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  1. Developement of placenta ,umbilical cord and membranes Directed by Esraa Hamdy Abo Zaid Under supervision Nashwa El shenawy Prof of Obstetrics and Gynecology
  2. Placenta Chorio – decidual membrane Embryology:  The development of placenta involves the following 1. Development of decidua basalis from endometrium. 2. Development of chorion. 3. Combination of decidua basalis ( from mother ) and chorion frondosum ( from fetus ) to form placenta.
  3. Decidua:  Specialized , Highly modified endometrium of pregnancy. Decidualization:  Transformation of secretory endometrium to decidua It is dependent on estrogen , Progesterone and factors secreted by the implanting blastocyst.  The special relationship that exists between the decidua and the envading trophoblast appears defies the law of transplantation immunology.
  4. Decidual structure:  It is classified into three parts based on anatomical location 1. Decidua basalis: decidua directly beneath blastocyst implantation is modified by trophoblast envision. 2. Decidua capsularis: overlies the enlarging blastocyst and initially separates the conceptus from the rest of the uterine cavity , It is prominent during the second month of pregnancy. 3. Decidua parietalis the remainder lining of uterus .
  5. During early pregnancy: • Three is space between capsularis & Parietalis because gestational sac does not fill the entire uterine cavity. By 14 to 16 Weeks gestation : • The expanding sac has enlarged to completely fill the uterine cavity, The resulting apposition of the decidua capsularis and parietalis creates decidua vera & The uterine cavity is functionally obliterated.
  6.  The decidua parietalis and basalis are composed of three layers: 1. Zona compacta : surface or compact zone. 2. Zona spongiosa : Middle portion or spongy zone. 3. Zona basalis : basal zone remains after delivery and gives rise to new endometrium. Zona compacta & spongiosa together form zone functionalis.
  7. Decidual blood supply 1. Decidua capsularis : As a consequence of implantation the blood supply to capsularis is lost as embryo grows. 2. Decidua parietalis : Supplied by spiral arteries which retain smooth muscle wall & endothelia and thereby remain responsive to vasoactive agents. 3. Decidua basalis : Spiral arterial system supplying decidua basalis is altered remarkably. these spiral arterioles and arteries are invaded by cytotrophoblasts , during this process.
  8. The vessel walls in basalis are destroyed only a shell with out smooth muscle or endothelial cells So these blood vessels ( uteroplacental vessels ) are not responsive to vasoactive agents conversely the fetal chorionic vessels which transport blood between placenta & fetus contain smooth muscle & thus do respond to vasoactive agents.
  9. Decidua basalis contributes to formation of placental basal plate and differs Histologically from decidua parietalis in two important respects. 1. Spongy zone of basalis consists mainly of Arteries and widely dilated veins and by term glands disappeared. 2. The decidua basalis is invaded by many interstitial trophoblast cells & trophoblastic giant cells which commonly penetrate the upper myometrium. The NitaBuch layer is a zone of fibrinoid degeneration in which invading trophoblasts meet the decidua basalis if decidua is defective as in placenta accreta the NitaBuch layer is usually absent.
  10. Development of chorion and formation of chorionic villi Human placental formation begins with trophectoderm which appears at morula stage, It gives rise to trophoblast cell layer encircling the blastocyst.
  11. Differentiation of trophoblast: By 8th day post fertilization, after initial implantation the trophoblast has differentiated into outer multi nucleated syncytium = primitive syncytiotrophoblast and an inner layer of primitive mononuclear cells = cytotrophoblast.
  12. Syncytio trophoblast Cytotrophoblast  Amorphous cytoplasm without cell borders  Nuclei are multiple and varies in size and shape  Well demarcated cell border  Single nucleus  Ability to undergo DNA synthesis and mitosis.
