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Neuroendocrinal regulation of menstrual cycle


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Neuroendocrinal regulation of menstrual cycle

  2. 2.  NEUROENDOCRINAL REGULATION OF MENSTRUAL CYCLE – is a complex, genetically determined system of inter-regulation of genitals, central nervous system and target organs. Formation of reproductive system starts antenatally and finishes at the age of 18-21.
  3. 3. 5 LEVELS OF MENSTRUAL CYCLE REGULATION. 1 Target organs. These include external and internal genital organs, mammary glands, bone tissue and skin. Target organs have receptors for steroid hormones. Influence of sex hormones on these organs leads to formation of secondary sexual character, cyclical processes in endometrium and vagina.
  4. 4. 2. Ovaries. Steroid hormones in the ovary are synthesized due to the action pituitary hormones. The hormones synthesis process inside the ovary is called steroidogenesis. Adrenal glands and adipose tissue synthesize steroid hormones too. Steroid hormones are synthesized from cholesterol and have the same nature. Schematically this process can be represented in the following way: cholesterol – pregnenolone – androgens – estrogens.
  5. 5.  Ovaries synthesize 3 types of hormones: estrogens, gestogens, androgens. Female organism produces 3 fractions of estrogens. Estradiol - is the most active estrogen and is produced by ovaries. Estrone – less active, mainly produced by adipose tissue. Estriol – is a result of transformation of estradiol, estrone and androgens of epinephroses. Estriol is produced only during pregnancy and has minimal hormonal activity.
  6. 6.  Progesterone – is the hormone of yellow body of ovary and is a gestogen. Major androgen of ovary is testosterone , which is produced by cells of internal theca. Testosterone is not very active. Under the influence of enzyme 5-α- reductase, it is transformed into a more active hormone – dehydrotestosterone.
  7. 7.  Most estrogens and androgens merge with sex steroid-binding globulin (SSBG). Smaller amount of estrogens merge with albumin and erythrocytes. Only one per cent of estrogens remains free and influences the target organs. SSBG is synthesized by liver, its quantity is proportional to estrogen level, and decreases under the influence of androgens. Today have been discovered 2 progesterone-binding proteins.
  8. 8. PHYSIOLOGIC EFFECTS OF ESTROGEN ON FEMALE ORGANISM Uterus. Estrogens determine the proliferation processes in endometrium, growth of myometrium and uterine tubes. Mammary glands. Stimulate growth. Bone tissue. Estrogens are parathormone antagonists. They hinder development of osteoporosis and condense growth zones in bones. Cardiovascular system - i ncrease the arterial pressure and vascular tone.
  9. 9.  Circulatory system. Increase the amount of fibrin. Mineral metabolism. Estrogens influence the natrium metabolism they attract sodium from tissues and can cause oedemas. Lipidic metabolism. Increases quantity of high-density β-lipoproteins; this has anti- atherosclerotic effect. Central nervous system. Estrogens form optimal neuropsychic condition. They change synthesis of pituitary and hypothalamus hormone.
  10. 10. PHYSIOLOGIC EFFECTS OF PROGESTERONE. Uterus. In case of sufficient concentration of estrogens, progesterone exerts influence upon tissues. Progesterone creates the evident anti- proliferative effect and conditions the secretion processes in endometrium. Besides, progesterone furthers myometrium growth. Mammary gland. Along with estrogens and prolactin, progesterone conditions tissue development. Progesterone also furthers lactation.
  11. 11.  Cardiovascular system. Progesterone decreases vessels tone and arterial pressure. Circulatory system. Progesterone does not influence the amount of fibrin. Mineral metabolism. Progesterone has diuretic effect. Central nervous system. Progesterone may cause depressions. It shows evident anti-gonadotrophic action.
  12. 12. EFFECTS OF ANDROGENS. - Androgens in normal concentration are synergists of estrogens. - In high concentrations androgens show evident anti-gonadotrophic action and further the development of secondary male sexual characters. - During antenatal and postnatal periods increase of their level causes change of central nervous system.
  13. 13.  3. Hypophysis. Hypophysis is divided into 2 lobes: anterior – adenohypophysis and posterior – neurohypophysis. Adenohypophysis consists of groups of cells, these groups of cells are responsible for the synthesis of the following hormones: growth hormone (somatotropic hormone – STH);
  14. 14.  thyrotropin (thyroid stimulating hormone – TSH); prolactin (PRL); follicle-stimulating hormone (FSH); luteinizing hormone (LH); adrenocorticotropic hormone (ACTH); melanotropic hormone (MH).
