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Phase 2: Reproduction, Nephrology and Urology > Lecture 4: Pregnancy and Pre-eclampsia > Flashcards

Lecture 4: Pregnancy and Pre-eclampsia Flashcards

1
Q

Describe the placenta?

A

A temporary organ that facilitates nutrient and gas exchange between maternal and foetus.

Brings the foetal/maternal circulations in close proximity allowing the exchange of gases, nutrients and waste.

Produces hormones e.g. human chorionic gonadotrophin (hCG) and oestrogen

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2
Q

What are the 2 sides of the placenta?

A

Chorionic plate

Basal plate

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3
Q

Describe the chorionic plate of the placenta?

A

The foetal side of the placenta

Umbilical cord is inserted in this side

Chorionic vessels are present on the surface of this side.

Covered in an avascular glossy amnion as a protection membrane.

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4
Q

Describe the basal plate of the placenta?

A

Maternal side of the lacenta

Basal surface is separated into lobes, known as cotyledons, that mark the positions of the underlying villous trees.

Comprised of: endometrial, trohoblast and fibrinoid.

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5
Q

Which layer in the blastocyst stage develops into the placenta?

A

A blastocyst is formed from the morula. It consists of a fluid filled cavity surrounded by a single layer of trophoblast cells. At one end of the blasocyst, there is a cell mass, known as the inner cell mass, that are the precursor of the embryo.

Trophoblast layer is the precursor of the placenta

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6
Q

Describe what happens during day 6-7?

A

Blastocyst attaches itself to the epithelial surface of the uterus

Trophoblast extensions penetrate between the uterine epithelial cells.

The embryo eventually becomes fully embedded by day 6-7.

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7
Q

Describe the changes in placenta development by day 9 of gestation?

A

Blastocyst is fully embedded into the uterus.

Trophoblast layer differentiates into: Cytotrophoblast and Syncytiotrophoblast.

Serious of fluid filled spaces known as lacunae begin to develop

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8
Q

Describe the cytotrophoblast?

A

Proliferating inner layer that continues to proliferate throughout pregnancy

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9
Q

Describe the syncytiotrophoblast?

A

Non-dividing outer layer

Multinucleated

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10
Q

Describe the lacunae?

A

Fluid filled spaces in the syncytiotrophoblast

Precursors of the intervillous space

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11
Q

Describe what happens during day 12 of placental development?

A

Maternal blood escapes from the spiral arteries

These pass into the lacunae before the mouths of the spiral arteries become blocked with extravillous trophoblast cells.

Important as it prevents maternal blood from entering the intervillous space

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12
Q

Describe spiral arteries?

A

Also known as coiled arteries

Supplies blood to the stratum functionalis of the uterus during the menstration cycle.

Become blocked by extravillous trophoblast cells. This causes the cells to remodel. Resulting in the vessels to become wider, high flow and low resistance

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13
Q

Because the placenta is not formed immediately, how does the foetus gain nutrients?

A

Particularly important in the 1st trimester (Weeks 1 -> 12)

Uterine gland secretions are the nutrient source for both the foetus and the placenta cells

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14
Q

Describe the next step in placenta development after the maternal blood passes into the lacunae?

A

Cytotrophoblast cells migrate, forming villous projections that extend towards the maternal basal plate.

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15
Q

What happens by the 3rd week of gestation, in relation to placenta development?

A

Tertiary villi have formed

Consist of:

An outer, monolayer of syncytiotrophoblast

Invaded by an inner layer of cytotrophoblast cells

Vascularised with fetal capillaries

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16
Q

Describe each step of placenta development?

A

Step 1:

Morula develops into a blastocyst

Consist of a single layer of trophoblast cells

Step 2:

Trophoblast extensions penetrate between uterine epithelial cells.

Blastocyst becomes embedded into the uterine wall

Step 3:

Trophoblast differentiate into:

Cytotrophoblast

Syncytiotrophoblast

Step 4:

Lacunae begin to develop in the syncytiotrophoblast

Step 5:

Maternal blood escapes from spiral arteries

Passes into the lacunae in the syncytiotrophoblast

Step 6:

Cytotrophoblast cells migrate forming villous projections that extend towards the maternal basal plate

Step 7:

Tertiary villi formation.

