Endometrium Hyperplastic Processes

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Endometrium Hyperplastic Processes

  1. 1. Endometrium Hyperplastic Processes BY ASSISTANT O.V.BAKUN
  2. 2. <ul><li>EHP - is a benign pathology of endometrium which is characterized by the development of clinical-morphological manifestations (from simple and complex hyperplasia to atypical precancerous conditions of endometrium) and which appears against the background of chronic anovulation when, in the absence or insufficient proliferative influence of progesterone, there takes place absolute or relative hyperestrogenia. </li></ul>
  3. 3. <ul><li>Etiopathogenesis of EHP </li></ul><ul><li>Causes and mechanisms of EHP development are regarded to be deviation variants from normal endocrine system functioning: </li></ul><ul><li>pathology of biosynthesis, </li></ul><ul><li>rhythm and cycling, </li></ul><ul><li>ejactions and disturbance in the ratio of hormone content; </li></ul><ul><li>functional disturbance of receptor cellular system, organs-targets in particular; </li></ul><ul><li>genetically determined “hormone-receptor” system pathology; </li></ul><ul><li>“ break-down” of immunological control of pathologically transformed cellular elimination; metabolism disturbance of sex hormones by pathology of hepatobiliary system and gastrointestinal tract; </li></ul><ul><li>failure of thyroid gland function. </li></ul>
  4. 4. <ul><li>EHP formation takes place in the conditions of stable hyperestrogenia against the background of reduced progesterone production. </li></ul>
  5. 5. <ul><li>Causes of hyperestrogenia: </li></ul><ul><li>Ovary disfunction (persistence or atresia of follicules); </li></ul><ul><li>Follicular cysts; </li></ul><ul><li>Stroma hyperplasia; </li></ul><ul><li>Theca-cells tumours; </li></ul><ul><li>Adrenal cortex hyperplasia; </li></ul><ul><li>Failure of pituitary body gonadotropic function; </li></ul><ul><li>Incorrect estrogen usage; </li></ul><ul><li>Changes in hormone metabolism (obesity, cirrhosis of the liver, hypothyrosis). </li></ul>
  6. 6. Normal anatomy
  7. 7. Normal anatomy
  8. 8. Normal anatomy
  9. 9. Normal anatomy
  10. 10. <ul><li>The appearance of hyperestrogenia is connected with anovulation in the reproductive period and premenopause as well as with obesity leading to the increased transformation of androstenendiona into esteron in fatty tissue. </li></ul>
  11. 11. <ul><li>The condition of endometrium receptory apparatus plays a great part in the development of EHP. In the norm the content of cytoplasmic receptors of progesterone and estradiol in endometrium under the influence of estrogens increases but under the influence of progesterone reduces. At the development of EHP the quantity of progesterone receptors comes down. A straight dependence of tumour differentiation upon the condition of receptor apparatus has been marked:the lower degree of differentiation the less receptors of endometrium to estrogens, progesterones and androgens and vice versa. </li></ul>
  12. 12. <ul><li>Among disharmonious conditions for EHP formation they single out a disturbance in physiologic secretion of thyroid hormones which are the modulator of estrogen action. </li></ul>
  13. 13. <ul><li>Not only estrogens but also biological amines, produced by cells of APUD-system take part in the regulation of cellular proliferation processes. Multiplied increase of their concentration has been found in malignant neuroendocrinal tumors. </li></ul>
  14. 14. <ul><li>Obesity is a special feature for patients with uterus cancer. Fatty and carbohydrate disbolism predispose EHP development. A high frequency of diabetes mellitus has been recorded in patients with glandular hyperplasia, atypical hyperplasia and cancer of endometrium in particular. </li></ul>
  15. 15. <ul><li>Failure of immune system is enormously significant in pathogenesis of precancerous processes. The quantity and functional activity of T-lymphocytes, peripheral B-cells have been recorded to fale, lymphopenia has been often observed. </li></ul>
