Pathology: Vulva, Vagina, & Cervix Flashcards

(18 cards)

1
Q

What is the vulva? What type of cell lines it?

A
  • the vulva is the skin of the genitalia external to the hymen
  • it is lined by squamous epithelium
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2
Q

What is a Bartholin cyst? How do patients present?

A
  • this is a cystic dilation of a Bartholin gland (lubricates the vestibule) due to inflammation and/or obstruction
  • patients present with a unilateral painful lesion in the lower vestibule, just adjacent to the vagina
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3
Q

What is a condyloma? What is it due to? Does it increase the risk for carcinoma?

A
  • a condyloma is a warty neoplasm due to infection with HPV serotypes 6 and 11 (these are the low-risk serotypes; types 16, 18, 31, and 33 are the high-risk ones)
  • these can occur anywhere in the lower genital tract (vulva, vagina, cervix)
  • it can very rarely progress to carcinoma
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4
Q

What type of cellular change is associated with an HPV infection?

A
  • koilocytic histology

- cells contain a clear halo around a crinkled pyknotic nucleus that resembles a raisin, and increased mitotic activity

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5
Q

What is lichen sclerosis? What about lichen simplex chronicus? How do patients present? Do either increase the risk for carcinoma?

A
  • lichen sclerosis: thinning of the epidermis and fibrosis of the underlying dermis; patients present with leukoplakia and parchment-like (very thin) vulvar skin
  • lichen simplex chronicus: hyperplasia of the squamous epithelium; patients present with leukoplakia and thick, leathery vulvar skin
  • ONLY lichen sclerosis is associated with a (slightly) increased risk of developing squamous cell carcinoma of the vulva
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6
Q

How do patients with vulvar carcinoma present? What are the major differentials for this presentation? What are the two pathways for vulvar carcinoma to develop?

A
  • patients with vulvar carcinoma present with leukoplakia
  • this is the same presentation as lichen sclerosis (slightly increased risk of malignancy) and as lichen simplex chronicus (completely benign); therefore, a biopsy is needed
  • 2 pathways: via HPV (serotypes 16, 18, 31, 33) or via long-standing lichen sclerosis
  • (patients with HPV carcinoma are usually younger, 40-50; patients with non-HPV carcinoma are usually older, 70+)
  • note that vulvar carcinoma is relatively rare (occurrence: endometrial then ovarian then cervical then vulvar and vaginal)
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7
Q

What is extramammary Paget disease? How does it present? What is the major differential and how do we rule it out?

A
  • this is the presence of malignant epithelial cells in the epidermis of the vulva (it is called extramammary because it usually occurs in the nipple)
  • it is associated with carcinoma in situ (nearly 100% association when in the nipple, but most cases in the vulva don’t involve cancer)
  • presents as erythematous, pruritic, ulcerated skin
  • must be distinguished from melanoma:
  • Paget: PAS positive, keratin positive, S100 negative
  • melanoma: PAS negative, keratin negative, S100 positive
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8
Q

What is adenosis and what is is highly associated with? What is rare but serious complication of this disease?

A
  • adenosis is the focal persistence of columnar epithelium in the upper 1/3 of the vagina (in the fetus: the lower 2/3 of the vagina is squamous epithelium and derived from the uro-genital sinus, the upper 1/3 is columnar and derived from the Mullerian duct; normally, the upper 1/3 gets replaced by squamous epithelium during development)
  • highly associated with DES (a drug no longer in use) exposure in utero
  • rare complication: vaginal clear cell adenocarcinoma
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9
Q

What is embryonal rhabdomyosarcoma? What cell type is involved? What is it also known as? How do patients present?

A
  • this is a very rare malignant mesenchymal proliferation of immature skeletal muscle cells (the rhabdomyoblast) of the vagina
  • it is AKA sarcoma botryoides because of it’s grape-like physical appearance
  • patients present as children with vaginal bleeding and a grape-like mass protruding from the vagina
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10
Q

What features/markers characterize rhabdomyoblasts?

