CLIPP summaries Flashcards

1
Q

Effects of tobacco on the fetus

A

Low birth weight (d/t placental insufficiency)

No characteristic facial abnormalities

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2
Q

Effects of alcohol on the fetus

A

NO SAFE AMOUNT

Facial abnormalities, growth deficiency, CNS dysfunction

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3
Q

Effects of heroin/opiates on fetus

A

Increases risk of fetal growth restriction, placental abruption, fetal death, preterm labor and intrauterine passage of meconium

NAS: uncoordinated sucking reflexes –> poor feeding, irritability, high-pitched cry

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4
Q

Effects of cocaine on fetus

A

vasoconstriction –> placental insufficiency –> low birth weight

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5
Q

Etiologies of SGA

A

Maternal factors

  • young and advance maternal age
  • maternal prepregnancy short stature and thinness
  • poor maternal weight gain during the latter third of pregnancy
  • cigarettes, cocaine
  • low SES
  • African-American
  • uterine and placental abnormalities
  • polyhydramnios

Fetal factors

  • chromosomal abnormalities and syndromes
  • metabolic disorders
  • congenital infections
  • structural abnormalities

Medications and other exposures

  • amphetamines
  • antimetabolites
  • bromides
  • cocaine
  • alcohol
  • heroin and other narcotics
  • hydantoin
  • isotretinoin
  • metal (mercury, lead)
  • phenylcyclidine
  • PCBs
  • propranolol
  • steroids
  • tobacco
  • toluene
  • trimethadione
  • warfarin

Uterine and placental abnormalities

  • avascular vili
  • decidual or spiral arteritis
  • infectious villitis
  • multiple gestation
  • multiple infarctions
  • partial molar pregnancy
  • placenta previa and abruption
  • single umbilical artery
  • umbilical thrombosis
  • abnormal umbilical vascular insertions
  • syncytial knots
  • tumors (chorioangioma, hemangiomas)
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6
Q

TORCH infections

A
Toxoplasmosis
Other: HIV, HBV, human parvovirus, syphilis, zika
Rubella 
CMV 
HSV2
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7
Q

RFs for GSB sepsis

A
  • prolonged ROM
  • prematurity
  • intrapartum fever
  • previous delivery of infant w/ GBS disease
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8
Q

Fever workup for ill-appearing newborn

A
  • CBC
  • blood culture
  • CXR
  • LP
  • IV antibiotics
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9
Q

Apgar score

A
  • Appearance
  • Pulse
  • Grimace (reflex irritability)
  • Activity (muscle tone)
  • Respiration

0-10
1 and 5 min

Does not identify birth asphyxia
Does not predict neurologic outcome or mortality

Score below 7 at 5 min –> continued resuscitation w/ reassessment every 5 min up to 20 min until get to 7

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10
Q

Symmetric vs asymmetric IUGR

A

Symmetric: congenital infection

Asymmetric (head sparing): poor delivery of nutrition to fetus (e.g. smoking)

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11
Q

Risks for SGA newborns

A
  • hypoglycemia
  • hypothermia
  • polycythemia
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12
Q

Prevent hemorrhagic disease of the newborn

A

IM vitamin K

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13
Q

If mom positive for HBsAg

A
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14
Q

Infants born to mothers not tested for HBsAg

A
  • give infant HepB vaccine

- wait to give HBIG until maternal HBsAg status is known

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15
Q

Routine newborn medications

A
  • vitamin K (IM)
  • HepB vaccine
  • erythromycin (topical)
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16
Q

Vitamin D supplementation

A

400 IU daily in breastfed infants

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17
Q

When to transition to cow’s milk

A

12mo

Cow’s milk may damage kidneys, cause GI bleeding, and doesn’t have all the nutrients needed (e.g., iron, vitC)

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18
Q

Caloric requirements for 1-2 m.o.

A

Very preterm: up to 150 kcal/kg/d
Preterm: 115-130
Term: 100-120

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19
Q

Do babies need water?

A

No, because breast milk/formula fulfills fluid requirements

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20
Q

When are infants expected to have regained their birth weight?

A

1-2 wks

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21
Q

When does the Moro reflex disappear?

A

4 mo

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22
Q

When can solid foods be introduced?

A

4-6mo

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23
Q

When do babies sleep through the night?

A

4-6mo

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24
Q

Prevent SIDS

A

Safe sleeping (sleep on back, alone, firm surface, without objects, in parents’ room)

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25
Q

When can kids sit in front car seat?

A

13 y.o.

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26
Q

Until when should kids sit in rear-facing car seat?

A

2 y.o.

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27
Q

Vaccines until 6

A
DTaP (5)
IPV (4)
Hib (3-4)
PCV13 (4)
MMR (2)
Varicella (2)
RotaV (2-3)
HepA (2)
HepB (3)
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28
Q

Flu shot

A

Every year in >6 m.o.

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29
Q

When will healthy infants double and triple their birth weight? Double length?

A

Double: 4-5 mo
Triple: 12 mo

Double length: 4 y.o.

