Chapter 7. Embryogenesis and fetal development. Will Obs

 Chapter 7. Embryogenesis and fetal development

BS. Nguyễn Hồng Anh

Contemporary obstetrics incorporates physiology an pathophysiology o the etus, an its evelopment an environment.

As a result, the etus is consiere a patient an is given the

same meticulous care provie or the mother. Section 6 is

eicate to the etal patient, however, virtually every aspect o

obstetrics can aect the eveloping etus.

GESTATIONAL AGE

Several terms ene pregnancy uration an thus etal age

(Fig. 7-1). Gestational age or menstrual age is the time elapse

since the rst ay o the last menstrual perio (LMP), a time

that actually precees conception. Tis starting time, which is

usually approximately 2 weeks beore ovulation an ertilization an nearly 3 weeks beore blastocyst implantation, has

traitionally been use. Embryologists escribe embryoetal

evelopment in ovulation age, or the time in ays or weeks

rom ovulation. Another term is postconceptional age, which is

nearly ientical to ovulation age.

Until recently, clinicians customarily calculate menstrual age, an with this, term pregnancy averages 280 ays

or 40 weeks between the rst ay o the LMP an birth.

Tis correspons to 9 an 1/3 calenar months. However,

menstrual cycle length variability among women reners

many o these calculations inaccurate. Tis realization, combine with the requent use o rst-trimester sonography, has

le to more accurate gestational age etermination (Duryea,

2015). Much o this change stems rom the accuracy o early

sonographic measurement. As a result, the American College

o Obstetricians an Gynecologists, the American Institute o

Ultrasoun in Meicine, an the Society or Maternal-Fetal

Meicine (2019) together recommen the ollowing:

1. First-trimester sonography is the most accurate metho to

establish or rearm gestational age.

2. In conceptions achieve with in vitro ertilization (IVF), the

embryo age an egg transer ate are use.

3. I available, the gestational ages calculate rom the LMP

an rom rst-trimester sonography are compare, an the

estimate ate o connement (EDC) is recore an iscusse with the patient.

4. Te best obstetrical estimate o gestational age at elivery is

recore on the birth certicate.

Te embryoetal crown-rump length in the rst trimester

is accurate ± 5 to 7 ays. Tus, i sonographic gestational

age iers by more than 5 ays prior to 9 weeks’ gestation,

or by more than 7 ays later in the rst trimester, the EDC is

change. Tese an iscrepant values in the secon an thir

trimester are iscusse urther in Chapter 14 (p. 248).

■ Naegele Rule

An EDC base on the LMP can be quickly estimate as ollows: a 7 ays to the rst ay o the LMP an subtract

3 months. For example, i the rst ay o the LMP was October 5, the ue ate is 10–05 minus 3 (months) plus 7 (ays)

= 7–12, or July 12 o the ollowing year. Tis calculation has

been terme the Naegele rule. Te perio o gestation can also

be ivie into three units o approximately 14 weeks each.

Tese three trimesters are important obstetrical milestones.

In aition to estimating the EDC with either Naegele rule

or “pregnancy wheels,” calculator tools in the electronic meical recor an smartphone applications can provie a calculate

EDC an gestational age. For example, the American College

o Obstetricians an Gynecologists (2020) has evelope a calculator application that incorporates sonographic criteria an

the LMP or embryo transer ate (Chap. 14, p. 248).

EMBRYONIC DEVELOPMENT

Te complexity o embryoetal evelopment is immense.

Figure 7-2 shows a evelopmental sequence o various organ

systems. New inormation regaring organ evelopment

continues to accrue. For example, imaging techniques help

to unravel the contributions o gene regulation an tissue

interaction to eventual three-imensional organ morphology

(Anerson, 2016). Others have escribe the sequence o gene

activation that unerlies cariac evelopment (p. 126).

■ Zygote and Blastocyst Development

During the rst 2 weeks ater ovulation an then ertilization,

the zygote—or preembryo—progresses to the blastocyst stage.

Te blastocyst implants 6 or 7 ays ollowing ertilization. Te

58-cell blastocyst ierentiates into ve cells—the inner cell

mass, which evelops into the embryo. Te remaining 53 cells

orm placental trophoblast. Details o implantation an early

evelopment o the blastocyst an placenta are escribe in

Chapter 5 (p. 86).

■ Embryonic Period

Te conceptus is terme an embryo at the beginning o the

thir week ater ovulation an ertilization. Primitive chorionic

villi orm, an this coincies with the expecte ay o menses.

Te embryonic perio, uring which time organogenesis takes

place, lasts 6 weeks. It begins the thir week rom the LMP

an continues through the eighth week. Te embryonic isc

is well ene, an most pregnancy tests that measure human

Embryonic Period

(Organogenesis) Fetal Period (Growth)

Crown-rump

length (cm)

Period: Implantation

1 2 3

Weight (g)

Brain

Weeks 4 5 6 7 8 9 12

6-7

Neural tube

12 16 21 25 28 32

110 320 630 1100 1700 2500

16 20 24 28 32 36 38

Hemispheres, cerebellum,

ventricles, choroid plexus Temporal lobe, sulci, gyri, cellular migration, myelinization

Lips, tongue, palate, cavitation, fusion

Canals, cochlea, inner ears, ossicles

Face

Eyes

Ears

Pinnae

Diaphragm

Lungs

Heart

Intestines

Urinary tract

Genitalia

Axial skeleton

Limbs

Skin

Optic cups, lens, optic nerves, eyelids

Pinnae

Transverse septum, diaphragm

Tracheoesophageal septum, bronchi, lobes

Primitive tube, great vessels, valves, chambers

Foregut, liver, pancreas, midgut

Glomeruli

Genital folds, phallus, labioscrotal swelling

Vertebral cartilage, ossification centers

Buds, rays, webs, separate digits

Vernix

Brows

Canaliculi Terminal sacs

Eyes open

Abdominal wall,

gut rotation

Mesonephric duct Metanephric duct collecting sytem

Fingernails

Penis, urethra, scrotum

Clitoris, labia

Lanugo hair

FIGURE 7-2 Embryofetal development according to gestational age determined by the first day of the last menses. Times are approximate.Embryogenesis and Fetal Development 123

CHAPTER 7

chorionic gonaotropin (hCG) become positive by this time.

As shown in Figure 7-3, the boy stalk is now ierentiate.

Tere are villous cores in which angioblastic chorionic meso-

erm can be istinguishe an a true intervillous space that

contains maternal bloo.

During the thir week, etal bloo vessels in the chorionic

villi appear. In the ourth week, a cariovascular system has

orme (Fig. 7-4) (Moore, 2008). Tereby, a true circulation

is establishe both within the embryo an between the embryo

an the chorionic villi. Partitioning o the primitive heart

begins. Also in the ourth week, the neural plate orms, an

it subsequently ols to orm the neural tube. By the en o

the th menstrual week, the chorionic sac measures approximately 1 cm in iameter. Te embryo is 3 mm long an can be

Yolk sac

Embryo

Amnion

Chorion

Body stalk Developing villi

Allantois

A C

Yolk

sac

Allantois

Body stalk Chorion

Amnion

Developing

neural groove

B

FIGURE 7-3 Early human embryos. Ovulation ages: A. 19 days (presomite). B. 21 days (7 somites). C. 22 days (17 somites). (After drawings

and models in the Carnegie Institute.)

Otic pit

Lens placode

Arm bud

Leg bud

E

Third

branchial arch

Hyoid

arch

Otic pit

Arm bud

Leg bud

D

Somites

Mandibular

arch

Heart

prominence

C

Neural fold

Rostral neuropore

Neural tube

Somites

Caudal neuropore

B

Neural fold

Rostral neuropore

Neural groove

Neural tube

Caudal neuropore

Somites

A

Mandibular

arch

FIGURE 7-4 Three- to four-week-old embryos. A, B. Dorsal views of embryos during 22 to 23 days of development showing 8 and 12

somites, respectively. C–E. Lateral views of embryos during 24 to 28 days, showing 16, 27, and 33 somites, respectively.124 Placentation, Embryogenesis, and Fetal Development

Section 3

measure sonographically. Arm an leg bus have evelope,

an the amnion is beginning to ensheathe the boy stalk, which

thereater becomes the umbilical cor. At the en o the sixth

week, the embryo is approximately 9 mm long, an the neural

tube has close (Fig. 7-5). Cariac motion is almost always

iscernable sonographically (Fig. 7-6).

Te cranial en o the neural tube closes by 38 ays rom

the LMP, an the caual en closes by 40 ays. Tus, the

neural tube has close by the en o the sixth week. An by

the en o the eighth week, the crown-rump length approximates 22 mm. Fingers an toes are present, an the arms

ben at the elbows. Te upper lip is complete, an the external ears orm enitive elevations on either sie o the hea.

Tree-imensional images an vieos o human embryos rom

the Multi-Dimensional Human Embryo project can be seen

at: embryo.soa.umich.eu/.

FETAL DEVELOPMENT AND PHYSIOLOGY

■ Fetal Period Epochs

Te transition rom embryonic to etal perios occurs at 7 weeks

ater ertilization, corresponing to 9 weeks ater the LMP. At

this time, the etus approximates 24 mm in length, most organ

systems have evelope, an the etus enters a perio o growth

an maturation. Tese phases are outline in Figure 7-2.

A B C

FIGURE 7-5 Embryo photographs. A. Dorsal view of an embryo at 24 to 26 days and corresponding to Figure 7-4C. B. Lateral view of an

embryo at 28 days and corresponding to Figure 7-4D. C. Lateral view of embryofetus at 56 days, which marks the end of the embryonic

period and the beginning of the fetal period. The liver is within the white, halo circle. (From Werth B, Tsiaras A: From Conception to Birth:

A Life Unfolds. New York, Doubleday, 2002.)

