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BRS > pregnancy & parturition > Flashcards

pregnancy & parturition Flashcards

1
Q

What is early embryo nutrition like? How does it happen?

A

It is histiotrophic (from breakdown of surrounding tissue). Syncitiotrophoblasts invade maternal endometrium breaking down maternal capillaries and glands which supply uterine milk (source of nutrients for development embryo)

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2
Q

What type of nutrition do we switch to in 2nd trimester? What does this involve?

A

Switch to haemotrophic support. Fetus derives nutrients from maternal blood. Haemochorial-type placenta (maternal blood directly contacts chorion).

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3
Q

When does activation of the placenta happen?

A

12th week gestation

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4
Q

How does fetal growth change in 2nd trimester compared to 1st trimester?

A

Great increase in rate of fetal growth in 2nd trimester

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5
Q

How is the placenta made?

A
  • Syncytiotrophoblasts invade endometrium breaking down maternal capillaries.
  • Amniotic sac surrounding/cushioning fetus.
  • Chorion surrounds whole conceptus unit.
  • Embryo develops connecting stalk - part of extra-embyronic tissue that grows from embryo & connecting conceptus to chorion.
  • Trophoblastic lacunae formed (large spaces filled with maternal blood formed by breakdown of maternal capillaries & uterine glands). These become intervillous spaces (maternal blood spaces)
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6
Q

What are fetal membranes?

A

Extraembyronic tissues that form tough but flexible sac encapsulating fetus & forming basis of maternal-fetal interface

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7
Q

What is the amnion and its role?

A

Inner fetal membrnae arises from epiblast. Doesn’t contribute to fetal tissues. Forms closed, avascular sac with developing embryo at one end. From 5th week secretes amniotic fluid that forms fluid filled sac encapsulating/protecting fetus

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8
Q

What is the chorion?

A

Outer fetal membrane formed from yolk sac derivatives & trophoblasts. Highly vascularised. Gives rise to chorionic villi that form basis of fetal side of placenta.

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9
Q

What is the allantois?

A

Outgrowth of yolk sac which grows along connecting stalk from embryo to chorion, becomes coated in mesoderm & vascularises to form umbilical cord

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10
Q

How is the amniotic sac made?

A

Expansion of amniotic sac by fluid accumulation forces amnion into contact with chorion, they fuse forming amniotic sac with 2 layers (amnion inside, chorion outside)

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11
Q

What are primary chorionic villi?

A

Cytotrophoblast forms finger-like projections through syncitiotrophoblast layer into maternal endometrium. Provide area of exchange of gases and nutrients

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12
Q

What are the 3 phases in chorionic villi development?

A
  1. primary: outgrowth of cytotrophoblasts & branching of extensions 2. secondary: growth of fetal mesoderm into primary villi 3. tertiary: growth of umbilical artery & vein into villus mesoderm providing vasculature. Growth of chorionic villi into maternal blood spaces
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13
Q

What is the terminal chorionic villus microstructure like and why? How do villi change in late pregnancy compared to early pregnancy & why?

A

Convoluted knot of vessels & vessel dilation slows blood enabling exchange between maternal and fetal blood. Whole structure coated with trophoblasts and there are blood vessels coming up through villus. Early pregnancy 150-200μm villi in diameter, 10μm trophoblast thickness between capillaries and maternal blood. In late pregnancy the villi thin out to 40μm, blood vessels within villi move closer to maternal blood supply & trophoblast layer shrinks so less diffusion distance needed

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14
Q

What is the maternal blood supply to the endometrium? What happens if there is no fertilization / or if there is fertilization?

A

Uterine artery branches -> arcuate arteries –> radial arteries –> basal arteries –> spiral arteries formed during menstrual cycle endometrial thickening. If no fertilisation loss of endometrium + regression of spiral arteries. If fertilisation happens spiral arteries stabilise and provide maternal blood supply to fetus

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15
Q

What happens in spinal artery remodelling? What is the outcome?

A

Extra-villus trophoblast cells (EVT cells) coating villi invade into maternal spiral arteries forming endovascular EVT. Breaks down endothelium & smooth muscle, despiralising them and making them straight channels - from highly convoluted high pressure vessels they become low-pressure high capacity vessels for maternal blood flow

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16
Q

What is the ultimate placental structure?

A

Spiral arteries supply maternal blood spaces (intervillous spaces). On fetal side chorionic villi invade maternal blood spaces - large surface exchange interface. umbilical vein taking oxygenated nutrient-rich blood from placenta to fetus & umblicial arteries carry deoxygenated blood back to placenta.

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17
Q

How is oxygen exchanged across the placenta?

A

Diffusion (high maternal O2 - low fetal O2 tension)

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18
Q

How is glucose exchanged across the placenta?

A

Facilitated diffusion via transporters on maternal side & fetal trophoblast cells

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19
Q

How is water exchanged across the placenta and where?

