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Mar 3

Sexual and Reproductive Anatomy, Class 12 - Pregnancy and Labor

The prenatal period begins with fertilization- when a secondary oocyte and sperm combine, and it ends approximately 38 weeks later with birth. The general term for the new organism is a conceptus, but there are multiple different terms are used during specific parts of the prenatal period.

Some physicians refer to pregnancy as a 40-week gestation period. This time frame is measured from the pregnant individual’s last period to the birth of the newborn, so fertilization does not occur until week 2 (when ovulation occurs). Physicians may use this reference because the individual knows when their last period was, but they may not know the day they ovulated and had a secondary oocyte fertilized. Even when the date of conception is known, typical pregnancy length may vary up to ±19 days from this average.

The prenatal period is broken down into three shorter periods;

The pre-embryonic period is the first 2 weeks of development (the first 2 weeks after fertilization), when the single cell produced by fertilization (called the zygote) becomes a spherical, multicellular structure (called the blastocyst). This period ends when the blastocyst implants in the endometrial lining of the uterus.

The embryonic period extends from the third through eighth weeks of development. It is a remarkably active time, during which rudimentary versions of the major organ systems appear in the developing body, which is now called an embryo.

The fetal period includes the remaining 30 weeks of development prior to birth, when the organism is called a fetus. During the fetal period, the fetus continues to grow, and its organs increase in complexity.

The latter two stages make up a process known as embryogenesis.

The pre-embryonic period in human development begins with fertilization, when the sperm penetrates the secondary oocyte, and the two unite to form a single diploid cell called the zygote. The zygote is the same size as the secondary oocyte, which typically is between 100-120 micrometers in diameter.

Fertilization combines the sperm and oocyte's genetic material, as well as restores the diploid number of chromosomes to the gamete. Fertilization occurs most commonly within the uterine tube, typically in the widest part, called the ampulla. Following ovulation, the secondary oocyte remains viable in the reproductive tract for no more than 24 hours, whereas sperm remain viable for an average of 3 to 4 days after ejaculation.

Sperm are not yet capable of fertilizing the secondary oocyte when they are ejaculated. Sperm must undergo capacitation, a physiologic conditioning, before they can accomplish fertilization. Capacitation occurs in the uterine tract and typically takes several hours. During this time, a glycoprotein coat and some proteins are removed from the sperm plasma membrane that overlies the acrosome of the sperm.

Typically, millions of sperm are deposited in the vagina during intercourse. However, only a few hundred reach the secondary oocyte in the uterine tube. Many sperm leak out of the vagina, and some are not completely motile. Other sperm do not survive the acidic environment of the vagina, and still more do not reach the uterine tube as they move through the uterus and get churned by its muscular contractions. Recall that each month, typically only one of the two ovaries will ovulate a secondary oocyte into a uterine tube. Only those sperm that enter the uterine tube containing the secondary oocyte have a chance at fertilization. Thus, although millions of sperm may be released during sexual intercourse, only a few hundred have a chance at fertilization.

The secondary oocyte and the cumulus oophorus cells surrounding the oocyte release chemicals to attract the sperm to its location. Specifically, the cumulus oophorus cells release progesterone, which binds to and opens calcium channels found on the flagella of sperm, which causes an influx of calcium ions (Ca2+). The influx of Ca2+ is necessary for calcium-dependent actions such as capacitation, the acrosome reaction needed to penetrate the oocyte, and fertilization.

All viable sperm that reach the secondary oocyte have the potential of fertilizing the secondary oocyte. However, only one sperm typically is able to fertilize the secondary oocyte at a time; the remaining sperm are prevented from penetrating the oocyte.

There are three phases of fertilization: corona radiata penetration, zona pellucida penetration, and fusion of the sperm and oocyte plasma membranes (followed by fusion of the ovum and sperm pronuclei).

The sperm that successfully reach the secondary oocyte are initially prevented entry by both the corona radiata and the zona pellucida. When sperm reach the corona radiata, their motility allows the sperm to push through the cell layers. Once the sperm have penetrated the corona radiata, they then encounter the more solid zona pellucida.

After the sperm have made a pathway through the corona radiata, digestive enzymes are released from the sperm acrosomes to penetrate the glycoproteins forming the zona pellucida. This release of enzymes (primarily hyaluronidase and acrosin) from the acrosome is known as the acrosome reaction. When one sperm successfully penetrates the zona pellucida and its nucleus enters the secondary oocyte, immediate changes occur to both the zona pellucida and the oocyte, in order to make it so that no other sperm can enter. In essence, the zona pellucida hardens, preventing other sperm from binding to and ultimately digesting their way through this layer. This process is necessary to ensure that only one sperm fertilizes the oocyte.

On very rare occasions, two or more sperm cell nuclei simultaneously enter the secondary oocyte, a phenomenon called polyspermy (poly meaning "many"). Polyspermy causes the fertilized oocyte to have 23 triplets (if two sperm enter) or 23 quadruplets (if three sperm enter) of chromosomes, instead of 23 pairs of chromosomes. These fertilized oocytes are not viable and result in spontaneous abortion.

When the sperm and oocyte plasma membranes come into contact, they immediately fuse. Only the nucleus of the sperm enters the cytosol of the secondary oocyte. The midpiece and flagellum of the sperm degenerate shortly thereafter and typically do not enter the fertilized cell. When the nucleus of the sperm enters the secondary oocyte, the secondary oocyte completes the second meiotic division and forms an ovum and a second polar body. The nucleus of the sperm and the nucleus of the ovum are called pronuclei because they each have a haploid number of chromosomes (23 single chromosomes). These pronuclei come together and fuse, forming a single nucleus that contains a diploid number (23 pairs) of chromosomes. The single diploid cell formed is the zygote.

Following fertilization, the zygote begins the process of becoming a multicellular organism. After the zygote divides once by mitosis and reaches the 2-cell stage, a series of further mitotic divisions called cleavage results in an increase in cell number, but not an increase in the overall size of the structure. The diameter of the structure remains about 120 micrometers, so the mitotic divisions produce greater numbers of smaller cells within this structure. The structure will not increase in size until it implants in the endometrial lining of the uterus and derives a source of nourishment from the carrier.

