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1. GYNACOLOGIC
ONCOLOGY
Arba Minch University
Department of Midwifery
For 3rd year Midwifery Students
BY YOSEF A.
(BSc.)

2. Introduction
Gynecologic oncology is a specialized field of
medicine that focuses on benign and cancers of
the female reproductive system, including ovarian
cancer, uterine cancer, vaginal cancer, cervical
cancer, and vulvar cancer.
*Pelvic mass-Pelvic masses may originate from gynecologic organs (cervix, uterus,
uterine adnexa) or from other pelvic organs (intestine, bladder, ureters, skeletal muscle,
bone).
*Adnexal mass-consist of the fallopian tube, ovary & broad ligaments.
Chapter Five- Benign & Malignant disorders of
the female Reproductive track
Chapter Six- The Breast

3. Definition of terms
• Tumor: An abnormal mass of tissue. Tumors are
a classic sign of inflammation, and can be benign
or malignant (cancerous).
• Neoplasm: (from Ancient Greek νεο- neo- "new"
and πλάσμα plasma "formation, creation"), also
commonly referred to as a tumor or tumour, is
an abnormal growth of tissue. This abnormal
growth usually but not always forms a mass.
• The terms,tumors and neoplasm, are used
interchangeably.

4. • The World Health Organization classifies
neoplasms into four main groups: benign
neoplasms, in situ neoplasms, malignant
neoplasms, and neoplasms of uncertain or
unknown behavior.
• Benign: refers to a condition, tumor, or growth
that is not cancerous. This means that it does
not spread to other parts of the body. It does
not change or destroy nearby tissue.
Sometimes, a condition is called benign to
suggest it is not dangerous or serious.

5. • Malignant: refers to cancerous cells that have the
ability to spread to other sites in the body
(metastasize) or to invade and destroy tissues.
Malignant cells tend to have fast, uncontrolled
growth due to changes in their genetic makeup.
• Malignant types of cells are generally called
CANCER.
• Hyperplasia is increased cell production in a
normal tissue or organ.
• Hypoplasia is an underdevelopment or incomplete
development of a tissue or an organ.

7. Anatomy Revision

8. External Genitalia
• The vulva refers to
those parts that are
outwardly visible
• The vulva includes:
– Mons pubis
– Labia majora
– Labia minora
– Clitoris
– Urethral opening
– Vaginal opening
– Perineum
Individual differences in:
Size
Coloration
Shape
are common

9. MONS PUBIS
• The triangular mound of fatty tissue that covers the pubic bone
• During adolescence sex hormones trigger the growth of pubic hair on the mons
pubis
• Hair varies in coarseness curliness, amount, color and thickness
LABIA MAJORA
• Referred to as the outer lips
• They have a darker pigmentation
• Protect the introitus and urethral openings
• Are covered with hair and sebaceous glands
• Tend to be smooth, moist, and hairless
LABIA MINORA
• Referred to as the “inner lips”
• Made up of erectile, connective tissue that darkens and swells during sexual
arousal
• Located inside the labia majora
• They are more sensitive and responsive to touch than the labia majora
• The labia minora tightens during intercourse
CLITORIS
• Highly sensitive organ composed of nerves, blood vessels, and erectile tissue
• Located under the prepuce
• It is made up of a shaft and a glans
• Becomes engorged with blood during sexual stimulation
• Key to sexual pleasure for most women
• Urethral opening is located directly below clitoris

10. Vaginal Opening - Introitus
• Opening may be covered by a thin sheath called
the hymen
• Using the presence of an intact hymen for
determining virginity is erroneous
• Some women are born without hymens
• The hymen can be perforated by many different
events

11. Perineum
• The muscle and tissue located between the vaginal opening
and anal canal
• Contains an abundance of nerve endings that make it
sensitive to touch
• An episiotomy is an incision of the perineum used during
childbirth for widening the vaginal opening

12. INTERNAL GENITALIA
The internal Genitalia
consists of the:
• Vagina
• Cervix
• Uterus
• Fallopian Tubes
• Ovaries

13. Vagina
• The vagina connects the
cervix to the external genitals
• It is located between the
bladder and rectum
• It functions
– As a passageway for the
menstrual flow
– For uterine secretions to
pass down through the
introitus
– As the birth canal during
labor
– With the help of two
Bartholin’s glands becomes
lubricated during sexual
arousal

