- Embryology and Fetology, Normal Placenta, Placental Hormone
- Teratology and Drug Categories in Pregnancy
- Normal Pregnancy Events
- Prenatal Management of Minor Ailments during Pregnancy
- Physiological Changes in Pregnancy, Postpartum, and Lactation
- Maternal and Perinatal Statistics
- Prenatal Laboratory Investigations
- Establishment of GA and History Taking Examination—Diagnosis of Pregnancy Including Fetal Orientation in Utero-Leopold Maneuvers
EMBRYOGENESIS AND FETAL DEVELOPMENT
Figure 1 depicts the fetal development.
ZYGOTE AND BLASTOCYST DEVELOPMENT
During the first 2 weeks after ovulation and then fertilization, the zygote or preembryo develops to blastocyst stage.
- After fertilization, the zygote—a diploid cell with 46 chromosomes—undergoes cleavage and zygote cells produced by this division are called blastomeres. In two-cell zygote, the blastomeres and polar body continue to be surrounded by zona pellucida. The zygote undergoes slow cleavage for 3 days while still remaining in fallopian tube. As the blastomeres continue to divide, a solid mulberry-like ball of cells—the morula—is produced. The morula enters the uterine cavity approximately 3 days after fertilization. Gradual accumulation of fluid between morula cells is the formation of early blastocyst.
- The blastocyst implants 6 or 7 days following fertilization. The 58-cell blastocyst differentiats into five embryo-producing cells—inner cell mass. The remaining 53 outer cells called 4the trophoectoderm are destined to form trophoblasts. With ovulation, secondary oocyte and adhered cells of cumulus-oocyte complex are freed from ovary.
- This mass of cells is released into peritoneal cavity; oocyte is quickly engulfed by fallopian tube infundibulum. Further transport through tube is accomplished by directional movement of cilia and tubal peristalsis. Fertilization which normally occurs in oviduct, must take place within a few hours, and not more than a day after ovulation. Because of narrow window, spermatozoa must be present in fallopian tube at the time of arrival.
- Almost all pregnancies result when intercourse occur 2 days preceding or on day of ovulation. Fertilization is highly complex. Molecular mechanisms allow spermatozoa to pass between follicular cells, through zona pellucida, which is a thick glycoprotein layer surrounding oocyte cell membrane and into the oocyte cytoplasm. Fusion of two nuclei and intermingling of maternal and paternal chromosomes creates the zygote. Early human development is described by days or weeks post-fertilization that is postconceptional.
- As early as 4–5 days after fertilization, the inner cell mass forms. The 107-cell blastocyst is found to be no larger than earlier cleavage stage, despite accumulated fluid within blastocyst cavity. At this stage 8 formative, embryo-producing cells are surrounded by 99 trophoblastic cells. Blastocyst is released from zona pellucida secondary to secretion of specifically proteases from secretory phase endometrial glands.
- Release from zona pellucida allows blastocyst produced cytokines and hormones to directly influence endometrial receptivity. IL-1α and IL-1β are secreted by blastocyst and these cytokines likely directly influence endometrial receptivity. Embryos also have been shown to secrete hCG, which may influence endometrial receptivity. Receptive endometrium is thought to respond by producing leukemia inhibitory factor (LIF), follistatin and colony-stimulating factor 1 (CSF-1). LIF and follistatin activate signaling pathways that collectively inhibit proliferation and promote differentiation of endometrial epithelia and stroma to enable uterine receptivity. At the maternal–fetal interface, CSF-1 has proposed immunomodulatory actions and proangiogenic actions that are required for implantation.
IMPLANTATION
Six or seven days after fertilization, blastocyst implants into uterine wall. This process can be divided into three phases:
- Apposition—initial contact of blastocyst to the uterine wall
- Adhesion—↑ physical contact between blastocyst and decidua
- Invasion—penetration and invasion of syncytiotrophoblast and cytotrophoblast into decidua, inner third of myometrium and uterine vasculature.
- Successful implantation requires a receptive endometrium appropriately primed with estrogen and progesterone by corpus luteum. Such uterine receptivity is limited to D 20–24 of cycle. Adherence is mediated by cell-surface receptors at implantation site that interacts with blastocyst receptors.
