Pediatric GI Pathology Flashcards

1
Q

Is atresia/stenosis more common in foregut or hindgut?

A

More common in foregut.

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2
Q

What other abnormality often co-occurs with esophageal atresia?

A

Tracheo-esophageal (TE) fistula: Most commonly… Lower esophagus, disconnected from upper esophagus, has fistula with the trachea.

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3
Q

Clinical presentation of esophageal atresia (with TE fistula)? On X-ray?

A

Aspiration, regurgitation, respiratory distress with initial feeds.
X-ray shows absence of GI gas.

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4
Q

Take home point about clinical pattern of esophageal atresia (with TE fistula)?

A

Often occurs as part of syndrome with many abnormality, such as trisomies.

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5
Q

Duodenal stenosis causes?
Presentation?
Classic X-ray presentation?

A

Web, or annular pancreas.
Presents with vomiting +/- bile (depending on if before or after ampulla of Vater)
Double-bubble.

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6
Q

Broad cause thought to be behind most jejuno-ileal atresias?

A

Intrauterine vascular accidents

including volvulus, hernias, NEC

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7
Q

What’s the division line for high vs. low anorectal atresia?

What tends to happen in high vs. low atresia?

A

Division line is levator sling.
High: fistula with GU tract.
Low: fistula out through skin

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8
Q

Do gastrointestinal duplications usually communicate?

A

No, but they do usually share a wall.

and they’re usually on the mesenteric side of the bowel…

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9
Q

When to GI duplications cause symptoms?

A

When mucous secretions build up -> cysts -> compress normal bowel.

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10
Q

What side of the bowel are diverticula usually on?

A

the anti-mesenteric side (remember all that penetrating artery weakness stuff?)

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11
Q

Where do diverticula come from? Most common form?

A

Remnants of vitelline duct (to yolk sac).

Meckel’s diverticulum is most common.

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12
Q

What’s the problem with Meckel’s diverticulum?

A

50% are symptomatic and do weird shit like develop gastric mucosa, secreting acid that damages small bowel mucosa.
(This is screened for when there’s rectal bleeding in an infant.)

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13
Q

What are neurenteric remnants or cysts?

Most severe complication?

A

Connections between the intestine and spinal cord that failed to obliterate.
Most severe complication is chemical meningitis.

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14
Q

Why is volvulus more likely to happen when normal rotation of the bowel doesn’t happen?

A

Things such as the cecum don’t get fixed retroperitoneally as they normally would. They’re free floating, or fixed in a bad area, and cause problems.

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15
Q

2 main categories of primary pseudobstruction?

A
Enteric neuropathies (esp. Hirschsprung)
Visceral myopathies
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16
Q

What does visceral myopathy affect in addition to intestinal motility?

A

Bladder contraction.

17
Q

Secondary causes of pseudobstruction?

A

Infections (esp Chagas), toxic megacolon, connective tissue disorders, muscular dystrophies, nervous problems, endo problems, metabolic, etc. etc.

18
Q

Where does Hirschsprung’s disease most often affect? How does this help for surgical treatment?

A

The distal hindgut.

Can cut out the affected, aganglionic bowel and bring remaining bowel to the anus.

19
Q

What’s actually missing in Hirschsprung’s?

A

Ganglia. There is still some other nervous tissue in Meisner’s and Auerbach’s plexuses.

20
Q

Who does necrotizing enterocolitis (NEC) affect?

A

Premature infants, most with very low birthweight.

21
Q

4 most important contributing factors for NEC?

A

Intestinal ischemia
Intestinal immaturity
Bacterial colonization of gut
Enteral feeding

22
Q

Signs of NEC? How does it look on radiology?

A

Abdominal distension, bloody stools, apnea.

Radiology: gas in bowel wall (pneumatosis)

23
Q

What does the histology of NEC look like?

A

Ischemic necrosis of the mucosa.

24
Q

What can happen when NEC heals?

A

Strictures and atresia.

25
Q

Treatment of NEC?

A

Resect involved segments of colon. If too much gone, can have Short Bowel Syndrome.
(if too much is gone, must do TPN and transplant)

26
Q

What’s intussusception? What’s the problem with that?

A

Invagination of one instestinal segnement into the other.

This constricts venous outflow, then arterial inflow -> ischemic necrosis.

27
Q

Common presentation of intussusception?

A

Colicky, intermittent pain. If there’s necrosis, will often have blood stool.
Kids will often draw their knees up to their chest.

28
Q

What are 3 things that can cause a “lead point” for intussusception?

A

Masses
Meckel’s Diverticulum
Lymphoid hyperplasia

29
Q

Intestinal manifestations of CF?

A

Thick meconium that obstructs bowel (ileus -(sometimes)-> perforation -> meconium peritonitis).
Dilated Brunner’s glands with thick secretion.

30
Q

Pancreas manifestations of CF?

A

Necrosis of acini of pancreas -> loss of exocrine function of pancreas.

31
Q

Liver manifestations of CF?

A

High LFTs, hepatomegaly, steatosis, cirrhosis, gall stones.