A B

FIGURE 7-6 A. This image of an 8-week, 3-day embryo depicts measurement of the crown-rump length, which is 1.93 cm at this gestational age. B. Despite the early gestational age, M-mode imaging readily demonstrates embryonic cardiac activity. The heart rate in this

image is 161 beats per minute.Embryogenesis and Fetal Development 125

CHAPTER 7

12 Gestational Weeks

Te uterus usually is just palpable above the symphysis pubis.

Fetal growth is rapi, an the etal crown-rump length is 5 to

6 cm (Fig. 7-7). Centers o ossication have appeare in most etal

bones, an the ngers an toes have become ierentiate. Skin

an nails evelop, an scattere ruiments o hair appear. Te

external genitalia are beginning to show enitive signs o male or

emale gener. Te etus begins to make spontaneous movements.

16 Gestational Weeks

Fetal growth slows at this time. Te crown-rump length is 12 cm,

an the etal weight approximates 150 g. Clinically, the sonographic crown-rump length is not measure beyon 13 weeks,

which correspons to approximately 8.4 cm. Instea, biparietal iameter, hea circumerence, abominal circumerence,

an emur length are measure. Fetal weight in the secon an

thir trimesters is estimate rom a combination o these measurements (Chap. 14, p. 248).

Eye movements begin at 16 to 18 weeks, coinciing with

mibrain maturation. By 18 weeks in the emale etus, the

uterus is orme an vaginal canalization begins. By 20 weeks

in the male, testicles start to escen.

20 Gestational Weeks

Tis is the mipoint o pregnancy as estimate rom the LMP.

Te etus now weighs somewhat more than 300 g, an weight

increases substantially in a linear manner. From this point

onwar, the etus moves approximately every minute an is

active 10 to 30 percent o the ay (DiPietro, 2005). Brown

at orms, an the etal skin becomes less transparent. Downy

lanugo covers its entire boy, an some scalp hair can be seen.

Cochlear unction evelops between 22 an 25 weeks, an this

maturation continues or 6 months ater elivery.

24 Gestational Weeks

Te etus now weighs almost 700 g. Te skin is characteristically wrinkle, an at eposition begins. Te hea is still

comparatively large, an eyebrows an eyelashes are usually recognizable. By 24 weeks, the secretory type II pneumocytes have

initiate suractant secretion (Chap. 32, p. 587). Te canalicular perio o lung evelopment, uring which the bronchi an

bronchioles enlarge an alveolar ucts evelop, is nearly complete. Despite this, a etus born at this time will attempt to

breathe, but many will ie because the terminal sacs, require

or gas exchange, have not yet orme. Although epenent

on racial an ethnic actors, an as iscusse in Chapter 45

(p. 785), the overall survival rate at 24 weeks barely excees 50

percent (Janevic, 2018). By 26 weeks, the eyes open. Nociceptors are present over all the boy, an the neural pain system is

evelope (Kaic, 2012). Te etal liver an spleen are important early sites or hemopoiesis (Fanni, 2018).

28 Gestational Weeks

Te crown-rump length approximates 25 cm, an the etus

weighs about 1100 g. Te thin skin is re an covere with vernix caseosa. Te pupillary membrane has just isappeare rom

the eyes. Isolate eye blinking peaks at 28 weeks. Te bone

marrow now becomes the major site o hemopoiesis. Te otherwise normal neonate born at this age has a 90-percent chance

o survival without physical or neurological impairment.

32 and 36 Gestational Weeks

At 32 weeks, the etus has attaine a crown-rump length

approximating 28 cm an a weight o about 1800 g. Te skin

surace is still re an wrinkle. In contrast, by 36 weeks, the

etal crown-rump length averages about 32 cm, an the weight

approximates 2800 g (Duryea, 2014). Because o subcutaneous at eposition, the boy is more rotun, an the previous

wrinkle acies are now uller. Normal etuses have a nearly

100-percent survival rate.

40 Gestational Weeks

Tis is consiere term, an the etus is ully evelope. Te

average crown-rump length measures about 36 cm, an the

average weight approximates 3500 g.

■ Central Nervous System Development

Brain Development

Te cranial en o the neural tube closes by 38 ays rom the last

menstrual perio, an the caual en closes by 40 ays. Hence,

olic aci supplementation to prevent neural-tube eects

must be in place beore this point to be ecacious (Chap. 9,

p. 168). Te walls o the neural tube orm the brain an spinal

cor. Te lumen becomes the ventricular system o the brain

an the central canal o the spinal cor. During the sixth week,

the cranial en o the neural tube orms three primary vesicles. In the seventh week, ve seconary vesicles evelop: the

telencephalon—uture cerebral hemispheres; iencephalon—

thalami; mesencephalon—mibrain; metencephalon—pons

an cerebellum; an myelencephalon—meulla. Tis is, in

part, controlle by Hox genes, an eects result in abnormal

signaling that leas to neuropathic anomalies (Arent, 2018).

Meanwhile, fexures evelop an ol the brain into its typical

FIGURE 7-7 This image of a 12-week, 2-day embryo depicts measurement of the crown-rump length. The fetal profile, cranium, and

a hand and foot also are visible in this image.126 Placentation, Embryogenesis, and Fetal Development

Section 3

conguration. Te en o the embryonic perio signies completion o primary an seconary neutralization.

At 3 to 4 months’ gestation, neuronal proliferation peaks.

As expecte, isorers in this cerebral evelopment phase

proounly worsen unction (Ortega, 2017; Volpe, 2018).

One example is Zika virus inection (Rothan, 2019). Neuronal migration occurs almost simultaneously an peaks at 3 to

5 months. Tis process is characterize by movement o millions o neuronal cells rom their ventricular an subventricular zones to areas o the brain in which they resie or lie

(Fig. 7-8). Upregulation o gene expression or neuronal migration has been escribe (Di Donato, 2017). Noninvasive methos to stuy etal neuroevelopment also have been reporte

(Goetzl, 2016; Wang, 2015).

As gestation progresses, the etal brain appearance steaily

changes. Tus, it is possible to ientiy etal age rom its external appearance (Volpe, 2018). Neuronal prolieration an

migration procee along with gyral growth an maturation (see

Fig. 7-8). Sequential maturation stuies using magnetic resonance (MR) imaging have characterize the eveloping etal

brain (Dubois, 2014; Meng, 2012; Wang, 2015).

Myelination o the ventral roots o the cerebrospinal nerves

an brainstem begins at approximately 6 months, but most

myelination progresses ater birth. Tis lack o myelin an

incomplete skull ossication permit etal brain structure to be

seen sonographically throughout gestation.

Spinal Cord

Whereas the superior two thirs o the neural tube give rise

to the brain, the inerior thir orms the spinal cor. In the

embryo, the spinal cor extens along the entire vertebral

column length, but ater that it lags behin vertebral growth.

Ossication o the entire sacrum is visible sonographically by

approximately 21 weeks (Chap. 15, p. 276). By 24 weeks, the

spinal cor extens to S1, at birth to L3, an in the ault to L1.

A B C

FIGURE 7-8 Neuronal proliferation and migration are complete at

20 to 24 weeks. During the second half of gestation, organizational

events proceed with gyral formation and proliferation, differentiation, and migration of cellular elements. Approximate gestational

ages are shown. A. 20 weeks. B. 35 weeks. C. 40 weeks.

Spinal cor myelination begins at migestation an continues

through the rst year o lie. Synaptic unction is suciently

evelope by the eighth week to emonstrate fexion o the

neck an trunk. During the thir trimester, integration o nervous an muscular unction procees rapily (Molina, 2017).

■ Cardiovascular System

Te embryology o the heart is highly complex. At its earliest

stages o ormation, the etal heart unergoes molecular programming, an more than a hunre genes an molecular actors are integral to its morphogenesis (Kathiriya, 2015; Moore,

2020). Tese molecular actors inclue the hypoxia-inducible

factor—HIF an homeobox (HOX)—amily.

o summarize its embryology, the straight cariac tube is

orme by the 23r ay uring an intricate morphogenetic

sequence, uring which each segment arises at a unique time.

Between 4 an 7 weeks the heart unergoes extensive growth

an morphological moication, leaing to the ormation o a

partially septate our-chambere heart with a set o primitive

valves (Sylva, 2014). Te valves evelop, an the aortic arch

orms by vasculogenesis. Chapter 8 o Hurst’s Te Heart has

a ull escription (orres, 2017). Late in etal lie, coronary

angiogenesis vascularizes the myocarium (Lu, 2021).

Fetal Circulation

Tis unique circulation is substantially ierent rom that o

the ault an unctions until birth, when it changes ramatically. For example, etal bloo is oxygenate by the placenta

an oes not nee to enter the pulmonary vasculature. Tus,

most o the right ventricular output bypasses the lungs. In aition, the etal heart chambers work in parallel, not in series.

Tis eectively supplies the brain an heart, compare with the

rest o the boy, with more highly oxygenate bloo rom the

ominant right ventricle.

Oxygen an nutrient materials require or etal growth

an maturation are elivere rom the placenta by the single

umbilical vein (Fig. 7-9). Te vein then ivies into the uctus

venosus an the portal sinus. Te uctus venosus is the major

branch o the umbilical vein an traverses the liver to enter

the inerior vena cava irectly. Because it oes not supply oxygen to the intervening tissues, it carries well-oxygenate bloo

irectly to the heart. In contrast, the portal sinus carries bloo

to the hepatic veins primarily on the let sie o the liver, an

oxygen is extracte. Te relatively eoxygenate bloo rom the

liver then fows back into the inerior vena cava, which also

receives more eoxygenate bloo returning rom the lower

boy. Bloo fowing to the etal heart rom the inerior vena

cava, thereore, consists o an amixture o arterial-like bloo

that passes irectly through the uctus venosus an less welloxygenate bloo that returns rom most o the veins below the

level o the iaphragm. Te oxygen content o bloo elivere

to the heart rom the inerior vena cava is thus lower than that

leaving the placenta.

Because the ventricles o the etal heart work in parallel, this

allows the right ventricle to account or two thirs o the total

cariac output. Well-oxygenate bloo enters the let ventricle,Embryogenesis and Fetal Development 127

CHAPTER 7

which supplies the heart an brain, an less oxygenate bloo

enters the right ventricle, which supplies the rest o the boy.

