introduction to human anatomy ame 102 ii.general …

INTRODUCTION TO HUMAN ANATOMY

AME 102

II. General EmbryologyBy

And

Staff members of Anatomy and Embryology departments

Faculty of Medicine Cairo University

PROF. DR. HODA EL AASARPROFESSOR & HEAD OF ANATOMY DEPARTMENT

Faculty of Medicine -MTI PROFESSOR OF ANATOMY - CAIRO UNIVERSITY

Contents

Page Introduction

Chapter 1 - Gametes

Male and female gametes

Formative Assessment

1

3

Chapter 2 – First Week Development

Fertilization

Cleavage and migration


4

8

10

Chapter 3 – Second Week of Development

Implantation

Decidua

Daily changes of blastocyst during 2nd week

11

15

16

Chapter 4 – Third Week of Development

Development of chorion

Gastrulation

Notochord

Intraembryonic mesoderm


21

24

27

31

34

Chapter 5 – Embryonic Period

Derivatives of ectoderm

Development of intraembryonic mesoderm

Derivatives of endoderm

Folding

Formative assessment

35

38

43

44

47

Chapter 6 – Fetal membranes

Chorion

Placenta

Amnion

Umbilical cord

Yolk sac


48

49

56

59

63

66

Chapter 7 – Fetal period

Fetal Period


67

69

INTRODUCTION

Embryology is the science which describes the

developmental process from a single cell (zygote) to a baby in 9

months. These studies are important because they provide

knowledge essential for creating health care strategies for better

reproductive outcomes. Thus, our increasingly better

understanding of embryology has resulted in new techniques for

prenatal diagnoses and treatments.

The process of progressing from a single cell (zygote)

through the period of establishing organ primordia (the first 8

weeks of human development) is called the period of

embryogenesis, the period from that point on until birth is called

the fetal period, a time when differentiation continues while the

fetus grows and gains weight. Scientific approaches to study

embryology have progressed over hundreds of years. Scientists

made comparisons between species and so began to understand

the progression of developmental phenomena.

Gametes 1

CHAPTER 1

ILOs:

By the end of this chapter, the student should be able to: ▪ Identify the morphology of mature sperm. ▪ Describe the mature ovum and its coverings.

Male & Female Gametes

Male gametes (sperms) and female gametes (ova) are the reproductive cells that are formed from primordial germ cells by a process known as spermatogenesis and oogenesis, respectively.

Site of formation: In the gonads (testis or ovary).

Time of formation: ▪ In males, it starts at puberty and continues till old age. ▪ In females, it starts in the intrauterine life, then arrested to be continued

from puberty to menopause through ovarian cycles. Ovulation occurs at the 14th day of the ovarian cycle.

Morphology of mature gametes: I-Sperm: (Fig.:I-1) A human sperm is 55 microns long and consists of:

▪ Head: It is 4 microns long that contains:

➢ Condensed nucleus which carries hereditary material of the father (22 autosomes & X- or Y- sex chromosomes) mostly covered by acrosomal cap that has enzymes that facilitate pentration of covering of the ova (fertilization).

➢ Minimal cytoplasm.

➢ Cell membrane. ▪ Neck: It is narrow part between head and middle piece.

▪ Middle piece: It is 6 micron long and composed of mitochondrial sheath which is the source of energy for sperm motility.

▪ Tail: It is 45 microns long and composed of axial filament with cell membrane around most of it. The tail directs the movement of sperms twards the ovum, then helps fertilization.

II- Ovum: (Fig.: I-2)

The diameter of mature ovum is about 120 microns. It consists of: A- Ootid which is the mature oocyte that carries:

▪ Nucleus that has the hereditary material of the mother (22 autosomes & X-Chromosome).

▪ Large cytoplasm which is the initial source of nutrition of the zygote.

Gametes 2

▪ Cell membrane. B- Zona pellucida: It is the glycoprotein coat around the ootid. It carries

sperm receptors that attracts sperms prior to fertilization. C- Corona radiate: it is the outer cover that is formed of follicular cells derived

from the ovary.

Fig.I-1: Morphology of sperm.

Nucleus

Cell membrane Corona radiata

Cytoplasm

Zona pellucida

Fig.I-2: Structure of mature ovum with its coverings.

Gametes 3


1. Mention site and time of formation of mature male & female

gametes.

2. What is the structure of the sperm?

3. Describe the structure of mature ovum and mention its

coverings.

4. Regarding the sperm, one of the following statements is correct:

a. Its length is about 6 microns.

b. The nucleus carries 22 autosomes and either X- or Y-chromosome.

c. It starts formation at birth.

d. Acrosomal cap covers most of the middle piece.

Answer: b

5- Regarding the ovum

a. Its diameter is about 12 microns.

b. The nucleus carries 22 autosomes and either X- or Y-chromosome.

c. It starts development at puberty.

d. Corona radiate is the outer cover of the ovum.

Answer: d

Key words:

1- Mature human sperm – morphology.

2- Mature human ovum – morphology - coverings.

First week 4

CHAPTER 2

ILOs:

By the end of this chapter the student should be able to:

▪ Identify the term fertilization and analyze its phases. ▪ Discuss the results of fertilization. ▪ Realize the meaning of cleavage and migration. ▪ Describe the formation of the blastocyst.

FIRST WEEK OF DEVELOPMENT

FERTILIZATION

Fertilization is the union between the male gamete (sperm) and the female gamete (ovum) to form the zygote.

Site: In the ampulla of uterine tube.

Mechanism: (Fig.II-1)

➢ Capacitation of the sperms: It is the process of removal of glycoprotein coat that covers the acrosomal regions of the sperms in the female genital system. It takes about 7 hours to be completed.

➢ Phase I (Penetration of corona radiata): Only 300 – 500 sperms out from 200 – 300 million sperm / ejaculation will reach the ovum and start dispersion of corona radiata.

➢ Phase II (Penetration of zona pellucida): One sperm only will

pass through the zona pellucida by the following steps: ▪ Sperms bind to the zona at specific binding sites (sperm

receptors). ▪ Sperms secrete acrosomal enzymes (acrosin- and trypsin-

like substances) that dissolve a passage through zona. Only one sperm will pass through the zona pellucida (acrosomal reaction) helped by movement of the tail.

▪ The head of the fertilizing sperm comes in contact with the plasma membrane of the secondary oocyte.

➢ Phase III (Penetration of cell membrane of the oocyte): It

occurs by the following steps: ▪ The plasma membranes of both sperm and ovum will fuse

together. ▪ Then, fused plasma membranes (of sperm and oocyte)

open to allow passage of sperm contents (nucleus, neck, middle piece and axial filament) to cytoplasm of the ovum, leaving sperm cell membrane on the outer surface of the oocyte.

First week 5

➢ Events that occur after entrance of the sperm to cytoplasm of the oocyte:

A. Cortical and zona reactions: (Fig.II-2) after entrance of the fertilizing sperm, the oocyte releases lysosomal enzymes from cortical granules. These enzymes prevent polyspermy through:

▪ Changing sperm binding sites of the zona pellucida to prevent binding and passage of more sperms.

▪ Making the plasma membrane of the fertilized oocyte impenetrable to other sperms.

B. The secondary oocyte completes the 2nd meiotic division to form mature ovum (ootid) (23 Ch.) and 2nd polar body (23 Ch.).

C. Male nucleus becomes larger (male pronucleus) and come to be in contact with nucleus of ootid (female pronucleus).

D. Nuclear membranes of both male and female pronuclei fuse together to form nucleus of the zygote.

Results of fertilization: 1. Formation of the zygote. 2. Determination of sex of the zygote either male (XY) or female

(XX). 3. Restoration of diploid number (46 Ch.).

4. Start of cleavage and migration of the zygote from site of fertilization to site of implantation in the uterine cavity.

Fig.II-1: Steps of fertilization.

First week 6

Fig.II-2: Cortical and zona reactions.

Artificial fertilization:

1-In vitro fertilization (IVF): (Fig.II-3) ▪ It is performed in case of a female suffering from obstructed

uterine tubes.

▪ Giving the mother gonadotropins to stimulate FSH secretion which induce multiple Graafian follicles formation in the ovary.

▪ Withdrawal of secondary oocytes from the Graafian follicles just before ovulation using laparoscope.

▪ Transfer of the secondary oocytes to a special culture medium, and then addition of the sperms.

▪ When fertilization occurs and the embryo reaches the 8-cell stage it is taken from the culture medium and is implanted in the endometrium.

