I. Pathogenesis The necessary conditions for prostatic hyperplasia are advanced age and functional testes, but the true etiology has not yet been elucidated. Currently, there are several theories: dihydrotestosterone, androgen-estrogen synergy, embryonic reawakening, stem cells, and mesenchymal-epithelial interactions. Among them, the role of dihydrotestosterone is the most emphasized, and various anti-androgen therapies are currently based on this theory. Second, the pathogenesis of the prostate is a male tubular gland, located between the bladder and the urogenital diaphragm, the shape of the prostate in adult men is like an inverted chestnut, which can be divided into the bottom, the body and the tip of the 3 parts, the longitudinal diameter of the prostate is 3cm, the transverse diameter is 4cm, the anterior and posterior diameter is 2cm, the bottom of the prostate is upward and thick, the front of the prostate is tightly connected with the neck of the bladder, the urethra is penetrated through, the back of the spermatogonial vesicle attached, the bottom is toward the downward direction. The tip of the prostate is directed downward, the tip is tiny and fused with the membranous part of the urethra, ending at the urogenital diaphragm. Between the bottom and the tip is the body, the front of the body is more convex, the back is flatter, there is a line of shallow grooves in the center, called the central groove of the prostate, this groove divides the back of the prostate into the left and right lobes, you can touch the back of the left and right lobes of the prostate and the central groove of the prostate through the anterior wall of the rectum by rectal palpation to understand the condition of the prostate, and the weight of the prostate gland of the adult is about 20g. 1, pathology The human prostate is mainly composed of glandular tissue and non-glandular tissue 2 parts, and the function and disease related to the prostate is mainly the glandular tissue part, Mcneal (1988-1990) will be the morphology of the prostate function and pathology of the prostate combined with the study of the prostate gland parts of the prostate named, the glandular part of the gland can be divided into 4 zones, peripheral zone accounted for 70% to 75% of the gland, the central zone, the central zone. The peripheral zone accounts for 70% to 75% of the gland, the central zone, accounting for 25% of the gland (both for the peripheral part of the prostate); the migratory zone accounts for 5% to 10% of the gland, and the periurethral zone accounts for less than 1%, the migratory zone, the periurethral zone is a specific part of the occurrence of prostate hyperplasia. Pathologically BPH, also known as prostatic nodular hyperplasia, is the most common symptomatic verrucous lesion of the prostate. Nodularity may begin as a spontaneous reversal of stromal cells to the embryonic stage, and its growth potential may be due to the synergistic effect of stromal-epithelial interactions, culminating in the formation of prostatic hyperplasia. This lesion is rare in individuals under the age of 50 years and increases with age until the age of 70 to 80 years, when nodular hyperplasia in the prostate gland begins to occur in the migrating zone of the prostate and in the periurethral tissues, where the nodules in the periurethral tissues are similar to the mesenchymal component of the embryonic stage and are of stromal composition, whereas the nodules in the migrating zone are of glandular composition. Prostatic hyperplasia grows in 3 separate processes: 1. Nodule formation. 2, Diffuse enlargement of the migratory zone. 3, Nodule enlargement. Patients aged 50 to 70 years old, although the migratory zone increased 1 times, but nodules only 14%, the migratory zone diffusely enlarged part of the people are younger than 70 years old, 70 years old, until the age of 80 years of age nodules significantly enlarged, is the main cause of prostate hyperplasia in this period of time. Gross observation: hyperplasia of the prostate is generally walnut or chicken egg large, or even larger, like the size of a goose egg, the surface is smooth, nodular, tough, elasticity, the normal prostate weighs about 20g, hyperplasia can be up to 30 ~ 80g, or even weigh more than 100g, in vivo, can be surrounded by normal prostate tissue extrusion, and the formation of fibrous “surgical peritoneum “; Surgical envelope is tough and elastic, and there is a clear demarcation between the nodular hyperplasia, which is helpful for peeling off the hyperplasia during surgery, but prostate cancer can still occur in the remaining prostate. Cutting view: some small nodules are mainly fibromuscular components, pale white, homogeneous, smooth cut surface, soft, can overflow a small amount of milky fluid, there are also nodules in the form of honeycomb or spongy, glandular vesicles are