Male Genital Tract

MALE GENITAL TRACT Professor Dr. Wahda M.T. Al- Nueimy Department of Pathology Faculty of Medicine University of Mosul 2013

prostate

Normal weights approximately 20 gm. Its a retroperitoneal organ. consist of 5 lobes: posterior, middle, anterior & 2 lateral lobes. Histology: it composed of 2 element Glandular element of large size lined by 2 cell layers. Fibro muscular stroma.

Relation of prostate and urethra

prostate
Diseases affecting: Inflammation. Nodular prostatic hyperplasia. Prostatic carcinoma.

Inflammation

Three categories: Acute bacterial prostatitis. chronic bacterial prostatitis. Chronic a bacterial prostatitis. 1- Acute bacterial prostatitis: Acute focal or diffuse suppurative inflammation. caused by various strains of E. coli, enterococci, gram negative rods & staphylococci. The m.o. become implanted in the prostate usually by intraprostatic reflux of urine from the posterior urethra, or by the lymphohematogenous routes from distant foci of infection. It may follow some surgical manipulations of the urethra or the prostate itself. Diagnosis : by clinical features &urine culture.


2- Chronic bacterial prostatitis: low back pain, dysuria, perineal & suprapubic discomfort. Common historical characteristic is recurrent UTI (cystitis & urethritis) caused by same organism. Diagnosis: leukocytosis in the expressed prostatic secretion with positive bacterial culture of the secretion also. 3- Chronic a bacterial prostatitis ( Lymphocytic Prostatitis). Most common type now a days. No history of recurrent UTI. Culture negative. Caused by sexual transmitted pathogens e.g., C. trachomatis, Ureaplasma urealyticum & mycoplasm. Micro: It should be differentiate from chronic lymphocytic leukemia.

TUBERCULOSIS

Its the result from hematogenous spread from the lungs, but it may also result from direct invasion from the urethra. Grossly : the lesions are usually bilateral.

Nodular prostatic hyperplasia

Extremely common disorder in men above 50 yr. Its regarded as normal aging process. Hyperplasia of both prostatic stroma & epithelial cells. It occurs in periurethral region so caused partial or complete obstruction of urethra. Pathogenesis: The cause of NPH is Unknown Dihydrotestosteron (DHT) a metabolite of testosterone act on nuclear androgen receptor on stromal & epithelial cells signals a transcription of a growth factors stimulate proliferation & growth. Estadiol (estrogen) level increase in elderly person which increase nuclear androgen receptor & possibly sensitize the prostate to the growth- promoting effects of DHT.

Nodular prostatic hyperplasia

Grossly: increase weight of prostate (60-100 gm) with gray-white firm nodules affecting periurethral & transitional zones. Histology: The earliest changes is a stromal proliferation in the periurethral portion of the prostate, this followed by glandular proliferation . Some glands are dilated or even cystic & often contain an inspissated secretion of glycoprotein nature (corpora amylacea) which is some times calcified. Foci of squamous metaplasia & small areas of infarction some times are seen. It is not consider as a premalignant lesion Presentation: Difficulty in urination & retention of urine, cystitis, UTI and renal stones.

BPH requires testicular androgen during prostatic development. Basic fibroblast growth factor, epidermal growth factor, keratinocyte growth factor, transforming growth factor-beta play some part in prostate growth. Decreased endogenous apoptosis in prostate cause abnormal tissue growth in prostate.

Tumors of the prostate

1-Primary into Benign & malignant. 2-Secondary involvement of the prostate occurs through direct extension by carcinoma of the urinary bladder, urethra, colorectal , anus & soft tissue tumors. Distant metastases have been seen from lung cancer & melanoma.

Prostatic carcinoma

Most common form of cancer in men, Followed closely by lung cancer. Second leading cause of cancer death. Approximately 70 % of men between 70-80 years have prostatic carcinoma. There are some remarkable & puzzling national & racial differences in the incidence of this disease. These differences are thought to be due to environmental influences. Etiology: Several risk factors e.g. age, race, family history, hormone levels (testosterone & androgen) & environmental influences are suspected of playing roles. Increased consumption of fats has been implicated, its influences the levels of hormones such as testosterone, which in turn affect the growth of prostate.

Prostatic carcinoma

Grossly: affecting peripheral zone of the gland classically in the posterior location. firm yellow with gritty cut sectionHistology: small closely packed glands (back-to-back) with single cell lining. These cells have large vesicular nuclei with prominent one or more nucleoli .Invasion of capsule with its lymphatic & vascular channels, perineural invasion or both.Grading & staging:Use Gleason’s grade. Grading particular importance because there is in general fairly good correlation between the prognosis & degree of differentiation.

Prostatic carcinoma

Clinical course: 60 % of patient presented with localized disease in the prostatic gland. 40 % of patient presented with invasion to the surrounded organ specially urinary bladder & tract causing urinary symptoms or metastases by lymphatic to the obturator lymph nodes. Or metastasis by blood to the axial skeleton especially to lumber spine, pelvis & thoracic spine producing osteoblastic reaction.

