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1B Development & Ageing > Pregnancy, Parturition and late foetal development: > Flashcards

Pregnancy, Parturition and late foetal development: Flashcards

1
Q

how is fetus nutrition provided?

A
  • early- histiotrophic
    • reliant on uterine gland secretions and breakdown of endometrial tissues
  • switch at start of 2nd trimester- haemotrophic
    • achieved through a haemochorial- type placenta where maternal blood directly contacts the fetal membranes (chorion)
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2
Q

what are the fetal membranes

A

extraembryonic tissue that forms a tough but flexible sac

encapsulates the fetus and forms the basis of the maternal-fetal interface

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3
Q

what are the types of fetal membrane?

A

amnion (inner fetal membrane)

chorion (outer fetal membrane)

allantois

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4
Q

what is the amnion?

A

arises from the epiblast (does not contribute to the fetal tissues)

forms a closed, avascular sac with the developing embryo at one eld

begins to secrete amniotic fluid for 5th week- forms a fluid-filled sac that encapsulates and protects the fetus

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5
Q

what is the chorion

A

outer fetal membrane

  • Outer membrane surrounding conceptus unit
  • Formed from yolk sac derivatives and the trophoblast
  • Highly vascularized
  • Gives rise to chorionic villi – outgrowths of cytotrophoblast from the chorion that form the basis of the fetal side of the placenta
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6
Q

what is the allantois?

A
  • Outgrowth of the yolk sac
  • Grows along the connecting stalk from embryo to chorion
  • Becomes coated in mesoderm and vascularizes to form the umbilical cord.
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7
Q

how does the amniotic sac form?

A

Expansion of the amniotic sac by fluid accumulation forces the amnion into contact with the chorion, which fuse, forming the amniotic sac

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8
Q

what is the composition of the amniotic sac?

A

2 layers

amnion on inside

chorion on outside

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9
Q

what is the makeup of the placenta?

A
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10
Q

what are primary chorionic villi formed from?

A

cytotrophoblast

forms finger-like projections through syncytiotrophoblast layer into maternal endometrium

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11
Q

what is the use for primary chorionic villi?

A

provide substantial surface area for exchange

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12
Q

what are the phases of chorionic villi developement?

A

3 phases:

Primary: outgrowth of the cytotrophoblast and branching of these extensions

Secondary: growth of the fetal mesoderm into the primary villi

Tertiary: growth of the umbilical artery and umbilical vein into the villus mesoderm, providing vasculature.

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13
Q

what is the terminal villus microstructure?

A
  • convoluted know of vessels and vessel dilation
  • slows blood flow enabling exchange between maternal and fetal blood
  • whole structure coated with trophoblast
  • change through pregnancy
    • in late pregnancy are thinner with less trophoblast separation from maternal blood
    • this allows reduction in transfer distance later in pregnancy
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14
Q

how is maternal supplied to endometrium?

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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15
Q

what is the function of spiral arteries?

A

provide the maternal blood supply to the endometrium

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16
Q

how do spiral arteries re-model?

A
  • 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 (replace maternal endothelium/SM)
  • Conversion: turns the spiral artery into a low pressure, high capacity conduit for maternal blood flow.
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17
Q

what is the structure of the placenta?

A
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18
Q

how does oxygen transport to fetus?

A

diffusional gradient (high maternal O2, low fetal O2 tension)

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19
Q

how does glucose transfer to fetus?

A

facilitated diffusion by transporters on maternal side and fetal trophoblast cells

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20
Q

how does water transfer to fetus?

A

placenta main site of exchange

some crosses amnion-chorion

majority by diffusion, some local hydrostatic gradients

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21
Q

how do electrolytes transport to fetus?

A

large traffic of sodium and other electrolytes across the placenta

combination of diffusion and active energy dependant co-transport

22
Q

how does calcium transport to fetus?

A

actively transported across a concentration gradient by magnesium APTase calcium pump

23
Q

how do amino acids transport to fetus?

A

reduced maternal urea excretion and active transport of amino acids to fetus

24
Q

how does maternal supply change during pregnancy?

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%
25
Q

what does the placenta and fetus absorb from maternal supply?

A
  • Placenta consumes 40-60% glucose and O2 supplied
  • But 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
26
Q

how does the circulatory system mature in late fetal development

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

27
Q

how does the respiratory system develop?

A

primitive air sacs form in the lungs around 20 weeks

vascularisation from 28 weeks

surfactant production begins around week 20, upregulated towards term

fetus spends 1-4hrs/day making rapid respiratory movements during REM sleep

28
Q

how does the GI system develop in late fetal development?

A

endocrine pancreas functional from start of 2T- insulin from mid-2T

liver glycogen progressively deposited- accelerates towards term

large amounts to amniotic fluid swallowed- debris and bile acids form meconium

29
Q

how does the nervous system develop in late fetal development?

