embryology- content from slides and book Flashcards
what are primordial germ cells (PGCs)? what are they derived from? where do they migrate?
the earliest cells that will eventually become eggs or sperm (give rise to gametes)
- derived from epiblast during gastrulation and migrate to the wall of the yolk sac in the 4th week and then to the indifferent gonad at the end of the 5th week
clinical correlation: teratomas UQ
type of tumor that contains various tissues like bone, hair, muscle, gut epithelia
- origin is disputed but some evidence suggests that these arise from PGCs straying from their normal migration path
- another origin could be pluripotent stem cells
when is DNA replicated during the cell cycle?
during interphase, or the S phase
- during this time, chromosomes are long and cannot be recognized by a light microscope
what process produces gametes?
gametogenesis
oogenesis in females and spermatogenesis in males
what is a major characteristic of meiosis I?
pairing of homologous chromosomes
number of chromosomes and amount of DNA in a gamete
23 chromosomes, 1N
sister chromatid vs chromosome
sister chromatid = duplicated version of the chromosome
analogy: you photocopy a piece of paper (chromosome) and staple it to the original. the 2 papers together are sister chromatids
- once you remove the staple and separate them, they are now individual papers (chromosomes) again!
structure of a duplicated chromosome
2 sister chromatids attached to a single centromere
- formed during the process of meiosis when DNA replication of each chromosome occurs
cell potency + 3 types (pluripotent, totipotent, & multipotent)
cell potency: cell’s ability to differentiate into other cell types
- more cell types it can differentiate into = greater the potency
totipotent: most powerful type, can become any cell in the body AND extra embryonic structures (like placenta)
- ex. zygote (fertilized egg) up to 1st few divisions
pluripotent: cells can become any cell in the body but NOT extra embryonic structures
- ex. embryonic stem cells
multipotent: more limited, can become only CERTAIN types of cells within a specific tissue
- ex. bone marrow stem cells can make different types of blood cells but not muscle or nerve cells
stem cell therapy
uses stem cells to treat or prevent a disease or condition
- as of 2024, the only FDA approved therapy is hematopoietic stem cell transplantation
- bone marrow
- peripheral blood stem cell
on the slides, not sure if need to know
what is induction and how does it lead to organ formation?
induction: diversification occurs in response to cues and interactions by means of chemical signals, interactants, etc.
- one group of cells causes another group of cells to change their fate
cell signaling is essential for induction
terminology:
- prenatal period
- gestational & fertilization age
- neonate
- embryonic & fetal period
- prenatal period: period before birth
- gestational age: calculated from the first day of menstrual cycle
- fertilization age: calculated from the time of fertilization
- neonate: baby aged one month or less
- embryonic period: extends from fertilization unto 8 weeks (56 days)
- fetal period: extends from 9th week up to birth
cell signaling: juxtacrine signaling + 3 types
unlike paracrine signaling, juxtacrine signaling requires direct cell-to-cell contact
three types:
Notch Signaling: protein on one cell binds to a receptor on an adjacent cell to send signals
Extracellular Matrix Signaling: cells attach to proteins like laminin (in the basal lamina) to receive signals
Gap Junctions: special channels directly connect two cells, allowing signals to pass.
primary vs secondary oocyte & mature ovum
primary oocyte: immature egg cell that has started meiosis I but is paused at the diplotene stage of prophase I
- remains in this stage from before birth until puberty
- at puberty, each menstrual cycle, a few primary oocytes resume meiosis I but only one completes it per cycle.
secondary oocyte: primary oocyte becomes secondary oocyte once it completes meiosis I
But DOES NOT finish meiosis II immediately—it pauses again, this time in metaphase II.
