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PATHOPHYSIOLOGY OF BPH

Introduction

Benign prostatic hyperplasia (BPH) is a very common urological problem seen locally
and it is estimated that approximately 20% of men above t he age of 50 years might
require treatment. Patient with BPH present with both obstructive and irritative
symptoms. Obstructive symptoms include hesitancy, poor stream, post micturition
dribbling and retention of urine. Irritative symptoms include frequency, dysuria,
urgency and nocturia. About 50% of our local patients with BPH will have an
enlarged prostate gland. However, the size of the prostate gland bears no
relationship with severity of obstruction.

Etiology

The exact etiology of BPH is still poorly understood. Various risk factors have been
implicated such as racial predilection, hypertension, liver cirrhosis and vasectomy but
none had been proven convincingly. Studies and observations have shown that both
increasing age and intact testes are important for BPH to develop as castration in
young age of the development of BPH later in life.

Microscopic BPH starts to develop as early as in the thirties but clinical BPH usually
present after the fifties. Studies of the various populations form different parts of the
world have shown that t he incidence of the disease is approximately the same
amongst the various races.

Anatomy of the Prostate Gland

Prostate gland is para reproductive organ of the male derives from the outpouching
of the urethra during early embryonic life. It weighs about 15 grams in adults and is
situated deep in the pelvis between the bladder and the external sphincter. It is an
organ, which consists of both glandular epithelium and fibromuscular stroma with
numerous ducts emptying into the prostatic urethra. Alkaline secretion is produced
during sexual stimulation by these glands. Two zones or prostate gland are
recognized on histological examination, the outer or the peripheral zone and the
inner or the central zone.

Pathology and Pathogenesis of BPH

With increasing age, the prostate gland undergoes benign enlargement first around
the prostatic urethra and later extends to involve the central zone. The weight of
prostate gland in BPH is usually tow to three times that of normal. Grossly, nodular
enlargements are seen in the prostate gland usually with cystic spaces due to
dilatation of the obstructed prostatic ducts.

Histologically, hyperplasia of both glandular and fibromuscular components are seen


in BPH. It is also important to note that with advancing age, carcinoma of the
prostate gland is also likely to occur and this commonly arise from the peripheral
zone. Both conditions present with symptoms of bladder outlet obstruction and can
sometimes coexist.

The pathogenesis of BPH is still largely unresolved. Several theories have been
postulated to explain it s development. These include: 1. Hormonal mechanism, an
increase in the level of dihydro testosterone (DHT) in the cells leads to stimulation of
cell growth. DHT is derived from testosterone by the enzymatic action of 5 alpha
reeducates 2. Stem cell theory, by reactivation of the stem cells and benign
enlargement of the prostatic gland 3. Stroma-epithelial interaction by growth factor
which stimulates cell proliferation.
Both mechanical enlargement of the prostate gland as well as an increase in the tone
of the prostatic urethra causes bladder outlet obstruction in BPH. The tone of the
prostatic urethra is regulated by smooth muscle which is innervated buy the alpha
adrenergic nerve fibres which are abundant in the prostate gland as well as in t he
bladder neck.

Sequelae of BPH

Bladder outlet obstruction causes hypertrophy of the detrusor muscle and thickening
of t he bladder due to increasing workload against the outflow resistance. Normal
person empties the bladder with a detrusor pressure below 30 cm H20 with a
maximal peak flow rate of more than 25 cc/sec. In the early phase of bladder outlet
obstruction, the flow rate is maintained with increase in the emptying pressure. This
is known as compensatory hypertrophy. As the obstruction progresses, the detrusor
pressure rises further and the flow rate decreases with large amount of residual urine
in the bladder, The detrusor muscle is replaced by fibrous tissue and become floppy
with poor tonicity. This late phase is known as decompensatory hypertrophy and t he
bladder is now suffering from irreversible damages.

In addition to thickening of the bladder wall, the increased detrusor pressure also
leads to trabeculation, saccule and diverticulum formation in the bladder. When the
obstruction is not relieved by appropriate treatment, hydronephrosis, hydroureter
and renal failure can occur. As a result of increased residual urine, stasis can lead to
stone formation in the bladder and is seen in about 10% of patients with BPH locally.
Infection is also commonly seen at this stage and would be difficult to eradicate until
obstruction is relieved. About 3-5% of patients with BPH present with chronic
retention and overflow incontinence is usually associated with impairment of renal
function. The response to treatment by TURP at this stage tends to be less
satisfactory due to decompensation and is also associated with higher morbidity.
Hence, to achieve optimal result of treatment for patient with BPH, timely
intervention is important.

Natural History of BPH

The symptom of BPH varies depending on the severity of obstruction. Though t he


symptoms generally progress with time, they do wax and wane along its course.
Studies have showed that about 25 to 30% of patients experience improvement in
their symptoms without treatment. Hence, strict objective criteria are needed in
evaluating newer treatment modalities for patients with BPH.

Those with severe symptoms and associated with complications such as retention of
urine, infection and renal impairment would require surgical treatment.

Conclusion

BPH is a common problem affecting the elderly male in our local population. It exact
etiologies still poorly understood but aging, dihydrostestostrone, growth factor and
epithelial – stroma interaction are believed to play an important role in its
development. Obstruction in BPH is contributed both mechanical and neurogenic
factors and surgical treatment is needed only in those with proven obstruction. With
availability of newer medications and less invasive modalities of treatment, both
physicians and urologists are now in a better position to tailor the choice of
treatment according to the severity of the obstruction.

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