Dr. Roopam Jain, Professor & Head, Dept. of Pathology & Blood Bank

1. The Male Reproductive System & Prostate
PATHOLOGY
DR. ROOPAM JAIN
PROFESSOR & HEAD, PATHOLOGY

2. The Male Reproductive
System & Prostate

3. DEVELOPMENTAL DISORDERS
CRYPTORCHIDISM
• Cryptorchidism or undescended testis is a condition in which the testicle
is arrested at some point along its descent.
• Its incidence is about 0.2% in adult male population.
• In 70% of cases, the undescended testis lies in the inguinal ring,
• in 25% in the abdomen
• and, in the remaining 5%, it may be present at other sites along its
descent from intra-abdominal location to the scrotal sac.

4. DEVELOPMENTAL DISORDERS
CRYPTORCHIDISM - ETIOLOGY
• 1. Mechanical factors e.g. short spermatic cord, narrow
inguinal canal, adhesions to the peritoneum.
• 2. Genetic factors e.g. trisomy 13, maldevelopment of the
scrotum or cremaster muscles.
• 3. Hormonal factors e.g. deficient androgenic secretions

5. DEVELOPMENTAL DISORDERS
CRYPTORCHIDISM
MORPHOLOGIC FEATURES
• Cryptorchidism is unilateral in 80% cases & bilateral in the
rest.
• Grossly, the cryptorchid testis is small in size, firm & fibrotic

6. DEVELOPMENTAL DISORDERS
CRYPTORCHIDISM
CLINICAL FEATURES
• As such, cryptorchidism is completely asymptomatic and is
discovered only on physical examination.
• significant adverse clinical outcome may result:
• 1. Sterility-infertility
• 2. Inguinal hernia
• 3. Malignancy

7. MALE INFERTILITY
• The morphologic pattern of testicular atrophy described above for
cryptorchidism can result from various other congenital or acquired
causes of male infertility.
• These causes can be divided into 3 groups:
• pre-testicular,
• testicular and
• post-testicular

8. MALE INFERTILITY
A. Pre-Testicular Causes
• 1. Hypopituitarism
• 2. Oestrogen excess
• 3. Glucocorticoid excess
• 4. Other endocrine disorders

9. MALE INFERTILITY
B. Testicular Causes
• 1. Agonadism i.e. total absence of the testes.
• 2. Cryptorchidism or undescended testis described above.
• 3. Maturation arrest
• 4. Hypospermatogenesis
• 5. Sertoli cell-only syndrome
• 6. Klinefelter’s syndrome
• 7. Mumps orchitis.
• 8. Irradiation damage

10. MALE INFERTILITY
C. Post-Testicular Causes
• 1. Congenital block e.g. absence or atresia of vas deferens.
• 2. Acquired block e.g. due to gonorrhoea and surgical
intervention.
• 3. Impaired sperm motility in the presence of normal sperm
counts e.g. immotile cilia syndrome

11. INFLAMMATIONS
• Inflammation of the testis is termed as orchitis and of epididymis is
called as epididymitis; latter being more common.
• A combination epididymo-orchitis may also occur.
• A few important types are
• NON-SPECIFIC EPIDIDYMITIS AND ORCHITIS
• GRANULOMATOUS (AUTOIMMUNE) ORCHITIS
• TUBERCULOUS EPIDIDYMO-ORCHITIS
• SPERMATIC GRANULOMA

12. ELEPHANTIASIS
• Elephantiasis is enormous thickening of the scrotal skin resembling the
elephant’s hide and results in enlargement of the scrotum.
• The condition results from filariasis in which the adult worm lives in the
lymphatics, while the larvae travel in the blood.
• The most important variety of filaria is Wuchereria bancrofti.
• The condition is common in all tropical countries.
• The vector is generally the Culex mosquito.
• The patients may remain asymptomatic or may manifest with fever, local
pain, swelling, rash, tender lymphadenopathy and blood eosinophilia.

13. MISCELLANEOUS
LESIONS

14. TORSION OF TESTIS
• Torsion of the testicle may occur either in a fully-descended testis or
in an undescended testis.
• The latter is more common and more severe.
• It results from sudden cessation of venous drainage and arterial
supply to the testis
• Torsion is common in boys and young men.

