BENIGN AND MALIGNANT

TUMORS OF
REPRODUCTIVE SYSTEM
MASTER PLAN
 CONTENTS
I. Benign lesions of the vulva and vagina
A. Vulval epithelial disorders
B. Vulval ulcers
C. Vulval cysts
D. Benign tumors of the vulva
E. Vaginal wall cysts
F. Vaginal adenosis
 CONTENTS
II. Benign lesions of the cervix
A. Cervical ectopy
B. cervical cyst
C. Cervical polyps
III. Benign lesions of broad ligament and parametrium
VI. Benign lesions of the uterus
D. Fibroids
E. Adenomyosis
F. polyps
 CONTENTS
V. Benign lesions of ovary
A. Non neoplastic enlargement
B. Benign ovarian neoplasm
VI. Premalignant lesions
C. Vulva
D. Vagina
E. Cervix
F. Endometrium
 CONTENTS
VII. Genital malignancy
A. Vulval
B. Bartholin’s gland
C. Vaginal
D. Cervical
E. Endometrial
F. Gestational trophoblastic disease
G. Sarcoma Uterus
H. Fallopian Tube
I. Ovary
 CONTENTS
• Nursing management
• Bibliography
General objective
At the end of the class students gets adequate knowledge regarding
benign and malignant tumors of reproductive tract and apply this
knowledge in their clinical settings
Specific objectives
At the end of the class students can able to
1. Describe Benign lesions of the vulva and vagina
2. Explain Benign lesions of the cervix
3. Describe Benign lesions of broad ligament and parametrium
4. Explain Benign lesions of the uterus
5. Describe Benign lesions of ovary
6. Explain Premalignant lesions
7. Explain malignant lesions of genital tract
8. Apply nursing management for benign and malignant tumors of genital tract.
 I. BENIGN LESIONS OF THE VULVA
AND VAGINA
A. NON NEOPLASTIC EPITHELIAL DISORDERS
Non neoplastic epithelial disorders of skin and mucosa of vulva refer to
a group of chronic diseases shown as female genital skin and mucosal
tissue degeneration and pigmentation change.
The main symptoms are vulval itching, squamous cell hyperplasia,
vulval and perianal skin atrophy or thinning, hypopigmentation.
 I. BENIGN LESIONS OF THE VULVA
AND VAGINA
A. NON NEOPLASTIC EPITHELIAL DISORDERS
Etiology
- Traumatic injury( scratching)
- Autoimmune disorders
- Allergic (atopic) disorders( asthma, eczema, hay fever)
- Irritation
- Nutritional deficiency(folic acid, vit.B12, riboflavin, achlorhydria)
 I. BENIGN LESIONS OF THE VULVA
AND VAGINA
A. NON NEOPLASTIC EPITHELIAL DISORDERS
Etiology
- Infection(fungus)
- Metabolic or systemic disorders
- Drugs
- Diabetes
- Common allergens : cosmetics, synthetic underwear's’, fragrances.
 I. BENIGN LESIONS OF THE VULVA
AND VAGINA
A. NON NEOPLASTIC EPITHELIAL DISORDERS
Classification
1. Lichen sclerosus
2. Lichen planus
3. Squamous hyperplasia( hyperplastic dystrophy)
4. Other dermatoses
 1. Lichen Sclerosus
• Most common white lesions of the vulva
• Occur at any age (common in postmenopausal women and before
puberty)
• Metabolically active epithelium.
 1. Lichen Sclerosus
CLINICAL FEATURES
- Decreased subcutaneous fat
- Marked shrinkage of labia minora
- Narrowing of the introitus to obscure the urethra
- Intercourse is impossible
- Lesion is bilateral and symmetrical in a figure of eight distribution
- Lesion is thin and white with a crinkled pattern with fissure or excoriation.
- Involve vulva as a italics encircling the vestibule and involving the
clitoris, labia minora, inner aspects of labia majora and perineal skin.
 1. Lichen Sclerosus
Symptoms
• Pruritus
• Dyspareunia
• Burning
• Sleeplessness
• Difficulty in micturition and urinary retention
 1. Lichen Sclerosus
Diagnosis
• Biopsy
Lesion is thin with hyperkeratosis
Flattening of the rete pegs with hyalinization
Lymphocyte and plasma cell may present
Risk of malignancy is about 1-4%
 1. Lichen Sclerosus
Treatment
• Topical steroids like clobetasol
• Bland emollients
 2.  Lichen Planus
General Appearance
• Erosive lesions at vestibule with or without adhesions resulting in
stenosis
• May have associated oral mucocutaneous lesions and desquamative
vaginitis
Symptoms
• irritating vaginal and vulvar soreness
• intense burning, pruritus
• dyspareunia with or post-coital bleeding
  2. Lichen Planus
Types
• Papulosquamous Lichen Planus
• Hypertrophophic Lichen Planus
• Erosive Lichen Planus
Treatment
• Intravaginal hydrocortisone suppositories BID x 2m
• Steroid creams (medium-high potency)
• Vaginal oestrogen cream if atrophic epithelium present
• Vaginal dilators for stenosis
• Surgery for severe vaginal synechiae
• Vulvar hygiene
• Emotional support
 3. Squamous hyperplasia

• This was formerly called Hyperplastic dystrophy

• Commonly seen in postmenopausal age group
Clinical features
• Pruritus
• Lesion appears thickened and hyperkeratotic.
• Usually discrete but may be multiple
• Confined to the inner aspect of labia majora, minora, introitus, prepause of
clitoris
• Area appears white with defined margin
• There may be acanthosis and hyperkeratosis
 3. Squamous hyperplasia

Diagnosis
• Biopsy
Treatment
• If there is no atypia, clobetasol cream are effective.
 4. Other Dermatoses
It includes
• Lichen simplex
• Contact dermatitis
• Eczema
• Psoriasis
 I. BENIGN LESIONS OF THE VULVA
AND VAGINA
B. VULVAL ULCERS
• Sexually transmitted infections
• Other infections like tuberculosis
• Non specific causes like Behcet’s disease, lichen planus and Lipschutz
ulcer
 I. BENIGN LESIONS OF THE VULVA
AND VAGINA
B. VULVAL ULCERS
Vulval ulcers are commonly due to sexually transmitted infections like
herpes simplex, syphilis, lymphogranuloma venereum and granuloma
inguinale.
 Behcet’s disease
• Rare chronic inflammatory disease characterized by recurrent Oral and
Genital ulcers with inflammation of eye.
• Etiology is not known
• There is no effective treatment
• Topical and systemic steroids can be used for relief of symptoms.
 Lipschutz ulcer
• Affect labia minora and introitus
• Etiology due to Epstein- Barr virus
• Associated lymphadenopathy and fever
• Treatment with antiseptic creams.
 I. BENIGN LESIONS OF THE VULVA
AND VAGINA
C.VULVAL CYSTS
a. Bartholin’s cyst
b. Sebaceous cyst
c. Cyst of the canal of Nuck
d. Skene duct cysts
 a. Bartholin Duct Cyst
Common vulvar lesions and due to occlusion of the Bartholin duct with
accumulation of mucus.
Causes
• Infection
• Trauma
• A wrongly directed episiotomy can injure the duct
• Cyst may get infected leading to abscess formation
• Typical location of the cyst is on the inner side of the labia majora at
the junction of the anterior two third and posterior one third.
 a. Bartholin Duct Cyst
MANAGEMENT
• Analgesia
• Antibiotics
• Surgical drainage by marsupialisation
 b. Sebaceous cyst
• Usually multiple and formed by accumulation of the sebaceous
material due to occlusion of the ducts.
• These are located in the labia majora
• If infected treatment is with antibiotics and surgical drainage.
 c. Cyst of the canal of Nuck
• The processus vaginalis, which accompanies the round ligament is
usually obliterated prior to birth.
• A part of it may persist and form a cyst in the anterior part of the
labium majus.
 d. Skene Duct Cysts
• These are cystic dilatations of the Skene glands, which are adjacent to
the urethra meatus in the vestibule.
• They are usually small and asymptomatic but can enlarge and cause
difficulty in urination when they will have to be removed. If
superadded infection occurs an abscess will result
 I. BENIGN LESIONS OF THE VULVA
AND VAGINA
D. BENIGN TUMORS OF THE VULVA
1. fibroma, lipoma, neurofibroma
• Fibroma is the most common benign solid tumor of the vulva. It arises
from the deeper connective tissue of the labia majora.
• Vulval fibroma grow slowly
• It may be small and malignant change is very low.
• Surgical removal is necessary as they produce discomfort.
 I. BENIGN LESIONS OF THE VULVA
AND VAGINA
D. BENIGN TUMORS OF THE VULVA
2. Hydradenoma
• It arises from the sweat gland in the vulva, usually located in the
anterior part of the labia majora.
• It rarely exceeds 1 cm.
• It is benign lesion but its reddish look and complex adenomatous
pattern on histology may be confused with adenocarcinoma.
• Simple excision and biopsy is adequate.
 I. BENIGN LESIONS OF THE VULVA
AND VAGINA
E. VAGINAL WALL CYSTS
Common cysts include
• Gartner duct cyst
• Epithelial inclusion cyst
 Gartner duct cysts
• Cysts of remnants of the mesonephric or Wolffian duct.
• Typical location is high up in the fornices on the anterio-lateral aspect
of the vaginal wall
• Usually asymptomatic and not require treatment
• If they are symptomatic produce dyspareunia
• Marsupalisation or excision can be done.
• Anterior vaginal wall cyst must be differentiated from a cystocele by
means of a catheter.
 I. BENIGN LESIONS OF THE VULVA
AND VAGINA
F. VAGINAL ADENOSIS
• It involve the presence of epithelium lined glands within the vagina
and is associated with in utero exposure to diethyl stilboestrol.
• Rarely in progress to vaginal cell adenocarcinoma.
 II. BENIGN LESIONS OF THE CERVIX
A.CERVICAL ECTOPY
• Also known as cervical erosion
• In this condition the squamous epithelium of the ectocervix is replaced
by columnar epithelium, which is continuous with the endocervix.
• It may be congenital or acquired
 Congenital cervical erosions

