Condition	Pathology	Clinical features	Morphology	
Vulva	
Bartholin Cyst	•	Results from inflammatory occlusion of the main ducts of Bartholine vulvovaginal glands.
•	Gonorrheal & other infections may have caused the inflammatory obstruction, which may produce abscesses that must be drained.	•		•	Uninflammed cysts are lined by transitional or flattened epithelium.	
Vestibular adenitis	•	Inflammatory condition of the minor vestibular glands.	•	Painful ulcerative lesions.	•		
Lichen sclerosus	•	Yellowish blue papules or macules that coalesce into thin, gray patchment-like areas.	•		•	Epithelial thinning & subepithelial fibrosis & mononuclear perivascular reaction.	
Squamous hyperplasia	•	Thickened hyperplastic epithelium, hyperkeratosis & leukocytic dermal inflammation.
•	Lesions appear as white plaques – leukoplakia	•		•		
Papillary hidradenoma	•	Benign tumor from modified apocrine sweat glands.
•	Presents as a sharply circumscribed nodule that consists of tubular ducts.	•		•	Tubular ducts are lined by nonciliated columnar cells underlain by a layer of flattened myoepithelial cells.	
Condyloma acuminatum	•	A wartlike, verrucous lesion that occurs on the vulva, perineum, vagina & cervix.
•	Lesions are sexually transmitted & induced by HPV types 6 & 11.	•		•	Lesions consist of a treelike proliferation of stratified squamous epithelium with a perinuclear vacuolization of squamous cells called koilocytosis.	
Vulvar dysplasia (vulvar intraepithelial neoplasia)	•	Presents as multicentric mucosal, raised lesions.
•	Degree of epithelial atypia vary – carcinoma-in-situ in severe form.
•	Untreated lesions may progress to invasive carcinoma.	•	Invasive vulvar carcinomas usually occur in women older than age 60.
•	Tumors metastasizing to regional lymph nodes indicate a poor prognosis.	•	Nuclear epithelial atypia.
•	Increased mitoses.
•	Lack of surface differentiation.	
Extramammary Paget disease	•	A red, crusted, sharply demarcated, maplike area on labia majora.
•	An underlying sweat gland adenocarcinoma in the vulva is uncommon in vulvar Paget disease. 	•		•	Large, anaplastic cells, vacuolized cells lying singly or in small clusters within epidermis & its appendages.
•	The tumor cells are mucin positive.	
Vagina	
Carcinoma	•	Primary carcinoma of the vagina is rare.
•	95% is squamous cell carcinoma, peak incidence between 60 & 70 years of age.
•	Lesions are plaquelike or fungating, invading the cervix & perivaginal structures.
•	Clear cell adenocarcinoma in young women associated with use of DES during pregnancy.	•		•		
Embryonal Rhabdomyosarcoma	•	An uncommon, highly malignant vaginal tumor consisting of embryonal rhabdomyoblasts in infants & children.
•	The tumors are polypoid, bulky masses with grapelike clusters that may protrude from the vagina.	•		•	The tumor cells are small, have oval nuclei, & have small protrusions of cytoplasm from one end (tennis-racket cells)	
Pelvic inflammatory Disease (PID)	•	An ascending infection that begins in the vulva or vaginal glands & spreads upward through the entire genital tract.
•	Causes: gonococcal / chlamydial infections.
•	Postabortal & postpartum PID usually caused by staphylococci, streptococci, coliform bacteria, or clostridium perfringens.
•	Gonococcal disease is characterized by an acute suppurative reaction confined to superficial mucosa & underlying submucosa.	•	Acute suppurative salpingitis may lead to salpingo-oophoritis, pyosalpinx (pus in distended tubes), & tubo-ovarian abscesses.
•	Untreated infection results in chronic salpingitis, with tubo-ovarian adhesions & fibrosis of fallopian tube, occlusion of its lumen, & resultant infertility. 
•	Complications: peritonitis, intestinal obstruction, infertility & ectopic tubal pregnancy.	•		
Cervix	
Acute & Chronic Cervicitis	•	Exogenous infection: gonococci, chlamydia, Trichomonas vaginalis, Candida & mycoplasma.
•	Endogenous infection: streptococci, enterococci, E.coli, staphylococci.	•	Acute cervicitis is most commonly encountered postpartally.
•	Chronic cervicitis is benign & is present to some degree in every cervix during the reproductive years. 	•	Acute cervicitis: acute infiltration of neutrophils beneath lining mucosa.
•	Chronic cervicitis: stenosis of cervical gland ducts, formation of nabothian cysts lined by columnar epithelium, squamous metaplasia of endocervical glands.	
Endocervical polyps	•	Benign tumors made up of connective tissue stroma harboring dilated glands & covered by endocervical epithelium.	•		•		
Intraepithelial & Invasive squamous cell neoplasia	•	One of the most common tumors in women.
•	Peak incidence is at 40-45 years old for invasive cancer.
•	Cervical carcinoma is usually preceded by cervical dysplasia (CIN)
•	Increased risk for cervical cancer: first intercourse at early age, multiple sex partners & high-risk male sex partners.
•	HPV is implicated as promoter of cervical carcinoma.
•	Of cervical carcinomas, 25% consist of adenocarcinomas, adeno-squamous carcinomas, & undifferentiated carcinomas.	•	Risk of progression to malignancy is proportional to grade of CIN.
•	Carcinoma in situ is a precursor of invasive carcinoma.

