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Peds Patho > GI > Flashcards

GI Flashcards

killin it!!

1
Q

gastroesophageal reflux

A

frequent postprandial regurgitation, ranging from effortless to forceful

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2
Q

most common infant symptom of gastroesophageal reflux

A

frequent postprandial regurgitation

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3
Q

what normal factors promote gastroesophageal reflux in infants?

A
  • -small stomach capacity
  • -frequent large-volume feedings
  • -short esophageal length
  • -supine positioning
  • -slow swallowing response to the flow of refluxed material up the esophagus
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4
Q

should GE reflux contain bile?

A

NO! bile may be sx of intestinal obstruction

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5
Q

2 types of intestinal obstruction seen in infants

A

1) malrotation w/volvulus

2) intussussception

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6
Q

classic sign of Sandifer Syndrome

A

neck contortions

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7
Q

GERD

A

GE reflux disease, that causes:

  • -failure to thrive
  • -food refusal
  • -colic
  • -rumination
  • -neck contortions
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8
Q

apneic spells especially occur when?

A

with position change after feeding

may be caused by GERD

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9
Q

when is GERD diagnosed?

A

when reflux causes persistent sx w/ or w/out inflammation of the esophagus

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10
Q

older children w/GERD may complain of:

A

adult-type sx:

  • -regurgitation into the mouth
  • -heartburn
  • -dysphagia
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11
Q

why does esophagitis occur?

A

can occur as a complication of GERD

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12
Q

how do you diagnose esophagitis?

A

requires endoscopy for diagnostic confirmation

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13
Q

what kids are at increased risk of GERD & esophagitis?

A

children w/:

asthma, cystic fibrosis, developmental handicaps, hiatal hernia, repaired tracheoesophageal fistula

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14
Q

what meds can we use in older children w/heartburn?

A

a trial of acid-suppressing medication

–can be both diagnostic & therapeutic

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15
Q

when does reflux usually resolve in infants? in what percentage of infants does it resolve?

A

by 12 mos of age in 85% of infants w/reflux

coincident w/assumption of erect posture & initiation of solid feedings

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16
Q

until reflux resolves, how can it be reduced?

A
  • -by offering small feedings at frequent intervals

- -by thickening feedings w/rice cereal (2-3 tsp/oz of formula)

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17
Q

do H2-receptor antagonists or proton pump inhibitors reduce the frequency of reflux?

A

no– but they may reduce pain

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18
Q

does GERD spontaneously resolve in older children?

A

less likely

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19
Q

how can we control pain from episodic heartburn in older children?

A

intermittent use of acid blockers

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20
Q

patients w/severe heartburn or esophagitis require:

A

chronic acid suppression

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21
Q

untreated GERD esophagitis may lead to:

A
  • -feeding dysfunction
  • -esophageal stricture
  • -anemia
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22
Q

Barrett esophagus

A
  • -rare in children
  • -precancerous condition
  • -can occur in pts w/v. long-standing esophagitis
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23
Q

3 types of disorders of the esophagus

A

1) Esophagitis
2) Stricture
3) Barrett’s

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24
Q

when will you see the esophagus sprinkled with pinpoint white exudates?

A

eosinophilic esophagitis

superficially resembles Candida

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25
Q

3 common features of eosinophilic esophagitis:

A

1) thickening
2) longitudinal muscle fibers
3) circumferential mucosal rings

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26
Q

on microscopic exam, what are the pinpoint spots seen in eosinophilic esophagitis made of?

A

they’re composed of eosinophils

basal cell layers of the esophageal mucosa are hypertrophied & infiltrated by eosinophils

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27
Q

eosinophilic esophagitis is also known as:

A

allergic esophagitis

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28
Q

eosinophilic esophagitis involves what type of reaction?

A

Type 1 hypersensitivity reaction:

antigens illicit an IgE-mediated allergic reaction causing infiltration of eosinophils

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29
Q

eosinophilic esophagitis is associated w/what conditions?

A
  • -esophageal strictures
  • -food impaction
  • -dysphagia
  • -heartburn
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30
Q

tx for eosinophilic esophagitis?

