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Flashcards in repro Deck (175):
1

Kartagener Syndrome

absence of dynein --> immotile sperm --> infertility for males

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TEXT-14

Testis-expressed gene 14: essential for cytoplasmic bridges in mice

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sperm - longer in meiosis I or II?

meiosis I takes much longer - which is wh yyou see many more primary spermatocytes

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Tunica Albiginea

fibrous capsule of connective tissue around testes. Divides testes into lobules

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haploid/diploid for primary/secondary spermatocyte

primary = diploid // secondary = haploid

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menstrual cycle length

24-35

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GnRH pulsatility for LH

HIGH amplitude, low frequency

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how many oocytes do you have?

@ 5 months gestation: 6 million --> 2 million @ birth --> 300k @ puberty --> 0 @ menopause

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follicles start to be recruited to mature starting at...

5 months in utero until menopause

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follicles become dependent on FSH at the....

secondary follicle stage (defined by formation of the antrum)

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hormones at the end of the menstrual cycle

decrease in E and P leads to an increase in FSH, which recruits next round of follicles

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actions of FSH on follice

stimulates granulosa cell prolif. stimulates aromatase activity, increases FSH AND LH receptors

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3 actions of p on uterus

limit growth, make glands more tortuous, coiling of b.v.

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LH surge (3 things)

resume meiosis II and extrude first polar body, ovulation occurs 36 hours after, switches hormone production: E --> E + P

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Corpus luteam makes E and P for...

8-10 weeks (Then placenta takes over)

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most common contraceptives

OCPs >> tubal sterilization >> male condom >> vasectomy

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timing of copper IUD

insert before 7 days after sex, good for 12 years

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medroxyprogesterone acete

progesterone only depot injection. Take every 3 months. Ver effect, but people quite because of irregular bleeding

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effect of combination pills on androgens

they decrease free T by 1. increasing the binding protein (SHBG), and 2. via (-) feedback --> lower LH and FSH

20

Patch - contraceptive

like OCP (combined) - similar efficacy. MOA: no ovulation. Replaced weekly

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vaginal ring

like OCP: combined, similar efficacy to OCP. change every 3 weeks. MOA: stops ovulation

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IUD

P only --> thickens cervical mucosa (woman still ovulates) Works for 5 years.

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Implanon

P only. Placed under arm. Works for 3 years. Rapid return to fertility (period within 3 months)

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Implanon

progesterone only LARC. Placed under arm - effect for 3 years

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Do OCPs increase risk of venous embolisms?

YES, but not to the extent of pregnancy

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Do OCP increase CV risk?

only in smokers

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How many pregnancies a year?

6 million pregnancies a year, 1/2 are unplanned, of the unplanned, 1/3 will abort

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% of women who have had induced abortions

40%

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strongest risk factor for abortion-related mortality

gestational age

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can use medical abortion..

up to 9 weeks (used in 1/4 of eligible abortions)

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mifepristone

blocks the P receptor --> decidual necrosis, increased prostaglandin receptors, cervical ripening

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misoprostal

prostaglandin E1 analog --> contractions and cervical ripening. Used with mifepristone, methotrexate, and by itself

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side effects of misoprostol

** responsible for most side effects of abortion. GI (nausea, vomiting, diarrhea), and systemic (fever/chills, HA)

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methotrexate

blocks cells division. Takes longer (3-45 days), used off label with misoprostal

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signs of perimenopause/menopause transition

irregular menses (fewer follicles to make E), and Sx (e.g., hot flashes)

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timing of perimenopause

median age is around 45 - 47.5 (MWHS), duration is 4-5 years (can last 2-8 years)

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What defines the onset of menopause?

follicular cohort + rate of atresia --> DECREASED ESTROGEN

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biochem profile of menopause

decreased estrogen --> increased and LH and FSH

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MOA of CVD and OP in post-menopausal women

lower estrogen leads to increased cholesterol & LDL levels, and increased bone lose

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smoking and estrogen

smoking increases the metabolism of estrogen --> faster onset of menopause

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sstreak gonads seen with

Turner's syndrome. Need both X's for normal ovarian function --> accelerated atresia, streak gonads , ovarian failiure

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HCG mimcs

LH

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endometrial receptivity window

Determined by progesterone. Day 20-24

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timing of implantation

at 7 days post-ovulation (blastocyst stage)

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when is embryo fully embedded in endometrial stroma?

7 days post-implantation (14 days post-ovulation)

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where does embryo implant?

usually mid-posterior of uterus.

