EMBRYOLOGY

EMBRYOLOGY NOTES HASAN BAJWA

N68

ACKNOWLEDGEMENT

This is solely a composing work.

Special thanks to Dr. Najeeb & drnajeeblectures.com
 EMBRYOLOGY
EMBRYOLOGY NOTES HASAN BAJWA
N68

USING THIS BOOK

These notes are intended to enable the students to easily learn embryology. As these are made
from the lectures of Dr. Najeeb, the entire focus is on concepts.
I recommend that you first see the respective lecture and then read the notes. These notes are
made out of utmost sincerity since I have prepared my professional exam with these. These are
comprehensive and you will not need to write anything more.
All diagrams drawn in the lectures are included in this. I have spent a lot of time making these
thinking it might help students in the future especially who don't want to write while listening
to the lectures.
I recommend these notes to my juniors of 1st-year MBBS (Especially those who find
embryology difficult and not understandable). Study these after listening lectures. Then read
supplements which I have made from Langman's embryology (Available on Facebook).
Insha Allah, you will not miss anything and it will be a piece of cake for you.
Wishing you all the best!

Regards
Hasan Bajwa
Nishtar Medical University, Multan
Session 2018-2023 (N68)
 EMBRYOLOGY
EMBRYOLOGY NOTES HASAN BAJWA
N68

To my parents and my teachers. They enabled me to be who I

am with their prayers and efforts.
 EMBRYOLOGY
EMBRYOLOGY NOTES HASAN BAJWA
N68

TABLE OF CONTENTS
1 CELL CYCLE AND GENES---------------------------------------------------- 01

2 GAMETOGENESIS------------------------------------------------------------05

3 FEMALE REPRODUCTIVE CYCLE-------------------------------------------11

4 FERTILIZATION----------------------------------------------------------------17

5 DEVELOPMENT UPTO 2ND WEEK------------------------------------------22

6 DEVELOPMENT UPTO 3RD WEEK------------------------------------------27

7 CNS DEVELOPMENT---------------------------------------------------------35

8 CVS DEVELOPMENT---------------------------------------------------------42

CELL CYCLE & GENES
INCLUDES:
• Cell cycle
• Detail about mitosis
• Certain genes that regulate
different steps during cycle
• Role of these genes in cancer
development
1 WHAT IS CELL CYCLE
How a cell passes through different phases to
divide into 2 daughter cells. Sequence of all these
changes through which a cell eventually divides 2
cells is called CELL CYCLE.
It has 2 parts: 1-Interphase 2-Mitosis
1.1 INTERPHASE
When cell gets a stimulus to divide, it will:
1- Duplicate genetic material.
2- Pass through mitosis.
3-increase its cytoplasm, proteins and organelles.
First of all cell duplicates its DNA. It does not start
replicating DNA directly. It has to produce a lot of
proteins, enzymes, increase cytoplasm, increase
organelles and replicating enzymes to be
produced.
1.1.1 S Phase
This is phase of DNA synthesis. DNA is synthesized
in this phase. DNA has been replicated semi-
conservatively. Every chromosome has become
double structured chromosome. 2n=4n.
n=23 chromosome haploid set.
1.1.2 G1 Phase
Phase before DNA synthesis is called
Presynaptic/G1/Growth phase 1. First cell enters
G1 and prepares itself at molecular and organelle
level to synthesize DNA. Then S phase will start.
EMBRYOLOGY
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1.1.3 G2 Phase
Cell should get ready to divide duplicated genetic
material for two daughter cells. After synthesis
phase, when cell is preparing itself to divide
genetic material equally into 2 daughter nuclei,
that preparatory phase is G2 phase. It is Post
synthetic/Pre-Mitotic phase.
Cell is getting ready to divide its duplicated DNA
into 2 daughter nuclei.
1.1.4 M Phase
Genetic material is divided and nuclear
membrane is eventually dissolved and genetic
material is moved to both sides of cell to go to
new daughter nuclei.
That phase in which nuclear duplicated material of
one nucleus id under process of division for 2
daughter nuclei is called Mitotic stage/M-phase.
After M-phase eventually cell has divided into:
1-2 cells
2-In some cells, it may enter next cell cycle.
3-In some cells it may take rest by entering G0
phase (out of proliferative cycle.
If proper stimulus given, cell may enter
proliferative phase again.
1.1.4.1 Labile Cells
Some tissues in which cells are multiplying
continuously, do not enter G0 phase.
e.g- Skin cells, GIT cells, Bone marrow
hematopoietic cells.
1.1.4.2 Stable Cells
Some cells, if tissue does not require more cells,
enter G0 phase. Now it is housekeeping function
by housekeeping genes. With stimulus these can
proliferate again by exiting G0.
E.g- Liver cells (if you cut liver, cells start dividing
and regenerate that part), Kidney nephrons,
Pancreatic cells.
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1.1.4.3 Permanent Cells

Cells go into G0 phase and never come out of it
and don’t multiply. 1.2 MITOSIS
For these to divide, stem cells should divide to Prophase➔Metaphase➔Anaphase➔Telophase
generate these cells. Once well differentiated, and
1.2.1 Before Prophase
performing general and specific functions, they
There will be G2 phase. DNA in form of loose
cannot multiply.
chromatin network and centrioles may be there.
e.g- Neuronal cells, skeletal and cardiac muscle
1.2.2 Prophase
cells.
➔Loose chromatin condenses because Histones
G1+S+G2=Interphase get dephosphorylated➔chromosomes more clear
and each is double structured.
1.1.5 Cytokinesis
Not part of mitosis. But takes place during mitosis. ➔Nuclear membrane starts dissolving because
Mitosis is about nuclear division. This is about laminin proteins get phosphorylated by enzymes.
cytoplasmic and organelle division. In this,
➔Centrioles move at two opposite poles
cytoplasm and organelles divide into 2 daughter
cells.

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1.2.3 Metaphase 1.2.6 What causes a cell to divide?

➔Nuclear membrane disappeared. Cell division is extremely regulated phenomenon.
It has checkpoints:
➔Microtubules and mitotic spindles formed.
➔If DNA of cell in G1 is already damaged, it should
➔Chromosomes (double structured) arranged on
be repaired before entering S phase. Cell will be
equatorial plate.
arrested at this checkpoint called G1-S checkpoint.
➔Tubular microtubules attach on Kinetochores.
If DNA is OK, it will be allowed to move forward.
1.2.4 Anaphase ➔G2-M Checkpoint→All DNA will be scanned to
➔Double structured chromosomes break at make sure no error during replication and every
centromere➔Two chromosomes start moving to chromosome is duplicated exactly.
opposite poles.
If anyone missing, arrested.
1.2.5 Telophase
➔Chromatids reach at poles. ➔M-Checkpoint→Make sure all DNA is properly
aligned on Metaphase Plate.
➔Nuclear membrane reappears.
➔Chromosomes decondense to chromatin.
➔Cell membrane invaginates (Cytokinesis).

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 EMBRYOLOGY
GAMETOGENESIS HASAN BAJWA
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1 OVERVIEW
→Specialized process occurring in primordial
germ cells.
→It is process by which early germ cells undergo
process of meiosis and cytodifferentiation
eventually convert into mature gamete. 2.1 SPERMATOGENESIS / GAMETOGENESIS
→Meiosis is a special type of cell division occurs in →Germ cells undergo meiotic division.
2 stages (Meiosis1 & 2). ➔Full set of 23 chromosomes=1n
→Chromosome no. is halved in final daughter ➔N=Amount of DNA in a given cell
cells. So, it is also called Reduction Division.
➔n=Number of chromosomes
➔InMales→Spermatogenesis→Meiosis+Cytodiff
erentiation→Mature sperm. ➔1N=23 chromosomes (single structured)

➔InFemales→oogenesis→Meiosis+Cytodifferent ➔2N=23 chromosomes (double structured)

iation→Mature ovum. ➔Primary Gamete: Pri. Spermatocyte & Pri.
Oocyte.
2 MEIOSIS ➔Germ cells replicate DNA before entering M1.
Primary gamete has double structured
→Early germ cells are… (1)Oogonia
chromosomes but number of chromosome
(2)Spermatogonia.
remains same (46) since it depends on centromere.
→46 chromosomes→23 from mother and 23 from
father. 2.2 DIFFERENCE BETWEEN MEIOSIS & MITOSIS
e.g= Ch#1 from mother and father both & son on →Normally Paternal and Maternal origin
for all chromosomes bcz these are in homologous chromosomes of a homologous pair lie randomly
pairs. in nucleus.

