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GIR Test 4 > B5.069 Development of the GI System > Flashcards

B5.069 Development of the GI System Flashcards

1
Q

when does this endoderm epithelium dramatically change shape?

A

day 20-26

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2
Q

components of endodermal epithelium at day 26

A 
foregut
midgut
hindgut
allantois
vitelline duct
yolk sac
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3
Q

only organ suspended by 2 mesenteries

A

stomach

dorsal and ventral mesenteries

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4
Q

stomach rotation

A

rotates 90 degrees clockwise, left vagus ends up anterior and right vagus posterior
original posterior portion grows larger forming the greater curvature

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5
Q

what do the mesenteries develop into?

A 
dorsal = greater omentum
ventral = lesser omentum
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6
Q

prevalence of pyloric stenosis

A

2 in 1000 births
2nd most common GI abnormality after Meckel’s
typically in males (4x more likely)
first 2-6 weeks of life

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7
Q

symptoms of pyloric stenosis

A

severe projectile non-bilious vomiting
dehydration and weight loss
hypochloremia due to loss of gastric acid in vomit

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8
Q

cause of pyloric stenosis

A

hypertrophy of pyloric sphincter muscles to the point of pyloric stenosis
no gastric contents can enter first portion of duodenum
can sometimes palpate “olive” in anterior abdominal wall caudal to xyphoid process

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9
Q

what organs are derives from foregut endoderm

A

(lungs)
liver
gallbladder
pancreas

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10
Q

what structure forms the diaphragm

A

septum transversum

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11
Q

what is the bare area of the liver

A

liver fuses with developing diaphragm resulting in bare area surrounded by coronary ligament

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12
Q

discuss the origin of the falciform ligament and lesser omentum

A

liver growth causes lower portion of the septum transversum to thin, leaving the falciform ligament anterior and lesser omentum posterior to the liver

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13
Q

where do pancreatic buds originate

A

dorsal and ventral buds form on opposite sides of the gut tube
during the 5th week smaller ventral pancreas migrates around and fusion forms definitive pancreas

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14
Q

what happens if dorsal and ventral pancreatic buds don’t fuse?

A

typically don’t cause problems until sometimes in adult lift

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15
Q

major pancreatic duct

A

Wirsung
more caudal
always present

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16
Q

accessory pancreatic duct

A

Santorini

superior if present

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17
Q

annular pancreas

A

thought to arise when two (bilobed) ventral pancreatic buds form and migrate in opposite directions constricting the duodenum

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18
Q

severity of annular pancreas

A

some only partly block lumen

typically obstruct bile flow and pancreatic juice flow into lumen

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19
Q

classification of annular pancreas

A

classified into 6 subtypes based upon the drainage site of the annular duct

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20
Q

prevalence of annular pancreas

A

rare, 1 in 15,000 newborns

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21
Q

symptoms of annular pancreas in newborns

A

may have complete blockage of duodenum leading to polyhydramnios
present with difficulty feeding after birth
non-bilious vomiting and nausea
abdominal distention

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22
Q

other pathologies associated with annular pancreas

A 
maternal polyhydramnios
Down syndrome
esophageal and duodenal atresias
imperforate anus
Meckel's diverticulum
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23
Q

what is duodenal atresia

A

congenital duodenal obstruction

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24
Q

presentation of duodenal atresia

A

early (within 24 hrs) with vomiting that may or may not contain bile, depending on atresia location
abdomen is not dilated bc distal intestines have not fully developed

