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Gynecology: Benign Disorders & Cervical Lesions Chart

Benign Disorders & Cervical Lesions
Congenital Anomalies of the Vulva & Vagina:
Occur in external genitalia, vagina, and cervix
Often associated with concomitant anomalies in the upper reproductive tract
And anomalies in the GU tract (renal agenesis, pelvic/horseshoe kidneys, irregular collecting ds. etc.)
Upper Genital Tract: Includes the endometrium, myometrium, uterus, fallopian tubes, ovaries, and peritoneal cavity
Lower Genital Tract: Includes the vulva, vagina, and cervix
Clinical Presentation
Exogenous cortisol 
Glucocorticoid provides (-)
feedback that ↓ ACTH release
21-hydroxylase deficiency
↑: androgens + DHEA
↓: aldosterone + cortisol
Benign Disorders of the Lower Genital Tract
Labial Fusion
Imperforate Hymen
Transverse Vaginal
1. Excess androgens:
- OR2. Enzymatic: ↑ androgens
M.C. type of error= 21hydroxylase deficiency
leading to CAH
Absence of opening in
hymen; results in
obstruction to outflow
Anomaly occur when
Müllerian tubercle is not
In neonates:
- Phenotypically = ambiguous or
masculinization of external
genitalia (enlarged clitoris, labial
fusion, labioscrotal masc.)
↑ 17hydroxyprogesterone
↑ Urine 17-ketosteroid
↓ Serum cortisol
Exogenous Aldosterone 
Mineralocorticoid added for
salt wasting (fludrocortisone
- Metabolically = salt wasting
(ADRENAL CRISIS – 75% pts),
hypotension, hyperkalemia and
Primary amenorrhea,
dysmenorrhea, abdominal pain
Before menarche: hydrocolpos
or mucocolpos = buildup of
secretion behind hymen
After menarche: hematocolpos/
hematometra: buildup of blood
behind hymen in vagina or
uterus (respectively)
Presents similar to imperforated
hymen, primary amenorrhea,
cyclic pelvic pain accompanied
by menstrual symptoms.
Physical examination:
Absence of an identifiable
vaginal lumen; tense
bulging hymen
Usually made at the time
of puberty in adolescents:
Often requires reconstructive
 Surgery to excise the extra
 Evacuate any obstructed
 Create a normal sized vaginal
Surgical correction → only
form of treatment
Differentials: imperforate
hymen, and vagina
Occurs at junction
between lower 2/3 and
upper 1/3 of vagina
Vaginal Atresia
Vagina is abnormally
closed or absent
Lower vagina fails to
develop (urogenital sinus
failure) and is replaced
with fibrous tissue
Normal external female
genitalia with short vagina that
appears to end in a blind pouch
Primary amenorrhea, cyclic
pelvic pain
Absence of introitus and
presence of vaginal dimple
Ultrasound and MRI:
thickness and location of
the septum.
