General Anatomy Module

Dr. Gamal Taha Abdelhady

Assistant Professor of Anatomy & Embryology

General
Embryology
– Part 5
 General Embryology
◼ By the end of this session the student should be able to:

1) Recognize the cord structure and function

2) Enumerate different parts of the embryonic membranes and its function

3) Know the common types of congenital chromosomal abnormalities and

their specific characteristics

4) Describe the term teratology and enumerate its causes

 Extraembryonic Mesoderm
◼ Migrate between the cytotrophoblast and yolk sac and
amnion

◼ Extraembryonic somatic mesoderm lines the

cytotrophoblast and covers the amnion.

◼ Extraembryonic somatic mesoderm also forms the

connecting stalk that is the primordium of the
umbilical cord.

◼ Extraembryonic visceral mesoderm covers the

yolk sac.
 Umbilical Cord
◼ Early, the connecting stalk (formed of
extraembryonic mesoderm, from
trophoblastic tissue) connects the
caudal end of the embryonic disc to the
chorion.

◼ It receives the allantois and the umbilical

vessels develop in it.
 Umbilical Cord
◼ After folding, the connecting stalk shifts ventrally
and fuses with the mesoderm around the
vitellointestinal duct leading to the early umbilical
cord which contains

1. Umbilical vessels: 2 arteries + 1 vein (the right

vein disappears early).

2. Rudimentary ducts: allantois & vitello-intestinal

duct (both atrophy).

3. Mesoderm.
 Umbilical Cord
◼ At birth, the cord:
1. Is 50 cm long and half cm in diameter.
2. Extends from the fetal umbilicus to the center of
the fetal surface of placenta.
3. Its surface is covered by amnion.

◼ Contains:
1. 2 umbilical arteries (carry unoxygenated blood
from the fetus) + 1 umbilical vein (carries
oxygenated blood from the placenta).
2. Allantois and Vitello intestinal duct.
3. Wharton’s jelly.
 Umbilical Cord
◼ Postnatal changes

1. Umbilical arteries lead to the formation of

medial umbilical ligaments.

2. Left umbilical vein leads to the formation of

ligamentum teres of the liver.

3. Allantois leads to the formation of urachus

then median umbilical ligament.
 Extraembryonic Membranes
Amnion:

◼ Develops on the dorsal aspect of the embryonic

disc above the epiblasts.

◼ Later, it becomes connected temporarily to the

yolk sac by the neuroenteric canal.

◼ During folding, it enlarges to surround the

fetus on the expense of yolk sac.
 Extraembryonic Membranes
Source:
Amnion

1. Secretion of
amniogenic
epithelium.

2. Foetal urine.
 Amniotic Fluid
◼ Amount: at birth= 1 liter

◼ Amniocentesis: Obtaining a sample of

amniotic fluid for chromosomal analysis
of the exfoliated cells of the fetus to detect
the presence of congenital anomalies early
 Amnion
◼ Oligohydraminos: abnormally poor
amount, leads to dry labor and occurs
with agenesis of fetal kidney.

◼ Polyhydraminos: abnormally excessive

amount more than one liter, occurs with
fetal esophageal atresia (fetus cannot
swallow the fluid)
 Extraembryonic Membranes
Amnion Function: amnion

1. Provides an environment that

protects the embryo, constant
homeostatic temperature

2. Allows freedom of movement

and prevents fusing parts

3. Amniotic fluid comes from

maternal blood, and later,
fetal urine
 Extraembryonic Membranes
Amnion Function:

4. Contains antibodies.

5. Keeps equal temperature around the fetus.

6. Nutritive (contains 98% water and 2% solids=

glucose + amino acids).

7. Swallowing of amniotic fluid leads to development

of suckling reflex.
 Extraembryonic Membranes
Amnion Function:

8. Medium for excretion of fetal urine.

9. During labor; It forms the bag of forewaters

which helps to dilate the cervix.