- If the blastocyst approaches endometrium after D24, potential for adhesion is ↓ because antiadhesive glycoprotein synthesis prevents receptor interactions. At the time of its interaction with endometrium, blastocyst is composed of 100–250 cells. The blastocyst loosely adheres to decidua by apposition—on upper posterior uterine wall.
- Attachment of blastocyst trophoectoderm to decidual surface by apposition and adherence appears to be closely regulated by paracrine interactions between two tissues. Successful endometrial blastocyst adhesion involves modification in expression of cellular molecules (CAMs). The integrins—one of four families of CAMs—are cell surface receptors that mediate cell adhesion to extracellular matrix proteins. Endometrial integrins are hormonally regulated and a specific set of integrins is expressed at implantation. Recognition site blockade of integrins needed for binding will prevent blastocyst attachment.
EMBRYONIC PERIOD
Conceptus is termed an embryo at the beginning of third week after ovulation and fertilization. Primitive chorionic villi form and this coincides with expected day of menses. Embryonic period, during which organogenesis takes place, lasts 6 weeks, and begins third week from LMP through 8th week. The embryonic disc is well defined, and most pregnancy tests that measure hCG become positive by this time. The body stalk is now differentiated. These are villous cores in which angioblastic chorionic mesoderm can be distinguished and a true intervillous space that contain maternal blood
FETAL DEVELOPMENT AND PHYSIOLOGY
Fetal period Epochs: Transition from embryonic to fetal period occurs at 7 weeks after fertilization, corresponding to 9 weeks after LMP. At this time, fetus is approximately 24 mm in length, most organ systems have developed and the fetus enters a period of growth and maturation.
PLACENTA
“It makes sense that the placenta almost looks like a tree with many branches—a tree of life—Richie Lake.”
Introduction
The placenta is a temporary organ that begins developing from blastocyst shortly after implantation. It plays the crucial role of facilitating nutrient, gas and water exchange between maternal and fetal circulations and is important endocrine organ producing hormones that regulate both maternal and fetal physiology during pregnancy. Human placenta is discoid in shape and hemochorial—direct contact of chorion with maternal blood (Figs. 2 and 3).
Fig. 3: Extravillous trophoblasts found outside the villus and can be subdivided into endovascular and interstitial.
Placental Embryology
Development of Trophoblast
Chorionic Villi
With deeper blastocyst invasion into decidua, solid primary villi arise from buds of cytotrophoblasts that protrude into primitive syncytium before 12 days post fertilization.
- Primary villi: These are composed of cytotrophoblast core covered by syncytiotrophoblast. As the lacunae join a complicated labyrinth is formed that is partitioned by these solid cytotrophoblastic columns. The trophoblast-lined channels form intervillous space and solid cellular columns form the primary villous stalks.
- Day 12 marks the invasion of solid trophoblast columns and form secondary villi. Once angiogenesis begins in mesenchymal cords, tertiary villi are formed. Maternal venosus sinuses are tapped early in implantation, maternal arterial blood does not enter intervillous space until D15.
- By 17th day, fetal vessels are functional and placental circulation is established. Fetal placental circulation is completed when blood vessels of embryo are connected with chorionic vessels. In some villi, angiogenesis fails from lack of circulation. They can be seen normally but exaggeration of this process is seen with hydatidiform mole. Villi are covered by an outer layer of syncytiotrophoblast and inner layer of cytotrophoblast which are known as Langhans cells. Cytotrophoblast proliferation at villous tips produces trophoblastic cells columns that form anchoring villi. They are not invaded by fetal mesenchyme and they are anchored to decidua from cell columns, covering shell of syncytiotrophoblast and maternal decidua of basal plate. Base of chorionic plate forms roof of intervillous space. It consists of two layers of trophoblasts externally and fibrous mesoderm internally. The “definitive” chorionic plate is formed 8–10 weeks as amnionic and primary chorionic plate mesenchyme fuse together. This formation is accomplished by expansion of amniotic sac which surrounds connective stalk and allantois and joins these structures to form umbilical cord.
