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GOATED BRS > Pregnancy, parturition, late fetal dev > Flashcards

Pregnancy, parturition, late fetal dev Flashcards

1
Q

What causes the early fetal acceleration in growth and when does this occur?

A

Change in support from histiotrophic to haemotrophic(Start of 2nd trimester)

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2
Q

How is the placenta able to support the fetus?

A

Haemochorial-type placenta where maternal blood directly contacts the fetal membranes.

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3
Q

What does histiotrophic mean?

A

Reliant on uterine gland secretions and breakdown of endometrial tissues

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4
Q

What is the role of the connecting stalk

A

Links developing embryo unit to the chorion

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4
Q

What is the function of the trophoblastic lacunae?

A

Large spaces filled with maternal blood formed by breakdown of maternal capillaries and uterine glands
Become intervillous spaces aka maternal blood spaces

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5
Q
A
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6
Q

Where is amniotic fluid secreted from and what is its role?

A

Secreted from amnion
-Begins to secrete amniotic fluid from 5th week – forms a fluid filled sac that encapsulates and protects the fetus

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7
Q

What forms the umbilical cord?

A

Allantois
-Grows along the connecting stalk from embryo to chorion
Becomes coated in mesoderm and vascularizes to form the umbilical cord.

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8
Q

What forms the chorionic villi?

A

Chorion(Outer fetal membrane)
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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9
Q

What is the structure of the amniotic sac?

A

2 layers
-Amnion on inside
-Chorion on outside

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10
Q

How are primary chorionic villi formed?

A

Cytotrophoblast forms
finger-like projections
through
syncitiotrophoblast layer

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11
Q

What are the phases of chorionic villi development?

A

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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12
Q

Describe the structure of the terminal villi microstructure

A
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13
Q

Describe the blood supply to the 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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14
Q

How is the endovascular EVT formed?

A

Extra-villus trophoblast (EVT) cells coating the villi invade down into the maternal spiral arteries, forming endovascular EVT.

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15
Q

What is the purpose of spiral artery remodelling in the endometrium?

A

Conversion: turns the spiral artery into a low pressure, high capacity conduit for maternal blood flow.

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16
Q
A
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17
Q

How are amino acids transported across the placenta

A

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

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18
Q

How is O2 transported across the placenta

A

Oxygen: Diffusional gradient (high maternal O2 tension, low fetal O2 tension)

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19
Q

How is glucose transported across the placenta

A

Glucose: facilitated diffusion by transporters on maternal side and fetal trophoblast cells.

20
Q

How is water transported across the placenta

A

Water: placenta main site of exchange, though some crosses amnion-chorion. Majority by diffusion, though some local hydrostatic gradients.

21
Q

How are electrolytes transported across the placenta

A

Electrolytes: large traffic of sodium and other electrolytes across the placenta – combination of diffusion and active energy-dependent co-transport.

22
Q

How is Ca2+ transported across the placenta

A

Calcium: actively transported against a concentration gradient by magnesium ATPase calcium pump.

23
Q

How is fetal O2 saturation similar to maternal saturation when O2 tension is low?

A

Fetal Hb has a high O2 affinity

24
Q

During pregnancy what occurs to:
Maternal cardiac output
Maternal peripheral resistance
Maternal blood volume
Maternal 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%

25
Q

How does the circulatory system mature in LFD?

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

26
Q

How does the respiratory system mature in LFD?

A

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

27
Q

How does the GI system mature in LFD?

A

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

28
Q

How does the nervous system mature in LFD?

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

29
Q

What kind of reaction is similar to labour and why?

A

Pro-inflammatory reaction
Immune cell infiltration
Inflammatory cytokine and prostaglandin secretion

30
Q

What occurs in the 3 stages of labour?

A
31
Q

How does the cervix alter during pregnancy?

A
32
Q

Describe the structure of the cervix and what traits allow its function

A

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.

33
Q

What fetal hormone is thought to have an impact on labour?

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

34
Q

What is the function 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

35
Q

What hormone in pregnancy retains uterine relaxation?

A

Progesterone

36
Q

What occurs to progesterone as term approaches?

A

As term approaches: 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

37
Q

What change related to oestrogen allows a shift in oestrogen progesterone ratio near birth?

A

Uterus becomes ‘blinded’ (non-responsive) to progesterone action and sensitized to estrogen action

Control of these changes unclear but likely leads to local changes in Estrogen-to-Progesterone (E:P) ratio in uterine tissues.

38
Q

What occurs to oxytocin production near/peri labour and what drives this?

A

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

39
Q

What receptor is responsible for the increase in oxytocin levels relative to progesteron/oestrogen

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

40
Q

Give the 3 functions of oxytocin to increase contactile force

A

Increases connectivity of myocytes in myometrium (syncytium)
Destabilise membrane potentials to lower threshold for contraction
Enhances liberation of intracellular Ca2+ ion stores

41
Q

How does estrogen increase the effects of prostaglandins?

A

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

42
Q

Function of PGE2?

A

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

43
Q

Function of PGF2 alpha?

A

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

44
Q

Function of PGI2?

A

myometrium relaxation
Promotes myometrial smooth muscle relaxation and relaxation of lower uterine segnment.

45
Q

What factors apart from prostaglandins are responsible for cervix remodelling?

A

Relaxin
NO

46
Q

How does CRH control labour?

A

Fetal cortisol stimulates placental DHEAS production
-
DHEAS drives up E2, which increases OXY
-
Increased OXY drives contraction, stimulating parturition

47
Q

Describe the contractions of the uterus

A

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

Describe the expulsion of the placenta and the purpose and outcome of u-cord clamping

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

GOATED BRS (56 decks)

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