5 September 2013 Dap Louw Urologist Life Beacon Bay Hospital.

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Presentation transcript:

5 September 2013 Dap Louw Urologist Life Beacon Bay Hospital

2 main components: 1.Epithelial compartment -luminal secretory cells 2.Stromal compartment - structural support -smooth muscle, connective tissue α1-receptors blockers has effect on prostatic stroma

Free testosterone (2% of total) converted to DHT by 5alpha reductase enzyme in prostate DHT 1,5-2 X as potent as free testosterone - major androgen regulating prostate growth and differentiation

5alpha reductase type I- skin, prostate epithelium + stroma typeII- prostate fibromuscular stroma Dutasteride (Avodart) inhibits type I&II Finasteride (Proscar) inhibits type II

Increase in stromal and epithelial cells in periurethral and transitional area Clinical symptoms not solely due to urethral resistance but also due to age related + outlet obstruction related detrusor dysfuntion ( detrusor instability and or decreased contactility) 25-30% of men will still urinary symptoms after releaving obstruction Active + passive forces play role in patophysiology. Alpha- blockade acts on active (dinamic) forces. Androgen blockade/surgery acts on passive forces (mechanical obstruction) Androgens do not cause BPH but is essential for development No correlation between prostate size, androgen concentration and urinary symptoms

Androgens- DHT not elevated but maintained in BPH. Androgen receptors and 5alpha reductase enzymes not downregulated with age Apoptosis Growth factors- VEGF,IGF,FGF,EGF. Hypoxia secondary to atherosclerosis induces HIF, FGF Inflammatory channels- source of growth factors Genetics – autosomal dominant (50% of men having surgery 60 yr). Higher prostate volume on average