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FEMALE GENITAL
SYSTEM - 1
DR. ROOPAM JAIN
PROFESSOR & HEAD, PATHOLOGY
MISCELLANEOUS
CONDITIONS
BARTHOLIN’S CYST & ABSCESS
• Inflammation of Bartholin’s vulvovaginal glands (Bartholin’s adenitis)
may occur due to bacterial infection, notably gonorrhoeal infection.
• Infection may be acute or chronic.
• Acute Bartholin’s adenitis occurs from obstruction and dilatation of the
duct by infection resulting in formation of a Bartholin’s abscess.
• Chronic Bartholin’s adenitis results from a less virulent infec tion so that
the process is slow and prolonged.
NON-NEOPLASTIC
EPITHELIAL
DISORDERS
• non-neoplastic epithelial disorders of the skin of vulva includes following
2 lesions:
• 1. Lichen sclerosus (older term: atrophic dystrophy).
• 2. Squamous hyperplasia or keratosis (older term: hyperplastic
dystrophy, or lichen simplex chronicus).
• The two types of lesions may coexist in the same patient called mixed
vulvar dystrophy.
Lichen Sclerosus
• more common and more extensive in the vulva in postmenopausal
women.
• Th e lesions appear as multiple, small, coalescent, yellowish-blue
macules or papules which produce thin and shiny parchment-like skin.
• The lesions may extend from vulva onto the perianal and perineal area.
• Clinically, the patient, usually a post-menopausal woman, complains of
intense pruritus which may produce excoriation of the affected skin.
• Eventually, there is progressive shrinkage and atrophy resulting in
narrowing of the introitus, clinically referred to as kraurosis vulvae
Lichen Sclerosus MORPHOLOGIC
FEATURES
• Microscopically, the follow - ing characteristics are seen (Fig. 22.1,A):
• 1. Hyperkeratosis of the surface layer.
• 2. Thinning of the epidermis with disappearance of rete ridges.
• 3. Amorphous homogeneous degenerative change in the dermal
collagen.
• 4. Chronic inflammatory infiltrate in the mid-dermis
Non-neoplastic epithelial
disorders of vulval skin
Lichen Sclerosus
Squamous Hyperplasia
• Squamous hyperplasia, or simply called keratosis, is characterised by
white, thickened vulvar lesions which are usually itchy.
• The cause is unknown
• symptomatic relief results from use of topical corticosteroids.
Non-neoplastic
epithelial disorders
of vulval skin
Squamous
Hyperplasia
VULVAL
TUMOUR
VULVAL TUMOUR
STROMAL POLYPS
• Stromal (fibroepithelial) polyps or acrochordons may form in the vulva or
vagina.
• There may be single or multiple polypoid masses.
• Histologically, they are covered by an orderly stratified squamous
epithelium. The stroma consists of loose fibrous and myxomatous
connective tissue with some adipose tissue and blood vessels.
PAPILLARY HIDRADENOMA
(HIDRADENOMA PAPILLIFERUM)
• This is a benign tumour arising from apocrine sweat glands of the vulva.
• Most commonly, it is located in the labia
Histologically
• the tumour lies in the dermis under a normal epidermis.
• The tumour consists of papillary structures
• covered by double layer of epithelial
CONDYLOMA ACUMINATUM
• Condyloma acuminata or anogenital warts are benign papillary lesions of
squamous epithelium
• transmitted venereally to male sex partner.
• They may be solitary but more frequently are multiple forming soft
warty masses.
• The common locations are the anus, perineum, vaginal wall, vulva and
vagina.
• They are induced by HPV, particularly types 6 and 11.
CONDYLOMA ACUMINATUM
Histologically
• they are identical to their counterparts on male external genitalia.
• The features consist of a tree-like proliferation of stratified
squamous epithelium, showing marked acanthosis,
hyperkeratosis, parakeratosis, papillomatosis & perinuclear
vacuolisation of epithelium called koilocytosis, indicative of HPV
infection.
• The papillary projections consist of fibro vascular stoma.
VULVAL INTRAEPITHELIAL NEOPLASIA
& INVASIVE CARCINOMA
• Vulval intraepithelial neoplasia (VIN) and invasive squamous cell
carcinoma are morphologically similar to those in the cervix and vagina.
• viruses in carcinogenesis, particularly high-risk HPV types 16 and 18
• VIN is often multifocal within vulva and may be multicentric as well
• Vulval carcinoma constitutes 3% of all female genital tract cancers.