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30
Q

Absent red reflex

A
  • dark skin (more gray than red)
  • cataracts
  • glaucoma
  • retinoblastoma
  • chorioretinitis
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31
Q

6mo developmental milestones

A

Gross motor

  • rolls over
  • sits unsupported
  • no head lag

Fine motor

  • reaches for objects
  • looks for dropped items

Language

  • turns toward voice
  • babbles

Social/adaptive

  • feeds self
  • demonstrates stranger recognition, the prelude to stranger anxiety
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32
Q

Acetaminophen before vaccines?

A

Decreased antibody concentration (although all still in protective range)

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33
Q

12mo developmental milestones

A

Gross motor
-stands alone (may also walk well)

Fine motor
-pincer grasp

Language
-mama, dada, one or two other words

Social/adaptive

  • hands a book to read
  • points when wants something
  • imitates activities
  • plays ball
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34
Q

Prognosis of stage 4S neuroblastoma

A

If <1 y.o., may spontaneously regress

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35
Q

Genetics of neuroblastoma

A

Familial: <1% of cases, autosomal dominant with low penetrance

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36
Q

Differential diagnosis for RUQ mass and pallor in 9 m.o. infant

A
  • hepatic neoplasm
  • hydronephrosis
  • neuroblastoma
  • teratoma
  • Wilms’ tumor (nephroblastoma)
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37
Q

What age toilet training

A

~3

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38
Q

3 y.o. developmental milestones

A

Socio-emotional

  • brushes teeth
  • feeds self

Communication
-2-3 word sentences (75% understandable)

Cognitive
-known name and use of cup, ball, spoon, crayon

Physical

  • throws ball overhand
  • rides tricycle
  • copies circle
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39
Q

4 y.o. developmental milestones

A

Socio-emotional

  • knows gender and age
  • friendly to other children
  • plays with toys/engages in fantasy play

Communication

  • states first and last name
  • sings a song
  • most speech clearly understandable

Cognitive

  • names colors
  • aware of gender
  • plays board games
  • draws person w/ 3 parts
  • copies cross
Physical
-hops on one foot
-balances for 2 sec
Pours, cuts, and mashes own food
-Brushes teeth
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40
Q

5 y.o. developmental milestones

A

Socio-emotional

  • listens and attends
  • can tell difference between real and make believe
  • shows sympathy and concern for others

Communication

  • articulates well
  • tells a simple story using full sentences
  • uses appropriate tenses and pronouns
  • counts to 10
  • follows simple directions

Cognitive

  • draws person w/ >6 body parts
  • prints some letters and numbers
  • copies squares and triangles

Physical

  • balances on one foot
  • hops and skips
  • ties a knot
  • has mature pencil grasp
  • undresses/dresses w/ minimal assistance
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41
Q

Treatment of eczema

A

Non-pharm

  • lubrication
  • avoiding triggers

Pharm

  • high potency topical steroids
  • topical calcineurin inhibitors
  • antihistanines (non-sedating: loratadine, fexofenadine, cetirizine; sedating: diphenhydramine, hydroxyzine)
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42
Q

Juice limit

A

No more than 4-6 oz/d

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43
Q

Discontinue bottle

A

12-15mo

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44
Q

Most common cause of iron deficiency anemia

A

Mlik drinking

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45
Q

BMI

A

kg/(m^2)

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46
Q

Adverse effects of ADHD meds

A
  • appetite suppression
  • insomnia
  • decrease in growth velocity
  • cardiovascular effects in kids with heart problems
  • may unmask tic disorders
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47
Q

Obesity complications

A
  • obstructive sleep apnea
  • dyslipidemia
  • HTN
  • SCFE
  • T2DM
  • steatohepatitis
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48
Q

Diagnosis of T2DM

A
  • HbA1c > 6.5%
  • fasting plasma glucose > 126
  • 2 hr 75g GTT > 200
  • random plasma glucose >200 w/ symptoms of hyperglycemia
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49
Q

DM screening

A

10 y.o. or onset of puberty, whichever is earlier
Screen every 3 yrs

Overweight plus 2:

  • Fh/o DM
  • race/ethnicity
  • signs of insulin resistance (acanthosis nigracans, PCOS, HTN, dyslipidemia)
  • maternal h/o DM or GDM
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50
Q

Weight gain vs endocrine disorder

A

Endocrine: limits growth –> short stature

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51
Q

Secondary HTN

A
  • umbilical arterial or venous line during perinatal period may predispose to renovascular disease
  • UTI –> renal scarring
  • catecholamine excess (pheochromocytoma or neuroblastoma)
  • coarctation of the aorta
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52
Q

Puberty in girls and boys

A

Girls

  • breast buds (10-11)
  • pubic hair (10-11)
  • growth spurt (12)
  • menarche (12-13)
  • adult height (15)

Boys

  • growth of testicles (12)
  • pubic hair (12)
  • growth of penis and scrotum (13-14)
  • first ejaculations (13-14)
  • growth spurt (14)
  • adult height (17)
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53
Q

von Willebrand disease

A

Most common hereditary bleeding disorder– autosomal dominant (types I and II, III is AR)

Sx

  • ecchymoses
  • epistaxis
  • menorrhagia
  • bleeding post-surgery
  • gingival bleeds