  16. 16. <ul><li>Data testifying to the inflammatory genesis of EHP have been obtained. Prolonged morphologic and functional changes in endometrium by chronic endometritis stipulate the possibility of pathologic afferentation in the structure of central nervous system, which regulate functioning of hypothalamolimbic system. Disturbances in it lead to the development of the second hypofunction of ovaries, formation of anovulation kind of absolute or relative hyperestrogenia and, consequently, EHP. </li></ul><ul><li>The role of hereditary factors in the development of EHP is really great. </li></ul>
  17. 17. <ul><li>Hyperplasia of endometrium (HE) with secretory tansformation : thickening of the basal layer spreads all over the mucous coat or has a local character. Thinning of the functional layer and subsiding of the cyclic processes have been recorded. The glands of the basal layer are narrow and straight. The stroma is thick, often fibrous. Vessels with thickened sclerosed walls like glomes are clearly distinguished. The given form of HE contributes to the development of endometrium polyps. </li></ul>
  18. 18. <ul><li>Polyps of endometrium arise from the pathologically changed basal layer of uterus. The thickened loci of this layer strengthen, lengthen and take shape of polyps which are located on the wide basis and then-under the influence of uterus contractions – on the thin one. </li></ul><ul><li>Polyps are formed in the result of local changes in the receptors of endometrium (the quantity of receptors to estrogens increases) and also because of the pathologixal vessel condition. </li></ul>
  19. 19. <ul><li>Polyps consist of stromal and glandular components and enlarged blood vessels with thickened sclerosed walls at their bottom or peduncle. The most frequent localization of polyps is the mucosa of the bottom and angles of the uterus . Polyps always have a peduncle unlike polipiform glandular HE. </li></ul>
  20. 20. <ul><li>Clinical classification of endometrium polyps </li></ul><ul><li>Polyps covered with functional layer of endometrium </li></ul><ul><li>Glandular (glandular – cystic) polyps </li></ul><ul><li>Fibrous polyps </li></ul><ul><li>Glandular – fibrous polyps </li></ul><ul><li>Adenomatous polyps </li></ul>
  21. 21. <ul><li>Polyps covered with functional layer of endometrium – are found only in women of reproductive age with the preserved two-phase menstrual cycle and are located in secretory endometrium </li></ul>
  22. 22. <ul><li>Small polyps near the tubal ostium. The clinical significance with regard to the patient’s fertility remains to be clarified. Probably, these very small structures are not related to the infertility of the couple. </li></ul>
  23. 23. <ul><li>Glandular (glandular – cystic) polyps - differ by predominance of glandular component over stromal. The glands are inactive located unevenly, unsystematically, of different form and size; lined with highly prismatic epithelium of indifferent or proliferative type. </li></ul>
  24. 24. <ul><li>In fibrous polyps glands are absent or there are some isolated, the epithelium is not functional. </li></ul><ul><li>In glandular – fibrous polyps stromal component prevails over glandular, moreover phasic transformations are not characteristic for the former. </li></ul>
  25. 25. <ul><li>Adenomatous polyps contain a lot of glands, their epithelium proliferates intensively possessing a high mitotic activity. The content of RNA in the cytoplasm is increased, the area of nuclei is enlarged as well as DRNA concentration in them. </li></ul>
  26. 26. <ul><li>Four examples of endometrial polyps, often the cause of spotting </li></ul><ul><li>or bleeding in between periods but sometimes also including </li></ul><ul><li>glandulocystic or adenomatous hyperplasia of the polyp’s endometrial layer. </li></ul>
  27. 27. <ul><li>Polyps with local adenomatosis: the epithelium of glandular component outside adenomatosis doesn’t function or shows some signs of slight proliferation. </li></ul>
  28. 28. Soft fleshy endometrial polyp seen prolapsing from the endometrial canal
  29. 29. <ul><li>Precancerous diseases of endometrium </li></ul><ul><li>Atypical hyperplasia of endometrium (EAH) </li></ul><ul><li>The following forms of EAH are distinguished: </li></ul><ul><li>1. EAH of functional and/or basal layers: </li></ul><ul><li>Slight form of precancerous changes </li></ul><ul><li>Acute form of precancerous changes </li></ul><ul><li>2. Focal adenomatosis in glandular (glandular – cystic) and basal hyperplasia, polyps, displastic, hypoplastic, atrophic and slightly changed functional and/or basal layers of endometrium </li></ul><ul><li>3. Adenomatous polyps. </li></ul><ul><li>Slight form of precancerous changes </li></ul><ul><li>Acute form of precancerous changes </li></ul>
