PH7.6 | PH7.6 | Androgens and Erectile Dysfunction Drugs — SDL Guide — Summary & Reflection

KEY TAKEAWAYS

Androgens and Erectile Dysfunction Drugs — Key Takeaways:

• Testosterone metabolism: DHT (via 5α-reductase in prostate/scalp) — targeted by finasteride/dutasteride; oestradiol (via aromatase in adipose) — explains gynaecomastia.
• Finasteride: reduces PSA by ~50% — double PSA when screening on finasteride; 1 mg for alopecia, 5 mg for BPH.
• TRT monitoring: serum T, haematocrit (polycythaemia), PSA, liver enzymes. Contraindicated in active prostate cancer.
• Anabolic steroid misuse: testicular atrophy (LH/FSH suppression), hepatotoxicity (17α-alkylated), polycythaemia, cardiovascular risk.
• PDE5 inhibitors: amplify NO/cGMP in penile smooth muscle — sildenafil (4–6 hr), tadalafil (17–36 hr, daily dose possible).
• ABSOLUTE CONTRAINDICATION: PDE5i + any nitrate (GTN, ISDN, isosorbide mononitrate) — severe hypotension.
• Alprostadil: PGE1 analogue, intracavernosal — effective even with poor NO signalling; risk of priapism.
• Anti-androgens: bicalutamide (prostate cancer, flare protection); cyproterone acetate (hirsutism, hypersexuality).

REFLECT

Consider the concept of androgen receptor (AR) targeting in prostate cancer. First-generation anti-androgens (bicalutamide) block AR competitively. Newer agents (enzalutamide) also prevent AR nuclear translocation. Abiraterone inhibits CYP17A1 — the androgen biosynthetic enzyme in the adrenal gland and intra-tumoral tissue. Reflect on the pharmacological arms race between prostate cancer cell evolution and new drug classes: why does castration-resistant prostate cancer (CRPC) emerge, and what does it tell you about the pharmacodynamics of resistance? Write two sentences on the mechanism of CRPC and why it is pharmacologically challenging to treat even with AR blockade.