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Cervix,Vagina, andVulva


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Here is a normal cervix with a smooth, glistening mucosal surface. There

is a small rim of vaginal cuff from this hysterectomy specimen. The

cervical os is small and round, typical for a nulliparous woman. The os

will have a fish-mouth shape after one or more pregnancies.


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This is normal cervical non-keratinizing squamous epithelium. The squamous

cells show maturation from basal layer to surface.


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The normal adult vaginal mucosa with a wrinkled appearance that is seen in

women of reproductive years appears at the left. The cervix has been opened to

reveal an endocervical canal leading to the lower uterine segment at the right

that has an erythematous appearance extending to the cervical os consistent

with chronic inflammation.


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Genital Infections

Sexually Transmitted Genital Infections

Infectious diseases of the female genital tract

are common and are caused by many

pathogenic organisms

Most of the important infectious diseasesaffecting the female genital tract are sexually

transmitted


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VIRAL INFECTIONS

Human Papillomavirus

Human papillomavirus (HPV) is a DNA virusthat infects a number of skin and mucosal

surfaces to produce wart-like lesions, referred

to as verrucae and condylomata (Fig. 18-2).

FIGURE 18 2 H ill i i d d d l t i f ti A


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FIGURE 18-2. Human papillomavirus-induced condylomatous infections. A.

Condyloma acuminatum on the cervix, visible with the naked eye as cauliflower-

like excrescences. B. A cervical smear contains characteristic koilocytes with a

perinuclear halo and a wrinkled nucleus that contains viral particles. C. Biopsy

of the condyloma shows koilocytes with perinuclear halos but lacking nuclear

atypia.


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More than 100 HPV serotypes are known,

one-third of which cause genital tract lesions.

In the United States, as many as two thirds of graduatingcollege women have genital HPV infections, which resultfrom sexual contact with an infected person.

Approximately 20 million people are currently infected withHPV in this country.

HPV types 6 and 11 are detected in more than 80% ofmacroscopically visible condylomata.

Several strains of HPV are the major etiologic factors forsquamous cell cancer in the female lower genital tract.

Types 16 and 18 are associated with about 60% of cases;

types 31, 33, 45, 52, and 58 account for most otheroccurrences of intraepithelial neoplasia and invasivecancer (see the section on the cervix below).


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Most cases of HPV are diagnosed by cervical Papsmear.

Tests that directly assay for HPV DNA are seeing

increasing clinical use. Treatment for HPV infection has been inadequate,

and most infections spontaneously disappear.

A recently approved prophylactic vaccine directed

against four common serotypes of HPV potentiallyprovides protection against the HPV strainsresponsible for 70% of cervical cancer and 90% ofcervical warts and is recommended for all females

between the ages of 9 and 26.


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This is chronic cervicitis at the squamo-columnar junction of the cervix.

Small round dark lymphocytes are seen in the submucosa, and there is

also hemorrhage. Chronic cervicitis is quite common.


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The normal cervical squamous epithelium at the left transforms to

dysplastic changes on the right. There is also underlying chronic

inflammation because abnormal epithelial surfaces do not provide the

same protective barrier as normal epithelial surfaces do.


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Cervical squamous dysplasia is seen at medium magnification, extending from

the center to the right. The epithelium is normal at the left. Note how the

dysplastic cell nuclei at the right are larger and darker, and the dysplastic cells

have a disorderly arrangement. This dysplastic process involves the full

thickness of the epithelium, but the basal lamina is intact, so this is a high grade

squamous intraepithelial lesion (HSIL) that can also be termed cervical


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Dysplasias may also involve the vulvar epithelium, seen here at the right with

overlying hyperkeratosis (producing an area of leukoplakia), with more normal

(but atrophic) keratinizing squamous epithelium at the left. Most cases of

vulvar intraepithelial neoplasia (VIN) do not progress to invasive cancer. Many

are multicentric, and some occur in association with cervical or vaginal


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This is a Pap smear. The cytologic features of normal squamous epithelial cells

can be seen at the center top and bottom, with orange to pale blue plate-like

squamous cells that have small pyknotic nuclei. The dysplastic cells in the

center extending to upper right are smaller overall with darker, more irregular


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This is why you do Pap smears--to prevent invasive squamous cell

carcinomas from occurring. With Pap smears, pre-neoplastic and neoplastic

cervical lesions can be detected when small and treated. Nests of squamous

cell carcinoma have invaded underlying stroma at the center and left.


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At high magnification, nests of neoplastic squamous cells are invaded

through a chronically inflamed stroma. This cancer is well-

differentiated, as evidenced by keratin pearls. However, most cervical

squamous carcinomas are non-keratinizing.


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This is the gross appearance of a cervical squamous cell carcinoma

that is still limited to the cervix (stage I). The tumor is a fungating red totan to ellow mass.


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Here is another cervical squamous cell carcinoma. Note the IUD string

protruding from the cervix. This implies that someone could have done

a Pap smear when it was inserted. There is a natural history of

progression of dysplasia to carcinoma, so don't leave dysplasias alone.


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This is a pelvic exenteration done for stage IV cervical carcinoma. At the left,

dark vulvar skin leads to vagina and to cervix in the center, where an irregular

tan tumor mass is seen infiltrating upward to the bladder. A slit-like endometrial

cavity is surrounded by myometrium at the mid-right. The rectum and sigmoid

colon are at the bottom extending to the right.


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This is another pelvic exenteration for cervical squamous cell

carcinoma. The irregular grey-brown tumor extends toward bladder


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VULVACYSTS

Bartholin Gland Cysts:

The paired Bartholin glands located immediately

posterolateral to the introitus produce a clear mucoidsecretion that continuously lubricates the vestibular surface.

