Pathology of

Female Genital System And Breast

2008

Contents:

Pathology of

       

Vulva Vagina Cervix Body of Uterus Fallopian Tubes Ovaries Diseases of Pregnancy Breast

VULVA
Diseases of vulva:  Vulvitis (more common but not serious).  Non-Neoplastic epithelial disorders.  Carcinomas (uncommon but life threatening).  Painful bartholin cysts (caused by obstruction of the excretory ducts of the glands).  Imperforate hymen in children.  Impeding secretions and menstrual flow later in life.

 Herpes genitalis (HSV1 or 2): causing vesicular eruption. .  Gonococcal suppurative infection  Syphilis: produce primary chancre at site of inoculation.Vulvitis Most important forms of vulvitis related to sexually transmitted disease:  HPV: produce condylomata acuminata and vulvar intraepithelial neoplasia.  Candidal vulvitis.

 Contact irritant dermatitis: presents as welldefined erythematous weeping and crusting papules and plaques. antiseptics. or alcohol. chemical treatments on clothing and other antigens. sops. .Vulvitis Contact dermatitis: the most dommon causes of vulvar pruritus is a reactive inflammation to an exogenous stimulus.  Contact allergic dermatitis: has similar gross appearance and may result from allergy to perfumes and other additives in creams. lotions. and soaps. May be a reaction to urine. whether an irritant or an allergen. detergents.

 Both may coexist in different areas in the same person. and both may appear macroscopically as depigmented white lesions.Non-Neoplasic epithelial disorders  The epithelium of vulvar mucosa may undergo atrophic thinning or hyperplastic thickening  There are two forms of non-neoplastic epithelial disorders: lichen sclerosus and lichen simplex chronicus. . referred to as leukoplakia.

 Lichen Simplex Chronicus End reaction of many inflammatory dermatoses. Generally. marked by epithelial thickening. Pathogenesis is uncertain. there is no inrecased predisposition to cancer. but suspiciously. .Non-Neoplastic epithelial disorders  Lichen Sclerosus: Characterized by atrophic epithelium. lichen simplex chronicus is often present at margins of established cancer of the vulva. autoimmune reaction may involved Carries an increased risk of developing squamous cell carcinoma. usually with dermal fibrosis. expansion of stratum granulosum and surface hyperkeratosis.

Non-Neoplastic epithelial disorders Lichen Sclerosus Lichen simplex chronicus Lichen Planus It‟s benign dermatoses .

Significant characteristic cellular morphology is: perinuclear cytoplasim vacuolization.Condylomata accuminata: (more common) may be papillary and distinctly elevated.Tumors  Condylomas and low-grade vulvar intraepithelial Neoplasian (VIN) Condylomas fall into two distinctive biologic forms: .Condylomata lata: (not commonly seen today). They occur anywhere on the anogenital surface. are flat. Vulvar cndylomas are not pre-cancerous but coexist with foci of intraepithelial neoplasia in vulva (VIN grade 1) and cervix. minimally elevated lesions that occur in secondary syphilis . . moist.

Condylomas Giant condyloma accuminata A vulva chancre and condylomata .

and 90% of them are HPV related.Non-HPV-related vulvar squamous cell carcinoma occorus in older women. and is associated with lichen sclerosus or other inflammatory conditions. . It is well differentiated and unifocal.Carinoma of vulva represent about 3% of all genital tract cancers in women. . and most common seen in relatively younger patients.Tumors (continued …)  High-grade vulvar intraepithelial neoplasia and carcinoma of the vuvla .90% of vulvar carcinomas are squamous cell carcinomas. .

vulvar Paget disease have no demonstrable underlying carcinoma. occasionally with invasion of underlying dermis . scaly plaque.Extramammary Paget Disease  Like that of breast. red.  Microscopically. is essentially a form of intraepithelial carcinoma. characterized by spread of malignant cells within the epithelium.  Unlike breast.

. C. E. A 75-year old woman presents with a pruritic vulvar lesion. B. Physical examination reveals an irregular white. D. If this leukoplakia is due to lichen sclerosis. A biopsy showed thinning of the epidermis with replacement of the underlying dermis by dense connective tissue. B. D. E. rough area involving her vulva. A 62 year old woman presented with stenosis (narrowing) of her introitus and symmetrical atrophic changes of the labia.Review Questions 1. C. These findings are most consistent with: Moderate dysplasia (VIN II) Squamous hyperplasia Condyloma acuminatum Verrucous carcinoma Lichen sclerosis 2. A. then biopsies will most likely reveal Atrophy of epidermis with dermal fibrosis Epidermal atypia with dysplasia Epithelial hyperplasia and hyperkeratosis Individual malignant cells invading the epidermis Loss of epidermis pigment A.

and primary tumors. and congenital small lateral Gartner duct cysts arising from persistent embryonic remnants.VAGINA  The vagina is seldom the site of primary disease. vulva.  Congenital anomalies are uncommon and include entities such as total absence of vagina. . vaginitis.  The only primary disorders discussed here are a few congenital anomalies. a separate or double vagina. more often it is secondarily involved in the spread of cancer or infection arising in cervix. or rectum. bladder.

Vaginitis  Relatively common clinical problem that is usually transient and not serious.  The frequent organisms are Candida Albicans and Trichomonas vaginalis. Candidal vaginitis produces a curdy white discharge. primary gonorrheal infection of the vagina is uncommon. However.  A large variety of organisms are implicated. it is present in about 5% of normal adults. and so the appearance of symptomatic infection always involves predisposing influences or sexual transmission of new aggressive strains. it may occur in newborn born to infected mothers. in adults. .

and so symptomatic infection usually represent a sexually transmitted new strain.Vaginitis (continued…)  T. vaginalis can also be identified in 10% of asymptomatic women. in which parasite can be identified microscopically. . T.  Nonspecific atrophic vaginitis may be encountered in postmenopausal women with preexisting atrophy and thinning of the squamous vaginal mucosa. vaginalis produces a watery. copious green discharge.  However.

usually encountered in young women in their late teens whose mothers took diethylstilbestrol during pregnancy. .  Risk factors are similar to those for carcinoma of the cervix (discussed later).Vaginal intraepithelial neoplaisa and squamous cell carcinoma  Extremely uncommon. overall risk is 1 per 1000 of those exposed in utero.  Vaginal clear cell adenocarcinoma. usually occur in women older than age 60 years.  Vaginal adenosis. appear as red glandular foci lined by mucus-secreting cell. from such inclusions rare clear cell adenocarciona arises.  Associated with HPV infection in most cases. are small glandular or microcystic inclusions appear in vaginal mucosa.

