Endocrinology (6) - reproductive - CL and pregnancy Flashcards
formation of CL - estradiol surge causes
increase LH receptor on granulosa - develop follicle and thecal cell role = main steroid forming rather than just steroid modifying = huge amount of steroids
formation of CL - taking huge amount of steroids
take cholesterol -> pregnenolone -> progesterone before FSH
modify androgenous from thecal cells = progesterone - downstream pathway = estradiol
formation of CL - LH signalling
larger and more active steroids
progesterone made by granulosa cells - after ovulation an luteal phase
increase progesterone effect Pit and hypo - -ve feedback
FSH decrease - 2nd follicle forming - stop cycle
decrease LH - block 2nd ovulation and maturation of 2nf follicle
change uterus for implantation
interact with its receptor - increase feedback problem therefore - hCG
in granulosa cells - spike of estradiol
LH expression - regulate enzymes = progesterone - active
oestrogen/progesterone act as contraceptive - -ve feedback - block Gn produced therefore no production and priming of new follicles
luteal stage
egg released and enter fallopian tube
enters nucleus - egg is 100-120 cells
myemetrium
outer layer of connective tissue and layer of smooth muscle
2-3 sheets - broken down
endometrium
inner surface - inner stromal and lining epithelial cells - change for embryo
day 6-7 contact
at upper region of epithelial and cervix closed by mucus plug (break at fertilisation and end of pregnancy)
proliferation - before ovulation
increase [estradiol] - endometrium responds - increase vascularity and thickness of epithelial cells
increase blood supply
secretory phase - after ovulation
increase progesterone + estradiol action = more activity = increase glycoprotein, sugar and a.a. - nutrients
7-10 days - embryo implanted
hCG by syncytiotrophoblast
blasist change and outer layer increases and grow through epithelium
embryo consists of 3 main cell types
outer trophoblastic - syncytiotrophoblast and cytotrophoblast
lining inner cell - hypoblast = yolk sac
epiblast - embryo in centre = all embryo proper
syncytiotrophoblast
=hCG and invasive - grown through epithelium
hCG
human chorionic Gonadotropin
hormones during pregnancy
LH, FSH, TSH and hCG
all have alpha
but all have different beta
LH and hCG
similar - 80% identical
bind to similar receptor and control on many roles but hCG has longer half life
maintain CL and function independent of LH receptors
CL need embryo to survive
LH from Pit decreases - cannot support CL after ovulation therefore dies
no embryo
no hCG produced = CL die - 10-14 days after
embryo present
hCG bind to CL - stops degeneration
binds to LH receptor as well - increase progesterone and estradiol
progesterone from CL = LH (off) and has no effect on hCG production
not pregnant
luteolysis - feedback loop - cell death of CL cell = decrease progesterone
= endometrium die and shed = period - increase FSH = another cycle
pregnant
increase progesterone - blocks follicle development and ovulation
cervix plug - prevent microorganism entering
induce uterine endometrium - nutrient rich food sources for embryo
continue increase
uterine myometrium - rested state - prevent contraction - damage embryo
4-7weeks
progesterone predominantly appear from CL
luteoplacental shifts
in primates - starts to produce progesterone
Mifeprotone
block progesterone receptor before 4-7 weeks
= active myometrium
drive abortion
early parturition
caused by infection/ twins - in effect 90% birth - 14 days of expected gestation - curve is tighter
parturition
timing of labour
from 1st pregnancy day - remarkably conserved
embryo drive timing of parturition
many species - progesterone/estrogen ratio
primates - related to CRH - corticotropin RH
P>E during but when E increases and P plateau and drops
cervical ‘ripening’ mucus lost - increase local prostaglandin
myometrial response to oxytocin
P to E stimulated by foetal cortisol
foetal adrenal gland grow - increase cortisol - stimulate conversion of progesterone to 17b-estradiol = P/E ratio decrease
P to E stimulated by foetal cortisol - upregulation of alpha 17 hydroxylase
aromase - estradiol synthetase -placenta - increases progesterone - rate limiting enzymes
= progesterone efficiently modified through pathway = estradiol
P decrease and E increases - P/E ration decrease = parturition
before pregnancy - level of progesterone
v. high pregnenolone and enzyme low- increase progesterone + little E
time of birth
in response to embryonic cortisol
enzyme increases = progesterone put into pathway = E
primate placenta
has not 17a hydroxylase - maternal side hypo-Ant -adrenal cortex cortisol - -ve feedback and cortisol cannot pass - inactive enzyme
foetal side of primate placenta
same pathway
cortisol passes in placenta bind to GR+ = CRH - +ve feedback
binds to Ant = +ve feedback loop - increase prostaglandin and oxytocin R expression
upregulates myometrium - increase muscle excitability
oxytocin released
endometrial myometrial contraction
uterus has many oxytocin R by
induced by signalling molecules like prostaglandin
due to CTRH
when baby grow - birth
stimulate nerves at cervix to pelvic to dorsal horn of spinal column to reflex loop into hypo
feed onto paraventricular superoctive nuclei - get excited
nerve end goes through Post. gland and release oxytocin = contraction of uterus
artificial inducing labour
increase levels of steroids, estrogen , prostaglandin
increase oxytocin at the very end
