Development
Gartner duct cysts
- mesonephric (Wolffian) duct rests that don’t
regress in the female
- in cervix & lateral vaginal wall
Infections of the female genital tract
Lower genital tract
- HSV
o involves cervix, vagina, vulva
o DNA viruses
o HSV-1 = oropharyngeal inf.
o HSV-2 = genital mucosa & skin (more
prone to recurrence)
o red papule  vesicle  painful ulcer
o latent in lumbosacral nerve ganglia
o transmission to offspring
o Dx: viral cytopathic effect on tissue
culture, PCR, ELISA, or antibody
o presence of serum anti-HSV =
recurrent/latent inf.
- Molluscum contagiosum – poxvirus
o MCV-1 to -4
o MCV-1 = MC
o MCV-2 = most often sex transmitted
o common in 2-12 years old (thru direct
contact or shared articles)
 MC areas = trunk, arms, legs
o adults = genitals, lower abdomen, butt,
inner thighs
o pearly dome-shamed papule w/ dimpled
center
o central waxy core contain
intracytoplasmic viral inclusion
- Fungal infections (Candida)
o DM, antibiotics, pregnancy,  cell-med
immunity
o vulvovaginal pruritus, erythema, swelling,
curdlike vaginal discharge
o wet KOH mount = pseudospores or
filamentous fungal hyphae
o not considered STI
- Trichomonas vaginalis
o large flagellated ovoid protozoa
o seen on wet mount or pap of discharge
o yellow, frothy vaginal discharge
o vulvovaginal discomfort, dysuria,
dyspareunia
o vaginal/cervical mucosa = fiery-red
o strawberry cervix
- Gardnerella vagnialis
o gram-neg bacillus
o main cause of BV
o thin, green-gray malodorous (fishy)
discharge
o pap = superficial & intermediate
squamous cells covered by shaggy coat of
multiple coccobacilli
o premature labor
- Ureaplasma urealyticum & Mycoplasma
hominis
o cause of vaginitis & cervicitis
o cause chorioamnionitis & premature
delivery
- Chlamydia trachomatis
o cervicitis
o may cause ascending inf.  PID
- Treponema palladium
o painless chancre
o condylomata lata
o fetal malformation
Pelvic inflammatory disease
- gonorrhea
o serious complication of gonorrhea
o involve endocervical mucosa
o acute suppurative salpingitis = tubes
o salpingo-oophoritis = ovaries
o may form tubo-ovarian abscess
o pyosalpinx = pus in tube lumen
- chlamydia
- puerperal inf.
o induced or spontaneous abortion
o abnormal deliveries
o surgical procedures of genital tract
o usually polymicrobial
o infect deeper layers (less mucosal
involvement)
- acute complications = peritonitis, bacteremia
(usually non-gonococcal)
- chronic complications = infertility,
hydrosalpinx, infertility, ectopic pregnancy,
intestinal obstruction from adhesions
VULVA
Bartholin cyst
- acute inflammation in the gland (adentis)
- may result in abscess
- common in all ages
Non-neoplastic epithelial disorders
Lichen sclerosis
- lesion characterized by:
o thinning of epidermis
o disappearance of rete pegs
o hydropic degeneration of basal cells
o superficial keratosis
o dermal fibrosis
- smooth white plaques or papules
- resembles parchment
- may constrict vaginal orifice
- MC in postmenopausal women
-  freq. of autoimmune disorders
-  risk of squamous cell carcinoma
Squamous cell hyperplasia
(lichen simplex chronicus)
- from rubbing or scratching of skin
- epithelial thickening
- significant surface hyperkeratosis
- area of leukoplakia
- no predisposition to CA
Benign exophytic lesions
- condyloma acuminatum = HPV (genital wart)
- condyloma latum = syphilis
Condyloma acuminatum
- STI
- verrucous gross appearance
- frequently multifocal
- branching, treelike cores of stroma covered by
squamous epithelium
- koilocytic atypia (nuclear enlargement w/
cytoplasmic perinuclear halo)
- HPV 6 & 11 (low oncogenic risk)
Squamous neoplastic lesions
VIN & vulvar carcinoma
- MC = squamous cell carcinoma
- Basaloid & warty carcinomas
o related to high oncogenic risk HPV
o develop from Classic VIN
 aka Bowen dz
 commonly occurs in repro. age
 most are HPV 16 positive
 discrete white (hyperkeratotic),
flesh-colored, slightly raised lesions
- Keratinizing squamous cell carcinoma
o not related to HPV inf.
