Late fetal development Flashcards
What is early embryo nutrition reliant on?
Where does it switch its nutrient source to at the start of second semester ?
it is Histotrophic
reliant on uterine secretions and breakdown of uterine lining
haemotrophic
achieved via a haemochorial- type placenta
where maternal blood supply directly contacts fetal membranes
What is the inner Fetal membrane?
what does it arise from?
what does it form?
what does it do?
the Amnion
epiblast
a closed avascular sac with the developing embryo at one end
fluid filled sac encapsulates the embryo to protect it
begins to secrete amniotic fluid by the 5th week
what is the outer fetal membrane
what is it formed from
what does it give rise to
the chorion
yolk sac derivatives and trophoblasts
chorionic villi- outgrowths of the cytotrophoblast from the chorion that form the basis of the fetal side of the placenta
what is the allantois
where does it grow to and from
what does it become
outgrowth of the yolk sac
down the connecting stalk from embryo to chorion
coated in mesoderm and vascularised to form umbilical cord
what are the foetal membranes
how is the amniotic sac formed
what are the two layers of the amniotic sac
Extraembryonic tissues that encapsulate the foetus by forming a tough but flexible sac, forms the basis of the maternal-foetal interface
amnion cells secrete fluid , causing fluid to accumulate and amnion cells to come into contact with the chorion, forms the amniotic sac
amnion cells on the inside, chorion cells on the outside
what is the chronic villi and what do they do?
what are the three stages of villi development?
finger like extensions of the chorionic cytotrophoblast, which undergo branching
provides a larger surface area for exchange
primary- when finger like cytotrophoblast projections form through the syncitiotrophoblast layer to the maternal endometrium layer. begin to branch
secondary- fetal mesoderm grows into villi
tertiary- vasculature is provided by the umbilical artery and vein growing into the villus mesoderm
why are the ends of the villi convoluted knots and more dilated vessels?
what is the difference in the villi between early and late pregnancy
slows down blood flow so more time for exchange between maternal and fetal blood
Early pregnancy: 150-200µm diameter, approx. 10µm trophoblast thickness between capillaries and maternal blood.
Late pregnancy: villi thin to 40µm, vessels move within villi to leave only 1-2µm trophoblast separation from maternal blood.
what is the order of arteries formed from maternal blood to fetal?
Uterine artery branches give rise to a network of arcuate arteries.
Radial arteries branch from arcuate arteries, and branch further to form basal arteries.
Basal arteries form spiral arteries during menstrual cycle endometrial thickening.
why are spiral arteries converted?
How are spiral arteries converted?
Conversion: turns the spiral artery into a low pressure, high capacity, to ensure continuous and extensive blood flow.
Extra-villus trophoblast (EVT) cells coating the villi invade down into the maternal spiral arteries, forming endovascular EVT.
Endothelium and smooth muscle is broken down – EVT coats inside of vessels
How are various nutrients transported across the placenta ?
Oxygen: diffusional gradient (high maternal O2 tension , low fetal O2 tension)
Glucose: facilitated diffusion by transporters on maternal side and foetal trophoblast cells.
Water: placenta main site of exchange, though some crosses amnion-chorion. Majority by diffusion, though some local hydrostatic gradients.
Electrolytes: large traffic of sodium and other electrolytes across the placenta – combination of diffusion and active energy-dependent co-transport.
Calcium: actively transported against a concentration gradient by magnesium ATPase calcium pump.
Amino acids: reduced maternal urea excretion and active transport of amino acids to fetus
how do the mothers…change ?
- cardiac output
- peripheral resistance
- blood volume
- pulmonary ventilation
Maternal cardiac output increases 30% during first trimester (stroke vol & rate)
Maternal peripheral resistance decreases up to 30%
Maternal blood volume increases to 40% (near term (20-30% erythrocytes, 30-60% plasma)
Pulmonary ventilation increases 40%
How much glucose and 02 does the placenta consume?
how is the 02 conc and glucose conc related to the maternal?
Which haemoglobin has a higher affinity- fetal or maternal?
Placenta consumes 40-60% glucose and O2 supplied
although fetal O2 tension is low, O2 content and saturation are similar to maternal blood.
Embryonic and fetal hemoglobins: greater affinity for O2 than maternal hemoglobin.
How does the circulatory system work in a developing fetus
Hints:
- placenta?
- vascular shunts?
- ventricles?
Placenta acts as site of gas exchange for fetus
Ventricles act in parallel rather than series
vascular shunts bypass pulmonary & hepatic circulation -> close at birth
How does the respiratory system work in a developing fetus?
Hints:
when do primitive air sacs form?
when does vascularisation occur?
when does surfactant production occur?
Primitive air sacs form in lungs around 20 weeks, vascularization from 28 weeks
Surfactant production begins around week 20, upregulated towards term
Foetus spends 1-4h/day making rapid respiratory movements during REM sleep
What is labour?
Safe expulsion of the fetus at the correct time
Expulsion of the placenta and fetal membranes
Resolution/healing to permit future reproductive events
How does labour have the characteristics of a pro-inflammatory reaction
Immune cell infiltration
Inflammatory cytokine and prostaglandin secretion
What happens in the first stage of labour?
what are the two stages within the first stage of labour?
First Stage: Contractions start, Cervix dilation
Latent Phase:
Slow dilation of the cervix to 2-3cm
Active Phase:
Rapid dilation of the cervix to 10cm
What happens in the second two stages of labour?
Second stage: Delivery of the fetus
Commences at full dilation of the cervix (10cm)
Maximal myometrial contractions
Third stage: Delivery of the placenta
Explusion of placenta and fetal membranes
Post-partum repair
what is the role of the cervix ?