Confirm the presence of
other parts of the
reproductive tract
Pelvic imaging w/
ultrasound and/or MRI 
large hematocolpos and
presence of upper tract
Normal ovaries, uterus,
cervix, and upper vagina
Vaginal Agenesis
Vagina is abnormally
closed or absent
Mayer-Rokitansky-Kü sterHauser (MRKH):
- Normal pheno/genotype
- Normal ovaries and fx
- Normal secondary sexual
- Congenital absence of
the vagina
- Absence or hypoplasia
of cervix, uterus, fallopian
and ovaries and kidneys
- Amenorrhea; normal external
and abnormal internal genitalia
- Rudimentary pouch of vagina
may be present
10% have normal uterus with
functioning endometrium
associated w/ urologic and
(rarely) skeletal anomalies
Can also have CARDIAC issues
Pelvic imaging with
ultrasound and MRI to
assess the:
 Vagina
 Uterus
 Ovaries
 Kidneys
Surgical correction:
Incision of the fibrous tissue,
evac of accumulated contents,
normal upper vagina sutured
to hymenal ring  vaginal
pull-through procedure
 Psychosocial support
 Counseling
 Nonsurgical and surgical
correction individualized to the
 Serial vaginal dilators used on
perineum or blind vaginal
pouch, may be used with or
without surgery
Differentials: Turner’s
pt’s genitalia can present
with similar genitalia,
imperforate hymen,
transverse septum
Benign Epithelial Disorders
Lichen Sclerosis
Age: women of all age
Major significance:
postmenopausal women in
50’s or 60’s→ associated
with 4% risk of vulvar skin
Lichen Planus
Women in their 50s or 60s
and it is associated with a
4% risk of vulvar skin
Associated with vaginal
adhesions and with erosive
Usually asymptomatic, may
cause pruritus and dyspareunia
Atrophy can cause resorption of
the labia minora
 Thinning of the vulvar skin,
and skin fragility
 Labial fusion
 Occlusion of the clitoris
 Contracture of introitus
- White coloration; often figure
8 pattern around vulva + anus
 Chronic eruption of shiny
purple papules with white
 Vaginal adhesions.
 Similar lesions are often found
on the mucous membrane of
the oral cavity and flexor
Histological confirmation
Topical steroids: clobetasol:
0.05% 1-2x/day 6-12 weeks
Biopsy if malignancy is
suspected (sclerosis and
Types of tx for
sclerosis + planus:
for post-inflammatory
sequela  adhesions and
Differentials: also includes
carcinomas such as
squamous cell, basal cell,
melanoma, sarcoma, and
Paget disease of the vulva
(presents w/ eczema)
 High potency topical
 Vaginal suppositories:
 Vaginal estrogens
 Surgical excision or vaginal
dilators for vaginal adhesions
 Skin disorder leads to a
scratch–itch cycle
 Intense pruritus →
usually unilateral &
circumscribed, may be
1. Atopic dermatitis
2. Neuropathic pain
3. Psychologic disorders
It may begin with something
that rubs, irritates, or scratches
the skin, such as clothing.
Thickened skin with skin
markings and excoriations →
due to chronic itching and
1) High potency topical
steroids: clobetasol or
halobetasol (1-2x/d for 612 weeks, then reduce to
once a week
2) Low dose vaginal
estrogen: Premarin - for
vaginal atrophy in
postmenopausal women
3) Surgical excision to
enlarge the introitus and
open adhesions
6 Ps: Purple, Pruritic, Papules,
Plaques, Polygonal, Planar
Lichen Simplex
Lesions should be
biopsied in older women
to rule out vulvar skin
4) Vaginal Dilators: to
widen the introitus
Topical steroids 2x/ 4-6 weeks
(medium-high potency)
Vulvar Psoriasis
Red, moist, scaly lesions
 Asymptomatic or pruritus
 Topical steroids
 Ultraviolet light
Benign Cysts or Tumors
Epidermal Inclusion
M.C. Tumor on the vulva
Cause: Occluded
pilosebaceous duct/ hair
Sebaceous Cysts
Apocrine Sweat Gland
May be found on vulva or
Solitary, small, mobile, nontender, filled with keratinaceous
If these become superinfected
and develop into abscesses
Multiple, non-tender, usually
appear yellow, usually
Filled with sebaceous
Sweat glands in the axilla,
mons pubis, and labia
majora can become
occluded and form cysts.
1. Fox-Fordyce disease:
Pruritic, inflamed, keratinplugged apocrine sweat
Skene’s Gland Cysts
Incision and drainage or
complete excision
2. Hidradenitis
suppurativa: apocrine +
sebaceous glands;
abscesses in underarms,
breasts, inner thighs,
groin, and buttocks.
