FEMALE GENITAL TRACT Dr.

Nerves 2012

Pathology of the FEMALE GENITAL TRACT

Nuclei showing "ground-glass" appearance. Multinucleation, nuclear molding,

and dense eosinophilic intranuclear inclusions surrounded by a halo are also
seen. "Ground-glass" appearance is due to intranuclear viral particles and
enhancement of nuclear envelope caused by peripheral chromatin margination.

Infections of the Female Genital Tract Molluscum contagiosum Infection

Molluscum contagiosum poxvirus

Common Female Genital Infections
4 types:
Organism VULVA VAGINA CERVIX CORPUS ADNEXA - MCV-1: most prevalent
Herpes Virus Herpetic Ulcers - MCV-2: sexually transmitted
Molluscum Molluscum Incubation period: 6 weeks
Contagiosum lesions
HPV Genital warts, intraepithelial Neoplasia, Invasive Carcinoma
Chlamyda Follicular Cervicitis, Endometritis, Salphingo-
trachomatis oophoritis
Neisseria Skenes gland Vaginitis Acute Acute Endometritis and
gonorrhoea adenitis in Cervici salphingitis
children tis
Candida Vulvo- LESION: pearly, dome-shaped papules with a dimpled center, 1-5 mm
vaginitis
Trichomonas Cervico-
vaginitis
Ureaplasma
urealyticum
Mycoplasma
Molluscum bodies
hominis (Henderson-
Paterson bodies)

Herpes Virus Infection

Affects cervix, vagina and vulva
DNA virus with 2 serotypes: Yeast (Candida) Infection
- HSV-1: oropharyngeal infection Predisposing factors to symptomatic infection:
- HSV-2: genital mucosa and skin - DM
HSV-2 infections are more likely to recur - antibiotics
Gravest consequence: Transmission to neonate during birth - pregnancy
(+) Anti-HSV antibodies: recurrent or latent infection - compromised cell-mediated immunity
Manifestation: marked vulvovaginal pruritus, erythema, swelling and
curdlike vaginal discharge

LESION: 3-7 days after sexual transmission red papules vesicles painful
coalescent ulcers

KOH/Pap smear: pseudospores or filamentous fungal hyphae

Trichomonas Infection
Trichomonas vaginalis: large, flagellated ovoid protozoan
Transmitted by sexual contact and develops within 4 days - 4 weeks
Epidermis being destroyed by herpes virus infection. The herpes virus causes
essentially complete destruction of the epidermis, and what is seen clinically is a
blister, the top of which is formed largely by the very thin stratum corneum.

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Clinical: asymptomatic or w/ yellow, frothy vaginal d/c, vulvovaginal
discomfort, dysuria and dyspareunia Syphilis

LESION: strawberry cervix

Koilocytotic changes in
cervical squamous
epithelium diagnostic of
HPV infection

Lymphogranuloma venereum

LGV - characteristic lesion is a raised, soft, beefy-red, superficial PAINLESS ulcer

Regional lymph nodes typically are spared or show only nonspecific reactive
changes

PAP SMEAR Micro: dermis

and subcutis are
infiltrated by
macrophages
and plasma cells
koilocytes
and by fewer
neutrophils and
lymphocytes
- Interspersed
macrophages
contain many
bacteria, termed
Donovan bodies
INFECTIONS OF THE VULVA
INFECTIOUS Causative organism MICROSCOPIC
DISEASE FEATURE
SYPHILIS (primary Treponema pallidum Ulcerated
lesion, chancre) epidermis, chronic
dermal
inflammation,
perivascular Donovan
inflammation body

Condyloma lata Treponema pallidum Similar to chancre,

(secondary but with epithelial Granuloma inguinale
Syphilitic hyperplasia
infection)
Granuloma Klebsiella(Calymmatobactrium) Ulcer, non
inguinale granulomas casseating
granuloma,
Donovan Bodies,
Pseudoepithelial
Hyperplasia
Lymphogranuloma Chlamydia Non-specific GC,
venereum lymphocytes,
plasma cells, no
organism seen
Chancroid H. ducreyi Ulcer, non-
casseating
granuloma, Gram (-
) bacilli
Tuberculosis M. tuberculosis Casseating
granuloma, acid-
fast bacilli

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PELVIC INFLAMMATORY DISEASE
Clinical
Char by pelvic pain, adnexal tenderness, fever & vaginal discharge
Caused by Neisseria, Chlamydia & enteric bacteria
Puerperal infections with PID: staphylococci, streptococci, coliform
bacteria & C. perfringens

Vulva
Bartholin glands in women are analogous to Cowpers (bulbourethral)
glands in men. They are also called GREATER vestibular glands.
Inflamation or obstruction to the ducts of these glands can cause cyst
formation.

BARTHOLIN CYST
Lesions arise from inflammatory scarring and obstruction of the duct
with accumulation of secretions and cystic dilatation
Squamous (most common), transitional, or low cuboidal, mucinous BENIGN EXOPHYTIC LESIONS
epithelial cyst lining CONDYLOMA ACUMINATUM
350% of patients with vulvar condyloma acuminatum have a cervical
NON-NEOPLASTIC EPITHELIAL DISORDERS HPV infection
Commonly associated with vaginitis, pregnancy, diabetes mellitus,
LICHEN SCLEROSUS oral contraceptive use, and immunosuppression
Clinical HPV 6 and 11
Dermatosis of unknown etiology Microscopic
Most frequently on the genitalia, but may affect the trunk or Koilocytotic cells: enlarged nuclei, wrinkled nuclear membrane, and
extremities perinuclear halos/cavitation
Most common in postmenopausal women Acanthosis, dyskeratosis, parakeratosis, hyperkeratosis, & prominent
Macroscopic granular layer
Pale, white, flat, plaque-like areas Squamous cells often binucleated and multinucleated
Vaginal mucosa is not involved Superficial dermal chronic inflammatory infiltrate often seen

Microscopic
Considerable variation related to the age of lesion, excoriation, and
treatment
Progressive thinning of the epithelium, with blunting or loss of rete
ridges
Homogeneous subepithelial edema with fibrin deposition
Underlying dermal zone of chronic inflammation

Macroscopic
Papillary, verrucous, or papular lesions
Almost always multiple; frequently confluent

GROSS: Pale, white, flat, plaque-like areas

SQUAMOUS CELL HYPERPLASIA

AKA: lichen simplex chronicus; hyperplastic dystrophy
Usually found in adult women, 3060 years of age Koilocytic cells
Macroscopic
SQUAMOUS NEOPLASTIC LESIONS
Gray-white or reddened, with adjacent gray-white epithelium
May be confined to a focal area, usually involving the labia majora
Vulvar Intraepithelial Neoplasia and Vulvar Carcinoma
Microscopic
Epithelial thickening with acanthosis SCC: most common histologic type
Hyperkeratosis and parakeratosis may be present SCC is divided into:
No significant inflammatory infiltrate a) Basaloid & warty carcinoma high oncogenic risk HPV
b) Keratinizing SCC not related to HPV infection
Classic VIN: most commonly occurs in reproductive age women
- Risk Factors:
a) young age at first intercourse
b) multiple sexual partners
c) male partner with multiple sexualpartners
- frequently multicentric in the vulva
- HPV 16 and 18