Prostatic carcinoma

Investigations: PSA : increase in prostatic carcinoma usually more than 10 ng/ml PAP : increase in cases with bony metastases Treatment: Surgery, radiotherapy & hormonal manipulation prognosis: depend on grading & staging but generally poor.

Penis

Disease included: Congenital anomalies. Inflammation. Tumors.

Congenital anomalies

Hypospadias & Epispadias Malformation of urethral groove & canal. Create abnormal opening either on the ventral surface of the penis (hypospadias) or the dorsal surface (epispadias) Hypospadias more common. May associated with undescended testis Complication: 1- UTI. 2-UT obstruction. 3- Abnormal ejaculation.

Phemosis

When the orifice of prepuce is too small to permit its normal retraction. Result in interference with cleanliness & accumulation of secretion under the prepuce. causes repeated attack of secondary infection. Complication: may result in tumor development.


Inflammation
Balanoposthitis: Infection of the glans & prepuce. Most common seen in uncircumcised newborns. Caused by pyogenic bacteria, anaerobic bacteria, Candida albicans , strept , staph. Syphilis Usually on glans. firm erythematous papule that ulcerate ( primary Syphilis). Condyloma lata (secondary syphilis). Gumas (granuloma) (tertiary syphilis)

Inflammation

Lymphogranuloma venereum Caused by Chlamydia trachomatis. Short live painless papule or ulcer. Associated with suppurative inflammation of inguinal lymph nodes.


Tumor Benign tumor Condyloma Acuminatum Caused by HPV type 6 & 11. Occurs on the external genital & peri anal. In penis occurs most often about the coronal sulcus & inner surface of the prepuce. Grossly: single or multiple sessile or pedunculated red papillary excrescencies from 1 to few millimeter. Histology: branching villous, papillary connective tissue stroma covered by epithelium with hyperkeratosis & koilocytosis (irregular nuclei &per nuclear vacuole).

Carcinoma In Situ

Epithelial lesions having cytological changes of malignancy confined to the epithelium with no evidence of local invasion or distal metastases. 3 types Bowens disease. Erythroplagia of Queyrat. Bowenoid papulosis.

Bowens Disease

Occurs in age over 15 years. Strong association with HPV 16 & 18 ( 80 %). Occurs in skin of shaft of penis & scrotum. Grossly: plaque with shallow ulceration & crusting. Histology: proliferation of epidermis with numerous mitosis & lack of orderly maturation. Cell are dysplastic with hyper chromatic nuclei. 10 % change to invasive squamous cell carcinoma .

Erythroplagia of Queyrat

Occurs on the glans & prepuce. Grossly: single or multiple, shiny red velvety plaque. Histology: as in Bowens disease.



Bowenoid papulosisSexually active young men (mean age 30), usually on skin of shaft, glans or scrotum.Associated with HPV 16 or 18.Almost never becomes invasive.May spontaneously regress.Gross: multiple, small, pigmented papular lesions, may resemble condyloma accuminatum.Micro: histologically resembles Bowen’s disease, but may have mild / heavy melanin pigmentation within the lesion; often spiky or flat appearance, may have less cytological atypia .

Squamous cell carcinoma

Occurs between 40 - 70 years. 10 - 20 % of male malignancies in some parts of Asia, Africa & south America. < than 1 % in U.S. Circumcision confers protection so it is rare in Moslems & Jews. 50 % of cases associated with HPV 16 & 18 Cigarette smoking is another risk factor.

Squamous cell carcinoma

Commonly occurs in glans or inner surface of the prepuce near the coronal sulcus. Grossly: either papillary or ulcerated lesion. Histology: invasion of nest of squamous cell of varying degree of differentiation with desmoplasia & inflammation. It is slowly growing tumor with early metastasis to the inquinal lymph node.

Testes & epididymis

Congenital anomalies. Inflammations. Tumors.

Congenital anomalies

Cryptorchidism (Undescended Testis) Found in approximately 1 % of 1 year-old boys. complete or incomplete failure of the intra abdominal testis to descend to the scrotal sac. Normally 2 phases transabdominal: from abdomen to the brim of the pelvis controlled by hormone (Mullerian-inhibitor substance) inguinoscrotal: controlled by androgen hormone from genitofemoral nerve. Transabdominal defect is uncommon (5-10%). Majority in inguinal canal. May associated with other anomalies.

Cryptorchidism (Undescended Testis)

Most common unilateral but in 25 % bilateral. Histological changes occurs as early as 2 years of age. Bilateral cases may result into sterility. Five folds to ten folds increase in testicular tumor in un descended.

Inflammation

More common in epididymis than in testis Four major specific types Gonorrhea. T.B. (mostly involve the epididymis). Mumps. Syphilis (affect first the testis).

Gonorrhea

Caused by Neisseria gonorrhea microorganism. Extension of infection from first the posterior urethra to the prostate, seminal vesicles & then to the epididymis. Causes epididymal abscess with extensive destruction.

Tuberculosis

Caused by Mycobacterium tuberculosis. Almost invariably begins in epididymis & may spread to the testis. Usually secondary extension from prostate or seminal vesicle. Causing granulomatous inflammation with caseation.