• VIN occurs in reproductive age
VULVAL INTRAEPITHELIAL NEOPLASIA
& INVASIVE CARCINOMA
• Grossly, VIN and vulval carcinoma in early stage is a ‘white’ lesion (leukoplakia)
while later the area develops an exophytic or endophytic (ulcerative) growth
pattern.
• The traditional VIN lesion, described as Bowen’s disease of the vulva, is
generally a slightly elevated, velvety, plaque lesion.
VULVAL INTRAEPITHELIAL NEOPLASIA &
INVASIVE CARCINOMA
Microscopically,
• VIN may also range from VIN I to VIN III, higher grade being also called
Bowen’s disease (in situ carcinoma).
• Vulvar cancer is squamous cell type with varying degree of anaplasia
and depth of invasion depending upon the stage (Fig.).
• HPV-positive tumours are more often poorly-differentiated squamous cell
carcinoma
• while HPV-negative are well-differentiated kerati nising type.
• Verrucous carcinoma is a rare variant which is a fungating tumour but is
locally malignant.
Vulval intraepithelial neoplasia (VIN) (Bowen’s disease)
There is hyperkeratosis, parakeratosis, acanthosis, koilocytosis and presence
of atypical anaplastic cells throughout the entire thickness of the epithelium.
Photomicrograph on right under higher magnification shows mitotic figures in
the layers of squamous epithelium.
• Clinical staging for vulval carcinoma based on tumour
size (< or > 2 cm) and extent of spread has been
described by International Federation of Gynaecology
and Obstetrics (FIGO staging)
FIGO staging of carcinoma of the vulva
VAGINA
VAGINITIS &
VULVOVAGINITIS
• Since vulva and vagina are anatomically close to each other, often
inflammation of one affects the other location.
• i) Bacterial e.g. streptococci, staphylococci, Escherichia coli,
Haemophilus vaginalis.
• ii) Fungal e.g. Candida albicans.
• iii) Protozoal e.g. Trichomonas vaginalis.
• iv) Viral e.g. Herpes simplex.
VAGINITIS &
VULVOVAGINITIS
• The most common causes of vaginitis are Candida (moniliasis) and
Trichomonas (trichomoniasis).
• The hyphae of Candida can be seen in the vaginal smears.
• Similarly, the protozoa, Trichomonas, can be identified in smears.
• These infections are particularly common in pregnant and diabetic
women and may involve both vulva and vagina.
• (adult vaginal mucosa is relatively resistant to gonococcal
infection because of its histology)
TUMOURS &
TUMOUR-LIKE
CONDITIONS
• Vaginal cysts such as Gartner’s duct (Wolffian) cyst lined by glandular
epithelium and vaginal inclusion cyst arising from inclusion of vaginal
epithelium are more common benign vaginal tumours
• Other uncommon benign tumours are papillomas, fi bromas, lipomas,
angiomas and leiomyomas
• Primary malignancies of the vagina are rare
• and include carcinoma (squamous cell carcinoma and adenocarcinoma)
• and embryonal rhabdomyosarcoma (sarcoma botryoides).
CARCINOMA OF VAGINA
• Primary carcinoma of the vagina is an uncommon tumour.
• Squamous cell dysplasia or vaginal intra epithelial neoplasia occur less
frequently as compared to the cervix or vulva and can be detected by
Pap smears.
• Invasive carcinoma of the vagina includes two main types:
• 1. Squamous cell carcinoma of vagina constitutes less than 2% of all
gynaecologic malignancies. The role of HPV types 16 and 18 in its
etiology
• 2. Adenocarcinoma of the vagina is much less frequent than squamous
cell carcinoma of the vagina. It may be endometrioid or mucinous type.
FIGO clinical staging of
carcinoma of the vagina
EMBRYONAL RHABDOMYOSARCOMA
(SARCOMA BOTRYOIDES)
• This is an unusual and rare malignant tumour occurring in
infants and children
• under 5 years of age.
• The common location is anterior vaginal wall.
EMBRYONAL RHABDOMYOSARCOMA
(SARCOMA BOTRYOIDES)
MORPHOLOGIC FEATURES
Grossly
• The tumour is charac terised by bulky and polypoid grape-like mass
(botryoides = grape) that fills and projects out of the vagina.
Histologically:
• 1. Groups of round to fusiform tumour cells are characteristically lying
underneath the vaginal epithelium, called cambium layer of tumour cells.