cystic; the size of prostatic hyperplasia is not proportional to the degree of urinary obstruction, i.e., prostate symptoms, but has a direct relationship with the location of the enlarged area, e.g., periurethral glandular area stromal nodules occurring in the periurethral glandular ducts Glandular follicles invade therein before slowly proliferating, more towards the proximal urethra, protruding into the bladder to form the so-called mesophyll hyperplasia type intraurethral hyperplasia, even when the gland is enlarged by less than 10g, it can also cause severe obstructive situations. Microscopic observation: the hyperplastic nodules include the original components of the prostate itself, glandular fibrous tissue and smooth muscle, but the hyperplasia is uneven, the earliest prostatic hyperplasia nodules are mesenchymal hyperplasia, the nodules of the mesenchymal smooth muscle increased and elastic fibers are reduced, followed by the glandular components of the hyperplasia, the gland is often irregularly dilated, or even cystic, and sometimes the lumen is a papillary protuberance, and the glandular lumen contains a reddish staining of proteinaceous secretion, sometimes forming calcified vesicles, glandular epithelium is flattened or columnar; the nucleus is regular, the nucleolus is not obvious, the cytoplasm is light stained, the gland is surrounded by intact basement membrane, there is no obvious fibrous periphery of the nodule, and there is no boundary with the normal prostate, in recent years, it has also been observed that the infarction of the gland is observed in nearly 25% of the enlarged glands, the infection of glandular ducts causes cellulitis, the dilatation of the adenoid follicles, and the obstruction of ducts causes the secretion trapping, and the focal type is observed. Atypical hyperplasia and epithelialization are meaningful pathological features of prostatic hyperplasia. 2.Pathological typing According to the different proportions of glandular epithelium and fibrous and smooth tissues of the hyperplastic glands, prostatic hyperplasia can be divided into several different subtypes: (1)Sclerosing adenopathy: similar to the homonymous lesion of the breast, with a clear boundary of the nodule, consisting of glands and epithelium of varying sizes and shapes, the glands are usually compressed, there is often a mucus-like mesenchymal formation, and there is a basilar membrane and basal lamina cells at the periphery of the epithelium-. (2) Fibroadenoma-like type: glands, smooth muscle and fibrous tissue are all proliferated. (3) Adenoma-like type: glandular hyperplasia predominates, resembling an adenoma, with less surrounding mesenchyme and no true surface envelope, so it is not a true adenoma. (4) Fibroproliferative type: fibrous tissue hyperplasia is dominant, glandular hyperplasia is relatively light, sometimes smooth muscle hyperplasia is dominant and fibrous hyperplasia is light, resembling smooth muscle tumor. These types are different stages of disease development and are often mixed together in the same case and cannot be categorized distinctly. Foci of infarction are seen in some of the tissues resected in BPH, ranging from a few millimeters to several centimeters. The healed lesions are replaced by fibrous scar tissue. Foci of squamous epithelial hyperplasia are often seen around the infarcts. 3, pathophysiology Prostatic hyperplasia caused by lower urinary tract obstruction can lead to a series of pathological changes in the bladder and upper urinary tract, the size of the prostatic hyperplasia and whether the symptoms of lower urinary tract obstruction is very relevant, prostatic hyperplasia in different parts of the symptoms caused by different severity is also different, such as both sides of the prostate lobe significant enlargement has not yet reached the degree of urethral pressure to make the prostatic part of the urethra flexion, elongation; clinical symptoms may be Is very mild, if the hyperplasia site in the urethral periphery, even if very mild hyperplasia can cause very serious obstruction symptoms, in the clinic can often have although there are very serious urinary difficulties, bladder outlet obstruction symptoms, but rectal diagnosis of prostate hyperplasia may not be significant, which can be referred to as the “non-prostatic hyperplasia of the prostate disease”. When prostatic hyperplasia causes bladder outlet obstruction, the bladder’s retention and voiding function can be affected accordingly, and the bladder reflexively establishes the process of stress-compensation-loss of compensation to overcome the outlet obstruction, and at the same time, the forced urethral muscle begins to proliferate, and when there is a high degree of irritation of the bladder, the patient may experience urinary urgency and urgency incontinence, etc. In the compensatory stage, the