Embryology 6 - Placenta and Membranes PDF

The embryo needs to establish a parasitic relationship with the mother for acquiring oxygen and nutrients and for eliminating wastes. The embryo must avoid being rejected as a foreign body. The placenta and the extraembryonic membrane have to mediate the communication with the mother The placenta a...

The embryo needs to establish a parasitic relationship with the mother for acquiring oxygen and nutrients and for eliminating wastes. The embryo must avoid being rejected as a foreign body. The placenta and the extraembryonic membrane have to mediate the communication with the mother The placenta and chorion originate from the trophoblast while the amnion, yolk sac, allantois and extraembryonic mesoderm originate from inner cell mass AMNIOTIC MEMBRANE and CAVITY (epiblast - ectoderm) —> during folding the amniotic sac covers the embryo completely Functions of the amniotic sac: Buffer against mechanical injury (liquid environment) Accommodates growth (the liquid increases while the embryo grows) Allows fetal movements (muscular development) Permits normal fetal respiratory movements (the fetus is not breathing, there are no gas exchanges but the lungs are moving as they will when the fetus will be born, he’s kind of practicing) Protects the fetus from adhesion to the wall of the chorionic cavity Acts as a barrier to infections as it has bacteriostatic properties Maintains a relative constant temperature Assists in maintaining homeostasis of fluids and electrolytes The amniotic membranes can be used for different things —> they can be used to cover wounds and burns (they have anti-inflammatory and anti-angiogenic properties so they allow a faster healing). They can be used in ophthalmic surgery too (to restore the cornea). In the amniotic membrane there are stem cells which are at the center of a field of research. Functions of the amniotic membrane: Contains a significant number of cytokines and essential GF Reduces pain when applied to a wound Increases and enhances the wound healing process Has antibacterial properties Is non-immunogenic (won’t be identified as foreign material) Provides a biological barrier Provides a matrix for migration and proliferation of cells Reduces inflammation Reduces scar tissue formation From the 11th week the amniotic fluid is mainly made up of the urine of the embryo. The fetus’ urine is different from ours —> It doesn’t contain wastes because those are secreted in the placenta. Lungs produce secretions that are released in the amniotic fluid as well. Before this, the amniotic fluid is made by diffusion of maternal plasma (from chorion to amniotic membrane). Up to the 20th week the skin is yet not keratinised (still water permeable) so the amniotic fluid is equal to the tissue fluid —> there is a bidirectional exchange between the AF and the fetal tissues. From the 11th week there is the addition of fetal urine and lung fluids (half a litre of fluid produced everyday). Towards the second trimester around 1L of fluid is made. Amniocentesis —> sampling of the amniotic fluid (usually done after the 15th week because there’s more fluid and so there are less chances of hurting the fetus). Used to detect chromosomalKaryotypeofthe fetus abnormalities, CNS abnormalities, omphalocele, duodenal or esophageal atresia (if the alpha fetoprotein is too high there are problems in conformation), fetal maturity (lectin-to-sphingomyelin ratio on plasma membranes) and Rn disease (erythroblastosis fetalis) In the third trimester there is a complete turnover of AF every three hours (500ml/h). The re absorption takes place throughout the amniochorionic membrane. Composition of the AF —> water, fetal epithelial cells, proteins, carbohydrates, hormones, enzymes, pigments, electrolytes, amino acids, lipids and fetal lungs fluids Disorders in amniotic fluid volume: Reduced amount of amniotic fluid —> oligohydramnions —> it can be caused by a diminished placental blood flow (placenta doesn’t receive enough blood), by a preterm rupture of the amniochorionic membrane (fusion between amniotic sac and chorion), by renal agenesis (kidneys don’t develop so there is no fetal urine added to the amniotic fluid) or by a urinary tract obstruction (same reason as renal agenesis). Fetal complications may involve pulmonary hypoplasia (because the fetus isn’t swallowing amniotic fluid and because it isn’t practicing respiratory movements), limb deformities and facial abnormalities (because the lack of amniotic fluid causes the restriction of movement + mechanical shock isn’t absorbed). Potter syndrome —> pulmonary hypoplasia + limb deformities + facial abnormalities. Caused by renal agenesis Increased amount of amniotic