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Pediatrics Board Exam > Board Exam > Flashcards

Board Exam Flashcards

1
Q

Reasons for high alpha-fetoprotein

A

RAIN: Renal (nephrosis, renal agenesis, polycystic kidney disease), Abdominal wal defects, Increased number of fetuses/Incorrect dates, Neuro (anencephaly and spina bifida)

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2
Q

Reasons for low alpha-fetoprotein

A

Trisomy 21 or Trisomy 18

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3
Q

What is a non-stress test and what does it measure?

A

Measures spontaneous fetal movements and heart rate; therefore, it measures fetal autonomic nervous system integrity

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4
Q

What is the contraction stress test and what does it measure?

A

Measures the fetal heart rate in response to uterine contraction; measures uteroplacental insufficiency and tolerance of labor

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5
Q

Most common cause of fetal bradycardia

A

Heart block, which may be seen with maternal lupus

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6
Q

When do you treat SVT in a fetus

A

With heart rates >240 bpm; treat with antiarrhythmic medication for the mother

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7
Q

What are the components of the biophysical profile?

A

Fetal movement, reactive heart rate, breathing, tone, volume of amniotic fluid

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8
Q

Causes of apnea in a neonate

A

APNEA: Abnormal metabolism (hypoglycemia, hypocalcermia, anemia, maternal medications); PDA and other cardiac causes; Neurological (seizures, intracranial hemorrhage, apnea of prematurity); Epidemiological/Infectious (sepsis, pertussis, RSV and other respiratory infections); Abnormal swallowing/GERD

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9
Q

Chest XR findings in RDS

A

Granular opacifications, air bronchograms, ground glass appearance. Typically symmetric appearance

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10
Q

One way to distinguish RDS from pneumonia secondary to GBS

A

Calculate the ratio of bands to total neutrophils; if greater than 0.2, sepsis or pneumonia is more likely. Also, temperature instability is a clue towards pneumonia

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11
Q

Interaction between bilirubin and RDS

A

When hyperbilirubinemia co-exists with RDS, the threshold for kernicterus is lowered

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12
Q

Factors that increase and decrease the risk of RDS

A

Increase: infants of diabetic mothers, c-section delivery, birth asphyxia; decrease: prolonged rupture of membranes, prenatally administered steroids

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13
Q

Changes expected after surfactant administration in RDS

A

Decreased oxygen requirement, reduced inspiratory pressure, improved lung compliance

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14
Q

Definition of chronic lung disease

A

Present in infants who still have an oxygen requirement 28 days after birth and/or continued oxygen requirement at 36 weeks corrected gestation

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15
Q

Typical CXR of BPD

A

Diffuse opacities as well as cystic areas with streaky infiltrates and ground glass appearance

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16
Q

How long should you monitor well appearing infants whose mothers had inadequately treated GBS?

A

48 hours

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17
Q

Drug of choice for treatment of proven GBS

A

Pencillin

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18
Q

Delayed detachment of the umbilical cord

A

Leukocyte adhesion deficiency or low WBC

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19
Q

Proper cord care

A

Wash with soap and water (Do not apply mercurochrome–can cause harm! and cases mercury)

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20
Q

What test should you do when you see a single umbilical artery?

A

Renal ultrasound

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21
Q

Should the obstetrician milk the cord?

A

No, it can lead to polycythemia

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22
Q

Physical findings in post-term babies

A

Dry skin that is peeling, long fingernails, and decreased lanugo on the back, the ears will have a strong recoil

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23
Q

Is bilateral ankle clonus normal in an infant?

A

Yes

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24
Q

CXR in meconium aspiration syndrome

A

Patchy areas of atelectasis alternating with areas of hyperinflation

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25
Q

Contraindications to phototherapy

A

Elevated direct bilirubin (can cause “Bronze Baby Syndrome”) or a family history of light-sensitive porphyria

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26
Q

Causes of indirect hyperbilirubinemia

A

YELLOW:
You never know: Gilbert Disease
Endocrine (hypothyroid-hypopituitarism)
Enterohepatic circulation increased (obstruction, pylori stenosis, meconium ileus, ileus, Hirshsprung’s)
Lucy Driscoll Syndrome
Lysed blood cells (hemolytic disease, defects of RBC metabolism, isoimmunization)
Overdrive (Galactosemia, tyrosinosis, hypermethionemia-cystic fibrosis)
Wasted blood (petechiae, hematomas, hemorrhages,cephalphematomas, swallowed maternal blood)

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27
Q

Risks in LGA infants

A

Hypoglycemia, polycythemia (possibly due to increased erythropoietin), hypoplastic left colon syndrome

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28
Q

When do full and preterm infants have their hemoglobin nadir?