Review Questions 3. Clear cell carcinoma D. Condyloma acuminatum B. Clear cell adenocarcinoma C. Squamous cell carcinoma 4. Embryonal rhabdomyosarcoma B. Cervical carcinoma C. Sarcoma botryoides E. Squamous carcinoma of the vagian . Vaginal adenosis D. Carcinoma of the endometrium E. Vaginal adenosis is most likely to precede the development of A. The most frequent malignancy of the vagina is: A.

CERVIX  Cervix is often the seat of disease. most cervical lesions are relatively banal inflammation  But cervix is also the site of the most common cancers in women. squamous cell carcinoma. .  Fortunately.

the columnar mucus-secreting epithelium of the endocervix meets the sqamous epithelial covering of the exocervix at the external os. squmocolumnar junction comes to lie visibly on the exocervix (condition called extropion). not visible by naked eye. Frequently. overgrowth of these epithelium blocks the orifices of endocervical glands in the transformation zone to produce small nabothian cysts. . regeneration of both squamous and columnar epithelium in region known as the transformation zone.Cervicitis  At birth.  In adult.  In young women.

enterococci. trachomatis represent 40% of cases of cervicitis encountered in sexually transmitted disease clinics. staphylococci.  These inflammation can be infectious or noninfectious cervicitis. . Ureplasma urelyticum. herpes simplex genitalis.  Microorganisms often present are indigenous. incidental vaginal aerobes and anaerobes.  Many of these organisms are transmitted sexually. Among these organisms.. vaginlais. streptococci. Neisseria gonorrheae. T. C. so cervicitis may represent sexually transmitted disease. and are associated with purulent vaginal discharge.Cervicitis (contiued …)  Inflammation of the cervix are extremely common. and HPV. Chlamydia trachomatis. Candida spp. Escherichia coli.

. It is important to know that nearly all invasive cervical squamous cell carcinoma arise from epithelial changes CIN. the incidence of cervical cancer has plummeted.Tumors of the cervix  Cervical carcinoma is one of the major causes of cancer-related deaths in women. the incidence precursor cervical intraepithelial neoplasia (CIN) has increased to more than 50.  Since introduction of the Papanicolaou (Pap) smear 50 years ago.  Over the same period.  The pap smear remains the most successful cancer screening test ever developed. despite improvements in early diagnosis and treatment.000 cases annually.

Cervical intraepithelial Neoplasia
 Cytologic examination can detect epithelial changes (CIN) before the development of an overt cancer by many years. However, only a fraction of cases of CIN progress to invasive carcinoma.  The peak incidence of CIN is about 30 years, whereas that of invasive carcinoma is about 45 years.  Risk factors for the development of CIN and invasive carcinoma are: -Early age at first intercourse -Multiple sexual partners -Male partner with multiple previous sexual partners -persistent infection by „„High-risk‟‟ HPV They point to the likelihood of sexual transmission of a causative agent, in this case HPV.

Cervical intraepithelial Neoplasia

Normal squamous epithelium of the cervix. There is weak positive cytoplasmic staining

Left, normal epithelium. Right, CIN2/3 Strongly positive staining nuclie

HPV

(additional information)

 High-risk HPV types: 16, 18, 45, and 31, account for the majority of carcinomas, smaller contributions by HPV33, 35, 39, 45, 52, 56, 58, and 59. The viral DNA integrates into the host genome and express E6 and E7 proteins which inactivate tumor suppressor genes p53 and RB, respectively.  Low-risk HPV types: 6, 11, 42, 44 which produce condylomas; the viral DNA does not integrate into the host genome.  The recently introduced HPV vaccine is very effective in preventing HPV infections and cervical cancers.  Many women harbor these viruses, only few develop cancer, suggesting other influences like cigarette smoking and exogenous or endogenous immunodeficiency.

 In some individual with aggressive intraepithelial changes. glandular lesions are not detected well by Pap smear. and small cell neuro-ednocrine carcinoma 5%. The only reliable way to monitor the course of the disease is with careful follow-up and repeat biopsies. . whereas in other women CIN precursors may persist for life.  The relative proportion of adenocarcinoma has been increasing in recent decades. the time interval may be considerably shorter. adenocarcinoma and adenosquamous carcinoma 20%.Invasive carcinoma of the cervix  The most common cervical carcinoma are sqamous cell carcinoma 75%.

leukorrhea. Tumors encircling the cervix and penetrate into the stroma produce a “barrel cervix”.Invasive carcinoma of the cervix (continued…)  advanced cases of cervical cancer are invariably seen in women who either have never had a Pap smear or have waited many years since the prior smear. Such tomors may be symptomatic.  Invasive carcinomas range from microscopic foci of early stromal invasion to grossly conspicuous tumors encircling the os. which can be identified by direct palpation. . painful coitus.  Detection of precursors by cytologic examination and their eradication by laser vaporization or cone biopsy is the most effective method of cancer prevention. called to attention by unexpected vaginal bleeding. and dysuria.

Herpes . Early age at first intercourse E. Risk factors for cervical cancer include all of the following except: A. Multiple sexual partners B. Mycoplasma E. All of the following are significant causes of acute or chronic cervicitis EXCEPT: A. Gonococci B. Endocervical polyps D.Review Questions 5. Chlamydia D. A male partner with multiple previous sexual partners C. Lactobacilli C. Cigarette smoking 6.

A. C. Which of the following statements concerning carcinoma of the cervix is true? Stage II disease is confined to the cervix Distant metastases accounts for most deaths Peak incidence is 20 to 25 years 85% associated with human papillomavirus Definitive diagnosis is made by Pap smear 8. A 31 year old woman was found to have abnormal cells on pap smear a separate sample of which were sent for HPV (human papillomavirus) typing.Review Questions 7. . D. Which of the following HPV types would put her at highest risk for subsequent development of squamous cell carcinoma of the cervix? (From additional information) 6 11 16 42 44 C. B. E. B. D. E. A.

Review Questions 9. Multiple small mucinous cysts of the endocervix that result from blockage of endocervical glands by overlying sqmaous metaplastic epithelium are called: A) Bartholines cysts B) Chocolate cyst C) Follicular cyst D) Gartners duct cyst E) Nabothian cyst .

Only the more frequent and significant ones are considered here. and sometimes disastrous. often chronic and recurrent.  Endometritis  Adenomyosis  Endometriosis  Dysfunctional uterine bleeding and endometrial hyperplasia  Tumors .BODY OF UTERUD Many disorders of this organ are common.

gonorrhoeae or C. Generally the diagnosis of chronic endometritis requires the presence of plasma cells. Acute endometritis is frequently due to N.Endometritis  Can be seen with pelvic inflammatory disease. They act as a nidus for infection. trachomatis.  It may be associated with foreign bodies or retained tissue subsequent to miscarriage or delivery. Removal of the foreign body and offending tissue typically results in resolution.  Endometritis is classified as acute or chronic based on whether there is a predominant neutrophilic or lymphoplasmacytic response. .

