Lecture 14: Fetal growth and Nutrition Flashcards Preview

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Flashcards in Lecture 14: Fetal growth and Nutrition Deck (21):

Importance of a healthy start to life?

Small babies < 2.5kg 

  • 6x increase in perinatal mortality and morbidity 
  • Average IQ is 8 points lower 
  • Inattention, hyperactivity, behavioral problems 
  • 20% of adults short in stature 
  • lower income 
  • Increased adult non-communicable disease (hypertension, diabetes, metabolic syndromes) 


Problems faced for large children?

  • Birth trauma 
  • increased neonatal admission 
  • increased adult non-commincable disease (childhood obesity, metabolic syndrome) 


Term gestation? Birth weight boundaries?

Statistical and clinical defnitions, is the point where infant mortality and morbidity is lowest around 39-40weeks. 



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Fetal growth features?

Is the increase in body size and mass from the end of organogenesis

Is largely hyperplasia (increase in cell number) than hypertrophy

Mean weight is 16-17g/kg/day

For: neurons, Skeletal muscle, SNT, Renal neohrons, heart muscle their hyperplasia is mostly done before birth and after birth these only undergo hypertrophy. 


Fetal Growth Restriction?

In utero growth potential limited by pathological process and is the decreased accretion of faat and lean tissue +/- skeletal growth

Most cases due to poor placentation and is a key risk factor for stillbirth, neoatal death and asphyxia

FGR>SGA and SGA is NOT the same as FGR


FGR in preterm babies?

FGR is a common cause of preterm births

10% of preterm babies are SGA but actually as much as 25% or preterm babies are growth restricted if we reference to a fetag growth curve. 


Determinants of fetal growth?

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Histiotrophic nutrition?

Period of organogenesis when the embryo is supported directly by secrestions from endometrial glands and growth of the embryo and chorionic sac are relatively consistent and autonomous

Maternal placental circulation established at the end of the first trimester where we see a 3 fold rise in intra-placental oxygen. Chorionic villous regression and formation of discoid placenta.


Fetus: haemotrophic nutrition. The fetal supply line? Where is the most likely place for a problem?

Problems are usually with the placenta as the placenta is a very good scavenger of the mothers blood so nutritional issues would have to be relatively severe to cause a decreased growth.

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Four main components of the fetal diet?

  1. Glucose through facilitated diffusion. Key oxidative fuel and also a carbon source. 
  2. Amino Acids through AT and some placental synthesis. Key role inmetabolic balance between oxidation and growth. Source of Carbon and nitrogen.
  3. lactate produced by the placenta. Mostly oxidised 
  4. Fatty acids readily cross by diffusion. For cell membranes, an energy store with limited oxidation.


Fetal growth hormones?

Have less of a role than in post natal life but do play a role in coordination. Especially the insulin-like growth factors and insulin (+glucocorticoids and growth factor)

IGFs are widely produced in fetal and placental tissues. They are potent mitogens and promoting protein anabolism acting through paracrine and endocrine action. 

IGF2: main circulating fetal IGF, constituent drive for embryonic and placental growth as well tissue diff in late gestation

IGF1: matches fetal growth to nutrient supply but is not regulated by growth hormone in fetus like it is post-natal. 


Actions and secretion of fetal insulin?

  • Increases glucose uptake
  • Fat deposition
  • protein anabolism
  • May promote placental growth 

Tissue accretion and fuel storage (+ stimulates fetal IGF1) 

Early pregnancy is sstimulated by AA and later by placental uptake of glucose and FFA


Growth hormone in the Fetus?

  • Ciculating concentrations are high but receptors absent in liver and present in other tissues
  • Does not regulate IGF1 so definciency has minimal effect
  • May cause shortness and alter fetal metabolism if lost


Glucocorticoids and fetal growth?

  • Fetal adrenal activtion near term
  • Turn on somatrophic axis by inducing expression of growth receptors in liver
  • Promote cell differentiation and tissue maturation
  • Derease DNA synthesis and cell devision


Placental barrier to maternal cortisol?

A functional barrier by enzymes stops cortisol getting into fetal circulation.

Reduced enzyme activity in: 

  • Maternal protein malnutrition 
  • Ischaemic placental disease

Increased passage of maternal cortisol prepares the fetus for preterm birth but may contribute to slowing of growth. 


Genetic effect in prenatal growth?

Race and sex account for <20% of variance 

Genetic factors have more influence on lean mass

Fetal growth is normally limited by constraint (non-genetic/non-pathological factors that limit fetal growth) 


Maternal constraint?

  1. Maternal size 
  2. Maternal age -adolescent pregnancy 
  3. Primiparous have lowest uteroplacental function 
  4. Short inter-pregnancy interval reduces function 
  5. Macronutrient imbalance 

Is during embryogenesis, events during early pregnancy can affect growth throughout gestation (twins, preiconceptual undernutrition) 


Fetal vs postnatal growth?

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Causes of fetal growth restriction?

Fetal undernutrition

  • Placental insufficiency (idiopathic or vascular disease) 
  • Maternal undernutrition 

Fetal pathology

  • Congenital malformation 
  • congential infection 
  • Toxins 
  • Chromosomal disorders 
  • Specific genetic disorders


Placental insufficiency?

Deficient trophoblast invasion and remodelling of the spiral arteries, with maldevelopment of terminal villi.

Reduced surface are, diffusing capacity, uterplacental and fetoplacental blood flow.

Placental inflammation, hypoxic/hyperoxic stress, antiagiogenic state, thrombo-occlusive damage. 


Genetic disorders affecting growth?

Genes regulating growth are commonly imprinted:

  • Maternally expressed genes supress growth 
  • paternally expressed genes promote growth

EG. Beckwith Wiedemann syndrome 

  • Maternal allele normally imprinted but here we get overexpression of IGF2 
  • Macrosomia (large tongue), Transverse ear crease, Hypoglycaemia, embryonal tumours

Russel Silver Sydrome 

  • SGA, normal head growth 
  • 60% due to reduced expression of IGF2 from hypoethylation od paternal allele.