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

REFERENCESLecture ppt, manual’s CD, lab (gross and histo) peekchas

Male Genital Tract Diseases

PENIS

CONGENITAL ANOMALIES

Hypospadias

Abnormal urethral orifices involving the VENTRAL aspect of the penis

Epispadias

Abnormal urethral orifices involving the DORSAL aspect of the penis

Phimosis

•Abnormally small orifice in the prepuce•Prepuce can’t be retracted

INFLAMMATIONS

• can be specific or non-specific • specific usually refers to sexually transmitted

infections

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

NEOPLASIA

Condyloma Acuminata

• Sexually transmitted tumor caused by human papilloma virus (HPV type 6 and 11)

• Gross: Thrives in any moist mucocutaneous surface of the external genitalia

Condyloma Acuminatum

Koilocytosis

Condyloma Acuminata

• Micro: Koilocytosis or perinuclear vacuolization is the pathognomonic lesion for this disease.

• Presence of nuclear atypia

Bowen’s Disease

• Involves the skin of the shaft and scrotum • Gross: solitary, thickened grey-white,

opaque plaque; can also be seen in the glans and prepuce as single or multiple shiny red, velvety plaques.• 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

Invasive Squamous Cell Carcinoma

• 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.

• Cigarette smoking also elevates the risk of developing penile cancer.

Infiltrating Squamous Cell Carcinoma

Flat lesions appear as areas of epithelial thickening accompanied by graying and

fissuring of the mucosal surfacepapillary SCC

TESTIS and EPIDIDYMIS

REGRESSIVE CHANGES

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.

Testicular Atrophy

• Ghosting or fibrosis of tubules• NO spermatogenesis• INCREASED interstitial cells of Leydig

Hydrocoele of infected Testis

Acute epididymitis

•Caused by gonococcal infection•The epididymis is replaced by abcess (seen on the left side)

VASCULAR DISEASES

Torsion

• Twisting of the spermatic cord which typically cuts off the venous drainage of the testis

• Bilateral anatomic defect where the testis has increased mobility giving rise to “bell-clapper” abnormality

• Infracted testicle and epididymis due to torsion

TESTICULAR TUMORS

Seminoma

• Typical seminomas produce bulky masses, sometimes 10 times the size of a normal testis.

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

• Generall, the tunica albuginea is not penetrated, but occasionally, it extends to the epididymis, spermatic cord, and scrotal sac.

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.

Embryonal Carcinoma

• Smaller than a seminoma. Does not replace the whole testis.

• On cut surface, mass is variegated, poorly demarcated, and punctuated foci or hemorrhage or necrosis.

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

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.

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 endodermal sisuses (perivascular formation around tumor cells).

PROSTATE

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

Granulomatous Prostatitis

• Can non-TB or TB-related• Escape/rupture of prostatic secretions granulomatous proliferation

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

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

Nodular hyperplasia, BPH

Glandular hyperplasia, no nucleoli. dilated acini, two cell layer, cuboidal

columnar

Benign Prostatic Hyperplasia

TUMORS

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.

Adenocarcinoma of the Prostate gland

Adenocarcinoma with perineural invasion

Metastatic osteoblastic prostatic carcinoma

• Within vertebral bodies•Haematogenous spread

Fibrous Pseudo tumor, Testes

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