- will only complete meiosis II IF fertilized by a sperm.
mature ovum: if sperm fertilizes secondary oocyte, finishes meiosis II to become a mature ovum (fully developed egg ready to combine with sperm)
- if no fertilization = secondary oocyte dies and is lost during menstruation
explain the whole process of release of an oocyte (primordial, primary follicle, Graafian follicle, atretic, granulosa cells, theca cells, zone pellucida)
primordial follicle: what is stimulated to become a primary follicle (remain in diplotene stage of prophase until puberty)
primary follicle: follicle in the ovary that has a single layer of cuboidal granulosa cells surrounding an oocyte (at puberty)
- FSH stimulates 15-20 primary-stage (prenatal) follicles to grow
- one of these follicles fully matures into Graafian follicle (which releases its oocyte during ovulation)
- cells starts to form a layer of granulosa cells (surround primary oocyte & nourish it, also produce estrogen) - Theca folliculi: layer of cells outside the granulosa cells, help make hormones (androstenedione) that granulosa convert into estrogen
- . the other follicles degenerate and become atretic = basically follicle dies & nutrients are reabsorbed by the body
- the degenerate is replaced by connective tissue forming a corpus atreticum - granulosa cells continue to divide and form multiple layers around the oocyte, and a glycoprotein layer called zona pellucida develops b/w oocyte & granulosa cells
granulosa cells proliferation is mediated by what
growth differentiation factor 9
from book
what 3 things happen directly as a result of the estrogen production from the granulosa cells?
- uterine endometrium enters the follicular or proliferative phase
- thinning of cervical mucus occurs to allow passage of sperm
- anterior lobe of pituitary gland is stimulated to secrete LH
at the middle of the ovarian (menstrual) cycle, there is an LH surge that results in 3 things:
- elevates conc. of maturation-promoting factor (MPF), causing oocytes to complete meiosis I and initiate meiosis II (tells egg to finally continue developing, while it was paused in meiosis I)
- stimulates production of progesterone by granulosa and theca cells (lutenization- helps prepare uterus for possible pregnancy)
- causes follicular rupture and ovulation - LH surge makes follicle burst open, releasing the mature egg
hormones/organs that act on the ovarian cycle to start UQ- ovarian cycle
gonadotropin-releasing hormone *GnRH) produced by hypothalamus → acts on cells of anterior lobe of pituitary gland to secrete gonadotropins (FSH & LH) → stimulate and control cyclic changes in the ovary
what major events occur in the second week of development? UQ
- trophoblast differentiates into inner (cytotrophoblast) and outer layer (syncytiotrophoblast)
- primitive uteroplacental circulation begins through the lacunar network
- inner cell mass (embryo blast) differentiates into epiblast and hypoblast = forms bilaminar disc
- amniotic and yolk sac cavities form
- extra embryonic mesoderm splits into somatic and splanchnic layers
why is the second week of development called the “week” of two’s?
- trophoblast differentiates into 2 layers: cytotrophoblast and synciotrophoblast
- embryo blast forms 2 layers: epiblast and hypoblast
- extra embryonic mesoderm splits into 2 layers: somatic & splanchnic layers
- 2 cavities form: amniotic and yolk sac cavities
when does implantation occur and because of which cells?
implantation occurs at the end of the first week and by the help of penetrating trophoblast cells
list the 3 phases of fertilization
UQ
- penetration of corona radiata
- penetration of zona pellucida
- fusion of the oocyte and sperm cell membranes
what are 4 functions of the syncytiotrophoblast?
syncytiotrophoblast: outer multinucleate layer of trophoblast that:
- secretes hCG - hCG maintains corpus luteum, which produces progesterone to sustain pregnancy
- facilitates implantation: helps blastocyst invade uterine wall by breaking down maternal tissues
- forms early placenta: contributes to formation of placenta, allowing nutrient and gas exchange b/w mother & embryo
- suppresses maternal immune response
how does a woman’s immune system change to accommodate pregnancy?
