Lecture 08.pdf Placenta Development PDF
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Square High School and College
Ruqaiya Al Jabri
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Summary
This lecture details the development of the placenta and membranes, including the formation of primary villi and the development of secondary and tertiary villi. It also covers aspects such as the structure of the placenta, its function, and changes during pregnancy.
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DEVELOPMENT OF PLACENTA AND MEMBRANES PART I: PLACENTA RUQAIYA AL JABRI Development of trophoblast: Formation of primary villi 3rd week Syncytiotrophoblastcells are highly invasive Blood lacunae ( spaces) are being formed in endometrium( maternal blood) Proliferating cytotrophoblasts in...
DEVELOPMENT OF PLACENTA AND MEMBRANES PART I: PLACENTA RUQAIYA AL JABRI Development of trophoblast: Formation of primary villi 3rd week Syncytiotrophoblastcells are highly invasive Blood lacunae ( spaces) are being formed in endometrium( maternal blood) Proliferating cytotrophoblasts invaginate into syncytiotrophoblasts Primary chorionic villi have formed DEVELOPMENT OF SECONDARY AND TERTIARY VILLI Primary villi are being invaded by extraembryonic mesoderm to form secondary villi Foetal blood vessels from chorionic plate and connecting stalk have penetrated the EEM forming definitive placental villi (tertiary villi) Capillaries in the tertiary villi connect with capillaries in the chorionic plate and in the connecting stalk These vessels establish contact with the intraembryonic developing vessels and heart Initially villi develop all around the chorion EMBRYO AND THE TROPHOBLAST AT THE END OF THE THIRD WEEK: THE CYTOTROPHOBLAST SHELL Cytotrophoblast cells penetrate the syncytiotrophoblast and surround the trophoblast They form a thin cytotrophoblast shell: Are in direct contact with the endometrium Attaches the chorion firmly to the maternal endometrium Intervillous spaces, are found throughout the trophoblast are between the chorionic villi The embryo is suspended in the chorionic cavity by means of the connecting stalk. At the embryonic pole, villi are numerous and well formed. This part of the chorion is known as chorion frondosum At the abembryonic ( opposite) pole, they are few in number and poorly developed. The rest of the chorion is known as chorion laevae (smooth)(As villi slowly disappear here) FOETAL PART OF PLACENTA : STRUCTURE Chorionic plate composed of Extra embryonic somatic mesoderm containing foetal blood vessels Cytotrophoblast Syncytiotrophoblast Tertiary Chorionic villi MATERNAL PART OF PLACENTA: DECIDUA BASALIS Functional layer of endometrium at site of implantation: Decidual reaction: -consists of a compact layer of large decidual cells derived from endometrial stroma. Cells filled with abundant lipids and glycogen (source of early nutrition) Maternal blood vessels-open into lacunae, intervillous spaces Endometrial glands Incomplete septa grow into intervillous spaces DECIDUA BASALIS & PLACENTAL CIRCULATION Incomplete decidual septa or partitions grow out of the decidual plate They do not reach chorionic plate These divide the maternal side of placenta into 15-20 placental lobules or cotyledons PLACENTAL MEMBRANE/BARRIER : SITE OF EXCHANGE: A SELECTIVE SEMI PERMEABLE MEMBRANE Formed by Endothelial cells of fetal blood vessels Extraembryonic Mesoderm Cytotrophoblast cells Syncytiotrophoblast cells Maternal and foetal blood does NOT mix PLACENTAL CIRCULATION Spiral arteries---branches of endometrial ( uterine) arteries deliver blood to placenta Enters intervillous spaces Cytotrophoblastcells ( from the shell) invade the terminal portions of spiral arteries Transform into endothelial cells lining maternal spiral arteries (epithelial –to-endothelial transformation) This invasion transforms these small diameter, high resistance vessels into large diameter, low resistance vessels-more blood can be delivered into intervillous spaces PLACENTAL CIRCULATION Blood enters intervillous spaces Bathes chorionic villi Exchange of nutrients, gases and metabolites occurs at placental membrane of free villi More free villi grow out into the intervillous spaces Endometrial veins carry waste products and CO 2 back into maternal circulation PLACENTA FUNCTIONS Facilitates nutrient, electrolyte and gas exchange by diffusion across placental membrane Exchange of metabolites Transmission of maternal antibodies-IgG (Immunity to fetus) Hormone production Progesterone, oestrogen, HCG, somatomammotropin (a growth-hormone-like substance) A semipermeable barrier-allows some bacteria, viruses, drugs to cross into foetal circulation BEYOND 4 MONTHS IUL Placental barrier begins to thin due to thinning of cytotrophoblastic layer to facilitate greater exchange Some mesoderm connective tissue also degenerates The barrier is only formed by syncytiotrophoblast sand capillary endothelium in some areas. Few remaining cytotrophoblasts do not participate in exchange Full term placenta: Diameter: 15-25 cms. Thickness: 3 cms. Weight: 500-600 gms. Attachment of umbilical cord is usually eccentric on Foetal side Foetal side of the placenta PLACENTAL CHANGES AT THE END OF PREGNANCY At the end of pregnancy, a number of changes that occur in the placenta reduced exchange between the two circulations. These changes include an increase in fibrous tissue in the core of the villus, thickening of basement membranes in fetal capillaries obliteration of small capillaries of the villi, deposition of fibrinoid on the surface of the villi in the junctional zone and in the chorionic plate. Excessive fibrinoid formation frequently causes infarction of an intervillous lake or an entire cotyledon. The cotyledon then assumes a whitish appearance. NORMAL POSITION OF PLACENTA ABNORMAL ATTACHMENT AND PENETRATION OF PLACENTA Placenta accreta: Anchoring placental villi attach to the myometrium rather than the decidua resulting in abnormally adherent placenta. Placenta increta Chorionic villi penetrate into the myometrium. Placenta percreta Chorionic villi penetrate through the myometrium to the uterine serosa or adjacent organs. CLINICAL APPLICATION: RH INCOMPATIBILITY Placental barrier is semipermeable allows harmful viruses like rubella, measles, polio and AIDS , some drugs, antigens etc. to enter foetal circulation If Rh–ve mother: Foetal RBCS of an Rh +ve (D or Rh antigen) foetus can enter maternal blood during delivery/trauma etc. stimulate anti-Rh antibodies (isoimmunisation) in mother. If antibody production is sufficient, antibodies attack and destroy fetal RBCs in next pregnancy : hemolytic disease of the newborn: Erythroblastosis foetalis The severe anaemia can cause tissue fluid accumulation and oedema Fetal hydrops Slide courtesy of Dr. Sadhana