Pregnancy/ Labour Flashcards

1
Q

When is the child viable?

A

end of second trimester

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2
Q

What are the main maternal changes?

A

General changes – abdominal changes in the mother only become apparent during the 2nd trimester +

Main maternal changes:

  • Increased weight
  • Increased hormone levels
  • Increased body temperature (possibly by role of progesterone. Also, mediated by increased foetal size)
  • Increased blood clotting (protective against losing blood at delivery)
  • Decreased BP (is lowest during 2nd trimester and is why pregnant women should not stand for long)
  • Increased breast size
  • Increased vaginal mucus
  • “Morning sickness”
  • Altered brain function (due to high levels of steroids, such as progesterone)
  • Altered appetite (due to +height of fundus, stomach may be impinged and mother may need smaller meals)
  • Altered fluid balance and urination frequencey (– kidney functions change -> ~50%+ in plasma fluid volume by term)
  • Altered emotional state (due to hormone levels and can vary in people)
  • Altered joints (changes in pelvis to make connections more flexible to permit child-birth)
  • Altered immune system
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3
Q

What causes increased weight?

A

(+10-15kg) – baby, placenta, amniotic fluid, increased fluid retention, increased stores

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4
Q

How do hormone levels change?

A

hCG – peaks 1st trimester and decreases thereafter

All other hormones (progesterone, oestrogens, lactogen) – slowly increase as the pregnancy progresses

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5
Q

What is the source of progesterone?

A

progesterone antagonists -> loss of pregnancy at ALL gestational ages

Progesterone source:

  • Fertilisation -> 8 weeks’ gestation – corpus luteum source via hCG
  • 8+ weeks – placenta supplies progesterone
  • The change-over = “Luteo-placental shift”
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6
Q

What is the source ofoestrogen?

A
  • Fertilisation -> Luteo-placental shift – corpus luteum
  • 8+ weeks – complex interplay between foetal/maternal adrenals and placenta
  • Human placenta – does not express the enzymes needed to convert pregnenolone -> androgens so this occurs in foetal adrenals
  • The weak androgen produced (DHEA) is sulphated to give DHEA-S which is inactive (so female foetus is not exposed to androgens) - DHEA-S goes to the placenta to be converted to 17b-oestradiol.

*High levels of oestriol are produced by a parallel mechanism including hydroxylation of DHEA-S in foetal liver to give 16OH-DHEA-S

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7
Q

What causes low FSH and LH throughout?

A

high steroidal levels supress HPG-axis

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8
Q

What causes an altered immune system?

A
  1. Production of factors – supress the maternal immune system from the utero-placental interface. This results in a reduction of Th1 responses and increased Th2 responses
  2. Placenta expresses unusual HLA – placental HLA are almost invariant (HLA-G has 5 known sequence variants – normal HLA-A and others have millions of variants) and very simple. This is thought to identify the tissue as human but due to its simplicity, no other information is given. HLA-G can also supress some leucocytes and down-regulate maternal immune responses
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9
Q

Define the following terms:

  • conceptus
  • embryo
  • foetus
  • infant
A
  • Conceptus – everything resulting from the fertilised egg
  • Embryo – the baby up to week 8 of development
  • Foetus – the baby for the rest of pregnancy
  • Infant – applied after delivery typically
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10
Q

How does the weight of the foetus?

A
  • First trimester – 50g
  • Second trimester – 1050g – viable at 500-820g stage (21-24 weeks)
  • Third trimester – 2100g
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11
Q

What are the functions of the placenta?

A
  • Separation of blood supplies of mother and baby
  • Exchange of nutrients (maternal to foetal) and waste products (foetal to maternal)
  • Connection (or anchorage)
  • Immunoregulation – allows the maternal immune system to switch off, allowing for pregnancy
  • Biosynthesis (e.g. progesterone, oestrogens and hCG)
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12
Q

Describe the anatomy of the placenta

A
  • Primary subunit is the placental villus that has the branches - provides a large surface area for exchange between the maternal and foetal vascular systems
  • the veins contain oxygenated blood and the arteries contain deoxygenated blood as the placenta carries out a parallel function to the lungs during pregnancy

Cotyledons – the maternal surface of the placenta is sub-divided into cotyledons (30-60/placenta). Each contains one or more villi

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13
Q

Describe the development of the placenta

A
  • Day 9 post-fertilisation, the conceptus is almost completely implanted within the endometrium
  • At this stage of development, the outer layer of the conceptus is multinucleated syncytiotrophoblasts
  • These syncytiotrophoblasts contain fluid-filled lacunae
  • The underlying layer of cytotrophoblast is proliferating adjacent to the embryo
  • This is where the placenta will develop.
  • Following implantation, the cytotrophoblast proliferate into the
  • First a columnar structure forms (cytotrophoblast column), which undergoes branching (villous sprouts)
  • At the centre of each villus are mesenchymal (extra-embryonic mesoderm) cells
  • From these cells, the villus vascular system develops
  • The branching process continues through out pregnancy, giving rise to the complex branched villi
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14
Q

How does part of the placenta cut itself off from maternal blood supply?

A
  • Cytotrophoblast cells block spiral arteries in the uterus
  • They are part of the way of remodelling the arteries
  • The arteries in the uterus normally have a vascular endothelium and a smooth muscle layer
  • The ability of the spiral arteries to carry large volumes of blood is limited (due to narrowness)
  • To get enough nutrients to the baby, it is necessary for these arteries to become wider
  • Spiral artery remodelling involves loss of endothelium and smooth muscle cells
  • You end up with distended, non-vasoactive vessels – can carry large volumes of blood at low pressure
  • More nutrients can be delivered to the baby, and it can be extracted easily by the placenta
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15
Q

What is labour?

A

uterus undergoes regular coordinated contractions - fundally domianted
cervical ripening and effacement

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16
Q

What happens during labour?

A
  • cervical ripening and effacement (increasing)
  • co-ordinated myometrial contractions (increasing)
  • rupture of foetal membranes
  • delivery of infant
  • delivery of placenta
  • contraction of uterus
17
Q

What can initiate labour preterm?

A
  • intrauterine infection
  • intrauterine bleeding
  • multiple pregnancy
  • stress (maternal)
18
Q

What happens during cervical ripening?

A
  • Change from rigid to flexible structure
  • Remodelling (loss) of extracellular matrix
  • Recruitment of leukocytes (neutrophils)
  • Inflammatory process
    > Prostaglandin E2, interleukin-8
    > Local (paracrine) change in IL-8
19
Q

What happens during coordinated myometrial contractions?

A
  • Fundal dominance
  • Increased co-ordination of contractions
  • Increased power of contractions
  • Key mediators
    > Prostaglandin F2a (E2) levels increased from fetal membranes
    > Oxytocin receptor increased
    > Contraction associated proteins
20
Q

What happens during rupture f fetal membranes?

A
  • Loss of strength due to changes in amnion basement component
  • Inflammatory changes, leukocyte recruitment
    > Modest in normal labour, exacerbated in preterm labour
  • Increased levels and activity of MMPs
  • Inflammatory process in fetal membranes