• At birth, in one third of the cases, the columnar epithelium of the

endocervix extends beyond the external os.
• This condition persists only for a few days until the level of estrogen
derived from mother falls.
• Thus congenital ectopy heals spontaneously
 Acquired cervical erosions
• The whole cervical mucosa including the crypts and stroma is
displaced.
• This is observed in pregnancy and in users of the estrogen
progesterone combine pills
• Chronic cervicitis may be associated with formation of cervical
erosions.
 A.CERVICAL ECTOPY
Clinical features
Signs
• Bright red area surrounding and extending the external os in the
ectocervix
• The outer edge is clearly demarcated.
 A.CERVICAL ECTOPY
Clinical features
Symptoms
• Excessively mucoid vaginal discharge
• Contact bleeding
• Cervicitis
• Backache
• Pelvic pain
• Infertility
 A.CERVICAL ECTOPY
Management
• Pap smear
• If smear is abnormal colposcopy and directed biopsy and endocervical
curettage
 II. BENIGN LESIONS OF THE CERVIX
B. CERVICAL POLYPS
• Usually mucous polyps arising from the cervical canal.
• Appear as a red vascular swelling with a pedicle attached to the endo-
cervical mucosa.
• They can be multiple
• Visualized on speculum examination
• Usual in the reproductive age group
• May be asymptomatic or can present as metrorrhagia or post ctal bleeding.
• Removed by avulsion
 II. BENIGN LESIONS OF THE CERVIX
B. CERVICAL CYSTS
• Nabothian cysts
• Endometriotic cysts
• Mesonephric cysts
 Nabothian cyst
• A nabothian cyst (or nabothian follicle) is a mucus-filled cyst on the
surface of the cervix. They are most often caused when stratified
squamous epithelium of the ectocervix (portion nearest to the vagina)
grows over the simple columnar epithelium of the endocervix (portion
nearest to the uterus).
• This tissue growth can block the cervical crypts, trapping cervical mucus
inside the crypts
• Nabothian cysts usually require no treatment and frequently resolve on
their own.
• Cryotherapy has been used to treat nabothian cysts but is rarely necessary.
 III. BENIGN LESIONS OF BROAD
LIGAMENT AND PARAMETRIUM
A. EPOOPHORON AND PAROOPHORON
• Remnants of the wolffian duct or mesonephric duct may be seen in the
broad ligament between the fallopian tube and ovary.
• The tubules of the upper part of the wolffian body are called
epoophoron or organ of Rosenmuller and are associated with duct
opening into it.
• The paroophoron are a number of blind tubular remnants seen near the
inner border of the ovary.
• Cyst can arise in the broad ligament from remnants of the mesonephric
duct and tubules.
 III. BENIGN LESIONS OF BROAD
LIGAMENT AND PARAMETRIUM
B. PAROVARIAN AND PARATUBAL CYSTS
• Retroperitoneal cysts lying in the broad ligament next to the ovary.
• They may arise from remnants of the mesonephric ducts or tubules or from
peritoneal inclusions or the tubal epithelium.
• The ovary is seen distinct from the cysts.
• The fallopian tube is usually stretched over the cyst and there may be
dilated vessels over the cyst.
• They may be small but can become very large.
• Cysts are unilocular and contain clear fluid
Treatment
• Laparotomy or laparoscopy
 III. BENIGN LESIONS OF BROAD
LIGAMENT AND PARAMETRIUM
B. PAROVARIAN AND PARATUBAL CYSTS
Paratubal cyst can also arise and the most common is the hydatid of
Morgagni, which is pedunculated and typically dangles from one of the
fimbria.
 III. BENIGN LESIONS OF BROAD
LIGAMENT AND PARAMETRIUM
C. BRAOD LIGAMENT MYOMAS
• These are common broad ligament tumors and can be true or false.
• True broad ligament fibroids are extremely rare and have no
attachment to the uterus. They originate from smooth muscle fibers in
the broad ligament.
• False broad ligament fibroids are more usual. They are sub serous
fibroids arising from the lateral uterine wall and grow between the
layers of the broad ligament.
 VI. BENIGN LESIONS OF THE UTERUS
A. UTERINE FIBROIDS
• Commonest benign tumor of the uterus
• Commonest benign solid tumor in female.
• Histologically, it composed of smooth muscle and fibrous connective
tissue, so named as uterine leiomyoma, myoma or fibromyoma.
 A. UTERINE FIBROID
Incidence
• At least 20 percent of women at the age of 30 have got fibroid
• Fortunately, most of them (50%) remain asymptomatic.
• The incidence of symptomatic fibroid in hospital outpatient is about 3 percent.
• A high incidence of 10 percent prevails in England.
• In colored races (black women), the incidence is even higher.
• These are more common in nulliparous or in those having one child infertility .
• The prevalence is highest between 35–45 years.
 A. UTERINE FIBROIDS
Origin
• The etiology still remains unclear.
• The prevailing hypothesis is that, it arises from the neoplastic single
smooth muscle cell of the myometrium.
• The stimulus for initial neoplastic transformation is not known.
 A. UTERINE FIBROIDS
Etiology
• Chromosomal abnormality
Mainly in the chromosome six, seven, twelve and fourteen
(rearrangements, deletions).
Somatic mutations in myometrial cells may also be the cause for
uncontrolled cell proliferation.
Cytogenetic abnormalities are seen in 50% of fibroids.
 A. UTERINE FIBROIDS
Etiology
• Ovarian steroids
Regulate the growth of fibroids
Steroid receptors especially estrogen receptors are present in higher
concentration in fibroids than in surrounding myometrium.
Also action of estrogen depends on growth factors like epidermal
growth factors and insulin growth factors,
Progesterone receptors are also increased in fibroids and stimulate
fibroid growth.
 A. UTERINE FIBROIDS
Etiology
• Bcl-2
an inhibitor of apoptosis is significantly increased in leiomyoma cells
and this is also influenced by the steroid hormones.
 A. UTERINE FIBROIDS
Etiology
• Role of polypeptide growth factors
Epidermal growth factor (EGF),
insulin-like growth factor-1 (IGF-1),
transforming growth factor (TGF),
stimulate the growth of leiomyoma either directly or via estrogen.
A positive family history is often present.
 A. UTERINE FIBROIDS
Growth
• It is predominantly an estrogen-dependent tumor.
• Estrogen and progesterone is incriminated as the cause.
Estrogen dependency is evidenced by:
Growth potentiality is limited during childbearing period.
Increased growth during pregnancy.
They do not occur before menarche.
Following menopause, there is cessation of growth and there is no new
growth at all.
 A. UTERINE FIBROIDS
It seems to contain more estrogen receptors than the adjacent
myometrium.
Frequent association of anovulation.
 A. UTERINE FIBROIDS
RISK FACTORS
1. Ethnicity
2. Early age of menarche
3. Nulliparity
4. Increasing body weight
5. Familial associations
6. Exogenous hormones
7. Smoking reduces risk
8. Hyperoestrogenic state
9. Multiparity also reduces the risk
 A. UTERINE FIBROIDS
TYPES
1. Interstitial or intramural
2. Subserous
3. Submucous
4. Cervical
5. Broad ligament
 A. UTERINE FIBROIDS
TYPES

Body(corporeal) Cervical

Interstitial(75%) Subserous(15%) Submucous(5%)

(intramural)

Subserous Broad ligament Wandering Sessile Pedunculated

(pseudo) (Parasiyic) (polyp)

