Subject: Pathology

Topic: 5. 05b-Vagina and Vulva

Lecturer: JANET LIM-DY ,MD. FPSP, DTMH
Date: January 13, 2015

OUTLINE the viral particle)

I. Infections of the Lower Female Genitalia Cervical and vaginal lesions present with purulent discharge and
a. Genital Herpes Simplex pelvic pain
b. Human Papilloma Virus Infection Urethral lesions cause painful urination and urine retention
c. Molluscum Contangiosum
d. Candidiasis
Complications
e. Trichomoniasis o Latent infection
f. Bacterial Vaginitis / Vaginosis o Transmission to the neonate during birth
g. Lymphogranuloma Venereum 2/3 of patients suffer recurrences
h. Granuloma Inguinale o HSV-2 more likely to recur
i. Syphilis o Very persistent infection
II. Infections of the Upper Female Genitalia
Factors that trigger the recurrence
a. Pelvic Inflammatory Disease
III. Non-Neoplastic Epithelial Lesions
o Stress (even sunlight)
a. Bartholins Duct Cyst o Hormonal changes
b. Vulvar Dystrophy o Reduced immune system surveillance
i. Lichen Sclerosus Transmission
ii. Squamous Cell Hyperplasia o In active or latent phase
IV. Neoplastic Tumors of the Vulva o Less likely transmission in asymptomatic carriers
a. Papillary Hidradenoma No effective treatment for latent HSV
b. Vulva Intraepithelial Neoplasia (VIN)
o Acyclovir and famiciclovir may shorten the length of symptoms
c. Carcinoma of the Vulva
i. Vulvar SCCA
ii. Invasive SCCA
d. Extramammary Pagets Disease
e. Malignant Melanoma
V. Vagina
a. Congenital Anomalies
b. Vaginal Intraepithelial Neoplasia (VaIN)
c. SCCA of Vagina
d. AdenoCa of Vagina
e. Embryonal Rhabdomyosarcoma
I. Infection of the Lower Genital Tract
The following organisms cause infections of the lower female
genitalia includes: Figure 1. Vaginal lesions are present and it shows red papules, vesicles,
o Candida pustules and ulcers. Sometimes with purulent discharge and pelvic pain.
o Trichomonas
o Gardnerella
o Gonorrhea
o Treponema
o Chlamydia
o Mycoplasma
o Virus: HPV, HSV and molluscum
Most of them are sexually transmitted causing STD

A. Genital Herpes Simplex

Caused by HSV 1 and 2 (usually type 2) Figure 2. A slide of Pap smear showing multinucleation and molding which
o HSV-1 oropharyngeal infection results to GROUND GLASS APPEARANCE of the nuclei.
o HSV-2 genital mucosa and skin
In the past decades, frequency has increased amongst teenagers
and young women
Results in the formation of:
o Painful vesicles
o Secondary ulceration with infection
Gross
o initial lesion is a red papule seen in the skin ->progresses to
become vesicles -> pustules -> ulcers
Microscopic
o Shows typical cytopathic effects of the virus that include Figure 3. A slide of Pap smear showing margination resulting to intranuclear
INCLUSION BODIES
nuclear homogenization (GROUND GLASS APPEARANCE) and
multi-nucleation with intranuclear inclusion bodies (represents

