female genital system

Pathology of the Female GenitalTract

DEPT OF PATHOLOGY

LOWER GENITAL TRACT

Vulva, Vagina, Cervix-

Infections and neoplasms

Embroyology and Anatomy

Female Genital Infections-

CandidaTrichomoniasis Gardnerella – most common

Gonnorrhoea,Chlamydia –female infertility

Mycoplasma –spontaneous abortion

Viruses asHPV- cancer

HSV Type II-cervix, vagina, vulva

Papules-vescicle-ulcersCx and vagina-- Leukorrhea

Latent InfectionRecurrenceTo neonates

Diagnosis-serology,microscopy

Trichomonas Vaginalis flagellated ovoid protozoanStrawberry CxMycoplasmaCandida species

Pelvic inflammatory disease

SymptomsOrganisms_Gonococcus,Chlamydia trachomatis, Clostridium PerfringensMode of infection and spread

Gonococcus-an intracellular diplococcusDiagnosis-culture, papsmear

Endometrium spared

Cl .features--A/c Suppurative salpingitis salpingo-oophoritis Tubo ovarian abscesses Pyosalpinx, Hydrosalpinx

Complications

Peritonitis

Intestinal obstn

Bacteraemia

Infertility

Vulva

Vulvitis

Bartholin Cyst

Vestibular Adenitis

Non-neoplastic lesions

Leukoplakia

Lichen sclerosus-subepithelial fibrosis

Lichen simplex chronicus-acanthosis, and hyperkeratosis

Squamous Hyperplasia

Vulvar Leukoplakia� Leukoplakia: A descriptive clinical term; refers to a white plaque or patch on a mucosal surface

� Causes of vulvar leukoplakia:

1.Vitiligo (loss of pigment)

2.Inflammatory dermatosis: p.e. psoriasis

3.Squamous intraepithelial neoplasms of the vulva (VIN) and invasive carcinoma

4.Paget’s disease

Leukoplakia

Tumors of Vulva

Benign-Papillary hidradenomaCondyloma accuminatum(HPV 6&11)Venereal Wart,Mucosal PolypSyphilitic Condyloma latumViral cytopathic effect-Koilocytic atypia

Premalignant and malignant neoplasms – SCC,BCC,melanomas or adenocarcinomas.

SCC-HPV related SChyperplasia

Vulvar Intraepithelial Neoplasia

Extramammary Paget Disease

Paget’s Disease

Melanoma

Vagina

VIN and Sq.cell carcinoma

Adenocarcinoma

Embryonal Rhabdomyosarcoma

Uterine Cervix

Cervicitis

Tumors

Cervicitis“Erosions” and development of the transformation zone

(T zone). Nabothian cysts.

Infectious and non-infectious cervicitis

Vaginal flora, Chlamydia trachomatis, Ureaplasma urealyticum, Trichomonas vaginalis, Candida species, Neisseria gonorrhoeae, Herpes simplex II, and HPV.

acute nonspecific: postpartum, Staphylococci/Streptococci

Nonspecific (chronic) cervicitis

Gross: reddening, swelling, and granularity around margins of external cervical os.

Microscopy: Hyperplasia and reactive atypia of epithelium, no dysplasia, glycogen depletion . Mononuclear cell infiltrate, nabothian cysts. Viral inclusions (HSV). Plasma cells in C. trachomatis.

CervicitisLeukorrhea

Culture interpretation*.If severe >>>differentiation from carcinoma:

colposcopy and biopsy.Subsoil for carcinogenesis?

May lead to sterility (fibrosis/ unfavorable medium for sperm).

Endocervical polyp Inflammatory polypoid masses, cm. Smooth surface composed of columnar

mucus-secreting cells (endocervical epithelium) with underlying cystically dilated glands filled with mucus. Stromal edema inflammatory mononuclear cells.

Squamous metaplasia and ulceration.

Cervical Intraepithelial Neoplasia (CIN) and Carcinoma

Cervical cancer was the most frequent form of cancer around the world.

Impact of Papanicolaou screening: Decrease incidence of invasive tumors and increase incidence in the detection of precursors (dysplasias/CINs) lesions.


Peak incidence1. CIN : 30 Y2. Invasive carcinoma: 45 yRisk factors1. Early age at first intercourse2. Multiple sexual partners3. A male partner with multiple previous

sexual partners


Higher incidence in lower socioeconomic groups

Genital infections

Exposure to oral contraceptives

Rarity among virgins

Multiple pregnancies


T zone

High grade dysplasia/HPV 16 and 18

Viral isolation and typing do not predict the course.