Dx

  • prolonged PFA
  • prolonged BT
  • mildly prolonged aPTT (maybe)
  • to confirm: vWF antigen and/or PFA and factor VIII levels

Tx
-intranasal desmopressin

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54
Q

HEEADSSS

A
Home
Education and employment
Eating disorder
Activities
Drugs
Sexuality
Suicide and depression
Safety
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55
Q

Causes of chest pain

A
  • precordial catch syndrome (sudden onset, sharp, L sternal border, exacerbated by deep inspiration)
  • costochondritis (hrs-ds)
  • GI (retrosternal, burning, non-raditiating, associated w/ meals)
  • asthma or exercise-induced bronchospasm (w/ cough, wheezing, resp distress)
  • cardiac (triggered by exertion, pressure or crushing sensation, 10-15 min, w/ syncope/palpitations, murmur/thrill/hyperdynamic precordium)
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56
Q

Adolescent vaccines

A

Tdap: first dose 11-12
MCV4: 11 w/ booster at 16
MenB: 16
HPV: first dose at 11, 3 shots over 6 mo

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57
Q

Diabetes control in pregnancy

A

Very important–major predictor of fetal outcome

Incidence of major malformations directly related to 1st trimester A1c levels

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58
Q

LGA complications

A
  • C-sections, forceps, vacuum extraction –> all have risk
  • birth injury (fractured clavicle, brachial plexus injury, facial nerve palsy)
  • hypoglycemia (esp. if DM mother)
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59
Q

SGA complications

A
  • hypothermia
  • inadequate glycogen stores –> hypoglycemia
  • polycythemia and hyperviscosity
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60
Q

Signs of respiratory distress in infants

A
  • tachypnea
  • retractions
  • grunting (serves to “auto-PEEP”)
  • paradoxical breathing
  • nasal flaring
  • head bobbing
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61
Q

Common problems in late pre-term infants

A

(34-36.6)

  • hypothermia
  • hypoglycemia
  • respiratory distress
  • apnea
  • hyperbilirubinemia
  • poor feeding
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62
Q

Symptomatic hypoglycemia in newborn

A

IV dextrose

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63
Q

Asymptomatic hypoglycemia in newborn

A

breastfeed

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64
Q

Level to keep sugars in infants

A

> 45 mg/dL

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65
Q

Features and risk factors for DDH

A

Features

  • partial or complete dislocation
  • instability of the femoral head

RFs

  • breech
  • F
  • FHx
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66
Q

Pediatrician follow up after newborn discharge

A

w/in 48h

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67
Q

TTN xray

A

“wet” looking lungs

no consolidation or air bronchograms

68
Q

RDS xray

A

diffuse reticulogranular appearance of the lung fields (“ground glass appearance”) and air bronchograms

69
Q

Diaphragmatic hernia xray

A

Most often a diaphragmatic hernia develops on the left side. A radiograph shows air-filled loops of bowel in the left side of the chest, displacing the heart and mediastinum to the contralateral side

70
Q

Where does most of the bilirubin in the newborn come from?

A

75% comes from the physiological breakdown of RBCs

The hemoglobin released from the red cells is converted to unconjugated bilirubin that is insoluble in aqueous solutions and binds to albuminin the blood stream.In the liver the bilirubin is extracted by the hepatocytes where it binds to cytosolic proteins and is then conjugated with glucuronide by uridinediphosphate glucuronyl transferase (UDPGT, also known as glucuronosyl transferase).The conjugated bilirubin is water-soluble and is excreted into the bile and then into the intestine.
In adults, most of the bile is metabolized by the intestinal flora to urobilin and excreted in the stool. The newborn infant, however, lacks thegastrointestinal flora to metabolize bile, which allows the β-glucuronidase present in the meconium to hydrolyze the conjugated bilirubin back to itsunconjugated form.The unconjugated bilirubin is then reabsorbed into the blood stream where it binds to albumin.Newborns absorb significant quantities of bilirubin through this process, known as enterohepatic circulat

71
Q

Kernicterus

A

Kernicterus is the pathological term used to describe staining of the basal ganglia and cranial nerve nuclei by bilirubin. “Kernicterus” also describesthe chronic clinical condition that results from the toxic effects of high levels of unconjugated bilirubin.Kernicterus res

72
Q

Physiologic jaundice

A

This is defined as a total bilirubin level ≤ 15 mg/dL (≤ 257 μmol/L) in full-term infants who are otherwise healthy and have no other demonstrable cause for elevated bilirubin.

Almost all newborn infants have hyperbilirubinemia, but it is benign and self-limited.

Physiologic jaundice in a full-term baby is usually first noticed on the second or third day of life, with the bilirubin level reaching its peak at day three or four of life.

