L18 - Placenta & Growth Restriction Flashcards

1
Q

FERTILISATION

i) which days does the morula form?
ii) which days does the early blastocyst form?
iii) which reaction stops more than one sperm fertilising an egg?
iv) which part of the blastocyst does the embryo arise from?

A

i) day 3-4
ii) day 4-5
iii) acrosome reaction
iv) inner cell mass

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2
Q

DAY 4-5 POST FERTILISATION

i) what does the morula develop into?
ii) what part of the structure becomes the start of the placenta?
iii) what do the rest of the cells become? what does this create?
iv) label picture

A

i) the blastocyst
ii) trophoblast becomes the placenta
iii) rest of the cells become the inner cell mass > embryonic pole

iv) A = inner cell mass
B = trophoblast
C = blastocele

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3
Q

DAY 6-7 POST FERTILISATION

i) what two layers does the inner cell mass differentiate into? are these layers in contact?
ii) which layer forms the extraembryonic membranes and the primary yolk sac?
iii) which layer forms the embryo?
iv) where does the amniotic cavity develop within?
v) label diagram

A

i) epiblast and hypoblast - in contact
ii) hypoblast forms extraembryonic membranes and primary yolk sac
iii) epiblast forms the embryo
iv) amniotic cavity develops withint the epiblast
v) A - syncytiotrophoblast, B - epiblast, C = hypoblast, D - cytotrophoblast, E - amniotic cavity

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4
Q

DAY 16+ POST FERTILISATION

i) what is the name of the process by which the three germ layers are formed from a bilaminar disk?
ii) what is this process initiated by?
iii) what does the epiblast become first?
iv) what happens to the hypoblast? what does this then become?
v) what happens after all layers have be formed?

A

i) gastrulation
ii) the primitive streak
iii) epiblast > ectoderm

iv) hypoblast is replaced by epiblast cells > endoderm
- then epiblast cells keep piling on top and form the mesoderm

v) the embryo folds to create the adult pattern

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5
Q

DEVELOPMENT OF THE PLACENTA

i) which area invades the endometrium?
ii) which structures do cytotrophoblast cells invade? what does this lead to?
iii) which germ layer develops into fetal vessels?
iv) name two things that are transferred across the placenta
v) in what condition may this process happen abnormally? what doesnt happen properly and what does this result in?

A

i) syncytiotrophoblast

ii) cytotrophoblast cells invade spiral arteries and veins which makes big blood filled spaces = lacunae
- lacunae fill up with materal blood

iii) mesoderm > fetal vessles
iv) nutrients and oxygen

v) pre eclampsia (high BP)
- syncytio doesnt invade the endometrium properly therefore spiral arteries are narrow
- this causes inc resistance and decreased blood flow to baby which can cause growth restriction

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6
Q

CELLS OF PLACENTAL DEVELOPMENT

i) which cells are undifferentiated stem cells and which cells are fully differentiated?
ii) which cells have direct contact with maternal blood and produce placental hormones?
iii) which cells invade the materal blood vessels and destroy the epithelium?
iv) which cells give rise to syncytiotrophoblast cells and reduce in number as pregnancy advances?
v) label diagram A-C

A

i) cytotrophoblast cells are stem cells
- syncytiotrophoblast cells are fully differentiated

ii) syncytio direct contact maternal blood and produce hormones
iii) cytotropho invade materal blood vessels
iv) cytotropho give rise to syncytiotropho cells and reduce as pregnancy advances

v) A - cytotrophoblast
B - syncytiotrophoblast
C - spiral artery

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7
Q

PLACENTA AS AN ENDOCRINE ORGAN

i) which hormone is released that maintains the corpus luteum of pregnancy?
ii) which two hormones are produced by the corpus luteum early on and then by the placenta?
iii) which hormone aids in growth, lactation etc

A

i) human chorionic gonadotrophin (HCG)
ii) oestrogen and progesterone
iii) human placental lactogen (HPL)

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8
Q

PLACENTAL BARRIER

i) which cells is maternal blood in the lacunae in direct contact with?
ii) what happens to the layer seperating fetal and maternal blood as the pregnancy advances? what does this allow for?
iii) how many cells thick is the layer that seperates the fetal and maternal blood?
iv) which cells decrease as pregnancy advances?

