Parturition: Normal Birth Flashcards
What exactly is labour?
Getting the fetus from the uterus to the outside world;
ie; uterine and cervical change which leads to the expulsion of the fetus and placenta.
Also prevention of haemorrhage so that mother survives, estabilshes lactation and nuture the newborn
What are the 3 P’s of labour?
- Passage: pelvis/birth canal
- Power: driving force pushing baby out
- Passenger: baby
Within a normal biological range, POWERS are the most important as the pelvis is very hard to get out
Challenges in Human Parturition?
- Quiescence: of uterus with growth, distension. pressure (fetus + amniotic fluid)
- Timing: for safe birth
- Activation: stimulation of uterine musculature changes in genital tract
- Birth: fetal-neonatal adaptations (sudden loss of placental life-line)
- Involution: homeostasis, establishing lactation
We can link the anatomical changes to the physiological changes of birth
Uterus: is quiet for ~280 days post LMP, and then changes itself from a tiny organ to a larger organ with two segments, and upper (muscular) and lower (part of cervix).
Then the myometrium is stimulated and forms many structures so that when the time is right they can expell a baby.
The cervix softens and shortens.
At some point the amniotic sac the baby’s in has to rupture.
Hormones allows the pelvis to move a bit “ligamentous laxity” : sacraliliac lig, and pubic symphysis moves!
How does the uterus stay “quiet” or at a point of quiescense??
In fact it’s not totally quiet, the uterus is contracting all the time (bc it s a muscle).
But these are weak, of low amplitude (<10mmHg) and low frequency.
Poorly coordinated and the cervix is firm and closed.
Called Braxton-Hicks contractions and occur throughout pregnancy.
What is the principle hormone to maintain quiescence?
Progesterone, produced from the corpus luteum (and placenta).
Although a multitude of hormones are required for this, it take more then >1 to be abnormal/removed before quiescence can be undone
What affects Gestation Length?
- Parity (if you’ve had kids before GL: shorter)
- Age: older you are GL: shorter
- Genetics (maternal and paternal)
- Race/ethnicity
How does being a human impact on gestation length?
- In addition to the other factors (age, ethnicity etc), we have stress (cytokines/steroid hormones) influence the length of gestation.
Extreme stress/infection → shorter GL
Despite of influences on GL, the _______ is relatively tight.
Timing
280 d from LMP (37-42 weeks)
268 d from conception
BUT the # of weeks with the least risk of still birth is 38 weeks.
What may activate the partuition
Activation involves the
- Fetal genome
- Uterine stretch-quadruplets preterm as can’t grow any more
- fetal HPA axis: if not these GL prolonged
- Upregulation of myometrium
- Melatonin and circadian rhythms
- ABNORMALLY if membranes rupture pre labour
How does upregulation of the myometrium during partuition work?
Increas in CAPS form gap junctions (from protein connexin 43) which bind the muscle together for a stronger contraction.
We can use the knowledge of myometrial contractility and CAPs to find drug targets
Increase myometrial contractility by….. antagonising Ca2= blockers eg Nifedipine
Increase myocyte excitability ion channels …….block B2 sympathomimetics eg salbutamol (to stop Ca2+flux)
increase intercellular connectivity gap junction…. antagonise with PG synthase inhibitors (COX1 and COX2)
Usually in homeostasis there are controlling negative feedback loops, but in partuation, once you reach a certain level of stimulation, what happens?
There is now a positive-feedback loop past this point, so once all the connections are ready, you just need a little stimulation and the process will commence and uterus will contract.
***Progesterone modulate this whole process! Doesn’t change/drop like animals, is thought instead P4 receptors are altered, and although the [p] is constant the receptivity changes (the uterus ‘hears’ less progesterone)
What happens once the uterus “hears” theres less progesterone (due to altering P receptors)
The prostaglandins are the effector that go into the uterus, it is said labour is an inflammatory event.
