KEY NOTES WK 1 Flashcards

1
Q

round ligament attachment

A

ovarian ligament and down to mons pubis and labia major

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2
Q

broad ligament

A

double layer peritoneum surrounding most other ligaments (cardinal, uterosacral, round, ovarian)

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3
Q

uterus position

A

anteverted (lie over bladder)h and ante flexed (angle at cervix)

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4
Q

ligaments to maintain anteverted and ante flexed uterus

A

cardinal and uterosacral ligaments

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5
Q

function for cortex and medulla of ovaries

A

cortex= follicles found

medulla= CT and blood vessels

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6
Q

opening of uterine tube to ovary is called and is lined with

and opening of uterine tube to uterus

A

infundibulum lined by fimbriae (fingers to draw oocytes in)

isthmus

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7
Q

where does fertilization occur

A

ampulla of uterine tube

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8
Q

cells of fallopian tube

A

cilia

peg cells (secrete glycoproteins to nourish and protect sperm and oocyte)

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9
Q

2 mucosal layers of the uterus

A

basal layer: not shed during menses, gives rise to functional layer

functional layer: shed, has spiral arteries and tortuous glands

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10
Q

spiral arteries in uterus are sensitive to

A

progesterone

progesterone withdrawal at end of cycle –> constrict and ischemia of functional layer or endometrium

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11
Q

transformation zone of the cervix

A

columnar –> stratified squamous (mouth of external os)

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12
Q

cervix differs from uterus

A

no spiral arteries or myometrium

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13
Q

vagina lacks

A

glands (moisture via cervical glands)

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14
Q

thickness of vaginal epithelium via

A

estrogen

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15
Q

external part of clitoris with nerve endings

A

glans clitoris (union of both corpora caverns)

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16
Q

body of clitoris (corpora caverns) is surrounded by what muscle

A

ischiocavernous muscle

enhance blood flow to clit and engorge

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17
Q

muscle surrounding vestibular organs and secrete fluid from vestibular gland for engorgement of bulboclitoral erectile organ

A

bulbosponguisum muscle

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18
Q

vestibular glands aka and function

A

bartholin glands (in labia minora)

release mucus to lubricate vestibule during sex

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19
Q

mechanisms behind PCOS

A
  • Inappropriate gonadotropin secretion
  • Insulin resistance with hyperinsulinemia
  • Excessive androgen production
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20
Q

GhRH pulsatility and LH:FSH ratio in PCOS

A

increase puslatility leads to high LH:FSH ratio

LH stimulates androgen production

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21
Q

in PCOS the altered gonadotropic prevents a ____ from devleoping

A

pdominant follicle (bc premature LH secretion)

no luteal phase and no progesterone; estrogen is unopposed

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22
Q

more androgens and estrogen in periphery in PCOS

A

decrease SHBG that bind androgens (from insulin resistance)

adipose tissue makes estrogen (chronically high throughout cycle)

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23
Q

anovulation in PCOS (infertility)

A

from GnRH altered pulsatility

androgens make many antral follicles (that aren’t maturing for ovulation- would do follicular atresia if dominant follicle developed)

metformin can help oligoovulation (insulin resistance)

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24
Q

altered menses in PCOS

A

amenorrhea, oligomenorrhea and heavy menstrual bleeding (leading to iron-deficiency anemia)

chronic unopposed estrogen thickens endometrium (too much?) and leads to unpredictable bleeding