not entirely understood but seems to be a shift from cell mediated immunity to humoral (antibody-mediated) immunity
- also places pregnant women at increased risk for certain infections, such as influenza
- cell-mediated conditions also show improvement in women though
abnormal implantations of the blastocyst + what symptoms look like UQ
- implantation in the internal os (closer to the cervix) = placenta previa → severe, even life threatening bleeding in second part of pregnancy and even delivery
- implantation outside of uterus = ectopic pregnancy → mostly in the ampulla (upper part of fallopian tube), but can also be in the abdominal (common location = pouch of Douglas) → can result in severe hemorrhaging (blastocyst usually dies)
hyadtidiform mole (aka molar pregnancy) UQ
mass of tissue grows in the uterus instead of normal embryo
happens when sperm fertilizes an egg missing a uterus
- moles secrete high levels of hCG and can produce benign or malignant (invasive mole, choriocarcinoma) tumors later if pieces are left behind during abortion or intrauterine termination
microdeletion on chromosome 15 of mother vs father causes what? UQ
on paternal gene = Prader-Willi syndrome (hypotonia, intellectual disability, hypogonadism, and obesity)
on maternal gene = Angelmann syndrome (seizures, little to no speech, constant laughter, severe intellectual disability)
gastrulation forms what and what do they form? imp UQ
gastrulation forms the 3 primary germ layers from the epiblast involving movement of cells through the primitive streak to form endoderm and mesoderm
ectoderm: forms skin, central nervous system, hair, nails, teeth
mesoderm: middle germ layer, forms blood vessels, bone, connective tissue, kidneys, reproductive organs
endoderm: innermost germ layer, forms the gut and its derivatives, lungs, liver, pancreas
sacrococcygeal teratomas UQ
tumors that arise in the embryo during gastrulation when the primitive streak doesnt properly diminish (tissues are derived from all 3 germ layers)
- can also arise from primordial germ cells that fail to migrate to the gonadal ridge
most common tumor in newborns
role of serotonin (5-HT) in laterality
activates transcription factor MAD3 that restricts NODAL to the left side
disrupting 5-HT can result in: situs invertus, heterotaxy, dextrocardia, & other heart defects
pregnant mothers should not take SSRIs (selective serotonin uptake inhibitors) which are antidepressants = birth defects in laterality of child
primitive streak, primitive node, primitive pit (3rd week of development) UQ
primitive streak: groove that appears on surface of embryonic disc, marking start of gastrulation
- cells migrate through this streak to form the 3 germ layers
primitive node: small circular structure at the front of the primitive streak
- controls movement of cells during gastrulation
primitive pit: small depression in the center of the primitive node
- cells move through this pit to form the notochord (which helps form the spine)
FGF8 (fibroblast growth factor 8)
protein (growth factor) that controls cell movement during gastrulation
- made by the primitive streak itself
works by down regulating E-cadherin (protein that normally binds epiblast cells together) - makes them loose so they move inward
prechordal plate (3rd week)
thickened area of cells in between the cranial end of notochord and the oropharyngeal membrane
- some of the firsts to pass through primitive streak and are important for forebrain induction using SONIC hedgehog as signaling molecule
oropharyngeal membrane & cloacal membrane (3rd week)
oropharyngeal membrane: that big circle on the right side (cephalic/cranial end)
- marks the future mouth
cloacal membrane: similar to oropharyngeal membrane but on the caudal end
- will form the anus
prenotochordal cells, notochordal plate, definitive notochord, neurenteric canal (3rd week) UQ
prenotochordal cells: special cells that come from primitive node and move through the primitive pit, moving forward towards the head of the embryo
- they help form the notochord
notochordal plate: once prenotochordal cells reach their destination, flatten out and become notochordal plate
- plate is temporary and will fold into the definitive notochord (sort of like a blueprint)
definitive notochord: notochordal plate forms into a tube, forming this
- notochord is a stiff rod that acts as signaling center for inducing the axial skeleton (neural plate, motor region of brain and spinal cord, & sclerotome portion of somites)
- major signal molecule for these phenomena is SONIC hedgehog (SSH)
neurenteric canal: temporary tunnel that connects amniotic cavity (outside embryo) with the yolk sac (inside embryo)
- this canal closes once notochord is complete
allantois (allantoenteric diverticulum)
small outpouch from the yolk sac that extends into connecting stalk
- seems to have no purpose in humans but may be involved in abnormalities of bladder development
the 3 body axes that are established in the third week of development
- **anterior posterior (A-P; craniocaudal)
- dorsal-ventral (D-V)