Numerous factors promote the increased enterohepatic circulation that results in physiologic jaundice:

  • Increased bilirubin production (from the breakdown of the short-lived fetal red cells)
  • Relative deficiency of hepatocyte proteins and UDPGT
  • Lack of intestinal flora to metabolize bile
  • High levels of β-glucuronidase in meconium
  • Minimal oral (enteral) intake in the first 2-4 days of life, resulting in slow excretion of meconium (especially common with breastfed infants)
73
Q

Breastfeeding jaundice

A
  • happens early in the first week of life and occurs when the milk supply is relatively or absolutely low, resulting in limited enteral intake.
  • This may be referred to as a “lack-of-breast milk jaundice” or “breastfeeding-associated jaundice.”
  • The low intake results in decreased gastrointestinal motility that in turn promotes retention of meconium.
  • The β-glucuronidase in meconium deconjugates bilirubin and the unconjugated bilirubin is reabsorbed via the enterohepaticcirculation, causing an elevation of serum levels.
  • Occasionally, persistently low volume of breast milk can cause the neonate to become dehydrated and malnourished.Breastfeeding jaundice is often difficult to distinguish from physiologic jaundice
74
Q

Breast milk jaundice

A
  • Begins in the first 4 to 7 days of life but may not peak until about 10 to 14 days.
  • Not the result of low breast milk volume.
  • While the cause is not completely understood, one explanation is that β-glucuronidase present in breast milk deconjugates bilirubin in the intestinal tract; the unconjugated bilirubin is then reabsorbed via enterohepatic circulation.
  • Breast milk jaundice can persist for up to 12 weeks, but total bilirubin concentration rarely, if ever, reaches concerning levels.
  • The time course of breast milk jaundice is quite different from that of physiologic jaundice
75
Q

Hemolytic causes of jaundice

A

Antibody-positive hemolysis is labeled “direct Coombs” or “direct antibody test (DAT)” positive.
The most common forms of antibody-positive hemolysis include:
-Rh incompatibility (mother is Rh-negative and baby is Rh-positive)
-ABO incompatibility (mother is type O and baby is type A or B)
-Incompatibilities with minor blood group antigens (much less common)

Antibody-negative hemolysis occurs in infants who have red blood cell membrane defects (e.g., spherocytosis) or red blood cellenzyme defects (glucose-6-phosphate dehydrogenase or pyruvate kinase deficiency).

76
Q

Non-hemolytic RBC breakdown

A
  • excessive bruising from birth trauma
  • large cephalohematoma or other hemorrhage (e.g. intracranial)
  • polycythemia
  • swallowed blood (large amounts) during delivery
77
Q

Metabolic causes of jaundice

A

Crigler-Najjar syndrome type 1 and type 2: is a rare (1;1,000,000 newborns) autosomal recessive condition that causes severe unconjugated hyperbilirubinemia starting in the first few days of life. It results from decreased bilirubin clearance caused bydeficient (type 2) or completely absent (type 1) UDPGT and can lead to kernicterus.

Gilbert Syndrome is a much less severe but more common cause of unconjugated hyperbilirubinemia than Crigler-Najjaar. The more common form of this condition involves the UGT1A1 gene and is inherited in an autosomal recessive pattern. The resulting decreased enzyme function interferes with glucuronidation and therefore the conjugation of bilirubin is slowed.Patients with Gilbert syndrome have intermittent, self-resolving episodes of unconjugated hyperbilirubinemia, usually beginningin adolescence.

Galactosemia and hypothyroidism also have jaundice as prominent clinical findings. Jaundice found in hypothyroidism may be caused by a combination of decreased rate of bilirubin conjugation, decreased gut motility and impaired feeding. These congenital disorders may be detected by neonatal screening.

78
Q

Typical infant breastfeeding pattern

A

A successfully breastfed baby typically nurses 8-12 times in 24 hours.

Feedings may initially last up to 60 minutes but gradually become shorter in duration, ~10-15 minutes at each breast. (Increasingly frequent or consistently lengthy feeding sessions may indicate a problem, especially if the infant is not gaining weight.)

79
Q

Biliary atresia

A

A healthy-appearing infant who develops jaundice, dark urine, and acholic (pale) stools between 3 and 6 weeks of age may have biliary atresia.

Any infant who develops jaundice after two weeks of age must be evaluated with fractionated bilirubin (i.e., total and direct bilirubin levels).

A patient suspected of having biliary atresia generally will be referred to a pediatric gastroenterologist or pediatric surgeon.

Treatment
When diagnosed early, biliary atresia can be treated surgically with the Kasai procedure (anastomosis of the intrahepatic bile ducts to a loop of intestine to allow bile to drain directly into the intestine).
If done early, the Kasai procedure will restore bile flow and prevent liver damage.

80
Q

Caput vs cephalohematoma

A

A caput succedaneum is an edematous swelling over the presenting portion of the scalp of an infant and is commonly seen in babies born vaginally in vertex position. Because the scalp overlies the periosteum, this boggy swelling crosses suture lines, easily differentiating it from a cephalohematoma.

81
Q

How often should young infants breastfeed?

A

8-12 feedings per 24h

About every 2-3h w/ 10-15min per breast

82
Q

Large fontanelles

A
  • Skeletal disorders (e.g., rickets, osteogenesis imperfecta)
  • Chromosomal abnormalities (e.g., Down syndrome)
  • Hypothyroidism
  • Malnutrition
  • Increased intracranial pressure can also result in large fontanelles and splitting of the sutures.
83
Q

Small fontanelles

A
  • Microcephaly
  • Craniosynostosis
  • Hyperthyroidism
  • A normal variant
84
Q

Sunken fontanelles

A

dehydration

85
Q

Bulging fontanelles

A
  • Meningitis
  • Hydrocephalus
  • Subdural hematoma
  • Lead poisoning
86
Q

CAH

A

The most common form of congenital adrenal hyperplasia, 21-OH deficiency, causes decreased production of cortisol and aldosterone.

