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Skye's ESA 4 > Repro 8.1 the placenta > Flashcards

Repro 8.1 the placenta Flashcards

1
Q

Why does the placenta take precedence in the beginning of pregnancy?

A

The whole pregnancy relies on this, it needs to be fully formed and functional to substain the embryo.

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2
Q

Why is week 2 of embryonic development known as the week of 2s?

A

-2 distinct layers form

outer cell mass

  • cytotrophoblast
  • syncytiotrophoblast

inner cell mass

  • epiblast
  • hypoblast
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3
Q

What cavities are present in week 2?

the time of the bilaminar disc?

A

blastocyst cavity

amniotic cavity

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4
Q

Which embryonic space grows substantially at the beginning of pregnancy?

A

The amniotic cavity- it grows to surround the developping embryo.

It’s growth compromises the space of the chorionic cavity.

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5
Q

When does the yolk sac disappear?

A

When the GIT forms

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6
Q

What is found on the chorionic membrane?

A

Villi like structures which act to increase the surface area and help with the transport needed for the embryo.

Chorionic villi.

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7
Q

What happens during implantation of the embryo?

A
  • It is interstitial- happens within a tissue
  • the conceptus breaches the uterine epithelium and implants within the stroma.
  • invasiveness of the process can cause some blood loss which can be mistaken for a menstrual period.
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8
Q

What happens as the needs of the foetus increase?

A

The placental membrane become progressively thinner, reducing the barriers to diffusion.

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9
Q

What does the term ‘heamomonochorial’ mean?

A

There is only one layer of trophoblast separating the maternal blood from the foetal capillary wall.

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10
Q

What are the aims of implantation?

A
  • To establish a basic unit of exchange between the foetus and the mother (Villi)
  • The anchor the placenta within the endometrium
  • to estabilsh as maternal blood flow within the placenta.
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11
Q

What are the features of the:
Primary villi
Secondary villi
Tertiary villi?

A

primary- just projections of the trophoblast, so made only of cytotrophoblast and syncitiotrophoblast

Secondary- develop a mesenchyme core, some vessels begin to develop allowing exchange to begin

tertiary- fetal vessels fully developped, exchange happening.

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12
Q

What is placenta previa?

A

implantation in the lower uterine segment

Can lead to haemorrhage in pregnancy, and fetus must be delivered by C section (Growing over the internal Os of the cervix, so the birth canal is occluded.

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13
Q

What are pre-decidual cells?

A

Cells within the endometrium which control the implantation, making sure it;s not excessive or too little.

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14
Q

What’s the effect of having no decidual cells within the fallopian tubes?

A

If an ectopic pregnancy occurs there is no control over implantation, so it’s excessive and can easily lead to rupture of the fallopian tubes and haemorrhage.

This paired with the fact the tissue of the fallopian tubes is not suitable to grow an embryo makes it an innaprpriate site for implantation.

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15
Q

What are the spiral arteries?

A

They are formed during the menstrual cycle and develop during pregnancy.
They aim to make a high flow (to meet demands of fetus) whilst maintaining a low resistance vascular bed.

This is ideal for the exchange needed to maintain the foetus.

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16
Q

What normally happens to the spiral arteries during pregnancy?

A

Trophoblast invades the spiral arteries, so they become lined by foetal tissue, which reduces the resistance and increases transport.

Helps to maintain the high flow, low resistance blood supply.

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17
Q

In pre-ecclampsia, what happens to the spiral arteries?

A

They are not modified enough, remodelling doesnt happen, so not properly lined with trophoblast tissue (invasion is not enough).

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18
Q

What is the effect of excessive invasion of the spiral arteries?

A

myometrium invasion,

at parturition this will result in improper shearing of the placenta.

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19
Q

What can happen if there is incomplete invasion?

A
  • pre-eclampsia

- placental insufficiency (will lead to poor growth and development of the feotus)

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20
Q

In monozygotic twinning, the sharing of the membranes can vary, discuss different variations and the impact of this on survival.

A
  • two amnions, two chorions
  • two amnions but only one chorion
  • shared chorion and shared amnion

The more sharing of membranes the increased risk of mortality.

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21
Q

When you look at the gross placenta, what features do you see?

A
  • shiny looking due to amnion coverring
  • large vessels (umbilical vessels radiate from around the umbillicus)
  • umbilicus comes from the placenta and is also coverred by amnion
22
Q

Give some differences of the first trimester placenta and the term placenta.

A
  • first trimester placenta has a relatively thick barrier, whereas at term this has diminished to only syncytiotrophoblast and endothelium of foetal capillaries.
  • in the first trimester, the cytotrophoblast layer is present under the syncytiotrophoblast, whereas this is lost in the term placenta.
  • The term placenta has a much higher SA than the first trimester placenta due to more villi.
23
Q

What is the function of the umbilical vein?

