Transcript The Female Genital Tract

The Female Genital Tract
Infections
Lower genital tract
HSV- latent, recurrence, transmission
to offspring, painful ulcers,
multinucleated giant cells
Molluscum contagiosum –pox virus,
umblicated papules
Fungal infections- Candida – DM,
antibiotics, pregnancy,
suppression of cell-mediated
immunity
Trichomonas vaginalis- frothy,
strawberry cervix
Gardnerella vaginalis – fishy odor,
clue cells
Ureaplasma – Preterm labor
Chlamydia –usually cervicitis
LGV in tropics
Syphilis – painless chancre,
condyloma lata, fetal
malformations
Toxic Shock – S. aureus, tampons,
PID
Ascending infection
GC- also pharyngitis, arthritis, proctitis, ophthalmia
neonatorum, Chlamydia – more mucosal
involvement
Puerperal infections – polymicrobial, more reaction in
the deeper layers
Acute salpingitis
Salpingo-oophoritis
Tubo-ovarian abscesses
Acute complications –peritonitis, bacteremia
Chronic complications- infertility, tubal obstruction,
intestinal obstruction, ectopic pregnancy
Vulva
Skin diseases – similar to other areas of body – infection,
inflammatory, cancers
Bartholin Cyst
Lichen sclerosus- thinning of epidermis, dermal fibrosis
Squamous cell hyperplasia (Lichen simplex chronicus)
Condyloma acuminatum-HPV 6 and 11, koilocytic (expanded
epithelial cells with perinuclear clearing) atypia
VIN and carcinoma – basloid and warty- HPV
keratinizing squamous cell- more common, not HPV
Papillary hiradenoma – sweat glands
Extramammary Paget disease
Vagina
Vaginal adenosis and clear cell
adencarinoma – DES
Vaginal intraepithelial neoplasia and
squamous cell carcinoma
Embryonal rhadomyosarcomasarcoma botryoides – “bunch of
grapes”
Cervix
Acute and Chronic Cervicitis
Intracellular gycogen
Lactobacillus – lower pH
May cause an abnormal PAP test
Endocervical polyps – may cause
vaginal bleeding
Cervix
High oncogenic risk HPVs are considered to be the
single most important factor in cervical
oncogenesis – 16 and 18
Other risk factorsMultiple sexual partners
Young age at first intercourse
High parity
Immunosuppression
Certain HLA types
Use of oral contraceptives
Use of smoking
Cervix
HPV
Most infections are asymptomatic
50% clear in 8 months
90% clear in 2 years
Persistent infection increases the risk of cervical dysplasia
and carcinoma
Can infect only the immature cells but replication occurs in
the maturing cells
Koilocytic atypia – nuclear atypia and perinuclear halo
Activate cell cycle by interference with Rb and p53
Cervix
Cervical Intraepithelial Neoplasia
CIN I – mild dysplasia (LSIL)
CIN II – moderate dysplasia (HSIL)
CIN III – severe dysplasia (HSIL)
Natural history
LSIL – 60% regress, 30% persist, 10%
progress to HSIL
HSIL – 30% regress, 60% persist,10%
progress to carcinoma
Cervix
Cervical cancer
80% squamous cell
15% adenocarcinoma
5% adenosquamous and neuroendocrine
Staging
stage 0 - carcinoma in situ (CIN III, HSIL)
stage I – confined to cervix
stage II – beyond the cervix but not to pelvic wall or lower 1/3
of
vagina
stage III – extended to the pelvic wall, lower 1/3 of vagina
stage IV – beyond the true pelvis, bladder or rectum or distant metastases
Screening and prevention
PAP smear
Removal of precancerous lesions - colposcopy
surgical removal of invasive cancers
HPV vaccine
HPV DNA testing
Endometrium
“Dating” the endometrium
Proliferative phase
Secretory phase
Exhaustion and disintegration
Hypothalmic-Pituitary-Ovarian Axis
Corpus luteum
Endometrium
Dysfunctional Uterine
Bleeding
Anovulatory Cycle
Menopausal changes
Atrophy
Inflammation
Acute endometritis
Retained
products of
conception
Chronic endometritis
