UTERINE CORPUS

Dr.N.Shayanfar M.D.
Endometrium
Myometrium
UTERINE WALL
HISTOLOGY OF THE
MENSTRUAL CYCLE
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Proliferative phase(first 2 weeks)
Secretory phase(last 2 weeks)
PROLIFERATIVE PHASE
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Growth of both glands and stroma
Glands:straight,tubular
Lining:pseudostratified columnar cells
Mitotic figures:numerous
Stroma:compact spindle cells with
scant cytoplasm & numerous mitotic
activity
EARLY POST MENSTRUAL
ENDOMETRIUM
PROLIFERATIVE PHASE
PROLIFERATIVE PHASE
SECRETORY PHASE
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Glands:
basal secretory vacuoles
secretion
tortusity of glands(serrated or saw-toothed
appearance)
Stroma:
Spiral arterioles Days 21-22
Stromal edema
Predecidual change Days 23-24
Leukocytic infiltration Days 27-28
EARLY SECRETORY
PHASE
SECRETOPRY PHASE
SECRETORY PHASE
DATING OF
ENDOMETRIUM
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Assess hormonal status
Causes of AUB
Causes of infertility
PATHOLOGY
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Functional endometrial disorders
Inflammations
Endometriosis
Adenomyosis
Endometrial polyps
Endometrial hyperplasia
Malignant neoplasms
ABNORMAL UTERINE
BLEEDING(AUB)
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Common
Menorrhagia: profuse or prolonged
bleeding at the time of period
Metrorrhagia: irregular bleeding
between the periods
Postmenopausal bleeding
Common causes: Polyps, leiomyomas,
hyperplasias, carcinomas, endometritis
ABNORMAL UTERINE
BLEEDING(AUB)

Dysfunctional uterine bleeding

Organic lesions
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Depends on the age of the patient
Age group
Causes
Prepuberty
Precocious puberty
Adolescence
Anovulatory cycle
Reproductive age
Complications of pregnancy
Organic lesions
Anovulatory cycles
Ovulatory dysfunctional bleeding
Perimenopausal
Anovulatory cycle
Irregular shedding
Organic lesions
Post menopausal
Organic lesions
Endometrial atrophy
DYSFUNCTIONAL
UTERINE BLEEDING
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Failure of ovulation(anovulatory cycle)
Inadequate luteal phase
Contraceptive induced bleeding
DEFINITION
Abnormal bleeding in the absence of a welldefined organic lesion in the uterus
ANOVULATORY CYCLES
Are very common at both ends of reproductive
life
 An endocrine disorder(thyroid,adrenal,
hypothalamic-pituatory axis)
 A primary lesion of the ovary(PCO,tumors)
 Generalized metabolic
disturbance(obesity,malnutrition,chronic systemic
disease)
 Severe physical or emotional stress
 Subtle hormonal imbalance
AN EXESS OF ESTROGEN RELATIVE TO
PROGESTRONE
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The endometrium goes through a
proliferative phase, not followed by
the normal secretory phase
Mild cystic changes or disorderly
appearance of endometrial glands
The endometrial stroma may be scarce
Prone to breakdown and abnormal
bleeding
INADEQUATE LUTEAL
PHASE
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Inadequate corpus luteum function
(fail to mature, regress prematurely)
Low progestrone output
Biopsy: Estimated secretory change
lags with respect to the expected date
Contaceptive-induced
bleeding
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Older OCPs
Lush decidua like stroma & inactive
nonsecretory glands
INFLAMMATIONS(ENDOM
ETRITIS)
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Acute endometritis(after delivery or miscarriage)
Chronic endometritis:
-chronic PID
-postpartal or postabortal
-IUDs
-tuberculosis
-in 15% no primary cause
Plasma cells.macrophages.lymphocytes & irregular
proliferation of endometrial glands
Clinically:AUB,pain,discharge,infertility
Adenomyosis
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Growth of the basal layer of the
endometrium down into the myometrium
Induces reactive hypertrophy of the
myometrium
Enlarged globular uterus
Do not undergo cyclic bleeding
Menorrhagia, dysmenorrhea & pelvic pain
ENDOMETRIOSIS
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Presence of endometrial glands or stroma in a locations
outside the uterus (endomyometrium)
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In 10% of women in their reproductive years, in nearly half
of women with infertility, 3rd & 4th decades
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Frequently multifocal, often involves pelvic structures
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Locations: ovaries, pouch of Douglas, uterine ligaments,
rectovaginal septum, tubes, pelvic peritoneum, laparotomy
scars, rarely umiblicus, vagina vulva or appendix
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Less frequently: LN, lungs, heart, SM, bone
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Origin: Regurgitation theory, Metaplastic
theory, vascular or lymphatic dissemination
theory
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Recent studies: Endometriotic tissue is not just
misplaced but is also abnormal

