Late fetal development Flashcards

1
Q

What is early embryo nutrition reliant on?

Where does it switch its nutrient source to at the start of second semester ?

A

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

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2
Q

What is the inner Fetal membrane?

what does it arise from?

what does it form?

what does it do?

A

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

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3
Q

what is the outer fetal membrane

what is it formed from

what does it give rise to

A

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

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4
Q

what is the allantois

where does it grow to and from

what does it become

A

outgrowth of the yolk sac

down the connecting stalk from embryo to chorion

coated in mesoderm and vascularised to form umbilical cord

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5
Q

what are the foetal membranes

how is the amniotic sac formed

what are the two layers of the amniotic sac

A

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

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6
Q

what is the chronic villi and what do they do?

what are the three stages of villi development?

A

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

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7
Q

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

A

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.

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8
Q

what is the order of arteries formed from maternal blood to fetal?

A

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.

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9
Q

why are spiral arteries converted?

How are spiral arteries converted?

A

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

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10
Q

How are various nutrients transported across the placenta ?

A

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

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11
Q

how do the mothers…change ?

  • cardiac output
  • peripheral resistance
  • blood volume
  • pulmonary ventilation
A

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%

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12
Q

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?

A

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.

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13
Q

How does the circulatory system work in a developing fetus

Hints:

  • placenta?
  • vascular shunts?
  • ventricles?
A

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

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14
Q

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?

A

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

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15
Q

What is labour?

A

Safe expulsion of the fetus at the correct time

Expulsion of the placenta and fetal membranes

Resolution/healing to permit future reproductive events

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16
Q

How does labour have the characteristics of a pro-inflammatory reaction

A

Immune cell infiltration

Inflammatory cytokine and prostaglandin secretion

17
Q

What happens in the first stage of labour?

what are the two stages within the first stage of labour?

A

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

18
Q

What happens in the second two stages of labour?

A

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

19
Q

what is the role of the cervix ?

What is the advantage of high rigidity connective tissue?

what is it made up of?

A

retains fetus in uterus

Provides rigidity and its stretch resistant

bundle of collagen fibres embedded in a proteoglycan matrix

20
Q

why does the cervix need to soften?

What are the four stages to cervix softening?

A

allow it to dilate
to open birth canal and let fetus through

Softening
Ripening
Dilation
Post partum repair

21
Q

What happens in each stage of cervical dilation?

A

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

22
Q

how does the foetus determine the timing of parturition?

what happens to CRH binding protein levels?

A

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

23
Q

What are the the functions of CRH in Labour?

A

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

24
Q

what does the high amount of progesterone do

what happens to the serum oestrogen: progesterone ratio

A

High progesterone through pregnancy maintains uterine relaxation

Serum oestrogen : progesterone ratio may shift in favour of oestrogen – this is unclear

25
Q

what happens to the progesterone receptors as term approaches ?

A

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

26
Q

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

A

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

27
Q

what receptor does oxytocin bind to

what are the hormonal changes that stimulate in increase in OXTR expression

A

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

28
Q

what are the functions of oxytocin

A

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

29
Q

what are the primary prostaglandins produced in labour

what two ways do rising estrogen levels stimulate release of prostaglandin

A

Primary PGs synthesized during labour are PGE2, PGF2alpha and PGI2.

Rising estrogen levels drive prostaglandin action in the uterus in two ways:

  1. Rising estrogen activates phospholipase A2 enzyme, generating more arachidonic acid for PG synthesis
  2. Estrogen stimulation of oxytocin receptor expression promotes PG release.
30
Q

what is PGE2 main function?

what three things does PGE2 stimulate

what other factors aid PGE2

A

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

31
Q

What is PGF2 alpha function?

how does it go about doing this?

A

PGF2alpha – aids myometrial contractions

Destabilises membrane potentials and promotes connectivity of myocytes (with Oxytocin

32
Q

what is PGI2 main function

why is this function important

A

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

33
Q

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

A

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

34
Q

Outline the process of fetal expulsion

A

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.

35
Q

Outline the process of placenta and fetal membrane expulsion

A

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

36
Q

why does the uterus remain contracted after delivery?

why does uterus involution and cervix repair occur?

A

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
37
Q

What are trophoblastic lacunae

A

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