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GI Midterm > Embryo > Flashcards

Embryo Flashcards

1
Q

what initiates specification of the gut?

A

retinoic acid gradient that causes TFs expressed in different regions of the tube

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2
Q

SOX2 specifies

A

esophagus

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3
Q

PDX2 specifies

A

duodenum and pancreas

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4
Q

CDXC specifies

A

small intestine

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5
Q

CDXA specifies

A

large intestine

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6
Q

what else is required for specification of gut tube into different components?

A

interaction b/w epithelium and mesenchyme initiated by SHH

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7
Q

what does the endoderm become?

A

epithelial lining and glands

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8
Q

what does the splanchnic mesoderm become?

A

lamina propria, submucosa, muscularis layers, serosa/adventitia

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9
Q

what supplies foregut?

A

celiac A

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10
Q

what supplies midgut?

A

SMA

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11
Q

what supplies hindgut?

A

IMA

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12
Q

where are preganglionic cell bodies for foregut and midgut?

A

brainstem

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13
Q

where are preganglionic cell bodies for hindgut?

A

S2-4

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14
Q

nerve of the foregut and midgut

A

vagus N

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15
Q

nerve of the hindgut

A

pelvic splanchnic N

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16
Q

tracheoesophageal fistula

A

i. lung buds develop from an outgrowth of the esophagus
1. should eventually lose the connection here except for in one area where you can regulate airflow at the tracheoesophageal junction
2. if the opening does not close, then we get a tracheoesophageal fistula
a. this is when we have an inappropriate connection with the esophagus somewhere along the trachea
b. often get atresia of the esophagus—the esophagus ends in a blind pouch

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17
Q

esophageal stenosis or atresia

A
  1. narrow or occluded esophagus due to incomplete recanalization, usually found in the lower 1/3
  2. may also be caused by vascular abnormalities or compromised blood flow
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18
Q

esophageal replacement

A
  1. the majority of esophageal procedures are performed on infants/children and are done for congenital esophageal atresia or acquired caustic strictures
  2. successful esophageal anastomoses may be performed in those few with long gap esophageal atresia b/w the proximal and distal esophageal remnants
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19
Q

colon interposition

A
  • type of esophageal replacement
  • section of colon is taken from normal position and transposed with its blood supply in tact into the chest, where it is joined by the esophagus above and the stomach below
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20
Q

gastric tube esophagoplasty

A
  • type of esophageal replacement

- longitudinal segment is taken from stomach, which is swung up into the chest and joined to the esophagus

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21
Q

gastric transposition

A
  • type of esophageal replacement

- whole stomach is freed, mobilized, and moved into the chest and attached to the upper end of the esophagus

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22
Q

diverticulum of the foregut

A

i. liver diverticulum
ii. cystic diverticulum
iii. dorsal pancreatic diverticulum
iv. ventral pancreatic diverticulum

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23
Q

growth of stomach

A

i. dorsal surface grows faster than ventral surface (causes c shape)
ii. the abdominal esophagus and stomach start as a straight tube suspended by dorsal and ventral mesentery
1. the dorsal (left) side of the tube grows rapidly expands and there is a CW rotation of 90 degrees
2. rotation of the stomach causes:
a. left side to lie anterior, right side to become posterior
b. left vagus becomes the anterior vagal trunk, right vagus becomes the posterior vagal trunk

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24
Q

hypertrophic pyloric stenosis

A
  1. usually presents 2-3 weeks after birth
  2. pyloric sphincter becomes overgrown
    a. doesn’t occur immediately after birth
    b. child comes in with non bilious (non green) projectile vomiting
  3. clinical: scaphoid stomach—distended
    a. also can feel an olive sized mass right of midline which is pyloric sphincter
25
Q

stenosis and atresia of the duodenum

A
  1. usually, recanalization should occur to reopen the gut tube after development
  2. stenosis—occur in 3 or 4 part
  3. atresia—occur in 2 or 3 part
    a. bile will get into this chyme, so it will be vomited green
26
Q

double bubble sign

A

gas distended stomach and proximal duodenum with no distal gas

27
Q

where does the liver develop?

A

ventral mesentery

28
Q

molecular regulation of the liver

A

a. all foregut endoderm has the potential to express liver specific genes and to differentiate into liver tissue
b. expression is blocked by unknown signals from the trunk mesoderm and ectoderm, restrict hepatic development in posterior endoderm
i. action of these inhibiting factors is blocked in the area of the liver by FGF2 secreted by cardiac mesoderm and BMPs secreted by the septum transversum
ii. cardiac mesoderm/septum transversum instruct the gut endoderm to express liver specific genes

29
Q

ductus venosus

A

shunts a portion of the left umbilical vein blood flow directly to the inferior vena cava. Thus, it allows oxygenated blood from the placenta to bypass the liver.

30
Q

ligamentum venosum

A

fibrous remnant of the ductus venosus

31
Q

ligamentum teres hepatis

A

obliterated left umbilical vein

32
Q

Extrahepatic biliary atresia

A

a. Incomplete canalization of the bile duct
b. 1/15000 live births
c. can’t get bile from liver down into the GI system
i. jaundice—high levels of bilirubin in bloodstream
ii. dark urine—bilirubin filtered by kidney and excreted in urine
iii. pale stool—no bile or bilirubin is being emptied into the intestine
d. TX: surgical correction or transplant

33
Q

where does the gallbladder and bile ducts develop?

A

ventral mesentery

34
Q

where does the pancreas develop?

