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Flashcards in Pregnancy and labour Deck (60)
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1

What are the trimesters of pregnancy defined by?

Defined by experience, not science

  1. 1st = 0-13 weeks
  • If you make it past the 1st trimester than the pregnancy is 90-95% likely to successfully continue to term
  1. 2nd = 13-26 weeks
  2. 3rd = 26-39
  • 26 weeks represents the earliest absolute limit of viability 
  • Modern medicine can push this limit to 22/23 weeks

2

How common are miscarriages?

  • Most common in the 1st trimester, its estimated 30-60% of pregnancies never survive to the 2nd trimester
  • In total its estimated nearly half of all pregnancies miscarraige

 

3

What does 'term' mean?

  • Normally refers to 280 duration of pregnancy (40 weeks)
  • Term = 37-41 weeks of pregnancy
  • Before this is pre-term
  • After this is post-term

4

What is the defined time course of pregnancy

Pregnancy = the first day of the last menstrual period to the day of delivery

5

What maternal changes in pregnancy are directional?

  • Increased weight
  • Increased blood clotting tendency
  • Increased basal body temperature
  • Increased breast size
  • Increased vaginal mucus production
  • Increased nausea and vomiting (‘morning sickness’)
  • Decreased blood pressure

6

What maternal changes in pregnancy are non-directional?

  • Altered brain function 
  • Altered hormones 
  • Altered appetite (quantity and quality) 
  • Altered fluid balance
  • Altered emotional state 
  • Altered joints 
  • Altered immune system 

7

Why do mothers crave certain foods?

  • If the baby is lacking something it will override the mothers need for it and take up all the mothers nutrient stores
  • The mother than craves foods high in those nutrients to provide for the baby and restore her own levels
  • E.g. iron levels when the baby is producing RBCs

8

Why do the mothers joints change in pregnancy?

They become more flexible in preparation for having to expand the pelvic girdle when giving birth.

9

When does the mother increase weight in pregnancy and why does this happen?

  • In the 2nd and (mainly) 3rd trimesters
  • Usually 10-15 kg.
  • This will include the weight of the fetus, amniotic fluid and placenta; increased fluid retention; increased nutritional stores (to feed the baby after delivery).

10

How do maternal hormone levels change in pregnancy?

  • HCG peaks in the 1st trimester at aprox 8 weeks then declines
  • Progesterone, oestrogens and placental lactogen increase throughout pregnancy and only decline once the placenta has been delivered

11

What is the significance of the high levels of progesterone and oestrogens in pregnancy?

  1. Progesterone is the key hormone in allowing the pregnancy to continue.
  • Low progesterone levels, or administration of a progesterone antagonist, will lead to loss of the pregnancy at all gestational ages.
  1. High levels of steroid hormones (progesterone and oestrogens) suppress the HPG axis 
  • Results in very low levels of LH and FSH throughout pregnancy, and hence no cyclic ovarian or uterine functions.

12

Define:

conceptus

embryo

fetus

infant

  • Conceptus – everything resulting from the fertilised egg (baby, placenta, fetal membranes, umbilical cord)
  • Embryo – the baby before it is clearly human
  • Fetus – the baby for the rest of pregnancy
  • Infant – less precise, normally applied after delivery

13

Where does the progesterone in pregnancy come from?

  1. From Fertilisation to 8 weeks gestation, the corpus luteum is the main source of progesterone
  • This production is sustained by hCG 
  • From about 6 weeks of gestational age, the corpus luteum gradually produces less progesterone despite the very high hCG levels
  • by about 9 weeks it has ceased to make steroids.
  1. The placenta also produced progesterone relative to its size as it grows during pregnancy
  • by 10 weeks of gestation, the placenta is the source of all progesterone.
  1. This change in the source of progesterone to sustain pregnancy is the ‘luteo-placental shift’.

14

When does the mother increase blood clotting tendency in pregnancy and why does this happen?