Plasma 17-OH progesterone is elevated with 21-OH deficiency because its production occurs prior to the block in the pathway of adrenal steroid formation.

The increased 17-OH progesterone with CAH is diverted to androgen formation.Thus, female patients with 21-OH deficiency are virilized.

Male patients with 21-OH deficiency may be harder to detect (virilization presents as increased penile length and darker pigmentation of the scrotum).

Decreased mineralocorticoid activity in 21-OH deficiency (the salt-wasting form) leads to hyponatremia and hyperkalemia, and may present with vomiting, dehydration, and shock in a newborn.

87
Q

Congenital hypothyroidism symptoms

A
  • Feeding problems
  • Decreased activity
  • Constipation
  • Prolonged jaundice
  • Skin mottling
  • Umbilical hernia

With time, if untreated, patients develop a large tongue, hoarse cry and puffy myxedematous facies.

CH is one of the most common preventable causes of intellectual disability. The longer treatment is delayed, the greater the risk

Newborns with a low T4 and elevated TSH on the newborn screen are considered to have CH until proven otherwise.

Because early treatment is critical for normal development, the patient should be started on levothyroxine (L-thyroxine) while waiting forconfirmatory measurement of serum T4 and TSH.

88
Q

Fevers w/ live vs killed vaccines

A

Live: 6-14d after

Killed: w/in a few days

89
Q

Pyelonephritis IV antibiotics

A
  • ampicillin/gentamicin
  • ceftriaxone
  • meropenem
  • ciprofloxacin
90
Q

Pyelonephritis oral antibiotics

A
  • cephalexin
  • TMPSMX
  • amoxicillin/clavulanate
91
Q

Causes of unilateral cervical adenopathy

A
  • reactive cervical adenitis
  • Kawasaki disease
  • bacterial cervical adenitis
  • cat scratch disease
  • Mycobacterial infection
92
Q

Causes of strawberry tongue

A
  • Kawasaki disease
  • Streptococcal pharyngitis
  • Toxic shock syndrome
93
Q

Kawasaki disease criteria and lab findings

A

5+ days of fever +4/5:

  • Changes in oral mucosa (i.e.: “strawberry tongue”)
  • Extremity changes (redness/swelling)
  • Unilateral cervical lymphadenopathy
  • Rash
  • Conjunctivitis (bilateral, nonpurulent)

The one least likely to be present is cervical adenopathy.

Though irritability is very common, it is not part of the diagnostic criteria.

[CRASH and BURN]

CBC

  • elevated WBC w/ neutrophilia
  • normochromic, normocytic anemia
  • thrombocytosis

CMP

  • elevated LFTs
  • low albumin

ESR and CRP elevated

UA
-sterile pyuria (from sterile urethritis) [see on clean catch, not bladder cath]

94
Q

Complications of Kawasaki disease

A
  • aseptic meningitis or other CNS manifestations [most common]
  • coronary artery aneurysm
  • liver dysfunction (elevated LFTs and low albumin)
  • arthritis
  • hydrops of gallbladder
95
Q

Treatment of Kawasaki disease

A
  • high dose ASPIRIN followed by low dose after defervescence
  • IVIG (decreases coronary artery aneurysms)

Follow-up

  • cardiology
  • flu and varicella vaccine (decreases risk of Reye syndrome from viral illness)
96
Q

Measles

A

After a prodrome of fever (over 38.3 C, or 101 F), cough, coryza, and conjunctivitis, this maculopapular rash starts on the neck, behind the ears,and along the hairline.

The rash spreads downward, reaching the feet in two or three days.The initial rash appears on the buccal mucosa as red lesions with bluish whitespots in the center (known as Koplik spots).

These have frequently disappeared by the time the patient presents to medical attention.

Immunization is very effective in preventing this infection.

97
Q

Rocky Mountain Spotted Fever

A
  • Fever
  • Headache
  • Rash (typically starts on ankles and wrists and progresses centrally and to palms and soles; may be macular or papular at first, quickly becoming petechial; in 5% of cases, there may be no rash)
  • Myalgia
98
Q

Scarlet fever

A
  • Fever
  • A diffuse, erythematous, finely papular rash (described as having a”sandpaper” texture) is pathognomonic
  • Rash often begins at neck, axillae, and groin and then spreads over trunk andextremities, typically resolving within four or five days
99
Q

Stevens-Johnson syndrome

A
  • Macular rash, or diffuse erythema, often tender, with subsequent vesicles or bullae that may progress to erythema multiforme. Nikolsky sign may bepresent.
  • Fever
  • Mucosal changes (e.g., stomatitis)
  • Conjunctivitis
100
Q

Varicella

A

Chicken pox:

  • rash starts on trunk and spreads to extremities and head
  • Each lesion starts as an erythematous macule, then forms a papule followed by a vesicle before crusting over
  • Lesions at various stages of development are seen in the same area of the body
  • Immunization is effective in preventing this infection
101
Q

Erythema infectiosum

A

Also called 5th disease

Low grade fever followed by a rash, which starts as a facial erythema to the face (“slapped cheek” appearance), which can spread to the trunk and extremities and appears lacy

Can lead to pain and swelling of the extremities, as well as development of transient pure red cell aplasia which can lead to severe anemia in patients with underlying hemolytic disease.

