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the ability to conceive children
not being able to achieve pregnancy after 1 year of having regular, unprotected intercourse, or after 6 months if woman > 35yrs
sperm count/quality, regularity of menstrual cycle, and possibility for implantation in uterus & maintenance of pregnancy over course of gestation
sex chromosomes, genes, and hormones
XX (female) or XY (male)
sex-determining region of the Y chromosome (partially directs formation of typical male sex organs)
XO (lack of second sex chromosomes)
XXY (extra X chromosome)
hypothalamus (GnRH) <-> anterior pituitary (LH & FSH) <-> gonads (androgens & estrogens) <-> effector tissues
Testosterone and dihydrotestosterone (DHT)
estrone & estradiol
cholesterol
aromatase
5-alpha-reductase
0-7 years
not changing (infertile?
LOWEST
FSH > LH
Approximately 8-14 years
Becoming physiologically capable of conceiving children
Initial menses in females and growth of testes in males
Onset of pulsatile GnRH
increase
LH > FSH
18-44 years
fluctuates w/ menstrual cycle (stays relatively high for sperm-producing individuals)
continue to increase
LH > FSH
45-55 years
menstruation becomes more sporadic/less frequent & decreases/changes in libido
decrease in estrogen levels
56+
cessation of menstrual cycle/decrease in sperm count/motility
HIGHEST
FSH > LH
cortisol inhibits HPG axis (which can lead to amenorrhea (absence of menses), low libido, & erectile dysfunction)
excitement, plateau, orgasm, resolution
increased blood flow to genitals (vasocongestion), vaginal lubrication & swelling of labia (females), testes swell & scrotum tightens (males)
sexual excitement continues to grow
climactic short phase of sexual response, sensation of orgasms across sexes does NOT differ, & some females can vacillate between plateau & orgasm many times
body slowly returns to its original unexcited states, refractory period occurs during male resolution phase (& for some females) in which individuals cannot becomes aroused for a period of time
leydig cells of the testes for testosterone production
sertoli cells of the testes for inhibin & androgen-binding protein production
theca cells of the ovaries for androgen (-> estrogen) & progesterone production
granulosa cells of the ovaries for estrogen & inhibin production
two meiotic divisions of one spermatogonium yield four spermatids which then develop into four mature sperm
more than 20 million/mL
less than 15 million/mL
Seminiferous tubules -> Epididymis -> Vas deferens -> Ejaculatory ducts -> None -> Urethra -> Penis (SEVEN-UP)
head (contains nucleus & acrosome (digestive enzymes for outer ovum)), midpiece (contains motor & mitochondria), tail (contains flagellum), & mucus (from semen, protects sperm during travel)
Nonoxynol-9
degrades acrosome & inhibits sperm motility
growth process where primary egg cells (ova) become mature ova
ovarian cycle & uterine cycle
follicular phase, ovulation phase, and luteal phase
follicular growth
one or more follicles have ripened; ovary releases oocyte(s)
secretes hormones that maintain uterine lining (in case of fertilization/implantation)
primordial -> primary -> secondary -> antral
FSH > LH (both low); progesterone & inhibin low, estrogen (estradiol) high & increasing
estrogen downregulates GnRH, LH, & FSH but promotes estrogen secretion by the follicle; LH stimulates androgen secretion from thecal cells, and FSH stimulates granulosa cells to produce estrogens from the androgens via aromatase & AMH
LH >> FSH (both spike); estrogen spikes before ovulation, after ovulation progesterone & inhibin rise
LH stimulates thecal cells to produce androgens, FSH stimulates granulosa cells for high estrogen output (via androgens & aromatase), inhibin secretion, and progesterone release; Inhibin suppresses FSH, while estrogen & progesterone promote GnRH & LH
surge of LH
follicle ruptures and egg (ovum) is released
LH > FSH (both very low), progesterone highest, estrogen & progesterone still @ moderate levels
Corpus luteum secretes increased estrogen progesterone, and inhibin, which shut off FSH & LH
estrogen, progesterone, and inhibin return to low levels, and LH & FSH begin increasing (FSH > LH)
Corpus luteum dies, which decreases estrogen and progesterone; as LH & FSH increase again, FSH stimulates new follicle development
fertilized egg
fertilized egg after a week that implants into uterine lining (endometrium) during pregnancy
an embryo
fetus
uterine/fallopian tube
SRY blocks DAX1 -> upregulates gene expression of SOX9 & SF1 which bind to the promotor region of AMH -> inhibits development of female reproductive tract (or Mullerian ducts)
no SRY gene, no blockage of DAX1 -> suppresses gene expression of SOX9 & SF1 -> AMH absent which enables development of female reproductive tract (Mullerian ducts)
make sperm (spermatogenesis)
store and concentrate sperm, increase sperm motility & fertility
supply fructose for energy
Produces alkaline fluid that enhances sperm motility & can neutralize vaginal secretions
secrete mucus for lubrication
secrete sex steroids (estrogen, progesterone, & inhibin) & produces oocytes
presence/absence of SRY gene, AMH, & testosterone (presence causes males (Wolffian ducts -> epididymis & vas deferens) & absence causes females (Mullerian ducts -> uterine tube & uterus))
presence/absence of strong androgens (DHT) (presence causes males (genital tubercle becomes glans of penis; labioscrotal fold becomes scrotum) & absence causes females (genital tubercle becomes clitoris; labioscrotal fold becomes labia majora))
complete androgen insensitivity syndrome (androgens present but no action - female phenotype but male internal structures)
SRY gene still present, so fetal testes develop, and AMH, DHT, & T are present but have no action so no Wolffian ducts or male reproductive tract development
no uterus so no menses, but no male secondary sex characteristics; breasts develop b/c aromatase & estrogen receptors are still working
5-alpha-reductase deficiency (T does not get transformed into DHT)
SRY present so fetal testes develop & AMH present (no Mullerian ducts), and T is present so Wolffian ducts develop into male internal repro tract, but no DHT so not strong enough response to develop penis, scrotum, and prostate
testes develop & eventually produce enough T to compensate for lack of DHT, leading to the development of penis & scrotum (external genitalia) at puberty
congenital adrenal hyperplasia (mutation in 21-hydroxylase, the enzyme that makes glucocorticoids)
no SRY, so fetal ovaries develop, & no AMH so Mullerian ducts present & develop into uterus, uterine tubes, & inner vagina; adrenal glands are stimulated to make excess androgens in absence of glucocorticoids which enlarges the external female genitalia
may experience early puberty (nothing else unordinary)
no SRY genes so fetal ovaries develop, but female repro tract is underdeveloped
relatively short stature, smaller breasts, and no menses
SRY present so male internal & external structures develop; testicular atrophy may occur
taller stature, breasts may develop, feminized hair growth