Benign prostatic hyperplasia
Introduction
Introduction Benign prostatic hyperplasia (BPH), formerly known as prostatic hypertrophy, is one of the common diseases in older men and is a benign lesion of the prostate. The cause of the disease is related to the imbalance of androgen and estrogen in the human body. The lesion originates from the glandular tissue, connective tissue and smooth muscle tissue of the middle or lateral lobes of the posterior urethra to form a mixed spherical nodule. It is obvious that both sides of the lobe and middle lobe hyperplasia protrude into the bladder or urethra, compressing the bladder neck or urethra, causing obstruction of the lower urinary tract. Long-term lesions can cause hydronephrosis and renal dysfunction. Can also be complicated by stones, infections, tumors and so on.
Cause
Cause
(1) Causes of the disease
The prostate is located in front of the rectum and resembles a chestnut. The bottom is close to the bladder neck and surrounds the posterior urethra. Normal adult male prostate has a transverse diameter of 4 cm, a longitudinal diameter of 3 cm, a anteroposterior diameter of 2 cm, and a weight of 20 g, which is the largest accessory gonad of male. It secretes a milky white pulpy liquid that is part of semen and contains sodium, potassium, calcium, chlorine, zinc, magnesium, sodium bicarbonate, citrate, protein and starch, as well as acid phosphatase and prostate specificity. antigen. When the prostate glandularizes, their serum levels increase significantly. The prostate secretion is an alkaline liquid, which makes the pH of the semen up to 7.3. It can buffer the acidic environment of the vagina and is suitable for the survival and activity of sperm, which is conducive to conception.
The size of the prostate varies with age. It is very small in young children, and the glandular tissue is underdeveloped. It is mainly composed of smooth muscle and connective tissue. The mature prostate is rapidly increased, especially the glandular tissue, and gradually degenerates into the old age, and the gland tissue shrinks. The development of benign prostatic hyperplasia in the elderly is a pathological phenomenon. The prostate can be divided into five leaves, namely the anterior, middle, posterior and bilateral leaves. Close to the benign prostatic hyperplasia is the middle and both sides of the leaf. Middle lobe hyperplasia often protrudes into the bladder neck, blocking the urethral opening causes difficulty in urinating. The leaves on both sides cling to the side wall of the urethra, and its hyperplasia can compress, prolong, and distort the urethra, resulting in difficulty in urinating. Because it is close to the front of the levator ani muscle, the anal finger examination is easy to touch, providing a way for the physician to examine and detect prostate lesions.
At present, the cause of benign prostatic hyperplasia is still not very clear. In a nutshell, the imbalance of sex hormones, including androgen and estrogen metabolism in older men, is the cause of benign prostatic hyperplasia. However, the specific links and mechanisms, although many years of basic and clinical research, are still not very clear. Previously, Carleton believed that prostate hypertrophy and excessive sexual life, lustful indulgence, sloppy life, post-urethral inflammation were not completely treated, urinary tract obstruction and testicular dysfunction. It seems difficult to say now what is the relationship. Virchow once described the hypertrophic prostate as a "fibroid" or "adenomas", using the doctrine of new organisms to explain the prostatic hypertrophy. Later, Deming (1935) and Moore (1943) and others objected to this doctrine and believed that the new organism It is an abnormal mass of tissue, which grows rapidly and irregularly; while hyperplasia is the hypertrophy of tissue cells, often to compensate for the loss of similar tissues, or to compensate for the lack of functions of similar tissues. A similar situation can be seen in the thyroid gland, adrenal cortex and pituitary gland. Others have arterial hard chemistry, infection theory, metabolism and nutritional condition theory, it is difficult to explain the essence of the problem, the more able to explain the problem is the endocrine theory.
