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CKPeds > Newborn > Flashcards

Newborn Flashcards

1
Q
  • The 1-minute score gives an idea of ______

* The 5-minute score gives an idea of _______

A

what was going on during labor and delivery.

response to therapy (resuscitation).

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2
Q

T or F

the Apgar score is not predictive of outcome

A

T

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3
Q

Part of the Newborn Care

A 
Vitamin K IM
• Prophylactic eye erythromycin
• Umbilical cord care
• Hearing test
• Newborn screening tests
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4
Q

MC skull Fx in NB

A

Linear

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5
Q

_______ C5–C6; cannot abduct shoulder; externally rotate and supinate forearm;

_____ C7–C8 ± T1; paralyzed hand ± Horner syndrome

A

Erb-Duchenne:

Klumpke:

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6
Q

Prognosis of Brachial Nerve Palsy

A

Most with full recovery (months); depends on

whether nerve was injured or lacerated; Rx

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7
Q

Position of birth prone to clavicular fx

A

Especially with shoulder dystocia in vertex

position and arm extension in breech

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8
Q

What is needed if no improvement after 3-6 mos in facial/brachial nerve injury

A

neuroplasty if no improvement (torn fibers)

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9
Q

Diffuse edematous swelling of soft tissues of

scalp; crosses suture lines

A

Caput succedaneum

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10
Q

Caput succedaneum may lead to?

A

may lead to molding for week

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11
Q

Subperiosteal hemorrhage: does not cross

suture lines

A

Cephalohematoma

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12
Q

COurse of Cephalohematoma

A

May have underlying linear fracture; resolve in 2

wk to 3 mo; may calcify; jaundice

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13
Q

Lacy, reticulated vascular pattern over most of body when baby is cooled; improves over first month; abnormal if persists

A

Cutis marmorata

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14
Q

Blue to slate-gray macules; seen on presacral, back, posterior thighs; > in nonwhite infants; arrested melanocytes; usually fade over first few years; differential: child abuse

A

Mongolian spots

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15
Q

Pale, pink vascular macules; found in nuchal area, glabella, eyelids; usually disappears

A

Salmon patch (nevus simplex)

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16
Q

Firm, yellow-white papules/pustules with erythematous base; peaks on second day of life; contain
eosinophils; benign

A

Erythema toxicum, neonatorum

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17
Q

CHaracteristics of superficial hemangioma

A

Superficial: bright red, protuberant, sharply demarcated; most often appear in first 2 months; most on face, scalp, back, anterior chest; rapid expansion, then stationary, then involution (most by 5–9 years of age);

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18
Q

CHaracteristics of deeper hemangioma

A

bluish hue, firm, cystic, less likely to regress; Rx: (steroids, pulsed laser) only if large and interfering with function

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19
Q

What to do if with Preauricular tags/pits

A

Look for hearing loss and genitourinary anomalies

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20
Q

Association of Coloboma of iris

A

CHARGE association

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21
Q

Hypoplasia of iris; defect may go through to retina; association with Wilms tumor

A

Aniridia

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22
Q

Enzyme deficiency of PKU

A

Phenylalanine hydroxylase; accumulation of PHE in body

fluids and CNS

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23
Q

Asscn of PKU

A

Fair hair, fair skin, blue eyes, tooth abnormalities,

microcephaly

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24
Q

Gal-1-P uridylyltransferase deficiency; accumulation of gal-1-P with injury to kidney, liver, and brain.

What condition?

A

Classic Galactosemia

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25
Q

SSx of Classic Galactosemia

A

Jaundice (often direct), hepatomegaly, vomiting,

hypoglycemia, cataracts, seizures, poor feeding, poor weight gain, mental retardation

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26
Q

Classic Galactosemia Association

A

Predisposition to E. coli sepsis; developmental delay, speech disorders, learning disabilities

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27
Q

T or F

May begin prenatally—
transplacental galactose from mother

A

T

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28
Q

Types of IUGR

A

symmetric and asymmetric

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29
Q

etiology of symmetric IUGR

A

Genetic syndromes, chromosomal abnormalities, congenital infections, teratogens, toxins

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30
Q

What is the reason for asymmetric IUGR

A

Relatively late onset after fetal organ development;
abnormal delivery of nutritional substances and
oxygen to the fetus

