Placenta Flashcards
PLACENTA AND FETAL MEMBRANES
PLACENTA
FETAL MEMBRANES
CHORION
YOLK SAC
AMNION
ALLANTOIS
PLACENTA
DUAL ORIGIN -HYBRID ORGAN FROM FETUS AND MOTHER
MATERNAL PART IS FROM ENDOMETRIUM
FETAL PART IS FROM CHORION
HAS LIFE SPAN OF 9 MONTHS
GROWS AND CHANGES AND AGES DURING PREGNANCY
FETAL MEMBRANES (DO YOU KNOW WHAT THEY ARE?)
ARE DERIVED FROM ZYGOTE BUT DO NOT FORM PART OF EMBRYO
EXCEPT FOR PART OF YS AND ALLANTOIS
most actual waste is excreted through the placenta. Placenta makes hCG
FUNCTIONS
NUTRITION
EXCRETION
RESPIRATION
ENDOCRINE
INDISPENSABLE FOR PERPETUATING OUR SPECIES
TERTIARY VILLI, INTERVILLOUS SPACE, DECIDUA BASALIS ARE THE BUSINESS END OF THE PLACENTA
HOW DOES PLACENTA DEVELOP?
ANATOMY OF THE PLACENTA AND THE UMBILCIAL CORD
MATERNAL AND FETAL VIEWS OF THE HUMAN PLACENTA
thousands of chorionic villi (From fetus) make up a cotyledon. Cotyledons are separated by septae(from the mother). This is on teh maternal side of the placenta (most visible)
Mesiderm goes into the pores of the villi, which then becomes blood vessels
Examples of real human placentas
FORMATION OF VILLI – the fetal component of the placenta
CHORION =
SYNCYTIOTROPHOBLAST
CYTOTROPHOBLAST
EESOMATIC MESODERM
THESE TISSUE GIVE RISE TO CHORIONIC VILLI
MANY OF THE VILLI GO ON TO FORM THE DEFINITIVE PLACENTA
EXPLAIN FORMATION OF VILLI
PRIMARY FORM AT END OF SECOND WEEK
SECONDARY AND TERTIARY FORM DURING THIRD WEEK
VILLI INITIALLY SURROUND ENTIRE CHORION
WEEKS 2- 3 - LACUNAE, INTERVILLOUS SPACE, AND VILLI
POSITION AND DEVELOPMENT OF CHORIONIC VILLI DURING THE THIRD WEEK
LACUNAE FORM - FUSE = INTERVILLOUS SPACE
WEEKS 3
SECONDARY AND TERTIARY VILLI FORM
LACUNAE HAVE FUSED = INTERVILLOUS SPACE
MATERNAL BL VESSELS EMPTY INTO INTERVILLOUS SPACE
HEART PUMPS BLOOD THRU VILLI BY END OF 3RD WEEK
AMNION EXPANDING, FORMATION OF THE AMNIOCHORIONIC MEMBRANE, AND EMBRYO FOLDING
AMNION ENLARGES FASTER THAN CHORION - EVENTUALLY AMNION AND CHORION FUSE
FORM AMNIOCHORIONIC MEMBRANE
DECIDUAL REACTION
DECIDUALIZATION
DECIDUA CELLS
THREE REGIONS
DECIDUA BASALIS
DECIDUA CAPSULARIS
DECIDUA PARIETALIS
STROMA CELLS OF ENDOMETRIUM ARE TRANSFORMED INTO DECIDUAL CELLS
DECIDUAL CELLS = LARGE PALE CELLS
PROVIDE NUTRITION FOR EMBRYO
PROTECT UTERUS AGAINST EXTENSIVE INVASION
PRODUCE HORMONES - PROLACTIN
DECIDUALIZATION OCCURS OVER ENTIRE SURFACE OF UTERUS
BEGINS WITH IMPLANTATION - WEEK 2 AND CONTINUES THRUOUT PREGNANCY
REGIONS OF DECIDUA
EXPLAIN THE REGIONS OF THE DECIDUA
EXPLAIN FUSIONS OF AMNION AND CHORION
AMNIOCHORIONIC MEMBRANE WITH WALL OF UTERUS
EXPLAIN DISTRIBUTION OF VILLI OVER TIME
VILLI COVER ENTIRE SURFACE OF CHORION TILL WEEK 8
VILLI ASSOCIATED WITH CAPSULLARIS DEGENERATE AND FORMS SMOOTH CHORION
VILLI ASSOCIATED WITH DECIDUA BASALIS INCREASE IN # AND BRANCH - FORM VILLOUS CHORION = FETAL PART OF PLACENTA
CAN YOU FIND DECIDUAL CELLS IN THE HISTO SECTION?
