Foetal Adaptations to Birth Flashcards

1
Q

Intrauterine environment - how is it different from outside world?

A
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2
Q

What is the basic direction of gas exchange across the placenta.

A

O2 + nutrients = from maternal blood –> into intervillous spaces –> into chorionic villi –> foetal blood
CO2 = from foetal blood –> into chorionic villi –> into intervillous space –> into maternal blood

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3
Q

Describe how O2 & nutrients are exchanged occurs across the placenta.

A

O2 & nutrients diffuse from spiral arteries (maternal blood) -> across trophoblast memb -> into branches of umbilical vein/chorionic vein (within placental villi) -> then flows into umbilical vein -> then through umbilical cord to foetal circulation  O2 & nutrients distributed to heart, brain & all foetal organs & tissues

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4
Q

Describe how CO2 is exchanged occurs across the placenta.

A

CO2 & other waste products from foetus body -> umbilical arteries (x2) -> branches of umbilical artery/chorionic artery (within placental villi) -> across trophoblast memb -> through uterine veins (maternal blood)

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5
Q

How does O2 transport occur - what facilitates it?

A

-Placenta has low resistance
-Maternal blood PO2 is higher than foetal -> so O2 readily diffuses across to foetus = pressure gradient set up

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6
Q

How does CO2 transport occur - what facilitates it?

A

-Placenta has low resistance
-Foetal blood PCO2 is higher than maternal -> so CO2 readily diffuses across to mother = pressure gradient set up

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7
Q

What else assists in the movement of CO2 across placenta?

A

Haldane effect = the increased capacity of deoxy blood to carry CO2 compared to oxygenated blood
-As foetal blood absorbs O2 to form oxyhaemoglobin – it has reduced affinity for CO2 – so releases this CO2 to mother
-Whereas waste products e.g., urea, uric acid, creatinine – diffuse passively due to conc grads – from foetal to maternal blood

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8
Q

How is foetal haemoglobin different from adult haemoglobin -> describe process involved?

A

-Foetal = x2 alpha + x2 gamma chains
-Adult = x2 alpha + x2 beta chains

-Foetal Hb = has higher affinity for O2 (so is shifted to left on oxyhaemoglobin dissociation curve) - more readily binds/associated O2 - higher O2 carrying capacity

-Adult Hb = has lower affinity for O2 (so curve is further to right) - more readily dissociates O2 - lower O2 carrying capacity

–> more 2,3-DPG at placenta - beta chains (in HbA) bind to 2,3-DPG more readily than alpha (= stabilises deoxygenated Hb by allosteric binding & facilitates O2 release at tissue)
–> so 2,3-DPG enables more O2 release from HbA at placenta - to HbF - so HbF can then deliver O2 to foetal tissues
(as HbF is unaffected by 2,3-DPG)

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9
Q

Why is foetal haemoglobin (HbF) different from adult haemoglobin (HbA)?

A

Foetal arterial oxygen pressures are lower than adult arterial oxygen pressures
–> so HbF requires the ability to associate with more O2 (as there is less of it!)

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10
Q

Describe foetal circulation (& shunts involved)?

A
  1. Blood from placenta –> flows to umbilical vein (oxygenated blood)
  2. Ductus venosus shunts blood from umbilical vein to inferior vena cava
  3. Inferior vena cava flows to right side of heart – RA
  4. Blood will bypass lungs (as lungs are filled with fluid not air – so pressure is too high to get blood to flow to them – need pressure gradient) by:
  5. Foramen ovale –> shunts blood from RA to LA (as right side of heart has higher pressure than left)***
  6. Flows down to LV
  7. Up aorta
  8. Down descending aorta
  9. Joins up with umbilical artery (deoxygenated blood)
  10. –> to placenta

*** Another shunt – called ductus arteriosus:
-As some blood flows from RA -> RV
–> so shunt moves blood up pulmonary artery & to the aorta (this bit is the shunt) –> to aorta –> down descending aorta –> joins up with umbilical artery –> to placenta

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11
Q

Name the 3 shunts in foetal circulation & where they shunt blood from & to.