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31
Q

Etiology of asymmetric IUGR

A

Uteroplacental insufficiency secondary to maternal diseases (malnutrition, cardiac, renal, anemia) and/or
placental dysfunction (hypertension, autoimmune disease,
abruption

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32
Q
  • Birth weight >4,500 grams at term
  • Predisposing factors: obesity, diabetes
  • Higher incidence of birth injuries and congenital anomalies
A

Large for Gestational Age (LGA)—Fetal Macrosomia

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33
Q

Post term is delivery after_____

A

42 weeks

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34
Q

Characteristics of post term babies

A 
− Increased birth weight
− Absence of lanugo
− Decreased/absent vernix
− Desquamating, pale, loose skin
− Abundant hair, long nails
− If placental insufficiency, may be meconium staining
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35
Q

• Maternal hyperglycemia (types I and II DM) → fetal ________

A

hyperinsulinemia

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36
Q

______ is the major fetal growth hormone → increase in size of all organs except the brain

A

Insulin

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37
Q

Infants of DM mothers are_____

A

large for gestational age and plethoric (ruddy).

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38
Q

Hypocalcemia in infants of DM mothers from?

A

(felt to be a result

of delayed action of parathyroid hormone)

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39
Q

Cadiomegaly from infants of DM mothers?

A

asymmetric septal hypertrophy (insulin effect, reversible)

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40
Q

infants of DM mothers

___________ (flank mass, hematuria, and thrombocytopenia) from polycythemia

A

Renal vein thrombosis

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41
Q

Increased incidence of congenital anomalies:

° Cardiac—especially ________

° _________ (transient delay in development of left side of colon; presents with abdominal distention)

° _________: spectrum of structural neurologic defects of the caudal region of spinal cord which may result in neurologic impairment
(hypo, aplasia of pelvis & LE)

A

VSD, ASD, transposition

Small left colon syndrome

Caudal regression syndrome

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42
Q

What is the problem with surfactant deficiency?

A

Inability to maintain alveolar volume at end expiration → decreased FRC (functional residual capacity) and atelectasis

43
Q

Xrays of Respiratory distress syndrome (RDS) from surfactant deficiency

A

ground-glass appearance, atelectasis, air bronchograms

44
Q

Most accurate diagnostic test—Respiratory distress syndrome (RDS) from surfactant deficiency

A

L/S ratio (part of complete lung profile; lecithin-to sphingomyelin ratio)
°° Done on amniotic fluid prior to birth

45
Q

Most accurate diagnostic test—Respiratory distress syndrome (RDS) from surfactant deficiency

–– Best initial treatment—________
–– Most effective treatment—_______

A

oxygen

intubation and exogenous surfactant administration

46
Q

Slow absorption of fetal lung fluid → decreased pulmonary compliance and tidal volume with increased dead space

A

TTN

47
Q

TTN association

A

Common in term infant delivered by Cesarean section or rapid second stage of labor

48
Q

Chest x-ray (best test) for TTN—

A

air-trapping, fluid in fissures, perihilar streaking

49
Q

Chest x-ray (best test) for MAS—

A

patchy infiltrates, increased AP diameter, flattening of diaphragm

50
Q

Cx of MAS

A

air leak (pneumothorax, pneumomediastinum)

51
Q

TX of MAS

A

Treatment—positive pressure ventilation and other complex NICU therapies

52
Q

Failure of the diaphragm to close → abdominal contents enter into chest, causing pulmonary hypoplasia

A

CDH

53
Q

PE of CDH

A

Born with respiratory distress and scaphoid abdomen

• Bowel sounds may be heard in chest

54
Q

Tx of CDH

A

immediate intubation in delivery room for known or suspected

CDH, followed by surgical correction when stable (usually days

55
Q

Umbilical hernia

Most are small and resolve in _______years without any treatment

A

1-2

56
Q
  • Failure of intestines to return to abdominal cavity with gut through umbilicus
  • Covered in a sac (protection
A

Omphalocele

57
Q

Genetic abn asstd with Omphalocele

A

Trisomy

58
Q

Mx of Omphalocele

A

Large defects need a staged reduction (use of a surgical Silo), otherwise respiratory failure and ischemia

59
Q
  • Defect in abdominal wall lateral to umbilicus (vascular accident)
  • Any part of the GI tract may protrude
  • Not covered by a sa
A

Gastroschisis

60
Q

Asstd problems with Gastroschisis

A

tresia, stenosis, ischemia, short gut

61
Q

Mx of Gastroschisis

A

Surgery based on condition of gut; if no ischemia, large lesions need a staged reduction
as with omphalocele

62
Q

What condition?

