T2 L17: Placenta & Intra-Uterine Growth Restriction, Abnormal Fetal Development Flashcards

1
Q

what happens in days 4-5 in development of the zygote

A

The morula develops a cavity and becomes known as a blastocyst.

Blastocyst thins out and becomes the trophoblast –start of the placenta

The rest of the cells move (are pushed up) to form the inner cell mass. This creates an embryonic pole.

The blastocyst has now reached the uterine lumen and is ready for implantation.

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2
Q

what happens in days 6-7 in development of the zygote

A

Inner cell mass differentiates into two layers: epiblast and hypoblast.

These two layers are in contact.

Hypoblast forms extraembryonic membranes and the primary yolk sac

Epiblast forms embryo

Amniotic cavity develops within the epiblast mass

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3
Q

what happens in days 16+ in development of the zygote

A

Bilaminar disc develops further by forming 3 distinct layers (this process is known as gastrulation.

Initiated by primitive streak.

The epiblast becomes known as ectoderm

The hypoblast is replaced by cells from the epiblast and becomes endoderm

The epiblast gives rise to the third layer the mesoderm.

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4
Q

describe the embryo in 3 germ layers

A

The hypoblast degenerates. The epiblast gives rise to all three germ layers.

The embryo folds to create the adult pattern

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5
Q

look at slide 9

A

how was it

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6
Q

describe the formation of the placenta

A

Syncytiotrophoblast invades decidua (endometrium)

Cytotrophoblast cells erodes maternal spiral arteries and veins

Spaces (lacunae) between the fill up with maternal blood

Followed by mesoderm that develops into fetal vessels

Aiding the transfer of nutrients, O2, across a simple cellular barrier

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7
Q

look at slide 11

A

how was it

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8
Q

describe the difference between CTB and STB cells

A
Cytotrophoblast cells (CTB):
Undifferentiated stem cells

Invade the maternal blood vessels and destroy the epithelium

Give rise to the syncytiotrophoblast cells (STB)

Reduce in number as pregnancy advances

Syncytiotrophoblast cells (STB):

Fully differentiated cells

Direct contact with maternal blood

Produce placental hormones

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9
Q

what is the function of the placenta as an endocrine organ

A

maintenance of corpus luteum of pregnancy

progesterone and oestrogen

Human placental lactogen HPL:

growth, lactation

carbohydrate and lipid
Many more!

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10
Q

describe the placental barrier

A

Maternal blood in the lacunae in direct contact with syncytiotrophoblasts

Mono layer of syncytiotrophoblast/cytotrophoblast/fetal capillary epithelium is all that separates the fetal and maternal blood

Cytotrophoblasts decrease as the pregnancy advances (not needed)

The barrier thins as pregnancy advances leading to a greater surface area for exchange (over 10m2 )

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11
Q

what components are transferred across the placenta

A

Gases – oxygen and carbon dioxide by simple diffusion

Water and electrolytes

Steroid hormones

Proteins poor – only by pinocytosis

Transfer of maternal antibodies IgG -starts at 12 weeks – mainly after 34 weeks therefore lack of protection for premature infants

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12
Q

look at slide 16

A

how was it

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13
Q

what is the Vasa praevia

A

velamentous cord insertion that runs across the cervical os

The fetal vessels within the umbilical cord pass over the internal os. As the internal os dilates in labour the vessels are stretched and exposed and can rupture leading to massive fetal blood loss and death.

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14
Q

what are the clinical aspects of the placenta

A

Position of the placenta within the uterus

  • Mainly fundal (at the top)
  • Anterior or posterior (front wall or back wall)
  • “low lying” or placenta praevia (near to the cervical os)

Placenta Praevia

-Massive bleeding in pregnancy
-Painless bleeding
-Fetal death
Maternal death

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15
Q

what does failure of trophoblastic invasion into maternal circulation at 12 & 18 weeks

A
  • Poor maternal fetal mixing of blood
  • Lack of oxygen and nutrients to the fetus
  • Leads to Fetal Growth Restriction
  • Pre-eclampsia (raised Blood Pressure)
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16
Q

look at slide 22-23

A

how was it

17
Q

what is placental abruption

A

Massive bleeding in pregnancy (often concealed)

Extremely painful

Fetal death

Maternal death

18
Q

look at slide 25

A

how was it

19
Q

what is the difference between development and growth

A

First 12 weeks fetal development occurs – organs formed

Then the baby needs to get bigger – fetal growth

20
Q

what are the 2 types of growth problems

A

1-Small for gestational age (SGA)
<5th centile
normal variant or growth restricted

2-Intra-uterine growth restriction (IUGR)
<5th centile
growth restricted (i.e. failure to achieve growth potential)
21
Q

look at slide 5 IUGR

A

how was it

22
Q

what can fetal growth restriction result in

A

Deficient placental invasion

Reduced placental reserve

Fetal need exceeds supply

IUGR

Hypoxia

Fetal vascular redistribution

Oliguria

Abnormal CTG

Fetal death

23
Q

how can you diagnose IUGR

A

Clinical suspicion – abdomen “looks smaller”

Clinical measurement of uterine size: Symphysis - fundal height (SFH)

24
Q

what is symmetrical growth restriction and why does it occur

A

both head and abdominal growth affected

Chromosomal anomaly (T21)

Viral infection (Rubella, CMV)

Severe Placental insufficiency

OR normal small baby (look at the parents)

25
Q

look at slides 9 10 12 & 13

A

how was it

26
Q

what is asymmetrical growth restriction and why does it occur

A

Asymmetrical Growth Restriction: just abdominal growth affected

Abdominal circumference reflects the size of the fetal liver

Causes:

Placental insufficiency – no excess glycogen being deposited within the liver

27
Q

what are the consequences of hypoxia in the fetus

A
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 O2)
28
Q

what do you find in US in IUGR

A
  • Small AC ( small liver)
  • Decreased amniotic fluid ( this is produced by the kidneys)
  • Increased blood flow to the brain (look at Middle Cerebral arteries in the brain – using the doppler effect scan
29
Q

what are the clinical features of IUGR

A
  • SFH smaller than expected
  • Baby’s movements lessen to conserve energy
  • Fetal heart rate changes as hypoxia develops (as seen on CTG)
  • Fetal death
30
Q

when do you wait or deliver in IUGR

A

wait- Low chance of survival

To give steroids

Reduce need for C/S

Deliver- >32 weeks

Doppler abnormality

Decreased movements

CTG abnormality

31
Q

what is the action of Betamethasone/dexamethasone

A
  • When given to the mother will cross the placenta and stimulate the aveoli cells to produce surfactant gene
  • Surfactant stops the collapse of the aveoli cells by coating the cells and reducing the surface tension
  • Helps prevent Respiratory Distress Syndrome which leads to neonatal death in premature babies
  • Produced from 24- 34 weeks and usually the baby will have enough by 34 weeks in preparation for a term delivery
  • In premature babies it is lacking
32
Q

look at slides 20-22

A

how was it