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170 Cards in this Set
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initation of labor:
what is increased in fetus? 4 other steps: |
fetal increased DHEA 1. placental conversion of estradiol--> estriol 2. inc decidual prostaglandin and gap junctions (more likely to myometrium to contract) 3. inc oxytocin and prostaglandin receptors 4. dec progesterone receptors (bc progesterone keeps uterus calm) |
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regulation of parturition: pathway |
inc CRH (placental)--> ACTH (fetal)--> DHEA (fetal)--> E3 (fetal) E3 causes inc oxytocin receptors, Inc PG, and Inc gap junctions which all leads to inc uterine contractions |
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during normal pregnancy what 3 things are happening? |
uterine quiescence immature fetus closed cervix |
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during partuirtion what 4 things happen? |
coordinated uterine activity maturation fo fetus maternal lactation progressive cervical dilation |
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oxytocin where is it produced? function? what induces oxytocin receptors on uterus |
produced from fetus (during second stage of labor) and from posterior pituitary it stimulates uterine contractions and stimulates prostaglandin production from amnion oxytocin receptors are in fundal location on uterus and are increased by estrogen |
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what hormones are inhibitors of contractions? (5) |
progesterone prostacycline relaxin nitric oxide parathyroid related peptide cortisol releasing hormone and human placental lactogen |
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what are uterotrophins that cause activation? (4) |
estrogne, progesterone, prostaglandins, CRH |
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what are uterotonins that cause stimulation? (help uterus contract) |
prostaglandins, oxytocin |
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what 2 hormones cause involution of uterus? |
oxytocin, thrombin |
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how far apart are normal contractions? how long do they last? what is adequate power? |
duration 30-60 sec occur every 2-5 minutes (so 3-5 contractions every 10 min) need >200-250 montevedeo units (measured by intrauterine catheter)-- add up peaks |
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what is considered preterm? what are risk factors for preterm? |
preterm: <37 weeks risk factors: prior PTB, multiple gestations, smoking, SES, fetal or uterine anomalies, short cervix, HTN |
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what can cause preterm birth? from maternal-fetal HPA axis? 3 others
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maternal-fetal H |
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what will present as a discrete, movable mass in the breast that is clearly circumscribed and smooth? |
fiboradenoma |
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which path presents with unilateral bloody discharge from the nipple? what does it look like macroscopically and microscopically? |
intraductal papilloma discrete subareolar intraductal mass micro: fibrovascular changes, ducts with papillas in them, cystic spaces |
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gynecomastia |
enlargement of adult male breast tissue caused by relative increase in the estrogen/androgen ratio intake of exogensou estrogen, or hormone secreteing adrenal or testicular tumor histo: you see ductal hyperplasia |
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what dx would you give with linear and branching calficiations on a mammogram? |
DCIS |
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what is comedonecrosis? |
high grade nuclie, central necrosis (comedo type DCIS) |
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what is a phyllodes tumro? |
like a larger fibroadenoma more cellular irregularity "feathers out" |
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pagets disease |
tumor cells infiltrating teh epidermis in smaller nests or singly with abundant pale cytoplasm and atypical nuclei |
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what are 3 benign breast tumors? |
fibroadenoma (younger), inc tenderness w/ estrogen intraductal papilloma: bloody nipple discharge phylodes tumor (older) |
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what is buzz word for endometriosis?
what is it? what are possible causes of it? |
chocolate cysts-- blood is being degraded and macrophages move in non-neoplastic endometrial glands/stroma outside of the endometrial cavity (ovary, pelvis, peritoneum) can be due to retrograde flow, metaplastic transformation of multipotent cells, transportation of endometrial tissue via lymphatic system cyclic pelvic pain, bleeding, dysmenorrhea, dypareunia, infertiltiy uterus is normal |
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adenoyosis |
extension of endometrial tissue into uterine myometrium caused by hyperplasia of basalis layer of endometrium |
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serous cystadenoma |
most common ovarian noplasm-- thin walled, smooth, lined with non-stratified fallopian like epithelium
simple (single layer) epithelial lining premenopausla |
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mucinous cystadenoma |
multiloculated, large, lined with mucus secreting epithelium |
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you need 2 of what 3 findings to histologically diagnose endometriosis? |
endometrial glands endometrial stroma evidence of hemorrhage or hemosiderin-laden macrophages |
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serous carcinoma |
malignant with stormal invasion papillary architecture: glands are no longer in one dimension with each other and have fibrovascular cores nuclear hobnailing-- nucleic bulge from cytoplasmic surface into glandular lumen high grade nuclei psammoma bodies |
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artificial induction of labor medical non-pharm
when should elective inductions be done? |
medical: oxytocin, prostaglandins non-pharm: nipple sitmulation, intercourse, castor oil, acupuncture
only do elective induction if after 39 weeks-- DONT DO IT PRIOR |
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how to dx ruptured membranes |
pooling on speculum exam ferning-- allow to dry (can get false pos from semen, cervical mucus, fingerprints false neg from prolonged PROM, dry swabs, blood
nitrazine-- check pH ultrasound |
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what is normal fetal HR? |
110-160 |
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what are 3 types of decelerations and what do they mean? |
late deceleration: uteroplacental insuffiicency, hypoxia - low O2 in CNS, increased sympathetic tone, increased BP, baroreceptor mediated bradycarida - myocardial depression
early: 5-10% of labors, due ot vagal reflex due to cervical compression on fetal head
variable: umbilical vein compression-- dec cardiac return, fetal hypotension, fetal increased HR
umbilical artery compression: inc SVR, dec fetal HR (protective |
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what is first stage of labor?
