Session 31 Male Reproductive System Pathology

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Lecture Notes

Session 31: Male reproductive system Pathology

Felician Sikujua (MD)

Learning tasks

At the end of this session, students are expected to be able to:

Explain diseases of penis.

Explain scrotal disorders.

Explain diseases of testis.

Explain diseases of prostate.

Inflammatory lesions of the Penis

Inflammatory lesion of the penis

Sexual Transmitted Infections.

Balanitis.

Posthitis.

Balanoposthitis.

Fungal infections, e.g. Candidiasis.

Congenital Malformations of Penis

Hypospadias.

Epispadias.

Chordee.

Penile agenesis.

Bifid penis.

Hypospadias

Abnormal opening of the urethra is on the ventral aspect of the penis

More common than epispadias

Result from incomplete closure of urethral folds on the underside of the penis during embryo dev.

Related to defect in production/metabolism of fetal androgens.

Epispadias

Urethral opening on the dorsal surface of the penis.

Failure of midline penile fusion much earlier in embryogenesis.

Associated with bladder extrophy.

Inflammatory Lesions

Balanitis is local inflammation of the glans penis.

Posthitis is local inflammation of overlying prepuce.

Balanoposthitis refers to local inflammation of the glans penis and of the overlying prepuce.

Among the more common agents are Candida albicans, anaerobic bacteria, Gardnerella, and pyogenic bacteria.

Most cases occur as a consequence of poor local hygiene in uncircumcised males.

Accumulations of desquamated epithelial cells, sweat, and debris, termed smegma, acting as a local irritant.

Sexual Transmitted Infections

Disease

Causative agent

Bacterial cause

Gonorrhoea

Neisseria gonorrhoeae

Bacteria vaginosis

Gardnerella vaginalis

Bacteroides

Mycoplasma hominis

Chancroid

Haemophilus ducreyi

Viral cause

Genital herpes

Herpes simplex

Genital warts

Human papilloma virus

AIDS

HIV

Hepatitis

HBV

Spirochaetes

Syphilis

Treponema pallidum

Protozoa

Trichomoniasis

Trichomonas vaginalis

Fungi

Genital candidiasis

Candida albicans

Chlamydia

Lymphogranuloma venereum

Chlamydia trachomatis

Phimosis

Phimosis represents a condition in which the prepuce cannot be retracted easily over the glans penis.

This occurs when the orifice of prepuce is small.

Although phimosis may occur as a congenital anomaly, most cases are acquired from scarring of the prepuce secondary to previous episodes of balanoposthitis.

Regardless of its origin, most cases of phimosis are accompanied by evidence of ongoing distal penile inflammation.

Paraphimosis

When a stenotic prepuce is forcibly retracted over the glans penis, the circulation to the glans may be compromised, with resultant congestion, swelling, and pain of the distal penis, a condition known as paraphimosis.

Condition in which the foreskin of the penis, once retracted, cannot return back to its original location.

In paraphimosis, foreskin becomes trapped behind the glans penis, and cannot be reduced (pulled back to its normal flaccid position covering the glans penis).

Urinary retention may develop in severe cases.

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Neoplasms of Penis

More than 95% of penile neoplasms arise on squamous epithelium.

Most cases occur in uncircumcised patients older than 40 years of age.

Risk factors

Poor hygiene (with resultant exposure to potential carcinogens in smegma).

Cigarette smoking.

Infection with human papillomavirus (HPV), particularly types 16 and 18.

Scrotum disorders

Inflammatory conditions.

The skin of the scrotum may be affected by local fungal infections and systemic dermatoses.

Fournier’s gangrene.

Necrotizing infection or gangrene affecting the perineum.

Caused by a mixed infection by both aerobic and anaerobic bacteria.

Fulminating lesion which affect the scrotum and completely destroyed the skin, testes are left exposed.

Other disorders of Scrotum:Scrotal enlargement

Hydrocele.

Accumulation of serous fluid within the tunica vaginalis.

Chylocele.

Accumulation of lymphatic fluid within the tunica vaginalis.

Hematocele.

Accumulation of blood within the tunica vaginalis.

Varicocele.

Dilatation, elongation and tortuosity of the veins in pampini-form plexus in the spermatic cord.

Neoplasms of the scrotum

Neoplasms of the scrotal sac are unusual.

Squamous cell carcinoma, the most common of these, observation of a high incidence of the disease in chimney sweeps.

Testicular disorders

Testicular diseases may be congenital, inflammatory, or neoplastic.

Manifest themselves in a variety of ways: infertility, testicular atrophy, testicular enlargement and testicular local pain.

Congenital abnormalities of testes including

Tunder development of testis (hypoplasia).

Absence and aplasia of testis.

Undescended testis (Cryptorchidism).

