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388 Cards in this Set
- Front
- Back
what happens during mitosis
|
diploid cells from diploid cells
|
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what happens during meiosis
|
production of haploid gametes
|
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what is progesterone bound to in circulation
|
corticosteroid binding globulin
|
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how many carbons do androgens have
|
19
|
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how many carbons is testosterone
|
19
|
|
how many carbons do estrogens have
|
18, loss of 1 C from androgens
|
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what does 5 alpha reductase do and where is it expressed
|
converts testosterone to DHT
mainly in testosterone target cells |
|
what is androstenedione a precursor of
|
extraglandular estrogens in men
|
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what cells produce testosterone
|
leydig cells of testes
|
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what supplies most of androgens in women
|
adrenals
|
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what cells produce estrogens
|
granulosa and thecal cells of ovary
|
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what produces progesterone
|
corpus luteum and later placenta
|
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where is GnRH produced
|
arcuate and preoptic area of hypothalamus
|
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how is GnRH produced
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as preprohormone --> prohormone --> decapeptide
|
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what secretes GnRH into portal circulation
|
neuron
|
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what does GnRH bind to
|
plasma membrane of gonadotrophs in pituitary
|
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what does GnRH stimulate
|
LH and FSH in men and women
|
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what do LH and FSH share with TSH and hCG
|
all are glycoproteins with alpha and beta subunits (beta - specificity)
|
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what does somatic refer to
|
external and internal genitalia
|
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what kind of cells do males and females have during 1st 5 weeks in utero
|
coelomic epithelial
mesenchymal stromal |
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what are coelomic epithelial cells precursors of
|
granulosa and sertoli cells
|
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what are mesenchymal stromal cells precursors of
|
theca and leydig cells
|
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what happens in males during weeks 6-7
|
seminiferous tubules form
sertoli cells enclose germ cells |
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what appears in males by weeks 8-9
|
leydig cellls appear
|
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when does differentiation begin in females
|
9 weeks
|
|
what happens at 9 weeks in females
|
both x chrs activated
mitosis forms oogonia meiosis in some oogonia |
|
what surrounds some oogonia in females in utero
|
granulosa cells and stroma
|
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what do theca cells develop from
|
stroma
|
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what are cells arrested in in the female in utero
|
late prophase
|
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what chr has genes encoding androgen receptors
|
X
|
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what does the fetus have prior to 6 weeks
|
indifferent gonads from genital ridges
|
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what invades the genital ridges
|
migratory germ cells
|
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what does the early embryo have, regardless of sex
|
wolffian duct
mullerian duct |
|
what does the wolffian duct become
|
male internal reprod. tract
|
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what does the mullerian duct become
|
female repro. tract
|
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what is required to stimulate wolffian duct formation
|
testes
|
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when are testes fully functional
|
weeks 14-16 gestation
|
|
what do wolffian ducts develop into
|
epididymis
vas def. seminal ves. ejac. ducts |
|
how does testosterone act upon wolffian ducts
|
paracrine manner
|
|
what do hormones are needed for dev of male internal genitalia
|
testosterone from leydig cells
MIH (AKA AMH) from sertoli cells |
|
what happens to the ducts in the absence of testosterone
|
wolffian ducts regress
mullerian --> fallopian tubees, uterus, cervix and upper 1/3 of vagina |
|
what is needed for dev of prostate penis and scrotum
|
5a reductase (to form DHT)
|
|
when do external genitalia develop
|
9-10 weeks
|
|
what determines which external genitalia develop
|
DHT
no DHT --> female DHT --> male |
|
what happens if there are no androgen receptors but the genotype is XY
|
testes
regressed mullerian duct regressed wolffian duct female ext. genitalia |
|
where does spermatogenesis happen
|
lumen of seminiferous tubules
|
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what does spermatogenesis proceed from
|
from basement membrane into lumen
|
|
what cells are in seminferous tubules
|
sertoli cells
|
|
when do sperm first appear
|
6-7 wks gestation
|
|
what does 1 spermatagonium give rise to
|
4 spermatids
|
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what is spermiation
|
release of spermatazoa into seminiferous tubules
|
|
how much LH and FSH are required for spermatogenesis in the adult
|
only low levels
|
|
where do sperm mature
|
epididymis
|
|
what moves spermatazoa forward
|
seminif. tube fluid and muscle contraction of epididy.
