Female Repro Flashcards
basic anatomy
- 2 ovaries
- repro tract : two fallopian tubes, uterus, cervix, vagine (last 3 = internal genitalia)
how m +f differ in urinary tract
men - urinary tract same tract as ejaculatory duct/internal genitalia.
f: urinary tract is separate from repro
fallopian tubes + ovaries - connected?
how to carry ovum thru?
not connected.
- finger-like projections called fimbriae brush over surface of ovaries. if ovum present, will be picked up and drawn into fallopian tubes.
fallopian tubes have cilia that beat in direction of uterus. movement coaxes ovum through the fallopian tube into the uterus
female external genitalia
- mons pubis
- labia majora (~scrotum)
- labia minora
- clitoris (~penis, has corpora cavernosa, can tumesce)
- vaginal vestibule (contains urethral opening + vaginal opening)
- vestibular glands
glands in F external genitalia
skenes glands = on either side of vaginal opening. produce milky white secretion (~prostate)
bartholin’s, closer to vaginal opening - mucoid type of secretion (~bulbourethral)
what is hymen?
thin fold of mucous membrane partly overlies the vaginal opening
–can remain if non-penetrative sex has been had. but can rupture in other ways.
ovary function (2 main)
- matures oocyte + endocrine function in follicles.
- ovulation
- eggless follicle differentiates into corpus luteum
fetal development +oogenesis
develops primordial germ cells in ovaries as fetus. quiescent until puberty. but oocytes will go thru apoptosis over time.
- at birth has 1-2 million
- at puberty has 300-400 thousand.
- each cycle, cohort of oocytes mature, the one with most FSH receptors will develop into mature ovum + be released/ovulated.
production of sex hormones by ovary
- E, P and Inhibin.
- some Androgens produced too + aromatized to E.
- uterus primed for baby with hormones from corpus luteum. CL releases hormones to prep + maintain endometrium. if no fertilization, endometrium sloughed + CL degrades
ovarian microanatomy
- primordial oocyte surrounded by granulosa cells = primordial follicles.
- primary follicles
- secondary follicles
- Graafian vesicle: one ovum picked to mature
- graafian becomes CL
ovarian medulla vs cortex
where arterial inflow and veinous drainage is.
- Autonomic nerves trace blood vessels.
cortex: oocytes and follicle development
hormonal control of ovarian function
- dependent upon pulsatile secretion of GnRH.
- frequency + amplitude of GnRH pulse changes over course of menstrual cycle
- change in GnRH = change in Gn (FSH,LH), E, P,I
where do FSH, LH act?
FSH - granulosa
LH - theca cells
support development of follicle, ovum + direct ovulation
when + how does ovulation occur?
- day 14 of menstrual cycle may differ btw women, btw periods
- thin walls of follicle + ovary ruptured by enzymatic digestion
- carried out of ovary by antral fluid (optimal enviro) - pushes ovum out with fluid pressure
- need LH surge*
cells around secondary oocyte?
zona pellucida + granulosa cells
noticing change in ovulation?
heaviness in abdomen, feel rupture, local inflammatory reaction
FSH actions on follicles?
acts on granulosa cells
- stimulate proliferation to develop + mature
- contain aromatase, thus producing E.
- granulosa produce antral fluid to expand follicle
= dominant follice = Graafian has increased FSH receptors = higher sensitivity to FSH = greater E production.
LH on follicles?
- act on theca cells. theca cells differentiate from granulosa cells.
- theca cells produce A, which diffuses into granulosa allowing conversion to E.
E on follicles?
produced by granulosa cells + stimulates granulosa cells to multiply + continue E production.
formation of the CL
@ovulation: discharge ovum + antral fluid
granulosa + theca cells undergo phenotypic change after ovulation.
- increase size, accumulate lipid (yellow colour)
- mini-endocrine gland: secrete E, P, I= support endometrium + maintain enviro for uterus
- maxes out at 10 days + degrades by apoptosis.
- loss of function triggers menstruation
what does inhibin do?
negative feedback on FSH
- inhibit follicle maturation/development.
- but FSH (+LH) maintain CL, so with too much (-) feedback CL degrades.
two phases of menstrual cycle?
follicular phase: uterine bleeding as follicles develop, ~day 7 follicle is dominant + chosen to mature.
ovulation at ~day 14
- luteal phase: corpus luteum functions for ~10 days, then degenerates
LH + FSH hormone patterns in normal menstrual cycle
FSH: increases early follicular phase, then steadily decreases until mid-cycle
LH: constant in follicular phase. surge triggers ovulation.
- peaks 18hr before ovulation, then rapidly declines.