Endocrine theory, it has long been observed that the development of the prostate is closely related to the testis. Excision of the testis on both sides can cause the prostate to shrink. The pituitary gland is destroyed before puberty, and the prostate also stops developing. A large number of females can cause prostate atrophy. Everyone acknowledges that the prostatic hyperplasia is due to a disorder of gonadal endocrine, but so far there is still lack of laboratory data to illustrate this problem. The details of the endocrine disorders are not well understood. For example, the content of testosterone in the blood of normal male spermatic vein is between 0.025 and 1.6 g%. This value is gradually reduced during the 30- to 80-year-old period (Finkelstein 1961). In addition, the amount of 17 keto alcohol excretion in urine was measured, and 50 to 70 years old was only 40 to 55% of the male youth discharge (Mac Donald 1962). However, the results of measuring male hormones in patients are very inconsistent, some are low, some are high, and some are unchanged. Lacssagne (1933) once thought that estrogen may be the cause of prostatic hypertrophy. Prostatic hypertrophy occurs in the "medullary part" of the lateral and middle lobe of the prostate without degrading the medulla; the "cortex" has no effect. Huggins believes that because the estrogen reduces the effect of androgen, which causes the medulla to degenerate; while the "cortex", the posterior lobe, has a low threshold for males, so it remains intact.
The male and female hormones in males are produced in both the testis and the adrenal cortex, and are controlled and regulated by the secretion of the pituitary to maintain their balance. From the perspective of the effect of treatment, the effect of female and phlegm on normal prostate and prostate cancer is more reliable. The effect on prostatic hypertrophy is not constant. The use of male or male females in combination with the treatment of prostatic hypertrophy can not achieve reliable results. In summary, the prostate hypertrophy is closely related to the disorder of gonadal endocrine, but the specific mechanism is still unclear. There are two necessary conditions for the occurrence of benign prostatic hyperplasia: one is advanced age, and the other is the presence of functional testes. As early as 90 years ago, it was pointed out that males who were castrated did not develop prostate hyperplasia.
(two) pathogenesis
1. Pathological changes in the prostate
The normal prostate is divided into the inner and outer layers: the inner layer is the urethral mucosa surrounding the urethra and the submucosal gland, also known as the transition zone, and the outer layer is the peripheral zone, with fibrous membrane separation between the two layers. When the prostate enlarges and changes, first, there are multiple central fibromuscular nodules and stromal hyperplasia in the submucosal gland of the prostate segment, and then there is glandular epithelial hyperplasia. Pathology can be divided into two types: glandular nodules and matrix nodules. If the nodules appear in the glandless area, matrix nodules are formed; then the adjacent epithelial cells are stimulated to proliferate and invade the hyperplastic nodules. Matrix adenoma. The hyperplastic tissue compresses the true prostate tissue to the periphery, and the extruded tissue undergoes degeneration and transforms into fibrous tissue, forming a gray-white hard pseudomembrane-surgical envelope.
(1) Pathological classification: Some people divide the different tissue components of hyperplasia into 5 types: fibromuscular hyperplasia, muscle hyperplasia, fibroadenoma-like hyperplasia, fibromuscular adenomatous hyperplasia and stromal hyperplasia. Matrix hyperplasia is an important feature of benign prostatic hyperplasia.
(2) Changes in structural composition: When prostate hyperplasia occurs, the proportion of interstitial (about 60%) is significantly higher than that of normal prostate (about 45%), and the structural components of interstitium also change. The area of smooth muscle to interstitial area It is significantly higher than normal prostate, and epithelial hyperplasia is characterized by hyperplasia of basal cells. Basal cells change from normal flat to cubic and short column. Smooth muscle cells were thick, dense, diffusely distributed in the interstitial, and the nuclear morphology did not change abnormally, but the activity of DNA and RNA in glandular epithelial cells increased, while the main features of elderly benign prostatic hyperplasia showed a decrease in vascular composition. .
(3) Pathological changes associated with symptoms: The symptoms of benign prostatic hyperplasia are related to the following three changes:
1 Detrusor lesions: Animal experiments have shown that after obstruction occurs, the bladder detrusor changes significantly, and the nerve endings in the detrusor muscle decrease, that is, partial denervation, the bladder volume increases, but the muscle contraction strength is relatively weakened. The activity of acetylcholinesterase was significantly reduced.
2 Prostate motility factors: The human prostate contains more 1-AR receptors, 98% of which are present in the glandular matrix. Human prostate muscle cells can stimulate the contraction of smooth muscle contraction by this receptor, causing obstruction of the bladder outlet.
3 prostate static factors: that is, the gradual increase of prostate volume caused pressure on the bladder neck and obstruction symptoms.
Prostate gland, connective tissue and smooth muscle tissue proliferate during prostatic hyperplasia, which can form multiple nodules. These histological processes begin in the prostate and other tissues around the urethra and then spread to the outer layer of the prostate. These nodules continue to grow, compressing the surrounding glandular tissue to form a pseudo-peric envelope, which is 2 to 5 mm thick, white and solid, and elastic.