➔No. of Chromosomes=No. of CENTROMERES. Mitosis Meiosis

No formation of
Homologous
homologous pairs
chromosomes
while replicating. replicate and come
together & pair with
each other length wise
and point to point
called Synapsis.
No synapsis & crossing Crossing over occurs.
over. Chromosomes of a
homologous pair
➔GENES are sequence of nucleotides which make exchange alleles or
a specific functional RNA. Those genes that are blocks of genes with
going to perform similar functions present on each other after
homologous chromosomes at same loci and are in crossing over.
specific relationship with each other. These are No chiasma formation. While separating,
called ALLELES of each other. Chromosomes remain

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attached at cross over 2.2.3 Chiasma formation

points and moving
away from elsewhere.
This is chiasma
formation.
No random Random assortment
assortment. occurs. Daughter cells
have maternal or
paternal
chromosomes bcz
they assort
independently.

2.2.1 Synapsis

2.2.4 Random assortment

2.2.2 Crossing over

→Due to crossover, Maternal chromosomes are

not purely maternal but have paternal genes also
(at cross over point) and vice versa.
→Crossing over and random assortment of
chromosomes leas to genetic variability and
diversity.
➔At end of Meiosis 1 we have:
(1) Secondary gamete→ Secondary spermatocyte
or Secondary oocyte + 1st Polar body.
➔ Chromosomes enter Meiosis 2 without
replicating DNA.
In M1→Homologous chromosomes go away.

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In M2→ Centromere breaks and Double

structured chromosome convert to 2 single
structured chromosomes.
➔End of Meiosis 2 we have→ 4 Spermatids or
Ovum + 2nd polar body and 1st & 3rd polar bodies.

2.3 PURPOSE OF MEIOSIS

• Specialized type of cell division.
• Occurs in germ cells.
• Makes them mature germinative cells.
• Makes sperm in males and ova in females.

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GAMETOGENESIS
3 OOGENESIS
→Formation of mature ovum from oogonia.
→Starts in prenatal life→ before birth.
3.1 PRENATAL DEVELOPMENT
→Most primitive germ cells→Primordial germ
cells. They appear in yolk sac around 4th week of
development. Keep dividing by mitosis to produce
oogonia and at same time keep migrating to
gonads of developing female.
3.1.1 Oogonia
→Surrounded by flat epithelial cells derived from
epithelium on surface of ovary.
→Oogonia also divide by mitosis to produce more
and more oogonia.
3.1.2 Primary Oocyte
→Many oogonia enlarge in size, stop mitotic
division, get ready for meiosis. These are pri.
Oocytes.
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3.1.3 Primordial Follicle
One oogonia enlarges and rest degenerate and
now one oogonium and sheath of flat epithelial
cells (follicular cells). This is Primordial Follicle.
→Before Pri. Oocyte starts M1, DNA replicates.
i.e=Duplicated 46 chromosomes.
→Primary oocytes during prophase of M1 at
diplotene stage get arrested. Stop progression of
M1.
→Before birth, all oogonia are converted to pri.
Oocytes arrested at diplotene.
→At birth, no Pri. Oogonia. Instead 2Million Pri.
Oocytes in diplotene.
→After birth, no new formation of pri. Oocytes.
➔At birth, All pri. Oocytes are surrounded by flat
epithelial cells called Primordial follicle (flat
epithelial cells + Pri. Oocyte in it).
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3.2 AFTER BIRTH UPTO PUBERTY 3.3.1 Ovarian / Primary /Pre-antral follicle
→Pri. Oocyte remains arrested. • Primary oocyte in diplotene stage.
• Some Connective tissue(c.t) cells
→Most of them degenerate.
start differentiation from ovarian
→Around puberty→40000 Primordial follicles stroma around cells layer.
(Pri-oocyte arrested in diplotene) present. • Oocyte secretes glycoprotein
outside. Follicular cells secrete
3.3 AT PUBERTY glycoprotein inside. This layer is
→Start of Menstrual cycle. zona pallucida between oocyte and
follicular cells.
→FSH stimulates Primordial follicles→Every
month 5 to 15 start growing but only one matures
into Graffian Follicle.
→Follicular cells become cuboidal (Growing
Follicle).
→then multi-layered (stratified cuboidal) called
Primary Follicle / Ovarian Follicle.

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suddenly becomes reactive and completes its

meiosis 2→Now it is Definitive / Fertilized ovum.
3.3.2 Secondary / Antral / Vesicular Follicle
• Follicular cells proliferate a lot. Follicles ➔Male and Female pronucleus swell up and fuse
become enlarged. to form zygote and become metabolically active.
• From the cells fluid secreted forms fluid
3.3.5 Function of Theca and Granulosa cells
filled spaces between follicular cells. These
➔Nourishment to ovum
fuse and form a single cavity called
Antrum. ➔Theca cells produce product (androgens) → go
• Some follicular cells remain around ovum to Granulosa cells → convert them to special
and zona pallucida called cumulus ooforus. products (estrogen) that goes to uterus and make
• C.T derived from ovarian stroma thickens, it prepared that there are chances of conception.
makes covering around growing follicle
3.3.6 Gametogenesis vs Meiosis
and is called Theca Folliculi. It starts
Gametogenesis Meiosis
forming at level of primary follicle. Inside
Oogonia→Mature Pri-oocyte→mature
part is Theca Interna (outside follicular
egg ovum
cells) & outside part is Theca Externa. Spermatogonia→Ma Pri-
• Pri. Oocyte still arrested in diplotene stage. ture sperm spermatocyte→Sperm
atids
3.3.3 Graffian / Mature Vesicular Follicle
• Now pri. Oocyte starts growing. M1
completed and 1st polar body lies b/w zona
pallucida and sec oocyte.
• Sec. oocyte enters M2 as soon as it is
formed.
• Fully mature secondary follicle also called
graffian follicle. It has sec. oocyte + 1st
polar body.
• 3 hours before ovulation sec. oocyte
arrested at Metaphase of Meiosis 2.
➔At ovulation, ovum + some cumulus ooforus
cells release and taken up by fallopian tubes. Polar
body is non functional cell and eventually
degenerates.
➔Remaining follicular cells and theca cells remain
and convert to yellow mass called corpus luteum.
➔Cumulus ooforus cells rearrange and look like a
crown called Corona Radiata.

3.3.4 Fate of Ovum

➔If fertilization does not occur→Ovum
disintegrates in fallopian tube and absorbed by its
epithelium. (After 24-48hrs that is life of ovum).
➔If fertilization occurs→as soon as sperm
touches membrane of sec. oocyte, sec oocyte

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Also called female monthly sexual cycle / 2 HYPOTHALAMIC ROLE

Menstrual cycle.

2.1 ARCUATE NUCLEUS

1 HIGHER CONTROL This is collection of neuronal cell bodies.
→Highest center playing a role in monthly cycles →These neurons are truly masters of female
is HYPOTHLAMUS. This is the commanding center. reproductive activity (with some help from pre-
→Monthly cycle can have 4 aspects: optic nucleus)

Limbic system effects hypothalamus→Ant. →These neurons release special chemical

Pituitary→Ovaries→Uterus substance called Gonadotropin hormone
releasing factor (GnHRF)
(1) Hypothalamus→Hypothalamic cycle
(2) Anterior pituitary→Pituitary cycle 2.2 GONADOTROPINS
➔Gonadotropins→Such hormones which have
(3) Ovaries→Ovarian
tropic action (growth action) on gonads.
(4) Uterus→Uterine
→These are FSH and LH.
→Hypothalamus controls endocrine system. It
controls all visceral, autonomic, reproductive, 2.3 VASCULAR CONNECTION
endocrine, sexual activities including mood. 4g in
Takes secretions (GnHRF) of hypothalamus to Ant.
weight.
Pituitary cells to secrete Gonadotropic Hormones.
➔Masters controlled by masters. i.e= Limbic
system (part of cerebral cortex controlling
3 HOW FSH & LH WORK
emotions, mood, perceptions) controls
hypothalamus ➔Average length of cycle is 28 days.
➔Normal range is 21 to 35 days.
➔Cycle length caries with age also.
➔If more than 35 days→Oligomenorrhea
➔If less than 21 days→Polymenorrhea
➔Menstrual bleeding remains for almost 1→4 or
5 days in start.

