Parturition and lactation Flashcards

1
Q

define partuition

A

the process of giving birth labour

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2
Q

what two anatomical elements are key from partuition and what must happen to them

A

ripening of cervix and uterine contractions

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3
Q

outline 3 stages of labour briefly

A

stage 1 - ripening of cervix and developing contraction and dilation of cervix

stage 2- cervix fully dilated strong uterine contraction baby delivered head first

stage 3- extremely strong contractions delivers placenta

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4
Q

what hormone is extremely important in stage 3 of labour delivering the placenta

A

Oxytocin ensure muscle clamps down on blood vessels to prevent hemorrhage

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5
Q

describe the 3 time frame stages that the cervix undergoes during gestation

A

quiescent is for 37 weeks, activation cervix starts to ripen and weaken a bit before labour and stimulation the cervix begins to dilate

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6
Q

why does the cervix remain closed for majority of gestation

A

because a closed cervix is essential to maintaining pregancy

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7
Q

how is the cervix ripened

A

through inflammation, cox 2 enzymes stimulate prostaglandin(PGE 2) production which activates immune response, contributes to metalloproteinases 2 and 9 breaking down collagen in cervix and immune cells and cytokines attacking cervix

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8
Q

what does cox 2 do

A

enzyme for prostaglandin production

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9
Q

what enzyme is most important for cervix ripening

A

metalloproteinases 2 and 9 breaking down the collagen in the cervix

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10
Q

what is functional progesterone hormone withdrawal

A

actual concentration of progesterone does not decrease it plateaus unlike other mammals and the cells stop being responsive to progesterone

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11
Q

whats causes inflammatory process in cervix

A

WHAT INSTIGATES THIS INFLAMMATORY PROCESS?

HORMONE CHANGES - Functional progesterone withdrawal - inflammation and influx of
immune cells, increased corticotrophin releasing hormone and oestrogen,
plus cervical distension → oxytocin → PGR (Ferguson reflex).

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12
Q

what are the clinical implications of cox 2 being increased at at term
and post partum

A

pge 2 used to ripen cervix in women who cervix is intact and not ripening

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13
Q

in the quiescent stage of gestation describe uterine contraction activity and why it is favorable to be like this

A

minimal and this is because the baby is not ready to come out yet and strong frequent contraction for 37 weeks could harm baby

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14
Q

why are there does uterine contractions begin to increase

A

in preparation for stimulation phase where their will be many strong contractions

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15
Q

describe innervation and vasculrisation of myometrium

A

lots of vessels good supply, sparsely innervated good due to pain that would be felt potentially

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16
Q

what physiological changes allow preparation of uterus myometrium for labour

A
contraction associated proteins’
induced: prostaglandin receptor
COX-2, oxytocin receptor,
gap junctions (connexins),
calcium signalling proteins and
ion channels
Myometrium primed for contraction
17
Q

for uterine contraction why is up regulation of connexons synthesis so important

A

so there is a greater conduction of electrical information between smooth muscles cells allowing for a more co-ordinated and strong contraction

18
Q

what does cervical distension caused by fetal movement do

A

Cervical distension due to fetal movement and development of uterine contractile activity also triggers
maternal oxytocin release (Fergusson reflex) and local prostaglandin production.

19
Q

what enzyme is responsible for PGE production

A

cox2

20
Q

what hormones and processes cause uterine myometrium contractility to increase

A

The initiation of these processes is likely to involve oestrogen, oxytocin, uterine stretch, inflammatory
agents, CRH, and functional progesterone withdrawal. Clinically this information has been translated
into the use of oxytocin as an agent for labour induction and augmentation.

