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Repro > Week 2 > Flashcards

Week 2 Flashcards

1
Q

naturally occurring steroidal estrogens

A

Estrone (E1), Estradiol (E2), Estriol (E3)

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2
Q

source of estrogen during pregnancy

A

during ovulation, corp luteum, then fetoplacental unit (fetal adrenals, placenta)

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3
Q

synthesis of female sex hormones

A

Androstenedione testosterone. Aromatase: Androsten –> Estrone (conversion to Estriol) and Testost –> Estradiol. Conversion is determined by presence of aromatase (mostly in liver)

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4
Q

Biological role of estrogen

A

Female maturation, Bone growth(!), growth of endometrium (follicular phase), Cardiovascular (protective? increase in coagulative factors but also increase in HDL and TGCs), Metabolic (increase leptin, binding globulins), Bone health (promotes apoptosis of osteoclasts).

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5
Q

sources of progesterone

A

non-pregnant: stimulated corp lut. pregnant: placenta.

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6
Q

feedback in female steroidogenesis

A

estrogen and progesterone both feed back (neg) on hypothal and anterior pituitary

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7
Q

co-activator/co-repressor

A

in estrogen-sensitive tissues co-activators lends estrogen full agonist nuclear action. co-repressors reduce action

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8
Q

general categories of estrogen response

A

non-genomic response (e.g. vascular smooth muscle) are autocrine/paracrine
genomic responses

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9
Q

estrogen of therapy

A

primary hypogonadism or secondary estrogen deficiency (HRT)
suppression of ovulation
post-menopausal HRT

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10
Q

Risks vs benefit of HRT for menopause

A

OK for short-term relief of menopausal Sx (t use long-term. Other drugs that can prevent bone loss.

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11
Q

SERMs

A

Selective antagonist in breast/uterus but agonist in bone.

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12
Q

Tamoxifen

A

suppresses E2 dependent growth of breast cancer (antagonist), agonist in uterus bone, CVS(?). tumoristatic and not tumoricidal (chemoprevention).
OK for women with hysterectomy or post-menopausal. Need to watch use in pre-menopausal (endometrial hyperplasia)

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13
Q

Raloxifene

A

antagonist in breast and uterus. Suppresses E2-dependent tumors without risk to uterus. OK for non-historectomized and pre-menopausal women.

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14
Q

aromatase inhibitors

A

block conversion of testosterone to estrogen. used for tumors of female genital tract

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15
Q

indications for progestin therapy

A

HRT in hypogonadism, contraception/IVF, endometriosis, dysfunctional uterine bleed,ing.
RU486 as progesterone antagonist for abortion

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16
Q

androgens and sources

A

potent: testis (test and DHT)
weak: adrenals (androstenedione and DHEA)–hair growth and bone maturation

much smaller quantities in women

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17
Q

androgen synthesis

A

all come from cholesterol, don’t worry about specifics

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18
Q

5-alpha reductase

A

converts testosterone to DHT (happens in many target tissues)

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19
Q

aromatase in men

A

liver and adipose tissue

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20
Q

ARA-70

A

testosterone/DHT co-activator. necessary for agonist action

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21
Q

Testosterone induced effects

A

sex drive, muscle mass, penile/scrotal growth, vocal cord thickening. Bind Androgen receptor!

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22
Q

DHT induced effects

A

secondary sex characteristics: facial/body hair, acne, prostate enlargement, decrease HDL, stimulate erythropoeitin and clotting factor. Binds Androgen Receptor!

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23
Q

synthetic androgens

A

17-beta esterification: complete androgens. used for severe anorexia
17-alpha alkylation: anabolic steroids. used by athletes. Dysregulation of HPA, feminization, liver toxicity..

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24
Q

finasteride

A

inhibits 5-alpha reductase type II (prostate, hair follicles). Increases T/DHT ratio. reduce BPH, male pattern baldness.

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25
Q

5 alpha reductase

A

Type I expressed in sebaceous glands: acne (may have more toxicity/deficiency in younger men).
type II: prostate, hair follicles

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26
Q

flutamide

A

androgen receptor antagonist used as hormone ablative therapy for prostate cancer

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27
Q

site of testosterone biosynthesis

A

Leydig cells

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28
Q

Criteria for PCOS

A
  1. Hyperandrogenism: hirsutism/acne/balding or biochemical
    and
  2. Ovarian dysfunction (oligo/anovulation or polycystic ovaries)
    and
  3. Exclusion of other androgen excess or related disorders (hypothyroidism/hyperprolactinemia)
    PCOS is an androgen excess disorder
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29
Q

prevalence of PCOS by ethnicity

A

same across ethnicity!