A

Mainly diffusion but also local hydrostatic gradients. Placenta main site of exchange but some crosses amnion-chorion

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20
Q

How are electrolytes (eg sodium) exchanged across placenta?

A

Combination of diffusion and active energy-dependent co-transport

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21
Q

How is calcium exchanged across placenta?

A

Actively transported against concentration gradient by magnesium ATPase calcium pump

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22
Q

How are amino acids exchanged across placenta?

A

With pregnancy progression reduced excretion of urea - amino acids more efficiently utilised and transported actively across placenta to fetus

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23
Q

What maternal changes occur in order to have maternal-fetal oxygen exchange?

A

Maternal cardiac output increases by 30%, peripheral resistance decreases by 30%, maternal blood volume increases to 40% (increase in RBC and plasma volume). Pulmonary ventilation increases 40%.

24
Q

How much oxygen and glucose does the placenta consume?

A

Placenta consumes 40-60% of glucose & O2 supplied.

25
Q

What is the fetal O2 tension, O2 content & saturation, and embryonic/fetal haemoglobins like?

A

Fetal O2 tension is low but O2 content & saturation similar to maternal blood. Embryonic & fetal haemoglobins have greater affinity for O2 than maternal haemoglobins

26
Q

When are most organ systems complete? When does organ maturation happen?

A

Most organ systems complete by first trimester. Organ maturation happens in 2nd and 3rd trimesters

27
Q

What is the circulatory system like in the fetus and why?

A

Placenta site for gas exchange for fetus, not lungs. Ventricles act in parallel not series because of prescence of vascular shunts allowing bypass of pulmonary & hepatic circulation. Heart drives oxygenated blood from placenta around body well (especially to head). Vascular shunts close at birth

28
Q

What is the respiratory system like in the fetus why does the fetus spend hours per day making rapid respiratory movements doing REM sleep?

A

Lung begins as bud around foregut and branching gives lung structures. Primitive air sacs in lungs at 20weeks, vascularisation from 28wks. Surfactant production wk20, upregulated towards term. Fetus spends 1-4h daily making rapid respiratory movements during REM sleep as practice for breathing reflex once it leaves uterus

29
Q

What is the GI system like in fetus? What is the meconium?

A

Gut tube forms from endoderm with contribution of yolk sac. Endocrine pancreas functional from start of 2nd T, insulin mid-2T. Liver glycogen progressively deposited (accelerates towards term). Large amounts of amniotic fluid swallowed by fetus containing debris & bile acids form first stool (meconium) which is delivered just after birth

30
Q

What nervous system responses does the fetus have? What doesn’t it have?

A

Fetal movement begins late 1T, detectable by mother from 14wks. Stress responses from 18wks, thalamus-cortex connections form by 24 wks. Fetus doesn’t show conscious wakefulness (mostly in slow-wave or REM sleep)

31
Q

What is organ maturation coordinated by?

A

Increase in fetal corticosteroids (exponential increase). Changes in surfactant production & liver glycogen deposition increase in parallel to corticosteroid increase

32
Q

What does labour involve and what kind of process is it?

A

Safe expulsion of fetus at correct time, and expulsion of fetal membranes followed by resolution and healing for future reproductive events. Labour is pro-inflammatory reaction with extensive immune infiltration into tissues of reproductive tract & increase in inflammatory cytokine & prostaglandin secretion (for timing of labour)

33
Q

What is phase 1 of labour?

A

Quiescence - uterus quiet and not contracting but cervical changes seen

34
Q

What is phase 2 of labour?

A

Activation - some activity of uterus & further development of cervix to allow delivery

35
Q

What is phase 3 of labour?

A

Active uterine contraction - cervical dilation

36
Q

What is phase 4 of labour?

A

Involution - uterine involution, cervical repair & lactation

37
Q

What are the 3 stages of labour?

A
  • 1st stage: contractions start & cervical dilation starts. Latent phase has slow cervical dilation to 2-3cm, active phase rapid dilation to 10cm.
  • 2nd stage: delivery of fetus & intense/frequent myometrial contractions (at full cervical dilation 10cm).
  • 3rd stage: delivery of placenta & fetal membranes. Allows post-partum repair
38
Q

What is the role and structure of the cervix and why?

A

Role to retain fetus within uterus. Has high connective tissue content providing rigidity & stretch resistance. Bundles of collagen fibres embedded in proteo-glycan matrix

39
Q

What process underlies cervical softening?

A

Changes in collagen bundle structure

40
Q

What are the 4 phases of cervical remodelling?

