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Rob's RDA > Foetal growth > Flashcards

Foetal growth Flashcards

1
Q

Define foetal growth

A

The increase in mass that occurs between the end of the embryonic period and birth.

(i.e. not development of structurs)

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2
Q

What is Symphysis Fundal Height (SPH)

A

the distance between the pubic symphysis and the top of the uterus, as shown in Figure 6.1

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3
Q

What might lead to lower values for the SFH at each week of development than should be the case

A

wrong last menstrual period date,

the baby in a transverse lie,

or complications including oligohydramnios (low levels of amniotic fluid)

or a baby that is small for gestational age (SGA).

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4
Q

Why might higher values be found for SFH than should be

A

wrong last menstrual period date,

multiple pregnancy,
or

maternal obesity.

Complications:

molar pregnancy, fibroids, polyhydramnios or a baby that is large for gestational age (LGA).

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5
Q

What can SFH detect

A

This simple and inexpensive measurement may identify gross changes in size, and hence gross complications in the pregnancy,

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6
Q

Why is SFH of limited use

A

many confounders, which include the problems listed above, as well as considerable inter-operator variability.

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7
Q

Why might the size of foestuses during miscarriage of pregnacy not be the best representation of normal foetal size at that age

A

did not take account of the possible causative relationship between low fetal growth leading to miscarriage, and hence such data may be inaccurate.

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8
Q

Differentiate changes in foetal height and foetal weight in pregnancy

A

It can be seen that fetal weight continues to increase during pregnancy, while fetal length changes less in the later stages.

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9
Q

Measure of length of foetus

A

Crown rump length

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10
Q

What was miscarriage data for foetal growth replaced with

A

in utero scanning

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11
Q

When is foetal growth fastest

A

Mid-third trimester

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12
Q

What is responsible for extent of foetal growth

A
  1. Genetic

2. Substrate supply

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13
Q

Outline the genetics as responsible for extent of foetal growth

A
  • derived from both parents
  • parents who are taller or bigger will have infants that are different in size to parents who are shorter or lighter in build.
  • mediated by factors under genetic control, including mediators such as the insulin-like growth factors.
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14
Q

Outline the substrate supply as responsible for extent of foetal growth

A

sufficient nutrients are essential to achieve genetic potential. This is primarily based on the placenta which is dependent upon both uterine and placental vascularity.

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15
Q

How is foetal growth assessed on ultrasound

A

Biparietal diameter (BPD),

Head Circumference (HC),

Abdominal Circumference (AC)

and

Femur Length (FL).

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16
Q

What is a composite measure of growth from ultrasound, what is it based on

A

Estimated Fetal Weight (EFW):

based on

Biparietal diameter (BPD),

Head Circumference (HC),

Abdominal Circumference (AC)

and

Femur Length (FL).

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17
Q

What can normative growth curves from ultrasound measurements be used for

A

They are used clinically to identify a normal intrauterine growth and detect risk of obstetric and neonatal complications.

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18
Q

What is ultrasound most importnat for

A

Note that ultrasound can also be used to assess fetal wellbeing, which can be a more important use of the technology

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19
Q

Why are centiles important and useful

A

allows compensation for different sizes of infants that are growing and developing normally.

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20
Q

How should the growth pattern for each of the 4 US variables look over time

A

For any infant, the changes in each parameter can be plotted, and the growth over time visualised. In a normal pregnancy, each parameter is expected to follow a centile, showing steady increases in size.

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21
Q

What are customised foetal growth charts

A
  • allow for a more individualised assessment
  • based on fetal weight curves for NORMAL pregnancies
  • adjusted to reflect maternal constitutional variation e.g. maternal height, weight, ethnicity, parity.
  • optimised by presenting a standard free from pathological factors such as diabetes and smoking.
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22
Q

What is growth velocity, and state patterns

A

Overall average rate at which an infant gains weight

14-15 weeks= 5g/day

20 weeks= 10g/day

32-34 weeks=30-35g/day

AFTER 34 WEEKS DECREASES: decreased velocity towards the end of pregnancy

GROWTH RATE HIGHEST MID-THIRD TRIMESTER

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23
Q

What are the 3 phases of foetal growth

A

Cellular hyperplasia (increased cell numbers): 4-20 weeks

Hyperplasia and hypertrophy (increased cell size): 20-28 weeks

Hypertrophy dominates: 28-40 weeks

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24
Q

Is hyperplasia or hypertrophy more important for foetal weight gain? How do we know

A

As the main increase in fetal weight occurs during the final trimester of pregnancy, hypertrophy is a key factor.