A

1) nutritional exclusion of offending allergens
- -> elemental diet, removal of allergenic foods
2) topical corticosteroids

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31
Q

how are corticosteroids delivered in tx for eosinophilic esophagitis?

A

puffed in the mouth & swallowed from a metered dose pulmonary inhaler

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32
Q

eosinophilic esophagitis most frequently occurs in…?

A

boys, of all ages

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33
Q

common initial sx of eosinophilic esophagitis in young children?

A

feeding dysfunction

vague nonspecific sx of GERD: abdom. pain, vomiting, regurgitation

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34
Q

what disease results from an esophageal motility disorder?

A

achalasia of the esophagus

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35
Q

what happens to motility in achalasia of the esophagus?

A

failure of smooth muscle fibers of the esophagus & LES to relax
–> results in increased LES tone & lack of peristalsis of the esophagus

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36
Q

what causes increased LES tone and lack of peristalsis seen w/achalasia of the esophagus?

A

failure of the smooth muscle fibers of esophagus & LES to relax

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37
Q

achalasia of the esophagus is characterized by:

A
  • -difficulty swallowing
  • -regurgitation
  • -sometimes: chest pain
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38
Q

when reflux/regurg causes FTT, colic, it is referred to as:

A

GERD

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39
Q

why does GERD resolve on its own as kid gets older?

A
  • -assumes more upright position

- -consumes solid food

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40
Q

if vomit contains bile, this indicates:

A

regurg. is coming from the intestines

- -> could be intestinal obstruction!

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41
Q

how do you r/o Barrett’s?

A

requires endoscopy

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42
Q

Barrett’s Esophagus

A

pre-cancerous metaplasia of mucosal cells lining the esophagus
–> simple squamous cells are replaced w/columnar cells interspersed w/Goblet cells
( creates mucosal lining more similar to what you’d see in the stomach)

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43
Q

why does metaplasia occur w/Barrett’s?

A

is an adaptive process d/t prolonged acid exposure

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44
Q

why is metaplasia w/Barrett’s worrisome?

A

bc metaplasia can –> dysplasia!

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45
Q

what is normal esophageal tissue composed of?

A

simple squamous epithelial cells:

flat, epithelial tissue

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46
Q

is Barrett’s esophagus common?

A

no! is relatively rare in children w/GERD

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47
Q

ultimately, what sx will you see w/eosinophilic esophagitis?

A

discomfort similar to heartburn, d/t inflammation

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48
Q

achalasia especially affects…?

A

the lower esophageal sphincter

(v. high muscle tone, fails to relax properly
- -> regurg, chest pain)

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49
Q

achalasia most commonly occurs in:

A

children older than 5

but cases in infancy have been reported

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50
Q

most common presenting sx of achalasia:

A

–dysphagia, postprandial vomiting, retrosternal pain, early satiety, wt. loss, solid food impaction

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51
Q

postprandial

A

post-meal

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52
Q

why does vomiting occur w/achalasia?

A
  • -pt eats slowly & requires lots of fluid when ingesting solid food
  • -> dysphagia is relieved by repeated forceful swallowing or vomiting
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53
Q

familial cases of achalasia may occur w/?

A

1) Allgrove syndrome

2) familial dysautonomia

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54
Q

Allgrove syndrome is characterized by?

A
  • -alacrima
  • -adrenal insufficiency
  • -achalasia
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55
Q

cause of Allgrove syndrome?

A

–is assoc. w/defect in AAAS gene on 12q13

codes for ALADIN protein

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56
Q

are mast cells involved w/pathogenesis of achalasia?

A

yes, perhaps! recent study showed electron micrographic evidence of mast cells in close proximity to nerve fibers

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57
Q

common sx of achalasia?

A

–chronic cough, wheezing, recurrent aspiration pneumonitis, anemia, poor wt. gain

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58
Q

stricture seen where w/achalasia?

A

esp. in LES

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59
Q

above area of LES stricture, what do we see w/achalasia?

A

above that, esophageal tube tends to dilate d/t build-up of pressure
–> see tapered beak appearance of dilated tube at the gastroesophageal junction

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60
Q

where does trapping of food tend to happen w/achalasia?

