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BRS 2 > development and ageing > Flashcards

development and ageing Flashcards

1
Q

how is development related to cancer?

A

usual processes: proliferation, apoptosis, migration, responsiveness to local signals and neighbouring cells

unrestrained processes underpin cancer pathophysiology

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2
Q

how is development related to common/ chronic diseases?

A

potential opportunities for tissue repair

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3
Q

what is the Barker hypothesis?

A

impact of the uterine environment ‘programmes’ foetus for postnatal life

e.g. low birth weight or premature birth associated with risk of cardiovascular disease in adulthood

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4
Q

what are some stressors that affect the uterine environment?

A

endocrine (cortisol)

nutritional (e.g. high fat low protein)

extrinsic toxicants (e.g. smoking)

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5
Q

how do stressors in the uterine environment affect health across the life course?

A

epigenetic modification – heritable changes to the DNA which do not alter the sequence of bases (i.e. genes are switched on and off)

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6
Q

how is child development charted (0-5 years)?

A

gross motor control

fine motor control

cognitive development

language development

social and emotional development

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7
Q

where does fertilisation occur?

A

fallopian tube

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8
Q

what does fertilisation trigger?

A

cortical reaction

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9
Q

what does the release of molecules from cortical granules cause?

A

degrade Zona Pellucida (e.g. ZP2 and 3)

therefore prevents further sperm binding (no receptors)

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10
Q

how does the conceptus develop?

A

continues to divide as it moves down fallopian tube to uterus (3-4 days)

receives nutrients from uterine secretions

free-living phase can last for 9-10 days

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11
Q

what is the attachment phase of implantation?

A

outer trophoblast cells contact uterine surface epithelium

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12
Q

what is the decidualisation phase of implantation?

A

changes in underlying uterine stromal tissue within a few hours of attachment phase

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13
Q

what hormonal change does implantation require?

A

progesterone domination in the presence of oestrogen

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14
Q

what is the function of leukaemia inhibitory factor (LIF) (and interleukin-11 (IL11)) in the attachment phase of implantation?

A

stimulates adhesion of blastocyst to endometrial cells

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15
Q

where are leukaemia inhibitory factor (LIF) and interleukin-11 (IL11) released from?

A

endometrial cells

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16
Q

what endometrial changes occur due to progesterone during the decidualisation phase of implantation?

A

glandular epithelial secretion

glycogen accumulation in stromal cell cytoplasm

growth of capillaries

increased vascular permeability (leads to oedema)

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17
Q

what factors are involved in the decidualisation phase of implantation?

A

interleukin-11 (IL11)

histamine

certain prostaglandins

TGFb (promotes angiogenesis)

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18
Q

how is time divided in embryo-foetal development?

A

fertilisation/conceptual age

gestational age

carnegie stage

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19
Q

when is fertilisation/conceptual age measured from?

A

time of fertilization (assumed to be +1 day from last ovulation)

difficult to know time of fertilization exactly (unless IVF)

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20
Q

when is gestational age calculated from?

A

beginning of last menstrual period (LMP)

determined by fertilization date (+14 days) if known, or early obstetric ultrasound and comparison to embryo size charts

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21
Q

how is the carnegie stage divided up?

A

23 stages of embryo development based on embryo features not time

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22
Q

what does the carnegie stage allow?

A

comparison of developmental rates between species

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23
Q

how long is the carnegie stage?

A

0-60 days fertilization age in humans

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24
Q

what 2 stages of embryo-foetal development make up the first trimester of pregnancy?

A

embryogenic stage

embryonic stage

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25
Q

how long does the embryogenic stage last?

A

14-16 days post-fertilization

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26
Q

what happens during the embryogenic stage?

A

establishing the early embryo from the fertilized oocyte

determining two populations of cells:

  • pluripotent embryonic cells
  • extraembryonic cells
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27
Q

what do pluripotent embryonic cells contribute to?

A

foetus

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28
Q

what do extraembryonic cells contribute to?

A

support structures (e.g. placenta)

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29
Q

how long does the embryonic stage last?

A

16-50 days post-fertilisation

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30
Q

what 2 things happen during the embryonic stage?

A

establishment of the germ layers and differentiation of tissue types

establishment of the body plan

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31
Q

what stage of embryo-foetal development makes up the second and third trimester of pregnancy?

A

foetal stage

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32
Q

how long does the foetal stage last?

A

~8 - ~38 weeks

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33
Q

what happens during the foetal stage?

A

major organ systems now present

migration of some organ systems to final location

extensive growth and acquisition of foetal viability (survival outside the womb)

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34
Q

how does the ovulated oocyte develop after fertilisation?

A

zygote (1 cell, fertilised)

cleavage stage embryos (2-8 cells)

morula (16+ cells)

blastocyst (200-300 cells)

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35
Q

when does maternal-to-zygotic transition happen?

A

4-8 cell stage

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36
Q

what 3 things happen during maternal-to-zygotic transition?

