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GENITAL TRACT
Developmental Disorders (Congenital)
• Mullerian Duct Anomalies
- Embryologic fusion anomalies Æ organ agenesis,
abnormal septation,
organ duplication : double vag/uterus (didelphys), etc.
• Gardner’Duct Cyst
- arise in women from remnants of the degenerated
mesonephric/wolffian duct
- Submucosa of anterolateral vaginal wall, 1-2 cm in size
• Imperforate Hymen
- May not be recognized until puberty Æ complain of
failure to menstruate
Æ retain blood: hematocolpos, hematometria,
hematosalpinx
Atresia,
Double vagina,
Double uterus.
VULVA
• Synonymous with EXTERNAL genitalia
• Everything ANTERIOR to the INTROITUS
• Usual classification of Degen., Inflam., Neopl.
• Common Diseases:
– BARTHOLIN Cyst
– Vulvar Vestibulitis
– Deg./Inflam. Epithelial: LICHEN diseases
– BENIGN tumors: Condyloma(ta)
– MALIGNANT tumors: VIN, SCC
Result from
Inflammation/Obstruction
of the Bartholin glands
(i.e., greater vestibular
glands)
Often result in abscesses
Surgical removal is
curative when local
procedures are
inadequate or often
recurrent
NEVER become
malignant
VULVAR VESTIBULITIS, assoc. w. vulvodynia
“LICHEN” DISORDERS
LICHEN Sclerosu(i)s (atrophic skin)
LICHEN Simplex Chronicus (hypertrophic skin)
Common features of
FIBROSIS and INFLAMMATION
Mucosal Atrophy
Fibrosis (sclerosis)
Inflammation
LICHEN SIMPLEX CHRONICUS
show HYPER-plastic mucosal changes are often regarded as being potentially
pre-malignant
Condylomas
-Condylomata lata: (not commonly seen today), are flat, moist, minimally
elevated lesions that occur in secondary syphilis
-Condylomata accuminata: (more common) may be papillary and distinctly
elevated, occur anywhere on the anogenital surface. Significant characteristic
cellular morphology is: perinuclear cytoplasim vacuolization. Vulvar cndylomas
are not pre-cancerous but may coexist with foci of intraepithelial neoplasia in
vulva (VIN grade 1) and cervix.
CONDYLOMA(TA)
VIN, SCC
• Like condylomas, HIGHLY linked to
HPV
• VIN=changes leading to SCC‐in‐situ,
look like “plaques”
• BEYOND VIN = INFILTRATION
VIN
EXTRAMAMMARY PAGET’S DISEASE
MALIGNANT
MELANOMA
VAGINA
• CONGENITAL: Parallel uterus anomalies
• INFLAMMATORY
– PRE‐menopausal: STD
– POST‐menopausal: ATROPHY
• BENIGN: Hidradenoma, Condyloma
• MALIGNANT: VIN, INFILTRATING SCC
VAGINITIS
• 90% Æbacterial vaginitis, candida, T. vaginalis
• Bacterial Vaginitis
• the most common cause of vaginitis,
accounting for 50% of vaginitis cases.
• caused by an overgrowth of organisms such as
Gardnerella vaginalis (gram‐variable
coccobacillus), Mobiluncus species,
Mycoplasma hominis, and Peptostreptococcus
species.
• Risk factors include pregnancy, intrauterine
device (IUD) use, and frequent douching.
Candida
• Candida species (C albicans, C tropicalis, and
C glabrata) are airborne fungi that are
natural inhabitants of the vagina in as many
as 50% of women,
• vaginal candidiasis is the second most
common cause of vaginitis.
• Risk factors include oral contraceptive use,
IUD use, young age at first intercourse,
increased frequency of intercourse, receptive
cunnilingus, diabetes, HIV or other
immunocompromised states, chronic
antibiotic use, and pregnancy.
T. vaginalis
• the third most common cause of vaginitis, is caused
by trichomonads.
• These organisms are flagellated protozoans.
Trichomonads primarily infect vaginal epithelium,
and they less commonly infect the endocervix,
urethra, and Bartholin and Skene glands.
• Trichomonads are transmitted sexually and can be
identified in as many as 80% of male partners of
infected women.