14. Cervix
• The cervix connects the
uterus to the vagina
• The cervical opening to
the vagina is small
• This acts as a safety
precaution against
foreign bodies entering
the uterus
• During childbirth, the
cervix dilates to
accommodate the
passage of the fetus
• This dilation is a sign
that labor has begun
(10 cm)

15. Uterus
• Commonly referred to as
the womb
• A pear shaped organ
about the size of a
clenched fist
• It is made up of the
endometrium,
myometrium and
perimetrium
• Consists of blood-
enriched tissue that
sloughs off each month
during menstrual cycle
• The powerful muscles of
the uterus expand to
accommodate a growing
fetus and push it through
the birth canal

16. Fallopian Tubes• Serve as a pathway for the
ovum to the uterus
• Are the site of fertilization
by the male sperm
• Often referred to as the
oviducts or uterine tubes
• Fertilized egg takes
approximately 6 to 10
days to travel through the
fallopian tube to implant
in the uterine lining
• Site of Ectopic Pregnancy
• Tubal Ligation:
Sterilization

17. Ovaries• The female gonads or sex
glands
• They develop and expel
an ovum each month
• A woman is born with
approximately 400,000
immature eggs called
follicles
• In a lifetime: about 400
to 500 fully matured eggs
for fertilization
• The follicles in the ovaries
produce the female sex
hormones, progesterone
and estrogen
• These hormones prepare
the uterus for
implantation of the
fertilized egg

18. It consists of
• Benign and malignant disorders of the female
genital track as a whole.
• Benign and malignant disorders of
1- the vulva
2- the vagina
3- the cervix
4- the uterus
5- the fallopian tube
6- the ovary

19. Benign disorders of the Vulva,
Vagina, & Cervix

20. Objectives
• List out the types of benign disorders of the
vagina vulva and cervix
• List out the types of malignant disorders of the
vagina vulva and cervix
• Explain the clinical features of the disorders
• Explain the diagnosis of those disorders
• Explain the management protocols of those
disorders

21. • Vulvular lesions
• Pigmentation abnormalities
• Vulvovaginal swelling
• Congenital anomalies

22. Vulvar lesions
• A wide spectrum of benign, premalignant, and
malignant lesions involve the vulva.
• The challenge is to differentiate among normal
variants, benign findings, and potentially serious
disease, which is not always easy.
• The most useful means of generating a differential
diagnosis of vulvar lesions is by morphologic findings
rather than by symptomatology, which is often nonspecific.

23. I. Vulvar intraepithelial disorders

24. 1.Lichen sclerosus
• Lichen sclerosus (LS):- a benign, chronic,
progressive dermatologic condition characterized
by:-
– marked inflammation,
– epithelial thinning, and
– distinctive dermal changes (fibrosis)
• The previous designation "et atrophicus" was
dropped because areas of thickening and
hyperplasia often occur (mixed dystrophy).

25. Continued…
• LS can develop on any skin surface,
– Anogenital region (85 to 98 %).
– Extra genital lesions in 15 to 20 percent of patients.
• Causes itching and pain
• Usually occurs in postmenopausal women,
– although men, children, and premenopausal women
may also be affected.
• It is one of the most common conditions treated
in vulvar clinics

26. Continued…
ETIOLOGY — The etiology of LS is unknown.
• A number of mechanisms have been proposed based
upon epidemiologic data.
1. Genetic factors
– A familial association between fathers and daughters,
mothers and daughters, sisters, and in identical and
fraternal twins has been reported .
– Trauma, injury, and sexual abuse have been
suggested as possible triggers of symptoms in
genetically predisposed individuals
2. Immunological abnormality
- Disorders of the immune system are more common

27. Continued…
3.Hormonal factors
– patients with LS have decreased serum levels of
dihydrotestosterone, free testosterone, and
androstenedione
4. Infection
– eg, Borrelia burgdorferi, variably acid fast bacteria,
HPV
5. Local factors
– a graft placed on the vulva developed LS and
– skin with LS from the vulva became normal when
grafted to the thigh
– This suggests local vulvar factors may facilitate

28. CLINICAL MANIFESTATIONS
A. Asymptomatic; careful inspection
B. Vulvar pruritus, is the hallmark of the disease, this
is not specific to LS
C. Pruritus ani, painful defecation, anal fissures, and
rectal bleeding are common
D. Dyspareunia is often a late symptom associated with
introital stenosis, fissures,
E. Dysuria and difficulty voiding
 symptoms = due to continuing inflammation and
anatomic changes and scarring from long-standing
active disease