Increased level of inflammatory mediators
(PGE2), increased estrogen production
(aromatase activity)

COX-2 inhibitors & Aromatase inhibitors
Ovarian Endometriosis
(Chocolate cyst)
Clinical Manifestations
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Depends on distribution of lesions
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Extensive scarring of oviducts and ovaries:
Discomfort in lower abdominal quadrants, Sterility
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Rectal wall involvement: painful defication
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Involvement of uterine or bladder serosa:
dyspareunia & dysuria
Dysmenorrhea, pelvic pain (intrapelvic bleeding &
periuterine adhesions)
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PROLIFERATIVE LESIONS OF
THE ENDOMETRIUM &
MYOMETRIUM
ENDOMETRIAL POLYP
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Sessile, hemispheric
0.5-3 cm
Endometrium resembling the basalis
Small muscular arteries
Stomal cells are monoclonal (6p21)
Most commonly: around the time of
menopause
AUB, rare risk of cancer
ENDOMETRIAL POLYP
ENDOMETRIAL
HYPERPLASIA(EIN)
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An important precursor endometrial carcinoma
Prolonged or marked excess of estrogen relative to progestin
Exaggerated endometrial proliferation (Hyperplasia)
Predisposing conditions: Failure of ovulation, PCO, Functioning GCT
of ovary, prolonged adminstration of estrogenic substances, obesity
Severity: Level & duration of estrogen excess
Simple, complex, atypical
Risk of developing carcinoma: Presence of cellular atypia 5% vs 2050%
Inactivating mutations of PTEN tumor suppressor gene (del,inact)

The endometrial cavity is opened to reveal lush fronds of
hyperplastic endometrium. Endometrial hyperplasia usually
results with conditions of prolonged estrogen excess and can
lead to metrorrhagia (uterine bleeding at irregular intervals),
menorrhagia (excessive bleeding with menstrual periods), or
menometrorrhagia.
Simple nonatypical
hyperplasia
Complex atypical
hyperplasia(EIN)
Loss of PTEN gene
ENDOMETRIAL
CARCINOMA
Adenocarcinoma
The most frequent invasive cancer
of the female genital tract
Molecular Pathogenesis
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Type I
Type II
Characteristics
Type I
Type II
Age
55-65 yr
65-75 yr
Clinical setting
Unopposed estrogen
Breast cancer
Atrophy
Thin physique
Obesity
Hypertension
Diabetes
Infertility
Morphology
Endometrioid
Serous carcinoma
80%
15%
Precursor
Hyperplasia
Endometrial intraepithelial
carcinoma
Molecular genetics
PTEN,mismatch repair
genes, p53 (uncommon)
P53,
Behavior
Indolent
Aggressive
Spreads via lymphatics
Intraperitoneal and
lymphatic spread
Type I Carcinomas
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The most common type (> 80% of all
cases)
Majority are well differentiated
(Endometrioid carcinoma)
Estrogen-secreting ovarian tumors
Associated with:1) obesity, 2) diabetes
, 3) hypertension, 4) infertility ,
5) unopposed estrogen stimulation
Morphology
Gross morphology:
* A localized polypoid tumor
* A diffuse (infiltrative) tumor
 Myometrial invasion, Dissemination to
the regional lymph nodes ,
metastasize to the lungs, liver, bones,
and other organs
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Microscopy
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Endometrioid adenocarcinomas
characterized by gland patterns resembling
normal endometrial epithelium
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A range of histologic types: Mucinous,
tubal (ciliated), & squamous differentiation
A three-step grading system is applied to
endometrioid tumors (I-III)
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This adenocarcinoma of the endometrium is more obvious.
Irregular masses of white tumor are seen over the surface of
this uterus that has been opened anteriorly. The cervix is at
the bottom of the picture. This enlarged uterus was no doubt
palpable on physical examination. Such a neoplasm often
present with abnormal bleeding.
ENDOMETRIAL
ADENOCARCINOMA