Before the 8-cell stage, none of the cells are tightly bound together. However, after the third cleavage division, the cells become tightly compacted into a ball. The process by which contact between cells is increased to the maximum is called compaction. These cells now divide again, forming a 16-cell stage, the morula. The cells of the morula continue to divide further.

Shortly after the morula enters the lumen of the uterus, fluid begins to leak through the degenerating zona pellucida into the morula. As a result, a fluid-filled cavity, called the blastocyst cavity, develops within the morula. The structure at this stage of development is known as a blastocyst, and it has two distinct components;

The trophoblast, an outer ring of cells surrounding the fluid-filled cavity. These cells will form the chorion, one of the extraembryonic membranes discussed later.

The embryoblast, or inner cell mass, is a tightly packed group of cells located only within one side of the blastocyst. The embryoblast will form the embryo proper. These early cells are pluripotent (pluris meaning "multi", potentia meaning "power"), which means they have the power to differentiate into any cell or tissue type in the body, except the placenta.

By the end of the first week after fertilization, the blastocyst enters the lumen of the uterus. The zona pellucida around the blastocyst has begun to break down as the blastocyst prepares to invade the proliferated functional layer of the endometrium of the uterus. Implantation is the process by which the blastocyst burrows into and embeds within the endometrium.

The blastocyst begins the implantation process by about day 7 (the end of the first week of development), when trophoblast cells begin to invade the functional layer of the endometrium. Simultaneously, the trophoblast subdivides into two layers: a cytotrophoblast, which is the inner cellular layer of the trophoblast, and an outer layer termed the syncytiotrophoblast. (The term syncytium refers to a multinucleate mass of cytoplasm formed from fused cells.) Over the next few days, the syncytiotrophoblast cells burrow into the functional layer of the endometrium and bring with them the rest of the blastocyst.

By day 9, the blastocyst has completely burrowed into the uterine wall and makes contact with the pools of nutrients in the uterine glands. Thus, implantation begins during the first week of development and is not complete until the second week.

The syncytiotrophoblast is responsible for producing human chorionic gonadotropin (hCG). Recall from prior lessons that hCG signals the corpus luteum (within the ovary) that fertilization and implantation have occurred. Thus, the corpus luteum does not degenerate but rather persists for another 3 months, producing large amounts of progesterone and estrogen that thicken and maintain the uterine lining.

By the end of the second week of development, sufficient quantities of hCG are produced to be detected in the carrier’s urine (from when it was filtered from the blood within the kidneys). The presence of hCG in urine indicates a pregnancy, and thus hCG is the basis for most modern-day pregnancy tests. For the first 3 months of pregnancy, hCG levels remain high, but after that they decline. When hCG declines, the corpus luteum degenerates. However, by this time, the corpus luteum is no longer needed because the placenta is producing progesterone and estrogen to maintain the pregnancy.

During the second week of development, as the blastocyst is undergoing implantation, changes also occur to the embryoblast portion of the blastocyst (the inner cell mass). By day 8, the cells of the embryoblast begin to differentiate into two layers. A layer of small, cuboidal cells adjacent to the blastocyst cavity is termed the hypoblast layer, and a layer of columnar cells adjacent to the amniotic cavity is called the epiblast layer. Together, these layers form a flat disc termed a bilaminar germinal disc, or blastodisc.

The bilaminar germinal disc and trophoblast produce extraembryonic membranes. These membranes first appear during the second week of development and continue to develop during the embryonic and fetal periods. They protect the embryo and assist in vital functions. These extraembryonic membranes include the following;

The yolk sac is the first extraembryonic membrane to develop. It is formed from and continuous with the hypoblast layer of the bilaminar germinal disc. In humans, it does not store yolk as it does in eggs of birds and reptiles, but is instead an important site for early blood cell and blood vessel formation.

The amnion is formed from and continuous with the epiblast layer of the bilaminar germinal disc. The amnion is a thin membrane that encloses the entire embryo in a fluid-filled sac called the amniotic cavity to protect the embryo from drying out. The amniotic membrane is specialized to secrete the amniotic fluid that bathes the embryo.

The chorion is the outermost extraembryonic membrane and is formed from both the rapidly growing cytotrophoblast cells and syncytiotrophoblast (both were formed from the trophoblast). These cells implant within the functional layer of the endometrium and together, these structures (chorion and functional layer) will form the placenta. The placenta is the site for providing oxygen (O2) and nutrients to the embryo/fetus and removing carbon dioxide (CO2) and other wastes from the embryo/fetus.

To develop into an embryo and then a fetus, the blastocyst must receive nutrients and respiratory gases from the maternal blood supply. The connection between the embryo or fetus and the mother is the richly vascular placenta. The main functions of the placenta are the exchange of nutrients, respiratory gases, and waste products between the maternal and fetal blood; transmission of maternal antibodies to the developing embryo or fetus; and production of progesterone and estrogen to maintain and build the uterine lining.

The placenta begins to form during the second week of development. The fetal portion of the placenta develops from the chorion, whereas the maternal portion of the placenta forms from the functional layer of the uterus. The early organism is connected to the placenta via a structure called the connecting stalk. This connecting stalk is the precursor to the future umbilical cord. The connecting stalk, which later helps form the umbilical cord, contains the umbilical vein and umbilical arteries that transport blood to and from the embryo or fetus, respectively.

Fingerlike structures called chorionic villi form from the chorion. The chorionic villi contain branches of the umbilical vessels. Adjacent to the chorionic villi is the functional layer of the endometrium, which contains maternal blood. Note that fetal blood and maternal blood do not mix- rather, the two bloodstreams are so close to one another that exchange of gases and nutrients can occur. The concentration of O2 and nutrients is higher in the maternal blood, and therefore these diffuse into the fetal blood. Conversely, the concentration of CO2 and waste products is higher in the fetal blood, so these materials diffuse from the fetal blood into the maternal circulation.

Although the placenta first forms during the pre-embryonic period, most of its growth and development occur during the fetal period (the last 30 weeks of development). When the placenta matures, it is disc shaped and adheres firmly to the wall of the uterus. Immediately after the baby is born, the placenta is also expelled from the uterus. The expelled placenta is often called the afterbirth

The placenta may be thought of as a selectively permeable structure. Certain materials enter freely through the placenta into the fetal blood, whereas other substances are effectively blocked. For example, respiratory gases and nutrients may freely cross the placental barrier, but many microorganisms (e.g., viruses, bacteria) and high levels of maternal hormones are prevented from crossing this barrier into the developing fetus. Unfortunately, a number of potentially harmful substances, such as some viruses (ex; HIV, rubella) and bacteria (ex; Treponema, the bacterium that causes syphilis) can cross the placental barrier, infecting the fetus and sometimes causing birth defects or death. Most drugs, alcohol, and the toxins from smoking also pass through the placental barrier.

