Fetal Adaptations To Pregnancy Flashcards

0
Q

Reasons for low birth weight

A

Preterm pregnancy
Multiple pregnancy
Genetics
IUGR

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1
Q

Factors influencing fetal growth

A
Fetal genome
Maternal height in relation to uterine capacity
Maternal nutrition
Placenta malfunction 
Fetal sex
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2
Q

Effects of insulin like growth factors

A

IGF1 and 2 produced by fetal cells including placenta
Synthesis increases through pregnancy
2-3x more IGF2
IGF1 produced in response to nutrient levels, decrease with nutrient levels
IFG1 productions also sensitive to insulin, thyroxine, glucorticoids-> match fetal growth to maternal nutrient supply
IGF2 stimulates placental growth and transport mechanisms
IGF2 paternally expressed
Increased recourse extraction from mother

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3
Q

Gradients that drive diffusion exchange

A

pO2 in umbilical vein is low compared to maternal blood
pCO2 high in umbilical artery compared to maternal blood
O2 saturation is high in fetal blood-> much lower pO2 still leads to similar O2 content-> fetal blood has higher O2 trapping capacity
2 gamma instead of beta chains-> doesn’t bind 2DPG
double Bohr effect-> fall in pH of maternal due to uptake of fetal CO2-> release of maternal O2 and rise in fetal due to CO2 removal
Switch to adult Haemoglobin happens several months after birth

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4
Q

Fetal CV system

A

Ductus venosus-> oxygenated blood in fetal vein-> two channels-> larger is ductus venosus-> bypasses hepatic circulation
Small amount of blood enters liver-> regulated by sphincter-> blood shunted here during uterine contraction
For amen ovale-> IVC carries blood to RA-> split into two streams by crista dividens-> larger through foremen ovale to LA
Ductus arteriosus-> smaller stream-> RA-> RV -> pulmonary artery-> ductus arteriosus-> aorta or small amount to lungs

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5
Q

CV changes at birth

A

Initiated at first breath
Closure of umbilical arteries-> contraction caused by thermal, mechanical and pO2 change
Closure of umbilical veins and ductus veinosus-> placental blood no longer reaches heart-> minutes after birth
Closure of ductus arteriosus-> contraction of muscular walls-> blood must go to lungs-> bradykinin released by lungs after initial inflation, complete obliteration takes 1-3 months
Closure of foramen ovale-> increased pulmonary blood flow-> increased pressure in LA-> decreased pressure RA

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6
Q

Respiratory system

A

Surfactant production starts 2 months before birth
No surfactant-> respiratory distress syndrome
Fetus makes rapid respiratory movements 1-4 per day
Moves amniotic fluid in and out of lungs-> lung development and resp muscle conditioning

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7
Q

Renal system

A
Kidneys are functional during pregnancy 
Produce amniotic fluid
Produce lots of hepatouric urine
Inefficient Na reabsorption 
Fetal urine-> 0.5l/day to amniotic fluid
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8
Q

Nervous system

A

Fetus can respond to extraneous stimuli form 2nd trimester
Loud noises, intense light, rapid temp decrease
Results in changed movement and increased heart rate
Pain detected at 29 weeks
Immature blood brain barrier-> opioids and nictine can produce dependence

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9
Q

Sub optimal intrauterine conditions

A
Poor maternal diet 
Maternal stress
Hypoxia 
Drugs
Endocrine disrupting chemicals 
Alcohol
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10
Q

Suboptimal intrauterine conditions lead to…

A
Placental insufficiency 
Poor placental growth 
Poor transport mechanisms
Impaired barrier
Vascular dysfunction 
Increased cortisol secretion 
Aberrant invasion of decidua and spiral artery re modelling
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11
Q

Consequences of placental insufficiencies

A
Small baby 
Intrauterine growth restriction 
Metabolic changes in infants
Obesity 
Impaired glucose tollerance 
Insulin resistance
Dyslipdemia 
Obesity 
Type 2 
Metabolic syndromes in adults
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12
Q

Barker hypothesis

A

The lower the weight of the baby at birth and infancy the higher the risk of CV disease

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13
Q

Dutch famine disease

A

Low birth weight associated with risk of hypertension, stroke and diabetes
Maternal diabetes and macro soma-> CV and metabolic disease

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14
Q

Evolutionary changes

A

Low birth weight babies-> survival value for selecting genes that reduce fetal growth in response to maternal nutritional stress as a way of preparing the offspring for optimised survival in resource poor world
However if recourses are fine-> catch up growth is bad of for health

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15
Q

Thrifty gene hypothesis

A

Early in evolutionary history-> genes that promoted fat deposition would’ve been useful to survive famine
In modern society these genes aren’t useful
Disease and diabetes
Early life metabolic adaptions help survival of organism by selecting appropriate growth trajectory in response to environmental ques

16
Q

Epigenetics

A

The mechanism of regulating gene expression without altering the DNA sequence

17
Q

Epigenome

A

The machinery that regulates gene expression-> alters phenotype
Histones-> wrapped around DNA-> controll when the complex opens so code can be read

18
Q

Epigenetic modification

A

DNA methylation-> addition of methyl groups to cytosine-> activate or repress genes
Histone modification-> methylation affects hi stones-> alters DNA wrapping and availability of genes to be activated

19
Q

Examples of epigenetic modification

A

Reprogramming during gametogenesis-> differ in spermatogenic and oogenic lineage-> uni parental imprinting
After fertilisation-> rapid demethylation of entire maternal nome and slower of paternal. Not on imprinted genes
Can be modulated throughout life

20
Q

Parental imprinting

A

For majority of genes expression is bilallelic
80-100 one parent silences their own gene-> parent specific monoallelic expression
IGF is paternal
Gnasxl paternally expressed-> suckling