Foetal Growth Flashcards

1
Q

What are the three phases of foetal growth and development?

A
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)
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2
Q

Define IUGR

A

Intrauterine growth restriction

- failure of the foetus to achieve his or her growth potential

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3
Q

Define small for gestational age (SGA)

A

Brith weight <10th centile for gestational age

  • centimes are based on local populations
  • can be adjusted for sex, parity, race, maternal weight and height
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4
Q

Define large gestational age (LGA)

A

birth weight >90th percentile

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5
Q

Define low birth weight

A

birth weight less than a certain threshold e.g. 2500g

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6
Q

What other neonatal indices can be measured to find out about foetal growth?

A
  • ponderal index, skin fold thickness, MAC/HC ratio (mid arm circumference, head circumference)
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7
Q

What are the consequences of foetal growth restriction?

A

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?

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8
Q

What is foetal programming/Barker hypothesis?

A
  • 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
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9
Q

-

A
  • have SGA babies

- have increase perinatal mortality

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10
Q

What are the 2 proposed mechanisms of transgererational effects of SGA?

A

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

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11
Q

What are the defining for large for gestational age (LGA)?

A
  • birth weight >90th gentile

- macrosomia - birth weight >4500g

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12
Q

What are the causes of LGA?

A
  • 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)
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13
Q

What is the pathophysiology of LGA and diabetes?

A
  • increased maternal glucose concentration
  • increased foetal insulin concentrations
  • increased foetal growth factors
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14
Q

How does LGA fit into the foetal programming/Barker hypothesis?

A
  • 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
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15
Q

What is placental and foetal growth regulated by?

A

by combination of substrate availability and endocrine or paracrine signalling
- IGF 1 and IGF 2 major stimulus

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16
Q

What maternal factors affect growth?

A
  • ethnicity
  • maternal stature/BMI
  • drugs: cigarettes, alcohol, drugs of abuse
  • nutrition
  • material hypoxia: cyanotic heart disease, chronic respiratory disease, altitide
17
Q

Describe the link between IUGR and perinatal mortality/morbidity in the developing world

A
  • maternal undernutrition

- synergistic with low age, maternal anaemia, chronic disease, HIV, placental malaria

18
Q

What foetal factors affect growth?

A
Genome
- chromosomal disorders
- trisomy 13, 18, 21 
Growth factors 
- insulin like growth factors, thyroxine 
Congenital infections
- CMV, toxoplasmosis, rubella
19
Q

What placental factors affect growth?

A
Primary placental problems 
- abnormality of placenta structure/function
Secondary placental problems 
- hypertension
- chronic renal disease
- vasculitis 
- pro-thrombotic disorders 
Multiple gestation 
- growth discordance
20
Q

Describe the process of malplacentation in IUGR

A
  • 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.
21
Q

Describe the difference sweeten asymmetrical and symmetrical patterns of IUGR
This can help you determine the cause

A

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

22
Q

IUGR is a combination of…

A
  • reducing growth velocity and placental insufficiency
23
Q

How can IUGR be identified on uterine doppler?

A

different uterine waveforms

abnormal - high resistance to flow, notch seen

24
Q

How do we asses foetal growth clinically?

A

Measure symphysiofundal height at each antenatal visit from 24 weeks
Ultrasound can calculate foetal weight using head, femur, abdominal measurements

25
Q

How can we assess foetal wellbeing in the long and short term?

A

Short term = cardiotocography, septal heart rate and contractions
Long term = umbilical artery doppler, middle cerebral artery doppler, ductus venous doppler, liquor volume

26
Q

What is gestational diabetes?

A
  • defined as any degree of glucose intolerance with its onset (or first recognition( during pregnancy
  • affect 5% of pregnancies
27
Q

How does gestational diabetes come about?
Pre-existing risk..
Pregnancy risk…

A

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

28
Q

How and when is gestational diabetes screened for?

A

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

29
Q

What are the maternal complications of GDM?

A
  • pre-eclampsia
  • pre-term labour
  • instrumental delivery/caesarean section
  • diabetes later in life
30
Q

What are the foetal complications of GDM?

A
  • macrosomia
  • shoulder dystocia
  • polyhydraminos
  • perinatal mortality and morbidity: neonatal hypogylcaemia, jaundice, polycythaemia, and hypocalcaemia
  • foetal programming and increased risk of adult disease
31
Q

How is GDM managed?

A

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

32
Q

What is obstetric management of GDM?

A
  • regular growth scans
  • regular BM (blood glucose measurement) monitoring
  • deliver around 38 weeks
  • offer GTT at 6 weeks postnatal