  • starts early in pregnancy, and is greatest at term
  • protective against losing too much blood at delivery,
  • May also be important for interactions between the placenta and maternal blood throughout pregnancy

15

What is the severe form of 'morning sickness' called?

hyperemesis gravidarum

16

What is thought to cause morning sickness and why?

  • hCG
  • Morning sickness worse in 1st trimester at aprox 8 weeks and declines in the 2nd trimester
  • This is the same pattern of hCG levels

17

Why is eating pattern changed during the latter stages of pregnancy?

  • As the size of the uterus increases during the later stages of pregnancy, it imposes steadily increasing pressures on the gastro-intestinal system, including the stomach.
  • This can decrease the distensibility of the stomach, and in late pregnancy the mother may need to have up to 6 smaller meals per day, rather than 3 bigger meals.

18

Why does urinary fucntion change in pregnancy?

  • Urinary frequency increases during the first trimester of pregnancy, generally normalises during the second trimester, and increases again in the third trimester.
  • The changes in the first trimester are generally thought to be due to changes in the maternal hormones, regulating altered kidney function.
  • By the third trimester, the greatly enlarged uterus will be exerting pressure on the bladder, decreasing the maximum size and volume of urine it can contain, so the mother will pass smaller volumes of urine more frequently.

19

why does kidney function change during pregnancy?

  • To increase fluid retention for a higher plasma volume.
  • By the end of pregnancy, maternal blood volume is ~50% higher than before pregnancy.

20

What is thought to be the cause of altered brain function and mood in pregnancy?

Increased levels of steroid hormones

21

What systems prevent the fetus from being rejected by the immune system?

  1. a number of factors that can suppress the maternal immune system are produced at the utero-placental interface.
  • decreasing the Th1 responses
  • increasing the Th2 system.
  1. HLA-G is expressed on the maternal side of the placenta
  • HLA-G has five known sequence variants so is almost invariant compared to most HLAs
  • It is very simplistic - shows the tissue as being human but not whether it is self or non-self, therefore the immune system doesn't attack it as its not non-self
  • can suppress the activity of some leukocytes
  • and can down-regulate the maternal immune system within the uterus.

22

How are oestogens produced during pregnancy?

  • Before the luteo-placental shift they're produced in the corpus luteum
  • After this there is a complex interaction between fetal and maternal adrenals, fetal liver and the placenta
  • The placenta doesn't express the CYP 17A1 enzyme that converts pregnenolone to androgens, so this part of biosynthesis takes place in the fetal adrenals
  • The weak androgen produced (dehydroepiandrosterone, DHEA) is sulphated as well to give DHEA-S, which is inactive.
  • Hence a female fetus is not exposed to any androgens during development.
  • The DHEA-S circulates to the placenta, where it is converted to 17beta-oestradiol.

23

What are the last 4 organ systems to develop?

  • the lungs,
  • the digestive system,
  • the immune system
  •  the brain.

24

When is the fetus at greatest risk in pregnancy?

  • 1st trimester is most vulnerable e.g to teratogens
  • 2nd trimester has little risks
  • 3rd trimester risks are the delivery itself

25

Before the umbilical cord develops, where does the embryo get its nutrients from?

Secretions of the fallopian tubes

26

What are the function of the placenta?

  1. Exchange of nutrients and waste material
  2. Anchorage
  3. Separation (of maternal and fetal vascular systems)
  4. Biosynthesis (2nd only to the liver)
  5. Immunoregulation

27

How do we know the placenta and not the uterus is the key to pregnancy?

  • Ectopic pregnancies (implantation at sites other than the uterus) can survive to term.
  • No pregnancy without a placenta is viable

28

What are the functional subunits of the placenta?

  • Cotyledon on the maternal side
  • Each cotyledon contains one or more placental vill

 

29

What is different about the umbilical blood supply?

Named relative to the fetal heart

2 umbilical arteries carrying deoxygenated blood away from the fetus

1 umbilical vein carrying oxygenated blood from the maternal blood supply to the fetus

30

What are the functions of the placental villi?