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25
oligo vs amenorrhea
oligo: <9 menses/year amen: no menses for 3+ months
26
menstural intervals
Menstrual intervals <20 or >45 days > 2 years after menarche or an interval >90 days at any time warrants further evaluation
27
signs of hyperandrogenism and signs that are not in PCOS and would be in androgen secreting tumor
PCOS: hirsutism, acne, alopecia rapid increase in androgen: increase muscle mass, deep voice, cliteromegaly (NOT IN PCOS)
28
hirsutism; testosterone into ____ via ______ and turns ____ hair into _____ hair
testosterone is converted by 5 alpha reductase to dihydrotestosterone (DHT) vellus --> terminal hair (in androgen sensitive follicles ie. chin)
29
alopecia in PCOS
excess 5 alpha reductase activity turning testosterone to DHT for terminal hairs that dont need androgens they transform to vellus and fall out
30
4 factors in pathogenesis of acne in PCOS
1. Blockage of the follicular opening by hyperkeratosis 2. Sebum overproduction 3. Proliferation of commensal bacteria (Propionibacterium acnes) 4. Inflammation testosterone --> DHT in sebaceous glands
31
acanthosis nigrigans in PCOS
hyperisulinemia --> keratinocyte growth
32
cancer risk in PCOS
endometrial hyperplasia/ neoplasia from anovulation and unopposed estrogen, hyperandrogenism, hyperinsulineamis, obesity, decreased SHBG
33
pregnancy complications in PCOS
miscarriage, hypertensive disorders, gestational diabetes (GDM), and preterm birth use fertility interventions can cause multi fetal gestations
34
ovulation to menses is __ days because of lifespan of _____
14 days, bc corpus luteum menstruation to ovulation can vary
35
GnRH released from where in hypothalamus
pre optic and arcuate nuclei
36
pulsatility of GnRH for LH and FSH
rapid= LH slower= FSH
37
2 cells in ovary and what hormones stimulate them and what hormones they make
theca cells (via LH and cholesterol): steroidogenesis; progesterone and androgens granulosa cells (via FSH, and some LH): convert androgens to estrogens (activins, inhibins, follistatin)
38
negative and positive feedback in menstrual cycle
negative: progesterone and estrogen inhibit GnRH positive: late follicular phase, estradiol promotes GnRH to create LH surge
39
what enzyme in granulosa cell to create the hormones
testosterone --> estradiole androstenedione --> estrone via aromatase enzyme ----------------- Estrone converted into estradiol via 17Beta-hydroxysteroid dehydrogenase
40
if too much androgens they will get converted into what in the grnaulosa cell
dihydrotestrone --> apoptosis of grnaulosa cell and follicular atresia
41
what phase does primary oocyte arrest in until ovulation during puberty
prophase
42
what do primary follciles develop into after puberty and due to exposure of what
into secondary follicles via LH and FSH
43
Just before ovulation, the antral follicle(s) will develop into
Graafian follicle(s) dominant follicle gets selected at ovulation via how much growth factors, oxytocin, steroids, peptides it has
44
dominant follicles releases _____ to trigger ____
estradiol ; LH surge (ovulation)
45
what does secondary oocyte arrest in until fertilization
metaphase
46
LH surge promotes release of ____ so follicle swells and basement membrane disintegrates then granulosa cells activate _____ so the rupture follicle ovum is released
release of histamine, prostaglandins and bradykinins, which cause vasodilation prostaglandins activate lysosomal enzymes to degrade ovarian wall Granulosa cells (FSH stimulation) release plasminogen activator→ get activated plasmin and with collagenases (LH stimulation) will digest the connective tissue matrix
47
when Graafian follicle collapses at ovulation if fills with blood and becomes ____ which releases ____. if not fertilized it apoptosis and necrosis and becomes ____
corpus luteum ; progesterone corpus albicans
48
if fertilized, maintain corpus luteum via
hCG and progesterone (reduce contractility)
49
follicular phase hormone levels
low LH, estrogen, progesterone, inhibin high FSH (stimulate granulosa cells, increase aromatase to make estradiol increase, increase LH receptors on growing follicle) day 5-7 pick dominant follicle via size and streoidogenic activity
50
late follicular phase
increase estradiol to cause LH surge reduce FSH
51
luteal phase
corpus luteum secretes progesterone (some estradiol), FSH and LH decline
52
endometrial cycle
1. proliferative phase [mid-late follicular phase] (estrogen causing hyperplasia, vascularize with spiral arteries) 2. secretory phase [ovulation and early-mid luteal phase] (coiled glands with glycogen, tortuous spiral arteries, thickest 1 week after ovulation, progesterone decreases and causes myometrial contraction to prep for implantation)
53
cervical mucus in follicular vs ovulation vs luteal
follicular: alkaline, viscose, elastic ovulation: most elastic for sperm to pass luteal: progesterone decreases amount and elasticity so sperm and infection cant enter
54
body temp increases
after ovulation bc of progesterone
55
mensturation
low progesterone and estradiol cause vasospasm of spiral arteries --> ishemia of endometrail layer --> necrosis and apoptosis --> macrophage and WBC invade to phagocytose ischemic tissue
56
autonomic nervous sytem for arousal
* Cerebral sympathetic stimulation→promotes desire * Peripheral parasympathetic stimulation→clitoral vasocongestion and vaginal secretions; both processes depend on nitric oxide
57
ovarian cyst
follicular cysts (if follicle doesnt rupture in ovulation) luteal cyst (if corpus luteum doesnt dissolve)
58
endometriosis
endometrial tissue in ectopic location
59
endometrial hyperplasia
Increase in endometrial gland to stroma ratio could be typical or atypical (cancer risk)
60
endometrial hyperplasia caused by
excess estrogen stimulation (anovulation, exogenous estrogen, PCOS, obesity)
61
fibroids- leiomyomas
benign tumor of myometrium sx: menorrhagia (heavy bleed)