29. Physical examination
Classic LS is expressed
– thin, white, wrinkled
skin localized to the
labia minora and/or
labia majora
– the whitening may
extend over the
perineum and around
the anus in a keyhole
fashion

30. Physical examination
• Excoriations and
lichenification may be
observed, often associated
with edema of the labia
minora and the prepuce.
• Relatively minor rubbing or
intercourse may lead to
hemorrhage and/or
petechiae with purpura and
ecchymoses due to the
fragility of the involved skin

31. Early versus late disease
Early LS= the vulvar
architecture remains intact.
Late LS= the distinction
between the labia majora
and minora is lost and the
clitoris becomes buried
under the fused prepuce
End-stage LS = results in a
pallid, featureless vulva
with midline fusion leaving
only a posterior pinhole
orifice.
– In contrast, the vagina and
cervix are not involved.

32. DIAGNOSIS —
The diagnosis of LS is based upon:-
• characteristic clinical manifestations plus
• histological (immunofluorescent staining).
– The epidermis is typically thinned, although areas
of hyperkeratosis may be observed,
– and there is acanthosis and flattening of the rete
pegs.
– The upper dermis is hyalinized with a band of
lymphocytes below this region.

33. Differential diagnosis —
• Estrogen deficiency
– is also associated with a thinned epidermis, labial
adhesion, and dyspareunia;
– failure to respond to topical estrogen within two
weeks of treatment should prompt a vulvar biopsy.
• Vitiligo
– produces whitening and can be confused with LS if
other manifestations of the disease are minimal.
• Anal fissure or hemorrhoids,
– Anal involvement with LS is sometimes confused
with leading to unnecessary surgery.
• SC Hyperplasia

34. ASSOCIATED MALIGNANCY
• The generally reported risk of associated SCC is 4 to
6 percent.
• SCC in patients with LS does not appear to be HPV
mediated
• The skin of patients with vulvar LS should be
examined at least yearly for the remainder of the
patient's life.

35. TREATMENT —
• Goal is to relieve symptoms and discomfort,
prevent further anatomical changes, and
possibly for prevention of malignant
transformation
• Therapy comprises
– patient education,
– behavioral modification and support,
– medication
– Surgery is reserved for a small subset of cases.

36. Medication — for all patients with LS,
1.Topical steroids —
– superpotent topical ointment
– (eg, clobetasol 0.05 % ointment daily 6-12wks then
1-3x/wk for maintenance)
2. Intralesional steroids -Thickened plaques
– 5 to 20 mg of triamcinolone
3. HRT - for PM vulvovaginal atrophy
Surgery
- is only indicated for the postinflammatory
sequelae of the disease and when malignancy
is present.

37. Abnormalities of pigmentation
• The color of vulva depends on:-
– Vascularity of the dermis
– Thickness of the epidermis &
– Amount of pigment (melanin, bd-pigment)

38. A. White lesions
• Melanocytes loose their ability to manufacture
melanine = depigmentation & subsequent
WHITE lesion:-
– Lichen Sclerosis
– SC-Hyperplasia
– Leukoderma
– Vitiligo
– Albinizm
– Neoplasia

39. B. Red Lesions
Red lesions are due to:-
- Thinning, ulceration, vasodilitation of
inflamation or immune response, or
neovascularization of neoplasia
• Infections
• Dermatitis
• Invasive epidermoid cancer
• Melanosis
• Psoriasis

40. C. Dark lesions
• Ca in situ of vulvar skin
• Acanthosis nigricans
• junctional nevi
• Dermatofibroma
• Extramammary breast
• Kaposi's sarcoma
• Dysplastic nevi and melanoma

41. Acanthosis nigricans
• typically appears as dark,
velvety plaques in axillary
and nuchal areas.
• Most affected patients are
obese.
• may be cutaneous
manifestation of systemic
illness (endocrinopathy or
malignancy)

42. Summary
• Generating a DDX = morphology than by SSX.
• In all patients, one or more vulvar biopsies if clinically
suspicious for malignancy
– (asymmetry, border irregularity, color variation, rapid change,
bleeding, non-healing).
• Most common white lesions are lichen sclerosus, leukokeratosis,
and vitiligo.
• Black, or red vulvar lesions can be due to a wide variety of
benign, infectious, inflammatory, and malignant conditions.
• General principles of treatment of vulvar disorders include good
hygiene and soaks for symptomatic relief.
• Specific hormonal, antimicrobial, immunomodulating,
antiinflammatory, or surgical therapies depend on the specific
diagnosis.