(paraurethral glands), located next to the urethra meatus
Chronic inflammation  obstruction of ducts + cystic dilation of the glands
If they become infected and
form multiple abscesses 
Excision or incision and
drainage are the treatments of
If an over-lying cellulitis is
present, antibiotics are
Cysts: generally, no
treatment required if
asymptomatic; if
antibiotics with
incision/drainage (I&D)
or excision
Bartholin’s Duct Cysts
and Abscesses
Mucous-secreting glands
that provide lubrication to
the vagina; opens just
external to hymenal ring
Location: at 4 and 8
o’clock positions near the
vaginal introitus
Gartner’s Duct Cysts
Can be asymptomatic if the cyst
remains small (1-2cm) – may
resolve on its own
1. Warm sitz baths several
times per day: pain relief and
to ↓ healing time.
Cysts can become large and
cause localizes pain,
dyspareunia, and pain with
walking  can lead to infection
(Bartholin abscess)
2. Adjunct antibiotic therapy:
If Neisseria gonorrhoeae (10%)
(Azithro, Doxy); If cellulitis or
an abscess, tx for S. aureus
Result from polymicrobial
infections, and is also
associated with STDs
Word Catheter (w/balloon):
emergent setting or office 
For drainage: 4-6 weeks
Obstruction  Cystic
Marsupialization: Indications:
1. Recurrent cysts 2. Abscesses
(infected cyst) 3. Word Cath
failed  prevents reformation
of the abscess 
1. Bartholin Abscess
2. Bartholin Cyst
3. Bartholin Cyst
carcinoma: < 1%
Remnants of Wolffian
 Most common location:
anterior lateral aspects of
the upper part of the
Most asymptomatic
May present in adolescence
with dyspareunia or difficulty
inserting tampon
Excision: potential for
significant bleeding during
excision  use vasopressin to
maintain hemostasis
If needs to be removed, IVP (IV
pyelogram) and cystoscopy 
locate bladder and urethra
Benign Cervical Lesions
Nabothian Cysts
Dilated retention cysts
Intermittent blockage of
mucinous endocervical
Normal variant
Clinical presentation:
M.C. in menstruating women;
most are asymptomatic.
No tx needed for most
Woman over 40 = risk for
Bartholin gland cancer 
biopsy cyst wall
1. Urethral diverticula
2. Ectopic ureters
3. Vaginal and cervical
Endometriosis Cysts
Cervical Polys
Cervical Fibroids
Cervical Stenosis
Can implant on/near cervix
Benign pedunculated or
broad-based (sessile)
growth from endocervix
or endometrium
Rarely: obstructs canal
Very rarely: (<1%) contain
Squamous Cell Carcinoma
or adenocarcinoma
Can arise In cervix or be
prolapsing from the
endometrial cavity
1. Congenital
2. Infection
3. Scarring (surgery,
cryosurgery, radiation)
4. Atrophy: secondary to
lack of estrogen
5. Obstruction: neoplasm,
polyp, fibroid (less
Cysts tend to be red or purple in
Endometriosis symptoms 
cyclic pain and dysperunia
Intermenstrual/ postcoital
No tx needed
Hysteroscopy 
distinguish cervical and
endometrial polyps
No pain
Removal to prevent masking of
abnormal bleeding  done
easily in office: twist off with
ring forceps in office
Not considered premalignant lesion
Dilation and curettage (D&C)
May need electrocautery
Dyspareunia, bladder pressure,
rectal pressure, pregnancy
problems (dilation, hemorrhage,
malpresentation, obstruction)
Typically asymptomatic
Does not affect menstruation or
fertility  unless passage from
uterus is completely blocked
Can cause difficult birth; of
obstruct certain procedures
Congenital Anomalies
Surgical removal if
Hysterectomy rather than
myomectomy may be required
 depending on location and
desire to preserve fertility
Generally, no tx necessary
Can use cervical dilators  can
leave catheter in cervical canal
for few days until stenosis
Obstructive lesions should be
Rule out possibility of
cervical cancer
Female Reproductive Organs Arise From:
1. Genital ridge: ovaries
2. Mü llerian system: Formed by fusion of paramesonephric (mü llerian) ducts: superior vagina, cervix, uterus,
fallopian tubes
3. Urogenital diaphragm: Lower one-third of the vagina
Uterine anomalies are EXTREMELY RARE  Incidence increased in women exposed to DES from 1940-1973
DES: Diethylstilbestrol: synthetic non-steroidal estrogen
- Given to woman with risk of spontaneous abortion (also given for postpartum laceration, atrophic vaginitis,
menopausal symptoms, adv breast cancer, etc.) - Female children later developed congenital anomalies
Isolated congenital anomalies of the cervix are rare
 Can cause uterine didelphys with a double vagina, a double cervix (bicollis) may be found, but not isolated.