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25
Q

What is last menstrual period an estmate of

A

Gestational age (i.e. PF plus around two weeks)

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26
Q

What are the confonding factors around LMP

A

Irregular length of periods; abnormal endometrial bleeding; the use of oral contraceptives; breastfeeding.

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27
Q

When is LMP less liley ot be precise

A

If couple weren’t planning pregnancy

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28
Q

Why is dating in pregnancy importnat

A

a change in the dates may lead to a pregnancy being inappropriately identified as Large or Small for gestational age

Clinical decisions about delivery timings and methods (induction or Caesarean section) may not be correct

glucocorticoids are given prior to preterm delivery to enhance lung surfactant production and subsequent lung function.

All pregnancies dated by CRL apart from IVF

HC used if scan done after 14wk

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29
Q

Ho can the pregnancy be dated by US, at what time and why

A

determining the Crown-Rump length of the fetus, preferably towards the end of the first trimester; variations in fetal size are more limited at this stage of development, so the gestational age of the infant can be estimated more precisely.

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30
Q

Maternal factos affecting foetal growth

A
  1. Poverty
  2. Mother’s age
  3. Drug use
  4. Alcohol
  5. Smoking and nicotine
  6. Diseases
  7. Mother’s diet and physical health
  8. Mother’s prenatal depression
  9. Environmental toxin
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31
Q

How can poverty affect foetal growth

A
  • more likely to have children at a younger age, which can result in low birth weight
  • Many of these expecting mothers have little education and are therefore less aware of the risks of smoking, alcohol, and drugs – other factors that influence the growth rate of a fetus.
  • Women in poverty are more likely to have diseases that are harmful to the fetus.
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32
Q

How can mother age affect foetal growth

A
  • Women over 35 are more inclined to have a longer labour period, could result in death of mother or fetus.
  • Women under 16 and over 35 have higher risk of preterm labour and this risk increases for women in poverty, African Americans, and women who smoke
  • Young mothers more likely to drink, smoke, drugs
  • Premature babies from young mothers increase likelihood of neuro defects influencing their coping
  • increased risk of Down syndrome for infants born to those aged over 40 years
  • Young teenaged mothers (younger than 16), and mothers over 35, are more exposed to the risks of miscarriages, premature births, and birth defects.
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33
Q

How do drugs reach the foetus

A

Maternal drug use occurs when drugs ingested by the pregnant woman are metabolized in the placenta and then transmitted to the fetus

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34
Q

What can maternal drug use lead to

A
  • greater risk of birth defects, low birth weight, and a higher rate of death in infants or stillbirths.
  • extreme irritability, crying, and risk for SIDS once the fetus is born
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35
Q

Effect of marijuana on foetal groth

A

Marijuana will slow the fetal growth rate and can result in premature delivery. It can also lead to low birth weight, a shortened gestational period and complications in delivery

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36
Q

Effect of heroin on foetal growth

A

interrupted fetal development, stillbirths, and can lead to numerous birth defects. Heroin can also result in premature delivery, creates a higher risk of miscarriages, result in facial abnormalities and head size, and create gastrointestinal abnormalities in the fetus. There is an increased risk for SIDS, dysfunction in the central nervous system, and neurological dysfunctions including tremors, sleep problems, and seizures. The fetus is also put at a great risk for low birth weight and respiratory problems.

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37
Q

Effect of cocain on foetal weight

A

maller brain, which results in learning disabilities for the fetus. Cocaine puts the fetus at a higher risk of being stillborn or premature. Cocaine use also results in low birthweight, damage to the central nervous system, and motor dysfunction.

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38
Q

Effect of alcohol on foetal growth

A

disruptions of the fetus’s brain development, interferes with the fetus’s cell development and organization, and affects the maturation of the central nervous system

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39
Q

What organs can alcohol use affect in foetus

A

heart and other major organ defects, such as small brain

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40
Q

What can result from brain defects due to alcohol use in pregnancy

A

Could affect the fetus’s learning behaviors. Alcohol use during pregnancy can cause behavioral problems in a child,

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41
Q

How can alcohol affect the foetus when it is a child

A

lcohol use during pregnancy can cause behavioral problems in a child, mental problems or retardation and facial abnormalities – meaning smaller eyes, thin upper lip, and little groove between the nose and lips.

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42
Q

T/F alcohol can also increase the risk of miscarriages and stillbirths, or low birth weight.

A

T

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43
Q

What is foetal alcohl sndrome

A

Children with FAS have a variety of distinctive facial features, brain abnormalities, and cognitive deficits.

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44
Q

How can smoking affect foetal growth

A

fetus is exposed to nicotine, tar, and carbon monoxide.