- left-right (L-R)
establishment of the cranial-caudal (A-P) axis (head to tail)
anterior visceral endoderm (AVE): plays key role in setting up this axis by transcription factors (OTX 2, LIM1, HESX1) and secreting factors (cerebrus, lefty 1 - both members of TGF- B) → inhibit NODAL → contribute to head development in the cranial end
- nodal not in the caudal end* → allows NODAL expression to continue → primitive streak maintained
establishment of the dorsal-ventral (D-V) axis (back to belly)
Nodal not in caudal end → streak established so NODAL then upregulates a bunch of genes that form dorsal & central mesoderm and head and tail structures
Bone morphogenetic protein 4 (BMP4): spreads throughout embryonic disc, pushing cells towards ventral (belly) fates
- causes mesoderm to ventralize to form intermediate mesoderm (kidneys) and lateral plate mesoderm (blood and body wall)
node acts as organizer, blocking BMP4 in the dorsal (back) side using chordin, noggin, and follistatin so all of the mesoderm isn’t ventralized
GOOSECOID regulates these inhibitors, ensuring proper head and back development
HNF-4B (beta)
maintains the node and later induces regional specificity of the forebrain and midbrain areas
- No HNF-4B → embryos dont gastrulate properly → lack forebrain and midbrain structures
BRACHYURY
gene that is essential for cell migration through primitive streak → regulates dorsal mesoderm formation in middle & caudal regions of embryo
- if missing, lower body doesn’t develop properly - “spine builder”
formation of the left-right axis
for left: FGF8: secreted by node and primitive streak cells → induces expression of NODAL → serotonin (5-HT) restricts expression of NODAl to the left side
genes that prevent NODAL from crossing to the right: SONIC HEDGEHOG, LEFTY1, ZIC3
for right: not as well understood, but SNAIL transcription factor is restricted to the right lateral plate mesoderm & most likely regulates development of the right side
- cilia on cells in node create a gradient of NODAL to left or by gap junctions
situs invertus, heterotaxy, situs ambiguus UQ
Situs inversus → Complete mirror image of normal organ positions (e.g., heart on the right)
Heterotaxy → Some organs are on the wrong side, while others are normal.
Situs ambiguus → Unclear organ placement, leading to congenital heart issues.
fate maps during gastrulation
fate map: like blueprint of embryo that shows which areas will develop into specific tissues & organs
cells migrating through the cranial-most part of the node → form the notochord
- those migrating more posteriorly → form paraxial mesoderm (somites and somi-mesodermtomeres)
- those migrating through the next portion of the streak → form intermediate mesoderm (urogenital membrane system)
- those migrating through more caudal regions
of the streak → form lateral plate mesoderm (body wall)
- those migrating through the caudalmost part of the streak → formation of extraembryonic
membrane mesoderm (chorion)
basically saying in to out
fate of the primitive streak
forms mesoderm until 4th week → then diminishes in size and remains in sacrococcygeal region
disappears by end of 4th week
caudal dysgenesis UQ
insufficient mesoderm in the caudal region → fusion of lower limbs, vertebral anomalies, missing or malformed kidneys and genitals
-diabetes in the mother increases this risk
holoprosencephaly UQ
brain fails to divide properly → eyes are close together, forebrain is small, structures in anterior midline are deficient
can be caused by high doses of alcohol during the gastrulation phase (which is only 4 weeks so mother might not even know she’s pregnant by then
primary, secondary, and tertiary villi UQ
- Primary Villi (Day 11-13): consist of cytotrophoblast cells covered by syncytiotrophoblast cells, look like small protrusions extending from the chorionic plate into the maternal tissue
-
Secondary Villi (Day 16-17): extraembryonic mesoderm invade the primary villi, making them thicker.
- prepares the villi for blood vessel development -
Tertiary Villi (By End of 3rd Week)- also called definitive placental villus: blood vessels form inside the mesodermal core, connecting to the fetal circulation.
- villi are now fully functional, allowing nutrient and oxygen exchange between mother and fetus.
anchoring vs free villi
anchoring villi: attach chorionic plate to the maternal tissue (decidua basalis)
- provide structural support for the placenta
free (floating) villi: extend into the maternal blood but do not attach to the uterus
- increase surface area for nutrient and gas exchange
outer cytotrophoblast shell
layer of cytotrophoblast cells that forms barrier b/w fetus and maternal tissue
- anchors placenta to the uterus
- prevents excessive invasion of fetal cells into the mother’s uterus
what is the main event that occurs during the 3rd-8th weeks (aka embryonic period)?
organogenesis: each of the 3 germ layers (ectoderm, mesoderm, endoderm) give rise to organs
- main organs have been established by the end of this period
when do the majority of birth defects occur?
