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what cell types make up the corpus luteum
leftover theca + granulosa cells (after the egg is released)
Granulosa cells
location in relation to egg
male adjacent cell
location in relation to egg- fixed to egg
male adjacent cell- sertoli
Theca cell
location in relation to egg
male adjacent cell
location in relation to egg- live around the egg/follicle
male adjacent cell- leydig
too many theca cells can lead to an increase in what hormone
androgens
what hormones does the corpus luteum synthesize
progesterone + low levels of estradiol
timing in the ovarian cycle
follicular phase: 0-14 days
luteal phase: 15-28 days
timing in the endometrial cycle
menses: 0-4 days
proliferative phase: 5-14 days
secretory phase: 15-28 days
what day does ovulation occur on
day 14
withdrawal of what hormone causes menstruation
progesterone
when is GnRH released or inhibited in response to progesterone levels (in comparison to estradiol)
low progesterone- released
high progesterone- inhibited
what effect does high estrogen have on FSH
it inhibits FSH
when does LH act on granulosa cells
during the luteal phase in preparation for ovulation (makes progesterone)
When does gametogenesis begin in males vs females
males- during puberty
females- during fetal life
What are the 6 hormones the placenta produces
chorionic gonadotropin (hCG)
placental lactogen (PL)
ACTH-like protein
PTH-related protein
hypothalamic-like releasing hormones
progesterone + estrogens
during fetal development, which organs does the placenta act as
lungs
GI tract
liver
kidneys
Internal female genitalia
ovary
fallopian tubes
uterus
vagina
external female genitalia
clitoris (equal to penis)
labia majora+ minora
secretory glands(bartholin)
where is ovary cortex located and what does it develop
cortex- outer
responsible for developing follicles, corpus lutea and stroma
where is ovary medulla located + what does it develop
medulla-inner
develops blood vessels + stromal elements
role of fallopian tubes
transport the ova from the ovary to uterus using cilia (beat egg towards uterus)
fimbriae at the distal ends
3 parts of the uterus
fundus
corpus-endometrial lining
cervix
menarche vs. thelarche vs. adrenarche
menarche- beginning of menstrual cycle
thelarche- breast development
adrenarche- increase in adrenal androgen secretion around 6-8yrs old
how are gonadotropin levels during childhood
they are low (high sensitivity to feedback inhibition by steroids)
when GnRH becomes pulsatile how does the sensitivity of gonadotrophs to estrogen change
they sensitivity decreases (less inhibitory effect)
How does GnRH lead to a period
increased pulsatility of GnRH causes LH surge, this marks initiation of 1st period (rise in LH and FSH levels produce androgen/estrogen that lead to period)
how often are gonadotrophins surging during our reproductive years
monthly
average age of puberty + what can delay it
9-10, but is decreasing in the US
exercise + obesity can delay it
during the luteal + follicular phase what type of feedback is given by estrogen/progesterone
luteal- negative feedback
follicular- positive feedback
which cells can LH act on
theca (to make androgens a precursor for estradiol) + granulosa (FSH can only work on granulosa cells)
which cell types are estrogen + androgens made in
estrogen- granulosa cells (bc they have aromatase)
androgens- theca cells (bc they have 17 alpha hydroxylase)
What are the main roles of LH and FSH in female reproduction
LH- progesterone synthesis
FSH-estrogen synthesis
Primordial cells
what are they
when do they appear in the fetus
when is a complete set made
what % of follicles do they represent
what are they- primary oocytes surrounded by single layer of pre-granulosa cells
when do they appear in the fetus- 6 weeks
when is a complete set made- 6 months after birth
what % of follicles do they represent- 95%
how does the number of primordial cells change between birth + puberty
it decreases to 400,000 at puberty
growth stages of follicles
primordial
primary
secondary (more granulosa layers, theca cells, make steroids bc of LH receptors)
tertiary (requires FSH, has antrum, gap junctions, desmosomes, granulosa cells differentiate)
graafian- dominant follicle
secretion of what from graafian follicles triggers LH surges
estrogen (E2)
What does follicular development require
FSH
Estrogen (E2)
LH
during childhood what does follicular development lead to
atresia
which follicle types undergo atresia
all except graafian
where are ovarian and endometrial cycles occuring
ovarian- in the ovaries
endometrial- in the uterus
Follicular phase
how long it lasts
follicle development stages
what type of feedback from estrogen
how long it lasts- 14 days
follicle development stages- primordial into graafian follicle
what type of feedback from estrogen- initially negative feedback on LH + FSH, but switches to positive and increases FSH+ LH around day 14
Luteal phase
follicle development stages:
what type of feedback are estrogen and progesterone exerting
follicle development stages- graafian follicle turns into corpus luteum
what type of feedback are estrogen and progesterone exerting- negative feedback to decrease FSH+LH release
what hormones does luteal cells secrete
estrogen + progesterone
