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184 Cards in this Set
- Front
- Back
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where do precancerous lesions and cervical carcinomas dvlp
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squamocolumnar jxn |
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HSV-1
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generally oropharyngeal infections result |
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HSV-2
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usually involves genital mucosa and skin |
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latency of HSV2
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lumbosacral nerve ganglia; more likely to recur than HSV1 |
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gravest consequence of HSV infection
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transmission to neonate during birth |
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Pelvic inflammatory disease (PIV)
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ascending infection that begins in vulva or vagina and spreads upward to involve most of the structures of female genital system |
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PIV due to gonococcus
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spreads upward to involve fallopian tubes and tubo-ovarian region; endometrium spared for unknown reasons |
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PIV due to non-gonococcus infections (after full term/abortion deliveries)
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spread from uterus upward through lymphatics or venous channels rather than mucosal surface-tend to produce less mucosal involvement, but more rxn within deeper layers of organs |
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why can hydrosalpinx dvlp in PIV
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consequence of fusion of fimbriae and subsequent accumulation of tubal secretions and tubal distension
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Bartholin duct cysts
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relatively common, all ages, due to obstruction of duct by inflammatory process; lined by ductal squamous metaplastic and/or epithelium; up to 3-5 cm, produce pain and local discomfort |
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leukoplakia of vulva
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white, opaque, plaquelike mucosal thickening that may produce itching and scaling
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what are different things leukoplakia can be
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1) inflammatory dermatoses 2) vulvular intraepithelial neoplasia, Paget disease, invasive carcinoma 3) epithelial disorders of unknown etiology |
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non-neoplasic epithelial disorders of unknown disorders fall into what categories
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1) lichen sclerosus and 2) squamous cell hyperplasia |
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Lichen sclerosus
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thinning of epidermis and disappearance of rete pegs, hydropic degeneration of basal cells, superficial hyperkeratosis, and dermal fibrosis with scant perivascular, mononuclear inflammatory cell infiltrate |
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possible cause of lichen sclerosus
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may be autoimmune mediated-association with other autoimmune disorders, presence of activated T cells in subepithelial inflammatory infiltrate |
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squamous cell hyperplasia (hyperplastic dystrophy or lichen simplex chronicus)
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nonspecific condition resulting from rubbing or scratching of skin to relieve itching; epithelial thickening, expansion of stratum granulosum, significant hyperkeratosis |
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Condyloma acuminatum
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PPV-induced lesion aka genital wart; benign, verrucous gross appearance; usually multifocal
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condyloma latum
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syphilitic lesion |
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most common histologic type of vulvar cancer
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squamous cell carcinoma-2 types: basaloid and warty carcinomas and keratinizing squamous cell carcinomas (not related to HPV-70% cases) |
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what do basaloid and warty carcinomas dvlp from
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precancerous in situ lesion called classic vulvar intraepithelial neoplasia (classic VIN) |
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majority of cases of classic VIN are positive for
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HPV 16, occasionally for HPV 18 or 31
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non-HPV related keratinizing squamous cell carcinomas
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immediate premalignant lesion is referred to as differentiated vulvar intraepithelial neoplasia aka differentiated VIN or VIN simplex |
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differentiated VIN is characterized by
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marked atypia of basal layer of squamous epithelium with apparently normal epithelial maturation and differentiation in superficial layers
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papillary hidradenoma
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sharply circumscribed nodule, most common on labia majora or interlabial folds, tendency to ulcerate
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papillary hidradenoma morphology
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identical in appearance to intraductal papillomas of breasts and consists of papillary projections covered with 2 layers of cells: columnar, secretory and myoepithelial cells
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extramammary paget disease diagnostic microscopic feature
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large tumor cells lying singly or in small clusters within epidermis and its appendages; clear halo in these cells, finely granular cytoplasm containing mucopolysacchride that stains with PAS, Alcian blue, or mucicarmine stains |
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gartner duct cyst
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relatively common lesions found along lateral walls of vagina and derived from walffian (mesonephric) duct rests; submucosal
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almost all primary tumors of vagina are
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squamous cell carcinomas associated with high oncogenic risk HPVs; usually upper posterior vagina at jxn of ectocervix
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lesions in lower 2/3 vagina metastisize to
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inguinal nodes
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lesions in upper vagina involve what nodes