Some fetuses may be more susceptible to materials that cross the placental barrier than other fetuses. Additionally, the dose of the material crossing the placental barrier and the timing of this crossing both affect fetus susceptibility. These facts help explain why some newborns are strongly affected by substances that cross the placental barrier, whereas other newborns are relatively unaffected.

Prior to implantation, the potentially harmful substances have little or no access to the developing embryo because the embryo is within the uterine tubes and is moving toward the uterus. However, once implantation begins, the developing organism is exposed to most of the substances to which the mother is exposed. For these reasons, individuals who are pregnant are strongly urged to do the following: a) quit smoking, because nicotine induces constriction of blood vessels including the umbilical vein, which decreases oxygen and nutrient to the developing embryo/fetus, and b) refrain from taking drugs and drinking alcohol, because most drugs and alcohol are potential teratogens, which can result in potentially harmful congenital deformities.

The embryonic period begins with the process called gastrulation, whereby the three primary germ layers (ectoderm, mesoderm, and endoderm) form. Once gastrulation is complete, a process called organogenesis occurs, whereby the basic composition of each organ is formed. By the end of the embryonic period (week 8), the main organ systems have been established, and the major features of the external body form are recognizable.

Gastrulation occurs during the third week of development immediately after implantation, and is one of the most critical periods in the development of the embryo. Gastrulation is a process by which the epiblast cells migrate and form the three primary germ layers, which are the cells from which all body tissues develop. The three primary germ layers are called ectoderm, mesoderm, and endoderm. Once these three layers have formed, the developing trilaminar (three-layered) structure may be called an embryo.

Gastrulation begins with formation of the primitive streak, a thin depression on the surface of the epiblast. The cephalic (head) end of the streak, known as the primitive node, consists of a slightly elevated area. Within the center of the primitive node is a depression called the primitive pit.

Cells detach from the epiblast layer and migrate through the primitive streak between the epiblast and hypoblast layers. This inward movement of epiblast cells is known as invagination. Migrating epiblast cells first displace the hypoblast and form the endoderm (endo meaning "inner", derma meaning "skin"). Next, more epiblast cells invaginate and form a new primary germ layer known as mesoderm (meso meaning "middle"). Cells remaining in the epiblast then form the ectoderm (ektos meaning "outside"). Thus, the epiblast, through the process of gastrulation, is the source of the three primary germ layers from which all body tissues and organs eventually derive.

The 3-week embryo is a flattened, disc-shaped structure. For this reason, the structure is also referred to as an embryonic disc. So how does this flattened structure develop into a three-dimensional human?

The shape transformation begins during the late third and fourth weeks of development, when cells are rapidly dividing, and certain regions of the embryo grow faster than others. This rapid division and growth of cells causes folding in two directions; thus, the embryonic disc starts to fold on itself and become more cylindrical. There are two types of folding that occur; cephalocaudal folding and transverse folding.

Cephalocaudal folding occurs in the cephalic (head) and caudal (tail) regions of the embryo. Essentially, the embryonic disc and amnion grow very rapidly, but the yolk sac does not grow at all. This differential growth causes the head and tail regions of the embryo to fold on themselves.

Transverse folding (or lateral folding) occurs when the left and right sides of the embryo curve and migrate toward the midline. As these sides come together, they restrict and start to pinch off the yolk sac. Eventually, the sides of the embryonic disc fuse in the midline and create a cylindrical embryo. Thus, the ectoderm is now solely along the entire exterior of the embryo, whereas the endoderm is confined to the internal region of the embryo. As this midline fusion occurs, the yolk sac pinches off from most of the endoderm (with the exception of one small region of communication called the vitelline duct).

Thus, cephalocaudal folding helps form the future head and buttocks region of the embryo, whereas transverse folding creates a cylindrical trunk or torso region of the embryo.

After the embryo undergoes cephalocaudal and transverse folding, the ectoderm is located on the external surface of the now-cylindrical embryo. The ectoderm is responsible for forming nervous system tissue in a process called neurulation. The ectodermal cells covering the embryo after neurulation form the epidermis. Ectoderm also forms the epidermal derivatives, sense organs, and pituitary gland. It forms the adrenal medulla, enamel of teeth, and lens of the eye. With a few exceptions, ectoderm gives rise to those organs and structures that maintain contact with the outside world.

The mesoderm subdivides into five different categories;

The tightly packed midline group of mesodermal cells, also called chordamesoderm, forms the notochord. The notochord serves as the basis for the central body axis and the axial skeleton and induces the formation of the neural tube.

Paraxial mesoderm is found on both sides of the neural tube. The paraxial mesoderm then forms somites, which are blocklike masses responsible for the formation of the axial skeleton, most muscle (including limb musculature), and most of the cartilage, dermis, and connective tissues of the body.

Lateral to the paraxial mesoderm are cords of intermediate mesoderm, which forms most of the kidneys, the ureters, and the internal reproductive organs.

The most lateral layers of mesoderm on both sides of the neural tube are called the lateral plate mesoderm. The lateral plate mesoderm will form the spleen, the adrenal cortex, the epithelial lining of blood vessels and lymph vessels, the heart, the serous membranes of the body cavities, and all the connective tissue components of the limbs.

The last region of mesoderm, called the head mesenchyme, forms connective tissues and musculature of the face.

Endoderm becomes the innermost tissue when the embryo undergoes transverse folding. Among the structures formed by embryonic endoderm are the epithelial linings of the respiratory, gastrointestinal (GI), urinary, and reproductive tracts. It forms the epithelial lining of the tympanic cavity (middle ear) and the auditory tube. Endoderm also forms most of the liver, the gallbladder, pancreas, portions of the palatine tonsils, thyroid gland, parathyroid glands, and thymus.

Once the three primary germ layers have formed and the embryo has undergone cephalocaudal and transverse folding, the process of organogenesis, or organ development, begins. The upper and lower limbs attain their adult shapes, and the rudimentary forms of most organ systems have developed by week 8 ofdevelopment.