|
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what do spermatozoa have
|
haploid chrs
acrosomal cap mito in middle piece principle piece for ATP storagee |
|
how many days are spermatozoa in seminf. tubes
|
50
|
|
what does maturation of spermatozoa consist of
|
increase in forward motility
maturation of acrosome aquisition of protein receptors for zona pellucida decreased cytoplasm |
|
what cell does de novo synth of cholesterol of gets it via LDL/HDL receptors
|
Leydig cell
|
|
what cell converts progesterone to androstenedione
|
leydig cells
|
|
what enzyme do leydig cells use to produce testosterone
|
17 beta HSD
|
|
where is testosterone concentrated
|
adluminal compartment of seminif. tubes
|
|
what receptors do sertoli cells express
|
androgen receptors
FSH receptors |
|
which cells produce MIH
|
sertoli cells
|
|
which cells convert testosterone to estradiol 17 beta
|
sertoli cells
|
|
what cells in men express LH receptor
|
Leydig
|
|
which cells lead to incr in testosterone
|
leydig
|
|
which cells in men incr nursing function of cell
|
sertoli
|
|
which cell synthesizes inhibin in men
|
sertoli
|
|
what does inhibin B do
|
neg feedback on FSH production
|
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what hormones influence production of male gametes in seminf. tubes
|
FSH and testosterone.
|
|
what influences androgen synth in leydig cells
|
LH
|
|
what does testosterone do neg feedback on
|
GnRH release
LH release |
|
what hormones inhibit LH more than FSH
|
testosterone, DHT and estrogen
|
|
what must testicular levels of testosterone be at for sperm dev
|
over 100x that in blood
|
|
what happens if exogenous testosterone is administered to men
|
inhibition of GnRH and pituitary gonadotrophs, specifically decreasing LH production
|
|
what happens when testosterone and DHT bind AR in cytoplasm
|
nuclear translocation of androgen-AR complex
binding to androgen response element results in transcription |
|
what effects does testosterone have upon the lipid profile
|
incr in VLDL
incr in LDL decr in HDL incr in lean mass incr in visceral abd. fat |
|
what does testosterone do to hematocrit
|
increases it
|
|
what is DHT involved in
|
secondary sex charac.
hair growth sebaceous glands |
|
how is estrogen produced in men
|
peripherally via testosterone's conversion in adipose and liver
|
|
what happens if there is a lack of estrogen or its receptors
|
tall stature due to delay in epiphyseal plate closure
|
|
how is testosterone circulated
|
most bound to ABP or SHBG
some bound to albumin 2% free |
|
how is testosterone excreted
|
conversion to ketosteroids (andosterone), added to intact androgen and conjugated androgens from liver
all excreted in urine |
|
what regulates testicular temp
|
scrotum
external cremaster tunica dartos |
|
what happens in men to GnRH as puberty approaches
|
GnRH secretion becomes more pulsatile
|
|
what leads to incr in testosterone in early and middle puberty
|
nocturnal peak in LH
|
|
what is responsible for primary sex charac. in male puberty
|
incr in LH --> incr in testosterone
incr in FSH --> incr in inhibin |
|
what is responsible for secondary sex charac. in male puberty
|
testosterone and adrenal androgens, GH
|
|
what stimulates GH
|
testosterone and estradiol
|
|
what seminal fluid
|
sperm plus seminal plasma from accessory glands
yellowish viscous alkaline fluid of fructose and prostaglandins |
|
why are there prostaglandins in seminal fluid
|
to decrease viscosity of cervical mucousq
|
|
what is the final pH of semen
|
7.3-7.7
|
|
what "Activates" sperm
|
prostatic fluid
|
|
what is prostatic fluid like
|
has citrate
has PSA (protease) - dissolvees seminal fluid coagulum |
|
when does prostatic fluid enter prostatic urethra
|
when prostatic smooth m. contracts during ejaculation
|
|
what do bulbourethral (cowper's) glands do
|
secrete alkaline fluid that neutralizes acidity and lubricates the penis
|
|
what is the sperm road map
|
lumen of semin. tube
rete testis epididimis tail vas def ampulla of vas def urethra ejaculation |
|
what does the ANS control in men
|
testes
vas def male accessory glands erectile tissue |
|
what does parasympathetic do in male
|
pelvic n to cavernous n of penis corpora
|
|
what receptors does ACh bind to in men
|
M3 muscarinic on endothelial cells
|
|
what does NO synthase do in men
|
release NO
stimulates cGMP to cause vasodilation |
|
what contributes to flaccidity
|
tonic symp tone
|
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somatic part of male erection
|
contraction of ischiocavernosus m increases pressure in corpora cavernosa to levels higher than systemic arterial pressure
|
|
what is emission
|
movement of ejaculate into prostatic or proximal pt of urethra
|
|
what does emission result from
|
rhythmic contractions of ampulla of vas def
|
|
are gonadal smooth muscle cells in close contact
|