  15. 15.  LH, FSH, PRL are major hormones which regulate menstrual cycle. But it is only possible under the condition of optimal concentrations of other pituitary hormones. Synthesis of pituitary hormones is realized due to stimulating impact of hypothalamus. PRL synthesis depends on dopamine concentration. PRL concentration increases when dopamine level decreases.
  16. 16.  Hormones are not synthesized in the posterior lobe of hypophysis. Oxytocin and vasopressin are synthesized in hypothalamus, but are accumulated in the posterior lobe of hypophysis.
  17. 17.  4. Hypothalamus. Nucleuses of hypothalamus synthesize the following neurohormones: libertines and statines. The libertines stimulate adenohypophysis, statines inhibit it. These hormones are called releasing hormones.
  18. 18.  Libertines include the following hormones: adrenocorticotropin-releasing hormone (ACTH-RG); thyrotropin-releasing hormone (TRG); gonadotropin-releasing hormone (GN- RG); growth hormone-releasing hormone (somatoliberin GH-RG); melanoliberin (M-RG)/
  19. 19.  Statines include the following hormones: somatostatin; dopamine (major prolactin- inhibiting factor).
  20. 20.  Neurohormones are synthesized not only in hypothalamus. Somatostatin is synthesized in tissues of thyroid gland, bowels. Other hypothalamus peptides – gastrin, cholecystokinin, enkephaline are synthesized by other tissues also. They create a regulation system called “diffused neuroendocrinal system of organism”.
  21. 21.  5. Extra-hypothalamic structures. Epiphysis, limbic system, celebrum tonsil and hippocampus influence the reproductive function. They are related to extra-hypothalamic structures. Function of hypothalamus can be stimulated or inhibited by enkephalins, endorphins, neuropeptides.
  22. 22. NEUROENDOCRINAL REGULATION OF MENSTRUAL CYCLE. At the age of 10-12 years the reproductive system starts its development.There are several theories, which explain activation of hypothalamo-pituitary-ovarian system. 1.Theory of late-pubescence. According to this theory sensitivity of hypothalamus to the steroid hormones changes with the age. Besides, sensitivity of ovaries to gonadotropin increases also.
  23. 23.  2.Theory of resonance. According to this theory the increase in electrical activity of hypothalamus nucleuses stimulates an increase of GN-RG level. 3.Theory of block release. According to this theory at the start of pubescence epiphysial function decreases and hypothalamic function increases.
  24. 24.  The activation of hypothalamus makes it oversensitive to decrease in estrogen concentration. Next, it synthesizes GN-RG, which stimulates production of FSH and LH. Gonadotropins influence the process of growth and development of follicle (“folliculogenesis”) in ovaries. This descending process is called direct relationship.
  25. 25.  The ovary of a newborn girl contains from 400.000 to 500.000 primary ovarian follicles. Only 400 follicles ripen and reach the ovulation. Under the influence of FSH the development of several primari ovarian follicles starts in the ovary. In the beginning they grow independently.
  26. 26.  Later on, their growth depends on the FSH level and the sensitivity of follicle to the FSH. Therefore, only one follicle reaches the size of pre-ovulatory, others atrophy. The wall of antrum-containing follicle has 3 sheaths: interstitial, internal theca and granulosis. These sheaths have different sensitivity to gonadotrophic hormones. Intersticium and theca are more sensitive to LH; granulosis is more sensitive to FSH.
  27. 27.  Follicle synthesizes steroid hormones. This process is called steroidogenesis. Theca and intersticium synthesize steroids up to androgen fraction; granulosis produces estrogens. Increase in estrogen concentration depresses the function of hypophysis. This process is called negative inverse relationship.
  28. 28.  It takes place in the early pubertal period when menstrual cycles are monophase. Positive inverse relationship is characterized by maximum estrogen concentration. Consequently honadotropines and libertines increase dramatically. Ovulation follows this process. The ovulation process is a histochemical process. Estrogens, prostaglandins and histamine influence the sheath of the follicle and cause its rupture.
  29. 29.  Granulosis cells are transformed into the yellow body under the influence of LH after ovulation. The yellow body synthesizes progesterone. Increase of progesterone inhibits the synthesis of LH. This causes the death of the yellow body.
  30. 30.  The ovarian cycle is a consistent process of growth and development of follicle, ovulation, development and death of the yellow body. Ovarian cycle is divided into 3 phases: Follicular phase is characterized by growth and development of follicle. It lasts 12-14 days. Ovulatory phase – lasts several hours. Lutein phase is characterized by development and functioning of the yellow body.