This is endometrial adenocarcinoma which can be
seen invading into the smooth muscle bundles of
the myometrial wall of the uterus. This neoplasm
has a higher stage than a neoplasm that is just
confined to the endometrium or is superficially
invasive.
MYOMETRIAL INVASION
Type II Carcinomas
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A decade later than type I carcinoma
Usually arise in the setting of
endometrial atrophy
Are by definition poorly differentiated
(grade 3) tumors
Approximately 15% of cases of
endometrial carcinoma
The most common subtype is serous
carcinoma
Morphology
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Large bulky tumors or deeply invasive
into the myometrium
All of the non-endometrioid carcinomas
are classified as grade 3 (high grade)
irrespective of histologic pattern
Form small tufts & papillae, much greater
cytologic atypia
High levels of p53 on IHC
Papillary serous
carcinoma
Clinical Course
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Irregular or postmenopausal vaginal
bleeding with excessive leukorrhea
Fixation to surrounding structures
Slow to metastasize
The prognosis depends heavily on the
clinical stage of the disease, its histologic
grade and type
Serous tumors: stage, cytology of peritoneal
washings
Staging
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I confined to the corpus
II Corpus & cervix
III extends outside the uterus but not
true pelvis
IV extends outside the true pelvis or
involving bladder or rectum
TUMORS OF THE
MYOMETRIUM
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Benign:Leiomyomas(fibroids)
Malignant:Leiomyosarcoma
LEIOMYOMA
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The most common benign tumors in
females
30-50% of women of reproductive age
Monoclonal
Rearrangement of chromosome 6 & 12
Estrogen & OCP: stimulate the growth
Shrink postmenopausally
MORPHOLOGY
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Sharply circumscribed
Firm gray masses
Whorled cut surface
More often multiple tumors,
intramural,submucosal, subserosal, parasitic
Histology
Foci of calcification fibrosis, degeneration
LEIOMYOMA
LEIOMYOMATA
LEIOMYOMA

Here is a very large
leiomyoma of the uterus that
has undergone degenerative
change and is red (so-called
"red degeneration"). Such an
appearance might make you
think that it could be
malignant. Remember that
malignant tumors do not
generally arise from benign
tumors, which is a good
thing, because leiomyomas
are so common (20% of
women will have at least
one). Postmenopausally,
leiomyomas tend to regress in
size and become fibrotic.
Clinical Manifestations
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Often are asymptomatic (incidental)
Menorrhagia (most frequent)
Palpable mass, or dragging sensation
Almost never transform into
sarcoma
LEIOMYOSARCOMA
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Arise de novo from the mesenchymal
cells of the myometrium
Almost always are solitary
Postmenopausal women (most often)
Soft, hemorrhagic necrotic mass
STUMP
Tumor necrosis, cytologic atypia &
mitotic activity
Recurrence, metastasis (lungs)
LEIOMYOSARCOMA
LEIOMYOSARCOMA
LEIOMYOSARCOMA
FALLOPIAN TUBES
HISTOLOGY
FALLOPIAN TUBE
HISTOLOGY
FALLOPIAN TUBES
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Inflammations(most common)
Ectopic pregnancy
Endometriosis
Tumors(uncommon) and cysts
INFLAMMATIONS
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Almost always microbial in origin
Gonorrhea, nongonococcal (chlamydia,
mycoplasma hominis), coliforms,
streptococci, staphylococci
Suppurative salpingitis (gonococcus,
chlamydiae)
Nongonococcal: blood-borne
Tuberculous salpingitis (important cause of
infertility)
PID
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Lower abdominal or pelvic pain, fever, pelvic
mass, vaginal discharge
Complications: Tubo-ovarian abscess,
Peritonitis, intestinal obstruction, tubal ectopic
pregnancy, infertility
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A remnant of tubal epithelium is seen here
surrounded and infiltrated by numerous
neutrophils. This is acute salpingitis.
Neisseria gonorrheae was cultured.
TUBO-OVARIAN ABSCESS
TUBO-OVARIAN ABSCESS
Salpingitis
Tumors and cysts
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Paratubal cyst(hydatid of morgani)
Adenomatoid tumor(mesothelioma)
Adenocarcinoma(rare)
Adenocarcinoma
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Serous or endometrioid types
Serous types are increased in women with
BRCA mutations
Prophylactic oophorectomies: 10% occult
foci of malignancy, usually in the fimbria
Frequently involve the omentum and
peritoneal cavity at presentation