1.

Endometrial polyps
a. Abnormal protrusions of friable tissue into the endometrial cavity
b. Can cause:
i. Menorrhagia
ii. Spontaneous bleeding during reproductive years
iii. Postmenopausal bleeding after menopause
c. Appear as focal thickening of endometrial stripe on US
d. More clearly recognized on saline infusion sonography or visualized directly by
hysteroscopy
e. Histological evaluation of polyp is imperative b/c although most are benign,
endometrial hyperplasia, endometrial carcinoma, and carcinosarcomas may also
present as polyps
2. Cervical Polyps
a. If symptomatic, they most commonly cause coital bleeding or menorrhagia
b. All specimens must be sent for pathologic examination b/c both SCC and
adenocarcinomas can present as polyps although incidence of malignancy is low (1%)
3. Asherman’s syndrome
a. Endometrium is denuded and endometrial cavity filled with adhesions
b. Irregular bleeding to amenorrhea depending on amount of intrauterine scraping
c. Scarring results from curettage (procedure using curette for scraping) in high-risk
settings
i. Postpartum hemorrhage
ii. Septic abortion
iii. Any vigorous scraping resulting in loss of endometrium and consequent
adhesion of opposing myometrial surfaces
d. Endometrial ablation procedures are designed to deliberately destroy endometrium and
create such scarring Can ONLY be officially diagnosed by surgical pathology!
4. Adenomyosis (Endometriosis interna)
Usually after hysterectomy
a. Defined as extension of endometrial glands and stroma into the uterine musculature
more than 2.5mm beneath basalis layer
b. Often an incidental finding. About 15% of patients have associated endometriosis
c. Pathology
i. Diffuse enlargement of the uterus with a thickened myometrium containing
characteristic glandular irregularities, with implants containing both glandular
tissue and stroma. No distinct margin can be detected between adenomyoma
and surrounding myometrium differentiating it from fibroid
d. Symptoms
i. Many are asymptomatic
ii. Secondary dysmenorrhea
iii. Menorrhagia
iv. Pain and tenderness
1. Prostaglandin release and local inflammation
v. Deep thrust dyspareunia
e. As opposed to endometriosis, islands of adenomyosis do NOT cycle in response to
ovarian hormonal stimulation!
f. Signs
i. “Boggy” uterus is classic term to describe uterus with adenomyosis during
pelvic exam
ii. Symmetrically enlarged
iii. Tender if premenstrual
g. Treatment
i. Conservative management with NSAIDs and hormonal control of the
endometrium are mainstays of therapy
ii. If woman not candidate for meds or if medical treatment not sufficiently
controlling symptoms, then hysterectomy may be indicated. Endometrial
ablation to control bleeding is another option
 1. Polycystic Ovary Syndrome
a. Chronic condition defined as anovulation or oligo-ovulation with clinical or
laboratory evidence of hyperandrogenism and without evidence of any other
underlying condition
b. Increased chance that first-degree female relatives are affected (heritable aspect)
c. Most common signs
i. Hirsutism (90%)
Combined OCP's contain estrogen which increases 1. Less likely in women who have used combined hormonal
serum SHBG which decreases free androgens
contraceptives for most of their postpubertal lives and for women
of East Asian ethnicity
ii. Menstrual irregularity (90%)
iii. Infertility (75%)
iv. Abdominal obesity (60% in US)
1. Varies widely by country
v. Insulin resistance/decreased insulin sensitivity (60-70%)
d. Ovaries contain multiple inactive follicular cysts arrested in mid-antral stage of
development located peripherally in the cortex

e. Ovarian stroma is hyperplastic and contains nests of luteinized theca cells that
produce androgens
f. Hyperandrogenism results from an overproduction of androgens (androstenedione
and testosterone) by ovarian theca cells due to increased LH pulse frequency
leading to higher circulating levels of LH which stimulates cholesterol desmolase
in theca cells
g. Anovulation mechanism
i. Increased androgens are converted to estrogen in the periphery via adipose
aromatase resulting in tonic estrogen levels higher than those found
normally in early follicular phase which suppress FSH release. Recall that
FSH secretion at this stage is what is supposed to be driving follicular
development and increasing estrogen secretion from granulosa cells.
Threshold level of estrogen isn’t reached and positive feedback
mechanism isn’t established hence LH/FSH surge doesn’t occur
h. Insulin resistance leads to insulin hypersecretion. Direct insulin stimulation of
theca cells results in androgen secretion. Elevated androgen and insulin levels
reduce hepatic production and secretion of SSBP/SHBG which can dramatically
increase amount of FREE testosterone with only a small/moderate increase in
total testosterone. This is why physical manifestations of hyperandrogenism in
PCOS may seem dramatic in relation to level of total testosterone
i. Long term effects
i. Insulin resistance may lead to increased risk for metabolic syndrome
ii. Unopposed estrogens may cause hyperplasia of endometrium and
occasionally endometrial carcinoma
j. Treatment
i. Combination contraceptives (estrogen-progestin) suppress gonadotropins
(LH/FSH) which allows regression of overproduction of testosterone and
androstenedione by ovary. Estrogen also stimulates production of SHBG
which decreases free testosterone levels
ii. Scheduled progestin-induced withdrawal of the endometrium to reduce
risk for developing endometrial hyperplasia and cancer if they are not
taking combined oral contraceptives
1. Medroxyprogesterone (Provera)