Congenital cariac eects may contribute to ysregulate

brain evelopment or placenta ysunction (Fantasia, 2018;

Laurisen, 2017).

Tese two separate circulations are maintaine by rightatrium anatomy, which eectively irects entering bloo to

either the let atrium or the right ventricle, epening on

its oxygen content. Tis separation o bloo accoring to its

oxygen content is aie by the pattern o bloo fow in the

inerior vena cava. Te well-oxygenate bloo tens to course

along the orsomeial aspect o the inerior vena cava an the

less oxygenate bloo fows along the lateral vessel wall. Tis

ais their shunting into opposite sies o the heart. Once this

bloo enters the right atrium, the conguration o the upper

interatrial septum—the crista dividens—preerentially shunts

LV

RV

RA

Ductus

arteriosus

LA

Superior vena cava

Foramen ovale

Inferior vena cava

Ductus

venosus

Portal

sinus

Portal v.

Aorta

Umbilical aa.

Umbilical v.

Hypogastric

aa.

Placenta

Oxygenated

Mixed

Deoxygenated

FIGURE 7-9 The intricate nature of the fetal circulation is evident. The degree of blood oxygenation in various vessels differs appreciably

from that in the postnatal state. aa = arteries; LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle; v = vein.128 Placentation, Embryogenesis, and Fetal Development

Section 3

the well-oxygenate bloo rom the meial sie o the inerior

vena cava through the oramen ovale into the let heart. Here,

it is irecte to the heart an brain (Dawes, 1962). Ater these

tissues extract neee oxygen, the resulting less oxygenate

bloo returns to the right atrium through the superior vena

cava. Bloo fow velocity in the superior vena cava rises rom

20 weeks until term (Steopoulou, 2021).

Te less oxygenate bloo coursing along the lateral wall o

the inerior vena cava enters the right atrium an is efecte

through the tricuspi valve to the right ventricle. Te superior

vena cava courses ineriorly an anteriorly as it enters the right

atrium, ensuring that less well-oxygenate bloo returning rom

the brain an upper boy also will be shunte irectly to the

right ventricle. Similarly, the ostium o the coronary sinus lies

just superior to the tricuspi valve so that less oxygenate bloo

rom the heart also returns to the right ventricle. As a result o

this bloo fow pattern, bloo in the right ventricle is 15 to 20

percent less saturate with oxygen than bloo in the let ventricle.

Almost 90 percent o bloo exiting the right ventricle

is shunte through the uctus arteriosus to the escening

aorta. High pulmonary vascular resistance an comparatively

lower resistance in the uctus arteriosus an the umbilical–

placental vasculature ensure that only about 8 percent o right

ventricular output goes to the lungs (Fineman, 2014). Tus,

one thir o the bloo passing through the uctus arteriosus is

elivere to the boy. Te remaining right ventricular output

returns to the placenta through the two hypogastric arteries.

Tese two arteries course rom the level o the blaer along

the abominal wall to the umbilical ring an into the cor

as the umbilical arteries. In the placenta, this bloo picks up

oxygen an other nutrients an is recirculate to the umbilical vein.

Circulatory Changes at Birth

Ater birth, the umbilical vessels, uctus arteriosus, oramen

ovale, an uctus venosus normally constrict or collapse. With

the unctional closure o the uctus arteriosus an the expansion o the lungs, bloo leaving the right ventricle preerentially

enters the pulmonary vasculature to become oxygenate beore

it returns to the let heart (Hillman, 2012). Virtually instantaneously, the ventricles, which ha worke in parallel in etal

lie, now eectively work in series. Te more istal portions

o the hypogastric arteries unergo atrophy an obliteration

within 3 to 4 ays ater birth. Tese become the umbilical ligaments, whereas the intraabominal remnants o the umbilical

vein orm the ligamentum teres. Te uctus venosus constricts

by 10 to 96 hours ater birth an is anatomically close by 2 to

3 weeks. Tis ultimately orms the ligamentum venosum (Fineman, 2014).

Fetoplacental Blood Volume

Although precise measurements o human etoplacental bloo

volume are lacking, Usher an associates (1963) reporte

values in term normal newborns to average 78 mL/kg when

immeiate cor clamping was conucte. Gruenwal (1967)

oun that the etal bloo volume containe in the placenta

ater prompt cor clamping average 45 mL/kg o etal weight.

Tus, etoplacental bloo volume at term is approximately 125

mL/kg o etal weight. Tis is important when assessing the

magnitue o etomaternal hemorrhage, which is iscusse in

Chapter 18 (p. 358).

■ Hemopoiesis

Embryo hemopoiesis begins in the yolk sac an enothelium, ollowe by the liver, an then spleen an bone marrow (Canu,

2021). ransitions are intricate an involve several genes an

protein complexes (Shao, 2018). Both myeloi an erythroi

cells are continually prouce by progenitors that erive rom

hemopoietic stem cells (Fanni, 2018; Heinig, 2015). Te rst

erythrocytes release into the etal circulation are nucleate an

macrocytic. Te mean cell volume is at least 180 L in the embryo

an ecreases to 105 to 115 L at term. Normal ault volume

ranges rom 80 to 95 L. Te erythrocytes o aneuploi etuses

generally o not unergo this maturation an maintain high

mean cell volumes, which average 130 L (Sipes, 1991). As etal

evelopment progresses, more an more circulating erythrocytes

are smaller an nonnucleate. With etal growth, both the bloo

volume in the common etoplacental circulation an hemoglobin

concentration increase. As shown in Table 7-1, etal hemoglobin

concentrations rise across pregnancy. For clinical purposes, the

Society or Maternal-Fetal Meicine (2015) recommens a cuto

etal hematocrit value o 30 percent to ene anemia.

Because o their large size, etal erythrocytes have a short lie

span, which progressively lengthens to approximately 90 ays

at term (Pearson, 1966). As a consequence, re bloo cell concentrations rise. Reticulocytes are initially present at high levels

but ecrease to 4 to 5 percent o the total at term. Fetal erythrocytes ier structurally an metabolically rom those in the

ault (Baron, 2012). Tey are more eormable, which serves

TABLE 7-1. Fetal Hemoglobin Concentrations Across

Pregnancy

Multiples of the Median

Weeks’

Gestation

1.16

(95th

percentile)

1.00

(median)

0.84

(5th

percentile)

grams per deciliter

18 12.3 10.6 8.9

20 12.9 11.1 9.3

22 13.4 11.6 9.7

24 13.9 12.0 10.1

26 14.3 12.3 10.3

28 14.6 12.6 10.6

30 14.8 12.8 10.8

32 15.2 13.1 10.9

34 15.4 13.3 11.2

36 15.6 13.5 11.3

38 15.8 13.6 11.4

40 16.0 13.8 11.6Embryogenesis and Fetal Development 129

CHAPTER 7

to oset their higher volume an viscosity. Tey also contain

several enzymes with appreciably ierent activities.

Erythropoiesis is controlle primarily by etal erythropoietin

because maternal erythropoietin oes not cross the placenta. Fetal

hormone prouction is infuence by testosterone, estrogen,

prostaglanins, thyroi hormone, lipoproteins, an importantly,

by etal hypoxia (eramo, 2018). Serum erythropoietin levels

rise with etal maturity.

Te etal liver is an important source until renal pro-

uction begins near term.

Te erythropoietin concentration in amnionic fui

correlates closely with that

in umbilical venous bloo

obtaine by corocentesis.

Ater birth, erythropoietin

normally may not be etectable or up to 3 months.

In contrast, platelet pro-

uction reaches stable levels

by mipregnancy, although

there is some variation across

gestation (Fig. 7-10). Te

etal an neonatal platelet

count is subject to various

agents, which are iscusse

in Chapter 18 (p. 359).

Fetal Hemoglobin

Tis tetrameric protein is

compose o two copies o

two ierent peptie chains,

95th

100,000

400,000

200,000

300,000

24 26 28 30 32 34 36 38 40 42

Gestational age (weeks)

Platelets (per µL)

50th

5th

FIGURE 7-10 Platelet counts by gestational age obtained the first

day of life. Mean values and 5th and 95th percentiles are shown.

(Data from Christensen RD, Henry E, Antonio DV: Thrombocytosis

and thrombocytopenia in the NICU: incidence, mechanisms and

treatments, J Matern Fetal Neonatal Med 25 Suppl 4:15, 2012.)

FIGURE 7-11 Hemoglobin types transition throughout pregnancy. Alpha (α) and zeta (ζ) globin chains

are interchangeable. The beta (β) globin chain can be replaced by epsilon (ε), gamma (γ), or delta ( δ)

globin chains. In embryonic life (stage I), ζ and ε globin chain production is gradually replaced by α

and γ globin chain production. Hemoglobin F is the main type in fetal life (stage II). After birth (stage III),

HbA1 predominates.

which etermine the type o hemoglobin prouce

(Fig. 7-11). Normal ault hemoglobin A1 is mae o α an

β chains. During embryonic an etal lie, various α an β

chain precursors are prouce. Tis results in the serial pro-

uction o several ierent embryonic hemoglobins. At least

17 genetic loci potentially regulate erythropoiesis (umburu,

2017). Genes or β-type chains are on chromosome 11, an

those or α-type chains on chromosome 16. Each o these

genes is turne on an then o uring etal lie, until α an

β genes, which irect the prouction o ault hemoglobin A1,

are permanently activate.

Te timing o prouction o each o these early hemoglobins

correspons to the site o hemoglobin prouction. Fetal bloo

is rst prouce in the yolk sac, where hemoglobins Gower 1,

Gower 2, an Portlan are mae. Erythropoiesis then moves

to the liver, where etal hemoglobin F is prouce. When

hemopoiesis nally moves to the bone marrow, ault-type

hemoglobin A1 appears in etal re bloo cells an is present

in progressively greater amounts as the etus matures (Lessar,

2018).

