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Year 1 - BRS > 10.4 - Pregnancy, Parturition and Late Foetal Development > Flashcards

10.4 - Pregnancy, Parturition and Late Foetal Development Flashcards

1
Q

How much does the embryo grow in the first trimester?

A
  • embryo-foetal growth during the first trimester is relatively limited
  • this is because early embryo is reliant on histiotrophic nutrition
  • it is reliant on uterine gland secretions (uterine milk) and breakdown of endometrial tissues and maternal capillaries (to derive nutrients from maternal blood)
  • the syncitiotrophoblasts that invade the maternal endometrium do this breakdown to fuel embryo development
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2
Q

As we go from the first to second trimester, how does the growth rate of the embryo change?

A
  • significant increase in rate of foetal growth
  • embryo changes to haemotrophic support at start of second trimester (around 12wks gestation)
  • this means the foetus starts to derive nutrients from maternal blood
  • achieved in humans through a haemochorial-type placenta where maternal blood directly contacts the foetal membranes
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3
Q

What happens in the early implantation stage (1)? (Origins of the placenta)

A
  • syncitiotrophoblasts are invading surrounding endometrium to breakdown cells to provide nutrients to support embryo
  • uterine gland secretions
  • maternal capillary breakdown to bathe embryo in maternal blood which gives nutrients too
  • amnion - derivative of epiblast which is the first of the foetal membranes and forms amniotic cavity
  • amniotic cavity expands to become amniotic sac which surrounds and cushions foetus in 2nd and 3rd trimesters
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4
Q

What happens in the next stage of development (2), a few days later?

A
  • invasion of syncitiotrophoblasts has become more extensive
  • amnion’s amniotic cells are secreting secretions into space in the middle which will start to expand
  • yolk sac formed from hypoblast
  • chorion is another key foetal membrane - outer membrane surrounding whole conceptus unit
  • embryo unit develops connecting stalk
  • formation of trophoblastic lacunae
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5
Q

What is the connecting stalk?

A

Links developing embryo unit to the chorion

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6
Q

What are trophoblastic lacunae?

A
  • large spaces filled with maternal blood formed by breakdown of maternal capillaries and uterine glands
  • later in development, become intervillous spaces aka maternal blood spaces
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7
Q

What are foetal membranes?

A
  • extraembryonic tissues that form a tough but flexible sac encapsulating the foetus and forms the basis of the maternal-foetal interface
  • amnion - inner foetal membrane
  • chorion - outer foetal membrane
  • allantois
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8
Q

Where does the amnion come from and what does it do?

A
  • inner foetal membrane
  • arises from the epiblast - but does not contribute to the foetal tissues
  • forms a closed, avascular sac with the developing embryo at one end
  • begins to secrete amniotic fluid from 5th week - forms a fluid-filled sac that encapsulates and protects the foetus
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9
Q

Where does the chorion come from and what does it do?

A
  • outer foetal membrane
  • formed from yolk sac derivatives and the trophoblast
  • highly vascularised (unlike amnion)
  • gives rise to chorionic villi - outgrowths of cytotrophoblast from the chorion that form the basis of the foetal side of the placenta
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10
Q

What does the expansion of the amniotic sac do?

A
  • expansion of the amnion by amniotic fluid accumulation forces the amnion into contact with the chorion, which fuse to form the amniotic sac
  • amniotic sac has two layers - amnion on inside, chorion on outside
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11
Q

What are the allantois and where do they come from?

A
  • outgrowths of the yolk sac
  • grows along the connecting stalk from embryo to chorion
  • becomes coated in mesoderm and vascularises to form the umbilical cord
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12
Q

What happens in the next stage of development (3)?

A
  • cytotrophoblast forms finger-like projections through syncitiotrophoblast layer into maternal endometrium
  • these are the primary chorionic villi and are an important part of the maternal-foetal interface
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13
Q

What are the chorionic villi important for?

A
  • provide substantial surface area for exchange
  • finger-like projections of the chorionic cytotrophoblast that then undergo branching
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14
Q

What are the three phases of chorionic villi development?

A
  • primary - outgrowth of the cytotrophoblast and branching of these extensions
  • secondary - growth of the foetal mesoderm into the primary villi
  • tertiary - growth of the umbilical artery and umbilical vein into the villus mesoderm, providing vasculature
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15
Q

Describe the blood network around each villus.

A
  • there is a convoluted knot of vessels that are dilated around each villus
  • this slows down the blood flow to enable exchange between maternal and foetal blood
  • they are surrounded by maternal blood in lacunae = facilitates exchange
  • whole structure coated with trophoblast
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16
Q

How does the villus change from early to late pregnancy?