Trans Group: Tan, Tasani, Tayo, Te Page 1 of 11

Edited By: Frances and Charm
B. Human Papilloma Virus Infection epithelium. Shows Acanthosis, parakeratosis and hyperkeratosis.
Sexually transmitted
Not considered as a premalignant lesion
Involved in the pathogenesis of vulvar, vaginal, and cervical
neoplasia and other squamous tumor of the skin and mucous
membranes
Cause of Condyloma acuminatum/acuminata
Koilocytediagnostic for HPV
Regress spontaneously within 2 years (infection is transient and
self-limiting)
Role of HPV in the pathogenesis of lower genital tract neoplasia
o HPV DNA detected by hybridization techniques in 85% of
cervical cancers and 90% of condylomas and precursor lesions
o There are many serotypes with most being relatively site-
Figure 7. HPV cytopathic changes (koilocytic atypia). Picture on the left
specific when they infect shows the biopsy histo. Picture on the right shows the Pap smear.
o Low risk types- 6, 11, 42, 44
Not associated with cervical carcinoma
C. Molluscum contagiosum
o High risk types- 16, 18, 31, 33
A DNA poxvirus infection
Associated with cervical carcinoma
Common self-limiting viral disease of skin spread by direct
o Types 6 & 11
contact
Cause condyloma
o Types 16 & 18 Common in young children (direct contact or sharing of
Causative agent for cervical and vulvar ca materials), adults (sexual intercourse)
4 types (only 2 were discussed)
o MCV1 most prevalent
o MCV2 sexually transmitted
Diagnosis
o Characteristic appearance of pearly, dome-shaped papules
with a dimpled center (CENTRAL UMBILICATION)
Microscopic
o Cup shaped lesion with eosinophilic intracytoplasmic
inclusions

Figure 4. A, B, C. Verrucous, papillary growth or may be sessile involving the

vulva, perineum, vagina and cervix. D. Shows a flat condyloma.

Figure 8. Multiple 2 to 4 mm dome shaped flesh colored firm papules caused

by Molluscum contagiosum are seen grossly at the left. They can be
umbilicated. They are often on the trunk and anogenital region, but may
appear elsewhere, as shown here on the face. The biopsy at the right
demonsrates a cup-like verrucous epidermal hyperplasia.

Figure 5. Gross appearance of HPV infection

Figure 9. Microscopic appearance. Cup shaped lesion with eosinophilic

intracytoplasmic inclusions
Figure 6. Papillary of branching tree like cores stroma, overlined by squamous

