{"paper_id":"1ea1d63b-6832-4a2c-94cf-17bde1d0982f","body_text":"Chapter 10\nCauses of Visiting Teenagers in the Pediatric and\nAdolescence Examining Room\nPanagiotis Tsikouras,\nTheodora-Eleftheria Deftereou, Anna Chalkidou,\nXanthoula Anthoulaki, Anastasia Bothou,\nBachar Manav, Zacharoula Koukouli,\nStefanos Zervoudis, George Iatrakis and\nGeorgios Galazios\nAdditional information is available at the end of the chapter\nhttp://dx.doi.org/10.5772/intechopen.72979\nProvisional chapter\n© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons  \nAttribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, \nand reproduction in any medium, provided the original work is properly cited. \nDOI: 10.5772/intechopen.72979\nCauses of Visiting Teenagers in the Pediatric and \nAdolescence Examining Room\nPanagiotis Tsikouras, Theodora-Eleftheria Deftereou, \nAnna Chalkidou, Xanthoula Anthoulaki, \nAnastasia Bothou, Bachar Manav, Zacharoula Koukouli, \nStefanos Zervoudis, George Iatrakis and \nGeorgios Galazios\nAdditional information is available at the end of the chapter\nAbstract\nAdolescence is the transitional period between childhood and adulthood. Depending on \nfemale gonads’ function and on hypothalamic-pituitary-ovarian axis activation, results \nin teenager’s body growth, in secondary sex characteristics’ development and finally in \ntheir reproductive potential. In adolescence, the negative feedback of gonadal steroids \non gonadotropins is disturbed. Teenagers presenting with dysfunctional bleedings are \nusually suspected of hemorrhagic ovarian cysts or endometriosis and require gyneco -\nlogic examination, evaluation, and hormone therapy. It is of great importance both for \nteenagers and their parents to understand that hormone therapy is the first line treatment \nfor bleeding disorders in these ages. A detailed medical history is necessary to determine \nthe appropriate treatment plan. Primary care includes the detection of adolescents with \nacute or chronic pelvic pain that may be associated with endometriosis or other patholo-\ngies like mullerian duct abnormalities, imperforate hymen, ovarian teratomas, ovarian \ntorsion, and vaginal absence or atresia. Mullerian duct abnormalities are associated with \nincreased rates of unexplained infertility, spontaneous abortions, and pathological con -\nditions of pregnancy. Specialists, should help teenagers in getting familiar to their bod -\nies, to their sexuality, inform them about the sexually transmitted diseases, and safety \noptions including vaccination and guide them in contraception issues.\nKeywords: adolescence, reasons for examination, menstrual disorders, contraception\n© 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative\nCommons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use,\ndistribution, and reproduction in any medium, provided the original work is properly cited.\n\n\n1. Introduction\nAdolescence is a period of rapid physical development triggering the simultaneous secretion of \nvarious growth hormones, sexual and thyroid hormones [1]. This period occurs in people aged \nbetween 10 and 19 years, in about 18% of the world’s population and this period between child-\nhood and adolescence, which causes physiological, psychological changes, and various other \nhealth problems and problems of menstruation, is of major importance [2]. During childhood \nand adolescence, it is necessary for the doctor to have appropriate behavior towards the young \ngirl and the parents when taking history and during gynecological examination. In general, it \nhas been found that all mothers co work to obtain information, but there is some mistrust and \nskepticism about gynecological examination. This mistrust largely subsides after discussions, \nin an appropriately configured practice environment, but in a small percentage it remains \naccompanied by fear and, even less, it turns into neglect in the gynecological examination. The \nusual reasons why young girls visit the teenage gynecology clinic are as following: amenor -\nrhea, dysfunctional bleeding, lower abdominal pain, to avoid pregnancy due to the presence \nand association to great problems, great early development of genital organs, breasts, hirsut-\nism, genital anatomy outgrowth, excretion from breast nipple, symptoms from the urethra or \nbowel, irritation and redness in the vulva, and pain or palpable lymph nodes in the vulva [3, 4].\n2. Amenorrhea\nThe main process that marks the start of adolescence is the onset of pulsatile excretion of \nGNRH. Breast growth (thelarche) is the first natural characteristic of puberty and occurs nor-\nmally in the 11th year whereas the menstrual is expected to be shown 1 year later. A range of \nvariations in the normal sequence of events among the different populations is observed. In \ngeneral, significant role plays the body weight and the nutritional balance [ 5, 6]. Typically, \nmenstruation begins after 2–3 years of thelarche at Tanner IV breast stage and rarely at Tanner \nIII stage. Approximately, 96–97% of adolescent women will have menstruation at the age of \n15 [6]. During the first year after menstruation, 50% of the cycles are anovulatory, also during \nthe next 2  years, the intervals between the menstrual cycles show wide variations ranging \nbetween 21 and 45  days. The classic definition of amenorrhea includes the absence of men -\nstruation after the 15th year. It is distinguished in primary with or without breast growth and \nsecondary. Amenorrhea in adolescence is a reasonable concern regarding the thorough inves-\ntigation in order to find the diagnosis and future fertility prognosis. Before the beginning of \nany hormonal therapy, it is necessary to exclude a certain number of pathological conditions \nin order to avoid a delayed diagnosis of all causes that in the mature reproductive age will be \ncharacterized as infertility [ 5]. In the case of primary amenorrhea without the development \nof secondary sex characteristics, the diagnosis can be made earlier, by the completion of the \n13th year and is indicative of hypogonadism [5, 7]. The occurrence of primary amenorrhea is \na disruption of the interaction of a large complex of processes that contribute to the appear -\nance and normal continuance of menstruation such as normal chromosomal composition, \nthe presence of a functioning hypothalamic-pituitary-ovarian axis, the normal endometrial \nFamily Planning186\n\nresponse, the anatomical integrity of the entire path of the output of the menstrual content, \nand sufficient supportive function of other endocrine glands such as thyroid gland and adre-\nnal glands. In the primary amenorrhea of adolescents, there is an increased probability that \nthe underlying pathology is the result of congenital malformations of the genital organs (60%) \nor endocrine disorders (40%). The most common causes of primary amenorrhea are normal \ndelay, important weight loss, intense exercise, and virginity hymen atresia.\n2.1. Clinical indications for investigation of amenorrhea in adolescence\nAbsence of menstruation at 15  years (complete development of the secondary sex character -\nistics) is an indication of amenorrhea investigation Absence of menstruation at 13  years with \nsimultaneous absence of secondary sex characteristics (non-start breast growth) (delayed \npuberty) should also be investigated [8–10]. Lastly, absence of menstruation at 14 years with \nsimultaneous coexistence of clinical disorders, such as nutritional disorders and clinical signs \nof hyperandrogenism needs further investigation.\nSecondary amenorrhea is characterized by the absence of menstruation for 6 months in teens \nwho previously had an unstable menstrual cycle for three or more consecutive cycles, in ado-\nlescents with a previous cycle of 21–45  days, and generally the interruption of menstruation \nsince it had previously begun [8–11]. The most frequent cause of secondary amenorrhea is the \npolycystic ovary syndrome (PCOS). The most common symptoms are infertility because of \nanovulation and hyperprolactinemia. Regardless of the type of amenorrhea, the presence of \nhypertrichosis and galactorrhea, the possibility of pregnancy, the pelvic pain as well as the \nhistory of sexual contacts should be thoroughly investigated. Other parameters to be inves -\ntigated also include height, body mass index, nutritional balance and estradiol, prolactin, \ntestosterone, AMH and FSH levels. The above investigation is considered really useful for the \ndiagnosis of underlying pathology and the distinction between hypogonadotropic hypogo -\nnadism (HH) and amenorrhea due to primary ovarian failure. At this point, hormone control \nplays an important role. Low levels of FSH, LH, and E2 are indicative of hypothalamic dam -\nage. High level of FSH and LH and low levels E2 are indicative of ovarian damage. High level \nof prolactin is indicative of prolactinoma [10–12].\nThe hypogonadotropic hypogonadism (HH) (hypothalamic amenorrhea) is accompanied by \nlow levels of FSH and E2 and can be hereditary or acquired, organic or functional. In primary \namenorrhea, the origin is usually genetic or even organic and the corresponding hypotha -\nlamic functional etiology is very rare [13–15]. In the last case, absence or delayed development \nof secondary sex characteristics is very helpful for the distinction. In the case of hypogonado-\ntropic hypogonadism, it is necessary to perform pituitary imaging to exclude or diagnose \nneoplastic pathology.