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Prostate, testis & haematuria flashcards

11 high-yield MRCP Part 1 cards from the Intellect Medicos Nephrology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.

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1. What is the first-line drug for moderate–severe bothersome LUTS due to benign prostatic hyperplasia?

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   An alpha-1 blocker (e.g. tamsulosin, alfuzosin).

   Why? It relaxes prostatic and bladder-neck smooth muscle (the dynamic component), working within days. Side effects: postural hypotension, dizziness, retrograde ejaculation.

2. What is the mechanism of finasteride in BPH, and how long does it take to work?

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   5-alpha-reductase inhibitor — blocks conversion of testosterone to dihydrotestosterone, shrinking the prostate over 3–6 months.

   Why? NICE suggests a 5-ARI for men with a prostate estimated above 30 g or PSA above 1.4 ng/mL and high risk of progression. Side effects include reduced libido and erectile dysfunction.

3. What is the first-line investigation for suspected clinically localised prostate cancer (before biopsy)?

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   Multiparametric MRI (mpMRI).

   Why? It identifies suspicious lesions, guides targeted biopsy and avoids unnecessary biopsies. Transperineal biopsy is preferred over TRUS because of lower infection risk.

4. After a UTI or prostatitis, how long should a PSA test be delayed?

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   At least 6 weeks after treatment.

   Why? Infection, recent ejaculation, vigorous exercise (cycling) and catheterisation all raise PSA falsely.

5. When starting a GnRH agonist (e.g. goserelin) for metastatic prostate cancer, what is given to prevent tumour flare?

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   A short course of an anti-androgen (e.g. bicalutamide), started before and continued for 2–4 weeks.

   Why? GnRH agonists first cause a testosterone surge before receptor down-regulation, which can worsen bone pain or cause cord compression.

6. Which type of androgen-deprivation drug is preferred in prostate cancer with impending spinal cord compression, and why?

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   A GnRH antagonist (e.g. degarelix, relugolix) — it suppresses testosterone immediately with no initial flare.

   Why? It blocks pituitary GnRH receptors directly, so there is no surge of LH.

7. What is the mechanism of abiraterone, and why is it given with prednisolone?

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   It inhibits CYP17, blocking androgen synthesis; prednisolone prevents mineralocorticoid excess.

   Why? Blocking CYP17 raises ACTH and mineralocorticoid production, causing hypertension, hypokalaemia and fluid retention.

8. Which testicular germ cell tumour NEVER raises AFP?

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   Pure seminoma.

   Why? Seminoma may mildly raise β-hCG. A raised AFP means non-seminomatous elements (yolk sac or embryonal). Choriocarcinoma produces very high β-hCG.

9. What is the most important risk factor for testicular germ cell cancer?

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   Cryptorchidism (undescended testis).

   Why? Others include family history, Klinefelter syndrome and previous testicular cancer. A testicular mass with gynaecomastia and normal markers suggests a Leydig cell tumour.

10. What is the treatment of epididymo-orchitis in a sexually active man under 35 (likely STI)?

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    Ceftriaxone 1 g IM single dose plus doxycycline 100 mg twice daily for 10–14 days.

    Why? Covers Neisseria gonorrhoeae and Chlamydia trachomatis; notify partners. If enteric organisms are likely (older men, no STI risk), ofloxacin for 14 days is used.

11. Which patients with haematuria should be referred on a suspected cancer pathway (formerly '2-week wait') for bladder cancer (NICE NG12)?

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    Age ≥45 with unexplained visible haematuria (no UTI) or visible haematuria persisting after UTI treatment; or age ≥60 with non-visible haematuria plus dysuria or a raised white cell count.

    Why? Visible haematuria is bladder cancer until proven otherwise. Refer to nephrology instead if there are glomerular features (proteinuria, hypertension, impaired function, red cell casts).