.S.Endometritis (continued …)  Endometritis may present with fever.  Granulomatous endometritis: seen in immunocompromised individuals in U. menstrual abnormalities. abdominal pain. infertility and ectopic pregnancy due to damage to the fallopian tubes. and in other countries where tuberculosis is endemic.

 Endometrial stroma. and pelvic pain before the onset of menstruation.  The uterine wall often becomes thickened and the uterus is enlarged. . Nevertheless.  Because they are drived from the stratum basalis of the endometrium. they do not undergo cyclical bleeding.Adenomyosis  It is the growth of basal layer of the endometrium down into the myometrium. glands are found well in the myometrium between the muscle bundles. adenomyosis may produce menorrhagia. dysmenorrhea.

Indeed. menstural endometrium is viable and survives when injected into the anterior abdominal wall. . It may present as a pelvic mass filled with degenerating blood.  Regurgitation theory: (currently most accepted theory) proposes menstrual backflow through the fallopian tubes with subsequent implantation.Endometriosis  It is characterized by endometrial glands and stroma in a location outside the endomyometrium.

Pain on defecation reflects rectal wall involvement. respectively. and dyspareunia (painful intercourse) and dysuria reflect involvement of the uterine and bladder serosa.  Almost in all cases. and eventually causes sterility. there is severe dysmenorrhea and pelvic pain as a result of intrapelvic bleeding and periuterine adhesions. Extensive scaring of the oviducts and ovaries produces discomfort in the lower abdominal quadrants. .Endometriosis (continued …)  Manifestations depend on the distribution of the lesions.

Common locations of endometriosis within the pelvis and abdomen .

Dysfunctional uterine bleeding  Abnormal bleeding in the absence of a well-defined organic lesion in the uterus is called dysfunctional uterine bleeding. Induce a variety of endometrial responses.Contraceptive-induced bleeding. Leads to an excess of estrogen relative to progesterone. . endometrial polyps. non-secretory glands. e. . .Inadequate luteal phase. Including chronic endometritis.Failure of ovulation. and leiomyomas.Endomyometrial disorders. Corpus luteum fail to mature normally. . It depends somewhat on the age of the women. leading to relative lack of progesterone. decidua-like stroma and inactive.  Various causes can be segregated into four groups: .g.

 Potential contributors include failure of ovulation.Endometrial hyperplasia  An excess of estrogen relative to progestin.  They can be classified into simple hyperplasia. which can be preneoplastic. complex hyperplasia and atypical hyperplasia. prolonged administration of estrogenic steroids.  Common risk factor is obesity. because adipose tissue processes steroid precursors into estrogens. and granulosatheca cell tumors of the ovary. polycystic ovaries (estrogen-producing ovarian lesion) cortical stromal hyperplasia. . The risk of developing carcinoma is dependent of the severity of the hyperplastic changes. induce hyperplasia.

risk of giving rise to a cancer (rare). They may occur at any age. but more commonly. usually hemispheric. frequently with small muscular arteries. . composed of endometrium resembling the basalis. clinical significance: . Histologically.production of abnormal uterine bleeding. but some have normal endometrial architecture. . they develop at time of menopause.Tumors  They tend to produce bleeding as the earliest manifestation. More often they have cystic dilated glands.  Endometrial polyps: sessile.

is menorrrhagia. More frequent in blacks than in whites. .They are often referred to as fibroids because they are firm. when present.Estrogens and oral contraceptives stimulate their growth.Tumors (continued…)  Leiomyoma: . they shrink postmenopausally. . They may become palpable to the woman or may produce a dragging sensation.They may be entirely asymptomatic. discovered on routine pelvic examination. conversely.The most common benign tumor in females and are found in 30% to 50% of women during reproductive life. .They rarely transform into sarcomas. with or without metrorrhagia. The most frequent manifestation. . .

Many metastasize.Diagnostic features include tumor necrosis. . .Almost always solitary tumors.They are frequently soft. typically to the lungs. Yielding a 5-years survival rate of about 40%. . hemorrhagic and necrotic.Recurrence after removal is common with these cancers. . cytologic atypia.Tumors (continued…)  Liomyosarcomas: . .Typically arise de novo from mesenchymal cells of the myometrium. . and mitotic activity.They present a wide range of differentiation .

and it is well recognized that prolonged estrogen replacement therapy and estrogen-secreting tumors increase the risk of this cancer.Appears most frequently between the ages of 55 and 65 years. .Well-defined risk factors for endometroid carcinoma: obesity-diabetes-hypertension-infertility . .S and other Western countries.These risk factors poin to increased estrogen stimulation. respectively). (endometroid and serous carcinoma of the endometrium. .There are two clinical stettings in which endometrial carcinomas arise: in perimenopausal women with estrogen excess and in older women with endometrial atrophy.Tumors (continued…)  Endometrial carcinoma: The most frequent cancer occurring in the female genital tract in the U. .

Two familial cancer syndromes that have an increased risk of the endometrioid type of endometrial carcinoma: 1. . a tumor suppressor gene). 2.Breast cancer occurs more frequently in women with endometrial cancer than by chance alone.These tumors are termed endometrioid because of their similarity to normal endometrial gland. hereditary nonpolyposis colon cancer syndrome. have mutations in PTEN. thyroid. Cowden‟s syndrome (carries an increased risk of carcinoma of the breast. . and endometrial carcinoma frequently arises on a background of endometrial hyperplasia.Tumors Endometrial carcinoma: (continued…) Many of these risk factors are the same as those for endometrial hyperplasia. . . and endometrium.

- . nearly all cases have mutations in the p53 tumor suppressor gene. With progression. these are usually latemetastasizing neoplasms. but dissemination eventually occurs. however. Mutations in DNA mismatch repair genes and PTEN are rare in serous carcinoma. uterus may be palpably enlarged. sometimes in the setting of an endometrial polyps. Marked leukorrhea and irregular bleeding are the fist clinical indication of all endometrial carcinoma. Fortunately.Tumors Endometrial carcinoma: (continued…) Serous carcinoma of the endometrium typically arises in a background of atrophy. and in time it becomes fixed to surrounding structures by extension of the cancer beyond the uterus.

Neither . _____ May result in pelvic adhesions A. Endometriosis B. Adenomyosis C. Endometriosis B. Both D.Review Questions 10. Neither 11. Adenomyosis C. _______Causes enlargement of the uterine wall A. Both D.

