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Year Ii Organ Systems - Reproduction Self-Study

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Year Ii Organ Systems - Reproduction Self-Study YEAR II ORGAN SYSTEMS - REPRODUCTION SELF-STUDY PATHOLOGY OF THE TESTES AND PENIS I. REQUIRED READING Kumar, Abbas, Fausto & Mitchell, Robbins Basic Pathology, 9th ed., Elsevier- Saunders, 2013; Ch. 17, The Male Genital System and Lower Urinary Tract; pp. 657-663. II. LEARNING OBJECTIVES Upon completion of the lecture, laboratory and required reading the student will be able to: 1. Describe the general morphological patterns and pathogenesis of testicular hypoplasia and atrophy with particular reference to the following: Cryptorchidism Klinefelter syndrome (XXY) Hypopituitarism Mumps and other causes of orchitis Alcoholic cirrhosis Androgen insensitivity syndrome Exposure to antiandrogens and other chemotherapeutics 2. Describe the major gross and microscopic features of the following tumors: Germ cell tumors of testis: Non-germ cell tumors of testis: seminoma Leydig embryonal carcinoma Sertoli yolk sac (endodermal sinus) tumor teratoma, mature and immature choriocarcinoma Carcinoma of penis 3. Correlate the pathologic features with the major symptoms produced by these tumors. III. NON-NEOPLASTIC DISEASES OF THE TESTES The gonads are homologous organs in the male and the female, and the diseases of the testis and ovary therefore are closely parallel. In the light of these homologies, a rational classification of diseases of the gonads can be made. Each gonad has a dual function: (1) production of gametes; and (2) the secretion of sex hormones. In clinical practice, however, male hypogonadism is a term generally used to mean deficient production of androgen by the testis (interstitial cells of Leydig), whereas the term infertility is applied when referring to deficient production of spermatozoa by the germinal epithelium. Pathology 1. Epididymitis and Orchitis Although inflammation of the epididymis is more common than that of the testis, epididymitis can spread to involve the testis. The morphological patterns are similar to inflammation elsewhere in the body: congestion; edema; and infiltration by neutrophils, macrophages, and lymphocytes. Typically, the initial inflammation is limited to the interstitium; however, this can extend to involve the tubules. In some cases, abscess formation may occur leading to significant loss of tissue; this may lead to tubular atrophy (see below). Often, the significant numbers of Leydig cells are spared, maintaining testosterone production. 31 2. Hypoplasia Hypoplasia is the condition of defective or incomplete development. The hypoplastic testis fails to develop at the usual time (puberty in the male should be completed by age 20) but instead remains small and retains infantile characteristics. Testis biopsy shows small tubules without lumens, containing undifferentiated germinal epithelium, immature Sertoli cells and an occasional spermatogonium. Some of the conditions that result in hypoplastic testis are given below. a. Cryptorchidism If the testes fail to descend, but instead remain within the abdominal cavity, the condition is known as cryptorchidism. The abdominal environment is unfavorable (presumably due to increased temperature), and the cryptorchid testis does not develop normally. Its overall dimensions are small and the tubules are less than normal diameter. Maturation of the germinal epithelium fails to occur, and Sertoli cells and spermatogonia make up the tubular lining. Leydig cells on the other hand are prominent or frankly hyperplastic. Opinions differ concerning the optimal management of cryptorchid testis, but if descent is delayed beyond puberty, there is little chance of normal gametogenesis. The risk of malignancy in an abdominal testis is increased, and the usual neoplasm is a germinal tumor. b. Male pseudohermaphroditism and androgen insensitivity syndrome (AIS) A true hermaphrodite has gonadal tissue of both sexes. In contrast, a pseudohermaphrodite either has testes or ovaries but not both, and the external genitalia are not congruent with the gonads. Instead, the external genitalia resemble those of the opposite sex. The condition is designated male pseudohermaphroditism if the gonads are male. Thus a male pseudohermaphrodite has testes but has female external genitalia and body habitus. Although the karyotype is 46,XY the patient resembles a normal woman, with unremarkable breasts, female external genitalia and sparse body hair. The gonads, which often are contained within inguinal hernias, resemble testes grossly. Microscopically, undeveloped tubules are seen in a fibrous stroma containing scattered clumps of interstitial cells. Incidence of gonadal tumors is said to be increased. Male pseudohermaphroditism derives from a defective virilization of the male embryo, usually