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Z YEAR 2 BRS Embryology > Pregnancy, Parturition and Late Fetal Development > Flashcards

Pregnancy, Parturition and Late Fetal Development Flashcards

1
Q

What is early embryo nutrition?

A

histiotrophic

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2
Q

What is the embryo also reliant on in 1st trimester?

A

on uterine gland secretions and breakdown of endometrial tissues

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3
Q

What is the support in the 2nd trimester?

A

haemotrophic support

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4
Q

How is haemotrophic support achieved in humans?

A

through a haemochorial-type placenta where maternal blood directly contacts the fetal membranes

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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 is the trophoblastic lacunae?

A
  1. Large spaces filled with maternal blood formed by breakdown of maternal capillaries and uterine glands
  2. Become intervillous spaces aka maternal blood spaces
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7
Q

What are fetal membranes?

A

extraembryonic tissues that form a tough but flexible sac encapsulates the fetus and forms the basis of the maternal-fetal interface

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8
Q

What is the amnion?

A

inner fetal membrane

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9
Q

What does the amnion arise from?

A

rom the epiblast (but does not contribute to the fetal tissues)

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10
Q

What does the amnion form?

A

closed, avascular sac with the developing embryo at one end

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11
Q

What does the amnion secrete?

A

amniotic fluid from 5th week – forms a fluid filled sac that encapsulates and protects the fetus

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12
Q

What is the chorion?

A

outer fetal membrane

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13
Q

What is the chorion formed from?

A
  • yolk sac derivatives

- the trophoblast

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14
Q

What is chorion like and what does it give rise to?

A
  1. Highly vascularized
  2. 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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15
Q

What is the allantois?

A

Outgrowth of the yolk sac

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16
Q

How does the allantois grow?

A

along the connecting stalk from embryo to chorion

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17
Q

What happens to the allantois?

A

Becomes coated in mesoderm and vascularizes to form the umbilical cord

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18
Q

How is the amniotic sac formed?

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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19
Q

What are the two layers of the amniotic sac?

A
  1. Amnion inside

2. Chorion outside

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20
Q

How are primary chorionic villi formed?

A 
Cytotrophoblast forms
finger-like projections 
through 
syncitiotrophoblast layer
into maternal
endometrium
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21
Q

What do the chorionic villi allow?

A

substantial surface area for exchange

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22
Q

What are chorionic villi?

A

finger-like extensions of the chorionic cytotrophoblast, which then undergo branching

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23
Q

What are the three phases of chorionic villi development?

A
  1. Primary: outgrowth of the cytotrophoblast and branching of these extensions
  2. Secondary: growth of the fetal mesoderm into the primary villi
  3. Tertiary: growth of the umbilical artery and umbilical vein into the villus mesoderm, providing vasculature.
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24
Q

What does the terminal villus microstructure allow?

A
  1. Convoluted knot of vessels and vessel dilation
  2. Slows blood flow enabling exchange between maternal and fetal blood
  3. Whole structure coated with trophoblast
    (missing here as capillary cast)
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25
Q

What is the terminal villus microstructure like in early pregnancy?

A
  1. 150-200µm diameter

2. approx. 10µm trophoblast thickness between capillaries and maternal blood

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26
Q

What is the terminal villus microstructure like in late pregnancy?

A
  1. villi thin to 40µm

2. vessels move within villi to leave only 1-2µm trophoblast separation from maternal blood

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27
Q

What do uterine artery branches give rise to?

A

a network of arcuate arteries

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28
Q

What branches from arcuate arteries?

A

radial arteries and branch further to form basal arteries

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29
Q

What do basal arteries form?

A

spiral arteries during menstrual cycle endometrial thickening

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30
Q

What do spiral arteries provide?

A

the maternal blood supply to the endometrium

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31
Q

What forms the endovascular EVT?

A
  1. Extra-villus trophoblast (EVT) cells coating the villi invade down into the maternal spiral arteries
  2. Endothelium and smooth muscle is broken down – EVT coats inside of vessels
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32
Q

What is conversion?

A

turns the spiral artery into a low pressure, high capacity conduit for maternal blood flo

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33
Q

How is oxygen exchanged across the placenta?

A

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

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34
Q

How is glucose exchanged across the placenta?

A

facilitated diffusion by transporters on maternal side and fetal trophoblast cells

35
Q

How is water exchanged across the placenta?

A
  1. placenta main site of exchange, though some crosses amnion-chorion
  2. majority by diffusion, though some local hydrostatic gradients
36
Q

How are electrolytes exchanged across the placenta?

