anatomy 2 final exam: reproductive system

seminiferous tubule structure

blindly ending tubules in the testes — kits for making sperm cells; millions made per day throughout entire life

• peritubular/myoid cells: smooth muscle-like cells on the outside — contract to move immature sperm cells into epididymis

• germ cells (spermatogonia): on the outer edge of the tubule

  • type A & type B — type B is committed to entering meiosis

  • undergo mitosis to replenish population (~30x before telomeres run out)

  • have telomerases that regenerate telomeres after mitosis (cancer cells also have this)

  • spermatogonia are diploid; sperm cells are haploid

• sustentacular cells (aka sertoli/nurse cells): span the seminiferous tubule; shaped like a christmas tree; envelop cells as they move through mitosis/meiosis

epididymis

tightly coiled structure where sperm cells mature, become functional, & develop motility

• caput (head) → corpus (body) → cauda (tail)

• becomes continuous w/ vas deferens → carries sperm to urethra

• vasectomy: cutting of ends of the vas deferens

spermatogenesis

production of sperm cells in seminiferous tubules

• spermatogonia → (differentiate) → primary spermatocytes

• primary spermatocytes → (meiosis 1) → 2 haploid secondary spermatocytes

• secondary spermatocytes → (meiosis 2) → 4 haploid spermatids

• spermatids → (differentiation/spermiogenesis) → spermatozoa (immature sperm cells)

• release from seminiferous tubule = cytogenous secretion (whole cell is released)

spermiogenesis

differentiation process from spermatid → spermatozoa

• acrosome: organelle that develops in the Golgi

  • during fertilization, interacts w/ zona pellucida (glycoprotein layer surrounding the oocyte)

  • drugs can contain antibodies that prevent acrosome from interacting w/ zona pellucida

• centrioles move to one pole → extend → form microtubules → develop into flagella

• mitochondria condense in the mid piece (for energy)

• excess cytoplasm is shed

hormonal regulation of male reproduction — HPG axis

hypothalamic-pituitary-gonadal axis

• hypothalamus releases GnRH → anterior pituitary releases:

  • LH (luteinizing hormone, also called ICSH in males — interstitial cell stimulating hormone):

    • stimulates Leydig cells (interstitial cells, outside seminiferous tubules) to produce testosterone

  • FSH (follicle stimulating hormone):

    • stimulates sertoli cells to secrete androgen binding protein (ABP) — binds testosterone bc spermatogenesis is testosterone-dependent

• testosterone: negative feedback on hypothalamus & anterior pituitary → ↓ GnRH, LH, FSH

• other androgen effects: ↑ muscle mass, ↑ larynx volume (lower voice), acne, ↑ aggression

• testosterone abuse:

  • can see low GnRH, LH, FSH on blood panel (negative feedback)

  • excess testosterone → aromatized into estrogen → gynecomastia (breast tissue development)

  • can take HCG to kickstart HPG axis back to normal levels

testosterone levels over male lifespan

• testosterone levels decline at ~25–35 yrs, but remain high enough to generate sperm throughout entire life

• one-step conversion: testosterone → 17-β-estradiol → suppresses osteoclast activity → bone density remains relatively high in males (reason why males experience less osteoporosis than females)

oogenesis

every egg cell is present at time of birth — production does NOT continue throughout life

• primary oocyte begins meiosis but is arrested in prophase 1 — nothing happens until puberty

• at puberty (every menstrual cycle): one primary oocyte continues meiosis → secondary oocyte (gives off 1st polar body)

• secondary oocyte arrested in metaphase 2 — will NOT finish meiosis unless fertilized by sperm

• if fertilized: finishes meiosis → ovum (mature egg cell) + 2nd polar body

• result: starts w/ 1 diploid → ends w/ 1 haploid ovum + 2 polar bodies (haploid)

• continues until menopause (~45–55): "halting of menstrual cycle"

ovarian follicle development (follicular phase)

from primordial → vesicular follicle takes ~350 days

• primordial follicle: present at birth; single layer of follicular cells surrounding primary oocyte

• primary follicle: larger; granulosa cells (cuboidal, in direct contact w/ oocyte); thecal cells (around granulosa cells)

• secondary follicle: larger; multiple layers of granulosa cells; antrum (pockets of follicular fluid)

• vesicular follicle (aka mature/graafian/tertiary follicle): capable of releasing egg during ovulation

  • contains: secondary oocyte, large fluid-filled antrum, corona radiata (crown of granulosa cells around oocyte), cumulus oophorus (stalk connecting oocyte to corona radiata)

• FSH causes 5–7 follicles to begin developing each cycle; only one becomes dominant

follicle numbers over female lifespan

• millions of follicles develop during fetal development

• at birth (per ovary): ~300,000 follicles

• 99.9% become atretic (degenerate & die)

• ~300 per ovary (600 total) continue

• menstrual cycle is circalunar (~28 days); 600/12 months ≈ 50 follicles per year → lasts until menopause

• endocrine disrupting chemicals: puberty onset has shifted from ~16 to ~10 yrs

• primary cause of menopause: follicles run out

ovarian cycle — 3 phases

• follicular phase (days 1–14): follicles develop under FSH stimulation

• ovulation phase (day 14):