no, so there is limited electrical coupling
|
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how are individual smooth muscle cells inervated in men
|
directly innervated so norepi release allows for fast responses to stimulation
|
|
what controls constriction of internal urethral sphincter
|
symp
|
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when is ejaculation spinal reflex triggered
|
when semen from the prostatic urethra enters the bulbous urethra
|
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what marks the onset of puberty in females
|
gradual incr in LH and FSH
|
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what marks the reproductive years in females
|
cyclic release of LH and FSH
|
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what marks menopause
|
sustained high levels of FSH and LH
|
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what does pulsatile release of GnRH result in
|
pulsatile release of LH and FSH leading to incr in estrogen and androgens from ovary
primary sex charac. |
|
what is thelarche
|
first sign of puberty -- breast dev
|
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what is adrenarche
|
incr in androgen secr --> pubic hair growth
|
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why does the growth spurt happen earlier in females
|
earlier onset of GnRH release
|
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what are the metabolic actions of estrogen
|
anabolic
anti-lipolytic (promotes fat storage) epiphyseal plate closure |
|
what is the last step of female puberty
|
maturation of HP-ovarian axis
decr in sensisitivy of gonadotrophs to feedback inh. by estrogen |
|
what is the functional unit of the ovarian
|
follicle
|
|
what are the 5 main functions of the ovarian follicle
|
maintains/nurtures oocyte
matures oocyte prepares vagina and fallopian tube prepares uterus hormonal support of fetus initially |
|
what is an ovarian follicle
|
1 germ cell completely surrounded by cluster of endocrine cells
|
|
what happens to some oogonia from 8-9 wks gestation to 6 mo after birth
|
enter prophase of meiosis I and become primary oocytes and remain in prophase I utnil sexual maturity
|
|
what do primary oocytes become
|
primordial follicles
|
|
what characterizes formation of 2ndary follicle from primary follicle
|
addition of thecal layer of cells
before, it's just granulosa cells |
|
when does graafian follicle dev begin
|
at puberty and continues in cycles
|
|
what do vesicles of 2ndary follicle coalesce to form
|
fluid filled antrum that is rich in estrogen produced by granulosa and thecal cells
|
|
what happens to the oocyte within the antrum
|
gets pushed to 1 side and sits on cluster of granulosa cells called cumulus oophorus
|
|
what is the most rapid stage of oogenesis
|
selection for ovulation
|
|
what determines what graafian follicle is selected for ovulation
|
the number of estrogen and FSH receptors
|
|
what hormones influeences ovulation
|
LH
|
|
what happens to oocytes during ovulation
|
1st meiotic div is completed --> 2ndary oocyte and 1st polar body
2ndary oocyte begins 2nd meiotic div but is suspended at metaphase II |
|
what happens to 2ndary oocyte after ovulation
|
traveels down ampulla of oviduct and sperm penetrates zona pellucida
|
|
what happens after sperm penetrates zona pellucida
|
2nd meiotic div completes --> ootid and 2nd polar body
|
|
what is the remaining follicle called at rupture
|
corpus hemorrhagicum
|
|
what forms the corpus luteum
|
granulosa and theca interna cells under the influence of LH
|
|
what happens to the corpus luteum if no pregnancy
|
it becomes the corpus albicans at the end of the luteal phase
|
|
what maintains arrested state of primary oocyte
|
high cAMP levels
|
|
when does the secondary oocyte complete meiosis
|
at fertilization
|
|
when does the oocyte complete meiosis I
|
just prior to ovulation
|
|
what kind of feedback do ovarian sex steroids provide
|
both positive and negative
|
|
what cells provide nursing function in females and what receptors do they express
|
Granulosa; FSH
|
|
Can granulosa cells make testosterone or estrogen? Why or why not?
|
They don't have the enzyme for conversion to androstenedione so they cannot make those hormones without the theca cell
|
|
which cell expresses the LH receptor and produces androgens
|
thecal cells
|
|
what do LH stimulate theca cells to do
|
increase synth of LDL and HDL receptors --> incr of androstendione synth by theca cells
|
|
how does androstenedione get to granulosa cells
|
it freely diffuses
|
|
what stimulates granulosa cells to produce aromatase
|
FSH via cAMP
|
|
what does aromatase do
|
converts androstenedione to estrone
|
|
what does 17betaHSD do
|
converts estrone to estradiol
|
|
how does estradiol get into blood vessels
|
diffuses
|
|
what does FSH induce expression of in late follicular phase and what is the result?
