Chapter 10 Flashcards

1
Q

Cylopamine effects

A

teratogen that causes craniofacial abnormalities

“cyclopia”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Valproic acid

A

antilepileptic
teratogen
disripts HOX protein
mimic features of valproic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Excessive retinoic acid as teratogen

A

retinoic acid embryopathy
involves CNA, cardiac and craniofacial defects
cleft lip, cleft palate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

PPROM

A

ROM rupture before 37 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

PROM

A

ROM rupture after 37 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Chorioamniocentesis

A

inflammation of the placental membrane in intrauterine infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Funisitis

A

inflammation of umbilical cord in intrauterine infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

TORCH infections

A

toxoplasmosis, rubella, cytomegalovirus, herpes,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Fetal infections

A

TORCH infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Proportionate FGR

A

when a small for gestational age baby has proportionate organ size to their body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can cause uteroplacental insufficiency? (5)

A
umbilical vascular abnormalities
placental abruption
placental thrombosis and infarction
placental infections
multiple gestations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Who has proportionate FGR

A

babies experiencing fetal abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Babies experiencing placental abnormalities

A

usually have asymmetric growth retardation of the fetus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Most common factors associated with SGA

A

vascular diseases and thrombophilias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Vascular diseases of maternal abnormalities

A

preeclampsia and chronic hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

3 common features of child born with untreated RDS

A

preterm, normal weight, associations with male, maternal diabetes, and C-section

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

2 complications of RDS

A
  1. retrolental fibroplasia

2. bronchopulmonary dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are recovery RDS patients at risk for?

A

patent ductus arteriosus, intraventricular hemorrhage, necrotizing enterocolitis

19
Q

Mediator of necrotizing enterocolitis

A

PAF which promotes mucosal permeability

20
Q

Clinical presentation of necrotizing enterocolitis?

A

bloody stools, abdominal distension, circulatory collapse

21
Q

Clinical presentation of necrotizing enterocolitis?

A

bloody stools, abdominal distension, circulatory collapse

22
Q

Two routes of perinatal infection

A

transcervical (ascending)

transplacental (hematologic)

23
Q

Sequelae for transcervical infection

A

ingesting amniotic fluid, pneumonia, sepsis, and meningitis

24
Q

Sequelae for transcervical infection

A

ingesting amniotic fluid, pneumonia, sepsis, and meningitis

25
Q

What does Parvovirus B19 do?

A

causes erythema infection

26
Q

TORCH clinical manifestations

A

fever, encephalitis, chorioretinitis, hepatosplenomegaly, pneumonitis, myocarditis, hemolytic anemia, vesicular or hemorrhagic skin lesions

27
Q

TORCH clinical manifestations

A

fever, encephalitis, chorioretinitis, hepatosplenomegaly, pneumonitis, myocarditis, hemolytic anemia, vesicular or hemorrhagic skin lesions

28
Q

Late onset perinatal sepsis

A

longer latent period of when organism enters and when it shows signs
*Listeria and Candida

29
Q

Late onset perinatal sepsis

A

longer latent period of when organism enters and when it shows signs
*Listeria and Candida

30
Q

Immune hydrops

A

hemolytic anemia caused by Rh blood group incompatability between mother and fetus
ex. Rh and ABO

31
Q

Immune hydrops

A

hemolytic anemia caused by Rh blood group incompatability between mother and fetus

32
Q

Cystic hygroma

A

localized edema or post nuchal fluid accumulation

33
Q

Maternal Rh isoimmunization

A

Rhesus immune globulin that contains anti-D antibodies

34
Q

2 consequences of destruction of red blood cells in a neonate

A
  1. Anemia

2. Jaundice

35
Q

Kernicterus

A

yellow discoloration of brain parenchyma

36
Q

3 causes of nonimmune hydrops

A
  1. structural and functional cardiovascular defects
  2. chromosomal anomalies
  3. fetal anemia
37
Q

3 causes of nonimmune hydrops

A
  1. structural and functional cardiovascular defects
  2. chromosomal anomalies
  3. fetal anemia
38
Q

Clinical signs of PKU (5)

A

strong musty diaper odor, sever mental retardation, seizures, decreased pigmentation of hair and skin, eczema

39
Q

Clinical signs of PKU (4)

A

sever mental retardation, seizures, decreased pigmentation of hair and skin, eczema

40
Q

Mechanism of maternal PKU

A

phenylalanine crosses the placenta and becomes teratogenic to the fetus

41
Q

Mechanism of maternal PKU

A

phenylalanine crosses the placenta and becomes teratogenic to the fetus

42
Q

Biochemical cause of PKU

A

phenylalanine can’t be converted to tyrosine due to lack to phenylalanine hydroxylase

43
Q

Lack of tyrosine

A

depigmentation of hair and skin

*tyrosine goes to melanin

44
Q

THB form of PKU

A

important because it can’t be treated with dietary restriction of phenylalanine