Benign prostatic

hyperplasia
aetiopathogenesis and
clinical features
Presented by Shalini Lalljee
Roll no 34
Definition
 Benign prostatic hyperplasia (BPH)
also known as benign prostatic
hypertrophy (technically a
misnomer), benign enlargement of
the prostate (BEP), and
adenofibromyomatous hyperplasia,
refers to the increase in size of the
prostate.
Etiology
 Presently the exact cause of BPH is
not known.
 However, there are a lot of theories
regarding it.
Theory 1
 Androgens and related hormones are
considered to play a PERMISSIVE
role, i.e they have to be present for
BPH to occur, BUT do not necessarily
cause them.
 Testosterone causes prostatic
proliferation.
 There are both pros and cons to this
theory.
 One pro factor is that if young boys
are castrated before attaining
puberty, they do not dev BPH.
 OTOH, even if we do administer
testosterone to men, it does not
necessarily mean that they will dev
BPH.
Theory 2
 Dihydrotestosterone ( DHT ), is a
metabolite of testosterone and is
produced by the action of 5-alpha
reductase type 2 on testosterone.
 DHT is mainly produced in stromal
cells.
 It can act autocrinally on the stromal
cells or paracrinally on epithelial cells.
 DHT binds to nuclear androgen
receptors and signals transcription
factors that are mitogenic to stromal
and epithelial cells causing a
hyperplasia of the prostate.
 DHT is more potent than testosterone
because it stays bound to the
receptor more.
 The importance of DHT in BPH is
demonstrated by the fact that
treatment with an inhibitor of the
enzyme decreases the prostatic
volume and sometimes the
symptoms.
Theory 3
 Effect of oestrogen is mainly
explained by its local conversion to
androgens, rather than by oestrogen
itself.
Theory 4
 Neoplastic theory which says that
there is proliferation of all the
elements of the prostate resulting in
fibromyoadenoma.
Theory 5
 This is a new theory published in a study in
1998 which reports on a newly discovered
venous route by which free (active)
testosterone reaches the prostate in
extremely high concentrations, promoting
the accelerated proliferation of prostate
cells, leading to the gland's enlargement.
The study suggests that BPH is caused by
malfunction of the valves in the internal
Spermatic veins manifesting as varicocele,
a phenomenon which has been shown to
increase rapidly with age.
 There is a 6 -8 fold increase in the
hydrostatic pressure which leads to a
retrograde venous drainage, allowing free
communication with the prostatic
circulation.
 The elevated venous pressure causes
hypertrophy and exposure to high
concentrations of free testosterone which
causes hyperplasia in the prostate.
Pathology
 BPH affects both glandular epithelium
and connective tissue.
 There occurs :
 1. adenosis : the abnormal
development of glandular tissue
 2. epitheliosis : proliferation of
epithelial cells
 3. stomal proliferation
 BPH affects submucous glands in the
transitional zone, forming a nodular
enlargement. This growth later
compresses the peripheral zone
glands into a false capsule, causing
lateral lobes to appear.
 When BPH affects subcervical central
zone glands, a middle lobe appears.
Secondary
effects of BPH
Urethral changes
 Urethra gets compressed narrow
longitudinal slit.
 This is more with middle lobe
development.
 Prostatic urethra is lengthened.
 The normal posterior curve may be
exagerated.
Bladder changes
 Obstruction bladder
musculature hypertrophies
trabeculations are formed.
 In b/w trabeculations, sacculations
( depressed areas ) are formed.
 As pressure increases, the thin sacculi
herniate outside causing diverticuli.
 In diverticuli, there is urinary stasis
causing infection and stone formation
Changes in ureter and kidney
 Bilateral hydronephrosis ( swelling of
kidneys )
 Bilateral hydroureter ( swelling of
ureter )
 Renal failure may develop.
Clinical features
of BPH
Frequency
 It means urinating more than usual.
 At first, it is only during the day,
followed by day and night.
 Due to ineffective emptying of
bladder.
 Results in residual urine in bladder
precipitating cystitis.
Urgency
 Prostate enlarges vesical
introversion of sensitive mucous
membrane of prostatic urethra within
the bladder internal sphincter
stretches prevents contraction.
 This results in a few drops of urine
trickling down the posterior urethra,
causing an URGENT DESIRE TO PASS
URINE.
Hesitancy
 Patient hesitates to pass urine
because micturition is so ineffective
due to obstruction.
Acute retention of urine
 Urinary retention is the inability to
empty the bladder.
 With acute urinary retention, you
can’t urinate at all, even though you
have a full bladder. Acute urinary
retention is a medical emergency
requiring prompt action.
Chronic retention of urine
 With chronic urinary retention, you
may be able to urinate, but you have
trouble starting a stream or emptying
your bladder completely. You may
urinate frequently; you may feel an
urgent need to urinate but have little
success when you get to the toilet; or
you may feel you still have to go after
you’ve finished urinating.
Haematuria
 This occurs RARELY.
 It is because of congestion of
prostatic venous plexuses resulting in
hyperemia and haematuria.
References
 Bailey and love TB of surgery
 Manipal manual of surgery
 Wikipedia
 National kidney and urological
diseases information clearinghouse