THE ENDOCRINOLOGIST'S CLINICAL PERCEPTION OF THE PATHOPHYSIOLOGY OF PITUITARY DISORDERS RELATED TO HYPOGONADOTROPHIC HYPOGONADISM

Abstract

Fertility is determined by the regulation of the pituitary hypothalamic axis coordinated by the regulation of the synthesis and release hormones, with it determines the production testosterone, and gonadotropins triggering the onset puberty. They are neuroendocrine hormone mediators which under normal conditions secrete gonadotropin to stimulate gonadal maturation. When there is an inactivation and deregulation the endocrine system, causing disturbance of this axis. leading in turn to the clinical correlations hypogonadotropic hypogonadism. A rare conditions congenital etiology primary origin, the testicles, and secondary by the failure of the hypothalamus to produce the hormones coursing with the delay or absence in the onset puberty, or due to autoimmune pathologies. Occurring as a result of the process failure this axis, and subsequently gonadal function and gonadotrophic distress, individuals hospitalized for this conditions have manifestations of androgens and serum testosterone, in addition to levels sex steroids and hormone-binding globulin. For a better clinical conduct, it is necessary to perform testosterone and estrogen dosages and, consequently hormone replacement therapy with adjusted doses to induce sexual control and the onset of the pubertal milestone. Objective: The purpose this study is to understand the possible etiologies the disturbance pituitary hypothalamic axis and the causes of the failure in occurrence of gonadotropin raising hypotheses in the possible treated conducts. Methodology: Articles in portuguese were used in the years 2012 to 2022, available in the following data sources: academic google and Scielo and Pubmed. In these articles, the authors were unanimous in demonstrating that the main manifestation of this pathology is associated with disturbing gonadal disorders. and hormone replacement therapy has been effective in preserving reproduction.