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Repro > Week 8.0 - Placenta > Flashcards

Week 8.0 - Placenta Flashcards

1
Q

When does the placenta begin to appear and how?

A
  • 2nd week

- Differentiation of outer cell mass into syncytiotrophoblast and cytotrophoblast

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2
Q

Which section of the placenta mediates implantation?

A

-Syncytiotrophoblast

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3
Q

What happens to the embryonic spaces in the developing embryo?

A
  • Yolk sac disappears

- Amniotic sac enlarges to fill the chorionic cavity and the two layers fuse together making the amniochorion

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4
Q

What happens to the chorionic villi during development of the placenta?

A

-Initially cover the entire outer surface of the chorion but eventually only present on the developed placenta and the chorion becomes smooth

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5
Q

Why is implantation described as interstitial?

A

-The uterine epithelium is breached and the conceptus becomes implanted within the stroma -> interstitial

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6
Q

Why is it important that the placental membrane become progressively thinner as the fetus enlarges?

A

-The needs of the fetus increase and diffusion across the membrane needs to be rapid

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7
Q

What is meant by the placenta being haemomonochorial?

A

-One layer of trophoblast separates maternal blood from capillary fetal wall

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8
Q

What are the aims of implantation?

A
  • Establish a basic unit of exchange between mother and fetus
  • Anchor the placenta
  • Establish maternal blood flow within the placenta
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9
Q

Describe the development of the placental villi

A
  • Primary villi -> cytotrophoblast cells project through syncytiotrophoblast
  • Secondary villi -> gastrulation occurs and the trophoblast villi become invaded by a mesenchyme core and expand to touch the lacunae
  • Tertiary villi -> Mesenchyme core develops into arteries, veins and supporting tissues which connect with embryonic vessels and from here on products pass across this placental barrier
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10
Q

What is meant by the change of the placenta from histiocytic to haemocytic?

A

-Change from simple diffusion to blood

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11
Q

What is an ectopic pregnancy? Why is it so dangerous?

A
  • Implantation of the embryo at a site other than uterine body, commonly the fallopian tube but can be in the peritoneum or ovary
  • Dangerous as there are no decidual cells to control invasion and complex network of vessels nearby are therefore all at risk of erosion as it can penetrate through the wall
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12
Q

What is placenta previa? What effect does it have on delivery? Why is it dangerous?

A
  • Implantation occurs low on the uterine wall in such a way that as the placenta grows it obstructs the growth canal
  • Highly vascularised structure growing across an opening -> risk of haemorrhage
  • Requires C-section as birth canal occluded
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13
Q

What are pre-decidual cells?

A

-Cells which are produced during the uterine cycle which become decidual cells upon pregnancy. These cells become an intransic part of the placenta and control the extent of invasion during implantation

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14
Q

What 2 major changes happen in the endometrium during the uterine cycle?

A
  • Pre-decidual cells develop

- Elaboration of arterial blood supply -> spiral arteries

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15
Q

What is decidualisation?

A

-The incorporation of decidual cells into the placenta to act as a control for invasion

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16
Q

In response to which hormone does decidualisaion occur?

A

-Progesterone

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17
Q

What is the function of the decidual cells within the placenta?

A
  • Control implantation

- Prevent the mothers immune system from attacking the fetus

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18
Q

What is the cause of excessive implantation within the endometrium?

A

-Faulty decidual cells -> can lead to placenta accreta (villus invasion of the myometrium

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19
Q

What is meant by the elaboration of the arterial supply in the maternal endometrium during the uterine cycle?

A

-The arteries spiralise in order ro develop a rich vascular supply

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20
Q

What is meant by remodelling of the spiral arteries? How does this help establish a sufficient uteroplacental circulation?

A

-The maternal endothelial lining of spiral arterioles is invaded by the cells of the cytotrophoblast layer at its opening. The invasion causes destruction of smooth muscle and replacement of some of the endothelium. This creates a low resistance vascular bed to maintain high blood flow

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21
Q

What is pre-eclampsia?

A
  • Implantation defect where there is inadequate modification of spiral vessel walls-> endothelial lining remains-> vascular bed is not sufficient to maintain high flow needed during pregnancy -> maternal circulation tries to compensate to drive placental transport
  • Spectrum
22
Q

Name 3 different ways you can get monozygotic twins and the effects on the placenta/amnion

A
  • Zygote spilts are morula stage producing two morulas, to blastocytes, two separate implantation sites, two placentas
  • Zygote splits at inner cell mass producing one placenta, two amnions but a shared chorion
  • Apprearance of a second primative streak -> one placenta, one amniotic sac
23
Q

What is a placental cotyledon?

A

-Separations of the decidua basalis by the placental septae which has a main stem of chorionic villus and its branches and capillaries (the cotyledon is surrounded by maternal blood and this is where diffusion takes place)

24
Q

How is the maternal blood supply established within the syncytiotrophoblast?

