SummaryThis document provides a comprehensive overview of male reproductive system pathologies, covering congenital malformations, inflammatory conditions, and
SummaryThis document provides a comprehensive overview of male reproductive system pathologies, covering congenital malformations, inflammatory conditions, and neoplasms of the penis, testis, epididymis, and prostate. It details conditions such as hypospadias, squamous cell carcinoma of the penis, cryptorchidism, testicular torsion, germ cell tumors, prostatitis, benign prostatic hyperplasia (BPH), and prostate carcinoma. Key risk factors, pathogenesis, clinical features, and management strategies are discussed for each pathology. Key Points- Hypospadias is the most common penile malformation, characterized by a ventral urethral opening, and is associated with increased UTI risk. Squamous cell carcinoma is the predominant penile neoplasm, with risk factors including poor hygiene, smoking, and HPV infection. Cryptorchidism significantly increases the risk of both sterility and testicular cancer, even in the contralateral descended testis. Testicular torsion is a urologic emergency caused by twisting of the spermatic cord, requiring prompt surgical intervention to prevent venous infarction. Germ cell tumors account for 95% of postpubertal testicular neoplasms, often presenting as painless masses, and are frequently associated with the molecular marker isochromosome i(12p). Benign Prostatic Hyperplasia (BPH) is an androgen-dependent proliferation of prostatic tissue in the transitional zone, causing obstructive and irritative urinary symptoms in many older men. Prostate carcinoma is the most common cancer in men, typically arising in the outer peripheral zone, and is graded by the Gleason system. Tumor markers like hCG, AFP, and LDH are crucial for the diagnosis and monitoring of testicular germ cell tumors. - Detailed Notes Congenital MalformationsMost penile malformations involve abnormal positioning of the distal urethral orifice. Hypospadias Urethral opening on the ventral (underside) of the penis Most common penile malformation — 1 in 300 live male births Constricted orifice → urinary obstruction + increased UTI risk Associated with inguinal hernia and cryptorchidism - Epispadias Urethral opening on the dorsal (top) of the penis Less common than hypospadias Severe cases associated with bladder exstrophy - Inflammatory LesionsBalanitis — inflammation of the glans penis Balanoposthitis — inflammation of the glans AND prepuce (foreskin) Organisms: Candida albicans, anaerobic bacteria, Gardnerella, pyogenic bacteria Most common in uncircumcised males with poor hygiene Smegma (dead skin, sweat, debris) acts as the local irritant - Phimosis Foreskin cannot retract over the glans Can be congenital; most cases acquired from scarring after balanoposthitis Perpetuates smegma accumulation, recurrent infection, and increased SCC risk - NeoplasmsOver 95% of penile neoplasms arise from squamous epithelium. More common in developing countries. Most cases occur in uncircumcised males over 40 years. Risk Factors for Squamous Cell Carcinoma (SCC) Uncircumcised males over 40 Poor hygiene — smegma exposure Smoking HPV infection, especially types 16 and 18 - Bowen Disease — SCC In Situ Solitary plaque on the shaft of the penis in older uncircumcised males Histology: malignant cells throughout the epidermis — no stromal invasion Progresses to invasive SCC in ~10% of cases - Invasive Squamous Cell Carcinoma Gray, crusted, papular lesion — most commonly on the glans or prepuce Infiltration produces an indurated, ulcerated lesion with irregular margins Histology: typical keratinizing SCC Prognosis is stage-dependent - Verrucous Carcinoma Variant of SCC with papillary architecture and virtually no cytologic atypia Rounded, pushing deep margins Locally invasive — does not metastasize - CryptorchidismFailure of complete testicular descent from the abdomen into the scrotum. Present in ~1% of 1-year-old males. Both bilateral and unilateral forms associated with tubular atrophy