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

1
Q

What is the embryo called 72 hours after fertilisation has occurred?

A

A morula

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2
Q

How many days after fertilisation does the blastocyst appear?

A

4 days

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3
Q

What happens to the embryo between days 4 - 5?

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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4
Q

What happens to the embryo between days 6 - 7?

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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5
Q

What happens to the embryo at day 16+?

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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6
Q

Which layer gives rise to all the germ layers in the embryo?

A

The epiblast

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7
Q

Name the germ layers present in the embryo

A

Ectoderm

Mesoderm

Endoderm

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8
Q

How is the placenta formed?

A

Syncytiotrophoblast invades decidua (endometrium)

Cytotrophoblast cells erodes maternal spiral arteries and veins

Spaces (lacunae) between them, fill up with maternal blood

Followed by mesoderm that develops into fetal vessels

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9
Q

What is the function of the foetal vessels?

A

They aid the transfer of nutrients, O2, across a simple cellular barrier

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10
Q

What happens in pre-eclampsia?

A

There is an abnormality of invasion by the (syncytiotrophoblast and the cytotrophoblast)

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11
Q

What are the cytotrophoblast cells (CTB)?

A

Undifferentiated stem cells

Invade the maternal blood vessels and destroy the epithelium

Give rise to the syncytiotrophoblast cells (STB)

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12
Q

What are the syncytiotrophoblast cells (STB)?

A

Fully differentiated cells

Direct contact with maternal blood (in the lacunae)

Produce placental hormones

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13
Q

What happens to the cytotrophoblast cells (CTB) as pregnancy advances?

A

They reduce in number

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14
Q

Is the placenta an endocrine organ?

A

YES

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15
Q

Name two hormones secreted by the placenta and their function

A

Human chorionic gonadotrophin (HCG)
-maintenance of corpus luteum of pregnancy which releases progesterone and oestrogen

Human placental lactogen (HPL)

  • growth, lactation
  • increases carbohydrate available for the foetus by increasing the use of lipolysis as an energy source in the mother
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16
Q

What forms the placental barrier?

A

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

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17
Q

What happens to the cytotrophoblasts as the pregnancy advances? Why?

A

They decrease as they are no longer needed

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18
Q

What happens to the placental barrier as pregnancy advances? What does this result in?

A

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

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19
Q

What structures/molecules 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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20
Q

Give the topographical name for different parts of the decidua (mucousal layer of the endometrium)

A

capsularis – overlying embryo and chorionic cavity

parietalis – side uterus not occupied by embryo

basalis – between uterine wall and chorionic villae

21
Q

What is placenta (or vasa) praevia?

A

Velomentous cord insertion that runs across the cervical os

The umbilical cord inserts into the fetal membranes (choriamniotic membranes), then travels within the membranes to the placenta (between the amnion and the chorion).

The exposed vessels are not protected by Wharton’s jelly and hence are vulnerable to rupture

22
Q

What are the different positions the placenta can take in the uterus?

A

Mainly fundal (at the top)

Anterior or posterior (front wall or back wall)

“low lying” or placenta praevia (near to the cervical os)

23
Q

What occurs during placenta praevia?

A

Massive bleeding in pregnancy

Painless bleeding

Fetal death

Maternal death

24
Q

What happens to the trophoblastic invasion in placenta praevia? What does this result in?

A

Failure of trophoblastic invasion into maternal circulation at 12 and 18 weeks

LEADS TO:

  • Poor maternal fetal mixing of blood
  • Lack of oxygen and nutrients to the fetus
  • Leads to Fetal Growth Restriction
  • Pre-eclampsia (raised Blood Pressure)
25
Q

What is placenta accreta?

A

The placenta inserts too deeply into the muscles of the uterus (placenta increta) or grow through the uterine wall (placenta percreta)

It is unable to separate at birth

26
Q

What complications can placenta accreta lead to?

