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Tuberculosis of the Genitourinary System Overview of GUTB
Marzo 29 2011
Overview of GUTB
Mycobacterium tuberculosis bacilli are inhaled through the lungs to the alveoli, where they are phagocytosed by polymorphonuclear leukocytes and macrophages. Although most bacilli are initially contained, some are carried to the region's lymph nodes. Eventually, the thoracic duct may deliver mycobacteriato the venous blood; this may result in seeding of different organs. In addition, multiple granuloma form at the site of metastatic foci.
Renal, ureteral, and bladder TB
In the kidneys, when multiple granuloma form at the site of metastatic foci, they are typically bilateral, cortical, and adjacent to the glomeruli, and they may remain inactive for decades. Although both kidneys are seeded,clinically significant disease, which is caused by capillary rupture and delivery of proliferating bacilli into the proximal tubules, usually develops in only one kidney. The medullary hypertonic environment impairs the phagocytic function.
Growing granuloma may erode into the calyceal system, spreading the bacilli to the renal pelvis, ureters, bladder, and other genitourinary organs. Depending onthe status of the patient's defense mechanisms, fibrosis and strictures may develop with chronic abscess formation. Extensive lesions can result in nonfunctioning kidneys. Hypertension in persons with renal tuberculosis (TB) is twice as common as it is in the general population.
Ureteral TB is an extension of the disease from the kidneys, generally to the ureterovesical junction, and develops inabout one half of all patients with renal TB. It only rarely affects the middle third of the ureter. Ureteral TB often causes ureteral strictures and, sometimes, hydronephrosis. Occasionally, severe cases can cause stricture of virtually the entire ureter.
Bladder TB is secondary to renal TB and usually starts at the ureteral orifice. It initially manifests as superficial inflammation withbullous edema and granulation. Fibrosis of the ureteral orifice can lead to stricture formation with hydronephrosis or scarification (ie, golf-hole appearance) with vesicoureteral reflux. Severe cases involve the entire bladder wall, where deep layers of muscle are eventually replaced by fibrous tissue, thus producing a thick fibrous bladder. Tubercles are rare in the bladder; if present, they usuallyappear at the ureteral orifice. Malignancy should be considered with any isolated tubercles away from the ureteral orifices.
Epididymal and testicular TB
The higher frequency of isolated epididymal TB lesions in children favors the possibility of hematologic spread of infection , whereas adults seem to develop tuberculous epididymoorchitis caused by direct spread from the urinary tract.[1] Theformation of a draining sinus is uncommon in developed countries, but epididymal induration and beading of the vas are common.
Involvement of the testis is usually due to direct extension. Infertility may result from bilateral vasal obstruction. Nodular beading of the vas is a characteristic physical finding, and orchitis and the resulting testicular swelling can be difficult to differentiatefrom other mass lesions of the testes.
Prostatic TB
Prostatic TB is also spread hematogenously, but involvement is rare; however, of those with affected, 85% also have renal TB. The affected prostate is nodular and not tender to palpation. Severe cases may cavitate and form a perineal sinus, although this development is rare. Decreased semen volume may indicate extensive prostatic disease orejaculatory duct obstruction.[3]
Genital and urethral TB
Urethral TB is secondary to genital TB. Patients with genital and urethral TB present with a superficial tuberculous ulcer on the penis or in the female genital tract secondary to mycobacteria exposure during intercourse. The penile ulcer may cause cavernositis that extends to the urethra. This form of TB may involve the uterus and fallopian...
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