URETHRA AND MALE GENITAL SYSTEM (PENIS & TESTIS)

DR.SAURAV SINGH

ANATOMY OF URETHRA

• In males – Urethra is 20 cm in length – three named regions– Prostatic urethra• Passes through the prostate gland

–Membranous urethra• Through the urogenital diaphragm

– Spongy (penile) urethra• Passes through the length of the penis

URETHRA IN FEMALES _4 cm in length

BOUND BY CONNECTIVE TISSUE TO ANTERIOR WALL OF VAGINA

URETHRAL ORIFICE EXITS BODY BETWEEN VAGINAL ORIFICE AND CLITORIS

URETHRA

Epithelium of urethra Transitional epithelium

At the proximal end (near the bladder) Stratified and pseudostratified columnar –

mid urethra (in males) Stratified squamous epithelium

At the distal end (near the urethral opening)

STRUCTURE OF URETHRA

Muscle layer

Submucosa layer

Mucosa

5

URETHRA

Inflammation (Urethritis) Causative agents: Gonococcal urethritis( N.gonococcus) Nongonococcal urethritis- E.coli/ other enteric bacteria C.trachomatis Mycoplasma Urethritis is often accompanied by cystitis in women and

prostatitis in men.

Symptoms: local pain, fever, itching and frequency.

Reiters syndrome: clinical triad of arthritis, conjunctivitis and urethritis.

Morphology: changes are typical of inflammation.

TUMOR AND TUMOR-LIKE CONDITIONS

Urethral caruncle

Present as a small, red ,painful mass about the external urethral meatus.

It may be covered with intact mucosa but is extremely friable and bleeds to slightest trauma.

Histologic examination- inflamed granulation tissue, polyp can be seen.

Benign epithelial tumors includes

Squamous and urothelial papilloma

Inverted urothelial papilloma

Condylomas

URETHRAL POLYP

These include:

Inflammatory polyp

Caruncle

Urothelial papilloma

Nephrogenic adenomas and polyp

Presentation:

Dysuria and hematuria

Histology

Polyps are lined by prostatic-type epithelium , may be solitary or multiple.

characterised by a papillary or filiform fibrovascular core covered by glandular epithelium.

The luminal layer is columnar whereas the basal layer is cuboidal or flat.

Polyps may also contain acini some with corpora amylacea.

Majority of these polyps stain strongly for PSA and PSAP using IHC techniques.

Histogenesis of these benign polyps is unclear but possibilities include:

Activation of embryonic nests Metaplasia Overgrowth of the urothelium by proliferating

prostatic epithelium.

CONGENITAL POSTERIOR URETHRAL POLYP / FIBROEPITHELIAL POLYPS

Seen in young boys who present with mild symptoms of bladder outlet obstruction and hematuria.

Located in the area of verumontanum.

Histologically, they are characterised by congested or edematous fibrovascular stroma lined by transitional epithelium.

CARCINOMA OF URETHRA

Male urethral cancer

Prostatic and membranous urethra: tumors arising are usually transitional type and most commonly associated with bladder tumors.

These do not express PSA or PSAP antigens and are not hormone sensitive.

Bulbous and membranous urethra: tumors are mostly squamous type and rarely associated with vesical neoplasm.

Female urethral cancer

Usually epidermoid.

Proximal two-thirds of female urethra: tumors arising are transitional cell type and associated often with vesical neoplasm's.

Distal one-third of urethra: are usually squamous cell type.

Adenocarcinomas of urethra

These are rare tumors and arise from the periurethral glands or through metaplasia of the surface urothelium.

ANATOMY OF PENIS

Consists of: foreskin, glans, shaft, & root

Penis - formed of three cylindrical masses of erectile tissue - enclosed in separate fibrous coverings - held together by a covering of skin

Root at base of penis, divides into crura which are attached to the pelvic bones

Glans is at the tip of the penis and is the most sensitive part for most men - covered by prepuce or foreskin which may be removed by a surgical procedure called circumcision

smegma - secretion that can accumulate under foreskin of penis

Corona (crown) - ridge between glans and foreskin Frenulum - connects glans to shaft on underside of penis

Two "corpora cavernosa" One "corpus spongiosum" which lies ventrally

in the penis and houses the spongy urethra. Expands at the end of the penis into the "glans penis.