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30
Q

relationship of obesity and PCOS

A

obesity magnifies complications; not part of diagnosis

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31
Q

pathophys of PCOS

A

Hypo/Pit: pulsatility of GnRH increases in frequency increasing LH/FSH ratio (underlying problem not known).
Ovary: theca increases androgen production. increased sensitivity to FSH. larger cohort of follicles
Insulin: Acanthosis Nigricans associated with PCOS, IR in muscle, adipose, liver (not in ovary) and insulin increases ovarian androgen production (no changes to insulin receptor, but increased phosphorylation)

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32
Q

Acanthosis Nigricans

A

raised, velvety, hyperpigmented skin in axilla, neck. sign of insulin resistance

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33
Q

Pregnancy outcomes in PCOS

A

reduced fertility; increased HTN, pre-eclampsia, gestational diabetes, pre-term birth, perinatal mortality

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34
Q

Tx of PCOS

A

OCPs, cyclic progesterone
Anti-androgens
Weight Loss
Insulin sensitizing agents

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35
Q

general relationship of HPV/Cervical cancer

A

HPV necessary but not sufficient (vast majority of pop has HPV, few get cancer

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36
Q

oncogenic HPV subtypes

A

16, 18

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37
Q

ASC-US

A

atypical squamus cells of undetermined significance

“Reflex” testing for High-risk HPV rather than just culposcopy.

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38
Q

HPV co-test

A

HPV with pap-smear inpatients >30 yo. if neg, can space intervals to every 5 yrs instead of 3 yrs.
increases detection of CIN 3+, decreases necessity for colposcopies.
Increases detection of adenocarcinoma

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39
Q

HPV tests

A

multiple FDA approved, lots that aren’t. Don’t want most sensitive test, want the one that picks up clinically significant infections!

40
Q

biggest risks for cervical cancer

A

lack of pap smear, failure to follow up on abnormal pap

41
Q

HPV tropism

A

glandular cells, squamous metaplastic cells, basal epithelium (not surface)

42
Q

Cervical cancer screening guidelines

A

start 21yo
3y paps 21-29
5y cotesting 30-65 (3y paps optional, not preferred)
stop 65yo if negative

43
Q

culposcopy procedure

A

can you see entire transition zone (glandular red epithelium all the way around)? Are there acetyl white lesions?

44
Q

Tx of CIN 2/3

A

excision (used to do ablation, but decreases detection of cervical cancer b/c don’t get sample). remain at increased risk of cervical cancer for at least 20 yrs.

45
Q

HPV vaccine

A

not a replacement for other preventative measures

should be part of adolescent visit

46
Q

reasons for endometrial biopsy

A
  • determine cause of uterine bleeding
  • work-up of patient with suspected ectopic pregnancy
  • determine response to hormone therapy
47
Q

features of proliferative endometrium

A
  • round, regular glands
  • mitoses
  • pink/purple stroma
  • stratified nuclei
48
Q

features of early secretory endometrium (first signs of ovulation) day 17

A
  • subnuclear vacuoles
  • edema in stroma
  • single row of nuclei
49
Q

features of post-ovulatory secretory endometrium (day 20-21)

A
  • marked stromal edema (“naked nuclei”)

- intraluminal secretions

50
Q

features of later secretory endometrium (day 23-24)

A
  • predecidual changes around spiral arteries (preparing for implantation)
  • prominent spiral arteries
51
Q

features of late secretory endometrium (day-26-27)

A

confluent sheets of predecidua with lymphos

52
Q

menorrhagia

A

excessive bleeding (amount and duration) at regular intervals

53
Q

metrorrhagia

A

bleeding at irregular intervals

54
Q

menometrorrhagia

A

excessive bleeding with prolonged period of flow and frequent and irregular intervals

55
Q

dysmenorrhea

A

painful menses

56
Q

postemenopausal bleeding

A

abnormal bleeding at least one year after menopause

57
Q

causes of abnormal vaginal bleeding

A 
anovulatory cycles
complications of pregnancy
organic lesions (fibroids, polyps, infection)
atrophy
hyperplasia
neoplasia
clotting disorders
58
Q

Dysfunctional Uterine Bleeding (DUB)

A
  • alteration of normal cyclical hormonal stimulation of endometrium with no underlying organic disorder (ovulatory dysfunction)
  • excludes postmenopausal bleeding and presence of specific pathologic process.
  • no progesterone –> no ovulation
  • path: stromal and glandular breakdown (outgrowing blood supply but no decidua, secretory changes). Stromal blue balls
59
Q

endometrial atrophy

A

lack of estrogen stimulation causes cystic change of glands and endometrial stripe. 25-50% of abnormal bleeding in postmenopausal women.