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regional iliac nodes
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sarcoma botryoides
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uncommon vaginal tumor seen in infants and kids <5 yrs; mostly malignant rhabdomyoblasts
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sarcoma botryoides growth
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polyploid, rounded, bulky masses that sometimes fill and project out of the vagina; grape-like clusters
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sarcoma botryoides histo
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small with oval nuclei, small protrusions of cytoplasm from one end resembling tennis racket
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endocervical polyps
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benign exophytic growths that occur in 2-5% adult women; produce irregular vaginal 'spotting'
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endocervical polyps typical location
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endocervical canal; vary in size up to 5 cm
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endocervical polyps morphology
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soft, almost mucoid composed of loose fibromyxomatous stroma harboring dilated, mucus-secreting endocervical glands
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what have high oncogenic reisk HPVs been found in
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vaginal squamous cell carcinomas and subset of vulvar, penile, anal, tonsillar, and other oropharngeal carcinomas
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cerival important HPV strains
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16 (60% cervical cancer cases) and 18 (10% cases)
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immune clearance of most HPV infections
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50% cleared within 8 months and 90% within 2 years
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what do HPVs infect
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immature basal cells of squamous epithelium in areas of epithelial breaks, or immature metaplastic squamous cells present at squamocolumnar jxn
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where does replication of HPV occur
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in maturing squamous cells and results in cytopathic effect (koilocytic atypia)
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what does koilocytic atypia consisting of
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nuclear atypia and cytoplasmic perinuclear halo
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how does HPV activate cell cycle to cause mitosis in maturing, nonproliferating squamous cells
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interferes with fxn of Rb and p53
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viral E6 and E7 of HPV
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promote cell cycle by binding RB and up-regulation of cyclin E (E7); interrupt cell death pathways by binding p53 (E6); induce centrosome duplication and genomic instability (E6 and 7); prevent replicative senescence by up-regulation of telomerase (E6)
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HPV E6 and p53
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enduces rapid degradation via ubiquitin-dependent proteolysis, reducing p53 2 to 3 fold
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HPV E7 and RB
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complexes with hypophosphorylated (active) form of RB and promotes proteolysis via proteosome pathway
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what does hypophosphorylated RB normally inhibit
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S-phase entry via binding to E2F transcription factor
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physical state of virus in cancers vs condylomata
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integrated into host DNA in cancers and free/episomal viral DNA in condylomata and most precancerous lesions
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chromosome abnormalities associated with HPV 16 cancers
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deletions of 3p, amplifications of 3q
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cervical intraepithelial neoplasia (CIN) classification (2 tier system)
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low-grade squamous intraepithelial lesion (LSIL) CIN I, CIN II and CIN III high-grade squamous intraepithelial lesion (HSIL)
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LSILs
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associated with productive HPV infection, but show no significant disruption or alteration of host cell cycle; most regress spontaneously
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HSILs
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progressive deregulation of cell cycle by HPV-results in increased cellular proliferation, decreased/arrested epithelial maturation, and lower rate of viral replication compared to LSIL; 1/10 at common as LSILs
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diagnosis of SIL is based on
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ID of nuclear atypia characterized by nuclear enlargement, hyperchromasia, presence of coarse chromatin granules, and variation in size and shape
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grading of high vs low SIL based on
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expansion of immature cell layer from its normal, basal location; confined to lower 1/3=LSIL, 2/3=HSIL
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Ki-67
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marker for cell proliferation, in normal squamous mucosa is confined to basal layer
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p16
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cell-cycle regulatory protein which inhibits cell cycle by preventing phosphorylation of RB; overexpression with oncogenic HPV
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most common histologic type of cervical cancer
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squamous cell carcinoma ~80% cases; cervical adenocarcinomas ~15%; adenosquamous and neuroendocrine remaining 5%
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peak incidence of invasive cervical cancer
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~45 yrs
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histo of squamous cell carcinomas of cervix
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nests and tongues of malignant squamous epithelium (keratinizing or not) invading underlying cervical stroma
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adenocarcinomas of cervix histo
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proliferation of glandular epithelium composed of malignant endocervical cells with large, hyperchromatic nuclei and relatively mucin-depleted cytoplasm (dark appearance in glands)
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adenosquamous carcinomas of cervix histo
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intermixed malignant glandular and squamous epithelium