 Women who were exposed in utero to DES (25%) have an associated abnormality of the cervix, including:
1. Cervical hypoplasia
2. Cervical collars (fig. 13-11)
3. Cervical hoods
4. Cock’s comb cervix
5. Pseudopolyps
Other risks of DES:
1. Increased risk of cervical insufficiency in pregnancy.
2. A very rare clear cell adenocarcinoma of the cervix and vagina.
 Cell adenocarcinoma of the cervix and vagina: Seen in young women <20; only occurs in 0.1% of DES-exposed pts
Non-Drug Related Cause = M.C. septate uterus due to: malfusion of müllerian ducts
Also associated with: Unilateral renal agenesis, pelvic/horseshoe kidneys, and irregularities in collecting system
Anomalies usually asymptomatic and most are discovered incidentally during OBGYN visits at onset of menarche, coitus, or when attempting pregnancy
Symptoms associated with anomalies of the uterus include:
 Menstrual abnormalities
 Dysmenorrhea
 Dyspareunia
 Cyclic and noncyclic pelvic pain
 Infertility
 Recurrent miscarriages
Mullerian Anomalies (CLASS):
 Class I – Hypoplasia/Agenesis: failure in müllerian duct fusion; can affect, vagina, cervix, fundal, tubal, or combined
- associated with Mayer-Rokitansky-Hauser-Kauser Syndrome (MRHK): absent vagina and uterus
- presents with amenorrhea and urinary tract anomalies
 Class II – Unicornuate uterus: may have communicating/non-communicating endometrial cavity or absent cavity; müllerian ducts fail to form  incomplete horn (banana shape)
 Class III – Uterine didelphys: double uterus; ducts fail to fuse and each become a separate uterus
 Class IV – Bicornuate uterus = M.C. can be complete, partial or arcuate (bow shape); ducts fail to fuse on top, resulting in two separate single horns sharing one cervix
 Class V – Septate Uterus: medium septate persists in the uterus; lacks adequate blood supply to facilitate placentation and maintain pregnancy; RISK = recurrent 1st trimester
 Class VI – Arcuate uterus/partial septate: normal in shape, small indentation in fundus; medium septum fails to dissolve completely; no negative effects in pregnancy
 Class VII – DES Related
Primary investigative tools for uterine abnormalities are:
1. Pelvic ultrasound
2. CT scan
3. MRI
4. Sonohistogram
5. Hysterosalpingogram
6. Hysteroscopy
7. Laparoscopy
TREATMENT: Many uterine anomalies require no treatment.
Treatment: when the defect causes significant symptoms such as:
 Pain
 Menstrual irregularities
 Infertility
Uterine septa:
 Can be excised with operative hysteroscopy
 Bicornuate uterus has to be ruled out first.
Bicornuate uterus
 When a viable pregnancy cannot be achieved:
- Surgical unification procedures is indicated.
- Viable pregnancies have been achieved after these surgeries.
- These pts will require cesarean to ↓ the risk of uterine rupture.