60
Q

endometrial polyps

A

focal growth with no malignant potential (sometimes cancer will form incidentally)

path: large tissue fragments with dense stroma and thick-walled arteries, irregular crowded glands. separate fragments of normal endometrium
- don’t respond to normal cycling

61
Q

Leiomyoma (def, incidence, etiology, classification by location, complications, typical gross cut surface, histology)

A
  • benign smooth muscle tumor. “fibroids”
  • > 40% women over 40, more common in African Americans
  • High sensitivity to estrogen/tamoxifen–tumors of reproductive period. enlarge during pregnancy, regress after menopause
  • subserosal: outer wall of uterus
  • intramural: within wall of myometrium
  • submucosal: underneath endometrium
  • torsion, infarction, separation (parasitic), infertility, spontaneous abortion
  • gross cut surface: well circumscribed, solid, white/tan, whorled, no necrosis or hemorrhage
  • histology: uniform, bland spindled cells with fascicular arrangement, uniform cigar-shaped nuclei
62
Q

leiomyoma vs endometrial polyp

A

leiomyoma: tumor arising from myometrium
polyp: hyperplasia arising from endometrium

63
Q

leiomyosarcoma (def, epi, gross features, histology)

A
  • malignant tumor of uterine sarcoma
  • > 40, African American, tamoxifen
  • loss of whorled pattern, irregular margin, yellow, necrotic, hemorrhage, less rubbery/bulging, invasive
  • hist: invasive, vascular, increased cellularity, nuclear atypia, increased mitosis, coag necrosis)
64
Q

endometriosis (def, epi, risk factors, protective factors, gross appearance, Sx)

A
  • endometrial tissue outside the uterine cavity
  • women in reproductive years
  • risk: genetics, increased exposure to menstruation
  • protective: multiparous, OCP use
  • gross: red/blue/black nodules on peritoneum, vesicle formation
  • Sx: secondary dysmenorrhea, dyspaneunia, pelvic pain, infertility. pelvic mass or ascites. no correlation with extent of disease(!)
65
Q

endometriotic cyst

A
  • endometriotic deposit on ovary
  • chocolate cyst
  • benign
66
Q

adenomyosis

A
  • endometrial tissue within muterine wall (myometrium) “boggy uterus”
  • remains in continuity with endometrium
  • menometrorrhagia, pelvic pain, dysmenorrhea, dyspareunia
67
Q

endometrial hyperplasia (def, cause, Sx, risk, protection, gross, imaging, histology, classification, complications)

A
  • non-physiologic non-invasive proliferation of endometrium
  • cause: increased unopposed estrogen effect
  • Sx: abnormal bleeding)
  • risk: exogenous (tamoxifen) or endogenous estrogen (obesity, HTN, nulliparity, smoking)
  • protective: progesterone! (lots of births, short premenopausal delivery-free periods)
  • gross: abundant, fleshy endometrium. diffuse process
  • ultrasound: thickened endometrial stripe
  • histology: diffuse process. more glands, irregular glands, mitosis.
  • Classification: w/ or w/o nuclear atypia. Simple vs complex (glandular complexity)
  • complications: complex with atypia confers 30% risk of endometrial cancer (regardless of hysterectomy)–gray zone.
68
Q

endometrial hyperplasia vs carcinoma

A
  • myometrial invasion

- invasion of endometrial stroma (desmoplastic response, cribiform glands, extensive papillary pattern)

69
Q

endometrial carcinoma (epi, risks, types, staging)

A
  • most common malignant tumor of female genital tract
  • risks: same as hyperplasia
  • Type I: estrogen dependent 80%. endometrioid type
  • Type II: non-estrogen dependent 20%. serous type/clear cell type. different pathogenesis
  • staging: I- confined to uterus, II-cervical involvement III-uterine serosa, adnexa, LN IV-invasion of bladder or bowel or distant metastases
70
Q

Type I vs Type II endometrial carcinoma

A

Type I: unopposed estrogen, pre-/peri-menopausal, precursor: atypical hyperplasia, low grade, variable invasion, endometrioid type, indolent, PTEN, K-ras, microsatellite
Type II: not estrogen-dependent, postmenopausal, precursor: intraepithelial carcinoma, high grade, variable deep myometrial invasion, serous/clear cell type, aggressive, P53!

