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

Pregnancy, Parturition & Late Fetal Development Flashcards

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
Q

How are electrolytes exchanged across the placenta?

A

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

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26
Q

How are amino acids exchanged across the placenta?

A

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

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27
Q

What maternal changes occur?

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%

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28
Q

How much oxygen and glucose does the placenta use?

A

40-60%

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29
Q

Where is the site of gas exchange for the fetus?

A

Placenta

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30
Q

What is the key difference in the ventricles in a fetus?

A
  • Ventricles act in parallel rather than series
    • vascular shunts bypass pulmonary & hepatic circulation
      • Closes at birth
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31
Q

When do the air sacs form?

A

20 weeks

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32
Q

When does vascularization occur?

A

28 weeks

33
Q

When is surfactant made?

A

production begins around week 20, upregulated towards term

34
Q

When does the endocrine function of the pancreas start?

A

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
Q

When do fetal movements develop?

A

begin late 1T, detectable by mother from ~14 weeks

36
Q

When does the stress response develop?

A

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

37
Q

What coordinates fetal development?

A

Cortico-steroids

38
Q

What is 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
39
Q

What are the phases of labour?

A

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
Q

What are the stages of labour?

A

1st, 2nd, 3rd

41
Q

What occurs in 1st phase?

A
  • Contractions start

- Cervix dilation

42
Q

What is the latent phase?

A

Slow dilation of the cervix to 2-3cm

43
Q

What is the latent phase?

A

Slow dilation of the cervix to 2-3cm

44
Q

What is the rapid phase?

A

Rapid dilation of the cervix to 10cm

45
Q

What is second stage?

A

Delivery of the fetus

46
Q

When does second stage begin?

A

Full cervical dilation

47
Q

What is third stage?

A

Delivery of the placenta

48
Q

What is the role of the cervix?

A

Retaining the fetus in the uterus

49
Q

How does the cervix fulfil its role?

A

High connective tissue content:

Provides rigidity

Stretch resistant

50
Q

How is stretch resistance achieved in the cervix?

A

Bundles of collagen fibres embedded in a proteo-glycan matrix

51
Q

What allows cervix softening?

A

Changes in collagen bundle structure

52
Q

What are the phases the cervix goes through?

A
  • 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
Q

What is the relationsip between CRH and the CRH binding protein as term approaches?

A

Availability of CRH is increasing as the conc^ increases and the conc^ of the binding protein decreases

54
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
55
Q

Why are there high levels of progesterone?

A

Maintains uterine relaxation

56
Q

What happens to the progesterone receptors as term approaches?

A

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
Q

What happens to the oestrogen receptors as term approaches?

A

Rise in their expression

58
Q

What is oxytocin?

A

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

59
Q

What drives an increase in expression?

A

Oestrogen levels

60
Q

What prompts oxytocin release?

A

Stretch receptors → Ferguson reflex

61
Q

How does oxytocin signal?

A

G coupled oxytocin receptor OTR/OXTR

62
Q

What is the effect of progesterone on OXTR expression?

A

Inhibits it keeping uterus relaxed, but rise in oestrogen leads to an increased expression of OXTR

63
Q

What are the functions of oxytocin?

A

Increases connectivity of myocytes in the myometrium (syncytium)

Destabilise membrane potentials to lower threshold for contraction

Enhances liberation of intracellular Ca2+ ion stores

64
Q

What are the primary prostaglandins in labour?

A

PGF2, PGFC2alpha, PGI2

65
Q

How does oestrogen drive PG action?

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.
66
Q

What is the role of PGF2?

A
  • Cervix re-modelling

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

67
Q

What is the role of PGF2alpha?

A

Myometrial contractions

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

68
Q

What is the role of PGI2?

A

Myometrium

Promotes myometrial smooth muscle relaxation and relaxation of lower uterine segment

69
Q

Which part of the uterus do contractions start from?

A

Fundus then spread down the upper segment

70
Q

What are brachystatic contractions?

A

fibres do not return to full length on relaxation

71
Q

What do brachystatic contractions allow?

A

Lower segment & cervix to be pulled up forming birth canal

72
Q

What is pre-eclampsia?

A

Hypertensive syndrome that occurs in pregnant womenafter 20 weeks’ gestation,consisting ofnew-onset, persistent hypertensionwith eitherproteinuriaor evidence ofsystemic involvement

73
Q

How is pre-eclampsia diagnosed?

A
  • 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
Q

Are there distinct forms of PE?

A
  • Early-onset
    • Associated with fetal and maternal symptoms
    • Changes in placental structure
  • Late-onset
75
Q

What maternal risk factors may pre-dispose to developing PE?

A
  • primiparity - a condition or state in which a woman is bearing a child for the first timeand/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
Q

What management options are available for women who develop PE during pregnancy?

A
  • Monitoring upon hospital delivery
  • Make a plan for delivery date & method of delivery
  • Corticosteroids → anti-hypertensive therapy
  • Treat seizures with MgSO4
77
Q

Are there preventative measures that can be taken to avoid PE from developing?

A
  • 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
Q

Are there any ongoing risks to the mother after pregnancy?

A

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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