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pediatrics II > PEDS GI > Flashcards

PEDS GI Flashcards

1
Q

why do infants get gastroesophagual reflux

A
  • reflux of gastric contents into the stomach
  • combination of lower esophageal sphincter immaturity, small stomach, and short esophagus
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2
Q

gastroesophagual reflux is common in infants at what age group

A

< 6 months

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3
Q

differentiate between gastroesophagual reflux (GER) and gastroesophagual reflux disease (GERD)

A
  • gastroesophagual reflux (GER) = “happy spitter”
    • growing well, healthy clinically
  • gastroesophagual reflux disease (GERD) = “unhappy spitter”
    • failure to thrive
    • fussy or irritable/ dystonic neck posturing
    • feeding refusal
    • occult blood in stool
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4
Q

what is esophageal atresia

A
  • upper esophagus does not connect with lower esophagus (+/- tracheoesophageal fistula)
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5
Q

treatment for infants with GERD

A
  • positional therapy: upright after feeding
  • elimination diet (milk) or change in formula
  • thickened feeds: rice in formula
  • don’t overfeed
  • medications
    • H2 blocker (ranitidine)
    • proton pump inhibitor (iansoprazole) > 1 yo
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6
Q

GERD prognosis

A

symptoms usually resolve by 9-12 months

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7
Q

what is Pyloric stenosis

A
  • Pylorus muscle thickening, causing stenosis of the pyloric channel and gastric outlet obstruction
  • M > F (4:1)
  • more common in first born children
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8
Q

clinical presentation

  • 3-12 week old infant with vomiting
  • Projectile vomiting after eating
  • non-billous vomitus
  • “hungry vomiter” infant is hungry
A

Pyloric stenosis

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9
Q

physical exam

  • upper abdomen distended after eating
  • prominent peristaltic waves moving from L to R
  • “olive” sized mass in RUQ
A

pyloric stenosis

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10
Q

test of choice to diagnose pyloric stenosis

A

ultrasound

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11
Q

if ultrasound is nondiagnostic, what test can be done if you expect pyloric stenosis? what do you expect to see on this test?

A
  • Upper GI series: The test uses barium contrast material, fluoroscopy, and X-ray.
  • “string sign”
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12
Q

treatment of pyloric stenosis and prognosis

A
  • treatment
    • IV fluids and electrolyte resuscitation
    • Pyloromyotomy
      • incision down to mucosa and fully across length of pylorus
  • prognosis: excellent
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13
Q

Define congenital atresia and name the different types

A
  • one or more segments of bowel may be absent and/or obstructed at birth
  • types
    • Duodenal atresia
      • trisomy 21 (30%)
    • Jejunoileal atresia
      • cystic fibrosis
    • Colonic atresia - least common
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14
Q

differentiate between etiology of Duodenal atresia and jejunoileal atresia

A
  • Duodenal atresia: secondary to events that occur during early development of gut (8-10 weeks of gestation)
  • jejunoileal atresia: utero vascular accident occuring 11-12 weeks
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15
Q

clinical presentation

  • bile stained vomiting
    • ​within first 24-48 hours of life
  • mild abdomen distension
  • failure to pass meconium (+/-)
A

Congenital atresia

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16
Q

“double bubble” sign is common of what condition

A
  • Duodenal atresia
  • due to gas and dilation in both stomach and duodenum
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17
Q

what will be characteristic of jejunoileal or colonic atresia on abdominal plain film

A
  • dilated loops of bowel and air fluid levels
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18
Q

how is congential atresia diagnosed

A
  • CMP: electrolytes, biliruben
  • abd plain film
  • Upper GI series/constrast enema
    • used to confirm diagnosis and identify area of obstruction
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19
Q

Etiology of midgut malrotation +/- volvulus

A
  • incomplete rotation of midgut during embryonic development
  • malrotation can result in
    • shortening of mesenteric root -> increases small bowel mobility which can lead to volvulus
  • volvulus: small intestine twists around SMA causing vascular compromise
  • **surgical emergency
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20
Q

clinical presentation

  • >50% present before 1 month of age
  • bilious vomiting, abdominal pain
  • +/- hematochezia
  • PE
    • abd distension
    • tenderness
    • visible peristalsis
A

midgut malrotation +/- volvulus

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21
Q

how is midgut malrotation +/- volvulus diagnosed

A
  1. abd xray: r/o bowel obstruction
  2. UGI
    1. “Corkscrew appearance” - proximal jejunum spiraling downward in the right or mid-upper abd
  3. barium enema: if diagnosis is in question
    1. will see cecum in RUQ instead of RLQ
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22
Q

