AP Ch39 PDF: Urinary Tract Obstruction & Infections

# Summary Review ## Urinary Tract Obstruction - Obstruction can occur anywhere in the urinary tract and may be anatomic or functional. - Examples include kidney stones, tumors, an enlarged prostate, or strictures of the ureter or urethra. - Most serious complications include: - Hydronephrosis...

# Summary Review ## Urinary Tract Obstruction - Obstruction can occur anywhere in the urinary tract and may be anatomic or functional. - Examples include kidney stones, tumors, an enlarged prostate, or strictures of the ureter or urethra. - Most serious complications include: - Hydronephrosis - Hydroureter - Ureterohydronephrosis - infection caused by the accumulation of urine behind the obstruction. - Tubulointerstitial fibrosis and dysregulated apoptosis can result in progression to chronic kidney disease in untreated obstructive uropathy. - Compensatory hypertrophy and hyperfunction of the opposite kidney compensate for loss of function of the kidney with obstructive disease. - Relief of obstruction is usually followed by postobstructive diuresis. - Causes of obstruction include: - Fluid and electrolyte imbalance - Kidney stones - Stones caused by supersaturation of the urine with precipitation of stone-forming substances, changes in urine pH, or urinary tract infection - Most stones are unilateral. - The most common kidney stone is formed from calcium oxalate and most often causes obstruction by lodging in the ureter. - Obstructions of the bladder are a consequence of neurogenic or anatomic alteration of the bladder or both. - A neurogenic bladder is caused by a neural lesion that interrupts innervation of the bladder. - Upper motor neuron lesions above the pontine micturition center result in detrusor hyperreflexia and uninhibited or reflex bladder. - Upper motor neuron lesions between C2 and S1 result in overactive or hyperreflexive bladder function and detrusor sphincter dyssynergia (lack of coordinated neuromuscular contraction). - Lower motor neuron lesions below S1 result in detrusor areflexia with underactive, hypotonic, or atonic bladder function. - OAB syndrome is an uncontrollable or premature contraction of the bladder that results in urgency with or without incontinence, frequency, and nocturia. - Anatomic obstructions to urine flow include: - Prostatic enlargement - Urethral stricture - Pelvic organ prolapse in women. - Partial obstruction of the bladder can result in overactive bladder contractions with urgency. - There is deposition of collagen in the bladder wall over time, resulting in decreased bladder wall compliance and ineffective detrusor muscle contraction. - Renal cell carcinoma is the most common renal neoplasm. - Larger neoplasms tend to metastasize to the lung, liver, and bone. - Bladder tumors are commonly composed of transitional cells with a papillary appearance and a high rate of recurrence. ## Urinary Tract Infection 1. UTIs are commonly caused by the retrograde movement of bacteria into the urethra and bladder. 2. UTIs are uncomplicated when the urinary system is normal or complicated when there is a defect or abnormality. 3. Host defenses that protect against urinary tract infection include: - High osmolality and acidic pH of urine - Mucus - Uromodulin - Other antimicrobial proteins that activate the immune response - Sphincters that prevent reflux, and urine flow that washes out bacteria. 4. Virulent uropathogens have pili or fimbriae, or both, that promote binding to the uroepithelium and retrograde movement in the urinary tract. 5. Formation of biofilms enhances colonization and resists host defenses and antimicrobial therapy. 6. Cystitis is an inflammation of the bladder commonly caused by bacteria and may be acute or chronic. 7. Manifestations of frequency, urgency, and dysuria are caused by inflammation. 8. Interstitial cystitis/painful bladder syndrome may be an autoimmune injury with increased permeability of the glycosaminoglycan layer of the bladder mucosa. 9. Pyelonephritis is an acute or chronic inflammation of the renal pelvis often related to ascending infection and obstructive uropathies and may cause abscess formation and scarring with acute or chronic kidney injury. ## Glomerular Disorders 1. Glomerular disorders are a group of related diseases of the glomerulus that can be primary and caused by immune injury, infection, ischemia, toxins or drugs, or vascular disorders or, secondarily, caused by systemic diseases. 