Outer monolayer of syncytiotrophoblast

Inner layer of cytotrophoblast cells

Vascularised with fetal capillaries

Step 8:

Subset of cytotrophoblast cells differentiate into extravillous trophoblast cells

These invade the maternal wall and remode lthe coiled vessels to become wider, high flow and low resistance channels.

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17
Q

Define the term villous tree?

A

Main structures of the placenta

Connects the foetal surface (chorionic plate) to the maternal surface (basal plate)

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18
Q

Define the term anchoring villi?

A

These are villi that become attached to the basal plate

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19
Q

What is the function of the tertiary villi of the villous tree?

A

The site of nutrient exchange

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20
Q

How many main stem villi are contained in the placenta?

A

60-70

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21
Q

Name the different parts of the villous tree?

A
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22
Q

Why are the tertiary villi a good site of nutrient exchange?

A

Because it has a large surface area.

Promotes good gas exchange

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23
Q

At term what separates the endothelium of the villous capillaries from the maternal circulation?

A

Syncytiotrophoblast

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24
Q

Describe the spiral/coiled arteries remodelling stage of placenta development?

A

Subset of cytotrophoblast cells differentiate into extravillous trophoblast cells

Extravillous trophoblast cells invade the maternal endometrium, myometrium and spiral arteries

The extravillous trophoblast cells remodel the spiral arteries by making them wider.

This causes the spiral arteries to change from:

Low flow + High resistance = High flow + Low resistance channels

This ensures sufficient blood flow to the foetus

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25
Q

At what point does the foetus receive nutrients from maternal vessels

A

End of week 13

The mouth of the spiral arteries are blocked with extravillous trophoblast cells creating a plug.

The extravillous trophoblast cells invades and remodel the vessels, from maternal endometrium to spiral arteries.

The plug is dissolved, allowing maternal blood to enter the intervillous spaces

Foetus now receives nutrients from mother.

26
Q

Define gestation?

A

Process of development between conception and birth

27
Q

Define pregnancy-induced hypertension?

A

Hypertension occuring in the 2nd half of pregnancy in the absence of proteinuria (protein in the uterine)

28
Q

Define proteinuria?

A

Presence of excess proteins in the urine.

29
Q

Define pre-eclampsia?

A

The new onset hypertension (systolic >140 or diastolic >90 mmHg) occurring after 20 weeks’ gestation with new proteinuria (excess protein in the urine) and associated with oedema (fluid retension)

30
Q

How do we distinguish between pregnancy-induced hypertension and pre-eclampsia?

A

PIH: usually associated with no proteinuria

Pre-eclampsia: proteinuira is present

31
Q

Define eclampsia?

A
  • Severe complication of preeclampsia.
  • The high blood pressure, associated with pre-eclampsia, results in fits or convulsions during pregnancy.
  • If severe, can cause maternal and/or fetal death
32
Q

When is the birth termed pre-term?

A

Delivery at < 37 weeks gestation

33
Q

Define Fetal growth restriction?

A

the failure of the fetus to reach its genetically predetermined growth potential

34
Q

What conditions is fetal growth restriction associated with?

A
  • Associated with abnormal umbilical artery blood flow
  • Associated with pre-eclampsia and other complications of pregnancy
35
Q

Fetal growth restriction increase the risk of ___

A

Stillbirth

36
Q

PE classically defined as new onset hypertension after what week of gestation?

A

After week 20

37
Q

What is the typical presentation of pre-eclampsia?

A

New onset hypertension (systolic >140 or diastolic >90 mmHg) occurring after 20 weeks’ gestation with new proteinuria.

However, many present with atypical presentation that does not fit this threshold.

38
Q

What happens if pre-eclampsia is not diagnosised?

A

Left untreated may progress to eclampsia, a life-threatening condition characterised by convulsions

39
Q

Name some of the risk factors for pre-eclampsia?

A
  • Genes
  • The placenta
  • The immune response
  • Maternal vascular disease
40
Q

What is the treatment plan for pre-eclampsia?

A

No cure- the only cure would be to deliver the baby and placenta (placenta being the most important thing)

Management options only.

41
Q

What is the long-term effects of hypertensive disorders (during pregnancy) on a mother?

A

More likely to develop heart disease in later life

42
Q

Why is pre-eclampsia a major cause of preterm birth?

A

As the only cure is to deliver the baby and placenta.

