24. Development of GI Function in Early Life Flashcards

1
Q

Breifly describe organogenesis of the GI tract.

What is the arterial supply of the foregut, midgut and hindgut?

What organs do the three regions of primitive gut tube give rise to?

A

Occurs 4-12w. Gut forms tube, ventral and dorsal pancreatic bud fuse. Primary interstinal loop herniates into umbilicus and rotates. Midgut rotates and retracts into abdomen. Ascending and descending colon attach to body wall. Liver also complete by 12w.

Foregut: celiac artery, Midgut: superior mesenteric artery, Hindgut: inferior mesenteric artery.

Foregut: pharynx to first 1/2 of duodenum, inc. liver parenchyma and hepatic duct epithelium, gallbladder, cycstic duct and common bile duct, dorsal and ventral pancreatic buds. Midgut: Second 1/2 of duodenum to first 2/3 of transverse colon, inc. appendix. Hindgut: distal 1/3 of transverse colon to rectum, inc. urogenital sinus.

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2
Q

What are some foregut developmental abnormalities?

What would happen if the oesophagus and respiratory tracy failed to seperate via a septum?

How would you detect this?

A

Oesophageal atresia/stenosis, tracheo-oesophageal fistulae, congenital hiatus hernia, pyloric stenosis, duodenal atresia.

Feed baby -> cough + splutter, may go blue. May have oesophageal atresia +/- tracheo-oesophageal fistulae (leads from oesophagus into trachea so cough/vomit).

X-ray, if atresia woud see no gas in stomach after birth but if atresia + fistula then would see air in stomach.

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3
Q

What causes GORD in neonates?

When does the midgut grow rapidly and leave the abdominal cavity, and when does it re-enter?

A

LOS sphincter pressure reduced when v young, gastric emptying delayed, slow mouth -> anus transit time. Premature babies = no suck reflex until 32w. GORD v common 1-3m, 5% at 12m and v few after 24m. More severe = GOR disease.

5-7w leaves, rotates and returns to abdo cavity at 10-11w. Rotates so caecum and appendix near top and need to move down to R iliac fossa.

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4
Q

What does this x-ray of a newborn show?

A

Duodenal atresia: see double bubbles: gastric bubble (black arrow) and big swollen duodenum with bubble (white arrow). If blockage in duodenum, presents with vomiting but takes longer than if oesophageal atresia.

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5
Q

What does this x-ray of a newborn show?

A

Diaphragmatic hernia. Baby has bowel in chest. As it developed, diaphragm had hole in it and bowel slipped up into pleural cavity so lung on R not developed. Baby: blue, tachycardia.

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6
Q

List some midgut developmental abnormalities.

How can a midgut abnormality cause gangrenous bowel?

Compare the position of the duodenum after normal development compared to after intestinal malrotation.

A

Jejunal atresia (takes longer to vomit + bile), malrotation (bowel rotates outside then reenters but doesn’t rotate properly), Meckel’s diverticulum, omphalocoele, gastrochisis. Different types of jejunal atresia and malrotation.

Malrotation - twists around the mesenteric artery and cuts of blood supply.

Normally duodenum lies across midline from R to L. If malrotation: failure of normal rotation and fixation - duodeum to R of spine and absent ligament of Treitz. Abnormal placement of mesenteric ligaments may obstruct 2nd portion of the duodenum (Ladd’s bands). [pic]

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7
Q

Differentiate between gastroschisis and omphalocele. (Congenital conditions)

A

Gastroschisis: defect in the anterior abdominal wall through which the abdominal contents freely protrude. No overlying sac/peritoneum. Almost always to R of umbilicus. Defect most likely due to a disruption of the blood supply to the developing abdominal wall.

Omphalocele: rare abdominal wall defect in which the intestines, liver, and occasionally other organs remain outside of the abdomen in a sac due to failure of normal return to abdominal cavity during 9th week of dev. Caused by malrotation of the bowels while returning to the abdomen. Some cases poss due to an underlying genetic disorder.

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8
Q

What is this condition?

A

Gastroschisis. Don’t want to put in back in right away or else baby can’t breathe b/c lungs and diaphragm splinted by pressure from reintroduced bowel, so have to do it slowly day by day.

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9
Q

What is this condition?

A

Omphalocele

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10
Q

What is Meckel’s Diverticulum?

What problem can it cause?

A

Vitelline duct normally obliterated and loses its connection to the midgut loop before the loop returns to the abdo cavity. If it persists = Merkel’s diverticulum, attached to terminal ileum near ileo-caecal junction, represents apex of midgut loop. Ectopic gastric mucosa or pancreatic tissue may be present in diverticulum.

Most people = no problems. Sometimes can get ulcers and bleeding, acute appendicitis, or intussusception = part of the intestine folds into the section next to it -> obstruction -> ischemia and gangrene.

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11
Q

Give an example of a hindgut abnormality.

What forms the enteric ganglia?

Describe Hirschprung’s disease.

A

Anorectal abnormalities - mouth and anus closed at first, problem if anus membrane does not open later. Also development of urogenital sinus (urethra and vagina both open into common channel). Imperforate anus - cloaca not opened.

Neural crest cell subpopulation migrate through embryo from lateral edges of neural plate and give rise to enteric ganglia. NC cells from occipitocervical region populate whole gut. NC cells from sacral region populate distal gut.

Failure of NC cells to migrate to the correct location leads to absence of ganglion cells. Absence of inhibitory innervation = tonic contraction and colonic obstruction. Presents after day or 2, distended abdo, constipation, delayed meconium. B/c ganglionic cells provide relaxation stimulation.

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12
Q

What produces the cells of the small intestinal epithelium?

How are small intestinal villi and crypts formed? How is SA increased?

When do most small instestine microvillus enzymes start to appear? How does lactase activity look throughout gestation?

A

Continuously produced from stem cells.

Via epithelial and mesenchymal reorganisation. Morphogenesis occurs from weeks 9-20. SA is increased by mucosa folding, villi formation and microvilli development.

8 weeks, increases up to birth e.g. sucrase, aminopeptidase. Lactase activity reaches max levels at end of gestation but lost lots by adulthood.

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13
Q

Label the following cell types in the small intestine.

A

A) Goblet cell

B) Absorptive cell

C) Crypt cell

D) Paneth cell

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14
Q

The 3 compartments of GALT are structurally and functionally mature at term - what are they?

List some parts of the GI tract that continue to mature postnatally.

What age can a baby suck, swallow and breathe?

When do teeth appear?

A

Intraepithelial lymphocytes, peyer’s patches, lamina propria cells.

Oesophagus (LOS, motility (reflux)), stomach (acid and intrinsic factor secretion), pancreas (fluid, bicarb and enzyme secretion), liver (enzyme changes, bilirubin/bile salt conjugation, secretion (neonatal physiological jaundice), SI (IgA synthesis, ileal bile salt carrier), LI (fermentative path for carb metabolism).

Sucking and swallowing present early (amniotic fluid), but unable to swallow and breathe before 32-34w of gestation.

6m of age.

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15
Q

Compare cow milk and breast milk.

How long should infant formula be used? At what age should weaning commence?

A

Breast milk: lower protein (whey > casein - more easily digested), lower minerals e.g Na = lower solute load, essential FAs (better absorbed), lipase, anti-infective (e.g. IgA), vits A/C/D greater, lower Ca and phosphorus (high phosphorus in cow’s milk can cause hypocalcemic tetany).

Formula until 12m. Weaning from 6m. Food known to be potentially allergenic can be introduced - eggs, gluten foods

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