  13. After implantation is complete:  Trophoblast further differentiate along two Extra villous trophoblasts Villous trophoblasts gives rise to = Not villi chorionic villi . transport O2, Migrate into decidua & Myometrium and nutrient and other compounds ALSO penetrate maternal vasculature. Between fetus & Mother Thus coming into contact ē various maternal stages primary Cell types classified into secondary Tertiary classified into Interstitial trophoblasts Endovascular Invade decidua & Myometrium trophoblasts to form placental bed giant cells which penetrate floating Anchoring they surround spiral arteries. Spiral Artery lumen villi villi
  14. All around chorionic vesicle finger like processes develop from syncytiotrophoblast and called syncytial trabeculae they are separated by spaces called lacunae.
  15. This occurs 12 days after conception. After invasion of superficial decidual capillary walls lacunae become filled ē maternal blood. Placental organization 1. Development of primary villi with deeper blastocyts invasion into the decidua cyto trophoblastic cells grow in the center of each syncytial trabeculum to form primary villous composed of core of cytotrophoblast surrounded by syncytiotrophoblast.
  16.  The cytotrophoblast cells pierce the distal ends of the syncytial trabeculae = primary villi and spared deep to decidua basalis and capsularis to meet & fuse with cytotrophoblast cells from adjacent trabeculae. As a result continuous layer called cytotrophoblast shell develops deep to decidua basalis & capsularis this shell separates the syncytiotrophablast of chorionic vesicle from decidua preventing more erosion of uterus by syncytiotrophoblast.
  17.  This cytotrophoblast proliferation at villous tips produce the trophoblastic cell columns that form anchoring villi which has no mesoderm or fetal vessels it is trophoblastic cell columns that are anchored to the decidua at basal plate.
  18. Development of secondary villi: These are formed when extraembryonic mesoderm grows in the center of cytotrophoblast cells of primary villi this occurs 12th day after fertilization. 3. Development of tertiary villi :This formed when villous mesoderm gives rise to Arterioles capillaries & venules which join the blood vessels of the umbilical cord & feotus.
  19. Decidual septa:  Number of decidual septa project into the intervillous spaces from the decidua basalis. These septa do not reach the chorionic plate. They have a core of decidua basalis in the center covered by cytotrophoblast & syncytiotrophoblast the septa incompletely divide placenta into 25 - 15 spaces called cotyledons.
  20. Trophoblast formation are divided to  Villous trophoblast : Trophoblast that arranged in villous pattern it is further divided to A. Anchoring villi formed of cyto & syncytiotrophoblast. B. Floating = free = branching villi formed of fetal vessels + Extraembryonic mesoderm + cyto + cyncytiotrophoblast.
  21. 2. Extra villous trophoblast this trophoblast does not form villi – it invades the decidua reaching the myometrium & invades decidual spiral arterioles and it is subdivided into A. Interstitial trophoblast B. Endovascular trophoblast
  22. Fate of chorionic villi All the chorionic vesicle is surrounded by villi in which 1. The villi related to decidua capsularis degenerate compression by the expanding chorionic vesicle. 2. The villi related to decidua basalis enlarge to form ( chorion frondosum ).
  23. Which chorion frondosum combine which decidua basalis to form placenta. Although maternal venous sinuses are tapped early in implantation maternal arterial blood does not enter the inter villous space until around day 15. Approximately at Day 17 fetal blood vessels are functional and placental circulation is established.
  24. Invasion of spiral Arteries These events occur in 1st half of pregnancy completed by 18 to 20 WKS. Spiral artery modification are carried out by two population of extra villous trophoblast. Interstitial trophoblast surround Arteries endovascular trophoblast penetrate spiral Artery lurnen. This remodeling converts narrow lumen, muscular Arteries into dilated, low resistance uteroplacental vessels.
  25. Placental Growth: • 1st trimester placental growth is more rapid than that of the fetus. • 17 postmenstrual weeks placental & fetal weights are approximately equal. • At term placental weight one sixth of fetal weight.
  26. Morphology of placenta Placental disc : 1. site of implantation:  Upper uterine segment posterior in 60%of cases and anterior in 40% , If inserted in lower uterine segment partial or total it is placenta previa. 2. Weight At term typical placental weighs 1/6 fetal weight = 500gm. 3. Shape discoid round to oval. 4. Diameter 18-22 cm in diameter.