\nIf the imaging test is negative, then hypogonadotropic hypogonadism may be congenital, func-\ntional, attributed to absorption disorders, or ultimately due to chronic underlying pathology \n(renal or hepatic failure) [ 13–15]. The congenital hypogonadotropic hypogonadism is statis -\ntically very rare. It may be appeared as independent pathological entity or associated with \npituitary insufficiency, either primary or as a demonstration of a syndrome. Independent HH \noccurs in 90% of cases with primary amenorrhea and is accompanied by absence or delayed \nCauses of Visiting Teenagers in the Pediatric and Adolescence Examining Room\nhttp://dx.doi.org/10.5772/intechopen.72979\n187\n\ndevelopment of secondary sex features [13–15]. The careful investigation of clinical signs and \nsymptoms such as anosmia or hypoxia when combined with congenital disorders in the palate \nor teeth is considered necessary because they may be manifestations of Kallman’syndrome. In \nthe case of hypoxia absence, some mutations that adversely affect the functioning of the hypo-\nthalamus may be responsible [14–16]. Moreover, some congenital HHs may be associated with \nother disorders of pituitary function and morphological abnormalities such as the presence of \nectopic pituitary tissue. Genetic mutations and polymorphisms are also involved in these cases.\nIn obese adolescents with amenorrhea, some rare genetic variations regarding the leptin gene \nor its receptor have been described. Finally, congenital HHs may be a part of various syn -\ndromes such as Prader Willi and Bardet-Biedl.\nThe functional hypothalamic amenorrhea is usually secondary. The abnormal background is \noften associated with nutritional disorders mainly related to lipid metabolism. This particular \npathological condition can be a part of a chronic pathological process or a severe emotional \nepisode that blocks the pulsatile secretion of GNRH.  The first priority in case of primary \namenorrhea with normal development of secondary sex features is the exclusion of pelvic \npain. That is the reason why it is widely recommended application of pelvic ultrasound as \nwell as hormone control (testosterone, estradiol, and FSH) [13–15].\nWhen pain is observed, the possible causes may be vaginal aplasia, presence of a transverse \ndiaphragm covering the vagina, and more often the virginity hymen atresia. In these cases, \nclinical examination of the abdominal wall reveals the existence of a painful mass that may \nbe caused by the distension of the endometrial cavity (hematometra). Presence of blood in \nthe vagina may also be seen. Ultrasound and MRI examinations always confirm the primary \ndiagnosis [13–15].\nWhen there is no pain, the possible diagnosis is uterine aplasia accompanied in many cases by \nvaginal aplasia as in Rokitansky syndrome. The incidence is very rare, 1/4000–1/5000 [13–15]. \nIt is a syndrome that reflects abnormal development of Muller’s ducts and sometimes abnor-\nmalities of the urinary tract, musculoskeletal as well as heart disorders are also observed. \nLevels of FSH, LH, estradiol, and testosterone hormones are normal. The ultrasound confirms \nthe absence of uterus [ 12–14]. Karyotype is always XX.  The differential diagnosis of uterine \naplasia includes androgen resistance syndrome, which is caused by mutations in testosterone \nreceptors, high plasma testosterone levels, and concomitant tubal aplasia as well as aplasia of \nthe upper part of the vagina. Karyotype in these cases is XY.\nIn the case of painless amenorrhea, with existing uterus confirmed by ultrasound and normal \nbreast growth, the most probable cause is polycystic ovary syndrome.\nFinally, according to a review of the American Reproductive Society, 40% of primary amenor-\nrhea is accompanied by the absence of secondary sex characteristics and high levels of gonad-\notropins, 30% are due to the absence of secondary sexual characteristics and low levels of \ngonadotropins and 30% are present with normal breast growth [17].\nSecondary amenorrhea is characterized by the absence of menstruation for a period of at least \n3 months in previously normally menstruating adolescents. In any case, the possibility of \npregnancy must first be excluded.\nFamily Planning188\n\nIt is also necessary to investigate the history of secondary sex characteristics develop -\nment, the nutritional balance, the psychological status, the weight ups and downs and the \nphysical fitness, or the presence of hyperandrogenic signs and the rapid increase of weight \nduring puberty. Special points are also hyperinsulinemia, galactorrhea-indicative sign of \nhyperprolactinemia, signs of hypercortisonemia, and black nozzle in the neck. Coexistence \nof hyperandrogenism is confirmed by elevated levels of total testosterone as well as of \n17-OH-progesterone. In cases that confirmed the lack of hyperandrogenic signs, proges -\nterone test, control of E2, prolactin, and FSH levels can be used for the determination of \ndiagnosis. Oligomenorrhea (less than 8  cycles during a year) undoubtedly raises the inter -\nest for further investigation. The most frequent causes of secondary amenorrhea are func -\ntional hypothalamic disorders and polycystic ovarian syndrome. Finally, the diagnostic plan \nshould always include the exclusion of less common causes that may also contribute to the \ndemonstration of oligomenorrhea [ 10–15].\n2.2. Therapy\nTherapy should be mainly based on the underlying cause. If any barrier exists to menstrual \nflow, surgery is inevitable. It is also necessary to surgically remove androgen-secreting tumors \nthat may be located either in the ovaries or in adrenal glands. Non -pharmaceutical hyper -\nprolactinemia should be treated by dopaminergic agonists. When amenorrhea is caused by \nfunctional hypothalamic etiology, the treatment should include changes in dietary habits and \npossible special psychological support. All other cases, except of Rokitansky and the andro -\ngen resistance syndrome where there is no hormonal disorder, require hormonal therapy.\nThe main target is either to restore estrogen deficiency or to prevent endometrial hyperplasia \nin cases of anovulatory cycles [10–16]. Replacement treatment also aims to prevent distressing \nconsequences such as osteoporosis and cardiovascular diseases.\nWhen primary amenorrhea is not accompanied by development of secondary sex charac -\nteristics, treatment initially includes the administration of small doses of estrogen to induce \npuberty onset. It is then required to progressively increase the above doses until satisfactory \nbreast growth is achieved. After the second year, it is recommended to add progestogen for \nat least 10 days/cycle.\nWhen amenorrhea is secondary with normal development of secondary sex characteristics, \nprogestogen is used to assess endogenous estrogen production. The positive test indicates \nadequate estrogen production and 10  days administration of progestogen allows the cycle’s \nnormalization. If the test is negative and there is also a need, treatment with contraception \ncan be administrated starting with a low dose. Basic condition is the absence of any familiar \nhistory of thromboembolic events. If contraception is not desired, then replacement therapy \nis administered. This includes 17β-estradiol either orally, as skin patch, or as gel for 25  days/\ncycle and progestogen 10–12 days/cycle. In case of hyperandrogenism in PCO syndrome, the \nadministration of acetate cyproterone at a dose of 50  mg/day is recommended for 21  days/\nmonth in combination with 17β-estradiol.\nThe presence of amenorrhea in adolescence should not be underestimated. It is advisable to \ninvestigate amenorrhea either after the 15th year or 3  years after breast growth has started. \nCauses of Visiting Teenagers in the Pediatric and Adolescence Examining Room\nhttp://dx.doi.org/10.5772/intechopen.72979\n189\n\nThe clinical examination always evaluates BMI, height, any hyperandrogenic, or galactor -\nrhea signs. Laboratory investigations include estradiol, hCG, FSH as well as testosterone, and \n17-OH progesterone levels.\nEarly diagnosis of genetic causes of hypogonadotropic hypogonadism occurs at <40%. The \nidentification of new genes may improve the scientific knowledge in the function of hypotha-\nlamic-pituitary-ovarian axis during puberty.\nIn the case of hypogonadism, long-term hormone replacement therapy is recommended and \nsometimes psychological support is also required.\n3. Polycystic ovary syndrome (PCOS)\nThe most frequent hormonal disorder in reproductive age’s women with oligo or anovula -\ntion and hyperandrogenemia is associated with PCOS in the majority of cases. Many factors \nsuch as psychological, social, and economic could play role in the disorder of the syndrome. \nMoreover, the association of PCOS with metabolic syndrome and its effects represent a new \nchallenge of interest of the syndromes in the general population. The major symptoms are:\na. Hyperandrogenemia or hyperandrogenism\nb. Oligo or anovulation\nc. Polycystic appearance of the ovaries during sonography [18, 19].