Tuesday, September 30, 2008

Testicular Tumours: Germ Cell Tumours

Germ Cell Tumours:
Germ cell tumour gives rise to either a seminoma (an undifferentiated germ cell tumour) or an embryonal carcinoma (a tumour of totipotent cells).
Embryonal carcinoma may undergo somatic differentiation and become a teratoma. Alternatively, extra-embryonic differentiation results in a yolk sac tumor (endodermal sinus tumour) or a choriocarcinoma.
Metastases of germ cell tumours may show a form of differentiation not present in the primary tumour.
Infants and children are most commonly afflicted with yolk sac tumours and teratomas. Choriocarcinomas are more frequent in the second or third decades, embryonal carcinoma in the third decade, and seminoma in the fourth decade.
Identification of tumour marker includes:
1. Chorionic gonadotropin : Typically found in patients with choriocarcinoma.
2. Alpha-fetoprotein: Found in patients with yolk sac tumour or embryonal carcinoma with yolk sac elements.
Important risk factors are the following:
1. Cryptorchidism: Associated with 10% of testicular tumours.
2. Genetic factors: Higher risk of testicular neoplasia among siblings of patients with testicular tumours ; some familial clustering reported. Significant racial differences also exist (rare in African blacks).
3. Testicular dysgenesis: Includes testicular feminization and Klinefelter syndrome.
Cytogenetic abnormalities involving chromosome 12 are common; i(12p) is present in 90% of testicular germ cell tumors. In the remaining cases, extra genetic material derived from 12p is found in other chromosomes, thus implicating genes located on the short arm of chromosome 12.
Incidence of germ cell tumours is approximately 6: 100,000 men annually, with peak incidence between ages 15 to 34 years.
Germ cell tumours account for 10% of cancer deaths in this age group. Incidence is higher in whites than in blacks in all geographic locations.
Classification and histogenesis:
Diverse classification schemes are based on different morphologic patterns and variable concepts of histogenesis. Testicular germ cell tumours may contain a single histological pattern (40% of cases) or a mixture of patterns (60% of cases).
Most tumours arise from a focus of intratubular carcinoma in situ.
The neoplastic germ cells may give rise to seminoma or transform into a totipotential neoplastic cell (embryonal carcinoma) capable of further differentiation.
Germ cell neoplasms accordingly may be divided into seminomas and non-seminomatous tumours.
General characters of Germ cell Tumors:
Clinically, most cases present with painless enlargement of the testis.
Neoplasia should be considered in the differential diagnosis of all testicular masses, even those that are painful. Clinical evaluation, however, does not reliably distinguish between the various types of germ cell tumours.
Clinical staging is accomplished via physical examination, radiographic imaging of the retroperitoneum and chest, and assay of various tumour marker.
Clinical stages are as follows:
Stage I: Tumour confined to the testis
Stage II: Metastases limited to retroperitoneal nodes below the diaphragm.
Stage III: Metastases outside the retroperitoneal nodes or above the diaphragm.
Metastases: Lymphatic metastases are most common in retroperitoneal para-aortic nodes but may occur in more distant sites (Example: mediastinal and supraclavicular nodes).
The lungs are the most common site for hematogenous metastases, followed by liver, brain, and bone.
Biological behaviour: Biological behaviour of nonseminomatous germ cell tumours (NSGCTs) is in general, more aggressive than that of seminomas. Roughly 70% of seminomas present with localized (clinical stage I) disease, in contrast, 60% of NSGCTs present with advanced stage (stage II or III) disease. Extensive metastases may be present even with small primary lesions, particularly in the case of choriocarcinoma.
Immunology: Several peptides may be produced by germ cell tumours and can be detected in body fluids by sensitive assays. AFP and HCG are the most commonly assayed. Lactate dehydrogenase although not specific for testicular tumours, is produced by the tumour cells, and the degree of elevation provides a rough measure of tumour burden.

