Pregnancy, Parturition and late foetal Dev + disorders

Question 1

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

Answer 1

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

Question 2

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

Answer 2

There is significant increase in rate of foetal growth + haemotrophic

Question 3

What is spiral artery remodelling?

Answer 3

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

Question 4

How does the remodelling work?

Answer 4

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.

Question 5

Failed conversion (spiral artery)

Answer 5

immune cells become embedded and RBCs occlude vessels

Question 6

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

Answer 6

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

Question 7

How is oxygen exchanged in the placenta?

Answer 7

diffusion

Question 8

How is glucose exchanged in the placenta?

Answer 8

Facillitated diffusion

Question 9

How is water exchanged in the placenta?

Answer 9

diffusion + hydrostatic gradients

Question 10

How is calcium exchanged in the placenta?

Answer 10

active transport

Question 11

4 ways the mothers circulation changes throughout pregnancy?

Answer 11

• incraesed ventilation
• increased cardiac output
• increased blood volume
• decreased resistance

Question 12

2 major things failed spiral artery remodelling causes?

Answer 12

• hyperplasia
• atherosis ( poor placentation)

Question 13

3 increased risks of Failed SAR

Answer 13

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

Question 14

Atherosis?

Answer 14

occurs in basal arteries that havent been remodelled

Question 15

What is Preeclampsia? How is it diagnosed

Answer 15

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

Question 16

Symmptoms of preeclampsia? (4)

Answer 16

• Odema
• Headache
• Seizures
• Abdo pain

Question 17

Severe cases of preeclampsia symptoms (3)

Answer 17

• Visual disturbances
• Breathlessness
• Risk of eclampsia (seizures)

Question 18

Risk factors? (7)

Answer 18

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

Question 19

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

Answer 19

• 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

Question 20

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

Answer 20

• Placental abruption
• Restriced growth
• Premature brith

Question 21

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

Answer 21

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

Question 22

What is PlGF?

Answer 22

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

Question 23

What is Flt1?

Answer 23

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

Question 24

What happens between PLGF and Flt1 in PE?

Answer 24

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

Question 25

What’s the only way PE can be resolved?

Answer 25

By delivery of the placenta

Question 26

What 2 ways can we detect PE with?

Answer 26

* PLGF alone * Flt1/PLGF

Question 27

What is given for management of PE? **(2)**

Answer 27

* Antihypertensive treatments * Corticosteroids for <34 weeks to promote foetal lung development before delivery

Question 28

What are the 3 main ways of preventing PE?

Answer 28

* 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

Question 29

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

Answer 29

- 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)

Question 30

What are the 2 subtypes of PE?

Answer 30

* Early Onset <34 * Late onset >34

Question 31

What else is thought to contribute to PE?

Answer 31

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

Question 32

MoA of EVs in PE

Answer 32

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

Question 33

Pathology of later onset PE

Answer 33

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

Question 34

Define Small Gestational Age

Answer 34

fetal weight: <10th centile Severe SGA: 3 centile or less

Question 35

Reasons for SGA

Answer 35

-> Small throughout pregnancy → Early growth normal but slows later (FGR/IUGR) → Non-placental growth restriction (genetic, metabolic)

Question 36

IUGR? sym vs asym (5)

Answer 36

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)

Question 37

Complications of IUGR: (3)

Answer 37

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