peds GI Flashcards

1
Q

Non-bilious projectile vomiting, dehydration, poor weight gain, afebrile – often looking ill with hypochloremic metabolic alkalosis and Exam may reveal “olive” (thick pylorus)

A

hypertrophic pyloric stenosis

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2
Q

hypertrophic pyloric stenosis

A

pyloric channel thickening that leads to gastric outlet obstruction. this causes vomiting and witht he loss of HCl leads to hypocholremic alkalosis with eventual hypokalemia

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3
Q

treatment of hypertrophic pyloric stenosis

A

srugical- pyloromyotomy to relieve tightening

  • prognosis is excellent
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4
Q

intussusception

A

proximal segment of bowel telescopes into the distal portion bringing the mesentary with it causing venous and lymphatic congestion leading to edema, ischemia and perforation

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5
Q

difference between adults and children with intussusception

A

addults have a leading point

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6
Q

“Classic” case = male under 10 months old

  • intermittent abdominal pain
    vomiting
    “currant jelly stool”-LATE finding!!
  • may reveal palpable mass in right mid-abdomen (“palpable sausage”)
A

intussusception

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7
Q

“doughnut” with hyperechoic mesenteric fat with vessels/nodes inside intussusception

A

intussusception

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8
Q

classic diagnosis for intussusception and treatment

A

therapeutic enema:

  1. Air (pneumatic) reduction = most popular, cleaner, less risk if perforates
  2. Water-soluble contrast (hydrostatic) reduction= better than barium
    * Success 80-95% success with either

** surgery may be indicated

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9
Q

recurrence with intussusception

A

yepppp

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10
Q

constipation may be associated with hypothyroidism, celiac disease, electrolyte abnormalities, Hirschsprung’s disease, neurologic disease (cerebral palsy, spina bifida), others…

A

organic

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11
Q

common between 6 months and preschool
trigger may be dietary transition – breastmilk to formula, liquids to solids, new food – and possibly milk allergy (especially in infants)

A

Functional constipation is the most common reason – no evidence of any organic disorder

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12
Q

traumatic defecation, i do not want to poop

A

functional constipation

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13
Q

prognosis of functional constipation

A

typically problematic x years, relapses >50%

affected children may become adults with IBS

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14
Q

Aka: congenital aganglionic megacolon
Consistent with embryonic enteric neuronal plexus development…HD always involves the rectum and extends proximally to area
where cephalad caudad nerve development ends

A

Hirschsprung’s disease

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15
Q

hirschsprung’s disease

  1. arrest of
  2. affects both
  3. genetics
  4. Adults appearance
  5. delayed passage of
  6. treatment
A
  1. arrest of neural crest cell migration
  2. affects both meissner’s submucosal and auerbach’s myenteric plexuses
  3. half of familial cases and 15% sporadic related to mutation in RET proto-oncogene
  4. short-segment
  5. meconium
  6. surgical- removal of affected portion
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16
Q

hirschprung’s diease

A

affected colon loses ability to relax (NO and other por-relaxation peptides no effect) leading to narrowed, collapsed contracted distally but portion that is proximal is dilated normal

17
Q

Outpouching results from incomplete obliteration of vitelline (omphalomesenteric) duct – connecting the midgut to the yolk sac

A

Meckel’s diverticulum

THE most common congenital abnormality of the GI tract

18
Q

Meckel’s diverticulum layers

A

it is ocnsidered a true diverticulum containing all layers of the ileal wall

19
Q

Meckel’s diverticulum symptoms formation

A

the ectopic gastric mucosa within the diverticulum affects the parietal cells which secrete HCl which injures the neighboring tissue causing bleeding, abdominal pain and obstruction

20
Q

The Rule of Twos…

  • Occurs in 2% of population
  • M:F ratio of 2:1
  • Within 2 feet of the ileocecal valve
  • Can be 2 inches in length, 2cm wide
  • Complications typically occur at < 2 years old
  • Approx 2-4% develop complications
A

meckel’s diverticulum

21
Q

how is meckel’s diverticulum diagnosed

A

technetium-99m pertechnetate scan

22
Q

Omphalocele and Gastroschisis

A

congenital defects in the abdominal wall and both are usually identified prenetaly then surgical repair

23
Q

large central defect that involves the intestines, liver, and other organs are outside the abdomen in a sac

A

omphalocele

24
Q

smaller defect, NOT involving umbilicus, usually bit to the right, and NO sac, no liverassociated with intestinal atresia in 10%

A

gastroschisis

25
Q

bubbles of air in intestinal wall

A

necrotizing enterocolitis

**“pneumotosis intestinalis” = air within bowel wall. air may track up into portal venous system

26
Q

prevalence of necrotizing enterocolitis

A

common!!! 7% and has a mortality of 20-30%

27
Q

Typically presents within first 2 weeks, with onset of enteral feeding – abdominal distension, vital sign changes

A

consider Necrotizing enterocolitis !!!!!

28
Q

necrotizing enterocolitis factors

A

it may be involved with prematurity, microbial overgrowth, mucosal immaturity, vascular factors leading to infarction that causes transmural necrosis, hemorrhage, subserosal air increasing perforation risk

29
Q

prevention of necrotizing enterocolitis

A

getting infant closer to term gestation

30
Q

treatment of necrotizing enterocolitis

A
  • bowel rest/antibiotics

- surgery

31
Q

what occurs in 10-35% of all cases mostly colonic origin in necrotizing enterocolitis

A

strictures