Digestive System

I. PRIMITIVE GUT TUBE. The primitive gut tube is divided into the foregut, midgut, and hindgut (Figure 7-1).

A. Formation. The primitive gut tube is formed by the incorporation of a portion of the yolk sac into the embryo during craniocaudal and lateral folding.

B. Histology. The epithelial lining and glands of the mucosa are derived from endoderm, whereas the lamina propria, muscularis mucosae, submucosa, muscularis externa, and adventitia/serosa are derived from mesoderm. The epithelial lining of the gut tube proliferates rapidly and obliterates the lumen. Later, recanalization occurs.

II. FOREGUT DERIVATIVES are supplied by the celiac artery.

A. Esophagus

1. Formation. The tracheoesophageal septum divides the foregut into the esophagus and trachea.

2. Clinical correlation: Esophageal atresia occurs when the esophagus ends as a blind tube owing to a malformation of the tracheoesophageal septum. It is associated with polyhydramnios and a tracheoesophageal fistula (see Chapter 10).

B. Stomach

1. Formation. The primitive stomach develops from a fusiform dilatation that forms in the foregut during week 4- The stomach rotates 90 degrees clockwise during its formation, causing the formation of the lesser peritoneal sac.

2. Clinical correlation. Hypertrophic pyloric stenosis occurs when the muscularis externa hypertrophies, narrowing the pyloric lumen. This condition is associated with projectile nonbilious vomiting and a small, palpable mass at the right costal margin.

C. Liver

1. Formation. The hepatic diverticulum sends hepatic cell cords into the surrounding mesoderm called the septum transversum. As the liver bulges into the abdominal cavity, the septum transversum is stretched to form the ventral mesentery. The septum transversum also plays a role in the formation of the diaphragm, which explains the close adult anatomic relationship of the liver and diaphragm.

2. Clinical correlation. Congenital malformations of the liver are rare.

D. Gallbladder and bile ducts

1. Formation. The connection between the hepatic diverticulum and foregut nar-

Foregut Hindgut Midgut Duodenum

Foregut

Esophagus, stomach, liver, gallbladder, pancreas, upper duodenum

Figure 7-1. Development of gastrointestinal tract showing the foregut, midgut, and hindgut along with the adult derivatives. The entire length of the endodermal gut tube is shown from the mouth to the anus. The fate of the lung bud (LB) is covered in Chapter 10. The fate of the pharyngeal pouches (1, 2, 3, 4) and the thyroid diverticulum (TD) are covered in Chapter 11. E = esophagus; ST = stomach; HD = hepatic diverticulum; GB = gallbladder; VP = ventral pancreatic bud; DP = dorsal pancreatic bud; CA = celiac artery; YS = yolk sac; VD = vitelline duct; AL = allantois; SMA = superior mesenteric artery; CL = cloaca; /MA = inferior mesenteric artery.

Hindgut

Distal third of the transverse colon, descending colon, sigmoid colon, rectum, and upper anal canal

Foregut

Esophagus, stomach, liver, gallbladder, pancreas, upper duodenum

Midgut

Lower duodenum, jejunum, ileum, cecum, appendix, ascending colon, proximal two thirds of the transverse colon

Figure 7-1. Development of gastrointestinal tract showing the foregut, midgut, and hindgut along with the adult derivatives. The entire length of the endodermal gut tube is shown from the mouth to the anus. The fate of the lung bud (LB) is covered in Chapter 10. The fate of the pharyngeal pouches (1, 2, 3, 4) and the thyroid diverticulum (TD) are covered in Chapter 11. E = esophagus; ST = stomach; HD = hepatic diverticulum; GB = gallbladder; VP = ventral pancreatic bud; DP = dorsal pancreatic bud; CA = celiac artery; YS = yolk sac; VD = vitelline duct; AL = allantois; SMA = superior mesenteric artery; CL = cloaca; /MA = inferior mesenteric artery.

rows to form the bile duct. Later, an outgrowth from the bile duct gives rise to the gallbladder and cystic duct.

2. Clinical correlation. Extrahepatic biliary atresia occurs when incomplete re-canalization leads to occlusion of the biliary ducts. This condition is associated with jaundice soon after birth, pale stool, and dark urine.