|
induces expression of LH receptors on granulosa cells in late follicular phase allowing granulosa cells to maintain high levels of aromatase as FSH falls and ensures cells will respond to LH surge
|
|
what phases is ovary involved in
|
follicular and luteal, separated by ovulation
|
|
what phase is uterus involved in
|
endometrial cycle: menstrual, proliferative and secretory phases
|
|
what is the monthyl pattern in females a result of
|
interaction of ovarian steroids and peptides
|
|
what begins the follicular phase
|
menstrual bleding
|
|
which phase is the most varibale in the cycle
|
follicular phase - 9 to 23 days
|
|
how long is the ovulatory phase
|
1-3 days
|
|
how long is the luteal phase
|
13-14 days
ends with menstrual bleeding |
|
what characterizes the follicular phase
|
recruitment and growth of the 15-20 antral follicles
|
|
what happens to the corpus luteum in the folli. phase
|
regresses
|
|
what are the levels of inhibin, estrogen and progesterone in follicular phase
|
they are low
|
|
what happens to gonadotroph and FSH in foll. phase
|
gonadotroph released from neg feedback --> incr in FSH secret.
|
|
what happens in foll. phase due to rise in which hormone
|
FSH incr --> recruitment of antral follicles that grow and produce low levels of E and inhibin B
|
|
what do E and inhibin B do during foll. phase
|
neg feedback on FSH secr
|
|
what happens to LH during foll phase
|
increase in synth and secretion
|
|
what happens to LH/FSH ratio during foll. phase
|
increases
|
|
what happens in foll phase due to decr in FSH
|
atresia of follicles except for 1 (the 1 with the most FSH receptors)
|
|
what happens in late follicluar phase
|
dom. follicle produces more E and inhibin --> + effect LH on FSH
|
|
when does follicle produce some P
|
2-3 days prior to ovulation
|
|
what does FSH stim very early in foll. phase
|
granulosa cell growth and estradiol synth in some primary follicles
|
|
what is step 2 of foll phase
|
local estradiol increases its own receptors and FSH receptors on granulosa cells
autocrine pos. feedback |
|
what happens ins tep 3 of foll phase
|
FSH stim GF production and granulosa cell prolifer.
FSH incr LH receptors augmenting responsiveness to LH |
|
step 4 of foll phsae
|
LH stim theca cell growth and androgen prod. androgen -->estradiol in granulosa cells
LH stim P prod in gran cells |
|
step 5 foll phase
|
dom follicle is primary producer of estradiol
|
|
step 6 foll phase
|
rising estradiol and potentiation by P acts on pituitary gland and hypothalamus to evoke preovul. surge of LH and FSH by pos. feedback
|
|
when does E secretion by dom follicle incr
|
near end of late foll phase
|
|
what does E secretion by dom foll promote
|
+ feedback of ant pit. and sensitizes it to GnRH
|
|
what does dom fol induce
|
LH surge
|
|
what terminates LH surge
|
loss of + feedback of estradiol and increasing P
|
|
what 3 events does the LH surge drive in the ovary
|
1mary oocyte to complete meiosis I and arrest in metaphase II
wall of foll and ovary broken down w release of cumulus-oocyte (ovulation) granulosa and thecal cells form CL |
|
when does germinal vesicle breakdown occur
|
30 hrs after LH surge
|
|
what does formation of CL involve
|
direct vascularization of gran cells and their differen. into E and P producing cells
|
|
what happens in early luteal phase
|
initial decr in E --> termination of + feedback on LH
levels of E and P rise again --> - feedback on LH and FSH |
|
what happens in late luteal phase
|
CL starts to regress leading to decr in P and E
|
|
what happens in luteal phase if no fertil.
|
CL regresses
Inhibin, E, P are low gonadotroph released frm neg feedback --> incr in FSH |
|
what kind of control can E and P exert on hypothalamus and pit.
|
both pos and neg
|
|
which uterine phase coincides with foll phase
|
proliferative
|
|
what induces all cell types in stratum basale to grow and divide
|
rising E levels in mid-late foll phase
|
|
when does the endometrial lining start to grow
|
proliferative phase
|
|
how does cell proliferation occur in prolif. phase
|
directly via ER
indirectly via prod. of GFs |
|
what phase has formation of uterine glands and incr in arteries
|
prolifer.