Decidul cells have a lot of cytoplasm…barrier to syncitiotrophoblast
gold=decidua basalis
decidua capsularis=uterine area (dark gold)
Lacunae fuse together to form the intervillous space (mother’s blood)
Week 4
PLACENTA 13 WEEKS
12 WEEK FETUS AND PLACENTA
PLACENTAL MEMBRANE
THESE ARE XS THRU VILLI (TERTIARY) BEFORE AND AFTER WEEK 20
GO OVER CHANGES IN STRUCTURE OF PLACENTAL MEMBRANE
YOU SHOULD BE ABLE TO INTERPRETE THIS HISTO SECTION - WHAT DO THE ARROWS POINT TO?
After 20 weeks, cytotrophoblast leaves
Placental membrane keeps circulatory systems separate
Anchoring villi hold to endometrium
PLACENTAL MEMBRANE CONTINUED
PLACENTAL MEMBRANE = WHAT SEPARATES MATERNAL BLOOD FROM FETAL BLOOD
DRUGS: TOBACCO, ETOH, COCAINE -EASILY CROSS PLACENTA
1990 350,00 NEWBORNS AFFECTED BY COCAINE
IN SOME CITIES 20% OF BABIES BORN TO COCAINE USERS
BABIES ARE BORN ADDICTED
MAY ALSO HAVE INFARCTION OF CEREBRAL CORTEX AND CARDIAC MALFORMATIONS
COCAINE USERS OFTEN HAVE PRETERM LABOR
THERAPEUTIC DRUGS:
VITAMIN A (RETINOIC ACID) -ACNE - CAN CAUSE NTD AND FACIAL ABNORMALITIES
WARFARIN - ANTICOAGULANT - MENTAL RETARDATION, CNS DEFECTS
VIRUSES:
RUBELLA (GERMAN MEASLES) - CAN CAUSE CATARACTS, CARDIAC DEFECTS, DEAFNESS
CYTOMEGALOVIRUS - MICROCEPHALY, HYDROCEPHALUS
HIV - INFANTS USUALLY DIE BY 3 YEARS -
BY 2000 THERE WILL BE 10 MILLION HIV INFECTED INFANTS WORLD WIDE
A SMALL NUMBER DO NOT DIE - NOT KNOWN WHY
Chorionic somatomammotropin: fetus makes it, increases mother’s glucose levels, the glucose goes to the fetus. too much can cause chemical diabetes
Progesterone/Estrogen
after 12 weeks, the corpus luteum isnt necessary (it remains anyway)
CIRCULATION THROUGH PLACENTA
More circulation
HORMONES OF THE PLACENTA
GONADOTROPINS
HCG
CHORIONIC
SOMATOMAMMOTROPIN
STEROIDS
PROGESTERONE
ESTROGEN
HCG
GONADOTROPIN
MADE IN SYNCYTIOTROPHOBLAST
MADE EARLY AND REACHES MAX BY WEEK 8, THEN DECLINES
RESCUES CL
PL
LIKE GROWTH HORMONE
MADE IN SYNCYTIOTROPOHOBLAST
MOBILIZES MATERNAL GLUCOSE - STIMULATES GROWTH OF FETUS
PROMOTES MATERNAL BREAST DEVELOPMENT DURING PREGNANCY
PROGESTERONE
MAINTAINS LINING OF UTERUS
PREVENTS PREMATURE UTERINE CONTRACTIONS
MADE IN SYNCYTIO
ESTROGEN
HELPS DEVELOP UTERINE MUSCLE TONE
WHY DOESN’T THE MOTHER REJECT THE FETUS? -THE CRRY KNOCK OUT
CRRY = COMPLEMENT RELATED GENE Y (MICE)
In humans:
Decay accelerating factor
Membrane cofactor protein
Discovered this past January!