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D. Lymphogranuloma venereum (LGV)
Chlamydia trachomatis serotypes L1, L2 & L3
Has 3 phases
o Phase 1: Initial, painless genital ulcer ordinarily pass away
unnoticed formation of small and usually painless ulcers
located at the site of the venereal contact
o Phase 2: Swelling & inflammation of the inguinal lymph node
(giving rise to the bubos) due to the stellate abscesses
surrounded by pale epitheloid cells
o Phase 3: Scarring (in chronic cases) -> lymphatic obstruction
with chronic lymphedema-> elephantiasis of the vulva
Diagnosis: Frei testo A delayed hypersensitivity skin test using
purified clamydial antigen
The histological picture is nonspecific and the organisms are not
seen histologically.
E. Granuloma inguinale
Caused by Calymmatobacterium donovani (however, the
organisms name was changed to Klebsiella granulomatis)
Gross: painless ulcers with rolled borders & a friable base
Microscopic: non-specific changes, granulomatous reaction
without caseation
Diagnosis: (+) Donovan bodies
o Small round encapsulated bodies inside cytoplasm of
histiocytes
o May be seen extracellularly within macrophages
Figure 10.1 Painless ulcers with a rolled borders and a friable base.
F. Syphilis
Caused by Treponema pallidum
Diagnosis: Dark filed microscope, fluorescence
Silver stain serology
Gross: painless shallow ulcer (chancre)
o Chancre is different from chancroid which is cause by
Haemophilus ducreyi
Microscopic: ulceration, chronic inflammation predominantly of
plasma cells, vasculitis
G. Chlamydial Infection (Chlamydia Trachomatis)
Most common bacterial STI in the US
Leading cause of infertility
Often asymptomatic
DIAGNOSTICS: amplified DNA, fluorescent monoclonal AB
screening
Figure 10.2 Beefy red mucosa of Chlamydial infection
II. Infections of the Upper Genital Tract
A. Pelvic Inflammatory Disease
Ascending type of infection which begins in the lower part of
genital tract, then spreads upward to invade most of the
structures (e.g. uterus, fallopian tubes etc.)
Causes: usually polymicrobial
o Neisseria gonorrhea/GC (most common)
o Chlamydia trachomatis
o Enteric bacteria & polymicrobial (Strep., Staph., Clostridium)
Associated conditions: abortions/puerperal infections (infections
after spontaneous or induced abortions and normal and abnormal
deliveries)
S/Sx: pelvic pain, fever, adnexal tenderness, vaginal discharge
(esp. in GC infection)
In GC infection: endocervix (most common site of involvement);
Bartholin gland, periurethral; spreads through mucosal surface
o GC infection ascends from the endocervix to the fallopian tubes
(FT). Once it reaches the FT, it causes Acute Suppurative
Salphingitis, which shows severe neutrophilic inflammation of
the mucosa. The lumen can be filled with pus/exudates that
could spill over through the fimbriae and reach the ovaries ->
Salphingo-oophoritis -> Tubo-ovarian abscess or infection of
the tubal lumen (pyosalpinx)
o Endometrium is spared
o Sequelae: chronic follicular salpingitis and hydrosalpinx
Non-GC infection (Staph or Strep): initial site is the uterus,
spreads upward thru lymphatics or venous channels, compared to
GC which is thru the mucosal surface.
o Less exudation, less involvement of mucosa
o Greater inflammatory response within deeper tissue layers
Complications: bacteremia and peritonitis
Complications:
o Acute usually in non-GC due to lymphatic spread of
microorganism
Peritonitis
Bacteremia
o Remote
Intestinal obstruction
Infertility and ectopic pregnancy (Fallopian tube injury may
lead to fibrosis narrowing)
III. Non-Neoplastic Epithelial Lesions
Benign epithelial cysts
Most common clinically important cystic lesions of the vulva.
A. Bartholins Duct Cyst
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 Figure 12 . Lichen sclerosus Gross: vulvar skin is dry, scaly, pale, narrowing
introitus secondary to extensive fibrosis. the labia becomes atrophied and
introitus narrowed. note: sclerosus refers to fibrosis of the underlying
Figure 11 . Bartholins Duct Cyst dermis. atrophicus refers to thin epidermis. lichen is greek for crusty
skin has a pale gray and parchment-like appearance. (Atrophy of the
Cystic dilation with accumulation of secretions epidermis. Dense sclerosis of dermis, absence of dermal appenadages and
Mononuclear infiltrates around the blood vessel)
Usually preceded by inflammation/ obstruction
Occurs in all ages
Characterized by thinning of the epidermis, disappearance of rete
Bartholin glands in women are analogous to Cowpers
pegs, hydropic degeneration of the basal cells, dermal fibrosis and
(bulbourethral) glands in men. They are also called greater
a scant perivascular mononuclear inflammatory infiltrate
vestibular glands.
Appears as smooth, white plaques (leukoplakia) or papules that in
o Inflamation or obstruction to the ducts of these glands can
time may extend and coalesce.
cause cyst formation.
Develops slowly, predisposes to acute infections
Swelling in the posterior aspect of the labium majus (up to 5 cm),
associated with pain and discomfort When entire vulva is affected, labia may become atrophic and
stiffened and vaginal orifice is constricted.
May result in abscess
Occurs in all groups but more common in postmenopausal
Never becomes malignant
women.
Pathogenesis is uncertain but maybe autoimmune in etiology due
B. Vulvar Dystrophy
to presence of activated T cells in the subepithelial Inflammatory
infiltrate and the increased frequency of autoimmune disorders in
1. Lichen Sclerosus
affected women.
Benign, however, may develop to squamous cell carcinoma of the
vulva in1-5% of women with symptomatic lichen sclerosus.

2. Squamous Cell Hyperplasia/ Lichen Simplex Hyperplasia

Figure 13 . Lichen Simplex Hyperplasia

This type of lichenoid disorder has HYPER-plastic epidermis, NOT atrophic.,
like most of the SKIN lichenoid disorders do. The hyperplasia is felt to be
related to itching or mechanical epidermal irritation. Biopsy is indicated in all
vulvar lesions.

