The causes and pathogenesis of prostate adenoma

Understanding the pathogenesis of prostate adenoma (prostate gland) is impossible without taking into account modern data on its anatomy and morphology. At the heart of the modern theory of prostate adenoma (prostate) is the zonal concept of the structure of the prostate, according to which in the prostate gland several areas are distinguished that differ in the histological and functional characteristics of their constituent cellular elements. These are the peripheral, central and transitional (transitory) zones, as well as the anterior fibromuscular stroma and preprostatic segment.

In the region of the seminal tubercle, the opening of the vas deferens opens. The wall of the proximal part of the urethra consists of longitudinal smooth muscle fibers. The preprostatic (genital) sphincter formed by a thick layer of smooth muscle fibers surrounds the proximal part of the urethra from the neck of the bladder to the apex of the seminal tubercle and prevents retrograde ejaculation.

Histological studies have shown that the growth of the prostate adenoma (prostate gland) begins in the central and transitional zones of the prostate. Transitory zone of the prostate consists of two separate glands located immediately behind the internal sphincter of the bladder. The inferior ducts of this zone are located on the lateral wall of the urethra near the seminal tubercle. The proximal transitional zone is the gland of the periurethral zone, they border on the inner sphincter of the bladder and are located parallel to the axis of the urethra. Adenomatous nodes can develop both in the transitional zone and in the paraurethral. In addition to nodular hyperplasia, the transitional zone tends to grow with age.

An important role in the development of symptoms of prostate adenoma (prostate) is the capsule of the prostate. So, in dogs the capsule of the prostate is poorly developed, and even with severe hyperplasia the symptoms of the disease develop rarely. The capsule transfers the pressure of enlarged prostate tissue to the urethra, causing an increase in urethral resistance.

Prostate adenoma (prostate gland): pathophysiology

Elongation and deformation of the prostatic part of the urethra to 4-6 cm and more occurs mainly due to the site of the posterior wall located above the seminal tubercle. The cervix of the bladder is raised and deformed, its lumen becomes slit-shaped. As a result, the natural curvature of the urethra increases, and with uneven development of the lateral lobes, the urethra is curved in the transverse direction, so that it can take a zigzag appearance. Ziyanie lumen of the neck of the bladder as a result of the failure of the urethral sphincter mechanism with detrusor compensation is clinically manifested by urinary incontinence.

The bladder also undergoes profound changes. His reaction to the development of obstruction goes through three stages: irritability, compensation and decompensation. At the first stage of the infravesical obstruction, the bladder responds by increasing detrusor cuts. Allowing temporarily to maintain the functional balance and ensure complete evacuation of urine. The further development of obstruction leads to compensatory hypertrophy of the wall of the bladder, which can reach a thickness of 2-3 cm. At the same time, it can acquire a trabecular appearance due to thickened and bulging muscle beams.

The initial stage of development of trabecularity is morphologically characterized by hypertrophy of smooth muscle cells. Progression of the process leads to the dissociation of hypertrophied muscle elements and the filling of spaces between them with connective tissue. Between the trabeculae are formed indentations, called false diverticula, the walls of which gradually become thinner from the increased intravesical pressure. Such diverticula are often multiple, sometimes reaching considerable sizes.

Elastic properties detrusora determines the presence of collagen, which in its smooth muscle tissue is 52% of the total protein. With the depletion of compensatory possibilities and the growth of atrophy, the walls of the bladder are thinning. Detrusor loses its ability to contract and stretches, resulting in a significant increase in the capacity of the bladder, reaching 1 liter or more. Concomitant inflammatory and trophic changes lead to a pronounced sclerosis of the muscular layer of the vesicle wall and a decrease in the collagen content. The content of connective tissue becomes equal to or exceeds the content of muscle elements.

The degree of restoration of the normal structure of the wall of the bladder depends on the duration of the existence of an obstruction to the outflow of urine. As a result of prolonged obstruction, irreversible morphological changes develop that lead to severe functional bladder disorders and can not be eliminated even after surgery. Pronounced infravesical obstruction leads to increased pressure in the bladder, impairment of urine outflow from the kidneys and the occurrence of vesicoureteral and renal reflux as well as pyelonephritis. Ureters dilate, lengthen, become sinuous, develop ureterohydronephrosis and chronic renal failure. The pathogenesis of changes in the kidneys and upper urinary tract in patients with prostate adenoma is complicated and depends on many factors: age-related changes, concomitant diseases affecting their functional capacity, development of obstructive uropathy.