what happens if egg is not fertilized
corpus luteum will degrade
decrease in estrogen + progesterone
does the luteal phase allow other follicles to develop
no, it inhibits follicles from developing + sustains uterine lining
what is occurring during the menstrual phase
oocyte is not fertilized (no pregnancy)
degeneration of corpus luteum (CL)
drop in estrogen + progesterone secretion
proliferative phase
what is happening to the endometrium
estrogen levels
what is happening to the endometrium- its thickening
estrogen levels- high, but decrease after ovulation (in response to progesterone)
secretory phase
what does the endometrium develop
what causes the endometrium to slough off
what is the layer left behind after menstruation
which hormone is dominant
what does the endometrium develop- secretory glands
what causes the endometrium to slough off- decreased estrogen + progesterone
what is the layer left behind after menstruation- zona basalis
which hormone is dominant- progesterone
what halts the proliferative phase
production of 17 beta HSD from progesterone
when is the effective implantation window
day 16-19 (lasts 3-4 days)
role of estrogen in female reproduction
positive + negative feedback on FSH/LH secretion
causes maturation + maintenance of fallopian tubes, uterus, cervix, vagina
causes development of female secondary sex characteristics at puberty
causes thelarche
upregulates estrogen, LH and progesterone receptors
role of progesterone in female reproduction
negative feedback on LH/FSH during luteal phase
increases secretory activity of uterus during luteal phase
maintains endometrial lining during pregnancy
decreases uterine contraction
4 stages of the female sex act
excitation- parasympathetic
plateau
orgasm- myotonic(muscle contraction)+ sympathetic
resolution- no refractory period
Menopause
what is it
average age
what is it- termination of reproductive functions
average age- 51 years
what causes menopause
progressive loss of ovarian follicular units
ovarian steroid levels fall + gonadotropin levels rise
high FSH +LH, low estrogen, progesterone and inhibin
how many germ cells do women start with
6-7 million at 20 weeks (only a few primary by menopause)
how does GnRH levels change during puberty
they increase which leads to rise in FSH + LH (increasing gonadal steroid production)
what are the “triggers” for the start of puberty
increased set point of hypothalamus + pituitary for gonadal steroid negative feedback (increased set point=increase circulating steroids)
what effect does estrogen have on progesterone receptors
estrogen increases the amt of progesterone receptors on uterine lining during secretory phase
Summary of events in the menstrual cycle (8 things)
FSH↑- follicular growth + estradiol secretion
Estradiol↑-proliferative growth of endometrium, inhibits FSH, stimulate LH surge
LH surge +smaller increase in FSH (ovulation + CL formation)
corpus luteum secretes progesterone + estradiol
estradiol+ progesterone ↑- inhibits FSH+ LH, secretory phase
corpus luteum degenerates if fertilization/implantation don’t occur
estradiol↓ + progesterone ↓- result in menstrual flow
estradiol ↓- FSH ↑ + cycle begins again
what effect does continuous GnRH have on LH/FSH levels
decreases LH/FSH (shutting down reproductive system)
How does birth control work
continuous secretion of synthetic estrogen/progesterone
blocks LH surge + ovulation + FSH needed for follicle development
mimics negative feedback of estrogen + progesterone
What contributes to the nucleus vs cytoplasm
nucleus- sperm + egg equally
cytoplasm- oocyte
where does energy from sperm motility come from
fructose in seminal vesicles
steps of fertilization
sperm cells weave past follicular cells + binds to zona pellucida and interacts with ZP3
increased Ca2+ causes acrosomal reaction that allows sperm to exocytose its acrosomal contents (hydrolytic enzymes) into zona pellucida
hydrolytic enzymes dissolve the zona pellucida + the tail pushes the sperm head towards the oocyte membrane
microvilli of the oocyte surround the sperm head, fuse + allow its contents into the oocyte
increased Ca2+ in the oocyte causes a cortical reaction hardening the zona pellucida (preventing another sperm from entering)
increase Ca2+ also causes completion of the oocytes 2nd meiotic division forming the 2nd polar body and a pronucleus
the sperm head enlarges + becomes the male pronucleus
the male + female pronuclei fuse together
Post-fertilization
what happens to the embryo
what happens to the inner cell mass
what happens to the trophoblasts
what happens to the embryo- it divides multiple times during its path to the uterus and becomes blastocyst
what happens to the inner cell mass- becomes the embryo proper
what happens to the trophoblasts- becomes the placenta (inner- cytotrophoblast + out-syncytiotrophoblast aka multinucleated cell)
steps of implantation (4)
hatching- zona pellucida of the blastocyst degenerates
apposition
adhesion- interaction between trophoblasts + uterine epithelial cells
invasion- blastocysts penetrate through epithelial layer via syncytiotrophoblast
placentation
what do syncytiotrophoblasts invade
where do lacunae form
what do lacunae fuse with
what do fetal blood vessels form from
what is the role of intervillous space