What is intussusception

A

invagination of one portion of intestine into another (usually near ileocecal junction)

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23
Q

What is the most frequent cause of intestinal obstruction in the first two years of life

A

intussusception

  • ** rare in newborns
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24
Q

What causes intussusception

A
  1. idiopathic (75%): no clear link
  2. stem from lead point
    • lesion/variation in intestine is dragged by peristalsis
      • Meckel’s
      • tumor
      • hematoma
      • vascular lesion
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25
Q

clinical presentation

  • intermittent, severe crampy abd pain
  • cries and draws legs up toward chest
  • vomiting
  • does not feed
  • “Currant jelly” stools
  • blood and mucous
  • triad (15%)
    • pain
    • palpable sausage shape
    • currant jelly stools
A

Intussusception

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26
Q

how is Intussusception diagnosed

A
  • abd ultrasound
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27
Q

managment of Intussusception

A
  1. urgent surgical consult
  2. air enema
    • can reduce with 74% success rate
    • US guided
    • risk: perforation
  3. sugical intervention
    • can be fatal if reduction is not performed
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28
Q

What is Meckel’s Diverticulum

A
  • embryonic remnant of vitelline duct
  • incomplete obliteration and diverticulum formed
  • located within 2 feet of Ileocecal valve
  • gastric acid produced -> damage
  • bleeding occurs from mucosal ulceration
29
Q

Meckel’s Diverticulum rule of 2’s

A
  • 2% of the population
  • 2:1 M:F ratio
  • 2% become symptomatic
30
Q

clinical presentation

  • Painless rectal bleeding
  • obstruction (volvulus or intussusception)
  • Diverticulitis (can mimic appendicitis)
A

Meckel’s Diverticulum

31
Q

how is Meckel’s Diverticulum diagnosed

A
  • Technetium-99 scan (Meckel’s scan)
32
Q

what is the most common pediatric surgical emergency

A

appendicitis

33
Q

appendicitis is most often caused by

A

obstruction of the appendiceal lumen leading to inflammation

34
Q

when does appendicitis become most prevelant

A
  • peaks 2nd decade of life
  • rare before 5 yo
35
Q

clinical presentation

  • anorexia
  • migrating abd pain (periumbilical to RLQ)
  • vomiting (after onset of pain)
  • fever
  • guarding
  • rebound tenderness
    • Rovsing sign
  • Obturator or ileopsoas sign
A

appendicitis

36
Q

how is appendicitis diagnosed

A
  1. US
  2. CT scan
37
Q

What is Hirschsprung’s disease

A
  • aka: congenital aganglionic megacolon
  • occurs secondary to absense of ganglion cells in mucosal and muscular layers of colon
  • begins in distal bowel (usually rectosigmoid)
  • peristaltic waves cannot extend beyond this zone of de-nervation and bowel may become obstructed
38
Q

what is the most common cause of lower bowel obstruction in neonates? is it more prevalent in males or females

A
  • Hirschsprung’s disease
  • M>F 3:1
39
Q

clinical presentation

  • 80% present within first 6 weeks of life
  • 20% develop enterocolitis
    • fever, vomiting, explosive diarrhea
  • newborns fail to pass meconium within 48-72 hr
  • bilious vomiting, abd distension
A

Hirschsprung’s disease

40
Q

older children with Hirschsprung’s disease may present with

A
  • chronic constipation
  • failure to thrive
  • *later diagnosis -> less severe disease : smaller segment of colon affected
41
Q

physical exam

  • abd distension
  • anal canal may feel narrow on rectal exam
  • anal canal and rectum devoid of fecal material​
  • explosive release of gas/stool when finger removed = “squirt” or “blast” sign
A