A

transcription of embryonic genes (zygotic genome activation)

increased protein synthesis

organelle maturation
(mitochondria, Golgi)

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37
Q

what does the embryo depend on during the first divisions?

A

maternal mRNAs and proteins synthesized and stored during oocyte development (i.e. pre-ovulation)

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38
Q

what can impair embryonic development (impacts first divisions specifically)?

A

failure to synthesise, store or interpret maternal mRNAs and proteins during oogenesis

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39
Q

what starts the formation of the first two cell types?

A

compaction

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40
Q

what 5 changes occur during the 8 cell stage or later?

A

outer cells become pressed against zona (compaction)

change from spherical to wedge-shaped

outer cells connect to each other through tight gap junctions and desmosomes

forms barrier to diffusion between inner and outer embryo

outer cells become polarised

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41
Q

what are the 2 distinct cell populations in a compacted morula?

A

inner

outer

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42
Q

how are the inner and outer cells of the morula change over time?

A

reorganisation with formation of blastocoel cavity (blastocyst)

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43
Q

what is the zona pellucida?

A

hard protein shell inhibiting polyspermy

protects early embryo

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44
Q

what is the blastocoel?

A

fluid-filled cavity formed
osmotically by
trophoblast pumping
Na+ ions into cavity

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45
Q

what makes up the inner cell mass of a blastocyst?

A

pluripotent embryonic cells (contribute to final organism)

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46
Q

what is the trophoectoderm?

A

(outer cells)

extra-embryonic cells (contribute to extraembryonic structures that support development)

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47
Q

what process must occur for implantation to take place?

A

hatching (day 5-6)

blastocyst must escape zona pellucida

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48
Q

how does hatching occur for the blastocyst to escape the zona pellucida?

A

enzymatic digestion

cellular contractions

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49
Q

what 2 lineages are produced from the inner cell mass of the blastocyst during peri-implantation events (day 7-9)?

A

epiblast (from which the foetal tissues will be derived)

hypoblast (forms yolk sac - extraembryonic structure)

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50
Q

what 2 lineages are produced from the trophoectoderm of the blastocyst during peri-implantation events (day 7-9)?

A

cytotrophoblast

syncitiotrophoblast

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51
Q

why do cytotrophoblast cells remain individual?

A

provide source of syncitiotrophoblast cells

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52
Q

how does the separation of the trophoectoderm aid implantation?

A

trophoblast cells fuse to form syncitiotrophoblast

syncitiotrophoblast invasion destroys local maternal cells in endometrium

creates interface between embryo and maternal blood supply

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53
Q

what is the final stage before gastrulation?

A

bilaminar embryonic disc formation

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54
Q

what hormone is secreted by syncitiotrophoblasts?

A

hCG

detection of beta hCG subunit in blood/urine is basis of pregnancy testing

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55
Q

how is the bilaminar embryonic disc formed?

A

some cells become separated from the epiblast by the formation of a new cavity (amniotic cavity)

two-layer disc of epiblast and hypoblast remains sandwiched between cavities (blastocoel and amniotic cavity)

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56
Q

what do amnion cells contribute to?

A

extra-embryonic membranes

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57
Q

what is gastrulation (day 15-16)?

A

bilaminar embryonic disc reorganised to form trilaminar disc

layers formed are precursors to foetus organs

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58
Q

what occurs during gastrulation?

A

thickened structure forms along midline of epiblast near caudal end of bilaminar embryonic disc (primitive streak)

primitive streak expands at cranial end to create primitive node containing circular depression (primitive pit)

primitive pit continues along primitive streak towards caudal end to form primitive groove

cells from epiblast migrate inwards towards primitive streak, detach and slip beneath into interior of embryo (invagination)

invaginating cells invade hypoblast and eventually fully displace cells - forms definitive endoderm

remaining epiblast cells = ectoderm (most distal layer)

invaginated epiblast cells remain in between endoderm and ectoderm (forms mesoderm)

epiblast cells no longer migrate towards primitive streak

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59
Q

what does the primitive streak define?

A

cranial and caudal ends

left and right sides of embryo

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60
Q

which direction does gastrulation occur in?

A

cranial to caudal end

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61
Q

which organs are formed from the endoderm?

A

GI tract

liver

pancreas

lung

thyroid

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62
Q

which organs are formed from the ectoderm?

A

CNS and neural crest

skin epithelia

tooth enamel

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63
Q

which organs are formed from the mesoderm?

A

blood (endothelial cells, red and white blood cells)

muscle (smooth, skeletal and cardiac)

gonads, kidneys and adrenal cortex

bone, cartilage

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64
Q

what is the function of the notochord?

A

acts as a key organizing centre for neurulation and mesoderm development

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65
Q

what is the notochord?

A

rod-like tube structure formed of cartilage-like cells

forms along the embryo midline, under the ectoderm (opposite direction to primitive streak)

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66
Q

what occurs during neurulation?

