week 3 Flashcards
Describe the endocrine regulation of lactation
progesterone and oestrogens stimulate mammary growth + prolactin secretion. but also inhibit milk secretion
in lactogenesis 2 (after birth) fall in progesterone + oestrogens reduces inhibition.
suckling stimulus releases prolactin driving milk synth.
suckling releases oxytocin - ejects milk.
State the components of breastmilk
secretory iga
lactoferrin
lysozyme
List the benefits of breastfeeding
significant impact on mortality and morbidity.
higher cognition for babies who are breastfed
Describe the processes by which milk is transferred from mother to baby and how it can go wrong
discuss drugs that can augment/ suppress lactation
Describe the normal physiological changes in pregnancy
serum HcG rises fast to maintain corpus leuteum.
prog and oestrogen rise much slower, placenta produces them after about 8 weeks. and they take over from HCG.
gain 9-13kgs during preg.
basal metabolic rate increases.
1st tri more insulin (greater no of pancreatic cells)- storing sugar. 2nd tri insulin resistance- from placental lactogen more serum glucose.
estrogen + progesterone are so high they act like mineralocorticoid (retain more sodium). placenta prod its own renin.
Differentiate between pathological states and normal physiology in the pregnant patient
have to know what was going on medically before. patients will have their own reference ranges/ heart ecg change etc.
respiratory changes during pregnancy
maternal blood changes during pregnancy
cvs changes in pregnancy
discuss thyroid changes in pregnancy
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discuss thyroid changes
Outline the general structure and function of the myometrium
3 layers of smooth muscle. outer longitudinal
middle figure of 8- wringing a towel- prevents blood loss.
inner circular fibres.
innervated by ANS - sympathetic nerves. also has some spontaneous contraction.
Outline effects of oestrogen and progesterone on the myometrium
Alpha receptors produces contraction (oestrogen, oxytocin, prostaglandins) . B2 receptors- relaxation (progesterone).
stronger contractions in labour as progesterone decreases. ratio changes.
Outline how synchronous contraction of the myometrium is achieved through coupling of interstitial cells of Cajal and smooth muscle cells
has a pacemaker mechanism- interstitial cells of cajal. generate elec activity + coordinate.
spreads to smooth muscle cells via electrical coupling (gap junctions connexin proteins)- oestrogen increases expression of gap junctions
can be modulated by external stimuli (e.g oxytocin) to go through gq pathway and contract via a rise in calcium
Describe the effects and uses of myometrium stimulants oxytocin, prostaglandins, and ergots
oxytocin- dependant on oestrogen. only effective at term. increases frequency and force of contractions.- induces labour - only at term (doesn’t soften cervix) rx post partum haemorrhage.
prostaglandins- 2x types- vasodilator and vasoconstrictor. both cause contractions. roles in dysmenorrhoea and menorrhagia (why nsaids are good for both) both inc freq/force of contraction, gap jct funct, inc synth of oxytocin.
key difference to oxytocin is that PG’s soften the cervix. (induce labour before term, induce abortion, rx postpartum bleeding). can cause systemic vasodilation- CVS collapse.
ergots- fungus. contains laods of stuff (histamine, tyramine, AcH) whn ingested- convulsions and abortion. powerful + prolongues uterine contraction (only when myometrium is relaxed) ? MOA is 5-HT/ adrenoreceptors.
used for post partum bleeding- NOT induction of labour
Describe the effects and uses of myometrium relaxants
used to delay delivery (48 hrs) aid fetal lung maturation etc.
B2 adrenoreceptor stimulants (sabutamol) relax uterine contractions by direct action on myometrium. dec strength of contraction in premature labour.
can also use Ca channel antagonists or magnesium sulfate.
oxytocin receptor antagonists.
COX inhibitors (dec prostaglandin)
Describe the process of implantation of the blastocyst
zona cannot impant.
has to be the blastocycst that has ‘hatched’ this happens on day 5. (if no cilia, or too fast cilia then ectopics)
need remodelling of maternal vessels to facilitate placenta circulation.
trophoblast needs to develop vessels also.
window of implantation - trophoblast produces HCG- binds corpus leuteum- rescues it- which then produces steroids.
decidualisation (secretory changes) under progesterone- thicker and more gloopy.
placental steriogenesis starts at week 7. HCG peaks week 9-11
Explain how the embryo signals its presence to the maternal system
shed loads of hcg. rescues the corpus leuteum and makes it continue to create steroids.