Chronic PID
Postpartum or
post-abortion
IUDs
TB
Non-specific
Endometrium
Endometriosis
Presence of endometrial tissue
outside the uterus
Adenomyosis
Presence of endometrial tissue
within the uterine wall
(myometrium)
Infertility
Dysmenorrhea Pelvic pain
Metastatic theory
Metaplastic theory
Activation of inflammatory
cascade
Upregulation of estrogen
production
Hyperplasia
Prolonged estrogen stimulation of
the endometrium
Relationship with endometrial
carcinoma
Inactivation of the PTEN tumor
suppressor gene
Simple hyperplasia + atypia
Complex hyperplasia +atypia
Endometrium
Endometrial carcinoma
Most common invasive tumor of the female genital tract
Post-menopausal bleeding
Type I
Unopposed estrogen
Obesity, hypertension, diabetes
Endometroid
Hyperplasia
PTEN
Indolent
Type II
Atrophy
Thin
Serous, clear cell, mixed mullerian tumor
Endometrial intraepithelial carcinoma
Aggressive
p53
-
Myometrium
Leiomyomas – fibroids
Leiomyosarcomas
Ovaries
Polycystic Ovarian disease
persistent anovulation
obesity
hirsutism
rarely virilism
Variety of enzymes involved in androgen
synthesis are poorly regulated
Ovarian Tumors
Surface Epithelialstromal
Most common
Most malignant
Most ovarian cancers are
detected when they
have spread beyond
the ovary; account for
a disportionate
number of deaths
Germ cell
Sex cord-stromal
Metastasis to ovarytumors of Mullerian
origin, breast, GI,
Krukenberg tumor
Surface Epithelial (Mullerian)
Most primary neoplasms
of ovary
Transformation of
coelmic epithelium
Lower abdominal pain,
enlargement
GI compliants, urinary
complaints,
pelvic pressure
CA-125, osteopontin
Types
Serous
Mucinous
Endometrioid
Clear cell
Brenner – transitional
cell
Cystadenofibroma
Serous
Lined by tall, columnar
ciliated and noniliated
epithelial cells
Filled with clear serous
fluid
BRCA1 and BRCA2
fimbriated end of
fallopian tube
Higher frequency of
malignancy in women
of low parity
Mucinous
KRAS
Pseudomyxoma
peritonei
Less frequently
bilateral
Endometrioid
PTEN. KRAS, betacatenin
Germ Cell Tumors
Types
Teratomas
Dysgerminoma
Endodermal sinus
(yolk sac)
Choriocarcinoma
Most are benign
cystic teratomas
Teratomas
Mature (benign)dermoid cyst
Immature (malignant)
Monodermal ( highly
specialized) –
strumi ovarii
(thyroid) and
carcinoid
Dysgerminoma
Equivalent to seminoma
Gonadal dysgenesis
Yolk sac
Alpha-fetoprotein and
alpha1- antitrypsin
Choriocarcinoma
HCG
Aggressive
Sex Cord-Stromal
Types
Fibroma – Meigs syndrome ( ovarian
tumor, hydrothorax, ascites), basal
cell nevus syndrome
Granulosa-theca cell – estrogen,
precocious puberty, endometrial
hyperplasia or carcinoma, Call-Exner
bodies
Sertoli-Leydig cell - masculinizing
Gestational and Placental Disorders
Early Pregnancy
Spontaneous abortion
Ectopic pregnancy
Late pregnancy
Twin placentas
Placental Implantation
abnormalities – previa and
accreta
Placental abruption
Placental Infections
Preeclampsia
Eclampsia
Preeclampsia
Widespread endothelial dysfunction, vasoconstriction, increased
vasopermeability
Hypertension, Edema, proteinuria
3-5% women
Last trimester
Primiparas
HELLP syndrome ( hemolysis, elevated liver enzymes, low platelets)
Abnormal placental vasculature- abnormal trophoblastic implantation is
the initial event – remodeling of vessels does not occur
Followed by endothelial dysfunction and imbalance of angiogenic and
anti-angiogenic factors
Coagulation abnormalities
Headache and visual changes – severe preeclampsia
Seizures - eclampsia
Gestational Trophoblastic Disease
Hydatidiform Mole
Complete
Partial
Invasive mole
Choriocarinoma
Placental-Site Trophoblastic Tumor