|
|
what primes the uterus to respond to P during luteal phase
|
E inducing expression of P receptors
in prolife. phase |
|
what is the 2nd uterine phase
|
secretory
|
|
what is the purpose of the secretory phase
|
prep for implantation (for a baby!)
|
|
what hormones influence secr. phase
|
P and E
|
|
what phase coincides with the luteal phase
|
secr.
|
|
what does P do in the secr. phase
|
induces differen. of epithelial and stromal cells
induces uterine glands to fill w glycogen vacuoles inhibits endometrial growth |
|
how does P inhibit endometrial growth in secr. phase
|
by downregulating the ER
|
|
how is active estradiol converted to inactive estrone in secr phase and what is the importance
|
P induces inactivating isoforms of 17B-HSD
protects endometrium from estrogen induced uterine cancer |
|
what happens in non-fertile cycle
|
CL dies and sudden withdrawal of P
loss of lamina functionalis menstruation |
|
what is the implantation window
|
brief period of time of endometrial receptivity for implantation
|
|
when is the implantation window
|
around early to mid secretory phase of uterine cycle
|
|
when does fert. usually occur
|
within 1 day of ovulation
|
|
what does the oviduct do during cycle
|
increases muscular and ciliary activity
|
|
What does E do in the vagina
|
stimulates prolif of epithelium and increases cell glyogen content
|
|
what does P do in the vagina
|
increases desquamation of epithelial cells
maintenance of acidic environment |
|
what hormones is responsible for incr in basal body temp
|
P
|
|
what does E do in the cervix
|
stimulates thin, slightly alkaline mucous (ideal for sperm)
|
|
what does P do in the cervix
|
stimulates viscous, acidic mucous (sperm don't like that)
|
|
what does E do to breasts
|
enhances duct growth
|
|
what does P do in breasts
|
alveolar dev.
|
|
what effects does E2 have on bone
|
anabolic bone effect and calciotropic effect
survival of osteoblasts and apoptosis of osteoclasts --> bone growth |
|
what effects does E2 have on intestinal and renal Ca functions
|
stim intestinal Ca absorption and renal Ca reabsorption
|
|
what does E do in liver
|
increases expr of LDL receptor
incr circulating HDL levels |
|
how do E and P maintain skin
|
incr collagen synth and suppress matrix metalloproteases (E and P)
incr GAG production (E) promote wound healing (E) |
|
what are the cardiovasc. effects of E
|
promotoes vasodilation via incr prod of NO
|
|
which hormone is neuroprotective
|
E!
|
|
what effects does E have on angiogenesis
|
pos effect
|
|
what alters thermoregulatory set pt
|
P, by acting on hypothalamus
|
|
what enzyme does E block to improve mood
|
MAO
|
|
how can P produce poor mood
|
by increasing MAO
|
|
what effects does P have on kidney
|
comp inhibitor of aldosterone (natriuretic)
that's why pregnant women have to pee a lot |
|
what effect does E have on adipose
|
lipolytic
decr LPL and incr HSL I don't understand that! Earlier Dr. G said it's anti-lipolytic ... wtf! |
|
how is E transported
|
mostly bound to SHBG, 20% free
|
|
how is P transported
|
bound to cortisol binding globulin mostly
|
|
where does peripheral aromatization of androgens to estrogen occur
|
in tissues such as breasts that have lots of aromatase
|
|
mechanism of action of E and P
|
pass thru cell mem to bind to receptors in cytosol
unbound receptors complexed w chaperones ligand binding dissociates receptors from chaperones and induces dimerization and nuclear translocation hormone receptor complex binds response element on DNA --> transcription |
|
what increases libido around ovulation
|
increased secretion of nadrogenic steroids
|
|
how are sexual sensations transmitted in the female
|
pudendal n and sacral plexus to cerebrum
|
|
what innervates the bartholin's glands to secrete mucous
|
PNS
|
|
what does the pit. secrete in female orgasm and what is the purpose
|
oxytocin
increases uterine contraction |
|
how many primary follicles remain at menopause
|
just a few
|
|
what causes menopause
|
loss of functional follicles --> decr in E and P and incr in LH and FSH
|
|
what is the chorion
|
extraembryonic membranes of the fetus
|
|
what is the decidua
|
endometrial tissue from mom
|
|
what does increased blood flow to female genitals produce
|
vaginal transudate that neutralizes acidic pH and increases O2
|
|
what does vaginal tenting do
|
draws cervix away from vagina creating local reservoir for sperm
|
|
what is capacitation and where does it occur
|
must occur before sperm can fertilizat egg
in oviduct unbinds sperm from epithelium of oviduct |
|
how does capacitation modify sperm
|
alters their membrane fluidity by removing cholesterol
removes proteins and/or carbs that may block egg binding sites changes membrane pot to assist Ca to enter sperm and facilitate acrosomal rxn protein phos. |
|
what 3 layers must sperm pass through to fertilize
|
cumulus
zona pellucida fusion of sperm w plasma mem of egg |
|
what is the chorion
|
extraembryonic membranes of the fetus
|
|
what is the decidua
|
endometrial tissue from mom
|
|
what is the cumulus layer mostly composed of
|
hyaluronic acid
|
|
how do sperm get thru cumulus
|
membrane bound hyaluronidase
|
|
what does increased blood flow to female genitals produce
|
vaginal transudate that neutralizes acidic pH and increases O2
|
|
what is the zona pellucida composed of
|
ZP1
ZP2 ZP3 glycoproteins |
|
what does vaginal tenting do
|
draws cervix away from vagina creating local reservoir for sperm
|
|
what is capacitation and where does it occur
|
must occur before sperm can fertilizat egg
in oviduct unbinds sperm from epithelium of oviduct |
|
how does capacitation modify sperm
|
alters their membrane fluidity by removing cholesterol
removes proteins and/or carbs that may block egg binding sites changes membrane pot to assist Ca to enter sperm and facilitate acrosomal rxn protein phos. |
|
what 3 layers must sperm pass through to fertilize
|
cumulus
zona pellucida fusion of sperm w plasma mem of egg |
|
what is the cumulus layer mostly composed of
|
hyaluronic acid
|
|
how do sperm get thru cumulus
|
membrane bound hyaluronidase
|
|
