General Embryology Book Final (1) Edit
General Embryology Book Final (1) Edit
Organ Function
6- Prostate gland. -Secretes an alkaline fluid for
neutralize acidity of vagina.
7- Bulbourethral -Secretes a mucoid fluid that
glands. lubricates the urethra and end of
penis.
8- Scrotum.
-Encloses and protects the testes.
.
Oligiospermia;
Necrospermia;
follicle luteinizing
stimulating hormone (LH)
hormone acts on Leydig
(FSH) stimulates
Follicle secretion of
hormone acts testosterone
upon the hormone by
Sertoli cells to Leydig cells
stimulate
spermatogene
sis.
Female reproductive system l
Superficial layer
Deeper layer
small cell called the first large cell called the secondary
polar body (which oocyte (23chromosomes.)
degenerates)
small cell called the second large cell called the mature
polar body (which degenerates) ovum (23chromosomes.)
Stages of oogenesis
Abnormal ovum:
yte.
Abnormal ovum
Main differences between spermatogenesis and oogenesis
Spermatogenesis Oogenesis
1- Site. • Seminiferous tubules •Ovaries.
of testis.
2- Time. • Start at puberty and •Start at puberty
continuous to old age until menopause (45-
50 years)
3- Occurrence. • Continuously occur. •Occur once every
month.
• One spermatogonium •One oogonium
4-Results.
four sperms, two of one mature ovum
[22+X chromosomes]
which have 22+X
chromosomes & two
contain 22+Y
chromosomes.
The process of oogenesis is controlled by TWO centers in the brain -
1- the hypothalamus which secretes gonadotropin-releasing hormone (GnRH) to
the anterior pituitary.
2- the anterior lobe of the pituitary gland. Which release
GnRH 4 Positive
8
feedback exerted
Travels via
portal blood by large in
estrogen
1 output.
Anterior pituitary
1 5
Progesterone
LH surge Estrogen
FSH LH 6
Inhibin
Ruptured
2 2 8
follicle
3 Slightly
elevated 7
estrogen Thecal
and rising cells
inhibin
levels. Granulosa Androgens Corpus luteum
cells Mature follicle Ovulated
Convert secondary
Inhibin androgens to 2 oocyte
estrogens Late follicular and
Early and midfollicular phases luteal phases
LH
FSH
Progesterone
Menstrual
flow
Functional layer
Basal layer
Days
Menstrual Proliferative Secretory
phase phase phase
(d) The three phases of the uterine cycle:
• Menstrual: Shedding of the functional layer of the
endometrium.
• Proliferative: Rebuilding of the functional layer of
the endometrium.
• Secretory: Begins immediately after ovulation.
Enrichment of the blood supply and glandular secretion of
nutrients prepare the endometrium to receive an embryo.
Both the menstrual and proliferative phases occur before ovulation, and
together they correspond to the follicular phase of the ovarian cycle. The
secretory phase corresponds in time to the luteal phase of the ovarian cycle.
FERTILIZATION
What is fertilization?
Sperm transport in the female genital system
.
3-
I:
After Ramasamy_Santhanam, schematic diagram for events of fertilization
Results of fertilization
Cleavage of zygote and
blastocyst formation
Zygote cleavage
Zygote Стоковые фотографии и лицензионные изображения
Morula
Blastocyst
Implantation
By. Prof. Saeed Abuel Makarem
By the 5th day the Zona pellucida degenerates.
Blastocyst begins implantation by the 6th day, (20 day of a 28 day menstrual
cycle).
Trophoblast cells penetrate the epithelium of the endometrium.
