Gyn, endometriosis ppt for reference purpose ....

1. Endometriosis

2. Definition Pathophysiology Molecular mechanism Classification Symptoms Diagnostics Treatment
Definition
Pathophysiology
Molecular mechanism
Classification
Symptoms
Diagnostics
Treatment

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Endometriosis is a common benign disorder defined
as the presence of endometrial glands and stroma
outside the normal location. Implants of
endometriosis are most often found on the pelvic
peritoneum, but other frequent sites include the
ovaries and uterosacral ligaments. Endometrial
tissue located within the myometrium is termed
adenomyosis, in case of ovarian location, ovarian
endometrial cysts – endometriomas are developed.

4. Definition Pathophysiology Molecular mechanism Classification Symptoms Diagnostics Treatment
 The definitive cause of endometriosis remains unknown,
but theories have been proposed;
 A more favored one describes retrograde menstruation
through the fallopian tubes;
 The stem cell theory, implicates undiferentiated
endometrial cells that initially reside in the
endometrium’s basalis layer. These cells diferentiate
into epithelial, stromal, and vascular cells as the
endometrium is routinely regenerated each cycle.

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 Aberrant lymphatic or vascular spread of endometrial tissue
 Coelomic metaplasia and suggests that the parietal peritoneum is
pluripotent and can undergo metaplastic transformation to tissue
histologically identical to normal endometrium.
 Because the ovary and the progenitor of the endometrium, the
müllerian ducts, are both derived from coelomic epithelium, such
metaplasia may help explain endometriosis involving the ovary.
 This process may also underlie cases of endometriosis in those
without menstruation, such as premenarchal girls and males
treated with estrogen and orchiectomy or prostate cancer.

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Endometriosis may develop anywhere within the pelvis and on other extrapelvic
peritoneal surfaces. Most commonly, endometriosis is found in the dependent areas of
the pelvis. As such, the anterior and posterior cul-de-sacs, other pelvic peritoneum, the
ovary, and uterosacral ligaments are frequently involved.
Additionally, the rectovaginal septum, ureter, and bladder and rarely, pericardium,
surgical scars, and pleura may be afected. Implants may be superficial or they may be
deep infiltrating endometriosis (DIE), that is, infiltrative forms that involve vital
structures such as bowel, bladder, and ureters.

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Other specific sites
Rectosigmoid lesions
Urinary tract lesions
Thoracic lesions (catamenial)

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Endometriosis is an estrogen-dependent, chronic
inflammatory disease with aberrant growth of ectopic
endometrial tissue. In this discussion, eutopic endometrium is
that which lines the uterine cavity, whereas ectopic
endometrium describes that outside the cavity.

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The molecular mechanism of endometriosis
include:
Estrogen and progesterone;
Inflammation;
Immune system;
Genetics.

10. Definition Pathophysiology Molecular mechanism Classification Symptoms Diagnostics Treatment
Estrogen plays a causative role in endometriosis
formation and is derived from multiple sources. First,
most estrogen in women is produced directly by the
ovaries. Second, peripheral tissues also produce
estrogens through conversion of ovarian and adrenal
androgens by the enzyme aromatase. Endometriotic
implants express aromatase and 17β-hydroxysteroid
dehydrogenase type 1, which are the enzymes
responsible or conversion of androstenedione to
estrone and of estrone to estradiol, respectively.

11. Definition Pathophysiology Molecular mechanism Classification Symptoms Diagnostics Treatment
In addition to an estrogenic environment, normal
progesterone effects are attenuated in
endometriosis. This progesterone resistance is
thought to stem from an overall low concentration of
progesterone receptors within implants.
Specifcally, pathological overexpression of estrogen
receptor β in endometriosis suppresses estrogen
receptor α expression.
This diminishes estradiol-mediated induction of the
progesterone receptor in endometriotic cells

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Namely, normal endometrium does not express
aromatase and has elevated levels of 17β-
hydroxysteroid dehydrogenase type 2 in
response to progesterone. As a result,
progesterone antagonizes the estrogen efects in
normal endometrium during the luteal phase.
Endometriosis, however, manifests a relative
progesterone-resistant state, which prevents this
antagonism in its implants.

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Progesterone resistance may also enhance
implantation of refluxed endometrium. Invasion
of the mesothelium can be aided by matrix
metalloproteinases (MMPs).
Progesterone represses MMP activity. Thus, in
affected patients, progesterone resistance within
these implants may augment the MMP
activity necessary or implant invasion.

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Inflammation
Prostaglandin E2 (PGE2) is the most potent inducer
of aromatase activity in endometrial stromal cells.
Estradiol produced in response to the increased
aromatase activity subsequently augments PGE2
production by stimulating the cyclooxygenase type 2
(COX-2) enzyme in uterine endothelial cells.

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Immune System
Macrophages;
NK cells;
T lymphocytes;
Endometrial antibodies IgG, IgA;
Cytokines.

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Genetic factors
The increased incidence in first-degree relatives suggests a
polygenic/multifactorial pattern. For example, in population studies, 4 to 8
percent of the female siblings or mothers of affected women had
endometriosis.
In one research it was revealed that women with endometriosis and an
affected first-degree relative were more likely to have severe endometriosis
(61 percent) than women without an affected first-degree relative (24 percent).
Studies also demonstrate concordance for endometriosis in monozygotic twin
pairs.

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• The primary method of endometriosis diagnosis is visualization of endometriotic
lesions by laparoscopy, with or without biopsy for histologic confirmation.
• One classification by the American Society for Reproductive Medicine (1997)
allows disease to be quantified.
• With this, endometriosis on the peritoneum, ovaries,
fallopian tubes, and cul-de-sac is scored at surgery. At
these sites, points are assigned for disease surface
area, degree of invasion, morphology, and extent of
associated adhesions. Also, endometriotic lesions are
morphologically categorized as white, red, or black. In
this system, endometriosis is classified as stage I
(minimal), stage II (mild), stage III (moderate), and
stage IV (severe).

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Physical examination
Laboratory testing
Diagnostic imaging
Diagnostic laparoscopy

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Combination of medical-surgery-medical
Surgery
Depends on:
• woman’s specific complaints;
• symptom severity;
• location of endometriotic lesions;
• goals for treatment;
• desire to conserve future fertility.

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Medical treatment
Expectant management
NSAID
COCs
Progestins (progestine pills, DMPA, NETA,
levonorgestrel containing IUD)
GnRH agonists (Leuprolide acetate, Gozerelin)
GnRH antagonists (cetrorelix)
Selective progesterone receptor modulators (SPRM) and progesterone receptor modulator-associated
endometrial changes (PAEC)
Androgens

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Surgery
• Lesion Removal and Adhesiolysis;
• Endometrioma Resection;
• Presacral Neurectomy;
• Laparoscopic Uterosacral Nerve Ablation;
• Hysterectomy;
• Oophorectomy.