  • Transmural intestinal necrosis
  • Greatest risk factor is prematurity; rare in term infants
  • Symptoms usually related to introduction of feeds:
A

NEC

63
Q

Abdominal Xray for NEC

A

Pneumatosis intestinalis on plain abdominal film is pathognomonic (air in bowel wall)

64
Q

(unconjugated bilirubin in the basal ganglia and brain stem nuclei) hypotonia, seizures, opisthotonos, delayed motor skills, choreoathetosis, and sensorineural hearing loss

A

kernicterus

65
Q

Work up for pathologic hyperbilirubinemia when:

A
  • It appears on the first day of life
  • Bilirubin rises >5 mg/dL/day
  • Bilirubin >13 mg/dL in term infant
  • Direct bilirubin >2 mg/dL at any time
66
Q

Causes of hyperbilirubinemia from Increased RBC production:

A

Chronic hypoxia, IUGR, post-mature; IODM,
Beckwith-Wiedemann syndrome (insulin effect); maternal Graves’ disease (transplacental antibodies); trisomies (? mechanism)

67
Q

Causes of hyperbilirubinemia from Extra RBCs entering the circulation:

A

delayed cord clamping, twin-twin transfusion,maternal-fetal transfusion

68
Q

Treatmentof jaundice form PV:

A

partial exchange transfusion with normal saline (dilutional)

69
Q

What test:

Jaundice + immune related hemolysis

A

labs: high unconjugated bilirubin, may be anemia, increased reticulocyte count, positive direct Coombs test)

70
Q

Causes of immune related hemolysis

i. Rh negative mother/Rh positive baby: ______
ii. _________: most common reason for hemolysis in the newborn
iii. Minor blood group incompatibility (Kell is very antigenic; Kell negative mother), uncommon

A

classic hemolytic disease of the newborn (erythroblastosis fetalis)

ABO incompatibility (almost all are type O mother and either type A or B baby)

71
Q

Smear of Non-immune mediated hemolysis

A

Smear shows characteristic-looking RBCs: membrane defect (most are either spherocytosis or elliptocytosis

72
Q

Smear of Non-immune mediated hemolysis,

normal looking RBC

DDx

A

(most are G6PD deficiency then pyruvate kinase deficiency)

73
Q

Bilirubin is then bound to albumin and carried in the blood; bilirubin may be uncoupled from albumin in the blood stream to yield free bilirubin in what conditions?

A

e.g. neonatal sepsis, certain drugs (ceftriaxone), hypoxia, acidosis

74
Q

Bilirubin is transported to the hepatocytes: within the hepatocytes is the conversion of unconjugated (laboratory indirect-acting) fat-soluble bilirubin to conjugated (glucuronide) water-soluble bilirubin (laboratory direct-acting) by the action of ______

A

hepatic glucuronyl transferase (GT).

75
Q

Conditions that may decrease activity of hepatic glucuronyl transferase (GT).

A

°° Normal newborn first week of life
°° Primary liver disease of systemic disease affecting the liver (sepsis, TORCH, metabolic
diseases)
°° No GT activity: Crigler-Najjar syndrome (type I)

76
Q

Transport through the intrahepatic biliary system to the porta hepatis for excretion into the duodenum; abnormalities of transport and excretion cause a_____________

A

conjugated (direct) hyperbilirubinemia (>2 mg/dL direct-acting bilirubin in the blood in the newborn

77
Q

(progressive obliterative cholangiopathy): obstruction at birth due to fibrosis and atresia of the extrahepatic ducts (and so no gall bladder); then variable severity and speed of inflammation and fibrosis of the intrahepatic system which ultimately leads to cirrhosis

A

Biliary atresia

78
Q

MC sx of Biliary atresia

A

Most present in first 2 weeks of life with jaundice (conjugated hyperbilirubinemia), poor feeding, vomiting, lethargy, hepatosplenomegaly, persistent acholic stools and dark urine

79
Q

Best initial test for Biliary Atresia:

A

U/S (triangular fibrotic cord at porta hepatis; no evidence of normal ductal anatomy; no gallbladder