43. Vulvovaginal Swellings
A. Cysts
1. Bartholini’s gland cyst / abscess
2. cyst of canal of Nuck
4. Gartner’s cyst
3. Sebaceous cyst
B. Tumors
1. Benign tumors (fibroma, lipoma, neurofibroma, endometriosis)
2. Hernias
3. Vulvar varicosities
4. Elephantiasis vulvae

44. A. Bartholini’s gland cyst / abscess
• Secrete mucus to provide moisture for the vulva;
• Homologue of bulbourethral glands in the male.
• Located bilaterally in four and eight o'clock positions on the
posterior-lateral aspect of the vaginal orifice.
• Each gland is approximately one-half centimeter (cm) in size
and drains into a duct 2.5 cm long.
• Occur in 2 percent of women; carcinoma is rare
• many vaginal and vulvar lesions mimic Bartholin's gland
disorders and should be considered in the differential diagnosis
of a vulvovaginal mass

45. Cause:-
• Inflammation/trauma
Diagnosis:-
• Usually asymptomatic
• Larger cysts - vulvar pain,
discomfort (sex)
• Dx is clinical and based
upon findings of a soft,
painless mass in the
medial labia majora or
lower vestibular area.

46. Treatment
1. Leave it if no SSX
2. Incision & drainage
– there is a tendency for cysts to
recur
3. Word catheter A’ 2”
– balloon-tipped device that can
be placed into the cyst cavity
immediately after incision and
drainage
– inflated and left in place for at
least two to four weeks
4. Sclerotherapy — Silver nitrate
sticks can be inserted into the cyst
cavity to necrotize the cyst wall
5. Marsupialization
6. Excision

47. Marsupialization —
• a new ductal orifice is created by
excising a 1 to 2 cm oval portion
of the vulvar roof of the cyst
behind the hymenal ring.
• The proximal duct wall is then
everted onto the introital mucosa
with sutures, thus creating a
fenestration for egress of
glandular secretions.
• performed with local anesthesia.
• We resort to this method after
failure of one or two placements
of a Word catheter.

48. Complication
• Bartholin’s Abscess
– Are polymicrobial infections, sts STI
– Should have both routine cultures (for anaerobic and
aerobic bacteria) and specialized tests for gonorrhea
and chlamydia taken of the abscess in conjunction
with surgical therapy (drain pus).
– Examination and treatment of partners
– Severe pain and swelling that they are unable to walk,
sit, or have sexual intercourse.
– On examination, the lesion appears as a large, tender,
soft or fluctuant mass

49. Treatment
• Immidiate surgical drainage
• Antibiotics
Ceftriaxone 125 mg IM stat or
Cefixime 400 mg orally
to cover E. coli and N. gonorrhoeae plus
Clindamycin (300 mg qid po 4x/day 7 days
to cover anaerobic organisms.
The regimen may have to be modified based
upon culture results

50. Congenital Abnormalities
• EMBRYOLOGY — The development of the
female genital tract begins at three weeks of
gestation and continues into the second
trimester of pregnancy.
• is a complex process dependent upon a series
of intricate events involving cellular
differentiation, migration, fusion, and
canalization.
• Failure of any one of these processes results in
a congenital anomaly.

51. • Uterus and fallopian tubes,& upper Vagina= müllerian
• Lower Vagina = urogenital sinus
 The development of the gonads occurs independent from
that of the genital tract;
 The formation of the reproductive tract is closely associated
with the development of the urinary system,
 Disruption of normal embryologic processes of the
müllerian ducts, such as
agenesis, failure of lateral fusion, or failure of
canalization,
 result in development of the various congenital anomalies

52. EMBRYOLOGY

54. ANOMALIES OF THE HYMEN
1. Imperforate hymen
• from incomplete
degeneration of the
central portion of the
hymen.
• infants = mucocolpos
• adolescent = cyclic pain
& hematocolpos
• Rx = elliptical incision

55. ANOMALIES OF THE VAGINA
1. Transverse vaginal septum
• failure of fusion and/or canalization of the urogenital sinus and müllerian
ducts,
• occurs in approximately 1 in 30-80,000
• These septa may be located at various levels in the Vx
• Clinical manifestations = same as above
• Ultrasonography or magnetic resonance
– Location & thickness;
– differentiate between a high septum and congenital absence of the
cervix.
• Rx = resection, followed by an end-to-end anastomosis of the upper and
lower vaginal mucosa.