- Chorionic development: In early pregnancy, the villi are distributed over entire periphery of chorionic membrane. As blastocyst with its surroundings trophoblasts grows and expands into decidua, one pole faces endometrial cavity, opposite pole forms placenta. Chorionic villi in contact with decidua basalis proliferate to form chorion frondosum/leafy chorion. As growth of embryonic and extraembryonic tissues continues, blood supply to chorion facing endometrial cavity is restricted. Because of this, villi in contact with decidua capsularis cease to grow and then degenerate. This portion of chorion becomes avascular fetal membrane that abuts decidua parietalis and is called the chorion leave/smooth chorion. This smooth chorion leave is composed of cytotrophoblasts and fetal mesodermal mesenchyme. Until end of third month chorion leave is separated from amnion by extracoelomic cavity. They are in intimate contact to form an avascular amniochorion. These two structures are important sites of molecular activity. They constitute an important paracrine arm of fetal–maternal communication system.
- Regulators of trophoblast invasion: Implantation and endometrial decidualization activate a unique population of maternal immune cells that infiltrate uterus and play critical functions in trophoblast invasion, angiogenesis, spiral artery remodeling, and maternal tolerance of fetal alloantigens.
- Decidual natural killer cells make up 70% of decidual leukocytes in first trimester and are found in direct contact with trophoblasts. In contrast to NK cells in peripheral blood, these cells lack cytotoxic functions. They produce specific cytokines and angiogenic factors to regulate invasion of fetal trophoblasts and spiral artery remodeling. These and other unique properties distinguish dNK cells from NK cells in endometrium before pregnancy. dNK cells express both IL-8 and interferon inducible protein-10 which bind to receptors on invasive trophoblastic cells to promote their decidual invasion toward spiral arteries. dNK cells produce angiogenic factors—VEGF and PlGF which both promote vascular growth in decidua. Trophoblasts also secrete specific chemokines that attract dNK cells to maternal–fetal interface. Thus both cell types simultaneously attract each other. Decidual macrophages account for approximately 20% of leukocytes in first trimester and elicit an M2-immunomodulatory phenotype. Remember M1 macrophages are proinflammatory and M2 macrophages counter proinflammatory responses and promote tissue 8repair. In addition to a role in angiogenesis and spiral artery remodeling, dNK cells promote phagocytosis of cell debris. Concurrent with critical role of maternal dNK cells and macrophages, T-cell subsets aid tolerance toward allogenic fetus. Regulatory T cells are essential for promoting immune tolerance. Other T-cell subsets are present, such as Th1, Th2, and Th17 although their functions are tightly regulated.
- Endometrial invasion: Extravillous trophoblast of first trimester placenta is highly invasive. This process occurs under low-oxygen conditions and regulatory factors that are induced under hypoxic conditions are contributory. Invasive trophoblast secretes numerous proteolytic enzymes that digest extracellular matrix and activate proteinases present in decidua (urokinase-type plasminogen activators converts plasminogen to plasmin and degrades matrix proteins and activates MMPs). The timing and extent of trophoblast invasion is regulated by balance between pro- and anti-invasive factors—invade maternal tissue in early pregnancy and limited invasiveness in late pregnancy (controlled by autocrine and paracrine trophoblastic and decidual factors). Trophoblasts secrete insulin-like GF2 that promotes invasion into decidua. Decidual cells secrete IGF-binding protein-4 which blocks this autocrine loop. Low estradiol levels in first trimester are critical for trophoblast invasion and remodeling of spiral arteries. Rise in second trimester estradiol levels suppresses and limits vessel remodeling by ↓ trophoblast expression of VEGF-specific integrin receptors. Extravillous trophoblasts express integrins receptors that recognize extracellular matrix proteins collagen 4, laminin, and fibronectin. Binding of these matrix proteins and integrin receptors initiates signals to promote trophoblast cell migration and differentiation. As the pregnancy advances, rising estradiol levels downregulate VEGF receptor expression. This represses and control extent of uterine vessels transformation.