Follow up: cytology, colposcopy (acetic acid test), biopsy*.

HPV: 85-90% of lesionsSerotypes: 1. High risk: 16, 18, 31, and 33.2. Low risk (associated with condylomas):

6, 11, 42, and 44.Integration of viral genes into host

genome>>transcription>>translation of specific proteins that inactivate p53 and retinoblastoma tumor suppressor genes.



Viral infection does not mean that a women will develop cancer.

10-15% HPV: negative

Other carcinogens, genetic factors, host immunity, cigarette smoking.


Importance of early detection, adequate follow up and management.

Histologic grading of precursor lesions:

1. CIN I: Mild dysplasia

2. CIN II: Moderate dysplasia

3. CIN III : Severe dysplasia/carcinoma in situ


Cytologic grading of precursor lesions1) LOW GRADE SQUAMOUS

INTRAEPITHELIAL LESIONS

[CIN I and Condylomas (koilocytosis)]

2) HIGH GRADE SQUAMOUS INTRAEPITHELIAL LESIONS

[CIN II, CIN III/CIS]


Natural History

Different studies = different populations = different results

CIN I: 50 to 60% regress, persists 30%, and progress to CIN III 20%. 1 to 5% become invasive.

CIN III: 33% regress, progression varies from 6 to 74%.

Schilling test

Invasive Carcinoma of the Cervix80-95%: Squamous cell carcinomas

Multifactorial disease

Preventable

Gross (macroscopic appearance)

Fungating (exophytic)

Ulcerative (endophytic)

Infiltrative

Invasive Carcinoma of the Cervix

ROUTES OF INVASION

Direct spread-adjacent stroma, vagina, pelvic wall.

Local and distant spread to lymph nodes

Distant metastasis to lungs , liver ,bone marrow etc

Invasive Carcinoma of the Cervix Squamous cell carcinoma

Well to poorly differentiated Adenocarcinomas Adenosquamous carcinomas Staging

Invasive Carcinoma of the Cervix CIS: Asymptomatic, Leukorrhea Carcinoma: Vaginal bleeding, leukorrhea,

painful coitus, and dysurea DX: Colposcopy: acetic acid test, Bx Mortality: Related to local extension*:

ureter obstruction or invasion of bladder or rectum.

Invasive Carcinoma of the Cervix Importance of early diagnosis Time….? 5-year survival rate:

1. Stage 0 (CIS): 100%

2. Stage I: 85% to 90%

3. Stage II: 70 to 75%

4. Stage III: 35%

5. Stage IV: 10%

Invasive Carcinoma of the CervixStage 0: Carcinoma in situStage I: Tumor confined to the cervixStage II: Tumor extends beyond the cervix but not

onto the pelvic side wallStage III: Tumor extends to the pelvic side wall or

to the lower one third of vagina, or causes hydronephrosis, or a nonfunctioning kidney

Stage IV: Tumor extends beyond true pelvis, or biopsy-proved involvement of bladder or rectal mucosa.

Invasive Carcinoma of the CervixManagement

LEEP Conization Hysterectomy Pelvic exenteration Radiotherapy

FEMALE GENITAL SYSTEM

Endometrium

Body of the Uterus

Endometritis

Adenomyosis

Endometriosis

Dysfunctional uterine bleeding

Endometrial hyperplasia

Endometrial polyps

Leiomyomas and leiomyosarcomas

Endometrial carcinomas

Endometritis Clinical settings:1. Chronic gonorrheal pelvic disease2. Tuberculosis3. Retained Product of conception4. IUD5. Spontaneously Histology: Irregular disposition and

proliferation of endometrial glands, plasma cells and lymphocytes in the stroma

Adenomyosis

Growth of the basal layer of endometrium (glands and stroma) down into the myometrium between the muscle bundles

Thick myometrium: reactive hypertrophy Nonfunctional: no bleeding* Menorrhagia, dysmenorrhea, and

premenstrual pain

Endometriosis Infertility, dysmenorrhea, pelvic pain. Foci of endometrial tissue in pelvis

(ovaries, pouch of Douglas, uterine ligaments, tubes, rectovaginal septum).

Sometimes in umbilicus, LNs, lungs, skin, heart, bone.