during the embryonic period (3rd-8th week)
- before that, any abnormalities are aborted by the body, also mother dont know at that time that they’re pregnant so they dont take care to avoid things they wouldn’t normally
which germ layer does neurulation occur from? UQ
occurs entirely from the ectoderm specifically from the neuroectoderm (specialized part of the ectoderm that forms the neural plate
what is neurulation? UQ
process where the neural tube forms → later develops into the brain & spinal cord
key parts:
1. neural plate formation: notochord from beneath (in the mesoderm layer) induces the upper ectoderm layer to differentiate and form the neural plate (aka neuroectoderm)
- lengthening of neural tube which eventually form the neural groove (ends are folded in, creating a groove in the center)
- neural tube formation: edges of the groove come together & fuse → this tube becomes the brain and spinal cord
what germ layer is the notochord present in? UQ- notochord
the mesoderm
what happens to the notochord later? UQ- notochord
disappears but leaves behind nucleus pulpous in adults (soft center of intervertebral discs in the spine)
important for MCQs
parts of the neural tube that close + when they close (imp) and what happens if they dont?
anterior neuropore: upper opening of the neural tube (hole at the top)
- closes at day 25
posterior neuropore: lower opening of the neural tube (hole at the bottom)
- closes at day 28
if not close properly → leads to neural tube defects (NTDs)
neuralation is complete once these 2 structures close
in making the neuroectoderm (neural plate) what genes are down regulated and which are unregulated?
inhibited: BMP4 (these levels have to be low wherever the neural plate is being formed, otherwise no neural plate will form)
unregulated: FGF (fibroblast growth factor), noggin, chordin, and follistatin
which 2 proteins are important in neurulation to induce caudal neural plate structures (hindbrain and spinal cord)?
WNT3a and retinoic acid (RA)
- the caudal region doesn’t have any notochord present underneath it so it’s not doing anything like the cephalic region is = so these proteins cause it to make structures for the spinal cord
what are neural crest cells (NCCs) and what are their derivatives? - UQ
very badmash cells that just leave the neural tube after it closes and go to other parts of the body
- also called fourth germ layer b.c of how many different structures in the body they contribute to
- move in 2 directions:
1. dorsal pathway → leave through dermis where they go form melanocytes in the skin and hair follicles (melanin)
- ventral pathway → through anterior half of each somite to become sensory ganglia, sympathetic and enteric neurons, schwann cells, cells of adrenal medulla (inner part of kidney)
also migrate from cranial neural folds → contribute to craniofacial skeleton, neurons for cranial ganglia, glial cells
4 derivatives of the ectodermal layer - v. imp
- central nervous system
- peripheral nervous system
- sensory epithelium of ear, nose, and eye
- epidermis (including hair and nails)
also glands:
1. subcutaneous glands
2. mammary glands
3. pituitary gland
4. enamel of the teeth
basically all the structures that maintain contact with the outside world
some of the derivatives of NCCs (neural crest cells)
- schwann cells
- sensory cells
- adrenal medulla cells
- bone & cartilage of the face
- parts of the skill
- melanocytes
clinical correlates: anencephaly and spina bifida + how to avoid UQ
both are neural tube defects if neural tube doesn’t close properly
anencephaly: failure of closure at cranial end (top hole) → absence of brain and skull
- fatal and has no treatment → not compatible with life
spina bifida: failure of neural tube closure at the caudal end (bottom hole) → defects in the spinal cord and vertebrae
- is compatible with life, but depending on severity, different amounts of neurological functions are lost
to avoid: 400 micrograms of folic acid daily beginning 3 months prior to conception continuing throughout pregnancy
- higher (4000 micrograms) for women who have a previous kid with neural tube defects
what 3 structures is the ectoderm giving rise to and how are they formed based on BMP levels?
3 main structures:
1. epidermis (skin)
2. neural tube (CNS- brain & spinal cord)
3. neural crest cells (NCCs - which migrate and form structures)
High BMP → epidermis (skin) created
Intermediate BMP → neural crest cells (NCCs)
Low BMP → neural plate (neuroectoderm formed)
How PAX3, WNT, FGF, SNAIL, and FOXD3 Regulate NCC Formation
intermediate conc. of BMP + FGF & WNT → induce PAX3 → expressed at neural plate border (where NCCs form) → these transcription factors induce SNAIL & FOXD3 (specify cells as neural crest) & SLUG (promotes crest cell migration from the neuroectoderm)
what do VANGL genes do
regulate convergent extension (process that lengthens the neural tube and is necessary for normal closure to occur)
what do somatic and splanchnic mean as words?
somatic → “related to the body wall”
splanchnic → “related to internal organs”
what are the name of the 3 layers that the mesoderm divides into during the embryonic period (3-8 weeks)?