second? third? |
onset of labor to complete dilatation: latent phase is 0-4 (slow), and active is 4-10
second: complete dilatation to delivery of neonate (if you have epidural it takes a little longer)
third is delivery of placenta-- mean is 6 min, and after 30 min you need dilatation and curatage |
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how do you assess uterine activity? |
observe and manual palpation external tocodynamometry internal uterine pressure catheter |
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steps from ovulation to implanation |
after ovluation, ovum remains in tube for 8-24 hrs- if not fertilization, it distegrates
days 1-3: if fertilized: it begins cell division in fallopian tube 4: moves to uterus wiht ongoing cellular division 8-9: implants |
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what are examples of highly effective reversible contraception (HERC) |
levonorgestrel IUD (mirena) copper IUD etonogestrel implant (nexplanon) |
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what are examples of short acting reversible contraception (SARC) |
medoxyprogesterone acetate (depo injection) combined OCP nuva rin transdermal patch progestin only pills condoms diaphragm
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tubal ligation: 3 ways biggest downfall: efficacy: risk: |
clip, severage, or band
regret-- up to 25% (risk: <30, change in marital status)
procedural risk: anesthesia, surg complications efficacy: failure risk persists over time, compare to other methods, ectopic risk (33%) |
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transcervical sterilization (essure) pros: conts: |
pros: highly effective, in office, quick
cons: may require second attempt (tubal spasm), no immediately effective, takes time to reverse
put coil in, tube scars up around coil-- takes time for scarring to occur
do a hysterosalpingogram to make sure that you are infertile (put dye in, see if it goes beyond fallopian tubes) |
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vasectomy pros cons |
mechanism: interrupting vas deferens
pros: simple, safer than female sterilization cons: not immediate, need to have semen evaluated to make sure sperm=0 |
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what are progestins MOA? estrogen? |
progestin: suppresses ovlulation, cervical mucus thickening, endometrial effects
estrogen just suppresses ovulation |
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how does levonorgestrel IUD (mirena) work?
pros cons? |
mech: thickens cervical mucus alters uterotubal mileiu impairing oocyte and sperm migration things endometrium, inhibits ovluation
pros: minimal bleeding, low maintenance, effective cons:: initial inc in spotting, possible amenorrhea, possible expulsion, possible perf with placement |
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paraguard T380 (copper IUD) |
mechanism: spermicidal effect of copper oins
pros: low maintenance, cost effective, last 10 years
cons: possibly heavier menses, possibly increased crampin, possible perf during placement |
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nexplanon (etonorgestrel) |
mech: thickens cervical mucus inhibits ovulation, lasts for 3 years
pros: low maintenance, oligomenorrhea, amenorrhea
cons: requires insertion and removal, irregular bleeding |
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dpo-provera shot |
mech: inhibits FSH and LH thickens cervical mucus thins endometrium dec tubal motility
pros: low maintenance (IM injection every 3 mo) amenorrhea with prolonged use improved dysmenorrhea (menstrual cramps)
cons: irregular bleeding possible weight gain reversible dec in bone density |
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combination oral contraceptive pill |
mech: inhibit ovulation, thicken cervical mucus, dec tubal motility, thin endometrium
pros: lighter periods, less dysmenorrhea, fewer ovarian cysts, protective against benign breast disease, ovarian cancer, endometrial cancer, colorectal cancer
cons: daily oral dosing, occasional SA (breast tenderness, HA) |
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when do you NOT use estrogen? |
pregnancy previous/active thrombocembolic disease smoking and age >35 undiagnosed genital bleeding hepatoma or serious active liver disease CAD
(relative if unctontrolled HTN, lupus, gallbladder dz, obesity) |
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ortho evra patch |
mechanism: same as OCP pros: weekly maintenance (better than OCP)
cons; application site irritation, more nausea and breast tenderness than OCP, lower efficacy in overweight women |
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nuvaring |
mech: same as OCP only requires insertion/removal-- lowest hormone dose of any combined method cons: 25% cycles w/ spotting, possible expulsion |
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condom: |
mech: barrier ONLY OCP TO PROTECT AGAINST STIs no hormonal side effects |
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emergency contraception protestin-only pills (plan B) |
use within 5 days combined oral contraceptive-- use within 5 days ella (ulipristal acetate)-- more effective, esp in obese women
copper IUD-- only one that has post contraceptive effect
EFFECTS ARE ONLY PRE-FERTILIZATION!
if taken before ovulation-- it disrupts follicular development and blocks LH surge so it inhibits ovulation may inhibit motility of ova and sperm
if taken after ovulation it has little effect |
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when do you do vacuum aspiration? |
up to 14 weeks can do manual (suction) or electric
dilate, aspirate with pressure, can use ultrasound guidance procedure complete when chorionic villi identified use local anesthetic |
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what abortion technique do you use over 14 weeks? |
dilation and evacuation dilation- for 1-2 days (laminaria-- osmotic dilators, seaweed or synthetic evacuation: requires adequate anesthesia, ultrasound guidance, uterine evacuation using suction and instraments- can do a paracervical block to dec blood loss can hemorrhage, give prophylactic AB for infection labor induction abortion (4% of time) |
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medication abortion what are actions of mifepristone? misoprostol? |
mifespristone is a 19-norsteroid that specifically blocks the receptors for progesterone and glucocorticosteroids
antagonizing effect blocks relaxation effects of progesterone-- results in uterine contractions, pregnancy disruption, dilation and softening of cervix takes 24-48 hrs to occur inc sensivitiy of uterus to prostaglandin analogues by 5x
misoprostol is a synthetic prostaglandin analogue taken orally-- effective at iniating uterine contactions, effective at inducing cervical ripening (given 24-48 hrs later)
evaluate with utrasound 13-16 days later to confirm completion
9-15 weeks med abortion is rare bc its more diff to do fetal expulsion with meds |
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many women will have an abortion by age 45?