2- Intracytoplasmic sperm injection (ICSI):(Fig.II-4) It is in-vitro injection of a single sperm into the cytoplasm of the

oocytes to cause fertilization. This procedure is done in case of low count of sperms or failure of its penetration to walls of oocyte. After formation of morula, it is implanted into the uterine endometrium using a catheter

First week 7

3- Gamete intrafallopian transfer (GIFT): In this technique oocytes and sperms are introduced into the

ampulla of the fallopian (uterine) tube, where fertilization takes place. Development then proceeds in a normal manner.

FigII-3: Natural& in-vitro fertilization.

Fig.II-4: Intracytoplasmic sperm injection.

First week 8

Cleavage and Migration

Zygote divides mitotically, inside the zona pellucida coat, giving rise to smaller blastomeres (46 Ch.) in the following manner (Fig. II-5):

• Two cell stage is formed in the 1st day. • Four cell stage is formed in the 2nd day. • 16 cell stage (morula) followed by 32 and then 64-cell stage is

formed in the 3rd day. During cleavage, the morula migrates inside the uterine tube to reach the uterine cavity at the 4th day by the following mechanisms:

1. Muscular peristalsis of the uterine tube.

2. The motion of the cilia of mucosal lining of the tube.

Formation of the blastocyst: (Fig. II-6)

▪ Zona pellucida starts to degenerate at the end of 5th day.

▪ Fluid pass through degenerating zona to form multiple spaces between cells of the morula.

▪ Gradually, those spaces fuse together to form a single cavity, called blastocele. This stage is named blastocyst.

▪ Blastocyst is composed of:

1. Outer cell mass (trophoblast) which is formed of a single layer of cells.

2. Inner cell mass (embryoblast) which is formed of a mass

of cells on one side of the inner aspect of trophoblast. 3. Blastocele is the cavity of the blastocyst.

4. Embryonic pole is the side of the outer surface of blastocyst that corresponds to the embryoblast.

5. Abembryonic pole is the opposite side of the embryonic

pole of the blastocyst.

First week 9

Fig.II-5: Cleavage and migration of the embryo.

Fig.II-6: Structure of the blastocyst.

First week 10


1- hat are the events that occur after the entrance of the sperm to the cytoplasm of the oocyte? 2- hat are the results of fertilization? 3-How is the blastocyst formed?

4-Which of the following cells contains a haploid number of chromosomes?

a) Primordial germ cells.

b) Somatic skin cell. c) Sperm.

d) Zygote. Answer: c

Key words:

1- Fertilization in human – cortical reaction – zona reaction.

2- Fertilization in human – results of fertilization.

3- Blastocyst in human – formation.

Second week 11

CHAPTER 3

ILOs:

By the end of this chapter the student should be able to:

▪ Define the term implantation. ▪ Describe its mechanism. ▪ Detect the abnormal sites of implantation and ectopic

pregnancy. ▪ Recognize different parts of "decidua” and the fate of each

part. ▪ Trace the events that occur in the blastocyst changing it into"

the chorionic vesicle. ▪ Describe the formation and structure of the chorionic vesicle.

SECOND WEEK OF DEVELOPMENT

IMPLANTATION

Definition: It is the process by which the blastocyst becomes

embedded in the endometrium.

Time: It starts at the 7th day and is completed at the 11th day.

Site: In the endometrium of the upper part of the posterior wall of the

uterus (near fundus), less frequent it occurs in the upper part of the anterior wall. N.B. During implantation, endometrium (lining of uterus) is at the secretory phase of endometrial (menstrual) cycle. This phase is characterized by increased thickness of endometrium, increased number and size of endometrial cells, glands are spiral and rich with secretion and arteries are spiral showing arterio-venous anastomoses.

Mechanism of implantation (Figs.III-1, 2 &3):

➢ It starts by adhesion of the blastocyst by its embryonic pole to the endometrium at the implantation site.

➢ Trophoblast proliferate at the embryonic pole to form a new layer of cells that has no cell walls and this layer is called syncytiotrophoblast. This new layer secretes proteolytic enzymes that erode the endometrium and form the implantation cavity.

➢ Blastocyst becomes embedded inside the implantation cavity.

➢ At the 9th day, the site of penetration by the blastocyst becomes blocked by fibrin clot (Fig.III-10)

Second week 12

➢ Two days later (11th day), endometrial epithelium overgrows and covers the fibrin clot.

Changes of blastocyst during implantation:

1. Trophoblast differentiates into outer syncytiotrophoblast and inner cytotrophoblast, starting at the embryonic pole then extends all over the blastocyst.

2. Formation of amniotic and yolk sac cavities. 3. Formation of double layered embryonic disc (epiblast and

hypoblast).

Abnormal sites of implantation: (Fig.III-4) A-P lacenta Previa: Implantation occurs at the lower segment of uterus. It is of three types:

1. Placenta previa parietalis: The margin of placenta is near the

internal os. 2. Placenta previa marginalis: The margin of placenta covers the

internal os. 3. Placenta previa centralis: The center of placenta covers internal

os. N.B.

• Internal os is the inner opening of cervical canal of uterus. • Placenta previa is life threatening as:

a. It leads to antepartum (before birth) maternal hemorrhage. b. It may lead to death of fetus.

So, cesarean section is highly recommended in case of placenta previa.

B-E opic pregnancy: (Fig.III-5) Blastocyst is abnormally implanted outside the uterus in the following sites:

▪ Tubal (Fig. III-6) in uterine tube which may occur in ampulla, isthmus or intramural parts. In this case, rupture of the tube is expected at the 8th week of pregnancy leading to severe internal hemorrhage.

▪ Ovarian on the surface of the ovary.

▪ Omental: in peritoneum (abdominal or pelvic).

Second week 13

Fig.III-1: Adhesion of the blastocyst to the endometrium.

Fig.III-2: Partial implantation of the blastocyst.

Fig.III-3: Implantation is completed.

Second week 14

Fig.III-4: Placenta previa: parietalis (A), marginalis (B) and centralis (C).

Fig.III-5: Ectopic pregnancy may occur in peritoneum (1), uterine tube {ampulla (2), isthmus (3), intramural part (4)}, internal os (5), ovary (6).

Fig.III-6: Ruptured uterine tube due to tubal pregnancy.

Second week 15

Decidua

It is the endometrium of the uterus after implantation of the blastocyst. It is called decidua as it sheds during labor (Latin word deciduus, meaning falling off or shedding). It is exaggerated secretory phase of endometrium.

Features of decidua: Features of decidua are increased thickness of endometrium, increased

number and size of endometrial cells, glands become spiral and full of secretions while arteries become spiral and show arterio-venous anastomoses.

Parts of decidua: (Fig.III-7)

1. Decidua basalis: It is the part of decidua that lies between the implanted embryo and myometrium.

2. Decidua capsularis: It is the part of decidua that covers the embryo, separating the embryo from uterine cavity.

3. Decidua parietalis: It is the part of decidua that lines the rest of

the uterine cavity.

Fate of decidua: (Fig.III-7) ▪ Decidua basalis: persists as the maternal part of placenta and is

known as decidual plate. ▪ Decidua capsularis and parietalis: come in contact and fuse

together obliterating uterine cavity. They degenerate at last.

Fig.III-7: Parts of decidua.

Second week 16

Daily events during the second gestational week

8th day: (Fig. III-9) ▪ Blastocyst is partially implanted.

▪ Trophoblast layer differentiates into inner cytotrophoblast and

outer syncytiotrophoblast, starting at the embryonic pole of the

blastocyst.

▪ Cells of the inner cell mass (facing the blastocele) become

cuboidal to form a layer known as hypoblast.

▪ Amniotic cavity appears within cells of the embryoblast. The cells

adjacent to cytotrophoblast secrete amniotic fluid and are known

as amnioblast cells. Amniotic cavity separates between

amnioblast and epiblast of the embryonic disc.

▪ Epiblast and hypoblast form the bilaminar embryonic disc.

9th & 10th days: (Fig. III-10) ▪ Blastocyst is completely implanted.

▪ Site of penetration is closed by fibrin clot.

▪ Flat cells (Heuser’s membrane) from hypoblast line the blastocele

which is transformed into primary yolk sac.

▪ Syncytiotrophoblast extends to surround the cytotrophoblast of

the whole blastocyst.

▪ Lacunae appear in the syncytiotrophoblast (Lacunar stage).

11th & 12th days: (Fig. III-11) ▪ Endometrial epithelium grows and covers the fibrin colt.

▪ Lacunae are filled with maternal blood to form utero-placental

circulation.

▪ Extra-embryonic mesoderm is formed between cytotrophoblast

(externally) and embryonic disc with amniotic and yolk sac

cavities (internally). Multiple spaces appear in the extraembryonic

mesoderm.

