Week 2 - Female Repro Flashcards

1
Q

Hormonal control of ovary

A

FSH (pituitary) mediated granulosa cells prolif and secretion. Also stimulates aromatase
LH (pituitary) stimulates theca cells androgen production and promotes follicle vascularization
Estrogen (ovarian follicles and CL) is anabolic and does lots of things

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2
Q

Estrogen Production

A

Theca cell: LH via cAMP stimulates cholesterol to pregnenolone to progesterone to androgens
Granulosa cell: can make progesterone like theca cells, but can also turn androgens into estrogens via aromatase (stim by FSH via cAMP)

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3
Q

Inhibins (role in cycle)

A

synthesized by granulosa cells
A: peaks in leuteal phase, suppresses FSH
B: index of granulosa cell volume in leuteal phase, suppresses FSH in midfollicular phase

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4
Q

Gonadal steroids (role in cycle)

A

Estradiol: increase in late follicular phase stimulates LH surge
Progesterone: increase in luteal phase suppresses GnRH pulses

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5
Q

Gonadotropins (role in cycle)

A

FSH: increase at end of luteal and beginning of follicular phase stimulates maturation of follicles
LH: surge stimulated by estrogen pos feedback stimulates ovulation

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6
Q

Effects of estrogen

A
Uterus: endometrium prolif
Ovary: mitotic effect on granulosa cells
Breast: ductal epithelium growth and differentiation
Liver: metabolic modulation
CNS: neuroprotective
Bone: anti-resorptive
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7
Q

Things about female puberty that warrant evaluation

A
  • breasts or pubic hair before 8yo
  • absence of 2ndary sex char by 14yo
  • absence of menstruation by 16yo
  • absence of menses with a hx of menses for 3 cycles or 6mo
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8
Q

Breast and pubic hair hormones

A

breast= estrogen (ovarian axis)

pubic hair= testosterone (adrenal axis)

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9
Q

Physiological efects of estrogen

A
female sexual maturation and growth
epiphyseal growth plate closure
feedback regulation of GnRH
positive effects on bone mass
plasma lipids: inc trigs, lowers chol, inc HDL, dec LDL
Increases coag, decreases anti-coag, increase fibrinolysis
alters bile
increases watery cervical mucus
Promotes endometrial prolif**
increases tubal contractility
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10
Q

Physiological effects of progesterone

A

decreases freq of GnRH pulses (supp gonadotropin)
decreases endometrial prolif
abrupt decline- end of cycle- onset of menstruation
maintenence of pregnancy
increases basal body temp mid-cycle
increases cervical mucus viscosity
decreases uterine contractions

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11
Q

Clomiphene

A

weak estrogen agonist and potent antagonist
induces ovulation
increases pulsitile gonadotropin release
reduces intracellular estrogen receptors, diminishes negative feedback, activates GnRH secretion
sides: hot flashes, multiple births

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12
Q

Tamoxifen

A

anti-estrogenic in the breast
treatment and prevention of breast CA
sides: hot flashes, risk of endometrial ca, thrombo ds

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13
Q

Raloxifene

A

estrogen agonist in bone
prophylaxis of osteoporosis
sides: hot flashes, thrombo, does not cause endometrial thickening

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14
Q

Aromatase inhibitors

A

Letrozole, Anastrozole (reversible)
Exemestane (irreversible)
tx breast ca
sides: hot flashes

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15
Q

Progestin drugs

A

Progesterone (low oral bioavail)
Medroxyprogesterone (ester, better)
Norethindrone and Norgestrel (oral, slower metabolism)
Drospirenone (spironolactone analog, monitor K)
Uses: pregnancy prevention, post-menopause hormone replacement (w/ estrogen)
Sides: breakthrough bleeding, androgenic action

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16
Q

Mifepristone

A

progesterone receptor antagonist
use: pregnancy termination (-49d)
usually given with misoprostol to ensure expulsion

17
Q

Ulipristal

A

selective progesterone receptor partial agonist
use: emergency contraception (-5d)
inhibits LH release- inhibits ovulation

18
Q

Leimyoma (uterine fibroids)

A
very common
meno/menometrorrhagia
intermenstrual spotting
mass sx
most prevalent during reproductive years
Tx: surgery (myomectomy)
19
Q

Benign neoplasms

A
endometrial polyps (endometrium)
endocervical polyps (cervical mucosa)
adenomyosis (invasion of endometrium into myometrium)
20
Q