A

notochord signals direct neural plate ectoderm to invaginate forming neural groove

creates two ridges (neural folds) running along cranio-caudal axis

neural crest cells specified in neural folds

neural folds move together over neural groove, fuse to form hollow tube

neural tube overlaid with epidermis (ectoderm)

migration of neural crest cells from folds

neural tube closure

  • head end day 23 (closure at head end precedes formation of brain structures)
  • tail end day 27
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67
Q

what is anencephaly?

A

absence of most of the skull and brain

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68
Q

what causes anencephaly?

A

failure of neural tube closure at head end

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69
Q

what is spina bifida?

A

open neural tube at birth (usually lower spine - failure to close neural tube at tail end))

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70
Q

what is neurulation?

A

formation of neural tube and CNS

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71
Q

how do neural crest cells contribute to development?

A

ectoderm-derived

plastic and migrate extensively during development to form various structures

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72
Q

what structures are formed from cranial neural crest cells?

A

cranial neurones

glia

lower jaw

middle ear bones (ossicles)

facial cartilage

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73
Q

what structures are formed from cardiac neural crest cells?

A

aortic arch/pulmonary artery septum

large artery wall musculoconnective tissue

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74
Q

what structures are formed from trunk neural crest cells?

A

dorsal root ganglia

sympathetic ganglia

adrenal medulla

aortic nerve clusters

melanocytes

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75
Q

what structures are formed from vagral and sacral neural crest cells?

A

parasympathetic ganglia

enteric nervous system ganglia

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76
Q

what are some defects that can arise as a result of neural crest migration/specification defects?

A

pigmentation disorders

deafness

cardiac defects

facial defects

failure to innervate gut

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77
Q

what is somitogenesis?

A

segmentation of body axis

formation of somites

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78
Q

what are somites?

A

arise from paired blocks of paraxial mesoderm flanking the neural tube and notochord

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79
Q

what occurs during somitogenesis?

A

blocks of paraxial mesoderm condense and bud off in somite pairs (one of each pair either side of the neural tube)

rate of ‘budding’ or appearance of somite pairs is species-specific, as is the number of pairs
(humans 1 pair/90 min, 44 pairs)

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80
Q

what direction does somitogenesis take place in?

A

commences at the head end

progresses down the long axis of the embryo

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81
Q

what are the 2 forms of embryonic tissue initially derived from somites?

A

sclerotome

dermomyotome

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82
Q

what does the sclerotome give rise to?

A

vertebrae, rib cartilage

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83
Q

the dermomyotome is subdivided into what 2 forms of embryonic tissue?

A

dermatome

myotome

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84
Q

what does the dermatome give rise to?

A

dermis of the skin

some fat

connective tissues of neck and trunk

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85
Q

what does the myotome give rise to?

A

muscles of the embryo

86
Q

what 2 types of folding in the embryo give rise to the primitive gut (day 16+)?

A

ventral folding (head and tail ends curl together)

lateral folding (2 sides of embryo roll)

87
Q

how does folding form the primitive gut?

A

pinches off part of yolk sac to form primitive gut

patterned into foregut, midgut and hindgut

88
Q

what structures are derived from the foregut?

A

oesophagus

stomach

upper duodenum

liver

gallbladder

pancreas

89
Q

what structures are derived from the midgut?

A

lower duodenum and remainder of small intestine

ascending colon

first two-thirds of transverse colon

90
Q

what structures are derived from the hindgut?

A

last third of the transverse colon

descending colon

rectum and upper anal canal

91
Q

what are the notable stages of the development of the heart?

A

begins as tube of mesoderm (~ day 19)

beating and pumping blood commences ~ day 22

foetal heartbeat detectable from ~6 weeks gestational age

92
Q

what are the notable stages of the development of the lungs?

A

arise from the lung bud, and endodermal structure adjacent to the foregut (4th week of development)

lung bud splits into two at the end of the 4th week, progressively branches through development

93
Q

what are the notable stages of the development of the gonads in XY embryos?

A

forms from mesoderm as bipotential (i.e. not committed to testis or ovary) structures known as gonadal/genital ridges

presence of SRY gene on Y chromosome directs gonadal cells to become Sertoli cells

triggers testis development, Leydig cell formation and testosterone production

94
Q

what are the notable stages of the development of the gonads in XX embryos?

A

forms from mesoderm as bipotential (i.e. not committed to testis or ovary) structures known as gonadal/genital ridges

absence of SRY leads to gonadal cells adopting a granulosa cell fate and ovary development

requires reinforcement by FOXL2

95
Q

what is likely to be the major driver of early pregnancy loss?

A

aneuploidy

exponential increase in risk of trisomic pregnancy with increasing maternal age

96
Q

why does increasing maternal age increase risk of miscarriage?

A

loss of cohesion between homologous chromosomes in oocyte with increasing age

loss of proteins (cohesins) holding homologues together

97
Q

how is recurrent miscarriage defined?

A

loss of 3+ consecutive pregnancies

98
Q

how is recurrent implantation failure defined?

A

3 failed IVF attempts with good quality embryos

99
Q

what is the key difference between recurrent miscarriage and recurrent implantation failure?