Endometrial carcinoma risk factors include all except: A Obesity B Hypertension C Diabetes mellitus D HPV infection E Infertility .Review Questions 12.

penetrate the wall of the tubes. They may result in tubo-ovarian abscess.  Salpingitis increase risk of tubal ectopic pregnancy. and sometimes the heart valves.FALLOPIAN TUBES  Salpingitis is the most common disease of the fallopian tubes.  Non-gonococcal infections are more invasive. and give rise to blood-borne infections and seeding of the meninges. And damage or obstruction of the tubal lumina may produce permanent sterility. almost always as a component of pelvic inflammatory disease. lower abdominal or pelvic pain. . It is almost always microbial in origin. or tubo-ovarian complex. joint spaces. and pelvic masses.  All forms of salpingitis may produce fever.

They seem to be increased in women with BRCA mutations. fallopian tube carcinomas frequently involve the omentum and peritoneal cavity at presentation. .FALLOPIAN TUBES (continued…)  Primary adenocarcinomas: may be of papillary serous or endometrioid histology. Because the lumen and fimbria of the fallopian tube have access to the peritoneal cavity.

Mucinous tumors .Serous tumors .Other tumors .Teratomas *Benign (mature) cystic teratomas *Immature malignant teratomas *Specilized teratomas .OVARIES (contents):  Follicle and luteal cysts  Polycystic ovaries  Tumors of the ovary .Endometrioid tumors .Brenner tumor .Surface epithelial-stromal tumors .

They may become palpable masses and produce pelvic pain. pressure may cause atrophy of these cells. . when they achieve diameters of 4-5cm. .OVARIES  Follicle and luteal cysts: .When small thy are lined by granulosa lining cells or luteal cells.Common place of physiologic variants.Originate in unruptured graafian follicles or in follicles that have ruptured and immediately sealed. but as the fluid accumulates.Sometimes these cysts rupture. . . . producing intraperitoneal bleeding and acute abdominal symptoms.

They are also called Stein-Leventhal syndrome. high concentration of LH. gray-white cortex. and sometimes obesity may appear in girls after menarche secondary to excessive production of estrogens and androgens by multiple cystic follicles in the ovaries. . studded with subcortical cysts. low concentration of FSH. with hypertrophic and hyperplastic luteinized theca interna. .The principal biochemical abnormalities are excessive production of androgens. And corpora lutea is absence. .Ovaries usually twice normal in size.Histologically.Oligomenorrhea. hirsutism. . thickened outer tunica. . infertility.OVARIES (continued…)  Polycystic ovaries: .

 Three cell types make up the normal ovary: the multipotential surface (coelomic) covering epithelium.  Neoplasms of the surface epithelial origin account for almost 90% of ovarian cancers. . Each of these cell types gives rise to a variety of tumors. the totipotential germ cells.Tumors of the ovary  Ovarian cancer is the fifth most common cancer in US women. and the multipotntial sex cord/stromal cells. It is also the fifth leading cause of cancer death in women.

.Prolonged use of oral contraceptives reduce the risk somewhat. mostly mucinous cystadenocarcinomas.Two of the most important are nulliparity and family history.A majority of hereditary ovarian cancers seem to be caused by mutations in the BRCA1 and BRCA2 genes.Tumors of the ovary (continued…)  Pathogenesis: several risk factors for epithelial ovarian cancers have been recognized. . .P53 is mutated in about 50% of all ovarian cancers. . . .HER2/NEU protein is overexpressed in 35% of ovarian cancers. with poor prognosis.K-RAS protein is overexpressed in up to 30% of tumors. .

Surface epithelial-stromal tumors  They are derived from the coelomic mesothelium that covers the surface of the ovary.  Malignant tumors may also be cystic (cystadenocarcinoma) or solid (carcinoma). . tumors of low malignant potential.  Benign lesions are usually cystic (cystadenoma) or have a stromal component (cystadenofibroma). forming small epithelial cysts.  There are also intermediate. They are lowgrade cancers with limited invasive potential. borderline category.  With repeated ovulation and scarring the surface epithelium is pulled into the cortex of the ovary.

spherical to ovoid.  Benign lesions are usually encountered between ages 30 and 40 years. cystic structures.  Grossly.  The prognosis for the individual with clearly invasive serous cystadenocarcinoma after treatment is poor and depends on the stage of the disease at the time of diagnosis. and malignant serous tumors are more commonly seen between 45 and 65 years of age. .Serous Tumors  These are the most frequent of the ovarian tumors. account for 60% of all ovarian cancers. but most are large.  Serous tumors are the most common malignant ovarian tumors. may be small.

.  Their incidence is much lower and they are less likely to be malignant than serous tumors. 80% are benign. accounting for about 10% of all ovarian cancers.Mucinous tumors  The differ essentially from serous tumors in that the epithelium consists of mucin-secreting cells simlar to tthose of the endocervical mucosa. but the stage is the major determinant of treatment success. 10% are of low malignant potential.  10% of them are malignant.  The prognosis is of mucinous tumors is better than for the serous counterpart.

 Microscopically. but sometimes they develop as a mass projecting from the wall of a cyst filled with chocolate-colored fluid.Endometrioid tumors  They may be solid or cystic.  Similar to endometrial cancer. formation of tubular glands. similar to those of the endometrium. endometrioid carcnoma have mutations in PTEN suppressor gene. .  They are usually malignant tumors. although benign and borderline forms also exist.  15-30% of women with these ovarian tumors have a concomitant endometrial carcinoma.

they are formed as nodules within the wall of a mucinous cystadenoma. most are benign. the nests are cystic and are lined by columnar mucus-secreting cell.  Occasionally. consisting of an abundant stroma containing nest of transitionl-like epithelium resembling that of the urinary tract. .  They are generally somoothly encapsulated. usually unilateral tumors. solid.Brenner tumor  They are uncommon.  They may arise from the surface epithelium or from urogenital epithelium trapped within the germinal ridge.  Rarely.

 They arise in the first two decades of life. the greater is the likelihood of malignancy  However. . more than 90% of these germcell are benign mature cystic teratomas.  Thy younger the person.Teratomas  Neoplasms of germ-cell origin constitute 15% to 20% of ovarian tumors. The immature malignant variant is rare.

foci of bone and cartilage. reveal a hairbearing epidermal lining. In about 1% of cases there is malignant transformation. producing an acute surgical emergency. On transection. when removed. Occasionally. Usually there is cysts lined by recognizable epidermis replete. they produce infertility for unknown reasons. Sometimes. they are often filled with sebaceous secretion and matted hair. usually taking form of a squamous cell carcinoma. Sometimes teeth protrude from nodular projection. these tumors are prone to undergo torsion.Benign (mature) cystic teratomas    They are marked by differentiation of totipotential germ cells into mature tissues representing all three germ cell layers. For unknown reasons.     . and other recognizable lines of development are also present. nests of bronchial or GIT epithelium.