Define the functions of the extra-embryonic structures and describe the key steps in their development
placenta has a very good adaptations to it.
maternal circulation is a low pressure system. big reserve.
trophoblast- makes placenta (two types- 1’ and 2’ invasion.) syncitiotrophoblast goes 1st. lots of neuclei- behind this cytotroblast more cell like structures. extraembryonic mesoderm then follows- turns into blood vessels.
Describe the functions of the placentally derived hormones
4 sorts of hormones– placental steroids are one of them.
all work in unison-
progesterone is a smooth muscle relaxant
decidulisation
mineralocorticoid effects.
breast development
estrogens do uterine hyertrophy. insulin resistance. CVS changes, breast dev.
CRH and cortisol- (cortisol) lung dev and insulin resistance.
CRH possibly labour induction
HPL- similar to GH. some lactate, some insulin resistance
functions of the amniotic cavity
and yolk sac
made up of fetal pee.
important for homeostasis
vital for limb and lung development
protection- physical and barrier- e.g infection trauma
yolk sac only important during early preg- folds around and gets closed up (3 weeks of gestatio)
Outline common complications of pregnancy in each trimester
1st trimester- miscarrage (1 in 6)
ectopic (1-2%)
hyperemesis gravidarum (1-2%)
2nd + 3rd- UTI, anaemia, pre-ecclampsia (4-5%) gestational diabetes. antepartum hemmorage.
premature (before 37/52)
interuterine growth restriction( less than 2.5 kgs at birth)
macrosomia (more than 4.5kgs)
Relate pathological conditions of pregnancy to normal physiology with reference to anaemia, gestational diabetes and pre-eclampsia
anaemia- 120-160 mg/dl normal
preg 10.5- 13
likely dilutional- inc in plas > inc in hb. max dilution at 28-30
gestational diabetes- comes on after 20 weeks gestation.- don’t mix well- increased risk of morbidity and mortality for both. if hba1c is 10% gives 25% congen abnormality risk. (baby tries to get rid of sugar and stores lots of fat)
pre-ecclampsia- significant rise in BP ( 30syss, 20 dys) OR 140/90 at 20 weeks or longer. on two measurements 4 hrs apart. + significant proteinuria. (systemic vasospasm- increacing TPR which then incs blood pressure)
what could cause a particularly small baby
abnormal placentation- 2nd wave of trophoblastic invastion
increaced endothelial activation of platelets
increaced extracellular space fluid
affects kidneys, live, cna, coagulation, placenta.
baby becoes very small and skinny- opposite to diabetes.
has reduced fetal transfer so less energy transfer.
reduced kidney function, oligohydramminos
only cure is delivery.
Describe the physiology and mechanism of normal labour
poorly understood. ? some neuronal feedback from cervical pressure.
CRH placental clock
imflammatory process in cervix.
Define and describe the three stages of labour
uterine contractions and and cervical dilatation that enables delivery of fetus and membranes. painful contractions, regular that have done something to cervix.
Describe management of each stage of normal labour
1st stage- (2 parts latent - up to 3cm dilatation. active 3-10 cm- cm an hour)- manage by encouragement, hydration, pain relief.
2nd- vulval bungling, anal dilatation, push urge, inc resp rate, unable to sit still.
3rd stage- IM syndtometrine (when ant shoulder comes)
L hand placed on symphasis pubis to guard ant wall of uterus.
controlled chord traction until placenta is delivered. placenta and chord checked for completeness. estimate blood loss. check tears/ suture.
Describe the common complications in each stage including “failure to progress” and postpartum haemorrhage
failure to progress - prolonged latent stage.
failure of uterus to constrict properly can lead to PPB
final stage is most dangerous, want to get it over quickyl, which is why IM med is given.
shoulder dystocia- when the shoulders get stuck.
Outline the management of common complications in each stage including “failure to progress” and postpartum haemorrhage
first stage- failure of membranes to break- can be induced with membrane sweep. may be offered oxytocin to speed things along.
2nd stage- shoulder dystocia- getting stuck and have to manually rotate the baby.