80
Q

Most accurate test for biliary atresia (next step):

A

percutaneous liver biopsy (is pathognomonic for this

process)

81
Q

Best initial Tx for Biliary Atresia:

A

hepatic portojejunostomy (Kasai procedure

82
Q

Best long term Tx for Biliary Atresia:

A

liver transplant

83
Q

Intestinal transport and excretion: most bilirubin is eliminated in the stool with final
products synthesized with help of colonic bacteria; some bilirubin is eliminated in the
urine, some is reprocessed in the liver due to _____

A 
enterohepatic circulation (along with bile
acids)
84
Q

______ hydrolyzes glucuronide-bilirubin bonds to yield
some unconjugated bilirubin, which is absorbed into the portal circulation and transported back to the liver to be acted upon by hepatic glucuronyl transferase

A

intestinal beta-glucuronidase

85
Q

means a baby is not nursing well and so not getting many calories.

This is common in first-time breast-feeding mothers. The infant may become dehydrated; however, it is lack of
calories that causes the jaundice.

Treatment is to obtain a lactation consultation and rehydrate the baby. The jaundice occurs in the first days of life

A

Breast-feeding jaundice

86
Q

________occurs due to a glucoronidase present in some breast milk. Infants become jaundiced
in week 2 of life. Treatment is phototherapy if needed.

A

Breast-milk jaundice

87
Q

Cx of hyperbilirubinemia

A

loose stools, erythematous macular rash, overheating leading to dehydration, and bronze baby syndrome

88
Q

(occurs with direct hyperbilirubinemia; dark, grayish-brown discoloration of the skin [photo-induced change in porphyrins, which are present in cholestatic jaundice])

A

bronze baby syndrome

89
Q

Tx of hyperbilirubinemia

________—if bilirubin continues to rise despite
intensive phototherapy and/or kernicterus is a concern

A

Double volume exchange transfusion

90
Q

RF for neonatal sepsis

A

– Prematurity
– Chorioamnionitis
– Intrapartum fever
– Prolonged rupture of membranes

91
Q

Most common organisms for neonatal sepsis:

A

group B Streptococcus, E. coli, and Listeria monocytogenes

92
Q

Tx of sepsis If no evidence of meningitis

A

ampicillin and aminoglycoside until 48–72-hour cultures are negative

93
Q

Tx of sepsis If meningitis or diagnosis is possible:

A

ampicillin and third-generation cephalosporin (not ceftriaxone)

94
Q

Outcomes of Toxoplasmosis

A

– Psychomotor retardation
– Seizure disorder
– Visual impairments

95
Q

Tx of Toxo

A

maternal treatment during pregnancy reduces the likelihood of transmission significantly (spiramycin)

96
Q

Tx of Toxo in childrne

A

Infants are treated with pyrimethamine, sulfadiazide, and leucovorin

97
Q

Congenital rubella

• Classic findings when maternal infection occurs in _________

A

first 8 weeks’ gestation

98
Q

Findings in Congenital Rubella

A

– Blueberry muffin spots (extramedullary hematopoiesis), thrombocytopenia
– Cardiac—PDA, peripheral pulmonary artery stenosis
– Eye—cataracts
– Congenital hearing loss
– Thrombocytopenia
– Hepatosplenomegaly

99
Q

Manifestations of HSV

A

• Keratojunctivitis, skin (5–14 days), CNS (3–4 weeks), disseminated (5–7 days)

100
Q

Prevention of HSV

A

Prevention is elective Cesarean section when active disease or visible lesions
are identified; however, this is not 100% effective

101
Q

Early manifestations of Congenital Syphilis

A

snuffles, maculopapular rash (including palms of soles,

desquamates), jaundice, periostitis, osteochondritis, chorioretinitis, congenital nephrosis

102
Q

Late manifestations of Congenital Syphilis

A

Hutchinson teeth, Clutton joints, saber shins, saddle

nose, osteochondritis, rhagades (thickening and fissures of corners of mouth)

103
Q

Neonatal Varicella happens when?

A

delivery occurs <1 week before/after maternal infection

104
Q

Neonatal Varicella is associated with?

A

Associated with limb malformations and deformations, cutaneous scars, microcephaly, chorioretinitis, cataracts, and cortical atrophy

CKPeds (20 decks)

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