Lecture 15: Normal Birth Flashcards
Define labour and the three stages
Uterine activity and cervical change which leads to expulsion of the fetus and placenta
S1: until full dilatation (10cm)
Has Latent phase ->24 hrs and Active phase ->cm an hour
S2: full dilatation until birth of baby- more descent of the baby down the ischial spine.
S3: birth of baby until delivery of placenta
What is 2 main functions of the uterus
- Be relaxed and quiescent but also have massive growth to support bb
- Initiate labour in line with fetal development which is highly coordinated, forceful activity, with sufficient relaxation for oxygenation but also keep sustained tension on cervix involution
What are the 3 layers of the myometrium and what is important about it
- Outer longitudinal
- Middle mesh like fibres- interwoven to allow force to be given in lots of directions
- Inner circular
Bulk of muscle is at the fundus to allow contraction to push down
What are the factors that promote and inhibit SM contraction of the myometrium due to Ca2+ uptake and release from intracellular storage
Promote: Oxytocin and Prostaglandins
Inhibit: Progesterone, cAMP, B-adrenergic agent
How is the tone/contractions of myometrium regulated and in what degree
Myometrium is spontaneously active even when relaxed but increases in frequency, amplitude and duration by cell surface receptors
–>endocrine, paracrine, autocrine factors.
The coordination of the contractions themselves is helped by Gap junctions
What are the 2 functions of the cervix
Keeps bb from falling out due to gravity and stops infections from getting inside. It undergoes softening in pregnancy in preparation for dilatation
Where is P2, E2, Oxytocin and Prostaglandins (PG) produced during pregnancy important for birth and what is its effect on the Uterus muscle
P2: Corpus Luteum (early), Placenta.
=Relaxant
E2: Placenta from fetal adrenal precursor DHEAS
= Uterotonic
Oxytocin: Hypothalamic production released from posterior pituitary
= Uterotonic
Prostaglandins: Decidua, placenta, membranes, neutrophils
= Uterotonic (PgE2, F2 alpha) and
= Relaxant (PgI2)
What are the 4 Physiological Phases for preparation of birth
Quiescence, Activation,
Stimulation and
Involution
What happens in Quiescence
Everything is relaxed; uterus is growing in capacity
- first wks: Myocyte hyperplasia, then stretch induced hypertrophy
- Pelvic Ligamentous laxity
- Cervix softens but remains firm and closed
- Myocyte contractions weak and uncoordinated
What happens in Activation
- Last 6-8 weeks of pregnancy
Undergoing cellular changes to prime for labour
- Lower segment forming
- myocytes becoming more excitable and contractions coordinated
What happens in Stimulation
- (280 days from LMP) 37-42 wks
A release from the inhibition on myometrial contraction
- Cervix is very soft now. It shortens and effaces,
- membranes rupture- release more Pg
- coordinated uterine activity
What happens in Involution
Period of retraction and remodelling of the uterus
- Placental separation
- Cleaving of decidua basalis
- Contractions to prevent PPH- increased sensitivity to oxytocin
- Later returns women to non pregnant state
What are the cell signalling factors that contribute to Quiescence
Mainly Progesterone (also PgI2, relaxin, pthrp, NO)
Causing:
- increased degradation of uterotonins, increased B-adrenergic receptors
- decreased intracellular Ca2+, Gap junctions, PG production
What are the cell signalling factors that contribute to Activation
- Increase in Contraction associated proteins (CAPS) - eg PG and oxytocin receptors
which leads to
- increased excitability, actin-myosin interaction and cross talk between myocytes - Upregulation of Connexin 43- gap junction which allow AP to propagate through myometrium.
- Estrogen
How come contractions can happen when Progesterone maternal, amniotic and fetus concentration elevates at birth/parturition
Functional progesterone withdrawal: Maybe
- change in isoform
- local inactivation of p2 by steroid metabolising enzyme
- altered expression of co-activator/repressors at the receptor
- post translational modification of P2 receptor
What is hormones trigger cervical ripening and what is the structural difference between cervix before and after ripening
- Triggered by functional progesterone withdrawal and increase in E2 around term which lead to increased COX-> PG acting locally at the cervix to get cervical remodelling
B4: 90% dense fibrous ECM, 10% blood vessels, immune, glandular cells
After:
- Collagen degrades,
- increased spacing between fibres,
- straight->wavy fibres,
- increased hyaluronic acid and immune cell infiltration
What factors precipitate the breaking of the membranes
- PGs, inflammation, stretch, shear force will increase MMP- matrix metalloproteinase which degrades collagen and weaken the membrane
- When its broken it will expose decidua which will leads to more PG release which set up a positive feedback
What are the steps that initiate the start of contractions at Stimulation
- Fetal stress-> leads to increased ACTH from ant pituitary
- Leads to increased cortisol release from adrenals
- Cortisol effects on the placenta:
- decreased P2 function
- increased E2, PG - uterotonic causing - Contraction and retractions of myocytes cause stretch on the lower cervix/uterus
- stimulation is started by triggering oxytocin and PG receptor which starts a positive feedback cascade
that leads to more contraction - Feeds back to the hypothalamus and posterior pituitary cause more oxytocin production and release which leads to more #4 which is a positive feedback cycle
- As the decidua is exposed, inflammation and rupture of membranes there is more increase of PG which further increases #4.
How do we clinically start labour
P2 antagonist used for non viable bb:
Mifepristone
More PG
- Stretch and sweep, finger in cervix sweep between decidua and chorion to release pg
- Break the water: ARM
- Misoprostal - pg analogue
- PGE2 gel in vagina - Most Common
How can you help a stalled labour clinically
Increasing oxytocin
-Syntocinon in IV
-Nipple stimulation (not rlly)
Reducing B-agonist receptor stimulation
-Presence of support person: less anxious, reduce length of labour
Increase PG: Amniotomy- more breaking water
What is given clinically to prevent PPH
- Injection of syntocinin (Oxytocin)
2. Carboprost: very potent, PG f2 alpha- tonic contraction, also causes diarrhoea
How to prevent a preterm labour clinically
Want uterus to relax
- Vaginal P2
- Insert a Cervical cerclage- stitch around cervix to help it remain competent
- Treating infections nearby
How can we slow down contractions after giving too much PG, syntocinin or Stop the contractions in pre-term labour to give medications to help the baby
TOCOLYTICS
Slow down
- Beta agonists eg. Terbutaline/salbutamol
Stop the contractions
- Ca channel blockers: nifedipine
Outside of NZ
- Atobisan - oxytocin receptor blocker not so effect
- Indomethacin - PG synthesis blocker - not so good for bb
What is the signals for Ductus arteriosus closure
Oxygen, Ach, Bradykinin, endothelin
How does the term bb keep warm for 30-60 min transitioning from fetus to neonate, what factors promote this process and what neonatal conditions hinder this
Non-shivering thermogenesis: lipolysis of brown fat which requires adequate oxygenation. This is accumulated in utero by ProstaglandinE2 and adenosine which inhibit lipolysis
Hypoxic bb and pre term bb
How does feeding change from fetus to neonate
Instead of constant supply of nutrients, there is now intermittent feeding- leading to risk of hypoglycaemia so needs to be fed early and frequent- breast feeding