Anterior Posterior Central Lateral

FIGO LEIOMYOMA CLASSIFICATION
 INTRAMURAL FIBROID
• Common fibroid(75%)
• Lie within the wall of the uterus.
• They are separated from the myometrium by a thin layer of connective
tissue, which forms a pseudo capsule or false capsule.
• It is through this plane that the fibroid is enucleated at myomectomy.
• The blood supply is through this capsule.
• Most fibroids are initially intramural and eventually some of them
grow outwards or inwards to become sub serous or sub mucous. Some
remain in the intramural location.
INTRAMURAL FIBROIDS WITH
PSEUDOCAPSULE
 SUBSEROUS FIBROIDS
• The fibroid which was initially intramural, projects outwards the
peritoneal cavity and is covered by peritoneum.
• The subserous fibroid can be sessile or pedunculated.
• These fibroids can attain huge sizes.
• They do not usually have menstrual symptoms.
• Pressure symptoms are common.
• Subserous tumours contain more of fibroid tissue.
 SUBMUCOUS FIBROIDS
• Constitute 5% of all fibroids
• The intramural fibroid grows into the uterine cavity distorting the cavity and is
covered by endometrium to form a submucous fibroid.
• In some cases a submucous fibroid may become pedunculated and protrude
out through the cervix as a polyp.
• A large fibroid polyp arise from the body of uterus and distended the entire
cervix, so that the cervix is thinned out and resembles a fully dilated cervix in
labour.
• Submucous fibroid produce the maximum menstrual symptoms and may also
be responsible for infertility and recurrent miscarriage.
• These tumours contain more of smooth muscle tissue than the sub serous.
• Sacromatous change is also more common in these tumors.
 CERVICAL FIBROID
• Rare type
• May be subserous, intramural or submucous.
• They can be anterior, posterior, lateral or central
• Cervical fibroids can become impacted in the pelvis causing
compression on the bladder and urinary retention
• They can also cause distortion of the pelvic anatomy by displacing the
ureter.
• In a central cervical fibroid, the uterus sits in top of the expanded
cervix. This is termed as lantern on the dome of St Paul’s.
 CERVICAL FIBROID
• These fibroids are surgical challenges due to their inaccessibility and
proximity to the bladder and ureters.
• Myomectomy may be extremely difficult and may even end in
hysterectomy.
• Preoperative GnRH agonists are useful to reduce bleeding and
facilitate surgery.
• Cervical fibroids, especially central one are extremely problematic in
pregnancy and labour.
• They may cause obstructed labour.
• In case of caesarean section LSCS is almost impossible and such cases
classical caesarean section is indicated.
 BROAD LIGAMENT FIBROIDS
• They can be of two types
True broad ligament fibroids
• They are rare and have no attachment to the uterus.
• They originate from smooth muscle fibres in the broad ligament.
 BROAD LIGAMENT FIBROIDS
False broad ligament fibroids
• They are more common
• They are subserous fibroids arising from the lateral uterine wall and grow
between the layers of the broad ligament.
• The difference between the two is the position of the ureter, which is
lateral to the fibroid in the false and medial in the true broad ligament
fibroids
• Submucosal fibroids produce maximal menstrual symptoms and can cause
infertility and recurrent miscarriage.
• Sarcomatous change is also more in submucous tumors.
 PATHOLOGY
• Fibroids can be single but are more commonly multiple.
• Consistency is firm and fibrous
• The major blood supply is through blood vessels running through the pseudo
capsule.
• The periphery of the fibroid is more vascular
• Central part is less vascular and likely to undergone degeneration
• Microscopically the tumour is composed of smooth muscle fibres and fibrous
tissue.
• Hence the correct term is fibromyoma and not fibroid.
• Endometriosis is found to be associated in 30%
 DEGENERATIONS
• Typical appearance of the leiomyoma may change if normal muscle
tissue is replaced with various degenerative substances following
haemorrhage and necrosis.
TYPES
1. Hyaline degeneration
Commonest type of degeneration
Central portion is more prone to degeneration
Firm become soft and elastic
 DEGENERATIONS
2. Cystic degeneration
Due to liquefaction in areas which undergone hyaline membrane
changes.
3. Calcification or calcareous degeneration
Due to circulatory impairement and common after menopause
Occur in subserous fibroid with narrow pedicle
Calcium carbonate or phosphate id deposited
 DEGENERATIONS
4. Red degeneration or carneous degeration
• Occurs in large fibroid usually in pregnancy or the puerperium.
• Cause is vascular and due to coagulative necrosis because of
thrombosis of blood vessels.
PAHTOPHYSIOLOGY
 CLINICAL FEATURES
SYMPTOMS
1. Abnormal uterine bleeding
• Common symptom
• Menorrhagia ( submucous fibroids)
• Metrorrhagia(ulcerated submucous fibroid or polyp)
• Menometrorrhagia (submucous and intramural)
 Mechanism of menorrhagia
• Increasing the endometrial surface area due to submucous and
intramural fibroids
• Increased vascularity
• Interference with normal uterine contractility
• Endometrial ulceration and haemorrhage over a submucous fibroid
• Compression of venous plexuses in the myometrium causing venostasis
• Associated endometrial hyperplasia and anovulation due to
hyperoestrogenism
• Increased production of growth factors.
 CLINICAL FEATURES
SYMPTOMS
2. Pressure symptoms
a. Pelvic discomfort or pressure
i. Occur with large fibroids
ii. Posterior fibroid cause low back pain
iii. Broad ligament fibroid compress the sciatic nerve leading to
sciatic nerve pain
 CLINICAL FEATURES
b. Urinary symptoms
• Cervical fibroid cause bladder compression and discomfort.
• Urinary frequency
• Voiding difficulties
• Incomplete emptying of bladder
• Urinary retention
• Hydronephrosis
 CLINICAL FEATURES
c. Other pressure symptoms
• Oedema over the limbs
• Venous stasis and DVT
• Difficulty in defecation and dyspareunia
• dyspnoea
 CLINICAL FEATURES
d. Pelvic pain
• Less common
• Acute pain
Causes
Torsion
Red degeneration
Expulsion of submucous fibroid
Haemorrhage into the fibroid
Acute retention of urine in the cervical fibroid.
 CLINICAL FEATURES
e. Abdominal Distension
f. Infertility
• Submucous and intramural fibroids distort or impinge upon the cavity
cause infertility
• Cornual myomas cause tubal occlusion
• Impaired gamete and embryo transport
• Altered relation between cervix and vaginal pool of semen
• Distortion of cavity
 CLINICAL FEATURES
g. Recurrent miscarriage
Early and second trimester miscarriage
h. Pregnancy and fibroids
 EFFECT OF FIBROIDS ON PREGNANCY
PREGNANCY
• Early and late miscarriage
• First trimester bleeding
• Preterm labour
• Abruption
• Placenta praevia
• PROM
• Malpresentations
• IUGR
EFFECT OF FIBROIDS ON PREGNANCY
LABOUR
