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128 Cards in this Set
- Front
- Back
list the stages of a ovulating follicle
|
primordial (primary oocyte)
primary (larger oocyte, gap junctions form) preantral (+zona pellucida) antral (has follicular fluid-->antrum) pre-ovulatory (GC differentiate-->cumulus) |
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what happens after ovulation?
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the granulosa and theca cells become luteal cells
the produce prog + estrogen Basal Lamina dissolves -Cell types intermingle -Blood vessels enter |
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what are the phases of the ovarian cycle?
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Follicular (10-22 days): Development of egg
Ovulatory (36 hours): Release of egg Luteal (14 days): Corpus luteum |
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phases of Uterine Cycle?
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Proliferative: Growth of endometrium
Secretory (14 days): Differentiate endometrium Menstruation (4-5 days): Shed endometrium |
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# C's of cholesterol, progesterone, androgens, estrogen
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27 (cholesterol)
21 (progesterone) 19 (androgens) 18 (estrogen) |
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which hormones are dominant in
follicular phase? luteal phase? |
follicular: estrogen
luteal: estrogen, progesterone + when hormone levels fall, corpus luteum dies |
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what's the Two Cell, Two Gonadotropin Theory
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Theca cells have LH receptors -->produce Androgens
ANDROGENS diffuse into the Granulosa Cells where it's converted to ESTROGENS Granulosa Cells have FSH receptors, FSH increases Aromatase which converts androgens to estrogens) (BUT: Granulosa Cells get LH receptors later ) |
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what are the 3 ovarian peptide hormones and what do they do?
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---INHIBIN (inhibits FSH
---ACTIVIN (stimulates FSH release, Augments FSH action in ovary) ---FOLLISTATIN (bind Activin, suppress activity) |
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where are inhibin, activin, and follistatin synthesized?
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granulosa Cells
-Secreted into follicular fluid -Endocrine & Paracrine signaling |
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FSH ______ Inhibin
Inhibin_______ FSH |
FSH stimulates Inhibin
Inhibin inhibits FSH |
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actions of inhibin (4)
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Blocks synthesis (FSH)
Blocks secretion (FSH) Reduces GnRH receptors Promotes Intracellular degradation of FSH |
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where is activin expressed?
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pituitary
granulosa (secrete into follicular fluid) |
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actions of activin
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augments FSH by:
inc GnRH receptors in pituitary inc FSH receptors in ovary (paracrine effects...granulosa secrete activin into follicular fluid) |
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what does follistatin do?
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binds activin
its a FSH-suppressing protein) |
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regulation of follistatin?
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activin stimulates follistatin
inhibin inhibits |
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high frequency GnRH pulses favor _____
low frequency favor _____ continuous pulses lead to |
LH
FSH desensitization |
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how can desensitization happen?
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--Uncoupling of receptor and signaling pathway
---Down-regulation of functional receptors (Internalization of receptors) |
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fxns of FSH
(in female) |
Promote GC Proliferation
Induce FSH receptors Induce Aromatase--> Estrogen Induce LH receptors |
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fxns of LH
|
Androgen production
Ovulation Supports corpus luteum (how does it do each of these??) |
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when does mitosis of oogonium (46XX) to form more oogonia (46XX) occur?
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only during fetal life
|
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oogonium-->(Meiosis) -->Primary Oocyte (46XX)
the primary oocyte is arrested in _____ until ovulation |
prophase 1
|
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t/f new oocytes form after birth
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FALSE
you have what you have |
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meiosis 1 converts 46XX (primary oocyte) to _______
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secondary oocyte (23X)
+ a polar body |
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what's atresia?
|
Degenerative process of oocytes
Via apoptosis (programmed cell death) in GC fetus: 6-7 million newborn: 1 million puberty: 300,000 menopause: NONE left! (start out with |
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primordial ---> preantral follicle
is hormone _________ |
independent
No FSH receptors on GC yet |
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Preantral --> Antral Follicle
is _________ dependent |
FSH
preantral follicles are responsive to FSH now! -FSH receptors ---> estrogen production |
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what does FSH + estrogen do to preantral follicles?
