Fetal Growth Flashcards

1
Q

What are the three phases of fetal growth ,and development?

A

There are three phases of fetal growth and development:

FIRST – 4-20 weeks: Increases in fetal weight, protein content and DNA content (cellular hyperplasia).

SECOND – 20-28 weeks: Increased in protein and weight and lesser increases in fetal DNA content (hyperplasia and concomitant hypertrophy).

THIRD – 28 weeks to term: Continued increases in fetal protein and weight but no further increase in DNA (hypertrophy).

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2
Q

Define fetal growth restriction (FGR).

A

Fetal growth restriction (FGR) (A.K.A IUGR): Failure of a fetus to achieve his or her growth potential.

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3
Q

What are the parameters for small for gestational age (SGA)?

A

Birth weight <10th centile for gestational age. Centiles are based on local populations and can be adjusted for sex, parity, race, maternal weight and height.

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4
Q

What is large for gestational age (LGA)?

A

Birth weight >90th centile.

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5
Q

What is low birth weight (LBW)?

A

Birth weight less than a certain threshold at a certain age e.g. 2500g.

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6
Q

What are neonatal indices?

A

These are other measurements to see if the baby has met their growth potential: Ponderal index, skinfold thickness, MAC/HC ratio.

Ponderal index = birth weight in g/length in cm³ x 100.

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7
Q

What are the consequences of fetal growth restriction?

A

Occurs in 3-10% of all births. Significant cause of perinatal mortality and morbidity. 85% of unexplained stillbirths may be due to FGR. LBW infants are more likely to die within the first year of life and suffer from neonatal problems such as birth asphyxia, hypoglycaemia, hypothermia, polycythaemia, neurodevelopmental defects, and cerebral palsy. FGR can be an origin of adult disease in later life.

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8
Q

What happens with most FGR?

A

Most with FGR show catch-up growth in childhood though may have smaller size in adulthood.

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9
Q

What is the ‘Barker hypothesis’?

A

Fetal programming → Barker hypothesis. GR (IUGR) can have lifelong impact - increase chances of having impaired glucose tolerance or diabetes or metabolic syndrome.

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10
Q

What does evidence show that those with FGR are at increased risk of in adult life?

A

Good evidence that those with FGR have an increased risk in adult life of obesity, type 2 diabetes, high BP, stroke, heart disease, secondary to changes in growth, metabolism, and vasculature. However, postnatal factors are also important.

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11
Q

Describe the intergenerational effect that can lead to FGR.

A

Mothers who were small for gestational age (SGA) themselves are more likely to have SGA babies and increased perinatal mortality. Rodent models show that maternal undernutrition (F0) increases adiposity, glucose intolerance, and cardiovascular risk in F1 and F2 generations.

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12
Q

What are the mechanisms for trans-generational effects?

A
  1. Epigenetics: Heritable changes in gene expression by mechanisms other than underlying DNA sequences (e.g., DNA methylation, histone modification, micro RNA).
  2. Maternal mitochondria: Food restriction can alter the number and function of mitochondria, directly passed onto offspring through ova.
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13
Q

Define LGA.

A

Large for gestational age (LGA) = Birth weight >90th centile. Macrosomia: birth weight >4500g.

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14
Q

What are the causes of LGA?

A

Gestational age; pregnancies that go beyond 40 weeks increase incidence. Fetal sex; male infants tend to weigh more than female infants. Excessive maternal weight gain and obesity. Multiparity increases size. Erythroblastosis fetalis - Hydrops Fetalis. Genetic disorders of overgrowth (e.g., Beckwith-Wiedemann syndrome, Sotos syndrome). Maternal diabetes (pre-existing or gestational).

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15
Q

What is the pathophysiology for diabetes causing macrosomia?

A

Increased maternal glucose concentrations lead to increased fetal insulin concentrations, which increases fetal growth factors and ultimately increases birth weight.

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16
Q

What is the fetal programming relation to LGA?

A

LGA babies have increased risk of impaired glucose tolerance, diabetes, or metabolic syndrome. Evidence suggests that curves may actually be U-shaped; very low and very high birth weight predispose you to these diseases.

17
Q

What is a major growth issue in the developing world?

A

In the developing world, IUGR is a major cause of perinatal mortality/morbidity, often due to maternal undernutrition, synergistic with low age, maternal anaemia, chronic disease/HIV, and placental malaria.

18
Q

What are the maternal factors for abnormal fetal growth?