A

To bring oxygenated blood from the placenta to the foetus.

24
Q

What is the function of the umbilical artery?

A

To take deoxygenated blood from the foetus to the placenta.

25
Q

How many umbilibal arterys and veins does one foetus have?

A

2 umbilical arteries

1 umbilical vein

26
Q

What functions does the placenta have?

A

Metabolism
Endocrine
Transport

27
Q

What metabolic function does the placenta have?

A

-production of fatty acids, cholesterol and glycogen.

28
Q

What is the significance of the placenta producing a lot of cholesterol?

A

It is the precursor for steroid hormones, and the placenta produces a lot of oestrogen and progesterone during pregnancy.

29
Q

What classes of hormones are produced by the placenta?

A
  • protein

- steroid

30
Q

Give examples of protein hormones produced by the placenta.

A
  • Human Chorionic gonadotrophin
  • Human chorionic somatomammotrophin
  • Human Chorionic thyrotrophin
  • Human chorionic corticotrophin.
31
Q

What is the function of hCG?

A

Helps to maintain the corpus leuteum in the first couple of months, to maintain progesterone production and keep the lining of the uterus from shedding.

This is what’s detected in pregnancy testing.

It is released and produced by the syncytiotrophoblast cells.

32
Q

What steroid hormones does the placenta produce?

A

Oestrogen

Progesterone

33
Q

What are examples of trophoblast disease?

A
  • Molar pregnancy

- Choriocarcinoma

34
Q

What is a molar pregnancy?

A

There is gross overgrowth of the placental tissue but no development of a foetus.

There will be high levels of hCG, so pregnancy tests will test positive but no foetus will grow.

35
Q

When does placental production of steroid hormones take over from the corpus luteum?

A

Around 11 weeks.

36
Q

What are the effects of placental hormones on maternal metabolism?

A

progesterone- increases appetite

-hCS/hPL increases glucose availbility to the foetus.

37
Q

What is hPL?

A

Human placental lactogen.

Another name for human chorionic somatomammotrophin.

breaks down maternal fats for the baby, and can lead to insulin and carbohydrate resistance for the mother.

38
Q

What forms of transport does the placenta use?

A
  • simple diffusion (Water, electrolytes, urea, gases)
  • facilitated diffusion (glucose transport)
  • active transport (amino acids, iron, vitamins)
39
Q

What is the gas exchange in the placenta limited by?

A

Flow, not diffusion.

40
Q

What are the foetal O2 stores like?

A

Minimal, therefore a maintained maternal-foetal circulation is essential.

41
Q

How does the feotus gain immunity?

A

Via passive immunity, the IgG of the mother can pass through the placenta and into the fetus.

It happens via receptor mediated endocytosis.

The fetus is likely to be contact with the same pathogens as the mother, so the mother lends some of her immunity.

42
Q

How doe IgG concentrations in the fetus and the mother differ?

A

They are higher in the foetus than in the mother.

43
Q

Discuss the steps involved in receptor mediated endocytosis of IgG.

A
  1. IgG receptor found over clathrin coated pit
  2. IgG bind and coaed pit invaginates
  3. Formation of a coated vesicle
  4. ATP used to uncoat the vesicle
  5. IgG and receptor transported to the endosome (pH has no effect on the receptor and IgG which remain coupled)
  6. IgG and receptor have to be physically cleaved apart.
  7. IgG released into fetal circulation.
44
Q

What else can cross the barrier apart from nutrients etc?

think pathology

A

Teratogens.

45
Q

Give examples of some teratogens.

A

Alcohol
Thalidomide
theraputic drugs
maternal smoking (harmful toxins)

46
Q

What is the rhesus blood group?

A

On top of having blood groups A, B, O etc, blood can also have an antigen known as the rhesus antigen (Rhesus positive) or not (rhesus negative).

47
Q

What is rhesus disease?

A

When the mother is rhesus negative but the fetus has inherited rhesus positive blood from the father.

The mother also has to have been sensitised to the resus positive antigen.

The mother will produce antibodies against the babys blood which can cause complications to the baby such as heart failure, jaundice, deaffness or even still birth.

48
Q

Why is rhesus disease now uncommon?

A

Women are screened for their blood group and the disease as part of antenatal testing.

If found to have rhesus disease the mother will be given prophylactic treatment.

49
Q

What infectious agents can cross the placenta and infect the embryo?

A
  • varicella zoster
  • treponema pallidum (syphillis)
  • rubella
50
Q

What are some of the effects of rubella syndrome infecting the child?

A
  • microcephaly
  • cateracts
  • PDA.

Skye's ESA 4 (48 decks)

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