Chapter 10: Pregnancy, Development, and Aging PDF

Enter word / phrase to search UBook text Automatic ZoomActual SizePage Width100%50%75%100%125%150%200%300%400% Chapter 10: Pregnancy, Development, and Aging 359 Lesson 10.4 **Gestation** Introduction **Gestation** (ie, pregnancy) generally lasts approximately 38 weeks, from ovulation until bi...

Enter word / phrase to search UBook text Automatic ZoomActual SizePage Width100%50%75%100%125%150%200%300%400% Chapter 10: Pregnancy, Development, and Aging 359 Lesson 10.4 **Gestation** Introduction **Gestation** (ie, pregnancy) generally lasts approximately 38 weeks, from ovulation until birth. However, the gestation period is often expressed as 40 weeks when considered from the beginning of the last menstrual cycle. During gestation, many maternal changes occur to support the growing fetus and to prepare the body for delivery (ie, parturition) and lactation (ie, synthesis and secretion of milk). This lesson provides an overview of gestation, fetal circulation, parturition, and lactation. 10.4.01 Pregnancy As discussed in Lesson 10.2, the first stage of gestation (the **embryonic period**) occurs within the first eight weeks following fertilization. The embryonic period begins with zygote formation (week two of pregnancy), and by the end of this period, the embryo has initiated the development of all major organ systems. The **fetal period** begins at the ninth week after fertilization (week 11 of pregnancy) and lasts until birth. Relatively few new structures are formed during the fetal period, but fetal growth is significant during this time. Gestation is generally divided into three equal parts known as **trimesters**. The first trimester (weeks 1--12) includes fertilization, implantation, the embryonic period, and the first stages of the fetal period. By the second trimester (weeks 13--26), the placenta is fully formed and functions to sustain the fetus while secreting pregnancy hormones (eg, human chorionic gonadotropin, estrogen, progesterone). The third trimester begins at week 27 and lasts until the end of pregnancy (weeks 38--40). A timeline of the development of select embryonic and fetal structures during gestation is shown in Figure 10.20. Chapter 10: Pregnancy, Development, and Aging 360 **Figure 10.20** Timeline of the development of select embryonic and fetal structures during gestation. 10.4.02 Fetal Circulation The fetus acquires oxygen (O2) and nutrients and eliminates carbon dioxide (CO2) and waste through the maternal circulatory system. Once the fetal circulatory system is functional, fetal-maternal materials are exchanged through the **placenta**. The placenta is attached to the fetus at the **umbilicus** (ie, navel) via the **umbilical cord**, which is derived from the embryonic yolk sac and allantois (see Concept 10.1.02). Typically, there is no mixing of maternal and fetal blood because the exchange of materials occurs via diffusion through capillary walls. Fetal red blood cells contain a specialized type of hemoglobin (**fetal hemoglobin** \[**hemoglobin F**\]), which has a greater O2 affinity than adult hemoglobin (**hemoglobin A**), thereby favoring O2 transfer from the maternal blood supply to fetal blood (see Concept 13.1.03). Embedded in the uterine wall, the placenta contains many small [blood vessels](javascript:void(0)) emerging from the umbilical cord and branching into capillaries in the **chorionic villi** of the placenta (Figure 10.21). O2 and nutrients are transported from a uterine artery into the **intervillous space** (ie, space around the chorionic villi), and eventually diffuse into fetal capillaries connected to the unpaired **umbilical vein**. CO2 and wastes from fetal blood are transported via paired **umbilical arteries** into fetal capillaries at the placenta and diffuse into the intervillous space and subsequently into a uterine vein. A diagram of stages of a baby Description automatically generated Chapter 10: Pregnancy, Development, and Aging 361 **Figure 10.21** Fetal and maternal circulation at the placenta. The placenta also functions as a protective barrier. Although most bacteria and viruses cannot cross the placenta, certain pathogens (eg, HIV, *Treponema pallidum* \[causes syphilis\], rubella virus \[causes German measles\]) can travel through the placenta, potentially leading to birth defects and/or fetal disease. Certain maternal [immunoglobulins](javascript:void(0)) (ie, antibodies) can cross the placenta, conferring partial pathogen immunity to the fetus, and are thought to function in fetal immune system \"training.\" Oxygenation of fetal blood occurs in the placenta, not the fetal lungs. Therefore, fetal circulation to and from the placenta is reminiscent of the [pulmonary circulation](javascript:void(0)), in which pulmonary veins carry oxygenated blood from the lungs to the heart and pulmonary arteries carry deoxygenated blood from the systemic circulation to the lungs (see Concept 13.1.07). After acquiring O2 and nutrients from the maternal circulation at the placenta, oxygenated fetal blood returns to the fetus via a single umbilical vein in the [umbilical cord](javascript:void(0)), and deoxygenated blood is transported into the placenta from the fetus via two umbilical arteries in the umbilical cord (Figure 10.22). Because some fetal organs (eg, lungs, liver) are not functional during gestation, there are several key differences between the fetal and postnatal circulatory systems. Oxygenated blood (ie, high O2 saturation \[SpO2\]) enters the fetus via the umbilical vein, which divides into two branches at the fetal liver. Most of the blood flows into one branch, the **ductus venosus**, which bypasses the liver and connects with the inferior vena cava. Deoxygenated blood (low SpO2) returning from the fetal systemic circuit enters the venae cavae, mixes with the oxygenated blood from the ductus venosus, and passes into the right atrium (Figure 10.22).  