  27. 5. Thickness at center 25mm. 6. Surfaces has 2 surfaces Maternal surface : that lies against uterine wall. It is basal plate which is divided by clefts into 15-20 portions = cotyledons. Fetal surface : chorionic plate into which umbilical cord insert typically near center visible large fetal vessels that originate from cord vessels then spread & branch a cross chorionic plate.
  28. In tracing these two features are clinically important •Fetal Arteries invariably cross over veins which is important when taking a fetal arterial blood sample. •Fetal vessels do not reach periphery of placenta important to determine that no other lobes are missed. Chorionic plate and it’s vessels are covered by thin amnion which can be easily peeled away from post- delivery specimen.
  29. Extra placental membranes Amnion amniotic epithelium covering the fetal surface of the placenta. Amnion & chorion that extend from placental edge. Abnormality in size = weight = thickness 1. Small placenta no universal definition but if <15cm diameter & it is associated é LBW.
  30. 2. Placentomegaly placenta thicker than 40mm by ultrasound. Causes : (a) large retro placental hematoma. (b) Collection of blood or fibrin é massive peri villous or inter villous fibrin deposition. (c) Villous enlargement due to maternal causes DM, Anemia or fetal causes Hydrops, anemia or infection by syphilis, toxoplasmosis, CMV, parvovirus.
  31. Variation in placental Morphology 1. Bilobate placenta = bipartite placenta = placenta duplex
  32.  The cord insert between two placental lobes either into a connecting chorionic bridge ( bilobate ) or into intervening membranes ( bipartite ) multilobate = more equivalently sized lobes is rare. 2. Placenta succenturiate placenta é small succenturiate lobe ( s ) that develop in membranes at a distance from main placenta.
  33. Clinical complication: 1. These lobes have vessels that pass through the membranes and if these vessels overlie the cervix and create vasa previa dangerous fetal He can follow vessel laceration. 2. An accessary lobe can also be retained in the uterus after delivery post partum Hge & atony. 3. Placenta membranacea :  This placenta é large diameter like amembrane and villi cover all or nearly all the uterine cavity.
  34. 4. Ring shaped placenta: May be a variant of placenta membrancea. This placenta is annular and a partial or complete ring of placental tissue is present. 5. Placenta fenestrate the central portion of placental disc is missing.
  35. 6. Placental mesenchymal dysplasia:  Cystic vesicles are seen é this rare condition correspond to enlarged stem villi but unlike molar pregnancy trophoblast proliferation is not excessive.
  36. 7. Circumvallate placenta the periphery of chorion is thickened , opaque , gray – white circular ridge composed of double fold of chorion & amnion.
  37. 8. Circummarginate placenta The chorionic membranes insert inward from the margin of placental edge unlike circumvallate placenta , the placental edge is not central depression & rolled up.
  38. Variation of placental site: Placenta previa partial or total encroachment of placenta on lower uterine segement a low lying , marginal previa , partial previa , complete previa. Placental calcification & grading  It occurs é advancing gestation , smoking , maternal serum ca levels.
  39. • These Hyperechoic deposit can easily be seen by U/S and aggrading scale from 0 to 3 reflects calcification é numerical grade. • Grade 0 placenta is Homogenous , lacks calcification and displays a smooth , Flat chorionic plate. • Grade 1 placenta scattered echogenicities , subtle chorionic plate. • Grade 2 placenta shows echogenic stippling at basal plate , large.
  40. Placental Abnormal attachment Abnormal placental adherence placenta accreta . Abnormal detachment placental abruption. Vascular pathologies of placenta Placental Fibrin deposition : (a) Subchorionic (b) Perivillous  Slow of maternal blood flow in the intervillous space. It appears as white, Firm, round elevated plaques with in placental fetal surface.  Slow of maternal blood flow around on individual villus result in fibrin deposition & can lead to diminished villous O2 .  They are small, yellow - white placental nodules are only visible with in parenchyma of a cut placenta.
  41. Infraction : chorionic Villi receive O2 solely from maternal Circulation supplied to the intervillous space any obstruction to this supply by uteroplacental disease can cause infarction. They are common lesions in mature placenta. Hematoma: several types of hematoma A. Retroplacental hematoma, between placenta & decidua e.g placental abruption is large & clinically significant. B. Marginal hematoma between chorion & decidua at placental periphery known clinically as subchorionic Hge. C. Sub amniotic hematoma from fetal blood vessels, beneath the amnion but above chorionic plate.