when is abortion safest?
how do risks compare to childbirth? |
1/3 women
safest when induced before 8 wks
risk with induced abortion are lower than childbirth |
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perimenopause |
gradual regression of ovarian follicular estrogen production median age of onset is 47 yrs, last 4 years characterized by menstrual irregularity-- have shortened follicular phase, then episodic ovulation |
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is metorrhagia (intramenstrual bleeding) ever normal? |
NO |
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menopause average age what determines it? what contributes? |
permanent cessation of menstruation caused by failure of ovarian follicular development in teh presence of high gonadotrophin levels
average age is 51-52 genetically predetermined smoking assoc w/ earlier menopause |
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hat happens before menopause (in terms of hormones) |
finite nubmer of ovarian follicles inhibin levels fall (which are produced by granulosa cells-- which are dwindling) so you have no neg feedback on FSH, which rises-- then estradiol levels rise, then they fall as no more follicles develop
so endometrium is no longer stimulated
you have HIGH FSH, LOW estradiol, LOW inhibin |
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in menopause what happens to estradiol: estrone ratio? estrogen: androgen? total testosterone? progesterone FSH: LH |
estradiol: estrone declines estrogen: androgen declines-- ovarian stroma still producing testosterone
will have slightly dec levels of total T but free T is unchanged undetectable progesterone FSH>>LH |
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what causes hot flushes? |
inc peripheral vascular perfusion, sweating
dec estrogen levels lead to changes in hypothalamic thermoregulation intensity proportional to BMI and acuteness of estrogen deficiency
acccompanied by inc in LH and cortisol occurs at night |
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what happens during menopause? (physical effects) |
inc in total body weight and fat, distribution of fat from peripheral sites to abdomen, reuduced breast cize, inc facial hair, loss of collagen, emotional liability, insomnia, genitourinary atrophy (itching, burning, irriation, dypareunia, frequent UTIS, pelvic organ prolapse, urinary urgency) |
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what happens to libido during menopause? |
libido only slightly reduced (free T is almost unchanged) if you get ovaries removed-- THEN you have LOW T vaginal dryness and dec lube-- so use astroglide vaginal estrogen cream is systemically absorbed |
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what are 4 health risks with menopause? |
osteoporosis CV effects breast, endometrial, ovarian, colon CA incontinenance and pelvic organ prolapse |
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when is greatest bone loss during menopause? what type of bone is lost |
greatest bone loss immediately after menopause-- 1-2% per year trabecular bone >> cortical bone
without HRT< lots of women will have spinal and hip fractures |
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what are osteoporosis risk facors? |
white or asian race alcohol caffeine sedentary lifestyle low BMI chronic steroid use premature menopause calc and vit D def |
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what does estrogen do with bone mass? |
cannot increase bone mass it reduces bone resorption by blocking action of PTH, inc calcitonin, stimulating osteoblast, inc Ca absorption |
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how iwll person who takes estrogen for 5 yrs then stops compare to someone who does not? if you do the measurement 10 yrs later? |
they will be the same bc after you stop HRT therpay you decline to the point where you would have been without therapy |
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how much bone loss does there have to be to be detected on X ray?