Te nal ault version o the α chain is prouce exclusively by 6 weeks. Ater this, there are no unctional alternative

versions, an the gene or the zeta (ζ) globin chain is ownregulate. I the gene coing the α globin chain unergoes

mutation, no alternate α-type chain can be substitute to orm

unctional hemoglobin. In contrast, at least two versions o the

β chain—δ an γ—remain in prouction throughout etal lie

an beyon. With a mutation in the gene coing the β globin

chain, these two other versions o the β chain oten continue

to be prouce, resulting in either hemoglobin A2 (α2δ2) or130 Placentation, Embryogenesis, and Fetal Development

Section 3

hemoglobin F (α2γ2), which substitute or the abnormal or

missing hemoglobin A1.

Genes are turne o by methylation o their control region,

which is iscusse in Chapter 13 (p. 322). In some situations,

methylation oes not occur. For example, in newborns o iabetic women, hemoglobin F may persist ue to hypomethylation o the γ gene (Perrine, 1988). With sickle-cell anemia,

the γ gene remains unmethylate, an large quantities o etal

hemoglobin continue to be prouce. As iscusse in Chapter

59 (p. 1053), elevate hemoglobin F levels are associate with

ewer sickle-cell isease symptoms, an pharmacological moi-

cation o these levels by hemoglobin F–inucing rugs is one

treatment approach (Pasricha, 2018).

Hemoglobins A an F unction ierently. At any given

oxygen tension an at ientical pH, etal erythrocytes that

contain mostly hemoglobin F bin more oxygen than o

those that contain nearly all hemoglobin A (Fig. 50-2, p.

886). Tis is because hemoglobin A bins 2,3-iphosphoglycerate (2,3-DPG) more avily than oes hemoglobin F.

Remember that 2,3-DPG is an intraerythrocyte phosphate,

an hemoglobin has a reciprocal anity or 2,3-DPG an

oxygen (Benesch, 1968). Tus, hemoglobin A’s greater

2,3-DPG bining lowers its oxygen anity compare with

hemoglobin F. Moreover, uring pregnancy, maternal 2,3-

DPG levels are greater, an because etal erythrocytes have

lower concentrations o 2,3-DPG, etal cells have increase

oxygen anity.

Te amount o hemoglobin F in etal erythrocytes begins

to ecrease in the last weeks o pregnancy. At term, approximately three ourths o total hemoglobin levels are hemoglobin

F. During the rst 6 to 12 months o lie, the hemoglobin F

proportion continues to ecline an eventually reaches the low

levels oun in ault erythrocytes (Pasricha, 2018).

Coagulation Factors

With the exception o brinogen, other hemostatic proteins o

not exist in embryonic orms. Te etus starts proucing normal, ault-type procoagulant, brinolytic, an anticoagulant

proteins by 12 weeks. Because they o not cross the placenta,

their concentrations at birth are markely below the levels that

evelop within a ew weeks o lie (Corrigan, 1992). In normal

neonates, the levels o actors II, VII, IX, X, an XI, an o protein S, protein C, antithrombin, an plasminogen, all approximate 50 percent o ault levels. In contrast, levels o actors V,

VIII, XIII, an brinogen are closer to ault values (Saracco,

2009). Maternal vitamin K eciency has been associate with

etal cerebral hemorrhage (Goto, 2018). Without prophylactic

treatment, the levels o vitamin K–epenent coagulation actors usually rop even urther uring the rst ew ays ater

birth. Tis ecline is amplie in breaste inants an may

lea to newborn hemorrhage (Chap. 33, p. 606). Schott (2018)

an Konstantinii (2019) an their colleagues have provie

thromboelastographic parameters or both healthy an sick

term newborns.

Fetal brinogen, which appears as early as 5 weeks, has the

same amino aci composition as ault brinogen but ierent properties (Klagsbrun, 1988). It orms a less compressible

clot, an the brin monomer has a lower egree o aggregation

(Heimark, 1988). Although plasma brinogen levels at birth are

less than those in nonpregnant aults, the protein is unctionally

more active than ault brinogen (Ignjatovic, 2011). Neonates

have higher cor plasma levels an bronectin-brinogen complexes compare with maternal levels (Lis-Kuberka, 2018).

Levels o unctional etal actor XIII (brin stabilizing actor)

are signicantly reuce compare with those in aults (Henriksson, 1974). Nielsen (1969) escribe low levels o plasminogen an elevate brinolytic activity in cor plasma compare

with that o maternal plasma. Platelet counts in cor bloo are

in the normal range or nonpregnant aults.

Despite this relative reuction in procoagulants, the etus

appears to be protecte rom hemorrhage, an etal bleeing is

rare. Even ater invasive etal proceures such as corocentesis,

excessive bleeing is uncommon. Ney an coworkers (1989)

have shown that amnionic fui thromboplastins an a actor(s)

in Wharton jelly combine to ai coagulation at the umbilical

cor puncture site.

Various thrombophilias may cause thromboses an pregnancy complications in aults (Chap. 55, p. 976). I the etus

inherits one o these mutations, thrombosis an inarction can

evelop in the placenta or etal organs. Tis is usually seen with

homozygous inheritance. One example is homozygous protein

C mutation, which causes purpura fulminans.

Plasma Proteins

Liver enzymes an other plasma proteins are prouce by the

etus, an these levels o not correlate with maternal levels

(Weiner, 1992). Concentrations o plasma proteins, which

inclue albumin, lactic ehyrogenase, aspartate an alanine aminotranserases, an γ-glutamyl transpeptiase, all

rise. Conversely, prealbumin levels ecline with gestational

age (Fryer, 1993). At birth, mean total plasma protein an

albumin concentrations in etal bloo are similar to maternal

levels. Tis is important because albumin bins unconjugate

bilirubin to prevent kernicterus in the newborn (Chap. 33,

p. 606).

■ Respiratory System

Lung maturation an biochemical inices o unctional etal

lung maturity are important preictors o early neonatal

outcome. Morphological or unctional immaturity at birth leas

to the evelopment o the respiratory distress syndrome (Chap.

34, p. 615). A sucient amount o surace-active materials—

collectively reerre to as surfactant—in the amnionic fui is

evience o etal lung maturity (Warburton, 2017). As Liggins

(1994) emphasize, however, the structural an morphological maturation o etal lung also is extraorinarily important to

proper lung unction.

Anatomical Maturation

Like the branching o a tree, lung evelopment procees along

an establishe timetable. As with other organ systems, gene

activation an eactivation control these unctions (Miller,

2019). Te lung primorium is an outgrowth rom oregut

enoerm at approximately 20 ays’ gestation. Te lung bu

arises at 25 ays an within this ramework, our essential lungEmbryogenesis and Fetal Development 131

CHAPTER 7

evelopment stages are escribe by Moore (2020). First, the

pseudoglandular stage entails growth o the intrasegmental bronchial tree between the 5th an 17th weeks. Te microvasculature begins to evelop, an the lung looks microscopically

like a glan. Secon, uring the canalicular stage, rom 16 to

25 weeks, the bronchial cartilage plates exten peripherally.

Each terminal bronchiole gives rise to several respiratory bronchioles, an each o these in turn ivies into multiple saccular ucts. Tir, the terminal sac stage begins ater 25 weeks.

During this stage, primorial alveoli give rise to primitive pulmonary alveoli, that is, the terminal sacs. Simultaneously, an

extracellular matrix evelops rom proximal to istal lung segments until term. Te ourth alveolar stage begins uring the

late etal perio an continues well into chilhoo. An extensive capillary network is built, the lymphatic system orms, an

type II pneumocytes begin to prouce suractant. At birth, only

approximately 15 percent o the ault number o alveoli is present. Tus, the lung continues to grow an a more alveoli or

up to 8 years.

Various insults can upset this process, an their timing

etermines the sequelae. During the embryonic phase, abnormalities in lung evelopment inclue esophageal an tracheal

atresia, tracheoesophageal stula, an pulmonary agenesis.

Another example is etal renal agenesis in which amnionic fui

is absent at the beginning o lung growth, an major eects

occur in all our evelopmental stages. Similarly, the etus with

membrane rupture an subsequent oligohyramnios beore 20

weeks usually exhibits nearly normal bronchial branching an

cartilage evelopment but has immature alveoli. In contrast,

membrane rupture ater 24 weeks may have minimal long-term

eect on pulmonary structure. Last, vitamin D is thought to be

important or several aspects o lung evelopment (Hart, 2015;

Ustun, 2020).

Pulmonary Surfactant

Ater the rst breath, the terminal sacs must remain expane

espite the pressure imparte by the tissue-to-air interace, an

suractant keeps them rom collapsing. Suractant is orme in

type II pneumocytes that line the alveoli. Tese cells are characterize by multivesicular boies that prouce the lamellar

boies in which suractant is assemble. During late etal lie,

at a time when the alveolus is characterize by a water-to-tissue

interace, the intact lamellar boies are secrete rom the lung

an swept into the amnionic fui uring respiratory-like

movements that are terme etal breathing. At birth, with

the rst breath, an air-to-tissue interace is establishe in the

lung alveolus. Suractant uncoils rom the lamellar boies an

spreas to line the alveolus to prevent alveolar collapse uring

expiration. Tus, the etal lungs’ capacity to prouce suractant establishes lung maturity.

Surfactant Composition. Gluck (1972) an Hallman (1976)

an their coworkers approximate that 90 percent o suractant

ry weight is lipi, specically glycerophospholipis. Proteins

account or the other 10 percent. Nearly 80 percent o the

glycerophospholipis are phosphatiylcholines (lecithins). Te

principal active component that constitutes hal o suractant

is a specic lecithin, which is ipalmitoyl phosphatiylcholine

(DPPC or PC). Phosphatiylglycerol (PG) accounts or another

8 to 15 percent. Its precise role is unclear because newborns

without PG usually o well. Te other major constituent is

phosphatiylinositol (PI).