A

i) syncytiotrophoblasts

ii) as preg advances the layer gets thinner
- allows for increased surface area for exchange

iii) one cell think (monolayer)
iv) cytotrophoblasts decrease as pregnancy advances

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9
Q

TRANSFER ACROSS THE PLACENTA

i) name two gases that pass across? by which mechanism does this happen?
ii) give three other things that pass
iii) by which mechanism do proteins cross?
iv) which week does transfer of maternal IgG antibodies start? when does this mainly happen? what implications does this have for premature infants

A

i) oxygen and co2 - by simple diffusion
ii) water, electrolytes, steroid hormones
iii) pinocytosis

iv) IgG transfer starts at 12 weeks and mainly happens after 34 weeks
- premature babies may lack protection

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10
Q

CLINICAL ASPECTS OF THE PLACENTA

i) where does the placenta usually sit in the uterus?
ii) where does a low lying/placenta praevia sit? which scan should this be checked on?
iii) is bleeding from placenta praevia painful or painless? what can it result in?
iv) what is vasa praevia? what can this result in?

A

i) fundal (at the top)

ii) placenta praevia sits near or across the cervical os
- check on 20 week scan

iii) placenta praevia - massive but painless bleeding
- can result in maternal/fetal death

iv) vasa praevia is when fetal blood vessels lay across the cervical os
- can result in haemmorhage when the membranes rupture and can be fatal for baby

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11
Q

CLINICAL ASPECTS OF PLACENTA CONT

i) at what weeks are the two waves of invasion of trophoblastic cells into the maternal circulation?
ii) if this doesn’t happen name three things this can cause? what two conditions can this ultimately result in?
iii) what happens in placenta abruption? what is the character of the bleeding? (2) what can this result in?

A

i) trophoblast invasion at 12 and 18 weeks

ii) if this doesnt happen - poor maternal and fetal blood mixing, lack of oxygen, lack of nutrients to fetus
- can lead to growth restriction and pre eclampsia

iii) placetal abruption - placenta starts to detach
- massive concealed bleeding that is very painful
- can result in fetal and maternal death

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12
Q

PLACENTA ACCRETA

i) what happens? what does this result in?
ii) give three things that can increase the risk of this?
iii) how is this treated?
iv) what is the most severe version called?

A

i) placenta is unable to seperate at birth as it has invaded the uterine wall
- can result in the uterus not contracting down and massive bleeding

ii) inc risk in caesarian, scarring, not first baby
iv) percreta - invasion through wall and to surrounding organs

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13
Q

PLACENTAL ABNORMALITIES

i) label A-D

A

A - vasa praevia

B - placenta praevia

C - placenta accreta

D - placental abruption

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14
Q

MONITORING FETAL GROWTH

i) name three things growth restriction is associated with
ii) what may growth restriction be associated with?

A

i) stillbirth, neonatal death, perinatal morbidity
ii) may be associated with sub optimal care

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15
Q

SMALL FOR GESTATIONAL AGE (SGA) FETUS

i) what is SGA based on? (2)
ii) what centile are SGA fetuses below on growth scan?
iii) is SGA synonymous with fetal growth restriction? give two other situations where a baby may be SGA
iv) which three measurements are used to calculate weight on ultrasound?

A

i) estimated fetal weight or abdominal circumference
ii) <10th centile

iii) SGA and FGR are not synonymous
- can just have a small baby or have a normal sized baby that is showing reduced growth

iv) abdominal circumference, head circumference and femur length

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16
Q

CAUSES OF SMALL BABIES

i) what are the three main groups of small for gestational age fetuses?
ii) what non placental cause may result in SGA? (3)
iii) give four conditions that placental mediated growth restriction may be associated with?
iv) which type of SGA can result in symmetrical IUGR? what does this mean?
v) which type of SGA can result in assymmetrical IUGR? which measurement is reduced here?

A

i) constitutionally small, placenta mediated or non placenta mediated
ii) non placental - structural or chromosomal abnormality, fetal infection, inborn error of metabolism
ii) placenta mediated - assoc pre eclampsia, autoimmune disease, thrombophilia, renal disease, diabetes

iv) small baby and non placental mediated > symmetrical
- symmetrical means all measurements are reduced in proportion

v) placenta mediated GR can result in asymmetrical IUGR
- only abdominal circumference is reduced

17
Q

RISK FACTORS

i) name three maternal factors that can increase risk of growth restriction
ii) which two pre-existing conditions can increase risk
iii) name two factors from previous pregnancy that can increase risk
iv) low levels of which protein at combined screening may increase risk?