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inc FSH receptors
inc GC mitosis---> growth! |
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what are traits of follicles that do not ovulated? ie the non-dominant ones?
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Not enough FSH receptors
Not enough aromatase Androgens--> atresia ----dec aromatase ----Inhibit LH receptor |
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Leydig cells produce
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testosterone
|
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t/f Leydig cells produces mineralocorticoids, glucocorticoids
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False!
Leydig cells dont' have 11B nor 21B, so can only produce androgens (testosterone)! |
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LH stimulates what enzyme?
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cholesterol desmolase
(just like ACTH in the adrenal gland) |
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what converts testosterone to dihydrotestosterone?
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5-alpha reductase
|
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LH acts on ___________
FSH acts on ___________ (in the male) |
Leydig (inc testosterone synthesis)
Sertoli (stimulate spermatogenesis) |
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t/f testosterone acts via intra-testicular paracrine mechanism to reinforce the spermatogenic effects of FSH on Sertoli cells
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True!
|
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________caues prenatal diffrentiation of the wolfiann ducts
_____________ diffrentiation of external genitalia (males) |
testosterone
dihydrotestosterone |
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__________causes pubertal growth spurt in males
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testosterone
|
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t/f dihyrotestosteone increases the size and secretory activity of the epididymis, vas deferens, prostate, and seminal vesicles
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true!
|
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t/f GnRH upregulates its own receptor in the ap
|
true!
|
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puberty initiated by _______-
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pulsatile GnRH release from the hypthalamus
|
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FSH > LH when in a person's lifespan?
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childhood + senescence
(puberty: the reverse, LH>FSH) |
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t/f estrogen inhibits prolactin secretion
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false!...
estrogen stimulates prolactin secretion (but blocks its action at the breast) |
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t/f both estrogen + progesterone maintain pregnency
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true!
|
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during __________ phase, progesterone has negative feedback effects on FSH & LH
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luteal phase
|
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t/f :
LH and FSH levels are up during follicular phase |
false! estrogen exerts negative feedback inhibition on the ap during follicular phase
|
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t/f the basal body temp increases during the follicular phase
|
false!
during the luteal phase (progesterone is + during luteal phase and it affects the hypothalamic thermoregulatory center) |
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what causes menses?
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sudden drop in estrogen + progesterone (bc the corpus luteum dies)
|
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after fertilization occurs, what rescues the corpus luteum from regression?
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human chorionic gonadotropin (HCG) which is produced by the PLACENTA
|
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in the first trimester, who's producing the estrogen + progesterone?
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the corpus luteum (stimulated by HCG)
|
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in the 2nd and 3rd trimester, what takes over estrogen + progesterone production after corpus luteum stops ?
(stops due to declining levels of HCG) |
well the PROGESTERONE is produced by PLACENTA
estrogens produced by interplay of fetal adrenal gland + the placenta |
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how is estrogen produced in the 2-3 trimesters?
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the FETAL ADRENAL GLAND synthesizes DHEA-S (dehydroepiandrosterone-sulfate)
hydroxylated in the fetal liver go to placenta, where enzymes remove sulfate and aromatize to estrogens |
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the major placental estrogen is _______--
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estriol
|
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what's human placental lactogen?
|
produced throughout pregnancy. actions are similar to those of GH and prolactin
|
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what inc threshold for uterine contraction?
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progesteron
|
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near term, the estrogen/prog ratio increases....resulting in?
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uterus becomes more sensitive to contractile stimuli
|
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do we know what the initiating even in parturition is?
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NO!
(interesting...) |
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why doesn't lactation occur during pregancy, despite the high levels of prolactin?
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estrogen, although it stimulates prolactin synthesis by ap, blocks its action at the breast (along with prog)
|
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why is ovulation suppresed during lactation?