A
  • early pregnancy - 150-200um diameter, approx 10um trophoblast thickness between capillaries and maternal blood
  • late pregnancy - villi thin to 40um, vessels move within villi to leave only 1-2um trophoblast separation from maternal blood - reduced diffusion distance between maternal and foetal circulation
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17
Q

Describe the maternal blood supply to the endometrium.

A
  • uterine artery branches to give rise to a network of arcuate arteries –> radial 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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18
Q

What is spiral artery remodelling?

A
  • spiral arteries provide the maternal blood supply to the endometrium
  • 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 spiral vessels
  • conversion - turns the spiral artery into a non-spiral low pressure, high conduit for maternal blood flow to feed the maternal blood spaces
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19
Q

Describe the final placental structure.

A
  • the maternal unit is on the bottom side with the maternal blood supply made up of spiral arteries
  • the spiral arteries supply the intervillous spaces, some of which drains from the maternal vein system
  • on foetal side, we get chorionic villi formation which invade the trophoblasts, become branched and vascularised
  • foetal circulatory system invade into chorionic villi which provide large SA between maternal blood and foetal chorionic villi
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20
Q

How is oxygen exchanged across the placenta?

A

Diffusional gradient (high maternal O2 tension, low foetal O2 tension)

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21
Q

How is glucose exchanged across the placenta?

A

Facilitated diffusion by transporters on maternal side and foetal trophoblast cells

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22
Q

How is water exchanged across the placenta?

A
  • placenta is main site of exchange
  • some crosses amnion-chorion
  • majority by diffusion, though some local hydrostatic gradients
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23
Q

How are electrolytes exchanged across the placenta?

A
  • large traffic of sodium and other electrolytes across the placenta
  • combination of diffusion and active energy-dependent co-transport
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24
Q

How is calcium exchanged across the placenta?

A

Actively transported against a concentration gradient by a magnesium ATPase calcium pump

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25
Q

How are amino acids exchanged across the placenta?

A

Reduced maternal urea excretion and active transport of amino acids that make up urea to foetus where they can be used

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26
Q

How does mother’s circulation change through pregnancy?

A
  • maternal cardiac output increases 30% during first trimester (stroke volume and rate)
  • maternal peripheral resistance decreases up to 30%
  • maternal blood volume increases to 40% (near term - 20-30% increase in erythrocytes, 30-60% increase in plasma)
  • pulmonary ventilation increases by 40%
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27
Q

What is the placenta/foetus’ O2 consumption like?

A
  • placenta consumes 40-60% glucose and O2 supplied
  • but although foetal O2 tension is low, O2 content and saturation are similar to maternal blood
  • embryonic and foetal haemoglobins - greater affinity for O2 than maternal haemoglobin
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28
Q

When are organs developed in embryos?

A
  • most organ systems are completed by end of 1st trimester
  • through 2nd and 3rd trimesters the organ systems mature
29
Q

How does the circulatory system develop?

A
  • begins with a tube of mesoderm that pumps blood by around day 22 of embryo development
  • by 2nd trimester, circulatory system is pretty much complete
30
Q

How does the foetal circulatory system differ to a neonate’s?

A
  • placenta acts as the site of gas exchange for foetus
  • ventricles act in parallel rather than series around same circulatory loop
  • vascular shunts bypass pulmonary and hepatic circulations to allow heart to drive oxygenated blood from placenta with greater efficiency –> close at birth
31
Q

How does the respiratory system develop?

A
  • lungs begin as a bud around the foregut which branches in first trimester
  • branches develop further in 2nd trimester and we get primitive air sacs at 20 weeks
  • surfactant production begins around week 20 and upregulated towards term
  • vascularisation of lungs at 28 weeks
  • foetus spends 1-4h a day making rapid respiratory movements during REM sleep (practise breathing reflex for when foetus born and strengthens diaphragm)
32
Q

How does the gastrointestinal system develop?

A
  • formed from endoderm and yolk sac
  • functional pancreas from start of 2T, insulin from mid-2T
  • liver develops from 23 days and through 2T&3T
  • liver glycogen progressively deposited - accelerates towards term
  • large amounts of amniotic fluid is swallowed by foetus - debris and bile acids form meconium (first stool)
33
Q

How does the nervous system develop?

A
  • foetal movements begin late 1T, detectable by mother from 14 weeks
  • stress responses from 18 weeks, thalamus-cortex connections form by 24 weeks
  • foetus does not show conscious wakefulness - mostly in slow-wave or REM sleep
34
Q

What do we think is the cause for the final development of these organ systems closer to term?