A

HEAVY VAGINAL BLEEDING - can cause a life-threatening condition that prevents maternal blood from clotting normally (disseminated intravascular coagulopathy), as well as lung failure (adult respiratory distress syndrome) and kidney failure. A blood transfusion will likely be necessary.

PREMATURE BIRTH - if placenta accreta causes bleeding during pregnancy, there may be need to deliver the baby early.

27
Q

How is placenta accretia treated?

A

Hysterectomy

28
Q

What is placental abruption?

A

Occurs when the placenta separates early from the uterus (separates before childbirth)

29
Q

What are the complication of placental abruption?

A

Massive bleeding in pregnancy (often concealed)

Extremely painful

Fetal death

Maternal death

30
Q

Give definitions for these 2 types of growth problems

  • Small for gestational age (SGA)
  • Intra-uterine growth restriction (IUGR)
A

Small for gestational age (SGA)

  • <5th centile
  • normal variant or growth restricted

Intra-uterine growth restriction (IUGR)

  • <5th centile
  • growth restricted (i.e. failure to achieve growth potential)
31
Q

List the factors that are indicative of foetal growth restrictions

A
  • Deficient placental invasion
  • Reduced placental reserve
  • Fetal need exceeds supply
  • IUGR
  • Hypoxia
  • Fetal vascular redistribution
  • Oliguria
  • Abnormal CTG
  • Fetal death
32
Q

How is foetal growth restriction clinically diagnosed?

A

Clinical suspicion – abdomen “looks smaller”

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

33
Q

How is the symphysis - fundal height (SFH) measured?

A

Measured in cm

From the pubic symphysis to the top most portion of the uterus

34
Q

What is the SFH used for?

A

Assessment of foetal growth

35
Q

What occurs in Symmetrical Growth Restriction?

A

BOTH head and abdominal growth affected

36
Q

What are the causes of Symmetrical Growth Restriction?

A
  • Chromosomal anomaly (T21)
  • Viral infection (Rubella, CMV)
  • Severe Placental insufficiency

OR normal small baby (look at the parents)

NOTE: Their head is often proportionate with the rest of their body

37
Q

What occurs in Asymmetrical Growth Restriction?

A

ONLY the abdominal circumference is reduced. Abdominal circumference reflects the size of the fetal liver

NOTE: Their head often looks disproportionate to their body

38
Q

What is the cause of Asymmetrical Growth Restriction?

A

Placental insufficiency – no excess glycogen being deposited within the liver

39
Q

What are the consequences of hypoxia in the foetus?

A

Blood flow (oxygen and nutrients) redirected to areas of greater importance e.g. the brain

Blood flow (oxygen and nutrients) redirected away from areas of lesser importance (organs that the foetus does not actively use) e.g

  • the gut (doesn’t eat!)
  • the kidneys (placenta clears waste products)
  • the lungs (placenta brings O2)
40
Q

Describe the ultrasound findings 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
41
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
42
Q

When and why should you wait/observe if the foetus shows signs of IUGR?

A

Low chance of survival (outside the womb)

To give steroids

Reduce need for C/S (Caesarean Section)

43
Q

When should the foetus be delivered if it shows signs of IUGR?

A

> 32 weeks

Doppler abnormality

Decreased movements

CTG abnormality

44
Q

What happens when betamethasone/dexamethasone is given to the mother?

A

The drug crosses the placenta and stimulates the aveoli cells to produce surfactant gene

45
Q

What is the effect on surfactant the foetal lung?

A

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

46
Q

When is surfactant produced in the foetus?

A

Produced from 24- 34 weeks

The baby will have enough by 34 weeks in preparation for a term delivery

47
Q

Do premature babies have surfactant?

A

NO

It is lacking

48
Q

What happens to the middle cerebral artery blood flow in a normal pregnancy?

A

The peak corresponds to systole of the heart and during diastole the flow is negative (or reduced)

49
Q

What happens to the middle cerebral artery blood flow in foetal growth restriction?

A

The blood flow is maintained during both systole and diastole – increasing blood flow.