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human development > implantation and placental function > Flashcards

implantation and placental function Flashcards

1
Q

where does fertilisation take place?

A

oviduct

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2
Q

where does implantation take place?

A

lumen of the uterus

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3
Q

when it reaches the uterus, how does the embryo communicate with the mother?

A

placentation

maternal recognition of pregnancy

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4
Q

what is placentation and why is it required?

A

establishes physical and nutritional contact – required for a supply of nutrients leading to growth

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5
Q

what is maternal recognition of pregnancy and why is it required?

A

signals its presence to mother – required to prevent luteal regression. In humans, this molecule is done by hCG.

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6
Q

what are the stages in implantation and placental development?

A

first differentation step
apposition
adhesion
invasion

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7
Q

what happens in the first differentiation step?

A

6 days after fertilisation, cells of blastocyst differentiate into trophectoderm (outer cell layer) and inner cell mass

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8
Q

what does the trophoectoderm differentiate into?

A

placenta

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9
Q

what does the inner cell mass of the trophoblast differentiate into?

A

fetus

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10
Q

when does apposition happen?

A

6-7 days after fertilisation

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11
Q

what happens during apposition?

A

Positioning of the blastocyst within the uterine cavity - must face the right way

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12
Q

what happens during adhesion?

A

• Cells of the trophoblast fix to maternal tissues and to each other

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13
Q

how does adhesion occur?

A

Done via a group of cell adhesion molecules (including laminin and fibronectin) together with cell surface receptors for these molecules

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14
Q

when the trophoectoderm attaches to the uterine wall, how does it differentiate?

A

differentiates into 2 types of cells - cytotrophoblast and syncytiotrophoblast

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15
Q

describe cytotrophoblasts?

A

have single nucleus and divide rapidly in vivo

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16
Q

describe syncytiotrophoblasts?

A

o Syncytiotrophoblasts are derived from fused cytotrophoblasts

Multinucleated cell which doesn’t divide in vivo

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17
Q

what happens during invasion?

A

Trophoblast penetrates into maternal decidua (pregnancy endometrium) and endometrial spiral arteries via proteolytic processes

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18
Q

how do trophoblasts reach the maternal spiral arteries?

A
  • Trophoblasts form villous structures
  • Cytotrophoblasts break through trophoblast shell
  • Invade through decidual tissue
  • Trophoblasts reach maternal spiral arteries
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19
Q

what happens when trophoblasts reach the maternal spiral arteries and why?

A

• Spiral arteries are converted from narrow to wide vessels  allows a much greater flow of maternal blood around the villi

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20
Q

what is the barrier between maternal and fetal circulation?

A

villous trophoblasts

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21
Q

why is it important that the embryo is in a hypoxic environment?

A

oxygen tension gradient is present

O2 tension increases towards the maternal side.

Invasion is partly regulated by this gradient

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22
Q

what molecules are involved in successful implantation and what do they do?

A
  • Cyclooxygenase-2 (COX-2) - converts AA to PGE2 promotes invasion and decidualisation
  • Heparin-binding epidermal growth factor (HB-EGF) - involved in attachment and invasion
  • Vascular endothelial growth factor (VEGF) - involved in angiogenesis
  • Human leukocyte antigen-G (HLA-G) - inhibits antigen-specific lymphocyte response & decreases NK cell function
  • Indoleamine 2,3-dioxygenase (IDO) - regulated by IFNs to promote anti-proliferative effects
  • Transforming growth factor β (TGFβ) - regulates invasion and proliferation
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23
Q

if fertilisation and implantation occur, why dont progesterone levels fall?

A
  • Corpus luteum does not degenerate because of hCG.
  • Progesterone levels don’t fall bc progesterone secretion is maintained by corpus luteum (oestrogen levels do not fall either)
  • Progesterone maintains the endometrium and becomes the decidua
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24
Q

when does the luteal:placental shift occur?