how does dual energy x ray absorptiometry (DEXA) work? |
25% is lost to be detected by x ray
DEXA: evualuate spine and femoral neck indicated for all women >65 or <65+ 1 risk factor |
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tx of osteoporosis (5 options)
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HRT: within 5 yrs of menopause and continued for 10+ yrs bisphosphonates: (end in "dronate"): inhibit osteoclast bone resorption calcium, vitamin D
SERMs: raloxifene (estrogen agonist on bone, agnatonist on bresat, endometriu, vagina) tamoxifen (estrogen agonist on bone, endometriu, antagonist on breast) |
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what is the number one killer of all women? |
heart disease! estrogen is controversial: it lowers LDL, inc HDL (good things!) but in increases blood clot so overall effect on CAD is not much |
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what do you need for HRT? |
need progestins to oppose estrogen effect in uterus benefits: hot flushes, prevent osteoporosis, redcued GU atrophy, improved lipid profile
but assoc w/ inc rates of CHD, breast CA, PE and stroke |
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what are adverse effects of estrogen? |
endometrial cancer gallbladder disease HTN and stroke clotting disorders breast tenderness vaginal bleeding
in women with a uterus, estrogen must always be accompanied by progesterone |
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what is fat necrosis of the breast? |
unilateral localized process assoc w/ trauma, breast surgery, and breast radiation can be confused with cancer due to induration, dystrophic calcification, irregular but its PAINFUL and cancer usually isnt |
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mastitis what is it caused by? |
almost always lactational assoc w/ engorgement and/ or loss of nipple integrity caused by skin flora (staph aureus, strep pneumo) can have accompanying fever, malaise
give AB/NSAIDs |
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fibrocystic change |
common between 30-55 cysts of various sizes surrounded by dense fibrotic tissue exaggerated physiologic response to changing hormone environment
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what is main risk for breast cancer? what is percentage of familial breast cancer? |
age 5-10% familal (AD dominant gene-- BRCA 1 and 2)-- 50-90% lifetiem risk breast and 20-50% ovarian |
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what are things to do for prevention of breast cancer |
maintain healthy body weight, exercise, low fat idet
for HIGH risk: SERMs-- selective estrogen receptor modulators lowers risk of breast CA by 50% absolute benefit depends on risk
BRCA 1 and 2-- screened for-- prophylactic mastectomy (95% red), prophylactic oophorectomy (50% reduction, SERMS
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can all breast CAs be found by mammograms? |
NO-- 15% of CA are mammographically occult ultrasound can be useful adjunct in examining palpable masses
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what are the screening requirements for breast CA? |
every 1-2 years age 50-70 (breasts are not as dense after menopause bc estradiol drops, you lose milk ducts and alveoli, easier to spot dense cancer) |
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what are 2 types of breast CA? |
ductal carcinoma in situ (noninvasive-- rarely spreads) invasive breast cancer-- |
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what are two surgical options for tx of breast cancer? |
mastectomy or breast conservation by lumpectomy/radiation JUST as good of outcomes |
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whta are cardinal movements of the fetus through the birth canal after engagement? |
engagement, then descent, flexion, internal rotation, extension, external rotation, expulsion |
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hat do you need to know for tumor stage and type for bresat CA? |
TNM: tumor size, node status, mets (outdated but used)
histology and tumor grade hormone receptors (estrogen and progesterone) HER-2 status
stage 1, 2, 3 is non-metastatic- breast only or regional lymph nodes stage 4: mets-- tumor elsewhere in body |
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what is sentinel lymphadenectomy? what is the value?
axillary dissection |
removal of first draining lymph node from a tumor if neg, no further surgery if positive, may need full axillar dissection >3 nodes
axillary dissection--surgical removal of lower lymph nodes (10 on average)-- dec lowcal recurrence |
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what are hormone therapies for breast CA (2)
biologic therapies?
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hormone therapy-- blocks or lower estrogen levels tamoxifen, oopherectomy, aromatase inhibitors
biologic therapies: anti-HER2 (trastuzumab-- kills breast CA cells) mTOR pathway: everolimus cyclin dependent kinase pathway |
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what is adjuvant systemic therapy? |
use chemo, hormone, or radiation therapy either before or after to destroy microscopic mets
PROPORTIONAL risk reduction of recurrence of 25-50% |
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3 types of breast cancer which one is the worst? how do you treat them? |
hormone receptor positive ER and/or PR and HER-2 neg (70%)-- endocrine therapy-- most relapse in >5 yrs
HER2 pos, any PR or ER (chemo AND anti-HER2 therpay) relapse in <5 yrs
ER/PR neg, HER2 neg-- chemo- most common in younger patients and AA patients, most relase in <5 yrs worst to have |
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what are cancer suvivorship issues? |
coordination of care, screening for new cancers, hot flashes, one issues, lymphedema, cardiac tox, venous thromboembolism, peripheral neuropathy, weight gain, fatigue, deperssion, infertilty, second cancers |
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what characterizes PCOS? |
inc LH LH: FSH >2 extra cysts due to degenerative follicle cells-- hormone imbalance thecal cells will produce androgen due to high LH androgen will go into blood-- create hirtuism (excess hair) in peripheral adipose tissue, androgen converted to estrone (tend to be obese)-- estrone will go back to pituitary and shut down FSH. will get degeneration of follicle bc they wont produce estrogen to maintain follicle. follicle will become cystic infertility, oligomenorrhea, hirsutism some pts have insulin resistance (will develop type 2 DM) inc risk for endometrial carcinoma (high circulating estrone levels) |
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what kind of tumors are serous and mucinous tumors?
what are benign tumors called? what age of women get these tumors? |
cystic
if full of water-- serous tumor
cystadenoma: composed of single cyst with simple, flat lining most commonly arises in premenopausal women (30-40)
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what is malignant serous or mucinous tumor of ovary called? (surface tumor) what is its lining composed of? what age women get them? |
cystadenocarcinoma composed of compelx cysts with thick, shaggy lining most commonly arises in post menopausal women (60-70 yo)
cells invade into connective tissue of cyst wall |
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borderline tumors of ovary? |
features of benign and malignant tumors better prognosis, but still carry metastatic protential |
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BRCA1 mutation carriers have an increased risk of getting what? |
increased risk of serous carcinoma of the ovary and fallopian tube
BRCA1 is breast and ovary serous subtype is most common |
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endometrioid surface ovarian tumor |
looks like endometrial cells usually malignant may be associated with endometriosis 15% of them will have separate endometrioid carcinoma in endometrium as well |
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what kind of cells do brenner tumor contain? |
eurothelium cells |
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what do surface ovarian tumors present with?
what serum marker can you use to monitor for tx response and recurrence? |
vague abdominal symptoms (pain, fullness) signs of compression (urinary frequency) ovary likes to spread locally and involve peritoneum poor prognosis
CA-125 (not good for screening, but good for recurrence monitoring
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germ cell tumors how common? what age?
