Adenomyosis with Posterior Wall Adenomyoma and Left Ovarian Cyst

Our patient has been diagnosed with adenomyosis accompanied by a posterior wall
adenomyoma and cysts in the left ovary. In the development of adenomyosis leading to
adenomyoma and ovarian cysts, the precise cause of these conditions is unknown or idiopathic,
however, one of the considered causes of adenomyoma and ovarian cysts is hormonal
imbalances, specifically the increase levels of estrogen.

And so what are the predisposing factors and precipitating factors that contribute in the
development of adenomyoma and ovarian cysts?

First, let's start with the predisposing factors.

First, we have Advancing Age. Women between the ages of 30 and 40 are statistically more
susceptible to adenomyoma and ovarian cysts. During this time, hormonal fluctuations occur,
such as an increase in estrogen levels. In addition, given their age, they have experienced
numerous menstrual cycles and hormonal changes, which may contribute to the development of
adenomyoma and ovarian cysts.

Second, being female is also a risk factor in the development of adenomyoma and ovarian
cysts. As we all know, menstruation is a unique biological process exclusive to women. During
menstruation, there is shedding and regrowth of the uterine lining, thereby increasing the risk of
adenomyoma, where endometrial tissue descends into the myometrium. Additionally, ovarian
cysts can develop from follicles that fail to release an egg during the menstrual cycle, which will
be tackled in the pathophysiology later on.

Third, we have prior uterine surgeries. A woman who has had previous uterine surgeries, for
example, a C-section, is at a higher risk of developing adenomyosis because these uterine
surgeries can disrupt the normal anatomy of the uterus, resulting in the formation of scar tissue
within the uterus, leading to the development of adenomyosis.

Fourth, we have genetics. Genetics can also play a role as a predisposing factor for
adenomyoma and ovarian cysts, because there may be a family history of these conditions,
which leads to a higher risk of experiencing them for the patient.

Last, we have early onset of menstrual periods. Early onset of menstrual periods, occurring at
age 10 or earlier, can be a predisposing factor for adenomyoma and ovarian cysts because it is
believed that early menstruation is often associated with an early onset of hormonal changes,
including estrogen production. This prolonged exposure to estrogen can increase the risk of
hormonal imbalances.

On the other hand, we have three risk factors under precipitating factors.

First, we have multiple pregnancies. Multiple pregnancies can serve as a precipitating factor for
adenomyoma and ovarian cysts as they can lead to again, hormonal fluctuations in the body,
particularly increases in estrogen and progesterone levels. Aside from that, during multiple
pregnancies, the uterus undergoes stretching to accommodate the growing fetus. This
stretching can disrupt the normal architecture of the uterine lining and increase the likelihood of
adenomyosis.

Secondly, we have stress. Stress can act as a precipitating factor for adenomyoma and ovarian
cysts. When the body is stressed, there will be the release of the stress hormone called cortisol.
If the stress becomes chronic, it can lead to increased levels of cortisol, which in turn can cause
hormonal imbalances and irregular menstruation.

Lastly, we have smoking and alcohol. Smoking and alcohol consumption can act as precipitating
factors for adenomyoma and ovarian cysts. Smoking and alcohol consumption can lead to
alterations in estrogen metabolism and clearance, resulting in elevated estrogen levels, which
promote the growth adenomyoma and contribute to the development of ovarian cysts.

Back to the disease process, let's assume that menstruation has already occurred and the
uterine lining has shed. Following menstruation, when the uterine lining sheds due to decreased
levels of estrogen and progesterone, the hypothalamus, a region of the brain, detects the low
levels of these hormones and releases gonadotropin-releasing hormone (GnRH) into the
bloodstream. GnRH stimulate on the anterior pituitary gland, stimulating it to release
follicle-stimulating hormone (FSH) and luteinizing hormone (LH).

Following the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from
the anterior pituitary gland, ovarian follicles in the ovaries begin to develop with the help of FSH.
And these ovarian follicles will undergo morphological changes. And eventually, there will be
one dominant follicle that continues to grow and mature.

As the dominant follicle grows, Granulosa cells inside the follicle will actively produce estrogen
in response to FSH stimulation. Therefore there will be increase levels of estrogen in response
to the production of estrogen from the Granulosa cells.

As estrogen levels rise, there will be thickening of the endometrium, preparing the uterus for
potential implantation of a fertilized egg. Due to increased levels of estrogen, there is excessive
proliferation of cells within the endometrium. This proliferation of cells can result in the
overgrowth of endometrial tissue. As the endometrial tissue overgrows, it invades the muscular
layer of the uterus, known as the myometrium. This invasion into the myometrium leads to the
development and formation of benign growths known as uterine fibroids (myoma uteri). The
medical management in the case of our patient is Total Abdominal Hysterectomy and Bilateral
Salpingo-Oophorectomy (TAHBSO). The removal of the uterus, cervix, ovaries, and fallopian
tubes through an abdominal incision is to help prevent the recurrence or further growth of
adenomyoma and ovarian cysts.