2. Changes in the urethra and bladder: The underlying cause of pathophysiological changes in benign prostatic hyperplasia is obstruction of the bladder outflow channel, on the basis of which bladder dysfunction, upper urinary tract dilatation and renal dysfunction occur.
(1) Obstruction of the bladder outflow channel: Prostatic hyperplasia first causes bladder outflow obstruction. Bladder outflow obstruction has mechanical obstruction caused by prostatic hyperplasia caused by decreased cross-sectional area of the urethra and prolonged urethra; dynamic obstruction caused by increased tension of the urethra, prostate tissue and prostate capsule of the prostate. In proliferating prostate tissue, smooth muscle tissue and markedly proliferating alpha receptors are major factors influencing this tension.
(2) abnormal bladder function: manifested as unstable bladder, bladder weakness and low compliance bladder. 52% to 82% of BPH has an unstable bladder. Unstable bladder is the main cause of frequent urination, urgency, and urge incontinence. Bladder detrusor weakness, decreased systolic function, can also cause dysuria, poor postoperative recovery.
Prostatic hyperplasia of the prostate can be elongated, distorted, and compressed after the urethra, the mid-lobe hyperplasia and even the bladder neck cause obstruction, leading to difficulty in urinating. If the prostate only proliferates to the periphery, and does not oppress the obstruction of the urethra and bladder neck, it does not cause difficulty in urinating. Therefore, it can be seen clinically that some elderly men have a marked increase in prostate, but urinating freely. Clinically, it has also been found that the degree of benign prostatic hyperplasia is not proportional to the symptoms of dysuria. Therefore, it is a factor that causes dysuria in patients with benign prostatic hyperplasia.
It is now clear that dysuria is also closely related to prostate capsule tension and bladder neck, prostate, and urethral smooth muscle tone. Increased tension and tension, increased symptoms of dysuria. The tension in these sites increases with increasing sympathetic excitability, and sympathetic excitability is regulated by the abundant alpha 1 receptors at these sites. Therefore, it is not difficult to explain that sympathetic nerve excitement such as anxiety, tension and cold will aggravate dysuria in patients with benign prostatic hyperplasia, and 1 blockers will alleviate the symptoms of dysuria in these patients. In addition, dysuria is also associated with the compliance and synergy of the bladder detrusor. Experiments have shown that any chronic disease that diminishes urinary flow can have an effect on the bladder. It is generally manifested by a thickening of the whole layer of the bladder (incidence of epithelial cells, smooth muscle connective tissue, and serosa), compliance, and reduced synergy.
Prostatic hyperplasia continues to progress, dysuria is intensified, bladder detrusor due to long-term excessive urine, eventually leading to damage, bladder wall from the initial compensation increased, to the final bladder wall thinning, covered with trabecular chamber, and even bladder diverticulum More exacerbated dysuria.
3. Pathological changes of the upper urinary tract: a large amount of residual urine, continuous intravesical pressure > 40cmH2O is the two basic causes of upper urinary tract expansion of benign prostatic hyperplasia, according to the main pathological features of the bladder are divided into:
1 high-pressure chronic urinary retention, characterized by low compliance bladder, intravesical pressure > 40cmH2O during storage, and upper urinary tract function recovery after upper urinary tract dilatation is also poor. 2 low-pressure chronic urinary retention, characterized by impaired bladder sensory function, a large number of residual urine, mostly associated with bladder weakness, and intravesical pressure during storage
If the lower urinary tract obstruction can not be treated properly, the bladder wall can lose compensatory capacity, the bladder enlarges, the bladder wall becomes thinner, and further development leads to weak muscle strength supporting the ureteral bladder wall segment, and damage to the valve at the entrance of the bladder ureter is damaged. Bladder ureteral reflux occurs, and bilateral renal pelvis and ureteral hydrops occur, the renal pelvis expands into a sac, gradually expanding; the renal parenchyma is gradually elongated and thin, and there is congestion, the renal pelvis expands and gradually enlarges, the kidney cone and the kidney The column is pressed and thinned and finally disappears. The glomerulus can still maintain urinary function, but due to tubular necrosis and loss of concentrated function, the proportion of urine is low, which can cause various pathological changes in the pathogenesis:
1 Reflux of the renal pelvis: After the hydronephrosis occurs, part of the urine can still be evacuated from the ureter, but another part will flow back to the vein around the kidney and the lymphatic vessels around the renal pelvis.