what do syncytiotrophoblasts invade- maternal blood vessels + kill and replace maternal endothelial cells
where do lacunae form- within syncytiotrtophoblasts
what do lacunae fuse with- maternal blood vessels to form intervillous space full of blood
what do fetal blood vessels form from- tertiary chorionic villi
what is the role of intervillous space- surrounds fetal vessels to supply gas/nutrients to fetus from mother
what prevents maternal blood from mixing w fetal blood
syncytiotrophoblast/placental barrier
when does the placenta develop
around 14 days post fertilization
what is the role of the placenta
creates hormones essential for growth/development of fetus
prevents mixing of maternal/fetal blood
nutrient exchange
Non-placenta counterparts + source
hCG
hPL
ACT-like protein
PTH-related protein
hypothalamic-like releasing hormones
progesterone/estrogens
hCG- LH+ pituitary
hPL- Gh, hPRL+ pituitary
ACT-like protein: ACTH+ pituitary
PTH-related protein: PTH+ pituitary
hypothalamic-like releasing hormones: GnRH, TRH,CRH, somatostatin + hypothalamus
progesterone/estrogens- ovary
insulin resistance during pregnancy
competition for food w baby so mother increases insulin following meals
if it takes longer for mother to take up glucose=more food for fetus (hPL acts on moms prolactin receptors to increase insulin resistance)
Gestational diabetes results if mother can’t produce enough insulin to lower blood sugar
how do the following parameters change during pregnancy
blood volume
RBC mass
arterial pressure
weight
breast size
cardiac output
blood volume- increase by 30%
RBC mass- increase
arterial pressure- decrease (progesterone/estrogen vasodilate)
weight- increase
breast size- double
cardiac output- increase by 30% (contributes to mild HTN + can lead to pre-eclampsia)
how does the fetus increase blood delivery
by increasing maternal blood pressure
hCG
what produces it
what does it do
what produces it- trophoblasts (trophoblast proliferation increases hCG)
what does it do- prevents regression/death of corpus luteum(maintains progesterone release to maintain uterine lining)
Luteal placental shift
at around 8 weeks the corpus luteum degrades + hCG decreases+ slight decrease in progesterone
the placenta takes over progesterone production and levels go back up
fetoplacental unit
maternal cholesterol is converted to progesterone in placenta
fetal DHAS is converted into estrogen in the placenta (via aromatase)
fetal DHAS is also transported to liver to become 16OH DHAS
fetal 16OH-DHAS gets transported to the placenta to form estriol
Quiescence- stage 0
uterus is relaxed + insensitive to uterotonins (prostaglandins/oxytocin)
braxton-hicks contractions occur at the end of pregnancy (weak + irregular)
steady progesterone (inhibits uterine contractions)
Transformation/activation-stage 1
switch to estrogen (begin to activate expression of uterotonins)
myometrium becomes more contractile via increase expression of CAPs
cervix expresses enzymes that break down collagen matric to facilitate dilation
Active labor-stage 2
forceful + rhythmic contractions associated w dilated
increased levels of prostaglandins(PGF2a + oxytocin)
increased myometrial cell interconnectivity
increased myometrial responsiveness to PGs + oxytocin
involution-stage 3
oxytocin causes sustained + forceful myometrial contractions after uterine contents are expelled
lactation (let down reflex)
suckling leads to oxytocin release from hypothalamus followed by post pit
inhibition of dopamine release to promote prolactin(PRL) secretion
oxytocin travels to myoepithelial cells in breast to release milk
circulation pathways in the fetus
placenta
ductus venosus- directs blood from left umbilical vein to inferior vena cava (oxygenated blood can bypass liver)
foramen ovale- shunts oxygenated blood from right to left atrium
ductus arteriosus- directs blood from pulmonary artery to aorta to by pass fetal lungs
what happens to these fetal circulation pathways at birth
ducts close + placenta is removed
how do the following values change after birth
vascular resistance
blood flow
arterial pressure
vascular resistance- decrease
blood flow- increase
arterial pressure- decrease
what triggers first breath
mild hypoxia/hypercapnia + tactile stimuli and cold skin
how do left atrial vs right atrial pressures change in newborns
left increases bc of increased systemic resistance
right decreases bc of decreases flow from closed ductus arteriosus (decreases venous return)
signals from the pituitary control what 3 things in ovarian follicle
formation of antral/graafian follicles
resumption of meiosis
ovulation
how does high levels of estrogen affect gonadotrophs sensitivity to GnRH
it enhances sensitivity
what is the climacteric
the transition period from being reproductive to non-reproductive (pre-menopausal)
tonic vs Gn regulated growth phases
tonic-class 1-4
Gn regulated- class 5-8
what 2 hormones causes maternal blood sugar to remain high after a meal
placental lactogen(PL)
GH
what is the role of RU486
a progesterone antagonist that induced labor +delivery
2 main evolutionary developments in humans
bipedalism(2 feet walking)
encephalization (big brains)
what effect does cortisol have on surfactant
it increases surfactant production