A
  • organ maturation is coordinated by foetal corticosteroids
  • increase in foetal corticosteroids from around mid-gestation to end of term
35
Q

What is labour?

A
  • safe expulsion of the foetus at the correct time
  • expulsion of the placenta and foetal membranes
  • resolution/healing to permit future reproductive events
36
Q

What type of reaction is labour and why?

A
  • labour has the characteristics of a pro-inflammatory reaction
  • immune cell infiltration
  • inflammatory cytokine and prostaglandin secretion
37
Q

What is phase 1 - quiescence - of labour?

A
  • prelude to parturition (happens from late 3T onwards)
  • contractile unresponsiveness
  • cervical softening
38
Q

What is phase 2 - activation - of labour?

A
  • preparation for labour
  • uterine preparedness for labour
  • cervical ripening
39
Q

What is phase 3 - stimulation - of labour?

A
  • actual process of labour - characterised by the three stages of labour
  • uterine contraction
  • cervical dilation
  • foetal and placenta expulsion
40
Q

What is phase 4 - involution - of labour?

A
  • parturient recovery
  • uterine involution
  • cervical repair
  • breast feeding
41
Q

What is the first stage of labour?

A
  • contractions start
  • cervical dilation
  • latent phase - slow dilation of the cervix to 2-3cm
  • active phase - rapid dilation of the cervix to 10cm
  • extensive stage (14h), latent and active phase roughly same duration
42
Q

What is the second stage of labour?

A
  • delivery of foetus
  • commences at full dilation of the cervix (10cm)
  • maximal myometrial contractions
  • relatively quick - 2h around
43
Q

What is the third stage of labour?

A
  • delivery of the placenta
  • expulsion of placenta and foetal membranes
  • post-partum repair
  • relatively quick (1-2h)
44
Q

How long do deliveries take for a woman’s first delivery and subsequent ones?

A
  • first delivery: 8-18h
  • subsequent deliveries: 5-12h
45
Q

What role does the cervix have when the foetus is being delivered?

A
  • cervix has critical role in retaining foetus in uterus
  • due to high connective tissue content to keep cervix closed, rigid, stretch-resistant
  • achieved through bundles of collagen fibres embedded in a proteoglycan matrix
  • near the time of delivery, cervical remodelling occurs - changes to collagen bundle structure underlie softening, but mechanisms unclear
46
Q

Softening - What is the first phase of cervical remodelling?

A
  • begins in first trimester
  • measurable changes in compliance but retains cervical competence to keep foetus in uterus
47
Q

Ripening - What is the second phase of cervical remodelling?

A
  • weeks and days before birth
  • monocyte infiltration and IL-6 and IL-8 secretion
  • hyaluronan deposition
48
Q

Dilation - What is the third phase of cervical remodelling?

A
  • increased elasticity
  • increased hyaluronidase expression –> hyaluronan breakdown
  • matrix metalloproteinases decrease collagen content and increase elasticity of tissue
49
Q

Post-partum repair - What is the fourth stage of cervical remodelling?

A

Recovery of tissue integrity and competency - allows subsequent pregnancies

50
Q

What do we think is the cause of initiation of labour?

A
  • the foetus determines the timing of parturition through changes in the foetal HPA axis
  • corticotrophin releasing hormone (CRH) levels rise exponentially towards the end of pregnancy
  • decline in CRH-binding protein levels, so bioavailable CRH increases
51
Q

What do we think these rising CRH levels do in labour?

A
  • promotes foetal ACTH release from pituitary which acts on foetal adrenal cortex to release cortisol
  • this increasing cortisol drives placental production of CRH - positive feedback
  • this stimulates DHEAS production by foetal adrenal cortex - substrate for oestrogen production
52
Q

What is the importance of high progesterone through pregnancy?

A
  • made by placenta and maintains uterine relaxation
  • maintains endometrium lining
53
Q

How does the relationship between oestrogen and progesterone levels near labour change?

A

There may be a shift in serum oestrogen:progesterone ratio in favour of oestrogen

54
Q

What happens to progesterone receptors closer to labour?

A
  • as term approaches, there is a switch from progesterone receptor A (PR-A) isoforms (activating) to PR-B and PR-C isoforms (repressive) expressed in the uterus
  • this causes functional progesterone withdrawal - where the level of progesterone is still high but type of receptor has changed so it cannot act properly anymore
55
Q

What happens to oestrogen receptors closer to labour?

