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FEMALE GENITAL TRACT NO increased predisposition to cancer

Benign Exophytic Lesions


INFECTIONS OF THE FEMALE GENITAL TRACT Condyloma acuminatum
Herpes Simplex Virus Infection Syphilitic condyloma latum
Common Fibroepithelial polyps (skin tags)
Involves cervix, vagina, and vulva Squamous papillomas
HSVs are DNA viruses that include two serotypes, HSV-1 and Condyloma acuminatum: HPV types 6 and 11, have verrucous
HSV-2 gross appearance, may be solitary but are more frequently
Initial lesions typically develop 3 to 7 days after sexual multifocal; koilocytic atypia
transmission and consist of red papules that progress to
vesicles and then to painful coalescent ulcers VAGINA
Developmental Anomalies
Molluscum contagiosum Septate or double vagina: uncommon anomaly that arises from
MCV-1 being the most prevalent failure of total fusion of the mllerian ducts and accompanies a
MCV-2 being most often sexually transmitted double uterus (uterus didelphys)
Infections are common in young children between 2 and 12 Manifestations of genetic syndrome or exposure in utero to DES
years of age and are transmitted through direct contact or Vaginal adenosis: a remnant of columnar, endocervical-type
shared articles epithelium; presents clinically as red, granular areas
Incubation period: 6 weeks contrasting with the normal pale-pink vaginal mucosa
Reported in 35% to 90% of women exposed to DES in utero
Pelvic Inflammatory Disease Rare cases of clear cell carcinoma arising in DES-related
Ascending infection that begins in the vulva or vagina and adenosis
spreads upward to involve most of the structures in the female Gartner duct cysts: relatively common lesions found along the
genital system, resulting in pelvic pain, adnexal tenderness, lateral walls of the vagina and derived from wolffian
fever and vaginal discharge (mesonephric) duct rests; 1- to 2-cm fluid-filled cysts that occur
Gonococcus and Chlamydia infection; infections after in the submucosal location, lined by cuboidal epithelium
spontaneous or induced abortions and normal or abnormal Other cysts i.e. including mucus cysts occur in the proximal
deliveries (called puerperal infections) vagina and endometriosis, are derived from mllerian
Gonococcal ingection: epithelium
o Endocervical mucosa is the most common site of initial
involvement CERVIX
o Smears of the inflammatory exudate disclose the Acute and Chronic Cervicitis
intracellular gram-negative diplococcus Maturation of the cervical and vaginal squamous mucosa and
o Definitive diagnosis requires culture, or detection of formation of intracellular glycogen vacuoles in the squamous
gonoccocal RNA or DNA cells at onset of menarche
Acute complications: peritonitis and bacteremia Glycogen - substrate for endogenous vaginal aerobes and
Sequelae : infertility and tubal obstruction, increased risk of anaerobes
ectopic pregnancy, pelvic pain, intestinal obstruction due to Lactobacilli - maintain pH below 4.5; at low pH, lactobacilli
adhesions between the bowel and pelvic organs produce bacteriotoxic H2O2
Antibiotics and salpingo-oophorectomy Infections by gonococci, chlamydiae, mycoplasmas and herpes
simplex virus may produce significant inflammation and are
VULVA important to identify due to their association with upper genital
Bartholin (Duct) Cyst tract disease, complications during pregnancy and sexual
Common transmission
Obstruction of Bartholin duct, usually from preceding infection Abnormal Pap test result
Accumulation of mucoid, or clear secretion
Epithelial lining: squamous, transitional, or cuboidal Endocervical polyps
Pain and local discomfort 2% to 5% of adult women
Management: excision or opened permanently Irregular vaginal spotting or bleeding
(marsupialization) Vary from small and sessile to large soft, almost mucoid,
lesions composed of a loose fibromyxomatous stroma
Non-neoplastic Epithelial Disorders harboring dilated, mucus-secreting endocervical glands, often
Leukoplakia - opaque, white, plaque-like mucosal thickening accompanied by inflammation
that may produce itching and scaling Simple curettage or surgical excision
Lichen sclerosus
Squamous cell hyperplasia (Lichen simplex chronicus) BODY OF UTERUS AND ENDOMETRIUM
Lichen sclerosus : a dermatosis of unknown etiology
characterized by thinning of epidermis and disappearance of Functional Endometrial Disorders (DUB)
rete pegs, hydropic degeneration of the basal cells, superficial AUB can have organic and functional causes
hyperkeratosis, and dermal fibrosis with a scant perivascular, DUB: clinical term for uterine bleeding not caused by any