Surfactant Synthesis. Biosynthesis takes place in the type II

pneumocytes. Te apoproteins are prouce in the enoplasmic reticulum, an the glycerophospholipis are synthesize

by cooperative interactions o several cellular organelles. Phospholipi is the primary surace tension–lowering component

o suractant, whereas the apoproteins ai the orming an

reorming o a surace lm.

Te major apoprotein is suractant A (SP-A), which is a glycoprotein with a molecular weight o 28,000 to 35,000 Da. It

is synthesize in the type II cells, an its content in amnionic

fui increases with gestational age an etal lung maturity.

SP-A gene expression is emonstrable by 29 weeks (Menelson,

2005). Specically, SP-A1 an SP-A2 are two separate genes on

chromosome 10, an their regulation is istinctive an ierent (McCormick, 1994).

Corticosteroids and Fetal Lung Maturation. Since Liggins

(1969) observe accelerate lung maturation in lamb etuses

given glucocorticosteroi prior to preterm elivery, many suggeste that etal cortisol stimulates lung maturation an suractant synthesis. It is unlikely, however, that corticosterois are the

only stimulus or augmente suractant ormation. But, when

these are aministere at certain critical times, they may improve

preterm etal lung maturation. Antenatal betamethasone an

examethasone or lung maturation an neonatal replacement

suractant therapy are iscusse in Chapter 34 (p. 617).

Breathing

Fetal respiratory muscles evelop early, an chest wall movements are etecte sonographically as early as 11 weeks (Koos,

2014). Breathing is essential or normal lung growth an

evelopment. From the beginning o the ourth month, the

etus engages in respiratory movement suciently intense to

move amnionic fui in an out o the respiratory tract. Some

extrauterine events have eects on etal breathing, or example,

maternal exercise stimulates it (Sussman, 2016).

■ Digestive System

Ater its embryogenic ormation rom the yolk sac as the primorial gut, the igestive system orms the intestines an various appenages. Te oregut gives rise to the pharynx, lower

respiratory system, esophagus, stomach, proximal uoenum,

liver, pancreas, an biliary tree. Te migut gives rise to the

istal uoenum, jejunum, ileum, cecum, appenix, an the

right colon. Te hingut evelops into the let colon, rectum,

an the superior portion o the anal canal that empties into the

cloaca (Kruepunga, 2018). Numerous malormations evelop

in these structures rom improper rotation, xation, an partitioning. A common example is one o the several types o

intestinal atresias (Moore, 2020; Stoll, 2017).

Swallowing begins at 10 to 12 weeks, coincient with

the ability o the small intestine to unergo peristalsis an132 Placentation, Embryogenesis, and Fetal Development

Section 3

to actively transport glucose (Kolovsky, 1965). As a correlate, neonates born preterm may have swallowing iculties

because o immature gut motility (Singenonk, 2014). Much

o the water in swallowe fui is absorbe, an unabsorbe

matter is propelle to the lower colon. Gitlin (1974) emonstrate that late in pregnancy, approximately 800 mg o soluble

protein is ingeste aily by the etus. Te stimulus or swallowing is unclear, but the etal neural analogue o thirst, gastric

emptying, an change in the amnionic fui composition are

potential actors (Boyle, 1992). Te etal taste bus may play

a role because saccharin injecte into amnionic fui increases

swallowing, whereas injection o a noxious chemical inhibits it

(Liley, 1972).

Fetal swallowing appears to have little eect on amnionic

fui volume early in pregnancy because the volume swallowe

is small compare with the total. However, term etuses swallow between 200 an 760 mL per ay—an amount comparable

to that o the term neonate (Pritchar, 1966). Tus at term,

amnionic fui volume regulation can be substantially altere

by etal swallowing. For example, as iscusse in Chapter 14

(p. 256), i swallowing is inhibite, hyramnios is common.

Hyrochloric aci an some igestive enzymes are present in the stomach an small intestine in minimal amounts

in the early etus. Intrinsic actor is etectable by 11 weeks,

an pepsinogen by 16 weeks. Te preterm neonate, epening

on its gestational age, may have transient eciencies o these

enzymes. Te small intestinal histological appearance is normal

(Meier, 2018).

Stomach emptying appears to be stimulate primarily by

volume. A ilate stomach suggests obstruction (McCormick,

2021). Movement o amnionic fui through the gastrointestinal system may enhance growth an evelopment o the

alimentary canal. Tat sai, other regulatory actors likely are

involve. For example, anencephalic etuses, in which swallowing is limite, oten have normal amnionic fui volume an

normal-appearing gastrointestinal tract.

Meconium

Fetal bowel contents consist o various proucts o secretion,

such as glycerophospholipis rom the lung, esquamate etal

cells, lanugo, scalp hair, an vernix. It also contains unigeste

ebris rom swallowe amnionic fui. Te ark greenishblack color orms rom bile pigments, especially biliverin.

Meconium can pass rom normal bowel peristalsis in the

mature etus or rom vagal stimulation. It can also pass when

hypoxia stimulates arginine vasopressin (AVP) release rom the

etal pituitary glan. AVP stimulates colonic smooth muscle

to contract, resulting in intraamnionic eecation (Rosenel,

1985). Meconium is toxic to the respiratory system, an its

inhalation can result in meconium aspiration syndrome.

Liver

Te hepatic iverticulum is an outgrowth o the enoermal

lining o the oregut. Epithelial liver cors an primorial cells

ierentiate into hepatic parenchyma. By 9 weeks, the liver

accounts or 10 percent o etal weight (Moore, 2020). Serum

liver enzyme levels increase with gestational age. As note, in

early gestation, etal hepatic hemopoiesis is a key source o

bloo an immune cells (p. 125) (Popescu, 2019).

Te etal liver has a gestational-age-relate capacity to conjugate bilirubin, which orms rom hemoglobin breakown

(Morioka, 2015). Because o hepatic immaturity, the preterm

newborn is at particular risk or unconjugate hyperbilirubinemia (Chap. 33, p. 606). An because the lie span o normal etal macrocytic erythrocytes is shorter than that o the

ault, relatively more unconjugate bilirubin is prouce. O

this unconjugate orm, only a small raction is conjugate

by the etal liver, an this is excrete into the intestine an

ultimately oxiize to biliverin. Instea, most o the unconjugate bilirubin is excrete into the amnionic fui ater

12 weeks an transerre across the placenta (Bashore, 1969).

Importantly, placental bilirubin transer is biirectional. Tus,

a woman with severe hemolysis has excess unconjugate bilirubin that reaily passes to the etus an then into the amnionic

fui. Conversely, conjugate bilirubin is not exchange to any

signicant egree between mother an etus.

Most etal cholesterol erives rom hepatic synthesis, which

satises the large eman or low-ensity lipoprotein (LDL)

cholesterol by the etal arenal glans. However, an estimate

20 to 50 percent o etal cholesterol originates rom the mother,

is transerre through the placenta, an release to circulating

etal apolipoproteins (Baarman, 2012; Pecks, 2014). Fetuses

with growth restriction have lower cholesterol levels ue to

iminishe etal synthesis rather than iminishe maternal

supply (Pecks, 2019).

Hepatic glycogen is present in low concentration uring the

secon trimester, but near term, levels rise rapily an markely to reach concentrations that are two- to threeol higher

than those in the ault liver. Ater birth, glycogen content alls

precipitously.

Pancreas

Tis glan arises rom orsal an ventral pancreatic bus rom

the enoerm o the oregut (Moore, 2020). Gene regulation o its evelopment has been reviewe (Jennings, 2015).

Insulin-containing granules can be ientie by 9 to 10 weeks,

an insulin is etectable in etal plasma at 12 weeks (Aam,

1969). Between 19 an 36 weeks, Kivilevitch an associates

(2017) were able to visualize the pancreas sonographically in

60 percent o etuses.

Te etal pancreas respons to hyperglycemia by secreting insulin (Obenshain, 1970). Islets o Langerhans are

enlarge in etuses o mothers with metabolic abnormalities

(Avagliano, 2019). Tese etuses likely can be ientie by

sonographic pancreatic hyperechogenicity (Akkaya, 2018).

Glucagon has been ientie in the etal pancreas at 8 weeks.

Although hypoglycemia oes not cause an increase in etal

glucagon levels, similar stimuli o so by 12 hours ater birth

(Chez, 1975).

Most pancreatic enzymes are present by 16 weeks. rypsin, chymotrypsin, phospholipase A, an lipase are oun in

the 14-week etus, an their concentrations increase with gestational age (Werlin, 1992). Amylase has been ientie in

amnionic fui at 14 weeks (Davis, 1986). Te exocrine unction o the etal pancreas is limite. Physiologically importantEmbryogenesis and Fetal Development 133

CHAPTER 7

secretion occurs only ater stimulation by a secretagogue such

as acetylcholine, which is release locally ater vagal stimulation (Werlin, 1992). Cholecystokinin normally is release

only ater protein ingestion an thus orinarily is not oun

in the etus.

■ Urinary System

Renal evelopment involves interaction between pluripotential

stem cells, unierentiate mesenchymal cells, an epithelial

components (Fanos, 2015). wo primitive urinary systems—

the pronephros an the mesonephros—precee evelopment o

the metanephros, which orms the nal kiney. Te pronephros

involutes by 2 weeks, an the mesonephros prouces urine at

5 weeks an egenerates by 11 to 12 weeks. Failure o these two

structures either to orm or to regress may result in anomalous

urinary system evelopment. Between 9 an 12 weeks, the ureteric bu an the nephrogenic blastema interact to prouce the

metanephros. Glomeruli evelop an ltration begins by week 9

(Moore, 2020). Te kiney an ureter evelop rom intermeiate mesoerm. Te blaer an urethra evelop rom the urogenital sinus. Te blaer also evelops in part rom the allantois.

Urogenital embryology is a ocus o Chapter 3.

By week 14, the loop o Henle is unctional an reabsorption occurs (Smith, 1992). New nephrons continue to be

orme until 36 weeks (Linström, 2018). In preterm neonates, their ormation continues ater birth. Although the etal

kineys prouce urine, their ability to concentrate an mo-

iy the pH is limite even in the mature etus. Fetal urine is

hypotonic with respect to etal plasma an has low electrolyte

concentrations.