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Macroscopic Vaginal Carcinoma
Discrete, white (hyperkeratotic), flesh-colored or pigmented, slightly Primary vaginal carcinoma: extremely uncommon (1% of malignant
raised lesions neoplasms of the FGT)
Microscopic 95% are squamous cell carcinoma
Nuclear enlargement, pleomorphism, and hyperchromasia Most are associated with HPV
Abnormal mitotic figures Risk factors:
Involves skin appendages in >50% of all cases - early age at onset of sexual activity
Grading depends on the extent of replacement of the epithelium by - number of sexual partners
abnormal cells in the most severely involved areas: - infection with HPV
VIN 1: mild dysplasia; lower 3rd of the epith Greatest risk factor: previous carcinoma of
VIN 2: moderate dysplasia; 1/22/3 of the epith the cervix or vulva
VIN 3: severe dysplasia; >2/3 of the epith
carcinoma in situ; full thickness, but not surface layers Adenocarcinoma
Clinical
Rare
Develops in about 0.14% of those exposed to DES
Median age = 19 years
Anterior wall of the vagina, usually upper two-thirds
Macroscopic
Varies in size from microscopic to large
Most are polypoid and nodular but may be flat or ulcerated.

Clear Cell Adenocarcinoma

Microscopic
Histologic patterns
a) solid sheets of clear cells
b) tubulocystic pattern most common
c) less common:
papillary pattern
Non-HPV-related SCC: arise from lichen sclerosus or squamous cell tubular pattern resembling em CA
hyperplasia pattern composed of cords of cells w/ eosinophilic cytoplasm
- Differentiated VIN/VIN simplex: premalignant lesion
- Risk Factor: chronic epithelial irritation Embryonal Rhabdomyosarcoma(Sarcoma Botryoides)
Invasive CA: metastatic spread is linked to Clinical
a) size of tumor Almost always in infants and children; rare in vulva and vagina beyond
b) depth of invasion 10 years of age
c) involvement of lymphatic vessels Usually arises in the perineal or labial area (classified as vaginal in
Lesions < 2 cm. 60-80% 5-yr survival rate origin if the labia minora is involved)
Macroscopic
Vagina Polypoid usually solid
May simulate a bunch of grapes (more common in the vagina)
Developmental Anomalies
The old name botryoid rhabdomyosarcoma, is still often used. Sarcoma
Double vagina failure of total fusion of the mullerian ducts botryoides, or botryoid sarcoma. IS botryoid the Greek root word for grape
Mesonephric Cyst (Gartners Duct Cyst) bunches? Ans: YES
Found along the lateral walls of the vagina
Derived from wolffian duct rests
Microscopic
Lined by low cuboidal, non-mucin-secreting cells devoid of
cytoplasmic mucicarmine or PAS (+) material Thin squamous epithelial surface overlying the edematous or
myxomatous tumor
Vaginal Intraepithelial Neoplasia (VaIN, Dysplasia, Carcinoma In Situ) Cambium zone: dense cellular subepithelial layer
Mean age = 53 years Embryonal rhabdomyoblasts: round to spindled-shaped cells,
Risk factors: eosinophilic cytoplasm, and pleomorphic nuclei
immunosuppresion Microscopic
HPV infection
Rhabdomyoblasts with cross-striations seen in <15% of all cases
squamous neoplasia elsewhere in the lower genital tract
irradiation and in utero DES exposure Cytoplasm of tumor cells usually reactive for myoglobin, desmin, and
5% of VAIN progress to invasive squamous CA muscle-specific actin
Macroscopic
In most cases there is no grossly identifiable lesion Cervix
Epithelium on occasion may appear raised and white or pink
Microscopic
Microscopic features of VAIN are similar to squamous intraepithelial Endocervical Polyp
lesions of the cervix. Most common new growths of the uterine cervix
S/Sx: profuse leukorrhea
Polypoid lesion with loose myxomatous stromal core, containing
vessels and dilated endocervical glands
Lined by mucus endocervical glandular epithelium or metaplastic
epithelium

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Nabothian Cyst Squamous Intraepithelial Lesions (SIL)
Clinical
Most common cervical cyst Microscopic: LSIL
Develop within the transformation zone due to obstruction from Includes condyloma and CIN1
squamous metaplasia overlying endocervical glands Thickened epithelium (acanthosis) and koilocytic atypia in the mid
Macroscopic and upper portions of the epithelium
Usually superficial Koilocytic atypia:
Yellow or white cysts; frequently multiple Nuclear atypia with variation in nuclear size & shape, perinuclear
Measure up to 1.5 cm in diameter cavity, wrinkled nuclear membrane, and binucleate forms
Microscopic Microscopic: HSIL
Cysts lined by a flattened, single layer of mucin-producing
(endocervical) epithelium Includes CIN2 and CIN3
Nuclear atypia in all layers of the epithelium, in at least a portion of
Cervical Squamous Intraepithelial Lesions (SIL)
the lesion:
Historically, classified as dysplasia (mild, moderate, and severe) and
carcinoma in situ or cervical intraepithelial (CIN, grades 13) neoplasia Lesions with koilocytic atypia or maturation are equivalent to CIN2
SIL encompasses the entire morphologic spectrum of preinvasive Lesions without discernible maturation are equivalent to CIN3
squamous lesions
Linked to HPV infection: detected in ~90% of HSIL lesions (usually HPV Invasive Squamous Cell Carcinoma
16)
HPVs infect immature basal cells of the squamous epithelium in areas RISK FACTORS:
of epithelial breaks, or immature squamous metaplastic squamous 1. multiple sexual partners
cells present in the squamocolumnar junction 2. male partner w/ multiple sexual partners
HPVs cannot infect the mature superficial squamous 3. young age at first intercourse
4. high parity
5. persistent infection w/ high oncogenic risk HPV
6. Immunosuppression
7. certain HLA subtypes
8. Use of oral contraceptives
9. use of nicotine
Clinical
Uncommon before age 30, but 1/2 of patients are <50 years old at
diagnosis
Cervical biopsy necessary for diagnosis
Begins in the transformation zone & replaces adjacent squamous and
glandular epithelium Macroscopic
Natural history of SIL: Either on ectocervix or in endocervical canal
~50% of LSIL regress Exophytic, infiltrative, or ulcerative
~10% progress to high-grade lesions Microscopic
~1% progress to invasive cancer Considerable morphologic variation
Fewer high-grade lesions regress and more progress to invasive cancer Usually nests of neoplastic squamous epithelium with keratinization
or necrosis
Macroscopic Nuclei vary from uniform to pleomorphic
Best seen grossly by colposcopic examination after application of 3 Increased mitotic figures; atypical mitoses common
5% acetic acid Subtyped into keratinizing and non-keratinizing: depends on presence
Variety of colposcopic patterns depending on epithelial changes and or absence of keratin pearls
underlying vasculature Prognosis and survival depends on:
Occurs twice as often on the anterior lip of the cervix as on the - stage at which CA is first discovered
posterior lip; rare laterally - cell type: small cell neuroendocrine tumors
very poor prognosis
Cervical Squamous Intraepithelial Lesions (SIL) 5-year survival:
95% for stage Ia
Microscopic 80-90% for stage Ib
Abnormal cellular proliferation beginning in the basal & parabasal 75% for stage II
< 50% for stage III
layers; increased immature parabasal cells variably extending into
intermediate and superficial layers
Abnormal maturation with loss of polarity and cellular disorganization
Degree of maturity inversely related to severity of lesion