o freq. arise from long-standing lichen
sclerosus or squamous cell hyperplasia
o mean age = 76 years
o develop from Differentiated VIN or VIN
simplex
o nodules in a background of vulvar
inflammation
- initial spread to inguinal, pelvic, iliac, and
periaortic lymph nodes
Glandular neoplastic lesions
Papillary hiradenoma
- benign tumor of specialized apocrine gland in
vulva
- sharply circumscribed painful nodule
- MC on labia majora or interlabial folds
- tendency to ulcerate
- papillary projections covered w/ 2 layers of
cells:
o top columnar secretory cells
o underlying flat myoepithelial cells (sweat
gland)
Extramammary Paget disease
- pruritic, red, crusted, sharply demarcated,
maplike area usually on labia majora
- large tumor cells lying singly or in small
clusters within the epidermis and its
appendages
- tumor cells surrounded by halo from
surrounding epithelial cells
- PAS positive
- apocrine, eccrine, keratinocyte differentiation
- confined to epidermis
- high recurrence rate
VAGINA
Development anomalies
- exposure to DES (diethylstilbestrol) in utero
o vaginal adenosis
o clear cell carcinoma can arise from DES
related adenosis
Premalignant & malignant neoplasms
- most benign tumors occur in reproductive age
o leiomyomas
o stromal tumors (polyps)
o hemangiomas
- MC malignant tumor of vagina = metastasis
from cervix
Vaginal intraepithelial neoplasia & squamous
cell carcinoma
- 1carcinoma of vagina is very rare
- most are squamous cell
- greatest risk factor is previous carcinoma of
cervix or vulva
- arises from vaginal intraepithelial neoplasia
- most often affect upper posterior vagina,
posterior wall
- lesions in lower 2/3 of vagina metastasize to
inguinal nodes
- upper lesions involve regional iliac nodes
Embryonal rhabdomyosarcoma
- aka sarcoma botryoides
- MC in infants and girls <5 years old
- polyploidy, rounded, bulky masses
- sometimes fill and project out of vagina
- grapelike clusters
- tumor cells = small w/ oval nuclei; small
protrusions of cytoplasm from one end (tennis
racket)
- invade locally; penetrate peritoneal cavity
CERVIX
Acute & chronic cervicitis
- intracellular glycogen vacuole sin squamous
cells provide substrate for bacteria
- lactobacillus dominate – produce lactic acid to
maintain pH below 4.5 (suppress others)
- anything causing pH can cause overgrowth of
other microbes  cervicitis
- infections caused by GC, chlamydiae,
mycoplasma, HSV can cause significant acute or
chronic cervicitis
- cervical inflammation can give abnormal Pap
test
Endocervical polyps
- may cause irregular spotting or bleeding
- most arise in endocervical canal
Premalignant & malignant neoplasms
- high oncogenic risk HPV = HPV 16 & 18
- risk factors for cervical CA:
o multiple sex partners
o young age at 1st intercourse
o high parity
o immunosuppression
o certain HLA types
o OC
o smoking
- HPV infections
o most asymptomatic
o 50% clear in 8 mo.; 90% by 2 years
o persistent inf.  risk of cervical dysplasia
& carcinoma
o can infect only immature cells in basal
layer of epithelium but replication occurs
in maturing squamous cells  koilocytic
atypia (nuclear atypia & perinuclear halo)
o activate cell cycle by interference w/ Rb
and p53
 E6 = binds p53 & interrupts cell
death pathways; rapidly degrades
p53
 E7 = binds RB & upregulates cyclin
E; degrades RB
Cervical intraepithelial neoplasia (CIN)
- CIN I – mild dysplasia (LSIL)
o productive HPV inf. w/out disruption of
cell cycle
o remain confined to lower 1/3 of
epithelium
o most regress spontaneously
- CIN II – moderate dysplasia (HSIL)
- CIN III – severe dysplasia (HSIL)
LSIL
60% regress
30% persist
10% become HSIL
HSIL
30% regress
60% persist
10% become carcinoma
Cervical carcinoma
- 80% squamous cell carcinoma
- 15% adenocarcinoma
- 5% adenosquamous & neuroendocrine
- staging
o 0 – carcinoma in situ (CIN III, HSIL)
o I – confined to cervix
o II – beyond cervix; before pelvic wall or lower