  30. 30. <ul><li>Histological picture of EAH </li></ul><ul><li>Structural transformation and intensive proliferation of glands are characteristic. Excess growth of twisted glands of quaint form is recorded by the slight form of precancerous changes. Mitotic activity in glandular epithelium is increased. </li></ul>
  31. 31. <ul><li>Acute form of precancerous changes is characterized by intensive glandular proliferation with acute atypia. Epiglandular component is multiseries, polymorphic. The cytoplasm of epitheliocytes is enlarged in volume, eosinophilic; cellular nuclei are big, pale. Clods of chromatin and big nuclei are identified. Typical for all degrees of EAH is very close location of glands with narrow layers of stroma between them. The glands lose their normal position, they are very different by form and size. In the glandular lumen there may appear papillae with a fibrous “peduncle” or by more acute degrees of proliferation consisted of piled epithelial cells. Sometimes there are small filial glands of microfollicular type around the big gland. Isolated glands with some growths pointed to the surrounding stroma look like clover leaves. </li></ul>
  32. 32. <ul><li>Morphological precancer transforms into adenocarcinoma in 10% of cases. Moreover, the possibility of endometrium hyperplastic processes transformation (which don’t belong to morphologic precancer) is significantly high in favourable conditions such as: endocrine system pathology (neuro-exchange-endocrine syndrome); the age (pre- and postmenopause); the character of hyperplastic process course. </li></ul>
  33. 33. <ul><li>Classification of endometrious precancer </li></ul><ul><li>Precancerous changes in the endometrium are reasonable to estimate according to the patient’s age, the clinical course of pathological process, failures of hormonal or metabolic character. In particular, endometrium atrophy accompanied by bleeding is classified as precancerous condition in postmenopause. That’s why the classification of endometrious precancer suggested by Savelyeva G.M and Serov V.N. (1980) has taken into account not only morphostructural disturbances but clinical signs of the disease as well: </li></ul><ul><li>Adenomatosis and adenomatous polyps at any age of the women </li></ul><ul><li>Glandular HE in combination with hypothalamic neuro-exchange-endocrine syndrome (hypothalamic syndrome of the type Itsenko-Kushing syndrome) at any age of the woman. </li></ul><ul><li>Glandular HE recurring in the menopause period </li></ul>
  34. 34. <ul><li>Endometrial carcinoma (EC) </li></ul><ul><li>Highly differentiated adenocarcinoma – I degree of histologic differentiation. The tumor is characterized by the conservation of glandular structure or formation of papillae structures. Cellular and nuclei polymorphism is expressed very slightly. The nuclei can be hypochromic with dust-like or small-grained chromatin or hypochromic with big-sized clods and sometimes homogeneous chromatin. In the part of glands there can be observed a slight form of multiseries nuclei and rare figures of mitosis. The cytoplasm is usually well developed, light, transparent and eosinophilic. </li></ul>
  35. 35. <ul><li>Moderately differentiated adenocarcinoma - II degree of histologic differentiation. This is the most common variant of EC. The tumor preserves a glandular structure and consists mostly of papillae growths. But unlike highly differentiated adenocarcinomas the glands very significantly as to the size and shape. Cellular and nuclei polymorphism is moderate or marked. The polarity of nuclei location is disturbed. The nuclei are oval, round or stretched more often hyperchromic with macrogranular or coldly chromatin. The cytoplasm is usually unclear and basophilic. </li></ul>
