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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
Q

duodenal atresia imaging findings

A

gas in stomach and 1st portion of duodenum, but not more distally (double bubble)
CT rules out annular pancreas and other associated congenital defects

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26
Q

prevalence of duodenal atresia

A

1 in 10,000 births

8% of downs syndrome infants

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27
Q

other pathologies associated with duodenal atresia

A

polyhydramnios in 50%

VACTERL in 50%

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28
Q

VACTERL

A 
vertebral abnormalities
anal atresia
cardiac defects
trachea-esophageal fistula
renal anomalies
limb abnormalities
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29
Q

discuss gut tube occlusion

A

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

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30
Q

recanalization error possibilities

A
  1. cysts
  2. duplications
  3. septa
  4. diverticuli
  5. failure to reopen lumen
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31
Q

true vs false diverticulum

A

true contains all layers of wall, false only has outpunching of certain layers

32
Q

most common locations of GI duplications

A

ileum and thorax

33
Q

what is a GI duplication

A

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
Q

midgut organs

A

primary intestinal loop

SMA axis

35
Q

formation of primary intestinal loop

A

rapid growth and elongation in 5th week
vitelline duct connects loop to yolk sac
90 degree rotation

36
Q

physiological herniation of the midgut

A

6th week to 10th week
intestines physiologically herniate out of the embryo
same time during filling and recanalization

37
Q

return of the intestine to the peritoneal cavity

A

end of 10th week
another 180 degree rotation, large intestines now “frame” small intestines”
vitelline duct lost around this time

38
Q

omphalocele

A

failure of gut to return to the peritoneal cavity

loops covered with the amnion which is attached to an enlarged umbilical cord

39
Q

prevalence of omphalocele

A

1 in 5,386 in US
small- SI only
large- can involve liver and spleen

40
Q

detection of omphalocele

A

often detected by prenatal ultrasound or as a consequence of elevated AFP levels

41
Q

when is AFP tests in pregnant women

A

14th-22nd week

most accurate 16-18th weeks

42
Q

association of omphalocele with other pathologies

A 
25-40%
heart defects
neural tube defects
diaphragmatic hernia
chromosomal abnormalities, nearly half have trisomy
43
Q

treatment of omphalocele

A

saran wrap over exposed intestines until surgery
organs returned to cavity with time and growth
umbilicus surgically closed

44
Q

risk factors for omphalocele

A

alcohol and tobacco
SSRIs
obesity

45
Q

when is international omphalocele awareness day

A

jan 31

so just be aware of that

46
Q

gastroschisis

A

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
Q

prevalence of gastroschisis

A

1 in 10,000

more frequent in young teenage mothers

48
Q

detection of gastroschisis

A

prenatal ultrasound
elevated AFP
as early as 14 weeks

49
Q

association of gastroschisis with other pathologies

A

NOT associated with other defects

inherited autosomal recessive

50
Q

risk factors for gastroschisis

A

young mothers
smoking
drug abuse
low birth weight

51
Q

treatment of gastroschisis

A

delivery by C-section at 36 weeks

placing man made materials over exposed intestines to limit volvulus prior to surgical repair

52
Q

success of surgery in gastroschisis

A

successful 90% of the time
small repaired 24 hrs after birth
larger may require more steps

53
Q

what are gut rotation abnormalities

A

malrotation of the intestines

54
Q

2 most common malrotations

A
  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
Q

volvulus

A

if normal rotation fails, there is spontaneous compromised blood supply to a section of the GI tract

56
Q

result of volvulus

A

intestinal atresia

57
Q

vascular accidents

A

most commonly atresias and stenosis
occur in 1 in 1500 births
most frequently in duodenum, least frequently in the colon

58
Q

termination of the vitelline duct and allantois

A

programmed cell death (apoptosis) in 10th week

59
Q

human umbilical cord at time of birth

A

2 umbilical arteries
1 umbilical vein
Wharton’s jelly protects vessels

60
Q

congenital vitelline duct defects

A

occur if vitelline (omphalomesenteric) duct does not undergo apoptosis
vitelline ligament
vitelline cyst
vitelline fistula

61
Q

Meckel’s diverticulum

A

remnant of where the vitelline duct was attached to the ileum

62
Q

appearance of Meckel’s diverticulum

A

2 inches long
2 feet proximal to ileocecal junction
2 types of ectopic tissue: gastric and pancreatic

63
Q

symptoms of Meckel’s

A

abdominal pain

blood in stool

64
Q

prevalence of Meckels

A

2% of the population
< age 2
2x as frequent in boys than girls

65
Q

what is Hirschsprung disease

A

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
Q

genetic component of Hirschsprung

A

failure of RET gene, tyrosine kinase receptor

67
Q

prevalence of Hirschsprung

A

1 in 5,000
males 4x more frequent than females
9% in downs individuals

68
Q

how is Hirschsprung identified

A

infants not dismissed until they have passed meconium
90% in first 24 hours
99% within 48 hours
Hirschsprung suspected after 48 hours

69
Q

symptoms of Hirschspring

A

abdominal distention

constipation

70
Q

diagnosis and treatment of Hirshsprung

A

barium enema or lower GI study showing non motile bowel section
generally must be removed surgically

71
Q

what is the urorectal septum

A

grows down to separate hindgut from cloaca

creates one space for urine (bladder), and one for fecal matter (rectum)

72
Q

what is imperforate anus

A

anal atresia
failure of anus to form or connect to the rectum
usually very obvious to detect

73
Q

prevalence of imperforate anus

A

1 in 5000
part of VACTERL
associated with trisomy 18 and 21

74
Q

treatment of imperforate anus

A

immediate surgical intervention which may involve a temporary colostomy

75
Q

why are most screenings done between 14-20 weeks?

A

this is after most of the fetal GI development has occurred

GIR Test 4 (20 decks)

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