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Medsci 312 > Lecture 13; Fetal Growth part Two > Flashcards

Lecture 13; Fetal Growth part Two Flashcards

1
Q

What is post natal growth determined by?

A

Growth is determined by genetic potential

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2
Q

What is post natal growth regulated by?

A

Provided that minimal nutritional requirements are
met, growth is regulated by endocrine status (GH
is important)

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3
Q

What is pre natal growth restrained by?

A

Constrained by maternal environment

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4
Q

What regulates pre natal growth?

A

• Provided minimal endocrine requirements are

met, growth is regulated by substrate supply

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5
Q

What hormone is not important in pre natal growth?

A

GH not important

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6
Q

How does age affect pre natal growth?

A

Maternal and paternal age appear to have
significant but poorly defined effects

– In humans, U-shaped relationship between
mother’s age and birth outcomes: optimal ~
20 to 28 years

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7
Q

What did sheep studies show about maternal age?

A

In sheep pregnancy during adolescence is

associated with fetal growth retardation

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8
Q

What are other maternal factors that may affect growth?

A

Smoking: >9 cigarettes per day associated
with 200g decreased birth weight

  • Starvation/undernutrition
    • Severe exercise in late gestation
    • Maternal health
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9
Q

What can poor maternal health lead to?

A

e.g. Chronic infection can lead to maternal
catabolism and thus, to nutrient competition
between mother and placenta

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10
Q

How does maternal size influence birth weight?

A

Most of the variation (60%) in birthweight
in humans is attributed to environmental
factors

The maternal environment has a major influence on fetal growth

i.e Temp, body fat, glucose, oxygen

Mother modifies fetal growth

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11
Q

How does the mum constrain fetal nutrition?

A

• Delivery of nutrients to the fetus is
actively constrained by mother;
– placental transport capacity
– diffusion area

• Hormones facilitate nutrition

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12
Q

What is the major regulator of fetal growth?

A

• The supply of nutrients to the fetus is the

major regulator of fetal growth

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13
Q

What does fetal growth late in gestation reflect?

A

Fetal growth in late gestation reflects

compartmentalisation of nutrients

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14
Q

What is IUGR?

A

Inter Uterine Growth Restriction

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15
Q

How can IUGR occur?

A

– Frank maternal malnutrition, starvation
– Placental dysfunction: e.g. infarction,
– impaired blood flow to the uterus: preeclampsia
– Smoking

Because mum is the supply of nutrients to the fetus

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16
Q

Whats the incidence of IUGR in nz?

A
  • In NZ -50,000 births/year

* 5000 SGA (=<10th percentile), of which 2000 IUGR infants/year

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17
Q

What is IUGR associated with?

A
  • Stillbirth rate is doubled
  • Perinatal mortality and asphyxia increased 6-fold
  • ~30% of neonatal unit admissions
  • 21% of short children
  • On average 8 IQ points lower by adolescence – problems with behaviour
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18
Q

What is the barker hypothesis?

A

IUGR has a Strong association with later insulin

resistance and diseases such as coronary artery disease

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19
Q

What is critical in fetal growth?

A

The effects of an insult are determined by the duration of that insult

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20
Q

What does the impact of nutritional deprivation depend on?

A

The impact of nutritional deprivation
depends on the gestational age when this
occurs and the severity of the insult

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21
Q

What is embryonic growth influenced by?

A

• Embryonic growth is influenced by nutrient

concentration

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22
Q

What does maternal under nutrition result in mid pregnancy?

A 
Maternal undernutrition after
conception and throughout the
1st and 2nd trimester of
gestation results in“symmetrical”
SGA by the 2nd trimester of
gestation;
  • Baby’s head and body are proportionately small
  • Weight, length + head circumference are all =<10th%tile
  • Ponderal index is normal.
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23
Q

What is symmetrical IUGR?

A
  • baby grew slowly through out pregnancy

* head circumference is proportionate to body

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24
Q

What does maternal undernutrition result in during late gestation?

A

• Nutritional deprivation later in pregnancy generally
results in asymmetric IUGR (head size is bigger
than body size)

• The effects of undernutrition in late gestation
depend on its duration

Ponderal index is low

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25
Q

Describe asymetrical or head sparing IUGR?

A 
• Head and brain are normal in size
but the abdomen is smaller
• Suggests last trimester
• Redistribution of cardiac output →
↑ flow to brain, adrenal and heart
at expense of splanchic circulation
• Liver size diminished

No fat

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26
Q

What happens to the fetus during malnutrition?