What is the advantage of high rigidity connective tissue?
what is it made up of?
retains fetus in uterus
Provides rigidity and its stretch resistant
bundle of collagen fibres embedded in a proteoglycan matrix
why does the cervix need to soften?
What are the four stages to cervix softening?
allow it to dilate
to open birth canal and let fetus through
Softening
Ripening
Dilation
Post partum repair
What happens in each stage of cervical dilation?
Softening - measurable changes in compliance but overall competence of cervix remains. Begins in first trimester
Ripening- hydraulon deposition, IL-6 and IL-8 secretion and monocyte infiltration
Dilation- MMPs (Matrix Metalloproteinase) decreases collagen content
Post partum repair- repair tissue integrity and competency
how does the foetus determine the timing of parturition?
what happens to CRH binding protein levels?
Current thinking: fetus determines timing of parturition through changes in fetal HPA axis
Corticotrophin Releasing Hormone (CRH) levels rise exponentially towards the end of pregnancy
Decline in CRH-binding protein levels, so bioavailable (free to signal) CRH increases
What are the the functions of CRH in Labour?
promotes fetal ACTH and cortisol release
Increasing cortisol drives placental production of CRH -> Positive feedback, more CRH
stimulates DHEAS production by the fetal adrenal cortex -> substrate for estrogen production
what does the high amount of progesterone do
what happens to the serum oestrogen: progesterone ratio
High progesterone through pregnancy maintains uterine relaxation
Serum oestrogen : progesterone ratio may shift in favour of oestrogen – this is unclear
what happens to the progesterone receptors as term approaches ?
Progesterone Receptor (PRs) expressed by the uterus switch from active signalling forms (PR-A) isoforms
to repressive isoforms (PR-B and PR-C) isoforms expressed in the uterus
functional progesterone withdrawal
Uterus is blinded to progesterone action and sensitised to oestrogen
how many amino acids does oxytocin contain and where is it synthesised
when does uterine oxytocin production increase
what are oxytocin expression and release driven by
Nonapeptide (9amino acid) hormone synthesized mainly in the utero-placental tissues and pituitary.
Uterine oxytocin production increases sharply at onset of labour
Expression increase is driven by increase in estrogen levels
Release promoted by stretch receptors -> Ferguson reflex. cervix is stretched- stretch receptors detect this so afferent neurones send signals to hypothalamus to release oxytocin
what receptor does oxytocin bind to
what are the hormonal changes that stimulate in increase in OXTR expression
Signals through G-coupled oxytocin receptor (OTR / OXTR)
Pre-labour: progesterone inhibits OXTR expression -> uterus relaxed
Rise in estrogen promotes large increase in uterine OXTR expression
what are the functions of oxytocin
Functions of Oxytocin:
Increases connectivity of myocytes in myometrium (syncytium)
Destabilise membrane potentials to lower threshold for contraction
Enhances liberation of intracellular Ca2+ ion stores
all of this helps to enable uterine contraction
what are the primary prostaglandins produced in labour
what two ways do rising estrogen levels stimulate release of prostaglandin
Primary PGs synthesized during labour are PGE2, PGF2alpha and PGI2.
Rising estrogen levels drive prostaglandin action in the uterus in two ways:
- Rising estrogen activates phospholipase A2 enzyme, generating more arachidonic acid for PG synthesis
- Estrogen stimulation of oxytocin receptor expression promotes PG release.
what is PGE2 main function?
what three things does PGE2 stimulate
what other factors aid PGE2
PGE2 – aids cervix re-modelling
Promotes leukocyte infiltration into the cervix, IL-8 release and collagen bundle re-modelling
peptide hormone relaxin and nitric oxide implicated in cervix remodelling
What is PGF2 alpha function?
how does it go about doing this?
PGF2alpha – aids myometrial contractions
Destabilises membrane potentials and promotes connectivity of myocytes (with Oxytocin
what is PGI2 main function
why is this function important
PGI2 - myometrium relaxation
Promotes myometrial smooth muscle relaxation and relaxation of lower uterine segment
relaxation is important between contractions as it allows blood flow to return to placenta and fetus
what is the name of the extensive gap junctions myometrial cells form and what does it do
where do contractions start and how does this form the birth canal
syncytium, transmits contractions across muscle
Contractions start from the fundus (top of uterus) , spread down upper segment
Muscle contractions are brachystatic –fibres do not return to full length on relaxation
This causes lower segment and cervix to be pulled up forming birth canal
Outline the process of fetal expulsion
Head engages with pelvic space 34-38wks
Pressure on fetus causes chin to press against chest (flexion)
Fetus rotates (belly to mother’s spine)
Head expelled first after cervix dilates
Shoulders delivered sequentially (upper first) followed by torso.
Outline the process of placenta and fetal membrane expulsion
Rapid shrinkage of the uterus after fetal delivery causes area of contact of placenta with endometrium to shrink
Uterine shrinkage also causes folding of fetal membranes – peel off the endometrium
Clamping of the umbilical cord after birth stops fetal blood flow to placenta -> villi collapse
Hematoma formation between decidua and placenta
Contractions expel placenta and fetal tissues
why does the uterus remain contracted after delivery?
why does uterus involution and cervix repair occur?
to facilitate uterine vessel thrombosis to aid the healing of the uterine vessel to prevent uterine bleeding
to restore non-pregnant state
- to Shield uterus from commensural bacteria in the reproductive tract and prevent them from going up into uterus
- Restore endometrial cyclicity in response to hormones to ensure the uterus is ready to allow implantation of another embryo if one comes along
What are trophoblastic lacunae
large spaces in trophoblast filled with maternal blood formed by the breakdown of maternal capillaries and uterine glands
become intervillous spaces aka maternal blood spaces