fluid —> polyhydramnions —> causes are unknown but there are some factors that may influence its development —> maternal factors: diabetes (or general difficulties in controlling body glucose, which then crosses the placental barrier and leads to fetal hyperglycaemia with polyuria), cardiac problems or infections. Fetal factors: oesophageal or duodenal atresia (not developed in the right way, the fetus can’t swallow the fluid so it accumulates in the placenta), anencephaly (non-developed brain, the fetus can’t swallow the amniotic fluid), infections or congenital diaphragmatic hernia. Polyhydramnions is often associated with defects of the caudal part of the neural tube (defects of the CNS) Complications of polyhydramnions: Preterm contraction of the uterine wall and possibly preterm labour Premature rupture of the amniochorionic membrane (sometimes followed by placental abruption) Fetal malposition  Maternal respiratory compromise (the diaphragm can work properly) Umbilical cord prolapse (it comes out of the uterine cavity into the uterine canal) Uterine atony (the uterus loses its tone) Postpartum haemorrhage (increased damaged due to the overall attachment of the placenta int he uterus) Fetal death Amniotic bands —> they are caused by a delamination of the amnion due to rupture or testing. The debris of the amniotic sac (band) floats in the amniotic fluid and eventually wraps around the body of the fetus. The band can constrict some parts of the body and lead to a malformation as the fetus grows The defected portion of the body has to be amputated YOLK SAC The yolk sac is lined internally by the endoderm and externally by a vascularised extraembryonic mesoderm. Initially the yolk sac is the major source of nutrition, but after a while it doesn’t serve that purpose anymore (replaced by mother). Histiotrophic nutrition —> absorption of nutrients through the tissue of the developing embryo by endocytosis (vitamins A, B12 and E + follic acid) vitelline During the folding of the embryo the vitelline sac is incorporated in the body of the embryo ad it gives rise to the primordial gut. The vitelline stalk or canal (communication between midgut and vitelline sac) is then formed and it is incorporated in the umbilical cord During the 3rd week undifferentiated mesodermal cells migrate to the wall of the vitelline sac and form blood islands. Extraembryonic hematopoiesis (and erythropoiesis) is performed up to 6th week in the yolk sac ALLANTOIS (endoderm) Protrusion (evagination) of the yolk sac into the body stalk. It is a vestigial organ in humans (eventually it degenerates as it is not useful). However the allantois is important because where it evaginates it triggers the formation of blood vessels. The umbilical circulatory arc is formed by arteries and veins that connect the embryo to the placenta (umbilical veins and arteries, then embedded in the umbilical cord) What remains of the Allantois that is not part of the umbilical cord will be connected with the cloaca of the intestinal tube and then it will become a ligament of the urinary bladder (urachus) UMBILICAL CORD It develops from the body stalk (initially attached to the caudal end of the embryonic disc) and the vitelline duct. It is located in the ventral surface of the curved (post folding) embryonic disc at the umbilical region The umbilical region initially is wider and then it becomes narrower as folding progresses and the vitelline duct and body stalk get closer (until they fuse together) Initial content of the umbilical cord —> body stalk (with Allantois and umbilical vessels) + vitelline duct (vitelline vessels) + extraembryonic coelom + intestinal loop (from 6 to 10 week) There is a time in which the intestine is outside of the embryo to develop, then it goes back inside the abdominal cavity. Umbilical cord at term —> 55-60cm and 2-2.5cm in diameter. It contains two arteries and one vein and it is surrounded by Wharton’s jelly. It is enclosed in the amnion if Zpatogies CHORION and PLACENTA They represent a cooperative effort between the extraembryonic tissues of the embryo (trophoblast) and the maternal endometrium (decidua) The placenta is formed by the cytotrophoblast + syncytiotrophoblast + extraembryonic mesoderm + villi + endometrium Chorionic plate —> region of mesoderm that is part of the chorion Formation of chorionic villi (very important for the formation of the placenta) —> they grow more on the side of the embryo (chorion frondosum, tertiary villi only form on this side) and less on the opposite side (chorion leave) network meson apiaries connected newsman vessels mesenangmae me p manoeuvre bananas useless between thesymatotronoven matneaecione nonrereeyrotropnobeest isinainecoconroat