Placental Physiology Flashcards

1
Q

What is the meaning of placenta in latin?

A

Flat cake!

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2
Q

Explain the umbilical vessels.

A

2 umbilical arteries takes waste and CO2 from the baby.

Umbilical vein - delivers O2, nutrients and hormones to the baby. Larger as less vascular tone, therefore less constricted.

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3
Q

Explain the fetal placenta components.

A

Syncytiotrophoblast (epithelial covering of villi, secretes progesterone, hCG and hPL).
Villous cytotrophoblasts.
Extravillous cytotrophoblast columns.
Endovascular trophoblast.

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4
Q

Explain the maternal placenta components.

A
Amnion (closest to fetus)
Chorion
Maternal blood in Sprial arteries (invaded by endovasular trophoblasts).
Endometrium
Myometrium
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5
Q

What are trophoblasts?

A

Placental epithelial cells which form the syncytiotrophoblast which is the site of nutrient transfer.

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6
Q

What happens when the blastocyst attaches to the trophoblasts?

A

Forms migrating columns and invades the endometrium to reach maternal vessles.

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7
Q

When and what do trophoblasts differentiate?

A
7 days.
To cytotrophoblasts (stem cell layer) and syncytiotrophoblasts (multinucleated and fused).
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8
Q

What does the synctiotrphoblasts form?

A

basis primary villi stems - framework for chorionic villi/outer layer.

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9
Q

Cytotrophoblats?

A

Colums that extend through the syncytiotrophoblasts.

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10
Q

Explain the shape of the human placenta.

A

It develops over the whole chorion then regresses to form the discoid placenta.

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11
Q

Explain the maternal endometrium at 6 weeks of gestation.

A

5-6nm, highly active glands…produce cytokines to stimulate placenta growth.
Glandular epithelium is stimulated by progesterone from the corpus luteum.

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12
Q

Why is there a 4 weeks delay before the placenta is fully functioning?

A

Because the baby needs to develop in hypoxic conditions 1st.

YES GOD!

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13
Q

Oxidative stress in normal pregnancies?

A

Yes, in the peripheral regions allows villous regression and formation of smooth chorion laeve. (No villi left by ~4 months).

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14
Q

Explain plugging of spiral arteries.

A

In early pregnancy the volume of the endovascular trophoblasts is such that it plugs the mouth of the spiral arteries preventing blood flow from mother to placenta.

Allows histiotrophic nutrition.

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15
Q

What changes to unplug the spiral arteries?

A

Loss of SM and elastic tissue from arterial walls as far as the inner 1/3 of the myometrium. This is mediated by invading trophoblasts from the placenta.

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16
Q

What are 4 functions of the placenta?

A

Hormones synthesis.
Respiratory organ.
Nutrient transfer.
Excretion of fetal waste products.

17
Q

Explain respiratory gas transfer.

A
pO2.
Maternal uterine artery = 95mmHg.
Intervillous space - pool of maternal blood. Localisation?
Fetal umbilical vein = 32 mmHg.
To heart, 02 extracted.
Fetal umbilical artery = 24mmHg.
Intervillous space and due to localisation...
Maternal uterine vein = 42 mmHg.

The foetus is relatively hypoxic.

18
Q

Explain the function of the syncytiotrophoblast.

A

Site of nutrient transfer.
CO2 - conc gradient.
AA - ATP dependent, AA specific, conc specific.
Glucose - Na+ dependent GLUT-1 transporters in the second half of the pregnancy.

19
Q

Explain glucose homoeostasis especially insulin.

A

The fetus can synthesise insulin from 9=11 weeks.
Fetal insulin is dependent on glucose metabolism.
Excess glucose - excessive fat deposition.
Inadequeate glucose - emaciation (bonyness/extreme leanness).

Glucose has to transfered across placenta as foetus has little capacity for gluconeogenesis - as the necessary enzymes don’t function at low pO2.

20
Q

Explain fatty acid transport.

Maternal to foetal.

A

Long chain PUFA are preferred.
Passive diffusion of membrane carrier proteins.
To the fetal circulation where it binds to alpha fetal protein…
…to the liver where it is re-esterified.
…re-enter the circulation with lipoproteins (mainly as TG).

21
Q

Billirubin?

A

Excreted after a long process between mother and foetus.

22
Q

Explain the production of hormones in the foetal, placental and maternal circulation.

A

Placenta - cholestrol to pregnenelone (to foetal) to progesterone (to maternal).

Foetal - pregnenolone to DHEA to DHEA sulphate to 16(OH)DHEA to (placental) 16-OH-DHEA to oestriol.

Maternal DHEA - placental DHEA to androstenedione to oestrone (to maternal) to oestradiol (to maternal).

23
Q

Role of oestrogens?

A

CV adaptations - remodel BVs.
Growth of uterus.
Priming of uterus for labour.
Weak anti-insulin activity (via increased cortisol)
Onset of labour (relative increase vs progesterone)
Cervical ripening.

24
Q

Role of progesterone.

A

Prepares and maintains endometrium to allow implantation.
From CL then from placenta.
Suppress immune response to fetal antigens.
Partuition
Substrate for adrenal gland production of glucocoriticoids and minerocorticoids.
Growht of mamillary glands.
Maintain pregnancy.
inhibit uterine contractions.
Prevent cervical ripening.
Induce overbreathing and decrease maternal CO2

25
Q

hCG?

A

Human chorionic gonadotropin.
Pregnancy test - ELISA of hCG.
Rescue and maintain function of CL
Stimulate maternal thyroid activity (binds TSH receptor and LH-hCR receptor).

26
Q

hPL?

A

Human Placental Lactogen.
Maternal lipolysis and increase maternal FFAs…energy for maternal metabolism and fetal nutrition.
Increase maternal insulin - favour protein synthesis - metabolise AA and glucose for the foetus.
Potent angiogenic hormone - formation of foetal vasculateur.

27
Q

CRH?

A
Corticotrophin releasing hormones.
Immunosuprresant.
Induce myometrial contractions.
Initiate patruition.
PG formation in placental, amnion and chorion.
Placental clock?
28
Q

Leptin.

A

From corticotrophoblast and syncytiotrophoblast.
Maternal levels are high cf non pregnant women/fetal circulation.
Stimulate AA and FA transport.
Fetal leptin levels correlate to birth weight.
Important role in growth and development.