\nIn PCOS, many symptoms included hirsutism, acne, alopecia, acanthosis nigricans, and obe -\nsity that are also linked to hyperinsulinemia [18–20]. One of seven teenagers (13%) has a major \nhealth problem because of obesity. Obesity is a major health problem affecting approximately \n13% of teenagers. Normal body mass index (BMI) values range from 19 to 24.9  kg/m2. Body \nmass index <19 kg/m2 characterizes underweight individuals. Body mass index ranging from \n25 to 29.9  kg/m2 characterizes overweight people, 30–40  kg/m2 characterizes obese people, \nand >40 kg/m2 characterizes severely obese individuals. Menstrual cycle disorders are related \nto obesity in childhood and in young women. As the abdominal adipose tissue increases, \nincrement of androgens aromatization is observed and subsequent endocrine abnormalities \nare appeared. Obesity is an independent factor aggravating PCOS endocrine abnormalities \nas subcutaneous abdominal tissue and liver contributes to extragonadal aromatization [ 21]. \nObese women with PCOS have two types of insulin resistance, one related to the syndrome \nand the other related to obesity. The pancreas is involved in the mechanism of insulin resis -\ntance by increasing the release of insulin, which leads to stabilization of the glucose level \nin the early stage of the disease [ 21]. During pregnancy, the morbitity is increased with an \nincrease in labor induction, urgent cesarean section, dystocia and abnormal presentation. The \nneonates are generally overweight and the risk for fetal death is increased. Moreover, diabe -\ntes during pregnancy is increased and needs follow-up. Recent data show an increased rate \nof overweight and obese women, specifically in the United States of the female population \n(64.1%) and obese women remain high (35.5%). In Europe, there is a diversity depending of \nthe countries: low rate (6.2%) in Western and Northern Europe, high rate in Central, East and \nSouth Europe (36.5%). Oral contraceptives are the major treatment of PCOS decreasing all the \nFamily Planning190\n\nclinical symptoms and the level of androgens. In obese adolescence, the oral contraceptive \npills have a different pharmacokinetic profile with a decrease of the estrogens and progesto -\ngen clearance, but in contrary an increased SHBG was observed [22–26].\nContraceptive pills constitute the cornerstone of hormone therapy, as they promote reduction \nof hyperandrogenemia, hirsutism, and acne [27].\nTherefore, there is a typical decreased effectiveness of contraceptive pills in obese adolescents, \ndespite there are superior to the contraception with condoms.\n3.1. Therapeutical strategy\nAny other known disorders, that they are possible to cause hyperandrogenemia and oligo \nor amenorrhea have to be excluded. These are often associated with: nutrition, exercise, \nmenstrual disorder treatment, metabolic syndrome and diabetes drug treatment and can be \ntreated by contraceptive pills having progestagen with antiandrogenic action, as cyproterone \nacetate, dienogest, drospirenone [28, 29].\n3.2. Functional uterine bleeding in adolescence\nIn adolescence, it is quite possible a disorder of negative regression of gonadotropins by \ngonadal steroids to be happened. The average age of menarche, based on recent data, has \nbeen reduced in developed as well as in developing countries over the last few decades and is \nattributed to various conditions, such as metabolic syndrome, eating disorders, gynecological \ncancer, and heart stroke diseases [30–33].\nDysfunctional bleeding is characterized by abnormal bleeding without functional impairment. \nIt is caused by ovarian dysfunction in 10% of the cases in women of reproductive. The inci -\ndence is 10–17% among adolescents and is mainly dependent on the immaturity of the hypo-\nthalamic-pituitary-ovarian axis. They are not attributable to structural damage of the genital \ntract. In addition, they are observed during all the years of reproductive age.\nIt constitutes an exclusionary diagnosis at the onset of reproductive age and it is anovulatory \nalmost in all cases (80–90%). The reason of the bleeding concludes the lack of cyclic secretion \nof progesterone resulting in continuous stimulation and endometrial hyperplasia of endog -\nenous estradiol. Throughout of this progress the endometrium is overpowered, its perfusion \ncapacities die resulting in necrosis, while in other places it continues to be repaired [34].\nThey are usually characterized as anovulatory cycles, even they can also be appeared in nor -\nmal cycles as well as they are almost the half of the total metrorrhagia cases.\nIn some cases, asymptomatic structural abnormalities also coexist, such as polyps and subse-\nrous or intramural fibroids. They usually do not affect the whole of the endometrium and are \noften of high intensity without excluding the possibility of remaining drooping for several \ndays. They are generally irregular with fluctuations in their intensity. It is quite often the first \nclinical manifestation of systemic hematological diseases especially in adolescents. The disor-\nders are limited just to one of the three phases of the hemostatic procedure. In thrombocyto -\npenia and von Willebrand’s disease, there is insufficient platelet clot formation (1st phase of \nhemostasis) resulting in metrorrhagia [9]. Menorrhagia may occur in the rare case of VIII, XIII, \nCauses of Visiting Teenagers in the Pediatric and Adolescence Examining Room\nhttp://dx.doi.org/10.5772/intechopen.72979\n191\n\nand fibrinogen deficiency (2nd phase of hemostasis), mutation of the M.T.H.F.R. (C677T) gene \n(LAME). In these cases, there is a lack of primary platelet clot and fibrin production. Finally, \nfibrinolysis (3rd phase of hemostasis) in endometrium can be also observed, especially in \ncases of unexplained or intense menorrhagia [9].\n4. Anovulatory cycles\nFemale genital hormone equilibrium disorders observed either in cases of hyperestrogenism \n(estrogen escape bleeding) or in cases of sudden subestrogenism (interruption of exogenous \nadministration – bilateral ovariectomy), or, finally, in cases of progesteronism (progester -\none bleeding bleeding-progesterone withdrawal contraceptive). Diagnosis is often raised \nby exclusions (malignant diseases, genital tract, PCO, and hypothyroidism liver cirrhosis). \nThe mechanisms involved in the pathophysiology of the above-mentioned bleeding cases \nare systemic in their nature, although it is possible to observe inadequacy of local hemo -\nstatic mechanisms resulting from the absence of cyclic production of progesterone and related \nendothelin-1, prostaglandins and other substances that contribute positively to local hemo -\nstasis of the endometrium [ 9]. Additionally, lack of ovulation causes unexpected bleeding, \nwhich adversely affects the quality of life of the patient. Functional hypothalamic or pituitary \ndisorders that cause suppression of gonadotropin production, anovulation, and the approach \nto perimenopausal age cause typical changes in the genital cycle.\nProgressively shorter cycles due to a gradual decrease in follicles and a corresponding fall in \novarian function lead to metrorrhagia [9].\n5. Insufficient follicular maturation\nIncreased FSH levels are associated with abnormal menstrual in duration and time. Impact \non adolescents is including 20–55% of the cycles in the first year and one-third of the cycles in \nthe third year after menstruation which are still anovulatory. Anabolism is the most common \ncause of dysfunctional hemorrhages in adolescence and indeed it can even lead to hospital \ncare [35]. This is due to functional immaturity of the hypothalamic-pituitary-ovarian axis.\nAdolescents whose menstruation appears before the 12th year of age have in 50% anovula -\ntory cycles during the first year, while those who are menopausal at the age of 12–13  years \nit is needed to pass a period of up to 3  years to make ovulation cycles. Hemorrhage due \nto hyperestrogenic cycles are usually characterized by histologically persistent produc -\ntive endometrium and hyperplasia caused by progesterone prolonged and progesterone \ndeficient estrogen mitotic activity [ 9]. The morphological changes in the endometrium are \nsimilar to those observed in women receiving estrogen replacement therapy. The origin of \nbleeding can be sought in the apoptosis of the layer accompanied by red blood cell extrava -\nsation, the formation of platelet thrombi and fibrin clots in the capillaries, and the existence \nof processes related to the reconstitution, including layer formation and hypertrophy of the \nregenerated epithelium. Morphological lesions are typically focal and located near or on the \nFamily Planning192\n\nsurface of the endometrium. In contrast, in cases of interruption of the E2/P relationship, \nthey are diffuse. The exact mechanism of tissue apoptosis in hyperestrogenic endometrium \nis unclear. The abnormal development of the endometrium includes additional qualitative \nand quantitative changes in microvascularization such as spiral arterial compression and \nvenous growth, which are often stretched, thus forming abnormal venous networks. Of par -\nticular interest is the fact that the process of neovascularization is inadequate in or near \nthe hemorrhage focal area while adjacent intact endometrium does not show an increase \nin microvascularization. The abnormal