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FEMALE REPRODUCTIVE CYCLE
➔First day of menstrual bleeding is first day of
cycle.
➔Each month 5→15 primordial follicles start
growing automatically (stimulated by local factors)
to form primary follicle.
➔In females Meiosis 1 starts before birth while in
men after puberty. However, M1 is completed
when primordial follicle is converted to sec.
follicle.
➔5→15→all into primary follicle→some into sec.
follicle→suddenly ova complete M1 and start M2.
➔FSH acts on Primary follicles. Converts it to sec.
follicle and sec to graffian follicle.
→Zona pellucida allows only Human Male sperms
to pass through. As soon as one sperm touches
ovum membrane, ovum releases substances that
modify zona pellucida so that no more sperms can
penetrate.
→If no FSH, Primary follicle degenerates.
→Uterus has 3 layers:
• Endometrium→inner most layer
• Myometrium→middle smooth muscle
layer
• Perimetrium→outside C.T
→Theca and Granulosa cells produce estrogen
and it prepares endometrium and thickens it. This
is proliferative stage of endometrium. At this time
blood is at estrogen stage and ovary at follicular
stage (graffian or sec).
4 DAY 1→14
Ovary→Follicular stage.
Blood levels of hormones→Estrogenic stage
Endometrium→Proliferative stage
➔Estrogen also acts on hypothalamus to dec FSH
secretion so FSH level decreases.
EMBRYOLOGY
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→Best growing follicle will grow on its own and
less grown ones still dependent on FSH die. These
are Atretic Follicles. (Negative feedback).
→Estrogen also suppresses LH. But at mid of cycle,
unexpectedly, under estrogen, Ant. Pituitary starts
producing more FSH(2 to 3x) and LH(10x). (Positive
Feedback). This is LH surge.
➔LH acts on graffian follicle causing:
• Blood vessels to dilate.
• Theca cells release destructive enzymes
(proteolytic & collagenases).
Graffian follicle becomes so big that it produces
elevation on surface of ovary (2→2.5cm). Due to
pressure blood flow lessens here. Avascular area
called Stigma.
• Due to more blood flow fluid inside also
decreases.
• Destructive enzymes (collagenases destroy
some collagen fibers so cover becomes
weak).
• LH has increased pressure inside follicle
and made cover weak. So, it will rupture
within a few hours. Ovum, zona pellucida
and corona radiata will come out.
➔Due to high FSH and LH, after ovulation,
fallopian tubes (finger like processes) come near
to ovary and start sweeping on ovary to find
stigma and capture ovum.
→Structure left behind collapses (contract). It has
theca and granulosa cells. LH works on these cells
as:
• Make them swell up
• SER becomes too much
• Accumulate a lot of fat globules which
means a cholesterol derived hormone is
going to be made. This is Progesterone.
Estrogen is still produced but Progesterone
in larger amounts.
• These cells look yellow colored. This is
Corpus Luteum. It is temporary endocrine
gland in female body. It’s total life is
10→12 days
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➔Just before ovulation, estrogen is at peak 4.2 IN NEXT CYCLE BEGINNING

and it causes cervical glands to release thin ➔Estrogen and progesterone low bcz of Corpus
mucus (normally thick) to increase chances for Albicans.
sperm.
➔Due to this, Hypothalamus produces more
➔Progesterone will act on endometrium: releasing factor and so, more gonadotropins are
produced.
• Arteries become coiled. More blood
flow. (Vascularization)
• More fluid in endometrium→more 4.3 IF FERTILIZATION OCCURS.
edema→E.M becomes swollen, warm Day 2 → Ovum 2 cell stage
and gets increased capability to
Day 3→ Morula and then enters uterus and zona
produce nutrition.
pellucida breaks down and fluid (uterine milk)
• Glands in wall become more tortuous. moves in. actually nutrition material. Fluid filled
This is Glandular/Vascular/Secretory cavity is Cyst. And structure is called Blastocyst.
phase of endometrium.
Day5→ Finger like protrusions and with their help,
blastocyst hangs with endometrium.
4.1 IF NO FERTILIZATION
→If no fertilization, ovum dies. It sends no signal.
Endometrium keeps on preparing for 10→12 days.
→After 10→12 days, Corpus luteum not received
any message. So, it will start degenerating and
become Corpus Albicans→Progesterone level
decreases dramatically.
➔Dec. progesterone causes:

• Vessels will undergo plasticity and shut

down. So, blood flow decreases.
Fingers secrete digestive enzymes and digest
Endometrium is ischemic. Cells start
endometrium wherever touch it. Endometrial cells
dying. Necrotic changes occur.
undergo digestion and release nutrition foe
• Necrotic materials slough away→Vessels
blastocyst while being digested.
are open. Bleeding starts→Menstruation.
• Estrogen and progesterone go It has gone inside Endometrium.
down→Ant. Pituitary starts next cycle.
5/6 day→start implantation.
➔Max bleeding time is 8days.
7/8day→Complete implantation.
➔Total bleeding volume is 20→80ml. If more or
Trophoblast area of Blastocyst sends message
less, there’s problem.
(special chemical substance HCG via blood) to
Endometrium has 3 layers: corpus luteum that causes it to multiply.

1. Basal layer→Outer Corpus luteum becomes big and starts producing

2. Glandular layer→Middle heavy amounts of estrogen and progesterone. It is
3. Compact layer→Inner corpus luteum of pregnancy. High estrogen and
progesterone inhibit FSH and LH release.
Glandular and Compact layers are called
Functional layers bcz these are lost in
menstruation while basal layer persists.
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HCG→Human Chorionic Gonadotropic Baby survival depends on continuous supply of

Hormone→appears in urine→released by estrogen and progesterone. After some time baby
trophoblast area. If in urine→means pregnant. develops special covering around it and placenta.

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Placenta is endocrine gland (starts producing its 6) Slough off and Menstruation.
own progesterone)→Estrogen progesterone inc.--
>baby independent→Corpus luteum degenerates
(3→4months).
During pregnancy, Estrogen and progesterone
7 FUNCTIONS OF HORMONES IN CYCLE
remains high. INDIVIDUALLY
➔Ovulation always occurs 14 days prior to start
of menstruation. First half of cycle is not fixed. 2nd 7.1 ESTROGEN
half is fixed. 1) From sec follicle→acts on uterus
endometrium and thickens it.
(proliferation)
5 1ST HALF SUMMARY 2) Acts on hypothalamus to dec FSH & LH.
1) FSH inc. 3) At mid cycle→ Inc FSH & LH.
2) Primary→secondary→graffian follicle. 4) At peak just before ovulation, causes
3) Estrogen inc. cervical glands to release thin mucus.
4) Endometrium→Proliferative stage.
5) First half is: ➔FSH dependent. ➔Follicular 7.2 FSH
stage of ovary. ➔Estrogenic stage 1) Pri follicle→Sec follicle→Graffian follicle
hormonally. ➔Proliferative stage of 2) After ovulation, causes fallopian tube
endometrium. processes sweeping action along with LH.

6 ON 14TH DAY 7.3 LH

1) Causes ovulation by increasing P inside
1) FSH and LH surge follicle and weakening its wall.
2) Ovulation 2) Acts on corpus luteum and makes it corpus
3) Remaining→Corpus luteum luteum (fat accumulation and inc SER) and
4) Make endometrium more secretory and secrete progesterone.
vascular. 3) After ovulation, causes fallopian tube
➔If fertilized: processes sweeping action along with FSH.

1) Product of conception reaches uterus and

7.4 PROGESTERONE
implant
1) Prepares endometrium by vacularization,
2) Release HCG that ➔supports corpus
swell, warm, tortuous glands and inc
luteum. ➔HCG to CNS and feels nausea.
nutrition.
➔HCG in urine, sign of pregnancy.
2) Dec will cause Menstrual Discharge.
3) No next cycle.
3) Maintains Pregnancy. 3→4 months by
➔If no fertilization: corpus luteum. Rest by placenta.

1) Ovum dies
2) Corpus luteum release progesterone for 7.5 HCG
10→12days. 1) To CNS→ causes Nausea
3) Prepare uterus 2) To blood→urine→Sign of pregnancy
4) No HCG→Corpus luteum degenerates 3) Supports corpus luteum and proliferates it.
5) Estrogen and Progesterone dec 4) Inc progesterone.
dramatically.
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FERTILIZATION
Process of fusion of male and female gametes.
1 DEFINITION
It is a coordinated sequence of molecular and
cellular processes which begins with contact of
oocyte and sperm and ends with the intermingling
of maternal and paternal chromosomes at
metaphase of first meiotic division of zygote.
➔Zygote is a unicellular embryo.
➔Most common site of fertilization in humans in
AMPULLA of Fallopian Tubes.
➔Infundibulum receives ovum. Fertilization
mostly in Ampulla. Fimbriae are processes.
2 HOW GAMETES REACH AMPULLA
Ovum is immotile and sperm is motile.
2.1 TRANSPORT OF OVUM
➔At time of ovulation, Graffian follicle ruptures
and ovum, zona pellucida & corona radiata release
on the surface of ovary, Due to inc FSH and LH.
➔Due to inc FSH and LH at ovulation, fimbriae
become active and sweeping over ovary and find
bulge(stigma) and pick up ovum.
➔Fallopian tubes have mucosa and cells are
ciliated. Cilia produce small fluid currents and help
in picking up ovum.
➔Ovum reaches ampulla and survives for 24 to
48hrs.
➔Meanwhile, it may be travelling towards uterine
cavity.
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2.1.1 Mechanism of transport of ovum in Uterine
tube
Little peristaltic movements that transport ovum
through fallopian tube.
2.2 TRANSPORT OF SPERM.
➔In one ejaculate, 200-500 million sperms.
(100million/ml according to Langman).
➔Semen is usually 2-6ml. 10% of it are sperms
and 90% are fluids from glands.
→Sperms are deposited in vagina. In semen, an
enzyme is activated here that causes some part of
semen to coagulate and stick to cervix so it may
not drain out. This is released by seminal vesicles.
Its name is Vesiculase enzyme.
2.2.1 Sperms more motile in uterus / Vagina
➔Vagina is acidic (helps to protect it from
microbes). So, sperms slow down.
➔Warm uterus has alkaline environment and
sperms become more motile. Sperms rapidly jump
from vagina to cervix.
➔Under estrogen just before ovulation, glands in
cervix release mucus that is thin, less viscid, stringy
and more abundant. Normally there is mucus plug
in cervix canal. This mucus is tested by doctor to
check ovulation
➔Tail of sperm propels sperm through cervical
canal into uterine cavity. For propulsion Energy
comes from Fructose in mitochondria to make
ATP. Fructose is in rich amounts in semen.
Mitochondria are in middle piece of sperm. All
mitochondria of spermatozoa come together and
make middle piece. Mucosal folds in cervical
canal→Some sperms hide here and keep sitting
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and start moving later on. So, sometimes after

some days, they are seen moving.