A

fetal movements begin late 1T, detectable by mother from 14 weeks

stress responses from 18 weeks, thalamus-cortex connections form by 24 weeks

fetus does not show conscious wakefulness- mostly in slow-wave or REM sleep

30
Q

what is organ maturation coordinated by?

A

fetal corticosteroids

31
Q

what is the point of 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

labour has the characteristics of pro-inflammatory reaction

32
Q

how does labour have the characteristics of pro-inflammatory reaction?

A

immune cell infiltration

inflammatory cytokine and prostaglandin secretion

33
Q

what are the phases of labour?

A

quinescence

activation

stimulation

involution

34
Q

what are the 3 stages of labor?

A
  • all occur in phase 3 of labour
  • first stage
    • contractions start
    • cervix dilated
    • latent phase (slow dilation of cervix to 2-3 cm)
    • active phase (rapid dilation of cervix to 10cm)
  • second stage
    • deliver of fetus
      • commences at full dilation of cervix
      • maximal myometrial contractions
  • third stage
    • delivery of placenta
    • expulsion of placenta and fetal membranes
    • post-partum repair
35
Q

how long does first delivery take?

A

8-18 hours

36
Q

how long do subsequent deliveries take?

A

5-12 hours

37
Q

how does the cervix change during pregnancy?

A

remodeling of cervix occurs

  • Cervix has a critical role in retaining the fetus in the uterus.
  • High connective tissue content:
    • Provides rigidity
    • Stretch resistant
  • Bundles of collagen fibres embedded in a proteo-glycan matrix
  • Changes to collagen bundle structure underlie softening, but mechanism unclear.
38
Q

how is labour initiated?

A
  • Fetus determines timing of parturition through changes in fetal HPA axis
  • CRH levels rise exponentially towards end of pregnancy
  • Decline in CRH binging protein levels, so CRH bioavailability increases
39
Q

what are the functions of CRH in labour?

A
  • promotes fetal ACTH and cortisol release
  • Increasing cortisol drives placental production of CRH -> Positive feedback!
  • stimulates DHEAS production by the fetal adrenal cortex -> substrate for estrogen production
40
Q

what are the levels of progesterone and estrogen in labour?

A
  • High progesterone through pregnancy maintains uterine relaxation
  • Serum estrogen:progesterone ratio may shift in favour of estrogen – this is unclear
  • As term approaches, switch from PR-A isoforms (activating) to PR-B and PR-C (repressive) isoforms expressed in the uterus -> functional prog. withdrawal
  • Rise in Estrogen Receptor Alpha expression
  • Uterus becomes ‘blinded’ to progesterone action and sensitized to estrogen action
  • Control of these changes unclear but likely leads to local changes in E:P ratio in uterine tissues.
41
Q

what is the role of oxytocin in labour?

A
  • NonapeHSptide (9aa) 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
  • 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
42
Q

what are the functions of oxytocin in labour?

A
  • Increases connectivity of myocytes in myometrium (syncytium)
    • Promotes formation of gap junctions to myometrium can act as a syncytium
  • Destabilise membrane potentials to lower threshold for contraction
  • Enhances liberation of intracellular Ca2+ ion stores
43
Q

what are the primary prostaglandins synthesised in labour?

A

PGE2

PGF2alpha

PGI2

44
Q

how do estrogen levels drive prostaglandin action in uterus in labour?

A
  • Rising estrogen activates phospholipase A2 enzyme, generating more arachidonic acid for PG synthesis
  • Estrogen stimulation of oxytocin receptor expression promotes PG release.
45
Q

what do prostaglandins do during labour?

A

PGE2 – cervix re-modelling

  • Promotes leukocyte infiltration into the cervix, IL-8 release and collagen bundle re-modelling

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

Other factors: peptide hormone relaxin and nitric oxide (NO) implicated in cervix re-modelling

46
Q

what is the hypothesis for the regulation of labour?

A
47
Q

how do myometrial contractions cause the formation of the birth canal?

A
  • Myometrial muscle cells form a syncytium (extensive gap junctions)
  • Contractions start from the fundus, 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
48
Q

what happens to the uterus after fetal delivery?

A

rapid shrinkage of uterus

causing area of contact of placental with endometrium to shrink

also causes folding of fetal membranes- peel off the endometrium

49
Q

what is the effects of clamping of the umbillical cord after brith?

A

stops fetal blood flow to placenta -> villi collapse

hematoma formation between decidua and plaenta

contractions expel placenta and fetal tissues

50
Q

what state does the uterus remain in after delivery?

A

contracted

to facilitate uterine vessel thrombosis

uterine involution and cervix repair restore the non-pregnant state, shielding uterus from commensural bacteria and restore endometrial cyclicity in response to hormones

51
Q

how does expulsion of the fetus occur?

A
52
Q
A

1B Development & Ageing (7 decks)

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