- Spiral artery invasion (Fig. 4): The extensive modification of maternal vasculature by trophoblasts, which are of fetal origin, occur in first half of pregnancy. They are integral to some pathological conditions—preeclampsia, FGR, and preterm birth. Spiral artery modifications are carried out by two populations of extravillous trophoblasts—endovascular trophoblasts, which penetrate spiral artery lumen, and interstitial trophoblasts, which surround the arteries. Interstitial trophoblasts penetrate decidua and adjacent myometrium and aggregate around spiral arteries. Their functions—vessels preparation for endovascular trophoblast invasion—first enter spiral artery lumens and form cellular plugs—destroy vascular endothelium via an apoptosis mechanism and invade and modify vascular media. Fibrinoid material replaces smooth muscle and connective tissue of vessel media—spiral arteries later regenerate endothelium. Invading endovascular trophoblasts can extend several centimeters along vessel lumen and migrate against arterial flow. Invasion by trophoblasts involves only decidual spiral arteries and not decidual spiral arteries or decidual veins. Uteroplacental vessel development proceeds in 2 waves/stages. The first wave occurs before 12 weeks post fertilization and spiral arteries are invaded and modified up to border between decidua and myometrium. Second wave, 12–16 weeks, involves some invasion of intramyometrial segments of spiral arteries. Remodeling converts narrow-lumen, muscular spiral arteries into dilated, low-resistance uteroplacental vessels.
- Molecular mechanisms of these crucial events, their regulation by cytokines, signaling pathways, and their significance in pathogenesis of preeclampsia, and FGR has been well established. Approximately after 1 month maternal blood enters intervillous space and the blood is propelled outside of maternal vessels and comes in direct contact with syncytiotrophoblasts. Villus branching: Although certain villi of chorion frondosum extend from 9chorionic plate to decidua to serve as anchoring villi, most villi arborize and end freely within intervillous space. As gestation proceeds short thick, early stem villi branch to form progressively finer subdivisions and greater number of smaller villi. Each of the truncal or main stem and their ramifications constitutes a placental lobule/cotyledon. Each lobule is supplied with a single chorionic artery and each lobule has a single vein so the lobule constitutes functional units of placental architecture.
- Placental growth and maturation: In the first trimester placental growth is more rapid than that of fetus. But by approximately 17 weeks GA, placental and fetal weighs are approximately equal. By term placenta weight is 1/6th of fetal weight. Viewed from maternal surface, number of slightly elevated convex areas called lobes-10 to 38. Lobes are incompletely separated by grooves of variable depth that overlie placental septa, which arise as upward projections of decidua. Total number of placental lobes remains same throughout gestation and individual lobes continue to grow less in final weeks. Grossly visible lobes—cotyledons. Lobules/cotyledons are functional units supplied by each main stem villus. As villi continue to branch and terminal ramifications become more numerous and smaller volume and prominence of cytotrophoblasts ↓. As the syncytium thins, fetal vessels become more prominent and lie closer to surface. In early pregnancy, branching connective tissue cells are separated by an abundant loose intercellular matrix. Later villous stroma becomes denser and cells are more spindly and closely packed. Another change in stroma—infiltration of Hofbauer cells/fetal macrophages—round with vesicular/eccentric nuclei and very granular or vacuolated cytoplasm. They are important mediators of protection at maternal fetal interface—phagocytic, immunosuppressive phenotype, can produce various cytokines and are capable of paracrine regulation of trophoblastic functions.
- Some histological changes that accompany placental growth and maturation improve transport and exchange to meet advancing fetal metabolic requirements → thinner syncytiotrophoblast, significantly ↓ cytotrophoblast no, ↓ stroma and ↑ number of capillaries with close approximation to syncytial surface.
- By 16 weeks apparent continuity of cytotrophoblasts is lost. At term, villi may be focally ↓ to a thin layer of syncytium covering minimal villous connective tissue in which thin-walled fetal capillaries abut the trophoblast and dominate the villi. There are some changes in placental architecture that can cause ↓ pl exchange efficiency if these are severe. These are thickening of basal lamina of trophoblast or capillaries, obliteration of certain fetal vessels greater villous stroma and fibrin deposition on villous surface.