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45
Q

How does nicotine and CO affect foetus

A

Nicotine results in less blood flow to the fetus because it constricts the blood vessels

Carbon monoxide reduces the oxygen flow to the fetus.

Eduction of blood and oxygen flow results in stillbirth, low birth weight, and ectopic pregnancy. There is an increase of risk of sudden death syndrome (SIDS) in infants.

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46
Q

What can increase ris of asthma for baby

A

smoking during pregnancy

ow birth weight and premature births can also increase the risk of asthma if a mother smoked during pregnancy because of the effects on the respiratory system of the fetus.

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47
Q

How can diseases affect foetal growth

A

If a mother is infected with a disease, the placenta cannot always filter out pathogens. Babies can be born with venereal diseases transmitted by the mother.

48
Q

How can mothers diet affect foetal health

A

An adequate nutrition is needed for a healthy fetus. A lack of iron results in anemia in the fetus, the lack of calcium can result in poor bone and teeth formation, and the lack of protein can lead to a smaller fetus and mental retardation.

49
Q

How can mother prenatal depression affect foetal growth

A

ower fetal growth rates. It appears that prenatal maternal cortisol levels play a role in mediating these outcomes.

50
Q

How can environmental toxins affect foetal growth

Give examples

A

higher rates of miscarriage, sterility, and birth defects

lead, mercury, and ethanol or hazardous environments.

51
Q

Feto-placental factors influencing foestal growth

A
  1. Gender

2. Hormones

52
Q

How does gender affect foetal growth

A

Males are usually bigger than females.

53
Q

How does preious pregnancy affect foetal growth

A

Generally infants are heavier in second and subsequent pregnancies, but this is based on large patient groupings, so extrapolating to an individual pregnancy is difficult, due to all the other potential variables.

54
Q

What is accretion

A

growth or increase by the gradual accumulation of additional layers or matter.

55
Q

What aspects of foetal growth do hormones impact

A

both tissue accretion and differentiation and enable a precise and orderly pattern of growth to occur during late gestation

56
Q

What are hormones action on growth mediated by

A

In part, their actions on growth may be mediated by other growth factors such as the insulin-like growth factors (IGFs).

57
Q

How does insulin control foetal growth

A

Insulin stimulates fetal growth by increasing the mitotic drive and nutrient availability for tissue accretion. It has little effect on tissue differentiation.

58
Q

How does cortisol affect foetal growth

A

the main effects of cortisol in utero are on tissue differentiation and maturation.

in contrast to insulin

59
Q

How does cortisol afffect foetal growth on a molecular level

A

Remember this is talking about differentiation so it makes sense

appears to act directly on the cells to alter gene transcription or post-translational processing of the gene products

-may also initiate the transition from the fetal to the adult modes of growth regulation by inducing the switch from IGF-II to IGF-I gene expression in the fetal liver. (remember these hormones are occurring late in the gestation period)

60
Q

How does thyroxine affect foetal growth

A

affects both tissue accretion and differentiation in the fetus by a combination of metabolic and non-metabolic mechanisms.

61
Q

T/F pituitary growth homone doesn’t control foetal growth or postnatal growth

A

Pituitary growth hormone, on the other hand, appears to have little part in the control of fetal growth, unlike its role postnatally.

62
Q

What promotes growth and development in the foetus

A

Fetal hormones, therefore, promote growth and development in utero by altering both the metabolism and gene expression of the fetal tissues

63
Q

Why are hormones needed to impact foetal growth rate?

A

These hormonal actions ensure that fetal growth rate is commensurate with the nutrient supply and that prepartum maturation occurs in preparation for extrauterine life.

64
Q

What are IGFs overall function

A

-Mitogenic, stimulating fetal metabolism and coordinating the feto-placental metabolism.

65
Q

What is the function of IGF1 and IGF2

A

IGF-II regulates early embryonic development while

IGF-I is responsible for the growth of the newborn.

66
Q

Role of foetal insulin on foetal growth (more detail)

A

plays an indirect role in

  • indirect role the regulation of fetal growth. It modulates the expression of the fetal IGF.
  • direct effects on adipose tissue + prolferation of fetus cells
  • Little effect on differentiation or prenatal maturation
67
Q

Affect of glucocorticoids (i.e. cortisol) on foetal growth more detail

A

affects tissue differentiation and prenatal development of the organs

68
Q

Glucocorticoids affect differentatin and development of which organs

A

lungs (maturation of the surfactant), liver (control of glycemia), as well as the intestines (maturation of the expression of digestive enzymes and proliferation of the villi)

69
Q

What other hormone do glucocorticoids work with

A

glucocorticoid, together with thyroid gland hormones, affects the maturation of the lungs and the nervous system

(remember thyroid hormones affect tissue accretion and differentiation)

70
Q

Effect of growth hormone on foetal growth

A

Growth hormone (GH) has no effects on prenatal growth. This explains the absence of growth deficiencies in congenital hypopituitarism.