witnemeaecione The villi anchored to the cytotrophoblasic shell are called anchoring villi while the other ones are called floating villi (floating in the blood of the lacunae). Villi are what allow maternal blood to circulate Cytotrophoblast from anchoring villi invades spiral arteries —> the wall of the arteries is substituted by the cells of the cytotrophoblast and this allows a high volume flow at low pressure (lots of blood passes through but without a lot of pressure). Fetal blood has a lower concentration of oxygen but fetal haemoglobin has a higher affinity with oxygen Inadequate transformation of maternal vessels by cytotrophoblast cells leads to poor placental perfusion and underlies preeclampsia (hypertensive disorder) and certain intrauterine growth restriction of the fetus Excessive proliferation and invasion of cytotrophoblast in cells is a hallmark of gestational trophoblastic neoplasia and choriocarcinoma (malignant tumour deriving from the chorion) Blood enters the intervillous spaces (lacunae) from spiral arteries, it spurts against the chorionic plate and slows down. Bathing of villi: exchanges. Blood exits through the open ends of the uterine veins that also penetrate the cytotrophoblastic shell. In lacunae there’s both blood from arteries and from veins Intervillous spaces contain 150ml of blood and are replenished 3-4 times/minute. If the utero-placental circulation doesn’t develop properly fetal hypoxia and intrauterine growth restriction (IUGR, can also develop due to polyhydramnions) may occur. Placental barrier —> barrier in between the fetal blood and the maternal blood. Until the 5th month it is made by —> endothelium lining capillaries + cytotrophoblast + syncytiotrophoblast From the 5th month on the barrier becomes thinner —> syncytiotrophoblast + endothelium of capillaries. Cytotrophoblastic cells disappear Antibodies pass through the barrier to provide the fetus with passive immunity Infectious diseases (es: zika virus) can pass through the placenta and through the birth canal at delivery (es: herpes) TORCH —> most common organisms that can cross the placenta (toxoplasma gondii, other, rubella virus, cytomegalovirus (CMV), herpes simplex virus (HSV)) The placenta is also an endocrine organ —> the placenta produces hCG to maintain the corpus luteum functional. Then from the 2nd trimester the placenta starts producing estrogens and progesterone (alongside the corpus luteum in the ovary). By the 3rd trimester the corpus luteum ceases its production. The fetal adrenal glands has to cooperate in the production of hormones Other factors produced by the placenta: Human chorionic somatotropin (or placental lactogen) —> produced by the syncytiotrophoblast and similar to GH. It helps regulate the maternal metabolism of glucose and helps with the preparation for lactation Prostaglandins The placenta protects the embryo from rejection as it doesn’t present foreign antibodies to mother’s immune system (lack of MHC in syncytiotrophoblast and villus cytotrophoblast, which is present in fetal tissues and placental stroma). The mother’s immune defence is lowered at the same time restriction intrauterinegrowth The decidual reaction of the endometrium forms the design is visibee decidual which can be divided into different regions in the aecionecapsueeris disappears relation to the embryo: too afterstretching much Decidua Basalis —> between the implanted embryo and the myometrium (where the chorion frondosum develop) Decidua Capsularis —> overlies the embryo and its chorionic cavity (it degenerates at the 3rd month) Decidua Parietalis —> rest of the decidua, it has nothing to do with the implanted embryo amnion war closer The chorion frondosum is on the side of the decidua of getting to theendometrium basalis while the chorion leave are at the abembryinic pole The amnion and the chorion get together to form the amniochorionic membrane (which will fuse with the decidua parietalis after the disappearance of the decidua capsularis). The rupture of the amniochorionic membrane is the “breaking of the waters” Mature placenta: Fetal side (umbilical cord attached to the foetus) —> it is shiny due to the amnion and it presents the chorion frondosum Maternal side (side attached to the decidua) —> it is the decidua basalis and it is covered by the fetally-derived cytotrophoblastic shell, it is dull and it is divided into cotyledons (compartments made by projections of the decidua basalis, around 15-20) The available surface of the placenta is of 10m3, the diameter is around 15-30cm, the thickness is of around 3cm and the sight around 0.5kg Pathological placenta PPP abnormal vaginal bleeding Two examples of pathological placenta: Placenta that