mononuclear inflammatory cell infiltrate underlying organic (structural) abnormality
Grossly, parchment-like epithelium o Anovulatory cycle
Most common in postmenopausal women o Inadequate luteal phase
Autoimmune reaction (?) o Endometrial changes caused by OCPs
NOT considered a pre-malignant condition o Menopausal and postmenopausal changes
Squamous cell hyperplasia: hyperplastic dystrophy or lichen Anovulatory Cycle - results in excessive and prolonged
simplex chronicus; nonspecific condition resulting from rubbing estrogenic stimulation without the counteractive effect of the
or scratching of the skin to relieve pruritus progestational phase that regularly follows ovulation; most
Marked by epithelial thickening with no atypia, expansion of the have no obvious cause, likely due to subtle hormonal
stratum granulosum, and significant surface hyperkeratosis imbalances; endocrine and metabolic disorder and ovarian
Increased mitotic activity in both the stratum basalis and tumor
spinosum and leukocytic infiltration of the dermis Anovulatory cycle - most common at menarche and in the
Grossly, leukoplakia perimenopausal period; microscopically seen as cystic
dilatation of glands and stromal breakdown
Inadequate luteal phase- stem from inadequate corpus luteum Has a relationship with endometrial carcinoma - common
function resulting in low progesterone output, with subsequent genetic alteration is inactivation of the PTEN tumor suppressor
early menses gene
Often manifests clinically as infertility, with either increased Risk of progression of endometrial hyperplasia
bleeding or amenorrhea; endometrial biopsy performed at an Type Progression rate
estimated postovulatory date shows secretory endometrium, SH 4.3% 0-10%
which, however, lags in its secretory characteristics expected CH 16.1% 3-22%
at that date SAH 7.4% 7-8%
Pill endometrium -discordant appearance between glands and CAH 47.0% 29-100%
stroma, usually with inactive glands amid a stroma showing
large cells with abundant cytoplasm reminiscent of the decidua SIMPLE
of pregnancy; these changes have been minimized with newer o Increased volume of glands and stroma
low-dose contraceptives o Cystic glands rounded, or with focal outpouchings
Menopausal and postmenopasusal changes: cystic atrophy o Epithelial lining proliferative type
COMPLEX
Endometriosis o Marked glandular crowding (back to back)
Presence of endometrial tissue outside of the uterus; most o Highly variable and irregular gland outlines
ATYPICAL
commonly consists of both endometrial glands and stroma, but
SIMPLE OR COMPLEX HYPERPLASIA + CYTOLOGIC ATYPIA
rarely consists only of endometrial stroma
o Large, rounded nuclei, varied in size
Involve the ovaries, uterine ligaments, rectovaginal septum, cul
o Prominent nucleoli
de sac, pelvic peritoneum, large and small bowel and appendix;
o Hyperchromasia
mucosa of the cervix, vagina and fallopian tubes; and
laparotomy scars o Increased N:C ratio
Most often in the third and fourth decades, affecting
approximately 10% of women Endometrial Polyps
Often causes infertility, dysmenorrhea, pelvic pain Exophytic masses of variable size that project into the
Two major theories for the development of endometriosis: endometrial cavity
metastatic theory (implantation in abnormal locations, Single or multiple and are usually sessile,, but are occasionally
retrograde menses) and metaplastic theory (metaplasia of large and pedunculated
coelomic epithelium) Asymptomatic or may cause abnormal bleeding
Specific abnormalities that distinguish normal endometrium (intramenstrual, menometrorrhagia, or postmenopausal)
from endometriotic tissue: Hyperplastic or atrophic or functional
o Activation of the inflammatory cascade characterized by Observed in association with the administration of tamoxifen
high levels of prostaglandin E2, IL-1, TNF and IL-6 Stromal cells in endometrial polyps contain chromosome (6p21)
o Upregulatd estrogen production rearrangements involving the HMGIY gene
Clinical signs and symptoms : severe dysmenorrhea,
dyspareunia and pelvic pain due to the intrapelvic bleeding and FALLOPIAN TUBES
periuterine adhesions; pain on defecation and dysuria Common disorders:
o Infections
Adenomyosis o Ectopic pregnancy
Defined as the presence of endometrial tissue within the - onset of severe abdominal pain, most commonly about
uterine wall (myometrium) 6 weeks after a previous normal menstrual period,
Clinical symptoms: menometrorrhagia (irregular and heavy rupture of a tubal pregnancy constitutes a medical
menses), colicky dysmenorrhea, dyspareunia and pelvic pain, emergency
particularly during the premenstrual period o Endometriosis