  42. D. Subchorial thrombus along roof of intervillous space & beneath chorionic plate. By U/S Hyperechoic to isoechoic in 1st wk after Hg. Hypoechoic at 1 to 2 WKS. Anechoic after 2WKs. Placental thrombosis : a) Intervillous collection of coagulated maternal blood normally found in the intervillous space + fetal blood from a break in a villus .  If recent rcd, around or oval vary in size up to > 1 cm.  old white-yellow round or oval. a) Fetal arteries thrombosis:  Fetal arteries that divide & send branches out across placental surface. this will obstruct fetal blood flow distal to obstruction affected portions of the villus become non functional.  there are thrombi limited numbers are normally found in mature placentas.
  43. C. Vascular lesions affecting villous capillaries 1) Chorangiosis number of capillaries with in terminal villi ≥ 10 capillaries to be present in ≥ 10 villi in ≥ 10 field through a 10x microscope lens. 2) Chorangiomatosis number of capillaries in stem villi But not terminal villi. Clinical significance remains unclear.
  44. Placental tumors : 1) Chorioangioma : Benign placental tumors have components similar to blood vessels & stroma of chorionic villus incidence 1%. In some cases fetal to maternal Hge across tumor capillaries leads to elevated level of maternal serum alpha – fetoprotein ( MSAFp). U/S well-circumscribed-rounded hypoechoic lesion lying near the chorionic plate & protruding into amniotic cavity. Cavity. By color doppler increase blood flow distinguish these lesions from other placental masses e.g hematoma.
  45. 2. Gestational trophoblastic neoplasia 3. Metastatic tumors  Maternal malignant tumor rarely metastasize to placenta Fetal malignant tumors rarely metastasize to placenta. Development of fetal membranes Fetal membranes are extra embryonic mesoderm Chorion Amnion
  46. Amnion:
  47. Early during development a space develops from the dorsal cell of inner cell mass (ectoderm). Epithelial cells of Amnion derived from Fetal ectoderm and called amnioblastic cells. Amnion 1st identifiable at 7th or 8th day of embryo development initially a minute vesicle small sac that covers the dorsal embryo surface. As amnion enlarges it engulfs the growing embryo which prolapses into cavity. Human amnion lacks smooth muscle calls, nerves, blood vessels and lymphatics.
  48. Amnion Epithelium is metabolically active & involved in solute & Water transport for amniotic fluid Hemostasis & produce Bioactive compounds é both autocrine & paracrine responses that include production of IL8, PGE2 , fetal fibronectin and collagenase. Proteoglycans are responsible for tensile strength of amnion. Such factors modulate change in membrane properties during labor.
  49. Amniotic fluid : Early pregnancy it is an ultrafiltrate of maternal plasma.  2nd trimester consists largely from extracellular fluid that diffuses through the fetal skin thus reflects composition of fetal plasma. After 20 Wks cornification of fetal skin prevents this diffusion and amniotic fluid is produced by . 1) Largely From Fetal urine ,kidneys produce urine 12 weeks by 18 weeks 7 to 14 ml per day. 2) Pulmonary fluid Small proportion of Amniotic volume. 3) Fluid filtering through placenta accounts for rest. 4) Desquamated fetal cells, vernix, lanugo bec these are hypotonic, the net effect is that amniotic fluid osmolality decreases é advancing gestation.
  50. Volume : Volume at each Wk is variable. Volume by 10 ml per week at 8weeks. Volume by 60 ml per week at 21 weeks. Then peaks at 34 weeks . At term average volume 1000 ml.  Functions :  Cushion to fetus, Musculoskeletal development protection from trauma, maintain temperature minimal nutritive function.
  51. •Chorioamnion abnormalities : 1.Chorioamnionitis . 2.Amnion nodosum numerous, small, light tan nodules on the amnion overlying the chorionic plate these may be scraped off the fetal surface & contain deposits of fetal squamous & fibrin reflects prolonged & severe oligohydramnious.