• Prolonged labour
• Increased chance of caesarean section
• Difficulty in delivery of the baby at CS
• Chance of classical CS in cervical fibroids
• Increased bleeding at CS
EFFECT OF FIBROIDS ON PREGNANCY
AFTER DELIVERY
• Postpartum haemorrhage
• Retained placenta due to a submucus myoma in the lower segment
• Puerperal sepsis
EFFECT OF PREGNANCY ON FIBROIDS
• Increase in size
• Red degeneration
• Torsion of a pedunculated subserous myoma
• Infection of a submucous myoma in the puerperium
 CLINICAL FEATURES
• SIGNS
Abdominal examination- pelvic mass with smooth or irregular surface
with firm consistency
Lowe border may not be palpated
Transmitted mobility
 INVESTIGATIONS
1.ULTRASOUND
• Confirm nature of pelvic mass
• Trans abdominal and trans vaginal ultrasound
• First mass is confirmed by its typical appearance( hypoechoic)
• Then number and location are assessed
• Adenomyosis should be excluded
• Ovaries are assessed separately
 INVESTIGATIONS
2. SONOHYSTEROGRAPHY
• Instillation of saline into the endometrial cavity during trans vaginal
ultrasound.
• To identify small submucous fibroid or fibroid polyp
 INVESTIGATIONS
3. HYSTEROSCOPY
• Combined diagnostic and therapeutic procedure for submucous
fibroids
4. HAEMATOLOGICAL INVESTIGATIONS
• Hb, PCV
 COMPLICATIONS
1.SACROMATOUS CHANGE
• Leiomyosarcoma is a malignant tumour of the smooth muscle of
uterus.
• Sarcomatous change is rare and can occur in about 0.1% leiomyomas
• Recurrence of fibroid polyp and postmenopausal bleeding is
associated with malignant transformation
 COMPLICATIONS
2. LEIOMYOMATOSIS
• Concurrent benign smooth muscle tumours.
• Three types
1. Intravenous leiomyomatosis
2. Benign metastasising leiomyomas
3. Disseminated peritoneal leiomyomatosis
 COMPLICATIONS
3. WANDERING FIBROIDS
• Subserous fibroid may outgrow its blood supply and get its
nourishment from omentum.
• In such cases the original pedicle may be disrupted and it may not
show any obvious attachment to the uterus. This is called wandering
parasitic fibroid
 COMPLICATIONS
4. INFECTION
Occur in submucous fibroids projecting into the uterine cavity and into
the vagina as surface epithelium becomes thinned out and sloughs off.it
usually occurs following delivery or abortion resulting in puerperal
sepsis
 COMPLICATIONS
5. TORSION OF A PEDUNCULATED FIBROID
6. PSEUDO MEIG SYNDROME
• Meig syndrome is defined as the ascites and pleural effusion that
accompanies a benign ovarian fibroma.
• Pelvic tumour including large cystic fibroid or other benign ovarian
cyst can cause this. Then it is termed as pseudo Meig Syndrome
Cause
• Discordancy between the arterial supply to and the venous drainage
from the fibroid
 COMPLICATIONS
7. POLYCYTHAEMIA
• Due to erythropoietin production by the fibroid
• Due to pressure on the ureters, causing an alteration on erythropoietic
function of the kidneys
 MANAGEMENT
1. EXPECTANT MANAGEMANT
2. SURGICAL MANAGEMENT
3. MEDICAL MANAGEMENT
4. UTERINE ARTERY EMBOLISATION
 EXPECTANT MANAGEMENT
CRITERIA
1. Absolute certainty of diagnosis( exclusion of ovarian mass)
2. Asymptomatic
3. No evidence of urethral compression
4. Size usually less than 12-14 weeks
5. Wiling for follow-up
 SURGICAL MANAGEMENT
• Traditional method
• Ovaries can be conserved if they appear normal
TYPES
• Myomectomy
• Abdominal hysterectomy
• Vaginal hysterectomy
• Laparoscopic hysterectomy
 MYOMETOMY
• It is an option for patients with symptomatic myomas who desire
further childbearing or wish to preserve the uterus.
Preoperative counselling
• Discussion of the risks and complications of myomectomy.
• Risk of recurrence (50% in 5 years)
• Risk for intraoperative bleeding
• Possibility for hysterectomy
 MYOMECTOMY
TYPES
• Open myomectomy
• Hysteroscopic myomectomy
• Laparoscopic myomectomy
• Vaginal myomectomy
 MYOMECTOMY
COMPLICATIONS OF MYOMECTOMY
Intraoperative
• Primary haemorrhage
• Injury to ureters in broad ligament and cervical fibroids
• Injury to bladder and rectum
• Conversion to hysterectomy
 MYOMECTOMY
COMPLICATIONS OF MYOMECTOMY
Postoperative
• Febrile morbidity or myoma fever due to tissue reaction
• Postoperative haemorrhage
• Re-Laparotomy
 MYOMECTOMY
COMPLICATIONS OF MYOMECTOMY
Sequelae
• Adhesions between uterus and rectosigmoid
• Peritubal adhesions leading to tuboperitoneal infertility
• Recurrence of fibroids and repeat surgery
• Persistence of menorrhagia in about 10%
 HYSTERECTOMY
Hysterectomy is the surgical removal of the uterus. It may also involve
removal of the cervix, ovaries (oophorectomy), Fallopian tubes
(salpingectomy), and other surrounding structures.
 HYSTERECTOMY -TYPES
There are five types of hysterectomy
• Total hysterectomy – where the uterus and cervix are removed
• Subtotal (partial) hysterectomy – where the uterus is removed, but the cervix is left
in place. While removal of the cervix is generally advised because it is a potential
cancer site, some women feel that it serves a purpose during penetrative sex. If the
cervix is kept, regular cervical screening is still necessary
• Hysterectomy and bilateral salpingo-oophorectomy – where the uterus, fallopian
tubes and ovaries are removed. This operation is performed if the woman has cancer
of the ovaries or the uterus, or for chronic pain due to recurrent pelvic infection or
recurrent endometriosis
HYSTERECTOMY -TYPES
• Radical hysterectomy – the most extensive version of the operation. It
involves the removal of the uterus, fallopian tubes, ovaries, upper part of
the vagina, and associated pelvic ligaments and lymph nodes. This is
performed if the woman has cancer of the cervix, ovaries, fallopian tubes
or uterus
• Hysterectomy with prophylactic bilateral salpingectomy –most doctors
now recommend removing the fallopian tubes at the time of hysterectomy
due to research suggesting that early ‘ovarian’ cancers originate in the
tubes.
HYSTERECTOMY – POTENTIAL
COMPLICATIONS
• A reaction to the anaesthetic during the operation, which may be due to
allergy
• Nausea and vomiting – post-anaesthetic or medication induced – for the first
one to three days
• Infection
• Internal haemorrhage (internal bleeding)
• Build-up of blood beneath the stitches (haematoma) or in the abdomen
• Internal scar tissue
• Blood clots (for example, thrombosis, deep vein thrombosis or pulmonary
embolism)
HYSTERECTOMY – POTENTIAL
COMPLICATIONS
• Difficulties with urination
• Injury to the bowel, bladder or ureters (tubes that carry urine from the kidneys to
the bladder) – rare
• Fistula (abnormal hole between internal structures, such as the bowel and vagina) –
rare
• Vaginal vault prolapse (when the top of the vaginal wall sags or bulges down)
• Decreased sexual desire (or you may have an increase in sexual desire due to the
treatment of your symptoms)
• Constant pelvic pain – rare, and post-operatively usually shows improvement