56. Transverse vaginal septa

57. Transverse vaginal septum

58. Longitudinal vaginal septum
2. Longitudinal vaginal septum
• typically associated with uterine anomalies, septate &
didelphys.
• septum may be partial or complete.
SSX =
• difficulty inserting tampons, persistent bleeding despite
tampon placement, dyspareunia, or she may be
asymptomatic.
Treatment —complete removal of the septum.

59. 3. Vaginal agenesis,
– müllerian aplasia or Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome,
• refers to congenital absence of the vagina with variable uterine
development.
• usually accompanied by cervical and uterine agenesis;
• incidence = 1 in 5000
• 25 to 50 percent have urologic anomalies
• 10 to 15 percent have skeletal anomalies
• CF = Amenorrhea + normal SSC

60. Vaginal agenesis

61. Intraepithelial Neoplasia of the
Vagina

62. Clinical Profile
• The incidence of vaginal intraepithelial
neoplasia (VAIN) is not well described. The
first report apparently was by Graham and
Meigs in 1952. They reported on three patients
with carcinoma of the vagina, two
intraepithelial and one invasive, that were
discovered 6, 7, and 10 years, respectively,
after total hysterectomy for CIS of the cervix.
The most recent analysis of the incidence of
VAIN in the United States, published in 1977,

63. Risk factors
• VAIN has many of the same risk factors
associated with cervical intraepithelial
neoplasia, including smoking, earlier age at
first intercourse, increased number of sexual
partners, and human papillomavirus (HPV)
infection.
• Patients with VAIN tend to have either an
antecedent or coexistent neoplasia in the lower
genital tract. This is the usual situation in at
least half to two thirds of all patients with
VAIN. In patients who have been treated for

64. Diagnosis
• The diagnosis is confirmed by biopsy. The extent
of the lesion can be evaluated with the colposcope
or with Lugol’s solution. Almost all lesions are
asymptomatic, although a patient will
occasionally have discharge or postcoital staining.
• Colposcopic examination Each of the four walls
should be examined from the apex to the introitus
as separate and sequential steps
• Small biopsy specimens are taken with a Tischler
or Kevorkian–Younge alligator-jaw forceps.
Normal vaginal epithelium is stained brown,
whereas dysplastic lesions with abnormal

65. Presentation
• The majority of VAIN is multifocal; even if a
lesion is identified, one must search the entire
vagina for coexisting, multiple lesions. Lesions
are more common in the upper third of the
vagina, but disease-free skip areas may be
encountered with additional VAIN in the lower
vagina.

66. Management
• Local excision of the involved area has been
the mainstay of therapy. In many cases, a
single isolated lesion can be removed easily in
the office with biopsy forceps. If larger areas
are involved, an upper colpectomy may be
necessary if the lesion is to be removed by
surgery.
• A dilute pitressin solution or lidocaine with
epinephrine can be injected submucosally at
the beginning of the procedure and will greatly

67. • As in CIN, outpatient modalities of therapy
have been investigated for VAIN. Many
patients have been treated historically with 5-
fluorouracil (5-FU), but toxicity has decreased
enthusiasm for this option
• More recently, experience with 5% imiquimod
cream in the management of VAIN has been
reported.
• Ultrasonic surgical aspiration has been
successfully used by Robinson, von

68. Intraepithelial Neoplasia
of the Vulva (VIN)

69. Classification
• Classification of Vulvar Intraepithelial
Neoplasia (Vin) of the vulva
• A ---VIN, usual type
• 1-Warty type
• 2-Basaloid type
• 3-Mixed (warty/basaloid) type
• B ---VIN, differentiated type

70. • Two distinct subtypes of VIN exist: usual type
and differentiated type. The two subtypes are
different in epidemiology, morphology, and
their association with vulvar cancer.
Differentiated type may also be called simplex
VIN, whereas usual type may be called warty,
basaloid, or undifferentiated VIN. In
comparison to usual type, differentiated type
tends to occur in older women, be unifocal and
unicentric, be found at the edge of vulvar
squamous cell carcinoma and in the setting of
lichen sclerosus or planus, and be less
associated with HPV. Usual type VIN, with
warty and basaloid subtypes, is found in