The ducts are prone to obstruction and consequent cysts.

In turn, cyst infection leads to abscess formation.

Staphylococci, chlamydia, and anaerobes are frequently thecause.

Treatment consists of incision, drainage, marsupialization, and

appropriate antibiotics.


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Follicular Cysts:

The follicular cyst recapitulates the most distal

portion

of the hair follicle.

Also termed epithelial inclusion cysts or

keratinous

cysts, follicular cysts frequently appear on thevulva,

especially the labia majora.

They contain a white cheesy material and


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Mucinous Cysts:

Mucinous glands of the vulva occasionally

becomeobstructed and subsequently cystic.

Mucinous columnar cells line the cyst and may

becomeinfected.


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Mal ignant Tumors and

Premal ignant Condi t ions

Vulvar Intraepithelial Neoplasia (VIN) is a Precurs or o f Invasive

Cancer

VIN reflects a spectrum of neoplastic changes that range from minimal

cellular atypia to the most marked cellular changes short of invasive

cancer.

Between 1983 and 2000, there has been about a twofold increase in the

frequency of VIN, much of which occurs in women under the age of 40years.

As with comparable lesions in the cervix (cervical intraepithelial neoplasia

[CIN]), VIN is a precursor of vulvar squamous cell carcinoma, of which at

least 30% to 40% of cases are caused by HPV.


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Pathology:

The lesions of VIN may be single or multiple, and macular,

papular, or plaque-like.

Microscopically, the grades are labeled VIN I, II, and III,

corresponding to mild, moderate, and severe dysplasia,respectively.

Grade III also includes squamous cell carcinoma in situ

(CIS).

VIN, even if locally excised, often recurs (25%), in whichcase it may progress to invasive squamous cell carcinoma

(6%).

Women with VIN may have squamous neoplasms similar to

VIN elsewhere in the lower genital tract.


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Squamous Cel l Carcinoma Fol lows

VIN

Squamous cell carcinoma of the vulva (Fig. 18-3) is the end result ofa multistep process that begins with VIN.

This tumor accounts for 3% of all genital cancers in women and isthe most common cancer of the vulva.

In the past, it mainly affected older women, but like VIN, it now

occurs with increasing frequency in younger women. Two thirds of larger tumors are exophytic; the others are ulcerative

and endophytic.

Pruritus of long duration is commonly the first symptom.

Ulceration, bleeding, and secondary infection may develop.

The tumors grow slowly and then extend to the contiguous skin,vagina, and rectum.

They metastasize to superficial inguinal and then deep inguinal,femoral, and pelvic lymph nodes.

The outlook correlates with the stage of disease and lymph nodestatus.

The prognosis of patients with vulvar cancer is generally good, withan overall 5-year survival rate of 70%.


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FIGURE 18-3. Squamous cell carcinoma of the vulva. A. The tumor is

situated in an extensive area of lichen sclerosus (white). B. Small nests

of neoplastic squamous cells, some with keratin pearls, are evident in

this well-differentiated tumor.


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Figure 18-4. Interrelations of naming systems in

premalignant cervical disease. This complex chart

integrates multiple aspects of the disease complex. It

lists the qualitative and quantitative features that become

increasingly abnormal as the premalignant diseaseadvances in severity. It also illustrates the changes in

progressively more abnormal disease states and

provides translation nomenclature for the

dysplasia/carcinoma in situ (CIS) system, cervicalintraepithelial neoplasia (CIN) system, and the Bethesda

system. Finally, the scheme illustrates the corresponding

cytologic smear resulting from exfoliation of the most

superficial cells, indicating that even in the mildest

disease state, abnormal cells reach the surface and are


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Endometrium


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This is the microscopic appearance of normal proliferative endometrium in the

menstrual cycle. The proliferative phase is the variable part of the cycle. In this

phase, tubular glands with columnar cells and surrounding dense stroma are

proliferating to build up the endometrium following shedding with previous


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Here is early secretory endometrium. The appearance with prominent

subnuclear vacuoles in cells forming the glands is consistent with

post-ovulatory day 2. The histologic changes following ovulation are

quite constant over the 14 days to menstruation and can be utilized to


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This is normal secretory phase endometrium. Note the larger tortuous glands

with secretions. The secretory phase follows a set 14 day course leading to

either implantation of a fertilized ovum or menstruation.


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The endometrial cavity is opened to reveal lush fronds of hyperplastic

endometrium. Endometrial hyperplasia usually results with conditions

of prolonged estrogen excess and can lead to metrorrhagia (uterine

bleeding at irregular intervals), menorrhagia (excessive bleeding with

menstrual periods), or menometrorrhagia.


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This is endometrial cystic hyperplasia in which the amount of

endometrium is abnormally increased and not cycling as it should. The

glands are enlarged and irregular with columnar cells that have some

atypia. Simple endometrial hyperplasias can cause bleeding, but are not

thought to be premalignant. However, adenomatous hyperplasia isremali nant.


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This uterus is not enlarged, but there is an irregular mass in the upper

fundus that proved to be endometrial adenocarcinoma on biopsy.

Such carcinomas are more likely to occur in postmenopausal women.

Thus, any postmenopausal bleeding should make you suspect that


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The endometrial adenocarcinoma is present on the lumenal surface of

this cross section of uterus. Note that the neoplasm is superficially

invasive. The cervix is at the right.


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This is endometrial adenocarcinoma which can be seen invading into

the smooth muscle bundles of the myometrial wall of the uterus. This

neoplasm has a higher stage than a neoplasm that is just confined to

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