A

Full term reach their nadir at 2-3 months (can go as low as 9-11), preemies reach it in 1-2 months (can go as low as 7-8)

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29
Q

What test is used to detect the presence of fetal cells in the mother’s blood and is used to evaluate neonatal anemia?

A

Kleihauer Betke Test

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30
Q

What Hgb is considered anemic at birth?

A

Less than 13

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31
Q

What is polycythemia and when and how should it be treated?

A

Central venous (not capillary) hematocrit of 65 or higher. Treat for 70 or higher with partial exchange transfusion. Polycythemia can lead to hypoglycemia, hyperbilirubinemia, and/or thrombocytopenia.

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32
Q

Lethargy, hypotonia, and irritability in an infant with a history of TTTS, delayed clamping of the cord, Down syndrome, or IDM

A

Hyperviscosity syndrome from polycythemia

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33
Q

What is the Apt Test?

A

Test if blood in the neonate’s gastric aspirate is actually maternal blood

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34
Q

What test should be performed in eery baby with omphalocele?

A

Echocardiogram

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35
Q

Treatment for neonatal seizures

A

Phenobarbital

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36
Q

Grading of IVH

A

Grade 1- Germinal matrix
Grade 2- IVH without dilation
Grade 3- IVH with dilation
Grade 4- Parenchymal involvement

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37
Q

What to watch for if mother is given terbutaline as tocolysis during labor?

A

Hypoglycemia (terbutaline stimulates fetal insulin)

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38
Q

Baby withdrawal symptoms if mother was using alcohol

A

Hyperactivity, irritability. May also see hypoglycemia

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39
Q

Baby withdrawal symptoms if mother was using cocaine

A

No official withdrawal or abstinence syndrome exists. But are at increased risk for cerebral infarctions, limb anoalies, and urogenital defects.

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40
Q

Baby withdrawal symptoms if mother was using marijuana

A

None

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41
Q

Baby withdrawal symptoms if mother was using amphetamine

A

None. Though are often irritable and easily agitated with routine environmental stimulation. Often experience IUGR, and are prone to developmental and cognitive impairment.

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42
Q

Baby withdrawal symptoms if mother was using barbituates

A

hyperactivity, hyperphagia, irritability, crying and poor suck swallow coordination

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43
Q

Baby withdrawal symptoms if mother was using opioids

A

Hyperirritability, tremors, jitteriness, hypertonia, loose stools, emesis, and feeding difficulties. Can also have seizures. May need methadone and/or oral morphine to manage withdrawal

44
Q

Sequence of male pubertal development

A

Testicular growth–> pubarche–> penile growth –> peak height velocity

45
Q

What testicular length indicates the onset of puberty

A

Greater than 2.5 cm

46
Q

What should you think about if there is pubic hair development and penis enlargement in the absence of testicular enlargement

A

Androgen stimulation from outside the gonadal area

47
Q

Sequence of female pubertal development

A

Breast budding–> pubarche –> peak height velocity –> menarche

48
Q

What is considered delayed puberty?

A

No pubertal signs by age 14 in boys and age 13 in girls

49
Q

Treatment of delayed puberty

A

Should be evaluated by endocrinologist. Monthly IM injections of testosterone for boys and oral estrogen for girls

50
Q

What is premature adrenarche?

A

The presence of androgenic sexual characteristics (axillary hair, pubic hair, acne, and/or adult body odor) without estrogenic sexual characteristics (breast development and menarche) and without the growth spurt of puberty

51
Q

Lab findings in premature adrenarche

A

Elevated serum DHEA and DHEA-S, Low testosterone

52
Q

Causes of premature adrenarche

A

exogenous androgen, endogenous androgen-secreting tumor, late-onset CAH, polycystic ovary syndrome

53
Q

What is the bone age in premature adrenarche or premature thelarche

A

Normal (no more than one year advanced)

54
Q

What is central precocious puberty

A

Development of secondary sexual characteristics accompanied by acceleration in linear growth or advanced bone age. Precocious if starts before 9 in boys or before 8 in girls

55
Q

What is the consequence of central precocious puberty?