Theories of genesis: Regurgitation, metaplastic, and lymphovascular

Endometriosis Functional endometrium: cyclic bleeding

Complications:Fibrosis,adhesions: pain, sterility

Gross: red-blue to yellow-brown nodules, chocolate cysts in ovaries

Microscopy: Endometrial glands, stroma, and hemosiderin deposition

Endometriosis

Theories of genesis:

1. Regurgitation: menstrual backflow through fallopian tubes and subsequent implantation

2. Metaplastic: metaplasia of coelomic epithelium

3. Lymphovascular dissemination

EndometriosissitesOvaries,ligaments,rectovaginal areas,pelvisscars,umbilicus,vagina,vulva&appendix

Dysfunctional Uterine Bleeding

abnormal bleeding with no organic lesion

Etiology of uterine bleeding varies with age :prepuberty

, adolescence,

reproductive age,

perimenopause, and postmenopause.

Dysfunctional Uterine BleedingThree functional groups (E/P)

1. Anovulatory cycles-metabolic disorders, ovarian lesions,sys diseases,unexplainable

2. Inadequate luteal phase-inadequate corpus leuteum

3. Contraceptive induced bleeding

Anovulatory Cycles Common at both ends of reproductive life Hypothalamic-pituitary axis, thyroid, or adrenal

dysfunction Functioning ovarian producing lesion,

malnutrition, obesity, stress, debilitating disease Persistence of proliferative “growth” until

endometrium collapse, spiral arteries rupture, and bleeding occurs.

Inadequate Luteal Phase Corpus luteum fail to mature normally or regress

prematurely: less progesterone is produced: delay and inadequate secretory phase

Contraceptive Induced Bleeding Imbalance in the ratio Estrogen/Progesterone

Endometrial Hyperplasia

estrogen>>>>Progesterone: Polycystic ovaries(Stein-Leventhal syndrome), cortical stromal hyperplasia, granulosa-theca ovarian tumors

Simple Hyperplasia Complex Hyperplasia without atypia Complex Hyperplasia with atypia: 20/25% risk of

carcinoma Continuum of changes based on duration and level of

estrogen excess Causes irregular uterine bleeding Biopsy and follow up

Endometrial Hyperplasia

Endometrial Polyps

Uterine bleeding

Gross: Sessile(rarely pedunculated) rounded lesions: 0.5 to 3 cm

Microscopy: Surface lined by columnar epithelium, stroma (monoclonal stromal cells with rearrangement of 6p21) with thick-walled vessels, and endometrial glands some of which appear cystically dilated.

Occur at any age, but common around menopause

Endometrial Polyp

Uterine Malignancy

Endometrial- glands

Stroma

Both glands and stroma

Myometrial-

Leiomyoma

Benign smooth muscle tumor

“Fibroids”, “Myomas”

30 to 50% of women during reproductive life.

Estrogen stimulates their growth

Involutes after menopause

Monoclonal, 40% have non-random chromosomal abnormalities

Leiomyoma

Gross: Well circumscribed, firm, gray, white mass. Whorled cut surface.

Singly or multiple. Few cm to large masses.

Intramucosal, intramural, and/or subserosal location. Parasitic leiomyomas

Microscopy: Interlacing bundles of smooth muscle cells. Foci of ischemic necrosis, fibrosis, cyst degeneration, hemorrhage, and calcification are not uncommon.

Leiomyoma

Leiomyoma

Leiomyoma

Asymptomatic

If Symptoms: Bleeding (menorrhagia) or “mass effect”

Progression to sarcomas?

Leiomyosarcoma

usually solitary tumorsDerived from mesenchymal myometrial cellsGross: 1. Bulky masses infiltrating uterine wall2. Polypoid lesions projecting into uterine

cavity3. Discrete tumors(~ leiomyomas)

Leiomyosarcoma

Leiomyosarcoma

Microscopy: Increased cellularity, mitosis, nuclear atypia, and necrosis.

Recurrence and metastasis are not uncommon

5 year survival rate: 40%

Leiomyosarcoma

Endometrial Carcinoma

Most frequent cancer of the female genital tract in USA

55 to 65 y (uncommon <40y)

Risk factors:1. Obesity: synthesis of estrogen in fat deposits2. Diabetes3. Hypertension4. Infertility: anovulatory cycles


Hyperestrinism : HRT, estrogen secreting ovarian tumors, etc.

