Placenta and Fetal Membrane Flashcards

1
Q

Placenta Week 3-4

A

o Trophoblast has differentiated into cytotrophoblast and syncytiotrophoblast cells
o Tertiary villi formed by cytotrophoblasts, syncytiotrophoblasts, and extraembryonic mesoderm which are enmesched and anchored into chorionic plate
o Tertiary villi formation = functioning extraembryonic vascular system
o Boundaries of placenta = chorionic plate and outer cytotrophoblastic shell
o Trophoblastic lacunae = intervillus space once arteries and veins form within

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2
Q

Chorion Structure Week 5-18

A

 Chorion frondosum (bushy chorion) – functional portion of chorion
• Majority overlies the embryonic pole of the conceptus
 Chorion leave – overlies the abembryonic pole of conceptus
• Eventually breaks down and loses tertiary villi and becomes smooth muscle

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3
Q

Maturation of Chorion Frondrosum Week 5-18

A

 4th month – placenta has 2 components (fetal and maternal)
• Fetal portion – composed primarily of chorion frondosum
• Maternal portion – composed primarily of decidua basalis
 Spiral arteries supply oxygen and nutrient rich maternal blood to intervillous space
 Endometrial veins – remove waste and deoxygenated blood
 Syncytiotrophoblast, cytotrophoblast cells, extraembryonic mesoderm, AND endothelial cells lining capillaries separate fetal and maternal blood
 Initial blood supply & vessels for embryo supplied by mesoderm of secondary yolk sac
 Week 18 – fetal blood flow through placenta is 500ml/min

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4
Q

Uterus Changes Week 5-18

A

 Decidua basalis – portion of decidua overlying and associating with chorion frondosum
• Cells are abundant in lipids and glycogen
• Decidua septa – 3rd month – decidua basalis grows in between intervillus spaces
o Cotyledons – compartments formed by septums
 Decidua Capsularis – portion of deciduas overlying the abembryonic pole
• 2nd month – tertiary villi expanding into deciduas capsularis disappear
• Disappears as embryo grows, leaving only the chorion laeve
• 3rd month – chorion laeve fuses with opposite wall of uterus

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5
Q

Placenta Functions

A

transport
barrier
hormones

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6
Q

Placenta Transport

A

 Gas Exchange: O2, CO2, CO
 Water, glucose, vitamins
 Steroid hormones
• hCG – feeds back on ovary to produce progesterone; keeps uterus from shedding
• stress (corticosteroids) hormones
 Electrolytes
 Maternal Antibodies – fetus does not make own antibodies until after birth
• Pinocytosis by syncytiotrophoblasts take up IgG
• Set up PASSIVE immunity against diphtheria, smallpox, measles
o NOT against: chickenpox or whooping cough
 Drugs and their metabolites
 Waste products
 Some infectious agents

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7
Q

Placenta Barrier

A

– molecular weight cutoff ~100,000 daltons
 Placental barrier blocks most viruses and all bacteria
 Cancer cells CAN penetrate the placenta but it is not common

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8
Q

Placenta Hormones

A

 hCG – by syncytiotrophoblasts
 PLGF
 Indoleamine 2,3 deoxygenase (IDO) - destroys tryptophans on maternal T cells rendering them inactive as they approach the placenta; makes maternal immune system unable to trigger response against developing placenta
 Somatomammotropin – decreases mother’s sensitivity to insulin so that more glucose will be in blood; gives fetus priority of maternal blood glucose; can cause mother to become temporary diabetic

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9
Q

Amnion/Amniotic Fluid/Amniocentesis

A

o Comprised of epithelial cells few layers thick
o Inner most fetal membrane
o Amniotic Fluid
 Derived from diffusion of water from maternal blood through the intervillus space
 Composed of electrolytes, proteins, lipids, carbs, and desquamated fetal epithelial cells
 Entire volume replaced every 3 hours
• Week 10 = 30mls, Week 20 = 350mls, 37 Weeks = 1000mls
 Function – cushion embryo from impacts; maintains consistent temperature; barrier to infections; provides consistent environment to fetus
• Bathes external areas inside embryo such as GI tract and lungs  without amniotic fluid the GI tract and lungs will be underdeveloped
o Amniocentesis – done after 13 weeks to test for genetic abnormalities and levels of fetal proteins

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10
Q

Umbilical Chord + Diagnostics

A

o Derived from growth of extraembryonic mesoderm at posterior end of bilaminar disc
o Connecting Stalk – formed by extraembryonic mesoderm; primary structure of umbilical chord
 Week 5 – connecting stalk contains: allantois, 2 arteries, 1 vein, vitelline duct
o Week 8 – amniotic membrane – surrounds entire structure and creates primitive umbilical cord
 Excess intestinal endoderm enters umbilical cord creating temporary umbilical hernia
o Week 10 – vitelline duct and allantois have been degraded leaving only the umbilical blood vessels and Jelly of Wharton (proteoglycan substance that cushions the blood vessels)
o Meckels diverticulum- intestines from umbilical hernia do not retreat back into embryo fully
o Color Doppler Ultrasonogram – measures blood flow direction and resistance

