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CARDIO TEST 3 > Lecture 10: Preeclampsia – Placental and Vascular Origins > Flashcards

Lecture 10: Preeclampsia – Placental and Vascular Origins Flashcards

1
Q

When is development of maternal blood supply to placenta complete?

A

End of 1st trimester - 12-13 weeks

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2
Q

What organs does the placenta substitute for?

A

Lungs, kidney, GIT

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3
Q

What are the vascular components of the placenta and what is contained in these?

A

Fetal - fetal arteries and veins in chorionic plate

Maternal - endometrial arteries and veins

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4
Q

What happens at the metal-maternal interface?

A

Umbilical arteries and veins move between mother and fetus

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5
Q

What happens to cytotrophoblasts in normal placental development?

A

Cytotrophoblast cells invade maternal spiral arteries and go from an epithelial to endothelial phenotype, allowing spiral arteries to enlarge to increase blood flow

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6
Q

What do invading trophoblast cells replace?

A

Endothelial cells and smooth muscle cells

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7
Q

How do uterine spiral arteries change in pregnancy?

A
  • Loss of vascular smooth muscle
  • Breakdown extracellular matrix
  • Loss of endothelial cells
  • Wider arteries
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8
Q

What happens if there is inadequate remodelling of the spiral arteries?

A

Abnormal placental development and reduced placental perfusion

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9
Q

What is preeclampsia and what are the features?

A

Pregnancy specific CVD characterised by hypertension >20 weeks gestation and excess serum proteins in urine (>300mg – proteinuria), general oedema

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10
Q

What % of Australian pregnancies are affected by preeclampsia?

A

5-8%

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11
Q

When do the symptoms of preeclampsia present?

A

Late in pregnancy (3rd trimester) – need hospitalisation

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12
Q

What happens in eclampsia?

A

Seizures, coma

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13
Q

What is the treatment for preeclampsia?

A

Early delivery - need to remove placenta

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14
Q

What happens to babies born to preeclamptic mothers?

A

Low birth weight and increased risk of adult disease

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15
Q

Where does preeclampsia begin and end?

A

Placenta to maternal edothelium, causing endothelial dysfunction

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16
Q

What things are thought to contribute to placental dysfunction?

A

Immune cells, genetic factors, placental oxidative stress and antibodies thought to cause placental dysfunction and hypoxia - releases factors that cause endothelial damage in organs and complications

17
Q

What things characterise placental dysfunction?

A
  • Abnormal vascular adaptations
  • Inadequate trophoblast invasion
  • Abnormal spiral artery remodelling
18
Q

What are the abnormal changes to spiral arteries in preeclampsia?

A
  • Invasion is shallow
  • Cytotrophoblasts fail to adopt invasive endothelial phenotype
  • Vascular smooth muscle intact
  • Arteries remain small, resistance vessels – blood flow and placental perfusion reduced
19
Q

What is the role of VEGF?

A

Angiogenesis and vascular relaxation

20
Q

How does sFlt affect blood vessels and VEGF?

A

Binds to VEGF and prevents relaxation action - stiffer vessels

21
Q

When do sFlt levels rise?

A

Towards end of pregnancy (2 fold increase in preeclamptic women)

22
Q

When are increases in sFlt detected and when do high levels indicate risk of preeclampsia?

A

Detected 5-8 weeks before development of preeclampsia, and high levels at 25-32 weeks pose high risk for preeclampsia

23
Q

What did treatment with sFlt cause?

A

Increased MAP, proteinuria, endothelial dysfunction

24
Q

How does sEng change with preeclampsia?

A

Increased levels in serum and placenta

25
Q

How does COMT1 change with preeclampsia?

A

Decreases

26
Q

What happens to 2-ME during normal pregnancy/preeclampsia?

A

Increases in normal pregnancy

Levels are low in preeclampsia at 22-29 weeks (low COMT expression)

27
Q

What happens if you knockout CMOT1?

A
  • Significant increase in sFlt

- Diminished uterine arteries

28
Q

What happens if COMT1 is present and woman is treated with 2-ME?

A

sFlt levels returned to normal (2-ME reduces COMT1)

29
Q

When is relaxin a predictor of preeclampsia?

A

Low circulating relaxin during first 13 weeks of gestation are a strong predictor of preeclampsia – 7 times more likely to develop preeclampsia

30
Q

What happens when there is a knockout of relaxin?

A
  • Increase creatinine levels, proteinuria

- Reduction in fetal weight

31
Q

What does relaxin treatment do?

A

Restores normal pregnancy vasodilatory phenotype in human arteries from women with preeclampsia

32
Q

What are the actions of relaxin?

A
  • Increase vasodilation (renal, mesenteric, uterine)
  • Increase NO pathway
  • Increase vasodilator sensitivity and reduce vasoconstrictor sensitivity
  • Decrease stiffness (renal, mesenteric)
33
Q

What does renin do in pregnancy?

A

Maintains endothelial function and remodels systemic and uterine vasculature

CARDIO TEST 3 (10 decks)

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