•
Day 8
Day 8
DAY 9
Twins
Types of twins
1. dizygotic twins (Fraternal, non-
identical twins):
Pygo-pagus
Cranio-pagus
wall of pharyngeal membrane
amniotic cavity
wall of yolk sa
primitive streak
endoderm ectoderm
(hypoblast) (epiblast)
2 germ layers: ectoderm
Development of intraembryonic mesoderm
prim
mesoderm
notochordal process
notochordal canaliculus
plate allantois
lateral
mesoderm
plate
derm
paraaxial mesoderm
intermediate mesoderm
canalis neurentericus nic
derm mesoderm
notochord
notochord
derm endoderm
mesoderm
extraembryonic mesoderm of
ectoderm amniotic cavity
notochord endoderm
mesoderm extraembryonic mesoderm of
yolk sac
3rd week
Paraxial mesoderm gives rise to somites (40-42) and these are divided into 3 parts:
1. Sclerotome – axial skeleton
2. Myotome – striated skeletal muscles
3. Dermatome – dermis of cutis
Intermediate mesoderm gives rise to male and female genital and urinary system.
2. Notochord fuses with the underlying visceral hypoblasts, and its inferior wall
degenerates and disappear.
3. Neuroenteric canal is formed between the amnion and yolk sac for a short time.
4. Definitív notochord develops from the cells of notochordal process between the
prechordal plate and cloacal membrane
Neuroenteric canal
DEVELOPMENT OF THE DEFINITIVE NOTOCHORD
Differentiation of the
intraembryonic mesoderm
MESODERM
Intermediate mesoderma
gononephrotom
Parietal mesoderm
somatopleura
splanchnopleura
DIFFERENTIATION OF THE MESODERM
17th day
paraxial mesoderm
lateral mesoderm .
- At the beginning of the 3rd week somites (or somitomeres) appear both side of
- Somites appear first cranially (around the 20th day), than develop caudally
(3 pair/day).
SCLEROTOM
gonads
From the somatopleura develops the body wall (PARIETAL LAYER OF THE SEROUS MEMBRANES).
From the splanchnopleura mesothelial cells, visceral layer of the serous membranes
develop. (pleura, pericardium, peritoneum).
neural tube
somite
intermediate mesoderm
kidney, ureter,
notochord male genital tract
somatic mesoderm
intraembryonic coelom → parietal layer of
body cavities (pericardium, serous membranes
pleura, peritoneum)
epiblasts primitive
streak
intraembryonic
mesoderm
hypoblasts yolk sac
endoderm
? endoderm
3. Neurulation: formation of the neural tube and crest (CNS AND PNS)
Neurulation
Development of the nervous system
m – in the midline,
and oropharyngeal
Neural crest
17. day
paraaxial
chord intermed
ectoderm mesoderm meso
mesoderm
yolk sac
intermed somite
amnion neural gro e
mesoderm
visceral
mesoderm
neural tube
endoderm of
yolk sac
parietal
mesoder
1. Neural plate
2. Neural groove
3. Neural crest
4. Neural tube
neu
so ive
no
prim eak
neura
heart
somit
som
amnio nion
neuroporus anterior
l otic pit
arch
branchial arches
eye placod
rt prominence
amnion rt
prominence upper
limb bu
funiculu
yolk sac s
umbilica
lis
neuropo
posterior
Development of the brain
telencephalon
diencephalon
mesencephalon
metencephalon cerebellum
pons Varoli
myelencephalon
medulla oblongata
Development of spinal cord
matter
ttt
outer marginal zone
next white matter
s int na
endoderm ectoderm
mesoderm
Germ layer derivatives
ECTODERM
1. Neuroectoderm
neural plate
neural crest
placodes
2. Surface ectoderm
NEURAL CREST
otic placode: epithelial and neural elements of the vestibulocochlear system (organs of hearing and equilibrium)
epibranchial placode: taste buds of the tongue, soft palate and laryngeal inlet, neurons and supporting cells of
taste-sensing ganglia of the facial glossopharyngeal and vagus nerves.