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functions of syncytiotrophoblasts

1. direct contact with maternal blood; 2. secrets hormones (HCG, P4, E2)

48

most common endocrine disorder in young, reproductive aged women

PCOS

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describe the hyperandrogenism in PCOS

chronic, low-grade elevation in androgens coming from ovaries (not adrenal glands, HEAD levels moderately elevated in 10-15% patients)

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Dx for PCOS

1. hyperandorgenism //2. anovulation or oligo-ovulation (<6-9/yr) // ultrasound - 12 follicles/ovary

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anti-Mullerian hormone in PCOS?

it's elevated = new marker? in PCOS, the granulosa cells are more sensitive to FSH - greater AMH production

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long term effects of PCOS

lifetime metabolic disorder, higher risk of endometrial cancer (lack of periods), increase risk of psych disorders

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E and P in PCOS

women will have normal E levels, but lower P levels (won't make P in the 2nd half of cycle) --> chronic relatively unopposed estrogen --> can see thickened endometrial stripe on ultrasound

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effect of estrogen on bone

decreases osteoclasts and determines the closure of the epiphyseal plates

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estrogen - CV effects

increases blood coagulability (BAD) but improves cholesterol profile: increases HDL, and decreases LDL (Good)

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Metabolic effects of estrogen

increases leptin (involved in fat redistribution also), and increases protein synthesis in liver --> including TBG!!!

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two roles of P

1. prepares uterus for implantation; 2. render uterus refractory to oxytocin until labr

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type 3-4 antagonist

mixed agonist/antagonist - binding of receptor to HRE can recruit co-activator or co-repressor

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type 2 antagonist

pure antagonist - binding of receptor to HRE recruits co-repressor

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Type 1 antagonist

pure antagonist - does not allow the receptor to bind the HRE

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exogenous estrogens and cancer risk

INCREASES endometrial and ovarian (E only) and breast (E+P) but DECREASES colon cancer (E+P)

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RU486

Progesterone receptor Type 2 antagonist

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hormone independent breast cancer

1/3 of cases --> do mastectomy then chemo + rad

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hormone dependent breast cancer

2/3 cases - can do adrenalectomy, aromatase inhibitors (part of chemo) or SERM (prophylactic Rx)

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SERM

selective estrogen receptor modulators. Are tumoristatic, can be used for prophylaxis Rx after treatment for breast cancer

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aromatase inhibitors

used as chemo for ER-positive tumors

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Tamoxefin

Type 4 SERM: ANTAGONIST: breast // AGONIST: bone, uterus (bad), maybe CV

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Raloxifene

type 3 SERM: ANTAGONIST in breast and uterus, AGONIST in bone and CV

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sperm can stay in the cervix for

80 hours.

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sperm capacitation

secretions for woman trigger sperm maturation (so it can fertilize egg). characterized by increased motility of sperm

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sperm penetrating the cumulus cells

assisted by sperm motility and enzymes (PH20 - hyaluronidase)

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What happens in the acrosome reaction?

the sperm adheres to ZP. ZP3 receptor on sperm is activated. Ca entry via T type Ca channels. Activates PLC and IP3. The sustained Ca triggers fusion of outer acrosome membrane with sperm plasma membrane

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hallmark of egg activation

Ca oscillations - lead to exocytosis of cortical granules and blocks polyspermy

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timing of egg activation

occurs AFTER fertilization. Egg finishes 2nd meiosis --> mitosis --> embryonic dev.

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globozoospermia

round headed sperm that don't have acrosome reaction - can't move past ZP. Can use ICSI, but success rate is low

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PESA and TESE

look at notes

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describe fertilization

penetrate cumulus --> penetrate ZP --> merge with egg plasma membrane --> fertilization (2 pro nu) --> egg activation --> block polyspermy

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drugs that can cause impotence

beta blockers, exogenous androgens

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initiating erection

CNS --> limbic system activates paraS system, which increases cGMP and causes vasodilation. Local reflex supports this

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MOA phosphodiesterase 5 inhibitrs

they inhibit phosphodiesterase 5, increase cGMP, MAINTAIN erection (still need the limbic system to initiate erection and get cGMP production)

81

metabolism of sildenafil

metabolized in liver by CYP3A4 to active metabolite (20% activity). Excreted via kidneys

82

can't use PD5 inhibitors with....

nitrates (anti-hypertensives) because both cause vasodilation (dizziness, hypotension, fatal events)

83

Timing of adrenarche

usually 2 years before secondary sex char (usually thelarche, then pubarche)

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timing of thelarche

usually between 8-13

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timing of menarche

average age =13 (after gonadarche, takes about 2 years to build up estrogen secretion and increase endometrial lining)

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estrogen and height

low levels == bone growth; high levels = close epiphyseal plates

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hormone levels in neonates

release from maternal E&P inhibition --> high LH and FSH --> high fetal E and P

88

sign of puberty

LH pulses at night (represent GnRH pulses because LH has a short half-life)

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what initiates pubertal changes?

the hypoT (arcuate nucleus) is released from inhibition --> starts GnRH pulses (This is NOT controlled by the gonads)

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signals that inhibit GnRH pulsatility (delay puberty)