During the embryonic period, the embryo is particularly sensitive to teratogens (teras meaning "monster", gen meaning "producing"), substances that can cause birth defects or the death of the embryo. Teratogens include alcohol, tobacco smoke, drugs, some viruses and bacteria, and even some seemingly benign medications, such as aspirin. Because the embryonic period includes organogenesis, exposure to teratogens at this time can result in the malformation of some or all organ systems.

Although rudimentary versions of most organ systems have formed during the embryonic period, different organ systems undergo peak development periods at different times. A peak development period is a time frame where most of the cellular organization and construction of the organ framework occurs. For example, the peak development for limb maturation is weeks 4 to 8, whereas peak development of the external genitalia begins in the late embryonic period and continues through the early fetal period. Teratogens cause the most harm to an organ system during its peak development period. So, a drug such as thalidomide (which causes limb defects) causes the most limb development damage if taken during pregnancy when the embryo is between weeks 4 to 8 of development.

The fetal period extends from the beginning of the third month of development (week 9) to birth. It is characterized by maturation of tissues and organs, and rapid growth of the developing fetus. Fetal length increases dramatically in months 3 to 5. The length of the fetus is usually measured in centimeters, either as the crown–rump length (CRL) or the crown–heel length (CHL). The 2.5-centimeter (1-inch) embryo will grow in the fetal period to an average total length of 53 centimeters (21 inches).

Fetal weight increases steadily as well, although the weight increase is most striking in the last 2 months of pregnancy. The average weight of a full-term fetus typically ranges from 2.5-4.5 kilograms (5.5–9.9 pounds).

Pregnancy is an approximately 9-month process that, if all goes well, leads to the birth of a healthy baby. However, pregnancy also has dramatic anatomic and physiologic effects on the carrier of the baby. Some of these changes can be very demanding, as the carrier’s body adapts to the changes associated with the pregnancy. A significant observation to keep in mind is that great variation exists in how individuals experience pregnancy.

The length of the pregnancy is subdivided into trimesters:

The first trimester encompasses the first 3 months of pregnancy (or the first 12 weeks of development of the embryo and fetus). During this time period, the zygote develops into an embryo and then into an early fetus.

The second trimester includes months 4 to 6 of pregnancy and is marked by growth of the fetus and expansion of maternal tissues.

The third trimester encompasses months 7 to 9 of pregnancy. During this time period, the fetus grows most rapidly and gains weight, and the mother’s body prepares for the eventual labor and delivery.

Individuals may experience their pregnancies very differently. For example, some may have little or no “morning sickness” that is common in the first trimester of the pregnancy, whereas others may have to be hospitalized due to extreme nausea and vomiting that last well past the first trimester, known as hyperemesis gravidarum. Some may have little weight gain, whereas others may gain a significant amount of weight. Even the length of the pregnancy is variable- some may deliver well before their projected due dates, whereas some may need to have labor induced because they are well past the due date. In addition, one individual may have a different experience for each of their pregnancies. One pregnancy may be uneventful, whereas another may have medical complications; or one birth may be long and difficult, and another relatively quick and not difficult. Please keep in mind that every pregnancy, and how it is experienced by the carrier, is unique.

Recall that when the blastocyst implants in the uterus, its syncytiotrophoblast begins secreting large amounts of human chorionic gonadotropin (hCG). During the first trimester of pregnancy, hCG levels remain high to maintain the corpus luteum (so it continues to produce progesterone and estrogen), but then hCG levels decline. When hCG declines, the corpus luteum degenerates as well—but by this time, the corpus luteum is no longer needed because the placenta is producing progesterone and estrogen to maintain the pregnancy.

In the second and third trimesters of pregnancy, the placenta is the major producer of progesterone and estrogen. The high levels of progesterone and estrogen suppress FSH and LH secretion, so the ovarian cycle and additional follicular development are arrested during the pregnancy. Progesterone is responsible for continued growth of the functional layer of the endometrium (and prevention of menstruation) during pregnancy. Both progesterone and estrogen facilitate uterine enlargement, breast enlargement, and fetal growth.

Progesterone and estrogen also have a dramatic effect on the integumentary system; many pregnant individuals report faster growing and stronger nails (likely due to increased levels of these hormones), and their hair tends to be fuller and thicker in response to these hormones (because the hormones prevent typical cyclical hair loss, and a greater percentage of hair follicles remain in the resting stage). In addition, estrogen is primarily responsible for relaxation of many ligamentous joints, such as the sacroiliac joints and pubic symphysis, in preparation for labor.

Relaxin is another hormone that is secreted by the corpus luteum and placenta. Despite its name, research suggests that this hormone is not responsible for the ligament relaxation seen in pregnancy. Rather, relaxin appears to promote blood vessel growth in the uterus. The placenta also becomes a major secretor of corticotropin-releasing hormone (CRH). Recall that small amounts of CRH are produced and released by the hypothalamus and stimulate the anterior pituitary to secrete adrenocorticotropic hormone (ACTH), which acts on the adrenal cortex to release glucocorticoids (ex; cortisol). The placenta also secretes CRH during pregnancy, but in much larger amounts than that of the hypothalamus. CRH is thought to play a role in regulating the length of pregnancy and the timing of childbirth. CRH also is responsible for the rise in aldosterone in the mother, which promotes fluid retention and an overall increase in blood volume during pregnancy. (Aldosterone increases sodium and water retention.) Thus, edema may be experienced by the carrier during the later stages of pregnancy.

Human placental lactogen (HPL), also known as human chorionic somatomammotropin (hCS), is secreted by the developing placenta— specifically, by the syncytiotrophoblast cells. The levels of this hormone rise linearly beginning the fifth week to maximum levels by the thirty-sixth week of development. Although this hormone is named for its effects on inducing lactation in mammals generally, its effects on human lactation have not been demonstrated. Specifically, HPL does affect the metabolism of certain nutrients— the carrier metabolizes more fatty acids instead of glucose, leaving greater glucose reserves for the fetus. HPL also inhibits the effects of insulin, so there are greater circulating levels of glucose in the blood (again, for use by the fetus).