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11
Q

Vasculogenesis vs. Angiogenesis

A

 Angiogenesis – branching of blood vessels from existing blood vessels
 Vasculogenesis – formation of blood vessels de novo

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12
Q

Vasculogenesis

A

o Occurs first in secondary yolk sac around week 2-3
o Also occurs later within the embryo around week 4 when mesoderm cells cluster due to low O2
 Cell in periphery will express fibroblast growth factor (FGFR) and will remain fibroblasts and become endothelial cells
 Cells in middle that see less oxygen express VEGF (Flk1 and Flt1) and PLGF
• Cells expressing Flk1 will become hemangioblasts and then mature RBCs
• Cells expressing Flt1 will become endothelial cells and form vessel wall
 Controlled by specific molecular switches
• VEGF genes A-D + 5 isoforms, FGF, Tie-2, PDGF, TGFbeta

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13
Q

Dizygotic Twins

A

– fraternal; 2/3rds of twins; 8 per 1000 births; increases with maternal age
 2 eggs released by ovary that are each fertilized by a separate sperm
• No more related than any other siblings
 Usually develop 2 completely separate placentas, chorions, and amnions
 Occasionally chorions will fuse; can lead to erythrocyte mosaicism (mixture of genetically different RBCs)

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14
Q

Monozygotic Twins

A

– maternal – 3-4 per 1000 births
 1 egg fertilized by single sperm
 3 Different Arrangements of Fetal Membranes
• Embryo splits prior to blastocyst formation  completely separate compartments
• Epiblast (inner cell mass) splits  shared placenta and chorion sac BUT separate amniotic sacs
• Embryo splits at gastrula stage (or neurula stage)  shared placenta, chorion sac, and amniotic sac
 Siamese twins – result from late stage splitting  neurula stage or later

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15
Q

Rh Incompatability

A

 IF fetus is + & mother is –  any fetal RBC that may leak into maternal blood will elicit antibody response in mother  maternal antibodies against fetal antigens return to fetus and breakdown fetal RBCs  erythroblastosis fetalis or hemolytic disease newborn
• May lead to intrauterine death
• Spectrophotometric analysis of amniotic fluid can be used to indicate severity
• Fetal mortality not as prevalent as past due to RH immunoglobulin given to at risk mother; Rh IgG binds to and removes Rh antibodies from maternal blood

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16
Q

Umbilical Cord Abnormalities

A

 Chord can wrap around neck causing difficulties at birth
 False knots can cause decreased blood flow
• Can cause cardiac and vascular defects if it goes on long enough

17
Q

Amniotic Banding

A

 Occasional tears in amniotic membrane can allow extremities/face to become constricted by the amniotic membrane; may result in amputation or craniofacial deformities

18
Q

Amniotic Fluid Abnormalities

A

 Hydramnios or Polyhydramnios – results from excess amniotic fluid
• Can cause maternal diabetes, anencephaly (improper skull formation), GI defects
 Oligohydramnios – results from decreased amount of amniotic fluids
• Can cause severe deformities of lungs and GI tract

19
Q

Placenta accreda + placenta percreta

A

o Placenta accreda – lack of decisua basalis

o Placenta percreta = chorionic villi penetrate myometrium

20
Q

Pre-Eclampsia Characteristics, Risk Factors, Effects on Mother and Fetus

A

o Caused by shallow implantation and occurs in 5% of all pregnancies
o 20% of all serious birth complication
o Risk factors: 1st pregnancy, overweight, IVF with donor egg, genetic predisposition
o Problems to Mother (mostly seen in 3rd trimester)
 Hypertension (very serious)
 Proteinuria
 Liver inflammation
 Edema
 Clot-plugging platelets
 Can progress to eclampsia  maternal brain swells convulsions and coma
o Problems to Fetus: premature birth

21
Q

Pre-Eclampsia Mechanism and Treatment

A

 Flt-1 (VEGF receptor) on endothelial cells responsible for blood vessel growth
• sFlt-1 – found circulating in blood
 PLGF – produced by placenta and binds to Flt-1 to enhance blood vessel growth during pregnancy (especially during 3rd trimester)
o Pre-Eclamptic Women have high sFLt-1 levels and low PLGF
 sFlt-1 hijacks PLGF leading to deterioration of existing blood vessels and inhibition of new one in placenta and other organs
o TREATMENT: flood mother with PLGF hormone