2 Kidney balance and compensation: After the occurrence of hydronephrosis, just like the loss of function of kidney tissue caused by other reasons, the remaining tissue can produce hypertrophy and compensate for some functions, but this effect increases with age. Attenuated, generally after 35 years of age, this compensatory function is almost lost, renal vasoconstriction, tubular atrophy, ureteral pressure is gradually reduced, renal blood flow is reduced, causing renal dysfunction, manifested as loss of appetite, anemia, elevated blood pressure, Drowsiness, dysfunction, and azotemia, these symptoms are not easy to be detected, and are often misdiagnosed as digestive tract diseases, so benign prostatic hyperplasia should be considered in elderly patients with unexplained renal insufficiency.
4. Other changes: Due to long-term dysuria, there are often residual urine in the bladder, which will cause secondary infection and stone formation, further aggravating dysuria and worsening kidney function. Due to the difficulty of urinating, it is necessary to contract the abdominal muscles and diaphragm muscles, and the pressure of the breath to promote the discharge of urine. In the long run, it is easy to cause complications such as sputum, sputum, emphysema, so the damage caused by prostate hyperplasia is systemic.
Examine
an examination
Related inspection
Prostate finger test semen viscosity prostate examination semen lactate dehydrogenase-X
Physical examination: When the urine is in the urine, the lower abdomen is bulging. The suprapubic area touches the filled bladder. Rectal examination, the prostate enlarges, the surface is smooth, elastic, and the central groove becomes shallow or disappears. Prostatic hyperplasia can be divided into 3 degrees according to the degree of gland enlargement. I degree enlargement: the prostate is 1.5 to 2 times larger than normal, the central groove becomes shallow, and the distance from the rectum is 1 to 2 cm; the second degree is enlarged: the gland is moderately enlarged, 2 to 3 times larger than normal, and the center The sulcus disappeared or slightly protruded, and it protruded into the rectum by 2 to 3 cm. The degree of swelling was 3 degrees: the gland was swollen and severely protruded into the rectum more than 3 cm. The central sulcus was prominent, and the finger could not touch the upper edge during the examination.
Laboratory inspection:
When long-term urinary retention affects renal function, creatinine and urea nitrogen are elevated. When combined with urinary tract infection, urine is routinely examined for red blood cells and pus cells.
PSA measurement: Although PSA can be increased at BPH, the significance of measuring PSA is not to diagnose BPH, but to detect prostate cancer at an early stage. Combined with free PSA, digital rectal examination, B-ultrasound can find most prostate cancer.
Other auxiliary inspections:
1. Imaging examination
(1) X-ray: In the IVU or bladder urethra angiography, the anterior and posterior and urinary conditions were taken. The bottom of the bladder was elevated, the arc density was reduced, and the length of the posterior urethra was increased. Such as the merger of diverticulum, tumors, stones can show filling defects. Late IVU can show vesicoureteral reflux, hydronephrosis or poorly developed kidneys or even no development.
(2) B-ultrasound: There are two methods of transrectal and transabdominal ultrasound, and transrectal B-ultrasound is preferred. The gland size, residual urine can be measured, and prostate cancer can be excluded according to the sonogram.
2. Cystoscopy: visible bladder neck protruding bulge, urethral orifice deformation. The bladder wall forms trabeculae, a small chamber, and even a diverticulum. For example, combined with bladder stones and bladder tumors can also be diagnosed together. This method is not routinely examined and is only performed when indicated.
3. Urodynamic examination: for non-invasive examination, the bladder volume should be >150ml when measured. The main indicators are: maximum urinary flow rate (Qmax, normal >15ml / s), bladder capacity (bladder capacity, normal male 350 ~ 750ml, female 250 ~ 550ml), detrusor contractility, etc., treatment options for benign prostatic hyperplasia And prognosis is important.
4. Residual urine volume measurement After the patient has urinated, the catheter is inserted into the urine, and the urine in the bladder is collected, and the volume of the urine is determined as the residual urine volume of the bladder. Ultrasound can also be used to measure the bladder capacity after urination and calculate the residual urine volume. Normal <50ml. When prostate hyperplasia occurs, the amount of residual urine often increases.