Preterm birth to remove the risk

43
Q

Pre-eclampsia is unique to which animal?

A

Humans

44
Q

Why is the pathogenesis hard to understand in pre-eclampsia?

A

PE is unique to humans therefore no animal studies to investigate the pathogenesis

45
Q

What are the symptoms of pre-eclampsia?

A
  • Headaches
  • Blurred/flashing vision
  • Pain in upper right abdomen
  • Nausea/vomiting
  • Heartburn that doesn’t go away with antacids
  • Rapid oedema

Overall, severe and varied symptoms

46
Q

Which needs to be removed for the symptoms of pre-eclampsia to regress?

A

The removal of the placenta is necessary for symptoms to regress

47
Q

Name some of the risk factors for pre-eclampsia?

A
  • Maternal age >40
  • Primigravidae
  • Weight (BMI > 35)
  • Hereditary
    • Link in the family
  • Existing medical conditions e.g. renal disease, hypertension

However, having these risk does not mean you will have PE. The majority who have these risks do not develop PE.

48
Q

1 BMI unit rise is equivalent of which percentage rise in pre-eclampsia incidence?

A

~ 0.5% incidence

49
Q

Name the three step hypothesis for pre-eclampsia

A
  1. Abnormal placentation
  2. Abnormal maternal response to placental trigger
  3. Organ/systems failure
50
Q

Describe the pathophysiological mechanisms that underlie pre-eclampsia

A

Normally, during implantation, placental trophoblasts invade the uterus and induce the spiral arteries to remodel. This results in the physiological changes in the spiral arteries (from low flow high resistance to high flow low resistance arteries).

In PE, this invasion of trophoblasts is abnormal, resulting in an impairment in the remodelling of the spiral arteries. Due to the reduction in remodelling, the blood flow to the placenta is reduced, resulting in the placenta being likely to be deprived of oxygen. Subsequently causes increased release of free radicals and inflammatory mediators in the syncytiotrophoblast. Ultimately, there is a maternal response to placental dysfunction = exaggerated inflammatory response and endothelial dysfunction

51
Q

What is the epidemiology of pre-eclampsia?

A

Leading cause of maternal and neonatal mortality and morbidity affecting 3-8% of pregnancies worldwide

52
Q

If a patient is pregnant or planning pregnancy. How do we clinically manage her risk of pre-eclampsia?

A

Reducing the risk of hypertensive disorders before and during pregnancy

53
Q

Which test could help in determining patients with pre-eclampsia?

A
  • PlGF-based testing
  • Used to help diagnose suspected PE
  • Rule out test
    • Recommended to help rule-out PE
    • Not used to diagnosis (rule-in) PE
54
Q

When should women who have PE be clinical assessed?

A
  • Carry out a full clinical assessment at each antenatal appointment for women with PE
  • Offer admission to hospital for surveillance and any interventions needed if concerns for the wellbeing of woman or baby
  • Look out for concerning signs:
    • Sustained high blood pressure (>160 systolic)
    • Signs of impending eclampsi
55
Q

What are the treatments options for pre-eclampsia?

A

No cure, except birth when the placenta is removed.

Treatment is to treat the symptoms.

For the hypertension, labetalol is used (beta-blocker) or if thats not suitable nifedipine.

56
Q

How do we monitor the fetal development in pre-eclampsia?

A
  • Cardiotocography
    • Recording the fetal heartbeat
  • Ultrasound
    • Assessing fetal growth and amniotic fluid volume
  • Umbilical artery Doppler velocimetry
    • Recording the blood flow to the fetus

Repeated monitoring every 2 weeks

57
Q

What levels of amniotic fluid volume is associated with pre-eclampsia?

A

Low levels of amniotic fluid

58
Q

Approx. 1 in ___ risk of pre-eclampsia recurrence in future pregnancies

A

1 in 5

59
Q

In women who had pre-eclampsia in a previous pregnancy, the likelihood of pre-eclampsia recurrence increases with inter-pregnancy interval of which time course?

A

with inter-pregnancy interval >10yrs

60
Q

Define the term “Primigravidae”?

A

Refers to a mother a woman who is pregnant for the first time, first time with a new partner or first pregnancy in 10 years

Phase 2: Reproduction, Nephrology and Urology (25 decks)

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