Exam 2: Placenta phys/TWINNING Flashcards
Prelacunar stage (days 6-8)
- implantation of blastocyst
- differentiation of tblasts –> inner CTB, outer sCTBs
do CTB divide? do sCTB divide?
CTB= inner layer, proliferate and eventually invade adjacent maternal tissue
sCTB= outer layer, NON MITOTIC
lacunar trabecular stage (day 9-12)
implantation is complete
villous stage (day 13-18)
appearance/ development of chorionic villi in 3 stages
Primary Villi
CTB core surrounded by sCTB
develops in week 2
secondary villi
extra-embryonic mesoderm core surrounded by CTB and sCTB
develops week 3
tertiary villi
- formation of arterio capillary network
- core of villous (fetal) caps surrounded by CTB and sCTB
- will become VILLOUS CHORIAN aka fetal component of placenta
floating villi
- nut/waste xchange
- majority of placental mass
anchoring villi
- site of invasive CTB development
- attaches to uterus, makes contact with decidua
CTB interstitial invasion –> CTB endovascular invasion
CTBs from anchoring cell column invade through decidua into inner 1/3 of myometrium –> remodel uterine spiral arteries
what is the purpose of CTB invasion?
modify arterioles to become low resistance, high flow to prevent growth restriction
route of O2 diffusion from mom to baby
maternal arterial blood in intervillous space –> sCTB layer –> CTB layer –> fetal endothelial cells of L umbillical v
amniotic fluid
= ultrafiltrate of maternal plasma + fetal urine + fetal lung secretions
- 250ml at 16weeks to 1L at 32weeks, decreases from there
- critical for lung development and MSK fx
causes of oligohydramnios?
- rupture of membranes
- congenital anomalies –> GU
- nephrotoxic drugs –> ACEi, NSAIDs
- poor placental perfusion
causes of polyhydramnios?
- congenital anomalies –> NTD, esophageal atresia
- gestational diabetes
diffusion limited transport
substances that cross placenta via diffusion cross SLOWLY
- RLS is characteristics of sCTB layer
- O2, CO2, H2O
- damage to sCTB can affect O2 to fetus!
flow limited transport
- dependent on plasma concentration and rate of blood flow
- can be altered by decreased uterin bf –> dec placental perfusion –> decreased transport
- ex: pregnany woman with aortic stenosis
why do we care about the types of placental transport
alterations lead to growth restricted fetuses
hCG
- earliest preg marker, peaks at 10weeks
- maintain corpus lut and prog until week 8, placenta takes over
- regulates CTB –> sCTB diff
hPL (human placental lactogen)
- produced by sCTB
- shifts maternal metab to fatty acid so carbs are available to fetus
- insulin resistance –> gestational diabetes
placental growth hormone
- similar to pit GH
- control maternal IGF1
- secretion regulated by glucose
- **low levels in IUGR
trophoblasts secrete _______
prog/est
immune cell of the placenta
hofbauer cells in villous core
what Ig does the fetus make? what Ig crosses?
- makes IgM
- IgG crosses via receptor mediated endocytosis
- flu vax/ Tdap to mom protects baby
maternal fetal placental unit
- req for steroid hormone synthesis
- placenta lacks P450c17, 16aOHase
- Fetus lacks P450 aromatase and 3bOH-dh
dizygotic vs monozygotic
di: 2 ova, 2 sperm; 70% of spont twins, 95% of ART
mono: 1 ovum, 1 sperm; 30% of spont twins
dichorionic, diamniotic chorionicity
- cleavage at 0-4 days
- MONO OR DIZYGOTIC
- separate chorionic cavities, amnion, placenta
- 20-30% of monozygotics
monochorionic diamniotic
- cleavage at 4-8 days
- shared chorion, sep amnions, one placenta
- only monozygotic
- 70%
monochorionic, monoamniotic
-cleavage at 8-12 days
-shared amnion and chorion
-only monozygotic
1%
what do we worry about with mono/mono chorionicity?
cord entanglement
- risk of mortality increase for BOTH babies
- can’t do much but admit mom to hospital and monitor fetal HR in case need to deliver emergently
when do we see conjoined twins?
monochorionic, monoamniotic morula that splits after 13 days
how to tell chorionicity on US?
di/di –> thick dividing membrane, twin peak/lambda sign
mono/di –> thin dividing membrane, t sign
mono/mono –> nothing
what do we worry about with monochorionic diamniotic twins?
twin-twin transfusion syndrome (TTTS)
what are risks of twinning?
- increase miscarriage in early preg
- increased hyperemesis (from inc bhCG)
- premies
- anueploidy
- prenatal screening is less sensitive, more difficult
- gestational diabetes (inc hPL)
- preeclampsia
- PPH
what is the average week of delivery for twins?
36 –> premie by definition.
TTTS
- unbalanced flow through connected vessels
- higher rate of discordance= higher rate of mortality
- donor death –> increased risk of brain damage to reciever
what type of vascular connection is implicated in TTTS?
artery/vein –> pressure difference
-can visualize with placental injection studies
what do you see on US with TTTS?
donor baby: small, reduced urine –> OLIGO
receiving baby: increases urine to reduce blood volume –> see large bladder, POLYhydro
implications of untreated TTTS?
- mortality of one twin 80-90%
- donor –> small placental vol, not enough nutrients to support fetal growth
- recipient –> polyhyd, early delivery, fetal hydrops due to diffuse edema
treatments for TTTS
1) reduction amniocentesis –> risk early delivery
2) microseptosomy –> create hole
3) laser ablation of anastomoses –> best survival rate