Cryptorchidism

Cryptorchidism represents a failure of testicular descent into the scrotum.

The cause of the cryptorchidism is unknown.

Because undescended testes become atrophic, bilateral cryptorchidism causes infertility.

However, even unilateral cryptorchidism may be associated with atrophy of the contralateral descended gonad and therefore may also lead to sterility.

It is associated with a 3- to 5-times increased risk of testicular cancer.

Causative factors for Cryptorchidism

Hormonal abnormalities.

Intrinsic testicular abnormalities.

Mechanical problems (e.g. obstruction of the inguinal canal).

However, most cases the cause of the cryptorchidism is idiopathic.

Testicular Atrophy

Atrophic changes similar to those in cryptorchid testes may be caused by several other insults:

Chronic ischemia.

Trauma.

Irradiation.

Antineoplastic chemotherapy.

Conditions associated with chronically elevated estrogen levels (e.g., Cirrhosis).

Intratubular germ cell neoplasia is not a feature of these conditions, however.

Inflammatory lesions of the Testis

Common in the epididymis than in the testis proper.

Sexually transmitted infections.

Other causes of testicular inflammation include nonspecific epididymitis, orchitis, mumps, and tuberculosis.

Nonspecific epididymitis and orchitis usually begin as a primary urinary tract infection.

The involved testis typically is swollen and tender.

Histologically: Predominantly neutrophils, lymphocytes in mumps, granulomatous infl. in TB.

Testicular torsion

Torsion, or twisting of the spermatic cord typically results in obstruction of testicular venous drainage while leaving the thick-walled and more resilient arteries patent, so that intense vascular engorgement and venous infarction follow unless the torsion is relieved.

There are two (2) types of testicular torsion.

Neonatal torsion occurs either in utero or shortly after birth. It lacks any associated anatomic defect to account for its occurrence.

Adult torsion typically is seen in adolescence and manifests with sudden onset of testicular pain.

Testicular Neoplasms

Testicular germ cell tumors are subclassified into seminomas and nonseminomatous germ cell tumors.

Seminomas germ cell tumor.

Most common tumor of the testes.

Non seminomas germ cell tumors.

Embryonal carcinoma.

Yolk cell tumor.

Choriocarcinoma.

Teratoma.

Mixed tumor.

Testicular Tumors

Germ cells are the source of 95% of testicular tumors, and the remainder arise from Sertoli or Leydig cells.

Germ cell tumors may be composed of a single histologic pattern (60% of cases) or mixed patterns (40%).

The most common “pure” histologic patterns of germ cell tumors are seminoma, embryonal carcinoma, yolk sac tumors, choriocarcinoma, and teratoma.

Mixed tumors contain more than one element, most commonly embryonal carcinoma, teratoma, and yolk sac tumor.

Testicular Tumors

Seminomas remain confined to the testis for a long time and spread mainly to paraaortic nodes—distant spread is rare.

Nonseminomatous tumors tend to spread earlier, by both lymphatics and blood vessels.

Human chorionic gonadotropin (hCG) is produced by syncytiotrophoblasts and is always elevated in patients with choriocarcinomas and those with seminomas containing syncytiotrophoblasts.

Alpha fetoprotein (AFP) is elevated when there is a yolk sac tumor component.

Risk factors for Testicular neoplasms

The cause of testicular neoplasms remains unknown.

Testicular tumors are more common in whites than in blacks.

Cryptorchidism is associated with the risk of cancer.

Intersex syndromes, including androgen insensitivity syndrome and gonadal dysgenesis.

Family history is important.

The development of cancer in one testis is associated with a markedly increased risk of neoplasia in the contralateral testis.

Prostate

The normal prostate contains glands with two cell layers, a flat basal cell layer and an overlying columnar secretory cell layer.

Surrounding prostatic stroma contains a mixture of smooth muscle and fibrous tissue.

It is involved by infectious, inflammatory, hyperplastic, and neoplastic disorders, of which prostate cancer is by far the most important clinically.

Prostatitis

Prostatitis is divided into four (4) categories

Acute bacterial prostatitis.

Chronic bacterial prostatitis.

Chronic nonbacterial (abacterial) prostatitis.

Asymptomatic inflammatory prostatitis.

Acute bacterial prostatitis

Acute bacterial prostatitis is caused by the same organisms associated with other acute urinary tract infections, particularly Escherichia coli and other gram-negative rods.

Most patients with acute prostatitis have concomitant infection of the urethra and urinary bladder (acute urethrocystitis).

In these cases, organisms may reach the prostate by direct extension from the urethra or urinary bladder or by vascular channels from more distant sites.

Chronic prostatitis

Chronic prostatitis may follow clinical episodes of acute prostatitis, or may develop insidiously, without previous episodes of acute infection.