15. VARICOCELE
• Varicocele is the dilatation, elongation and tortuosity of the veins of the
pampiniform plexus in the spermatic cord.
• It is of 2 types: primary (idiopathic) and secondary. ”
• Primary or idiopathic form is more frequent and is more common in
young unmarried men. ”
• Secondary form occurs due to pressure on the spermatic vein by
enlarged liver, spleen or kidney. It is commoner in middle-aged people.

16. HYDROCELE
• A hydrocele is abnormal collection of serous fluid in the tunica vaginalis.
• It may be acute or chronic, congenital or acquired.
• The usual causes are trauma, systemic oedema such as in cardiac failure
and renal disease, and as a complication of gonorrhoea, syphilis and
tuberculosis.

17. HAEMATOCELE
• Haematocele is haemorrhage into the sac of the tunica vaginalis.
• It may result from direct trauma, from injury to a vein by the needle, or
from haemorrhagic diseases.
• In long-standing cases, the tunica vaginalis is thickened with dense
fibrous tissue coated with brownish material due to old organised
haemorrhage and occasionally may get partly calcified (Fig.)

18. Haematocele
testis
Sectioned surface of the sac shows thick wall coated
internally by brownish, tan and necrotic material which
is organised blood clot (arrow

19. TESTICULAR
TUMOURS

20. Classification
of testicular
tumours

21. • all testicular tumours are divided into 3 groups:
germ cell tumours,
sex cord-stromal tumours
mixed forms.
• Vast majority of the testicular tumours (95%) arise from
germ cells or their precursors in the seminiferous tubules,
while less than 5% originate from sex cord-stromal
components of the testis.
• From clinical point of view, germ cell tumours of the testis
are categorised into 2 main groups—
seminomatous
non-seminomatous

22. Distinguishing features of seminomatous
(SGCT) & non-seminomatous (NSGCT) germ
cell tumours of testis

23. TESTICULAR TUMOURS
ETIOLOGIC FACTORS
• 1. Cryptorchidism
• 2. Other developmental disorders
• 3. Genetic factors
• 4. Other factors
i) Orchitis
ii) Trauma
iii) Carcinogens

24. HISTOGENESIS
4 Classification, incidence and histogenesis of testicular tumours

25. CLINICAL FEATURES AND DIAGNOSIS
• The usual presenting clinical symptoms of testicular
tumours are gradual gonadal enlargement and a dragging
sensation in the testis.
• Metastatic involvement may produce secondary symptoms
such as pain,
• lymphadenopathy,
• haemoptysis and
• urinary obstruction

26. SPREAD
• Since testicular germ cell tumours originate from totipotent germ cells, it
is not unusual to find metastases of histologic types different from the
primary growth.
• Testicular tumours may spread by both lymphatic and haematogenous
routes:
• 1. Lymphatic spread occurs to retroperitoneal para-aortic lymph nodes,
mediastinal lymph nodes and supraclavicular lymph nodes.
• 2. Haematogenous spread primarily occurs to the lungs, liver, brain and
bones.

27. TUMOUR MARKERS
• Germ cell tumours of the testis secrete polypeptide hormones and
certain enzymes which can be detected in the blood. Two tumour
markers widely used in the diagnosis, staging and monitoring the
follow-up of patients with testicular tumours are: human chorionic
gonadotropin (hCG) and alpha-foetoprotein (AFP). In addition,
carcinoembryonic antigen (CEA), human placental lactogen (HPL),
placental alkaline phosphatase, testosterone, oestrogen and
luteinising hormone may also be elevated.
• 1. hCG is synthesised by placental syncytio-trophoblast such as in
various non-seminomatous germ cell tumours of the testis (e.g. in
choriocarcinoma, yolk sac tumour and embryonal carcinoma).
However, ectopic hCG production may occur in a variety of non-
testicular non-germ cell tumours as well.
• 2. AFP is normally synthesised by the foetal liver cells, yolk sac and
foetal gut. Its levels are elevated in testicular tumours associated
with yolk sac components. However, elevated serum AFP levels are
also found in liver cell carcinoma.

28. PROGNOSIS
• For selecting post-orchiectomy treatment (radiation, surgery,
chemotherapy or all the three) and for monitoring prognosis, 3 clinical
stages are defined:
• Stage I: tumour confined to the testis.
• Stage II: distant spread confined to retroperitoneal lymph nodes below
the diaphragm.
• Stage III: distant metastases beyond the retroperitoneal lymph nodes.