Similar to Lichen Sclerosus

Histologically: Hyperplasia of the vulvar squamous epithelium

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 (particularly of the stratum granulosum) with hyperkeratosis
Consequence of irritation, often caused by pruritus related to an
underlying inflammatory dermatosis.
Appears as an area of leukoplakia
May be associated with cancer especially if atypia is present

IV. Neoplastic Tumors of the Vulva

This may be in situ or invasive. The frequency of progression of in
situ disease to invasive is uncertain but has been estimated as 2%
to 10%.
The term vulvar intraepithelial neoplasia (VIN) has now largely
replaced other designations for in situ squamous proliferations of
the vulva

A. Papillary Hidradenoma

Figure 14 . Papillary Hidradenoma : Complex papillary glandular pattern

with stratification. Benign proliferation of sweat glands, tubular ducts lined
by columnar cells and surrounded by myoepithelial cells.

in Labia majora or minora

GROSS: small, well circumscribed nodules covered by normal skin.
Occasionally it ulcerates thru skin and clinically may mimic
carcinoma.
Modified apocrine sweat gland
Histologic appearance is similar to intraductal papilloma of the Figure 15. Vulvar Intraepithelial Neoplasia (VIN)
breast Gross appearance of VIN: Intraepithelial neoplasia in the labia majora (VIN).
Lesion is grayish white, elevated, slightly polypoid, with irregular borders.
B. Vulvar Intraepithelial Neoplasia (VIN) Normal Histology of vulva and intraepithelial lesions.The maturation pattern,
nuclear aberrations such as enlargement, hyperchromasia, pleomorphism,
mitoses differentiate LOW from HIGH.
1. Normal
2. VIN I- abnormal cellular changes only affects the basal layer (<1/3)
3. VIN III- involves almost the entire thickness of the epithelium; more marked
atypia
4. VIN II- affects more than 1/3 but not more than 2/3

The spectrum of abnormalities seen in atypical proliferative

squamous lesions of the vulvar skin
Subdivided into:
o VIN I
o VIN II
o VIN III
Premalignant vulvar lesion
This may be in situ or invasive.
The term vulvar intraepithelial neoplasia (VIN) has now largely
replaced other designations for in situ squamous proliferations of
the vulva
Clinical & pathologic - basis of subdividing