Two (2) types

Chronic bacterial prostatitis.

Chronic abacterial prostatitis

Account for most cases of chronic prostatitis.

Morphology of Acute Prostatitis

Acute prostatitis is characterized by the presence of an acute, neutrophilic inflammatory infiltrate, congestion, and stromal edema.

Neutrophils are initially most conspicuous within the prostatic glands.

As the infection progresses, the inflammatory infiltrate destroys glandular epithelium and extends into the surrounding stroma, resulting in the formation of microabscesses.

Morphology of Chronic Prostatitis

Lymphoid infiltrate, evidence of glandular injury, and, frequently, concomitant acute inflammatory changes.

Evidence of tissue destruction and fibroblastic proliferation, with inflammatory cells, such as neutrophils.

Granulomatous prostatitis include multinucleate giant cells and variable numbers of foamy histiocytes, sometimes accompanied by eosinophils.

Caseous necrosis is only seen in the setting of tuberculous prostatitis.

Benign prostatic hyperplasia (Nodular hyperplasia)

BPH is characterized by proliferation of both stromal and epithelial elements, with resultant enlargement of the gland and, in some cases, urinary obstruction.

The cause of BPH remains incompletely understood.

Excessive androgen-dependent growth of stromal and glandular elements has a central role.

BPH does not occur in males castrated before the onset of puberty or in men with genetic diseases that block androgen activity.

Pathogenesis of Benign Prostatic Hyperplasia

Androgens (testosterone and related hormones) are considered to play a permissive role in BPH.

Dihydrotestosterone (DHT), a metabolite of testosterone, is a critical mediator of prostatic growth

Synthesized in the prostate from circulating testosterone by the action of the enzyme 5α-reductase, type 2.

This enzyme is localized principally in the stromal cells, hence, those cells are the main site for the synthesis of DHT.

Pathogenesis of Benign Prostatic Hyperplasia cont…

DHT binds to nuclear androgen receptors and signals the transcription of growth factors that are mitogenic to the epithelial and stromal cells.

An inhibitor of 5α-reductase reduces prostate volume.

Estrogens also play a role in the etiology of BPH

Because BPH occurs, in general, elevated estrogen levels and relatively reduced free testosterone levels, and when prostate tissue becomes more sensitive to estrogens and less responsive to DHT

Morphology-BPH

The affected prostate is enlarged, circumscribed nodules that bulge from the cut surface.

The nodules may appear solid or contain cystic spaces.

The urethra is usually compressed by the hyperplastic nodules.

Microscopically the hyperplastic nodules are composed of proliferating glandular elements and fibromuscular stroma.

The hyperplastic glands are lined by tall, columnar epithelial cells and a peripheral layer of flattened basal cells.

Carcinoma of the Prostate

It is predominantly a disease of older males, with a peak incidence between the ages of 65 and 75 years.

Although the cause of carcinoma of the prostate remains unknown.

Hormones (androgens), genes, and environment all have a role in its pathogenesis.

Risk factors

Hereditary

American blacks than in whites, Asians, or Hispanics.

Environmental influence.

A diet high in animal fat.

Carcinoma of the Prostate cont…

Classification of Prostate cancer

Latent carcinoma

Incidental carcinoma

Clinical carcinoma.

Histologic Types of Prostatic Cancer

Adenocarcinoma (most common).

Transitional.

Squamous cell carcinoma.

Undifferentiated carcinoma.

Key points

Balanoposthitis refers to local inflammation of the glans penis and of the overlying prepuce.

Phimosis occurs when prepuce cannot be retracted easily over the glans penis.

Smegma, cigarette smoking and HPV 16,18 are the risk factors for penile carcinoma.

Complications of cryptorchidism include testicular cancer and infertility.

Seminomas (one of the germ cell tumor) is the commonest testicular tumor.

Dihydrotestosterone (a metabolite of testosterone) is a critical mediator of prostatic growth.

Review questions

Differentiate between hypospadias from epispadias.

List five (5) causes of scrotal swelling.

Explain fournier’s gangrene.

List five (5) causes of testicular atrophy.

Explain pathogenesis of benign prostate hyperplasia.

References

Goljan E.;(2007): Rapid Review Pathology (2th Ed.) Elsevier Saunders, USA. Pg. 433-442.

Kumar V. ; Abbas A. K. ; Aster J. C.;(2013): Robbins and Contran Pathologic Basis of Disease (9th Ed.) Elsevier Saunders, USA. Pg. 657-665.

Mohan H.;(2010): Text book of Pathology (6th Ed.) Jaypee Brothers Medical Publishers, India. Pg. 703-718.

Xiu P.;(2012): Crash Course Pathology (4th Ed.) Elsevier Saunders, USA. Pg. 217-222.

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Session 31 Male Reproductive System Pathology

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