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
  1. ) 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
  2. ) 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
  3. ) 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
  4. ) 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)
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2
Q

2 features of CO2 transfer

Lower pCO2 in Maternal Blood
Double Haldane Effect

A
  1. ) Lower pCO2 in Maternal Blood - due to progesterone driving hyperventilation so mother has lower CO2
    - this creates a conc gradient between mother and fetus
  2. ) 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
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3
Q

4 fetal responses to hypoxia

Fetal Haemoglobin
Flow Distribution
Heart Rate
Chronic Hypoxaemia

A

1.) Increased HbF

  1. ) Redistribution of Flow - towards the heart and brain
    - reduces supply to the GI, kidneys, and limbs
  2. ) 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
  3. ) Chronic Hypoxaemia - impact on development
    - causes asymmetrical growth restriction because of the redistribution of blood flow
    - can also cause behavioural changes
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4
Q

3 features of fetal growth

Hormones Required x6
Cell Growth Mechanisms (and weeks)
Effect of Malnutrition

A
  1. ) 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)
  2. ) Cell Growth Mechanism
    - 0-20 weeks: hyperplasia
    - 20-28 weeks: hyperplasia and hypertrophy
    - 28 weeks+ : hypertrophy
  3. ) Malnutrition - can cause symmetrical or asymmetrical growth restriction
    - nutritional and hormonal status during fetal life can influence health in later life (unknown mechanism)
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5
Q

5 features of amniotic fluid

Function
Composition
Production and Recycling
Amniocentesis
Amniotic Fluid Volume
A
  1. ) Function - protection of the fetus
    - also contributes to the development of the lungs
  2. ) 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
  3. ) 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
  4. ) Amniocentesis - sampling of amniotic fluid
    - allows for collection of fetal cells
    - used in fetal karyotyping
  5. ) 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)
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