21
Q

why is oxytocin not that useful in encouraging contractions in premature preganancy

A

because oxytocin receptors are poorly expressed as the stage due to down regulation as you do not want baby to be delivered early in non pathogenic circumstances

22
Q

pro relaxation occurs for majority of pregnancy, what characterizes this period in smooth muscle cells

A

calcium in cell is low and extremely negative resting membrane potential not excitable

23
Q

when are smooth muscle cells in uterus converted from pro relaxation to pro contraction

A
Pro-contraction pathways up-regulated in labour - Contraction in smooth muscle involved influx of
calcium through voltage gated ion channels and receptor operated channels involving the release of
inositol trisphosphate (IP3) which amplifies the response by releasing calcium from the SR
24
Q

what drug can be used to inhibit uterine contraction and delay labour

A

nifediprine calium voltage gate inhibitior

25
Q

during pregancy what happens to resting membrane potential of myometrium

A

becomes more and more positive from -75 to -45

26
Q

prior to labour what receptor increases its protein synthesis and why

A

oxytocin so it is ready to respond

27
Q

how does ethnicity affect when a child is born

A

slight variation of timing of birth with white ethnicties taking slightly longer

28
Q

what is the normal time for a fetus to be born

A

between 37-41 weeks

29
Q

why do babies in uk never exceed gestation of more than 42 weeks

A

medical intervention at this point

30
Q

why are babies born between 37-41 weeks normally

A

because mother cant support growth of baby anymore, ageing placenta , balanced against fetus maturation size and ability to survive in environment makes 37-41 weeks ideal for birth

31
Q

why do pregnancy with multiple children twins triplets tend to give birth earlier

A

increased amniotic fluid, increased stretch and distension, two placentas

32
Q

what are the four main theories about what causes regulates timing of labour in humans

A

Several related hypotheses:
1. Placental CRH production is key driver
2. Fetal HPA, cortisol and PGE2
plus a drive for estrogen production (from dehydroepi-androsterone sulphate, DHEAS) plays a key
role,
3. Functional progesterone withdrawal, and
4. Fetal maturation (fetal lung) initiates surfactant
production which stimulates inflammatory response in uterine tissues, this increases cytokine output
and suppresses progesterone transcription events and favours pro-contraction gene regulation

33
Q

outline this theory about Fetal HPA, cortisol and PGE2 and its role in pregnancy timing

A

fetus hpa axis develops and secretes crh, causes acth release which causes cortisol release in mother acting on uterus promoting inflammation and pge 2

34
Q

when are female breast capable of producing milk

A

from about 16 weeks of pregnancy but they don’t at this stage

35
Q

why do females only lactate after pregnancy though the breast have been ready since 16 weeks

A

inhibited by progesterone and estrogen which decrease in conc after removal of placenta

36
Q

prolactin hormone conc after pregnancy drops is this normal

A

yes it was initially high because of inhibition by progesterone and estrogen, but it will rise with suckling

37
Q

why is suckling so important even with no milk delivery

A

Prolactin concentrations also
drop, but there is a steady maintained plateau after pregnancy as long as there is suckling. Without
suckling, prolactin remains at lower levels for a few weeks - milk production, but scant. Suckling
ensures that prolactin production is maintained and that full lactogeneisis can occur.

38
Q

How does suckling ensure milk production?

A

Neuroendocrine reflex, suckling induces an impulse via the spinal cord and brain stem to stimulate
vasoactive intestinal peptide (VIP) production from the paraventricular nucleus in the hypothalamus.
This induces prolactin synthesis in the anterior pituitary and release into the maternal circulation.
Suckling also suppresses dopamine production (dopamine inhibits prolactin production) therefore
increasing prolactin release. The strength and duration of suckling will determine the subsequent level
of prolactin production.

39
Q

How does this milk get to the baby’s mouth

A

Suckling again
stimulates this milk ejection reflex. Suckling signals via the spinal cord and brain stem to the
hypothalamus. Suckling stimulates the supraoptic and paraventricular neurones to produce oxytocin
production and stimulate oxytocin release into the maternal circulation. The oxytocin stimulated the
myoepithelial cells that surround the alveoli lobules storing the milk. The cells contract, pushing milk
into the ducts and increasing intra-mammary pressure (let down reflex) enabling the suckling infant
to draw the milk out through the nipple