At the first stage of development of obstructive uropathy, the preservation of the fornicative apparatus of the calyx and the integrity of the epithelium of the collecting tubules of the papillae prevent the development of the renal tubular reflux and the penetration of the infection into the kidney parenchyma by the ascending pathway. With the development of ureterohydronephrosis, a structural deformation of the calyx arches occurs, which creates favorable conditions for the development of tubular-tubular, and later lohanno-venous and lochnoco-lymphatic refluxes.

As a result of increased intra-local pressure and pulmonary-renal reflux, the hemodynamics of the kidney is significantly impaired, followed by the development of structural changes in the intra-arterial arteries in the form of obliteration and diffuse stenosis. Hemodynamic disorders lead to serious metabolic changes and severe ischemia of the renal tissue. Due to obstructive uropathy, there is an increasing deterioration in all indicators of the functional state of the kidneys. A characteristic feature of this process is the early violation of the concentration ability of the kidneys, which is primarily manifested by a sharp decrease in the reabsorption of Na ions and an increase in their excretion in the urine. Abnormal kidney function in stage I prostate adenoma is observed in 18% of patients. In the II stage of chronic renal failure complicates the course of the disease in 74%, and 11% of them mark the terminal stage. Chronic renal failure was detected in all patients with Stage III prostate adenoma, with an intermittent stage being observed in 63%. And terminal - in 25% of those surveyed.

Urinary tract infection is of fundamental importance in the pathogenesis of renal impairment in prostate adenoma and significantly complicates the course of the disease. Pyelonephritis and kidney failure account for up to 40% of the cause of death of patients with prostate adenoma. Chronic pyelonephritis in patients with prostatic adenoma is observed in 50-90% of cases.

Inflammation of bacterial origin occurs mainly in the interstitial peritubular tissue. In the pathogenesis of secondary pyelonephritis in prostate adenoma, the main role is played by urostasis. Development of vesicoureteral and pulmonary-renal reflux. Infection enters the kidney ascending from the bladder. Urinary tract infection accompanies most cases of prostate adenoma. Chronic cystitis was observed in 57-61% of outpatients and 85-92% of inpatients. In this regard, the pathogenesis of chronic pyelonephritis in patients with prostate adenoma can be represented as follows: infravesical obstruction → bladder dysfunction → cystitis → incompetence of vesicoureteral jaws → vesicoureteral reflux → chronic pyelonephritis.

Great importance in the formation of the clinical picture in prostate adenoma is the presence of a concomitant inflammatory process in the prostate. The frequency of chronic prostatitis in prostate adenoma according to laboratory, operating and sectional data is 73, 55.5 and 70%, respectively. Venous stasis, compression of the excretory ducts of the acini with hyperplastic gland tissue and its swelling are prerequisites for the development of chronic inflammation. Morphological study of the operating material showed that in most cases the inflammatory process was localized at the periphery of the gland. Concomitant chronic prostatitis can clinically manifest dysuria, which requires differential diagnosis with urinary disorders due to the actual prostate adenoma. Its presence also leads to an increase in the number of early and late postoperative complications, which calls for measures to identify and repair chronic prostatitis at the stage of conservative treatment or preparation for surgery.

Stones of the bladder in adenoma are formed again due to a violation of emptying the bladder. They are detected in 11.7-12.8% of patients. They usually have a regular rounded shape, can be single or multiple, and in terms of chemical composition it is urate or phosphate. Kidney stones accompany prostate adenoma in 3.6-6.0% of cases.

The frequent complication of prostate adenoma is the complete acute retention of urination, which can develop at any stage of the disease. In some cases, this is the culmination of the obstructive process in combination with the decompensation of the detrusor's contractile ability, and in others it develops suddenly against the background of mild symptoms of urinary disorders. Often this is the first clinical manifestation of prostate adenoma. According to the literature, this complication is observed in 10-50% of patients, most often it occurs on stage II of the disease. The provoking factors of the development of this complication can be a violation of diet (taking alcohol, spices), hypothermia, constipation, untimely emptying of the bladder, stressful conditions, taking certain medications (anticholinergics, tranquilizers, antidepressants, diuretics).

The main factors of the development of acute urination delay are the growth of hyperplastic tissue, functional changes in the tone of the cervix and the muscle of the bladder, impaired microcirculation of the pelvic organs with the onset of edema of the prostate.

In the initial stage of acute urinary retention, an increase in the detrusor contractile activity leads to an increase in intravesical pressure. At subsequent stages, due to dilatation of the wall of the bladder and a decrease in its contractility, the intravesical pressure falls.