10. Its rupture releases the sterile amniotic fluid

which cleans the birth canal.
 Extraembryonic Membranes
2. Yolk sac: a sac that
hangs from the ventral
surface of the embryo

◼ Forms part of the

digestive tube

◼ Source of the earliest

blood cells and blood
vessels, nourishment
for non - placentals Yolk sac
 Extraembryonic Membranes
3. Allantois:

A small outpocketing (an

endodermal outgrowth
from the yolk sac ) at the Allantosis
caudal end of the yolk sac Chorion

◼ Structural base for

the umbilical cord

◼ Becomes part of the

urinary bladder
 Allantois
◼ The allantois stores urinary waste, and
helps with the exchange of gases in
general, which makes it a crucial structure
since it delivers oxygen to the embryo.

◼ It also has a very important role in egg-

laying animals, including all birds, as it
serves as the embryo’s respiratory organ
together with the chorion.
 Allantois
◼ Somewhere between the fifth and seventh
weeks of embryonic development, the
allantois becomes a fibrous cord that is
referred to as the urachus

◼ After birth and persists in the body as the

median umbilical ligament
 Extraembryonic Membranes
4. Chorion:

cytotrophoblast and
syncytiotrophoblast as the
blastocyst invades into the
endometrium Allantosis
Chorion
Along with the maternal
endometrium forms the
(Decidua)

Helps form the placenta

Encloses the embryonic body and

all other membranes
 Extraembryonic Membranes
At the site near the
embryo, they will form the
chorion frondosum
because of the presence of
“feathery villi” and forming Allantosis
the fetal contribution to the
placenta. Chorion

On the side opposite the

embryo, they will become
the chorion laeve, which
means “smooth chorion”
due to the absence of villi.
 Decidua
◼ In addition there are different names for each region of the
endometrium depending upon its relationship to the fetus.
Decidua basalis forms the maternal component of the
placenta.

◼ Decidua capsularis encapsulates the fetus and is fused with

chorion laeve.

◼ Decidua parietalis describes the endometrium of the rest of

the uterine wall.

Note that by the end of the third month, the amnion, chorion
laeve, decidua capsularis and decidua parietalis are all fused
together and the uterine lumen is all but obliterated.
 Congenital Anomalies
◼ These are the malformations or congenital
anomalies which may be structural, behavioral,
functional, or metabolic disorder present at birth.

◼ Major structural anomalies occur in 2 to 3% of

live-born infants, and an additional 2 to 3% are
recognized in children by age 5 years, for a total
of 4 to 6%.

◼ Birth defects are the leading cause of infant

mortality, accounting for approximately 21% of
infant deaths.
 Congenital Anomalies
Causes
In 50% of persons with birth defects, the cause is
unknown.

1. Genetic factors (15%):

A. Chromosome abnormalities (7%)

B. Mutant genes (8%).

1. Environmental factors: 10%.

2. Multifactorial inheritance (a combination of

genetic and environmental influences): 25%.
 Chromosomal Abnormalities
◼ Numerical abnormalities:

◼ Monosomy: loss of a chromosome due to

nondisjunction of a pair of chromosomes
during gametogenesis:
A. Monosomy of an autosome: Fatal.

B. Monosomy of a sex
chromosome:99%→ Death.
 Chromosomal Abnormalities
◼ Remaining 1%→ Turner Syndrome (44+ XO).

◼ Incidence: 1/5000 females.

◼ Causes: nondisjunction or deletion of X

chromosome.

◼ Manifestations: Short stature, webbed neck, low

set ears, wide chest with spaced nipples, primary
amenorrhea (due to ovarian agenesis) &
congenital heart malformations.
 Chromosomal Abnormalities
◼ Trisomy:
◼ Trisomy of autosomes:

◼ Trisomy 21= Down’s syndrome, incidence

increase with maternal age, at age of 45,
incidence is 1:25.

◼ Trisomy 18= Edward’s syndrome.

