Benign prostatic hyperplasia (BPH) also known as benign prostatic hypertrophy (technically a misnomer), benign enlargement of the prostate

(BEP), and adenofibromyomatous hyperplasia, refers to the increase in size of the prostate. Properly, BPH involves hyperplasia rather than hypertrophy, but the nomenclature is often interchangeable, even amongst urologists.[1] It involves hyperplasia of prostatic stromal and epithelial cells, resulting in the formation of large, fairly discrete nodules in the periurethral region of the prostate. When sufficiently large, the nodules compress the urethral canal to cause partial, or sometimes virtually complete, obstruction of the urethra, which interferes the normal flow of urine. It leads to symptoms of urinary hesitancy, frequent urination, dysuria (painful urination), increased risk of urinary tract infections, and urinary retention. Although prostate specific antigen levels may be elevated in these patients because of increased organ volume and inflammation due to urinary tract infections, BPH is not considered to be a premalignant lesion. Adenomatous prostatic growth is believed to begin at approximately age 30 years. An estimated 50% of men have histologic evidence of BPH by age 50 years and 75% by age 80 years. In 4050% of these patients, BPH becomes clinically significant.[2]

The prostate gets larger in most men as they get older, and, overall, 45% of men over the age of 46 can expect to suffer from the symptoms of BPH if they survive 30 years. Incidence rates increase from 3 cases per 1000 man-years at age 4549 years, to 38 cases per 1000 man-years by the age of 7579 years. Whereas the prevalence rate is 2.7% for men aged 4549, it increases to 24% by the age of 80 years.[43] For some men, the symptoms may be severe enough to require treatment.

Signs and symptoms

Benign prostatic hyperplasia symptoms are classified as storage or voiding. Storage symptoms include urinary frequency, urgency (compelling need to void that cannot be deferred), urgency incontinence, and voiding at night (nocturia). Voiding symptoms include urinary stream, hesitancy (needing to wait for the stream to begin), intermittency (when the stream starts and stops intermittently), straining to void, and dribbling. Pain and dysuria are usually not present. These storage and voiding symptoms are evaluated using the International Prostate Symptom Score (IPSS) questionnaire, designed to assess the severity of BPH.[3] BPH can be a progressive disease, especially if left untreated. Incomplete voiding results in stasis of bacteria in the bladder residue and an increased risk of urinary tract infection. Urinary bladder stones are formed from the crystallization of salts in the residual urine. Urinary retention, termed

acute or chronic, is another form of progression. Acute urinary retention is the inability to void, while in chronic urinary retention the residual urinary volume gradually increases, and the bladder distends. Some patients that suffer from chronic urinary retention may eventually progress to renal failure, a condition termed obstructive uropathy.

[edit] Cause
A study published in 2008 in the journal of andrology "Andrologia"[4] reports on a newly discovered venous route by which free (active) testosterone reaches the prostate in extremely high concentrations, promoting the accelerated proliferation of prostate cells, leading to the gland's enlargement. The study suggests that BPH is caused by malfunction of the valves in the internal spermatic veins manifesting as varicocele, a phenomenon which has been shown to increase rapidly with age,[5][6] roughly equal to 10-15% each decade of life. The 6- to 8-fold elevated hydrostatic pressure then leads to retrograde venous drainage, allowing free communication with the prostatic circulation. Having measured a concentration of free testosterone of some 130-fold above serum level in the internal spermatic vein (the testes being the main source and the blood being undiluted in systemic circulation), the authors conclude that the elevated venous pressure causes hypertrophy and exposure to high concentrations of free testosterone causes hyperplasia in the prostate. The study also proposes a treatment method (GatGoren Technique) similar to that used in treating varicocele, which restores normal pressure in the venous drainage system, effectively reducing the volume of the prostate and clinical manifestation of BPH. Most experts consider androgens (testosterone and related hormones) to play a permissive role. This means that androgens have to be present for BPH to occur, but do not necessarily directly cause the condition. This is supported by the fact that castrated boys do not develop BPH when they age. On the other hand, administering exogenous testosterone is not associated with a significant increase in the risk of BPH symptoms.[citation needed] Dihydrotestosterone (DHT), a metabolite of testosterone, is a critical mediator of prostatic growth. DHT is synthesized in the prostate from circulating testosterone by the action of the enzyme 5-reductase, type 2. This enzyme is localized principally in the stromal cells; hence, those cells are the main site for the synthesis of DHT. DHT can act in an autocrine fashion on the stromal cells or in paracrine fashion by diffusing into nearby epithelial cells. In both of these cell types, DHT binds to nuclear androgen receptors and signals the transcription of growth factors that are mitogenic to the epithelial and stromal cells. DHT is 10 times more potent than testosterone because it dissociates from the androgen receptor more slowly. The importance of DHT in causing nodular hyperplasia is supported by clinical observations in which an inhibitor of 5-reductase is given to men with this condition. Therapy with 5-reductase inhibitor markedly reduces the DHT content of the prostate and, in turn, reduces prostate volume and, in many cases, BPH symptoms.[citation needed] Testosterone promotes prostate cell proliferation,[7] but relatively low levels of serum testosterone are found in patients with BPH.[8][9] One small study has shown that medical castration lowers the serum and prostate hormone levels unevenly, having less effect on testosterone and dihydrotestosterone levels in the prostate.[10]

While there is some evidence that estrogen may play a role in the etiology of BPH, this effect appears to be mediated mainly through local conversion of estrogen to androgens in the prostate tissue rather than a direct effect of estrogen itself.[11] In canine in vivo studies castration, which significantly reduced androgen levels but left estrogen levels unchanged, caused significant atrophy of the prostate.[12] Studies looking for a correlation between prostatic hyperplasia and serum estrogen levels in humans have generally shown none.[9][13] On a microscopic level, BPH can be seen in the vast majority of men as they age, in particular over the age of 70 years, around the world. However, rates of clinically significant, symptomatic BPH vary dramatically depending on lifestyle. Men that lead a western lifestyle have a much higher incidence of symptomatic BPH than men that lead a traditional or rural lifestyle. This is confirmed by research in China showing that men in rural areas have very low rates of clinical BPH, while men living in cities adopting a western lifestyle have a skyrocketing incidence of this condition, though it is still below rates seen in the West. Much work remains to be done to completely clarify the causes of BPH.

Patients should decrease fluid intake before bedtime, moderate the consumption of alcohol and caffeine-containing products, and follow timed voiding schedules.

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. Stromaepithelial 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 35% 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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