A

i) maternal age >40, first baby, low or high BMI
ii) diabetes and renal disease
iii) previous SGA or stillbirth
iv) low levels of PAPP-A

18
Q

RESPONSE TO FETAL GROWTH RESTRICTION

i) why is blood space allowing exchange of nutrients etc low?
ii) how does the fetus respond to hypoxia?
iii) which monitoring can be used?
iv) if not recognised - what can happen?

A

i) blood space low due to deficienct placental invasion
ii) hypoxia > fetal vascular redistribution
iii) use CTG
iv) fetal death

19
Q

DIAGNOSIS OF GROWTH RESTRICTION

i) what may arouse clinical suspicion?
ii) which two measurements are taken to measure uterine size? what should this height roughly correspond to?
iii) what imaging may be used?
iv) how can growth restriction patterns be visualised?

A

i) abdomen looks smaller

ii) symphysis to fundal height (SFH)
- should roughly correspond to number of weeks of pregnancy

iii) ultrasound
iv) plot on growth chart

20
Q

FETAL GROWTH CHARTS

i) what is expected to be seen on a growth chart in symmetrical GR?
ii) what is expected to be seen on asymmetrical GR?
iii) what does the abdominal circumference reflect? which type of growth restric is this solely affected in?
iv) what may cause reduced abdominal circumference?

A

i) head and abdo circumference are following eachother
ii) only the abdominal circumference is lower (head is still normal)

iii) abdo circumference reflects liver size
- solely affected in assym growth restric

iv) placental insufficiency can result in no excess glycogen in the liver therefore small size and small abdo circumference

21
Q

CONSEQUENCES OF HYPOXIA/US FINDINGS

i) where is blood flow redirected to?
ii) name three areas where blood flow is directed away from?
iii) what can low fluid levels on a scan be a sign of?
iv) which artery can be looked at to see inc blood flow?

A

i) the brain
ii) kidneys, GI and lungs
iii) low fluid levels = placental insuffiency as kidneys are struggling
iv) look at middle cerebral artery in brain

22
Q

CLINICAL FEATURES OF IUGR

i) which measurement may be smaller than expected?
ii) how may babys movements change? why
iii) what may also change to conserve oxygen? how is this monitored?
iv) what could this ultimately result in?

A

i) SFH
ii) decreased movements to conserve energy

iii) fetal heart rate change
- can monitor using CTG

iv) can result in fetal death

23
Q

MANAGEMENT/MONITORING OF IUGR BABY

i) name two things serial ultrasound should monitor?
ii) name two things timing of delivery can depend on?
iii) what do fetal dopplers allow? (3)
iv) what is the first artery looked at on fetal doppler? what may be seen if there is growth restriction?
v) if that artery is abnormal, which artery is looked at next? what would be seen in growth restriction?
vi) which type of doppler can show abnormalities in flow that may result in expediting delivery?

A

i) fetal growth and liqor volume
ii) gestational age and doppler studies
iii) dopplers allow non invasive assess of fetal circulation, identifies GR, guides timing of intervention

iv) first look at umbilical artery
- should be low resis but in GR has high resis

v) if umbilical artery has high resis then look at MCA
- usually ceb arteries are constricted but in GR are dilated

vi) ductus venosus doppler

24
Q

MIDDLE CEREBRAL ARTERY

i) what can be used to measure flow here?
ii) at which two times is pressure in this artery measured?
iii) in a healthy baby - what is seen on the graph?
iv) what is seen in a GR baby? why?

A

i) doppler
ii) look at pressure in systole and diastole
iii) healthy - big differences in pressures at systole and diastole
iv) in GR there isnt much difference between systole and diastole as the arteries are dilated

25
Q

DELIVERY AND SURFACTANT

i) after how many weeks are you more likely to deliver? name three implications for early delivery
ii) name two steroids that can be given to mum if needing to deliver early? what cells do these stimulate in the fetus when it crosses the placenta? what does this cause them to produce?
iii) how does surfactant help the fetus?
iv) which syndrome can be prevented by increasing surfactant?
v) between which weeks is surfactant produced? by how many weeks does the baby have enough to survive?
vi) which group of babies is surfactant lacking in

A

i) >32 weeks
- doppler abnormality, decreased movement, CTG abnormality

ii) betamethasone and dexmethasone
- stimulates alveoli cells in fetus to produce surfactant gene

iii) surfactant stops collapse of alveoli cells by coating the cells and reducing surface tension
iv) surfactant can help prevent respiratory distress syndrome > neonatal death

v) surfactant produced 24-34 weeks
- baby will usually have enough by 34 weeks

vi) surfactant is lacking in neonates