A
  1. large traffic of sodium and other electrolytes across the placenta
  2. combination of diffusion and active energy-dependent co-transport
37
Q

How is calcium exchanged across the placenta?

A

actively transported against a concentration gradient by magnesium ATPase calcium pump

38
Q

How are amino acids exchanged across the placenta?

A
  1. reduced maternal urea excretion

2. active transport of amino acids to fetus

39
Q

What are the maternal changes for maternal-fetal oxygen exchange?

A
  1. Maternal cardiac output increases 30% during first trimester (stroke vol & rate)
  2. Maternal peripheral resistance decreases up to 30%
  3. Maternal blood volume increases to 40% (near term (20-30% erythrocytes, 30-60% plasma)
  4. Pulmonary ventilation increases 40%
40
Q

What are the placenta and fetus changes for maternal-fetal oxygen exchange?

A
  1. Placenta consumes 40-60% glucose and O2 supplied
  2. But although fetal O2 tension is low, O2 content and saturation are similar to maternal blood
  3. Embryonic and fetal hemoglobins: greater affinity for O2 than maternal hemoglobin
41
Q

How is the circulatory system matured in late fetal development?

A
  1. Placenta acts as site of gas exchange for fetus
  2. Ventricles act in parallel rather than series
  3. vascular shunts bypass pulmonary & hepatic circulation -> close at birth
42
Q

How is the respiratory system matured in late fetal development?

A
  1. Primitive air sacs form in lungs around 20 weeks, vascularization from 28 weeks
  2. Surfactant production begins around week 20, upregulated towards term
  3. Fetus spends 1-4h/day making rapid respiratory movements during REM sleep
43
Q

How is the gastrointestinal system matured in late fetal development?

A
  1. Endocrine pancreas functional from start of 2T, insulin from mid-2T
  2. Liver glycogen progressively deposited – accelerates towards term
  3. Large amounts of amniotic fluid swallowed –debris and bile acids form meconium
44
Q

How is the nervous system matured in late fetal development?

A
  1. Fetal movements begin late 1T, detectable by mother from ~14 weeks
  2. Stress responses from 18 weeks, thalamus-cortex connections form by 24 weeks
  3. Fetus does not show conscious wakefulness – mostly in slow-wave or REM sleep
45
Q

What does labour involve?

A
  1. Safe expulsion of the fetus at the correct time
  2. Expulsion of the placenta and fetal membranes
  3. Resolution/healing to permit future reproductive events
46
Q

What does labour have the characteristics of?

A
  • pro-inflammatory reaction
    1. Immune cell infiltration
    2. Inflammatory cytokine and prostaglandin secretion
47
Q

What happens in the first stage of labour?

A
  1. Contraction starts

2. Cervix dilates

48
Q

What happens in the latent phase in the first stage of labour?

A

slow dilation of the cervix (2-3cm)

49
Q

What happens in the active phase in the first stage of labour?

A

rapid dilation of the cervix to 10cm

50
Q

What happens in the second stage of labour?

A
  • Delivery of fetus
    1. Commences at full dilation of the cervix (10cm)
    2. Maximal myometrial contraction
51
Q

What is the third stage of labour?

A
  • Delivery of placenta
    1. Expulsion of placenta and fetal membranes
    2. Post-partum repair
52
Q

What does the cervix do?

A

critical role in retaining the fetus in the uterus

53
Q

What is the cervix made of?

A
  1. High connective tissue content:
    - Provides rigidity
    - Stretch resistant
  2. Bundles of collagen fibres embedded in a proteo-glycan matrix
  3. Changes to collagen bundle structure underlie softening, but mechanism unclear
54
Q

What are the stages in the re-modelling of the cervix?

A
  1. Softening: begins in first trimester
  2. Ripening: weeks and days before birth
  3. Dilation: increased elasticity
  4. Post-partum repair
55
Q

What happens in the softening stage?

A

Measurable changes in compliance but retains cervical competence

56
Q

What happens in ripening stage?

A
  1. Monocyte infiltration and IL-6 and IL-8 secretion

2. Hylaluron deposition

57
Q

What happens in dilation stage?

A
  1. Increased hyaluronidase expression -> HA breakdown

2. MMPs decrease collagen content

58
Q

What happen in post-partum repair?

A

Recovery of tissue integrity and competency

59
Q

What determines timing of parturition?

A

fetus determines timing of parturition through changes in fetal HPA axis

60
Q

What happens to CRH in initiation of labour?