Serum markers are of value to:
i) Evaluate testicular masses
ii) Stage germ cell tumours
iii) Assess tumour burden
iv) Monitor the response of a germ cell tumour to therapy.

Treatment includes radiation and chemotherapy, depending on the histologic type of the tumour (seminoma versus NSGCT) and the stage of the disease, chemotherapy, in particular, has dramatically improved the prognosis of patients with NSGCT.

Abstracts: Germ cell tumors of the gonads: a selective review emphasizing problems in differential diagnosis, newly appreciated, and controversial issues.Mod Pathol. 2005 Feb;18 Suppl 2:S61-79.
Gonadal germ cell tumors continue to be the cause of diverse, diagnostically challenging issues for the pathologist, and their correct resolution often has major important therapeutic and prognostic implications. They are academically interesting because of the biological diversity exhibited in the two gonads and variation in frequency of certain neoplasms. The most dramatic examples of the latter are the frequency of dermoid cyst in the ovary compared to the testis and the reverse pertaining to embryonal carcinoma. Within the teratoma group, there is strong evidence that ovarian and prepubertal testicular teratomas are derived from benign germ cells, a pathogenesis that likely applies also to the rare dermoid cysts and uncommon epidermoid cysts of the testis. In contrast, postpubertal testicular teratomas derive from malignant germ cells, specifically representing differentiation within a preexistent nonteratomatous cancer. As expected, given the foregoing, teratomas in boys are clinically benign, whereas in postpubertal males they are malignant, independent of their degree of immaturity. On the other hand, immaturity is an important finding in ovarian teratomas, irrespective of age, although its significance in children has recently been challenged. It is usually recognized on the basis of embryonic-appearing neuroepithelium, which shows mitotic activity and apoptosis in contrast to differentiated neuroepithelial tissues, which may occur in mature ovarian teratomas. Rarely it is based on the presence of cellular, mitotically active glial tissue. Fetal-type tissues alone are not sufficient for a diagnosis of immature teratoma. Further differences between the teratomatous tumors in the two gonads are the relative frequency of monodermal teratomas in the ovary in contrast to the testis, where only one subset, carcinoids, is seen with any frequency. When uncommon somatic-type malignancies (usually squamous cell carcinoma) occur in mature cystic teratomas of the ovary, this is a de novo form of malignant transformation; similar tumors in the testis, a very rare event, represent overgrowth of teratomatous elements that originated from malignant, nonteratomatous germ cell tumors and, therefore, had previously undergone malignant transformation. Germinomas may have several unusual features in each gonad; these include microcystic arrangements that suggest yolk sac tumor, tubular patterns that mimic Sertoli cell tumor, apparent increased cytological atypia that causes concern for embryonal carcinoma, and prominent syncytiotrophoblast giant cells that suggest choriocarcinoma. Awareness of these variants, good technical preparations, the retained typical cytological features of germinoma cells, and the judicious use of tailored panels of immunohistochemical stains resolve these dilemmas in virtually all instances. Two aspects of germinomas are unique to the testis. Firstly, intertubular growth of small seminomas may cause them to be overlooked. Secondly, the distinctive spermatocytic seminoma occurs only in the testis. A newly recognized aspect of this tumor is the propensity for some to be relatively monomorphic, making them apt to be mistaken for usual seminoma or embryonal carcinoma, although the characteristic polymorphic appearance in some foci, absence of intratubular germ cell neoplasia, unclassified type, and immunohistochemical stains should prevent this error. Cytoplasmic membrane immunoreactivity for placental alkaline phosphatase and CD117, with usual negativity for AE1/AE3 cytokeratins, is helpful in the diagnosis of germinoma. The recently described marker, OCT3/4, a nuclear transcription factor, is especially helpful in the differential of germinoma and embryonal carcinoma with other neoplasms. Yolk sac tumor continues to be confused occasionally with clear cell carcinoma of the ovary. Glandular ('endometrioid-like') yolk sac tumors mimic endometrioid carcinomas; predominant or pure hepatoid yolk sac tumors cause concern for metastatic hepatocellular carcinoma or, in the ovary, primary hepatoid carcinoma, and solid patterns, especially in limited samplings, may be misinterpreted as germinoma. The usually younger age of patients with yolk sac tumors helps with the differential considerations with the nongerm cell tumors, as do other clinical and microscopic features and selected immunohistochemical stains. Choriocarcinoma is rare in both gonads, and those in the ovary must be distinguished from metastatic tumors of placental origin. Syncytiotrophoblast cells alone, admixed with other forms of germ cell tumor, still are confused with choriocarcinoma, but this phenomenon, which is much more frequent than choriocarcinoma, lacks the plexiform arrangement of different trophoblast cell types that typifies the latter. Mixed germ cell tumors (which may show almost any combination of components) are common in the testis but rare in the ovary. A separately categorized, rare form of mixed germ cell tumor seen in both gonads is the polyembryoma. It is perhaps the most photogenic of all gonadal germ cell tumors and is also intriguing because of its distinctive, organized arrangement of yolk sac tumor and embryonal carcinoma elements and recapitulation of very early embryonic development, even to the extent of having in its fundamental unit, the embryoid body, a miniature yolk sac, and amniotic cavity. These tumors, which are constituted by innumerable embryoid bodies, almost always contain teratomatous glands in minor amounts, and one way of viewing the polyembryoma is to consider it the most immature form of teratoma. Embryoid bodies are also common as a minor component of many mixed germ cell tumors, particularly in the testis, and the diffuse embryoma is another variant that has a particular arrangement of yolk sac tumor and embryonal carcinoma elements. Regression of gonadal germ cell tumors is a phenomenon restricted to the testis, for unknown reasons. These so-called 'burnt-out' germ cell tumors can be recognized by a distinctive constellation of findings, including sometimes minor foci of residual recognizable germ cell neoplasia, a well-defined zone of scarring (often having residual ghost tubules), associated lymphoplasmacytic infiltrate, intratubular calcification and, in about 50%, of in situ germ cell neoplasia.

