Obgyn - Path Of Vulva, Vagina, Cervix

Front 1

Bartholin Glands
- function?
- how do cysts/abscesses form?
- tx?

Back 1

Function: produce mucoid secretions that lubricate the vestibule

Cyst: due to obstruction of the gland
Abscess: due to secondary infection of the obstructed gland

Tx: surgical incision and drainage; antibiotic tx

Front 2

Lichen Sclerosis
- what is?
- population?
- associated with?
- gross appearance?
- histo appearance?
- clinical presentation?
- at risk of? %?

Back 2

= Inflammatory disorder of vulva, often extending to perianal region

- Most common in post-menopausal women

- Often ass'd with autoimmune disorders - e.g., vitiligo, pernicious anemia, thyroiditis

- Gross: whitish plaques, resembles parchment

- Histo: hyperkeratosis, atrohy of rete ridges, homogenous zone of superficial dermis

- Clinical: vulvar itching and dyspareunia

- 15% risk for subsequent SCC of vulva

Front 3

Vulvar Intraepithelial Neoplasia (VIN)
- what is?
- can lead to?
- associated with? %?
- grading?
- tx?

Back 3

= preneoplastic --> risk for SCC --> invasive carcinoma

- associated with HPV 16 (20-40%)

- 3 Grades (mild, moderate, severe dysplasia) based on epithelial cell nucleas size/atypia, mitotic activity, maturation
- Note: younger women usually have more undifferentiated form - warty/basiloid; older women usually more differentiated

- Tx: surgical excision --> may recur (25%)

Front 4

Squamous Cell Carcinoma of the VULVA
- % of genital tract cancers?
- associated with?
- gross appearance?
- histo appearance?

Back 4

= most common malignancy in vulva
- 3% all genital tract cancers

- preceded by VIN in most cases

- Gross: exophytic or ulcerative tumors; tendency to invade vagina, rectum... to inguinal, femoral and pelvic lymph nodes

Histo: varying degrees of differentiation; often KERATIN PEARL FORMATION

Front 5

Verrucous Carcinoma
- what is?
- associated with?
- gross appearance?
- histo appearance?
- prognosis

Back 5

= distinct type of vulvar SCC
- assocaited with HPV 6 or 11
- gross: large fungating/condyloma-like mass
- histo: well-differentiated
- prognosis: slow-growing; better prognosis than other SCCs

Front 6

Extramammary (Vulvar) Paget Disease
- population
- gross appearance?
- associated with???
- differential dx?

Back 6

- When in vulva, usually older women with history of pruritis or vulvar burning

- Gross: red, moist, sharply demarcated

- Histo: large atypical cells with abundant clear cytoplasm

- **Rarely associated with adenocarcinoma (UNLIKE IN BREAST)

- differential dx: melanoma

Front 7

Atrophic Vaginitis
- due to?
- presentation?

Back 7

- Due to post-menopausal decrease in E2 levels --> thinning and atrophy of vaginal squamous epithelium; dryness

- Presentation: vaginal bleeding, dyspareunia

Front 8

Vaginal Adenosis
- due to??
- what is it/how develops?
- gross appearance?
- can lead to?

Back 8

- Due to DIETHYLSTILBESTROL (DES) taken in high-risk pregnancies in mid-20th century --> caused vaginal adenosis in DAUGHTERS

- Normally, in 10th wk gestation, squamous epith from urogenital sinus replaces embryonic glandular epith of vagina; DES inhibits this!
- Glandular epith perisits - either endocervical type (mucin-producing) or fallopian tube type (ciliated)

- gross: mucosa red and granular

- can lead to squamous metaplasia...
- can lead to clear cell adenocarcinoma (usually between ages 17-22)

Front 9

Squamous Cell Carcinoma of VAGINA
- % of vaginal malignancies?
- cause?
- peak incidence in what pop?
- location?
- prognosis?

Back 9

= 90% of vaginal malignancies (most common)

- often arises from VAIN - vaginal intraepithelial neoplasia
- HPV may play a role

- peak incidence: 7th and 8th decades

- upper third of anterior vaginal wall

- prognosis related to time of diagnosis

Front 10

Embryonal Rhabdomyosarcoma
- aka
- gross appearance?
- peak incidence?
- derivision of tumor/histo?
- clinical presentation?
- progression
- tx

Back 10

- aka: Sarcoma Botryoides - looks like cluster of grapes arising from vagina

- most cases in girls <4 yo

- derived from mesenchymal cells, composed of primitive spindle cells with cross-striations (indicitive of SKELETAL MUSCLE CELLS)
- cambium layer (directly below vaginal epithelium) has dense band of tumor cells
- deep to cambium is spaced out tumor cells separated by mycomatous stroma

- clinical pres: vaginal bleeding

- highly aggressive/ metastisizes widely
- but responds well to surgery and chemo

Front 11

Cervicitis
- cause?
- acute v. chronic? -- descrip, histo... which one is more common?

Back 11

- due to chronic exposure to variety of bacteria present in the vagina

ACUTE:
- cervix red and edematous
- purulent exudate
- histo: neutrophils make up infiltrate

CHRONIC
- more common
- mucosal hyperemia and focal erosion
- histo: lymphocytes and plasma cells; germinal centers; squamous metaplasia

Front 12

Benign Endocervical Polyps
- clinical presentation?
- histo?
- tx?