Renal vascular resistance is high, an the ltration raction

is low compare with ault values (Smith, 1992). Fetal renal

bloo fow an thus urine prouction are controlle or infuence by the renin-angiotensin system, the sympathetic nervous system, prostaglanins, kallikrein, an atrial natriuretic

peptie. Te glomerular ltration rate increases with gestational age rom less than 0.1 mL/min at 12 weeks to 0.3 mL/

min at 20 weeks. In later gestation, the rate remains constant

when correcte or etal weight (Smith, 1992). Hemorrhage or

hypoxia generally ecreases renal bloo fow, glomerular ltration rate, an urine output.

Urine usually is oun in the blaer even in small etuses.

Te etal kineys start proucing urine at 12 weeks. By 18 weeks,

they are proucing 7 to 14 mL/, an at term, this increases

to 650 mL/ (Wlaimiro, 1974). Maternally aministere

urosemie augments etal urine ormation, whereas uteroplacental insuciency, etal-growth restriction, an other etal

isorers can lower it. Obstruction o the urethra, blaer, ureters, or renal pelves can amage renal parenchyma an istort

etal anatomy (Müller Brochut, 2014). Pathological correlates

an prenatal therapy o urinary tract obstruction are iscusse

in Chapter 19 (p. 376).

Kineys are not essential or survival in utero but infuence control o amnionic fui composition an volume. Tus,

abnormalities that cause chronic etal anuria are usually accompanie by oligohyramnios an pulmonary hypoplasia (Cotton, 2017).

■ Endocrine Gland Development

Te etal enocrine system is unctional or some time beore

the central nervous system reaches maturity (Mulchahey, 1987).

Pituitary Gland

Te anterior pituitary glan evelops rom oral ectoerm—the

Rathke pouch—whereas the posterior pituitary glan erives

rom neuroectoerm. Embryonic evelopment involves a

complex an highly spatiotemporally regulate network o

signaling molecules an transcription actors (Bancalari, 2012;

Montenegro, 2019).

Anterior and Intermediate Lobes. Te aenohypophysis, or

anterior pituitary, ierentiates into ve cell types that secrete

six protein hormones. O these types, lactotropes prouce prolactin (PRL), somatotropes prouce growth hormone (GH),

corticotropes prouce arenocorticotropic hormone (ACH),

thyrotropes prouce thyroi-stimulating hormone (SH), an

gonaotropes prouce luteinizing hormone (LH) an olliclestimulating hormone (FSH).

ACH is rst etecte in the etal pituitary glan at 7

weeks, an GH an LH have been ientie by 13 weeks. By

the en o the 17th week, the etal pituitary glan synthesizes

an stores all pituitary hormones. Moreover, the etal pituitary

is responsive to tropic hormones an is capable o secreting

these early in gestation (Grumbach, 1974). Te etal pituitary

secretes β-enorphin, an cor bloo levels o β-enorphin

an β-lipotropin rise with etal arterial partial pressure o carbon ioxie (Paco2) (Browning, 1983).

Te intermeiate lobe in the etal pituitary glan is well

evelope. Te cells o this structure begin to isappear beore

term an are absent rom the ault pituitary.

Neurohypophysis. Te posterior pituitary glan or neurohypophysis is well evelope by 10 to 12 weeks, an oxytocin an

arginine vasopressin are emonstrable. Both hormones probably

unction in the etus to conserve water by actions irecte largely

at the lung an placenta rather than kiney. Vasopressin levels in

umbilical cor plasma are strikingly higher than maternal levels

(Char, 1971).

Thyroid Gland

Te thyroi primorium arises rom the enoerm o the primorial pharynx (Moore, 2020). Te thyroi migrates to its

nal position, an the obliterate thyroglossal uct connects to

the oramen cecum o the tongue.

Te pituitary–thyroi system is unctional by the en o the

rst trimester. By 10 to 12 weeks, the thyroi glan is able to

synthesize hormones, an thyrotropin, thyroxine, an thyroi-

bining globulin (BG) have been etecte in etal serum as

early as 11 weeks (Bernal, 2007). Tyroi ollicles have orme

an colloi is present. Te placenta actively concentrates ioine

on the etal sie, an by 12 weeks an throughout pregnancy,

the etal thyroi concentrates ioine more avily than oes

the maternal thyroi. Tus, maternal aministration o either

raioioine or appreciable amounts o orinary ioine is hazarous ater this time (Chap. 66, p. 1174). Normal etal levels

o ree thyroxine (4), ree triioothyronine (3), an BG rise134 Placentation, Embryogenesis, and Fetal Development

Section 3

steaily throughout gestation (Ballabio, 1989). Compare with

ault levels, by 36 weeks, etal serum concentrations o SH

are higher, total an ree 3 concentrations are lower, an 4

is similar. Tis suggests that the etal pituitary may not become

sensitive to eeback until late pregnancy.

Fetal thyroi hormone plays a role in the normal evelopment o virtually all etal tissues, especially the brain (Anersen,

2018; Jansen, 2019). Congenital hypothyroiism is a heterogenous isorer or which several caniate genes have been ientie (Moore, 2020). With hypothyroiism, it was previously

believe that normal etal growth an evelopment provie

evience that 4 was not essential or etal growth. It is now

known, however, that growth procees normally because small

quantities o maternal 4 prevent antenatal cretinism in etuses

with thyroi agenesis (Forhea, 2014; Vulsma, 1989). As iscusse in Chapter 61 (p. 1098), the etus with congenital hypothyroiism typically oes not evelop stigmata o cretinism

until ater birth (Abuljabbar, 2012). Because aministration

o thyroi hormone will prevent this, by state law, all newborns

are teste or high serum levels o SH (Chap. 32, p. 594).

Te placenta prevents substantial passage o maternal thyroi hormones to the etus by rapily eioinating maternal

4 an 3 to orm reverse 3, a relatively inactive thyroi hormone. Several antithyroi antiboies cross the placenta when

present in high concentrations (Pelag, 2002). Tose inclue

the long-acting thyroi stimulators (LAS), LAS-protector

(LAS-P), an thyroi-stimulating immunoglobulin (SI).

Congenital hyperthyroiism evelops when maternal thyroi-

stimulating antiboy crosses the placenta to stimulate the etal

glan to secrete thyroxine (Donnelley, 2015). Tese etuses

evelop large goiters as shown in Figure 61-3 (p. 1092). Tey

also isplay tachycaria, hepatosplenomegaly, hematological

abnormalities, craniosynostosis, an growth restriction. As chil-

ren, they have perceptual motor iculties, hyperactivity, an

reuce growth (Johns, 2018).

Immeiately ater birth, thyroi unction an metabolism

unergo major change. Cooling to room temperature evokes

a suen an marke increase in SH secretion. Tis in turn

causes a progressive increase in serum 4 levels that are maximal

24 to 36 hours ater birth. Tere are nearly simultaneous elevations o serum 3 levels.

Adrenal Glands

Tese glans evelop rom two separate tissues. Te meulla

erives rom neural crest ectoerm, whereas the etal an

ault cortex arise rom intermeiate mesoerm. Te glan

grows rapily through cell prolieration an angiogenesis,

cellular migration, hypertrophy, an apoptosis (Ishimoto,

2011). Expression o the Kiss1R gene, alone or in concert

with corticotropin-releasing hormone, stimulates etal arenal growth (Katugampola, 2017). Fetal glans are enormous

in relation to boy size an are 10 to 20 times larger than

ault glans (Karsli, 2019; Moore, 2020). Te bulk is mae

up o the inner or etal zone o the arenal cortex an involutes rapily ater birth. Tis zone is scant to absent in rare

instances in which the etal pituitary glan is congenitally

absent. Te unction o the etal arenal glans is iscusse

in Chapter 5 (p. 102).

■ Immunological System

Inections in utero have provie an opportunity to examine

mechanisms o the etal immune response (Chap. 67, p. 1182).

Evience o immunological competence has been reporte as

early as 13 weeks (Stabile, 1988). In cor bloo at or near

term, the average level or most components approximates hal

that o the ault values.

B cells ierentiate rom pluripotent hemopoietic stem cells

that migrate to the liver (Berthault, 2017; Melchers, 2015).

Despite this, in the absence o a irect antigenic stimulus such

as inection, etal plasma immunoglobulins consist almost

totally o transerre maternal immunoglobulin G (IgG). Tus,

antiboies in the newborn most oten refect maternal immunological experiences (American College o Obstetricians an

Gynecologists, 2019). Te interaction between maternal an

etal  cells is escribe in Chapter 5 (p. 93).

Immunoglobulin G

Maternal IgG transport correlates with placental Fc receptor

expression (Lozano, 2018). Fetal transport begins at approximately 16 weeks an increases thereater. Because the bulk o

IgG is acquire uring the last 4 weeks, preterm neonates are

poorly enowe with protective maternal antiboies. Newborns begin to slowly prouce IgG, an ault values are not

attaine until age 3 years. In certain situations, the transer o

IgG antiboies rom mother to etus can be harmul rather

than protective. Te classic example is hemolytic isease o the

etus an newborn resulting rom Rh-antigen alloimmunization (Chap. 18, p. 353).

Immunoglobulins M and A

In the ault, prouction o immunoglobulin M (IgM) in

response to an antigenic stimulus is supersee in a week or so

preominantly by IgG prouction. Similarly, very little IgM

is prouce by normal etuses not expose to inection, but

with inection, the IgM response preominates an remains so

or weeks to months in the newborn. An, because IgM is not

transporte rom the mother, any IgM in the etus or newborn is

that which it prouce. Tus, specic IgM levels in umbilical cor

bloo may be elevate in those with congenital inection. Accor-

ing to the American College o Obstetricians an Gynecologists

(2019), elevate IgM levels are usually oun in newborns with

congenital inection such as rubella, cytomegalovirus inection,

or toxoplasmosis. In inants, ault levels o IgM are normally

attaine by age 9 months.