⅓ of vagina
o III – extends to pelvic wall; involves lower ⅓ of
vagina
o IV – beyond true pelvis; bladder, rectum,
distant metastases
- small-cell neuroendocrine tumors have very
poor prognosis
- screening & prevention
o Pap smear (1st screen at 21 years or
within 3 years of 1st sexual encounter)
o colposcopic exam (acetic acid on lesion
can highlight abnormal areas)
o HPV vaccine (types 6, 11, 16, 18)
o HPV DNA testing
BODY OF UTERUS & ENDOMETRIUM
Endometrial histology in the menstrual cycle
Dating the endometrium
- cycle begins w/ shedding of upper ½ - 2/3 of
endometrium (functionalis)
- Proliferative phase: under influence of estrogen,
bottom 1/3 (basalis) of endometrium
undergoes extremely rapid growth of glands &
stroma
- at ovulation, endometrium slows in growth and
ceases mitotic activity 
- Secretory phase: postovulation, secretions
discharged into gland lumens; glands are
dilated
- Exhaustion & disintegration: by 4th week,
serrated or saw-toothed appearance &
shrinking of glands
Corpus luteum
- produces progesterone in addition to estrogen
after ovulation
- dissolutes when there is no implantation
- lack of progesterone causes disintegration of
functionalis
Hypothalamic-pituitary-ovarian axis
- endometrium undergoes changes in response
to sex hormones produced by ovary
- ovary is influenced by hormones produced by
the pituitary
Dysfunctional uterine bleeding
- uterine bleeding not caused by any underlying
organic (structural) abnormality
Anovulatory cycle
- excessive & prolonged estrogenic stimulation
w/o counteractive effect of progesterone phase
that regularly follows ovulation
- most common at menarche and in
perimenopausal period
Inadequate luteal phase
- inadequate corpus luteum function low
progesterone output  early menses
- infertility
- increased bleeding or amenorrhea
Menopausal changes
- characterized by anovulatory cycles
- ovarian failure
- atrophy of endometrium
Inflammation
Acute endometritis
- bacterial inf. after delivery or miscarriage
- retained products of conception
- GAS, staph
Chronic endometritis
- may occur due to:
o chronic PID
o post-partum or post-abortion
o IUD
o TB (miliary spread or drainage of TB
salpingitis)
- nonspecific chronic endometritis
o Chlamydia may be involved
o abnormal bleeding, pain, discharge,
infertility
o key histo finding = plasma cells
Endometriosis & adenomyosis
- presence of endometrial tissue outside the
uterus
- ovary is MC site
- usually made of glands & stroma
- often causes infertility, dysmenorrhea, pelvic
pain
- metastatic theory = endometrial tissue
implanted at abnormal locations thru
retrograde menstruation thru fallopian tubes
- metaplastic theory = arises directly from
coelomic epithelium from which müllerian
ducts & ultimately the endometrium itself
originate during embryonic development
- morphology:
o nodules w/ red-blue to yellow-brown
appearance
o chocolate cysts (cystic masses on ovaries
filled w/ brown fluid from hemorrhage)
- abnormalities of endometriotic tissue:
o activation of inflammatory cascade
o upregulation of estrogen production
- adenomyosis
o endometrial tissue w/in myometrium
o menorrhagia (irregular, heavy)
o colicky dysmenorrhea
o dyspareunia
o pelvic pain
Endometrial polyps
- exophytic mass of variable size that project into
endometrial cavity
- usually single & sessile
- may cause abnormal bleeding
Endometrial hyperplasia
- common cause of abnormal bleeding
-  proliferation of endometrial glands relative to
stroma
- assoc w/ prolonged estrogen stimulation of
endometrium
- risk for endometrial carcinoma
- inactivation of PTEN tumor suppressor gene is
common
o Cowden syndrome (germline mutation in
PTEN) have high incidence of endometrial
carcinoma
- simple hyperplasia without atypia
o cystic or mild hyperplasia
o glands of various sizes & irregular shapes
w/ cystic dilation
o response to persistent estrogen
stimulation