A

-Foramen ovale - shunts blood from RA to LA
-Ductus arteriosus - shunts blood up pulmonary artery & to aorta
-Ductus venosus - shunts blood from umbilical vein to inferior vena cava

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12
Q

What facilitates the movement of blood from right to left side of heart?

A

*Higher pressure on right side compared to left
-High pulmonary vascular resistance
-Hypoxaemia – pulmonary vasoconstriction

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13
Q

Why are the lungs bypassed in foetal circulation?

A

As lungs are filled with fluid not air – so pressure is too high to get blood to flow to them – need pressure gradient

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14
Q

What occurs at birth to baby’s circulation - simple description?

A

-Change in circulation occurs in first few breaths as infants makes a transition to extrauterine life
–> this occurs as umbilical cord is cut

-Pink lips & tongue, rest cyanosed (blue) as lower oxygen saturation in utero – takes several hours for peripheral circulation to make full transition

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15
Q

Give the process of the circulatory changes at birth.

A

-Circulatory changes – once umbilical cord is cut –> then gas exchange is no longer from placenta

-First breaths transforms circulation in infant
Inflation of lungs reduces pulmonary vascular pressure
-Gas exchange at lungs = rise in PO2
–> causes vasodilatation of pulmonary vasculature (factor causing higher pressure in right side than left – enabling blood shunts)
–> significantly reduces pulmonary vascular resistance (factor causing higher pressure in right side than left – enabling blood shunts)
-Reversal in interatrial pressure gradient causing a valve over foramen ovale to close = functional closure – leaves fossa ovalis (small depression)
-Reversal in pressure gradient between pulmonary artery & aorta causes flow to reverse through ductus arteriosus
-Loss of placental PGE2 & the increased aortic PO2 triggered by respiration also triggers contraction of ductus arteriosus – causing a functional closure of ductus arteriosus = forms ligamentum arteriosum
-Ductus venosus closes = forms ligamentum venosum

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16
Q

What must happen prior to the circulatory changes that occur at birth?

A

-Lungs full of amniotic fluid before birth = v. high pressure
–> infant must replace lung fluid with air - by resisting lung vol - i.e., to lower pressure in lungs - so that blood can flow to them (pressure gradients must go high to low)

17
Q

How is lung pressure lowered (i.e., how is amniotic fluid removed from lungs & how it it replaced by air)?

A

-During birth -> squeezes body by vaginal birth = replaces lungs with air
-Surge in glucocorticoids, catecholamines & ADH = causes secretion of lung fluid to be switched off
-Crying at birth = removes fluid from lungs

18
Q

Why is it easier for foetus to breath compared to newborn?

A

-Pulmonary compliance = measure of lung expandability

-Foetus - lungs filled w/ fluid - compliance w/ fluid is higher
-Newborn - lungs are uninflated - compliance w/ air is much lower

=> so is much harder for lungs of newborn to expand
–> so need much higher pressure to have same change in vol (compared to in foetus)

19
Q

What is the foetal adaptations for birth to assist in breathing?

A

-Surfactant is produced by Type 2 pneumocytes
–> stimulated by surge in maternal glucocorticoid hormones & thyroid hormones = cortisol! - which increases no. of type 2 pneumocytes & increase in enzymes that make surfactant
–> @ around 30-32 weeks gestation
–> lowers surface tension (at the newly formed air-water interface) & increases pulmonary compliance (makes it easier to expand lungs)

20
Q

Why do babies lose heat rapidly once they are born?

A

-Large SA ratio (SA:Vol) - including proportionately bigger head
-Wet
-Small
-Naked
-Poor thermal insulation by adipose tissue
-Can’t shiver to make heat, or move to warmer envs or put clothes on themselves

21
Q

How do babies lose heat when they are born?

