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Endocrinology & Reproduction > Prevention and treatment of preterm labour > Flashcards

Prevention and treatment of preterm labour Flashcards

1
Q

what is preterm labour

A

labour between 24 and 37 weeks

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2
Q

what induces preterm labour

A

contractions or short cervix

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3
Q

what triggers early activation of normal labour process

A
  • placental/vascular problems
  • inflammation and infection
  • maternal stress
  • hormonal signals and uterine stretch
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4
Q

what category are the majority of preterm births

A

60% are spontaneous pre term births

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5
Q

SPTB

A

spontaneous preterm births

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6
Q

how common are medically induced preterm births

A

40%

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7
Q

rates of birth <30 weeks

A

less than 1% , but they account fo 80% of neonatal deaths

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8
Q

what is survival of PTB associated with

A

disability

  • cerebral palsy
  • severe sensory & cognitive impairment
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9
Q

are there many causes of preterm labur

A

yes; a syndrom of multiple aetiologies

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10
Q

causes of preterm labour

A
  • spontaneous pre term labour

- preterm premature membrane rupture which increases risk of infection and so labour is induced

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11
Q

influecing factors of PTL

A
  • infection <32 weeks (40-80%)
  • cervical weakness / shortening
  • multiple foetus’
  • BV
  • maternal age
  • genetics
  • prenatal BMI & deit
  • environment
  • stress
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12
Q

impact of maternal stress on labour

A

increased cortisol stimulates activation stage earlier than normal

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13
Q

impact of placental haemorrhage on labour

A
  • thrombin directly activates the uterus

- contration associated proteins in the uterus are activated causing PTL

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14
Q

effect of thrombin in PTL

A

directly activates the uterus

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15
Q

what do blood and thrombin do in PTL

A

induce uterine contractions through a COX-1 and COX-2 independent mechanism

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16
Q

how are uterine contractions induced independent of COX-1 and COX-2

A

by blood & thrombin

happens by placental haemorrhage

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17
Q

impact of muliple foetuses on PTL

A

increased foetal hormone sectretion causing stimulation f activation stage earlie than normal (P and O)
earlier uterine stretch which induces COX-2

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18
Q

Impact of infection and inflammation on PTL

A

inflammatory response comes before functional progesterone withdrawal instead of after and so becomes the driver of the system
- causes increase in COX-2 which drive activation

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19
Q

BV and PTL

A

evidence of sub clinical infection

  • cytokines raised in tissues from women with PTL
  • cytokines induce PG and MMPs
  • influx of immune cells in tissues from PTL women
20
Q

MMPs

A

matrix metalloproteinases, ripen cervix

21
Q

treatment aims of PTL

A
  • stop uterine contractions
  • revesal of cervix softening/ripening
  • prevential of inital PTL
22
Q

treatment approaches of PTL

A
  • smooth muscle relaxaction to inhibit contraction
  • treat infection
  • stop bleeding or response to bleeding
  • inhibit inflammation releated event (COX/PGR)
  • increase progesterone
23
Q

thrombin

A

clotting protein released in respose to bleeding e.g hemorrhage, but induces contractions

24
Q

what is a medication used to treat PTL

A

Tycolytics

25
Q

tycolytics

A

use to treat PTL

26
Q

are tycolytics effective

A

they do not improve the outcome of PTL but they give time for the baby to be given steroids to try and make foetal lungs develop as much as possible preterm for survival

27
Q

retigabine

A

researched into treatment for PTL

28
Q

what medication is being researched for treatment of PTL

A

retigabine

29
Q

how does retigabine supposedly work

A

keeps K+ channels open which keeps smooth musle in relaxation state

30
Q

what is retigabine

A

a Kv7 activator which keeps K+ channels open

31
Q

what is the way forward for PTL

A

early prevention of PTL needing early identification

challenge is identifying who needs treatment

32
Q

what is the challenge of treating PTL

A

knowing who needs treatment and when treatment is needed

33
Q

what is prophylactic treatment

A

preventative

34
Q

exampls of PTL prophylactic treatment strategies

A
  1. treat infection
  2. inhibit inflammatory events
  3. prevent progesterone withdrawal
  4. maintain active cAMP system
35
Q

how can infection be prevented in PTL

A

prophylactic antibiotics

36
Q

how can inflammatory events be prevented in PTL

A

COX-2 inhibitors, TLR anatagonists, PG receptor inhibitors

37
Q

how can progesterone withdrawal events be prevented in PTL

A

synthetic or natural progesterone

38
Q

how can active cAMP system be maintained to prevent PTL

A

inhibit PDE activity

39
Q

why is COX-2 inhibitor thought to be good for treating PTL

A
  • COX-2 increases in labour and PTL
  • COX 2 synthesise PGs
  • PGs cause contractions
  • COX-2 stimulates cytokins whch are high from inflammation in PTL
40
Q

How would COX-2 inhibitor help PTL

A

with reduce the increased PGs, and cytokines from inflammation

41
Q

example of COX2 inhibitor

A

rofecoxib

42
Q

what is Rofecoxib

A

COX-2 inhibitor

43
Q

results of Rofecoxib study

A
  • mean gestation was 32 comapred to 34 for placebo
  • increased deliveries with R at <37 weeks
  • decrease birth weight in R
  • increase in premature rupture of memebrane in R
44
Q

why is Rofecoxib not working

A

dont understand enough about the mechanisms and process/timing of PTL

  • could have affected the good PG pathways
  • may have been given at wrong stage
  • may be completely unrelated to PTL
45
Q

rational for using progesterone to prevent PTL

A
  • delays the effects of functional progesterone withdrawl
  • shown to prevent PTL in animals
  • thought to be anti-inflammatory
  • progesterone antagonists induce labour
46
Q

why would you not want to use progesterone for PTL

A

levels are already high in pregenent women. May not be a good idea to add more

47
Q

current study findings of progesteron use in PTL

A
  • not associated with reduced risk of SPTB
  • no long term benefit or harm at 2 years of age
    study on going

Endocrinology & Reproduction (15 decks)

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