➔Fastest speed→ sperms reach in 5 minutes. (30
minutes acc to LANGMAN)
➔Slowest→45 minutes. (6 days acc to
LANGMAN).
➔Out of 500 million, 200-500 only reach and the
rest disintegrate on the way and absorbed by
mucosa.
➔Tail propulsion and Contraction of smooth
muscles in uterus move sperm forward. Cilia also
play a minor role.
➔In semen, prostaglandins are present which
stimulate contraction of uterine tube to pass them
3 CHANGES IN SPERM BEFORE FUSION
to ovum in ampulla when they reach fallopian Two main changes:
tubes.
• Capacitation reaction.
➔After reaching Intrauterine part of fallopian
• Acrosome reaction.
tube, they stop.
➔If ovum released, ovum and its cells (Corona 3.1 CAPACITATION REACTION:
Radiata) release substances that are →Special type of conditioning of sperm within
chemoattractant. Sperms detect them and move female reproductive tract→Takes about 7hrs.
there restarting movement.

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→Only capacitated sperms pass through corona
radiata.
Following changes occur:
• Glycoproteins and seminal plasma proteins
are washed off→Conditioning
• Cilia and enzymes of mucosa digest and
clear this in uterine tube.
➔Hyaluronic acid b/w corona radiata cells keep
cells together.
➔Capacitated sperms easily pass through corona
radiata.
➔Enzymes are Acrosin/Trypsin like substances or
Hyaluronidases.
➔Zona pellucida has ZP3 protein. It binds sperm
to zona pellucida as well as induces acrosome
reaction.
➔Ovum has integrins and sperm has disintegrins
on membrane. Membranes lockup due to
interaction of integrins and disintegrins. This
ensures sperms do not fall away.

3.2 ACROSOMAL REACTION

➔Induced by Zona Pellucida when sperm touches
it.
→This reaction is about fusion of acrosomal
➔Many sperms reach zona pellucida. In
Fusion b/w oocyte and sperm cell
membrane, post part of head of sperm
involved (head region membrane is lost in
acrosome reaction).

3.3 CORTICAL & ZONA REACTION

As soon as sperm membrane and ovum
membrane touch each other, cortical part
of ovum (has lysosomal enzymes) releases
lysosomal enzymes in cortical granules that
are release on surface of ovum. This is
cortical reaction. These enzymes cause
zona pellucida and ovum impermeable to
remaining sperms. This is Zona reaction.
membrane and and cell membrane at multiple
➔Species specific receptors (on zona pellucida
points. Due to fusion holes are
that allow only human male sperms to pass
produced→Enzymes released out of it that digest
through) are inactivated in zona reaction.
zona pellucida.

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➔Reaching inside sperm will undress (leave

membrane out). Only sperm goes in leaving
membrane.

• Tail degenerates after it gets in.

• M2 is completed in ovum bcz before this
sperm had single structured 23
chromosomes while ovum had double
structured 23 chromosomes. Almost all
cytoplasm of ovum after M2 goes to ovum.
Now this is definitive ovum.
• Cytoplasm also disappears.
• Pro-nuclei double their DNA. (Double
structured chromosomes).
• Come together and fuse.
4 HOW OVUM RESPONDS IF SPERM
TOUCHES OVUM AND ENTERING IT
• Cortical & Zona reaction.
• Completion of M2
• Metabolic activation of ovum induced by
sperm.
4.1 FUSION OF NUCLEI
• When touch each other both dissolve
nuclear membrane.
• Now we have 46 double structured
chromosomes.

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• Mitosis starts. In metaphase, these are

rearranged on metaphase plate.
• Centromere breaks and two cells formed
ultimately. Chromatids move opposite
poles.
• After new nuclear membrane → called
Chromosomes.

5 MAIN RESULTS OF FERTILIZATION

• Establishment of diploid number. (2n)
• Determination of sex of zygote.
• Metabolic activation of ovum and initiation
of cleavage.

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close. This is compaction. They develop electrical

1 OVERVIEW
As ovum is metabolically active, it will not undergo
apoptosis. Fertilized ovum will undergo cleavage.
Previously chromosomes were arranged on
metaphase plate. Now, chromosomes start
contacts (gap junctions) with each other bcz at
multiple points membranes fuse. Metabolic
products, signals, ions can go through and cells can
communicate. This compact inner cell mass will
make baby. Outer mass will make covering of baby
and placenta. Inner cells are going to make

segregating. Break at centromere longitudinally. embryo proper.

Chromatids move to opposite poles. During this,
cell develops deep furrow. When chromatids
reach poles, furrow deepens and cell divides. Both
cells have 46 double structured chromosomes.
First division completes in fallopian tubes within
zona pellucida.
➔Day 1→Fertilization.
➔Day 2→After 30hrs of fertilization→2 cell stage.
➔During 2nd day→4 cell stage.
➔3rd day beginning→8 cell stage.
➔Morula floats in uterine fluid for 2 days. 4th and
5th day.
➔Around 4th day→fluid starts going in through
zona pellucida→Fluid filled cavities→join and
push inner cell mass to outside. This fluid filled
cavity is cyst. Cells are rapidly multiplying→Blast.
This structure is hence Blastocyst.
➔Early stage embryoblast still has zona pellucida.
Inner cell mass is called embryoblast now. Outer
cell mass is trophoblast.
➔Zona pellucida starts degenerating. Blastocyst
comes out as chicken comes out of a shell (hatch
out). This is 5th day.
This blastocyst has to attach to endometrium. This
is about 20th day if ovulation happened at 14th day.
Corpus luteum is producing progesterone.
➔Day 6→Time of implantation. At that time
status of endometrium is as in table:

➔Around end of 3rd day→16 cell 1st half (Pre- Ovulation 2nd half (Post-
stage→resembles melburry→so called early Ovulation) (14th day) Ovulation)
morula stage. High FSH and FSH and LH Low FSH and
LH surge. LH
Uptill now ovum is in fallopian tube. Ovary: -- Ovary: Luteal
➔Around end of 3rd and start of 4th day→Morula Follicular stage
will fall into uterine cavity→Morula has outer and stage
inner cell mass→Central/inner cells come very

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Blood: High -- Blood: High 3 DAY 6-12

estrogen estrogen but
even more  Day 6→Attachment
Progesterone.  Day 7th, 8th, 9th→Getting in
Endometrium: -- Endometrium:  Day 10th and 11th→gone deep
Proliferative Glandular and
 Digested endometrium area closed by
Secretory
fibrous plug.
 Day 12→New mucosal layer develops.
➔Most commonly, Implantation in Anterior and
Posterior wall of Uterus. Less commonly in
Fundus.
4 CHANGES IN TROPHOBLAST &
➔Trophoblastic cells express special molecular
EMBRYOBLAST WHILE GETTING IN
hooks (Selectins) →hook with other molecules ➔End of 1st week→Implantation started.
(Receptors for selectins) on surface of
endometrium. Receptors are special type of ➔End of 2nd week→Completes implantation.
sugars. Blastocyst loosely attaches with sugar
molecules by Selectins. 4.1 2ND WEEK OF DEVELOPMENT
Rule of 2
➔Now blastocyst has to move in→ It induces
programmed cell death of endometrium and will  Trophoblast develops 2 layers.
go deeper and gets nutrition from dead cells. Cytotrophoblast and Syncytiotrophoblast.
Starts implanting in b/w Glandular structures and  Embryoblast develops 2 layers. Epiblast
also gets nutrition from here. and Hypoblast.
 Two cavities. Amniotic cavity and
Chorionic cavity.
2 DECIDUAL REACTION  Extracoelomic mesoderm develops 2
Happens only if implantation starts. layers. Splanchnopleuric and
Somatopleuric.
Endometrium cells around
site of implantation:

• Becomes polyhedral.
• Accumulate lot of
glycogen, lipids as
source of nutrition
and becomes
edematous.
• This change spreads
to all endometrium.
➔Powerful attachment of Blastocyst with
integrins and integrates into endometrium.
➔Fibronectins and leminins help it to migrate
within endometrium and attach to it respectively.