A

Rise in oestrogen receptor alpha expression

56
Q

What do the changes in oestrogen and progesterone receptors at labour mean?

A
  • uterus becomes ‘blinded’ (non-responsive) to progesterone action and sensitised to oestrogen action
  • control of these changes is unclear but likely leads to local changes in oestrogen:progesterone ratio in uterine tissues
57
Q

What is oxytocin?

A

A nonapeptide (9 amino acid) hormone synthesised mainly in the utero-placental tissues and pituitary

58
Q

What happens to oxytocin levels closer to labour and why?

A
  • uterine oxytocin production increases sharply at onset of labour
  • expression increase is driven by increase in oestrogen levels
  • release promoted by stretch receptors (Ferguson reflex) - as foetus bears down on cervix, stretch receptors send signals to hypothalamus which acts on posterior pituitary to release oxytocin to act on uterus and myometrium
59
Q

What does oxytocin signal through?

A
  • G-coupled oxytocin receptors (OTR/OXTR)
  • pre-labour - high progesterone inhibits OXTR expression in uterus = uterus relaxed
  • rise in oestrogen promotes large increase in uterine OXTR expression
60
Q

What are the functions of oxytocin in pregnancy?

A
  • increases connectivity of myocytes in myometrium - the myocytes form a syncytium and oxytocin promotes gap junction connections between myocytes
  • destabilise membrane potentials to lower threshold for contraction
  • enhances liberation of intracellular Ca2+ ion stores
61
Q

What are the primary prostaglandins (PGs) synthesised during labour?

A
  • PGE2 - cervix remodelling - promotes leukocyte infiltration into cervix, IL-8 release and collagen bundle remodelling
  • PGF2alpha - myometrial contractions - destabilises membrane potentials and promotes connectivity of myocytes (with oxytocin)
  • PGI2 - myometrium - promotes myometrial smooth muscle relaxation and relaxation of lower uterine segment
62
Q

How do rising oestrogen levels drive prostaglandin action in the uterus?

A
  1. rising oestrogen activates phospholipase A2 enzyme, generating more arachidonic acid for PG synthesis
  2. oestrogen stimulation of oxytocin receptor promotes PG release
63
Q

What other factors are involved in cervical remodelling?

A
  • peptide hormone relaxin
  • nitric oxide (NO)
64
Q

What is the integrated hypothesis for regulation of labour?

A
  • production of CRH by foetal pituitary which acts on foetal adrenal glands to produce cortisol
  • cortisol transferred to placenta where it triggers production of more CRH - positive feedback
  • CRH on foetal adrenal promotes DHEAS which is converted to oestrogen
  • oestrogen acts on myometrium, promoting expression of OXTR = uterus becomes sensitive to pituitary production of maternal oxytocin = triggers contractions
  • oestrogen also promotes local production of oxytocin which stimulates contraction and promotes PG production
  • PGs important for mediating myometrial contractions and helping soften/ripen cervix so dilation can occur
  • progesterone inhibits OXTR in non-labour state to stop premature contractions
65
Q

How do myometrial contractions work?

A
  • myometrial muscle cells form a syncytium (extensive gap junctions) - transmits contractions across muscle of upper segment of uterus
  • contractions start from fundus (top) and spread down upper segment
  • these contractions are brachystatic - fibres do not return to full length on relaxation
  • these contractions act to pull up the lower segment and cervix to form birth canal
66
Q

Describe how the baby emerges?

A
  • head engages with pelvic space at 34-38 weeks
  • as labour occurs, pressure on foetus from myometrial contractions causes chin to press against chest (flexion)
  • foetus then rotates so the belly faces the mother’s spine
  • head expelled first after cervix dilates
  • shoulder delivered sequentially (upper first) followed by torso
67
Q

Describe how the placenta is expulsed and repaired?

A
  • rapid shrinkage of the uterus after foetal delivery causes area of contact of placenta with endometrium to shrink
  • uterine shrinkage also causes folding of foetal membranes - peel off the endometrium
  • clamping of the umbilical cord after birth stops foetal blood flow to placenta –> villi collapse
  • haematoma forms between decidua and placenta
  • contractions expel placenta and foetal tissue
68
Q

What happens after placenta expulsion?

A
  • uterus remains contracted after delivery to facilitate uterine vessel thrombosis
  • uterine involution and cervix repair restore non-pregnant state - why is this important?
  • to shield the uterus from commensural bacteria
  • to restore endometrial cyclicity in response to reproductive hormones to allow uterus to accept another embryo if egg is fertilised

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