morphology of microvascularization accompanies \nor is the cause of endometrial hemostasis disorders. Because of the lack of the arachidonic \nacid precursor, prostaglandin production is inadequate. Prostaglandins cause more dilation \nthan contraction, and angiotensin-2 production is reduced. All of the above leads to the con -\nclusion that bleeding, in these cases, is caused by vascular density disorders accompanied \nby structural abnormalities leading to rupture or degradation of the microvascular system. \nThis process is followed by the release of lysosomal proteolytic enzymes from the epithe -\nlial and stromal cells and from endometrial migrating leukocytes and macrophages, while \ngranulocytes and activated NK cells secrete perforins. In addition, the ability of contraction \nof basal and myometrial vessels is inadequate or absent. All of the above changes contribute \nto the inadequate structure and layout and ultimately to the degradation of the capillary \nnetwork and constitute the major agents of extensive hemorrhage. Based on the above, the \nbest therapeutic results are obtained when the bleeding hypertrophic-hyperplastic endo -\nmetrium is excluded by performing suction biopsy or scraping. In these cases, an extensive \nstripping of the base layer is created followed by vasoconstriction of the arteries and arte -\nrioles as well as by tissue reconstruction. Functional hemorrhage due to progesteronism \nmanifests as escape bleeding in women taking progestogens or using contraceptive tablets. \nThe intensity, duration, and other features of these cases’ bleeding depend on: type, dose \nand duration of progestogen administration, the estrogen-progestogen relationship, endog -\nenous estradiol levels and the particular endometrial response to hormonal administration  \n[7, 9]. Endometrial histology in these cases is predominantly influenced by progesterone and \nranges between atrophy with or without cortical conversion of the layer and mixed appear -\nance of productive and secretory elements. The greater the dose and the duration of admin -\nistration, the more pronounced is the secretory type atrophy with a pronounced pro-stratum \ngland-layer relationship. In this case there is a corrugated endometrial layer especially in the \ninitial periods of use containing migratory lymphocytes and macrophages as well as granu -\nlar endometrial cells. All of the above lesions are associated with abnormalities of endome -\ntrial angiogenesis. These changes are accompanied by structural lesions and vasodilation \nleading to bleeding during the first months of use. The increased concentration of migratory \nleukocytes and other cells associated with immunity and the imbalance between metallo -\nproteinases (proteolytic MMP enzymes that cause an intrauterine extracellular matrix) and \ntheir inhibitors against them, cause even greater vasodilation [ 7, 9]. In conclusion, the devel-\nopment of an abnormal and fragile network of microvascular surfaces in combination with \nthe release of proteolytic enzymes and poor vasoconstriction due to reduced production of \nvasoconstrictors as a result of increased degradation by endopeptidase is the key factor in \nthe manifestation of the above functional bleeding. Fortunately, the continuation of contra -\nceptives decreases the frequency with the end result being usually observed only during the \nfirst 6–12 months of use.\nCauses of Visiting Teenagers in the Pediatric and Adolescence Examining Room\nhttp://dx.doi.org/10.5772/intechopen.72979\n193\n\n6. Ovulatory cycles\nThey are related to disorders or inadequacy of local hemostasis mechanisms and decreased \nspiral arteriolar density. Endometrial histology varies from productive and secretory to \nmenstrual, and the changes are not different from the corresponding premenstrual women \nwith normal cycles. There is an increased blood flow to the endometrium whereas the lev -\nels of circulating ovarian steroids are normal. The endometrial prostaglandin production \nis increased with a priority to vasodilator PGF2a and angiopathic PGE2 types. Prolonged \nvasodilation leads to decreased platelet aggregation and increased overexpression of \npotential parathyroid-related vasodilatory protein. High proteolytic activity of lysosomal \nenzymes in the endometrium as well as fibrinolysis through increased local secretion of \nagents with heparin analog activity. The mechanism that triggers all these disorders is pres -\nent unknown [ 9, 35].\n6.1. Diagnostic approach\nHistory, gynecological examination, laboratory test such as blood generation, coagulation factors, \nβhCG, ultrasound through genital organs, parthenoscopy, magnetic resonance, and laparoscopy.\n6.2. Treatment\nAdolescent medium degree functional disorders of uterus: Hb  > 9gr cyclic providing of \nprogesterones, contraceptive pills, and iron preparations. In cases of Hb  < 9gr, intravenous \nhydration, blood transfusion, high dosage of contraceptive pills per os, potential intravenous \nproviding available estrogens continuing usage of contraceptive pills, and iron preparations.\nActivity of the estrogen-progesterinoides agents in haemostasis led to:  increasing of TXA2, \nplatelet agglutination, prothrombin, Factors VIII and X,  r eduction of fibronolysis, PGI 2 in \nendometrium.\n7. Adolescent functional disorders of uterus\nMetrorrhagia is a symptom, not a specific disease entity. The effectiveness of treatment is \nbased on proper diagnosis. It is very important to establish the stabilization of ovulation \ncycles. Therapeutic intervention always takes seriously the young of the age [36, 37].\n8. Dysmenorrhea\nIt is a Greek word that has prevailed in the international bibliography as painful menstrual \nbleeding 2–3 years after menstruation with onset of ovulation. Frequent disturbance of ado-\nlescence ED has primary—no organic damage to the pelvis and secondary—painful ER due to \npelvic conditions such as endometriosis, pelvic inflammation, and congenital abnormalities \nof the genital system [38, 39].\nFamily Planning194\n\n9. Explanatory theories\nTheory of Hippocrates: Cervical lumen stenosis and the induced posture of stomach blood are \nresponsible for the occurrence of dysmenorrhea. Myometric factor: increased myometrial activ-\nity and increased endometrial pressure. Neuromic factors: changing neuromuscular activity \nin the uterus after pregnancy may explain the reduction in menstruation pain after childbirth.\n• Hormonal effect: women with anorexic cycles do not show painful menstruation.\n• Prostaglandins: high levels of PGs are currently the most accepted causal theory\nIncreased levels of PGF2a and PGE2 and increased PGF2a/PGE2 ratio are observed in ado -\nlescents with PD.  Also increased levels of LTC4, LTD4, and LTE4 angiotensins, stimulation \nof myometrial contractility, and increase in plasma hormone concentrations in women with \ndysmenorrhea [38, 39].\n9.1. Psychological factors\nSubjectivity and fluctuation of the pain, dysmenorrhoea very often presented in family \nhistory.\n9.2. Clinical features of dysmenorrhea\nSubabdominal pain, nausea, vomiting, diarrhea, irritability, headache, flatulence payment of \nforces, depression, and inability to concentrate are clinical features of dysmenorrhea.\n9.3. Treatment of dysmenorrhea\nPGs synthetase inhibitors, non-steroidal anti-inflammatory agents act by lowering levels of PGs \nby reducing levels of PGs, tolfenamic acid, naproxen, and mefenamic acid. The release of PGs \ninto the menstruation blood is maximal in the first 48–72  hours of EGFR. Contraceptive pills \nreduce the amount of menstruation blood, through the controlled increase of the thickness of \nendometrial tissue. By inhibiting of ovulation, an endocrine environment with low levels of \nPGs is maintained.\nOther therapeutic proposals are spasmolytics, analgesics, calcium inhibitors, progesterone, \nmagnesium, GnRH analogues, leukotriene antagonists, cervical curettage, acupuncture, elec-\ntricity stimulation, and psychotherapeutic methods [39, 40].\n9.4. Pelvic pain\nPrimary care of the gynecologist specialized in child and adolescent gynecology is the inves-\ntigation of women with chronic pelvic pain. The rate of disease varies among teenagers \nbetween rarity and 19–47% [ 41, 42]. Typical forms of chronic pelvic pain are relatively com -\nmon and non-recognition may underestimate their incidence. Mostly have primary second -\nary dyspnea and dysmenorrheal. In girls, the gynecological examination is not feasible and \nthe rectal examination provides little information. The ultrasound provides information on a \nCauses of Visiting Teenagers in the Pediatric and Adolescence Examining Room\nhttp://dx.doi.org/10.5772/intechopen.72979\n195\n\npossible chocolate cyst, hematosalpinx, and free fluid in the Douglas space. In non-response \nto NSAID medication, MRI and laparoscopic approaches are recommended with a detection \nrate in the specific cases of endometriosis approaching approximately 50%. Endometriosis \nsymptoms in this age group are not specific, not related to adults, but gives continuous pain \nand a normal menstrual cycle. Atypical forms of endometriosis are more common in teenag -\ners and their non-recognition may underestimate their frequency [43–45].