• Feelings of grief and loss – if not counselled appropriately before the hysterectomy.
SELF-CARE AFTER HYSTERECTOMY
• Rest – try to rest as much as possible for at least two weeks. Should
avoid driving during this time. Always rest lying down
• Exercise – continue with the light exercises. Should aim to go for a
walk each day, unless advised otherwise by your doctor
• Standing – avoid standing for more than a few minutes at a time in the
early post-operative period. Can increase standing time as patients
recovery progresses
• Lifting – avoid heavy lifting and stretching
SELF-CARE AFTER HYSTERECTOMY
• Constipation – to avoid constipation, drink plenty of fluids and eat
fresh fruits and vegetables. Patient may be advised to take stool
softeners for the first few days
• Medication – if patient have been prescribed antibiotics, make sure
they take the full course, even if they feel well
• Sex – it is advised that patient avoid vaginal sex until after the post-
operative check (about four to six weeks after the operation) to make
sure the vagina is fully healed. If vaginal dryness is a problem, it may
be helpful to use a lubricant, or sweet almond oil or olive oil.
 LONG-TERM OUTLOOK AFTER
HYSTERECTOMY
• After hysterectomy, patent will no longer need contraception or have
menstrual periods. If patients ovaries were removed, patient may
experience menopause symptoms starting within a few days of your
surgery. 
• If patient were still having periods before her hysterectomy, should discuss
oestrogen replacement therapy or other options with her. How long patient
might need oestrogen replacement therapy will depend on patient’s age.
• Hysterectomy can be an effective treatment for gynaecological conditions
such as fibroids, endometriosis and adenomyosis, though sometimes
endometriosis may recur. 
 LONG-TERM OUTLOOK AFTER
HYSTERECTOMY
• If patient had a hysterectomy to treat cancer, depending on the stage of
the cancer patient will need to have regular check-ups to make sure
patients are cancer free. Patient may need to have a regular vault
smear test – similar to a cervical screening test but involving cells
from the top of patients vagina instead of the cervix.
• If patient have had a subtotal hysterectomy (uterus removed but cervix
retained) then she will need to continue having cervical screening.
 MEDICAL MANAGEMENT
OBJECTIVE
• Reduction in tumour size and relief of symptoms like menorrhagia
DRUGS
• GnRH agonists
• GnRH Antagonists
• Antiprogestins
• Levonorgestrel Intrauterine System(LNG-IUS)
 GnRH AGONISTS
• Reduce the size of the fibroids and lead to amenorrhoea.
• This is by gonadal suppression and hypooestrogenism.
• Discontinuation of drug lead to regain of the original size.
• Best used preoperatively and just before the menopause
• Optimal duration prior to surgery is 3 months
• Therapy should be started in the midluteal phase
• Dose – goserelin 3.6 mg or leuprolide 3.75 mg as monthly
subcutaneous depot injection
 GnRH AGONISTS
Side effects
1. Hypooestrogenism
2. Hot flushes
3. Osteoporosis
4. Vaginal dryness
 GnRH ANTAGONISTS
• Direct gonadal suppression and have the same effect on agonists.
• Example- cetrorelix and ganirelix
ANTIPROGESTINS
• RU486 or mifepristone is an antiprogesterone used mainly in medical
abortion. It can be given continuously in doses of 25-50mg daily to
achieve shrinkage of the myoma and amenorrhoea.
 LNG IUS
• Marked reduction of bleeding
UTERINE ARTERY EMBOLISATION
• Also called embolotherapy
Prerequisites
• Accurate pretreatment diagnosis
• No suspicion of malignancy as in sarcoma or endometrial carcinoma
• The patient should be warned of the possibility that the procedure may
fail and hysterectomy may be needed later
• Informed consent
UTERINE ARTERY EMBOLISATION
Contraindications
1. Pregnancy
2. Pelvic infection
3. Pelvic malignancy
4. Contrast medium allergy
5. Coagulopathy
6. Adenomyosis
7. Pedunculated submucous fibroids
8. Infertility
UTERINE ARTERY EMBOLISATION
Complications
1. Failure to cannulate the uterine arteries
2. Local haematoma or femoral artery damage
3. Severe pain due to infraction of the fibroid
4. Postembolism syndrome include fever nausea and vomiting and
subside with in 1 week
5. Infection
6. Exposure to radiation
7. Persistent vaginal discharge
NURSING MANAGEMENT
DISTURBED BODY IMAGE RELATED TO PERCEIVED LOSS OF FEMINITY
AND FUTUTRE INABILITY TO CONCIEVE
Determine patients body image expectations to establish need and
plan for intervention
Determine patient and family’s perceptions of the alterations in body
image vs reality to provide accurate facts and decrease fear of
consequences of hysterectomy
Identify supportive group
Assist patient to discuss stressors
NURSING MANAGEMENT
2. Acute pain related to surgical procedures
3. Ineffective breathing pattern related to abdominal surgery
4. Fluid volume deficit
5. Risk for infection
6. anxiety
7. Risk for complications
 B. ADENOMYOSIS
• A benign ingrowing of the endometrium (both the glandular and
stromal components) into the myometrium.
• Previously called endometriosis interna
 PATHOLOGY
• Uterus diffusely enlarged due to myometrial hyperplasia.
• Enlargement is asymmetrical and more on the posterior wall.
• Size is not usually more than 12-14 weeks of a gravid uterus.
• Growth may be localised as an adenomyoma
• There is no capsule as in fibroid
CLINICAL FEATURES
• Usually asymptomatic
Symptoms
• Menorrhagia or menometrorrhagia and congestive dysmenorrhoea
Signs
• Enlarged uterus not more than 14 weeks
• Uniform uterine enlargement with no restriction of mobility
• Uterus may be softer than normal.
 INVESTIGATIONS
• Ultrasound
• MRI
 MANAGEMENT
• Depend upon patient age and desire for future fertility
• Secondary dysmenorrhoea can be treated with NSAIDs or oral
contraceptives
• GnRH agonists
• LNG IUS
• Total hysterectomy
 C. POLYPS
• Polyps are usually begin, but can rarely be malignant. They can arise
from the uterus or cervix
TYPES
1. Mucous
2. Fibroid
3. placental
 MUCOUS POLYPS
• Arise from either the cervix or the uterus
• Polyp contains stroma, glands and vascular channels.
• Malignant change is rare
• Symptoms are intermenstrual and postcoital bleeding, discharge per
vaginum.
• Removal is by avulsion if visible
• Other wise hysteroscopic removal
FIBROID POLYPS
• Arise from the body of the uterus or the cervix
• Occur due to extrusion of a submucous fibroid into the uterine cavity.
• Fibroid become pedunculated and may lie in the cervix or vagina
• Microscopy is similar to vagina
• Symptoms are intermenstual bleeding, colicky pain and sensation of
mass coming down
 PLACENTAL POLYP
Retained placental tissue adhere to the uterine wall and become
organised with surrounding blood clots.
Symptoms
• Irregular bleeding and offensive vaginal discharge
 BENIGN LESIONS OF OVARY