Now, uterine fibroids may form in different sites of the uterus. They may be beneath the inner
lining of the uterus (submucosal layer), within the muscular wall of the uterus (intramuscular
layer), or beneath the outer covering of the uterus (subserosal layer). In the case of our patient,
the adenomyoma forms on the posterior wall; therefore, it is under the intramuscular layer.

Once formed, uterine fibroids can grow gradually over time because of increased levels of
estrogen. As these fibroids grow, they can cause compression and exerts pressure on the
uterine cavity. As the uterine cavity becomes compressed, the normal flow of menstrual blood
may be obstructed/impeded, leading to the accumulation of blood within the uterus.

It can result in symptoms such as spotting, which refers to light vaginal bleeding between
menstrual periods. Additionally, due to the prolonged accumulation of blood inside the uterus, it
can lead to heavy menstrual bleeding and the passage of large blood clots, also known as
menorrhagia. Furthermore, because of the increased pressure within the uterine cavity, it can
cause pain and discomfort during menstruation, known as dysmenorrhea.

If heavy bleeding continues, it can lead to significant blood loss over time. As the bleeding
becomes increasingly severe, it can result in a condition known as hemorrhage, where there is
rapid and excessive loss of blood from the body. Since there is active blood loss, it can rapidly
deplete the body’s blood volume, leading to a state of hypovolemic shock. Hypovolemic shock
occurs when there is insufficient blood circulating in the body to meet the body’s oxygen and
nutrient needs. In severe cases, untreated hypovolemic shock can lead to death.

Aside from the compression and increasing pressure of the uterine cavity, as fibroids grow, they
can exert pressure on surrounding tissues, including blood vessels and the iliac arteries that
supply blood to the pelvic region. Additionally, the presence of growing fibroids can distort the
normal architecture of the uterus. This compression, increasing pressure, and distortion of the
uterus's architecture can impede the normal flow of blood in the blood vessels, leading to
ischemia. Since there is insufficient blood supply, the amount of oxygen and nutrients reaching
the uterus and ovaries will be reduced, leading to tissue hypoxia. Without sufficient oxygen, the
uterine tissue may become damaged and necrotic, a condition known as uterine necrosis.

Now, how about the formation of ovarian cyst? Let's go back to the disease process on the top.
Again, granulosa cells inside the dominant follicle will actively produce estrogen in response to
FSH stimulation. Therefore, there will be increased levels of estrogen. Because of this, there is
stimulation of the anterior pituitary gland to increase secretion of luteinizing hormone (LH).
Luteinizing hormone is the hormone responsible for the final maturation of the ovarian follicle.
As the follicle becomes mature, it will rupture and eventually collapse, releasing the egg from
the ovary into the fallopian tube, which is the process we know as ovulation.

After the rupture and collapse of the follicle, the remains of the collapsed follicle undergo a
transformation into a temporary endocrine structure known as the corpus luteum. The corpus
luteum secretes progesterone. I forgot to mention earlier, Progesterone also helps to thicken the
endometrial lining of the uterus, preparing it for potential implantation of a fertilized egg.

Now, let's assume that the follicle did not rupture and collapse. Instead, the follicle continues to
grow and fills with fluid, forming a cyst within the ovary. As the cyst grows, it can compress the
ovarian capsule and nearby structures such as the fallopian tubes, intestines, and bladder. It
can also exert pressure on surrounding tissues and organs. This pressure can lead to pelvic
pain. In the case of our patient, she was experiencing gnawing pain in her left iliac region. It can
also lead to symptoms of constipation, a sensation of fullness, nausea, urinary frequency, and
urgency.

Aside from the compression and increasing pressure to the surrounding tissues and organs, it
can also lead to stretching of the abdominal wall. As the cysts within the abdominal cavity grow
in size, they occupy more space and exert pressure on the abdominal walls. This pressure can
cause stretching of the abdominal muscles and tissues, leading to abdominal distention or the
enlargement of the abdomen beyond its normal size. As the cysts continue to enlarge, they will
continue to exert more pressure against the abdominal walls, causing them to protrude outward
and expand. This expansion of the abdominal walls contributes to an increase in abdominal
girth, or the circumference of the abdomen.

And lastly, as the cyst grow and enlarge, it can lead to rupture of the cyst itself because of the
exerting pressure. When a cyst ruptures, its fluid and contents spill into the pelvic cavity. The
presence of foreign material and bacteria within the pelvic cavity can lead to the development of
pelvic infection, also known as pelvic inflammatory disease (PID). Pelvic infection is
characterized by inflammation and infection of the reproductive organs, including the uterus,
fallopian tubes, and ovaries. If PID is left untreated, the bacteria may enter the bloodstream,
causing sepsis and eventually leading to death.