Fetal Growth and Nutrition

Question 1

What is fetal growth?

Answer 1

Increase in body size and mass from end of organogenesis (8-10 weeks).
Fetal hyperplasia versus child hypertrophy

Question 2

What cells in the body undergo hyerplasia and stop before birth?
What does this determine

Answer 2

Neurons, skeletal muscle fibres, seminiferous tubules. renal nephrons, pancreatic beta cells, heart muscle.
Pulmonary will keep growing for a bit after birth (few months)
This determines the metabolic capacity, so limited fetal growth can limit the metabolic capacity

Question 3

What is fetal growth restriction, cause, result of it and risk?

Answer 3

In utero growth potential being limited by a pathological process, typically due to poor placentation.
Results in less fat and lean tissues
Risk of still birth and asphyxia

Question 4

Weights and sizes of small babies?

Answer 4

LBW: <2500g
SGA: <10th centile

Question 5

Distinguishing SGA and FGR

Answer 5

They are not the same. Not all SGA babies have had FGR. Signs of FGR are less fat accretion etc

Question 6

FGR and pre term babies

Answer 6

Is very common

Question 7

What determines fetal growth?

Answer 7

In order of priority

Nutrition; Hormones; Genetics

Question 8

How does the embryo grow early?

Answer 8

Uterine glands secrete secretion high in carbs and lipids. Growth is autonomous an consistent. Period of organogenesis
Histiotrophic nutrition

Question 9

When does haemotrophic nutrition begin and what does it involve?

Answer 9

2nd trimester, Fetal nutrtion from placenta.
Influenced by maternal diet, maternal metabolic and endrocrine status, uterine blood flow, plaental transport and metabolism, umbilical blood flow and then fetal status

Question 10

What does the fetal diet consist of, how are these transported and what is their role?

Answer 10

Glucose: Facilitated diffusion by GLUT1; Fetal has limited gluconeogenesis so relies on glucose for fuel and carbon source

Protein: Active transport, and glutamate and glycine made in placenta. Some is shuttled from fetus to placenta too; role in metabolic balance between oxidation and growth. Also C, N, nuceltides etc

Lactate: made by placenta; oxidised

FA: Diffusion: energy store and cell membranes

Question 11

What are the two most fetal growth hormones?

Answer 11

Insulin-like growth factor (IGF’s, most important) and insulin

Question 12

What do IGF’s do?

Answer 12

Are potent mitogens and cause protein anabolism that act in a paracrine and endocrine manner. Made in placenta and fetal tissues

Question 13

IGF1 vs IGF2

Answer 13

IGF1: Matches fetal growth to nutrient supply; not regulated by GH
IGF2: Embryonic and placental growth, the constitutive drive for growth (more of this)

Question 14

Action of fetal insulin

Answer 14

Increases glucose uptake, fat deposition, protein anabolism and may promote placental growth, stimulate fetal IGF1

In early pregnancy, AA stimulates insulin

Question 15

Growth hormone in the fetus

Answer 15

Is high, deficiency causes little change to weight (some change in length so short). No regulation of IGF1. No receptors in liver.

May alter fetal metabolism

Question 16

What do glucocorticoids do in fetal growth?

Answer 16

Near term due to adrenal activation, promote tissue differentiation and maturation.
Decreased DNA synthesis and cell division, slowing babies growth
Turn on somatotrophic axis, causing GH receptor expression in the liver

Question 17

How does the placenta create a barrier to maternal cortisol?

Answer 17

11 beta HSD2, reduction occurs n maternal protien malnutrition and disease like preeclampsia. Too much cortisol exposure can cause later effects

Question 18

What is the typical reason for limited fetal growth?

maternal; embryogenesis

Answer 18

Constraint:
Main is maternal- ability of placenta to supply oxygen and nutrients, e.g placental size, maternal size and age(adolescent), parity, short inter pregnancy interval, macronutrient imbalance

Embryogenesis: twins and periconceptual undernutrition

Question 19

Fetal versus postnatal growth

Answer 19

Fetal: normally constrained by maternal environ, if endorcrine status is okay, growth is normally regulated by amount of substrate

Postnatal: Normally to genetic potential, if nutrition is adequate, growth is normally regulated by endocrine status

Question 20

What are some causes of FGR?

Answer 20

Fetal Undernutrition: Placnetal insufficiency or maternal undernuturion

Fetal pathology: congenital malformation, toxins, chromosomal etc

Question 21

What is Beckwith Wiedmann syndrome?

note maternal genes suppress growth, paternal promote

Answer 21

Overexpression of IGF2 (maternal gene imprinted), causing macrosomia/macroglossia. Transverse ear crease, omphalocoele, hypoglycaemia, hemihypertrophy

Opposite (less IGF2) Russel silver syndrome with SGA and normal head growth.

Question 22

Placental insufficiency

Answer 22

Leading cause of FGR, due to deficent trophoblast invasion and remoddeling of spiral arteries. Maldevelopment of villi.
Reduced SA for perfusion.
May also have placental inflammation

Question 23

Long term effects of FGR

Answer 23

Have a thrifty phenotype, so low nephron mass, low muscle mass, endothelial dysfuncntion etc

Predisposing you too: hypertension, IHD, diabetes, stroke etc

Question 24

Gestational diabetes

Answer 24

Excess maternal glucose and FFA increases fetal insulin leading to increased fetal growth.

Leads to preeeclampsia in mother, and fetal problems such as RDS, neonatal jaundice> increases risk of mather to get type 2 diabetes and risk of diabetes and obesity in offspring