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neuroendocrine carcinomas of cervix histo
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similar to small-cell carcinoma of lung
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where do advanced cercival carcinomas spread
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paracervical tissues, urinary bladder, ureters, rectum, vagina
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Stage 0 cervical cancer
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carcinoma in situ (CIN III, HSIL)
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Stage 1 cervical cancer
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confined to cervix; 4 divisions: 1a=preclinical, microscopy diagnosis; 1a1=stromal invasion <3mm deep and <7 mm wide; 1a2=>3mm deep <5mm deep, horizontal <7 m; 1b=invasive carcinoma confined to cervix
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Stage 2 cervical cancer
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extends beyond cervix but not to pelvic wall, involves vagina, but not lower 1/3
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Stage 3 cervical cancer
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extends to pelvic wall; involves lower 1/3 vagina
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Stage 4 cervical cancer
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beyond true pelvis or involves mucosa of bladder/rectum; metastatic dissemination
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false-neg error rate of Pap test
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~10%-20%; usually due to sampling errors
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when should Pap tests be done
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starting at age 21 or within 3 years onset sexual activity, then on annual basis; after 30 if 3 normal in a row, screen every 2-3 years
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myometrium is composed of
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tightly interwoven bundles of smooth muscle that form the wall of the uterus
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functionalis
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hormonally responsice upper zone of endometrium
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glands during proliferative phase
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straight, tubular structures lined by regular, tall, pseudostratified columnar cells; mitotic figures numerous-no evidence of mucus secretion or vacuolation
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postovulatory endometrium
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marked by secretory vacuoles beneath the nuclei in the glandular epithelium; most prominent during 3rd week of cycle
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by what day of cycle are there prominent spiral arterioles
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by days 21 to 22
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days 23-24 of cycle
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considerable increase in ground substance and edema btwn stromal cells
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predecidual change
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stromal cell hypertrophy with accumulation of cytoplasmic eosinophilia; occurs days 24-28
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what does most of hormonal action of estrogen and progesterone act through
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cognate nuclear receptors (estrogen receptor alpha and progesterone receptor A and B)
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cross-talk btwn glands and stroma
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much of estrogen effect on glandular proliferation occurs via stromal cells, which produce GFs in response to estrogen
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progesterone responses
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inhibits proliferation in both glands and stroma initially; promotes differentiation of glands and causes profound alterations of stroma; leads to decrease in estrogen receptor expression in both glands and stroma |
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dysfunctional uterine bleeding (DUB)
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bleeding not caused by any underlying organic (structural) abnormality; most common form of uterine bleeding
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anovulatory cycle results in
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excessive and prolonged estrogenic stimulation without the counteractive effect of progestational phase that regularly follows ovulation |
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when are anovulatory cycles common
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at menarche and in perimenopausal period; also in endocrine disorders (thyroid, adrenal, or pituitary diseases/tumors); primary lesion of ovary, polycyctic ovaries; generalized metabolic disturbance (obesity, severe malnutrition, or any chronic systemic disease)
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inadequate luteal phase
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inadequate corpus luteum fxn resulting in low progesterone output with subsequent early menses
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endometrial changes induced by oral contraceptives
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discordant appearance btwn glands and stroma, usually with inactive glands amid a stroma showing large cells with abundant cytoplasm reminiscent of decidua of pregnancy; minimized with newer low-dose contraceptives
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menopausal and postmenopausal changes
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ovarian failure and atrophy of endometrium
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acute endometritis
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uncommon and limited to bacterial infections that arise after delivery/miscarriage
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chronic endometritis occurs when
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1) suffering from chronic PID 2) postpartum or post-abortion patients with retained gestational tissue 3) IUD 4) TB from miliary spread or drainage from tuberculous salpingitis
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endometriosis
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presence of endometrial tissue outside of the uterus
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most common sites of endometriosis
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1) ovaries 2) uterine ligaments 3) rectovaginal septum 4) culde sac 5) pelvic peritoneum 6) large and small bowel and appendix 7) mucosa of cervix, vagina, and fallopian tubes 8) laparotomy scars
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metastatic theory of endometriosis
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endometrial tissue implanted at abnormal locations; retrograde menstruation through fallopian tubes occurs regularly and could mediate spread
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metaplastic theory of endometriosis
