S7) Foetal Physiology Flashcards

1
Q

Where does materno-foetal exchange occur?

A

Materno-fetal exchange happens at the placenta

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2
Q

Identify the vascular structures involved in materno-foetal exchange

A
  • Umbilical arteries
  • Umbilical vein
  • Fetal capillaries within chorionic villi
  • Uterine arteries
  • Uterine veins
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3
Q

Describe the foetal blood supply and drainage

A
  • Oxygenated blood carried via the umbilical vein
  • Deoxygenated blood carried via the umbilical arteries
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4
Q

Identify the factors increasing foetal pO2 content

A
  • Fetal haemoglobin variant
  • Fetal haematocrit (proportion of red blood cells) is increased over that in the adult
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5
Q

What is necessary for gas exchange to occur at the placenta?

A
  • Gradient of partial pressures required
  • Maternal pO2 increases only marginally, so fetal pO2 must be lower than maternal pO2
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6
Q

What is the value of foetal pO2 compared to maternal pO2?

A
  • pO2 approx. 4kPa compared to normal adult pO2 of 11 – 13kPa
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7
Q

Identify 3 additional factors promoting oxygen exchange to the foetus at the placenta

A
  • Increased maternal production of 2,3 BPG
  • Fetal haemoglobin
  • Double Bohr effect
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8
Q

Why is there an increased maternal production of 2,3 BPG?

A

Secondary to physiological respiratory alkalosis of pregnancy

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9
Q

The predominant form of haemoglobin from weeks 12 is HbF.

Describe how its structure is adapted to its function

A
  • HbF consists of 2 alpha subunits & 2 gamma subunits
  • HbF has a greater affinity for oxygen as it doesn’t bind 2,3-BPG as effectively as HbA
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10
Q

The double Bohr effect speeds up the process of O2 transfer.

Describe how this process works

A

MATERNAL:

  • As CO2 passes into intervillous blood, pH decreases (Bohr effect)

⇒ Decreasing affinity of Hb for O2

PATERNAL:

  • At the same time, as CO2 is lost, pH rises (Bohr effect)

⇒ Increasing affinity of Hb for O2

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11
Q

Explain how maternal physiological adaptations to pregnancy promotes CO2 transfer from the foetus

A
  • Progesterone-driven hyperventilation lowers pCO2 in maternal blood
  • Concentration gradient created
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12
Q

Describe how CO2 is transferred to the maternal blood from the foetus through the Double Haldane effect

A
  • As maternal Hb gives up O2, it can accept increasing amounts of CO2
  • Foetus gives up CO2 as O2 is accepted
  • No alterations in local pCO2 occur
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13
Q

Briefly, outline foetal circulation

A
  • Receives oxygenated blood from mother via placenta in umbilical vein
  • Lungs are non-functional so blood by-passes the lungs
  • Returns blood to the placenta via umbilical arteries
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14
Q

In terms of foetal shunts and vasculature, describe the anatomical course of foetal circulation in detail

A
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15
Q

In terms of foetal shunts and vasculature, label the key structures of foetal circulation in the diagram below

A
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16
Q

Why is the ductus venosus needed?

A
  • DV connects umbilical vein carrying oxygenated blood to the IVC so blood enters right atrium
  • By ensuring shunting of blood around the liver, saturation is mostly maintained
17
Q

Why is the foramen ovale needed?

A
  • Right atrial pressure > left atrium
  • Forces leaves of FO apart and blood flows into left atrium
18
Q

Why is the ductus arteriosus needed?

A
  • DA joins aorta distal to the supply to the head (and heart)
  • DA shunts blood from right ventricle and pulmonary trunk to aorta, minimising drop in O2 saturation
19
Q

Describe the foetal response to hypoxia

A
  • Foetal chemoreceptors detect decreased pO2 or increased pCO2
  • Redistribution of flow (reduced to limbs & intestines) to protect supply to heart and brain
  • Vagal stimulation leads to bradycardia to reduce O2 demand
  • hbF and increased Hb
20
Q

What are the effects of chronic hypoxaemia on the foetus?

A
  • Growth restriction
  • Behavioural changes
  • Impact on development
21
Q

Identify some hormones necessary for foetal growth

A
  • Insulin
  • IGFI
  • IGFII
  • Leptin (placental production)
  • EGF
  • TGFa
22
Q

Distinguish between IGF I and II

A
  • IGF II nutrient independent, dominant in first trimester
  • IGF I nutrient dependent, dominates in second and third trimester
23
Q

Nutritional and hormonal status during foetal life can influence health in later life.

What is the effect of malnutrition on foetal growth?

A

Malnutrition can cause symmetrical or asymmetrical growth restriction

24
Q

Identify and describe the dominant cellular growth mechanisms at different stages of pregnancy

A
25
Q

What is the structure and function of the amniotic sac?

A
  • Structure: encloses embryo / fetus in amniotic fluid
  • Function: protection and also contributes to development of lungs
26
Q

What is the volume of aminiotic fluid?

A

Approximately:

  • 10 ml at 8 weeks
  • 1 litre at 38 weeks
27
Q

Most of the amniotic fluid is swallowed.

Identify the structures involved in the production and recycling of amniotic fluid

A
  • Foetal urinary tract (urine production by 9 weeks)
  • Foetal lungs
  • Foetal GI tract
  • Placenta and foetal membranes
28
Q

Describe the composition of amniotic fluid

A
  • 98% water
  • 2% electrolytes, creatinine, urea, bile pigments, renin, glucose, hormones and fetal cells, lanugo and vernix caseosa
29
Q

What is amniocentesis and what does it do?

A

Amniocentesis is a useful diagnostic test involving the sampling of amniotic fluid and allows for collection of fetal cells

30
Q

Debris accumulates in the foetal gut and the presence of meconium in amniotic fluid during delivery is a sign of foetal stress and asphyxia.

What is meconium?

A

Meconium is debris from the amniotic fluid and intestinal secretions including bile

31
Q

In terms of bilirubin metabolism during pregnancy and after birth, explain why physiological jaundice is common in infants

A
  • During gestation: clearance of foetal bilirubin is handled efficiently by the placenta as foetus cannot conjugate bilirubin
  • At birth: the liver, intestinal processes for metabolism, conjugation and excretion are immature
32
Q

what is olgiohydramnios?

A
  • too little amniotic fluid
  • placental insufficiency
  • premature rupture of membranes
  • pre eclampsia
33
Q

what is polyhydramnios?

A
  • too much amniotic fluid
  • fetal abnormality
  • gestational diabetes
  • fetal anemia
  • multiple pregnancy