A

right above LES, in dilated tube

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61
Q

how can we treat achalasia?

A

1) botulinum toxin (Botox) can be used to try to force muscle to relax (paralyzes LES & temporarily relieves obstruction)
2) endoscopy can be used to stretch open LES
3) surgical techniques to try to relax the muscle

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62
Q

is prognosis good w/achalasia tx?

A

recurrence rates of stricture are high w/all tx’s

–> prognosis better if tx’d at younger age

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63
Q

where do you see tapered beak w/achalasia?

A

at gastroesophageal junction

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64
Q

w/achalasia, will you see esophageal dilation in infants?

A

maybe not, bc of the short duration of distal obstruction

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65
Q

relapse rates of botox tx for achalasia?

A

greater than 50%

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66
Q

how long does pneumatic dilation of LES provide relief of achalasia?

A

may last weeks to years

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67
Q

how does surgery w/achalasia work?

A

by surgically dividing the LES (Heller myotomy)

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68
Q

recurrence rates of obstructive sx w/myotomy tx for achalasia?

A

as high as 27%

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69
Q

is prognosis for return/retention of normal esophageal motor function after achalasia surgery better for adults or children?

A

children have better prognosis bc there is less secondary dilation of the esophagus
(–> d/t the shorter duration of esophageal obstruction)

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70
Q

hiatal hernia

A

the protrusion (or herniation) of the upper part of the stomach into the thoracic cavity through a tear or weakness in the diaphragm

71
Q

3 basic types of hiatal hernias:

A

1) paraesophageal hernia
2) sliding hiatal hernias
3) combination of 1 & 2

72
Q

paraesophageal hiatal hernia

A

the esophagus & gastroesophageal (GE) junction are in their normal anatomic position, but the gastric cardia is herniated through the diaphragmatic hiatus alongside the GE junction

73
Q

what part of the stomach is usually herniated with a paraesophageal hiatal hernia?

A

the fundus

a portion of the stomach just past the LES gets through

74
Q

most common type of hiatal hernia?

A

sliding hiatal hernia

often complication of a procedure, e.g. Nissen fundoplication

75
Q

sliding hiatal hernia

A

the GE junction & a portion of the proximal stomach are displaced above the diaphragmatic hiatus

76
Q

what happens w/a sliding hiatal hernia?

A

slides up:
creates a sucking pressure moving acid from the stomach to the esophagus
–> v. difficult to treat GERD w/hiatal hernias!

77
Q

are congenital paraesophageal hernias common in childhood?

A

no! rare

78
Q

how would a pt. w/paraesophageal hernia present?

A

–recurrent pulmonary infections, vomiting, anemia, FTT, dysphagia

79
Q

most common cause of paraesophageal hernia?

A

previous fundoplication surgery

80
Q

how to make dx of paraesophageal hernia?

A

typically w/an upper GI series or a CT scan of chest & abdomen

81
Q

sx of sliding hiatal hernias?

A

usually no sx!

may see GE reflux

82
Q

when is fundoplication indicated w/hiatal hernias?

A

if paraesophageal or sliding hiatal hernias produce persistent sx
(but, presence of a preop hiatal hernia triples the risk of recurrent GERD following fundoplication)

83
Q

what is a fundoplication?

A

fundus taken & wrapped around esophagus

  • -> reinforces the tension
  • -> done on pts w/persistent GERD, to reinforce the LES
  • -> not too complicated, us. done endoscopically
84
Q

long-term results of fundoplication?

A

by 10 years or so, us. undo themselves

–> sliding hiatal hernia as complication

85
Q

sliding hiatal hernias are often assoc. w/?

A

gastroesophageal reflux

–> esp. in developmentally delayed children!

86
Q

is medical tx for hernias directed at the hernia?

A

no–tx is directed at the reflux

unless failure of tx prompts correction of the hernia at the time of fundoplication

87
Q

pyloric stenosis: pathology

A
  • -narrowing of the opening from the stomach to the duodenum

- -d/t hypertrophy of the pyloric sphincter

88
Q

common sx w/pyloric stenosis?