Microscopic
Microscopic grading of SIL:
Based on extent of replacement of epithelium by abnormal
proliferating parabasal cells, degree of nuclear atypia, and quadrivalent human bivalent human
papillomavirus papillomavirus
level at which mitotic figures are found recombinant recombinant vaccine
vaccine
Most clinically important distinction is between LSIL and
HSIL

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Verrucous Carcinoma Microscopic
Glands: sparse, focally dilated, and irregularly distributed; lined by
Type of well-differentiated squamous cell carcinoma that recurs atrophic, inactive, or proliferative endometrium
locally but does not metastasize Stroma: either focally or diffusely fibrotic; may contain variable
More common on vulva amounts of smooth muscle (classified as adenomyoma if stroma is
Associated with HPV 6 predominantly smooth muscle)
Uterus Characteristic thick-walled blood vessels, usually dilated

Endometrial Hyperplasia
Acute & Chronic Endometritis
Increased proliferation of endometrial glands relative to the stroma
Usually result from ascending infection through the cervix
Associated with prolonged estrogen stimulation
Cervical barrier is compromised during parturition, abortion, menses,
Condition associated with hyperplasia:
and instrumentation
a) obesity
Clinically significant acute endometritis is usually associated with
b) menopause
pregnancy or abortion
c) polycystic ovarian disease
- usually caused by Streptococcus, Staphylococcus, Neisseria
d) functioning GCT of the ovary
gonorrheae, or Clostridium welchii
e) excessive cortical function
Chronic endometritis occurs in:
f) prolonged administration of estrogen therapy
a) pts sufferring from chronic PID
b) postpartum or post-abortion pts w/retained gestational tissue
Genetic alteration: inactivation of the PTEN tumor suppressor gene
c) women with IU contraceptive device
(>20% of hyperplasias and in 30-80% of endometrial CA)
d) women with TB

Endometriosis / Adenomyosis
ENDOMETRIOSIS:
endometrial tissue outside of the uterus
- occurs in the ovaries, uterine ligaments, rectovaginal septum, cul
de sac, pelvic peritoneum; large and small bowel & appendix; mucosa of the
cervix,vagina, and FT; laparotomy scars

ADENOMYOSIS:
Common non-neoplastic condition where endometrial glands and
stroma are found within the myometrium
Simple Hyperplasia
Commonly associated with abnormal menstrual bleeding, dysmenorrhea, and Cystically dilated glands with glandular outpouchings
uterine enlargement, but may be asymptomatic In some cases, the glands are focally crowded but only minimally
Abnormalities that distinguish normal from endometriotic tissue: dilated
a. profound activation of the inflammatory cascade high levels of Pseudostratified columnar cells without cytologic atypia line the
PGE2, IL-1B, TNF and IL-6 glands
b. estrogen production by endometriotic stromal cells is upregulated due Variable mitotic activity
to high levels of aromatase
Complex Hyperplasia
Abnormalities are related to epigenetic changes in key genes that encode 2 Crowded glands with little intervening stroma
nuclear receptors steroidogenic factor-1 and estrogen receptor-beta Characteristically have back-to-back glands with papillary intraluminal
infoldings
Macroscopic Variable mitotic activity, usually <5 mitotic figures per 10 high-power
Usually moderately enlarged uterus fields
Myometrium usually thickened, with a trabeculated cut surface No cytologic atypia
Lesions may be visible grossly as small, soft, pink or gray-white areas
within the myometrium Simple/Complex Hyperplasia with ATYPIA
Hemorrhagic foci and small cysts may be seen Simple or complex glandular architecture
Microscopic Glands lined by cytologically atypical cells (increased
Presence of endometrial glands & stroma within the myometrium nuclear:cytoplasmic ratio, prominent nucleoli, nuclear stratification)
Usually inactive or proliferative endometrium Confluent glands
Variable mitotic activity

Endometrial Polyp
Clinical Endometrial Carcinoma
One of the most common pathologic lesions of the uterine corpus
Benign nodular lesion above the endometrial surface
Most common invasive CA of the FGT
Due, in part, to estrogenic stimulation Accounts for 7% of invasive CA in women
Usually seen in perimenopausal or postmenopausal women
Peak incidence: 55-65 y/o
Macroscopic Classification:
Sessile or pedunculated; usually solitary Type I carcinoma
Located anywhere within the uterine cavity
Type II carcinoma
Surface usually smooth, tan, and glistening
May have focal erosions, hemorrhage, and/or necrosis

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Characteristics Type I Type II Pain, dysmenorrhea, menorrhagia, metrorrhagia, or constipation may