 Differ from benign teratomas insofar as they are often bulky.  Uncommonly.Immature malignant teratomas  They are found early in life. one of the cystic foci may contain sebaceous secretion. the distinguishing feature is an immature areas of differentiation toward cartilage. the mean age is 18 years. and other feature similar to those in the mature teratoma. and predominantly solid or near-solid on transection. and other structure.  Microscopically. . hair. muscle.  Particularly ominous are foci of neuropithelial differentiation. because they are aggressive and metastasize widely. nerve. bone. and are punctuated by areas of necrosis.

 Struma ovarii and carcinoid may combined in the same ovary. One of these elements may become malignant. solid.Specialized teratomas  Struma ovarii is composed entirely of mature thyroid tissue that may hyperfunction and produce hyperthyroidism. unilateral brown ovarian masses.  They appear as small. Specialized teratoma .

Tomors of the ovary Serous tumor Mucinous ovarian tumor Brenner tumor Endometrioid tumor Mature (benign) teratoma Immature (malignant) teratoma .

The most likely diagnosis: A Granulosa cell tumor B Polycystic ovary disease C Thecal luteal cysts D Bilateral cysts of Morgagni E Bilateral Brenner tumors . Ultrasound shows bilateral 8 cm ovaries with multiple small cortical cysts.Review Questions 13. A 27 year old nulliparous woman presents with hirsutism and oligomenorrhea.

Ectopic pregnancy .DISEASES OF PREGNANCY  Diseases of pregnancy and pathologic conditions of the placenta are important causes of intrauterine or perinatal death. maternal death.Gestational trophoblastic disease * hydatidifrom mole: complete and partial * invasive mole * choriocarcinoma * placental site trophoblastic tumor .Placental inflammations and infections . congenital malformations and growth retardation.Preeclampsia/eclampsia (toxemia of pregnancy) .  Some disorders: . and morbidity for both mother and child. premature birth.

Choriomnion shows polymorph leukocytic infiltration with edema and congestion of the vessels. they are bacterial and are associated with premature birth. . it may cause acute vasculitis of the cord. Candida. They are caused by mycoplasms. When it extends beyond the membranes. The most common.Placental inflammations and infections  Infections reach placenta by two pathways:  Ascending infections through the birth canal. and bacteria of the vaginal flora.

Histologically. . listeriosis. tuberculosis.Placental inflammations and infections (continued…)  Hematogenous spread. rubella and cytomeglaovrius and herpes simplex viruses can all cause placental villitis. .Syphilis. toxoplasmosis. . .Transplacental infections can affect the fetus and give rise to the so-called TORCH complex. the villi are most often affected (villitis).

implantation is in the oviducts (tubal pregnancy) other sites include the ovaries. and the intrauterine portion of the oviduct. such obstruction is based on chronic inflammatory changes in the oviduct. the abdominal cavity.Ectopic pregnancy  It is implantation of the fertilized ovum in any site other than the normal uterine location.  In 90% of these cases. .  In half of tubal pregnancy no anatomic cause can be demonstrated. In adult half of the cases. although tumors and endometriosis may also retard passage of the ovum.  Occurs as many as 1% of pregnancies.  Any factor that retard the passage of an ovum from oviduct to uterus predispose to ectopic pregnancy.

 Rupture of an ectopic pregnancy may be with sudden onset of intense abdominal pain. .  Gestation within the abdominal cavity occurs when the fertilized eggs drops out of the oviduct and implants on the peritoneum. Prompt surgical intervention is necessary.  Until rupture occurs. the endometrium (in 50% of cases) undergoes the characteristic changes. an ectopic pregnancy may be indistinguishable from a normal one. (although there is absence of elevated gonadotropin levels). often followed by shock.  Under the influence of the placental hormones.Ectopic pregnancy (continued…)  Ovarian pregnancies result when ovum is fertilized within its follicle just at time of rupture.

Invasive mole .  All elaborate human chorionic gonadotropin (hCG). most of which are benign.Hydatidiform mole .  The fall or rise in the level of the hormone can be used to monitor the effectiveness of treatment. to the highly malignant choriocarcinomas. .Choriocarcinoma  They range in aggressiveness from the dydatidiform moles. which can detected considerably higher than those found during normal pregnancy. The titers progressively rising from hydatidiform mole to invasive mole to choriocarcinoma.Gestational trophoblastic disease  They are divided into three overlapping morphologic categories: .

Hydatidiform mole It is a voluminous mass of swollen.  Elevation of hCG in the maternal bllod and absence of fetal parts or fetal heart sound are typical. uncommonly.XX or. has some normal chorionic villi. appears as grapelike structures.  .  The swollen villi are covered by varying amounts of normal to highly atypical chorionic epithelium. .Partial hydatidiform: compatible with early embro formation. and a history of the condition increases the risk in subsequent pregnancies.Complete hydatidiform: does not permit embryogenesis therefore never contain fetal parts. chorionic villi.  Two distinctive subtypes of moles have been charaterized: . and the chorionic epithelial cells are diploid (46.XXY). and is almost always triploid (69.XY). sometimes cystically dilated. rarely give rise to choriocarcinoma  Moles are most common before age 20 years and after age 40 years. 46. All of the chorionic villi are abnormal.

which penetrate the uterine wall deeply. such as lungs or brain. . but they do not constitute true metastases and may actually regress spontaneously.  Hydropic villi may embolize to distant organs.  Because of the greater depth of invasion into the myometrium. and therefore serum hCG may remain elevated.Invasive mole  They are complete moles that are more aggressive locally but do not have the aggressive metastatic potential of a choriocarcinoma.  An invasive mole retains hydropic villi. causing rupture and sometime life-threatenining hemorrhage.  Local spread to the broad ligament and vagina may also occur. an invasive mole is difficult to remove completely by curettage.