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bc prolactin is high and it:
-inhibits hypothalamic GnRH secretion -inhibits the action of GnRH on teh ap....so dec LH, FSH -antagonizes actions of LH and FSH on ovaries |
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list functions of the follicle
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-provide nutrients to the developing oocyte
-release oocyte @ proper time (ovulation) -prepare vagina and tubes to aid in fertilization by sperm -prepare lining of uterus for implantation of the fertilized egg -in the event of fertilization, maintain hormone production until placenta takes over |
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by 6 months of birth, all oogonia have become _____________ suspended in Prophase I
|
oocytes
|
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what happens to follicle that released its egg
1) after fertilization 2) no fertilization |
becomes corpus luteum (nurtures developing zygote)
becomes corpus albican (a scar) |
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with ovulation, the _________ is completed, and the resulting __________ oocyte enters the fallopian tubes where it begins the _________________
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first mieotic division
secondary oocyte second mieotic division |
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in both the testes and ovary____________ is the major hormone produced
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testosterone
|
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female:
_______________ cells are the only cells with FSH recepters |
granulosa
|
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over course of menstrual cycle, __________ precedes progesterone, preparing the target tissues to respond to progesterone
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estrogen
|
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without__________, progesterone doesn't have that much activity!
|
estrogen
|
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what does estrogen do in follicular phase?
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-growth of endometrium
-growth of glands + stroma -cervical mucus: watery, elastic |
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progesterone _______ quantity of cervical mucosa
|
dec
the opportunity of fertilization has passed....the cervical mucus doesn't have to be penetrable by sperm |
|
(female)
LH stimulates __________ FSH stimulates __________ |
cholesterol desmolase
aromatase |
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theca cells produce both ___________ + testosterone
|
progesterone
|
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estradiol causes the endometrial lining to proliferate
__________ stimulates secretory activity of the endometrium and increase its vascularity (it's preparing the endometerium to recieve a fertilized egg) |
progesterone
|
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how many days after ovulation does HCG "rescue" the corpus luteum?
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10 days
|
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fertilization of the ovum takes place wi ________ of ovulation
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24 hrs
|
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when does the blastocyst implant in the endometrium?
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5 days after ovulation
|
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without fertilization and the stimulation by __________, the corpus luteum regresses 12 days after ovulation, at which point it stops producing steroid hormones and menses occurs
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HCG
|
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what hormone is tested in a pregnancy test?
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HCG
|
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pregnancy lasts ______ wks counting from ________
(or 38 wks from the date of the last ovulation) |
40
last menstrual period |
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how is progesterone produced by the placenta?
remember that placenta is the only organ that can't make cholesterol from scratch (ie from acetate) |
cholesterol enters the placenta from the maternal circulation
placenta converts it to progesterone |
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estriol synthesis in 2nd and third trimester?
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cholesterol from maternal blood goes to placenta-->pregnenolone--> goes to the fetal adrenal gland-->DHEA-sulfate-->fetal liver--> 16-OH DHEA-sulfate------> goes back to placenta---(sulfatase, aromatase)---> ESTRIOL
|
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the contraceptive effect of progesterone alone is based primarily on its effects on ____________
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cervical mucus and tubal motility
|
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during which period of the menstrual cycle does the dominant follicle produce most of its estrogen?
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5-14 days
|
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in a genetic male with deficiency of 5a-reductase, which of the following is present:
testes muscle mass male hair distribution epididymis deepening of the voice |
testes
muscle mass epididymis deepening of the voice (all except male hair distribution) |
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what is dihydrotestosterone responsible for?