Monday, September 29, 2008

Testis and Epididymis: Spermatic Granulomas

Spermatic granulomas result from an intense inflammatory response to sperm that enter into the interstitial tissue of epididymis.
The cause of extravasation of the sperm is not clear but trauma or infection may play a role.
Clinically, patients present with scrotal pain and swelling of weeks or months duration.
Microscopically, a mixed inflammatory cell infiltrate is associated with numerous extravasated sperm fragments and phagocytosis of sperm by histiocytes. Ultimately the inflammatory process results in interstitial fibrosis and ductal obstruction.

Testis and Epididymis: Miscellaneous Lesions of Tunica Vaginalis

Miscellaneous Lesions of Tunica Vaginalis :
Conditions include the following:
Hydrocele: Accumulation of serous fluid within the tunica vaginalis, either secondary to generalized edema or due to incomplete closure of the processus vaginalis. A hydrocele may become secondarily infected.
Hematocele: Accumulation of blood within the tunica vaginalis secondary to trauma, torsion, or hemorrhage; a generalized bleeding diathesis; or, rarely, invasion of the tunica by neoplasms.
Chylocele: Accumulation of lymphatic fluid within the tunica vaginalis, secondary to lymphatic obstruction (Example: In patients with elephantiasis).
Spermatocele: Local accumulation of semen in the spermatic cord, generally within a dilated duct in the head of the epididymis.
Varicocele: Local accumulation of blood within a dilated vein in the spermatic cord (internal spermatic veins that drain the testicle).It is a very common condition present in 15% of the general male population and 40% of men evaluated for infertility. A varicocele develops because of defective valves that normally allow for blood to flow away from the testicle toward the abdomen. Testicular injury occurs due to abnormal back flow of blood from the abdomen into the scrotum and this creates a hostile environment for sperm development.

