Urological Tumours and PSA: Prostate, Kidney and Testis | Part 1 | 泌尿 | OET Music

Dr Allison Lu · Pip & Barnaby · Medical English

本頁提供本曲完整英文歌詞與影片搭配的繁中醫學提示。歌詞保留原演唱文字;遇到過度簡化或舊門檻,請搭配下方提示與原始資料閱讀。這是概念學習材料,不替代個別醫療評估。

Lyrics · 完整歌詞

Benign prostatic obstruction reflects both a structural component, arising from glandular enlargement,
and a dynamic component, determined by smooth-muscle tone.
The static arm runs from testosterone through 5-alpha-reductase to dihydrotestosterone,
which drives glandular growth.
Finasteride and dutasteride block the enzyme, but the gland shrinks slowly,
so benefit takes three to six months
and is significant only above about 40 mL.
These drugs halve the PSA,
so the measured value is doubled when cancer is being followed.
The dynamic arm depends on alpha-1A receptors,
about 70 per cent of prostatic alpha-1 receptors;
tamsulosin and silodosin block them within days at any gland size.
Alpha-1D receptors, in the detrusor and spinal cord,
are not tamsulosin's main target.
Creatinine and renal ultrasound are the least urgent initial tests
unless obstruction is suspected.

PSA is organ-specific, not cancer-specific.
Prostatitis, infection, digital examination, cycling, ejaculation and benign enlargement all raise it.
A raised PSA with pyuria of 50 to 60 leucocytes per high-power field is
inflammation
until proven otherwise:
treat, then repeat the PSA before any biopsy.
A raised PSA with a free-to-total ratio below 15 per cent
and a hypoechoic lesion points to cancer and warrants MRI-guided
or transrectal biopsy.
PSA is insensitive for nodal spread, below 40 per cent,
so staging relies on pelvic CT or MRI
and a bone scan for osteoblastic metastases.

Post-prostatectomy erectile dysfunction follows injury to the parasympathetic cavernous nerves in the posterolateral neurovascular
bundle.

Benign prostatic obstruction reflects both a structural component, arising from glandular enlargement,
and a dynamic component, determined by smooth-muscle tone.


Renal cell carcinoma is usually clear cell,
linked to VHL on chromosome 3p and to smoking.
It is the internist's tumour: erythropoietin causes polycythaemia,
PTHrP hypercalcaemia and renin hypertension.
Stauffer syndrome is hepatic dysfunction without hepatic metastases,
driven by interleukin-6 and reversible after nephrectomy.
VEGF tyrosine kinase inhibitors treat advanced disease;
their commonest adverse effect is hypertension, not hypothyroidism.
Angiomyolipoma declares itself by fat density on CT; it is benign,
associated with tuberous sclerosis, and treated only above 4 cm.
A filling defect in the renal pelvis or ureter suggests urothelial carcinoma,
linked to smoking, phenacetin and aristolochic acid.
Bladder cancer is urothelial, not adenocarcinoma; smoking is the dominant risk,
Schistosoma haematobium drives squamous carcinoma, and painless haematuria is the presentation.

Testicular germ cell tumours divide into seminoma and non-seminoma.
Seminoma is radiosensitive and never raises AFP.
Non-seminomatous tumours raise AFP through yolk sac or embryonal elements
and are treated with orchidectomy and BEP chemotherapy.
Bleomycin scars the lung, and cisplatin injures the kidney and cochlea.
Cryptorchidism raises cancer risk, and orchidopexy does not lower it;
it only makes the testis examinable.

Erection begins with nitric oxide,
which raises cyclic GMP and relaxes cavernosal smooth muscle.
PDE5 degrades cyclic GMP, so sildenafil sustains the erection;
slight inhibition of retinal PDE6 explains transient blue vision.
Nitrates also raise cyclic GMP,
so their combination causes profound hypotension and is an absolute contraindication.
Rifampicin induces CYP3A4 and merely weakens the drug;
it is not a contraindication.
Myocardial infarction within six months,
severe hypotension and aortic stenosis remain serious cautions.

Benign prostatic obstruction reflects both a structural component, arising from glandular enlargement,
and a dynamic component, determined by smooth-muscle tone.