Second week 17

13th day: (Fig.III-12) ▪ Fusion between spaces in the extraembryonic mesoderm leads

to formation of extraembryonic coelom (chorionic cavity). Now the

blastocyst is termed chorionic vesicle and its wall is called

chorion. The Chorionic cavity separates between somatic and

splanchnic mesoderm. Somatic mesoderm lines cytotrophoblast

and covers amniotic cavity while splanchnic mesoderm covers

yolk sac.

▪ Connecting stalk is the part of the extraembryonic mesoderm that

connects the caudal end of embryonic disc with the chorion.

▪ New generation of cells from hypoblast line the primary yolk sac

to form secondary yolk sac.

▪ Pinching off a large part of the secondary yolk sac with marked

reduction of its size.

▪ Formation of allantois that extends from caudal wall of yolk sac.

▪ Primary chorionic villi start to appear from the chorion.

N.B. Chorion: is the wall of chorionic vesicle. It secretes chorionic gonadotropin (CG) which maintains the corpus luteum (source of progesterone in the ovary) for 4 months. It is composed of (from internal to external):

➢ Somatic extraembryonic mesoderm. ➢ Cytotrophoblast. ➢ Syncytiotrophoblast.

Fig.III-8: Start of implantation at the 7th day.

Second week 18

Fig.III-9: Partial implantation of the embryo at the 8th day.

Fig. III-10: Implantation of blastocyst at the 9th& 10th days.

Second week 19

Fig.III-11: Changes of blastocyst at the 12th day.

Fig.III-12: Formation of chorionic vesicle at the 13th day.

Second week 20


1- Explain why menstruation stops if pregnancy occurs? 2- Describe the wall of the chorionic vesicle. 3- Mention parts and fate of decidua.

Key words:

1- mplantation of blastocyst in human. 2-Decidua. 2- horionic vesicle in human.

Third week 21

CHAPTER 4:

ILOs

By the end of this chapter, the student should be able to:

• Trace the changes that occur in the embryo during the 3rd week of

pregnancy.

▪ Describe the development of the chorionic villi at different stages

(primary, secondary and tertiary).

▪ Cite the different parts of the 3ary villus and point to the function of each.

▪ Recognize the different parts of the chorion and indicate the fate of each.

▪ Define and describe gastrulation.

▪ Describe the different stages of formation of the notochord, discuss its

important functions and indicate its fate.

▪ Review the site and differentiation of the extraembryonic mesoderm.

▪ Distinguish the different areas of the embryonic disc by the end of the 3rd

week.

THIRD WEEK OF DEVELOPMENT

The most characteristic events that occur during the third week of gestation are development of chorion and gastrulation of the embryonic disc.

Development of Chorion

• The chorion is the wall of the chorionic vesicle. (Figs.III-11&12)

• Chorion is composed of somatic extraembryonic mesoderm, cytotrophoblast and syncytiotrophoblast (from internal to external).

• Chorionic villi are formed starting from the end of 2nd week. They are projections from the wall of chorionic vesicle (chorion).

Chorionic Villi Time of formation:

They start formation at the end of the 2nd gestational week then continues during the 3rd week.

Third week 22

Types: ▪ Primary villi: Cytotrophoblast cells proliferate and push

syncytiotrophoblast to form the primary villi which are separated from each other by lacunae filled with maternal blood.

▪ Secondary villi: They are formed when somatic extraembryonic mesoderm enters the core of the primary villi. They are formed at the middle of the third week.

▪ Tertiary villi: They are formed when fetal blood vessels appear in the mesoderm of secondary villi at the end of the third week. They are separated by intervillous spaces filled with maternal blood. Cytotrophoblastic shell is formed when cytotrophoblast cells penetrate syncytiotrophoblast at the apices of the stem villi and extend to surrounds chorionic villi and the intervillous spaces.

Parts of the tertiary villus: (Fig.IV-2)

Each villous is composed of: 1. Stem (anchoring) villus: It is the stem of the villous that extends

between chorion and decidua basalis. 2. Free (floating or absorbing) villi: They are side branches from

the stem villous that float in the maternal blood inside the intervillous spaces. They are responsible for exchange of nutrient and gases with maternal blood.

Parts of chorion: (Fig.IV-3) A. Chorion frondosum (chorionic plate): It is the part of the

chorion that carries well developed tertiary villi that face decidua basalis.

B. Chorion laeve: It is the rest of the chorion that carries

degenerating tertiary villi which are covered with decidua capsularis.

Fate of chorion:

Chorion frondosum (chorionic plate) persists to share in the formation of placenta while chorion laeve degenerates.

Third week 23

Fig. IV-1: Development of chorionic villi.

Fig.IV-2: Parts of tertiary chorionic villi.

Third week 24

Fig.IV-3: Parts of chorion.

Gastrulation

Gastrulation is the transformation of bilaminar embryonic disc into trilaminar disc. It starts by development of primitive streak and primitive node in the epiblast layer. (Figs. IV-4&5)

Primitive streak: It appears in the midline of the caudal part of the embryonic disc

as a median narrow groove with bulging sides. It is developed from proliferation and migration of epiblast cells towards the primitive groove. After its appearance, it is possible to identify the embryo’s cranio-caudal axis, ventral and dorsal aspects as well as its right and left sides.

Primitive node: It is a rounded bulge in the cephalic end of the primitive streak

with middle depression known as primitive pit. Invagination: (Fig. IV-6)

Epiblast cells migrate towards the primitive groove to pass through it towards the hypoblast to form:

• Endodermal layer that replaces the hypoblast.

• Intra-embryonic mesoderm which forms middle layer in the

Third week 25

embryonic disc. • Notochord in the median region of the embryonic disc.

The remaining epiblast layer is called ectoderm and its junction with amnion is called amnio-ectodermal junction.

• Finally, the embryonic disc becomes formed of 3 germ layers (ectoderm, mesoderm and endoderm).

Buccopharyngeal membrane

It is a rounded area of fusion between ectoderm and endoderm at the cranial part of the embryonic disc.

Cloacal membrane

It is a rounded area of fusion between ectoderm and endoderm at the caudal part of embryonic disc.

Shape change of the embryonic disc

At the beginning of the third week, the disc is oval in shape then due to spread of intraembryonic mesoderm, the cranial part becomes broader than the caudal part giving the disc the pear shape. (Fig.IV- 5)

Fig.IV-4: Formation of primitive streak and primitive node.

Third week 26

Fig.IV-5: Change in the shape of the embryonic disc.

Fig.IV-6: Invagination of epiblast cells through the groove of the

primitive streak (Gastrulation).

Third week 27

Notochord

Notochord is the temporary axial skeleton of the embryonic disc.

Development :( Figs.IV-7,8,9,10,11,12&13)

➢ Prenotochordal process: It is formed by invagination of solid cord of cells from primitive pit. Prenotochordal process extends cranially in the midline between ectoderm and endoderm till the buccopharyngeal membrane.

➢ Notochordal canal: Primitive pit extends into the process transforming it into a canal. Its roof is in contact with the ectoderm while the floor is fused with endoderm.

➢ Neurenteric canal: It is temporary communication between amniotic cavity and yolk sac due to degeneration of floor of the canal together with median endoderm fused with it.

➢ Notochordal plate: It is the persisting roof of the canal that fuses

with the remaining endoderm. ➢ Definitive notochord: Notochordal plate becomes folded upon

itself to form solid cord (definitive notochord). Endoderm regenerates so amniotic cavity and yolk sac regain their separation from each other.

Importance of notochord

1. It is a temporary axial skeleton of the embryonic disc. 2. During folding, its firmness limits head fold. 3. Vertebral column is formed around it.

Fate of notochord

Vertebral column and intervertebral discs are formed around the notochord which persists as nucleus pulposus inside the intervertebral disc.

Third week 28

Fig.IV-7: Median LS of embryo showing the formation of prenotochordal process.

Fig.IV-8: Median LS of embryo showing the formation of notochordal canal.

Third week 29

Fig.IV-9: Median LS of the embryo showing degeneration of floor of the notochordal canal with underlying endoderm.

Fig.IV-10: Median LS of the embryo showing the neurenteric canal.

Third week 30

Fig.IV-11: TS of the embryo showing the fusion between notochordal plate with endoderm.

Fig.IV-12: TS of the embryo showing folding of notochordal plate.

Third week 31

Fig.IV-13: TS of the embryo showing the formation of definitive notochord.

Intra-embryonic mesoderm

Cells of intraembryonic mesoderm originate from the epiblast

cells that migrate to primitive streak and primitive node. Then they slip through primitive groove and pit to invaginate between ectoderm and endoderm. Intraembryonic mesoderm forms the middle layer of embryonic disc transforming it into trilaminar disc (gastrulation) (Figs.IV- 14,15&16). Intra-embryonic mesoderm is not present at the following sites:

1. Buccopharyngeal membrane.

2. Cloacal membrane. 3. Site of notochord. 4. Site of neural tube.

At 17th day, intraembryonic mesoderm is divided into paraxial-, intermediate- and lateral plate-mesoderm. (For details see chapter V).