Immunoglobulin A (IgA) ingeste in colostrum provies

mucosal protection against enteric inections. Tere is only a

small amount o etal secretory IgA oun in amnionic fui

(Quan, 1999).

Lymphocytes and Monocytes

Te immune system evelops early, an B lymphocytes are

erive rom primorial stem cells an appear in etal liver

by 9 weeks an in bloo an spleen by 12 weeks (Moore,

2020).  lymphocytes begin to leave the thymus at approximately 14 weeks. Despite this, the newborn respons poorly

to immunization, an especially poorly to bacterial capsularEmbryogenesis and Fetal Development 135

CHAPTER 7

polysaccharies. Tis immature response may stem rom a

ecient response o newborn B cells to polyclonal activators

or rom a lack o  cells that prolierate in response to specic stimuli (Haywar, 1983). In the newborn, monocytes are

able to process an present antigen when teste with maternal

antigen-specic  cells. DNA methylation patterns are evelopmentally regulate uring monocyte-macrophage ierentiation an contribute to the antiinfammatory phenotype in

macrophages (Kim, 2012).

■ Musculoskeletal System

Te origin o most muscles an bones is mesoermal. MYOD

is a member o the amily o myogenic regulatory actors that

activates transcription o muscle-specic genes (Moore, 2020).

Te limb bus appear by the ourth week. Most skeletal muscle

erives rom myogenic precursor cells in the somites. Te skeleton arises rom conense mesenchyme—embryonic connective tissue—which eventually orms hyaline cartilage moels o

the bones. Osteoclasts arise rom erythro-myeloi progenitors

(Jacome-Galarza, 2019). By the en o the embryonic perio,

ossication centers have evelope, an bones haren by enochonral ossication.

ENERGY AND NUTRITION

Because o the small amount o yolk in the human ovum,

growth o the embryoetus is epenent on maternal nutrients uring the rst 2 months. During the rst ew ays ater

implantation, blastocyst nutrition comes rom the interstitial

fui o the enometrium an the surrouning maternal tissue.

Maternal aaptations to store an transer nutrients to the

etus are iscusse in Chapter 4 an summarize here. Tree

major maternal storage epots are the liver, muscle, an aipose

tissue. Tese maternal epots an the storage hormone insulin are intimately involve in the metabolism o the nutrients

absorbe rom the gut. Maternal insulin secretion is sustaine

by increase serum levels o glucose an amino acis. Te net

eect is maternal storage o glucose as glycogen primarily in

liver an muscle, retention o some amino acis as protein,

an storage o the excess as at (Abeysekera, 2016). Storage o

maternal at peaks in the secon trimester an then eclines as

etal energy emans rise in the thir trimester (Pipe, 1979).

Interestingly, the placenta appears to act as a nutrient sensor,

altering transport base on the maternal supply an environmental stimuli (Jansson, 2006b, Wesolowski, 2017).

During times o asting, glucose is release rom glycogen, but maternal glycogen stores cannot provie an aequate

amount o glucose to meet requirements or maternal energy

an etal growth. Augmentation is provie by cleavage o triacylglycerols, store in aipose tissue, which results in ree atty

acis an activation o lipolysis.

■ Glucose and Fetal Growth

Although epenent on the mother or nutrition, the etus also

actively participates in proviing its own nutrition. At mi-

pregnancy, etal serum glucose concentration is inepenent

o maternal levels an may excee them. Glucose is the major

nutrient or etal growth an energy. Logically, mechanisms

exist to minimize maternal glucose use so that the limite maternal supply is available to the etus. As one example, human placental lactogen (hPL) is a hormone normally abunant in the

mother but not the etus an has an insulin antagonist eect. It

blocks the peripheral uptake an use o glucose, while instea

promoting mobilization an use o ree atty acis by maternal

tissues (Chap. 5, p. 98). Tis hormone is also iabetogenic as

iscusse in Chapter 60 (p. 1068). Last, intrinsic epigenetic

changes play a role (Hansen, 2017). For example, nonalcoholic

atty liver isease (NAFLD) is associate with etal macrosomia

(Lee, 2019).

Glucose Transport

Te transer o d-glucose across cell membranes is accomplishe

by a carrier-meiate, stereospecic, nonconcentrating process

o acilitate iusion. Tere are 14 glucose transport proteins

(GLUs) encoe by the SLC2A gene amily an characterize

by tissue-specic istribution (Joshi, 2021). Several o these

are expresse by trophoblast (Stanirowski, 2017). GLU-1,

GLU-3, an GLU-4 primarily ai glucose uptake by the

placenta an are locate in the plasma membrane o the syncytiotrophoblast microvilli (Acosta, 2015; James-Allan, 2019).

DNA methylation regulates expression o placental GLUT

genes, with epigenetic moication across gestation (Novakovic, 2013). Methylation increases as pregnancy avances an

is inuce by almost all growth actors.

In aition to its transport role, the placenta uses glucose or

its metabolic unctions. Fetal an placental glucose consumption are inversely relate. Tus, placental glucose use is a key

moulator o maternal-etal transer (Michelsen, 2019).

Lactate is a prouct o glucose metabolism an transporte

across the placenta also by acilitate iusion. By way o

cotransport with hyrogen ions, lactate is probably transporte

as lactic aci.

Fetal Macrosomia

Te precise biomolecular events in the pathophysiology o

etal macrosomia are not ene. Nonetheless, etal hyperinsulinemia is clearly one riving orce (Luo, 2012). As iscusse

with etal-growth isorers in Chapter 47 (p. 824), insulin-like

growth actor an leptin an other aipokines are important

regulators o placental evelopment an unction (Gao, 2012).

Maternal obesity begets etal macrosomia. In aition, theories suggest that maternal obesity aects etal cariomyocyte

growth that may result in etal cariomyopathy or even congenital heart isease (Roberts, 2015).

■ Leptin

Tis polypeptie hormone was originally ientie as a pro-

uct o aipocytes an a regulator o energy homeostasis by

curbing appetite. It also contributes to angiogenesis, hemopoiesis, osteogenesis, pulmonary maturation, an neuroenocrine,

immune, an reprouctive unctions (Bria, 2015). Leptin is

prouce by the mother, etus, an placenta. It is expresse

in syncytiotrophoblast an etal vascular enothelial cells. O136 Placentation, Embryogenesis, and Fetal Development

Section 3

placental prouction, 5 percent enters the etal circulation,

whereas 95 percent is transerre to the mother (Hauguel-e

Mouzon, 2006).

Leptin concentrations peak in amnionic fui at mipregnancy (Scott-Finley, 2015). Fetal serum leptin levels begin

increasing at approximately 34 weeks an are correlate with

etal weight. Tis hormone is involve in the evelopment an

maturation o the heart, brain, kineys, an pancreas, an its

levels are ecrease with etal-growth restriction (Bria, 2015;

Yalinbas, 2019). Abnormal levels are associate with etalgrowth isorers, gestational iabetes, an preeclampsia, but

not maternal obesity (Allbran, 2018; Gurugubelli, 2018).

Postpartum, leptin levels ecline in both the newborn an

mother. Perinatal leptin is associate with the evelopment o

metabolic synromes later in lie (Bria, 2015).

■ Free Fatty Acids and Triglycerides

Te term newborn has a large proportion o at, which averages 15 percent o boy weight (Kimura, 1991). Tus, late in

pregnancy, a substantial part o the substrate transerre to the

human etus is store as at. Although maternal obesity raises

placental atty aci uptake an etal at eposition, it oes not

appear to aect etal organ growth (Dubé, 2012). Neutral at

in the orm o triglyceries oes not cross the placenta, but

glycerol oes. Despite this, evience supports that abnormal maternal concentrations o triglyceries—both low an

high levels—are associate with major congenital anomalies

(Neerlo, 2015).

Tere is preerential placental-etal transer o long-chain

polyunsaturate atty acis (Fonseca, 2018). Lipoprotein lipase

is present on the maternal but not on the etal sie o the placenta. Tis arrangement avors hyrolysis o triacylglycerols in

the maternal intervillous space yet preserves these neutral lipis

in etal bloo. Fatty acis transerre to the etus can be converte to triglyceries in the etal liver.

Te placental uptake an use o LDL is an alternative mechanism or etal assimilation o essential atty acis an amino

acis (Chap. 5, p. 100). LDL bins to specic receptors in the

coate-pit regions o the syncytiotrophoblast microvilli. Te

large LDL particle, measuring about 250,000 Da, is taken up

by a process o receptor-meiate enocytosis. Te apoprotein an cholesterol esters o LDL are hyrolyze by lysosomal

enzymes in the syncytium to yiel: (1) cholesterol or progesterone synthesis; (2) ree amino acis, incluing essential amino

acis; an (3) essential atty acis, primarily linoleic aci.

Interestingly, maternal cholesterol is obligatory or steroi hormone synthesis, but increasing levels are associate with etal

aortic atherogenesis (e Nigris, 2018).

■ Amino Acids

Te placenta concentrates many amino acis in the syncytiotrophoblast, which are then transerre to the etal sie by

iusion. In corocentesis bloo samples, the amino aci concentration in umbilical cor plasma is greater than in maternal

venous or arterial plasma. DNA methylation serves to regulate

transporter gene expression (Simner, 2017). ransport system

activity is infuence by gestational age an environmental actors. Tese inclue heat stress, hypoxia, uner- an overnutrition, an hormones such as glucocorticois, growth hormone,

an leptin (Bria, 2015). rophoblastic mammalian target o

rapamycin complex 1 (mORC1) regulates placental amino

aci transporters an moulates transer across the placenta

(Jansson, 2012). In vivo stuies suggest an upregulation o

transport or certain amino acis an a greater elivery rate o

these to the etuses o women with gestational iabetes associate with etal overgrowth (Jansson, 2006a).

