caudal ends of the gut tube.
Artery of the foregut
Celiac Artery (minus pharynx, resp. tract, intrathoracic esophagus)
Artery of the Midgut
Superior Mesenteric Artery
Artery of the Hindgut
Inferior Mesenteric Artery
Adult derivatives of the foregut
Pharynx, lower respiratory system, esophagus and stomach, superior duodenum, liver, biliary system, pancreas
Esophageal atresia
tracheo-esophageal septum deviates posteriorly, causing the esophagus to end as a closed tube. One third of patients also have other congenital defects (VACTERL)
Esophageal stenosis
Resultant from failure of the esophageal septum to recanalize
Associated with Polyhdramnios
Development of curvatures of the stomach
- Dorsal stomach wall grows faster than ventral wall, resulting in greater and lesser curvatures
Rotation of Stomach
- Stomach rotates 90 degrees clockwise
- left side becomes ventral surface, right side becomes dorsal
- left vagus supplies ventral wall, right vagus supplies dorsal wall
Mesogastrium
- Suspends stomach from dorsal and ventral abdominal walls
- Has dorsal and ventral portions
Dorsal Mesogastrium
- Becomes Greater omentum, gastrosplenic and splenorenal ligaments in adults
- Spleen is derived from mesenchymal cells between layers
Omental bursa
- “lesser sac” formed posteriorly to stomach by rotation of the dorsal mesogastrium
- Accessible to rest of peritoneal cavity through epiploic foramen
Ventral Mesogastrium
- becomes the lesser omentum
- connects lesser curvature of the stomach to liver and duodenum
- Liver develops within and is encased by it
- bc of this, forms falciform ligament and livers visceral peritoneum
Hypertrophic pyloric stenosis
- marked hypotrophy and hyperplasia of the 2 muscular layers of the pylorus, channel is lengethened and thickened.
- diluted stomach
- presents with projectile vomiting with feeding and palpation of small knot @ right costal margin “the olive”, NO bile in vomit.
- increased incidence in infants with erythromycin
- Treatment– hypokalemic, hypocholoremic metabolic alkalosis treated first; then pyloromytomy
Development of the Duodenum
- forms from caudal foregut and cranial midgut
- attachment of bile duct forms just proximal to this junction
- the two segments grow and form c shaped loop projecting ventrally toward the umbilical cord
Effect of stomach rotation on duodenal loop
- rotation turns ventrally projected duodenal loop to the right
- both pancreas and duodenum are pushed into secondarily retroperitoneal position
Recanalization of the duodenum
- Epithelium proliferates and occludes lumen
- recanalization occurs by 8-9 weeks
Duodenal Stenosis
- Lumen is narrowed as a result of failed recanalization
Duodenal atresia
- lumen is occluded as a result of failed recanalization,
- strong association with Trisomy 21
- bilious vomiting (most obstructions are distal to ampulla of vater)
- no abdominal dissension
- often associated with polyhydramnios due to low intestinal reabsorption of amniotic fluid
Double bubble sign
- characteristic of duodenal occlusion in prenatal ultrasonography
- first bubble is stomach
- second stomach is post pyloric and PRE-STENOTIC dilated duodenal loop
Pancreas germ layer origin
- endoderm of the foregut
- dorsal and ventral pancreatic buds form as two outgrowths into dorsal and ventral mesentery
Effects of rotation on forming pancreas
- Duodenal rotation carries ventral pancreatic bud posterior to dorsal bud and they fuse
- Duodenal and gastric rotation cause pancreas to become secondarily retroperitoneal
Derivatives of each pancreatic bud
- Ventral bud - Head, uncinate process, most of main pancreatic duct
- Dorsal bud - rest of pancreas (neck, body, tail, distal duct)
Formation of main pancreatic duct
- forms from ventral bud duct and distal dorsal bud duct
- proximal dorsal bud duct usually degenerates, but can remain patent as accessory pancreatic duct
Annular Pancreas
- ventral pancreatic bud splits to fuse both dorsally and ventrally, forming ring of pancreatic tissue around duodenum
- presents as duodenal obstruction shortly after birth
Hepatic Diverticulum germ layer
- Ventral outgrowth of caudal foregut endoderm into surrounding mesoderm of the septum transversum
Formation of the Liver
- Cranial portion of the hepatic diverticulum
- Hepatic cords from endoderm, fibrous Kupffer cells and hematopoietic cells from mesoderm of septum transversum
- Hematopoiesis begins week 6, bile production in week 12
Caudal portion of hepatic diverticulum
- forms gallbladder and cystic duct
- endoderm of gallbladder proliferates and occludes cystic duct, followed by recanalization
- Common stalk connecting haptic and cystic ducts to the duodenum becomes the bile duct
Extrahepatic biliary atresia
- Presents with obliteration of the biliary ducts and jaundice soon after birth
-Failure of the biliary tree to reanalyze
Persistant jaundice (despite therapy), acholic stools, dark urine, enlarged firm liver, normal growth during first few weeks, develop failure signs to survive.