Third week 32

Fig.IV-14: Formation of intraembryonic mesoderm.

Fig.IV-15: Transverse section of embryonic disc showing differentiation of intraembryonic mesoderm

Third week 33

Fig.IV-16: Differentiation of intraembryonic mesoderm.

Third week 34


1- Describe the structure of the 3ary chorionic villus. Mention its

parts and its function. 2- Explain why the epiblast is the mother layer of all three germ

layers. 3- Mark the following sentences as right (ے) or wrong (X):

a- The primitive streak results from migration of the epiblast cells.( ) b- The buccopharyngeal membrane is formed of three germ layers.(

) c- The notochord persists in the whole adult vertebral column.( ) d- The amniotic cavity and yolk sac never communicate.( )

Key answer of Right or Wrong statements 3 –

a) Right. b) Wrong. c) Wrong. d) Wrong.

Key words 1. Chorionic villi – structure – functions. 2. Epiblast – germ layers of embryonic disc.

Embryonic period 35

CHAPTER 5

ILOs:

By the end of this chapter, the student should be able to: ▪ Determine the embryonic period and its significance. ▪ List the different structures and organs derived from each of the three

germ layers; ectoderm, mesoderm and endoderm. ▪ Trace the steps of formation of the central nervous system out of

ectoderm. ▪ Follow the differentiation of subtypes of intraembryonic mesoderm

(paraxial, intermediate and lateral plate) and cite the fate and derivatives of each subtype.

▪ Describe the process of folding of the embryonic disc and discuss its results.

EMBRYONIC PERIOD (4TH- 8TH)

The embryonic period, or period of organogenesis, occurs from the 4th to the 8th week of development. It is the time when each of the three germ layers of the embryo gives rise to a number of derivatives.

A-Derivatives of Ectoderm

I-Central nervous system: (Figs.V-1&2)

Formation of central nervous system (Neurulation) is induced by growth factors secreted from developing notochord. It is developed through the following steps:

➢ Neural plate: It is the thickened median region of ectoderm

which is formed by change of the shape of ectodermal cells to be columnar. It is formed at the median region between primitive node and buccopharyngeal membrane dorsal to notochord. Two strips of cells known as neural crest are present on both sides of the neural plate.

➢ Neural groove: It is a median depression in the neural plate with two elevated neural folds on both sides. Neural crests are present on both sides of neural folds.

➢ Fusions: Fusions between three structures occur as follows:

1. Neural folds fuse together, starting at the neck and extending in cranial and caudal directions to form a neural tube. The last parts to be fused are cranial neuropore

Embryonic period 36

(closes at the 25th day) and caudal neuropore (closes at the 27th day).

2. Neural crest strips fuse together dorsal to the neural tube. Then it splits into two columns, dorsolateral to the neural tube.

3. The rest of ectoderm fuse together to cover the neural crest and neural tube forming surface ectoderm.

Fate of neural tube: It forms the central nervous system (brain inside the skull and spinal cord in the vertebral canal).

II-Neural crest: (Fig.V-3) They are two strips of ectodermal

cells on both sides of neural plate. Development:

➢ During fusion of the neural folds, the two neural crests bands fuse together to form median single strip dorsal to neural tube that is covered by surface ectoderm.

➢ Then it divides into two longitudinal columns of cells on the dorsolateral aspect of neural tube.

Derivatives: Neural crest cells migrate to give rise to the

following derivatives: • Ganglia (sensory, sympathetic and parasympathetic). • Cells (Schwann, glial, melanoblast and pigmented

epithelium of iris). • Adrenal medulla, arachnoid and pia mater. • Some bones of the skull and enamel of teeth. • Septum between ascending aorta and pulmonary trunk.

III- Otic and lens placodes

They are ectodermal thickenings at the cranial part of the embryo.

• Otic placode forms otic vesicle and then the internal ear. • Lens placode forms lens of the eye.

IV- Other derivatives of ectoderm

• Peripheral nerves. • Sensory epithelium of ear, nose, eye, and epidermis of

skin. • Pituitary gland.

• Anterior part of oral cavity and lower part of anal canal.

Embryonic period 37

Fig.V-1: Dorsal aspect of an embryo showing formation of neural

tube.

Fig.V-2: Dorsal (A) and lateral (B) views of an embryo showing terminal steps of neural tube formation.

Embryonic period 38

Fig.V-3: Cross sections showing the formation of neural tube and neural crest.

B-D evelopment of intraembryonic mesoderm

It is the layer that separates between ectoderm and endoderm.

Origin: Intraembryonic mesoderm cells originate from epiblast cells that invaginate through the groove of primitive streak and primitive pit (Fig.IV-14).

Site: It is present between ectoderm and endoderm except in the

following sites: a) Buccopharyngeal membrane. b) Cloacal membrane.

c) Median region which is occupied by developing notochord and neural tube.

Differentiation: (Figs. IV-14,15&16)

At the 17th day, the intraembryonic mesoderm is divided into 3 parts:

Embryonic period 39

1. Paraxial mesoderm: It is the part of intraembryonic mesoderm that is present on both sides of notochord and neural tube.

2. Intermediate mesoderm: It is present between paraxial and lateral plate mesoderm.

3. Lateral plate mesoderm: It is the most lateral part of intraembryonic mesoderm.

N.B.

• Cells from cranial part of primitive streak form paraxial mesoderm.

• Cells from middle part of primitive streak form intermediate mesoderm.

• Cells from caudal part of primitive streak form lateral plate mesoderm.

1- Paraxial mesoderm: (Figs.V-4,5,6&7)

It is the part of the intraembryonic mesoderm on both sides of notochord and neural tube.

Segmentation: Paraxial mesoderm divides transversely into segments known as somites. Segmentation starts at the occipital region and extends caudally. Smaller segments of paraxial mesoderm are present cephalic to the first occipital somite and are called somitomeres. (Fig.V-6)

Somites: They are segmented masses of the paraxial mesoderm. Time of segmentation:

First pair appears in the 20th day, and then three pairs are formed per day till the 30th day (somite period). Then segmentation continues in a slower rate till the 35th or 40th day. Number:

They are 42 – 44 pairs of somites. Determination of the age of the embryo (Somite period)

Number of somites - 1 Age in days = + 20

3 Regional classification:

4 occipital, 8 cervical, 12 thoracic, 5 lumbar, 5 sacral and 8 – 10 coccygeal somites.

Embryonic period 40

Differentiation of somites: (Figs.V-5&6) Each somite is divided obliquely into:

1. Sclerotome: It is the ventromedial part of the somite

that: ▪ Migrates medially and surrounds the notochord to

form the vertebral bodies and intervertebral discs. ▪ Migrates medially and surrounds neural tube to

form the neural arch of vertebrae. 2. Dermomyotome: It is the dorsolateral part of the somite that is further subdivided into:

a) Dermatome: It forms the dermis of the skin whereas epidermis is formed from ectoderm.

b) Myotome: It divides into dorsal part that forms skeletal muscles of the back of the body and ventral part that forms skeletal muscles of anterolateral aspect of body and limbs. N.B. Each spinal nerve divides into dorsal and

ventral primary rami to supply divided parts of the myotomes (Fig.V-6)

Fig.V-4: Segmentation of paraxial mesoderm (somites).

Embryonic period 41

Fig.V-5: Fate of paraxial mesoderm.

Fig.V-6: Fate of myotomes.

Embryonic period 42

2-Intermediate mesoderm (Fig.IV-15&16)

• It lies between paraxial mesoderm and lateral plate mesoderm.

• It is partially segmented.

• It forms the urogenital system.

3- Lateral plate mesoderm (Fig.IV-15&16)

• It is the part of intra-embryonic mesoderm that lies lateral to intermediate mesoderm.

• Lateral plate mesoderm on both sides are continuous together cranial to buccopharyngeal membrane.

• It is continuous with the extra-embryonic mesoderm at the margin of the disc.

Intra-embryonic coelom: (Fig.V-7)

• It is a horse shoe cavity that is formed in the lateral plate mesoderm.

• Its caudal ends communicate with extra-embryonic coelom at the margin of embryonic disc.

• It is divided into

a) Pericardial cavity in median cranial part of the coelom.

b) Peritoneal canals in the lateral part of the coelom. c) Pleural cavities between pericardium and

peritoneal canals. • Lateral plate mesoderm is split by intraembryonic

coelom into: 1. Somatopleuric (somatic) mesoderm: It is the

mesoderm that is present in contact with ectoderm. It forms connective tissue of anterolateral walls of the body as well as parietal layer of pleura, pericardium and peritoneum.