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 VIN I VIN II VIN III or Bowen Disease. Classic VIN is characterized by nuclear
Corresponds to mild Corresponds to Corresponds to atypia of the squamous cells, increased mitoses, and lack
dysplasia moderate dysplasia sever dysplasia or of cellular maturation. It is analogous to cervical
carcinoma in situ squamous intraepithelial lesions (SILs)
Atypical proliferation Atypical proliferation Atypical proliferation o VIN is frequently multicentric in the vulva, and 10% to
does not exceed 1/3 exceeds 1/3 but esceeds 2/3 the 30% of patients with VIN also have vaginal or cervical
the epithelial does not exceed 2/3 epithelial thickness HPV-related lesions. The majority of cases of classic VIN
thickness of the epithelial are positive for HPV 16, and less frequently for other
thickness high-risk HPV types, like HPV 18 or 31.
Note: the frequency of progression of in situ disease to invasive is o Spontaneous regression of VIN lesions has been
uncertain but have been estimated as 2% to 10%. reported, usually in younger women. The risk of
progression to invasive carcinoma is higher in women
NEW CLASSIFICATION: older than 45 years of age or in women with
1.CLASSIC VIN 2.KERATINIZING/DIFFERENTIATED immunosuppression.
(Carcinoma in situ/ Bowens Most commonly occurs in reproductive-age women
disease) o Risk factors are the same as those associated with
-nuclear atypia of the -marked parabasal atypia vaginal and cervical squamous cell carcinoma (e.g. young
squamous cells -normal maturation age at first intercourse, multiple sexual partners, male
-increased mitoses -not HPV related partner with multiple sexual partners), since both
-lack of cell maturation -over expression of p53 cervical squamous intraepithelial lesions and classic VIN
-slightly elevated, plaque-like are related to HPV infection
with red velvety appearance
-occurs in reproductive-age SECOND GROUP (KERATINIZING SQUAMOUS CELL CARCINOMA)
women Associated with long standing vulvar dystrophy (lichen
-related to HPV infection in 90% sclerosis and squamous cell hyperplasia hyperkeratotic,
-multi-centric flesh colored or pigmented, slightly raised lesions)
-5% progress to invasive Not associated with HPV but preceded by premalignant
carcinoma lesion called Differentiated VIN
-10-30% associated with vaginal o Differentiated VIN is characterized by: marked atypia of
and cervical carcinoma the basal layer and normal maturation and
differentiation in the superficial layers
More common compared to Basaloid type; accounts for 70%
C. Carcinoma of the Vulva Affects elderly women with a mean age of 76 years
Uncommon (3% of all female genital cancers) Associated with mutations of p53
Mostly occur in elderly women over the age of 60 Worse prognosis
The majority (85%) are squamous cell carcinoma because the vulva
is lined by squamous cell epithelium 2. Invasive Squamous Cell Carcinoma of the Vulva
15% (melanoma, adenocarcinoma, and basal cell carcinoma) Exophytic fungating mass or endophytic ulcerating lesion
The prognosis and behavior of this malignancy is based on the Look for evidence of keratinization (keratin pearls) and intercellular
presence of regional node involvement and the size of the lesion bridges
(not so much based on the histologic type/appearance) Look for evidence of frank stromal invasion (delineating point
o Lesions <2cm five-year survival rate is about 80% between invasive and in-situ)
o Larger lesions (>2cm) with positive nodes five-year survival
rate is reduced to just about 10% Note:
65% have metastasized to regional nodes (inguinal, pelvic) at time SCCA can be in situ or invasive
of diagnosis Rare variants of squamous cell carcinoma include verrucous
carcinomas which are fungating tumors resembling condyloma
1. Vulvar Squamous Cell Carcinoma acuminatum, and basal cell carcinomas, which are identical to their
Two groups of squamous cell carcinoma differ in etiology, counterparts in the skin. Neither tumor is associated with
pathogenesis and clinical presentation: papilloma viruses. Both tumors rarely metastasize and are
successfully cured by wide excision.
FIRST GROUP (BASALOID/WARTY)
Accounts for 30% of all vulvar squamous cell carcinoma
Associated with HPV infection, high oncogenic risk (16, 18/31)
Almost always preceded by vulvar intraepithelial neoplasia
(classic VIN)
From 2016B trans:
o Invasive basaloid and warty carcinomas develop from a
precancerous in situ lesion called classic vulvar
intraepithelial neoplasia (classic VIN). This form of VIN
includes lesions designated formerly as carcinoma in situ

