Benign prostatic hyperplasia (BPH), also known as benign prostatic hypertrophy, is a histologic diagnosis characterized by proliferation of the cellular elements of the prostate. Chronic bladder outlet obstruction (BOO) secondary to BPH may lead to urinary retention, renal insufficiency, recurrent urinary tract infections, gross hematuria, and bladder calculi. The image below illustrates normal prostate anatomy.
Signs and symptoms
When the prostate enlarges, it may constrict the flow of urine. Nerves within the prostate and bladder may also play a role in causing the following common symptoms:
Nocturia- Needing to get up frequently at night to urinate
Hesitancy - Difficulty initiating the urinary stream; interrupted, weak stream
Incomplete bladder emptying - The feeling of persistent residual urine, regardless of the frequency of urination
Straining - The need strain or push (Valsalva maneuver) to initiate and maintain urination in order to more fully evacuate the bladder
Decreased force of stream - The subjective loss of force of the urinary stream over time
Dribbling - The loss of small amounts of urine due to a poor urinary stream as well as weak urinary stream
See Presentation for more detail.
Digital rectal examination
The digital rectal examination (DRE) is an integral part of the evaluation in men with presumed BPH. During this portion of the examination, prostate size and contour can be assessed, nodules can be evaluated, and areas suggestive of malignancy can be detected.
Urinalysis - Examine the urine using dipstick methods and/or via centrifuged sediment evaluation to assess for the presence of blood, leukocytes, bacteria, protein, or glucose
Urine culture - This may be useful to exclude infectious causes of irritative voiding and is usually performed if the initial urinalysis findings indicate an abnormality
Prostate-specific antigen - Although BPH does not cause prostate cancer, men at risk for BPH are also at risk for this disease and should be screened accordingly (although screening for prostate cancer remains controversial)
Electrolytes, blood urea nitrogen (BUN), and creatinine - These evaluations are useful screening tools for chronic renal insufficiency in patients who have high postvoid residual (PVR) urine volumes; however, a routine serum creatinine measurement is not indicated in the initial evaluation of men with lower urinary tract symptoms (LUTS) secondary to BPH 
Ultrasonography (abdominal, renal, transrectal) is useful for helping to determine bladder and prostate size and the degree of hydronephrosis (if any) in patients with urinary retention or signs of renal insufficiency. Generally, they are not indicated for the initial evaluation of uncomplicated LUTS.
Endoscopy of the lower urinary tract
Cystoscopy may be indicated in patients scheduled for invasive treatment or in whom a foreign body or malignancy is suspected. In addition, endoscopy may be indicated in patients with a history of sexually transmitted disease (eg, gonococcal urethritis), prolonged catheterization, or trauma.
The severity of BPH can be determined with the International Prostate Symptom Score (IPSS)/American Urological Association Symptom Index (AUA-SI) plus a disease-specific quality of life (QOL) question. Questions on the AUA-SI for BPH concern the following:
Flow rate - Useful in the initial assessment and to help determine the patient’s response to treatment
PVR urine volume - Used to gauge the severity of bladder decompensation; it can be obtained invasively with a catheter or noninvasively with a transabdominal ultrasonic scanner
Pressure flow studies - Findings may prove useful for evaluating for BOO
Urodynamic studies - To help distinguish poor bladder contraction ability (detrusor underactivity) from BOO
Cytologic examination of the urine - May be considered in patients with predominantly irritative voiding symptoms
See Workup for more detail.
Agents used in the treatment of BPH include the following:
Alpha-adrenergic receptor blockers
Phosphodiesterase-5 enzyme inhibitors
5-alpha reductase inhibitors
Transurethral resection of the prostate (TURP) - The criterion standard for relieving BOO secondary to BPH
Open prostatectomy - Reserved for patients with very large prostates (>75 g), patients with concomitant bladder stones or bladder diverticula, and patients who cannot be positioned for transurethral surgery
Minimally invasive treatment
Transurethral incision of the prostate (TUIP)
Laser treatment - Used to cut or destroy prostate tissue; multiple laser types are available, including green light, holmium, and thulium, and each has its own strengths and weaknesses
Transurethral microwave therapy (TUMT) - Generates heat that causes cell death in the prostate, leading to prostatic contraction and volume reduction
Transurethral needle ablation of the prostate (TUNA)
High-intensity ultrasonographic energy therapy - Currently in the clinical trial stage
Prostatic stents - Flexible devices that expand when put in place to improve the flow of urine past the prostate
Implanted devices to relieve prostatic obstruction (eg, UroLift)
Prostate artery embolization - Performed by a radiologist; this technique is still in the early stages of development and usage
Benign prostatic hyperplasia (BPH), also known as benign prostatic hypertrophy, is a histologic diagnosis characterized by proliferation of the cellular elements of the prostate. Cellular accumulation and gland enlargement may result from epithelial and stromal proliferation, impaired preprogrammed cell death (apoptosis), or both.
BPH involves the stromal and epithelial elements of the prostate arising in the periurethral and transition zones of the gland (see Pathophysiology). The hyperplasia presumably results in enlargement of the prostate that may restrict the flow of urine from the bladder.
BPH is considered a normal part of the aging process in men and is hormonally dependent on testosterone and dihydrotestosterone (DHT) production. An estimated 50% of men demonstrate histopathologic BPH by age 60 years. This number increases to 90% by age 85 years.