102
Q

Roseola

A

Exanthem subitum Also called sixth disease

Erythematous macules start on trunk and spread to arms and neck (less commonly face and legs)Rash is typically preceded by 3 to 4 days of high fevers, which end as the rash appears

Usually occurs in children under age 2 years

103
Q

Pertussis stages

A
  1. Catarrhal (1-2 wks): URI-like
  2. Paroxysmal (4-6 wks): repetitive, forceful coughing episodes followed by massive inspiratory effort, which results in the characteristic “whoop.”
  3. Convalescent (months- “hundred day cough”): episodic cough that eventually resolves
104
Q

Biggest complication of pertussis

A

apnea

105
Q

Epiglottitis

A

due to H. influenzae type b (Hib)

  • fever
  • stridor
  • drooling
  • dysphonia
  • dysphagia
  • respiratory distress

Toxic appearing and head in “sniffing position”

More likely in unimmunized

106
Q

If suspect epiglottitis

A

immediate securing of airway

do not examine or disturb child for risk of acute decompensation

107
Q

Radiology of epiglottitis

A

Xray: thickening of the epiglottis (the “thumb sign”) and thickening of the aryepiglottic folds

108
Q

Diphtheria

A

pharyngitis and a low-grade fever, particularly if stridor or hoarseness is present

Diagnosed clinically with characteristic gray pseudomembrane in pharynx

More likely in unimmunized

109
Q

Which bugs cause pneumonia in which ages?

A

Most common cause of pneumonia in kids is a respiratory virus (adenovirus, RSV, parainfluenza, influenza)

In the neonatal period, bacteria transmitted from the maternal genital tract must be considered, including Group B streptococcus, E.Coli, and Klebsiella.

Pneumonia due to Chlamydia pneumoniae usually presents with a staccato cough between 4 and 12 weeks of age.

Streptococcus pneumoniae is the most common bacterial cause of pneumonia in the U.S. among infants beyond the neonatal period and children up to 5 or 6 years of age.In school-aged and older children,

Mycoplasma pneumoniae is the predominant cause, followed by S. pneumoniae.

110
Q

Croup

A

Laryngotracheobronchitis

Mostly due to parainfluenza, but can also be due to RSV, influenza, and rhinovirus.

Peak incidence 2y

Cough and stridor: Croup often starts with cold-like symptoms (congestion, coryza, sore throat, cough, and fever). This may progress to inspiratory stridor and a “seal-like” or “barky” cough

CXR: narrowing in the subglottic region (“steeple sign”)

Tx: supportive
Breathing humidified air or mist therapy can improve laryngospasm. Racemic aerosolized epinephrine can beused for acute improvement, and oral or IM dexamethasone can reduce the severity of symptoms

111
Q

Foreign body aspiration xray

A

PA film (with the child in a sitting position): Right hemidiaphragm is flattened, suggesting unilateral hyperexpansion on the right.

Right decubitus: With child on her right side, the mediastinal structures remain in the midline, rather than shifting towards the right lung due to gravity, further demonstrating the fixed hyperinflation of the right lung.

Left decubitus: With child on her left side, the mediastinal structures shift towards the left lung as expected.

112
Q

TB presentation in kids

A

Often asymptomatic or mild. Radiology is also mild [hilar adenopathy most common]. Often discovered only by contact tracing.

113
Q

Bacterial causes of acute otitis media

A

Streptococcus pneumoniae
Haemophilus influenzae, nontypeable
Moraxella catarrhalis
Streptococcus pyogenes

114
Q

Antibiotics for acute otitis media

A

Amoxicillin, or amoxicillin-clavulanate

Treat if (6mo-2yrs unilateral OR >2 uni or bilat):

  • toxic appearing, OR
  • persistent ear pain for 48h, OR
  • fever >39 C w/in past 48h
115
Q

Pyloric stenosis metabolic abnormality

A

hypochloremic, hypokalemic metabolic alkalosis

116
Q

Maintenance fluid calculation

A

4-2-1 (first 10, second 10, all other 1)

117
Q

Fatal complication of DKA

A

cerebral edema

118
Q

Metabolic disturbances in DKA

A

Anion gap metabolic acidosis

Total body potassium depleted but serum high, normal, or low

Hyponatremia [make sure to correct Na+ when glc is very high]

119
Q

DKA presentation

A
  • Vomiting
  • Weight loss
  • Dehydration
  • Shortness of breath
  • Abdominal pain
  • Change in the level of consciousness

Diagnostic criteria:
A random blood glucose of > 200 mg/dL (> 11.1 mmol/L), and
A venous pH < 7.3 or serum bicarbonate < 15 mEq/L (< 15 mmol/L), and
Moderate or large ketonuria or ketonemia.