GABA (in girls) and Neuropeptide Y (in boys)

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Leptin and puberty

leptin promotes puberty (and decreases NPY). It is NECESSARY for gonadarche, but doesn't prompt the start of GnRH pulsatility

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Kisspeptin receptor

GPR54

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Kisspeptin

simulates GnRH neurons (in the arcuate nu of the hypoT) -sudden appearance o kisspeptin fibers surround GnRH neuron just before onset of puberty

94

why is the ureter vulnerable to injury during pelvic surgery? 1

1. in a hysterectomy, the uterine artery crosses the ureter ~2" over the ischial spines; 2. the LEFT ureter comes close to the lateral cervix 3. the ureter lies close to the ovarian vessels

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what procedure is commonly performed through the rectouterine pouch?

oocyte retreival

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what ligaments support the uterus and vagina?

uterosacral and cardinal ligaments

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what is the major cause of infertility in females and how to Dx?

tubal obstruction. Dx with hysterosalpingography (radiography)

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perineal body

fibromusclar mass anterior to retum. Can tear during labor to enlarge vaginal orfice. Increases chance of vaginal prolapse

99

when do you start to dev gonads?

6 weeks gestation (from last menses)

100

prev of mullerian abnormalities in the general pop

4%

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most common mullerian abnormality

septated uterus

102

inhibin

produced by granulosa and Sertoli cells. Decrease pituitary GnRH receptors --> decrease FSH secretion. Increase LH receptors on thecal cells

103

Klinefelter Syndrome

47XXY. bilateral atrophic testes. Congenital cause of primary hypogonadism

104

Kallman Syndrome

GnRH precursor doesn't migrate from nose to hypoT. no LH/FSH (need supplementation), and altered smell

105

males and infertility

15% couples are infertile. males account for 30% of blame (females - 50%; combined 20%)

106

5 alpha reductase

turns testosterone into DHT (external virilization and sexual maturation at puberty)

107

most common location for BPH

around the proximal urethra (transitional zone)

108

definition of BPH

nodular prostate enlargement due to proliferation of glands, stroma, or both, that LEADS TO lower urinary tract Sx

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PCA epidemiology in the US

most common malignancy in men, 2nd most deadly after lung cancer

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PCA epidemiology in the word

6th MOST COMMON cancer

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high serum PSA levels signal

that the PCA has broken through the basement membrane

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The Sx you see with PCA

** most often asymptomatic. Sx = obstructive bladder Sx, pelvic pain, bone pain

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origin of PCA

75-80% from peripheral zone / 15-25% from transitional zone. Central zone can be secondarily involved

114

Chlamydia vs. Gonorrhea

Chlamydia is an IC org --> fewer Sx --> more common than G

115

Dx for PID

1. lower abdominal pain 2. adnexal tenderness, 3. cervical motion tenderness.

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ectopic pregnancies are most common in,.

the ampulla

117

what makes the vagina resistant to micro-org?

Vagina has lactobacilli which make H2O2 --> acidic environment = resistant to many STIs

118

dysfunctional uterine bleeding

LACK OF OVULATION - means no progesterone & secretory endometrium. Estrogen causes proliferation - outgrows blood supply - breakdown/bleeding

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Endometrial atrophy

Lack of estrogen causes endometrium to break down --> common cause of abnormal uterine bleeding in post-M women

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three things to know about polyps

they arise from Basalis layer // they are benign (but have different morphology - thick-walled arteries and enlarged glands) // they are focal (sessile or pedunculated)

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most frequent tumor in female genital tract

leiomyoma

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leiomyoma and hormones

we know hormones have an effect - tumors increase in preg and decrease after menopause. They are sensitive to estrogen (Tamoxifen)

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endometriosis

endometrial tissue (glands & stroma) outside of uterus - usually in ovaries or peritoneal cavity

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Adenomyosis

endometrial tissue in uterine wall (myometrium)

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most common malignant tumor of female genital tract

endometrial carcinoma

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Estrogen dependent endometrial carcinoma

during pre-menopause, perimenopause / myometrial invasion is variable, us/minimal, low tumor grade, indolent behavior, genes: PTEN, K-ras

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features of endometrial carcinoma, not hyperplasia,

invasion into myometrium, desmoplastic response, cribriform glands, extensive papillary pattern

128

mutation found in Type 2 endometrial carcinoma

non-estrogen dependent. p53 mutation (can statin for it)

129

is type 1 or type 2 more common for endometrial carcinoma?