and sterility. Microscopic tubular atrophy evident by age 5–6 years; hyalinization by puberty Foci of intratubular germ cell neoplasia develop within atrophic tubules — precursors to germ cell tumours Carries 3–5 fold increased risk of testicular cancer; history of cryptorchidism found in ~10% of all testicular cancer cases Contralateral descended testis also carries increased cancer risk Treatment: Orchiopexy — reduces risk of both sterility and malignancy - Note: Similar atrophic changes occur with chronic ischemia, trauma, irradiation, chemotherapy, and elevated estrogen states (e.g. cirrhosis) — but these do not produce intratubular germ cell neoplasia. Inflammatory LesionsNonspecific Epididymitis and Orchitis Spreads from UTI via vas deferens or spermatic cord lymphatics Testis: swollen and tender Histology: predominantly neutrophilic inflammatory infiltrate - Mumps Orchitis Complicates mumps in ~20% of infected adult males; rare in children Testis: oedematous and congested Histology: lymphoplasmacytic infiltrate Severe cases → necrosis, tubular atrophy, fibrosis, and sterility - Tuberculous Epididymo-orchitis Most common cause of granulomatous orchitis Usually begins as epididymitis → secondary testicular involvement Histology: granulomatous inflammation with caseous necrosis — identical to TB elsewhere - Vascular Disturbances — Testicular TorsionTwisting of the spermatic cord obstructs venous drainage while arteries remain patent → venous infarction. A urologic emergency — must be relieved within 6 hours to preserve viability. Neonatal Torsion Adult Torsion --- --- --- Timing In utero or shortly after birth Adolescence Anatomic defect None identified Bell-clapper abnormality — increased testicular mobility Onset — Sudden pain; may awaken patient from sleep Management: Surgical exploration + manual untwisting. Contralateral orchiopexy performed routinely to prevent torsion on the other side. Testicular NeoplasmsEpidemiology ~6 per 100,000 males; more common in whites Brothers of affected males have 8–10 fold increased risk Cryptorchidism → 3–5 fold increased risk; present in ~10% of all testicular cancer cases Intersex syndromes (androgen insensitivity, gonadal dysgenesis) also increase risk Key molecular marker: isochromosome i(12p) — found in virtually ALL germ cell tumours regardless of histologic type - Classification 95% of postpubertal testicular tumours arise from germ cells — all malignant Sex cord-stromal tumours (Sertoli, Leydig cell) — uncommon and usually benign - Germ Cell Tumour Summary Tumour Peak Age Morphology Tumour Markers --- --- --- --- Seminoma 40–50 Sheets of uniform polygonal cells, clear cytoplasm, lymphocytes in stroma hCG elevated in 10% Embryonal Carcinoma 20–30 Poorly differentiated pleomorphic cells in cords, sheets, or papillary formation Negative (pure form) Yolk Sac Tumour <3 years Poorly differentiated endothelium-like cuboidal/columnar cells AFP elevated in 90% Choriocarcinoma 20–30 Cytotrophoblast + syncytiotrophoblast, no villus formation hCG elevated in 100% Teratoma All ages Tissues from all 3 germ layers, variable differentiation Negative (pure form) Mixed Tumour 15–30 Variable depending on mixture hCG + AFP elevated in 90% Clinical Features of Testicular Tumours- Present as a painless, non-translucent testicular mass — non-translucence distinguishes it from hydrocele Biopsy risks tumour spillage → standard management is radical orchiectomy Seminomas — remain confined to testis for long periods; metastasize to iliac and para-aortic lymph nodes; haematogenous spread occurs late Nonseminomatous tumours — metastasize earlier via lymphatic and haematogenous routes; commonest sites are liver and lungs - Tumour Markers — Clinical Importance Useful in both diagnosis and monitoring treatment response hCG — always elevated in choriocarcinoma; also elevated when syncytiotrophoblastic cells present in other tumours AFP — elevated indicates yolk sac tumour component LDH — correlates with overall tumour burden - ProstatitisFour recognized categories: Category Frequency K