what is the zona pellucida composed of
|
ZP1
ZP2 ZP3 glycoproteins |
|
what does sperm bind to first on ZP and what does it induce
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ZP3
triggers acrosomal rxn and enzymes to digest ZP |
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what does sperm bind to 2nd on ZP
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ZP2 and sperm held in place
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what part of sperm enters egg for fert.
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the whole thing!
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what triggers the cortical rxn in the egg and what does it prevent
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fusion
prevent polyspermy |
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when does the egg finally become haploid
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fusion
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what triggers the egg waking up and fusion events
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Ca++ release
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What does increased Ca stimulate in fert.
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stims egg to enter cell cycle and stimulates recruitment of stored maternal mRNAs
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what does binding of ZP3 to sperm initiate
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signal transduction
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what are trophoblasts and what do they form
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they are a layer of cells from the blastocyst
they form the chorionic villi |
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what is important in formation of chorionic villi
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prostaglandins and histamine
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what does the blastocyst secrete
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immunosuppressive agents
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what does hCG do
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sustains CL
immunosuppressive promotes trophoblast growth and placental dev |
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what invades endometrium in fert and dev
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trophoblasts
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what is required before implantation can occur
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hatching -- degenration of ZP
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where does apposition occur and why
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at site where ZP is lysed -- trophoblast can make direct contact w cell membranes of endometrium
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which way should cell mass point
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toward endometrium
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what are the 3 stages of implantation
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apposition
adhesion invasion |
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what is adhesion step of implantation
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interactions of integrins --
intracellularly they interact w cytoskeletal elements extracell -- receptors for matrix proteins |
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what is invasion stage of implantation
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trophoblasts differen. into 2 layers: syncytiotrophoblasts and cytotrophoblast
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describe the syncytiotrophoblast
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outer layer
multinucleated w no cell boundarie protrusions bw uterine epithl. cells |
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what cells eventually penetrate the basement membrane of uterine epithelial cells
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?
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where do the decidual cells degenerate and what do they release
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in region of invading syncytio.
release lipids and glycogen to provide nutrients for embryo |
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what does the cytotrophoblast layer initially provide
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layer of continuously dividing cells
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when does endocrine function of dev begin
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at implantation when syncytio. start secreting hCG
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what does hCG do
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maintains LH
secretes P |
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what happens to syncytio. by 10 wks
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becomes steroiogenic and make P
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what do syncytio. do
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make enzymes for modifying and converting hormones
gas transfer, facilitated transport, and pinocytosis/transcytosis |
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what is decidualization
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engorgement of stromal cells as they fill with lipid and glycogen
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what does the decidua form
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epithelial sheet w adhesive junctions to inhibit migration of implanting embryo
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what does the decidua secrete
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factors that moderate activity of syncytiotrophoblastic-derived hydrolytic enzymes: regulates invasion of embryo
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what covers the outer surface of the mature chorionic villus
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thin layer of syncytio.