 50% of choriocarcinoma arise in complete hydatidiform moles. accompanied by a rising titer of hCG. 25% after abortion. The more abnormal the conception the greater is the risk of developing gestational choriocarcinoma. .  Rare in western countries.  The risk is greater before age 20 years and after age 40. less frequently. from totipotential cells within the gonads or elsewhere.  In most cases there is a bloody. and the remainder occur during a normal pregnancy.  Arises from gestational chorionic epithelium or. and much more common in Asian and African countries. brownish discharge.Choriocarcinoma  It is very aggressive malignant tumor.

there is relatively poor response to chemotherapy in chocriocarcinoma that arise in the gonads (ovary or testis). maternal immune response against paternal antigens helps by acting as an adjunct to chemotherapy. Nearly 100% of cases can be cured  By contrast.Choriocarcinoma (continued…)  By the time most choriocarcinomas are discovered. present-day chemotherapy has achieved remarkable results. . vagina. which made them nearly fatal in the past. there is usually widespread dissemination via the blood most often to lungs. Lymphatic invasion is uncommon. This striking difference may related to the presence of paternal antigens on placental choriocarcinoma but not gonal lesion.  despite extreme aggressiveness of these neoplasms.

Placental site trophoblastic tumor  These uncommon tumors are diploid.  They produce human placental lactogen.  Intermediate trophoblasts do no produce large amount of hCG. so hCG concentration is only slightly elevated. are often XX in karyopte. . they are not sensitive to chemotherapy. derived from the placental site or intermediate trophoblast.  Typically arise a few months after pregnancy.  They are indolent and have favorable outcome if confined to endometrium. However. and the prognosis is poor if they spread beyond the uterus.

particularly with first pregnancies in women older than age 35 years.  Preeclampsia and eclampsia are referred to as toxemia of pregnancy. the blood pressure mounts.  In those severely affected.  Occurs in 5% to 10% of pregnancies. renal function is impaired.Preeclampsia/eclampsia (toxemia of pregnancy)  Preeclampsia is the development of hypertension. convulsive seizures may appear. accompanied by proteinuria and edema in third trimester of pregnancy. the symptom complex is then termed eclampsia. .

Preeclampsia/eclampsia (toxemia of pregnancy) (continued…)
 Full-blown eclampsia may lead to disseminated intravascular coagulation, with widespread ischemic organ injuries, and so eclampsia is potentially fatal. However, early recognition and treatment of preeclampsia has now made eclampsia rare.  The basic feature underlying all cases is inadequate maternal blood flow to the placental secondary to inadequate development of spiral arteries of the uteroplacental bed.  Recent studies suggest imbalance between proangiogenic and antiangiogenic factors. Increase in the antiangiogenic factor sFlt1 and reduction in the level of the proangiogenic factor VEGF have been noted.

Review Questions
14.Triploid Karyotype A. Complete mole B. Partial mole C. Both A and B D. Neither 15.Fetal parts may be present A. Complete mole B. Partial mole C. Both A and B D. Neither

Review Questions
16.Edematous changes of all the villi A. Partial hydatiform mole B. Complete hydatiform mole C. Invasive mole D. Choriocarcinoma E. Placental site trophoblastic tumor 17. _____ Admixture of edematous and normal villi A. Complete mole B. Partial mole C. Both D. Neither

Neither .Elevated HCG in serum A.Review Questions 18. Both A and B D. Complete mole B. Partial mole C.

 Some of them produce palpable “lumps”. Estrogenic therapy and oral contraceptives do not seem to increase the incidence of these alterations.  They may cause nodularity.  Lumps that are produced by the various patterns of fibrocystic change must be distinguished from cancer.BREAST Fibrocystic changes:  Different changes range from those that are innocuous to patterns associated with an increased risk of breast carcinoma. only a small minority represent forms of epithelial hyperplasia that are clinically important.  This range of changes is the consequence of an exaggeration and distortion of the cyclic breast changes that occur normally in the menstrual cycle. .

The nonproliferative lesions include cysts and/or fibrosis without epithelial cell hyperplasia (simple fibrocystic change). . .  They tend to arise during reproductive period of life but may persist after menopause.  Nonproliferative changes are so common. . that they almost constitute physiologic variants.Fibrocystic changes (continued…)  They can be subdivided into nonporliferative and proliferative patterns.The proliferative lesions include a range of innocuous to atypical duct or ductular epithelial cell hyperplasias and sclerosing adenosis. being found at autopsy in 60% to 80% of women.

myxomatous appearance.  A stromal lymphocytic infiltration is common in this and other variants of firbrocystic change. having lost in their normal delicate. .Nonproliferative change Cysts and fibrosis:  Characterized by an increase in fibrous stroma associated with dilation of ducts and formation of cysts of various size.  The stroma is usually compressed fibrous tissue.

rising fears about cancer. the terminal ducts. and sometimes the lobules of the breast.  Occasionally it produces microcalcifications on mammography.Proliferative change Epithelial hyperplasia:  It is proliferative lesion within the ductules.  But there is more florid atypical hyperplasia that carry significantly greater risk. and carry little risk of carcinoma.  Some of the epithelial hyperplasia are mild and orderly.  The epithelial hyperplasia are often accompanied by other histologic variants of fibrocystic change. .

.  Although it is difficult to differentiate from carcinoma. it is associated with only a minimally increased risk of pregression to carcinoma.  They contain marked intralobular fibrosis and proliferation of small ductules and acini.Proliferative change (continued…) Sclerosing adenosis:  This variant is less common than cysts and hyperplasia. but it is significant because its clinical features are smilar to those of carcinoma.

It is uncommon. . and during acute stages usually cause pain and tenderness in the involved areas.Inflammations  They are uncommon.  Mammary duct ectasia is significant because it leads to induration of the breast substance mimicking the changes caused by some carcinomas.  Mammary duct ectasia (periductal or plasma cell mastitis) is nonbacterial chronic inflammation of the beast associated with inspiration of breast secretions in the main excretory ducts.  They are not associated with increased risk of cancer. and encountered in women in their 40s and 50s who have borne children.  In this category there are several forms of mastitis and traumatic fat necrosis.

Tumors of the breast  They may arise from either connective tissue or epithelial structures. That latter give rise to common breast neoplasms. .

 Smiliar lesions may appear with fibrocystic changes. the peak incidence is in the third decade of llife.  An increase in estrogen activity is thought to contribute to its development. movable mass. . They almost never become malignant. discrete. Usually appear in young women.Fibroadenoma  It is the most common benign neoplasms of the female breast.  They usually present as solitary. They may enlarge late in the menstrual cycle and during pregnancy.

and invasion of adjacent breast tissue by malignant stroma. they remain localized and are cured by excision. Only the most malignant (15% of cases) metastasize to distant sites. In the past they had the name cystosarcoma phyllodes. distending the breast. They may be small or grow to large massive size.even malignant tumors also tend to remain localized.  . The most ominous change is the appearance of increased stromal cellularity with anaplasia and high mitotic activity. an unfortunate name because they are benign.Phyllodes tumor       They are much less common than fibroadenomas. Some become lobulated and cystic. Arise from the periductal stroma and from preexisting fibroadenomas. accompanied by rapid increase in size. that is why they called phylodes tumors. on gross section they exhibit leaflike clefts and sliits.

wherease the solitary papilloma almost always remain benign.Intraductal papilloma  It is a neoplastic papillary growth within a duct. . These lesion sometimes become malginant.Appearance of serous or blody nipple discharge .Nipple retraction (rare).  Most are solitary. found within the principal lactiferous ducts or sinuses.  Present clinically as a result of .Precence of small subareolar tumor .  In some cases there are multiple papillomas in several ducts (intraductal papillomatosis).