The complement system
antibodies attach to antigens on invading cells
this attracts a series of complement proteins
a membrane attack complex opens a hole in the membrane
water enters and the cell explodes
Complement receptor-related gene Y (CRRY) encodes protein called crry
Crry acts to prevent two complement proteins C3 and C4 from marking and attacking foreign cells so crry blocks above reaction.
They tried to KO crry in mice
They made heterozygotes but found no ko in 245 births
discovered all -/- embryos died 10 days after conception
Conclude that the absence of crry left embryo vulnerable to its mothers immune system
Wild type mice express lots of crry on trophoblast – crry here prevents attack by complement proteins
Then made knockouts lacking both crry and complement proteins.
These mice were born and normal except they were crry deficient
No complement – no danger
Complement activation must be controlled on the surface of a placenta for embryo to survive
Humans do not have crry but do have decay accelerating factor (DAF) and membrane cofactor protein (MCP)
These are now being tested to see if they play the same role in humans.
Stem Cells in The Placenta and Cord
Placenta and cord blood is a rich source of stem cells
These stem cells are multipotent - give rise to blood lineages
Can be banked for future use
Stem Cells in The Amniotic Fluid and Amnion
Both amnion and amniotic fluid are sources of stem cells
These stem cells appear to be pluripotent
Amazing finding
“A pregnancy lasts forever, because every woman who has been pregnant carries these little souvenirs (fetal cells) of the pregnancy for the rest of her life.”
Diana Bianchi
THE PLACENTAL MEMBRANE- JUST HOW LEAKY IS IT? –
Fetal cells can breach the placental membrane
Fetal cells can be found in the mother years after pregnancy- fetal cell microchimerism
First found in the 1990s by Dr. Diana Bianchi and not initially believed
Fetal cell types identified in mother include immune cells, mesenchymal stem cells, placental cells
THE BAD NEWS – MICROCHIMERISM- HAS BEEN ASSOCIATED WITH AUTOIMMUNE DISEASE
Fetal cells left over from a pregnancy can linger in mothers body for decades
If these cells are from the fetuses immune system they can attack the mothers tissue and cause diseases previously thought to be autoimmune
e.g. systemic sclerosis – thickening extends to joints arteries and internal organs (heart, kidneys, lungs etc)
aggressive forms kill within 5 years. Only 50% live 10 years after diagnosis
scleroderma – excess CT, hard skin, taut skin can restrict movement
Cells with Y chromosomes have been found in skin lesions of patients with these diseases. Are rare in patients without disease.
Cause may be due to retention of fetal cells by mom. These cells may secrete cytokines that activate the immune system. Arise from fetal stem cells that cross over to mothers circulation then mature.
Could revolutionized therapy for patients.
Benefits of fetal microchimerism
There is evidence that fetal cells can populate various organs of the mother’s body
They are sometimes found in high number in diseased organs (not autoimmune disease) where they may be repairing damaged tissue
They have been found in mouse models in the brains of females after birth where they increase in number over time!
Has lead to the hypothesis that fetal stem cells may help mother repair organs and battle disease
Fetal cells may remain in the mother for decades after birth.