A

causes severe projectile, non-bilious vomiting

89
Q

when does pyloric stenosis occur?

A

most often occurs in the first few mos. of life

90
Q

how can you palpate the pyloric sphincter hypertrophy that occurs with pyloric stenosis?

A

classically felt as an olive-shaped mass (5-15mm) in the middle upper part or the right upper quadrant of the abdomen
–esp. felt after vomiting/eating: when muscle tone is highest
(but only present in 13.6% of pts!)

91
Q

where is the pyloric sphincter located?

A

at the junction of the stomach & the duodenum

92
Q

what does bilious emesis indicate?

A

that it is coming from the intestine

93
Q

pyloric stenosis is what type of d/o?

A

congenital disorder

94
Q

what happens in children born w/pyloric stenosis?

A

significant hypertrophy of the pyloric sphincter

–> it stays v. tightly closed & allows little, if any, stomach contents into the duodenum

95
Q

cause of postnatal pyloric muscular hypertrophy?

A

unknown

96
Q

why does pyloric stenosis become more obvious as time goes on?

A

muscle tone along the GI tract is fairly low @ birth

–> as it increases, stenosis becomes more and more obvious

97
Q

incidence of pyloric stenosis?

A

1-8 per 1000 births

98
Q

who is more likely to have pyloric stenosis?

A

males, 4:1

99
Q

is pyloric stenosis r/t family history?

A

yes: 13% of pts have a positive family hx

100
Q

drug related to pyloric stenosis?

A

erythromycin in neonatal period is assoc. w/a higher rate of pyloric stenosis in infants < 30 days

101
Q

mean age at dx for pyloric stenosis?

A

43.1 days

102
Q

when does projectile vomiting w/pyloric stenosis usually begin?

A

b/t 2-4 weeks of age

but may start as late as 12 weeks

103
Q

how often does vomiting start at birth w/pyloric stenosis?

A

10% of cases

104
Q

when may you see onset of sx delayed in pyloric stenosis?

A

sx may be delayed in preterm infants

105
Q

is vomitus from pyloric stenosis bilious?

A

no (rarely), but may be blood-streaked

106
Q

what sx will an infant w/pyloric stenosis have?

A
  • -frantically nursing bc food not getting through–can’t absorb those calories
  • -st constipation, wt. loss, fretful, dehydrated
  • -finally –> apathy
107
Q

signs of infant w/pyloric stenosis?

A
  • -upper abdomen may be distended after feeding

- -prominent peristaltic waves from left to right may be seen

108
Q

classic metabolic findings of pyloric stenosis?

A

hypochloremic alkalosis w/potassium depletion
(but: low chloride in as few as 23%
alkalosis in as few as 14.4%

109
Q

dehydration in infants w/pyloric stenosis causes:

A

elevated hemoglobin & hematocrit

110
Q

other complication of pyloric stenosis?

A

mild unconjugated bilirubinemia seen in 2-5% of cases

111
Q

how do you dx pyloric stenosis?

A

barium GI upper series: see retention of contrast in the stomach & a long narrow pyloric channel w/a double track of barium

112
Q

tx of choice for pyloric stenosis?

A

Ramstedt pyloromyotomy:
incision down to the mucosa along the pyloric length
(*MUST treat dehydration/electrolyte imbalance before surgical tx–even if it takes 24-48 hrs)

113
Q

outlook after pyloric stenosis surgery?

A

excellent!

although–pts may show as much as 4 times greater risk for development of chronic abdominal pain of childhood

114
Q

peptic ulcers

A
  • -gastric & duodenal ulcers

- -consist of defects or breaks along the mucosal lining of the stomach & duodenum

115
Q

where in the stomach lining do peptic ulcers usually occur?

A

usually in the antrum, where most HCl is produced

116
Q

when do peptic ulcers usually occur?

A

at any age!

boys more than girls

117
Q

what are most gastric/duodenal ulcers assoc. w/in the US?

A

underlying illness (esp. traumatic injury), toxins, or drugs that cause breakdown in mucosal defenses

118
Q

what happens when there is a break in the mucosal lining of stomach/duodenum?

