NICU Boards Review 1 Flashcards

1
Q

In this autoimmune disease, the body makes antibodies against acetylcholine receptors

A

Myasthenia Gravis

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2
Q

What percentage of neonates born to mothers with Myasthenia Gravis will develop transient neonatal myasthenia gravis?

A

10-20%

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3
Q

Pathophys of transient neonatal myasthenia gravis

A

Results from placental passage of maternal antibodies (IgG) to acetylcholine receptors

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4
Q

Symptoms of neonatal myasthenia gravis include….
These symptoms last for how long…?

A

Symptoms: weak cry, hypotonia, poor oral feeding (due to difficulty swallowing due to weak oropharyngeal muscles from the acetylcholine receptors getting attacked by maternal IgG antibodies to these receptors)

Symptoms show up early (by 72 hours of life) and peak around 3 weeks. Almost always resolved by 2 months of age, but sometimes (for 10% of infants) takes up to 4 months. But MOST infants will be symptom free by age 2 months.

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5
Q

Infant has stippled bone epiphyses. Mom took what drug between 6-12 weeks gestation?

A

Warfarin

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6
Q

Describe the clinical findings of a neonate affected by early (6-12 wks gestation) maternal warfarin use:

A

-depressed nasal bridge and nasal hypoplasia
-low birthweight
-stippled bone epiphyses
-can also have seizures and cognitive disabilities

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7
Q

What is the maternal quad screen–what tests does it consist of, and when should it be performed?

A

Quad screen: AFP, unconjugated estriol, b-hCG, inhibin A

Optimal timing: 16 weeks (but can be done between 14-20 weeks)

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8
Q

Ileal atresia is associated with this in utero drug exposure

A

cocaine

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9
Q

Early decels are caused by

A

fetal head compression

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10
Q

Why do early decels happen, what causes them?

A

Fetal head gets compressed
This causes fetus to vagal
which causes fetal heart rate to get lower

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11
Q

What causes variable decels?

A

umbilical cord compression

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12
Q

Pathophys of variable decels

A

Caused by umbilical cord compression
This leads to either a baro or chemoreceptor vagal response that causes the HR to drop, OR, it causes more direct fetal myocardial depression

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13
Q

The most common cause of late decels is

A

placental insufficiency

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14
Q

Describe the 2 mechanisms (both of which lead to placental insufficiency) that cause late decels in a fetus:

A
  1. Placental insufficiency leads to fetal hypoxemia–> chemoreceptors respond by increasing alpha adrenergic activity–> fetal blood pressure goes up–> fetal HR goes down (baroreceptor/parasympathetic response to the hypertension)
  2. Placental insufficiency–> fetal hypoxemia–>myocardial depression–> HR slows
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15
Q

Placental insufficiency leads to this kind of decel:

A

Late

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16
Q

Cord compression leads to this kind of decel:

A

variable

17
Q

What is the incidence of a single UA (aka 2 vessel cord)?

A

<1% of the population

18
Q

Fetal head compression leads to this kind of decel:

A

early

19
Q

This maternal medication increases the risk of neonatal PPHN

A

Indomethacin

20
Q

Bad effects that maternal indomethacin use can have on neonate (aka why prolonged maternal use is not recommended):

A

PPHN
renal insufficiency
ileal perforation
NEC

21
Q

What is indomethacin used for in obstetric care? MOA?

A

= a prostaglandin synthase inhibitor
used as a tocolytic (aka to stop contractions in PTL)

22
Q

Congenital heart defect associated with lithium

A

Ebstein’s anomaly

23
Q

What is the most common complication of pregnancy?

A

pre eclampsia

24
Q

Incidence of pre-eclampsia

A

5-10% of pregnant women

25
Q

Name 5 risk factors for pre-eclampsia:

A

Primaparity
Twin/multiple gestation
Chronic hypertension
Obesity
Diabetes

26
Q

Define pre-eclampsia

A

= hypertension that develops after 20 weeks gestation with associated proteinuria

27
Q

HELLP syndrome stands for

A

H emolysis
E levated L iver enzymes
L ow P latelets

28
Q

Which is more common, transient neonatal myasthenia gravis, or congenital myasthenia gravis?

A

Transient neonatal myasthenia gravis is much more common. This occurs in 10-20% of infants born to moms with MG. Congenital MG on the other hand is rare, and shows up later in childhood.

29
Q

In transient neonatal myasthenia gravis, do maternal antibody titers and the severity of maternal disease affect how severe the neonate’s disease will be?

A

Nope. No correlation.

Instead it’s just related to how well the maternal antibody against maternal acetylcholine receptor binds to the FETAL acetylcholine receptor.

30
Q

Does the severity of NAS symptoms correlate with the amount of drug (dose) or duration of intake by the mother?

A

NO

Although I mean come on, one dose of morphine won’t be the issue.
It must be somewhat sustained use. So sure. But the point here is the dose does NOT correlate with how severe the NAS symptoms are, oddly enough.

31
Q

What is the palpebral fissure

A

= distance between the medial and lateral corners of one eye

32
Q

Short palpebral fissures, smooth area between nose and mouth (philtrum), and thin upper lip =

A

Fetal alcohol syndrome

33
Q

Describe the physical features of a newborn with fetal alcohol syndrome:

A

Dysmorphic facies (thin vermillion border of upper lip), smooth philtrum, short palpebral fissures, microcephaly, and low birth weight. Later on, intellectual disability.

VSD or other cardiac defects also common ish.

34
Q

Is twin to twin transfusion syndrome more common in mono di or mono mono twins?

A

Mono di

Can occur in mono mono twins but the risk is lower than in mono di twins. huh.

35
Q
A