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OB/GYN > Reproductive AP > Flashcards

Reproductive AP Flashcards

1
Q

Ovarian and Uterine blood supply?

A
  • ovarian artery comes off of the aorta: feeds ovary, fallopian tube, uterus, anastomes with uterine artery
  • internal iliac artery feeds uterine, vaginal, middle rectal, and internal pudendal artery
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2
Q

Relationship of uterine artery and ureter?

A
  • ureter is underneath the uterine artery
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3
Q

Anatomic variations in position of the uterus?

A
  • mid-position
  • anteverted (MC variation)
  • anteverted and anteflexed
  • retroverted
  • retroverted and retroflexed
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4
Q

Why are there so many diff uterine anomalies?

A
  • b/c in fetal development first mullerian or paramesonephric ducts form fallopian tubes and then fuse caudally to form uterus, cervix, and upper vagina
  • usually don’t notice any problems until pregnancy (early labor, miscarriage)
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5
Q

What are gartner’s duct and cyst?

A
  • remnants of male reproductive system - from : sites of mesonephric duct remnants - epoophoron (by ovaries), cervix, and vagina
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6
Q

DES was assoc with what?

A
  • b/t 1941-71 given to 3 mill preg ladies to decrease miscarriages
  • in 1971 - fetal exposure in daughters assoc with rare clear cell adenocarcinoma vaginal cancers in girls 14-22
  • later assoc with uterine anomalies (T shaped uterus) which increased preg. complications and infertility as well as increased risk of cervical and breast cancer
    (women now 45 and older)
  • exposed sons: increased risk of cryptorchidism, hypogonadism, and epidymal cysts
  • mothers have modest increase risk of breast cancer
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7
Q

Pelvic types?

A
  • round = gynecoid
  • wedge = android
  • oval = platypelloid
  • oval-long = anthropoid
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8
Q

How many eggs are left at puberty? How many get the chance to develop? How many ovulations are in a lifetime?

A
  • 500,000 eggs left at puberty
  • only 8,000 have chance to develop
  • 400-500 ovulations in a lifetime
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9
Q

Where is hypothalamus located? Circulation to anterior pituitary?

A
  • located at base of brain, just above junction of optic nerves
  • hypothalamic-hypophyseal portal circulation: blood supply of anterior pituitary originates in hypothalamus - no direct nerve connections
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10
Q

5 hormones that hypothalamus releases?

A
  • GnRH - gonadotropin releasing hormone
  • TRH - thyrotropin releasing hormone
  • SRIF - somatotropin release inhibiting factor
  • CRF - corticotropin releasing factor
  • PIF - prolactin release- inhibiting factor = dopamine
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11
Q

What are anterior and posterior pituitaty glands derived from? Main fxns?

A
  • anterior (adenohypohysis): derived from ectoderm, diff cell types that produce 6 diff hormones
  • posterior (neurohypophysis): derived from neural tissue, transports oxytocin and vasopressin
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12
Q

Hormones produced by anterior pituitary?

A
  • FSH - gonadotrophs (ovaries)
  • LH - gonadotrophs (ovaries)
  • TSH - thyrotrophs
  • prolactin - lactotrophs (breast)
  • GH
  • ACTH - MSH (melanocyte stim hormone - Addison’s)
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13
Q

Effect of secretion of GnRH from (arcuate nucleus) hypothalamus?

A
  • stim by NE
  • inhibited by dopamine (PIF)
  • influenced by endogenous opioids
  • low pulse frequency triggers FSH
  • high pulse frequency triggers LH
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14
Q

How does GnRH reach the anterior pituitary? What does this stimulate?

A
  • by hypothalamic pituitary portal vascular system and stimulates secretion of FSH and LH
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15
Q

What does low levels of LH stimulate?

A
  • stimulate secretion of androgens (testosterone and androstenedione) from theca cells, these androgens are converted to estrogens in granulosa cells
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16
Q

What does FSH stimulate?

A
  • secretion of estrogens (estradiol and estrone) by granulosa cells of ovarian follicles
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17
Q

When does FSH and LH spike?

A
  • LH spikes 36 hrs b/f ovulation
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18
Q

When does estrogen spike? Progesterone?

A
  • estrogen spikes - during end of follicular proliferative phase (the granulosa cells of chosen follicle is making estrogen)
    ovulation occurs 36 hrs after LH surge
  • progesterone spikes during luteal secretory phase
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19
Q

Feedback mechanism of estrogen and LH?

A
  • initially estrogen creates negative feedback to pituitary to decrease LH and FSH
  • in late follicular phase, peak estradiol levels from dominant follicle trigger a midcycle surge of LH needed for ovulation and preparing the ovary to make progesterone
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20
Q

What secretes progesterone? What phase of menstrual cycle begins?

A
  • with ovulation, dominant follicle becomes a progesterone secreting cyst called corpus luteum and luteal phase of menstrual cycle begins?
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21
Q

Negative feedback of progesterone?

