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PA28.1-6 | Male Genital Tract — PBL Case
CLINICAL SETTING
Rajan, a 24-year-old farm labourer from a small village in Tamil Nadu, arrives at the surgery outpatient of the district government hospital. He has been ignoring a swelling of his right testis for nearly four months, initially dismissing it as 'just a knock' from heavy work. His wife, worried by the increasing size and his recent unexplained weight loss, persuaded him to make the three-hour bus journey to town. He has no history of trauma, no fever, and denies pain — the lump is firm, heavy, and 'silent,' which is precisely why he ignored it for so long. On examination, the right testis is replaced by a hard, non-transilluminable mass roughly 7 cm in diameter; the left testis is normal. He has no palpable inguinal lymphadenopathy, but there is a faint, soft fullness in the right iliac fossa.
Trigger 1: The Silent Swelling
The casualty medical officer performs a detailed history. Rajan had an undescended right testis as a child; his mother recalls the 'small operation' performed at a rural health post when he was around 3 years old, though records are unavailable. He reports no recent infections, no urinary symptoms, and no gynecomastia. On scrotal palpation, the mass is hard, arises within the testis (not the epididymis), and is separate from the spermatic cord. Transillumination is negative. A baseline scrotal ultrasound is ordered and shows a 6.8 cm hypoechoic intratesticular mass with internal vascularity on Doppler. The radiologist notes the absence of haemorrhage or cystic change within the mass.
DISCUSSION POINTS
- Why does a painless firm testicular mass in a young man demand immediate investigation rather than a 'wait and watch' approach? What pathological process does this presentation most strongly suggest?
- Rajan had a history of cryptorchidism corrected in early childhood. How does cryptorchidism increase the risk of germ cell tumours, and does successful orchiopexy eliminate that risk entirely?
- Based on the ultrasound description — hypoechoic, homogeneous, no haemorrhage or cystic areas — which testicular tumour type fits best? What is the significance of the absence of internal haemorrhage on ultrasound?
- What is the correct approach to biopsy a suspected testicular tumour, and why must a trans-scrotal biopsy be avoided? How does the lymphatic drainage of the testis differ from that of the scrotum, and why does this matter surgically?
Click to reveal Trigger 2: Markers, Pathology, and Spread (discuss previous trigger first!)
Trigger 2: Markers, Pathology, and Spread
Serum tumour markers drawn before surgery return: AFP 18 IU/mL (normal <10), beta-hCG 420 mIU/mL (mildly elevated), LDH 680 U/L (elevated). A CT scan of the abdomen and pelvis reveals two enlarged para-aortic lymph nodes at the level of L2, the largest measuring 2.1 cm. There is no retroperitoneal mass and no visceral metastases. Chest X-ray is clear. Radical inguinal orchiectomy is performed. The pathologist receives a 7.2 cm testis: the cut surface is homogeneous, creamy-white, and lobulated with fibrous septa — no haemorrhage, no necrosis. Histology shows sheets of large, uniform polygonal cells with clear glycogen-rich cytoplasm, prominent nucleoli, lymphocytic stroma, and fibrous septa. AFP on immunostaining is negative in the tumour cells.
DISCUSSION POINTS
- The AFP is mildly above normal and the beta-hCG is mildly elevated in a patient whose histology shows a pure seminoma. The surgical pathologist states 'if AFP were significantly elevated, I would have looked harder for a non-seminomatous component.' Explain the AFP rule for seminoma and its clinical implications.
- The tumour has spread to para-aortic lymph nodes at L2. Trace the lymphatic pathway from the right testis to explain why this is the first nodal station, and contrast this with the lymphatic drainage that would change if scrotal skin were involved.
- Using the CT findings and pathology, assign a clinical stage to this patient. What are the criteria for Stage I, IIA, and IIB in testicular seminoma?
- Which serum marker — AFP, beta-hCG, or LDH — is most useful for monitoring recurrence after treatment in pure seminoma, and why is a rising AFP in a 'treated seminoma' always an alarm signal?
Click to reveal Trigger 3: Treatment Decision and Long-Term Outlook (discuss previous trigger first!)
