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BIOL30001 reproductive biology > W7L1 Mon Parturition > Flashcards

W7L1 Mon Parturition Flashcards

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1
Q

Hormonal control: human chorionic gonadotropin (hCG)

A
  • produced by the placenta after implantation.
    -support the function of the CL, a temporary structure important in early pregnacy
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2
Q

Hormonal control: progesterone

A

-helps establish the placenta.
-stimulates growth of blood vessels that supply the womb and inhibits contraction of the uterus so it grow as the baby does
-strengthen pelvic wall muscle for labor

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3
Q

Role of progesterone in paturition

A
  • Maintains uterine quiescence
  • Decreases myometrial contractility
  • Regulates nitric oxide (NO) synthase, relaxin
    Inhibits
  • Gap junction formation (Connexin-43)
  • CAPs (prostaglandin synthesis, oxytocin receptor affinity)
  • Calcium mobilisation
  • Oestrogen receptor expression
  • Pro-inflammatory cytokine synthesis
    Stimulates:
  • Prostaglandin degradation
  • Source of progesterone varies between species (corpus luteum or placenta)
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4
Q

Role of relaxin in paturition

A
  • Relaxes pelvic ligaments
  • Softens cervix
  • Contributes to placental development
  • Prevents contraction of the uterus
  • Acts through nitric oxide production
    Some species it is only produced by the corpus luteum (not the placenta)
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5
Q

Hormonal control: key difference between humans and other mammals

A
  • in animals, increase in progesterone but the decrease before birth
    -in human and other species, continues increase of pregesterone
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6
Q

Hormonal control: drop in progesterone levels at parturition and the cause

A

Transition from quiescence (Phase 1) to activation (Phase 2) marked by change in ratio of oestrogen : progesterone
* In many animals, there is an abrupt withdrawal of progesterone from maternal circulation before parturition
* Caused by luteolysis (degradation of the corpus luteum) by prostaglandins

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7
Q

Hormonal control: functional progesterone withdrawal in humans

A
  • There are two progesterone receptor (PR) isoforms: PR-A and PR-B
  • PR-B inhibits oestrogen working through the ER-⍺ – this oestrogen signalling is “pro-labour”
  • Progesterone withdrawal in humans depends on the ratio of PR- A and PR-B in the myometrium
    -When progesterone starts signalling through PR-A, it inhibits PR-B, which in turn prevents the inhibition of ER-⍺
    -Oestrogen can now signal through the ER-⍺
    -Increases production of contraction-associated genes
    -Increases contractility and excitability of myometrial muscle cells
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8
Q

Hormonal control: oestrogen (phase 2)

A

Oestrogen
* Induces expression of contraction-associated protein (CAPs) receptors in myomentrium
* e.g. oxytocin receptor, prostaglandin receptors, gap junction proteins
* Makes myometrium more sensitive to CAPs
* Promotes cervical ripening

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9
Q

Key event of phase 2

A

i) Activation of uterine contractions
ii) Softening and ripening of the cervix
iii) Activation of fetal membranes

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10
Q

Phase 2: activation of uterine contraction :Myometrium

A
  • Muscular wall of the uterus
  • Increases in size during pregnancy
  • Smooth muscle cells (called myocytes)
  • Contractile machinery (actin and myosin)
    -Myometrial contractility is calcium dependent
  • Prostaglandins and oxytocin inhibit intracellular cAMP (inhibitors of Ca2+) or stimulate local release of Ca2+ ions
  • Binding of oestrogen to the oestrogen receptor (ER) triggers calcium mobilisation from internal stores in endoplasmic reticulum
  • Oestrogen receptor (ER) can also act in the nucleus to increase transcription of contraction associated protein (CAP) genes
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11
Q

gap juction between myometrium

A

-Gap junction proteins enhance connectivity between myocytes in myometrium
-Stimulation of myometrial gap junction (called connexin-43) formation enables rapid and efficient spread of electrical impulses through the uterine muscle to facilitate the strong, coordinated contractions characteristic of active labour

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12
Q

Phase 2: stage of cervix change

A
  • at the beginning of labour, the cervix has thinned
    -during labour, the cervix opens
    -at the end of the first stage of labour, the cervix is fully dilated (10cm)
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13
Q

Phase 2: Cervical changes in preparation for birth

A
  • Change in the state of collagen fibers
  • Collagen breakdown and rearrangement of fiber bundles (number and size)
  • Changes in the relative amount of GAGs (e.g. hyaluronic acid) and the capacity of the cervix to retain water
  • Dermatan sulfate (collagen fiber crosslinking)
  • Nitric oxide
  • Cytokine production called matrix metalloproteinases (MMPs) → degrades collagen
    → Enables cervical dilation (first stage of labour)
  • Largely regulated by inflammatory factors such as cytokines released from leukocytes (immune cells)
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14
Q

Immune control of pregnancy and parturition

A

-Balance between pro-inflammatory and anti-inflammatory
-At parturition, transitions from anti-inflammatory to pro-inflammatory
-activation of macrophages in the amniotic fluid
-neutrophils and macrophages infiltrate myometrium and cervix
-§ ↑PGs = myocyte calcium entry increase + myometrial contractions
§ ↑MMP = collagen breakdown + cervical ripening

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15
Q

Phase 2: Activation (preparation for labour) | fetal role

A
  • The fetus controls the onset of labour through hormonal and mechanical signals:
    i. Fetal hypothalamus-pituitary- adrenal (HPA) axis
    ii. Mechanical stretch (fetal size)
    iii. Lung maturation (shown in rodents)
    Hormonal:
  • Release of CRH (cortisol releasing hormone)
  • Source of CRH differs depending on species
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16
Q

role of cortisol

A

a) accelerates production of oestrogen
b) increases production of prostaglandins
c) helps mature fetal organs