Medical Notes · 醫學學習提示

  1. 良性攝護腺阻塞涉及腺體組織與平滑肌張力
  2. 症狀不只由腺體大小決定,也要評估膀胱功能
  3. 五α還原酶將睪固酮轉為雙氫睪固酮
  4. 雙氫睪固酮參與攝護腺生長與維持
  5. 五α還原酶抑制劑逐漸減少腺體體積
  6. 效果需數月,通常長期使用才能充分評估
  7. 大腺體較受益,但四十毫升並非所有藥物的絕對界線
  8. 使用六至十二個月後,PSA 常下降約一半
  9. 須依療程校正 PSA 並看新基線;不能機械式一律乘二
  10. 攝護腺平滑肌張力與 α1A 受體有關
  11. 約七成是教學估值,比例依組織與研究而異
  12. α 阻斷劑較快改善症狀,但不能保證每人數日見效
  13. 其他 α1 亞型也參與泌尿道與神經調控
  14. 坦索羅辛也作用於 α1D;不可解讀為完全無作用
  15. 腎功能與超音波依腎損傷、殘尿及手術評估需求安排
  16. 疑滯留、腎積水或腎損傷時不可延誤評估
  17. PSA 並非癌症專屬;良性原因也可能升高
  18. 感染等可升高 PSA;一般肛診不造成顯著升高
  19. 膿尿支持發炎可能,但不能單憑白血球數排除癌症
  20. 須結合症狀、尿培養與其他原因評估
  21. 感染與癌症也可能並存,不能視為互斥
  22. 有感染才依證據治療;勿只為無症狀 PSA 高而給抗生素
  23. 游離比偏低增加疑慮,但不是固定切片門檻
  24. 結合 MRI、PSA 密度與整體風險決定是否切片
  25. 可用影像標靶切片;現行常優先經會陰以降低感染
  26. PSA 不能單獨判定淋巴轉移;四成不是通用敏感度
  27. 分期依風險選影像,適用時 PSMA PET 更敏感
  28. 骨轉移評估依風險與症狀,不是每人都要骨掃描
  29. 術後勃起功能可能受海綿體神經損傷影響
  30. 神經束位於攝護腺後外側;保留也不保證功能不變
  31. 透明細胞型最常見,但腎細胞癌仍有多種亞型
  32. VHL 路徑與透明細胞型相關;吸菸是重要風險
  33. 部分腎癌可分泌 EPO,引發紅血球增多
  34. 副腫瘤表現可能含高血鈣或高血壓,並非人人都有
  35. Stauffer 症候群指無肝轉移的副腫瘤性肝功能異常
  36. 常與 IL6 相關,治療腫瘤後可改善但非必然
  37. 晚期腎癌依風險使用免疫治療、VEGF 標靶或合併療法
  38. 高血壓與甲狀腺異常皆須監測;最常見副作用依藥而異
  39. 典型血管肌脂肪瘤含脂肪,但有脂肪少或特殊亞型
  40. 四公分不是唯一治療門檻;症狀、出血與動脈瘤也重要
  41. 充盈缺損須鑑別腫瘤、血塊、結石等原因
  42. 吸菸與馬兜鈴酸等暴露會增加上泌尿道癌風險
  43. 膀胱癌多為尿路上皮型,但仍有腺癌等少見亞型
  44. 血吸蟲相關鱗癌;無痛血尿須評估,並非癌症特有
  45. 睪丸生殖細胞腫瘤主要分精原與非精原型
  46. 純精原瘤不分泌 AFP;升高須查混合成分或其他來源
  47. AFP 可由卵黃囊或胚胎癌成分升高,但非所有非精原型都有
  48. 通常先根治性腹股溝睪丸切除;BEP 依分期與風險選用
  49. 博來黴素有肺毒性風險;順鉑須監測腎功能與聽力
  50. 更正:青春期前固定術可降低癌症風險,但無法恢復至一般水平
  51. 早期手術也有助生育潛能,且便於後续檢查
  52. 性刺激引發一氧化氮訊號,促進勃起
  53. 經 cGMP 使海綿體平滑肌放鬆與血流增加
  54. PDE5 抑制劑延長 cGMP 作用,仍需性刺激
  55. 對視網膜 PDE6 的作用可造成短暫色覺改變
  56. 硝酸鹽也增強 NO 與 cGMP 相關作用
  57. PDE5 抑制劑與硝酸鹽禁併用,可能造成嚴重低血壓
  58. 利福平可誘導 CYP3A4,降低西地那非暴露與效果
  59. 不是同硝酸鹽般禁忌,仍須由醫師評估交互作用
  60. 近期心肌梗塞須個別心血管評估,不能只看六個月界線
  61. 低血壓及嚴重流出道阻塞等需審慎評估性活動與用藥

References