Amenorrhea (Gynecologists' Lecture)

There are many causes of secondary amenorrhea, and when they occur before menarche, all of these can also cause primary amenorrhea.
The most common cause of secondary amenorrhea is pregnancy.
Next, there’s functional hypothalamic amenorrhea, which is when there is a decrease in GnRH secretion, leading to low levels of LH, FSH, and estrogen.
Often, this is due to weight loss from anorexia, nutritional deficiencies like excessively low fat consumption, prolonged periods of strenuous exercise, or severe physical or emotional stress.
Another condition that affects the hypothalamic-pituitary-ovarian axis and can be responsible for secondary amenorrhea is
Now, it’s not clear exactly what causes PCOS, but there seems to be an imbalance between LH and FSH levels.
Specifically, ovulation doesn’t occur, so progesterone levels don’t rise enough to inhibit LH production.
This leads to an increase in the production of LH compared to FSH, so there’s an elevated LH to FSH ratio.
Additionally, because there is post-ovulatory rise and fall in progesterone, there is no menstruation.
Issues with the pituitary gland can also cause secondary amenorrhea.
One cause is hyperprolactinemia, or excessive prolactin secretion by pituitary lactotroph cells, which is frequently seen with a benign pituitary tumor called a prolactinoma.
High prolactin levels inhibit hypothalamic GnRH production, therefore inhibiting ovulation and menstruation.
Interestingly, hypothyroidism - a condition in which there’s low levels of thyroid hormones - can also cause amenorrhea.
This is because low thyroid hormone levels signal the hypothalamus and pituitary to release more thyrotropin releasing hormone, or TRH, and thyroid stimulating hormone, or TSH, respectively.
Incidentally, TRH also stimulates prolactin release - so hyperprolactinemia and amenorrhea ensue.
Now, sometimes secondary amenorrhea can occur because of premature ovarian failure - which is when the ovarian follicles undergo accelerated atresia and get depleted before the age of 40, resulting in early menopause. This leads to low serum estrogen and high FSH and LH.
Finally, a structural cause of secondary amenorrhea is intrauterine adhesions, or Asherman syndrome, which is when there is scar tissue inside the uterine cavity, typically in a female that has undergone uterine instrumentation in the past.
Amenorrhea can occur because there is so much scar tissue that there’s no functional endometrium left, or because the presence of scar tissue makes the endometrium refractory to hormonal stimulation.
The one symptom of both primary and secondary amenorrhea is, well, the absence of menstruation.
Additional symptoms depend on the cause.
Individuals with Turner syndrome have a short stature, absent secondary sex characteristics, and a wide, or webbed, neck.
Müllerian agenesis might cause dyspareunia, or painful sexual intercourse, and infertility.
With androgen insensitivity syndrome, individuals typically have sparse body hair, and little to no pubertal acne.
With Kallmann syndrome, there may be anosmia, or absent sense of smell, because the neurons responsible for olfaction are closely related to the ones that release GnRH.
With functional hypothalamic amenorrhea due to anorexia, there’s significant weight loss and decreased bone density and fractures.
With polycystic ovary syndrome, the ovarian follicles secrete too much testosterone, causing hirsutism, or excessive hair growth on the chin and upper lip, chest, and back.
With a prolactinoma, there might be galactorrhea, or abnormal milk production.
With premature ovarian failure, there may be additional symptoms like hot flashes and vaginal dryness.
With intrauterine adhesions there could be infertility.
First step when evaluating primary or secondary amenorrhea is to rule out pregnancy with a pregnancy test.
If that’s negative, diagnosis requires serum levels of FSH, LH, estrogen, prolactin, TSH and testosterone.
A karyotype can be done for Turner syndrome and androgen insensitivity syndrome.
An ultrasound can show if there are structural issues with the vagina or the uterus, which suggests Müllerian agenesis, or, if there is no uterus, and intra abdominal testicles are found, that suggests androgen insensitivity syndrome.
Intrauterine adhesions can be visualized through hysteroscopy.
Treatment depends on the underlying condition.
Hormone replacement therapy, like combined oral contraceptives may be useful for individuals with Turner syndrome, polycystic ovarian syndrome or premature ovarian failure.
For a prolactinoma, dopamine agonists like cabergoline can be used - because they inhibit prolactin secretion just like dopamine naturally would, and they shrink the adenoma.
Surgery can be used to remove intrauterine adhesions, and to help correct some of the structural issues in Müllerian agenesis.
In some cases, psychotherapy can also be useful, as well as treatment for the related fertility issues.

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