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what is under the syncytio. layer of mature chorionic villus
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cytotrophoblasts
mesenchyme fetal blood vessels |
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what forms chorionic membrane
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cytotrophoblasts
mesenchyme fetal blood vessels |
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where does maternal blood get trapped
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intervillous space -- bw decidua capsularis and fetal villi
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where do spiral arteries from mom drain
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directly into intervillous space
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what drains the intervillous space
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maternal veins
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what does the original uterine endometrium become
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decidua parentalis
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what provides early nutrition for fetus
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trophoblastic digestion
absorption from endometrium |
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what provides later nutrition for fetus
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diffusion through placental membrane
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what is the mean PO2 of maternal blood in placental sinus near end of pregnancy
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about 50 mmHg
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what is mean PO2 of fetus after oxygenation
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about 30mmHg
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does fetus have greater [Hb] or less
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50% greater
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what kind of Bohr shift in fetus
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double
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what are the endocrine functions of the placenta
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maintain pregnancy
stimulate breast growth adapt maternal met. and phys. regulate fetal dev. regulate birth |
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when do trophoblast cell form hypothalamic pit. type unit
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when they differentiate
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what does CT layer of placenta do
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seceretes releasing and inhibiting hormones (hypothalamic actions)
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what does SCT layer of placenta do
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secretes gonadotropin like hormones (FSH, LH) (pituitary action)
secretes hCG and hCS |
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what kind of cells produce hCG
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placental cells
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what subunits does hCG have and which one is identical to what other hormones
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alpha and beta
alpha same as FSH, LH, TSH |
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what stimulates hCG secretion
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LHRH from CT layer (paracrine action)
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when does hCG peak
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9-12 wks
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what supports the CL until the placenta can produce E and P
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hCG
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does any hCG enter fetal circ.
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Yes, but just a little
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what does hCG do in male fetuses
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stimulates leydig cells to produce testo.
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when is hCS detected and how does it change during pregnancy
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detected at 5 wks
rises throughout pregnancy w weight of placenta |
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what does hCS have similar functions to
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PRL and GH
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what effects does hCS have on insulin and glucose
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decreases insulin sens.
descreases glucose utilization in mom --> directs to fetus --> increas in maternal serum glucose |
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what effect does hCS have on mammary glands
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stimulates dev
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what does relaxin do
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relaxes pubis
helps dilate cervix |
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what produces relaxin
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placenta and CL
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what is needed for E synth in pregnancy
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both placenta and fetus
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what enzymes do SCT cells produce and what kind of receptors do they have
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produce lots of 3B-HSD
do NOT produce 17a-hydroxylase have LDL receptors |
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what is the importance of P produced by placenta
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maintains quiescent myometrium and pregnant uterus
maintains decidual lining |
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what is the regulation of P produced by placenta
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completely independent of fetus -- unregulated
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what might placental P modulate
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secretion of hCG and hCS
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whjat is placental P converted to
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cortisol and aldosterone for fetal use
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what does placental P stimulate decidual liniing to do
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secrete PRL
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how does P quiet uterine contraction
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inhibits PGs
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what effect does placental P have on mom
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increases capacity of alveolar pouches to hold milk
stimulates resp center to get rid of excess CO2 |
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how much of placental P is used by fetus
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only 10%, rest is used by mom
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which placental cells produce E
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SCT
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what cells are SCT similar to and why
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gran cells bc both lack 17b-hydroxylase
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where do fetal androgens come from
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fetal adrenal cortex
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what does the fetal zone of the adrenal gland resemble and why
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zona reticularis
expresses little or no 3b-HSD |
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what does the fetal adrenal cortex release during gestation
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DHEA-S
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what is production of fetal DHEA dependent on
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release of ACTH from fetal pit.
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what can the placenta convert DHEA into
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estriol
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what is used to assess fetal well being
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estriol
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what effects do estrogens have on placenta
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increase blood flow
increas LDL receptors in SCT induce factors for parturition |
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what does E stimulate in uterus during pregnancy
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growth of uterine muscle
softens pelvis enlargement of external genitals |
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what does E do to breasts during pregnanct
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increases duct system
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what effect does pregnancy E have upon P
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augments its synth
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what does E stimulate placental conversion of
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cortisol to cortisone
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what maintains appropriate E and P levels during pregnancy
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mother, placenta, and fetus
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what are pregnancy levles of E and P compared to normal cyclic levels
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much higher
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who contributes most of intiial cholesterol for steroid synth in pregnancy
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mom
|
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can placenta make androgens?
