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Embryology, Anatomy, and Physiology of the Male Reproductive System
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Mesonephric (Wolffian) ducts are the embryological origin of the male reproductive system.They form the epididymis, vas deferens, seminal vesicles, and the central zone of the prostate.
Pediatric Hematocolpos
Published in Botros Rizk, A. Mostafa Borahay, Abdel Maguid Ramzy, Clinical Diagnosis and Management of Gynecologic Emergencies, 2020
Omar M. Abuzeid, Mostafa I. Abuzeid
During the indifferent stage of embryo development, from 5 to 8 weeks, both Wolffian and Müllerian ducts coexist in all embryos. During embryo development, there is an intimate relationship between the Müllerian and Wolffian ducts. Therefore, it is not surprising that renal anomalies occur in approximately one-third of patients with Müllerian anomalies.
Mesenchymal-Epithelial Interactions as a Mechanism for Regulating Hormonally Induced Epithelial Differentiation and Growth
Published in Takao Mori, Hiroshi Nagasawa, Toxicity of Hormones in Perinatal Life, 2020
G. R. Cunha, R. M. Bigs, P. S. Cooke, A. A. Donjacour
The male genital tract develops from two embryonic anlagen: the Wolffian ducts and urogenital sinus (UGS). The Wolffian duct, whose epithelium is mesodermal in origin, gives rise to the epididymis, ductus deferens, seminal vesicle, and ejaculatory ducts. The urogenital sinus, whose epithelium is derived from endoderm, gives rise to the prostate, bulbourethral glands, urethra, and periurethral glands, and contributes substantially to the urinary bladder.89 Within the prostatic complex each lobe (ventral, dorsolateral, and coagulating gland) has a unique pattern of ductal branching, while the seminal vesicle has its own distinctively folded mucosa.10,11
Moyamoya syndrome in a male pseudohermaphrodite patient with congenital adrenal hyperplasia – a rare association. Case report and review of literature
Published in British Journal of Neurosurgery, 2023
Remesh Chirayil Vasudevan, Reshma Vachali Madayi, Rohit Ravindranath Nambiar
CAH is a rare disorder that results from defective biosynthesis of steroid hormones in the adrenal cortex. CAH with 17 alpha-hydroxylase and 11 beta-hydroxylase deficiencies is associated with hypertension. Pathogenesis of CAH is due to various genetic mutations in the enzymes involved in steroid synthesis. As a result, cortisol production is reduced and the negative feedback control on adrenocorticotropic hormone (ACTH) is lost. Elevated ACTH level results in overproduction and accumulation of steroids precursors prior to the enzyme defect.6 There is hyperplasia of adrenal cortex. The clinical features depend on the level of enzyme defect. Patients with ambiguous genitalia, hypogonadism, hypertension and associated hypokalemia should be evaluated for possible CAH. In CAH due to 17 alpha-hydroxylase deficiency, both adrenal and gonadal steroid hormones production will be impaired. In male patients, lack of testosterone will impair Wolffian duct development. They will have gonads but no internal genitalia.7 High 11 deoxycorticosterone levels will cause sodium retention, potassium loss and hypertension due to potent mineralocorticoid action.
Genitourinary syndrome, local oestrogen therapy and endometrial pathology: a single-centre, randomised study
Published in Journal of Obstetrics and Gynaecology, 2022
Stefan Miladinov Kovachev, Miladin Stefanov Kovachev
The genitourinary syndrome affects 20% to 45% of postmenopausal women (Kim et al. 2015; Kagan et al. 2019; Kozma et al. 2019). It includes a combination of symptoms due to low oestrogen levels, such as genital dryness, burning irritation, dyspareunia, genital discomfort and pain, recurrent uroinfections, and urination disorders (dysuria, urgency, dysuria) (Kagan et al. 2019). The embryonic origin of general genital and urinary system complaints should be sought in the Mullerian and Wolffian ducts and the impaired function of oestrogen receptors located in them (Kim et al. 2015). To treat this syndrome, local and oral phytoestrogens, local lubricants and moisturisers, selective oestrogen receptor modulators (SERM), local lasers, and mainly local and oral oestrogens can be used (Tempfer et al. 2007; Kim et al. 2015; Bruyniks et al. 2017; Kagan et al. 2019; Kozma et al. 2019). Oral and transdermal oestrogen therapy, according to the data from various studies, leads to 1%–28% of all cases of endometrial hyperplasia (benign or atypical) and 0.2%–3% of all cases of endometrial neoplasia (Brinton and Felix 2014; Chandra et al. 2016). Topical vaginal oestrogens do not have the same stimulating effect on the endometrium as oral ones, and therefore the association between them and endometrial hyperplasia or cancer has not been established categorically. Vaginal oestrogens cause 0% to 2% of all cases of endometrial hyperplasia and cancer, according to various clinical studies (Simon et al. 2010; Constantine et al. 2019).
The XY Female: Exploring Care for Adolescent Girls with Complete Androgen Insensitivity Syndrome
Published in Comprehensive Child and Adolescent Nursing, 2020
The 46, XY classification is complex, and usually encompasses diagnoses and presentations of ambiguous or female external genitalia, and either the absence or presence of Mullerian structures (Mendonca, Costa, Belgorosky, Rivarola, & Domenice, 2010). Mullerian structures involve the fallopian tubes, uterus, the cervix, and part of the vagina, whereas the Wolffian structures will develop into the epididymis, the two vas deferens, and the seminal vesicles in the male reproductive system. However, abnormalities of karyotype, formation of gonads, androgen synthesis and androgen action are the principle causes that result in under-virilization—that is, under masculinization of ‘biological’ XY individuals (Massanyi, Dicarlo, Migeon, & Gearhart, 2013). Sometimes, the Wolffian ducts may not form properly in the early stages of embryological development, resulting in a non-endocrine-related picture, and also gonadal dysfunction and hypogonadism can be the result of insufficient testosterone. Disorders of androgen synthesis, such as 5-α-reductase deficiency are found in individuals with female or ambiguous genitalia at birth who later virilize at puberty, which can sometimes lead to a personal decision to change gender (Michala & Creighton, 2010). However, Complete Androgen Insensitivity Syndrome results from androgen receptor dysfunction (Mongan, Tadokoro-Cuccaro, Bunch, & Hughes, 2015), and is the most common condition leading to the presentation of an XY female, with an estimated incidence of 1 in every 40,000–60,000 births (Michala & Creighton, 2010).