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 Figure 16. Infiltrating or invasive squamous cell carcinoma
The vulva has been replaced by large exophytic, yellow-white mass na halos
nakain na yung vulvar skin and the tumor has already infiltrated the
underlying soft tissue. If you measure this mass, maybe this is around 8-9cm in
greatest dimension.
Figure 17. LEFT: Basaloid Vulvar Carcinoma HPV+ infiltrating tumor
characterized by nests of tightly-packed or tightly-cohesive malignant
squamous cells lacking maturation. These neoplastic cells have a very large
hyperchromatic nuclei and scanty to absent cytoplasm infiltrating the
underlying soft tissue. RIGHT: Well differentiated or keratinizing SCC Marked
atypia, prominent central keratin pearl with areas showing normal maturation
and differentiation. The tumor is composed of nests and tongues of neoplastic
squamous cells which are also considered invasive because they infiltrate the
underlying stroma. The tumor arises from the overlying skin mucosa.
If the patient is young, the more common will be Basaloid type. But
if you are dealing with an older patient, the common type of SCCA
that you will get is the Keratinizing type because it is not associated
with HPV.
Note:
Important features to look for before giving SCCA as the diagnosis:
Aside from nests and tongues of neoplastic cells, there are also
prominent pearl keratinization or central pearl formation (you dont
see this in adenocarcinoma or even in melanoma) exclusive for
SCCA
Cytoplasm is abundant and eosinophilic
At HPO, you may appreciate the intercellular bridges
D. Extramammary Pagets Disease (Pagets Disease of the Vulva)
Gross: Pruritic, red, scaly, crusted plaque sharply demarcated
lesion on the surface of the labia majora
Histology: Similar to Pagets Disease of the breast, clusters of
anaplastic tumor cells confined to the epidermis of the skin
o In Extramammary Pagets Disease, these Paget cells or
Pagetoid cells have abundant vacuolated cytoplasm
(micropoly-saccharide) making them (+) for mucin creates
a halo
o In Pagets Disease of the breast, Paget cells are (-) for mucin
Figure 18. Histologic appearance of Extramammary Pagets Disease: Pagets
cells are large anaplastic cells with clear cytoplasm, hyperchromatic and large
nuclei, lying in the epidermis. Often occurs in clusters, but may also seen
singly.
Note:
This is the second vulvar disease/condition which has a breast
counterpart. Remember the first one? Yep, Papillary Hidradenoma
Its because the vulva contains modified apocrine sweat glands which
are also present in the breast. Clinical presentation and microscopic
changes are exactly the same. The only difference is the location (one
is from the breast and the other one is from the vulva. Thats why you
have to specify the source of the biopsy specimen when sending them
out for analysis)
Thats why if you see white, plaque-like lesions in the vulva, biopsy
is indicated or mandatory in order to arrive at a specific diagnosis
since there are lots of lesions or diseases of the vulva that present
that way
NO DEMONSTRABLE UNDERLYING VULVAR CARCINOMA
Arise from primitive germinal cells of the mammary-like gland
Very good prognosis rarely metastasize
Note: (from 2016B trans)
In contrast to Pagets Disease of the breast/nipple in which 100% of
patients show an underlying ductal breast carcinoma, vulvar lesions
are most frequently confined to the epidermis of the skin and
adjacent hair follicles and sweat glands. Pagets Disease is treated
with wide local excision and shows a high recurrence rate. Typically,
Paget cells spread beyond the confines of the grossly visible lesion,
and therefore are frequently present beyond the margins of surgical
excision. But, Intraepidermal Pagets Disease may persist for many
years, even decades, without invasion or metastases.
E. Malignant Melanoma
Very aggressive and highly malignant tumor
Rare tumor (5% of all vulvar cancers)
Peak incidence is 6-7 decades
Histologic and biologic characteristics are similar to melanomas
elsewhere
Histology: Cells round, ovoid to spindly, with large nuclei and
prominent nucleoli. Presence of brown to black intracytoplasmic
melanin pigments
Gross: Tumor is red to brown black in color (presence of melanin
pigment will be reflected in the color of the tumor. But there is
what we call amelanotic melanoma wherein you dont see
melanin pigment. If thats the case, it will become difficult to
diagnose)
To diagnose, look for the melanin pigment. If you suspect
melanoma but do not see any melanin pigment, request for special
stains/immunohistochemistry stains: HMB-45 (specific for
melanoma) or S-100
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 Figure 21. Individual squamous cells may be covered by a layer of coccobacilli,
Figure 19. Gross appearance of malignant melanona particularly along the margin of the cell membrane, forming so-called clue
cells

2. Candidiasis
Figure 20. GROSS: Radical Vulvectomy specimen. HISTO: Tumor cells are round
to ovoid to spindly, with large hyperchromatic nuclei and prominent nucleoli,
contains melanin pigment in the cytoplasm. Note: if melanin pigment is not
seen within the tumor cells, order an S-100 and HMB-45 immunostain which is
specific for melanoma (since it stains the melanin pigment).
Caused by Candida albicans (yeasts) which is a normal vaginal
microflora
Second most common cause of vaginitis
Disturbance in the patients vaginal microbial ecosystem (hormonal
imbalance, diabetes, antibiotics, pregnancy) infection
Extremely common
Clinical manifestation: curdlike vaginal discharge associated with
severe pruritus (vulvovaginal pruritus, erythema, swelling)
In severe cases of cervicovaginal candidiasis: mucosal ulcers
Dx: presence of the organism (Candida albicans pseudospores or
hyphae) in KOH mount/Pap smear
NOT considered as an STD

