The female genital tract Flashcards
What is the fundamental reproductive unit in females?
What is it composed of?
What is it surrounded by?
-
single ovarian follicle
- composed of one germ cell (oocyte)
- surrounded by endocrine cells
Avg age of menarche
11-13
Female monthly sex cycle controlled by?
gonadotropins
- only single ovum released
- endometrium prepared for implanation
Describe the ovarian cycle?
follicular phase - 15 days
Ovulation -occurs day 14
Luteal phase -13 days
Phases of endometrial growth and menstration
proliferative phase (11 days) (cells of endometrium are proliferating and becoming thicker)
secretory phase (12 days) (thicking even more)
menstrual phase (5 days) (shed)
Describe the Hierarchies of homrones of the female hormonal system?
- Hypothalamus -GnRH
- Anterior pituitary -FSH & LH
- The ovarian hormones- Estrogen (FSH) and Progesterone (LH)
A surge in LH is required for?
Ovulation
when are estrogen and progesterone at their highest during the cycle?
estrogen: after menses → ovulation
progesterone: after ovulation → menses
when are FSH and LH high during the cycle?
- FSH: early follicle maturation, a bit higher than LH on either side of ovulation, spikes but lower than LH at ovulation
- LH: spikes at ovulation
what hormone contributes to early follicular maturation?
FSH
what hormones contribute to late follicular maturation?
FSH, LH, estrogen
How does LH surge cause ovulation?
causes granulosa and theca cells produce more progesterone → transition to luteal phase
which anterior pituitary hormone stimulates estrogen and which progesterone?
FSH → estrogen
LH → progesterone
Body temperature and ovulation?
-spikes to 98.6 at ovulation, slowly returns to 96.8 over the rest of the luteal phase
what happens physiologically during the menstrual cycle?
6 - 12 follicles develop, but only 1 follicle matures → ovulation releases ovum → corpus lutem degrades → corpus albicans
what is endometriosis?
- chronic, estrogen-dependent, inflammation w/ varying degree of severity (can be all over or localized)
- Characerized by the presence and growth of endometrial tissue outside the uterine cavity
uterine tissue outside the uterus
what are the clinical features of endometriosis?
mod - severe pain, lower back pain, infertility, dysmenorrhea
what are the most common sites of endometriosis?
ovaries, cul-de-sac, broad ligaments
⇒cul de sac refers to the rectouterine pouch (the pouch of Douglas)
can be anywhere in the peritoneum
pathogenesis of endometriosis is:
multifactoral
-ectopic endometrial tissue, inflammation, imbalanced cell prolif/apoptosis, angiogenesis, genetic factors
what are the 2 theories of endometriosis?
Sampson’s theory of retrograde menstruation: endometrial cells flow backwards thru fallopian tubes into peritoneal cavity during menses (can be due to obstruction)
Pre-Menarcheal endometriosis: undifferentiated mullerian cells seed the peritoneal cavity & differentiate into endometrial tissue
what are the 3 main players in the pathogenesis of endometriotic pain?
- endometriotic lesions → directly stimulate sensory nerves → nociceptive pain signal
- innate immune system release → proinflamm mediators and pro-nociceptive mediators such as nerve growth factor (NGF )→ stimulate sensory nerve endings
- peripheral nervous system → spinal cord
what are uterine leiomyomas?
fibroids: benign myometrial tumors (created from smooth muscle cells of the myometrium)
what is the most common pelvic tumor in women?
fibroids (confined & non-malignant) from uterus
what are the clinical presentation/clinical significance of fibroids?
alters function/structure → excessive bleeding in uterus
How does an Uterine Leiomyoma form?
-transformation of normal myocytes (cells of the smooth muscle) into abnormal myocytes
-growth of abnormal myocytes into clinically apparent, confined tumors (affect structure and function- not malignant)
which 5 factors contribute to leiomyomas?
- genetics
- steroid hormones (estradiol & progesterone) → mitogenic stimuli
- stem cells
- angiogenesis
- ↑ fibrotic factors (ECM, collagen, abnormal fibrotic GFs)
what is PCOS?
intraovarian androgen excess & insulin resistance → polycycstic ovaries
triad of insulin resistance to keep in mind with PCOS?
triad of insulin resistance to keep in mind with PCOS
- DM2
- Obesity
- CVD
what is the clinical triad of PCOS?
- an/oligovulation
- hirsutism - due to hyperandrogenism
- polycystic ovaries
what causes PCOS?
2 Hit:
- genetic/acquired predisposition (maternal drugs, nutritional disorders affecting fetus)
- insulin resistant hyperinsulinism (obesity, t2dm)
Unified Minimal Model of PCOS patho
-Functional Ovarian Hyperandrogenism (FOH): accounts for all features of PCOS, most important factor
-Hyperinsulinism and Obesity
-LH Excess: secondary to FOH, no negative feedback
what does hyperinsulinism do to PCOS?
In the ovary hyperinsulism increas androgen production in theca cells by sensitizing them to LH AND prematurely luteinizes granulosa cells
Excess insulin combined w. LH excess, aggravates ovarian dysfunction
what is PMS?
biopsychological disorder
physical/behavioral symptoms in second half of menstrual cycle (luteal phase) for at least 2 consecutive cycles
what is the clinical triad of PMS?
tender breasts
abdominal bloating
headaches
What is the pathogenesis of PMS?
What is the common treatment?
- abnormal NT (serotonin) response to normal hormonal changes
- normal flucuations in hormones through out the cycle, just abnormal response to hormones
- SSRI’s
Development of menopause
getting periods→ menopausal transition (irregular periods) → menopause (no period consectively for one year)
which 3 things contribute to menopause?
- hypothalamic & ovarian aging
- environmental/genetic/lifestyle
- systemic diseases
what does hypothalamic aging have to do with menopause?
desynchronized GnRH production & an abnormal surge of LH→this leads to no ovulation