be seen with larger or multiple leiomyomas
Age 55-65 years old 65-75 years old 40% have chromosomal abnormality
Clinical Setting Unopposed Estrogen Atrophy Malignant transformation is extremely rare
Obesity Thin Physique Macroscopic
Hypertension Solitary or multiple (multiple in 2/3 of patients)
DM Well-circumscribed
Morphology Endometrioid Serous May be submucosal, intramural, or subserosal:
Clear Cell Firm pearly white to tan cut surface with whorled trabecular pattern
Mixed Mullerian Degenerative changes: hemorrhage, hyalinization, necrosis,
Tumor calcification, and myxoid or cystic changes
Precursor Hyperplasia Endometrial Microscopic
intraepithelial Composed of smooth muscle cells arranged in anastamosing whorled
Carcinoma fascicles
Molecular Genetics PTEN P53 Nuclei are uniform, elongated, and cigar-shaped, with blunt or
PIK3CA Aneuploidy tapered ends
KRAS PIK3CA Usually more cellular than the surrounding myometrium
MSI Mitotic figures infrequent or absent (<5 mitotic figures/10 HPF)
B-Catenin
P53 LEIYOMYOSARCOMA
Behaviour Indolent Aggressive Clinical
Spreads via Lymphatics Intraperitoneal and Represents ~30% of all uterine sarcomas
Lymphatic spread Usually occurs in postmenopausal women, average age = 52 years (a
Classification of endometrial carcinoma decade older than women with leiomyoma)
Endometrioid adenocarcinoma: Presenting symptoms include abnormal bleeding, lower abdominal
Villoglandular pain, or pelvic or abdominal mass (occasionally rapidly growing)
Secretory Macroscopic
Ciliated cell Usually large, solitary, poorly circumscribed
Endometrioid adenocarcinoma with squamous differentiation Most are intramural
Serous carcinoma Soft fleshy appearance with variegated cut surface
Clear cell carcinoma Gray-yellow or pink with hemorrhagic and/or necrotic areas
Mucinous carcinoma May grossly extend beyond the uterus
Squamous carcinoma Microscopic
Mixed types of carcinoma Very cellular tumor composed of intersecting fascicles of large atypical
Undifferentiated carcinoma spindled cells
Atypical hyperchromatic nuclei with rounded ends, coarse chromatin,
ENDOMETRIAL CANCER and prominent nucleoli
Clinical Multinucleated giant cells found in 50% of cases
Endometrial carcinomas are the most common invasive malignant Hemorrhagic and necrotic foci may be prominent
tumors of the female genital tract Many have at least focal infiltration into adjacent myometrium
Risk factors include: Microscopic
Unopposed estrogen stimulation, including ovarian lesions Three main criteria for diagnosis:
associated with increased estrogen production Mitotic activity: usually have 10 or more mitotic figures/high-power field
Obesity Significant nuclear atypia
Nulliparity or low parity Hypercellularity
Hypertension
Possible diabetes mellitus Fallopian Tube
Most occur in perimenopausal and postmenopausal women
Almost always present with abnormal bleeding ACUTE SALPINGITIS
Clinical
Macroscopic Usually due to the direct passage of bacteria from uterine cavity into
Almost all histologic subtypes look similar grossly tubal lumen, but may spread via lymphatic or hematogenous route
More frequently seen on posterior than anterior wall Polymicrobial etiology: N. gonorrhoeae, C.
Surface often focally ulcerated with soft, friable, gray white tumor trachomatis, anaerobic bacteria, E. coli and others
mass below Typically, onset of pain several days after menses
Microscopic Recurrent infections result in chronic salpingitis
Endometrioid CA is the most common type seen Close association with chronic endometritis
Comprised of small, round, fairly uniform glands Macroscopic
The glands of a well-differentiated endometrioid carcinoma are Enlarged, edemetous, erythematous tube(s)
usually lined by uniform cells with single or moderately stratified Frequently show fibrinopurulent serosal and luminal exudate
nuclei May be adherent to adjacent structures, including ovary
Occasionally may see increased nuclear atypia Tubo-ovarian abscess may result
Mitotic activity variable Microscopic
Initial marked neutrophilic transmural and mucosal infiltration with
LEIYOMYOMA intraluminal exudate
benign smooth muscle tumor Associated congestion and edema
Most common neoplasm of the uterus Possible tubal mucosal ulceration
Occurs in ~2040% of women >30 years of age Subsequent lymphoplasmocytic infiltrate
Rare in women <18 years of age Surface fibrin deposition resulting in adherence of mucosal plicae

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CHRONIC SALPINGITIS Usually postmenopausal, sixth or seventh decade
Caused by chronic, recurrent infections Classic triad seen in <50% of cases:
Large dilated tube with shaggy lining and thick walls Pain
Healing and organization lead to permanent bridging between plicae Vaginal discharge
with resulting follicular salpingitis (adherent tubal plicae, variably- Palpable adnexal mass
sized follicle-like spaces) Macroscopic
Fimbriae may occlude completely and form pyosalpinx Swollen tube due to marked intraluminal growth
Microscopic Lumen usually filled and dilated by solid or papillary growth
Multiple tuboovarian adhesions; may progress to tuboovarian abscess Frequently bilateral
Resolution of purulent salpingitis: Microscopic
Severely scarred tube Usual histologic appearance similar to that of an invasive papillary
Hydrosalpinx: serous adenocarcinoma of the ovary:
Obliterated fimbriated end with dilated tube Branching papillae covered by epithelium with enlarged,
Clear serous fluid within tube pleomorphic, hyperchromatic nuclei
Low cuboidal epithelial lining with occasional remaining plicae Increased and atypical mitoses
Unlikely recovery of tubal function; often bilateral May see abrupt transition from normal to neoplastic epithelium

SALPINGITIS ISTHMICA NODOSA

Clinical PART II
Average age at diagnosis = 30 years
Single or multiple diverticula of tubal epithelium in the isthmic region
Possibly adenomyosis-like process, but exact etiology unknown
Ovaries
Associated with infertility and ectopic pregnancy
Macroscopic
Yellow-white nodular swellings in the isthmus, 12 cm in diameter
Smooth serosa
Bilateral in up to 85% of cases
Microscopic
Cross-sectioned diverticula appear as isolated glands lined by tubal
epithelium and separated by broad bands of smooth muscle
Usually no connection with serosal surface

ECTOPIC PREGNANCY
Clinical
12% of all conceptions are ectopic
>95% occur in the fallopian tube
Majority (7580%) occur in the ampulla, 1015% isthmic, 5% at the The CORTEX is the site of developing follicles.
fimbriae The MEDULLA is relatively free of developing follicles, and rich in connective
Previous history of pelvic inflammatory disease in 3545% of all cases tissue (stroma) and blood vessels.
If not recognized, rupture typically occurs around the eighth
gestational week
Macroscopic
If unruptured, grossly seen as irregular dilation of bluish-colored tube
(from hematosalpinx)
Chorionic villi usually identified within blood-filled, dilated lumen
~2/3 contain identifiable embryo (grossly or microscopically)
Microscopic
Chorionic villi and extravillous trophoblast can grow intraluminally or
penetrate deeply into the muscularis
Evidence of chronic salpingitis found in ~50% of all cases
Tubal wall should be examined for evidence of salpingitis isthmica GREAT whole mount to demonstrate overall cortex vs. medullary differentiation.
nodosa
FOLLICLE CYST
PARATUBAL CYST Clinical
Mesothelial or paramesonephric (mllerian) in origin: Common after menarche
Mesothelial cysts: Seen in childhood to menopause
Includes large majority of paratubal cysts >3 cm May be seen in cases of precocious puberty
Lined by flat cells and surrounded by thin fibrous wall Benign
Paramesonephric cysts: Macroscopic
Also known as hydatids of Morgagni Corpus follicle:
Small (210 mm) round cysts attached by pedicle to the fimbriae Physiologic secondary ovarian follicle <1 cm
Thin translucent wall containing clear serous fluid Cystic follicle:
Lined by ciliated and nonciliated cells Physiologic secondary follicle 13 cm in size
Follicular cyst:
INVASIVE ADENOCARCINOMA Unilocular smooth-walled cyst or cysts 310 cm
Clinical Microscopic
Rare; accounts for <1% of primary genital tract malignancies Cyst wall lined by inner theca layer and outer granulosa layer
Direct tubal extension by uterine or ovarian carcinoma is 10 times
more common
Diagnosis rarely made preoperatively

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Polycystic Ovarian Disease (PCOD) / Multiple Follicular Cysts / Stein-Leventhal Macroscopic
Syndrome Bluish-red macules on serosal surfaces or chocolate cysts in ovary
Microscopic
Young women presenting with symptoms / signs of ovarian failure: Three components: endometrial type glands, endometrial stroma, and
Oligomenorrhea or amenorrhea hemorrhage/hemosiderin-laden macrophages
Infertility
Hirsutism (50%) Neoplasms of the Ovary
- Obesity (40%)
Affects 3-6% of reproductive age women
Pathogenesis: enzymes involved in androgen biosynthesis are poorly
regulated
Macroscopic
Normal to slightly enlarged ovaries
Multiple cysts usually <1 cm
Often no coropora lueta or follicular cysts
Microscopic
Fibrous hypocellular ovarian cortex
Multiple cysts with inner layer(s) of nonluteinized granulosa cells and
prominent outer layer of luteinized theca cells
Hyperthecosis often present
Primordial follicles can be identified.

