male repro

1. MALE GENITAL TRACT Pathology: A Reviewer for the 3rd Practical Exams How to Use: 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. Best viewed as a slide show 

2. REFERENCES Lecture ppt, manual’s CD, lab (gross and histo) peekchas

3. Male Genital Tract Diseases

4. PENIS

5. CONGENITAL ANOMALIES

6. Hypospadias Abnormal urethral orifices involving the VENTRAL aspect of the penis

8. Epispadias Abnormal urethral orifices involving the DORSAL aspect of the penis

13. Balanoposthisis Non-specific infection of the glans penis and prepuce Causative factors Candida Anaerobes Gardnerella Pyogenic organisms Role of smegma (white exudates) – chronic accumulation account for symptom

14. NEOPLASIA

17. CondylomaAcuminatum

18. Koilocytosis

19. CondylomaAcuminata Micro: Koilocytosis or perinuclear vacuolization is the pathognomonic lesion for this disease. Presence of nuclear atypia

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.

26. Infiltrating Squamous Cell Carcinoma Flat lesions appear as areas of epithelial thickening accompanied by graying and fissuring of the mucosal surfacepapillary SCC

27. TESTIS and EPIDIDYMIS

28. REGRESSIVE CHANGES

29. Testicular Atrophy Atherosclerotic narrowing of the blood supply in old age The end stage of an inflammatory orchitis, whatever the etiologic agent. Possible causative factors: cryptorchidism hypopituitarism generalized malnutrition or cachexia irradiation prolonged administration of female sex hormones, as in treatment of patients with carcinoma of the prostate Cirrhosis 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.

31. Testicular Atrophy Ghosting or fibrosis of tubules NO spermatogenesis INCREASED interstitial cells of Leydig

33. Hydrocoele of infected Testis

38. TESTICULAR TUMORS

40. It is homogenous, gray-white in color, lobulated cut surface, usually devoid of hemorrhage or necrosis.

42. Seminoma Sheets of uniform cells into poorly demarcated lobules by delicate septa of fibrous tissue. 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. Polygonal cells with distinct borders and clear cytoplasm due to glycogen content Pathognomonic here is the lymphoid stroma.

46. Embryonal Carcinoma Cells grow in alveolar or tubular patterns, sometimes papillary convolutions Undifferentiated sheets of cells may be appreciated. Two cell lines: syncitio- and cyto-trophoblast Syncitiotrophoblasts- bizaare looking; elaborates the tumor marker: HCG; Cytotrophoblasts- paler looking Highly malignant form

48. Choriocarcinoma Highly malignant form of testicular tumor comprised of both cytotrophoblasts and syncytiotrophoblasts Syncytiotrophoblast appears as a large cell having many irregular or lobular hyperchromatic nuclei and an abundant eosinophilic vacuolated cytoplasm Cytotrophoblasts are more regular and polygonal with distinct borders and clear cytoplasm.

50. Yolk Sac Tumor The most common testicular tumor in infants and children up to 3 years with very good prognosis Lace-like (reticular) network of medium-sized cuboidal or elongated cells. Pathognomonic lesion is the presence of Schiller-Duval bodies, which resemble the primitive glomeruli and other endodermalsisuses (perivascular formation around tumor cells).

51. PROSTATE

53. Prostatitis May be acute, caused by the same pathogens as those implicated in UTI; lot of neutrophilic infiltrates May be chronic, usually abacterial or from recurrent or persistent acute infections ; lymphocytic infiltration

57. Benign Prostatic Hyperplasia Glandular and stromal hyperplasia resulting to formation of large, fairly discrete nodules in the periurethral region of the prostate. Associated with old age Associated with urinary obstruction, frequency, bladder hypertrophy and bladder trabeculations Micro: glandular hyperplasia. NOTE: no nucleoli

59. Benign Prostatic Hyperplasia Etiopathogenesis: 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. 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 DHT does not increase cellular epithelial proliferation but instead inhibits death of the epithelial cells

61. Nodular hyperplasia, BPH Glandular hyperplasia, no nucleoli. dilated acini, two cell layer, cuboidal columnar

63. Benign Prostatic Hyperplasia

64. TUMORS

65. Prostatic Adenocarcinoma Prostatic carcinoma with lots of nucleoli. Presence of nucleoli distinguishes this from BPH. Etiology Androgens play an important role in prostate cancer the growth and survival of the cancer cells depend on the androgens The androgens bind to the androgen receptors and induce the expression of pro-growth and pro-survival genes.

68. Adenocarcinoma of the Prostate gland

69. Adenocarcinoma with perineural invasion

73. Fibrous Pseudo tumor, Testes

75. ACKNOWLEGDEMENTS We would like to thank our lecturers for their ppts. Monique and Erica for their lab pictures  And most especially Abby, Armi, Daph, Den, Domar, FX, and Kenji for making this reviewer. Go 2012! Study hard, work harder, party hardest 