Prolactin and oxytocin levels also increase. Prolactin is produced by the anterior pituitary and is responsible for milk production. Prolactin levels increase 10-fold during pregnancy to ensure that lactation occurs after giving birth. Oxytocin is produced by the hypothalamus and is involved in uterine contractions as well as milk expulsion from the mammary glands of the breast. Oxytocin levels increase in the second and third trimesters, in response to rising estrogen levels, and peak during labor.

The uterus undergoes a dramatic metamorphosis during pregnancy. Prior to pregnancy, the uterus is approximately 8 cm by 5 cm (3 inches by 2 inches) and located within the pelvic cavity. Once implantation occurs, the uterus begins to enlarge and expand as its muscle cells hypertrophy and undergo hyperplasia. Uterine enlargement can be detected during a vaginal exam by 4 weeks after fertilization, and by 12 weeks (the end of the first trimester) the uterus is just superior to the level of the pubic symphysis and is about the size and shape of a large grapefruit. As the uterus expands, it impinges on the space occupied by the urinary bladder, so more frequent urination during this trimester is common. Recall that the developing fetus has a crown-to-rump length of only 9 cm at this time, so the bulk of the enlargement is due to myometrium muscle hypertrophy and hyperplasia, placental growth, and amniotic fluid production.

By 16 weeks (4 months), the uterus has expanded into the abdominal cavity and its fundus typically is at a midpoint level between the pubic symphysis and umbilicus. The uterus continues to expand and reaches the level of the umbilicus by about week 22. During this second trimester, the superior growth of the uterus temporarily decreases pressure on the urinary bladder, so the frequent need to urinate may lessen during this trimester.

The expansion continues during the third trimester, as now the fetus is preparing for its own rapid growth sequence. By about 28 weeks (7 months), the fundus of the uterus is superior to the umbilicus, and by the ninth month the fundus of the uterus is at the level of the xiphoid process of the sternum. The enlarged uterus pushes against the diaphragm and compresses many of the abdominopelvic organs, often resulting in certain gastrointestinal (GI) ailments (described in the next section). In addition, now the uterus is so large that it compresses the bladder, so frequent urination is once again an issue.

The breasts typically are tender and sore during the first trimester due to the increasing levels of estrogen and progesterone. The placenta secretes melanocyte-stimulating hormone (MSH), which is in part responsible for the darkening of the areolae and nipples during this time. MSH also is responsible for a darkening of the linea alba, the ligamentous connection between left and right rectus sheaths, turning it into a temporary vertical dark line called the linea nigra. Mammary glandular tissue grows and additional acini develop, especially under the influence of prolactin. It is typical during pregnancy to increase one bra cup size due to breast growth.

Human placental lactogen (HPL), which is secreted by the placenta, affects how a pregnant individual utilizes glucose by stimulating cells to use fatty acids instead of glucose; this increases the amount of available glucose for the developing fetus. The elevated levels of HPL, as well as higher levels of corticosteroids (ex; cortisol), estrogen, and progesterone, also result in increased insulin resistance in the pregnant person. This increased insulin resistance in some cases can lead to gestational diabetes.

Many carriers may experience morning sickness during the first trimester of their pregnancy. Contrary to its name, morning sickness does not occur just in the morning, although typically symptoms tend to be most severe then. There are several hypotheses about the cause of morning sickness, one hypothesis suggesting that morning sickness is an evolutionary adaptation to protect the developing fetus from harmful toxins in food. Individuals with morning sickness tend to prefer bland carbohydrates (which may be less likely to be spoiled or have toxins) and may have aversions to meat and eggs (which may be more likely to have toxins or be spoiled with pathogens). Another hypothesis suggests that high levels of selected circulating hormones may be the cause of nausea and vomiting associated with pregnancy. Until recently, many researchers believed that high levels of hCG hormone were the culprit, although several research studies have not been able to prove this. A 2024 research study implicates GDF15 (growth differentiation factor 15), a hormone that is produced by many body cells inresponse to a stress on the body and acts on the brainstem to stimulate nausea and vomiting. This research study found a strong positive correlation between GDF15 maternal circulation and severity of pregnancy-related nausea and vomiting symptoms, with those experiencing hyperemesis gravidarum (HG) having some of the highest GDF15 levels.

The higher circulating levels of progesterone result in relaxed smooth muscle and thus slowed intestinal motility, so digested materials remain in the GI tract for longer periods of time. In the later stages of pregnancy, the expanding uterus compresses the abdominal organs and may impinge on part of the intestines. All of these factors may result in heartburn and indigestion, as well as an increased risk of constipation. Chronic constipation, as well as problems with venous circulation (caused by compression of the lower veins by the fetus) also can lead to hemorrhoids.

During the pregnancy, an additional 300 calories typically are needed to meet the metabolic needs of both the mother and fetus. Adequate levels of folic acid, calcium, protein, and iron are especially important during pregnancy. Weight gain typically occurs during pregnancy, but only about 20 pounds of this weight gain is due to the fetus, placenta, breast and uterine enlargement, and fluid retention. Any additional weight gain typically is additional adipose tissue, fluid retention, or both.

Because of the needs of both the expectant carrier and the embryo/fetus, the cardiovascular system of the carrier undergoes dramatic changes throughout pregnancy. The carrier’s respiratory system function also becomes altered to meet increased requirements for gas exchange.

The carrier’s cardiovascular system must distribute respiratory gases and nutrients to both the mother and the growing fetus. More blood is needed, so plasma volume increases by about 50% throughout pregnancy. The heart must work harder to circulate the increased blood volume. Cardiac output (amount of blood pumped per minute) increases 30–50% beginning at week 6 of pregnancy and peaks about weeks 24–28 of pregnancy, before dropping slightly. To increase cardiac output, the body increases both heart rate (on average an increase of 10 to 20 beats per minute) and stroke volume.

The increase in blood volume may initially cause an increase in blood pressure during the first trimester. However, by the second trimester the blood pressure drops because of a decrease in peripheral vascular resistance that results from both a decrease in blood viscosity (hematocrit levels typically are lower during pregnancy due to relatively greater proportion of plasma to erythrocytes) and a decreased sensitivity to the hormone angiotensin II, which is a potent vasoconstrictor.

By the third trimester, the uterus and fetus compress the abdominal blood vessels, so venous return from the lower part of the body may be impaired. Thus, pregnancy may cause the development of varicose veins, hemorrhoids, and edema in the lower limbs.