- paraxial mesoderm plate
- lateral plate
- intermediate mesoderm layer
mesoderm derivative: paraxial mesoderm UQ
- the cells close to the midline start to proliferate (right next to the notochord- and they get bigger)
give rise to somites which further differentiate into: sclerotome, myotome, dermatome
somites + what they give rise to + neuromeres UQ
made from paraxial mesoderm
differentiate into:
Sclerotome → Vertebrae & ribs
Myotome → Muscles
Dermatome → Skin of the back
neuromeres: cephalic end somites combine with neuroectoderm to form neuromeres (which form the head- prominent in the hindbrain)
where do the first pair of somites come from and how are the number of somites used?
they come from the occipital region and they can help determine the fetal age by counting the number of somites
mesoderm derivatives: lateral plate mesoderm + 2 divisions and what they form UQ
the outermost of mesoderm (all the way at the ends)
- cavities form in the lateral plate to divide it into 2:
somatic (parietal) mesoderm: covers the amniotic sac
- forms the body wall (bones, connective tissue, muscles of limbs), and dermis of the skin in the body wall
splanchnic (visceral) mesoderm: covers the yolk sac
- forms the gut wall and coverings of the internal organs (heart, blood, vessels etc.)
mesoderm derivative: intermediate mesoderm
lies in between the paraxial mesoderm and the lateral plate mesoderm
forms the urogenital structures (urinary and reproductive systems)
in the cervical and upper parts → nephrotomes (temporary, segmented early kidney structures that mostly disappear later in development)
in the more caudal region → nephrogenic cord (continuous structure that forms the actual kidneys)
mesothelial membranes & serous membranes (serosa)
Mesothelial Membranes: thin layers of specialized epithelial cells (mesothelial cells) that cover internal body cavities and organs, originate from mesoderm
- reduce friction by secreting a lubricating fluid
Serous Membranes (Serosa): thin, double-layered membranes that line closed body cavities and cover organs inside them
Vasculogenesis vs. Angiogenesis
both are involved formation of blood vessels, but happen at different stages and in different ways
Vasculogenesis: formation of new blood vessels from scratch during early embryonic development
- happens only during embryonic development
Angiogenesis: growth of new blood vessels from pre-existing ones
- happens throughout life, especially in wound healing, tissue repair, and cancer growth.
Involves sprouting, branching, and remodeling of blood vessels
hemangioblasts
precursor cells
found in blood islands that arise from mesoderm cells in the yolk sac during early development
give rise to hematopoietic stem cells that form blood cells
clinical correlates: capillary hemangiomas
benign tumor of capillaries that is caused by abnormal growth of endothelial cells (which line blood vessels)
appear red or purple, raised or flat, and commonly associated with craniofacial structures
endoderm derivaties UQ
forms the gastrointestinal tract
endoderm gives rise to (straight from book):
- epithelial lining of the respiratory tract
- parenchyma of the thyroid, parathyroids, liver, and pancreas
- reticular storm of the tonsils and the thymus
- epithelial lining of urinary bladder
preeclampsia UQ
happens when mother develops high blood pressure and signs of organ damage, usually affecting kidneys and liver
- leading cause of maternal deaths in the US
can lead to ecplampsia (seizures) if untreated
in regards to the villuses, where is the maternal and fetal blood present?
maternal is in the intervillous space (derived from lacunae)
fetal is in the villi always
only exchange, never intermingling between the 2 bloods in normal, healthy pregnancies
- exchange happens at the branches b/w mom and baby
the 3 classifications of decidua based on their locations UQ
decidua: modified uterine lining (endometrium) that plays role in supporting embryo and forming placenta
decidua basalis: located beneath implanted embryo, directly interacts with chorionic villi, helping form placenta
touches the mother
decidua capsularis: located on the outer side of the embryo, opposite the decidua basalis
- covers the embryo but disappears as the pregnancy progresses (fuses with decidua parietalis)
decidua parietalis: rest of endometrium that is not directly involved with the embryo
- ventually fuses with the decidua capsularis, eliminating the uterine cavity
smooth & bushy chorion
chorion: outer fetal membrane that forms part of the placenta and helps protect and nourish the developing embryo
Smooth Chorion (Laeve): part of chorion that does not form the placenta
- villi have degenerated here thats why its smooth
- located on opposite side of placenta
Bushy Chorion (Frondosum): part of chorion that contributes to placenta, contains numerous chorionic villi that helping exchange between mother and fetus