2. Splanchnopleuric (splanchnic) mesoderm: It is the mesoderm that is present in contact with endoderm. It forms smooth muscles and connective tissue of gut and respiratory tract, cardiac muscles as well as visceral pleura, pericardium and peritoneum.

N.B.

▪ Cardiogenic area is the splanchnic mesoderm related to pericardium.

▪ Septum transversum is a mass of mesoderm cranial to pericardium (before folding) and caudal to pericardium (after folding).

Embryonic period 43

Fig.V-7: Divisions of intraembryonic mesoderm and of the intraembryonic coelom.

C-Derivatives of Endoderm

Endodermal layer gives rise to: 1. Lining epithelium of :

▪ Digestive system except its beginning and end.

▪ Respiratory tract. ▪ Most of urinary bladder and urethra.

▪ Tympanic cavity and Eustachian tube. 2. Glandular epithelium:

▪ Parenchyma of liver, pancreas, thyroid, thymus, tonsils (palatine & nasopharyngeal) and parathyroid glands.

Embryonic period 44

FOLDING

It is the process by which the embryonic disc becomes folded upon itself.

Time of folding: It starts at the end of 3rd week and is completed at

the end of 4th week.

Types of folding: 1. Cephalo-caudal folding: forming head and tail folds. 2. Lateral folding: It is the folding of sides of the embryonic

disc.

Causes of folding: 1. Increase of longitudinal length of the embryonic disc due

to growth of neural tube and somites leads to cephalo- caudal folding.

2. Expansion of amniotic cavity leads to folding in all directions.

Limitations of head & tail folds:

Head fold is limited by relatively firm cranial end of notochord while tail fold is limited by relatively firm primitive streak.

Steps of folding: (Figs.V-8&9)

➢ Expansion of amniotic cavity leads to ventral shift of amnio- ectodermal junction towards endoderm with subsequent incorporation of a part of yolk sac inside the folded embryo. The embryonic disc gradually bulges into the amniotic cavity.

➢ The embryo thus acquires a cylindrical shape;

▪ The ectoderm becomes on the outer surface of the embryo.

▪ It contains a cavity that is lined with endoderm called gut.

▪ The primitive umbilical ring is present on the ventral body wall and is surrounded by the amnioectodermal junction.

▪ The embryo becomes completely surrounded by the amniotic cavity bathing in the amniotic fluid.

➢ Cranio-cuadal elongation of the embryonic disc by the growth of neural tube and somites leads to formation of head fold and a tail fold due to cephalo-caudal folding.

Results of folding:(Figs.8,9&10)

a. The embryonic disc changes into cylindrical shape which has a body cavity.

b. Amniotic cavity surrounds the cylindrical embryo.

Embryonic period 45

c. Formation of primitive umbilical ring by ventral shifting of the amnio-ectodermal junction. It contains the connecting stalk, allantois and the vitelline duct.

d. Formation of the gut that is lined with endoderm; foregut in the head fold, midgut in the middle and hindgut in the tail fold.

e. Formation of the definitive yolk sac which is the part of the yolk sac that remains outside the abdomen in the umbilical cord. The midgut is connected to the definitive yolk sac by the vitelline duct.

f. Formation of forebrain bulge in the head fold which is separated from pericardial bulge by stomodeum. Buccopharyngeal membrane separates stomodeum from foregut.

g. Peritoneal canals of intraembryonic coelom surround the gut with subsequent formation of the mesenteries.

h. Reversal of position: 1. Heart and pericardium become cranial to septum

transversum (before folding, septum transversum was the most cranial).

2. Connecting stalk and allantois become ventral and cranial to cloacal membrane instead of being the most caudal before folding.

Fig.V-8: Lateral folds of the embryo.

Embryonic period 46

Fig.V-9: Cranio-caudal folding of the embryo.

Fig.V-10: Median longitudinal section of folded embryo.

Embryonic period 47


1- Discuss paraxial mesoderm regarding site, segmentation

and fate.

2- Regarding formation of central nervous system, mark the

correct statement:

a) It is derived from ectoderm.

b) It is not induced by the underlying notochord.

c) The neural groove results from depression of the

neural crest.

d) The first area of the neural tube to close is its caudal

end.

Key answer of MCQ

2- a

Key words:

1. Paraxial mesoderm.

2. Germ layers of embryonic disc – fate.

Fetal membranes 48

CHAPTER 6

ILOs:


▪ Define the chorion and describe the steps of its formation.

▪ Define the placenta.

▪ Describe the external features and structure of full term placenta.

▪ Identify the placental circulation and barrier.

▪ List the functions of placenta.

▪ Describe the malformations of placenta.

▪ Define the amnion and describe the steps of its formation.

▪ Figure out the features of amniotic fluid.

▪ Enumerate the functions of amniotic fluid.

▪ Recognize the abnormalities of amniotic fluid.

▪ Define the umbilical cord and describe its morphology at full term.

▪ Recognize the functions of the umbilical cord.

▪ Describe the steps of formation of the umbilical cord.

▪ Identify the abnormalities of umbilical cord.

▪ Define the yolk sac and describe its different stages of development.

▪ List the functions of yolk sac.

Fetal Membranes

They are structures that are developed from the zygote but do not share in the formation of a part of the embryo, they are:

1- Chorion and placenta. 2- Amnion. 3- Umbilical cord. 4- Yolk sac.

Chorion

Definition: Chorion is the wall of chorionic vesicle.

Formation: (Figs.III-11&12)

• At the 12th day, extra-embryonic mesoderm is formed on the inner aspect of cytotrophoblast.

• Chorionic vesicle is formed when spaces in the extraembryonic

Fetal membranes 49

mesoderm fuse to form extra-embryonic coelom (chorionic cavity) with subsequent division of the mesoderm into:

1. Somatic mesoderm which lines the cytotrophoblast and covers the amniotic cavity.

2. Splanchnic mesoderm which covers the yolk sac.

Layers of chorion: It is composed of the following layers (from external

to internal): 1. Syncytiotrophoblast. 2. Cytotrophoblast.

3. Extraembryonic somatic mesoderm.

Chorionic villi: see chapter IV.

Placenta

Definition: It is the organ through which exchange of materials occurs

between maternal and fetal blood.

External features of full-term placenta Shape: Disc shape.

Weight: 500 – 600 gm. Diameter: 15 – 20 cm

Thickness: 3 cm.

Site: Mostly in the upper segment of posterior wall of the uterine

cavity, near fundus (Fig.VI-1). Surfaces: It has 2 surfaces (Fig. VI-1)

1. Fetal surface: It is the surface that faces the fetus. It is smooth and covered with transparent amnion. Umbilical cord is attached near its center.

2. Maternal surface: It is the surface that lies in contact with internal surface of uterine wall. It shows the presence of 15 – 20 elevations named cotyledons which are separated from each other by grooves. It is covered by a thin layer of decidua basalis.

Formation of placenta: Placenta is formed by union between two main parts:

1. Maternal Part: This is the decidual plate (decidua basalis). 2. Fetal part: This is the chorionic plate (chorion frondosum).

Structure of placenta: (Fig. VI-2)

Placenta is composed of: 1. Chorionic plate: which is formed of (from external to internal):

a) Amnion. b) Somatic extraembryonic mesoderm. c) Cytotrophoblast.

Fetal membranes 50

d) Syncytiotrophoblast. 2. Decidual plate: which is formed of (from internal to external):

a) Syncytiotrophoblast which lines the intervillous space. b) Cytotrophoblastic shell. c) Decidua basalis.

3. Chorionic villi: which are tertiary villi of the chorion frondosum and are composed of the following layers:

a) Syncytiotrophoblast is the outer layer.

b) Cytotrophoblast. c) Somatic extraembryonic mesoderm.

d) Endothelium of fetal blood vessels. Parts of the chorionic villi: a) Stem (anchoring) villi: It is the main part of the villous that

extends between chorionic and decidual plates. b) Floating (absorbing or free) villi: They are side branches from

stem villi that float in maternal blood in the intervillous spaces to allow exchange of food material and gases between fetal and maternal blood.

4. Intervillous space: It is formed of intercommunicating spaces

that separate between stem villi and extend from chorionic plate to decidual plate. Maternal arterioles and venules open into the spaces through the decidual plate.

5. Placental (decidual) septa

▪ They are septa that extend from decidual plate to the cavity of intervillous spaces.

▪ They appear during 4th and 5th months.

▪ They are incomplete septa that do not extend to the chorionic plate.

▪ Each septum is composed of a core of decidua basalis, covered with cytotrophoblast and syncytiotrophoblast.

▪ Cotyledons on the maternal surface are separated by grooves that correspond to inwards extension of the placental septa.

