Implantation Flashcards

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1
Q

what do we need for implantation to occur?

A

A fully developed blastocyst and a receptive endometrium.

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2
Q

Describe the structure of the blastocyst

A

The blastocyst is made up of two lineages:

  • Trophoblasts (form the placenta) and Embryoblast/ inner cell mass (forms the foetus).
  • Blastocoel is a fluid filled cavity inside the blastocyst.
  • The embryoblast is concentrated at the ‘embryonic pole’ while the opposite pole is known as the ‘abembryonic pole’ (trophoblast concentrated).
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3
Q

what must occur with the blastocyst and the endometrium for implantation to occur?

A
  • The blastocyst must be fully expanded and hatched out from the ZP.
  • The endometrium must show a thickened endometrial lining and exhibit the expression of embryo receptivity markers.
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4
Q

briefly go over the stages of embryo development

A

The blastocyst bathes in uterine fluid and begins to hatch at the end of day 5. After full blastocyst expansion the ZP becomes thinner and enzymes that dissolve ZP at the abembryonic pole and a series of rhythmic expansions achieve hatching and contractions, which enable the blastocyst, herniate and bulge out of ZP.

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5
Q

what are the 3 stages of implantation?

A

1) Apposition – positioning of blastocyst close to endometrium surface.
2) Attachment – blastocyst attaching to the endometrium.
3) Invasion – trophoblast starts to grow, divide and multiply and invade endometrium until submerged.

  • Implantation normally takes place in the upper uterus. The endometrium is not necessary for initial implantation stages (i.e. ectopic pregnancy – implantation disorders – recurrent miscarriage).
  • The junctional zone is the circulatory foundation for the formation of the placenta.
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6
Q

Describe days 7-8, days 9-11 and day 12 of implantation

A

days 7-8: Blastocyst attaches itself to the surface of the endometrial wall (decidua basalis). Trophoblast cells start to assemble to form a syncytiotrophoblast in order to facilitate invasion of the decidua basalis.

Days 9-11: Syncytiotrophoblast further invades the decidua basalis and by day 11 its almost completely buried in the decidua.

Day 12: Decidual reaction occurs. 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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7
Q

what happens on day 14 of implantation?

A

Cells of the syncytiotrophoblast start to protude out to form tree-like structures known as primary Villi, which are then formed all around the blastocyst.

Decidual cells between the primary villi begin to clear out, leaving behind empty spaces known as lacunae.

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 is known as the junctional zone

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8
Q

who creates the placenta?

A
  • The placenta is co-created by the mother and foetus, with contributions from endometrial as well as embryonic cells/tissue.
  • It is typically formed in the upper uterus.
  • On an ultrasound, chorionic cavity shows up as a large dark space. It is used to identify a pregnancy even before a foetus can be seen.
  • The lining of the villi (also acts as a barrier) and the endothelial cell wall is separating the maternal and foetal blood vessels.
  • The umbilical cord contains two arteries and one vein.
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9
Q

what happens on day 17?

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.

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10
Q

what are the function of the placenta?

A
  • Provision of maternal oxygen, CHO, fats, amino acids, vitamins, minerals and antibodies.
  • Metabolism e.g. synthesis of glycogen.
  • Barrier to bacteria, viruses and drugs etc.
  • Removal of foetal waste products like carbon dioxide, urea, ammonia and minerals.
  • Endocrine secretions e.g. hCG, oestrogens, progesterone, HPL and cortisol.

Placenta functions as a barrier to toxins and drugs etc but it not safe all the time i.e. some things make its way through

The placenta is adapted to carry out its function as it has a huge maternal uterine blood supply which operates at low pressure, a huge surface area in contact with maternal blood and a huge reserve in function.

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11
Q

name disorders of the placenta

A

Placental insufficiency
Pre-eclampsia
Placental abruption
placenta previa

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12
Q

Describe placental insufficiency

A

inadequate maternal blood flow to the placenta during pregnancy. This in turn compromises the transfer of necessary nutrients to support the development of the foetus. Pre-eclampsia usually occurs after around twenty weeks gestation. However, it could still develop after delivery (up to six weeks after).

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13
Q

Describe pre-eclampsia

A
  • 3-4% of pregnancies
  • happens at around 20 weeks gestation (or more)–> can occur even 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.
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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14
Q

what is the cause of pre-eclampsia and what is it characterised by?

A

Primary cause is still unclear.

Characterised by the narrowing of the maternal spiral arteries supplying blood to the placenta.

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15
Q

describe placental abruption

A

premature separation of all or part of the placenta. Symptoms include vaginal bleeding and pain in the back and abdomen.

Risk factors:

  • blunt force trauma e.g. car crash, fall
  • smoking and recreational drug use- risk of vasoconstriction and increased blood pressure
  • multiple gestation
  • maternal age more than 35 yo
  • previous placental abruption
  • hypertension from severe pre-eclampsia
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16
Q

what causes placental abruption?

A

Caused by the degeneration of maternal arteries supplying blood to the placenta.

Degenerated vessels rupture causing haemorrhage and separation of the placenta.

17
Q

what are the maternal complications that arise from placental abruption?

what about the foetal complications that arise from placental abruption?

A

Maternal complications: Hypovolemic shock, Sheehan Syndrome (Perinatal Pituitary Necrosis), Renal failure and Disseminated Intravascular Coagulation (from release of thromboplastin).

•The mothers pituitary will degenerate due to not enough blood supply so it will undergo necrosis and it wont function properly thus symptoms such as irregularities in the menstrual cycle, small breasts and loss of hair can be seen.

Foetal complications: Intrauterine hypoxia and asphyxia and premature birth.

18
Q

describe placenta previa

A

Overgrowth of placental cells on to the uterus (hydatiform mole).

  • placenta implants in lower uterus, fully or partially covering the internal cervical os.
  • associated with increased chances of pre-term birth and foetal hypoxia
  • causes still unclear- maybe the endometrium in the upper uterus is not well vascularised?

Risk factors:

  • previous caesarean delivery
  • previous uterine/endometrial surgery
  • uterine fibroids
  • previous placenta previa
  • smoking and recreational drug use
  • multiple gestation
  • maternal age >35 yo
19
Q

Describe the hormonal changes in pregnancy

A
  • The continued presence of the low oestrogen: progesterone ratio supresses’ maturation of other follicles in the ovary.
  • BhCG can be detected in the bloodstream as early as day nine and is the basis of urinary pregnancy tests (qualitative).
  • Serum BhCG (quantitative) is useful for monitoring early pregnancy complications e.g. ectopic pregnancy and miscarriage.
  • Serum hCG hits peak levels by nine to eleven weeks.
  • The placenta takes over around week seven where it synthesises oestrogens from foetal androgens from the foetal adrenal cortex. It also synthesises progesterone from maternal cholesterol.
20
Q
  • Movement between foetal, placenta and mother and vice versa
  • Progesterone: have a reserve of cholesterol (and LDLs that package it) in placenta that makes its way from mother (and foetus if needed)
  • Progesterone secreted from the steroidogenic pathway (pregnenolone–> progesterone secreted from placenta).
  • Adrenal androgens before remodelling are secreting DHEA and DHEAS–> make their way from foetus into placenta= go through a series of steroidogenic pathways to form oestrogens (secreted during pregnancy when placenta is taken over)
  • HPL: secreted in mitochondria of syncytiotrophoblast cells–> synthesised and secreted directly through the mother as well.
A

• Oestrogen and progesterone work alongside other hormones to trigger the physiological changes observed during pregnancy as seen in the above diagram.