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4 Male Genital Tract

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4 Male Genital Tract

  1. 1. MALE GENITAL TRACT Pathology: A Reviewer for the 3rd Practical Exams<br />How to Use: <br />Identify the images on the slide. Disease names, pathognomonic lesions, and other important info that may be asked in the projection part are on the next slide.<br />Best viewed as a slide show <br /><br />
  2. 2. REFERENCES<br />Lecture ppt, manual’s CD, lab (gross and histo) peekchas<br />
  3. 3. Male Genital Tract Diseases<br />
  4. 4. PENIS<br />
  5. 5. CONGENITAL ANOMALIES <br />
  6. 6. Hypospadias<br />Abnormal urethral orifices involving the VENTRAL aspect of the penis<br />
  7. 7.
  8. 8. Epispadias<br />Abnormal urethral orifices involving the DORSAL aspect of the penis<br />
  9. 9.
  10. 10. Phimosis<br /><ul><li>Abnormally small orifice in the prepuce
  11. 11. Prepuce can’t be retracted</li></li></ul><li>INFLAMMATIONS<br />can be specific or non-specific <br />specific usually refers to sexually transmitted infections <br />
  12. 12.
  13. 13. Balanoposthisis<br />Non-specific infection of the glans penis and prepuce <br />Causative factors <br />Candida<br />Anaerobes<br />Gardnerella<br />Pyogenic organisms <br />Role of smegma (white exudates) – chronic accumulation account for symptom<br />
  14. 14. NEOPLASIA<br />
  15. 15. CondylomaAcuminata<br /><ul><li>Sexually transmitted tumor caused by human papilloma virus (HPV type 6 and 11)</li></ul>Gross: Thrives in any moist mucocutaneous surface of the external genitalia<br />
  16. 16.
  17. 17. CondylomaAcuminatum<br />
  18. 18. Koilocytosis<br />
  19. 19. CondylomaAcuminata<br />Micro: Koilocytosis or perinuclear vacuolization is the pathognomonic lesion for this disease. <br />Presence of nuclear atypia<br />
  20. 20.
  21. 21. Bowen’s Disease <br /><ul><li>Involves the skin of the shaft and scrotum
  22. 22. Gross: solitary, thickened grey-white, opaque plaque; can also be seen in the glans and prepuce as single or multiple shiny red, velvety plaques.
  23. 23. Micro: surface cells are not much different from the base cells, this is defined as a “loss of maturation” pattern, and is quite typical of squamous CIS everywhere</li></li></ul><li>
  24. 24. Invasive Squamous Cell Carcinoma<br /><ul><li>Risk in developing penile carcinoma is related to genital hygiene since exposure to carcinogens that may be concentrated in the smegma increases the likelihood of infection which may carry the potential oncogenic type HPV 16 which is detected in 50% of patients with penile carcinoma.
  25. 25. Cigarette smoking also elevates the risk of developing penile cancer.</li></li></ul><li>
  26. 26. Infiltrating Squamous Cell Carcinoma<br />Flat lesions appear as areas of epithelial thickening accompanied by graying and fissuring of the mucosal surfacepapillary SCC<br />
  27. 27. TESTIS and EPIDIDYMIS<br />
  28. 28. REGRESSIVE CHANGES<br />
  29. 29. Testicular Atrophy<br />Atherosclerotic narrowing of the blood supply in old age<br />The end stage of an inflammatory orchitis, whatever the etiologic agent. Possible causative factors:<br />cryptorchidism<br />hypopituitarism<br />generalized malnutrition or cachexia<br />irradiation<br />prolonged administration of female sex hormones, as in treatment of patients with carcinoma of the prostate<br />Cirrhosis<br />Normal testes (left) and atrophic testes (right). In testicular atrophy, there is ghosting or fibrosis of tubules, no spermatogenesis, and increased interstitial cells of Leydig.<br />
  30. 30.
  31. 31. Testicular Atrophy<br />Ghosting or fibrosis of tubules<br />NO spermatogenesis<br />INCREASED interstitial cells of Leydig<br />
  32. 32.
  33. 33. Hydrocoele of infected Testis<br />
  34. 34.
  35. 35. Acute epididymitis<br /><ul><li>Caused by gonococcal infection
  36. 36. The epididymis is replaced by abcess (seen on the left side)</li></li></ul><li>VASCULAR DISEASES<br />
  37. 37. Torsion<br />Twisting of the spermatic cord which typically cuts off the venous drainage of the testis<br /><ul><li>Bilateral anatomic defect where the testis has increased mobility giving rise to “bell-clapper” abnormality</li></ul>Infracted testicle and epididymis due to torsion<br />
  38. 38. TESTICULAR TUMORS<br />
  39. 39. Seminoma<br /><ul><li>Typical seminomas produce bulky masses, sometimes 10 times the size of a normal testis.
  40. 40. It is homogenous, gray-white in color, lobulated cut surface, usually devoid of hemorrhage or necrosis.
  41. 41. Generall, the tunica albuginea is not penetrated, but occasionally, it extends to the epididymis, spermatic cord, and scrotal sac.</li></li></ul><li>
