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BIOL1025 - Fundamentals of cell biology and physiology > Endocrinology (6) - reproductive - CL and pregnancy > Flashcards

Endocrinology (6) - reproductive - CL and pregnancy Flashcards

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1
Q

formation of CL - estradiol surge causes

A

increase LH receptor on granulosa - develop follicle and thecal cell role = main steroid forming rather than just steroid modifying = huge amount of steroids

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2
Q

formation of CL - taking huge amount of steroids

A

take cholesterol -> pregnenolone -> progesterone before FSH

modify androgenous from thecal cells = progesterone - downstream pathway = estradiol

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3
Q

formation of CL - LH signalling

A

larger and more active steroids

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4
Q

progesterone made by granulosa cells - after ovulation an luteal phase

A

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

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5
Q

change uterus for implantation

A

interact with its receptor - increase feedback problem therefore - hCG

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6
Q

in granulosa cells - spike of estradiol

A

LH expression - regulate enzymes = progesterone - active
oestrogen/progesterone act as contraceptive - -ve feedback - block Gn produced therefore no production and priming of new follicles

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7
Q

luteal stage

A

egg released and enter fallopian tube

enters nucleus - egg is 100-120 cells

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8
Q

myemetrium

A

outer layer of connective tissue and layer of smooth muscle

2-3 sheets - broken down

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9
Q

endometrium

A

inner surface - inner stromal and lining epithelial cells - change for embryo

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10
Q

day 6-7 contact

A

at upper region of epithelial and cervix closed by mucus plug (break at fertilisation and end of pregnancy)

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11
Q

proliferation - before ovulation

A

increase [estradiol] - endometrium responds - increase vascularity and thickness of epithelial cells
increase blood supply

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12
Q

secretory phase - after ovulation

A

increase progesterone + estradiol action = more activity = increase glycoprotein, sugar and a.a. - nutrients

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13
Q

7-10 days - embryo implanted

A

hCG by syncytiotrophoblast

blasist change and outer layer increases and grow through epithelium

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14
Q

embryo consists of 3 main cell types

A

outer trophoblastic - syncytiotrophoblast and cytotrophoblast
lining inner cell - hypoblast = yolk sac
epiblast - embryo in centre = all embryo proper

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15
Q

syncytiotrophoblast

A

=hCG and invasive - grown through epithelium

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16
Q

hCG

A

human chorionic Gonadotropin

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17
Q

hormones during pregnancy

A

LH, FSH, TSH and hCG
all have alpha
but all have different beta

18
Q

LH and hCG

A

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

19
Q

CL need embryo to survive

A

LH from Pit decreases - cannot support CL after ovulation therefore dies

20
Q

no embryo

A

no hCG produced = CL die - 10-14 days after

21
Q

embryo present

A

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

22
Q

not pregnant

A

luteolysis - feedback loop - cell death of CL cell = decrease progesterone
= endometrium die and shed = period - increase FSH = another cycle

23
Q

pregnant

A

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

24
Q

4-7weeks

A

progesterone predominantly appear from CL

25
Q

luteoplacental shifts

A

in primates - starts to produce progesterone

26
Q

Mifeprotone

A

block progesterone receptor before 4-7 weeks
= active myometrium
drive abortion

27
Q

early parturition

A

caused by infection/ twins - in effect 90% birth - 14 days of expected gestation - curve is tighter

28
Q

parturition

A

timing of labour

from 1st pregnancy day - remarkably conserved

29
Q

embryo drive timing of parturition

A

many species - progesterone/estrogen ratio

primates - related to CRH - corticotropin RH

30
Q

P>E during but when E increases and P plateau and drops

A

cervical ‘ripening’ mucus lost - increase local prostaglandin
myometrial response to oxytocin

31
Q

P to E stimulated by foetal cortisol

A

foetal adrenal gland grow - increase cortisol - stimulate conversion of progesterone to 17b-estradiol = P/E ratio decrease

32
Q

P to E stimulated by foetal cortisol - upregulation of alpha 17 hydroxylase

A

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

33
Q

before pregnancy - level of progesterone

A

v. high pregnenolone and enzyme low- increase progesterone + little E

34
Q

time of birth

A

in response to embryonic cortisol

enzyme increases = progesterone put into pathway = E

35
Q

primate placenta

A

has not 17a hydroxylase - maternal side hypo-Ant -adrenal cortex cortisol - -ve feedback and cortisol cannot pass - inactive enzyme

36
Q

foetal side of primate placenta

A

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

37
Q

oxytocin released

A

endometrial myometrial contraction

38
Q

uterus has many oxytocin R by

A

induced by signalling molecules like prostaglandin

due to CTRH

39
Q

when baby grow - birth

A

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

40
Q

artificial inducing labour

A

increase levels of steroids, estrogen , prostaglandin

increase oxytocin at the very end

BIOL1025 - Fundamentals of cell biology and physiology (21 decks)

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