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DEVELOPMENT UPTO 2
4.2 CYTO AND SYNCYTIO? 8TH DAY
4.2.1 Cytotrophoblast
 Clearly defined cells.
 Each having membrane.
 Each having one nucleus.
4.2.2 Syncytiotrophoblast
 These are Mitotic figures.
 New cells move outward from
cytotrophoblast→Loose membranes and
their protoplasm fuses (syncytium).
 Nuclei present but cells not visible.
 Produces lot of digestive enzymes.
 Develops more on embryonic pole.
➔Around 9th day→Fluid filled cavities called
Lacunae form on Syncytiotrophoblast. Lacunae get
connected around 10th and 11th day.
➔While moving in, Syncytiotrophoblast may
digest dome of capillaries (sinusoids)→Blood may
come into lacunae→Some lacunae connected to
venules so blood seeps in and out. This is
establishment of Uteroplacental
th
circulation→Around 11 and 12 day.th
➔So, If around 13th day, area of digested
endometrium is not plugged, little blood may
drain. This is 27th day, Time of menstruation also.
It may result in wrong calculation of expected date
of delivery.
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➔Around 14th day→Cytotrophoblastic cells make
columns of cells moving into Syncytiotrophoblast.
These are called Primary Villi.
4.3 EMBRYOBLAST
➔Cells of embryoblast facing cystic cavity make
layer of cells. These cells make cuboidal cell layer
facing cavity. These are called HYPOBLAST.
➔Above, Cells make columnar cell layer called
EPIBLAST.
➔Some cells above it also. They develop fluid
filled cavities→Later fuse to form Amniotic cavity
and layer pushed up→Amnioblast. Columnar cells
facing newly developed cavity. Cuboidal cells
facing Blastocystic cavity. Amniotic cavity is lined
by Amnioblast and Epiblast.
➔Hypoblast cells move down and enclose a cavity
called Primary yolk sac. In b/w Primary yolk sac
and amniotic cavity, we have Bilaminar germ disc
having Epiblast and Hypoblast.
➔Downwards, Hypoblastic cells start secreting
Connective tissue between yolk sac and
cytotrophoblast. This connective tissue moves up
as well between Amnioblast and Cytotrophoblast.
Since this C.T is outside embryo (Proper germ
layer), this is called extraembryonic mesoderm.
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Cytotrophoblast+Syncytiotrophoblast+Somatopl
euric layer=Chorionic Plate
➔Real baby comes out of 2 layers (Bilaminar disc).
➔Connected outside by Connecting Stalk which
develops into umbilical cord in future. Also
connected to chorionic cavity by same stalk.
➔Syncytiotrophoblast produces hCG.
➔Sec Yolk sac disappears lateron.

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DEVELOPMENT UPTO 3
1 GASTRULATION
In the beginning of 3rd week of development,
Bilaminar disc→Trilaminar disc.
Bilaminar Trilaminar
embryonic Gastrulation embryonic
disc disc
➔Embryo having 3 layers is called Gastrula.
➔Bilaminar disc formed during 2nd week. (bi for 2)
➔Trilaminar germ disc formed during 3rd week.
(tri for 3).
Looking embryo/disc from above we see:
➔We see very flat disc in the beginning. An area
of thickness called prechordal plate at cephalic
end. This is area where both layers are very close
to each other.
➔From caudal to cephalic end, cells start
proliferating along central axis and a longitudinal
streak (Line) appears. This is Primitive streak. Its
anterior part is more wide→Primitive Node. Cells
from center of Primitive streak and Primitive node
disappear. Line within primitive streak where cells
are deficient is called Primitive groove. Central
depression in primitive node is called Primitive pit.
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1.1.1 Purpose of groove
➔Cells from epiblast start proliferating and
migrating to primitive groove/streak. Why?
➔Primitive streak and node cells start producing
chemical substances (Fibroblast growth factor 8)
(a protein) that attract cells to it. This substance
moves laterally and neighboring cells proliferate
rapidly and then migrate. Hypothalamic cells held
by E-Cadherins(Sticky). FGF8 reduces reduces
concentration of E-Cadherins to make migration of
cells possible.
➔Cells moving towards groove then move down
through groove→After coming down they
become flask shaped cells and move laterally and
forwards to cephalic end→Mix with hypoblast
cells→Hypoblast cells start degenerating and
these cells take place of hypoblast→Hypoblast
replaced by a new layer called Endoderm.
Endoderm derived from Epiblast.
➔Once it is made, another generation of cells
start migrating in the same way→Coming
down→spread to place in b/w epiblast and
endoderm→this is Mesoderm. This is present
everywhere b/w ecto and endoderm except 3
places:
• Prechordal plate.
• Posterior/caudal part of disc.
• Buccopharyngeal membrane.
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DEVELOPMENT UPTO 3
Mesoderm is derived from epiblast.
➔Layer of remaining part of epiblast is ectoderm.
Remaining layer of Epiblast which has already
made endoderm and mesoderm.
Ectoderm is derived from epiblast.
1.1.2 Cells moving through Primitive Node
➔Primitive streak present only on posterior
aspect (caudal) of plate. Because cells are moving
forward also, so, caudal end area around primitive
streak is truly loosing cells and cephalic end area
ahead of primitive streak truly gaining the
cells→Caudal end becomes narrow and Cephalic
end becomes broad with the passage of time.
Initially almost round then longitudinal and then
like a sleeper.
➔From this circular pit cells will move in and
migrate down and forward because below is
hypoblast. As they go down circularly, a tube like
arrangement is formed b/w epi and hypoblast.
➔These cells in tube arrangement move from
primitive node upto prechordal plate between
epiblast and endoderm. This tube is Notochordal
tube / canal. Derived from primitive pit. This tube
acts as central axis of body/ embryo. Vertebra will
develop from it.
Longitudinal section as shown in 2nd row in above
figure.
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Mesoderm can be seen absent in 3 areas
described earlier. These are:
1. Cloacal plate & Caudal end→Ecto and
Endo held together.
2. Buccopharyngeal membrane (Future
mouth area) & prechordal plate→Just
cephalic to prechordal plate.
3. Where something else is present in
between→ Notochordal tube.
➔Notochordal tube is opening above into
amniotic fluid. With passage of time, floor of tube
fuses with endoderm and both disintegrate.
Temporarily, fluid of amniotic cavity gets
connected with yolk sac. This is established
through Neuroenteric Canal.
Why this canal is called so?
Because later on, area above→Nervous system
develops from it. Area below→ GIT develops from
it. Canal is from part of disc going to develop
nervous system to part of disc going to develop
GIT. Roof of tube in contact with Epiblast.
Transverse section (Figure ahead)
After loosing floor, tube changes to plate
intercalated with endoderm (roof of yolk sac).
Neuroenteric canal will disappear.
➔Notochordal plate detaches endoderm and
proliferates a lot and make solid mass of cells.
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DEVELOPMENT UPTO 3
➔Endoderm will proliferate also and fill gap. Now,
this solid rod is definitive notochord.
Role of notochord:
• Plays very important role in development
of nervous system.
• Causes cells in ectoderm to proliferate by
producing products. These cells will form
Neural plate.
• Involved in Paraxial mesoderm formation.
In center of Intervertebral disc, there is nucleus
pulposus. It is remanent of notochord in adults.
2 IN THE END OF 3RD WEEK
• A trilaminar disc formed.
• Has endoderm, mesoderm (except 3
places) and ectoderm.
Disc will roll up→Folds go laterally→Ends fuse.
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Ectoderm→Skin
Mesoderm→ Muscles, Urogenital system, Bones
Endoderm→GIT
Notochord→Causes development of vertebral
column and spinal cord around it.
➔From ectoderm, we pull out material for limbs
(Ectodermal skin, nails, hair) and mesoderm
(Muscles, ligaments, tendons) also goes there.
In the end of 3rd week and beginning of 4th week,
Gastrulation is Completed. When gastrulation is
completed, Primitive streak disappears.
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DEVELOPMENT UPTO 3
3 PROBLEMS OCCURING IN
GASTRULATION
Damage to the embryo during its early
development is called Teratogenesis. Substances
that produce teratogenesis are called teratogenic
substances.
Many toxins and drugs are teratogenic. e.g= High
Alcohol intake at time of development of
trilaminar germ disc damages development of
embryonic tissue.
Female may be unaware of pregnancy or think
that periods are delayed and not take precautions.
If she takes high doze of alcohol, it will damage
trilaminar disc.
By now, trilaminar disc is programmed about what
tissues will be made from three layers.
➔2rd-8th week most dangerous time because
layers will start forming tissues and organ systems.
Upto 8th week, most of body tissues and organ
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systems are made. After this, further is usually
maturity of organ system. At this stage (2-8week),
a little damage to embryo may produce a very big
damage to developing system.
3.1 HOLOPROSENCEPHALY
➔Alcohol is highly lipid soluble. It will be rapidly
absorbed in GIT and go into the blood. Any
substance that is highly lipid soluble will efficiently
cross placenta. Placenta is not established yet. So,
we say it product of conception.
➔Alcohol→GIT→absorb→Dissolve
into blood→dissolve into biological barriers and
cross them to reach upto product of
conception→Destroy cells of midline from
prechordal plate and anteriorly (to cephalic end)
because these cells are very sensitive to high doses
of alcohol. They also destroy cells in notochordal
tube area→ This area folds lateron and forms
front of head and neck. So, there can be:
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• Eyes may be abnormal→Central/midline
structures may underdevelop and eyes
more near to each other→Hypotelorism.
• Underdevelopment of forebrain specially
central area. In CNS there are ventricles
(CSF produced). From lateral ventricle,
fluid to central area (3rd vent.) and then a
duct and then into 4th vent. Central area
underdeveloped so, both laeral ventricles
more near→Fuse.
WHOLE THIS COMPLICATION IS CALLED
HOLOPROSENCEPHALY.
1. Lower limbs ma not form properly and may
fuse. (Hypoplasia of lower limbs).
2. Abnormal vertebral column (lumbar and
Sacral region) →caudal intermediate
mesoderm in this area also less so
structures from it also
abnormal→Urogenital system (Many parts
of this system derived from intermediate
mesoderm.
3. Renal agenesis
4. Genital abnormalities
5. Imperforate anus. The is no perforation of
anus.

