L17 - Placenta & Intra-Uterine Growth Restriction, Abnormal Fetal Development Flashcards

1
Q

zygote to blastomere: what are there steps

what happens at day4-5

day 6-7?

days 16+?

A

zygote, 2 cell, 4 stage 8, then morula after 72 hours then blastocyte after 4 days

days 4-5
bastocyte is when there is a cavity. blastocyte thins out and becomes trophoblast – start of placenta
rest of cells move up and become INNER CELL MASS - creates EMBRYONIC POLE
blastocyte then reaches uterine lumen, ready for implantation

day 6-7 inner cell mass becomes epiblast and hypoblast.
Epiblast forms embryo
Amniotic cavity develops within epiblast mass

days 16+?
3 layers forms from bilaminar disc - gastrulation
– primitive streak initiate
– epiblast –> ectoderm
– hypoblast –> replaced by epiblast cells, become endoderm
– epiblast –> mesoderm

THEN EMBRYO FOLDS

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2
Q

how does the placenta form

A

syncytiotrophoblast invades decidua
cytotrophoblast erodes maternal spiral arteies and veins
spaces between (lacunae) fill up with maternal blood
this is followed by mesoderm that develops into fetal vessels
this aids transfer nutrients of O2 across simple cellular barrier

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3
Q

what is the difference between cytotrophoblast cells and synctiotrophoblast cells

A
CTB
undifferentiated
they invade maternal blood and destroy epithelium
they give rise to STB
reduce in no as pregnancy goes on

STB
they are fully differentiated
are in direct contact with maternal blood
they produce placental hormones

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4
Q

how does the placenta act as an endocrine organ

A

HCG

    • human chorionic gonadotrophin
    • maintains corpus luteum in pregnancy
    • progesterone and oestrogen

HPL

    • human placental lactogen
    • growth, lactation
    • carb and lipods

also more

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5
Q

what is the placental barrier like

what goes across this barrier

A

maternal blood in the lacunae is in direct contact with syncytiotrophoblasts

there is just a monolayer of STB, CTB and fetal capillary epithelium separating fetal and maternal blood

as pregnancy advances, barrier thins leas to greater surface area for exchange

  • -gases (o2 co2)
  • -water electrolytes
  • -steroid hormones
  • -proteins poor - pnly via pinocytosis
  • -transfer of maternal
  • -antbodies IgG starts at 12 weeks – mainly after 34 weeks SO premature infants LACK protection
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6
Q

Parts of the decidua

A

decidua capsularis: overlay embryo and chorionic cavity

decidua parietalis: side uterus not occuped by embryo

decidua basalis: between uterine wall and chorionic villae

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7
Q

Vasa praevia
what is it
how is it diagnosed
how is it managed

how is this different to placenta praevia

A

fetal vessels within umbilical cord pass over internal os. when this dilates in labour the vessels are stretched and exposed – can rupture, massive fetal blood loss and death

with ultrasound using colour dopplers

m - delivery by c section when fetus is 34 readings

PLACENTA PRAEVIA
–massive, painless bleeding, fetal and meternal death

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8
Q

what happens if the trophoblast fails to invade the maternal circulation at 12 and 18 weeks?

A

poor maternal and fetal mixing of blood,
lack od o2 and nutrients to fetus,
leads to fetal growth restriction
pre-eclampsia (raised BP)

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9
Q

what are the different types of placenta accreta

what is the consequence of this

A

normal, acceta, increta, percreta

Placenta cannot seperate, stays within uterus. uterus cannot contract down, massive bleeding - hysterectomy is req

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10
Q

PLACENTAL ABRUPTION

what is it like and what can happen as csq

A

massive bleeding in preg - often concealed.
separation of placenta during pregnancy.

extremely painful
fetal death
maternal death

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11
Q

how can the placenta differ in multiple pregnancies (from what to what)

A

morula cleavage
dichorionic / diamniotic

blastoyte cleavage
monochorionic / diamniotic

implanted blastocyte
monochorionic / monoamniotic

formed embryonic disc
conjoined twins

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12
Q

what are the two types of growth problems for fetuses

A

SGA
small for gestational age
– less than 5th centile
– normal variant or growth restricted

IUGR
Intra-uterine growth restriction
–less than 5th centile
– growth restricted: failure to achieve growth potential

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13
Q

Fetal growth restiction

what can happen as a result of this

A
Fetal growth restriction 
Deficient placental invasion 
Reduced placental reserve 
Fetal need exceeds supply 
IUGR 
Hypoxia 
Fetal vascular redistribution 
Oliguria 
Abnormal CTG 
Fetal death
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14
Q

diagnosis of fetal growth restriction

A
    • looks smaller
    • clincial measurement of uterine size: symphysis - fundal height SFH

SFH - weeks +/- cms

also ultrasound scan

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15
Q

symmetrical vs asymmetrical growth restriction?

whar are causes of early fetal growth restriction for BOTH of these

A

SYMMETRICAL
BPD - biparietal diameter of head and abdominal circumference are all reduced
CAUSES: chromosoma anomaly (T21), viral (rubella, CMV), severe placental insufficiency OR normal small baby

in asymmetrical ONLY abdominal circum is reduced
CAUSES– abdominal circum reflects size of fetal liver.
PLACENTAL INSUFFICIENCY - no xs glycogen being deposited within the liver

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16
Q

what are consequences of hypoxia in the fetus

A

Consequences of hypoxia in the fetus
‘ Blood flow (oxygen and nutrients) redirected to areas
of greater importance
‘ Brain
‘ Blood flow (oxygen and nutrients) redirected away
from areas of lesser importance

’ Gut (doesn’t eat!)
‘ Kidneys (placenta clears waste products)
‘ Lungs (placenta brings 02)

17
Q

what are ultrasound findings in IUGR

clinical features of IUGR

A

small AC - small liver
decr amniotic fluid - prod by kidneys
incr blood flow to the brain
— middle cerebral arteries in doppler effect scan
——- blood glow maintained during both systole and diastole, incr blood flow. remains high

clinical:

  • -SFH smaller
  • -baby’s movements lessen to conserve energy
  • -fetal HR changes as hypoxia develops - seen on CTG
  • -fetal death
18
Q

what are the factors to consider when waiting or delivering a baby with IUGR

A

WAIT
low chance of survival
to give steroids
reduce need for C/S

DELIVER
over 32 weeks
doppler abnormality
decr movements
CTG abnormality
19
Q

what is given to prevent respiratory distress syndrom

A

in premature babies, surfactant is lacking (prod from 24-34 weeks)

BETAMETHASONE AND DEXAMETHASONE will cross placenta and stimulate alveoli cells to produce surfactant GENE

this surfactant prevents alveoli cells from collapsing by coating the cells and reducing surface tension