Leukemia (Blood Cancer)

 

In this blog, I will be continuing the discussion on uterine pathologies so last time I spoke about polyps, adenomyosis, and fibroids. In this blog, I will be discussing endometrial cancer, and congenital uterine abnormalities so starting off with endometrial cancer first. Endometrial cancer is most commonly adenocarcinoma of columnar epithelial gland cells basically in around 90% of cases and meets with cancer is the most common kinda malignancy and is the 4^th most common malignancy in women. Now the cause of endometrial cancer is most often related to excess estrogen so when you have high levels of unopposed estrogen now I will say unopposed that we mean that we don't have progesterone to counteract the effects of estrogen. Estrogen will result in the proliferation of the endometrium which can result in hyperplasia and malignancy which we're going to discuss. So now we're going to look at those risk factors which cause high levels of unopposed estrogen so we've got obesity because the adipose tissue results in the conversion of androgens to Estrogen so with a lot of adipose tissue we'll you and have a lot of Estrogens, We've also got patients to have many menstrual cycles so of course the more menstrual cycles you have in your lifetime then the more estrogen is being exposed to the endometrium so in cases where you've got early menarche which is the age of the first menses late menopause or nulliparous women. These patients will have many menstrual cycles and therefore are at an increased risk.

Next, we have polycystic ovarian syndrome so basically, over here the ovary is full of cystic follicles which are all secreting an estrogen now most of these follicles don't ovulate so the corpus luteum which secretes progesterone is not formed so excess estrogen is secreted without being balanced out by progesterone. So we've also got Estrogen secreting tumors. Charles granulosa cells tumors of the ovaries estrogen-only HRT is also a risk factor because progesterone is not given as part of the HRT regimen to balance out the estrogen so you have excess unopposed estrogen tamoxifen can also result in excess estrogen so basically, tamoxifen is a breast cancer medication which blocks estrogen receptors in the breast but activates its gene receptors in the uterus, other risk factors include diabetes, hypertension and no physical activity which have also been linked to endometrial cancer, finally, we've got a genetic condition called hereditary nonpolyposis colorectal cancer which is also known as Lynch syndrome which is high risk for developing colon cancer and endometrial cancer.  

                There are also some protective factors for developing endometrial cancer so like I said before many menstrual cycles increase your risk over here few menstrual cycles will act as a protective factor and we can see this in multiparous women and women on the oral contraceptive pill exercise was also found to be protective as well as smoking. So now before moving on with the discussion of endometrial cancer we need to talk a bit about endometrial hyperplasia. Endometrial hyperplasia is basically a premalignant disease that can eventually result in endometrial cancer so essentially this is excessive proliferation of the endometrium and again this is caused usually by excessive unopposed estrogen levels. There are two types of hyperplasia so we've got simple hyperplasia and complex hyperplasia and here we're going to take a look at their histology. Simplified hyperplasia 

has a cystic branching pattern with a normal stroma to gland ratio complex hyperplasia has crowded and closely opposed glands so it has a high gland so Marines show this has a higher risk of progressing into cancer now when we talk about atypical hyperplasia we are saying that there are atypical cells so abnormal cells which have abnormal nuclei it is. These atypical cells increase the risk of progression to malignancy so you can have simple hyperplasia of the atypia or complex hyperplasia with a TPM and both of these carry a greater risk of developing into malignancy.  So that is a short side note on endometrial hyperplasia.

Now, barrows so different types of individual cancer we've got type one which is the most commonly referred to as endometrial carcinoma and this includes around 80% of endometrial cancers it occurs as a result of unopposed estrogen, and in patients with a high BMI it is low-grade and has a relatively good prognosis, on the other hand, type 2 when the material cancer affairs to a serious form of carcinoma this is actually secondary to endometrial atrophy it is high-grade and has a poor prognosis, so now how do endometrial hyperplasia and endometrial cancer typically presents so the classic presentation is of postmenopausal bleeding so this refers to bleeding after one year of not seeing any periods so once menopause has been reached 10% of women presenting at postmenopausal bleeding will, in fact, have endometrial cancer.