A

failure to implant or sustain pregnancy by natural conception vs. failure of transferred embryo to implant/sustain pregnancy (RIF)

100
Q

what is the initial diagnostic approach for recurrent miscarriage and recurrent implementation failure?

A

check for uterine anatomical defects or presence of fibroids/polyps that might disrupt implantation

determine presence of auto-immune antibodies (anti-nuclear, anti-phospholipid antibodies)

test for paternal DNA sperm integrity/fragmentation?

101
Q

what signalling pathways may underpin recurrent miscarriage or recurrent implementation failure?

A

LIF - leukaemia inhibitory factor (cytokine) promotes decidualisation of human endometrial stromal cells in culture

normal embryo development but failed implantation in LIF-deficient mouse models

reduced LIF in uterine secretions of subfertile women

102
Q

what is endometrial scratching?

A

use of pipette or hysteroscope to damage endometrial mucosa before embryo transfer in IVF

103
Q

what is thought to be the benefit of endometrial scratching?

A

thought to stimulate immune cell infiltration and wound healing cytokine production

104
Q

is endometrial scratching effective?

A

some studies suggest no benefit

possible benefit in selected group (e.g. recurrent implementation failure)

105
Q

what are some adaptations of the fallopian tube that aid function?

A

smooth muscle – contractions drive embryo along fallopian tube

epithelium coated in cilia (microvilli) -promote fluid movement

106
Q

how does smoking impact the fallopian tube and therefore pregnancy?

A

cotinine (component of cigarette smoke) regulates PROKR1 expression - regulator of fallopian tube smooth muscle contractility

cotinine increases expression of pro-apoptotic proteins in fallopian tube explants

tobacco smoke inhibits ciliary function - reducing transit of the embryo through the tube

increased risk for tubal pregnancy in smokers

107
Q

how does cannabis impact the fallopian tube and therefore pregnancy?

A

fallopian tube expresses CB1 and CB2 cannabinoid receptors

CB1 reduced in ectopic pregnancy patients, and CB1 KO in mice causes embryo retention in the fallopian tubes

levels of endocannabinoids elevated in ectopic pregnancy fallopian tubes

some components (e.g. THC) disrupt embryo environment by acting directly on the fallopian tube to:

  • perturb transit
  • alter balance of endocannabinoids (‘endocannabinoid tone’)
108
Q

what is foetal growth acceleration associated with?

A

changes in support

growth relatively limited during 1st trimester, increases after 2nd trimester

109
Q

what kind of support is present during the first trimester/early embryo?

A

histiotrophic

reliant on uterine gland secretions and breakdown of endometrial tissues

110
Q

what kind of support begins at the beginning of the 2nd trimester?

A

haemotrophic

achieved in humans through a haemochorial-type placenta - maternal blood directly contacts the foetal membranes

111
Q

what are the 2 key foetal membranes that lead to formation of the placenta?

A

chorion

amnion

112
Q

what is the connecting stalk?

A

links developing embryo unit to the chorion

113
Q

what are the trophoblastic lacunae?

A

large spaces filled with maternal blood

114
Q

how are trophoblastic lacunae formed?

A

breakdown of maternal capillaries and uterine glands

115
Q

what do trophoblastic lacunae develop into?

A

intervillous spaces

aka maternal blood spaces

116
Q

what are the foetal membranes?

A

extraembryonic tissues

form tough, flexible sac encapsulating foetus

forms basis of the maternal-foetal interface

117
Q

what is the function of the amnion?

A

arises from epiblast (does not contribute to foetal tissues)

forms closed, avascular sac with the developing embryo at one end

begins to secrete amniotic fluid from 5th week – forms a fluid filled sac to encapsulate and protect foetus

118
Q

what is the function of the chorion?

A

formed from yolk sac derivatives and the trophoblast

highly vascularized

gives rise to chorionic villi – outgrowths of cytotrophoblast from the chorion that form the basis of the foetal side of the placenta

119
Q

what is the allantois?

A

grows along the connecting stalk from embryo to chorion

becomes coated in mesoderm, vascularizes to form umbilical cord

120
Q

how is the amniotic sac formed?

A

expansion of the amniotic sac by fluid accumulation forces the amnion into contact with the chorion, which fuse, forming the amniotic sac

2 layers; amnion inside, chorion outside

121
Q

what are the primary chorionic villi?

A 
cytotrophoblast forms
finger-like projections 
through 
syncitiotrophoblast layer
into maternal
endometrium (surface area for exchange)

undergo branching

122
Q

what occurs during the primary phase of chorionic villi development?

A

outgrowth of the cytotrophoblast

branching of these extensions

123
Q

what occurs during the secondary phase of chorionic villi development?

A

growth of foetal mesoderm into the primary villi

124
Q

what occurs during the tertiary phase of chorionic villi development?

A

growth of the umbilical artery and umbilical vein into the villus mesoderm, providing vasculature

125
Q

how can terminal villus microstructure be described?

