17. Placenta and intra-uterine growth restriction Flashcards
Fertilisation
Sperm and Ovum meet in Fallopian Tube (Uterine Tube) (usually ampulla) 12-24 hours after ovulation.
Fusion occurs and 2nd meiotic division occurs
Acrosome reaction makes ovum impermeable to other sperm
End- Zygote- has diploid (46 chromosomes)
Days 4-5
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.
Day 6-7 bilaminar disc of the embryo
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
Days 16+
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.
The 3 germ layers of the embryo
The hypoblast degenerates. The epiblast gives rise to all three germ layers.
The embryo folds to create the adult pattern
The development of the placenta
Syncytiotrophoblast burrows into the myometrium of the uterus – the syncytiotrophoblasts invading the maternal spiral arteries and starting the formation of the primary/secondary and tertiary villi
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
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
The placenta as an endocrine organ
Human chorionic gonadotrophin (HCG) maintenance of corpus luteum of pregnancy progesterone and oestrogen Human placental lactogen HPL growth, lactation carbohydrate and lipid Many more!
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 )
Transfer 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
Named parts of the decidua
Topographical names
capsularis – overlying embryo and chorionic cavity
parietalis – side uterus not occupied by embryo
basalis – between uterine wall and chorionic villae
What is vasa praevia?
velomentous 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.
Diagnosed on Ultrasound using colour dopplers
Management deliver by Caesarean Section when the fetus is above 34 weeks.
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 and 18 weeks lead to?
Failure of trophoblastic invasion into maternal circulation at 12 and 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)
Placenta Accreta
Placenta unable to separate at birth – uterus can not contract down and massive bleeding. Treatment hysterectomy.
The placenta has invaded too deep into the myometrium and thus after birth the placenta can not separate and stays within the uterus. As a consequence the uterus can not contract down and massive bleeding can occur leading to the requirement to do a hysterectomy.
Placental abruption
Massive bleeding in pregnancy (often concealed)
- Extremely painful
- Fetal death
- Maternal death
Separation of the placenta during pregnancy. Leads to disruption of the blood to the fetus leading to fetal distress and death
Bleeding can be concealed ie not seen via the vagina but the uterus fills up with blood. Different to Placenta praevia where the blood is seen from the vagina.
Make one about placenta in multiple pregnancies
dont forget
Development vs growth
Development vs Growth
First 12 weeks fetal development occurs – organs formed
Then the baby needs to get bigger – fetal growth
Definitions: 2 types of growth problems
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)
Foetal growth restriction
Deficient placental invasion Reduced placental reserve Fetal need exceeds supply IUGR Hypoxia Fetal vascular redistribution Oliguria Abnormal CTG Fetal death
Diagnosis
Clinical suspicion – abdomen “looks smaller”
Clinical measurement of uterine size: Symphysis - fundal height (SFH)
SFH = weeks +/- cms
Ultrasound scan
Symmetrical foetal growth restriction
In symmetrical growth restriction the Head Circumference, The BPD ( biparietal diameter of the Head() and the abdominal circumference are ALL reduced
Early foetal growth restriction
Symmetrical Growth Restriction: both head and abdominal growth affected
Causes:
Chromosomal anomaly (T21)
Viral infection (Rubella, CMV)
Severe Placental insufficiency
OR normal small baby (look at the parents)
Asymmetrical foetal growth restriction
In asymmetrical growth restriction ONLY the abdominal head circumference is reduced.
Foetal growth restriction
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
Consequences of hypoxia in the foetus
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)
Ultrasound findings 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
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
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
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
Foetal growth restriction middle cerebral artery
In growth restriction the blood flow is maintained during both systole and diastole – increasing blood flow.
