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Module 5 (Pediatrics) > GI Dysfunctions in Newborn > Flashcards

GI Dysfunctions in Newborn Flashcards

1
Q

Distribution of ______ changes with growth

A

water

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2
Q

Water and electrolyte imbalances occur more frequently and more rapidly at what age?

A

infants and through early children

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3
Q

Do children adjust to these water distribution changes quick or slow?

A

less quickly

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4
Q

Total Water in the body

A

75% in term newborn
decrease to 45% in adolescents
Premature more than 75%

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5
Q

The amount of water ingested approximates what

A

urine to be excreted in 24 hours
I&O balance

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6
Q

Factors of fluid loss

A

Insensible fluid loss (perspirations, sweating, respirations, fluid in feces)
Increased Body surface area (
Basal metabolic rate
Kidney function
Fluid requirements

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7
Q

With body surface area, what do you need to remember with size of the patient?

A

The smaller the patient the greater the BSA
- the baby has more skin than body weight and dehydration can come on more quickly

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8
Q

Basal Metabolic Rate in children

A

higher to support cellular and tissue growth
** Any condition with the metabolism causes increased heat production and insensible water loss to increase in relation**
- rapid growth

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9
Q

The kidney function of a newborn

A

functionally immature at birth
inefficient in excreting waste products of metabolism
harder time to concentrate and dilute urine
- higher fluid requirements

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10
Q

Maintenance fluid requirements in a newborn have to include

A

water and electrolytes (balanced)

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11
Q

2/3 of insensible fluid loss is through

A

the skin (sweating)

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12
Q

1/3 of insensible fluid loss is through

A

respirations

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13
Q

Infants are more prone to

A

infections due to weakened immune system

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14
Q

What condition causes a large amount of insensible water loss to occur? and Why?

A

infection
fever and sweating (2/3 of insensible)
fever causes tachypnea (1/3 of insensible from respiration)

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15
Q

Isotonic Dehydration

A

water and electrolytes are decreased in balanced proportions

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16
Q

Isotonic dehydration sodium level

A

stays the same

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17
Q

Hypotonic dehydration sodium level

A

decrease of Na

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18
Q

Hypertonic dehydration sodium level

A

increase of Na

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19
Q

Water Intoxication Causes

A

water without electrolytes
increase serum sodium
worsen dehydration
consistent tap water enemas (GI is longer)
- absorb more water
Incorrect formula balance
- little powder and more water
Hypotonic IVF admin - less solute and more water

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20
Q

Dehydration Causes

A

the infection affects the water loss
incorrect mixing formula (too much powder and little water)

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21
Q

Hypotonic Dehydration

A

electrolyte deficit exceeds the water deficit

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22
Q

Hypertonic Dehydration

A

water loss in excess of electrolyte loss

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23
Q

What is the most important determinant of total body fluid loss in infants & young children?

A

Daily weights
- goes up = retaining
- goes down = dehydration
same scale, time, and nude

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24
Q

What is the earliest detectable sign of dehydration?

A

tachycardia

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25
Q

Compensatory mechanisms

A

heart is bounding
overtime till it stops
pulse ox low (blood towards vital organs)

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26
Q

S/S of dehydration

A

lethargic
dark urine
dry mucous membranes
skin turgor slow
no tears
reduce cap
fast hr
decrease sunken fontanels
cool extremities
low pulse Ox

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27
Q

When should you be concerned about a pedi pt changing weight

A

day or 2 different
trends

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28
Q

A very late sign of dehydration is

A

drop in BP (heart is overworked)

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29
Q

Tx for severe isotonic and hypotonic dehydration

A

initial IV therapy of rapid fluid replacement
Bolus or 2

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30
Q

Tx of hypertonic dehydration

A

slow infusion of IV fluids

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31
Q

Why do you not do a rapid infusion of IVF on a hypertonic dehydration patient?

