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RDA > Lecture 14 - 2018/2017 > Flashcards

Lecture 14 - 2018/2017 Flashcards

1
Q

What are the problems of small babies?

A
  1. Around 8500 are born each year.
  2. There is a 6 fold increase in perinatal mortality and morbidity.
  3. 30% neonatal admissions.
  4. The average IQ of small babies is 6 points lower.
  5. They can have behavioural problems when older, have a smaller attention span and may be hyperactive.
  6. 20% of those small babies as adults will have short stature.
  7. Decreased employment when older.
  8. Increased adult cardiovascular and metabolic disease.
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2
Q

Define small babies?

A

<2.5 kg.

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3
Q

Define pre-term?

A

<37 weeks.

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4
Q

Define early term?

A

37-38 weeks.

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5
Q

Define term?

A

39-41 weeks.

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6
Q

Define post-term?

A

41 weeks onwards.

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7
Q

What are the problems of large babies?

A
  1. Birth trauma.
  2. Increased neonatal admissions.
  3. Increased adult non-communicable disease:
    - childhood obesity.
    - metabolic syndrome.
    - depends on neonatal body composition.
    - interaction with maternal diabetes.
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8
Q

Define low birth weight (LBW)?

A

<2.5kg.

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9
Q

Define very low birth weight (VLBW)?

A

<1.5kg.

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10
Q

Define extremely low birth weight (ELBW)?

A

<1kg.

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11
Q

Define macrosomia?

A

> 4.5kg.

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12
Q

Define appropriate for gestational age (AGA)?

A

10-90th percentile.

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13
Q

Define small for gestational age (SGA)?

A

<10th percentile.

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14
Q

Define large for gestational age (LGA)?

A

> 90th percentile.

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15
Q

When is infant mortality and morbidity at its lowest?

A

39-40 weeks.

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16
Q

What is fetal growth?

A

Increase in body size and mass from the end of organogenesis (10-12 weeks).

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17
Q

What is the mean weight gain of fetal growth?

A

16-17g per kg per day.

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18
Q

What occurs in fetal growth?

A

Hyperplasia (cell number) is exceeding hypertrophy (cell size) to allow metabolic capacity to be built. After birth (when fetal growth has stopped) hypertrophy is exceeding hyperplasia to develop metabolic load.

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19
Q

What happens to your metabolic capacity if you grow poorly as an infant?

A

Your metabolic capacity will be restricted - growth at beginning of life determines how your body functions.

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20
Q

What is fetal growth restriction (FGR)?

A

Some pathological process that is limiting growth in utero. FGR does not = SGA.

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21
Q

What occurs in FGR?

A

Typically there is decreased accretion (growth by gradual accumulation of additional layers) of fat and lean tissue +/- skeletal growth.

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22
Q

What can cause FGR?

A

Most cases are due to poor placentation.

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23
Q

What is FGR a key risk factor for?

A
  1. Still birth.
  2. Neonatal death.
  3. Asphyxia.
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24
Q

Is FGR the same as SGA?

A

No. Many small babies are growth restricted, and some SGA are not. There are quite a few FGR babies that aren’t SGA and are within the gestational weight (10-90th percentile).

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25
Q

What are the four birthweight centile charts?

A
  1. Population reference.
  2. Population standard.
  3. Fetal growth curves.
  4. Customised birthweight.
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26
Q

Describe the population reference birthweight centile chart?

A

Sample - actual birth weights across population.
Issue - preterm centiles too low.
Example - fenton 2013.

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27
Q

Describe the population standard birthweight centile chart?

A

Sample - actual birth weights in optimal pregnancy conditions.
Issue - few preterm babies.
Example - intergrwoth-21.

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28
Q

Describe the fetal growth curves birthweight centile chart?

A

Sample - Serial ultrasound biometry of healthy fetuses born at term.
Issue - small samples.
Example - WHO 2017.

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29
Q

Describe the customised birthweight centile chart?

A

Sample - models that incorporate maternal size, ethnicity, parity, fetal growth velocity.
Issue - ethnicity, interpretation of upper centiles.
Example - UK perinatal institute.

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30
Q

What are the determinants of fetal growth?