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25
duodenal atresia imaging findings
gas in stomach and 1st portion of duodenum, but not more distally (double bubble) CT rules out annular pancreas and other associated congenital defects
26
prevalence of duodenal atresia
1 in 10,000 births | 8% of downs syndrome infants
27
other pathologies associated with duodenal atresia
polyhydramnios in 50% | VACTERL in 50%
28
VACTERL
``` vertebral abnormalities anal atresia cardiac defects trachea-esophageal fistula renal anomalies limb abnormalities ```
29
discuss gut tube occlusion
6th-9th week gut tube goes from hollow to occlusion of the lumen by endodermal cell proliferation 1-2 weeks later recanalized and hollow again
30
recanalization error possibilities
1. cysts 2. duplications 3. septa 4. diverticuli 5. failure to reopen lumen
31
true vs false diverticulum
true contains all layers of wall, false only has outpunching of certain layers
32
most common locations of GI duplications
ileum and thorax
33
what is a GI duplication
developmental duplication of a segment of the GI tract may occur anywhere along the tract, though certain sites are more common may be cystic or tubular on mesenteric side of bowel share common wall but do not communicate with intestine
34
midgut organs
primary intestinal loop | SMA axis
35
formation of primary intestinal loop
rapid growth and elongation in 5th week vitelline duct connects loop to yolk sac 90 degree rotation
36
physiological herniation of the midgut
6th week to 10th week intestines physiologically herniate out of the embryo same time during filling and recanalization
37
return of the intestine to the peritoneal cavity
end of 10th week another 180 degree rotation, large intestines now "frame" small intestines" vitelline duct lost around this time
38
omphalocele
failure of gut to return to the peritoneal cavity | loops covered with the amnion which is attached to an enlarged umbilical cord
39
prevalence of omphalocele
1 in 5,386 in US small- SI only large- can involve liver and spleen
40
detection of omphalocele
often detected by prenatal ultrasound or as a consequence of elevated AFP levels
41
when is AFP tests in pregnant women
14th-22nd week | most accurate 16-18th weeks
42
association of omphalocele with other pathologies
``` 25-40% heart defects neural tube defects diaphragmatic hernia chromosomal abnormalities, nearly half have trisomy ```
43
treatment of omphalocele
saran wrap over exposed intestines until surgery organs returned to cavity with time and growth umbilicus surgically closed
44
risk factors for omphalocele
alcohol and tobacco SSRIs obesity
45
when is international omphalocele awareness day
jan 31 | so just be aware of that
46
gastroschisis
failure of body wall closure followed by gut herniation failure of the anterior body wall typically occurs to the right of the umbilicus herniate intestines are NOT covered with a membrane
47
prevalence of gastroschisis
1 in 10,000 | more frequent in young teenage mothers
48
detection of gastroschisis
prenatal ultrasound elevated AFP as early as 14 weeks
49
association of gastroschisis with other pathologies
NOT associated with other defects | inherited autosomal recessive
50
risk factors for gastroschisis
young mothers smoking drug abuse low birth weight
51
treatment of gastroschisis
delivery by C-section at 36 weeks | placing man made materials over exposed intestines to limit volvulus prior to surgical repair
52
success of surgery in gastroschisis
successful 90% of the time small repaired 24 hrs after birth larger may require more steps
53
what are gut rotation abnormalities
malrotation of the intestines
54
2 most common malrotations
1. only initial 90 degrees of rotation occurred: small intestines to the right of large 2. revere rotation of initial 90 degree rotation, duodenum falls in front of colon
55
volvulus
if normal rotation fails, there is spontaneous compromised blood supply to a section of the GI tract
56
result of volvulus
intestinal atresia
57
vascular accidents
most commonly atresias and stenosis occur in 1 in 1500 births most frequently in duodenum, least frequently in the colon
58
termination of the vitelline duct and allantois
programmed cell death (apoptosis) in 10th week
59
human umbilical cord at time of birth
2 umbilical arteries 1 umbilical vein Wharton's jelly protects vessels
60
congenital vitelline duct defects
occur if vitelline (omphalomesenteric) duct does not undergo apoptosis vitelline ligament vitelline cyst vitelline fistula
61
Meckel's diverticulum
remnant of where the vitelline duct was attached to the ileum
62
appearance of Meckel's diverticulum
2 inches long 2 feet proximal to ileocecal junction 2 types of ectopic tissue: gastric and pancreatic
63
symptoms of Meckel's
abdominal pain | blood in stool
64
prevalence of Meckels
2% of the population < age 2 2x as frequent in boys than girls
65
what is Hirschsprung disease
failure of enteric neural crest cells to migrate around the developing intestines resulting in a non-motile portion of the bowel lack of parasympathetic innervation
66
genetic component of Hirschsprung
failure of RET gene, tyrosine kinase receptor
67
prevalence of Hirschsprung
1 in 5,000 males 4x more frequent than females 9% in downs individuals
68
how is Hirschsprung identified
infants not dismissed until they have passed meconium 90% in first 24 hours 99% within 48 hours Hirschsprung suspected after 48 hours
69
symptoms of Hirschspring
abdominal distention | constipation
70
diagnosis and treatment of Hirshsprung
barium enema or lower GI study showing non motile bowel section generally must be removed surgically
71
what is the urorectal septum
grows down to separate hindgut from cloaca | creates one space for urine (bladder), and one for fecal matter (rectum)
72
what is imperforate anus
anal atresia failure of anus to form or connect to the rectum usually very obvious to detect
73
prevalence of imperforate anus
1 in 5000 part of VACTERL associated with trisomy 18 and 21
74
treatment of imperforate anus
immediate surgical intervention which may involve a temporary colostomy
75
why are most screenings done between 14-20 weeks?
this is after most of the fetal GI development has occurred

GIR Test 4 (20 decks)

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