A
  1. Ethnicity: Certain ethnic groups are at increased risk of having SGA babies.
  2. Maternal stature/BMI: Taller genetics result in increased birth weight.
  3. Maternal Nutrition: Availability of Vit D, Folic acid, and a well-balanced diet are important in preventing SGA.
  4. Maternal hypoxia: Conditions like cyanotic heart disease increase the likelihood of FGR.
  5. Drugs: Cigarettes, alcohol, and drugs of abuse increase the risk of FGR.
19
Q

What are the fetal factors for abnormal growth?

A
  1. Genome: Chromosomal disorders (e.g., Down syndrome).
  2. Growth factors: Insulin-like growth factors, thyroxine.
  3. Congenital infection: Cytomegalovirus (CMV), Toxoplasmosis, rubella.
20
Q

What are the placental factors for abnormal growth?

A
  1. Primary placental problems: Abnormality of placenta structure/function.
  2. Maternal problems that have secondary placental problems: Hypertension, chronic renal disease, vasculitis, pro-thrombotic disorders.
  3. Multiple gestation causes: Growth discordance, e.g., two fetuses sharing one placenta.
21
Q

Describe malplacentation in IUGR (FGR).

A

Majority of blood flow to the uterus is supplied by uterine arteries. Poor trophoblast invasion of maternal spiral arteries results in increased impedance to flow and decreased placental perfusion.

22
Q

What is uterine artery Doppler waveforms and what can it be used for clinically?

A

Uterine artery Doppler waveforms measure blood flow from the uterine artery into the placenta. Notching in the waveform can indicate decreased blood flow into the placenta during diastole, which can predispose to FGR and preeclampsia.

23
Q

How do we monitor fetal growth during pregnancy?

A

Fetal growth is monitored during ultrasound (USS) by taking measurements of head and abdominal circumference and femur length.

24
Q

How do we monitor fetal growth during pregnancy?

A

We monitor fetal growth during pregnancy using ultrasound (USS). We take measurements of head circumference, abdominal circumference, and femur length to estimate fetal weight.

25
What is uteroplacental insufficiency?
Uteroplacental insufficiency leads to decreased glycogen stores in the baby, resulting in decreased abdominal circumference while head circumference growth is maintained. This results in asymmetrical growth, indicating a fetal growth pathology.
26
What is symmetrical growth restriction?
In symmetrical growth restriction, both head circumference and abdominal circumference grow but at a reduced velocity. This can indicate early growth insult, chromosomal issues, or viral infections.
27
Are symmetrical/asymmetrical patterns of IUGR useful predictors?
These patterns are observed but are generally not helpful in predicting cause or outcome. It is important to distinguish between small but healthy and small but not well (IUGR).
28
What are the causes of abnormal fetal growth?
Causes of abnormal fetal growth include maternal, fetal, and placental factors.
29
What occurs at each antenatal visit?
At each antenatal visit, gestational age is recorded, blood pressure and urine are measured to assess the risk of pre-eclampsia, and fetal movements are discussed.
30
What is involved in fetal growth assessment?
Fetal growth assessment involves measuring symphsio-fundal height, which is plotted on a graph. If there is tailing growth, a referral to USS is made. High-risk women undergo USS surveillance.
31
What occurs in fetal wellbeing assessment?
Fetal wellbeing assessment can be done immediately via CTG. Long-term wellbeing is measured using Doppler indices and liquor volume. Abnormalities in these measurements indicate growth restriction.
32
What are the risk factors for SGA during pregnancy?
Risk factors for SGA include diabetes, previous SGA, previous stillbirth, low maternal weight gain, vigorous exercise, cocaine use, and maternal age over 40.
33
What is gestational diabetes?
Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with its onset during pregnancy, occurring in 5% of all pregnancies.
34
What happens to GD as pregnancy advances?
As pregnancy advances, insulin resistance increases due to hormonal and inflammatory changes.
35
When do you screen for GD in pregnancy?
Screen from 16-18 weeks if there is a past history of GDM. Screen from 24-26 weeks for family history, PCOS, BMI > 30, certain ethnicities, previous macrosomia, or unexplained stillbirth.
36
What are maternal complications of GDM?
Maternal complications include pre-eclampsia, preterm labor, increased risk for instrumental delivery or cesarean section, and diabetes in later life.
37
What are fetal complications of GDM?
Fetal complications include macrosomia, shoulder dystocia, polyhydramnios, perinatal mortality, and increased risks of adult diseases.
38
What is the management for GDM?
Management involves a multi-disciplinary approach including obstetricians, diabetologists, and dieticians, with regular growth scans, blood glucose monitoring, and dietary control.