  36. 36. <ul><li>Glandular-solid adenocarcinoma – III degree of histologic differentiation. The tumor consists of solid layers or cords of polygonal or stretched cells which alternate with areas of glandular structure. Nuclei cellular polymorphism is usually marked. The nuclei of tumor cells are oval or round, but sometimes they are of irregular shape with macrogranular or clodded chromatin. The degree of cytoplasm development may be different and the colour of it very from light to basophilic or eosinophilic. </li></ul>
  37. 37. <ul><li>Solid (low-differentiated) adenocarcinoma - IV degree of differentiation. The tumor consists of cords or layers of polygonal cells, rarely stretched or of irregular form. Cellular and nuclei polymorphism in the tumor is marked. Multinuclei cells may occur. Sometimes the tumor takes a sarcoma-like structure, but in this case one can distinguish glandular structures by thorough investigation. </li></ul>
  38. 38. <ul><li>In tumors with different degree of differentiation there can be found so-called pseudoplanocellular nodules more often in moderately differentiated or highly differentiated adenocarcinomas. In scientific literature such tumors are usually called adenoacanthomas, but it is more correct to define such tumors as adenocarcinomas with the instruction to the degree of their histologic differentiation and the focus of adenoacanthoma. </li></ul>
  39. 39. <ul><li>A rare variant of malignant epithelial uterus tumor are lightcellular adenocarcinomas which consist of cells with a light transparent cytoplasm and distinct cellular boundaries. Such adenocarcinomas may be mostly glandular, papillae or glandular-solid and solid structure. </li></ul>
  40. 40. <ul><li>Clinic of hyperplastic processes in endometrium </li></ul><ul><li>Bohman Y.B. distinguished two clinical variants of EHP: </li></ul><ul><li>1. The first (hormone-dependent) variant . It is found in 60-70% of patients with AHE and characterized by marked hyperestrogenia and metabolic disturbances (especially of fatty and carbohydrate metabolism). Anovular uterus bleedings, infertility, signs of ovary polycystosis (Shtein-Levental syndrome), uterus myoma (by obesity and diabetes) have been recorded in patients. </li></ul><ul><li>At the same time together with AHE there are polyps with enlarged degenerative ovaries at the expense of hyperplasia of theca-cells. </li></ul>
  41. 41. <ul><li>2. The second autonomous variant. It is recorded in 30-40% of patients. Endocrine disturbances are not marked or are absent. AHE together with polyps are develops against the background of atrophic processes of endometrium together fibrosis of ovarian stroma. There are signs of immunodepression by that. Hypoestrogenia the rise of hydrocortisone level and the fall in the cellular receptors content in the endometrium at the marked depression of T-lymphocytes have been recorded. </li></ul>
  42. 42. <ul><li>Complaints of patients with EHP can be divided into 3 groups: </li></ul><ul><li>connected with the failure of menstrual function (bloody discharged from genitals), </li></ul><ul><li>conditioned by pain syndrome or contact bloody discharge </li></ul><ul><li>produced by metabolic or endocrine failures. </li></ul>
  43. 43. <ul><li>The main clinic sign of all variants of EHP are functional uterus bleedings. At reproductive age patients complain of bloody discharge from genitals in intermenstrual period. In climacteric period women complain of irregular menstruations with smearing to follow (at polyposis) or bleeding (at glandular hyperplasia and adenomatosis). At the menopause patients complain of scarce, short in time or very long bloody discharges. Sometimes patients suffer from moderate aches at the lower part of abdomen or contact bleeding. </li></ul>
  44. 44. <ul><li>Complaints caused by metabolic or endocrine failures come from patients with adenomatosis in particular. The most peculiar for them are complaints against headache, overweight, pathological pilosis, sleep disorders, periodical thirst, rosy striae, low capacity for work, irritability. Obesity and arterial hypertension are often singled out among extragenital diseases. According to the rate the second place comes to the diseases of liver. </li></ul>
