Implantation, placentas and hormonal changes in pregnancy Flashcards

1
Q

What is the trophoblast?

A
  • Cells of the blastocyst that invade the endo and myometrium (days 5-6).
  • Also secrete hCG
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2
Q

What is the chorion?

A

The layer that becomes the placenta

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3
Q

What is the amnion?

A

The layer that becomes the amniotic sac

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4
Q

Give a brief process of implantation

A
  • Start with fertilised oocyte
  • Divides into 2,4, then 8 cells
  • Then becomes a morula, which will undergo a lot of reorganisation
  • A blastocoele cavity will form and the inner cell mass orientates itself in the blastocyst
  • These are very tightly regulated events with critical timings - if something goes wrong it can lead to misccarriage
  • Blastocyst then hatches as it enters the uterus and implants - it loses the ZP and it will begin the next stage of implantation
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5
Q

How and why does the menstrual cycle change the endometrium?

A
  • In order to implant you have to have a receptive endometrium so that the blastocyst can implant
  • During the follicular phase, the oestrogen levels gradually rise, causing proliferation of the endometrium
  • After ovulation (caused by the LH surge), the Luteal phase starts
  • The CL releases lots of progesterone, which causes the endometrium to differentiate into a secretory lining, ready for implantation of the foetus.
  • If there is no fertilisation, the CL will die after 14 days, meaning that there is no P produced, causing the endometrium to shed as mensies.
  • If there is fertilisation, the foetus will produce hCG, which will rescue the CL, and continue the Progesterone production.
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6
Q

What are the main stages of implantation and placentation?

A
  • Differentiation of the trophoblast
  • Trophoblastic invasion of the decidua and myometrium
  • Remodelling of the maternal vasculature in the utero-placental circulation - If not pregnant, you will have spiral arteries in the endometrium (dont have huge vessels otherwise would bleed to death when menstruate). If pregnant, there will be remodelling of vasculature to allow oxygen/nutrients etc
  • development of vasculature within trophoblast - foetus has to develop its own vasculature
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7
Q

When does implantation occur?

A

Day 5-6

- A very tight window of implantation - 24-36hrs

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8
Q

What changes are there when implantation occurs?

A
  • trophoblast produces hCG = maternal recognition of pregnancy
  • Allows maintenance of the CL - P production
  • Without hCG from the viable embryo, you will shed the endometrium
  • Decidualisation under P
  • Vital until placental steroidgenesis is established
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9
Q

What is beta hCG?

A
  • Basis of urinary pregnancy tests - detects beta sub-unit of hormone
  • Uses a MoAb that will bind and produce a colour change
  • Maximal levels by 9-11 weeks (high for remainder)
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10
Q

How can b-hCG be used for monitoring?

A
  • Serum b-hCG useful for monitoring early pregnancy complications such as ectopic pregnancy
  • If nothing shows up on US scan, but there is hCG, you know that there is a trophoblast somewhere, just where it shouldn’t be.
  • If trophoblast tissue there, but no rise in hCG -> miscarriage
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11
Q

What are the functions of the placenta?

A
  • Steroidogenesis - oestrogens, P, HPL, cortisol
  • Provision of maternal oxygen, CHO, Fats, AAs, vitamins, minerals, Abs
  • Removal of CO2, urea, NH4, minerals
  • Barrier against bacteria, viruses, drugs etc
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12
Q

Why is the placenta good at its job?

A
  • Huge maternal uterine blood supply - low pressure (about 750ml/min)
  • Huge reserve in function
  • Huge SA in contact with maternal blood
  • Highly adapted ad efficient transfer system
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13
Q

What happens at 14-15 days?

A
  • Connective stalk will become umbilical cord
  • Little ball in the middle is the ICM - will grow to become the foetus
  • Outside layer has cytotrophoblastic cells (base layer of placenta), these columns will grow into the maternal decidua
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14
Q

How does the implantation develop over time?

A
  • Most successful pregnancies will implant in the upper part of the uterus around the fundus
  • It completely envelops, burrowing in and invades deeply into the maternal decidua
  • As it grows it will fill the uterine cavity
  • At term, you get a disc like structure of placenta
  • The chorion leavae will regress and become the amniotic sac with thin fibrous layer of regressed cells on top.
    Chorion frondosum will proliferate and grow into the folded structure
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15
Q

How do the villi develop?

A
  • Primary stem villi - folded structure of cells, layer of cytotrophoblasts will fuse to form syncytium - makes the bulk of the villi
  • Secondary stem villi - get a core network of foetal capillaries in amongst this
  • Tertiary stem villi - have a little arteriole feeding in, a network of capillaries, and a vein feeding out of the villus. Also have a layer of cytotrophoblast, and a thin layer of syncytiotrophoblast - this villus then sits in a pool of maternal blood.
  • By the 3rd trimester you get a lot more complex folding and an increase in SA to get as much nutrient transfer as possible.
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16
Q

What are the functions of the amniotic cavity?

A
  • Its the sac that the baby sits in - what ruptures when waters break
  • Homeostasis of temperature, fluid and ions
  • Vital for development of certain structures - limbs and lungs
  • Protection - physical barrier - ascending infection
17
Q

What are some disorders of the placenta?

A
  • Miscarriage - majority caused by chromosomal abnormalities (trisomy 9,11,16), causes rejection by the placenta. Repeated miscarriages caused by placental ‘recognition system’
  • Pre-eclampsia - mums get high BP and protein in pregnancy - may be due to the way the placenta implants
  • Hydatidiform mole - inherit too many copies of paternal chromosomes. End up with abnormally developed embryo and over-proliferation of placental tissue
  • Placental insufficiency - small babies, need early delivery
  • Transfer of drugs, toxins or infections
18
Q

What are some disorders of the amnion?

A
  • Polyhydramnios - excess of amniotic fluid - often problem with control mechanism of fluid. If have bowel atresia, the fluid doesnt pass normally through foetal bowel, get recycled or taken out by placenta, it just accumulates. Neuromuscular condition may also it because of inability to swall for example
  • Oligohydramnios - deficiency of amniotic fluid - baby’s kidney may be malformed
  • Premature rupture of membranes - normal at 34/35 weeks, but if happens early on it can be dangerous
19
Q

What are the 4 main categories of hormonal changes?

A
  • Placental steroids
  • maternal steroids
  • Foetal steroids
  • Placental peptide hormones
20
Q

Why do P levels change?

A
  • Placental steroidogenesis - active from 7-8 weeks
21
Q

What does the increase in P levels cause?

A
  • Decidualisation (CL)
  • Smooth muscle relaxation (uterine quiescence)
  • Mineralocorticoid antagonist - lower BP
  • Breast development
22
Q

What does the increase in oestrogen cause?

A
  • Uterine hypertrophy
  • Metabolic changes - insulin resistance
  • CVS changes
  • Breast development
23
Q

What are the changes in placental CRH and cortisol?

A
  • Both increase in 2nd trimester onwards
  • Cortisol causes metabolic changes (insulin resistance) and foetal lung maturity
  • CRH is probably involved in labour initiation
24
Q

What does human placental lactogen (HPL) do?

A
  • similar to GH
  • metabolic changes (insulin resistance) - placenta makes mum insulin resistance allowing lots of lipids and carbohydrates for foetus
  • Possibly some role in lactation
25
Q

What does prolactin do?

A
  • increases through pregnancy

- Breast development for lactation