A
  • negative feedback on pituitray secretion of LH and FSH causes decreasing E and P to be made in corpus luteum
22
Q

What occurs to progesterone levels if there is no conception?

A
  • lifespan of corpus luteum is then 9-11 days, and then progesterone levels fall
  • menstrual period is triggered
  • negative feedback for FSH secretion stops and FSH levels start to rise b/f onset of menses
23
Q

What occurs to progesterone levels if there is implantation?

A
  • HCG (human chorionic gonadotropin) from zygote sustains corpus luteum for 6-7 wks until placenta takes over
  • this is time when a lot of miscarriages occur, hard to transition with change in hormones
24
Q

Characteristics of follicular (proliferative) phase - what hormone dominates?

A
  • estrogen dominates
  • development of mature follicle
  • culminates with LH surge preceding ovulation (LH surge necessary for ovulation)
25
Q

Characteristics of luteal (secretory) phase - what hormone dominates?

A
  • reqrs that ovulation has occurred
  • progesterone dominant
  • elevated basal body temp
  • further prepares uterine lining (endometrium) to receive fertilized egg
26
Q

Importance of estrogen - on diff parts of body?

A
  • breast: pubertal development
  • endometrium: stim cell growth (proliferative phase)
  • cervix: stimulates abundant, clear mucus at mid cycle (helps with motlity of sperm)
  • vagina: growth and maturation of epithelium, lubrication
  • bone: helps to maintain density, estrogen receptors in osteoblasts
  • brain: we don’t really know
27
Q

Importance of progesterone on diff parts of body?

A
  • thermogenic effects at level of hypothalamus: increase BBT by 0.5-1.F
  • cervical mucus thickens and decreases in amt (prevents sperm from easy travel)
  • breasts: stim of ducts, nipple and areola contributes to fullness and tenderness
  • fallopian tubes: decrease mucus and causes relaxation to speed transport of ovum
28
Q

What are diff ways to tell if ovulation has occurred?

A
  • track length of menstrual cycles
  • serial transvaginal US to follow follicular development from dominant follicle to corpus lute
  • measure LH surge (OTC urine kits):
    ovulation 36 hrs after LH surge, LH shows up in urine 12 hrs after surge
  • LH also increased with PCOS, POI, and menopause
  • BBT rises 0.5-1.0 defree F
  • measure serum progesterone at mild luteal phase: expect more than 6 ng/ml
  • ovulation to menses: 12-14 days
  • menses to ovulation - more variable
29
Q

What is the reproductive physiology of breasts - when does it present, what occurs during pregnancy? What is thelarche?

A
  • both males and female infants may have palpable breast tissue at birth. Some will have galactorrhea - an effect of maternal hormones
  • by 2-3 months of age, the breast tissue regresses
  • thelarche: onset of breast development starts at 12.5 in US in 95% of girls
  • growth during pregnancy from hormones including: prolactin, estrogen, progesterone, cortisol, insulin, thyroid hormones, and growth hormone
30
Q

Composition of the breasts?

A
  • nipple
  • areola
  • milk glands (lobules)
  • ducts: transport milk from glands
  • connective (fibrous) tissue that surrounds the lobules and ducts
  • fat
31
Q

What happens to the breasts during pregnancy?

A
  • breasts increase in size: increase in lobules= alveoli lined by milk secreting epithelial cells
  • the release of estrogen and progesterone from the placenta and prolactin from the anterior pituitary causes breast development
  • breast milk production: inhibited during pregnancy by effect of progesterone on prolactin
32
Q

lactation physiology?

A
  • colostrum produced first 3-6 days
  • milk production stimulated by prolactin, prolactin release stimulated by direct stimulation of the nipple
  • milk ejection results from nipple stimulation: neuro endocrine reflex with release of oxytocin
  • neuro-endocrine reflex disturbed by maternal tension resulting in problems with nursing
33
Q

What are diff causes of galactorrhea?

A

this is non-physiologic milky d/c from nipples

  • idiopathic
  • meds: tranquilizers, antidepressants, antiHTN meds, herbal supplements, birth control pills
  • hypothyroidism
  • pituitary tumors
  • stimulation of breasts
  • chest surgery, burns, nerve damage from injury
  • spinal cord injury
34
Q

Duration of the menstural cycle? Define Menarche and menopause?

A
  • majority are b/t 24-35 days and are ovulatory
  • about 15% are 28 days
  • less than 1% are less than 21 or more than 35 days
  • menarche: first menses
  • menopause: final menses
35
Q

Diff phases of menstrual cycle?

A
  • follicular: begins with onset of menses and ends with LH surge
    ovulation occurs w/in 36 hrs of LH surge
  • luteal phase: begins with LH surge and ends with onset of next menses
  • day 1 is 1st day of menses and date used in LMP
36
Q

Usual age of first menses? What is this the onset of?