Stages of cervical cancer:
•	0: Carcinoma in situ
•	I: Carcinoma confined to the cervix
•	II: Carcinoma extends beyond cervix but not into pelvic wall; into vagina, but not lower third.
•	III: Carcinoma extends to pelvic wall or lower third of vagina.
•	IV: Carcinoma has extended beyond pelvis	Classification of precancerous lesions:
•	CIN I: atypia is predominantly in superficial cell layers with preservation of epithelial maturation.
•	CIN II: atypia is conspicuous in both superficial & basal cell layers, but with decreasing maturation.
•	CIN III: atypia is in all cell layers but little or no maturation (carcinoma in situ).

Invasive cervical carcinoma:
•	exophytic or fungating, ulcerating & infiltrative.
•	65% of tumors are large cell, nonkeratinizing & moderately well differentiated.
•	25% are large & keratinizing; rest are composed of small, undifferentiated squamous cells.	
Body of Uterus and Endometrium	
Dysfunctional Uterine Bleeding	Prepuberty: precocious puberty (hypothalamic, pituitary or ovarian origin)

Adolescence: anovulatory cycle
•	Endocrine disorder: thyroid or adrenal disease
•	Primary lesion of ovary: functioning estrogenic ovarian tumor or polycystic tumors.
•	Generalized metabolic disturbance: obesity or malnutrition. 

Reproductive age: 
•	Complications of pregnancy: abortion, trophoblastic disease, ectopic pregnancy.
•	Organic lesions: leiomyomas, adenomyosis, polyps, endometrial hyperplasia, carcinoma
•	Anovulatory cycle
•	Ovulatory dysfunctional bleeding: inadequate luteal phase

Perimenopause:
•	Anovulatory cycle
•	Irregular shedding
•	Organic lesions: carcinoma, hyperplasia, polyps