resulting from impaired androgen synthesis or action (or both). The most common form of male pseudohermaphroditism is the familial disorder known as complete androgen insensitivity syndrome (AIS). c. Klinefelter syndrome or aneuploidy X (47,XXY). Klinefelter syndrome is the result of genetic abnormality, and the usual karyotype is 47,XXY. The affected adult is a phenotypic male with small testes and eunuchoid proportions; gynecomastia and mental dullness may be present. At puberty, the testes fail to develop; instead, a distinctive form of testicular tubular sclerosis occurs, characterized by hyalinization of tubules and failure of development of germinal epithelium. Large clumps of interstitial cells appear. Urinary gonadotrophin is elevated. Chromosomal variants of the syndrome include mosaicism (47,XXY/46,XY) and other karyotypes (48,XXXY and 49,XXXXY). In most cases of Klinefelter syndrome, sterility is absolute, with azoospermia. d. Destruction of pituitary If pituitary destruction occurs in childhood, gonadotrophic hormone will fail to be secreted, puberty will not occur and the testes will remain immature. Dwarfism may also be present as a result of deficiency of growth hormone. e. Selective failure of gonadotrophin secretion In this condition, puberty fails to occur at the expected time and secondary sexual development is absent. With failure of testosterone production by the testis, epiphyses fail to close, skeletal growth continues and body habitus becomes eunuchoid (length from pubis-to-crown is less than pubis-to-heel; span exceeds height). Body hair is scant and voice remains high pitched. 3. Absent Germ Cells (Sertoli Cell-Only Syndrome) 32 Germ cells are absent in the testes, and the tubules are lined only by Sertoli cells. The testes are slightly smaller than normal, but in all other respects, physical findings are normal, and the patient is not eunuchoid. However, semen analysis reveals azoospermia, and the patient is sterile. Biopsy is required for diagnosis. In most cases the etiology is unknown (idiopathic), although in some cases it has been linked with genetic lesions on the Y chromosome. Sertoli only syndrome may also be seen in the context of other diseases, such as cryptorchidism, Klinefelter syndrome, radiation therapy; and history of severe trauma. 4. Atrophy Under this designation will be discussed some of the conditions manifested by bilateral shrinkage of the fully developed testes, or by diminution of their component tissues. Etiologies are diverse, and in some cases, unknown. The degree of atrophy need not be great to cause profound functional effects, since a relatively small loss of cells from the germinal epithelium may result in infertility. Semen analysis and testicular biopsy are sensitive indicators of the status of the germinal epithelium and interstitial tissue. a. Destruction of pituitary Hypophyseal damage occurring postpuberally, after the testes are fully developed, results in testicular changes which may range from hypospermatogenesis to advanced atrophy, depending upon the extent of injury to the pituitary. b. Hypospermatogenesis (proportional hypoplasia) In hypospermatogenesis, all cell types of the germinal epithelium are present in the usual proportion, but the number of cells of each type is reduced. Leydig cells are intact. This condition is an important cause of infertility. Endocrinologic status is otherwise apparently normal. c. Inflammatory orchitis, especially associated with mumps Mumps may be complicated by orchitis, and though usually unilateral, both testes may be involved. The incidence of orchitis is low in children but rises with adolescence. The acute stage, with leukocytic infiltration of tubules, vascular engorgement, hemorrhage and edema, rarely is seen by the pathologist. Not all tubules are involved to the same extent. With healing, the tubules may undergo atrophy and sclerosis, but fortunately, a significant degree of atrophy occurs in only about half the cases. Other causes of inflammatory orchitis may lead to testicular atrophy. d. Irradiation The germinal epithelium is a radiosensitive tissue, and severe radiation injury may cause permanent loss of the germ cells, tubular sclerosis and interstitial fibrosis. With less intense irradiation exposure, destruction is not complete and regeneration of the germinal epithelium may occur. e. Chemotherapeutic agents Substances that inhibit cell division or prevent differentiation or both can damage the germinal epithelium by interfering with mitosis or preventing differentiation of the post-mitotic cells into spermatozoa (i.e., cause maturation arrest). Among these compounds are many of the drugs used to treat cancer and leukemia, including alkylating agents, folic acid antagonists, antibiotics, alkaloids, colchicine and urethane. f. Cirrhosis and alcohol use In cirrhosis
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