SURFACE ECTODERM
Epithelium and glands of the oral and nasal cavity, enamel of the teeth, salivary glands
Mammary glands
Epithelium and glands of the anus, epithelium of the spongy part of the male urethra
MESODERM
Intermediate mesoderm → epithelium of the kidney, ureter and the male genital tract
(epididymis, ductus deferens, seminal vesicle)
MESENCHYMAL TYPE
Circulatory system, including the endothelium of blood and lymph vessels, cardiac muscle,
formed elements of blood and lymphatic cells
Microglia
ENDODERM
Epithelium and glands of the GI tract (including liver, gallbladder and pancreas)
Epithelium of the urinary bladder, the prostate, the prostatic part of the male urethtra
Epithelium and glands of the airways (trachea, bronchi and alveoli of the lungs)
Thymus, tonsills
SUMMARY
Fetal membranes
Fetal membranes means all the
structures that developed from
the zygote but not form parts of
the embryo. After birth they
expelled from the uterus as “
afterbirth ”. These include [1]
chorion [2] amnion [3] yolk sac
[4] connecting stalk, and [5]
AMNION
Source of amniotic fluid
Excretion of the fetal Secretion of the
kidneys amniotic cells
*
Congenital abnormalities of amnion and
amniotic fluid
1- Polyhydramnios (poly-much) if the volume more than 1500-2000
ml.
Causes of Polyhydramnios
The cause of this condition cannot always be determined, but it is
often associated with:
Twins
Gestational diabetes (in some cases, if diabetes is the cause of
polyhydramnios, the baby may be unusually lardge for its
gestational age)
Gut atresia, a blockage in the baby’s digestive system that can interfere
with the absorption of amniotic fluid (this will usually require surgery
after the baby is born)
Rh diseases, an incompatibility between maternal and fetal blood
types
Twin-to-twin transfusion syndrome, a condition in which a pair of
identical twins in separate sacs share the placenta and one twin does
not receive
Risks of Polyhydramnios
Congenital anomalies of the amnion:
Amniotic band syndrome: .
primary chorionic villi develop on the entire surface of the chorionic sac - they appear as
local masses of the cytotrophoblast
secondary chorionic villi occur on day 13 to day 14, when the extraembryonic mesoderm
proliferates and grows into cytotrophoblast masses forming a core of loose connective tissue
tertiary chorionic villi are vascularized , they contain already anlage blood vessels
chorionic villi was originally developed around the
entire surface of implanted conceptus
later with the growth of conceptus
villi adjacent to capsular and marginal decidua become
rare and shorter up to evetually disappear
while
villi adjacent to basal decidua become long and branched
by this way, the chorion is divided into regions of different
surface
villous chorion /chorion frondosum/ - against the basal
decidua
smooth chorion/ chorion laeve - against the marginal and
capsular deciduae
Chorionic sac - 4th month Placenta - 6th month
maternal aspect
Placenta
a membrane-like and temporary organ that develops between the 3 - 8 weeks
the site of nutrient and gas exchange between the mother and fetus
the full term human placenta is a discoid, a diameter 15 - 25 cm and 2- 3 cm thick
it weighs 500 to 600 g
the human placenta is hemochorionic - the blood of mother enters the intervillous space and
flows slowlyaround the villi, allowing an exchange metabolic and gaseous products with fetal
blood
shortly after birth a baby, the placenta and fetal membranes are expelled from the uterus as
the afterbirth
2 parts close associated each other of the placenta:
the fetal part or villous chorion - smooth with insertion of umbilical cord and outlines of
umbilical vessels that are seen through the amnion
project into the intervillous space (is deriving from the lacunae developed in the
syncytiotrophoblast during the 2nd week)
chorionic villi may be either free or anchored to the decidua basalis = main stem villi, one main
stem villus forms a unit of the fetal part of the placenta known as - the cotyledon, they are
separated each other by septa of placenta
maternal blood
circulates through
the intervillous
space, bringing
nutritive and other
substances
necessary for
embryonic and
fetal growth, and
taking away the
waste products of
fetal metabolism
Structure of villi:
a connective tissue core deriving from the extraembryonic mesoderm