A

convoluted knot of vessels and vessel dilation

structure coated with trophoblast

126
Q

how does terminal villus microstructure change between early and late pregnancy?

A

early pregnancy: wider diameter, more trophoblast thickness between capillaries and maternal blood

late pregnancy: villi thin, vessels move within villi to leave minimal trophoblast separation from maternal blood

127
Q

how does maternal blood supply to the endometrium develop?

A

uterine artery branches give rise to a network of arcuate arteries

arcuate arteries branch into radial arteries

radial arteries branch further to form basal arteries

basal arteries form spiral arteries during menstrual cycle endometrial thickening

128
Q

how does implantation affect spiral arteries?

A

spiral arteries stabilised

provide maternal blood supply to foetus

129
Q

how does lack of implantation affect spiral arteries?

A

loss of endometrium

regression of spiral arteries

130
Q

when happens to spiral arteries during implantation and placental development?

A

extensive remodelling

131
Q

how are spiral arteries remodelled during implantation and placental development?

A

extra-villus trophoblast (EVT) cells coating villi invade down into the maternal spiral arteries

outgrowth of trophoblast - grow into spiral arteries

forms endovascular EVT

132
Q

what is the role of endovascular EVT (extra-villus trophoblast)?

A

replace maternal endothelium of blood vessels

133
Q

how does endovascular EVT (extra-villus trophoblast) form a new endothelial layer (conversion)?

A

breaks down maternal endothelium and underlying smooth muscle

134
Q

why is conversion important during placental development?

A

replacement of endothelium causes conversion of spiral arteries into relatively straight arteries

results in low pressure, high capacity conduit for maternal blood flow

135
Q

what conditions may conversion underly?

A

pre-eclampsia

uterine growth retardation

136
Q

how can the structure of the placenta be described?

A

maternal unit - maternal arteries give rise to spiral arteries, supply intervillous spaces (lacunae) with blood (some drained through venous system)

foetal unit - formation of chorionic villi, trophoblast invades branch and become vascularised

invasion of foetal circulatory system into chorionic villi provides surface for exchange

137
Q

what are the 3 different ways that substances cross the placenta?

A

simple diffusion

facilitated diffusion (through formation of concentration gradients or via transporter proteins)

active transport (blood flow or energy dependent co-transporters)

138
Q

how does oxygen cross the placenta?

A

simple diffusion - high maternal oxygen tension and low foetal oxygen tension causes diffusional gradient

139
Q

how does glucose cross the placenta?

A

facilitated diffusion - via transporters on maternal side and foetal trophoblast cells

140
Q

how does water cross the placenta?

A

majority via diffusion

some local hydrostatic gradients

(placenta is main site of exchange but some crosses amnion-chorion)

141
Q

how do electrolytes cross the placenta?

A

large traffic of sodium and other electrolytes across placenta

combination of diffusion and active energy-dependent co-transport

142
Q

how does calcium cross the placenta?

A

active transport against concentration gradient by magnesium ATPase calcium pump

143
Q

how do amino acids cross the placenta?

A

reduced urea excretion as pregnancy progresses

active transport of amino acids across placenta

144
Q

what physiological changes occur maternally in maternal-foetal oxygen exchange?

A

cardiac output increases 30% during first trimester (increased rate and stroke volume)

peripheral resistance decreases up to 30%

blood volume increases to 40% near term - increase in erythrocytes, increased plasma volume (20-30% erythrocytes, 30-60% plasma)

pulmonary ventilation increases 40%

145
Q

what physiological changes occur in the placenta and foetus in maternal-foetal oxygen exchange?

A

placenta itself consumes 40-60% glucose and oxygen supplied

although foetal oxygen tension is low, oxygen content and saturation are similar to maternal blood.

embryonic and foetal haemoglobins: greater affinity for oxygen than maternal haemoglobin

146
Q

how does the circulatory system act in late foetal development?

A

placenta acts as site of gas exchange (not lungs)

ventricles act in parallel, not in series (blood driven around same circulatory loop)

147
Q

how can ventricles act in parallel rather than in series during late foetal development?

A

vascular shunts allow circulatory system to bypass pulmonary and hepatic circulation

permits heart to drive oxygenated blood from placenta around body more efficiently - delivers nutrients and gas supply, especially to the head

shunts close at birth to give standard circulatory system

148
Q

how does the respiratory system act in late foetal development?

A

lungs begin as a bud around foregut - branches during first trimester to give lung structure

primitive air sacs form around week 20, vascularised from week 28

surfactant produced around week 20 - upregulated towards term

foetus spends 1-4 hours a day making rapid respiratory movements during REM periods

149
Q

why may the foetus spend 1-4 hours a day making rapid respiratory movements during REM periods?

A

within amniotic sac - lungs are not site of gas exchange

probably practice for breathing reflex once leaving the uterus

may be important for diaphragm development

150
Q

how does the gastrointestinal system act in late foetal development?