Congenital Anomalies

1. Epispadias & Hypospadias =Malformations of the urethral groove: • Epispadias - opening on the Dorsal surface of

penis • Hypospadias - More common(1 in male 300

births)- opening on ventral surface of penis

• Complications: Urinary obstruction ↑ risk of ascending UTI, can’t ejaculate properly infertility.

1. HYPOSPADIAS & EPISPADIAS

HYPOSPADIASopening in the ventral surface of penisMore common

EPISPADIASopening in the DORSAL surface of penis

↑ risk of infectioncan’t ejaculate properly

2. Phimosis =Abnormally narrow prepuce – prevents normal retraction;

Results in Urinary obstruction, ↑ risk of recurrent infections, ↑ risk of cancer.

3. Paraphimosis = forcible retraction of the prepuce in cases of

Phimosis, extremely painful, severe congestion of the Glans, acute urinary obstruction

PHIMOSIS & PARAPHIMOSIS

• Inflammations

• 1. Balanitis : Inflammation of the Glans, Commonly caused by

Phimosis. • 2. Balanoposthitis : Infection of the Glans and prepuce.

• Both caused by-pyogenic bacteria including gonococcus, anaerobic bacteria

– Fungi – Candida (seen in diabetics)

– Mycoplasma, Chlamydia, gardnerella

Most often consequence of poor local hygiene in uncircumcised males & underlying systemic disorder such as Diabetes.

3. Specific STD’s

• Syphilis• Gonorrhea • Chanchroid • Granuloma inguinale • Lymphogranuloma venereum • Herpes (HSV-2)• HPV

PENILE FIBROMATOSIS (PEYRONIE'S DISEASE)

Mostly affects men between ages 40-60. A history of penile trauma and urethritis is

present in some instances, suggesting a sclerosing inflammatory process in the genesis of the lesion.

It presents as an indurated plaque or indentation in the corpora cavernosa.

30% of cases are associated with erectile dysfunction.

TUMORS OF PENIS• Benign tumors

• Condyloma Accuminatum (genital warts) = Benign, HPV (types 6 & 11)

Gross: Occurs as a papillary excrescence at coronal sulcus or inner surface of the prepuce.

Histologically: Papillae covered by- Hyperplastic Hyperkeratotic ( acanthosis) Stratified squamous epithelium of orderly

maturation sequence Koilocytosis (vacuolation) of scattered

superficial cell.

CONDYLOMA ACCUMINATUM

koilocytosis

MALIGNANT

• Carcinoma in Situ( CIS)- includes:

- Bowen disease- Seen in both men and women over the age of 35

years. Strongly associated with HPV especially type 16.

In men it involves the skin of the shaft of the penis an scrotum.

Gross- solitary thickened gray white opaque lesion.

Erthroplasia of Queyrat- clinical variant of bowen disease presenting as a shiny red velvety plaque.

shiny red plaque•

Histology Epidermis shows proliferation with

numerous mitosis , markedly dysplastic cells with large hyperchromatic nuclei and lack of orderly maturation.

However, the dermal-epidermal border is sharply delineated by an intact basement membrane.

Bowenoid papulosis Occurs in sexually active adults Presence of multiple reddish brown

papular lesions. Histologically similar to bowen disease

and is also related to HPV 16 But virtually never develops into

invasive carcinoma.