A

• The fetus becomes less reliant on maternally
supplied glucose during fasting and must
consume other substrates

Starts to use AA (doubles in rate) but No change in umbilical uptake of a.a. from placenta or other potential substrates such as lactate

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27
Q

What was found across species in terms of oxygen consumption?

A

Very similar rate across species for the fetus

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28
Q

What is the equation for the fetal substrate/oxygen quotient?

A

Substrate/O2 quotient = ((v-a)substrate X n) / ((v-a) O2)

n = number of moles O2 required for complete oxidation of a substrate.

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29
Q

What does the fetal substrate/oxygen quotient mean?

A

• The demonstration of a substrate – oxygen quotient near or equal to 1.0
suggests that if the particular substrate measured were completely oxidised it
could provide 100% of the carbon for the measured fetal O2 consumption.

30
Q

What is the extent of glucose oxidation responsible for oxygen consumption?

A

Non-ruminants have a greater
dependence on glucose metabolism than
ruminants
• Under physiological conditions, not all glucose is
oxidised
• Therefore, glucose carbon only accounts for 25-
30% of the total rate of fetal O2 consumption

31
Q

Describe the major AA metabolism during fetal under nutrition;

A

Fasting → glucose fell by 40%

Glucose O2 quotient fell from 1.20 → 0.621. (using other substrates)

Fasting saw significant changes in net
balance of several amino acids

32
Q

What particular AA are metabolised during fasting?

A

Both alanine & glutamine, which
demonstrated a +ve uptake by fetus when
fed, showed an efflux during fasting

• observations consistent with fetus adapting
to a diminished supply of glucose from the
mother by enhanced amino acid catabolism
and, possibly, proteolysis with subsequent
release of gluconeogenic precursors in the
form of alanine and glutamine

33
Q

Describe the rate of fetal growth;

A

Fetal growth is exponential

34
Q

Describe the rate of placental growth;

A

Placental weight increases at a much slower rate and

does not parallel the steep rise in fetal weight

35
Q

Why do post term babies stop growing?

A

Placenta determines the rate of nutrient supply thus at post term it cannot provide enough nutrients to sustain growth

Thus post term babies stop growing

36
Q

What is the slow growth of the placenta in the second trimester compensated by?

A

increased exchange area in the placenta to sustain nutrient delivery:

  • Increased total villous surface area of the placenta 
  • Decreased proliferation and dilation of the fetal capillaries
  • Decreased resistance of the feto-placental vasculature
37
Q

What placental factors are released that aid fetus growth?

A
  • Placental lactogen (hPL)
  • Growth Hormone (GH)
  • Insulin-like growth factors (IGFs)
  • Insulin-like binding proteins (IGFBPs)
38
Q

What is the dominant source of alternative GH in the second trimester and what is the effect of this?

A

By end of first trimester of human pregnancy, the placenta is the dominant source for an alternate form of GH (placental GH or GH-2 ie GH-variant) which suppresses pituitary GH (GH-1)

39
Q

Where is GH2 in circulation?

A

GH-2 only secreted into maternal circulation

40
Q

What creates a state of relative insulin resistance?

A

Both hPL and GH-2 are believed to create a state of relative maternal insulin resistance

= Increased glucose for the baby

41
Q

What is the other function of GH2?

A

• GH-2 may also directly affect placental function or development

42
Q

What is the role of IGF in the placenta?

A

• IGF-I and IGF-II are produced in the placenta as
well as the fetus
• Across a group of normal and diabetic
pregnancies, placental IGF-II mRNA was
positively correlated with placental weight

43
Q

In what instance is IGF1 increased?

A

• Placental expression of IGF-I is increased in

some cases of IUGR

44
Q

What is a key enzyme in the placental barrier?

A

11βHSD2

45
Q

What does 11βHSD2 do?

A

Converts cortisol (active) into cortisone (inactive)

maternal cortisol would cause differentiation and maturation of tissues prematurely

46
Q

What happens if the fetus is exposed to high levels of glucocorticoids?

A

Exposure of the fetus to high

levels of glucocorticoids negatively impacts on growth

47
Q

What are the key fetal factors in fetal growth?

A

 Growth hormone
 IGFs
 Insulin
 Thyroid hormones

48
Q

When do GHs act?

A

Post birth

49
Q

Describe the levels of GH prior to birth;

A

GH levels are much higher before birth… and yet have relatively little effect on fetal growth….

Lack of GH receptors in liver?

50
Q

What happens to those with congenital GH deficiency?

A

Children with congenital GH deficiency can also be average length at birth and don’t begin to experience growth problems until
about six months of age

51
Q

Does insulin cross the placenta?

A

No

52
Q

Is insulin an important fetal growth factor?