■ Proteins

Placental transer o larger proteins is limite, but there are

exceptions. As iscusse, IgG crosses the placenta in large

amounts via enocytosis an trophoblast Fc receptors. IgG

transer epens on maternal levels o total IgG, gestational

age, placental integrity, IgG subclass, an antigenic potential

(Palmeira, 2012). Conversely, the larger immunoglobulins—

IgA an IgM—o maternal origin are eectively exclue rom

the etus.

■ Ions and Trace Metals

Calcium an phosphorus are actively transporte rom

mother to etus. Calcium is transerre or etal skeletal mineralization (Olausson, 2012). A calcium-bining protein is

prouce in placenta. Parathyroi hormone–relate protein

(PH-rP), as the name implies, acts as a surrogate PH in

many systems (Chap. 5, p. 99). PH is not oun in etal

plasma, but PH-rP is present, suggesting that PH-rP

is the etal parathormone (Martin, 2016). Te expression

o PH-rP in cytotrophoblasts is moulate by the extracellular concentration o Ca2+ (Hellman, 1992). It seems

possible that PH-rP synthesize in eciua, placenta, an

other etal tissues is important in etal Ca2+ transer an

homeostasis.

Another example is the uniirectional transer o iron. ypically, maternal plasma iron concentration is much lower than

that in her etus. Even with severe maternal iron-eciency

anemia, the etal hemoglobin mass is normal.

Ioine transport is clearly attributable to a carrier-meiate,

energy-requiring active process. An, as iscusse in Chapter

61 (p. 1097), the placenta concentrates ioine (Velasco, 2018).

Te concentrations o zinc in the etal plasma also are greater

than those in maternal plasma. Conversely, copper levels in

etal plasma are less than those in maternal plasma. Tis act

is o particular interest because important copper-requiring

enzymes are necessary or etal evelopment.

Placental Sequestration of Heavy Metals

Te heavy metal–bining protein metallothionein-1 is

expresse in human syncytiotrophoblast. Tis protein bins

an sequesters a host o heavy metals, incluing zinc, copper,

lea, an camium. Despite this, etal exposure is variable

(Caserta, 2013). For example, lea enters the etal environment at a level 90 percent o maternal concentrations. In contrast, placental transer o camium is limite (Kopp, 2012).Embryogenesis and Fetal Development 137

CHAPTER 7

Te most common source o environmental camium is cigarette smoke.

Metallothionein also bins an sequesters copper in placental tissue. Tis accounts or the low copper levels in cor

bloo (Iyengar, 2001). It is possible that camium provokes

metallothionein synthesis in the amnion. Tis may cause copper sequestration, a pseuocopper eciency, an in turn,

iminishe amnion tensile strength.

■ Vitamins

Te concentration o vitamin A (retinol) is greater in etal than

in maternal plasma an is boun to retinol-bining protein

an to prealbumin. Retinol-bining protein is transerre rom

the maternal compartment across the syncytiotrophoblast. Te

transport o vitamin C—ascorbic aci—rom mother to etus

is accomplishe by an energy-epenent, carrier-meiate

process. As a result, the concentration o ascorbic aci is two

to our times higher in etal plasma than in maternal plasma

(Morriss, 1994). Levels o principal vitamin D metabolites,

incluing 1,25-ihyroxycholecalcierol, are greater in maternal plasma than in etal plasma. Te 1β-hyroxylation o

25-hyroxyvitamin D3 is known to take place in placenta an

in eciua.

PLACENTAL ROLE IN EMBRYOFETAL

DEVELOPMENT

Te placenta is the organ o transer between mother an etus.

Within this biirectional maternal-etal interace, maternal

oxygen an nutrients transer to the etus, whereas CO2 an

metabolic wastes are irecte back to the mother. Fetal bloo,

which is containe in the etal capillaries o the chorionic villi,

has no irect contact with maternal bloo, which remains in

the intervillous space. Instea, biirectional transer epens

on processes that allow or ai the transport through the syncytiotrophoblast that lines chorionic villi (Michelsen, 2017).

With this system, breaks in the chorionic villi permit escape

o etal/placental cells an other bloo-borne material into the

maternal circulation. Tis leakage is the mechanism by which

some D-negative women become sensitize by the erythrocytes

o their D-positive etus (Chap. 18, p. 353). Te escape o

etal cells can also lea to etal microchimerism rom entrance

o allogeneic etal cells, incluing trophoblast, into maternal

bloo an other organs (Rijnink, 2015). Volumes are estimate

to range rom 1 to 6 cells/mL at mipregnancy. Some etal

cells become “immortal” in that they persist in the maternal

circulation an organs ollowing pregnancy. As iscusse in

Chapter 61 (p. 1109), the clinical corollary is that some maternal autoimmune iseases such as Hashimoto thyroiitis may be

provoke by such microchimerism.

Last, cell-ree DNA (cDNA) is release rom syncytiotrophoblast uring normal physiological cell turnover. Ater 10

weeks, 10 to 15 percent o all cDNA in maternal plasma is

trophoblastic DNA (Norton, 2015; Shaer, 2018). Tis phenomenon unerlies one maternal-serum screening metho or

etal aneuploiy, which is iscusse in Chapters 16 an 17

(pp. 327 an 335).

■ The Intervillous Space

Maternal bloo within the intervillous space is the primary

source o maternal–etal transer. Bloo rom the maternal spiral arteries irectly bathes the trophoblast layer that surrouns

the villi. Substances transerre rom mother to etus rst enter

the intervillous space an are then transporte to the syncytiotrophoblast. As such, the chorionic villi an intervillous space

unction together as the etal lung, gastrointestinal tract, an

kiney.

Circulation within the intervillous space is escribe in

Chapter 5 (p. 92). Intervillous an uteroplacental bloo fow

increases throughout pregnancy, an at term, the resiual volume o the intervillous space approximates 140 mL. Moreover, uteroplacental bloo fow near term ranges rom 700 to

900 mL/min, an most o this bloo apparently goes to the

intervillous space (Pates, 2010).

■ Placental Transfer

In the terminal villi, substances that pass rom maternal to

etal bloo must rst traverse the syncytiotrophoblast, the

attenuate cytotrophoblast layer, the thinne villous stroma,

an nally, the etal capillary wall. Although this histological barrier separates maternal an etal circulations, it is not

a simple physical barrier. First, throughout pregnancy, syncytiotrophoblast actively or passively permits, acilitates, an

ajusts the amount an rate o substance transer to the etus.

As iscusse in Chapter 5 (p. 92), the maternal-acing syncytiotrophoblast surace is characterize by a complex microvillus

structure. Te etal-acing basal cell membrane is the site o

transer to the intravillous space. Finally, the villous capillaries

are an aitional site or transport rom the intravillous space

into etal bloo, or vice versa. In etermining the eectiveness

o the human placenta as an organ o transer, several variables

are important an shown in Table 7-2. Epigenetic placental

changes brought about by methylation o genes engage in

nutrient transer also play a role (Kerr, 2018).

Mechanisms of Transfer

Most substances with a molecular mass <500 Da pass reaily

through placental tissue by simple iusion. Tese inclue

TABLE 7-2. Variables of Maternal-Fetal Substance

Transfer

Maternal plasma concentration

Maternal carrier-protein binding

Maternal blood flow rate through the intervillous space

Trophoblast surface area size available for exchange

Physical trophoblast properties to permit simple diffusion

Trophoblast biochemical machinery for active transport

Substance metabolism by the placenta during transfer

Fetal intervillous capillary surface area size for exchange

Fetal blood concentration of the substance

Fetal carrier-protein binding

Villous capillary blood flow rate

DNA methylation of transporter genes138 Placentation, Embryogenesis, and Fetal Development

Section 3

oxygen, CO2, water, most electrolytes, an anesthetic gases

(Carter, 2009). Some low-molecular-weight compouns

unergo transer acilitate by syncytiotrophoblast. Tese are

usually those that have low concentrations in maternal plasma

but are essential or normal etal evelopment.

Insulin, steroi hormones, an thyroi hormones cross

the placenta, but very slowly. Te hormones synthesize in

situ in the syncytiotrophoblast enter both the maternal an

etal circulations, but not equally (Chap. 5, p. 86). Examples

are hCG an hPL concentrations, which are much lower in

etal plasma than in maternal plasma. High-molecular-weight

substances usually o not traverse the placenta, but there are

important exceptions. As iscusse, one is IgG—molecular

weight 160,000 Da—which is transerre by way o a specic

trophoblast receptor–meiate mechanism (Stach, 2014).

Although simple iusion is an important metho o

placental transer, the trophoblast an chorionic villus unit

emonstrate enormous selectivity in transer. As iscusse,

important in this regar is DNA methylation o transporter

genes (Kerr, 2018; Simner, 2017). Te net results are ierent

metabolite concentrations on the two sies o the villus.

Transfer of Oxygen and Carbon Dioxide

Placental oxygen transer is bloo fow limite. Using estimate

uteroplacental bloo fow, Longo (1991) calculate oxygen

elivery to be approximately 8 mL O2/min/kg o etal weight.

Because o the continuous passage o oxygen rom maternal

bloo in the intervillous space to the etus, its oxygen saturation

resembles that in maternal capillaries. Te average oxygen saturation o intervillous bloo is estimate to be 65 to 75 percent,

with a partial pressure (Pao2) o 30 to 35 mm Hg. Te oxygen

saturation o umbilical vein bloo is similar but has a somewhat lower oxygen partial pressure (Ramsay, 1996). As note

earlier, etal hemoglobin has a higher oxygen anity than ault

hemoglobin.

Te placenta is highly permeable to CO2, which traverses

the chorionic villus by iusion more rapily than oxygen.

Near term, the partial pressure o carbon ioxie (Paco2) in the

umbilical arteries averages 50 mm Hg, which is approximately

5 mm Hg higher than in the maternal intervillous bloo. Fetal

bloo has less anity or CO2 than oes maternal bloo, thereby

avoring CO2 transer rom etus to mother. Also, mil maternal hyperventilation results in a all in Paco2 levels, avoring a transer o CO2 rom the etal compartment to maternal bloo.



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