Pathology: The prostate is divided into the peripheral zone, central zone, migratory zone and periurethral glandular region. All prostatic hyperplastic nodules occur in the migratory zone and periurethral glandular region. The nodules in the early periurethral glandular region are entirely mesenchymal in composition, whereas the nodules in the early migratory zone show mainly hyperplasia of glandular tissue with a relative decrease in the amount of mesenchyme. The anatomical envelope of the prostate gland is closely related to the lower urinary tract symptoms, and due to the presence of this envelope, the hyperplastic gland is compressed and expands into the urethra and bladder thus aggravating the urinary tract obstruction. After prostate enlargement, the enlarged nodules compress the rest of the gland to form a “surgical envelope” with a clear demarcation between the two. After the hyperplasia is surgically removed, the compressed gland is left behind, so the prostate gland can still be detected during postoperative rectal examinations and imaging. Pathophysiological changes: Prostatic hyperplasia leads to lengthening of the posterior urethra, deformation of pressure, narrowing and increased urethral resistance, resulting in bladder hypertension and associated voiding symptoms. As bladder pressure increases, compensatory hypertrophy of the bladder forcing muscles occurs, and instability of the forcing muscles and associated storage phase symptoms occur. If the obstruction is not relieved for a long time, the forceps muscle loses its compensatory capacity. The main causes of upper urinary tract changes secondary to prostatic hyperplasia, such as hydronephrosis and renal impairment, are urinary retention and ureteral reflux due to bladder hypertension.