A. Non neoplastic enlargement

B. Benign ovarian neoplasm
 NON-NEOPLASTIC
The non-neoplastic enlargement of the ovary is usually due to accumulation of
fluid inside the functional unit of the ovary.
The causes are:
• Follicular cysts.
• Corpus luteum cyst.
• Theca lutein and granulosa lutein cysts.
• Polycystic ovarian syndrome.
• Endometrial cyst (chocolate cyst).
• Except the last one, all are functional cysts of the ovary and are loosely called
cystic ovary.
 NON-NEOPLASTIC
The features of the functional cysts are:
a. Related to temporary hormonal disorders.
b. Rarely becomes complicated.
c. Sometimes confused with neoplastic cyst but can be distinguished by :
a. Usually 6–8 cm in diameter.
b. Usually asymptomatic.
c. Spontaneous regression usually following correction of the functional disturbances to
which it is related.
d. Unilocular.
e. Contains clear fluid inside unless hemorrhage occurs.
f. Lining epithelium corresponds to the functional epithelium of the unit from which it
arises.
 FOLLICULAR CYSTS
• Follicular cysts are the commonest functional cysts.
• They are usually multiple and small as seen in cases of cystic glandular hyperplasia
of the endometrium or in association of fibroid.
• Cause Hyperestrinism
• An isolated cyst may be formed in unruptured Graafian follicle, which may be
enlarged but usually not exceeding 5 cm.
• The cyst is lined by typical granulosa cells without lutein cells or the cells may be
flattened due to pressure.
• In majority of cases, the detection is made accidentally on bimanual examination,
sonography, laparoscopy or laparotomy.
• The cyst may remain asymptomatic or may produce vague pain.
 FOLLICULAR CYSTS
Management
• A follicular cyst < 3 cm requires no further investigations.
• A simple cyst, < 8 cm, unilocular, echo free without solid areas or
papillary projections, with normal serum CA 125 should be followed
up with repeat ultrasound in 3 to 6 months time.
• Whenever a cyst persists or grow, it should be removed by
laparoscopy/laparotomy.
 CORPUS LUTEUM CYSTS
• Corpus luteum cyst usually occurs due to overactivity of corpus luteum.
• There is excessive bleeding inside the corpus luteum.
• In spite of the blood filled cyst, the progesterone and estrogen secretion
continues.
• As a result, the menstrual cycle may be normal or there may be amenorrhea or
delayed cycle.
• It is usually followed by heavy and/or continued bleeding.
• It is then confused with a case of threatened abortion or else, if the intracystic
bleeding is much, it may rupture producing features of acute intraperitoneal
hemorrhage with clinical picture simulating disturbed tubal ectopic pregnancy.
 CORPUS LUTEUM CYSTS
• It may often be associated with pregnancy and persists for about 12
weeks.
• Unless complicated, spontaneous regression is expected.
• If features of acute abdomen appears, laparotomy with enucleation of
the cyst is to be done along with resuscitative measures as in disturbed
tubal pregnancy.
• These two types of cysts are rather uncommon in women taking oral
contraceptive pills. As such, if the cyst persists after three months of
pill therapy, it is more likely to be a neoplastic cyst.
 LUTEIN CYSTS
• Lutein cysts are usually bilateral and caused by excessive chorionic
gonadotropin secreted in cases of gestational trophoblastic tumors.
• These may also be formed with administration of gonadotropins or
even clomiphene to induce ovulation.
• These are usually lined either by theca lutein cells, called theca lutein
cyst or by granulosa lutein cells, called granulosa lutein cyst.
• Spontaneous regression is expected within few weeks following
effective therapy of the tumors with the gonadotropin level returning
back to normal
 BENIGN OVARIAN NEOPLASMS
Incidence
• The incidence of ovarian tumor amongst gynecologic admission varies from 1–3%.
About 75% of these are benign.
Classification
• The ovarian tissues are constantly in a dynamic state.
• They are under the action of the gonadotropins and have got steroidogenic
potentialities.
• Even before puberty and after menopause, the ovarian tissues remain in a dynamic
state.
The principal ovarian tissue components are:
• Epithelial cells derived from the celomic epithelium.
BENIGN OVARIAN NEOPLASMS
The principal ovarian tissue components are:
• Epithelial cells derived from the celomic epithelium.
• Oocytes derived from the primitive germ cells.
• Mesenchymal elements from the gonadal stroma
BENIGN OVARIAN NEOPLASMS
WHO classification
1. Mucinous cyst adenoma
2. Serous cyst adenoma
3. Brenner tumor
4. Dermoid cyst
5. Endometrioid tumors
6. Clear cell tumors
These cysts constitute about 80 percent of the primary ovarian tumors and
are called ovarian cysts as opposed to cystic ovaries in functional ones
MUCINOUS CYST ADENOMA
• Origin
It arises from the totipotent surface epithelium of the ovary.
Its association with Brenner tumor suggests its origin as mucinous
metaplasia of the epithelioid cells.
Pathology
These are quite common and account for about 20–25 percent of all
ovarian tumors. The tumors are bilateral in about 10 percent cases. The
chance of malignancy is about 5–10 percent.
SEROUS CYST ADENOMA
Origin
Serous cyst arises from the totipotent surface epithelium of the ovary. It
is quite common and accounts for about 40% of ovarian tumors. It is
bilateral in about 40 percent and chance of malignancy is about 40%.
Pathology
The cysts are not so big as that of mucinous type. As the secretion is not
abundant, there is more chance of proliferation of the lining epithelium
to form papillary projection. As such, intracystic hemorrhage is more
likely. Often, the papillary growth projects outwards perforating the cyst
wall in about 15% cases.
BRENNER TUMOR
• Brenner tumor account for 1–2 percent of all ovarian tumors, 8–10 percent are bilateral
and usually seen in women above the age of 40.
• Majority are solid and are less than 2 cm in diameter.
• It usually arises from squamous metaplasia of surface epithelium.
• Gross picture of Brenner is similar to that of fibroma.
• Histologically islands of transitional epithelium (Walthard nests) in a compact fibrous
stroma are seen.
• The cells look like “coffee bean” as the nuclei have longitudinal grooves.
• They are usually benign in nature.
• Estrogen is secreted by the tumor and the woman may present with abnormal vaginal
bleeding.
• Unilateral oophorectomy in a young woman and total hysterectomy and bilateral
salpingo-oophorectomy in elderly women is the treatment choice
DERMOID CYST
Origin:
• Dermoid cyst arises from the germ cells arrested after the first meiotic division.
Pathology:
• Dermoid cyst constitutes about 97 percent of teratomata.
• Its incidence is about 30–40 percent amongst ovarian tumors.
• The tumor is bilateral in about 15-20 percent.
• It constitutes about 20–40 percent of all ovarian tumors in pregnancy. Torsion is
the most common (15–20%) and rupture is an uncommon (1%) complication.
• The chance of malignancy is about 1–2 percent. Squamous cell carcinoma is the
commonest.
 CLINICAL FEATURES OF BENIGN
TUMORS
Age
• Benign tumors predominantly manifest in the late childbearing period.
• Dermoid (90%) specially with mucinous cyst adenoma, is common in
the reproductive period.
• The dermoid is more common during pregnancy (10 percent).
Parity:
There is no correlation with parity of the patient (c.f. Fibroid — more
related with nulliparity
 CLINICAL FEATURES OF BENIGN
TUMORS
Symptoms:
Most tumors are asymptomatic.
These are detected accidentally by a general physician to find a lump in the lower abdomen
during routine abdominal palpation or by a gynecologist to find a tumor during pelvic
examination, laparoscopy or laparotomy.
• Heaviness in the lower abdomen.
• A gradually increasing mass in lower abdomen (ovarian tumor grows in months — c.f.
fibroid).
• Dull aching pain in lower abdomen.
• In neglected cases, the tumor may be big enough to fill whole of the abdomen.
• It then produces cardiorespiratory embarrassment or gastrointestinal symptoms like nausea
or indigestion.
 CLINICAL FEATURES OF BENIGN
TUMORS
• Menstrual pattern remains unaffected unless associated with hormone producing
tumors — menorrhagia or postmenopausal bleeding or precocious puberty in
feminizing tumorlike granulosa cell tumor or amenorrhea in masculinizing tumor-
like Sertoli-Leydig cell tumor
• Signs
• General condition remains unaffected.
• In huge mucinous cyst adenoma, the patient may be cachetic due to protein loss
• Pitting edema of legs may be present when a huge tumor presses on the great
veins.
• Abdominal examination: An ovarian tumor which is enlarged sufficiently so as to
occupy the lower abdomen presents with the following
 CLINICAL FEATURES OF BENIGN
TUMORS
• Abdominal examination: An ovarian tumor which is enlarged
sufficiently so as to occupy the lower abdomen presents with the
following
• Inspection: There is bulging of the lower abdomen over which the
abdominal wall moves freely with respiration. The mass may be
placed centrally or in one side. At times, the mass fills the entire
abdominal cavity everting the umbilicus with visible veins under the
skin; the flanks remain flat (c.f. Flanks are full with ascites)
• Palpation Feel is cystic or tense cystic. Benign solid tumors such as
fibroma, thecoma, Brenner tumor are rare.
 CLINICAL FEATURES OF BENIGN
TUMORS
• Percussion
• Percussion note is dull in the center and resonant in the flanks (c.f. In
ascites — just the opposite). A fluid thrill may be elicited when the
walls are thin and the content is watery. Co-existing ascites may be
present even in a benign solid tumor (fibroma) and is called Meigs’
syndrome.
 CLINICAL FEATURES OF BENIGN
TUMORS
• Auscultation: A friction rub may be present over the tumor (Hissing
sound over a vascular fibroid, gargling sound in ascites and FHS over a
pregnant uterus).
INVESTIGATIONS
• Ultrasonography
• MRI
• S. CA125
• EUA.
• Laparoscopy
• Straight X-ray of the abdomen over the tumor
• Laparotomy
• Cytology — When the patient presents with ascites or pleural effusion, cytological
examination of the aspirated fluid is done for malignant cells. Ultrasound guided
cyst aspiration for cytological diagnosis of malignancy is not recommended.
Complications Of Benign Ovarian Tumors
• Torsion of the pedicle (axial rotation)
• Intracystic hemorrhage Infection
• Rupture
• Pseudomyxoma peritonei
• Malignancy
Pseudomyxoma Peritonei
It is a condition of mucinous ascites usually secondary to mucinous
tumor of intra-abdominal organ. Its exact nature of origin is not known.
But it is often associated with mucinous cyst adenoma of the ovary,
mucocele of the appendix and gallbladder and intestinal malignancy.
Pseudomyxoma Peritonei
Spontaneous perforation of mucinous cyst may lead to implantation of
the cells of low grade malignancy on the peritoneum. Or else, the
mesothelium of the peritoneum is converted to high columnar
epithelium with secretory activity. The cell type is similar to mucinous
cyst adenoma.
MANAGEMENT OF A BENIGN OVARIAN
TUMOR
Once an ovarian tumor is diagnosed, the patient should be admitted for
operation — sooner the better. This is because, the complication can
occur at any time and the nature of the tumor cannot be assessed
clinically. A clinically benign tumor may turn into a malignant one at
operation. In others, even a benign tumor removed may be proved
malignant on histological examination.
VI. Premalignant lesions

• Premalignant vulval lesions include:

♦ Vulval intraepithelial neoplasia (VIN).
♦ Paget’s disease .
♦ Lichen sclerosus .
♦ Squamous cell hyperplasia .
♦ Condyloma accuminata
Vulval intraepithelial neoplasia (VIN).
• The different degrees of VIN are:
• VIN–I: Corresponds to mild cellular atypia. The lesion is limited to the
deeper one-third of the epithelium.
• VIN–II: Corresponds to moderate cellular atypia. The lesion is limited
up to middle-third of the epithelium.
• VIN–III:Corresponds to severe cellular atypia and carcinoma-in-situ.
The abnormal cells involve whole thickness of the epithelium. There is
no stromal invasion.
Vulval intraepithelial neoplasia (VIN).
• The chief complaints may be pruritus vulvae, lump or bleeding from a
vulval ulcer. It may be even symptomless.
Treatment of VIN
• Medical Medical treatment is done for young woman to control the
symptoms. Topical fluorinated steroid ointment can be applied twice
daily for a period of about 6 months. . Commonly used preparations
are 0.1 percent triamcinolone acetonide, or 0.1 percent
betamethasone valerate.
Vulval intraepithelial neoplasia (VIN).
• Surgery: The following are the types of surgery:
• ♦ Local excision
• ♦ Laser therapy
• ♦ Simple vulvectomy
PAGET’S DISEASE
This is a special type of VIN. The lesion grows horizontally within the
epidermis. The rete ridges tend to push into the dermis without
actually penetrating it.
PAGET’S DISEASE
The characteristic histologic picture is presence of Paget cells in the
epidermis. The cells are large— round or oval in shape with abundant
pale cytoplasm. There may be presence of mucopolysaccharides in
most of the cells. Nuclear mitotic figures are rare.
PAGET’S DISEASE
Symptoms are mainly pruritus, vulvar soreness, pain or bleeding. Local
examination reveals—labia majora appear red, scaling, with elevated
lesion. There may be associated white lesions. The skin is usually
indurated.
PAGET’S DISEASE
Treatment Simple vulvectomy is done. Multiple biopsies are to be taken
to exclude associated adenocarcinoma of the apocrine glands. If it is
found positive, bilateral lymph node dissection should be done at a
second stage.
Genital Malignancy
1. Vulval carcinoma
Incidence the lesion is rare, about 1.7 per 100,000 females. The distribution varies
from 3-5 percent amongst genital malignancies.
Etiology the etiology remains unclear. But the following factors are often related.
• Usually occurring in postmenopausal women with a median age of 60. ™ More
common amongst whites.
• Increased association with obesity, hypertension, diabetes and nulliparity. ™
Associated vulval epithelial disorders (lichen sclerosus) specially of atypical type
are the risk factors.
• Human papilloma virus (HPV) DNA (type 16, 18) has been detected in patients
with invasive vulval cancer.
1. Vulval carcinoma
• Vulval cancer may have a causal relation with condyloma accuminata
(HPV 6, 11), syphilis and lymphogranuloma venereum.
• Chronic pruritus usually preceds invasive vulval cancer. ™ Chronic
irritation of the vulva by chemical or physical trauma associated with
poor hygiene may be a predisposing factor.
• Other primary malignancies have been observed in about 20 percent
of cases with vulval cancer. Cervix is most commonly affected; other
sites are breast, skin or colon
1. Vulval carcinoma
• Pathology Sites: The commonest site is labium majus followed by
clitoris and labium minus. Anterior two-third are commonly affected.
Malignant ulcer on the contralateral side may be multifactorial
1. Vulval carcinoma
CLINICAL FEATURES
• Patient profile: The patients are usually postmenopausal, aged about 60 years often with obesity,
hypertension and diabetes.
• symptoms :
Asymptomatic
Pruritus vulvae
Swelling with or without offensive discharge
Difficulty in urination
Vulval ulceration
bleeding
inguinal mass
Pain
1. Vulval carcinoma
Signs
• Vulval inspection reveals an ulcer or a fungating mass on the vulva. The
ulcer has a sloughing base with raised, everted and irregular edges and
it bleeds to touch. Surrounding tissue may be edematous and indurated.
• Associated vulval lesions mentioned earlier may be present.
• Inguinal lymph nodes of one or both the sides may be enlarged and
palpable. The enlargement may also be due to infection.
• Clinical examination of the pelvic organs, including the cervix, vagina,
urethra and rectum must be done. This is due to the coexistance of
other primary cancers in the genital tract
1. Vulval carcinoma
STAGING
The staging is based on clinical examination and includes only the primary
carcinoma, excluding melanoma. The FIGO classification is widely used.
CAUSES OF DEATH
• Uremia—from ureteric obstruction due to enlarged common iliac and
paraaortic nodes.
• Rupture of the femoral vessels by the overlying involved inguinal lymph
glands
• Sepsis.
1. Vulval carcinoma
MANAGEMENT
Prophylactic
• Adequate therapy for non-neoplastic epithelial disorders of the vulva
• Adequate therapy for persistent pruritus vulvae in postmenopausal
women
• Frequent use of multiple biopsies in conservative treatment of VIN.
• Liberal use of simple vulvectomy in postmenopausal women with VIN
where follow-up facilities are not available.
1. Vulval carcinoma
MANAGEMENT
DEFNITIVE TREATMENT
• Microinvasive lesion
There is increased incidence of lymph node involvement in lesion of
more than 1 mm invasion.
It is thus prudent to perform radical vulvectomy with bilateral groin
node dissection in all cases of stromal invasion more than 1 mm.
If the invasion is less than 1 mm, wide local excision with or without
ipsilateral groin lymphadenectomy may be done with follow up.
1. Vulval carcinoma
MANAGEMENT
DEFNITIVE TREATMENT
• Microinvasive lesion
There is increased incidence of lymph node involvement in lesion of
more than 1 mm invasion.
It is thus prudent to perform radical vulvectomy with bilateral groin
node dissection in all cases of stromal invasion more than 1 mm.
If the invasion is less than 1 mm, wide local excision with or without
ipsilateral groin lymphadenectomy may be done with follow up.
1. Vulval carcinoma
If the general condition is poor and/or in presence of medical diseases The following
principles may be adopted:
• Two stage operation is preferred.
• Total vulvectomy followed by at a later date, bilateral inguinofemoral lymphadenectomy.
• Total vulvectomy followed by full pelvic and groin irradiation (megavoltage therapy).
• neoadjuvant chemotherapy—chemotherapy followed by surgery, radiotherapy or both.
• Technically inoperable or recurrent lesion
− Chemotherapy (cisplatin, bleomycin, 5-FU) can be used as radiation sensitizer.
− Chemoradiation therapy may be combined as primary therapy or following surgical
excision of the tumor.
− Radiotherapy can be used as a primary therapy for advanced disease.
BARTHOLIN’S GLAND CARCINOMA
The surgery is like that of squamous cell carcinoma of the vulva. In
addition, part of the lower vagina, levator ani and the ischiorectal fat are
to be removed.
Prognosis in a case of Bartholin gland carcinoma is similar to squamous
cell carcinoma when compared stage for stage of the disease.
 VAGINAL CARCINOMA
Incidence
• The incidence of primary vaginal carcinoma is very rare (about 0.6 per
100,000 women). It constitutes about 1 percent of genital
malignancies.
 VAGINAL CARCINOMA
• The primary site of growth is in the vagina.
• The cervix and the vulva must not be involved.
• There must not be clinical evidence of metastatic disease.
 VAGINAL CARCINOMA
Etiology:
• Exact etiology is unknown.
• HPV may have a causal relationship.
• Progression from vaginal intraepithelial neoplasia (VAIN).
• Women with history of cervical cancer (multicentric neoplasia).
• Diethyl stilboesterol (DES) is related with clear cell adenocarcinoma of the vagina.
This is found in those who had history of intrauterine exposure to diethyl stilboesterol.
• Previous irradiation therapy to the vagina or immunosuppression.
• Prolonged use of pessary.
• More common amongst whites than blacks.
CLINICAL FEATURES:
The mean age of the patient is about 55 years.
Symptoms
• May be asymptomatic, being accidentally discovered during routine screening
procedures.
• Abnormal vaginal bleeding including postcoital bleeding is conspicuously
present as an early symptom.
• Foul smelling discharge per vaginum.
Signs
• Speculum examination reveals an ulcerative, nodular or exophytic growth.
• The cervix looks apparently normal.
CLINICAL FEATURES:
diagnosis
• During cytology, screening procedure to detect abnormal cells.
Colposcopic examination and targeted biopsy are helpful for patients
with abnormal cytology or unexplained vaginal bleeding.
• Cystourethroscopy, proctosigmoidoscopy, CT/ MRI (for nodes), are
done.
• Biopsy from clinically suspected lesion
STAGING
Staging of vaginal carcinoma figo (1995)
Stage-0 carcinoma in situ
Stage-I carcinoma is limited to the vaginal wall.
Stage-II carcinoma has involved subvaginal tissue but has not extended to the
pelvic wall
Stage-III carcinoma has extended to the pelvic wall
Stage-IV carcinoma has extended beyond the true pelvis or has involved the
mucosa of the bladder or rectum.
a. Adjacent organs are involved (bladder, rectum)
b. b. Distant organs are involved
TREATMENT
Radiotherapy or surgery or the combination is the accepted modality of therapy for invasive
primary carcinoma of the vagina.
Choice depends on the clinical stage, anatomical location and size of the lesion.
Stage I
• Growth limited to the upper-third Radical hysterectomy, partial vaginectomy and bilateral
pelvic lymphadenectomy is the treatment of choice (as that of stage IB carcinoma cervix).
• Growth limited to the lower-third Radical vulvectomy with removal of bilateral
inguinofemoral lymph nodes along with vaginectomy.
Stage II–iv
• Radiation by external beam therapy with intracavity or interstitial radiation. Care is to be
taken to prevent bladder or rectal injury.
• Pelvic exenteration operation is done when there is failure with radiation therapy
RADIOTHERAPY
• Radiation therapy is widely used as a primary treatment for invasive
vaginal cancer.
• External radiation with 4500 to 5000 cGy is administered on the pelvis
encompassing the vagina. Additional 3000 to 4000 cGy is delivered
locally in the form of interstitial therapy (brachytherapy) with iridium