|
-external male genitalia (penis + scrotum)
-stimulation of hair follicles -male pattern baldness -activity of sebaceous glands -growth of the prostate |
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Addison's disease: (inc/dec)
cortisol ___ ACTH ___ blood glucose ____ |
dec
inc dec |
|
nephrogenic diabetes insipidus: (inc/dec)
ADH urine osmolarity |
inc
dec |
|
Conn's syndrome (inc/dec)
serum K+ blood pressure renin |
dec
inc dec |
|
cushing's disease (inc/dec)
ACTH cortisol blood glucose |
all high
|
|
surgical hypoparathyroidism (inc/dec)
serum Ca serum Phosphate urinary cyclic AMP |
dec
inc dec |
|
car accident that severs the hypothalamic pituitary stalk
prolactin ADH serum osmolarity PTH |
prolactin (increased) due to loss of tonic inhibition of dopamine
ADH (decreased) serum osmolarity (increased) PTH (no change) |
|
autoimmune destruction of the thyroid
inc/dec T4 TSH basal metabolic rate |
dec
inc dec |
|
21B-hydroxylase deficiency
inc/dec ACTH cortisol DOC (deoxycorticosterone) aldosterone DHEA urinary 17-ketosteroids |
ACTH (inc)
cortisol (dec) DOC (deoxycorticosterone) (dec) aldosterone (dec) DHEA (inc) urinary 17-ketosteroids (inc) |
|
giving dexamethasone to a normal person
(inc/dec) ACTH cortisol |
dec
dec |
|
17a-hydroxylase deficiency
inc/dec blood pressure blood glucose DHEA aldosterone |
inc
dec dec dec |
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what are the three male accessory glands (that produce seminal fluid)?
|
seminal vesicles, bulbourethral glands, prostate gland
|
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path of sperm from testicular lobule to urethra?
|
seminiferous tubules -> tubuli recti -> rete testis -> efferent ducts -> epidymis -> vas deferens -> ejaculatory ducts -> urethra
|
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until how many weeks of gestation are female/male gonads still bipotential?
|
7 weeks
|
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where are sertoli and leydig cells located in relation to the basal lamina that surrounds the seminiferous tubules?
|
sertoli: inside, where sperms develop;
leydig: outside in interstitium -> makes testosterone |
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what cells does FSH bind in male? function?
|
FSH binds sertoli cells -> inc. ABP
|
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what type of cells does LH bind in male? function?
|
LH binds leydig cells -> inc. testosterone (test -> dec. LH)
|
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what are the functions of sertoli cells?
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nurture sperms, makes ABP (upon binding FSH), makes inhibin B (inhibits FSH), has 5a reductase -> makes DHT; forms blood/testis barrier
also during development, makes AMH -> mullerian duct regression |
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what converts testosterone to DHT?
|
5 alpha reductase (type I: adult; II: fetus)
(DHT more potent, made at site of action, little in circulation) |
|
what are the differential effects of DHT vs testosterone?
|
DHT:
maturation of UG tract; differential of external genitalia; phallic growth; pubic hair; temporal hair regression Test: stimulate wolffian duct to become UG tract; muscoskeletal growth; spermatogenesis; gonadotropin regulation |
|
what is the role of estradiol in male?
|
neg feedback (made from testosterone by aromatase); epiphyseal closure
|
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what happens with DHT deficiency in an XY individual?
|
ambiguous external genitalia
1. still has testosterone to maintail wolffian duct, so still has testes, vas deferens etc 2. still has sertoli cells to secret AMH -> mullerian duct regression -> no uterus, but has blind vaginal pouch 3. no DHT to stimulate male external genitalia development |
|
how are estrogen and testosterone transported in blood?
|
~70% with SHBG; ~30% with albumin
|
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how are DHT, androstenedione and DHEA transported in blood?
|
70-90% with albumin; 10-30% with SHBG; trace soluble.
|
|
what increases SHBG (sex hormone binding globulin)?
|
hyperthyroidism, pregnancy, estrogen treatment
|
|
what decreases SHBG?
