Implantation, the Placenta and Hormonal Changes in Pregnancy Flashcards

1
Q

What do we need for implantation to occur in regards to the blastocyst?

A

A fully developed blastocyst
- Fully expanded
- Hatched out from the zona pellucida
A blastocyst is an embryo at the stage ready for implantation 5 days after fertilisation
By then it would have developed the embryoblast which gives rise to the foetus
The trophoblast cells give rise to the placenta
The blastocoel is the fluid filling inside

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2
Q

What do we need for implantation to occur in regards to the uterus?

A

A receptive endometrium
- Thickened endometrial lining.
- Expression of embryo receptivity markers.
A fully developed blastocyst will be able to interact with the embryo receptivity markers

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3
Q

How do we get from a fertilised egg to a blastocyst ready for implantation?

A

At day 2 all the cells are identical in the organism called a blastomere but by day 5 cells are differentiating
The zona pelucida starts to get thinner as the blastocyst forms
You would also see a series of expansions and contractions before the blastocyst stays in its expanded state
The reason for this is because at the abembryonic pole you start to have digestive enzymes that start to digest the zona to assist with the hatching process
The blastocyst senses that and starts to undergo a series of expansions and contractions to be able to herniate out of the area being digested
Somehow it knows not to digest the region on the other side, the embryonic pole
Once hatched, its ready for implantation

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4
Q

What are the stages of implantation?

A
  1. Apposition- the positioning of the blastocyst close to the endometrium
    1. Attachment- blastocyst attaches to the endometrium
    2. Invasion- blastocyst borrows into the endometrium to implant itself
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5
Q

Give an implantation timeline from day 7 to day 12.

A
  • Blastocyst attaches itself to the surface of the endometrial wall (decidua basalis).
    • Trophoblast cells start to assemble to form a Syncytiotrophoblast, a version of a syncytium which is a fusion of multiple cells to form a multinucleated cell mass, in order facilitate invasion of the decidua basalis.
    • It is a continuous syncytium because as trophoblast cells die off more are being added to it
      Day 9-11:
    • Syncytiotrophoblast further invades the decidua basalis and by Day 11 its almost completely buried in the decidua.
      Day 12:
    • Decidual reaction occurs.
    • This is a remodelling of the cells of the endometrium in response to the invading blastocyst driven by progesterone
    • High levels of progesterone result in the enlargement and coating of the decidual cells in glycogen and lipid-rich fluid.
    • This fluid is taken up by the Syncytiotrophoblast and helps to sustain the blastocyst early on before the placenta is formed.
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6
Q

What happens around day 14 of the implantation timeline?

A

Around Day 14:
- Cells of the Syncytiotrophoblast start to protrude out to form tree-like structures known as Primary Villi, which are then formed all around the blastocyst.
- Primary villi are differentiated from the trophoblast
- Decidual cells between the primary villi begin to clear out, leaving behind spaces known as Lacunae.
- These spaces are initially filled with uterine secretions
- Maternal arteries and veins start to grow into the decidua basalis.
- These blood vessels merge with the lacunae – arteries filling the lacunae with oxygenated blood and the veins returning deoxygenated blood into the maternal circulation.
- Blood-filled lacunae merge into a single large pool of blood connected to multiple arteries and veins.
- This single large pool is known as the Junctional Zone, the circulatory foundation for the placenta
This is the point of end of the implantation stage

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7
Q

How is placenta formed?

A

Around day 17, foetal mesoderm cells start to form blood vessels within the villi – a basic network of arteries, veins and capillaries.
Capillaries connect with blood vessels in the umbilical cord (formed around week 5).
Villi grows larger in size, develops into the Chorionic Frondosum.
At this point, endothelial cell wall and Syncytiotrophoblast (villi) lining separate maternal and foetal red blood cells.

In the 4TH & 5TH months of pregnancy, decidual septa form as they divide the placenta into 15-20 regions known as Cotyledons.
Numerous maternal spiral arteries supply blood to each cotyledon, facilitating the maternal-foetal exchange.

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8
Q

What is the placenta’s role in maternalfoetal exchange?

A
Within the umbilical cord you will usually have two arteries and one vein
Through the placenta the foetus takes up:
Nutrition- O2 and glucose
Immunoglobulins
Hormones
Toxins (in some cases)
And it drops off:
CO2
Waste products
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9
Q

What are the functions of the placenta and how is it suited for them?