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No
initially DHEA from mom later from fetus |
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what happens to maternal prolactin levels during preg.
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rise due to incr in E
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what happens to LH and FSH during preg.
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decr do to - feedback from high E and P
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what happens to thyroid during preg
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increase in size
T4 and T3 incr TBG incr |
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what changes happen to adrenal gland during preg
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liver increases cortisol bindign glob --> incr in serum cortisol
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when is there a surge in cortisol prod and why
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late in preg for initiation of lactation
|
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what happens to cardiac output during preg and why
|
increases a lot during 1st trimester and then slowly after
due to mostly incr in SV |
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where is incr in CO seen/not seen
|
40% incr in renal flow
15% in uterine incr flow to heart, skin, breasts no change in flow to: brain gut skeleton |
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what happens to MAP during preg and why
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decreases during mid preg but incr in 3rd trimester (still at or below normal though) due to decr in PVR and vasodilation from E and P
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what positional changes affect CO
|
highest with mother in lateral recumbent position
i |
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what happens if preg woman is supine
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fundus of uterus rests on IVC impeding venous return
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what happens toblood vol during preg and why
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increases during 2nd and 3rd trimesters due to inc in plasma vol and RBCs
helps meet demand due to hypertrophied vascular system |
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what are vol changes in resp during preg
|
diaphragm rises due to effects of P
net decr in RV with no change in VC |
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what happens to alveolar vent during preg and what does it cause
|
pulm resistsance falls
incr in TV and alveolar vent creates decr in maternal PCO2 |
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what additional dietary needs are there during preg
|
much more protein
more iron folate |
|
intrauterine weight gain
|
fetus - 3.3 kg
placenta - 0.7 kg amniotic fluid - 1 kg |
|
maternal weight gain
|
most from adipose and breasts
|
|
stages of labor
|
dilation and thinning of cervix
delivery of fetus delivery of placenta |
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what causes the 1st stage of labor
|
uterine contractions force fetus against cervix
|
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what does cortisol from fetus do
|
maturation of lungs
incr in liver glycogen storse incr in intestinal transport |
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what does PG from uterus, placenta, and fetus do
|
stim contraction of uterus
forms gap junctions to potentiate contractions induced by OXY effacement of cervix |
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what does oxytocin do
|
stim contraction of uterus
bonds receptor on decidual cells --> PG prod maternal OXY maintains labor fetal OXY may initiate labor |
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what does relaxin do during preg
|
keeps uterus quiet
|
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what produces relaxin
|
CL, placenta, decidua
|
|
what hormone is relaxin related to
|
insulin
|
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what does estrogen do in regards to birth
|
increases OXY receptors in myometrium and decidual layers
|
|
what marks the dilation stage of birth
|
contractions
|
|
what marks the expulsion stage of birth
|
active labor
|
|
what is mammogenesis
|
prolif of alveolar and duct cells
|
|
what is lactogenesis
|
milk prod by alveolar cells
|
|
what is lactation
|
lactogenesis and milk let down (galactokinesis)
|
|
what does lactogenesis rely on
|
PRL
|
|
what does milk let down rely on
|
oxytocin
|
|
what does breast glandular tissue consist of
|
alveoli and ducts
|
|
what do lactiferous ducts do
|
carry secretions to outside
|
|
what is prenatal mammary gland dev like
|
mammary sensitive to estrogen
|
|
what are mammary glands like at birth
|
rudimentaryt duct system
|
|
what happens to breasts from birth thru puberty
|
growth of secretory tissue and dev of supporting adipose
|
|
what happens to breasts during puberty
|
E, P, GH and PRL extend duct growth
lobules and epithelial buds at duct terminus |
|
what happens to breasts during menstrual cycle
|
foll phase - duct maintenance
luteal phase - lobular/alveolar maintenance |
|
what happens to breasts during preg
|
high E, P and hCS cause lots of growth of lobular/alveolar and duct systems
|
|
how does PRL concentration change during preg
|
increases progressively
|
|
what is PRL essential for
|
for P and E to have mammotropic effects
|
|
what does PRL stimulate
|
lactogenic apparatus
|
|
what prevents lactation during preg
|
excess P and E
|
|
what initiates milk synth after birth
|
decr in P and E
|
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what maintains levels of PRL for lactation
|
suckling
|
|
what effects does PRL havee on GnRH
|
inhibits GnRH keeping LH low
|
|
what is suckling require for
|
stimualting release of PRL
maintaining ongioing lactogenesis |
|
how does OXY result in milk let down
|
causes contraction of myoepithelial cells
|