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LALALA-LALA

DYSMENORRHEA

Defined as a severe, painful, cramping sensation in


the lower abdomen often accompanied by other
biologic symptoms such as sweating, tachycardia,
headaches,
nausea,
vomiting,
diarrhea,
tremulousness, all occurring just before the menses

Positive correlation seen between severity of


dysmenorrhea & duration, amount of menstrual flow &
early menarche

2.

Primary
Dysmenorrhea
< 20 y/o
Few months after
menarche

Oral contraceptives (OC)


May relieve symptoms of primary dysmenorrhea
Suppress ovulation & endometrial proliferation +
progestin component blocks production of
precursors to prostaglandins
Low dose OCs (ex. ethinyl estradiol)
Side effect: breakthrough bleeding

3.

Levonorgestrel releasing intrauterine system (LNG


IUS)
Results to an atrophic endometrial lining
Reduces menstrual pain

4.

Nifedipine
Blocks uterine contractility
Rarely used

5.

Transcutaneous electrical nerve stimulation (TENS)


May relieve dysmenorrhea but not as effective as
analgesics
Relieves pain w/o decreasing intrauterine
pressure

Onset

Pathogenesis

Diagnosis

Pain before/during
menses

Secondary
Dysmenorrhea
> 20 y/o
Years
after
menarche or after
years of painless
menses
Throughout whole
menstrual period

Elevated PGF2 =
uterine
hypercontractility,
severe cramping

Pain is secondary
to a pathologic
process of certain
conditions:

Contractions
=
decrease in uterine
blood
flow
=
ischemia
&
sensitization
of
pain fibers
History & PE

Cervical stenosis
Endometriosis
Pelvic
inflammation
Pelvic congestion
syndrome
Consider in px who
do not respond to
NSAIDs or OC

Midline,
crampy
lower
abdominal
pain
Pain may involve
back & thighs

Pelvic exam
Treatment

Resolves after 12
72 hrs
Normal; (-) pelvic
pathology
NSAIDs
(mefenamic acid*
>
ibuprofen,
naproxen, etc)

(+)
pathology

pelvic

COX 2 inhibitors
(coxibs) not used
widely bcos of
cardio
adverse
events
Oral
contraceptives
*mefenamic acid more effective than ibuprofen, indomethacin,
naproxen
Notes on Treatment Modalities for Primary Dysmenorrhea
1. NSAIDS
Standard therapy for primary dysmenorrhea
Give 1 day prior to expected menses or at onset
of menses
Do not give to px with hx of NSAID
hypersensitivity

C/I: nasal polyps, angioedema, bronchospasm,


chronic ulceration/inflammation of upper/lower
GIT, pre-existing renal disease

Conditions Associated with Secondary Amenorrhea


1. Cervical stenosis
Severe narrowing of the cervical canal (at level of
internal os) = impedance of menstrual flow =
increase intrauterine pressure
May also cause endometriosis if severe
Etiology: congenital or acquired (cervical injury
electrocautery, cryocautery, operative trauma)
Hx & PE: scant menstrual flow + severe
cramping; hematometra or pyometra may occur
Dx: inability to pass a thin probe of mm diameter
through internal os OR by a hysterosalpingogram
Tx: D&C, laminaria tents, pregnancy & vaginal
delivery (more lasting cure)
2.

Endometriosis
Hx: pain becoming more severe during menses;
may have dyspareunia and infertility
High levels of prostaglandins found in
endometriosis may increase pain
More on this later

3.

Pelvic inflammation
Pelvic infections (gonorrhea, Chlamydia, etc) ->
inflammation, abscess -> healing -> adhesions &
tubal damage = pelvic pain
Pelvic inflammatory disease

4.

Pelvic congestion syndrome


Results from the engorgement of pelvic
vasculature
May be due to past pregnancy or past
inflammatory pelvic pathology
Burning/throbbing pain, worse at night, worse
after standing
May reveal vasocongestion of vagina & cervix
with uterine enlargement & tenderness
Dx: observation + laparoscopy

LALALA-LALA
ENDOMETRIOSIS

Presence of endometrial glands & stroma in abnormal


sites (ectopic sites: outside the uterus)
o Most common site: ovaries

Other
common
sites:
pelvic
peritoneum over uterus, anterior &
posterior cul-de-sac, uterosacral,
round, broad ligaments, cervix,
vagina, fallopian tubes

