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Development & Ageing > Pregnancy, Parturition & Late Fetal Development > Flashcards

Pregnancy, Parturition & Late Fetal Development Flashcards

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1
Q

Embryo-fetal growth is limited during the first trimester. Why does this occur?

A

Nutrition is histiotrophic - reliant on uterine gland secretions and breakdown of endometrial tissues.

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2
Q

When does the change in nutrition occur?

A

Start of the 2nd trimester

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3
Q

What is the source of nutrition in the second trimester?

A

Haemotrophic - Achieved in humans through a haemochorialtype

placenta where maternal blood directly contacts the fetal membranes.

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4
Q

Why does more growth occur in the second trimester?

A

Switch in nutrition allows growth to be supported

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5
Q

What are the fetal membranes?

A

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

  • Amnion
  • Chorion
  • Allantois
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6
Q

What is the amnion?

A
  • Arises from the epiblast (but does not contribute to the fetal tissues)
  • Forms a closed, avascular sac with the developing embryo at one end
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7
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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8
Q

What is the chorion?

A
  • Formed from yolk sac derivatives and the trophoblast

- Highly vascularized

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9
Q

What does the chorion form?

A

chorionic villi – outgrowths of cytotrophoblast from the chorion that form the basis of the fetal side of the placenta

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10
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

Amniotic sac: 2 layers; amnion on the inside, chorion on the outside

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11
Q

What is the allantois?

A

The 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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12
Q

What is the role of cytotrophoblasts?

A

finger-like projections through syncytiotrophoblast layer into maternal endometrium

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13
Q

What are the chorionic villi?

A

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

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14
Q

What is the role of the chorionic villi?

A

Provides SA for exchange

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15
Q

What are the phases of chorionic 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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16
Q

Which arteries supply the endometrium?

A

Basal

Spiral

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17
Q

What is the effect of the menstrual cycle on the arteries?

A

They grow during the cycle if implantation doesn’t occur then they regress

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18
Q

What are the extra-villus trophoblasts?

A

cells coating the villi invade down into the maternal spiral arteries, forming endovascular EVT

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19
Q

What is the role of the EVT cells?

A

When the endothelium and smooth muscle is broken down – EVT coats inside of vessels

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20
Q

What is conversion?

A

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

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21
Q

How is oxygen exchanged across the placenta?

A

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

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22
Q

How is glucose exchanged across the placenta?

A

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

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23
Q

How is water exchanged across the placenta?

A

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

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24
Q

How is calcium exchanged across the placenta?

A

actively transported against a concentration gradient by magnesium ATPase calcium pump