A

-Radiation -> as env is much colder than intrauterine
-Convection -> as may be drafts in room
-Conduction -> stimulated by wrapping in cold towels/placing on cold surfaces
-Evaporation -> as they are wet

22
Q

What is the foetal adaptation to birth to assist keeping warm?

A

= Brown adipose tissue (BAT) production - enabling non-shivering thermogenesis
-Production of brown adipose tissue (BAT) prior to birth – (@ ~26 weeks gestation)
-BAT – found centrally – in intrascapular region & around clavicles, heart, aorta, trachea, kidney & pancreas
-BAT – has inc amount of mitochondria, is highly vascularised & is well innervated by sympathetic NS
–> Mitochondria = convert fat into heat
–> Highly vascularised & well innervated by symp NS = regulates rate of heat generation
-Also has increased lipase activity & free fatty acid production
==» So BAT - can double metabolic heat production during cold exposure

23
Q

Define non-shivering thermogenesis?

A

= inc. in metabolic heat production not associated w/ muscle activity – occurs mainly by metabolism in BAT

24
Q

Give the 10 steps that can be taken to prevent heat loss from neonate - WHO guidance = ‘warm chain’?

A
  1. Warm delivery room
  2. Immediate drying
  3. Skin-to-skin contact
  4. Breast Feeding
  5. Bathing & weighing postponed
  6. Clothing newborn
  7. Mother & baby together
  8. Warm transportation
  9. Warm resuscitation
  10. Training & awareness raising
25
Q

Where do newborns get their nutritional supply?

A

-Placenta nutritional source is stopped
-Period of fasting - if don’t feed immediately - rely on ‘stores of nutrition’
-Breastfeeding - milk supply

26
Q

How to newborns get their nutritional supply immediately after birth?

A

Glucagon, catecholamine & cortisol – help mobilise glycogen
-Decreased plasma glucose conc
= triggers increase in glucagon & adrenaline
-> these hormones promote glycogenolysis (glycogen -> glucose)
-Adrenaline – also inhibits insulin secretion & stimulates glucagon release from pancreatic islets
-Adrenaline & glucagon = promote lipolysis – providing fatty acids

27
Q

How do newborn get their nutritional supply 12 hours after birth -> once glycogen supply has run out?

A

PEPCK (enzyme) activity increases (due to decreased plasma glu conc – but doesn’t immediately increase – hence the previous process taking place 1st) – enables onset of gluconeogenesis
-Cortisol promotes lipolysis = glycerol
-Cortisol promotes gluconeogenesis of non-carb substrates = fatty acids & AAs & glycerol = forms glucose (& can also be used to store more glycogen)
-So glycogen can again undergo glycogenolysis
–> = glucose
*
-Cori cycle forms lactate which can then undergo gluconeogenesis (promoted by cortisol) or convert to glycogen stores (then undergo glycogenolysis)
–> Cori cycle also converts glucose back to lactate (so Cori cycle recycles)

28
Q

How do newborns get their nutritional supply 12 hours after birth?

A

-Ketogenesis = production of ketone bodies – by breaking down fatty acids & (ketogenic) AAs
-So same processes as above – fatty acids & AAs can either undergo gluconeogenesis or be converted to glycogen (& later undergo glycogenolysis to form glucose)
-Lactate Cori cycle still occurring
But now fatty acids (& AAs?) can undergo B-oxidation
= this is where fatty acids are converted into acetyl CoA in mitochondria of liver
-x2 of these acetyl-CoA molecules are combined -> forming ketone bodies
-Ketone bodies are used to supply energy to brain, heart & skeletal muscles

29
Q

Summarise the importance (i.e., the roles) of endocrine hormones in foetal maturation.

A
30
Q

From what I now know - why are premature babies so unwell?

A

-No fat stores -> BAT stores not build up yet = hypothermia risk
-Little glycogen -> not built up yet = little energy supply for when born
-No surfactant -> lungs can’t expand as well (low compliance) & higher surface tension
-Persistence of foetal circulation = shunts still in heart - bypass lungs