Pathophysiology

O The symptoms and signs of BPH are due to static, dynamic, and/or detrusor factors. The static factor refers to anatomic obstruction of the bladder neck caused by an enlarged prostate gland. As the gland grows around the urethra, the prostate occludes the urethral lumen. The dynamic factor refers to excessive stimulation of aiA-adrenergic receptors in the smooth muscle of the prostate and urethra, which results in smooth muscle contraction. This reduces the caliber of the urethral lumen. The detrusor factor refers to bladder detrusor muscle instability, in which bladder muscle fibers have decompensated as a result of excessive, prolonged hypertrophy in response to prolonged bladder outlet obstruction. Patients with detrusor muscle instability will develop irritative voiding symptoms, such as urinary urgency and fre-quency.1 Detrusor muscle fibers are embedded with a1D-receptors. Therefore, it has been proposed that some a1D-adrenergic antagonists may be particularly useful for controlling these symptoms.3,4

In an enlarged gland, the epithelial/stromal tissue ratio is 1:5.1 Androgens stimulate epithelial, but not stromal tissue hyperplasia. Hence, androgen antagonism does not induce a complete reduction in prostate size to normal. This explains one of the limitations of the clinical effect of 5a-reductase inhibitors.

Stromal tissue is the primary locus of a1-adrenergic receptors in the prostate. An estimated 98% of the a-adrenergic receptors in the prostate are found in prostatic stromal tissue. Of the a1-receptors found in the prostate, 70% of them are of the a1A-subtype.4 This explains why a-adrenergic antagonists are effective for managing symptoms of BPH.

Symptoms of BPH are classified as obstructive or irritative. Obstructive symptoms result from failure of the urinary bladder to empty urine when the bladder is full. The patient will complain of reduced force of the urinary stream, urinary hesitation, dribbling, and straining to empty the bladder. Irritative symptoms result from the failure of the urinary bladder to store urine until the bladder is full. With longstanding bladder outlet obstruction, detrusor muscle fibers undergo hypertrophy so that the bladder can generate higher pressure to overcome the bladder outlet obstruction and empty urine from the bladder. Once maximal bladder muscle hypertrophy occurs, the muscle decompensates. The detrusor becomes irritable, contracting abnormally in response to small amounts of urine in the bladder. As a result, the patient complains of urinary frequency and urgency.

The natural history of untreated BPH is unclear in patients with mild symptoms. It is estimated that up to 38% of untreated men with mild symptoms will have symptom improvement over a 2.5- to 5-year period.5 It may be that such patients attribute their symptoms to aging, grow tolerant of their symptoms, or adopt behavioral changes in their lifestyle that minimize their voiding symptoms. On the other hand, a significant portion of patients with mild symptoms will likely experience disease progression. In one Veterans Affairs study, approximately one-third of men with mild BPH symptoms, who were initially randomized to watchful waiting, developed progressive symptoms and required surgical intervention within 5 years of initial diagnosis.6 Patients with moderate to severe symptoms can experience a decreased quality of life as daily activities are adjusted because of urinary incontinence. Also, such patients may develop complications of BPH, which include acute refractory urinary retention, renal failure, urinary tract infection, urinary incontinence, bladder stones, large bladder diverticuli, and recurrent gross hematuria. Predictors of disease progression include an enlarged prostate of at least 30 g (1.05 oz) or PSA of at least 1.5 ng/mL (1.5 mcg/ L)7-9

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