• 2. The central core of polypoid masses is composed of loose and myxoid
stroma with many infl ammatory cells.
FEMALE GENITAL SYSTEM PATHOLOGY

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FEMALE GENITAL SYSTEM PATHOLOGY

  • 1. FEMALE GENITAL SYSTEM - 1 DR. ROOPAM JAIN PROFESSOR & HEAD, PATHOLOGY
  • 3. BARTHOLIN’S CYST & ABSCESS • Inflammation of Bartholin’s vulvovaginal glands (Bartholin’s adenitis) may occur due to bacterial infection, notably gonorrhoeal infection. • Infection may be acute or chronic. • Acute Bartholin’s adenitis occurs from obstruction and dilatation of the duct by infection resulting in formation of a Bartholin’s abscess. • Chronic Bartholin’s adenitis results from a less virulent infec tion so that the process is slow and prolonged.
  • 5. • non-neoplastic epithelial disorders of the skin of vulva includes following 2 lesions: • 1. Lichen sclerosus (older term: atrophic dystrophy). • 2. Squamous hyperplasia or keratosis (older term: hyperplastic dystrophy, or lichen simplex chronicus). • The two types of lesions may coexist in the same patient called mixed vulvar dystrophy.
  • 6. Lichen Sclerosus • more common and more extensive in the vulva in postmenopausal women. • Th e lesions appear as multiple, small, coalescent, yellowish-blue macules or papules which produce thin and shiny parchment-like skin. • The lesions may extend from vulva onto the perianal and perineal area. • Clinically, the patient, usually a post-menopausal woman, complains of intense pruritus which may produce excoriation of the affected skin. • Eventually, there is progressive shrinkage and atrophy resulting in narrowing of the introitus, clinically referred to as kraurosis vulvae
  • 7. Lichen Sclerosus MORPHOLOGIC FEATURES • Microscopically, the follow - ing characteristics are seen (Fig. 22.1,A): • 1. Hyperkeratosis of the surface layer. • 2. Thinning of the epidermis with disappearance of rete ridges. • 3. Amorphous homogeneous degenerative change in the dermal collagen. • 4. Chronic inflammatory infiltrate in the mid-dermis
  • 8. Non-neoplastic epithelial disorders of vulval skin Lichen Sclerosus
  • 9. Squamous Hyperplasia • Squamous hyperplasia, or simply called keratosis, is characterised by white, thickened vulvar lesions which are usually itchy. • The cause is unknown • symptomatic relief results from use of topical corticosteroids.
  • 12. VULVAL TUMOUR STROMAL POLYPS • Stromal (fibroepithelial) polyps or acrochordons may form in the vulva or vagina. • There may be single or multiple polypoid masses. • Histologically, they are covered by an orderly stratified squamous epithelium. The stroma consists of loose fibrous and myxomatous connective tissue with some adipose tissue and blood vessels.
  • 13. PAPILLARY HIDRADENOMA (HIDRADENOMA PAPILLIFERUM) • This is a benign tumour arising from apocrine sweat glands of the vulva. • Most commonly, it is located in the labia Histologically • the tumour lies in the dermis under a normal epidermis. • The tumour consists of papillary structures • covered by double layer of epithelial
  • 14. CONDYLOMA ACUMINATUM • Condyloma acuminata or anogenital warts are benign papillary lesions of squamous epithelium • transmitted venereally to male sex partner. • They may be solitary but more frequently are multiple forming soft warty masses. • The common locations are the anus, perineum, vaginal wall, vulva and vagina. • They are induced by HPV, particularly types 6 and 11.
  • 15. CONDYLOMA ACUMINATUM Histologically • they are identical to their counterparts on male external genitalia. • The features consist of a tree-like proliferation of stratified squamous epithelium, showing marked acanthosis, hyperkeratosis, parakeratosis, papillomatosis & perinuclear vacuolisation of epithelium called koilocytosis, indicative of HPV infection. • The papillary projections consist of fibro vascular stoma.
