Benign Prostatic Hyperplasia

  • Also called nodular hyperplasia and is very common in men over 50
  • Characterised by hyperplasia of prostatic stromal and epithelial cells resulting in large discrete nodules in the periurethral region of the prostate
  • May compress the urethra causing partial or complete obstruction

 

Incidence

  • 20% of men aged 40, 70% aged 60 and 90% aged 70
  • Only 50% of those with microscopic evidence of nodular hyperplasia have any detectable enlargement of the prostate and only 50% of these individuals have any symptoms

 

Aetiology and pathogenesis

  • Dihydrotestosterone (DHT), a metabolite of testosterone, is the ultimate mediator of prostatic growth
  • It is synthesised in the prostate from testosterone by 5a-reductase type 2, which is localised principally in the stromal cells
  • DHT has a mitogenic effect on epithelial and stromal cells
  • DHT is 10 times more potent than testosterone as it dissociates more slowly from the androgen receptor
  • Oestrogen also plays a role, possibly by rendering cells susceptible to the action of DHT
  • There is also smooth muscle contraction of the prostate mediated by the a1-adrenergic receptor in the prostatic stroma
  • Inhibitors of 5a-reductase decrease prostatic volume and urinary obstruction

 

Morphology

  • Prostate can weigh 60-100g
  • Nodules can be stromal or epithelial in origin
  • The nodules may encroach on the urethra
  • In some cases the nodular enlargement may project up into the floor of the urethra which is clinically termed ‘median lobe hypertrophy’
  • Fibroepithelial nodules can contain glandular tissue from which may ooze white prostatic fluid
  • BPH typically occurs in the transition zone of the prostate
  • Can also contain foci of squamous metaplasia

 

Clinical course

  • Symptoms relate to 2 effects;
    • Compression of the urethra with difficulty in urination
    • Urinary retention resulting in bladder hypertrophy, urinary infection, cystitis and renal infections
  • In some cases sudden acute retention occurs which requires catheterisation
  • The inability to empty the bladder completely resulting in increased susceptibility to infection
  • Many secondary changes occur to the bladder;
  • Hypertrophy
  • Trabeculation
  • Diverticulum formation
  • Hydronephrosis, or acute rentention, with secondary urinary infection and azotemia and uraemia can develop
  • Nodular hyperplasia is not considered to be a premalignant lesion
  • Treatment is with a1 adrenergic blockage which relaxes the smooth muscle and inhibition of DHT

 

 

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Disclaimer: These notes are my own personal study aid - DO NOT use them for medical advice!