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Dev ad Ageing BRS2 > Pregnancy, Parturition and late foetal Dev + disorders > Flashcards

Pregnancy, Parturition and late foetal Dev + disorders Flashcards

1
Q

How much does the embryo grow in the first trimester? + why?

A

Its growth is relatively limited + histiotrophic nutrition (uterine gland secretions)

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2
Q

As we go from first to second trimester, how does the growth rate of the embryo change?

A

There is significant increase in rate of foetal growth + haemotrophic

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3
Q

What is spiral artery remodelling?

A

Extra-villus trophoblasts (EVTs) remodel the artery to form chorionic villi for fetal blood supply

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4
Q

How does the remodelling work?

A

Remodelling occurs when the EVT cells invade down into the maternal spiral arteries to endovascular EVTs. As they invade, they break down the endothelium and smooth muscle and replace them to coat the inside of the spiral artery vessel through immune cell recuirtment (chemokines) +eEVT’s secrete fibrinoid.

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5
Q

Failed conversion (spiral artery)

A

immune cells become embedded and RBCs occlude vessels

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6
Q

How enviornemnt is psiral artery remodelling trying to create + name of process?

A

conversion- turns into a low pressure, high capacity conduit for maternal blood flow

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7
Q

How is oxygen exchanged in the placenta?

A

diffusion

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8
Q

How is glucose exchanged in the placenta?

A

Facillitated diffusion

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9
Q

How is water exchanged in the placenta?

A

diffusion + hydrostatic gradients

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10
Q

How is calcium exchanged in the placenta?

A

active transport

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11
Q

4 ways the mothers circulation changes throughout pregnancy?

A
  • incraesed ventilation
  • increased cardiac output
  • increased blood volume
  • decreased resistance
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12
Q

2 major things failed spiral artery remodelling causes?

A
  • hyperplasia
  • atherosis ( poor placentation)
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13
Q

3 increased risks of Failed SAR

A
  • Local hypoxia bc of turbulent flow,
  • free radical damage
  • insufficient nutrient delivery
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14
Q

Atherosis?

A

occurs in basal arteries that havent been remodelled

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15
Q

What is Preeclampsia? How is it diagnosed

A

New onset hypertension:
-> BP over 140/90
-> after 20 weeks gestation

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16
Q

Symmptoms of preeclampsia? (4)

A
  • Odema
  • Headache
  • Seizures
  • Abdo pain
17
Q

Severe cases of preeclampsia symptoms (3)

A
  • Visual disturbances
  • Breathlessness
  • Risk of eclampsia (seizures)
18
Q

Risk factors? (7)

A
  • Maternal Age
  • Co morbities (renal irregularities, T2DM, Hypertension)
  • Fx
  • Previous preganancies with PE
  • BMI
  • IVF
19
Q

What risk does preeclampsia pose to the mother? (4)

A
  • Damage to kidneys, liver, brain and other organ systems
  • Possible progression to eclampsia (seizures, loss of consciousness)
  • HELLP syndrome (haemolysis, Elevated Liver enzymes, Low platlets)
  • Placental abruption
20
Q

What risk does it pose to the foetus? (3)

A
  • Placental abruption
  • Restriced growth
  • Premature brith
21
Q

How deep does remodelling usually go? What happens to this in PE -> causes?

A

Remodelling in decidual and myometrium
this is limited to decidual -> placental perfusion decreased -> ischaemia

22
Q

What is PlGF?

A

Placental growth factor
- Vascualr Endotheliam Growth Factor related
- Pro-angiogenic factor release in large amounts by placenta

23
Q

What is Flt1?

A

Soluble receptor for VEGF-like factors which binds soluble angiogenic factors to limit their bioavailability

24
Q

What happens between PLGF and Flt1 in PE?

A

Distressed Placenta ives off fLT1 > SO DECREASE IN READILY AVAILABLE PLGF AND VEGF (Vascular endothelial growth factor)

25
Q

What’s the only way PE can be resolved?

A

By delivery of the placenta

26
Q

What 2 ways can we detect PE with?

A
  • PLGF alone
  • Flt1/PLGF
27
Q

What is given for management of PE? (2)

A
  • Antihypertensive treatments
  • Corticosteroids for <34 weeks to promote foetal lung development before delivery
28
Q

What are the 3 main ways of preventing PE?

A
  • Weight loss (esp if BMI>35)
  • Exercise throughout pregnancy (seems to work independent of BMI)
  • Low dose aspirin (from 11-14 weeks) for high risk groups- but may only prevent early onset
29
Q

What are the long term impacts of PE on maternal health? (2)

A
  • Elevated risk of cardiovascular disease, T2DM and renal disease after PE
    • Roughly 1/8 risk of having preeclampsia in next pregnancy (greater if early onset)
30
Q

What are the 2 subtypes of PE?

A
  • Early Onset <34
  • Late onset >34
31
Q

What else is thought to contribute to PE?

A

Extracellular Vesicles:
Vesicles containing microRNAs can cause local changes . These were observed as decrease of placental, increase in endothelial and overall increase

32
Q

MoA of EVs in PE

A

Placental ischaemia causes trophoblast apoptosis and EV release. These cause endothelial dysfunction, inflam, hypercoag. They inhbit vasodilation and eNOS

33
Q

Pathology of later onset PE

A

existing maternal genetic pre-disposition to CVD which manifests during the stress of pregnancy

34
Q

Define Small Gestational Age

A

fetal weight: <10th centile

Severe SGA: 3 centile or less

35
Q

Reasons for SGA

A

-> Small throughout pregnancy

→ Early growth normal but slows later (FGR/IUGR)

→ Non-placental growth restriction (genetic, metabolic)

36
Q

IUGR? sym vs asym (5)

A

IUGR is a clinical definition with fetuses with malnutrition despite what they are born with.

  • Sym:
    • earlier gestation → everything shrinks (20/30%)
    • Genetic disorder
    • cell no reduced but size is normal
    • difference in head/chest → more equal
  • Asym:
    • later on in gestation
    • placental disorder
    • head normal but adbominal abnormal
    • cell no normal, cell size shrinks (because cell size increases growth later on)
    • length and head cirumference normal (brain Sparing Growth)
37
Q

Complications of IUGR: (3)

A
  • CV: fetal cardiac hypertrophy
    • Resp: poor maturation of lungs
    • Nuero: motor defects

Dev ad Ageing BRS2 (3 decks)

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