Background of endometrial hyperplasia

20%: no Hyperestrinism and no hyperplasia: older patients, poor prognosis


Gross:Diffuse thickening of uterine wall: Infiltrative

Exophytic form

Filling of the endometrial cavity with a firm to soft partially necrotic tumor.

Myometrium invasion/ serosa/ LN


Adenocarcinomas (Adenocarcinomas with squamous metaplasia, Adenoacanthoma, Adenosquamous carcinoma)

Endometrioid

Papillary serous carcinoma

Clear cell adenocarcinoma


Grade: Degree of cytologic differentiation. GH1, G2, and G3

Stage: Spread of the tumor

1. I: Confined to corpus2. II: Extension to cervix3. III: Extension outside the uterus , but still

confined to pelvis4. IV: Extension outside the pelvis


Leukorrhea and irregular bleeding in a postmenopausal patient

Enlargement of uterus and fixation to surrounding structures

Late metastasizing neoplasm to LN and other organs5-year survival rate:1. Stage I: 90%2. Stage II: 30 to 0%3. Stage III and IV: less than 20%

Mixed Mullerian Tumors

adenofibromaadenosarcomaCarcinosarcoma

with or withoutdifferentiation(Cartilage,bone&muscle)


FALLOPIAN TUBES AND OVARY

Fallopian tube

Common affliction is inflammation, pelvic inflammatory disease

gonorrhea, chlamydia, mycoplasma, streptococci and staphylococci

fever, lower abdominal pain and pelvic mass

•Tubal pregnancy

•Adenocarcinoma

Ovary

Normal ovary measures 3-5 x 1.5-3 x 0.6-1.5 cm and weighs 5-8 grams during reproductive age.

Newborn ovaryNote presence of numerous primordial follicles filling the cortex

Four Primordial Follicles and two primary follicles

Mature follicle, Granular cells, marked by an arrow, produce estradiol.(diameter 4-5mm)The preovulatory folliclereaches a diameter of 15-25mm.

Corpus LuteumThe cells produce progesterone.

Degenerating Corpus luteum

Hilar cells of ovarian medulla,these cells are mainly responsiblefor androgen production.

Luteinized stromalcells

Stromal luteinization (stromal hyperthecosis) are associated withandrogenic or estrogenicmanifestation.

Normal Cycle of Endometrium Proliferative phase: Active growth of

glands, stroma and vessels influenced by estradiol production by granular cells in the follicles ( follicular phase).

Secretory phase: reflects the effect of the combined production of progesterone and estradiol by luteinized granulosa and theca cells of the corpus luteum (luteal phase).

PAROVARIAN/PARATUBAL (MESONEPHRIC) CYST

Common lesions, vary in size, often bilateral

Large cysts may become palpable, undergo torsion with/without infarction, and cause pelvic pain

They are benignmesonephric cysts: lined by cuboidal cells;usually arise in ovarian hilumparamesonephric cysts: lined by columnar tubal - type epithelium; adjacent to fallopian tube

FOLLICLE AND LUTEAL CYSTS OF OVARIESFunctional Cysts

Very commonOriginate in unruptured Graffian follicles or in

follicles which have ruptured and resealedOften multiple, they are located immediately

subjacent to the serosaLined by granulosa cells or by luteal cellsUsually small (1 - 1.5 cm), filled with clear fluidOccasionally larger, up to 5cm, and may then be

palpableOccasionally rupture, causing pain and

intraperitoneal bleeding

FOLLICULAR CYST OF OVARY

CORPUS LUTEUM CYST OF OVARYCorpus luteum of pregnancy can be up to 20 cm.

Polycystic Ovarian Disease

Ovarian Neoplasms Clinical Presentation

Despite their considerable pathologic diversity, the clinical presentation of ovarian neoplasms is similar:Usually asymptomatic until large enough to cause pressure symptoms (pain, GI complaints, urinary frequency)30% are discovered incidentally during routine GYN exams

Ovarian Neoplasms Clinical Presentationlarge masses may cause increased

abdominal girthOccasionally, the masses undergo torsion

severe abdominal pain and acute abdomen

Fibromas and malignant epithelial tumors can cause ascites

mucinous tumors can cause pseudomyxoma peritonei

tumors may cause endocrinopathies

Surface Coelomic Ovarian Neoplasm

SEROUS TUMORSMUCINOUS TUMORSENDOMETRIOID TUMORS - Most are

malignant; adenocarcinoma of endometrium present in 15-30% of cases

BRENNER TUMORS- Most are benign

Surface Coelomic Ovarian NeoplasmMost surface tumors present with

nonspecifically low abdominal pain and/or abdominal mass

Malignant tumors grow through capsule and widely seed the peritoneal cavity with tumor nodules and ascites; also distant metastases

Surface Epithelial TumorsThey are derived from coelomic

epithelium.They can be strictly epithelial, e.g.

serous, mucinous or endometroid.They can also have a distinct stromal

component, cystadenofibroma or Brenner tumor.

