Robbins Ch 22 - Lecture 2 Flashcards
shedding of the functionalis
menses
straight tubular glands line with regular, tall pseudostratified columnar cells w/ no evidence of mucus secretion or vacuolation
proliferative phase
appearance of secretory vacuoles beneath the nuclei in the gladular epi
postovulation
spiral arterioles, increase in ground substance and edema btwn stromal cells
late secretory phase
predecidual change occurs in the
late secretory phase
drives the prolideration of both glands and strom
estrogen
down-regulates expression of estrogen receptor in glands and stroma
progesterone
causes differentiation of the glands and function changes in stromal cells
progesterone
most frequent cause of dysfunctional uterine bleeding
anovulation
stromal condensation, eosinophilic epithelial metaplasia w/out glandular secretory changes and stromal pre-decicualization
anovulation
infertility ass’d with increased bleeding or amenorrhea d/t inadequate progesterone production during post-ovulatory period
inadequate luteal phase
acute endometritis is caused by
GAS, staphlyococci or another bacteria post delivery or miscarriage
ectopic endometrial tisse at a site outside of the uterus
endometriosis
5 MC sites of endometriosis
ovaries> uterine ligaments > rectovaginal septum > cul de sac > pelvic peritoneum
MC age group of endometriosis
active reproductive age - 3rd/4th decade
endometric implants in endometreosis show
release of proinflammatory factors, increased estrogen production by stromal cells
genetic changes in endmetriosis indicating possible clear cell ovarian cancer
PTEN, ARID1A
chocolate cysts
endometriosis that has cause fibrosis of the ovaries
presence of endometiral tissues within the uertine wall
adenomyosis
endometrial polyps have been ass’d with
tamoxifen
important cause of abnormal bleeding and frequent precursor to MC type of endometrial carcinoma
endometrial hyperplasia
inactivation of PTEN tumor suppressor in common genetic alteration in
endometrial hyperplasia and carcinoma
ass’ with prolonged estrogenic stimulation of the endometrium
endometrial hyperplasia
WHO classifications of endometrial hyperplasia
non-atypical and atypical hyperplasia
most common mutation acts to increase signaling though the PI3K/AKT pathway
hallmark of type 1 endometeroid carcinoma
clinical settings of type 1 endometrial carcinoma (4)
unopposed estrogen, obesity, HTN, DM
DNA mismatch repair gene defects
endometrial carcinomas in women with fam hx of HNPCC
well differentiated tumors may be distinguised from hyperplasias by
lack of intervening stroma
carcinoma that is confined to the corpus uteri
stage I
carcinoma that involves the corpus and cervix
stage II
carcinoma that extends outside the uterus but not outside the true pelvis
stage III
carcinoma that extends outside the true pelvis or involved the mucosa of the bladder and rectum
stage IV
usually arise in the setting of endometrial atrophy
type II endometrial carcinoma
most common subtype of type II endometrial carcinoma
serous carcinoma
most prevalent mutation in type II endometrial carcinomas
TP53
PI3K and PP2A mutations are also common in
type II endometrial carcinoma
precursor liesion of type II endometrial carcinoma
serous endometrial intraepithelial carcinoma
peak incidence of endometrial carcinomas
postmenopausal F, 55-65yo
endometrial adenocarcinomas with a malignant mesenchymal component
malignant mixed mullerian tumors
MMMT mets usually only contain
epithelial components
bulky polypoid mass that may protude out of the cervical os composed of both malignant epi and stromal components
MMMT
large, broad-based endometrial polypoid growth with malignant-appearing stroma coexisting with benign, abnormally shaped endometrial glands
adenosarcoma of the endometrium
estrogen-sensitive and responds to oophorectomy
adenosarcoma of the endometrium
JAZF1 SUZ12 translocation
low-grade endometrial stromal sarcoma
12q14 and p6 rearrangements
uterine lieomyoma
well differentiated, regular, spindle-shaped smooth mm cells ass’d with hyalinization
leiomyoma
rare variant leiomyoma that extends into vessels and can spread to other sites - MCly the lung
benign metastasizing leiomyoma
dissmeniated peritoneal leiomyomatosis presents as
multiple small peritoneal nodules
MED12
leiomyomas, lieomyosarcomas
peak incidence on lyeiomyosarcomas
before and after menopause, 40-60yo
spread of lyeiomyosarcoma and MC met sites
hematogenously; lungs, bone, brain