Diagnosis
Differential diagnosis
Differential diagnosis
The disease should be differentiated from bladder neck contracture (Marion's disease), prostate cancer, neuropathogenic bladder, bladder tumor, prostate tuberculosis, prostatic calculus, prostate cyst, ureteral hypertrophy, stones, foreign body and so on.
Bladder neck contracture
Bladder neck contracture is secondary to inflammatory lesions. Bladder neck smooth muscle is replaced by connective tissue, and it may also be abnormal in the bladder neck muscle during development, so that the neck cannot be opened when the bladder detrusor contracts. During cystoscopy, the posterior lip of the bladder neck is raised, and the contraction of the posterior urethra and the bladder triangle becomes shorter.
2. Prostate cancer
The prostate has nodules, PSA>4ng/ml, and the hypoechoic area in the prostate can be seen by rectal ultrasound. CT showed irregular shape of the prostate, the angle of the seminal vesicle disappeared, and the shape of the seminal vesicle changed. A biopsy can confirm.
3. Neuropathic bladder
All ages can occur, with obvious history and signs of neurological damage, often accompanied by lower limb sensation and movement disorders, sometimes accompanied by anal sphincter relaxation and reflexes disappear. The rectal examination is not large, and the urodynamic examination can be used for identification.
4. Bladder cancer
Bladder cancer near the bladder neck can be manifested as bladder outlet obstruction, often with hematuria, cystoscopy can be identified.
5. Urethral stricture
There are many medical history such as urethral injury and infection.
The above diseases can be identified in most cases by physical examination, laboratory tests, anal finger examination and cystoscopy. Only prostate cancer in atypical cases, according to the aforementioned examination methods, it is difficult to draw conclusions, the following methods can be used to assist differential diagnosis:
1. Determination of serum acid phosphatase: The prostate tissue contains high acid phosphatase, and when the cancer is cancerous, the content increases. This principle is used for this test. The normal value of serum acid phosphatase is 1 to 5 units according to King-Armsstrong, according to Bodansky. It is 0.5 to 2 units, and its value is determined to be 0.7KA units since the new inspection method in 1950. More than half of patients with prostate cancer are above normal. Note that false positives can occur after applying testosterone or prostate massage.
2. Serum phosphatase assay: When there is bone metastasis, serum phosphatase is elevated, normal value Bodahsky 2 ~ 4.5 units, King-Armstrong 8 ~ 14 units, but must pay attention to false positive.
3. Prostate biopsy: prostate biopsy can be performed by perineal or rectal.
4. Seminal ejaculation angiography: Prostate hypertrophy can only be seen with symmetry expansion, neat edges; prostate cancer can be seen with narrow, irregular, marginal, or defective.
diagnosis
Urinary frequency
Frequent urination is the earliest manifestation, first of all for frequent urination at night, followed by frequent urination during the day. After the decompressive decompression of the bladder, the residual urine increased, and the effective capacity of the bladder decreased, which also made the urinary frequency more serious.
2. Dying dysuria
Progressive dysuria is a prominent feature of the disease. Symptoms can be divided into two types: obstruction and irritation; obstructive symptoms include urinary fistula, intermittent, terminal drip, fine and weak urinary tract, and urinary incontinence. The irritating symptoms are frequent urination, nocturia, urgency, and dysuria. Symptoms can be aggravated by cold, alcohol, and the use of anticholinergics and psychotropic drugs. Long-term obstruction can lead to uremia symptoms such as fatigue, lethargy, nausea and vomiting.
3. Hematuria
Capillary hyperemia and small blood vessel dilatation on the prostate mucosa, and rupture and bleeding due to bladder filling and contraction. Hematuria also occurs when bladder tumors are combined.
4. International Prostate Symptom Score (IPSS) Ask the patient about 7 questions about urination, and rate each question according to the severity of the symptoms (0 to 5 points), with a total score of 0 to 35 points (asymptomatic to very severe symptoms) ). Among them, 0 to 7 are classified as mild symptoms, 8 to 19 are classified as moderate symptoms, and 20 to 35 are classified as severe symptoms. Although IPSS analysis attempts to quantify the extent of symptom changes, it is still subject to subjective factors.