The voiding dysfunction that results from prostate gland enlargement and bladder outlet obstruction (BOO) is termed lower urinary tract symptoms (LUTS). It has also been commonly referred to as prostatism, although this term has decreased in popularity. These entities overlap; not all men with BPH have LUTS, and likewise, not all men with LUTS have BPH. Approximately half of men diagnosed with histopathologic BPH demonstrate moderate-to-severe LUTS.
Clinical manifestations of LUTS include urinary frequency, urgency, nocturia (awakening at night to urinate), decreased or intermittent force of stream, or a sensation of incomplete emptying. Complications occur less commonly but may include acute urinary retention (AUR), impaired bladder emptying, the need for corrective surgery, renal failure, recurrent urinary tract infections, bladder stones, or gross hematuria. (See Presentation.)
Prostate volume may increase over time in men with BPH. In addition, peak urinary flow, voided volume, and symptoms may worsen over time in men with untreated BPH (see Workup). The risk of AUR and the need for corrective surgery increases with age.
Patients who are not bothered by their symptoms and are not experiencing complications of BPH should be managed with a strategy of watchful waiting. Patients with mild LUTS can be treated initially with medical therapy. Transurethral resection of the prostate (TURP) is considered the criterion standard for relieving bladder outlet obstruction (BOO) secondary to BPH. However, there is considerable interest in the development of minimally invasive therapies to accomplish the goal of TURP while avoiding its adverse effects  (see Treatment).
The prostate is a walnut-sized gland that forms part of the male reproductive system. It is located anterior to the rectum and just distal to the urinary bladder. It is in continuum with the urinary tract and connects directly with the penile urethra. It is therefore a conduit between the bladder and the urethra. (See the image below.)
The gland is composed of several zones or lobes that are enclosed by an outer layer of tissue (capsule). These include the peripheral, central, anterior fibromuscular stroma, and transition zones. BPH originates in the transition zone, which surrounds the urethra.
Prostatic enlargement depends on the potent androgen dihydrotestosterone (DHT). In the prostate gland, type II 5-alpha-reductase metabolizes circulating testosterone into DHT, which works locally, not systemically. DHT binds to androgen receptors in the cell nuclei, potentially resulting in BPH.
In vitro studies have shown that large numbers of alpha-1-adrenergic receptors are located in the smooth muscle of the stroma and capsule of the prostate, as well as in the bladder neck. Stimulation of these receptors causes an increase in smooth-muscle tone, which can worsen LUTS. Conversely, blockade of these receptors (see Treatment and Management) can reversibly relax these muscles, with subsequent relief of LUTS.
Microscopically, BPH is characterized as a hyperplastic process. The hyperplasia results in enlargement of the prostate that may restrict the flow of urine from the bladder, resulting in clinical manifestations of BPH. The prostate enlarges with age in a hormonally dependent manner. Notably, castrated males (ie, who are unable to make testosterone) do not develop BPH.
The traditional theory behind BPH is that, as the prostate enlarges, the surrounding capsule prevents it from radially expanding, potentially resulting in urethral compression. However, obstruction-induced bladder dysfunction contributes significantly to LUTS. The bladder wall becomes thickened, trabeculated, and irritable when it is forced to hypertrophy and increase its own contractile force.
This increased sensitivity (detrusor overactivity), even with small volumes of urine in the bladder, is believed to contribute to urinary frequency and LUTS. The bladder may gradually weaken and lose the ability to empty completely, leading to increased residual urine volume and, possibly, acute or chronic urinary retention.
In the bladder, obstruction leads to smooth-muscle-cell hypertrophy. Biopsy specimens of trabeculated bladders demonstrate evidence of scarce smooth-muscle fibers with an increase in collagen. The collagen fibers limit compliance, leading to higher bladder pressures upon filling. In addition, their presence limits shortening of adjacent smooth muscle cells, leading to impaired emptying and the development of residual urine.
The main function of the prostate gland is to secrete an alkaline fluid that comprises approximately 70% of the seminal volume. The secretions produce lubrication and nutrition for the sperm. The alkaline fluid in the ejaculate results in liquefaction of the seminal plug and helps to neutralize the acidic vaginal environment.
The prostatic urethra is a conduit for semen and prevents retrograde ejaculation (ie, ejaculation resulting in semen being forced backwards into the bladder) by closing off the bladder neck during sexual climax. Ejaculation involves a coordinated contraction of many different components, including the smooth muscles of the seminal vesicles, vasa deferentia, ejaculatory ducts, and the ischiocavernosus and bulbocavernosus muscles.
BPH is a common problem that affects the quality of life in approximately one third of men older than 50 years. BPH is histologically evident in up to 90% of men by age 85 years. As many as 14 million men in the United States have symptoms of BPH.  Worldwide, approximately 30 million men have symptoms related to BP5.
The prevalence of BPH in white and African-American men is similar. However, BPH tends to be more severe and progressive in African-American men, possibly because of the higher testosterone levels, 5-alpha-reductase activity, androgen receptor expression, and growth factor activity in this population. The increased activity leads to an increased rate of prostatic hyperplasia and subsequent enlargement and its sequelae.
In the past, chronic end-stage BOO often led to renal failure and uremia. Although this complication has become much less common, chronic BOO secondary to BPH may lead to urinary retention, renal insufficiency, recurrent urinary tract infections, gross hematuria, and bladder calculi.
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