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Peds > peds4 > Flashcards

peds4 Flashcards

1
Q

bronchopulm displasia

A

chronic complication of RDS; pathologic changes that affect lung growth

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2
Q

diagnosis of bronchopulm dysplasia

A

mechanical ventilation during the first 2 weeks of life; clinical signs of respir compromise persistent beyond 28 days of life; need for supplemental oxygen beyond 28 days of life; characteristic CXR

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3
Q

prognosis for infant with RDS

A

with aggressive treatment in the NICU, >90% survive

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4
Q

persistent pulm hypertension of the newborn occurs most freq in what GA?

A

full term or post-term

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5
Q

most common causes of persistent pulm hypertension of the newborn

A

perinatal asphyxia and meconium aspiration syndrome

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6
Q

hypoxemia is a potent pulm vasoconstrictor

A

which explains why perinatal asphyxia is a cause of pulm hypertension

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7
Q

ECMO

A

extra-corporeal membrane oxygenation

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8
Q

inhaled NO

A

may be used as a potent pulm vasodilator

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9
Q

what does CXR look like in infants with meconium aspiration syndrome?

A

increased lung volume with diffuse patchy areas of atelectasis and pulm infiltrates alternating with areas of hyperinflation

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10
Q

a couple of bad consequencees of meconium aspiration syndrome?

A

pneumothorax and pneumomediastinum; also persistent pulm htn of the newborn, bacterial pneumonia, and lont term reactive airway disease

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11
Q

apnea of prematurity

A

resp pause lasting 15-20 sec OR resp pause of any duration resulting in cyanosis or ox desat as evidenced on pulse ox

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12
Q

most frequent type of apnea in the newborn

A

mixed (of central and airway obstruction), not either one on its own

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13
Q

incidence of idiopathic apenea of prematurity

A

frequency increases with decreasing gestational age; as high as 85% in infants less than 28 weeks and 25% in infants 33-34 weeks

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14
Q

management of apnea

A

respiratory stimulant medications (caffeine or theophylline), ventillation as needed, CPAP as needed

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15
Q

direct bilirubin

A

bilirubin is conjugated in the liver; most of it goes into bile and into the small intestine

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16
Q

indirect (unconjugated)bilirubin

A

this is the bilirubin as a result of hemoglobin breakdown; it has not gone to the liver yet

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17
Q

physiologic jaundice

A

often occurs during the first week of life; most freq caused by indirect (unconjugated) hyperbilirubinemia

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18
Q

visible jaundice occurs at what bilirubin level

A

5 mg/dL

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19
Q

direct hyperbilirubinemia

A

when the conjugated form is greater than 15% of the total bilirubin level; this is always pathologic in neonates

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20
Q

breastfeeding jaundice

A

causes indirect hyperbilirubinemia; occurs within the first week; related to suboptimal milk intake; decreased stooling leads to decreased passage of bilirubin in the stool; note that breastfeeding is associated with higher peak bilirubin levels than formula feeding

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21
Q

breast milk jaundice

A

causes indirect hyperbilirbinemia; typically occurs after the first week; likely related to breast milk’s high levels of beta-glucuronidase and high lipase

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22
Q

when should jaundice be evaluated

A

when it appears in a baby less than 24 hours after birth; when bilirubin rises more than 5-8 mg/dL in a 24 hour period; the rate of rise of bilirubin exceeds 0.5 mg/dL per hour (suggestive of hemolysis)

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23
Q

exchange transfusion

A

performed for rapidly rising bilirubin levels secondary to hemolytic disease

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24
Q

when indirect bilirubin gets so high that it passes through the BBB, where dies it most freq localize? Note that it is Indirect that gets into the brain

A

basal gang, hippocampus, and brainstem nuclei

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25
Q

clinical features of bilirubin getting into your brain

A

choreoathetoid cerebral palsy, hearing loss, opisthotonus, seizures, and oculomtor paralysis

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26
Q

most common signs in infants with drug abusing mothers

A

jitteriness and hyperreflexia, with irritability, tremulousness, feeding intolerance, and excessive wakefulness

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27
Q

what is the most common type of esophageal atresia?