  • secondary oocyte released from vesicular follicle w/ corona radiata

  • ruptured follicle fills w/ blood → corpus hemorrhagicum → corpus luteum

  • LH (+ enzymes) breaks the wall of the ovary to release the follicle

  • released onto fimbriae (finger-like projections on end of fallopian tube) → captured & moved toward uterus

• luteal phase (days 14–28):

  • corpus luteum: remnant of ruptured follicle; secretes progesterone & estrogen in high concentrations

  • if no fertilization → corpus luteum → corpus albicans (degenerates)

hormonal regulation of HPG axis in females — 2 cell 2 gonadotropin model

• hypothalamus releases GnRH → anterior pituitary releases LH & FSH

• LH: causes cells of ovarian follicles to generate androgen

• FSH: increases aromatase production → cells convert androgen → estrogen

• ovarian follicles also produce inhibin → negative feedback on GnRH & gonadotropins

• estrogen acts differently depending on timing:

  • early: stimulates dominant follicle to mature → produces large amounts of estrogen → positive feedback on HPG → LH surge (+ FSH peak) → triggers ovulation

  • after ovulation: negative feedback — inhibits LH secretion; estrogen & inhibin ↓ FSH secretion; inhibits GnRH secretion

uterine (endometrial) cycle — 3 phases

circalunar cycle (~28 days); ovulation at day 14

• menstrual phase:

  • stratum functionalis sloughs off / detaches from stratum basalis

  • ↓ thickness of endometrium

  • caused by loss of progesterone → ischemia of spiral arteries → stratum functionalis sheds

• proliferative phase:

  • under influence of estrogen: new stratum functionalis develops

  • endometrial glands develop; spiral arteries develop

  • endometrium rebuilds

• secretory phase:

  • spiral arteries convert stratum functionalis → secretory mucosa

  • endometrial glands secrete uterine milk — makes endometrium "lush" to sustain possible fertilized egg

  • almost entirely due to progesterone ("pro-gestational hormone")

  • endometrium reaches peak thickness at end of 28-day cycle

  • if no pregnancy: corpus luteum stops functioning → loss of progesterone → ischemia → menstrual phase begins again

big picture — ovarian & uterine cycle overlap

• follicular + menstrual phase (days 1-5): GnRH → ↑ FSH & LH → multiple follicles start to develop; low progesterone → stratum functionalis sheds (stratum basalis stays intact)

• follicular + proliferative phase (days 6-14): dominant follicle selected → ↑ estrogen → endometrium rebuilds (glands & spiral arteries)

• ovulation (day 14): continued high estrogen → positive feedback on HPG → LH surge → dominant follicle ruptures → secondary oocyte + corona radiata released; FSH also peaks; endometrium is thickest

• luteal + secretory phase (days 14-28): collapsed follicle → corpus luteum → ↑ progesterone → endometrium becomes secretory mucosa; progesterone peaks then drops ~day 24 if no fertilization → cycle restarts

human chorionic gonadotropin (HCG)

produced by developing embryo/placenta

• keeps corpus luteum functioning → corpus luteum continues generating progesterone

• progesterone effects during pregnancy:

  • maintains stratum functionalis of endometrium

  • firms the cervix (creates mucus plug)

  • induces uterine relaxation (allows expansion for growing embryo)

• detected in urine via pregnancy tests (antibodies attach to HCG → produce line)

• HCG peaks in 1st trimester, then levels decline

• estrogen & progesterone slowly increase over course of pregnancy

• just before week 40: progesterone levels drop → induces contractions & delivery

oxytocin

made by hypothalamus

• estrogen causes oxytocin receptors to develop on the uterus

• oxytocin stimulates smooth muscle of uterus (myometrium) to contract

• also stimulates placenta to make prostaglandins → cause more vigorous contractions → positive feedback loop

oral contraceptive pill

contains progesterone (21 days progesterone + 7 days placebo to induce menstruation)

• progesterone (along w/ ↑ estrogen & inhibin) inhibits FSH & LH release & blocks GnRH → no follicles develop → no ovulation

• progesterone also forms mucus plug at base of cervix to block sperm entry

• ~80% effective

permanent birth control methods

• tubal ligation: uterine tubes cut & ligated

  • ovarian steroid hormone production still happens

  • ovulation still occurs — egg just can't reach oviduct

• vasectomy: vas deferens severed, ends cut & cauterized

menopause

"halting of menstrual cycle" (~45–55 yrs); primary cause: follicles run out

• generation of estrogen & progesterone halted → systemic consequences (steroid hormones have huge role in entire body)

• perimenopause (period before): hot flashes, insomnia, mood changes, memory impairment, weight gain

• postmenopause (period after): fatigue/mood swings improve; ↑ risk of osteoporosis, heart disease, Alzheimer's

• women's health initiative study: tested giving back estrogen/progesterone — stopped bc saw ↑ risk of breast cancer, ↑ cognitive impairment/dementia, cardiac arrest

  • some positives: reduced osteoporosis

estrogen as a vasodilator

• estrogen ↑ nitric oxide (NO) synthesis → NO causes smooth muscle relaxation → vasodilation

• estrogen also ↑ opening of K+ channels in vascular smooth muscle → vasodilation

• paradox: when estrogen is given exogenously (as in HRT), it can act as a vasoconstrictor