Pathophysiology of BPH

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Pathophysiology of BPH1,2

In a given organ, the number of cells, and thus the volume of the organ, is
dependent on the equilibrium between cell proliferation and cell death (Isaacs and
Coffey, 1987). An organ can enlarge not only by an increase in cell proliferation but
also by a decrease in cell death. Although androgens and growth factors stimulate cell
proliferation in experimental models, the relative role of cell proliferation in human
BPH is questioned because there is no clear evidence of an active proliferative
process. Androgens not only are required for normal cell proliferation and
differentiation in the prostate but also actively inhibit cell death. The development of
BPH requires the present of testicular androgens during prostate development,
puberty, and aging although androgens don’t cause BPH.
BPH develops in the transition zone. It is truly a hyperplastic process resulting
from an increase in cell number. Microscopic evaluation reveals a nodular growth
pattern that is composed of varying amounts of stroma and epithelium. Stroma is
composed of varying amounts of collagen and smooth muscle. The differential
representation of the histologic components of BPH explains, in part, the potential
responsiveness to medical therapy. The prostatic stroma, composed of smooth muscle
and collagen, is rich in adrenergic nerve supply. The level of autonomic stimulation
thus sets a tone to the prostatic urethra. Use of alpha-blocker therapy decreases this
tone, resulting in a decrease in outlet resistance.

Picture 1. Pathophysiology of BPH


The irritative voiding
complaints of BPH result from the
secondary response of the bladder
to the increased outlet resistance.
Bladder outlet obstruction leads to
detrusor muscle hypertrophy and
hyperplasia as well as collagen
deposition. Although the latter is
most likely responsible for a
decrease in bladder compliance,
detrusor instability is also a factor.
Clinical Manifestations2
The symptoms of BPH can be divided into obstructive and irritative
complaints. Obstructive symptoms include hesitancy, decreased force and caliber of
stream, sensation of incomplete bladder emptying, double voiding (urinating a second
time within 2 hours of the previous void), straining to urinate, and post-void
dribbling. Irritative symptoms include urgency, frequency, and nocturia.

Complications3
If the conditions still continue, urine residue will remain in the bladder. In the
end, patient can’t urinate anymore because total obstruction is occurred (urine
retention). Pressure in the bladder will increase. And then, when the pressure in the
bladder is higher, overflow incontinence is occurred. Urine will be reflux to the
ureter, and then hydroureter, hydronephrosis, dan renal failure will be occurred.

1. Campbell
2. Smith
3. Gaol HL, Mochtar CA. Kapita Selekta Kedokteran Jilid I. Edisi 4. Jakarta :
Media Aesculapius; 2014.

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