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!!!!! BRS YR2 !!!!! > Age + Dev - Placentation + Pregnancy > Flashcards

Age + Dev - Placentation + Pregnancy Flashcards

1
Q

How does the embryo gain nutrition and grow in the first trimester?

A

Histiotrophic

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2
Q

What is histiotrophic support?

A

Gaining nutrients from the breakdown of endometrial tissues and uterine gland secretions for growth and development

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3
Q

Give an example of histiotrophic growth in early foetal development.

A

Synctiotrophoblasts invading maternal endometrium - this breakdown of local tissues + maternal capillaries fuels some of the embryo’s development

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4
Q

What type of support does the embryo switch to at the start of the 2nd trimester?

A

Haemotrophic support

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5
Q

What haemotrophic support?

A

Deriving nutrient directly from the maternal blood

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6
Q

Why does embryo support switch from histiotrophic to haemotrophic?

A

Needs to switch to maintain the increasing rate of growth of the embryo from 1st trimester to 2nd

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7
Q

How is haemotrophic support achieved?

A

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

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8
Q

What are trophoblastic lacunae?

A

→ Large spaces filled with maternal blood formed by breakdown of maternal capillaries + uterine glands
→ become intervillous spaces AKA maternal blood spaces

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9
Q

What are fetal membranes?

A

Extra embryonic tissues that form a tough but flexible sac encapsulates the foetus and forms the basis of the maternal-fetal interface

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10
Q

What are the 4 different fetal membranes?

A

→ Innermost = Amnion
→ Outermost = Chorion
→ Allantois
→ Yolk Sac or Umbilical Vesicle

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11
Q

What is the amnion?

A

→ Innermost fetal membrane
→ Arises from the Epiblast but doesn’t contribute to the fetal tissues
→ Forms a closed avascular sac with the developing embryo at one end
→ Begins to secret amniotic fluid around the 5th week to fill the amniotic sac

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12
Q

What is the chorion?

A

→ Outer fetal membrane
→ Firmed from yolk sac derivatives and the trophoblast
→ Highly vascularised
→ Gives rise to the chorionic Villi

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13
Q

What is the connecting stalk?

A

Links developing embryo unit to the chorion

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14
Q

What is the allantois?

A

→ Outgrowth of the yolk sac
→ Grows along the connecting stalk from embryo to chorion
→ Becomes coated in mesoderm + vascularises to form the umbilical chord

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15
Q

What is the amniotic sac?

A

→ Inner membrane = amnion
→ Outer membrane = chorion
→ Fluid filled sac formed by the production of amniotic fluid
→ Encapsulates and protects the foetus
→ Forces amnion into contact with the chorion

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16
Q

What are chorionic villi?

A

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

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17
Q

What is the main function of chorionic villi?

A

Provide substantial surface area for exchange

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18
Q

What are the 3 phases of chorionic villi development?

A

→ Primary
→ Secondary
→ Tertiary

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19
Q

What is the primary phase of chorionic growth?

A

Outgrowth of the cytotrophoblast and branching of its extensions

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20
Q

What is the secondary phase of chorionic villi growth?

A

Growth of the fetal mesoderm into the primary villi

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21
Q

What is the tertiary phase of chorionic villi growth?

A

Growth of the umbilical artery + vein into the villus mesoderm, providing vascular use

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22
Q

What is the microstructure of the terminal chorionic villus?

A

→ Convoluted knots of vessels with vessel dilation
→ Slows blood flow enabling exchange between maternal and fetal blood
→ Whole structure coated with trophoblast

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23
Q

What are the difference in terminal villus microstructure in early pregnancy and late pregnancy?

A

Villi become much thinner, vessels move within the villi to leave less trophoblast separation between maternal blood and capillaries

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24
Q

What arteries does the blood supply to the endometrium consist of?

A

→ Uterine artery give rise to network of Arcuate arteries in the myometrium
→ Arcuate arteries branch into Radial arteries
→ Radial arteries further branch into Basal arteries in the endometrium
→ Basal arteries form Spiral arteries during the menstrual cycle endometrial thickening

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25
Q

How do spiral arteries remodel to become the maternal blood supply during pregnancy?

A

→ Extra-villus trophoblasts (EVT) cells coating the villi invade down into the maternal spiral arteries, forming endo vascular EVT
→ Endothelium and smooth muscle is broken down - EVT coats the inside of vessels
→ Turns spiral artery into low pressure, high capacity conduit for maternal blood flow

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26
Q

What is the process of spiral artery remodelling in pregnancy called?

A

Conversion

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27
Q

How is oxygen exchanged across the placenta?

A

diffusional gradient (high maternal O2 tension, low O2 fatal tension

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28
Q

How is glucose exchanged across the placenta?