  45. 45. <ul><li> EHP diagnosis </li></ul><ul><li>Patient’s complaints </li></ul><ul><li>Life history (disorders of fatty and carbohydrate metabolism, hypertension, liver disease). </li></ul><ul><li>Ginecological history (disorders of menstrual cycle with bleedings, infertility, myoma of uterus, mastopathy </li></ul><ul><li>Ginecological examination </li></ul><ul><li>Bacteriological and bacterioscopic examination </li></ul><ul><li>Hormonal examination (estrogens, progesterones, hormones of thyroid gland and adrenal glands. </li></ul>
  46. 46. <ul><li>Hysteroscopy is performed both before curettage – for the sake of making the character of endometrial pathological transformation more precise – and after it – with the aim of supervision whether the operation was thoroughly performed. </li></ul><ul><li>Simple hyperplasia : the endometrium is unevenly thickened, it has a folded structure; the base of folds is wide, the top is thin with uneven edges, the colour of folds varies from light pink to bright red. There is a peculiar sign of “submarine plants” – wave-like movements of mucous membrane by pressure changes in the uterus during its stretching with liquid media. The mucous height is 10-15 mm. Vascular pattern is distinctly marked. Withdrawing ducts of tubal glands are clearly visualized and evenly located. Uterine openings of the oviduct are free. </li></ul>
  47. 47. <ul><li>Cystic form of glandular HE is characterized by multiple cystic cavities, located in the projection of superficial blood vessels of the mucosa and having different thickness (a “trap” phenomenon). The diameter of cystic structure is 2-3 mm. </li></ul>
  48. 48. <ul><li>Polypoid form of HE is characterized by the appearance of a multitude of polypoid growths (spherical structures on the broad basis) of pale-pink or blue-purple colour, hanging into the lumen of the uterus, their size fluctuating from some mm to 1-1,5 cm. Uterine openings are not identified. Withdrawing ducts of glands are not distinguished. Vascular pattern is sharply marked. </li></ul>
  49. 49. <ul><li>Polyps covered with functional layer have smooth surface and pale-pink colour. They locate at the fundus and uterine angles. </li></ul><ul><li>Glandular and glandular-fibrous polyps are pale pink or pale grey, locate at the fundus or uterine angles. Vascular pattern is sharply marked (peripheric vessels are dilated) </li></ul>
  50. 50. <ul><li>Fibrous polyps: spherical or oval, pale pink or pale yellow with smooth surface and a wide base. Vascular pattern is not identified. The size of polyps is 15 mm, as a rule they are isolated. </li></ul><ul><li>Polyps with local adenomatosis have the same endoscopic picture as glandular or glandular-fibrous polyps. </li></ul>
  51. 51. <ul><li>Adenomatous polyps : dull grey formations with rough surface. The size is 5-30 mm. Some times the surface is of purple-bluish colour ( local disorder of circulation) or marked vascular pattern (multiple dilated capillaries). </li></ul>
  52. 52. <ul><li>Endometrial carcinoma: papillomatous growths of grey or dirty-grey colour with areas of hemorrhage and necrosis. The vascular pattern is intensified with the change of volume of the administered liquid the tissue easily decays, bleeds and crumbles. </li></ul>
  53. 53. <ul><li>9. Ultrasound examination with the usage of transvaginal unit. When hyperplastic process or uterine carcinoma are suspected then special attention is paid to the study of median uterine echo (m-echo) – reflection from the endometrium and walls of the uterine cavity. Its form, contours and inner structure are estimated. The value of antero-posterior size of m-echo is determined. </li></ul><ul><li>The main criterium of hyperplastic process in endometrium in reproductive age is its thickening in the second phase of M.C. of 16-18 mm and during menopause – more than 5 mm </li></ul>
  54. 54. <ul><li>USE – indications for morphologic study: </li></ul><ul><li>In premenopause and reproductive period: rise in the thickness of endometrium more than 16 mm; endometrial-uterine coefficient (EUC) – that is the ratio of endometrial thickeness to the value of anteroposterior size of uterus>0,33. </li></ul><ul><li>In postmenopause: rize of endometrial thickness>5 mm; EUC>0,15; enormous squamous differentiation; inflammatory processes in endometrium. </li></ul>
