Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
21 Cards in this Set
- Front
- Back
|
Definition of endometriosis |
Endometriosis is the occurrence of functional endometrial glands and stroma outside the uterine cavity and myometrium. It was previously referred to as endometriosis externa. |
|
|
Definition of adenomyosis |
Adenomyosis is defined as the presence of endometrial tissue within the myometrium. It was previously referred to as endometriosis interna but presently it is regarded as a seperate entity . |
|
|
Sites/location of endometriosis |
The commonest sites are Ovaries, POD and utero- sacral ligaments. Virtually every system is involved•Rep. system: uterine serosa, broad ligament, fallopian tubes, utero vesical fold and rectovaginal septum•GIT: Sigmoid colon, caecum, appendix, liver, S.I. GIT is the commonest site outside the reproductive system. •Urinary system: Bladder, ureters •Skin: umbilicus, perineum, surgical scars e.g. episiotomy site•Resp. system: lungs •CNS: Brain •MSK: thighs, buttocks. |
|
|
Epidemiology of endometriosis |
•Reproductive age. •Commonest b/w ages 30 and 45 yrs •Mostly regresses after menopause but can be maintained by HRT in menopausal women. •Exact prevalence rate is difficult to get b/c definitive diagnosis can only be made via surgical procedures like laparoscopy and laparotomy thus it varies from place to place, h/v a prevalence of 10% has been estimated. It increases in areas where the practice of laparoscopy is higher. •NB: Endometriosis has been reported in males. |
|
|
Risk factors for endometriosis |
Risk factors include – increase exposure to menstruation, caffeine and alcohol intake, family hx of endometriosis |
|
|
Etiology of endometriosis |
No single theory can explain the occurrence in various sites however there are 3 main etiological theories1. Coelomic metaplasia: Mullerian duct, peritoneum, pleura and ovarian surface epithelium all developed from the primitive coelomic epithelium. This shows that coelomic cells can differentiate into endometrial tissue in response to appropriate stimuli. This explains the presence of endometriosis in the pelvis, at distant sites, in males and in women without uterus. 2. Implantation theory: Retrograde menstruation, iatrogenic dissemination as in surgeries, Lymphatic and haematogenous spread. Retrograde menstruation explains why it is commoner in people with increase menstrual exposure or in people with mullerian duct outlet obstruction e.g. impeforate hymen. Also lesions occur in more dependent areas eg. POD. 3. Induction theory: Combination of the 1st two theories. Release of a certain factor by implanted endometrial tissue induces the undifferentiated mesenchyme in that area to form endometriotic tissue. |
|
|
Pathology of endometriosis |
•Histology of the lesion may show the following:--Endometrial glands, endometrial stroma and hemosiderin pigments. -Diagnosis is made if 2 out of the above 3 are present. •Early lesions in the peritoneum may appear macroscopically as reddish- blue, dimpled or raised lesion.•You can also have the classical powder burns lesion which later depigments into white plaques. This leads to chronic inflammation leading to adhesion formation •Ovarian lesion forms a chocolate cyst from repeated cyclical bleeding. This can also lead to adhesion to the peritoneum and tubes leading to kinking of the tubes. |
|
|
Symptoms of endometriosis |
•Pain: Dysmenorrhoea, dyspareunia,dysuria,dyschesia, chronic back-aches, low abdominal/pelvic pain. •Acute abdomen from rupture of an endometriotic cyst. •Infertility: Impairment of tubal function and coital problems due to dyspareunia •Menstrual abnormalities: dysmenorrhoea,(Menorrhagia?). •Unusual symptoms like cyclical rectal pain and bleeding, cyclical dysuria and heamaturia, cyclical haemoptysis, pleuritic chest pain and haemothorax, cyclical pain and bleeding from umbilicus, cyclical headaches and seizures, right hypochondrial cyclical pain and jaundice |
|
|
Signs of endometriosis |
•There may be no physical finding on examination depending on the site. •Cystic lesion in the involved area e.g. surgical scars. •Pelvic exam may reveal tender nodules in the uterosacral ligament and rectovaginal septum, retroverted and fixed uterus, tender adnexal masses. |
|
|
Investigation for endometriosis |
•This is to confirm the suspicion from history and examination. These include •Laparoscopy: Gold standard and may involve taking biopsy for histology.•Pelvic USS for endometriotic ovarian cyst. •MRI: More sensitive than USS and can diagnose endometriosis obscured by adhesions. Used in monitoring response to medical therapy. •Others e.g. infertility work-up depending on the presentation. |
|
|
Differential diagnosis of endometriosis |
Differential Diagnosis: PID, schistosomiasis, bladder cancer, bowel cancer, UTI, PTB, lung cancer, SOL. (NB : cyclicity helps in differentiation) |
|
|
Staging of endometriosis |
Depends on location, depth of invasion & degree of adhesion formation. STAGE I (Minimal) 1----5 STAGE II (Mild) 6----15 STAGE III (Moderate) 16---40 STAGE IV (Severe) >40 |
|
|
Factors considered before institution of treatment for endometriosis |
•age •symptoms •stage •infertility |
|
|
Treatment of endometriosis |
1. Medical 2. Surgical |
|
|
Medical treatment of endometriosis |
MEDICAL:- This attempts to create pseudo-menopause or pseudo-pregnancy. These conditions impair the growth and development of the endometrial tissues. It also suppresses the implants but cannot remove them. Cannot be used if there is associated infertility problem. 1. Synthetic androgens e.g. Danazol and gestrinone. Danazol causes anovulation by inhibiting the mid-cycle LH surge and increases the serum conc. of testosterone. Gestrinone decreases both estrogen and progesterone receptor concentration. Also reduce the mid- cycle gonadotrophin surge. 2. Gossypol:Also reduces FSH/LH Level 3. Progestogens or combined estrogen/ progesterone eg. Medroxy progesterone acetate and C.O.C. 4. Gn RH agonist: Decrease FSH &LH when given continuously e.g. goserelin, buserelin, leuprorelin. These cause menopausal symptoms and thus their use is not prolonged. ‘Add back’ regimen of estrogen/progesterone can minimize side effects and encourage prolonged use. 5. NSAIDS for pain. |
|
|
Surgical treatment of endometriosis |
SURGICAL: can be conservative or radical. 1. Conservative aims at removal of visible deposits and retaining reproductive function. It can be via laparoscopy or via laparotomy. 2. Radical involves TAH, BSO and removal of implants. Done in severe cases or where other Rx have failed or the pt has completed her family. HRT may be given at a risk of the endometriosis reoccurring. 3. Uterosacral nerve ablation and presacral neurectomy for pain relief |
|
|
Adenomyosis: features, risk factors, incidence |
Menorrhagia and dysmenorrhoea. •Risk factors: D&C, C/S and endometrial hyperplasia. May be diffuse or localized. Commoner in multiparous women. •Incidence widely varies from 5-70% |
|
|
Diagnosis of adenomyosis |
Diagnosis by TVS, MRI, Laparoscopy & biopsy for histology. |
|
|
Treatment of adenomyosis |
•Local resection if localized or TAH if diffuse. •Symptomatic Rx is by using Medical Rx to induce amenorrhoea hence stopping menorrhagia & dysmenorrhoea. |
|
|
Differential diagnosis of adenomyosis |
Uterine fibroid |
|
|
Prognosis of endometriosis |
•Recurrence of endometriosis is about 50% within 1yr after medical treatment while after surgery it is about 28% after 18months. •HRT increases the chances of recurrence. •There is also a possibility of malignant transformation hence take biopsy in any recurrent case for histology. |