A

facilitated diffusion by transporters on maternal side `+ fetal trophoblast

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29
Q

How is water exchanged across the placenta?

A

→ placenta is main site of exchange, though some H2O crosses at the amnion-chorion border
→ majority is by diffusion, with some local hydrostatic gradients

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30
Q

How are electrolytes exchanged across the placenta?

A

large traffic of sodium + other electrolytes across the placenta - combo of diffusion + active energy-dependent co-transport

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31
Q

How is calcium exchanged across the placenta?

A

actively transported against a conc. gradient by magnesium ATPase calcium pump

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32
Q

How are amino acids exchanged across the placenta?

A

reduced maternal urea excretion + active transport of AAs to foetus

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33
Q

What are the maternal changes when the maternal-fetal oxygen exchange occurs`?

A

→ maternal cardiac output increase 30`% during first trimester (stroke volume & rate)
→ maternal peripheral resistance decreases up to 30%
→ maternal blood volume increases to 40%
→ pulmonary ventilation increases 40%

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34
Q

What are the fetal changes when the maternal-fetal oxygen exchange occurs`?

A

→ placenta consumes 40-60% glucose and oxygen supplied
→ fetal O2 tension is low
→ O2 content + saturation are similar to maternal blood
→ embryonic + fetal haemoglobins have a greater affinity for O2 than maternal haemoglobin’s

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35
Q

Describe how the circulatory system matures from 1st trimester to 2nd trimester.

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

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36
Q

Describe how the respiratory system matures from 1st trimester to 2nd trimester.

A

→ Primitive air sacs form in lungs around 20 weeks, vascularization from 28 weeks
→ Surfactant production begins around week 20, up-regulated towards term 2
→ Fetus spends 1-4h/day making rapid respiratory movements during

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37
Q

Describe how the gastrointestinal system mature from 1st trimester to 2nd trimester.

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

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38
Q

Describe how the nervous system mature from 1st trimester to 2nd trimester.

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

39
Q

How is feral organ maturation co-ordinated?

A

fetal corticosteroids

40
Q

What is the purpose of 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

41
Q

What are the 4 phases of pregnancy from conception to fertility restoration?

A

→ phase 1 : QUIESCENCE : prelude to parturition
→ phase 2 : ACTIVATION : preparation for labour
→ phase 3 : STIMULATION : processes of labour
→ phase 4 : INVOLUTION : parturient recovery

42
Q

What are the characteristics of Phase 1?

A

→ between conception and initiation of parturition
→ contractile, unresponsiveness
→ cervical softening

43
Q

What are the characteristics of phase 2?

A

→ between initiation of parturition and onset of labour
→ uterine preparedness for labour
→ cervical ripening

44
Q

What are the characteristics of phase 3?

A 
→ between onset of labour and delivery of conceptus
→ uterine contraction
→ cervical dilation
→ fetal and placenta expulsion
→ involves 3 stages of labour
45
Q

What are the characteristics of phase 4?

A

→ between delivery of conceptus and fertility restoration
→ uterine involution
→ cervical repair
→ breast feeding

46
Q

What type of reaction does labour share the characteristics of? Why?

A

pro-inflammatory reaction
→ immune cell infiltration
→ inflammatory cytokine + prostaglandin secretion

47
Q

What are the 3 stages of labour?

A 
1 = contractions start + cervix dilation
2 = delivery of fetus
3 = delivery of the placenta
48
Q

What can the first stage be divided into?

A

→ latent phase

→ active phase

49
Q

What is involved in the latent part of the first stage?

A

slow dilation of the cervix to 2-3cm

50
Q

What is involved in the active stage of the first stage?

A

rapid dilation of the cervix to 10cm

51
Q

What is involved in the second stage of labour?

A

→ commences at full dilation of the cervix (10cm)

→ maximal myometrial contractions

52
Q

What is involved in the third stage?

A

→ expulsion of placenta + fatal membranes

→ post-partum repair

53
Q

How long is the first delivery typically?

A

8-18 hrs

54
Q

How long are subsequent deliveries typically?

A

5-12 hrs

55
Q

What is the role of the cervix?

A

retains fetus in uterus

56
Q

What features does the cervix have in order to be able to complete 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

57
Q

What are the 4 phases of cervix remodelling?

A

→ softening
→ ripening
→ dilation
→ post-partum repair

58
Q

What is involved in the softening of the cervix?

A

→ begins in first trimester

→ measurable changes in compliance but retains cervical competence

59
Q

What is involved in the dilation of the cervix?

A

→ Increased hyaluronidase expression -> HA breakdown

→ MMPs decrease collagen content

60
Q

What is involved in the ripening of the cervix?