Postmenopause:
•	Organic lesions: carcinoma, hyperplasia, polyps.
•	Endometrial atrophy	•			
Chronic endometritis	Occurs in:
•	Patients suffering from chronic PID
•	Tuberculosis of the female genital tract
•	Postabortal or postpartal endometrial cavities as a result of retained gestational tissue.
•	Patients with intrauterine contraceptive devices.	•	Abnormal endometrial bleeding	•	Infiltration of plasma cells & macrophages into the endometrium.	
Adenomyosis	•	Nests of endometrium in the myometrium of the uterine wall.	•	Uterine enlargement & irregular thickening of the uterine wall.	•	Diagnosed histologically by the finding of endometrial stroma & glands in the myometrium.	
Endometriosis	•	Presence of endometrial glands or stroma in abnormal locations outside the uterus.
•	Involves the ovaries, uterine ligaments, rectovaginal septum, pelvic peritoneum & laparotomy scars.	•	Presents clinically as severe dysmenorrhea & pelvic pain.
•	Common cause of female infertility. 	A definite histologic diagnosis requires two of the three following:
•	Endometrial glands in ectopic lesions.
•	Stroma in ectopic lesions.
•	Hemosiderin pigment in ectopic lesions.	
Endometrial polyps	•	Sessile tumors composed of endometrial glands & stroma.
•	Associated with hyperestrogenism or tamoxifen therapy.
•	Usually benign but may harbor endometrial hyperplasia or cancer.	•		•		
Endometrial Hypherplasia	•	Occurs as a result of a variety of disordered glandular & stromal growth patterns.
•	Associated with hyperestrogenism	•	Abnormal uterine bleeding	Low-grade hyperplasia:
•	Simple hyperplasia without atypia: benign hyperplastic glands become cystically dilated.
•	Complex hyperplasia: glands of varying size are crowded together into clusters, but there is no cellular atypia.

High-grade hyperplasia:
•	atypical hyperplasia
•	glandular complexity is accompanied by cellular atypia of hyperplastic epithelium.	
Carcinoma of endometrium	•	7% of all invasive cancers.
•	Peak incidence: 55-65 years.
•	Associated with obesity, diabetes, hypertension & infertility.	•	Abnormal uterine bleeding.
•	Prognosis is excellent in patients in whom carcinoma is confined to corpus uteri itself.	•	Presents either as a localized polypoid tumor or as a diffuse spreading lesion involving the entire endometrial surface.
•	Most endometrial carcinomas are adenocarcinomas.
•	Less aggressive tumors: well-differentiated carcinomas with squamous, secretory or mucinous differentiation.
•	More aggressive tumors: poorly differentiated carcinomas – clear cell & papillary serous carcinomas.	
Mesenchymal tumors	•	Rare tumors derived from primitive stromal cells.
•	Consist of glandular & stromal elements; the latter show muscle, cartilage, & osteoid differentiation.
•	Tumors protrude into endometrial cavity & vagina & are bulky & polypoid.	•	Occur in postmenopausal women & are associated with postmenopausal bleeding.
•	Highly malignant & have a 5-year survival rate of 25%.	•	Benign stromal nodules: nodules of stromal cells within myometrium.
•	Low-grade stromal sarcoma: masses of well-differentiated endometrial stroma that penetrate lymphatic channels.
•	Endometrial stromal sarcoma: cells display atypia & mitoses; capable of widespread metastases.	
Leiomyoma	•	Most common tumors in women.
•	Composed of benign masses of smooth muscle cells.
•	Most common in women in active reproductive life & are related estrogenic stimulation.	•	May be asymptomatic or associated with abnormal uterine bleeding, pain, urinary bladder disorders, & impaired fertility.
•	Malignant transformation is rare.	•	Lesions are sharply circumscribed, discrete, round, firm, gray-white nodules that occur within myometrium beneath serosa or endometrium.
•	May undergo cystic degeneration & calcification.	
Leiomyosarcomas	•	Uncommon malignancies that form bulky, fleshy masses in the uterine wall.	•	Tumors disseminate throughout abdominal cavity & metastasize.
•	5-year survival rate is 40%.	Differentiated from benign leiomyomas by presence of:
•	more than 10 mitoses per 10 high-power fields, with or without atypia.
•	5-10 mitoses per 10 high-power fields with cellular atypism.	
Fallopian Tubes	
Inflammations	•	Suppurative salpingitis: infection with pyogenic organisms, e.g. streptococci, staphylococci & gonococci & is a part of PID.
•	Tuberculous salpingitis: hematogenous spread of tuberculosis into the tubes. 	•	Both forms of salpingits are associated with infertility.		
Ovaries	
Non-neoplastic cysts	•	Follicular & luteal cysts are common, measure 1 to 8cm in diameter, & are lined by follicular or luteinized cells.
•	Polycystic ovarian syndrome is a disorder of young women.	•	Follicular/luteal cysts: asymptomatic or may rupture, causing a peritoneal reaction & pain.
•	Polycystic ovarian syndrome: oligomenorrhea, infertility, hirsutism, obesity, persistent anovulation & fibrotic cystic ovaries – important cause of infertility.	Polycystic ovarian syndrome:
•	ovaries are large & white.
•	subcortical cysts 0.5 to 1cm in diameter.
•	covered by a thickened, fibrosed outer tunica.	
Tumors:
•	Common forms of neoplasia in women.
•	Arise from the surface epithelium, germ cells, or sex cord-stroma.
•	Malignant tumors account for 6% of all cancers in women.
•	Risk factors: nulliparity & family history.	
Tumors of Surface Epithelium	
Serous tumors	•	Most common cystic neoplasms
•	Lined by tall, columnar, ciliated epithelial cells & filled with serous fluid.
•	Benign (60%), frankly malignant (25%) & of low malignant potential (15%)	All epithelial tumors cause similar symptoms:
•	lower abdominal pain.
•	abdominal enlargement.
•	gastrointestinal & urinary complaints.