It is thought that these are a type of stem cell that can replenish itself over long time intervals
Some data suggest that these fetal “stem cells” may be beneficial to the mother
Two-way traffic- Mothers cells can also go into fetus = Maternal microchimerism
Mothers cells enter fetal circulation and can remain for years
At least one autoimmune disease has been linked to maternal cells in the fetus
Dermatomyositis (inflamed muscle) – mothers cells found in the muscle
2012 2/3 of mothers aged 37-59 had traces of male Y chromosome in their brains.
Mothers cells found in offspring but les frequent (25-35% of offspring carry mothers cells.
Mothers brains had part of Y chromosome – did qPCR on autopsied brains found Y chromosome gene in 63% of females
Placental leakiness and prenatal diagnosis
Fetal cells/proteins that leak into maternal blood can be used in prenatal diagnosis
About 1000 fetal cells per quart of mothers blood vs 10 million maternal cells in same volume
However there is a lot of fetal DNA in mothers blood and this can be studied by sequencing. Can be isolated and analyzed.
Emerging market for Downs syndrome and other trisomies e.g. Harmony Prenatal Test – introduced in US in 2011
Not yet as versatile as amniocentesis
Fetal proteins in mothers blood can also be monitored – for hCG, PAPP-A (pregnancy-associated plasma protein A) , alpha fetoprotein.
Differences in methylation can be used to distinguish fetal and maternal DNA in blood of mother. Fetal DNA can then be sequenced.
hCG – can be used to see if pregnancy established and if there is trophoblastic disease such as hydatidiform mole
PAPP-A if low may indicate Down’s syndrome
AFP – open neural tube defects
Nuchal translucency – measured early in pregnancy – nuchal fold measured later – relates to thickness of soft tissues in nape of the neck. Down syndrome fetuses tend to have more fluid in nape of neck.
ABRUPTIO PLACENTA
OFTEN SEEN IN WOMEN WHO SMOKE
Part of placenta becomes necrotic. generally because tha portion is disconnected from the uterus.
Fragile X-mental retardation gene
CGG repeats if there are less than 40, you’re okay. more than 200, the individual has fragile x syndrome. More visible in males than females
ABNORMALITIES OF THE PLACENTA
Placenta previa occurs in about 1 in 200 pregnancies
More common in women who smoke, use cocaine or are over 35
Placenta Accreta
difficult to deliver-deep implantation of placenta. placenta percereta is even deeper
The Umbilical Cord
UMBILICAL CORD STRUCTURE
Whorton’s jelly is largely hyaluronic acid. provides support for blood vessels
prolapse~.5% deliveries. cord in front of fetus
UNUSUAL INSERTIONS OF THE CORD
VELEMENTOUS INSERTION:
IF BLASTOCYST IMPLANTS SIDEWAYS OR UPSIDE DOWN
CORD RUN THRU FETAL MEMBRANES TO PLACENTA
CAN LEAD TO TEARING OF CORD VESSELS
UNUSUAL INSERTIONS OF THE CORD continued
ABNORMALITIES OF THE CORD
KNOTS
BATTLEDORE
SINGLE UMBILICAL ARTERY
PROLAPSE
CORD = 1-2 CM IN DIAMETER; 50-55 CM LONG
KNOTS : MAY BE TRUE OR FALSE
TRUE ABOUT 1 % OF DELIVERIES
LONG CORDS LIKELY TO CAUSE KNOTTING
CAN KILL FETUS IF KNOW BECOMES TIGHT
TORSION = TWISTING OF CORD
BATTLEDORE:
CORE INSERTS AT ONE EDGE OF PLACENTA INSTEAD OF NEAR CENTER
MORE EASILY RUPTURED DURING DELIVERY
1 ARTERY
1% OF ALL CORDS
15-20% OF THESE BABIES HAVE CARDIAC DEFECTS
PROLAPSED: 0.5% F ALL DELIVERIES
AT DELIVERY CORD PROTRUDES THRU CERVIX AHEAD OF FETUS
IF IT BECOMES COMPRESSED O2 WILL BE CUT OFF FROM FETUs