Inflammation Acute Endometritis Inflammation


Uncommon Suppurative salpingitis - caused by any of the pyogenic
Limited to bacterial infections that arise after delivery or organisms; 60% is due to gonococcus followed by chlamydiae;
miscarriage; retained products of conception are the usual part of pelvic inflammatory disease
predisposing influence Tuberculous salpingitis
Causative agents include group A hemolytic streptococci,
staphylococci OVARIES
Inflammatory response is chiefly limited to the interstitium and Follicle and Luteal Cysts
is entirely nonspecific. Cystic follicles -unruptured graafian follicles or in follicles that
Completion curettage, accompanied by antibiotic therapy have ruptured and immediately sealed -- cysts are usually
multiple. They range in size up to 2 cm in diameter, are filled
Inflammation Chronic Endometritis with a clear serous fluid, and are lined by a gray, glistening
Occurs in the following settings: (1) chronic PID; (2) in membrane
Corpus luteum cysts - cysts are lined by a rim of bright yellow
postpartum or post-abortion patients with retained gestational
tissue; (3) in women with IUDs and (4) in women with tissue containing luteinized granulosa cells; occasionally
tuberculosis rupture and cause a peritoneal reaction
Associated with abnormal bleeding, pain, discharge, and
Polycystic Ovarian Disease
infertility
In about 15% of cases no cause is obvious Stein Leventhal syndrome
Plasma cells, macrophages and lymphocytes are seen affects 3% to 6% of reproductive-age women
Chlamydia - associated with both acute and chronic Pathologic abnormality is numerous cystic follicles or follicle
inflammatory cell infiltrates cysts, often associated with oligomenorrhea
Antibiotic therapy Persistent anovulation, obesity (40%), hirsutism (50%), and
rarely, virilism
Endometrial Hyperplasia Ovaries 2x the normal size and have a smooth, gray-white
An important cause of abnormal bleeding outer cortex studded with subcortical cysts 0.5 to 1.5 cm in
diameter.)
Increased proliferation of the endometrial glands relative to the
stroma, resulting in an increased gland-to-stroma ratio when
compared with normal proliferative endometrium
Histologic examination, there is a thickened, fibrotic superficial 10% of women develop HELLP syndrome (hemolysis, elevated
cortex beneath which are innumerable follicle cysts associated liver enzymes and low platelets)
with hyperplasia of the theca interna (follicular hyperthecosis Placenta plays a central role in the pathogenesis of the
Increased secretion of luteinizing hormone may stimulate the syndrome
theca-lutein cells of the follicles, to produce excessive Critical abnormalities in preeclampsia are diffuse endothelial
androgen (androstenedione), which is converted to estrone dysfunction, vasoconstriction (leading to hypertension) and
Insulin resistance increased vascular permeability (resulting in proteinuria and
edema)
Stromal Hyperthecosis Principal pathophysiologic aberrations appear to be the
Cortical stromal hyperplasia following:
Disorder of ovarian stroma most commonly seen in o Abnormal placental vasculature
postmenopausal women o Endothelial dysfunction and imbalance of angiogenic and
Uniform enlargement of both ovaries (up to 7 cm), which has a anti-angiogenic factors -high levels of sFlt1 and soluble
white to tan appearance on sectioning endoglin bring about a decrease in angiogenesis much
Microscopically shows hypercellular stroma and luteinization of earlier than in normal pregnancy