•	Benign tumors are resected with cure.
•	Carcinomas grow slowly & are first seen when no longer confined to ovary with metastases to lymph nodes & distant organs.
•	Carcinomas can seed peritoneal cavity causing massive ascites. 	•	Present grossly as large (up to 40cm in diameter), spherical or ovoid masses.

Benign cystadenomas:
•	smooth & glistening inner lining.
•	composed of a single layer of tall, columnar, ciliated epithelial cells with small papillae.

Malignant cystadenocarcinomas:
•	small, mural, solid nodularities.
•	papillary projections & capillary invasion.
•	multilayered epithelium with many papillary areas & formation of large, solid epithelial masses with atypical cells invading stroma.

Tumors of low malignant potential show epithelial atypia & solid areas but no obvious invasion of stroma.	
Mucinous tumors	•	80% are benign, 5-10% are malignant.
•	Can seed the peritoneal cavity with multiple implants, filling it with mucinous secretions to produce pseudomyxoma peritonei.	•		Gross:
•	the tumors tend to produce large cystic masses.
•	multiloculated & filled with sticky, gelatinous fluid.

Histology:
•	tumors are lined by tall, columnar epithelium showing atypical mucinous vacuolation.
•	cystadenocarcinomas: papillary projections are numerous, mural nodules are present, & epithelial cells show atypia & invade capsule.	
Endometrioid tumors	•	20% of all ovarian cancers.	•		•	Gross: lesions are a combination of solid & cystic masses.
•	Histology: glandular patterns bear strong resemblance to endometrial adenocarcinoma.	
Brenner tumor	•	Encountered in wall of mucinous cystadenomas.
•	Majority are benign.	•		•	Small, solid tumors characterized by dense fibrous stroma & nests of transitional cells. 	
Germ Cell Tumors:
•	15-20% of all ovarian tumors.
•	Arise from totipotential germ cells capable of differentiating into the three germ cell layers	
Mature (benign) Teratomas	•	Dermoid cysts
•	Lined by skin with adnexal structures.
•	Filled with hair-bearing sebaceous secretion.
•	Reveal epidermis, hair follicles, tooth, cartilage, bone & thyroid tissue.	•	Clinically benign.
•	Cured by resection.	•		
Specialized Teratomas	•	Monodermal teratomas differentiate along the line of a single abnormal tissue.
•	Most common is struma ovarii, composed entirely of thyroid tissue.	•		•		
Immature (malignant) Teratomas	•	Elements derived from more than one of the three germ layers are usually present.
•	Most common in adolescents & young women.
•	Grow rapidly & metastasize widely.	•		•	Gross: tumors are bulky & solid with areas of necrosis & hemorrhage.
•	Histology: varied amounts of immature tissue differentiating toward cartilage, glands, bone & muscle.	
Dysgerminoma	•	Tumors are solid, yellowish white to gray-pink.
•	Tumors are uncommon & may occur in childhood or in the teens & twenties.	•		•	Consists of sheets & cords of large vesicular cells separated by scant fibrous stroma.	
Endodermal Sinus Tumor	•	Derived from multipotential embryonal carcinoma cells differentiating toward yolk sac structures. 
•	Occur in children & young women.
•	Grow rapidly & aggressively.	•		•	Consists of cystic spaces into which protrude papillary projections with central blood vessels enveloped by immature epithelium.	
Choriocarcinoma	•	Arises in the ovary from the teratogenous development of germ cells.
•	Highly malignant & metastasize widely.	•		•		
