human labour and delivery Flashcards
define miscarriage *
delivery of a non-viable infant <23wks of gestation
why do miscarriages happen at end of trimester 1 *
there is a switch in the contact of the placenta - blood that was being kept away from the placenta can now access it
therefore if the placenta is not anchored properly it cant cope with the pressure and is dislodged = miscarriage
what is preterm delivery *
23-37 weeks of gestation
this is because difficult to stop labour once it has started so can be preterm labour
or preterm caesarean - when baby/mum medically comprimised eg by high BP - preterm caesarian can be fine but there can be risks
what is the size of a baby at term
head size of adult hand
should fit on forearm
what is term delivery *
delivery at 27-41 wks - either by labour or elective caesarian
what is the result of a preterm delivery *
all the structural features are there
but some features might not have developed properly
small
define labour *
fundally dominant contractions - myometrium was relaxed in pregancy to allow expansion - changes to contracting so that the baby is pushed out
cervical ripening and effacement - change in tissue structure from firm to soft and flexible - become open space so that the baby can get out
summarise the process of labour *
it is independant of gestational age
- cervical ripening and efficacement (increasing)
- co-ordinated myometrial contractions (increasing)
- rupture of fetal membranes - amniotic fluid leaks - this is water breaking
- delivery of infant
- delivery of placenta
- contraction of the uterus
describe the stages in labour *
pregnancy is having 39weeks not in labour
latent stage is 8wks - uterus beginning to change - parts contract and then relax - otherwise rapid contraction wouldnt work at term
labour - 12-48hrs - increasing contractions
- phase 1 is many hours (longer in 1st pregnancy) - beginning of onst of contractions through the period of dilation of the os uteri, rupture of fetal membrane, changes to uterus and cervix
- phase 2 is hours - contractions and cervical changes
- phase 3 - 30mins - baby delivered and placenta and fetal membrane delivered
what can slow down delivery *
if baby is bottom 1st
emergancy delivery is needed
what causes initiation of labour at term *
not sure
eostrogen
perhaps low progesterone, or CRH or oxytocin
what causes initiation of labour preterm *
intrauterine infection
intrauterine bleeding
multiple pregnancy
stress - maternal
other fators
describe cervical ripening and effacement in pregnancy *
change from rigid to flecible structure
remodelling (loss) of ECM
recruitment of leukocytes (neutrophils)
it is an inflammatory process involving PGE2, IL-8, and a local (paracrine) change in IL-8
describe the coordinated myometrial contractions in labour *
driven inside uterus
fundal dominance
there is increased coordination and power of contractions
inflammatory cascade - key mediators
- PGF2alpha (E2) levels increased from fetal membranes
- oxytocin receptor increased
- contraction associated proteins
describe the rupture of fetal membranes in labour *
loss of strength due to changes in amnoin basement component
inflammatory changes and leukocyte recruitment - this is modest in normal labour and exacerbated in preterm
there is inreased activity of MMPs
inflammatory process in fetal membranes
interleukins and prostaglandins are involved
describe the role of NFKb in labour *
it is a pro-inflammatory transcription factor - it controls the production of endpoints:
- COX-2
- cPLA2
- IL1B
- IL6
- IL8
IL-1b especially, is inviolved in increasing levels of NFKb - it is a feedforward mechanism
this is what makes it difficult to stop labour once it has started
summarise the inflammatory cascade that is labour *
many initiators cause production of NFKb
NFKb is a transcription factor upregulating many genes than are mostly inflammatory
- COX2
- PGs
- IL8
- IL1B
- MMPs
- oxytocin receptor
- PG receptors
- contraction associated proteins
these drive the changes that occur in labour
what is the supporting evidence for the fact that NFKb is a key part of labour *
almost all pro-labour genes have NFKb binding domains in their promotors - ie NFKb upregulates all the factors involved in labour, in the same way at the same time
modification of the NFKb sites in the promotor sequence leads to loss of expression of cells or in expression vectors
infection (ie intrauterine infection/UTI) drives up inflammation and is very linked to preterm labour
describe PGE2 synthesis in vitro with addition of NFKb *
when tissues in vitro - they produce some PGE2, this is increased when NFKb is added
however when fetal membrane at term is not in labour - there is no increase in PGE2 production when NFKb is added - it is already at max production - the tissues have biochemically switched into labour
what is the hypothesis for the control of term labour *
CRH and PAF are the key drivers of the biochemical change in labour
CRH rises in the last 3 weeks of labour
COX-2 increases in amnion and chroion-decidus tissue in last 3 weeks of pregnancy - COX2 is what makes the PGs that drives the endometrium and cervix
PAF (platelet activating factor) is part of lung surfactant which is produced by the maturing lung before birth - lung is last tissue to mature - the PAF signal is involved in initiation of labour and its levels in amniotic fluid rise near term - surfactant is a fetal signal of maturity
CRF and PAF stimulate production of PGs and COX-2
also upregulate production of IL-1B which is a pro-inflammatory cytokine and drives production fo the molecules needed for labour
summarise the overall hypothesis for partuition (labour) *
CRH is made in the placenta - this stimulates the cascade that occurs in the fetal membrane and goes into the umbilcal cord
it works on the pituitary gland of the fetus causing release of ACTH which works on adrenal gland = cortisol production
cortisol goes through the umbilical cord to the placenta and upregulates CRH production - feedforward mechanism
CRH activates labour by causing production of IL and PGs
adrenal glands also produce steroids that mature lungs and cause production of PAF that contributes to labour
adrenal glands also make the precurser to oestrogen (DHEA) - oestrogen causes th myometrium to contract
what are things that follow from this theory of labour *
anything that increases CRH may predispose to labour - stress, multiple infants
anuting that increases muscle contraction may predispose to labour - excess stretch of uterus
anything that activates inflammatory cascades may predispose to labour
this all applies to preterm labour - intrauterine infection, bleeding, twins
what is the role of progesterone in pregnancy *
it is needed to sustain preg - if block the prog receptors = loss
the prog levels stay high until after the delivery of the placenta
in pregnancy have high PR which binds to NFKb - means that progesterone can act, also that NFKb is inactive
in labour there is an increase in NFKb and a decrease in progesterone receptor
therefore there is more NFKb present to act and drive labour
PAF, CRP and hence COX-2 are affected by progesterone
describe the progesterone receptor *
PR-B mediates the effects of progesterone via gene expression
PR-A is less able to mediate these effecys
ratio of PRA:PRB increases at term - therefore there is ‘functional progesterone withdrawal’ - there is still progesterone just no PR to mediate the effects