the stromal cells, which are visible as discrete nests of cells o Coagulation abnormalities decreased endothelial
with vacuolated cytoplasm production of PGI2
Lutein hyperplasia of pregnancy - physiologic condition
mimicking PCOD and SH syndromes -- proliferation of theca Pre-eclampsia Morphology
cells and expansion of the perifollicular zone Placenta reveals various microscopic changes: placental
infarcts, ischemic changes in the chorionic villi (increased
GESTATIONAL AND PLACENTAL DISORDERS syncytial knots and the appearance of accelerated villous
Disorders of Early Pregnancy Spontaneous Abortion maturity); retroplacental hematomas ; thrombosis, fibrinoid
Miscarriage, is defined as pregnancy loss before 20 weeks of necrosis or acute atherosis of decidual vessels
gestation Liver, renal and cerebral findings
Causes are both fetal and maternal
Chromosomal anomalies such as aneuploidy, polyploidy, and Pre-eclampsia Clinical Features
translocations are present in approximately 50% of early Most commonly starts after 34 weeks of gestation
abortuses For term pregnancies, delivery is the treatment of choice
Maternal factors include luteal-phase defect, poorly controlled For preterm pregnancies, where delivery may not be in the best
diabetes, and other uncorrected endocrine disorders interest of the fetus, patients with mild disease can be
Physical defects of the uterus may prevent implantation managed expectantly with close monitoring of the mother and
adequate to support fetal development fetus
Systemic disorders affecting maternal vasculature, Proteinuria and hypertension usually disappear within 1 to 2
coagulopathies and hypertension weeks after delivery
Infections with bacteria such as Toxoplasma, Mycoplasma, and 20% of women develop hypertension and microalbuminuria
Listeria, as well as viral infections -- ascending infection is within 7 years of a pregnancy complicated by preeclampsia.
particularly common in second-trimester losses Two-fold increase in the long-term risk of vascular diseases of
the heart and the brain

Disorders of Late Pregnancy


Twin placentas
o Monozygotic
o Dizygotic
3 types of twin placentation
Monochorionic placentas imply monozygotic (identical) twins
One complication of monochorionic twin pregnancy is twin-twin
transfusion syndrome

Abnormalities of Placental Implantation


Placenta previa is a condition in which the placenta implants in
the lower uterine segment or cervix, often with serious third-
trimester bleeding
Placenta accreta is caused by partial or complete absence of
the decidua with adherence of the placental villous tissue
directly to the myometrium and failure of placental separation;
an important cause of postpartum bleeding; common
predisposing factors are placenta previa and history of previous
cesarean section

Placental Infections
Two pathways: (1) ascending infection through the birth canal
most common and almost always bacterial (2) hematogenous
(transplacental) infection e.g. TORCH (toxoplasmosis and others
[syphilis, tuberculosis, listeriosis], rubella, cytomegalovirus,
herpes simplex)

Pre-eclampsia and Eclampsia


Preeclampsia refers to a systemic syndrome characterized by
widespread maternal endothelial dysfunction presenting
clinically with hypertension, edema, and proteinuria during
pregnancy
3% to 5% of pregnant women, usually in the last trimester
more common in primiparas
Severe form - eclampsia