Placental circulation: It is the circulation of blood inside the placenta

and is composed of: 1- Maternal part (circulation of maternal blood) • Arterial blood flows to the intervillous spaces through 80 – 100

decidual arterioles. • Full term placenta contains about 150 ml of maternal blood which

is changed 3 – 4 times/min. • Maternal blood flows back towards the decidual plate to leave the

intervillous space through maternal venules.

Fetal membranes 51

2- Fetal part (inside fetal blood vessels) • Umbilical arteries leave the abdomen of the fetus through

umbilical cord. They reach the fetal surface of placenta where they branch to enter the tertiary villi inside the placenta.

• After the exchange between fetal and maternal blood the fetal blood is carried through left umbilical vein to the fetal heart where it is distributed to the body of fetus.

Placental barrier (membrane): It is the membrane that separates

between fetal blood (inside the tertiary villi) and maternal blood (in the intervillous spaces). Early placental barrier is composed of the following layers:

a. Endothelium of the fetal blood vessels. b. Somatic extraembryonic mesoderm. c. Cytotrophoblast.

d. Syncytiotrophoblast. Late placental barrier (from 4th month) it is composed of:

a. Endothelium of fetal blood vessels. b. Syncytiotrophoblast.

So, the placental membrane becomes thinner in the second half of pregnancy to allow rapid exchange of nutrition and gases to give adequate supply to the larger fetus.

Functions of placental barrier: a. It separates between fetal and maternal blood. b. It permits gaseous, nutritive and waste products exchange. c. It prevents passage of bacteria and most of viruses (except

Human Immunodeficiency Virus (HIV), poliomyelitis, rubella, cytomegalovirus, and measles.

d. It prevents passage of most toxic material and most of maternal hormones (except some synthetic hormones e.g. progestin and diethylstilbestrol).

Fetal membranes 52

Fig.VI-1: Fetal (A) and maternal (B) surfaces of placenta.

Fig.VI-2: Structure of the placenta

Fetal membranes 53

Functions of placenta:

1. Exchange of metabolic products, as it allows transmission of nutritive substances from maternal to fetal blood and in the opposite direction waste products are transmitted from fetal to maternal blood.

2. Exchange of gases; giving oxygen to fetus and receiving CO2 from fetal blood.

3. Transmission of maternal antibodies to the fetus starting from 14th

week, so the fetus will gain immunity since this time. 4. It has an endocrine function as it produces:

a) Progesterone hormone which maintains the endometrium of pregnancy.

b) Estrogen hormone which stimulate uterine growth and development of mammary gland.

c) Human chorionic gonadotropins (HCG) which maintains the corpus luteum till the 4th month. It is used to detect pregnancy.

d) Somatomammotropin gives fetus the priority on maternal blood glucose. It also promotes breast development.

5. Placenta has a protective role as it prevents passage of bacteria and most of viruses from mother to fetus.

6. Placenta has excretory function as it gets rid of fetal urea and creatinine.

Abnormalities of Placenta

1- In position (placenta previa): (Fig.III-4) due to implantation of the embryo in the lower segment of the uterus, forming placenta previa. Types of placenta previa:

a) Placenta previa parietalis: the margin of placenta is above the internal os.

b) Placenta previa marginalis: the margin of placenta covers the internal os.

c) Placenta previa centralis: the central part of placenta covers the internal os.

2- In shape: Placenta may be bilobed or trilobed.

3- In number: a) Twin placenta: Two identical placentae with two umbilical cords. b) Accessory placenta: The main placenta is accompanied with

small placenta (Fig.VI-3). 4- In attachment of umbilical cord:

a) Velamentous placenta: The umbilical cord is attached to placenta

Fetal membranes 54

through membranes (Fig.VI-4). b) Battle door placenta: the cord is attached to the margin of

placenta (Fig.VI-5). 5- n diameter: Thinner and wider placenta is called placenta membranacea. 6- In infiltration: (Fig.VI-6) Deep infiltration of placenta to the myometrium or even to the covering peritoneum is known as placenta accreta, increta (myometrium) or percreta (peritoneum).

Fig.VI-3: Accessory placenta.

Fig.VI-4: Velamentous placenta.

Fetal membranes 55

Fig.VI-5: Battle door placenta.

Fig.VI-6: Placenta accreta, increta and percreta.

Fetal membranes 56

Amnion

Definition: Amnion is the wall of amniotic cavity. After folding the

amniotic cavity surrounds the fetus.

Formation of amniotic cavity: (Figs. VI-7&8)

• Amniotic cavity appears at the 8th day within the embryoblast cells.

• It separates between the amnioblasts (adjacent to cytotrophoblast) and epiblast (adjacent to hypoblast).

• Amnioblast cells start production of amniotic fluid. • In the third week, the junction between ectoderm and amnion is

called amnio-ectodermal junction.

Expansion of the amniotic cavity: (Fig:VI-9) leads to:

• After folding, the amnioectodermal junction is shifted ventrally and surrounds the primitive umbilical ring.

• With more expansion, amnion surrounds the umbilical cord and covers the fetal surface of placenta.

• At the 3rd month, the amnion comes in contact with chorion to form amniochorionic membrane with obliteration of chorionic cavity.

• By the end of the 3rd month, amniochorionic membrane covered with decidua capsularis comes in contact with decidua parietalis obliterating uterine cavity.

Amniotic fluid

▪ It is clear, watery fluid which is mainly composed of water, electrolytes, proteins, carbohydrates, lipids, phospholipids, and urea.

▪ It is partially produced by amnioblast cells but primarily it is derived from maternal blood by osmosis through the amnion. After kidney development, fetal urine is added to the amniotic fluid starting from the fifth month.

Volume of amniotic fluid: It reaches 1.0 – 1.5 liter starting from

the 37th week till birth.

Amniotic fluid and stem cells: Recent studies show that

amniotic fluid contains a considerable quantity of stem cells. These amniotic stem cells are pluripotent and able to differentiate into various tissues, including brain, liver and bone.

Fetal membranes 57

Functions of amniotic fluid: A-At early pregnancy: 1. It acts as shock absorbent protecting the fetus against external

trauma. 2. It acts as heat insulator keeping constant fetal temperature.

3. It prevents adhesion of the embryo to the wall of uterus. 4. It prevents adhesion of fetal parts together e.g. limb to the body. B-At late pregnancy:

1. It gives a space for fetal movements which is essential for development of fetal muscle.

2. It gives a space for accumulation of urine.

3. At the beginning of 5th month, the fetus starts to swallow the amniotic fluid and this helps the fetus to learn suckling.

C-During delivery: 1. It protects the fetus against uterine contractions. 2. Forebag of amniotic sac helps gradual dilatation of cervical canal.

3. Rupture of forebag of amniotic sac is the sign of start of labor. 4. Sterile amniotic fluid washes vagina just before passage of the

fetus.

Abnormalities of amniotic fluid 1-Polyhydramnios

▪ It is the increase of amniotic fluid volume to be more than two liters at full term.

Causes:

a) Unknown cause in 35 % of cases. b) Maternal diabetes. c) Congenital malformation as esophageal atresia that interferes

with normal fetal swallowing. d) Congenital malformation of central nervous system. e.g.

anencephaly. 2-Oligohydramnios

▪ It is the decrease of the amniotic fluid volume to be less than 400 ml at full term.

Causes:

• It may result from renal agenesis or obstruction of urinary tract. 3-Premature rupture of amniotic sac

It is the rupture of amniotic sac before start of uterine contractions. It is the most common cause of preterm labor. No cause could be identified for this condition.

Fetal membranes 58

Fig.VI-7: Start of formation of amniotic cavity.

Fig.VI-8: Expansion of amniotic cavity.

Fetal membranes 59

Fig.VI-9: Expansion of amniotic sac leads to obliteration of chorionic

and uterine cavities.

Umbilical Cord

Definition: It is the cord that connects between fetus and placenta.

Morphology of umbilical cord: ➢ Attachments: It extends between fetal surface of placenta and ventral

aspect of fetal abdominal wall. (Fig. VI-10) ➢ Length: 50 – 60 cm. ➢ Structure: (Fig.VI-11) It contains two umbilical arteries and one

umbilical vein embedded in Wharton’s jelly and covered with amnion.

Functions of umbilical cord: 1. It contains umbilical vessels that transmit fetal blood between the

fetus and the placenta. 2. It allows free mobility of the fetus.

Development of the umbilical cord: A-Formation of primitive umbilical ring: (Fig.VI-12) ▪ Expansion of amniotic cavity, leads to folding of the embryonic

disc (during 4th week) with ventral shifting of amnio-ectodermal junction with subsequent formation of primitive umbilical ring.

Fetal membranes 60

Contents of the primitive umbilical ring: 1. Connecting stalk that contains allantois and umbilical vessels. 2. Vitelline duct and vitelline vessels.