A

opens up trapped wall to autodigestion: acid & digestive enzymes begin to eat away at wall of stomach/duodenum

119
Q

most common cause of gastric & duodenal ulcer worldwide?

A

infection of gastric mucosa w/ Helicobacter pylori (H pylori)

120
Q

how does H pylori cause ulcers?

A

produces an endotoxin that triggers inflammation

  • -> irritates mucosal lining
  • -> can cause ulceration on its own or w/physiological stress causes
121
Q

h pylori infection causes:

A

1) nodular gastritis

2) duodenal or gastric ulcer

122
Q

long-standing h pylori infection is assoc. w/:

A
  • -gastric lymphoid tumors

- -adenocarcinoma

123
Q

what %age of N. Amer. children have antibodies against h pylori?

A

10-20%

in some developing countries, over 90% of schoolchildren have serologic evidence of past or present infection

124
Q

antibody prevalence of h pylori increases w/:

A

age, poor sanitation, crowded living conditions, family exposure

125
Q

how are non-H. pylori ulcers diff. from h. pylori ulcers?

A
  • -occur as frequently in girls as in boys
  • -present at a younger age
  • -are more likely to recur
126
Q

endoscopy has shown what in regards to ulcers & etiology?

A

5.4% of 1000 children had ulcers:
47% d/t h. pylori
16.5% r/t NSAIDs
35.8% unrelated to either h. pylori or NSAIDs

127
Q

illnesses predisposing to secondary ulcers:

A

–CNS disease, burns, sepsis, multiorgan system failure, chronic lung disease, Crohn disease, cirrhosis, rheumatoid arthritis

128
Q

most common drugs causing secondary ulcers:

A

aspirin, alcohol, NSAIDs

129
Q

severe ulcerative lesions in full-term neonates are assoc. w/:

A

maternal antacid use in the last month of pregnancy

130
Q

what can happen when ulcers become v. deep?

A
  • -> penetrates through muscle completely
  • -> perforates the organ
  • -> perforating ulcers run high risk of peritonitis
131
Q

s&s of ulcers in children < 6 yrs?

A
  • -vomiting

- -GI bleeding

132
Q

older children s&s of ulcers?

A

abdominal pain

133
Q

how can ulcers cause anemia?

A

chronic blood loss may –> iron-deficiency anemia

deep penetration of ulcer may erode into a mucosal arteriole–> cause acute hemorrhage

134
Q

when are you more likely to see penetrating duodenal ulcers?

A

during cancer chemo, immunosuppression, & in ICU

–> can perforate deodenal wall, causing peritonitis or abscess

135
Q

most accurate diagnostic exam for ulcers?

A

upper GI endoscopy

also allows for ID of other causes of peptic sx: esophagitis, eosinophilic enteropathy, celiac disease

136
Q

mainstay of ulcer tx?

A

acid suppression or neutralization:
–H2-receptor antagonists & proton-pump inhibitors usually cause healing in 4-8 weeks
(**liquid antacids in volumes needed to neutralize gastric acid are us. unacceptable to children!)

137
Q

tx of h pylori infection?

A

eradication of organism

spontaneous clearance of infection may occur

138
Q

when should we see healing w/use of H2-receptor antagonists & proton pump inhibitors in tx of ulcers?

A

4-8 weeks

139
Q

what is a risk of chronic use of NSAIDs?

A

increased risk of ulcers

140
Q

intestinal atresia

A

congenital malformation where there is a absence of a portion of either the large or small intestine

141
Q

intestinal stenosis

A

congenital malformation where there is a narrowing of a portion of either the large or small intestine

142
Q

atresia

A

absence/failure to develop

143
Q

stenosis

A

narrowing

144
Q

what else will you see w/intestinal atresia & stenosis?

A

about half the time (54%), there is also another congenital defect
–> esp. heart defects (30% w/atresia)

145
Q

what is an impt. cause of intestinal obstruction, that must be treated surgically right away?

A

intestinal atresia/stenosis

146
Q

what accounts for 1/3 of all causes of neonatal intestinal obstruction?

A

intestinal atresia/stenosis

147
Q

how can you dx intestinal stenosis?