V. VAGINA
The vagina is seldom the site of primary diseases. It is most often
involved by diseases arising from the nearby structures like vulva
and cervix.
Therefore, primary diseases in the vagina are very uncommon, the
most serious of which is primary vaginal cancer and still, this is not
common.

A. Infection of the Vagina or Vaginitis

Figure 22. Candida albicans
Common causes:
Bacteria 3. Trichomoniasis
Candida
Caused by Trichomonas vaginalis
Trichomonas o Pear-shaped cyanophilic organism ranging in size from 15-30
m
1. Bacterial Vaginitis / Vaginosis o Nucleus is pale, vesicular, and eccentrically located
Gardnerella vaginalis (main cause of bacterial vaginosis) Third most common cause of vaginitis
Overgrowth of multiple gram negative coccobacilli colonizing Develops within 4 days 4 weeks
bacteria in the vaginal canal NOT an STD Sexually-transmitted infection involving vagina and cervix (not the
Most common cause (50%) vulva)
Gross: Thin, green-gray, fishy odor vaginal discharge May be asymptomatic or complain of copius, yellow, frothy vaginal
Dx: Pap smear superficial and intermediate squamous cell discharge
covered by shaggy coat of multiple coccobacilli S/Sx: discomfort, dyspareunia (painful intercourse), dysuria
Squamous cells are covered by coccobacilli particularly among the Gross: Fiery red appearance of the mucosa and severe dilatation of
margin of the cell membrane, forming so-called CLUE CELLS the mucosal vessels strawberry cervix
In pregnant patient, has been implicated in chorioamnionitis Dx: Large, flagellated, ovoid protozoan in wet mounts of vaginal
(infection involving coverings of the placenta) because it can trigger discharge or Pap smear
premature rupture of bag of water

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 Figure 23. Trichomonas vaginalis. Flagellated, ovoid protozoan. Pear-shaped
cyanophilic organism 15-30 nm in size. Nuclei is pale, vesicular, and
eccentrically located

B. Congenital Anomalies
Figure 23: Gross of VaIN
Garthners duct cysts
o Common
o Derived from Wolffian (mesonephric) duct rests
o Located on lateral wall of vagina (upto 2cm), occurs in
submucosal cyst
o No clinical significance (Nice to know)
Mucous cyst
o Derived from Mullerian epithelium
Atresia
Total Absence of Vagina
Double Vagina
o Failure of total fusion of Mullerian duct

C. Premalignant and Malignant Neoplasm

Benign
Figure 24: Left: Normal Histology of the Vagina, lined with non-
o Hidradenoma keratinizing squamous cell epitherium. Right: VaIN1 has enlarged
o Condyloma tubules/ nuclei of epithelial cell, hyperchromatic.
Malignant
o Primary carcinoma of the vagina is extremely uncommon (1%)
o assoc. with high oncogenic risk HPVs
o Arises vaginal intraepithelial neoplasia (VaIN)
o SCCA (95%)
o Inv. Upper posterior / proximal 3rd
o Risk factors ---similar to those of cervical Ca
o Most common malignancy is secondary to carcinoma of the
cervix or vulva.

