GI embryology, transesophageal anomalies Flashcards

1
Q

What are the developmental defects that can be seen in the anterior abdominal wall?

A

rostral fold closure: sternal defects
lateral fold closure: omphalocele, gastroschisis
caudal fold closure: bladder exstrophy (part of bladder is facing the outside world)

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2
Q

What are the different intestinal atresias? What causes them?

A

atresia (failure of recanulization) may be seen at any point in the intestines.
duodenal atresia is usually associated with trisomy 21
atresia in the jejunum, ileum, or colon is usually due to a vascular accident

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3
Q

Describe midgut development, including weeks

A

week 6: the gut herniates through the umbilical ring

week 10: the fetus is big enough to hold the gut, so it returns to the abdominal cavity and rotates around the SMA

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4
Q

gastroschisis vs. omphalocele

A

gastroschisis: extrusion of abdominal contents through the abdominal folds. NOT covered by peritoneum
omphalocele: persistence of herniation of abdominal contents into the umbilical cord; sealed by peritoneum. associated with additional abnomalities; liver may also be involved.

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5
Q

What is the most common cause and clinical manifestations of a tracheoesophageal anomaly? What are the imaging abnormalities, and what is the diagnostic test? When does it present?

A

esophageal atresia with distal tracheoesophageal fistula is the most common.
presents as vomiting, drooling, and choking with the first feeding. the TEF allows air to enter the stomach, which can be seen on CXR. there may be cyanosis secondary to laryngospasm as the lung tries to protect itself from reflux-related aspiration.
test: failure to pass an NG tube into the stomach

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6
Q

Pure esophageal atresia vs. pure transesophageal fistula

A

pure EA: CXR will show gasless abdomen

pure TEF: aka H-type.

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7
Q

What is congenital pyloric stenosis? What are the clinical findings? Who is most at risk? When does it present?

A

pyloric hypertrophy causes obstruction. presents around 2-6 wks of age with nonbilious, projectile vomiting and a palpable “olive” mass in the epigastric region.
most common in firstborn males

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8
Q

How does the pancreas develop? Which parts of the pancreas come from the vental bud? Which parts come from the dorsal bud?

A

the pancreas begins as two separate buds, the dorsal and ventral bud. the ventral bud rotates to be near the dorsal bud, and they should fuse around week 8 of development.
most of the pancreas comes from the dorsal bud. the ventral bud contributes the main pancreatic duct, the head of the pancreas and the uncinate process (it is the only contributor to the uncinate process).

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9
Q

Annular pancreas: which bud is involved? what is a complication?

A

this is a problem with the migration of the ventral pancreas. it abnormally encircles the duodenum and can cause duodenal narrowing.

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10
Q

pancreas divisum: what is the problem and when does it arise?

A

the pancreas fails to fuse at 8 wks

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11
Q

Where does the spleen come from? How is it different from the rest of the GI tract, and how is it similar?

A

spleen comes from the mesentary of the stomach and therefore is of mesodermal origin (remember that the liver and pancreas parenchyma and the epithelial lining of the GI tract are all of endodermal origin).
It is supplied by the celiac artery, however.

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12
Q

What is the definition of a retroperitoneal structure? What can happen with injury to a retroperitoneal structure?

A

retroperitoneal structure: GI structures without a mesentary; non GI structures in that region. injuries can cause blood or gas accumulation in the retroperitoneal space.

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13
Q

What are the retroperitoneal structures?

A

SAD PUCKER:
suprarenal (adrenal) glands, aorta and IVC, duodenum (2nd-4th parts), pancreas (except tail), ureters, ascending and descending colon, kidneys, lower 2/3 of esophagus, part of rectum.

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