Type 1 = 80-85% // type 2 = 15-20%

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in a post-menopausal women with bleeding, consider....

endometrial hyperplasia (most common) or endometrial carcinoma - type 2 (most concerning)

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endometroid endometrial carcinoma

type 1 - it was similar to complex atypical hyperplasia. Saw cribriform plates

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Serous endometrial carcinoma

type 2 form (can be mixed with clear cell form). Saw complex papillae structure. Can see calcification (psammoma bodies)

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staging of endometrial cacner

look at notes

134

prognosis for ovarian cancer

5 year survival is 30-50%. Staging is the most impt prognostic factor

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most common malignant ovarian tumor (overall)

serous carcinoma

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genetics seen in serous carcinoma

LOW GRADE: K-ras or BRAF // HIGH GRADE: BRCA1 or BRCA2 --> usually due to +p53

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endometroid ovarian carcinoma

genetics: PTEN, K-ras, microsatellite instability (think type 1 endometroid carcinoma). 15-20% accompanied by endometriosis

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Origin of germ cell tumors

the oocyte (in the follicle)

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malignant transformation of dermoid cyst

can turn into any kind of cancer. Common = squamous cell carcinoma

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Dysgerminoma makes up a sig. % of malignant tumors in...

during pregnancy (20-30%), and before age 30 (80%)

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prognosis for dysgerminoma

excellent prognosis - 80-90% survival for high-stage disease

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cystadenoma

benign form of surface epithelial carcinoma. See a cyst lined by one layer of cells, filled with fluid. Smooth, thin cyst wall.

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Call-Exner bodies

seen in adult granulosa - sex-cord stroma tumors. The granulosa tumor cells are trying to form follices!

144

what kind of ovarian carcinoma can make estrogem?

adult granulosa (sex-cord stroma) --> endometrial hyperplasia and carcinoma (type 1)

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4 side effects of PD5 inhibitors

1. vasodilation (don't use with nitrates) 2. CV - hypotension, tachycardis, decreased platelets; 3. GI - heartburn and indigestion 4. eyes - see blue/green

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site of 1st lesions - cervical cancer

squamo-columnar junction (transition zone). As you get older, the transition zone moves higher into the cervical canal

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high risk HPV strains

16 & 18

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Reflex HPV testing

take the residual liquid from the Pap smear, do high risk-HPV testing. (+) = colposcopy , (-) = Pap smear in 1 year

149

Co-Test

cytology (papsmear) + high risk HPV testing simultaneously. Used in women >30. (-) = come back in 5 years.

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cervical cancer subtypes

squamous cell (80%+), adenocarcinoma (glandular - 15%), other (5%)

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biggest factor in cervical cancer deaths

never been screened (50% cervical cancer cases)

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worst - HPV 16 or 18?

HPV 16 = more carcinogenic (60% all cervical cancers). HPV 18 = 15% - more in adenocarcinomas

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how many cases of cervical cancer a year?

15K in the US - 450K in the world

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principle age for HPV vaccine

12-Nov

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most common cause of abnormal pap dx

ASC-US --> do reflex testing (if women is 25+)

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Timing of testing for cervical cancer

START screening at 21. Can do reflex testing at 24. Can to co-test at 30. You don't want to start earlier because younger women have higher levels of HPV but lower levels of CIN 3

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Cases: LSIL on papsmear, no high risk testing

answer: colposcopy (assume the high risk testing could be positive)

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Clue: cyclic bleeding

suggest that ovaries/hormones are in tact (even if duration of cycle if abnormal)

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19-year old presenting with malignant cancer

think: dysgeminoma

160

breast changes during puberty

ductal elongation, driven by estrogen. mitotic rate of glandular epithelial cells is greatest in luteal phase (E+P)

161

what stimulates the differentiation of breast glands

progesterone and prolactin - prepare glands to lactate

162

what suppresses the lactogenic action of prolactin?

Estrogen and progesterone

163

supernumerary nipples (polymastia)

secondary to incomplete regression of milk streak

164

2 etiologies of galactorrhea

1. increased prolactin (amenorrhea) 2. increases sensitivity of breasts to prolactin (regular prolactin levels & regular menses)

165

Sheehan's syndrome

infarction of pituitary during labor/delivery --> no lactation, etc.

166

Gynecomastia - causes

due to imbalance between E and androgens. See it transiently in newborns (mother's E), transiently during puberty (E production before androgens), in elderly - taking drug that decreases androgens

167

seminal vesicles add...

fructose

168

alkylation at 17 alpha

makes androgens with more ANAbolic properties - JUICING

169

Esterification @ 17-beta

makes regular androgens (similar in potency to T and DHT)

170

what's a common OTC male hormone supplement?

DHEA

171

the adrogen potencies

DHEA and androstenedione=weak // testosterone = moderate.// DHT = very potent (but you make very little)

172

ARA70

it's a coactivator for AR-testosterone and AR-DHT

173

which androgen increases prostate size?

DHT

174

flutamide

its a receptor antagonist. It prevents the binding of the receptor complex to ARA70

175

Finasteride

blocks 5-alpha reductase TYPE 2 - can decreased BPH and male pattern baldness (both are caused by 5-DHT)