1. Vaginal Intraepithelial Neoplasia (VaIN)

Goss: epithelium may appears rise and has white or pink
Microscope: loss of maturation, nuclear atypical increased
mitotic activity.
Figure 25: Gross and microscopic specimen for VaIN3, more atepia,
hyperchromatic nuclei and prominent pleomorphism with intact
VaIN 1 VaIN 2 VaIN 3 basement membrane. Gross appearace, with elevated whitish
Mild dysplasia Moderate dyspasia Severe dysplasia/ Ca- mucosa in the epithelial layer
in-situ
Atypical proliferation Atypical proliferation Atypical proliferation 2. Squamous Cell Carcinoma (SCCA)
does not exceed 1/3 exceeds 1/3 but exceeds 2/3 the 90% of malignant lesions of the vagina
the epithelial does not exceed 2/3 epithelial thickness Associated with high oncogenic gene (HPV16)
thickness of the epithelial Must be located in the vagina without clinical of histologic
thickness evidence of involvement of the cervix or vulva
Most originates from proximal 3rd of the vagina
Arises from a premalignant lesion, vaginal intraepithelial
neoplasia, analogous to cervical squamous intraepithelial
lesions (SILs) [Robbins and Cotran, 8th ed]
Invasive tumor affects the upper posterior vagina (along
posterior wall at the junction with the ectocervix) [Robbins
and Cotran, 8th ed]

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 Lesions in the lower two thirds of vagina metastasize to the
ingunal nodes, where upper lesion tends to involve regional
ileac nodes. [Robbins and Cotran, 8th ed]
Figure 26: Gross of Vaginal SCCA
Figure 27: Microsopic: keratinizing or non-keratinizing irregular-shaped nests
or clusters of squamous cells invading stroma, often w/ eosinophilic
cytoplasma typical nuclei w/ coarse chrom prominent nuclei
Gross:
o Polpyoid
o Fungating
o Indurated or ulcerated
Remember!!!
Difference between the VIN and VaIN from invasive carcinoma is
the neoplastic cells are confined within the epidermis, so there no
capacity to metastasize, because basement membrane are still intact
(Dr.Dy, 2015)
Invasive Carcinoma
- once there is a break in basementmembrane the neoplastic cell
start to invade and infiltrate the underlying strom
- being a squamous cell carcinoma or adenocarcinoma are capable
of metastasizing at distant site (Dr. Dy, 2015)
Epithelial neoplasia being Vaginal, Vulvar or Cervical neoplastic
process is confined within the epidermis, therefore they dont
metastasize (Dr. Dy, 2015)
3. Vaginal Adenocarcinoma
Rare tumor.
Increased frequency (0.14%) of clear cell adenocarcinomas
in young women (15-20 years) whose mothers had been
treated with diethylstilbestrol (DES) during pregnancy (for
threatened abortion).
Composed of vacuolated, glycogen-containing cells (clear
cell).
Vaginal adenosis is a possible precursor.
Careful follow-up of all DES-exposed women is mandatory.
Surgery and radiation (80% eradication rate).
Figure 28: Several histologic patterns : a. solid sheets of clear cells
b. tubulocystic pattern most common clear , glycogen containing
cells
4. Embryonal Rhabdomyosarcoma
Aka Sarcoma Botryoides
Very uncommon vaginal tumor.
Mostly seen in infants and children (under age of 5 years),
consists predominantly of malignant rhabdomyoblasts.
skeletal muscle sarcoma
tends to grow as polypoid, rounded, bulky masses that
sometimes fill and projected out of the vagina [Robbins and
Cotran, 8th ed]
Gross : soft, gray or tan, & nodular tumors, polypoid lesions
like a bunch of grapes
Histologically: small round to spindle cells with cytoplasmic
extensions from one end ( tennis racket),abundant pink
cytoplasms
cambium layersubepithelial dense zone
Locally invasive and may cause death by penetration into
peritoneum or obstruction of urinary tract.
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Figure 29: Polypoid, rounded, bulky masses that sometimes fill and project out
of the vagina; they have the appearance and consistency of grapelike clusters
(hence the designation botryoides = grapelike).

Figure 30. Histology: Left: Note zone of cellularity (cambmium layer) beneath
the epithelial mucosa. This layer consists of tumor cells which round, ovoid, to
spindle with abundant pink cytoplas. Right: tennis racket shape cell

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