Repro17 - Fetal Physiology Flashcards
1
Q
4 factors promoting oxygen exchange to the fetus at the placenta
Partial Pressure Gradient
Maternal Production of 2,3-DPG
Fetal Haemoglobin
Double Bohr Effect
A
- ) Large Partial Pressure Gradient - fetal blood pO2 is only 4kPa compared to 11-13kPa in the mother
- this means maternal haemoglobin easily gives up oxygen to the fetus - ) Increased Maternal Production of 2,3 DPG - caused by physiological respiratory alkalosis in pregnancy
- shifts maternal curve to the right so the maternal haemoglobin has lower affinity for oxygen - ) Fetal Haemoglobin - HbF, 2 alpha, 2 gamma subunits
- doesn’t bind w/ 2,3 DPG so fetal curve doesn’t shift to the right so HbF has greater affinity for oxygen than HbA - ) Double Bohr Effect - speeds up O2 transfer due to CO2 leaving the fetus and going to the mother
- mother receiving CO2 lowers the pH, causing the maternal curve to shift to the right (less affinity)
- fetus losing CO2 increases the pH, causing the fetal curve to shift to the left (more affinity)
2
Q
2 features of CO2 transfer
Lower pCO2 in Maternal Blood
Double Haldane Effect
A
- ) Lower pCO2 in Maternal Blood - due to progesterone driving hyperventilation so mother has lower CO2
- this creates a conc gradient between mother and fetus - ) Double Haldane Effect - as maternal haemoglobin gives up O2, it can accept more CO2
- fetus gives up more CO2 as more O2 is accepted
- leads to no alterations in local pCO2
3
Q
4 fetal responses to hypoxia
Fetal Haemoglobin
Flow Distribution
Heart Rate
Chronic Hypoxaemia
A
1.) Increased HbF
- ) Redistribution of Flow - towards the heart and brain
- reduces supply to the GI, kidneys, and limbs - ) Bradycardia - less O2 demand for the heart
- fetal chemoreceptors detect change in pO2 or pCO2 to cause vagal stimulation which leads to bradycardia
- in adults, it is vagal inhibition –> tachycardia - ) Chronic Hypoxaemia - impact on development
- causes asymmetrical growth restriction because of the redistribution of blood flow
- can also cause behavioural changes
4
Q
3 features of fetal growth
Hormones Required x6
Cell Growth Mechanisms (and weeks)
Effect of Malnutrition
A
- ) Hormones Required - insulin, IGF1/2, leptin, EGF, TGF
- IGF2 is nutrient independent and dominates T1
- IGF1 is nutrient dependent and dominates T2 and T3
- leptin is needed for placental production
- EGF (epidermal GF) and TGF (transforming GF) - ) Cell Growth Mechanism
- 0-20 weeks: hyperplasia
- 20-28 weeks: hyperplasia and hypertrophy
- 28 weeks+ : hypertrophy - ) Malnutrition - can cause symmetrical or asymmetrical growth restriction
- nutritional and hormonal status during fetal life can influence health in later life (unknown mechanism)
5
Q
5 features of amniotic fluid
Function Composition Production and Recycling Amniocentesis Amniotic Fluid Volume
A
- ) Function - protection of the fetus
- also contributes to the development of the lungs - ) Composition - 98% water
- contains electrolytes, creatinine, urea, bile pigments, renin, gluose, hormones, fetal cells, lanugo, vernix
- volume: 10ml at 8 weeks, 1 litre at 38 weeks - ) Production and Recycling - produced by the placenta in the first 9 weeks then the fetal urinary tract afterwards
- fetus swallows amniotic fluid so it enters the GI tract to be digested and then recycled as urine
- debris accumulates in the gut which is meconium
- meconium is only passed after delivery - ) Amniocentesis - sampling of amniotic fluid
- allows for collection of fetal cells
- used in fetal karyotyping - ) Amniotic Fluid Volume - diagnostic sign
- oligohydraminos is caused by placental insufficiency (pre-eclampsia) or fetal renal impairment
- polyhydraminos is caused by the inability to swallow (no recycling)