A

rapid may lead to cerebral edema (central pontine myelinolysis)

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32
Q

Mild to Moderate Dehydration starts with rehydration methods

A

Enteral (PO) - pedilyte
Oral replacement therapy over 4-6 hours
= replacement of continuing losses
= Provide least minimum fluid replacements

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33
Q

Severe Dehydration starts with rehydration methods

A

Parenteral (IV)
unable to keep fluid and electrolytes down
- meet daily physiological needs
- replace previous deficits
- replace ongoing abnormal losses

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34
Q

How do we know if rehydration methods are working on a pedi pt?

A

urine output is meeting the minimum acceptable urine output

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35
Q

Acute diarrhea

A

self-limiting
less than 14 days
viral infections

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36
Q

Chronic diarrhea

A

more than 14 days
cause is usually chronic (IBD; lactose intolerance)

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37
Q

If children are having intense and long periods of diarrhea, what should the main interventions be?

A

dehydration - replenish fluids
return to normal diet (better nutrients regardless of increase stool output)

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38
Q

Rotavirus is known as the

A

c.diff of the infant

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39
Q

What is the most common cause of acute diarrhea in children less than 5 y/o?

A

rotavirus

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40
Q

Rotavirus is more severe in infants less than

A

6 months

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41
Q

Immunization of Rotavirus is taken by

A

mouth

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42
Q

Transmission of Rotavirus

A

fecal-oral route
person-to-person

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43
Q

S/S of Rotavirus

A

Fever
Vomiting
Watery diarrhea (severely dehydrating)
distinct foul smell
2-7 days of diarrhea

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44
Q

Infection of the rotavirus does not mean

A

immunity just less severe

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45
Q

Nursing Teachings of Severe Diarrhea

A

handwashing
diapers need to be changed more frequently and disposed of properly
Do not give antidiarrheal medications because the virus is expelled through the diarrhea and just keeping it inside them prolongs the virus
no fruit juices, no sugar or carbonation
no Na

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46
Q

Good forms of fluid replacement for diarrhea

A

Pedialyte
no fruit juices, no sugar or carbonation
no Na

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47
Q

Constipation

A

decrease in bowel movement frequency or trouble defecating for more than 2 weeks

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48
Q

Reasons of constipation

A

failing to pass meconium
hypothyroidism
Hirshsprung Disease
imperforated anus
stricture or anal fissures
stress and school

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49
Q

Strictures

A

the small opening of the rectum in which the bowel mvmt can not pass

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50
Q

Anal fissures

A

tears in the rectum

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51
Q

Who has a higher stool output (frequency) breastfeed or formula feed

A

Breastfed
- educate if a change in food to formula and whole milk

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52
Q

The majority of constipation issues can be addressed with

A

dietary modifications
- Cereals, veggies, and fruits increase fiber
- increase fluid intake
- no cheese

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53
Q

If constipation continues even with dietary modifications, then the pediatrician usually recommends

A

stool softeners

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54
Q

Hirschsprung aka

A

Congenital Aganglionic Megacolon

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55
Q

Hirschsprung is usually misdiagnosed

A

chronic constipation

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56
Q

What is Hirschsprung Disease?

A
  • anomaly results from mechanic obstruction from inadequate motility of the bowels caused by the absence of ganglion cells (nerve cells coordinate peristalsis)
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57
Q

Pathology of Hirschsprung

A

absence of ganglion cells
no peristalsis
loss of rectosphicteric reflex
stool accumulation
Megacolon
Intestinal ischemia may develop
Enterocolitis (damage to the mucosal cells lining the intestinal walls)
- decreases blood supply and leads to cell death

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58
Q

Enterocolitis

A

damage to the mucosal cells lining the intestinal walls
= decreases blood supply and leads to cell death

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59
Q

Diagnose Hirschsprung

A

Xray assists distended colon
Rectal Bx - looking for ganglion cells

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60
Q

Infants S/S of Hirschsprung

A

Failure to pass meconium
Abdominal distension
Feeding intolerance/Vomiting

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61
Q

Older children s/s of Hirschsprung

A

Constipation, diarrhea, and/or watery or ribbon-like
foul-smelling stools
Easily palpable stool mass