B-Formation of primitive umbilical cord: (Fig.VI-13) ▪ Expansion of the amniotic cavity leads to collecting the contents

of primitive umbilical ring inside a sheath of amnion to form the primitive cord.

Contents of primitive umbilical cord: 1. Definitive yolk sac, vitelline duct and vitelline vessels.

2. Connecting stalk, remnant of allantois and umbilical vessels. 3. At the 6th week, intestinal loop herniates in the proximal part of

the umbilical cord (physiological hernia).

C-Formation of definitive umbilical cord: ▪ Intestinal loop returns to the abdominal cavity by the 3rd month. ▪ Obliteration of vitelline duct, allantois, and extra-embryonic parts

of vitelline vessels. ▪ Degeneration of right umbilical vein with persistence of the left

vein. ▪ Formation of Wharton’s jelly from the mesoderm of

the connecting stalk.

Abnormalities of umbilical cord: 1. Short cord: leads to limitations of movements of the fetus and

premature separation of placenta. 2. Long cord: The long cord may encircle the neck of the fetus. 3. Congenital umbilical hernia (omphalocele): the cord contains

coils of intestine which failed to return to abdominal cavity. 4. Degeneration of one umbilical artery with persistence of one

artery. 5. Abnormal attachment of the umbilical cord which may be

attached to the margin of placenta (battledore) (Fig.VI-5) or through membranes (velamentous) (Fig.VI-4).

6. True knots which leads to obstruction of umbilical vessels with subsequent death of the fetus. False knots are sites where umbilical vessels become tortuous which do not interrupt blood flow.

Fetal membranes 61

Fig.VI-10: Umbilical cord connects placenta with ventral aspect of fetal abdominal wall.

Fig.VI-11: TS of the umbilical cord.

Fetal membranes 62

Fig.VI-12: Primitive umbilical ring with its contents.

Fig.VI-13: Physiological umbilical hernia inside primitive umbilical cord.

Fetal membranes 63

Yolk Sac

Definition: It is the sac that replaces the blastocele of the blastocyst. Development of the yolk sac:

Yolk sac passes through 3 stages: 1- Primary (primitive) yolk sac: (Fig. VI-14)

At the 9th day, Heuser’s membrane is developed from hypoblast cells and migrates to line the blastocele transforming it into primary yolk sac. 2- Secondary yolk sac: (Fig. VI- 15&16) It is formed at the 13th day due to the following changes: ▪ New generations of cells from hypoblast line the Heuser’s

membrane. ▪ Reduction of the size of yolk sac due to pinching off a part that is

known as exocoelomic cyst. ▪ Formation of allantois which is a diverticulum that extends from

the caudal part of yolk sac inside the connecting stalk. (Fig. VI- 14)

3- Defenitive yolk sac: (Fig. VI-17)

▪ During the 3rd week, the hypoblast layer is replaced by endodermal layer.

▪ After folding (during 4th week), yolk sac shares in the formation of the gut. The remaining part in the primitive umbilical cord is called definitive yolk sac.

▪ Definitive yolk sac is connected to the mid-gut by vitello-intestinal (vitelline) duct.

Fate of yolk sac: Definitive yolk sac and vitelline duct are gradually reduced in size

and finally degenerate.

Functions of yolk sac:

a) Formation of gut: Endodermal lining of the yolk sac shares in the formation of mucosa of foregut, midgut and hindgut after folding of the embryonic disc.

b) Formation of a part of urinary bladder from proximal part of allantois.

c) Formation of primordial germ cells: (Fig.I-1) at the 2nd week,

epiblast cells migrate to the wall of the caudal part of yolk sac to form primordial germ cells.

d) Vitelline vessels develop in the mesoderm around the vitelline duct. Intra-embryonic parts of vitelline vessels will remain and

Fetal membranes 64

form arteries and veins of the gut while the extraembryonic parts disappear.

e) Blood cells develop in the mesoderm of the yolk sac in early

pregnancy.

Fig.VI-14: Formation of primary (primitive) yolk sac.

Fig.VI-15: Formation of secondary yolk sac.

Fetal membranes 65

Fig.VI-16: Formation of allantois from caudal part of secondary yolk sac.

Fig.VI-17: Formation of definitive yolk sac and vitelline duct.

Fetal membranes 66


1. Describe the structure of placenta. 2. List the functions of yolk sac.

3- olume of amniotic fluid at full term ranges between: a) 1000 – 1500 ml. b) 500 – 600 ml. c) 2000 – 3000 ml.

d) 800 – 1000 ml.

Answer of MCQ: 3- a

Key words:

1. Placenta - structure. 2. Placenta - malformations. 3. Amniotic fluid – functions.

4. Umbilical cord – development. 5. Polyhydramnios. 6. Umbilical cord – malformations.

7. Yolk sac – functions.

Fetal period 67

CHAPTER 7

ILOs:

By the end of this chapter, the student should be able to: ▪ Identify the fetal period. ▪ Describe how to measure the fetus at different stages of growth.

FETAL PERIOD

It is the period from the beginning of the ninth week till birth is known as the fetal period. It is characterized by maturation of tissues and organs as well as rapid growth of the body (Fig.VII-1). The length of the fetus is usually indicated as the crown-rump length (CRL) (sitting height) or as the crown-heel length (CHL), the measurement from the vertex of the skull to the heel (standing height). These measurements, are correlated with the age of the fetus in weeks (Table 1).

Age (weeks)

C-R length (cm)

Weight (grams)

9 - 12 5 – 8 10 – 45

13 - 16 9 - 14 60 - 200

17 -20 15 - 19 250 - 450

21 – 24 20 - 23 500 – 820

25 – 28 24 – 27 900 – 1300

29 – 32 28 – 30 1400 – 2100

33 – 36 31 – 34 2200 – 2900

37 – full term 35 – 36 3000 – 3400

Table 1: growth changes during fetal life.

Relative size of head to body :( Fig. VII- 2) • At the beginning of the 3rd month, the head is 1/2 the CR length. • At the beginning of the 5th month, the head is 1/3 the CH length. • At birth, the head is 1/4 of CH length.

Changes in external features:

• Face becomes human looking during the 3rd month. • Limbs become longer at the 3rd month.

Fetal period 68

• External genitalia are differentiated at the end of 3rd month. • Lanugo hair covers the fetus starting from the 4th month. • Skin of the fetus is covered by fatty substance called vernix

caseosa at the 5th month. • The skin is wrinkled till the end of 6th month due to absence of

subcutaneous fat. • Testes descend to scrotum just before birth.

Fetal movements: • Clearly recognized since the 5th month.

Time of birth

The duration of pregnancy is about 280 days (40 weeks) starting from the first day of last menstruation or more accurately 266 days (38 weeks) after fertilization.

Fig.VII-1: Fetal growth.

Fig.VII-1: Fetal growth.

Fetal period 69

Fig.VII-2: Relation between length of head and length of fetus.


1. What is meant by crown-rump length?

2. Fetal movements are normally perceived by the mother starting from

a) Third month. b) Fifth month.

c) Seventh month. d) Ninth month.

Key answer of MCQ: 2- b

Key words: 1- Human fetus – fetal measurements.

Twins & birth defects 70

CHAPTER 8

ILOs:


▪ Define the twins.

▪ Recognize the differences between variable types of twins.

▪ Define the birth defects.

▪ Realize the factors responsible for birth defects.

▪ Recognize different methods of fetal therapy.

TWINS

It is giving birth to more than one baby.

Types of twins:

1- Dizygotic (fraternal) twins: ➢ Cause: Formation of two zygotes by simultaneous

ovulation of two oocytes and fertilization by two sperms. ➢ Incidence: It is the commonest type. It represents 0.7 –

1.1% of the total births. ➢ Features:

▪ Each embryo implants separately. ▪ Each embryo develops its own amnion, chorion

and placenta. ▪ Offspring are not identical in shape and may be of

same or different sex. 2- Monozygotic (identical): (Fig. VIII-1) ➢ Cause: Splitting of a fertilized ovum at variable stages

of development. ➢ Incidence: 0.3 – 0.4 % of the total births. ➢ Features:

▪ Offspring are identical in shape and sex. ▪ Fetal membranes are variable according to the

stage at which splitting occurs. A. Splitting of the morula

• Morula divides into two morulae which develop into 2 separate balstocysts.

• Each embryo has its own amnion, chorion and placenta.

B. Splitting of the inner cell mass of early blastocyst • Single blastocyst which has 2 inner cell

masses. • Each embryo has its own amnion. • Both embryos have a common chorion and


placenta. C. Splitting of the embryonic disc of late blastocyst

• Single blastocyst which has 2 embryonic discs.

