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Flashcards in fetal growth and nutrition Deck (33):

problems faced by small babies

- 6-fold increase in perinatal mortality and morbidity

- average IQ 8 points lower

- intention, hyperactivity, behavioural problems

- lower income

- increased adult non-communicable disease

- 20% of adult short stature


problems face by large for babies

- birth trauma
- increased neonatal admissions
- increased adult non-communicable disease
-e.g. childhood obesity, metabolic syndrome
-(depends on neonate body composition, interaction with maternal diabetes)


define full term and benefits

39-40 weeks

- lowest risk for respiratory distress, cerebral palsy and childhood mortality


how is pregnancy dated?

first trimester ultrasound looking at the crown rump length
-(95% confidence interval +/- 5 days)

accurate dating important for improving outcomes


birth size (number definitions)

LBW = <2500g

VLBW = <1500g

ELBW = <1000g

appropriate for gestational age = between 10-90%


fetal growth

increase in body size & mass from end of organogenesis

- hyperplasia (not hypertrophy)

mean weight gain = 16-17g/kg per day


life course epidemiology (duration of hyperplasia)

key body organs undergo hyperplasia before birth

e.g. neurons, skeletal muscles, kidneys, heart, pancreas (metabolic)

therefore what you're born with is largely what you maintain for life (+ hypertrophy)


fetal growth restriction

- pathological process limiting growth in utero
- decreased adipose tissue and lean tissue
- can make baby shorter

- majority due to poor placental function
- key risk factor for stillbirth, neonatal death, asphyxia


relationship between FGR and SGA

fetal growth restriction and being small are not the same thing

can be growth restricted and still in the normal birth weight

can be small and not growth restricted


4 possible references to compare babies birth weight too

population reference
- actual birthweight across population
(preterm centile too low)

population standard
- actual birthweight in optimal pregnancy conditions
(few preterm babies)

fetal growth curves
- serial ultrasound biometry of healthy fetuses born at term
(small samples)

customised birthweight
- models that incorporate maternal size, ethnicity, parity, fetal growth velocity
(ethnicity, interpretation of upper centiles)


determinants of fetal growth

1. nutrition
2. hormones
3. genetics



nutrition in fetal growth

histiotrophic nutrition
-endometrial glands
- growth 'autonomous'

maternal placenta circulation established end of 1st trimester (3-fold rise in intra-placental O2)

haemotrophic nutrition
- 10-12 weeks (proper)
- fetal supply line


'fetal diet' of glucose
what is its placental transport and role?

= facilitated diffusion (GLUT1)

= key oxidative fuel
carbon source for tissue accretion
limited fetal glucogenesis therfore needs to be constant


'fetal diet' of amino acids
what is its placental transport and role?

active transport
some synthesized by placenta

key role in metabolic balance between oxidation vs growth

carbon & nitrogen for tissue accretion, nucleotides


'fetal diet' of lactate
what is its placental transport and role?

produced by placenta

mostly oxidised (energy)


'fetal diet' of fatty acids
what is its placental transport and role?

readily cross placenta by diffusion

role = cell membranes, energy store, limited energy supply


hormones for fetal growth

serve to coordinate fetal growth with the supply of nutrition

e.g. insulin-like growth factors and insulin


insulin-like growth factors (IGF)

is the major growth hormone in the fetus
- produced in all fetal tissues and placenta
- regulated by fetal nutrition



actions of fetal insulin

- increased glucose uptake
- fat deposition
- protein anabolism
- may promote placental growth
- stimulates fetal IGF1

key role = tissue accretion and fuel storage


secretion of fetal insulin

early pregnancy = amino acids

late pregnancy = placental uptake of glucose and free fatty acids


genetic influences on fetal growth

- race and sex account for <20% variance in birthweight

- genetic factors have more influence on lean mass

- fetal growth is normally limited by constraint from mother (e.g. non-genetic or non-pathological)


maternal constraint

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

- maternal size
- maternal age (young less utero-placental function)
- parity
- short inter-pregnancy interval
- macro-nutrient imbalance


fetal growth constraints

fetal growth is normally constrained
- constrained below optimal for survival
- best chance is born around 80-90th centile


fetal vs postnatal growth

- normally constrained by maternal environment
- if endocrine status is adequate growth is normally regulated by substrate supply

- is normally to genetic potential
- if nutritional status is adequate growth is normally regulated by endocrine status


causes of FGR (fetal growth restriction)

fetal under-nutrition
- placental insufficiency
- maternal under-nutrition

fetal pathology
- congenital malformation
- congenital ingection
- toxins
- chromosomal disorders
- specific genetic disorders


placental insufficiency

- deficient trophoblast invasion and remodelling of spiral arteries with maldevelopment of terminal villi
- reduced SA, diffusing capacity, BF
- placental inflammation, hypoxic stress etc


genetic disorders affecting fetal growth

genes regulating growth are commonly imprinted:
- maternally expressed genes suppress growth
- paternally expressed genes promote growth


beckwith wiedemann syndrome

- overexpression of IGF2 (maternal allele imprinted)
-overexpression of paternal gene
- large tongue and ears etc


russell silver syndrome

- SGA, short, normal head
- 60% due to reduced expression of IGF2


long-term effects of FGR

- low nephron mass
- low lean mass
- insulin resistance
- exaggerated stress response
- endothelial dysfunction

-ischaemic heart disease
-metabolic syndrome


gestational diabetes and consequence

- glucose intolerance developing in pregnancy

excess substrate + excess insulin -> excess growth


what determines fetal growth

substrate supply via the fetus


what contributes to adult non-communicable disease

fetal under- and over-growth