is surrounded by the cytotrophoblast and the syncytiotrophoblast
the cytotrophoblast disappears cca in a half of pregnancy while the syncytiotrophoblast
is retained to the end
fetal and maternal blood streams in the placenta are separated by the placental
membrane (barrier)
a composite membrane consisting of
protrudes between
individual
cotyledons as
placental septa
Placental circulation
Fetoplacental circulation: Deoxygenated blood leaves the fetus and passes through the 2
umbilical arteries to the placenta, arteries branch and ultimately give rise to capillaries of
chorionic villi, oxygenated fetal blood returns to the fetus through the one umbilical vein
Maternal-placental circulation: 80 to 100 spiral arteries (are branches of the uterine artery)
open in the middle of the placenta; blood flows into the intervillous space and passes over villus
surfaces toward the chorionic plate; the maternal blood leaves the intervillous space through
the endometrial veins (located near the periphery of the placenta)
normally, no intermingling of fetal and maternal blood occurrs
Placental activities
has three main functions: metabolic, transport of gases and nutrients, and endocrine secretion
Placental metabolism - placenta, in particular during early pregnancy, synthesizes glycogen,
cholesterol, and fatty acids that all serve as a source of nutrients and energy for the embryo
Placental transport - is bidirectionally (between the placenta and maternal blood and vice versa)
gases, nutrients, hormones, electrolytes, antibodies, wastes, and also several drugs are transported
across the placental membrane
4 main transport mechanisms are utilized: simple cell diffusion, facilitated diffusion, active
transport, and pinocytosis
Placental endocrine secretion: the syncytiotrophoblast is endocrine active and produces
hormones of 2 categories:
protein hormones: human chorionic gonadotropin (hCG), human chorionic
somatomammotropin (hCS) or placental lactogen, human chorionic thyrotropin (hCT), and
human chorionic corticotropin (hCACTH)
steroid hormones: progesterone + estrogens
What Are Birth Defects?
Birth defects are defined as abnormalities of structure,
function, or body metabolism that are present at birth.
These abnormalities lead to mental or physical disabilities
or are fatal. There are more than 4,000 different known birth
defects ranging from minor to serious, and although many
of them can be treated or cured, they are the leading cause
of death in the first year of life.
According to the March of Dimes, about 150,000 babies are
born with birth defects each year in the United States. The
American College of Obstetricians and Gynecologists
(ACOG) says that out of every 100 babies born in the United
States, three have some kind of major birth defect.
Birth defects can be caused by genetic, environmental, or
unknown factors.
Spina bifida is determined during the first
trimester of pregnancy. As the embryo
forms, the bones in the spinal column
come together and tissue grows around
the vertebrae, closing it. In the case of
spina bifida, an opening remains. The size
of the opening varies from almost
pinpoint to several inches.
Current research links the nutrient FOLIC ACID to this birth defect. It is
imperative that the mother has an adequate supply of this nutrient prior to
AND in the early stages of pregnancy. Oranges are a common source of this
nutrient, as well as many enriched breads and cereals products. For this
reason, spina bifida would be considered as having an environmental cause.
The top arrow points
to a part of the spine
that is properly
closed.
The area where the The bottom arrow
bones are not properly points to an area that
closed allows the is improperly closed…
cord, tissue, and/or spina bifida.
fluids to protrude.
The location of the
“opening” on the
spine is critical. Areas
and functions below
the hole are affected.
Some areas above the
hole may be affected
as well, especially the
brain, as it is
connected to the
spinal cord and
nervous system.
Various degrees of
leg and foot
deformities are
found in spina bifida
patients, depending
on the size of the
improper spinal
closure.
The rarest form of spina bifida is when the spinal tissue actually
protrudes from the body. This only occurs in 10% of all cases.
Marfan's syndrome is a disorder
of connective tissue which causes
skeletal defects typically
recognized in a tall, lanky person.
