7. Implantation and Placental Function Flashcards
Where does fertilisation and implantation take place?
On reaching the uterus the conceptus will ‘talk’ to the mother in what two ways?
What are the 4 key stages in implantation and placental development?
Describe stage 1.
Fertilisation: in oviduct. Impantation: uterus.
1) Placentation: establishes physical and nutritional contact
2) Maternal recognition of pregnancy: signals presence to mother to prevent luteal regression
First differentation step, apposition, adhesion, invasion.
6 days after fertilisation, blastocyst cells will have differentiated into the outer cell layer (trophoectoderm) and inner cell mass. The trophoectoderm will become the placenta and the inner cell mass the foetus.
Describe stage 2.
Describe stage 3.
How does the trophoblast differentiate at day 6-7?
Appostion: positioning of blastocyst within uterine cavity. Inner cell mass is the side that goes down onto endometrium (called decidua)
Adhesion: cells of trophoblast fix to maternal tissues and to each other via group of adhesion molecules, including laminin and fibronectin
Blastocyst attached to uterine wall. Trophoectoderm differentiates into cytotrophoblast (single nucleus, divides rapidly in vivo) and syncytiotrophoblast (derived from fused cytotrophoblasts, multinucleated cell, doesn’t divide in vivo).
Describe stage 4.
Describe placental formation.
What forms the barrier between maternal and foetal circulation?
Invasion: trophoblast penetrates into maternal decidua and endometrial spiral arteries via proteolytic proceses.
Trophoblasts form villous structures, cytotrophoblasts break through trophoblast shell and invade through decidual tissue to reach maternal spiral arteries. They are converted from narrow to wide vessels allowing greater maternal blood flow around villi.
Villious trophoblast
What drives the formation of spiral arteries?
What is spiral artery remodelling?
How many umbilical veins and arteries are there?
Hypoxic enviroment, oxygen tension gradient, O2 tension increases towards maternal side.
Reform spiral artery: big, wide open structure allowing blood to pool around villus. Trophoblasts replace SM and endothelium of spiral arteries.
2 umbilical arteries (carry deoxygenated blood -> placenta), 1 umbilical vein (carries oxygenated blood -> foetus)
In terms of hormones, what happens if fertilisation and implantation occur?
What is the luteal:placental shift? What happens if it goes wrong?
Corpus luteum does not degnerate b/c of hCG secreted by placenta. Progesterone levels do not fall b/c progesterone (and oestrogen) secretion maintained by corpus luteum. Progesterone maintains endometrium which becomes decidua.
hCG secreted by placenta early on, detected about 4w, shoots up, then down and maintained. As placenta matures and starts to produce its own progesterone, shift from corpus luteum to placentral progesterone at around 3m. Mismatch can occur here = endometrium breaks down and miscarriage.
What is an ectopic pregnancy?
What is placenta praevia?
What is the difference between the foetal and maternal placenta surfaces?
Implantation is not in lumen of uterus, most common in oviduct. As it grows it expands, causing massive bleeding. Lots of other possible sites but rarer.
Placenta forms across exit to uterus - woman will need C-section. Normally placenta on posterior wall (2/3) or anterior wall (1/3)
Foetal: smooth, glistening, covered in amnion, umbilical cord in centre with vessels radiating from it. Maternal: dull, greyish, divided to 15-20 cotyledons.
Label A-E.
a) placenta
b) myometrium
c) chorionic villi
d) chorion
e) amnion
What are the 3 different regions of decidua?
Describe foetal circulation in the mature placenta.
Describe maternal circulation in the mature placenta.
Decidua basalils: beneath implantation site. Decidua capsularis: layer covering developing embryo. Decidua parietalis: remaning endometrium. *don’t need to worry about…*
2 umbilical arteries (CO2 and waste) to the placenta, smaller branches to chorionic villi. Main site of exchange are capillary networks in terminal branches of chorionic villi. Vessels consolidate -> larger venous branches -> umbilical vein leaves placenta (O2, nutrients and hormones).
80-100 spiral arteries open directly into intervillous spaces, low blood pressure, villi bathed in maternal blood, return via venous pathways in decidual plate of placenta
Why is the placenta necessary?
How is gas exchanged across the placenta?
The placenta is a barrier but also allows what through?
Foetus requires nutrition. Placenta: site of gas and molecular exchange between maternal and foetal blood, nutrient (glucose, H2O, electrolytes, AAs, FAs, hormones, vitamins, minerals) and waste (CO2, urea, creatinine, billirubin, hormones) exchange, synthesis of proteins and enzymes. Luteal regression prevented.
Simple diffusion. HbF has more affinity and carrying capacity than adult Hb. Diffusion rate depends on maternal/foetal gas gradient and blood flow, placental permeability and placental SA.
IgG Abs, hormones, antibiotics, sedatives, some viruses e.g. rubella, some organisms e.g. treponema pallida (syphilis). It won’t let large molecules e.g. insulin through.
What foetal cells can cross the placenta?
Why are rhesus factors important in pregnancy?
Trophoblast cells, granulocytes, gametocytes, lymphocytes, primitive counterparts, nucleated RBC
If 1st pregnancy and mum R -ve and baby R +ve, mum is sensitised and makes antibody in response to R+ anrigen. If then have 2nd R+ pregnancy, Abs from mum pass to baby and destroy RBCs of baby. Now anti D given.
Describe the protein and steroid hormones that the placenta, an important endocrine organ, produces.
1) hCG: maintains corpus luteum -> progestrone and oestrogen secretion during early pregnancy. Resembles LH
2) hPL (human placental lactogen): promotes foetal growth and mammary duct proliferation, inhibits GNG, increases free FA by lipolytic action, exhibits lactogenic effects, resembles GH
3) Oestrogen and progesterone: from cholesterol precursors, by end of 1st trimester can produce enough and corpus luteum not needed
4) Human placental growth hormone: like GH, regulation of maternal blood gluocse levels
5) Insulin-like growth factors: stimulate proliferation and differentiation of cytotrophoblast
6) Relaxin: from decidual cells, softens cervix and pelvic ligaments for birth
7) Hypothalamic and pituitary-like hormones: e.g. GnRH, CRF
What factors regulate trophoblast invasion and spiral artery remodelling?
Why is the foetus not rejected by the maternal immune system?
What are some pathologies associated with abnormal placental development?
Growth factors, cytokines, matrix metalloproteinases, adhesion molecules
1) Trophoblasts express HLA G which is not recognised by ‘host’ immune system
2) Infiltrating leucocytes secrete IL-2 which regulates the immune system
3) Decidual reaction when decidual cells become swollen and tightly compacted together around foetus = barrier between mum and embryo
Pre-eclampsia, intrauterine growth restriction, early miscarriage
List some placental complications.
1) Placenta completeness: retained placental tissue associated with postpartum hemorrhage and infection
2) Placental size: <2.5cm = intrauterine growth retardation of foetus, >4cm = maternal diabetes mellitus, foetal hydrops and infections
3) Placental consistency and surfaces: maternal surface pallour = foetal anaemia. Thick membrane rings on foetal surface = circumvallate placenta -> prematurity/bleeding
4) Cord knots: may cut off blood supply to foetus during birth - asphyxia
5) Cord vessels: if only 1 artery and 1 vein
6) Thromboses