A

Short adult height

56
Q

What should you think of with precocious puberty and cafe au lait spots?

A

McCune Albright Syndrome.

Other signs include Cushing syndrome in infants

57
Q

Treatment of precocious puberty

A

Leuprolide (GnRH agonist)

58
Q

What syndromes can have panhypopituitarism?

A

Prader-Willi, Kallmann, and septooptic dysplasia

59
Q

Genetics of androgen insensitivity syndrome?

A

X-linked

60
Q

Why do patients with androgen insensitivity syndrome have a vagina ending in a blind pouch?

A

Because Mullerian inhibiting factor is still produced by the Y chromosome, so no uterus or ovaries develop

61
Q

What should you think of if a newborn male has excessive scrotal pigmentation?

A

Congenital adrenal hyperplasia

62
Q

What levels are high in 21-hydroxylase deficiency?

A

17-hydroxyprogesterone

63
Q

What are the two main hormones produced by the adrenal glands and what do they do?

A

Aldosterone, which helps control the amount of salt and fluid in the body, and cortisol, which helps control how the body uses sugar and how it responds to stress

64
Q

How do you treat adrenal crisis?

A

20 mL/kg of D5NS (with NO potassium) IV over one hour. Then add IV hydrocortisone. Then add glucocorticoid replacement.

65
Q

What is the cosyntropin stimulation test (ACTH stimulation test)?

A

Used to test the adrenals.
With primary adrenal deficiency–> no rise in cortisol levels (b/c adrenals are broken and can’t respond)
With secondary disease–> the adrenal usually have normal cortisol stores and cortisol will be released during the test

66
Q

What is the difference between Cushing syndrome and Cushing disease?

A

Cushing syndrome refers to glucocorticoid excess of any origin. Cushing disease speciically refers to the excessive production of corticotropin by the pituitary gland, which leads to excess cortisol production by the adrenal gland

67
Q

How does Cushing syndrome present in children?

A

Increased BMI with growth arrest. Will also have delayed bone age

Can also see classic acne, purple striae, hirsuitism, virilization, and buffalo hump.

68
Q

Labs to test for Cushing syndrome?

A

24 hour urine free cortisol excretion, midnight sleeping plasma cortisol level (greatest sensitivity of all tests for CS in children), dexamethasone suppression (should lead to undetectable plasma cortisol levels after dexamethasone administration

69
Q

What two hormones is the posterior pituitary responsible for?

A

ADH and oxytocin

70
Q

What presents as diabetes insipidus, exophthalmos, and lytic bone lesions?

A

Langerhans cell histiocytosis

71
Q

Bone age in children with growth delay due to hypothyroidism

A

Delayed

72
Q

Clues to Marfan syndrome in a patient with tall stature

A

Disproportionately long arms (arm span to height ratio >1.05) and significantly long tapering fingers described as arachnodactyly, or spider fingers

73
Q

What is the most common preventable cause of intellectual disability worldwide?

A

Hypothyroidism

74
Q

How should babies take levothyroxine?

A

Crushed and mixed in formula, human milk, or water, but NOT with soy formulas because it reduces absorption

75
Q

How is thyroxine binding globulin deficiency inherited?

A

X-linked

76
Q

Antibodies seen in Hashimoto’s

A

Anti-thyroglobulin and anti-thyroid peroxidase antibodies

77
Q

What antibodies are seen in Graves disease?

A

Thyroid-stimulating immunoglobulin

78
Q

Signs and symptoms of Graves disease?

A

Bulging eyes, emotional lability, weight loss, sleep disturbance, and/or heat intolerance, lid lag, increased appetite with weight loss, decreased muscle strength or endurance, itching, tremors, sweating, increased urination at night, decreased menstrual flow and/or decreased frequency of menses

79
Q

First line agent for Graves and how does it work

A

Methimazole, blocks the organification of iodide and so decreases thyroid hormone synthesis

80
Q

Symptoms of neonatal thyrotoxicosis

A

Irritability, tremors, and tachycardia, failure to thrive, feeding problems, and hyperbilirubinemia

81
Q

What causes neonatal thyrotoxicosis?