Trigger 3: Treatment Decision and Long-Term Outlook
Post-orchiectomy, the oncology team reviews the case. The para-aortic nodes regress completely after a short course of radiotherapy, and all tumour markers normalise to within reference range. Rajan is discharged on a surveillance protocol. Three months later, at follow-up, his wife brings up a new concern: she notices Rajan has developed mild bilateral breast enlargement, which embarrasses him. Examination reveals soft, rubbery bilateral subareolar tissue. A 17-year-old cousin of Rajan, seen in the same clinic the same day, presents with a testicular mass that is variegated on ultrasound with haemorrhagic areas, AFP of 4,800 IU/mL, and beta-hCG of 82,000 mIU/mL.
DISCUSSION POINTS
- Explain the pathological mechanism by which a testicular germ cell tumour can cause gynaecomastia. Which tumour type is the classical culprit, and how does hormone mimicry via the LH receptor explain this phenomenon?
- The cousin's tumour has a variegated cut surface with haemorrhage, markedly elevated AFP, and very high beta-hCG. Contrast the gross pathology and marker profile of this non-seminomatous germ cell tumour with Rajan's seminoma. What component of the cousin's tumour is responsible for the very high beta-hCG?
- Seminoma is highly radiosensitive and responds well to platinum-based chemotherapy. What histological feature of seminoma underlies its radiosensitivity, and how does this differ from the biology of non-seminomatous GCTs?
- Describe the morphological features a pathologist uses to identify GCNIS (germ cell neoplasia in situ) on testicular biopsy, and explain its significance as a precursor lesion for invasive GCTs.
Group Task Assignments
Group 1: Classification and risk factors for testicular germ cell tumours
- Construct a table classifying testicular tumours by cell of origin, age group, typical gross appearance, and serum marker profile.
- Prepare a two-minute oral summary explaining to a patient why cryptorchidism — even corrected — remains a risk factor for germ cell tumours.
Competencies: PA28.1
Group 2: Morphological identification — seminoma vs NSGCT
- Draw and annotate the gross and microscopic features that distinguish a seminoma from a mixed non-seminomatous germ cell tumour.
- Describe the immunohistochemical profile (PLAP, CD117, OCT3/4, AFP, beta-hCG) that differentiates the major GCT subtypes.
Competencies: PA28.1, PA28.6
Group 3: Prostate pathology — BPH, prostatitis, and carcinoma
- Create a comparison chart of BPH vs prostate carcinoma covering zone of origin, hormonal dependence, gross morphology, microscopic features, PSA pattern, and complications.
- Explain the NIH classification of prostatitis with one clinical vignette per category.
Competencies: PA28.3, PA28.4, PA28.5
Group 4: Penile carcinoma and HPV spectrum
- Produce a diagram showing the HPV risk spectrum from condyloma acuminatum through PeIN subtypes to invasive squamous cell carcinoma, with the HPV types responsible for each step.
- Identify the risk factors for penile SCC in the Indian context and explain why circumcision is protective.
Competencies: PA28.2, PA28.6
Group 5: Gleason grading and staging of prostate carcinoma
- Draw and label Gleason patterns 1 through 5 and explain how the Gleason score is calculated from a needle biopsy specimen.
- Summarise the TNM staging of prostate carcinoma and list the features that upstage a T2 tumour to T3 or T4.
Competencies: PA28.4, PA28.6
Learning Issues
Research these questions and bring your findings to the discussion.
- [PA28.1] What is the WHO classification of testicular tumours, and how do pathogenesis, gross morphology, tumour markers, lymphatic spread, and prognosis differ between seminoma and non-seminomatous germ cell tumours?
- [PA28.2] What is the role of HPV in the pathogenesis of penile squamous cell carcinoma, what are the premalignant penile lesions, and how does penile SCC spread and present in the Indian clinical context?
- [PA28.3] What is the hormonal pathogenesis of benign prostatic hyperplasia, which zone does it arise in, and how do its gross and microscopic morphology explain the lower urinary tract symptoms it produces?
- [PA28.4] How does prostatic adenocarcinoma differ from BPH in zone of origin, morphology, and hormonal dependence, and how are the Gleason grading system and PSA used together for diagnosis, staging, and prognosis?
- [PA28.5] What are the four NIH categories of prostatitis, what organisms cause acute bacterial prostatitis, and why can prostatitis cause a dramatic but transient rise in serum PSA?
- [PA28.6] What are the key gross and microscopic features — including immunohistochemical markers — that allow practical identification of seminoma, non-seminomatous GCT subtypes, BPH, and prostatic adenocarcinoma on pathology slides?