  55. 55. <ul><li>10. Radioisotope examination of the uterus. The essence of the method lies in the value of the degree of radioactive preparation consumption by tissues depending upon the activity of proliferative processes. The intensity of radioactive preparation consumption by tissues at HE is higher than by normal endometrium, and by AHE (atypical hyperplasia of endometrium) higher than by glandular-cystic hyperplasia. Radioactive phosphorus is used more often, its accumulation in the uterus rises in the following consequence: the second phase of normal menstrual cycle – benign forms of hyperplasia. Processes of endometrium (EHP)-adenomatosis-cancer. </li></ul><ul><li>11. Determination of fermental activity in nucleotide exchange. </li></ul>
  56. 56. <ul><li>Treatment of EHP </li></ul><ul><li>Consists of 4 stages </li></ul>
  57. 57. <ul><li>1. stage of treatment – arrest of bleeding </li></ul><ul><li>The method of bleeding arrest at a juvenile age is determined by the general condition of a patient, the amount of hemorrhage and amnesia. At a satisfactory state hormonal hemostasis is commonly used: </li></ul><ul><li>estrogen-gestagen preparations ( logest, femoden, zhanin, yarina and other ) in hemostatic regime (on the first day 3-5 tablets with the following consequent reduction of the dose to one tablet in a day with the whole period of administration of 21 days). Girls admitted to the hospital in critical condition and abundant bleeding, posthemorhagic anemia (content of Hb<70g/l and fall of hematocrit to 20%), AP-falling down and tachycardia should have the uterine mucosa scraped under histeroscopic supervision and preliminary prevention of hymen rupture (local injection of 64 units of lydasa with 0,25% solution of Novocain). Curettage is performed after the parents content in a written form or that by close relatives and guardians. </li></ul>
  58. 58. <ul><li>Hemostasia of uterine bleedings in women at reproductive or climacteric age is performed by means of endometrial curettage with a a histologic study to follow. </li></ul><ul><li>Uterotonic means are also used : cold at the bottom of abdomen, oxytocin, water pepper tincture, nettle-brew/water. </li></ul><ul><li>Antianemic therapy : transfusion of blood and packed red cells, plasma, usage of iron preparations (fercoven, ferroplex, tardiferron, ferum-lec). Infusion therapy for improvement of rheologic properties of blood and normalization of water-electrolyte balance: stabizol, refortan, reopolyglukin, zhelatinol, saline isotonic solutions, 5-10% solution of glucose. </li></ul>
  59. 59. <ul><li>Hemostatics: 10% solution of calcium gluconate – 10 ml i/v or in tablets: 0,5g 3-4 times a day; 5% solution of apsilon-amino-kapron acid in the doze of 100 ml i/v or 2-3 g in powder 3 times a day; 1% solution of vicasol in the dosage of 3 ml i/m during 3 days; dicinon – 250 mg 3 times a day. </li></ul><ul><li>Vitamins and energizers: vitamin B12-200 mg a day i/m; vitamin B6-1 tabl (5 mg) 2-3 times a day or 1 ml 5% solution i/m; folic acid 1 tablet (1mg) 2-3 times a day, 5% solution of ascorbic acid 5-10 ml once a day i/v or 250 mg 2 times a day; rutin – 1 tablet (2 mg) 3 times a day; cocarboxylase 50 mg i/v or i/m; ATF- in the dosage of 2 ml i/m. </li></ul>
  60. 60. <ul><li>2 stage – hormone-therapy with the aim to suppress endometrium. </li></ul><ul><li>“ Clean” gestagens (EHP) treatment with pathogenetic grounds). The course of treatment lasts during 3-6 months from the 16-th until the 25-th day of menstrual cycle; from the 5-th until the 25-th day of MC or uninterrupted regime depending upon the woman’s age </li></ul><ul><li>norcolut, primolut-nor, norluten (noretisteron acitat)-5 mg from 16 to 25 day of the cycle </li></ul><ul><li>progesterone – 10 mg (1 ml 1% solution) i/m from 16 to 25 day of the cycle </li></ul><ul><li>17 OPC – 125 mg (1 ml 12,5% solution) i/m on the 14 th and 25 th days of the cycle. The course dosage 750-155 mg </li></ul><ul><li>Utrozhestan – 100 mg 2-3 times from 16-th day of MC during 10-14 days. </li></ul><ul><li>Dufaston – (didrogesteron) 10 mg once a day from 16-th till 25-th day MC. </li></ul><ul><li>Provera (medroksiprogesteron acetate) – 10 mg from 16 to 25 </li></ul><ul><li>Depo-provera – 200 mg i/m on the 14 and 21 day of MC </li></ul><ul><li>Depostat (gestonoron caproat) 200 mg i/m once a week </li></ul>