A

gut tube formed in early embryo development from endoderm and some contribution from yolk sac

second trimester - functional endocrine pancreas, secretes insulin from mid pregnancy

liver progressively develops, glycogen progressively deposited (accelerates towards term)

151
Q

how is the first stool after birth (meconium) produced?

A

foetus inhales and swallows large amounts of amniotic fluid in utero

debris from fluid, bile acids and cells sloughing from inside of developing intestine form the meconium

152
Q

how does the nervous system act in late foetal development?

A

movements begin late in first trimester, detectable by mother from ~week 14

stress responses present from week 18 but thalamus-cortex connections only present from week 24 (sensory inputs probably only processed from mid-pregnancy onwards)

no conscious wakefulness - mostly in slow-wave or REM sleep

153
Q

how is organ maturation co-ordinated?

A

increase in foetal corticosteroid towards end of pregnancy

triggers production of surfactant from lungs, deposition of liver glycogen etc. (increases in parallel with corticosteroid)

154
Q

what are the 3 aims of labour?

A

safe expulsion of foetus at correct time

expulsion of placenta and foetal membranes (empty for future reproductive events)

uterus has gone through extensive tissue remodelling and distension - resolution and healing period needed to ensure uterus is suitable for future pregnancy

155
Q

what are the 2 characteristics of a pro-inflammatory reaction that can be seen in labour?

A

immune cell infiltration into tissues of reproductive tract

inflammatory cytokine and prostaglandin secretion (probably to orchestrate timing and sequence of events during labour)

156
Q

what occurs during the first phase of labour? (quiescence)

A

prelude to parturition

uterus not contracting but some cervical changes (cervical softening)

late first trimester onwards

157
Q

what occurs during the second phase of labour? (activation)

A

preparation for labour

preparing uterus for labour, cervical ripening (ready to dilate to allow delivery)

158
Q

what occurs during the third phase of labour? (stimulation)

A

processes of labour

3 stages: uterine contraction, cervical dilation, expulsion of foetus and placenta

159
Q

what occurs during the fourth phase of labour? (involution)

A

parturient recovery

restoration of uterus to original size (involution), cervical repair, onset of lactation

160
Q

what happens during the first stage of labour (during stimulation)?

A

contractions begin, cervical dilation

latent phase - slow dilation of cervix to 2-3 cm

active phase - rapid dilation of cervix to 10cm

161
Q

what happens during the second stage of labour (during stimulation)?

A

delivery of foetus

begins at full dilation of cervix (10cm)

intense and frequent myometrial contractions

162
Q

what happens during the third stage of labour (during stimulation)?

A

delivery of placenta

expulsion of placenta and foetal membranes

allows onset of postpartum repair

163
Q

how long is the entire delivery process?

A

8-18 hours (first delivery)
5-12 hours (subsequent deliveries)

0-8 hrs - latent stage 1

8-14 hrs - active stage 1 (equal parts acceleration, maximum slope and deceleration)

14-16 hrs - stage 2

16+ hrs - stage 3

164
Q

what is the role of the cervix during pregancy?

A

retains foetus within uterus

165
Q

what features of the cervix allow it to carry out its function?

A

high connective tissue content

keeps cervix closed - provides rigidity, stretch resistant

properties caused by collagen fibres embedded in proteoglycan matrix - changes to collagen bundle underlie softening (exact mechanism unclear)

166
Q

what happens during the first phase of cervical remodelling? (softening)

A

begins in first trimester

changes in compliance (less stretch resistant)

retains cervical competence (cervix remains closed, keeps foetus inside uterus)

167
Q

what happens during the second phase of cervical remodelling? (ripening)

A

weeks and days before birth

monocyte infiltration, IL-6 and IL-8 secretion

extensive immune cell infiltration of cervix (macrophages, neutrophils)

hyaluron deposition

168
Q

what happens during the third phase of cervical remodelling? (dilation)

A

increased elasticity (cervix needs to open up to allow transit of foetus)

increased hyaluronidase expression - breaks down hyaluron (deposited during ripening phase)

influx of immune cells leads to production of matrix metalloproteinases (collagen breakdown, allows increased tissue elasticity)

169
Q

what happens during the fourth phase of cervical remodelling? (post-partum repair)

A

recovery of tissue integrity and competency

170
Q

how does the foetus determine the time of parturition according to current thinking?

A

changes in foetal HPA axis

corticotrophin-releasing hormone (CRH) levels rise exponentially towards end of pregnancy

concomitant decline in CRH binding proteins increases CRH bioavailability

171
Q

what is the function of corticotrophin-releasing hormone (CRH) during labour)?

A

increased CRH levels act on foetal adrenal cortex - promotes foetal ACTH and cortisol release

increased cortisol drives placental CRH production (positive feedback)

CRH stimulates dehydroepiandrosterone sulphate (DHEAS) production by foetal adrenal cortex - substrate for increased placental oestrogen production

172
Q

how do oestrogen and progesterone change during pregnancy?

A

both concentrations increase during pregnancy (oestrogen : progesterone ratio may shift in favour of oestrogen in association with onset of labour, unclear)

173
Q

what is the function of progesterone in pregnancy?