Feature Bowen’s Disease(Carcinoma in situ )

Bowenoid Papulosis

Age >30 yrs <30 yrs

lesions Solitary, Gray- white Multiple, reddish brown

Behavior ↑risk of invasive carcinoma (10% cases)

Never

Visceral malignancies

↑risk of visceral malignancies

No

Histology Carcinoma in situ(HPV-16)

Same as Bowen’s(HPV-16)

CARCINOMA IN-SITU

MALIGNANT CANCER OF PENIS

• Invasive carcinoma • Age- 40 to 70yrs• Almost exclusively seen in non-circumcised

males (Possible carcinogens in smegma); • Cause : HPV types 16 & 18; • Cigarette smoking elevates the risk.• Circumcision confers protection.

Clinical features Slow growing locally invasive lesion,

usually non-painful unless there is secondary ulceration and infection.

Progressive growth Spreads to inguinal & iliac lymph nodes, Later by blood.

Prognosis: Overall 5-year survival rate is <50% (with positive nodes<30%).

Morphology Usually begins on the glans or inner

surface of prepuce near the coronal sulcus. Two macroscopic patterns :1. Papillary lesion- simulate condyloma

acuminata , produces a cauliflower-like fungating.

2. Flat lesions- areas of epithelial thickening along with graying and fissuring of the mucosal surface

.

Histology- Both types are squamous cell carcinomas with varying degrees of differentiation.

Majority of the usual SCC show infiltrating keratinization with moderate degrees of differentiation.

Verrucous carcinoma- exophytic well differentiated variant of SCC that has low malignant potential.

Other less common subtypes of penile SCC includes

Basaloid Warty( condylomatus) Papillary Sarcomatoid Pseudohyperplastic Pseudoglandular( adenoid) Adenosquamous variants

SQUAMOUS CELL CARCINOMA

ANATOMY OF THE TESTIS

Testis are paired oval structures about 4 cm in the longest (vertical) diameter lying in the scrotal sac

Epididymis , mass formed by tortuous tubules lies on its posterior border- It has a Head , Body and Tail

Tunica vaginalis – outermost layer ,closed sac covering testis and epididymis , has visceral and parietal layers

Tunica albuginea- deep to tunica vaginalis formed by a dense fibrous membrane

Substance of the testis divided into lobules containing highly convoluted seminiferous tubules involved in spermatozoa production

Each testis has about 200 lobules, one to three seminiferous tubules in each lobule

Tubules enter the fibrous tissue in posterior part of testis to form a network called rete testis

Tunica vasculosa lies deep to tunica albuginea, layer of vascular tissue

• Congenital anomalies• Cryptorchidism : Failure of descent of testis from the abdominal cavity

through the inguinal canal.

• Causes: Most common idiopathic

epidemiology about1% of males right > left, 25% bilateral

Pathogenesis Hormonal abnormalities Testicular abnormalities Mechanical problems

CLINICAL COURSE When unilateral, may see atrophy in

contralateral testis. sterility concomitant inguinal hernia increased risk of testicular malignancy

Orchiopexy ( Placement in the scrotal sac) May help prevent atrophy May not decrease risk of malignancy.

Morphology – Atrophic changes by 2 yrs of age; – Arrest in the development of germ cells– Hyalinization and thickening of seminiferous

tubules & interstitial fibrosis– Sparing Leydig cells which become prominent– With progressive tubular atrophy the testis

becomes small and firm in consistency.– Similar changes - contralateral descended

testis

TESTICULAR ATROPHY

Atrophy is a regressive change affecting scrotal testis It is the end stage of an inflammatory orchitis Possible causative factors: Atherosclerotic narrowing of the blood supply in old

age cryptorchidism hypopituitarism generalized malnutrition or cachexia irradiation prolonged administration of female sex hormones, as

in treatment of patients with carcinoma of the prostate Cirrhosis

klinefelters syndrome.

Associated with decreased fertility, hypospermatogenesis, maturation arrest and sometimes vas deferens obstruction.

Histology: Hyalinization of seminiferous tubules & interstitial

fibrosis

Sparing of Leydig cells.