  • 16. VULVAL INTRAEPITHELIAL NEOPLASIA & INVASIVE CARCINOMA • Vulval intraepithelial neoplasia (VIN) and invasive squamous cell carcinoma are morphologically similar to those in the cervix and vagina. • viruses in carcinogenesis, particularly high-risk HPV types 16 and 18 • VIN is often multifocal within vulva and may be multicentric as well • Vulval carcinoma constitutes 3% of all female genital tract cancers. • VIN occurs in reproductive age
  • 17. VULVAL INTRAEPITHELIAL NEOPLASIA & INVASIVE CARCINOMA • Grossly, VIN and vulval carcinoma in early stage is a ‘white’ lesion (leukoplakia) while later the area develops an exophytic or endophytic (ulcerative) growth pattern. • The traditional VIN lesion, described as Bowen’s disease of the vulva, is generally a slightly elevated, velvety, plaque lesion.
  • 18. VULVAL INTRAEPITHELIAL NEOPLASIA & INVASIVE CARCINOMA Microscopically, • VIN may also range from VIN I to VIN III, higher grade being also called Bowen’s disease (in situ carcinoma). • Vulvar cancer is squamous cell type with varying degree of anaplasia and depth of invasion depending upon the stage (Fig.). • HPV-positive tumours are more often poorly-differentiated squamous cell carcinoma • while HPV-negative are well-differentiated kerati nising type. • Verrucous carcinoma is a rare variant which is a fungating tumour but is locally malignant.
  • 19. Vulval intraepithelial neoplasia (VIN) (Bowen’s disease) There is hyperkeratosis, parakeratosis, acanthosis, koilocytosis and presence of atypical anaplastic cells throughout the entire thickness of the epithelium. Photomicrograph on right under higher magnification shows mitotic figures in the layers of squamous epithelium.
  • 20. • Clinical staging for vulval carcinoma based on tumour size (< or > 2 cm) and extent of spread has been described by International Federation of Gynaecology and Obstetrics (FIGO staging)
  • 21. FIGO staging of carcinoma of the vulva
  • 23. VAGINITIS & VULVOVAGINITIS • Since vulva and vagina are anatomically close to each other, often inflammation of one affects the other location. • i) Bacterial e.g. streptococci, staphylococci, Escherichia coli, Haemophilus vaginalis. • ii) Fungal e.g. Candida albicans. • iii) Protozoal e.g. Trichomonas vaginalis. • iv) Viral e.g. Herpes simplex.
  • 24. VAGINITIS & VULVOVAGINITIS • The most common causes of vaginitis are Candida (moniliasis) and Trichomonas (trichomoniasis). • The hyphae of Candida can be seen in the vaginal smears. • Similarly, the protozoa, Trichomonas, can be identified in smears. • These infections are particularly common in pregnant and diabetic women and may involve both vulva and vagina. • (adult vaginal mucosa is relatively resistant to gonococcal infection because of its histology)
  • 26. • Vaginal cysts such as Gartner’s duct (Wolffian) cyst lined by glandular epithelium and vaginal inclusion cyst arising from inclusion of vaginal epithelium are more common benign vaginal tumours • Other uncommon benign tumours are papillomas, fi bromas, lipomas, angiomas and leiomyomas • Primary malignancies of the vagina are rare • and include carcinoma (squamous cell carcinoma and adenocarcinoma) • and embryonal rhabdomyosarcoma (sarcoma botryoides).
  • 27. CARCINOMA OF VAGINA • Primary carcinoma of the vagina is an uncommon tumour. • Squamous cell dysplasia or vaginal intra epithelial neoplasia occur less frequently as compared to the cervix or vulva and can be detected by Pap smears. • Invasive carcinoma of the vagina includes two main types: • 1. Squamous cell carcinoma of vagina constitutes less than 2% of all gynaecologic malignancies. The role of HPV types 16 and 18 in its etiology • 2. Adenocarcinoma of the vagina is much less frequent than squamous cell carcinoma of the vagina. It may be endometrioid or mucinous type.
  • 28. FIGO clinical staging of carcinoma of the vagina
  • 29. EMBRYONAL RHABDOMYOSARCOMA (SARCOMA BOTRYOIDES) • This is an unusual and rare malignant tumour occurring in infants and children • under 5 years of age. • The common location is anterior vaginal wall.
  • 30. EMBRYONAL RHABDOMYOSARCOMA (SARCOMA BOTRYOIDES) MORPHOLOGIC FEATURES Grossly • The tumour is charac terised by bulky and polypoid grape-like mass (botryoides = grape) that fills and projects out of the vagina. Histologically: • 1. Groups of round to fusiform tumour cells are characteristically lying underneath the vaginal epithelium, called cambium layer of tumour cells. • 2. The central core of polypoid masses is composed of loose and myxoid stroma with many infl ammatory cells.