\nPrimary care is the detection of adolescents with chronic pelvic pain experienced by endometriosis \nor other pathology. Irritable bowel syndrome is a common bowel dysfunction without attributing \nto specific etiology. It is characterized by recurrent chronic abdominal and pelvic pain combined \nwith bowel dysfunction either as diarrhea or constipation. It is found in 50–80% of women with \nchronic pelvic pain and diagnostic criteria are proposed for diagnosis criteria against Rome ii.\nAnother cause of pelvic pain is congenital abnormalities of the genital system. Clinical symp-\ntoms are amenorrhea, metrorrhagia, dysmenorrhea, endometriosis, repetitive abortions, in \ncases of pregnancy, abnormal position and presentation of fetus, and premature birth [43–45]. \nTreatment of abdominal pain is a challenge for the specialized gynecologist especially when \nan exact diagnosis has not been made. Particularly in these young people, there is a major \nharmonic relationship between a young doctor and his/her parents in order to find an organic \ncause of the reported symptomatology or in cases where there is no finding of a treatment \nanalogous to the subjective cause [43, 44].\n10. Contraceptive methods\nThe purpose of contraception is to prevent fertilization of the ovum from the sperm or to prevent \nimplantation of the fertilized egg in the uterus. There are many methods of contraception for every-\none to be educated. The ideal method of contraception attaches to the prevention of an unwanted \npregnancy but also protects against sexually transmitted diseases. Of approximately, 3 million \nunwanted pregnancies that occur in the United States, 54% of these do not use contraception.\n10.1. Contraceptive methods\nNatural methods: withdrawal method (coitus interruptus) of approximately 57% is used in \nadolescent women with a failure rate of about 22% and lack of protection against sexually \ntransmitted diseases.\n1. Reversible (small time action) [46–49].\n• Men’s condoms\n• Hormonal methods (contraceptive tablets, vaginal ring, transdermal patches)\n• Other methods (contraceptive diaphragm, cervical cap)\n2. Reversible (long time action) [46–49].\n• Intrauterine device \n• Implants\nFamily Planning196\n\n3. Irreversible\n• Tubal ligation\n• Seminal duct ligation\n4. Emergency contraception\n• Levonorgestrel\n• Ulipristal acetate [46–49].\n11. Contraceptive pills\nIt is a complex issue that causes family embarrassment to healthcare professionals in govern-\nment officials in civil servants and young people themselves. There has been extensive effort \nto increase the use of contraceptive methods and in particular the condom to avoid pregnan-\ncies and sexual transmitted diseases.\nDefinitely it is necessary to set up Family Planning Centers for Teenagers, which must become a \npriority for each government. Basic award principle for contraceptive pills, as long as necessary, as \nlittle as possible [50]. Contraceptive capacity of contraceptive pills is estimated by the Pearl Index \n(Pearl Index). All formulations with combined oral hormonal contraception have Pearl index ≤1.25 \nwomen (years). There are several differences regarding the hormonal components contained in \neach formulation which may vary depending on the type, composition, quantity, and number \nof active tablets. Single-phase formulations contain active tablets with the same constant amount \nof estrogen and progestogen ratio. In contrast, the above ratio changed in the multiphase pills. \nBiphasic have two different combinations, the three phase and recently there are also four phases \nwith successive decrease in the estrogen ratio and corresponding increase in the progestogen ratio. \nContraceptive pills have not been associated with weight gain and mood changes. It is recom-\nmended to take single-phase pills in teenagers for their menstrual bleeding disorders [51–55].\nContraindications of contraceptive pills are BP ≥160/100 mmHg, liver disease, migraines with \nfocal neurological symptoms, diabetes, nephropathy, neuropathy, retinopathy, or angiopathy \ncomplications are also included.\nHistory of thromboembolism (particularly with third generation pills with drospirenone), \nthrombophilia, factor V Leiden mutation, factor II mutation (G20210A allele), antiphospho -\nlipid antibodies, protein C deficiency, protein S deficiency, antithrombin III deficiency, undiag-\nnosed vaginal bleeding, and estrogen-dependent breast cancer compromise contraindications \nfor contraceptive pills. Smoking is a relative contraindication for the use. According to FDA \n(April 2012), revision of contraceptive pills guidelines with drospirenone increases three times \nthe risk of thrombosis compared to other progestogens. Clots are caused by contained estrogen.\n11.1. Impact of thrombophilia\n• Total population: 1 per 10,000 woman years per year.\n• Contraceptive pills: 4 per 10,000 woman years per year.\n• Pregnancy: 10–20 per 10,000 woman years per year [56].\nCauses of Visiting Teenagers in the Pediatric and Adolescence Examining Room\nhttp://dx.doi.org/10.5772/intechopen.72979\n197\n\n11.2. Positive actions\nCirculation disorders such as hypermenorrhea, hypomenorrhea, metrorrhagia restoring a \nnormal menstrual cycle, and prolong the menstrual cycle. Dysmenorrhea decreases through \nthe action of prostaglandin synthesis. They also improve the presence of premenstrual syn -\ndrome, premenstrual edema, irritability, anxiety, and depression.\nOvary cancer risk is decreased by about 20% per 5 years of use and 50% for 15 years.\nThere is no protective action for mucosal ovarian cancer. They decrease the risk of endome -\ntrium cancer by 50% every 4 years of use and 70% after 12 years. Cancer of cervix represents \nan independent factor with a relative risk probably due to co-factors (HPV, intercourse with-\nout condoms). According to the WHO, there is a slight increase in the relative risk for users \nof contraceptive pills over a period of >4 years. Higher relative risk is increased for users over \n10 years. The above may be affected by the use of non-barrier methods by the number of sex \npartners by multiparity and alcohol consumption.\nIt is believed that hormonal contraception, especially estrogen as mitotic agents, enhances neo-\nplastic process particularly in women with HPV infection. Estrogenic probably affects specific \nDNA sequences.\nAdditionally, there is a direct interaction between estrogen receptors and HPV E6 and E7 \nprotein. The problem of the possible relationship between breast cancer and hormone therapy \nis still largely unresolved.\nThe results that are available now suggest that relatively short-term treatment (less than \n5 years) does not increase the risk.\nFor a treatment with longer duration, the existing results based primarily on estrogen mono-\ntherapy do not allow clear conclusions without excluding the possibility that the frequency \ncould increase under these conditions. It is difficult to evaluate the role of progestogen added \nto the above treatment. So, it is preferable to utilize steroid hormones with anti-mitotic activ-\nity. It is known that hydroxyprogesterone derivatives such as medroxyprogesterone acetate \ncan inhibit tumor growth activities.\nThere are indications that use of contraceptive pills over a period of 10 years can cause a mod-\nerate increase of the relative risk (24%) to the oncogenic progression for breast cancer . With \ndiscontinuation, this risk decreases to 0% in 10 years. It is also gained ground the aspect that \nthis risk is greater in women with a family history, with the risk of being limited to second \ndegree relatives. It is unlikely, however, to incriminate only estrogen because of the fact that \nthere are minimal estrogen receptors in normal breast epithelial cells.\nThe progesterone may promote the mitotic process and cause atypia. It is known that the \nmitotic action on MCF-7 cells of human breast cancer of 19 nor-progestogen (norethindrone, \ngestodene, and 3-ketodesogestrel) [56–60].\nIn conclusion, progestogen should be emphasized that any attempt to adapt to the clinical \npractice of the experimental anti-mitotic action of a pregestogen should be done very care -\nfully. Only well-tested prospective clinical trials may answer the question whether the protec-\ntive effect found in the laboratory has the potential clinical application.\nFamily Planning198\n\nContraceptive pills advantages include ovarian cysts treatment, endometriosis, dysmenor -\nrhea, dyspareunia, metrorrhagia, acne and decreased androgen synthesis, hirsutismus, spe -\ncific activity of estrogen and antiandrogens, mastodynia, symptom reduction mastopathy, \nreduction of benign mastopathy, and bone increase density [60, 61].\nWhat do women think about birth control pills from our own child and adolescent gynecol -\nogy center housed in the Democritus University Family Planning Laboratory. Positive effects: \npositive effect on sexual life, reliability, easy to use/comfort, less bleeding, regulation of men-\nstruation, and less painful periods.\nNegative effects: nausea, headaches, changes in mood, feeling of tension on the breasts, and \nincrease of weight.\n11.3. Action mechanism of contraceptive pills\n• Suspension of implantation\n• Ovulation inhibition\n• Thickening of cervical mucus\n• Sperm motility disorder [62, 63].