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17  Male Genital Tract   497


             •	  The prostate is divided into two parts depending on the hormone responsiveness, the
               inner  periurethral  part  which  is  sensitive  to  oestrogen  and  androgens  and  an  outer
               subcapsular part that is sensitive to androgen.

             Q.  Write  briefly  on  the  aetiopathogenesis,  clinical  features  and
             morphology of nodular hyperplasia of prostate (NHP).
             Ans.  NHP (benign prostatic hyperplasia) is defined as hyperplasia of prostatic stromal and
             epithelial cells, resulting in the formation of discrete nodules in the transitional and inner
             periurethral zones (prostate is divided into several zones namely, peripheral, central, tran-
             sitional  and  periurethral).  The  nodules  compress  the  prostatic  urethra  to  produce  the
             clinical symptoms of NHP.
             •	  NHP was earlier called ‘benign hypertrophy’, which is a misnomer because the funda-
               mental lesion is a hyperplasia and not hypertrophy.
             •	  Age	group  affected is more than 50 years; incidence increases with increasing age.

             Pathogenesis (Flowchart 17.1)



                                             Testosterone
                                                  5      ­reductase
                                          Dihydrotestosterone
                             (DHT constitutes 90% of the total androgens in the prostate)

                           Binds to nuclear androgen receptors in stromal and epithelial cells


                                         Release of growth factors
                                            •  Autocrine action
                                            •  Paracrine action
                                          • Stromal cell hyperplasia
                                          • Epithelial cell hyperplasia
                                 FLOWCHART 17.1.  Pathogenesis of NHP.




             •	  Testosterone  is  converted  into  DHT	  by	  5a-reductase  type  II  enzyme  specifically
               located	in	the	stromal	cells.
             •	 DHT	is	10	times	more	potent	than	testosterone, as it dissociates slowly from androgen
               receptors.
             •	  DHT thus produced, acts on nuclear	receptors	to	produce	growth	factors  that are
               mitogenic to epithelial	and	stromal	cells.
             •	  Testosterone acts similarly, but is very	weak.
             •	  Oestrogen  increases the expression of androgen receptors, thus providing DHT more
               sites for action. Oestrogen levels increase with age, making its role significant.

             Clinical Features
             •	  Clinical	symptoms	are	seen	in	10%	of	affected	patients.
             •	  Early	  changes:  Compression  of  urethra  leading  to  increased  frequency,  nocturia
               (urgency), problem in starting and stopping the stream of urine, overflow dribbling and
               painful micturition.
             •	  Late	  complaints:  Retention  of  urine  in  the  bladder  causing  urinary  tract  infection
               (UTI), cystitis, hypertrophy or trabeculation in urinary bladder and hydronephrosis may
               occur.






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