A
  • age of first menses: US median age: 12.5
  • one of final events in continuum of puberty: onset of puberty signals reactivation of hypothalamic-pituitary gonadal axis with pulsatile Gn-RH secretions
37
Q

What is puberty?

A
  • endocrine process that influences physical, sexual and emotional transition from childhood to adulthood
  • triggers for onset not well defined
  • US: puberty starting 6-12 months earlier than last century
38
Q

Sequence of events in puberty?

A

sexual maturation extends about 4.5 yrs

  • growth acceleration
  • breast development (thelarche) - in US by age 12.5 in 95%
  • pubic hair development (pubarche): preceded by increased adrenal androgen production (adrenarche), and axillary hair development
  • max growth rate
  • menarche (further ht limited to about 2.4 in)
  • ovulation
39
Q

What is onset of puberty influenced by?

A
  • ethnic background: African American earlier, then Mexican American, then white and then Asian American
    (black girls begin around 8-9 but can be as early as 6, white girls around 10 but as early as 7 is normal)
  • BMI: higher the earlier onset - possible effect of leptin (from adipocytes) on pulsatile GnRH secretion
  • genetics
  • possible role of enviro toxins acting as endocrine disruptors (pesticides, fertilizers)
40
Q

Role of estrogens in puberty?

A
  • augments accrual of bone during puberty. 2 estrogen receptors (alpha and beta) mediate the actions of estrogen, and presence of both has been demonstrated in growth plate
  • contributes to growth plate fusion at end of puberty
  • stimulates breast development
41
Q

What hormone causes pubertal growth spurt?

A
  • Growth Hormone
  • pulsatile release from pituitary
  • both GH and sex steroids contribute to growth and epiphyseal fusion
  • stimulates secretion of IGF-1
42
Q

What is delayed puberty?

A
  • absent or incomplete seual maturation by age at which 95% of girls started pubertal development:
  • absence of secondary sexual characteristics by age 13
  • absence of menarche by 15-16
  • no menarche 5 yrs after onset of thelarche (breast development)
43
Q

Causes of delayed puberty?

A
  • hypergonadotrophic hypogonadism: FSH greater than 35 - gonadal dysgenesis (turner’s syndrome)
  • hypogonadotropic hypogonadism: FSH and LH less than 10 -
    constitutional (physiologic delay) of HPO. Suppression of HPO axis by illness, malnutrition or excessive exercise
    Elevated prolactin (certain drugs, pituitary tumors)
    Kallman syndrome (genetic)
  • anatomic:
    Imperforate hymen/transverse vaginal septum
    Mullerian agenesis: absence of uterus, cervix, and upper vagina
44
Q

What is precocious puberty? What is this caused by?

A
  • onset of secondary sexual characteristics b/f age 6 in black girls and prior to 7 in white girls (or more than 2 SD from normal)
  • caused by early sex hormone production
45
Q

Evaluation goals of precocious puberty?

A
  • define cause, determine if tx is necessary and minimize psychosocial impact
  • hx and exam (tanner staging)
  • xray of non-dominate wrist and hand for bone age: premature closure of epiphyseal plates limits stature
  • lab
  • pelvic sono
  • MRI of brain
46
Q

Causes of GnRH-dependent (central) precocious puberty?

A

early activation of HPO with both breast and pubic hair development

  • 90% idiopathic (dx of exclusion: MRI)
  • CNS lesions (tumor, hydrocephalus), trauma, inflammatory disease
  • severe hypothyroidism: high TSH activates FSH receptor
  • generally tx with GnRH agonist
47
Q

Causes of Gn-RH independent (peripheral) precocious puberty?

A
  • autonomous fxnl ovarian cysts
  • McCune-Albright syndrome (rare genetic disorder)
  • adrenal pathology: nonclassical congenital adrenal hyperplasia (CAH). May mimic PCOS due to accompanying hyperadrogenism, adrenal tumors
  • exposure to exogenous estrogens or xenoestrogens (endocrine disruptors which mimic estradiol)
48
Q

What is menopause? Median age?

A
  • permanent cessation of menses: retrospective dx: no period for 12 months w/o other explanation = post menopause
  • median age: 51.4, primary ovarian insufficiency (premature ovarian failure): cessation of menses prior to 40, confirmation of infertility is a common concern
49
Q

What is happening with the hormones in menopause?

A
  • ovaries are no longer listening to brain - the oocytes are resistant to FSH:
    this represents depletion (or near depletion) of follicles
    FSH, although elevated is seldom needed for dx unless confirmation of infertility is a concern
50
Q

What occurs secondarily to estrogen loss in postmenopause?

A
  • urogenital atrophy
  • increase in LDL and decrease in HDL
  • decrease in bone density: estrogen acts to maintain the appropriate ratio b/t bone-forming osteoblasts and bone-resorbing osteoclasts in part through the induction of osteoclast apoptosis
  • vasomotor sxs (hot flashes)

OB/GYN (17 decks)

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