\nOral contraceptive pills (OCPs) perform their action through a variety of mechanisms, through \nthe inhibition of the mesocyclic peak of gonadotropin secretion resulting in the suppression \nof ovulation.\nContraceptive action is mainly exercised through the progesterone of OCPs, which cause ovu-\nlation suppression by multiple mechanisms:\n• ↓ Luteinizing hormone (LH).\n• The thickening of the cervical mucus and ↓ of the sperm penetration.\n• ↓ of fertilization capacity of the semen, the disturbance of normal motility and occlusion of \nthe fallopian tubes.\n• Obstruction of implantation due to endometrial perforation [62, 63].\nEstrogens exert their contraceptive action, but they are dose-dependent, by inhibiting the \nsecretion of gonadotropins (FSH and LH), cause the uterus to change its secretory capacity of \nthe cellular structure of the endometrium.\nThere are several differences regarding the hormonal components contained in each formu -\nlation which may vary depending on the type, composition, quantity, and number of active \ntablets. Single-phase formulations contain active tablets with the same constant amount and \nestrogen and progestogen ratios. In contrast to multiphase, the above ratio changes of bipha-\nsic have two different combinations, the three phase have three and recently, there are also \nfour phases with successive reductions in the estrogen ratio and a corresponding increase in \nthe progesterone ratio [62, 63].\nCauses of Visiting Teenagers in the Pediatric and Adolescence Examining Room\nhttp://dx.doi.org/10.5772/intechopen.72979\n199\n\nWith regard to the first few generations because the dosage did not decrease at the appro -\npriate time, side effects such as unwanted bleeding or spotting often occurred. The second \ngeneration was more effective and longer half-life, but with increased androgenic action that \nhelped to sexual desire, however, it could lead to hypertrichosis, acne, and dyslipidemia. The \nthird generation retains the effectiveness of the progestogen while reducing its androgenic \neffect. Smaller androgenic effect also makes estrogen more effective. This however entails a \ngreater risk for thromboembolic events [62, 63].\n11.4. 4th generation contraceptive pills\nThe widespread use of a combination of estrogen and progesterone as a contraceptive or \nhormone replacement therapy has made it possible to complete large epidemiological studies \nthat have made it possible to assess the benefits and risks that may have arisen.\nAmong the major advantages of use, are included primarily the reduced incidence of endo -\nmetrium cancer, attributed mainly to the antimitotic progesterone activity, and secondly, the \nreduced frequency of ovaries cancer, due anti-gonadotropic action combination [62, 63].\n11.5. Contraceptive vaginal ring\nIt releases daily and for 21  days 120 μg of etonogestrel and 15  μg of ethinylestradiol (nesto -\nrone ring study 15–20 μg EU  + 150–200 μg nestorone).\nIt remains in place for 3 weeks and the fourth week it is removed for bleeding to escape. It is \npossible to be removed during sexual intercourse.\nExisting progesterone: etonogestrel (3-keto desogestrel) 19-nortestosterone derivative.\nNestorone belongs to the norprogesterone family and is weakly active by oral administration. It \ndoes not bind significantly neither to the androgen receptor, nor to the estrogen receptor. It is a \nflexible, transparent silicone ring. It secrets daily 15 μg ethinylestradiol and 120 μg etonogestrel. \nIts diameter is 53 mm with cross section 4 mm. The duration of usage is 1 month, 3 weeks/1 week.\nIt is direct start fitting and has possibility to maintain up to 35  days. The next placement can \nbe without delay. There is less interruption for a shorter duration of menstruation. Tampons, \nspermicide nonoxynol-9, or intravaginal miconazole should not to be used at the same time. \nIt can be removed in less than 3 hours. It does not affect in sexual contact.\nIt causes breast tenderness, headaches and nausea, spotting, vaginal intolerance or hyperse -\ncretion, and unconceivable loss or misuse. There are no studies evaluating its effect on ado -\nlescent bones. There is no evidence of VTE in relation to low-dose OCPs. Ease of use has not \ndemonstrated increased compliance or prolonged use (<30% in 6 months) [64, 65].\n11.6. Evra patch contraceptives\nThey release EE 600 μg with norelgestromin 6 mg. They remain placed for 7 days for 3 consecu-\ntive weeks followed by 1 week without patch. It is a useful alternative method for women who \nhardly remember daily taking the pill because if they forget there is a 2  day error margin. It \nshould be avoided when weight greater than 90 kg. The increased exposure to estrogen compared \nto oral contraceptive pills creates 1.6 and 1.2–2.2 higher probability of deep thrombosis [65, 66].\nFamily Planning200\n\n11.7. Implants\nThey modify cervical mucus (viscosity in reduced amount) prevent sperm penetration and \nsuppress endometrial growth which becomes inappropriate for implantation.\nIt is an ideal contraceptive method for teenagers who do not want to deal with contraception \noften [65].\n11.8. Injectable contraceptive preparations\nInjectable contraceptive preparations medroxyprogesterone acetate depot, intramuscular \nprotection 3 months with efficacy 99.7%.\nMonthly combined contraceptives estradiol cypionate and medroxy progesterone acetate \ndepot, valerian estradiol, and norethrone acetate.\nThey improve dysmenorrhea increase the risk of thromboembolic events and may cause men-\nstrual disorders [65].\n11.9. Transdermal contraceptive patches evra\nTransdermal contraceptive patches evra release ethinyl estradiol 600  μg with norelgestro -\nmin 6 mg. They remain placed for 7  days for 3 consecutive weeks followed by 1 week with -\nout patch it is a useful alternative for women who hardly remember daily taking the tablet \nbecause if they forget there is a 2  day error margin. They should be avoided when weight of \nthe woman is greater than 90 kg. There is an increased exposure to estrogen compared to oral \ncontraceptive pills 1.6 and 1.2–2.2 with higher probability of deep vein thrombosis [65, 66].\n11.10. Subdermal implants\nThey modify cervical mucus (viscosity in a reduced amount), prevent sperm penetration, and \nsuppress endometrial growth which becomes inappropriate for implantation. It is an ideal \ncontraceptive method for teenagers who do not want to deal with contraception often [65].\n11.11. Injectable progestogens\nInjectable progestogens contain depot medroxyprogesterone acetate, intramuscular site of \ninjection and they offer protection for 3 months with efficacy 99.7%.\nCombined oral contraceptive pills estradiol cypionate and depot medroxyprogesterone acetate, \nvalerian estradiol, and norethrone acetate.\nThey improve dysmenorrhea, increase the risk of thromboembolic events, and may cause \nmenstrual disorders [67].\n11.11.1. Barrier methods\n• Male condoms.\n• Female condoms.\nCauses of Visiting Teenagers in the Pediatric and Adolescence Examining Room\nhttp://dx.doi.org/10.5772/intechopen.72979\n201\n\n• Sponge.\n• Diaphragm.\n• Birth control rings.\n• Spermicides.\nFrom contraceptive barrier methods, the most widespread, economic, easy to use, well \naccepted by both partners, with the greatest contraceptive success and the greatest protection \nagainst sexually transmitted diseases is the male condom, 75% of adolescents report using a \ncondom with a failure rate of 18% [68].\n11.12. Intrauterine contraception\nCopper intrauterine device is the most effective reversible method of contraception in terms \nof cost-effectiveness which is the first method of contraception with a coil used in the world.\nMirena, which was released in 1997, is a type of intrauterine device with levonorgestrel that \ncontains 52 mg levonorgestrel and yields 20 μg/24  h for 5 years.\nThey can cause amenorrhea or oligomenorrhea.\n11.13. Innovations\nForming new IUD with less levonorgestrel that will be easily applied to nulliparous women \n(Femilis and Femilis slim) are under construction and they are another IUD without side \narms, for easy adjustment to various sizes of uterus IUD (SPRM) (ulipristol).\nAims of intrauterine devices:\n• Contraception.\n• Menorrhagia.\n• Endometrial protection.\n11.14. Side effects\nThe use of IUD can cause tempοrarily edema, headache, tenderness, depression and breast \ntenderness, acne or other skin lesions. There are may also be appeared: abdominal pain in \nthe lower part of the abdomen, vaginal discharge, nausea, functional ovarian cysts and rarely \nspotting, especially in the first months [69].\n11.15. Mirena\nMirena is an intrauterine device effective in relation to the main indication of its usage which \nis contraception. It could be also used as a reliable therapeutic method of menorrhagia. In \nmany cases, reduce dysmenorrhea. It reduces the risk of pelvic inflammatory disease and \nectopic pregnancies.\nFamily Planning202\n\nFinally, it protects woman in perimenopausal and postmenopausal periods who are under \nhormonal replacement therapy with estrogens from endometrial hyperplasia indicated in \npuerperium.\nContraindications conclude pelvic inflammatory disease. HIV and immunosuppressant are \nnot contraindications. Risk of expulsion in women of reproductive age is 3–5% and in ado -\nlescents 5–22%.