• Both embryos have a common amnion, chorion and placenta.

Fig.VIII-1: Types of monozygotic twins; divisions of the embryo at morula (A) stage, at early blastocyst stage (B) and late blastocyst stage(C).

Siamese (fused) twins: (Fig. VIII-2)

• It occurs due to incomplete split of the embryonic disc. • Twins may be fused at the head (craniopagus), at the

thorax (thoracopagus) or the pelvis (pygopagus).

• Success of surgical separation depends on the site of fusion and the organs in common between the twins.

Twin defects: Twins may suffer from increased incidence of

prematurity, low birth weight or high mortality rate.


FIG.VIII-2: TYPES OF SIAMESE TWINS.

BIRTH DEFECTS

They are structural abnormalities and / or functional disorders present at birth. They are caused by environmental or genetic factors acting independently or together. (Fig.VIII- 3)

Fig.VIII-3: Different causes of birth defects.


Risky gestational period (Fig. VIII-4)

The most sensitive time is the embryonic period (3rd to 8th week). During the fetal period (9th week to full term), the risk for gross structural defects are decreased, but organ systems may still be affected.

Fig.VIII-4: Graph showing high risk gestational period.

Factors Responsible for Birth Defects

A-E vironmental factors (teratogens) The effect of teratogens varies according to: ▪ Developmental stage at the time of exposure.

▪ Dose and duration of exposure of the teratogen. 1- Infectious agents

• Viruses: as German measles, cytomegalovirus, herpes simplex, varicella and HIV (AIDS).

• Bacteria: as Syphilis. • Parasites: as toxoplasma.

2-Radiations

Ionizing radiation (x-ray and gamma rays) has teratogenic effects because:

1. They kill rapidly proliferating cells.

2. They lead to genetic alteration of germ cells with subsequent fetal malformations.

3- Drugs and chemicals ▪ Most of drugs have teratogenic effects especially in the

first 3 months. ▪ Alcohol and nicotine have also a teratogenic effect.

4- Maternal causes

a) The incidence of congenital malformations is 3 – 4 times higher in the offspring of diabetic mother.


b) Iodine deficiency in maternal diet leads to baby cretinism. c) Obese mother give birth to babies with neurological

defects. d) Pregnant mothers above 40 years old have the higher

possibility to give birth to a child suffering from Down syndrome.

e) Mothers with cyanotic heart disease and those living in high altitude may give birth to small size infants with no gross congenital anomalies.

f) Hyperthermia (increased body temperature) either caused secondary to bacterial infections or externally as exposure to hot sun or sauna may affect neurulation leading to anencephaly or spina bifida.

5- Paternal causes

a) Exposure to chemicals and radiation can cause mutations in male germ cells. b) Advanced age may lead to chromosomal defects in male gametes with subsequent anomalies in the offspring e.g. Down syndrome.

B-C hromosomal abnormalities

1-Numerical

The offspring has abnormal chromosomal number. It could be autosomal or in sex chromosomes. I-Autosomal

• Trisomy 21 (Down syndrome or mongolism): (Fig. VIII-5 A) In this case there is an extra chromosome 21 so the chromosomal number is 45 + XX or XY. This occurs due to non-disjunction of chromosomes 21 during 1st meiotic division of the oocyte. The possibility of a child with Down syndrome increases with the increase of the age of the mother. Mongol child has specific facial features with mental retardation.

• Trisomy 13, 15, 17 or 18: are less common and the infant suffers from many congenital anomalies and usually dies by the age of 2 months after birth.

II-Sex-chromosomes

• Klienfelter syndrome (44 + XXY): It occurs due to non- disjunction of X-chromosomes during division of oocyte. Male child suffers from gynecomastia and infertility.

• Turner syndrome (44 + X0): (Fig. VIII-5 B) this occurs due to non-disjunction of sex chromosomes during division of either male or female gametes. A female child suffers from webbed neck and infertility due to agenesis of ovaries.


2- Structural chromosomal abnormalities They result from breaking of a chromosome due to

exposure to viruses, radiations or drugs. A. Cri-du-Chat syndrome (Fig. VIII-6 A) In this case there

is a partial deletion of short arm of chromosome 5. This child suffers from cat like cry, microcephaly, mental retardation and congenital heart disease.

B. Angelman syndrome (Fig. VIII-6 B) In this case there is partial deletion of long arm of chromosome 15. This child suffers from mental retardation, inability to speak, poor motor development and prolonged period of laughter.

Prevention of birth defects

Many birth defects can be prevented. For example, supplementation of salt or water supplied with iodine, eliminates mental retardation and bone deformities resulting from cretinism. Folate supplementation lowers the incidence of neural tube defects, such as spina bifida and anencephaly, and also reduces the risk for hyperthermia-induced abnormalities. Avoidance of alcohol and other drugs during all stages of pregnancy reduces the incidence of birth defects.

Prenatal diagnosis of fetal malformations

To assess the growth and development of the fetus in utero, routine ultrasonography examination, maternal serum screening (level of alpha feto-protein), amniocentesis (for genetic analysis of sloughed fetal cells), and chorionic villus sampling (sample from placenta for genetic analysis) should be performed when there is a suspicious fetal malformation.


Fig.VIII-5: Photographs showing two children with Down (A) and Turner (B) syndromes.

Fig.VIII-6: Photographs of children with Cri-du chat (A) and Angelman (B) syndromes.


FETALTHERAPY

1. Fetal transfusion

In cases of fetal anemia produced by maternal antibodies or other causes, blood transfusion to the fetus can be performed. Ultrasound is used to guide insertion of a needle into the umbilical cord vein, and blood is transfused directly into the fetus.

2. Fetal medical treatment

Treatment of infections, fetal cardiac arrhythmias and other medical problems is usually provided to the mother and reaches the fetus through maternal blood after crossing the placenta. In some cases, however, agents may be administered to the fetus directly by intramuscular injection into the gluteal region or via the umbilical vein.

3. Fetal surgery

Because of advances in ultrasound and surgical procedures, operating on fetuses has become possible. It could be done either by open fetal surgery or by minimally invasive fetoscopic surgery (fetendo) that uses small incisions and is guided by fetoscopy and sonography However, because of risks to the mother, infant, and subsequent pregnancies, procedures are only performed in centers with well-trained teams and only when there are no reasonable alternatives.

It is indicated in cases of repairing congenital diaphragmatic hernia, congenital heart defects or even neural tube defects.

4. Stem cells therapy

Stem cells have two important characteristics that distinguish them from other types of cells. First, they are unspecialized cells that renew themselves for long periods through cell division. The second is that under certain physiologic or experimental conditions, they can be induced to become cells with special functions such as the beating cells of the heart muscle or the insulin- producing cells of the pancreas. Scientists primarily work with two kinds of stem cells from animals and humans; embryonic stem cells and adult stem cells.

Because the fetus does not develop any

http://en.wikipedia.org/wiki/Fetendo

http://en.wikipedia.org/wiki/Fetoscopy

http://en.wikipedia.org/wiki/Medical_ultrasonography


immunocompetence before 14 weeks’ gestation, it may be possible to transplant tissues or cells before this time without rejection. Research in this field is focusing on hematopoietic stem cells for treatment of immunodeficiency and hematologic disorders.

5. Gene Therapy

Gene therapy is an experimental technique that uses genes to treat or

prevent disease. In the future, this technique may allow managing a

disorder by the following:

▪ Replacing a mutated gene that causes disease with a healthy copy

of the gene.

▪ Inactivating a mutated gene that is functioning improperly.

▪ Introducing a new gene into the body to help fight a disease.


1. Compare between dizygotic and monozygotic twins. 2-

Down syndrome occurs due to: a) Extra chromosome 13 b) Partial deletion of long arm of chromosome 15

c) Partial deletion of short arm of chromosome 5 d) Extra chromosome 21

Key answer of MCQ:

2- d Key words

1. Twins – monozygotic – dizygotic- Siamese. 2. Birth defects – environmental causes - maternal causes-

chromosomal abnormalities- Neural crest.


References

1. Gray C.Schoenwolf, Steven B. Bleyl, Philip R.Brauer, Philippa H. Francis (2014).: Larsen’s human embryology, 5th edition, Churchill livingstone, Edinburgh, London, Melbourne, New York.

2. Larry R. Cochard (2012): Netter’s Atlas of Human Embryology, 1st

edition. 3. Sadler, T.W. (2010): Langman's Medical Embryology, 11th Edition.

Philadelphia, PA, Lippincott Williams & Wilkins. 4. Sadler, T.W. (2012): Langman's Medical Embryology, 12th Edition.

Philadelphia, PA, Lippincott Williams & Wilkins.

introduction to human anatomy ame 102 ii.general …

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