Female GU Path - Genital Tract, Vulva, Vagina, Cervix, Body of Uterus/Endometrium, and Fallopian Tubes Flashcards
In the micro cards, we delve into details about the etiology and consequences of HPV, but we do not delve into the pathology as related to the GU system for females.
Where does HPV hit the female GU system, and what can it potentially lead to?
Infects the lower GU ract, especially the cervix transformational zone. It is usually eradicated by acute inflammation and the immune system.
It can lead to LSIL and HSIL (low/high grade squamos intraepithelial lesions = abnormal cells on pap smear)
Low vs high risk HPV subtypes and what they lead to
Low risk = 6 and 11 = condylomas
High risk = 16, 18, 31, 33 = dysplasia and carcinoma
How does the high risk HPV work?
High risk HPV produce E6 and E7 proteins which destroy tumor suppressor proteins (p53 and Rb, “6 before 7, p before rb”) leading to dysplasia
How do we stain/test for HPV?
- DNA sequencing
- ki67 and p16 staining
Discus the histology of an HPV infected cell
koilocytic change (raisin nuclei) with disordered cellular maturation and mitotic activity
As we discuss in the micro cards, HSV (not HPV) is a bigger virus. What do we see on gross inspection and on histology?
Gross - desquamated epthelium with marked inflammation in the ulcer bed.
Histo - Multinucleated squamos cells containing eosinophilic to basophilic viral inclusions with a “ground glass” appearence.
Squamos cells with 3 M’s: multinucleation, nuclear molding and margination of the chromatin.
Strawberry cervix is caused by:
Trichomonas vaginalis
If my patient presents with fishy green discharge, what does she have?
Bacterial vaginosis - Gardnerella (think a green garden) vaginalis - gram positive bacillus.
What exactly causes pelvic inflammatory disease and how does it present?
PID is an infection that begins in the vulva/vagina and spreads to involve most genital system
sx: pelvic pain, adnexal tenderness, fever, and vaginal discharge.
cause: Neisseria gonorrhoeae
We have all felt the Bartholin glands during the ICS session. What causes one of these to go cystic and who is at risk for it? What do we need to be careful of?
sx: Enlarged unilateral lesion in lower vestibule adjacent to the vaginal canal
cause: STD/STI or infection=inflammation & obstruction of ducts causing back-up
risk: women of reproductive age
can lead to: abscess
Compare lichen sclerosus to lichen simplex chronicus (also called squamos cell hyperplsia)
These are both benign non-neoplstic epithelial disorders.
Lichen sclerosus is a thinning epidermis that becomes fibrotic with disappearence of rete pegs (the epidermal extensions that dip down into the dermis at the ED junction). LSC (hyperplasia) is the opposite, we see hyperplasia of vulvar squamos epithelium.
Due to their different results, they appear different as well, with the thinning slcerosus looking like a leukoplakia thin like parchment and the hyperplasia lookling like thick leathery white vulvar skin.
Sclerosing is something that happens with age (skin gets thinner) so we see it more often in post menopausal women, putting them at a higher risk for squamos cell carcinoma (SCC). Thickening with hyperplasia, as per usual, happens due to constant irritation, and thus has no increased risk of development for SCC.
What is the fancy name for genital warts, what causes them, and how do they present?
Condyloma Acuminatum
STD that causes red/pink warty growths on anogenital skin due to HPV 6/11
What does a genital wart look like under histology?
Histology:
- branching/villous, papillary CT stroma covered by epithelium
- hyperkeratosis & acanthosis (thickening)
- koilocytosis (Cytoplasmic vacuolization of squamous cells = wrinkly raisin nucleus)
- squamous cells with enlarged, hyperchromatic nuclei with perinuclear halo
- condensed peripheral rim of plasma membrane
What is VIN and how does it present?
VIN = Vulvar intraepithelial Neoplasia
This is dysplasia in vulvar squamos epithelial lining.
Sx are a huge range, appearing very similar to condyloma acum. We see a Bowenoid papule (pigmented keratinized lesion, similar to the raised white warty papules of cond.), possibly a leukoplakia, and in general squamos hyperplasia.
DANGER - Distinguish from condyloma, because this guy is queued up to cause invasive SCC
Discuss the usual type of VIN vs the differentiated type
Normal type is a warty, basaloid mixed type that is multifocal, presenting with pruitis, pain and/or bumpy skin lesion. Unlike the differentiated type, this one is caused by high risk HPV (16, 18, 31). Oddly though, between the two, this one puts the patient at a lower risk for invasive SCC, so to treat it we can do a small excision without fear of missing material. We see this type in premenopausal women or those being immunosuppressed.
The differentiated type os unifocal mass in postmenopausal women not associated with HPV. Chronic dermatological issues, vichen sclerosis or erythroplasia of Queyrat (red nonkeratinized epithelium in the vestibule) lead to this. This guy has an increased chance of developing to SCC so to treat it we do a wide excision.
Vulvar carcinoma is a malignant neoplasm of vulvar squamous epithelium lining. What causes it and how does it present?
This is a relatively rare cancer that presents as a leukoplakia.
Two general patterns of cause:
40-50yo: HPV (high risk 16,18, 31, 33) –> VIN in about 10-15 years→ VC.
70+yo: long standing lichen sclerosus= inflamm→ VC
Discuss papillary hidradenoma of the breast as far as what it is and what it looks like under histology, which is really the extent of what you need to know.
This mimics intraductal papillomas of breast
histo: papillary projections w/ top columnar secretory cells & underlying flattened myoepithelial cells
What is the deal with this extramammary paget disease? How does it present?
Malignant epithelial cells in vulvar epidermis
sx: red, pruitic ulcerated skin
carcinoma in situ (Usually no underlying carcinoma)
When diagnosing EPD, how do we do it, and what must we do?
dx: Must distinguish from melanoma:
carcinoma (Paget cells) = S100(-), PAS(+) keratin(+), (mucus secreting epithelial cells)
Melanoma = S100(+) (classic sign), PAS(-), Keratin(-), (no mucus secreting epithelial)
Discuss the developmental pathology behind adenosis. Who is at risk?
persistence of columnar epithelium in the upper 1/3 of the vagina
patho: Lower ⅓ of canal is stratified squamous, upper ⅔ columnar. Over time, squamous should move up and replace columnar. Persistence of columnar = adenosis.
risk: Females exposed to DES (estrogen drug) while in utero
