fetal growth and nutrition Flashcards
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
- nutrition
- hormones
- genetics
(pyramid)
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?
transport
= facilitated diffusion (GLUT1)
role
= 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
IGF1 & IGF2
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
fetal
- normally constrained by maternal environment
- if endocrine status is adequate growth is normally regulated by substrate supply
postnatal
- 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
- hypertension
- ischaemic heart disease
- stroke
- diabetes
- 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
