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Life cycles > Exam 2: Placenta phys/TWINNING > Flashcards

Exam 2: Placenta phys/TWINNING Flashcards

1
Q

Prelacunar stage (days 6-8)

A
  • implantation of blastocyst

- differentiation of tblasts –> inner CTB, outer sCTBs

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2
Q

do CTB divide? do sCTB divide?

A

CTB= inner layer, proliferate and eventually invade adjacent maternal tissue

sCTB= outer layer, NON MITOTIC

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3
Q

lacunar trabecular stage (day 9-12)

A

implantation is complete

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4
Q

villous stage (day 13-18)

A

appearance/ development of chorionic villi in 3 stages

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5
Q

Primary Villi

A

CTB core surrounded by sCTB

develops in week 2

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6
Q

secondary villi

A

extra-embryonic mesoderm core surrounded by CTB and sCTB

develops week 3

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7
Q

tertiary villi

A
  • formation of arterio capillary network
  • core of villous (fetal) caps surrounded by CTB and sCTB
  • will become VILLOUS CHORIAN aka fetal component of placenta
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8
Q

floating villi

A
  • nut/waste xchange

- majority of placental mass

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9
Q

anchoring villi

A
  • site of invasive CTB development

- attaches to uterus, makes contact with decidua

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10
Q

CTB interstitial invasion –> CTB endovascular invasion

A

CTBs from anchoring cell column invade through decidua into inner 1/3 of myometrium –> remodel uterine spiral arteries

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11
Q

what is the purpose of CTB invasion?

A

modify arterioles to become low resistance, high flow to prevent growth restriction

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12
Q

route of O2 diffusion from mom to baby

A

maternal arterial blood in intervillous space –> sCTB layer –> CTB layer –> fetal endothelial cells of L umbillical v

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13
Q

amniotic fluid

A

= 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
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14
Q

causes of oligohydramnios?

A
  • rupture of membranes
  • congenital anomalies –> GU
  • nephrotoxic drugs –> ACEi, NSAIDs
  • poor placental perfusion
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15
Q

causes of polyhydramnios?

A
  • congenital anomalies –> NTD, esophageal atresia

- gestational diabetes

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16
Q

diffusion limited transport

A

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!
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17
Q

flow limited transport

A
  • 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
18
Q

why do we care about the types of placental transport

A

alterations lead to growth restricted fetuses

19
Q

hCG

A
  • earliest preg marker, peaks at 10weeks
  • maintain corpus lut and prog until week 8, placenta takes over
  • regulates CTB –> sCTB diff
20
Q

hPL (human placental lactogen)

A
  • produced by sCTB
  • shifts maternal metab to fatty acid so carbs are available to fetus
  • insulin resistance –> gestational diabetes
21
Q

placental growth hormone

A
  • similar to pit GH
  • control maternal IGF1
  • secretion regulated by glucose
  • **low levels in IUGR
22
Q

trophoblasts secrete _______

A

prog/est

23
Q

immune cell of the placenta

A

hofbauer cells in villous core

24
Q

what Ig does the fetus make? what Ig crosses?

A
  • makes IgM
  • IgG crosses via receptor mediated endocytosis
  • flu vax/ Tdap to mom protects baby
25
Q

maternal fetal placental unit

A
  • req for steroid hormone synthesis
  • placenta lacks P450c17, 16aOHase
  • Fetus lacks P450 aromatase and 3bOH-dh
26
Q

dizygotic vs monozygotic

A

di: 2 ova, 2 sperm; 70% of spont twins, 95% of ART
mono: 1 ovum, 1 sperm; 30% of spont twins

27
Q

dichorionic, diamniotic chorionicity

A
  • cleavage at 0-4 days
  • MONO OR DIZYGOTIC
  • separate chorionic cavities, amnion, placenta
  • 20-30% of monozygotics
28
Q

monochorionic diamniotic

A
  • cleavage at 4-8 days
  • shared chorion, sep amnions, one placenta
  • only monozygotic
  • 70%
29
Q

monochorionic, monoamniotic

A

-cleavage at 8-12 days
-shared amnion and chorion
-only monozygotic
1%

30
Q

what do we worry about with mono/mono chorionicity?

A

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
31
Q

when do we see conjoined twins?

A

monochorionic, monoamniotic morula that splits after 13 days

32
Q

how to tell chorionicity on US?

A

di/di –> thick dividing membrane, twin peak/lambda sign
mono/di –> thin dividing membrane, t sign
mono/mono –> nothing

33
Q

what do we worry about with monochorionic diamniotic twins?

A

twin-twin transfusion syndrome (TTTS)

34
Q

what are risks of twinning?

A
  • 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
35
Q

what is the average week of delivery for twins?

A

36 –> premie by definition.

36
Q

TTTS

A
  • unbalanced flow through connected vessels
  • higher rate of discordance= higher rate of mortality
  • donor death –> increased risk of brain damage to reciever
37
Q

what type of vascular connection is implicated in TTTS?

A

artery/vein –> pressure difference

-can visualize with placental injection studies

38
Q

what do you see on US with TTTS?

A

donor baby: small, reduced urine –> OLIGO

receiving baby: increases urine to reduce blood volume –> see large bladder, POLYhydro

39
Q

implications of untreated TTTS?

A
  • 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
40
Q

treatments for TTTS

A

1) reduction amniocentesis –> risk early delivery
2) microseptosomy –> create hole
3) laser ablation of anastomoses –> best survival rate

Life cycles (16 decks)

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