A
  1. CRH levels rise exponentially towards the end of pregnancy
  2. Decline in CRH binding protein levels, so CRH bioavailability increases
61
Q

What are the functions of CRH in labour?

A
  1. promotes fetal ACTH and cortisol release
  2. Increasing cortisol drives placental production of CRH -> Positive feedback!
  3. stimulates DHEAS production by the fetal adrenal cortex -> substrate for estrogen production
62
Q

What does progesterone do during pregnancy?

A

High progesterone through pregnancy maintains uterine relaxation

63
Q

What happens to estrogen at labour?

A

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

64
Q

What ha[[ens to estrogen and progesterone as term approaches?

A
  1. As term approaches, switch from PR-A isoforms (activating) to PR-B and PR-C (repressive) isoforms expressed in the uterus -> functional prog. withdrawal
  2. Rise in Estrogen Receptor Alpha expression
  3. Uterus becomes ‘blinded’ to progesterone action and sensitized to estrogen action
  4. Control of these changes unclear but likely leads to local changes in E:P ratio in uterine tissues
65
Q

What is oxytocin?

A

nonapeptide (9aa) hormone synthesized mainly in the utero-placental tissues and pituitary

66
Q

When does uterine oxytocin production increase sharply?

A

at onset of labour

67
Q

How does the expression of uterine oxytocin increase?

A
  1. Expression increase is driven by increase in estrogen levels.
  2. Release promoted by stretch receptors -> Ferguson reflex
  3. Signals through G-coupled oxytocin receptor (OTR / OXTR)
68
Q

What does oestrogen and progesterone do to OXTR expression?

A
  1. Pre-labour: progesterone inhibits OXTR expression -> uterus relaxed
  2. Rise in estrogen promotes large increase in uterine OXTR expression
69
Q

What are the functions of oxytocin?

A
  1. Increases connectivity of myocytes in myometrium (syncytium)
  2. Destabilise membrane potentials to lower threshold for contraction
  3. Enhances liberation of intracellular Ca2+ ion stores
70
Q

What are the primary PGs synthesised during labour?

A

PGE2, PGF2alpha and PGI2

71
Q

What does rising estrogen levels drive prostaglandin action in the uterus?

A
  1. Rising estrogen activates phospholipase A2 enzyme, generating more arachidonic acid for PG synthesis
  2. Estrogen stimulation of oxytocin receptor expression promotes PG release
72
Q

What does PGE2 do?

A
  • cervix re-modelling

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

73
Q

What does PGF2alpha do?

A
  • myometrial contractions

- Destabilises membrane potentials and promotes connectivity of myocytes (with Oxytocin)

74
Q

What does PGI2 do?

A
  • myometrium

- Promotes myometrial smooth muscle relaxation and relaxation of lower uterine segnment

75
Q

What other factors are implicated in cervix re-modelling?

A
  • peptide hormone relaxin

- nitric oxide (NO)

76
Q

What do myometrial muscle cells form?

A

form a syncytium (extensive gap junctions)

77
Q

Where does contraction start and spread?

A

start from the fundus, spread down upper segment

78
Q

What are the muscle contraction likes? What does this form?

A
  1. muscle contractions are brachystatic –fibres do not return to full length on relaxation
  2. causes lower segment and cervix to be pulled up forming birth canal
79
Q

What is the process of fetal expulsion?

A
  1. Head engages with pelvic space 34-38 weeks
  2. Pressure on fetus causes chin to press against chest (flexion)
  3. Fetus rotates (belly to mother’s spine)
  4. Head expelled first after cervix dilates
  5. Shoulders delivered sequentially (upper first) followed by torso
80
Q

What happens to the uterus after fetal delivery?

A
  1. Rapid shrinkage of the uterus after fetal delivery causes area of contact of placenta with endometrium to shrink
  2. Uterine shrinkage also causes folding of fetal membranes – peel off the endometrium
81
Q

What does clamping of the umbilical cord form?

A

1, Clamping of the umbilical cord after birth stops fetal blood flow to placenta -> villi collapse

  1. Hematoma formation between decidua and placenta
  2. Contractions expel placenta and fetal tissues
82
Q

Why does the uterus remain contracted after delivery?

A

to facilitate uterine vessel thrombosis

83
Q

How does uterine involution and cervix repair restore non-pregnant state?

A
  1. Shielding uterus from commensural bacteria

2. Restore endometrial cyclicity in response to hormones

Z YEAR 2 BRS Embryology (10 decks)

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