- simple hyperplasia with atypia
o uncommon
o cytologic atypia w/in glandular epithelial
cells
- complex hyperplasia without atypia
o increase in # & size of glands
o marked gland crowding
o branching glands
- complex hyperplasia with atypia
o looks like well-differentiated endometrioid
adenocarcinoma
o greatest risk for CA
o managed w/ hysterectomy
Malignant tumors of endometrium
Endometrial carcinoma
- MC invasive tumor of female genital tract
- mainly in postmenopausal women
- cause abnormal (postmenopausal) bleeding;
allows early detection
Type I carcinoma
- MC type
- well-differentiated
- arise from endometrial hyperplasia
- assoc w/ obesity, diabetes, HTN, infertility,
unopposed estrogen stimulation
- PTEN mutation
- p53 mutation is a late event
- MC = endometrioid adenocarcinomas
- grade 1 = well differentiated w/ easily
recognizable glandular patterns
- grade 2 = moderately differentiated with wellformed glands mixed w/ solid sheets of
malignant cells
- grade 3 = poorly differentiated; sheets of cells
w/ barely recognizable glands; nuclear atypia &
mitotic activity
Type II carcinoma
- arise from endometrial atrophy
- occur a decade later than type I
- poorly differentiated (grade 3) tumors
- p53 mutation (90%)
- Serous carcinoma
o MC subtype
o endometrial intraepithelial carcinoma
(EIC) = precursor
o mutation of p53 is early event
o often spread beyond uterus at dx
o has propensity for extrauterine
(lymphatic or transtubal) spread
o large bulky invasive tumors
Malignant mixed Müllerian tumors
- endometrial adenocarcinoma w/ malignant
changes in the stroma
- stroma differentiates into malignant
mesodermal components (muscle, cartilage,
osteoid)
- occur in postmenopausal women (bleeding)
- morphology:
o fleshier than adenocarcinomas
o sometimes protrude thru cervical os
- highly malignant
Endometrial tumors w/ stromal differentiation
Adenosarcoma
- malignant-appearing stroma
- coexists w/ benign but abnormally shaped
endometrial glands
- 4-5th decades
- low-grade malignancy
Stromal tumors
- Benign stromal nodules
- Endometrial stromal sarcomas
Tumors of the myometrium
Leiomyoma (fibroids)
- MC tumor in women
- benign smooth m. neoplasm
- morphology:
o whorled pattern of smooth m. bundles
o red degeneration
o within myometrium of corpus
o may be intramural, submucosal, or
subserosal
o oval nucleus & long slender bipolar
cytoplasmic processes
- clinical:
o may be asymptomatic
o abnormal bleeding
o compression of bladder  urinary
frequency
o sudden pain
o impaired fertility
o spontaneous abortion in pregnant
women
o malignant transformation very rare
- rare variants:
o benign metastasizing leiomyoma
o disseminated peritoneal leiomyomatosis
Leiomyosarcoma
- arise de novo from myometrium or
endometrial stromal precursor cells
- 2 distinct patters:
o bulky fleshy masses that invade uterine
wall
o polyploid masses that project into uterine
lumen
- wide range of atypia, zonal necrosis
- more than ½ metastasize hematogenously to
distant organs (lungs, bone, brain)
- equally common before & after menopause
- peak at 40-60 years old
FALLOPIAN TUBES
Suppurative salpingitis
- may be caused by an pyogenic microbe
- MC = gonogoccus (>60%)
- chlamydiae less common
Paratubal cyst
- MC 1 lesion of the fallopian tube (excluding
endometriosis)
- filled w/ clear serous fluid
Hydatids of Morgagni
- larger cysts near fimbriated end of tube or in
broad ligaments
OVARIES
Non-neoplastic & functional cysts
Follicle and luteal cysts
- so common, they’re considered normal
- unruptured graffian follicles or follicles that
have ruptured & immediately sealed
- filled w/ clear serous fluid
- lined by gray glistening membrane
- may cause pelvic pain
- granulosa luteal cysts (corpora lutea) normally
present in ovary; may rupture & cause
peritoneal rxn
Polycystic ovarian disease (PCOD)
- aka Stein-Leventhal syndrome
- numerous cystic follicles or follicle cysts assoc
