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Transcript
Yeasting Nov. 11, 2009; Development of Trilaminar Disc
Implantation- in growth of trophoblast into endometrium.
Endometrium alters and is known as deciduas; maternal BVs empty into intervillous space,
which were originally lacunae; these coalesced and became larger, leaving synctitiotrophoblast
suspended/hanging from fetal aspect of developing placenta to the maternal aspect of
developing placenta.
Cytotrophoblasts grow into these areas of synctiotrophoblasts, extraembryonic mesoderm
grows in a BVs develop within this (embryonic fetal cardiovascular system) (see figure 4.17 &
4.16—longitudinal section through a villus)
anchoring villi- when synctitiotrophoblasts are reinforced, anchor from fetal aspect to
maternal; side branches develop from this as free villi—these do not bridge entire distance btw
fetal aspect and maternal aspect (does not attach to maternal aspect); bridging villi hold things
together
Fig. 4.15 primary villi (cytotrophoblast growing into synctitiotrophoblastic elements) , secondary villi—
when extraembryonic mesoderm grew in, tertiary villi (embryonic/fetal BVs developing in villi)
We can tell that above picture of chorionic villus is a free villus bc we see fetal aspect but not the
maternal surface; there are many BVs in here which is important for increasing the surface area for
transmission diffusion from maternal blood to fetal blood and vise versa.
Early on in pregnancy—(first half); placental barrier consists of fetal endothelial cells, extraembryonic
mesoderm, cytotrophoblasts, synctitiotrophoblast. Diffusing back and forth- diffuse long distance and
through several different cell layers (this occurs at early pregnancy); early on this is ok bc embryo is
small and doesn’t need as much nutrients or waste products ridding; Early pregnancy is indicated by
completed cytotrophoblastic layer
Mid pregnancy—cytotrophoblasts drop away and run out; fetal BVs move to the sides of the villi and
come in contact with syncytiotrophoblast through respective basal laminae (diffusion barrier has been
reduced, very thin layer for diffusion to pass through); this is good bc the fetus is getting large at this
point so we need more oxygen and nutrients to pass through readily and fetus needs to get rid of waste
prdocucts (back diffusion) to get into maternal blood (this occurs before circulation happens)
Components of maternal blood—has nutrients (good) and toxins (bad ) which can easily diffuse through
the membrane; embryo/fetus gives up fetal waste which diffuses from high conc in fetal blood into low
conc of maternal blood (fetal waste products then go with maternal blood and are eliminated either
through maternal lungs as CO2 or nitrogenous wastes eliminated through the maternal kidneys)
Immunoglobulins from mom to fetus can make it through and do not react to fetus, but give fetus some
passive immunity so that when fetus is born it has some immunity to what mom has been exposed to.
More harmful immunoglobulins and bacteria normally do not make it through membrane to fetus (so
fetus is sequestered/hidden from maternal immune system)
Tears in placenta- (occasionally this occurs) fetal blood is released in intervillus space; (fetal cells then
circulate and are no longer hidden; fetus cells in mom’s body) mom might have immune response if
have diff types of blood (different RH factors btw mom and child); maternal antibodies move across the
placental membrane and begin to destroy fetus’ red cells.
Other cells that migrate from fetal circulation into maternal circulation: ex. Fetal cells from
male child can migrate to mom’s thyroid; male cells are found within thyroid bc thyroid is a
vascular area and cells like it mom may have thyroid problems due to the immune response
to these migrated cells.
Trophoblast grows larger and larger, expands and grows into uterine lumen into Decidua capsilaris
eventually it outgrows it’s blood supply; villi growing toward uterine cavity will decrease in size and
degenerate as they lose a blood supply (thus these original villi are lost and smooth chorion remain)
2 portions of chorion (outer membrane)1) Villus portion= placenta
2) Smooth chorion (outer layer of extraembryonic membrane; this has lost it’s original villi)
VIlli develop where there is a rich oxygen supply; where there is less O2, villi do not develop; start out
with thin placenta, as villi get larger and more villi are formed, this takes up space; as this occurs, villi
push further into underlying deciduas—syncio and cytotrophoblasts are pushed farther into deciduas.