Sunday, September 28, 2008

Testis and Epididymis: Vascular Disturbances -Testicular Torsion

Vascular disturbances : Testicular torsion
Torsion occurs secondary to twisting of the spermatic cord, resulting in venous obstruction.
Arteries may also be occluded but often remain patent due to thicker walls.
Torsion typically occurs in patients with preexisting structural lesions, such as incompletely descended testis, absence of scrotal ligaments, or testicular atrophy.
Torsion is generally precipitated by physical trauma or other violent movement.
Changes range from congestion and interstitial hemorrhage to extensive hemorrhagic necrosis, depending on the duration and severity of the process.

Testis and Epididymis: Specific Inflammations -Syphilis

Syphilis always begins as orchitis with secondary involvement of the epididymis.
It may present as isolated orchitis without involvement of adnexal structures.
Orchitis may occur in both congenital and acquired syphilis.
Microscopically, syphilis may produce nodular gummas ( Syphilitic Gumma ) or diffuse interstitial inflammation. Interstitial changes include edema, lymphocytic and plasma cell infiltration and typical obliterative endarteritis with perivascular cuffing of lymphocytes and plasma cells. Gradually, there is complete loss of seminiferous tubules and interstitial cells.

Testis and Epididymis: Specific Inflammations -Tuberculosis

Tuberculosis almost always begins in the epididymis and may spread to the testis.
Tuberculosis of testis is usually unilateral and may occur at any age.
They are commonly associated with the tuberculosis of lungs and genitourinary tract.
Discrete tubercles in the testis may be seen in generalized military tuberculosis.
Commonly earliest lesion is seen as an area of granuloma with caseous necrosis in the globus minor due to retrograde infection via vas deferens from seminal vesicle.
Blood-borne infection commences on the globus major.
This lesion usually regresses and becomes calcified.
Progressive lesion shows involvement of the entire epididymis.
Tunica vaginalis serves as a barrier against extension into the testis. It is often seen that there is complete destruction of the epididymis with no invasion of the testis.
Clinically, a firm often painless mass is felt behind the testis.
In 30% cases secondary hydrocele may be present.

Testis and Epididymis: Specific Inflammations - Mumps

Mumps is a systemic viral disease that most commonly affects school-aged children.
In adult males orchitis typically develops in about 1 week after onset of parotid inflammation, rarely, it may precede parotitis or occur in the absence of parotitis.
Orchitis occurs as a complication in 20 to 30% of cases of mumps and on 70% cases there is unilateral testicular involvement. Due to unilateral involvement and patchy interstitial inflammation, it is usually, not associated with sterility,
Grossly, The testis is enlarged with punctate hemorrhages in the tunica albuginea.
Microscopically, there are acute inflammatory cells together with infiltration of histiocytes in the interstitial tissue. Seminiferous tubules show no evidence of spermatogenesis and the cells in the lumen are Sertoli cells.
Neutrophils are usually not prominent but in the more intense inflammatory response, frank suppuration may develop with tubular lumen distended with pus.

Saturday, September 27, 2008

Testis and Epididymis: Specific Inflammations - Gonorrhea

1. Most cases of gonorrhea are due to retrograde extension of infection from the posterior urethra to prostate, seminal vesicles, and epididymis.
2. The inflammatory pattern is identical to that seen in nonspecific epididymitis and orchitis.
Infection may extend to the testis and produce suppurative orchitis in untreated cases.

Friday, September 26, 2008

Testis and Epididymis : Granulomatous (Autoimmune) Orchitis

Granulomatous (Autoimmune) Orchitis:
Granulomatous orchitis is an uncommon cause of unilateral testicular enlargement in middle-aged men. It has a possible autoimmune origin.
Clinically, most cases present with sudden onset of tender testicular mass, sometimes associated with fever. It may be painless in some patients and difficult to distinguish from testicular neoplasia.
Microscopically, non-caseating granulomas occur within testicular tubules and adjacent connective tissue, accompanied by occasional plasma cells and neutrophils.
Epithelioid cells may originate from Sertoli cells.
Lesions must be differentiated from granulomas of tuberculosis.
Grossly, the testis is enlarged, grayish-white or brownish in colour with normal or thickened tunica albuginea.

