Lecture 2: Developmental Origins of Cardiovascular Disease Flashcards Preview

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Flashcards in Lecture 2: Developmental Origins of Cardiovascular Disease Deck (22)
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1
Q

What is the placenta responsible for?

A

Transport of nutrients and waste exchange from the foetus

2
Q

What hormones promote fetal growth?

A

IGFs, thyroid hormones and insulin

3
Q

What effect do glucocorticoids have?

A

Inhibit fetal growth

4
Q

When are glucocorticoids released?

A

In stressful situations

5
Q

What is the figure for small for gestational age and what % of babies is this?

A

Less than 2500g - 2%

6
Q

What % of birth size is dependent on genotype and sex?

A

15%

2%

7
Q

What is low term birth weight and what % of babies have this?

A

2SD below population mens - 10%

8
Q

What % of babies die due to being born small?

A

2-10%

9
Q

What is intrauterine growth restriction caused by in western and 3rd world societies?

A

Placental insufficiency

Maternal undernutrition

10
Q

What is the common feature of the causes of IUGR?

A

Reduced nutrient delivery across the placenta

11
Q

What is fetal programming?

A

Exposure of the fetus to a suboptimal environment causes adaptations that may help the fetus to survive in the short term but leads to increased susceptibility of developing some diseases in adulthood. If there is a reduction in nutrient transport across the placenta the baby will keep brain developing normal and restrict development of other organs - disease occurrence

12
Q

What is prepartum maturation?

A

Maturation after organogenesis but before birth

13
Q

What are adult disease associated with?

A

Suboptimal intrauterine conditions in humans

14
Q

What cardiac conditions are adults born small susceptible to?

A

Cardiac hypertrophy, hypertension, coronary heart disease and altered cardiac genes

15
Q

What corticoid changes are present in adults who were born small?

A

Higher plasma cortisol, altered mineralo and glucocorticoid receptos

16
Q

What are the changes in nephrons in adults born small?

A

Reduced nephron endowment, low nephron number, high BP

17
Q

When do cardiomyocytes transition to binucleate form?

A

Late development and around birth (reduced binucleate cardiomyocytes when born small)

18
Q

What does uteroplacental insufficiency lead to?

A
  • Offspring born small (10% reduction in birth weight)
  • Altered maternal endocrine environment (reduced progesterone)
  • Impaired mammary development during pregnancy
  • Triggers early lactogenesis (increases milk protein genes)
  • Reduced milk quality and quantity during lactation: impaired lactational nutrition compromises postnatal growth with consequences for adult disease development
19
Q

What are the sex specific differences associated with being born small?

A

Males more susceptible to disease development in adulthood, whereas females are relatively protected - even after being subjected to the same in utero restriction. Males develop hypertension at 6 months and females don’t develop hypertension even by 18 months

20
Q

What % of babies born small have accelerated growth in the first 6 months?

A

90%

21
Q

When is accelerated growth good and bad?

A

Protective if early and detrimental if late

22
Q

What happens when you cross foster a restricted male with a control mum?

A

Improved postnatal body weight due to adequate lactational nutrition