E+P hormone patterns in normal menstrual cycle
both low during menstruation. *no follicles/CL to produce
- no neg feedback allows FSH + LH to increase.
- need some follicle development/differntiation for E to form.
- E rises before ovulation = (-) feedback on ant.pit and hypothal - FSH declines, but E supports follicles to continue E production.
- if high E sustained for 24-36 hours, switches to (+) feedback [E action on kisspeptin neurons] = pronounced increase in FSH, especially LH = LH surge.
- P increases in luteala phase
- E high in luteal phase, but not enough for (+) feedback.
= both E+P = negative feedback, suppressing FSH +LH thus preventing maintenance of CL.
CL maintained in pregnancy?
placenta produces hCG to saave CL and maintain it’s function.
cycles vary - quick point?
average cycle is 28 days.
- can be 20 days or 40 days.
menstrual cycle uterine changes
day 1: menstrual flow + beginning of menstrual phase.
- endometrium degenerates; sloughs off all but thin base layer (needs to be intact for endometrium development)
- at end of menstruation (average 5 days, can be 2-15) E increases thus endometrium proliferates + thickens until ovulation. = proliferative phase
- post-ovulation = secretory phase: phenotypic change in cells to enrich endometrial tissue. E+P increase secretion of glycogen, glycoproteins, mucopolysacch = uterine fluid is nutrient rich.
- allows for implantation: conceptus digests endometrial tissue + absorbs nutrients
4 phases of menstruation
- constriction of uterine blood vessels [when E+P are high, inhibit PG. as P decreases at end of luteal phase/menstruation phase PG increases; PG constricts blood vessels = no O2, nutrients -> degeneration. also effect cramping + GI changes]
- disintegration of uterine lining [low O2 and nutrients = degenerates endometrium, except for thin base layer]
- rhythmic contractions of uterine smooth muscle [PG overproduction = contraction, cramping = helps endometrial shedding]
- dilation of endometrial arterioles [ source of blood in menstruation - hemmorrhave thru capillary walls. increase permeability + hydrostatic pressure. blood + endometrial tissue exits vagina]
why menstruate if high energy input?
- endometrium takes a lot of energy to maintain.
- no point to hang on if endomet is unused. more energy efficient to get rid of + re-build.
- cleanse repro tract
- menstruation is passive due to CL decline.
- may be role in immune system to shed uterine lining.
typical E effects?
- paracrine effects in ovaries: local and feedback loop in follicle.
- modulates ant. pit + hypothal (-) feedback, except _ feedback before ovulation
- uterine actions: proliferation of endometrium. if no endometrium priming = problems w implantation + sustaining that.
- pro-progesterone effects: E increases expression of P receptors.
typical P effects?
- inhibits PG thus maintains quiescence of uterus in case of fertilization.
- effects include: vaginal dryness, atrophy, increased basal body temp = sign of ovulation
- anti-E effects: reduces E receptors to limit endometrium proliferation
negative feedback of E
on ant.pit
- decrease FSH + LH
- can do (+) feedback on LH
hypothal
- decrease GnRH impulse + amont secreted.
*inhibin acts to inhibit FSH secretion = FSH more inhibited
female sexual response - physiological responses
- significant increases in blood flow + muscular contractions (engorged breasts, nipple erection, increase clitoral diameter/length, increased vaginal blood flow + mucal lubrication
phases of sexual response on female breasts
excitement: increase breast size, nipple erect, veins distinct, areola darkens
plateau + orgasm phases:
- greater size increase, areola increases, less erect, sex flush on breasts
resolution phase:
- detumescence of areola, return to unaroused size
orgasm in females
- pleasurable sensation
- increase skeletal muscle activity
- increase HR + BP
- rhythmic contraction of vagina + uterus
- minimal function in facilitating fertilization
orgasm + fertilization
- not facilitative
- won’t hinder
- orgasm may create vacuum to help sperm move thru uterus + oviducts.
- orgasm widens cervical opening and cervix dips down, potentially facilitating sperm movement
female sexual response at repro organs
excitement: clit, labia swell as increased blood flow. vaginal lubrication
plateau: uterus increases/lifts to facilitate deeper penetration.tighten orgasmic platform (lower 1/3)
orgasm: rhythmic contractions of uterus + orgasmic platform.
resolution: uterus lowers, re-stimulation can happen.
female ejaculation
in F: emission of fluid from skenes gland.
- some women void large amount of liquid - call “ejaculation”
- small study found as women reach orgasm, bladder collects fluid + voids.. = involuntary voiding of bladder assoc with rapid filling of bladder during sexual activity