A

Provision of maternal O2, CHO, fats, amino acids, vitamins, minerals, antibodies.
A site of metabolism e.g. synthesis of glycogen from the maternal substrates
Barrier e.g. bacteria, viruses, drugs etc.
Removal of foetal waste products e.g. CO2, urea, NH4, minerals.
Endocrine secretion e.g. hCG, oestrogens, progesterone, HPL, cortisol.

Why is the placenta good at it’s job?

- Huge maternal uterine blood supply – blood is coming in at low pressure allowing for an efficient filtration system
- Huge surface area in contact with maternal blood
- Huge reserve in function.
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10
Q

What is pre-eclampsia?

A

3-4% of pregnancies.
≥20 weeks gestation (up to 6 weeks after delivery).
Results in placental insufficiency – inadequate maternal blood flow to the placenta during pregnancy.
Causes new onset maternal hypertension and proteinuria.
Symptoms range from mild to life-threatening.
Primary cause is still unclear.
Characterised by the narrowing of the maternal spiral arteries supplying blood to the placenta.

Preeclampsia affects other organ systems:
Reduced blood flow to kidney -> Glomerular damage › Proteinuria

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11
Q

What are the risk factors of pre-eclampsia?

A
RISK FACTORS:
	- First pregnancy
	- Multiple gestation
	- Maternal age >35yo
	- Hypertension
	- Diabetes
	- Obesity
	- Family history of pre-eclampsia
Pre-eclampsia + seizures = Eclampsia.
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12
Q

What is placental abruption?

A

Premature separation of all or part of the placenta
Symptoms include vaginal bleeding and pain in the back and abdomen
Caused by the degeneration of maternal arteries supplying blood to the placenta.
Degenerated vessels rupture causing haemorrhage and separation of the placenta.

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13
Q

What are the risk factors of placental abruption?

A
Blunt force trauma e.g. car crash, fall
Smoking & recreational drug use – due to risk of vasoconstriction and increased blood pressure. 
Multiple gestation
Maternal age >35yo
Previous placental abruption
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14
Q

What are the maternal and foetal complications of placental abruption?

A

COMPLICATIONS – MATERNAL:
Hypovolemic shock- not enough circulating blood from haemorrhaging
Sheehan Syndrome (Perinatal Pituitary Necrosis)- from lack of blood to brain particularly the pituitary, seen as loss of secondary sexual characteristics e.g. loss of axillary and pubic hair and shrinking of breasts
Renal failure
Disseminated Intravascular Coagulation (from release of thromboplastin)- leads in formation of blood clots
COMPLICATIONS – FOETAL:
Intrauterine hypoxia and asphyxia
Premature birth

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15
Q

What is placenta previa?

A
PLACENTA PREVIA (meaning placenta first):
Placenta implants in lower uterus, fully or partially covering the internal cervical is.
Associated with increased chances of pre-term birth and foetal hypoxia.
Cause still unclear.
	- Endometrium in the upper uterus not well vascularised so placenta moves to more vascularised lower uterus
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16
Q

What are the risk factors of placenta previa?

A
RISK FACTORS:
Previous caesarean delivery- following uterine surgeries those areas are expected to be less vascularised
Previous uterine/endometrial surgery- "
Uterine fibroids- "
Previous placenta previa 
Smoking & recreational drug use
Multiple gestation
Maternal age >35yo
17
Q

What are the hormonal changes in pregnancy at the beginning?

A

So we know implantation has occurred
Cells from the foetal placenta produce hCG
Because hCG had LH properties it can bind to the LH receptors on the corpus luteum, resulting in the production of oestrogen and progesterone
These are produced in a low oestrogen to progesterone ratio, so oestrogen at a much lower quantity than progesterone
This ration is necessary for maintaining a pregnancy

18
Q

How do hormone levels change from week 7?

A

At week 7 the placenta takes over so hCG levels drop but oestrogen and progesterone continue to be produced by the placenta
You also see an increase around that time in human placental lactogen (hPL) which counteracts the effects of maternal insulin so that there is enough glucose for both mother and foetus
The production of hPL is also the reason for gestational diabetes

19
Q

How are steroids converted between the mother, placenta and foetus?

A

It all starts with cholesterol and LDL making its way to the placenta from the mother
You have the establishment of a cholesterol reserve in the placenta
Cholesterol is converted to pregnenolone and then progesterone which is then secreted back to the mother
Oestrogens are synthesised via conversion from foetal adrenal androgens so in the adrenal gland of the foetus you have DHEA and DHEA-S being produced and then via a series of steroidogenic conversions, these are converted to the oestrogens; estrone, oestradiol and estriol
These are secreted back to the mother
hPL is synthesised by the syncytiotrophoblast cells and secreted back to the mother