Sex Cord-Stromal Tumors: originate either from the sex cords of the embryonic gonad or from the stroma of the ovary.	
Granulosa-Theca cell tumors	•	Composed of various continuation of granulosa & theca cells.
•	Two thirds occur in postmenopausal women.
•	Tumors are usually unilateral & solid with white-yellow coloration.
•	Clinical malignancy: 5-25%
•	Pure thecomas are benign.	•	Potential of producing large amounts of estrogen & of precocious sexual development & endometrial hyperplasia.	•	Granulosa cell component: small, cuboidal-to-polygonal cells growing in cords, sheets, or strands.
•	Theca cell component: sheets of plump spindle cells; contain lipid droplets.	
Fibromas	•	Common forms of ovarian neoplasms.
•	Unilateral, solid, hard, gray-white masses.
	•	40% associated with hydrothorax & ascites (Meigs syndrome).	•	Well-differented fibroblasts	
Sertoli-Leydig cell tumors	•	Recapitulate cells of testes
•	Usually unilateral	•	Produce masculinization or defeminization.	•	Consists of tubules composed of tubular Sertoli cells or Leydig cells interspersed with stroma.	
Gestational and Placental Disorders	
Ectopic pregnancy	•	Implantation of embryo in any site other than uterus, most commonly the fallopian tubes (90%), others in ovary or abdominal cavity.
•	Predisposing factors: PID with chronic salpingitis & peritubular adhesions.
•	Characterized by acute abdominal pain & shock.
•	Early diagnosis is critical: suggested by high HCG levels & ultrasonographic findings.	Outcome of tubal pregnancy:
•	Intratubal hemorrhage with formation of hematosalpinx.
•	Tubal rupture with intraperitoneal hemorrhage.
•	Spontaneous regression
•	Extrusion into abdominal cavity.	•	Endometrial biopsy specimen show decidual changes & absent chorionic villi.	
Placental infections	•	Occurs by ascending through birth canal or hematogenous.
•	Ascending infections are common & associated with premature rupture of membranes.
•	Bacterial infection results in chorioamnionitis characterized by a neutrophilic infiltration of chorion, amnion & acute vasculitis in umbilical cord.		•		
Toxemia of pregnancy	•	Symptom complex characterized by hypertension, proteinuria & edema.
•	Eclampsia is severe form associated with convulsions & coma.
•	Occurs in 6% of pregnancies, usually in last trimester.	Preeclampsia occurs after 32nd week of pregnancy & is characterized by hypertension, edema, proteinuria, headaches, & visual disturbances.
Mild toxemia can be controlled by bed rest, diet & antihypertensive agents.	•		
Gestational Trophoblastic Disease	
Hydatidiform Mole	•	Characterized by cystic swelling of the chorionic villi, accompanied by trophoblastic proliferation.
•	Common precursor of choriocarcinoma	•	Present in the fourth or fifth month of pregnancy with vaginal bleeding. 
•	Diagnosed by ultrasound examination & analysis of serum HCG.	•	Gross: masses of thin-walled, translucent, cystic, grapelike structures.
•	Histology: complete moles show hydropic swelling of villi, inadequate vascularization of villi & trophoblastic proliferation.	
Choriocarcinoma	•	Malignant tumor in pregnancies. 
•	Metastasizes to the lungs, bone marrow, liver and other organs.	•	Vaginal bleeding & discharge.
•	High HCG levels.
•	Highly sensitive to chemotherapy.	•	Gross: tumor is large, soft, yellowish white, & fleshy with areas of necrosis & hemorrhage.
•	Histology: abnormal proliferations of cytotrophoblasts & syncytiotrophoblasts.