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Ca Prostate MB6.pptx
- 1. PROSTATE CANCER Dr WinstonMakanga, M.B.Ch.B, M.MEd (Surg) Consultant General and Laparoscopic Surgeon
- 2. Objectives of thelecture • Surgical anatomy • Physiology and functions • Epidemiology • Etiology • Work-up (screening, diagnosis, staging) • Treatment
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- 5. Physiology and function •Testosterone is trophic to the prostate • DHT is the active form after conversion by 5 alpha reductase • LH production by pituitary responds to pulsatile release of GnRH • Function = production of seminal fluid, hormone production and sphincteric function
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- 7. Etiology • High bodymass index • Physical activity • Smoking • African-American race • Positive family history
- 8. Pathology • Microscopic: adenocarcinoma •Types • Latent disease found on autopsy • Incidental disease on TURP/open prostatectomy • Localized cancer • Locally advanced • Metastatic disease • Spread • Local to seminal vesicles, trigone, membranous urethra, ureters • Metastatic: by blood to lumbar vertebrae/pelvis/ribs • Lymphatic: internal and external iliac nodes, para-aortic, mediastinal
- 9. Presentation • Mostly asymptomatic(screening or opportunistic PSA testing) • LUTS • BOO, pain, hematuria, renal failure • Symptoms due to metastatic disease • DRE: nodule, hard, irregular, fixed rectal mucosa, sulcus obliteration
- 10. Investigation • General bloodtests • CBC, UEC, LFTs • PSA • Trucut biopsy • Radiology • CXR, Lumbar and pelvic XR • Ultrasound - TRUS • MRI • Bone scan
- 11. Gleason’s score Mostprevalent gland types Second most common gland type 1 1 2 2 3 3 4 4 5 5 High risk disease >7 (4+3)
- 12. Staging • Clinical vsPathological staging; Based on TNM • Nodes: N1 – N2 – N3 (<2-5> cm) • Met: M0 and M1 (abc)
- 13. Treatment options • Activesurveillance • Radical prostatectomy • Androgen suppression therapy • Chemotherapy • Radiotherapy • Palliation
- 14. Active surveillance • Forlow risk disease • Low PSA • Small focus • <Gleason 6 on histology • Involves: • 3 monthly DRE and PSA • Repeat trucut if/when needed • Avoid use of Alpha reductase inhibitors to treat LUTS • ~ 30% will require radical treatment in ~3-5 years
- 15. Surgery • Ideally forT1, T2 and ?T3a • Radical prostatectomy offers potential cure • Open (perineal/retropubic) vs laparoscopic vs robotic • Highly dependent on case load, life expectancy, performance status and lifestyle • Likely complications: • Erectile dysfunction • Incontinence • Hemorrhage
- 16. Radiotherapy • External beamor internal – brachytherapy (T1,T2) • Can be offered for localized disease • OS similar to radical prostatectomy • Complications • Radiation Cystitis &/or proctitis • urinary frequency, urgency • urge incontinence • Diarrhea
- 17. Androgen deprivation therapyADT • Used in advanced disease or poor performance status • As adjuvant therapy in locally advanced disease • Lessens risk of metastatic advancement • Controls local and general symptoms • Combine GnRH agonist with androgen receptor blockers ARB at initiation • Prevents flare up of mets at initiation of therapy • Combined androgen blockade for locally advanced disease = long term GnRH agonist + ARB* • Abiraterone may be an option in castrate resistance * Time to CRPC is ~ 5-15 years in CAB
- 18. Chemotherapy • In castrateresistant ca prostate • Main option = taxanes (docetaxel) • Early introduction may have better outcome • Response is generally poor
- 19. Palliation • Radiotherapy forfocal mets (pain and risk of fracture) • Orchidectomy for imminent risk of cord compression in poor status • Channel TURP for BOO • Manage castration induced osteoporosis with Vit D, calcium and bisphosphonates (Alendronate….)
- 20. Overview of treatment AgeLow risk Intermediate High risk Metastatic >70 Watchful waiting Palliate BOO Androgen suppression Palliate BOO Androgen suppression Palliate BOO Androgen suppression Focal radiotherapy <70 Active surveillance Radical prostatectomy Radiotherapy Androgen suppression Radical prostatectomy Radiotherapy Androgen suppression Chemotherapy Focal radiotherapy Palliate BOO
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