TAILIEUCHUNG - Ebook Blueprints obstetrics & gynecology (6E): Part 2
(BQ) Part 2 book “Blueprints obstetrics & gynecology” has contents: Benign disorders of the upper genital tract, endometriosis and adenomyosis, pelvic organ prolapse, urinary incontinence, puberty, the menstrual cycle, and menopause, abnor malities of the menstrual cycle, and other contents. | Part II Gynecology Chapter 13 Benign Disorders of the Lower Genital Tract BENIGN LESIONS OF THE VULVA, VAGINA, AND CERVIX This chapter encompasses an overview of the many congenital anomalies, epithelial disorders, and benign cysts and tumors of the vulva, vagina, and cervix. Infections of these structures are covered in Chapter 16, and premalignant and malignant lesions are covered in Chapter 27 (vulva and vagina) and Chapter 28 (cervix). CONGENITAL ANOMALIES OF THE VULVA AND VAGINA A variety of congenital defects occur in the external genitalia, vagina, and cervix including but not limited to labial fusion, imperforate hymen, transverse vaginal septum, longitudinal vaginal septum, vaginal atresia, and vaginal agenesis. Congenital anomalies of the female genital tract are associated with concomitant anomalies in the upper reproductive tract as well as anomalies in the genital urinary (GU) tract such as unilateral renal agenesis, pelvic or horseshoe kidneys, or irregularities in the collecting system. LABIAL FUSION Labial fusion is associated with excess androgens. Most commonly, the etiology is the result of exogenous androgen exposure but may also be due to an enzymatic error leading to increased androgen production. The most common form of enzymatic deficiency is 21-hydroxylase deficiency (Chapter 23) leading to congenital adrenal hyperplasia. This may be phenotypically demonstrated in the neonate with ambiguous genitalia, hyperandrogenism with salt wasting, hypotension, hyperkalemia, and hypoglycemia. The neonates often present in adrenal crisis with salt wasting seen approximately 75% of the time. This autosomal recessive trait occurs in roughly 1 in 40,000 to 50,000 pregnancies. The diagnosis is made by elevated 17α-hydroxyprogesterone or urine 17-ketosteroid with decreased serum cortisol. Because cortisol is not being made in the adrenal cortex, the treatment for this disorder is exogenous cortisol. The exogenous cortisol then negatively feeds back on .
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