T2 L17: Placenta & Intra-Uterine Growth Restriction, Abnormal Fetal Development Flashcards
what happens in days 4-5 in development of the zygote
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.
what happens in days 6-7 in development of the zygote
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
what happens in days 16+ in development of the zygote
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.
describe the embryo in 3 germ layers
The hypoblast degenerates. The epiblast gives rise to all three germ layers.
The embryo folds to create the adult pattern
look at slide 9
how was it
describe the formation of the placenta
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
look at slide 11
how was it
describe the difference between CTB and STB cells
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
what is the function of the placenta as an endocrine organ
maintenance of corpus luteum of pregnancy
progesterone and oestrogen
Human placental lactogen HPL:
growth, lactation
carbohydrate and lipid
Many more!
describe the placental barrier
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 )
what components are transferred across the placenta
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
look at slide 16
how was it
what is the Vasa praevia
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.
what are the clinical aspects of the placenta
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
what does failure of trophoblastic invasion into maternal circulation at 12 & 18 weeks
- Poor maternal fetal mixing of blood
- Lack of oxygen and nutrients to the fetus
- Leads to Fetal Growth Restriction
- Pre-eclampsia (raised Blood Pressure)
look at slide 22-23
how was it
what is placental abruption
Massive bleeding in pregnancy (often concealed)
Extremely painful
Fetal death
Maternal death
look at slide 25
how was it
what is the difference between development and growth
First 12 weeks fetal development occurs – organs formed
Then the baby needs to get bigger – fetal growth
what are the 2 types of growth problems
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)
look at slide 5 IUGR
how was it
what can fetal growth restriction result in
Deficient placental invasion
Reduced placental reserve
Fetal need exceeds supply
IUGR
Hypoxia
Fetal vascular redistribution
Oliguria
Abnormal CTG
Fetal death
how can you diagnose IUGR
Clinical suspicion – abdomen “looks smaller”
Clinical measurement of uterine size: Symphysis - fundal height (SFH)
what is symmetrical growth restriction and why does it occur
both head and abdominal growth affected
Chromosomal anomaly (T21)
Viral infection (Rubella, CMV)
Severe Placental insufficiency
OR normal small baby (look at the parents)
look at slides 9 10 12 & 13
how was it
what is asymmetrical growth restriction and why does it occur
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
what are the 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 O2)
what do you find in US in IUGR
- 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
what are the clinical features of IUGR
- SFH smaller than expected
- Baby’s movements lessen to conserve energy
- Fetal heart rate changes as hypoxia develops (as seen on CTG)
- Fetal death
when do you wait or deliver in IUGR
wait- Low chance of survival
To give steroids
Reduce need for C/S
Deliver- >32 weeks
Doppler abnormality
Decreased movements
CTG abnormality
what is the action of Betamethasone/dexamethasone
- 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
look at slides 20-22
how was it