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2nd most common ovarian tumor (15% of cases) usually occur in woman of reproductive age |
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what are the germ cell tumors? (5) |
cystic teratoma
embyronal carcinoma yolk sac tumor placenta--> choriocarcinoma germ cell tumor (dysgerminoma)
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cystic teratoma |
cystic tumor that contains different embyrologic layers (hair, teeth, bone, gut, thyroid) most common germ cell tumor in females, sometime bilateral |
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what does immature tissue in a teratoma mean?
what is struma ovarii |
malignant contain neuroectoderm tissue of teratoma can also have a cancer ex: in skin of teratoma, you can have a squamous cell melanoma-- called a somatic malignancy
also struma ovarii-- cystic teratoma composed of thyroid tissue, so you have hyperthyroidism |
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dysgerminoma
what is its counterpart in males? |
composed of large cells with clear cytoplasm and central nuclei most common malignant germ cell tumor overian counterpart of testicular seminoma composed of primordial germ cells
good prognosis, responds to radiotherapy serum LDH may be elevated nests of cells, composed of round cells |
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endodermal sinus tumor yolk sac tumor |
malignant tumor that mimics yolk sac most common germ cell tumor in kids serum AFP often elevated (just like yolk sac)
schiller-duval bodies are seen on histology glomeruloid like structures blood vessel in center and cells organizing around it in ring like pattern |
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choriocarcinoma |
malignant proliferation of placenta like tissue villus, blood vessel that runs through villus-- cells that surround villus is cytotrophoblast and synciotrophoblast choriocarcinoma-- malignant proliferation of trophoblast, synctiotrophoblasts- no villi small, hemorrhagic tumor w/ hematogenous spread (tiny primary in ovary, but spread all over blood) high beta- hCG (made by syncytiotrophoblasts) poor response to chemo |
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embryonal carcinoma what is it composed of? |
composed of large primitive cells aggresive with early mets
when cells are primitive, they have the ability to move and srpead |
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sex cord stroma tumors
granulosa: what histo features? fibroma: histo features, what is it associated with? |
resemble sex cord stroma tissues of ovary
granulosa theca cell tumor: neoplasm of granulosa and theca cells, often produce estrogen, presents with signs of estrogen excess can have abnormal uterine bleeding (can also cause precocious puberty in kids, abnroaml uterine bleeding, and postmenopausal bleeding in adults) call-exner bodies (coffee bean nuclei)
sertoli-leydig cell tumor sertoli cells form tubules leydig cells contain reinke tisssues will produce androgen- can get hisutism or virilization
fibroma: benign tumor of fibroblasts, assoc w/ pleural effusion and ascites (meigs syndrome) spindle cells and collagen on histo (benign tumor of fbiroblasts) |
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krukenberg tumor |
gastric carcinoma (from diffuse subtype) signet ring cells-- nucleus pushed off to edge of cell bc mucin displaces nucleus
can also come from breast or colon cancer will usually involve both ovaries |
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what is most common site of ectopic pregnancy? what are key risk factors?
what is presentation? |
lumen of fallopian tube scarring-- PID (inflammation of upper portion of female genital tract) or endometriosis
presentation: lower quadrant abdominal pain always do pregnancy test |
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sponatenous abortion what age how does it present? |
miscarriage of fetus (20 weeks before gestation)
common vagianl bleeding, cramp like pain, pass fetal tissue due to chromosomal anomalies or hypercoagulable state (lupus anticoagulant) exposure to teratogen |
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placenta previa |
implantation of placenta in lower uterine segment-- it will give you a "preview" of the placenta placenta overlies the cervical os 3rd trimester bleeding, need a C section |
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placental abruption |
placenta abruptly begins to separate from decidua (uterine wall) prior to delivery
common cause of still birth cut off baby's source of oxygen-- fetal distress, fetal insufficiency you will also get bleeding between placenta and uterus you will see blood on maternal surface with clots |
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placenta accreta |
improper implantation of placenta directly into myometrium with little or no intervening decidua decidua is endometrium under affect of progesterone) if no decidua, placenta attaches to myometrium presents with difficult delivery of placenta and post-partu bleeding requires hysterectomy |
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preeclampsia |
emergency induced HTN, proteinuria, and edmea arises in 3rd trimester due to abnormality of maternal-fetal vascular interface in placenta will get very high blood pressure, can get fibrinoid necrosis in vessels of placenta if you remove placenta, it will resolve |
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eclampsia |
preeclampsia-- with seizures need to deliver |
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HELLP |
H: hemolysis EL: elevated liver enzymes LP: low platelets
example of thrombotic microangiopathy involving liver |
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hydatidiform mole what is it? what is passed? what does it look like on ultrasound? |
abnormal conception characterized by swollen and edematous villi with proliferation of trophoblasts uterus expands as if normal pregnancy is present beta hCG will be higher than you expect, baby will be bigger than you expect
women would begin to pass grape like masses through vaginal canal-- in early 2nd trimester- if not prenatal care villi are edematous, surrouned by trophoblasts- these are what are passing through
dx by routine ultrasound in early first trimester, fetal heart sounds are absent "snow storm" appearance on ultrasound |
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what is genetics of partial mole? complete mole? fetal tissue in which one? which one has higher risk of choriocarcinoma?