Earlier we mentioned that in the last trimester of pregnancy, the expanding uterus prevents the diaphragm from fully flattening inferiorly when contracted, and the lungs from fully expanding with air. To partially compensate for these vertical dimensional changes of the thorax, chest width increases (due to ribs not completely depressing) so total lung capacity is preserved. Dyspnea is shortness of breath and may occur during periods of exertion. Increased estrogen levels may cause increased blood circulation and fluid retention in the nasal cavity mucosa, resulting in nasal congestion. The expectant carrier also may experience epistaxis (nosebleeds) and bleeding of the gums due to the increased blood circulation.

Progesterone increases the sensitivity of chemoreceptors to blood carbon dioxide (CO2) levels, ultimately functioning to lower the blood CO2 levels. These lower blood CO2 levels facilitate the diffusion of gases across the placenta from the fetal blood to the carrier’s blood. To lower the blood CO2 levels, the tidal volume increases by 30–40%, and minute volume increases due to this increased tidal volume and unchanged respiration rate. Additionally, the carrier’s oxygen consumption increases about 20–30% to meet the oxygen demands of both mother and fetus. These alterations provide enough oxygen to mother and fetus, as well as facilitate gas exchange between the placenta and the maternal blood.

Metabolic waste produced by both the carrier and the fetus are eliminated by the expectant carrier’s urinary system. In addition, up to 50% more plasma volume must be filtered by the kidneys. Thus, glomerular filtration rate increases about 30–50% during pregnancy, and urine output increases slightly.

Recall that compression by the expanding uterus on the urinary bladder can lead to frequent urination in both the first and third trimesters. In contrast, the uterus places relatively less pressure on the bladder during the second trimester.

Progesterone causes smooth muscle relaxation in the ureters, which may cause expansion of the ureters and renal pelvis of the kidneys. This dilation and the increased urine volume may result in urine stasis (slowing or stopping) from the kidneys to the urinary bladder. In addition, compression of the ureter or kidney by the uterus can result in urine drainage issues. All of these factors greatly increase the risk for urinary tract infections (UTIs), which are perhaps the most common type of bacterial infection during pregnancy.

Labor is also known as parturition, and is the process of physical expulsion of the fetus and placenta from the uterus. True labor typically occurs at 38 weeks for a full-term pregnancy, but not all uterine contractions lead to true labor.

Throughout the pregnancy, as the uterus enlarges and stretches, the uterine myometrium prepares itself for uterine contractions. In the later stages of pregnancy, the increasing levels of estrogen counteract the inhibiting effects of progesterone on the uterine myometrium and increase the uterine myometrium sensitivity. In addition, the rising levels of estrogen stimulate the production of oxytocin receptors on the smooth muscle cells of the uterine myometrium, so as the levels of oxytocin also rise, more receptors are available on the uterus for binding this hormone.

All of these factors result in the uterine myometrium becoming more sensitive and “irritable” in the later stages of pregnancy, and contractions begin to occur. These contractions typically are weak and irregular, but as levels of estrogen and oxytocin continue to rise in the later stages, they become more intense and frequent. Thus, weak contractions may occur and be noticed as soon as the second trimester of pregnancy.

Premature labor refers to labor that occurs prior to 38 weeks. Premature labor (and giving birth to a premature infant) is not desirable because the infant’s body systems, especially the lungs, may not be fully developed. Very premature infants are at greater risk for morbidity and mortality due to their underdeveloped organ systems. Thus, the ideal outcome is for labor to begin as close as possible to full term.

False labor is defined as uterine contractions that do not result in the three stages of labor and the expulsion of the fetus. The contractions of false labor are known as Braxton-Hicks contractions, named for a nineteenth-century gynecologist. It may be difficult for a person to know whether they are experiencing Braxton-Hicks contractions or true labor contractions, and it is not uncommon for Braxton-Hicks contractions to be mistaken for true labor contractions.

In general, Braxton-Hicks contractions have the following characteristics;

They tend to be irregularly spaced and do not become more frequent as time passes.

The pain from these contractions is usually limited to the lower abdomen and pelvic region, instead of radiating through the entire abdominal region and back (as with true labor contractions).

The pain from the contractions may change or stop in response to movement, like going for a walk.

They tend to be relatively weak, and do not increase in intensity.

They do not lead to the cervical changes seen in the three stages of labor.

True labor is defined as uterine contractions that increase in intensity and regularity, and that result in changes to the cervix. The carrier and the fetus both have an active role in initiating true labor.

As the pregnancy nears term, the carrier’s hypothalamus triggers the posterior pituitary to release increasing levels of oxytocin. (This increase in oxytocin levels is in response to a cascade of changes in both fetal and maternal hormones responsible for maintaining preg- nancy.) Near the beginning of true labor, the fetus’s hypothalamus is also triggering release of oxytocin from the fetus’s posterior pituitary. Oxytocin from both the mother and fetus causes two primary effects: a) contraction of the smooth muscle of the uterus and b) stimulation of the placenta to secrete prostaglandins. Prosta- glandins are eicosanoids that act as local hormones to stimulate smooth muscle contraction, most notably uterine muscle contraction. Prostaglandins are also responsible for the softening and dilating of the cervix. The combined actions of maternal oxytocin, fetal oxytocin, and the rising levels of prostaglandins initiate the rhythmic contractions of true labor.

In comparison to Braxton-Hicks contractions, true labor contractions have the following characteristics;

They tend to be regularly spaced and increase in frequency over time. For example, contractions that begin with a frequency of roughly every 15 minutes eventually will increase in frequency to about every 5 minutes.

Contractions increase in intensity as labor progresses.

The pain from the contractions tends to radiate from the upper abdomen inferiorly to the lower back (or vice versa), instead of being localized in the lower abdomen or groin (as with Braxton-Hicks contractions).

The pain from the contractions does not go away or change in response to movement.

The contractions facilitate cervical dilation and expulsion of the fetus and placenta

True labor also initiates a positive feedback mechanism. The more intense uterine contractions result in the fetus’s head pushing against the cervix, stimulating the stretching and dilation of the cervix. This manual stretching of the cervix and uterine contractions initiate sensory input to the hypothalamus, causing it to stimulate the posterior pituitary to secrete more oxytocin. In addition, uterine contractions stimulate the placenta to secrete more prostaglandins, which also result in more intensive uterine contractions. Thus, true labor intensifies until the fetus is expelled from the uterus. Once the fetus and placenta are expelled (and thus the major source of prostaglandins is removed from the body) and the uterus and cervix are no longer fully stretched, oxytocin levels drop and labor ceases.