A

can st see in utero (antenatal ultrasound): polyhydramnios, bc fetus is constantly swallowing & vomiting amniotic fluid

148
Q

polyhydramnios

A

excess of amniotic fluid in the amniotic sac

149
Q

are babies w/intestinal atresia usually preemies?

A

52% are delivered preterm

150
Q

which has a worse prognosis: jejunal or ileal atresias?

A

jejunal atresias have a much less favorable prognosis than ileal atresias:
when atresias happen in the jejunum, they’re more likely to have a severe dilation above that level, & loss of peristaltic activity
–> needs surg. intervention v. quickly!

151
Q

w/intestinal atresia/stenosis, what will you see w/in first 48 hrs of life?

A
  • -bile-stained vomiting

- -abdominal distention

152
Q

why will you see bile-stained vomiting & abdominal distention w/intestinal atresia/stenosis?

A

multiple sites in the intestine may be affected

–overall length of the sm. intestine may be significantly shortened

153
Q

what will we see on radiograph w/intestinal atresia/stenosis?

A
  • -dilated loops of sm. bowel

- -absence of colonic gas

154
Q

intussusception

A

part of the intestine has invaginated into another section of the intestine (telescope-like collapse)

155
Q

is intussusception a malformation?

A

no! is not congenital or a malformation

–> is a complication of something else

156
Q

most frequent cause of intestinal obstruction in the first 2 years of life?

A

intussusception

157
Q

intussusception is most common in…?

A

females (3x more common)

158
Q

what is cause of intussusception?

A

in 85% of cases, cause is not apparent

159
Q

possible causes of intussusception?

A
  • -small bowel polyp
  • -Meckel diverticulum
  • -omphalomesenteric remnant
  • -duplication
  • -Henoch-Schonlein purpura
  • -lymphoma
  • -lipoma
  • -parasites
  • -foreign bodies
  • -viral enteritis w/hypertrophy of Peyer patches
160
Q

w/what other diseases can you see intussusception?

A

w/celiac disease & cystic fibrosis

–> r/t the bulk of the stool in the terminal ileum

161
Q

most common cause of intussusception in children older than 6?

A

lymphoma

162
Q

can intussusception cause intermittent abdominal pain?

A

yes, but rarely

intermitterent small bowel intussusception is a rare cause of recurrent abdominal pain

163
Q

how does intussusception manifest in its usual form?

A

it starts just proximal to the ileocecal valve & extends varying distances into the colon
–> the terminal ileum telescopes into the colon

164
Q

ileocecal valve

A

small tube leading into a larger tube

anything causing pressure can cause a telescoping effect

165
Q

what may occur w/intussusception?

A
  • -swelling, hemorrhage, incarceration, vascular compromise, & necrosis of the intussuscepted ileum may occur
    (also: intestinal perforation & peritonitis)
166
Q

clinical findings of intussusception?

A

infant is thriving from 3-5 mos: then all of a sudden develops abdom. pain
(w/screaming & drawing up the knees)
–vomiting & diarrhea may occur soon after (90% of cases)
–bloody bm’s w/mucus appear w/in next 12 hrs (50%)
–child: lethargic, may be febrile, tender/distended abdomen
–st can palpate sausage-like mass in upper abdomen

167
Q

paroxysm

A

sudden fit/attack/worsening of sx

168
Q

in older children, sudden attacks of abdom. pain may be r/t…?

A

chronic recurrent intussusception

169
Q

can intussusception persist for several days?

A

yes: if obstruction is not complete

- -pts may present w/intermittent attacks of enterocolitis

170
Q

what combination of s/s has a sensitivity of 95% in identifying intussusception in children?

A

–abdom. pain, lethargy, vomiting, & a suspicious abdom. radiograph

171
Q

can you use an abdominal ultrasound to dx intussusception?

A

can be used as an initial screening study

172
Q

use of barium & air enema for intussusception?

A

both diagnostic & therapeutic

173
Q

prognosis for intussusception?

A

relates directly to the duration of the intussusception before reduction
–> if sx duration was > 24 hrs, successful reduction by enema decreased from 59% to 36%

Peds Patho (8 decks)

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