Epidemiology and risk factors:  Geographic distribution: there are differences among countries in the incidence and mortality rates of breast cancer. almost one-fourth of women who develop these neoplasms will die of the disease. but after the menopause the slope of the curve is almost plateous. These difference seems to be environmental rather than genetic in origin. only 5% are younger than the age 40.  75% of women with breast cancer are older than age 50. The risk is significantly higher in North America and northern Europe than in Asia and Africa.  Age: uncommon in women younger than 30 ys.Carcinoma  Despite advances in diagnosis and treatment. the risk steadily increase throughout life. .

Less common genetic diseases associated with breast cancer are the Li-Fraumeni syndrome (mutations in p53).5% to 10% of breast cancer are related to inherited mutations.Half of women with hereditary breast cancer have mutations in gene BRCA1 and one-third have mutations in BRCA2. . Cowden disease (mutations in PTEN). or have a family history. have other associated cancer like ovarian cancer.Women are more likely to carry a breast cancer susceptibility gene if they develop breast cancer before menopause. . have bilateral cancer. These genes function in DNA repair. .Carcinoma (continued…)  Getetics and family history: . and carriers of ataxia-telangiectasia gene. .

prevents or delays the onset of osteoporosis. Other less well-established risk factors: obesity. use of combined estrogen plus progestin hormone therapy is associated with an increased risk of breast cancer. diagnosis at more advanced stage. 20% to 30% of women irradiated for Hodgkin lymphoma in their teens and 20s develop breast cancer. but the risk for women treated later in life is not elevated. Only women irradiated before age 30. and more abnormal mammograms. Oral contraceptives: they have been suspected of increasing the risk of breast cancer. However. and a diet high in fat. alchohol consumption. seem to be affected. Ionizing radiation to the chest increases the risk of breast cancer. .Carcinoma  (continued…)    prolonged exposure to exogenous estrogens postmenopausally: know as a hormone replacement therapy.

three set of influences seem to be important:  Genetic change: . . however. .Overexpression of the HER2/NEU proto-oncogene. the cause of breast cancer remain unknown. found to be amplified in up to 30% of invasive breast cancers.Mutation of the tumor suppressor genes RB and p53 may also be present.Amplification of RAS and MYC genes has also been reported in some breast cancer. .Carcinoma (continued…) Pathogenesis: as with all cancers. .Mutations affecting proto-oncogenes and tumor supressor genes in breast epithelium contribute to the oncogenic transformation process.

Many risk factors (mentioned before) imply increased exposure to estrogen peaks during the menstrual cycle.Most likely. . multiple acquired genetic alterations are involved in the sequential transormation of a normal epithelial cell into a cacerous cell. basal-like.  Hormonal influences: . luminal B. . These subtypes are reproducible and are associated with difference outcomes.Endogenous estrogen excess or hormonal imbalance has a significant role.Gene expression profiling can stratify breast cancer into five subtypes: luminal A. . HER2/NEU overexpression. and normal breast like.Carcinoma - (continued…) A large number of genes including the estrogen receptor may be inactivated by promoter hypermethylation.

Important environmental variables include irradiation and exogenous estrogens. may interact with growth promoters to create an autocrine mechanism of tumor development.They are suggested by the variable incidence of breast cancer in genetically homogeneous groups and the geographic differences in prevalence.Carcinoma - (continued…) Functioning ovarian tumors that elaborate estrogens are associated with breast cancer in postmenopausal women. .Estrogens stimulate the production of growth factors by normal breast epithelial cells and by cancer cells. Enviornmental variables: . Estrogen and progesterone receptors are present in breast epithelium and in breast cancer cells. .

Lymph node metastasis are present in about 40% of cancers presenting as a palpable masses. Outer quadrant and centrally located lesions typically spread to the axillary nodes. spleen. but they become involved only after the axillary and internal mammary nodes are affected. adrenals brain. Matastases may appear many years after apparent therapeutic control of the primary lesion. The supraclavicular nodes are sometimes the primary site of spread. Those in the inner quadrants often involve the lymph node along the internal mammary arteries. such as lungs. liver. skeleton. and pituitary.Carcinoma    (continued…) Spread of breast cancer:    Occurs through lymphatic and hematogenous channels. sometimes 15 years later. . Metastatic involvement maybe to any organ.

 With mammographic screening. involvement of regional lymph nodes is already present in about half of patients. painless.Carcinoma (continued…) Clinical course:  Breast cancer is often discovered by the woman or physician as a discrete.  Magnetic resonance imaging is being studied in highrisk young patients with dense breasts that are difficult to image by mammography. solitary. . carcinomas are frequently detected before they become palpable. and only 15% of these have nodal metastases. and movable mass. At this time.

Invasive carcinoma smaller than 1cm have an excellent prognosis in the absence of lymph node metastases. The most common grading system for breast cancer evaluates tubule formation. and mitotic rate to divide carcinomas in to three groups.Carcinoma  1. Well-differentiated or poor differentiated or moderately differentiated. (continued…) 3. The grade of the carcinoma. . 5-year survival rate is 90% with no axillary node involvement. Patient who develop hematogenous spread are rarely curable. Lymph node involvement and the number of lymph nodes involved by metastases. The survival rate is decreases with each involved lymph node and is less than 50% with 16 involved nodes. nuclear grade. 4. Prognosis is influenced by the following variables: The size of the primary carcinoma. 2. Distant metastases.

. However. Carcinoma with an abnormal DNA content have a slightly worse prognosis. (continued…) 7. adenoid cystic. medullary. The proliferation rate of the cancer. The reason for determining their presence is to predict the response to anti-estrogen therapy. Ovexpression is associated with poorer prognosis. the importance of evaluating HER2/NEU is to predict resposne to monoclonal antibody “Herceptin” to the gene product. Overexpression of HER2/NEU. High proliferative rates are associated with a poorer prognosis. 8. All specialized types of breast carcinoma (tubular. The presence of receptors confers a slightly better prognosis. The histologic type of carcinoma. 6. The presence or absence of estrogen or progesterone receptors. Aneuploidy. 9. and mucinous) have a better prognosis than carcinomas of no special type (ductal carcinoma).Carcinoma 5. cribriform.