They are traditionally divided into benign, low malignant potential or malignant.

Serous Tumors60% Benign, 15% borderline (LMP),

and 25% malignant.Size ranges from 5-40cm.Unilocular or multilocular containing

clear serous fluid.Benign forms show smooth glistening

surface.The surface of the malignant forms

appears multinodular.

Serous Tumors of the Ovary

Single most common group of ovarian tumorsbenign and borderline: ages 20 - 50 yearsmalignant: ages 40 - 60+ years

Usually at least partially if not entirely cystic:“cystadenomas; cystadenocarcinomas”

Serous Tumors of the Ovary

Behavior depends on degree of differentiation and distribution

May occur on the ovarian surface, occasionally arises from peritoneal

surface

Serous Tumor of Low Malignant potential

Serous Tumor of Low Malignant Potential Papillary Tufting No evidence of

stromal invasion

Borderline Vs. Malignant Serous Tumors

Both may penetrate (or arise from) the ovarian surface, shedding cells which implant on peritoneal surfaces and produce ascites

Only malignant serous tumors invade the ovarian stroma and metastasize to lymph nodes or other sites

If confined to ovary, survival at 5 years: Borderline - 100% ;

Malignant - 70%

Serous Cystadenocarcinoma of OvaryThese tumor show stromal invasion

Cause elevated CA125 in serum

Serous Cystadenocarcinoma Involving both Ovaries

Mucinous tumors

Benign tumors usually occur between 3rd. And 5th. Decade of life

Most common tumor seen during pregnancy

most often associated with acute abdomen due to torsion

Mucinous Tumors of Ovary10% BENIGN - only 5% bilateral10% BORDERLINE10% MALIGNANT - only 20% BILATERAL

Note that Mucinous tumors are much less likely to be bilateral and to be malignant than serous tumors!

Often larger and more likely multiloculated than Serous tumors; lack psammoma bodies

have endocervix-like or intestine-like lining cells

Mucinous tumors

Benign

Low malignant potential

Malignant

Mucinous Tumors of the Ovary

5% of cases are complicated by pseudomyxoma peritonei:

peritoneal cavity becomes filled with gelatinous mucinous fluid (similar to cyst contents), which mats together the abdominal viscera.

Rx is surgical, and repeated operations are sometimes required

Benign Mucinous Tumor of Ovary

Mucinous tumor of low malignant potential10-15% of all mucinous tumors

6-8% of intestinal subtype are bilateral, Vs. 40% of endocervical type

100% long term survival in patients with stage I mucinous tumor of LMP ( no malignant potential)

Mucinous tumor of low malignant potential

10-15% of all mucinous tumors

6-8% of intestinal subtype are bilateral, Vs. 40% of endocervical type

100% long term survival in patients with stage I mucinous tumor of LMP ( no malignant potential)

Mucinous tumor of low malignant potential

Mucinous Carcinoma

Destructive stromal invasion, resemble mucin secreting adenocarcinoma of intestinal tract

Mucinous Carcinoma

Endometroid tumorsBenign, unilateral masses, occurring in

older patient>57 Y/OEndometroid tumor of low malignant

potential, rare, defining criteria are not well established

Endometroid carcinoma, second most common of ovarian epithelial malignancy

Endometroid adenocarcinoma

Occur in 5th. and 6th. DecadeAbout 15-25% are associated with similar

lesion in the endometriumCan arise from endometriotic cyst, usually in

younger womenSynchronous or metachronous endometroid

adenocarcinoma of cervix has been reportedPrimary extraovarian site has been reported

Clear cell tumorBenign, rareLow malignant potential, rareMalignant can arise from areas of endometriosis, have

been seen in association with endometroid adenocarcinoma, both in ovary and endometrium. They can also be associated with hypercalcemia

Clear cell carcinomaThese tumors have the highest association

with pelvic endometriosis and Para endocrine hypercalcemia.