3.2 SIRENOMELIA / CAUDAL DYSGENESIS THIS IS CAUDAL DYSGENESIS OR SIRENOMELIA.

➔If a drug/toxin causes damage to posterior end

(caudal end)→Caudal area does not develop 3.3 CILIOPATHIES / SITUS INVERSUS /
well→Caudal dysgenesis. KARTAGENER'S SYNDROME
➔During formation of gastrula, gene is damaged
Mostly occurs in children of those females who
that is encoding for dynins.
have diabetes mellitus.
➔Cilia on ventral aspect of endoderm alter
➔There is underdevelopment of caudal
concentration of certain substances (produced by
mesoderm.
disc) →which determine which side of fetus will be
3.2.1 Problems right or left and also play a role in pattern
development on left/right side of body.

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➔Endoderm is on visceral side. Here, viscera of Abnormal dilation of bronchial passages and full of
thorax and abdomen will form. infection→Bronchiactitis.
Cephalically→Heart, Respiratory system. ➔Sperms→ non motile→Male infertility.
Caudally → GIT along liver/Pancreas/Other Situs Inversus with all additional problems is called
structures in abdomen. Kartagener’s Syndrome.
➔Rarely, heart lies on left side called
dextrocardia. Normally heart on left along with
spleen and stomach. Liver on right side.
➔A patient may have all organs on opposite sides
in abdomen called Situs Inversus → Site of viscera
are transpositioned in thorax and abdomen.
Patient may have no problem.

3.3.1 What is the Problem?

➔When patient in stage of development of
gastrula (Product of conception in gastrulation at
trilaminar disc stage).
➔Additional problems include:
1. Chronic sinusitis
2. Bronchiactitis
3. Male infertility (Male specific)
Most of structures in adult body with cilia like
structures, their cilia will dysfunction.
Cilia have special proteins DYNINS that are
abnormal in these (genetic problem). This may
also lead to situs inversus.
➔Paranasal sinuses→Cilia→force mucus to go to
nose. If cilia not working well, mucus collects here.
Bacteria settle and proliferate and cause chronic
sinusitis.
80% patients have no problem. In these cases we
say this is Primary ciliary dyskinesia.
20% have additional problems. Cilia have
dysfunctioned during development.
➔Cilia in respiratory passages→ some cells
produce mucus here→cilia push mucus to pharynx
and then to stomach/esophagus. If not working
well, mucus accumulates and bacteria
settle→Infection→bronchial walls weak. So,

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1 INTRODUCTION
➔Mid-cycle→ LH surge→ Ovulation→ ampulla→
Fertilization→ definitive/Fertilized ovum (cell
memb, zona pellucida and corona radiata)→
Meiosis-2 completed→ Zygote→ Blastula→
Morula→ Blastocyst→ Embryoblast and
Trophoblast→ villi at embryonic pole→Cyto and
cyncytiotrophoblast. • From center to cephalic & caudal→ some
➔Almost at 1 week→ villi→ destructive cells separate from tube→ neural crest
enzymes→ dissolve endometrium→ start cells
implantation→ uterus secretory/ luteal stage→ • Anterior & posterior neuropores close at
implants in superior and posterior wall mostly. 25th and 27th day respectively.
10→12 days life of corpus luteum→ hCG by • Notochord:
cytotrophoblast→ corpus luteum of pregnancy 1. Produces substances that develop
(also called Corpus luteum gravidarium)→ keeps neural tube.
endometrium secretory. 2. Major role in development of CNS.
3. Ramanant as Nucleus pulposus in
➔At 2nd week: intervertebral disc.
• hCG detectable in urine after 10 days.
• Bilaminar disc formation.
• Amniotic cavity and yolk sac.
• Epiblast and hypoblast tightly held at
prechordal plate. A site of future mouth
of baby.
➔3rd week

• Primitive streak and node→

gastrulation→ 3layers.
• Trilaminar disc formation.
• Ectoderm, endoderm and mesoderm.
• Notochord formation between ecto and
endoderm form primitive pit upto
prechordal plate at mesoderm area since
there mesoderm is absent.
• Notochord releases chemicals→
ectoderm rapidly proliferates→
Additional layer of cells→ longitudinal
thickness→ Neural Plate→ Starts folding
and depressing down→ edges raising→
center depressing→ neural folds and
grooves→ folds fuse eventually. ➔At 25/27 day there should be sufficient folic acid
in blood. This time first period in missed usually. If

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NERVOUS SYSTEM DEVELOP.
anterior neuropore does not close properly→
Anencephaly occurs:
• Rudimentary brain stem.
• Upper part of CNS not formed.
• Baby not capable of extrauterine survival.
• Born dead or dies after birth.
If posterior neuropore does not close in time→
problems occur in lower back area (e.g= Spina
Bifida).
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2 NEURAL TUBE DERIVATIVES
➔At cephalic end of tube→ 3 swellings called
Primary Vesicles appear→ Make future brain.
1. Prosencephalon (Forebrain).
2. Mesencephalon (Midbrain).
3. Rhombencephalon (Hind Brain).
This tube is having CSF filled cavity throughout. In
upper part, it will make brain ventricles. Lamina
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terminalis→ structure in adult brain here anterior 2.3.2 Myelencephalon

neuropore closed. → Medulla Oblongata.

2.1 PROSENCEPHALON 2.4 TELENCEPHALON

→very rapidly growing except mid portion that is
slow. So, prosencephalon divides into 2 vesicles
telencephalon and diencephalon.
Telescopes converging on Diana Princess.
2.2 MESENCEPHALON
→remains same.
2.3 RHOMBENCEPHALON
→2 vesicles:
1. Metencephalon at cephalic end.
2. Myelencephalon at caudal end.
2.3.1 From posterior side of metencephalon
→ special plate develops→ structures develop
backward→ cerebellum hemispheres develop.
What remains anteriorly is Pons.
→ rapidly developing. It has one area
underdeveloped located above diencephalon
called Insula. Rest of telencephalon grows around
INSULA:
• Forward→ Frontal lobe
• Upward→ Parietal lobe
• Backward→ occipital lobe
• Downward and turns→ temporal lobe
2.5 DIENCEPHALON
is thalamus, hypothalamus and other structures
around it.

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2.6 CNS CORRELATES

➔From nasopharynx→ epithelial cells grow up
and back→ ruthke,s pouch→ convert into
hypophysis (Anterior pituitary).
➔Retina, uveal tract (choroid, ciliary body and
iris) of eye, optic nerve, chiasma, optic tract all
develop from diencephalon.
➔Optic nerve not actually a nerve but a CNS
tract derived from diencephalon.
➔Lateral geniculate body on sides of
thalamus→here optic tract ends.
➔Anterior pituitary does not develop from
neural ectoderm.

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3 SPINAL CORD • Go upward→ tracts (Dorsal).

• Laterally and up→ lateral tracts.
Cross section: • Cross to opposite side anteriorly and go
up→ Anterior tracts.
3.1 GREY MATTER So, we get:
➔Layer of cells multiplying (neuroblasts) develop
on posterolateral sides→ ALAR (means ear) 1. Dorsal column
plates→ sensory grey matter. 2. Lateral column
3. Anterior column
➔Anterolateral development→ basal plates→ 4. Anterior spinal fissure
play role in motor system→ motor grey matter. 5. Dorsal sulcus
➔Grey matter from center to anterolateral and ➔Fluid filed cavity→ cells proliferate→ grey
posterolateral sides. matter→ basal and alar plate→ motor and
sensory grey matter→ Motor (to
tissues) and sensory (projections
to cns. Actually receiving from
ganglion.)
➔Dorsal Root Ganglion:
→peripheral (skin, joints,
proprioception)→ dorsal root →
directly back and go up and relay
at upper level OR relay here and
n2d order neuron cross and go
lateral or to anterior side.