Phospholipases release lots of arachodonic acid from decidua and cell membranes, but forming PG’s is the activator to this
What do Prostoglandins have to do with labour; and how do we stimulate labour with this knowledge
- Increase myometrial (muscle) contractility
- Lead to cervical changes
- associated with membrane rupture
So How do we induce labour from this?
So we can give PG as gel or tablet
Artifically rupture membranes → let the amniotic fluid run out
Put finger up to cervix, move finger around and take membranes off → PG release
Describe the model of cervical ripening
Can be due to preterm (eg infection) or fullterm (normal) and sets off a cascade of events that slowly leads to cervical change.
Starts with an inflammatory even that leads to the ECM of cervix being completel degraded, and cervix effectively “disappears” so baby can come out
Describe the visual and structural differences between
- Normal Firm uneffaced cervix
- Softened, ripened cervix
During pregnancy: Normal, firm uneffaced, long cervix
ECM: collagen (type I 70%, type II 30%) , Proteoglycans and elastin
Cells: SM, fibroblasts, BV’s, epithelium
Strong fibrous tough structure.
During partuation: Softened, ripened cervix
What are the membranes that are ruptured for labour?
The amnion and chorion. (strong and fused during pregnancy)
- Site of PG production
- so rupture of membranes ⇒ large PG release
- Rupture isn’t essential for labour (near the cervix)
- Rupture occurs at zone of altered morphology
- Amniotomy in normal labour has little effect on progress
Therefore by manually trying to rupture/tear membranes ⇒ release PGs ⇒ clinically induce labour
Learn and describe this summary of changes during parturition
All of these changes need to occur in the different locations for normal birth to occur.
1st Stage of labour; describe the latent and active phase
Latent Phase: nothing really happening (2-3cm) for many hours
Active Phase: cervix opens ~1cm/hour
When cervix is fully open at 10cm, there is pressure on the pelvic floor and mum wants to push!
How does pariety change the first stage of Labour?
Takes significantly longer if this is you first baby, then if you’ve had 1 or more.
The 1st stage of labour, what actually happens?
- CONTRACTIONS:
- last ~90 seconds, a pressure rise wave, with 45 seconds of pain in the middle past a specific high Pressure
- Cervical effacement and dilatation (to 10m)
- Descent of the presenting part into birth canal
- SRM- spontaneous rupture of membrane
- ROM- Rupture of membranes
- PROM- premature ROM
What’s important to remember with the pain portion of uterine contractions?
This is when the pressure is extremely high, and the baby is effectively “holding it’s breath’ because the intervillous blood flow is being cut off.
The 3-4 minutes between contractions flushes out the CO2 and a reoxygenation of the baby.
Dangerous if not a healthy strong baby!
Like snorkelling!
Where/ how does the baby “descend’ during the first stage
Into the pelvis (hopefully) curled up into a ball head first.
Partogram watches progress.
- Baby come into pelvic inlet transversely
- Does 90º turn in pelvic cavity
- Comes out
Whats a therapeutic technique of correcting asphyxia in newborns (to avoid hypoxia/metabolic acidosis)
Head Cooling:
- Have to meet certain criteria
- SHows a significant benefit of hypothermia
- ___________ acts as a labour “brake”
- There’s a _________ clock in humans (that requires an intact fetus)
- Placental ________ increases CRH (key to winding up the clock, but levels don’t predict labour)
- Progesterone “withdrawal” (via altered _______ levels) increase C43 to increase Gap junctions
- PGs stimulate Progesterone receptor __ (fire up system)
- Activation of________ signalling (babies born at night/early morning)
- Progesterone acts as a labour “brake”
- There’s a placental clock in humans (that requires an intact fetus)
- Placental estrogens increases CRH (key to winding up the clock, but levels don’t predict labour)
- Progesterone “withdrawal” (via altered receptor levels) increase C43 to increase Gap junctions
- PGs stimulate Progesterone receptor A (fire up system)
- Activation of circadian signalling (babies born at night/early morning)