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62
Q

Tx of Hirschsprung

A

Hirschsprung’s Endorectal Pull-through

https://www.youtube.com/watch?v=9QjZe6zZpRA

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63
Q

Pre-Op Considerations for Endorectal Pull-Through

A

Nothing per Rectum
monitor stool output and abd girth,
IV and prophylactic antibiotics

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64
Q

Post-Op Considerations for Endorectal Pull-Through

A

IV and prophylactic antibiotics
Pain meds and activity

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65
Q

Gastroesophageal Reflux defincition

A

transfer of gastric contents into the esophagus

usually outgrow after 1 year

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66
Q

Reason for Gastroesophageal Reflux

A

diet is liquid as an infant but start eating solids at 4-6 months it decreases and usually outgrows after 1 year
- relaxed esophageal sphincter
- delayed gastric emptying

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67
Q

Diagnosis for Gastroesophageal Reflux

A

H&P mainly
Upper GI series (anatomic abnormalities)
24-hr intraesophageal monitoring
Endoscopy with biopsy (presence and severity of esophagitis)
Scintigraphy - gold standard (detect radioactive substances in the esophagus after feedings)

68
Q

Difference between Gastroesophageal Reflux and GERD

A

GERD is environmental overtime and chnage the cell lining
If only reflux as an infant = spit up and regurgitate much more

69
Q

Infants s/s of Gastroesophageal Reflux

A

Spitting up/vomiting
Irritability
Arching of back
Poor weight gain
Choking with feedings
Respiratory (aspirations)

70
Q

Child/Adolescent s/s of Gastroesophageal Reflux

A

Heartburn
Abdominal pain
Chronic cough/clearing
Dysphagia
Recurrent vomiting
trouble eating
Hx asthma - respiratory with aspiration pneumonia

71
Q

Tx for Gastroesophageal Reflux

A

H2 Antagonist (Ranitidine and famotidine)
Proton Pump Inhibitors (Esomeprazole (Nexium); lansoprazole (Prevacid); omepraxole (Prilosec); pantoprazole (Protonix))
Nissen Fundoplication surgery

72
Q

Foods to avoid with Gastroesophageal Reflux

A

citrus fruits
tomatoes
alcohol
peppermint
fried
spicy

73
Q

Infants with Gastroesophageal Reflux need

A

smaller but more frequent feedings
give iron-fortified cereal in formula
= makes it more difficult to suck through the nipple to get nutrients
breastfed - pump and give smaller and more frequent
special formulas
Positioning - elevate HOB, sit up in chair

74
Q

if after all interventions for Gastroesophageal Reflux the kid is still going down on wt and falling off track, then the doctor will Rx?

A

H2 Antagonist
Proton Pump Inhibitors

75
Q

H2 Antagonist

A

Suppresses the secretion of gastric acid by selectively blocking H2 receptors

76
Q

H2 Antagonist meds

A

Ranitidine (Zantac) and famotidine (Pepcid)

77
Q

Proton Pump Inhibitors (PPI)

A

Reduce gastric acid secretion

78
Q

Proton Pump Inhibitors (PPI) meds

A

Esomeprazole (Nexium); lansoprazole (Prevacid); omepraxole (Prilosec); pantoprazole (Protonix)

79
Q

Nissen Fundoplication is for what pts

A

severe complication of Reflux

80
Q

Nissen Fundoplication process

A

fundus of the stomach is placed behind the esophagus; encircles the distal esophagus
strengths the sphincter and prevent regurgitation

81
Q

Post-Op for Nissen Fundoplication

A

NG Tube (do not replace if pulled out)
- decompress stomach
Monitor for gastric distension

82
Q

Imperforate Anus

A

Absence of analopening
occurs during the development
fistula connection - stool passes through increases UTIs

83
Q

With an imperforated anus, what would happen

A

Inability to visualizerectal opening
No meconium is passed
Gradual abdominaldistention
May have fistula

84
Q

Imperforated anus is fixed with

A

surgery (Analplasty)
with Colostomy afterwards

85
Q

Appendicitis

A

Inflammation of the vermiform appendix caused by an obstruction of the lumen of the appendix or viral

86
Q

Appendicitis average age

A

12-18 y/o

87
Q

S/S of appendicitis

A

Pain starts in the middle of the abdomen and moves to RLQ (Mcburney’s point)
Rigid abdomen
Decreased/absent BS
Fever
Possible vomiting

88
Q

Where is McBurnery’s Point?