A

at 12 weeks

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25
Q

what is the luteal:placental shift?

A

Progesterone goes from being made by the corpus luteum to being made by the placenta

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26
Q

what happens if the placenta and corpus luteum levels of progesterone dont match up?

A

miscarriage can occur

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27
Q

what is an ectopic pregnancy?

A

pregnancies which implant in the oviduct of the fallopian tube

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28
Q

what is the risk if an ectopic pregnancy occurs in the uterine lumen?

A

placenta previa

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29
Q

what is placenta previa?

A

placenta lies low in the uterus and partially/completely covers the cervix

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30
Q

what complications can occur in placenta previa?

A

haemorrhage can occur during labour –> puts mother and baby’s life in risk

31
Q

how should the baby be delivered in placenta previa?

A

caesarean

32
Q

describe the structure of the mature placenta

A
  • discoid shape - diameter of 15-20cm
  • weighs approx 500g and 2.5cm thickness
  • found in the upper uterine segment
  • anterior or posterior
  • fetal and maternal surface
33
Q

describe the fetal surface of the placenta

A

o Smooth, glistening covered in amnion

o Umbilical cord inserted in the centre with vessels radiating from it

34
Q

describe the maternal surface of the placenta

A

o Dull, greyish and divided into 15-20 cotyledons (lobes)

o Each cotyledon is formed of branches of one main villus stem covered by the decidua basalis

35
Q

what is the decidua?

A

uterus endometrium that forms in preparation for pregnancy

36
Q

what are the three layers of the decidua and where are they found?

A 
decidua basalis (layer below the implantation site)
decidua capsularis (encapsulates the growing fetus)
decidua parietalis (all the remaining uterine mucosa)
37
Q

describe the fetal circulation of the placenta

A
  • 2 x umbilical arteries from baby to the placenta to carry away waste and CO2
  • 1x Vein takes oxygen and nutrients to the baby
  • Smaller branches to chorionic villi
38
Q

what is the main site of exchange in the placentaa?

A

capillary networks in terminal branches of chorionic villi

39
Q

describe the maternal circulation of the placenta

A
  • 80 - 100 spiral arteries open directly into the intervillous spaces
  • Low pressure blood (10mmHg in the relaxed uterus)
  • Villi bathed in maternal blood (exchanged 3-4 x/min)
  • Return via venous pathways in decidual plate of placenta
40
Q

why is the placenta necessary?

A
  • Fetus requires nutrition

* Luteal regression needs to be prevented

41
Q

what are the functions of the placenta?

A
  • Site for exchange of gases (02 and C02) and other molecules between maternal and fetal blood
  • Nutrient exchange
  • Waste exchange – urea, bilirubin etc.
  • Synthesis of proteins, hormones and enzymes
42
Q

how do O2 and CO2 cross the placenta?

A

simple diffusion

43
Q

how does fetal haemoglobin compare to adult haemoglobin?

A

has greater affinity and carrying capacity

44
Q

what does the rate of diffusion across the placenta depend on?

A

o maternal/fetal gases gradient
o maternal and fetal blood flow
o placental permeability
o placental surface area

45
Q

what substances cross the placenta and how?

A
  • H20 and electrolytes - simple diffusion
  • Glucose - facilitated diffusion via glucose transporter proteins (GLUTs)
  • Amino acids - active transport via transporter proteins (accumulative or exchangers)
  • Fatty acids – simple diffusion
  • Large proteins and cells – pinocytosis
  • Waste products, eg urea – simple diffusion
46
Q

what non-nutrients with the placenta allow to pass through?

A
  • IgG antibodies
  • hormones
  • antibiotics
  • sedatives
  • some viruses, eg rubella
  • some organisms, eg treponema pallida (syphilis)
47
Q

what molecules wont the placenta allow through?

A

large molecules e.g. heparin and insulin

48
Q

what fetal cells can cross the placenta?