Brenner TumorOver 95% are diagnosed between the ages of

30-70.

Are usually unilateral and benign.

Fibroma Any age Unilateral Solid grey Most hormonally inactive Can produce hydrothorax and ascites

(Meigs Syndrome) Rarely malignant

Ovarian Fibroma

Thecoma

Any age Unilateral Yellow Can elaborate estrogen resulting in excess

endogenous estrogen Can also elaborate androgen resulting in

hirsutism

Sertoli Leydig Cell Tumor All ages Unilateral, usually small Gray to yellow brown Composed of tubuli or cords and plump

pink leydig cells Most are androgenic Small percentage are malignant

Leydig Cell TumorThese tumors are usually

yellow in color, high lipid content.

Uniform cell population, presence of crystals of Reinke are diagnostic.

Granulosa cell tumorAny age, two different type, adult form and

juvenile formUnilateralMost elaborate large amount of estrogen5-25% are malignant, adult form onlyComposed of mixture of cuboidal Granulosa

cells in cords, sheets, or strands with spindled or plump lipid laden theca cells

Granulosa cell tumorNote presence of Call Exner Bodies

Granulosa cell tumorDiffuse pattern

Germ Cell Tumors Dysgerminoma can occurs with gonadal

dysgenesis Mature teratoma (dermoid cyst) Immature teratoma Choriocarcinoma Endodermal sinus tumor (yolk sac tumor)

Dysgerminoma Peak incidence: 2nd and 3rd decade. 80-90% unilateral Gross: Solid small or large gray mass Micro: Sheets and cords of large cleared

cells separated by scant fibrous strands. Stroma contains lymphocytes.

Prognosis: malignant, but only 1/3 aggressive and spread; all radiosensitive with 80% cure

DysgerminomaAre occasionally encountered in phenotypic

females with gonadal dysgenesis.

Teratoma of the Ovary

BENIGN (MATURE) CYSTIC TERATOMAHistologically mature

IMMATURE MALIGNANT TERATOMAAverage age 18 yearsMost are predominantly solidFoci of immaturity, usually of neuroepithelial typeAggressive, metastasize widely

SPECIALIZED TERATOMASStruma ovarii: mature thyroid tissue; may cause

hyperthyroidismCarcinoid: may cause carcinoid syndrome

Mature (benign) Cystic Teratoma (“DERMOID CYST”) Unilocular cyst, bilateral in 10% of cases Lined by epidermis with all adnexal structures bone, cartilage, thyroid, and other organoid

formations including tooth anlage, bronchi, gut, brain, eye, etc. often present

Rarely exceed 10 cm diameter Young women (late teens, 20’s); present most often

as asymptomatic ovarian masses on PE or X-ray 10-15% undergo torsion, present as acute abdomen Karyotype of benign cystic teratoma always 46,XX Malignant transformation in 1%, squamous cell ca.

Mature Teratoma

Immature TeratomaUsually cause large solid

or partially cystic masses.

Show immature neural elements consisting of neuroepithelial tubules

Specialized TeratomaStruma ovarii can cause hyperthyroidism.

Endodermal Sinus TumorYolk Sac Tumor

Predominantly in young patients Large partially cystic ovarian mass Aggressive behavior, survival rate for

stage I tumors are 70-90% and 30-50% for higher stage tumors.

Endodermal Sinus tumorSerum AFP (alfa fetoprotein) is elevated in

almost all patients.

commonly show Shiller Duval Bodies.

Metastases to Ovary

Older women

Usually bilateral

Tumors can be up to 20 cm

Common primary sites include breast, lung, gastrointestinal tract

Krukenberg Tumor

Other tumors of the ovary Embroyonal carcinomas

Mixed germ cell tumors

Gonadoblastoma


PLACENTA

Gestational Trophoblastic Disease Hydatidiform mole, complete and partial Invasive mole Choriocarcinoma Persistent trophoblastic Disease”

All elaborate human chorionic gonadotropin HCG, which can be detected in the blood and the urine.

Hydatidiform MoleIs a voluminous mass of swollen , sometimes

cystically dilated, chorionic villi, appearing grossly as grape like structures.

The swollen villi are covered by varying amount of banal to highly atypical chorionic epithelium.