2. Acute glomerulonephritis commonly results from inflammatory damage to the glomerulus as a consequence of immune reactions including deposition of circulating immune complexes, antibodies reacting in situ to planted antigens, antibodies directed against the glomerular basement membrane, and complement activation. 3. The urine sediment may contain large amounts of protein (nephrotic sediment) or have red and white blood cells and protein (nephritic sediment). 4. Acute postinfectious glomerulonephritis is commonly associated with immune complex deposition in the glomerulus or in situ formation. 5. Lupis nephritis is caused by the formation of autoantibodies against double-stranded DNA (dsDNA) and nucleosomes in the glomerulus, causing inflammation and injury. 6. IgA nephropathy is the binding of abnormal IgA to mesangial cells in the glomerulus resulting in injury and mesangial proliferation. 7. Focal segmental glomerulosclerosis is a scarring lesion that involves some but not all glomeruli (focal) and some but not all of the glomerular capillaries (segmental). 8. Membranous nephropathy is complement-mediated glomerular injury with increased glomerular permeability and glomerulosclerosis. 9. RPGN is associated with injury that results in the proliferation of glomerular capillary endothelial cells and a rapid loss of renal function. 10. Mesangial proliferative glomerulonephritis is usually idiopathic and involves deposits of immune complex in the mesangium with mesangial cell proliferation. 11. Membranoproliferative glomerulonephritis involves mesangial cell proliferation, complement deposition, and crescent formation. 12. Chronic glomerulonephritis is related to a variety of diseases that cause deterioration of the glomerulus and a progressive loss of renal function over a period of months to years, including diabetic nephropathy and lupus nephritis. 13. Diabetic nephropathy develops from metabolic, inflammatory, and microvascular complications associated with chronic hyperglycemia. 14. Lupus nephritis is caused by the formation of autoantibodies against dsDNA and nucleosomes in the glomerulus, causing inflammation and injury. 15. Nephrotic syndrome is the excretion of at least 3.5 g of protein (primarily albumin) in the urine per day primarily because of glomerular injury with increased capillary permeability and loss of membrane negative charge. 16. The principal signs are hypoproteinemia, hyperlipidemia, and edema. 17. The liver cannot produce enough protein to adequately compensate for urinary loss. 18. Nephritic syndrome is hematuria and red blood cell casts in the urine and less severe proteinuria. ## Acute Kidney Injury 1. AKI is the sudden decline in kidney function with decreased glomerular filtration and an increase in serum creatinine, cystatin, and BUN levels. 2. AKI is considered in three categories as prerenal, intrarenal, and postrenal and is usually accompanied by oliguria with elevated plasma BUN and plasma creatinine levels. 3. Prerenal acute renal failure is caused by decreased renal perfusion with a decreased GFR, ischemia, and tubular necrosis. 4. Intrarenal acute renal failure is associated with several systemic diseases or to drug toxicity but is commonly related to ATN. 5. Postrenal acute renal failure is associated with diseases that obstruct the flow of urine from the kidneys. 6. Oliguria is a urine output of less than 400 mL per day and can be caused by alterations in renal blood flow, tubular obstruction, tubular fluid backleak, or by a combination of these events. ## Chronic Kidney Disease 1. Chronic kidney disease is a progressive loss of renal function. Plasma creatinine levels gradually become elevated as GFR declines, sodium is lost in the urine, potassium is retained, acidosis develops, activation of vitamin D declines, calcium and phosphate metabolism are altered, and erythropoietin production is diminished. 2. Symptomatic changes usually do not become evident until renal function declines to less than 25%. 3. Glomerular hypertension, hyperfiltration, and tubulointerstitial inflammation and fibrosis contribute to the progression of chronic kidney disease. 4. Proteinuria and angiotensin II promote the pathologic changes of chronic renal injury. 5. Uremic syndrome is a proinflammatory state with the accumulation of urea and other nitrogenous compounds as well as toxins and alterations in fluid, electrolyte, and acid-base balance that result from chronic kidney failure. 6. All organ systems are affected and contribute to disease symptoms.