A

maintains pregnancy

maintains uterine relaxation until labour

174
Q

what is progesterone produced by?

A

placenta

175
Q

how does progesterone signalling change as term approaches?

A

switch in progesterone receptors

moves from PR-A isoform (activating) expression in uterus to PR-B and PR-C isoforms (repressive)

causes functional progesterone withdrawal

176
Q

what is the effect of functional progesterone withdrawal on oestrogen?

A

rise in oestrogen receptor expression within uterine tissues

although both progesterone and oestrogen levels stay high, uterus becomes ‘blinded’ to progesterone action and sensitised to oestrogen action

causes local shift in oestrogen : progesterone ratio in uterine tissue

177
Q

what kind of hormone is oxytocin?

A

nonapeptide (9aa)

178
Q

where is oxytocin synthesised?

A

predominantly in pituitary

also mainly in utero-placental tissues

179
Q

what is increased oxytocin release driven by?

A

sharp increase in uterine oxytocin production at onset of labour

expression promoted by increased oestrogen levels

Ferguson reflex for main production of oxytocin from maternal pituitary

180
Q

what is the Ferguson reflex?

A

neuroendocrine stretch reflex to promote oxytocin release

stretch receptors in cervix and vagina signal hypothalamus

firing of hypothalamus onto posterior pituitary triggers release of oxytocin from pituitary into maternal circulation

181
Q

by what method does oxytocin signal?

A

through G-protein coupled oxytocin receptor (OTR/OXTR)

progesterone inhibits OXTR expression pre-labour (for uterus relaxation)

rise in oestrogen near term promotes increased OXTR expression

182
Q

what are the functions of oxytocin?

A

increased connectivity of myocytes in myometrium (promotes formation of extensive gap junctions, myometrium can act as syncytium)

destabilise membrane potentials, lower threshold for contraction

enhance liberation of intracellular Ca2+ stores (aid contraction)

183
Q

oxytocin acts in conjunction with what key effectors of labour?

A

prostaglandins

PGE₂, PGF₂ alpha, PGI₂: primary prostaglandins synthesised during labour

184
Q

how do rising oestrogen levels affect prostaglandins in the uterus?

A

drives synthesis during labour

increased oestrogen activates phospholipase A2 enzyme, generates arachidonic acid for prostaglandin synthesis

oestrogen stimulation of oxytocin receptor (OXTR) expression promotes some prostaglandin release through oxytocin signalling

185
Q

what is the primary function of PGE₂ during pregnancy?

A

cervix remodelling

promotes leukocyte infiltration into cervix, IL-8 release - allows remodelling of collagen bundles and therefore cervix ripening

186
Q

what is the primary function of PGF₂ alpha during pregnancy?

A

acts on myometrium to promote contraction

destabilises membrane potential, promotes connectivity of myocytes (with oxytocin)

187
Q

what is the primary function of PGI₂ during pregnancy?

A

acts on myometrium

promotes smooth muscle relaxation, relaxation of lower uterine segment

relaxation allows blood flow into uterus and placenta for foetus

188
Q

what factors (other than prostaglandins) are implicated in cervix remodelling?

A

peptide hormone relaxin (levels increase sharply towards term)

nitric oxide (NO)

189
Q

how can an integrated hypothesis for the endocrine regulation of labour be described?

A

production of CRH (corticotrophin releasing hormone) by foetal pituitary acts on foetal adrenal gland to produce cortisol and DHEAS

cortisol transferred to placenta - triggers increased CRH production (positive feedback)

DHEAS converted to oestrogen in placenta

oestrogen acts on myometrium to promote oxytocin receptor expression in uterus (previously inhibited by progesterone)

uterus sensitised to maternal pituitary oxytocin - triggers contraction

oestrogen promotes local production of oxytocin - oxytocin stimulates contraction, promotes placental prostaglandin production

prostaglandins (e.g. PGF₂ alpha) mediate contractions, soften cervix, stimulate placenta to produce more prostaglandins (positive feedback)

(in non-labouring state - prostaglandins inhibit oxytocin receptors to prevent premature contraction - positive feedback)

190
Q

how can the uterus be divided up into functional segments?

A

fundus (top of uterus) (active)

upper segment (active)

lower segment (passive)

cervix (passive)

191
Q

how do myometrial contractions take place?

A

myometrial muscle in fundus and upper segment form syncytium (extensive gap junctions) so contractions can be transmitted across whole muscle

contractions start in the fundus, spread down upper segment (active contraction)

lower segment and cervix pulled upwards (passive contraction)

formation of larger, open birth canal

192
Q

what characteristic of myometrial contractions aids formation of the birth canal?

A

brachystatic contraction - muscle fibres do not return to full length upon relaxation (retain some shortening)

therefore each contraction progressively opens cervix and lower segment more until full dilation

193
Q

what are the stages of foetal delivery?