Testis and Epididymis : Nonspecific Epididymitis and Orchitis

Nonspecific epididymitis and orchitis:
Nonspecific epididymitis and orchitis are often associated with infection of the urinary tract, with secondary infection of the epididymis via vas deferens or lymphatics of the spermatic cord.
Causes vary with the age of the patient and include:
i) In pediatric patients it is usually associated with genitourinary malformations.
ii) In sexually active men, younger than age 35 years of age, the sexually transmitted pathogens, Chlamydia trachomatis (Chlamydial Infection; Chlamydial Infection of the Genital Tract) and Neisseria gonorrhoea are the frequent organisms.
iii) In older age, Escherichia coli and Pseudomonas species are responsible for most infections.
Microscopically, nonspecific interstitial congestion, edema and neutrophilic infiltrates occur in the early stage, with subsequent involvement of tubules. Severe cases may progress to generalized suppuration of the entire epididymis. Inflammation may extend to the testis via efferent ductules or local lymphatic channels. Scarring of the testis and epididymis may occur with resultant infertility. Leydig cells are less severely affected and sexual activity generally is not disturbed.

Thursday, September 25, 2008

Testis and Epididymis : Inflammations

Inflammatory conditions are more common in the epididymis than in the testis; however, some infections notably syphilis (syphilitic gumma) , may begin in the testis with secondary involvement of the epididymis.
Inflammatory diseases include nonspecific epididymitis and orchitis, granulomatous (autoimmune) orchitis, and several specific infectious diseases (Eg: Gonorrhea, mumps, tuberculosis, syphilis) .

Testis and Epididymis : Atrophy

Atrophy of the Testis:
Atrophy is the regressive change affecting the testis.
Causes include:
1. Progressive arteriosclerotic narrowing of the blood supply in old age.
2. End stage of orchitis
3. Cryptorchidism
4. Hypopituitarism
5. Generalized malnutrition or cachexia
6. Obstruction to the outflow of semen
7. Irradiation and chemotherapy
8. Prolonged administration of female sex hormones as in the treatment of carcinoma prostate.
9. Persistently elevated levels of follicle-stimulating hormone,
10. Primary developmental abnormality in patients with Klinefelter syndrome.
Gross and microscopic alterations are identical to those in cryptorchidism.

Testis and Epididymis: Cryptorchidism

1. Cryptorchidism affects 1% of 1-year-old boys.
2. It is the failure of descent and testes may be found anywhere along the normal path of descent, from abdominal cavity to the inguinal canal.
3. Most cases are idiopathic; other causes include:
i) Genetic abnormalities (e.g., trisomy 13)
ii) Hormonal abnormalities
4. Most cases are unilateral; 25% are bilateral.
5. Microscopically, the changes may be apparent, as early as 2 years of age, including decreased germ cell development, thickening and hyalinization of seminiferous tubular basement membrane, interstitial fibrosis, and relative sparing of Leydig cells. Spermatogenesis is lacking but Sertoli cells fill the lumen of the seminiferous tubules (Fig 19-3). Regressive changes may also occur in the contralateral descended testis.
6. Clinically, cryptorchidism is asymptomatic and it is found only when the scrotal sac is discovered not to contain the testis. Its significance is related to high prevalence of inguinal hernia, sterility, and a 5- to-10-fold increased incidence of testicular neoplasms.
Surgical correction (orchiopexy) decreases the likelihood of sterility, if performed early but does not decrease the risk of neoplasia, which may occur in either testis.

Testis and Epididymis: Congenital Anomalies

Congenital Anomalies:
Anomalies include cryptorchidism, aplasia, fusion (synorchism) and a variety of developmental cysts.