A

Midway point between the superior anterior iliac crest and ileus

89
Q

Dx of appendicitis

A

Ultrasound
CT scan
basic labs

90
Q

Tx of appendicitis

A

appendectomy
prophylactic antibiotics

91
Q

If the patient is suspected of having appendicitis and is in the pain stage, BUT now has no pain at all, what happened?

A

ruptured
then the pain gradually starts up again
start the central line and start strong antibiotics

92
Q

nursing care for appendicitis

A

child life
post-op: pain control and activity

93
Q

Biliary Atresia

A

progressive inflammatory process that results in intrahepatic & extrahepatic bile duct fibrosis, resulting in ductal obstruction
- bile trapped in liver
- causes damage and starring to cells in the liver
- untreated leads to liver failure and death within 1st 3 years of life

94
Q

S/S of biliary atresia

A

Jaundice persisting beyond 2 weeks of age
most common early sx
Putty-like white or gray stools
-the absence of fat
Tea colored urine - bilirubin and bile salts
Intense itching & irritability - cholesterol deposits and malabsorption of fat
Malnutrition leads to severe growth failure
- fall off growth chart

95
Q

The Bile duct of the Liver does what

A

bile ducts remove waste from the liver
carries salts to help the small intestine break down fat

96
Q

Dx of Biliary atresia

A

Abd Ultrasound - look at it
percutaneous liver biopsy (most useful) in true dx

Exploratory laparotomy or intraoperative cholangiogram

97
Q

Biliary atresia results if untreated

A

excessive cirrhosis of the liver
death of the hepatic cells by 3

98
Q

Tx of Biliary Atresia

A

Hepatoportoenterostomy (Kasai procedure)
- connect the liver to s. intestine goal to drain bile
- improves condition BUT not a cure
Liver Transplant
- Most still need
Nutitional support (formula vs. TPN)
- nutritional support with fat-soluble vitamins

99
Q

What is the only cure for Biliary atresia?

A

liver transplant

100
Q

Nursing Considerations of Biliary Atresia

A

emotional support - child life and religious
education with G and D
s/s of infection or liver failure

101
Q

Esophageal Atresia

A

failure of the esophagus from developing as a continuous passage

102
Q

TEF

A

Tracheoesophageal fistula
- failure of the trachea and esophagus to separate into 2 district structures

103
Q

T/F: EA can occur separately or with TEF.

A

True
mostly together

104
Q

Esophageal atresia cause

A

unknown, but is associated with:
- maternal polyhydramnios- too much amniotic fluid
- Midline anomalies (cardiac)
- VATER/VACTERL syndrome (50%)
- higher risk: low birth weight, preterm birth

105
Q

S/S of Esophageal Atresia

A

Excessive frothy mucus from nose and mouth
The 3 C’s:
- Coughing
- Choking
- Cyanosis
Apnea spells
Respiratory distress during feeds
Abdominal distension

106
Q

Dx of Esophageal Atresia

A

History & physicalassessment
Radiographicstudies todetermine:
- esophageal patency
- catheter till hits the wall
X-ray = Presence ofa blind pouch with gas in the stomach orsmall bowel indicates TEF

107
Q

If there is gas in the stomach this indicates a

A

TEF

108
Q

Pre-Op for Esophageal Atresia

A

Position baby to facilitate drainage
- supine with HOB up at 30
- suction out secretions

109
Q

Cleft Lip & Cleft Palate

A

Defects in cell migration failing the maxillary & premaxillary processes to merge between the 4th & 10th weeks of embryonic development
- incomplete closure of the lip and/or palate

110
Q

T/F: Cleft anomalies can occur by themselves or be associated with a syndrome.

