Endometrial Cancer and Hyperplasia for USMLE
Endometrial Hyperplasia there is proliferation of the endometrium which becomes very thick. Primarily the hormonal trigger for endometrial proliferation is estrogen. The hormone that blocks the effects of estrogen on endometrium is progesterone.
ETIOLOGY
Obesity can cause this because there is increased aromatase which converts more testoserone to estrogen. Polycystic Ovarian Syndrome (PCOS) which has a high estrogen and testosterone and there is no ovulation and therefore there is no corpus luteum and therefore no progesterone. Tumors that release estrogen releasing. Hormone replacement therapy in post menopausal women.
Two types of hyperplasia, simple and complex. Normally there is small amounts of gland and lots of stromal tissue. In simple there are more glands, but not touching each other. In complex the glands are touching each other. In Atypia there are abnormal nucleus which is really large and it is a very bad sign. Complex atypia has a 30% chance of become endometrial cancer.
Sign and symptoms is abnormal heavy bleeding due to lack of ovulation. Diagnosis is done initially by doing a transvaginal ultrasound looking for endometrial thickness. If less than 5mm than 95% can rule out endometrial hyperplasia. Biopsy is done with a pipelle, however it can miss areas of cancer because small sample. Dilation and curretage and hysteroscopy. Treatment depends on the pathology report. If there is no atypia you can give mirena and MPA which causes enodmetrium to go back to normal. Atypia requires hysterectomy. Type 1 endometrial cancer is endometroid adenocarcinoma.
Endometrial Carcinoma
Most common gyne cancer in women, especially in post menopausal. Type 1: Endometroid Adenocarinoma, due to estrogen secondary to endometrial hyperplasia. Type 2 is clear cell, serous carcinoma and there is no precursor, no precursor, more agressive and occurs much later (70s and 80s). Risk Factors related to unopposed estrogen. Risk factors are Cancers (Breast, Ovarian, Colon Cancer). Obesity, Late Menopause, Diabestes Mellitus, HTN, Nulliparity, Unopposed Estrogen due anovulation, Hormone replacement and tamoxifen. However, COC is protective.
Signs and Symptoms in type 1 is postmenopausal bleeding. In type 2 there is bloating, bowel dysfunction, pelvic pressure. Staging is done by direct extension myometrium, serosa, bladder and large bowel. Or down cervix and vagina and finally fallopian tube. Lympahtic spread can go to pelvic para-aortic lymph nodes. Fallopian tube and into peritoneum. Hematogenous spread is liver and lungs. Stage 1 is when only in uterus. Stage 2 goes into cervix Stage 3 is when it goes into adjacent strucutres. Stage 4 is beyond pelvic cavity.
Investigations are Transvaginal Ultrasound, Biopsy with pipelle, Dilation and curretage, and hysteroscopy. Treatment depends on staging, surgery of hysterectomy with bilateral salpingo-oopherectomy (BSO), pelvic wash and lymph nodes. Omentectomy and this can be done laparoscopy. If there is metastasis then also do chemotherapy and if it recurs than perform radiation therapy
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