Corpus Luteoma / Corpus Luteum Cyst

Clinical
Most common during reproductive years
Rarely reported to be seen at birth
Rare rupture with hemoperitoneum
Macroscopic
Often yellow coloration of cyst wall and/or hemorrhage
Corpus luteum/cystic corpus luteum 12.5 cm (physiologic)
Corpus luteum cyst >2.5 cm Surface Epithelial-Stromal Tumors
Microscopic General
Physiologic cyst lined by luteinized granulosa cells and theca layer 2/3 of all ovarian tumors; 90% of all malignant ovarian tumors
and/or hemorrhage and central necrosis Thought to originate from surface epithelial invaginations

Serous Tumors
GENERAL
Serous tumors account for ~30% of all ovarian neoplasms
Approximately 70% of serous tumors are benign, 25% are carcinomas,
and 5% to 10% are borderline tumors
Serous CA: account for approx. 40% of all cancers of the ovary
- MOST COMMON malignant ovarian tumors
ENDOMETRIOSIS
RISK FACTORS for Malignant Serous Tumors:
1. nulliparity
2. family history
3. heritable mutations mutations in BRCA1 and
BRCA2
Serous Ovarian CA divided into:
a) Low-grade: mutations in KRAS & BRAF oncogenes; rare p53
b) High-grade: p53 mutations; (-) mutations in KRAS & BRAF oncogenes

Clinical
Women in reproductive years
Ovary is the most common site of involvement
Often present with pain and fertility problems
May give rise to hyperplasia or carcinoma as in uterus
Hormonal therapy is often initial treatment

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Benign Serous Tumors Malignant Serous Tumors
General Classification Based on Atypia

BENIGN BORDERLINE MALIGNANT

Single layer Papillary architechture Papillary, solid
Papillary
Uniform, non- Cell atypia present Cell atypia present
stratified
No stromal invasion No stromal invasion Stromal invasion
present

Macroscopic
Predominantly unilateral (bilateral in 30% to 50% of cases)
Unilocular thin-walled cyst, occasionally multilocular, 130 cm
Thin watery to slightly viscous fluid
Moderate size
And/or small polypoid excrescenses

Clinical
Occur at slightly older age than benign serous lesions, 5060 years
Bilateral ovaries in 2/3 of cases
Most patients present with advanced stage disease
Macroscopic
Any size from few millimeters to >20 cm
Cystic, papillary with turbid and hemorrhagic fluid, necrosis
Surface papillae may be present.
Psamomma bodies usually present ~70%
Microscopic
Tumors with stromal invasion, nuclear atypia, numerous mitoses, and
complex architectural features (slitlike glandular lumina, tight nests,
etc.)

Mucinous Tumors
GENERAL
30% of ovarian tumors
Borderline Surface Tumors of the Ovary 85% of mucinous tumors are benign
Atypical proliferating, of low malignant potential Bilateral in 10% to 20% of cases
Show intermediate features between benign and malignant Molecular pathogenesis: mutation in KRAS proto-oncogene
neoplasms
Epithelial proliferation greater than that in benign tumors Pseudomyxoma peritonei: defined by extensive mucinous ascites, cystic
Cellular stratification with epithelial budding and tufting: epithelial implants on the epithelial surfaces, adhesions and frequently mucinous
Cellular buds may appear detached fr lining tumors involving the ovaries
May have cribriform patterns
Mild-moderate nuclear atypia Benign Mucinous Tumors
Mitotic figures rare to prominent
Absence of stromal invasion
Up to 40% may have cystic/papillary serous lesions arising in
omentum, lymph nodes, or pelvic organs (implants), which does not
change prognosis

Clinical
Adnexal mass
Most frequent around 3050 years (borderline mucinous tumors 40
70 years)
Association with Brenner tumors, Peutz-Jehgers syndrome,
pseudomyxoma peritonei (intestinal type), and teratoma
Macroscopic
Tendency toward larger size when compared to serous tumors (up to
50 cm)
Often multilocular with thin-walled cysts and thick mucinous fluid
Papillations not a prominent feature

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Microscopic Macroscopic
Cyst wall lined by columnar epithelium with basal nuclei similar to Solid and/or cystic mass
endocervix or intestinal-type lining (borderline tumors) with Often hemorrhagic
occasional goblet cells, Paneth cells, or mixed types May grossly resemble adenofibroma
Stroma shows variable degrees of fibrous component, usually not Microscopic
prominent Tubular glands resembling endometrial adenocarcinoma/hyperplasia
Minor nuclear atypia may be seen in mucinous tumors without other Pseudostratified, non-mucinous epith
features of borderline tumors/carcinomas +/-squamous differentiation (30%)
- usually benign occasionally malignant
Secretory change may be present
Borderline Mucinous Tumors
Variants
Benign
- cystadenoma w/ squamous difftn
- adenofibroma or cystadenofibroma +/- squamous difftn
Borderline (rare)
- Adenofibroma
- Cystadenofibroma
Malignant
Clinical
- Adenocarcinoma
Peak incidence around 30 years
- Cystadenocarcinoma
Microscopic
- Adenocarcinofibroma / cystadeno-carcinofibroma
Greater epithelial proliferation than benign mucinous tumors
- Endometrial stromal sarcoma
Borderline tumors more likely to have solid areas or excrescences
- Mesodermal mixed tumors (carcinosarcoma)
Lining epithelium more likely to be intestinal type (89%); mllerian
(15%)
Malignant Mixed Mullerian Tumor (MMMT)
Microscopic
Postmenopausal women
Tumors of intestinal type associated with pseudomyxoma peritonei
Similar macro- and microscopic appearance as in uterus
Mllerian type associated with extraovarian implants
Stage most important but poor prognosis overall
Some tumors may show foreign body giant cell reaction due to mucin
Mullerian adenosarcoma: malignant stroma and benign glandular
extravasation
component
Malignant Mucinous Tumors

Clinical
Women 4070 years
10% to 20% bilateral
Pseudomyxoma peritonei:
Synchronous tumor of appendix usually identified
Consider metastasis if appendiceal primary present
Macroscopic
Necrosis and hemorrhage more commonly associated with carcinoma
Solid areas and mural nodules more common
Microscopic
Malignant tumors show nuclear atypia, epithelial stratification, Clear Cell (Mesonephroid) Tumor
architectural complexity, and invasion
CEA positivity seen in 100% malignant mucinous tumors as compared
to 30% of endometrioid and serous types

Endometrioid Tumors
GENERAL
15% to 25% of ovarian tumors; account for 10-20% of ovarian CAs
Most (>75%) are malignant with benign and borderline endometrioid
tumors rare
Clinical
Origin in endometriosis in 10% of cases
Uncommon (5% of ovarian tumors)
May be assoc w/ independent uterine CA or represent spread fr
Benign, borderline, and malignant categories
uterus (33%)
Most commonly occur in ages 50-70
Most carcinomas are well-differentiated, low stage with good
Usually unilateral, infrequently bilateral
prognosis
Prognosis based on stage
Pathogenesis: 15-20% of cases with endometrioid CA coexist with
Macroscopic
endometriosis
Gross resemblance to adenofibromas with white/yellow color and/or
Molecular pathenogenesis: mutations in PTEN tumor suppressor
hge, necrosis; may be spongy or cystic
genes, KRAS and B-catenin oncogenes and microsatellite instability
Average diameter = ~15 cm.

