Pathology-Female GU Path Flashcards
(120 cards)
A 22 year old woman present with a unilateral painful lesion at the lower vestibule adjacent to the vaginal canal. What is the most likely cause of her condition?
Bartholin cyst. This is a cystic dilation of the Bartholin gland that arises due to inflammation and obstruction of the gland; commonly in women of reproductive age.

A 34 year old woman presents with a large warty lesion of the vulvar skin. Biopsy of the lesion is shown below. What is causing her condition?

Condylomas are most commonly due to HPV 6 or 11. They are characterized by koilocytic change (crinkled or raisinoid nucleus) on biopsy. Note that these rarely progress to carcinoma because HPV 6 and 11 are low risk infections.

Typical areas affected by HPV 6 or 11 in females
Vulvar, vaginal canal and cervical (lower genital tract) condylomas
How do you know whether a woman is infected with high risk or low risk HPV infection?
DNA sequencing (because HPV is a DNA virus). Low risk are serotypes 6 and 11. High risk are serotypes 16, 18, 31 and 33
Typical areas affected by HPV 16, 18, 31 and 33 in females
Dysplasia over time that can eventually become carcinoma in the cervix, vagina and vulva.
A 60 year old post-menopausal woman presents with parchment-like (very thin) leukoplakia on the vulvar skin. What is likely causing her condition?
Lichen sclerosis. This is a thinning of the epidermis and fibrosis of the underlying dermis. This is a benign lesion but has a SLIGHT increased risk of squamous cell carcinoma.
A 60 year old post-menopausal woman presents with thick leathery leukoplakia on the vulvar skin. What is likely causing her condition?
Lichen simplex chronicus. This is hyperplasia of vulvar squamous epithelium due to chronic irritation and scratching. Note that these are benign and have NO increased risk of squamous cell carcinoma as Lichen Sclerosis does.
A patient presents with leukoplakia on the vulvar skin. Biopsy shows cancer. What is the most likely diagnosis?
Vulvar carcinoma. This arises from the squamous epithelium lining the vulva. Note that it is rare and accounts for a very small percentage of female genital cancers.
What are the two etiologies of vulvar carcinoma?
HPV-related (40-50 year old patient has high risk HPV which results in vulvar intraepithelial neoplasia that progresses to carcinoma) and non-HPV-related (elderly patient has long-standing lichen sclerosis, chronic inflammation and irritation leads to carcinoma).
A patient presents with erythematous, pruritic and ulcerated skin around the nipple and vulva. The biopsy is shown below. How would you narrow your diagnosis?

Paget Disease of the nipple and vulva (carcinoma) or malignant melanoma. Note the malignant epithelial cells present in the epidermis of the vulva. If the cells were PAS+, keratin+ and S100- it is Paget Disease of the nipple and vulva (carcinoma) If it is PAS-, keratin- and S100+, it is melanoma. Note that this represents carcinoma in situ, with no underlying carcinoma in the vulva.
Why are you more concerned about a patient with Paget Disease of the nipple vs a patient with Paget Disease of the vulva?
Nipple usually means there is underlying cancer in the breast. Vulva usually means no underlying carcinoma.
Where does the lower 1/3 of the vagina originate from? The upper 2/3?
Lower 1/3 = Urogenital sinus. Upper 2/3 = Mullerian duct.
What drug can cause a woman to have this vaginal biopsy?

She has adenosis. Normally, the stratified squamous epithelium from the lower 1/3 of the vaginal canal proliferates and replaces the columnar epithelium in the upper 2/3 of the vagina. Adenosis is a focal persistence of columnar epithelium in the upper vagina, with increased incidence in females exposed to DES in utero. Note the two glands persisting with columnar epithelium.
Why is exposure to DES in utero such a big deal that people stopped using it?
A rare complication of DES-associated vaginal adenosis is clear cell adenocarcinoma.
Aside from adenosis and/or clear cell adenocarcinoma, what other complications may arise from DES?
Abnormal smooth muscle formation in the uterine tube carries a complication of ectopic pregnancy and infertility. Mothers who took DES is related to increased estrogen and increased risk for breast cancer.
A <5 year old girl presents with bleeding and a grape-like mass protruding from the vagina. What is the most likely diagnosis?

This is embryonal rhabdomyosarcoma. This is a malignant mesenchymal proliferation of immature skeletal muscle and is rare.
A <5 year old girl presents with bleeding and a grape-like mass protruding from the vagina. What is the key cell in this lesion? How do you distinguish them?
Rhabdomyoblasts are the key cells in defining rhabdomyosarcoma. These cells have cytoplasmic cross-striations and will stain positive for desmin (intermediate filament in muscle cells) and myogenin (nuclear transcription factor in immature muscle cells) with immunohistochemistry.
What is a patient at risk for if they have vaginal intraepithelial neoplasia?
Vaginal carcinoma. This arises from squamous epithelium lining the vaginal mucosa. It is related to high-risk HPV and the precursor lesion is vaginal intraepithelial neoplasia (VAIN).
Lower 1/3 vaginal carcinoma spreads to what nodes? Upper 2/3 vaginal carcinoma spreads to what nodes?
Lower 1/3 = inguinal. Upper 2/3 = regional iliacs.
What defines the boundary between the exocervix and the endocervix?
Exocervix = squamous epithelium. Endocervix = columnar epithelium. This division is called the zone of transition.

HPV’s favorite place to infect in the lower genital tract. What happens in the 1% of time that persistent infection occurs?
Zone of transition. With persistent infection, cervical intraepithelial neoplasia occurs and can transform to carcinoma.
What is it about HPV 16, 18, 31 and 33 that make them high risk?
They make pro-oncotic proteins: E6 increases destruction of p53 (normally promotes DNA repair & apoptotic mechanisms) and E7 increases destruction of Rb (normally inhibits E2F so transcription does not go rampant)
What checkpoint is regulated by p53?
G1 -> S phase transition via checking for DNA damage, repairing it and inducing apoptosis if repair is not possible.
What checkpoint is regulated by Rb?
G1 -> S phase transition via suppression of E2F.






