patient’s symptoms may be reduced, and the patient’s symptoms will be more severe. In the compensatory phase, the patient’s symptoms begin to develop and urination appears hesitant, that is, because the bladder changes pressure to overcome the bladder outlet obstruction. Interruptions of urination, divergence of the urinary line, and dribbling after urination occur because of forceful contraction of the urethra muscle. When there are changes in the bladder wall, the muscles of the deltoid region and the interureteral ridge proliferate, the interureteral ridge extends to the sides, and the ureter is displaced to the posterior and lateral directions, which increases the resistance in the lumen of the ureter and produces stenosis, thus causing bilateral ureterocele, and likewise there is a varying degree of hyperplasia in the detrusor muscle, which creates a beam-like protuberance in the wall of the bladder, as a compensatory hypertrophy. When urinating, intravesical pressure can reach 50-100cmH2O, which prompts the formation and development of bladder diverticulum, and the persistence of these factors makes the detrusor muscle lose its compensatory function, as a result of which the residual urine increases, the effective bladder capacity decreases, presenting atonic dilatation, and the bladder wall thins, and the hypertrophy of the bladder detrusor muscle lengthens the wall segment of the ureteric bladder, which can lead to ureteral obstruction, and the wall segment of the ureter can be shortened after bladder loss of compensation. After bladder failure, the ureteral wall segment can be shortened, the residual urine volume in the bladder increases, and even urinary retention occurs; at this time, it is accompanied by serious symptoms and filling incontinence can occur; because of the increasing intravesical pressure, the ureteral orifice loses the function of sphincter and urine reflux occurs, then the ureter and renal pelvis dilate, and the pelvis becomes hydrated, which affects the renal function. Long-term hydronephrosis and the increase of the intra-pelvic pressure make the renal cortex become thin, and the renal function is impaired, and even the occurrence of infections, stones and renal failure. Renal failure. Patients develop significant hypertension, water retention and other clinical manifestations of uremia. Prostatic hyperplasia is mainly manifested in bladder outlet obstruction (BOO), which means that bladder outlet obstruction is the root cause of the pathophysiologic changes of prostatic hyperplasia, on the basis of which abnormal bladder function occurs, and the dilatation of the ureter leads to severe impairment of renal function. Prostatic hyperplasia first caused bladder outlet obstruction has mechanical factors, and also dynamic factors. Mechanical factors for prostate hyperplasia caused by urethral transverse area reduction and urethral lengthening caused by kinetic factors for the prostate urethra, prostate tissue and prostate envelope tension caused by α receptor affects the main factors of this tension, through the physiological and pharmacological studies have proved that the human prostate myocytes can be stimulated through the α1 receptor contraction of the smooth muscle, the increased tension caused by the bladder outlet obstruction. The human prostate contains a high number of α1 adrenergic receptors, and 98% of all α1 receptors are found within the prostate stroma. An important part of prostatic hyperplasia is stromal (smooth muscle and connective tissue) hyperplasia, with smooth muscle predominating. Some scholars have studied patients with clinical symptoms of prostatic hyperplasia, biopsy was performed before drug treatment to determine the density of smooth muscle per unit area of the prostate; after that, α-blockers were used for treatment, and the improvement of patients’ symptoms was related to the density of smooth muscle per unit area of the prostate, and the improvement of maximal urinary flow rate (QMX) was also consistent with the improvement of symptoms, which suggests that bladder outlet obstruction is mainly caused by the contraction of smooth muscle of the prostate, which is the main cause of bladder outlet obstruction. This result suggests that bladder outlet obstruction is mainly caused by prostate smooth muscle contraction and increased tension, and the severity of urinary symptoms is not proportional to the size of the prostate. Sympathetic α1 receptor blockers can effectively relax the bladder neck and prostate smooth muscle without affecting the function of the urethral muscle; thus, they can rapidly relieve the obstructive symptoms of prostatic hyperplasia. Vascular endothelin, the strongest known smooth muscle contraction agent in the human body, can cause slow but strong contraction of prostate smooth muscle, which can not be eliminated by α-blockers.