And areas without high growth are left in btw—cotelydons develop (these develop because of rich O2
supply by maternal vessels cause villus growth; in areas where there is not a lot of blood supply, partial
septa develop in btw these go up toward the chorionic plate); fuzziness in coteyldon is due to the villi
that have broken in; fetal BVs lie within the villus
Tertiary villus has fetal BVs
Early pregnancy indicated by complete trophoblastic layer; cyto and syncitio
Red cells can only come in contact with here (in above pic) are either maternal endothelial cells or
syncitiotrophoblasts; syncitiotrophoblasts and cytotrophoblasts will grow down around the ends of the
open vessels to form a cap to prevent leakage.
Maternal blood comes in, shoots all the way through the chorionic plate through the villi and then
perculates back down across villi and then out through maternal veins
Fig 4.18 stem villi extended from chorionic plate; figure 3.2
Maternal aspect of placenta—see cotyledons; break cotelydon open and see numerous fetal BVs lying
within the villus; fetal aspect—see villi; chorionic tissues can develop well without the presence of a
fetus (this is not a good thing if there is not a fetus there)
Proof that all of this really does occur!
When conceptus is invading in, it invades into glands which are good nutrient sources for developing
fetus; maternal BVs are just under here and it will eventually invade into those too; initially there are villi
that develop all around the conceptus; later on some of those villi will be lost; outer portion of
extraembryonic membrane becomes known as the chorion this part will become stretched as
conceptus enlarges which will decrease profusion; decidual capsilaris degenerates and chorion loses it
villi which had originally developed. Villus chorion will become the placenta; placenta is always
examined at the time of birth to make sure that the maternal aspect is intact and all the maternal
placenta tissue has moved out of maternal body; this is important because chorionic tissues can develop
well without fetus; if placental elements are retained, these may continue to develop and function and
this is not a good thing.
What occurs inside trophoblast:
Extraembryonic coelom= chorionic cavity (cavity outside the embryonic proper; has fluid inside of it);
hanging in chorionic cavity is the:
1) embryonic disc, 2) the amnion and the cavity that the amnion surrounds which is fluid filled;
and the 3) umbilical vesicle (empty bubble, aka yolk sac; there is a primary and
secondary/definitive yolk sac; there is actually no yolk in humans hence the name has been
changed) also hangs within chorionic cavity, develops on other side of embryonic disc from
the amnion. (see pic on page 1)
Connecting stalk- largely extraembryonic mesoderm and some intraembryonic mesoderm
(mesenchyme); connects intercell mass to the chorion
Allantois diverticulum of yolk sac; vessels that supply this become umbilical vessels; when “shrink
wrapped” by amnion it is known as umbilical chord
See figure 2.10 and 3.1
Inner cell mass/embryoblast develops into 2 layers: 1) epiblast 2) hypoblast (hence we have a 2 layer
disc) this is occurring during the 2nd week of development.
Within the epiblast, a small cavity develops which becomes the amnionic cavity. Original
epiblastic cells start separating bc of formation of epiblastic cavity into an epiblast proper
(remains in same location) and amnioblasts (have moved out).
Hypoblastic cells- on inferior aspect of epiblast; these stick into the original blastocyst cavity
and with time the amnionic cavity enlarges, hypoblastic cells have proliferated and are growing
down into inside of trophoblastic cells, forming an exoceolomic membrane (another layer now
covers the original blastocele; 2 layers now exist—exocoelomic membrane of hypoblastic origin
and trophoblastic cells). Hypoblastic cells migrate down on inside or trophoblasts and
proliferate externally and this population of cells forms cellular layer of tissue known as
extraembryonic mesoderm (has a lot of extracellular space, cells are stellate and have
processes; fills space btw trophoblast and extracoelomic membrane and space btw trophoblasts
and amnioblasts)  grows into villi as they form to form secondary stage of villus formation
(see figure 3.4); extraembryonic mesoderm completely surrounds the embryo proper/bilaminar
discs and the 2 vesicles (amnion and primary yolk sac) forming within this.
Everything in extraembryonic mesoderm will divide, except…the one place where extraembryonic
mesoderm does not divide will become the connecting stalk.
At same time as extraembryonic mesoderm spits, another generation of cells grow out of embryonic
disc, making a new lining for the upper portion of the primary yolk sac.