• Risk factors include tobacco use, unprotected
intercourse with multiple sexual partners, and the
use of an IUD.
VAGINAL NEOPLASIA
• VIN
• INFILTRATING SCC
• ADENOSIS (D.E.S.) Æ
• ADENOCARCINOMA (Di‐
Ethyl‐Stilbestrol)
NORMAL VIN
SCC
CHILDHOOD EMBYRONAL
RHABDOMYOSARCOMA
CERVIX
• NORMAL
• METAPLASIA
• INFLAMMATION
• POLYPS
• DYSPLASIA
• CIN
• INFILTRATING SCC
DYSPLASIA / CIN / SIL
INFILTRATION
How have we “CURED” Cervical Carcinoma?
ENDOMETRIUM
• FUNCTIONAL HISTOLOGY
• D.U.B. (Dysfunctional Uterine Bleeding)
• INFLAMMATION
• ADENOMYOSIS/ENDOMETRIOSIS
• POLYPS/HYPERPLASIA
• ADENOCARCINOMA and/or STROMAL
• LEIOMYOMYOMAS, ‐SARCOMAS
• MITOSES differentiate benign from malignant
MITOSES (Glandular and Stromal) = PRE-ovulatory
VACUOLES/SECRETION = POST-ovulatory
DYSFUNCTIONAL UTERINE BLEEDING
(DUB)
• Anovulatory Cycle
• Inadequate Luteal Phase
• Oral Contraceptives
• Menopause
• Post‐Menopause
INFLAMMATORY DISEASE
A. Acute endometritis
• Post‐abortion, post‐partum states with retaind
placental parts
• Suppurative inflammation + microabscess Æ
pyometra Æ obstruction of endocervical canal
B. Chronic endometritis
• Contination of acute endometritis, could be
associated with IUD, 15% with unknown etiology
• Pelvic pain, abnormal bleeding, infertility
• Characteristic: infiltration by plasma cells
ADENOMYOSIS
• Defined as normal endometrial glands deep
within the myometrium
Endometriosis
• Presence of endometrial tissue outside uterus
(ectopic)
– Found on ovaries, ligaments, colon, sometimes lungs
• Responds to cyclic hormonal variations
– Grows and secretes then degenerates, sheds and bleeds
– Blood irritating to tissues = inflammation and pain
• Recurs with every cycle with eventual fibrous tissue
– Causes adhesions and obstruction
• Diagnosis confirmed with laparoscopy
Endometriosis
• Infertility results from
– Adhesions pulling uterus out of normal position
– Blockage of fallopian tubes
• “chocolate cyst” develops on ovary
– Fibrous sac containing old brown blood
• Primary manifestations
– Dysmenorrhea
• More severe every month
– Painful intercourse if vagina and supporting ligaments
affected by adhesions
Endometriosis
“CHOCOLATE” CYST
ENDOMETRIAL POLYPS
5% Prevalence
Anovulation
Oligomenorrhea
Obesity
Hirsutism
Polycystic Ovaries
OVARY
12/04/2013 tums‐pafkugm 91
OVARIAN TUMORS
• MÜLLERIAN (MAJORITY)
– Serous (Benign, Borderline, Malignant)
– Mucinous (Benign, Borderline, Malignant)
– Endometroid (Benign, Borderline, Malignant)
– Adenosarcoma (Carcinoma AND Sarcoma)
– Mesodermal Mixed (MULTIPHASIC Sarcoma)
– Clear Cell
– Brenner (almost always benign)
– Transitional (almost always look like Brenner)
• Germ Cell
• SEX‐CORD/STROMAL
• METASTATIC
OVARIAN TUMORS
• Solid vs. Cystic
• Functional vs. NON‐functional
• Benign vs. Malignant
• First clinical presentation may be ascites
• Malignant ascites in a woman is ovarian cancer
until proven otherwise
• CA‐125 is THE important tumor marker in ovarian
cancer, especially as a follow up.
