Lower Urinary Tract & Ureter Pathology: Obstruction & Tumors

Explore lower urinary tract anatomy, ureter pathology including UPJ obstruction, urothelial carcinomas, calculi, and sclerosing retroperitoneal fibrosis.

--- DISORDERS OF THE LOWER URINARY TRACT — PART 1 --- CLINICAL ANATOMY Definition: The renal pelves, ureters, urinary bladder, and urethra (except the terminal portion) are lined by a special transitional epithelium called urothelium . Structure: Composed of 5–6 cell layers with oval nuclei and linear nuclear grooves Surface layer = large, flattened "umbrella cells" with abundant cytoplasm Bladder Wall Layers — ⚠️ Know This: Muscularis mucosa — wisps of smooth muscle in the lamina propria; discontinuous Detrusor muscle (muscularis propria) — deeper, well-defined, larger bundles Bladder cancers are staged based on invasion of the detrusor muscle — the two must not be confused Obstructed urine flow → ↑ intravesical pressure → bladder musculature hypertrophy Clinical Relationships: Ureters are entirely retroperitoneal → retroperitoneal tumours or fibrosis can entrap and obstruct them Women (middle-aged/older): pelvic support relaxation → uterine prolapse → bladder floor descends → cystocele (bladder protrudes into vagina; fails to empty properly during micturition) Men: prostate lies posterior/inferior to bladder neck → prostatic enlargement = major cause of urinary tract obstruction --- URETERS --- A. CONGENITAL ANOMALIES Incidence: Found in ~2–3% of all autopsies; most clinically insignificant. UPJ (Ureteropelvic Junction) Obstruction: Most common cause of hydronephrosis in infants and children In children: preferentially affects males ; bilateral in 20% of cases; often associated with other anomalies; minority have agenesis of the contralateral kidney In adults: more common in women ; most often unilateral Cause: abnormal smooth muscle bundle organisation OR excess collagen deposition at UPJ OR (rarely) extrinsic compression by abnormal renal vessels --- B. TUMOURS AND TUMOUR-LIKE LESIONS Benign Tumours: Rare; generally of mesenchymal origin Fibroepithelial polyp — tumour-like lesion; common in children; composed of loose, vascularised connective tissue overlaid by urothelium Malignant Tumours: Primary malignant ureteral tumours resemble those of the renal pelvis, calyces, and bladder Majority are urothelial carcinomas Peak incidence: 6th–7th decade of life → cause obstruction of the ureteral lumen Commonly occur concurrently with urothelial carcinomas of the bladder or renal pelvis --- C. OBSTRUCTIVE LESIONS Overview: Intrinsic and extrinsic lesions may obstruct ureters → hydroureter, hydronephrosis, pyelonephritis Unilateral obstruction → proximal intrinsic or extrinsic causes (e.g., stones, neoplasms) Bilateral obstruction → distal causes (e.g., nodular hyperplasia of the prostate) Intrinsic Causes: Calculi — typically of renal origin; usually ≤5 mm; impact at narrowings (UPJ, iliac vessel crossing, bladder entry) → excruciating renal colic Strictures — congenital or acquired Tumours — urothelial carcinomas; rarely benign tumours/fibroepithelial polyps Blood clots — from massive haematuria due to renal calculi, tumours, or papillary necrosis Neurogenic — interruption of neural pathways to the bladder Extrinsic Causes: Pregnancy — physiologic smooth muscle relaxation OR uterine fundus pressure on ureters at the pelvic brim Periureteral inflammation — salpingitis, diverticulitis, peritonitis, sclerosing retroperitoneal fibrosis Endometriosis — pelvic lesions with scarring Tumours — cancers of rectum, bladder, prostate, ovaries, uterus, cervix; lymphomas; sarcomas --- D. SCLEROSING RETROPERITONEAL FIBROSIS Definition: Rare fibrotic proliferative inflammatory process that encases retroperitoneal structures → causes hydronephrosis . Epidemiology: Middle to late age; more common in males Aetiology: Subset linked to IgG4-related disease → elevated serum IgG4; fibroinflammatory lesions rich in IgG4-secreting plasma cells; affects multiple organs Other causes: drug exposures (ergot derivatives, β-adrenergic blockers), inflammatory conditions (vasculitis, diverticulitis, Crohn disease), malignancies (lymphomas, urinary tract carcinomas) Most cases: no obvious cause → idiopathic (Ormond disease) Morphology (Histology): Fibrous tissue with prominent infiltrate of lymphocytes (often with germinal centres), plasma cells (frequently IgG4+), and eosinophils Treatment: Initially: corticosteroids If resistant → ureteral stents or surgical ureterolysis (freeing ureters from surrounding fibrosis) --- URINARY BLADDER --- A. CONGENITAL ANOMALIES Vesicoureteral Reflux: Most common and serious congenital bladder anomaly Predisposes to ascending pyelonephritis and loss of renal function Abnormal connections between bladder and vagina/rectum/uterus → congenital vesicouterine fistulae Diverticula: Pouch-like invaginations of the bladder wall; <1 cm to 10 cm in diameter Congenital — focal failure of musculature development OR obstruction during foetal development Acquired — most often from prostatic hyperplasia → ↑ intravesical pressure → outpouching of wall Most are small and asymptomatic Complications: urinary stasis → infection
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