Vulvar, Vaginal, and Cervical Pathology - Behmaram Flashcards

1
Q

Describe the two epithelia found in the cervix.

What separates them?

A

Stratified (non-keratinizing) squamous and simple columnar.

Separated by the squamocolumnar junction in the transformation zone (in turn within the cervical os)

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2
Q

Besides squamous epithelium, what other cell types may be found in the cervix?

How does the stroma compare to that of the uterus?

A

Endocervical glands (this will comprise a subset of cervical cancers), leukocytes, vessels, muscles blahblah.

More fibrous, with fewer muscle fibers.

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3
Q

What can be found on a pap smear?

A

Primarily used to find cervical squamous dysplasia (not great for finding adenoid dysplasia) but can also identify infectious elements.

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4
Q

Describe the structure of an endocervical polyp.

What are its complications?

A

A mass of glandular or squamous tissue protruding through the cervix.

It may bleed. That’s it–no malignant potential.

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5
Q

What is the single greatest risk factor for cervical (and vaginal, and vulvar) neoplasia?

What behaviors increase this risk?

A

Persistent infection with high-risk HPV (16, 18, 31, 33).

Sexual exposure at a young age, promiscuity in general.

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6
Q

How common are HPV infections?

Where, specifically, does it infect?

A

Almost ubiquitous, 75-80% acquire it before age 50, about half of reproductive-age women (large spike in incidence in 20s-30s)

Infects the basal layer of the epithelium (stratum basale?)

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7
Q

HPV-related cervical (and vaginal, and vulvar) dysplasia is graded based on the thickness of epithelial involvement. Name 4 of these stages and distinguish between them.

How do they exchange with one another?

A

CIN I (involves less than the basal 1/3; “LSIL”), CIN II (less than 2/3), CIN III (almost all), CIS (full-thickness).

They may progress or regress. Note that more advanced dysplasia is less likely to regress.

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8
Q

What are the hallmarks seen on pap smear of HPV infection?

Name some immunostains that can ID HPV.

A

Koilocytes (in low-risk or in Condyloma acuminatum), increased N:C ratio, smaller cells, more atypia and mitoses.

HPV DNA, Ki-67, p16INK4.

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9
Q

Cervical cancer usually involves squamous epithelium, but may involve glandular tissue (adenocarcinoma).

How common is this?

What is the main risk factor?

What challenges does this present?

A

Only comprises about 15-20% of cervical cancers.

Still HPV infection!

Pap smears are of reduced sensitivity since adenoid tissue is not shed as readily.

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10
Q

What is the rarest subtype of cervical carcinoma?

How are they all treated?

A

Small cell carcinoma.

Radical hysterectomy!

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11
Q

Who should receive a pap smear? How often?

What should be done upon a positive pap result?

A

Anyone between 21 and 65 (except those with hysterectomies). Every 3-5 years.

Follow up with colposcopy and biopsy.

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12
Q

Describe the structure of an HPV vaccine.

Describe the two vaccine preparations.

What should women receive following their vaccines?

A

Recombinant L1 protein (capsid) with aluminum adjuvant.

Gardasil (quadrivalent) protects from 6/11/16/18, Cervarix (bivalent) protects from 16/18.

Continued pap smears! Not every serotype is covered.

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13
Q

What serovars of HPV are “high-risk”?

What makes them high risk?

A

16, 18, 31, 33.

These express the genes E6 and E7, which respectively inhibit p53 and Rb (important tumor-suppressors). They are also more likely to integrate into the host cell genome and persist.

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14
Q

What are Bartholin’s glands? Where are they located?

What epithelium lines the vestibule?

A

Vestibular glands which produce mucus. Located at “4 and 8 o’clock”.

Non-keratinizing stratified squamous.

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15
Q

The external vulva is essentially skin. Therefore, any skin condition can manifest there.

Name 3 besides squamous cell carcinoma.

A

Basal cell carcinoma

Melanoma

Contact dermatitis (and probably a thousand other dermatites)

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16
Q

Between lichen sclerosus and lichen simplex chronicus, which:

  1. Is a secondary process?
  2. Features thinning of the epidermis?
  3. Appears with leukoplakia?
  4. Feels like leather?
  5. Occurs mainly in the premenarchal or post-menopausal?
  6. Can develop into squamous cell carcinoma?
A
  1. Lichen simplex chronicus
  2. Lichen sclerosus
  3. Both!
  4. Lichen simplex chronicus
  5. Lichen sclerosus
  6. Lichen sclerosus
17
Q

Both vulvar and vaginal dysplasia can result from infection with high-risk HPV serovars. Describe their classifications.

What are the long-term consequences?

A

Follows the same grading based on epithelial depth of involvement as in cervical dysplasia (CIN).

Abbreviated VIN, VAIN.

Both can progress to cancer or fully regress.

18
Q

Describe the appearance of cells in extramammary paget’s disease.

IHC hallmarks?

A

Red, scaly plaques with epidermal malignancy (usually no underlying mesenchymal cancer). Large and pale cells.

Mucin, cytokeratin (CK7)

19
Q

Unlike in cervical cancer, adenocarcinomas of the vagina arise from a teratogen exposure.

What is the teratogen, and what is the condition (and cancer) called?

A

DES exposure in utero causes vaginal adenosis which predisposes for clear cell carcinoma!

20
Q

A 4-year old boy presents to your clinic with a soft, polypoid mass on his penis. Histology reveals “primitive cells”.

What is the diagnosis?

A

This is embryonal rhabdomyosarcoma (sarcoma botryoides). Note it can occur in either the vagina of young girls or the penis of young boys!