71
Q

cervical cancer (subtypes, Sx, risk, precursor lesions, epi)

A
  • squamous (80%) adeno (15%), other rare types
  • Sx: bleeding, post-coital bleeding
  • risk: HPV 16/18, smoking, immunosuppression,
  • precursor lesions: dysplasia of increasing severity (pap smear/histo)
  • US: 2nd leading COD women 20-39, disproportionate impact
  • global: 1st most common gynecologic malignancy, 3rd cause of cancer death in women
72
Q

condyloma acuminatum

A

genital warts caused by low risk HPV (6/11)

73
Q

Transformation zone

A

squamous metaplasia point squamous –> columnar

tropism of HPV

74
Q

precursor lesions of cervical cancer

A 
Cyt: 
CIN 1: <50% of epithelium  abnormal
CIN 3: 100% epithelium abnormal
Microinvasion
pap:
ASC-US: borderline
LSIL: abundant cytoplasm, weird nuclei
HSIL: large nuclei, not a lot of cytoplasm
Squamous cell carcinoma: atypical, fragmented nuclei, blood
75
Q

types of ovarian tumors

A

surface epithelial 70%
germ cell 15%
sex-cord stromal 10%
metastatic (other primary) 5%

76
Q

surface epithelium tumors of ovary (subtypes, classification)

A
  • serous: ciliated epithelial cells (lining of tube)
    mucinous: (cells with intracytoplasmic mucin)
  • benign, malignant, borderline
77
Q

ovarian cystadenoma

A

benign surface epithelium tumor lined by single layer of bland epithelial cells (serous or mucinous types). ovulation –> inclusion cysts

78
Q

ovarian carcinoma (types, spread, Sx, staging, risk, genetics

A
  • serous, mucinous, endometrial, clear cell
  • spreads by peritoneum and omentum
  • no Sx in early stage, most pts present with late stage
  • Staging: I- ovaries II- tubes/pelvis III- LN, outside the pelvis IV- distant metastasis
  • risk: nulliparity, family hx, BRCA1/2
  • genetics: low grade serous KRAS or BRAF. high grade serous p53. almost all carcinomas in BRCA1/2 women are high-grade and are tubal.
79
Q

borderline epithelial ovarian tumor

A

more proliferation/atypia than cystadenoma. more complex lining than cystadenoma. not quite carcinoma. much better prognosis than carcinomas. may have extraovarian lesions (implants) but NO STROMAL INVASION
prognosis: stage I 100% survival. tumors with invasive implants behave like low grade carcinoma (30-60% survival)

80
Q

dermoid cyst

A

most common germ cell tumor of ovary. benign.

prone to torsion, infection, perforation, rupture, malignant transformation (rare). can have any kind of tissue.

81
Q

dysgerminoma

A

looks like seminoma. most common malignant germ cell tumor.

82
Q

sex cord-stromal tumors

A

arise from granulosa or thecal cells. have malignant potential but rarely metastasize. can produce estrogens–> endometrial hyperplasia and Type 1 carcinoma (!)

83
Q

ovarian fibroma

A

solid white/tan surface
no hormone production!
meigs’ and gorlin’s syndromes

84
Q

normal menstruation

A

periods: 24-35 day
duration: 4-7 days
amount: 30 mL

85
Q

anovulatory bleeding

A

dysynchronous shedding due to unopposed estrogen

86
Q

DDx abnormal vaginal bleeding

A

PALM-COEIN
uterine: Polyp, Adenomyosis, Leiomymoma, Malignancy and hyperplasia
non-uterine: Coagulopathy, Ovulatory dysfunction, Endometrial (infection, inflammation), Iatrogenic (IUD), Not classified

Structural (uterine, cervical, vaginal) vs hormonal (ovarian, systemic)

87
Q

abnormal bleeding hormone vs structural

A

regularity?

88
Q

abnormal bleeding post menopause

A

think cancer!

89
Q

gonadotropins during childhood

A

quiescent

90
Q

gonadotropins during pre-puberty

A

GnRH pulsatile (so is LH…FSH has long half-life so doesn’t look pulsatile). Night-time pulsing.

91
Q

gonadotropins at midpuberty

A

pulsatility all day

92
Q

gonadotropins in neonate period

A

high

93
Q

adrenarche

A

increase in androgen secretion from adrenal glands leading to hair growth. not under ACTH control. Can undergo w/o gonads

94
Q

Gonadarche

A

Activation of sex steroid secretion by the ovary or testis–> breast/sexual maturation

95
Q

telarche

A

breast development

96
Q

breast development flags

A

if 13 requires evaluation

97
Q

signal for onset of puberty

A

increasing pulsatile GnRH (intrinsic suppression of hypothal in childhood). extra-gonadal control. control of hypothal not well understood (GABA, NPY , Kisspeptin etc). factors are nutrition, toxins, stress, etc

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