Penis: Malignant tumours

Squamous cell carcinoma:
The frequency of squamous cell carcinoma shows a marked geographic variation, with the highest incidence in Asian countries, Africa, and Central America. The variation in frequency has been associated with personal, social, and religious practices, including personal hygiene and the practice of circumcision. In USA it accounts for about 1% of cancers in men between the ages 40 and 70 years. Carcinoma of the penis is extremely rare in Jews and Moslems.
Potential causes are carcinogens within smegma accumulating under the foreskin and HPV types 16 and 18 infection.
Grossly, it presents as epithelial thickening on the glans or inner surface of the prepuce near the coronal sulcus, progressing to ulceroinfiltrative or exophytic growth eroding the penile tip, shaft, or both.
Microscopically, it is identical to squamous cell carcinomas involving other cutaneous sites.
Clinically, it is characterized by slow growth with metastases to regional (inguinal and iliac) lymph nodes; distant metastases are common. This progression can be expected within 2 years of the initial diagnosis.
The 5-year survival rate is 66% for lesions confined to penis and 27% with regional node involvement.
Verrucous carcinomas:
Verrcous carcinomas, also called giant condyloma or Buschke-Lowenstein tumor, is an uncommon, well-differentiated form of squamous cell carcinoma with low malignant potential. This is seen with greater frequency in the larynx. The carcinoma cells show minimal atypia. Large penile carcinomas cause complete destruction of penis.

Penis: Bowenoid Papulosis

Bowenoid Papulosis
Grossly, bowenoid papulosis presents as a multiple, pigmented (violet) papules in the penile shaft. It may mimic condyloma acuminatum grossly. Patients are generally two decades younger than those with Bowen's disease.
Bowenoid papulosis is histologically indistinguishable from Bowen's disease, but, in contrast to Bowen's disease, evolution into invasive carcinoma is rare.

Penis: Erythroplasia of Queyrat

Erythroplasia of Queyrat:
Erythroplasia of Queyrat generally appears on the glans or prepuce as a single or multiple, shiny-red, sometimes velvety plaques. Histologic features and evolution are comparable to those of Bowen's disease. There is no association with visceral malignancy.

Penis: Bowen's Disease

Bowen's disease
Bownen's disease may occur in the genital region in both men and women, generally those older than 35 years of age. In men it mainly involves the shaft of the penis and the scrotum.
Grossly, it appears as a solitary, thickened, gray-white, opaque plaque with shallow ulceration and crusting.
Microscopically, there is marked epidermal proliferation with numerous mitosis, some atypical. There is complete loss of normal surface maturation but the basement membrane is intact and there is no invasion of underlying stroma. Transition to invasive squamous cell carcinoma is estimated to occur in about 10% of cases; there is a possible association with visceral malignancies (about one-third of patients).

Penis: Carcinoma in situ

Carcinoma in situ:
Carcinoma in situ is the histologic term used to describe cytologic evidence of malignancy (e.g. marked dysplasia, hyperchromasia, pleomorphism) confined to the epithelium with no invasion of underlying connective tissue or distant metastasis.
It shows extensive or patchy parakeratosis, hyperkeratosis, papillomatosis with broad epidermal papillae, thinning of the granular layer.
A chronic inflammatory cell infiltrate in the subjacent dermis is characteristic.
Variants include Bowen's disease ; Eryhtroplasia of Queyrat and Bowenoid papulosis.

Penis: Benign tumours - Condyloma Acuminatum

Condyloma Acuminatum:
1. Condyloma acuminatum is a benign epithelial proliferation caused by human papilloma virus (HPV), especially type 6 and 11.
2. Condyloma acuminatum may involve mucocutaneous genital surfaces of either sex. Sexual contact is the most likely mode of transmission. It is most common after puberty. Its presence in prepubertal child should arouse suspicion of sexual abuse.
3. Grossly, the lesion is a sessile or pedunculated papillary excrescence. In male, it often involves the coronal sulcus or inner surface of the prepuce. Large condylomas are cauliflower-like in appearance and small ones require colposcopic detection.
4. Microscopic characteristics include branching fibrovascular stromal papillae covered by hyperplastic stratified squamous epithelium, often associated with prominent hyperkeratosis. Vacuolation of superficial epithelial cells (koilocytosis) is common. Maturation of epithelial cells is orderly, in contrast to carcinoma in situ.
5. Most lesions remain benign. They may recur due to persistence of HPV infection.
6. It has association with and possible etiologic role in the development of cervical dysplasia, carcinoma in situ, and squamous cell carcinoma. Type16, 18, and 31 have been found in the vast majority of high-grade precancerous lesions and invasive carcinomas.