E. Pancreas

1. Formation. The ventral pancreatic bud forms the uncinate process and part of the head of the pancreas. The dorsal pancreatic bud forms the remaining part of the head, body, and tail of the pancreas. Acinar cells, duct epithelium, and islet cells are derived from endoderm.

2. Clinical correlations a. Annular pancreas occurs when the ventral and dorsal pancreatic buds form a ring around the duodenum, thus causing an obstruction of the duodenum.

b. Macrosomia (increased birthweight) occurs when fetal islets are exposed to high glucose levels such as those present in a pregnancy involving an uncontrolled diabetic woman. Glucose freely crosses the placenta and stimulates fetal insulin secretion, which causes increased fat and glycogen deposition in fetal tissues.

F. Upper duodenum. The upper duodenum develops from the caudal portion of the foregut. The junction of the forcgut and midgut is just distal to the opening of the common bile duct.

III. MIDGUT DERIVATIVES are supplied by the superior mesenteric artery.

A. Lower duodenum

1. Formation. The lower duodenum develops from the cranial portion of the midgut.

2. Clinical correlation. Duodenal atresia occurs when the lumen of the duodenum is occluded owing to failed recanalization. This condition is associated with polyhydramnios, bile-containing vomitus, and distended stomach.

B. Jejunum, ileum, cecum, appendix, ascending colon, and proximal two thirds of the transverse colon

1. Formation. At week 6, the midgut loop herniates through the primitive umbilical ring and causes a physiologic umbilical herniation. At week 11, :he midgut loop rotates 270 degrees counterclockwise around the superior mesenteric artery as it returns to the abdominal cavity, thus reducing the physiologic umbilical herniation.

2. Clinical correlations a. Omphalocele occurs when the midgut loop fails to return to the abdominal cavity. In the newborn, a light gray shiny sac protruding frorr. the base of the umbilical cord is apparent (Figure 7-2A).

b. Ileal (Meckel's) diverticulum occurs when a remnant of the vitelline duct persists, thus forming a blind pouch on the antimesenteric border of the ileum. This condition is often asymptomatic but occasionally becomes inflamed or contains ectopic gastric, pancreatic, or endometrial tissue, which may produce ulceration.

C. Vitelline fistula occurs when the vitelline duct persists, thus forming a direct connection between the intestinal lumen and the outside of the body at the umbilicus. This condition is associated with fecal (meconium) discharge from the umbilicus.

d. Malrotation of the midgut occurs when the midgut undergoes only partial rotation and results in the abnormal position of abdominal viscera. This condition may be associated with volvulus (twisting of intestines), which can compromise blood flow and result in gangrene.

e. Intestinal atresia or stenosis occurs as a result of failed recanalization.

Aganglionic Megacolon

Figure 7-2. (A) Photograph of a newborn infant with an omphalocele that is covered by amnion and contains loops of intestine. (B) A lateral view radiograph of the colon after a barium enema in a 3-year old girl with aganglionic megacolon (Hirschsprung's disease). The upper segment of normal colon (*) is distended with fecal material. The distal segment of the colon (**) is narrow and is the portion of colon where the myenteric plexus of ganglion cells is absent. (A, Courtesy of Dr. S. Shaw, Department of Surgery, University of Virginia. From Sadler TW: Langmans Medical Embryofogy, 7th ed. Baltimore, Williams & Wilkins, 1995, p 264; B, From Wyl-lie R: Congenital aganglionic megacolon [Hirschsprung's diseasej. In Behrman RE, Kliegman RM, Jenson HB [eels]: Nelson Textbook of Pediatrics, 16th ed. Philadelphia, WB Saunders, 1999.)