A

atresia of the esopagus (proximal pouch) with a distal tracheoesophageal fistula

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28
Q

associated malformations are found in what percent of infants with esoph atresia

A

50%

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29
Q

most cases of diaphragmatic hernias involve which side of the diaphragm?

A

the left

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30
Q

scaphoid abdomen

A

abdominal contents in the abdomen; sign of diaphragmatic hernia

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31
Q

omphalocele

A

abdominal organs covered with a peritoneal sac herniate centrally through the umbilical ring area; there is an increased risk of other congenital anomalies

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32
Q

gastroschesis

A

fissure of the anterior abdominal wall (usually right side) ; there is no peritoneal sac covering the bowel is the only viscera that herniates; no increased risk of other congenital anomalies

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33
Q

what is the most common type of intestinal obstruction?

A

intestinal atresia

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34
Q

volvulus

A

loops of intestine twist, can lead to restricted circulation and gangrene;

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35
Q

hirschrpung disease- more common in males or females?

A

males

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36
Q

diagnosis of hirschsprung disease

A

rectal biopsy showing absence of ganglion cells

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37
Q

management of hirschsprung

A

resection of the affected segment

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38
Q

NEC clinical features

A

abdominal distension and tenderness; residual gastric contents, billous aspirate, bloody stools, abdominal erythema

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39
Q

NEC may lead to what?

A

thrombocytopenai, DIC, and death

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40
Q

classic radiograph findings in NEC

A

abdominal distension, air-fluid levels, thickened bowel walls, pneumatosis intestinalis (air in the bowel wall) and venous portal gas

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41
Q

pneumoperitoneum

A

suggestive of NEC that perforated

42
Q

definition of hypoglycemia

A

serum glucose less than 40 mg/dL

43
Q

small left colon syndrome

A

condition that occurs exclusively in infants of diabetic mothers; they present with abdominal distension and failure to pass meconium due to decreased caliber of left colon

44
Q

definition of polycythemia

A

central venous hematocrit greater than 65% (22-ish hgb)

45
Q

increased risk of NEC with polycythemia

A

TRUE

46
Q

management of polycythemia

A

partial exchange transfusion, in which blood is removed and replaced with saline

47
Q

cause of direct hyperbilirubinemia

A

choledochal cyst (cystic dilation of the bile duct)

48
Q

soap bubble on abdominal radiograph

A

meconium ileus

49
Q

fragile x syndrome

A

unstable repeat sequences (number of specific nucleotide copies within a gene increases)

50
Q

genomic imprinting

A

the expression of the gene depends on which parent you inherited that chromosome from; example is 11q region on chrom 15 (prader willi vs angelman)

51
Q

marfan syndrome

A

autosomal dominant connective tissue disorder; affects the ocular, cardiovascular, and skeletal systems; gene defect is fibrillin on chrom 15; decreased upper to lower segment body ratio

52
Q

ocular findings in marfans syndrome

A

upward lens subluxation and retinal detachment

53
Q

diagnosis of marfans?

A

mostly on clinical findings, but, interestingly, homocystinuria has similar findings so you need to rule that out first;

54
Q

marfans syndrome patients are at increased risk for endocarditis

A

right

55
Q

prader willi genetics

A

absence of paternally derived part of chrom 15

56
Q

craniofacial findings of prader willi

A

almond shaped eyes and fishlike mouth

57
Q

growth problems in prader willi syndrome

A

failure to thrive initially followed by obesity as a result of hyperphagia; also short stature with small hands and feet

58
Q

other features of prader willi

A

hypogonadism, hypotonia (in infancy that can lead to poor feeding), mental retardiation

59
Q

what percent of alveolar development occurs after birth?

A

90 percent

60
Q

alveoli increase in number until what age

A

8 yo

61
Q

three reasons that infants are more prone to resp problems than older kids and adults

A

smaller air passages, less compliant lungs with more compliant chest wall, less efficient pulm mechanisms

62
Q

inspiratory stridor suggests what kind of obstruction?