120
Q

Kocher criteria

A

For septic hip

  • fever
  • non-weight bearing
  • ESR >40
  • WBC >12

If all 4, 93%

If add CRP and have all, 97.5%

121
Q

If suspect septic arthritis

A

tap joint

  • Turbid appearance
  • Increased white cell count, predominantly polymorphs
  • Gram stain positive for bacteria
122
Q

Septic hip bugs

A

Staphylococcus aureus
Streptococcus (neonate: group B; infant and older child: Group A and Streptococcus pneumoniae)
Haemophilus influenzae type b (in unimmunized children)
Neisseria gonorrhea (adolescents)
Kingella kingae (in children less than 4 years)

123
Q

Transient synovitis treatment

A

rest and ibuprofen

124
Q

Infant CHF signs and symptoms

A
  • dyspnea with feedings
  • diaphoresis
  • poor growth
  • an active precordium
  • hepatomegaly
125
Q

ASD presentation

A

Often first detected 3-5 y.o.

Widely split, fixed S2

126
Q

Coarctation of the aorta presentation

A

murmur, hypertension in the upper extremities, and a discrepancy between the upper and lower extremity blood pressures.

Poor femoral pulses, brachiofemoral delay, and occasionally a murmur medical to the left scapula

127
Q

VSD presentation

A

Holosystolic murmur beginning with S1 with a blowing quality

Often not picked up in nursery because PVR is still elevated so there is no shunting

128
Q

PDA presentation

A

Continuous ‘machine-like’ murmur and bounding pulses (from a widened pulse pressure)

129
Q

Pediatric CHF medications

A
  • furosemide
  • digoxin
  • elanapril
130
Q

EKG in VSD

A

prominent biventricular forces (high voltage QRS complexes in leads V1 and V2),suggesting both LV volume overload and RV pressure overload.

131
Q

Simple vs complex febrile seizures

A

Simple (more common): <15 min, once in 24h, generalized

Complex (rarer): >15 min, more than once in 24h, focal

132
Q

Roseola etiology

A

HHV-6

133
Q

Primary HHV-6 infection may lead to what in 20-30% of kids?

A

Febrile seizures

134
Q

Post-infectious cerebellitis

A

Autoimmune post-viral

occurs several weeks after a viral infection (e.g., varicella or coxsackie virus).

Onset is sudden and consists of ataxia, vomiting, nystagmus in about half of the patients and dysarthria in some.

CSF may be normal or have a pleocytosis; eventually the CSF protein is elevated.

135
Q

Infectious cerebellitis

A

May be viral or bacterial in etiology.

Fever is often an accompanying symptom.

Mental status changes are often observed.

Examples of pathogens include mumps, enteroviruses and Epstein-Barr virus.

Bacterial pathogens include those that cause bacterial meningitis (e.g., Streptococcus pneumoniae, Neisseria meningitidis and Haemophilus influenzae type B.

136
Q

Opsoclonus-myoclonus syndrome

A

A paraneoplastic syndrome that occurs most often with neuroblastoma, generally occurs in the younger child (6months-3 years).

Ataxia is accompanied by intermittent jerking movements (myoclonus) and erratic, jerky conjugate movements of the eyes (opsoclonus).

137
Q

Features of HSP

A
  • non-thrombocytopenic purpura
  • renal involvement (hematuria)
  • arthritis or arthralgia
  • colicky abdominal pain (can also get intestinal bleeding)
  • recent URI
138
Q

Steroids in HSP?

A

reduce GI manifestations

139
Q

Intusussception in HSP

A

usually ileo-ilial, which can’t be reduced w/ enema and thus needs surgery

140
Q

Classic presentation of intusussception

A

-Paroxysms of severe abdominal pain with inconsolable crying
-Passage of “currant jelly” stool containing blood and mucus
Palpation of a “sausage-shaped” mass in the right abdomen

141
Q

Treat intusussception

A

air or barium enema

142
Q

PID

A

Minimum Criteria:

  • cervical motion tenderness
  • uterine tenderness
  • adnexal tenderness

Supportive Criteria (enhance specificity of minimum criteria):

  • oral temperature > 101 F (38.3 C)
  • abnormal cervical mucopurulent discharge or cervical friability
  • presence of abundant numbers of WBC on saline microscopy of vaginal fluid
  • elevated ESR
  • elevated CRP
  • laboratory documentation of cervical infection with N. gonorrhoeae or C. trachomatis
143
Q

Antibiotics for PID

A

azithromycin + ceftriaxone

consider also adding metronidazole

144
Q

Late sign of shock in kids

A

hypotension

145
Q

Meningococcal prophylaxis

A

Adults: cipro (rifampin, CTX, azithro are alternatives)

Kids: rifampin or CTX

146
Q

Treat Nisseria meningitis

A

Penicillin G

then needs to be put on abx to eliminate carrier state (rifampin or CTX)

147
Q

Cholinergic toxicity

A

e.g., organophosphates

  • Miosis and blurred vision
  • Increased gastric motility (nausea, vomiting, diarrhea)
  • Excessive tearing, salivation, sweating and urination
  • Bronchorrhea and bronchospasm
  • Muscle twitching and weakness
  • Bradycardia
  • Seizures
  • Coma

