Endometriosis

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Introduction0:00–1:20

Endo- means internal and -metrium means womb, so endometrium is the innermost layer of the womb, and endometriosis is where these endometrial cells grow outside of the womb.
The female internal sex organs are the ovaries, which are the female gonads; the fallopian tubes, two muscular tubes that connect the ovaries to the uterus; and the uterus, which is the strong muscular sack that a fetus can develop in.
It’s a hollow organ that sits behind the urinary bladder and in front of the rectum. The top of the uterus above the openings of the fallopian tubes is called the fundus, and the region below the openings is called the uterine body.
The uterus tapers down into the uterine isthmus and finally the cervix, which protrudes into the vagina. It’s is anchored to the sacrum by utero-sacral ligaments, to the anterior body wall by round ligaments, and it’s supported laterally by cardinal ligaments as well as the mesometrium, which is part of the broad ligament.
The wall of the uterus has three layers: the perimetrium, which is a layer continuous with the lining of the peritoneal cavity, the myometrium, which is made of smooth muscle that contracts during childbirth to help push the baby out, and the endometrium, a mucosal layer, that undergoes monthly cyclic changes.

Pathology1:20–5:07

In endometriosis, the cells that make up the endometrium migrate and implant themselves in other parts of the body. Once there, they will set up camp and start growing to form a mass of endometrial tissue.
Most often, this affects the ovaries, fallopian tubes, and uterine ligaments. But it can also affect other structures in the pelvis and abdomen like the perimetrium, the rectovaginal septum, the recto-uterine pouch, also called the pouch of Douglas, and even the intestines or bladder!
Although we are unsure of the exact cause of the endometrial cell migration, There are at least five main theories that try to explain this phenomenon.
First, retrograde menstruation theory says that during menstruation, some blood carrying endometrial cells will flow backwards into the fallopian tubes and implant into nearby tissue.
Sometimes, there could also be a patented fallopian tube, meaning there’s an opening in it, so the adventurous endometrial cells could actually escape and travel to the other pelvic and abdominal structures!
Now, because retrograde flow is much more common than endometriosis, other factors probably come into play. So the second theory is that there’s a dysfunction with the immune system where B and T cells don’t respond to endometrial implants and allow it to grow.
Third, the metaplastic theory suggests that cells of the peritoneum, which come from the same cell line as endometrial cells, can transform spontaneously into endometrial tissue.
This theory explains how in rare cases, a woman that underwent a hysterectomy, where the uterus was surgically removed, can still develop endometriosis.
The fourth and fifth theories are especially useful for explaining how endometrial implants show up in places like the lungs or heart.
Benign metastases theory says that endometrial cells can travel to distant organs through the lymph and blood, while extrauterine stem cell theory says that stem cells in the bone marrow differentiate into endometrial cells and then travel to other parts of the body.
In addition to these proposed causes, there are some risk factors for developing endometriosis. These include a family history of endometriosis, never having been pregnant, early menarche, and late menopause.
Now, whatever the cause, endometriosis implants are benign so they don’t grow out of control like cancerous cells. However, because they’re functionally the same as the epithelial cells found within the uterus, they have the same estrogen receptor.
So they go through the same proliferation, secretion, and menstruation cycle just like the normal endometrial cells. But, there are two key differences between normal endometrial cells and endometriosis implants.
First, the implanted cells contain high levels of the enzyme aromatase, which allows them to produce their own estrogen.
Second the implanted cells release pro-inflammatory factors which causes inflammation and scarring. These scars could cause adhesion which is the binding of different organs or structures to each other, affecting their normal anatomical placement.
Both the pro-inflammatory factors and estrogen also promotes the growth of new blood vessels which nourish the implant. Now, changes in hormone levels and the chronic inflammation will cause the implant to bleed, especially during menstruation.
If the implant is on an ovary, it could form an endometriomas, or chocolate cysts, which contains the old, dark blood and shed tissue.
When these get too large, they will rupture and spill their contents, resulting in a lot of pain and even more inflammation.
Endometrioma cells also tend to develop mutations in certain genes, including PTEN and ARID1A, which increase the risk of developing ovarian carcinoma.

Symptoms and diagnosis5:07–6:37

The symptoms of endometriosis can be quite debilitating and are related to the location of the endometrial cells. Most commonly, endometriosis on the reproductive organs will causes pelvic pain, bleeding, dysmenorrhea, or painful menstruation, and dyspareunia, or painful sexual intercourse.
If it involves the pouch of Douglas, a section of the peritoneum located between the rear wall of the uterus and the rectum, it can cause dyschezia, or pain with defecation.
It can also cause urgent, frequent and sometimes painful urination if it involves the bladder, and abdominal pain if involves the intestines.
All of these symptoms will often vary with the hormone changes throughout the menstrual cycle, and often gets worse during menstrual periods.
About 30-40% of women with endometriosis are subfertile. The exact link between infertility and endometriosis isn’t totally clear.
It’s believed that the inflammation that comes with endometriosis can damage or scar the reproductive structures, thus inhibiting the release of the egg or its movement through the fallopian tube.
Damage to the uterus can also make the implantation of the gamete more difficult. The good news is that pregnancy is often still possible, depending on the severity of the endometriosis and the effectiveness of the treatment.
The best way to diagnose endometriosis is through laparoscopy, and the diagnosis can be confirmed with a biopsy. Treatment is focused on managing pain, trying to limit the progression of the implants, and addressing the associated subfertility.

Treatment6:37–7:51

Common hormonal medications that are used to treat pain include: combined estrogen-progesterone oral contraceptive pills, which relieve pain through ovarian suppression; progesterone analogs like medroxyprogesterone and levonorgesterol, which inhibit growth of the endometrium; danazol, which is a steroid that inhibits mid-cycle surges of follicular stimulating hormone and luteinizing hormone and prevents steroidogenesis in the corpus luteum; and gonadotropin-releasing hormone modulators, which cause a decrease in estrogen levels.
Surgical options are available for severe cases. If the woman still wants to have children, the surgery involves only excision of endometrial implants, endometriomas, and adhesions.
If she has completed her childbearing or if the pain is too debilitating, a hysterectomy and oophorectomy with excision of any other endometrial implants is done.
Whatever the treatment, once menopause hits and hormone levels fall, the symptoms generally goes away. All right, as a quick recap, endometriosis is when cells of the endometrium grow outside the uterus.

Review7:51–8:15

These cells follow the same hormonal cycle as normal endometrial tissue, including secretion and bleeding. This causes inflammation, scarring, adhesions, and endometriomas.
Common symptoms include pelvic pain and bleeding that gets worse during menstruation, and infertility.