 Many women are able to carry a pregnancy to fruition, with risk ↑ of:
- Preterm labor
- Preterm delivery
Benign Disorders of the Upper Genital Tract
uterine fibroid)
Proliferation of the smooth muscle cells of the myometrium; vary in size
It is unclear if fibroid have malignant potential; however, leiomyomas and leiomyosarcomas typically exist concurrently (with rare exception)
Leiomyosarcoma thought to be new neoplasms and not a degeneration of an existing benign fibroid
Factors that play a role in the formation and growth of uterine fibroids:
1. Genetic predisposition
2. Steroid hormone factors
3. Growth factors
4. Angiogenesis
 Responsive to both estrogen & progesterone but the relationship is complex. 1
Reproductive age women: fibroids can grow and shrink at differing rates
During menopause the tumors:
 Usually stop growing
 May atrophy in response to naturally ↓endogenous estrogen levels
Risks to develop leiomyoma by age 50.
 Whites: 70%
 African American: > 80% 5x more likely (also more likely to be diag. younger, have larger or more fibroids, bleed heavily, and develop severe anemia)
Fibroids become problematic only when their location results in:
 Heavy or irregular bleeding
 Reproductive difficulties.
 Large enough to cause a mass effect on other structures resulting
1. Pelvic pain and pressure
2. Urinary frequency
3. Constipation
 50-65% → Have no clinical symptoms
 M.C. symptom = abnormal uterine bleeding:
Typically presents as:
 Menorrhagia: increasingly heavy periods of longer duration
 Postcoital spotting: spotting after intercourse.
 Metrorrhagia: bleeding between periods
 Menometrorrhagia: heavy irregular bleeding
Blood loss from fibroids can lead to:
1. Chronic iron-deficiency anemia
2. Dizziness
3. Weakness
4. Fatigue
Pelvic Pain:
 Present if vascular compromise is present.
 Most common in subserosal pedunculated fibroids.
 Secondary dysmenorrhea: when menorrhagia or menometrorrhagia are present.
Pressure-related symptoms:
Vary depending on the number, size and location of leiomyomas.
 Pelvic pressure
 Constipation
 Hydronephrosis
 Venous stasis
 Urinary frequency
 Urinary retention
Depending on their location and size:
Leiomyomas can sometimes be palpated on:
1. Bimanual Pelvic examination: a nontender irregularly enlarged uterus with “lumpy-bumpy” or cobblestone protrusions that feel firm or solid on palpation.
2. Abdominal examination.
(3) Types of Uterine Fibroid
 Subserosal: can impact implantation, placentation & ongoing pregnancy; resection of submucosal fibroids in
pts diagnosed with infertility does lead to increased conception rates.
 Intramural & Submucosal: are both unlikely to affect conception or pregnancy loss except when multiple
fibroids are present.
1. Differentials: depends on the pt symptoms
2. Pelvic ultrasound: M.C. – can be seen as areas of hypoechogenicity among normal myometrial material
Valuable tools in identifying submucosal fibroids and in distinguishing fibroids from polyps:
3. Hysterosalpingogram (HSG)
4. Sonohysterogram (saline infusion sonogram)
5. Hysteroscopy
6. MRI: especially helpful in distinguishing fibroids from adenomyosis as well as for surgical planning.
1. Expectant therapy:
 Most cases with close follow up, they ↓ size after menopause
 Pts with actively growing fibroids: Follow every 6 months to monitor the size and growth.
2. Nonhormonal options
- Nonsteroidal anti-inflammatory drugs
- Anti-fibrinolytics: tranexamic acid
- Are limited at treating:  Dysmenorrhea  Heavy prolonged bleeding  Anemia
3. Hormonal options:
 Combined oral contraceptive pills  Progestins (medroxyprogesterone acetate  Mirena IUD
 Norethindrone acetate  Mifepristone  Androgenic steroids: danazol and gestrinone
 GNRH agonists: nafarelin acetate, leuprolide acetate depot
4. Uterine Artery Embolization 
 Less invasive, for treating symptomatic fibroids.
 Interventional radiologist catheterizes the femoral artery under local anesthesia in
order to inject an embolizing agent into each uterine artery.
 Goal: decrease the blood supply to the fibroid.