- Placental circulation: Placenta is functionally an intimate approximation of fetal capillary bed to maternal blood, its anatomy primarily concerns vascular relations. The fetal surface is covered by transparent amnion, beneath which chorionic vessels course. A section through placenta includes amnion, chorion, chorionic villi and intervillous space, decidual (basal) plate, and myometrium.
- Fetal circulation: Deoxygenated venous-like fetal blood flows to placenta through two umbilical arteries (UA). As the cord joins placenta, these umbilical vessels branch repeatedly beneath amnion as they run across chorionic plate. Branching continues within villi to ultimately form capillary networks in terminal villous branches. Blood with significantly higher oxygen content returns from placenta via a single umbilical vein (UV) to fetus.10
- Branches of umbilical vessels traverse along fetal surface of placenta in chorionic plate or chorionic vessels. These vessels are responsive to vasoactive substances, and anatomically, morphologically, histologically, and functionally, unique. Chorionic arteries always cross over chorionic veins. Truncal arteries are perforating branches of surface arteries that pass through chorionic plate. Each truncal artery supplies one main stem villus and thus one cotyledon. As the artery penetrates chorionic plate, its wall loses smooth muscle, and its caliber ↑. Loss of muscle continues as the truncal arteries and veins branch into their smaller rami. Before 10 weeks, there is no end-diastolic flow (EDF) pattern within UA at end of fetal cardiac cycle. After 10 weeks EDF appears and is maintained throughout pregnancy.
- Maternal circulation: Mechanisms of placental blood flow must allow blood to leave maternal circulation; flow into space lined by syncytiotrophoblast, rather than endothelium; and return through maternal veins without producing arteriovenous-like shunts that would prevent maternal blood from remaining in contact with villi long enough for adequate exchange. Maternal blood enters through basal plate and is driven high up toward chorionic plate by arterial pressure before laterally dispersing. After bathing external microvillous surface of chorionic villi, maternal blood drains back through venous orifices in basal plate and enters uterine veins. Maternal blood traverses placenta randomly without preformed channels. The previously described trophoblast invasion of spiral arteries creates low-resistance vessels that can accommodate massive ↑ in uterine perfusion during gestation. Generally, spiral arteries are perpendicular to and veins are parallel to uterine wall. This arrangement aids closure of veins during uterine contraction and prevents exit of maternal blood from intervillous space at term. These discharge blood in spurts that bathes adjacent villi. After 30th week a prominent venous plexus lies between decidua basalis and myometrium and helps develop cleavage plane needed for placental separation after delivery. Both inflow and outflow are curtailed during uterine contractions. USG during normal labor shows placental length, thickness and surface area grew during contractions—due to distension of intervillous space by impairment of venous outflow compared with arterial inflow.
- During contractions, larger volume of blood is available for exchange and diastolic flow velocity in spiral arteries is ↓ (Doppler velocimetry). Principal factors regulating intervillous space blood flow—arterial BP, intrauterine pressure, uterine contraction pattern, and factors that act specifically on arterial walls.
- Breaks in placental “Barrier”: The placenta does not maintain absolute integrity of fetal and maternal circulations—examples of trafficking cells between mother and fetus in both directions. → erythrocyte D antigen alloimmunization. Fetal cell admixtures likely are small in most cases, although rarely fetus exsanguinates into maternal circulation. Fetal cells can also engraft in mother during pregnancy and can be identified decades later.
- Amnion: At term, amnion is a tough and tenacious but pliable fetal membrane and is contiguous with amnionic fluid.
- Function: (1) Amnion provides tensile strength of fetal membranes. (2) Its resilience to rupture is vitally important to successful pregnancy outcome.
- Bourne (1962) described five separate amnion layers. The inner surface, bathed by amnionic fluid, is an uninterrupted, single layer of cuboidal epithelium (Fig.) attached firmly to a distinct basement membrane that is connected to an acellular compact layer composed of interstitial collagens. On outer side of compact layer, there is a row of fibroblast-like mesenchymal cells, widely dispersed at term and a few fetal macrophages in amnion. The outermost amnion layer is relatively acellular zona spongiosa, which is contiguous with second fetal membrane, the chorion laeve. The human amnion lacks smooth muscle cells, nerves, lymphatics, and blood vessels.