  31. 31.  Uterine cycle is a cyclic process in the ovary, which causes cyclic changes in the endometrium. It has 4 phases: Desquamation. Decrease of steroid hormones causes spasm, ischemia and rejection spiroid artery of decidual sphere of endometrium. First day of desquamation corresponds to the first day of menstruation and menstrual cycle. Regeneration. It corresponds to the early period of follicular phase in the ovary. Regeneration lasts 4-5 days. It starts with epithelization of endometrium.
  32. 32.  Proliferation. It lasts 5-7 days and results in ovulation. It corresponds to the late period of follicular phase in the ovary. Is characterized by proliferation of epithelium and development of spiroid arteries. Secretion. It corresponds to lutein phase in the ovary. It lasts 10-12 days. The process of proliferation is superseded by secretion. If pregnancy did not take place, cyclic processes in the system uterus-ovaries-hypothalamic- pituitary system repeat.
  33. 33. MENSTRUAL DISORDERS ETIOLOGY Nervous diseases. Mental diseases. Malnutrition. Some occupational hazards. Systemic and gynecologic inflammatory diseases. Illness of the haemopoiesis, cardiovascular and other systems. Gynecologic operations. Puberty disorders. Age-specific reconstruction of the functional state in hypothalamic-pituitary-ovarian axis in the menopause.
  34. 34. AMENORRHOEA Pathological primary amenorrhoea – when the patient has never menstruated. Pathological secondary amenorrhoea – when the periods are absent for more than 6 months. Physiological amenorrhoea – before puberty, during pregnancy and lactation, and after the menopause. False amenorrhoea – when the flow does not escape because of some obstruction. True amenorrhoea – when the endometrial cycle is absent.
  35. 35. TRUE PATHOLOGICAL AMENORRHOEA 1.Uterine disorders. the uterus may be congenitally defective; the endometrium atrophies after irradiation with X-ray or radium, and hysterectomy.
  36. 36. 2. Ovarian disorders. failure of ovarian development occurs in cases of gonadal dysgenesis; Stein-Leventhal syndrome is a disorder of unknown cause. After some years of normal menstruation amenorrhoea occurs with hirsuties. Both ovaries are enlarged and contain multiple small follicular cysts. There is a block in the normal conversion of progesterone to estrogen so that an intermediate androgen substance androstendione appears in excess. The urinary excretion of estrogens is normal or low, while that of pregnantriol (a metabolic product of certain androgens) is raised; arrhenoblastoma is a very rare cause of amenorrhoea; ovarian infections or new growths as processes destroying all ovarian tissue.
  37. 37. 3. Pituitary disorders. There is of production of gonadotrophic hormones. Amenorrhoea is one aspect of general disorders and the gynecologist is seldom responsible for treatment. Pituitary infantilism (Levi-Loraine syndrome). The adult resembles a child. No effective treatment is known. Pituitary cachexia (Simmond’s disease). This is usually due to ischemic necrosis of the pituitary glands (hypophysis) due to thrombosis of pituitary vessels after postpartum hemorrhage and collapse. Failure of lactation is followed by genital atrophy, loss of pubic hair, weakness, anorexia.
  38. 38.  Treatment with cortisone, thyroxin and anabolic steroids may cause some improvement. Adipogenital dystrophy is characterized by dwarfing, adiposity and genital infantilism, and is usually caused by a craniopharyngioma that involves the pituitary gland and hypothalamus. The treatment is surgical. In acromegaly the eosinophilic adenoma of the pituitary gland may destroy the gonadotrophic cells, and the same may happen with other pituitary tumors. Small pituitary adenoma may secrete prolactin and cause amenorrhoea with galactorrhoea.
  39. 39. 4.Other endocrine disorders. Amenorrhoea occurs: in severe cases of hyperthyreoidism, myxoedema and cretinism; in some cases of diabetes; in Addison’s disease; with adrenocortical tumors or hyperplasia.
  40. 40.  5. Nervous disorders (stress or hypothalamic amenorrhoea). This is the commonest type of secondary amenorrhoea, and may be the result of emotional disturbances.
  41. 41.  6.Disorders of general health and nutrition. Any chronic or severe illness (including nutritional deficiency) will cause amenorrhoea. 7.Oral contraception. A delayed first period is common after stopping oral contraception. More prolonged amenorrhoea sometimes occurs.
  42. 42. DIAGNOSIS General examination; Special gynecologic examination; Ultrasonic; X-ray; Hormonal tests.
  43. 43. TREATMENT Sedative therapy; Vitamin therapy; Adequate nutrition, a special diet intended to decrease the body weight; Physiotherapy (endonasal electrophoresis with 2% solution of vitamin B1, 0.25% solution of dyphenhydramine hydrochloride). Drugs suppressing prolactin secretion (bromocriptine, parlodel, dostineks). Hormonal therapy of the cyclic hormones (estrogens followed by progesterone).
