path of uterus 12/10 Flashcards
during proliferative phase
see increased mitotic figures in endometrium
after ovulation
See subnuclear vacuoles in ednometrium
also called piano keys
Day 21 of cycle
see increased stromal edema and secretions in glands
Day 23 (pre-implantation)
see pre-decidua around vessels
Day 26
entire stroma is decidualized
changes in usterus during the cycle

anovulatory bleeding
most common cause of DUB
excess estrogen and no progesterone–> endometrial hyperplasia and cells grow out of their blood supply and bleed
most are due to subtle hormonal changes
additional causes od DUB
inadequate luteal phase: inadequate progesterone from corpus luteum–> menstruation 6-9 days after LH surge
irregular shedding: heavy bleeding due to extended secretion of progesterone, see proliferative and secretory phases together
congenital usterus anomalies
septate: wedges of fibrous tissue dividing uterine cavity
asherman’s syndrome: adhesions (band-like) formations crossing the lining of uterus
bicornuate: incomplete uniting of uterus
leiomyoma
submucosal ones are most responsible for abnormal bleeding and infertility
histology of leiomyoma
whorled bundles of smooth muscle cells that resemble uninvolved myometrium
cells uniform in size and shape and have characteristic oval nucleus and long, slender ‘cigar-shaped’ cytoplasm
benign metastasizing leiomyoma
extend into vessels and migrate to other sites, most commonly lungs (benign)
disseminated peritoneal leiomyomatosis
multiple small nodules on peritoneum (benign)
endometrial hyperplasia
also endometrial intraepithelial neoplasia (EIN)
can cause abnormal bleeding
can progress from simple–>atypical–>carcinoma
conditions promoting EIN
menopause
PCOS
functioning granulosa cell tumors of ovary
excessive cortical function
estrogen replacement therapy
high grade or atypical EIN
from inactivation of PTEN tumor suppressor gene through deletion or inactivation
simple hyperplasia without atypia
lowest grade out of 4
increase in glands:stroma
rarely malignant
caused by persistent estrogen stimulation and usually becomes cystic atrophy if estrogen is withdrawn
simple hyperplasia with atypia
uncommon
cells of glands are rounded and lose their perpendicular orientation to BM
8% progresses to CA
complex hyperplasia without atypia
increase in number and size of glands
glands crowded and show branching:back-to-back with little stroma and lots of mitotic figure
epithelial cells normal
complex hyperplasia with atypia
hard to distinguish from well-differentiated endometroid adenocarcinoma
35% of pts have CA of uterus
can treat with progestin if keeping uterus is important
endometrial hyperplasia with squamous metaplasia
less easily classified
endometrial adenocarcinoma
most common invasive CA of femal genital tract
mainly in post-menopausal as abnormal bleeding
risk factors for endometrial adenocarcinoma
obesity
diabetes
HTN
infertility (anovulatory cycles)
2 pathogenetic groups of endometrial CA
type I: in background of estrogen stimulation and endometrial hyperplasia
type II: sporadic