Mumps

It is a systemic viral disease that commonly affecting school-aged children. Testicular involvement is extremely uncommon in this age group. In post puberty 20 - 30 % of cases can involve the testis one week after the onset of parotid swelling.

Syphilis

Caused by Treponema pallidium. Almost invariably affecting testis. Either produce gamma (granuloma) or diffused interstitial inflammation with endarteritis obliterance & perivascular cuffing by lymphocytes & plasma cells.

Testicular tumors

Divided into 2 major categories Germ cell tumor (95 %). Non Germ cell tumor derived from stroma or sex cord. Most Germ cell tumors are highly aggressive cancer capable of rapid wide dissemination. generally non Germ cell tumors are benign .

Germ cell tumors

Age affected between 15-34 years. In this age group they constitute the most common tumor in male & account approximately 10 % of all cancer death. Much more common in whites than in blacks in ratio of 5:1. Divided into 2 categories: Seminoma (usually pure 40 %) Non seminomatous (usually mixed 60 %) these are: Embryonal carcinoma yolk sac tumor Teratoma Choriocarcinoma

Germ cell tumors

Pathogenesis Several influences may be important 1-Cryptorchidism: 10 % of testicular tumor associated with undescended testis. 2-Genetic predisposition: blacks more affected than whites. familial clustering (10 folds increase risk in close relative). 3-Testicular dysgenesis: testicular feminization & klinefilter syndrome increase risk. 4-Isochromosome 12 (i 12p) are found commonly in these tumors.

Seminoma

Divided into Classical (85 %). Anaplastic (5-10 %). Spermatocytic seminoma (4-6 %). Grossly: homogenous, gray-white, lobulated cut surface devoid from necrosis & hemorrhage. Histology: sheets of uniform cell with clear cytoplasm contain glycogen with infrequent mitosis these cells arrange in poorly demarcated lobules by delicate septa of fibrous tissue contain T-lymphocytes.

Embryonal carcinoma

More aggressive than seminoma. Grossly: small, variegated poorly demarcated at the margin with foci of necrosis & hemorrhage. Histology: sheets of large anaplastic, angry-looking cells with high mitotic count grow in glandular or alveolar or tubular pattern.

Yolk sac Tumor (endodermal sinus tumor)

Most common testicular tumor in infants& children up to 3 years of age with very good prognosis. In adult usually occurs in combination with embyronal carcinoma with bad prognosis. Grossly: homogenous, yellow-white, mucinous appearance Histology: lacelike network of cuboidal cells with Schiller-Duval bodies (glomeruli-like structure), with central capillary & mesodermal core. Cell contains eosinophilic, hyaline-like globules in which AFP can be demonstrated.

Choriocarcinoma

Highly malignant form of testicular tumor that is composed of both cytotrophoblast & sycytotrophoblast commonly occurs in mixture with other germ cell tumors. Grossly: small nodule with foci of hemorrhage & necrosis, rapidly growing. Secrete HCG Histology: mixture of syncytotrophoblast (large cell with many irregular hyper chromatic nuclei & abundant eosinophilic cytoplasm which is + ve for HGC) & trophoblast (polygonal cell with clear cytoplasm & single uniform nucleus).

Teratoma

Group of complex tumor derived from more than one germ cell layer. pure form are fairly common in infant & children. In adults occur in combination with other Germ cell tumor mostly embryonal carcinoma. Grossly: heterogeneous large mass with solid sometime cartilaginous & cystic areas. Histology: 3 types 1- Mature teratoma: different type of mature tissue e.g., neural, muscle, cartilage, bits of intestinal wall, bronchial epithelium, thyroid, skin...

Teratoma

2- Immature teratoma: elements of 3 germ layers but incompletely differentiated e.g., poorly formed cartilage, neuroblasts, loose mesenchyme & cluster of glandular structure. They consider as malignant variant. 3- Teratoma with malignant transformation: focus of clear cut squamous cell ca, adenocarcinoma, carcinoid or sarcoma.

Tumors of sex cord-gonadal stroma

Two main types Leydig cell tumor. Sertoli cell tumor.

Leydig cell tumor

Occurs between 20-60 years of age. common presenting features are testicular swelling, gynecomastia & sexual precocity in children. Tumor elaborate androgens or androgen & estrogens. Most are benign. Only 10 % invasive Grossly: homogenous golden brown circumscribed nodule Histology: polygonal cell with abundant granular eosinophilic cytoplasm with lipofuscin pigment & rod-shaped Reinke crystalloids.

Sertoli cell tumor

Same age group as Leydig cell tumor. May composed entirely of Sertoli cells or may have a component of granulosa cells. Some induced endocrinologic changes, either androgen or estrogen may be elaborated. Most are benign but 10 % are malignant. Grossly: firm small nodule with homogenous gray-white to yellow cut surface. Histology: uniform cells arrange in cord-like structures resembling immature seminiferous tubules.



Testicular Lymphoma
Account for 5 % of testicular neoplasm & constitute the most common form of testicular cancer in men over the age of 60 years. Grossly: Gray-white homogenous mass. Histology: almost all cases of diffused large cell lymphoma. Prognosis: extremely poor.

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