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endometrium arises directly from coelomic epithelium (mesothelium of pelvis or abdomen)
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abnormalities of endometriosis endometrial tissue
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profound activation of inflammatory cascade (high E2, IL-aB, TNF, IL-6); estrogen production upregulated (steroidogenic enzyme aromatase-absent in normal endometrium)
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chocolate cyst or endometriomas
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ovaries distorted by large cystic masses filled with brown fluid resulting from previous hemorrhage
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adenomyosis
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presence of endometrial tissue within the uterine wall (myometrium)
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endometrial polyps
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exophytic masses of variable size that project into the endometrial cavity
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atrophic polyps
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most in postmenopausal women, most likely due to atrophy of hyperplastic polyp
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common genetic alteration in endometrial hyperplasias
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inactivation of PTEN-dephosphorylates lipis and protein molecules
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PIP3 fxn
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blocks phosphorylation of AKT-central factor in PI3K regulatory pathway; PTEN inactive=AKT phosphorylation enhanced
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PTEN and estrogen
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loss of PTEN may activate pathways normally activated by estrogen
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Simple hyperplasia without atypia aka cystic/mild hyperplasia
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glansa of various sizes and irregular shapes with cystic dilation; mild increase in gland-to-stroma ratio; largely reflect response to persistent estrogen stimulation
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simple hyperplasia with atypia
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uncommon; loss of polarity, vesicular nuclei, prominent nucleoli; cells rounded and lose normal perpendicular orientation to BM; 8% progress to carcinoma
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complex hyperplasia without atypia
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increase in size and # of endometrial glands, marked crowding, and branching of glands; little intervening stroma and abundant mitotic figures; glands distinct and nonconfluent and epithelial cells cytologically normal; 3% progression to carcinoma
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Complex hyperplasia with atypia
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overlap with well-differentiated endometrioid adenocarcinoma morphology; 23-48% have carcinoma when hysterectomy performed
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endometrial carcinoma
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most common invasive cancer of female genital tract; 7% of invasive cancer in women (excluding skin cancer)
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Type I endometrial carcinomas (aka endometrioid carcinoma)
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most common 80% cases; well differentiated and mimic proliferative endometrial glands
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PTEN mutations in type I
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30-80%
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PIK3CA fxn
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catalytic subunit of PI3K (lipid kinase that phosphorylates PIP2 to PIP3) directly antagonizing action of PTEN; found in 39% endometrial tumors with and without PTEN mutations
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endometrioid adenocarcinoma
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~80% endometrial carcinomas on histo; grades 1 (well differentiated) to 3 (poorly differentiated); includes only glandular differentiation, no squamous differentiation included
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endometrioid adenocarcinoma grade 1
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well-differentiated, less than 5% solid growth
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endometrioid adenocarcinoma grade 2
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moderately differentiated with partly (<50%) solid growth
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endometrioid adenocarcinoma grade 3
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poorly differentiated with predominately solid growth >50%
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Type II endometrial carcinomas
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arise in setting of endometrial atrophy; defined by poorly differentiation (grade 3) tumors; 15% endometrial carcinomas
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serus type II endometrial carcinoma mutation
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p53 in ~90%
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serus type II endometrial carcinoma precursor
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endometrial intraepithelial carcinoma (EIC); cells identical to serous carcinoma, but lacks identifiable stromal invasion; p53 in 75%
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what causes poorer prognosis in serus endometrial carcinomas
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propensity to exfoliate, undergo transtubal spread, and implant on peritoneal surfaces like ovarian counterparts
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clinical presentation of endometrial carcinomas
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irregular or postmenopausal vaginal bleeding with excessive leukorrhea
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Malignant mixed mullerian tumors (MMMTs) aka carcinosarcomas
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endometrial adenocarcinomas with malignant changes in the stroma; carcinomas with sarcomatous differentiation |
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changes of stroma in MMMTs
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variety of differentiations including mucle, cartilage, and even osteoid
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Staging of types I and II of endometrial adenocarcinomas and MMMTs
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1:confined to corpus uteri; 2:involves corpus and cervix; 3:extends outside uterus but not outside ture pelvis; 4:outside true pelvis or mucosa of bladder/rectum
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adenosarcomas of endometrium
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present commonly as large, broad-based polyploid growths that may prolapse through os; malignant appearing stroma with benign/abnormally shaped endometrial glands
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treatment of adenosarcoma
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oophorectomy since estrogen sensitive