Anovulation and abnormal uterine bleeding

A

common at extremes of reproductive ages
result of chronic estrogen without cyclic postovulatory progesterone
endometrium becomes abnormally thickened
results in asynchronous shedding of endometrium unaccompanied by vasoconstriction
predisposes to endometrial hyperplasia and cancer

21
Q

Endometrial atrophy

A

“spotting”
hypoestrogenism
must be eval bc looks similar to cancer

22
Q

Endometriosis

A

presence of endometrial glands and stroma outside of endometrial cavity and uterine musculature
can cause adhesions, pain, infertility, inflammation
can have chocolate cysts
Tx: hormonal suppression (oral contraception, GnRH agonists, aromatase inhibitors), NSAIDs

23
Q

Ovarian reserve

A

“biological clock”
inversely proportional to LH/FSH levels
proportional to antimullerian hormone (secreted by granulosa cells)

24
Q

Anatomic causes of hypogonadotropic hypogonadism (2ndary amenorrhea)

A

tumors (craniopharyngioma)
infiltrative ds
cranial irradiation
Sheehan syndrome (pituitary ischemia postpartum)
lymphocytic hypophysitis (pituitary infiltration of lymphocytes)

25
Q

Endocrine causes of hypogonadotropic hypogonadism (2ndary amenorrhea)

A

hyperprolactinemia
thyroid ds
hypercortisolism
hyperandrogenism

26
Q

Uterine cervical lesions

A

Cervicitis (infxns, STDs)
Neoplasia (squamous or glandular, caused by HPV)
Non-HPV (benign polyps, cysts, leiomyoma, sarcomas)

27
Q

HPV

A

super common, peaks in 20s-30s, have vaccine now
6,11= low risk= condyloma
16,18= high risk= CIN(mucosa)- higher grade- invasive carcinoma- metastasis
stains with p16

28
Q

Lichen sclerosis (vulva)

A
increased risk of squamous cell carcinoma
usually non-menstruating
painful, itchy
epithelial thinning, inflammation
white plaques
29
Q

Lichen simplex chronicus (vulva)

A

no risk of cancer
epithelial thickening
white plaques

30
Q

Neoplasms of vulva

A

condylomas (dysplasia, warty)
carcinoma (VIN) (squamous cell or adeno) (HPV-assoc)
Paget disease (glandular cells in epidermis, LMCK:CK7)
Mesenchymal lesions

31
Q

Vagina pathology

A
vaginitis
rare stuff: 
squamous dysplasia and carcinoma(VIN) (HPV)
clear cell carcinoma (DES exposure)
Sarcoma botryoides (young kids)
32
Q

Fallopian tube pathology

A

inflammation (salpingitis) (plasma cells)
ectopic pregnancy
endometriosis
tumors: BRCA assoc, serous carcinoma

33
Q

Ovary pathology

A

follicle and luteal cysts
polycystic ovarian disease
tumors: surface epithelial, sex cord, germ cell

34
Q

Functional cysts of ovary

A

follicular
luteal
inclusion
hemorrhagic

35
Q

Ovarian neoplasms

A

usually in reproductive age, usually benign, 20% malignant
Surface epithelial: most common, inc risk with obesity, estrogen use
also: germ cell (teratoma(mature,capsule), yolk sac (a-fetoprotein)) and sex-cord (estrogenic, thecoma, granulosa cell, steroid, )
Most are sporadic, 10% are familial
Type 1: low grade, most common, genetically stable, KRAS, BRAF, PTEN, ERBB2
Type 2: high grade, genetically unstable, p53, Her2, AKT
can be papillary serous (psammoma bodies)
or clear cell
CA125 is blood test marker (non-specific)

36
Q

Fallopian tube tumors

A

cause ovarian cancer too
BRCA-1 assoc
also p53

37
Q

Abnormal uterine bleeding DDX

A
uterine polyps
leiomyomas (fibroids)
adenomyosis
endrometriosis
ectopic pregnancy
blood dyscrasias
medical/endocrine disorders
other tumors
38
Q

Endometrial adenocarcinoma

A

Type 1: estrogen dependent, hyperplasia-carcinoma sequence
assoc with obesity
endometrial hyperplasia (excess estrogen)
(microsatellite path, PTEN, KRAS, B-catenin)
Type 2: usually atrophic background, older women, more aggressive, p53
Also assoc with HNPCC (lynch), Cowden’s syndrome