17
Q

Phase 2 fetal role in human: activation of cortisol

A

-In humans, fetal tissues and placenta can produce and secrete corticotropin-releasing hormone (CRH) which signals to the fetal pituitary gland to bring about secretion of adrenocorticotropic hormone (ACTH)
* ACTH then acts on the fetal adrenal to make cortisol
* Maternal stress can also have an additive effect on placental CRH

18
Q

Phase 2 fetal role in sheeps

A
  • Fetal stress (space limits), leads to activation of the HPA axis to release of fetal cortisol (the stress hormone)
  • Cortisol:
  • downregulates progesterone (P4) and increase of oestrogen (E2)
    o leads to prostaglandin (PGE 2 ) production which activates the enzyme that converts progesterone to oestrogen
    o increases PGF 2a which leads to luteolysis (destruction of corpus lutem)
    – no more progesterone produced (not in humans)
  • Ratio of oestrogen:progesterone changes
  • Oestrogen leads to downstream signalling causing uterine contraction
19
Q

Phase 2: Activation (preparation for labour) | fetal role in rodent

A
  • In rodents, timing of birth controlled by events in the maternal tissues leading to luteolysis (destruction of corpus luteum) and a drop in progesterone levels
    o increases PGF 2a which leads to luteolysis
    → reduction in progesterone produced (note: not in humans)
  • Ratio of oestrogen:progesterone changes
  • Oestrogen leads to downstream signalling causing uterine contraction
  • Signal may be transduced by the mother (e.g. uterine volume), the fetus (nutrient restriction, developmental transition), or the placenta (increased fetal demand for nutrients)
20
Q

Lung maturation (shown in rodents)

A

Ø Foetal lung produces surfactant protein A (SP-A) which matures lungs + interacts with macrophages in amniotic fluid → ↑NFkB → ↑PGF2a → luteolysis + ↓P4 → labour

21
Q

Phase 2: Activation (preparation for labour) | fetal role mechanical strech factor

A
  • As the fetus(es) increases in size, there is a mechanical stretch effect
  • Nervous system detects (pressure on cervix or myometrium) and sends signals to maternal hypothalamus
  • Leads to release of oxytocin by maternal pituitary gland
  • ↑ Contractility by ↑ expression of CAP receptors (e.g. oxytocin receptor and gap junction proteins) within the uterus
  • Stretch induces pro-inflammatory cytokine production
  • Movements of the fetus → intermittent contractions
  • Faster growth and more stretch at the end of pregnancy → stronger contractions
  • Twins → more stretch → earlier birth
22
Q

Phase 2: activation in marsupials

A

-Possible that parturition occurs when the limit of placental transfer is reached
-Leads to cortisol release and the cascade of prostaglandin signalling (Mesotocin is the oxytocin equivalent in the Tammar Wallaby)

23
Q

Role of oxytocin in stage 3: stimulation

A
  • Peptide hormone Released by pituitary gland in mother
  • Receptors increase throughout pregnancy,particularly during labour (+ increased receptor sensitivity)
  • Increases intracellular calcium (Ca2+)
  • Stimulates prostaglandins (PGE2 and PGF2a ) synthesis and release from the amnion and decidua
  • Sufficient to induce contractions and birth in most vertebrates (used in labour inductions in humans)
24
Q

Role of prostagladins in phase 3: stimulation and test to see the effect

A
  • Small lipid molecules which Regulate luteolysis
  • Placenta is major source in most animals
  • Synthesised from arachidonic acid enriched in the fetal membranes (humans)
  • Can induce parturition in mammals
  • Prostaglandin gel applied to cervix via vagina can be used to induce labour in pregnant individuals
  • Studies shown that PG receptor inhibitors prolong gestation
  • Key prostaglandins (PGs) in parturition: PGE2 and PGF2a
25
Q

Phase 2+3: water breaking

A
  • Fetal membranes are the amnion and the chorion
  • Rodent models suggest that there is a weakening of membranes prior to labour
  • “Water-breaking” = rupture of the amniotic sac
  • Normally, it occurs spontaneously at term either during or at the beginning of labour
  • Caused by pressure of baby or by uterine contractions
    Pre-term premature rupture of membranes (PPROM)
  • can increase risk of prematurity and neonatal or perinatal complications
  • once the membranes are ruptured, bacteria may ascend and could lead to amnionitis or fetal infection
26
Q

The 3 stages of birth

A

-dilation of cervix
-expulsion of fetus
-after birth

27
Q

Parturition in marsupials: from uterus to pouch

A
  • Gestational period of marsupials is very short (in the uterus)
  • Kangaroos: 28 to 33 days
  • Tammar wallaby: 25 to 28 days
  • Newborns are born undeveloped, no hair, premature eyes and ears
  • Newborns crawl instinctively from the vagina to the pouch
  • They rush to a teat in the pouch and feed for 7-9 months before being able to leave the pouch and fend for itself
28
Q

Preterm Birth

A
  • Foetal stress: uteroplacental insufficiency
    § Activation of foetal HPA axis → ACTH → DHEAS converted into oestrogen → ↑myometrial OTR, PGs, MLCK, calmodulin, gap junctions → rupture of membranes
  • Maternal stress:
    § Maternal HPA axis activation → cortisol → CRH → prostaglandins → contractions/cervical change

BIOL30001 reproductive biology (33 decks)

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