A

True

111
Q

Cleft lip symmetry

A

asymmetrically
symetrically

112
Q

Cleft lip dx by

A

prenatally in ultrasound
around 13-14 weeks

113
Q

Cleft palate identified through

A

physical exam of the oral cavity after birth
partial or complete up the lip and to the nose

114
Q

Cleft deformities are a combination of factors

A

genetic
environmental
- exposure to alcohol, anticonvulsants, cigarettesmoke, retinoids, or steroids is associated with a higher rate of oralclefting
- folate deficiency

115
Q

Folate dose for mom

A

0.4 mg

116
Q

Immediate problems of clefts

A

the reaction of parents and family if unaware
feeding and sucking (breastfeeding will conform to the cleft but if formula then get special nipples)
- if the palate more challenging
- different positioning helps - upright with supported head

117
Q

Cleft Lip surgical repair

A

2-3 months
require rhinoplasty

118
Q

Cleft Palate repair

A

before 12 months for speech development
- 2nd surgery possible
- prosthetic mgmt in the meantime

119
Q

Post-Op of cleft repairs

A

No objects in mouth (protect suture site and no pressure on site)
NPO with NG tube
Elbow immobilizers
Resume feeding (7-10 days)
Pain control
Upright positioning

120
Q

Long-term considerations of Cleft repairs

A

Speech therapy
Dental
Hearing loss (otitis media)
Social/Academic

121
Q

Umbilical Hernia

A

Intestine protrudes through the abdominal wall at the umbilicus

122
Q

S/S of Umbilical Hernia

A

protrusion at umbilicus
- gets bigger when they cry or force out
- can poke in and out

123
Q

Tx of Umbilical Hernia

A

no treatment for small hernia
closes itself after 3-5 years old
surgical repair only after 5 or strangulation of tissue

124
Q

Omphalocele

A
  • Abdominal contents are herniatedthroughthe umbilicalcord
  • Exposed abdominal contents are covered by atranslucent two-layer membrane sac
125
Q

Dx of omphalocele and gastroschisis can often be made

A

prenatally at 14 weeks
delivered C section

126
Q

Omphalocele is usually associated with

A

Trisomy 14,18,21 or cardiac defects (syndromes)

127
Q

Tx of Omphalocele (small or large)

A

paint and wait
- sac is painted with antibiotic cream with zinc (skin cell production) and skin grows over the defect and is covered in sterile gauze
surgical reduction
- if small, put the organs back in

128
Q

Zinc stimulates

A

skin cell production

129
Q

Pre-Op of Omphalocele

A

Maintain thermoregulation
Protect defects from trauma or drying
warm, sterile, saline-soaked dressing
top dressing with a layer of sterile plastic wrap
NPO - NGT
IVF AND Antibiotics

130
Q

Post-Op of Omphalocele

A

Routine postop care
Pain management
NGT
IVF
Monitor the return of bowel function

131
Q

Gastroschisis

A

Abdominal contents herniated outside of the abdominal wall
- no covering membrane
the umbilical cord is intact

132
Q

Pre-Op Gastroschisis

A

Maintain thermoregulation
NPO, IVF, Antibiotics, NGT
Observation of exposed bowel
- supine
Prosthetic silo
allows a gradual return of intestines to the abdominal cavity over 5 – 10days, then closure of the abdomen

133
Q

Prosthetic Silo

A

allows a gradual return of intestines to the abdominal cavity over 5 – 10days, then closure of the abdomen
- squeeze the contents into the body slowly and then close up

134
Q

Post-Op of Prosthetic Silo

A

Routine postop care​
NGT​
Pain management​
Lower extremity pulses​ 0 vena cava compression
Return of bowel function​

https://youtu.be/Zo3cZH_7BRs

135
Q

Hypertrophic Pylori Stenosis

A

Narrowing of the pyloric canal producing outlet obstruction

136
Q

Hypertrophic Pylori Stenosis pathology

A
  • thickening of the pylorus muscle
  • elongation and narrowing of the pyloric channel
  • partial obstruction of the lumen
  • edema and inflammation eventually lead to complete obstruction
137
Q