  52. 3. Amniotic band sequence : Amnion bands Constrict or amputate fetal parts. U/S : often identifies the sequelae of this sequence rather than the bands them salves. Management : Fetoscopic laser interruption of band in highly selected antepartum cases .
  53. 4. Amnionic sheet normal amniochorion draped over a preexisting uterine synechia . It poses little fetal risk.
  54.  Development of umbilical card :
  55. •At first Embryo is 3 layer flattened disc (trilaminar embryo) interposed between Amnion (fetal ectoderm side) & yolk sac (fetal endoderm side). Fetal dorsal surface=ectoderm grows faster than the ventral surface = endoderm resulting in folding of the embryo in all direction such that the ectoderm is now on the outer surface of the whole embryo then the mesoderm in the middle and the endoderm in the center of the embryo.
  56.  The amniotic sac enlarges as well, squeezing & forming the umbilical card.  As pregnancy advances yolk sac become smaller & it’s pedicle relative longer.  By the 3rd month (middle of it) the expanding amnion fuses with chorion leave & covers the pulging placental disc & lateral surface of body stalk = called umbilical card.
  57. Primitive umbilical card : 1. Connecting stalk containing allantois and 4 umbilical vessels (2 Arteries , 2 veins). 2. Yolk stalk is covered by vitelline vessels and surrounded by extraembryonic coelom which contains loops of intestine if persist umbilical hernia.
  58.  Definitive umbilical cord: Some structures disappear Loops of intestine return into the abdomen. The extraembryonic coelom is closed. The allantois, yolk stak and vitelline vessels are obliterated. Rt umbilical vein disappears.  At term Umbilical card contain , 1 vein + 2 Arteries.
  59. Umbilical card abnormalities :  Length: A. excessive long card cord entanglement, prolapse and fetal anomalies. B. shorts cord < 30 cm failure of engagement descant, malpresentation.
  60. Vessel number: four vessel cord- rare, e congenital anomalies. The most common aberration is that single umbilical artery (SUA) which is associated e fatal anomalies.  Cysts: A. True cysts: are epithelium-lined remnants of allantoic or vitelline duct - located closer to fetal insertion B. Pseudocysts: more common, from local degeneration of Wharton jelly, and where along cord.
  61.  Insertion of cord: 1. Eccentric insertion: no identifiable fetal risk. C. Marginal insertion: common, called battledore placenta cord anchors at placenta margin. D. Velamentous insertion: vessels (umbilical) travel with the membrane before reaching the placental margin incidence 1% - twin 6% - more common é placenta previa. 4. Furcate insertion: umbilical vessels lose their protective Wharton jelly shortly before insertion, they are covered by amnion sheath, prone to compression, twisting, thrombosis.
  62. Vasa previa: fetal vessels travel within the membranes and overlie cervical os. They can be torn é cervical dilatation or membrane rupture antepartum Hge from rapid fetal bleeding.
  63.  Vascular abnormalities: Cord hematoma: rare, follow rapture of umbilical vessel Still birth, intrapartum abnormal fetal Heart rate. Umbilical cord vessel thrombosis: rare, 70% venous 20% venous & arterial, 10% arterial still birth, fetal growth restriction, intrapartum fetal distress. Umbilical vein varices by color Doppler Umbilical Artery Aneurysm d.t congenital thinning vessel wall é decrease support from Wharton jelly fetal compromise & death.
  64. Knots, strictures & loops True knots 1% of births, formed from fetal movement if found in singleton fetuses – still birth 4 to 10 fold False knots: focal redundancy & folding of vessels Cord strictures: focal narrowing of diameter usually near fetal cord insertion site.
  65. cord loops: common coiling & round various fetal parts during movement Nuchal cord: common vaginal delivery is suitable since despite their frequency nuchal cord & cords wrapped around body are not associated é greater rates of adverse perinatal outcome. Funic presentation :umbilical cord is presenting part in lab uncommon, associated with malpresentation identified by U/S color flow Doppler overt or occult cord prolapse at term cesarean delivery is recommended.
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