Complete Hydatidiform mole All of the chorionic villi are abnormal Chorionic epithelial cells are diploid, 46 XX or

uncommonly 46XY. An empty egg is fertilized by two spermatozoa. Incidence is 1-1.5/ 2000 pregnancies in US, higher

incidence in Asian countries. More common before age of 20 and after age of

40.

Complete hydatidiform mole The condition is usually discovered in 4th month

of gestation. Ultrasound studies show a diagnostic pattern

which resembles snowflakes. Fetal heart tone is usually absent.

The uterine cavity is filled with a delicate friable mass of thin-walled translucent cystic structures.

Striking proliferation of cytotrophoblasts and syncytiotrophoblasts present.

Markedly elevated serum HCG 2% progress to choriocarcinoma

Partial hydatidiform mole Is developed as the result of fertilization of

a normal egg by two spermatozoa. Is always triploid (69XXY). Villous edema is only seen in some villi. Trophoblastic proliferation is focal. Serum HCG level is less elevated. Rarely progresses to choriocarcinoma.

MOLAR PREGNANCY

Curettage produced this specimen, which consisted of 300 cc of bloody tissue.

GESTATIONAL TROPHOBLASTIC DISEASE:HYDATIDIFORM MOLE, COMPLETE TYPE

Swollen, avascular villi covered by chorionic epithelium (trophoblast) of varying atypia

Gross appearance is that of a voluminous mass of grape like structures

GESTATIONAL TROPHOBLASTIC DISEASE: COMPLETE VERSUS PARTIAL HYDATIDIFORM MOLE

FEATURE COMPLETE PARTIAL

Karyotype 46, XX (rare XY) 69, XXY

Villous edema all villi some villi

Trophoblast Pro- diffuse; circum- partial liferation ferential

Atypia often absent

serum HCG elevated less elevated

HCG in tissue ++++ +

Behavior 2% get chorio- rare chorio-

carcinoma carcinoma

GESTATIONAL TROPHOBLASTIC DISEASE:PARTIAL HYDATIDIFORM MOLE

A fetus or fetal parts may also be present

Some villi are normal

Almost always triploid

Normal egg + two spermatozoa 69,XXY

Rarely becomes malignant

Invasive Hydatidiform Mole An invasive mole retains hydropic villi, which

penetrate the uterine wall. Can cause uterine rupture and can be life

threatening. Hydropic villi may embolize to distant organs,

but this tumor does not have metastatic potential. Cure is possible by hysterectomy or

chemotherapy.

Choriocarcinoma Is very aggressive malignant tumor arises

either from gestational chorionic epithelium or less frequently, from totipotential cells within gonads or elsewhere.

Incidence is 1/ 30,000 pregnancies in US. More common in Asian and African

countries.

ChoriocarcinomaIncidence In US 1/30,000 pregnancies

50% follow complete molar pregnancy, 25% following abortion, remainder following normal pregnancy

In Asia and Africa can be as high as 1/2,000 pregnancies

Choriocarcinoma Most cases are discovered by the appearance of a

bloody, brownish discharge, accompanied by a rising titer of HCG, particularly the beta subunit.

Usually appear as very hemorrhagic, necrotic masses within the uterus.

The tumor is entirely composed of cytotrophoblasts and syncytiotrophoblasts.

Widespread dissemination via blood, lung (50%), vagina (30-40%), brain, liver and kidney.

Choriocarcinoma

Chemotherapy results in almost 100% cure or remission in all patients except some who have high risk metastatic trophoblastic disease.

Many of the cured patients have subsequent normal pregnancies.

By contrast, non-gestational choriocarcinoma are much more resistant to therapy.

Drug of choice is methotrexate.

GESTATIONAL TROPHOBLASTIC DISEASE: CHORIOCARCINOMA

CHORIOCARCINOMA

Placental Site Trophoblastic Tumor

Placental Site Trophoblastic Tumor

PLACENTA ACCRETA DEFINITION: Partial or complete absence of the decidua,

with adherence of the placental villi directly to the myometrium:

placenta increta - extends part way thru myometrium

placenta percreta - extends thru entire wall of uterus CLINICAL IMPORTANCE:

1. 60% of cases associated with placenta previa, in which implantation is in lower uterine segment or cervix ante partum bleeding; many cases occur in C-section scars

2. Postpartum bleeding, often life threatening, due to failure of placental separation

PLACENTA ACCRETA

PLACENTA ACCRETA, PERCRETA TYPE, WITH UTERINE RUPTURE

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