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stromal nodule
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well-circumscribed aggregate of endometrial stromal cells in myometrium that does not penetrate myometrium and is of little consequence
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chromosomal translocation (7;17) in stromal sarcomas
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leads to fusion of JAZF1 and JJAZ1 with anti-apoptotic properties; fusion of these is found in normal stromal cells by stitching together mRNAs
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Leiomyomas aka fibroids
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benign smooth muscle neoplasms, usually multiple; 40% have chromosomal abnormality
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Leiomyomas morphology
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sharply circumscribed, discrete, round, firm, gray-white, variant in size; usually within myometrium of corpus
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Leiomyomas histo
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whorled pattern of smooth muscle bundles on cut section; mitotic figures scarce
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leiomyosarcomas
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uncommon; arise de novo from myometrium or endometrial stromal precursor cells; complex, highly variable karyotypes
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morphology of leiomyosarcomas
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bulky fleshy masses that invade uterine wall OR polyploid masses that poject into uterine lumen
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how are leiomyosarcomas distinguished from leiomyomas
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nuclear atypia, mitotic index (>10 per 10 HPFs), and zonal necrosis
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most common disorders in fallopian tubes
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infections leading to inflammatory conditions, ectopic pregnancy, and endometriosis
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common agents in suppurative salpingitis
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gonococcus 60%, chylamydiae
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most common primary lesion of fallopian tubes
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minute .1-.2 cm translucent cysts filled with clear serous fluid (paratubal cysts)
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hydatids of Morgagni
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larger variety of paratubal cysts found near fimbriates end of tube or broad ligaments; arise in remnants of mullerian duct-little significance |
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3 main histologic components of ovary
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1) surface mullerian epithelium 2) germ cells 3) sex cord-stromal cells |
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cystic follicle in ovary
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so common, considered virtually normal; originate in unruptured graafian follicles or in follicles that have ruptured and immediately sealed
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Polycystic ovarian disease (PCOD) aka Stein-Leventhal syndrome
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3-6% reproductive age women; numerous cystic follicles of follicle cysts-often associated with oligomenorrhea |
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dysfxn in PCOD
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variety of enzymes involved in androgen synthesis are poorly regulated |
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stromal hyperthecosis
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usually postmenopausal women, but blends with PCOD in younger women; uniform enlargement of ovary |
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theca lutein hyperplasia of pregnancy
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proliferation of theca cells and expansion of perifollicular zone occurs; as follicles regress, concentric theca-lutein hyperplasia may appear nodular
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wher do tumors of the ovary tend to arise
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1) surface epithelium derived from coelomic epithelium 2) germ cells 3) stroma of ovary
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3 main histologic types of surface epithelial neoplasms in ovary |
Serous, mucinous, and endometrioid tumors |
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serous tumors of ovary
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lined by tall, columnar, ciliated and nonciliated cells-filled with clear serous fluid; 70% benign
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BRCA-1 and 2 associated serus tumors in ovary
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high-grade, commonly with p53, and arise from epithelium lining the fimbriated end of fallopian tube
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mucinous tumor of ovary breakdown
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middle life-rare b4 puberty and after menopause; 80% borderline or benign, 15% malignant; 30% ovarian neoplasms
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KRAS and mucinous tumors of ovary
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58% benign mucinous cystadenomas, 75-86% mucinous borderline tumors, and 85% primary ovarian mucinous carcinomas |
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how do mucinous tumors differ from serous tumors of ovary
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rarity of surface involvement and less frequently bilateral; larger cystic masses; multiloculated tumors filled with sticky, gelatinous fluid rich in glycoproteins
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mullerian mucinous cystadenoma
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benign/borderline mucinous tumors in endometriosis; resembles endometrial or cervical epithelium |
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pseudomyxoma peritonei
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excessive mucinous ascites, cystic epithelial implants on peritoneal surfaces, adhesions, and frequently mucinous tumor involving ovaries
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endometrioid tumors of ovary
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uncommon for benign/borderline; 20% ovarian carcinomas
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endometrioid tumors of ovary are distinguished from other ovarian tumors by
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presence of tubular glands bearing close resemblance to benign or malignant endometrium |
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molecular studies of endometrioid tumors of ovary
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PTEN and KRAS along with B-catenin; microsatellitle instability
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clear cell adenocarcinoma of ovary
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VERY rare as benign/borderline and uncommon as carcinoma; large epithelial cells with abundant clear cytoplasm similar to hypersecretory gestational endometrium |