Penis: Tumours

Tumours of the penis include: Benign tumours ; Carcinoma in situ ; and malignant tumours.

Penis : Peyronie’s disease

Peyronie’s disease is of unknown etiology and is characterized by focal asymmetric fibrosis induration of the shaft of the penis without significant change of the overlying skin.
Fibrosis results in curvature and discomfort of the penis at the time of erection.
It occurs in a young or middle aged man.
Rarely, it may be inherited with an autosomal dominant transmission.
Microscopically, dense dermal fibrosis focally replaces the muscle in the septum of the corpus cavernosum. Occasionally the fibrous tissue undergoes ossification.
No reliable therapy has emerged.

Penis: Balanoprosthitis

Balanoprosthitis is the nonspecific infection of the glans penis and prepuce, generally associated with phimosis or a redundant prepuce, and resultant chronic accumulation of smegma.
It may be caused by a wide variety of bacteria, fungi, mycoplasmas and chlamydiae (Chlamydial Infection ; Chlamydial Infection of the Genital Tract) .
Such inflammation, if neglected may lead to ulceration of the mucosal surface of the glans.

Penis: Inflammations

Inflammations characteristically involve both the glans penis and the prepuce.
Nonspecific inflammatory processes and specific sexually transmitted diseases (Example: Syphilis , gonorrhea, chancroid, lymphogranuloma venereum, genital herpes, granuloma inguinale) occur.

Penis : Congenital Anomalies

Penis is the site of many congenital anomalies only some of which have clinical significance.
A variety of abnormalities occur in size and form, including aplasia or hypoplasia; hypertrophy; duplication; pin-hole meatus, and more commonly, hypospadias, epispadias, and phimosis.
Hypospadias and Epispadias:
Malformation of the urethral groove and urethral canal causes abnormal openings either on the ventral surface of the penis (hypospadias) or on the dorsal surface (epispadias). These may be associated with other urogenital malformations, including undescended testes.
Its clinical significance is as follows:
i) Constriction of this abnormal opening may produce partial urinary obstruction with spread of infection from penile urethra to bladder and the entire urinary tract.
ii) When the orifice is situated at the base of the penis, normal ejaculation and insemination are hampered or totally blocked producing sterility in men.
Phimosis is the inability to retract the prepuce because of an abnormally small preputial orifice. It may arise as a primary developmental defect but is more commonly secondary to inflammatory scarring of the prepuce. Phimosis predisposes to secondary infection and carcinoma, due to chronic accumulation of secretions and other debris under the foreskin.
Paraphimosis is the abnormal painful swelling of the glans penis after forceful retraction of a phimotic prepuce. It may cause urethral obstruction.
Circumcision is effective therapy for phimosis and the complication of balanoposthitis.

Anatomy and Embryology of Male Genital Tract

Anatomy and Embryology:
In embryo, urinary system develops in 3 attempts (pronephros, mesonephros, metanephros).
Pronephros is replaced by mesonephros.
Metanephros utilizes only the distal mesonephric duct to complete the development of urogenital system.
Metanephros forms kidney with nephrons, renal pelvis, ureter, urinary bladder and urethra.
Mesonephros forms gonads, vas deferens, seminal vesicle, and ejaculatory duct.
Prostate is developed from the proximal part of urethra and composed of urethral (metanephros), urogenital sinus, mesonephros and paramesonephric tissue.