Stage 4. invasive carcinoma 2cm. without nodal involvement (5-year survival rate: 87%) .Stage 0. invasive carcinoma 5cm with four or more involved axillary nodes.Carcinoma (continued…)  The major prognostic factors are used by the American Joint Committee on Cancer to devide breast cancer into clinical stages as follows: . breast cancer with distant metastases (5year survival rate: 13%) .Stage 3. DCIS or LCIS (5-year survival rate: 92%) . with up to 3 involved axillary nodes (5-year survival rate: 75%) . (5-year survival rate: 43%) .Stage 1. invasive carcinoma 5cm.Stage 2.

They resemble invasive carcinoma in females both morphologically and biologically. Other causes include Klinefelter syndrome. Gynecomastia: male breast are also subject to hormonal influences. Carcinoma: frequency ratio to breast cancer in the female of 1:125.Male breast   Only two disorders occur in male breast with sufficient frequency. with consequent inability of the liver to metabolize estrogens. digitalis therapy. Gynecomastica may occur in response to estrogen excess. estrogen-secreting tumors. estrogen therapy. Morphologic features are simlar to intraductal hyperplasia. Physiologic gynecomastia occurs in puberty and in old age. It occurs in advanced age. Because of scant amount of breast substance in males.  . Almost half have spread to regional nodes and more distant sites by the time they are discovered. The most important cause is cirrhosis of the liver. the tumor rapidly infiltrates the skin and underlying thoracic wall. but they are less sensitive than are female breasts.

A) Fibrocystic change B) Acute mastitis C) Fibroadenoma D) Carcinoma E) Pagets disease of the breast 20. except: A) High-fat diet B) Positive family history C) Obesity D) Early menarche E) multiparity .Review Questions 19.All of the following are associated with carinoma of the breast. The most likely cause of 1 cm mass in the upper outer quadrant of the breast of 65 year old woman.

.Additional informations Infectious disorders:  Candidiasis: most common form of vagnitis  Trichomoniasis: second most common type of vaginitis.  Shyphilis: 1st stage: chancre.  Herpes simplex virus infection: produce small viscels and shallow ulcers.  Chlamydial infection: clymedial cervicitis – lymphogranuloma venereum.  Chancroid: soft and painful ulcerated lesion. Caused by haemophilus dureyi  Granduloma inguinale: characterized by donovan bodies. 2nd stage: condyloma lata.  Garnerella vaginitis: “clue cell” are characteristic cells  Toxic shock syndrome: associated with use of tampons. Cased by calmmatobacterium granulomatis.  Gonorrhea: frequent cause of pelvic inflammatory disease.

All of the following condition correctly matched with the appropriate association. except: A) Endometriosis: severe menstrual pain B) Endometrial hyperplasia: excess estrogen stimulation C) Leiomyoma: postmenopausal decrease in size D) Endometrial carcinoma: multiparity E) Ectopic pregnancy: hematosalpinx 22.Review Test 21.HPV infection is not associated with: A Vulvar intra epithelial neoplasia (VIN) B Vaginal intra epithelial neoplasia (VAIN) C Cervical intra epithelial neoplasia (CIN) D Endocervical glandular dysplasia E Paget's disease of the vulva .

Review Test 23. caused by (from additional information) A. Squamous cell carcinoma C. Vaginal intraepithelial neoplasia (VAIN) B. Candida D. Trichomonas B. Which of the following neoplasms of the vagina has been associated with in utero exposure to diethylstilbestrol? A. Clear cell adenocarcinoma E. Herpes E. Embryonal rhabdomyosarcoma D. "clue cells”. Leiomyoma . Gardnerella C. Gonorrhea 24. Fishy odor.

Review Test 25. otherwise normal E Hypertension. ovary B. You would expect to find which constellation of findings on your evaluation: A Hypertension.The most common site of an ectopic pregnancy: A. endometrial cavity E. otherwise normal C Glucose intolerance. A 21 year old woman is at week 25 of her first pregnancy. otherwise normal D Glucose intolerance. endocervical canal D. otherwise normal B Hypertension and proteinuria. peritoneal cavity C. Her gynecologist tells you she has pre_eclampsia. and hypertension. proteinuria and peripheral edema . fallopian tube 26.

Mature cystic teratoma E. Dysgeminoma B. A 32-year-old woman with a history of hyperthyroidism was found to have a left adnexal tumor composed entirely of the tissue as depicted microscopically. Yolk sac tumor C. A 27 year old woman had a palpable right ovary which an x-ray was found to contain a well developed molar tooth.Review Test 27. Krukenberg tumor B. Ovarian carcinoid E. Denturoma . Sertoli-Leydig cell tumor D. The most likely diagnosis would be: A. The best diagnosis is: A. Struma ovarii C. Immature teratoma D. Strumal carcinoid 28.

Which of the following would not be consistent with that diagnosis? A.HCG A.Review Test 29. Fibroma C. Granulosa cell tumor D.Elevated beta . Immature teratoma 30. Hypertension B.A 21 year old woman was diagnosed as having pre-eclampsia. Proteinuria D. Endodermal sinus tumor E. Convulsions C. Edema . Choriocarcinoma B.

Vulva 32. Nehprotic syndrom E. Liver C. A 26-year old female in the third trimester of her first pregnancy develops persistent headaches and swelling of her legs and face. The most common primary sites for the oringin of Paget‟s disease are the nipple and the A.Review Test 31. Nehritic syndrom D. Nasopharynx D. Penis E. Eclampsia B. Her blood pressure is 170/105 mmHg and urnialysis reveals slight proteinuria. Gestational trophoblastic disease C. Anal canal B. preeclampsia . What is the diagnosis A.

The size of the tumor D.Review Test 33. The presence of estrogen receptors.The most important factor related to the prognosis of breast cancer is A. . the presence of activated oncogenes B. The histologic type and grade C. The status of axillary lymph nodes E.

11-A. 19-D. 13-B. 10-B. 20-E. 32-A. 7-D. 23-B. 14-B.Answers 1-E. 29-A. 17-B. 25-E. 6-B. 3-E. 33-E. 4-C. 28-D. 12-D. 16-B. 2-A. 24-D. 26-E. 9-E. 31-E. 18-C. 30-B. 8-C. 22-E. 27-B. 21-D. . 5-C. 15-B.

com . contact us at ali_hisham@windowslive.For your comments.

Sign up to vote on this title
UsefulNot useful