or cobalt.
• Teletherapy (external radiation) reduces the tumor volume and
sterilizes the regional (pelvic and inguinofemoral) lymph nodes.
• Complications of radiotherapy include vaginal stenosis, bladder and
rectal fistula.
SECONDARY
Secondary vaginal malignancy follows carcinoma vulva, cervix or
urethra by direct spread. Metastases in the lower-third of the anterior
vaginal wall or vault occur in cases of choriocarcinoma or endometrial
carcinoma.
CARCINOMA CERVIX
Magnitude of the problem
• incidence of cervical cancer is steadily declining in the developed world.
• Pap smear has reduced the incidence of cervical cancer by nearly 80
percent and death by 70 percent.
• Cervical cancer is an entirely preventable disease as the different screening,
diagnostic and therapeutic procedures are effective.
• At present throughout the globe, there are nearly 1 million women each
year having cervical cancer.
• Cancer cervix is the most common cancer in women of the developing
countries where screening facilities are inadequate
ENDOMETRIAL CARCINOMA
Etiology:
• estrogen—persistent stimulation of endometrium with unopposed estrogen is the
single most important factor for the development of endometrial cancer.
• age—about 75 percent are postmenopausal with a median age of 60 (c.F.
Carcinoma cervix is more common in perimenopausal period). About 10 percent
of women with postmenopausal bleeding have endometrial cancer.
• parity—it is quite common in unmarried and in married, nulliparity is associated
in about 30 percent. (C.F. – Carcinoma cervix is associated more with multiparae).
• late menopause—the chance of carcinoma increases, if menopause fails to occur
beyond 52 years.
• corpus cancer syndrome — encompasses – obesity, hypertension and diabetes.
ENDOMETRIAL CARCINOMA
• Obesity leads to high level of free estradiol as the sex hormone
binding globulin level is low.
• Unopposed estrogen stimulation --in conditions such as functioning
ovarian tumors (granulosa cell) or polycystic ovarian syndrome
(PCOS) is associated with increased risk of endometrial cancer.
Unopposed estrogen replacement therapy in postmenopausal women is
associated with increased risk of endometrial cancer. Use of cyclic
progestin reduces the risk. Prior use of combined oral contraceptives
reduces the risk significantly (50%).
ENDOMETRIAL CARCINOMA
• Tamoxifen is antiestrogenic as well as weakly estrogenic. It is used for
the treatment of breast cancer. Increased risk of endometrial cancer is
noted when it is used for a long time due to its weak estrogenic effect.
• Family history or personal history of colon, ovarian or breast cancer
increases the risk of endometrial cancer. Genetic inheritance (Lynch 11
syndrome family) is currently thought of
• Fibroid is associated in about 30 percent cases.
• Endometrial hyperplasia precedes carcinoma in about 25 percent
cases.
CLINICAL FEATURES
• Patient profile:
The patient is usually a nullipara, likely to be postmenopausal. There
may be history of delayed menopause. She may be obese; likely to have
hypertension or diabetes .
CLINICAL FEATURES
symptoms
• Postmenopausal bleeding (75%) which may be slight, irregular or
continuous. The bleeding at times may be excessive
• In premenopausal women, there may be irregular and excessive
bleeding.
• At times, there is watery and offensive discharge due to pyometra.
• Pain is not uncommon. It may be colicky due to uterine contractions
in an attempt to expel the polypoidal growth.
• Few patients (< 5%) remain asymptomatic.
CLINICAL FEATURES
Signs: There may be varying degrees of pallor
Pelvic examination: Speculum examination reveals the cervix looking
healthy and the blood or purulent offensive discharge escapes out of the
external os.
Bimanual examination reveals—The uterus is either atrophic, normal or
may be enlarged due to spread of the tumor, associated fibroid or
pyometra. The uterus is usually mobile unless in late stage, when it
becomes fixed.
Rectal examination corroborates the bimanual findings.
Regional lymph nodes and breasts are examined carefully
DIAGNOSIS OF ENDOMETRIAL
CARCINOMA
• history and clinical examination are to be recorded, as mentioned
earlier.
• endometrial biopsy
• papanicolaou smear is not a reliable diagnostic test for endometrial
carcinoma. It is positive only in 30 percent cases of endometrial
cancer.
• Ultrasound and color Doppler (TVS)
• Hysteroscopy
• Fractional curettage
DIAGNOSIS OF ENDOMETRIAL
CARCINOMA
• Computed Tomography (CT)
• Magnetic Resonance Imaging (MRI)
• Positron Emission Tomography
 MANAGEMENT OF ENDOMETRIAL
CARCINOMA
• ♦ Preventive
• ♦ Curative
 MANAGEMENT OF ENDOMETRIAL
CARCINOMA
• Preventive:
primary prevention includes
 strict weight control beginning early in life
To restrict the use of estrogen after menopause in nonhysterectomized women. If at
all it is needed, cyclic administration of progestogen preparations are added and
continued under supervision.
Education as regard the significance of irregular bleeding per vaginum in
perimenopausal and postmenopausal period.
Secondary prevention
• Screening of ‘high risk’ women at least in menopausal period to detect the
premalignant or early carcinoma is a positive step.
TREATMENT MODALITIES OF
CARCINOMA ENDOMETRIUM
• Surgery
• Radiotherapy
• Chemotherapy
• Combined therapy
RADIOTHERAPY
The primary treatment by radiotherapy is indicated in:
• Women found unfit for surgery
• Women with significant medical comorbidities.
• Surgically inoperable disease
• Those with high-risk of recurrence
• Patients with advanced disease for pallation therapy.
RADIOTHERAPY
Contraindications of radiotherapy:
Presence of a pelvic mass, pelvic kidney, pyometra, pelvic abscess,
previous laparotomies and/or adhesions with bowel and prior pelvic
radiation.
SARCOMA UTERUS
Incidence
• Sarcoma of the uterus is rare and constitutes about 3 percent of
uterine malignancy
Classification of uterine sarcomas (gynecologic oncology group)
• Leiomyosarcomas
• Endometrial stromal sarcomas
• Malignant mixed müllerian tumor (homologous and heterologous)
• Other uterine sarcomas.
SARCOMA UTERUS
Spread
blood borne: this is the commonest mode of spread. The organs
involved are liver, lungs, kidneys, brain, bones, etc.
directly to the adjacent structures.
lymphatic spread to the regional lymph glands.
SARCOMA UTERUS
Clinical features
• patient profile: the age is usually between 40 and 60 years. There may be
history of pelvic irradiation either for induction of menopause or malignancy.
• Symptoms:
there is no specific symptom.
irregular premenopausal or postmenopausal vaginal bleeding.
abnormal vaginal discharge — offensive, watery associated at times with
expulsion of fleshy necrotic mass.
abdominal pain — due to involvement of the surrounding structures
Pyrexia, weakness and anorexia.
SARCOMA UTERUS
Suspected sarcomatous change in a fibroid is evidenced by:
• postmenopausal bleeding.
• rapid enlargement of fibroid.
• recurrence following myomectomy or polypectomy. Pelvic
examination: there is no specific finding. The uterus may be enlarged
and irregular.
• Parametrium may be thickened and indurated.
• Speculum examination may reveal a polypoidal mass protruding out
through the external os.
SARCOMA UTERUS
Treatment
Total hysterectomy with bilateral salpingo-oophorectomy is to be done.
This should be followed by external pelvic radiation.
CARCINOMA FALLOPIAN TUBE
Primary
• primary carcinoma of the fallopian tube is very rare. The incidence of
tubal carcinoma is less than 0.5 percent of gynecological
malignancies.
• Predisposing factors are: infertility, nulliparity and family history of
ovarian cancer. Women with BRCA1 or BRCA2 mutations are at high
risk.
CARCINOMA FALLOPIAN TUBE
Clinical features:
patient profile — the patients are usually post-menopausal and nulliparous.
History of infertility and pelvic infection may be there.
Symptoms
• vaginal (postmenopausal) bleeding.
• intermittent profuse watery discharge (hydrops tubae profluens).
• colicky pain in lower abdomen.
Signs:
• bimanual examination reveals a unilateral mass which may be tender. If reduced in
size on compression, along with a watery discharge through the cervix, it is very much
suspicious.
CARCINOMA FALLOPIAN TUBE
Treatment
prophylactic
• surgery in high risk cases needs bilateral salpingo-oophorectomy once
child bearing is completed.
• Actual treatment: total hysterectomy with bilateral salpingo-
oophorectomy along with omentectomy. This should be followed by
platinum based combination chemotherapy as an adjuvant therapy. In
advanced cases, radiotherapy is considered .
CARCINOMA FALLOPIAN TUBE
Secondary
this is more common (90%) than the primary.
The common primary sites are ovary, uterus, breast and gastrointestinal
tract.
The mode of spread from the ovary or uterus is probably by lymphatics
rather than a direct one.
MALIGNANT OVARIAN TUMORS
• Incidence
ovarian malignancy constitutes about 15–20 percent of genital
malignancy.
MALIGNANT OVARIAN TUMORS
• Clinical features patient profile:
although no age is immune to ovarian malignancy, but about 60
percent of ovarian neoplasms in postmenopausal and about 20 percent
in premenopausal women are malignant.
There is increased association of nulliparity and with a family history.
MALIGNANT OVARIAN TUMORS
• Symptoms:
• In its early stage, ovarian carcinoma is a notoriously silent disease
(asymptomatic).
• The presenting complaints are usually of short duration and insidious
in onset.
• Symptoms are not specific.
• Feeling of abdominal distension and vague discomfort.
• Features of dyspepsia such as flatulence and eructations
MALIGNANT OVARIAN TUMORS
• Loss of appetite with a sense of bloating after meals.
• In pre-existing tumor. − Appearance of dull aching pain and tenderness over one area.
− Rapid enlargement of the tumor. Gradually, more pronounced symptoms appear.
These are:
1. Abdominal swelling which may be rapid.
2. Dull abdominal pain.
3. Sudden loss of weight.
4. Respiratory distress — may be mechanical due to ascites or due to pleural effusion.
5. Menstrual abnormality is conspicuously absent except in functioning ovarian
tumors (mentioned later in the chapter).
Signs: The following are the findings in an established case of ovarian malignancy.