A

Insulin is a key mediator/facilitator of fetal growth & metabolism

• Fetal islet tissue mass is correlated with body weight in newborn human infants

53
Q

What does a pancreatectomy in sheep show?

A

That growth is halted, unless analogous insulin is given in which case growth recovers

54
Q

What secretes IGF in the fetus and what are its effects?

A

IGF-I and IGF-II, are peptides primarily secreted by the fetal liver, that
circulate in the blood - have a sequence similar to insulin and can bind
insulin receptor

55
Q

What does IGF1 promote?

A

IGF-I + amino acids promote growth and differentiation of cells and tissues
– Combination of insulin+IGF-1 is highly anabolic

56
Q

Which IGF is the primary growth factor?

A

IGF-2 is the primary growth factor involved in embryonic growth, whereas the dominant fetal growth regulator in late gestation is IGF-1 as well as postnatally

Ironically, fetal growth is more closely related to IGF1 levels rather than IGF2

57
Q

What is the role of fetal produced GH?

A

GH has a limited role in the regulation of fetal growth, because of receptor immaturity, but begin to exert a limited influence after 36 weeks’ gestation

58
Q

What regulates these growth factors?

A

Fetal IGF-1 levels are regulated not by GH but by fetal insulin

59
Q

What is the role of thyroxine post natally and to the fetus?

A
  • Postnatally, most of the effects of thyroxine are secondary to stimulation of O2 consumption
  • Thyroxine is anabolic in the fetus – Critical for brain development
60
Q

How does cortisol and catecholamines affect fetal metabolism?

A

In late gestation, normally cortisol and adrenaline are maturational rather than nutritional signals, but still have metabolic effects

Promote increased fetal [glucose] during adverse nutritional conditions

61
Q

How much do maternal genes contribute to fetal growth?

A

25%

62
Q

How much does paternal genes influence fetal growth?

A

– 1-2%
– at least in part: imprinting
– IGF2 gene is paternally expressed in the fetus and placenta → crucial for placental development and fetal growth

Note: imprinting is the epigenetic phenomenon by which genes are expressed in a parent-of-origin- specific manner

63
Q

What is IUGR?

A

a condition in which a fetus is unable to achieve its genetically determined potential size

64
Q

Write some notes on IUGR;

A

• SGA ≠ IUGR
– Not all small fetuses are
• ~40%insufficientnutrition= IUGR
• ~40%healthy&normal
• ~20%intrinsicallysmalle.g. • trisomy 21
• cytomegalovirus infection • fetal alcohol syndrome

65
Q

What is the Russell Silver syndrome?

A

pre- and post-natal asymmetrical growth restriction and relative macrocephaly

66
Q

Describe the genetic mutations in Russell silver syndrome;

A

– 30%-50% chromosome 11p15.5-related
– Loss of methylation at paternal IC1 (imprinting control 1 region)biallelic expression of H19 and biallelic silencing of IGF-2
– abnormalities of spontaneous growth hormone (GH) secretion and subnormal responses to GH stimulation

67
Q

Define large for gestational age and some causes;

A

LGA: just >90th percentile for gestational age, i.e.> 4kg at term
– Macrosomia: a subset of LGA
– All organs, including head are large; + fat
• e.g. poorly controlled diabetes in mother

68
Q

What results in maternal diabtetes?

A

Pregnancy is ‘catabolic’:

– favours reduced use of glucose & a.a. by mother
• Placental GH-2 and hPL (human placental lactogen)- normally raises maternal glucose & makes her body less sensitive to insulin
– 30% increase in insulin requirements

69
Q

What does maternal diabetes before 20 weeks result in?

A

– fetal islet cells cannot respond

– fetus is exposed to unregulated hyperglycemia – typically decreased fetal growth

70
Q

What happens in maternal diabetes to the fetus in the 2nd trimester

A

• the fetus can respond to hyperglycemia: – pancreatic beta-cell hyperplasia
– increased fetal insulin levels
– Increased fetal amino acid transfer

71
Q

What does high levels of insulin for the fetus result in, during the second trimester?

A

Insulin favours glycogen + fat deposition:

 hepatosplenomegaly (enlarged liver and spleen) and cardiomegaly (enlarged heart)

72
Q

Describe what can happen after birth if the mother has had late gestation diabetes

A

Insulin is mitogenic as well.
• Insulin+IGF-1 powerful
• stimulants of increased cell proliferation
• At birth baby still has islet cell hyperplasia What happens?
– Hypoglycemia!
- Increase  basal metabolism
 Fetal hypoxia,
-  Increased Hematocrit (Hct) ie “Polycythemia

Medsci 312 (28 decks)

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