Benign prostatic hyperplasia
Lower urinary tract symptoms consequent upon bladder outlet obstruction due to BPH are predominantly due to 2 components
A static component related to an increase in benign prostatic tissue narrowing the urethral lumen
A dynamic component related to an increase in prostatic smooth muscle tone mediated by alpha-adrenergic receptors
Symptoms related to bladder outlet obstruction may also be contributed by bladder over-activity. 
Age over 50 years
Histological and lower urinary tract voiding symptoms increase with age. 
Men with an affected family relative, diagnosed with BPH before age 60 years, are at an increased risk.
In addition, twin studies indicate a 3.3-fold higher risk in monozygotic twins with affected siblings. 
A US study showed that Asian men have smaller prostates at any given age with less need for invasive surgery compared with white or black men. 
Male pattern baldness
A potential causal relation has been associated with lower urinary tract voiding symptoms. 
Frequent urge to urinate with possible incontinence and nocturia.
Fever, suprapubic or low back pain, tender, enlarged prostate gland on rectal examination is more consistent with prostatitis.
Abnormal digital rectal examination with prostate nodules or asymmetry is more consistent with prostate cancer
Presence of fever, dysuria, suprapubic or low back pain is more consistent with UTI.
Haematuria, suprapubic pain, bladder spasms with abnormal voiding, history of tobacco abuse, unknown major risk factor is more consistent with bladder cancer.
Storage abnormality in patients with involuntary bladder contractions.
Usually seen in patients with vascular disease, Parkinson disease, multiple sclerosis or diabetes mellitus with neuropathy. 
History of straddle injury or prior urological surgery with obstructive symptoms is more consistent with urethral stricture.
Global differences in epidemiology statistics are somewhat dependent upon how BPH is defined.
However, the prevalence of histological BPH does increase with age
Afects approximately 42% of men between the ages of 51 and 60 years, and 82% of men between the ages of 71 and 80 years. 
In 2000, BPH generated $1.1 billion in healthcare costs and accounted for over 4.4 million office visits, 117,000 emergency department visits and 105,000 hospitalizations in the US. 
Hyperplasia of the epithelial and stromal compartments, particularly in the transitional zone, may be attributed to various factors
Including shifts in age-related hormonal changes creating androgen/oestrogen imbalances
Changes in prostatic stromal-epithelial interactions that occur with ageing and increases in prostatic stem cell numbers are also aetiological considerations
Progression from pathological BPH to clinical BPH (i.e., the presence of symptoms) may require additional factors
Such as prostatitis, vascular affects, and changes in the glandular capsule. 
Frequency, urgency, and nocturia
Weak stream, hesitancy, intermittency, straining, incomplete emptying, and post-void dribbling
Fever with dysuria
Suggestive of complicated UTI
BPH involves hyperplasia of both epithelial and stromal prostatic components.
A key characteristic of BPH is increased stromal:epithelial ratio.
Over time, prostatic hyperplasia can result in bladder outlet obstruction.
Obstruction has both:
a prostatic component due to increased epithelial tissue, particularly in a transition zone
a dynamic component due to increases in stromal smooth muscle tone
A large number of alpha-adrenergic receptors are present in the prostate capsule, stroma, and the bladder neck.
The predominant alpha-1 receptor in prostatic stromal tissue is the alpha-1A receptor.
Treatment of symptomatic BPH is mainly accomplished via:
reduction of the size of the glandular component
following inhibition of the formation of dihydrotestosterone (DHT) by 5-alpha-reductase inhibitors
relaxation of smooth muscle tone
Select surgical intervention (e.g., transurethral resection) alleviates symptoms of urinary obstruction by reduction of prostatic bulk
pyuria (pus in urine)
elevation greater than age guideline
International Prostate Symptom Score (IPSS)
score of 0 to 35 to define severity of symptoms
global bother score
score 0 to 6 dependent on degree of bother
diary of frequency of voiding
hydronephrosis, mass, urolithiasis
mass, hydronephrosis, urolithiasis
mass, stone, stricture
less than 20 mL/second
abnormal bladder pressure, abnormal bladder voiding
behavioural management programme
Limitation of fluids
bladder training focused on timed and complete voiding
treatment of constipation
Alpha-blockers work through smooth muscle relaxation in the prostate and bladder neck.
The predominant receptor type in the prostate and bladder is the alpha-1A receptor
Alpha-blockers specific for this receptor are more prostate selective and have less vascular effects
Long-acting alpha-1 antagonists include terazosin and doxazosin
Alfuzosin is a modified release alpha-1A antagonist
Tamsulosin and silodosin are a long-acting sub-type (alpha-1A) selective alpha-blocker
5-alpha-reductase inhibitors work through reduction of serum dihydrotestosterone (DHT)
Inhibit DHT formation, reducing prostate volume by 20% to 25%
They have been shown to reduce the risk for acute urinary retention and the need for invasive therapy by approximately 50%
Finasteride is a type II 5-alpha-reductase inhibitor that reduces serum DHT by 75%
Dutasteride is a type I and II 5-alpha-reductase inhibitor with 90% to 95% reduction of serum DHT
Minimally invasive therapy
transurethral needle ablation
transurethral microwave therapy
visual laser ablation
interstitial laser coagulation
Transurethral resection of the prostate (TURP) or transurethral vaporisation (TUVP)
Open prostatectomy or holmium laser enucleation (HoLEP)
The majority of patients with BPH can expect at least moderate improvement of their symptoms with a decreased bother score and improved quality of life
Lower urinary tract symptoms (LUTS), secondary to BPH, may affect sexual wellbeing including erectile function
Medical therapy for BPH may also effect sexual function, beneficially and harmfully, so this must be considered on an individual basis
Some studies suggest that patients with a low risk for progression may be able to discontinue first-line therapy with alpha-blockers after several months of therapy
However, the majority of patients will require ongoing therapy.
Clinical progression of BPH (as defined by symptom progression >3 points) occurs in approximately 20% of patients
Approximately 2.5% of patients will develop acute urinary retention and another 6% will require invasive therapy over a 5-year time-frame
Risk for BPH progression is increased in patients with higher prostate volumes and PSA levels
Risk reduction of clinical BPH progression has been demonstrated by 39% in patients on doxazosin and 34% in patients on finasteride
Patients on combination therapy had a 66% reduction in clinical BPH progression