  1. Villi have large surface area for exchange between fetal and maternal blood supplies
  2. Anchors the placenta (and hence the baby) securely - no anchorage = miscarriage in 1st trimester

31

When does the conceptus implant and what does it implant into?

9 days post fertilisation

maternal decidualising endometrium

32

How does the placenta develop?

  • At implantation, there exists an outer layer of syncytiotrophoblasts containing fluid-filled lacuna
  • The underlying layer of cytotrophoblast is proliferating adjacent to the embryo: this is where the placenta will develop.
  • the cytotrophoblast proliferate into the syncytium
  • first a columnar structure is formed (cytotrophoblast column),
  • which then undergoes branching (villous sprouts).
  • At the centre of each villus are mesenchymal (extra-embryonic mesoderm) cells, from which the villus vascular system develops

33

How does the placenta change during pregnancy?

  • fewer cytotrophoblast present at term, so that there can be a closer apposition between the syncytium and the placental capillaries.
  • This will maximise the efficacy of nutrient transfer into the fetal blood, and enhance fetal growth in later pregnancy.

34

How does the placenta receive nutrients?

  • The decidual glands hypertrophy during the first trimester 
  • these provide the nutrients for the placenta and developing baby
  • After the breakdown of the cytotrophoblast plugs the maternal blood provides nutrition

35

How does the contact of the conceptus and maternal blood supply change during pregnancy?

  • At the earliest stages of pregnancy, the conceptus is in contact with maternal endometrial cells
  • As it grows, it makes transient contact with the maternal capillaries
  • Rapidly proliferating cytotrophoblast cells form a shell around the conceptus isolating it from maternal blood by 4 weeks post fertilisation.
  • The cytotrophoblast shell remains in place until 8 weeks post-fertilisation (10 weeks GA)
  • the spiral arteries are blocked by cytotrophoblast plugs.
  • During weeks 10-12 (GA), the cytotrophoblast plugs gradually break down,
  • spiral arteries now provide maternal blood to the placenta

36

What can cause late 1st trimester miscarriage?

  • When the cytotrophoblast plug is broken down 10-12 weeks GA
  • if the placenta is not fully anchored to maternal decidua,
  • the increase in pressure as it is exposed to the maternal arterial supply can detach the placenta and lead to miscarriage 

37

What is the significance of spiral artery re-modelling?

  • Vascular endothelium and smooth muscle cells are replaced with cytotrophoblast cells 
  • This remodelling process begins during the first trimester, and continues until weeks 16-18 of gestation.
  • This widens the arteries as they dont respond to vaso-constrictors
  • they can transport very large volumes of maternal blood to the placenta, and hence provide the quantities of nutrients needed

38

Explain the maternal risks of pregnancy

  • Labour and delivery is major risk
  • Spiral artery remodelling means that these vessels can lose relatively large volumes of blood after delivery
  • contraction of the uterus after the placenta has been delivered diminishes the blood loss
  • Placental tissue is relatively inflexible, and any left within the uterus will prevent the contraction of uterine tissue, and permit continued blood flow through the spiral arteries into the uterine lumen

39

What are the major defects in gametes?

  • Autosomal loss is non-viable
  • Only autosomal trisomy are trisomy 21 (downs syndrome) trisomy 18 (edwards syndrome) and trisomy 13 (patau's syndrome)
  • Extra sex chromosomes are normally viable with mild phenotypic changes
  • Loss of sex chromosomes is serious  XO (turners) being infertile with strong phenotypic changes and YO inviable

40

What are the most serious placental problems?

  • Incomplete anchorage leading to miscarriage or early delivery
  •  

41

What happens in the 1st stage of labour?

 

  1. Increasing Cervical ripening (becoming softer and flexible) and dilatation/effacement (becoming thinner and being stretched sideways) 
  • Requires extensive ECM remodelling that takes many hours but is sped up by the increasing pressure of the baby's head
  1. Recruitment of neutrophils
  2. Increasing Co-ordinated myometrial contractions from the fundus down 
  3. Rupture of fetal membranes

42

What happens in the 2nd stage of labour?

