patho sheet 4th of Dr faisal - Mohammad H. Bustani

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patho sheet 4th of Dr faisal - Mohammad H. Bustani

Post by Shadi Jarrar on 24/4/2011, 1:29 pm

بسم الله الرحمن الرحيم

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Lecture # 17 ((20.03.2011))
بسم الله الرحمن الرحيم
UTERUS
Last lecture we talked about cervix, today we are going to talk about the uterus. The first few minutes of the lecture wasn’t recorded unfortunately, so am going to mention the introduction from the book.
The uterine corpus with its lining endometrium is the principal seat of female reproductive tract disease. Many disorders of this organ are common, often chronic and recurrent, and sometimes disastrous. Only the more frequent and significant ones are considered here.
ENDOMETRITIS
Inflammation of the endometrium is seen as part of the wider spectrum of pelvic inflammatory disease, a condition with consequences on the integrity of the fallopian tubes and subsequent fertility.
Endometritis may be associated with retained products of conception subsequent to miscarriage or delivery, or a foreign body such as an intrauterine device
All of the following pieces of information are from the recording.
Just for your knowledge: Usually there is (1) moderate or severe degree of acute inflammatory infiltrate, neutrophilic infiltrate in the stroma. (2) Sometimes there are micro-abscesses (a collection of neutrophils in the stroma which causes micro-abscesses) and within the endometrial glands there is micro-abscesses and (3) destruction of the glandular epithelium, any of these might go into acute endometritis, but few neutrophilic infiltrate within the stroma are not enough to cause endometritis.
Retained products of conception (RPOC): RPOC -remnants of the placenta after pregnancy- should be evacuated or else it will cause acute then chronic endometritis.
CHRONIC ENDOMETRITIS
Pelvic inflammatory disease (PID): might be associated with a range of events in the tube and ovary and if it remains untreated it will cause chronic endometritis.
Postpartum
Intrauterine contraceptive devices (IUD): mainly it causes low-grade chronic endometritis.
TB in the endometrium: (1) it's not common, and it is usually secondary to TB salpingitis (TB in the fallopian tube –primary for the FGT- then it goes to endometrium –secondary-) and TB salpingitis in general is secondary to TB elsewhere (mainly secondary to pulmonary TB, renal TB or intestinal TB). (2) There is no well-formed granuloma because the endometrium is shed every month in menstruation. So there is no chronic granuloma, where we can find centric caseation necrosis bounded by langhans' giant cells (multi-nucleated) attended by lymphocytes and plasma cells. And there is discomfort, pain and vaginal bleeding.

ENDOMETRIOSIS
It is the presence of endometrial glands, stroma or both (and might be associated with hemorrhage) elsewhere other than the luminal aspect of the uterus -its proper place-.
Endometriosis is found mainly in females in their mid 20's and 30's.
There are many sites of endometriosis: uterine ligaments, fallopian tube, and appendix … but mainly in ovaries (70- 80 %).
There are a lot of theories to explain endometriosis;

1. The regurgitation/implantation theory
The blood is normally supposed to go down but instead it retrogrades back to the fallopian tubes and goes out of the pelvis into the peritoneal cavity.
2. The metaplastic theory
Metaplasia means changing from one type of tissue to another.
Endometrium could arise from any other tissue by metaplastic means.
3. The vascular or lymphatic dissemination theory
Dissemination through pelvic veins and lymphatics would explain the presence of endometriotic lesions in any part of the body but mainly in places near the uterus. And it is the most acceptable theory.
Endometriosis is most probably hormone responsive, it responds to estrogen and progesterone, which means that it might go into menstruation – menses in the place of endometriosis – and blood outside the CVS is considered as a foreign body and it will cause (1) dysmenorrhea (pain during menstruation) and (2) infertility and adhesions when it is in the ovaries. And this blood may be encysted and is called chocolate cyst. So, chocolate cyst is an endometriosis in the ovaries which became encysted.

ADENOMYOSIS
Is almost the same as endometriosis, but adenomyosis is within the body of the uterus.
Myometrium itself can be studied with endometrial foci (in the myometrium, you can find foci of endometrium). If it is more than 2 mm dipping within the myometrium, it is considered adenomyosis.
Usually all of the symptoms of endometriosis are applied on adenomyosis BUT Adenomyosis is not responsive to hormonal effect.
((There is 2 layers of endometrium: functionalis (superficial) & basalis (deep). The basalis layer is not responsive to ovarian hormones. The functionalis layer is shed every month and the basalis layer replaces the functionalis layer.))
To diagnose adenomyosis or endometriosis any of these combinations should be observed: Stroma and bleeding, endometrial glands and bleeding or endometrial glands and stroma.

ENDOMETRIAL POLYPS
They are named according to their appearance and the age. ((Premenopausal, postmenopausal, functional, hyper-plastic & atrophic – after menopause-))... New schools prefer not to categorize them because there is a huge overlap between each type and the other.