Rare sites: umbilicus, episiotomy


scar, bladder, kidney, lungs, arms,
legs, nasal mucosa, spinal column
o Growth of these glands & tissues are
estrogen = dependent

Significance? This means that


endometriosis will only occur in
patients who are already ovulating
or are in their reproductive years

Postmenopausal endometriosis is
due to exogenous estrogen
o May be deep or superficial lesions

Deep: penetrations of >5mm =


more progressive disease
o Evolution of lesions:

New lesions: bleblike, <1cm, raised

Red blood filled lesions: most active


phase of disease

Chocolate
cysts:
areas
of
endometriosis after some time
become a light/dark brown color

Older lesions: white & retracted


from surrounding tissue
o Progression from RED to
WHITE lesions: correlate
with age

Benign disease but may act as malignant: locally


infiltrative, invasive, widely disseminating

Typical patient w/ endometriosis: mid 30s,


nulliparous, involuntarily infertile, w/ symptoms of
secondary dysmenorrhea & pelvic pain

Classic symptom of endometriosis: CYCLIC


PELVIC PAIN & INFERTILITY
o However, some px may not present
classically

3 cardinal histologic features of endometriosis:


o Ectopic endometrial glands
o Ectopic endometrial stroma
o Hemorrhage into adjacent tissue

Adenomyosis
o Growth of endometrial glands & stroma into
the myometrium, at least 2.5mm from
basalis layer of endometrium
o Aka internal endometriosis

THEORIES ON ENDOMETRIOSIS
1. Retrograde Menstruaton (Sampson)
Most popular theory
Endometriosis was due to implantation of
endometrial cells shed during menstruation
Summary: During menstruation, there is tubular
regurgitation of menstruation. Upon reaching site
of predilection, there will be proliferation of
endometrial tissue.
o Upon reaching peritoneal cavity, the
endometrial cells adhere to the surface

producing an inflammatory reaction (in


response to foreign bodies)
o Inflammation + cell growth + secretion of
prostaglandin = fibrosis, scarring (w/c
may lead to adhesions), PAIN
Most common site: posterior region, between
the uterus & rectum (cul de sac)

Why here? Because majority of


endometrial
implants
are
in
dependent portions of pelvis

2.

Coelomic Metaplasia
Endometriosis arises from metaplasia of
coelomic epithelium or proliferation of embryonic
rests
Theory suggests that coelomic epithelium retains
its ability for multipotential development
o Metaplasia occurs after induction
phenomenon
has
stimulated
multipotential cell
Explains endometriosis in prepubertal girls,
women w/ congenital absence of uterus, men
(very rarely)

3.

Lymphatic & Vascular Metastasis


Endometrium
transplanted
via
lymphatic
channels & the vascular system: explains remote
sites of endometriosis (ex. spinal column, nose)
Endometriosis far from the reproductive tract
During menstrual period, blood vessels &
lymphatics are open
o Sloughed off endometrial cells may
enter vascular & lymphatic systems

4.

Iatrogenic Dissemination
Aka direct implantation theory
Implantation of endometrial glands & stroma in
certain areas
o Pain on episiotomy scar

May be due to failure to wash


hands or follow antiseptic
methods
o Endometriosis of anterior abdominal
wall after CS delivery

Presence of a wound where


baby, lochia, and endometrial
tissue will pass through and
may be implanted on the
wound site

5.

Immunologic Changes
Explains why some women with retrograde
menstruation do not develop endometriosis while
some do
o Due to altered function of immune
related cells w/c are associated with
endometriosis:

Larger peritoneal macrophages

Decreased cytotoxicity of NK
cells

(+) Endo 1 in endometriosis


epithelial cells

Increased IL-6, IL-8, PDGF,


VEGF

Increased estrogen though


aromatase activity

LALALA-LALA
6.

Genetics
(+) family hx of endometriosis in first degree
relatives = high likelihood of getting disease
earlier in life & having more advance disease

DIAGNOSIS
Symptoms
Cyclic pelvic pain (due to
swelling & extravasation of blood
into surrounding tissue)

a.