\n12. Conclusion\nFrom the above mentioned, we conclude that with the preventative gynecological control in \nfemales of young age, a prompt diagnosis and appropriate treatment, in particular congenital \nabnormalities of the genitals and investigation of clinical symptoms of these individuals, can \nbe made.\nEarly diagnosis and treatment of ovarian tumors despite their small incidence of genital can-\ncers up to 18 years of age is of major clinical importance because they are not always accom -\npanied by a characteristic clinical picture.\nAcknowledgements\nMany thanks to Professor Efthimios Deligeoroglou , Head of the Division of Pediatric —\nAdolescent Gynecology and Reconstructive Surgery, Cherman of 2 nd Department of  \nObstetrics and Gynecology — Medical school, University of Athens, Aretaieion Hospital,  \nGreece for his scientific support due to his great experience and knowenlege in this area. \nMany thanks to midwives (Mrs Maria Strofali and Mrs Stavroula Falaga)  of family plan -\nning center, Democritus University of Thrace, Greece for their clinical support and examina -\ntion of teenagers.\nAuthor details\nPanagiotis Tsikouras1*, Theodora-Eleftheria Deftereou1, Anna Chalkidou1, \nXanthoula Anthoulaki1, Anastasia Bothou2, Bachar Manav1, Zacharoula Koukouli1, \nStefanos Zervoudis2,3, George Iatrakis3 and Georgios Galazios1\n*Address all correspondence to: ptsikour@med.duth.gr\n1 Department of Obstetrics and Gynecology, Democritus University of Thrace, Greece\n2 Department of Obstetrics and Mastology, Rea Hospital, Athens, Greece\n3 Technological Educational Institute of Athens, Department of Midwifery, Athens, Greece\nCauses of Visiting Teenagers in the Pediatric and Adolescence Examining Room\nhttp://dx.doi.org/10.5772/intechopen.72979\n203\n\nReferences\n[1] Al-Sahab B, Ardern CI, Hamadeh MJ, Tamim H. Age at menarche and current substance \nuse among Canadian adolescent girls: Results of a cross-sectional study. BMC Public \nHealth. 2012 Mar 16;12:195. DOI: 10.1186/1471-2458-12-195\n[2] Chan SS, Yiu KW, Yuen PM, Sahota DS, Chung TK.  Menstrual problems and health-\nseeking behaviour in Hong Kong Chinese girls. Hong Kong Medical Journal. 2009 \nFeb;15:18-23\n[3] Cavanaugh RM Jr. Screening adolescent gynecology in the pediatrician's office: Have a \nlisten, take a look. Pediatrics in Review. 2007 Sep;28:b332-b342\n[4] Tsikouras P, Dafopoulos A, Trypsianis G, Vrachnis N, Bouchlariotou S, Liatsikos SA, \nDafopoulos K, Maroulis G, Galazios G, Teichmann AT, Von Tempelhoff GF. Pregnancies \nand their obstetric outcome in two selected age groups of teenage women in Greece. The \nJournal of Maternal-Fetal & Neonatal Medicine. 2012 Sep; 25:1606-1611. DOI: 10.3109/  \n14767058.2011.648242\n[5] Duranteau L.  Adolescent amenorrhea. Journal de Pediatrie et de Puericulture. 2013;  \n26:308-321\n[6] Basak S, Prakash A. Obstetrics gynecology and reproductive. Medicine. 2013:23364-23369\n[7] Balen AH, Morley LC, Misso M, Franks S, Legro RS, Wijeyaratne CN, Stener-Victorin E, \nFauser BC, Norman RJ, Teede H. The management of anovulatory infertility in women \nwith polycystic ovary syndrome: An analysis of the evidence to support the develop -\nment of global WHO guidance. Human Reproduction Update. 2016 Nov;22:687-708\n[8] Practice Committee of American Society for Reproductive Medicine. Fertility and Sterility. \n2008 Nov;90(5 Supple):219-225\n[9] Deligeoroglou E, Creatsas G.  Menstrual disorders.  Endocrine Development.  2012;22: \n160-170. DOI: 1159/000331697. Epub 2012 Jul 25\n[10] Deligeoroglou E, Athanasopoulos N, Tsimaris P, Dimopoulos KD, Vrachnis N, Creatsas \nG. Evaluation and management of adolescent amenorrhea. Annals of the New  York \nAcademy of Sciences. 2010 Sep;1205:23-32. DOI: 10.1111/j.1749-6632.2010.05669.x\n[11] Bothou A, Koutlaki N, Iatrakis G, Mastorakos G, Tsikouras P, Liberis V, Galazios G, \nLiberis A, Lykeridou A, Zervoudis S.  Antimullerian hormone as indicator of ovarian \ndysfunction. Acta Endocrinologica (Buc). 2017;XIII(2):237-245\n[12] Tsimaris P, Vrachnis N, Iliodromiti Z, Deligeoroglou E.  Long-term followup of adoles -\ncent and young adult females with hypergonadotropic hypogonadism. International \nJournal of Endocrinology. 2012; 2012:862892. DOI: 10.1155/2012/862892. Epub 2011 \nDec 10. Erratum in: Int J Endocrinol. 2012;2012:680569. Pantelis, Tsimaris [corrected to \nTsimaris, Pantelis]; Nikolaos, Vrachnis [corrected to Vrachnis, Nikolaos]; Zoe, Iliodromiti \n[corrected to Iliodromiti, Zoe]; Efthymios, Deligeoroglou [corrected to Deligeoroglou]\nFamily Planning204\n\n[13] Meczekalski B, Podfigurna-Stopa A, Warenik-Szymankiewicz A, Genazzani AR. Functional \nhypothalamic amenorrhea: Current view on neuroendocrine aberrations. Gynecological \nEndocrinology. 2008 Jan;24:4-11. DOI: 10.1080/09513590701807381\n[14] Vescovi JD, Jamal SA, De Souza MJ. Strategies to reverse bone loss in women with func-\ntional hypothalamic amenorrhea: A systematic review of the literature. Osteoporosis \nInternational. 2008 Apr;19:465-478. DOI: 10.1007/s00198-007-0518-6 Epub 2008 Jan 8\n[15] Jayasinghe Y, Grover SR, Zacharin M. Current concepts in bone and reproductive health \nin adolescents with anorexia nervosa. BJOG : An International Journal of Obstetrics and \nGynaecology. 2008 Feb;115:304-315. DOI: 10.1111/j.1471-0528.2007.01601.x\n[16] Deligeoroglou E, Tsimaris P, Deliveliotou A, Christopoulos P, Creatsas G. Menstrual dis-\norders during adolescence. Pediatric Endocrinology Reviews. 2006 Jan;3(Suppl 1):150-159\n[17] Vescovi JD, Scheid JL, Hontscharuk R, De Souza MJ. Cognitive dietary restraint: Impact \non bone, menstrual and metabolic status in young women. Physiology & Behavior. 2008 \nSep 3;95:48-55. DOI: 10.1016/j.physbeh. 2008.04.003\n[18] Carmina E, Rosato F, Jannì A, Rizzo M, Longo RA. Extensive clinical experience: Relative \nprevalence of different androgen excess disorders in 950 women referred because of \nclinical hyperandrogenism. The Journal of Clinical Endocrinology and Metabolism. 2006 \nJan;91:2-6\n[19] Silfen ME, Denburg MR, Manibo AM, Lobo AR, Jaffe R, Ferrine M, Levine LS, Oberfield \nSE. Endocrine, metabolic and sonographic characteristics of PCOS: Comparison between \nnonobese and obese adolescents. The Journal of Clinical Endocrinology and Metabolism. \n2003;88:4682-4688\n[20] Ehrmann DA, Liljenquist DR, Kasza K, Azziz R, Legro RS, Ghazzi MN.  PCOS/\nTroglitazone study group. Prevalence and predictors of the metabolic syndrome in \nwomen with polycystic ovary syndrome. The Journal of Clinical Endocrinology and \nMetabolism. 2006 Jan;91:48-53\n[21] Agacayak E, Tunc SY, Sak S, Basaranoglu S, Yüksel H, Turgut A, Gul T. Levels of Neop-\nterin and other inflammatory markers in obese and non-obese patients with polycystic \novary syndrome. Medical Science Monitor. 2015 Aug 20; 21:2446-2455. DOI: 10.12659/\nMSM.894368\n[22] González-Jiménez E, Montero-Alonso MA, Schmidt-RioValle J, García-García CJ, Padez \nC. Metabolic syndrome in Spanish adolescents and its association with birth weight, \nbreastfeeding duration, maternal smoking, and maternal obesity: A cross-sectional study. \nEuropean Journal of Nutrition. 2015 Jun;54:589-597. DOI: 10.1007/s00394-014-0740-x\n[23] Huynh MH, Borrell LN, Chambers EC. Nativity status/length of stay in the US and exces-\nsive gestational weight gain in New  York City teens, 2008-2010. Journal of Community \nHealth. 2015 Feb;40:161-166. DOI: 10.1007/s10900-014-9914-y\n[24] Chasan-Taber L, Silveira M, Lynch KE, Pekow P, Solomon CG, Markenson G.  Physical \nactivity and gestational weight gain in Hispanic women. Obesity (Silver Spring). 2014 \nMar;22:909-918. DOI: 10.1002/oby.20549\nCauses of Visiting Teenagers in the Pediatric and Adolescence Examining Room\nhttp://dx.doi.org/10.5772/intechopen.72979\n205\n\n[25] Marshall NE, Guild C, Cheng YW, Caughey AB, Halloran DR. Racial disparities in preg-\nnancy outcomes in obese women. The Journal of Maternal-Fetal & Neonatal Medicine. \n2014 Jan;27:122-126. DOI: 10.3109/14767058.2013.806478\n[26] Heslehurst N, Sattar N, Rajasingam D, Wilkinson J, Summerbell CD, Rankin J.  Existing \nmaternal obesity guidelines may increase inequalities between ethnic groups: A national \nepidemiological study of 502,474 births in England. BMC Pregnancy and Childbirth. \n2012 Dec 18;12:156. DOI: 10.1186/1471-2393-12-156\n[27] Falsetti L, Gambera A, Tisi G. Efficacy of the combination ethinyl oestradiol and cyprot-\nerone acetate on endocrine, clinical and ultrasonographic profile in polycystic ovarian \nsyndrome. Human Reproduction. 2001;16:36-42\n[28] Tsikouras P, Spyros L, Manav B, Zervoudis S, Poiana C, Nikolaos T, Petros P, Dimitraki \nM, Koukouli C, Galazios G, von Tempelhoff GF. Features of polycystic ovary syndrome \nin adolescence. Journal of Medicine and Life 2015 Jul-Sep;8:291-296\n[29] Orsino A, Van Eyk N, Hamilton J.  Clinical features, investigations and management \nof adolescents with polycystic ovary syndrome. Paediatrics & Child Health. 2005 \nDec;10:602-608\n[30] Pathak PK, Tripathi N, Subramanian SV.  Secular trends in menarcheal age in India-\nevidence from the Indian human development survey. PLoS One. 2014 Nov 4;9:e111027. \nDOI: 10.1371/journal.pone.0111027. eCollection 2014\n[31] Yermachenko A, Dvornyk V. Nongenetic determinants of age at menarche: A systematic \nreview. BioMed Research International. 2014;2014:371583. DOI: 10.1155/2014/371583\n[32] Morris DH, Jones ME, Schoemaker MJ, McFadden E, Ashworth A, Swerdlow AJ.  