S/S of Hypertrophic Pylori Stenosis

A

Olive-like mass in the upper abdomen
Vomiting after feedings
eventually projectile vomiting
Dehydration
Metabolic alkalosis
Growth failure

138
Q

Dx of Hypertrophic Pylori Stenosis

A

H&P - Ultrasound to confirm

139
Q

Tx of Hypertrophic Pylori Stenosis

A

Transpyloric tube
Pyloromyotomy
- longitudinal incision through the circular pylorus muscle to widen the opening to pressure let off

140
Q

Intussusception

A

Occurs when one segment of bowel telescopes into another segment

141
Q

Intussusception PATHO

A

segment of bowel telescopes into another
mesentery compressed and angled
lymphatic and venous obstruction
edema increase
Pressure within the area of intussusception increases
When the pressure equals the arterial pressure, arterial blood flow ceases
ischemia
pouring of mucous into the intestines

142
Q

Intussusception ages

A

3 months to 6 years

143
Q

Intussusception s/s

A

Acute, severe, intermittent abdominal pain
Tender, distended abdomen
Palpable mass in RUQ
Empty RLQ
Vomiting
Lethargy
Red, currant jelly-like stool

144
Q

Intussusception MGMT

A

Water-soluble contrast enema
air pressure
and carbon dioxide
Barium enema

145
Q

Surgical Interventions of Intussusception

A

Manual reduction
removal of dead tissue if needed

146
Q

Pre-Op and Post-Op

A

IV access and antibiotics
Pain control
abd distension
active bowel sounds
bowel mvmts

147
Q

Giardiasis is a

A

protozoa

148
Q

Giardiasis is ingested in how

A

cysts are ingested & eventually excreted in stool
- lives in the intestines and excreted out in feces

149
Q

Mode of transmission of giardiasis

A

person-to-person
improperly prepared infected food
contaminated water
animals

150
Q

Giardiasis can survive outside the body for how long

A

weeks or months

151
Q

Giardiasis s/s

A

Infants:
diarrhea
vomiting
not wanting to eat
Older:
abdominal cramps
foul-smelling greasy stools

152
Q

How to Dx parasites in stool

A

stool sample

153
Q

Tx Giardiasis

A

Flagyl
Metronidazole (Flagyl)
Tinidazole (Tindamax)

154
Q

Enterobiasis is also known as

A

Pinworms (small white roundworm)
most common in the US

155
Q

Enterobiasis transmission

A

hand-to-mouth inhalation of eggs
eggs hatch in the upper intestines
larvae migrate to the cecum
pregnant females migrate out to the anus to lay eggs at night

in daycares, schools

156
Q

S/S of Pinworms

A

intense itching
scratch butts

157
Q

Dx of pinworms

A

Tape Test
- before getting out of bed parent places tape on anus
- 2-3 days for collection and place in jar

158
Q

Tx of Pinworms

A

Pyrantel pamoate (Pinrid)
albendazole
all members of the household need 2 doses
initial dose and dx
2nd at 2 weeks
deep clean house

159
Q

Ascariasis

A

Round Worms

160
Q

Ascariasis in children ages

A

1-4 years old

161
Q

Ascariasis transmission

A

eggs in stool
hatch in small intestines
may move to the lungs
ascend to pharynx
swallow repeat

162
Q

Ascariasis transmission simplified

A

hand to mouth

163
Q

Ascariasis prevalent in

A

warm climates and developing countries

164
Q

Ascariasis mild s/s

A

asymptomatic
- cramping

165
Q

Ascariasis severe leads to

A

intestinal obstruction, peritonitis, pneumonitis

166
Q

Education of Ascariasis

A

Examine stools 2 weeks after treatment & monthly for 3 months
Treat family members as needed
clean fingernails and handwashing and clean house

167
Q

Tx of Ascariasis

A

albendazole
mebendazole
regardless of symptoms

Module 5 (Pediatrics) (27 decks)

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