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Often unilocular, thick-walled cyst with solid nodules in cyst wall Usually unilateral, 15% bilateral
May arise in endometriotic cyst Good prognosis, >95% survival rate
Microscopic Macroscopic
Clear cell adenofibroma: Solid, grayish white surface w/ fibrous capsule
- fibrous stroma w/ glands lined by flat to slightly Focal hemorrhage & necrosis can be seen
hobnail cells and clear cells
Clear cell carcinoma:
- fibrous stroma w/ prominent hobnail cells and clear cells Yolk Sac Tumors
- complex papillae w/ hyalinized cords (Endodermal Sinus Tumors)
- diffuse, tubulocystic, papillary, trabecular patterns
- hyaline bodies may be present (25%)

Transitional Cell Tumor

BRENNER TUMOR:
Clinical
Adenofibromas in which the epithelial component consists of nests of
transitional-type epithelial cells resembling those lining the urinary
bladder
< 2% of all ovarian tumors Young patients, most <20 years
Women 40-80 years old Derived from differentiation of malignant germ cells along the extra-
Slow-growing neoplasm, often incidental finding embryonic yolk sac lineage
Most are benign with <2% borderline or malignant Elevated serum AFP and A1-AT
Microscopic Highly aggressive tumor with tendency for widespread metastasis;
Nests of round/polygonal cells surrounded by dense fibroblastic stage most important prognostic factor
stroma Macroscopic
Transitional cell-like cells w/ sharply defined borders, clear Smooth external surface, partially cystic
cytoplasm, & distinct nucleus w/ longitudinal groove Foci of necrosis & hemorrhage
Average size ~15 cm.
Malignant Brenner tumors: with invasion and identifiable benign Brenner Microscopic
component Cuboidal cells with loose reticular pattern and microcystic areas; solid
undifferentiated areas
Schiller-Duval bodies (glomerulus-like structure composed of a central
blood vessel enveloped by germ cells within a space lined by germ
cells)

Embryonal Carcinoma

Germ Cell Tumors

Clinical
Young patients, <20 years
Elevated serum AFP
Elevated hCG
Aggressive malignant tumor with early metastasis
Macroscopic
Median size = 17 cm.
Smooth external surface, predominantly solid
Variegated cut surface with necrosis and hemorrhage
Microscopic
Dysgerminoma Sheets or nests of large, undifferentiated cells with abortive glandular
formations
Large and prominent centrally located nucleus
Numerous mitoses

Choriocarcinoma
Clinical
Most ovarian choriocarcinomas represent metastases from the uterus
May arise as choriocarcinomatous differentiation in germ cell tumor
or pure ovarian primary
Clinical Young women
Young patients (children and young adults <30) Elevated hCG
+/- elevated hCG
Arise in both normal and abnormal gonads (gonadoblastoma)
Female counterpart of seminoma in males

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Teratoma Microscopic
MATURE TERATOMA Normal to nodular thyroid tissue that can show features of thyroiditis,
hyperplasia or carcinoma
Cystic changes may be prominent

Sex Cord Stromal Tumors

General
Approximately 5% of all ovarian tumors
Tumors that show differentiation towards sex cords and stroma
Undifferentiated gonadal mesenchyme eventually produces structures
of specific cell type in both male (Sertoli and Leydig) and female
(ganulosa and theca)

Granulosa Theca Cell Tumors

Mature Teratoma, cystic type:

Most common childhood ovarian neoplasm
Usually unilateral
Multiloculated mass with teeth (Rokitanskys protuberance), hair & Ovarian neoplasms composed of varying proportions of granulosa and
caseous-like keratin material theca cell differentiation
Microscopically composed of mature, adult tissues 5% of all ovarian tumors
2/3 occur in postmenopausal women
Fetiform Teratoma: cystic teratomas w/ identifiable body-like structures Associated with symptoms of hyperestrinism (metrorrhagia) &
endometrial hyperplasia
Epidermoid Cyst: cystic teratomas with skin epithelium, without skin adnexae or Clinical importance of GCT:
other elements 1. potential to elaborate large amts of estrogen
2. small but distinct hazard of malignancy
IMMATURE TERATOMA (Malignant) All GCT are potentially malignant (5-25%)
Elevated tissue and serum levels of inhibin (a product of granulosa
cells)
Macroscopic
Unilateral > 90%
Solid mass with smooth external surface
Small cysts with thin fluid sometimes present
Cysts occasionally large
Yellow cut surface tumors that are hormonally active due to IC lipids
Microscopic
Adult and primitive, embryonal-type tissues seen microscopically
Variable architectural patterns with microfollicular (Call-Exner bodies),
Grossly solid, solid and cystic, or mostly cystic
macro-follicular, diffuse, trabecular
Immature neural type tissue most often seen but any immature tissue
Nuclei with folds or grooves coffee-bean nuclei
from ectoderm, mesoderm, or endoderm can be encountered
Variable luteinization
Prognosis based on amount & type of immature components
Fibroma/Thecoma/Fibrothecoma
Grading:
Composed of either fibroblasts (fibroma) or plump spindle cells with
Grade 1 predominantly mature tissues w/ loose mesenchymal tissue,
lipd droplets (thecomas)
immature cartilage, & tooth anlage
Any age; ~4% of ovarian tumors
Grade 2 fewer mature tissues; focal neuroepithelial tissue w/ mitotic figures
Arise from ovarian stromal cells
<3/HPF
Unilateral; benign clinical course
Grade 3 few to no mature tissues and abundant neuroepithelium
Associated with
- Meigs Syndrome (fibroma, ascites,pleural effusion/hydrothorax)
Monodermal or Specialized Teratoma: Struma Ovarii
- Gorlins syndrome (basal nevus cell syndrome)
Macroscopic
Firm, solid, white-colored mass; ave. size = 12 cm.
Some with cystic or myxoid change
Microscopic
Spindle cells with storiform pattern or intersecting bundles
Cellular fibromas: hypercellular fibromas
Mitoses should not exceed >3 mitoses/10HPF
Inhibin +
Overgrowth of thyroid tissue in association with teratoma
Associated w/ Brenner tumor, mucinous cystadenoma, and carcinoid
tumors
Macroscopic
Gross appearance of thyroid tissue with red, meaty consistency
Occasionally cystic

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Sertoli-Leydig Cell Tumors (Androblastoma / Arrhenoblastoma) Mucin-laden, signet-ring cells strewn individually and in small clusters
within a hypercellular ovarian stroma (occasionally with storiform
pattern).