Body \nmass index, exercise, and other lifestyle factors in relation to age at natural menopause: \nAnalyses from the breakthrough generations study. American Journal of Epidemiology. \n2012 May 15;175:998-1005. DOI: 10.1093/aje/kwr447\n[33] Review AAT. Reproductive factors and the risk of endometrial cancer. International Journal \nof Gynecological Cancer. 2014 Mar;24:384-393. DOI: 10.1097/IGC.0000000000000075\n[34] Deligeoroglou E, Tsimaris P.  Menstrual disturbances in puberty. Best Practice & \nResearch. Clinical Obstetrics & Gynaecology. 2010 Apr;(2):157-171. DOI: 10.1016/j.\nbpobgyn.2009.11.001\n[35] Comité Nacional de Endocrinología, Escobar ME, Pipman V, Arcari A, Boulgourdjian E, \nKeselman A, Pasqualini T, Alonso G, Blanco M. Menstrual cycle disorders in adolescence. \nArch Argent Pediatr. 2010 Aug;108(4):363-369. DOI: 10.1590/S0325-00752010000400018\n[36] Dowlut-McElroy T, Williams KB, Carpenter SL, Strickland JL.  Menstrual patterns and \ntreatment of heavy menstrual bleeding in adolescents with bleeding disorders. Journal \nof Pediatric and Adolescent Gynecology. 2015 Dec; 28:499-501. DOI: 10.1016/j.jpag.  \n2015.03.001\nFamily Planning206\n\n[37] Warner PE, Critchley HO, Lumsden MA, Campbell-Brown M, Douglas A, Murray \nGD. Menorrhagia II: Is the 80-mL blood loss criterion useful in management of com -\nplaint of menorrhagia? American Journal of Obstetrics and Gynecology. 2004 May; 190: \n1224-1229\n[38] Warner PE, Critchley HO, Lumsden MA, Campbell-Brown M, Douglas A, Murray \nGD. Menorrhagia I: Measured blood loss, clinical features, and outcome in women \nwith heavy periods: A survey with follow-up data. American Journal of Obstetrics and \nGynecology. 2004 May;190:1216-1223\n[39] Harel Z. Dysmenorrhea in adolescents. Annals of the New  York Academy of Sciences. \n2008;1135:185-195. DOI: 10.1196/annals.1429.007\n[40] Harel Z. Dysmenorrhea in adolescents and young adults: An update on pharmacologi -\ncal treatments and management strategies. Expert Opinion on Pharmacotherapy. 2012 \nOct;13:2157-2170. DOI: 10.1517/14656566.2012.725045\n[41] Rodgers AK, Falcone T. Treatment strategies for endometriosis. Expert Opinion on Phar-\nmacotherapy. 2008 Feb;9:243-255. DOI: 10.1517/14656566.9.2.243\n[42] Hansen KA, Chalpe A, Eyster KM. Management of endometriosis-associated pain. Clinical \nObstetrics and Gynecology. 2010 Jun;53:439-448. DOI: 10.1097/GRF.0b013e3181dbda06\n[43] Tsikouras T, Liberis V, Galazios G, Sarri S, Teichmann AT.  Contribution of laparos -\ncopy in young women with abdominal pain. Clinical and Experimental Obstetrics & \nGynecology. 2007;34:168-170\n[44] Liatsikos SA, Tsikouras P, Souftas V, Ammari A, Prassopoulos P, Maroulis G, Liberis V.  \nDiagnosis and laparoscopic management of a rudimentary uterine horn in a teenage girl, \npresenting with haematometra and severe endometriosis: Our experience and review of \nliterature. Minimally Invasive Therapy & Allied Technologies. 2010 Aug; 19:241-247. \nDOI: 10.3109/13645701003644491\n[45] Joensson IM, Siggaard C, Rittig S, Hagstroem S, Djurhuus JC.  Transabdominal ultra-\nsound of rectum as a diagnostic tool in childhood constipation. The Journal of Urology. \n2008 May;179:1997-2002. DOI: 10.1016/j.juro.2008.01.055\n[46] Satterwhite CL, Ramaswamy M. Let's talk about sex (again): Advancing the conversation \naround long-acting reversible contraception for teenagers. Womens Health (London). \n2015 Nov;11(6):841-850. DOI: 10.2217/whe.15.66 Epub 2015 Dec 2\n[47] Diedrich JT, Klein DA, Peipert JF. Long-acting reversible contraception in adolescents: A \nsystematic review and meta-analysis. American Journal of Obstetrics and Gynecology. \n2017 Apr; 216(4):364.e1-364.e12. DOI: 10.1016/j.ajog.2016.12.024. Epub 2016 Dec 28. \nReview\n[48] Francis JKR, Gold MA. Long-acting reversible contraception for adolescents: A review. \nJAMA Pediatrics. 2017 Jul 1; 171(7):694-701. DOI: 10.1001/jamapediatrics.2017.0598. \nReview\nCauses of Visiting Teenagers in the Pediatric and Adolescence Examining Room\nhttp://dx.doi.org/10.5772/intechopen.72979\n207\n\n[49] Hubacher D, Spector H, Monteith C, Chen PL, Hart C. Long-acting reversible contracep-\ntive acceptability and unintended pregnancy among women presenting for short-acting \nmethods: A randomized patient preference trial. American Journal of Obstetrics and \nGynecology. 2017 Feb;216(2):101-109. DOI: 10.1016/j.ajog.2016.08.033. Epub 2016 Sep 20\n[50] Zapata LB, Steenland MW, Brahmi D, Marchbanks PA, Curtis KM. Patient understand-\ning of oral contraceptive pill instructions related to missed pills: A systematic review. \nContraception. 2013 May;87:674-684. DOI: 10.1016/j.contraception.2012.08.026\n[51] Schaffir J, Worly BL, Gur TL. Combined hormonal contraception and its effects on mood: \nA critical review. The European Journal of Contraception & Reproductive Health Care. \n2016 Oct;21:347-355. DOI: 10.1080/13625187.2016.1217327\n[52] Sirakov M, Tomova E. Oral contraceptives and mood/sexual disorders in women. Akush \nGinekol (Sofiia). 2015;54:34-40\n[53] Bhuva K, Kraschnewski JL, Lehman EB, Chuang CH.  Does body mass index or weight \nperception affect contraceptive use? Contraception. 2017 Jan; 95:59-64. DOI: 10.1016/j.\ncontraception.2016.09.003\n[54] Shakerinejad G, Hidarnia A, Motlagh ME, Karami K, Niknami S, Montazeri A.  Factors \npredicting mood changes in oral contraceptive pill users. Reproductive Health. 2013 Sep 9; \n10:45. DOI: 10.1186/1742-4755-10-45\n[55] Lidegaard O, Nielsen LH, Skovlund CW, Løkkegaard E. Venous thrombosis in users of \nnon-oral hormonal contraception: Follow-up study, Denmark 2001-10. BMJ. 2012 May \n10;344:e2990. DOI: 10.1136/bmj.e2990\n[56] Amate P, Luton D, Davitian C.  Contraception and adolescence. Archives de Pédiatrie. \n2013 Jun;20:707-713. DOI: 10.1016/j.arcped.2013.03.002\n[57] Lauring JR, Lehman EB, Deimling TA, Legro RS, Chuang CH.  Combined hormonal \ncontraception use in reproductive-age women with contraindications to estrogen use. \nAmerican Journal of Obstetrics and Gynecology. 2016 Sep; 215:330.e1-330.e7. DOI: \n10.1016/j.ajog.2016.03.047\n[58] Küçük M, Aksu H, Sezer SD.  Misconceptions about the side effects of combined oral \ncontraceptive pills. Gynecological Endocrinology. 2012 Apr; 28:282-285. DOI: 10.3109/  \n09513590.2011.613502\n[59] Kiatiyosnusorn R, Suprasert P, Srisomboon J, Siriaree S, Khunamornpong S, Kiet -\npeerakool C.  High-grade histologic lesions in women with low-grade squamous \nintraepithelial lesion cytology from a region of Thailand with a high incidence of cervical \ncancer. International Journal of Gynaecology and Obstetrics. 2010 Aug;110:133-136. DOI: \n10.1016/j.ijgo.2010.03.022\n[60] Gold MA, Duffy K. Extended cycling or continuous use of hormonal contraceptives for \nfemale adolescents. Current Opinion in Obstetrics & Gynecology. 2009 Oct; 21:407-411. \nDOI: 10.1097/GCO.0b013e32832e493e\nFamily Planning208\n\n[61] Nickles MC, Alderman E.  Noncontraceptive use of contraceptive agents. Pediatrics in \nReview. 2014 Jun;35:229-42; quiz 242. DOI: 10.1542/pir.35-6-229\n[62] De Leo V, Fruzzetti F, Musacchio MC, Scolaro V, Di Sabatino A, Morgante G. Effect of a \nnew oral contraceptive with estradiol valerate/dienogest on carbohydrate metabolism. \nContraception. 2013 Sep; 88(3):364-368. DOI: 10.1016/j.contraception.2012.09.003. Epub \n2013 Jun 13\n[63] Edelman A, Micks E, Gallo MF, Jensen JT, Grimes DA. Continuous or extended cycle vs. \ncyclic use of combined hormonal contraceptives for contraception. Cochrane Database \nof Systematic Reviews. 2014 Jul 29;7:CD004695. DOI: 10.1002/14651858. CD004695.pub3\n[64] Verhoeven CH, Dieben TO.  The combined contraceptive vaginal ring, NuvaRing, and \ntampon co-usage. Cochrane Database of Systematic Reviews. 2013 Apr 30; 4:CD003552. \nDOI: 10.1002/14651858. CD003552.pub4\n[65] Ott MA, Sucato GS. Committee on adolescence. Pediatrics. 2014 Oct;134(4):e1257-e1281. \nDOI: 10.1542/peds.2014-2300.Contraception for adolescents\n[66] Massaro M, Di Carlo C, Gargano V, Formisano C, Bifulco G, Nappi C. Effects of the con-\ntraceptive patch and the vaginal ring on bone metabolism and bone mineral density: A \nprospective, controlled, randomized study. Contraception. 2010 Mar;81(3):209-214. DOI: \n10.1016/j.contraception.2009.09.011. Epub 2009 Oct 29\n[67] Hofmeyr GJ, Singata-Madliki M, Lawrie TA, Bergel E, Temmerman M. Effects of inject-\nable progestogen contraception versus the copper intrauterine device on HIV acquisition: \nSub-study of a pragmatic randomised controlled trial. The Journal of Family Planning \nand Reproductive Health Care. 2017 Jul;43(3):175-180. DOI: 10.1136/jfprhc-2016-101607. \nEpub 2017 Apr 5\n[68] Curtis KM, Tepper NK, Jatlaoui TC, Berry-Bibee E, Horton LG, Zapata LB, Simmons KB,  \nPagano HP, Jamieson DJ, Whiteman MK.  U.S. medical eligibility criteria for contracep -\ntive use. MMWR - Recommendations and Reports. 2016 Jul 29;65(3):1-103. DOI: 10.15585/ \nmmwr.rr6503a1\n[69] Daniele MAS, Cleland J, Benova L, Ali M . Provider and lay perspectives on intra-uter -\nine contraception: a global review. Reprod Health. 2017 Sep 26; 14(1):119. DOI: 10.1186/\ns12978-017-0380-8\nCauses of Visiting Teenagers in the Pediatric and Adolescence Examining Room\nhttp://dx.doi.org/10.5772/intechopen.72979\n209","source_license":"CC0","license_restricted":false}