* located near decidua basalia*
**Chorionic Plate → The fetal part of the placenta where fetal blood vessels develop.
chorionic plate
- fetal side of the placenta
- forms the roof of the intervillous space, where maternal blood flows
- contains fetal blood vessels that connect to the umbilical cord.
amniochorionic membrane
formed when amniotic cavity (amnion) and chorion (outer fetal membrane) fuse together
- what ruptures when “water breaks”
functions:
- protects the fetus against infections and external trauma
- maintains the amniotic fluid
- breaks during labor
order of how oxygenated blood gets to the fetus
chorionic veins → umbilical veins → fetus
arteries and veins in fetus
opposite
arteries carry deoxygenated blood to the fetus (AWAY from the mother)
and veins carry oxygenated blood to the fetus
primitive umbilical ring imp
`primitive umbilical ring: opening in the early embryo where important structures pass to and from the fetus
allows passage of:
Umbilical vessels (bring oxygen and nutrients).
Vitelline duct (connects to the yolk sac, disappears by week 6-7).
Allantois (helps with waste removal, later forms the urachus).
4 functions of the placenta
- Exchange of gases
- Exchange of nutrients and electrolytes
- Transmission of maternal antibodies
- Hormone production
clinical correlates: hydraminos/polyhydraminos & oligohydraminos
UQ
hydraminos/polyhydraminos: excess of amniotic fluid [1500-2000 ml]
- causes: idiopathic (unknown), maternal diabetes, congenital malformations that prevent fetus from drinking the water
oligohydraminos: decreased amount of amniotic fluid [<400 ml]
- may result from renal agenesis
- can result in lung hypoplasia bc not enough space for the fetus to “breathe”
2 processes that sperm (spermatozoa) need to undergo before they can fertilize
capacitation & acrosome reaction
acrosome reaction UQ
occurs after binding to the zona pellucida
- induced by zona proteins
- culminates in release of enzymes need to penetrate the zona pellucida including acrosin and trypsin like substances
amnion
large sac containing amniotic fluid in whic fetus is suspended by its umbilical cord
functions:
- absorbs jolt
- allows fetal movements
- prevents adherence of embryo to the amnion
parts of umbilical cord
2 umbilical arteries, 1 umbilical vein, and wharton jelly that acts as protective cushion for the vessels
diff b/w dizygotic vs monozygotic twins + conjoined twins UQ
monozygotic: 2 amnions, 1 chorion, and 1 placenta
dizygotic: have 2 of each
conjoined twins: fetuses are not entirely split- 1 amnion, 1 chorion, and 1 placenta
What characterizes pre-eclampsia?
Pre-eclampsia is characterized by maternal hypertension and proteinuria (protein in urine), potentially leading to severe complications during pregnancy.
what is the purpose of placental lactogen (somatomammotropin)?
Placental lactogen prioritizes maternal blood glucose for the fetus and promotes mammary gland development for lactation.
What is considered low birth weight?
Low birth weight is defined as a weight of less than 2500 grams at birth, regardless of gestational age.
What is the significance of primary ossification centers in fetal development?
Primary ossification centers appear in almost all long bones and the skull by the 12th week, indicating bone development.
What is the amniochorionic membrane?
The amniochorionic membrane is formed by the fusion of the amnion and chorion and ruptures during childbirth, commonly referred to as the “water breaking”.
What is a physiological umbilical hernia?
occurs when intestinal loops protrude through the umbilical ring during normal gut development
abdominal wall is damaged and you can see the skin poking out
What is the vanishing twin phenomenon?
death of one fetus in a multiple pregnancy, often due to unequal blood supply
What is the appearance of the fetus’s skin towards the end of pregnancy?
Towards the end of pregnancy, the fetus’s skin is covered with vernix caseosa, which protects and moisturizes the skin.
What is endovascular invasion in placentation?
penetration of cytotrophoblasts into maternal spiral arteries to remodel them for increased blood flow