  61. 61. <ul><li>Agonists of gonadorealizeng hormone (for correction metabolic-endicrine disorders, CNS and vegetative nervous system normalization): </li></ul><ul><li>Gozerelin (zoladex) – 3,6 mg subcutaneously once every 28 days </li></ul><ul><li>Buserelin – 3,75 g once every 28 days </li></ul><ul><li>Buserelin spray nasal 900 mg a day every day </li></ul>
  62. 62. <ul><li>Indications for agonists GRH usage for women with EHP: </li></ul><ul><li>Simple atypical EHP in peri- and postmenopause; </li></ul><ul><li>Recurrence of simple atypical EHP at reproductive age after monotherapy with gestagens; </li></ul><ul><li>Atypical complex EHP at reproductive age and perimenopause; </li></ul><ul><li>Simple and complex EHP at reproductive age; </li></ul><ul><li>EHP in combination with leiomyoma of the uterus or adenomyosis </li></ul>
  63. 63. <ul><li>Agonists of GRH in combination with gestagens are administered for 3 months and if necessary (when atrophy of endometrium is absent at the control histological examination of endometrium after 3 months – long therapy) – for up to 6 months. In case endometrial atrophy is corroborated in 3 months then monotherapy with gestagens is administered for 3 further months. </li></ul>
  64. 64. <ul><li>Monophasic estrogen-gestagen preparations are administered at the dosage of 1 tablet from the 5-th to 25-th days of the cycle in women of reproductive age: </li></ul><ul><li>Rigevidon (0,15 mg levonorgestrel and 0.03 mg ethynilestradiol); </li></ul><ul><li>Marvelon (dezogestrel-0,15 mg ethynilestradiol – 0,03 mg); </li></ul><ul><li>Miniziston (0,125 mg levonorgestrel, 0,03 mg ethynilestradiol); </li></ul><ul><li>Femoden (ethynilestradiol-0,03 mg, gestoden – 0,075 mg); </li></ul><ul><li>Logest (0,02 mg ethynilestradiol and 0,075 mg gestoden); </li></ul><ul><li>Zhanin (0,03 mg ethynil-estradiol and 2 mg dienogest); </li></ul><ul><li>Anovlar (0,05 mg ethynilestradiol and 1 mg of noretisteron); </li></ul><ul><li>Non-ovlon (0,05 mg ethynilestradiol and 1 mg norestiron), unlike other monophasic COC, it is used beginning of the 16-th up to the 25-th days of the cycle. </li></ul>
  65. 65. <ul><li>Triphasic contraceptives are administered from the 1-th up to the 28-th days of the cycle in women of reproductive age: </li></ul><ul><li>Tricvilar (1 phase – 6 troches – 0,05 mg levonorgestrel, 0,03 mg ethynilestradiol; 2 phase – 5 troches – 0,075 mg levonorgestrel and 0,04 mg ethynilestradiol; 3 phase – 10 troches – 0,125 mg levonorgestrel and 0,03 mg ethynilestradiol); </li></ul><ul><li>Tristep (1 phase – 6 tabl. – 0,05 mg levonorgestrel and 0,05 mg ethynilestradiol; 3 phase – 10 tablets – 0,125 mg levonorgestrel and 0,04 mg ethynilestradiol); </li></ul><ul><li>Triziston (1 phase – 6 tablets, containing 0,05 mg levonorgestrel instead of gestagen, 0,03 mg ethynilestradiol as estrogen; 2 phase – 6 tablets – 0,075 mg of levonorgestrel and 0,04 mg of ethynilestradiol; 3 phase – 9 tablets – 0,125 mg of levonorgestrel and 0,03 mg ethynilestradiol. </li></ul>
  66. 66. <ul><li>III stage of treatment - optimization of hormonal status with the aim of hyperestrogenia prevention (recovery of biphase menstrual cycle in women of reproductive age and stable menopause in climatic period). </li></ul>
  67. 67. <ul><li>In young women : </li></ul><ul><li>1. Stimulation of ovulation with clomifen and chorionic gonadotropin: clomifen – 1 tabl (50 mg) from the 5-th to 9-th days of the cycle. Under the effect of clomifen numerous follicles simultaneously mature. </li></ul>
  68. 68. <ul><li>Chorionic gonadotropin is prescribed to intens absence of effect the dosage of clomifen can be 2 times enlarged (in the 2-th cycle) or 3 times (in the 3-th cycle) under the supervision of ovarian size (USE). At the beginning of ovulation against the background of hypoprogesteronemia gestagens are allowed to be prescribed in the 2 phase of the cycle for 10 days: pregnin – 0,02 g sublingually 2 times a day; noretisteron – (norcolut) – 0,005 g 2 times a day; orgametril (linestrenol) – 0,005 g in a day; progesterone – 1 ml of 2,5% solution i/m in a day for 5 days; 17-OPC – 1 ml of 12,5% solution i/m once; didrogesteron (dufaston) – 10-20g; utrozhestan – 200-300 mg a day two times ( 1 capsule in the morning 1 hour after breakfast; 1-2 capsules in the evening). The course of treatment – 6 cycles. </li></ul><ul><li>Control over ovarian hyperstimulation! </li></ul>