What was a large space is now changing into 2 smaller spaces (hour-glass shaped, somewhat);
endodermal cells coming out of the embryo proper push hypoblasts aside; one space will
ultimately be lined with endoderm and other small space will be pinched off (2ndary yolk sac
becomes related to embryonic disc and remnant sac will be lost). What was primary yolk sac is
now dividing into secondary yolk sac and remnant. Thus, a cavity is created inside chorion
(chorionic cavity) in which bilaminar embryo surrounded by amnionic cavity and yolk sac are
susepended into;
Trophoblastic structures (chorion ) is growing rapidly at this point and claiming space. Later on it
will reduce it’s growth rate, then amnion and embryo will grow to fill this cavity.
BVs develop within extraembryonic mesoderm related to chorion and within the connecting
stalk and embryo proper. 3 major sets of vessels:
1) placental vessels
2) umbilical vessels (within what will become umbilical cord, derived from allantoids)
3) intraembryonic vessels.
As embryo grows , it changes from a disc to a modified cylindar. Amnion enlarges; amnion is initially
attached to the edge of the amnionic disc; edge of amnion disc becomes the circumference of umbilical
chord (naval). Embryo pulls the amnion around as it changes from a disc to a modified cylinder; it’s still
attached to edge of disc which is the circumference of the umbilicus.
This will put the cylindrical embryo into the amnionic cavity; amnion will then grow rapidly, it will
“shrink wrap” around the connective stalk bc this is also at the umbilicus. The 2ndary yolk sac sticks out
through the umbilicus. As amnion increases in size it grows from the umbilicus down along the
connective stalk wrapping together the connective stalk tissue and its contained BVs and a portion of
the definitive yolk sac (2ndary yolk sac) creating the umbilical cord!!
As amnion increases in size and amnionic cavity increases in size, chorionic cavity decreases in size.
Amnionic cavity creates the fluid filled space that the little one develops in.
Ultimately the chorionic cavity and amnionic cavity fuse and the chorionic cavity
(extraembryonic coelom) is eliminated; outer surface of the amnion (extraembryonic
mesoderm) fuses with the inner aspect of the chorion (extraembryonic mesoderm) and they
come together IF YOU WILL. Decidua parietalis gets stretched and is eliminated so that smooth
chorion ultimately comes in contact with the decidua parietalis and fuses. When placenta and
other extraembryonic membranes are delivered at the time of partuition, placenta comes out
and a layer of deciduas. Chorion and amnion fused together and come out and a layer of
decidua related to this amnionic-chorionic membrane.
Allantois-(along with chorion and amnion, another extraembryonic membrane)
outgrowth of yolk sac; grows into the connective stalk; in animals who develop in shells (reptiles
and birds), the allantois is a reservoir for waste products; in humans this will become part of
the urinary bladder. BVs that supply the allantois become the vessels that develop within the
connective stalk (become the umbilical vessels) connect intraembryonic circulation to
placental circulation.
When there is enough amnionic fluid- This can be sampled to tell the health of the little one (look at cell
composition; cells from the amnionic fluid can be used for genetic testing (trophoblastic cells can also be
use for this from biopsies of placenta or abdominal wall or even through the vagina/cervical canal to
biops tissues there); placental tissue (extraembryonic tissue) have the same genetic makeup as the little
one. Ultra sound is used to know that you are not sticking the little one.
Implantation Problemsif there is a hold up (delay) in the conceptus, it implants in the uterine tube. When ZP
dissolves(at about 5 days after fertilization) the conceptus will implant there (wherever it is, normally
this is the uterine cavity, but if delayed it is the uterine tube). Uterine tube does not have the ability to
expand like the uterine cavity (uterine tube is well vascularized). Uterine tube till rupture (vasculature
will be torn open; fatal to little one; life threatening to mom);
can also implant in isthmas portion of uterine tube (slightly further along)- uterus cannot expand
as well here either so will rupture here also.
Conceptus can also implant on other tissues such as the stomach; lt implants on BVs here. (fetus
can be born from this and other extrauterine tissues; problem arises at time of birth/partuition; can get
little one out through c-section but getting the placenta out is the problem; it should not be left in (bc it
has such a big blood supply!) In uterus, blood supply to placenta is pinched off during uterine
contraction so with partuition uterus gets smaller and BVs passing through here to the placenta are
pinched off and there is partuition hemmorage
@12 days post fertilization; synctitiotrophoblasts gets nutrients from endometrial glands and then into
maternal BVs (small ones first); see fig 3.4;
Conceptus releases early pregnancy factors as it moves through uterine tube.