A
  1. Nutrition.
  2. Hormones.
  3. Genetics.
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31
Q

Describe histiotrophic nutrition (embryo)?

A

Before the formation of placenta occurs, the embryo receives nutrients from the endometrial glands (secretions rich in carbs and lipids) directly via chorion plate.

32
Q

Why is the histiotrophic nutrition important?

A

The growth of the embryo and the chorionic sac are consistent, which is needed during this period - as this is the period of organogenesis (10-12 weeks).

33
Q

Describe haemotrophic nutrition (fetal)?

A

Around 10-12 weeks/end of first trimester the maternal placental circulation is established. There is a sudden rise (3-fold ris) in intra-placental oxygen. This causes chorionic villous regression and formation of discoid placenta.

34
Q

Describe the fetal supply line (fetus haemotrophic nutrition)?

A

Maternal diet -> metabolic endocrine status ->uterine blood flow to placenta -> transport and metabolism (occurs in placenta) -> umbilical blood flow to fetus -> metabolic and endocrine status (occurs in fetus) -> FETAL GROWTH.

35
Q

What are the substrates in the fetal diet?

A
  1. Glucose.
  2. Amino acids.
  3. Lactate.
  4. Fatty acids.
36
Q

What is the role of glucose in the fetal diet?

A
  1. Key oxidative fuel (80% energy).
  2. Carbon source for tissue accretion.
    [Fetus has limited ability to make glucose].
37
Q

How is glucose transported across the placenta?

A

Facilitated diffusion (GLUT1).

38
Q

What is the role of amino acids in the fetal diet?

A
  1. Key role in metabolic balance between oxidation VS growth.
  2. Carbon and nitrogen for tissue accretion, nucleotides.
39
Q

How is amino acids transported across the placenta?

A

Active transport - some amino acids are synthesised by the placenta (glutamate and glycine). Some amino acids are transported via the feto-placental shuttle.

40
Q

What is the role of lactate in the fetal diet?

A

Mostly oxidised.

41
Q

How is lactate transported across the placenta?

A

It is produced by the placenta - placenta coverts glucose to lactate and gives to fetus.

42
Q

What is the role of fatty acids in the fetal diet?

A
  1. Cell membranes.
  2. Energy store.
  3. Limited oxidation.
43
Q

What are the hormones involved in fetal growth?

A
  1. Insulin-like growth factor.
  2. Insulin.
  3. Growth hormone.
  4. Thyroid hormone.
  5. Corticosteroids.
  6. Sex steroids.
  7. Placental lactogen.
  8. Prolactin.
  9. Catecholamines.
44
Q

What are insulin-like growth factors (IGFs)?

A

These are the major growth hormones in the fetus.

45
Q

Where are IGFs produced?

A

In fetal tissues and placenta:

  • potent mitogens, protein anabolism.
  • paracrine and endocrine hormones.
46
Q

Describe IGF1?

A
  1. Matches fetal growth to nutrient supply.

2. Not regulated by growth hormone in fetus.

47
Q

Describe IGF2?

A
  1. Embryonic and placental growth.
  2. Main circulating fetal IGF.
  3. Constitutive drive for growth.
  4. Tissue differentiation in late gestation.
48
Q

What does insulin do in fetal growth?

A
  1. Increases glucose uptake.
  2. Fat deposition.
  3. Protein anabolism.
  4. May promote placental growth.
49
Q

What happens in fetal pancreatectomy?

A

Insulin drops and the growth rate slows.

50
Q

How is fetal insulin secreted?

A
  1. In early pregnancy amino acids stimulate fetal insulin secretion.
  2. In later pregnancy secretion of fetal insulin is primarily controlled by placental uptake of glucose and FFA.
51
Q

How is glucose transported from the mother to the placental?

A

There is minimal effect on fetal weight if there is a decrease in growth hormone.

52
Q

When does fetal adrenal activation occur?

A

Near term.

53
Q

What doe glucocorticoids do in fetal growth?

A
  1. Promote tissue maturation and cell differentiation.
  2. Decreased DNA synthesis and cell division.
  3. It turns on somatrophic axis -inducing expression of growth hormone receptors in the liver.
54
Q

Describe what happens around term birth with glucocorticoids?