Figure 7-2. (A) Photograph of a newborn infant with an omphalocele that is covered by amnion and contains loops of intestine. (B) A lateral view radiograph of the colon after a barium enema in a 3-year old girl with aganglionic megacolon (Hirschsprung's disease). The upper segment of normal colon (*) is distended with fecal material. The distal segment of the colon (**) is narrow and is the portion of colon where the myenteric plexus of ganglion cells is absent. (A, Courtesy of Dr. S. Shaw, Department of Surgery, University of Virginia. From Sadler TW: Langmans Medical Embryofogy, 7th ed. Baltimore, Williams & Wilkins, 1995, p 264; B, From Wyl-lie R: Congenital aganglionic megacolon [Hirschsprung's diseasej. In Behrman RE, Kliegman RM, Jenson HB [eels]: Nelson Textbook of Pediatrics, 16th ed. Philadelphia, WB Saunders, 1999.)

IV. HINDGUT DERIVATIVES are supplied by the inferior mesenteric artery.

A. Distal third of the transverse colon, descending colon, and sigmoid colon

1. Formation. The cranial end of the hindgut forms the distal third of the transverse colon, descending colon, and sigmoid colon.

2. Clinical correlations. Aganglionic megacolon (Hirschsprung's disease) results from the failure of neural crest cells to form the myenteric plexus in the sigmoid colon and rectum. (See Figure 7-2B.) This condition is associated with the loss of peristalsis, fecal retention, and abdominal distention.

B. Rectum and upper anal canal. The terminal end of the hindgut is a pouch called the cloaca. The cloaca is partitioned by the urorectal septum into the rectum, upper anal canal, and urogenital sinus (Figure 7-3A, B).

V. ANAL CANAL

A. Formation. The upper anal canal is a hindgut derivative, whereas the lower anal canal

Rectovesical Fistula

Rectovesical fistula

Rectovesical Fistula

Cloacal

Rectovaginal

Rectovaginal fistula

Cloacal

Rectovesical fistula

Rectourethral D fistula

Rectovaginal fistula

Figure 7-3. (A, B) Partitioning of the cloaca. The cloaca (CL) is partitioned into the rectum and upper anal canal and urogenital sinus (UG) by the urorectal septum (UR). The arrow indicates the direction of growth of the UR toward the body surface where it fuses at the perineal body. The surface ectoderm invaginates to form the proctodeum, which eventually forms the lower anal canal. The upper and lower anal canal meet at the anal membrane. AL = allantois. (C, D, E) Defects associated with abnormal UR septum formation. (C) Rectovesical fistula. (D) A rectourethral fistula, which generally occurs in males, is associated with the prostatic urethra and is sometimes called a rectoprostatic fistula. (E) Rectovaginal fistula. (C-E redrawn from Larsen WJ: Human Embryology, 2nd ed. New York, Churchill Livingstone, 1997, p 268.)

develops from an envagination of surface ectoderm called the proctodeum. The junction between the upper and lower anal canal forms the anal membrane and is marked in the adult by the pectinate line.

B. Clinical correlations (see Figure 7-3 C, D, E)

1. Anorectal agenesis occurs when the rectum ends as a blind sac above the pub-orectalis muscle owing to abnormal formation of the urorectal septum. This condition may be accompanied by a rectovesical fistula, rectourethral fistula, or rectovaginal fistula.

2. Anal agenesis occurs when the anal canal ends as a blind sac below the puborec-

Perineal Membrane
membrane

Perineal body anal

B canal and upper part of the anal canal membrane membrane

Perineal body anal

B canal

Table 7-1

Deiivationof Adult Mesenteries

Embryonic Mesentery

Adult Mesentery

Ventral mesentery

Lesser omentum (hepatoduodenal and hepatogastric ligaments),

falciform ligament, coronary ligament, and triangular ligament

Dorsal mesentery

Greater omentum (gastrorenal, gastrosplenic, gastrocolic, and

splenorenal ligaments), mesentery of the small intestine,

mesoappendix, transverse mesocolon, sigmoid mesocolon

talis muscle owing to abnormal formation of the urorectal septum. This condition may also be accompanied by a rectovesical fistula, rectourethral fistula, or rectovaginal fistula.

VI. MESENTERIES. The primitive gut tube is suspended within the peritoneal cavity of the embryo by a ventral and dorsal mesentery from which all adult mesenteries are derived (Table 7-1).

Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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Responses

  • tony
    What is clinical conrelate of digestive system?
    1 year ago
  • tolman
    What is clinical correlation of the digestive system?
    1 year ago

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