TESTICULAR ATROPHY

•Focal atrophy infection (mumps)•↑ in space

Atrophy

Normal

Normal Atrophyhyalinized

REGRESSIVE CHANGES

VASCULAR DISORDERS

TORSION Twisting of the spermatic cord which typically

cuts off the venous drainage of the testis. There is intense vascular engorgement

which may lead to hemorrhagic infarction• Bilateral anatomic defect where the testis

has increased mobility giving rise to “bell-clapper” abnormality

Neonatal torsion: occurs either in utero or just after birth.

Adult torsion: typically seen in adolescence. C/f- sudden onset tesicular pain, often

without any inciting injury. Testis should be surgically explored and

manually untwisted within 6 hours to maintain its viability.

Contralateral un-affected one should surgically fixed

( Orchiopexy )

Morphology Depends on the duration of the process. Intense congestion Extravasation of blood into the interstitial

tissue Haemorrhagic testicular infarction Late stages: marked enlargement of

testis sac of soft, necrotic, hemorrhagic

tissue

TORSION OF TESTICLE

INFLAMMATION

• 1. Nonspecific Epididymitis & Orchitis• Infection reaches the epididymis and

testis from the urinary tract through either the vas deferens or via lymphatics of spermatic cord.

• causative agents:– children- Gram negative rods– 15-35 year old (sexually active males)-

Chlamydia & Neisseria– Older men- E. coli & Pseudomonas;

• Histology: – Early stage: Acute suppurative inflammation

characterised by congestion, edema and infiltration by neutrophils, macrophages and lymphocytes.

– Later stages: Fibrosis & hyalinization

sterility– Leydig cells - not affected (normal sexual

activity)

• 2. Granulomatous Orchitis- – Also called “Autoimmune Orchitis”– Presents in middle age – Sudden onset of tender testicular mass; fever may be seen if painless and of insidious onset, may mimic

testicular tumor

Histology: Granulomas within seminiferous tubules

SPECIFIC INFLAMMATIONS

1. Gonorrheal Epididymo -Orchitis- Retrograde infection from the posterior

urethra to prostate, seminal vesicles and then to epididymis causing suppurative Epididymitis.

may lead to development of frank abcesses and finally destruction of epididymis.

In untreated cases, spread to testis (suppurative Orchitis)

2. Mumps Orchitis-

1 week after onset of parotitis; seen in postpubertal males testicular involvement is rare in school

aged children Orchitis is unilateral in 70% of cases.

Histology: Interstitial inflammation with mononuclear cellular infiltrate

Recovery is complete

3. Tuberculous Epididymo - Orchitis- Primarily Epididymitis, with secondary

spread to the testis.

– Histology: – Caseating granulomas. – sinuses on the dorsal surface of the scrotum

4. Syphilitic Orchitis- Starts in the testis rarely spreading to epididymis

Histology: production of Gummas or

Diffuse interstitial inflammation with lympho plasmacytic infiltrate and

obliterative endarteritis with perivasular cuffing of lymphocytes and plasma cells.

SPERMATIC CORD AND PARATESTICULAR TUMORS

Lipoma of spermatic cord common lesion affecting the proximal

spermatic cord usually diagnosed at the time of inguinal

hernial repair not a true neoplasm, rather represents

retroperitoneal adipose tissue that has been pulled into the inguinal canal along with hernial sac

Adenomatoid tumor most common benign paratesticular tumor involves the epididymis and also

spermatic cord presents as painless , firm, intrascrotal

mass typically , head of epididymis is affected

Gross : Well circumscribed , firm, white to tan nodule , usually less than 2 cm.

Microscopy characteristic solid to cystic tubules and

cords of vacuolated cells cells lining the tubules are flattened to

cuboidal with a prominent intervening fibrous stroma.

the cellular vacuoles may yield a signet ring-like appearance

cytoplasm is typically abundant and eosinophilic with vesicular nuclei.

IHC shows positivity for CK, EMA and Calretinin

Malignant paratesticular tumors

in children: Rhabdomyosarcoma in adults: liposarcomas

located at the distal end of spermatic cord.

References : Robin – pathologic basis of disease. Sternberg. Urinary MG WHO. Internet.