SEROUS, BENIGN
MUCINOUS, BENIGN
PSAMMOMA bodies are dried up papillae of papillary adenocarcinomas, usually in
the thyroid, but in ANY papillary adenocarcinoma
OTHER MÜLLERIAN
• ENDOMETRIOD, malignant
– (looks like endometrium)
• CLEAR CELL, malignant
– (clear cells, reminiscent of renal clear cell ca.)
• CYSTADENOFIBROMA, benign
– (BENIGN “FIBROUS” COMPONENT)
• BRENNER TUMOR, benign
– (transitional cell nests)
• CARCINOMA with SARCOMA
– (adenosarcoma, mixed Müllerian)
Histogenesis and inter‐relationship of
tumors of germ cell origin
“GERM CELL” Tumors
• Teratomas (usually benign in ovary), i.e.,
“mature” cystic teratoma or dermoid cyst
• “Immature” teratomas are regarded as
malignant
• Dysgerminoma (look exactly like the testicular
seminoma), malignant
• Endodermal Sinus (Yolk Sac), malignant, Just
like testicular
• Choriocarcinoma, malignant, just like
testicular or placenta
Dysgerminoma:Female::Seminoma:Male
ENDODERMAL SINUS TUMOR
(YOLK SAC TUMOR)
CHORIOCARCINOMA,
Just like testis or placenta
SEX‐CORD/STROMAL TUMORS
• Chiefly benign and NON‐cystic, i.e.,
“solid”, often functional (hyper‐
estrogen‐ism)
• Granulosa‐Theca
• Fibroma‐Theca
• Sertoli‐Leydig (Androblastoma)
CALL-EXNER
BODIES
Krukenberg Tumor
DISEASES of PREGNANCY
• EARLY Pregnancy
• SPONTANEOUS ABORTION
• ECTOPIC PREGNANCY
• LATE Pregnancy
Spontaneous Abortion
• 15% ‐ 35%
• Fetal Causes
–Usually Genetic
• Maternal Causes (placental, uterus
infections or trauma)
–Toxo, Mycoplasma, Listeria
–Trauma
Ectopic Pregnancy
• Chiefly TUBAL, but ovarian or abdominal
rare
• 1% OF NORMAL WOMEN
• 35%‐50% OF WOMEN with previous
SALPINGITIS/PID
• + HCG, Abdominal pain, 1st trimester,
ultrasound
LATE PREGNANCY
• PLACENTAL ANOMALIES
• TWIN PLACENTAS
• PLACENTAL INFLAMMATIONS
• TOXEMIA (ECLAMPSIA/PRE‐ECLAMPSIA)
• INTRAUTERINE GROWTH RETARDATION
PLACENTAL ANOMALIES
• Accessory Lobes
• Bipartite Placenta
• Circumvallate Placenta
• Placenta Accreta, chorion going
DIRECTLY to the myometrium
CIRCUMVALLATE
PLACENTA ACCRETA
NO DECIDUA BETWEEN VILLI AND MYOMETRIUM
MONOCHORIONIC = MONOZYGOTIC
(PRE‐eclampsia)
• Hypertension
• Proteinuria
• Edema
• Related to Placental Ischemia
• Risk for DIC, convulsions (eclampsia)
Intrauterine Growth Retardation
• Fetal causes: Genetic, malformations
• Maternal Causes, vascular diseases,
toxemia, infections, placental diseases
• Placenta size (350‐700g) ~ Fetal size
Placental Infections
• Villitis vs. chorionamnionitis vs. funisitis
• ASCENDING vs. hematogenous
• ASCENDING are usually bacterial, and
chorionamnionitis
• HEMATOGENOUS are often
TORCH, and villitis
Placental Neoplasms,
i.e. gestational trophoblastic disease
• Benign: MOLES (Hydatidiform moles)
• Malignant: CHORIOCARCINOMA
• BOTH are associated with increased or
persistent levels of the placental hormone
HCG
Hydatidiform Mole
• 1/1000 in USA
• 1% in Indonesia
• Also called NON‐invasive mole in its
most common benign variant, but can
also be “invasive”
• Complete (2% chorioCA incidence) or
partial (0% incidence)
• Grapelike clusters, i.e., swollen villi
The MAIN thing differentiating benign from malignant
from worrisome trophoblastic neoplasms is
INVASIVENESS of the trophoblast
Terima kasih