digs too deep into the uterine wall (the syncytiotrophoblast erodes too much and goes beyond the endometrium) —> 1. Placenta accreta: abnormal adherence of chorionic villi to myometrium (partial or complete absence of the decidua basalis). The placenta is normal during pregnancy but then it fails to detach during labour and the attempt to remove it might cause haemorrhages 2. Placenta increta: penetration of the myometrium 3. Placenta percreta: complete penetration of the myometrium to reach the perimetrium (it can invade the nearby organs like the rectum or the bladder), a caesarean hysterectomy has to be performed immediately after birth. These can all cause bleeding in the 3rd trimester due to an erosion of blood vessels (the myometrium is highly vascularised) Placenta forms in the wrong place —> Placenta previa: attachment at the level of the internal uterine os. This leads to vessel rupture and thus to 3rd trimester bleeding. The mother may bleed to death and the foetus might suffer because of reduced blood supply. A caesarean section is necessary Something can happen to the placenta leading to the development of a pathological placenta —> Placenta abruption: premature separation (partial or complete) of the placenta from uterine wall. It can be caused by trauma (es: car accident), smoking (vasoconstriction), hypertension (vasoconstriction of peripheral blood vessels), preeclampsia (the mother becomes hypertensive during pregnancy) or use of drugs. The abrupt causes a painful bleeding during 3rd trimester (when the placenta is bigger it is easier for it to get damaged), possible DIC (diffuse intra vascular coagulation), maternal shock and fetal distress. It can be deadly (mother may bleed to death and foetus my die) Bleeding can be internal —> an hematoma forms but no outer bleeding is detected ma Vasa previa —> umbilical blood vessels run over or in close proximity to the cervical os. This leads to painless vaginal bleeding and fetal bradycardia. Vessels may rupture leading to fetal death Choriocarcinoma —> carcinoma of the trophoblast during normal or ectopic pregnancy. It can either be metastatic (it can spread to liver and brain)or non metastatic. It can happen during abortion or in case of Hydatiform mole Hydatiform mole —> It is a problem in the formation of the chorionic villi (they are very dilated and look like grapes). This happens due to a genetic problem that prevents the formation of an embryo (there is only the formation of a placenta). There is no fetal tissue at all and only paternal chromosomes are expressed. Complete mole: no fetal tissue, 2% risk of evolving into a choriocarcinoma. Partial mole: some fetal tissue, choriocarcinoma development is rare Hydatiform mole can lead to an overproduction of hCG and it is usually of paternal origin (the oocyte is inactive). Some moles may develop after delivery or after spontaneous abortion. Hydatiform mole can lead to vaginal bleeding, uterine enlargement, pelvic pressure, hyperthyroidism and hyperemesis (very acute nausea and vomiting, this and hyperthyroidism are due to the overproduction of hCG) matermeDna iseliminated TWINNING Dizygotic twins —> 2 oocyets are ovulated and fertilised at the same time and later implant in the uterus. 2 placentae, 2 chorionic cavities, 2 amnions… The placenta and chorions can may fuse if the blastocysts implant close. Anastomosis: one embryo steals blood from the other (may cause congestive heart failure due to an excessively high blood pressure or death of the other embryo) The twins can have different sex and they express a different genome (as brothers and sisters) Monozygotic twins —> they have the same genetic material. The most common type of twinning begins at the blastocyst stage by the end of the 1st week (the formation of twins may happen at different times) —> the inner cell mass splits into two (1 blastocyst, 2 inner cell mass). There is 1 placenta, 1 chorionic sac and 2 amniotic sacs (because there are 2 epiblasts). Other type of separation: one blastocyst divides into two blastocyst that then develop on their own (2 blastocysts, 2 placentae, 2 chorionic sacs and 2 amniotic sacs). Other type of separation: at the embryonic disc stage (bilaminar), the disc splits in two so there is 1 placenta, 1 amniotic sac and 1 chorion. If the embryonic disc doesn’t divide completely conjoined twins may develop. The twins may develop a parasitic relationship (one twin is just a part of the other twin). Conjoined twins may be caused by wrong signalling during the formation of the primitive streak. Es: Goosecoid activates chordin and noggin which, if ectopically expressed, may lead to the formation of a second primitive streak and thus a secondary body axis