Pediatric GI Pathology Flashcards

1
Q

What is the clinical presentation of esophageal atresia or TEF?

A

Aspiration, regurgitation and respiratory distress noted with initial feeds

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2
Q

What are things that are seen with esophageal atresia?

A

50% have other congenital abnormalities (i.e cardiac)

Observed with VATER, trisomy syndromes

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3
Q

Where are most cases of duodenal stenosis observed?

A

In the proximal portion, close to the ampulla of Vater

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4
Q

What are two causes of duodenal stenosis?

A

Web or annular pancreas

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5
Q

How does duodenal stenosis present? Both clinical signs and imaging

A

Vomiting at birth; if billous, stenosis is distal to ampulla

On imaging see a “double-bubble”

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6
Q

How many jejunoileal atresias are single? How many are multiple?

A

85% single

15% multiple

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7
Q

What is the cause of most jejunoileal atresias?

A

Most cases are due to intrauterine vascular accidents or vascular insults such as volvulus, hernias or necrotizing enterocolitis

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8
Q

What is the clinical presentation of jejuno-ileal atresias? Describe for proximal and distal

A

Proximal atresia result in vomiting

Distal atresias manifest with abdominal dissension and dilated loops on radiographs

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9
Q

What is the difference between low and high anorectal atresias?

A

Low atresia associated with perineal fistula
High atresia associated with fistula of GU tract
Both result in imperforate anus

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10
Q

What is an omphalocele? What is its etiology?

A

Extruded intestine covered by an amniotic sac through the umbilicus due to a failure of retraction through the abdominal wall. It is corrected by surgery

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11
Q

What is gastroschisis?

A

Intestinal extrusion through umbilicus. There is no amniotic sac covering so prognosis is worse

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12
Q

What are complications of omphalocele and gastroschisis? (4)

A

Infection
Atresia
Necrosis
Short gut

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13
Q

What is short bowel syndrome ? How is it treated?

A

Massive loss of bowel resulting in decreased fluid/electrolyte reabsorption, chronic diarrhea, nutrient deficiency.
It is treated with total parental nutrition or bowel transplantation

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14
Q

GI Duplications: which side does it usually appear?

A

On the mesenteric side of the bowel; it shares common wall with intestine but does not communicate with it.

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15
Q

What are two types of GI duplications?

A

Tubular duplication– often asymptomatic

Cystic duplication: secretes fluid and causes obstruction of primary organ

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16
Q

On which side are most Gi diverticula observed? What is the most common form?

A

Gi diverticula are the result of a failure in vitelline obliteration. They are usually on anti mesenteric side of bowel

Meckel’s diverticulum is the most common form

17
Q

What is the presentation of Meckel’s diverticulum?

A

Meckel’s diverticula can have gastric mucosa– results in gastric acid secretion that causes abdominal pain, rectal bleeding and sometimes perforation

18
Q

Neurenteric remnants/cysts:

A

Persistence of neural tissue from GI tract in cervical/lumbar area: can cause GI obstruction, respiratory distress, paralysis, infectious/chemical meningitis

19
Q

What are clinical consequences of malrotation of bowel?

A

Bad looping can lead to volvulus, vascular insults due to internal strangulations

20
Q

What is pseudobstruction? Name some primary and secondary causes

A

Symptoms of obstruction without mechanical obstruction

Primary: Hirschsprung disease, visceral myopathies
Secondary: Infections, CT disorders, muscular distrophies

21
Q

What are three plexuses of GI Tract?

A

Meissner’s plexus: superficial submucosa
Henley’s plexus: Deep submucosa
Auerbach’s plexus: Between smooth muscle layers

22
Q

What is clinical finding of hirschsprung disease?

A

Failure to pass meconium

23
Q

How far is the extent of angangliosis in most Hirschsprung patients?

A

75% is rectosigmoid

17% is long segment

24
Q

What are genetics of Hirschsprung?

A

Many cases involve RET mutation

10% incidence in Down’s syndrome

25
What are important contributing factors to necrotizing enterocolitis?
90% of infants are premature and have very low birthweight Contributing factors: intestinal ischemia, intestinal immaturity, bacterial colonization of gut, enteral feeding
26
What is clinical presentation of necrotizing enterocolitis?
Appears during first two weeks of life with abdominal distension, blood in stools, apnea Radiology: shows gas in bowel wall
27
What areas are most commonly affected in necrotizing enterocolitis?
Can affect any segment but terminal ileum, cecum, ascending colon most frequently involved (watershed areas)
28
What are consequences of necrotizing enterocolitis?
Healing leads to fibrous strictures, atresia/stenosis Loss of intestine due to necrosis or resection results in short bowel syndrome
29
What is the pathogenesis of intussusception?
Invagination of one intestinal segment into another
30
What are some of the "lead points" of an intussusception? (3)
Masses, meckel's diverticulum, lymphoid hyperplasia
31
What are GI abrnormalities associated with CF?
Intestinal: Meconium ileus, distal intestinal obstruction, rectal prolapse Pancreatic: insufficiency, pancreatitis Hepatic: chronic hepatic disease, cirrhosis Nutritional: failure to thrive, hypoproteinemia
32
What is CF effect on pancreas?
Acinar destruction and fibrosis with diffuse fatty replacement leads to loss of exocrine function
33
What are common results of CF on the liver?
Raised LFTs Hepatomegaly Hepatic steatosis