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partial: 69 XXY or 69 XXX (normal egg from mom, 2 sperm from dad) complete: 46XX (completely from dad)-- sperm go into empty egg, all villi edematous, complete proliferation of trophoblast fetal tissue in partial, not complete risk for choriocarcinoma more in complete mole |
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tx of molar pregnancy
how does choriocarcinoma arise? which one responds to chemo? |
dilatation and curettage measure beta-hCG to ensure adequate mole removal and to screen for development of choriocarcinoma
may arise as complication of gestation or as spontaeneous germ cell tumor gestation pathway responds well to chemo; germ cell pathway does not |
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adenomyosis |
endometriosis into the myometrium |
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what does endometriosis cause?
what are features it can have? |
increased risk of carcinoma, esp when it involves the ovary
implants can appear as powder burns, clear vesicles, red flame areas, adhesions or scarring, -- CHOCOLATE CYSTS
caused by retrograde flow, occurence and porgression
presents with dysmenorreha, dypareunia, chronic pelvic pain, infertility (last 3 are from adhesions)
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endometrial hyperplasia
what causes it? what population gets it?
what is most important predictor to progression? |
hyperplasia of endometrial glands relative to stroma consequence of unopposed estrogen presents as postmenopausal uterine bleeding
cellular atypia predicts progression to carcinoma
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what is endometrial carcinoma? how will it presetn? how does it arise? (2) |
malignant proliferation of endometrial glands presents as postmenopausal bleeding arises via two distinct pathways: hyperplasia and sporadic (get cancer from an atrophic endometrium-- its papillary serous-- driven by p53, elderly)
when it comes from hyperplasia-- its called endometrioid (cancer looks like normal endometrium) |
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hyperplasia pathway: type 1
sporadic pathway: type 2
ages, pathway, markers? |
type 1: carcinoma arises from endometrial hyperplasia risk factors are related to estrogen exposure average age is 60 yo histology is endomtrioid markers: PTEN, PI3KCA, ER/PR+, KRAS2
type 2: carcinoma arises in atrophic endometrium no evident precursor lesion, high grade/atypical histology average age is 70 yrs histology is usually serous p53, PI3KCA, Her2-neu, P16, ER/PR- papillae psammmoma bodies, aggressive you will get fibroblastic cords |
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leiomyoma
how does it compare to leiomyosarcoma |
benign proliferation of smooth muscle arising from myometrium related to estrogen exposure-- enlarge during pregnancy pre-menopausal women often multiple, well defined white whorled masses usually asymptomatic (but can present with abnormal uterine bleeding, infertility, and pelvic mass) multiple: more likely to be benign leiomyosarcoma: only one, hemorrhage, postmenopausal women, arises denovo (not from leiomyoma), malignant single lesion with necrosis and hemorrhage, mitotic activity, cellular atypia |
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epidemiology of HPV risk factors microbiology of cervical cancer
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risk factors: sex, smoking, immunosuppression, DES exposure double stranded circular DNA that affects epithelial |
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what is epidemiology of HPV?
low risk? high risk? |
most common STI, most get it and clear it away in 8-24 mos low risk: 6, 11 high risk: 16, 18, 31, 33, 39, 45-- may cause cervical dysplasia and cervical cancer |
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when is PAP smear recommended? official recommendations for HPV testing? |
less than 21, no PAP screen neeed 21-29- PAP smear every 3 years 29-65: cytology every 3 years plus HPV testing if >25, HPV testing is approved as primary screening test every 3 years |
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what is colposcopy? when is it recommended? |
looking at cervix under microscope apply ascetic acid (dehydrates cells, so abnormal areas appear white due to decreased glycogen)
lugols solution (iodine taken up by normal cells with high glyogen content-- cells that dont stain are abnormal
done when PAP smear is abnormal |
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what is transformation zone?
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columnar epithelium is replaced by squamous epithelium through metaplasia (this is the zone where the two come together)
squamo-columnar junction: where the 2 cells are visible |
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recommendations for tx for HPV |
CIN1: follow up in 1 yr with PAP CIN2: tx except in young women, pap/colpo in 6 mos CIN3: always treat, can observe in adolescents Adenocaricinoma in situ: CKC Cervical cancer: referral to GYN ONC |
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what is colposcopy? what 2 stains do you use and what do they show? |
Colposcopy: looking at cervix under microscope, apply ascetic acid (dehydrates cells, so abnromal areas appear white due to decreased glycogen) or lugols solution (iodine taken up by normal cells with high glycogen content; cells that don’t stain are abnormal) to see dysplastic changes |
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treatments of CIN when do you definitely use CKC? |
Observation Ablation of abnormal cells (cryotherapy-- freezes), CO2 laser therapy which desiccates tissue Diagnostic excisional procedures: LEEP: loop electro diathermy excisional procedure: convenient, but difficult to assess margins cold knife cone biopsy: OR procedure, larger specimen possible, non-cauterized margins, always for ACIS |
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CIN progression |
CIN1: 90% regression CIn2: 50% regression CIN3: 90% persistance/progression-- average 10 years to invasive CA takes 10 years to get to cancer |
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what are 2 vaccines for HPV? what do they protect agianst? |
Prophylactic HPV vaccines: Gardasil: recombinant L1 proteins using yeast, 100% effective in preventing HPV/CIN2+: HPV 6, 11, 16, 18 Cevarix: recombinant L1 proteins using baculovirus, 91-94% effective in preventing HPV/CIN 2+ HPV 16, 18 ONY PROPHYLACTIC, NOT TREATMENT! |
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difference between prophylactic and therapeutic vaccines |
prophylactic HPV vaccines Target extracellular virus, epitopes of native proteins-- viral-like particles, Produce antibodies, Humoral immunity: CD4/MHC II
Therapeutic: target viral infected cells, epitopes of MHC procesesd peptides, produce CTLs, cellular immunity: CD8/MHC1 |
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4 cell layers of ectocervix what is endocervix composed of? which layer is infected by HPV?
