Lower Urinary Tract Disorders: Ureters, Bladder, Obstruction

DISORDERS OF THE LOWER URINARY TRACT — Revision Notes --- CLINICAL ANATOMY Urothelium Lines renal pelves, ureters, bladder, and urethra (except terminal portion) 5–6 cell layers; oval nuclei with linear nuclear grooves Surface layer = large flattened "umbrella cells" with abundant cytoplasm Bladder Wall Layers Lamina propria contains wisps of smooth muscle forming a discontinuous muscularis mucosa Muscularis propria (detrusor muscle) = deeper, larger, well-defined muscle bundles IMPORTANT: Bladder cancers are staged based on invasion of the detrusor muscle Obstruction raises intravesical pressure, causing muscle hypertrophy Key Anatomical Relationships Ureters are retroperitoneal — vulnerable to entrapment by retroperitoneal tumors or fibrosis Women: uterine prolapse pulls bladder floor down, creating a cystocele (bladder protrudes into vagina, fails to empty properly) Men: prostate lies posterior/inferior to bladder neck — enlargement is a major cause of urinary obstruction --- URETERS### Congenital Anomalies- Found in 2–3% of autopsies; most are clinically insignificant UPJ (Ureteropelvic Junction) Obstruction — most common cause of hydronephrosis in infants and children - Early-life cases: predominantly male, bilateral in 20%, often associated with other anomalies (including contralateral renal agenesis in a minority) Adult cases: more common in women, usually unilateral Cause: abnormal smooth muscle organization, excess collagen deposition at UPJ, or rarely extrinsic compression by abnormal renal vessels Tumors and Tumor-Like Lesions- Primary ureteral tumors are rare Benign tumors = mesenchymal origin; e.g., fibroepithelial polyp (loose vascularized connective tissue overlaid by urothelium, common in children) Malignant tumors = mostly urothelial carcinomas; peak in 6th–7th decade; cause ureteral obstruction; commonly concurrent with bladder or renal pelvis urothelial carcinomas Obstructive Lesions Obstruction leads to hydroureter, hydronephrosis, and pyelonephritis Unilateral obstruction = proximal intrinsic or extrinsic causes Bilateral obstruction = distal causes (e.g., prostatic nodular hyperplasia) Intrinsic Causes Calculi (renal origin, usually <5 mm; impact at UPJ, iliac vessel crossing, or bladder entry — causes renal colic) Strictures (congenital or acquired) Urothelial carcinomas Blood clots (from calculi, tumors, or papillary necrosis) Neurogenic (interruption of neural pathways to bladder) Extrinsic Causes Pregnancy (smooth muscle relaxation or pressure from enlarging uterus) Periureteral inflammation (salpingitis, diverticulitis, peritonitis, retroperitoneal fibrosis) Endometriosis with scarring Tumors (rectum, bladder, prostate, ovaries, uterus, cervix, lymphomas, sarcomas) Sclerosing Retroperitoneal Fibrosis Rare; fibrotic inflammatory process that encases retroperitoneal structures → hydronephrosis Middle to late age; more common in males A subset is IgG4-related disease (elevated serum IgG4, fibroinflammatory lesions rich in IgG4-secreting plasma cells, affects multiple organs) Other causes: ergot derivatives, beta-blockers, vasculitis, Crohn disease, lymphomas, urinary tract carcinomas Most cases = idiopathic (Ormond disease) Microscopy: fibrous tissue with lymphocytes (germinal centers), plasma cells (IgG4-positive), eosinophils Treatment: corticosteroids first; resistant cases need ureteral stents or ureterolysis --- URINARY BLADDER### Congenital Anomalies Vesicoureteral Reflux Most common and serious congenital bladder anomaly Predisposes to ascending pyelonephritis and loss of renal function Diverticula Pouch-like invaginations of the bladder wall (<1 cm to 10 cm) Congenital: focal failure of muscle development or fetal obstruction Acquired: most often due to prostatic hyperplasia → raised intravesical pressure → outpouching Usually small and asymptomatic; cause urinary stasis → infection and calculi Rarely, carcinoma arises in diverticula — typically more advanced due to absent/thin muscularis propria Exstrophy Developmental failure of anterior abdominal wall and bladder → bladder communicates with abdominal surface Exposed mucosa undergoes colonic glandular metaplasia, prone to chronic infection Associated with increased risk of adenocarcinoma Urachal Anomalies Urachal canal connects fetal bladder to allantois; normally obliterated at birth If fully patent = fistulous urinary connection between bladder and umbilicus If partially patent (central region only) = urachal cyst (lined by urothelial or glandular epithelium) Urachal cysts: increased risk of neoplastic transformation; account for 20–40% of bladder adenocarcinomas (though only 0.1–0.3% of all bladder cancers) --- Inflammation (Cystitis) Acute and Chronic Cystitis Bacterial cystitis often precedes pyelonephritis via retrograde spread Predisposing factors: bladder calculi, urinary obstruction, diabetes mellitus, instrumentation, immunodeficiency Most common organisms: E. coli, then Proteus, Klebsiella, Enterobacter Women mor