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Repro > SGW - 8 (pregnancy) > Flashcards

SGW - 8 (pregnancy) Flashcards

1
Q

tissue constitute placenta barrier in 1st trimester?

A

syncytiotrophoblast
cytotrophoblast
connective tissue (around foetal capillaries)
fetal capillary (circles)

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2
Q

placenta barrier in 3rd trimester?

A

syncytiotrophoblast

foetal capillary endothelium

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3
Q

when does hCG peak?

A

at 8 weeks of pregnancy
rises from 4th week
then trails off from 8th week

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4
Q

effects of maternal smoking on placenta?

A

reduced placental blood flow

therefore poorer foetal nutrition will REDUCE BIRTH WEIGHT (by about 200g)

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5
Q

how does alcohol cross the placenta? causing?

A

by diffusion - lipid soluble (also small molecule)
can cause FAS - low foetal weight and growth retarded
(possibly mental retardation, head + facial abnormalities)

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6
Q

why might cytomegalovirus be a health hazard in pregnancy? (normally common cold)

A

can cause teratogenesis

process by which congenital malformations are produced in an embryo or fetus

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7
Q

what is given to prevent haemolytic disease of the new born?

A

anti-D therapy (antibodies) - prophylaxis given to mother
to neutralise the antigens in the mother’s blood
otherwise causes rapid haemolysis when bind to foetal RBC

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8
Q

what is shed in the 3rd stage of labour?

A

the placenta
maternal tissue: decidua
(foetal: amniochorion membrane)

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9
Q

where does IgG in foetal blood derive from?

A

mothers blood

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10
Q

why can’t a neonatal immune disease by mediated by IgM?

A

only IgG can cross the placenta (via pino-endocytosis)

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11
Q

why are the maternal adaptations to pregnancy required?

A
  1. provide suitable environment for nutrition, growth and development of foetus
  2. prepare mother for birth
  3. prepare mother for support of new born
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12
Q

where is hCG released and when does it peak?

A

from syncytiotrophoblast of blastocyst

peaking at 10 weeks gestation (pregnancy)

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13
Q

function of hCG?

A

mimics LH on corpus luteum - preventing degeneration to maintain endometrium lining to support pregnancy via release of progesterone (and oestrogen)

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14
Q

hormones involved in maintaining pregnancy?

A

oestrogen and progesterone (steroids)

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15
Q

where is hCG released from? function?

A

cells of developing FERTILISED OVUM

stimulates CL’s released of BOTH progesterone and oestrogen to maintain endometrium, therefore pregnancy

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16
Q

what does hCG mimic?

A 
luteal phase (LH) of menstrual cycle (post ovulation)
menstrual cycle = ovarian (oestrogen + progesterone) + uterine cycles (endometrium lining, stratum functionalis + basalis)
17
Q

what does hCG reduce? why?

A

maternal IgA, IgG, 1gM
humeral immunity is depressed - stop rejection of placenta
BUT mother - more susceptible to viral infections

18
Q

function of progesterone? effects on mother?

A

relaxes SM

can lead to GI: reduced motility –> heartburn + constipation

19
Q

which oestrogen hormone in maternal serum/urine would best indicate foetal progress? why?

A

oestriol (E3)
this hormone is dependent on foetal ADRENAL and LIVER metabolism as well as placental function
low oestriol = foetal distress, early delivery may be desirable

20
Q

which hormones from the anterior pituitary stimulate breast growth?

A

oestrogen, progesterone, prolactin

21
Q

how does inhibin (from CL + placenta) prevents further pregnancies?

A

suppress FSH secretion - blocking follicular growth

22
Q

what are the changes in glucose which occur during pregnancy to the mother?

A
  1. reduction in maternal glucose + AA CONC.
  2. diminished maternal RESPONSE to insulin (insulin resistance) in 2nd 1/2 pregnancy (save glucose for foetus)
  3. increase maternal free FATTY ACID, ketone, triglyceride levels (ALTERNATIVE metabolic fuel)
  4. increased insulin RELEASE to a normal meal
23
Q

how are the changes to the maternal concentration of glucose achieved in pregnancy?

A

through combined actions of:
hPL (hCS)
oestrogen, progesterone, prolactin (all anterior pit.)

24
Q

function of progesterone on maternal appetite during pregnancy?

A

stimulates appetite in 1st half of pregnancy

diverts glucose into FAT SYNTHESIS

25
Q

function of oestrogen in pregnancy on maternal appetite?

A

stimulates an increase in prolactin release (anterior pituitary) - +ve feedback

26
Q

which hormones generate maternal resistance to insulin?

A 
prolactin (stimulated by oestrogen)
hPL (increase maternal appetite)
glucose
cortisol (stress hormone, release more fatty A - alternative fuel)
(possibly oestrogen and progesterone)
27
Q

what are the effects on maternal glucose usage from all the hormonal changes?

A

maternal glucose usage declines
gluconeogenesis increases
maximising availability of glucose to foetus

28
Q

in later pregnancy, how are maternal energy needs met?

A

by metabolising PERIPHERAL fatty acids

29
Q

function of progesterone in early pregnancy?

A

stimulates appetite
increase maternal deposition of fat (divert glucose to fat synthesis)
(about 3kg of fat accumulated by mother)

30
Q

how is the 25% of maternal weight gain (about 3kg) from progesterone in early pregnancy beneficial to the mother in later pregnancy and after birth of baby?

A

maternal preparation e.g. breast growth (for lactation - why prolactin involved) and also may provide a reserve (fatty acids) for later pregnancy when foetal demands are greater (for glucose)

31
Q

what is the transport of glucose across the placenta limited by?

A

FLOW - simple diffusion

therefore maternal supply

32
Q

describe the effects of hPL (hCS) on mother during pregnancy

A

reduced uptake of glucose into maternal cells (from increase PERIPHERAL insulin resistance) - favour foetal supply
hPL LOW in early pregnancy, but increases as placenta grows (released from placenta)
has diabetogenic effect

33
Q

describe what happens after a maternal meal due to the effects of hPL (hCS) released from placenta? what can it lead to?

A

maternal meal –> transient maternal HYPER glycaemia –> INCREASE maternal insulin release from pancreas –> (hPL + other hormones) –> DECREASE uptake into maternal cells –> INCREASE availability of glucose to foetus
(can lead to maternal HYPO glycaemia BETWEEN meals)

34
Q

aside from insulin resistance, what else does hPL (hCS) promote?

A

lipolysis

35
Q

how does hPL promote lipolysis?

A

lipids and ketones released are avaliable for energy
in early pregnancy, PROGESTERONE increases maternal APPETITE and promotes STORAGE of glucose in fat stores
(lipolysis of mother = more glucose for foetus)

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