Fetal Growth and Nutrition Flashcards
What is fetal growth?
Increase in body size and mass from end of organogenesis (8-10 weeks).
Fetal hyperplasia versus child hypertrophy
What cells in the body undergo hyerplasia and stop before birth?
What does this determine
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
What is fetal growth restriction, cause, result of it and risk?
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
Weights and sizes of small babies?
LBW: <2500g
SGA: <10th centile
Distinguishing SGA and FGR
They are not the same. Not all SGA babies have had FGR. Signs of FGR are less fat accretion etc
FGR and pre term babies
Is very common
What determines fetal growth?
In order of priority
Nutrition; Hormones; Genetics
How does the embryo grow early?
Uterine glands secrete secretion high in carbs and lipids. Growth is autonomous an consistent. Period of organogenesis
Histiotrophic nutrition
When does haemotrophic nutrition begin and what does it involve?
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
What does the fetal diet consist of, how are these transported and what is their role?
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
What are the two most fetal growth hormones?
Insulin-like growth factor (IGF’s, most important) and insulin
What do IGF’s do?
Are potent mitogens and cause protein anabolism that act in a paracrine and endocrine manner. Made in placenta and fetal tissues
IGF1 vs IGF2
IGF1: Matches fetal growth to nutrient supply; not regulated by GH
IGF2: Embryonic and placental growth, the constitutive drive for growth (more of this)
Action of fetal insulin
Increases glucose uptake, fat deposition, protein anabolism and may promote placental growth, stimulate fetal IGF1
In early pregnancy, AA stimulates insulin
Growth hormone in the fetus
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
What do glucocorticoids do in fetal growth?
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
How does the placenta create a barrier to maternal cortisol?
11 beta HSD2, reduction occurs n maternal protien malnutrition and disease like preeclampsia. Too much cortisol exposure can cause later effects
What is the typical reason for limited fetal growth?
maternal; embryogenesis
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
Fetal versus postnatal growth
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
What are some causes of FGR?
Fetal Undernutrition: Placnetal insufficiency or maternal undernuturion
Fetal pathology: congenital malformation, toxins, chromosomal etc
What is Beckwith Wiedmann syndrome?
note maternal genes suppress growth, paternal promote
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.
Placental insufficiency
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
Long term effects of FGR
Have a thrifty phenotype, so low nephron mass, low muscle mass, endothelial dysfuncntion etc
Predisposing you too: hypertension, IHD, diabetes, stroke etc
Gestational diabetes
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