Back 12

- clinical pres: vaginal bleeding or discharge

Histo:
- polyps lined by mucinous columnar epithelium - same as endocervix
- contain foci of squamous metaplasia and mucosal erosion

- Tx: surgical excision or curettage

Front 13

What is the normal cell type of the:
- Vagina?
- Cervix?
- Fallopian Tubes?

Back 13

Vagina: squamous epithelium

Cervix: glandular epithelium = mucinous simple columnar

Fallopian Tubes: ciliated

Front 14

Microglandular Hyperplasia
- histo?
- cause?
- main problem??

Back 14

- Histo: uniform closely-packed glands without intervening stroma; surrounded by neutrophilic infiltrate

- cause: Progestin stimulation (during pregnancy and post-partum AND oral contraception)

= BENIGN!
- BUT migh be confused with well-differentiated adenocarcinoma (via pap smear)

Front 15

Squamous Cell Carcinoma of CERVIX

- history of the disease
- progression/description
- location
- peak incidence - pop
- risk factors
- prognosis
- tx

Back 15

- historically, leading cause of cancer death in American women... no longer due to pap smears (mortality decreased 50-80%)

- progression: sequence of intraepithelial changes - mild atypia to dysplasia to carcinoma in situ
= CERVICAL INTRAEPITHELIAL NEOPLASIA (CIN) (name for these changes, collectively)

...Early phase = microinvasion of basement mem

... Fully invasive phase = exophytic and/or ulcerating
- keratinizing or non-keratinizing
- direct invasion of adjacent structures (parametrium, bladder rectuym)
- lymphatic spread (paracervical, hypogastric, ext iliac nodes)

- location: most often in squamocolumnar junction/transformation zone

- peak: age 40-60 [CIN generally detected <40 y.o.]

RISKS
- HPV 16, 18
- mult sex partners
- early age of first sex
- cigarettes

- prognosis: related to stage at detection

- tx: radical hysterectomy with or w/o adjuvant radiation (most common tx)

Front 16

Cervical Intraepithelial Neoplasia (CIN)
- what is?
- location
- classification?
- dx?

Back 16

= collection of epithelial changes that occur leading to SCC (in ~10 yrs) - atypia, lack of maturation

- occurs mostly at transformation zone/squamocolumnar junction of cervix

- DX: often with colposcopy - can see abnormal mucosal vasculature (mosaic or punctuate pattern)

- classified by extent of dysplasia
... low grade: koilocytes, mild atypia
... high grade: full thickness changes, prominent atypia

Front 17

Transformation Zone of Cervix
- aka
- describe
- location

Back 17

= squamocolumnar junction

- Ectocervix = squamous
- Endocervix = glandular simple columnar --> produces mucin under hormonal control

**Transformation zone migrates throughout life
- birth- at cervical os
- then moves into endocervical canal
- menarchy- back to cervical os (increased estrogen)
- menopause- back up to endocervical canal (decreased estrogen)

Front 18

HPV
- types? strains??

Back 18

Episomal form
= HPV 6, 11
- Active replication and accumulation of virus (koilocytes)
- Low grade lesions

Integrative form
= HPV 16, 18
– Viral incorporation into genome --> synthesis of viral proteins
- **Inactivation of tumor suppressor genes
- High grade lesions

Front 19

HPV Vaccine
- function?

Back 19

= quadrivalent vaccine covering strains 6, 11, 16, 11
= 70% cervical cancers

- unsure of optimal time to administer and duration of functioning

Front 20

Adinocarcinoma of Cervix
- peak incidence: pop?
- risk factors?
- histo?
- spread?
- prognosis?

Back 20

- peak: age 50-60 (mean: 56)

- risks: same as scc of cervix (including HPV 16, 18)
- often precursor lesions = cervical glandular intraepithelial neoplasia (CGIN)

- histo: variable differentiation

- spread via lymphatics

- slightly worse prognosis than scc - bc often detected late!

Front 21

Koilocytes

Back 21

= enlarged squamous cells with prominent perinuclear clearing of the cytoplasm (due to virus accumulation)and minimal nuclear atypia

- found in low grade HPV lesions

Front 22

What is the typical latency period for maturation of CIN to carcinoma in situ?

Back 22

~10 years

Front 23

What percent of high grade HPV lesions develop into carcinoma in situ within 10 years?

Back 23

20%

Front 24

What is Microinvasion?

Back 24

- Earliest phase of SCC
- small nests of cells have just barely invaded through epithelial basement mem
- limited potential for vascular invasion and lymph node metastasis

Front 25

How does SCC of the cervix metastisize?

Back 25

Via lymph nodes: paracervical, hypogastric, and external iliac nodes

Front 26

What is CGIN?
- location?

Back 26

Cervical Glandular Intraepithelial Neoplasia
= precursor lesions to many cervical adenocarcinomas
- usually originate near squamocolumnar junction --> extend proximally into endocervical canal

Front 27

In what percent of cases does high grade CIN coexist with CGIN?

Back 27

40% of cases