Female Genital Tract – Vulva, Vagina & Cervix

Question-and-Answer flashcards covering anatomy, benign and malignant disorders of the vulva, vagina, and cervix; key pathogens, risk factors, pathogenesis, and clinical features relevant to exam preparation.

What anatomic organs are included in the female genital tract (FGT) pathology lectures?

Vulva, Vagina, Cervix, Body of Uterus, Fallopian Tubes, Ovaries, and Diseases of Pregnancy.

Which vulvar condition is common but not serious, yet causes painful cysts by obstructing gland ducts?

Bartholin (greater vestibular) cyst.

What is the usual treatment and prognosis for a Bartholin cyst?

Simple surgical excision; lesions are benign and never become malignant.

Name the two main non-neoplastic epithelial disorders of the vulva.

Lichen sclerosus and lichen simplex chronicus.

What histologic triad characterises lichen sclerosus?

Epithelial atrophy, dermal fibrosis (sclerosis), and chronic inflammation.

Does lichen sclerosus increase the risk of vulvar squamous cell carcinoma?

Yes, it carries an increased risk.

What microscopic changes define lichen simplex chronicus?

Epithelial thickening (acanthosis), expansion of the stratum granulosum, and marked surface hyperkeratosis.

Are patients with lichen simplex chronicus at increased cancer risk?

Generally no, but the lesion is often found at the margins of established vulvar carcinomas.

What are the two biologic forms of condyloma?

Condylomata lata (secondary syphilis; flat, moist) and condylomata acuminata (HPV-related; papillary, elevated).

Which HPV types are most often linked to condylomata acuminata?

Low-risk HPV types 6 and 11.

Key cytopathic change seen in condylomata acuminata?

Perinuclear cytoplasmic vacuolisation (koilocytosis).

Define VIN.

Vulvar intraepithelial neoplasia – dysplastic changes confined to vulvar epithelium (SCC in situ).

What infection is highly associated with VIN and vulvar SCC?

High-risk HPV infection (especially type 16).

Age groups: HPV-related vs non-HPV-related vulvar SCC.

HPV-related: younger women; Non-HPV-related: older women (often with lichen sclerosus).

Describe extramammary Paget disease of the vulva.

Intraepithelial adenocarcinoma presenting as red, scaly plaque; usually without underlying carcinoma.

Microscopic composition of a papillary hidradenoma of the vulva.

Benign papillary projections lined by columnar secretory epithelium overlying myoepithelial cells.

Most likely biopsy finding in leukoplakia due to lichen sclerosus.

Epidermal (epithelial) atrophy with dermal fibrosis.

List four congenital vaginal anomalies.

Imperforate hymen, vaginal/uterine atresia, septate vagina, and double vagina/uterus (didelphys).

Typical discharge in candidal vaginitis.

Curdy, white discharge.

Typical discharge in Trichomonas vaginalis infection.

Watery, copious, green discharge with motile parasites.

What precipitates nonspecific atrophic vaginitis?

Post-menopausal estrogen loss causing epithelial thinning and dryness.

Most common malignant vaginal tumour in childhood.

Embryonal rhabdomyosarcoma (sarcoma botryoides).

What is the transformation zone of the cervix?

Area where columnar endocervical epithelium is replaced by squamous metaplasia; site of most CIN and SCC.

Why did cervical cancer incidence fall dramatically over the last 50 years?

Introduction and widespread use of the Papanicolaou (Pap) smear screening test.

Peak ages: CIN vs invasive cervical carcinoma.

CIN peaks ~30 yrs; invasive carcinoma peaks ~45 yrs.

Four key sexual risk factors for CIN/invasive cervical carcinoma.

Early age at first intercourse, multiple sexual partners, male partner with many prior partners, persistent high-risk HPV infection.

High-risk HPV types most often causing cervical cancer.

16, 18, 31, and 45 (with smaller roles for 33, 35, 39, 52, 56, 58, 59).

Oncogenic proteins expressed by high-risk HPV and their targets.

E6 protein inactivates p53; E7 protein inactivates RB tumour suppressor.

Do low-risk HPV types integrate into the host genome?

No; they remain episomal and chiefly produce condylomas.

Effectiveness of the HPV vaccine.

Highly effective in preventing infection by high-risk HPV types and thus reducing cervical cancers.

Which listed condition is NOT a risk factor for cervical cancer: multiple sexual partners, cigarette smoking, early first intercourse, or endocervical polyps?

Endocervical polyps.

What histologic threshold separates VIN from invasive vulvar SCC?

Invasion beyond the basement membrane into underlying stroma.

What size criterion (in cm) is often used to stage microinvasive cervical carcinoma?

Invasion depth up to 5 mm and width ≤7 mm (Stage IA).

Why do only a minority of high-risk HPV infections progress to cancer?

Additional cofactors—e.g., cigarette smoke, immunodeficiency (HIV, transplant), or hormonal influences—are required for malignant transformation.