  42. 42. Seminoma<br />Sheets of uniform cells into poorly demarcated lobules by delicate septa of fibrous tissue.<br />Classic seminoma is large and round to polyhedral and has a distinct cell membrane, a clear or watery-appearing cytoplasm, and a large central nucleus with one or two prominent nucleoli.<br />Polygonal cells with distinct borders and clear cytoplasm due to glycogen content<br />Pathognomonic here is the lymphoid stroma. <br />
  43. 43.
  44. 44. Embryonal Carcinoma<br /><ul><li>Smaller than a seminoma. Does not replace the whole testis.
  45. 45. On cut surface, mass is variegated, poorly demarcated, and punctuated foci or hemorrhage or necrosis.</li></li></ul><li>
  46. 46. Embryonal Carcinoma<br />Cells grow in alveolar or tubular patterns, sometimes papillary convolutions<br />Undifferentiated sheets of cells may be appreciated.<br />Two cell lines: syncitio- and cyto-trophoblast<br />Syncitiotrophoblasts- bizaare looking; elaborates the tumor marker: HCG; Cytotrophoblasts- paler looking<br />Highly malignant form<br />
  47. 47.
  48. 48. Choriocarcinoma<br />Highly malignant form of testicular tumor comprised of both cytotrophoblasts and syncytiotrophoblasts<br />Syncytiotrophoblast appears as a large cell having many irregular or lobular hyperchromatic nuclei and an abundant eosinophilic vacuolated cytoplasm<br />Cytotrophoblasts are more regular and polygonal with distinct borders and clear cytoplasm.<br />
  49. 49.
  50. 50. Yolk Sac Tumor<br />The most common testicular tumor in infants and children up to 3 years with very good prognosis<br />Lace-like (reticular) network of medium-sized cuboidal or elongated cells.<br />Pathognomonic lesion is the presence of Schiller-Duval bodies, which resemble the primitive glomeruli and other endodermalsisuses (perivascular formation around tumor cells). <br />
  51. 51. PROSTATE<br />
  52. 52.
  53. 53. Prostatitis<br />May be acute, caused by the same pathogens as those implicated in UTI; lot of neutrophilic infiltrates<br />May be chronic, usually abacterial or from recurrent or persistent acute infections ; lymphocytic infiltration<br />
  54. 54.
  55. 55. GranulomatousProstatitis<br /><ul><li> Can non-TB or TB-related
  56. 56. Escape/rupture of prostatic secretions granulomatous proliferation </li></li></ul><li>
  57. 57. Benign Prostatic Hyperplasia<br />Glandular and stromal hyperplasia resulting to formation of large, fairly discrete nodules in the periurethral region of the prostate.<br />Associated with old age<br />Associated with urinary obstruction, frequency, bladder hypertrophy and bladder trabeculations<br />Micro: glandular hyperplasia. NOTE: no nucleoli<br />
  58. 58.
  59. 59. Benign Prostatic Hyperplasia<br />Etiopathogenesis:<br />Androgen Related. Conversion of testosterone by enzyme type 2 5∞-reductase to DHT (dihydrotestosterone). This enzyme is located entirely on the stromal cell whereby the stromal cell is responsible for androgen-dependent prostatic growth.<br />DHT binds to androgen receptors both present on the stromal and epithelial cell; DHT serves as an indirect mitogen on prostate (stromal) cells. DHT will induce increase production of several growth factors which will increase no. of stromal cells<br />DHT does not increase cellular epithelial proliferation but instead inhibits death of the epithelial cells<br />
  60. 60.
  61. 61. Nodular hyperplasia, BPH<br />Glandular hyperplasia, no nucleoli. <br />dilated acini, two cell layer, cuboidal columnar<br />
  62. 62.
  63. 63. Benign Prostatic Hyperplasia<br />
  64. 64. TUMORS<br />
  65. 65. Prostatic Adenocarcinoma<br />Prostatic carcinoma with lots of nucleoli. Presence of nucleoli distinguishes this from BPH. <br />Etiology<br />Androgens play an important role in prostate cancer the growth and survival of the cancer cells depend on the androgens<br />The androgens bind to the androgen receptors and induce the expression of pro-growth and pro-survival genes.<br />
  66. 66.
  67. 67.
  68. 68. Adenocarcinoma of the Prostate gland<br />
  69. 69. Adenocarcinoma with perineural invasion<br />
  70. 70.
  71. 71. Metastatic osteoblastic prostatic carcinoma <br /><ul><li> Within vertebral bodies
  72. 72. Haematogenous spread</li></li></ul><li>
  73. 73. Fibrous Pseudo tumor, Testes<br />
  74. 74.
  75. 75. ACKNOWLEGDEMENTS<br />We would like to thank our lecturers for their ppts. Monique and Erica for their lab pictures <br />And most especially Abby, Armi, Daph, Den, Domar, FX, and Kenji for making this reviewer.<br />Go 2012! Study hard, work harder, party hardest <br />

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