71
Q

Other factors than insulin (and IGFs) and cortisol and thyroxine affecting foetal growth

A

EGFs

TGFs

FGFs

Embyronic colinesterase (ChE) - morphogenesis

Interleukins 1 - implantation

Sexual hormones (for differentiation of reproductive tissue).

72
Q

Role of EGFs on foetal growth

A

strongly mitogenic and form a group of molecules that bind to the same receptors (tyrosine kinase)

73
Q

Role of TGFs on foetal growth

A

super-family that numbers more than 30 members (TGFb, activin, BMP [bone morphogenetic proteins], GDNF [glial-derived neurotropic factor]).

74
Q

Role of FGFs in foetal growth

A

There are 20

75
Q

Role of ChE in foetal growth

A

Enzyme that is active in morphogenesis.

Depending on their developmental stage embryonic cells express muscarinic receptors on their surfaces for acetylcholine and synthesize cholinesterase, which is able to inactivate neurotransmitters.

76
Q

When are interluekins 1 important in foetal growth

A

They play an important role during implantation.

77
Q

Why are sexual hormones importnat

A

Sexual hormones of embryonic origin are essential for differentiation of reproductive tissues

78
Q

Define small for gestational age (SGA)

A

The infant has a birth weight <10th centile (also called ‘Small for dates’).

79
Q

Define itrauterine growth restriction (IUGR)

A

Failure of the infant to achieve its predetermined (genetic) potential for a variety of reasons.

80
Q

Define low birth weight

A

Less than 2,500g at delivery. Currently ~7% of live births (UK).

81
Q

Define very low birth weight

A

Less than 1,500g at delivery. Currently ~1% of live births (UK).

82
Q

Defie extremely low birth weight

A

Less than 1,000g at delivery. Currently ~0.2% of live births (UK).

83
Q

T/f low/very low etc birthweight take account of gestational age

A

F

hey simply refer to the weight of the infant at delivery. This is very important – for example, an infant of 2,500g at term would be considered SGA, whereas if delivered at 33 weeks this would be an appropriate weight for a normal infant

84
Q

Why does birth weight matter

A

Infants who are inappropriately small at delivery are at increased risk of a range of neonatal complications. In many cases, treatment is best started as soon as possible, so identifying the at-risk infants is important.

85
Q

Differentiate the type of low birthweight

A
  1. infants born preterm, who are of low birthweight simply because they have been born early
  2. those who are growth restricted
86
Q

Which type of low birthweight baby has greater risk of morbiites and mortalities after delivery

A

those who are growth restricted (not those who have just been born early)

87
Q

Which type of low birthweight baby is more common

A

One that has been born early (not one who has been growth restricted)

88
Q

When looking at IUGR, which centile on a weight/weeks of gestation is most sensitive and which most spefici

A

Use figure 1.1

Small for gestational age changes depending on when the baby was born

The ELBW/VLBW/LBW does not change depending on when baby was born.

10th centile most sensitive

3rd centile most specific

89
Q

What is the benefit and problem with using 10th centile of birth weights for determining IUGR?

A

will capture all babies with IUGR, but will also include those babies that are just small for gestational age, i.e. you get a number of false positives.

just because a baby is SGA doesn’t mean they have IUGR (IUGR depends on what they were supposed to be )

90
Q

What is the benefit and problem with using 3rd centile of birth weights for determining IUGR?

A

All babies recorded using the third centile will have IUGR, but some IUGR babies may be missed, i.e you get a number of false negatives.

91
Q

Measurements of birth weight and centiles etc take account of parents

A

Note that none of these measurements take parental characteristics into account, so there is no consideration of the importance of genetic factors.

92
Q

What is the best way to measure growth restriction

A

The term IUGR should only be used for fetuses with definite evidence that growth has altered.

it can only be assessed by serial observation.