A

ventral and dorsal mesentery

35
Q

PDX1

A

pancreas and duodenum

36
Q

paired homeobox genes specify

A

endocrine cell lineages

37
Q

PAX4

A

cells secreting insulin, somatostatin, and pancreatic polypeptide

38
Q

PAX6

A

cells secreting glucagon

39
Q

islets of langerhans

A

3rd fetal month

40
Q

insulin secretion

A

5th fetal month

41
Q

what causes the 2 parts of the pancreas to fuse?

A

stomach rotation

42
Q

annular pancreas

A

a. Ventral and dorsal pancreatic buds form a ring around the duodenum
b. Presents as duodenal obstruction

43
Q

accessory or ectopic pancreatic tissue

A

a. Can be found from distal esophagus thru the primary intestinal loop (roughly distal part of transverse colon)
b. Most common in stomach or ileum (ileal or Meckel’s diverticulum)

44
Q

Gut atresias and stenosis

A

i. May occur anywhere along intestine
ii. In upper duodenum—usually due to failure to recanalize
iii. Caudal to duodenum—due to vascular compromise

45
Q

apple peel atresia

A
  1. 10% of all atresias
  2. occurs in proximal jejunum
  3. intestine is short and portion distal to defect is coiled around mesenteric remnant
    a. part of gut has died and has tobe removed
  4. associated with low body weight and other abnormalities
46
Q

rotation and fixation of the midgut

A

i. rapid growth of midgut starts at about 6 weeks
ii. produces a normal physiologic herniation
iii. gut loops into the umbilical cord
iv. as this happen, the loop rotates 90 degrees CCW around SMA
v. at about the 10th week, the herniated loops return to the abdominal cavity and rotate an additional 180 degrees
vi. returns to abdominal cavity

47
Q

malrotation

A
  1. partial rotation only
  2. abnormally positioned viscera
  3. increased risk of entrapment of portions of the intestine
  4. usually presents within first week as duodenal obstruction with bilious vomiting
  5. infants—recurrent abdominal pain, intestinal obstruction, malabsorption/diarrhea, peritonitis/septic shock, solid food intolerance, common bile duct obstruction, abdominal distention, and failure to thrive
48
Q

ladd’s bands

A

a. connection b/w gut tube and abdominal wall that shouldn’t be there
b. this may compress a part of the gut tube that is underneath the Ladd band

49
Q

volvulus

A
  1. abnormal twisting of the intestine causing obstruction

2. compromises the intestines or the blood flow

50
Q

intussusception

A
  1. enfolding of one segment of the intestine within another
  2. characterized and initially presents with recurring attacks of cramping abdominal pain that gradually become more painful
51
Q

omphalocele

A

i. herniation of abdominal contents thru enlarged umbilical ring
1. this Is normal if it is temporary
2. the gut should return into the abdomen as the embryo grows
ii. midgut does not return to the abdominal cavity
iii. pale, shiny sac protrudes from base of umbilical cord

52
Q

gastroschisis

A

i. failure of anterior abdominal wall musculature to close during folding
ii. gut contents not surrounded by membrane
iii. 1-2/10000 but frequency increasing in young women possibly due to drug use
iv. not associated with chromosomal abnormalities or malformations
v. survival rate is excellent

53
Q

prune belly syndrome common triad of features

A
  1. anterior abdominal wall—musculature is deficient or absent
  2. urinary tract anomalies—mega-ureters, large bladder
  3. bilateral cryptorchidism—undescended testes
54
Q

2 hypotheses of etiology of prune belly syndrome

A
  1. urinary tract obstruction—causes overdistention of the bladder and upper urinary tract which stretches the abdominal wall and causes damage to abdominal musculature and interferes with descent of testicles
  2. primary mesodermal developmental defect—an insult b/w 6-10 weeks gestation which disrupts the development of the intermediate and lateral plate mesoderm which give rise to both abdominal wall and genitourinary tract
55
Q

ill diverticulum

A

i. Meckel’s diverticulum
ii. Remnant of vitelline duct
iii. Asymptomatic
iv. Gastric or pancreatic tissue in the diverticulum
v. Failure of vitelline duct to close
vi. Rule of 2’s
1. 2% prominence, 2:1 female predominance, location 2 feet proximal to ileocecal valve in adults, half of those who symptomatic are younger than 2 years old
vii. causes fecal discharge thru umbilicus

56
Q

hirschsprung’s disease

A

i. Congenital aganglionic megacolon, is a motor disorder of the colon that causes a functional intestinal obstruction
ii. Both plexuses are affected
iii. Occurs in 1/5000 infants with male to female predominance of 4:1
iv. Pathogenesis of the disease is failure of migration of the neural crest cells that form the colonic ganglion cells
v. Without PS innervation, the colon cannot relax or undergo peristalsis, which causes a functional obstruction

57
Q

tx of HD

A
  1. Surgery is only proven, effective tx for HD
  2. Procedure is called pull through surgery and involves removing the section of the colon that has no ganglia cells, then connecting the remaining healthy end of colon to rectum
58
Q

imperforate anus

A
  1. Malformation of the anorectal region that may occur in several forms
  2. The recutm may end in a blind pouch that does not connect with the external environment, or it may have openings to urethra, bladder, or vagina
  3. Stenosis, or narrowing of anus, or absence of anus may be present
  4. Symptoms:
    a. Absence or misplaced anal opening
    b. Anal opening very near the vaginal opening in the female
    c. No passage of first stool within 24-48 hours
    d. Stool passed by vagina, scrotum, penis
    e. Abdominal distention
59
Q

Anorectal malformations are on a spectrum of high or low

A
  1. Anal canal ends as bling pouch below pelvic diaphragm—LOW
    a. Anal agenesis
    b. Rectum thru diaphragm so have some skeletal muscle we can use for fecal continence
  2. Rectum ends as blind pouch above the pelvic diaphragm—HIGH
    a. No muscle to use to control

GI Midterm (12 decks)

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