◼ Trisomy 13= Patau’s syndrome.

Down Syndrome – Trisomy
21
 Chromosomal Abnormalities
Trisomy of sex chromosomes:

◼ Kleinfelter’s syndrome: 44+XXY:

incidence, 1:1080

◼ Triple X syndrome: 44+XXX

◼ Supermale: 44+XYY
◼ Trisomy X
syndrome

Gemma Ward

She is an Australian
actress, model, and
fashion designer who
was discovered when
she was 14
(Unconfirmed
Info.).
 Super Male Syndrome
◼ XYY syndrome (supermale)

◼ 1 in 1,000 males

◼ First published by Avery A. Sandberg in Buffalo, New York-1961

◼ Increase risk of learning disabilities (slight lower IQ), tall with

increased acne, aggressive behavior (debatable)

◼ Some studies show a higher % of supermales are in prisons

◼ Normal sexual development and are fertile

◼ Some medical geneticists question whether the term

"syndrome'' is appropriate for this condition because its
phenotype is normal
 Teratology
◼ Factors determining the capacity of an agent
to produce birth defects are the principles of
teratology:

1. Genotype of the embryo and how this genetic

composition interacts with the environment. The
maternal genome is also important (drug
metabolism, resistance to infection…ect.)

2. Dose and duration of exposure to a

teratogen.
 Teratology
3. Critical period (time of exposure to the
teratogen):

A. Exposure during the first 2 weeks: either abortion or

no effect.

B. During 3-9 weeks (period of organogenesis): this is

the critical period generally. However each system
has its own critical period e.g. the brain up to 16
weeks.

C. During the fetal period: growth retardation (nervous

system is still in the critical period).
 Teratogens
◼ Viruses:

1. Rubella (german measles): first teratogen to be identified

(1941). It causes a Triad: Cataract, deafness & patent
ductus arteriosus. The earlier the infection during pregnancy,
the greater is the damage: 1st month infection----50%
anomalies, 2nd month-----20%, 3rd month----4%, after 5th
month-----rare.

2. Cytomegalovirus is a serious threat (CMV). Often, the mother

has no symptoms, but the effects on the fetus can be
devastating. The infection is often fatal, and if it is not,
meningoencephalitis caused by the virus produces mental
retardation, cerebral calcification, blindness. 30% of infected
infants die.
 Teratogens
3. Herpes simplex (HSV), varicella (chicken
pox), and human immunodeficiency
viruses (HIV).

Malformations following maternal infection

with measles, mumps, hepatitis,
poliomyelitis, ECHO virus, Coxsackie virus,
and influenza virus have been described.
 Teratogens
◼ Other teratogenic pathogens

◼ Toxoplasmosis: Poorly cooked meat, domestic

animals, especially cats; and feces in contaminated
soil can carry the protozoan parasite. Causes still
birth or nervous system malformations (mental
retardation, cerebral calcifications, hydrocephaly,
microcephaly, microphthalmia).

◼ Syphilis: deformed teeth & bones, blindness &

deafness. The organism crosses placenta after
20th wk, so early treatment is of great benefit
 Teratogens
Others:

1. Smoking: Intrauterine growth retardation

(IUGR) & premature birth.

2. Cocaine: microcephaly, cerebral infarction,

abnormal sleep, tremor, poor feeding,
irritability & seizures.

3. Alcohol
 Teratogens
4. Heavy metals: Mercury (present in cheap
cosmetics): mental retardation & blindness and
Lead

5. Ionizing radiation (X-rays, radioactive

substances, atomic bombs.)

6. Hyperthermia (high fever, hot tubs, sauna).

7. Diabetes mellitus: caudal regression syndrome

(sacral agenesis & hind limb hypoplasia).
◼ For further inquiries PLZ feel free
to contact at any time through
email

gamaltaha@med.asu.edu.eg
gamal.abdelhady@yu.edu.jo