Foetal Growth Flashcards
What are the three phases of foetal growth and development?
First = 4-20 weeks, increases in foetal weight, protein content and DNA content (cellular hyperplasia) Second = 20-28 weeks, increased in protein and weight and lesser increases in foetal DNA content (hyperplasia and concomitant hypertrophy) Third = 28 weeks - term, continued increases in foetal protein and weight but no increase in DNA (hypertrophy)
Define IUGR
Intrauterine growth restriction
- failure of the foetus to achieve his or her growth potential
Define small for gestational age (SGA)
Brith weight <10th centile for gestational age
- centimes are based on local populations
- can be adjusted for sex, parity, race, maternal weight and height
Define large gestational age (LGA)
birth weight >90th percentile
Define low birth weight
birth weight less than a certain threshold e.g. 2500g
What other neonatal indices can be measured to find out about foetal growth?
- ponderal index, skin fold thickness, MAC/HC ratio (mid arm circumference, head circumference)
What are the consequences of foetal growth restriction?
LBW infants are more likely to:
- die within first year of life
- suffer from neonatal problems (birth asphyxia, hypoglycaemia, hypothermia)
Foetal origin of adult disease?
What is foetal programming/Barker hypothesis?
- most show catch p with n childhood though may have smaller size in adulthood
- however, IUGR can have lifelong impact
Increased risk of: - diabetes, obesity, BP, stoke, CVD
“Thrifty phenotype” programming: evolved to offer advatage in ‘famine environment’ but proves in industrialised society
-
- have SGA babies
- have increase perinatal mortality
What are the 2 proposed mechanisms of transgererational effects of SGA?
Epigenetics
- heritable changes in gene expression by mechanisms other than underlying DNA sequences
- DNA methylation, histone modification, micro RNA
Maternal Mitochondria
- food restriction can alter number and function
- these are directly passed onto offspring through ova
What are the defining for large for gestational age (LGA)?
- birth weight >90th gentile
- macrosomia - birth weight >4500g
What are the causes of LGA?
- gestational age, increased incidence of pregnancies over 40 weeks
- foetal sex, male infants tend to weight more
- excessive maternal weight gain and obesity
- multiparty
- erythroblastosis fettles - hydrops details
- genetic disorders of overgrowth e.g. Beckwith-Wiedemann syndrome, Sotos syndrome
- maternal diabetes (prepexisignt of gestational)
What is the pathophysiology of LGA and diabetes?
- increased maternal glucose concentration
- increased foetal insulin concentrations
- increased foetal growth factors
How does LGA fit into the foetal programming/Barker hypothesis?
- evidence suggests that curve may actually be u-shaped
- babies born to GDM mothers in adulthood are at increased risk of IGT, diabetes and obesity
- early exposure to insulin levels leads to metabolic and epigenetic differences
What is placental and foetal growth regulated by?
by combination of substrate availability and endocrine or paracrine signalling
- IGF 1 and IGF 2 major stimulus
What maternal factors affect growth?
- ethnicity
- maternal stature/BMI
- drugs: cigarettes, alcohol, drugs of abuse
- nutrition
- material hypoxia: cyanotic heart disease, chronic respiratory disease, altitide
Describe the link between IUGR and perinatal mortality/morbidity in the developing world
- maternal undernutrition
- synergistic with low age, maternal anaemia, chronic disease, HIV, placental malaria
What foetal factors affect growth?
Genome - chromosomal disorders - trisomy 13, 18, 21 Growth factors - insulin like growth factors, thyroxine Congenital infections - CMV, toxoplasmosis, rubella
What placental factors affect growth?
Primary placental problems - abnormality of placenta structure/function Secondary placental problems - hypertension - chronic renal disease - vasculitis - pro-thrombotic disorders Multiple gestation - growth discordance
Describe the process of malplacentation in IUGR
- majority of blood flow to uterus is suppled by uterine arteries (supplying arcuate and spiral arteries)
- shape of uterine artery waveform in unique and changes with gestation: early –> high vascular impedance and low flow, mid –> high flow, low resistance
- poor trophoblast invasion of maternal spiral arteries
- increased impedance to flow and decreased placental perfusion
- change in Dopper indices, raaiend RI, diastolic notch etc.
Describe the difference sweeten asymmetrical and symmetrical patterns of IUGR
This can help you determine the cause
Asymmetrical
- uteroplacental insufficiency
- decreased glycogen shoes, so decreased abdominal circumference
Symmetrical
- early growth insult, chromosomal, viral infection - disrupted
- regulation of growth processes or disruption at cell hyperplasia stage
IUGR is a combination of…
- reducing growth velocity and placental insufficiency
How can IUGR be identified on uterine doppler?
different uterine waveforms
abnormal - high resistance to flow, notch seen
How do we asses foetal growth clinically?
Measure symphysiofundal height at each antenatal visit from 24 weeks
Ultrasound can calculate foetal weight using head, femur, abdominal measurements
How can we assess foetal wellbeing in the long and short term?
Short term = cardiotocography, septal heart rate and contractions
Long term = umbilical artery doppler, middle cerebral artery doppler, ductus venous doppler, liquor volume
What is gestational diabetes?
- defined as any degree of glucose intolerance with its onset (or first recognition( during pregnancy
- affect 5% of pregnancies
How does gestational diabetes come about?
Pre-existing risk..
Pregnancy risk…
Pre-existing risk
- pancreatic B cell dysfunction on background chronic insulin resistance present before pregnancy
Pregnancy
- is a state of insulin resistance - hormonal, inflammatory, cytokines, adipokines changes,
- resistance increases with advancing gestation
How and when is gestational diabetes screened for?
Screen from early pregancy 16-18 weeks if - PMH of GDm or glucose intolerance
Screen from 24-26 weeks if: family history, BMI>30, ethnicity, previous macrosomia, previous unexplained stillbirth, on steroids
Screen urgently if arises in current pregnancy: significant glyosuria, polyhydraminons and macrosomia
Screen via: OGTT (overnight fast then 75g glucose load, test at 2 hrs), random blood glucose profile >36 weeks
What are the maternal complications of GDM?
- pre-eclampsia
- pre-term labour
- instrumental delivery/caesarean section
- diabetes later in life
What are the foetal complications of GDM?
- macrosomia
- shoulder dystocia
- polyhydraminos
- perinatal mortality and morbidity: neonatal hypogylcaemia, jaundice, polycythaemia, and hypocalcaemia
- foetal programming and increased risk of adult disease
How is GDM managed?
MDT: obstetrician, diavetologist, diabetic nurse, dietician
Regular monitoring and strict control - blood sugars up to 7 times per day
Medical management: diet, oral agents e.g. metformin, insulin
What is obstetric management of GDM?
- regular growth scans
- regular BM (blood glucose measurement) monitoring
- deliver around 38 weeks
- offer GTT at 6 weeks postnatal