True labor involves three stages: the dilation stage, the expulsion stage, and the placental stage.

The dilation stage begins with the onset of regular uterine contractions and ends when the cervix is effaced (thinned) and dilated (expanded) to 10 centimeters in diameter. This is the longest of the three stages and is the stage marked by the greatest variability. Individuals who are nulliparous (those who have never given birth before) generally experience a longer dilation stage—on average, 8 to 24 hours—than do parous individuals (those who have given birth previously). The dilation stage in parous individuals may range from 4 to about 12 hours.

The dilation stage starts with regularly spaced uterine contractions that increase in intensity and frequency. Each time the uterus contracts, the baby’s head pushes against the cervix and causes it to efface and dilate slightly, until the cervix dilates from 1 cm to 10 cm in diameter.

This stage is also marked by the rupture of the amniotic sac and the release of amniotic fluid, also commonly known as the water breaking. If the amniotic sac doesn’t rupture on its own by the end of this stage, the obstetrician or other birth practitioner will manually rupture the sac in preparation for the expulsion stage.

The expulsion stage begins with the complete dilation of the cervix and ends with the expulsion of the fetus from the carrier’s body. This stage may last as little as several minutes but typically takes 30 minutes to several hours. As with the dilation stage, nulli parous people typically have a longer expulsion stage than parous people. The uterine contractions help push the fetus through the vagina.

When the first part of the baby’s calvarium dis tends the vagina, this is referred to as crowning. The head is then followed by the rest of the body. If there is difficulty in expelling the baby from the vagina, then an episiotomy may be performed, in which is where the perineal muscles are surgically incised to create a wider opening for the baby to pass through. This cut is sutured after the birth. When the baby’s body is fully expelled, the umbilical cord is clamped and tied off.

The placental stage occurs after the baby is expelled. The uterus continues to contract, and these contractions help compress uterine blood vessels and help displace the placenta from the uterine wall. The placenta and remaining fetal membranes collectively are referred to as the afterbirth. The expulsion of the afterbirth typically is completed within 30 minutes. The obstetrician or other birth practitioner carefully examines the afterbirth to make sure all portions of the placenta have been expelled from the uterus, because fragments of placenta left in the uterus can lead to extensive bleeding or other postpartum complications.

Once the fetus is expelled from the uterus, it is now known as a newborn, or neonate (neo = "new", natalis = relating to birth). A variety of respiratory and cardiovascular changes must occur quickly after birth in order for the neonate to adjust to life outside of the uterus.

Prior to birth, respiratory gases were exchanged between maternal and fetal circulation at the placenta. The fetal lungs are not fully inflated because they are not yet fully functional. However, within about 10 seconds after being born, the neonate typically takes its first breath. This first breath is thought to be caused by the central nervous system responding to the change in environment and temperature. This process may be facilitated by a general respiratory acidosis (caused by clamping of the umbilical vessels and constriction of the umbilical vessels prior to birth), but note that the first breath typically occurs regardless of whether the umbilical vessels have been clamped or not.

Once this first breath is taken, the lungs become inflated and the surfactant that is present in the alveoli keeps the alveoli open. Thus, every breath after the first is easier now that the alveoli remain open. Preterm infants born earlier than 28 weeks are not producing sufficient levels of surfactant to keep their alveoli open, so these infants may need to be placed on a ventilator until their lungs mature.

Given that the fetal lungs are not functional, other pathways (ex, ductus arteriosus, foramen ovale) shunt blood away from the non-functional lungs and directly to the fetal circulation. As a result, the fetal cardiovascular system has some structures that are modified or that cease to function once the fetus is born.

At birth, the fetal circulation begins to change into the postnatal pattern. When the neonate takes its first breath, pulmonary resistance drops, and the pulmonary arteries dilate. As a result, pressure on the right side of the heart decreases and the pressure is then greater on the left side of the heart, which handles the systemic circulation.

Postpartum refers to the first 6 weeks after giving birth. During this time, a carrier’s body undergoes additional transformative changes to both feed the neonate and return to pre-pregnancy form and function.

Within a few days after giving birth, estrogen and progesterone levels plummet, because the uterine lining no longer needs to be maintained for pregnancy. Many experts believe this precipitous drop in sex hormone levels may account for the "baby blues", feelings of varying degrees of sadness and depression some individuals experience immediately after giving birth.

As estrogen and progesterone levels plummet, the integumentary system is affected. Recall that high levels of these hormones prevent the regular cyclical hair loss. After giving birth, the hair reverts back to its regular cyclical growth and hair loss cycle. And, in fact, some of the hair that was prevented from falling out during pregnancy may fall out rather abruptly for some mothers after giving birth. A peak in hair loss may be experienced by some about 3 to 4 months after delivery, and it may take up to 12 months for the regular cyclical hair growth and loss cycle to resume. Thus, many new parents may experience temporary hair thinning during this time.

The decrease in progesterone also affects the respiratory system. Without the high levels of progesterone, the chemoreceptors are less sensitive to CO2 levels. As a result, tidal volume and minute ventilation return to pre-pregnancy levels.

Additionally, the levels of corticotropin-releasing hormone (CRH) drop dramatically, now that there is no longer a placenta producing copious amounts of this hormone. Recent research has suggested that high levels of CRH during pregnancy are associated with an increased risk of postpartum depression, a serious disorder in which the mother experiences severe depression and possibly suicidal thoughts; this condition should be treated as soon as possible.

Prolactin levels and oxytocin levels drop after birth as well. However, because both of these hormones are involved in lactation, periodic surges occur in these hormone levels each time a baby nurses.

A great deal of fluid is retained within the body throughout the 9 months of pregnancy. In addition to the fluid retained in the amniotic sac and some excess fluid found in the interstitial spaces, most additional fluid is due to the increased blood volume acquired during pregnancy. After giving birth, there no longer is a need for this additional fluid and it must be expelled in a relatively quick and efficient manner. The amniotic fluid is quickly expelled by the end of the first stage of labor. But what about the rest?

