vulva + vagina + cervix + uterine + ovarian Flashcards
round ligament of uterus terminates here
labia majora
skene glands are located around the
urethra
bartholin glands located
near vagina opening
ducts at 5 o’clock and 7 o’clock
obstruction of duct → cyst → infected cyst = abscess (I & D)
provide lubrication for intercourse
part of cervix in vagina
ectocervix
part of cervix closer to uterus is
endocervix
histology of vulva
stratified squamous epithelium labia majora (exposed): keratinized labia minor (moist): non-keratinized
histology of vagina
stratified squamous epithelium (non-keratinized)
histology of ectocervix
stratified squamous epithelium (non-keratinized)
histology of endocervix
simple columnar epithelium (mucous-secreting cells prevent infection to uterus)
where does most cervical cancers occur
squamocolumnar junction of the transformation zone (transitions between ectocervix and endocervix)
HPV can infect and replicate well here
squmocolumnar junction is located in
transformation zone
metaplastic cells transform from columnar (endocervix) → squamous epithelium (ectocervix) here
depends on age + hormonal status of women
transformation zone
histology of body of uterus
simple columnar epithelium (ciliated or secretory, long tubular glands)
histology of fallopian tube
simple columnar epithelium (mostly ciliated, some secretory (peg) cells - nutrition to egg)
histology of ovary
simple cuboidal epithelium (germinal epithelium)
most ovarian cancer come from what epithelium
simple cuboidal epithelium
most common type of vulvar cancer
squamous cell carcinoma of vulva
pre-pubertal or post-menopausal female benign, inflammatory lesion of vulva thinning of epidermis smooth, white plaques pruritic, pain, dyspareunia
lichen sclerosus
treatment of lichen sclerosus
topical corticosteroids
vulvar lesion associated with increased risk of squamous cell carcinoma of vulva
lichen sclerosus
most common type of vulvar cancer
squamous cell carcinoma of vulva
increased risk of squamous cell carcinoma of vulva if:
HPV infection (koilocytes present) -30% cases chronic inflammation (most cases) - like lichen sclerosus
HPV infection (oncogenic strains: 16, 18, 31) can cause
squamous cell carcinoma of: (vulvar and vaginal cancer are secondary to cervical SCC - have same risk factors) cervical cancer vulvar cancer vaginal cancer
koilocytosis (enlarged nuclei, white cytoplasmic clearing)
squamous cells infected with HPV (viral replication occurring here)
intraepithelial cancer of vulva (occurs in skin)
can be associated with underlying malignancy of vulva or non-vulvar (breast, GI)
red, well-demarcated lesion
pruritic (like eczema)
Paget disease of vulva
intraepithelial cancer of vulva (occurs in skin)
can be associated with underlying malignancy
Paget disease of breast
types of vaginal cancers
squamous cell carcinoma
clear cell adenocarcinoma
sarcoma botryoides
vaginal cancer associated with high-risk HPV strains (16, 18, 31)
squamous cell carcinoma
vaginal cancer associated with in utero
diethylstilbestrol (DES) exposure
clear cell adenocarcinoma of women in utero during exposure:
DES was given in 40/50’s to prevent miscarriage
SE of DES exposure
clear cell adenocarcinoma of vagina of women in utero during exposure
mullerian duct anomalies: T-shaped uterus
vaginal adenosis (patches of columnar epithelium on ectocervix + vagina)
vaginal cancer in infants and children
sarcoma botryoides (embryonal rhabdomyosarcoma)
progression of cervical cancer
infection of squamocolumnar junction of the transformation zone with high-risk HPV 16 and 18 have oncogenes E6 + E7 → mutated cells → cervical dyplasia (screen for this) → cervical cancer
risk factors for cervical dysplasia + cancer
persistent infection with high-risk HPV strain (16 + 18 = 70% of cervical cancers)
early coitarche: ↑ risk of exposure to HPV
multiple sexual partners
immunosuppression (HIV): can’t clear infection
smoking: impairs immunity
OCP use: don’t protect against HPV infection
history of STDs
Rb is a tumor suppressor that
G1 → S checkpoint
binds to and inactivates E2F TF (transcribes genes for DNA replication)
at G1→S
E7 protein
binds and inactivates Rb → activated E2F TF → DNA replication (G1 →S)
p53 is a tumor suppressor that controls
senses DNA damage at G1→S or G2→M
stop cell-cycle for DNA repair
if no repair possible: p53 induces apoptosis of cell
E6 protein
binds to p53 →degradation of p53 →DNA damage → cancer
types of cervical cancer
squamous cell carcinoma (most common)
adenocarcinoma
CIN describes
how far dysplastic cells extend
CIN: bottom 1/3 of epithelium
CIN II: 2/3 or full thickness involvement
invasive cervical carcinoma
invasion through BM
more common grading scheme
low grade and high grade SIL
(squamous intraepithelial lesions)
LSIL: = CIN I (mild dysplasia) HSIL = CIN II (moderate dysplasia) /III (severe or CIS)
most LSIL’s
regress
tx: just monitor
most HSIL’s
are precancerous
tx: need excision
cervical cancer screening
Pap smear: catches cervical dysplasia (koilocytes, darkening of nuclei, ↑N/C) before progressive to invasive carcinoma
if >30 yo: HPV DNA test + Pap smear allows to space out the screening interval
HPV vaccines
prevent HPV infection and cervical dysplasia
bivalent: 16 + 18
quadravalent: 16 + 18, 6 + 11 (90% of genital warts)
abnormal vaginal bleeding (poist-coital) due to friable tissue in cervix
nonspecific vaginal discharge
pelvic or low back pain
bowel or bladder symptoms
ureteral obstruction → pyelonoephritis, uremia, renal failure
cervical cancer
staging and treatment of cervical cancer
staged clinically (not surgically) treatment depends on stage: surgery +/- chemoradiation
3 layers of uterus
perimetrium: outer serosal
myometrium: smooth muscle
endometrium: glandular, grows via estrogen
4 layers of endometrium
stratum spongiosum + stratum compactum: sheds every month (due to low estrogen/progesterone) stratum basale (base layer): doesn't shed with menstruation
estrogen causes the endometrium to
proliferate and become thicker during 1st have of cycle