A 
o	Trophoblast cells
o	Granulocytes
o	Gametocytes
o	Lymphocytes
o	Nucleated red blood cells
o	Primitive counterparts
49
Q

what is rhesus factor?

A

protein found on the surface of your RBCs

50
Q

what do Rh+ and Rh- mean?

A

o Rh positive – your blood cells have the protein

o Rh negative – you lack the protein

51
Q

what happens if there is Rh incompatability between the mother and baby? (mother is - and baby is +)

A
  • Small amount of baby’s blood can come into contact with maternal blood and cause mother to produce Rh antibodies
  • In the second pregnancy if the baby is Rh positive, antibodies from the mother will cross the placenta and destroy the fetal RBCs
52
Q

what treatment is given in Rh incompatability?

A

Anti-D immunoglobulin can be given to remove any fetus Rh+

53
Q

what type of hormones does the placenta make?

A

protein and steroid hormones

54
Q

when does synthesis of hCG begin?

A

before implantation

55
Q

what does hCG do?

A

maintains corpus luteum –> progesterone and oestrogen secretion during early pregnancy

56
Q

what does human placental lactogen (hPL) do?

A 
o increases free fatty acids by its lipolytic action
o inhibits gluconeogenesis
o it promotes fetal growth
o it promotes mammary duct proliferation
o exhibits lactogenic effects
o resembles GH
57
Q

how does the placenta produce oestrogen and progesterone?

A

Placenta produces progesterone and oestrogen from cholesterol precursors and in concert with the fetal adrenal gland

58
Q

what is the human placental growth hormone needed for?

A

o Similar to growth hormone

o Regulation of maternal blood glucose levels to ensure adequate fetal glucose supply

59
Q

what do insulin like growth factors do?

A

o Similar structure to insulin

oStimulates proliferation and differentiation of the cytotrophoblast

60
Q

what produces relaxin and what does it do?

A

o Produced by decidual cells

o Softens the cervix and pelvic ligaments in preparation for childbirth

61
Q

why is the fetus not rejected by the maternal immune system?

A

1) HLA expression - Trophoblast cells express HLA G which isn’t recognised by ‘host’ immune system so Cells not rejected
2) Infiltrating leucocytes secrete IL-2 which regulates the immune system
3) Decidual reaction - decidual cells become swollen and compact around developing fetus so there’s a barrier between the mother and the implanting embryo

62
Q

what pathologies are associated with abnormal placental development?

A
  • Pre-eclampsia
  • Intrauterine growth restriction
  • Early miscarriage
63
Q

what placental complication can occur with placental completeness?

A

retained placental tissue associated with haemorrhage and infection after birth.

64
Q

what complications can arise from the size of the placenta?

A
  • less than 2.5 cm: intrauterine growth retardation of the fetus.
  • More than 4cm: association with maternal diabetes mellitus
65
Q

what colour should the maternal surface of the placenta be in a term infant?

A

dark maroon

66
Q

what colour should the maternal surface of the placenta be in a premature infant?

A

light maroon

67
Q

what does paleness of the maternal surface of the placenta indicate?

A

presence of fetal anaemia  sign of haemorrhage

68
Q

what do clots on the maternal surface of the placenta indicate?

A

shows placental abruption

69
Q

what does a thick ring of membrane on the placenta show?

A

prematurity and prenatal bleeding

70
Q

how does a true cord knot occur?

A

occurs when fetus passes through a loop of the umbilical cord (usually in early pregnancy)

71
Q

when and how does a cord knot cause compromise?

A

sufficient tension on the cord before or during delivery/labour then blood flow may be cut off and signs of fetal asphyxia may occur

72
Q

what happens if the umbilical cord only has 1 artery and 1 vein?

A

fetal anomaly rate is nearly 50%

73
Q

what cord complications can occur?

A

cord knots
cord vessels
thromboses

human development (20 decks)

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