- Amnion development, early during implantation, is a space develops between embryonic cell mass and adjacent trophoblastic cells. Small cells that line inner surface of trophoblasts called amniogenic cells—precursors of amniotic epithelium. Amnion is first identifiable on 7th or 8th day of embryo development and initially a minute vesicle develops into a small sac 11that covers dorsal embryo surface. It gradually enlarges and engulfs growing embryo, which prolapses into its cavity. Distension of amniotic sac eventually brings it into contact with interior surface of chorion leave. Apposition of chorion leave and amnion near end of first trimester caused obliteration of extraembryonic coelom. Amnion and chorion leave although slightly adhered are never intimately connected and can be separated easily. Placental amnion covers placental surface and is in contact with adventitial surface of chorionic vessels. Umbilical amnion covers umbilical cord. With MCDA placentas, there is no intervening tissue between fused amnions. In conjoined portion of membranes of DADC placenta, amnions are separated by fused chorion leave. Amniotic fluid fills this amniotic sac. Until 34 weeks normally clear fluid ↑ in volume as pregnancy progresses. After this volume declines. At term, amniotic fluid average 1,000 mL but may vary in abnormal conditions.
- Amnion mesenchymal cells: Functions of mesenchymal cells of amniotic fibroblast layer—synthesis of interstitial collagens that compose compact layer of amnion—the major source of its tensile strength takes place in mesenchymal cells. At term, generation of cortisol by 11β-hydroxysteroid dehydrogenase may contribute to membrane rupture via ↓ of collagen. Mesenchymal cells also synthesize cytokines that include IL-6, IL-8, and MCP-1. Cytokine synthesis rises in response to bacterial toxins and IL-1 useful in amniotic fluid study of labor-associated accumulation of inflammatory mediators. Mesenchymal cells may be a greater source of PGE2 than epithelial cells in case of PROM.
- Tensile strength: During tests of tensile strength, decidua and then chorion leave give way long before amnion ruptures. Membranes are elastic and can expand to twice normal size during pregnancy. The amnion tensile strength resides in compact layer—composed of cross-linked interstitial collagens I and III and lesser amount of collagens V and VI. The ratio of collagen III to collagen I in walls of highly extensible tissues—amniotic sac, blood vessels, urinary bladder, bile ducts, intestine, and gravid uterus—is greater in nonelastic tissues.
- Amnion tensile strength is regulated in part by fibrillar collagen assembly. This process is influenced by interaction fibrils with proteoglycans such as decorin and biglycan. ↓ of these proteoglycans is reported to perturb fetal membrane function. Fetal membranes overlying the cervix have a regional shift in gene expression and lymphocyte activation that set in motion an inflammatory cascade. This may contribute to tissue remodeling and loss of tensile strength in amnion.
- 12Metabolic functions: Amnion is metabolically active, involved in solute and water transport for amnionic fluid homeostasis, and produces array of bioactive compounds. Amnion is responsive to mechanical stretch, which alters amnionic gene expression. This may trigger autocrine and paracrine responses—production of MMPs, IL-8, and collagenase. Such factors may modulate changes in membrane properties during labor.
SOURCES OF AMNIOTIC FLUID
Composition:
- Water: 98.4% and solid component 1.6%
- Organic constituents:
- Proteins (albumin): 0.2–0.3 mg/dL
- Glucose: 10–20 mg/dL
- Urea: 30–35 mg/dL
- Nonprotein nitrogen: 30–35 mg/dL
- Lipids (phospholipids, lecithin, sphingomyelin)
- Hormone (insulin, prolactin, cortisol, estrogen)
- Inorganic constituents: Sodium, potassium, and chloride
- Solid particles: Lanugo, desquamated fetal skin cells, vernix caseosa, shedded amniotic cells, and epithelial cells
10 weeks: 20 mL. 20 weeks: 400 mL. 28 weeks: 750 mL. 36 weeks: 800–1,000 mL (Max). Term: 700 mL
UMBILICAL CORD
The yolk sac and the umbilical vesicle into which it develops are prominent early in pregnancy. At first, embryo is a flattened disc interposed between amnion and yolk sac. Its dorsal surface grows faster than ventral surface, in association with elongation of its neural tube. Embryo bulges into amnionic sac, and the dorsal part of yolk sac is incorporated into embryo body to form gut. The allantois projects into base of body stalk from caudal wall of the yolk sac and later, from anterior wall of hindgut.