Dyspareunia
(endometriosis
in
cul-de-sac)
b. Secondary
dysmenorrhea (most
common symptom)
Infertility (pathologic tubooverian pathway: adhesions
block passageway)
1/3: asymptomatic
Abnormal
bleeding
(premenstrual spotting and
menorrhagia)
Ovulatory
dysfunction
(anovulation
or
luteal
dysfunction)
GIT
symptoms
(diarrhea/feeling of defecation
at time of menses)
Massive ascites (rare, but
impt because it mimics
ovarian CA)

Signs
Classic
finding:
fixed
retroverted (fixed posteriorly)
uterus
w/
scarring
&
tenderness posterior to uterus

TREATMENT
2 short term goals in treatment of endometriosis:
1. Relieve pain
2. Promote fertility
Long term goal: Prevent progression or recurrence of disease
process
Medical Therapy

Suppress lesions & associated symptoms (ex. pain)

Menstrual suppression w/o causing hypoestrogenism

Medical therapy may suppress symptoms & prevent


progression BUT it does NOT provide long lasting
cure
1.

Danazol
Ind: benign cystic mastitis, menorrhagia,
hereditary angioneurotic edema
Attenuated androgen that is active when given
orally
Effect: hypoestrogenic, hyperandrogenic (on
steroid sensitive organs); pseudomenopause
Given at start of menses (duration: 6 9 mos)

2.

GnRH Agonists
Ex. leuprolide acetate (IM), nafarelin acetate
(nasal spray), goserelin acetate (SC implant)
Produce extremely low levels of estrogen +
amenorrhea
o Chronic use -> medical oophorectomy

Dramatic decrease in estrone,


testosterone,
and
androstenedione
in
levels
similar to oophorectomized
women
pseudomenopause
No androgenic side effects but with menopausal
symptoms (hot flushes, vaginal dryness,
insomnia)
If given in follicular phase of menstrual cycle,
amenorrhea is induced w/in 6 8 wks
If given in luteal phase, amenorrhea is induced in
4 5 wks
Better px compliance than in Danazol due to less
side effects
May arrest growth of endometriosis
o Greatest
therapeutic
effect
in
endometriosis <1cm in diameter

3.

Oral Contraceptives
Low estrogen with high progestin potency
Continuous daily oral contraceptives for 6 12
months
Potential risk: risk of rupture if a large
endometrioma is present (may lead to surgical
abdomen)
Produces amenorrhea & pseudopregnancy

4.

NSAIDs
For pain relief & improves bleeding control

5.

Progestogens (medroxyprogesterone acetate)


Give only if unable to tolerate high dose estrogen
in OC or estrogen therapy
Produces prolonged amenorrhea
Best for woman who has completed childbearing

Enlarged & tender ovaries

Beaded/Nodular uterosacral
ligaments
Lateral deviation of cervix
(mod severe endometriosis)
Time of maximum swelling in
areas of endometriosis: 1st or
2nd day of menstrual cycle

Diagnostic Tests:
1. Laparoscopy
Allows direct visualization of endometriosis,
scarring & adhesions
Gold standard?
2. Ultrasound
No specific pattern for endometriosis
Helps differentiate solid from cystic lesions
(endometrioma vs adnexal abnormalities)
3. MRI
Best diagnostic tool for endometriosis but not
always practical
Hyperintensity (T1W); hypointensity (T2W)
Course of Disease
Serial pelvic exams: poor indicator of disease
progression
CA 125: marker for endometriosis
o Increases in response to advancing
stages
o Not specific; also increases in
leiomyoma and other pelvic conditions
Endometriosis does not necessarily improve with
pregnancy
Risk for ovarian cancer may increase
With natural menopause, symptoms disappear
since endometriosis is highly dependent on
ovarian hormones.

LALALA-LALA
Surgical Therapy
For moderate to severe endometriosis, w/
adhesions, or involvement of nonreproductive
organs
Conservative Surgeries:
o Laparoscopy
o Oophorectomy/Right
salphingooophorectomy
o Oophorecystectomy
o Adhesiolysis
-

Definitive Surgeries:
o TAH
o Bilateral salpingo-oophorectomy
o Removal of all visible endometriosis

1.

Laparoscopy
Diagnostic & therapeutic
Advantage: Px may be treated at time of
diagnosis
Endometriosis may be coagulated, vaporized,
resected
Can also be used for tx of ovarian
endometriomas
Preferred over laparotomy due to shorter
recovery period & reduction in extent of
subsequent adhesions

2.

Total Abdominal Hysterectomy with preservation of 1


or more ovaries
Form of definitive surgery (given to px w/
continuous pain despite medical & conservative
surgery)
For women who have completed childbearing
(late 20s or 30s)
Usually for far advanced disease

Sources:
th
Comprehensive Gyne (Katz, et al) 6 ed
Dra. Dee notes
Dr. Castros notes
JM :D