Amenorrhea of thyroid genesis is often caused by primary or secondary hypothyroidism. Under conditions of deficiency of thyroid hormones, the growth of gyreotrophs is increased, producing an increased amount of TSH, the function of pituitary cells that produce LH is suppressed, the ratio of FSH / LH increases. A further decrease in the level of thyroid hormones leads to inhibition of the activity of the ovaries, an increase in degenerative changes in them. In subclinical and mild forms of hypothyroidism, a deficiency of the luteal phase is observed, with moderate and severe hypothyroidism – amenorrhea. When hypothyroidism in children is possible as premature sexual development, the hook and its delay.
Hyperthyroidism can lead to an increase in the basal level of LH, suppression of the ovulatory peak of hormones, an increase in the reactivity of the gonads in response to the action of LH and FSH. All of these factors contribute to anovulation and amenorrhea. During long-term hyperthyroidism under the influence of an excess of thyroid hormones, changes occur in the target organs (fibrous mastopathy, uterine contraction, degenerative changes in the granular layer in the ovaries).
Symptoms of mild hypo-and hyperthyroidism are not specific. Patients can be long and unsuccessfully treated by various specialists for vegetative-vascular dystonia, neuro-endocrine syndrome, amenorrhea of unknown origin.
Uterine form of amenorrhea
Uterine form of amenorrhea is observed when the impact of damaging factors on the uterus or in congenital malformations of internal genital organs.
Functional causes leading to amenorrhea are associated with traumatic injuries of the basal layer of the endometrium with frequent and rough curettage of the mucous membrane of the uterus.
As a result of removal of the basal layer of the endometrium, intrauterine adhesions (Asherman syndrome) may occur. One of the causes of intrauterine adhesions is genital tuberculosis (see Chapter 12, “Inflammatory diseases of the female genital organs”). Adhesions can lead to partial or complete fusion of the uterus. When the uterus cavity is fully invaded, secondary amenorrhea occurs. Fouling of the uterus in the lower third or in the region of the cervical canal during normal functioning of the endometrium in the upper sections leads to the development of hematometers. Extensive and tight adhesions cause secondary amenorrhea and secondary infertility as a result of occlusion of the fallopian tubes, impeding the fertilization process. The addition of an infection in case of injury to the uterine mucosa during curettage also contributes to the formation of intrauterine synechia. The adhesive process in the uterine cavity may occur after myomectomy, metroplasty, diagnostic curettage, electroconization of the cervix, endometritis, insertion of the IUD. The formation of intrauterine synechia in postmenopausal is a physiological process. Trophic disorders of the injured endometrium and secondary shutdown of the hypothalamic regulation of the menstrual cycle can lead to early climax.
Congenital malformations of the uterus and vagina – Rokitansky-Kyustner syndrome (uterus and vagina in the form of thin connective tissue cords), agenesia, aplasia, atresia of the vagina – are described in Chapter 4 “Malformations of the genital organs”.
These defects are accompanied by false amenorrhea and severe pain. False amenorrhea is also observed in atresia of the cervical canal due to its traumatic injury during intrauterine manipulation or due to inflammatory processes.
Determination of the level and nature of the lesion of the system of regulation of menstrual function with amenorrhea. General principles of therapy
Examination of a patient with amenorrhea provides for the gradual determination of the level of the lesion. The direction of the diagnostic search can be established on the basis of complaints, anamnesis and clinical manifestations. Sometimes a properly collected history allows you to identify the cause of amenorrhea before the clinical examination and additional studies (amenorrhea after stress or rapid weight loss).
In general examination, it is possible to form an idea of a possible pathology, since for each level of damage there are certain clinical manifestations: body type, obesity and distribution of adipose tissue, the presence or absence of somatic abnormalities, virilization and masculinization symptoms.
Appearance, development and distribution of subcutaneous fat in patients with hypothalamic-pituitary disorders have their own characteristics: obesity with the deposition of fatty tissue on the abdomen in the form of an apron, on the shoulder girdle or weight loss by 15-25% of the age norm, “moon-shaped” face purple-red color, hyperpigmentation of the skin of the elbows and skin folds, stretch marks, dry skin with a marble pattern, hypoplasia of the mammary glands.
When ovarian disorders, obesity develops in patients with the central form of PCOS, the distribution of adipose tissue is even. Obesity is not typical for congenital and organic disorders of ovarian genesis. Characteristic appearance in patients with congenital ovarian pathology – gonadal dysgenesis (see the section “Pediatric gynecology”).
Obesity is also unusual for patients with adrenal amenorrhea. Pronounced clinical manifestations were noted in patients with congenital adrenal cortex dysfunction (the classic form of AHS), they lead to pathology of the external genital organs and the wrong sex determination at birth.
In uterine form of amenorrhea, there are no typical changes in physique and metabolism. Patients have a normal female body type. In case of congenital abnormalities, the uterus may be absent, the vagina is a blind bag. The development of female secondary sexual characteristics correct and timely. Genital infantilism and anomaly of the development of the external genital organs can be identified by gynecological examination.
The severity of virilization also depends on the level of the lesion. The most noticeable androgenic disorders in patients with adrenal amenorrhea (post-pubertal forms of AHS, adrenal tumors): hirsutism, androgenic body type, alopecia, androgenic dermatopathy, reduced mammary glands and uterus. In patients with PCOS, hirsutism is more often observed with a mixed form of the disease; in the central form, virilization appears against the background of obesity. Structural changes in the ovaries and adrenal glands (hormonally active tumors) are accompanied by the progression of the virilization symptoms (clitoral hypertrophy, figure defeminization, decrease in the tone of the voice).
The high frequency of genetic abnormalities and hereditary diseases, especially in primary amenorrhea, requires genetic studies, including the definition of sex chromatin and karyotype.
The results of the clinical and anamnestic stage of examination determine the range of additional instrumental and laboratory methods. Further examination involves the identification or elimination of organic causes of amenorrhea at all levels of the regulation of the menstrual cycle. For this purpose, radiographs of the Turkish saddle and skull, echography of the pelvic organs and the thyroid gland, hysteroscopy with histological examination of scrapings, hysterosalpingography, laparoscopy are necessarily used. MRI of the brain is prescribed for indications.
If necessary, adjacent specialists are involved in examining patients: an ophthalmologist (examination of the fundus, peripheral and color fields of vision), a therapist, an endocrinologist, a neurologist, a psychiatrist, a psychologist.
After exclusion of tumors and congenital pathology of the reproductive system organs, hormonal studies and functional tests are carried out to assess its functional state. It is important to determine the level of FSH, LG, prolactin, TSH, T3, T4, estradiol, progesterone, DHEA and DHEA-C, testosterone, cortisol. Functional tests promote differential diagnosis and are designed to stimulate or suppress the activity of the endocrine glands (see Chapter 2, “Neuroendocrine regulation of the menstrual cycle”).