A

foetus head engages with pelvic space/cervix 34-38 weeks (final weeks of pregnancy)

onset of labour - myometrial contractions puts pressure on foetus, causing flexion (chin pressed against chest)

foetus rotates (stomach faces mother’s spine)

head expelled first after full cervical dilation

sequential delivery of shoulders (upper shoulder first), followed by torso

194
Q

what is the process of placental expulsion?

A

rapid shrinkage of uterus after foetal delivery causes:

  • shrinkage of area of contact between placenta and endometrium
  • folding of foetal membranes, causing them to peel off the endometrium

clamping umbilical cord stops foetal blood flow to placenta, causing villi to collapse

haematoma formation between decidua and placenta triggered

myometrial contractions expel placenta and foetal tissues

195
Q

how does uterine repair happen?

A

uterus remains contracted after placental delivery - facilitates thrombosis and healing of uterine vessels (prevents intrauterine bleeding)

eventual involution of uterus and repair of cervix to restore non-pregnant state

196
Q

why is restoration of the uterus important?

A

shields uterus from commensal bacteria in reproductive tract

restore endometrial cyclicity in response to hormones (ready to allow future embryo implantation)

197
Q

when does a mother’s emotional state have a long lasting effect on a child?

A

during pregnancy

early postnatal period

(can have as many symptoms of depression and anxiety during pregnancy as postnatally)

198
Q

why may pregnancy cause strain when expecting?

A

increased domestic abuse

increased relationship strain

199
Q

what is foetal programming?

A

concept that environment of the womb during different sensitive periods for specific outcomes (e.g. caused by mother’s emotional state) affects development of foetus and potentially all the way through to adulthood

200
Q

how can foetal programming be counteracted?

A

sensitive early mothering

helps attachment

counteracts some of what happens in utero

201
Q

how can the foetal brain be considered “under construction” and how does this continue during its lifetime?

A

250 000 neurons a minute through gestation

proliferation - 5 weeks gestation to 18 months after birth

(migration, differentiation, synaptogenesis)

neural pruning - continues through puberty

202
Q

what are some types of prenatal stress reportedly associated with increased risk of changes in a child’s cognitive development and behaviour?

A

(not just extreme/toxic stress, diagnosed mental illness)

maternal anxiety and depression

maternal daily hassles

pregnancy specific anxiety

domestic abuse; partner or family discord (lack of support too)

distress caused by war

experience of acute disasters, e.g. freezing ice storm, hurricane or 9/11

203
Q

what are some neurological/emotional conditions for which risk is increased by associated prenatal stress?

A

increased levels of anxiety, depression

behavioural issues - ADHD, conduct disorder

impaired cognitive development

neonatal behaviour

more difficult infant temperament

victimisation in childhood (are bullied)

schizophrenia (only very severe stress in first trimester)

autism spectrum

personality disorder

204
Q

why may schizophrenia be caused by stress in the first trimester?

A

altered pattern of migration of neurones during first trimester - gestation period affected

205
Q

what are some physical conditions for which risk is increased by associated prenatal stress?

A

reduced birthweight and gestational age

preterm delivery

mixed handedness

decreased telomere length (decreased longevity)

asthma

altered immune function

altered microbiome (in meconium)

206
Q

how can we tell that there is a causal relationship between the womb environment and later events (rather than genetic or postnatal factors?

A

animal studies - research literature shows direct effects, translatable to humans

effects of natural disasters - children all affected (no possibility of genetic transmission, children were all exposed to same event)

studies allow for confounders

underlying mechanisms (investigation)

207
Q

what is an example of a study investigating the effects of the uterine environment?

A

ALSPAC (Avon Longitudinal Study of Parents and Children)

large prospective birth cohort (~14 000 pregnant women recruited 1990-1991)

complete data obtained n=~7000

208
Q

what did ALSPAC show?

A

top 15% of most anxious/depressed women in pregnancy - rate of probable mental disorder doubled (6 to 12%) at 13 years

(after multivariate analysis allowing for a wide range of possible confounders)

attributable load of probable mental disorder in whole population due to prenatal anxiety/depression
~10%

209
Q

why are some children affected by womb environment and not others?

A

gene-environment interactions

different genetic predispositions
- e.g. COMT gene inactivate catecholamines (dopamine, adrenaline, noradrenaline), some COMT variations mean more vulnerability to anxiety in conjunction with womb environment

210
Q

what is the underlying mechanism behind maternal stress affecting uterine environments?

A

maternal stress, anxiety, mental illness triggers increased levels of cortisol, pro-inflammatory cytokines

transplacental passage of cortisol affects foetus

211
Q

how does the foetus control levels of cortisol received from the mother?

A

foeto-placental unit rich in placental 11beta-HSD2 enzyme (convers cortisol to cortisone)

(more anxious mothers have lower 11beta-HSD2 expression - significant correlation with state of anxiety, trend with depression)

212
Q

how does stress affect how much cortisol moves from a mother to the foetus?

A

stress downregulates 11beta-HSD2

more cortisol moves across placenta to foetus

BRS 2 (10 decks)

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