A

→ increased elasticity

çmonocyte infiltration and IL-6 and IL-8 secretion hylaluron deposition

61
Q

What is involved in post-partum repair?

A

recovery of tissue integrity and competency

62
Q

How does a fetus determine timing of parturition?

A

→ through changes in fetal HPA axis
→ corticosteroids-releasing hormone rise exponentially towards the end of pregnancy
→ decline in CRH binding protein levels so CRH bioavailability increases

63
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

64
Q

What is the progesterone level throughout pregnancy? Explain.

A

high progesterone = uterine relaxation

65
Q

How does the oestrogen to progesterone ratio change towards the end of the pregnancy?

A

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

66
Q

What type of hormone is oxytocin?

A

nonapeptide (9aa) hormone

67
Q

Where is oxytocin produced?

A

→ utero-placental tissues

→ pituitary

68
Q

When does uterine oxytocin production increase?

A

sharply at the onset of labour

69
Q

What is oxytocin expression driven by?

A

oestrogen levels

70
Q

What is oxytocin release promoted by?

A

stretch receptors (Ferguson reflex)

71
Q

What is the Ferguson Reflex?

A

neuroendocrine reflex in which the fetal distension of the cervix stimulates a series of neuroendocrine responses, leading to oxytocin production

72
Q

What receptors respond to oxytocin in the uterus?

A

G-coupled oxytocin receptor (OTR / OXTR)

73
Q

What inhibits the expression of OXTRs / OTRs pre-labour?

A

progesterone (keeps the uterus relaxed)

74
Q

What increases OTR / OXTR expression?

A

rise in oestrogen

75
Q

What are the functions of oxytocin during labour?

A

→ increases connectivity of myocytes in myometrium (syncytium)
→ destabilise membrane potentials to lower threshold for contraction
→ enhances liberation of intracellular Ca2+ ion stores

76
Q

What are the key effectors of labour?

A

prostaglandins

77
Q

What are the 3 primary prostaglandins synthesised during labour?

A

→ PGE2
→ PGF2-alpha
→ PGI2

78
Q

What drives prostaglandin action in uterus?

A

rising oestrogen levels

79
Q

In what 2 ways does oestrogen drive prostaglandin action in the uterus?

A

→ rising oestrogen activates phospholipase A2 enzyme = generating more arachidonic acid for PG synthesis
→ oestrogen stimulation of oxytocin receptor expression promotes prostaglandin release

80
Q

What are the functions of PGE2?

A

→ cervi xremodelling

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

81
Q

What are the functions of PGF2-alpha?

A

→ myometrial contractions

→ destabilises membrane potentials + promotes connectivity of myocytes (w/ Oxytocin)

82
Q

What are the functions of PGI2?

A

→ promotes myometrium smooth muscle relaxation

→ relaxation of lower uterine segments

83
Q

What are some other factors involved in cervix remodelling?

A

→ peptide hormone RELAXIN

→ NO - nitric oxide

84
Q

What do myometrial muscle cells form?

A

synctium (multi-nucleate cell formed from unicellular cells) with extensive gap junctions

85
Q

Where do contractions of the myometrium start? Where do they spread?

A

→ fundus

→ spread down upper segment

86
Q

How are the myometrial muscle contractions described?

A

brachystatic

→ fibres don’t return to full length on relaxation

87
Q

What do the brachystatic contractions of the myometrium form?

A

lower segment + cervix get pulled up = forms birth canal

88
Q

What happens to the uterus after fetal delivery?

A

rapid shrinkage of uterus

89
Q

What does uterus shrinkage cause?

A

→ area of contact of placenta with endometrium shrinks

→ folding of fetal membranes (they peel off the endometrium)

90
Q

What does the clamping of the umbilical cord lead to?

A

→ stops fetal blood flow to placenta

→ causes villi colapse

91
Q

What forms between the decidua and placenta after fetal delivery?

A

hematoma

92
Q

How are the placenta + fetal tissues expelled from the uterus after fetal delivery?

A

→ uterus rapidly shrinks after delivery
→ area of contact between placenta + endometrium shrinks
→ fetal membranes begin to fold + peel off the endometrium
→ hematoma forms between placenta + decidua
→ contractions expel placenta + fetal tissues

93
Q

Does the uterus contract or relax after delivery? Why?

A

→ contracted

→ to facilitate uterine vessel thrombosis

94
Q

How is the non-pregnant state of the uterus restored?

A

→ uterine involution + cervix repair
→ shielding uterus from commensurate bacteria
→ restore endometrial cyclicity in response to hormones

!!!!! BRS YR2 !!!!! (72 decks)

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