Mnemonic: “SLUDGE” (salivation, lacrimation, urination, defecation, GI motility, emesis) or: DUMBBELLSS

148
Q

Anticholinergic toxicity

A

e.g., antihistamines, TCAs

  • Mydriasis (dilated pupils) “blind as a bat”
  • Dry skin “dry as a bone”
  • Red skin (flushed) “red as a beet”
  • Fever “hot as Hades”
  • Delirium and seizures “mad as a hatter”
  • tachycardia
  • urinary retention
  • ileus
149
Q

Sedative hypnotic toxicity

A

e.g., barbituates, benzodiazepines

  • Blurred vision (miosis or mydriasis)
  • Hypotension
  • Apnea and bradycardia
  • Hypothermia
  • Sedation, confusion, delirium, coma
150
Q

Opioid toxicity

A
  • Miosis (constricted pupils)
  • Respiratory depression
  • Bradycardia and hypotension
  • Hypothermia
  • Depressed mental status (sedation, confusion, coma)
151
Q

Sympathomimetic toxicity

A

e.g., cocaine, amphetamines, pseudoephedrine

  • Mydriasis
  • Fever and diaphoresis
  • Tachycardia
  • Agitation and seizure
152
Q

Bronchopulmonary dysplasia

A

BPD is a chronic lung disease of premature infants resulting from damage to immature and insufficently flexible alveolar tissue associated with intubation, positive pressure ventilation, and oxygen toxicity.

BPD (or chronic lung disease) may cause poor growth in part due to increased caloric requirements, repeated pulmonaryinfections or congestive heart failure.

Development in these infants may be delayed because of prolonged or repeated hospitalization due to illness, underlying neurological disease, or both.

153
Q

Retinopathy of prematurity

A

ROP is characterized by extraretinal fibrovascular proliferation and, in severe cases, may cause retinal detachment and blindness.

All premature infants, particularly those weighing less than 1500 g are at risk of ROP.

Approximately 50% of infants weighing less than 1200 g develop ROP.

Development in children with ROP may be delayed depending on the degree of visual impairment

154
Q

Periventricular leukomalacia

A

PVL is the result of damage to the white matter surrounding the ventricles in the brain as a result of hypoxia, ischemia,and inflammation.

It is correlated with intraventricular hemorrhage (bleeding from the delicate vessels of the neuronal and glial proliferationzone-germinal matrix-that surrounds the lateral ventricles in preterm infants and fetuses); it is likely that damage to the white matter is actually more widespread, but not easily visualized using current clinical imaging techniques.

PVL with cysts (cystic PVL) is highly correlated with cerebral palsy

155
Q

Key feature of CP

A

NON-PROGRESSIVE motor and postural dysfunction

156
Q

Risk factors for CP

A
  • prematurity (most significant)
  • IUGR
  • chorioamnionitis
  • perinatal asphyxiation
157
Q

Features of Down syndrome

A
  • Upslanting palpebral fissures
  • Small ears (usually less than 34 mm at maximum dimension in a term infant)
  • Flattened midface
  • Epicanthal folds
  • Redundant skin on back of neck (nuchal skin)
  • Hypotonia [most consistent finding in infants with Down syndrome]

Others: small brachycephalic head, Brushfield spots, small shaped mouth, single transverse palmar crease, shortfifth finger with clinodactyly, and wide spacing and a deep plantar groove between the first and second toes.

158
Q

RF for Down syndrome

A

AMA

Although most kids with DS are born to mothers younger

159
Q

Turner syndrome findings

A
  • Webbed neck
  • Low ear placement
  • Edema of the hands and feet
  • Hyperconvex nails
  • “Shield” chest, with widely spaced nipples

Coarctation of the aorta is found in about 20% of affected girls.
Short stature is common, and some girls are not diagnosed until early adolescence when they present with short stature and delayed sexualmaturation (due to gonadal dysgenesis).
Most have a normal IQ

160
Q

Trisomy 13 (Patau syndrome)

A
  • Microphthalmia
  • Microcephaly
  • Severe intellectual disability
  • Polydactyly
  • Cleft lip and palate
  • Cardiac and renal defects
  • Umbilical hernias
  • Cutis aplasia
161
Q

Trisomy 18 (Edwards syndrome)

A

-Severe intellectual disability
-Prominent occiput
-Micrognathia
-Low-set ears
-Short neck
-Overlapping fingers
-Heart defects
-Renal malformations
-Limited hip abduction
Rocker-bottom fee

162
Q

Common surgeries for sickle cell kids

A

tonsillectomy and cholecystectomy

163
Q

Prevention of sepsis in sickle cell

A

Penicillin until 5 or 6

164
Q

Complications of sickle cell disease

A

Jaundice
Anemia (fatigue, etc.; baseline 6-9 Hgb)
Stroke
Respiratory problems (pneumonia, acute chest syndrome)

165
Q

When to transfuse in sickle cell disease

A
  • A fall in hemoglobin from baseline
  • Increasing respiratory rate
  • Worsening chest symptoms
  • Declining O2 sats
  • Progressive infiltrates on chest x-ray
166
Q

Treatment of nephrotic syndrome

A
  • corticosteroids
  • sodium restriction
  • IV furosemide and albumin (careful!)