w/ oligomenorrhea
- persistent anovulation, obesity, hirsutism,
virilism (rare)
- ovaries are 2x normal size
- variety of enzymes involved in androgen
biosynthesis are poorly regulated in PCOD
Stromal hyperthecosis
- aka cortical stromal hyperplasia
- commonly seen in postmenopausal
- uniform enlargement of ovary
- usually bilateral
- clinical presentation similar to PCOD but
virilization may be striking
Theca lutein hyperplasia of pregnancy
-  gonadotropins (pregnancy hormones) 
proliferation of theca cells + expansion of
perifollicular zone
- as follicles regress, hyperplasia may appear
nodular
OVARIAN TUMORS
- 80% of tumors are benign tumors that occur in
young women
- malignant tumors more common in older
women
- most ovarian CA detected when they have
spread beyond ovary  low survival rate
- arise from one for 3 ovary components:
o surface epithelium
o germ cells (migrate from yolk sac;
pluripotent)
o stroma of ovary (incl. sex cords)
- some are hormonally active but most are
nonfunctional
- produce mild symptoms until massive size
- MC symptoms:
o abdominal pain/distention
o urinary/GI symptoms (compression)
o vaginal bleeding
Surface (Müllerian) epithelium
- MC 1 ovarian neoplasm
- 3 main types: serous, mucinous, endometroid
- derived from coelomic epithelium
- lower abdominal pain, enlargement
- GI complains, urinary frequency, dysuria, pelvic
pressure
- ascites common if carcinoma extends thru
capsule of tumor to seed peritoneal cavity
- CA-125 & osteopontin are serum markers
- fallopian tubal ligation & OC therapy assoc w/ 
risk
- may be benign, borderline, or malignant
Serous tumors
- lined by tall columnar ciliated & nonciliated
epithelial cells
- filled w/ clear serous fluid
- serous carcinoma = MC malignant ovarian
tumor
- higher freq in low parity
- BRCA1 and BRCA2
o increased risk of ovarian CA
o assoc. w/ high-grade tumor
o many arise from epithelium lining of
fimbriae
- morphology:
o commonly bilateral
o micropapillary carcinoma = precursor to
low-grade serous carcinoma
o psamomma bodies (concentric
calcifications)
o propensity to spread to peritoneal
surfaces  ascites
Mucinous tumors
- occur mostly in middle adult life
- rare before puberty and after menopause
- 80% benign or borderline; 15% malignant
- smoking is risk factor
- KRAS mutation common
- rare surface involvement
- bilaterality less common
- large cystic mass
- multioculated tumors filled w/ sticky,
gelatinous fluid rich in glycoproteins
- mullerian mucinous cystadenoma = benign or
borderline mucinous tumor arising in
endometriosis
- may form precursor for cystadenocarcinoma
- pseudomyxoma peritonei = mucinous ascites,
cystic epithelia implants on peritoneal surfaces,
adhesions; may be from mucinous tumor
involving ovaries or appendix
Endometrioid tumors
- tubular glands with close resemblance to
benign or malignant endometrium
- 15-20% coexist w/ endometriosis (occurs
decade earlier)
- PTEN, KRAS, β-catenin, microsatellite
instability
- carcinomas = combo of solid + cystic areas
- 40% involve both ovaries
Benign tumors
- Clear cell adenocarcinoma
- Cystadenofibroma
- Brenner tumor
o adenofibromas in which epithelial
component consists of nests of
transitional-type epithelial cells
resembling those lining the bladder
o solid or cystic
o usually unilateral
o coffee bean
Germ cell tumors
- most are benign cystic teratomas
Teratomas
- mature (benign)
o MC ovarian germ cell tumor
o aka dermoid cyst
o common in active reproductive years
o assoc. w/ inflammatory limbic
encephalitis
o uniocular cysts; contain hair & cheesy
sebaceous material
o may contain tooth structures & hair
o 1%  malignant (MC squamous cell
carcinoma)
- immature (malignant)
o like embryonal & immature fetal tissue
o aggressive; grow rapidly
o found mainly in prepubertal adolescents
o hair, sebaeceous material, cartilage, bone,
calcifications may be present
- monodermal (specialized)
