Fetal Physiology Flashcards

1
Q

How does gas exchange at the placenta work -

A

• Diffusion barrier
– Small, and decreases as pregnancy
proceeds
• Gradient of partial pressures required
• Maternal pO2 increases on marginally
• Therefore to make the gradient work, fetal pO2 must be lower than maternal pO2

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2
Q

Compare fetal to adult pO2

A

Fetal blood = low pO2 ~4kPa compared to normal adult 11-13 kPa
But factors increasing fetal o2 content
– Fetal haemoglobin variant
– Fetal haematocrit is increased over that in the adult
Ss

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3
Q

What are factors promoting O2 exchange at placenta

A

• Increased maternal production of 2,3 DPG
– Secondary to physiological respiratory alkalosis of pregnancy
• Fetal haemoglobin
• Double Bohr effect
– Fetal haemoglobin variant
– Fetal haematocrit is increased over that in the adult
– 0.513 – 0.56 l/l cf 0.4 – 0.54 l/l in adult males
– Fetal Hb = 166 – 175g/L cf , 95 – 140 g/L at 2 years and 130 – 180 g/L in adult males

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4
Q

Describe fetal Hb

A
  • Predominant form from weeks 12 – term is HbF
  • 2 alpha subunits plus 2 gamma subunits
  • Greater affinity for oxygen because it doesn’t bind 2,3-DPG as effectively as HbA
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5
Q

Describe teh double Bohr effect

A
  • Speeds up the process of O2 transfer
  • As CO2 passes into intervillois blood, pH decreases
  • Bohr effect
  • Decreasing affinity of Hb for O2
  • At the same time, as CO2 is lost from fetal circulation, pH rises
  • Bohr effect
  • Increasing affinity of Hb for O2
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6
Q

Describe CO2 transfer

A
  • Maternal physiological adaptation to pregnancy
  • Progesterone-driven hyperventilation
  • Hence lower pCO2 in maternal blood - blows of CO2
  • Concentration gradient
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7
Q

Descrbe ethe double haldane effect

A
  • Double Haldane effect
  • As Hb gives up O2, it can accept increasing amount of CO2
  • Fetus gives up CO2 as O@ is accepted
  • No alterations in local pCO2
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8
Q

Describ efetal circulation

A

• Receives oxygenated blood from mother via placenta in umbilical vein
• Lungs are non-functional
• By-passes the lungs
• Returns to the placenta via umbilical arteries
Shuts around liver - wrong side of heart 0 shunted to left side - round body

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9
Q

What are teh fetal circulation shunts

A

Ss

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10
Q

Why is the DV needed

A

• DV connects umbilical vein carrying oxygenated blood to the IVC
• Blood enters right atrium
• By ensuring shunting of blood around the liver, saturation is mostly maintained
– Drops from 70% to 65

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11
Q

Why is the FO needed

A

• Right atrial pressure is greater than that in
the left atrium
• Forces leaves of FO apart and blood flows into LA
• Free border of septum secundum forms a “crest” – crista dividens
• Creates to streams of blood flow
• Majority flows to LA
• Minor proportion flows to RV, mixing with blood from SVC (deoxygenated)

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12
Q

What happens in the left atrium

A

• Small amount of pulmonary venous return
– doxygenated
• Blood reaching left atrium has saturation approx. 60%
• Pumped by LV to aorta
• Heart and brain get lion’s share of oxygen

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13
Q

Why is the DA needed

A
  • Shunts blood from RV and PT to aorta
  • NB: joins aorta distal to the supply to the head (and heart)
  • Minimising drop in O2 saturation
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14
Q

Describe the fetal response to hypoxia

A

• Adaptations to manage transient decreases in oxygenation
• HbF and increased [Hb]
• Redistribution of flow to protect supply to heart and brain (reducing supply to GIT, kidneys,
limbs)
• Fetal heart rate SLOWS in response to hypoxia to reduce O2 demand
• Fetal chemoreceptors detecting decreased pO2 or increased pCO2
– Vagal stimulation leading to bradycardia
– cf adult where vagal inhibition leads to tachycardia
• Chronic hypoxaemia
– Growth restriction
– Behavioural changes
• Impact on development

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15
Q

What are teh hormones necessary for fetal growth

A

– Insulin
– IGFI and IGFII
– IGF II nutrient independent, dominant in first trimester
– IGF1 nutrient dependent, dominates in T2 and T3
– Leptin
• Placental production
– Plus EGF, TGFa

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16
Q

What are the effects of nutrition on fetal growth during pregnancy

A

• maternal Malnutrition can cause symmetrical or asymmetrical growth restriction (Symmetrical 0 every part of the fetus body is affected. Asymmetrical - varies eg head could be norma but rest of body growth restricted)
• Nutritional and hormonal status during fetal life can influence health in later life
– “developmental origins of health and disease hypothesis”
– Mechanisms not well understood
• ?placental adaptive responses to alterations in hormonal and / or nutritional status

17
Q

What is the role of amniotic fluid

A

• Amniotic sac encloses embryo / fetus in amniotic fluid
• Protection
• Also contributes to development of lungs
• Volume
– 10 ml at 8 weeks
– Approx 1 litre at 38 weeks (term)
– Falls away post-EDD (estimated date of delivery)- lace tall senescence?

18
Q

Describe the production and recycling of animatic fluid

A

• Fetal urinary tract
– urine production by 9 weeks - functional metanephros
– Up to 800 ml/day in T3
• Fetal lungs
• Fetal GI tract
• Placenta and fetal membranes (intramembranous pathway)

19
Q

Describe the composition of amniotic fluid

A

• 98% water
• Plus electrolytes, creatinine, urea, bile pigments, renin, glucose, hormones and fetal cells, lanugo (fine hair covering fetus) and vernix caseosa (waxy substance giving emus a degree of protection)
• then Swallowed
• gi tract Absorbs water and electrolyes
• Debris accumulates in gut
– Meconium
• Debris from AF plus intestinal secretions including bile

20
Q

Wha is amniocentesis

A
Amniocentesis
• Sampling of amniotic fluid 
• Allows for collection of fetal cells 
• Useful diagnostic test
– E.g. fetal karotyping
21
Q

Describ ebilirubim metabolism

A
  • During gestation clearance of fetal bilirubin is handled efficiently by the placenta
  • Fetus cannot conjugate bilirubin
  • Immaturity of liver and intestinal processes for metabolism, conjugation and excretion
  • Physiological jaundice common - normally transient