(sex hormone binding globulins) |
Glucocorticoids
Androgens Progesterone Growth Hormone/IGF-1 Insulin |
|
how many sperms are produced each day?
|
~200 million!!!! ahhhh... life!
|
|
spermatogonia -> spermatozoa pathway?
|
Spermatogonia
1˚ Spermatocyte -> MI 2˚ Spermatocyte -> MII Spermatids (Haploid) Differentiating Spermatids Spermatozoa |
|
how long does it take for a sperm to mature?
|
70 days
|
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t/f
more mature sperms are closer to the lumen of the testicular lobule |
TRUE; least mature on periphery
|
|
t/f
spermatogenesis requires both LH and FSH |
TRUE; LH -> leydig cells -> produce testosterone
FSH -> sertoli cells -> ABP (maintains testosterone level), also makes DHT |
|
what is capacitation for sperms?
|
maturation process when sperms reach female reproductive tract,
Removal and/or modification of molecules on the sperm membrane for the acrosomal reaction and to bind Zona Pellucida |
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when does implantation occur?
|
5-6 days after fertilization
|
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what are the steps of fertilization?
|
1. sperm binds to zona pellucida (mainly through ZP3)
2. acrosomal rxn 3. digest ZP 4. membrane fusion 5. nucleus of sperm enters ovum |
|
what happens to cumulus cells when sperm encounters ovum?
|
cumulus cells expand to increase chance of receiving sperms (but no acrosomal rxn occurs)
|
|
what happens to ZP3 and ZP2 receptors on sperm membrane during acrosomal rxn?
|
ZP3 R degraded as acrosomal rxn dissolves outer sperm membrane -> exposes ZP2 R on inner membrane -> grabs onto ovum and maintain contact
|
|
what are the events in egg activation?
|
1. cortical rxn -> degrades ZPs -> prevents polyspermy
2. inc. synthetic activity (to prepare for mitosis of embryo) 3. ovum completes MII |
|
progesterone during pregnancy
|
Prepares and maintains endometrium
--Supports early pregnancy Immunosuppressant --Suppresses maternal immunological response to fetal antigens Maintains uterine quiescence ---Antagonizes uterine smooth muscle contractions Substrate for fetal adrenal steroidogenesis Inhibits gonadotropins (FSH, LH) --Prevents further ovulations |
|
predominant estrogen in pregnancy
|
estriol
|
|
what does Human Placental Lactogen do?
|
Glucose for fetus
Lipolysis Glucose uptake Risk of diabetes during pregnancy (gestational diabetes) |
|
in Primary hypothyroidism
low T3/4-->inc TRH...inc TSH what happens to prolactin? |
increases
(bc TRH inc prolactin!!) (prolactin is tonically inhibited by dopamine) |
|
symptoms of Hyperprolactinemia
|
Hyperprolactinemia
-Suppress GnRH -Hypogonadism -Amenorrhea -Menstrual irregularities -Infertility --No ovulation --Inadequate corpus luteum |
|
common causes of hyperprolactinemia?
|
Adenomas (benign tumors) of the pituitary that secrete prolactin (prolactinomas)
Hypothryoidism Medications that interfere with dopamine secretion |
|
how does the cervix/cervical mucus affect fertility?
|
Cervical Mucous
--Captures sperm --Filters sperm --Excludes seminal secretions --Removes abnormal sperm Cervix --Sperm reservoir |
|
HCG and _____ bind to the same receptor
|
LH
|
|
theca cells produce _________ (stimulated at the first step by LH)
which diffuses to the nearby granulosa cells which contain aromatase and convert testosterone to _________ (aromatase stimulated by FSH) |
theca cells produce TESTOSTERONE (stimulated at the first step by LH)
which diffuses to the nearby granulosa cells which contain aromatase and convert testosterone to ESTRADIOL (aromatase stimulated by FSH) |
|
what's the big deal that FSH stimulates Sertoli cells to make ABP (androgen binding protein)?
|
Androgen-binding protein (ABP) is a glycoprotein (beta-globulin) produced by the Sertoli cells in the seminiferous tubules of the testis that binds specifically to testosterone (T), dihydrotestosterone (DHT), and 17-beta-estradiol.
By binding to T and DHT these hormones are made less lipophilic and become concentrated within the luminal fluid of the seminiferous tubules. The higher levels of these hormones enable spermatogenesis in the seminiferous tubules and sperm maturation in the epididymis. |