o MC = struma ovarii and carcinoid
o always unilateral
o struma ovarii – mature thyroid tissue
(may present as hyperthyroidism)
o carcinoid – may cause carcinoid
syndrome
Dysgerminoma
- equivalent to seminoma of testis
- 2nd-3rd decades
- some occur in pts w/ gonadal dysgenesis
- some produce HCG
- c-KIT (dx marker & therapeutic target)
- all are malignant
- usually unilateral
- responsive to chemo
Endodermal sinus (yolk sac) tumor
- rich in AFP and α1-antitrypsin
- Schiller-Duval body (glomerulus-like structure)
= characteristic
- hyaline droplets
- children or young women
- abdominal pain, rapidly growing mass
- unilateral
Choriocarcinoma
- placental origin
- most exist in combo w/ other germ cell tumors
(pure choriocarcinomas very rare)
- aggressive (wide metastases at Dx)
- high HCG
- ovary origin = unresponsive to chemo, fatal
Sex cord-stromal tumors
- derived from ovarian stroma (which is derived
from sex cords of embryonic gonad)
- may be masculinizing (Leydig cell tumors) or
feminizing (granulosa-theca cell tumors)
Granulosa-theca cell tumors
- may be all granulosa or granulosa-theca mix
- 2/3 occur in postmenopausal women
- usually unilateral
- hormonally active tumors = yellow
- pure thecomas = solid firm tumors
- Call-Exner bodies (small, gland-like structures
filled w/ acidophilic material)
- may produce large amts of estrogen
- young girls = functional tumors can cause
precocious puberty
- adults = endometrial hyperplasia, cystic dz of
breast, endometrial carcinoma
- granulosa cells are potentially malignant
-  inhibin (product of granulosa cells)
Fibromas, thecomas, fibrothecomas
- fibroma = fibroblasts
- spindle cells w/ lipid droplets = thecomas
- fibromas usually unilateral
- most are pure fribromas
- pelvic mass
- Meigs syndrome = ovarian tumor + hydrothorax
+ ascites
- Basal cell nevus syndrome
Sertoli-Leydig cell tumors (androblastoma)
- cause masculinization or defeminization
- 2nd-3rd decades
- unilateral
- tubules of Sertoli cells or Leydig cells
interspersed w/ stroma
Other sex cord-stromal tumors
- Hilus cell tumors
o pure Leydig cell tumor
o unilateral, large, lipid laden cells w/
distinct borders
o Reinke crystalloids
o masculinization & hirsutism
o  17-ketosteroid excretion lvl
unresponsive to cortisone suppression
- pregnancy luteoma
o resembles corpus luteum of pregnancy
o virilization in pregnant pts & female
infants
Metastatic tumors
- MC = tumors of müllerian origin (uterus,
fallopian tube, contralateral ovary, or pelvic
peritoneum)
- MC extra-müllerian = breast & GI tract
- pseudomyxoma peritonei = from appendix
tumors
- Krukenberg tumor = from GI; B/L metastases;
mucin-producing, signet-ring CA cells
GESTATIONAL & PLACENTAL DISORDERS
Disorders of early pregnancy
Spontaneous abortion
- pregnancy loss before 20 wks gestation
- most occur before 12 wks
- 50% caused by chromosomal anomalies
- maternal factors: luteal-phase defect, poorly
controlled DM, uncorrected endocrine
disorders
- infections: Toxoplasma, Mycoplasma Listeria,
viral, ascending inf. common in 2nd trimester
losses
Ectopic pregnancy
- MC site = fallopian tubes (90%)
- most important predisposing risk = PID
- previous surgeries, endometriosis, IUDs
- tubal pregnancy = MC cause of hematosalpinx
- severe abdominal pain
Disorders of late pregnancy
Twin placentas
- twin-twin transfusion syndrome = complication
of monochorionic twin
Placental implantation
- placenta previa
o implant in lower uterine or cervix
o serious 3rd trimester bleeding
o complete placenta previa covers internal
cervical os (requires C section)
- placenta accreta
o partial or complete absence of decidua 
adherence of placental villous tissue
directly to myometrium  failure of
placental separation
o important cause of postpartum bleeding
(potentially life-threatening to mother)
Placental infections
- ascending or hematogenous (transplacental)
- MC = bacterial ascending inf.