5. Surgery:
 Myomectomy: preserves fertility
1. Laparoscopy
2. Laparotomy
 Hysterectomy: definitive treatment for leiomyomas when fertility is completed
1. Abdominal: TAH
2. Vaginal: TVH
GnRH agonists may be used to:
 Presurgical shrinkage: GnRH agonist for 3-6 months.
 Stop bleeding
 ↑ the hematocrit prior to surgical treatment of uterine fibroids
Unfortunately, the tumors usually resume growth after the medications are discontinued.
Women nearing menopause: txs may be used as a temporizing measure until their own endogenous estrogens decrease naturally
More commonly associated with:
1. African American heritage
2. Early menarche
3. Nulliparity
4. Perimenopause
5. Nonsmoking
6. Increased alcohol use
7. Hypertension
Localized benign overgrowths of
endometrial glands and stroma.
Clinical Presentation
Diagnostic Evaluation
They vary in size from
millimeters to several
May be:
3. Hysteroscopy
 Any polyp will be removed
in postmenopausal pts
 Premenopausal women
require removal of
symptomatic polyps 
 Pedunculated or sessile
Benefit of hysteroscopy:
 Single or multiple •
 Is the possibility of
immediate treatment.
 Women’s age ≥ 45 with
abnormal bleeding from
endometrial polyps should
 Within the endometrial
 prolapse through the
endocervical canal.
evaluated with endometrial
biopsy prior to removal.
 Most commonly in women 4050 years old
 Women taking tamoxifen are at
risk for developing polyps  Most
commonly present symptom:
metrorrhagia: bleeding between
menstrual cycles.
 Any bleeding in a
postmenopausal woman needs
Definition: Abnormal
proliferation of both elements of
the endometrium: 1. Glandular
Prolonged exposure to
exogenous/endogenous estrogen
in absence of progesterone
Classification of Hyperplasia and
Endometrial Cancer (EC)
 Majority are benign
 Polyps can be malignant or
premalignant in:
Depends on the:
Pathogenesis: Cause:
Risk of infertility
Endometrial cancer
 5% of postmenopausal
 1% to 2% of premenopausal
Fast facts about Endometrial
Asymptomatic polyps that
should be removed: those at:
Long periods of
oligomenorrhea or
amenorrhea followed by
irregular or excessive
uterine bleeding.
Uterine bleeding in a
woman should raise
suspicion of
 Method of choice for
evaluation of abnormal
uterine bleeding:
Endometrial biopsy
 When an office
endometrial biopsy cannot
be obtained: Do a D&C in
the operating room
1. Histologic variant of the
why an endometrial biopsy
cannot be obtained;
 Control abnormal bleeding
Simple and complex
2. Age of the patient.
Goal of treatment:
 Prevent progression of
Endometrial hyperplasia is
clinically important because it is:
 A source of abnormal uterine
 Link to endometrial cancer.
 Simple Hyperplasia: no atypical
cytology; 1% risk to become EC
 Complex Hyperplasia: no
atypical cytology; 3% risk
 Atypical Simple: cytologic atypia
present; 10% risk
 Atypical Complex: cytologic
atypia present; 30% risk
Risk factors
1. Chronic anovulation 2. Obesity
3. Nulliparity
4. Late menopause
5. Unopposed estrogen use
6. Hypertension: independent risk
7. Diabetes mellitus: independent
risk factor
8. Lynch II syndrome:
hyperplasia or
carcinoma until proven
Physical Examination:
• Pelvic examination is
• Pts may also have
signs associated with
chronic anovulation
such as:
 Abdominal obesity 
 Acne
 Hirsutism
because: 1. Insufficient
hyperplasia without atypia:
Progestin 3 to 6 months
2. Patient discomfort 3.
Cervical stenosis
 Depo-Provera
 Oral (Provera)
 megestrol (Megace)
 norethindrone (Aygestin)
 Followed by resampling of
the endometrium
D&C is also recommended
for women
 ≥ 45
 Younger women with risk
factors for hyperplasia and
 Pts with atypical complex
hyperplasia on biopsy (30%
will have endometrial cancer
Atypical complex hyperplasia
treatment of choice =
Ovarian masses can be divided
1. Functional cysts
2. Neoplastic growths
Follicular Cysts < 2.5
cm simple cysts are
physiologic, but they
size vary from 3-8 cm
 When > 4 cm can:
occurs during the proliferative
(estrogen-dominant) phase of the
Unopposed estrogen stimulation
may be from two sources:
Exogenous: M.C. source = estrogen
hormone replacement without
Endogenous: M.C. seen in obese
excess adipose tissue results in ↑
peripheral conversion of
androgens: androstenedione and
testosterone to estrogens: estrone
and estradiol by aromatase in the
This excess endogenous estrogen
stimulation can then stimulate
overgrowth of the endometrium
resulting in:
endometrial hyperplasia and even
 Hereditary nonpolyposis
colorectal cancer
 Have>10-fold ↑ lifetime risk of
endometrial hyperplasia &
Ovarian Cysts
 Endometrial proliferation is a
normal part of the menstrual cycle
Diagnositc Work Up:
1. Pregnancy test 2. UA
3. CBC
4. Pelvic US
Follicular Cysts
 Management:
Functional cysts of the ovaries:
 Most common types of ovarian
cysts: no treatment necessary 
Results from normal physiologic
functioning of the ovaries
 Divided into:
1. Follicular cysts → most
common functional cyst 2. Corpus
luteum cysts
Follicular Cysts
 MC functional cyst
 Results from unruptured
follicles during the follicular phase
of the cycle.  Usually unilateral
and resolve spontaneously in 6090 days
Estrogens dominate the follicular
phase of menstruation
Corpus luteum cysts
 Functional cysts that occur
during the luteal phase of the
menstrual cycle.  Corpus luteum
fails to regress after 14 days and
becomes either:
 Enlarged ˃ 3 cm
 Hemorrhagic (corpus
Theca Lutein Cysts
 Large bilateral cysts filled with
clear, straw-colored fluid.
 Result from stimulation by
 Cause a tender
palpable ovarian mass
5. Culdocentesis
 Lead to ovarian
Differential Diagnosis:
1. Ectopic pregnancy 2. PID
3. Torsed ovary
4. Endometriosis
Corpus luteum cysts A
delay in menstruation
and dull lower quadrant
pain.  A ruptured
corpus luteum cyst can
present with:
5. Appendicitis
6. UTI
7. Tubo-ovarian abscess 8.
Renal stone
9. Fibroids
10. Ovarian neoplasms
1. Observation for 8-12 weeks
2. Oral Contraceptives Pills: to
suppress future cyst
formation 3. Repeat pelvic
Corpus luteum cysts
 Signs of
hemoperitoneum late in
the luteal phase.
 Pain meds
 Cysts usually resolve
 May be suppressed with
oral contraceptives if
recurrent  Cysts that do not
resolve spontaneously in 60
to 90 days
Physical Exam:
Bimanual exam
Require further evaluation
and treatment
 Acute pain
 Follicular cysts usually
< 8 cm, simple or
unilocular in structure 
Lutein cysts:
 Usually larger than
follicular cysts
 Feel firmer or more
solid on palpation.  A
ruptured cyst can
 Pain on palpation
 Acute abdominal pain
 Rebound tenderness.
abnormally ↑ ß-human chorionic
gonadotropin  eG: From a
1. Molar pregnancy
2. Choriocarcinoma
3. Ovulation induction therapy
 Arise from the growth of ectopic
endometrial tissue within the: 
 Adnexa
 Cul-de-sac.
 Also called “chocolate cysts”
from the thick brown old blood
contained in them.  Findings:
symptoms of endometriosis such
 Pelvic pain
 Dysmenorrhea  Dyspareunia
 Infertility
 Torsed adnexa, the
classic presentation is: 
Nausea and vomiting
 Waxing and waning
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