Female pathology Flashcards
proliferative endometrium normal
Test tube shaped glands, abundant stroma, mitosis in the glands and stroma
Follicular phase
Secretory endometrium
Wiggly jiggly , cleared out stroma, spacing of the nuclei
Progestin effect on endometrium
inactive endometrium, stroma>glands, pseudodecidualized stroma
Endometritis
inflammation of endometrium (acute- neutrophils, chronic- plasma cells)
PID, Retained products of conception, intrauterine device (IUD), Mass lesion (leiomyoma, polyps)
Endometrial polyps
Benign biphasic neoplastic growths, proliferation of glands and stroma, dysfunctional bleeding
Most common with menopause
HMGIC or HMGIY- 12 q 15, or 6 p 21 rearrangement
Leiomyoma
mosst common benign tumors in females, Blacks> whites
asymptomatic, abnormal bleeding, ussually multiple, sharply demarcated tumors, submucosal, intramural, and subserosal, monoclonal proliferation of benign smooth muscle cells, complex genotypes
Adenomyosis
Growth of endometrium in the myometrium, often seen with endometriosis, enlarged, nodular myometrium with cysts, may be hemorrhagic, abnormal uterine bleeding infertility
Endometriosis
Presence of endometrial glands and stroma outside of uterus, cyclic bleeding, can become blood filled cysts (chocolate cyst), discharge of blood leads to reactive changes, fibrosis and adhesions, histology (endometrial glands and stroma with hemosiderin)
Endometrial disorders
Hyperplasia (Glandular proliferation, Gland/Stroma >50%, abnormal Glandular Architure, )
Without atypia lower risk of carcinoma
With atypia- higher rist of carcinoma- endometrial intraepithelial neoplasia (EIN)
Unopposed Estrogen
Prolonged excess estrogen
Obesity (peripheral estrogen production by adipocytes), anovulation (Polycustic ovariaan Syndrom, perimenopause)
Estrogen producing tumors (Granulosa cell tumor of ovary), exogenous hormones
Endometrial Adenocarcinoma Type 1
In a background of endometrial hyperplasia (estrogen dependent, Lots of mutations)
Low grade endometrioid and mucinous adenocarcinoma, hyperplasia- carcinoid sequence, Genetic alterations (mutation in Mismatch repair sporadic- hereditary cdanncers 90% survival for low stage tumors
PIK3CA, PTEN, KRAS, ARID 1a, CTNB1
Back to back glands`
Endometrial adenocarcinoma type2
usually atrophic background, independent of endometrial hyperplasia (TP53 mutations)
Older women- more aggressive, high grade endometrioid carcinoma, serous carcinoma, clear cell carcinoma, undifferentiated/dedifferentiated carcinoma, carcinosarcoma
Some nuclei are huge and very high not basal
very aggressive, 50%
Leiomyomasarcoma
Denovo from myometrial mesenchymal cells, post menopausal, solitary, soft, hemorrhagic, necrotic mass, pathological diagnostic features (tumor necrosis cytologic atypia and mitosis
Recurrence and mets are common, pelvic organs, soft tissue and bondes
Ovary normal structure
surface epithelium/ specialized mesothelium (coelemic epithelium), serum, mucinous, transitional, endometriod, clear cell tumors
Cortex- follicles, oocyte (germ cell), sex cord (granulosa cells), stromal cells (give rise to thecomas and fibromas)
Medulla/hilum (hilar/leydig cells), adrenal cortical rest, rete ovaril (mesonephric tubules), stromal cells/smooth muscle/fat, thick walled vessels
OOcyte in the middle, cortex is granulosa cells/sex cord cells making estrogen, and theca cells
functional cysts
inclusion cysts (cortical cyst), follicular cyst in follicles), luteal cyst (corpus luteum), hemorrhagic (corpus luteum)
PCOS
hyper androgenism, menstrual abnormalities, polycystic ovaries, chronic Anovualtion, decreased fertility, enlarged ovaries, thickened fibrotic capsule, innumerable cystic follicles, absence of corpora lutea
Risk factors for ovarian epithelial neoplasms
most common neoplasms of the ovary,
Things that reduce risk: high parity, use of oral contraceptives
Increased risk: obesity, estrogen usage for>10 y Family history (germline mutations in tumor suppressor gene
Family history- 5-10% of b=ovarian cancers are familial, BRCA1 and BRCA2 tumor suppressor genes, 30% lifetime risk of ovarian cancer in BRCA 1 carriers, Slightly lower risk for BRCA 2
lynch syndrome- mismatch repair gene mutation
Lifraumeni- Tp53 mutation
Somatic mutations in tumor suppressor genes- BRCA1 and 2 inn 8-10% of sporadic ovarian cancers, tp53
type 2 starts at the fimbrae
high grade serous carcinoma
poor prognosis, even after surgery and chemotherapy, prognosis depends heavily on the stage of the disease at diagnosis, the 5 yr survival for women with carcinoma confined to one ovary is about 90%, falls to less than 40% with high stage
Endometrioid Tumors
Solid/cystic, may be associated with endometriosis, usually malignant, bilateral 30%, concurrent endometrial carcinoma 15-30%
Mutation of PTEN suppressor gene and genes that upregulate PI3K AKT signaling
Brenner tumors
Uncommon, solid usually unilateral , incidental finding, nests of transitional type epithelium, mostly benign, borderline and malignant extremely rare