A

Exposure to maternal thyroid stimulating antibodies crossing the placenta. Be careful that mom may be on synthroid from having thyroid ablated, but still has circulating antibodies

82
Q

How to correct sodium for elevated glucose

A

Corrected (actual) Na= measured Na +0.3(glucose-5.5)

83
Q

What should you think about if sodium does not increase as glucose falls during treatment for DKA?

A

Overzealous fluid correction. This represents as increased risk for cerebral edema. Important if there is a patient with mental status change during DKA correction

84
Q

When do you put dextrose in the fluids during DKA correction?

A

After glucose drops below 300

85
Q

Definition of metabolic syndrome

A
  1. Hyperinsulinemia or insulin resistance
  2. Dyslipidemia
  3. Hypertension
  4. Obesity, particularly central adiposity
86
Q

Treatment of metabolic syndrome

A

Weight loss, regular exercise. NO recommendation for the use of metformin

87
Q

Definition of hypercalcemia

A

Serum calcium greater than 11 mg/dL

88
Q

Causes of hypercalcemia

A

WISH:
Williams syndrome
Ingestion (vitamin D and A intoxicaton, thiazide diuretics), Immobilization
Skeletal disorders (dysplasias and immobilization/body casts)
Hyperparathyroidism

89
Q

Treatment of hypercalcemia

A

High volume fluid, lasix, and EKG monitoring. In rare cases calcitonin is used.

90
Q

Presentation of hypocalcemia

A

Painful muscle spasms, generalized seizures (can be resistant to diazepam), vomiting, prolonged QT interval on EKA, Chvostek and Trousseau signs, hypomagnesemia

91
Q

Causes of hypocalcemia

A

PINK:
Pseudohypoparathyroidism (peripheral tissue resistant to the effects of PTH)
Intake (nutritional deficiency), Immune deficiency (DiGeorge syndrome)
Nephrotic syndrome (with a lowered albumin level, there is a lower calcium level)
Kidney (renal insufficiency results in higher phosphate, lower calcium, and a secondary hypoparathyroidism

92
Q

What should you think of if you see hypocalcemia and hypophosphatemia?

A

Vitamin D deficiency

93
Q

What do you see on XR of patients with longstanding hypoparathyroidism?

A

Short 4th and 5th metacarpals and metatarsals and calcification of the basal ganglia

94
Q

When might calcium be needed emergently?

A

Hypocalcemia, hyperkalemia, hypermagnesemia, calcium channel blocker ingestion

95
Q

What is rickets?

A

The deficient mineralization of bone at the growth plate. Thus, it cannot occur after the growth plates are closed.

96
Q

What is the alk phos level in rickets?

A

Elevated in all forms of rickets

97
Q

Signs and symptoms of rickets?

A

Bone pain, anorexia, decreased growth rate, widening of the wrist and knees, delayed eruption of teeth, bowed legs, enlarged costochondral junctions (“rachitic rosary”), and softening of the skull bones (craniotabes)

98
Q

Causes of calcipenic rickets?

A

Vitamin D deficient rickets, vitamin D dependent rickets, hereditary vitamin D resistant rickets

99
Q

Why might you see rickets in chronic liver disease?

A

Usually a result of reduced availability of bile salts in the gut and subsequent decreased absorption of vitamin D

100
Q

What causes vitamin D dependent rickets?

A

Inadequate renal production of 1,25 dihydroxy vitamin D. (Autosomal recessive disorder). Also known as pseudo-vitamin D resistant rickets

101
Q

Treatment of vitamin D dependent rickets?

A

Vitamin D2 and 1,25-dihydroxy vitamin D

102
Q

What is hereditary vitamin D resistant rickets?

A

Autosomal recessive hereditary condition due to end organ resistance to vitamin D

103
Q

How do you treat wound botulism?

A

Antitoxin, then penicillin or metronidazole

104
Q

What are the non-treponemal tests for syphillis?

A

RPR and VDRL

105
Q

When do you treat the infant for syphillis if the other had syphillis?

A

If the mother was treated within the past month; if she was treated with erythromycin (does not cross the placenta); or if the baby’s tigers are higher than the mothers

106
Q

Treatment of corynebacterium diphtheria

A

Antitoxin and antibiotics (penicillin or erythromycin)

107
Q

What should you think of in a baby with positive reducing substances in the urine?

A

Galactosemia

Pediatrics Board Exam (1 decks)

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