**Shrunken or absent gallbladder, HIDA scan
Structures of the Midgut
- Small intestine (minus proximal duodenum)
- Cecum and Vermiform appendix
- Ascending Colon
- Right half - 2/3 of transverse colon
Midgut Loop
- U shaped ventrally projecting structure that forms from the elongation of the midgut around the central axis of the superior mesenteric artery
- Dorsal mesentery lengthens as midgut elongates
Physiological Midgut Herniation
- The embryonic peritoneal cavity is not large enough (due to the large size of the liver and kidneys) for the midgut to fully differentiate within it. - Because the intraembryonic coelom is still in communication with the extraembryonic coelom at the level of the umbilical cord, the growing midgut loop moves into the extraembryonic space bw weeks 6 and 10
Cranial Limb of the Midgut Loop
- grows rapidly with many intestinal loops that develop into jejunum and upper ileum
Caudal Limb of the Midgut
- grows very little and does not coil
- Develops into lower ileum, ascending colon, proximal half - 2/3 of transverse colon
Cecal Diverticulum
- Appears on the caudal limb in the 6th week
- Develops into Cecum and Vermiform Appendix
First rotation of midgut loop
- While in the umbilical cord, midgut loop rotates counterclockwise 90 degrees so cranial is on the right and caudal is on the left
Reduction of the midgut hernia
- occurs as liver and kidneys decrease in size relative to abdomen
- Cranial limb returns first
- As Caudal limb returns, it rotates an additional 180 degrees to frame the small intestine
- Cecum returns last
Return of Colon to the abdomen
- Presses duodenum and pancreas against posterior wall, making them secondarily retroperitoneal
- Dorsal mesentery of ascending and descending colon fuses with peritoneum of posterior abdominal wall, making them secondarily retroperitoneal as well
- Caudal greater omentum fuses with itself and with the mesentary of the transverse colon
Malrotations of the Midgut
- Present with intestinal obstruction shortly after birth
- Predispose infant to volvulus
Volvulus
-Twisting of intestines around a short mesentery, often interfering with intestinal blood supply.
produces obstruction and ischemia
Symptoms–vomiting, abdominal distension, and bilious vomiting
Acute onset bilious vomiting AND abdominal distention
Ladd’s procedure
Congenital omphalocele
- Persistence of midgut herniation in the umbilical cord (failure of reduction to occur)
- Herniated intestine fails to return to the abdominal cavity (bowel and liver), midline
- Herniated gut is enclosed in the epithelium of the umbilical cord (amnion)
associated abnormalities (more to omphalocele than gastroschisis)–pentology cantrell, CHD, chromosomal abnormalities.
Umbilical Hernias
- Midgut hernia reduces normally, but herniates again through imperfectly closed umbilicus either pre or postnatally
- Herniated bowel is enclosed by subcutaneous tissue and skin
premature ingants, infants of african descent,
most resolve spontaneuously
Gastroschisis
- results from defect in the anterior abdominal wall. involution of right umbilical vein. (usually on right side)
- Abdominal viscera extrude through the abdominal wall without umbilical cord involvement (right side)
- abdominal contents (small bowel, NOT liver)
- no sac/covering
- incomplete embryonic folding
- prematurity, younger maternal age, vasoconstrictive agents (cocaine)
- nonrotation of the midgut without volvulus
Ileal (Meckel’s) Diverticulum
- persistence of the proximal yolk stalk (omphalomesenteric duct, vitalline duct)
- one of the most common anomalies of the GI tract
-Rule of 2’s– 2 feet proximal to ileocecal valve, 2 types of ectopic tissue (gastric and pancreatic)
2 inches long - May become inflamed and present like appendicitis
- Sometimes contain portions of gastric mucosa, producing ulceration and bleeding
Clinical Diagnosis–
painless rectal bleeding or melena
Most asymptomatic
Meckel scan.
Cranial Hindgut
- Develops into distal 1/2-1/3 of transverse colon, descending and sigmoid colon
Terminal hindgut
- Endoderm lined pouch called the Cloaca, which develops into the rectum and superior anal canal
Cloacal membrane
- Point where Cloaca contacts surface ectoderm
- LLies at the base of the depression called the proctodeum (anal pit)
Urorectal Septum
- Divides cloaca into dorsal and ventral regions
- Develops in angle between allantois and the hindgut
- Forms Urogenital Sinus and Anorectal Canal along with urogenital membrane and anal membrane
Perineal Body
- Site where urogenital septum fuses with cloacal membrane
- The Taint
Epithelium of superior anal canal
- Derived from hindgut endoderm
Lower Anal Canal
- Develops from proctodeum’s ectoderm
Pectinate line
- Junction of upper and lower anal canal
- Important landmark when considering the characteristics and metastasis of anorectal tumors
Congenital megacolon/ Hirschsprung’s disease
- neurological dysfunction affecting the colon; absence of ganglion cells in the distal bowel beginning at anus and extending proximally
-failure of migration, differentiation, or survival of neural crest cells. - Abnormality of autonomic ganglia causes failure of peristalsis in aganglionic segment
- Intestinal contents accumulate proximal to this point, enlarging the colon
Clinical– absence of myenteric and submucosal nerve plexus… gut is unable to relax.
functional bowel obstruction, dilation of proximal bowel
failure to pass meconium. constipation. abdominal distention
rectal biopsy
Anorectal Agenesis
- Condition in which the rectum ends too far superior, either blindly or with fistula to bladder (rectovesical fistula), urethra (rectourethral), vagina (rectovaginal), or vestibule (rectovestibular)
Splanchnic Mesoderm
Develops connective tissue and muscle of the gut
Ladd bands
duodenal obstruction is determined by Ladd bands which attach cecum to abdominal wall. an abnormal insertion into the mesentary.
Ladd’s procedure
conterclockwise de-torsion of gut.
Liver Biopsy
most reliable study for diagnosis of biliary atresia
Intestinal Atresia
later intrauterine mesenteric vacsular accident: complication of volvulus, intusseception, internal hernia, or strangulation from a tight omphalocele/gastroschises defect
abdominal distension
Lower GI with water soluble contrast, rule out other causes of obstruction
Imperforate anus
urorectal septum fails to completely separate allantois and handgun embyrologic cloaca in females only. low type-- rectum below elevator muscle high type-rectum able elevator muscle VACTREL low type--dialation high type--colostomy