A
  • 1st phase: cervical softening (starts in 1st trimester) with change in compliance but retains cervical competence to keep fetus inside.
  • 2nd phase: ripening (weeks/days before birth) - monocyte infiltration & IL-6/IL-8 secretion, hylauron deposition.
  • 3rd phase (dilation): increased hyaluronidase expression so breaks down hylauron. Influx of immune cells (MMP - metalloproteinases) break down collagen content increasing elasticity.
  • 4th phase: post-partum repair - recovery of tissue integrity and compliance
41
Q

What determines the timing of delivery? What increases and what decreases?

A

Timing of delivery determined by increase in corticosteroids. As we approach term exponential increase of CRH (corticotrophin releasing hormone) by fetus & decrease in CRH binding protein so CRH bioavailability increases.

42
Q

What are the functions of CRH (corticotrophin-releasing-hormone?

A
  1. promotes ACTH & cortisol release increasing cortisol and driving more placental production of CRH (positive feedback).
  2. stimulates DHEAS production by fetal adrenal cortex (substrate for greater oestrogen production by placenta)
43
Q

What happens to oestrogen and progesterone to prepare for labour?

A
  • Levels of oestrogen & prog increase steadily during pregnancy, high prog maintains uterine relaxation.
    1. As term approaches shift from PR-A isoforms (activating) to PR-B and PR-C (repressive) isoforms of progesterone receptor causing functional progesterone withdrawal (change in receptor blinds uterus to prog actions).
    2. Increase in oestrogen receptor alpha expression so uterus becomes sensitized to estrogen actions.
44
Q

Where is oxytocin made and when does it increase? What drives oxytocin increase in each place? How does it signal?

A
  • Made in pituitary and uterine placental tissues.
  • Uterine oxytocin production increases at onset of labour, driven by increase in oestrogen levels.
  • Stretch receptors in cervix signal maternal pituitary gland to release oxytocin (baby pushes on cervix). Can act back on uterus and myometrium (fergunson reflex - oxytocin causes contractions).
  • Signals through G-coupled oxytocin receptor OXTR. Pre-labour progesterone inhibits OXTR expression so uterus relaxes. Rise in oestrogen promotes large increase in uterine OXTR expression
45
Q

What are the functions of oxytocin?

A
  1. increases connectivity of myocytes in myometrium (syncytium).
  2. destabilises membrane potentials to lower threshold for contraction
  3. enhances liberation of intracellular calcium (aiding contraction)
46
Q

What are the prostaglandins made in labour? What does each prostaglandin do?

A
  • PGE2 (cervix remodelling - promotes leukocyte infiltration, IL-8 release and collagen bundle remodelling).
  • PGF2 alpha (myometrial contractions - destabilises membrane potentials & promotes connectivity of myocytes)
  • PGI2 (promotes myometrial smooth muscle relaxation & relaxation of lower uterine segment)
47
Q

What drives prostaglandin action in uterus and how?

A

Rising estrogen levels drive PG action in uterus because 1. rising oestrogen activates phospholipase A2 enzyme making more arachidonic acid for PG synthesis 2. oestrogen stimulation of oxytocin receptor expression promotes PG release

48
Q

What other factors are involved in cervix remodelling?

A

Relaxin & nitric oxide

49
Q

Summary of chemicals involved in labour?

A

CRH increase - positive feedback loop more cortisol produced. Promotes production of DHEAS (in placenta converted to oestrogen). Oestrogen increases expression of oxytocin receptor and promotes local production of oxytocin. More oxytocin & oestrogen -> more prostaglandins (cervix remodelling and myometrial contractions)

50
Q

What are myometrial contractions like in labour? Where do they occur? What do they cause?

A

Driven by fundus of uterus. Cervix dilates, lower segment of uterus passive (no contribution), upper segment of uterus contracts (myometrial muscle cells form syncytium). Contractions start in fundus & spead down upper segment to pull up cervix and dilation making space for fetus.
-Contractions are brachystatic meaning no complete relaxation of muscle fibres after each contraction. Lower segment pulled up forming birth canal

51
Q

How is the baby expelled and at what position?

A

Fetus head engages with cervix in final weeks. Pressure form contractions & head on cervix cause head flexion so fetal chin presses against chest, fetus rotates so belly at mothers spine. Head expelled first & followed by torso.

52
Q

What happens to the uterus after delivery? What does this cause?

A

Uterus shrinks down, area of contact with placenta with endometrium shrinks, folding of fetal membranes that peel off endometrium

53
Q

What does clamping umbilical cord after birth do?

A

Stops fetal blood flow to placenta (villi collapse)

54
Q

What forms between decidua & placenta and why?

A

Haematoma formation between decidua and placenta (these contractions expel placenta & fetal tissues)

55
Q

Why does uterus remain contracted after delivery?

A

To facilitate uterine vessel thrombosis

56
Q

What does uterine involution (shrinkage) & cervix repair contribute to? Why are they important processes?

A

To restore non-pregnant state.
-Important to stop commensal bacteria in reproductive tract getting into uterus and to restore endometrial cyclicity in response to hormones.

BRS (81 decks)

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