93
Q

Most common identifiable factor in babies who are still-born

A

IUGR

Note that IUGR babies are at greater risk of coplications, and those complications aare likely to be more severe in growth restriction

94
Q

Short term outcomes of IUGR

A 
Respiratory distress
Intraventricular haemorrhage
Sepsis
Hypoglycaemia
Necrotising enterocolitis
Jaundice
Electrolyte imbalance
95
Q

What is medium term impact of IUGR

A

Respiratory problems
Developmental delay
Special needs schooling

96
Q

What are long term impacts of IUGR

A

Fetal programming

97
Q

When does IUGR normally develop

and what factors can it be due to overall

A

IUGR generally develops in the second and third trimesters of pregnancy

  • maternal medical
  • maternal behavioural
  • foetal
  • placental
98
Q

Some maternal medical factors linked to IUGR and SGA fetus

A 
Chronic hypertension
Connective tissue disease
Severe chronic infection
Diabetes mellitus
Anaemia
Uterine abnormalities
Maternal malignancy
Pre-eclampsia
Thrombophilic defects
99
Q

Some maternal behavioural factors linked to IUGR and SGA fetus

A 
Smoking
Low booking weight (<50 kg)
Poor nutrition
Age <16 or >35 years at delivery
Alcohol
Drugs
High altitude
Social deprivation
100
Q

Some foetal factors linked to IUGR and SGA fetus

A 
Multiple pregnancy
Structural abnormality
Chromosomal abnormalities
Intrauterine (congenital) infection
Inborn errors of metabolism
101
Q

Placental factors leading to IUGR and SGA fetus

A 
Impaired trophoblast invasion
Partial abruption or infarction
Chorioamnionitis
Placental cysts
Placenta praevia
102
Q

What is the cause of pre-exclampsia (=pre-eclamptic toxaemia, PET)

A

the main cause of pre-eclampsia is diminished remodelling of the spiral arteries by cytotrophoblast, which causes decreased blood flow and hence decreased nutrient supply to the placenta and fetus.

103
Q

What is PET associated with

A

There is a close link between pre-eclampsia (pre-eclamptic toxaemia, PET) and IUGR, so that these complications often occur together.

104
Q

Criteria for pre-eclampsuia

A
  1. gestational hypertension of at least 140/90 mmHg on two separate occasions ≥4 hours apart
  2. Significant proteinuria

arising de novo after the 20th week of gestation in a previously normotensive woman and resolving completely by the 6th postpartum week.

105
Q

T/F IUGR only occurs with PET

A

f IUGR can occur independently of pre-eclampsia

106
Q

When could IUGR occur without PET

A

sometimes this may be because of altered placental function, without any maternal symptoms, but mostly it will be the result of some complication within the fetus itself.

107
Q

Risk factors for preterm devliery

A

pre-eclampsia and IUGR are both risk factors for preterm delivery.

108
Q

Is it easy to treat complications of PET/IUGR or reverse impact?

A

Once IUGR or pre-eclampsia have been identified, it is very difficult to treat these complications and reverse their impact on the infant.

109
Q

What can be used to monitor foetus in pre-eclampsia

A

Evidence of fetal compromise on CTGs or abnormal Dopplers/ultrasound finding / maternal compromise.

110
Q

What is the ultimate treatment for pre-eclampsia

A

as the placenta is the primary cause, the ultimate ‘treatment’ is delivery.

111
Q

How is delivery timed in pre-eclampsia

A

Timing delivery in these pregnancies depends on balancing the risks to the fetus if it remains in utero and the hazards from the prematurity, which decrease as the gestation advances.

112
Q

What could be the result of pre-eclampsia for some pregnancies

A

In some pregnancies, the health of mother or infant (or both) can deteriorate rapidly, making an emergency Cesarean section a necessity.

113
Q

How can uterine artery doppler screening help

A

Because if there is high resistance in the uterine arteries (hich occurs due to impaire cryptoblast invasion of spiral arteries)

then you get an early diastolic flow notch then a poor diastolic flow (i.e. when the heart isnt pumping there is hardly any blood going through the artery)

114
Q

T/F Increased pressure in a uterine artery duppler is only associated with PET , not FGR

A

f It’s associated wit both, because PET is a cause of FGR

115
Q

Sequence of events in FGR

A

Uerine artery pressure increases

Umbilical artery resistance increases

Middle cerebral artery in the foetus’ brain has reduced blood flow and dilates to try to get more (so low resistance)

Increased pressure in venous sytem

ACIDOSIS can lead to interuterine death

116
Q

What occurs in resonse to hypoxia with babies e.g. in pre-eclampsia

A

Aortic body chemoreceptor stimulation –> redistribution of caridac output (more to brain/heart/adrenals, less to lungs, kidneys and gut)

or

CNS dysfunction leads to poor tone, altered breathing altered movement patterns and change in heart rate

117
Q

Pre-eclampsia features

A

HTN
Oedema
Proteinuria

Rob's RDA (10 decks)

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