Hirschsprung’s disease

42
Q

how is Hirschsprung’s disease diagnosed

A
  • rectal biopsy is gold standard
43
Q

managment of Hirschsprung’s disease

A
  1. resection of aganglionic segment
  2. colostomy
  3. colorectal anastomosis performed later
  • over prognosis is good
44
Q

inflammatory bowel disease consists of what two conditions

A
  • Crohn’s disease
  • ulcerative colitis
45
Q

inflammatory bowel disease is most prevalent in what patient population and age group

A
  • peak incidence: 10-25 yo
  • 20-30% present before age 20
  • whites > african americans > hispanics
46
Q

smoking has what effect on risk for inflammatory bowel disease

A
  • doubles risk of crohn’s disease
  • halves risk for ulcerative colitis
47
Q

clinical presentation

  • diarrhea, abd pain, +/- hematochezia
  • weight loss
  • growth failure
  • arthritis, sacroileitis, uveitis, anemia
A

inflammatory bowel disease

48
Q

Crohn’s disease affects what part of intenstine

A
  • transmural inflammation
    • can occur from mouth to anus
    • ileum most commonly affects
49
Q

colonoscopy that reveals skip lesions and cobblestone appearance is indicative of

A

Crohn’s disease

50
Q

ulcerative colitis affects what part of intestine

A
  • involvement of rectum and large colon
    • mucosal layer only
  • starts from rectum and extends proximally
51
Q

colonoscopy that reveals erythematous and friable mucosa with small erosions is consistent with

A

ulcerative colitis

52
Q

ulcerative colitis greater than 10 years puts a person at a high risk for

A

colon CA

53
Q

treatment of inflammatory bowel disease

A
  • 5-ASA (sulfasalazine)
  • immunomodulating agents (6-MP)
  • biologics (remicade)
  • steroids
    • used during flares
54
Q

what is the definition of diarrhea

A

> 3 loose watery stools/day

55
Q

diarrhea that is diet related can be due to what

A
  • toddler’s diarrhea: fruit juice
  • cow’s mil/soy protein enteropathy
56
Q

what are the red flags to look for when a patient complains of diarrhea

A
  • fever
  • severe abd pain
  • blood in stool
  • vomiting
  • dehydration
  • leukocytosis
  • persistent symptoms
  • growth and development affected
57
Q

evaluation and management of diarrhea

A
  1. focus on hydration
  2. pursue further if red flags
    • labs
    • stool cx
58
Q

functional diarrhea has a high prevelance at what age

A
  • 5-6 yo
  • functional: no anatomical biochemical abnormality
    • voluntary withholding of stool
  • often at times of change
    • intro to solid foods
    • toilet training
    • start of school
59
Q

encopresis

A

stool incontinence

60
Q

differential diagnosis for constipation

A
  • Hirschsprung
  • neuropathic disorders (spina bifida)
  • hypothyroidism
  • cystic fibrosis
  • medications
  • psychological
61
Q

managment for constipation

A
  • decrease cow milk intake
  • if encopresis -> releive impaction (polyethylene glycol)
  • laxative therapy
62
Q

clinical jaudice is defined at what level

A

biliruben greater than 3 mg/dl

63
Q

neonatal jaundice

A
  • elevation of indirect biliruben
64
Q

breast milk jaundice

A
  • benign
  • appears in breast fed infants - 1st week of life
  • inhibition of conjugation of biliruben -> increase in indirect biliruben
  • resolves spontaneously
  • may be contributed to Gilbert’s syndrome
65
Q

what is pathological jaundice defined as

A
  • hyperbilirubinemia that requires intervention
  1. clinical jaundice appearing in first 24 hours
  2. clinical greater than 14 days of life (in term infant)
  3. total bili higher than 95% on nomogram
66
Q

what are the causes of < 24 hours pathological jaundice

A
  1. severe hemolysis
    • ABO incompability
    • Rh iso-immunisation
    • sepsis
67
Q

coombs test

A

detect antibodies on the baby’s red cells

68
Q

biliary atresia

A
  • rare disease that destroys bile ducts, resulting in obstruction to bile flow which damages liver
69
Q

clinical presentation

  • jaundice
  • dark urine
  • light stools
A

post hepatic jaundice- biliary atresia

pediatrics II (4 decks)

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