A
  • (rhabdomyoblasts are the immature skeletal muscle cells involved in the malignant proliferation known as embryonal rhabdomyosarcoma)
  • these cells have cytoplasmic cross-striations and have positive IHC staining for desmin (intermediate filaments found in skeletal muscle) and myoglobin
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11
Q

What causes vaginal carcinoma? Which lymph nodes does the cancer tend to spread to?

A
  • vaginal carcinoma is relatively rare (occurrence: endometrial then ovarian then cervical then vulvar and vaginal)
  • is it usually related to infection with high-risk HPV (16, 18, 31, 33), in which case it develops from the precursor lesion VAIN (vaginal intraepithelial neoplasia)
  • carcinoma of the lower 2/3 of the vaginal canal (derived from the urogenital sinus) spreads to the inguinal lymph nodes
  • carcinoma of the upper 1/3 (derived from the Mullerian duct) spreads to the regional iliac lymph nodes
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12
Q

Where is the most common site of HPV infection?

A
  • (HPV can infect the lower genital tract: vulva, vagina, and cervix)
  • it most commonly infects the cervix at the site of the transformation zone (when the exocervix becomes the endocervix; stratified squamous becomes columnar)
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13
Q

What action of HPV causes the intraepithelial neoplasia? Which serotypes are involved?

A
  • this involves the high-risk HPV serotypes: 16, 18, 31, and 33, as these cause the dysplasia that can progress into carcinoma
  • these serotypes have an E6 and E7 virulence factor; E6 destroys p53 and E7 destroys Rb
  • this results in intraepithelial neoplasia (in the cervix this is CIN, vagina: VAIN, vulva: VIN)
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14
Q

How do we classify the level of intraepithelial neoplasia in the cervix due to HPV infection? Which classifications are still reversible?

A
  • classification of CIN is based on how much of the cervical wall is involved in the dysplasia
  • CIN 1: 1/3 is dysplastic; 66% chance of reversal
  • CIN 2: 2/3 is dysplastic; 33% chance of reversal
  • CIN 3: greater than 2/3; unlikely to reverse but possible
  • carcinoma in situ (CIS): whole wall; neoplastic, so no chance of reversal, will likely invade the basement membrane to become cervical carcinoma
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15
Q

What is the major risk factor for developing cervical carcinoma? What are two other risk factors? What is this cancer’s relationship to HIV/AIDS?

A
  • major risk factor is persistent infection with high-risk HPV serotypes 16, 18, 31, or 33
  • other risk factors: smoking and immunodeficiency
  • cervical carcinoma is one of the AIDS defining illnesses
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16
Q

How do patients with cervical carcinoma classically present? How do advanced tumors present?

A
  • most common age group is 40-50 (patients get infected in their 20’s and the dysplasia and neoplasia develop slowly over the next 20 or so years)
  • presents as abnormal vaginal bleeding, malodorous discharge, and postcoital bleeding
  • cervical carcinoma tends to grow locally and invade local structures rather than metastasize, so advanced tumors often invade the bladder; patients present with blockage of ureters and hydronephrosis with eventual post-renal azotemia/failure (renal failure is actually a major cause of death in these patients)
17
Q

What are the two types of cervical carcinoma? How do we detect this carcinoma?

A
  • 2 types: squamous cell (much more common; 85%) and adenocarcinoma (15%)
  • BOTH types are associated with HPV
  • we screen for cervical carcinoma with the pap smear (used to determine the CIN classification); the pap smear is VERY good at detecting squamous cell carcinoma, but is not nearly as good for adenocarcinoma
  • positive pap smears are followed up with colposcopy and biopsy
18
Q

Which gynecological malignancies are more common? Which have better prognoses?

A
  • (breast is more common than all)
  • incidence: endometrial (MC), then ovarian, then cervical
  • prognosis: endometrial (best), then cervical, then ovarian (worst)