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stratified squamous epithelium superficial, intermediate, parabasal cells, basal cells endocervix: columnar mucinous epithelium |
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what happens to uterine cervix at birth? young adult? adult? |
birth: endocervix is high up YA: endocervix grows out beyond sqamocolumnar junction, exposed columnar epitehlium adult: sqamous cells take back over the area, transformation zone with regrowth of squamous epithelium |
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which subtype is most commonly assoc with endocervical glandular neoplasia (adenocarcinoma/ACIS)
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•HPV 18
16 and 18 are assoc with squamous cell carcinoma |
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steps of HPV mediated carcinogenesis |
HPV infects basal cells at the transformation zone HPV integrates into host DNA HPV viral oncogenes E6 and E7 are overexpressed E6 and E7 oncoproteins bind and lead to destruction of proteins encoded by p53 and Rb genes, respectively Proliferating cells acquire additional genetic errors Clonal selection leads to malignant phenotype |
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main issues with false negative results in PAP test |
•Failure to sample dysplastic cells •e.g. high endocervical lesions and small focal lesions •Failure to detect dysplastic cells on slide •e.g. only rare abnormal cells present or obscured by blood or inflammatory cells •Failure to properly categorize dysplastic cells •e.g. misinterpret dysplastic/carcinoma cells as benign reactive changes |
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what do you do with false neg pap smears? |
•If a lesion is suspicious clinically, it must be evaluated further irrespective of negative Pap test findings |
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what are reasons to have unsatisfactory specimen for bethesda system? |
•Too few squamous cells (#1 reason) •Obscured by blood or inflammation •Excessive lubricant •Specimen rejected -- e.g. mislabeled |
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candida what do you seeon pap smear? |
•Common finding •See pseudohyphae (sticks) and yeast forms (stones) •Effect on Pap smear •Nuclear enlargement, ASCUS-like cells, but chromatin not dark •Hyperkeratosis •Inflammation |
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what are coccobacilli involved in? what kind of organism causes bacterial vaginosis? |
•Clue cells •Indicative of shift in normal flora (fewer lactobacilli) and suggest bacterial vaginosis •Primary organism is Gardnerella vaginalis •Changes are not specific •Changes can be seen in the absence of clinical symptoms |
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3 Ms of herpes simplex |
•The 3 M’s •Multinucleation of nuclei •Molding of nuclei •Margination of chromatin •If patient is pregnant, call clinician to report this finding |
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what will you see with trichomonas? what can it be mistaken for? what must you see to dx on pap? |
Oval or pear-shaped organism, 8-30 microns Must see nucleus to diagnose on Pap Cytoplasmic red granules are supportive Infection may induce reactive atypia Cytoplasmic halos Increased background inflammation
can be mistaken for dypslastic changes |
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what are actinomyces assoc w/? what do they look like on pap? |
•Gram positive, long, filamentous, irregularly beaded bacteria•Often associated with IUD use |
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what do squamous intraepithelial lesions on cytology correspond to on PAP? |
•Cytology (Pap): squamous intraepithelial lesion (SIL)
SIL CIN Low grade SIL CIN 1 (mild) High grade SIL CIN 2 (moderate) High grade SIL CIN 3 (severe)
•Histology (Tissue): squamous intraepithelial lesion (SIL) AND cervical intraepithelial neoplasia (CIN) |
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which organisms cause gainitis? |
•Vaginitis•Very common•Infectious: fungi (Candida), bacteria (vaginosis - Gardnerella), Trichomonas vaginalis•Atrophic: postmenopausal women, loss of estrogen |
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what does DES put you at higher risk for? |
Congenital anomalies of cervix and/or vagina Vaginal adenosis Clear cell adenocarcinoma |
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what are 3 primary tumors of the vagina? |
•Squamous cell carcinoma (95%) •Arises from dysplasia, termed vaginal intraepithelial neoplasia (VAIN) •Graded VAIN 1-3, using similar criteria as CIN in cervix •DES-associated clear cell adenocarcinoma •Sarcomas should be considered when evaluating vaginal masses in children (rhabdomyosarcoma- small round blue cell tumor- looks like a bunch of grapes |
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what is lichen sclerosis? |
•may be painful, pale white plaques, cause unknown |
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condyloma acuminatum gross and histology features: |
vulva:
Gross Cauliflower/papillary lesions Histology Papillomatosis with fibrovascular cores Marked epidermal hyperplasia Koilocytes (HPV effect)
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extrammammary pagests disease what is special about it? |
•Positive intracytoplasmic staining for mucin (helps to distinguish from melanoma)•Most cases are NOT associated with an underlying adenocarcinoma (unlike Paget disease of the breast)need to stain with S100, HIM-45, Mlean A to distinguish from melanomamelanoma is mucin neg |
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what are 4 mullerian abnormalities? |
Bicornuate = failure of dissolution
Didelphys = failure of fusion-- 2 of everything (2 uteri, 2 cervixes
agenesis: failure of formation of both ducts unicornuate: agenesis of 1 duct |
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what do the bladder and lower vagina form from? the upper vagina, cervix, and uterus what do the wollferian structures form? |
from cloaca--> urogenital sinus upper UG tract: from mullerian duct wolfferian ducts: form testes, vas def, seminal vesicles, epididymis |
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uterine leiomyomata when is it most common? features? what population of people? how would you describe fibroid? role of estrogen and progesterone? |
fibroids
Well circumscribed, non-encapsulated, benign smooth muscle tumors of the myometrium
•30% of U.S. women by age 35 •Hormonally responsive : Estrogen states = prevalence •Most common in 4th & 5th decades of life •More common in African- American than Caucasian
•Each fibroid is monoclonal – cells derived from a single progenitor cell in which a mutation took place •Estrogen and progesterone important to growth §Increased levels of estrogen and progesterone receptors present §Estrogen induces proliferation of smooth muscle cells Progesterone produces proteins which prohibit apoptosis
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types of uterine leiomyomas?