  44. 44. DISFUNCTIONAL UTERINE BLEEDING Disfunctional,or anovulatory uterine bleeding is associated with anovulation caused by impaired or unestablished functional relationships in the hypothalamic-pituitary-ovarian axis.
  45. 45. Classification In juvenile age; In reproductive age; In the premenopausal period.
  46. 46.  Dysfunctionaluterine bleedings may be divided into anovulatory and ovulatory ones.
  47. 47.  Anovulatory bleedings are induced by the absence of ovulation and luteal phase of the cycle. Anovulatory uterine bleeding develops in patients with: persistence of an ovarian follicle; persistent follicles release a large number of estrogens; atresia of a few follicles; atresia of some small follicles is associated with hypoestrogenism.
  48. 48.  Both account for continuous, monotonous secretion of estrogens. Ovulation does not occur and the corpus luteum fails to form. Excessive proliferation of the endometrium occurs as a result of prolonged exposure to estrogens in both processes. Persistent and atretic follicles undergo involution. The level of hormones (estrogens) is decreased in the blood, and bleeding develops.
  49. 49.  Circulation in the endometrium is impaired, the capillary permeability is decreased, and the sites of dystrophy and necrosis are manifested. The necrotic mucosa is rejected slowly, which causes prolonged bleeding. Dysfunctional uterine bleedings are not attended with pain.
  50. 50. CLINICAL PICTURE Amenorrhoea: in 4-8 weeks in persistent follicle; 3-4 months in atretic follicles; Bleedings are more abundant in persistent follicles, being occasionally profuse; Anemia; Decrease the patient’s working capacity; General fatigue; Headache; Poor appetite; Sleep; Pale skin; Tachycardia; Decreased blood pressure.
  51. 51. DIAGNOSIS Diagnosis is based on general and gynecologic examination. At general examination one should pay attention to the typical sings: bleedings that follow the suppression of menses; monophase basal body temperature; high or low karyopycnotic index.
  52. 52.  Dysfunctional uterine bleedings should be differentiated from many disease forms that are attended with bleedings: abortions; interrupted fallopian pregnancy; tumors of the uterus.
  53. 53.  TREATMENT Thedoctor’s tactics largely depend on the patient’s age.
  54. 54. Juvenile bleedings. Conservative treatment (use coagulants, hemostatic agents, stimulants of uterine contractility). Hormonal haemostasis (“medicamentous curettage” synthetic estrogen-progesteron drugs (logest, yrina, dgaz, ganin) are prescribed in a dose of 5-6 tablets daily is gradually decreased to 1 tablet per day ( the total couse of drug administration is 21 days). Diagnostic curettage of the uterine mucosa. When bleeding has been arrested, cyclic hormone therapy is administered for 6 or 9 cycles.
  55. 55. In the child-bearing age. Diagnostic curettage of the uterine mucosa. Conservative treatment. Hormonal haemostasis (“medicamen-tous curettage” synthetic progestins (norcolut, orgametril, utrogestan, dyphaston) are prescribed in a dose of 5-6 tablets daily is gradually decreased to 1 tablet per day ( the total couse of drug administration is 21 days). When bleeding has been arrested, cyclic hormone therapy is administered for 6 or 9 cycles.
  56. 56. Premenopausal and menopausal age Diagnostic curettage of the uterine mucosa. Conservative treatment. Hormonal haemostasis (“medicamen-tous curettage” synthetic progestins (norcolut, orgametril, utrogestan, dyphaston) are prescribed in a dose of 5-6 tablets daily is gradually decreased to 1 tablet per day ( the total couse of drug administration is 21 days). The therapy is directed at regulating the menstrual function ( in women under 45 years) or its suppression ( in women over 45 years).
  57. 57.  DYSMENORRHOEA (ALGOMENORRHOEA) This term is used to painful menstruation. Pain may develop before the onset of menstruation and continue throughout the period of menstrual flow.
  58. 58.  Sometimes, pain is severe and attended by nausea, vomiting and other disturbances, which reduce the patient’s working capacity. In many cases dysmenorrhoea is just a manifestation of systemic diseases. It may be attributed to retroflexion or anteflexion of the uterus, cicatricial changes, and narrowing of the cervical canal.
  59. 59.  Primary and secondary forms of dysmenorrhoea are distinguished. The formes does not appear to be linked to any organic disease and is congenital. The latter develops in women with previously normal menstruations. Secondary dysmenorrhoea may be related to inflammatory processes, endometriosis, and genital tumors.
  60. 60. Treatment. Anti-inflammatory drugs. Hormonal drugs. Surgical treatment. Sedative drugs. Vitamin therapy.