A

Glucocorticoids have a potent effect around term birth. However, the placenta produces 11-beta-HSD2 to create a functional barrier to cortisol.

55
Q

What are the genetic influences on fetal growth?

A
  1. Race and sex account for <20% variance in birth weight.
  2. Genetic factors have more influence on lean mass.
  3. Fetal growth is normally limited by constraint - non-genetic/non-pathological factors that limit fetal growth.
56
Q

What is maternal constraint?

A

This is the major constraining factor and is the ability of the utero-placental unit to supply oxygen and nutrients.

57
Q

What contributes to maternal constraint?

A
  1. Maternal size - the smaller you are the less space you have for baby.
  2. Maternal age - e.g. adolescent pregnancy.
  3. Parity - primiparous (if you are young for your first pregnancy).
  4. Short inter-pregnancy interval - not much time between pregnancies.
  5. Macronutrient imbalance.
58
Q

What is constraint during embryogenesis?

A

These are events during pregnancy which can persistently affect growth throughout gestation.

59
Q

What can cause constraint during embryogenesis?

A
  1. Twins.

2. Periconceptial undernutrition - restrict nutrition around/before conception.

60
Q

What is fetal growth constrained by normally?

A

Maternal environment.

61
Q

What happens to fetal growth if endocrine status is adequate?

A

Growth is normally regulated by substrate supply.

62
Q

What is post-natal growth constrained by normally?

A

Genetic potential.

63
Q

What happens to post-natal growth if nutritional status is adequate?

A

Growth is normally regulated by endocrine status.

64
Q

What are the causes of fetal growth restriction?

A
  1. Fetal undernutrition.

2. Fetal pathology.

65
Q

What can cause fetal undernutrition?

A
  1. Placental insufficiency - idiopathic, vascular disease.

2. Maternal undernutrition (<1500kcal.day).

66
Q

What can cause fetal pathology?

A
  1. Congenital malformation.
  2. Congenital infection.
  3. Toxins.
  4. Chromosomal disorders.
  5. Specific genetic disorders.
67
Q

Describe placental insufficiency?

A

Deficient trophoblast invasion and remodelling of the spiral arteries, with maldevelopment of the terminal villi. Reduced surface area, diffusing capacity, uteroplacental and fetoplacental blood flow.

68
Q

What can cause placental insufficiency?

A
  1. Placental inflammation.
  2. Hypoxic/hyperoxic stress.
  3. Anti-angiogenic state.
  4. Thrombo-occlusive damage.
69
Q

Describe genetic disorders affecting fetal growth?

A

Genes regulating growth are commonly imprinted:

  1. Maternally expressed genes suppress growth.
  2. Paternally expressed genes promote growth.
70
Q

What is Beckwith Wiedemann syndrome?

A

Over-expression of IGF2 (maternall allele normally imprinted). It is usually due to paternal uniparental disomy.

71
Q

What are the features of beckwith wiedemann syndrome?

A
  1. Macrosomia, macroglossia.
  2. Hemi-hypertrophy (24%).
  3. Transverse ear crease.
  4. Omphalocoele.
  5. Hypoglycaemia (50%).
  6. Embryonal tumours.
72
Q

What are the long-term health effects of FGR?

A
  1. Thrifty phenotype.

2. Health risks.

73
Q

What is a thrifty phenotype?

A
  1. Low nephron mass.
  2. Low lean mass.
  3. Endothelial dysfunction, arterial stiffness.
  4. Insulin resistance.
  5. Dyslipidaemia, central adiposity.
  6. Exaggerated stress response.
74
Q

What are the health risks associated with long-term effects of FGR?

A
  1. Hypertension.
  2. Ischaemic heart disease.
  3. Stroke.
  4. Diabetes.
  5. Metabolic syndrome.
  6. Osteoporosis.
75
Q

What is gestational diabetes?

A

Glucose intolerance that develops in pregnancy (usually in the third trimester).

76
Q

What is the effect of gestational diabetes on fetal growth?

A

Excess fetal substrate (glucose and free fatty acids) can cause excess fetal insulin. Excess substrate + excess insulin can cause excess growth.

RDA (19 decks)

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