4 RHOMBENCEPHALON
Going up→ spinal cord converts
into pons and medulla.
Arrangement throughout brainstem:
3.2 WHITE MATTER Motor grey matter→ center
➔From anterolateral sides→ Fibers come out
Sensory grey matter→ sides
from tails of cells→ motor fibers→ eventually in
motor nerves. ➔top of brain→ motor fibers coming down→
crossing the medulla→ major sensory fibers will
➔Neural crest cells proliferate→ dorsal root
cross at different levels in brainstem speccialyy
ganglion→ some connection to periphery and
medulla→ so motor and sensory horns
some to sensory side. Neurons in DRG initially
fragmented. These fragments→ nuclei (may be
bipolar→ fuse→ unipolar→ one central process to
motor or sensory).
center and one peripheral process to periphery.
➔Hypoglossal nucleus→ motor nucleus→ basal
➔some neural crest cells form cranial nerve
plate. Trigeminal sensory nucleus→ ALAR plate.
ganglia and peripheral spinal nerve ganglia.
➔Posterolateral side fibers:

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5 NEURAL CREST CELLS DERIVATIVES • Respiratory system structures

• Digestive system structures
• Thyroid gland
5.1 NAJEEB’S WAY • Parathyroid gland
• Initially on sides of neural tube. • Tonsils
• Spread throughout ectoderm→ skin→ • Thymus
melanocytes.
• Some scatter around neural tube and its ➔in Abdomen:
derivatives (around all CNS)→ Pia and • Liver
arachnoid matter (leptomeninges). Dura • Pancreas
matter from mesoderm. • Lining of urinary bladder
• Some made aggregates around spinal
cord→ ganglia (sensory or autonomic, 5.2.3 Mesoderm
cranial or spinal) • Muscles→ smooth, cardiac, skeletal.
• Bones in neurocranium • Vessels→ CVS, lymphatic.
• Sympathetic ganglia put together and lost • Reproductive→ testes, ovaries, etc.
axons→ gland--. Adrenal medulla. • Urinary system→ bladder etc.
• Parafollicular C-cells in thyroid gland
(Produce calcitonin).
• Teeth→ odontoblasts
• Conotruncal cushions and
aorticopulmonary septum
• Schwan’s cells (PNS).
• Mesenchyme of pharyngeal arches.

5.2 SELFLESS MEDICOSE METHOD

5.2.1 Ectoderm
➔Outside structures:

• Skin/epidermis
• Hair
• Eyes
• Nose
• Ears
• Nails
• Teeth enamel
• Mammary glands
➔3 inside structures:

• CNS
• PNS
• Pituitary gland

5.2.2 Endoderm
➔in the NECK:

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1. Outer cells→ called angioblasts→ make

endothelial cells.
1 OVERVIEW 2. Inner cells→ separate→ blood cells.
1. Arterial system
2. Venous system
3. Fetal circulation
➔CVS develops from→ mesoderm→
Intraembryonic and extraembryonic (specially
connecting stalk mesoderm).
➔Multiple islands of cells communicate (grow to
➔Extraembryonic mesoderm present/consist of: each other and become continuous) then canalize
by disintegration→ blood vessels. This is
1. Mesoderm in connecting stalk
Vasculogenesis.
2. Around yolk sac and amniotic cavity
3. Chorionic layer
➔in Extraembryonic mesoderm:
1. Blood vessels mainly in connecting stalk
2. Some Around yolk sac
3. Some In chorionic mesoderm ➔Make vessels→ 2 ways→
➔Major role in CVS development→ 1. Vasculogenesis
splanchnopleuric intraembryonic mesoderm. 2. Sprouting of previous vessels.
Other parts also involved→ somites, intermediate
➔Angiogenesis→ from wall of these vessels→
mesoderm, somatopleuric mesoderm.
cells proliferate and form cords→ central walls
degenerate and branches form.

2 ARTERIAL SYSTEM
1. Pharyngeal arches
2. Rest of body

2.1 PHARYNGEAL ARCHES

➔Around pharynx→ mesoderm→ proliferates→
moves forward and down→ pharyngeal arches.
How mesenchymal cells make vascular system & Multiple develop bilaterally.
blood? ➔Proliferated solid mass of mesoderm that
➔Mesodermal cells proliferate→ Masses→ grows anterolateral to pharynx and moves
differentiate: forward and downward as paired structures

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(Right & Left). Each has its own nerve and arterial this arterial system descends down, it pulls this
supply. nerve down. Larynx is up and nerve going down
which was originally straight. But still connected to
➔Heart developing in neck ventrally→ this is
larynx but course is reverse→ Recurrent laryngeal
Truncus Arteriosus. Distal part of truncus is called
nerve.
Aortic sac.
➔Dorsally→ 2 dorsal aortae. Aortic sac→ vessels
sprout to pharyngeal arches and fuse with dorsal
aorta of respective side. 5th pharyngeal arch→
vessel does not develop or regresses very rapidly.
➔Every arch having its own artery (Paired).
Ventrally→ Aortic sac. Dorsally→ Dorsal aorta.
These vessels as paired structures connecting
aortic sac with dorsal aorta are called Pharyngeal
or Aortic arches.

➢ First pharyngeal/ aortic arch ramanant→
Maxillary artery.
➢ 2nd→ stapedial artery (Stapes bone relation).
➢ 3rd→ carotid system (Common, internal and
external).
➢ 4th→ ➔Aorta of one side except its proximal
part and proximal part of pulmonary artery
(these are from truncus arteriosus).
➔Subclavian artery.
➢ 6th→ vessels related to lungs. (Pulmonary
artery)
First make sexy steps then call for aortic arch and
sleep with lungs
➔Right side→ distal part of 6th arch degenerates.
Left side→ continue as left pulmonary artery and
ductus arteriosus.
➔Vagus nerve gives branch that is below and
behind 6th arch. Going to developing larynx. When
➔from 6th arch→ ductus arteriosus. So, after
birth→ ligamentum arteriosum. (left side). On
right side→ 6th degenerates so nerve hooks
around 4th. From 4th→ right subclavian artery. So
recurrent laryngeal nerve hooks around right
subclavian artery on right side and ligamentum
arteriosum on left side.
➔At T4 Dorsal aortae fuse and form dorsal aorta.
➔Initially, dorsal aortae around respiratory and
digestive system.
➔Sometimes anomaly. Right side dorsal aorta
does not regress and two aortic arches form.
These enclose esophagus and trachea causing
dysphagia and dyspnea.

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2.1.1.1 PRE DUCTAL

1. Left ventricle to aorta→ blood cannot go
2.1.1 COARCTATION OF AORTA
properly
• just before/ just after ductus arteriosus
2. Arch and its branches→ increased blood
• distal to origin of left subclavian artery→ aorta
pressure and flow.
may become narrow or constricted.
3. Reduced blood downstream→ reduced
• Congenital anomaly oxygen.
• Problem primarily with tunica media. 4. At reduced oxygen→ductus arteriosus
• Smooth muscles in ductus arteriosus are may remain open. Blood moves from
transferred to smooth muscle layer of aorta.
Since ductus arteriosus closes at high O2,
this may also close causing constriction.
• Primarily, media of aorta constrict.
• Secondarily, intima inside also
proliferates→ more constriction.
• Before duct→ pre-ductal coarctation.
After duct→ post-ductal coarctation
(Mostly).
• Associated with cardiac abnormalities,
turner syndrome. More common in boys.
➔Effects→ blood cannot go down.

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pulmonary artery to aorta distal to ➔Lateral branches→ kidneys (renal vessels).

obstruction.
2.1.1.2 Post ductal:
1. Bp high as before in arch and branches.
2. But ductus arteriosus closes because O2 is
good
3. Downstream→very reduced blood flow
and bp.
4. So blood takes collateral path. Blood→
aorta→ left subclavian→ internal thoracic
(dilates)→ intercostal arteries (reverse
direction)→ distal part of aorta. Intercostal
arteries→ pulsations→ damage ribs
development→ notched ribs.
5. May also go via periscapular anastomoses
because it is also connected with
intercostal arteries.
6. Inc. bp in upper limbs.
7. Dec. bp in lower limbs.
8. Palpate radial and femoral pulse
simultaneously→ little delay in femoral
pulse.
9. Auscultate chest→bruit is heard. Because
collateral vessels have increased blood
pressure audible. Abnormal audible sound
heard due to abnormally high blood flow
through arteries is called bruit.
10. Treatment→ surgically removed.
11. Increased risk of stroke because increased
bp to head may lead to burst of small
vessels in CNS.
12. Abnormal blood flow→ infection→
endocarditis.
Renal vessels also supply suprarenal glands and
gonads because gonads originally develop on sides
of aorta in abdominal cavity. Later on ovaries
descend to pelvis and testis to scrotum.
➔Ventral branches→ Vitelline arteries originally.
Because in embryo→ front→ yolk sac and git. And
aorta at the back.
1. They have many branches looking like sun.
so called sunciliac (actually CILIAC)
artery→ foregut.
2. Superior mesenteric→ upper git artery→
midgut.
3. Inferior mesenteric→ lower git artery→
hind gut.
4. Some ventral branches also come down→
2 arteries→ move forward→ upward→
enter umbilical cord→ umbilical arteries.
5. When aorta develops in lower part→
divides→ two→ common iliac arteries→
external and internal iliac arteries.
1,2,3 are derivatives of vitelline arteries.