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cystadenofibroma
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more pronounced proliferation of fibrous stroma that underlies columnar lining epithelium; benign, small and multilocular |
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Brenner tumor
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adenofibromas in which epithelial component consists of nests of transitional-type epithelial cells resembling those lining urinary bladder |
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CA-125 marker
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high MW glycoprotein in serum of more than 80% patients with serous and endometrioid carcinomas; elevations can occur with nonspecific irritation of peritoneum |
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osteopontin
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expressed at significantly higher levels in ovarian cancer patients |
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what reduces risk of ovarian cancer
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oral contraceptives and fallopian tubal ligation
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germ cell tumors of ovary
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15-20% ovarian tumors; most benign cystic teratomas |
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teratoma 3 categories
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1) mature (benign) 2) immature (malignant) 3) monodermal or highly specialized
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mature teratomas aka dermoid cysts
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young women during reproductive years; bilateral 10-15%
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morphology of mature teratomas
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unilocular cysts containing hair and cheesy sebaceous material; thin wall lined by opaque, gray-white, wrinkled epidermis
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karyotype of almost all benign ovarian teratomas
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46, XX-may arise from ovum after first mitotic division |
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monodermal or specialized teratomas
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rare; struma ovarii and carcinoid most common; always unilateral |
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struma ovarii
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composed entirely of mature thyroid tissue-may hyperfxn
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immature malignant teratomas
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rare; component tissues resemble embryonal and immature fetal tissue; found in prepubertal adolescents and young women
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immature malignant teratoma morphology
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bulky, smooth external surface; solid structure on section; areas of necrosis and hemorrhage
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immature malignant teratoma grading
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I to III; based onproportion of tissue containing immature neuroepithelium
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Dysgerminoma
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ovarian counterpart of seminoma of testis; composed of large vesicular cells with clear cytoplasm, well-defined boundaries, and central nuclei; 75% occur in 2nd and 3rd decades, can occur in childhood; all malignant-only 1/3 aggressive
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Dysgerminoma useful markers
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express Oct3, Oct4, and Nanog like seminomas (maintenance of pleuropotency); c-KIT
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endodermal sinus (yolk sac) tumor
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rare; may be derived from differentiation of malignant germ cells along extra-embryonic yolk sac lineage; rich in alpha-fetoprotein and a1-antitrypsin
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characteristic histo feature of endodermal sinus (yolk sac) tumor
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glomerulus-like structure composed of a central blood vessel enveloped by germ cells within a space lined by germ cells (Schiller-Duval body); intracellular and extracellular hyaline droplets
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presentation of endodermal sinus (yolk sac) tumor
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kid/young women with abdominal pain and rapidly dvlp pelvic mass |
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Choriocarcinoma
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more commonly of placental origin; extra-embryonic differntiation of malignant germ cells; most exist in combination with other germ cell tumors in ovary; aggressive; high levels of gonadotropins
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Granulosa-Theca cell tumors
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~5% ovarian tumors; any age-predominately postmenopausal (2/3)
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clinical importance of granulosa cell tumors
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1) potential to elaborate large amounts of estrogen 2) small but distinct hazard of malignancy in granulosa cell forms
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tumors composed predominately of theca cells
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almost never malignant |
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inhibin
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product of granulosa cells-can be elevated in tissue and serum and is useful as biomarker
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fibromas of ovary
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unilateral 90%; solid, spherical or slightly lobulated, encapsulated, hard, gray-white masses covered by glistening, intact ovarian serosa |
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fibromas of ovary histo
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well-differentiated fibroblasts and scant interspersed collagenous CT
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Meigs syndrome
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ovarian tumor, hydrothorax, and ascites
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Androblastomas (sertoli-Leydig cell tumors)
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masculinization or defiminization, but have few estrogenic effects; women of all ages; unilateral; may resemble granulosa-theca cell neoplasms |
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Androblastomas (sertoli-Leydig cell tumors) morphology
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solid; gray to golden brown; well-differentiated show tubules compsed of Sertoli cells or Leydig cells interspersed with stroma |
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Krukenburg tumor
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metastatic GI neoplasia to ovaries; bilateral masses composed of mucin-producing, signet-ring cancer cells most often of gastric origin |
