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Hypergonadotropic hypogonadism (HH), also known as primary or peripheral/gonadal hypogonadism or primary gonadal failure, is a condition which is characterized by hypogonadism which is due to an impaired response of the gonads to the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and in turn a lack of sex steroid production. [1]
This activation can lead to symptoms of hyperandrogenism such as acne, hirsutism, polycystic ovarian syndrome, or prostate enlargement. In the canonical pathway, dihydrotestosterone is directly synthesized from testosterone by the enzyme 5α-reductase , primarily in tissues like the prostate gland , hair follicles , and skin.
The symptoms of hypogonadotrophic hypogonadism, a subtype of hypogonadism, include late, incomplete, or lack of development at puberty, and sometimes short stature or the inability to smell; in females, a lack of breasts and menstrual periods, and in males a lack of sexual development, e.g., facial hair, penis, and testes enlargement, deepening ...
The ovary is thus formed mainly from the genital ridge and partly from the mesonephros. Later the mass is differentiated into a central part, the medulla of ovary, covered by a surface layer, the germinal epithelium. Between the cells of the germinal epithelium a number of larger cells, the immature ova, are found.
Physical activity may slightly reduce physical symptoms of chronic prostatitis but may not reduce anxiety or depression. Transrectal thermotherapy, where heat is applied to the prostate and pelvic muscle area, on its own or combined with medical therapy may cause symptoms to decrease slightly when compared with medical therapy alone. [7]
The ovary is differentiated into a central part, the medulla of ovary, covered by a surface layer, the germinal epithelium. The immature ova originate from cells from the dorsal endoderm of the yolk sac. Once they have reached the gonadal ridge they are called oogonia. Development proceeds and the oogonia become fully surrounded by a layer of ...
The prostate, like the external male genitalia, cannot masculinize in the absence of androgen receptor function, and thus remains in the female form. [18] [36] [37] [38] The Müllerian system typically regresses the same way it does in unaffected male fetuses due to anti-Müllerian hormone originating from the Sertoli cells of the testes. [19]
Right, Habitus after 3.5 years of androgen treatment. [17] Partial androgen insensitivity syndrome is diagnosed when the degree of androgen insensitivity in an individual with a 46,XY karyotype is great enough to partially prevent the masculinization of the genitalia, but is not great enough to completely prevent genital masculinization.