71. • According to a SEER data analysis by Judson
and colleagues, the incidence of vulvar CIS
increased 411% between 1973 and 2000
• This is due to increased physician awareness
and evaluation of vulvar disease, increased
prevalence of smoking among women, and
increased HPV prevalence.
• Women with a history of preinvasive cervical
disease or cervical cancer are at increased risk
of preinvasive vulvar dysplasia. HPV is a risk
factor for vulvar disease, but the progression

72. • HPV is strongly associated with VIN usual
type, but it is less commonly associated with
VIN differentiated type.
Sn
• The disease is asymptomatic in more than 50%
of cases. In the remainder of cases, the
predominant symptom is pruritus. The
presence of a distinct mass, bleeding, or
discharge strongly suggests invasive cancer.
The most productive diagnostic technique is
careful inspection of the vulva in bright light
during a routine pelvic examination followed

74. Management
• Surgical excision has been the mainstay of
therapy for VIN, although laser is a frequently
used technique and immune modulators have
gained recent prominence. Occasionally, a
skinning vulvectomy is indicated.
• Excision, Laser, Cavitational Ultrasonic
Surgical Aspirator, Imiquimod.

75. Congenital cervical anomalies
and benign cervical lesions

76. DEVELOPMENTALABNORMALITIES
- occurs:-
• If one or both müllerian ducts fail to fuse,
• or if development of one or both ducts does
not occur, or is incomplete,
– complete absence or
– duplication of the cervix can occur.

77. 1. Duplications
• can exist with two distinct cervixes or can be more
subtle with two fused cervixes.
• Coexistent UT- abnormalities are common
• Nonobstructive duplication of the cervix is usually
asymptomatic and does not require treatment.
• Obstructive lesions require surgical therapy if they
result in hematometra or pyometra.

78. Duplications

79. Cervical agenesis and hypoplasia
2. Cervical agenesis and hypoplasia
• are rarely encountered.
• With complete agenesis, both the cervix and the upper vagina must
be absent
• When hypoplastic, the vagina can be normal
• Adolescents = primary amenorrhea, cyclic or chronic
abdominopelvic pain, and possibly a pelvic mass
• differentiate between a high transverse vaginal septum and cervical
agenesis,
• Rx = hormone suppressive therapy (GnRH agonist)
– she can maintain her uterus with the plan for ART & a
planned abdominal delivery of the child

80. Cervical agenesis and hypoplasia

81. 2. ECTROPION —
- replacement of squamous cells on the portio of
the cervix by overgrowth of columnar epithelium
• Dynamic SCJ – EE2 dep.
– Neonates, pill users, pregnancy, infection
• reddish appearance covered by a yellow turbid
discharge.
• treated if excessive mucous discharge
– acid-buffered vaginal jelly.
– Ablation = cryocautery or electrocautery

82. ECTROPION

83. Cervical cysts
1.Nabothian cysts
• cystic structures that form when a cleft of tall,
columnar epithelium becomes covered with
squamous cells and cells continue to secrete
mucoid material.
• The cysts vary from microscopic to several
centimeters in size.
• pain or feeling of fullness in the vagina.

84. Nabothian cysts

85. Cervical cysts
• 2. Mesonephric cysts
- forms a cyst that may be confused with a Nabothian cyst.
- They seldom reach a size greater than 2.5 cm, and are usually
located at the three and nine o'clock points,
• 3. Endometriosis
- May form cystic structures on the portio vaginalis that appear
as red or blackish areas ("powder burns")
4. Adenosis
- is characterized by columnar epithelium with surrounding
fibromuscular stroma,
- can be associated with intrauterine (DES) exposure

86. Neoplasms
1.Cervical Polyp
• commonly occur during the reproductive years.
• The etiology is unknown.
• Chronic inflammation & hormonal factors
• usually arise from the endocervical canal, but
can also originate from the portio.
• The size is typically less than 3 cm
• Malignant change is rare.

87. Neoplasms
2. Leiomyoma
• rare to find it isolated to the cervix.
• can be subserosal, intramural, or submucous
and can distort the cervical canal or upper
vagina.
• symptoms such as bladder or bowel
dysfunction, bleeding, or dyspareunia
• A type of smooth muscle tumors conditions

88. Cervical Elongation
• Vaginal or supravaginal can be affected
A. Supravaginal – ass with P-relaxn.
– Asymptomatic, shallow fornix, long canal
B. Vaginal – Congenital / chronic cervicitis
– Dyspareunia, fullness, infertility
– Deep fornix,

89. Others
• 1. cervical traumas
• 2. cervical stenosis
• 3. STI