These patients can also present with other forms of abnormal uterine bleeding such as intermenstrual bleeding or heavy menstrual bleeding sometimes on the routine smear test CGIN (cervical glandular intraepithelial neoplasia) can be identified which may point towards an endometrial pathology so side note on CGIN and is basically as a logical result obtained from a smear test so in the cervix we have two types of cells we've got squamous cells which line the ectocervix and we've got glandular columnar cells which are present in the endocervix, both of these can be abnormal resulting in CGIN, so when abnormal columnar cells are present this reports an endometrial abnormality since this epithelium is continuous with the endometrium now to diagnose endometrial cancer we first perform a transvaginal ultrasound to take a look at how thick the endometrial lining is so usually an endometrial thickness greater than 4.0mm in a postmenopausal woman is considered to be thick and therefore we need to carry out further investigations which involves taking a sample so an in Demetrius supper can be taken using a propel but the gold standard for the diagnosis of endometrial cancer is by performing a hysteroscopy DNC.

Where we take a look at the lining and take a sample which is then sent to the lab if you have confirmed endometrial cancer then we need to stage the patient appropriately and perform some imaging such as a chest x-ray and MRI so essentially staging refers to how much cancer has spread and we tend to use the Figo staging so in stage 1, the lesion is still confined to the uterus in one you've got less than one-half of the myometrium which is involved and in what be you've got more than one half of the myometrium invaded. In stage 2 the lesion has spread to the cervix but has not gone beyond the uterus. In stage 3 the tumor has now spread beyond the uterus so in entry A the tumor has invaded the serosa or at next say in 3b, the tumor has spread to the vagina and possibly the Paramecium to entry c1 the pelvic nodes are involved and entry c2 the periodic nodes are involved in stage for a tumor has spread to the bladder or bowel and in 4b there is distant metastasis.

So I look at the treatment now so for simple hyperplasia will treat with progestogens this can be an oral progestin or an intrauterine system such as life on our guest intrauterine system called my arena now if the characteristics of individual hyperplasia are pointing towards high risk for malignancy such as atypical hyperplasia then a hysterectomy is performed. Now within mutual cancer, if it is still in the stages one or two a hysterectomy is performed but if the disease is more advanced the patient is given radiotherapy. So that's all you need to know about endometrial cancer now we're going to move on to congenital uterine abnormalities so to understand is contingent uterine anomalies we need to take a look back to embryology so during the third week the embryo will consist of three layers the ectoderm mesoderm and endoderm and between the third and fifth week the mesoderm will differentiate into proximal arm intermediate minute arm and lateral place means a term and over here we are interested in the intermediate mesoderm because this is where the reproductive system arises from the intermediate mesoderm gives rise to the urogenital range.

Now the Eurasian the range is further divided into the Gonadal Ridge which gives rise to the ovaries or testes the nephrogenic cord which gives rise to the kidneys and the paramesonephric/Mullerian duct and the mesonephric or Wolffian ducts so here we can see the gonads, the paramesonephric ducts and the mesonephric ducts the paramesonephric ducts give rise to the fallopian tubes, uterus and upper two-thirds of the vagina while the mesonephric ducts give rise to the ureters, the epididymis vas deferens, and seminal vesicles. Now hormones produced by the female will result in the paramesonephric ducts persisting and the mesonephric ducts regress the paramesonephric ducts will grow further and eventually fuse in the midline at around 10weeks with a septum. 

Then the septum is resorbed at around 20weeks so now that we have this background knowledge on the embryology we can take a look at the UH nominees to understand at which stage the error has occurred to know which process has gone wrong so first of all we've got errors in fusion so we've got a bicornuate uterus where we have a partial fusion of the ducts creating an indent in the fundus with a unicorn uterus there is an asymmetric lateral fusion defect with the other duct being poorly developed didelphys is when two Mullerian ducts fail to fuse causing duplication of reproductive structures. Now there can also be errors of septal resorption so a septated uterus has a normal external surface of the fundus with incomplete resorption of the septum between the two millennion ducts and an arcuate uterus is when there is a slight midline septum with minimal and broad funnel cavity indentation. So these are the most important congenital abnormalities you should know.  

Thank You