Chapter 10: Pregnancy, Development, and Aging 362 **Figure 10.22** Fetal circulatory system. An opening in the fetal heart called the **foramen ovale** acts as a one-way valve that connects the right and left atria. Most of the oxygenated blood entering the right atrium (ie, from the ductus venosus) passes through the foramen ovale into the left atrium and joins the systemic circulation via the aorta. The small amount of blood that passes into the right ventricle (rather than moving via the foramen ovale) is pumped into the pulmonary trunk and directly into the **ductus arteriosus**, a vessel that bypasses the lungs, connecting the pulmonary trunk directly to the descending aorta. This deoxygenated blood mixes with the O2-rich blood in the descending aorta, sending moderately oxygenated blood to the lower body of the fetus. Deoxygenated blood returning from the fetal systemic circulation is transported back to the placenta via the umbilical arteries (Figure 10.22). A summary of fetal circulatory structures and their functions can be found in Table 10.3. A diagram of the human body Description automatically generated Chapter 10: Pregnancy, Development, and Aging 363 **Table 10.3** Fetal circulatory structures. Directly following birth, the infant takes its first breaths, and O2 in the now-functional lungs signals the cessation of placental blood flow. In addition, breathing via the lungs leads to pressure changes that cause the ductus arteriosus, ductus venosus, and foramen ovale to close, a process that typically begins 12-24 hours after birth. 10.4.03 Parturition Typically, when a pregnancy has reached full term (38--40 weeks), the fetus exits the uterus through the vagina, a process known as **parturition** (ie, childbirth). **Labor** is the process by which childbirth occurs and is triggered by hormones from both the placenta and the fetus, along with mechanical cues. The initiation of labor is not well understood, but the process likely depends on a combination of maternal and fetal signals. When labor begins, increased pressure on the cervix causes impulses to be sent to neurosecretory glands in the hypothalamus, causing the hormone [oxytocin](javascript:void(0)) to be secreted via the posterior [pituitary](javascript:void(0)) [gland](javascript:void(0)). Oxytocin secretion stimulates the release of **prostaglandins** in the uterine myometrium, causing uterine contractions. A **positive feedback** loop is thus initiated: Each contraction causes more pressure on the cervix, sending increased signals for oxytocin release. When the infant is born, the positive feedback loop is broken because pressure on the cervix is relieved, as illustrated in Figure 10.23.  Chapter 10: Pregnancy, Development, and Aging 364 **Figure 10.23** Hormonal control of parturition. Labor can be divided into three stages, as shown in Figure 10.24: 1.**Dilation of the cervix:** From the onset of regular uterine contractions, cervical dilation typically lasts 6--12 hours. During this time, the amniotic sac (ie, fluid-filled sac surrounding the fetus) is usually ruptured. Dilation of the cervix is considered complete at 10 cm. 2.**Expulsion:** Delivery of the infant through the vagina typically occurs within 10 minutes to several hours after complete cervical dilation. 3.**Delivery of the placenta:** The placenta separates from the uterine wall and is typically delivered via the birth canal within minutes to an hour after birth of the infant. A diagram of a baby in uterus Description automatically generated Chapter 10: Pregnancy, Development, and Aging 365 **Figure 10.24** Stages of labor. 10.4.04 Lactation Following childbirth, an infant can no longer rely on the placenta for nutrition and must depend instead on external sources, including breast milk. During puberty, the breasts develop under the influence of estrogen, but do not **lactate** (ie, produce milk). Near the end of pregnancy, the milk-producing **mammary glands** of the breasts develop further and are converted into secretory structures. Fully developed mammary glands are composed of 15--20 lobes, which secrete milk when stimulated. Before delivery, when estrogen and progesterone are high, the mammary glands produce small amounts of a thin, low-fat secretion called colostrum. Within days of delivery, when estrogen and progesterone are decreased, the mammary glands produce milk with a higher fat and calcium concentration than colostrum. Mammary glands also secrete immunoglobulins (ie, antibodies), providing passive immunity to the infant. When the infant latches to the breast, stimulation of mechanoreceptors in the nipples sends signals to the hypothalamus, which stimulates the anterior pituitary gland to secrete **prolactin** and the posterior pituitary gland to secrete **oxytocin**. Prolactin stimulates milk production, whereas oxytocin stimulates the **let-down reflex**, a positive feedback loop resulting in the ejection of milk through milk ducts in the nipples. When the infant stops suckling, the stimulus for hormone release ends, and milk is no longer ejected (Figure 10.25). Enter word / phrase to search UBook text Automatic ZoomActual SizePage Width100%50%75%100%125%150%200%300%400% Chapter 10: Pregnancy, Development, and Aging 367 Lesson 10.5 **Cellular Regeneration and Senescence** Introduction Fetal development ends at birth, but growth and development continue throughout the lifespan of the organism. The ability of a fully developed organism to regenerate tissues varies throughout life, declining with age. In response to cellular injury or damage, an organism may initiate a program of **tissue regeneration** or repair. Alternately, older or damaged cells may enter a **senescent** (ie, growth-arrested) state, with senescent cells accumulating as the organism ages. This lesson discusses the regenerative capabilities of mammalian tissues, as well as the effects of aging and senescence at both the cell and organism levels. 10.5.01 Regeneration With the assistance of adult stem cells, many [tissues](javascript:void(0)) possess self-renewing and self-repairing capabilities. **Tissue regeneration** is a program of cell proliferation and growth that renews some structures and tissues throughout life (eg, [endometrial lining](javascript:void(0)), [red blood cells](javascript:void(0)), [epidermis](javascript:void(0))) or restores damaged tissues with the same functional tissue present before the injury. For example, when the epidermis is injured, a series of regenerative steps leads to the ultimate [replacement](javascript:void(0)) of the damaged area with functional (ie, identical) epidermal tissue. However, some tissues (eg, nerve cells) cannot be replaced. Likewise, when certain tissues (eg, [cardiac muscle](javascript:void(0))) are injured, the injured tissue is replaced with scar (ie, fibrotic) tissue instead of functional tissue during **repair**. Figure 10.26 illustrates the differences between tissue regeneration and repair. **Figure 10.26** Tissue regeneration and repair. In general, mammalian tissues have limited regenerative capabilities. For example, it is impossible for humans to regenerate an amputated limb, but healing near the area of amputation via thick scar tissue is possible. In addition to healing bone fractures and replacing lost blood, humans can also regenerate several other tissues in the body (eg, liver). Although tissue renewal and repair involve the [differentiation of stem cells](javascript:void(0)), regenerating tissues are formed from local stem cell populations in the context of a fully developed organism, rather than in the context of [embryonic development](javascript:void(0)). The potency of adult stem cells is much more restricted than the potency of embryonic stem cells. Mammalian tissues are limited in their regenerative potential due to differences between the embryonic and adult cellular environments.  Chapter 10: Pregnancy, Development, and Aging 368 10.5.02 Cell and Organism Aging **Senescence** is a cellular response that limits the proliferation of aged or damaged cells (Figure 10.27). Although senescence plays a physiological role in tissue homeostasis during normal development, it is also a stress response triggered by events associated with aging (eg, [telomere shortening](javascript:void(0)), genome instability, mitochondrial dysfunction). For example, cells are limited to a finite number of divisions due to the shortening of telomeres with each round of cell division and when telomere lengths are shortened past a critical point, a program of cellular senescence may be initiated. Cellular senescence involves a series of programmed events including [chromatin remodeling](javascript:void(0)), metabolic changes, and increased [autophagy](javascript:void(0)), culminating in stable growth arrest of the senescent cell. Senescent cells often secrete pro-inflammatory [cytokines](javascript:void(0)), leading to both short- and long-term consequences (Figure 10.27). Senescence has numerous physiological roles. For example, a cellular senescence program can be implemented during normal embryonic development, in response to cellular injury, or in transformed (ie, cancerous) cells to prevent potential detrimental effects. **Figure 10.27** Short- and long-term effects of cellular senescence. A diagram of a cell Description automatically generated Chapter 10: Pregnancy, Development, and Aging 369 The role of senescence in cancer development is paradoxical. Senescence can be considered a mechanism of [tumor](javascript:void(0)) suppression, *limiting* the development of cancerous cells by removing the cells from the [cell cycle](javascript:void(0)). However, accumulation of senescent cells may also play a role in *promoting* tumor progression through the secretion of pro-inflammatory cytokines, increasing cancer incidence with age. In addition, cancer cells may begin expressing the enzyme [telomerase](javascript:void(0)), which can replenish telomere ends. Telomerase expression allows cells to divide indefinitely, thereby preventing a protective senescent state. Senescent cells are sometimes eliminated (ie, via [apoptosis](javascript:void(0))), but, in many cases, senescent cells can accumulate over time, leading to decreased organism function. The accumulation of senescent cells is thought to be a contributing factor in organism aging, likely due to the secretion of pro-inflammatory factors by senescent cells (Figure 10.27). As more and more cells enter a senescent state, stem cell numbers decline, leading to the tissue deterioration associated with aging