Synctitiotrophoblast releases gonadotrophins (“feeding gonads”), (hCG), which comes from the
chorion gets into maternal circulation and circulates throughout the body; this stimulates the CL
(which would normally diminish at this time) to continue to be maintained and enlarge; thus
progesterone is still produced which maintains endometrium/decidua. This occurs for about 3
months. After this point, synctitiotrophoblasts produce enough placental estrogen and
progesterone and other hormones to maintain pregrancy. If syncytiotrophoblasts do not
produce hCG at this time (during first 3 months), sloughing will occur which allows normal
menstruation to occur and little one is lost 
TRILAMINAR DISC:
Day 13—(fig 3.7)- there is a bilaminar disc; fluid filled cavities surround it; before circulation has been
established. Cut edge of amnion apprears to edge of disc, which is somewhat oval in shape; there is a
proliferation of cells within the embryoblast;
Around Day 18 a streak/mound eventually forms (“primitive streak”) (see figure 4.2); will become the
caudal end of the embryo (away from the head);
Cells will migrate away from the primitive streak and drop down deeper into the epiblastic layer and
migrate in btw here and hypoblast creating a new layer of cells (mesoderm). During migration, point
where they take off deepens and is called the “primitive goove” (as they migrate away this depression is
created). The cranial end will become a pit-like area (deepening) of the primitive groove known as the
“primitive node”; there is not a uniform widening (as embryo disc gets wider, it adds predominately to
the caudal end, rather than the cranial end); tissue migrates away but mainly adds to caudal end
(locally).
Above is day 16 embyro; to the right is the cranial portion of the embryonic disc
3 areas where regular mesoderm does not go: 1) buccopharyngeal membrane (=oropharyngeal
membrane); 2) cloacal membrane; 3) notochord (in midline btw oropharyngeal membrane and primitive
node) (has same origin of mesoderm but has special properties therefore not considered mesoderm,
notochord is controller)
Oropharyngeal membrane (buccopharyngeal membrane)- (relating to mouth and pharynx; beginning of
digestive tract) temporary membrane which forms the area of fusion of ectoderm and endoderm (non
mesoderm in btw; thirs layer of cells does not migrate into this area), lies at cranial end
Cloacal membrane- at the tail end (cloaca) of the membrane (sewer end of digestive tract); no
mesoderm goes in btw here also
Prechordal plate (=prochordal cells)- group of early migrating epiblastic cells that localize immediately
caudal to the oropharyngeal membrane; organizing center for the head area
Prenotochordal cells- epiblastic cells that drop down into what will become the mesodermal area (btw
epiblast and hypoblast) and take up residency there
Notochordal process- (prechordal cells are added to, to become this); usually depicted as a hollow rod
(cylinder) of cells; was originally solid cells and tube developed within it (notochordal canal).
Mesenchymal cells that have ingressed through the streak and aquire mesodermal cell fate which then
go onto migrate cranially from the primitive node and pit forming this median cellular chord
Notochordal plate-(notochordal process opens up and flattens out to form this) ventral aspect of
notochordal process opens up inferiorly blends with adjacent endoderm, flattens out and now becomes
this. Arises once notochordal process elongates and the primitive pit extends from this to form
notochordal canal (cellular tube which extends cranially from primitive node to prechordal plate); floor
of notochordal process fuses with underlying embryonic mesoderm; these fused layers undergo
degeneration and notochordal canal can communicate with umbilical vesicle; floor of notochordal canal
disappears remains of notochordal process forms a flattened grooved notochordal plate
Neurenteric canal- ventral aspect of notochordal process breaks up and becomes open to the yolk sac;
sides of cylinder are now continuous with endoderm on top of yolk sac; this is a temporary
opening/communication between yolk sac cavity and amnionic cavity; if this persists in some
individuals it becomes a fistula between tissue around spinal cord and lumen of digestive tract.