(1) Don’t categorize.
(2) Any polyp of the endometrium associated with bleeding or not associated with bleeding should be sampled.
(3) Malignancy in the endometrial polyp is very rare.

After menopause, any endometrial polyps should be sampled. Because some of these polyps undergo trauma (some has a long pedicle, extends out of the cervical canal and may undergo trauma) and might undergo ulceration, infection or bleeding. So bleeding after menopause might be caused by cancer and therefore the polyp should be sampled.
Malignancy rate is usually < 1% and reach maximum of 5 %. But one kind of endometrium carcinoma is polypoid so it should be sampled not to confuse between benign polyps and polypoid endometrium carcinoma.

Tamoxifen: a therapeutic agent that is usually used for the cancer of the breast. Act as estrogen antagonist in breast and as agonist in FGT. So, most of tissues and disorders (such as polyps, endometrial hyperplasia, endometrial sarcoma, endometrial carcinoma …) of FGT which depend on estrogen might be affected by Tamoxifen.


ENDOMETRIAL HYPERPLASIA
Generally, it is an increase in the number or the mass of the glands in relation to the stroma, gland stromal ratio is increased associated with no other changes. Endometrial hyperplasia mainly depends on estrogen. Hyperestrinism (increase in estrogen, its effect or tissue response to estrogen) causes endometrial hyperplasia.
Estrogen might be endogenous or exogenous;
1- Endogenous; because of anovulatory cycle - ovaries do not release an oocyte, and estrogen remains in the second half of the cycle without being opposed by progesterone-, anovulatory cycle is one of the most causes of hyperestrinism. Polycyctic ovary (PCO) -or Stein-Leventhal syndrome- was described by 2 Jewish scientists (Stein and Leventhal) in 1930's, usually found in both ovaries and has increased tendency in obese people. PCO is usually associated with lack of menstruation or dribbling of menstruation and with some hormonal changes that cause verilization, hirsutism and menstrual abnormalities.PCO is not malignant but it is estrogen dependent. An ovarian tumor called granulosa cell tumor which secretes estrogen – this tumor is usually malignant if not treated-
2- Exogenous; HRT (hormone replacement therapy to treat hot flashes and osteoporosis in postmenopausal women).
Peak of incidence of endometrial hyperplasia is at the two extremities of active reproductive age, after puberty and before menopause. Increased incidence in obese.
((POC morphology: Ovaries usually are full of fibrous tissue especially at the cortex of the ovary so any ovum to be extruded won't make it because of the fibrous tissue. POC treatment: was by wedge resection of the ovary and now it is treated medically))


Classifications of endometrial hyperplasia:
By WHO ((Simple with no atypia, Simple with atypia, Complex with no atypia and Complex with atypia)) but we are not concerned about it.
By FIGO, the simplest:
(1) Simple endometrial hyperplasia or cystic
Endometrial glands goes cystic dilatation with no atypia, regress with treatment. Simple type has no malignant potential. ((In England, it was called Swiss cheese endometrial glands))
(2) Complex endometrial hyperplasia
Increased irregularities of the glands (folded, intra-luminal tufting, out pouching …), might be associated with little atypia. Complex type has very low malignant potential.
(3) Atypical endometrial hyperplasia
Or called complex with atypia, glands, cells, nucleus and mitosis are atypical (high N:C ratio, hyper-chromatic …). Atypical type has a high malignant potential (20 – 30 %).
Atypical endometrial hyperplasia might be confused with endometrial adenocarcinoma due to the huge overlap. So all atypical should be treated and you have to know the underlying source of estrogen to treat it.

ENDOMETRIAL CARCINOMA
There are two forms of endometrial carcinoma and the majority is dependent on estrogen is called endometrioid or adenocarcinoma of the endometrium, it is usually premenopausal. Preceded by hyperplasia and usually associated with nulliparity (haven't given birth to a child).
The other form is more aggressive and it’s not because of hyperestrinism (estrogen independent) called serous or papillary serous, usually in older age than endometrioids.
>> GENERALLY, Endometrial carcinoma is mainly caused by hyperestrinism. And it is mainly adenocarcinoma.
In some books you can find obesity, diabetes mellitus and hypertension as causes of endometrial carcinoma but these are minor causes.

STAGING OF ENDOMETRIAL CARCINOMA
Stage 1: confined within the uterus
Stage 2: reaching cervix
Stage 3: extending out of the cervix into the pelvis
Stage 4: extending out of the pelvis
>> Stages might correlate with the prognosis, treatment and management.
Stage 1: 90 % five years survival, while stage 4: < 20% five years survival.




CORRECTIONS ARE WELCOMED

Written by: Mohammad H. Bustani
Patho. Lect. #17 on 20.03.2011
4th lecture for Dr. Faisal Kamal
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Shadi Jarrar
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تاريخ التسجيل : 2009-08-28
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