  • Delivery of infant

43

What happens in the 3rd stage of labour?

  • Huge rise in maternal oxytocin levels
  • Very powerful contractions of uterus and rapid decrease in size of the uterus (involution)
  • Delivery of the placenta
  • Involution is vital to stop the flow of blood through the spiral arteries

44

What regulates the changes in the cervix seen in labour?

  • Prostaglandin E2,
  • Matrix metalloproteinases (MMPs)
  • interleukin-8 -> neutophil recuirtment -> MMP 
  • COX-2 -> PGE2 

45

What regulates the changes in the myometrium seen in labour?

  • Prostaglandin F2α levels increased from fetal membranes
  • Oxytocin receptor increased
  • Contraction associated proteins increased
  • IL1 & IL-6 -> COX-2 -> PGF2a

46

What regulates the changes in the fetal membranes seen in labour?

  • Inflammatory process in fetal membranes
  • Prostaglandins, interleukins, Matrix metalloproteinases (MMPs)

47

What can increase the risk of extreme pre term labour?

intrauterine infection or bleeding

48

What is the main mediator of inflammation in pregnancy?

  • NF-kB: a pro-inflammatory transcription factor

49

What does NFkB upregulate?

Many genes, mostly ‘inflammatory’:

  • COX-2 (prostaglandins - PGs),
  • IL-8,
  • IL-1b, 
  • MMPs,
  • Oxytocin receptor,
  • PG receptors;
  • contraction-associated proteins

50

How does NFkB create a positive feedback loop?

IL-1ß is upregulated by NFkB and it in turn upregulates NFkB

51

What are the main drivers of term labour?

CRH (corticotrophin releasing hormone)

PAF (platelet activating factor)

52

What do CRH and PAF upregulate?

  1. CRH
  • IL-8 -> neutrophils -> MPPs
  • COX-2 -> PGE2 & PGF2a
  • IL-1 & IL-6 -> COX-2 & IL-8
  1. PAF
  • IL-1 & IL-6
  • IL-8

53

Why does it make sense that PAF is an activator of labour?

PAF is a part of lung surfactant

Produced by a maturing lung 

Lung is the last tissue to mature before delivery

Sign of fetal maturity

54

What can in advertanly initiate labour?

  • Anything that increases CRH may predispose to labour (stress, multiple infants)
  • Anything that increases muscle contraction may predispose to labour (excess stretch of uterus)
  • Anything that activates inflammatory cascades may predispose to labour

55

What is 'functional progesterone withdrawal'?

 

  • PR-B mediates the main effects of progesterone via gene expression
  • PR-A is less able to mediate these effects
  • Ratio of PR-A : PR-B increases at term
  • Loss or change in PR may lead to ‘functional progesterone withdrawal’ even though progesterone levels remain high

56

What is the PAF CRH pathway for initiating labour systemically?

  1. PAF is produced by the maturing lungs
  • PAF is eventually produced in sufficient quantities to activate inflammatory processes in the fetal membranes of the uterus
  1. The placenta is the source of CRH in the maternal system
  • Placenta upregulates CRH production 
  • This upregulates inflammatory process in the fetal membranes
  • Also stimulates ACTH production in the fetus
  • This stimulates the adrenals to produce cortisol
    • Cortisol stimulates lung maturation
    • Cortisol travels to the placenta where it upregulates CRH production in a positive feedback loop
  • ACTH also stimulates DHEA production in the adrenals 
    • DHEA is converted to oestrogens which are important for labour

57

What is the definition of pre-eclampsia?

  • Maternal hypertension
  • Maternal proteinuria

58

What might happen as a result of pre-eclampsia?

  • Maternal oedema
  • Fetal distress late in the pregnancy

59

What causes pre-eclampsia?

  • Failure of cytotrophoblasts to remodel the spiral arteries
  • Subsequent narrowing of spiral arteries 
  • Hypertension to compensate
  • Hypertension causes glomerular damage allowing protein to leak into the urine

60

What is eclampsia?

Onset of seizures in a woman with pre-eclampsia