Lecture 14: The placenta and support of pregnancy Flashcards

1
Q

When does the placenta begin to develop?

A

2nd week of development
-in early development there is focus on ensuring development of the ‘fetal membranes’: sacs that support the embryo/fetus and the placenta
(there can’t be a healthy pregnancy without a healthy placenta)

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2
Q

What parts of the embryo develop into the fetal membranes?

A

Outer cell mass: syncytiotrophoblast (goes onto make hCG, maintains corpus luteum) and cytotrophoblast

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3
Q

When does implantation begin?

A

Blastocyst and endometrium merge
Day 6: syncytiotrophoblastic cells move into endometrium
Day 9: blastocoele has moved entirely into the endometrial layer

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4
Q

What happens to the embryonic spaces in early embryonic development?

A

-yolk sac disappears (some forms part of the primordial gut)
-amniotic sac enlarges
-chorionic sac is occupied by the expanding amniotic sac
(amniotic membrane and chorionic membrane then fuse and join forming the amniochorionic membrane- this membrane breaks in labour releasing the amniotic fluid)

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5
Q

What does implantation achieve?

A

-establish the basic unit of exchange
(villi structures establish units of exchange)
-anchor the placenta
-establish maternal blood flow within the placenta

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6
Q

What happens to the placental membrane as the needs of the fetus increase?

A

The placental membrane gets progressively thinner, as metabolism of the fetus increases (optimal movement of nutrients in and waste out)

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7
Q

Do the fetal and maternal blood ever mix?

A

No

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

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8
Q

What is a chorionic villus?

A
The placenta is a sepcialisation of the chorionic membrane
Finger like projections:
-high surface area to volume ratio
-thin
-capillary like networks at end of villi
=good for exchange
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9
Q

What are some implantation defects?

A
Implantation in the wrong place
-ectopic pregnancy (peritoneal/ovarian)
-placenta praevia (implantation in the lower uterine segment)
Incomplete invasion
-placental insufficiency
-pre-eclampsia
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10
Q

What is the decidua?

A

The endometrium is transforms into this in the presence of a conceptus
-the decidual reaction provides the balancing force for the invasive force of the trophoblast (enzymes released): so depth of implantation is just right

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11
Q

What is wrong with the decidua in an ectopic pregnancy?

A

In an ectopic pregnancy there is NO DECIDUA (in the fallopian tube), therefore no control, so the trophoblast works it way into the peritoneal region, which can damage blood vessels= haemorrhage

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12
Q

What happens where the decidual reaction is sub-optimal?

A

Leads to a range of adverse pregnancy outcomes, where the pregnancy is not maintained, or preeclampsia occurs

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13
Q

What can lead to preeclampsia?

A

Shallow implantation of the trophoblast into the endometrium

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14
Q

What is the morphology of the placenta which attaches to the mother?

A

-cobblestone appearance
-can see cotyledons (functional units which contain the chorionic villi)
(you want to ensure all the cotyledons are removed when you give birth to the child)

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15
Q

What is the structure of the chorionic villus?

A

-arteries and veins run in them forming arteriocapillary venous network

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16
Q

How does the barrier of the chorionic villus change along the trimesters?

A

First trimester: thick barrier (cytotrophoblast and syncytiotrophoblast) betwen the maternal and fetal blood, as metabolic requirements of baby aren’t as great
Third trimester: barrier at optimal thinness, to meet energy requirement for much larger fetus (loss of syncytiotrophoblastic layer, and thinning of the cytotrophoblastic layer)

(you also get marginalisation of the fetal capillaries so they meet right up close to the villus surface)

17
Q

What are the umbilical cord vessels?

A

2 umbilical arteries: take deoxygenated blood from fetus to placenta
1 umbilical vein: taking oxygenated blood from placenta to fetus

18
Q

What is the maternal circulation in the placenta?

A

Endometrial veins and arteries- cotyledons are bathed in this blood
-high flow rate of blood (for diffusion and active transport)
(these also help to anchor the villi)

19
Q

What are the hormones produced by the placenta?

A

Steroid hormones: progesterone and oestrogen (at the end of the first trimester, the placenta will take over from the corpus luteum)
Protein hormones: hCG

20
Q

What is hCG?

A

Human Chorionic Gonadotrophin
-produced during the first 2 months of pregnancy
-produced by the syncytiotrophoblast so is pregnancy specific
(excreted in maternal urine, can also be detected in serum in blood, so therefore used as basis for pregnancy testing)

21
Q

Whatis the function of hCG?

A

Supports the secretory function of the corpus luteum

22
Q

What is a marker for trophoblastic disease?

A

High levels of hCG

  • choriocarcinoma
  • molar pregnancy
23
Q

What is the purpose of placental steroid hormones?

A

Progesterone and oestrogen are responsible for maintaining the pregnant state

  • placental production takes over from the corpus luteum by the 11th week
  • progesterone also increases appetite and releases energy from maternal fat stores
24
Q

What is hCS?

A

Human chorionic somatomammotrophin (placental
hormone)
-increases glucose availability to fetus

25
Q

What are the transport functions of the placenta?

A

Simple diffusion (molecules moving down a conc gradient)
-water
-electrolytes
-urea and uric acid
-gases: gas exchange (flow limited, not diffusion limited)
(rapid good, blood flow and thin membrane for good diffusion)

Facilitated diffusion
-applies to glucose transport (important for fetal brain which has a high energy requirement)

26
Q

Why do you need an adequate uteroplacental circulation?

A

Fetal oxygen stores are small therefore maintenence of adequate flow is essential (often fetus is in marginally hypoxic state)
-contractions in birth can limit uteroplacental circulation, causing loss of fetal oxygen= stress on baby in delivery

27
Q

What active transport occurs at the uterplacental barrier?

A

Specific transporters are expressed by the syncytiotrophoblast

  • AA’s
  • iron
  • vitamins
28
Q

What is the transfer of passive immunity?

A
  • receptor mediated endocytosis pathway, maturing as pregnancy progresses
  • fetal immune system is immature
  • IgG antibodies cross only (IgG concentrations in fetal plasma exceed those in maternal circulation)
29
Q

What is a teratogen?

A

Anything that can disturb the fetal/embryonic developmental process
-teratogens can access the fetus via the placenta as the placenta is not a true barrier (can be physiological: rhesus incompatibility causing RBC destruction)

30
Q

What are some harmful substances to the placenta?

A
  • thalidomide (originally prescribed to prevent morning sickness): limb defects
  • alcohol: fetal alcohol syndrome, alcohol related neurological delay
  • theraputic drugs: anti-epileptic drugs, warfarin, ACEI
  • drugs of abuse (dependency in fetus and newborn)
  • maternal smoking
31
Q

What are the periods of susceptibility to teratogenesis?

A

Pre-embryonic: lethal effects
Embryonic: ++sensitive
Fetal: +/-sensitive
After the embryonic period risk of structural defects are low, expect CNS