1. URETHRA AND MALE
GENITAL SYSTEM (PENIS
& TESTIS)
DR.SAURAV SINGH

2. 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

3. 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


4. 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)

5. STRUCTURE OF
URETHRA
 Muscle
layer
 Submucosa
layer
 Mucosa
5

6. URETHRA

Inflammation (Urethritis)
Causative agents:
Gonococcal urethritis( N.gonococcus)
Nongonococcal urethritisE.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.

7. 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

8. 
URETHRAL POLYP
These include:
Inflammatory polyp
Caruncle
Urothelial papilloma
Nephrogenic adenomas and polyp
Presentation:
Dysuria and hematuria

9. 
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.

10. 
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.




12. 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.

13. 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.

14. 
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.

15. 
Adenocarcinomas of urethra
These are rare tumors and arise from the periurethral
glands or through metaplasia of the surface urothelium.

19. ANATOMY OF PENIS
Consists of:

foreskin, glans, shaft, & root

20. 
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

22. 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.


23. 
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.

24. 1. HYPOSPADIAS & EPISPADIAS
HYPOSPADIAS
opening in the ventral
surface of penis
More common
EPISPADIAS
opening in the DORSAL
surface of penis
↑ risk of infection
can’t ejaculate properly

25. 
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

26. PHIMOSIS & PARAPHIMOSIS

27. •
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.

28. 3. Specific STD’s
•
•
•
•
•
•
•
Syphilis
Gonorrhea
Chanchroid
Granuloma inguinale
Lymphogranuloma venereum
Herpes (HSV-2)
HPV

29. 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.


30. 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.

31. Histologically:
Papillae covered by
Hyperplastic

Hyperkeratotic ( acanthosis)

Stratified squamous epithelium of orderly
maturation sequence

Koilocytosis (vacuolation) of scattered superficial
cell.


32. CONDYLOMA ACCUMINATUM
koilocytosis

34. MALIGNANT
•
Carcinoma in Situ( CIS)- includes:
- Bowen diseaseSeen 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
•

35. 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.

36. 
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.

37. 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)

38. CARCINOMA IN-SITU

39. 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.

40. 
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%).

41. 
1.
2.
.
Morphology
Usually begins on the glans or inner surface of
prepuce near the coronal sulcus.
Two macroscopic patterns :
Papillary lesion- simulate condyloma acuminata
, produces a cauliflower-like fungating.
Flat lesions- areas of epithelial thickening along
with graying and fissuring of the mucosal surface

42. 
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.

43. 
Other less common subtypes of penile SCC
includes
Basaloid
Warty( condylomatus)
Papillary
Sarcomatoid
Pseudohyperplastic
Pseudoglandular( adenoid)
Adenosquamous variants

45. SQUAMOUS CELL CARCINOMA

48. 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

50. 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


51. •
•
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

52. 
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.


53. 
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

55. 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.

56. Associated with decreased
fertility, hypospermatogenesis, maturation arrest and
sometimes vas deferens obstruction.
Histology:
Hyalinization of seminiferous tubules & interstitial fibrosis
Sparing of Leydig cells.

57. TESTICULAR ATROPHY
Normal
Normal
Atrophy
•Focal atrophy 
infection (mumps)
•↑ in space
Atrophy
hyalinized

58. REGRESSIVE CHANGES

59. 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

60. 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 )

61. 
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

62. TORSION OF TESTICLE

64. 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;

65. •
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)
–

66. •
2. Granulomatous OrchitisAlso 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

68. SPECIFIC INFLAMMATIONS

1. Gonorrheal Epididymo -OrchitisRetrograde 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)

70. 2.
Mumps Orchitis1 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

71. 3. Tuberculous Epididymo - OrchitisPrimarily Epididymitis, with secondary spread to
the testis.
–
–
–
Histology:
Caseating granulomas.
sinuses on the dorsal surface of the scrotum

72. 4. Syphilitic OrchitisStarts 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.

73. 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

74. 
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.

75. 
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 ringlike appearance
cytoplasm is typically abundant and
eosinophilic with vesicular nuclei.
IHC shows positivity for CK, EMA and Calretinin

78. 
Malignant paratesticular tumors
in children: Rhabdomyosarcoma
in adults: liposarcomas
located at the distal end of spermatic cord.

79. 
References :
Robin – pathologic basis of disease.
Sternberg.
Urinary MG WHO.
Internet.