- hematogenous inf. classically caused by TORCH
o toxoplasmosis
o others [syphilis, TB, listeriosis]
o rubella
o CMV
o HSV
Preeclampsia
- widespread maternal endothelial dysfunction,
vasoconstriction  HTN,  vascular
permeability  proteinuria & edema
- present with HTN, edema, proteinuria
- 3-5% of pregnancies
- occurs in 1st trimester
- more common in primiparas
- severe preeclampsia  HELLP syndrome
(hemolysis,  liver enzymes, low platelets)
- abnormal placental vasculature
o initial event is abnormal trophoblastic
implantation  lack of development of
physiologic changes in maternal BVs
required for adequate perfusion of
placental bed
- endothelial dysfunction
o hypoxia causes ischemic placenta to
release factors into maternal circulation
 imbalance in circulating angiogenic &
anti-angiogenic factors
o placenta derived factors sFltl & endoglin
rise   in angiogenesis earlier than
normal pregnancy  defective vascular
development in placenta
- coagulation abnormalities
- preeclampsia most often starts after 34 weeks
of gestation
- headaches & visual disturbances = severe
preeclampsia
- eclampsia = preeclampsia + convulsions
- Tx = delivery of fetus
Gestational trophoblastic disease
Hyatidiform mole
- cystic swelling of chorionic villi accompanied
by variable trophoblastic proliferation
- classic appearance = delicate mass of thinwalled, translucent, cystic, grapelike structures
composed of edematous villi
- higher risk at far ends of reproductive life
(teens or 40-50)
Complete mole
- fertilization of an egg that has lost its
chromosomes (genetic material completely
paternal)
- risk of choriocarcinoma
- all or most of villi enlarged
- abnormally high HCG
- no expression of p57 (paternally imprinted and
maternally transcribed)
Partial mole
- fertilization of an egg w/ 2 sperm
- karyotype is triploid or tetraploid
- only portion of villi are enlarged
- fetal parts more common
- express p57
Invasive mole
- mole that perforates or penetrates the uterine
wall
- invasion of myometrium by hydropic chorionic
villi
- vaginal bleeding and irregular uterine
enlargement
- persistently  serum HCG
Choriocarcinoma
- malignant neoplasm of trophoblastic cells
derived from previously normal or abnormal
pregnancy
- rapidly invasive; metastasizes widely
- responds very well to chemo
- 50% arise in hyatidiform moles
- others from previous abortions & normal
pregnancies
- present w/ irregular vaginal spotting of bloody,
brown fluid
- HCG elevated above hyatidiform mole lvls
- widespread metastases characteristic (lung &
vagina)
Placental-site trophoblastic tumor (PSTT)
- malignant neoplastic proliferation of
extravillous trophoblast
- aka intermediate trophoblast
- presents as uterine mass w/ abnormal uterine
bleeding or amenorrhea
- moderate  β-HCG
- composed of malignant trophoblastic cells
diffusely infiltrating endomyometrium
- may be preceded by normal pregnancy,
spontaneous abortion, or hyatidiform mole