Gestational and Placental Disorders

Spontaneous Abortion
Pregnancy loss before 20 weeks of gestation
CAUSES:
1. Fetal
Clinical - chromosomal anomalies (aneuploidy,polypoidy and
Uncommon tumor (< 0.5%) translocations)
Young women, rarely postmenopausal 2. Maternal
Predominantly unilateral - luteal-phase defect; poorly controlled diabetes
Symptoms of androgen excess (hirsutism, acne, balding, etc) in 30- 3. Physical defects of uterus
40% of cases submucosal leiomyoma, uterine polyps or uterine
Relatively good prognosis, most Stage I malfotns (prevent implantation)
Macroscopic 4. Systemic dso affecting maternal vasculature
Solid and cystic mass, 5 15 cm. (APAS, coagulopathies and HPN)
Lobulated, capsulated, yellow, tan 5. Infections (Toxoplasma, Mycoplasma, Listeria, viral)
Rare: hemorrhage and necrosis
Microscopic Ectopic Pregnancy
Tubules composed of Sertoli cells or eosinophilic Leydig cells Implantation of the fetus in any sire other than a normal IU location
interspersed with stroma Fallopian tube - most common site (90%)
Hilus cell tumors (pure Leydig cell tumors): large, lipid-laden cells with Other sites: ovary, abdominal cavity, IU portion of the FT (Cornual
distinct borders pregnancy)
- (+) Reinke crystalloids Most important predisposing condition: previous PID chronic
- elevated 17-ketosteroid excretion level unresponsive to follicular salpingitis
cortisone suppression Other conditions predisposing to peritubal scarring & adhesions:
Gynandroblastoma appendicitis, endometriosis and previous surgery
Rare
Sex cord-stromal tumor with Sertoli-Leydig cells and granulosa cell Preeclampsia and Eclampsia
components in similar proportions PREECLAMPSIA: systemic syndrome char by widespread maternal
endothelial dysfunction presenting clinically with HPN, edema, and
Gonadoblastoma proteinuria during pregnancy
Clinical - occurs in 3-5% of pregnant women
Composed of a combination of germ cells & sex cord-stromal cells CRITICAL ABNORMALITIES of Preeclampsia
Occurs in individuals with gonadal dysgenesis (XY gonadal dysgenesis - Diffuse endothelial dysfunction
and XO-XY mosaicism) - Vasoconstriction (leading to HPN)
Macroscopic - Increased vascular permeability (resulting in proteinuria
Bilateral in 1/3 cases and edema)
Small mass, may be incidental finding

Microscopic
Mixture of germ cells and sex cord-stromal elements with features of
granulosa or sertoli cells
Calcification and or hyalinization present
Dysgerminoma: 50%

Metastatic Tumors
Most common metastatic tumors of the , ovary: tumors of mullerian
origin (uterus, FT, contralateral ovary or pelvic peritoneum)
Most common extramullerian primaries: breast & GIT (colon,
stomach, biliary tract & pancreas)
- Pseudomyxoma peritonei (appendiceal tumor)
- Krukenberg tumor (gastric tumor)

Krukenberg Tumor
Average age: ~ 45 years
Bilateral in 80% or more cases.
Source in 70% - 100% is a gastric carcinoma, usually arising in pylorus
Next most common primary sites are large intestine, appendix and
breast
90% of patients have symptoms related to ovarian involvement, most
commonly abdominal pain and swelling
Typically form rounded or reniform, firm, white masses that may be
bosselated, yellow or white on cut section.
Fleshy, gelatinous or spongy areas are common.

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Gestational Trophoblastic Disease

Partial Hydatidiform Mole

Clinical
Trophoblastic hyperplasia results from unbalanced overexpression of
paternal gene products
Presentation:
- late 1st or early 2nd TM spontaneous abortion
- Occasionally presents with elevated maternal hCG
Overall prevalence: 1/39 spontaneous abortions
Macroscopic
Spongy villous tissue with small 1-2mm fluid-filled vesicles (as in
hydropic abortus & complete H-mole)
Abnormal placentation in preeclampsia. Fetal fragments or malformed fetus may be seen occasionally
Microscopic
Exchange of oxygen, nutrients, and waste products between the fetus and Diagnostic criteria:
the mother depends on adequate placental perfusion by maternal vessels. In Villous trophoblast hyperplasia (usually predominantly
normal placental development, invasive cytotrophoblasts of fetal origin invade syncytiotrophoblast)
the maternal spiral arteries, transforming them from small-caliber resistance Dimorphic popn of large & small villi w/o intermediate forms
vessels to high-caliber capacitance vessels capable of providing placental o Hydropic villi > 0.5 mm.
perfusion adequate to sustain the growing fetus. During the process of vascular Irregular villous contour often w/ multicellular trophoblast
invasion, the cytotrophoblasts differentiate from an epithelial phenotype to an inclusions within villous stroma
endothelial phenotype, a process referred to as "pseudovasculogenesis" (upper
panel). In preeclampsia, cytotrophoblasts fail to adopt an invasive endothelial Complete Hydatidiform Mole
phenotype. Instead, invasion of the spiral arteries is shallow and they remain
small caliber, resistance vessels (lower panel). This may result in the placental
ischemia.

PRINCIPAL pathophysiologic aberrations:

a) abnormal placental vasculature
b) endothelial dysfunction and imbalance of angiogenic and anti-
angiogenic factors
c) coagulation abnormalities preeclampsia is associated with
hypercoagulable state thrombosis of arterioles & capillaries
throughout the body Clinical
a. related to reduced endothelial production of PGI2 Trophoblastic hyperplasia results from an overexpression of
(antithrombotic factor) and increased release of paternally-derived gene products &/or lack of maternally-derived
procoagulant factors gene products
Early presentation (< 8 weeks):
Microscopic: - anembryonic missed abortion by UTZ
1) placental infacrts Late presentation (> 8 weeks):
2) increased frequency of retroplacental hematomas due to bleeding - Large for dates
and instability of uteroplacental vessels - elevated hCG
3) thrombosis, lack of normal physiologic conversion, fibrinoid necrosis - vaginal bleeding
or intraintimal lipid deposition in the decidual vessels Incidence of persistent GTD requiring chemotherapy = 20-30%
Rate of subsequent choriocarcinoma is approximately 1/40
Macroscopic
Usually a discohesive collection of swollen, grape-like molar villi up to
5-10mm
Microscopic
Diffuse, circumferential villous trophoblast hyperplasia
Involves both cytotrophoblasts & syncytiotrophoblasts
Uniformly hydropic villi, many with well-defined central cisterns
Lack of fetal vessels & nRBCs