  69. 69. <ul><li>2. Stimulation of ovulation by fenobarbital: fenobarbital – 200 mg a day during 6 weeks with the following switch to 50 mg a day. </li></ul><ul><li>3. Stimulation of ovulation by means of FSH (gonal – F, menopausal gonadotropin, metrodin, urofollitropin), and chorionic gonadotropin (choriogonin, profasa, pregnil). Menopausal gonadotropin (metrodin, urofollitropin, gonal – F) is prescribed from the first days of the beginning of menstrual reaction in the dosage of 75 MU duringdotropin 7-12 days (USE control). In the absence of effect the dose is enlarged to150-225 MU. When the follicle is ripening (d-22-25 mm) ovulation and yellow body formation are being stimulated by chorionic gonadotropin: 10 000 MU of prophase on the 14-th day or 3 000 MU of choriogonin on the 12, 14, 16 days or 5 000 MU of pregnil on the 13-th or 15-th day. </li></ul>
  70. 70. <ul><li>4. Stimulation of ovulation by means of FSH or LH (pergonal, humegon, pergogrin) and chorionic gonadotropin (horiogonin, pregnil, prophase): pergonal, humegon (75 MU FSH and 75 MU LH) i/m in the dose of 1 ml from the beginning of menstrual reaction in the course of 7-12 days. Pergogrin (75 MU FSH and 35MU LH) – the same scheme. </li></ul><ul><li>When the follicle is growing mature the ovulation and yellow body formation are stimulated with chorionic gonadotrophin: 10 000 MU of prophase on the 14-th day or 3 000 MU of chorigonin on the 12-th, 14-th, 16-th days. </li></ul>
  71. 71. <ul><li>In climacteric period stopping of menstrual cycle is possible with preparations of male sex hormones: </li></ul><ul><li>Methyltestosteron: 10-15 mg a day during 3 month; </li></ul><ul><li>Testosterone propionat – 20-25 mg a day during 3 months; </li></ul><ul><li>Sustanon – 250 (omnadren- 250) 1 ml once a month during 3 months. </li></ul>
  72. 72. <ul><li>In the course of a long hormonal therapy it is reasonable to prescribe preparations which improve the function of liver, hyposensibilization means as well as vitamin therapy. </li></ul><ul><li>In case of ineffectiveness of conservative therapy of hyperplastic processes in endometrium there are indications for surgical treatment. By inatypical forms of EHP, especially in women of reproductive age, there are indications for hysteroscopic resection or ablation of endometrium, and by atypical forms – extirpation of uterus. </li></ul>
  73. 73. <ul><li>Indications for surgery for patients with EHP </li></ul><ul><li>1. In reproductive period: atypical complex EHP with no effect from conservative therapy during 3 months; simple atypical and complex inatypical EHP by ineffective therapy during 6 months. </li></ul><ul><li>2 . In climacteric period: complex atypical hyperplasia; simple atypical and complex inatypical EHP. </li></ul>
  74. 74. <ul><li>With the recurrence of polyps in endometrium there are indications for endoscopic surgery in the place of growth (at the peduncle of a polyp), and namely cryodestruction, lazervaporation or resectoscopy. </li></ul>
  75. 75. <ul><li>Ablation of endometrium </li></ul><ul><li>Patients without preliminary preparation undergo curettage or vacuum-aspiration of endometrium 3-5 days in advance before ablation. </li></ul><ul><li>The destruction of endometrium is performed hysteroscopically by means of high frequency current, making use of the effect of dissection, carbonization and drying. The dissection of tissues is performed due to the combination of thermoeffect and sparking incision. Due to the carbonization of tissues hemostasis takes place here. At the level of close contact of the electrode with the tissue there a drying process takes place with a crust formation, and in the underlying layers of the tissue – evaporation of intracellular liquid. </li></ul>
  76. 76. <ul><li>The technique of electrodestruction: coagulation of endometrium at the uterine fundus along the line connecting uterine openings of the oviduct, successive coagulation of posterior anterior uterine walls not reaching 1sm till the level of orificium internum uteri. </li></ul>
  77. 77. <ul><li>IV stage – successive dispensary supervision during 5 years after effective hormonal therapy and 6 months after surgery </li></ul>
  78. 78. THANK YOU!

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