As pregnancy advances, the yolk sac becomes smaller and its pedicle relatively longer. By middle of third month, expanding amnion obliterates extraembryonic coelom, fuses with chorion laeve, and covers bulging placental disc and lateral surface of body stalk. The latter is called umbilical cord—or funis. The cord at term normally has two arteries and one vein. The right umbilical vein disappears early during fetal development, leaving only one vein.
The umbilical cord extends from fetal umbilicus to fetal surface of placenta—chorionic plate. Blood flows from umbilical vein toward fetus. Blood then takes a path of least resistance via two routes within fetus. (1) Ductus venosus which directly empties into IVC; (2) Numerous smaller opening into hepatic circulation. Blood from liver flows into IVC via hepatic vein. Resistance in ductus venosus is controlled by a sphincter that is situated at origin of ductus at umbilical recess and is innervated by a vagus branch. Blood exits fetus via two umbilical arteries, branches of internal iliac artery and become obliterated after birth to form medial umbilical ligaments (Fig. 5).
Fig. 5: Cross-section of umbilical cord. Large umbilical vein carries oxygenated blood to fetus. To its left two smaller umbilical arteries, carrying deoxygenated blood from fetus to placenta.
NORMAL PLACENTA
At term, the typical placenta weighs 470 g, is round to oval with a 22 cm diameter, and has a central thickness of 2.5 cm. It is composed of a placental disc, extraplacental membranes, and three-vessel umbilical cord. The disc surface that lies against uterine wall is basal plate, which is divided by clefts into portions—termed cotyledons. The fetal surface is chorionic plate, into which umbilical cord inserts, in center. Large fetal vessels that originate from cord vessels then spread and branch across chorionic plate before entering stem villi of placenta parenchyma. In tracing these, fetal arteries cross over veins. The chorionic plate and its vessels are covered by thin amnion, which can be easily peeled away from a postdelivery specimen. Placental location and relationship to internal cervical os are recorded during prenatal USG. As visualized USG—normal placenta is homogenous and 2–4 cm thick, lies against 13myometrium, and indents into amnionic sac. The retroplacental space is a hypoechoic area that separates myometrium from basal plate and measures <1–2 cm. The umbilical cord is imaged, its fetal and placental insertion sites and its vessels are counted. Many placental lesions can be identified grossly or by USG, but other abnormalities require HPR clarification.
PLACENTAL HORMONES
Hormones | Function | Cytochemical origin | Maximum at GA |
|---|---|---|---|
hCG | Relaxation and quiescence of myometrium | Syncytiotrophoblast | 8-10 weeks |
Corticotropin RH | Fetal lung maturation Timing of parturition | Cytotrophoblast and syncytiotrophoblast | |
Human placental lactogen | Mediates insulin resistance | Syncytiotrophoblast | 36 weeks |
Progesterone | Suppresses uterine contraction Promotes cervical mucus formation and prevents infection | Before 7 weeks-corpus luteum After 7 weeks-placenta | Term (40 weeks) |
Estrogen | Stimulates growth of myometrium, ↑ uterine strength for parturition. Prepares mammary glands for lactation | Fetoplacental unit | Term (40 weeks) |
PAPP-A | Immunosuppressant | Syncytiotrophoblast | |
Human chorionic somatotropin | ↓maternal use of glucose and promotes breakdown of stored fat | Syncytiotrophoblast | |
Relaxin | Softens cervix in preparation for cervical dilatation at parturition | Corpus luteum, decidua, placenta | |
Placental growth factors (IGF-1 and 2, TGF, epidermal GF) | Immunosuppressive, paracrine and steroidogenic | Syncytiotrophoblast |