Notochord- when notochordal plate rises back up again to form a solid rod of cells (not a cylinder
despite pic) it is known as the notochord; it is a very important controlling structure; organizes through
induction and inhibition the tissue surround it to determine the fates of the cells surrounding this
structure (helps develop a lot of axial structures). A cellular rod-like structure; extends from
oropharyngeal membrane to primitive node; it will degenerate as the bodies of the vertebrae form;
small portions persist forming the nucleus pulposus of each intervertebral disc.
See fig 4.3, figure 4.12
Summary: epiblastic cells dropping down to the underlying hypoblastic layer; some cells take up
residency here (become endoderm), others stay in area btw (become mesoderm) ; others will migrate
through the primitive groove. 3 areas where mesoderm does not go: oropharyngeal membrane, cloacal
membrane, notochord.
There is a new layer of cells that replace hypoblastic cells= “intraembryonic endoderm”; these push
hypoblastic cells aside; early on the migration of these cells is haphazard, then it becomes more
organized and majority of migration takes place through primitive streak/primitive groove area.
Epiblastic cells become known as ectoderm, mesodermal cells, and then endodermal cells!
Mesoderm:
3 major areas of organization: 1) para-axial (closests to the notochord; “next to axis”) gives rise
to somites 2) intermediate area- lateral to para-axial; gives rise to urinary and reproductive
systems 3) lateral plate mesoderms-most lateral of the mesoderm areas; gives rise to body wall
structures, CT, gut (digestive tract), internal organs
Migration of cells is not willy nilly (see fig 4.11)- migrate into these 3 areas of mesoderm (can have
deficits in some areas and not other areas)
Lateral plate mesoderm this will cleft; forms areas of enlarged intracellular or extracellular spaces
which eventually coalesce forming the body cavities (“intraembryonic coelom”). Before this para-axial
and intermed develop.
Para-axial-- Somites develop give rise to axial skeleton, skull, vertebral bodies, and muscles related to
these areas, nervous system, also muscles of limb muscles and body wall (see fig 4-9)
Lateral plate mesoderm forms a coelom that is intraembryonic;
divided into 2 regions by coelom:
1) somatic mesoderm- overlying ectoderm which contributes to body wall and soma,
skeletal muscle, bone, cartilage
2) visceral/splanchnic mesoderm- yolk sac; gives rise to CT or muscle related to central
organs, glands
Combining terms:
Somatopleure= somatic mesoderm + ectoderm
Splanchnopleure= visceral mesoderm + endoderm
Notochord controls tissue development around it. Epiblastic cells dorsal to notochordal structure will
be transformed/maintained and become neural tissue. Neural tissue forms a groove as it folds, groove
deepens, ultimately comes together and neural tissue breaks free and becomes central portion of
nervous system. Ectoderm comes together and is fused to form epidermis
Neural crest tissue= Specialized tissue developing btw regular ectoderm and neural tissue; was at crest
of neural fold; this will break free and is free to migrate and develop into whatever it wants to do (fig
5.3)
Primitive streak/groove should turn off it’s proliferation- if not, a sacro-coccuygeal teratoma may arise
**New individual is of epiblastic origin!! Bc this replaces hypoblast (moves them aside) to become
endoderm, or forms mesoderm; hypoblast contributes to extraembryonic structures.
Ectodermsurface ectoderm: epidermis; gives rise to epidermal structures (skin, nails, hair, glands)
Endodermgives rise to epithelium of digestive tract and organs of digestive tract (lungs, liver,
pancreas, urinary system, etc.)
Mesodermfills in everything in btw!
Neural crest (ectodermal origin) ganglia, sensory neurons, medulla of supernal glands, a lot of CT
cells within head and neck; neural ectoderm becomes central portion of nervous system
Folding process of the embryo:
-Embryo starts as a disc (intraembryonic coelom within it), growth processes related to
development of the nervous system are accentuated, occurring rapidly
-disc eventually folds so that it folds over its margins; center area grows more rapidly than
peripherally (so it will rise up and overflow)
-a head and tail fold will develop and lateral body folds develop at the same time.
-Becomes a modified cylinder. Portion of 2ndary yolk sac is taken up into cylinder becoming
precursor of digestive tract beginning at the oropharyngeal membrane and ending at the
cloacal membrane