female repro- histology Flashcards
ovary surrounding layer
germinal epithelium
layer most ovarian cancer is from
germinal epithelium
what is in the cortex of the ovary
ovarian follicles
oocyte
the actual germ cell
makes proteases
granulosa/follicle cells
surround the oocyte
release estrogen converted from precursors
zona pellucida
inner glycoprotein layer surrounding the oocyte
stroma cells
outer layer of granulosa cells that will become theca cells
primordial follicle
oocyte arrested in meiosis 1 from birth to puberty
has 1 layer of granulosa cells
ovarian cycle
begins at puberty due to a rise in FSH levels
1-20 follicles begin maturing, but only 1 is ovulated
phases of ovarian cycle
follicular
ovulatory
development of corpus luteum
primary follicle
oocyte surrounded by zone pellucid and granolas cells
theca interna
secrete estrogen precursors
theca externa
flat connective tissue cells
secondary follicle
small antrum forms
antrum formation
follicle cells secrete liquor follicle and small spaces form which coalesce to form an antrum
graafian follicle
large antrum
cumuluc oophus and corona radiata
which stage do granulosa cells only have FSH receptors
primary follicle
which stage do granulosa cells gain LH receptors
graafian follicle
what is cumulus oophus
lots of follicle cells around an oocyte
coronoa radiata
single layer of follicle cells around the zone pellucida
what stage follicle starts meiosis 2
graafian follicle
when does meiosis 2 start
right before ovulation
what triggers ovulation
LH surge
what happens during ovulation
oocyte with 2 layers detaches and floats in the antrum
increased antrum pressure pushes the follicle against the wall of the ovary
blood supply to the wall is cut off–> ischemia
proteolysis and degeneration of the surface follicle and theca cells leads to the follicle rupturing and releasing the oocyte
theca lutein cells
release progesterone and androstenedione
from theca cells
stimulated by LH
granulosa lutein cells
release progesterone and some estrogen
from follicle cells
stimulated by FSH
corpus albicans
formed after no fertilization by the invasion of the corpus lute by connective tissue
factors are released that induce corpus lutem apoptosis
follicle atresia
degeneration of the rest of the follicles that begin maturing and don’t make it to ovulation
luteal cyst
from the follicle
germinal inclusion cyst
from germinal eipthelium
polycystic ovarian disease
high androgen secretion results in high estrogen which leads to no ovulation, no corpus lute formation, no progesterone secretion, and no uterine secretory phase
common ovarian cancer metastasis sites
colon
stomach
breast
where is fertilization
ampulla
lining of ovaducts
simple columnar epithelium with cilia
salpingitis
infection in uterine tube with bacteria from the uterus
pelvic inflammatory disease
spread of infection from uterine tube to pelvic cavity
ectopic pregnancy
implantation somewhere other than the uterus
endometrium lining
simple columnar epithelium
layers of the endometrium
functionalis- surface layer with spiral arteries that is shed during menstruation
basalis- bottom layer that is kept, has stem cells for endometrial regeneration
uterine phases
proliferative
secretory
menstrual
proliferative uterus
governed by follicle
functionalism layer built up
straight glands
secretory uterus
governed by corpus lute
uterine glands become disorganized
glands secrete fluid
menstrual uterus
corpus luteum regresses
coiled arteries contract and glands degenerate
see shedding of top layer
endometrial hyperplasia
high estrogen stimulate cells to replicate which leads to continuous bleeding without a full menstrual cycle
endometriosis
endometrial tissue outside the uterus
adenomyosis
endoderm grows backward into myometrium
endometrial carcinoma
cancer of uterine glands
fibroids
benign smooth muscle tumors in myometrium
parts of the cervix
internal os- opening into uterine canal
cervix
external os- opening into cervix
significance of external os
junctional zone- where the epithelium switches from simple columnar to stratified squamous
susceptible to dysplasia which can progress into neoplasia
nabothian cysts
blocked cervical galnds
cervical ectropia
metaplasia from simple columnar to stratified squamous epithelium in the cervix during menstrual cycle or pregnancy
human papilloma virus
dysplasia
high risk- invasive squamous cell carcinoma
low risk- condyloma acuminatum
veneral warts
condyloma acuminatum
grades of a pap smear
CN1- low grade squamous cell lesion, mild dysplasia due to hormones or infection
CN2- high grade squamous cell epithelial lesion, higher grade dysplasia with a larger nucleus
CN3- high grade, small cells, very close to neoplasia
vaginal mucosa
simple squamous epithelium with glycogen which is used by lactobacillus which lowers the vaginal pH
how are mammary proteins/sugars released
merocrine secretion
how are mammary lipids released
apocrine secretion
placental hormones during pregnancy
proliferation of glandular cells and terminal ducts
prolactin
milk secretion
oxytocin
milk ejection via myoepithelial cell contraction
fibrocystic changes in the breast
cystic dilation of ducts
glandular metaplasia
fibrosis of stroma
ductal hyperplasia
usually benign
fibroadenoma
most common benign tumor
fibrosis in the duct
lobar carcinoma
cancer in a lobe
ductal adenocarcinoma
tumor in a duct
