Flashcards in Exam 3 - reproductive system Deck (48):
Sex hormones are synthesized where?
What are the phases of the menstrual cycle?
Brief hormone stuff about menstrual cycle.
Estrogen starts it all. Causes LH to spike. this spike causes ovulation.
Proliferative phase (menstrual cycle)
- 1-14 days
-proliferation of glands
-mediated by estrogen. spike causes LH to peak and FSH (When LH goes up, so does FSH)
-at day 14-16
-mature follicle in the ovary releases an egg
-signs: inc temp, subnuclear vacuoles in endometrial cells, mittelschmerz "pelvic pain"
-at day 14/16-28 (depends on ovulation)
-mediated by PROGESTERONE
-histology: inc gland tortuosity and secretion, edema of stromal cells
-fertility work-ups: at day 21
-serum estrogen and progesterone drop
-causes endometrial cell apoptosis
What is FSH's function in the menstrual cycle?
-prepares follicle of the month - inc follicle size
-inc aromatase synthesis
-inc synthesis of LH receptors
What is LH's function in the menstrual cycle?
-testosterone synthesis: aromatase converts it to estradiol in granulosa cells
-LH surge: due to estrogen. causes ovulation when LH>FSH. moves follicle from meiosis I prophase to meiosis II metaphase
-progesterone synthesis (for secretory phase)
Pregnancy hormone changes: hCG
-hCG: human chorionic gonadotropin
-made in placenta
-analogue of LH (maintains corpus luteum)
Pregnancy hormone changes: progesterone
-until 10 weeks = made in corpus luteum
-after 10 weeks = made by placenta
-if progesterone drops: possible spontaneous abortion
How does OCPs work?
-usually mix of estrogen and progestins
-baseline estrogen prevents estrogen surge (prevents LH surge, prevents ovulation)
-progestins stop proliferative phase (gland atrophy, inhibit LH which prevents LH surge)
Menopause: definition and onset
Def: no menses for 1 year after age 40 (avg age =51)
onset: genetically determined. Earlier with smokers
-decrease in ovarian function.
-decreased estrogen levels overall
*she said this was all we need to know. slide 16)
What is the treatment for menopause? and why is it controversial?
-treatment = estrogen replacement. Helps inc overall levels
controversial: long-term severe risks of CAD, stroke, clots, etc. Should only do for a year or 2 at a time
Menorrhagia (Menstrual dysfunction)
>80 ml blood loss
Dysmenorrhea (Menstrual dysfunction)
-primary type (inc prostaglandins or uterine contractions)
Dysfunctional uterine bleeding
-abnormal. no anatomical cause
-typically hormone imbalances
-most are postmenarchal or perimenopausal
-90% anovulatory (no egg release)
Anovulatory DUB (dysfunctional uterine bleeding) causes
-excessive estrogen relative to progesterone (absent secretory phase)
-inadequate luteal phase (inadequate progesterone)
-irregular shedding of endometrium (persistent luteal phase)
-regular normal intervals
-excessive flow and duration
-regular normal intervals
(metro = "time")
- irregular intervals
-excessive flow and duration
-irregular or excessive bleeding during menstruation and btwn periods
-menses at intervals > 35 days
-menses at intervals <21 days
What is primary amenorrhea?
-absence of menses by 16 y/o
-constitutional (growth) delay = most common cause
What is secondary amenorrhea?
-no menses for >6 months in pt who has had normal menses
-MCC = pregnancy
-hypothalamic or pituitary disorder (dec LH and FSH synthesis => Dec estrogen and progesterone)
-ovarian disorder (dec estrogen and progesterone synthesis. FSH and LH inc)
-end-organ disorder (blood flow obstruction (normal FSH, LH, progesterone, estrogen)
Polycystic ovary syndrome: disease associations and clinical findings
-acanthosis nigricans (skin stuff, skin folds)
Clin find: oligomenorrhea, hirsutism(hair)- due to inc testosterone, infertility, obesity, DM etc
Polycystic ovary syndrome: pathology
*** increased LH secretion by anterior pituitary (**LH/FSH > 3)
*** dec pituitary FSH secretion
FSH and LH as male sex hormones
-FSH = stim spermatogenesis (seminiferous tubules)
-LH = stim testosterone (leydig cells)
Male hormones: testosterone
Male hormones: sex hormone binding globulin
-binds testosterone and estrogen (greater affinity for testosterone)
-made in liver
-dec testosterone production
-resist to testosterone
-primary or secondary
Primary hypogonadism (what causes, hormone effects)
(leydig cell, seminiferous tubule)
- dec testosterone secretion
-( dec T, inc LH)
secondary hypogonadism (what causes. hormone effects)
-pituitary (tumor) or hypothalamic (Kallmann's syndrome) dysfunction
- (dec T, dec or normal LH)
-decreased sperm count (leydig, seminiferous tubule, pituitary, or hypothalamus dysfunction)
-end-organ dysfunction (obstruction, dysfunction of accessory organs/ejaculation)
Infertility labs: seminiferous tubule dysfunction
-testosterone = normal
-FSH = inc
Infertility labs: Leydig cell dysfunction
- testosterone = dec
- LH = inc
Infertility labs: pituitary dysfunction
-testosterone = dec
-LH = dec
-FSH = dec
Infertility labs: end-organ dysfunction
-normal hormone levels
-variable sperm count
What do you look for with a sperm analysis?
serum hormone levels
What are the 3 causes of ED?
-psychogenic (nocturnal penile tumescence test)
-vascular insufficiency (atherosclerosis, leriche syndrome - butt and genital area)
In what zones does benign prostatic hyperplasia occur?
-***transitional and periurethral zones
benign prostatic hyperplasia: pathology
-inc sensitivity of prostate to DHT (dihydrotestosterone)
-DHT causes hyperplasia
-get nodules due to hyperplasia of glandular and stromal cells. (yellow-pink, soft)
-most common cancer in adult males
-90% of 90y/o have it
-asymptomatic until advanced
-DHT -dependent and ***development in peripheral zone
pt has LBP, pelvic pain, obstructive uropathy, and possible spinal cord compression. what does he have?