A

extrathoracic

63
Q

two examples of extrathoracic obtruction

A

croup and laryngomalacia

64
Q

what is laryngomalacia

A

softening of the laryngeal cartilage that collapses into the airway, esp when patient is in a supine position

65
Q

expiratory wheezing suggests what?

A

intrathoracic obstruction like asthma and bronchiolitis

66
Q

crackles or rales suggest what

A

parenchymal disease like pneumonia or pulm edema

67
Q

epiglottitis most common in what age? What gender?

A

2-7 year olds; equal in boys and girls

68
Q

epiglottitis is caused by what?

A

HIB (hemophilus influenzae type B) was most common; also group A strep, strep pneumonia, and staph

69
Q

clinical features of epiglottitis

A

abrupt onset of upper airways disease without prodrome

70
Q

what do lab studies of epiglottitis reveal?

A

leukocytosis with left shift; blood culture will show HIB

71
Q

what is classix xray finding of epiglottitis?

A

thumb print epiglottis on lateral x ray

72
Q

what should the airway look like?

A

cery red swollen epiglottis

73
Q

management of epiglottitis

A

medical emergency! Controlled nasotracheal intubatio; avoid examining the throat as this might cause resp distress

74
Q

antibiotic therapy for epiglottitis

A

2nd or 3rd gen cephalosporin; if epiglottitis is secondary to HIB then give rifampin to non-immunized house-hold contacts less than 4 yo

75
Q

laryngotracheobronchitis (aka croup)

A

inflamm and edema of the subglottic larynx, trachea and bronchi

76
Q

two forms of croup

A

viral and spasmodic

77
Q

what is the most common cause of stridor

A

viral croup

78
Q

age of croup

A

3 months to 3 years; male to female ratio is 2:1

79
Q

season for croup

A

late fall and winter

80
Q

most common cause of viral croup

A

parainfluenza; but can also be caused by RSV, rhinovirus, adeno , influenza A and B, and mycoplasma pneumoniae

81
Q

cause of spasmodic croup

A

hypersensitivity reaction

82
Q

clinical feature of viral croup

A

begins with URI for 2-3 days followed by stridor and cough; eventually barky cough; can last 3-7 days

83
Q

what does xray show for croup?

A

“steeple sign” of subglottic narrowing

84
Q

treatment for spasmodic croup

A

resolves without treatment

85
Q

management of viral croup

A

supportive care (col mist and fluids), systemic corticosteroids such as IM dexamethasone, nebulized budesonide, or oral corticosteroids

86
Q

children with resp distress from croup get treated how?

A

should be hospitalized; racemic epinephrine aerosols, which vasoconstrict subglottic tissue

87
Q

bacterial tracheitis

A

uncommon, but can be a cause of stridor

88
Q

causes of bacterial tracheitis

A

staph aureus, strep, HIB

89
Q

clinical features of bacterial tracheitis

A

abrupt onset; high fever, and mucous and pus in the trachea

90
Q

management of bacterial tracheitis

A

anti-staph agent and airway support

91
Q

bronchiolitis

A

inflamm bronchiolar obstruction

92
Q

most common cause of bronchiolitis

A

RSV

93
Q

less common causes of bronchiolitis

A

parainflluenza, adeno, rhino, mycoplasma pneumoniae

94
Q

bronchiolitis predominantly affects what age

A

kids less than 2 yo

95
Q

clinical features of bronchiolitis

A

onset is gradual with URI sx then tachypnea, fine rales, wheezing; liver and spleen may be enlarged due to lung hyperinflation

96
Q

cxr for bronchiolitis

A

hyperinflation with air trapping; patchy infiltrates and atelectasis

97
Q

will babies have recurrent wheezing after they recover from bronchiolitis?

A

yes

98
Q

when do babies with bronchiolitis usually recover by?

A

2 weeks

99
Q

what is a complication of bronchiolitis?

A

apnea

100
Q

management of bronchiolitis

A

primarily supportive; you can try nasal bulbs, nebulized racemic epinephrine may be helpful, aerosolized ribavirin (against RSV) may possibly help but evidence is lacking

Peds (99 decks)

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