A portion of the blood volume, as well as mucus and hypertrophied endometrial tissue, is released from the uterus as lochia. Lochia is similar to a menstrual period, in that blood and some endometrial tissue are expelled from the uterus via the vagina. However, lochia results in much heavier bleeding than a typical menstrual period, because the uterine lining buildup occurred over a 9-month period, instead of a typical 28-day cycle. Thus, the first 5 days of lochia typically result in very heavy bleeding, after which it lightens but progresses for at least 2 to 3 weeks. For some, it may take 4 to 6 weeks before the flow finally stops. As the blood volume decreases, cardiac output returns to pre-pregnancy levels.

Excess fluids also may be expelled by increased urination. The decline in CRH after birth results in a decline in aldosterone, which precipitates the overall drop in blood volume and interstitial fluid levels. The lymphatic system cycles some of the excess interstitial fluid into the blood circulation, where it may be filtered by the kidneys and secreted as urine. Within about 24 hours after giving birth, most individuals experience copious, frequent urination, the result of the kidneys “working overtime” in filtering out this excess fluid. Urination levels typically return to pre-pregnancy levels by the end of the first week after birth.

Another common symptom new parents experience is profuse sweating for the first 2 weeks after giving birth. This abundant sweating is yet another way the body eliminates the excess fluid gained during pregnancy.

Lactation refers to the production and release of breast milk from the breasts. Prolactin is produced by the anterior pituitary and is responsible for milk production. In nonpregnant women and in men, the secretion of significant amounts of prolactin is inhibited by prolactin-inhibiting hormone (also known as dopamine), secreted by cells in the hypothalamus.

High levels of estrogen positively influence the secretion of prolactin, so as estrogen levels rise during pregnancy, so do prolactin levels. Both estrogen and prolactin cause mammary gland acini proliferation and branching of the lactiferous ducts. Paradoxically, the high levels of estrogen and progesterone are also responsible for preventing breast milk secretion until after birth. It is not until levels of estrogen and progesterone drop that prolactin works unopposed to stimulate breast milk production.

During late pregnancy and for the first few days after birth, the substance produced by the mammary glands is not breast milk per se. It is a watery, yellowish, milklike substance called colostrum, and it has lower concentrations of fat than true breast milk but is rich in immunoglobulins, especially immunoglobulin A (IgA). By drinking colostrum, the infant acquires passive immunity from the parent. IgA resists breakdown in the infant’s stomach and is believed to protect the infant against ingested pathogens. Colostrum also has a laxative effect and facilitates the infant’s first bowel movement shortly after birth

A few days postpartum, the true breast milk starts to be produced. It has a higher fat content than colostrum, and it contains several growth factors, essential fatty acids (needed for optimal brain growth and development), specific enzymes to aid in digestion of the milk, and an array of immunoglobulins. Breast milk typically is more easily digestible for an infant than other types of breast milk substitutes (cow’s milk, soy milk) and it remains the optimal source of nutrition for an infant, if the parent is able to breastfeed. One vitamin that is not abundant in breast milk is vitamin D, and recently physicians have recommended that infants that are breastfed receive a vitamin D supplement.

Lactation requires both prolactin for breast milk production and oxytocin for breast milk release. Although prolactin levels drop after birth by about 50%, surges in prolactin continue as long as the baby continues to breastfeed. Thus, the continual production and release of breast milk is a positive feedback mechanism that is maintained by regular breastfeeding.

The release of breast milk is referred to as milk letdown, or the letdown reflex, because it involves this positive feedback mechanism. When the infant suckles at the breast, mechanoreceptors in the nipple and areola are stimulated, and they send sensory input to the hypothalamus. The hypothalamus is stimulated to produce oxytocin, and the posterior pituitary is stimulated to release oxytocin into the blood. The oxytocin targets special cells in the mammary glands called myoepithelial cells, which surround the mammary acini. Specifically, oxytocin stimulates the myoepithelial cells to contract, thereby releasing breast milk from the mammary acini. As milk is released from the breast, the infant may continue to nurse. Milk will continue to be released from the breast as long as the infant continues to nurse. Once the infant stops suckling (and the nipple and areola are no longer being mechanically stimulated), oxytocin levels drop and milk letdown stops.

Milk letdown may be initiated in some parents simply in response to hearing a baby cry. Note that since a baby usually cries when it is hungry, the mother’s milk letdown response may have developed to prepare for the eventual feeding of this baby.

As the infant breastfeeds, prolactin-inhibiting hormone (dopamine) release is inhibited. This decreases prolactin-inhibiting hormone secretion, resulting in the anterior pituitary secreting large amounts of prolactin. Spikes, or peaks, in prolactin production occur each time a baby breastfeeds. This prolactin promotes new breast milk production, so a new supply of breast milk will be available to the baby at the next feeding.

Those that regularly breastfeed (more than four to five feedings a day) usually do not ovulate at this time. Researchers believe that either the hormones or the sensory stimuli that send sensory input to the hypothalamus involved with breastfeeding inhibit release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. If GnRH is not released, then FSH and LH will not be released by the anterior pituitary, and so ovulation is prevented. This mechanism may have evolved as a way of spacing births, so that a nursing mother’s body will not be additionally burdened by a new pregnancy. However, breastfeeding is not a reliable form of birth control because ovulation can and does occur in breastfeeding individuals, especially those who may have reduced numbers of breastfeedings, and it is difficult to determine that ovulation has occurred. Thus, most lactating individuals are encouraged to use some form of birth control if they do not want to become pregnant again at that time.

The uterus increases in size due to both hypertrophy and hyperplasia during the 9 months of pregnancy. It takes 6 weeks following birth for the uterus to shrink to close to its pre-pregnancy size. Oxytocin facilitates this shrinkage by stimulating uterine contractions. These contractions tend to be most severe the first week after giving birth and are referred to as afterpains. Afterpains may be most severe and noticeable during breastfeeding, since oxytocin is involved in milk ejection. After the first week, these contractions will continue but typically will be less noticeable.

The spike in oxytocin that occurs with each breastfeeding event not only expels the milk but also stimulates uterine contractions. Thus, regular breastfeeding facilitates rapid, efficient shrinkage of the uterus. Although these contractions occur in postpartum individuals who don’t breastfeed, they may not be as frequent or as efficient, and the uterus may not return to its pre-pregnancy size as quickly.

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