symptoms? |
pedunculated (stalk)/non submucosal, intramural, subserosal
Bleeding symptoms •Menorrhagia – heavy bleeding •Metrorrhagia – bleeding between menses •Dysmenorrhea – painful menses
Bulk symptoms •Pelvic pressure •Urinary frequency •Infertility and/or recurrent pregnancy loss many women are asymptomatic
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tx of benign gyn disease |
endometriosis, lyomyoma
oral contraceptives, progestins, GnRH agonists (continuous admin will desensitize LH/FSH receptors, results in hypothalamic, hypogonadal state) side effects; hot flashes, vaginal atrophy, bone loss or you can excise disease or female repro organs |
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exogenous risk factors for type 1 endometrial cancer what are protective?
what is biggest risk factor? |
pelvic irradiation unopposed estrogen tamoxifen
protective: combination OCPs
atypical hyperplasia progestin therapy |
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who needs endometrial biopsy (5) |
postmenopausal bleeding or endometrial cells on pap premenopausal intermenstrual bleeding or abnormal bleeding w/ anvoluation risk such as DM or obesity thickened endometrial stripe family history of lynch syndrome-- only indication for routine screening |
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what give you increased risk for ovarian cancer?
symptoms |
personal history of breast, endometrial, colon cancer-- BRCA 1/2 more estrogen over lifetime BRCA 1 and 2
bloated feeling, urgent need to urinate, increaseing abd girth
(pain/pressure in lower adomen, difficulty eating normally, constipation/diarrhea, nausea, indigestion/gassiness, unexplained weight loss |
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what needs to be tested fo sho? (key sign for ovarian cancer) |
any woman who presents with ascites in the absence of liver disease) ultrasound: bliateral masses, irregular borders, papillations, solid components, ascites |
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what can ultrasound tell you about ovarian cancer? what about CA-125? |
it can tell you if there is NOT cancer
CA 125 only detects 50-60% of early stage ovCA better post menopausal, but not specific |
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risk factors for vulvar cancer?
symptoms |
mostly postmenopausal cigarrette smoking vulvar dysplasia HPV 16 HIV diabetes
symptoms: itching, burning, bleeding, no healing ulcer, presistant lump, pain
history cervical/vaginal neoplasia |
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what 2 places do you ues the sentinel node biopsy technique? |
breast and vulvar cancer |
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serum tumor markers:
serous/endometrioid mucinous yolk sac tumor choriocarcinoma granulosa cell tumor |
serous/:endometrioid: CA125 mucinous: CEA yolk sac tumor: AFP choriocarcinoma: hCG granulosa cell tumor: inhibin |
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dysfunctional uterine bleeding
what is most common cause? |
abn uterine bleeding resulting from alterations in teh normal cyclic changes of the endometrium in teh absence of structural or organ pathologic processes (NOT polyps, inflammation, hyperplasia, carcinoma, exogenous hormones, complications of pregnancy)
most common: excessive estrogen-- anovulatory cycles-- ovarian follicles devleop but ovulation does not occur, follclesl continue to produce estrogen also: luteal phase abnormalities (CL develops iproperly or regresses prematurely), persistant CL) hypothalamic-pituitary-ovarian axis disturbances
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what is the difference between breakthrough bleeding and withdrawal bleeding? |
breakthrough: endometrium is proliferative, disordered, bulky, outgrows structureal support and vessels
withdrawal bleeidng: rapid involution of stimulatory follicle, estrogen rapdily declines and endomtrium sheds (example-- after you treat anvolatory cycle w/ birth control) |
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what causes endometritis? acute chronic what will you see histologically?
what is pyometra? |
clinical: pain, bleeding, infertility
acute (bacterial, gonorrhea and clamydia)-- (spont abortion, post partum neutrophils chronic: PID, IUD, retained products of conception, TB
pyometra: accumulation of pus in endometrial cavity |
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adenomyosis |
abnormal bleeding and apin endometrial glands and stroma within myometrium |
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leiomyoma vs leiomyosarcoma which one is hormone dependent? menopausal status number gross margin histo |
leiomyoma is hormone dependent leiomyoma is pre and peri menopausal leiomyosarcoma is post menopausal myoma-- multiple, sarcoma: one gross: white whorled (myoma) vs red and soft (sarcoma) myoma: no atypia, mitoses, necrosis sarcoma: atypia, mitoses, necrosis |