2.2 DEVELOPMENT OF OTHER ARTERIES

➔initially around 4th and 5th week→ 2 dorsal
aortae. Eventually fused→ one dorsal aorta. From
dorsal aorta→ branches→ posterolateral
branches and lateral branches.

2.2.1 Posterolateral Branches:

1. To upper limbs
2. Intercostal arteries ➔From aorta to yolk sac→ vitelline artery→
3. Lumbar Loose connection with aorta→ move down in
4. Sacral origin→ internal iliac artery.
5. Lower limb
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In developing heart, venous input system is sinus

venosus. Initially during 4th and 5th week, all 3
systems go to sinus venosus.
CUVVUC
➔Cardinal veins→ draining upper body→
Anterior Cardinal veins
➔cardinal veins→ draining lower part of body→
Posterior cardinal veins.
Both come together before draining in sinus
venosus to form common cardinal vein (for a short
distance).

➔Originally, umbilical arteries→ from aorta. With

development→ Origin down→ separate and
come down as internal iliac. Connected with villus
vasculature in placenta.
In adults, umbilical arteries degenerate, close and
become fibrotic→ called Medial umbilical
ligament.
➔Adult remnants of umbilical arteries:
1. Going inside→internal iliac
2. Just above urinary bladder→ vesicle artery. Mostly, right sided system develops more than
3. Remaining→ fibrotic→ MUL→ just inside left side (regresses) because caval system on right
anterior abdominal wall. side.
➔As further development→ system should
3 VENOUS SYSTEM modify such that it should drain on right side and
sinus venosus→ originally symmetrical→
3 venous systems developing. becomes asymmetrical and bilateral to unilateral.
1. Which is draining yolk sac→ vitelline With time, left horn of sinus venosus→ regresses
veins→ 2 (right and left) and change. Somehow, most of venous system
2. Which is bringing blood from placenta to connects to right side.
embryo or fetus→ umbilical venous
system.
3.1 VITELLINE SYSTEM
3. Head & neck, upper limb and other
developing body→ cardinal venous system
(right and left). ➔Septum transversum, GIT also developing.
Initially, 2 umbilical veins. But later on, only one.

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CARDIOVASCULAR SYSTEM DEV
➔Two vitelline veins coming from yolk sac→ go
near duodenum/ developing git and around
duodenum→ Make a plexus.
➔On the way to sinus venosus→ pass through
septum transversum. (here liver bud comes and
develops). Liver bud becomes so large that
vitelline vein has to pass through liver.
➔While passing through liver→ break down into
smaller vessels→ sinusoids (wide bore capillaries).
Recollect and go out as hepatocardiac channels (R
& L)→ carry from liver to heart.
➔Modification starts→ left side→ degenerates or
fuses with right vitelline. So, left vitelline largens→
hepatic portal vein.
Why Portal?
3 derivatives of vitelline arteries come to GIT.
Recollect into portal system. This again breaks up
into microcirculation. So, it is connecting two
microcirculations→ portal.
➔Inferior mesenteric vein→ splenic vein.
Splenic vein + superior mesenteric vein→ hepatic
portal vein→ breaks into 2 sinusoids derived from
right and left vitelline veins.
Actually, left sided Sinus Venosus regresses. Left
hepatocardiac channel→ degenerate & its plexus
connects to right hepatocardiac channel. So RHCC
enlarges.
3.1.1 MAJOR DERIVATIVES OF VITELLINE VEIN
• Portal vein draining superior mesenteric
vein and splenic vein (draiing inf.
Mesenteric)
• Hepatic sinusoids
• Right hepatocardiac channel→ enlarges→
hepatic portion of inferior vena cava.
• Right hepatocardiac channel→ right
hepatic vein
• Left hepatocardiac channel→ left hepatic
vein→ degenerate.
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3.2 UMBILICAL VEINS
➔initially, 2 umbilical veins→ bringing blood to
sinus venosus.
➔As liver enlarges→ right and left umbilical veins
also have to connect to liver.
Also break into sinusoids. So, microcirculation of
liver is derived from 2
• Mainly, vitelline veins
• Partly, umbilical veins
Recollect and mix with sinusoids of vitelline veins.
By 2nd month of pregnancy→ all right umbilical
vein, except a little part of sinusoids, degenerates.
➔Left umbilical vein→ distal part going to sinus
venosus also degenerates. Its proximal part
making sinusoids is left. This part connects
placenta (oxygenated Blood) to liver.
Proximal end→ sinus venosus end.
Distal end→ placenta end.
WHY UMBILICAL VEINS GO TO LIVER?
Because their function is to provide nutrients to
baby just like portal vein of git.
➔Blood from mother in umbilical vein already
processed. So, it does not need much processing.
Ductus venosus→ special channel connecting
umbilical vein with Inferior vena cava.
Most of blood→ ductus venosus
Little blood→ sinusoids
➔A special type of sphincter in ductus venosus.
During delivery→ uterus contracts→ puts
pressure and squeezes placenta→ Lot of blood
comes to Ductus venosus and heat may overload.
➔As soon as its ductus venosus stretches→
sphincter contracts→ blood diverted to sinusoids
and slowly. So, heart may not overload.
➔After birth, we do not need umbilical vein. We
cut it at naval point/ umbilicus.
So, it will close→ no blood in this.
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Fibroblasts invade→ put collagen→ fibrotic
cord→ connecting umbilicus to liver. This is called
round ligament of liver or ligamentum teres.
➔Ductus venosus not needed also→ fibrotic→
ligamentum venosum
3.3 CARDINAL VEINS
➔Anterior and Posterior cardinal veins join near
sinus venosus to form Common cardinal veins.
➔Left side of cardinal system degenerates.
➔right side overdevelops and contributes to rest
of inferior vena cava.
➔Posterior cardinal system degenerates and new
cardinal system develops for lower limbs.
3 new cardinal systems develop for posterior
cardinal system. These are:
1. Supracardinal system.
2. Subcardinal system.
3. Sacrocardinal system.
3.3.1 ANTERIOR CARDINAL SYSTEM
Anastomosis between anterior cardinal veins
➔For anterior cardinal system➔ channel
develops→ moves blood from left to right side→
becomes wide→ superior vena cava.
Superior vena cava develops from
1. Right anterior cardinal vein
2. Right common cardinal vein
This anastomosis is called left brachiocephalic
vein.
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3.3.2 ANOMALY
Sometimes there is left sided superior vena cava.
This happens when right anterior cardinal vein
disintegrates and left persists. Left part of sinus
venosus remain intact. But it will drain into right
atrium via coronary sinus. Blood draining from
right to left.
3.3.3 ANOMALY
Sometimes both right and left anterior cardinal
systems do not degenerate and there are two
superior vena cavas. Right and left. No
anastomosis needed.
3.3.4 POSTERIOR CARDINAL SYSTEM
A part of IVC was developed from right vitelline
vein.
3.3.4.1 Supracardinal system
• Starts draining intercostal veins
• Thoracic duct drains into this system
• Right supracardinal vein→ connected to
superior vena cava. (Azygous vein)
• Right side→ 4 to 11th intercostals
• Left side→ 4th, 5th, 6th, 7th intercostals
• Anastomosis develops (Hemiazygous
system).
• Left supracardinal vein loses connection
with left horn of sinus venosus because it
degenerates.
• So, left drains into right supracardinal vein.
• From left supracardinal vein→
hemiazygous system.
• From right→ Azygous system
3.3.4.2 Subcardnial system
• Located on sides with kidneys
• Taking blood from renal, suprarenal and
gonads.
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• A channel connects left with right (left

renal vein shunting).
• Left side will degenerate.
• Right enlarges→ Inferior vena cava (RENAL
PART)
• Left gonadal vein→ left renal vein
• Right gonadal vein→ Inferior vena cava
directly.

3.3.4.3 Sacrocardinal system

• Receive blood from lower limbs through
right and left sacrocardinal system
• Shunt develops from left sacrocardinal to
right sacrocardinal system. This shunt→
part of left common iliac vein
• Left degenerates.
IVC develops from 3 sources
1. Hepatic part→ right vitelline vein
2. Renal part→ right subcardinal venous
system
3. Post-renal part→ From right
sacrocardinal system
Throughout body, shunts are present.
1. Left brachiocephalic vein
2. Hemiazygous system
3. Azygous system

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