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25
How are electrolytes exchanged across the placenta?
large traffic of sodium and other electrolytes across the placenta – combination of diffusion and active energy-dependent co-transport.
26
How are amino acids exchanged across the placenta?
reduced maternal urea excretion and active transport of amino acids to fetus
27
What maternal changes occur?
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%
28
How much oxygen and glucose does the placenta use?
40-60%
29
Where is the site of gas exchange for the fetus?
Placenta
30
What is the key difference in the ventricles in a fetus?
- **Ventricles act in parallel rather than series** - vascular shunts bypass pulmonary & hepatic circulation - Closes at birth
31
When do the air sacs form?
20 weeks
32
When does vascularization occur?
28 weeks
33
When is surfactant made?
production begins around week 20, upregulated towards term
34
When does the endocrine function of the pancreas start?
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**
35
When do fetal movements develop?
begin late 1T, detectable by mother from ~14 weeks
36
When does the stress response develop?
Stress responses from 18 weeks, thalamus-cortex connections form by 24 weeks
37
What coordinates fetal development?
Cortico-steroids
38
What is labour?
- Safe expulsion of the fetus at the correct time - Expulsion of the placenta and fetal membranes - **Resolution/healing to permit future reproductive events**
39
What are the phases of labour?
Quiescence - contractile unresponsiveness, cervical softening Activation - Uterine preparedness for labour, cervical ripening Stimulation - Uterine contraction, cervical dilation, fetal and placenta expulsion Involution - Uterine involution, cervical repair, breast feeding
40
What are the stages of labour?
1st, 2nd, 3rd
41
What occurs in 1st phase?
- Contractions start | - Cervix dilation
42
What is the latent phase?
Slow dilation of the cervix to 2-3cm
43
What is the latent phase?
Slow dilation of the cervix to 2-3cm
44
What is the rapid phase?
Rapid dilation of the cervix to 10cm
45
What is second stage?
Delivery of the fetus
46
When does second stage begin?
Full cervical dilation
47
What is third stage?
Delivery of the placenta
48
What is the role of the cervix?
Retaining the fetus in the uterus
49
How does the cervix fulfil its role?
**High connective tissue content:** Provides rigidity Stretch resistant
50
How is stretch resistance achieved in the cervix?
Bundles of collagen fibres embedded in a proteo-glycan matrix
51
What allows cervix softening?
Changes in collagen bundle structure
52
What are the phases the cervix goes through?
- Softening - change in compliance but same competence - Ripening - monocyte infiltration, IL 6 & 8 secretion, hylaluron deposition - Dilation - more hyaluronidase expression -> HA breakdown, MMPs decrease collagen content - Repair - recovery of tissue integrity & competency
53
What is the relationsip between CRH and the CRH binding protein as term approaches?
Availability of CRH is increasing as the conc^ increases and the conc^ of the binding protein decreases
54
What are the functions of CRH in labour?
- 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
55
Why are there high levels of progesterone?
Maintains uterine relaxation
56
What happens to the progesterone receptors as term approaches?
As term approaches, switch from PR-A isoforms (activating) to PR-B and PR-C (repressive) isoforms expressed in the uterus -> functional prog. withdrawal
57
What happens to the oestrogen receptors as term approaches?
Rise in their expression
58
What is oxytocin?
Nonapeptide (9aa) hormone synthesized mainly in the utero-placental tissues and pituitary.
59
What drives an increase in expression?
Oestrogen levels
60
What prompts oxytocin release?
Stretch receptors → Ferguson reflex
61
How does oxytocin signal?
G coupled oxytocin receptor OTR/OXTR
62
What is the effect of progesterone on OXTR expression?
Inhibits it keeping uterus relaxed, but rise in oestrogen leads to an increased expression of OXTR
63
What are the functions of oxytocin?
Increases connectivity of myocytes in the myometrium (syncytium) Destabilise membrane potentials to lower threshold for contraction Enhances liberation of intracellular Ca2+ ion stores
64
What are the primary prostaglandins in labour?
PGF2, PGFC2alpha, PGI2
65
How does oestrogen drive PG action?
1. **Rising estrogen activates phospholipase A2 enzyme, generating more arachidonic acid for PG synthesis** 2. **Estrogen stimulation of oxytocin receptor expression promotes PG release.**
66
What is the role of PGF2?
- Cervix re-modelling Promotes leukocyte infiltration into the cervix, IL-8 release and collagen bundle re-modelling
67
What is the role of PGF2alpha?
Myometrial contractions Destabilises membrane potentials and promotes connectivity of myocytes (with Oxytocin)
68
What is the role of PGI2?
Myometrium Promotes myometrial smooth muscle relaxation and relaxation of lower uterine segment
69
Which part of the uterus do contractions start from?
Fundus then spread down the upper segment
70
What are brachystatic contractions?
fibres do not return to full length on relaxation
71
What do brachystatic contractions allow?
Lower segment & cervix to be pulled up forming birth canal
72
What is pre-eclampsia?
Hypertensive syndrome that occurs in pregnant women after 20 weeks' gestation, consisting of new-onset, persistent hypertension with either proteinuria or evidence of systemic involvement
73
How is pre-eclampsia diagnosed?
- New onset hypertension BP >140mmHg systolic and or diastolic > 90mmHg - Occurring after 20 weeks' gestation - Reduced fetal movement and/or amniotic fluid (by US) in 30% of cases - Oedema is common → not discriminatory - Headaches ~40% - Abdominal pain ~15% - Visual disturbances, seizures & breathlessness → severe cases
74
Are there distinct forms of PE?
- Early-onset - Associated with fetal and maternal symptoms - Changes in placental structure - Late-onset
75
What maternal risk factors may pre-dispose to developing PE?
- primiparity - a condition or state in which a woman is bearing a child for the first time and/or has given birth to an offspring at one time. - BMI > 30 - Hx of PE - Increased maternal age (>40, <20) - Gestational hypertension/previous hypertension - Pre-existing conditions: diabetes, PCOS, renal disease, subfertility, autoimmune disease - Non-natural cycle IVF
76
What management options are available for women who develop PE during pregnancy?
- Monitoring upon hospital delivery - Make a plan for delivery date & method of delivery - Corticosteroids → anti-hypertensive therapy - Treat seizures with MgSO4
77
Are there preventative measures that can be taken to avoid PE from developing?
- Low-dose aspirin reduces the incidence & severity - Optimise treatment for hypertension & renal disease prior to pregnancy - Controlled weight loss & exercise in pregnancy - Particularly if BMI > 35 - Maintain calcium levels with supplements if necessary - If pre-diagnosed hypertension increase the frequency of corticosteroids
78
Are there any ongoing risks to the mother after pregnancy?
after pregnancy - should be normal after 6 weeks but are more likely to develop IHD, hypertension, more venous thrombi and stroke permanent damage to kidneys and liver; damage to lungs, pulmonary effusion, seizures

Development & Ageing (4 decks)

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