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 FEMALE GENITAL TRACT Dr. Nerves 2012
Feature Complete Mole Partial Mole Sometimes, it takes a painful experience to make us change our ways.Hindi lahat ng nagpapakita
ng sweetness sayo e mahal ka na. may mga tao lang talaga na gawa sa candy at nababalot ng plastic. Its not
Karyotype 46 xx (46 xy) Triploid about what you did in the past, its about the effort you made to make things right again.There will always be a
sunshine after the rain.
Villous edema All villi Some Villi
1. Pag kinikilig, in love agad? Di ba pwedeng naiihi muna?!
Trophoblast Diffuse; Focal;slight
2. Pag mahaba ang hair ligawin na agad? Di ba pwedeng Sadako muna?!
proliferation Circumferential 3. Pag malaki boobs Ethel agad? Di ba pwedeng Carlos Agassi muna?!
Atypia Often present Absent 4. Pag mahaba ang mga biyas supermodel na agad? Di ba pwedeng lastikman muna?!
Serum hcg Elevated Less elevated 5. Pag nagbigay ng bulaklak nanliligaw na? Di ba pwedeng nakikiramay muna?!
6. Pag nagsusuka, buntis agad? Di ba pwedeng nakita ka lang muna?
HCG in tissue ++++ + 7. Pag adik, sa drugs na agad? Di ba pwedeng sa'yo muna?!
Behavior 2% Choriocarcinoma Rare Choriocarcinoma 8. Pag walang kibo, behaved na agad? Di ba pwedeng comatose muna?!
9. Pag payat ang babae model na agad? Di ba pwedeng may TB muna?!
Invasive Mole 10. Pag hot yung babae sexy na agad? Di ba pwedeng may dengue muna?!
Microscopic 11. Pag di nakatulog, may insomnia na agad? Di ba pwedeng iniisip ka muna?!
Aka: chorioadenoma destruens 12. Pag di pinansin, hindi na mahal agad? Di ba pwedeng nag papa-miss muna?!
A hydatidiform mole in which villi penetrate deeply the myometrium 13. Pag abnormal Budoy na kagad? Di ba pwedeng ikaw muna?!
14. Pag lalaki naka-make up, bakla agad? Di ba pwdeng clown muna?!
and/or its vessels
15. Pag namumula ang mukha, blushing agad? Di ba pwedeng nasampal lang muna?!
16. Pag gwapo, sa iyo na agad? Di ba pwedeng pumila ka muna?!
Choriocarcinoma 17. Pag maraming chicks, babaero agad? Di ba pwedeng friendly muna?!
Clinical 18. Pag walang Boyfriend panget agad? Di ba pwedeng choosy muna?!
Rapidly growing and invasive, with frequent metastases
Can follow any pregnancy at any stage BANAT TIME
Frequency of preceding pregnancy types: Dugo ka ba?
Ikaw kasi tinitibok ng puso ko.
- H-mole = 45%
- Term pregnancy = 25% Nakalunok ka ba ng kuwitis?
- Spontaneous abortion = 25% Kasi pag ngumiti k may spark!
- Ectopic pregnancy = 5%
Macroscopic Boy : Ayoko sa mga taong nakapaligid sa mundo ko!
Girl: Pati ba ako? :(
Grossly hemorrhagic , ill-defined lesions within the uterovaginal wall Boy : Ikaw kaya yung mundong tinutukoy ko.
or in the parenchyma of other organs GirL : Anung Pangarap mo
Often difficult to detect nonhemorrhagic tumor tissue Boy : Ang Mapag isa
Microscopic Girl : SUNGET NAMAN !!!!!!!!!!!!
Biphasic tumor composed of malignant villous cytotrophoblast and Boy : wee ! Gusto Ko Mapagisa Ang Puso Nating Dalawa
syncytiotrophoblast Boy: Miss pwede makahiram ng ballpen?
Girl: Sure, eto oh.
Classic Pattern: Boy: Ayaw naman sumulat e.
- groups of 10-50 cytotrophoblasts Girl: Meron yan. Kakagamit ko lng kanina nian.
Boy: Cge nga, isulat mo nga number mo jan.
Uniformly enlarged central nuclei,prominent nucleoli, and
margination of chromatin BOY: Mayabang ba ako?
Scant, watery clear cytoplasm GIRL: Hindi naman. Bakit?
- Surrounded by a wreath-like arcade of multinucleate syncytiotrophoblast BOY: Sabi kasi nila mayabang ako..
Enlarged irregular, hyperchromatinc nuclei and glassy E ikaw lang naman pinagyayabang ko. :)
eosinophilic cytoplasm sana patay na lng ang ilaw.!
para tau nalng mag on )
Placental Site Trophoblastic Tumor BOY: miss, salamin ka ba?
Neoplastic proliferation of extravillous trophoblasts (intermediate GIRL: huh? bakit? kasi masarap ako titigan?
trophoblasts-produce HPL) BOY: hinde! putek! sarap mong basagin!
BOY: miss, salamin ka ba?
Rare, generally indolent tumors GIRL: huh? bakit? kasi masarap ako titigan?
15-20% manifest malignant behavior BOY: hinde! putek! sarap mong basagin!
Moderate elevation of B-HCG
Preceded by a normal pregnancy (1/2), spontaneous abortion (1/6) or Boy: Martes ka ba?
H-mole (1/5) Girl: Bakt?
Boy:Kase Lunes ako
Macroscopic At ikaw ang kinabukasan ko. :>
Presents as a uterine mass; generally nodular or polypoid
Occasionally diffusely infiltrative Boy: Alam mo, pag ksma kita inaantok ako
Microscopic Girl: Bakit? Boring ba ako?
Boy: Kasi masarap magpahinga sa tabi mo eh
Cohesive sheets of mononuclear intermediate trophoblasts
Often assoc with zonal necrosis& prominent vascular invasion & Boy: Maliit pla ung kamay mo
remodeling Girl: Oo nga eh
Enlarged, round to oval nuclei with coarse, clumped chromatin & Boy: Bakit ganun? maliit nga kamay mo
prominent nucleoli pero paano mo hinawakan ung mundo ko?
Tumors with a mitotic rate of > 5/10 HPF, prominent necrosis, & less Girl: anung tinitingin tingin mo?
dense, eosinophilic cytoplasm may have a worse prognosis Boy: kamukha mo kasi yung panlimang girlfriend ko eh.
END Girl: nice! naka ilang girlfriends ka na ba?
Boy: apat

Drama blues.. Boy: musta na buhay mo?

THERE ARE CERTAIN THINGS IN LIFE THAT ARE BETTER OFF UNKNOWN. Things that Girl: ok lang naman. ikaw, musta buhay mo?
you wish you never saw, never asked, never heard and sometimes, never felt. Appreciate life even if it gives Boy: eto kausap ko..
you the greatest heartaches, because after your great fall, a new you will be formed, which would probably be
stronger than before. Humps kba ?
kasi pagnakikita kita napapahinto ako ..

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