A person with Marfan's syndrome
may exhibit long limbs and
spider-like fingers, chest
abnormalities (inversion of the
septum), curvature of the spine
and a particular set of facial
features including a highly arched
palate, and crowded, crooked
teeth.
en invaluable e treatment
e in 1,0 rths in Cauc
often in
People who have CF produce abnormally
thick, sticky mucus, which clogs the lungs
and leads to recurring lung and sinus
infections and difficulty breathing.
Reduced oxygen in the blood also leads to
a characteristic rounding and enlargement
of the nail bed in the fingers and toes,
called clubbing. Those with the disease
may also develop a barrel-shaped chest as a
result of their increased work to breathe.
These repeated infections often lead to
fleshy growths inside the nose, called nasal
polyps.
The thick mucus also obstructs the ducts
of the pancreas, preventing digestive
enzymes from reaching the intestines. So
those with CF do not absorb nutrients
from their food well, and they eliminate
nondigested food through the bowel,
resulting in very large stools. Because so
little food is absorbed, those with CF have
difficulty gaining and maintaining weight,
despite a healthy appetite and diet.
This mother pounds on her
daughter’s chest several times a day
in order to dislodge the thick mucous
from lung sacs and give some
Cystic Fibrosis is a breathing relief.
genetic disorder, with
over 95% of all cases
diagnosed in
Dwarfism is a genetic/genetic linked
disorder. All forms of dwarfism are
characterized by small stature. The
overwhelming majority of these
individuals enjoy normal intelligence,
normal life spans, and reasonably good
health. Medical problems are often
linked to orthopedic complications.
When sickled cells clog blood vessels, pain most commonly affects the joints. A severe
crisis can also disrupt the work of the brain, the lungs, the heart, the kidneys, and the
spleen—sometimes with fatal consequences. Leg ulcers in the ankle region may persist for
years. Children risk seizures or strokes. Those with sickle-cell anemia are especially prone
to infectious diseases, since the disorder weakens natural defenses. Infection is a common
cause of death.
Prenatal Diagnosis
Prenatal Diagnosis
General Caveats about
Prenatal Diagnosis
• All couples have ~3% risk of having a child with congenital problems requiring
intervention
• No 100% guarantees - even if prenatal tests are ‘normal’
• All couples bring unique ethnocultural, moral, and/or religious perspectives to the process
• Use of non-judgmental, non-directive genetic counseling is important in helping families
make the best choice for them
• The decision to terminate or continue a pregnancy based on prenatal diagnostic findings is
never an easy decision
Goals of Prenatal Diagnosis and Counseling
• Assess pregnancy
• Determine specific risks to fetus
• Evaluate prenatal diagnostic options
• Diagnosis fetus when desired and possible
• Educate family about diagnosis, likely outcomes, potential and management
options
• Discuss risks, benefits, and uncertainties
• Explore family concerns
• Provide risk assessment for other family members
• Provide psychosocial support and follow-up
Who benefits from prenatal diagnosis?
• Older women (> 35) at increased risk of chromosome disorders
• Individuals in populations at increased risk of a genetic disease:
– Tay-Sachs: Ashkenazi Jews, French Canadians
– Sickle cell anemia: Africans, Mediterraneans, Arabs, Turks, Indo-Pakistanis
– Thalassemias: Mediterraneans, Arabs, Turks, Indo-Pakistanis, Southern and
Southeast Asians
– Cystic Fibrosis: Caucasians
– Fragile X syndrome: All women (?)
• Family history of a genetic disease/chromosome disorder
• Maternal disease associated with increased risk of birth defects (diabetes,
phenylketonuria)
• Known teratogen exposure during pregnancy
• Abnormal screening tests or ultrasounds
• Women who are concerned/worried
Prenatal Diagnosis Techniques
• Maternal Serum Screening Tests
– Triple screen (alpha-fetoprotein, beta-HCG, and estriol) for neural tube
defects and chromosome trisomies