A
  • lytic activity of the syncytiotrophoblast
  • maternal capillaries are eroded and anastomose with the trophoblast lacunae, forming the sinusoids.
  • At the end of the pregnancy the lacunae communicate with each other and form a single, connected system that is delimited by the syncytiotrophoblast and is termed the intervillous space.
25
Q

What constitutes the placental barrier in the first trimester?

A
  • Fetal vessel endothelium
  • Loose connective tissue which surrounds the endothelium
  • Cytotrophoblast
  • Syncytiotrophoblast
26
Q

How does the cytotrophoblast layer around the fetus develop?

A

-The cytotrophoblast cells of the villus expand further until a cytotrophicblastic layer exists between the syncytiotrophoblast and the uterine endometrium

27
Q

During transition from a first trimester placenta to a term placenta, what happens to the cytotrophoblast layer? Why is this significant?

A
  • Cytotrophoblast cells reduce in number in the villus wall but remain in the cytotrophoblast layer
  • Reducing the cytotrophoblast cells in the tertiary villi decreases the diffusion distance of the placental barrier
28
Q

What is the relationship between the spiral arteris, the lacunae and the placental villi?

A

-The placental villi project into the lacunae of the syncytiotrophoblast. The lacunae are supplied by the spiral arterioles, which are continuously pulled into the lacunae and modified to allow high blood flow into the placenta

29
Q

What are the two zones of decidua basalis?

A
  • Zona compacta

- Zona spongiosa

30
Q

Why is it that in early embryonic development placental development takes precedence?

A

-Placenta is important for establishment and maintenance of the pregnancy

31
Q

What is the difference between a first trimester placenta and a term placenta?

A
  • First trimester has thick placental barrier and cytotrophoblast layer within the villi
  • term placenta has thin placental barrier with hardly any trophoblast cells in villus
32
Q

What constitutes the placental barrier in a term placenta?

A
  • arterial and venous capillary endothelium pushed upto syncytiotrophoblast
  • few cytotrophoblast cells
  • Thin syncytiotrophoblast layer
33
Q

What is meant by thinning of the placental barrier during placental development?

A

-Loss of undifferentiated mesoderm and cytotrophoblastic cells from tertiary villi

34
Q

What constitutes the umbilical cord?

A

-Two umbilical arteries wrapped around an umbilical vein

35
Q

Regarding metabolism, what are the 3 main things that the placenta synthesises?

A
  • Glycogen
  • Cholesterol
  • Fatty acids
36
Q

Regarding the endocrine function of the placenta, what hormones are produced?

A
  • Progesterone
  • Oestrogen
  • human chorionic gonadotrophin
  • human chorionic somatomammotrophim
  • human chorionic thyrotrophin
  • human chorionic corticotrophin
  • human placantal lactogen
37
Q

What is hCG an analogue of? what is its function?

A
  • LH
  • Support the corpus luteum until the placenta is well enough established to produced sufficient progesterone and oestrogen (11th week)
38
Q

What is the function of progesterone and oestrogen produced by the placenta?

A
  • Control the HPG axis to prevent further follicular development
  • Maintain the pregnant state
39
Q

For how long is hCG produced?

A

-for approximately 4 months (highest in first 2-3 months)

40
Q

Where is hCG produced?

A

-syncytoitrophoblast

41
Q

What is a hydrotidiform mole (molar pregnancy)?

A

-Pregnancy where there is no fetal tissue as conceptus is only outer cell mass

42
Q

What is a choriocarcinoma?

A

-Malignancy of the chorion which produces hcg so is used as a marker

43
Q

Which hormones influence maternal metabolism?

A
  • Progesterone increases appetite

- hCS/hPL increase glucose availability to fetus (even at expense of mother)

44
Q

Which molecules move across the placenta by:

i) simple diffusion
ii) Facilitated diffusion
iii) active transport?

A

i) water, electrolyes, urea, gases
ii) glucose
iii) amino acids, irons and vitamins

45
Q

Why do you have to take care regarding fetal oxygen during delivery?

A

-Fetal O2 stores are small therefore maintainance of placental flow is essential
(compression of cord by contractions)

46
Q

What is passive immunity?

A
  • Fetal immune system is immature but gains immunity by IgG crossing the placenta into the fetal circulation by a receptor-mediated process
  • Wanes over time as fetal immune system develops
47
Q

What is a teratogen?

A

-Molecule which crosses placental barrier and interrupts fetal development eg drugs, poisons, CO, viruses

48
Q

Why is alcohol a teratogen?

A

-Small and easily diffusible across placenta interrupting pharyngeal pouch and CNS development

49
Q

What is haemolytic disease of the newborn?

A
  • Rhesus blood group incompatibility between mother and fetus
  • Occurs when rh -ve mother has been exposed to blood from a previous rh +ve baby
  • Rh antibody created, passes across placenta and attacks baby
  • Not common due to prophylaxis
50
Q

Name 3 viruses which can cross the placenta

A
  • Zika virus
  • Rubella
  • CMV

Repro (24 decks)

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