L17 - Pregnancy Flashcards
(18 cards)
Role of the placenta
- Interface btween maternal and foetal plasma
- Oxygen and nutrients
• Hormones
o hCG, hPL, pGH
Human Chorionic Hormone (hCH) - (structure and production (model and where)
Dimeric, related to LH (can bind to receptors), produced by 2-cell model
GnRH produced at cytotrophoblast – GnRH stimulates syncytotrophoblast to produce hCG
Endocrinology of pregnancy (hCG) - (visible/ detectable, signals, rescue and result, maintain and regression)
visible at 8 cell stage – double ever 2/3 days to week 9
Signals conception and rescues corpus luteum – secretion of progesterone by ovary = endometrium lining maintained
Detectible in maternal serum (day 8)
o Low – non-viable / high more than more embryo
- HGC maintain progesterone production by placenta
- Stimulates steroid production by fetal gonads
- CL – regress= normal – progesterone production taken over in placenta.
Progesterone (production and week, dependence, regulation, 3 functions, indicator)
Produced in the syncytotrophoblast (9th week)
Dependent on maternal cholesterol – placenta lacks enzymes (no cholesterol from acetate)
Regulated by hCG
Large amounts into maternal circulation
o Maintain decidual lining of uterus
o Decreases prostaglandins formation = relaxes myometrium
o Suppresses T-lymphocyte-mediated tissue rejection
• Good indicator of good health (high) – low = miscarriage (10ng = 80%)
Oestrogen (how many types, production complications, 3 functions)
- 3 types
- Placenta production alone insufficient – aromatase abundant
- Vasodilatary – utero-placental blood flow
- Foetal adrenal gland development
- Mammary gland development
Placental Growth Hormone (need, its release and control, 3 regulation roles)
- No necessary for foetal growth – mum GHD = normal growth
- No pulsatile or regulated by GnRH
• Regulate fetal growth; influences maternal (takes over pituitary GH):
o IGF-I production
o Gluconeogenesis and lipolysis
o pGH increases as placental grows
• Increase in maternal circulation – feedback to APG/Hypo to suppress GH levels – swapped by pGH
Human Placental Lactogen (hPL) (production, rise, 2 actions)
- Exclusively in placenta
- Rises through pregnancy (>1g/ day by term)
- Metabolic – regulate maternal glucose (via IGF-I)
- Stimulates onset of maternal behaviours after birth – neurogenesis.
Remember oestrogen chart
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Parturition (Inhibitors and Activators
Inhibitors:
Progesterone
hPL
Activators:
Estrogen
Prostaglandins
oxytocin
Contraction associated proteins:
Prostaglandin R
Oxytocin R
Connexins: gap junctions = coordinated contractions
Trigger for parturition? (Ratio, withdrawal, increase synthesis of (3), stimulus?
change in E:P ratio (E increase)
functional progesterone withdrawal? - switch in receptor isotope - P levels still the same
Increased estrogen (estriol) synthesis by placenta?
- increased fetal adrenal androgens
- increased placental aromatase activity
• stimulus for increased androgen production?
o placental corticotrophin releasing hormone (CRH)?
Once parturation initiated (2)
increased prostaglandin synthesis
increased oxytocin receptors / activity
Breast development
Atrophic duct
- E, GH Adrenal steroids
Duct growth
- P, Prolactin
Lobulo-aveolar growth
- E, P, Prolactin, hPL
Milk secretion
Lactation (regulation, suppression, stimulation)
Regulated by prolactin (anterior pituitary) = levels are high in pregnancy
Suppressed by high steroid & hPL levels
Suckling maintains prolactin levels after birth
- activates neural pathways to suppress dopamine
- milk ejection (into ducts) requires oxytocin (posterior pituitary) stimulate myoepithelial cells to contract
- conditioned reflex: suckling also inhibits GnRH suppression menstrual cycle
How does foetal endocrinology differ? 3
- T3 & T4
- adrenal hormones
- growth hormone
Throid hormones (Initially from where and time frame, why is T3 low and what happens at birth?)
Thyroxine (T4) from wk 18 from mother at first then fetus does it
• Tri-iodthyronine (T3) low due to:
- low type 1 deiodinase (liver)
- high type 3 deiodinase (placenta)
- preferential production of reverse T3 (inactive)
At Birth:-
• TSH, T3 & T4 rise rapidly
• Adult levels achieved within a few weeks
Cardiovascular chnages after birth
Thermogensis - not good stimaulted by drop in temp - may need brown fat = T3
Adrenal horomones (gland size at birth, what zone produces DHEA, medulla function, increase at parturition)
Glands disproportionally large in fetal life due to fetal zone of cortex (involution after birth)
Fetal zone produces DHEAs -> estriol
Medulla initially norepinephrine function in fetus?
increase at parturition neonate function? Thermogenesis surfactant release blood pressure
Growth hormones (Controlled by…., k/o which hormones and consequences of high/low levels)
Controlled by: genetic factors; placental function – nutrient uptake, hormone production e.g. placental GH and placental lactogen, insulin like growth factors
• Human IGF-I “k/o”:
- low birthweight
• IGF-I levels:
- decreased in Fetal Growth Restriction
- increased in Large-for-Gestational-Age
Neonate growth changes
- GH receptors increase
* IGF responsive to pituitary GH
